Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2 v2 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is ischaemic bowel disease?

A
  • Ischaemia/infarction in the GI tract due to reduced blood flow.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two most common causes of mesenteric ischaemia?

A
  • Embolism (over 50%)

- Hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which artery is most commonly occluded in mesenteric ischaemia?

A
  • Superior mesenteric artery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 main types of ischaemic bowel disease?

A
  • Acute mesenteric ischaemia.
  • Chronic mesenteric ischaemia.
  • Colonic ischaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do both acute and chronic mesenteric ischaemia present?

A

Abdominal pain out of proportion to the clinical findings.

- Acute will be rapid onset, whereas chronic will be insidious.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the presentation of colonic ischaemia?

A
  • Bloody, loose stools (due to mucosal damage).

- Usually left sided abdominal pain/tenderness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How are colonic ischaemia and mesenteric ischaemia differentiated?

A
  • Bloody stools indicative of colonic ischaemia rather than mesenteric.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the first line investigation for suspected bowel ischaemia?

A
  • CT scan.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the treatment for ischaemic bowel disease?

A
  • Fluids + oxygen.
  • Consider antibiotics (if there is perforation of the mucosal wall, gut flora can spread and cause infection).
  • Surgical intervention (bowel reconstruction/segment resection).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the investigations used for perianal disorders?

A
  • DRE + physical exam.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the four main types of perianal disorder? Brief description of each.

A
  • Haemorrhoids. Enlarged/swollen hemorrhoidal cushions so they protrude outside the anal canal.
  • Perianal abscess. Infection of the soft tissues around the anus.
  • Perianal fistula. Tunnel between the anus and the perianal skin.
  • Anal fissure. Split perianal skin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the clinical presentation of haemorrhoids?

A
  • PAINLESS rectal bleeding.

- Pain on shitting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the two types of haemorrhoids?

A
  • Internal or external.

- Differentiated by position in relation to the dentate line.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the treatment for haemorrhoids?

A
  • Increased dietary fibre.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the presentation of perianal abscess?

A
  • Perianal pain.

- Fever common (infective element).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What disease is commonly associated with perianal abscess/anal fistula?

A
  • Crohn’s disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is perianal abscess treated?

A
  • Abscess drainage.

- NOT ANTIBIOTICS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is usually the proceeding condition for an anal fistula?

A
  • Perianal abscess.

- When drained, may leave an anal fistula in its place.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical presentation of anal fistula?

A

Blood and pain on shitting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is an anal fistula treated?

A

Surgery. Normally a fistulostomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the clinical presentation of an anal fissure?

A
  • Pain on shitting (like glass)
  • Burning pain 1-2 hours after.
  • Small amount of bright-red blood on surface of stool
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is anal fissure treated?

A

GTN (topical) until fissure resolves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is pilonodial disease?

A
  • Hair follicles become inserted into the skin at the crease of the buttocks, creating a sinus/cyst.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Who is most likely to be affected by pilonodial disease?

A
  • Men aged 18-40.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the treatment for pilonodial disease?

A

If asymptomatic:
Keep area clean and hair free (shave/laser hair removal).

If symptomatic:
Consider surgical sinus excision.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is gastritis?

A
  • Stomach lesions that involve gastric mucosal inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is gastropathy?

A
  • Stomach lesions that with little to no evidence of mucosal inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the most common causes of gastritis?

A
  • H. Pylori infection.
  • Alcohol use.
  • NSAID use.
  • Autoimmune gastritis (but this is rarer).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What us the pathophysiology of autoimmune gastritis?

A
  • Anti-parietal cell antibodies (ACAs) and anti-intrinsic factor (IFAs) are produced, which stimulate inflammation and necrosis of the parietal cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the diagnostic factors for gastritis?

A
  • Presence of risk factors.
  • Dyspepsia (indigestion).
  • Epigastric discomfort.

BE AWARE OF RED FLAG SYMPTOMS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the risk factors for gastritis?

A
  • H. Pylori infection.
  • NSAID use.
  • Alcohol abuse.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What investigations are used if H.Pylori gastritis is suspected?

A

1st line - Urea breath test or Faecal antigen testing.

GOLD STANDARD - Endoscopy + mucosal biopsy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the investigation used for NSAID/alcohol-induced gastritis?

A
  • None needed.

- Stop NSAID or alcohol, and see if symptoms improve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What investigations are used for autoimmune gastritis?

A
  • IFAb (Intrinsic factor antibody) testing. Will be +ve in autoimmune gastritis.
  • Serum B12 (reduced in B12 deficiency, a common complication of gastritis).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the treatment for H.Pylori gastritis?

A
  • Triple therapy (Omeprazole + amoxicillin + clarithromycin) for 14 days.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the treatment for NSAID/Alcohol gastritis?

A
  • If possible, stop NSAIDS/alcohol use.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the treatment for autoimmune gastritis?

A
  • GIve B12 supplementation IM/IV.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the common complication of gastritis? Which forms of gastritis cause it?

A
  • Peptic ulceration.

- Caused by H. pylori and NSAID forms of gastritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is diverticular disease?

A
  • Refers to the presence of diverticula.

- These are small herniated portions of bowel that span through the mucosa, submucosa and muscle in the bowel wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is diverticulitis?

A
  • Inflammation of the diverticula, usually due to infection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are pseudodiverticula?

A

Diverticula that have not breached the muscle wall, only the mucosa and submucosa.

42
Q

What is the clinical presentation of diverticulitis?

A
  • Left lower quadrant pain (including guarding and tenderness).
  • Fever.
  • Painless rectal bleeding.
43
Q

What are the risk factors for diverticular disease?

A
  • Over 50.

- Low fibre diet.

44
Q

What are the investigations used for diverticular disease?

A
  • FBC with differential. POLYMORPHONUCLEAR LEUKOCYTOSIS.
  • CRP raised. (marker of acute inflammation).

IF ACUTE DIVERTICULITIS SUSPECTED:
- 1st line is contrast CT (provided kidney function is adequate).

45
Q

What is the management of diverticular disease?

A

If just diverticulosis: Increase fibre in diet + paracetamol (if symptomatic).

If acute diverticulitis: Amoxicillin +clavulanate (for infection) and paracetamol (for analgesia).

AVOID NSAIDS IN DIVERTICULITIS - THEY INCREASE RISK OF BOWEL PERFORATION.

46
Q

What is the histological presentation of coeliac disease?

A
  • Villous atrophy with crypt hyperplasia.
47
Q

What is appendicitis?

A
  • Acute inflammation of the appendix, most likely due to blockage of the lumen.
48
Q

What is the clinical presentation of appendicitis?

What is the sign associated with appendicitis?

A
  • Severe, acute umbilical pain that migrates to the right iliac fossa.
  • Vomiting/nausea.
  • Rovsing’s sign. Tenderness in the RIF on palpation of the LIF.
49
Q

What are the risk factors for appendicitis?

A
  • Low fibre diet (increased risk of faecolith formation due to constipation).
  • Improved hygiene (reduces the functionality of the gut flora).
  • Smoking.
50
Q

What is the pathophysiology of appendicitis?

A
  • Blockage of the appendix lumen.
  • Mucus builds up behind the blockage, causing an increased pressure inside the appendix.
  • Bacteria (normally E. coli) multiply in the appendix..
51
Q

What are the investigations used for appendicitis?

A
  • FBC - High WCC.
  • CRP - Raised (marker of acute inflammation).

Consider imaging (MRI abdomen, CT abdomen).

52
Q

What is the treatment for appendicitis?

A
  • 1st line for most is laparoscopic appendectomy.

- Prophylactic dose of antibiotics should be given prior to the surgery (just one dose).

53
Q

What is Gilbert’s disease?

A

An inherited condition where the unconjugated bilirubin is high due to deficiency of conjugating enzymes in the liver.

Characterised by ISOLATED raised bilirubin.

54
Q

What are the characteristic features of Crohn’s disease?

A
  • Transmural inflammation of the GI tract.
  • Contains skip lesions.
  • Cobblestone appearance.
  • Can occur anywhere in the GI tract.
  • Contains non-ceasating granulomas.
55
Q

What is the clinical presentation of Crohn’s disease?

A

Can be very generalised due to the potentially diffuse nature of the disease. Symptoms include:

  • Abdominal pain (RIF commonly).
  • Prolonged diarrhoea (may be bloody or non-bloody).
  • Fatigue (malnutrition).
  • Perianal lesions (present in 25% of Crohn’s patients).
56
Q

What are the risk factors for Crohn’s disease?

A
  • FH of Crohn’s.

- White.

57
Q

What investigations are commonly used for Crohn’s disease?

A
  • ESR/CRP - Raised due to active inflammation.
  • Faecal calprotectin - +ve in IBD (excludes IBS).

GOLD STANDARD - Colonoscopy + biopsy of mucosa. Look for classical histological signs of Crohn’s. This is diagnostic.

58
Q

What is the treatment for Crohn’s disease?

A

Inducing relapse:
1st line - Prednisolone.
2nd line - Add azathioprine (DMARD) or infliximab (tnf-a inhibitor).

Maintaining relapse:
1st line: azathioprine (DMARD).
If infliximab (tnf-a inhibitor) worked particularly well, consider continuation of that.
59
Q

What are the common differentials for Crohn’s disease? How are they different?

A

UC:

  • UC is limited to mucosa, continuous, no non-ceasating granulomas.
  • UC always involves the rectum, Crohns may do but no guarantee.
  • UC is more likely to cause left abdominal pain (descending colon).

IBS:

  • Negative faecal calprotectin.
  • Pain relieved by defecation.
  • No blood in stool.
60
Q

What are the common complications of Crohn’s disease?

A
  • Anaemia (due to malabsorption).
  • Bowel obstruction (bowel wall thickens due to inflammation).
  • Adenocarcinoma of the bowel.
61
Q

What are the key features of UC?

A
  • Inflammation of the GI tract limited to the mucosa.
  • Always involves the rectum and spreads proximally.
  • Inflammation is continuous (no skip lesions).
  • Pseudopolyps may develop.
62
Q

What is the clinical presentation of UC?

A
  • BLOODY DIARRHOEA.
  • Faecal urgency.
  • Abdominal pain (often left sided).
63
Q

What are the risk factors for UC?

A
  • Family history of IBD.
  • HLA-B27.
  • Infection (this can trigger relapse).

SMOKING IS PROTECTIVE.

64
Q

What are the investigations used for UC?

What is a common cause of acute exacerbation of UC?

A
  • Faecal calprotectin is raised in IBD.
  • GOLD STANDARD. Endoscopy + biopsy and look for UC histology.
  • C. diff a common cause of an acute exacerbation of UC.
65
Q

What is the treatment for UC?

A

Inducing remission:
1st line - Mesalazine (aminosalicylate)
2nd line - naproxen.
Consider going straight to naproxen if UC flare-up severe.

Maintaining remission:
1st line: mesalazine.
2nd line: azathioprine (DMARD).
Consider colectomy if disease severe.

66
Q

What are the differentials for UC? How are they differentiated?

A

Crohn’s - Skip lesions, transmural inflammation (histology), “cobblestone bowel”, more likely to extend past the splenic flecture.

IBS - Will have a negative faecal calprotectin, and relief with defecation.

67
Q

How does PSC relate to UC?

A
  • 70% of PSC patients will have UC.
68
Q

What is coeliac disease and what are the key features?

A
  • Systemic autoimmune disease triggered by gliadin, a product of gluten metabolism.

Key features:

  • Villous atrophy.
  • Crypt hyperplasia.
  • Increased lymphocytes in the mucosa.

Cause malabsorption.

69
Q

What is the clinical presentation of coeliac disease?

A
  • Diarrhoea.
  • Bloating.
  • Abdominal pain/cramping.
  • Fatigue.
  • Iron deficiency anaemia.
70
Q

What are the risk factors for coeliac disease?

A
  • FH of coeliac.
  • IgA deficiency.
  • Type 1 diabetes.
  • Down’s syndrome.
  • Hashimoto’s thyroiditis.
71
Q

What are the investigations used for coeliac disease?

A

Key investigations:
1st line: IgA-tTG - Raised titre in coeliac.
GOLD STANDARD: Duodenal biopsy - Classical histology of coeliac present.

Other options:

  • IgA serology. Low.
  • EMA. High titre.

Both EMA and IgA are more specific but less sensitive than IgA-tTG is.

72
Q

What is the management of coeliac disease?

A

1st line: Gluten free diet + ergocalciferol (vit D) + calcium carbonate.

If iron also low, give iron supplements.

73
Q

What is the main differential for coeliac disease?

A

IBD - Has a positive faecal calprotectin.

74
Q

What are the main complications of coeliac disease?

A
  • Osteoporosis (low calcium).
  • Iron-deficiency anaemia.
  • Dermatitis herpetiformis (itchy, blistering skin).
75
Q

What is GORD?

A

Reflux of gastric contents into the oseophagus.

76
Q

What is the clinical presentation of GORD?

A
  • Heartburn.
  • Regurgitation.
  • Often gets worse with lying down/bending over.
77
Q

What are the alarm symptoms when suspecting GORD? What are the alarm symptoms potentially suggestive of?

A
  • Anaemia
  • Haematemesis.
  • Blood in faeces.
  • Persistent vomiting
  • Weight loss
  • Progressive dysphagia.
  • Oesophageal cancer.
78
Q

What is the pathophysiology of Barrett’s oesophagus?

A
  • Conversion of stratified squamous epithelium (typical of the oesophagus) to simple columnar epithelium (more typical of the stomach).
79
Q

What are the investigations for GORD?

A
  • Typically no investigations. Just a trial of PPI (omeprazole).
  • If symptoms worrying/atypical, use of endoscopy indicated (Oesophagus, stomach and duodenal imaging).
80
Q

What is the treatment for GORD?

A

PPI (omeprazole).

Lifestyle changes:

  • Weight loss.
  • Stop smoking.
  • Tilt up bead head to sleep.
81
Q

What are the potential differentials for GORD?

A
  • Achalasia. Usually has more prominent, non-specific dysphagia (equal for solids and liquids).
  • Oesophageal cancer. Associated with progressive dysphagia.
82
Q

What is a peptic ulcer? What are the two types of peptic ulcer?

A
  • A break in the mucosal lining of the stomach/duodenum.
  • Stomach ulcer = gastric ulcer.
  • Duodenal ulcer = duodenal ulcer!
83
Q

What is the main complication of a peptic ulcer?

A
  • Upper GI bleed.

- If occurs, urgent endoscopy + ED management (potential blood transfusion).

84
Q

What are the risk factors for peptic ulcers?

A
  • Excessive NSAID use.
  • H. Pylori infection.
  • Smoking.
  • Old age.
85
Q

What are the investigations used for peptic ulcers?

A
  • Gold standard is endoscopy. This can find the ulcer, and check if it is H. Pylori related. If it is, biopsy can be taken and urea tested.
  • Can also do urea breath test/stool antigen test if something less invasive is better.
86
Q

What is the treatment for peptic ulcers?

A

IF BLEEDING: urgent endoscopy + blood transfusion + PPI (omeprazole).

IF STABLE:

  • Stop NSAIDS if possible
  • PPI (omeprazole) 1st line, H2 antagonist (famotidine) 2nd line.

IF CAUSED BY H. PYLORI:
- 7 days of triple therapy (amoxicillin + clarithromycin + omeprazole).

87
Q

What is the most common type of gastric cancer?

A
  • Gastric adenocarcinoma.
88
Q

What is the typical presentation of gastric cancer?

A
  • Weight loss.
  • Fatigue.
  • Persistent abdominal pain.
89
Q

What is the investigation used for suspected gastric cancer

A
  • Endoscopy + biopsy.
90
Q

What is the treatment for gastric cancer?

A
  • Resection of the tumour (often laparoscopic).
91
Q

What are the most common types of oesophageal cancer?

A
  • Adenocarcinoma.

- Squamous cell carcinoma.

92
Q

What are the key presenting complaints for oesophageal cancer?

A
  • Progressive dysphagia.

- Pain on swallowing.

93
Q

What is the first line investigation for oesophageal cancer?

A
  • Upper GI endoscopy + biopsy.
94
Q

What is the treatment for oesophageal cancer?

A
  • Surgical resection of the tumour.
95
Q

What is the most common type of colorectal cancer?

A
  • Colonic adenocarcinoma.
96
Q

What is the key red flag symptom for colorectal cancer?

A
  • Blood in stool.
97
Q

What is the investigation of choice for suspected colorectal cancer?

A
  • Colonoscopy + biopsy.
98
Q

How is colorectal cancer treated?

A
  • Excision of the tumour.
99
Q

What is the investigation for intestinal obstruction?

A
  • URGENT CT scan.
100
Q

What are the main potential causes of intestinal obstruction?

A
  • Hernia
  • Surgical adhesions.
  • Volvulus (twisting)
  • Intussusception (telescoping).
  • Bowel cancer.
101
Q

What are the symptoms of bowel obstruction?

A
  • Intermittent abdominal pain.
  • Bowel distension
  • Nausea/vomiting
  • Absolute constipation.

Phase 2 v2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions