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ACEM Viva > Pathology - GI > Flashcards

Pathology - GI Flashcards

1
Q

What are the causes of chronic gastritis

A

h pylori
chronic bile reflux
nsaid
autoimmune
allergic response
radiation
stress
coffee, alcohol

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2
Q

Describe the features and complications of h pylori induced chronic gastritis

A
  • predominantly antral
  • characterised by increased acid production
  • bacteria secretes urease which generates ammonia (used to detect presence)
  • bacteria makes phospholipases that damage surface of epithelial cells, disrupting normal mucosal defense mechanisms

complications: peptic ulcer disease, bleeding, perforation, obstruction, gastric adenocarcinoma, gastric lymphoma

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3
Q

By what mechanisms may h pylori cause peptic ulcers

A 
H. pylori contributes to peptic ulcers by weakening the mucosal barrier, inducing inflammation, increasing acid production, releasing toxins, and interfering with the healing process.
  • secretion of urease which generates ammonia
  • production of phospholipase that directly damages epithelial cell surface
  • enhancement of gastric acid secretion
  • h pylori proteins are immunogenic and evoke a strong inflammatory response
  • release toxins, directly damage mucosal cells
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4
Q

What complications may arise from peptic ulcer disease

A
  • bleeding = 25% of ulcer deaths, most common complication (15-20% of patients)
  • perforation = 5% of patients, 2/3 of ulcer deaths
  • obstruction = 2% of patients, from oedema and scarring due to pyloric ulcer
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5
Q

What are the pathological features and complications of crohns disease

A
  • transmural inflammation occurring anywhere in the GI tract
  • skip lesions are sharply delineated disease areas with sparing of interspersed mucosa
  • non-caseating granulomas and fibrotic strictures and fistulas may be present

complications: strictures, fistulas, malabsorption syndrome, extra-intestinal manifestations, neoplasia (adenocarcinoma)

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6
Q

What are the extra-intestinal manifestations of crohns disease

A

cholangitis
migrating polyarthritis
sacroiliitis
ankylosing spondylosis
erythema nodosum
uveitis

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7
Q

What are the pathological features of ulcerative colitis

A

-ulcerating inflammation extending only into mucosa and superficial submucosa
-limited to colon and rectum, does not involve small bowel, no skip lesions
-ulcers are superficial and broad based, no fistulas
-inflammatory pseudopolyps and crypt abscesses are present, no granulomas

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8
Q

Extra-intestinal manifestations of ulcerative colitis and Complications

A

extra-intestinal manifestations: same as crohns disease, more common in ulcerative colitis

complications: toxic megacolon, primary sclerosing cholangitis, neoplasia

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9
Q

What are the common causes of bowel obstruction

A

adhesion
hernia
malignancy
volvulus
intussusception
mesenteric infarct
strictures

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10
Q

How does a hernia form and cause a bowel obstruction and describe the important clinical sequelae of ongoing obstruction

A

-weakness or defect in the abdominal wall allows for protrusion of serosa lined pouch of peritoneum (hernia sac)
-viscera (small bowl, large bowel, omentum) may then protrude through the area of weakness
-viscera may get entrapped in the hernia sac if narrow necked
-ongoing obstruction leads to venous stasis and edema, leading to incarceration and strangulation and ischaemia

complications: perforation, ischaemia, sepsis, abscess, electrolyte disturbance, death

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11
Q

What conditions can lead to infarction of bowel

A

1) Occlusive ischaemia:
-arterial thombosis = atherosclerosis, vasculitis, aortic dissection, OCP
-arterial embolism = endocarditis, aortic thromboembolism
-mesenteric venous thrombosis = hypercoagulation state, OCP, post operation
-mechanical = volvulus, stricture

2) Non-occlusive ischaemia:
-shock, cardiac failure, dehydration

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12
Q

What parts of the bowel are most susceptible to ischaemic injury

A

-watershed zones are areas located at the end of arterial supply = splenic flexure, sigmoid colon, rectum
-villi are more at risk than crypts

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13
Q

Describe the intestinal response to an acute ischaemic insult

A

1) initial hypoxic injury
-at onset of vascular compromise, epithelial cells lining intestine are relatively resistant
2) reperfusion injury
-initiated by restoration of blood supply, due to leakage of gut lumen bacterial products into systemic circulation
-characterised by free radical production and neutrophil infiltration

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14
Q

Describe the morphology of acute ischaemic bowel injury

A

-initial congestion, followed by edema and haemorrhage in wall
-lumen contains bloody fluid
-coagulative necrosis of muscularis propria occurs in 1-4 days, during which time perforation may occur
-neutrophils present at time of reperfusion
-bacterial superinfection
-metabolic and cardiovascular derangement

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15
Q

What are the clinical features and outcomes of ischaemic bowel

A

clinical: severe pain, tenderness, peritonism, nausea, vomiting, bloody diarrhoea, shock, sepsis

outcomes: strictures, segmental patchy mucosal degeneration, death

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16
Q

What are the common causes of infective gastroenteritis

A

-viral: rotavirus (most common cause of diarrhoea in children), adenovirus, norovirus
-bacterial:
ingestion of preformed toxin = staph aureus, cholera
ingestion of toxigenic organism that proliferates in lumen and forms enterotoxin = enterotoxic e coli, vibrio cholerae
infection by enteroinvasive oragnisms = shigella, salmonella
-parasites: giardia lamblia, entamoeba histolytica

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17
Q

What is the difference between endotoxin and exotoxin

A

-endotoxin: LPS in outer membrane of gram negative bacteria, cause injury via the host immune response

-exotoxin: proteins secreted by bacteria that cause direct injury

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18
Q

What is the causative organism of cholera and describe the pathogenesis

A

-cholera is caused by vibrio cholerae, a gram negative bacteria, non-invasive, has flagella proteins for attachment
-transmitted by drinking contaminated water and causes secretory diarrhoea (rice water)
-vibrio does not enter epithelia cells itself, but produces a pre-formed cholera enterotoxin:
1) B subunit binds to intestinal epithelial cells
2) A subunit transfer to cytoplasm, act on G protein, cause CFTR to open and Cl- secretion into lumen and massive water shift

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19
Q

What bacterial class does escherichia coli belong to and what types of infections can they cause

A

-e coli is a gram negative rod, facultative anaerobe, normal GI pathogen

infections: UTI, prostatitis, epididymo-orchitis, infectious enterocolitis, cholecystitis, bacterial peritonitis

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20
Q

List the e coli enteritis types and describe their features

A

-ETEC = enterotoxic, produce a toxin, causes travellers diarrhoea
-EPEC = enteropathogenic, causes endemic diarrhoea
-EHEC = enterohaemorrhagic, produces a shigella like toxin, causes bloody diarrhoea
-EIEC = enteroinvasive, not toxin producing, invades epithelial cells and causes colitis
-EAEC = enteroaggregative, produce shigella like toxin, cause non-bloody diarrhoea

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21
Q

What is pseudomembranous colitis, the risk factors for developing and the clinical features

A

-formation of pseudomembrane (adherent layer of inflammatory cells and debris) overlying mucosal injury
-associated with antibiotic use causing disruption of normal flora and overgrowth of bacteria
-epithelial denudation, lamina propria with infiltrate of neutrophils and damaged crypts coalesce to form pseudomembrane
-caused by c diff, salmonella, c perfringens and staph aureus

risks: advanced age, hospitalisation, antibiotic treatment

clinical: fever, leukocytosis, abdominal pain, watery diarrhoea

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22
Q

What are the c diff toxins

A

Toxin A = stimulates chemokine production and recruitment of leukocytes
Toxin B = causes cytopathic effects and is used to diagnose c diff

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23
Q

What type of bacteria is salmonella and describe the pathogenesis and clinical features of typhoid fever

A

-gram negative bacillus, flagellated, food and water born, cause typhoid fever and non-typhoid fever infections

-typhoid fever pathogenesis: cause by salmonella typhi and paratyphi
travel in India, Mexico, Phillipines, Pakistan, humans only reservoir, transmission through contaminated food and water
organisms are resistant to gastric acid and invade M cells and disseminate via lymphatics and blood vessels
infection causes expansion of Peyers patches and draining nodes, liver shows typhoid nodules
-typhoid fever clinical: initial dysentery followed by bacteraemia, fevers, abdominal pain

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24
Q

What is the causative organism and pathogenesis of salmonella dysentery (gastroenteritis)?

A
  • Cause: Salmonella enteritidis and typhimurium
  • Pathogenesis: ingestion, adhesion invades epithelium (type III secretion system to inject effector protein), taken up by macrophages, gut wall inflammation, activates neural reflex pathway (adrenergic, host protective mechanism) , abdo pain/diarrhoea to wash out the infection
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25
Q

What are the clinical features of liver failure

A

-jaundice, icterus, pruritis, fetor hepaticus, palmar erythema, spider angiomata, hypogonadism, gyanecomastia

-encephalopathy, coagulopathy, hepatorenal syndrome, hepatopulmonary syndrome, portal hypertension

26
Q

What are the causes of acute liver failure

A

A (acetaminophen, hep A)
B (hep B)
C (hep C)
D (hep D, drugs such as tetracyclines)
E (hep E)
F (fatty change)

27
Q

What is hepatorenal syndrome

A

-renal failure in a patient with severe chronic liver disease and no obvious cause of renal failure, exact mechanism complex/not fully understood, likely due to renal ischaemia
-features: Na+ retention, impaired water excretion, decreased renal perfusion and GFR

28
Q

What are the causes and clinical consequences of portal hypertension

A

causes:
1) pre-hepatic = thrombosis, splenomegaly, portal vein narrowing
2) hepatic = cirrhosis, massive fatty change
3) post-hepatic = right sided heart failure, constrictive pericarditis, hepatic vein obstruction

consequences: ascites, portosystemic shunts, splenomegaly, hepatopulmonary syndrome, portopulmonary HTN

29
Q

What are the mechanisms involved in the formation of ascites?

A
  • hepatic sinusoidal hypertension (elevated hydrostatic pressure)
  • hypoalbuminaemia (reduced oncotic pressure)
  • percolation of hepatic lymph into peritoneal cavity
  • systemic and splanchnic vasodilation: activation of RAAS leads to renal retention of sodium and water
30
Q

Describe the pathological features of the liver in alcoholic liver disease and which are reversible

A

1) hepatic steatosis: reversible, fatty change marked by microvesicular lipid droplets within hepatocytes
2) alcoholic hepatitis: reversible, liver cell necrosis, Mallory body formation and inflammation
3) cirrhosis: irreversible, bridging fibrosis, parenchymal nodules, destruction of parenchymal architecture
4) hepatocellular carcinoma

31
Q

What are the morphological features of cirrhosis

A

Occurs diffusely throughout the liver
featured by:
- parenchymal nodules made of regenerating hepatocytes
- surrounded by dense bands of fibrous scar
- disorganised architecture
- vascular and portosystemic shunting
- elements of progression and regression

32
Q

What are the possible causes and sequelae of cirrhosis

A

cause: alcoholic liver disease, viral hepatitis, biliary disease

outcome: portal HTN, bleeding, hepatic failure, coagulopathy, HCC, hepatorenal syndrome, encephalopathy

33
Q

What changes occur at the cellular level in alcoholic hepatitis

A

hepatocyte swelling and necrosis
mallory-denk body formation
neutrophilic reaction
fibrosis

34
Q

In the end stage of alcoholic liver disease, what are the potential causes of death

A

hepatic failure and coma
massive GIT bleed
intercurrent infection
hepatorenal syndrome
hepatocellular cancer

35
Q

What is the causative agent of hepatitis A and how is it transmitted, diagnosed, clinical course and outcomes

A

cause: hepatitis A virus, single stranded RNA virus

transmission: faecal to oral route

diagnosis: anti-HAV IgM in serum indicates acute infection

course: incubation period of 2-6 weeks
-faecal shedding of anti-HAV IgM for 2-12 weeks (presence indicates acute infection, persists for months))
-IgG appears as IgM declines and persists for years (conferring lifelong immunity)

clinical features: mild febrile illness, nausea and vomiting, lethargy, dehydration, rarely fulminant hepatitis
outcomes: vaccine available, does not cause chronic liver disease, no carrier state, no association with HCC

36
Q

What is the causative agent of hepatitis B and how is it transmitted, diagnosed and clinical course and outcomes

A

cause: hepatitis B virus, double stranded DNA virus

transmission: parenteral, sexual contact, perinatal during child birth, blood transmission

diagnosis: anti-HBV IgM indicates active or recent infection

course: incubation period of 2-26 weeks
-HBsAg (surface antigen) = appears before symptoms, declines over months, presence indicates carrier state
-HBeAg (viral protein) = present during active infection, persistence indicates chronic infection

clinical features: 65% subclinical, cirrhosis and coagulopathy may lead to upper GI bleeding
outcomes: self-limiting with recovery, chronic with cirrhosis, fulminant with necrosis, HCC

37
Q

How does hepatitis B lead to upper GI bleeding

A

-cirrhosis and portal hypertension leading to oesophageal varices
-coagulopathy due to loss of synthetic function

38
Q

What are the complications of hepatitis B induced cirrhosis

A

jaundice
hepatorenal syndrome
hepatic encephalopathy
splenomegaly
HCC

39
Q

What is the causative agent of hepatitis C and how is it transmitted, diagnosed and clinical course and outcomes

A

cause: hepatitis C virus, single stranded RNA

transmission: IVDU, multiple sexual partners, needle stick, unknown

diagnosis: anti-HCV antibodies or PCR

course: incubation period of 4-26 weeks
-HCV RNA in blood for 1-3 weeks during acute infection
-anti-HCV antibodies occur in most acute infections

outcomes: potentially curable, most common cause of liver disease, cirrhosis, fulminant hepatitis is rare

40
Q

What features of hepatitis C make developing a vaccine difficult

A

highly stable core with extremely variable envelop
genomic and antigenic variability
frequent mutations

41
Q

What is the causative agent of hepatitis D and how is it transmitted, diagnosed and clinical course and outcomes

A

cause: hepatitis D virus, single stranded RNA

transmission: parenteral

diagnosis: anti-HDV antibodies and PCR

course: incubation period of 2-26 weeks
-HDV RNA in blood before and during early infection
-IgM anti-HDV indicates recent exposure (most reliable marker)
-IgM anti-HBAg suggests acute HBV co-infection

outcomes: can only cause infection when also have HBV, may develop chronic liver disease

42
Q

How does hepatitis D cause hepatitis

A

-hepatitis D virus is defective and can only cause infection when it is encapsulated by HBsAg
-superinfection occurs if patient is a HBV carrier

43
Q

What are the clinical syndromes possible following exposure to hepatitis in a patient without immunity

A

1) Acute asymptomatic infection with recovery
2) Acute symptomatic infection with recovery
-phases = incubation, symptomatic pre-icteric, symptomatic icteric, convalescence
-symptoms = constitutional, serum sickness, liver symptoms
3) Chronic hepatitis
-symptoms or relapsing disease for 6 months or more
-may be non-progressive, progressive to cirrhosis or asymptomatic carrier
4) Fulminant hepatitis
-develops over 2-3 weeks with necrosis and encephalopathy

44
Q

Describe the morphology of acute hepatitis

A
  • acute enlarged red (green) liver, injured hepatocytes are eosinophilic and rounded with shrunken nuclei
  • kupffer cell hyperplasia, portal tract inflammation
  • scant mononuclear infiltrates, ballooning degeneration, macrophage aggregates, cholestasis
45
Q

What are the risks for developing cholesterol stones and what is the pathogenesis

A

risks: age>80, women>men, genetics, pregnancy, obesity, rapid weight loss

pathogenesis: requires 4 conditions:
1) bile supersaturated with cholesterol
2) gallbladder hypomobility
3) cholesterol nucleation in bile
4) mucus hypersecretion traps crystals, permitting aggregation into stones

46
Q

What is the pathogenesis of acute calculous cholecystitis

A
  • overall chemical irritation of gallbladder by retained bile acids leading to an inflammatory response
  • mucosal phospholipases hydrolyse luminal lecithins to toxic lysolecithins
  • protective mucus layer is disrupted, allowing bile salts to have detergent action on exposed mucosal epithelium
  • prostaglandins contribute to inflammation
  • gallbladder dysmotility causes distension and increased intraluminal pressure
  • compromising blood flow
  • bacterial infection may follow
47
Q

How does acalculous cholecystitis differ from calculous cholecystitis?

A
  • rarer, seen in predisposed individuals, slower process
  • due to reduced blood flow in cystic artery circulation (end arteries) causing ischaemia
  • other promoting features: sludging micro-crystals, stasis, local inflammation, distension, sepsis, trauma
48
Q

What conditions are associated with acute acalculous cholecysitis

A

post-operation major surgery
severe trauma
severe burns
sepsis
post-partum

49
Q

What are the clinical features of cholecystitis

A

right upper quadrant pain, epigastric pain, mild fever, anorexia, tachycardia, sweating, nausea, vomiting

50
Q

How are the clinical features of acalculous different from calculous cholecytitis

A

-calculous: often more sudden but can be mild and self-limiting
-acalculous: insidious, may have no GB symptom, usually in patients with other illness, higher risk of complications

51
Q

What are the complications of cholecystitis

A

bacterial infection, cholangitis, sepsis, perforation, biliary fistula

52
Q

Outline the normal metabolism and elimination of bilirubin

A

-bilirubin is produced from heme breakdown
-binds to serum albumin for transport to liver as unconjugated bilirubin
-taken up by liver and conjugated to water soluble form
-conjugated bilirubin is secreted into bile and then into the intestine
-3 outcomes in the intestine after deconjugation to urobilinogens by bacteria
1) reabsorption in ileum and colon and returned to liver
2) small amount reabsorbed and excreted in urine
3) oxidised by bacteria to stercobilin and excreted in faeces

53
Q

What are the causes of jaundice

A

1) Unconjugated (indirect) hyperbilirubinaemia: water insoluble, uncharged
-excess bilirubin production = haemolytic anaemia, pernicious anaemia, thalassemia
-reduced hepatic intake = hepatitis, cirrhosis
-impaired conjugation = physiological jaundice of newborn (because liver is not mature)

2) Conjugated (direct) hyperbilirubinaemia: water soluble, charged
-decreased hepatocellular excretion = drug induced dysfunction, damage from infection (hepatitis)
-impaired intra/extra-hepatic bile flow = gallstones, primary sclerosing cholangitis, biliary atresia, malignancy
-hereditary syndromes = dublin syndrome

54
Q

What are the causes of pancreatitis

A
  • metabolic: ETOH, hypercalcaemia, drugs (frusemide, thiazide diuretics)
  • mechanical: gallstones, trauma, ERCP
  • genetic: mutation in trypsin genes, autoimmune, CF
  • gender: males more than females
  • vascular: shock, atheroembolism
  • infection: mumps, coxsachie virus, helminth infection
55
Q

What is the pathogenesis of pancreatitis

A

-overall inappropriate release and activation of pancreatic enzymes leading to autodigestion of pancreatic substance
-due to the activation of trypsin from trypsinogen, which causes downstream activation of inflammatory mediators
-3 mechanisms for initiation of pancreatic enzyme activation:
1) pancreatic duct obstruction
2) primary acinar cell injury by alcohol, mumps, trauma, drugs
3) defective intracellular transport of proenzymes within acinar cells

56
Q

Describe the morphology of pancreatitis

A

oedema due to vascular leakage
fat necrosis
acute inflammation
proteolytic destruction of pancreatic substance
necrosis

57
Q

What are the complications of pancreatitis?

A

Acute pancreatitis:

Locally
- necrotising pancreatitis/diffuse fat necrosis
- infection
- fluid sequestration
- bleeding/haemorrahge

Systemic
- SIRS/shock/death
- ARDS
- Renal ATN
- Haemolysis/DIC

Chronic pancreatitis:
- pancreatic insufficiency
- diabetes
- strictures/obstructions
- pancreatic pseudocyst

58
Q

What are the lab findings of acute pancreatits

A

raised amylase in first 24 hours
raised lipase in 72-96 hours
hypocalcaemia
glycosuria
metabolic acidosis

59
Q

What are the morphological features of chronic pancreatitis

A

-replacement of pancreatic acinar tissue with fibrous connective tissue
-sparing of islet of langerhans cells until late stage
-pancreas becomes hard with focal calcification
-duct dilatation

60
Q

What are the clinical consequences of chronic pancreatitis?

A
  • silent or recurring attacks of pain or jaundice
  • precipitated by ETOH
  • malabsorption/steatorrhea, diabetes, pseudocyst

ACEM Viva (39 decks)

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