Hepatic Pathology Flashcards

(34 cards)

1
Q

Liver failure

A

-deficiency in metabolic or synthetic capacity of the
-acute =quick onset
-chronic=slow onset
-many causes

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2
Q

Acute Liver Failure

A

-rare
-rapid necrosis of hepatic tissue (7-28 day) (without pre-existing disease)
- Coagulopathy and encephalopathy
-toxicity common cause

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3
Q

Acetaminophen (paracetamol toxicity)

A

-Inhibits COX in brain
-modulate endogenous cannabinoid system
-liver metabolism - half life 4hrs
-overdose in self harm 235 deaths in 2020
-NAPQI build up (metabolite)

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4
Q

Hepatic Encephalopathy

A

-altered consciousness due to liver failure
-acute and chronic liver failure
(40% of chronic)
-nitrogenous waste products cause
(ammonia)
-astrocytes increased osmotic pressure
- G-aminobutyric acid, less neurone energy

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5
Q

Chronic Liver Failure Causes

A

-over 6 months
 Alcoholism.
 Viral hepatitis.
 Haemochromatosis.
 Wilson’s disease.
 Autoimmune disease

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6
Q

Chronic Liver Disease Classes of Symptoms

A

 Chronic liver disease associated.
 Decompensation.
 Cause.

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7
Q

Viral Hepatitis

A

-virus has strains, A, B, C, D and E
-IV = C, D, B
-Faecal oral= A, E
- mucous membranes= B and D

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8
Q

Hepatitis A

A

-45% have Abs against
-contaminated food and water
-4-6 week incubation
-faecal shedding in 2 weeks before onset of symptoms

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9
Q

Hepatitis C

A

-Parenteral transmission (40% IV drug users)
-2% of world infected
-sRNA
-7 genotypes, no.1 70% of cases

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10
Q

Pathology of liver destruction by Hepatitis

A

-Viral infection of hepatocytes results in necrosis.
-Kupfter hyperplasia
-mononuclear cells in liber =fibrosis
(Cytotoxic T cells, NK cells)

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11
Q

Ledipasvir (drug)

A

-inhibits HCV protein NS5A
 RNA binding protein.
 Sub-cellular localization of HCV.
 Modulates host cell interferon response

100% cure rate when used with nucleoside analogues= sofosbuvir, ribavirin

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12
Q

Vaccine

A

-HepB vaccine 2 months of age dose.
-HepA for travelling to high risk countries
-Inactivated virus vaccines
-HepC no simple vaccine

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13
Q

Clinical Course of Viral Hepatitis

A

-prodromal phase (in 2 weeks)
-icteric phase (2-8 weeks)
-recovery phase (in 8 weeks)

chronic hepatitis if persists= viral antigen and abnormal liver functions

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14
Q

Portal Hypertension

A

-usually 3mmHg, hypertension above 10mmHg
-cirrhosis impeding blood flow
classes: intrahepatic, post hepatic and prehepatic

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15
Q

Symptoms associated with chronic liver disease

A

 Nail clubbing.
 Anaemia.
 Caput medusae.
 Testicular atrophy.
 Spider nevi.
 Jaundice.
 Ascites.
 Oedema.
 Bruising

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16
Q

Ascites

A

-Accumulation of fluid in the peritoneal cavity
-complication of portal hypertension
[Increased capillary hydrostatic and hepatic sinusoidal pressure, decreased oncotic]
-hypovolaemia, RAAS activation
-Transudate, fluid increase, hepatic portal vein pressure increase
-Exudate= inflammation

17
Q

Peritonitis

A

-inflammation of peritoneum
-emergency
-common in ascites (Spontaneous bacterial peritonitis)
-host defences compromised= bacteraemia (complement)
-gram negatives (E.coli, K. pneumoniae)

18
Q

Paracentesis

A

-sample fluid in peritoneal cavity
-remove fluid too

19
Q

Diuretics

A

-salt reduction in diets and potassium sparing diuretics can reduce fluid build up
-furosemide (Na K Cl cotransporter inhibitor, loop diuretic)
-vasopressin receptor 2-antagonists

20
Q

Hepatorenal Syndrome

A

-renal failure from liver failure (co -morbidity of ascites
-Arterial dilation in the splanchnic vasculature main cause (systemic hypotension, renal hypotension and reduced GFR)
-Compensation can occur due to limited renal vasoconstriction (angiotensin clearance poor)

21
Q

Chronic Liver disease neuropathy

A

-caused by alcohol

22
Q

Chronic Liver disease Kayser-Fleshier Rings

A

-Caused by Wilson’s

23
Q

Dupuytren’s Contracture

A

-alcohol
-genetics, Viking’s disease, WNT mutations
-Age= fibrotic response to fatty tissue damage, circulatory damage, changes in prostaglandin production

24
Q

Liver carcinoma Rates

A

-5700 new cases, 5091 deaths
-under 40 only 25% survive 5 years
-over 80 only 5% survive 5 years

25
Liver Carcinoma Associated Risk Factors
 Chronic viral hepatitis infection.  Chronic alcoholic liver disease.  Mycotoxin exposure - Aflatoxins.  Smoking.  Non-alcoholic fatty liver disease.  Hepatic iron overload.
26
Hepatocellular Carcinoma
-chronic cirrhosis and hepatitis (chronic hepatitis 80% cases) -infection causes Hepatocellular Carcinoma, oxidative stress, cytokine stimulation -nodular or infiltrative
27
Aflatoxins
-aspergillus (mold) produces (flavus and parasiticus -most potent carcinogen -improperly stored vegetables, grain, crops -14 distinct ones:B1 worst (no animal immune) -intercalate into DNA alkylating bases (third base of codon 249 in p53
28
Cholangiocellular carcinoma
-bile duct epithelia -liver parasites:  Clonochis sinensis.  Opisthorchis viverrini -mutations in codon 12 of KRAS gene  G12A  G12D  G12V
29
Clonochis sinensis
-Most prevalent human trematode infection in Asia (30 million cases) -raw uncooked fish transmission -lives in bile duct induces hyperplasia
30
Iron Overload
- iron stored liver prior to use -haemochromatosis primary (genetic) or secondary
31
Primary haemochromatosis
HFE gene classical type 1 haemochromatosis. - haemojuvelin, hepcidin, transferrin and ferroportin mutations also possible
32
Type 1 Haemochromatosis
-autosomal recessive disorder - HFE protein is a negative regulator of transferrin receptor mediated uptake of iron. C28Y mutation homo. C28Y/H63D mutation hetero. -celtic pops. high prevalence -tissue damage only noticeable after 30
33
Secondary Haemochromatosis
-Blood transfusion -dietary overload -supplements, - Acute iron toxicity most common cause of fatal poisoning in children.
34
Gallstones
-iron-overloading anaemias -Haemolytic anaemia -composition of stones vary cholesterol or bilveridin