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General Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are some causes of (non-fatty) osmotic diarrhoea?

A

Ingestion of PO4, Mg, SO4
Carb indigestion (disaccharide deficiency e.g., lactase –> lactose intolerance)

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2
Q

What are some causes of steatorrhea?

A

Pancreatic insufficiency
Damage to SI mucosa e.g., coeliac disease, CD, giardia, mesenteric ischaemia
Short bowel syndrome, small bowel bacterial overgrowth, post-resection diarrhoea

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3
Q

What are causes of inflammatory diarrhoea?

A
  1. Infectious: shigella, salmonella, campylobacter, EHEC (0157: H7), vibrio cholera, clostridium difficile (pseudomembranous colitis), yersinia, entamoeba histiolytica
  2. Inflammatory bowel disease, radiation colitis
  3. CRC Ca or lymphoma
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4
Q

What are causes of secretory diarrhoea?

A

Enterotoxins e.g., enterotoxigenic bacteria
Laxative abuse
Ileal bile acid malabsorption
VIPoma, villous adenoma, diabetic autonomic neuropathy, thyrotoxicosis, vasculitis

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5
Q

Most common cause of factitious diarrhoea

A

Surrepticious laxative abuse

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6
Q

Clinical features of factitious diarrhoea

A

Chronic watery diarrhoea - high frequency and volume + 50% have nocturnal bowel mvmts (uncommon in IBS) + cramping, abdo pain, weight loss, +/- N&V in anorexia/bullimia

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7
Q

Features of factitious diarrhoea Ix and Dx

A

Stool analysis: increase in fecal osmolar gap (laxatives containing magnesium, sorbitol, lactose etc.), plasma osmolality > stool suggests watering down with water (if opposite consider urine added esp. if high creat, Na, urea), high stool Mg suggests Mg containing laxatives
A can detect some stimulant laxatives
Endoscopy: melanosis coli (dark discolouration of colon with lymph follicles shining through as pale patches) + rarely cathartic (dilated) colon)

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8
Q

What toxins are implicated in C Diff diarrhoea

A

Toxin A and toxin B (more poitent)

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9
Q

What does pseudomembranous colon refer to

A

Endoscopic appearance of scattered white-yellow mucosal plaques in colon (esp. C. Diff)

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10
Q

What risk factors are associated with C diff infection

A

Antibiotic exposure (current/recurrent use), advanced age, hospitalisation, IBD (must rule out before starting immunosuppressive agents), PPI use, comorbid illness

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11
Q

Clinical features of C Diff infection

A

Fever
Abdominal tenderness
Frequent semi-formed/watery non-bloody diarrhoea
Dehydration
Risk of ileus, toxic megacolon, shock, peritonitis in fulminant disease
Secondary PLE –> hypoalbuminaemia –> peripheral oedema/ascites

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12
Q

Diagnosis of C Diff infection

A

Stool PCR (can do stool EIA for toxins too)

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13
Q

Endoscopic findings with C diff

A

Pseudomembranes = yellow-white mucosal plaques in colon
Patchy erythema
Friability
Ulcers

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14
Q

Treatment of C diff: 1st infective episode

A

Mild-moderate: Metronidazole 400mg PO or enterally 8hourly for 10 days
Severe: Vancomycin 125mg PO or enterally 6 hourly for 10 days +/- metronidazole 500mg IV 8 hourly for 10 days

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15
Q

Treatment of C diff: 1st recurrence/refractory disease

A

Vancomycin 125mg PO or enterally 6 hourly for 10 days

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16
Q

Treatment of C diff+ recurrences/ongoing refractory disease

A

Faecal microbiota transplantation via colonoscopy or enema with goal of restoring normal faecal microbiota (vancomycin as above for 14 days if unavailable)

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17
Q

Is follow-up testing required after Tx of C diff

A

Only if still symptomatic. Tests remain +ve for > 1mo even after effective Tx

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18
Q

Mechanisms of malabsorption

A

Infective agents
Structural deformities
Mucosal abnormalities
Enzyme deficiencies
Systemic disease affecting GIT

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19
Q

MCC of malabsorption

A

Celiac disease
Lactase deficiency
Chronic pancreatitis
Crohn Disease
Gastretcomy

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20
Q

Characteristcis of malabsorption

A

Weight loss, steatorrhea/frequent stooling, fatigue, nutrient deficiencies

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21
Q

Screening of patients of malabsorption

A

Albumin, Fe, Ca, carotene, cholesterol = low
PT/INR = prolonged
If abnormal as above do tests for specific aetiology

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22
Q

Less common causes of malabsorption

A

Whipple disease
Tropical sprue
Small intestinal bacterial overgrowth (SIBO)
Short bowel syndrome
Microscopic colitis
Eosinophilic gastroenteritis

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23
Q

What is the causative organism in Whipple disease

A

Tropheryma whipplei = GP actinomycete

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24
Q

Risk factors for Whipple disease

A

Male, 4th-6th decade, farm-related trades

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25
Q

Whipple disease clinical features

A

Diarrhoea/steatorrhea
Abdo pain, bloating, anorexia, LG fever, lymphadenopathy, malaise
Joints; Migratory polyarthralgia/chronic peripheral arthritis (seronegative)
Neuro: dementia, myoclonus, paralysis of gaze
Cardiac: pericardial friction rub, murmurs, pleural friction rub
Fatal if untreated

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26
Q

How to Dx Whipple disease

A

Small bowel biopsy:
- Lamina propria infiltrated by PAS+ MOs containing GP AFBs
- Lymphatic dilation (malabsorption secondary to obstruction of lymphatics)
Confirmed by PCR

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27
Q

DDx for Whipple disease

A

Celiac, lymphoma, mycobacterium avium complex

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28
Q

Treatment of Whipple disease

A

Trimethoprim-sulfamethoxazole = cotrimoxazole 800mg BD for a year (rpt biopsy after Tx to confirm eradication)

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29
Q

Microscopic colitis characteristics

A

Chronic diarrhoea w/out bleeding
Abdominal pain
+/- weight loss, fecal incontinence
No increased cancer risk

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30
Q

Ix findings of microscopic colitis

A

Colonoscopy = macroscopically normal but biopsies = reveal lymphocytic (intraepithelial lymphocytosis) or collagenous picture (intraepithelial lymphocytosis and thickened supepithelial collagen band)

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31
Q

Typical microscopic colitis pt

A

Middle age, female, autoimmune Hx

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32
Q

Tx microscopic colitis

A

Stop medications assoc. with onset e.g., SSRI, PPI, NSAIDs
Enteric coated budesonide preparing in morning –> refractory/not tolerated –> cholestyramine

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33
Q

Characteristics of tropical sprue

A

Occurs after prolonged (> 6 weeks) travel to tropics
Steatorrhea, diarrhoea, abdominal pain, weight loss, anorexia
Megaloblastic anaemia (folate then B12): glossitis, fatigue
Nutritional deficiencies
NB. folate deficiency is more common in TS vs IDA in celiac disease and does not improve with gluten free diet

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34
Q

Tx of tropical sprue

A

Tetracycline for 3-6mo

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35
Q

Mechanisms maintaining normal gut flora vs mechanisms of SIBO

A
  1. Gastric acid and pancreatic enzyme secretion, small intestinal motility, intact intestinal immune system, structural integrity of GIT
  2. Alteration in gut structural integrity or secretory, motor, or immune Fx
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36
Q

Clinical features of SIBO (including normal bloods)

A

Diarrhoea, abdo bloating/distension, florid malabsorption
Nutritional deficiencies: B12 (megaloblastic anaemia, peripheral neuropathy), fat soluble vitamins (vitamin A; follicular hyperkeratosis)
NORMAL serum levels: Vitamin K and folate secondary to bacterial synthesis

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37
Q

SIBO Dx

A

Refer to gastro based on clinical features: steatorrhea, elevated folate, low B12
Radio-labelled carbon breath test or small bowel aspirate

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38
Q

SIBO Tx

A

Antibiotics e.g., rifaximin or augmentin

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39
Q

Causes of eosinophilic gastroenteritis

A

Primary: idiopathic (and no extraintestinal organ involvement)
Secondary: celiac disease, hypereosinophilic syndrome, vasculitis (eosinophilic granulomatosis with polyangitis, polyarteritis nodosa, scleroderma), Crohn’s disease, parasites, hypersensitivity

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40
Q

Tx of eosinophilic gastroenteritis

A

Dietary elimination and corticosteroids

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41
Q

What is Chronic Idiopathic Intestinal Pseudo-obstruction and who does it effect

A

Rare syndrome characterised by recurrent and progressive symptoms of intestinal obstruction and dilatation of affected areas of SB/LB on imaging without identifiable anatomical cause
Young people

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42
Q

Causes and Dx of Chronic idiopathic intestinal pseudoobstruction

A

Neuropathies and myopathies
SB or colonic transit studies +/- full thickness biopsies (abnormal enteric NS/interstitial cells of cajal)

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43
Q

Tx of chronic idiopathic intestinal pseudoobstruction

A

Nutritional supplementation and cautious use of promotility agents
Severe: parenteral nutrition and surgery
Poor prognosis

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44
Q

What is short bowel syndrome

A

Short bowel syndrome occurs when an inadequate length of intestine is available for nutrient absorption

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45
Q

What causes short bowel syndrome and what factors determine whether it develops

A

MCC in adults: surgical resection of diseased bowel most commonly secondary to Crohn’s disease followed by bowel obstruction with strangulation, and mesenteric infarction
MCC in children: congenital causes or resection following NEC
Factors affecting development:
- length of SB remaining
- presence/absence of colon
- mucosal integrity of remaining SB

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46
Q

What length of bowel is adequate to avoid short bowel syndrome?

A

100cm of SB if colon is present
200cm of SB if colon is absent with long period of adaption
NB. adaptation takes years

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47
Q

What Tx is required if intestinal failure (failure to absorb sufficient nutrients) occurs secondary to short bowel syndrome

A

TPN

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48
Q

What is a better predictor of intestinal failure than length of remaining gut after resection

A

Plasma citrulline concentration = sensitive measure of absorptive capacity

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49
Q

What are the dietary measures for patients adapting to a short gut

A

Small frequent nutrient rich meals +/- carb-containing isotonic fluids +/- nocturnal nutritional supplementation (NG/gastrostomy)

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50
Q

Clinical parameters of malnutrition

A

Biochemical markers e.g., low albumin, micronutrient deficiencies e.g., vitA/D/zinc etc.
Body weight < 70% of ideal or > 20% weight loss in 6mo (beware of fluid e.g., ascites in chronic liver disease)
Inadequate dietary intake
Weak hand grip strength (poor protein status)
Body fat and lean muscle assessed using anthroprometric measurements: low triceps skinfold thickness, mid-arm muscle circumference
Functional capacity

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51
Q

Clinical features of Vit A deficiency

A

Xerophthlamia + Bitot’s spots –> night blindness
Poor bone growth
Impaired immune system
Follicular hyperkeratosis

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52
Q

Vit A deficiency: causes, Dx, Tx

A
  1. low intake (vitamin A = animals, provitamin A = plants)
  2. serum retinol
  3. vitam A supplementation
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53
Q

Clinical features of Vit B12 deficiency

A

Megaloblastic anaemia
Glossitis
Subacute combined degeneration of SC
Peripheral sensory neuropathy
Dementia

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54
Q

Vit B12 deficiency causes

A

Low intake
Pernicious anaemia
Terminal ileum disease e.g., resection, Crohn’s
Gastrectomy

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55
Q

Vit B12 Tx

A

Initial: hydroxocobalamin 1000ug IM on alternate days for 2 weeks
Maintainance:
Hydroxocobalamin 1000ug IM on every 2-3 mo/sublingual or oral cyanocobalamin or mecobalamin daily
Must correct B12 deficiency first if concomitant B12 and folate deficiency to avoid subacute combined spinal degeneration

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56
Q

Pyridoxine deficiency clinical features

A

Vit B6
Glossitis and angular stomatitis
Vomiting
Seizures
Scrotal dermatitis

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57
Q

Causes and Dx of vit B6 deficiency

A

MC = drugs e.g., isoniazid, phenobarbital, penicillamine

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58
Q

Tx (+ Tx SE) for B6 deficiency

A

Supplementation
SE = over supplementation can result in impaired position and vibratory sense

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59
Q

Riboflavin deficiency clinical features, causes, and Tx

A

Vitamin B2
1. seborrheic dermatitis in perianal area, nose; glossitis, angular stomatitis, normochromic normocytic anaemia, sore throat and magenta tongue
2. TCAs and phenothiazines
3. supplementation

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60
Q

Thiamine deficiency clinical consequences

A

Vitamin B1
- Wet beriberi = heart failure secondary to cardiomyopathy
- Dry beriberi = neuropathy
- Wernicke’s encephalopathy = gaitataxia, nystagmus, ophthalmoplegia, confusion (reversible)
- Korsakoff syndrome = confabulation, anterograde and retrograde amnesia, personality changes (irreversible)
- Periphereal neuropathy

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61
Q

Causes and Dx of thiamine deficiency

A

Low dietary intake
Alcoholism
Chronic dialysis
Dx = serum thiamine

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62
Q

What can precipitate Wernicke’s encephalopathy

A

Glucose: give thiamine before glucose

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63
Q

Vitamin C deficiency clinical features

A

Scurvy:
Petechial haemorrhage, ecchymoses, bleeding and swollen gums, periosteal haemorrhage, haemorrhage into joints and nail beds
Loose teeth, weak bones, impaired wound healing, coiled hairs, hyperkeratotic papules
Sjrogren’s syndrome

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64
Q

Vit C deficiency causes, Tx and SE of Tx

A

Low intake
Supplementation
Large doses -> oxalate renal stones and impaired B12 absorption

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65
Q

Iodine deficiency consequences, causes, Tx

A
  1. Hypothyroidism
  2. Low dietary intake, drug and alcohol abuse
  3. Improve dietary intake
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66
Q

Niacin deficiency clinical features

A

Vitamin B3
Pellagra = dermatitis(sun-exposed areas) /hyperpigmentation/glossitis/stomatitis, diarrhoea, dementia/psychosis/depression

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67
Q

B3 deficiency causes and Tx

A

Tryptophan is used in body to make niacin
- low dietary intake
- carcinoid syndrome: tryptophan used up
- isoniazid: excess excretion of trypotphan (give with B6)
Replacement

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68
Q

Zinc deficiency clinical features

A

Rash, skin ulcers, alopecia
Impaired immunity
Night blindness
Diarrhoea
Decreased spermatogenesis

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69
Q

Zinc deficiency causes and Tx

A

Low dietary intake and supplementation

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70
Q

Vitamin E deficiency clinical features

A

Peripheral sensory and motor neuropathy
Haemolytic anaemia
Dry skin
Retinal degeneration

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71
Q

Vitamin E deficiency Tx and Tx SE

A

Supplementation
Large doses can potentiate effects of oral anticoagulation

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72
Q

Vitamin K deficiency clinical features and Tx

A
  1. bleeding tendency & easy bruising
  2. supplementation
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73
Q

Vitamin K deficiency causes and Dx

A

Low dietary intake
Systemic disease that cause fat-soluble vitamin malabsorption
Dx: coag profile (INR and PT)

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74
Q

Vitamin D deficiency conquences

A

Rickets in children and osteomalacia in adults due to impaired bone mineralisation, hypocalcaemia, secondary hyperparathyroidism –> phosphaturia

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75
Q

Vitamin D deficiency causes and Dx

A

Reduced sun exposure (e.g., pigmented skin, skin coverings)
Decreased intestinal absorption
Kidney disease
Systemic diseases causing fat malabsorption
Serum 25(OH)D

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76
Q

Tx of vitamin D deficiency

A

Increase casual sunlight exposure
Vitamin D supplementation
-25(OH)D = ostelin 1000
- activated vitamin D = calcitriol for renal disease pts

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77
Q

Clinical features of vitamin D toxicity

A

Short term: Hypercalcaemia, confusion, polyuria, dehydration, polydipsia, anorexia, vomiting, muscle weakness
Long term: bone demineralisation and pain

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78
Q

Why is enteral nutrition preferred

A

It sustains the digestive, absorptive and immunological barrier functions of the GIT.

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79
Q

When is TPN indicated including examples

A

For pts who are malnourished/at risk of malnutrition with a non-functioning or inaccessible GIT. Used when all avenues of oral feeding have been exhausted.
- Postoperative (bowel surgery/protracted recovery)
- Severe IBD
- Severe acute radiation/chemo enteritis
- Pre-op (severely malnourished only)
- Severe acute pancreatitis
- Enterocutaneous fisula
- Short gut syndrome

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80
Q

What are the components of TPN

A

Essential and non-essential AAs, glucose, fats, electrolytes, micronutrients

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81
Q

What are the access/catheter-related complications of TPN?

A

Pneumothorax/haemothorax/chylothorax from line insertion
Cardiac arrhythmia
Cardiac tamponade
Venous thrombosis/pulmonary embolism/thrombophlebitis
Air embolism
Infection (candida, pseudomonas, klebsiella; if longterm coagulase negative staph)
Subacute bacterial endocarditis

82
Q

Early systemic complications of TPN

A

Hypophosphataemia (refeeding syndrome), hypomagnesaemia, hypokalaemia, hypoglycaemia/hyperglycaemia
Thiamine deficiency
Hyperchloraemic metabolic acidosis
Volume overload and cardiac failure

83
Q

Late systemic complications of TPN

A

Azotaemia, hyperosmolality, TPN-related nephropathy
Liver dysfunction (hepatocellular/cholestatic/fatty liver)
Acalculous cholecystitis
Cholelithiasis with gallstones and gallbladder sludge
Vitamin and mineral deficiency (rare), essential FA deficiency
Metabolic bone disease (rare)

84
Q

What is refeeding syndrome

A

Clinical syndrome characterised by potentally fatal electrolyte and fluid shifts occurring in a person who has been severely malnourished or malnourished for a long period of time upon refeeding

85
Q

Describe the pathogenesis of refeeding syndrome

A

During starvation intracellular electrolyte and phosphate stores are depleted and main energy source is fat
Upon refeeding metabolism switches to using carbohydrates as key energy source and basal metabolic rate increases with increased production of insulin and IC uptake of phosphate, magnesium, potassium, glucose, and thiamine causing significant deficiencies and affecting multiple organs

86
Q

High risk groups for refeeding syndrome

A

Directly related to amount of weight loss that has occurred and rapidity of weight restoration
- Eating disorder pts
- Chronic malnutrition
- Prolonged fasting period
- Prolonged IV hydration therapy

87
Q

Complications of refeeding syndrome

A

Electrolyte disturbance
Rhabdomyolysis, muscle weakness, tetany
Cardiac failure, volume overload, arrhythmia/bradycardia, labile BP
Respiratury failure secondary to muscle weakness from hypophosphataemia
Seizures, coma, death

88
Q

What is the criteria for IBS

A

Diagnosis of exclusion
Rome IV:
Recurrent abdominal pain at least one day per week for past 3 months with 2+ of following:
1. Relieved/worsened with defecation
2. Altered consistency/form of stool
3. Altered frequency of stool

89
Q

Treatment of IBS

A

Reassurance, explanation, reduce stressors
Non-pharmacological
- education
- exercise
- IBS specific/low FODMAP diet
- hypnotherapy and CBT
Constipation:
- Bulking agent e.g., psyllium
- Laxatives (osmotics then bisacodyl)
- Secretagogue
Diarrhoea
- Antidiarrheals e.g., loperamide
- Bulking agent
- Bile salt binder (cholestyramine)
- Rifaximin
- TCA low dose
Pain
- Antispasmolytics e.g., peppermint oil, anticholinergics, mebeverine
- TCA low dose

90
Q

What worsens IBS

A

Eating and stress

91
Q

What baseline tests are done in pt with IBS Sx and no red flags

A

FBC, TSH, coeliac serology, +/- CRP

92
Q

What are red flags in a pt presenting with IBS Sx and what should be done

A

Weight loss
Anaemia
Presentation 50yo+
Low albumin
High CRP
Fever
*Do colonoscopy

93
Q

Pathogenesis of IBS

A

Genetic and environmental triggers
Abnormal intestinal motility
Visceral hypersensitivity
Food sensitivity
Abnormal gut microbiota

94
Q

Define constipation

A

Decreased frequency of stools (<3/week)
Excessive straining to open bowels
Passage of hard stools
Feeling of incomplete evacuation

95
Q

Initial investigations for constipation

A

Exclude DM, hypothyroidism, hypercalcaemia
- TSH
- Fasting BSL or oral GTT, HbA1C, insulin
- Ca
- Consider plan AXR
NB. rectal exam compulsory: fecal impaction, fissures, pelvic floor dysfunction, rectal prolapse can be detected

96
Q

Causes of constipation

A

General
- Inadequate fibre intake
- Immobility
Functional
- Idiopathic slow transit
- IBS
Endocrine/metabolic
- Hypothyroidism
- Hypercalcaemia
- Diabetes mellitus
- Porphyria
- Pregnancy (progesterone, pressure, iron)
Psychological
- Depression
- Anorexia Nervosa
- Repressed urge to defecate
Medications
- Calcium channel blockers
- Opiates
- Antimuscarinics
- Iron
- TCAs
GIT Disease
- Intestinal obstruction/pseudoobstruction
- Aganglionosis e.g., Hirschprung/Chagas disease
- CRC/stricture
- Diverticular disease
- Anal fissures/other painful anal conditions/anal stenosis
Defecatory conditions
- Rectal prolapse
- Mucosal prolapse intussusception
- Solitary rectal ulcer syndrome
- Large rectocoele
- Megarectum
- Pelvic floor dyssynergia (paradoxical contraction on straining)
Neuro
- Spinal cord disease e.g., MS, spina bifida
- Diabetic autonomic neuropathy
- Parkinson Disease

97
Q

How to ID pelvic floor dyssynergia as a cause of constipation

A

Rectal exam with and without straining
Refer for anal manometry and biofeedback

98
Q

Special investigations for constipation

A

If no cause established and no response to Tx
Colonic transit study (radio-opaque markers used to determine transit time)
Dyssynergia: Balloon expulsion +/- anorectal manometry
Barium or MRI defecogram to define anatomy in difficulty cases

99
Q

Constipation treatment

A

Trial of basic treatment
- increased dietary fibre
- osmotic laxatives e.g., polyethylene glycol
Biofeedback if dyssynergia

100
Q

Laxative types and examples

A

Bulk-forming: psyllium, sterculia
Stool softeners: docusate
Osmotic: lactulose, sorbitol, macrogol, Mg salts
Stimulant: senna, bisacodyl
Prokinetic: prucalopride

101
Q

How do bulk forming agents work

A

Increase bulk and moisture in stool stimulating colonic activity

102
Q

How do osmotic laxatives work

A

Draw water into, or keep water in, colon –> expands and softens stool

103
Q

How do stimulant laxatives work

A

Stimulate intestinal motility

104
Q

How do stool softeners work

A

Incorporate fluid and fat into stool –> softening

105
Q

How do prokinetic laxatives work

A

5HT4 R agonist

106
Q

Explain stepwise laxative therapy approach

A
  1. Marogol e.g., movicol/osmolax
  2. Bisacodyl or docusate and senna
  3. Prucalopride
107
Q

What is a diverticulum

A

Sac-like outpouching of colonic wall continuous with lumen

108
Q

What are the types of diverticular disease

A

Diverticulosis
Diverticulitis
Diverticular colitis
Diverticular bleeding

109
Q

What is diverticulosis

A

Presence of (false) diverticula within colon (esp. sigmoid)

110
Q

What is diverticulitis

A

Inflammation of diverticula (+ thickening of wall)

111
Q

Diverticular colitis

A

Inflammation of colon in area of diverticula

112
Q

Pathogenesis of diverticulosis

A

High intraluminal pressure –> pouches of mucosa extrude through thickened msucular wall at points of weakness (where vasa recta penetrate)
Related to low dietary fibre

113
Q

Pathogenesis of diverticulitis

A

Faeces obstruct neck of diverticulum –> stagnation –> multiplication of bacteria –> inflammation

114
Q

Clinical features of diverticular disease

A

Asymptomatic/incidental finding on colonoscopy
Intermittent left iliac fossa pain/discomfort
Erratic bowel habit
Severe: luminal narrowing –> pain and constipation

115
Q

Investigations for diverticular disease

A

Colonoscopy or barium enema with flexible sigmoidoscopy

116
Q

Management of uncomplicated symptomatic diverticular disease

A

Well balanced (soluble and insoluble) fibre diet +/- analgesia e.g., paracetamol +/- antispasmodic

117
Q

Clinical features of acute diverticulitis

A

Severe pain in left iliac fossa
Fever
Constipation
Tachycardia
Abdo exam: tenderness, guarding, rigidity on L abdomen +/- palpable tender mass in LIF

118
Q

Ix acute diverticulitis

A

FBC, UEC, CRP, ESR
CT colonography: colonic wall thickening, diverticula, pericolic collections/abscesses, fat stranding
USS can be done quickly: thickened bowel and large pericolic collections
Colonoscopy and sigmoidoscopy are not performed during acute attack

119
Q

Mx acute diverticulitis

A

Uncomplicated: analgesia, low residue diet e.g., paracetamol +/- antispasmodic +/- PO ABx if systemically unwell/comorbidities/not responding to Tx/immunosuppressed = PO amoxicillin+clavulanate 875+125 mg orally, 12-hourly for 5 days
Complicated:
- CT/USS guided drainage of abscess > 3cm
- Perforation: Laparoscopy/washout/lavage/resection if faecal peritonitis (Hartmann’s procedure = resection of bowel with end stoma) or colectomy with primary anastamosis
- + analgesia (paracetamol, tramadol, morphine), low residue diet and IV ABx (gentamicin + metronidazole + amoxicillin/ampicillin)

120
Q

Complications diverticular disease

A

Perforation (acute diverticulitis) –> paracolic/pelvic abscess or generalised peritonitis
Fistula formation: colovesical –> pneumaturia, e. coli UTIs, dysuria; colovaginal –> fecal discharge/incontinence
Bleeding can be massive (colonoscopy/angiography/urgent colectomy)
Mucosal inflammation –> segmental colitis

121
Q

Mx of recurrent diverticulitis

A

Consider elective colectomy

122
Q

Why is colonoscopy contraindicated in acute diverticulitis

A

Air introduced during colonoscopy –> microperforation –> major perforation –> peritonitis

123
Q

Define Crohn’s Disease

A

A type of chronic idiopathic inflammatory bowel disease characterised by transmural granulomatous inflammation and skip lesions (of normal mucosa) affecting anywhere in the GIT but most commonly the terminal ileum and colon

124
Q

Define Ulcerative Colitis

A

A type of chronic idiopathic inflammatory bowel disease characterised by contiguous mucosal inflammation limited to the colon from the rectum (proctitis) and extends proximally

125
Q

Epidemiology of Crohn’s disease

A

2nd/3rd decade = MC
5th and 7th decades have a smaller peak
Slight F > M

126
Q

Risk factors for Crohn’s Disease

A

Smoking
Genetics
Colder climate
FHx

127
Q

Classify Crohn’s disease as per disease behaviour

A

Inflammatory
Stricturing
Fistulising (enteroenteral, enterovaginal, enterovesical, perianal)

128
Q

Clinical features of Crohn’s Disease

A

General: chronic diarrhoea, abdominal pain, fever, weight loss
Specific
- Perianal fistulas +/- abscesses: fever, perianal pain and drainage
- Colonic disease: haematochezia (more common in UC)
- Stricturing disease: obstructive Sx (upper or lower GIT)
- Gastric/duodenal disease: epigastric pain, voitinh, nausea, GOO
- Oesophageal/upper GIT: dysphagia, odynophagia, chest pain (all v. rare)

129
Q

Diagnosis of Crohn’s Disease

A

Clinical features
Labs
- Bloods: FBC, UEC, CRP, ESR, LFT, Fe, B12, vit D
- Serology: ASCA, pANCA (UC > CD)
- Stool: fecal calprotectin, stool MC&S, PCR, and C diff toxin EIA (rule out infection before immunosuppressive Tx)
Endoscopy
- Colonoscopy: focal inflammation with patchy/skip lesions, cobblestoning/polypoid changes, ulcerations (aphthous, serpiginous, deep transmural), strictures, fistulas
- Video capsule enteroscopy for SB imaging that cannot be seen with scope (CI if strictures –> stuck and surgical removal)
Histology:
- acute inflammatory infiltrate, crypt abscesses –> chronic inflammation, crypt distortion and abscesses, non-caseating granulomas
Imaging
- CT/MR/USS to assess extent and complications

130
Q

When is capsule endoscopy contraindicated

A

GIT strictures: risk it will get stuck and need surgical removal

131
Q

MC acute complications of Crohn’s Disease

A

Bowel obstruction
Bowel perforation
Cholelithiasis
Nephrolithiasis

132
Q

What is induction therapy for Crohn’s Disease

A

Mild-moderate
- Prednisolone 40-50mg PO in morning until clinical response then taper over 6-8 weeks to stop
- Ileocecal: enteric coated budesonide (entocort) 9mg PO in morning for 4-8 weeks
then taper over 2-4 weeks
Severe
- IV hydrocortisone 100mg 6hourly (or methylprednisolone 60mg daily) usually for 3-7 days then oral switch when disease activity has subsided
- VTE prophylaxis +/- fluid/electrolyte/blood replacement
- Radiological drainage of abscess and ABx
- Surgery for fistulas/BO and ABx

133
Q

What is maintenance therapy for Crohn’s Disease

A

1ST LINE
Azathiopurine 2-2.5mg/kg PO daily or mercaptopurine 1-1.5mg/kg PO daily (shunting of thiopurines can be reversed with allpurinol)
2ND LINE
Methotrexate 10-25mg SC or PO or IM one day a week + folic acid 5-10mg one day a week (different day to methotrexate)
3RD LINE
Biologics e.g., TNFa inhibitors (adalimumab/infliximab)

134
Q

Perianal fistulising in Crohn’s Disease management

A

Metronidazole 400mg PO 12 hourly or ciprofloxacin 500mg PO 12 hourly
Consider surgical exploration, local drainage, placement of setons

135
Q

Lifestyle measures in Crohns

A

NSAID avoidance (precipitate flares)
Smoking cessation

136
Q

UC epidemiology

A

Bimodal: 20s-30s and 50-60s
Males = Females

137
Q

Risk factors in UC

A

Smoking cessation
FHx
NSAIDs

138
Q

Classify UC into 3 phenotypes

A
  1. Proctitis
  2. Left-sided colitis (to splenic flexure)
  3. Extensive colitis (past splenic flexure)
139
Q

How is UC Dx

A

Clinical picture
Labs
- Bloods: FBC, UEC, CRP, ESR, LFT, Fe, B12, vit D
- Serology (not routine): pANCA ( UC > CD), ASCA
- Stool: fecal calprotectin, MC&S, PCR, and C diff toxin EIA (rule out infection before immunosuppressive Tx)
Endoscopy
- contiguous/circumferential erythema, friability/granularity, loss of vascular pattern, ulceration, pseudopolyps/mucosal bridging
- involves rectum and extends proximally
Histology:
- chronic inflammation with crypt distortion and abscesses on biopsy
Imaging:
- rule out Crohn’s
- colonic bowel wall thickening

140
Q

Clinical features of UC

A

Diarrhoea, haematochezia, tenesmus, urgency

141
Q

Features of severe and fulminant UC

A

Severe: > 6 bloody stools daily, anaemia (Hb < 105g/L), elevated ESR >30/CRP, fever > 37.8, tachycardia > 90bpm
Fulminant: > 10 bowel movements per day, persistent GI bleeding, systemic toxicity, blood transfusion requirement, abdominal tenderness and distension, colonic dilatation on AXR

142
Q

Treatment of acute severe UC

A

Admit to hospital
Exclude GI infection (esp. CMV, C. diff, common bacterial pathogens)
Initial Mx: hydrocortisone 100mg IV 6 hourly (or methylprednisolone 60mg IV daily) for 3-5 days –> oral switch
VTE prophylaxis +/- electrolyte/fluid/blood replacement
Flexible sigmoidoscopy within 48 hours of admission
Routine monitoring of daily stool count, FBE, CRP, UEC
AXR for colonic dilatation at admission and if Sx change
If response not achieved in 3 days –> salvage therapy or colectomy
Salvage therapy
- infliximab 5mg/kg by IV infusion over 2 hours
- or ciclosporin 2mg/kg IV as 24hour infusion
- followed by ongoing Tx if effective

143
Q

UC Induction Tx

A

Distal colitis/proctitis:
1. Oral and rectal (enema/suppository) 5ASA e.g., mesalazine
2. If ineffective add rectal corticosteroid
3. If ineffective add oral prednisolone 40-50mg PO
Extensive UC:
1. Rectal mesalazine + oral mesalazine/ASA
2. If ineffective add PO prednisolone

144
Q

UC Maintenance Tx

A

Oral and rectal 5-ASA
If ineffective consider azathiopurine/mercaptopurine
If ineffective consider biological

145
Q

Pouchitis

A
146
Q

CI to cyclosporin

A

HTN, renal disease, seizure history, total low cholesterol

147
Q

Indications for surgery in UC

A

Severe colitis not responding to IV steroids or rescue therapy
Fulminant colitis with or without toxic megacolon
Exsanguinating haemorrhage
Perforation
Pt unable to tolerate medication SEs
High grade dysplasia
Cancer

148
Q

MC urgent/acute UC operation

A

Total colectomy with formation of ileostomy

149
Q

MC elective UC operation

A

Panproctocolectomy with ileal pouch anal anastamosis

150
Q

What is a complication of IPAA for UC

A

Pouchitis (acute < 4 weeks/chronic > 4 weeks)

151
Q

Dx of pouchitis

A

Clinical: Increase in stool frequency (> 8-10/day), urgency, incontinence, increase in night-time seepage, perianal/abdominal pain
Pouchoscopy: erthyma, oedema, granularity, friability, loss of vascular pattern, mucous exudates, ulcerations
Histology: inflammation with crypt distortion and crypt abscess
Stool cultures: rule out C diff, CMV, bacteria

152
Q

Tx of pouchitis

A

Cirpofloxacin and metronidazole orch amoxicillin and clavulanic acid
If chronic rotate antibiotics and pouch endpscopic surveillance for neoplasia

153
Q

IBD acute/subacute complications

A

UC: GIT bleeding, toxic megacolon, toxic fulminant colitis
CD: perforation, strictures/inflammation –> SBO/LBO, abscesses (intra-abdominal, perianal)

154
Q

IBD longterm complications

A

UC: CRC, iron deficiency
CD: fistula formation (perianal, enteroenteric, enterovaginal, enterovesical), fibrostenotic strictures, CRC, iron deficiency, B12 deficiency, cholelithiasis (impaired bile acid reabsorption in terminal ileum), nephrolithiasis (impaired oxalate absorption –> kidney excretion), oral ulcers

155
Q

IBD extraintestinal complications

A

Episcleritis, scleritis, uveitis
Erythema nodosum, pyoderma gangrenosum
Primary sclerosing cholangitis, cholangiocarcinoma, autoimmune hepatitis
Anaemia
Prothrombitic state
Sacroilitis, ankylosing spondylitis, peripheral arthritis
Osteopaenia, osteoporosis

156
Q

Risk factors for CRC in UC

A

Duration of colitis
Backwash ileitis
Extensive colitis
Severe inflammation
Pseudopolyps
Primary sclerosing cholangitis
FHx CRC
Dysplasia

157
Q

CRC screening timeframes and actions in IBD

A

8-10yrs after Dx if extensive in UC or > 30% colitis in CD
15 years after left-sided colitis
At Dx of PSC then every 1-2 years
Flat lesions
- LG dysplasia: colectomy or close surveillance
- HG dysplasia: colectomy
Polypod lesions: complete removal and vigilant follow up

158
Q

Name benign and pre-malignant polyps

A

BENIGN
Inflammatory pseudopolyps
Hyperplastic polyps
PREMALIGNANT
Adenomas (tubular/villous/tubulovillous)
Serrated

159
Q

High risk features of polyps

A

Adenomas or sessile serrated polyps with HG dysplasia/villlous type/3+ in number/10mm+ in size, flat/depressed lesion

160
Q

Risk factors for CRC

A

Age
Hx of adenomatous colon polyps
FHx
DM
IBD
Genetic syndromes: FAP, Peutz Jeghers, Gardner, HNPCC

161
Q

How is CRC screened for in Aus?

A

FOBT (immunochemical test utilises antibodies for 50-74years every 2 years

162
Q

Who is ineligible for FOBT?

A

Recent colonoscopy, blood in stool, bleeding haemorrhoids, menstruating within last 3 days

163
Q

What is familial adenomatosis polyposis

A

Hereditary syndrome characterised by presence of thousands of CR adenomas that usually develop in adolescence –> without proctocolectomy (by ~age 20) CRC always develops (~mean 40yo)

164
Q

Extracolonic features of FAP

A

Duodenal adenomas
Gastric fundic gland hyperplasia
Mandibular osteoma
Supernumerary teeth

165
Q

What is Lynch Syndrome/HNPCC

A

MCC inherited colon cancer
Mismatch repair gene mutations

166
Q

What other cancers are associated with HNPCC

A

Uterine, ovarian, genitourinary, small bowel, hepatobiliary

167
Q

Amsterdam criteria for HNPCC

A
  1. At least 3 relatives with confirmed CRC/endometrial Ca/SB Ca
  2. At least 2 successive generations
  3. At least one Dx before 50yo
  4. At least one 1st degree relative
168
Q

What are the characteristics of Peutz Jegher Syndrome

A

Multiple hamartomatous polyps in GIT
Mucocutaneous pigmentation (lips, buccal mucosa, nose, perianal area, genitals)
Increased risk of malignancy (GI, gynae, testicular, breast, pancreas)

169
Q

MCC UGI Bleeding

A

Peptic ulcer disease
Oesophago-gastric varices
Mallory Weiss tear (longitudinal mucosal tear of oesophagus at GEJ 2˚ violent vomiting/coughing/sudden increase in IAP
Erosive oesophagitis
Gastritis
Gastric cancer
GAVE = gastric antral vascular ectasia
Dieulafoy lesion = submucosal vessel eroded into epithelium
Hereditary Haemorrhagic Telangiectasia (Osler-Weber-Rendu syndrome –> epistaxis, cerebral AVM, GI bleeding)
Aortic graft surgery with fistula (aortoenteric fistula)
Exacerbated by anticoagulation

170
Q

How does UGI bleeding present

A

Malaena
Haematemesis
Haemodynamic instability/collapse/shock
- tachycardia,hypotension
If rapid and heavy possibly haematochezia

171
Q

Initial management of UGI bleeding

A

Take Hx, Ex, monitor vitals, risk stratificaton
Airway positioning +/- suction/adjuncts
O2
2 wide bore cannulas placed:
- FBC, UEC, G&XM (2U), LFT, coag screen
- IV crystalloids for fluid resus +/- blood transfusion if Hb < 70g/L or < 100g/L and clinically unstable
- IV PPIs (e.g., omeprazole 80mg followed by infusion for 72 hr)
- Stop anticoagulant/antiplatelet medication including NSAIDs
- Keep NPO
Urgent endoscopy after resuscitation

172
Q

Peptic ulcer bleeding Mx

A

Resuscitation
Endoscopy: haemostasis with 2 or 3 methods (adrenaline injection into tissue + thermal coagulation with heater or laser or argon plasma coagulation + endoscopic clipping), risk stratification, H. Pylori testing (active bleeding can result in false -ve rapid urease test so do histology)
High dose PPI to prevent rebleed –> PPI continued for 4 weeks to ensure ulcer healing
Bleeding not controlled –> angiography for embolisation or surgery
Surgery only indicated if bleeding cannot be controlled endoscopically, bleeding secondary to gastric cancer, perforated ulcer, or refractory ulcer
Eradication of H. pylori if indicated (confirm)

173
Q

Variceal bleeding Mx

A

IV octreotide/terlipressin (constriction of splanchnic vessels)
IV prophylactic antibiotics due to high risk of bacterial sepsis
Endoscopy: band ligation or injection sclerotherapy
If bleeding not controlled: balloon catheter for compression of gastric/oesophageal varices
Insertion of transjugular intrahepatic portosystemic shunt reverses portal HTN and can be used for acute bleeding Mx and to prevent re-bleeding
propranolol???????

174
Q

GI vascular lesion and UGI Ca bleeding Mx

A

Argon plasma coagulation (ablates vessel)
Starch spray/haemostatic powder/radiotherapy for cancers

175
Q

Risk factors for UGI rebleeding and death

A

Age
Comorbidities (cardiac failure, IHD, CKD, malignant disease, liver disease)
Presence of clinical features of shock (pallor, hypotension, tachycardia, cold peripheries)
Endoscopic Dx and endoscopic stigmata of recent bleeding

176
Q

Rockall assessment for UGIB risk stratification

A

Age: < 60, 60-79, > 79
HR: < 100bpm, > 100bpm
BP: > 100mmHg < 100mmHg
Comorbidities: none, _, cardiac/other major, CKD/liver failure/disseminated malignancy
Endoscopic Dx: Mallory Weiss tear/no lesion, everything else, malignancy
Major stigmata of recent haemorrhage: none/dark spots, _, blood in UGIT, adherent clot, spurting vessel

177
Q

Mallory Weiss Tear Mx

A

Usually minor and resolve in 24 hours
If large can do endoscopic clipping (surgical oversewing of tear rarely needed)

178
Q

Causes of LGI bleeding

A

CRC
CR polyps
Colitis: infective, IBD, ischaemic
Angiodysplasia
Diverticulosis
Hemorrhoids
Anal fissure
Hookworm is MCC worldwide of chronic GI blood loss

179
Q

Dx of acute LGI bleeding

A

Hx, Ex including DRE
Ix: proctoscopy for anorectal disease esp. haemorrhoids, flexible sigmoidoscopy/colonoscopy (IBD, diverticular disease, ischaemic colitis, cancer, angiodysplasia), video capsule endoscopy, angiography (angiodysplsia/vascular abnormality)

180
Q

Chronic GI bleeding Dx

A

Hx and Ex may indicate site otehrwise both gastroscopy (duodenal biopsies for coeliac disease) and colonoscopy (biopsies) should be performed
Unprepared CT for colon ca in frail pts
CT colonography
Capsule endoscopy if no cause found
- Tx lesions with baloon assisted enteroscopy
Treat anaemia

181
Q

What separates UGI and LGI bleeding

A

Ligament of Treitz

182
Q

What are the 4 clinical scenarios associated with inadequate blood supply to colon

A

Acute mesenteric ischemia (MC)
Chronic mesenteric ischemia
Colonic ischaemia
Mesenteric venous thrombosis

183
Q

What are the causes of acute mesenteric ischaemia

A

Acute mesenteric artery embolism: MCC = embolic occlusion due to AF (also MI/valvular disease) and most commonly involves SMA
Acute mesenteric artery thrombosis: risk factors include visceral atherosclerosis, arteritis, aortic aneurysm, aortic dissection, prothrombotic disorders and hypercoagulability from cancers
Non-occlusive acute mesenteric ischaemia: critically ill pts with low CO
Mesenteric venous thrombosis

184
Q

Prognosis for acute mesenteric ischaemia

A

Life-threatening
Poor unless prompt radiologically guided revascularisation or resection of affecetd bowel

185
Q

Presentation of acute mesenteric iscahaemia

A

Severe abdominal pain out of proportion to relatively minor abdominal tenderness/lack of peritoneal signs on examination
High serum lactate

186
Q

Imaging features of acute mesenteric ischaemia

A

Pneumatosis intestinalis
Thumbprinting
Bowel wall oedema
All are late signs

187
Q

Causes of chronic mesenteric ischaemia

A

Atherosclerotic occlusion of main mesenteric vessels (coeliac, SMA, or IMA) - symptoms do not occur unless occlusion of 2/3 main vessels has occurred

188
Q

Clinical features of chronic mesenteric ischaemia

A

Postprandial abdominal pain, fear of eating, weight loss
Occassionally abdominal bruits

189
Q

How should chronic mesenteric ischaemia be investigated

A

Mesenteric USS doppler and/or an angiogram

190
Q

How is chronic mesenteric ischaemia treated

A

Endoluminal revascularisation or surgical bypass procedures
Optimisation of vascular risk factors

191
Q

What is the cause of mesenteric venous thrombosis

A

Occlusion of blood outflow usually due to local swelling, infection, masses or pro-thrombotic states

192
Q

What is standard therapy for mesenteric venous thrombosis

A

Bowel rest and anticoagulation

193
Q

What is ischaemic colitis

A

Acute or chronic hypoperfusion of the colon that is typically transient and self-limited but can also result in severe acute ischemia with bowel infarction

194
Q

What causes ischaemic colitis

A

Usually non-occlusive disease e.g., systemic hypotension, microvascular disease
Colonic bleeding occurs due to sloughing of necrosed mucosa mostly from watershed areas of colon (splenic flexure and rectosigmoid junction) prone to hypoperfusion during low flow states as in dehydration/reduced CO

195
Q

Risk factors for ischaemic colitis

A

Advanced age, haemodialysis, DM, hypoalbuminaemia

196
Q

Clinical presentation of ischaemic colitis

A

Sudden onset of abdominal pain (MC LLQ) followed by passage of maroon stools

197
Q

Investigation of ischaemic bowel disease

A

FBC, ABG (acidosis) with serum lactate, UEC, LFT, amylase, coags, group & hold/XM

ECG

Urgent CT with contrast/CT angiogram: bowel wall thickening, bowel dilation, pneumatosis intestinalis, portal venous gas, occlusion of mesenteric vasculature, bowel wall thickening with thumbprinting sign suggestive of submucosal oedema or haemorrhage

Sigmoidoscopy/colonoscopy if no peritoneal signs/surgery not urgent

198
Q

Diverticular bleeding presents as

A

Bright red rectal bleeding or red blood mixed with stool (haematochezia) or darker maroon stools

199
Q

What is angiodysplasia

A

Fragile, superficial BVs in colon that easily bleed esp. in cecum

200
Q

Tx angiodysplasia

A

Endoscopic ablation

201
Q

Ix of obscure GI bleeding

A

May present as IDA (replacement –> returns :( )
Upper and lower GI endoscopy
CT angio and isotope-labeled red cell scans both require active bleeding at time of scan
Video capsule endoscopy (risk = capsule retention can result in bowel obstruction)

General Medicine (3 decks)

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