Gastrointestinal 2 Flashcards

1
Q

functions of the liver

A
  • Synthesis: Of albumin, growth factors, urea, coagulation factors, complement, c-reactive protein, specific binding proteins (iron, copper, vitamin A). Excretes bilirubin from RBC turnover.
  • Storage: Of vitamins, glycogen, and lipids. Controls the absorption and transport of lipids (bile salts and lipoproteins)
  • Metabolism: Biotransformation, Metabolizes amino acids, Regulates hormones: insulin, thyroxin, androgen, estrogen.
  • Regulates blood glucose.
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2
Q

what characterized non-alcoholic fatty liver disease?

A

excess lipid accumulation in the liver.

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3
Q

frequency of non-alcoholic liver disease

A

40% in developed countries

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4
Q

NAFLD is a major complication of ______ and _______

A

obesity and insulin resistance

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5
Q

what can non-alcoholic fatty liver disease progress to?

A
  • Progresses to NASH – Non-Alcoholic Steatohepatitis
    (Now is fat plus inflammation and scarring.)
  • Cirrhosis (is a non-alcoholic cause of this)
  • Which can then cause/develop into liver failure or hepatocellular carcinoma
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6
Q

are there drugs available for NAFLD?

A

no but it is preventable and partially reversible

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7
Q

components in the pathogenesis of NAFLD?

A
  • Excess fatty acids in liver: from diet + adipose tissue +lipogenesis > metabolism + secretion
  • Adipose tissue releases inflammatory adipokines like leptin that promote steatosis and fibrosis.
    (Release many pro-inflammatory that have a predominant effect on the liver.)
  • Liver releases hepatokines that promote lipid accumulation and inflammation.
  • Obesity alters intestinal microbiome and increases permeability: bacteria enter portal blood.
  • Kupffer cells activate, release cytokines, initiate inflammation.
  • Stellate cells activate, initiate fibrosis – so scarring in the liver.
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8
Q

forms of bilirubin

A
  • Bilirubin from normal turnover or RBCs is not water soluble and is bound to albumin for transport.
  • Liver conjugates bilirubin to water-soluble glucuronides which are excreted in the bile.
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9
Q

what is jaundice?

A
  • Excess plasma level of either form of bilirubin can lead to tissue deposition: jaundice.
    o Yellow sclera is an obvious indicator – useful for someone with dark skin since melanin can mask the yellow in the skin.
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10
Q

when does hemolytic jaundice occur?

A
  • Occurs when there is a lot of bleeding.
  • liver overloaded, so excess of unconjugated bilirubin, which is not water soluble.
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11
Q

what happens in extrahepatic biliary obstruction?

A
  • excess of conjugated bilirubin, which is water soluble, so can be excreted in urine.
  • Intestinal bacteria normally convert a small fraction of the conjugated bilirubin to a brown pigment; so, obstruction can produce colorless stool – cannot go from the liver to the intestine.
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12
Q

what can cause the obstruction in extrahepatic biliary obstruction?

A

o Congenital biliary atresia: born with a section that is not open.
o Stone
o Tumor that is compressing it
o Enlargement of a lymph node

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13
Q

therapy for extrahepatic biliary obstruction

A
  • Bile duct obstruction requires surgical correction.
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14
Q

what is gilbert’s syndrome and what is the prevalence?

A
  • intermittent jaundice due to reduced transcription glucuronyl transferase (UGT)
    (mutation in the promoter region of the UGT gene. still works but doesn’t work as well – high stress can trigger it.)
  • Up to 10% of the population,
  • symptom onset in early adulthood
    o more common in males.
  • harmless
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15
Q

how does neonatal jaundice occur and what is the therapy?

A
  • newborn often have increased RBC hemolysis + lower synthesis of liver enzymes and albumin (still immature) + immature BBB,
  • which allows free bilirubin to enter the brain with deposition in the basal ganglia and neuronal degeneration: Kernicterus.
    (Causes neurodegeneration in the basal ganglia – neural necrosis.)
  • Prevented by treatment with blue light: photoconversion of bilirubin to a soluble derivative.
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16
Q

incubation period for hepatitis?

A

weeks – months between exposure and illness.

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17
Q

symptoms of viral hepatitis

A

o symptoms usually include fatigue, weakness, GI problems (nausea, vomiting, diarrhea, loss of appetite)
o may include fever, jaundice, and dark urine.
o B, C, and D can also cause skin rash, weight loss, joint pain, loss of inclination to smoke.

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18
Q

Hepatitis viruses are very small so can squeeze through the ____________

A

sinusoid in the liver

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19
Q

viral hepatitis is a risk factor for _____

A

HCC

20
Q

transmission of hepatitis A

A
  • Transmission fecal-oral.
  • Easily crosses intestine, so gets in the blood, liver, bile, and then stool, which can go in the water and contaminate it.
  • Common in situations with poor hygiene, easily spread.
21
Q

progression of hepatitis A

A

Don’t have the capacity to cause a chronic disease.

22
Q

therapy for hepatitis A

A

vaccine for travel

23
Q

symptoms for hepatitis A

A

usually mild, usually fatigue, GI problems, fever.
Due to the immune response in the liver but it can be resolved.

24
Q

transmission of hepatitis B

A
  • Highly contagious; virus in blood and all body fluids
  • Major spread through sexual activity.
25
Q

life cycle and effect of hepatitis B

A
  • Viral reproduction makes new virions plus non-infectious particles with only surface antigens, used as a “decoy” against the immune system.
  • Immune response, both innate and adaptive, causes liver injury—immune reaction destroys hepatocytes to stop the spread of the virus.
  • 90% of people recover.
26
Q

what happens when infants get hepatitis B

A

have lower immune defense and fewer symptoms, but most become carriers.

27
Q

progression of hepatitis B

A
  • Can cause acute liver failure.
  • Chronic infection is a major risk for cirrhosis and liver carcinoma.
  • 10% become chronic asymptomatic carriers who spread disease and who often progress to cirrhosis.
  • Primary liver disease almost always caused by this virus.
28
Q

therapy for hepatitis B

A
  • Vaccination is now universal in Canadian children; but infection is still widespread in poor countries.
  • 3 injections during 6 months (usually done in grade 4 in Canada)
29
Q

transmission of hepatitis C

A

Main route of transmission currently is IV drug use but can also be spread sexually.

30
Q

progression/life cycle of hepatitis C

A
  • Majority progress to chronic disease with eventual cirrhosis (20% of people with chronic disease will progress) and significant risk of carcinoma.
  • Increase in monocytes, fibrosis, and necrosis.
  • Virus enters hepatocyte by attachment to CD81 and SRB1 (scavenger receptor) on cell surface, then is endocytosed.
  • Virus reproduces in ER of hepatocyte, then attaches to a protective lipoprotein, makes a lipoviralparticle.
  • Thought to protect it against immune system.
  • Also helps it to easily be transported into the blood.
  • It hijacks the hepatocyte synthesis of lipoproteins.
31
Q

therapy for hepatitis C

A
  • Previous therapy was toxic with low success rate.
  • Ability to now cure Hepatitis C (block reproduction) – need for liver transplant shifting to cirrhosis and cancer from NASH instead of Hepatitis C.
32
Q

transmission of hepatitis D

A
  • Transmitted by bodily fluids.
33
Q

progression/life cycle of hepatitis D

A
  • Delta virus.
  • Requires Hepatitis B to produce the viral envelope.
  • Requires its surface envelopes (takes the non-infectious particles).
  • Superinfection produces severe symptoms: Causes the most severe chronic hepatitis due to greater immune response, leading to extensive necrosis
34
Q

therapy for hepatitis D

A
  • No cure.
  • Prevention: immunize against hepatitis B
35
Q

transmission of hepatitis E

A
  • Transmission fecal-oral.
    o Epidemics in poor countries – contamination in water.
36
Q

most common subtypes of hepatitis E

A
  • HEV 1 and 2 subtypes are the most common.
37
Q

effect of hepatitis E

A
  • Recovery is the major outcome.
  • Many are asymptomatic.
  • Linked to neurological syndromes in a small fraction of patients.
  • High risk in pregnancy: 20-30% death.
  • Don’t have the capacity to cause a chronic disease.
38
Q

what does chole mean?

A

bile

39
Q

what does cystis mean?

A

bladder

40
Q

what does dochos mean?

A

duct

41
Q

what does lithos mean?

A

stone

42
Q

what are gallstones and the types?

A
  • Ingredients in bile may precipitate within the gallbladder, producing stones.
  • Composed of pigment (bilirubin salts), cholesterol, or a mixture.
  • There are two major types: pigment and cholesterol gallstones. (Most are cholesterol (80%))
43
Q

gallstones are related/caused by ____

A

low fiber and high fat diet

44
Q

risks of gallstones

A

obesity, rapid weight loss, and chronic hemolysis

45
Q

what causes the pain of gallstones

A

related to irritation of gallbladder or progression through the bile duct

46
Q

treatment of gallstones

A
  • often surgical – laparoscopic cholecystectomy (take gallbladder out).
  • Another strategy is to try to dissolve the stone with shock waves
47
Q

potential complications of gallstones

A
  • Acute cholecystitis:
    inflammation of gallbladder following obstruction, can cause obstructive jaundice., may be accompanied by infection. Elevated pressure may relocate the stone.
    Risk for abscess, perforation, peritonitis. Reversible with surgical correction.
  • Choledocholithiasis (“bile/duct/stone”): causes cholestasis, (“bile/stops flowing”) and obstructive jaundice.
  • Ulceration of gall bladder, fistula to duodenum.
  • Pancreatitis, intestinal obstruction