Fat

emeh

PATHOPHYSI
OLOGYOFTHELI
VER

St
udent
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oup_
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a__
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Not
ion Def
ini
ti
on

Li
verf
ail
ure Hepatic insufficiency is a totality of syndromes, connected with
adisturbance of the liver ability to fulfill its functions

Gl
ycogenoses Splitting of glycogen (glycogenolysis) may be disordered in two oppositedirections. Primary
disorder is underlied by lack of phosphorilase andglocoso-6-phosphotase. Intracellular (in
hepatocytes) retention of glycogenin determined by enzymopathy (disease of accumulation)

Hepati
c
encephal
opat
hy, is a damage of the central nervous system function as
hepati
ccoma a result of thedisturbance of the antitoxic function of
the liver.
Jaundi
ce is a yellow coloration of the skin, mucous membranes and
sclera as a resultof bilirubin content increase in the blood
(bilirubinemia) and a deposition ofthe bile pigments in them
Bloodlevel
sof
total
bil
ir
ubin
anditsfr
acti
ons

Cholemic
is a totality of the symptoms, connected with the entering of
syndrome the bilecomponents into the blood
Achol
ic
is a totality of the symptoms, connected with nonentrance of bile components
syndr
ome into the duodenum and disturbance of a digestion.

Dy
schol
i
a Is syndrome in which the bile aquires lithogenic properties that
determines the formation of the gall calculi in the gallbladder and bile
duct,contributes to development of the cholelithiasis
Portal Increased blood pressure in the portal system results in development of
hypert
ensi
on collateral blood circulation and opening of porto-caval and cava-caval
anastomoses. The dilated vessels are visible on the frontal abdominal
wall while an observation of a patient (so-called kaput medusea ).

Answert
hequest
ions:

•
Classi
fi
cat
ionofl i
v erfail
ur e(bypathogenesi s):
1)hepatocellular(dystrophic and necrotic lesions of the hepatocytes)

2)excretory or cholestaticdisturbance of cholepoiesis and cholekinesis)

hepatovascular(in blood circulation disturbance in liver due to
3)
thrombosisor embolism of portal vein,…)
4)combined(due to combination of several mechanism in the process of
development of functional hepatic insufficiency)
 Fat
emeh

•
Disor
der
s of car
bohy
drat
e met
abol
i
sm i
nli
ver f
ail
ure(
eti
ology
,pat
hogenesi
s,
manif
est
ati
ons)
:
• Etiology: acquired or hereditary .Pathogenesis:1)inhibition of glycogenesis fromglucose_6_phosphate dehydrogenase 2)biosynthetase and breakdown the glycogen 3)glyconeogenesis 4)formation of
glucuronic acid 5) Reduction of glycogen synthesis; 6)Violation of the glycogen splitting; 7)Unstable blood glucose levels (hypoglycemia, hyperglycemia) Manifestations:Glycogen synthesis (glycogenes)
gets suppressed and a glycogen content in the liver is reduced. Primary disorder is determined by diminished enzymal activity, the secondary by hormonal disorders as a conversion of glucose
into glycogen is controlled by insulin .Splitting of glycogen (glycogenolysis) may be disordered in two opposite directions. Primary disorder is underlied by lack of phosphorilase and
glocoso-6-phosphotase. Intracellular (in hepatocytes) retention of glycogen in determined by enzymopathy (disease of accumulation). It is called glycogenosis and leads to hepatocytes degeneration.
Splitting of glycogen into glucose is controlled by hormones – glucagon, adrenaline and thyroxin.
•Di
sor
der
soff
atmet
abol
i
sm i
nli
verf
ail
ure(
eti
ology
,pat
hogenesi
s,mani
fest
ati
ons)
:

•Etiology: acquired or hereditary • Pathogenesis:Violation of atherogenic form cholesterol

transformation to less atherogenic Violation of the phospholipids synthesis with antyatherogenic
effect Increase the level of free cholesterol deposits in the walls of its vessels, the
development of atherosclerosis. Manifestation: 1)the transport hyperlipemia 2)hypercholesterolemia
3)hypocholesterolemia 4)hyperketonemia and ketonuria 5)lipid hepatosis 6)steatorrhea
• Di sorder s of pr otein met abolism i n l i
ver f ai
lure (etiology, pathogenesis,
mani festati
ons) :

•Ty
pesofj
aundi
ce,
thei
rcauses
1) Hemolytic jaundice: hemolysis of red blood cells (anemia, hemoglobinuria 2) Obstructive
jaundice(mechanical,posthepatic): violation of the bile secretion from the bile capillaries of
the gall bladder or its duct; 3)hepatic jaundice:disorder of bilirubin capturing by hepatic
epitheliocytes developmen
TASKSFORSELF- ASSESSMENT

Task.A 55- y earol d pat i

entwas admi t
ted t ot he surgicaldepar tment.
He l
ooks
exhausted,hi sski nandscl eraareyellow-saffron.Labor atoryfi
ndingsi ncl
udeserum
bil
i
rubinl evelsi s160 μmol/ L,colorl
ess f eces,dar k uri
ne (“coca-cola”uri
ne)
.On
examinationt umorofpancr easwasr evil
ed.Answert hefoll
owi ngquestions:
•Whatty peofj aundi ceoccur si
nthepat ient?
1.Pr ehepat ic
2.Hemol y tic
3.Par enchy mal
4.Hepat i
c
5.Chol est at i
c
•Whatisacauseofj aundiceinthepatient?
6.Hemol y sisofRBCs
7.Impai redconj ugati
onofbili
rubi
ni nhepat ocytes
8.Hepat ocy t enecrosis
9.Hepat ocy t eapoptosis
10.Obst ruct iont obilefl
ow
•Whatist hecauseofi mpaireddigest
ioni ntheintest i
neinthisdisorder?
11.Achol ia
12.Hy pochol i
a
13.Chol emi a
14.Mal digest ia
15.Mal absor bti
on
•Whatbi l
epi gmentpr ovidesfordarkcolorofur ineint hepatient
?
16.Bi l
ir
ubi n- albumincompl ex
17.Indirectbi li
rubin
 Fat
emeh

18.
Directbi
lirubi
n
19.
Mesobi l
inogen
20.
Stercobi
linogen
•Whatbil
epigmentabsencei
sacauseofcol
orl
essf
ecesi
nthepat
ient
?
21.
Hemogl obi n
22.
Directbi
lirubi
n
23.
Indir
ectbilir
ubi
n
24.
Stercobi
linogen
25.
Bili
verdi
n

Task4.Hy per bili

r ubinemi aduet oani ncreasei nbot hdirectandi ndi
rectbili
rubinwas
rev eal
edi npat ient ’
sbl oodser um. Hisur i
nalysi
sshowsdi r
ectbili
rubin,urobil
i
nogen, bi
l
e
acids.Hi sf ecesar ehy pocholic.Ther eisal sohy pocholest
erolemia( 1.2mmol/L) ,
hy poprot einemi a
(totalpr otein-30g/L)andi mpai redbl oodclotting.Answert hefoll
owi ngquest i
on:
1)Whatt ypeofj aundi ceoccur si nthepat i
ent ?
Hemolytic jaundice
2)Whatcausesani ncr easei ndirectandindi rectbi
li
rubinlev
elsi npatient
’sblood?
because of increase breaking of RBC and then hemoglobin in blood we will have high indirect bilirubin and
it lead to high level of direct bilirubin production in hepatocyte
3)Whatsy ndr omesoccuri nthepat ient?

4)Whatot
herchangescandev
elopi
npat
ient
’sbl
ood?Why
?

Fi
lli
nthet
abl
e.Mar
k“+”
,ift
hesy
mpt
om i
spr
esent
,or“
-“,
ifi
tisabsent

Sy
mpt
oms,
syndr
omes Mechani
calj
aundi
ce Hemol
yti
cjaundi
ce

Yellowi shski n + +
Achol icsy ndrome + _
Chol emi csy ndrome + _
Discol oratedf aces + _
Clay edf aces + _
Putref actedf aces + _
Disor derofl i
pidssuct i
on + _
Avitami nosis + _
Hemor r
hage
_
+
Disor derofdi gestion + _
Skini tching + _
Arter i
alhy potension + _
Brady car di
a + _
Met eor i
sm + _
Fat
emeh

Li
verpat
hol
ogy
V-3

1.Apat i
entwitht hejaundi
cehashy perbil
ir
ubinemiainaccountofconjugatedand
unconj
ugat edbil
irubinum,intheurine–conj ugat
edbili
rubi
num, urobi
li
nogen.Evi
dent
acti
onofbi l
eacidsi salsopresent.Hypercholest
erol
emia,hypoprotei
nemia,sl
owblood
cl
otti
ng.Whatt ypeofj aundicethesechangesar ecommonf or?
A.Par enchymat ous
B.Mechani c
C.Haemol yti
c
D.Mi xed
E.Nucl ear

2.Apat i
entwit
hthejaundicehadfol
lowingchanges:
incr
easedbi
li
rubi
num cont
enti
n
bl
ood,bi
li
rubi
nuri
ne,hyper
cholest
erol
emia,achol
iaandbil
eacidsi
nblood.Whatt
ypeof
j
aundi
cethesechangesarecommonf or?
A.Mechani c
B.Parenchymatous
C.Haemol yt
ic
D.Mixed
E.Nuclear

3.Apat i
entwi t
hthehepat i
cpat
hologyhaddev el
opedsignsoft hehemorr
hagic
syndrome.Whatpossi blemechanism ofthehemor r
hagicsy ndr
omedev el
opment?
A.Er yt
hrocyte’
shaemol ysisfr
om thebil
epigments
B.I ncr
easedv essel
s’permeabili
tyfrom t
hebil
epigment s
C.Augment ati
onofthev onWil
lebr
and’sfact
orformati
on
D.Di sorderoftheprothrombineformati
on
E.Augment ati
onofthet hrombocytescapabi
li
tyforadhesionandaggregati
on

4.Apat ient
,withthehepat icfailure,begantor
egi
stersl
eepi
ness,opaci
ty
consciousness, andthent hedeepf ainti
ngwasdev
eloped.Whatpathol
ogical
-genet
ic
mechani sm inthehepat i
cf ai
lurei sleading?
A.I ncreasedglucosel evelinblood
B.Toxi cact i
onoft heglucuroni de
C.Themet abolical
kalosisdev elopment
D.Ammoni aaccumul ati
on
E.Hy poxia

5.Apat i
entwit
ht hel i
verci
rr
hosi shasf l
uidaccumulat
ioni
ntheabdomi
nal
cav
ity
.
Whatmechanism oft heasci
tesdev elopment?
A.Incr
easedoncot icbloodpr essure
B.Incr
easedpressur eofthepor talveinsystem
C.Decreasedproduct i
onoft helymph
D.Decreasedsecr et
ionoftheant i
diuret
ichormone
E.Decreasedaldosteronesecr eti
on
 Fat
emeh

PAHOLOGYOFKI
DNY ANSWERTHEQUESTI
ONS

1.Renalf
ail
urei
smani
fest
edbyt
hef
oll
owi
nghomeost
ati
cal
ter
ati
ons:

(A)Changesofexcr etoryfuncti
onar e (B) Changesofi ncretoryf uncti
ons
mani fest
edbydi sturbances: causet
hedev el
opment :
a)a)wat erhomeost asis a)Hemodynamic
b)acid-base balance (isohydria). b)Hemopoietic (erythropoietic)
c)electrolytes (isoionia) c)Hemostatic
d)osmotic concentration (isotonia)
e)nitrous metabolism (urea, acid,
ammonia, creatinine)

2.Acut
erenalf
ail
urei
schar
act
eri
zedby
:
• disorder of homeostasis as a result of significant and quick decrease of the rate of the glomerular filtration. •
associated with acute suppression of renal function, • accompanied by reduction of the 24-hour urinary output to 400 ml or
less or • total its cessation (up to 1-10 ml/min comparatively with 125 ml/min in norm).
I
tset
iol
ogyi
sconnect
edwi
thact
ionofi
ntr
arenalf
act
ors(
li
st)
:
1. Local disorders of blood circulation (ischemia, thrombosis, DIC-syndrome) 2. Injury by nephrotoxic poisons (salts of
heavy metals, arsenic, phosphorus, and snake poison, endogenous intoxication in diabetic coma, sepsis, peritonitis,
hepatic insufficiency), 3. Immune nephrotoxic factors, 4. Severe diffuse glomerulonephritis, 5. Acute tubular necrosis
(pyelonephritis
andext
rar
enalf
act
ors(
li
st)
:
1. Shock, collapse accompanied by acute blood hypotension (decrease of the arterial blood pressure less than 40 mm Hg). 2. Blood loss,
incontrollable vomiting, profuse diarrhea, the diuretics abuse resulting in acute decrease of the intravascular and extracellular fluids volume. 3.
hemolysis of erythrocytes ( hemotransfusion mismatched) 4. trauma of tissues (crush-syndrome, large cutaneous burns) 5. Acute (myocardial
infarction) and chronic (hypertrophy of myocardium, cardiosclerosis) cardiac insufficiency 6. Postrenal part: 7. obstruction of urine flow and
retention of the urine at the level of urinary tract like calculi in the ureter, tumors, hypertrophy of the prostate
Pat
hogenesi
sofacut
erenal
fai
l
urei
sconnect
edwi
th:

(
A)Pr
erenal
fact
ors(
alt
erat
ionsofr
enal
bloodci
rcul
ati
on;

(
B)
Renal factors
C) Post renal factors
(

3.Chr
oni
crenalf
ail
urei
sther
esul
tof…
progressive and irreversible loss of functional parenchyma Chronic renal insufficiency is the end result of a variety of renal diseases and is
the major cause of death from renal pathology. It develops gradually due to heavy disorders of renal processes and the main renal functions
as a result of: .decrease of a number of acting nephrons, .substitution of parenchyma by connective tissue .puckering of the kidney. connected
with azotemia, water-electrolyte and acid-base disbalance.
I
tset
iol
ogyi
sconnect
edwi
th…
• most frequently are intrarenal. • chronic progressing diseases of the kidneys of inflammatory (chronic
glomerulonephritis, chronic pyelonephritis, etc.) • vascular (arterial hypertension) and metabolic (diabetes mellitus,
amyloidosis, gout) origin. Connection between chronic renal insufficiency and diabetes mellitus during long term (15 to
20 years) is significant. Half patients die because of diabetic glomerulosclerosis
I
npat hogenesi sofchr oni cr enalf ai lur et hef ol lowi ng4st agesar ei
ndi
cat
ed:
1.
• Latent, which can last for many years without any clinical manifestations;
2.
• Initial, or stage of the polyuria that develops after more 50 % of the nephron death and is
characterized by the polyuria as a result of the decreased sodium and water reab- sorption;
3.
• The oliguria and anuria that occurs, when more 70 % of the nephron death and the GFR
4.
decreasing less 20 % of normal;
• The uremia, which develops, when the GFR decreases less 10 % of normal.

4.Li
stt
hesi
gnsofr
enalf
ail
ure:
Fat
emeh

(A)Decr easeofcl ear ance( t

o40- 15 (
F)
ml /min Hypertension
(
B)decrease in amount of glomeruli in both (
G)
kidneys up to 25 30% and lower Anemia
(
C) (
H)Uremia
Polyuria
(
D) (
I)
Hypernitrogenemia Disorder of all organs and systems

(
E)Acidosis

5.Whatki
ndsofar
ter
ialhy
per
tensi
oncanoccuratr
enal
diseases?

(
A)Hy
per
tensi
ondependi
ngf
rom v
olume (
C) Hypertension depending on
renin_angiotensin Secretion
(
B) Hypertension depending on Resistance

6.Whatmechani
smscauseanemi
aatr
enalf
ail
ure?

(
A) Bleeding (
C) Deficit of erythropoietins

(
B) Hemolysis

7.Whatchangesofurineproduct i
on In case of Polyuria: high amount of urine
are the basic of polyuri
a at Hyperglycemia: high amount of glucose in
hydremia, hyper
glycemi a, urine and high amount of urine in total ADH:
hyperpr
oduct
ion of ant i
diureti
c Less amount of urine in total as a result of
absorbed water
hormone?

8.Consequencesf ort heor gani sm f

rom t
hepr
otei
nur iaatnephr iticsy ndr omear
e:
(A)Hypooncot icst at e, edemas (
E) Endocrine disturbances

(B)
Propensi ty t o t hr omboses and ( F)
thr
omboembol ism Predisposition to atherosclerosis
(C) Hemorrhage syndrome (
G)Deficiency of Fe, Zn, Cu
(D) Decreased resistance to infection

9.Gl
omer
ulonephr
it
isi
sbilateral diffusive infectious-allergic disease of the kidneys of the inflammatory origin
with the preferred damage of the glomeruli It may be primary and secondary (as a
complication of other diseases more often diffuse lesions of the connective tissue) as
well as acute and chronic
10.Mainpat
hogenet
icvari
ant sofacut
egl
omer
ulonephr
it
isar
e:
(A) Immune complex initiated

(
B) Nephrotoxic
Fat
emeh

TESTSWI
THMANYCORRECTANSWERS

13.Speci f
ylinksofpat hogenesi sofacut ediff
useglomerul
onephr
it
is(
5)
1)Fixati
onant igen-antibodycompl exesi ntheglomerul
arbasementmembraneof
ki
dney
2)Immunei nfl
ammat ionofki dneyglomer ularbasementmembrane
3)renalglomer ularmicr ovascularthr
ombosi s
4)For mati
onofr enalcy tot
oxicantibodies
5)For mati
onofant i-
streptococcalantibody
6)Streptococcemi a
7)hypocoagul ati
on
8)polyuria
9)Oliguri
a

14.Whatchangesi nt
heur
inear
echar
act
eri
sti
cofnephr
it
icsy
ndr
ome?(
3)
1)Glycozuria
2)Proteinuri
a
3)ketonur i
a
4)urobil
inuria
5)cyli
ndr ur
ia
6)Macr ohemat ur
ia
7)Microhemat uri
a

15.Arterialhyper t
ensioninchroni cdiff
usegl omerulonephri
ti
sdev elopsasaresul
tof
:
(3)
1)Blockingofr enal t
ubulesbyt hecy l
indersandt heproductsoferythrocy
teshemol
ysi
s
2)Activationoft he"reni
n-angi
ot ensi
n-aldosterone-
vasopressi
n"system
3)Decreasedpr oductionoftypeAandEpr ost
aglandi
nsbyt hekidneys
4)Incr
easedpr oductionofF-typepr ostaglandi
nbyt hekidneys
5)Reduct ionoft hekidneysproduceski nins
6)Incr
easi ngoft hekininsproduct i
onbyt hekidneys

16.Identifyt
hefactor
sofedemadev elopmenti nlesiontherenal
par
enchy
ma(
6)
1)Reduct i
oninglomerularfi
lt
rat
ionofbl oodpl asma
2)Increaseinthecontentofsodium ionsi nthetissues
3)Act i
vati
onofADHsecr et
ion,i
ncreasedt ubulesensiti
vi
tytoit
4)Increasedpermeabili
tyofthetissuemi crovasculat
urewalls
5)Mi crohematur
ia
6)Hy poonkiaofthebl
ood
Fat
emeh

7)Hy
per
onki aoft
hebl
ood
8)Hy
povolemia
9)Hy
per
v olemi
a

17.Whatf actor sdet erminet hedevelopmentofur o-andnephrol

it
hiasi
s?(5)
1)Reduct i
oni nbl oodsol ubili
zers
2)Increasei nbloodsol ubi
lizers
3)Infectionoft her enalparenchy maandur i
narytract
4)Increaset hesal tconcent rati
oninurine
5)Hy popr ot einemi a
6)Prot ei
nur ia
7)Ret entionofur ine
8)Pol yuri
a
Kidneypathology
V–8
1.Apat i
entwi t ht hemul t
iplemy el
omahadur ine-test
,wheretheprotei
nhasbeen
found.Whatpr oteinuriaform hasplace?
A.Supr ar enal
B.Renal gl omer ul ar
C.Renal tubul ar
D.Subr enal v
esi cular
E.Subr enal urethr al

2.Apat ientwithanacut ehear tinsuff

ici
encyoliguri
aarose.Whatmechani
sm oft
his
ef
fect
?
A.Decr easedquant it
yofthef unct i
onalnephrons
B.Increasedoncot icbloodpressur e
C.Increasedpr essureintheglomer ul
us’scapsule
D.Augment at
ionoft hehy dr
ost ati
cbloodpr essure
E.Augment at
ionoft heglomer ulus’smembr aneper meabi
li
ty

3.Apat i
ent,whoi ssuf f
er i
ngwi t
ht hesyst
emicl
upuseryt
hematosus,
devel
oped
azotemi aatmoder atepol yuri
a.Whati st
hemainlinki
nthepat
hogenesi
softhese
chronicrenal fail
uresy mpt oms?
A.I ncreaseft heglomer ulus’
sfil
trati
on
B.I ncreaseoft hetubule’ssecreti
on
C.Vasopr essindefici
ency
D.Di sor deroft heglomer ulus’
sfil
terpermeabi
li
ty
E.Decr easeoft hefunctionalnephrons’
smass

4.Apat i
entwiththeacut egl omerulonephrati
s.I
nhisur i
net
estwasdet ect
eda
si
gni
fi
cantquant i
tyofpr otein(10g/l)withthemolecularmasshigher70000D.What
di
sor
derhasbeenpr ovokedt hi
seffect?
A.Disorderofproteinreabsor pti
on
B.Changeoft hepol yanions’schargeoft heglomerul
us’smembr ane
C.Washoutoft hepol yani ons’
sfrom theglomerul
us’smembr ane
D.Damageoft heglomer ulus’
smembr ane
E.Decreaseoft hefunct i
onal nephronsmass

5. Astheresul
toft
heacuterenalf
ail
ureapat
ienthasdev
elopedol
i
gour
ia.Whatdai
l
y
di
uresi
siscommonf ort
hissy
mpt om?
A.50–100ml
Fat
emeh

B.1500–2000ml
C.1000–1500ml
D.500–1000ml
E.100–150ml