Cirrohsis Flashcards by Iseoluwa Ojo

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

4.5

9.5

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

fifty million

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

alcohol, NASH and viral hepatitis

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Cirrhosis is a chronic liver disease characterized by:

(1)____________ with __________/_________

(2)Diffuse _______________ varying between _______ - __________

(3)Disruption of the _____________.

Bridging fibrosis

delicate bands/septae.

parenchyma regenerative nodules

<3mm - >3mm

normal architecture

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Focal injury followed by fibrosis is cirrhosis

T/F

Focal injury followed by fibrosis is not cirrhosis

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Cirrhosis

The injury & fibrosis are ___________ and ____________

diffuse and irreversible

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Cirrhosis

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

reorganization of vascular channels

abnormal interconnections

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Classification of cirrhosis

 Morphological-

based on __________

(Can or Cannot?) distinguish the aetiological agents

____________
________________

size of nodule

Cannot

Micronodular

macronodular

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Classification of cirrhosis

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

viral hepatitis. {B,C,D}.

Alcoholic liver

Biliary

Obesity; insulin resistance

Metabolic

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Classification of cirrhosis

Metabolic disorders:

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

haemochromatosis

Wilson’s

Alpha 1 antitrypsin

Venous outflow

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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 __________

deposition of collagen; progressive

Ito; hepatic stellate ; space of Disse

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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 _____

Ito

Ito cells

myofibroblast-like

collagen

I & III

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Normally ito cells stores _____

Vitamin A

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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 _______.

toxins; cytokines

kupffer; endothelial

disruption of ECM

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Cirrhosis

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

lobule

delicate fibrils

broad fibrous septae

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

 These form ________ separated by the ____________

damage of hepatocytes and fibrosis

nodules; fibrous septae

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Fibrosis + nodules lead to :

Impaired _________

Impaired ______________ and _______ functions

Impaired ____________(________)

blood supply

hepatocyte secretory; synthetic

bile flow (cholestasis)

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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 ___________

osteoporosis, debilitation; liver

oxygenation

pulmonary blood flow

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complications of Cirrhosis

 Progressive _________
____________ carcinoma
________________
 ________________________

liver failure

Hepatocellular

Portal hypertension

Porto-systemic shunt

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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 _____________

increase resistance

sinusoids; compression

fibrosis

regenerating nodules.

Portal hypertension

It can be subclassified into:

 Pre-hepatic – _______________ to ________

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

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

Obstruction to portal vein thrombosis

cirrhosis, schistosomiasis, fatty change, sarcoidosis

constrictive pericarditis

Portal hypertension
PHT presents as:

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

ascites

splenomegaly

portosystemic venous

encephalopathy

Ascites-pathogenesis in cirrhosis

> _____mls of peritoneal fluid.

It is serous with ____g/dl protein.

500

Ascites-pathogenesis in cirrhosis

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

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

hypertension ; perfusion pressure of intestinal capillary

lymphatic; thoracic duct capacity

leakage to peritoneum

Ascites-pathogenesis in cirrhosis The mechanism include: Hypoalbuminemia leads to _____ ease plasma oncotic pressure _________ ————————

decr secondary hyperaldosteronism.

Porto-systemic shunts Increased portal pressure leads to development of ________ wherever ________ and ________________ share a ______________.

bypasses portal and systemic circulation common capillary beds

Porto-systemic shunts The sites are: _________ _________________ junction ____________ _______________+ ____________

Rectum Cardio-oesophageal Retroperitoneal peri-umbilical +abdominal wall collaterals

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

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

Other features of hepatic failure ________ hypo________________  Hyper________________

Jaundice albuminaemia ammonaemia

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

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

Features of hepatic failure Hepato-renal syndrome: ____________ in severe liver disease  Hepatic ______________

acute renal failure encephalopathy

Hepatic encephalopathy- impaired __________, hyper______ _________,________

consciousness; reflexia rigidity, asterexis

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

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

neurotransmission in CNS & NMS increase ammonia levels

Cirrhosis is an end stage of any chronic liver disease T/F

The three main morphologic characteristics of cirrhosis are: ________ (Focal or Diffuse?) parenchyma ____________ (between ______-______) Loss of _______

Fibrosis Diffuse ; regenerating Nodules <3mm - >3mm Architecture

The three main morphologic characteristics of cirrhosis are: Fibrosis (______ Fibrosis) Diffuse parenchyma regenerating Nodules (between <3mm - >3mm) Loss of Architecture

Bridging

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

Regular; small less than 3 mm

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

Variable Irregular larger than 3 mm

Mixed Cirrhosis It consists of ____________________________

both micronodules and some macronodules.

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)

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

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

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

Sodium Spironolactone Potassium-sparing Loop paracentesis

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

aldosterone distal tubule

Most effective drug for ascites is ??

Spironolactone

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Cirrohsis Flashcards

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