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Abdominal Flashcards

1
Q

Complications of fistula

A
  • Clotting
  • Ulceration/poor healing
  • Failure (up to 40% before ever used)
  • Steal syndrome in 10% (blood stolen from artery = cold/numb hand)
  • High output cardiac failure (is L to R shunt. May have up to 2L flow/min)
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2
Q

RIF mass differential

A
  • Renal transplant
  • Caecal carcinoma
  • Ovarian tumour
  • Ileocaecal mass (amoebic, TB, appendicular mass, ileal carcinoid or lymphoma)
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3
Q

LIF mass differential

A
  • Carinoma of sigmoid
  • Diverticular mass/abscess
  • Faeces
  • Ovarian tumour
  • Renal transplant
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4
Q

Epigastric mass differential

A
  • Left (caudate) lobe of liver (HCC, alcoholic hepatitis)
  • Carcinoma of stomach or pancreas
  • Lymphoma
  • AAA
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5
Q

Nail signs for CKD

A
  • Leukonychia
  • Half-and-half nails
  • Absent lunulae
  • Mees’ and Beau’s lines (transverse lines)
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6
Q

Causes of leukonychia

A
  • Hypoalbumin (malabsorption, nephrotic syndrome)
  • Familial
  • Sulphonamides
  • Heavy metal poisoning
  • Idiopathic
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7
Q

Causes of koilonychia

A
  • IDA
  • Poor peripheral circulation
  • Exposure to solvents
  • Altitude
  • Familial
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8
Q

Causes of clubbing

A
  • IBD
  • Cirrhosis
  • Coeliac
  • Hyperthyroidism (thyroid acropachy)
  • Idiopathic/familial (autosomal dominant) are most common!
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9
Q

Cause of unilateral clubbing

A
  • Arteriovenous fistula
  • Other vascular malformations
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10
Q

GI cause of Virchow’s node

A
  • Stomach adenocarcinoma
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11
Q

Causes of acanthosis nigricans

A
  • Paraneoplastic (stomach cancer)
  • Insulin-resistant T2DM
  • Hypo/hyperthyroid
  • Cushing’s
  • Obesity
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12
Q

Drug causes of gynaecomastia

A

DISCO
- Digoxin
- Isoniazid
- Spironolactone
- Cimetidine
- Oesotrogens

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13
Q

Causes of gynaecomastia

A
  • Drugs (DISCO)
  • Liver disease
  • CKD
  • Thyrotoxicosis
  • Secretory malignancies (hCG)
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14
Q

Causes of abdominal distension

A

5 F’s
- Fat
- Fluid
- Flatus,
- Faeces
- Fetus

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15
Q

How much fluid needed to diagnosed ascites clinically

A
  • 1500ml (USS can detect 500ml)
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16
Q

Signs of portal hypertension

A
  • Splenomegaly
  • Caput medusae (dilated superior epigastric veins)
  • Oesophageal varices
  • Ascites
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17
Q

Sites of portosystemic anastomoses

A

(In brackets = which portal vein joins which systemic vein)
- Oesophageal (left gastric vein –> azygos vein)
- Rectal (superior rectal vein –> middle/inferior rectal veins)
- Umbilical (paraumbilical vein –> superior epigastric vein)

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18
Q

3 most common causes of chronic liver disease

A
  • Alcohol
  • Hep B (abroad), Hep C (IVDU)
  • Non-alcoholic hepatic steatosis (overweight)
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19
Q

Types of hepatorenal syndrome

A

Due to liver not breaking down vasoactive substances (e.g. prostaglandins)–> excess renal vasoconstriction

  • Type 1: doubling in Cr/halve in Cr clearance in 2 weeks –> 50% mortality after 1month. Should improve with vasoconstrictors and volume expanders
  • Type 2: slower progression - starts with ascites and then diuretic-resistant ascites (kidneys can’t secrete enough sodium)
  • May need combined liver-renal transplant if pre-morbid eGFR <30 (as immunosuppression post-transplant will reduce eGFR…)
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20
Q

What is hepatopulmonary syndrome (with diagnosis and treatment)

A
  1. Liver failure
  2. Unexplained hypoxaemia
  3. Intrapulmonary vascular dilation (liver does not excrete NO)
  • Diagnosis: contrast echo (microbubbles pass through dilated pulmonary vessels into left atrium)
  • Treatment: liver transplant
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21
Q

Features of decompensated liver disease

A
  • Ascites
  • Encephalopathy
  • Hepatorenal/hepatopulmonary syndrome

(won’t come up in exam!)

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22
Q

Grades for hepatic encephalopathy

A
  • Grade 0: normal (mild changes on psychometric tests)
  • Grade 1: mild confusion; short attention span; disordered sleep
  • Grade 2: disorientated to time/place occasionally; lethargy; personality change
  • Grade 3: very disorientated; somnolent but rousable to speech; amnesia
  • Grade 4: comatose (no response to pain)

Test for it with constructional apraxia (ask pt to draw a 5-pointed star)

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23
Q

How to grade severity of cirrhosis

A

Modified Child-Pugh Score- based on ABCDE
- Albumin
- Bilirubin
- Clotting (INR)
- Distension (ascites)
- Encephalopathy

(Modify bilirubin scores in PSC/PBC as expect high bilirubin)

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24
Q

Management of ascites due to Chronic Liver Disease

A

Aim weight loss 1kg/day
1. No-added salt diet (5.2g a day/90mmol)
2. Spironolactone 100-400mg OD (if not getting hyperkalaemia)
3. Add furosemide 40-160mg OD
4. Ascitic drain (PleurX drain for malignant ascites)
5. Transjugular intrahepatic portosystemic shunt (TIPSS) = shunt from portal vein to hepatic vein, giving another route for portal blood to go to systemic circulation- increases encephalopathy risk as nitrogenous waste bypasses liver

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25
Q

Causes of ascites

A

Transudative
- Cirrhosis with portal HTN = commonest cause in PACES
- CCF
- Nephrotic syndrome (reduced oncotic pressure)
- Portal vein thrombosis
- Budd-Chiari Syndrome (occlusion of hepatic vein which drains liver to IVC)

Exudative
- Malignancy (metastatic GI, liver, ovarian, peritoneal mesothelioma)
- TB peritonitis
- Pancreatitis

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26
Q

Budd-Chiari Syndrome is triad of

A
  • Abdo pain
  • Ascites
  • Hepatomegaly
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27
Q

Types of Budd-Chiari Syndrome

A

Primary (75%) = thrombosis of hepatic vein
- Polycythaemia
- Pregnancy
- COCP

Secondary (25%) = occlusion of hepatic vein
- Tumour

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28
Q

Cause of ascites in Chronic Liver Disease

A

1.
- Renal hypoperfusion –> renin from juxtaglomerular apparatus –> aldosterone
- Liver failure means aldosterone not broken down–> salt/water retention

    • Hypoalbumin reduces oncotic pressure–> increased portal pressure

1+2 = ultrafiltration of fluid into abdominal cavity

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29
Q

How differentiate between exudative and transudative cirrhosis

A
  • Exudate: low serum:ascites albumin gradient (SAAG) <11g/L = loss of protein from serum into ascites
  • Transudate: high serum:ascites albumin gradient (SAAG) >11g/L
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30
Q

Causes of hepatomegaly

A

DINMCO
Drug-induced
-Alcohol/drugs

Infective
- Hepatitis
- Tropical (malaria, leishmaniasis)
- Infectious mononucleosis

Neoplastic
- Hepatocellular carcinoma
- Lymphoma

Metabolic
- NAFLD
- Haemochromatosis

Cardiac
- CCF

Other
- Sarcoidosis

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31
Q

Scoring systems to assess severity of acute alcoholic hepatitis

A
  • Modified Maddrey’s discriminant function test
  • Mayo End Stage Liver Disease (MELD) score
  • Glasgow Alcoholic Hepatitis score - do on Day 1
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32
Q

Treatment for acute alcoholic hepatitis

A
  • Adequate nutrition
  • Maddrey’s discriminant function test >32 = pred 40mg for 4/52 and then taper
  • IV NAC if severe
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33
Q

Histological stages of alcoholic liver disease

A
  • Hepatic steatosis (fat in liver cells)- reversible
  • Alcoholic hepatitis (inflammation liver cells–> necrosis) - reversible
  • Hepatic cirrhosis
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34
Q

Hepatic amyloidosis affects which clotting factors

A
  • Factor IX and X
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35
Q

Differentiate been palpable spleen and palpable left kidney

A
  • Spleen cannot be balloted, is dull to percussion, has a notch and you should not be able to ‘get above’ it
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36
Q

Causes of isolated splenomegaly

A

Massive (>8cm)
- Myeloproliferative (CML, myelofibrosis)
- Tropical (chronic malaria = p. vivax/ovale, visceral leishmaniasis a.k.a kal-azar)

Moderate (4-8cm)
- Infiltrative (amyloid)

Tip (<4cm)
- Portal hypertension
- Acute infection (EBV, CMV, endocarditis)
- Felty’s Syndrome (rheumatoid arthritis)
- Haemolytic anaemia

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37
Q

Features of Felty’s Syndrome

A

SANTA
- Splenomegaly
- Anaemia
- Neutropenia
- Thrombocytopaenia
- Arthritis (rheumatoid)

Unknown cause

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38
Q

Presenting symptoms for hepatosplenomegaly

A
  • Anaemia: fatigue/SOB
  • Thrombocytopaenia: easy bruising
  • Abdo pain referred to left shoulder
  • Constitutional symptoms
  • Febrile illness
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39
Q

Causes of hepatosplenomegaly

A
  • Cirrhosis with portal HTN
  • Infection (chronic malaria, visceral leishmaniasis, schistosomiasis)
  • Myeloproliferative (CML, polycythaemia, myelofibrosis)
  • Lymphoproliferative (CLL, lymphoma)
  • Metabolic (Wilson’s, haemochromatosis)
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40
Q

Important differential for hepatosplenomegaly

A
  • Bilateral large kidneys (PCKD)!
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41
Q

Cause of Wilson’s Disease (inc chromosome)

A
  • Autosomal recessive
  • Mutation of the adenosine triphosphatase 7B ( ATP7B) gene on chromosome 13
  • Copper accumuates in liver –> blood –> urine
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42
Q

Tests for Wilson’s Disease

A
  • Low serum caeruloplasmin (acute phase protein so may be raised abnormally!) = protein which binds to copper in serum
  • High 24hr urine copper
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43
Q

Features of Wilson’s Disease

A

Present in 2nd decade of life
- Gastro: chronic liver disease and cirrhosis
- Neuro: Parkinsons, tremor, dysdiadochokinesia
- Renal: Fanconi Syndrome
- Cardiac: cardiomyopathy
- Psych: emotion labile, psychotic

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44
Q

Signs of Primary Biliary Cirrhosis

A
  • Middle aged female with CLD –> always include PBC in differential!
  • Scratch marks
  • Orbital xanthelasma
  • Hepatosplenomegaly
  • Jaundice
  • Most asymptomatic and diagnosed incidentally at cholecystectomy!
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45
Q

Antibody in Primary Biliary Cirrhosis

A
  • Anti-mitochondrial antibodies
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46
Q

Antibodies in autoimmune hepatitis

A
  • ANA
  • Anti-smooth muscle
  • Anti-dsDNA
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47
Q

Differential for Primary Biliary Cirrhosis

A
  • Autoimmune hepatitis
  • Primary Sclerosis Cholangitis
  • Cholestatic sarcoidosis (-ve anti-mitochondrial antibody)
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48
Q

Management of Primary Biliary Cirrhosis

A
  • No alcohol
  • Fat-soluble vitamins (ADEK)
  • Ursodeoxycholic acid: reduced cholestasis/liver function decline
  • Cholestyramine: less itchy
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49
Q

Prevalence of haemochromatosis

A
  • 1 in 200
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50
Q

Symptom triad for haemochromatosis

A
  • Fatigue
  • Arthralgia
  • Sexual/gonadal dysfunction
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51
Q

Complications of haemochromatosis

A

GI
- Increased liver cancer risk

Endo
- T1DM (pancreatic failure)- 2/3 of patients
- Anterior pituitary dysfunction–> hypothyroid (TSH, ACTH)

Cardio
- Dilated cardiomyopathy (+/- arrhythmia)

Skin
- Bronze skin

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52
Q

Cause of haemochromatosis (inc mode of inheritance)

A
  • Autosomal recessive
  • Mutation in genes regulating iron metabolism (HFE gene on chromosome 6)
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53
Q

What speeds up iron overload in haemochromatosis

A
  • Excess alcohol consumption
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54
Q

Management of haemochromatosis

A
  • Weekly venesection (1unit a week until iron deficient, then 4x a year)
  • Desferrioxamine (binds to free iron–> excreted in urine)
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55
Q

Complications of liver transplantation

A
  • Infection: typical (LRTI) and atypical (PCP, CMV, varicella)
  • Malignancy: solid organ (bowel), lymphoproliferative (post-transplant lymphoproliferative disease), skin (SCC or BCC)
  • Metabolic: post-transplant diabetes and hyperlipidaemia
  • Cardiovascular: IHD
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56
Q

Palpable mass in left loin for liver transplant patient

A
  • Simultaneous liver-kidney transplant (paracetamol overdose)
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57
Q

Survival following liver transplant

A
  • Over 60% over 15yrs
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58
Q

King’s College criteria for liver transplant in paracetamol overdose

A
  • pH <7.3 after 12hrs resuscitation
  • Or all 3 of: INR > 6.5, creatinine > 300, encephalopathy (grade III or IV)
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59
Q

King’s College criteria for liver transplant in non-paracetamol overdose

A
  • Arterial lactate >3.5 4h after resuscitation
  • Or INR > 6.5
  • Or any 3 of: INR > 3.5, age<10 or > 40 years, bilirubin
    >300, jaundice > 7 days, caused by drug reaction
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60
Q

Types of liver support system

A
  • Bio-artificial: Extracorporeal Liver Assist Device (ELAD) = remove blood–> pass through ultrafiltration generator which separates blood from plasma–> pass through semi-permeable membrane to remove toxins
  • Artificial: Molecular Absorbents Recirculation System (MARS) = in 1st circuit, blood exposed to albumin, which binds to toxins –> in 2nd circuit, remove bound toxins from albumin
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61
Q

Prevalence of IBD

A
  • 250 per 100,000 in West
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62
Q

Extra-abdominal signs of IBD

A
  • Clubbing = extensive small bowel Crohn’s
  • Uveitis
  • Sacroiliitis
  • Skin: pyoderma gangrenosum, erythema nodosum
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63
Q

Palpable mass in RIF in IBD

A
  • Could be acute exacerbation
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64
Q

Differences between Crohn’s and UC

A

Crohn’s
- Non-bloody diarrhoea
- Mouth-to-anus skip lesions
- Full thickness wall inflamed
- Granulomas
- Fat malabsorption (affecting ADEK vitamins) - because affects small bowel
- Peri-anal disease (ulceration, fistulas)

UC
- PR bleeding + tenesmus (feeling incomplete defecation)
- Colon continuous inflammation
- Partial thickness wall inflamed
- Crypt abscesses
- Dilated terminal ileum (“backwash ileitis”)

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65
Q

Truelove and Witt’s criteria for IBD exacerbation

A
  • Mild: <4 poos a day, normal ESR, no systemic symptoms
  • Moderate: >4 poos a day, mild systemic symptoms
  • Severe: >6 bloody poos a day, ESR >30 or fever/tachy/anaemic
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66
Q

Management of Crohn’s

A
  • Ileocaecal: budesonide if mild and pred is more severe –> move on to immunosuppressants (azathioprine) or biologics (infliximab or adalimumab = anti-TNF)
  • Colonic disease but non-fistulating: prednisolone if mild and pred + azathioprine if more severe –> consider biologics
  • Perianal fistulae: surgery and infliximab
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67
Q

Management of UC

A

Acute = induce remission
- Mild: topical mesalazine if proctitis –> oral mesalazine if more extensive colitis
- Moderate/severe: oral prednisolone (or can do azathioprine + infliximab)
- Severe: IV hydrocortisone 100mg QDS –> add on infliximab if no response within 3 days

Maintain remission
- Proctitis: topical mesalazine
- More extensive: azathioprine +/- infliximab

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68
Q

Indications for surgery in acute IBD

A
  • Toxic megacolon (colon >6cm or caecum >9cm)
  • Stools >8/day or CRP >45 after 3 days of IV hydrocortisone
  • Fistula/perforation/obstruction
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69
Q

Which IBD is more commonly associated with Primary Sclerosis Cholangitis

A
  • UC
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70
Q

Management of Primary Sclerosis Cholangitis

A
  • ADEK vitamins
  • Stent fibrotic bile duct
  • Liver transplant
71
Q

Presenting features of Adult Polycystic Kidney Disease

A
  • Asymptomatic (proteinuria, blood tests)
  • Recurrent UTIs
  • Abdo pain
  • Subarachnoid haemorrhage
72
Q

Signs of Adult Polycystic Kidney Disease

A
  • Large kidneys with bruit over them (increased perfusion or vascular tumour e.g. angiomyolipoma)
  • Hepatomegaly- irregular (cysts)
  • Anaemia/HTN/CKD/dialysis signs
73
Q

Causes of unilateral kidney enlargement

A
  • Polycystic Kidney (other not palpable because had nephrectomy - look for scar!)
  • Tumour
  • Hydronephrosis
  • Horseshoe kidney
74
Q

Types of Adult Polycystic Kidney Disease

A
  • Type 1 and Type 2 (milder)
75
Q

Mechanism of Adult Polycystic Kidney Disease (including mode of inheritance and chromosomes affected)

A
  • Autosomal dominant mutation –> abnormal cilia function –> cysts form and replace kidney tissue
  • Type 1 = PKD1 gene on Chromosome 16 (85%)
  • Type 2 = PKD2 gene on Chromosome 4 (15%)
  • Type 2 is less severe/later onset
76
Q

Ultrasound diagnostic criteria for Adult Polycystic Kidney Disease

A
  • 15–39yrs: 3+ cysts in the kidneys (unilaterally or
    bilaterally).
  • 40–59yrs: 2+ cysts in each kidney.
  • > 60yrs: 4+cysts in each kidney.
77
Q

Complications of Adult Polycystic Kidney Disease

A
  • Mitral valve prolapse (also MR, TR, AR)
  • Cysts elsewhere (liver, pancreas, arachnoid)
  • Intracranial berry (saccular) aneurysm
  • HTN (excess renin)
  • Polycythaemia (excess EPO)
78
Q

Causes of new abdominal pain in Adult Polycystic Kidney Disease

A
  • Infected cyst
  • Haemorrhage into cyst
    (also diverticulitis, kidney stones, AAA rupture)
79
Q

Complications of chronic immunosuppression (e.g. transplant)

A
  • Infection (PCP, CMV, EBV, BK virus)
  • Malignancy (solid organ, lymphoproliferative, skin)– look for surgical/radiotherapy scars
  • Metabolic (diabetes, anaemia, HTN)
  • CVD
  • CKD (ciclosporin/tacrolimus)
80
Q

Cause of end-stage renal failure if no signs

A
  • Glomerulonephritis
81
Q

Patient wearing hearing aids in Abdominal station

A
  • Alport’s disease (glomerulonephritis, hearing loss, vision changes)
  • Aminoglycoside (gentamicin) induced nephrotoxicity and ototoxicity
82
Q

Things to check when assessing functional status of renal transplant

A
  • HTN
  • Fluid overload
  • Ongoing dialysis
83
Q

Complications of CKD

A
  • Anaemia (EPO)
  • Renal osteodystrophy (secondary hyperparathyroidism)
  • CVD
  • Hyperkalaemia
  • Pulmonary oedema
84
Q

Causes of end-stage renal failure

A
  • Diabetes
  • Adult Polycystic Kidney Disease
  • Chronic glomerulonephritis
  • HTN in blacks only! (association in other races less established)
85
Q

Issue with renal transplant in Alport’s Syndrome

A
  • Defect in type IV collagen –> transplant exposes to new antigens –> develop anti-GBM antibodies (Goodpasture’s!)
86
Q

Complications of specific immunosuppressants

A
  • Seborrheic wart (azathioprine)
  • Fine tremor (tacrolimus)
  • CKD (tacrolimus, ciclosporin)
87
Q

Presenting features of Hereditary Haemorrhagic Telangiectasia

A
  • Epistaxis
  • Anaemia (not melaena/UGI bleeding)
  • Telangiectasia on fingers, face, lips, tongue, buccal
    mucosa, conjunctiva and nose
  • High-output cardiac failure due to large AVM
  • Stroke (cerebral AVM) and lung haemorrhage (lung AVM)
88
Q

Difference between Hereditary Haemorrhagic Telangiectasia and Peutz-Jeghers syndrome

A
  • HHT = telangiectasia
  • Peutz-Jeghers = macules
89
Q

Difference between Hereditary Haemorrhagic Telangiectasia and Systemic Sclerosis

A
  • Systemic Sclerosis has thickened skin
90
Q

Common sites for AVM in Hereditary Haemorrhagic Telangiectasia

A
  • Brain, lung, liver, bowel, spine
91
Q

Cause of Hereditary Haemorrhagic Telangiectasia

A
  • Autosomal dominant mutation (chromosome 9– relates to TGFb signalling)
92
Q

Features of Peutz-Jeghers Syndrome

A
  • Mucucutaneous pigmented macules (lips, hands, feet)
  • Benign hamartomas in GI tract
  • Increased risk of malignancy (not related to hamartoma)
93
Q

Surface marking of abdominal aorta

A
  • Just left to midline
  • Bifurcates at L4/5 (umbilicus)- less reliable if fat
94
Q

Surface marking of gallbladder

A
  • Right costal margin in mid-clavicular line
95
Q

Surface markings of kidneys

A
  • Lowest point of left and right costal margins (L1)
96
Q

Surface anatomy of liver

A
  • Left upper border = just medial to left nipple
  • Right upper border = 5th rib at mid-clavicular line
  • Lowest point of liver = 0.5inch below right costal margin in mid-axillary line
97
Q

Gold-standard investigation for Primary Sclerosis Cholangitis

A
  • MRCP (Magnetic Resonance Cholangiopancreatography)
98
Q

Causes of palmar erythema

A
  • Cirrhosis
  • Hyperthyroidism
  • Pregnancy
  • Polycythaemia
  • Rheumatoid arthritis
99
Q

Indications for splenectomy

A
  • Trauma (including intraoperative damage)
  • Rupture
  • ITP (platelets destroyed in spleen)
  • So massive that destroys RBCs/platelets
100
Q

Post-splenectomy management

A
  • Vaccination against encapsulated bacteria 2 weeks BEFORE: pneumococcal, meningococcal, Hib
  • Lifelong penicillin
  • Medic alert bracelet
101
Q

Patient with large kidneys and long-term catheter

A
  • Hydronephrosis
102
Q

3 commonest causes for liver transplant

A
  • Cirrhosis
  • Acute liver failure (paracetamol, Hepatitis A/B)
  • Cancer
103
Q

Differentiate caput medusae between portal HTN and IVC obstruction

A

Press vein below umbilicus
- Drains away from umbilicus = portal HTN
- Drains towards umbilicus = IVC obstruction

104
Q

Areas to cover when presenting renal patient

A
  • Cause for CKD
  • Current RRT
  • Previous RRT
  • Immunosuppression evidence
  • Volume status
105
Q

Causes of dysphagia

A

Inflammatory
- Tonsillitis
- Oesophagitis
- Candidasis

Mechanical
- Luminal: foreign body, food
- Mural: cancer, benign stricture (Plummer Vinson)
- Extramural: goitre, mediastinal Lymph nodes, lung cancer

Motility:
- Achalasia
- Stroke
- MND
- Myasthenia gravis

106
Q

Eradication therapy for H. Pylori

A
  • Omeprazole 20mg BD
  • Amoxicillin 1g BD
  • Clarithromycin 500mg BD
107
Q

Causes of jaundice

A

Pre-hepatic = excess bilirubin
- Haemolytic anaemia
- Ineffective erythropoiesis

Hepatic- Unconjugated
- Reduced bilirubin uptake: drugs (rifampicin), CCF
- Reduced bilirubin conjugation: Gilbert’s (autosomal dominant), Crigler-Najjar (autosomal recessive

Hepatic - Conjugated
- Liver failure (congenital e.g. Wilson’s, infectious, toxins, autoimmune)

Post-hepatic
- Gallstones
- Cancer head of pancreas
- PSC/PBC

108
Q

Medication causes of liver injury/jaundice

A

Haemolytic
- Methyldopa
- Penicillin
- Anti-malarials

Hepatitis
- TB meds RIP
- Valproate
- Statins

Cholestatic
- Co-amoxiclav
- Flucloxacillin
- COCP
- Chlorpromazine

109
Q

Deficiency in Gilbert’s Syndrome

A
  • UDP-glucuronyl transferase
110
Q

Investigations for pre-hepatic jaundice

A
  • Blood film
  • Coomb’s test (direct = antibodies attached to RBCs- shows haemolytic anaemia is immune-related; indirect = antibodies against foreign RBCs- do before transfusion)
  • Hb electrophoresis (thalassaemia)
111
Q

Diagnosis of spontaneous bacterial peritonitis

A
  • Ascitic fluid polymorphonuclear cells >250mm3
112
Q

Hepatitis B antibodies

A
  • Surface antigen = acute infection
  • Anti-HBc IgM = acute infection
  • e Antigen = high infectivity
  • Core antibody = previous infection
  • Surface antibody = immunity
113
Q

Features of carcinoid syndrome

A

FIVE HT
- Flushing
- Intestinal diarrhoea
- Valve fibrosis (TR, PS)
- whEEze

  • Hepatic involvement
  • Tryptophan deficiency = niacin precursor –> pellagra (diarrhoea, dermatitis, dementia)
114
Q

Definition of pathological dilation on AXR

A

3-6-9
- 3cm small bowel
- 6cm large bowel
- 9cm caecum

115
Q

Cancer screening in IBD

A
  • Active disease for 10 years –> regular endoscopy to identify pre-malignant changes
116
Q

Features of dermatitis herpetiformis rash

A
  • Itchy
  • Symmetrical
  • Extensor surfaces
  • Vesicular –> can erupt, leaving crusted lesions
117
Q

Treatment for dermatitis herpetiformis if first-line management (gluten-free) does not work

A
  • Dapsone (sulphonamide antibiotic which has anti-inflammatory properties)
118
Q

Investigations for dermatitis herpetiformis

A
  • Anti-TTG (also FBC, haematinics, LFTs etc)
  • Skin biopsy: dermal papillae infiltrated with micro-abscesses containing eosinophils, neutrophils, fibrin
119
Q

Investigations for coeliac disease

A
  • Anti-TTG (also FBC, haematinics, LFTs etc)
  • Duodenal biopsy: villous atrophy and high lymphocytes (should be on a gluten diet!)
120
Q

Causes of renal transplant failure

A

SCARI
- Structural (transplant artery stenosis)
- Calcineurin toxicity
- Antibody
- Recurrence (focal segmental glomerulosclerosis)
- Infection

121
Q

General management of chronic liver disease

A

MDT approach!
- Alcohol abstinence
- Nutrition (thiamine)
- Laxatives (3 soft poos a day)
- Avoid hepatotoxic meds
- Propranolol if varices

122
Q

How does peritoneal dialysis work

A
  • Dialysate fluid is infused via peritoneal catheter into abdo cavity
  • Toxins diffuse across the peritoneum and into the dialysate fluid
  • Dialysate fluid removed while patient sleeps (automatic peritoneal dialysis) or up to 6 times throughout the day (continuous ambulatory peritoneal dialysis)
123
Q

Advantages for AV fistula over tunnelled line

A
  • Faster flow rates = shorter dialysis sessions
  • Less infection
  • Longer lifespan
124
Q

Complications of haemodialysis

A
  • Dialysis washout (remove too much fluid –> hypotension)
  • Infection
  • Bleeding (heparin used in dialysis)
125
Q

Complications of peritoneal dialysis

A
  • Infection (peritonitis)
  • Hernias
  • Hyperglycaemia (sugar in dialysate fluid)
126
Q

4 things must ask yourself if see a transplant

A
  • Which organ
  • Why done
  • Is it working
  • Complications
127
Q

Important blood test in organ transplant rejection

A
  • Immunosuppressant levels!
128
Q

See ileostomy which has been reversed- what 2 surgeries has patient had

A
  1. Pan-proctocolectomy with end-ileostomy
  2. Reversal of ileostomy with J pouch formation (part of jejunum attaches to rectal stump)
129
Q

Important panel of investigations in liver failure

A
  • Non-invasive liver screen!
  • Also AFP
130
Q

Hepatomegaly with fluid overload

A
  • Congestive hepatopathy! (right-sided heart failure –> hepatomegaly)
131
Q

Management of Wilson’s Disease

A
  1. Copper-chelation (penicillamine or trientine hydrochloride)
  2. Zinc once copper levels stable (stimulates protein in gut which binds to copper and prevents its reabsorption)

Also:
- Less copper in diet
- Liver transplant (nuts, shellfish, organ meats)

132
Q

Alcohol effects on other systems

A

Cardio
- Alcoholic cardiomyopathy
- Arrythmias

Haem
- Macrocytic anaemia
- Coagulopathy

CNS
- Peripheral neuropathy
- Cerebellar

133
Q

When to do SBP prophylaxis and which drug to use

A
  • Ascitic protein content <15g/L or previous SBP
  • Ciprofloxacin
134
Q

Commonest cause of SBP

A
  • E.coli (then staph and strep)
135
Q

CKD stages in terms of eGFR

A
  • 1: >90
  • 2: 60-89
  • 3: 30-59
  • 4: 15-29
  • 5: <15
136
Q

Referral criteria for dialysis in CKD

A
  • eGFR <30 (CKD stage 4 or 5)
  • eGFR 30-60 but rapidly progressing (reducing by 15 in 1yr)
  • Nephrotic syndrome and rapidly reducing eGFR <60
137
Q

Risk of breast/ovarian cancer with BRCA1 and BRCA2

A
  • BRCA1: 80% breast cancer, 40% ovarian cancer
  • BRCA2: 40% breast cancer
138
Q

1-year survival based on Child-Pugh grades

A
  • A: 100%
  • B: 80%
  • C: 45%
139
Q

Which IBD patients are eligible for screening colonoscopies (checking for cancer)?

A
  • UC (not proctitis alone)
  • Crohn’s involving >1 segments of colon
140
Q

Frequency of screening colonoscopies (checking for cancer) in IBD

A
  • Low risk: 5 years.
  • Intermediate risk: 3 years.
  • High risk (severe inflammation, PSC, colonic stricture): 1 year.
141
Q

Management of ascitic drain after insertion

A
  • 100ml 20% HAS for every 2L drained
  • Max 6hrs or 10L drained, whichever comes first
142
Q

Management of Polycystic Kidney Disease

A
  • Low salt, high fluid diet (suppresses vasopressin levels)
  • HTN control
  • Tolvaptan (vasopressor receptor antagonists) for rapidly progressive disease
  • RRT
143
Q

Indications for nephrectomy in Polycystic Kidney Disease

A
  • To make room for transplanted kidney
  • Renal cell carcinoma
  • Chronic pain/haematuria
  • Recurrent UTIs
144
Q

Indications for liver transplant

A
  • Acute (King’s criteria)
  • Cirrhosis with high UK End-Stage Liver Disease score >49
  • Hepatocellular carcinoma (e.g. tumour <5cm)
  • “Variant syndromes”: PBC with intractable pruritus, hepatopulmonary syndrome
145
Q

Absolute contraindications for liver transplant

A
  • Ongoing alcohol/drug use
  • Untreated HIV
  • Previous/active extra-hepatic cancer
  • Severe irreversible lung disease
146
Q

When to refer for renal transplantation

A
  • CKD stage 4+ (eGFR <30) who may need dialysis within next 6 months
147
Q

Definition of end-stage renal failure

A
  • eGFR <15ml/min
148
Q

Absolute contraindications for renal transplantation

A
  • Untreated malignancy
  • Untreated HIV
  • Deep-seated infection
149
Q

Investigations in haemochromatosis

A
  • Raised ferritin and transferrin saturations
  • HFE gene mutation testing (but variable penetrance so not everyone with mutation will have the condition)
150
Q

Meig’s Syndrome components

A
  • Ascites (transudative)
  • Pleural effusion
  • Benign ovarian tumour
151
Q

Tests to send for ascitic fluid

A
  • Albumin (calculate Serum: Ascites Albumin Gradient)
  • Polymorphonuclear leukocyte count >250/mm3
  • Amylase (raised in pancreatitis)
  • MC&S inc Gram Stain
  • Cytology (?malignant)
152
Q

Indications for haemachromatosis screening

A
  • 1st-degree relatives (check ferritin and transferrin saturations)
153
Q

Mechanism of Hereditary Spherocytosis (inc mode of inheritance)

A
  • Autosomal dominant on Chromosome 8 (can be recessive!)
  • RBCs are spherical = more prone to rupture = haemolytic anaemia
154
Q

Presenting symptoms of Hereditary Spherocytosis

A
  • Splenomegaly
  • Jaundice
  • Lethargy
155
Q

Complications of Hereditary Spherocytosis

A
  • Aplastic crisis (triggered by infection)
  • Gallstones
156
Q

Investigations for Hereditary Spherocytosis

A
  • Blood smear (check for haemolysis)
  • Reticulocytes
  • EMA-binding test = reduced fluorescence as reduced binding of eosin to the RBCs (do Osmotic Fragility Test if this is not available)
  • Haemolysis screen (LDH, split bilirubin, Coomb’s, haptoglobin)
157
Q

Management of Hereditary Spherocytosis

A
  • Folic acid
  • Regular transfusions for anaemia
  • Severe: splenectomy as stops haemolysis of RBCs in the spleen
  • Cholecystectomy for gallstones
158
Q

Foods which contain gluten

A
  • Wheat
  • Rye (flour, bread, beer)
  • Barley (cereal, porridge)
159
Q

Types of renal transplant

A
  • Live
  • Cadaveric (circulatory death or neurological death)
160
Q

Types of renal transplant rejection and treatment for each

A

Hyperacute = within minutes/hours (pre-existing antibodies in recipient attack the transplant e.g. ABO)
- Plasmapheresis and IVIG
- May need to remove the transplanted kidney!

Acute = antibody or T-cell mediated
- Antibody: Plasma exchange –> IVIG. Rituximab (anti-CD20)
- T-cell: IV methylprednisolone

Chronic = usually antibody (may be non-compliance to immunosuppression) = irreversible usually
- Immunosuppressants

161
Q

Complications of pancreatitis

A

Acute pancreatitis
- SIRS –> ARDS

Chronic pancreatitis
- Pseudocysts –> can obstruct pancreas/duodenum
- Portal vein thrombosis

162
Q

Symptoms of chronic pancreatitis

A
  • Chronic grumbling pain (usually epigastric, radiates to back, better sitting up)– some patient experience attacks
  • Steatorrhoea (fat malabsorption)
  • Weight loss
163
Q

Management of chronic pancreatitis

A
  • Stop triggers (stop alcohol/smoking)
  • Creon with PPI to improve absorption
  • Endoscopic drainage of pseudocysts
  • ERCP stenting of calcified ducts
164
Q

Genetic causes of chronic pancreatitis

A
  • CF!
  • SPINK1 mutation
  • PRSS1 mutation
165
Q

Investigations for chronic pancreatitis

A
  • Magnesium (low)
  • Faecal elastase (low)
  • IGG4 in autoimmune pancreatitis
  • CT abdo-pelvis
  • EUS with fine needle biopsy if suspect cancer (as may be difficult to differentiate cancer from pancreatitis on CT)
166
Q

Mechanism of sickle cell disease (inc mode of inheritance)

A
  • Autosomal recessive: sickle cell trait = 1 gene, disease = both genes
  • Valine replaces glutamic acid at the sixth amino acid of the beta globin chain–> have sickled HbS instead of normal HbA
167
Q

Complications of sickle cell disease

A
  • Painful vaso-occlusive crises (bone, chest, priapism)
  • Splenic sequestration (sickled RBCs build up –> splenomegaly and splenic failure = drop in RBCs)
  • Aplastic crisis (triggered by parvovirus B19)
  • Hyposplenism –> encapsulated infections
  • Stroke/MI
  • Gallstones
  • Avascular necrosis
168
Q

Investigations in sickle cell disease

A
  • Blood film (Howell-Joly bodies = hyposplenism)
  • Reticulocytes (high)
  • Hb electrophoresis
169
Q

Management of sickle cell disease

A
  • Hydroxycarbamide reduces crises by increasing fetal Hb (HbF)
  • Crizanlizumab (monoclonal against P-selectin) reduces vaso-occlusive crises
  • Splenectomy (sequestration crises)
170
Q

Types of glomerulonephritis

A

Non-proliferative
- Minimal change disease: nephrotic syndrome wibtoit changes on light microscopy. Steroid responsive
- Focal segmental glomerulosclerosis: steroids but half end in CKD
- Membranous glomerulonephritis: 1/3 stable, 1/3 remit, 1/3 end stage renal failure

Proliferative = increased cells in glomerulus
- IgA nephropathy: includes HSP
- Post-infectious: esp strep pyogenes (1 week after)
- Rapidly progressive

171
Q

Nephritic syndrome symptoms

A

Triad of
- Haematuria
- Oligouria
- HTN

172
Q

Definition of oligouria

A

<0.5ml/kg/hr

173
Q

Definition of anuria

A

<100ml/day

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