Cirrohsis Flashcards
Global prevalence of cirrhosis from autopsy studies ranges from ___% to ___% of the general population.
4.5
9.5
Estimates - more than _______ adult in the world would be affected with chronic liver disease.
fifty million
Globally, ________,_______, and ___________ currently are the most common causative factors.
alcohol, NASH and viral hepatitis
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
Focal injury followed by fibrosis is cirrhosis
T/F
F
Focal injury followed by fibrosis is not cirrhosis
Cirrhosis
The injury & fibrosis are ___________ and ____________
diffuse and irreversible
Cirrhosis
Parenchyma damage leading to ___________ of ___________ with _____________ between vascular inflow and outflow channels
reorganization of vascular channels
abnormal interconnections
Classification of cirrhosis
Morphological-
based on __________
(Can or Cannot?) distinguish the aetiological agents
____________
________________
size of nodule
Cannot
Micronodular
macronodular
Classification of cirrhosis
Aetiological
____________
________ disease
______ disease
_______, _______________
________ disorders
viral hepatitis. {B,C,D}.
Alcoholic liver
Biliary
Obesity; insulin resistance
Metabolic
Classification of cirrhosis
Metabolic disorders:
Primary ___________,
_______ disease
__________ deficiency
________ obstruction
Cryptogenic
Others-galactosemia, tyrosinosis, drug induced.
haemochromatosis
Wilson’s
Alpha 1 antitrypsin
Venous outflow
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
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
Normally ito cells stores _____
Vitamin A
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
Cirrhosis
The collagen are deposited in the ____ forming _________ and later to __________
lobule
delicate fibrils
broad fibrous septae
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
Fibrosis + nodules lead to :
Impaired _________
Impaired ______________ and _______ functions
Impaired ____________(________)
blood supply
hepatocyte secretory; synthetic
bile flow (cholestasis)
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
complications of Cirrhosis
Progressive _________
____________ carcinoma
________________
________________________
liver failure
Hepatocellular
Portal hypertension
Porto-systemic shunt
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
<3
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
T
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.
7
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
