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House AMP > Cirrohsis > Flashcards

Cirrohsis Flashcards

1
Q

Global prevalence of cirrhosis from autopsy studies ranges from ___% to ___% of the general population.

A

4.5

9.5

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2
Q

Estimates - more than _______ adult in the world would be affected with chronic liver disease.

A

fifty million

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3
Q

Globally, ________,_______, and ___________ currently are the most common causative factors.

A

alcohol, NASH and viral hepatitis

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4
Q

Cirrhosis is a chronic liver disease characterized by:

(1)____________ with __________/_________

(2)Diffuse _______________ varying between _______ - __________

(3)Disruption of the _____________.

A

Bridging fibrosis

delicate bands/septae.

parenchyma regenerative nodules

<3mm - >3mm

normal architecture

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5
Q

Focal injury followed by fibrosis is cirrhosis

T/F

A

F

Focal injury followed by fibrosis is not cirrhosis

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6
Q

Cirrhosis

The injury & fibrosis are ___________ and ____________

A

diffuse and irreversible

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7
Q

Cirrhosis

Parenchyma damage leading to ___________ of ___________ with _____________ between vascular inflow and outflow channels

A

reorganization of vascular channels

abnormal interconnections

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8
Q

Classification of cirrhosis

 Morphological-

based on __________

(Can or Cannot?) distinguish the aetiological agents

____________
________________

A

size of nodule

Cannot

Micronodular

macronodular

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9
Q

Classification of cirrhosis

Aetiological
____________
________ disease
______ disease
 _______, _______________
________ disorders

A

viral hepatitis. {B,C,D}.

Alcoholic liver

Biliary

Obesity; insulin resistance

Metabolic

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10
Q

Classification of cirrhosis

Metabolic disorders:

 Primary ___________,
_______ disease
 __________ deficiency
________ obstruction
 Cryptogenic
 Others-galactosemia, tyrosinosis, drug induced.

A

haemochromatosis

Wilson’s

Alpha 1 antitrypsin

Venous outflow

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11
Q

Pathogenesis of Cirrhosis

 The major process in cirrhosis is ___________ in the liver which is ________.

 The source of this is ___ cells ( __________ cells)found normally in the __________

A

deposition of collagen; progressive

Ito; hepatic stellate ; space of Disse

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12
Q

Pathogenesis

______ cells have been implicated as the major source of excess collagen formation in cirrhosis.

 During the process of cirrhosis, _______ become transformed to ________ cells.

 They lay down _______ types _____ and _____

A

Ito

Ito cells

myofibroblast-like

collagen

I & III

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13
Q

Normally ito cells stores _____

A

Vitamin A

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14
Q

Hepatic stellate cells are stimulated by

 directly by _______
 indirectly through ________
 activated by endogenous cells like _____ cells, _______ cells, hepatocytes or bile ductular epithelial cells can also produce cytokines
 _________ of _______.

A

toxins; cytokines

kupffer; endothelial

disruption of ECM

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15
Q

Cirrhosis

The collagen are deposited in the ____ forming _________ and later to __________

A

lobule

delicate fibrils

broad fibrous septae

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16
Q

Hepatocyte regeneration
 With the continuous ________ of ________ and __________ the remaining hepatocytes are stimulated to regenerate

 These form ________ separated by the ____________

A

damage of hepatocytes and fibrosis

nodules; fibrous septae

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17
Q

Fibrosis + nodules lead to :

Impaired _________

Impaired ______________ and _______ functions

Impaired ____________(________)

A

blood supply

hepatocyte secretory; synthetic

bile flow (cholestasis)

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18
Q

Clinico-pathologic correlation/complications

 Asymptomatic

 Symptomatic - non specific symptoms such as anorexia, weight loss, weakness, _________,_________, features of _____ failure

 Hepato-pulmonary syndrome-impaired _________ due to imbalance of ___________

A

osteoporosis, debilitation; liver

oxygenation

pulmonary blood flow

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19
Q

complications of Cirrhosis

 Progressive _________
____________ carcinoma
________________
 ________________________

A

liver failure

Hepatocellular

Portal hypertension

Porto-systemic shunt

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20
Q

Portal hypertension
 Portal HT is one of the complications of cirrhosis when there is __________ to portal blood flow through the ________ and _________ of the central veins by _______ and _____________

A

increase resistance

sinusoids; compression

fibrosis

regenerating nodules.

21
Q

Portal hypertension

It can be subclassified into:

 Pre-hepatic – _______________ to ________

 Intra-hepatic-_______,________,_______,_________etc

 Post-hepatic- RHF, ___________, Hepatic vein out flow obstruction.

A

Obstruction to portal vein thrombosis

cirrhosis, schistosomiasis, fatty change, sarcoidosis

constrictive pericarditis

22
Q

Portal hypertension
PHT presents as:

_________,
 congestive _________
 __________ shunt,
 hepatic _________

A

ascites

splenomegaly

portosystemic venous

encephalopathy

23
Q

Ascites-pathogenesis in cirrhosis

> _____mls of peritoneal fluid.

It is serous with ____g/dl protein.

A

500

<3

24
Q

Ascites-pathogenesis in cirrhosis

The mechanism include:
 sinusoidal ______ that leads to Increased ________ of __________ =>leakage.

 increased hepatic _______ flow leads to increased —————— leading to __________ to _______

A

hypertension ; perfusion pressure of intestinal capillary

lymphatic; thoracic duct capacity

leakage to peritoneum

25
Q

Ascites-pathogenesis in cirrhosis

The mechanism include:

Hypoalbuminemia leads to _____ ease plasma oncotic pressure

_________ ————————

A

decr

secondary hyperaldosteronism.

26
Q

Porto-systemic shunts

Increased portal pressure leads to development of ________ wherever ________ and ________________ share a ______________.

A

bypasses

portal and systemic circulation

common capillary beds

27
Q

Porto-systemic shunts

The sites are:
_________
_________________ junction
____________
_______________+ ____________

A

Rectum

Cardio-oesophageal

Retroperitoneal

peri-umbilical +abdominal wall collaterals

28
Q

Porto-systemic shunts

The sites are:
 Rectum , leads to ________
 Cardio-oesophageal junction leading to _______ (_______________ in 65% of cases )
 Retroperitoneal/peri-umbilical +abdominal wall collaterals leading to __________

A

hemorrhoids

varices; haemorrhage & death

caput medusae

29
Q

splenomegaly

 Increased ______________________________ leads to congestion and enlargement of the spleen

 This results in secondary haematologic abnormality due to __________

A

backflow of blood into the splenic vein

hypersplenism

30
Q

Other features of hepatic failure

________
hypo________________
 Hyper________________

A

Jaundice

albuminaemia

ammonaemia

31
Q

Other features of hepatic failure

_________________________ (musty, sweat & sour body odour)due to mecarptans from git bacteria action on sulphur containing amino acids

 Impaired oestrogen metabolism leading to increase _________ , leading to ___________,___________,_________, and ___________

 Impaired synthesis of ________________

A

Fetor hepaticus

oestrogen level

palmar erythema, spider angiomas, gynaecomastia and hypo-gonadism

clotting factors 2,7,9, 10

32
Q

Other features of hepatic failure

 Fetor hepaticus(_____,______,_____, and ____ odour)due to ______ from git bacteria action on ______ containing amino acids

A

musty, sweat & sour body

mecarptans; sulphur

33
Q

Features of hepatic failure

Hepato-renal syndrome: ____________ in severe liver disease

 Hepatic ______________

A

acute renal failure

encephalopathy

34
Q

Hepatic encephalopathy-

impaired __________, hyper______

_________,________

A

consciousness; reflexia

rigidity, asterexis

35
Q

asterexis

Is a (slow or rapid?) (Rythmic or non-rhythmic?) ————- and ________ movement of ________ and _______ especially when extended arms and wrist are __________.

A

Rapid; non-rhythmic

extension & flexion

head & extremities

dorsi-flexed

36
Q

asterexis

It is due to abnormal ______________ in ________ and _______ due to ___________

A

neurotransmission in CNS & NMS

increase ammonia levels

37
Q

Cirrhosis is an end stage of any chronic liver disease

T/F

A

T

38
Q

The three main morphologic characteristics of cirrhosis are:

________
(Focal or Diffuse?) parenchyma ____________ (between ______-______)
Loss of _______

A

Fibrosis

Diffuse ; regenerating Nodules

<3mm - >3mm

Architecture

39
Q

The three main morphologic characteristics of cirrhosis are:

Fibrosis (______ Fibrosis)
Diffuse parenchyma regenerating Nodules (between <3mm - >3mm)
Loss of Architecture

A

Bridging

40
Q

Micronodular CirrhosisIt is characterized by (regular or irregular?) and (small or large?) nodules measuring ________ in diameter.

A

Regular; small

less than 3 mm

41
Q

Macronodular CirrhosisIt is characterized by the presence of nodules of(constant or variable?) size, more (regular or irregular?) than in the micronodular cirrhosis and usually ________ in diameter

A

Variable

Irregular

larger than 3 mm

42
Q

Mixed Cirrhosis

It consists of ____________________________

A

both micronodules and some macronodules.

43
Q

Causes of cirrhosis?!!

Mnemonic??

A

HEPATIC

H-haemochromatosis
E-enzyme deficiency (alpha-1-antitrypsin)
P- post hepatic( infection + drug)
A-Alcoholic
T-Tyrosinosis
I-indigenious people in America (galactosemia)
C-cardiac/cholestatic/cancer/copper(Wilson)

44
Q

The clinical features of cirrhosis range widely:

Initial phase: It is termed as “_________” cirrhosis, the patient may be ________.

Later phase: It is termed as “ _________” cirrhosis, presents with complications of __________ or ___________(or both).

A

compensated; asymptomatic

decompensated

portal hypertension or liver dysfunction

45
Q

Portal hypertension is defined as the elevation of the hepatic venous pressure above ___mm Hg.

A

7

46
Q

Ascites Treatment•_____ restriction•__________ (drug of choice)•___________ diuretic•______ diuretics (2nd line)• Large volume ________

A

Sodium

Spironolactone

Potassium-sparing

Loop

paracentesis

47
Q

Ascites Treatment• Spironolactone (drug of choice)• Blocks ________ action at the _______•

A

aldosterone
distal tubule

48
Q

Most effective drug for ascites is ??

A

Spironolactone

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