Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > liver pathophysiology > Flashcards

liver pathophysiology Flashcards

1
Q

what is jaundice?

A

Yellow discolouration of sclera and skin – due to hyperbilirubin (>50umol/L)

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

what is the cause of pre-hepatic jaundice?

A

excessive RBC breakdown – overwhelming livers ability to conjugate bilirubin and causes unconjugated hyper bilirubin
- can not bind bile and hence remains in blood stream

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

what conditions can lead to pre-hepatic jaundice?

A

haemolytic anaemia, gilberts syndrome, criggler- Najjar

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

how does stool and urine present with pre hepatic jaundice?

A

normal

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

what is hepatocellular jaundice?

A

dysfunction of hepatic cells. liver loses ability to conjugate bilirubin.
- Can come cirrhotic and this compresses intra-hepatic portions of biliary tree and causing obstruction
- Can have both unconjugated and conjugated bilirubin

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

what conditions can cause hepatocellular jaundice?

A

alcoholic liver disease, viral hep, iatrogenic, HH, autoimmune hep, primary biliary cirrhosis or PSC, hepatocellular carcinoma

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

what does the stool and urine present as with hepatocellular jaundice?

A
  • Dark urine + normal stools
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the aetiology of post hepatic jaundice?

A

obstruction of biliary drainage. Bilirubin will not be excreted even though it is conjugated by the liver.

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

what type of bilirubin is seen in post hepatic jaundice?

A

conjugated hyperbilirubin

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

what type of hyper bilirubin is seen in hepatocellular jaundice?

A

mixed - unconjugated and conjugated

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

what would urine and stools present with post hepatic jaundice?

A

dark urine and pale stools

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

what conditions cause post hepatic jaundice?

A

gallstones, drug induced cholestasis, pancreatic cancer or abdo masses

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

how is jaundice treated?

A
  • Symptomatic: often needed for itching caused by hyperbilirubin – obstructive may need cholestyramine and others may need anti-histamine
  • Monitor for complications: coagulopathy, constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what can cause drug induced hepatotoxicity?

A

can be acute or chronic liver injury secondary to drugs or herbal compounds

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

what is intrinsic drug induced hepatoxicity?

A

both predictable and reproducible from drugs known to cause liver injury in dose dependent manner with short latency period eg acetaminophen toxicity

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

what is idiosyncratic drug induced hepatotoxicity?

A

unpredictable course and not reproducible, has variable latency periods. Can be further divided into immune mediated (allergic) from hypersensitivity or non immune mediated metabolic – mitochondrial injury

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

what is ALT?

A

alanine transaminase

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

what is alkaline phosphatase?

A

ALP

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

where is high ALT found normally?

A

within hepatocytes - enters following hepatic injury

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

where is ALP high?

A

particularly high in liver, bile and bone tissues. Often raised in liver pathology due to increases synthesis of cholestasis

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

what ALT/ ALP numbers would indicate hepatocellular injury?

A
  • Greater than 10 fold in ALT + less than 3 fold increase in ALP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what ALP/ ALT scores would indicate cholestasis?

A
  • Less than 10 fold increase in ALT + more than 3 fold increase in ALP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is GGT?

A

gamma-glutamyl transferase

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

when would you check GGT?

A

is rise in ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what can GGT indicate?

A
  • Can suggest biliary epithelial damage and bile flow obstruction
  • Can also be raised in response to alcohol and drugs such as phenytoin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does raised GGT and raised ALP indicate?

A

cholestatsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what would isolated raise in ALP indicate?

A

non-hepatobiliary pathology
- Causes of isolated raise in ALP: bony metastases/ primary bone tumour, vitD deficiency, recent bone fracture, renal osteodystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what condition is most likely if raise in bilirubin (NO ALP/ ALT RAISE)

A

gilberts syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is gilberts syndrome?

A

mild liver genetic disease - can not metabolise bilirubin as normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what investigations can be done to assess liver function?

A

serum bilirubin, serum albumin, prothrombin time (PT), serum blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the function of albumin?

A

synthesised in the liver – helps bind water, cations, fatty acids ad bilirubin – plays key role in maintaining oncotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how can cirrhosis effect albumin?

A

liver disease resulting in decreased production of albumin (cirrhosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how does cirrhosis effect albumin?

A
  • Inflammation triggering acute phase response which temporarily increases livers production of albumin
  • Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does PT measure?

A

Prothrombin time (PT): measure of blood coagulation tendency – specifically extrinsic way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does ALT > AST indicate?

A

chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what does AST > ALT indicate?

A

cirrhosis and acute alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

does gluconeogenesis become impacted by liver disease?

A
  • Gluconeogenesis tends to be one of last functions to become impaired in context of liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are common causes of acute hepatocellular injury?

A
  • Poisoning (paracetamol overdose)
  • Infection – hepA and B
  • Liver ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are common causes of chronic hepatocellular injury

A
  • Alcoholic fatty liver disease
  • Non-alcoholic fatty liver disease
  • Chronic infection – Hep B/ C
  • Primary biliary cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are less common causes of chronic hepatocellular injury?

A

alpha -1-antitrypsin deficiency, wilsons, HH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what would increase in PT/ INR and decrease in platelets indicate?

A

chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what factors can contribute to decreases platelets?

A
  • Many factors contribute to give low platelet: decreased production – bone marrow suppression which can be caused by alcohol, iron overload, drugs and chronic liver injury, splenic sequestrian – hypersplenism which is a consequence of portal hypertension, increased destruction - liver cirrhosis owing shear stress, fibrinolysis and bacterial translocation, autoimmune dysfunction can also result in platelet destruction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how does liver disease tend to progress?

A

Liver disease tends to progress silently with no symptoms until later stages.

44
Q

what symptoms are commonly seen in Pts with autoimmune hep?

A

fatigue, nausea, anorexia (general symptoms)

45
Q

what other conditions are common with autoimmune hep?

A

Inflammatory bowel disease (UC and Chron’s)

46
Q

what are common causes of acute liver failure?

A

hepatitis and drugs

47
Q

is acute liver failure an emergency?

A

Acute liver failure – fulminant hepatic failure – can cause serious complications including bleedings and increased pressure in the brain – medical emergency.

48
Q

what are complications of acute liver failure?

A

cerebral oedema, bleeding, infections, kidney failure, mulitorgan failure

49
Q

what is the consequence of cerebral oedema?

A

too much fluid causing pressure to build up in your brain – can lead to disorientation, severe mental confusion and seizures. Intracranial hypertension

50
Q

can can acute liver failure result in bleeding?

A

failing liver cannot make enough clotting factors, which help blood to clot. Bleeding in GI is common with this condition may be difficult to control

51
Q

what infections can be linked to acute liver failure?

A

sepsis, resp, UTI are common – bacteraemia, pneumonia, urosepsis, cellulitis, fungal infections are typically quite severe and often end up being the immediate cause of death

52
Q

when is kidney failure common within acute liver failure?

A
  • Kidney failure: occurs after liver failure – especially in acetaminophen overdose
53
Q

how can acute liver failure cause multi organ failure?

A
  • Multiorgan failure: if the patients failure does not begin to regenerate soon or does not respond to treatment and if they can not receive liver transplant – all critical body systems begin to malfunction and ultimately fail – CVS failure, pulmonary failure, kidney failure and then death
54
Q

what is alcoholic cirrhosis?

A

liver made up of scar tissue
causes by excessive alcohol exposure - meaning liver can not regenerate

55
Q

what is autoimmune hepatitis?

A

: idiopathic disease characterised by immune mediated hepatocyte injury associated with destruction of liver cells causing inflammation, liver failure and fibrosis – associated with autoantibodies

56
Q

what is the autoimmune hep aetiology?

A

genetic variants, environmental factors and epigenetic modifications

57
Q

what is the pathophysiology of AI hep?

A

: interaction between specific genetic traits, impaired immunoregulatory mechanisms (including CD4+, Treg as well as cytotoxicity by CD8+ and B cells)

58
Q

what is hereditary haemochromatosis?

A

includes several inherited disorders of iron homeostasis characterised by increased gastrointestinal iron absorption and tissue iron deposition. Hemochromatosis is defined by abnormal increase in body iron stores with consequent tissue pathology.

59
Q

which gene is responsible for HH?

A

faulty HFE gene - homozygous C282Y mutation

60
Q

where does iron absorption occur?

A

in the duodenum - can be absorbed as ionic iron (ferrous state) or haem

61
Q

how is iron brought into enterocytes?

A
  • Ferrous iron is then crosses apical membrane via divalent metal transporter 1 (DMT1)
  • Iron taken up by enterocyte may be stored as ferritin or transferred across basolateral membrane to plasma via ferroprotin channel
62
Q

what controls iron absorption?

A
  • Liver is responsible for producing hepcidin  this inhibits iron release by binding to ferroprotein causing its internalisation
63
Q

what is the overall pathophysiology of HH?

A

liver produces less hepcidin - more iron in cells- needs deposited somewhere
- Tends to deposit in liver, eyes, heart

64
Q

what is A1AT?

A

Alpha 1- antitrypsin (A1AT) deficiency: abnormality in the gene for protease inhibitor called alpha-1-antitrypsin

65
Q

what is the aetiology of A1AT?

A

: genetics- autosomal recessive conditions on Chr14

66
Q

what is the pathophysiology of A1AT?

A

elastase is an enzyme secreted by neutrophils – this enzyme digests connective tissue.
- A1AT is mainly produced in the liver and travels around the body inhibiting neutrophil elastase

67
Q

what does A1AT do to the liver?

A

cirrhosis

68
Q

what does A1AT do to the lungs?

A

bronchiectasis and emphysema

69
Q

what primary tumour makes up 90% of liver?

A

primary hepatocellular carnicoma

70
Q

what can cause primary hepatocellular carcinoma?

A

: Hep B, Hep C, alcoholic liver disease, non-alcoholic liver steatohepatitis are all aetiological factors for the development of hepatocellular carcinoma

71
Q

what is a major contribution into the pathophysiology of primary hepatocellular carcinoma?

A

cirrhosis

72
Q

what are the types of non alcoholic fatty liver disease?

A
  1. hepatic steatosis
  2. steatohepatitis
  3. fibrosis and cirrhosis
73
Q

what is hepatic steatosis?

A

accumulation of fat globules within hepatocytes

74
Q

what is steatohepatitis?

A

necrosis of hepatocytes, neutrophil-dominant inflame reaction. Mallory bodies: eosinophilic accumulation. Continued exposure causes development of fibrosis mainly around central vein

75
Q

what is alcoholic liver disease?

A
  1. Prolonged alcohol exposure – steatonis/ fibrosis , alcoholic steatohepatitis
  2. Can progress to liver cirrhosis and then onto liver cancer
76
Q

what does activation of stellate cells in cirrhosis do?

A

fibrogenesis, angiogenesis, parenchymal extinction (usually secondary to ischaemia)

77
Q

what microvascular changes occur within cirrhosis?

A

sinusoidal remodelling, intra-hepatic shunts, endothelial dysfunction – reduced nitric oxide and increased vasoconstrictive substances

78
Q

define portal hypertension?

A

hepatic venous pressure gradient (HVPG) greater than 5mmHg

79
Q

what is liver disease A?

A

initiation and progression of liver damage – increase HR
- Higher platelet count

80
Q

what is liver disease B?

A

: change in matrix structure/ composition and IH vascular bed. Splanchic blood pooling, impairment of enteropathy circulation of bile acids and dysboids.
- Endoscopy required to assess elastrography of liver and spleen and platelet count
- Imaging can help visualise

81
Q

what is liver disease C?

A

further increase of HR , further splanchnic blood pooling, renal sodium retention and ascites formation – further enlargement of collaterals with high risk bleeding

82
Q

how do you investigate liver disease C?

A
  • Imaging required and measure HVPG (pressure of portal vein)
83
Q

how do you decrease portal hypertension?

A
  • Decrease portal hypertension by stent shunts – transjugular intrahepatic portosystemic shunt (TIPSS)
84
Q

what can a high reading on ascitic fluid tap indicate?

A

portal hypertension (liver cirrhosis, heart failure, portal vein thrombosis, Budd-chiari syndrome)

85
Q

what can a lower reading on ascitic tap indicate?

A

TB, pancreatitis, infections, peritoneal malignancy

86
Q

when would spontaneous bacterial peritonitis be suspected?

A

suspected in anyone who presents with complication/ decompensation in hepatic cirrhosis

87
Q

what is spontaneous bacterial peritonitis usually caused by?

A

E.coli

88
Q

what symptoms are manifested by spontaneous bacterial peritonitis?

A

fever, pain, general deteroration

89
Q

what causes encephalopathy?

A

build up of ammonia - toxic to neurones
liver can not filter properly

90
Q

how do you treat encephalopathy?

A

treat underlying cause, lactulose + daily enemas (aim for 3 bowel movements a day). Rifaximin – non-absorptive antibiotics that reduces gut bacteria and hence gut ammonia production. Used in second episode of encephalopathy

91
Q

what can be the underlying cause of hepatic encephalopathy?

A

sedatives, constipation, dehydration, infection, GI bleed, TIPSS

92
Q

what is type 1 hepatorenal syndrome?

A

Type 1: rapidly progressive
- Insult to kidneys (infection, NSAID, diarrhoea, paracentesis) – on top of compensating renal function

93
Q

what is type 2 hepatorenal syndrome?

A

steady deterioration
- General decline in renal function and liver cirrhosis progresses

94
Q

what is hepatopulmonary syndrome?

A

generalised systemic vasodilation causing ventilation/ perfusion mismatch and hypoxia. Can lead to hepatorenal syndrome

95
Q

what is UKELD?

A

UK model for end-stage liver disease – predicts one year mortality

96
Q

what is modified maddrey discriminant?

A

determines prognosis in alcoholic hepatitis + need for steroids

97
Q

how do you manage liver cirrhosis?

A

General: lose weight (obese), stop ALL alcohol, all vaccinations up to date (hep A, B, influenza, pneumococcal), stop smoking, anti-oxidant, treat underlying cause

98
Q

what can decompensated liver cirrhosis lead to?

A

Decompensated: ascites, encephalopathy, jaundice

99
Q

what medical management is used within liver cirrhosis?

A
  • Aim for 3 bowel movements a day – lactulose
  • Ascitic tap
  • Reduce hyponatreamia/ AKI – 20% albumin, terlipressin
  • Upper GI bleed: prophylactic AB
  • Correct anticoagulation: vitK if INR> 1.8 or prothrombin complex/ cryoprecipitate
100
Q

what can be investigated within a liver screen?

A
  • Viral hepatitis – anti HBs, HBaAg, HCV – EBV and cytomegalovirus (CMV)
  • Coper and cueroplasmin
  • Iron, ferritin, TIBC (total iron binding capacity)
  • Alpha 1-anti- trypsin levels – protease inhibitor
  • Auto-antibodies: anti smooth muscle, anti-mitochondrial
  • Ultra-sound liver
101
Q

what are symptoms of HH?

A

vertigo, hair loss, memory loss, heart degermation (arrythmias, cardiomyopathy), hepatomegaly: (elevated liver enzymes, cirrhosis), bronze skin, diabetes mellitus, testicular atrophy (decrease in FSH, LH secretion), arthritis

102
Q

when is the onset of HH?

A
  • usually between 40-60yrs and women usually after menopause
    passed it on before realising you have it?
103
Q

what is wilsons disease?

A

inherited disorder of excessive amounts of copper accumulating in the body – particularly liver, brain and eyes

104
Q

what does wilsons disease pathophysiology?

A
  • kidneys Proximal renal tubular dysfunction
  • liver: hepatomegaly, jaundice, acute hepatitis, fulminant hepatic failure, portal hypertension, bleeding varices, cirrhosis.
  • Bone: Arthritis rickets
  • Haemolysis
  • Central nervous system: deterioration in school performance, behavioural changes, inco-ordination (handwriting deteriorates), resting and intention tremors, dystonia, dysarthria, excessive salivation, mask like facies, dysphagia
  • Eyes- copper ring
105
Q

when is the onset for wilsons disease?

A

between 6-45 - earlier onset

GI (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions