Gastroenterology Flashcards

1
Q

Crohn’s Disease

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
  • Complications
A

Pathophysiology
- Skip lesions (normally terminal ileum/colon) w/ transmural inflammation –> strictures, fistula, adhesions
- Cobblestone appearance
- Non-caseating granulmatous infection, goblet cells

Presentation
- late teens
- weight loss, lethargy, diarrhoea, abdo pain, perianal skin tags/ulcers, oral aphthous ulcers
- Crohn’s colitis -> bloody diarrhoea
- Extra-intestinal features:
Related to disease activity: arthritis, erythema nodosum, episcleritis, osteoporosis
Unrelated to disease activity -> arthritis, uveitis, pyoderma gangrenosum, clubbing

Investigations
- Faecal calprotectin - used to confirm acute flare
- Colonoscopy w/ biopsies
- can be low vit B12 (terminal ileum) +Vit D

Management
- Stop smoking

  • Inducing remission (flares):

Generally:
- 1st line: steroids OR elemental diet (eg. in children if worry re SE of steroids)
- 2nd line: 5-ASA (e.g. mesalazine)
- + azathioprine, mercaptopurine or methotrexate (add ons, not used as monotherapy)

Refractory/fistulating:
- infliximab

Isolated peri-anal disease:
- metronidazole

Maintaining remission
- Stop smoking
- 1st line Azathioprine or mercaptopurine
- (check TPMT activity before starting)
- 2nd: methotrexate

Surgery:
- Stricturing terminal ileal disease -> ileocaecal resection
- Segmental small bowel resection
- Stricturoplast
- Perianal fistulae: MRI to Ix. If syptomatic - PO metronidazole +/- anti-TNF (infliximab), draining seton
- Perianal abscess (incision + drainage + abx therapy)

Complications
- Fistulae, fissures, strictures, obstruction
- Small bowel cancer
- Colorectal cancer
- Osteoporosis

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

Ulcerative Colitis
- Pathophyiology
- Presentation
- Investigation
- Management

A

Pathophysiology
- Diffuse continuous mucosal inflammation (mucosa only), spreads proximally
- Non-granulomatous inflammation, crypt abscesses, goblet cell hypoplasia

Presentation
- Proctitis (confined to rectum) w/ PR bleeding + mucus discharge, increased frequency/urgency of defaecation + tenesmus
- If more extensive - bloody diarrhoea, malaise, anorexia, low grade pyrexia
- Severe abdo pain - ?fulminant colitis, toxic megacolon (CXR to confirm- transverse colon >6cm diameter) or perforation (CT)
- Extra-intestinal: arthritis, erythema nodosum, episcleritis, ant. uveitis, primary sclerosing cholangitis

Mild
- <4movements/day, minimal blood, no pyrexia, HR <90, no anaemia

Mod
- 4-6 movements, mild-sev blood, no pyrexia, tachy or anaemia

Severe
- >6 movements, visible blood, pyrexia, pulse >90 or anaemia

Investigations
- Colonoscopy + biopsies (although avoid in severe colitis as can -> perforation)
- Barium enema: loss of haustrations, superficial ulceration, drainpipe colon
- Faecal calprotectin

Management
- Inducing remission
Proctitis
- rectal aminosalicylate (mesalazine).
- no remission in 4/52: add PO aminosalicylate
- still no rem: add topical or PO steroids

Proctosigmoiditis/left-sided UC:
- rectal aminosalicylate
- no rem in 4/52: add high-dose PO aminosalicylate +/- topical steroid
- if not: stop topicals + give both PO

Extensive disease
- topical AND high-dose PO aminosalicylate
- no rem in 4/52: stop topical + give both high-dose PO

  • Extensive disease - topical aminosalicylate AND high-dose PO aminosalicylate
  • (if no remission in 4/52
  • Severe colitis - hospital admission - IV steroids +/- ciclosporin +/- surgery

Maintaining remission
Following mild/mod flare
- proctitis/proctosigmoiditis: rectal and/or PO aminosalicylate OD or intermittent
- left sided/extensive: low dose PO aminosalicylate

Following severe or 2 or more exac in a year
PO azathioprine + PO mercaptopurine

Complications
- Increased risk of colorectal Ca if UC for >10yrs - colonoscopy w/ biopsies every 1-5yrs

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

Side Effects of Aminosalicylate drugs e.g. mesalazine, sulfasalazine
(used in Tx of UC and Crohn’s)

A
  • Haematological: Agranulocytosis (need to do FBC in unwell patients)
  • Sulphasalazine: rash, oligospermia, megaloblastic anaemia, lung fibrosis
  • Mesalazine: pancreatitis, Gi upset, headache, interstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clostridium Difficile
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology
- Clindamycin and Cephalosporins high risk (cephalexin, cefuroxime, ceftriaxone) also PPIs

Presentation
- Diarrhoea, abdo pain
- raised WCC
- If severe –> toxic megacolon

mild - normal
Mod - elevated WCC (But <15), 3-5 stools/day
Sev - elevated WCC (>15) OR acutely raised Cr OR temp >38.5 OR abdo or radiological signs
Life-threatening: Hypotension, partial/complete ileus, toxic megaolon or CT evidence of severe disease

Investigations
- C. Diff toxin in stool

Management
1st episode
1st line: PO vancomycin 10d
2nd: PO fidoxamicin
3rd: PO vanc +/- IV metro

Recurrent episode
within 12/52 of sx resolution: PO fidoxamicin
after 12/52: PO vanc or fidoxamicin
2 or more prev episodes ?faecal microbiotca transplant

Life-threatening
PO vanc AND IV metronidazole
+ specialist advice, ?surgery

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

Irritable Bowel Syndrome
- Presentation
- Investigation
- Management

A

Presentation
- Abdominal pain, Bloating, Change in bowel habit
- Diagnosis if abdo pain w/ relief w defaecation or altered bowel freuency plus 2 of:
- Altered stool passage (strain, urge, incomplete evacuation)
- Abdo bloating (more in women)
- Sx worse w/ eating
- passage of mucus

Red Flags: PR bleed, unexplained weight loss, fam hx bowel/ovarian ca, onset >60yo

Investigations
FBC, ESR/CRP, coeliac screen (tissue transglutaminase antibodies)

Managament
- 1st line depends on main feature
- Pain: antispasmodic e.g. buscopan, mebeverine
- constipation: laxatives
- Diarrhoea: loperamide
- Can try TCAs and SSRI if above ineffective

  • General dietary advice: eat: oats, linseed. Avoid: food hard to digest e.g. broccoli + cabbage, sorbitol
  • Can try peppermint oil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Coeliac Disease
- Pathophysiology
- Presentation
- Investigation
- Management
- Complications

A

Pathophysiology
- autoimmune sensitivity to gluten -> villous atrophy -> malabsorption

  • People w/ following should be screened:
  • Symptoms (below)
  • Autoimmune thyroid disease
  • Dermatitis herpetiformis
  • IBS
  • T1DM
  • 1st degree relatives w/ coeliac

Presentation
- chronic/intermittent diarrhoea
- failure to thrive (children)
- unexplained n+v
- Prolonged fatigue
- Recurrent abdo pain, cramping, distension
- Sudden/unexpected weight loss
- unexplained IDA/other anaemia

Complications/Extra-intestinal manifestations
- Anaemia: iron, B12, folate (folate def more common than B12)
- Hyposplenism
- Osteoporosis, osteopenia, osteomalacia
- Lactose intolerance
- T-cell lymphoma of small intestine, rarely oesophageal + other malignancy
- Subfertility
- Arthritis + arthralgia
- Neuro: intractable epilepsy, cerebellar ataxia
- Chronic hepatitis

Investigation
- serology:
TTG antibodies + IgA antibodies
Endomyseal antibodies (look IgA def which would give false -ve coeliac result)
(other: anti-gliadin, anti-casein)

  • Endoscopic intestinal biopsy (done in all w/ suspected coeliac)
  • duodenal +/- jejunal biopsies (vilous atrophy, crypt hyperplasia, lymphocytes)

Management
- Gluten free diet-

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

Dyspepsia (epigastric discomfort)
- Differentials
- Investigation
- Management

A

Differentials for Dyspepsia
- Oesophageal: GORD, Ca, acahalsia
- Gastric: peptic ulcer, gastritis, H.pylori, gastric Ca
- Duodenal: ulcer, Ca
- Pancreas: acute/chronic pancreatitis, Ca
- HPB: cholangitis, stones, Ca

Investigation -
- Urgent (2ww) endoscopy:
Dysphagia
Upper abdo mass
>55 w/ weight loss AND either: upper abdo pain, reflux, dyspepsia

  • Non-urgent endoscopy
    >55 w/:
    Treatment resistant dyspepsia
    Upper abdo pain + low Hb
    Raised platelets or n+v w/ any one of: weight loss, reflux, dyspepsia, upper abdo pain
  • If not meeting referral criteria = undiagnosed dyspepsia
    1. Reivew meds
    1. Lifestyle Advice
    1. Trial full dose PPI for 1/12 OR ‘test and treat’ H.pylori
      (if sx persist try the alternative approach)

N.B. stop PPI 2/52 prior to endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is H.Pylori Tested for?
How is it treated?
What are possible complications of H.pylori infection?

A

Investigations
- Urea breath test: not within 4/52 of treatment w/ abx or PPI. Although eradication not routinely checked for if you were to test would use this.
- Rapid urease test
- Serum antibodies (remains +ve post eradication)
- Gastric biopsy culture
- Stool antigen test

Management
- 7 days of triple therapy:
- PPI + amoxicillin + clarithromycin or metronidazole
- (if pen allergin ppi + clari + metro)

Complications
- peptic ulcer disease (95% of duodenal + 75% of gastric ulcers)
- Gastric cancer
- B-cell lymphoma of MALT (H.pylori eradication -> regression of lymphoma in 80%)
- Atrophic gastritis

N.B. unclear relationship w/ GORD + no role for eradication in GORD management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

GORD
- Pathophysiology
- Presentation
- Investigations
- Management
- Complications

A

Pathophysiology
- Due to reflux of stomach acid into lower oesophagus
- RFs: smoking, alcohol, obesity, age
Presentation
- burning retrosternal/chest pain
- Worse after meals, lying down/bending over
- belching, odynophagia, chronic cough
- Red Flags: dysphagia, weight loss, early satiety, malaise, loss of appetite

Investigation
- Manage as per dyspepsia guidelines until endoscopy done
- GI endoscopy if: >55, Sx >4/52 or resistant to Tx, dysphagia, relapsing sx, weight loss

Management
- Endoscopically proven oesophagitis:
Full dose PPI 1-2/12
if response -> low dose tx as needed; if no response -> double dose for 1/12

  • Endoscopically -ve reflux disease:
  • Full dose PPI for 1/12
  • if response -> PRN low dose
  • If no response -> H2RA or prokinetic for 1/12

PPI Side effects: hyponatraemia + hypomagnesaemia, osteoporosis, microscopic colitis, increased risk of C.diff

Complications
- Oesophagitis, ulcers, anaemia, benign strictures
- Barrett’s oesophagus (metalplasia) -> high dose PPI; endoscopical surveillance w/ biopsies every 3-5yr, if dysplasia - endoscopic intervention (ablation or mucosal resection)
- Oesophgeal adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pernicious Anaemia

Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- Autoimmune disorder -> vit B12 def.
- Antibodies to intrinsic factor +/- gastric parietal cells
- Vit B12 normally produces red cells + myelinates nerves –> megaloblastic anaemia + neuropathy

RFs: female, other autoimmune conditions, blood group A

Presentation
- Anaemia: lethargy, pallor, SOB
- Neuro:
>Peripheral neuropathy
>Subacute combined degeneration of spinal cord –> progressive weakness, ataxia, paraesthesia –> spasticity + paraplegia
>Neuropsych: memory loss, poor concentration, confusion, depression
>Increased risk gastric Ca

Investigations
- FBC - macrocytic anaemia
- low B12 + folate
- Ab to intrinsic factor (only seen in 50%)

Management
- B12 replacement IM
no neuro features: 3 per week for 2/52, then 3 monthly
(if neuro features need more frequent)

+/- folic acid replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Oesophageal Cancer

Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- SCC - upper 2/3rd oesophagus + seen more in less developed countries
- RF: smoking, alcohol, achalasia
- Adenocarcinoma - lower 1/3rd - more in developed countries
- RF: GORD, Barrett’, smoking, achalsia, obesity

Presentation
- Dysphagia - solid then liquid (rapid progression)
- Anorexia + weight loss
- Vomiting
- Odynophagia, hoarseness, melaena, cough

Investigation
- Upper GI endoscopy + biopsy
- CT staging

Management
- Operable disease: surgical resection + chemo
- risk of anastamotic leak + mediastinitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Achalasia

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
- failure of oesophageal peristalsis + failure of relaxation of lower oesophageal sphincter

Presentation
- Dysphagia to BOTH solids + liquids
- Heartburn
- Regurgitation of food (can -> cough, aspiration, pneumonia)
- malignant change in small no.
Investigation
- Oesophageal manometry - excessive LOS tone
- barium swallow - expanded oesophagus, fluid level, ‘birds beak’ appearance
- CXR - wide mediastinum, fluid level
Management
- 1st line: Pneumatic dilation
- 2nd: surgery - Heller cardiomyotomy

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

Haemachromatosis

  • Pathophysiology
  • Presentation
  • Investigations
  • Management
A

Pathophysiology
- Autosomal recessive disorder –> iron accumulation
- HFE gene mutation inheritance.
Presentation
- Often asymptomatic in early disease then initial non-specific symptoms
- Fatigue, erectile dysfunction, arthralgia, DM
- ‘bronze’ skin pigmentation
- Liver: chronic liver disease, hepatomeg, cirrhosis, hepatocellular deposition
- HF (dilated cardiomyopathy)
- Hypogonadism

Liver cirrhosis, DM, hypogonadism, arthropathy = non-reversible

Investigations
- Transferrin saturation = most useful
- genetic testing for HFE mutation

Typically:
- Transferrin sat >55% men, >50% women
- Raised ferritin >500 + iron
- low TIBC

Management
- 1st: venesection
- keep transferrin sat below 50% + ferritin conc below 50
- 2nd: desferrioxamine

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

Wilson’s Disease

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
- Autosomal recessive disorder w/ excessive copper deposition in tissues

Presentation
- Age 10-25yo. Children - present w. liver disease. adults w/ neurological disease.
- Liver: hepatitis, cirrhosis
- Neuro: - basal ganglia degeneration in brain, speech, behavioural, psych probs. Asterixis, dementia, parkinsonism.
- Kayser-Fleisher rings
- Renal tubular acidosis
- Haemolysis

Investigations
- Serum reduced caeruloplasmin and reduced total copper
- High 24h urinary copper excretion
- confirmed w/ genetic analysis

Management
- Penicillamine (chelates copper)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the causes and consequences of the following vitamin deficiencies:

  • Vitamin B6 (pyridoxine)
  • Vitamin B1 (thiamine)
  • Vitamin A
A

Vitamin B6 (pyridoxine)
- Causes: Isoniazid therapy
- Consequences: peripheral neuropathy, sideroblastic anaemia

**Vitamin B1 (thiamine) **
- Causes: Alcohol excess and malnutrition
- Consequences - it is needed by highly aerobic tissues to signs seen in brain (wernicke-korsakoff) + heart (wet beriberi):

  • Wernicke’s Encephalopathy
    Signs:
    ataxia **
    – oculomotor dysfunction ( nystagmus + ophthalmoplegia (lateral rectus palsy))
    – encephlopathy (
    confusion,** disorientation)
    – peripheral sensory neuropathy)
    Ix
  • decreased red cell transkelotase
  • MRI

*Korsakoff syndrome *
- Above plus antero- and retrograde amnesia w/ confabulation

Treatment of wernicke’s/korsakoff w/ B1 - pabrinex
N.B. Glucose infusion can trigger wernicke’s in chronic thiamine deficiency

Dry beriberi: peripheral neuropathy

Wet beriberi: dilated cardiomyopathy

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

What is the difference between the following conditions. Include causes, presentation, investigation and management.

  • Primary Biliary Cholangitis
  • Primary Sclerosing Cholangitis
A

Primary Biliary Cholangitis
Chronic liver disorder seen in middle-age females.
Interlobular ducts damaged by chronic inflammation –> progressive cholestasis –> cirrhosis

Presentation
- Early: asymptomatic (raised ALP on LFTs), fatigue, pruritis
- Cholestatic jaundice, hyperpigmentation, RUQ pain, xanthelasma, clubbing, hepatomegaly
- Late –> liver failure

Diagnosis
- Anti Mitochondrial antibodies (M2 - m for middle aged)
- Raised serum IgM
- Imaging: MRI or USS (to ro/ extrahepatic biliary obstruction)

Management
- 1st: ursodeoxycholic acid
- pruritis: cholestyramine
- Fat soluble vitamin supplements
- Liver transplant (if bilirubin >100)

Complications
Cirrhosis –> portal HTN –> ascits, haemorrhage
hepatocellular carcinoma
osteoporosis

Primary Sclerosing Cholangitis
Unknown cause. Fibrosis + inflammation of intra- and extra-hepatic ducts
Associations: UC, chrons, HIV
(UsClerosing)

Presentation
-similar to above

Investigation
ERCP or MRCP (biliary strictures give beaded appearance)
pANCA can be +ve
Liver biopsy can show onion skin appearance

Management
- ursodeoxycholic acid
- ?liver transplant (only curative)

Complications:
Cholangiocarcinoma
Increased colorectal cancer risk

17
Q

Gallstones and their complications
Describe the cause/presentation/management of the following:
- Asymptomatic Gallstones (found incidentally)
- Biliary Colic
- Cholecystitis
- Gallbladder abscess
- Ascending Cholangitis
- Gallstone ileus
- Acalculous cholecystitis

A

Asymptomatic gallstones
- In gallbladder: reassure, no management needed
- In CBD: surgical management (risk of complications - cholangitis or pancreatitis)

Biliary Colic
- Cause: gallstones in gallbladder, obstruction when gallbladder contracts -> pain
- RF: fat, forty, fertile, female
- Presentation: colicky intermittent RUQ pain, worse after eating fatty foods
- Elective laparoscopic cholecystectomy

Acute Cholecystitis
- Cause: infection/inflammation of gallbladder
- Presentation: RUQ pain, Fever, murphy’s sign on exam (RUQ pain on inspiration during palpation), mildly deranged LFTs
- Imaging + cholecystectomy ideally within 48h of presentation

Gallbladder abscess
- prodromal illness then RUQ pain, swinging pyrexia, systemically unwell
- USS +/- CT
- Surgery or if unfit then percutaneous drainage

Cholangitis
- CBD stone w/ infection
- Triad: Jaundice, Fever, RUQ pain or Pentad: plus confusion and shock (low BP/tachy)
- USS
- IV abx + ERCP after 24-48h to relieve obstruciton

Gallstone ileus
- rare complication. Mechanical ileus due to impaction of gallstone in intestinal tract (gallstone enters via fistula between gallbladder + duodenum)
- Can –> intermittent SBO
- Lapraotomy + removal of gallstone

Acalculous cholecystitis
- Gallbladder inflam with no stones
- Seen in those w/ intercurrent illness (eg. CM, organ failure) - systemically unwell w/ pyrexia
- Fit patient: cholecystectomy
- or percutaneous cholecystectomy if unfit

18
Q

Pancreatitis
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology
- Acute causes: Iatrogenic, Gallstone, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion, Hypertriglyceridaemia/Hypercalcaemia/Hypotherami, ERCP, Drugs (azathioprine, mesalazine, steroids etc)

  • Chronic: alcohol, CF, haemachromatosis, duct obstruction (tumour, stone, structural abnormalities)

Presentation
- Acute: epigastric pain radiating to back, n+v, retroperitoneal haemrrhage (cullens + grey turner), hypocalcaemia (due to fat necrossi)
Mild - no organ failure or local complications
Mod- no/transient organ failure, possible local complications
Severe - persistent (>48h) organ failure, poss local

  • Chronic: pain worse 15-30mins after eating, steatthorea, DM

Investigation
Acute: amylase/lipase (>3x upper limit), LFTs (may be concurrant cholestatic element)

Chronic: CT (pancreatic calcification), functional test (e.g faecal elastase)

Management
- Acute:
- Fluid resus- aim u/o >0.5ml/kg/hr
- Analgesia
- Not routinely made NBM or given abx (unless pancreatic necrosis suspected)
- Only surgery if: gallstones (to remove), necrossi w/ worsening organ dysfunction (debridement)

  • Chronic:
  • pancreatic enzyme supplements, analgesia, anti-oxidants
19
Q

Pancreatic Cancer
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology
- RFs; smoking, increasing age, DM, chronic pancreatitis, hereditary non-polyposis colorectal Ca, multiple endocrine neoplasia, BRCA2, KRAS gene mutation

Presentation
- Painless jaundice - pale stool, dark urine, pruritis, cholestatic LFTs
- weight loss, epigastric pain, anorexia
- loss of exocrine func -> steatthroea
- loss of endocrine func -> diabetes
- Migratory thrombophlebitis

Courvoisier’s Law - palpable gallbladder w/ painless obstructive jaundice -> malignant obstruction of CBD (cholangiocarcinoma or pancreatic Ca)

Investigation
- High resolution CT. Can have ‘double duct’ sign - dilation of common bile duct + pancreatic duct

Management
- most unsuitable for surgery (can do Whipple’s if suitable but can –> dumping syndrome, peptic ulcer disease)
- ERCP for palliation

20
Q

What are the following:
- Melanosis Coli
- Peutz-Jehger Syndrome
- Gilbert Syndrome

A

Melanosis Coli
- Pigmentation of bowel wall. Histology shows pigment laden macrophages.
- Due to laxative abuse (esp senna)

**Peutz-Jehger Syndrome **
- Autosomal dominant -> numerous hamartomatous polyps in GI tract + freckles on lips, face, palms + soles
- polyps are NOT pre-malignant BUT the condition is associated w/ increased GI malignancy
- Polyps can present w/ SBO/intusussception
- Managed conservatively unless complications develop

Gilbert Syndrome
- autosomal recessive - defective bilirubin conjugation
- –> unconjugated hyperbilirubinaemia. Jaundice only in intercurrent illness/exercise/fasting
- Ix - rise in bilirubin w/ fasting or IV nicotinic acid
- No Treatment needed

21
Q

Describe typical features of diarrhoea caused by the following:
- E.Coli
- Giardiasis
- Cholera
- Shigella
- Staph aureus
- Campylobacter
- Bacillus cereus
- Amoebiasis

Which organisms cause bloody dirrhoea?

A

E.Coli
- Common in travellers. Watery stools w/ abdo cramps + nausea.

Giardiasis (>7d onset)
- Prolonged diarrhoea

Cholera
- Profuse watery diarrhoea, severe dehydration –> weight loss
- (not common in travellers)

Shigella
- Bloody diarrhoea, vomiting, abdo pain

Staph aureus (1-6h onst)
- Severe vomiting, short incubation period

Campylobacter
- Flu-like prodome –> crampy abdo pain, fever, diarrhoea (+/- blood) (can mimic appendicitis)
- Complications: Guillain-Barre

Bacillus cereus (rice) (1-6h onset)
- vomiting within 6 hours
- diarrhoeal illness after 6 hours

Amoebiasis (>7d onset)
- Gradual onset, bloody diarrhoea, abdo pain, tenderness (can last weeks)

Causes of bloody diarrhoea - SEECSY

S - salmonella
E - E.Coli
E - Entamoeba (protozoa)
C - campylobacter
S- Shigella
Y - Yersinea Enterocolitica

22
Q

What are the following?

  • Cyclical Vomiting Syndrome
  • Budd-Chiari Syndrome
  • Bile-acid Malabsorption
A

Cyclical Vomiting Syndrome
- Rare, more in children + females, often comorbid migraines
- Presentation:
- Episodes: prodrome of sweating/nausea. Then sudden vomiting lasting hours-days. Well in between times.
- Can –> weight loss, reduced appetite, dizziness, headache, photophobia
- Ix- clinical, preg test in women, bloods (r/o underlying cause)
- Manage:
- -Prophylactic: amitryptiline, propanolo, topiramate
- Acute: ondansetron, prochlorperazine, triptans

**Budd-Chiari Syndrome ** = hepatic vein thrombosis/obstruction
- Causes: polycythaemia rubra vera, thrombophilia, pregnancy, COCP
- Features: sudden onset severe abdo pain, ascites, tender hepatomegaly
- Ix - Doppler USS

Bile-acid Malabsorption
- Causes: primary or secondary eg. cholecystectomy, coeliac, small bowel bacterial overgrowth
- –> chronic diarrhoea, steatorrhoea + vit ADEK malabsorption
- Ix: SeHCAT (nuclear medicine test)
- Manage w/ bile acid sequestrants eg. cholestyramine

23
Q

Alocohol Misuse

  • Screening tools

Describe the following complications and their management
- Alcoholic ketoacidosis
- Alcoholic liver disease
- Korsakoff Syndrome and Wernicke’s Encephalopathy
- Alcohol Withdrawal

A

Screening Tools
- AUDIT- 10 questions, score 0-40. >8 in men or >7 in women = harmful drinking, >15m >13f = dependence.
- FAST - 4 questions, score 0-16, >3 = hazardous
- CAGE (not thought to be so helpful anymore)

Alcoholic Ketoacidosis
- Euglycaemic ketoacidosis
- Due to malnourishment –> fat breakdown -> ketones w/ normal/low glucose + elevated anion gap

Alchoholic Liver Disease
This includes:
- Alcoholic fatty liver disease - asymptomatic + reversible w/ abstinence
- Alcoholic Hepatitis - RUQ pain + jaundice –> riased GGT + AST:ALT >2
- Cirrhosis - can co-exist w/ hepatitis (irreversible) + can -> portal vein HTN, hepatic encephalopthy, hepato-renal syndrome

  • Management
  • Abstinence, good nutrition, treat any complications e.g. ascites, SBP, encephalopathy
  • For alcoholic hepaitits:
  • Steroids e.g. pred in some acute episodes (depends on prothrombin time + bilirubin level)

Korsakoff + Wernicke’s
- Korsakoff (earlier) –> altered mental state, ophthalmoplegia, ataxia
- Wernicke’s encephalopathy -> amnesia + confabulation, ataxia, visual problems

Withdrawal
- Symptoms start 6-12h: tremor, sweating, tachy, anxiety
- 36h: seizures (not as responsive to phenytoin as other seizures)
- 48-72h: Delirium tremens: coarse, confusion, delusions, auditory + visual hallucinations, fever, tachycardia

Complex withdrawal needs admission until stable (any seizures or delirium tremens)
- Long=acting BDZ eg. chlordiazepoxide (more in hostp) OR diazepam (out of hosp OR in liver failure) - reducing regime

24
Q

Hepatorenal Syndrome

  • Pathophysiology
  • Presentation
  • Management
A

Pathophysiology
- Progressive kidney failure in someone w/ cirrhosis
- Thought to be due to vasoactice mediators –> splanchnic (gut) vasodilation + so underfilling of kidneys –> kidneys compensate by activating RAAS + causing renal vasoconstriction BUT this isn’t enough to counter the vasodilation

Split into:
- Type 1: rapidly progressive, doubling of serum Cr to >221 OR halving of CrCl to <20 over less than 2 weeks (++ bad prognosis)
- Type 2: slowly progressive, poor prognosis but not quite as bad

Presentation
- Cirrhosis w/ ascites
- Absence of parenchymal kidney disease (no protein or haematuria)

Management
-Vasopressin analogues e.g. terlipressin (cause vasoconstriction of splanchnic circulation)
-Volume expansion w/ 20% albumin (HAS)
Transjugular intrahepatic portosystemic shunt

25
Q

Describe the following oesophageal disorders
- Oesophageal spasm
- Mallory Weiss Syndrome
- Plummer Vinson Syndrome
- Boerhaave Syndrome

A

Oesophageal spasm
- rare. elderly women.
- Diffuse (uncoordinated spasm -> dysphagia) or nutcracker oesophagsu (coordinated but excessive -> severe, crushing, central retrosternaal chest pain episodes)

Mallory Weiss Syndrome
- severe vomiting –> painful mucosal lacerations at gastroesophageal junction -> haematemsis
- Common in alcoholics. Self-resolving.
- Ix as per any cause of upper GI bleed

Plummer-Vinson Syndrome (unknown cause)
- Triad: Dysphagia (due to oesophageal webs); Glossitis, IDA
- Treat w/ iron supplementation + dilation of webs

Boerhaave Syndrome
- Severe vomiting or iatrogenic-> oesophageal rupture/perforation
- severe sudden onset retrosternal chest pain, resp distress, subcut emphysema following severe vomiting/retching (mackler’s triad)
- CXR- pneumomediastinum + intra-thoracic air-fluid levels
- CT w contrast - air/fluid in mediastinum or pleural cavity w/ leak of contrast from oesophagus
- Manage: Resus + surgery to control leak

26
Q

Give the following key features of Hepatitis A-E

  • Route of transmission
  • Does it progress to chronic disease?
  • Does it increase hepatocellular carcinoma risk?
  • Is there a vaccine?
  • How is it treated?
A

All present in acute phase w/ jaundice, RUQ pain, hepatomegaly, fever, raised LFTs, flu-like prodrome

Hepatitis A
Route: faecal-oral
Course: acute + self-limiting
Chronic disease: No
Cancer: No
Vaccine: Yes (given to at risk e.g. travel, MSM, IVDU, chronic liver disease, some occupation)

Hepatitis B
Route: infected body fluid, vertical
Chronic: Yes (but only 10%)
Cancer: yes
Vaccine: Yes (given as part of routine schedule and then again to at risk groups. Healthcare workers + CKD have Anti-HbS checked to check response (>100 adequate, 10-100 needs further dose, <10 = non-responder, needs to repeat course)
Management: Pegylated interferon

Hepatitis C
Route: body fluid, vertical
Chronic: Yes in >50% –> cirrhosis, sjogren’s arthralgia, porphyria cutanea tarda
Cancer: yes
Vaccine: No
Management: interferon based (95% clearance)

Hepatitis D
Route: same as B (so often co-infection); can also have superinfection (start w/ B then later D infection)
Chronic: yes (higher risk in superinfection)
Cancer: Yes
Vaccine: No
Treatment: interferon

Hepatitis E
Route: faecal-oral
Chronic: No
Cancer: No
Vaccine: No
Management: supportive

27
Q
  • Autoimmune hepatitis -investigation results, management
  • Drug-induced liver disease causes
  • Non-Alcoholic Fatty Liver Disease - subtypes, risk factors, investigation, management
A

Autoimmune Hepatitis
- Mostly in young women
- Presentation: chronic liver disease or acute hepatitis; amenorrhoea (common)
- Ix: ANA, SMA, LKM1 antibodies, IgG raised, inflammation + piecemeal/bridging necrosis on biopsy
- Mx: steroids, immunosupressants, transplant

Drug-Induced Liver Disease
Hepatocellular picture: paracetamol, alcohol, statins, amiodrone, Anti-TB (except ethambutol), Antiepileptics

Cholestatic picture: COCP, abx (fluclox, co-amox, erythromycin), steroids, sulphonylureas

Cirrhosis: methotrexate, methyldopa, amiodarone

Fatty Liver
- Types: steatosis, steatohepatitis, cirrhosis/fibrosis
- RF: obesity, T2DM, raised lipid
- Present: normally asymptomatic, hepatomegaly
- Ix ALT>AST (whereas alcoholic AST>ALT), increased echogenicity on USS, ELF (blood test to look for enhanced fibrosis or fibroscan if blood test not available)
- Management: Life-style changes + monitoring

28
Q

Liver Failure

Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
Live failure = inability to perform normal function
Can be: acute, acute-on-chronic or chronic
Causes: drugs, autoimmune, infection, fatty liver or pregnancy

Presentation
- May be signs of chronic liver disease: clubbing, palmar erythema, duputrens, spider naevi, gynaecomastia
- Acutely:
- Jaundice
- Hepatic encephalopthy - confusion, altered GCS, asterixis, constructional apraxia. Treat cause + give lactulose or rifaximin
- Coagulopathy
- Low Albumin
- Hepatorenal syndrome
- Hypoglycaemia
- Ascites
- Cerebral oedema
- Increased infection risk (treat w/ IV ceftriaxone)

Investigations - to determine cause + check liver/renal function/coag
Coagulopathy :
- Mostly low clotting factors –> increased bleeding risk –> increased PT, APTT + low fibrinogen
- BUT factor VIII is high (as good hepatic function needed to clear it) SO at paradoxically increased VTE risk
- Also in chronic liver disease there is less synthesis of protein C + S and anti-thrombin (these are all anticoags so –> increased thrombosis risk)

Management
- ITU supportive care +/- transplant

29
Q

Ascites
- Give possible causes of ascites and outline the management

A

Causes of ascites can be split into two groups:
- Serum-ascites albumin gradient (SAAG) >11 = due to portal HTN
Pre-hepatic: portal vein thrombosis

Hepatic: cirrhosis, alcholic liver disease, liver mets, fibrosis (wilsons, haemochromatosis)

Post-hepatic: hepatic vein thrombosis, budd chiari

  • SAAG <11
    e.g. hypoalbuminaemia; malignancy, infection (Tuberculous peritonitis), pancreatitis, bowel obstruction, serositic in connective tissue disease

Management
- Reduce dietary Na, fluid restirction
- Spironolactone +/- loop diuretics
- ?drainage in tense ascites
- Prophylactic abx (protects from SBP) if ascities protein <15 until the ascites has resolved

30
Q

Spontaneous Bacterial Peritonitis
- Pathophysiology
- Presentation
- Diagnosis
- Management

A

Pathophysiology
- Infection of ascites
- Mostly E.Coli

Presentation
- Ascites, abdo pain, fever

Diagnosis
- Neutrophils >250 cells/ul in ascitic fluid

Management
- IV cefotaxime

Prophylactic ciprofloxacin or norfloaxcin in patients w/ ascites protein <15 OR previous SBP

31
Q

Hepatocellular Carcinoma
- Pathophysiology
- Presentation
- Investigation
- Managment

A

Pathophysiology
- Risk Factors:
- Chronic Hepatitis B (main worldwide) + C (main in Europe)
- Liver cirrhosis - secondary to alcohol, haemaochromatosis, primary biliary cirrhosis
- Other: Alpha 1 antitrypsin deficiency, aflatoxin, COCP, steroids, male, DM, metabolic syndrome
BUT Wilson’s doesnt cause it

Presentation
- Tends to present late w/ features of liver cirrhosis or failure: jaundice, ascites, RUQ pain, hepatomegaly, pruritis, splenomegaly
- Can present as decompensation in someone w/ chronic liver disease
- Raised AFP

Investigation
- Screening w/ USS +/- AFP in high risk patients: liver cirrhosis secondary to Hep B, C or haemochromatosis, men w/ liver cirrhosis secondary to alcohol

Management
- Early: surgical
- Liver tranplsnt, ablation, transarterial chemoembolisation, chemo

32
Q

Gastric Cancer
Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- RF: age, H.pylori, atrophic gastritis, diet (salt + nitrates), smoking, Blood group A

Presentation
- Abdo pain (vague, epigastric, dyspepsia)
- Weight loss + anorexia
- Nausea + vomiting
- Dysphagia: esp if in prox stomach
- Overt upper GI bleeding in minority
- Virchow’s node
- Periumbilical node (sister mary joseph nodule)

Investigation
- OGD + biopsy (can see signet ring cells)
- CT for staging

Management
- Surgical: endoscopic mucosal resection, partial/total gastrectomy
- Chemo

33
Q

Carcinoid Tumours
Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- Carcinoid syndrome due to tumour release of serontonin into systemic circulation

Presentation
- Flushing (often earliest sign)
- Diarrhoea
- Bronchospasm
- Hypotension
- Right heart valvular stenosis
- Pellagra
- ACTH/GNRH may also be release -> cushing

Investigations
- Urinary 5-HIAA
- Plasma chromogranin Ay

Management
Somatostatin analogues eg. ocreotide

34
Q

Ischaemic to lower GI tract

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
Ischaemia to lower GI tract falls into:
- Acute or chronic mesenteric ischaemia
mesenteric ischaemia - typically small bowel, due to emboli, sudden onset severe sx needing urgent surgery

  • Ischaemic colitis
  • colitis typically large bowel, multifactorial, transient compromise of blood flow more likley in watershed areas e.g. splenic flexure. less severe sx. Bloody diarrhoea. Thumbprinting on imaging. Conservatively managed.

Common risk factors: age, AF, CVS disease, cocaine, sources of emboli e.g. endocarditis

Presentation
- Abdo pain - in acute MI tends to be sudden + severe + out of keeping w/ examination
- PR bleeding
- Diarrhoea
- Fever
- Bloods - raised WCC w/ lactic acidosis
- Chronic MI - rare, vague sx, ‘intestinal angina’

Investigation
- CT
- AXR shows thumbprinting in ischaemic colitis due to mucosal oedema/haemorrhage
Management
- Acute mesenteric ischaemia -> urgent surgery
- Ischaemic colitis - supportive +/- surgery if peritonitis, perforation or ongoing haemorrhage

35
Q

Angiodysplasia - what is this, how does it present
Ferritin - give causes of raised or reduced levels

A

Angiodysplasia
- Vascular deformity of GI tract - predisposes to bleeding + IDA. Typically in elderly or in hereditary haemorrhagic telangiectasia.
- Presentation: asymptomatic, painless occult PR bleeding (most), acute haemorrhage (10% - depends on location of malformation can -> haematemesis, melaena, PR blood)
- Diagnosis: colonscopy or mesenteric angiography if acutely bleeding
- Mx: endoscopic cautery, tranexamic acid, ?oestrogens

Ferritin
- Raised ferritin WITHOUT iron overload
Inflammation (acute phase reactant)
Alcohol
Liver disease
CKD
Malignancy

  • Raised WITH iron overload
    Hereditary haemochromatosis
    Secondary to repeat transfusions

Transferring saturation helps determine if iron overload is present. If <45% in females or <50% in males then no overload present.

  • Low ferritin
  • Iron deficiency anaemia
36
Q

Appendicitis

Pathophysiology
Presentation
Investigation
Management

A

Pathophysiology
- Lymphoid hyperplasia or faecolith obstructs appendiceal lumen -> oedema, ischaemia +/- perforation
Presentation
- Periumbilical abdo pain, migrates to RIF
- N+V, occassioanlly diarrhoea, mild pyrexia, anorexia
- worse on coughing. can’t hop.

Examination
- localised or generalised peritonitis
- Rosving’s (palpation of LIF causes pain in RIF)
- Psoas sign (pain on extending hip if retrocaecal appendix)

Investigation
- Raised inflammatory markers (mostly neutrophils)
- ?USS - eg. in females where differential is pelvic organ pathology
- ?CT

Management
- Appendicectomy + prophylactic IV abx
- If peritonitis/perforation/appendix mass - broad spectrum abx
N.B. in older patients need to consider underlying caecal malignancy or perforated sigmoid diverticular diseas

37
Q
  • Diverticulosis
  • Diverticular Disease
  • Diverticulitis
A

Diverticulosis
- Multiple outpouchings of bowel wall, mostly in sigmoid colon
*- Asymptomatic *
- RFs: age, low fibre fiet

Diverticular Disease
- Symptomatic diverticulosis
- Altered bowel habit, colicky left sided abdo pain
- Managed w/ high fibre diet

Diverticular bleed
- Diverticulum erodes into vessel –> large volume painless bleed
- most self-limiting + conservatively managed. May need embolisation or surgical resection if not.

Diverticulitis
- Infected diverticular –> LIF pain/tenderness, anorexia, N+V, diarrhoea, fever, raised inflammatory markers
- Complications: abscess, peritonitis, obstruction (stricture), perforation, fistula
- Management:
- Mild - PO abx
- Other: hospital - NBM IVI + IV abx (cephalosporin + metronidazole)
- If performation –> hartmann’s procedure (+ abx etc)

38
Q

Upper GI bleeding
- Causes
- Presentation

A

Causes
Oesophageal
- Varices - often haemodynamic compromise. May stop spontaneously but re-bleeds common.
- Oesophagitis - hx of GORD, low vol fresh blood
- Cancer - small vol, unless preterminal erosion of large vessels.
- Mallory Weiss Tear - small-mod vol following vomiting

Gastric:
- Ulcer - small vol bleed + IDA. OR can erode vessel -> haemorrhage + haematemesis
- Cancer- frank haematemesis w/ altered blood
- Diuelafoy lesion - AV malformation -> no prodrome -> haematemsis + melaena
- Diffuse erosive gastritis - triggered by NSAID use -> haematemesis + epigastric discomfort -> large vol bleed w/ haemodynamic compromise

Duodenal
- Ulcer - pain several hours after eating, haematemesis, melaena, epigastric discomfort
- Aorto-enteric fistula - rare but high mortality

Presentation
- Melaena, Haematemesis, Raised urea
- Plus signs of underlying cause
- Dysphagia/weight loss - cancer
- Dyspepsia - ulcer
- Stigmata of chronic liver disease - varices

39
Q

Outline the management of acute variceal and non-variceal upper GI bleeding

A

Both
Risk assess w/:

  1. Glasgow -Blatchford (pre-endoscopy)
    - Takes into account: urea, Hb, BP, pulse, co-morbidities, syncope, melaena
    - score = 0 - early discharge
  2. Rockall Score (after endoscopy) - gives % rebleeding + mortality

Resuscitate
- ABC
- Platelets transfusion (if active bleed + plt <50)
- FFP (fibrinogen <1 or PT/APTT >1.5x normal)
- Prothrombin complex if on warfarin + actively bleeding

Endoscopy (within 24h for any major bleed)

Non-variceal
- No PPI pre-endoscopy
- BUT if endoscopy shows recent haemorrhage then give PPI

Variceal
- Terlipressin and prophylactic abx (IV quinolone) pre-endoscopy
- Band ligation for oesophageal varices OR injection of N-butyl-2-cyanoacrylate for gastric (if not successful - TIPS or sengstaken blakemore tube)

  • Prophylaxis of variceal haemorrhage:
  • Propanolol
  • Band ligation every 2/52 until all varices eradicated w/ PPI cover