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Jonah's Med Notes > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What is the difference between Dysphagia and Odynophagia?

A

Dysphagia = Difficulty in swallowing

Odynophagia = Pain on swallowing

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2
Q

What are the key questions in Dysphagia?

A

Difficulty in starting swallowing?

Associated symptoms? (regurgitation, change in voice pitch, weight loss)

Solids, liquids, or both?

Intermittent or progressive?

History of heartburn?

Change in eating habits/diet?

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3
Q

What is Barrett’s Oesophagus?

A

Barrett’s oesophagus is a condition characterised by partial replacement of the normal squamous epithelium of the lower oesophagus by a metaplastic columnar epithelium containing goblet cells (intestinal metaplasia).

Barrett’s oesophagus is important clinically because those afflicted are predisposed to oesophageal adenocarcinoma.

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4
Q

How is Barrett’s Oesophagus managed?

A

Acid suppressive therapy with high-dose PPI indefinitely (or surgical fundoplication)

Surveillance gastroscopy every 3 years if no dysplasia

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5
Q

Most likely source of source of a significant gastrointestinal bleed occuring as a complication of peptic ulcer disease?

A

Gastroduodenal Artery

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6
Q

Epigastric pain that is relieved by eating.

A

Duodenal Ulcer - Peptic Ulcer Disease (PUD)

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7
Q

Epigastric pain that is worsened by eating.

A

Gastric Ulcers

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8
Q

Name 3 features of Crohn’s disease over UC (CD)?

A

Upper gastrointestinal symptoms, mouth ulcers, perianal disease

Skip lesions may be present. ‘Cobble stone appearance’

Inflammation in all layers from mucosa to serosa - increased goblet cells, granulomas

Non-bloody diarrhoea

Obstructions and fistulae may occur

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9
Q

Name 5 features of UC over Crohns?

A

Bloody diarrhoea more common
Abdominal pain in the left lower quadrant

Tenesmus - feeling you need to go

Risk of colorectal cancer high in UC than CD

Inflammation always starts at rectum and never spreads beyond ileocaecal valve

Continuous

No inflammation beyond submucosa (Crypt abcesses and pseudopolyps form)

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10
Q

How is synthetic capacity of liver tested? (Liver function)

A

ABC

Albumen

Bilirubin

Coagulation (Prothrombin Time)

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11
Q

What is the problem if ALT, AST > 5x upper limit; and ALP, GGT <5x upper limit?

A

Most likely Hepatocellular damage

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12
Q

What is the problem if ALP, GGT > 5x upper limit; and ALT, AST <5x upper limit?

A

Most likely Obstructive

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13
Q

What are the risk factors for PUD? (4)

A

NSAID use

H Pylori infection

Smoking

Hx, Fam Hx.

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14
Q

What are 90% of duodenal ulcers also positive for?

A

H. pylori

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15
Q

How is PUD investigated?

A

Endoscopy -> gold standard. Must biopsy due to malignancy risk.

FBC, EUC -> ~anaemia, malabsorption

H. Pylori Investigation

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16
Q

How is H. Pylori investigated? (3+3)

A

Non-invasive:

Urea breath test -> highly specific + sensitive. Expensive.

Serology -> rapid, but lacks specificity + no Ddx b/w past and current infection.

Faecal antigen testing -> cheap, specific (>95%)

Invasive (w/ antral biopsy):

Histology -> specific. False -ve’s, time.

Rapid urease tests -> cheap, quick, specific. Poor sensitivity.

Culture -> gold standard. Slow, laborious, insensitive.

Histology -> specific.

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17
Q

What are the ddxs of PUD?

A

Coeliac disease

Gastric cancer

Chronic pancreatitis

Biliary disease

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18
Q

How is PUD treated?

A

Heal ulcer -> H. Pylori eradication. PPI 8-12wks.

Maintenance therapy (reduce risk) -> stop NSAIDs, smoking. PPI/H2RA in some.

Treat complications -> surg.

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19
Q

How is H. Pylori treated?

A

Eradication of H. Pylori - Triple therapy:

2x Abx, 1x PPI

Amoxycillin + clarithromycin + esomeprazole. ~1wk.

Confirm eradication w/ breath test

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20
Q

What are the signs of impaired liver function?

A

Jaundice -> poor bilirubin clearance

Encephalopathy -> failure to clear by-products of metabolism

Bleeding -> impaired clotting factors

Hypoglycaemia

21
Q

What are the signs of Chronic liver injury?

A

Catabolic status (+/- poor nutrition)

  • Skin thinning*
  • Loss of muscle bulk*
  • Leukonychia*

Impaired albumin synthesis -> reduced oncotic pressure

Reduced aldosterone clearance -> Na+ retention

Reduced oestrogen clearance -> mild feminisation

22
Q

What are ascites?

A

Accumulation of free fluid in peritoneal cavity. -> distension, shifting dullness. ~hernia, abdominal vein distension.

23
Q

What are the causes of ascites?

A

Common

Cardiac failure, hepatic cirrhosis (2nd to splanchnic v. dilation), malignant hepatic/peritoneal disease.

Others:

Pancreatitis, lymph obstruction, hepatic vein obstruction (Budd-Chiari, veno-occlusive disease), infection.

Hypoproteinaemia -> nephrotic syndrome, malnutrition, protein losing enteropathy.

24
Q

What are the current alcohol guidelines?

A

No more than 2 a day and no more than 4 on a single occasion.

25
Q

What is NAFLD made up of?

A

Simple steatosis (Fatty Liver) and non-alcoholic steato-hepatitis (NASH)

26
Q

How is fatty infiltration of the liver confirmed?

A

Ultrasound, MRI or Liver Biopsy

27
Q

What co-morbidity most commobly exists with NAFLD?

A

Metabolic Syndrome

28
Q

What is the management of NAFLD?

A

Weight control

Reduction in cardiovascular risk factors such as smoking, diabetes,
hypertension and dyslipidaemia.

Referral to Cardiologist, Dietician, Endocrinologist

Statins

29
Q

Which is more common in Australia - IBS or IBD?

A

IBS (approx. 50 times more)

30
Q

What suggests IBD over IBS? (5)

A

Weight loss
Elevated C-reactive protein (CRP)
Nocturnal diarrhoea (especially if wakes patient
from sleep)
Blood in stools
Fever
Obstructive symptoms
Anaemia
Iron deficiency
Low albumin.

31
Q

Which are more likely to have fistulas - Crohns or UC?

A

Crohns

32
Q

What is smoking a risk factor for - Crohns or UC?

A

Crohns

Protective in UC

33
Q

Which is more likely to have bloody + mucus diarrhoea - Crohns or UC?

A

UC

34
Q

What are 5 possible signs of Crohns on physical?

A
  • *Iron deficiency anaemia ->** Koilonychia, pallor, angular stomatitis, glossitis
  • *Abdo ->** tenderness + masses (inflammation)
  • *Perianal ->** skintags, fissures, fistulas

MSK -> arthritis, osteoporosis.
Crohn’s w/ HLA-B27 -> sacroilitis + ank spond
Eye -> conjunctivitis, iritis, uveitis
Erythema nodosum - red lumps on shins
Hepatobiliary:
Primary sclerosing cholangitis
Fatty liver
Autoimmune hepatitis
Haem:
VTE + ATE
Autoimmune haemolytic anaemia

35
Q

What is first line therapy for IBD?

A

Mesalazine - 5-aminosalicyclic acid (5-ASA)

36
Q

What is Adalimumab and when is it used?

A

TNF inhibitor

Used in IBD, RA, other HLAB27s

37
Q

Name 4 different drug types used for IBD flaires?

A

Aminosalicylates (5-ASA)
Corticosteroids
Immunomodulators (azathioprine, 6-mercaptopurine
and methotrexate)
Biologic agents (infliximab, adalimumab, vedolizumab
and ustekinumab)
Antibiotics (metronidazole, ciprofloxacin and others).

38
Q

What 3 complications of IBD should be monitored?

A

Osteoporosis
Iron deficiency anaemia
Colon cancer

39
Q

What is the most common cause of acute nausea/vomiting?

A

Viral gastroenteritis or bacterial food poisoning.

40
Q

What are serious causes of nausea and vomiting not to be missed? (5_

A

Surgical causes
• Pancreatitis
– cholecystitis
– appendicitis
– small bowel obstruction
• Diabetic ketoacidosis
• Addisonian crisis
• Raised intracranial pressure (usually with other neurological features)
• Hepatitis
• Ingestion of irritants/allergens

41
Q

How should acute nausea and vomiting be investigated?

A

Electrolytes and renal function
Full blood count
Pancreatic and liver enzymes
Glucose.

42
Q

What investigations could be considered in chronic nausea and vomiting?

A
43
Q

The two most common causes of acute pancreatitis are:

A

Gallstones and Alcohol

44
Q

How is acute pancreatitis diagnosed?

A

Diagnosis is established by the presence of two of the
three criteria:

  • acute upper abdominal pain;
  • serum amylase and/or lipase levels greater than three
    times the upper limit of normal; and/or
  • findings on CT, MRI, or ultrasound
45
Q

What is more specific in Acute pancreatitis?

A

Lipase - if 3x upper limit suggestive

46
Q

Why is serum calcium important in Acute Pancreatitis?

A

Hypercalcemia may cause pancreatitis, which may then, in turn, cause hypocalcemia!

47
Q

What is the management of Acute Pancreatis?

A

“PANCREAS”

Perfusion (fluid replacement), Analgesia, Nutrition, Clinical (observation), Radiology (imaging), ERC (endoscopic stone extraction), Antibiotics, Surgery (surgical intervention, if necessary).

48
Q

How is Liver Cirrhosis Assessed?

A

A - Albumin

B - Bilirubin

C - Coagulations (PT)

Ascites and Encephalopathy

49
Q
A

Jonah's Med Notes (8 decks)

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