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.

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
Ascites-pathogenesis in cirrhosis The mechanism include: Hypoalbuminemia leads to _____ ease plasma oncotic pressure _________ ————————
decr secondary hyperaldosteronism.
26
Porto-systemic shunts Increased portal pressure leads to development of ________ wherever ________ and ________________ share a ______________.
bypasses portal and systemic circulation common capillary beds
27
Porto-systemic shunts The sites are: _________ _________________ junction ____________ _______________+ ____________
Rectum Cardio-oesophageal Retroperitoneal peri-umbilical +abdominal wall collaterals
28
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 __________
hemorrhoids varices; haemorrhage & death caput medusae
29
splenomegaly  Increased ______________________________ leads to congestion and enlargement of the spleen  This results in secondary haematologic abnormality due to __________
backflow of blood into the splenic vein hypersplenism
30
Other features of hepatic failure ________ hypo________________  Hyper________________
Jaundice albuminaemia ammonaemia
31
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 ________________
Fetor hepaticus oestrogen level palmar erythema, spider angiomas, gynaecomastia and hypo-gonadism clotting factors 2,7,9, 10
32
Other features of hepatic failure  Fetor hepaticus(_____,______,_____, and ____ odour)due to ______ from git bacteria action on ______ containing amino acids
musty, sweat & sour body mecarptans; sulphur
33
Features of hepatic failure Hepato-renal syndrome: ____________ in severe liver disease  Hepatic ______________
acute renal failure encephalopathy
34
Hepatic encephalopathy- impaired __________, hyper______ _________,________
consciousness; reflexia rigidity, asterexis
35
asterexis Is a (slow or rapid?) (Rythmic or non-rhythmic?) ————- and ________ movement of ________ and _______ especially when extended arms and wrist are __________.
Rapid; non-rhythmic extension & flexion head & extremities dorsi-flexed
36
asterexis It is due to abnormal ______________ in ________ and _______ due to ___________
neurotransmission in CNS & NMS increase ammonia levels
37
Cirrhosis is an end stage of any chronic liver disease T/F
T
38
The three main morphologic characteristics of cirrhosis are: ________ (Focal or Diffuse?) parenchyma ____________ (between ______-______) Loss of _______
Fibrosis Diffuse ; regenerating Nodules <3mm - >3mm Architecture
39
The three main morphologic characteristics of cirrhosis are: Fibrosis (______ Fibrosis) Diffuse parenchyma regenerating Nodules (between <3mm - >3mm) Loss of Architecture
Bridging
40
Micronodular Cirrhosis It is characterized by (regular or irregular?) and (small or large?) nodules measuring ________ in diameter.
Regular; small less than 3 mm
41
Macronodular Cirrhosis It 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
Variable Irregular larger than 3 mm
42
Mixed Cirrhosis It consists of ____________________________
both micronodules and some macronodules.
43
Causes of cirrhosis?!! Mnemonic??
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
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).
compensated; asymptomatic decompensated portal hypertension or liver dysfunction
45
Portal hypertension is defined as the elevation of the hepatic venous pressure above ___mm Hg.
7
46
Ascites Treatment •_____ restriction •__________ (drug of choice) •___________ diuretic •______ diuretics (2nd line) • Large volume ________
Sodium Spironolactone Potassium-sparing Loop paracentesis
47
Ascites Treatment • Spironolactone (drug of choice) • Blocks ________ action at the _______•
aldosterone distal tubule
48
Most effective drug for ascites is ??
Spironolactone