EXAM 1 CONTENT

Let the studying begin!

Cellular
Adaptatio
n, Injury,
& Death

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It all begins with a cell.

Cellularadaptation
___________ is how our bodies
accommodate + fight injury.
Cellular injury, malfunction, and death is
how ALL diseases occur.

CELL

Na/K ATPase
Na Na Na

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Cellular Adaptation

Change in
_____, #,type
or _____ of cell
size
Change is proportional
stimulus
to ____________
Change in
SIZE or #

NORMAL
cells

Change in
TYPE

HYPERTROPH
Y

METAPLASIA

HYPERPLASI
A

DYSPLASIA

ATROPHY

Cellular Adaptation Size or #

ATROPHY= ___size
in ________
From demand
__________ or nutrient supply
(atherosclerotic occlusive dz)
= ____
sizein ________
HYPERTROPHY
From demand
_________
Skeletal m, cardiac m, + neurons undergo
this why?
B/c once theyre gone, theyre gone
Figure out how to make them replicate $$$$$$$$$$$$

#
$$
demand
HYPERPLASIA
= ____ in _________

From _________

Cellular Adaptation Change in Type

METAPLASIA = changeNormal
from cells
reversible
______________ to
another; ALWAYS
______________
Messed up

DYSPLASIA = ___________ cells

Different, order, size, &/or characteristics
Different than anaplasia
inflammation
Can be reversible if _____________ stops!

Metaplasia

From chronic
irritation
___________inflammation
+
_______________
tougher
New cell type is _____________, better able
to function under
changed
Esophagus
conditions
Barrett
BEST EXAMPLE = __________s _______________,
in which
cells change to columnar epithelium
REVERSIBLE
in GERD

ALWAYS _____________

Dysplasia

From chronic
irritation
____________inflammation
+
______________
New cell types are jumbled & dont fxn
Dysplasia
well.
Inflammation
Inflammation
STOPS

NORMAL cells

continues

ANAPLASIA/CA
NCER

Intracellular Accumulation +
Calcification

Cellular Buildup

Hemolytic anemia bilirubinjaundice

____________
Alcoholism or DM fat fatty liver disease
Hypercholesterolemia LDL atherosclerosis

Calcification
METASTATIC:

normal
In _________
tissue
hyper
From ______calcemia
E.g. hyperparathyroidism

DYSTROPHIC:
diseased

In ___________ tissue
breakdown
From cell ___________
E.g. aortic stenosis, atherosclerosis, pancreatitis

Cellular Injury - Causes

Physical agents
Radiation
Chemicals
Nutritional Imbalances
Anything that hurts us, hurts our cells
first

Cellular Injury - Mechanisms

Fluid
Electrolyte
_______
& __________
imbalances

Often the result of hypoxia

_______________
injury
Free Radical
Hypoxic injury
Which, in turn, can create
Free______________s
Radical

Anaplasia
Reversion of cells into
a _____ differentiated
less
form

Cellular Injury Free Radicals

Normally kept in check by lysosomes,

neutrophils, and macrophages
Too many abnormal
chain
______ reactions
Damage to
_____ & cell membranes
DNA
Inactivation of enzymes

Reperfusion Injury
Regaining of blood flow after ischemia causes
introduction of these free radicals

Cellular Injury Hypoxic Injury

Due to an imbalance between O supply

+ demand
anaerobic
Change from aerobic
to __________
metabolism

ATP

Lactic acid
buildup

Na K ATPase fails to
___/__
fxn

Metabolic
acid
_____osis
w/ a
high
________
anion
gap

K
intracellular
___

intracellularNa
___

Cells swell/shrivel +

Cellular Injury - Outcomes

Reversible Injury, cell recovery, return to

fxn
Apoptosis, programmed cell death
Cell death/necrosis

Cellular Injury - Outcomes

Reversible Injury
Cellular swelling
Na
K
ATPase
From broken
___/____
_________
This is an early sign

Fatty Change
Due to intracellular fat accumulation
E.g. fatty liver disease (steatosis) remember, this is
reversible

Cellular Injury - Outcomes

Apoptosis
= programmed cell death
= Suicide + cellular cannibalism
Inflammation, or no inflammation?
Cell fragments are phagocytized by other
cells
Without apoptosis, humans would have
webbed feet.

Cellular Injury - Outcomes

NECROSIS
= Unregulated cell death
Cell products get released to surrounding
space, inflammation
thus causing ________________.
New cells often do/do not replace necrotic
cells
Always pathologic
Necrosis = bad

Inflammati
on
&
Healing

Inflammation

=
nonspecific
_______________ response
of
vascularized
_____________ tissue to injury
= itis
NOT a specific response!
Anything that causes injury to tissue
inflammation

ACUTE inflammation

Almost immediate response that resolves

Lasts minutes to days
Main cell types
macrophages
= ____________
&
neutrophils
_____________
2 Stages to acute inflammation:
Vascular stage
Cellular stage

5 CARDINAL SIGNS

RUBORRedness
= _____________
TUMORSwelling
= _____________
CALOR Heat
= _____________
DOLORPain
= _____________
FUNCTIO LAESA
= of
_________________
Loss
Fxn

Acute inflammation Vascular stage

Momentary vaso___________
constriction followed by...
(purpose is to control blood loss)

Rapid vaso_____________
dilation
From injured cells releasing prostaglandins +
histamines
calor
rubor
Causes ________ (think blood) & ___________ (think
blood) cardinal signs
healing
Purpose = bring in ___________ cells

capillary permeability
From release of prostaglandins & histamines
swelling
Causes ___________, pain, & impaired function
dilute
Purpose = _________ offending agent by
swarming via tons of diapedesis

Acute inflammation Cellular stage

WBCs move in & work their magic

Key Players:
Neutrophils
_______________ &Monocytes
_____________
Via diapedesis

Inflammatory mediators
INFLAMMATORY
MEDIATOR

PHYSICAL EFFECT

HISTAMINE &
PROSTAGLANDINS

Vaso___________
dilation &
permeability

Cytokines, lysosomes

Tissue damage &

necrosis

CYTOKINES (IL-1,
TNF)

__________ & Acute

Fever
Phase Response

Chronic inflammation

Continual response, lasts days to years.

Main cell types
= ____________ (B, T, NK
lymphocytes
fibro
cells), macrophages,
& _____blasts (think
scar tissue)
EXAMPLES:
Inflammatory Bowel Disease (Crohns, UC)
RA

Inflammation Local S/Sx

5 Cardinal Signs
Exudate (due to vascular permeability)
Serous
__________ = Clear, watery, thin
Chlamydia

Serosanguinous = watery but

has _____ in it
RBCs
(pink)
Hemorrhagic
Purulent
______________ = bloody
___________ = WBCs aka pus
Gonorrhea

Inflammation Systemic S/Sx

Acute Phase Response

_________,
Fever
hypermetabolism, muscle
catabolism, lethargy
Due to
_____,
_____, and
_____ cytokines
IL-1
IL-6
TNF

LEUKOCYTOSIS
From cytokines & CSF hematopoiesis

LEUKOPENIA
From WBCs being used upBone
whenmarrow
______________ cant keep up w/ demand

Systemic S/Sx

Lymphadenitis
Nearby lymph nodes reacting to
inflammation, making more cells to mount an
attack

Scar Formation
chronic

Often in _________ inflammation

Sepsis & Septic Shock

Widespread
systemic reaction leading to
vasodilation
diffuse _______________ response to infection

Tissue Regeneration

Replaces dead tissue w/ more of the

same
functional
PARENCHYMA = ___________ tissue

ONLY if cells are able to enter cell cycle

i.e. skin, G.I.
Liver can be stimulated to enter cycle

Scar Formation

If parenchyma cant be formed,

stroma _______
gets formed.
Occurs w/ cells that cant enter cell cycle,
or,cardiac
neural
___________ cells
___________ cells

Happens
if there is too much tissue
Fibroblasts
damage
______________ are key scar-forming cells
Lay down ECM & collagen

Wound Healing

INFLAMMATORY phase
Vascular + Cellular stages of acute
inflammation

PROLIFERATIVE
phase
fibro
epithelial

_________blasts, _____________ cells (skin)

REMODELING phase
Scar architecture changes to give most
strength
(80% of original)

Wound Healing is IMPAIRED if

MALNUTRITION
Need good nutrition!

BLOOD FLOW
Inflammation only occurs
in _____________
vascularized
tissue
Need blood to transport the healing cells
(vasodilation step of vascular phase)

OXYGEN
IMPAIRED IMMUNITY
INFECTION
OLD AGE

Neoplas
ia

Differentiation

= dividing cells are transformed into

specialized
more
_______________ cell types
Stem cells are
undifferentiated
__________________
They can become almost any type of cell

B-cells & pneumocytes are differentiated

They have matured & their function is set

More MALIGNANT = more/less

DIFFERENTIATED

Neoplasia

Neoplasm = new growth

Uncoordinated, uncontrolled growth that
CONTINUES WITHOUT A STIMULUS.

Benign vs. Malignant =

Cell characteristics
Rate of growth
Manner of growth
Potential of metastasizing
Ability to produce generalized effects
Tendency to cause tissue destruction
Capacity to cause death

BENIGN vs. Malignant

_______-differentiated
well
Early/late in differentiation? More/less
mature?
slowly

Grows ___________
Grows by expansion + does not infiltrate
Well-defined or poorly-defined margins?

Metastasizes/does not metastasize?

Effects
are
local/systemic?
Mass
______ effect

Only hurts tissue if mass causes vessel

impingement

Benign vs. MALIGNANT

poorly
_______-differentiated
Early/late in differentiation? More/less mature?

Grows quickly
___________ (_____
cells in cell cycle)
MORE
Grows at periphery + invades surrounding
tissue
Well-defined or poorly-defined margins?
What male cancer do we know grows @
periphery?
Prostate
CA

Metastasizes/does not metastasize?

Effects are local/systemic/both?
Paraneoplastic syndromes

Causes tissue destruction as it invades

Usually causes death

Etiology what causes it?

Heredity
Immunologic Mechanisms
Oncogenic Viruses
Radiation
Esp. those who are undergoing it to already
treat cancer

Chemical Carcinogens
Hormones

Etiology - Molecular

Cancer has effect on

Genes that regulate DNA repair /?
Genes that control cell replication +
proliferation
Proto-oncogenes /?
or
Tumor-suppressor genes /?
p53 suppressor, BRCA1

Genes
that control healthy cell death
Apoptotic
/?
= ______________ genes

Clinical Manifestations

Changes in
_______ function
organ
Physical Effects
________
Mass effect

__________
Cachexia + Fatigue
= wasting
Why? B/c body is busy replicating tons of
cells!

Paraneoplastic
Syndromes
SIADH
_________, hypercalcemia

Tissue Breakdown
From invasion, compression,

Staging vs. Grading

STAGING
To determine
___________ cancer is
where
TNM system
T___________
umor
N__________
odes
M__________
etastasis

GRADING

= what the cancer

_____________
Looks
like
Must do abiopsy
___________ to see them
Grades I IV; higher # = more anaplastic =
less differentiated

Hematopoies
is +
Hematostasi
s

Hematopoiesis

= how our bodies grow RBCs, WBCs, &

platelets Bone marrow
Starts in the ________________

All blood cells start from the same

pluripotent stem cell

Phys Review - Platelets

Aka thrombocytes
________________
No nucleus
Their growth & release is stimulated
TPO by
_____
Which is made in the liver when low plt #s

Make plt plug & activate the coagulation

cascade
A megakaryocyte = young platelet
Megakaryocyte gets broken up to make many
plts

-philia, -osis, & -penia

-philia or osis
= ____ in # beyond nml
range

thrombocytosis = ___ # of plts E.g.

E.g.
eosinophilia = ____ in # of eosinophils

-penia = ___ in # beyond

nml range

E.g. thrombocytopenia = ___ in # of plts

I could tell you the way I remember this, but
it is pretty immature. I will leave it at that.
I bet you will never forget which one is which now

Mechanism of Hemostasis

5 STAGES
Platelets get made inBone
the marrow
______________
Clotting factors (fibrinogen) + proteinsliver
made
in _______
folate
K
Vitamin
Spasm
___ and ____ crucial
1. Vessel ______
Platelet
2. Formation Plug
of
_______________
Insoluble
fibrin
clot
3.
Formation
of
______________,
activation of
Intrinsic
Extrinsic
_____________
or ____________ pathway
Retraction
4. Clot ______________
Dissolution
5. Clot ______________

1. Vessel Spasm

First rxn to injury

Less than 1 min
______________
is released from injured
Thromboxa
ne
endothelium
plt aggregatio
_____________
n

2. Formation of Platelet Plug

RBCs change from smooth discs spiny

spheres
Von Willy
plts
NeedWonka
____ _____________ factor to connect the
_____ to the subendothelium

Cluster Together
TxA
w/ the help of ______ released from platelets

NSAIDs + Aspirin inhibit this step!!!!

P.S. Von Willy
Wonka factor
= von
Willebrand

3. Formation of Insoluble Fibrin Clot

Blood coagulation starts w/ coag cascade

Need coag. Factors + vit. K + Ca2+
Factor 8 needsvWF
_____ to circulate

Ends w/ plasma proteinfibrinogen

_____________ from liver
converting into insoluble
_________ meshwork
fibrin
Next comes intrinsic & extrinsic pathway
Intrinsic p. = slow
______, begins in the
_________
blood
Extrinsic p. =fast
______, begins w/ vessel or
________
trauma
___________ factor is key to activation

Tissue
Final common pathway

Then Factor ___ activates ___________ from

10
thromb
prothrombin
in
Thrombin activatesfibrin
________ from fibrinogen
Fibrin cross-links

3. Formation of Insoluble Fibrin Clot

Most anticoagulants fxn by inhibiting this

step
Natural anticoagulants =
Heparin
Plasmin
_________
tPA (tissue plasminogen activator) = primary
treatment to dissolve blood clots after ischemic
stroke

Drug anticoagulants =
Warfarin
Heparin

4. Clot Retraction

Occurs within
20___-___
60 minutes after clot
forms
Fibrinolysis
Also called ______________
Lets
blood flow resume to prevent
Plasmin
ischemia!
fibrin
_________Dis key
enzyme to digest
Dimers
insoluble ________ links
Produces
__-_______ when it works, which
D Dimers
we can measure in blood
__-________
= clot retraction
plasminogen
plasmin
So, while thrombin
fibrin activates fibrinogen,

Hypercoagulability Platelet Activity

Anything that damages
_____________
endothelial
cells, induces
____ activity
plt
Atherosclerosis
Diabetes
Smoking
High cholesterol

What about plt #?

Thrombo__________
cytosis
From or bone marrow production
From or plt destruction

Hypercoagulability Clotting Cascade

Activity
Inherited disorders
Factor5___ Leiden mutation
Factor 5 cant beTurned
____________
& keeps clotting cascade
OFF
going

Acquired
disorders

___ blood flow

Bed rest, post-op, pools blood components together

and allows them to activate

Cancer,
Sepsis,
Tissue
factorCrush Injuries

_________________
gets released from damaged cells,
extrinsic
sparks ____________ pathway.

___ Estrogen

From pregnancy or OCP

liver
coag. Factor synthesis in the ________.

Bleeding disorders

= conditions that lead to

_____active
hypo
hemostasis & inhibited coagulation
From Platelet Function
If plts cant work, clots cant form
Defective plt receptors
______
vWFdisease (normally fxns to join plts to other cells)
Too many NSAIDs & aspirin

What will plt # be?

Thrombocyt_________
openia
Due to plt consumption (low plt count in early or late
DIC?)
From / bone marrow production?
From / destruction or sequestration of plts?

spleen

The _________ recycles/sequesters them

Bleeding disorders

From Platelet Fxn

S/Sx:

Chronic bleeding in small/large vessels?

Petechiae
Purpura (small bruises)
Bleeding from
Mucous
___________________
membranes

OVERALL, s/sx from plt fxn will be SMALLER /

LARGER than the s/sx from clotting cascade
activity ?

Bleeding disorders

From Clotting Cascade Activity

1. Impaired Coag. Factor Synthesis
liver
Failure of the
________!
2. Vitamin
or
K ___ Deficiencycalcemia
Hypo____________
Needed for coag. Factors to work

3. Inherited Disorders
vWF
Hemophilia (aka low or bad
Factor 8/9)
vWF
_____ Disease
(aka low Factor
or bad ____)
plts
8

. this allows _____ to clot and ___________ to circulate

4. Clotting Factor late

Consumption
Which would manifest in ________ DIC

Bleeding disorders

S/Sx from Coag. Cascade Activity

BleedingLARGER
in ___________ vessels
Major/long bleeds after
________ traumas
minor
Ecchymoses/hematomas (big bruises)
Melena & Hematochezia
Melena black
= _____ color,
_____ in GI tract

Hematochezia
= ______
_____ in GI tract
Bright
red color,

Hematuria (blood in urine)

Hemearthrosis (blood in joints)
s risk for RA or OA???

Disseminated Intravascular Coagulation

= DIC
= Death is Coming
Disorder of hemostasis where there is
widespread ___________ followed
by
clotting
bleeding
widespread
__________.
secondary
It is always a _____________ disease

DIC how?

Early DIC
Coag. Cascade is activated in vessels
throughoutclotting
the body more ___________

Late DIC
Morebleeding
__________ than clotting

DIC How?

Some stimulus causes damage to the

cells in the body. These Tissue
cells then
release
factor
thrombin
____________. This triggers
the activation
of _________. This then leads to
Deposition fibrin
of _________ to begin the insoluble
clot
plasmin
fibrin
Activation of bleed
___________, which begins
______olysis and leads to ______ing.
thrombocyto
platelet
Consumption of _________s,
leading to
bleed
________penia, and even more _______ing.

DIC S/Sx

Clots + Infarctions
Petechiae & Purpura
Hemorrhage
Shock
Signs of respiratory, renal, or circulatory
failure
Seizures, coma
ALL RELATED TO BLEEDING OR
VESSEL OCCLUSION

DIC Treatment Goals

Treat the CAUSE

Manage the primary injury

Treat the
______ing
Clott
Heparin drip

Treat theBleed
_______ing
Replace clotting components

Treat the COMPLICATIONS

E.g. help heart or renal fxn

Immun
e
Disorders

Components of Immunity

Antigen
Processing an antigen initiates the immune
response
Helps define what is the body, and what isnt
Major Histocompatibility Cells (MHCs)
T-Cell Receptors (TCRs)

Antibodies
immuno

Aka ________globins

Lymph System
Cytokines
QUICK:IL-1
WhichIL-6
cytokines
TNFare responsible for
APR & Fever??? ____, _____, & ______

Antigens

= immunogen
Anything that can stimulate an immune
response
receptors
Recognized by binding to ___________ on
immune cells & to antibodies
MHC TCR
Foreign vs. Body determined by ________

MHC

=Receptors
____________ on the surface of immune
cells that presents antigen
pieces of ____________
T& bind to ___-cell receptors
Hence,
_____-_____
MHC
TCR complex

= determine self vs. non-self

Along w/ cytokines, MHCs allow immune
cells to interact w/ eachother

The Response
Antigen is processed
by a ________phage, Bmacro
cell, or other Antigen Presenting Cell.

An APC,macrophage
e.g. _____________, binds toTHelper __cell thanks
to our
MHC
TCRfavorite _____-_____ complex

CD4+ T-cell, aka cytotoxic / helper T-cell,

orchestrates immune response
Decides whether its

Cell-mediated response
(CD8+ aka cytotoxic /

OR

Humoral-mediated
B
response

Cells of Immunity

Monocytes Macrophages (APCs)

T Lymphocytes
CD4+ aka
___________ T-cells
aka __________decision
Helper
makersCytotoxic
CD8+ aka ___________T-cells

B Lymphocytes
B-cells

plasma
Which produce
__________ cells
antibodies

Which produce _______________

Myeloma
Multiple
Which, when production
of them skyrockets, leads to
_______________ _______________
disease
lesionshyper
Which causes bone _________, ________calcemia, &
bone pain

Cells of Immunity

Monocytes Macrophages
Big eaters
Function to present
___________ antigens to T-cells

Aka _____s
APC
Have MHC molecules on their surface
Macrophage + MHC _____ T-cell How should
CD4+
we attack?

Along withneutrophils
______________, are crucial in early
________________ response, as well as chronic inf.
inflammatory
Also clean up damaged sites (phagocytize debris)
Whats it called when a macrophage or other cell stimulates the synthesis of
cytokines to attract other immune cells?------------- ___________________
chemotaxis
Whats it called when macrophages eat up lipids in the vessels? _______ cells

Foam

Cells of Immunity

T Lymphocytes (T-cells)
Mature in the
_________, which atrophies in
thymus
puberty
TCR
MHC
Help w/ self vs. non-self thanks to its _____
binding to _____s.
CD4+ HELPER
Ts =cell
DECISION makers
humoral
Determine
___________cytotox
vs. ______-mediated
antibodies
response

Aka, _________________ vs. _______ killer T cells.

viral
CD8+ CYTOTOXIC Ts = cell-mediated
response
End _______ infections, kill bacteria & fungi

We also have Memory T-cells, which have

Cells of Immunity

B Lymphocytes (aka B-cells)

humoral
___________-mediated immunity
Key to killing
_________________ bacteria
encapsulated
What else is key for doing this????
_____________
spleen
Plasma cell = B-cell that
makes
antibodies
_________________
Many different kinds IgM, IgG

Memory B-cells to provide a quick, efficient

response to particular antigens that theyve
seen before

Antibodies

= bind to ___________s
antigen
IgM = short-term
IgG = long-term
immunity
Function to
Let
B-cells bind to an antigen
neutralize
_____________ toxins by binding their active
sites
IgG
Form complexes
In RA, Rheumatoid Factor forms complex w/ ____
Ab, which is long term

Cytokines

= proteins secreted by cells during

inflammatory & immune reactions
= chemical talkers
Function to
Attract other cells (aka
______________)
chemotaxis
Promote other cells to proliferate
(____s stimulate
CSF
the bone marrow)
Activate other cells (macrophages cytokines
CD4)
Produce symptoms

APR

E.g. ______, fever

QUICK what are those 3 cytokines that cause the above
TNF
IL-6
IL-1
s/sx?
_____, _____, & _____

Cytokine Chart

CYTOKINE

FXN

IL-1

Acute Phase Response

IL-4

Growth + Differentiation of B & T

cells

IL-6

Acute Phase Response

INTERFERON (IFN)
TNF
CSFs

viruses

Activate macrophages, esp.

against ________
Acute Phase Response

Differentiation & multiplication of

cells

Mother-Infant Immunity

A fetus typically does NOT make Ab

Only
____ from the mother crosses the
IgG
placenta
Long term
Is thisIgG
a short or long3term6Ab???

Maternal ____ ___-___ mo after birth

Baby starts making its own

When
a baby
be at risk for
Firstmight
3-6 after
birth
infection?
___________________________
baby

fightin
infecti
If there is a presence
g of IgM in fetus
on or

AIDS

HIV
CD4+
= acquired disorder where
_____ virus infects
_____
cells & patient becomes unable to mount a good
immune response
200< CD4+
= diagnosed when an HIV + patient has
____
AIDS
defining
_____ cells &/or shows ______-__________ illness.
E.g. infection, pneumonia, lymphoma, cancers, &
especially wasting/cachexia

Affects both cell & humoral-mediated responses,

and bacterial, virual, fungal infections are common
IMMUNE SURVEILLANCE

HIV transmission

HIV can be contracted through

sexual
____________ contact
blood
_________-to_________
contact
blood
Mother-to-infant contact!breastmilk
(e.g. _____________)

HIV cannot be contracted through

Casual contact (to blood or membranes)
Insect bites

Has not been contracted through saliva

AIDS How?
Transmission of HIV via blood, semen,
breastmilk, etc
HIV binds toCD4+
_____ cells via their
_____
TCR
HIV attaches, inserts
its RNA, and
using
Reverse
transcriptase
_______________________, RNA DNA integrated into
hosts chromosome
T cell enzymes begin to make
viral __________s, which get
protein
assembledvirion
into __________s

virion
_________s lyse their host CD4 cells and get released,
spreading further and causing CD4 helper T-cell count

From Infection AIDS

WINDOW period =
Patient has become infected, but tests show
HIV _____ __ Time between INFECTION and SEROCONVERSION
Seroconversion = from testing
__ to
+ ___

Lasts 1-3 months

Can absolutely transmit disease during this time
Testing HIV + means body has produced ____ to HIV

Ab

AIDS status, again, determined by

______________

CD4+ OR
count

____________________

AIDS-defining illness

3 Phases of AIDS

Primary Infection
Latency
____________ (Chronic Asymptomatic)
Overt
________ AIDS

AIDS - Primary Infection

Lasts only 2-4 weeks

Fast / slow viral replication
CD4+ Helper T-cell counts
___,then ___

B/c of viral loads, and CD8+ cells initially

kill all HIV-infected cells in their path
CD4+s then rebound
+

This is the usually time to go from HIV __

to ___
HIV Acute Clinical Syndrome sore
Fever
Mononucleosis-like
throatlymphadenopathy
S/Sx of both Acute HIV & Mono = _______,

AIDS Latency (chronic asymptomatic)

8__-___
10 years!
Viral replication held in check by immune
system low
Viral load = ___

CD4+ helper T-cell counts slowly ___

Due to general, prolonged immune response
and gradual inability
of
body
to
continue
lymphadenopathy
making them

Main s/sx of LATENCY =

____________________

AIDS Overt AIDS

2__-__3 years
Viral replication and viral loadboth ____
steadily
CD4+
B/c _____ count is plummeting, viral load cant
be held in check
200

Diagnosed by CD4+ count < _____

and/or
AIDS-defining
illness
__________________________

Transplant Problems

Host vs. Graft

Graft. vs. Host
Matching
______ types is key to success
MHC

Host vs. Graft

HOST is attacking NEW TRANSPLANT

TISSUE
organ

Usually involves _____________ donor & a

healthy recipient
T

Undesired ___-cell response

Graft vs. Host

GRAFT tissue is attacking HOST

Usually involves
______________
& an
Bone
marrow
immunocompromised recipient
UndesiredT___-cell response
of
donor
_____________

Immunological Tolerance

= the ability of the body to distinguish

self from non-self
So what are the key molecules involved in
this?
MHC
TCR
______ and its corresponding _____

If tolerance is lost IMMUNE ATTACK!

Mechanisms of Autoimmune Dz

3 likely mechanisms that cause body to

attack self
Tolerance (anergy)

Cells escape
_____________
tolerance
Cells lose _______________
Aka, lose MHC
their anergy
TCR

Inappropriate _____-_____ activation

EXAM 2 CONTENT

Fluids
+
Electrolyte
s

Intracellular vs. Extracellular

Intracellular electrolytes =
K
____
Mg+
____
PO ____
4

Extracellular

VESSELS

Plasma located in the _________

CELLS
Interstitial located between ________
Third
Space
Transcellular aka ________ _________
EXTRACELLULAR
ELECTROLYTES =
Na
_____
Ca2+
_____
Cl
_____
HCO
(bicarbonate)
_____

Fluid Exchange
OU
Hydrostatic/Filtration pressure pushes
T
_____
H

Via force ofO _________

IN

Particles (i.e.
Osmotic/Colloidal
pressure pulls ______

Via force ofalbumin)

_____________.

EDEMA
INTERSTITIAL
Expansion of
____________ fluid volume
Lymphadema = edema due to
LYMPH
obstruction
of __________ vessels
GRAVITY
Dependent Edema = edema
from
__________FILTRATION
causing ___________ pressure

EDEMA

Connect the arrows:

Cause:
Liver Failure
Sepsis
Breast Cancer
Failure

Due to:
Capillary Filtration
Pressure
Capillary Osmotic
Pressure
Capillary
Permeability
Lymph Flow
Obstruction

EDEMA

4 ways to treat edema

Diuretics
___________
__________
Elevation
Pressure Stockings
____________
IV
ALBUMIN

EDEMA

For ALL F&E disorders

Disease identified via.
History
Manifestations
_______
(###)
LABS

Treatment begins with.

Short term = Target#s
the ____
Long term = Target Underlying
the ____________
causes
____________

SODIUM y WATER

An equal, proportional change in Na &

VOLUME
HO results in
a change in ___________ of
fluid
A disproportional
hypernatremia
change in Na & HO
hyponatre
resultsmia
in either ___________ or
_____________.

SODIUM y WATER

BP, Na _________
+ Na sensed
filtration
Juxtaglomerular
by
______________ cells
EN
IN
Leads to releaseRof
_________

Renin converts
________Angiotensin
to ________
Angiotens
in
Ang. I gets converted
the ______
A by
C EI ________ in
lungs
into Ang. II

Ang. II functions to cause

vasoconstriction
______________
aldosterone
and the release
of ___________
Aldosterone tells kidneys to Na
renal ____
_______________
reabsorption

Water Regulation
exhalation
Insensible Losses
= _________
+
perspiratio
ntachypnea
_____________

Increased with fever + _____________

hypothala
controlledPosterior
bymus
the ________________
pituitary

Thirst is
ADH released by the ______ ____________
The dipsias describe thirst
Adipsia = No thirst
Hypodipsia = Not thirsty enough
Polydipsia = Too thirsty

Na & Water

Diabetes Insipidus
Lack of production or response
no _________ to ADH

SIADH
Excessive amounts of ADH

Do these cause a VOLUME or SODIUM

SODIUM b/c it causes a disproportional change
problem?^^
____________
2.2

1L water = _____ lbs

Equal Na & HO changes

Hypovolemia aka Isotonic Fluid Deficit

CAUSES:
MANIFESTATIONS:
fluid intake
insensible losses
Third spacing

----

Acute weight loss

ADH & Aldosterone
___
in HCT
___

Hypervolemia aka Isotonic Fluid Excess

CAUSES:
MANIFESTATIONS:
Na & HO elim.
CHF
Renal failure

Fluid in > Fluid out

-- Weight gain
--__ interstitial fluid vol.
--__ in HCT

Unequal Na & HO Changes

Hyponatremia = serum 13
Na < ____
5
mEq/L
14
Hypernatremia = serum5 Na > ____
mEq/L

Hyponatremia

dilutio
Usually a _____________
problem

hypertoni hyponatremia
nal
Except in _______________

c hyponatremia
Hypervolemic

blood circulation, due to

HO flow but ____
CH
_____
renal
_______
F failure
Liver failure

Euvolemic hyponatremia
Normal ECF volume, usually due to

SIAD
____________

H
Hypovolemic
hyponatremia

in total body HO volume, due to

___
diuretics
____________
Sweating
Vomiting, diarrhea

Hyponatremia

CAUSES:
_______
losing Na fluid

Replacing fluids w/ just water or

low-Na fluid
Water in __ water out

> or SIADH?
Diabetes

LABS?
____ (determine hydration)
HCTlevels
____
ADH
MANIFESTATIONS:
___ in HCT

Hypernatremia

CAUSES:
HCT
Diab. Insipidus or SIADH? ADH

___
HO loss
Diarrhea

HO in<__ HO out

MANIFESTATIONS:
___
in HCT
___
serum osmol.
___
ADH (compensatory)

Pedialyt
e

P o t a s s i u m - Regulation

kidneys
Primarily regulated through
the ________
nerves
Function in
_______ and
__________
Muscle
_____________.
Contractions (e.g. CARDIAC muscle
Aldosterone exchanges
Na ____for K
Aldosterone
K____ secretion
Aldosterone ____
K
Aldosterone ____
H
alkalosis

Transcellular K Shift

Too high
K moves into cells when [K]
= ___
K leaves cells when [K]
Too =
low
____
K exchanges H
with ____ when moving
in and out of cells.
pH during hypokalemia
goes ____
pH during hyperkalemia
goes ____
K moves in/out of cells during alkalosis
K moves in/out of cells during acidosis

Hypokalemia

3.5

= [K] < ____ mEq/L

CAUSES:
___ renal loss
Diuretics
___ GI loss
______osis

MANIFESTATIONS:
ALKA
___ pH
GI
Paralytic Ileus
Neuromuscular
Atrophy, cramps
Cardiovascular
Arrythmias
EKG change
LABS?
___
____

pH
EKG

Hyperkalemia
Serum [K]> ____
CAUSES:

5.0

___ renal loss

______failure
Adrenal insuff.
____ inhibitors

fibrillati
on

renal

b/c Aldosterone = ___ in K

Intracellular release
Trauma

_______osis

ACE

Manifestations:

___ pH
Cardiovascular problems
Ventricular __________
EKG changes

ACID

LABS?
pH
EKG

TREATMENT?
________ if renal failure

Dialysis

CALCIUM

REGULATION
Primarily via
GI___ _______
Only30
Tract
___-___
is absorbed
50%
Inhibited by tanninstea
in ____
Primary LOSS via
___________
kidneys
Thebones
_______ act as a buffer system
Tightly related with
__________ Magnesi
and
Phospha
_____________
um
te
Active Vitamin D aka 1,25-dihydroxy-vitamin
D

C A L C I U M Vitamin D

Vitamin D made active

kidneys
in _________
Aka calcitrol
If KIDNEYS
________ fail, Ca2+

Ca2+ absorption occurs

in ____________
intestine
s
Very little Ca2+breastmi
in _______________
Need supplements
lk

C A L C I U M - PTH

Ca2+ is released from

bone______
Ca2+ reabsorbed inkidney
the ____________

PTH Disorders

Hypoparathyroidism
Low PTH leads to low
_____
Ca2+

Hyperparathyroidism
Primary: PTH
_____ leads to Ca2+
Secondary: Ca2+ leadsPTH
to _____
Almost always due
to _______ __________
Renal
failure

Hypocalcemia

Hypocalcemia =
8.5___mg
Serum [Ca]<

CAUSES:
___
release from bone
Hypo or hyperPTH?
Also neck surgery

___
intake/absorption
Vitamin
_____ ___
___
loss
D
renal
Pancreatic sequestration

MANIFESTATIONS:

hypo

Hypocalcemia

LABS?
______
____ levels
PO4 andMg2+
3-

TREATMENT
Acute onset of hypocalcemia requires
EMERGENT treatment with infusions, usually
with oral supplements.

Hypercalcemia

= serum [Ca]>____mg
10.5
CAUSES:

___intake/absorp.
Milk-Alkali Syndrome
penia

___
bone resorption
>___
90%of cases!
Hypo or HyperPTH?

HYPER

1 or 2??

Kidney
stones

Neoplasms
Bone resorption

PO4
3-

B
P

Mg2
+

Acids
&
Bases

Physiology Review

LUNGS
Respiratory control
_______
SHORTterm
RegulateCO
_______

Long
HCO

Physiology Review

Buffer System
Combines with acids or bases to prevent
Large swings in pH
_____________________________.

Anion Gap
= Unmeasured
______________ ________
(i.e. lactic acid,
anions
proteins,etc)
=Na
____ ____
Cl _______
HCO
An increase/decrease? In anion gap
means that something
negati with a
_______________ charge
ve
HCO(other than
chloride)
is replacing
________ in the
Na
+
blood & balancing _____s ____ charge.

Normal Physiological Ranges

pH =7.35
7.45
_____-______
= ____-____
mmHg
42
PaCO 38
24

31

HCO = ____-____ mEq/L

10 14

ANION GAP = ___-___ mEq/L

Significance of PaCO & HCO

PaCO
Theacidic
_____ component in the blood
Regulated by the
L u__________
ng
s
HCO (Bicarbonate)
Thebasic
_____ component
Regulated by the
__________
Kidneys
(metabolic)

Four-Step Acid-Base Problem

1. Is the patient acidic or alkalotic?

2. Is PaCO high, low, or nml? Is HCO?
3. Does the PaCO or HCO value make
sense?
4. Is there any compensation?

An example

Acidic or Alkalotic?
PaCO hi, lo, or nml?
HCO hi, lo, or nml?
Which makes sense? HCO
Compensation?

Yes

metab
olic
respirator
y

Metabolic Acidosis

HCO
= Low
_____ pH & low
_______
Lungs compensatehyperventilati
via __________________
on
Anion
________ _____ helps differentiate cause
gap
High
Nml

Metabolic Acidosis w/ HIGH ANION GAP

Gap >12
____ mEq/L
presence ofUnmeasured
_______________ __________
anions
Drug
chemical overdose
Often due to _____ or ____________
ethanol poisoning (varnish, shellac)
M _________
remia
U ________ (renal failure)
iabetic
D _________ ____________
ketoacidosis
araldehyde
P _____________ poisoning
ntoxication
I ________________
Actic
acidosis
L _______ ______________ (tissue hypoxia)
antifreeze
thylene
glycol
E ________ ________ poisoning (___________)
alicylate
S _________ poisoning (aspirin)

Metabolic Acidosis w/ NORMAL ANION

GAP

Gap =10
___-___
14 mEq/L

Causes:
Intestinal loss of HCO
______________
diarrhea
Renal loss of HCO
Acute Tubular Necrosis
Adrenal Insufficiency

TREATMENT:
w/ _____
Cl solutions

It is often called
_______________ met.
HYPERCHLOREMI
acidosis
C

Metabolic Acidosis Manifestations

S/Sx from the cause

S/Sx from acidosis
________
Nausea+ __________
vomiting
____________
Depressed neural activity
_____
cardiac contractility + output

Hypo or hyperkalemia?

S/Sx from
____________ compensation
respiratory
Hypo or hyperventilation?
___________
Kussmaul respirations

Metabolic Acidosis Treatment

Stabilize the patient

Target the underlying cause
NaHCO3
Addbase
______ to the blood

Metabolic Alkalosis

=HIGH
_____ pH HIGH
+ _______ HCO
Lungs compensatehypoventilation
via ___________________
To increase levelCO
of ______
(acid)

Metabolic Alkalosis

CAUSES:
ExtraHCO
______ in the blood
__________s
antacid
IV fluids (Ringers Lactate)
Blood transfusions

____
H Loss &/or HCO conservation
___________
Vomitin + gastric suction
___________
g
Adrenal excess/insufficiency +
hypovolemia
What
ALDOSTERONE
is secreted from the adrenals???
_________________

Metabolic Alkalosis - Manifestations

S/Sx from the cause

S/Sx from the alkalosis
_____
LESSsymptomatic than acidosis!
slow ________ than
HCO crosses blood-brain barrier
CO hyperactivity
er
Neural ________________
Cardiac arrythmias
Hypo or hyperkalemia?

S/Sx from respiratory compensation

Hypo or hyperventilation?

Metabolic Alkalosis - Treatment

Stabilize the patient

Target underlying cause
KCL
Often added to IV fluid
K helps to solve
______kalemia
hypo

Respiratory Acidosis

low pH & high

____
CO
_____
Kidneys compensate slowly by
RetainingHCO
______
_____
Excreting
H

Respiratory Acidosis - Causes

Anything leadingto ____ alveolar

ventilation
Acute
CNS
Depressed _____
Chest injury
Airway obstruction
Lung disease

Chronic
COP

______
Hypoxic
drive
D
CO retainers depend on ________ _______

Respiratory Acidosis - Manifestations

S/Sx from the cause

S/Sx from the acidosis
___________
Depress neural activity
ed
Depends
timeframe
on
___________ on onset
Often accompanied by Sx
hypoxemia
of ______________
Why? b/c if CO, an easy diffuser, is having a hard
time diffusing, then O is definitely going to have
a hard time

S/Sx from renal compensation

Acidic or alkalotic urine?

Respiratory Acidosis - Treatment

Stabilize the patient

VENTILATION
Careful with O supplementation if the patient is a
CO retainer, b/c it would take away
their _________
Hypoxic
drive
______!

Target the underlying cause

Respiratory Alkalosis

High pH &LOW
_____
_____ CO
Kidneys compensate by
RetainingH
____
ExcretingHCO
_____

Commonly associated hyper

with
______ventilation

Respiratory Alkalosis - Causes

acute
Almost always
______
Anything leadingto ____ alveolar
ventilation
Anxiety + panic attacks
Over breathing
Hypoxemia that causes ____-_____________
Fever
Sepsis
Pain
Mechanical ventilation

OVER

Respiratory Alkalosis - Manifestations

S/Sx from the cause

S/Sx from the alkalosis
Neuralhyper
______activity
Cardiac arrythmias

S/Sx from renal compensatoin

Acidic or alkalotic urine?

Respiratory Alkalosis - Treatment

Stabilize the patient

Target the underlying cause
The _______
____
Paper
bag effect

Endocrin
e
Disorders

Hormone Actions

Hormones = chemical messengers

They can only act when free, aka, unbound
to carrier proteins

There are multifunctional and

redundant hormones.

Hormone Regulation

Series of chain reactions that starts in the

CNS, specifically,
the ______________, and
hypothalamus
pituitary
then
________________.
Feedback mechanism
= ______________
negative

Hypo vs. Hyper

HYPOfunction = not enough hormone

action
________ Make it
Gland cant ____________
Congenital
Destruction
Aging, etc.
Respond to it

Cells cant ______________

No receptor
No binding

Hypo vs. Hyper

HYPERfunction = Too much hormone

action
Too much
Gland makes ___________
Broken feedback
Inappropriate receptor activation (Antibodies may
do this)
source
Enlarged gland

New hormone __________ (aka ectopic)

Neoplasia (whats the term for this?? Para.)

Where does the problem start?

PRIMARY
Problems starts w/ the glandmakes
that the
_________________.
hormone

SECONDARY

feedback
Problem starts w/ broken _____________
OR
wrong
Problem starts w/
__________________
of
amounts
pituitary
stimulating/releasing hormone (usually from
the ___________)

Thyroid Hormones

Triiodothryonine = T3
Thyroxine = T4
Thyroid Stimulating
Anterior Hormone (TSH):

Secreted
by the
_______________T3
T4
pituitary
thyroi
Tells d
__________ to make and release ___ & ___

T3 & T4 lead to

____
metabolic rate
____
protein + bone turnover
____ response to catecholamines (SNS)

Hypothyroidism - Congenital

Neonatal screening done regularly

Could cause growth + mental retardation
Babies look normal at birth (b/c mom has
been providing thyroid for baby up until
delivery)

Treatment must be done early via

artificial thyroid hormone

Hypothyroidism - Acquired

Acquired hypothyroidism may be

primary or secondary
be ___ and T3/T
In primary, TSH will
4 will be
____

In secondary, TSH will be ___ and T3/T4 will

be ___

Acquired Hypothyroidism - CAUSES

_____________
Hashimotos disease
Most common cause
_____________
the
autoimmunedisease that destroysthyroid
__________
This is a primary/secondary disease
hyperthyroidis
Overtreating
m _______________
Thyroidectomy or thyroid radiation
Drugs that block hormone synthesis in the
Pituitary
thyroid

__________ or hypothalamic dysfunction

Stroke, tumor, etc.
This is a primary/secondary disorder

Acquired Hypothyroidism S/Sx

________________________
Big, Slow, &
2 Cold
basic mechanisms that cause the above
phraseBMR
=
1. response
____
2. ___________ to SNS

Myxedema
= non-pitting edema due to
connective
sugars
buildup of ________ in _______________
tissue
Myxedematous Coma:
Extreme of hypothyroidism; life threatening

Acquired Hypothyroidism Dx, Tx

Diagnosed by history, s/sx, and lab values

E.g. T3
____ & ____
T4
TSH level depends on whether condition is
primary
____________
or secondar
___________
y
Presence of
antibodi
_____________
to thyroid tests
es
indicates
______________
disease!
Hashimo
tos
Treatment?
Artificial thyroid hormone

Hyperthyroidism

___________
Graves
disease
Most common cause
_______________
autoimmune process stimulates
TSH_____
receptors
on the ___________
thyroid
1/3 of patients have exophthalmos

Multinodular goiter
Tumor
Overtreating
_________________
hypothyroidis
m

Hyperthyroidism S/Sx

______________________
Small, Fast,

Hot
2and
basic
mechanisms that cause the above
phraseBMR
=
1. _____
SNS
2.toxicosis
response to _____

Thyro_____________

Highly symptomatic consequence of

Crysis
hyperthryoid

Thyroid Storm aka Thyroid ________

Extreme form of hyperthyroidism
Triggered by infection, trauma, surgery, etc.
tachycardia
Life-threatening

Hyperthyroidism Dx, Tx

Diagnosed by history, s/sx, and labs

T3 & ____T4
____
levels

Treated with
Radioactive
_______
iodine
Attempt to partially kill overactive tissue

Thryoidectomy
Drugs that block thyroid hormone synthesis
______-blockers
Beta
To _____
SNS receptors

Adrenal Products: Cortex vs. Medulla

Adrenal cortical hormones:

Mineralocorticoids (aldosterone)
Glucocorticoids (cortisol = glucocortisone)
Sex Hormones (androgens)

Adrenal medullary catecholamines

(SNS):
Epinephrine
Norepinephrine

Adrenal Cortical Hormones

Sex hormones
Little direct effect, insufficiency + excess only symptomatic in
women
____________

Mineralocorticoidsaldosterone
(_________________)
aldosterone =

reabsorption
Sodium _____________
Secretion+excreti
Potassium _____________
Secretion+excreti
on
Hydrogen ______________

on (cortisol)
Glucocorticoids
sleep cycle
Regulate _________
metabolis (catabolic or anabolic?)
Regulate ______________

gluconeogenesis
mglucose production, aka, ________________
___ hepatic

___ glucose use by the body

NET EFFECT = ___ in blood glucose

___ protein/fat breakdown, ___ fat deposition

Antiflammatory
Thus making you susceptible to infection

Quick Test Adrenal Hormones

Hypothalamus

Anterior Pituitary

ACTH
______________
Adrenal Gland

Cortisol
______________

Target Organs

Adrenal Cortex Insufficiency

PRIMARY cortical insufficiency =

______________
disease (pretty rare)
Addisons
ACTH levels will
be ____
Adrenal Hormones willbe ____

SECONDARY cortical insufficiency =

ACTH levels will
be ____
Adrenal hormones willbe ____

Adrenal Cortex Insufficiency - Causes

PRIMARY Addisons
= _____________ disease
From destruction Adrenal
of ______________
gland
_______________
response
autoimmune
Tuberculosis
Cytomegalovirus
AIDS

SECONDARY =

From Low
__________________
output
pituitary
After long-term glucocorticoid use (steroids to
replace diminished cortisol, patients
withdrawals
experience ____________ and
must therefore
taper
gradually ________ off steroids.

Adrenal Cortex Insufficiency S/Sx

Often not symptomatic until

90% ___ is gone
Mineralocorticoid deficiency (
aldosterone):
Hypo/hypernatremic?
Hypo/hypervolemic?
Hypo/hypertension?

Hypo/hyperkalemic?
Acidotic or alkalotic?
If acidotic, HIGH or NML anion gap?

Quick Quiz! HIGH Anion Gap Causes

M ethanol
_________ poisoning (varnish, shellac)
U remia
________ (renal failure)
D iabetic
_________ ____________
P _____________
araldehydepoisoning
ketoacidosis
I ntoxication
________________
L actic
_______ ______________ (tissue hypoxia)
E acidosis
________ ________
poisoning
antifreeze
thylene
glycol
(___________)
alicylate
S _________ poisoning (aspirin)

Adrenal Cortex Insufficiency S/Sx

Glucocorticoid deficiency ( cortisol):

Hypo/hyperglycemic?
Mood/energy levels?
low

Sex hormone deficiency ( androgens):

Remember, really only affects women
/ axillary + pubic hair?

ACTH excess (primary or secondary A.C.

insuff?)pigmentation

Hyper________________ (weird-looking suntan)

Adrenal Cortex Insufficiency Dx, Tx

Diagnosed by history, s/sx, lab values

/ aldosterone, cortisol, androgens
ACTH level depends on primary or
secondary insuf.
TREATMENT:
w/ hormone replacement
Regular daily, low-stress schedule
With
acute adrenal crisis, replace the 3 Ss:
ugar
S_____________
alt
S_____________
teroids
S_____________

Adrenal Cortical Excess - Causes

Cushings
_______________
syndrome
= too much
cortisol
__________
Interchangeable with hypercortisolism

_________ic
Iatrogen Cushings Syndrome
Due to steroid
______________ treatment

Cushings Disease

From too much

________ (thus, problem
is in
ACTH
pituitary
________)
Primary or secondary?

Ectopic Cushings
ACTH

ACTH
From too much _______ as result of an _____

Adrenal Cortical Excess S/Sx

Glucocorticoid excess ( cortisol):

Hypo/hyperglycemic?
Fat_________
pads (buffalo hump)
Subclavicular
Moon facies (round face)
Large abdomen
Thin skin & striae (due to protein breakdown)
/ muscle strength?
/ bone structure?
/ risk of infection?
/ mood/energy/activity level? (Possible
psychosis)

Adrenal Cortical Excess S/Sx

Mineralocorticoid excess (
aldosterone):
Hypo/hypernatremic?
Hypo/hypertension?
Hypo/hyperkalemic?
Acidotic vs. alkalotic?

Sex hormone excess ( androgens):

Females get hirsutism + menstrual
irregularities

Adrenal Cortical Excess Dx, Tx

Diagnosis, again, done by history, labs,

s/sx
TREATMENT:
INSULIN
____________
Potassium could be used for hyperglycemia
___________ electrolyte needs tobeta
be replaced
Blood pressure could
be treated with _____infection
blockers
Must
protect against ______________
Iatrogenic
Adjust steroid treatment!
_____________ Cushings Syndrome

Diabet
es
Mellitus

Review

Jobs of the Pancreas

ENDOCRINE:
Makes _________,
insulinwhich moves glucose from
_______________
to the _______
bloodstrea
cells

EXOCRINE:
m

Makes digestive enzymes for breakdown of proteins,

carbs, and fats

In pancreatitis, cells release these digestive

enzymes to surrounding tissue
Thus destroying _______ ________glycemia

insulin
Liver functions to.

hyper

Store glucose as ____________ for glycemic regulation

glycogen events
If liver fails, ________glycemic

hypo

Endocrine

Glucocorticoids (i.e. cortisol =

hydrocortisone)
metabolis
m_____________
Regulate
/ hepatic glucose breakdown, / glucose
use by the body
/ protein breakdown, / fat deposition?

In hypo
Addisons disease
_____glycemic events

In Cushings syndrome
/ insulin sensitivity insulin resistance

Review

Normal fasting glucose

80 = ___-___ mg/dL
90
Bld glc rises after
________
when food is
eating
absorbed from intestines
blood into the ______
Bodys response to B.G. is to secrete
insulin
________ pancre
from the __________
Returnsas
B.G. to normal by
Using glc for energy in cells (ATP production)
Storing extra glc in liver
the ______glycog
as ____________.
Storing glc fat
as _____
en

Metabolism Review

Glucose
Amino Acids
Free Fatty Acids

Liver can convert

these into
glucose and
ketone bodies
(acidic)

ANABOLISM
via INSULIN,ANABOLIC
STEROIDS
CATABOLISM
via GLUCAGON,EPINEPHRINE,
CORTISOL

Release into
bloodstream

Glycogen
Proteins
Triglycerides

Metabolism

1st source of ATP =

Glucose
From ingesting it, or from
____________
glycogen
breakdown

2nd source of ATP =

Glucose
gluconeogenes
liver
From is
_________________________ in the ________

3rdfat
and last source of ATP =

____ breakdown
liver
From beta-oxidation, done also by the _______

Insulin vs. Glucagon

INSULIN = anabolic or catabolic?

/glucose transport into muscles + fat
/ glycogen synthesis
b/c glycogen is storage form of glucose

/ gluconeogenesis

GLUCAGON = anabolic or catabolic?

/ glycogen breakdown
/ gluconeogenesis
Moves sugar from
the
cel _______ tobloodstream
_______________ ls

Diabetes Mellitus - Definition

= endocrine disorder of carb, protein, +

fat metabolism that results from an
deman
imbalance between insulin availability
d
and insulin _____
Type 1 or Type 2
Due to:
deficienc
y ___________
Absolute
insulin
Pancreas
___________ cant
make it
release

Impaired
insulin __________ relative to
pancreas
demand
response
___________ cant secrete enough
receptor
Inadequate
or defective _____________ of
s

Type 1

Loss ofpancreatic
____________ fxn insulin
deficiency
Previously calledyoun
juvenilethin
diabetes
g ________ + ______
Patients are usually
when dx
Really have no idea how it starts other
than genetics
Drastic
Require insulin
injections or pumps
fluctuations
Type 1 = more ________________________ in
B.G.

Type 1
Genetics + Trigger + immune reaction to
pancreas
Beta cells cant produce insulin

INSULIN DEFICIENCY

No hormone to give cells the glucose they

need; cells starve.

Fatty acid
oxidation in liver
KETOSIS

Gluconeogenesis
in liver
_________GLYCEMI
hyper
A

Type 2 INSULIN RESISTANCE

Relative lack of insulin, or impaired

A ______________
release__________
insulin
Impaired ability of the
tissues
_________ to use
insulin
older
obese
Patientsgeneti
usually ________ + _________ at dx
c ___________ links
STRONG
Treated w/releas
insulin straight up, or w/ drugs
that
Sensit e
ize
insulin
_________ from pancreas
gluconeogenes
______________
cells to insulins effects
is
Inhibit ____________________

Gestational Diabetes

Special type that occurs during

pregnancy
risk
for pregnancy
complications
Gestation
Larg
al LGA (______ for
e
including
death,
____________
Age), abnormalities
II
Women w/ GDM are at risk of
developing Type ___ 5-10 years after
delivery
Basically, baby gets the moms excess
glucose BIG BABY

Testing for Hyperglycemia

Diagnostic
Random blood glucose Very unreliable
Fasting blood glucose Should100
be
______
mg/dL
Glucose tolerance test

Tracking
Blood glucose diaries
Glycated Hb (aka
_________)
HBA
1C
Based on tracking a RBC over its120
lifespan -
______ days. IfHBA
there is an in ________, then
there is excess glucose in the bloodstream.
1C
Hence, glycated hemoglobin.

DM Early S/Sx

All related to cellular

_____________ &
starvation
___________
osmotic effects of hyperglycemia
More ______
onset w/ Type 1 or Type 2?
acute
Poly________
phagia
Usually w/ Type 1
___
Feel hungry often due to glucose delivery to
hungry cells

Poly______
uria

Frequent urination
_____________ b/c _________
cant handle
kidneys
excess glucose, and, as we know, H2O follows
solute.

dipsia
Poly_______

thirst

urination is going to result in _______

DM Complications + Late S/Sx

Occur when B.G. is not well-controlled

Acute
Chronic

ACUTE Complications

Diabetic Ketoacidosis aka DKA

Hyperosmolar Hyperglycemic State
aka Hyperglycemic Hyperosmolar
Nonketotic Syndrome
Hypoglycemia

DKA

Severely low insulin 3 metabolic

problems:
hyper
_______glycemia
ket
____osis acidosis
Metabolic ____________ (w/ a normal / high
anion gap) cata

Cells are starving, so metabolic pathways

thatFatty
get activated = ______bolic ketone
Gluconeogenesis
for glucose & ATP
acid
___________ oxidation makes ATP and
________s

HHNK/HHS

insulin resistance
carbo
+ ______ load
hyperglycemia
massive
________________
B.G. >600
_____mg/dL

B/c of _______glycemia,
blood is also
hyper
__________osmolar
hyper
Can thus get hypertonic hypo/hypernatremia?

Glucoses osmotic pull pulls

dilutes
H2Oin ____ +Na+
_____

How is
this different from DKA?
Metabolic

NO acidosis
_____________________ in HHNK
Why? b/c the cells are still able to pull in
some glucose for energy

HHS
Insulin resistance + Carbo
load
Massive hyperglyce
_______________ +hyperosmol
_________________

mia

arity

Osmotic diuresis
H2O follows
glucose
Dehydration,
electrolyte
imbalance

Hypertonic
Hyponatremia
nerve firing

SHOCK, COMA,
CONFUSION

Hypoglycemia

= low blood glucose from relative

excess
__________ of insulin
injecting
Usually from
______________ too much

= aka INSULIN REACTION

Due to:
Miscalculation
Not eating
exercise (takes glucose out of bloodstream
for mm)
Change in insulin site
Alcohol (s gluconeogenesis)

Hypoglycemia S/Sx

S/Sx from glucose to BRAIN:

_____________
Headache
Behavior change
Fatigue
Blurred/spotty vision

S/Sx from autonomic activation

(epinephrine):
HR
______________
Tremor, anxiety, shaking
Diaphoresis
Epi is functioning to take glucose FROM CELLS and
INTO BLOODSTREAM in order to supply enough for
muscles

Acute Complications: Somogyi Effect

= rebound hyper
_______glycemia duehypo
to
______glycemia
night
Often occurs at __________
Caninsulin
get initial hypoglycemia from
__________ reaction
Nightly fasting

HYPER follows HYPOglycemia

Somogyi Effect

Hypoglycemia can lead to hyperglycemia

because, at some set point, the body
decides that it does not have enough
glucose in its bloodstream. In response,
pinephrin
anabolic/catabolic
hormones, such
as
lucago
ortisol
n
G__________,
C___________, ande
cells
E__________,
becomebloodstre
activated,
am
functioning to pull glucose
from the ______
and into the ______________.

Chronic Complications - Theories

Glycosylation:
The idea that extra glucose gets stuck to
body structures (vessels, etc), and over time,
this causes these structures to malfunction
and lose their fxn.

Chronic complications

MICRO

N____________
europathies
S________
ensor
yotor
M_______
A________
GI, Bladder problems)
utono (_____TN,
hypo
mic
N____________
ephropathies
Leading cause Chronic
of ____________________!
renal
failure
Monitored via micro____________
albuminuria - determines
glomerular fxn
If theres albumin in the

R_____________
etinopathies

urine, then the

kidneys/glomeruli arent
doingin
their
job!
______________
U.S.

Leading cause blindness

of

Chronic complications - MACRO

Most common cause of death in DM =

________________________
Atherosclerosis
PVD
Coronary Heart Disease
Chronic Ischemic Heart Disease
Acute Coronary Syndromes

Cerebrovascular Disease
TIAs + Strokes

Chronic complications - Infections

Diabetes essentially causes:

A ______________
immune system
weakened
Very slowhealing
___________ by the body
Possibly due to poor blood supply.

Chronic complications Foot Ulcers

Common end result neuropathy

of ___________ +
macrovascular problems
+
immuno
__________suppression.
Neuropathy causes fxn of peripheral
muscles and venous valves poor
drainage and poor circulation, thus, will
result
in pressure on the weightweakened
bearing parts of the foot. With a
_______________ immune system, healing
the ulcers is extremely difficult.

Urinary
+
Renal

ELIMINATION jobs of the kidney

Regulate blood volume

Balance electrolytes
Control pH
ExcreteH
_________, reabsorb
___________
HCO

Excrete waste products

_______
Urea = breakdown product of protein
Creatinin
________ = product of
____________ muscle
skeletal
e

ENDOCRINE jobs of the kidney

RAAS
Makeserythropoietin
_________________, which stimulates
bone marrow to produce
______
RBCs
Activates
Vitamin
D
___________
____
Ca2+______
Which effects this electrolyte:

Kidney Depends On

How much blood the pumps each

20 25
minute
Kidney gets ___-___% of the CARDIAC
OUTPUT!
urine

Glomerular Filtration
glomerulu

Bowmans
scells ______
Space
the start of making
& cleaning blood
protein
Filters blood from __________
renal into ___________
__________
ultrafiltrate no _______, no _________ get filtered
Creatinine

GFR = a
of _______ fxn
Cr,measurement
BUN,

Normal GFR = 125 ml/min

______________ clearance is the standard for GFR
_____________ in bloodstream = renal fxn

Urinary Tract Infections

Where do the bugs come from?

GI ________
Tract
____
Wipe front to back
Lol

_________
Urethra
Vagina area
Bloodstream

COMMON UTI BUG:

___
E. ________
Coli

UTIs are Sexist

Why FEMALES > MALES?

SHORTE urethra easier for bacteria to
__________
R
climb
Easier bacterial
transfer (smaller distance)
CLEAN
Harder
SEX to keep _______
_____ = bugs

What keeps the UTI bugs out?

Climb
Its hard to
______ ____________.
upstream
WASH OUT
phenomenon
Drink water kids!

Bugs vs. Bugs

Normal flora vs. bad bugs

________
MUCIN
Protective layer
by release of
_____________
estrogen

What lets the bugs in?

OBSTRUCTION
REFLUX
ANTIBIOTICS
HYGIENE

Old folks w/incontine

_______________
MUCIN
__________ nce
Weakened by
____________ and age
menopaus
e
Thus, old women
susceptible

UTIs and REFLUX

URETHROVESICAL reflux
Backflow from
urethra
_________ bladder
to ____________

VESICOURETERAL reflux
Backflow from
___________ ureters
to _____________
bladder

Made worse with

_________________
OBSTRUCTION

Reflux + Obstruction = bad news

UTIs in HOSPITALS

_______________!!!
Catheters
Remove as soon as possible

High-Risk Populations for UTIs

Why diabetics?
_______
nerve fxn
immune system
Neurogenic Bladder Dysfunction
_______
not well controlled food source
__
E. for
Coli
Glucose
_____

Why Kids?

VESICOURE
Congenital anomaly which allows
TAL
_____________ reflux
mucin

Why the Elderly?

prostate
Thin _______ layer
Enlarged __________ (presses against bladder)

UPPER vs LOWER UTIs

CYSTITIS =
L o w e UTI
r
_______

upper

renal

(located in
bladder
________)
Dysuria
Frequency
Urgency
Incontinence
Low pelvic/back ache

cytokine
s

UTIs S/Sx

CHILDREN (esp. babies)

Cystitis or pyelonephritis?
_______
Weight______, anorexia, diarrhea, septic
shock,
Thrive, ____________ fever
unexplain
loss Failure to
ed

ELDERLY
Cystitis or pyelonephritis?
Change in
________ status, anorexia, fatigue,
mental
weakness
Frequency, urgency, incontinence are normal
even without a UTI.

Renal

Failure

= GFR <
125 ____mL/min
20____% of its normal
Results in toxic blood (circle one)
Hi vs. low urine output?
/ BUN & Creatinine?
Acidosis vs. Alkalosis?
Hypokalemia vs. Hyperkalemia?
Fluid overload
/ RBC count?
Weak vs. Strong bones?

Failure can be ACUTE or CHRONIC.

ACUTE renal failure

Comes in 3 types
1. PREREN
_____________
AL-The most common!
2. INTRAREN
___________ or Intrinsic
AL

3. POSTRENA
_____________
L-Always due obstructio
to _____________
n of all renal failure
-Only 10-20%

PRERENAL

before the kidney

Due to______________________________
arterial blood flow to
kindey
WITHOUT
causing renal
___________
ischemia
Can be due to
_______________
Hypotension
Hypovolemia
Dehydration, blood loss

<3 Failure

Prerenal How?

1. Hypotension, hypovolemia, CHF, shock..

2. effective blood volume
3. renal blood flow
4. Glomerular capillary hydrostatic pressure
5. GFR
6. /? BUN + Creatinine - /? FENa

FENa Fractional Excretion of Na

FENa is LOW (<1%) because renal blood

Aldoster
Na ____
flow release
of __________
retention. one

Thus, LESS Na is excreted.

INTRARENAL

= Instrinsic Acute Renal Failure

From damage Renal
to ______ ____________ (i.e.
structures
___________,
tubule,
interstitium) caused
glomerul
usIschemic
by
____________
damage
Drugs
toxins
________/______
(Aminoglycosides)
Inflammation/Immune Rxn

Acute Tubular Necrosis describes the

mechanism.

Acute Tubular Necrosis

how most intrarenal processes go

Renaltubular
_________ cells are highly
dependent
on _________ & very vulnerable
oxygen
to toxins (b/c its their job to filter them!)
Injury is REVERSIBLE if caught early
enough

Acute Tubular NecrosisHow?

Tubular
__________
cells are damaged (ischemia,
drugs,etc)
These cells, which normally transport
ions, slough CLOG
off
urine
Sloughed cells ______ tubules and _______
cannot be passedhydrostatic
This intratubular _____________
pressure
weak
This
leakalso leaves tubule walls _____ + allows
fluid to ______ (backleak)

in tubular hydrostatic pressure = /

in GFR

Intrarenalwhy is FENa >1%?

Tubula
Because the
________ cells are damaged,
r
they are inable
to do their job and HOLD
IN Na!

Thus, MORE sodium is excreted!

POSTRENAL

Obstructive
=__________________
acute renal failure
From BLOCK
to
__________________
flow causing
urine
pressure
backup. May occur in the
___________
Ureters
Kidney stones
Pregnancy, tumor (mass effect)

Bladder
Neurogenic bladder (diabetes, age)

Urethra
BPH

PostrenalHow?

1. _____________
Obstruction in the ureters, bladder, or
urethra
2. Urine cant flow out
Bowmans
3. Hydrostatic pressurespace
in __________

________
4. GFR

CHRONIC Renal Failure

Causes
1.
2.
3.
4.
5.
6.

Diabetes
________________
________________
Hypertensi
on
Pyelonephritis
(upper or lower?)
Glomerulonephritis
Interstitial nephritis
Cystic Kidney Dz

4 STAGES of chronic renal failure

reserve
Based on the idea of renal
__________
To compensate for fxn, surviving nephrons
hypertrophy to maintain GFR

Just like heart, there are few S/Sx until

over HALF of the nephrons are destroyed
% decrease GFR
in _____ defines the 4
stages

4 stages

1. Renal Impairment
Diminished renal
reserve
_________
GFR but >
50____% normal
NORMAL
BUN
Cr
_____ + ______

2. Renal Insufficiency
GFR =
___-___%
20
50 normal
Some S/Sx

3. Renal Failure
GFR 5___-___%
20 normal

4. End-Stage Renal Disease

GFR < ___% normal
5

Chronic Renal Failure Man of Fistations

Aka manifestations
=Accumulationnitrogenous
of ____________ wastes
Kidneys usually
Excrete nitrogenous wastes in urine
UREA (BUN) from________________________
protein
CREATININE (Cr) skeletal
from ______________ muscle
breakdown

But, if kidneys are failing

AZOTEMIA = levels of BUN & Cr in
bloodstream
Can lead to

UREMIA = Azotemia + SYMPTOMS

Chronic Renal FailureManifestations

IMBALANCES
Kidneys are usually supposed to
Concentrate/dilute urine, change fluid status
ADH(via
_____) H
HCO
Secrete ____ & reabsorb
________
aldosterone
Secrete K (via ______________)
or Na excretion? (via same mechanism as
above)

But if the kidneys fail at balancing

Metabolic acidosis or alkalosis?
Hypo or hyperkalemia?
Impaired Na regulation

Chronic Renal FailureManifestations

Mineral + Bone Disorders

Kidneys usually
D ____
Activate Vitamin
ReabsorbCa
______ (w/ the help
of _____)
PT
H
But if the 2+
kidneys are failing
Hypo or hypercalcemia
Hypo or hyperparathyroidism?
Primary or Secondary?

Renal osteodystrophy weak or strong bones?

WHY??? -----hint: PTH + bone resorption

Chronic Renal Failure Manifestations

Hematologic Disorders
Kidneys usually.
Make erythropoietin
________________
But if they are failing
Low or high RBC count?
Term for this anem
= __________

What other RBC

ia lab will be low?
______
HCT

Chronic Renal Failure Manifestations

Cardiovascular Disorders
Kidneys usually.
Regulate blood pressure (RAAS) + blood volume

If theyre failing
Hypo/hypertension
Do FAILING kidneys want or blood flow?
Does failing heart want or blood flow?

Chronic Renal Failure Manifestations

The rest of the effects are related to the

TOXIC effects of u r e m i a, which as we
know,
=
SYMPTOMS
AZOTEMIA
_______________ + _______________

CRFProblem w/ Medication

Adverse drug rxns + dosing

B/c the kidneys & liver process drugs to make
them inactive
Kidneys excrete toxic metabolites
If they kidneys arent working, should doses
be or ?
Depends haha.

CRF in the ELDERLY

Slow decline GFR

in ____ throughout life
Creatinine level is completely relative
High for a frail old woman is normal for Chuck
Norris
Are Chuck Norris jokes still funny?
Idk

CRF Dialysis

Dialysis cleans the blood

osmosis
Toxins removed by
____________
Semipermeable membrane
What molecules do NOT get diffused?
__________
+ ______________
Cells
proteins
2 types
of dialysis
HEMODIALYSIS
Patient gets a fistula put in, gets hooked up to
machine
Wow. Do not Google Image fistula.

PERITONEAL DIALYSIS
Abdominal peritoneum serves as natural diffuser
of blood

EXAM 3 CONTENT

GI
Disorders:
I

Anatomy Review

UPPER
Mouth, esophagus, stomach

MIDDLE
Small intestine
duoden
jejunum
ileum
(____________,
__________,
um
________)

LOWER
Large intestine aka colon, rectum

EXTRAS
Salivary glands, pancreas, liver, gallbladder,
appendix

GI S/Sx

Anorexia
Loss of appetite

Nausea
Feeling sick

Vomiting
-emesis
To empty GI tract

GI Tract Bleed

Often monitored through BP & HR why?

Likely a / In BP and subsequent / in HR
Hematemesis = vomiting blood (coffee
grounds)
Melena = dark, tarry, foul-smelling stool
Due to acute bleed higher/lower in GI tract; blood
gets partially digested

Hematochezia = Bright red blood, per

rectum
Due to acute bleed higher/lower in GI tract
chronic

Occult
= hidden
Iron-deficiency

From __________ bleed that usually leads to

_____________________ anemia.

GI - Abdominal Pain

From non-well-defined organ involvement

visceral
Term for this is
_____________
What if the pain is sensed on the skin at a
distant
site?
referre
____________
pain.
d

From peritoneal
involvement
SHARP

Pain = _________
Patient will want to lie very still

Gastroesophageal Reflux Disease

= GERD
= chronic backward movement of gastric
esopha
contents
into the __________ caused by
lower gus __________
incompetent
esophageal
sphinct
_____________ (LES). er
Vagu
LES is opened by the PNS or SNSsvia the
________ nerve

Can be a problem in babies due to small

stomachs, but usually resolves within 2
years.

GERD How?
y
ol
Fatt s
h
l
o
mea Alc
e
in
t
co
i
N

PN
We
S
a
dia k
He phra
rni
ati gm
on

LES
Relaxation
Low pH stomach contents
esophagus
Esophageal i n f l a m m a t i o n +
erosion

Aspirati
on

burping
heartbur
Bronchial
n
Stricture
inflammation,
s
Barretts Esophagus (metaplasia) pneumonia risk

GERD S/Sx

Acute: From immediate irritation, usually

night at _______
meals
worse
or after ________
Burping
Heartburn (dyspepsia)

Chronic: From long-term irritation +

_______________
inflammatio changes over time
n____________
Strictures can cause dysphagia (difficulty
swallowing due to scar tissue formation)
Barretts Esophagus increases risk of
cancer
Cells go from squamous columnar epithelium
(like the stomach)

Peptic Ulcer Disease

= disease characterized by erosions or

Mucosal
breaches
in the _________________ of the
barrierstomach,
esophagus,
duodenum&/or
_______________***
GI tract basically digests itself

*** = MOST COMMON LOCATION!!!!

Peptic Ulcer Disease - Causes

H. ____________
___

Pylori
Gram negative bacteria that LOVES acidic
environment
inflammatio
n __________ response by enterocytes
Induces
NSAIDS
DrugsGASTRI
injuring the GI lining (_________,
ASA) N

Excess ____________

Hyperacidic
Tumors may secrete it

P.U.D. Mechanism + S/Sx

barrier
Anything that disrupts mucosal
________
acidity
or causes
hyper________ allows acid to
reach enterocytes
Mucosal barrier normally protects GI tract
from autodigestion
No barrier no protection

Acid to enterocytes causes

Pain on a full/empty(?) stomach
Erosion
Scar --- Hematemesis, melena, occult
blood
tissue
PERFORATIO
____________ formation strictures
N

Inflammatory Bowel Disease

Category of 2 chronic disorders of

pain
diarrhe
nonspecific GI inflammation
causing
a
_______, _____________, and weight
loss.
1. Crohns Disease
2. Ulcerative Colitis
We dont know what causes them.

IBD What they have in COMMON

Both Crohns and UC

Are inflammatory
_______________
Cause the classic triad
paiof ______,
diarrh
__________,
Weight
n
ea
______________.
loss up in family clusters
Show
Most often diagnosedYoung
in ___________________
adults
Involve remissions and
exacerbations
Have no clear cause
Have systemic
____________ manifestations
Arthritis, skin problems, anemia,
hypercoagulability

Crohns Disease

part of the GI tract

AffectsAny
_________
anus
From mouth
________ to
__________
MOST COMMONLY inileum
the _________

Crohns Disease - Features

SUBMUCOS
_______________
layer is most hardly
AL
affected
May continue thru to muscularis + serosa
Islands
though

__________ of inflammation
Cobbleston
eSkip lesions

_______________ appearance
Due to fissures + crevices
Bowel wall thickness or ?
Absorption + Secretion or ?

scarring

Crohns Disease S/Sx

Related to location and extent of

lesions
RLQ

Colicky pain, usually ______ quadrant (why

there?)
melena
Diarrhea
absorption
Bloody, often dark (we know this as ________), fatty
absorptio
(why?)

Weight loss (due to ____________)

Malaise, fatigue, weakness (again due to
_________)
Nutritional deficiencies
Steatorrhea (excess fat in stool)
Fat is harder to digest than other nutrients.

Crohns Disease - Complications

Fistulas
____________
Abnormal openings or communications
New tubes or holes
Allow GI contents to bypass segments of
intestine via erosions
serosa of the ___________ (hint:
certain layer)

Intestinal Obstruction
+ Strictures
Scar

Due to edematissue
& _______________ formation

IBD Ulcerative Colitis

rectu
colon
Affects ONLY the
_________
+ _________
mrectu
Usually starts at
the ________ & spreads
m
Inflammation process,
unlike Crohns, is
__________________
continuou
s
Affects
the
____________ layer
mucosal

Ulcerative Colitis - Features

Mucos
___________
layer most hardly affected
al
Inflammatory
lesions conflue
are _____________
nt
Friable (crumbly) appearance

Due tonecrosi
____________ + ulceration
s
What happens
to the bowel wall?
______
scar formation, strictures

Seeing that UC manifests mainly in

COLON, what will be the tell-tale
symptom?
diarrhe
a
_____________
bleedin
Often withg__________

Ulcerative Colitis S/Sx

Related to the extent of colon + rectal

involvement
Mild abdominal cramping
Diarrhea,
hydrati
possibly up to 30-40 BMs/day!
Yikes.on
De___________
Bright blood + mucous

Weight loss
Malaise, weakness, fatigue
Low grade fever
Fecal incontinence

Ulcerative Colitis - Complications

Colo
_________
cancer

n
Risk = by 20-30 x

Crohns vs. UC

CHARACTERISTIC

CROHNS

ULCERATIVE
COLITIS

Layer?

Submucosal

Mucosal

Lesion pattern

Cobblestone

Confluent

GI Segments

ALL, mainly ILEUM

Colon + rectum

Hematochezia?
Melena?

Melena

Hematochezia

Steatorrhea?

Yes

No

Fistulas?

Yes

No

Strictures?

Yes

Yes

Cancer?

Nah

Yes

Diverticular Disease

colo
= condition of the
________ characterized
n
byweakenings
___________________
of the wall, leading
to outpouchings of the mucosa
Asymptomatic = diverticul_____
osis
Symptomatic = diverticul______
itis

Usually in younger/older/neither? patients

Diverticular Disease How?

wea
Diverticula usually form
at _______ points
k
colo
in
______ wall
n
Herniations
develop over time
Age
pressure

Diverticula may get _________, infected, +

blocke
inflamed__________________
PERFORATIO
d
N!
Thus, DIVERTICUL_____
itis
This is an emergency!

Diverticular Disease S/Sx

Diverticulosis
Often accidentally diagnosed
Has nonspecific GI symptoms (stomach ache)

Diverticulitis
____Q
LL pain + tenderness (why there?)
Nausea, vomiting (emesis, remember)
__________
(due to cytokine response)
Fev
What will WBC count likely be? or ?
er
Peritonitis

Intestinal Obstruction

failur
= mechanical blockage
or __________ of
e GI contents from
peristalsis that prevents
Moving
_____________________.
forward

GI Paralysis (akaperistalsis
lose _____________)
=adynamic obstruction

Adhesions
Incarcerated Hernia

Intestinal Obstruction How?

Nausea/vomi
ting
F/E
disorders

Obstruction

No
movement

Distensio
n

PAI
N

Ischemia
Necrosis
Perforat
ion

Bacterial
Overgrowth

Causes of Perforation

Thus far, there are 3 diseases that can

lead to PERFORATION: (in alphabetical
Diverticular
order)
1.
2.
3.

Intestinal
_____________________
disease
Obstruction
Peptic Ulcer _________________
______________
________________________ disease

GI
Disorders:
II
The Extras

Jobs of the Gallbladder + Pancreas

Gallbladder
Concentrates and stores
bile _______

Pancreas
ENDOCRINE: Makes
insuli
__________
moves glucose n
from
_____________
to ____________
bloodstre
cells
EXOCRINE: Makes
_____________ to break
am
enzymes
down proteins, fats, + carbs for absorption
Primarilyamylase
__________ and
_____________
lipase

Jobs of the Liver

Synthesizer
Makes

Clotting (from hemostasis)

_________________
albumin
________________
factors (creates osmotic pressure)

Detoxifier

alcohol drugs, + other toxins

Converts ___________,

Metabolizer

glycogenfor glycemic reg.

Stores glucose as _____________
Amino acidsinto urea
Breaks down ___________________

Secretor

bile to secrete into ____________

duodenum
fat
Makes _______
for intestinal _____
absorption
Bilirubin goes along for the ride
enzymes

Hepatocytes need _________ to do their job, which is where

Alanine aminotransferase (ALT) &
Aspartate aminotransferate (AST)

LIVER

come into play. If these 2 enzymes are ._______________.

Review Where do all the RBCs go?

RBCs live 120

________ days
Old RBCs get trapped (senesced)spleen
in the
________
Phagocytized by splenic macrophages
Amino
Globin from hemoglobin acids
_______________
iron

Spleen
releases 2 heme breakdown
bilirubin
products
__________
__________

If the bone marrow is stimulated, new

More about Bilirubin

RBCs break down, Hb gets released,

hem into
broken
e
globin and
________
__________

The
first blank
breaks further into
iron
bilirubi
________ & ____________
n

Free = unconjugated
=liver
insoluble
albumi
n
bilirubin
Must bind to ___________ in _________ to be
bile
excreted
Bilirubin is thus conjugated and soluble

the importance of bilirubin

It causesjaundi
___________, which we can
measure ce
What if conjugated bilirubin is ?
Problem must be before/after? the liver
If bile cant be excreted, stools become
lighter

Jaundice

biliru
=accumulation of
__________ in the blood,
bin
which deposits in
tissues, leading to
yellow skin + sclerae
CAUSES:
Cirrhosis
Tumor obstruction of biliary tree
Liver failure
Choledocholithiasis
Hemolysis
Pancreatitis

Jaundice

Prehepatic = before the liver

Extra bilirubin released heme
from _____ breakdown

Intrahepatic = in the liver

Cant remove or conjugate bilirubin

Posthepatic = after the liver

Whats after the liver?
What color will stools be?

Alcohol-Induced Liver Disease

= sequence of liver problems caused by

excess firewater
Fatty liver disease
Alcoholic hepatitis
Alcoholic cirrhosis

Alcohol-Induced Liver Dz

Alcohol + the Liver

Liver processes most of alcohol ingested

Alcohol
_______________________
is the key enzyme
Dehydrogenase
Gets or ? Regulated upon more alcohol

Produces acetaldehyde
Free
+ radicals
__________________
The latter cause ATP
cellular damage
Acetaldehyde
stops _________ production,
fibrogenesis
cells swell, and _________________.

Alcohol-Induced Liver Disease SEQUENCE

Fatty Liver

=Steatosis
___________
From altered cellular metabolism
Is this reversible or irreversible?
Usually symptomatic or asymptomatic?

Alcohol-Induced Liver Disease SEQUENCE

Alcoholic Hepatitis

= diffuse liver
inflammation
________________necrosis
& ____________
chronic
usually caused by acute binge
+ ___________
alcohol ingestion
From toxic damage to hepatocytes +
inflammatory
nonspecific
_______________ response
S/Sx:
_______
_________, those of liver failure +
RUQ pain,
fever
portal HTN

Can progress rapidly to liver failure

Alcohol-Induced Liver Disease SEQUENCE

Alcoholic Cirrhosis

= liverfibrosi
_________ caused by chronic alcohol
s
ingestion
= End-Stageinflammati
Alcoholic Liver Disease
From
chronic
scarring
on______________ leading to diffuse
_____________.
How is this different from hepatitis? (hint: scarring)

Fibrous tissue replaces function

stroma/parenchyma(?)
Presence of nodules + constrictive bands

hepato
S/Sx:

RUQ

________megaly, _____ pain, those of liver failure,

portal HTN

Cirrhosis

= liver scarri
__________ that usually leads to
ng
Portal
__________________
andliver
________ failure.
#1HTN
cause alcoholis
= _____________ (obvious)
m
S/Sx:
______________
Hepatome
galy
_____
RUQ pain
Those of portal
______
HTN
Those of liver failure

Portal HTN

= pressure in the portal

(arterial/venous?) system that causes
blood to backup to other abdominal
organs
Many causes
Alcoholic hepatitis
Cirrhosis
Left or right-sided heart failure?
Portal vein thrombosis

Portal HTN

Mechanism:
Prehepatic
Intrahepatic
Posthepatic

Normal path of blood flow = abdominal organs liver

The HOW of S/Sx

Portal HTN

hydrostatic
pressure in
peritoneal
capillaries

Splenomeg
aly

Portosystemic
shunting of blood

Ascit
es

Anemi
a

Hemorrhoi
ds

Hepatic
encephaly

Leukopeni
a

Thrombocytope
nia

Liver Failure

= loss of
80___-___% of hepatocyte fxn
90
Hepatocyte
damage
+ _____
AS____AL
enzymes
T
T

Due to:
Alcoholic damage
Other toxic damage (acetominophen)
Cirrhosis
Hepatitis
Metastasis
Genetic disorder

Liver Failure S/Sx

TONS of signs and symptoms due to

disorders of
Synthesis and storage fxn and
Metabolic and excretory fxn

Gallbladder Problems

Cholelithiasis
Gallston
_______________
in the gallblad
________________
es
der
Cholecystitis
________________
inflammati of thegallbladde
______________
on
r
Choledocholithiasis
_________________
gallstones
in thebiliary
___________ tree

Cholangitis
_______________
of thecystic
_______ &/or common
inflammati
bile
on duct

Gallbladder Problems

Cholecystitis is caused by some sort of

obstruct
______________
that leads to bile
________
stasis
+ion
inflammation
May be caused by
cholelithiasis
___________________
Can become infected

Cholangitis is caused
by
choledocholith
iasis
__________________
obstruction
Stones cause _____________
which leads to
inflammation
bile stasis which leads to pressure and
_________________

Gallbladder S/Sx

Cholelithiasis is often
symptomatic/asymptomatic
Choledocholithiasis is almost always
symptomatic/asymptomatic
Cholecystitis
RUQ
+ Cholangitis
_____ pain, especially
Right after fatty meals
Referred to the
__________________
shoulder
Vomiting
Fever
Leukocytosis or cytopenia?
Hyperbilirubinemia (conj or unconj?) + AST
& ALT

Gallbladder problems may lead to

PANCREATITIS

= inflammation of the pancreas

Due to
Choledocholithiasis (obstructs
Biliary
_______________!)
tree
Infection
Surgical trauma
Drugs
Alcoholism

Pancreatitis S/Sx

Something causes pancreatic

inflammation
If ampulla (Sphincter of Oddi) is
AST
obstructed, s/sx
may include
hyperbilirubinemia (conj or unconj?) AND
ALT
liver enzymes ____ +
_____

Pancreatitis How?

Cells release digestive enzymes to

surrounding tissue
amylase+lipase
_________
____________ autodigestion
These enzymes destroy pancreatic
insulin__________making cells hyper/hypoglycemia?
Also activate pathways leading to dystrophic
calcification hypo/hypercalcemia?
Causes more inflammation
SHARP pain radiating
to ______
BACK
Fever, vomiting

Leads to diffuse vasodilation + fluid loss

_____________,
hypotensi tachycardia, hypovolemic + septic
shock

Cardiovascula
r

Arteries

Thick walls
Highly elastic, stretchy
_______
pressure
high
Lowvolume
__________

Artery Disease

blood flow to / from tissues

Common end result = I s c h e m i a

Atherosclerosis

Paste-like changes leading to hardened

arteries
Causes these
Coronary Artery Disease
Chronic Ischemic Heart Disease
Acute Coronary Syndromes

Congestive Heart Failure

Cerebrovascular Accident (stroke)
Peripheral Vascular Occlusive Disease

40

> ____% of deaths in US

Atherosclerosis COMMON VESSELS

1.abdominal
___________ aorta & iliac arteries
2. Proximal
___________ artery
coronary
3. thoracic
___________ aorta, femoral, popliteal
aa.
4. Internal carotid artery

Atherosclerosis Risk Factors

#1 risk factor
=
HYPERCHOLESTEROLEMIA
_________________________
Smoking, HTN, Diabetes Mellitus, male
sex, older age, family hx

Atherosclerosis Vessel Changes

_________
streaks
Fatty
Macrophages + smooth
_________ muscle cellslipids
+ _______ =
Foam
__________ cell.

atheromatousplaque
Fibro_____________
Foam
_______ cells continue to necrose, fatty core grows,
highly unstable

Complicated Lesion
From the plaque breaking open
ISCHEMIA
ANEURYSM (balloon-like bulge in vessel)
THROMBOSIS (subsequent EMBOLISM)
ACUTE OCCLUSION of VESSELS due to IMMUNE
RESPONSE

Atherosclerotic Occlusive Dz

= PVOD, PVD
= Atherosclerosis
in ____________ vessels
peripheral
__________ of vessel & subsequent
stenosis
ischemia of any tissue downstream.
W H E R E?
__________
is most common
LEGS
femoral
_____________ &
______________ arteries
popliteal
60-70 y.o. males
Smokers, hypercholesterolemia, Diabetes,
HTN

PVOD Manifestations

No s/sx appear until

50 ___% stenosis!!!!
S/sx are gradual & progressive,
starting w/
claudication
Intermittentskin
_______________
Cool,pulse
thin, pale _______
Weak ___________
S/sx develop
into
rest
Pain @ ________ skin
ischemia
Necrotic,
cold,
purple
______
thanks
to
absent
__________

Acute Arterial Occlusion

Unlike PVOD which is over decades, this

is acute blockage of an artery
THE SEVEN Ps of Acute Arterial
Occlusion
Istol
shot
P______
allor ________ (acute onset)
P_________
(pale)
olar
ulseless
P_________ (cold)
P______ ness
Parasthesias
Pain
Paralysis

Veins

thin
_______ walls

_______
volume
high
_______
pressure
low
Must oppose gravity, and thus utilize
valves & muscle pumps.

Chronic Venous Insufficiency

= peripheral veins are unable to return

right
blood to the _______ side of the heart
Often due to
hrombosis
D_______
eep
einV_____
T_____________
Mm. pumps & valves
fail RETROGRADE
pressure
flow
thanks to gravity __________
fluid
buildup, _________ backup.

Chronic Venous Insufficiency

Pressure & Fluid buildup EDEMA,

CONGESTION
Impaired tissue nutrition
DERMATITIS

STASIS _______________
Minor injury
ULCERS

STASIS __________

CVI - Manifestations

Frequently occurs onmedial

the _________ aspect
of lower
__________ legs ! ! ! !
Stasis
_____________
dermatitis
Thin, shiny, purple-ish grandma legs
Thanks to blood not being recycled and just sitting
there, tissue not getting need nutrients

Stasis
_________
ulcers
Painful or painlesspainless
?

Why? Id guess b/c blood is not able to get to the

damaged tissue & bring along its healing factors, which
are what bring pain, and which manifests
itself in the
vascular
___________ stage of inflammation
to
capillarythanks
permeability
____________ _______________.

Tx w/ pressure dressings & grafts

Pressure Ulcers

= Decubitus ulcers
= Bedsores
WHO???
Anyone Decreased
mobility
w/ ___________________.
Worsened by poor nutrition, poor blood flow, & poor
sensation
Assisted living
ICU patients
Surgery
Fracture
Diabetes (via blood flow)
NOTICE, OBESITY is NOT on here The adipose
tissue literally serves as a cushion to prevent trapped
blood flow and oxygen deprivation.

Pressure Ulcers Where?

>95
___% occur in thelower
________ half of body
Sacrum
___________
Coccyx
___________
Ischial Tuberosities (butt bones)
Posterior heels

PREVENTION
Identify those @ risk
Position
change(at least q 2 hours)
Frequent
__________________
Soft surfaces (one benefit of obesity)
Hydration, nutrition

TREATMENT
Alleviate pressure (duh) & address the risk factors
Moist dressings
Surgical debridement (removal of nasty dead tissue)

Cardiovascula
r

II

Freidhoffs Favorite Formula

BP = CO
_____ x PVR
_______

BP=
x _____)
x
SV(____HR
PVR
_______

Basics of BP Regulation

Short Term
neural
___________ & some hormonal activity

Long Term
Days, weeks, months
_____________
hormonal via kidneys, adrenal, etc.
SHORTTERM

BP
Stimulate baroreceptors
SNS

-1
activation

_____________

HR
(which
CO)

BP

-1
activation
vasosconstriction
_____________
(which
PVR)

BP Regulation Short-term Hormonal

Renin-Angiotensin-Aldosterone System
RENIN
Released by
kidneys
____________ in response to B.
Flow
Angiotensin I
angiotensin
Fxns to convert ______________ to
________________
lungs
ACE
Ang II

ANGIOTENSIN I/II

vasoconstriction
Ang. I ____ enzyme in _______ _________
aldosterone
Ang. II fxns to cause ________________, & also
stimulate _____________ release

..BP Regulation Short-term Hormonal

ALDOSTERONE
Released from
___________ gland
adrenal
Causes
_____ reabsorption, and thus
Na
H2O
_____ retention.
Causes
K____ &
H____ secretion & excretion
from renal tubule

ANTI-DIURETIC HORMONE (aka ADH or

VASOPRESSIN
)
Posterior
pituitary
Released from __________ ____________,
stimulated
by blood volume
vasoconstrict
Fxns to ______________
H2O
Fxns to ________ retention & thus dilute

Hypertension

= high blood pressure

NML = systolic- <120/ diastolic - <80
REVIEW: Systole = ventricular
_____________
contraction
REVIEW: Diastole = ventricular
_____________
Relaxation/filling

PRE-HTN = SBP @ 120-139, DBP @ 8089

STAGE 2 HTN = SBP @ >160, DBP @
>100

HTN - Types

Primary, essential
aka ___________, accounts for
95% of HTN
There is also Secondary HTN (from a
previous disorder), and Malignant HTN,
which is rare but life-threatening

Essential HTN Risk Factors

_________ ___________
Family
History
Age
_____
Race
_________
More prevalent & severe
in __________ people
black

Metabolic
_______________ Syndrome X
risk factors)

(just a group of

hyper
Insulin resistance, leading to
________glycemia
TG
HDL, LDL cholesterol
Abdominal obesity
Atherosclerosis/Coronary Artery Disease

Essential HTN Lifestyle Factors

Salt Intake
Diet
(______
DASH diet Dietary Approach to Stop
HTN)

Obesity
Apple shape

Excessive Alcohol
> 3 drinks/day

Oral Contraceptives
Stress
Activates SNS

Most Effective Ways to HTN

1Weight
loss
= _________ _______
2 DASH
= ________
diet
3 = Na intake
4 = Physical Activity
5 = Moderate Alcohol Consumption
actually helps

Essential HTN - Manifestations

Basically,
no_____ s/sx
Effects appear only after long-term
damage.

BRAIN
EYES
HEART
BLOOD VESSELS
KIDNEYS

Orthostatic Hypotension

= postural hypotension
BP uponstanding
_______________
How do S/Sx happen?
From activation of BP Regulators,-1
i.e. _____
&
-1
_____ receptors, which activate
the _____________
sympathetic
nervous system
(_____ fxn to cause vasoconstriction,
____ fxn to cause
-1
-1
HR)
Causes HR, anxiety, sweating

Cerebral

Flow

From _____________ Blood ________

Causing dizziness, nausea, headache, spinning, white
out

Orthostatic Hypotension

What goes Wrong?

Blood Volume, aka

______________
Hypovolemia
Not enough blood returning to the heart

Drug-induced
ACE
______-inhibitors (b/c they dont allow angiotensin to
get converted and do its
job of ________________)
vasoconstriction
Aging
Mm. pumps & valves fail cant return enough blood!

Bed Rest
Weaker muscles/muscle pumps
blood vessel tone

ANS Dysfunction
B/c it doesnt allow for proper
_____ response
SNS
E.g. Guillan-Barre

Coronary Blood Flow

Coronary arteries basically start at the

level of the aortic valve and spread
distally down the heart from there

Coronary Artery Dz & Chronic

Ischemic Heart Dz

Coronary artery disease is broken down

chronic
into two categories,
_________
or
acute
___________.
If ACUTE Acute Coronary Syndrome
(MI, unstable angina)
If CHRONIC Chronic Ischemic Heart
Disease
Stable Angina
Silent Myocardial Ischemia

Coronary Artery Dz

Stable/Fixed plaque
75(___% stenosis) Stable
angina
__________, silentischemia
___________
Unstable plaque
Minor disruption Unstable Angina
MAJOR disruption MI
Disruption of any kind is going to lead to aggregation
of platelets and healing factors to stop the lesion,
s/sx depend on how large of a disruption &
subsequent healing response
lipid ruptures? Stress,
What causes these plaque
cap and esp. the size of the ________ core
degredation,
relative to its weak fibrous _____.

Chronic Ischemic Heart Dz

Ischemia
____________ = pathological in blood
flow which affects organ fxn
____________
Angina
= to strangle or choke
The
______ that results ischemia
from _____________
pain

Chronic Ischemic Heart Dz

Stable Angina

= chest
______ at times of cardiac
pain
oxygen __________
demand
Relieved by
rest
_________

Due to Fixed
a _____________________
plaque
atherosclerotic
causing ischemia
Coronary artery stenosis must 75
reach ____%
Incredible how well the heart can compensate

Chronic Ischemic Heart Dz Silent Ischemia

= ischemia without
_________ (aka pain)
angina
NOTE, there is a huge difference between
ischemia and infarction.

Acute Coronary Syndrome

= acute results from ______________s

of
disruption
unstable atherosclerotic plaques.
Unstable Angina
Non-ST-Segment Elevation MI
St-Segment Elevation MI

ACS Unstable Angina & Non-STElevation

= chest painrest
at _______ or w/ minimal
exertion
Cardiac enzymes

MI occurs if there is presence of

___________, which indicate cellular
damage (aka necrosis) has taken place.

enzymes
NON-ST-Segment MI =minor
MI, so presence
of _________, but is a result of a _________
plaque disruption & response Just a

ACS ST-Segment-Elevation MI

Ischemic death of cardiac tissue

causing severe, crushing angina pectoris
= Heart attack
Necrotic myocardium releases
__________
enzymes
Creatine kinase, myoglobin, troponin

FromM_________
A J O R plaque rupture leading to
_____________
thrombosis & acute occlusion
Thickness of
the __________cap
______ is crucial
Fibrous
Tissue factor stimulates the
fast ___________
extrinsic
pathway, and
the slow ____________ pathway
intrinsic
goes along for the ride too.

ACS ST-Segment-Elevation MI

S/Sx:
Severe angina (referred to jaw & left arm)
Tachycardia
Dyspnea
Fatigue, weakness
Hypotension
Pale, cool skin

Cardiovascula
r

III

Review

Cardiac Output = Measure of cardiac

efficiency
5
Average adult CO ___ L/min
reserve
% increase above normal = cardiac
____________

Stroke Volume
Volume of blood pumped w/ each contraction
(aka systole)

HR
Ifdiastole
HR gets too high, what happens?
There isnt as much time for the heart to refill with
blood, aka _________

Cardiac Principles

PRELOAD =
__________ ___________,
___________ the
Blood
volume which
stretches
cardiac muscle
Occurs at the end of diastole, or diastole
systole?
____________
SV
Activates Frank-Starling mechanism to
___
Blood

pressure

AFTERLOAD =

systole
_________ ___________ needed to move that
load
Occurs at the start of diastole, or systole?

Cardiac Principles

CONTRACTILITY = Mechanical
performance of the heart based simply
myosin
on
the strength & # of _________ fibers in
the cardiocytes.

Heart Failure

= the heart cant pump enough blood

forward to meet the bodys needs
Supply < Demand
Can be characterized as all of the
following
-output vs. -output
Systolic vs. Diastolic
Right-sided vs. Left-sided
Compensated vs. Uncompensated

 output & output heart failure

Output refers to cardiac output

HIGH () output failure
More or less common?
less _______
Caused bydemand
____________, not a bad heart
muscle
E.g. hyperthyroidism
Graves
Whats the primary hyperthyroid dz? ___________ Disease

LOW () output failure

Caused
by disorders
Pumping
ability that impair the
______________________ of the heart
Chronic Ischemic Heart Dz, Acute Coronary
Syndrome

Systolic vs. Diastolic heart failure

SYSTOLIC
Due to impaired
_______________ &/or
contractility
pressure
SV
Ejection fraction (aka ____) gradually as
ventricular fxn
Think about it as the heart having to work
against abnormally hard load over a span of
decades
Chamber
size
DIASTOLIC
Tachy
filling
Due to smaller ventricular ___________
________
_________cardia less diastolic ________ time

Right-sided vs. Left-sided <3 failure

First, lets get the blood flow down

R.
Ventricle

________
LUNGS

Pulm.
___________
arteries

atrium
L.

Vent.
L.

______

______

Pulm.
veins
___________

BOD
Y

R.
Vent.

Right-sided vs. Left-sided <3 failure

RIGHT-sided

lungs
Aka restricted blood flow into the
_________
Wait, how does that make sense?
If its hard to get blood into the lungs for whatever reason, that right
ventricle is going to work its ass off to try and get blood into the
lungs. Over time, it will work too hard, fxn will , and fail.
ventricles do not have asses

Common cause?left
______ sided-heart failure
Wtf how does that make sense?

The left ventricle pumps blood to the whole body, via the arteries. If it
gets way too hard for the left ventricle to overcome the pressure
needed to effectively pump blood throughout the whole body (e.g.
HTN), then blood that normally would have gotten dispersed
everywhere doesnt get pushed far enough and just chills. One of the
places it chills is going to be in the lungs, b/c, as you know, blood
goes from the lungs LV body.
Blood does not literally chill
Or does it?
Probably not.

Right-sided vs. Left-sided <3 failure

RIGHT-sided
Can also be due to a right ventricular
infarction
cor
pulmonale
Can also be due to pulmonary HTN, aka ____
_____________.

MANIFESTATIONS:

veins
All from blood backup in the ____________
Think about it where does the RV normally get
its blood from?
Peripheral2.2
edema
1 L H2O = ______ lbs

Full jugular veins

Organ engorgement

Right-sided vs. Left-sided <3 failure

LEFT-sided
Aka restricted blood flow into
the
arteries
_____________ b/c of way too much resistance
Chronic Ischemic Heart Disease

MANIFESTATIONS
Are all going to be due to blood backup
lungs in
_______ & tissue perfusion
We talked about this if the LV cant overcome the
pressure to effectively pump blood through the
aortic valve, where is the blood going to chill?

Compensated vs. Decompensated <3 failure

Its ALL ABOUTS/Sx

THE _______
COMPENSATED
Body is able to respond to heart fxn
or maintain the
CO ____ to meet the demand
______________atic
Asymptom

DECOMPENSATED
Mechanisms have given all they can; failing
or maxed CO
Symptom
______________atic

<3 Failure

Compensatory Mechanisms

Frank-Starling Mechanism
Heart failure CO

SV ____ (aka ejection fraction)

End-diastolic volume

Pre-load
_________load (hint: volume)

myofibers stretching
SV _________ CO.

<3 Failure

Compensatory Mechanisms

Sympathetic nervous system

compensation
BP
baroreceptors
Stimulate
_______________
SNS
-1
activation
HR
_____________
(which
CO)

-1
activation
vasoconstrict
_____________
(which venous
ret)
BP

Whichpre

______load

Had to throw this in somewhere

BP = CO
PVR
_____ x _______

BP=
x _____)
x
SV(____HR
PVR
_______

<3 Failure

Compensatory Mechanisms

RAAS in words
The heart is failing. As a result, the kidneys arent getting
enough blood. To try and combat this, they release an
enzyme named renin. Renin is going to circulate in the
blood, find angiotensin, and convert it into angiontensin
I. Angiotensin I literally doesnt do anything, until it finds
its way to the lungs to get converted by ACE (angiotensin
converting enzyme) into angiotensin II. Angiotensin II
actually does something. It is going to cause
vasoconstriction, as well as function to stimulate the
release of aldosterone, a mineralocorticoid that gets
released from the adrenal cortex. Aldosterone will
further help the cause by telling the kidneys to reabsorb
(keep) Na, and thus H2O, and tell it to get rid of
(secrete/excrete) K & H. All of this to blood volume
and get the heart delivering blood to where it needs
delivering. Very neat.

<3 Failure

Compensatory Mechanisms

Myocardial Hypertrophy &

Remodeling
larger
A ___________ muscle can do more workin
theory
Result of long-term compensation
(left) ventricular
Doesnt work out too well in the end..
Ventricular hypertrophyafter
can lead to
___________ dysfunction pre
Pressure overload ________load
Volume overload _________ load
LEFT side!!!!!!!!!

Acute Pulmonary Edema what sided

SHOCK

= circulatory failure
= Vascular system cant get enough
blood to the body organs & peripheral
tissues
CLASSIFICATIONS:
Cardiogenic
Hypovolemic
Septic
plus a few more

Shock How?
Cardiogenic

failure
<3
_________________
causes terrible perfusion
PVR attempts to regain perfusion worsens failure

Hypovolemic

___ _________________
blood volume

causes terrible perfusion

Septic

infection
Systemic response to
_____________ leads to
Diffusevaspodilation
________________, therefore terrible perfusion
Essentially anti-Frank-Starling mechanism b/c it
pre
_____load
QUICK: What are the 3 steps of acute vascular inflam. stage?
vasoconstriction vasodilation
___________________, __________________,
capillary permeability
_____________________________________

Shock - Manifestations

Thirst
Tachycardia
Cool, pale extremities
Capillary filtration pressure
___ capillary
<
osmotic press. Pulled in, sucked up
So interstitial fluid gets ____________________.

Diaphoresis
Tachypnea
Hypotension
Stupor

Shock - Complications

Acute Respiratory Distress Syndrome

Aka shock lung
24
___-___
48hrs after trauma
Diffuse inflammatory reaction in body
damages lungs
>50% mortality
Renal

Acute _________ Failure

GI Problems

b/c the GI system is dispensable

DIC
Multiple Organ Dysfunction Syndrome

Respirato
ry
Disorders

Mechanics of Breathing
The main stimulus to breath is
___ _______
PaCO
COPD
_______ sufferers are the exception to this!
They depend on
___ oxygen
_______ to drive breathing

INSPIRATION
Negativeintrapleural
________________ pressure is key
The small space between the visceral and parietal pleura

EXPIRATION
Elastic recoil, thanks to elastin

Thediaphragm
____________ is the main breathing muscle

Flattens with inspiration more thoracic space

intrapleural pressure atmospheric air wants to equalize
that pressure
Innervated by thephrenic
__________ nerve -C3
___,___,___,
keep you
C4 to
C5
alive
Accessory muscles = inercostals, abs, neck muscles

Lungs: Compliance vs. Resistance

COMPLIANCE
inflate
= how easily the lungs
_____________
elastin =compliance
_____________
collagen, scar tissue
= ___ compliance

Surface Tension
= force causing the alveoli
to _____________
collapse
surfactant
A ____________ is a molecule that surface
tension
surfactant
___________ = surf. Tension = ___
surfactant
compliance
___________ is low in premie babies so its
hard for them to breath

Lungs: Compliance vs. Resistance

RESISTANCE
How easily
________________________
Air flows
through the tubes
Proportional to 1/4r
Aka, if the radius gets cut in half, resistance 16
x. Yikes.

Thats why when you aspirate, or mucous

secretion , it gets a LOT harder to breathe

S
The __NS dilates the airways to ___ resistance

P
The __NS & histamines constrict airways, __
resistance

Lung Volumes

TIDAL volume
Volume of air inhaled & exhaled w/ each
breath

VITAL capacity

exhale
The max amount of air you can _______ after
full respiration

RESIDUAL volume

exhalation
The amount of air left after maximum
V C
_____________
Aka left over after __.__.
Residual volume
Vital Capacity

TOTAL LUNG capacity

____________________ + ______________________

Ventilation vs. Perfusion

VENTILATION
Gettingair
______ to
____________
alveoli
PERFUSION
Getting
_______ to
____________
blood
tissue
Abbreviated as Q

Unique feature to the lungs = hypoxic

_________________
vasoconstriction
Why?
B/c alveoli = socialists. They want to redistribute
the wealth; when alveoli arent getting the O they need,
they share it with other, better O-supplied alveoli by
telling their surrounding vessels to vasoconstrict. This
redirects O blood to better ventilated (air) alveoli,
which are then able to effectively maintain a V/Q ratio

Respiratory Disorders S/Sx

Dyspnea labored
= _____________ breathing
Orthopnea

Lying
down
Dyspnea when
_________ _________
Relieved by upright position

Paroxysmal Noctural Dyspnea

Sudden dyspea night

@ _________
LV
Due to acute pulmonary edema (LV or RV failure?
_____)

Kussmaul respirations

Verydeep
______ breathing often fast
Fast breathing =
______ventilation = compensation for
aci
metabolic
_____osis.

d
Cheyne-Stokes
Respirations

Sporadic deep & shallow breaths

Due to problemsbrainstem
w/ __________ (which controls breathing)
Head injury

Ventilation vs. Pneas

Hypoventilation & hyperventilation
Describe how much air reaches the
__________
alveoli
Aka depth of breath
HYPOventilation _________capnea
hyper
HYPERventilation_________capnea

hypo

How I think of it:

If you arent taking deep enough breaths and allowing
the CO to be exchanged in the capillaries and effectively
released, it is just going to stay stuck in the alveoli. Think
of holding your breath the ultimate form of
hypoventilation and what it is that, after 2 minutes,
builds up and causes you to exhale, gasping for oxygen..

Ventilation vs. Pneas

Apnea & Tachypnea

Describe the
rate______ of breathing
Apnea = not breathing
Tachypnea = fast breathing

Resp. S/Sx Cough + Cyanosis

Major protective mechanism activated in the upper
airways.
opiods
Cough stimulus is suppressed by __________!
Productive cough = produces
sputum
blood
HEMOPTYSIS = coughing up ________
Due to damage to lung tissue & vessels

vomiting

HEMATEMESIS = ___________ blood (a GI problem)

CYANOSIS

blue
________-colored
skin from severe hypoxemia
Oattached (absorbs different spectra,
Hb without ____
From ____
hence color-chance, when O is/isnt attached
Sickle
celldisease orThalassem
Sufferers of
_______ ________
_________ia may be
severely hypoxemic, as evidenced by excruciating ischemic
pain, but may not be cyanotic b/c they dont haveHb
enough
____ cells in the first place for us to see their color.

Results of Pulmonary Dz/Injury

HYPOXEMIA
HYPERCAPNEA
PLEURAL EFFUSION
ATELECTASIS
PNEUMOTHORAX

Results of
Pulmonary Dz:

Hypoxemia & Hypercapnea

= PaO
arterial
______ in the
___________ blood
Dont confuse this with hypoxia, which is
O to _______
cells
HYPERCAPNEA
= PaCO
______ in the
___________ blood
arterial
Almost always from diffuse
hypo
______ventilation
Brainstem injury
Diffuse V/Q mismatch

acid

primary respiratory _______osis

Results of
Pulmonary Dz:

Pleural Effusion

= excess fluid in the pleural cavity

FLUID

SEROUS

NAME

Hydrothorax
______________

PUS

Empyema
______________

LYMPH

Chylothorax
______________

BLOOD

Hemothorax
______________

Results of
Pulmonary Dz:

Pleural Effusion

= excess fluid in the pleural cavity

MECHANISM:

TYPE OF PE:

capillary hydrost.
Hydrothorax
______________
pressure
capillary osmotic
Hydrothorax
______________
pressure
cap. permeability
Infx, inflammation

Empyema
______________

lymph drainage
Hemorrhage

______________
Chylothorax

Hemothorax
______________

Results of
Pulmonary Dz:

Pleural Effusion

S/Sx
The
_____________ is much more important
timeframe
than
the fluid ____________
amount

Results of
Pulmonary Dz:

Atelectasis

= Lung
____________
collapse
May be total or partial
Due to.
Obstruction
________________
Very common after surgery

________________
Compression

Ultimate result of these 2 causes is a

loss of ___ pressure
in the
alveoli
____________,
causing them to
collapse
____________.

Pneumothorax

Results of
Pulmonary Dz:

= air
_____ in the space around the lungs (pleural
cavity)

Normally, ____ pressure in the pleural cavity keeps

the lungs inflated

If the pleural cavity is compromised and you lose this

___ pressure, the atmospheric pressure is going to flood
in to equalize the pressure, causing collapse/shriveling
of the lung

May occur from the INSIDE

COPD, Mechanical Ventilator

Or from the OUTSIDE

Trauma

Results of
Pulmonary Dz:

Open vs. Closed Pneumothx

OPEN pneumo = Communicating

Air enters on inspiration, exits on expiration
May have a same side,
or ________________
ipsilateral
mediastinal shift
From trauma (stab wound, GSW)
Google Image if you dont believe me.

TENSION pneumo - EMERGENCY

Air enters upon inspiration,
but leave
Doesnt
________________contralateral
Severe atelectasis & _______________
mediastinal shift
Think about itif one side of the chest can keep

Pneumonia

= inflammation ofalveoli
the ___________,
interstitium,
bronchiole& ____________s.
From microbes
Bacteria, viruses, etc.

From Irritants
Aspiration, inhalation

Pneumonia

Why do some ppl get sick, but not others?

Big reason = impaired defenses
Nasopharyngeal
1. __________________ defense
Up high/nose area

2.
_________!
Cough

Prevent aspiration

3.
______________ blanket
Mucocilliary
Remove bad stuff from respiratory tract

4. Pulmonary
______________
macrophages

Phagocytize bad stuff from lungs

Pneumonia Typical vs. Atypical

Describeswhere
______ infx & infl. occurs in lungs
TYPICAL

WBCs, exudate, & necrosis inalveoli

____________
bacterial
From ____________
infection
more
More or less severe than atypical?
_______ severe
Due to worse V/Q mismatch

ATYPICAL akaWalking
___________ pneumonia

WBCs, fluid in outside thealveoli

____________
Patchy Latticework
viral infection
From ___________
less
More or less severe than typical?
_________ severe

alveoli

Why? b/c _____________ arent as affected

MEMORY TRICK? Atypical aint as awful as alveoli arent affected (as much)

Pneumonia

Community vs. Nosocomial

Currently used way to classify pneumonia

COMMUNITY acquired pneumonia
From organisms found outside the hospital
_________ ____________
Strep
pneumoniae
Thick capsule prevents effective phagocytosis
Sowhat do we need to kill encapsulated
bacteria???
Ab
spleen
B
___-cells to make ____, & a functional __________

H-flu, mycoplasma, viruses

Pneumonia

Community vs. Nosocomial

HOSPITAL acquired pneumonia

Aka,
_______________
nosocomial
Pseudomonas aeruginosa
Staph aureus
E. Coli (very common hospital bacteria; also
primary suspect
UTI in _____s)
Diagnosed > 48 hrs after admission
HIGH mortality, difficult to treat
Why? These bugs are floating around a place that
is flooded with medication, medication, and more
medication. For them to have survived long
enough means they have developed resistance to
many of these antibiotics and medications.

Pneumonia

Community vs. Nosocomial

NOSOCOMIAL risk factors

NG tubes
Post-op
Mechanical vent
Pain meds, opioids
i.e. __________
Why? They suppress
the _______ defense reflex
cough
The 3 other defenses
= _________________,
______________
nasopharyngeal
mucocilliary
blanket, & ___________________
Pulmonary
macrophages

Pneumonia in the Immunocompromised

From organisms that dont usually cause

sickness in normal people
AIDS plays huge role in this!!!!!!

Pneumonia Manifestations

Fever, myalgias, anorexia

Hemoptysis
Pleural effusion
Just about everything else

Respirator
y
Disorders
II

Quick Review

TIDAL volume
Volume of air inhaled & exhaled w/ each
breath

VITAL capacity

exhale
The max amount of air you can _______ after
full respiration

RESIDUAL volume

exhalation
The amount of air left after maximum
V C
_____________
Aka left over after __.__.
Residual Volume
Vital Capacity

TOTAL LUNG capacity

____________________ + ______________________

Obstructive vs. Restrictive disorders

OBSTRUCTIVE
COPD
_______________
Emphysema
Chronic
______________
Bronchitis

Aint nobody got time for that

RESTRICTIVE

Obstructive disorders

= lung disease causing

______________
resistance
& difficult __________ation.
expir
Remember what resistance = ?
Problem lies in bronchiole
the __________s
& ____________
alveoli

= lung diseasing causing

_________
residual
volume+TLC
Think, chronic air trappers

Obstructive - Asthma

chronic disorder characterized by

hypersensitive
__________________
airways causing
broncho_______________
& airway inflam.
constriction
TRIGGERS
Allergens
Smoke
Gases
Cold air
Exercise (Im allergic to this)
Infection

Asthma

A trigger fxns to cause 2 things

1.Mast
_______ cells coated w/ IgE get activated
Release cytokines

2. __NS
gets activated bronchospasm
S

What if inflammation lasts too long

Airway
________________
remodeling
Not good

Asthma=bronchospasm
____________________ via sm. muscle of
bronchioles

+ mucus + inflammation =
OBSTRUCTION

Asthma Tx

How would a -1 agonist work?

S
__NS
and thus cause broncho______________
dilation

How would leukotriene inhibitors work?

Suppress
___________ portion of inflammation
cytokine

How would corticosteroids (cortisol) work?

Suppress the
__________ system
immune

Obstructive - Emphysema

= obstructive lung disorder due to loss of lung

_________
________ fibers), destruction of
elasticity(akaelastin
alveolar walls, & enlarged air spaces
Dysfunctional
_________, which helps hold
elastin
airways open
Without it, airways collapse upon _________ation
expir
Pursed
__________ lips help bronchial pressure to force
airways open
Dyspnea ___________ tachypnea

without

In order to make breathing most effective and allow

ventilation?

#1 causesmoking
= ______________
Always have RV & TLC barrel-chested

Obstructive Chronic Bronchitis

=obstructive lung disorder due to

inflammation
mucous
continual airway ________________,
causing
productive
excess ________, a ___________ cough, &
THICK airway walls
Obstruction from mucus plugs &
narrowed, remodeled airways
Pursed lips
help widen airways
without
Dyspneasmoking
___________ tachypnea
#1 cause = _____________________

Obstructive Disorders Overview

The pathology of obstructive disorders is

airways & ___________.
always in ___________
alveoli
Always causesresidual
_________ volume & TLC
Air trappers aka barrel chesters

= asthma, emphysema, & chronic

bronchitis

Restrictive Disorders
= lung diseases causing
_________ changes to lung
fibrous
tissue & difficultinflation
_____________
Pathology lies in the gross lung
_________, not the
tissue
airways & alveoli that = obstructive disorders.
Always have___ vital capacity
Dyspnea __________
tachypnea
with

Why? My logic = b/c lung tissues simply cant hold as

much O as usual (COPD pts can actually hold much
more) so, just like the heart would respond to BP by
HR, the lungs respond to TLC by breathing rate.

Effect on Lung Volumes

LUNG VOLUME

OBSTRUCTIVE
disorder

RESTRICTIVE disorder

Tidal Volume

Nml or
___

Usually
___

Vital Capacity

Nml or
___

___

Residual
Volume
Total Lung
Capacity

____ (trapped air)

___

(trapped air)
____

___

Pulmonary Embolism
thrombus
= small
______ (embolism = dislocated
thrombus) that has traveled through
blood stream in the pulmonary vessels
Thinkwhich circulation must this
embolism have
come
Veno
u s from? _____________
circulation

Why wouldnt it go to the brain, for

example?
venous
B/c it would never get the chance; the lungs
are the last stop for embolisms originating in

PE Risk Factors

Stasis
Venous
___________
Bed rest
Post-op
Inactivity

Endothelial
______________ Injury
Diabetes
Surgery
Smoking

coagulability
Hyper_______________
Pregnancy, OCP
Cancer, smoking, Factor V Leiden mutation
osis
Thrombocyt_____

Pulmonary HTN S/Sx

Dyspnea
Fatigue
Possible s/sx of right or left-sided heart
failure?
RIGHT
right
_______, b/c the _________ ventricle is
struggling to push against a high fluid force in
the lungs in order to get rid of CO, O
blood

Secondary Pulmonary HTN

= pulmonary
artery
___________ pressure
caused by other disease
Pulmonary Embolism
Microthrombi in Lungs (DIC)
Pulmonary fibrosis (which would
be a
restrictive
_________ dz)
LEFT
COPD
_______-sided heart failure left
b/c it isnt getting sucked out by the ______
ventricle to get sent throughout the body

Secondary Pulm. HTN

draw the lines

Pulmonary embolism
Pulm. microthrombi
Pulmonary fibrosis
COPD

think hypoxic drive

Hypoxic
Vasoconstricti
on
Pulmonary
Cong.

altitude
Left-heart failure
Mitral valve stenosis

Pulmonary
Vascular
Obstruction

Cor Pulmonale

= RIGHT
______-sided heart failure due to
pulmonary artery pressure (pulmonary
HTN)
If blood is backed up in the lungs, which side
of the heart is not going to like that? aka,
have a hell of a time pumping against it over
long spans of time?
MEMORY TIP:
Cor is Latin for of the heart
To remember which side of the heart it causes
failure of, look at the last letter in cor
corrrrrrrrrright-sided <3 failure

after
Will this pressure backup result in

Acute Respiratory Distress Syndrome

= diffuse inflammatory
___________ &
alveolar
pulmonary capillary damage leading to
resp. failure
= Huge reaction involving tiny
structures
Acute cellular
Never a primary
dz damage
HOW?
Diffusecytokine
___________ release
Influx of
_________________
inflammatory
cells to the LUNG
More
______________ get released in the lungs,
cytokines
Free
radicals form
many
_______________

ARDS - Tx

Lungs will look

__________ on x-ray thanks
white
to huge amounts of inflammatory cells
Tx is supportive only mechanical
ventilator..

Respiratory Failure
= lungs cant exchange
O ___ &
CO
____ at alveolarcapillary membrane leading to hypoxemia &
hypercapnea
Out of
B/c normally, O wants to diffuse _______ the alveoli in
order to get into the vessels and
intointo the body that needs
it
CO normally wants to diffuse _____ the alveoli so it can
get out of our bodies and into the atmosphere

= PaO < 50mmHg & PaCO > 50 mmHg

hypoxic

Cannot use this diagnosis w/ COPD pts b/c they live

based on their __________ drive and chronically O

ALWAYS leads to hypoxemia, but not always

local
hypercapnea

diffuse
Hypercapnea
is determined by whether it is a _______ or
___________ affliction.

Respiratory Failure Hyper CO

I M P O RTA N T
HYPERCAPNEA occurs
based on whether it
occurs as a LOCAL or D I
F F U S E problem.

EXAM 4 CONTENT

Musculoskelet
al
Disorders

Quick Review

Ligaments connect
bone
_________bone
to __________
muscle
bone
Tendons connect
__________ to
__________
Strains apply muscle
tendon
to
s
____________/_____________
ligame
nts
Sprains apply
to _______________
build
Osteoblasts ___________ bone
Create bone matrix matrix
Responsible
for making a _______ of collagen
Crush/reabs
+ bone orb
PTH

Osteoclasts ___________ bone

matrix
Release calcium into blood via _____

Strains

= Stretch injurymuscles
tendons
to _________
or
___________
back
Most common
overuse in the upper or lower
________
Due to ___________, not really an acute
injury
S/Sx:

NORMAL

Some pain, still fxnl

External appearance =
Usually doesnt show on xray

Sprains

ligament
= Stretch injury to
a ___________
Stretch, torn, ruptured, may pull bone with it
lateral
Most common in the
medial
________ knee
&

________ ankle
From acute movement or chronic
ACUTE!!! think sports injuries
damage?
(e.g. basketball & football

S/Sx:
Pain

Rapid swelling
______, ______________, heat, bruising, limited
fxn
Dont get confused
though, bones are
More severe than strain, longer
healing time
very well

Meniscal Injury

= tear or avulsion of C-shaped plates

femur
tibia
between
the
_______ & _______
Usually from
______________ movement
rotatio
nal
Plant & pivot

Often occur w/ sprains

Unhappy Triad
= _____,
&
MC
Medial
ACL ______,
_______________L
meniscus

S/Sx:

Instabili
Clicking Locking
Pain, swelling, __________, ___________,
&
ty
osteoarthr
_________
itis

Fractures
Transverse
Across the bone

Greenstick

Periosteum intact; breaks lengthwise (common inkid

____)

s
Child
twistininjuries; possible ________
Around the bone; ___________
abuse
Comminuted g
major like GSW
Many
_______________;
from _______________
trauma
pieces
Compression
crushing
vertebrae
From ___________
(most often in _____________)
osteoporopts
Commonly seen in _______________
Open/Compound sis
Bone fragment breaks through the skin (risk of infection
__________)
Pathologic

Spiral

Fracture due to previous lesion (e.g. tumor, cancer)

Which cancer freq. radiates to the back (and lungs)???PROSTAT

Stages of Bone Healing

________________
formation
Hematoma
CellularProliferatio
____________ &
_________
Callus
n
formation
Ossification
_________________
Remodeling
_________________

1. Hematoma Formation

First 1-3 days

From torn blood vessels essentially
pooling blood
Remember, bone is very well vascularized
Clot

_______ forms a meshwork for bone cells

to work

Steps 2 & 3

Callus
Cellular Proliferation
& _________
Formation
3 4
__-__
weeks
Osteoclasts
______________ destroy
matrix
dead bone, clean up
site
Ossific
Osteoblasts make a ________ of collagen +
bone

________ation

callus
resorb
1-2 months
Take the cast off now
Osteoclasts __________ the
P.S.__________
callus = a temporary
formation of fibroblasts &
Osteoblasts begin to make
new bone, hence,

Bone Healing - Remodeling

Up to6___-___
9 months later
Continuation of ossification
Important to utilize bones/motion in order
to dictatedirection
the ___________ of the bone
fibers & determine
the __________ of the
STRENGTH
new bone

Fractures - Complications

Compartment Syndrome
pressure in a confined space that impairs
= ___________
ischemia
circulation and causes
_____________!
Muscle edema, pressure buildup beneath the
_________
fascia that covers it, nerves + muscles then
become ischemic
Similar to brain hematoma sometimes remove part of
skull
Cut the fascia to release pressure & let muscle swell

S/Sx:
Limb will look nml, pulse will be normal why?
superficial
B/c
arteries
are __________ to the muscle/fascia
parasthesi
Pai
______, ___________,
numbness, loss of fxn
as
n
Fasciotemy if acute

Fractures - Complications

Fat Embolism Syndrome

= fat lobules that travel to organs
other _________ &
lodge in small blood vessels
SEVERE
Usually occur after
_________, ___________
MAJOR
fractures
S/Sx:
Cerebral:
Disorientation, seizures, focal deficits

Pulmonary:
Chest pain, tachycardia, resp. failure

Dermatological:
Petechial rash, thrombocytopenia, bleeding

Osteoporosis

= in bone massdensity
or _________ when bone
> ___ bone reformation.
reabsorption
T or F: the remaining bone is normal
TRUE.
Risk Factors:
Female (especially
Post-menopausal
___________________)
Family Hx
Older Age
White
Smoking
Low calcium high phosphates (drinking too
much pop)

Osteoporosis - Mechanism

___
osteoclasts fxn and
__ osteoblast fxn
Acquiring peak bone mass 30
age ___ is
key

Menopause = ___
estrogen = __
osteoclast activity
physical activity = __ osteoblast fxn &
bone mass
blast
clasts
Role of OSTEOPROTEGRIN
(is this good
s

or bad?)

Osteoporosis S/Sx

UsuallyNON
______ untilfxa ___ occurs!
E

Fx common in:
_______,
HIPS humerus, radius
Vertebrae compression
(____________ fracture)

Decrease in
__________
height
______osis
aka hunchback.
Kyph

Osteoporosis Dx & Tx

Dx
Bone mineral density scans

Tx
Prevention is best
Calcium supplements & Vitamin D
Estrogen & Selective Estrogen Receptor
Modulators endomet
May risk forrial
_____________ cancer though
Calcitonen & Bisphosphates
PTH
clast

Fxn to counteract _______, and thus osteo_______

activity

Future treatment hopes to target

Rheumatoid Arthritis

= Systemic
autoimm
____________ disease causing
une
connectiv
chronic inflammation
of the joint
e
synovium
_____________
tissue, especially
the
__________ (lines the synovial cavity)
Joints
PIP (unilaterally/bilaterally) affected
____
MCP(basically your first finger joints)
____ (make up your palm)
Wrists
Knees
Ankles, Vertebrae

Rheumatoid Arthritis How?

________
Genetic trigger
HelperT__-cells initiate the autoimmunity
Body then makes
rheumato
___________ factorIgG
and
id
____
inflammato
ry_____________ response
cytokines
Subsequent
___________, TNF, IL-1
Neutrophils, Macrophages, Lymphocytes

Chronic jt inflammation
Formation &
ofangiogenesis
new blood
vessels
Angiogenesis
=
____________________________
pannus

Rheumatoid Arthritis S/Sx

Cardinal Signs of Inflammationaka
1.
2.
3.
4.
5.

Redness
Pain
(dolor)
(rubor)
Swelling (tumor)
Heat (calor)
Loss of Fxn

Pannus
__________

angiogenes
From the new vessels, aka _____________,
formed during inflammation
scar
issynovium
Essentially _____
tissue of the
Unique to RA
Lock up
Causes joint to ___________

Joint Subluxation (partial dislocation) & Deformities

(Morning/Evening) Pain & Stiffness?
Fatigue, weakness, anorexia, anemia, fever
Due to chronic autoimmune response

Osteoarthritis

noninflamma
= mostly
________________ disease causing
erosion tory
ofArticular
_________________
cartilage
_____________
joint disease, aka Wear &
Degenerative
Tear
Unilateral/Bilateral
joint affliction?
DIP (distal interphalangeal
jt)
_____
HIPS
Lumbar spine
Knees
joint replacement (think
OA = #1 causehips
of __________________
& DIPs!)

Osteoarthritis How?

As opposed to RA, OA instead is usually

caused by a ___________ of joint damage
history
Sports injury
Overuse
Obesity
E.g. anything more chronic

Subsequent lossarticular
of ____________ cartilage,
loss of shock absorbing surface
Formation of
___________, aka bony spikes.
osteophytes
Can lead to synovial irritation and then
joint
effusion
_________.
Joint mice

Osteoarthritis S/Sx

OA = inflammatory / noninflammatory
NO cardinal signs

Osteo_______
phytes
Spikey growths

Crepitus & Grinding

Leading to
______-___-______
- ouch.
bone
on
bone
Joint Effusion
__________
Extrafluid
______ in the joint space (synovial
cavity) from synovial irriation

Morning / Evening Pain & Stiffness?

RA vs. OA

RA =
____
OA =
____
RA =
____
RA =
____
OA =
____
RA =
____
OA =
____
RA =
____
OA =
____

RA = Formation of pannus
____
OA = morning pain & stiffness
____
____ = osteophytes, grinding, effusion

RA
DIPs)

more inflammatory
no genetic linkage
mostly bilateral affliction
affects proximal interphalangeal jts
affects hips
affects metacarpophalangeal jts
affects distal interphalangeal jts
produces RH & Cytokines
main cause of jt replacements ( think hips &

Male
Genitourinar
y

Hypospadias & Epispadias

= Congenital disorder where the

Urethral meatus is in a weird location.
__________________
Often associated with other congenital
anomalies:
Chordee
Cryptorchidism
Inguinal hernia
Exstrophic bladder
Female masculinization

Hypospadias

Urethral meatus is onventral

the ________ side
Is this more/less common than
epispadias?
Corrected w/ surgery
May just be cosmetic
Done around 6-12 months of age

Epispadias

Urethral meatus is ondorsal

the ________ side of
penis
More/less common than hypospadias?
Surgery is often difficult:
Larger urethral opening & possible
Exstrophic bladder
(Exposed bladder)

Erection & Ejaculation

Somatic
____________
Senses
Feels physical contact

_________________
ParasympatheticPoints
oxide
endothelium
______________
releases Nitric
_______________
vasodilation
Acts on smooth muscle to cause
________________
arterial blood flow to corpus cavernosum &
spongiosum
Sympathetic Shoots & Sighs
_______________
Causes Ejaculation/contractions
____________________
Stops Nitric Oxide release + its breakdown
After ejaculation, opens venous channels
Detumescence

Erectile Dysfunction

= inability to achieve & maintain an

erection sufficient to permit satisfactory
sex.
Due to
Depression/stress
Parkinsons
Stroke
Diabetes
Atherosclerosis

ED - Mechanisms

Problems w/ the nerves & CNS

/ in PNS/SNS?

Problems w/ hormones
Low androgens (libido)

Problems w/ drugs or chemicals

____________
Inhibition of NO formation
/ NO breakdown

Problems w/ the
______________
vessels
Stenosis
SMOKING, DIABETES, ATHEROSCLEROSIS

ED - Treatment

Assess for cardiovascular disease

Major category of drugs that inhibit NO
breakdown
Viagra
Levitra
Cialis

nitrates

Cant use these with ____________ (for

chest pain)
Why??
vasodilation
Drop
in
BP
Because these nitrates,
combined with the preexisting heart medications, cause _______________

Priapism

=abnormally prolonged + painful erection

> 3 hours usually

Due to:
Too much blood in
Not enough blood out ISCHEMIA!!!!!!

EMERGENCY
Bloodstasis
_______Ischemiafibrosis
impotence

Treatment
Pain control
Sedation

Cryptorchidism

=failure of one or both

teste_________ to move
s
down from the abdomen
into the
scrotu
m
___________
=Undescended testes
Directly premat
related to birth weight +
ure age
gestational
5
30% of _______________ boys get it
___% of full-term boys get it

Cryptorchidism - Consequences

Testes cant be palpated in scrotum

May descend over the next 6 months
though
Increases the risk of:
Infertility
Inguinal Hernia
Neoplasms due to detection ability
E.g. testicular cancer

Inguinal Hernia

= outpouchingintestines
peritoneum
of ___________
+
______________ through a
weakening at
Inguinal
canal
the ______________.
If its incarcerated, aka
necrosis
strangulatedEMERGENCY
blood supply to bowel ischemia
__________

Due to:
Cryptorchidism
Congenital weakness
Sports trauma/lifting

Inguinal Hernia - Manifestations

______________
or palpable mass
Swelling
Reducible vs. irreducible

PAIN (acute &/or chronic)

May radiate to groin, may be visceral

GI Symptoms
Possiblebowel
________ obstruction

Treatment is always
___________ to reduce
surgical
hernia & reinforce the inguinal ring

Testicular Torsion

= twisting of the
________ on the
testes
Vascular
_______________
leading to
Spermatic
occlusion
cord
________________.
EMERGENCY!!!!!!!!!!!!
Due to:
Cryptorchidism
May be spontaneous or related to trauma

Testicular Torsion S/Sx

EDEMA
_____________
From venous occlusion, leading to an in
hydrostatic pressure
_______________
ACUTE PAIN
From arterial occlusion ischemia necrosis

ELEVATION
Testes want to be closer to the body; Cremasteric &
dartos muscles contract.

TREATMENT:
_________________
Manual
Surgical detorsion, bilateral
detorsion
Must be detorsed within ___ hours to prevent
necrosis
6
_________!

Benign Prostatic Hyperplasia

anaplastic
= age-related, non-____________
INTERIOR of the __________ prostate
enlargement
periurethr
numbe
gland
characterized
by in _________ of
al cells.
r
_________________
=BPH

BPH S/Sx

Difficult starting stream

Weak stream
Dribbling
Incontinence
Can encourage
UTI_____s!

Urinary frequency
Nocturia
Renal failure
_____________
Postrenal acute renal failure

Prostate Cancer

Anaplastic
=______________
changes of prostate cells
that usually occurs
in the _____________ of
periphory
the prostate.
UNRELATED to BPH.

cell proliferation
cell differentiation, fxn

Prostate Cancer S/Sx

May not be any symptomslate

until ______
Due to growth of cellsperiphory
on ___________ of
prostate

Many are diagnosed incidentally

Similar s/sx of BPH if neoplasm is large
enough
To thus effect the urethra

Hematuria

lung
bone
B/c malignant cells spread & infiltrate blood
BACK
vessels

Metastatic effects on _________ + ________

STIs

Who?

Anyone who has unprotected or partially

protected sex is at risk
women
___________
are usually at greater risk
(because they are receiving the fluids)
Bimodal distribution of incidence among
TEENS
ELDERLY

VIRAL STIsUNCURABLE
= _______________
HPV, HSV

BACTERIAL STIs
= _____________
CURABLE
Gonorrhea, chlamydia

Genital Warts

= HPV
Due to:
Infection w/ human papillomavirus

________
transmission rates
Very high
Transmission can occur whenasymptomat
pt is
ic
____________
Transmitted to infants during vaginal birth
if active lesions.

HPV - Manifestations

warty
Most common s/sxPainless,
= ____________________
lesions
Cauliflower-like
Many infected = asymptomatic
Positive association between HPV
&
cancer
cervical
____________
Especially ____________

Even stronger association between

smokers w/ HPV and neoplasms
Messes up the DNA

HPV - Vaccination

Developed not for HPV but

Cervical
for _________
cancer
_______
Not 100% effective
4
Protects against only ___
most common
Cervical
cancer
types of HPV that are associated
w/
9 26
__________ ________
Vaccine recommended for females aged
__-__

CAN PREVENT CERVICAL CANCER!

HPV Vaccine

Uses recombinant DNA technology to

Capsid for a ________________ that the
encode
protein
body
will mount a response to.
Essentiallyhollow
a _________ virus.
DNA fragment is inserted into bacteria,
bacteria then multiply and produce the
protein.
replication
DNAtranscriptio
_____________ DNA
DNAn_____________
mRNA
translation
mRNA____________Protein

Genital Herpes

= HSV
Due to infection with herpes simplex
virus
asymptomat
icpt is
Transmission may occur when
_____________
Can be given to fetus in utero or to
infant

HSV How?

HSV gets transmitted during sexual

contact
Mucus
membranes
HSV penetrates
_______________
lesions
systemi
Replicates, causing ________
c &DRG
__________ s/sx
HSV infects
Spinal & travels up nerves to _____,
cordto the _______.
proximal
Lies
Then replicates and
dormant
_____________
nerves

HSV travels back down the __________ and

reactivates to cause an outbreak of
local lesions.

HSV Manifestations

_____________,
___________, neuropathic
Parasthesias itching
pain
nerves
Due to virus travelling
along ___________
pustules

Eruption of small __________, aka herpetic

lesions, which causes dysuria and
dyspareunia.
Fever
aka hurts to pee and hurts to have sex

_________,
cytokinesmalaise, myalgias, and
lymphadenopathy from immune cells
releasing ______________.

HSV - Manifestations

Initial symptoms are usuallysevere

more
________ & last longer, due to typical
massive immune response.
Recurrent
HSV outbreak results from
reactivation
_____________ of the virus
# of recurrences every 2-4 months
Often
with/without systemic manifestations?
parasthesias
____________
& pain precede the outbreak of
lesions
lesions
___________ occur in a dermatomal
distribution.

Chlamydia

= a group of infectious syndromes

caused by Chlamydia trachomatis
Transmission can when whenasymptomat
pt is
ic
____________
Easily transmitted togonorrhea
infants during L&D
Pts often co-infected
w/ ______________
conjuctivitis
pneumonia
Infants may suffer ____________ &/or
__________
asymptomat
KEY DIFFERENCES
W/ GONORRHEA:
ic
clear serous
Pt is usually ________________
Discharge is _______/__________ fluid

Chlamydial Infection

Many patients,
50>___%, are asymptomatic
Many same s/sx with gonorrhea; if
infected w/ one, automatically get treated
for both.
Untreated infection I n f e r t i l i t
y
serous

Again, chlamydia characterized by

________ discharge.

Gonorrhea

= a group of infectious syndromes caused by

gonococci
Due to infection w/pus
Neisseria gonorrhoeae
purulen

These bacteria form _____, and subsequent ___________

t
discharges/exudate.

pregna
Again, easily transmitted during
________
ncy
Patients often co-infected w/ chlamydia
Baby may sufferconjunctiv
___________ but not pneumonia.
itis
KEY DIFFERENCES W/ CHLAMYDIA:
Patients are usually _____________
symtomati
_______, ___________ discharge

c
white purulent

Gonorrhea

Most patients,90
>___%, symptomat
are
ic
purulent
_________________
___________, pus-filled discharge

Many same s/sx as chlamydia

Untreated infection I n f e r t i l i t
y

Female
Reproductiv
e Disorders

Female Endocrine Control

Hypothalamus

Anterior Pituitary
FSH

LH

OVARY
Theca Interna (Follices)
Corpus Luteum

ESTROGEN

PROGESTERO
NE

Menstrual Cycle

Menses occurs every

days
25 ___-___
35
3 phases:
_______________
phase
Follicular
________
occurs,ovarian
____________________
menses
follicles develop
_______________
phase
Ovulatory
Dominant follicle
_____________
Releases
egginto fallopian tubes
Stage when fertilization can occur

_______________
phase
Luteal

Dominant follicle
___________ into
_________
Corpus
collaps
__________
luteum
Endometrium
es
_________________ grows

FSH from the Pituitary

FSH =
Follicle-Stimulating Hormone
Stimulates the development of ovarian
follicles
_________, which will eventually release an
egg
estrogen
Stimulates ____________ secretion by the
developing follicles
Negative feedback
via estrogen
fxns to /
follicul
estroge
FSH?
ar
n
FSH, and thus __________, peak at ___________
phase

LH from the Pituitary

= Luteinizing hormone
Its peak causes theejection
_______________
of an from the
dominant follicle
egg

= ovulation
Left over tissue from ejection =Corpus
_________________

Neg. feedback via progesterone

fxns to / LH?
luteum
LH peaks in the _____________ phase
ovulatory
Why? So _____ can be ejected
egg
So, how do female contraceptives work?
They contain progesterone, which causes negative
feedback inhibition of LH at the anterior pituitary
no spike in LH means no egg ejection.

Estrogen

Secreted by the ovaries before egg is

released to help:
Re-growth of the
_______________
endometrium
Growth ofEggs
________
and
breasts
Fertilization
by making cervical watery
mucus
_________ for easy transport of sperm to the
fallopian tubes
FOLLICULAR

ESTROGEN = HIGHEST DURING

___________ phase

Progesterone

Secreted by the
_______ after the egg is
ovary
released from the dominant follicle
Secreted most duringluteal
the _________ phase
Main fxn = promote
_____________
endometrial
changes
THICK
As well as create _________ cervical mucus

If fertilization occurs, / levels of

progesterone
continue to cause the
glcyogen
endometrium to secrete ___________ &
support implantation
If no fertilization, / levels of progest.

Stages

Preovulation =
____
in estrogen/progesterone leading to
growth in superficial layer

Postovulation =
____
in estrogen/progesterone? Leads to
secretions

Menstrual
=

____ in estrogen/progesterone? Leads to

sloughing off of superficial layer

Cervical Mucus Changes

Estrogen
_____________
large amounts of clear,
__________
mucus (easily penetrable)
watery

_____________
Progesteron reduces mucus
e
secretions
&viscous
makes it more ____________
This hormone also during the luteal phase
b/c it comes from
the ________ __________!
Corpus
luteum

Thus, easiest time to get a girl pregnant

is when
she is in ___________ phase
follicular

Menopause

= No menstruation for a fullyear

_____ &/or VERY
HIGH
FSH _____ level
Usually @ ages 48-55 y.o.
Females are born w/ all the eggs theyll ever
have
Ovaries eventually stop working, cant produce
follicles anymore, which normally produce
estroge
____________
n
FSH
Thus, a high ____ level indicates menopause
because there is no longer any estrogen present
in the body to provide negative feedback to the
anterior pituitary; without that feedback, the
pituitary will continue to secrete FSH

Menopause HRT Controversy

Since women have fewer CV problems,

estrogen seems to have protective effect
Womens CV risk after menopause
Researchers actually found a small in
CV risk in women on Hormone
Replacement Therapy
MI due to thrombosis due to estrogen)

Dysfunctional Menstrual Cycle

= Abnormal bleeding patterns

=Bleeding too much, too little, or,
without ovulation (most common).
Occurs when the hormonal support of the
____________
is altered.
enodmetrium
What effect does estrogen have on
endometrium?
Endometrial proliferation

What effect does progesterone have on

endometrium?
Secretion of glycogen ( levels lead to

Dysfunctional Menstrual Cycle - Causes

Primary disorders of ovaries

the ____________
Polycystic ovarian disease, perimenopause,
ovarian neoplasms

Problems external to ovaries

the ____________
_______________,
leiomyomas coag disorder, endometriosis

Secondary to
_____________-____________
Hypothalamic
pituitary
axis
Stress, big weight change, pituitary
neoplasms

Dysfunctional Menstrual Cycle -

Mechanism

Progesterone deficiency
or __________
estrogen
excess
Unopposed
estrogen
______________
____________ induces
development of thicker/thinner?
endometrial layer with a richer blood
supply

LH
Thus
causes
lighter/heavier menses?
Ant.
pituitary

What causes ovulation?? ____ _____

So, ______________ dysfunction can mess

things up
As caused by stress

Uterine Disorders - Overview

Endometriosis
Leiomyomas
Endometrial Cancer

Endometriosis

= condition in which functional

endometrial
_______________ectopic
tissue is found in
__________ sites
=increase in endometrium
Due to:
Retrograde menses?
Cells misplaced in fetal development?
Dont really know

Endometriosis Where?

__________
Ovaries
_____________
of ovaries & uterus
ligaments
Pelvis
Vagina
Vulva
Anywhere beside the brain and spinal
cord!

Endometriosis How?

Bits of endometrial tissue when there is

estrogen =
THICKENING of the endometrium
Watery, clear fluid secretions

progesterone =
Cause endometrium to secrete glycogen
THICK cervical mucus to promote implantation
after egg release!

progesterone =
Weakening of the endometrium, collapse into
corpus luteum
MENSES

Endometriosis How?

_____________
into the surrounding
Bleeding
structures can cause pain with defecation
and with sex, may also cause pelvic
Chocolate
scarring
+ ovarian cysts, aka
cysts
____________
________
CLASSIC TRIAD:
Infertility
Dyspareunia
Dysmenorrhea

Leiomyomas

= Benign
____________________
neoplasms in the
smooth
___________
muscle mostly dx in women > 35 yo
uterus
Why? Because estrogen is gradually declining
Usually regress withmenopause
______________

= myomas
= fibroids
Due to:

???
Size + growth likely related to changing hormone
levels, especially
___________
estrogen
Perimenopause & pregnancy

Closer to menopause = uterine fxn, estrogen, FSH from pit

huge spike in estrogen in last-ditch effort by failing ovaries

Leiomyomas - Manifestations

50% =
__________________
asymptomatic
S/Sx develop slowly
Mass
__________
effects
Constipation
Polyuria & urinary urgency (b/c uterus is atop
bladder)

Dysfunctional menstrual cycle

Heavy
Especially
________ ________
menses

Endometrial Cancer

= anaplastic
_____________ changes of the
endometrium most often in pre/post?
menopausal women
It is the most common pelvic cancer

Due to:

Unopposed
#1
estrogen
risk factor = prolonged ____________
_____________ stimulation
All
other risk factors trace back to creating
estrogen
___________________ levels.
Obesity, early menarche, late menopause,
estrogen-HRT, estrogen-secreting neoplasms

Endometrial Cancer How?

The main s/sx is abnormal

_________
painless
____________
bleeding
General s/sx of cancer usually not seen
b/c most endometrial cancersearly
are
diagnosed _________
Why?? b/c pts are
95bleeding AFTER
MENOPAUSE!
5 yr survival rate = ___%
Cure?
Remove the uterus

Breast Disorders

Galactocele
Fibrocystic Breast Disease
Fibroadenoma vs. Breast Cancer

Galactocele vs. Mastitis

Both of these disorders are most common

in
____________ _____________
Lactating
women
______________
= rare
Mastitis
BOTH are easily treated
Breastfeeding should continue for babies
until
old!
One ________
year

Galactocele

= local collectionmilk
of ______ in the breast
due
to ____________
obstruction
plugged duct
Due to:
______________
cells & other debris obstructing
epithelial
a duct in a lactating breast
Epithelial cells slough
off
Obstruction in the ductile
system

Breast develops hard,

tender, masses (from
trapped milk), which
pressure in the duct

Almost always spontaneously

Galactocele - Tx

Encourage the woman

Continue
to
____________________ breastfeeding
Milk towards the nipple to help re-open
the obstructed duct
Especially effective while baby is feeding

Mastitis

= inflammation
breast
_______________ of the
__________
Usually occurs during lactation b/c of
Skin trauma
Mothers hands/skin

Due to:
______________
Ascending ______________ w/ Staph or
Strep
infection
Skin trauma +
staph/strep
Travels up, causes
inflammation
_____________ &
obstructs a duct

Breast develops hard,

tender, red, swollen
mass + systemic s/sx
of infection
Without tx, area
becomes walled off &
abscess forms, may

Mastitis - Tx

Encourage the woman

to
Continue
___________________ breastfeeding
How
do we treat bacterial infections??
antibiotics
________________

Fibrocystic Breast Disease

= nodular, tender breast changes that

fluctuate
w/ the
_____________ luteal
(often
Menstrual
cycle
worse in _________ phase the time of
PMS)
progesterone
Which hormone peaks in this phase?
_____________

Fibrocystic
cysts changes
3 mainFibrous
pathologic
characteristics:
tissue
_________
(fluid-filled sacs)
epithelial

in ___________________
_______________ proliferation ( breast cancer risk!)

FBD - Manifestations

Vary w/ the menstrual cycle

_____________
breast nodules + masses
Bilateral
___________
breasts
tender

Most common cause of lumps in women

Usually free-moving, well-defined lumps
Sometimes painful
Again, worse during
_________ phase
luteal

Fibroadenoma

= Single
_________ mass
= Benign
____________ breast tumor
MANIFESTATIONS:
Typical manifestations of a benign tumor
i.e. mass effects

Easy/hard to move?
Well or poorly-defined edges?
Usually painful/painless?

Breast Cancers

= Anaplastic
___________ changes of breast tissue,
most often
in ductile ______________
epithelium
It is theMost
________________
cancer in women
common
About10
___% are hereditary
Autosomal recessive/dominant?

Mutation to
________,
BRCA1 which normally inhibits estrogen
receptors and acts as a Tumor Suppressor
Gene
HER2
_______, which encourages growth

Breast Cancers Risk Factors

Sex, age, alcoholism, obesity, radiation

What hormone is of concern?
estrogen
___________ b/c it breast growth
Early menarche, late menopause, etc

Risk factor = 1st pregnancy

30 >___ years old
Risk factor = Family history
If you have 2 first-degree relatives, risk
increases from 1/8 to 5/8!!!!!!!!!
Since so few cases are hereditary, many
women with breast CA have no risk factors
other than being an aging female

Breast Cancer - Tx

Herceptin
Fxns to block
_______ protein activity to
HER2
growth
Estrogen
Progestero

____________ & _______________

blockers
ne
Prophylactic Bilateral Mastectomy
For inherited forms
Angelina Jolie

Sentinel Node Biopsy

Inject dye to track lymphatic drainage for
possible metastatic routes

NEUROLOGIC
DISORDERS

Upper Motoneuron Lesion

= a disruption that stops signal

brain
transmission
of _______ nerves
that start
motor
in the _______
and synapse in the
Spinal
cord
_________________.
contralater
al
Above the brainstem affects
_______________
ipsilateral
side
Below the brainstem affects _______________
weakness
side.
spasticity

S/Sx

LMN
Initial ____________ followed by hypertonicity
and ____________.
= OVER reaction by
Lose UMN modulation but UPPER
_____
reflexes stay
body

Lower Motoneuron Lesion

= a disruption that stops

motor_______ nerve
Spinal
transmissions that start in
the
cord
muscles
______________
and synapse
on
____________.ipsilateral
Always affects ____________ side.
S/Sx
flaccid
Weak or ________Muscles
paralysis
Lose LMN signal but
________ remain intact
atrophy
Muscle denervation __________
Hypo
or hyperreflexia?
fascicul
_________ations.
LOWER = LIMP

Amyotrophic Lateral Sclerosis

= Progressive
ascending
____________ degenerative
disorder of (upper, lower, or both?)
inflammati
motoneurons that
shows NO SIGNS of
on
_________________.
intact
Sensation,
thought, memory and autonomics
2
5 entirely ________.
remain
___-___ year prognosis

AKA Lou Gehrigs Disease

We dont know why it is caused

ALS How?

From UMN involvement

Spastic
Clonus
Hypo or hyperreflexia?

From LMN involvement

Fasciculations
Limpness (LOWER = LIMP)
Muscle atrophy
Hypo or hypereflexia?

Cause of Death?
__________
phrenic nerve cant contract diaphragm

ALS - Treatment

No cure, only supportive

What happens when it reaches C3, C4,
C5?
Death

What
may happen to the skin with
Pressure
ulcers
immobility?
_______________

What could happen in the veins w/

immobility?
Edema, hypotension, DVT valve failure

Must catheterize b/c external sphincter =

Guillan-Barr Syndrome

= Self-limiting polyneuropathy peripheral

of the
___________
m______, s________,
utonomicand
otor
ensory
a___________ nerves.
Different from ALS because this can affect
more/less?
than ALS.
Epstein
Linked tobarr
________-_____ virus, which also

plays a role in mononucleosis and

Hodgkins Disease.

Guillan-Barre How?

Peripheral lower motor nerve involvement

Symmetric, ascending
_________ paralysis
flaccid
Starts in the
_______ + ________
hands
feet
Peripheral sensory
nerve involvement
_____________
Parasthesi and numbness
a
Peripheral
autonomic nerve involvement
Postural hypo/hypertension? (Baroreceptor
reflex)
retention
Urinary ___________
Cardiac arrythmias
flushing
___________ + sweating

GBS - Treatment

Now may administer IVIg (antibodies) to

help
Death if reaches C3, C4, C5
Again, risk for pressure ulcers, edema,
and the patient must be catheterized.

Basal Ganglia

middle
In the deep
______ of the brain
Aka Movement
________________________.

modulator
Coordinate
sensory + motor inputs for
smooth,
______________ movements,
voluntary
particularly of peripheral muscle groups

Also has role in memory

+ __________
thought

Parkinsons Disease

= degenerative neuro disorder of the

Basal
________________
that disrupts
movement
ganglia
paralysis
_______________
but
does NOT cause
dementia
_______________!
Substantiaisnigra
___________
also very common among PD
patients.dopamine
_____________________ loses its pigment.
Due to ________________.

PD S/Sx

Restingtremor
_________
_____-_____ing
Pill
roll
Feet, face, lips, jaws

___________
RIGIDITY
Cogwheeling or ratcheting along with
movement
BRADY

_______kinesia aka cant start movement

Lack of coordination
Short, shuffling steps

Dementia

Cerebellum

athlete brain
The _________s
Like theBasal
________________, it is a
ganglia
movement
modulator
Coordinates sensory + motor inputs for
finely-tuned
voluntary _______________ and involuntary
movements exact
Helps with _________ness of motion in space +
time
Stops motion by overcoming momentum

Cerebellar Disorders

= anything disrupting cerebral fxns of

movement coordination
Infection
Tumor
Degenerative
Etc. etc.

Cerebellar Disorders S/Sx

__________
Intention tremor
Dysmetriapast
- _______-pointing
Dysdiadochokinesis hand flip-flop
cant perform rapid (hand) movement
_________
- Gross incoordination
Ataxia
Dysphagia difficulty
_______________
swallowing
VERY HARD TO EAT

Dysarthria difficulty
_______________
speaking

Myelin

= WHITE insulation wrapping around

nerves oligodendrocyte
s___________________ in the CNS
Made bySchwann
Made by___________
cells in the PNS
nerve travel
Helps tospeed
_______________________.

Multiple Sclerosis

= De____________
myelinatio
disease of central
the
n
___________
nervous system
Common in
________ adults
young
Who gets it?
Women > or < men?
High or Low altitude birthplace?

Due to
______________
Genetics
Immune-mediated?

MS How?

_____________
+ immune attack
myelin
on
Inflammati
on
____________
Myelin thus breaks down plaques
Lesions
of demyelination are called
plaques
___________
scar
These ___________ are often scattered

Reactive _______ forms (aka gliosis)

Nerve signals subsequently slowed or
blocked.

MS S/Sx

Depend onlocation
___________ of demyelination
neuritis
Optic nerve? Vision loss and optic
____________
Motor nerves? Mostly (UMN or LMN?) s/sx
diplopia
DOUBLE VISION aka
___________

parasthesi
Sensory nerves?
_____________, numbness
a
Autonomic nerves?
Bladder, sexual dysfunction
Cerebellum? Incoordination
Cortex?mood
_______, memory, thought, concentration

Usuallyrelapsing
___________-remitting
Get better, then a lot worse, then better, etc

May be primary-____________
progressiv
(gets worse
e
and worse)

Skull + Meninges

Skull contains brain cells, blood, and CSF

It protects, but cannot expand
drain
or __________.
___________
Brain cellsfluctuate the least, and thus are
most prone to injury
Space-Occupying lesions, aka TUMORS.

Skull + Meninges

Meninges = several CT layers

surrounding the brain + spinal column
Meningitis = inflammation of the meninges

They form a P.A.D. from the inside out.

S K U L L
Spaces between them hold different
-____________
Dura
mater
vessels
Arachnoid
Subarachnoid
= _________________-____________
ARTERIES
Pia
mater
SubduralBridging
= _____________________
-____________
Epidural ARTERIES
= _____________________ mater
VEINS
B

Traumatic Head Injury

= anything causing damage to structures

of the head
MAIN CAUSES:
_________-_____________
Motor
vehicle accidents
Falls
Assaults

THJ Epidural Hematoma

________
F A S T bleeding into the epidural space
Why? b/c it contains (arteries/veins?)

Often theMiddle
____________________ artery
meningeal
Associated
with skull fracture
S/Sx
Bleeding, again,fast
is ________
Victim initially
_________________
unconscious
Then awake
Then rapid
____________________
deterioration

Opposite side deficits (why? b/c UMN are

downstream)
dilation
Pupil ________________

Subdural Hematoma

= ssllooww
_______ bleeding in the subdural space
Why? b/c it contains (arteries/veins?)
Associated w/ brain movement in skull

S/Sx
Bleeding, again,
is __________
ssllooww
May be asymptomatic for long time!
S/Sx fluctuate over time
Confusion,headache
_____________, altered
consciousness

Cerebral Circulation

Tight autoregulation
Can maintain perfusion well
Crucual b/c brain depends on continuous
_________
glucose
delivery

Local Metabolic Regulation

Stroke

= acute focal neurological disorder

Blocked blood
resulting
from _____________________
or
bleeding
flow
___________
into brain tissue
= Cerebrovascular Accident (CVA)
Transient Ischemic Attack (TIA) = mini stroke

2 types:
Ischemic
Hemorrhagic

Stroke Risk Factors

Anything that risk atheroscle

of _________________
will risk of stroke rosis

Ischemic Stroke

From Blood
________________
flow
to brain
CAUSES:
Stenosis
Almost always related to atherosclerosis

________osis
Thromb

Almost always related to atherosclerotic

_________
plaque
rupture

Embol
________ism

From what side

leftof the heart + circulation?

Must be the _______ side; if an embolism began in the

venous circulation, it would eventually return through
the Vena Cava Right Atrium Right Ventricle
Pulmonary Arteries LUNGS from here, blood vessels
get
smaller and smaller until they turn into tiny
pulmonary

Ischemic Stroke & Reperfusion

Ischemia causes cellular damage and also

creates
Free __________________.
radicals
Blood
flow needs to be restored, but in
doing so, will Free
carry these _______________
radicals
downstream.
Free
These __________________
radicals
can then attack
other cells and
cause further damage!
reperfusio
This is called
n ______________ injury.

Hemorrhagic Stroke

From bleeding
_____________ into brain tissue
CAUSES:
Rupturedaneurysm
___________ (out-pouching)
HTN + Diabetes + smoking atherosclerosis
_______
a ______________
subarachn
Berryaneurysm causes
hemorrhage
oid

Trauma
Tumors
Arteriovenous Malformation
Bleeding disorder

Hemorrhagic Stroke aka Aneurysmal

Subarachnoid
= small outpouching, usually in the
Circle of
_____________________,
that bursts open and
Willis bleeding
causes
Aka Berry
________ aneurysm
Often occur with HTN and smoking

Special S/Sx not in other strokes

Sudden
_______________
- Mule kick headache!
onset
Nausea/vomiting
Neck stiffness (due to meningeal irritation)
Photo
_______phobia
Dizziness
MAY BE MISTAKEN FOR MIGRAINE!

Stroke S/Sx

Focal Neurological Deficits are key

Use these specifics deficits to backtrack +
locate the problem

Motor + Sensory deficits are going to be

(ipsi/contralateral?)
Dysarthria + Aphasia

Stroke MOTOR deficits

Weakness or paralysiscontralater
on ____________
al
side
UMN or LMN?
Flaccid or Spastic?
Hyporeflexic or hyperreflexic?

Stroke SENSORY deficits

Parasthesia or numbnesscontralater
on ___________
al
side

Stroke Dysarthria + Aphasia

Dysarthria = dysfunction motor

of the _________
part of language
Can think of the words, but form
cant _____ them

Aphasia = dysfunction ofcomprehensi

the
on
_____________ part of language
understandin
Can form words, but trouble
_______________
g
them

Stroke Other Problems

Hemineglect for example, being

told to draw a basic house and only
drawing half.
Senses
Problem solving
Memory
Behavior
Personality

Integumenta
ry

Lesions + Rashes Flat & Nonpalpable

_________
Macule
Aka freckle
Size =small
_______

_________
Patch
Aka birthmark
Size =
_______
large

Ls & Rs Elevated, Palpable, Solid

____________
Papule
Aka mole
Size =small
__________

___________
Plaque
Aka tinea, psoriasis, HPV
Size =
__________
large

___________
Wheal
E.g. hives
NOT DETERMINED BY SIZE
Always due to
_______________ or an allergic
hypersensiti
rxn
vity

Ls & Rs Elevated, Palpable, Fluid-Filled

____________
Vesicle
Aka HSV
Size =
small
_________

__________
Bulla
E.g. 2nd degree burn or blister. (Blister =
bulla)
large
Size = __________
Pustule

___________

E.g. acne, impetigo

NOT DETERMINED BY SIZE
Pus
____-filled

UV Radiation & Skin Cancer

UV effects on the skin

Cause Cross
______-_________ of DNA
Cantlinking
be read properly
Burnt skin cells release further chemicals that
damage surrounding cells
Inhibits cutaneous immune cells

Sunburn
2nd & 3rd degree burns cause blistering (ex.
of ______),
bulla
temperature regulation problems,dehydration
& ______________
Base tan = dumb.
PREVENTION =
SPF ___-___
15 30
Reapply every2
___ hours
Never go outside ever for any reason

Skin Cancer

_________
Basal
cell carcinoma is better Squamous
than
________ cell carcinoma which is better
than
________________________.
Malignant
melanoma

Skin CA: Basal Cell

=Most
__________________ skin ca
common
Very
good
______ rate
cure
Low metastatic potential
Main risk factorSun
= _________________
exposure
Common areashead
= ________, neck
TREATMENT:
Cut it off

Basal Cell Whats it Look Like

EARLY:
Smooth, fleshy papule (which
is _______,
palpa
elevat
solid
________,
& ________) surrounded
by
ble
small
ed
superficial vessels

LATE:

depression
Raised
ulcer
Ring
ofw/ central _____________ & waxy
border,
aka ___________________
pearls

Skin CA: Squamous Cell

Second most common skin ca

Curable
Medium metastatic potential
exposure
Main risk factor, again, Sun
is _______________
Also linked to occupational exposure
arsenic
to
tar
__________,
____, & coal

Common areas = head, hands

WHAT IT LOOKS LIKE:
Red papule orplaque
________
Often scaling &crusting
___________
( Normal / Irregular ) border
No superficial vessels

Skin CA: Malignant Melanoma

Rarest form of skin ca

Most fatal
Extremely
____________
metastatic
Only moderately associated
w/exposure
Sun
________________
back
Common areas = ______, arms, legs

Malignant Melanoma 6 Risk Factors

Hx
1. F____
2. White w/ blond/red hair
3. Upper back freckles
4. Hx of 3
> ___ bad burns before
20 age ___
5. Hx > 3 years of outdoor job as a teen
6. Actinic
__________
keratoses
If you have 2/6 of these, risk
3.5 = ____ times
greater
20
If you have 3/6 of these, risk = ___ x
greater!!!!!

Malignant Melanoma Looks Like

______
BLACKor dark brown papule or plaque
elevate
solid
Which are small or large,
___________,
&
d
________

Irregular border
Uneven surface
Usually
from a previous mole that
ssymetr
changes
y
order

A_____________
olor
B_____________ irregularity
iameter
C_____________ change + variation
D_____________ (size of about pencil eraser)

SKIN INFECTIONS

Fungal = mycotic =
TINEA
CANDIDIASIS

Bacterial
IMPETIGO

Viral
Herpes SIMPLEX
Herpes ZOSTER

Skin Infx Tinea (ringworm)

Named by Location
___________
TINEA + latin
Corporis = Body
Faciale = Face
Head
Capitis =
Foot
Pedis =
Manus = Hand
Unguium = Nails
Dead cells
keratin
These fungi live off ___________ & digest _______
Hence, discoloration of afflicted area!

capitis
Pain, itching, scaling, hair loss if tinea ________
immunocompromi
risk in __________________
sed
Athletes Foot
Tinea Pedis more commonly called _____________

Skin Infx - Candidiasis

From Candida albicans
These are nml flora in mouth & vagina

toxins
Causes rash + sx by releasing
________

patch w/ ________-defined
well
Appears as red _________
borders
WHIT
_______
if occurses
in mouth (aka thrush)
E scale
May
Satellite
__________________ are KEY!
lesions

NOT SEEN IN TINEA!

Itchy & burning

dar war
mois
Loves _____, ______, & _______ skin foldsAbx
k
m
t

risk in immunocompromised and pts on ____!

TREATMENT?
Topical cream

Cortisol
__________
_______
epinephri
glucagon
catabolic
_________ to suppress
immune system
& inflammation
bloodstre
ne cells & __________,
This , along w/ _____________
are __________
am
Move glucose from ______________ to _____________

Impetigo

strep or ________
staph
From _______
Common ininfants
______ &kids
___________
Easily transmitted by
__________
TOUCH
Most common onface
_________
VERY ITCHY
_________
LOOKS LIKE
EARLY:
Vesicle or Bulla (whats the dif?) that ruptures to
release serous (clear) fluid

LATE:
_______-colored
crusty lesions that have not yet
Honey
burst
___________
Looks glued on very defined borders

VIRAL Infx

Herpes Simplex
HSV
Cold sores
Genital Herpes

Herpes Zoster
Varicella Zoster Virus
Aka Chickenpox Shingles

Both fxn by implanting inDorsal

the root
________________ of the spinal
cord
ganglion

HSV

Primary infection
________,
Fever malaise, local vesicles & ulcers
Production of antibodies at this time
S/sx are ( better / worse ) than recurrent infx
S/sx are ( more / less ) widespread than recurrent infx

Recurrent infection
Burning & _________ occur before visible skin signs
parasthesias
y?
DRGand must travel down the
Because HSV lives in the ____
________
before manifesting itself in the skin
nerves
S/Sx more local why?
Because the body has by now produced __________
memorycells to
control major outbreaks

Lasts 10-14 days

.HSV cont

Cure?Nope
____
Prevent recurrencesstress
via _______
management, sunscreen, & acyclovir,
which inhibits HSV replication
HSV may weaken local skin defenses,
allow strep & staph to infect,
& thus
IMPETIGO
cause __________
When defenses are weakened, these 2
fungi
could also infect:
Candidiasis
___________________
Tinea
_________

VZV - Shingles

Caused by varicella-zoster virus

Starts w/ virus exposure usually in
childhood
Aka chickenpox DRG

Virus, again, livesstress

in ______
Virus reactivation via ______, illness,
steroids orTchemo
Frequent in ___-cell compromised pts

VZV Shingles

Reactivation causes
Dermatomal
___________
Prodrome
_____________
Symptoms
dermatomal
that precede symptoms
Pain in a ___________ distribution
Burning, parasthesia, itching, b/ c of nerve
involvement
unilateral

Vesicles + Bulla occur in dermatomal

pattern

MOST COMMONLY ____________ on trunk/face

Neuralgia
Possible to transmit virus at this time
Clear in 2-3 weeks
nerves

Acne Vulgaris

= chronic
inflammatory
____________ disorder of the
pilosebaceous unit
P. unit =Hair
____________ sebaceous
+ _____________ gland
________
Sebumfollicle
is made when gland cells break
down
androgens
Responsive to ___________ (hence, acne
during puberty)

HOW?
Family Hx Sebaceous androgens
Response of
g.___________ to _____________
Infx due to trapped Propionibacterium acnes

Acne Vulgaris - Tx

Topical Creams
Steroidal, antibiotic

Oral Antibiotics & Hormones

estrogen
Oral Contraceptives (
__________ & thus fight
androgen
__________)
Retinoids unclog pores
Skin Management
Dont pop them.
Basic hygiene
Fun Fact: All standard acne meds active ingredient
= salicylic acid the same negative ion than can
cause high anion gap metabolic acidosis

Atopic Eczema

= Atopic dermatitis
=inflammatory skin disorder caused by
hypersensitive
__________________
allergic rxn
Highly associatedasthma
w/ _______ & other
allergic responses (hay fever)
Cause/pathophys = u n k n o w n
Onset usually before 5age ___

Atopic Eczema S/Sx

Usually starts Infants

on _________ face
Red, shiny vesicles
Slapface

ITCHY

Later present on
_________ surfaces
flexor
Dry, red, crusting, dull rash

Often w/ s/sx of other allergies

Broncho___________
constriction
_________
mucus production
Runny nose, itchy eyes

Psoriasis

autoimmun
=T___-cell mediated
______________
e thick,
plaques
disease that causes
scaling skin
___________, which are elevated, big, &
solid
T-cells respond to unknown antigen, produce
cytokines that stimulate
RAkeratinocytes and
cause inflammation
autoimmun

Moderate association w/
e _____

25
Duhthink about it..both are _____________
5

Onset usually before age ___

Whereas eczemas onset is before age ___

Psoriasis S/Sx

Usually on
__________ surfaces
extensor
Whereas eczema is usually
flexor
on __________
surfaces
Thick, red,
well-defined plaques
silvery
Overlying _________ scales!
Like eczema, its ITCHY

May be accompanying RA (both are

autoimmune)