UNIT (14) : Disease Of 456. Describe columnar epithelial cells by gross cyst about 20 cm 6.

gross cyst about 20 cm 6.Histological variants of disease [Grave’s disease]?

Genital Tract & Breast
452. Name types of
ectopic pregnancy? (p=3)
• tubal
• ovarian
• abdominal
453. Name types of tubal
pregnancy according to
sites of fetus
implantation. (p=3)
• ampular
• interstitial
• frimbrial
454. What is placenta
polyps? (p=3)
• Tissue masses of variable
size with polypous
structure
• surrounded by
hyperplastic trophoblast
may have necrosis
• projects into myometrium
455. What is hiditidiform
mole? How does it affect
pregnancy? (p=3)
• gestational trophoblastic
disease
• appear as mass of
hydrophic swelling
[swollen]
• cystically dilated
chorionic vili covered by
proliferating
cytotrophoblast and
syncytial trophoblast.
• fetus is absent is called
complete hidatidform
mole: or dying not later
than 4th
month of gestation called
partial hydtidiform mole.
microscopic composition
of the choriocarcinoma.
(p=5)
• choriocarcinoma is
malignant tumour develop
from complete
hydi;diform mole. from
ar;ficial abor;on or after
normal pregnancy.
• only epithelial cells with
anaplas;c cuboidal
syncy;otrophoblast and
cytotrophoblast with ;ssue
atypism.
• stroma vessel and vili are
absent
• invading surrounding
structure with hemorrhage
and necrosis.
*457. Specify most
typical complicaHons of
uterus carcinoma. (p=6)
• cachexia
• hemorrhage
• thrombosis of pelvic vein
• peritoni;s
• appearance of uterus
fistula
*458. Peritoneal
pregnancy was found.
IdenHfy possible variants
of its origin. (p=2)
459. During vagina
examinaHon there is
found a broad bright red
crown near
External orifice of
cervix .the crown does
not give hemorrhages by
Instrumental spatula
touch. During
microscopic examinaHon
there are
covering vaginal surface in endocervicosis=papillary,g (p = 4)
with numerous glands in diameter with fluid & landular,mixed • star shaped follicles
its heavy pappilary (hypertrophy &
thickness. Give your projecHon with white 7.Disease of hyperplasia of follicular
diagnosis. (p=2) cauliflower Hssue epithelium)
pregnancy=GTD,Gestosis(t
• Diagnose:endocervicosis remainder. • papilla of epithelium
of neck of uterus oxemia),Abortion,Ectopic
Microscopically papillaries of the tumor are covered by projec@ng into follicular
columnar epithelium with nuclearpregnancy,placental polyps lumen
ADDITIONAL hyperchromia & mitosis. • pale colloid
QUESTIONS: On separate secHons 8.Cervical • lymphoid infiltra@on of
1. In post‐mortem adenous complex grows carcinoma=squamous,aden stroma
examinaHon of elderly through cysHc wall. osquamous,undifferentiate 382. Name histology types
man there are found the Specify the tumor. (p=3) of colloid goiter. (p = 3)
d.
enlargement of the • Malignant tumor of • microfollicular
prostate to papillary cystoadenoma • macroflollicular
9.Endometrial carcinoma
marked degree and its • mixed
compression of urethra precursor=endometrial 383. Name causes of
1.Possible setting for
lumen. Mucous hyperplasia, adenomatous death with paLents of
chronic endometritis=using
membrane of the bladder polyps Basedov’s disease. (p = 4)
of IUD,TB,Chronic
is • heart insufficiency
dull.hyperemic with gonorrheal 10.COD • liver failure during toxic
hemorrhages. The ureter disease,PID,Postpartum/po eclampsia=respiratory hepatitis
is enlarged.pelvis are stabortal,no apparent insufficiency,coma,renal • acute adrenal
filled with pus.on cut reason, insufficiency during
failure and hepatic failure,
surface thyroectomy
of the kidney small cerebral hemorrhage • cacchexia
2.Classification of
abseccess are 384. Name common
Leiomyoma(localization)= 11.Leiomyosarcoma,Lung(
observed.what is the symptoms of diabetes
Submucous,subserous,Intra hematogenic),Hemorrage,c mellitus. (p = 6)
disease of urinary tract
described mural achexia. • hyperglycemia
here.what is the • polyuria
pathogenesis”? (p=3) 3.Schirrous, metastasis to: 12.Lobular,ductal(infiltrati • glucosuria
• disease: ascending axillary nodes, ve/non),nipple,areolar • polydypsia
pyelonephrits infra/supraclavicular • ketonuria, ketoacidosis
• pathogenesis: stagna;on nodes,parasternal,anterior • hyperlipidemia
13-Fibrocytic
of urine and nodular hype • polyphagia
mediastinal disease=infiltrative/non
rplasia of prostate. 385. Name changes of
2. Specify preinvasive infiltrative…precancerous Langerhan’s islets found
4.CIN=cervical
form of exocervical process to carcinoma of in diabetes mellitus. (p =
carcinoma in the uterus. intraepithelial neoplasia, breast… 2)
(p=1) CIN1/2/3=mild,moderate,s • decrease number of beta‐
• Cancer in situ evere Unit (15) : Diseases of cells
Endocrine • atrophy
3. The ovary has been 5.GTD=Hydatidiform 381. Which are typical 386. Name causes of
supplied as a biopsy mole, invasive mole, microscopic changes in death in paLents with
samples. It is presented choriocarcinoma, thyroid gland in diabetes mellitus. (p = 4)
Basedov’s • diabe@c coma
• sepsis
• heart failure
• uremia
387. Name clinical
morphologic changes of
Icenko‐Cushing’s
disease. (p = 6)
• coentaneous striae
• arterial hypertension
• glucosuria
• hyperglysemia
• hirsu@sm
• polydipsia
• weight gain (buffalo
hump)
• arrested sexual
development
388. Give the definiLon
of “parathyroid
osteodystrophy” concept.
(p = 4)
• parathyroid
osteodystrophy is a disease
associated with increase
parathyroid hormone
produc@on.
• disturbance in calcium
and phosphate exchange
lead to hypercalcemia &
hypophosphataemia.
• marked destruc@on of
bony @ssue and defect of
bone
structure( osteodystrophy).
*389. Specify basic
changes in bone Lssue in
hyperparathyreosis. (p =
6)
390. 55 yrs old male of
112cm height is
proporLonally built and
his mental progress is
adequate to his age. Give
your diagnosis. Specify
the character and the
localizaLon
of pathologic process. (p
= 6)
• diagnosis: pituitary
dwarfism
• characteris@c: decrease
produc@on of growth
hormone by somatotrophic
producing cells
• localiza@on: anterior
pituitary gland
• causes: ‐pituitary tumour
in childhood
‐necrosis in pituitary in
childhood
‐hemorrhage into pituitary
in childhood
‐retarded sexual
development, but normal
intelligence
1-Case=Addison
Disease,Increase(ACTH n
MSH)..hyperkalemia,hypo
natremia,hypotension,hypo
volaemia…
COD=Dehydration,hypote
nsion,Convulsion,confusio
n/psychosis,lethargy…
2-Complications of
acromegaly=cardiomyopat
hy,angina
pectoris,myocardial
infarction,DM,hypertensio
n,heart failure,kidney
failure.
3-
Hyperparathyroidism=Oste
oporosis,osteitis cystic
fibrosa,osteomalacia,bone
resorption,osteoclast
avtivation,hypercalcemia,o
steodystrophy
4-Graves
disease=organ(thyroid),fun
ctional
state(hyperparathyroidism)
,Gross
appearance(Enlarged),Clini
cal
manifestation(thyrotoxicos
is,heart
failure,opthalmopathy,liver
failure,cachexia)
5-COD DM=diabetic
coma,ketoacidosis,gangren
e,MI,heart
failure,uremia,sepsis
6-Acromegaly=endocrine
disease caused by
Eosinophilic cell adenoma
(somatotropinoma)..with
excess production of
Growth hormone…
irregular growth of soft
tissue,bones,cartilage,visce
ral organ,face hand feet
and jaw…
7-Etiology of
Addison=autoimmune
adrenalitis,metastasic
carcinoma,TB,AIDS,sarcai
dosis,hemachromatosis.
8-Histological findings of
graves disease=star shaped
follicles,hyperplasia n
hyperotrophy of thyroid
epithelial cells,formation
of small papillae projecting
into follicular lumen,pale n
pink colloid,lymphoid
infiltration of stroma.
9-Diabetec
glomerulosclerosis=diffuse
,nodular
10-DMtype1=Endocrine
disease characterized by
destruction of B-cell of
pancreas…leads to
insufficiency of insulin
production…and clinically
characterized by
Hyperglycemia….etiology
=autoimmune
insulinitis,genetic,virus….
11-
1’hyperparathyroidism=Ad
enoma,adenocarcinoma,hy
perplasia of parathyroid
gland.
12-Addison’s
disease=chronic adrenal
insufficiency..destruction
of adrenal
cortex..etiology…clinical
manifestation….
UNIT (16) : Rheuma1c
fever & Congenital heart
disease
332. Give defini1on of
rheuma1sm.(p=3)
• rheuma'sm is an
immunologically mediated
inflamma'on with systemic
disorganiza'on of
connec've
'ssue.
• as acute and chronic
disease with damage of
many organs but prefers
cardiovascular system.
333. Specify clinical
anatomic forms of
rheuma1sm.(p=4)
• cardiovascular form
• cerebral form
• arthri'c form
• nodosal form
334. What is the main
organ involved in
rheuma1c pathology.
(p=1)
• heart
335. Designate forms of
rheuma1c endocardi1s
according to the process
localiza1on and to the
character of
morphologic changes.
(p=7)
• According to localiza'on:
 Valve
 Chordal
 Visceral
• According to
morphologic changes:
 Valvuli's
 Fibroplas'c endocardi's
 Acute verruceous
endocardi's
 Recurrent verruceous
endocardi's
336. Name
thromboendocardi1s
types.(p=2)
• polypous‐ulcerate
• verruceous
337. What is valvuli1s?
Give its morphologic
signs.(p=6)
• valvuli's is diffuse
endocardi's characterized
by dystrophic changes in
valvular CT without
affec'ng
endothelium , no thrombus
forma'on.
• morphologic sign:
 inflamma'on
 sclerosis
 mucoid & fibrinoid
swelling (in vessel)
 fibrinoid necrosis
338. Show most typical
localiza1on of rheuma1c
granulomas in the
myocardium.(p=1)
• At perivascular connec've
'ssue(in the auricle of leI
atrium) OR leI ventricular
auricle,posterior wall
of leI ventricle and
ventricle septa.
339. Give forms of
rheuma1c myocardi1s.
(p=2)
• Nodular prolifera've
inflamma'on
(granulomatous)
• Local and diffuse
exuda've inters''al
*340. Name forma1on
stages of rheuma1c valve
disease.(p=4)
341. Specify clinical
anatomic forms of
rheuma1c mitral valve
disease.(p=2)
• Stenosis mitral valve
• Mitral insufficiency
342. Specify forms of
rheuma1c aor1c valve
disease leading to the
hypertrophy of leW
ventricular of the
heart.(p=2)
• Stenosis of aor'c valve
• Insufficiency of the valve
*343. Specify forms of
valve insufficiency
according to the
pathogenesis.(p=2)
344. Specify results of
connec1ve 1ssue
disorganiza1on within the
skin due to scleroderma.
(p=2)
• Sclerosis
• Hyalinosis
• Petrifica'on of heart
345. What are LE‐cells?
(p=2)
• Lupus cells are
leukocytes with
autoimmune an'nuclear
an'bodies.
• Take up calls with
destroyed DNA.Usually
found within vesicle of
phagocy'c macrophages.
346. Specify diseases
leading to the forma1on
of valvular heart disease.
(p=6)
• Rheuma'sm
• Athesclerosis
• Brucellosis
• Trauma
• Mitral valve prolapse
• Systemic lupus
erythromatosus with
Libman’s Sacks lupus
endocardi's
• Arterial endocardi's
347. Name most frequent
forms of congenital heart
disease.(p=4)
• Stenosis of pulmonary
artery
• Tetralogy of fallots
• Pathologic patent ductus
arteriosus (channel
between pulmonary artery
and aorta)
• Atrial and ventricle septal
defect
Copyright reserved@
group 39~2008
3
348. Name anatomic
changes of the heart with
tetralogy of fallot.(p=4)
• Dextra posi'on of aorta
• Stenosis of pulmonary
artery
• Ventricular‐septal defect
• Hypertrophy of right
ventricle myocardium
349. During postmortem
examina1on,sclerosis and
growth into one of cusps
are found in mitral
valve.The
oblitera1on of pericardial
cavity with calcified
deposits in the lesion are
found.Name changes
found and
disease to developed
them.(p=3)
Changes:
• Oblitera'on of pericardial
cavity with connec've
'ssue.
• Petrifica'on of Calcium in
pericardium(shell heart)
• Endocardi's lead to
stenosis
Disease: rheuma'sm
350. During postmortem
examina1on of the child
there are found stenosis
of pulmonary
artery,hypertrophy
of the right ventricular
myocardium,ventricular
septal defect and
dextraposi1on of
aorta.What is your
diagnosis?
• Tetralogy of fallot
1-Congenital heart
disease=Tetralogy Fallot,
Atrial septal
defect,ventricular septal
defect,patent ductus
atriosus,transposition of
great arteries,congenital
obstructivel lesion
2-component of tetralogy
of fallot=right ventricular
hypertrophy, ventricular
septal defect,
dextraposition of aortic
root, right ventricular
outflow obstruction
3-Rheumatic fever,
changes=vessel(vasculitis),
joint(arthritis),kidney(GN),
skin(erythema
marginatum),heart(verruco
us endocarditis)
4.SLE,diagnostic
criteria=Immunological
disorder,antinuclear AB,
Renal disorder, skin lesion,
arthritis,serositis,
hematological disorder,
neurological disorder
5.Acute rheumatic
fever=Mucoid/fibrinoid
swelling, edema,
….fibrinoid necrosis…
HE=basophilia…
toluidin=Metachromasia.
6.Left to right shunt=Atrial
septal defect, ventricular
septal defect, patent ductus
arteriosus.
7.Hemodynamic
consequences of tetralogy
falot=Right to left shunt,
decreased outflow to the
lung, increase outflow to
aorta
8.Valvular heart
disease=fatty infiltration,
cyanotic induration,
nutmeg liver, brown
induration.
9.Case=Mitral stenosis,
rheumatic fever, mucoid n
fibrinoid swelling,
thrombotic
vegetation..verrucous
endocarditis
10-Outcomes
scleroderma=hyalinosis,scl
erosis
11-
Dermatomyositis=systemic
disease characterized by
immunological mediated
muscle n skin injury and
inflammation.
12-Case=SLE…
morphology(increased
cellularity throughout
glomerulus, rigid wired
loops, foci of acute
capillary necrosis, fibrinoid
deposit, intracapillary
thrombi)
….complication=lupus GN
and libman sack
endocarditis.
13-cyanotic congenital
heart disease=tetralogy of
fallot, transposition of
great arteries
14-Rheumatic
fever=acute,immunological
ly mediated,multisystem
inflammatory disease that
follows after a few weeks,
episode of group A strep
pharyngitis
15-Rheumatic
pancarditis=inflammatory
changes in all 3 layers…
fibrinous pericarditis, hairy
heart..
16-complication of
RA=clawlike deformation,
ulnar deviation of finger,
ankylosis, amyloidosis,
osteoporosis
17-Valvular
endocarditis=valvulitis,ver
ucous
endocarditis,recurrent
verucous
endocarditis,fibroplastic
endocarditis
18-Valve
disease=obstruction or
regurgitation or both cause
major hemodynamic
burden….increased
susceptibility to infection
19-Case=TOF…right to
left shunt,,increased
bloodflow thru
aorta,,,decrease bloodflow
to lung
20-Rheumatic
granuloma=focus of
inflammation within CT of
heart…left heart
auriculum,,,central
fibrinoid necrosis
surrounded by Mphage n
anitshkow cell…Aschoff
body
21-Type of rheumatic
fever=Cardiovascular,nodo
sal,cerebral,arthritic
22-Rheumatic
myocarditis=granulomatou
s, diffuse interstitial
exudative, focus interstitial
exudative.
UNIT (17) :
Atherosclerosis &
Ischemic heart disease
314. Give the defini@on
of atherosclerosis. (p=6)
• Atherosclerosis is a
chronic disease with
abnormal lipid and protein
metabolism
• and destruc?on of large
artery & aorta(elas?c &
myoelas?c type)
• with forma?on of
atherosclero?c plaque
called fibro‐faGy plaque in
the in?ma of muscular
elas?c artery (large artery :
aorta)
315. Give successive
names of progress stages
of atherosclerosis
according to the view of
scien@sts
suppor@ng infiltrate
(combina@ve) theory of
atherosclerosis. (p=6)
• Prelipidosis
• Lipidosis
• Liposclerosis
• Artheromatosis
• Ulcera?on
• Artherocalcinosis
316. Give pathological
anatomic characteris@cs
of the atherosclero@c
plaque and specify its
localiza@on.
(p=5)
• Cells components
(smooth muscle cells,
macrophages, leukocytes)
• Extracellular matrix
(collagen, elas?c fibres,
proteoglycans)
• Intracellular &
extracellular lipids
Localiza?on: aorta & large
arteries (elas?c & myoelas?
c type)
317. Specify histological
findings in
atherosclero@c (primary
wrinkled) kidney. (p=4)
• Atherosclero?c plaque in
large arteries
• Sclerosis of stroma
• Narrowing of lumen
• Hyalinosis & sclerosis of
small arteries
• • Post infarc?on
318. What are
complica@ons connected
with the ulcera@on of
atherosclero@c plaques
on the aorta? (p=4)
• Aneurysm of aorta
• Rupture of aorta with
hemorrhage
• Thrombosis &
thromboembolism
• Cholesterol embolism
319. What is the ischemic
heart disease? (p=3)
• Ischemic heart disease is
group of closely related
disease with abnormality
of cardiac blood
circula?on
• Caused by imbalance vast sec@on of the wall is vasospasm,embolism,acute nal type,malignant clinical failure,congestive heart
between myocardium near morphology changes of course,acute renal failure. failure,uremia
oxygen demand & blood the top of the heart and is plaque(hemorrhage,disrupt 11-Outcomes of MI=Local Unit (17) : Arterial
supply (absolute rela?ve gray‐yellow color, soY ion) cardiosclerosis,acute n Hypertension.Hypertensi
insufficiency) consistency, blood‐ 3-Morphological finding in chronic ventricular on
320. What coronary layered. Primary wrinkled aneurysm,external rupture disease.Cerebrovascular
arteries changes lead →What is the disease kidney=hyaline of infarct disease.
most frequently to the described here according arteriolosclerosis, arteriolar 12-Secondary 324. Give the definiBon
progress of myocardial to modern interna@onal narrowing, diffuse hypertension=increase BP of the hypertonic crisis.
infarc@on? (p=4) classifica@on of diseases? nephrosclerosis, as a result of adrenal, (P=4)
Copyright reserved@ →What is its symmetrical contraction of cardiovascular disorder, • Exacerba=on of
group 34~2008 manifesta@on of this kidney, glomerulosclerosis. neurologic disease, renal hypertension
2 case? 4-EH=comlex disorder disease and other disease. • Characterized by rapid
• Steno?c atherosclerosis →What is the direct manifests by increased 13-EH eleva=on of in arterial
• Thrombosis cause of death? blood pressure, initiated by forms=cerebral,renal,cardi hypertension due to
• Spasm of vessel for →Name background disturbances in any factors ac generalized spasm of
long ?me disease. (p=6) which control the blood 14-atherosclerotic arterioles which
• Embolism • Disease: ischemic heart pressure, and act in plaque=hallmark of AS, leads to morphological
321. Specify results of disease genetically predisposed developed within intima of changes in wall of
myocardial infarc@on. • Manifesta?on: transmural individual. the elastic and myoelastic arterioles.
(p=4) myocardial infarc?on with 5-Case CHF with essential arteries, n have essentially • Characterized by rapid
• Acute aneurysm (necro?c rupture of heart hypertension=cardial type.. 3 components(cellular,CT eleva=on in arterial blood
?ssue undergoes rupture at • Direct cause of death: morphology fibers n matrix,lipid) pressure with lesion of the
any case) from hemotamponade of changes=myocardial 15-Malignant organ, especially within
• Rupture of heart with heart hypertrophy,fatty hypertension, arterioles brain.
hemorrhage into • Background disease: infiltration, changes=arteriolovasospas 325. Name stages of
pericardial cavity hypertension 6-IHD=MI,angina,sudden m,plasmorhagia,fibrinoid hypertensive disease
• Chronic aneurysm Addi@onal Ques@on cardiac death,chronic IHD necrosis,microaneurysm,m (primary arterial
(connec?ve ?ssue) 1. Name forms of with congestive heart icrothrombosis,hemorrrhag hypertension). (P=3)
valvular heart deficiency failure. e. • Func=onal changes of
cardiosclerosis according to the 7-Complication of 16- arteries and small arterioles
322. What are typical pathogenesis. (p=2) atherosclerotic Case=IHD,MI,pericardial • Changes in walls of small
changes of the brain due • Func?onal plaque=calcification,fissuri hematotamponade arteries and arteriole
to atherosclerosis of the • Organic ng,ulceration of luminal 17-MI • Changes within organs
cerebral arteries? (p=2) surface,rupture of stages=Ischemic,necrosis,o 326. What morphological
• Ischemic white infarc?on 1-Atherosclerosis=chronic plaque,cholesterol rganization changes in small vessels
of brain disease, which produced embolism,superimposed 18-COD MI=Cardiogenic of the brain due to
• Atrophy of brain (with by fat n protein thrombosis,hemorrhage shock,hematamponade,Vfi hypertensive disease
encephalopathy &↓ metabolism disorder, and into plaque,aneurysm. b,asystole,acute heart (primary arterial
memory) characterized by intimal 8-IHD=A group of closely failure, hypertension). (P=4)
323. During postmortem plaque that protrudes related syndromes caused 19-EH stage=functional • Increase vascular
examina@on fluid blood lumen of elastic arteries by imbalance btw vasoconstriction,blood permeability with
and clots of the blood are and myoelastic arteries and myocardial blood supply vessel disease,changes in plasmorrhagia
found in pericardial weaken underlying media and oxygen demand. organ. • Fibrinoid necrosis of wall
cavity. and undergo series of 9-CVA=transient ischemic 20-COD of • Microaneurysm
Heart weights 650g. The complications. attack, ischemic infarct. EH=cerebrovascular • Hemorrhage
thickness of the wall of 2-Coranary changes caused 10- disorder,acute heart • Vasospasm
leY ventricle is 2.5cm. MI=thrombosis, Case=Hypertension(EH),re
327. Name outcome of insufficiency mechanism 351. Name two basic 357. Name basic immunocomplex in the 364. Name stages of
arterial changes of of vascular dilata=on groups of diffuse morphologic types of epithelial cells of the development of acute
hypertensive disease 330. What are the most nephropathies. (p=2) chronic basal membrane renal failure. (p=4)
(primary arterial frequent causes of death • Tubulopathy glomerulonephriDs. 361. What is the renal • IniCal
hypertension). (P=2) due to hypertensive • Glomerulopathy (p=6) amyloidosis? What are • Oliguria (maintainence)
• Hyalinosis disease (Primary arterial 352. Name general • Membranous renal structures with • Polyuria
• Sclerosis hypertension)? mechanisms of proliferaCve amyloid deposiDon? • Recovery
(atherosclerosis) (P=3) glomerulonephriDs glomerulonephriCs What are groups of 365. Specify causes of
• Lipidosis and narrowing • Cardiac insufficiency/ development. (p=3) • Mesengial proliferaCve symptoms to give clinical death paDents with
of lumen cardiac • Deposit of glomerulonephriCs manifestaDons of this necroDc nephrosis. (p=2)
328. Name signs that are failure(acute,chronic) immunocomplex • Rapidly progressive process? (p=7) • Uremia
typical for malignant • Uremia (circulaCon/ cell‐ glomerulonephriCs • Renal amyloidosis is a • Acute heart insufficiency
hypertension having in • Stroke (Cerebral vascular mediated) or anCbodies • Mesengial capillary disease with deposiCon of 366. Designate
mind; the frequency of accident) • Glomerulosclerosis glomerulonephriCs amyloid into the renal microscopical renal
crisis; the nature 331. In anamnesis, the • Leukocytes infiltraCon • Focal segmental structure. changes typical for acute
of morphological changes paBent had firm 353. Specify typical renal glomerulonephriCs • Structure: ‐ glomerular renal failure of toxic
in small vessels; cause of elevaBon of blood symptoms of the • GlomerulonephriCs ‐ vessels nature:
death. (P=3) pressure during of long glomerulonephriDs. associated with nephroCc ‐ stroma (intersCCal a) bleeding filling in the
• Frequency: ORen crisis duraBon with repeated (p=4) syndrome peritubular Cssue) cortex, b) the condiDon
• Nature of morphological crisis of the brain has • NephroCc syndrome 358. Name • Symptoms: ‐ chronic of intersDDal Dssue, c)
changes in small vessels:‐ right sided hemiplegic. • Proteinuria glomerulopathies of non renal failure the condiDon
‐ Fibrinoid necrosis Death is of heart • Hematuria inflammaDon character ‐ nephroCc syndrome of epithelial cells in the
‐ Microaneurysm decompensaBon. What is • Casturia frequently found in clinic ‐ hypoalbunemia convoluted tubules, d) the
‐ Increase permeability the disease described 354. Specify typical extra and accompanied by ‐ hyperlipidemia condiDon of the tubular
with plasmarrhagia here? What possible renal symptoms of the nephroDc syndrome. ‐ edema lumen.
• Cause of death : Uremia, macroscopic (gross) glomerulonephriDs. (p=3) ‐uremia ( p=4)
Ischemic infarct of brain. changes are found in the (p=6) • Nephropathy during 362. Name most frequent • a) ischemia of cortex
Copyright reserved@ heart, the brain? What is • Hypoalbuminemia pregnancy renal diseases that • b) edematous of
group 37~2008 the localizaBon of • Hypertension • DiabeCc nephropathy leading to secondary intersCCal Cssues
2 changes in brain? (P=6) • Azotemia & Uremia • Amyloidosis contracted kidneys. • c) epithelial cells of
329. Give the definiBon • Disease: Hypertension • Generalized edema 359. Define morphologic ( p=3) proximal tubular are
of hypertensive disease (primary arterial • Hyperlipidemia substrate of primary • Chronic necrosis
(primary arterial hypertension) • edema nephroDc syndrome glomerulonephriCs • d) granular casts are seen
hypertension). (P=4) • Macroscopic changes:‐ 355. Specify forms of the (lipoid nephrosis) .(p=3) • Chronic pyelonephriCs in the enlarged tubular
• Chronic disease with ‐Heart: hypertrophy of leR glomerular nephriDs • Characterized by minimal • Amyloid nephrosis lumen
eleva=on of arterial ventricle and myogenic according to the process changes of glomerular • Chronic renal failure *367. Name most
pressure dilata=on, fa[y dystrophy localizaDon. (p=2) filtraCon 363. Specify most frequent types of chronic
• When rela=onship btw ‐Brain: hemorrhagic • Intracapillary • Expressed by loss of frequent causes of hereditary tubulopathies.
blood volume and total infiltra=on and hematoma • Extracapillary podocytes and small development of acute (p=3)
peripheral resistance is with cyst forma=on 356. Name morphologic branches renal failure. (p=5) • cystiuria
altered • Localiza=on of changes phases of development of 360. Give the • HemolyCc & Massive • phosphaCc diabetes
• Without connec=on with in brain: LeR Hemisphere acute characrerisDcs of basic loss of blood • oxcalaturia
lesion of organs due to right sided glomerulonephriDs. electronic microscopic • Trauma • syndrome of Debra de
• Due to disturbances of (p=3) sign of membranous • Burn Toni Fancon
hemiplegia.
nerve regula=on, due to • Changes to chronic glomerulopathy. (p=4) • Sepsis 368. Give the definiDon
constric=on of artery and glomerulonephriCs • Membranous • poisoning of the pyelonephriDs.
Unit (18) : Renal Disease • Sclerosis of kidney transformaCon associated (p=4)
altera=on of vessels,
• Recovery with deposiCon of
• PyelonephriCs is renal • Atrophy → What is the turbid fluid. Parenchyme hemorrhages. The ureter 4. Name of 2 general
disorder with purulent • Purulent nephriCs designaDon of renal of kidneyis thinned is theories of stone
inflammaCon affecCng • Pyonephrosis complicaDon? replaced by fibrous enlarged. Pelvis is filled formaDon in urinary
stroma, calyx,tubules, • Replacement of kidney → What is the origin of Dssue. In the with pus. On cut surface tract. (p=2)
intersCCal with fa`y Cssue mechanisms? enlarged pelvis and cups, of the kidney small • Matrix
and renal pelvis. 374. Name most frequent → What is the term for parDally the stone goes abscesses are • Colloid crystal
• Cause by bacteria renal diseases that renal changes? (p=3) into ureter mouth. Pelvis observed.
infecCon leading to • DesignaCon: Chronic membrane has → What is the disease of 1-GN=group of disease of
369. Name diseases nephrosclerosis. (p=7) renal failure hyperemia, it is rough urinary tract described infectious,allergic or
frequently leading to • Chronic glomerular • Origin of mechanism: and dull. here? unknown nature,which
ascending pyelonephriDs. nephriCs Kidneys can’t regulate → Give your diagnosis. → What is the
have bilateral inflammation
(p=4) • IntersCCal nephriCs volume and soluble → What is process most pathogenesis? (p=3)
• Stones of ureter • PyelonephriCs composiCon of urine frequently associated by *380. Give the definiDon and clinically manifested
• ConstricCon of ureter • Atherosclerosis • Glomerular filtraCon rate that disease? of Addison’s disease. by renal n extrarenal
• Sclerosis of ureter & • Amyloid nephrosis is less than 20% → What is (p=3) syndromes.
urethra • Hypertension • Renal changes: secondary microorganism most AddiDonal QuesDons:
• Hypertrophy of prostate • Diabetes mellitus wrinkled kidney frequently induces it? 1. What are typical 2-Nephrotic
• Tumor in urethra, ureter 375. Give the definiDon 377. A[er taking the → Name renal changes morphologic syndrome=Lipoid
or prostate of the uremia. (p=4) soluDon of sublimate by according to the process. manifestaDons of acute nephrosis,Focal
370. Name most severe • Uremia is a pathologic mistake paDent has → What is common exudaDve and
manifestaDons of acute condiCon associated with anuria , very high urea diseas with the source as proliferaDve glomerulosclerosis,
purulent pyelonephriDs. azotemia and a and creaDnine. this associated process? intracapillary membranous GN,
(p=3) constellaCon of clinical → What disease is it? (p=6) glomerulonephriDs? membranousproliferative
• Pyonephrosis signs and Copyright reserved@group • Diagnose: (p=3) GN.
• Urogenic sepsis symptoms of organs and 39~2008 Hydronephrosis • Development of
• Papillonecrosis biochemical alteraCon 5 • Microbes: E.coli pathological process in the 3-Membranous
• SuppuraCve (including uremic → What are microscopic • Kidney changes: vessels of glomerular GN,morpho=diffuse
paranephriCs gastroenterocoliCs, changes of renal pyelonephriCs, • ProliferaCon of cells in
thickening of GBM,
• Aponematous nephriCs neuropathy, structures? pyonephrosis glomerular
*371. Give the definiDon uremic fibrinous → Where are they • Common disease: ‐calculi • LeukocyCc infiltraCon presence of subepithelial
of urolithias disease. pericardiCs). involved? (p=4) ‐ tumor 2. What exudaDve Ig-contained deposit,nestle
(p=5) 376. Due to teminal stage • Disease: necroCc ‐ congenital atresia of glomerular nephriDs against GBM n separated
372. Specify stones of the glomerular nephrosis urethra types do u know? (p=3) by spikelike protrusion of
structures most nephriDs, paDent had • Microscopic changes : ‐ spinal cord damage with • Serous GBM matrix,podocyte loss
frequently found in the oliguria and azotemia. ‐ dystrophy of tubular paralysis of bladder • Fibrinous their foot process.
kidney according to their He died. During ‐ necrosis of the epithelial • General disease: • Hemorrhagic
composiDon.( p=3) postmortem cells Urosepsis 3. Give the definiDon of
4-Rapidly progressive
• Calcium oxalate and examinaDon, there were ‐ cylinder /cast in *379. During postmortem nephrolithias disease.
phosphate stone found very small (p=5) GN=distinctive crescents
glomerular and tubular examinaDon of elderly
• Magnesium ammonium contracted ‐ edema of stroma man, there are found the • Nephrolithias disease is formed by proliferation of
phosphate stones kidneys, fibrinous 378. For histology essay, enlargement chronic disease parietal cells and by
• Uric acid stone tracheal bronchiDs, extracted kidney was of prostate to marked • FormaCon of stones in migration of monocyte into
• CysCne stone pericardiDs and delivered. There is super degree and its kidney calyces, pelvis, bowman space, fibrin
373. Name variants of enterocloliDs with effects enlarged kidney. compression of urethra ureter exudation.
macroscopic (gross) types of On cut it is expressed by lumen. Mucous • Stones is of different
of kidney with the hemorrhage diathesis. mulDchamber membrane of the bladder sizes, structure and
5-Thyroidization=Chronic
uroliDasis. (p=5) formaDon. Chambers are is dull, hyperemic with chemical composiCon
• Hydronephrosis pyelonephritis, dilation or
filled with slightly
contraction of tubules,
atrophy of lining
epithelium, tubules contain
pink to blue, glassy colloid
cast.
6-
Hydronephrosis=dilatation
of renal pelvis n calyxes,
atrophy of parenchyma,
caused by obstruction of
urine outflow.
7-Lipoid Nephrosis=with
lipid, loss of foot process
of podocyte.
8-Acute Tubular
Necrosis=severe trauma,
pancreatitis, mismatched
blood transfusion n
hemolytic crisis,
septicemia, multitude
drugs, poison, organic
solvents, myoglobinuria.
9-Renal stones=calcium
oxalates, calcium
phosphate, urate, cysteine,
Mg Ammonium phosphate.
10-Renal
syndromes=Oliguria,
proteinuria, hematuria,
urinary cast.
11-Pyelonephritis
route=Hematogenic and
ascending infections.
12-RPGN=clinicalpath
syndrome characterized by
rapid and progressive loss
of renal fx associated with
oliguria n death from renal
failure.
13-Extrarenal
syndromes=Hypertension,d
yproteinemia, azotemia,
severe edema.
14-Immune mech in
GN=ag-ab rx,glomerular
deposit of IG n
complement component,
cell mediated immune.
15-Membranous
proliferative=proliferation
of mesangial cells n
infiltrating leukocyte,
GBM is thickened,
glomerulocapillary wall
show double
countour(tramtrack)
appearance,subendothelial
or intramembranous
electron dense deposit.
16-PN=suppurative
inflammation of kidney n
renal pelvis caused by
bacterial infections
17-Cause of urine outflow
obstruction=Calculi,tumor
of bladder prostate
uterus,inflammation,neuro
genic paralysis,normal
pregnancy
18-Chr.PN=interstitial n
calyxes fibrosis n
inflammatory infiltrates of
lymphocyte n plasma cell,
dilatation or contraction of
tubules, atrophy of lining
epithelium(thyroid)
19-GN=lipoid
nephrosis,membranous,me
mbranous
proliferative,RPGN,acute
diffuse
proliferative,chronic GN.
20-Nephrotic=Proteinuria,
generalized edema,
hypoalbuminemia,
hyperlipidemia, lipiduria.
21-Acute PN causative
agent=E.coli,proteus,pseud
omonas,enterobacter,kliebs
iella.
22-ATN=clinical path
entity characterized by
destruction of tubular
epithelial cells n clinically
by acute suppression of
renal fx.
23-Acute renal failure
cause=ATN,RPGN,diffuse
renal vessel disease,acute
papillary necrosis
associated with acute
pyelonephritis, acute drug
induced interstitial
nephritis, diffuse cortical
necrosis.
24-Urolithiasis=calculus
formation at any level of
urinary collecting system
25-Secondary wrinkled
kidney=kidney is
symmetrically contracted,
surface is red-brown and
diffusely granular,
microscopically advanced
scarring of glomerulus n
bowman’s space,complete
replacement or
hyalinization marked by
interstitial fibrosis,atrophy
n replacement of many
tubules of cortex.
UNIT ( 19 ) : Liver
diseases
415. Name etiologic
varieties and types of
primary acute viral
hepatitis according to
them. (P=6)
• HAV, HBV, HCV, HDV,
HEV, HGV
416. Specify 3 general
an7gen determinants of
hepa77s B virus and
name current methods to
detect for
hepa77s B an7gens in the
7ssue. (P=6)
• HBs Ag : (ground-glass
hepatocyte)histological
method
• HBc Ag : (Sanded-Nuclei
Hepatocyte)immunohistoc
hemical method
• HBeAg :(HBeAg-
Antibodies)
immunomorphological
method
417. What is the
difference between
concept of <infec7ous>
and <serum> hepa77s?
Name their synonyms.
(P=6)
• InfecGous – is termed
virus hepaGts A , has got
fecal-oral transmission and
doesn’t cause chronic
hepatitis.
• Serum – virus hepaGGs
B (D,C) has parenteral
transmission and can cause
chronic hepatitis.
418. What is viral
hepa77s A? Give its
morphological changes in
liver. (P=4)
Infectious type of Hepatitis
• Viral hepaGGs A is an
epidermis hepaGGs
transmiOed through fecal
oral way caused by RNA
picornavirus.
• Morphological change in
liver‐ dystrophy, necrosis,
proliferaGon of stromas.
It doesn’t cause chronic
hepatitis.
419. Name clinic
morphologic forms of
acute viral hepa77s B.
(p=4)
• A. cyclic jaundice
• B. without jaundice
• C. fulminant hepaGGs
• D. cholestaGc form
420. What are
morphologic macro‐
microscopic signs
characteris7c of viral
hepa77s with acute
massive liver
necrosis? (P=5)
• Fulminant hepatititis,
ballooning and foamy
degeneration,
necrosis,Leukocyte
infiltration…Enlarged and
reddening liver.
*421. Specify
morphological signs of
viral an7gens (markers)
of hepa77s B. (p=3)
• Ground glass
hepatocytes(HBs Ag)
• Sanded nucleus
hepatocytes (HBc Ag ).
• Councilman’s body
422. Name possible
outcome of acute viral
hepa77s B. (p=3)
• Recovery
• Acute hepaGc & renal
failure with death
• Chronic hepaGGs
• Cirrhosis of liver
423. Specify morphologic
forms of chronic viral
hepa77s. (P=2)
• Chronic persistent viral
hepaGGs
• Chronic acGve
aggressive viral hepaGGs
424. What is lipoid
hepatosis [steatosis]?
Name 4 basic causes of its
origin. (P=7)
• lipoid hepatosis is chronic
disease of liver
characterized by
predominance of fatty/lipid
degeneration of hepatocyte
• causes : i. intoxicaGon :
drugs, alcohols
o ii. metabolic
insufficiency : DM
o iii. diet insufficiency :
obesity
o iv. hypoxia
425. What is pigment
hepatosis? (P=5)
•is termed
hemachromatosis…it is a
liver disease with error of
metabolism and
accumulation of Iron
pigments.
.
426. Give the defini7on of
the hepa7c cirrhosis.
(P=5)
• is a chronic disease
characterized by :
 .fibrous septa bridging
 .pseudolubules
 . disrupGon of enGre
liver structure
427. Name morphologic
signs of hepa7c cirrhosis.
(P=5)
• ‐a. Necrosis
• ‐b. Fibrosis
• ‐c. Inflammation
• ‐d. Pseudolobules
• ‐e. Vascular derangement
f. Hepatocellular
degeneration
428. Specify types of
hepa7c cirrhosis
according to their
ac7vity. (P=3)
• Non active
• Mild active
• High Active
429. What is the
mechanism of forma7on
of hepa7c postnecro7c
cirrhosis? Describe its
morphogenesis. (P=4)
• Formation of
macronodular cirrhosis.
Nodules separated from
each other by connective
tissue septa. Triads are
close to each other with
proliferation of bile ducts.
. septum.
430. Name hepa7c
cirrhosis according to
their morphogenesis.
(P=3)
• ‐portal cirrhosis
• postnecroGc cirrhosis
• mix cirrhosis
431. Define 2 basic
mechanisms of new
forma7on of connec7ve
7ssue in hepa7c cirrhosis.
(p=2)
• Post-Necrosis,Portal
mechanisms
432. What is mechanism
of the forma7on of portal
hepa7c cirrhosis? Give its
morphogenesis. (P=5)
• Developing fibrous septa
is delicate and extend
through sinusoids from
Central Vein to portal
regions and from one
Portal tract to another.
433. Name basic sec7ons
[link] of the pathogenesis
of primary biliary
cirrhosis? (P=6)
• primary biliary cirrhosis
is rare chronic cholestaGc
inflammaGve disease.
• Its eGologic agent are
autoimmune reacGons.
• It’s characterized by
granulomatosis,
inflammaGon of small
biliary ducts & their
destrucGon.
• involving of the
inflammatory process at
the liver parenchyma with
hepaGc destrucGon.
• regeneraGon
proliferaGon of the
hepatocytes &
organizaGon of the fibrosis
• develop chronic epithelial
cell in bile duct acquire
anGgen properGes.
• lymphocytes cytolyse
epithelial cell
• regeneraGon
proliferaGon of
cholangiGs & periductal
fibrosis.
434. Explain ascites and
peritoni7s origin in
hepa7c cirrhosis. (P=3)
• AsciGes develop during
the portal‐ hypertension-
Accumulation of fluid in
abdominal cavity.
• PeritoniGs developed as a
result of influx of
Neutrophil with secondary
infections along lymphatic
way.
435. Designate basic
origin of hepa7c cerebral
syndrome. (P=3)
•Hepatocerebral syndrome
is termed hepatargia. It is
seated complication of
acute and chronic liver
insufficiency with 1-
Metabolic disorder 2-
Chunting of blood 3-
Severe loss of
hepatocellular functions..
436. Name most
significant portal
anastomoses in hepa7c
cirrhosis according to
clinical morphologic
rela7onship. (P=5)
• Esophageal-Cava Shunt,
abdominal-cava shunts and
rectal-cava shunts
437. Name clinical
morphological signs of
the hepatarrhia. (P=6)
• Hepatorenal failure or
intoxication, Neuropsychic
disfunction, hepatic coma
438. Specify most
frequent causes of pa7ent
death due to hepa7c
cirrhosis. (P=5)
• hemorrhage as a result of
dilated vein of esophagus
• tumour (hepatocellular
carcinoma)
• hepatorenal syndrome
• hepatic failure
• intercurrent infections
439. Give the
characteris7cs of
principal morphologic
changes progressing in
alcoholic liver. (P=10)
• Fibrosis, micronodular
cirrhosis, Mallory bodies,
necrosis, hepatocyte
swelling, hepatic steatosis,
neutrophilic reactions.
440. Give the defini7on of
<nutmeg liver> concept?
(P=3)
• Chronic passive
congestion of the liver.
441. What is <<goose
liver>>? (P=3)
• Figurative name for fatty
liver( hepatic steatosis).
442. What is <<icing
liver>>? (P=3)
• Figurative name for
hyalinosis of liver.
443. What is <<silicon
liver>> ? (p=3)
• is the liver affected in
congenital syphilis. Its
surface is hillocked, gray‐
brown in color & rocking
in
consistence.
* 444. A blood vomi7ng
has suddenly been
appeared before ,pa7ent
died. In postmortem
examina7on there
was found decreased
dense liver with fine hilly
surface. There were
verrucous enlarged
vessels in lower third
of the oesophugus. The
stomach overfilled with
blood and grume.
Diagnose and designate
morphologic form
of disease. Account for
varicose veins of
eosophagus. Name the
immediate cause of
death. (P=5)
-Portal cirrhosis of liver,
Esophageal-Cava Shunts.
Rupture of varices of
esophageal veins.
445. Pa7ent has ini7al
enlarged belly volume
with enlarged veins seen
near round navel. Soon ,
pa7ent dies.
During postmortem
examina7on, there are
found solid, small dense
liver with decreased size
and marked thin
layers of connec7ve
7ssue. Then there are
found enlarged spleen
and about 5 liters of
transparent fluid. Give
your diagnosis with
specifica7on of
morphologic form of the
disease. Name typical
extra hepa7c signs. (P=5)
• diagnosis : portal
cirrhosis of the liver
• morphological form :
collateral hyperemic
venous flow in the
abdominal wall (head of
medusa)
• complicaGon of
extrahepaGc –
splenomegaly, ascites
(portal hypertension)
450. What can take place
in the gallbladder when a
stone obstructs cys7c
duct? (P=2)
• hydrops (fluid in lumen)
• empyema (pus in lumen)
Addi7onal ques7ons :
1. Name the complica7on
of gastric ulcerous
disease. (P=5)
• PerforaGon
• PenetraGon
• PeritoniGs
• Bleeding
• Stenosis
• MalignisaGon
2. Type of chronic
hepa77s according to
their ac7ng. (p=3)
• minimal acGng
• middle acGng
• severe acGng
UNIT (20) : GIT Diseases
391. Specify types of
gastri>s.(p=3)
• acute
• chronic
• special
392. Define morphologic
signs of gastri>s. (p=5)
• Chronic inflammations,
Atrophy of gland,
Metaplasia, Sclerosis,
Neutrophilic infiltrations.
393. Give special forms of
gastri>s.(p=5)
• Eosinoplilia,
Granulomatosis,
tuberculous, fungal, drug
induced.
394. What cells are
involved in progress of
inflamma>on in gastri>s?
(p=4)
• lymphocytes
• plasma cells
• macrophages
• neutrophils
395. Name basic
morphologic parameter
of gastri>s ac>vity. (p=2)
• Neutrophils occurs in
inflammatory infiltrates
396. Give the defini>on of
stomach ulcerous disease
with calcula>on of its
basic
signs. (p=3)
• is a chronic disease with
a breach in mucosa with
extend as a deeper defect
of
membrane of stomach into
the submucous layer.
@ • Congenital
• Chronic disease in
clinical cyclic course and
the sign is chronic
recitaHve ulcer of stomach
397. Which factors take
part in dynamics of
ulcerous disease of
stomach? (p=3)
• H.pylori infecHon
• neural regulaHon
imbalance
• Exposure to gastric acid
and pepsin
398. Name complica>ons
of gastric ulcerous
disease.(p=5)
• hemorrhage
• fibrinous suppuraHve
peritoniHs
• scar with narrowing of
gastric lumen (stenosis)
• malignizaHon
• penetraHon &
perforaHon of ulcer
• melena & hematemesis
399. What is ulcera>on
penetra>on? (p=3)
• is termed lesion of gastric
wall and bottow of ulcer
into another organ
400. Name the types of
coli>s. (p=5)
• Ischemic colitis
• Crohn’s disease
• Infectious Colitis
• Pseudomemranous • diverHculiHs • purulent inflammaHon of 446. Name clinic • perforaHon and
• Non specific • anal fissura / cleW the cavity wall of appendix morphologic form of peritoniHs
401. Name morphologic 407. Give the defini>on of with the accumulaHon of acute cholecys>>s. (p=4) 451. What stones are
diver>cula types. (p=2) the appendici>s term. pus in the • catarrhal formed in the gall
• Acquired (p=2) cavity (lumen) or in the • purulent/ suppuraHve bladder most frequent by
•Congenital • inflammaHon of space of the appendix. • gangrenous according to their
402. Define variants of appendix 412. Appendix is • diphtheric chemical composi>on?
diver>cula according to 408. Name morphologic thickened. 447. What is empyema of (p=4)
e>ology and condi>ons of form of acute Its serous membrane is the gall bladder? What • cholesterol stone (yellow
origins. (p=4) appendici>s. (p=6) dull, injected by vessels. bile duct involved ion green color : cholesterol)
• Acquired • simplex Green colour mucous observing • pigmented stone (black
• superficial membrane and melted on obstruc>on? (p=3) brown : bilirubin salt‐
• Multiply • destrucHve cut surface. • empyema of gall bladder calcium bilirubinate)
• Meckel’s Diverticulum ( phlegmonous ) Give your diagnosis. is a purulent(suppuraHve) • calciferous (calcium salt)
403. Define causes • gangrenous (p=2) inflammaHon of the wall • mixed stone (cholesterol‐
inducing progress of • apostematous • phlegmonous with pigmented‐calciferous)
diver>culous disease. • phlegmonous + ulcerous appendiciHs accumulaHon of pus in the
(p=4) 409. Specify theories of 413. During cavity & duct. UNIT ( 21 ): Diseases of
• reduced dietary fibre beginning of appendici>s. appendectomy, there is • CysHc bile duct ( ductus the Lung
• retenHon of defecaHon (p=3) found thickened choledocus cysHcus) & 471. Specify clinical
• relaxaHon of intesHnal • invasive of m/o appendix covered with common bile duct ( ductus morphologic
wall of elderly ( coprostasis theory ) – massive choledocus classificaCon of acute
404. Name complica>ons obstrucHon with aprostasis fibrinous films, easily communis) involved in pneumonia. (p=3)
of diver>culosis. (p=5) and involve of m/o taken off. Mucous observed obstrucHon • Croupous Pneumonia
• lumen obstrucHon • disintegraHon of nervous membrane is gray colour, 448. What is hydrops of • Bronchopneumonia
• perforaHon system of appendix partly gall bladder? Give its • Inters>>al pneumonia
• diverHculiHs ( angioneuron theory )+ melted on cut surface. e>ology.(p=3) *472. Give definiCon of
• peritoniHs Neurohumoral theory Give your diagnosis • hydrops : accumulaHon lobar (croupous)
• suppuraHon • infecHons ( 2ndary taking into considera>on of fluid into lumen of gall pneumonia. Name the
• hemorrhage generalizaHon of serous bladder synonyms. (p=8)
405. Name diseases which infecHous disease ) changes? Name possible • eHology : stone within Defini>on : is an acute
most frequently bleeding Mixed complica>ons. (p=4) cysHc duct ( without infec>ous allergic
from upper sec>on of 410. Defini>on of • Diagnosis : jaundice ) inflammatory disease of
diges>ve primary gangrenous phlegmonous‐ulceraHve of 449. What are most the lungs characterized by
tract. (p=4) appendici>s. Real causes the appendix frequent complica>ons of fibrinous
• esophageal varices veins of it. (p=3) • ComplicaHon : cholecys>>s in bile duct inflamma>on. Involving 1
• Errosive gastrities • It is a necrosis of the perforaHon and peritoniHs a[er stone or more lobes of the lung.
• gastric carcinoma appendix, characterized by abscess of liver obstruc>on of common It may involve pleura.
• Gastric and duodenal grey black colour, empyema of appendix bile duct? What are most Synonyms : a. lobar
ulcer fibrinous suppuraHve 414. Appendix is sent to frequent complica>ons in pneumonia
film on the serous pathologic anatomy gall bladder wall with b. crupous pneumonia
406. Diseases which most membrane of the appendix. laboratory. It is black availability of stones in c. pleuropneumonia
frequently bleeding from • causes : with dull serous the gall bladder? (p=3) 473. Name atypical forms
lower sec>on of diges>ve thromboembolism of membrane. Give your • empyema of gall bladder if croupous pneumonia.
tract. (p=5) a.mesenterica of appendix diagnosis. (p=3) • mechanical jaundice due (p=5)
• ischemic coliHs 411. What is empyema of • Diagnosis : gangrenous to thromboembolism of • Central
• carcinoma appendix? (p=3) appendiciHs bile duct • Massive
• hemorrhoids • Total
• Migra>ve non‐specific pulmonary
• Klebsiella pneumonia disease. (p=5)
474. Name • Cor pulmonale
extrapulmonary • Amyloidosis
complicaCons in lobar • Bronchopneumonia
(croupous) pneumonia. • Atelectasis
(p=5) • Pneumofibrosis
• Purulent meningi>s *480. Give the definiCon
• Purulent Endocarditis of “destrucCve (saccular)
• Purulent peritoni>s bronchioecstasis”
• Purulent arthri>s concept. (p=3)
• Purulent medias>ni>s • Destruction of muscle
*475.Specify causes of and elastic supporting
death in tissue
pleuropneumonia.(p=1) • Resulting from chronic
Respiratory insufficiency necrotizing infection.
476. Name the synonym *481. Specify typical
of local pneumonia. (p=1) extra‐pulmonary
• Bronchopneumonia complicaCons by chronic
477. Give the definiCon chronic non specific
of “aspirate pneumonia” pulmonary consumpCon.
concept. (p=2) (p=2)
• Aspirate pneumonia is a • Amyloidosis
form of local pneumonia • Cor pulmonale
• Developed as a 482. Name the significant
consequence of aspira>on complicaCons in
of foreign body, vomitus anthracosis (p=5)
and food. • Black lung disease
478. Name morphologic • TB
signs of pulmonary • Carcinoma Lung
emphysema taking into • Pneumofibrosis
considerqaCon: the size • Chronic Obs lung disease
of the lung Cor Pulmonale
condiCon of alveolar 483. Name sites
ducts and lumen, accumulaCng coal dust in
condiCon of septa anthracosis. (p=4)
between alveoli, he • Pulmonary lymph nodes
condiCon of capillary • CT along bronchi
bed. (p=4) • Macrophage
• Size: Voluminous • Lymphatic vessels
• Enlarged 484. What is black
• Septa: Thinning consumpCon? Give its
• Capillary bed: morphology and clinical
Diminished manifestaCons (p=4)
479. Name pulmonary • It is final stage of
and extra‐pulmonary antrachosis
complicaCons in chronic • Characterized by
formation of fibrosis tissue
and necrosis foci leads to
cavernous cavity
appearance. Clinically
manifest by Cardio-
pulmonary insufficiency.
485. What is silicosis?
(p=3)
• It is a lung disease termed
as type of pneumoconiosis
which caused by
inhala>on of crystalline
silicon dioxide (silica)
486.What is radiaCon
sickness?(p=3)
• Is injury produce by
ioniza>on radia>on over
limi>ng permissible dose.
499. Name types of severe
grippe form? (p=2)
• Toxic, influenza with
pulmonary complica>ons.
*500. What are the forms
of inflammaCon
observed in respiratory
tract in viral bacterial
grippe? (p=3)
• Fibrinous
• Hemorrhage
• Necro>c
• catarrhal
501. Give figuraCve
name of lung with viral
bacterial grippe
(influenza).
• Large mo]led lung
502.What are common
causes of death in
grippe(influenza) with
complicaCons?(p=4)
• Intoxica>on
• Purulent mediastinis,
purulent pericarditis
• Glomerulonephri>s
• Purulent encephali>s
• purulent meningi>s
503. In life Cme, paCent
suffered from acute
fibrinous hemorrhage
tracheiCs, bronchiCs,
and hemorrhagic
pneumonia. What is the
disease suspected?
Specify cause of death.
(p=2)
• Disease : influenza
• Cause of death :
Pulmonary and extra
pulmonary complications,
intoxications
504. During postmortem
examinaCon, there are
found numerous airless
small and large
inflammaCve foci of
dark red colour
protruded over cut
surface. Name the
process and possible
causes of their origin.
(p=4)
• Hemorrhagic
bronchopneumonia,
associate with other
diseases like Grippe
• plaque and ulcer.
(staphylococcus,
streptococcus,
pneumococcus)
• Hemorrhagic fever
• Influenza
505. Name possible types
of the inflammaCon in
measles bronchiCs. (p=2)
• purulent
• Necro>c
506. What are the
mechanisms of
bronchioecstasis process
complicated by measles?
(p=3)
• Necrosis of bronchial
wall, purulent
inflammation of wall, lysis
of elastic bronchial wall
• Lead to destruc>ve
saccular bronchiectasis
507. Noma? It’s progress • Is the disease with
mechanism in measles? chronic cough and with
(p=4) inflamma>on of the
• Noma is termed wet bronchus and bronchioles.
gangrenous necrosis as a 6. Types of emphysema
complication of infection according to anatomic
in immunity decreasing in form.
debilitated children. • Compensatory
AddiConal quesCons • Serinille
1. Name significant • Obstruc>ve
complicaCons in • Intersi>al
anthracosis. 7. pulmonary
• Pneumonia complicaCon.
• Abscess in lung • Cor pulmonale
• Hemapthoe • Secondary amyloidosis
• Cor pulmonale • Hemorrhage
• Chronic bronchi>s • Pyepneumothorax
2. Give examples of
chronic non specific Unit (22):Intes-nal infec-
pulmonary disease. ons.Typhus
• Chronic bronchi>s fever,syphilis,poliomyeli-s
• Emphysema 460.Explain the
• Bronchioecstasis pathogenesis of
• Bronchial asthma dysentery.(p=3)
• Chronic Inters>>al • Shigella bacteria have
pneumonia (pneumoni>s) oral-fecal direct
• Adult RDS transmission.
• Chronic abscess • damages rectum,sigmoid
3. Give histological form colon and descending
of status asthmaCcus. colon
• Occlusion of bronchi and •.invade colon and enter
bronchioles colonocyte with
• Thick membrane of the destruction of epithelium…
bronchi toxic with vasoparalytic
• Mucous plaque in the effect.
lumen of bronchus 461.Present anatomic
• Eosinophilic infiltra>on characteris-c of dysentery
in the wall of bronchus stages.(p=4)
• Patching necrosis and • Catarrhal coliEs,
shading of the epithelium fibrinous coliEs, ulcerated
4. Types of coliEs, regeneraEon
pneumoconiosis 462.Give
• Asbestosis macro,microscopic
• Silicosis characteris-c of changes
• Anthracosis in large intes-ne in the 1st
• Bituminosis stage of dysenteric
*5. DefiniCon of chronic coli-s.(p=4)
bronchiCs. • Name: catarrhal coliEs
• Macroscopic: mucosa
swelling, hyperemia,
hyperproduction of
mucous
• Microscopical :
Hyperplasia and the
atrophy of crypts.
463.Name and describe
macro‐,microscopic ini-a-
on changes in large intes-
ne in second stage of
dysentery coli-s.(p=5)
• Name: fibrinous coliEs.
• Macroscopic: Mucosa
swelling and hyperemic
covered with gray-brown
films, deep necrosis under
it.
• Microscopic: deep
necrosis & ulcers, fibrin
and neutrophilic
infiltrations
464.Name the intes-nal
complica-on of dysentery.
(p=3)
• perforaEon
• peritoniEs
• melena
• phlegmon
• fibrous stenosis
465.Mucous membrane
of large intes-ne is
swell,hyperaemic,covered
with gray brown film
taken off
with difficulty.Name the
process in large intes-ne
and specify it.(p=5)
• Name: fibrinous
coliEs(2nd stage of
dysentery) diphtheritic
type
• Process=deep ulcer
formation after films flake
off.
466.Name the stages of
changes of follicular
groups(Peyer’s patches)
in typhoid fever.(p=5)
• brain‐like swelling
• necrosis
• ulceraEon
• clearance of ulceraEon
• healing,regeneraEon
467.Specify most typical
colon complica-ons of
typhoid fever.(p=3)
468.Specify colon
complica-ons of typhoid
fever.(p=3)
469.Give the defini-on of
amebiasis.(p=4)
• Contamination infectious
disease with large
intestinal lesions and
caused by E.hystolytica.
470.During post‐mortem
examina-on ,there are
found some small,gray‐
green colour ulcers with
irregular
form cecum.Ulcer edges
are dug,overhung.During
histology examina-on
necrosis
,leukocytes,macrophages
infiltrates and amebas
are found.
→Name the disease and
process in large intes-ne.
→Explain the cause of
vast disintegra-on of
-ssues .
→Name extra and intra
intes-nal complica-ons in
the disease.(p=8)
• Disease: Amebiasis
• Process: necroEc‐
ulceraEon of coliEs
• Cause: Invade crypts of
colonic glands,burrowing
through the tunica
propria,stopped by
muscular mucosa.Then
antameba fent out laterally
to create flask shaped ulcer
with a
narrow neck and broad
base.
• ExtraintesEnal: numerous
abscess within the
organs(liver,lung,
brain,heart,spleen)
• IntraintesEnal:
hemorrage(melena),perfora
Eon,peritoniEs,stenosis.
508.Name clinical
anatomic form of paraly-
c Poliomyeli-s.(p=4)
509.Pathogenesis of
typhus fever.(p=5)
• Louse feces of RickeNsii
prowazekii invade the skin
and penetrate blood
stream.
• It enter endothelium &
smooth muscular cells of
the vessels.
• produce endotoxins and
activate thrombosis
•formation of granuloma
surrounding vessel..
510.What is typhus fever
granuloma?(p=3)
• Composed of
proliferative glial,
adventicial, and endolial
cell near small vessel.
511.Name types of typhus
fever vasculi-s.(p=4)
• Hemorrhagic, destructive,
proliferative, destructive-
proliferative
515.Give the structure of
gumma.What are the
stage and disease to be
observed?(p=6)
• Central caseous necrosis
surrounded by epitheloid
cell, lymphocyte and
plasma cell.
• stage of disease: terEary
stage.
• disease: syphilis
516.Name the
morphological changes of
inflamma-on by ter-ary
syphilis.(p=2)
• necroEc inflammaEon
• proliferaEve
inflammaEon
517.During post‐mortem
examina-on ‘’lobatum
hepar’’,aneurysm of aor-
c arch ,gummas in the
brain
are found .What is the
disease involved,its
period amd form?(p=3)
• disease: syphilis
• period: terEary syphilis
• form: gumma
formation(organ changes)
Addi-onal ques-ons
1)Extraintes-nal
complica-ons of typhoid
fever.(p=7)
a) bronchopneumonia
b) osteomyeliEs
c) muscle abscess
d) purulent perichondriEs
of larynx
e) necrosis of abdomen
muscles
f) typhoid sepsis
g) serous arthriEs
2)Present clinical
morphogical (anatomic)
classifica-on of
poliomyeli-s.(p=4)
• Spinal, bulbar, pontines,
mixed
UNIT (23) : Tuberculosis
518. What are the <ssue
reac<ons observed in
tuberculosis? (p=3)
• Alterative
• Prolifera)ve (produc)ve)
• Exuda)ve
519. What does primary
tuberculosis affect
designate peritoneal
inflamma<on
morphologically? (p=3)
• There is local exudative
pneumonia(alveolitis)
which undergoes caseous
necrosis and surrounded by
perifocal serous
inflammation
520. Name most typical
localiza<on of primary
tuberculosis affect. (p=2)
• Lung
• Intes)ne
521. Name principal
forms of tuberculosis
dynamics. (p=4)
• Hematogenous
• Lymphogenous
• Direct growth of primary
effect
522. Name hematogenic
tuberculosis forms with
principal defect of lung.
(p=2)
• miliary TB of lung
• Hematogenic
disseminated large local
TB
523. What do reinfec<ve
foci represent in
secondary tuberculosis
morphologically?
What is the author’s
terminology? (p=5)
• Foci of acinar and lobular
caseous
bronchopneumonia with
tuberculous granula)on of )
ssue in
apex of lung. It contains
epitheloid cells,
lymphocyte, and piragov
langhans cell,
• Author’s terminology:
Abricosov focal
524. Specify forms of
secondary tuberculosis.
(p=8)
• Acute focal / localized
TB
• Fibrous focal TB
• Infiltra)ve TB (Assman‐
Redelev foci)
• Tuberculoma
• Caseous pneumonia
(acute)
• Acute cavernous
(cavitated) TB
• Fibrous cavernous
(cavitated) TB
• Cirrho)c TB
525. What anatomical
pulmonary structure is
involved first of all in
ini<a<on of
secondary tuberculosis?
Specify its size,
localiza<on and character
of process.
(p=4)
• Localized in apex of one
or both upper lobes
• Size : Focus consolida)on
less than 2 cm in diameter
• Character of process :
Tuberculous
endobronchitis,
mesobronchitis,
panbronchitis, acinar and
lobular caseous
bronchopneumonia.
526. What is the form of
secondary tuberculosis
that tuberculoma
originate from?
What is morphologic
structure of
tuberculoma? (p=3)
• Infiltra)ve pneumonic
form
• Morphology : Massive
small focal caseous
necrosis surrounded by
capsule
527. Name progression
form of infiltrate
pneumonic tuberculosis.
(p=2)
• Caseous pneumonia
• Tuberculoma
528. What is the wall
composi<on of chronic
tuberculous cavity? (p=3)
• Internal wall : pyogenic
(caseous necrosis)
• Middle wall : tuberculous
granula)on of the )ssue
• External wall : connec)ve
)ssue fibers layer
529. What are infiltra<ve
pneumonic foci of
tuberculosis
morphologically? (p=3)
• Lobar focal caseous
pneumonia surrounding the
wide zone of non specific
perifocal inflammation.
530. Name causes of
death in acute cavity
tuberculosis. (p=3)
• Lung bleeding
• Intoxica)on
• Pneumothorax
531. Name causes of
death of secondary
tuberculosis. (p=5)
• cachexia
• Uremia caused by
amyloidosis
• Lung bleeding
• Lung and heart
insufficiency
• Pneumothorax
532. During postmortem
examina<on there is
found white focus of
stony density,
a pea (of 1 cm in dm)
size, seVled under pleura
in third segment of the
lung.
Give diagnosis and
author’s name of focus.
(p=3)
• Diagnosis : primary TB
undergoes healing process
• Author’s name : Ghon
focus
533. A 3‐year‐old child
died due to tuberculosis.
During postmortem
examina<on, there are
found inflates “fluffy”
lung, pleura and <ssue
with
numerous millet‐like
hillocks, sand felt and so]
meningeal sheath of
basilar
brain infiltrate by
exudates with separate
analogous hillocks. Name
the
form of tuberculosis and
changes of meningeal
sheath according to the
localiza<on. (p=3)
• Form of TB : acute
miliary TB
• Changes : Tuberculous
basal meningi)s
534. Adolescent had
primary tuberculosis in
childhood. Tuberculosis
spondyli<s
is detected. What kind of
TB manifesta<on is it?
What is direct process
localiza<on in vertebra?
(p=3)
• Kind of TB
manifesta)on :
Hematogenous TB mainly
with
extrapulmonary changes
• Localiza)on : Corpus
vertebra
535. The corpse is
delivered from hathist
hospital to pathological
anatomy
department. During
postmortem examina<on
cavi<es with solid walls in
right lung are found. The
lung is deformed with
sclero<c fields. <Sago
spleen> is detected. What
is the form of
tuberculosis and the
complica<ons
involved? (p=2)
• Form : fibrous cavernous
TB of lung
• Complica)on :
amyloidosis,
536. A 40‐year‐old male
is diagnosed for
“periferic carcinoma of
lung”
intravitally. He died.
During postmortem
examina<on, there are
found the
focus of caseous necrosis,
“pigeon egg” (of 2‐3 cm
in dm) size, surrounded
by
connec<ve <ssue capsule.
The focus is found in
second segment of right
lung.
Give your diagnosis.
(p=1)
• Diagnosis : tuberculoma
Addi<onal Ques<on
1. 12‐month‐old infant
with growth retarda<on
chest pigeon deformity,
overgrowth of car<lage
and
osteoid bone <ssue in
ostochorndral junc<on.
Name type of mineral
disorders and its e<ology.
What disease is to be
involved in diagnosis?
(p=4)
• Type : rickets with
deficiency of vit D
• Disease : Disturbances of
bone development results
from
enchondral bone forma)on
with plenty of osteoid
forma)on, disturbances of
calcium and phosphorus
exchange.
Unit 23 : Sepsis And
Meningoccosis
487. What is sepsis? (p=3)
• Polye9ologic non‐
contagious disease with
generalized infec9on and
acyclic
clinical course caused by
the severe bacteremia
infec9ons from local site
with background of
altera9on of
immunoreac9vity.
488. What is cryptogenic
sespsis? (p=2)
• Form of sepsis with
unknown entry of infec9on
*489. What spleen
changes are observed in
sepsis?( p=3)
490. What is
sepFcaemia? Give the
characterisFc of changes
in sepFcaemia? (p=6)
• Form of sepsis with
hyperreac9on of organism
with DIC syndrome,
jaundice,hemorrhagic
diathesis,necrosis of
organs,reversible injury
Of organs.
• bacteria are in blood
stream,lymph organs and
other organs,marked by
intoxica9on.
491. What is
sepFcopyemia and what
are its morphologic
signs? (p=4)
• Sep9copyemia is a form
of sepsis with microbial
embolism into organs and
appearance of numerous
abscesses within organs
which have suppura9ve
metastasis at different
organs.
• Morphological signs:
primary sep9c focus,
embolism,purulent
thrombophlebi9s then
lymphangi9s,
lymphadeni9s with
mul9ple bacteriosta9c
abscess in different organs.
*492. Describe
microscopic picture of
the cardial valves
changes in sepsis lenta.
(p=6)
493. Give clinical
anatomic forms of
gyneacologic sepsis.when
does it begin?(p=4)
• Sep9caemia
• Sep9pyemia
• It happens few days aPer
abor9on or delivery
Purulent fibrinous
endometritis and
thrombophlebitis.
494. Name changes in
entrance gate and
peculiariFes of clinical
anatomic forms of
umbilical sepsis (p=4)
• Connected with
suppura9ve
thrombophlebi9s and
thromboarteri9s of
umbilical vessel
which can pass through the
type of sep9caemia and
like sep9copyemia
consequence
characterized by peritoni9s
& liver abscess.
495. The uterus is
enlarged to a marked
degree .its wall is
thickened,cavity
widened.mucous
membrane is
saturated with yellow‐
green exudates and films.
Name uterus disease
according to uterus size.
What is the
complicaFon of process?
(p=5)
• Uterus disease‐post
partum fibrinous purulent
endometri9s
• Complica9on‐
sepsis,lyphangi9s,lymphad
eni9s,mul9ple abscess of
liver.
496. PaFent with prostate
hypertrophy died due to
urosepsis.explain the
pathogenesis of
urosepsis?(p=5)
• Purulent
inflammation..later
decompesation process
follow and then urinary
refluxion leads to
secondary infection to
urinary bladder,urosepsis
497. PaFent perished due
to chronic heart and
vascular failure.
According to anamnesis
got treatment for
sepsis lenta 3 years
ago.name most typical
changes in the heart
found by pathologist in
post‐mortem
examinaFon. Specify the Waterhouse‐Friderchsen HIV INFECTION lyphodenopha8a during • neurologic manifestaIons o cell proliferaIon and
connecFon of changes syndrome,toxic 537. Specify basic second AIDS 548. What is the meaning diffuse intersIIal lung
with sepsis lenta in bacterial shock. pathways of HIV Period. (p=2) of opportunis8c fibrosis.
paFent (p=4) • Hemorrhage within infec8on transmission. (p ‐affecIng more than 2 infec8ons? (p=2) Addi8onal ques8ons :
• Typical changes: aor9c & bilateral adrenal gland =4) groups of lymph node • infecIon by 1.what does CNS
mitral valve sepsis 514 . During post‐ • sexual contact within more than 3 months protozoa.bacteria,virus,fun involvement syndrome in
• Connec9on of changes: mortem examinaFon of • infected blood Period gus persisIng in AIDS include? (p=3)
result of polypous brain,there are found • from mother to infant 544. What are immunocompetent host • meningoencephaliIs
ulcera9on endocardi9s. smoothed brain 538. Which are HIV characteris8cs [clinical without clinical • tumors
498. On the second day gyri,super enlarged infec8on carriers? (p=2) and morphological] of significant disease • demenIa
aZer childbirth [delivery] ventricle,atrophic brain • mother with HIV third AIDS period? 549. Name infec8ous 2. Specify most typical
the women had sudden Fssue, it is known from • drug abuser (p=5) agents causing malignant tumors in
chill[about 41 celcius] morbid history that 539. Name groups of • immune containing of opportunis8c infec8ons in AIDS. (p=2)
then paFent had acute popula8on belonging to virus AIDS. (p=4) • Kaposi sarcoma
appeared point of infecFon with the risk HIV infec8on group. • persistent • protozoal and helminIc • Non‐Hodgkin Lymphoma
hemorrhages on the skin changes of pia mater.give (p=6) lymphadenopathy • fungal infecIon [Burki\s lymphoma]
and mucous membranes your diagnosis.(p=3) • homosexual • asymptomaIc • bacterial infecIon 3. Specify most frequent
and jaundice.2 days later • Chronic hydropic brain • bisexual • decrease CD4 count • viral infecIon causes of death due to
the women aPer having • IV drug abusers • hypergammaglobulin *550. What are the HIV infec8on [p=2]
died. During post‐ meningococcal infec9on. • hemophiliacs 545. Name clinical and characteris8c features of • opportunisIc infecIon
mortem AddiFonal quesFons • recipient of blood who morphological changes of opportunis8c infec8ons in • neurologic syndrome
examinaFon,there was 1.What changed are are not hemophiliacs fourth AIDS period. AIDS? (p=4)
found the evidence of observed in sepsis . (p=3) • heterosexual contact of (p=4) 551. Name basic
expressed dystrophy in • Dystrophy other high risk group Copyright reserved@ manifesta8ons of gastric
organs,enlarged diffluent • Hyoperplasia 540. Specify AIDS group 38~2008 intes8nal syndrome in
spleen……... (p=4) • Inflamma9on progress. (p=4) 2 AIDS. (p=2)
• Diagnosis: 2.Define meningococcal • early acute phase • breakdown host defense • diarrhea
gyneocological post‐ infecFon. Which is the • middle chronic phase • viremia • exhausIon
partum sepsis nature of inflammaFon in • final crisis phase • destrucIon lymph node 552. What infec8ons
• Clinical morphologic it? Specify its 541. Specify dura8on of • neoplasm condi8on progress of
form: sep9caemia localizaFon.(p=4) AIDS infec8on period. • opportunisIc infecIon gastric intes8nal
• • Acute infec9ous disease (p=2) 546. The most typical syndrome in AIDS. (p=4)
Changes:endometri9s,thro caused by meningococcus • iniIal stage: 4 to 6 weeks clinical variants of AIDS. • shigella
mbophlebi9s of uterine which can develop • middle stage: 7 to 10 (p=4) • helicobacter
vessels purulent years • AIDS with opportunisIc • campylobacter
512.Name forms of inflamma9on of pia mater. 542. Name and specify infecIon and tumors • clostridia
meningococcal infecFon . • Localisa9on: mucous of second AIDS period • AIDS associated complex 553. Give clinical and
(p=3) nose and pharynx clinically and characterized by absence morphological
• Purulent ependyma99s • Meninges of brain morphologically .(p=6) of clinically significant characteris8c of
• Nasopharyngi9s • Appendyma of ventricles • non specific symptoms manifestaIon pulmonary AIDS variant.
• Purulent leptomeningi9s • Blood • high concentraIon viral in • persistent generalized (p=4)
• Meningococcemia plasma lymphadenopathy • clinical:
513. Name causes of COD in • viral specific 547. Name typical o fever and cough with
death in fulminate meningococcemia=jaundic immunoresponse morphologic changes in poor auscultaIve syndrome
meningoccemia. (p=2) e,hemorrhagic • normal CD4 count AIDS. (p=4) o pneumonia
• Acute adrenal 543. Name morphological • Severe opportunisIc • morphological:
syndrome,DIC,acute manifesta8on of infecIon o eosinophilic exudaIon
insufficiency described as
adrenal insufficiency. • secondary neoplasm within alveoli