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Progress Test > Digestive > Flashcards

Digestive Flashcards

1
Q

What are two key histological findings in Crohn disease?

A
  • Transmural inflammation (mucosa to serosa)

- Non-necrotising granuloma

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2
Q

Why might patients with Crohn disease present with anaemia and/or iron and B12 deficiency?

A
  • Anaemia due to bleeding from chronic inflammation

- Iron/B12 deficiency if small intestine is affected, less efficient absorption

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3
Q

Which part of the GI tract is affected by Crohn disease?

A

Entire tract can be affected, most commonly ileum + colon

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4
Q

What is the most commonly used anti-inflammatory for Crohn disease?

A

5-ASA

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5
Q

Which investigations are most commonly used for structural conditions of the oesophagus?

A

Gastroscopy and barium swallow

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6
Q

Which investigations are most commonly used for functional conditions of the oesophagus?

A

Manometry and pH study

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7
Q

How would a baby with an oesophageal fistula present?

A

Frequent vomiting following feeding

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8
Q

A patient presents with:

  • Heartburn
  • Regurgitation
  • Bitter taste in the mouth
  • Exacerbation when lying down

What GI pathology could this relate to?

A

GORD

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9
Q

What is Barrett’s Oesophagus?

A

Transition from stratified squamous to columnar, glandular epithelium in the oesophagus following chronic acid exposure

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10
Q

What are key symptoms of reflux oesophagitis?

A
  • Pain/discomfort in chest
  • Bleeding (haematmesis)
  • Dysphagia
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11
Q

Chronic GORD can lead to which conditions?

A
  • Reflux oesophagitis
  • Peptic stricutration
  • Oesophageal cancer (AdenoCa)
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12
Q

Anatomically, where are you most likely to find oesophageal SqCC?

A

High in the oesophagus

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13
Q

Which form of oesophageal cancer is associated with smoking, alcohol and poor diet?

A

SqCC

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14
Q

What is Zenker’s diverticulum?

A

A pouch that develops at the weakest portion of the pharynx due to excessive pressure

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15
Q

What are viral causes of oesophageal ulceration?

A

Herpes simplex, cytomegalovirus

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16
Q

What are pill induced causes of oesophageal ulceration?

A

Dioxycycilne and bisphosphonates

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17
Q

What is a characteristic macroscopic feature of eosinophilic oesophagitis?

A

Rings/circles/fissures in the oesophagus

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18
Q

What is achalasia?

A

Degeneration of the myenteric plexus and LOS inhibitory nerve

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19
Q

What causes the ‘bird beak’ appearance of an x-ray of a patient with achalasia?

A
  • Loss of peristalsis in distal oesophagus

- Failure of LOS to relax with swallow

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20
Q

How does scleoderma affect the oesophagus?

A
  • Absent peristalsis
  • LOS has no tone
  • Weak contraction
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21
Q

Why would manometry show high amplitude of contraction for nutracker oesophagus?

A

Normal peristalsis but amplitude of contraction is too strong

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22
Q

Why is vomiting of patients with congenital hypertrophic pyloric stenosis non-billous?

A

Stomach contents do not enter the duodenum due to thickening of pyloric wall

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23
Q

Which gastric tumour produces excess gastrin, causing destruction of gastric mucosa?

A

Gastrinoma

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24
Q

Which cell type is destroyed in pernicious anaemia?

A

Parietal cells

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25
Q

What are the symptoms of peptic ulcer disease?

A
  • Burning epigastric pain
  • Bleeding
  • Perforation
  • Obstruction
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26
Q

Which antibiotics comprise ‘triple therapy’ for peptic ulcer disease?

A
  • Omeprazole
  • Clarithromycin
  • Amoxycillin
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27
Q

Which gastric cells secrete HCl?

A

Parietal cells

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28
Q

Why are cramping and diarrhoea symptoms of rapid gastric emptying?

A

Due to osmotic effect of large particles and fluid in the small intestine

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29
Q

What is the mechanism of H2 antagonists?

A
  • Bind to H2 receptors on parietal cells for histamine

- Prevents parietal cell stimulation

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30
Q

What is the most commonly used H2 receptor antagonist?

A

Ranitidine

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31
Q

Why are H2 antagonists not effective for heartburn/oesophagitis?

A

Don’t allow mucosal healing - acid still secreted

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32
Q

What is the mechanism of action of PPIs?

A

Irreversibly bind to an activated proton pump

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33
Q

What are consequences of prolonged acid inhibition (e.g. chronic use of PPIs)?

A
  • Bacterial overgrowth
  • Lack of sterilisation
  • Impaired absorption
  • ECL hyperplasia
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34
Q

Increase in unconjugated bilirubin would be indicative of what kind of problem?

A

Vascular - bilirubin is not able to travel to the liver to become conjugated

35
Q

What are symptoms of increase in conjugated bilirubin?

A
  • Dark urine

- Obstructive jaundice

36
Q

What causes steatorrhoea?

A

Loss of bile -> inability to break down fats

37
Q

Which type of hepatitis is benign?

A

Hepatitis A

38
Q

What is the incubation period of hepatitis A?

A

2-6 weeks

39
Q

What are the causes of hepatitis A?

A

Poor sanitation and hygiene

40
Q

What is the mechanism of hepatitis B?

A

Viral antigens expressed on hepatocytes -> immune response -> damage of liver cells

41
Q

What is the current treatment for hepatitis C?

A

Direct acting antiviral agents (tablets)

42
Q

What is the mechanism of alcoholic liver disease?

A

Repeat exposure to alcohol -> alterations in lipid metabolism -> decreased export of lipoproteins

43
Q

What is haemochromatosis?

A

Abnormality in iron absorption -> excessive iron deposits on organs

44
Q

What is Budd-Chiari syndrome?

A

Acute thrombosis of hepatic veins -> restriction of blood outflow from liver -> liver damage

45
Q

A patient presents with:

  • Acute, rapidly progressive severe abdominal pain
  • Hepatomegaly
  • Ascites
  • Hepatic encephalopathy

What could be a suspected diagnosis?

A

Budd-Chiari syndrome

46
Q

How is Budd-Chiari syndrome treated?

A
  • Portocaval shunting
  • Anticoagulants
  • Diuretics
47
Q

Which enzyme is affected by Gilbert syndrome?

A

UDP glucuronyl transferase

48
Q

Oesophageal varices, splenomegaly and intestinal congestion are indicative of which kind of portal blood flow restriction?

A

Prehepatic (impaired inflow)

49
Q

Which liver enzymes are indicative of liver inflammation?

A

ALT and AST

50
Q

Which liver enzymes are indicative of biliary/cholestatic pathology?

A

ALP and GGT

51
Q

Which liver enzyme does alcohol induce?

A

GGT

52
Q

Which is more liver specific, ALT or AST?

A

ALT

53
Q

Where is albumin produced?

A

The liver

54
Q

What is the prothrombin ratio?

A

Reflects the rate of clotting factor synthesis

Liver failure or vitamin K deficiency

55
Q

How is excessive ammonia causing encephalopathy treated?

A

Lactulose

56
Q

How does lactulose treat hepatic encephalopathy?

A
  • Converts ammonia into a non-soluble molecule
  • Inhibits ammonia synthesis by bacteria
  • Increases bowel transit
57
Q

What does CEA test for?

A

A cancer marker

58
Q

Why might albumin levels be normal in an acute hepatic pathology?

A

Half life is 3 weeks (not enough time for levels to drop)

59
Q

What is choledocholithiasis?

A

Gall stone blockage in the biliary tree

60
Q

What would be the expected findings of a blood test for a patient with acute cholecystitis?

A
  • Neutrophil leucocytosis

- Raised bilirubin, ALP, GGT

61
Q

Why might a patient with prolonged biliary obstruction be vitamin K deficient?

A

Fat soluble vitamin - loss of bile means fat absorption is impaired

62
Q

What controls enzyme release from the pancreas?

A

CCK

63
Q

What are the most common causes of acute pancreatitis?

A

Alcohol consumption and gall stones

64
Q

Why would oedema be seen on a CT in an individual with acute pancreatitis?

A

Accumulation of fluid -> active enzymes cause fat necrosis -> oedema and local inflammation

65
Q

Which enzymes are expected to be elevated in acute pancreatitis?

A

Serum amylase and lipase

66
Q

How do you treat chronic pancreatitis?

A

Oral administration of pancreatic enzymes

67
Q

What are the symptoms of pancreatic adenocarcinoma?

A
  • Obstructive jaundice
  • Pain
  • Weight loss
  • Pancreatitis
  • Thrombophlebitis
68
Q

What is thrombophlebitis?

A

Blood clotting in a vein causing inflammation and pain

69
Q

Why might IBS occur after an episode of gastroenteritis?

A
  • Disruption of normal gut flora

- Upregulation of nociceptors

70
Q

A patient presents with

  • Swinging bowel habit
  • Abdominal pain relieved by defecation
  • Feelings of incomplete evacuation
  • Abdominal bloating

What could these symptoms be associated with?

A

Irritable Bowel Syndrome (IBS)

71
Q

IBS symptoms should have been present for at least ___ months prior to diagnosis

A

6

72
Q

What is loperamide?

A

An anti-motility drug for bowel frequency

73
Q

What is used for pain management in IBS?

A

Low dose tricyclics

  • Amitriptyline
  • Nortriptyline
74
Q

The genetic mutation in Coeliac disease is HLA ___ and ____

A

DQ2 and DQ8

75
Q

In coeliac disease antibodies are created against ____

A

Gliadin

76
Q

Which histological changes occur in coeliac disease?

A
  • Villous atrophy
  • Hypertrophy of crypts
  • Intraepithelial lymphocytes
77
Q

What is dermatitis herpetiformis?

A

Skin manifestation of coeliac disease

78
Q

Why may individuals with coeliac be iron and/or folate deficient?

A

Due to lack of absorption in the duodenum

79
Q

What is the recommended antibody test for coeliac disease?

A

Anti-TTG

80
Q

Why can small intestinal bacterial overgrowth cause maldigestion?

A

Bacteria deconjugate bile acids so fats cannot be digested

81
Q

What distinguishes ulcerative colitis from Crohn disease?

A

Affects mucosa and submucosa of large intestine only

82
Q

What pattern of inflammation is followed in ulcerative colitis?

A

Circumferential and continuous

83
Q

Ulcerative colitis/Crohn disease shows small ulcers on the gut mucosa (cobblestone appearance)

A

Crohn disease

Progress Test (5 decks)

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