Abdomen Flashcards

1
Q

what are the causes of hepatomegaly only?

A

malignancy

  • primary
  • haematological
  • metastases

alcoholic liver disease (early)

vascular

  • right heart failure
  • budd-chiari syndrome
  • sickle cell disease

infective

  • viral hepatitis
  • hydatid disease
  • toxoplasmosis
  • amoebiasis

other

  • polycystic liver
  • infiltration (amyloid, sarcoid)
  • syphilis
  • acute fatty liver of pregnancy
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2
Q

which tumours commonly metastase to the liver?

what are the common benign liver tumours?

A

metastasise to liver

  • CRC
  • oesophagus, stomach
  • lung

benign

  • cavernous haemangioma
  • hepatic adenoma (COCP use)
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3
Q

what are the infective causes of acute hepatitis?

A
  • HAV/HBV/HCV/HEV
  • EBV/CMV
  • toxoplasmosis
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4
Q

painless jaundice, normal liver, splenomegaly, anaemia

diagnosis?

A

extravascluar haemolysis 2ary haematological malignancy

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5
Q

what are the causes of splenomegaly (+/- hepatomegaly)?

A
  • portal hypertension 2ary chronic liver disease (33%)
  • haematological malignancy (27%)
    • lymphoproliferative disorder (with widespread lymphadenopathy)
    • myeloproliferative disorder (pallor, bruising)
    • lymphoma
    • CML
  • infection (23%)
    • domestic - HIV, EBV/CMV
    • tropical - visceral leishmaniasis
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6
Q

what are the causes of decompensation in chronic liver disease?

A

sedatives, constipation and dehyration

(occult) GI bleeding

any infection, including spontaneous bacterial peritonitis

AKI, hypokalaemia, hepatorenal syndrome

development of HCC

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7
Q

what are the important questions about stool pattern in inflammatory bowel disease?

A

are you woken up at night with the need to poo? (yes = IBD)

urgency - when you get the feeling of needing to poo, are you able to hold it? (yes = IBD)

have you ever lost continence of stool? (yes = rectal inflammation)

do your stool flush properly? (no = steatorrhoea, malabsorbtion)

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8
Q

what is a good question to guage the degree of control in IBD?

A

frequency and severity of relapse(s)

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9
Q

what is the most common fistula in crohn’s disease?

A

perianal fistulae

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10
Q

in IBD, how to you clarify the difference in pain from a flare of inflammation versus stricture/obstruction

A

flare = contant pain, feeling unwell most of the time

obstruction = colicky pain consistently related to their meals, depending on how far along the bowel the obstruction is

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11
Q

what is the most common biologic therapy for IBD?

A

anti-TNF = infliximab or adalimumab

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12
Q

what should you think with IBD, stricture and new explosive foul green diarrhoea?

A

small intestinal bacterial overgrowth

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13
Q

what is the most common presentation of coealic disease in adults?

A

iron-deficiency anaemia

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14
Q

what is the antibody likely to be positive in PSC?

A

pANCA

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15
Q

what is the management for PSC?

A

ursodeoxycolic acid

and yearly colonoscopic surveillance program (if it is associated with colitis)

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16
Q

how many spider naevi are pathological ?

how do you know it is a spider naevus?

A

>5

fills from the inside to out

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17
Q

what is a finding on clinical examination that differentiates oedema 2ary to RHF or 2ary to hypoalbuminaemia?

A

RHF - JVP elevated

hypoalbuminaemia - JVP low

low protein means you are intravascularly deplete

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18
Q

what are the signs of chronic liver disease, portal hypertension and decompensated liver failure?

A

chronic liver disease

  • palmar erythema
  • gynaecomastia
  • spider naevi
  • dupytren’s contracture

portal hypertension

  • distended abdominal veins/caput medusae
  • ascites
  • splenomegaly

decompensated liver disease

  • jaundice
  • bruising
  • hepatic encephalopathy
  • asterixis
  • fetor hepaticus
  • oedema & low JVP
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19
Q

what is the presenting symptoms of crohn’s disease in children and adults?

A

children - abdo pain

adults - diarrhoea (+/- blood)

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20
Q

how do you diagnose AKI?

A

increase in serum Cr by more than 26.5 mmol/L in 48 hours

increase in serum Cr to 1.5x baseline

UO <0.5 mL/kg for 6 hours

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21
Q

which is the most common form of inherited colorectal cancer?

A

HNPCC

22
Q

how do you diagnose PSC?

A

ERCP - characteristic beaded appearance of multiple biliary strictures

23
Q

define cirrhosis

A

irreducible liver damage; histologically characterised by fibrosis, scarring and nodular regeneration of the liver parenchyma

24
Q

what are the causes of liver cirrhosis?

A
  • chronic alcohol abuse
  • infection: HBV or HCV
  • genetic: wilson’s disease, haemochomatosis, alpha1-antitrypsin deficiency
  • hepatic vein: Budd-Chiari
  • metabolic: non-alcoholic fatty liver disease
  • autoimmune: PSC, PBC, autoimmne hepatitis
  • drugs: amiodarone, methyldopa, methotrexate
25
Q

what is the significance of thrombocytopenia in cirrhosis?

A

would normally expect clotting dysfunction to come from decreased synthetic function (decreased PT on clotting screen)

consumption of platelets indicates sequestration in an enlarged spleen (splenomegaly) and decreased synthesis of TPO in the liver

26
Q

in patients with cirrhosis under 40 years old and no significant alcohol history, what weird and wonderful tests should you order?

A

hepatitis serology

ferritin/TIBC/transferrin, serum caeruloplasmin, alpha1-antitripsin levels

ANCA, AMA, anti-SMC antibodies

27
Q

what finding on ascitic tap would indicate spontaneous bacterial peritonitis?

A

neuts >250 cells/mm3

28
Q

which common medications should be avoided in cirrhosis?

A

NSAIDs, opiates, sedatives

29
Q

how do you treat spontaneous bacterial peritonitis?

what are the common organisms?

A

need antibiotics immediately - tazocin tds for 5 days

E. coli, Klebsiella, streptococcus

30
Q

what is colestyramine used for in cirrhosis?

A

treats pruritis

31
Q

how would you treat PBC?

A

bile acid analog - e.g. ursodeoxycholic acid
prevents progression of disease and lengthens time to transplant

anti-inflammatory - prednisolone 20 mg OD

anti-pruritis - colestyramine

eventually, liver transplant for end-stage liver disease

32
Q

what is the management of ascites ?

A

conservative

  • fluid (<1.5 L/day) and salt restriction (40-100 mmol/day)
  • daily weights, aiming for 0.5 kg/day loss

medical

  • spironolactone (max 400 mg/day)
  • add furosemide (max 120 mg/day) if needed
    • have to monitor Na+ closely

surgical

  • therapeutic paracentesis
    • must infuse albumin as well (6-8 g per L fluid removed)
33
Q

what is the role of lactulose in hepatic encephalopathy?

A

for treatment or prophylaxis

  1. increases gastric motility, decreasing the amount of time ammonia-producing bacteria have to aminate the gut
  2. forms low pH stool, which discourages the growth of ammonia-producing bacteria
34
Q

what are the extraintestinal manifestations of UC?

A
  • clubbing
  • aphthous oral ulcers
  • conjunctivitis, episcleritis, scleritis, iritis
  • pyoderma gangrenosum, erythema nodosum
  • sacroilitis, ankylosing spondylitis, arthritis
  • primary sclerosing cholangitis
35
Q

what are the investigations for UC?

A

blood: FBC & CRP (inflammation is diagnostic, assess anaemia), U&E (diarrhoea), LFT (?PSC), blood culture (?infective colitis)

faecal calprotectin

lower GI endoscopy + biopsy

in acute presentation, limited flexible sigmoidoscopy to establish the diagnosis. when flare is under control, a colonoscopy is indicated to assess the extent of involvement of the bowel.

36
Q

what are the main acute and chronic complications of UC?

A
  • *acute** - toxic megacolon, large bowel >6 cm on AXR, risk of perforation
  • these patients are also at risk of VTE and hypokalaemia*

chronic - development of CRC, related to disease severity and total time flared up
these patients are monitored with surveillance colonoscopy + multiple biopsy q1-5 years depending on risk factors

37
Q

what are the management steps in UC?

A

mild

  • 5-ASA (mesalasine) = induce remisison/maintenance

moderate flare

  • steroids
    • PR for proctitis
    • PO for more extensive disease

severe flare

  • admit - supportive care, fluids, VTE prophylaxis, investigate for infective cause (C diff toxin), blood transfusion if Hb <80 g/L
  • IV steroids (hydrocortisone, methylpred)
  • rescue after 3-5 days with ciclosporin or infliximab
    • ciclosporin = AZA for maintenance
    • infliximab = infliximab for maintenance
  • surgical resection of disease after 7-10 days

immunomodulation

if many/severe flares then needs AZA/MTX or biologic therapy (infliximab, adalimumab, vedolizumab, ustekinumab)

38
Q

when do you use 5-ASA in crohn’s colitis?

A

there is no role for 5-ASA in crohn’s

5-ASA is only for UC

39
Q

how do you manage the diet of a crohn’s patient?

A

ideally they remain on enteral nutrition, TPN is last resort

diets that help control symptoms, induce remission and cure strictures:

  • elemental diet
  • low residue diet
40
Q

what is the rate of surgical intervention in crohn’s disease?

what is a complication of repeated surgical bowel resection?

A

50-80% of patients will have at least 1 surgery in their lives on the bowel

indications:

  • resection of the affected bowel
  • fistulae
  • GI obstruction from stricture

risk when bowel <150 cm = short bowel syndrome
diarrhoea, malabsorbtion, ADEK/Fe/B12 deficiency.
hyperoxaluira (renal stones), bile salt wasting (gallstones)

41
Q

small bowel villous atropy…

A

coeliac disease

42
Q

what is the skin manifestation of coeliac disease?

A

dermatitis herpetiformis

43
Q

what are the HLA types accociated with coeliac?

A

HLA-DQ2 (95%)

rest are HLA-DQ8

44
Q

what are the anti-spasmodics used in IBS?

A

meberevine or hyoscine

both OTC

45
Q

what is the name of the low sugar/alcohol diet used to reduce bloating/flatulence in IBS?

A

FODMAP diet

low in fermentable, poorly absorbed saccharides and alcohols

46
Q

what are the findings on ascitic tap that would indicate antibacterial prophylaxis against SBP?

what antibiotic would you give them?

A

ascites protein <15 g/L

oral ciprofloxacin

47
Q

in what portion of the oesophagus are tumours most likely to occur?

what is the typical tumour subtype?

A

middle third

likely adenocarcinoma 2ary to GORD/Barrett’s

48
Q

how do you diagnose AKI?

A

according to the KDIGO:

  • Cr rise of >26 mcmol/L within 48 hours
  • Cr rise to >1.5x baseline within 7 days
  • UO <0.5 mL/kg/hr for >6 hours
49
Q

a patient with a long-term catheter is found to grow bacteria on MC&S.

what are the management considerations?

A

do not use dipstick or microscopy for the diagnosis of UTI in catheterised patients. only send for culture and sensitivity.

do not regularly give antibiotic prophylaxis for patients with long-term catheters.

if symptomatic, change the catheter and give antibiotic treatment.

if asmyptomatic, do not treat the bacteriuria.

50
Q

what is the first line test for hepatitis C infection (chronic)?

A

1st = anti-hepatitis C antibodies
a.k.a. enzyme immnoassay (EIA)

confirm with NAATs