ADULT & ELDER 3: KAPLAN INTEGRATED REVIEW

Treatment of hip fracture

May be used prior to surgery
Little boot around lower leg (traction & weight)
Make sure weight is NOT on floor
DO NOT turn side to side
Bucks Trapeze can be used to help the patient move (sit upright more)
Traction No pins
Assess skin
Look at circulation
May need to reposition
Insufficient amount of cortisol
Rare
Medical emergency
Commonly cause by autoimmune response destroying adrenal tissue
Metabolism issuegive cortisol
Effects both genders equally, common in ages 30-60
Clinical manifestations
o Symptoms not evident until 90% of adrenal cortex is
destroyed
o Insidious onset
o Progressive weakness, fatigue, weight loss, anorexia,
abdominal pain
o Skin hyperpigmentation (bronze skin)
o Hypotension, hyponatremia, hyperkalemia, anemia, n/v, &
diarrhea
Diagnostic tests
o Subnormal levels of cortisol or levels fail to rise over basal
levels with ACTH stimulation test
Addisons o Abnormal lab findings
Disease Hyperkalemia
Hypoglycemia
Hyponatremia
Anemia
Increased BUN
Decreased urine cortisol level
o CT & MRItumors or calcifications, or enlargement
Treatment
o Replacement therapy
Cortisone
Hydrocortisone
Prednisone
Fludrocortisone
Nursing management
o Frequent V/S & fluid/electrolyte balance
o Daily weight
o Monitor for signs/symptoms of Addisonian Crisis
Life-threatening emergency
Caused by stress or sudden withdrawal of hormones
Neuromuscular, CV, GI, skin
o Fluid balance
o Prevent dehydration
o Prevent hypoglycemia
o Prevent hypotension, dysrhythmias
Traumatic Brain Injury#1 cause of death in those < 40 years old
Causes:
Head injury o MVCs
 o Falls (older adults)
o Firearms
o Assaults
o Sports-related
o Recreational accidents
Primary Head Injury (what actually happened)
o Contusions, hematomas, shearing injuries, diffuse white
matter injuries, & lacerations to the brain
Secondary Head Injury (happened as a result of the primary ie:
inflammation)
o Contributes to further brain injury
o Exacerbation from hypoxia, hypercapnia, systemic HTN,
intracranial HTN, ischemia, age, previous medical history
o Hypertonic salineprevents secondary injury, monitor
sodium & serum osmolarity
Mechanism of Injury
o Acceleration/Deceleration
Acceleration
Stationary brain is suddenly & rapidly moved
in 1 direction along linear path
Brain doesnt move as fast, hits front of head
Deceleration
Brain stops rapidly in the cranial vault, as
skull ceases movement, the brain continues
to move until hits skull
Head stop, brain keeps moving
Coup-contrecoup
Acceleration & deceleration
Coupaffects cerebral tissue directly under
point of impact
Countrecoupoccurs in a line directly
opposite the point of impact
o Rotational
Force impacting head transfers energy to brain in a
non-linear fashion
Shearing forces exerted throughout brain
Brain itself may twist
o Penetrating
Foreign object invades the brain
Most common is gun shot wounds
Skull Fractures
o Linear skull fractures
Minor traumatic injury
Diagnosed by CT scan
Not life-threateningheals overtime without
intervention
o Depressed skull fractures
May be visible & palpable
May tear meninges of brain & extend into brain
tissue
Surgical repair of fracture & meninges
May have to evacuate hematoma
Pain & neurological assessment q1h
o Open/Compound skull fractures
Depressed skull fracture with scalp laceration
Risk for infection (skin is broken, bone is
protruding)
 Surgical repair & debridement of wound
Pain management, antibiotics
o Basilar skull fractures
Fracture of 1 of the bones that make up base of
skull
Periorbital ecchymosis (raccoon eyes)
Mastoid ecchymosis (Battles sign)blood
behind ears
Facial nerve paralysis
Otorrhealeakage of CSF from ear
Rhinorrhealeakage of CSF from nose
Dextrostix or Tes-Tape Strip
See if glucose is present
Halo/ring signblood moves to center &
yellow ring encircles blood if CSF present
Medical management
Allow CSF to drain & dura close on its own
Surgery if not healed in 1-2 weeks
Nursing management
Neurological & pain assessment
Monitor for infectionif leaking CSF, gives
access for something to work its way up
Change dressings with aseptic technique
Cotton to absorb CSF leak/raise HOB to
decrease CSF pressure (help to drain)
Precautions
o DO NOT stand or sit for long periods
o DO NOT flex hips more than 90 degrees
o Abduction pillow
o Avoid internal rotation
Total Hip Prevention of complications
Replacement o Continuous Passive Movement (CPM)
Give pain medication before
o Assess for neurovascular compromise
o Manage pain
o Progression of activityup & moving post-op day 2
o Promotion of self-careOT
Leading cause of cancer deaths
Poor long-term survival because of late-stage diagnosis
Bronchogenic carcinomas
Staged to assess size & extent of disease
Warning signs
o Hoarseness
o Change in respiratory pattern
o Persistent cough
o Blood in sputum
o Chest pain/tightness
o Shoulder pain
o Recurrent pneumonias
o Dyspnea
o Wheezing
Lung Cancer o Weight loss
o Possible JVD & edema in upper extremities
Management
o Can be curative (if caught early) to increase survival time,
and/or palliative
o Chemotherapy
 o Targeted therapy (to de-bulk, then do in & remove it)
o Radiation therapy (to de-bulk, then do in & remove it)
o Photodynamic therapy
o Wedge resection
o Lobectomy
o Pneumonectomy
o Postoperative care
Chest tube placement (except for pneumonectomy)
Sterile technique
Place drainage system below level of patient
Look for kinks
Tidaling
Vaseline dressing
Pain management
Respiratory management (mechanical ventilation)
Interventionsto maintain quality of life, ADLs, IADLs
o Oxygen therapy
o Drug therapy
o Radiation therapy
o Thoracentesis (remove fluid from pleural space)
o Pleurodesis (injection to close off pleural space so fluid
cant get it)
o Dyspnea management
o Pain management
o Hospice care (~6 months)

Elevated
body
temperature

o Inflammation of vermiform appendix, obstruction

o Most common requiring surgery
o Clinical manifestations
Vomiting
Fever
RLQ pain
McBurneys point
Periumbilical pain
Rebound pain
Anorexia
Irritable, uncomfortable, apprehensiveJump test
Appendicitis Sudden relief from pain could occur after
perforation!
o Diagnostic tests
CT scansee if appendix is inflamed (but lots of
radiation)
Ultrasound
o Nursing management
Surgical removal
Laproscopy vs. laparotomy
Pre & post operative care
Antibiotic therapy
Possible NG tube placement
Pain management
Can have appendicitis againthere is a stump that
can get infected
pH: 7.35-7.45
 CO2: 35-45
HCO3-: 22-26
Fully compensated
o pH normal
ABGs Partially compensated
o pH abnormal
o Then CO2 & HCO3- BOTH go toward acidic or basic side
Uncompensated
o pH abnormal
o Either CO2 or HCO3- abnormal & other is normal
Gastrectomy Surgery to remove part or all of stomach

A surgical procedure to create an opening in the neck for direct

Tracheostomy access to the trachea (breathing tube)bypass obstructed upper
airway
Performed because of airway obstruction, problems with secretion,
and efficient O2 delivery
o Inflammation of large intestine
o Mainly rectum & rectosigmoid colon
o Can occur at any age, but most common in mid 30s
o Women affected younger/men more middle & older age
o Mild, severe, or fulminant
Bleedingerosionsulcers
Abscesses
Partial bowel obstruction
o Bowel movements bloodyhematochezia (BRBR) = bright
red blood in rectum
o Assessment
Family history (tends to run in families, yet no
genetic link)
Treatment
Surgery
Nutrition history
Bowel patterns
Timing of diarrheameals, distress, activity
Recent antibiotics (2-3 months)
Traveling to tropical areas
Recent NSAID usehigh risk for bleeding
Extraintestinal symptoms
Ulcerative Arthritis
Colitis Mouth sores
Vision or skin problems
*Some autoimmune thing going on
*More systemic
Psychosocial assessment feel tied to toilet,
anxious
Fever (can have even without inflammation)
Abdominal distention along coloninflammation
(edema, intestine will be swollen)
Abdominal tenderness
Signs/symptoms of peritonitis
Inflammation of peritoneal cavity
Severe inflammation of large intestine, so if
perforated & leaks into perotineum
-Belly pain (1st symptom)
-Guarding
-Fetal position
 Hgb, Hct (issue with bleeding)
Low hematocrit leads to fatigue, pallor, &
tachycardia
If really lowmay need blood transfusion
Platelets
WBC (infection)
C-reactive protein
ESR (indicative of inflammation)
Electrolytes (due to blood loss)
Potassium (heart/dysrhythmias)
Increased BUN, creatinine, MG
Worry about fluid depletionrisk for
hypovolemic shock
Albumin
Normal is 3.4-5.4 g/dl
Not great to use, but can see if any
absorption issue (nutrition)
o Diagnostic tests
Sigmoidoscopy or
Colonoscopy (GOLD STANDARD)
Scope with camera to visualize lining of
colon
Dont want to scope right away because it
can increase inflammation or perforation
CT scan
Barium enema
Radiopic dye via rectum & x-rays done
Good to dx Crohns vs. Ulcerative colitis
Positive stool cultures
o Treatment (Drug Therapy)
Aminosalicylates (5-ASA)
Anti-inflammatory drugs
Increase doses during flares
Decrease during remission
PO or rectal
Corticosteroids
For acute exacerbation & then taper them off
Decrease inflammation
But its side effectsincrease risk for
infection from suppressed immune system
Alters glucose (increases), Cushings, lots of
metabolic complicationsnot used long term
Immune modifiers
May use to decreased steroid dosage
Antibiotics
If infection occurring with disease
Biologic therapies
Anti-diarrhea medications
Sometimes used in extreme cases, but not
routinely
o Priorities
ABCs
Vitals
May need O2
Dyspnea on exertion
Pain
Opioids
 Treat underlying problem such as spasming
Rest the bowelNPO, would need to bypass gut to
provide nutrition
Look for infection process
Address issues of fatigue
Camode
Sleep is vital
Most common health care acquired infection
Most common cause of sepsis in hospitalized patients
Women at risk because of anatomy
Other causes: Sexual intercourse, pregnancy, BPH, or any
obstruction
UTI classification:
o Upper tract: renal parenchyma, pelvis, ureters
o Signs/symptoms
Fever
Chills
Flank pain
o Lower tractno usual systemic manifestations, more
localized
Better outcometreat it & dont let it ascend
Sites of infection
o Pyelonephritis (kidney punch, some hospitalization, some
IV fluids)
o Cystitis (more outpatient)
o Urethritis
Clinical manifestations:
o Polyuriadue to inflammation
o Painful urination (dysuria)
o Urgency
o Bloodinflammatory process
o Cloudy urine
o Odor
o Suprapubic discomfort
o Elderly can present with mental status changes, poor
appetite, falls, new incontinence, & less likely to have a fever
Predisposing factors:
o Anything that increases urinary stasis
Obstruction (intrinsic or extrinsic)
Urinary retention
o Foreign bodies
Urinary calculi
CAUTI
o Anatomical factors
UTIs
Congenital defects leading to obstruction or urinary
stasis
Fistula exposing urinary stream to skin, vagina, or
fecal stream
Shorter urethra
o Sexual intercourse
o Immunosuppression
o Functional disorders
Possible impairment of free flowing urine
Constipation
Voiding dysfunction
o After menopause, less estrogen, more atrophy= increases
risk
 Diagnostic tests:
Urinalysis (clean-catch preferred, or catheterization immediately
when you put it in since thats when its most sterile, or suprapubic
needle aspiration)
o *Nitrates
o *Leukocytes
o Protein
o WBCs
o Mucus, bloody, cloudy, etc.
Urine culture & sensitivity
o Must be sterile!
o See how many bacteria
o Greater than 10^5 indicates infection, but still want to look
at the patient
o This helps indicate what agent will work to eradicate
infection
o This is done BEFORE antibiotics
Imaging studies (in some cases)
o IVP or abdominal CT when obstruction is suspected
Treatment:
Trimethoprim-sulfamethoxazole or nitrofurantoin (Septra)
o Used to treat empiric uncomplicated UTI
o Want to make sure patient adheres to regiment
Pyridium
o OTC, provides soothing effect on urinary tract mucosa
o Stains urine reddish orange (even tears)will not
eradicate the infection!
Prophylactic or suppressive antibiotics
o For patients with repeated UTIs
o Prevent recurrence, or a single dose prior to events likely to
cause UTIs
Special considerations for pregnant women
Complicated UTIs in elderly, diabetics, and those that are
immunosuppressed
Nursing management:
Avoid unnecessary catheterization & early removal of indwelling
catheters
Aseptic technique & hand washing
Wear gloves
Avoid incontinent episodes by answering call light, offering bedpan,
etc.
Peeing after sex
Cotton underwear
Fluidsflush out the bacteria
Educate on proper wiping
Educate patient of taking full dose of medications despite
disappearance of symptoms
Instruct patient about drug & side effects
Central The pressure of blood in the thoracic vena cava near the right atrium
Venous of the heart
Pressure Reflects the amount of blood returning to the heart & the ability of
(CVP) the heart to pump it into the arterial system

Chamber 1collects fluid draining from patient

Chamber 2water seal, prevents air from entering patients pleural
space
Chest tubes Chamber 3suction control of the system

*If test tube falls out air can go in and lead to a tension pneumothorax
 *BEST INTERVENTION= tape sterile gauze on three sides and notify HCP
*Dont clamp chest tubestraps air!
*If changing chest tube drainage system, clamp, put in sterile water, &
change quickly
o Stage 1non-blanchable redness, skin intact
o Stage 2blisters, partial thickness
o Stage 3full thickness, subcutaneous fat may be visible
o Stage 4full thickness, bone, tendon or muscle exposed,
slough or eschar present
o Unstageablefull thickness, depth unknown, completed
obscured by slough and/or eschar
o Deep Tissue Injurypurple or maroon localized area of
discolored intact skin due to damage of underlying soft
tissue from pressure and/or shear
o Location:
Where is it anatomically located?
o Measurements:
Length x width x depth
Greatest length (head to toe)
Pressure Greatest width (side to side)
ulcer Depthuse cotton tipped applicator, note/mark
depth & hold against ruler
o Wound Characteristics:
Describe by % of type of tissue
Granulation
Red
Cobblestone appearance
Filing-in appearance
Necrotic
Slough
o Eschar
Undermining
Separation of tissue from the surface under
the edge of the wound
Describe by clock face
Tunneling
o Wound Drainage & Odor:
Exudate
Scant, light, moderate, heavy, copious
Clear
Sanguineous (red, thin, watery)
Serosanguineous (thin, watery, clear-pink)
Purulent (sign of infection, green/yellow)
Odor
Most wounds have an odor
Clean well prior to assessing odor
o Periwound
Protection is important!
Assess color, texture, temperature, & skin integrity
o Infection
All wounds are contaminated, but not necessarily
infected
Contamination on wound surface
Colonization
Infection invades soft tissueleads to systemic
response
Look for inflammation, pus, increased/different
 exudate, fever, pain, & delirium
Sterile technique during dressing changes
Other factors that contribute to wound healing
o Nutrition/hydration (especially protein)
o Circulation (pressure relief, oxygenation, no smoking)
o Edema
o Glucose control
o Delayed wound healingadvanced age, type-2 diabetes,
smoking, etc.
Nursing management:
o Prevention!
Minimize friction, sheer, & pressure
Incontinence
Nutrition
Education
o Relieve pain
Use appropriate pain scale
Try to alleviate pressure where the pressure ulcer is
Administer pain before debridement or dressing
change
Encourage communication when uncomfortable
o Proper positioning
Turn & reposition (regardless of support surface)
Avoid positioning on bony prominences with existing
non-blanchable erythema
Dont keep on bedpan too long
30 degree titled side-lying position
Moving and shifting in chair
Do not use donut-shaped devices
Should not use these devices to elevate heels:
Synthetics sheepskin pads
Cutout, ring, or donut-type devices
IV fluid bags
Water-filled gloves
Use specialized cushioned boots
o Proper nutrition
Assess ability to swallow
Ask patient food preferences
Ensure a high protein diet (supplements like Ensure
or Boost)
Education of patient and family/caregiver
Hydration
Consult with registered dietitian
30-35 kcalories/kg body weight with 1.25-1.5 grams
protein/kg of body weight
Consider enteral or parenteral nutrition when oral
intake is inadequate
Older adults we really want BMI above 21 even
though normal is 18.5-25older adults are very frail
o Relieve pressure
Support surfaces
o Enhanced pressure redistribution, shear
reduction, & microclimate control such as air-
loss or air fluidized mattress for those with
Stage 3, 4, or unstageable pressure ulcers
o Foam mattressesstage 1 or 2
o Fill in dead space if wound is deep
 o Protect skin from incontinence
o Protect periwound skin
o DO NOT USE WET to DRY Dressings
o Clean wound with saline or wound cleaner
o Debridement
Wound will not heal with presence of necrotic tissue
Necrotic tissue increases bioburden
Firm, dry, stable eschar should not be debrided from
heels
Autolytic, enzymatic, sharp, & biological
Dressing Selection:
o Manage drainage while maintaining a moist wound healing
environment
o Dressing Types:
1) Firms
2) Hydrogel
Doesnt have a lot of drainage, but has lots
of granulation tissue that you want to protect
while healing
3) Hydrocolloids
Shallow stage 3, non-infected, most common
4) Alginates
Heavy exudate
5) Foams
Lots of exudate, stage 2/shallow stage 3
6) Gauze
Pressure ulcers that have been
cleaned/debrided
7) Silicone
To prevent periwound tissue injury when area
is fragile
8) Silver-Impregnanted
Very infectedsilver helps kill
9) Honey-Impregnanted
Stage2/3promote wound healing
10) Cadexomer Iodine
Those that have lots of exudate
Be carefulrelates to thyroid
A lot of people are allergic to iodine
Be cautious in those with impaired renal
function
11) Collagen Matrix
Stage 3 or 4 to help heal
o Specialty Dressings
Antimicrobial dressings
o Vacuum-assisted wound treatments (NWPT)
o No recommended in:
Inadequately debrided
Necrotic, or malignant wounds
Where vital organs are exposed
Wounds with no exudate
Individuals with untreated coagulopathy,
osteomyelitis or local/systemic clinical
infection
Actively bleeding wounds
Wounds in close proximity to major blood
vessels
o Hyperbaric oxygen treatment
 Most common injury in older adults
High mortality rate
Especially concerned with femoral neck fracturecould lead to
avascular necrosis of the femoral head
Clinical manifestations:
o Injured leg shortened
o Externally rotated
o Extreme pain prevents movement
Treatment:
o Immobilize immediately to prevent further damage
o Bucks traction may be used before surgery
Little boot around lower leg (traction & weight)
Make sure weight is NOT on floor
DO NOT turn side to side
Trapeze can be used to help the patient move (sit
upright more)
No pins
Assess skin
Look at circulation
May need to reposition
Hip fracture
o Surgery is treatment of choice
Open Reduction Internal Fixation (ORIF)
Femoral neck fracture repairs = pins
Intertrochanteric fracture repairs =
bidirectional
o Surgical procedure depends on
Type of injury
Condition of the person
Preexisting orthopedic conditions
o With acute or chronic diseases the risk of surgery may be too
greatmedical management may be preferred
Nursing management:
o ABCs!
o Pain assessment
o Skin assessment
o Body alignmentabduction pillow
o Ambulation
Provide analgesic before first time out of bed
o Education to return home
o Monitor for complications
Dislocation of the device
Avascular necrosis
Infection
Delayed healing
PEfrom DVT or fracture surgery, fat embolism or
something else from rupturing the tissue, etc.
DVTdue to immobility
Compartment Syndrome
Due to lack of perfusion
Reduced circulation in an area due to edema
Pain, pressure, paralysis, parathesia, pallor,
pulselessness (use Doppler)
Notify HCP!
Poor alignmentdislocation of the prosthesis
Infection
Skin alterations
Hazards of immobility
 o Tick borne illness
o Deer ticks
o 2 weeks till symptoms really manifest so treat right away if
suspected
o 3 Clinical stages
1. Erythema migrans at site of bite (or within one
month of bite)
2. Multiple erythema migrans lesions, some
Lyme Disease neurological & cardiac findings
3. Arthritis involving one or a few large joints (ie: knee)
and/or neurological problems (ie: encephalopathy)
o Clinical manifestations:
EM lesionannular red rings
Serologic test IgM antibodies & IgG antibodies to B.
burgdorferi
o Treatment
Treatment is 14-21 days
Prevention is important!
Light colored clothing (so ticks can be
spotted)
Tuck pant legs into socks
Wear long sleeve shirts tucked into pants
Perform regular tick checks
Chronic, autoimmune disease affecting myelin sheath &
conductive pathway of CNS
One of the leading causes of neurological disability in young adults
Periods of exacerbations & remissions
o As severity & duration progresses, exacerbation > frequent
Relapsing-remitting most common type of the 4 types
Major concernlong time to diagnose because
signs/symptoms can be non-specific & vague
Cause unknown, tends to occur among family members
Usually occurs between ages 20-40
Women affected twice as much as men
Normal life expectancy & does not always lead to severe disability
Signs/symptoms
o Early symptoms vague & nonspecific
o Vision, mobility, & sensory changes
o Ask if fatigue, stress, overexertion, temperature extremes, or
hot baths/showers aggravate these symptoms
Multiple o Because location of damage is so variable, no two people
Sclerosis have same outcomes or results
Clinical manifestations
o Fatigue, weakness
o Abnormal reflexes (absent or exaggerated)
o Visual disturbances
Impaired, diplopia, or nystagmus
o Motor dysfunction
Weakness, tremors, incoordination
o Sensory dysfunction
Parasthesias, impaired vibration, & position
o Impaired, slurred speech
o Urinary dysfunction
Hesitancy, frequency, urgency, UTI
o Neurobehavioral symptoms
Depression, emotional inability
Diagnostic tests
o No specific procedure
 o Collective results of variety of tests
Abnormal CSF (cerebrospinal fluid)
Gather info/date about 2 attacks separated in time &
space
MRI consistent with MS
Treatment/Management
o Acute attacks:
Corticosteroids200mg prednisone for 1st weeks,
then taper off
Immunosuppressive agents
Some subQ injections that patients can administer
themselves
Anticholinergics for bladder (ie: Oxybutin)
o Chronic symptom management:
Treatment of spasticity
Control of fatigue
Treatment of depression with antidepressants &
counseling
Bladder management with anticholinergics &
intermittent catheterization
Bowel managementstool softeners, bulk laxatives,
suppositories
Multidisciplinary rehab approach
Involve physical therapists in
interdisciplinary care
Dystonia, abnormal posturemake sure patient is
balanced and/or has assistive devices when
ambulating
MEN erection issues prescribed ED drug
WOMEN vaginal dryness water based lubricants
Nursing interventions
o Promote motor function
Muscle stretching
Frequent rest periods, avoid sudden position
changes
Ambulation & activity with assistive devices
Change positions
o Minimize fatigue
Brief rest periods in day
Avoid overheating, overexertion
o Optimize sensory function
Eye patch for double vision
Orientation to environment, remove obstacles
o Maintain urine elimination
Adequate intake, voiding schedule
o Normalize family processes
o Promoting sexual functioning
o Involves siliconized rubber catheter placed into abdominal
cavity for infusion of dialysate
o Renal replacement therapy
o Using peritoneal membrane as filter instead of
outside
o Most common
o Less risk
o Catheter directly into peritoneum=infectionhospital is a
DANGER ZONE!
Peritoneal o Types:
 dialysis Continuous ambulatory (CAPD)
Infusion sits there, does its thing, then
connect back to drain
Automated (Cycler)
Intermittent
Continuous cycle
o Sterile technique in the hospital
o Catheter is surgically put in
o Clamp, leave, reattach, drain
o Monitor Is & Os
Weight is very important in dialysiswant to weigh
the person everyday at the same time, same clothes,
etc. an increase in weight may indicate fluid
retention
o Complications:
Risk for infection (peritonitis)
Clear then cloudy may indicate infection
Leaking from catheter site is another big risk
for infection
Electrolyte imbalances
Painfeeling of abdominal fullness or pain at site
Exit site/tunnel infections
Dialysate leakage
Poor dialysate flowmay need to change
position, palpate abdomen

Nursing Priorities:
Evaluate baseline vitals, weight, & lab tests BEFORE treatment
Continuously monitor patient for respiratory distress, pain, &
discomfort
Monitor prescribed indwell time & initiate outflow
Observe outflow amount & pattern of fluid

Cerebrovascu
lar Accident
(CVA)

Migraine
Headaches

o Autosomal recessive
o Affects all exocrine glands and organs
o Progressive lung disease due to infection, inflammation and
mucus plugging
Airtrapping, bronchiectasis and atelectasis
o Pancrease involvement
Deficient enzymesmalabsorption, oily stools and
cramping
Vitamin A,D,E, & K deficiencies
o Liver
Gallstones and cirrhosis
 Cystic o Intestinal
Fibrosis Meconium ileus at birth and obstructions
o Skin
Salt in sweat
Hyponatremic, hypochloremic, metabolic alkalosis
o Reproductive
Sterile males
Thick vaginal mucus blocks sperm from implanting in
females
o Clinical Manifestations
FTT
Salty tasting skin
Frequent pulmonary infections
Digital clubbing
Greasy stools
o Diagnostic tests
Newborn screening
Elevated sweat chloride test (>60)
o Treatment
Chest physiotherapy
Antibiotics
Mucolytics
Asthma treatment (if they have asthma)
Creon (pancreatic supplement)- allows fat to be
absorbed
Increased caloric intake and vitamins
o Nursing Management
Oxygen, nebulizers CPT
Medications and supplements
Nighttime enteral feedings
Can happen through heat (dry/moist), contact burns, chemical,
electrical, or from radiation
Depth of burn injury
o 1st degreesuperficial
o 2nd degreesuperficial partial thickness, deep partial
thickness
o 3rd degreefull thickness, deep full thickness
Priorities
1. Stop burn
2. Cool burn
3. Cover (prevent infection
4. Treat pain
5. Antimicrobials
Early response to burn is inflammation
Burns o Will have swelling (edema), redness, warmth, & erythema
Vascular changes
o Fluid shift: third spacing or capillary leak syndrome, fluid
imbalance, electrolyte (hyperkalemia & hyponatremia), acid-
base, & hemoconcentration
o Fluid remobilization: 48-72 hours after injury, diuretic stage
begins
Assessment
o Neurological
LOC, assess for sedation, pain management
o Cardiovascular
Shock (septic/hypovolemic), V/S, hemodynamics
o Pulmonary
 Airway (worry about smoke inhalation), pulmonary
edema, ABGs
o Renal
Urine output, renal function
Urine color, odor, & presence of particles
o Gastrointestinal
Ulcerscritically ill patientsbodys compensatory
responsealtered perfusionslows peristalsis
(decreases motility)acid sits there for longer
periods of time
Put them on a proton pump inhibitor

Rule of 9s
Surgical interventions
o Escharotomycut open to remove fluids (blood)
o Skin autograft
When a blood clot blocks one or more of your veins
Typically in legs
Can be caused by surgery, trauma, or prolonged inactivity
Signs/symptoms:
Thrombophle o Warmth
bitis o Tenderness
o Pain
o Redness
o Swelling
Clusters of nerve cells in the brain signal abnormally, which may
briefly alter LOC, movement, or actions
Two or more unprovoked (primary) seizures
Provoked (secondary) seizures
o Brain tumor
o Metabolic disorder
o Acute alcohol withdrawal
o Electrolyte disturbance
o High fever
o Stoke
o Head injury
o Substance abuse
Seizures o Heart Disease
o Treat underlying cause & give anti-seizure medications
Generalized Seizures
o Tonic-clonic aka Grand malfall to floor, jerking, shaking
o Absence
o Myoclonic
o Atoniccollapse to floor, complete loss of muscle tone, may
have helmet on, worry about falls & head injuries
 Partial Seizures
o Simple
Remain conscious
May have an aura
May spread
May be sensory
Can be muscle related
o Complex
Loss of consciousness (eyes still may be open)
Syncope
Safety risk, may do something they arent aware of
Nursing interventions (Seizures)
Padded bed rails
Place on side to prevent aspiration
Stay with patient
Monitor for status epilepticus
o Prolonged seizure (> 5 minutes) or keep seizing over 30
minutes
o Medical emergency!
o Notify HCP
o Will burn up all sugar in the brain
o Lorazepam (Ativan)
o Have suction equipment available
o Monitor vitals
o Provide oxygen
Seizure documentation
When seizure started
Body part 1st involved
Changes in pupil size or eye deviation?
Changes in LOC?
Presence of apnea, cyanosis, salivation?
Incontinence?
Movement/progression of motor activity?
Tongue or lip biting?
When seizure ended
*Medical management (Seizures)
For all types of seizures
o Divalproex (Depakote)
All seizures
Therapeutic range: 50-100 mcg/ml
Side effects: Hair loss, tremor, increased liver
enzymes, bruising, & N/V
o Valproic acid (Depakene)
All seizures
Therapeutic range: 50-125 (total), 6-22 (free)
Side effects: Hair loss, tremor, increased liver
enzymes, bruising, & N/V
o Phenytonin (Dilantin)
All types of seizures EXCEPT absence, myoclonic, &
absence
For status epilepticus
Therapeutic range: 10-20 mcg/ml, 1-2 mcg/ml (Free)
Low= seizures
High= toxicity
Side effects: Gingival hyperplasia
o Worry about toxicity
o Must taper off
 o Can have GI issues & exacerbate depression
For partial & general tonic-clonic seizures
o Carbamezapine (Tegretol)
Partial or generalized tonic-clonic seizures
Therapeutic range: 4-12 mg/L
Side effects: H/A, dizziness, diplopia, blurred vision,
N/V, & leukopenia
o Phenobarbital (Barbita)
Generalized tonic-clonic seizures or partial seizures
Therapeutic range: 10-40 mg/L
Side effects: Sedation, overdose can be fatal,
monitor for drowsiness, sleep disturbances, cognitive
impairment, & depression
o Primidone (Mysoline)
Partial seizures, tonic-clonic seizures
Therapeutic range: 5-10 mg/L
Side effects: Monitor for vertigo & lethargy
Turn a hair dryer on a cool setting & aim it under the cast
Cast care Can take OTC antihistamine if still itchy
Do not stick objects inside the cast to scratchcould cause an injury
or infection
Obstruction of the intestine due to paralysis of the intestinal muscles
Signs/symptoms:
Paralytic o Constipation
Ileus o Abdominal distention
o N/V
o No bowel sounds
Paracentesis Removal of fluid from a body cavity via a needle (ie: remove ascites)
Can be used as a diagnostic or treatment

Pain
management

Pump failing or not working effectively

Hearts inability to pump amount of oxygenated blood need to meet
metabolic requirements of the body
2 main ways to classify people with heart failure
1. Shortness of breath
2. Activity intolerance
Is not a disease, but a syndrome
Associated with long standing HTN & CAD
Most common reason for hospitalization in adults > 65
Risk factors:
o CAD & its risk factors
Smoking
Obesity
Sedentary lifestyle
o Age
Heart failure HF is the most common reason for hospitalization for
those > 65
o HTN
To compensate for increased blood pressure the
heart muscle thickens
Over time force of heart muscle contraction
weakens, preventing normal filing of the heart with
blood
 o High cholesterol
o African American descent
Related to higher incidences of diabetes & HTN
Have 30% higher mortality rate
Etiology:
o May be caused by an interference with normal mechanisms
regulating cardiac output (CO)
CO is influenced by:
Preload
-Volume of blood in the ventricle at
the end of diastole
Afterload
-Force ventricle must develop to
eject blood into the circulatory
system
Myocardial contractility
Heart rate
Types:
o Left-sided failure
Most common
Blood back up through left atrium into pulmonary
veins
Signs/symptoms:
Pulmonary congestion/edema
Paroxysmal nocturnal dyspnea
Cough
Crackles
Wheezes
Blood-tinged sputum
Restlessness
Confusion
Orthopnea
Tachycardia
-Compensatory mechanism from
SNSwill be short lived & cause
more problems
Exertional dyspnea
Cyanosis
o Right-sided failure
Backflow to right atrium & venous circulation
Results in diseased right ventricle
Signs/symptoms:
Fatigue (related to decreased CO)
Increased peripheral venous pressure
Ascites
Hepatomegaly/splenomegaly
Distended jugular veins
Anorexia & complaints of GI distress
Swelling of hands/fingers
Dependent edema

Care after
death

Lupus
Erythematos
 us

o Inadequate supply of dietary iron

o Generally preventable (iron-fortified cereals/formulas)
o Adolescents at increased risk because of rapid growth & poor
eating habits
o Symptoms
Fatigue
Pallor
Iron
o Treatment
Deficiency
Increase iron intake (food)
Anemia
Beef, clams, oysters, turkey, chicken, fish
Bok choy, brussel sprouts, broccoli
Dried fruits
Iron supplements
Do not take with milk
Can cause constipation
Take with citric acid
Change in stool color & consistency
Stains teeth (brush after taking)
Hypospadias Condition of male genitalia in which the opening of the urethra is on
the underside of the penis instead of the tip
Usually repaired with surgerymales eventually have normal adult
sexual function

Abdominal
pain

Chest pain not relieved

Classic sign: left-sided, crushing pain, radiating to left arm, & jaw,
diaphoresis due to sympathetic system response, nervousness,
anxiety, flushing of skin
Atypical presentation: can have back pain, fatigue, SOB (elderly),
change in mental status, epigastric pain
Diabetics can have peripheral neuropathy leading to atypical
presentationSilent heart diseasescreen more often!
N/V
Fever
High HR, low/high BP
Dysrhythmias are the biggest risk factor for MI
Priorities:
1. ABCs
2. Other physiological issues
3. Psychosocial
Treatment:
Morphine
Myocardial o Relaxes smooth muscles
Infarction o Vasodilation
o Usually 2mg to start
o Can cause respiratory depression
o If given too muchgive NARCAN
Oxygen
Nitroglycerin
o Vasodilation
o Allow more blood & O2 to heart
o Lowers BP so check before & after 3 doses at 5 minutes
 apart
o If become hypotensive give fluids & lower head
o Headaches common
Aspirin
o 325mg or 4 baby aspirin
Glycoprotein (GP) IIB/IIIa inhibitors
Once-a-day beta blockers
o Most reason for beta blockers is for CAD, not to lower BP
o Slows HR & lowers workload of the heart
ACE inhibitors or ARBs
o Preventing remodeling of heart or alterations in left ventricle
from MI
o Prevents Angiotensin 1 to 2, blocks aldosterone release so
Na+ excreted & K+ retained
Calcium Channel Blockers
o MI patients cant tolerate beta blockers or those in more
advanced disease
o Decreases preload
Coronary stent: holds plaque up against the arterycreates
passage way for perfusion
CABG: 4 vessels occluded or major occlusion
o NPO before surgery
o Anxiolytic meds, integrative cardiac meds, sleep meds
Goals:
Oxygen supply will meet demand
Pain relief
No progression of MI
Immediate & appropriate treatment
Cope effectively with associated anxiety
Cooperation of rehab plan
Modify or alter risk factors
Nursing Interventions (MI):
Administer O2, positioning
Continuous ECG monitoring
Frequent vital signs
Pain relief, rest, & comfort
Emotional relief/anxiety relief
Prevent complications and/or progression of MI
o Most common complication of MI is dysrhythmias
o Heart failurecan come from cardiogenic shock, pulmonary
edema, or come later on
o Cardiogenic shock
Nursing Interventions (Post CC/PCI):
Patients usually supine after femoral coronary stick
Want to look at back (retroperitoneal bleed)
Can have compartment syndrome; occlusion of blood flow & new MI
can happen
Check puncture sight, distal pulses, skin color/temp., capillary refill,
urine output (to see how kidneys are perfused)
Most common urinary diversion
Incontinent urinary diversion (need an
appliance)
Taking tissue from ileum & making a makeshift
bladder
Ileal conduit Stoma brought through the skin
This is where the urine flows (incontinent diversion)
Must be connected to a bag for drainage
Tremendous impact on life
 Worry about infectionskin care must be
maintained
Social well-being
Sexuality
If not drainingPROBLEM
Mode of transmission: fecal-oral
Usually through ingestion of contaminated
foods/liquids
Common in underdeveloped countries, overcrowding,
& poor sanitation
Hepatitis A Infected food handler can spread
diseaseTravelers
Commonly spread person to person, rarely by blood
transfusion
Incubation period 15-50 days (average 4 weeks)
Self-limiting
No chronic infection
With supportive treatment, should get better on
their own

Respiratory
alkalosis

Detatched
retina

Cardiac
catheterizati
on

Hemorrhagic
o GI bleed
o Trauma
o Massive hemoptysis
o AAA rupture
o Ectopic pregnancy
o Post Partum bleeding
*PRIORITIES
1. Stop bleeding
2. Stop underlying problem
3. Give fluids
Non-Hemorrhagic
o Vomiting
o Diarrhea
o Bowel obstruction
Fluid volume
deficit o Pancreatitis
o Burns
o Dehydration
Signs/symptoms
o Confusion
o Increased HR
o Increased RR
 o Decreased cardiac output
o Decreased BP
o Cool skin
o Decreased body temperature
o Decreased Hgb & HCT
Interventions
o No pharmacotherapy unless severeneed fluid replacement
o Fresh whole blood
o Colloids
o Lactated Ringers, 0.9% Normal Saline, 3% NaCl
Synchronized counter-shock
Used in emergencies for unstable ventricular/supraventricular
dysrhythmias
Cardioversion Invasive, but relatively quick (1 hour)
Hold digoxin
Usually in a more controlled setting
To shock their rhythm back
External electrical activity
Want them anti-coagulated
No single cause
Reflux of gastric contents into lower esophagus = irritation
Clinical manifestations
o Heartburn (greater than 1 week, increasing severity,
waking up at night, burning, tightening in chest sternum
upwards)
o Bitter/sour liquid into mouth
o Post meal bloating
GERD o N/V
o Wheezing, coughing, dyspnea, hoarseness of voice
Diagnostic tests
o Barium swallow
o Endoscopy
o Biopsy & cytologic specimensto differentiate carcinoma
from Barretts esophagus
o Esophageal manometric studies
Treatment
o H2 receptor blockers
Zantax, Pepsid, Tagament, more than 1x/day,
promote healing of inflamed tissue, short term
o Proton pump inhibitors
Protonics, Prylosec, long-acting, 1x/day
o Antacids
Short-acting, not used daily, increased risk for
hemorrhage
Nursing interventions/management
o Avoid milk products at night, late snacks or meals, caffeine,
alcohol, citrus fruits, chocolate, & high-fat foods
o HOB > 30 degrees
o Stay upright for 2 hours after eating
o No eating 3 hours before bed
o Sleeping on right side can increase heartburn
o Sleeping on left side decreases acid from coming up
Complications
o Ulcers
o Risk for esophageal cancers
o Strictures
o Hiatal Hernia
Opening of diaphragm where esophagus passes
 through becomes enlarged & part of stomach tends
to come through lower part of thorax
Flap of lower esophageal sphincter is relaxed, muscle
goes through opening
Clinical manifestations:
Heartburn
Dysphagia
Regurgitation
However, 50% are asymptomatic
Nursing interventions/management:
Small/frequent feedings
Keep upright 1 hour after meals
Possible surgery
-Nissen Fundoplication:
laprascopic anti-reflux surgery,
reinforces valve between esophagus
& stomach, wraps upper portion of
stomach around esophagus (fundus
of stomach wraps around the
esophagus when esophagus
sphincter is weak)
*Patient teaching post-op:
Splinting to prevent
dehiscence, rest, look at
color/pallor, hypovolemic
shock r/t bleeding

Sickle Cell
Anemia

Air or gas in the pleural space that causes the lung to collapse
Common risks
o Blunt chest trauma
o Penetrating chest wounds
o Closed/occluded chest tube
Pneumothora Signs & symptoms
x o Pleuritic pain
o Respiratory distressincrease RR, increased HR, hypoxia,
cyanosis, dyspnea, use of accessory muscles
o Tracheal deviation to unaffected side= CLASSIC SIGN
o Asymmetrical chest wall movement
o Anxiety
o Percussion
Hyperresonance (Pneumothorax)
Dullness (Hemothorax)
o Subcutaneous emphysema
Rice Krispies under skin
Diagnostic tests/procedures:
ABGs
Chest X-ray
Thoracentesis (to confirm hemothorax)
Nursing Interventions:
Assess & monitor respiratory status
Monitor chest tube drainage
Give meds as ordered
o AnxiolticsLorazepam (Ativan) or Midazolam (Versed)
o AnalgesicsMorphine or Fentanyl
 Provide emotional support
Cholecystogr X-ray to evaluate gallbladder
am Contrast medium swallowed
o Autoimmune disorderbeta cells destroyed
o Cant prevent it
o Onset usually < 30 years old, but can happen at any age
Type-1 o Insulin deficiencyalways requires exogenous insulin
diabetes o PO agents are ineffective
o Etiology viral infection
o Skinnier/underweight
Epidural Hematoma
o Between dura mater & skull from high impact to temporal
areas of brain
o 90% associated with linear fracture
o Classic presentation:
Brief loss of consciousness
Followed by AOx3
Loss of consciousness again
o Surgical evacuation of hematomaget rid of blood
o Nonreactive & dilated pupil on side of injury=
EMERGENCY
Subdural Hematoma
Closed head o Between dura & arachnoid layers
injury o Typically venous injury
o Types:
Acute SDH
< 48 hours from injury
Often associated with sudden deceleration
injuries (ie: MVCs)
Manifestations
o Drowsiness
o H/A
o Confusion
o Slowed thinking
o Agitation
Sub-acute SDH
48 hours to 2 weeks from injury
Rare & harder to detect, education important
Neurological deterioration does not occur for
days/weeks
Chronic SDH
> 2 weeks from injury
Usually from low impact injury
Manifestations
o H/A
o Lethargy
o Projectile vomiting
o Seizures
o Pupil changes
o Hemiparesis
Subdural drain placement
Surgical evacuation of hematoma
Monitor LOC
Pain management
Subarachnoid Hematoma
o Between arachnoid layer of meninges & the brain
o Common in severe brain injuries (ie: aneurysm)
 o Nuchal rigidity & headache
o Placement of an intraventricular catheter & monitor ICP
o Look at quantity & color of CSFmay have blood in it
Intracerebral Hematoma
o On brain itself
o Hemorrhagic stroke
o Accumulation of blood in the brain parenchyma
o From uncontrolled HTN, ruptured aneurysm, or trauma
o Manifestations
H/A
Decreasing LOC
Dilation of one pupil
Hemiplegia
o Medical management
Manage ICP (Normal: 7-15 mmHg)
Elevate HOB
Hypertonic saline, Mannitol, protein
Manage oxygen
Manage carbon dioxide in blood
Complications of Closed Head Injury
o Diabetes Insipidus (DI)
> 200 cc/hr., losing too much urine
Pressure on pituitary gland & loss of ADH secretion
Dilute urine
Increased serum sodium
Treatment
Vasopressinantidiuretic to decrease urine
output
If improvingwill have decreased urine
output & increased specific gravity
o SIADH
Excess secretion of ADH
Oliguria
Concentrated urine
Decreased serum sodium
Increased ICP
Treatment
Fluid restriction
o Cerebral Salt Wasting (CSW)
State of hypovolemia with low sodium & urine
osmolality
Often mistaken for SIADH
SIADH is too much fluid, CSW is low fluid
Treatment
Sodium replacement
o Herniation
Brain pushes through foramen magnum
o Seizures
Irritation in brainanti-seizure meds
Bronchospasm & dyspnea
Tissue damage is not reversible & increases in severityeventually
respiratory failure
Leading cause of morbidity & mortality worldwide
Associated with significant economic burden
Onset in mid-life
Symptoms slowly progress
 Long smoking history
Risk factors:
o Cigarette smoking
Smoking cessation!
ASK
ADVISE
ASSESS
ASSIST
ARRANGE
o Alpha 1 antitrypsin (AAT) deficiency
Helps breakdown enzymes around alveoli
COPD If not working they will breakdown alveoli =
emphysema at younger age with no PMH of smoking
o Air pollution
o Gender
o Age
o Respiratory infections
o Socioeconomic status
o Asthma/bronchial hyperreactivity
o Chronic bronchitis
o Emphysema
Complications
o Hypoxemia
o Acidosis
o Respiratory infections
o Lung cancer
o Diabetes
o Osteoporosis
o Cardiac failure, especially cor pulmonale (hypertrophy/right-
sided heart failure)
Air trapping = taking up more space = more
resistance = more pressure = right ventricle working
harder to pump blood
o Cardiac dysrhythmias
Hypertrophy of heartincreases distance electrical
conduction has to travel
o Ventilation failure (not getting air in/out)
o Oxygenation failure (not getting O2 to blood)
o Or Combination
o Anxiety & depression
Diagnostic tests
o Dyspnea assessment tool
o ABGs
o Sputum samples (culture & sensitivity, infection?)
o CBC (hemoglobin/hematocrit)
o Serum electrolyte levels (dilutional hyponatremia)
o Serum AAT levels (Alpha 1 Antitrypsin deficiency?)
o Chest x-ray
o Pulmonary function test
o Spirometry: required to establish diagnosis
Should be performed after administration of dose of
short-acting inhaled bronchodilator to minimize
variability
FEV1/FVC < 0.70 confirms airflow limitation
2 or more incidences that FEV1 < 50% OR 1 +
hospitalizations for COPD exacerbations = HIGH RISK
Treatment
o Pulmonary rehab
 Incentive spirometer 10x/hour
Chest physiotherapy
Hydrationif not fluid overloaded
Exercise
o Beta-adrenergic agents
o Cholinergic antagonists
o Methyxanthines
o Corticosteroids
o Mucolyticsto get mucus out
o Want to stop Robitussin or any other cough suppressants
stop cough, which will prevent them from removing
secretions
o Lung transplantationfor end-stage
Large midline incision or a transverse anterior
thoracotomy
Management
o Ineffective breathing
Breathing techniques
Positioning to help alleviate dyspnea or drainage
Energy conservationnot doing too much at one
time
Encourage patient to pace activities
Do not rush through morning activities
Gradually increase activities
o Ineffective airway clearance
Possible suctioning
Controlled coughing
Chest physiotherapy with postural drainage
Hydration via beverage & humidifier
Flutter-valve mucus clearance devices
Tracheostomy
o Risk for imbalance nutrition
Often in a hyper-metabolic stateneed more calories
Prevent protein-calorie malnutrition through dietary
consultation
Monitor weight, skin condition, & serum pre-albumin
levels
Dyspnea management
Food selection to prevent weight loss
o Prevent anxietythis can worsen symptoms
o Risk for pneumonia & other respiratory infections
Avoid large crowds
Pneumonia vaccine
Yearly influenza vaccine
Incompetent valves of deep veins, venous obstruction
Usually caused by HTN
Perfusing the extremities, but blood not coming back up & edema
occurs
Peripheral Pulses still present
Vascular Edema occurs because RBCs infiltrate surrounding tissues
Disease o Skin thick, hard, & contracted
(PVD) o Brown leathery skin
o Hyperpigmentationenzymes break down RBCs
o Stasis dermatitiscellulitis, infection
Ulcers develop above the ankle
Gravity will keep blood from getting back to heartwant to ELEVATE!
Collaborative care
 o Elevate extremity
o Compression
o Moist dressing
o Observe for infection
o Good nutrition
ABI less than 0.9 suggest PAD
Can have bothusually patients with long-standing HTN
Featur Arterial Ulcers Venous Ulcers Diabetic Ulcers
e
Claudicatio Chronic Diabetes
n after non-healing Peripheral
History walking ulcer neuropathy
1-2 blocks No No
Rest pain claudicatio claudication
Pain at ulcer n or rest
site pain
Ankle/leg
swelling
End of toes Ankle Plantar
Between toes Brown foot
Ulcer Deep pigmentati Pressure
locatio Ulcer with on points
n even edges Ulcer bed Deep
& look Little pink Pale
granulation Uneven Even edges
tissue edges Little
Granulation granulation
tissue tissue
present
Cool Ankle Pulses
NO pulses discoloratio present
Hair loss n & edema Cool or
Other Pallor with No warm foot
finding elevation neurological Painless
s Dependent deficits
rubor Pulses
Possible present
neurological Scarring
deficits (ulcers that
have
healed)
Changes in mental ability severe enough to interfere with ADLs
Memory loss & cognitive decline
Not curablewill lead to death eventually
DSM V: Decline in memory and one of the following
o Expressive or receptive aphasia
o Unable to identify objects in hand
o Difficulty with motor activities
o Inability to think abstractly, make sound judgments, and
plan & carry out complex tasks
Alzheimers
Warning signs of Alzheimers
Disease
o Poor judgment/decision making
o Inability to manage a budget
o Losing track of the date or season
o Difficulty having conversation
o Misplacing things and being unable to retrace steps to
find them
Risk factors
o Age
 o Family history (if someone has early onset)
o Genetics (some people that cant get rid of proteins that
make the plaques & tangles are at increased risk)
o Head trauma, DM, depression
o Higher education, greater social networksliving longer
Behavioral symptoms
o Psychomotor agitationwandering, not being able to
sit still
o Psychosishallucinations, delusions
o Aggressionverbal or physical
o Apathynot wanting to do anything all of a sudden
o Depression
o Sleepdaytime sleepiness, sundowning, want to keep
them awake during the day
*Stages of Alzheimers
o Early
Mild cognitive decline
Noticeable deficits in demanding job
situations
o Mild
Deficits with complicated tasks
Moderate cognitive decline
Denial & withdrawal from challenging
situations
Poor attention
Apathy
Depression
Word finding difficulty
o Moderate
Deficits with choosing proper attire
Moderate severe cognitive decline
Disorientation
Increasing memory loss
Insomnia
Wandering
Speech difficulty
Restlessness
o Moderately Severe
Deficits with ADLs
Severe cognitive declinetotal dependence
o Severe
Declined speech ability
Loss of ability to walk, sit up, smile, hold
head up
No verbal or self abilities
Agnosiacant identify things in hand
Apraxiaunable to move tongue to speak
Aggression
Agitation
Incontinence
Poor ADL function
Gait disturbance
Types:
o Pre-renal
Comes before the kidney
Ischemic process
 Decreased blood flow to kidneys
Ex: hypovolemic shock
Acute Renal o Intra-renal
Failure At kidneys
Ex: glomerulonephritis, cancer, medications,
substances (radiopic dye)
o Post-renal
Below the kidneys
Ex: BPH leading to hydronephrosis, tumor/stone in
bladder (obstructions)
Pre-renal azotemia
o Dehydration, buildup of nitrogenous wastes
Possible causes:
o Hypovolemic shock
o Heart failurealtered perfusion to the kidneys
Rapid decrease in kidney function can lead to collection of metabolic
wastes in the body
Phases of AKI:
o Onset
o Oliguric
o Diuretic
o Recovery
May be reversible with prompt intervention!

Bone marrow
biopsy

Resting tremor
Bradykinesiaslowness of movement
Rigiditycogwheeling
Postural instabilityleaning forward, disturbed balance
Loss of flexibility
Aching
Fatigue
Sleep disturbances
Drooling, sweating, weight loss
Orthostatic hypotension
Depression, dementia, psychosis, personality changes
Micrograhpia (very small handwriting)
Good way to diagnose PDif dopamine makes symptoms better
Risk factors
o Age
Parkinsons o Family history & genetics
Disease o Race/ethnicity (Caucasian)
o Gender (male)
o Declining estrogen levels
o Agricultural work
o Head trauma
Preventive measures?
o Smoking
o Alcohol
o High cholesterol
o High caffeine intake (GUYS WERE GOOD! )
Types
o Idiopathic PD
No identified cause
 Insidious onset
o Acquired Parkinsonism
Caused by infection, drug toxicity (ie: Haldol), or
trauma

Diagnostic tests (PD)

Medical history & clinical featuresno disease specific biological
marker
Positon Emission Tomography (PET) or Single-photon Emission
Computed Tomography (SPECT) with dopaminergic radioligands
Rule out secondary causes
Treatment (PD)
Levadopa
o Most effective, but less effective over time
o Long term use= high risk of dyskinesias (involuntary
movement/spasm)
Dopamine agonists
o Less effective
o Less likely to cause dyskinesias
o Frequently causes troubling side effects
COMT inhibitors, Dopamine Releaser, MAO-B Inhibitor
Dopamine does not cross the blood brain barrier

Intracranial
tumor

Peripheral facial nerve paralysis (cranial nerve 7)

Benign, unilateral
All ages
Cause unknowncause may have to do with herpes simplex virus
Patients rarely hospitalized
Can last about 48 hours (50% of patients)5 days
Flaccidity of affected side of face with drooping of mouthvery
similar to stroke
Recover within a few weeks or months
Signs/symptoms
Bells palsy o Increased pain in making facial expressions
o Inability to close eyes
o Loss of taste
o Decreased chewing
o Drooping of mouth
o Fever
o Tinnitus
Treatment
o Drug therapy
Prednisone (30-60 mg one time a day for the first
week)
Zorivax
Nursing Interventions
o Pain management
o Moist heat
o Protect face
o Good nutrition (chew on unaffected side, oral hygiene)
o Dark glasses
o Artificial tears
o Eye patch & eye drops if they cant close their eye
o Psychosocialbody image disturbed
 o As the muscle tone improves, you want them to wrinkle their
brows, & puff their cheeks 3-4 times a day in front of the
mirror
Removal of thyroid gland by surgery
Thyroidectom Thyroid responsible for producing hormones that regulate
y metabolism
Used to treat hyperthyroidism or goiter
Progressive opacity or clouding of the lens
Size, site, and density vary among individuals (can be different in
persons two eyes
Risk factors:
o Increased age
o Smoking
Cataracts o Alcohol use
o Diabetes
o Hyperlipidemia
o Eye trauma
o Exposure to the sun & UVB rays
o Long-term corticosteroid use
o Caucasian
Signs/symptoms:
o Blurry vision (becomes darker over time)
o Glare
o Halos around objects
o Double vision
o Difficulty sensing contrasting colors
o Poor night vision
Nursing management
o Surgery is treatment of choice (outpatient, lens
replacement)
o If both eyes have cataractswill do one at a time

Wound
healing/diet

Inflammation of meninges
Pathogenic organisms cross blood brain barrier & enter CNS
Viral usually self-limiting
Bacterial may be life-threatening, fungal is less
Can be caused by HSV-1
DROPLET PRECAUTIONS!
Clinical manifestations
o Severe headache, fever, N/V
o Classic: nuchal (neck) rigidity, positive Kernigs (flexing
the patients hip 90 degrees then extending the patients
Meningitis
knee causes pain) & Brudzinskis (flexing the patients neck
causes flexion of the patients hips and knees)
o Photophobia, symptoms of increased ICP
o Decreased LOC (using Glasgow scale), seizures, rash
(enterovirus)
Complications
o Cranial nerve dysfunction
o Hemiparesis, dysphasia, hemianopsia (half of visual field is
not seen)
o Cerebral edema seizures, bradycardia
Diagnostic tests
o Lab findings:
CSF analysis by lumbar puncture most significant
 Viral clear
Bacterial cloudy
LP patient is on one side, back is arched,
they can be relaxed and eupnea, just apply
band-aid over site once done, dont
necessarily need an anesthetic
CT scan
CBC with differential
Serum electrolytes
May have dilutional Na++ R/T SIADH (water
is retained)
Nursing interventions
o Follow ABCs!!!!!
o V/S, neuro checks, lungs, skin
o Reduce fever fever cerebral edema
Cooling blankets, Tylenol, sponge baths
o Manage fluid balance (I & O)
o Enhance Cerebral perfusion
o Reduce pain
o Optimal level of functioning
Rehab
Passive to active exercises
o Prevention:
Meningococcal vaccine for at risk patients
Dont share drinks, food, dont kiss
Common in close quarters/dorms/jails
Disorder of inner ear that causes spontaneous episodes of vertigo,
fluctuating hearing loss, ringing in the ear (tinnitus), & sometimes
pressure/fullness in ear
Usually unilateral
Menieres More common in 40-50, but can get at any age
Disease Chronic condition
May be on diuretic to reduce fluid retention, motion sickness
medication, or anti-nausea meds
Rehab for balance, hearing aid, Meniett device (application of
positive pressure to middle ear to improve fluid exchange), &
surgery
Total Hypertonic solution
Parenteral Central vein used
Nutrition ***Long term for people who cannot tolerate oral feedings
(TPN)
Progressive disorderpancreas makes < insulin over time
Insulin resistance
Etiology unknown
Type-2 Peaks at 50 years old, may occur earlier
diabetes 60%-80% obese
Insulin therapy required for 20%-30%
Oral agents effective for most

Pancreatitis

Progressive, irreversible kidney injurykidney function does not

recover
There are 5 stages of CKDEnd-stage kidney disease = Stage 5
o Based on GFR
Chronic Renal Normal (90-120)
Failure < 15 (need dialysis)
As we age our GFR decreases
Azotemia
o Nitrogenous wastes in the urinecan damage organs,
metabolic acidosis
Uremia
Uremic syndrome
Fluid buildup= edema, pulmonary congestion, electrolyte imbalances
Increase preload can lead to problems with the heartwhich can
affect kidneys
Stages of CKD:
o Reduced renal reserve
o Reduced GFR
o ESKD
o Kidney changes
o Metabolic changes
Urea & creatinine
o Electrolyte changes
Sodium
Potassium
Acid-base balance (metabolic acidosis)
Calcium & phosphorus
o Cardiac changes
Hypertension
Hyperlipidemia
Heart failure
Pericarditis
Can have strict renal diet (individualized)
o Hematologic changes
Decreased RBC production, which leads to anemia
Pallor
Dyspnea
IschemiaMI or infarct
Concurrent anemiacan give synthetic
erythropoietin
o GI changes
N/V
Decreased appetite
See nephrologist
Clinical manifestations:
o Neurologic
Increased nitrogenous wastes can lead to confusion
o Cardiovascular
Increased preload can lead to heart failure
o Respiratory
Dyspnea
o Hematologic
Altered erythropoietin
o Gastrointestinal
N/V, decreased appetite
o Skeletal
Osteoporosis (with Vitamin D deficiency)
o Urinary
Oliguria
End stagemay have no urine
o Skin
Uremiacrystals can come through skin
 Prurituscan be painful
Priority Assessments:
ABCs!
o Excess fluid volume
o Decreased cardiac output
Dietary restrictions
Uremic frost
Muscle strength/energy
Family members
Recombinant human erythropoietin
Interdisciplinary team
Treatment:
Hemodialysis
Peritoneal dialysis
o PRIORITY ASSESMENTS:
Postdialysis assessment
Hypotension
Headache
N/V
Malaise, dizziness
Muscle cramps, bleeding
Post dialysis disequilibrium
Difficult to arousewiped out
Make sure patient is moving during the 3
hours dialysis
Want BUN & creatinine to decrease after
dialysis
Watch for decreased BPDont want to
give digoxin, etc. BEFORE dialysis because
decreased BP
-Talk to HCP
-Dialysis may remove things like
antibiotics
Hypovolemic Shock: Loss of intravascular fluid volume, blood volume
insufficient to meet metabolic demands of tissues
Shock Hemorrhagic
o GI bleed
o Trauma
o Massive hemoptysis
o AAA rupture
o Ectopic pregnancy
o Post Partum bleeding
*PRIORITIES
4. Stop bleeding
5. Stop underlying problem
6. Give fluids
Non-Hemorrhagic
o Vomiting
o Diarrhea
o Bowel obstruction
o Pancreatitis
o Burns
o Dehydration
Signs/symptoms
o Confusion
o Increased HR
o Increased RR
o Decreased cardiac output
 o Decreased BP
o Cool skin
o Decreased body temperature
o Decreased Hgb & HCT
Interventions
o No pharmacotherapy unless severeneed fluid replacement
o Fresh whole blood
o Colloids
o Lactated Ringers, 0.9% Normal Saline, 3% NaCl

Cardiogenic Shock:
Cardiac failure leads to decreased tissue perfusion
Heart is damaged & unable to supply sufficient blood to body
PRIORITIES
1. Deliever more O2
2. Decrease metabolic O2
3. Fix underlying problem
Signs/symptoms
o Impaired cerebral perfusionanxiety & delirium
o Increased HR
o Increased RR
o Decreased BP
o Pulmonary congestioncrackles
o Cyanosis, pallor, cool clammy skin
o Decreased capillary refill
o Decreased renal blood flowdecreased urine output (retain
Na+ & water)
Interventions
o Sympathomimetics
o Vasopressors
o Vasodilators
o Diuretics

Anaphylactic Shock: caused by a severe systemic response to an allergen

resulting in massive vasodilation, decreased perfusion, decreased venous
return, & decreased cardiac output
Acute life-threatening reaction
Signs/symptoms
o Syncope
o Swelling of lips & tongue
o Angioedema
o Wheezing & stridor
o Decreased BP
o Increased HR
o Chest pain
o Flushing
o Pruritis
o Urticaria
o N/V
***TREAT WITH EPINEPHRINE

Septic Shock: overwhelming bloodstream infection, systemic inflammatory

response
Vital organs may not function properly or may fail
Occurs in people with underlying disease
o Immunosupressed (HIV/AIDS)
o Chemo patients
o Transplants
o Central lines
 o Urinary catheters
o Older adults with chronic disease= MOST COMMON
Sign/symptoms
o Decreased BP
o Decreased blood flow
Interventions
o Antibiotic therapy
o Fluids
o Vasopressor drugs

Neurogenic Shock: vasodilation as a result of loss of balance between

parasympathetic & sympathetic stimulation
Common causes
o Spinal cord injury
o Spinal anesthesia, medications
o Nervous system damage
Signs/symptoms
o Decreased SVR
o Decreased BP
o BRADYCARDIA
o Syncope
o Dry, warm skin
Interventions
o Heparin
o Osmotic diuretics, glucose, steroids
Diagnostic tests/procedures:
ABGs
Urine output
BUN to assess renal perfusion
Blood glucose
Electrolyte levels
Blood cultures
WBC & ESR may increase due to infection

*FOR SHOCK(S): Place victim in shock position, keep warm &

comfortable, turn head to one side if neck not injured or
suspectedat risk for aspiration
CPR Life-saving technique used when someones breathing or heartbeat
has stopped

Status Severe, life-threatening, acute episode of airway obstruction

Asthmaticus If not reversed patient may develop pneumothorax and cardiac or
respiratory arrest
Clinical manifestations (that asthma attack worsening)
o Cyanosis
o Inspiratory wheezing
o Altered LOC
o Use of accessory muscles
o Check ABGs or O2 saturation
Treatment
o IV fluids
o Potent systemic bronchodilator
o Steroids
o Epinephrine
o Oxygen
Glandular units in the prostate increase in the number of cells,
leading to enlargement of the prostate
Usually develops on outer part of the prostate
 Prostate produces the fluid that carries sperm
Surrounds the urethra (if enlarged it can obstruct urine flow)
Can effect a persons sexual health
During palpation of the prostate it is more spongy
Symptoms:
o Hyperirritable bladder
o Urgency & frequency
o Hypertrophied bladder wall muscles
o Cellules & diverticula
o Hydroureter
o Hydronephrosis
o Overflow urinary incontinence
o Incomplete emptying of the bladder=stagnant
urine=INFECTION
o Urinary dribbling
o Low stream
Diagnostic tests:
Benign Digital rectal exam
Prostatic Urinary analysis & culture
Hypertrophy Serum creatinine & BUN
(BPH) PSA (Prostate Specific Antigen)
Urodynamic flow studies
Cystourethroscopy
Treatment:
Drug therapy
o Hormonal manipulation
Proscartrying to block androgen
DO NOT GIVE WHEN PREGNANT (Category X)
Alpha-adrenergic blockers
o Promote relaxation of smooth muscle
o Examples:
Minipress
Cardura
Hytrin
o Side effects:
Orthostatic hypotension
Dizziness
o Give meds at bedtime & titrate them
Conservative therapy
o Stents, prostatic balloon
o Foley catheters
These can cause trauma to someone with
BPHleads to infection
o These are usually not long term
Invasive therapy
o TURPreduces tissue compressing the urethra
o Prostatectomy
Suprapubic
Retropubic
Perineal
Priority Assessments:
GOAL of treatments: to decrease symptoms & increase function
Want to restore bladder drainage
Treat complications (when it becomes problematic for the patient)