Liver Stuff Flashcards

1
Q

THE Largest solid organ in the body is __________

A

The liver

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2
Q

THE LIVER

Weighs about ____-___ kg in adults

Only organ capable of ______ after damage or partial hepatectomy

A

1.o – 1.5

complete regeneration

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3
Q

THE LIVER

Performs numerous complex functions including:

•____genesis, _____lysis, _____genesis and ___genesis

•Manufacture of _____ proteins

•______production

Detoxification, _____ metabolism, ____ genesis

A

Glyco; glycogeno

gluconeo; Leto

plasma

Bile; lipid; urea

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4
Q

Structure of the Liver

The liver is made up of liver lobules (the ________ of the liver).

Each lobule is constructed around a _____ that empties into the _____________ which then drain into the _______

A

functional units

central vein

right and left hepatic veins

vena cava.

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5
Q

Structure of the Liver

The lobule is composed of _______ that radiate from the central vein.

Each cellular _____ is _____ cells thick and between the two cells are (small or large?) _________ that empty into _______

A

cellular plates

plate; two

Small; bile canaliculi

terminal ducts.

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6
Q

Structure of the Liver

Blood enters the liver from two sources, the _________ and ____________

A

hepatic portal vein and the hepatic artery.

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7
Q

Structure of the Liver

____% of perfusing blood is from the hepatic portal vein, ____% is from the hepatic artery

A

60

40

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8
Q

Liver structure

At each corner of the ____gonal liver lobule is a group of _____ structures:

List them !… and it’s all called ??

A

hexa

three

a branch of the hepatic portal vein, a branch of the hepatic artery, and a bile duct

portal triad

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9
Q

Liver structure

As the two blood vessels leave the portal triad, they empty into the ______ where the blood from the two sources mix. It percolates through the that, toward the ____________ where the _________ is located.

It passes through a series of veins that collect from many lobules to enter the _________ and _____ which empty into the inferior vena cava.

A

sinusoids

center of the lobule

central vein

right and left hepatic veins

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10
Q

Liver structure

The venous sinusoids are lined with _____ different cell types:

List them

A

two

endothelial cells
Kupffer cells

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11
Q

Liver structure

The venous sinusoids are lined with two different cell types:

endothelial cells - have (small or large?) pores, allows H2O and plasma proteins to pass freely.

Kupffer cells - are ______ cells capable of ___________ and other foreign matter in the blood.

A

Large

reticuloendothelial

phagocytizing bacteria

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12
Q

Formation of bilirubin from Heme

RBCs have a life span of ______

Heme is degraded in the ____ system especially ______ and ____

_____% is from RBCs and ____% from turnover of immature RBCs and cytochromes

A

120 days

RE

Liver and spleen

85

15

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13
Q

Bilirubin metabolism and jaundice
Formation of bilirubin from Heme

Heme→ _______ ( ______ )→ ______(_____)

Enzyme:_________

A

biliverdin; green

Bilirubin ; red/orange

Heme oxygenase

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14
Q

Bilirubin metabolism and jaundice
Formation of bilirubin from Heme

Bilirubin is bound to ____= (conjugate or unconjugated?) bilirubin or (direct or indirect?) bilirubin.

A

albumin

unconjugated

indirect

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15
Q

Bilirubin metabolism in the liver

______ of bilirubin by ———-

______ of bilirubin

———- of bilirubin into _____

A

Uptake; hepatocytes

Conjugation

Excretion; bile

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16
Q

Bilirubin metabolism in the liver

Uptake of bilirubin by hepatocytes

Bilirubin ________ from its carrier _______ and enters hepatocytes

A

dissociates

albumin

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17
Q

Bilirubin metabolism in the liver

Conjugation of bilirubin

In hepatocytes, bilirubin is conjugated with __________ by the enzyme _________

A

two molecules of glucuronic acid

glucoronyl transferase

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18
Q

Bilirubin metabolism in the liver

Excretion of bilirubin into bile

Conjugated bilirubin (bilirubin _________) is transpoted into ______ and then into _____.

A

diglucoronide

bile canaliculi

bile

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19
Q

Excretion of bilirubin into bile is not energy dependent

T/F

A

F

Process is energy dependent and is impaired in liver disease.

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20
Q

Bilirubin metabolism in the intestine

Conjugated bilirubin is excreted through the _______ into the _____.( Ampulla of ____).

Gut ______ break it down to _______. Which is _______ by the _______ circulation as it is water (soluble or insoluble ?) into the circulation and is excreted by the kidneys as _____ a ____ pigment in urine.

The rest is converted to ________ the ____ coloured pigment and is excreted in faeces.

A

common bile duct; duodenum; Vater

bacteria; urobilinogen

reabsorbed; enterohepatic

soluble; urobilin; yellow

stercobilinogen; brown

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21
Q

Jaundice is a clinical term .

T/F

A

T

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22
Q

Jaundice

It is the ________ discoloration of skin, nail beds, sclera and mucous membranes as a result of ———secondary to increased bilirubin levels in blood. ( ___________ )

A

yellow

deposition of bilirubin

hyperbilirubinaemia

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23
Q

Types of Jaundice

_______ jaundice
_________ jaundice
_________ jaundice

A

Haemolytic

Obstructive

Hepatocellular

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24
Q

Haemolytic jaundice

Caused by _____ of _______ in haemolytic anaemias like sickle cell anaemia

____ is produced at a rate faster than the rate of _________ by the ______

A

massive lysis; RBC

Bilirubin

conjugation by the liver.

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25
Q

Haemolytic jaundice

____eased blood unconjugated (indirect) bilirubin

Urobilinogen is ______ in urine

A

Incr

increased

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26
Q

Haemolytic jaundice

Presence of bilirubin in urine

T/F

A

F

No bilirubin in urine as it is bound to albumin.

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27
Q

Haemolytic jaundice

colour of urine is _______.

_______ stools due to increased ———, produced from increased _____.

A

normal

Dark coloured

stercobilinogen

urobilinogen

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28
Q

Obstructive Jaundice: In bile obstruction;

__________ is prevented from passing into the intestine.

A

Conjugated bilirubin

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29
Q

Obstructive Jaundice

_________ is regurgitated into the blood increasing ________ in blood.

Excessive ________ is filtered in ____ and excreted in urine giving the ___________ colour of urine.

A

Conjugated bilirubin

conjugated bilirubin

conjugated bilirubin; urine

yellowish brown

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30
Q

Obstructive Jaundice

In Blood.

Increased _________.

Elevation of ____________.

____ is normal or mildly elevated.

A

conjugated bilirubin

GGT and ALP

ALT

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31
Q

Obstructive Jaundice

In Urine.

______ appears in the urine giving _________ urine.

_______ is reduced in urine.

A

Bilirubin

yellowish brown

Urobilinogen

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32
Q

In obstructive jaundice , stool color is unaffected

T/F

With reason

A

Stool is pale as a result of low stercobilinogen.

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33
Q

Hepatocellular jaundice

FIRST.

Caused by _____ as a result of _____.

Damage to ______ causes low ______ efficiency leading to increased ___________ in _______

A

liver damage

hepatitis; hepatocytes

conjugation

unconjugated bilirubin in blood.

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34
Q

Hepatocellular jaundice

SECOND!

Conjugated bilirubin is __________. So it enters the circulation increasing conjugated bilirubin in blood.

A

not efficiently secreted into bile

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35
Q

Hepatocellular jaundice

IN Blood

Increased ________________.

______________ are markedly elevated.

A

BOTH conjugated and unconjugated bilirubin

ALT and AST

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36
Q

Hepatocellular jaundice

IN Urine.

________ is present in urine.

Urine colour is ________.

Stool is _______ . (___________)

A

Bilirubin

yellowish brown

Pale; low stercobilin

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37
Q

JAUNDICE IN NEWBORNS

In newborns especially ______ ones,
Bilirubin accumulates as liver enzyme _____________ is low at birth.

The enzyme reaches adult levels in about ________.

A

premature; bilirubin glucoronyl transferase

4 weeks

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38
Q

JAUNDICE IN NEWBORNS

Treatment.

Exposure of the newborn’s ______ to _______ which ________________________

These isomers can be _____ into ____ without __________

A

skin

blue fluorescent light

converts bilirubin to more polar and hence water soluble isomers.

excreted; bile

conjugation to glucuronic acid.

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39
Q

JAUNDICE IN NEWBORNS

Accordingly,_______ is increased in blood.

Elevated bilirubin in excess of the _______ capacity of _______, can diffuse into the ———— and cause toxic ________( ________)

A

unconjugated bilirubin

binding ; albumin

basal ganglia; encephalopathy

kernicterus

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40
Q

Congenital Hyperbilirubinaemia

Mention 4

A

CRIGLER- NAJJAR SYNDROME
GILBERTS SYNDROME
Dubin-Johnson syndrome
ROTOR SYNDROME

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41
Q

Congenital Hyperbilirubinaemia
CRIGLER- NAJJAR SYNDROME

Low _____ of _________________

It is a (common or rare?) inherited disease.

There is severe _______ in neonates – ____________.

It is complicated by ______ and early death.

A

activity

glucoronyl transferase

Rare

hyperbilirubinaemia

unconjugated hyperbilirubinaemia

kernicterus

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42
Q

Congenital Hyperbilirubinaemia

GILBERTS SYNDROME

_______ production or expression of ______.

(Common or Rare?) autosomal (autosomal or dominant?) trait.

More common in (men or women?) .

Usually (symptomatic or asymptomatic ?) hyperbilirubinaemia.

A

Decreased

glucoronyl transferase

Rare; dominant ; men

asymptomatic

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43
Q

Congenital Hyperbilirubinaemia

ROTOR SYNDROME.

Rare __________

(benign or malignant?), autosomal (dominant or recessive?) disorder characterised by ________ jaundice due to chronic elevation of predominantly ______.

A

mixed hyperbilirubinaemia

benign; recessive

non haemolytic ; conjugated bilirubin

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44
Q

Congenital Hyperbilirubinaemia

Dubin-Johnson syndrome.

Defect in ________________________________.

__________hyperbilirubinaemia.

A

transfer of conjugated bilirubin into the biliary canaliculi

Conjugated

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45
Q

In Gilbert’s syndrome, Liver function tests are not normal.

T/F

A

F

Liver function tests are normal.

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46
Q

Congenital Hyperbilirubinaemia

ROTOR SYNDROME.

Caused by impaired _______________________ that leaks into plasma causing hyper bilirubinaemia.

A

hepatocellular storage of conjugated bilirubin

47
Q

Difference between ROTOR SYNDROME.
And Dublin-Johnson syndrome

A

Almost like DJ but liver has black pigmentation in Dubin Johnson that Rotor does not have.

48
Q

Diseases of the liver

Classified according to aetiology

For clinical purposes, sub-classification defines the stage of the disease process (______,______,_______etc.) and the pathological state of the liver (assessed ________, ______, or _________) is also included.

A

acute, subacute, chronic

clinically, histologically or radiologically

49
Q

Aetiology of liver disease: Viral

Hepatitis viruses ______

_________ virus
_______virus

A

A to E

Epstein-Barr

Cytomegalo

50
Q

Aetiology of liver disease: Metabolic

______________

_______ disease

_________ hyperbilirubinemias

A

Hemochromatosis

Wilson

Hereditary

51
Q

Aetiology of liver disease: Autoimmune

________ hepatitis

_______________

A

Autoimmune

Primary biliary cirrhosis

52
Q

Aetiology of liver disease: Neoplastic

________
___________

A

Primary
Secondary

53
Q

The liver has only a limited number of responses to various pathological insults, these include:

__________ and ______

Acute _______ and its sequelae ____

_____

______failure (related)

A

Cholestasis and jaundice

hepatitis; Chronic liver disease

Ascites

Renal

54
Q

Biochemistry and hematology tests

__________ tests play a valuable role in monitoring the progress of established liver disease and in assessing the response to treatment.

A

Liver function

55
Q

Biochemistry and hematology tests

The standard LFTs include the following groups:

_______ measurements in ______ and ___

___________ activities

_________: total protein, albumin, globulins

Measures of _____: ________ time

A

Bilirubin; blood and urine

Plasma enzyme

Plasma proteins

clotting; prothrombin

56
Q

Infectious liver disease

Most important epidemiological causes of infectious liver disease are _____,______, and _______ infections.

A

viral, trematode and cestode

57
Q

Infectious liver disease

________ is the commonest cause of acute hepatitis.

A

Viral infections

58
Q

Infectious liver disease

Viral infections the commonest cause of acute hepatitis.
Range of responsible viruses very broad but those of greatest importance are the —————- ____________

A

hepatitis viruses A, B, C, D and E.

59
Q

VIRAL HEPATITIS

Distinguished from each other by ______, modes of transmission and propensity for development of ________

A

morphology

chronic infections.

60
Q

VIRAL HEPATITIS

A and E transmitted via ________, cause (acute or chronic?) hepatitis, long- term sequelae is (common or rare?).

B, C and D viruses _______-transmitted, associated with development of (acute or chronic?) hepatitis following ________

A

faecal-oral route; Acute; rare

parenterally

Chronic

initial acute phase.

61
Q

VIRAL HEPATITIS

WHO estimates ________ carriers of hepatitis B virus,________ chronically infected with hepatitis C virus.

A

350 million

300 million

62
Q

Biochemical tests

Plasma biochemical changes are different for all hepatitis viral infections.

T/F

A

F

Plasma biochemical changes similar for all hepatitis viral infections.

63
Q

Biochemical tests: viral hepatitis

During _______ phase (even before _________), plasma aminotransferases begin to rise, may reach concentrations more than _____ times reference limits.

A

early acute

development of symptoms

50

64
Q

Biochemical tests : viral hepatitis

In contrast to alcoholic hepatitis, plasma (ALT or AST?) usually higher than (ALT or AST?).

As _____ illness subsides, ALT and AST activities return to normal, though they may continue to be slightly elevated for weeks/months in protracted cases/ _____ infections

A

ALT

AST

acute

chronic

65
Q

Biochemical tests: viral hepatitis

Plasma bilirubin concentrations rise more (slowly or rapidly ?) compared to plasma enzymes , peak at _______ times the reference limit.

A

Slowly

10 – 20

66
Q

Biochemical changes: viral hepatitis

ALP and GGT activities are not elevated

A

F

ALP and GGT activities only mildly elevated.

67
Q

Biochemical changes: viral hepatitis

Mild to moderate ________ is a frequent finding, various _______ may become detectable.

A

hyperglobulinemia

autoantibodies

68
Q

Viral hepatitis
Sequence of events following infection varies widely, depends on ________, _______ and _______ infection is acquired, ________ and ________ to it.

A

which virus is involved

how and at what age

viral load and the host’s response

69
Q

Viral hepatitis

In all stages, after a period of incubation (___-____ depending on the virus), ____ phase sets in, begins with general malaise, nausea, loss of apetite, fatigue, abdominal pain/discomfort, _____-like illness, followed by appearance of ____ urine, _____ faeces and the development of _____.

A

2 – 26 weeks

acute; influenza

dark; pale

jaundice

70
Q

Viral hepatitis

Acute phase oftentimes is entirely asymptomatic or can be severe, proceding to ________ and coma, with high mortality.

Acute phase usually gradually resolves over period of _______ to _______

A

acute liver failure

several weeks to months.

71
Q

Viral hepatitis

Mechanisms of liver damage in acute/chronic hepatitis virus not fully understood, may be due to ______ against virus-infected cells, though in ________ infections, virus-induced _______ may also play a role.

A

host reactions

A and B

autoimmune reactions

72
Q

Hepatitis B

Transmission occurs mainly during ____, injection of blood products, though screening in most countries for HBV, development of vaccination programs has led to reduction in infections acquired this way, while monitoring of HBV-positive mothers and therapeutic intervention has led to reduction in

A

blood transfusion

73
Q

Hepatitis B

Elsewhere, vertical transmission maintains high level of infection. Most neonates that acquire the infection become (acutely or chronically?) infected, very rarely clear virus in their lifetime.

A

chronically

74
Q

Hepatitis B

Others will have florida liver damage that progresses to cirrhosis. About ___% of patients with cirrhosis due to HBV develop hepatocellular carcinoma each year

A

5

75
Q

Hepatitis A
RNA virus. Transmission via _____, mainly through personal contact (especially in _______), drinking of contaminated water, consumption of _____ from sewage-contaminated waters. Clinical course is (benign or malignant?) , chronic infections seem not to occur, prognosis excellent.

A

faecal-oral route

children

shellfish

Benign

76
Q

Hepatitis C
Transmitted ———-, though in about ___% no history of parenteral exposure obtained. Route of transmission unknown.

Acute and chronic HCV clinically (mild or severe?), usually silent.

Plasma aminotransferases are _______________. Other biochemical parameters usually normal or slightly abnormal. Mild to moderate hypergammaglobulinemia frequent finding.

A

parenterally

50
Mild

only moderately elevated

77
Q

Hepatitis D
HDV wholly dependent on ______, acquired by same routes either as __________ or _______.

Infection can be acute or chronic.

Co-infection can lead to _________ hepatitis, first episode due to ____, second to _____.

A

HBV

co-infection or super-infection

biphasic acute ; HBV; HDV

78
Q

Hepatitis E

_____-borne virus, infections acquired mainly through ________. Clinically similar to ______ but tends to be (more or less?) severe, greater propensity for development of _______, particularly in women infected in the ____ trimester.

Biochemical liver test results typical of acute viral hepatitis. Rapid elevation of plasma aminotransferases before or during appearance of jaundice.

A

Water; drinking feces- contaminated water

HAV; more ; acute liver failure

3rd

79
Q

Hepatitis D

Super- infection often leads to (acute or chronic?) HDV infection which is associated with (more or less?) severe liver disease and a (more or less?) rapid progression to cirrhosis.

Occasionally HDV infections are very severe, lead to _____ failure which carries a high mortality.

A

Chronic

More

More

acute liver

80
Q

Acute hepatitis and its sequelae

Acute inflammation of the liver associated with hepatocellular damage is most often caused by ______ or ______ including _____ and ______

Symptoms depend on the ______ of the process and the individual’s ____ to the damaging agent.

A

viruses or toxins

drugs and alcohol.

severity; response

81
Q

Acute hepatitis and its sequelae

There are three main possible outcomes:

__________

Progression to _________ of varying severity

______________

A

Complete resolution

chronic liver disease
Acute liver failure (ALF)

82
Q

Acute hepatitis and its sequelae

The distinction between acute and chronic liver disease is a ______ one. The usual yardstick is persistence of signs and symptoms, clinical or biochemical for more than ________.

A

temporal

six months

83
Q

Chronic liver disease

The initial onset is (easy or difficult?) to define.

For example ________ and ________ have no recognizable acute phases and develop (slowly or rapidly ?) with few symptoms over many months or years.

A

Difficult

primary biliary cirrhosis and hemochromatosis

Slow

84
Q

Chronic liver disease

In chronic hepatitis ___, initial viral infection is clinically _____ and disease may not become apparent for ____ to _____

A

C

silent

20 or 30 years.

85
Q

Chronic liver disease

Chronic hepatitis was previously classified on histological criteria as

•Chronic active hepatitis (CAH), which has a high propensity to progress to
_______ and/or _______ and

•Chronic persistent hepatitis, a more (benign or malignant ?) form which could occasionally progress to ____.

A

cirrhosis; liver failure

benign

CAH

86
Q

Chronic liver disease
Chronic hepatitis was previously classified on histological criteria as

__________
And
____________

This classification is not in use anymore as it seems they __________________________

A

Chronic active hepatitis (CAH)

Chronic persistent hepatitis

represent extremes of a continuous spectrum of changes in the liver.

87
Q

Chronic liver disease

Chronic active hepatitis has been supplanted by the term _____ hepatitis, ______

A

interface

cirrhosis

88
Q

Following a single short-lived insult the liver can recover completely with normal architecture.

T/F

A

T

89
Q

Cirrhosis

When the cause of the damage _______ e.g in ______ viral infection, the capacity of the ________ process to keep pace with the liver cell death may be exceeded.

A

persists; chronic; regenerative

90
Q

In Cirrhosis
A number of events ensue:

•__________ supporting liver cell plates collapses and condenses to form ____________

•____ cells, _____ cells and _____ which promote _____ become activated through the influence of various cytokines.

•As more fibrous tissue forms, architecture of the liver become disrupted and this disruption affects the ________, leads to further cell death. This is the _____________ result of any chronic process which involves recurrent waves of cell death and attempts by the liver to regenerate.

A

Reticulin framework; fibrous scar tissue.

Ito; perisinusoidals; lipocytes; fibrogenesis

blood vessels; irreversible end

91
Q

Compensated cirrhosis

Even when cirrhosis has developed there may be sufficient tissue for the liver to continue performing most of its normal functions, patients may have no symptoms.
Cirrhosis in these cases said to be (poorly or well ?) compensated.

In other cases there may be rapid deterioration (________) with development of _______ and _______

A

Well

decompensation

complications and liver failure.

92
Q

Portal hypertension

Increased blood pressure in the _____ due to increased resistance to the flow of blood through the _____ as a result of extensive _______ deposition in the liver with patients with _______.

A

portal vein ; liver

fibrous tissue ; cirrhosis

93
Q

Portal hypertension

Consequence of this increased portal pressure is blood is diverted into lower pressure _____ especially the veins around the upper end of the stomach and lower end of esophagus, also around the rectum and anterior abdominal wall (_____________).

A

systemic circulation

portal-systemic shunting

94
Q

In Portal hypertension

Spleen becomes enlarged due to back pressure created in the ________ which drains into the _____

A

splenic vein

portal vein

95
Q

Clinical importance of portal hypertension

•Hemorrhage from _____ or _____

•Natural ______ and _____ functions of the liver are bypassed, this increases risk of developing hepatic ________

A

esophageal or gastric varices

filtering and detoxifying

encephalopathy

96
Q

Clinical importance of portal hypertension

Hypersplenism is associated with ___________ in the spleen and the resulting ____ and _______ in the systemic circulation decreases the patient’s resistance to infections.

A

sequestration of WBCs

neutropenia and thrombocytopenia

97
Q

Ascites
Excessive accumulation of _____ in the _________.

Usually a Complication of ________

A

ECF

peritoneal cavity

advanced cirrhosis

98
Q

Ascites Can also develop as a result of other non-hepatic conditions

T/F

With example

A

T

Mechanism due to Na retention as a result of secondary hyperaldosteronism compounded by hypoalbuminemia, fluid is localized in the peritoneal cavity because of portal hypertension.
Urine in such patients virtually Na free

99
Q

Ascites

Treatment of ascites includes bed rest, _____,____, and ______

However careful monitoring is required to ensure serious complications (_______ of the ascites) do not occur.

A

salt restriction, diuretics and paracentesis.

bacterial infection

100
Q

Renal failure
Renal failure is an ever present risk in patients with ________, usually precipitates _______.

Onset indicated by rising plasma concentrations of ______ and _____ and a decreased _______.

A

advanced cirrhosis

encephalopathy

creatinine and urea

urine output

101
Q

Renal failure

Hyper_______ is a particularly lethal complication

The _______ syndrome is an idiopathic form of renal failure associated with advanced liver disease, ascites and encephalopathy.

A

kalemia

hepatorenal

102
Q

Renal failure

Characteristic feature of hepatorenal syndrome is that kidneys are histologically ______ but there is disturbance of ______.

Precipitating event is _______ leading to decreased ________ and reduced ________

A

normal

function

renal vasoconstriction

renal blood flow

glomerular filtration rate

103
Q

In hepatorenal syndrome

there is (rising or dropping ?) plasma creatinine and urea concentrations.

Most dramatic feature which distinguishes it from acute tubular nephrosis is dramatic increase in _________

A

Rising

sodium retention

104
Q

Tests of chronic liver disease

Low _____, impaired ______ and raised _____ are features associated with poor prognosis in patients with chronic liver disease.

A

albumin; clotting; bilirubin

105
Q

Tests of chronic liver disease

Scoring systems also exist which can help in selecting patients for liver transplantation e.g _____________________ includes:

Extent of ______
Grade of ________
Plasma _______ and plasma ______

A

Child Pugh score for cirrhosis

ascites; encephalopathy

albumin; bilirubin

106
Q

Tests of hepatic fibrosis

Most important test of fibrosis is _______ but ___________ exist, the most important being the ______ terminal ________________________

A

histology

biochemical markers

amino-terminal pro-collagen type III peptide (PIIINP)

107
Q

PIIINP is used in the monitoring of patients with _______ therapy where ______ can occur.

A

chronic methotrexate

108
Q

Other markers of hepatic fibrosis include

_____,______,______ and ________

A

prolyl hydroxylase, laminin, fibronectin and type 7S collagen.

109
Q

With the exception of _____ which measures the ______, and _____ which measures ______ and ______, most LFTs are indicators of liver _____ rather than ______.

A

albumin; synthetic function

bilirubin

conjugation and excretion

damage; function

110
Q

Tests of hepatocellular activity (quantitative liver function tests)

Quantitative assessment of the functional hepatic mass would allow the hepatologist to judge when patients with ________ disease are __________ and plan therapeutic interventions such as ____________ accordingly.

A

chronic liver

nearing end-stage hepatic failure

liver transplantation

111
Q

Tests of hepatocellular activity (quantitative liver function tests)

Various tests have been proposed based on the ability of the liver to ____________________

A

clear exogenous compounds from the body.

112
Q

Quantitative tests for hepatocellular activity include:

___________ capacity

________ breath test

____________ clearance

______________ formation test

A

Galactose elimination

Aminopyrine

Indocyanine green

Monoethylglycineexylidide

113
Q

Reference intervals

AST- ___-___
ALT- ___-____
ALP- ___-____

A

5-30

6-37

30-90