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Phase 2 GI and Surgery > 2. Abdominal Pain, Altered Bowel Habit and Dyspepsia/Indigestion > Flashcards

2. Abdominal Pain, Altered Bowel Habit and Dyspepsia/Indigestion Flashcards

1
Q

Describe the underlying mechanisms and potential causes of the following types of diarrhoea

  1. osmotic
  2. secretory
  3. inflammatory
A
  1. large quantities of non-absorbed hypertonic substances in the lumen draws out water by osmosis
    - ingestion of non-absorbable substance
    - generalised malabsorption
    - specific absorptive defect
  2. decreased absorption + active secretion of fluid and electrolytes
    - enterotoxins
    - bile salts (ileal resection; bile acid malabsorption)
    - fatty acids
  3. damage to intestinal mucosa → loss of fluid and blood into the lumen + decreased absorption
    - infection
    - IBD
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2
Q

Name causes of abnormal gut motility that can cause diarrhoea (3)

A
  • diabetic neuropathy
  • post vagotomy
  • hyperthyroidism
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3
Q
  1. After how many days should cause of diarrhoea be investigated?
  2. How is the cause investigated (2)
A
  1. 5-7

2. stool culture; flexi sig

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4
Q

How is constipation defined? (4 points)

A

2+ of the following in the last 12 weeks:

  • infrequent passage of stools
  • straining >25% of the time
  • passage of hard stools
  • incomplete evacuation and sensation of anorectal blockage
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5
Q
  1. Name 3 metabolic/endocrine conditions associated with constipation
  2. name 5 drugs associated with constipation
A
  1. diabetes, hypercalcaemia, hypothyroidism

2. opiates, antimuscarinics, Ca channel blockers, tricyclic antidepressants, Iron salts

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6
Q

Describe the MOA of the following types of laxative, and give examples:

  1. Osmotic Laxatives
  2. Bulk forming Laxatives
  3. Irritant and Stimulant Laxatives
  4. Faecal softeners
A
  1. osmotically active saccharides hold water in gut lumen. LACTULOSE
  2. increases bulk of stooks thus aids peristalsis. ISPHAGHULA HUSK
  3. increase water and electrolyte secretion from colonic mucosa. SENNA. BISACODYL
  4. act to decrease surface tension thus increase penetration of intestinal fluid into the faecal mass CO-DANTHRUSATE
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7
Q

How does colorectal cancer alter bowel habit

A
  • inflammatory diarrhoea
  • constipation due to obstruction
  • bleeding
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8
Q
  1. describe the GI manifestations of IBS
A
  • abdo pain/cramping/bloating; relieved or partly relieved by opening bowels
  • excess gas
  • diarrhoea or constipation
  • mucus in stool
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9
Q
  1. What kind of diet can help relieve symptoms of IBS?

2. what kind of pharmacological agents can be useful in managing IBS symptoms?

A
  1. FODMAP
  2. loperamide (reduce diarrhoea)
    smooth muscle relaxants - peppermint oil; mebeverine
    antidepressants
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10
Q

Define the following:

  1. diverticula
  2. diverticulosis
  3. diverticulitis
  4. Diverticular colitis
A
  1. outpouches of the colonic wall
  2. presence of diverticula
  3. inflammation of diverticula(e)
  4. cresenteric inflammation on the folds in areas of diverticulosis. May/may not be associated with diverticulitis
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11
Q
  1. Describe the pathogenesis of diverticulosis

2. Why is the sigmoid colon particularly susceptible to the formation of diverticulae

A
  1. low fibre diet increases intestinal transit time and decreases stool volume, resulting in increased intralumenal pressure and colonic segmentation
    high intralumenal pressures cause pouches of mucosa to extrude through the muscular wall through weakened areas near blood vessels
  2. small diameter - larger pressures
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12
Q

Name risk factors associated with the formation of diverticulae

A
  • LOW DIETARY FIBRE
  • decreased physical activity
  • obesity
  • increased red meat consumption
  • excessive alcohol and caffiene
  • steroids and NSAIDs
  • smoking
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13
Q

Describe the general management of diverticulosis

A
  • high fibre diet
  • adequate fluid intake
  • weight loss + smoking cessation
  • bulk forming laxatives
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14
Q
  1. What is acute diverticulitis? Describe its pathogenesis
  2. How does it present?
  3. Examination findings?
A
  1. acute inflammation of diverticula. Faeces obstructs neck of diverticulum, causing stagnation and allowing bacteria within the diverticulum to multiply

2, similar presentation to acute appendicitis but on the left side

  • severe LIF pain
  • fever
  • general malaise
  • constipation
  1. left sided tenderness and guarding.
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15
Q

Name 5 complications of acute diverticulitis/diverticular disease:

A
  1. perforation (typically in association with acute diverticulitis)
  2. fistula formation - into bladder or vagina
  3. obstruction (usually after repeated episodes of acute diverticulitis, which can lead to the formation of colonic structures)
  4. bleeding
    5, mucosal inflammation - can give appearance of segmental colitis
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16
Q

What is an oesophageal stricture?

A

a tightening of the oesophagus that causes swallowing difficulties

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17
Q
  1. What are the majority of benign oesophageal strictures associated with?
  2. Name some other causes of benign oesophageal strictures
A
  1. long standing/poorly controlled GORD (inflammation and fibrosis)
  2. eosinophillic oesophagitis
    radiotherapy
    sclerotherapy of oesophageal varices
    prolonged NG intubation
    drug induced oesophagitis
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18
Q
  1. How do malignant strictures cause dysphagia?

2. How do patients with malignant strictures commonly present?

A
  1. mass effect; occluded oesophagus
  2. progressive dysphagia to solids
    odynophagia
    weight loss
    anorexia
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19
Q
  1. What is achalasia?

2. What is thought to be the underlying pathophysiology of achalasia?

A
  1. oeophageal motility disorder characterised by oesophageal aperistalsis and impaired relaxation of the LOS
  2. inflammation of the myenteric plexus of the oesophagus, with reduction in ganglion cell numbers
    Oesophagus is dilated
20
Q
  1. How do patients with achalasia usually present?

2. Name 5 tests useful in the investigation of achalasia

A
  1. long hx of intermittent dysphagia.
    regurgitation of food from the oesophagus
    aspiration pneumonia
  2. CXR - dilated oesophagus
    barium swallow - lack of peristalsis. lower end shows “birds beak” as LOS fails to open
    OGD - exclusion of CA
    CT - exclude CA
    Manometry - shows aperistalsis and failure of the LOS to relax
21
Q

Describe the pathophysiology of GORD

A
  • more frequent transient relaxations of the LOS - allow gastric acid to flow back into the oesophagus
22
Q
  1. How can a hiatus hernia lead to GORD?
  2. How does increased intra-abdominal pressure predispose to GORD?
  3. Name some other risk factors associated with GORD
A
  1. impairs the support provided by the gastric folds and the crural diaphragm at the LOS
  2. easier to overcome LOS
3. obesity
    smoking
    drugs - antimuscarinics, Ca blockers, nitrates
    alcohol
    systemic sclerosis
23
Q
  1. Name 3 occasions when heart burn associated with GORD is better/worse
  2. Name 3 clinical features of laryngopharyngeal reflux
A
  1. exacerbated by lying or bending down
    worse with hot drinks or alcohol
    relieved by antacids
  2. cough
    hoarse voice
    post-nasal drip
24
Q

Name examples of the following drugs used to manage GORD:

  1. dopamine antagonists
  2. H2 antagonists
  3. PPIs
  4. How do alginate containing antacids help relieve symptoms of GORD?
  5. Name a side effect of alginate containing antacids
A
  1. metoclopramide; domperidone (enhance peristalsis and speed gastric emptying)
  2. ranitidine
  3. omeprazole; lanzoprazole
  4. create a foam raft with gastric contents to reduce refluz
  5. Mg containing compounds cause diarrhoea
    Al containing compounds cause constipation
25
Q

Describe the metaplastic change in Barrett’s Oesophagus

A

squamous to columnar

26
Q

What are peptic ulcers?

A

breaks in the superficial epithelia of the stomach/duodenum, which penetrate down into the muscularis mucosa

27
Q
  1. Name 3 clinical features of peptic ulcers

2. Name 7 GI irritants which the patient may have a recent hx of using

A
  1. recurrent, burning epigastric pain
    nausea
    anorexia and weight loss
2. NSAIDs
    Steroids
    bisphosphonates
    doxycycline
    alcohol
    coffee
    smoking
28
Q

Name 4 investigative tests for H pylori infection

A
  • serological tests - IgG
  • CLO TEST
  • stool antigen test
  • endoscopic biopsy with histology and culture
29
Q

Name 5 functional oesophageal disorders

A
  1. globus - sensation of lump in the throat
  2. Functional chest pain of presumed oesophagel origin
  3. Functional Dyspepsoa
  4. Functional Vomiting
  5. Gastroparesis
30
Q

Describe the 3 mechanisms of bacterial GI infection

A
  1. NON-INFLAMMATORY - bacteria don’t induce inflammation themselves, but produce toxins which tend to affect the proximal small bowel
  2. INVASIVE - pathogens invade the gut wall and/or produce toxins. Primarily affect the colon
  3. PENETRATING - bacteria induce phagocytosis, enabling them to partially evade the immune system. Primarily affect the distal small bowel
31
Q

Define the following in terms of foodborne disease:

  1. infection

2. intoxication

A
  1. microbial agent is ingested, colonises the gut and causes infection by toxin production or by inducing inflammation
  2. bacteria produce toxins in the food before it is ingested.
32
Q
  1. How does staphylococcus cause foodborne illness?
  2. how quickly does it produce gastroenteritis symptoms?
  3. How long does it take signs and symptoms to resolve?
A
  1. intoxication - produces enterotoxins
  2. 1-6 hours
  3. 24-48 hours
33
Q
  1. What type of mechanism underlies shigella infection? (infection or intoxication?)
  2. how can shigella infection cause fluid loss?
  3. what is a severe complication of shigella infection?
A
  1. infection
  2. cause intestinal ulceration
  3. haemolytic uraemic syndrome
34
Q
  1. What type of mechanism underlies Salmonella infection? (infection or intoxication?)
  2. When do signs and symptoms typically resolve?
  3. What is NOT a predominant symptom of salmonella infection?
A
  1. infection and intoxication
  2. ~1/52
  3. vomiting
35
Q
  1. Which E. coli strain is associated with haemolytic uraemic syndrome?
  2. Are all strains of E. coli pathogenic
A
  1. E. coli O157:H7

2. No (most strains are part of the commensal microbiome)

36
Q

What is the time to onset of symptoms of Bacillus cerus infection?

A

a few hours following ingestion

37
Q

Name the 5 bacterial causes of bloody diarrhoea

A
  1. Campylobacter
  2. Haemorrhagic E. coli
  3. entameba histolytica
  4. shigella
  5. salmonella
38
Q

Define the following terms used to describe hernias:

  1. reducible
  2. Irreducible/incarcerated
  3. obstructed
  4. strangulated
A
  1. contents of hernia can be manipulated back into its original position through the defect from which it emerges
  2. hernia is compressed by the defect, causing it to be irreducible
  3. contents of hernia are compressed to the extent that the bowel lumen is no longer patent, causing bowel obstruction
  4. compression around the hernia prevents blood flow to the herniated viscus, causing ischaemia and pain
39
Q
  1. Within what structure does the inguinal canal run in?
  2. What 2 structures does this structure (1) rub in between?
  3. Where does the deep inguinal ring lie?
  4. Where does the superficial inguinal ring lie?
A
  1. inguinal ligament
  2. anterior superior iliac spine and pubic tubercle
  3. mid point of inguinal ligament (midway between ASIS and pubic tubercle)
  4. above and medial to pubic tubercle
40
Q
  1. What is an inguinal hernia?
  2. What is a direct inguinal hernia?
  3. In what type of patients do they more commonly occur?
  4. Where do these hernias occur?
  5. What is an indirect inguinal hernia?
  6. How do you distinguish clinically between direct and indirect inguinal hernias?
A
  1. abdominal cavity contents herniate into the inguinal canal
  2. bowel enters inguinal canal directly through a weakness in the posterior wall of the canal
  3. older patients
  4. medial to the deep inguinal ring
  5. bowel enters the inguinal canal via the deep inguinal ring
  6. if you press the deep ring and the hernia still protrudes, then the hernia is emerging via a defect in the posterior wall, and is therefore a direct hernia.
41
Q

Name the 2 main mechanisms which lead to the development of inguinal hernias

A
  • weakness of abdominal muscles

- increased intra-abdominal pressure

42
Q
  1. What is a femoral hernia?
  2. Why do these hernias have a high rate of strangulation
  3. Which sex are more prone to femoral hernias and why?
A
  1. abdominal viscera herniate through the femoral ring into the potential space of the femoral canal
  2. narrow neck of femoral ring
  3. women, due to the wider anatomy of the pelvis
43
Q

describe the anatomy of the femoral canal, lateral to medial

A 
femoral Nerve
femoral Artery
femoral Vein
femoral canal (Empty space)
Lymph canal
44
Q

Other than gender, name 3 other risk factors for the development of inguinal hernias

A
  • pregnancy/multiparity
  • raised intra-abdominal pressure
  • increased age
45
Q

How can you distinguish between femoral and inguinal hernias clinically?

A
  • femoral hernias are found INFEROLATERAL to the pubic tubercle
  • inguinal hernias are found SUPEROMEDIAL to the pubic tubercle
46
Q

Describe the following hiatus hernias:

  1. Sliding
  2. rolling/non-sliding
A
  1. gastro-oesophageal junction slides through the oesophageal hiatus into the chest
  2. gastro-oesophageal junction remains fixed; another portion of the stomach moves up through the stomach (can lead to gastric obstruction)

Phase 2 GI and Surgery (10 decks)

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