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GI > Liver > Flashcards

Liver Flashcards

1
Q

2 blood supplies to the liver

what’s the benefit?

A 
Hepatic artery (bringing oxygenated blood)
Hepatic portal vein (bringing everything from gut, still has a bit of O2 in it)

don’t get big infarcts like in other organs!

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2
Q

portal triad

A
  1. bile duct
  2. hepatic artery
  3. hepatic portal vein

2&3 will empty into sinusoids, gets to centre of lobule and drain into terminal hepatic venule –> hepatic vein –> vene cava –> systemic

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3
Q

Difference in cells in periphery of lobule vs. central?

A

oxygen concentrations

synthesis will occur centrally (eg. protein) ZONE 3

degradation/metabolism will occur on periphery (where conjugation enzymes will be) ZONE 1

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4
Q

Why do we get portal hypertension?

A

eg. due to alcohol
fibrosis/lose cells in Zone 3 will cause venule to get less blood, pressure required to get blood in through will increase = portal hypertension

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5
Q

Three main functions of liver

A

Synthesis (albumin, clotting factors, complement)
production (bile through conjugation of bilirubin)
breakdown (of any foreign substance eg. drug, insulin ammonia)

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6
Q

Role of Kupffer cells

A

sitting in the sinusoids acting like macrophages.

phagocytose old RBCs, bacteria and foreign materials from the blood or gut

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7
Q

what’s the bilirubin concentration to be classified as jaundice?

A

over 40umol/L

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8
Q

Why is jaundice associated with intense itch?

A

It’s not to do with bilirubin - it’s the accumulation of bile acids. Tells you about where the jaundice occurred (ie. at a point where the liver wasn’t able to properly excrete the bile acid ie. at the bile duct or distal to that. OBSTRUCTIVE).

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9
Q

Unconjugated vs conjugated jaundice

A

unconjugated: water insoluble
Conjugated: water soluble (can be excreted in urine so urine will be DARK)

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10
Q

3 classifications of jaundice

A

pre-hepatic: haemolysis (maybe sickle cell disease, exposure to a toxin, autoimmune disease, causing RBCs to break down) -> release of bilirubin from RBCs
but bili isn’t getting conjugated, normal urine (can’t solubilise it in kidney to throw it out)

Intrahepatic: liver disease destroys hepatocyte -> excess bilirubin in liver and bloodstream

Post-hepatic (obstructive) - obstruction of bile outflow –> dark urine and pale stools SMELLY (and itch)

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11
Q

BARNEY GUMBLE

Causes

A

Acute Liver Injury
Causes: viral infection, ALCOHOL, adverse drug reactions, biliary obstruction (gallstones)

Presentation: jaundice, malaise.
Raised serum bilirubin and transaminases.
Liver failure: decreased albumin, ascites, bruising, encephalopathy

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12
Q

Where does alcohol-induced hepatocyte injury usually occur?

A

zone 3

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13
Q

Where will autoimmune hepatitis injuries usually occur?

A

zone 1 (mostly cell mediated and antibody)

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14
Q

Steatosis leads to what

A

steatosis: fat build up which alters metabolism. Get big fat globule (with messed up metabolism) messes up cytoskeleton into Mallory’s hyaline.

can lead eventually to cirrhosis (liver becomes scarred and lumpy. fibrosis bridges from structures. Regeneration abnormal.
can lead to liver failure)

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15
Q

Describe alcohol hepatitis pathology

A

acute inflammation of bits of the liver (spotty necrosis)
Kupffer (macros) sat and fibroblast precursor sitting waiting to create fibrosis. little bits of fibrosis eventually merge (after many binges over time)
regeneration occurs, expanding cells but scar tissue resitricts the expansaion. continuous scar tissue creates CIRRHOSIS

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16
Q

Define cirrhosis

A

continuous scar tissue.

recurrent inflammation with fibrosis (collagen) and regeneration

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17
Q

What’s in alcohol that causes hepatocyte damage?

A

acetaldehyde binds to hepatocytes causing damage, inflammatory reaction, fibrosis

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18
Q

Complications of cirrhosis

A

Liver failure: can’t detoxify things! (hepatic encephalopathy (ammonia), build up of steroid hormones –> hyperoestrogenism (palmar erythema and gynaemastia)

Portal hypertension (increased hepaticvascular resistance, AV shunting –> oesophageal varices, haemorrhoids, caput medusea)

Hepatocellular carcinoma

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19
Q

KRUSTY

A

drug-induced liver injury
10% drug reactions involve liver
Hepatocellular damage from paracetamol dose
Injury to cholestatic cells (bile production/secretion) - methyl testosterone

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20
Q

PATTY AND SELMA

A

have ACUTE BILIARY OBSTRUCTION
usually due to gallstones
causes collicky pain and jaundice (waves as peristalsis is trying to get it out)

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21
Q

Complication of acute biliary obstruction

A

infection of the blocked CBD = cholangitis

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22
Q

why might we want to do an ultrasound rather than xray in someone with acute biliary obstruction?

A

as gallstones can be radiolucent (as mostly cholesterol)

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23
Q

what type of jaundice would you get with acute cholesistitis (patty/selma)

A

dark urine and pale stools (would be obstruction +/- secondary infection)

24
Q

Definition of chronic hepatitis

A

liver inflammation lasting more than 6 months

sustained elevation of transaminases (but liver biopsy will classify cause)

25
Q

Causes of chronic hepatitis

A

viral
autoimmune
drugs
alcohol (but is chronic recurrent acute injury, not chronic)

26
Q

Which ways would we classify chronic hepatitis

A

Type (aetiology)
Grade (degree of inflammation)
Stage (degree of fibrosis)

27
Q

COMIC BOOK GUY

A

NASH/NAFLD
non-alcoholic steatohepatitis/fatty liver disease
associated with METABOLIC SYNDROME (DM II, hypertension, HDL and triglycerides increased)
fat deposition in hepatocytes (can lead to cirrhosis)

28
Q

LISA SIMPSON

A

Autoimmune Chronic Active Hepatitis
females > males
mid to late teens
interface hepatitis (plasma cells and swollen hepatocytes. fibrosis from zone 1-zone 1 cirrhosis

29
Q

diagnosis of lisa simpson/autoimmune chronic active hepatitis

A

presence of
ANA
SMA (smooth muscle antibodies) *** key diag!
often serum IgG and transaminases are raised as it’s an immune response
anti-LKM (liver-kidney-microsomal)

30
Q

Treatment of Lisa Simpson/Autoimmune Chronic Active Hepatitis

A

steroids

more serious -> immunosuppression

31
Q

MARGE SIMPSON

A

PRIMARY BILIARY CHOLANGITIS/CIRRHOSIS
females > males (40-50 y/o)
Stages:
- autoimmune destruction of bile duct epithelium (dense lymphocytic infiltration and granulomas)
- proliferation of small bile ducts
- architectural disturbance: portal and bridging fibrosis
- cirrhosis

32
Q

Diagnosis of Primary Biliary Cholangitis/Cirrhosis

A

Jaundice, pruritis, xanthelasma

Raised ALP and IgM, AMA

33
Q

Primary Sclerosing Cholangitis

A

inflammation in bile ducts (cholangitis) which results in hardening (sclerosis) and narrowing of ducts as result.
Bile cannot be released properly and builds up in liver where prolonged exposure results in liver damage

34
Q

3 differences between PBC and PSC

A

Age/gender (>50, F vs. any age, M)
Serum immunoglobulins (inc IgM vs. none)
Autoantibodies (AMA, ANA vs. none)
Bile duct injury (small ducts vs. large ducts and obliterative fibrosis of them)
Portal inflammation (prominent vs. absent)

35
Q

GROUNDSKEEPER WILLIE

A

Haemochromatosis
- iron deposition in the liver causing alteration of architecture –> fibrosis –> cirrhosis
Autosomal recessive (mutation in liver cells HFE gene - so a major RF for cancer)

36
Q

Treating haemochromatosis/Groundskeeper Willie

A

Regular venesection - test iron and ferritin levels

37
Q

alpha-1-antitrypsin deficiency

A 
autosomal recessive disorder 
low levels of alpha-1-trypsin
proteins build up in hepatocytes as hyaline 
can lead to cirrhosis 
associated with emphysema
38
Q

CRAZY CAT LADY

A

WILSON’S DISEASE
young women
autosomal recessive disorder
failure of liver to excrete copper in bile –> build up of copper in liver –> cirrhosis
also deposits into brain and cause neurological dysfunction
get KAYSER FLEISCHER rings

39
Q

Diagnose Wilson’s disease

A

low caeruloplasmin

Kayser Fleischer rings in eyes

40
Q

Examples of developmental/hamartomas liver tumours

A

cysts

hamartomas

41
Q

Examples of benign liver tumours

A

incidental finding
adenoma, haemangioma
liver cysts

42
Q

Examples of malignant liver tumours

A

metastases COMMON
primary: hepatocellular carcinoma
cholangiocarcinoma

43
Q

aetiology of hepatocellular carcinoma

A

aflatoxins - fungal origin
hepatitis B and C
cirrhosis (of any cause)

44
Q

2 examples of congenital malformations of biliary system

A

atresia

choledocal cysts

45
Q

Other name for gallstones

A

cholelithiasis

46
Q

Cholangiocarcinoma

A

arises from bile duct epithelium anywhere in biliary system
associated with UC
causes obstructive jaundice, itch weight loss, lethargy

can lead to rupture of common bile duct or gallbladder (poor prognosis)

47
Q

Risk factors for gallstones
Types
Complications

A 
female
fat
fair
forty 
fertile 
diabetes mellitus

Cholesterol, bile pigment or mixed

cholescystitis, obstructive jaundice, cholangitis, pancreatitis, cholangiocarcinoma

48
Q

what is cholecystitis usually caused by?

A

gallstones

49
Q

symptoms of cholecystitis

A

RUQ pain (biliary colic)
fever
nausea/vomiting

50
Q

MAGGIE SIMPSON

A

HAS annular pancreas occurs in 2nd part of duodenum (wraps around SI)
causes OBSTRUCTION: polyhydramnios, low birth weight, poor feeding

51
Q

HOMER SIMPSON

A

has pancreatitis
Acute: causes catastrophic metabolic consequences (decreased calcium, decreased albumin, increased glucose)

massive fluid losses can lead to SHOCK

52
Q

diagnose acute pancreatitis

A

serum amylase

53
Q

chronic pancreatitis

A

multiple episodes of acute
causes fibrosis of pancreas: may lead to diabetes mellitus
reduced production of enzymes (require supplements)

54
Q

MONTY BURNS

A

has PANCREATIC CARCINOMA
an adenocarcinoma
associated with smoking and diabetes mellitus
presents with painless, progressive jaundice
weight loss
poor prognosis

operable if small and close to ampulla

55
Q

adenocarcinoma

A

starts in mucous secreting glandular cells (breast, colorectal, lung, pancreatic, prostate)

GI (9 decks)

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