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Pathology > GI ( 5% ) + HPB ( 10% ) > Flashcards

GI ( 5% ) + HPB ( 10% ) Flashcards

1
Q

In acute pancreatitis

  • Less than 5% are idiopathic.
  • 35% of patients with gallstones develop pancreatitis.
  • gallstones are present in 80% cases
  • trypsin plays a central role in the activation of the kinin system
A

trypsin plays a central role in the activation of the kinin system

  • About 15% are idiopathic.
  • 5% of patients with gallstones develop pancreatitis.
  • Alcohol + gallstones together account for 80% of cases
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2
Q

which of the following can occur in acute pancreatitis

  • hypercalcaemia
  • glycosuria
A

glycosuria

  • hypocalcaemia
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3
Q

In acute pancreatitis

  • Fat necrosis occurs in other intra-abdominal fatty depots
  • Trauma is the precipitating cause in 30%
  • Erythromycin has been implicated in severe cases
  • Kallikrein converts trypsin to activate the complement system
  • Alcohol is directly toxic to the islets of Langerhan
A

Fat necrosis occurs in other intra-abdominal fatty depots

  • All cause except alcohol and gallstones only account for <20%
  • Thiazides, frusemide, oestrogen can cause acute pancreatitis
  • Kallikrein converts trypsin to activate the complement system
    • ??
  • Alcohol is directly toxic to acinar cells
    • ​islets are the insulin etc
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4
Q

In acute pancreatitis

  • The 2 commonest causes are most often seen in males
  • Pathogenesis does not include diuretic use
  • Is idiopathic in 40%
  • Can be caused by Ascaris.
  • Is associated with hypocalcaemia
A

Is associated with hypocalcaemia

  • Gallstones and alcohol most common 2 causes, gallstones more common in women*
  • Idiopathic in 15%*
  • Thiazides and frusemide can cause pancreatitis*
  • Ascaris is a parasitic nemotode of the GI tract*
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5
Q

pancreatitis can be caused by all except

  • Coxsackie virus
  • frusemide
  • Henoch-Schonlein purpura induced ischaemia
  • Ascaris lumbricoides
  • Streptococci
A

Streptococci

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6
Q

acute pancreatitis

  • may be caused by Helminth infection
  • causes hypercalcaemia.
  • develop in 50% people with gallstones.
  • leads to inhibition of elastase.
  • involves acinar cell injury as a late event.
A

may be caused by Helminth infection

  • causes hypocalcaemia
  • develop in 5% people with gallstones
  • leads to inappropriate activation of enzymes including elastase
  • involves acinar cell injury as an early event
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7
Q

Acute pancreatitis

  • Is associated with increased serum amylase without a rise in serum lipase.
  • Occurs most often in later life.
  • Occurs in about 5% people with gallstones
  • When associated with alcohol is not usually preceded by chronic pancreatitis.
  • Is often associated with hypercalcaemia.
A

Occurs in about 5% people with gallstones

  • Is associated with increased serum amylase and a rise in serum lipase.
  • Occurs most often in younger age
  • Alcoholic chronic pancreatitis is usually preceded by acute pancreatitis.
  • Is often associated with hypocalcaemia.
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8
Q

Regarding pancreatitis

  • The 2nd commonest cause is infectious agents
  • Trypsin is implicated as an activator of the kinin system
  • Elastase is the only pancreatic enzyme that acts to limit pancreatitis
  • The chronic form is usually due to gallstones.
  • Duct obstruction is not the mechanism of injury in alcoholic pancreatitis
A

Trypsin is implicated as an activator of the kinin system

  • Gallstones and alcohol most common causes=
  • Elastase is the only pancreatic enzyme that acts to limit pancreatitis
    • Pretty sure elastase breaks down the pancreas
  • The chronic form is usually due to Alcohol
  • Duct obstruction is one of the mechanism of injury in alcoholic pancreatitis - inflammation causes tissue swelling which obstructs ducts
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9
Q

In acute pancreatitis

  • Alcohol induced injury may be caused by defective intracellular transport
  • Trypsin does not have a central role
  • Hyperlipoproteinaemias (type I and V) are a common cause
  • Male to female ratio is 3:1 in biliary tract disease
  • Serum lipase is elevated in the first 12 hours.
A

Alcohol induced injury may be caused by defective intracellular transport

  • Trypsin does have a central role - one of the pancreatic enzymes that is inappropriately activated
  • Male to female ratio is 1:3 in biliary tract disease.
  • Serum lipase is elevated in the first 72 hours
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10
Q

The complications of chronic pancreatitis include all except

  • Duct obstruction
  • DIC
  • Pseudocyst
  • Malabsorption
  • Secondary diabetes
A

DIC

Seen in acute pancreatitis

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11
Q

Chronic pancreatitis

  • Has equal prevalence between the sexes
  • Is predisposed to by hyperlipoproteinaemia
  • Does not commence until adulthood
  • Always has an identifiable precipitant
  • Always can be diagnosed by elevated amylase
A

Is predisposed to by hyperlipoproteinaemia

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12
Q
  1. Regarding oesophagitis
  • a. The severity of symptoms is closely related to the degree of reflux oesophagitis present
  • b. Radiation oesophagitis is characterized by mucosal fibrosis and thickening
  • c. Barrett’s oesophagus occurs in less than 5% of patients with symptomatic reflux
  • d. SCC of the oesophagus occurs more often in drinkers of beer than of spirits
  • e. May be due to aspergillosis in immunocompromised patients.
A

e. May be due to aspergillosis in immunocompromised patients.

Most common infectious cause is HSV, also CMV. Of fungal infections, candidiasis is most common, but aspergillosis and mucormycosis also occur (as per R&C)

  • a. The severity of symptoms is poorly correlated to the degree of reflux oesophagitis present
  • b. Radiation oesophagitis is characterized by mucosal fibrosis and thickening
  • c. Barrett’s oesophagus occurs in 5-15% of patients who seek tx for GORD
  • d. SCC of the oesophagus occurs more often in drinkers of beer than of spirits
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13
Q

oesophageal varices

  • occur in 1/3 of all cirrhotic patients
  • account for more than 50% of episodes of haematemesis
  • are most often associated with Hep C cirrhosis
  • have a 40% mortality during the first episode of rupture
  • lie primarily in the middle portion of the oesophagus
A

have a 40% mortality during the first episode of rupture

  • occur in 50% of all cirrhotic patients.
  • account for a small proportion of episodes of haematemesis
  • are most often associated with alcoholic cirrhosis (schistosomiasis second cause worldwide)
  • lie primarily in the distal portion of the oesophagus
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14
Q
  1. Regarding peptic ulceration
  • a. It occurs most commonly in the antrum of the stomach.
  • b. It has a strong genetic influence
  • c. H. pylori infection of the mucosa in 50% of patients with duodenal ulceration
  • d. It is more frequent in patients with chronic obstructive pulmonary disease
  • e. Gastric acid is the only prerequisite for the formation of ulcers. Can have impaired protective mechanisms
A

d. It is more frequent in patients with chronic obstructive pulmonary disease

Associated with smoking, obesity, and alcohol

  • a. Adenocarcinoma occurs most commonly in the antrum of the stomach.
  • b. It has a strong genetic influence
  • c. H. pylori infection of the mucosa in 50% of patients with duodenal ulceration
  • e. Gastric acid is not the only prerequisite for the formation of ulcers. Can have impaired protective mechanisms, NSAID use, autoimmune disease etc
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15
Q

Acute Appendicitis:

  • a. In preschool children is usually present with the so-called “classic” signs and symptoms.
  • b. Is associated with appendiceal obstruction in 10% of cases.
  • c. Histologically shows neutrophilic infiltration of the muscularis layer
  • d. Clinical diagnosis is falsely positive in about 50% of cases
  • e. It cannot cause liver abscesses
A

c. Histologically shows neutrophilic infiltration of the muscularis layer

  • a. Tends to have an atypical presentation in young children
  • b. Is associated with appendiceal obstruction in 75% of cases.
  • d. Clinical diagnosis is falsely positive in less than 50% of cases.
    • Is generally a diagnosis made clinically, which wouldnt happen if there was 50% false positives
  • e. It can cause liver abscesses if there is a high-riding posterior appendix abutting the liver (I assume)
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16
Q
  1. With regards to viral enteritis
  • a. It is commonly caused by a rhinovirus.
  • b. transmission of rotavirus is faecal-oral
  • c. rhinovirus accounts for 50% of all childhood diarrhoeas.
  • d. Norwalk agent (aka norovirus) more commonly cause infection in children compared with adults.
  • e. Norwalk agent have an incubation period of 72 hours.
A
  • a. It is commonly caused by a rhinovirus. Rotavirus
  • b. transmission of rotavirus is faecal-oral
  • c. rhinovirus accounts for 50% of all childhood diarrhoeas. Rotavirus
  • d. Norwalk agent (aka norovirus) more commonly cause infection in children compared with adults. Opposite
  • e. Norwalk agent have an incubation period of 72 hours. Viral enteritis incubation is 48 hrs
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17
Q
  1. The most common cause of traveller’s diarrhoea is
  • a. rotavirus
  • b. E. coli
  • c. Shigella
  • d. Salmonella
  • e. Giardia
A

b. E. coli

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18
Q
  1. Regarding ulcerative colitis all are true except
  • a. Inflammation extends in a continuous fashion proximally from the rectum
  • b. Mural thickening does not occur.
  • c. Has associations with ankylosing spondylitis
  • d. Toxic dilatation develops rarely with acute attacks
  • e. Onset of disease peaks between age 30-40 years.
A

e. Onset of disease peaks between age 20-25

  • a. Inflammation extends in a continuous fashion proximally from the rectum
  • b. Mural thickening does not occur - Atrophy/thinning does
  • c. Has associations with ankylosing spondylitis
  • d. Toxic dilatation develops rarely with acute attacks
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19
Q
  1. Features of ulcerative colitis include.
  • a. Skip lesions
  • b. Superficial ulcers
  • c. Early strictures
  • d. Thickened bowel wall
  • e. Granulomas
A

b. Superficial ulcers

Chrohns:

Skip lesions, strictures, thick wall, transmural inflammation, deep ulcers, granulomas

UC:

Colon only, diffuse, rare strictures, thin walls, mucosal inflammation only, marked pseudopolyps, no granulomas

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20
Q
  1. Which is not a feature of acute Crohn’s disease
  • a. Segmental lesions
  • b. Serosal involvement
  • c. Fissures penetrating deep into the wall of the affected mucosa
  • d. Inflammatory pseudo-polyps
  • e. Epithelioid granulomas
A

d. Inflammatory pseudo-polyps.

Occurs in Ulcerative colitis

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21
Q

A young baby presents with jaundice, dark urine and pale stools, most likely the problem is

  • Physiologic jaundice of the newborn
  • Breast milk jaundice
  • Gilbert’s syndrome
  • Biliary atresia
  • None of the above
A

Biliary atresia

Listed as a possible obstructive cause in children.

Dark urine and pale stools = conjugated hyperbilirubinaemia

Most babies will get unconjugated jaundice, as the conjugation machinary is not yet working properly (Physiologic jaundice of the newborn), and this can be exacerbated by breast milk.

Gilbert Syndrome will also cause an unconjugated jaundice

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22
Q

Splenic rupture

  • Can occasionally occur spontaneously in normal spleens
  • Often causes little blood loss
  • Is encountered most commonly in infectious mononucleosis
  • May result in speniculi
  • Must be considered in ITP
A

Is encountered most commonly in infectious mononucleosis

Most common cause is blunt trauma, but infectious mononucleosis is the most common predisposing condition

Can rupture spontaneously, but never in ‘normal’ spleens - always an underlying cause of fragility

Often cause massive haemorrhage requiring splenectomy to prevent death

No mention made of spleniculi (accessory spleens, which are congenital), nor of ITP in R&C. I think the answer above is the ‘best’ answer.

23
Q

Regarding cirrhosis

  • Focal changes can constitute cirrhosis
  • Delicate tracts of type II collagen are deposited.
  • Shunts occur in the rectum, oesophagus, retroperitoneum and falciform ligament.
  • The dominant intrahepatic cause of portal hypertension is massive fatty change.
  • Hypoalbuminaemia is initially due to decreased production
A

Shunts occur in the rectum, oesophagus, retroperitoneum and falciform ligament. ​

  • Diffuse fibrosis constitutes cirrhosis (not focal changes)
  • Delicate tracts of type I + III collagen are deposited (IV is normal in the liver)
  • The dominant intrahepatic cause of portal hypertension is Cirrhosis
  • Hypoalbuminaemia is initially due to ?
24
Q

Conjugated hyperbilirubinaemia

  • Occurs when greater than 80% of bilirubin is conjugated
  • Is a feature of Gilbert’s
  • Is rarely associated with cholestasis
  • Is often seen in β thalassaemia.
  • Is often associated with a clinical picture of jaundice, pruritis and xanthomata
A

Is often associated with a clinical picture of jaundice, pruritis and xanthomata

Water soluble so can deposit in tissues

  • Occurs when greater than 80% of bilirubin is conjugated
  • Unconjugated Is a feature of Gilbert’s (hepatocellular cause)
  • Is rarely associated with cholestasis. Cholestasis is a common cause
  • Is often seen in β thalassaemia. Unconjugated
25
Q

The following are true for cirrhosis except

  • It is among the top 10 leading causes of death in the western world
  • The central pathogenic process is progressive fibrosis
  • It may be clinically silent
  • Alcoholic liver disease is the aetiology in 30% cases
  • Collagen type I and III are deposited in all parts of the lobule
A

Unclear what answer is right

Chronic liver disease is the 12th leading cause of death in the US (and not all CLD is cirrhotic)

Alcoholic liver disease is the aetiology in ??? cases - percentages not given in current text book (2/3 in old book, likely remains higher than 30%)

26
Q

Ascites

  • is due to lymphatic obstruction
  • involves percolation of hepatic lymph into the peritoneal cavity
  • does not involve renal retention of sodium and water
  • involves increased vascular permeability.
  • is not associated with hepatic sinusoidal hypertension. Opposite
A

involves percolation of hepatic lymph into the peritoneal cavity

  • is due to Excess lymph production which overwhelms drainage capacity
  • does involve renal retention of sodium and water.
  • Does not involve increased vascular permeability - Transudate promoted by sinusoidal hypertension and hypoalbuminaemia
  • is associated with hepatic sinusoidal hypertension.
27
Q

Unconjugated bilirubinaemia

  • Is soluble in aqueous solution.
  • Is not protein bound.
  • When present in excess is readily excreted in urine.
  • Can cause kernicterus if present in excess in neonates
  • Is the major form of bilirubin elevated in gallstone obstruction. Conjugated
A

Can cause kernicterus if present in excess in neonates

  • Is insoluble in aqueous solution.
  • Is Always protein bound as its otherwise insoluble
  • When present in excess is not excreted in urine, as it can’t pass glomerular filter if albumin bound
    • ​Hence why dark urine is a sign of conjugated bilirubinaemia
  • Conjugated Is the major form of bilirubin elevated in gallstone obstruction.
28
Q

regarding cirrhosis

  • 30% caused by viral hepatitis
  • type I and III collagen are deposited in all portions of the lobule
  • the central pathogenesis is progressive nodule formation
  • Ito cells are considered as a minor source of collagen excess
  • Chronic inflammation has no role in its pathogenesis
A

type I and III collagen are deposited in all portions of the lobule

  • Probably <30% caused by viral hepatitis (old text stated that 2/3rds were alcoholic, so given there are other causes hepatitis likely <30%)
  • the central pathogenesis is progressive fibrosis
  • Chronic inflammation has a major role in its pathogenesis
29
Q

Ascites

  • is commonly associated with hyperproteinaemia
  • is a rare complication of cirrhotic liver disease
  • is diagnosed clinically by the presence of generalized oedema.
  • is associated with hepatic sinusoidal hypertension
  • occurs as an early complication of congestive heart failure
A

is associated with hepatic sinusoidal hypertension

  • is commonly associated with _hypo_proteinaemia
  • is a common complication of cirrhotic liver disease
  • is diagnosed clinically by the presence of generalized oedema.
  • occurs as a late complication of congestive heart failure
30
Q

In cirrhosis

  • Fibrosis is confined to delicate bands around the central veins.
  • Nodularity is uncommon.
  • Vascular architecture is preserved.
  • The Ito cell is a major source of excess collagen
  • The left lobe of the liver is the most affected.
A

The Ito cell is a major source of excess collagen

  • Fibrosis Links portal tracts to central veins
  • Nodularity is a Hallmark
  • Vascular architecture is Disrupted
  • Diffuse diease affecting the entirity of the liver
31
Q

conjugated hyperbilirubinaemia results from

  • Gilbert’s
  • Physiological jaundice
  • Excess production of bilirubin
  • Decreased hepatic uptake
  • Cholestasis
A

Cholestasis

32
Q

Regarding hepatic failure

  • Occurs with the loss of functional liver capacity of approximately 60%.
  • Encephalopathy is a result of increased ammonia formation.
  • The liver is the predominant site of the synthesis of albumin
A
  • Occurs with the loss of functional liver capacity of approximately 60%. 85%
  • Encephalopathy is a result of increased ammonia formation. Decreased metabolism
  • The liver is the predominant site of the synthesis of albumin
33
Q

With regard to jaundice

  • Conjugated bilirubin causes kernicterus in adults.
  • Unconjugated bilirubin does not colour the sclera
  • Unconjugated bilirubin is tightly bound to albumin
  • Unconjugated bilirubin produces bilirubin in urine
  • Conjugated bilirubin is tightly bound to albumin
A

Unconjugated bilirubin is tightly bound to albumin

Conjugated produces dark urine, and only causes kernicterus in neonates

34
Q

In viral hepatitis

  • The majority of cases of acute hepatitis B infection result in a carrier state, without clinical evidence of disease.
  • Anti HBs appears in the first week of infection
  • Anti HCV IgG does not confer immunity to Hep C
  • The major cause of death from Hep B is hepatocellular carcinoma.
  • Hep A has an outer surface envelope of protein, lipid and carbohydrate
A

Anti HCV IgG does not confer immunity to Hep C

  • The majority of cases (95%) of acute hepatitis B infection result viral clearance
  • Anti HBs takes months to develop
    • ​HBs-Ag, HBe-Ag, and HBV DNA appears first, 4-26 weeks after infection
  • The major cause of death from Hep B is Cirrhosis
  • Hep A is an unenveloped virus
35
Q

Regarding serum markers in hepatitis

  • IgM in HAV provides life long immunity.
  • In HBV, HBeAg, HBV DNA and DNA polymerase appear before HBsAg.
  • Carrier state in HBV is defined by the presence of HBsAg in serum for 6/12 or longer after initial detection
  • Anti HBe indicate active viral replication.
  • In HEV, serum transaminase precede elevation of IgM anti HEV.
A

Carrier state in HBV is defined by the presence of HBsAg in serum for 6/12 or longer after initial detection

  • IgG in HAV provides life long immunity.
  • In HBV, HBeAg, HBV DNA and DNA polymerase appear at the same time as HBsAg.
  • HBeAg indicates active viral replication.
  • In HEV, serum transaminase follows elevation of IgM anti-HEV.
36
Q

Hepatitis C virus

  • Is a DNA virus.
  • Has core antigens as serum markers.
  • Is the ‘kissing disease’
  • Persistent infection and chronic hepatitis are the hallmarks
  • Has a low rate of cirrhosis
A

Persistent infection and chronic hepatitis are the hallmarks

  • Is a ssRNA virus.
  • Has RNA as a serum marker (and antibodies are against an envelope protein)
  • EBV/infections mononucleosis Is the ‘kissing disease’
  • Has a low rate of cirrhosis
37
Q

Which of the following indicates immunity to Hepatitis B virus

  • RNA polymerase
  • IgM anti-HBc
  • Anti-HBs
  • HBeAg
  • HBV-DNA
A

Anti-HBs

  • IgM anti-HBc = is a marker of acute infection
    • ​Anti-HBc (IgG) = marker of past or present infection - does not distinguish acute, chronic, or cleared infection, but can distinguish vaccinated (not present) vs immune tolerance (present)
  • HBeAg = marker of active viral replication
  • RNA polymerase =
  • HBV-DNA =
38
Q

Hepatitis B virus

  • Is an unenveloped particle. Opp
  • Is an RNA virus. Opp
  • Is a member of the hepadnaviridae family
  • Results in chronic hepatitis in 30% acute infections. 10%
  • Has an incubation period of 2-6 weeks. 2-26 weeks
A

Is a member of the hepadnaviridae family

  • Is an partially dsDNA enveloped particle
    • Hep A is ssRNA, unenveloped
  • Is a DNA virus.
  • Results in chronic hepatitis in 10% acute infections.
  • Has an incubation period of 2-26 weeks
39
Q

Hep C infection

  • Is associated with sexual contact
  • Carries a 40% risk of cirrhosis.
  • Is idiopathic in 10% cases.
  • Carries a >50% risk of chronic progressive hepatitis
A

Carries a >50% risk of chronic progressive hepatitis

  • Is associated with sexual contact
  • Carries a 15% risk of cirrhosis (80% -> chronic, of which 20% develop cirrhosis)
  • Is idiopathic in 33% cases.
40
Q

In hepatitis B

  • Acute infection causes sub-clinical disease in 65% cases
  • The majority of cases of persistent infection result in cirrhosis
  • HBsAg appears soon after overt disease.
  • Infection does not play a role in the development of HCC.
  • Anti HBs appears soon after HBsAg. Opp
A

Acute infection causes sub-clinical disease in 65% cases

  • The 20-30% of cases of persistent infection result in cirrhosis
  • HBsAg appears before overt disease.
  • Infection plays a role in the development of HCC - Can develop HCC in absence of cirrhosis
  • Anti HBs appears a good few weeks-months (I assume) after HBsAg - Anti-HBs represents immunity, whereas HBsAg represents acute infection
41
Q

hepatitis C

  • is acquired by faecal – oral transmission.
  • has its highest seroprevalence in haemodialysis patients.
  • transmission by sexual contact is at a high rate.
  • causes chronic hepatitis at a higher rate than hepatitis B
  • exposure confers effective immunity to subsequent infection
A

causes chronic hepatitis at a higher rate than hepatitis B

80% of cases become chronic

  • is acquired by Parenteral​ transmission.
  • has its highest seroprevalence in IV drug users
  • transmission by sexual contact is at a low rate.
  • exposure does not confer effective immunity to subsequent infection, due to antigenic mutation
42
Q

Regarding hepatitis C

  • Has a high association with sexual transmission.
  • Transmission is increased in pregnancy
  • Greater than 50% become chronic
A

Greater than 50% become chronic

More like 80%

  • Has a low association with sexual transmission. Low
  • Transmission is increased in pregnancy
43
Q

with hepatitis E infection

  • it is transmitted primarily parenterally
  • it accounts for a > 20% mortality in pregnant mothers
A

it accounts for a > 20% mortality in pregnant mothers

Transmitted enterically

44
Q

Hepatitis A (pg 844)

  • is a benign, self-limiting disease.
  • has a mean incubation period of 1-4 months.
  • frequently causes fulminant hepatitis.
  • IgM is not a reliable marker of acute infection.
A

is a benign, self-limiting disease.

  • has a mean incubation period of 2-6 weeks
  • Never causes fulminant hepatitis.
  • IgM is a reliable marker of acute infection - over time it is replaced with IgG
45
Q

Hepatitis B can produce all of the following EXCEPT

  • acute hepatitis
  • helper-independent latent infection
  • non-progressive chronic hepatitis
  • an asymptomatic carrier state
A

helper-independent latent infection

Can lead to:

  • 1) acute hepatitis followed by recovery and clearance
  • 2) non-progressive chronic hepatitis
  • 3) progressive chronic disease ending in cirrhosis
  • 4) Acute hepatic failure with massive liver necrosis
  • 5) An asymptomatic ‘healthy’ carrier state
46
Q

Which of the following is NOT a single stranded RNA virus

  • HAV
  • HBV
  • HCV
  • HDV
A

HBV​

Is partially dsDNA

47
Q

Which is the correct match of mode of transmission with geographical areas for Hepatitis B

  • High prevalence regions – unprotected intercourse.
  • Low prevalence regions – perinatal transmission.
  • Intermediate prevalence regions – horizontal transmission
  • High prevalence regions – transfusion related spread.
A

Intermediate prevalence regions – horizontal transmission

  • Low prevalence regions – unprotected intercourse
  • High prevalence regions – perinatal transmission
  • Now rare anywhere – transfusion related spread.
48
Q

Which is INCORRECT with regards to hepatitis C (pg 847/849)

  • HCV is a major cause of liver disease worldwide.
  • Progression to chronic liver disease occurs in the majority of HCV-infected individuals.
  • HCV is the most common indication for liver transplantation in the US.
  • HCV has a high mortality rate among pregnant women.
A

Hepatitis E has a high mortality rate among pregnant women (20%).

No mention made of liver transplantation rates but the US rate of HCV serology being positive is 1.3%

49
Q

Hepatitis D (pg 848/849)

  • is dependant for its life cycle on HBV.
  • coinfection of HDV + HBV is clinically distinguishable from acute HBV.
  • has fecal-oral mode of transmission
  • Vaccination for HBV does not prevent HDV infection.
A

is dependant for its life cycle on HBV.

  • coinfection of HDV + HBV is clinically _in_distinguishable from acute HBV.
  • has exposure to serum containing HBV/HDV as a mode of transmission
  • Vaccination for HBV does prevent HDV infection.
50
Q

Hepatitis E (pg 844/849)

  • is a partially double stranded DNA virus.
  • is diagnosed via PCR for HEV RNA and detection of serum IgM and IgG antibodies.
  • frequency of chronic liver disease is 80%
  • route of transmission is sexual contact
A

is diagnosed via PCR for HEV RNA and detection of serum IgM and IgG antibodies.

  • is a positive-standed unenveloped RNA virus.
  • frequency of chronic liver disease is: NEVER
  • route of transmission is sexual contact
51
Q

Clinicopathologic syndromes of viral hepatitis do NOT include (pg 850)

  • acute asymptomatic infection with recovery
  • acute symptomatic hepatitis with recovery
  • chronic hepatitis with progression to cirrhosis
  • fulminant hepatitis with recovery
A

fulminant hepatitis with recovery

52
Q
  1. In regards to gallstones
  • a. Cholesterol stones arise exclusively in the gallbladder and consist of 50-100% cholesterol
  • b. About 1% of black stones are radio-opaque
  • c. There are no hereditary factors involved.
  • d. In the west, about 80% are crystalline cholesterol monohydrase and 50% are cholesterol stones
  • e. Rapid weight reduction is not a risk factor for gallstone formation
A

a. Cholesterol stones arise exclusively in the gallbladder and consist of 50-100% cholesterol

  • b. About 75% of black stones are radio-opaque
    • Cholesterol stones - 20%
    • Brown stones - 0%
  • c. There are definitely hereditary factors involved.
  • d. In the west, about 80% are radiolucent, remaining 20% contain enough calcium salts to be radioopaque
  • e. Rapid weight reduction _i**s_ a risk factor for gallstone formation, as is obesity itself
53
Q
  1. Cholelithiasis
  • a. Gallstones always produce symptoms
  • b. Rapid weight loss reduces the risk of gallstones.
  • c. Cholesterol stones are the predominant type of gallstone.
  • d. Brown stones are usually visible on xray.
  • e. Crohn’s disease is associated with the development of gallstones
A

e. Crohn’s disease is associated with the development of pigment gallstones

  • a. Gallstones often dont produce symptoms
  • b. Rapid weight loss increases the risk of gallstones.
  • c. Cholesterol stones are the predominant type of gallstone - In developed nations (90%), but pigment stones more common in Asians
    • ​**Difficult question, as it does not say which is more prevalent worldwide, though it is worded as if cholesterol are
  • d. Black stones are usually visible on xray, brown are not

Pathology (15 decks)

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