Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MEDS5009 > Liver Pathophysiology > Flashcards

Liver Pathophysiology Flashcards

(88 cards)

Start Studying
1
Q

functions of liver

A
  • production of bile salts
  • elimination of bilirubin
  • metabolism of steroid hormones
  • metabolism of drugs
  • CHO metabolism (stores glycogen and synthesises glucose from amino acids and lactic acid and glycerol)
  • fat metabolism (formation of lipoproteins, conversion of CHO and protein to fat, synthesis, recycling and elimination of cholesterol, formation of ketones from FA)
  • protein metabolism (deamination of proteins, formation of urea from ammonia, synthesis of plasma proteins, synthesis of clotting factors)
  • storage of vitamins and minerals
  • filtration of blood and removal of bacteria and matter by Kupffer cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

bile production

A

essential for absorption and digestion of dietary fats and fat soluble vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

bile

A

contains water, bile salts, bilirubin, cholesterol and by-products of metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

bile salts

A

emulsify dietary fats and formation of micelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cholestasis

A

decrease in bile flow through the canaliculi and reduction in secretion of water, bilirubin and bile acids from hepatocytes, resulting in these products accumulating in the blood

dilation of canaliculi, followed by rupture and extravasation of bile and degenerative changes in surrounding hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

intra-hepatic cholestasis

A

intrinsic liver disease, primary biliary cirrhosis or primary sclerosing cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

extra-hepatic cholestasis

A

obstruction of bile ducts, cholelithiasis, common duct strictures or cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

prolonged cholestasis

A

fatty changes, destruction of connective tissue, accumulation of bile products and debris, biliary tract fibrosis and end-stage biliary cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pruritus

A

related to accumulation of bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

skin xanthomas

A

related to impaired cholesterol metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

bilirubin

A

final product of breakdown of heme contained in aged RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

free bilirubin

A

found in albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hepatocyte role in bilirubin elimination

A

formation of conjugated bilirubin (with glucuronic acid), which is soluble in bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

intestine role in bilirubin elimination

A

50% bilirubin converted to highly soluble urobilinogen by bacteria, 20% of which is absorbed into portal circulation and remaining is excreted in the faeces and urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

direct bilirubin

A

conjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

indirect bilirubin

A

unconjugated, free

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

jaundice

A

yellow discolouration of skin and deep tissues as result of high level of bilirubin the blood coming from an imbalance between production and excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

clinically evident jaundice

A

serum bilirubin levels between 2 - 2.5mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pre-hepatic jaundice

A

RBC destruction in excess of capacity of removal from liveR

Mild jaundice, elevated unconjugated bilirubin, normal colour stool, no bilirubin in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

intra-hepatic jaundice

A

impaired capacity of liver to remove bilirubin from blood or conjugate it.

Gilbert’s disease

No symptoms but slightly elevated bilirubin and mild jaundice. Intefers with all phases of bilirubin metabolism.

Both conjugated and unconjugated bilirubin is elevated and urine is dark due to presence of bilirubin, serum alkaline phosphatase elevated slightly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

post-hepatic jaundice

A

cholestatic jaundice

bile flow obstructed at any point between hepatic duct and intestine

conjugated bilirubin levels usually elevated, sttol clay colour due to lack of bilirubin in bile, urine dark, serum alkaline phosphatase elevated, aminotransferase levels slightly increased.

in obstructive jaundice, bile acids in blood is elevated and as bile accumulates in blood, pruritus develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

causes of prehepatic jaundice

A

haemolytic blood transfusion reaction, hereditary disorders of RBC (sickle cell disease, thalassemia, spherocytosis), acquired haemolytic disorders, autoimmune hemolytic anemias, hemolytic disease of newborn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

causes of intrahepatic jaundice

A

decreased bilirubin uptake by liver, decreased conjugation of bilirubin, hepatocellular liver damage (hepatitis, cirrhosis, cancer of liver), drug-induced cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

causes of post-hepatic jaundice

A

structural disorders of bile duct, cholelithiasis, congenital atresia of extra hepatic bile ducts, bile duct obstruction caused by tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
test of hepatobiliary function
history and physical exam, liver function tests, liver enzymes, protein levels and prothromin time, liver biopsy, selective angiography of arteries to visualise hepatic or portal circulation, imaging, gamma-glutamyltransferase, alkaline phosphatase and 5'-nucleotidase
26
liver function tests
useful in diagnosis of disease, differentiate between different disorders, determine severity of present disease and monitor responses to established treatment
27
liver enzymes
alanine aminotransferase (ALT) and aspartate aminotransferase (AST) can indicate hepatocellular injury
28
Hepatocellular injury
hepatitis, hypoxic, ischemic injury, toxic injury
29
serum protein levels and prothromin time
reflects liver synthetic capacity
30
hypoalbuminemia
due to depressed synthesis and can complicate severe liver disease
31
alkaline phosphatase and 5'-nucleotidase
present in membranes between liver cells and bile duct and are released by disorders affecting the bile duct
32
gamma-glutamyltransferase (GGT)
helpful in diagnosing alcohol abuse and indicator of hepatobiliary disease
33
hepatitis
inflammation of liver caused by hepatotropic viruses that primarily affect hepatocytes, autoimmune mechanisms or reactions to drugs or toxins. secondary to other systemic disorders
34
hepatocytes
liver cells
35
hepatitis - mechanisms of damage
1. direct injury 2. indiction of immune responses against the viral antigens
36
hepatitis clinical course
1. asymptomatic infection with only serological evidence 2. acute hepatitis 3. carrier state without clinical presentation or with chronic hepatitis 4. chronic hepatitis with or without progression to cirrhosis 5. fulminating disease with onset of acute liver failure
37
prodromal phase
first stage of acute viral hepatitis manifestation abrupt to insidious, general malaise, myalgia, arthrlgia, easy fatigability, anorezia, GI symptoms serum levels AST and ALT increase and preceed to rise in bilirubin and accompanies onset of icterus or jaundice
38
icterus phase
second phase of acute viral hepatitis manifestation, follows prodromal phase by 7-14 days. tenderness around liver area, mild weight loss, spider angiomas
39
recovery phase
final phase of acute viral hepatitis manifestation increased wellbeing, return of appetite, disappearance of jaundice. symptoms subside after 2-12 weeks but full recovery 1-4 months depending on type
40
infection with HBV and HCV
produce carrier state - person harbours virus and can transmit disease but no symptoms
41
increase risk of becoming carrier
time of infection, age, immune status
42
hepatitis A
caused by HAV fecal-oral transmission also transmitted through contaminated water and food, and asymptomatic children. brief incubation 14-28 days, virus replicated in liver, excreted in bile and passes into stools. not associated with carrier or chronic status vaccine
43
acute hepatitis A
presence of IgM anti-HAV
44
past infection of hepatitis A
presence of IgG anti-HAV
45
HAV
small, unenveloped single stranded RNA virus
46
symptoms of hepatitis A
acute onset fever, malaise, nausea, anorexia, abdominal discomfort, dark urine, jaundice severity increase with age, last around 2 months
47
Hepatitis B
caused by double-stranded DNA, producing acute hepatitis, chronic hepatitis, progression of chronic hep into cirrhosis, fulminant hep with massive hepatic necrosis, and carrier state transmitted through inoculation with infected blood or serum (also other body secretions) vaccine, immunoglobin available
48
certain indicator of hep B
presence of viral DNA in serum
49
persistent HBsAG
beyond 6 months indicates infectivity and risk of chronic hepatitis
50
IgM anti-HBc
detectable before onset of symptoms, concurrent with onset of elevation in serum transaminases
51
Anti-HBe
detected after disappearance of HBsAg, signals onset of resolution
52
IgG anti-HBs
specific antibody of HBsAg, occurs after clearance of HBsAg
53
development of anti-HBs
signals recovery from HBV infection, non-infectivity and protection from future HBV infection (present in vaccinated person)
54
hepatitis C
most common cause of chronic hepatitis, cirrhosis and hepatocellular cancer transmitted by high risk drug use and sexual behaviours incubation 2-26 weeks, mostly asymptomatic but most develop chronic hep directly measured of HCV in serum single stranded RNA virus with 70+ subtypes (= difficult to develop vaccine)
55
consequences of chronic hep C
progressive liver fibrosis leading to cirrhosis, end-stage liver disease, hepatocellular cancer increased risk due to older age at onset, male sex, immunosuppressed state, concurrent HBV infection, alcohol consumption and hepatotoxic medications
56
chronic hepatitis
chronic inflammatory reaction in liver lasting longer than 3 months. Characterised by elevated liver enzymes and histological finding on liver biopsy major cause of cirrhosis and hepatocellular carcinoma, chief reason for liver implant (no other simple treatments)
57
symptoms of chronic hepatitis
fatigue, malaise, loss of appetite, possible jaundice
58
liver transplant
treatment option for end-stage liver disease due to viral hepatitis
59
alcohol liver disease
by-products of alcohol (lactic acid, NADH, depletion of NAD and acetaldehyde) contribute to liver damage binding acetaldehyde to other molecules impairs detoxification of free radicals and synthesis of proteins. lesions concentrated in centro-lobular area which surround central vein and where the pathway for alcohol metabolism is
60
fatty changes ALD
changes that occur with alcohol consumption, that do no produce symptoms and are reversible after alcohol intake has been discontinued
61
phases of ALD
1. fatty changes 2. alcoholic hepatitis 3. cirrhosis
62
alcoholic hepatitis
inflammation and necrosis of liver cells characterised by hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites and liver failure
63
micronodular / laennec cirrhosis
one fine, uniform nodules on surface seen in early cirrhotic liver
64
non-alcoholic liver disease (NFALD)
caused by metabolic dysfunction that affect liver ranges from simple steatosis to non-alcoholic steatohepatitis
65
simple steatosis
fatty infiltration of liver
66
non-alcoholic steatohepatitis
steatosis with inflammation and hepatocyte necrosis
67
conditions associated with fatty liver disease
obesity, T2DM, metabolic syndrome, hyperlipidaemia
68
cause of NFALD
lipid accumulation in hepatocytes and formation of free radicals
69
symptoms of NAFLD
usually asymptomatic but can involve fatigue, discomfort in right upper quadrant elevated AST, ALT, abnormal lab findings, hypoalbuminemia, prolonged prothrombin time, hypoerbilirubinemia
70
NAFLD diagnosis
requires liver biopsy and exclusion of alcohol as a cause of disorder
71
treatment of NAFLD
aim to slow progression and prevent liver-related illness weight loss and exercise improve insulin resistance and recommended with conjunction of other treatment associated with metabolic disturbances (Including avoiding alcohol)
72
cirrhosis
end stage of chronic liver disease and much of functional tissue has been replaced by fibrous tissue increased deposition of minerals in liver due to infectious and non-infectious diseases and metabolic disorders fibrosis and formation of nodules - balance between regenerative capacity and scarring clinical manifestations range from asymptomatic hepatomegaly to hepatic failure
73
cirrhosis fibrous tissue
forms constrictive bands that impact vascular and biliary flow leading to complications of portal hypertension and biliary stasis
74
symptoms of cirrhosis
weight loss, weakness, anorexia, diarrhoea, jaundice, abdominal pain (due to hepatomegaly) bleeding related to decreased coagulation, thrombocytopenia due to splenomegaly, gynecomastia due to testicular atrophy, spider angiomas, palmar erythema and encelopathy with asterixis
75
hepatomegaly
enlarged liver
76
signs of portal hypertension
splenomegaly, ascites, porto-systemic shunts
77
portal hypertension
increased resistance to flow in portal venous system and sustained portal vein pressure
78
ascites
large accumulation of fluids in abdominal cavity treatment - sodium restriction and diuretics
79
paracentesis
removal of large volume of liquid but also vascular volume expanders (albumin) given to avoid activation of renin-aldosterone system
80
splenomegaly
shunting of blood into splenic vein
81
hypersplenism
decrease in lifespan of all formed elements of blood and subsequent decrease in their numbers, leading to anemia, thrombocytopenia and leukopenia
82
portosystemic shunts
collateral channels to relieve pressure most important are ones connecting portal and coronary veins that lead to reversal of flow and formation of thin-walled varicosities in submucosa of oesophagus (subject to rupture, producing massive and sometimes fatal hemorrhage). impaired hepatic synthesis of coagulation factors and decreased platelet levels due to splenomegaly further complicate control of bleeding
83
portal hypertension treament
prevention of initial hemorrage, management of acute hemorrhage and prevention of recurrent hemorrhage pharmacologic therapy use to lower portal venous pressure and prevent initial hemorrage main treatment is shunts (surgical)
84
B-adrenergic-blocking drugs
reduce portal venous pressure by decreasing splanchnic blood flow and decrease blood flow in collateral channels
85
methods used to control acute hemorrhage
admin of ocetreotide, balloon tamponade, endoscopic injection slcerotherapy, vessel ligation, esophageal transection
86
surgical portosystemic shunt procedures
creation of opening between portal vein and systemic vein TIPS procedure involves insertion of expandable metal stent between branch of hepatic vein and portal vein
87
liver failure
most severe consequence of liver disease. Results from sudden or massive liver destruction (fulminant hep) or from progressive damage to liver (alcoholic cirrhosis) 80-90% hepatic functional capacity lost
88
fetor hepaticus
musty, sweetish odour of breath in person with advanced liver failure, resulting from metabolic by-products of intestinal bacteria

MEDS5009 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions