Abdominal Flashcards

Question

How would you manage SBP? (BSG)

Answer 1

Managed by gastroenterology team IV antibiotics (guided by tap culture, most common E. Coli) **In patients with a rising serum creatinine, albumin infusion is recommended** Consider ITU if unstable --- Secondary prophylaxis

Answer 2

A Glasgow Score of >9 or a Maddrey’s score >32 defines severe AH and predicts worse outcomes

Answer 3

-Cardiac: alcoholic cardiomyopathy -GI: **cirrhosis**, pancreatitis, peptic ulceration, UGI Ca -Neurological: cerebellar atrophy, polyneuropathy, Wernicke's/Korsakoff's

Answer 4

3Cs (as in ascites): -Cirrhosis -Cancer (primary or secondary usually colorectal)* -Hepatic congestion (as in heart failure)* Less commonly (IIIVAP): -Infectious (viral hepatitis B and C)* -Immune (PBC) -Infiltration (amyloid) -Alcoholic hepatitis* -Vascular* -Polycystic liver disease *may cause tender hepatomegaly

Answer 5

Mass in RUQ which moves with respiration that you are not able to get above and is dull to percussion Estimate size in finger breadths below diaphragm Smooth or craggy/nodular (malignancy/cirrhosis)? Pulsatile (TR)? Bruit (HCC)?

Answer 6

-Hepatitis A, B, E (sometimes C) -EBV and CMV -Toxoplasmosis -HSV

Answer 7

"CHIPS" (ensure P comes first) -Portal HTN (33%) -Haematological malignancy (lymphoma, leukaemia) (27%) -Infection (HIV, endocarditis, EBV) (23%) -Congestion (e.g. cardiac failure) -Primary splenic disease (e.g. splenic vein thrombosis) Less commonly ("MATH") -Haemolytic anaemia -Autoimmune (SLE, RA, Felty's syndrome) -Thalassaemia -Myeloproliferative disorders (such polycythaemia rubra vera) -Infiltrative (Gaucher's, amyloid) Massive splenomegaly >8cm (3Ms and leishmaniasis) -CML -Myelofibrosis -Malaria -Visceral leishmaniasis

Answer 8

Thick and thin films Also rapid diagnostic tests ID team input needed!

Answer 9

History (bleeding or bruising, anaemia symptoms, infective symptoms, autoimmune disease, liver disease, foreign travel, family history) FBC, LFTs, blood film, haemolysis screen, autoimmune screen, **TFTs**, HIV/EBV/HBV/HCV screen, **malaria screen, B12 and folate** USS abdomen CT-TAP (malignancy) +/- BM biopsy +/- LN biopsy Further investigations guided by ID, haematology or rheumatology teams

Answer 10

LUQ mass which moves infero-medially with respiration, has a notch, dull to percussion, cannot get above nor ballot

Answer 11

40% patients will have B-symptoms (fever, weight loss >10% over 6 months, night sweats) If one present, staging is altered accordingly

Answer 12

Philadelphia chromosome in 95% Translocation between chromosome 9 and 22 Increased oncogene activity

Answer 13

Splenic infarction/splenic artery thrombosis Coeliac or other autoimmune disease **Sickle cell disease**

Answer 14

-Rupture -ITP, hereditary spherocytosis -Haematological malignancy --- Vaccination (2/52 prior to proect against encapsulated organisms): pneumococcus, meningococcus, Haemophilus influenzae Prophylactic antibiotics (lifelong) Medic alert bracelet

Answer 15

N.B. First three are the same --- Bilateral: -PKD -Bilateral RCC -Bilateral HN -Tuberous sclerosis (renal angiomyolipomata and cysts) -Von-Hippel-Lindau (cysts and RCC) -Amyloidosis --- Single: -PKD (contralateral nephrectomy or other kidney not palpable) -RCC -HN due to ureteric obstruction -Simple cysts -Hypertrophy of single functioning kidney

Answer 16

BP, urinalysis and urine cytology U+Es USS abdomen CT if ?RCC Genetic studies (ADPKD) Echo (MV prolapse) and consider cerebral angiogram

Answer 17

Progressive replacement of normal kidney tissue by cysts leading to renal enlargement and renal failure (accounts for **5% ESRD in UK and affects 1:1000**) --- ADPKD1 accounts for 90%, mapped to chromosome 16 ADPKD2 has been mapped to chromosome 4 (later onset, fewer cysts) ARPKD is rare presents in infancy

Answer 18

Presents as part of familial screening or with complications such as: HTN Recurrent UTI or macroscopic haematuria Acute abdominal pain if haemorrhage, torsion or infection (also stones occur in 20%) Abdominal/back pain due to stretching of capsule or traction of the renal pedicle

Answer 19

HTN, infection, pain (as above) Polycythaemia ESRD by 40-60 years Hepatic cysts in 70% or cysts elsewhere Intracranial Berry aneurysms causing SAH MV prolapse Diverticular disease

Answer 20

Managed by renal team Control HTN Control other CV risk factors (e.g. statins) and Na restriction **Genetic counselling and family screening** Tolvaptan to slow progression (start in CKD 2 or 3 with evidence of rapidly progressive disease) Nephrectomy for recurrent bleeds/infection Manage ESRD (treat anaemia (only EPO when HTN controlled), phosphate binders, vitamin D etc.) and early specialist referral for RRT (dialysis and renal transplantation) --- N.B Cyst aspiration not done as does not improve renal function N.B. PD not used in PKD due to bulk of kidney alongside dialysate fluid causing discomfort and increased risk of cyst infection

Answer 21

Autosomal recessive fashion Usually due to HFE gene mutation on chromosome 6 (most homozygous for C282Y genetic variant, some H63D) Males affected at earlier age as women protected by menstrual loss

Answer 22

Commonly incidental diagnosis of raised ferritin or family screening of first degree relatives Fatigue, arthralgia and sexual dysfunction Or later features: CLD, T1DM, bronze pigmentation, CM

Answer 23

Secondary iron overload e.g. in repeated transfusions

Answer 24

Ferritin and transferrin (ferritin is less specific >200 females >300 males, TSATS >40% women >50% in men) FBC (polycythaemia), LFTs (can be normal), U+Es, HbA1c **HFE gene testing for C282Y and H63D (variable penetrance)** Liver US **For complications:** -Liver USS 6 monthly and variceal screening at time of diagnosis if cirrhotic -Retinopathy screening and urine ACR if diabetic -ECG/CXR/echo (can cause restricted or dilated cardiomyopathy, MRI is most sensitive) -Plain films of joints (chondrocalcinosis) Liver biopsy not required for diagnosis but may help evaluate degree of fibrosis

Answer 25

Managed by haematology +/- gastroenterology teams Phlebotomy (1 unit twice weekly initially, then once every 3 months when transferrin falls <50%) **Avoid alcohol** May need specialist input to manage complicating DM, CM, joint involvement Surveillance for HCC (200x risk if cirrhotic, 6 monthly USS) and variceal screening if cirrhotic Screening for first degree relatives --- N.B. Desferrioxamine second line

Answer 26

Survival equivalent to general population provided venesection started in a patient before cirrhosis and DM develops

Answer 27

1) Fatigue 2) Pruritus 3) Sicca Liver disease occurs late and is rarely a presenting feature

Answer 28

-LFTs showing cholestasis -AMA present in 95% -Liver biopsy portal tract granuloma progressing to cirrhosis -US and ERCP/MRCP to exclude extra-hepatic cholestasis

Answer 29

Managed by gastroenterology team **-Supplement vitamin ADEK** **-Treat bone disease and hypercholesterolaemia** -Ursodeoxycholic acid may slow progression -Pruritis management with bile acid sequestrants (rifampcin second line) and topical symptomatic therapy -Fatigue management with lifestyle adjustments and support -Sicca symptoms with artificial tears or saliva **-If cirrhotic: surveillance imaging every 6 months and variceal screening at time of diagnosis -If bilirubin >50 or decompensation: transplant**

Answer 30

Other autoimmune diseases (CSST): -Coeliac -Sjögren’s -Scleroderma -Thyroid disease

Answer 31

Up to 83% have IBD Associations including (CSSTT): -Coeliac -Sjögren’s -Scleroderma -Thyroid disease -Type 1 diabetes mellitus

Answer 32

Diabetes (34%) GN (21%) HTN (12%) Also less commonly PKD, reflux nephropathy and analgesic nephropathy

Answer 33

Diabetes GN ADPKD

Answer 34

Treat any reversible causes: -Identifying and treating glomerular disease (with biopsy) -Cessation of nephrotoxic drugs -Exclusion of obstructive uropathy and renovascular disease (with imaging) Slowing disease progression: -Manage HTN, blood sugar, dyslipidaemia and smoking cessation -ACEi and SGLT-2 inhibitors (slow progression independent of BP and glucose) -If diabetic kidney disease, **Finerenone** can slow progression Treatment of complications: -Anaemia: treat iron-deficiency, then EPO (aim 100 to 110) -Volume overload: Na restriction and loop diuretics -Hyperkalaemia: K restriction, loop diuretics, sodium bicarbonate -Hyperphosphataemia: phosphate binders -Metabolic acidosis: sodium bicarbonate -Renal osteodystrophy: vitamin D and phosphate binders, consider parathyroidectomy -Malnutrition: dietician input Early referral for consideration of RRT with doctors/nurses/dieticians/psychologists MDT approach and holistic manner

Answer 35

UKKA guidance suggests patients should be referred to nephrologist and discussion surronding RRT commenced when GFR falls below 30ml/min and is declining Indications are (AEIOU) for AKI/CKD: -Refractory acidosis -Refractory hyperkalaemia -Volume overload refractory to diuretics -Pericarditis/pleuritis/encephalopathy due to uraemia --- In addition, for CKD: -Progressive deterioration in nutritional status refractory to dietary intervention -Intractable pruritus -Inability to control hypertension --- In addition, for AKI: -Removal of toxins e.g. lithium, salicylates

Answer 36

Absolute (SHAME): -Untreated active infection (sepsis) -Untreated HIV infection or AIDS And -Untreated malignancy -Poor life expectancy --- Relative: -Obesity -Chronic hepatitis B or C or HIV infection -Previous malignancy -Age >65 years -Comorbid condition/untreated coronary artery disease

Answer 37

Early surgical: -Wound complications -Haemorrhage/thrombosis -Urine leak And later: **-Ureter obstruction** -Transplant renal artery stenosis --- Medical: -Delayed graft function -Hyper-acute (within hours), acute (highest risk in first 3 months, T-cell) or chronic allograft injury -Immunosuppression-related: **CNI nephrotoxicity, DM (steroids and CNI), transplant bone disease (steroids)** -Cardiovascular disease -Malignancy: PTLD, skin cancer -Infection: bacterial, viral (CMV, HSV, EBV or BK polyoma virus), fungal (PCP) -Recurrent disease

Answer 38

95% 1 year graft survival 50% 15 year graft survival

Answer 39

Infections (bacterial, fungal, viral) Malignancy including PTLD and skin Ca -Steroids: DM, hypertension, weight gain, osteoporosis -Tacrolimus: DM, tremor, nephrotoxicity -Ciclosporin: DM, hypertension, gum hypertrophy, hirsutism, nephrotoxicity

Answer 40

OE: Fluid overload and signs of uraemia Tenderness over graft HTN (although could be IS-related) May be current dialysis evidence As per KDIGO: -Declining renal function (high Cr and urine protein, low or high UO) -Not due to recurrence of disease or other recognized causes -IFTA on biopsy (in CAI)

Answer 41

In HD (DD HHCCAA): -Dialysis disequilibrium syndrome (acute cerebral oedema secondary to the rapid shifting of urea from the blood) -Dialyser reactions (reaction between blood components and the semi-permeable membrane of the dialysis machine, may present with anaphylaxis-like symptoms) -Haemorrhage from vascular access -Hypotension -Cardiovascular disease (the leading cause of death) **-Catheter-related bacteraemia** -Acute intravascular haemolysis (can be from reactions to contaminants in the dialysate or from mechanical forces) -Dialysis-related amyloidosis due to decreased clearance of beta-2 microglobulin -Psychological --- In PD specifically: -PD catheter obstruction (causes include constipation) -Infection of the exit site or tunnel, which may progress to bacterial peritonitis

Answer 42

Splanchnic vasodilation RAS activation Na and H20 retention

Answer 43

As per KDIGO guidelines when eGFR <30

Answer 44

Adynamic bone disease: due to reduced bone turnover, patients have low PTH Osteomalacia: decreased mineralisation mainly due to aluminium-containing phosphate binders Osteitis fibrosis: increased bone turnover due to secondary hyperparathyrodism, 'brown tumours' may develop

Answer 45

Tunnelled CVC more prone to infection, thrombosis, shorter lifespan and lower blood flow rate However, don't need to wait to mature

Answer 46

History (decreased intake, increased output, infective symptoms, medication history) Examination (volume assessment, evidence of obstruction, BP) -Urinalysis (protein or blood), **culture, osmolality and Na** -Bloods (inflammatory markers, U+Es, LFTs, clotting) -Renal immunology screen (ANCA, GBM, ANA, C3, C4, immunoglobulins and myeloma screen) **-CXR (overload, pulmonary haemorrhage)** -Renal tract US (hydronephrosis) -Consider renal biopsy

Answer 47

**A rise in Cr of >26 micromol/L** within 48 hours A >50% rise in Cr over past 7 days A fall in UO to <0.5 mL/kg/hour for >6 hours

Answer 48

-Current RRT -Previous RRT -Evidence of complications of ESRD or dialysis (laparotomy scar, parathyroidectomy scar)? -Aetiology of ESRD? -Adequacy of current RRT? To complete, perform fundoscopy

Answer 49

-Cirrhosis -Hyperthyroidism -RA -Pregnancy

Answer 50

Cirrhosis IBD

Answer 51

-Physiological (puberty and senility) -Cirrhosis -Drugs (spironolactone or digoxin) -Testicular tumour **-Klinefelter's** -Endocrinopathy (hyperthyroidism, hypothyroidism, Addison's)

Answer 52

Subtotal colectomy with end ileostomy End ileostomy with mucous fistula (usually emergency) Proctocolectomy and end ileostomy Proctocolectomy with ileo-anal pouch reconstruction

Answer 53

Cirrhosis (ALD, NAFLD, viral, AI, HH, Wilson's, alpha-1 antitrypsin) HCC Acute fulminant liver failure: paracetamol OD, hepatitis A and B **Also variant syndromes: hepatopulmonary syndrome, polycystic liver disease**

Answer 54

Liver transplant Hepatic resection for neoplastic disease Gastrectomy Oesopageal Ca Whipple's procedure

Answer 55

Absolute CI (SHAME): -Ongoing extra-hepatic sepsis -Untreated HIV -Ongoing alcohol misuse/illicit drug use -Active or previous extra-hepatic malignancy -Severe extrahepatic disease with poor life expectancy (including psychiatric disorder) -Liver cancer outside criteria --- Relative CI: -BMI >40 kg/m2 -Inadequate social support or poor adherance -Smoking Certain anatomical variants render some patients not ameanable e.g. extensive previous abdominal surgery

Answer 56

UKELD (Na, creatinine, INR, bilirubin) >49 indicates survival advantage King's College criteria in paracetamol

Answer 57

► Arterial pH <7.30 or HCO3 <18 **► INR >3.0 on day two or >4.0 thereafter** ► Oliguria and/or AKI ► Altered level of consciousness ► Hypoglycaemia ► Elevated arterial lactate (>4mmol/L) unresponsive to fluid resuscitation I.e. King's criteria

Answer 58

Encephalopathy, jaundice and coagulopathy appearing in a patient who, **less than 6 months ago, had no evidence of advanced liver disease** -Paracetamol -Viral hepatitis -Drug induced -Ischaemic

Answer 59

Signs CLD (although gynaecomastia and Dupuytren's may persist) Signs portal HTN such as caput medusae and splenomegaly (though spleen may remain large) ***Signs of decompensation such as asterix, jaundice and ascites (and other signs decompensation)*** N.B If transplant is palpable this may mean just there's a size mismatch N.B. Jaundice post-transplant raises question of graft dysfunction versus extra-hepatic causes

Answer 60

Surgical complications include 'Woo! HPB': -Wound complications -Haemorrhage/thrombosis -Post-operative AKI or chest infection **-Biliary complications** --- Medical: -Primary graft dysfunction -Hyper-acute, acute or chronic rejection -Immunosuppression-related: CNI nephrotoxicity, DM (steroids and CNI), osteoporosis (steroids) -Cardiovascular disease -Malignancy: PTLD, skin cancer -Infection: bacterial, viral (CMV, EBV, HCV), fungal -Recurrent disease

Answer 61

Survival 90% at one year 80% at 5 years

Answer 62

An autosomal codominant genetic disorder (i.e., one allele is inherited from each parent and each allele is expressed equally) Allele mutations cause ineffective activity of alpha-1 antitrypsin, the enzyme responsible for neutralising neutrophil elastase Manifestations include emphysema, COPD, bronchiectasis, and cirrhosis Intravenous AAT augmentation therapy benefits some patients

Answer 63

**Autosomal-dominant, neurocutaneous, multi-system disorder** Presentations are epilepsy, cognitive impairment, ash leaf spots, ungal fibromas, facial angiofibromas, renal angiomyolipomas and giant cell astrocytomas Lymphangioleiomyomatosis in women (cystic lung disease) Ix: Genetic testing Brain imaging EEG Abdominal US/MRI PFTs and HRCT

Answer 64

Autosomal dominant condition characterised by multiple vascularised tumours, particularly cerebellar, retinal or visceral

Answer 65

An inherited (mostly **dominant**) abnormality of the red blood cell, caused by defects in structural membrane proteins Most common form of inherited haemolytic anaemia in the US and northern Europe May be diagnosed at any age May be newly diagnosed in children who present with aplastic crisis due to parvovirus infection; may present with pallor, jaundice, splenomegaly or gallstones; may also be completely asymptomatic Splenectomy is the treatment of choice in patients with severe HS --- Investigations: -FBC and blood film -LDH, unconjugated bilirubin, reticulocytes high -Haptoglobin decreased -Coombs to rule out immune mediated -**EMA binding test** (previously osmotic fragility test) --- Treatment: -Transfusions for symptomatic anaemia -Folic acid supplementation -Splenectomy virtually eliminates haemolysis, sometimes combined with cholecystectomy -Will need vaccinations for encapsulated organisms and post-operative pneumococcal prophylaxis

Answer 66

G: gallstones E: ETOH T: trauma S: steroids M: other causes of ductal obstruction e.g. malignancy or mumps virus A: autoimmune S: - H: hypertriglyceridaemia/calcaemia or hereditary (cystic fibrosis, haemochromatosis) E: ERCP D: drugs (steroids, azathioprine)

Answer 67

Acute: -SIRS -ARDS or effusion -Ascites <4 weeks: collections, necrosis, abscesses and vascular complications (e.g. thrombus or haemorrhage) >4 weeks: pseudocyst -Recurrent AP or chronic pancreatitis -In chronic: **exocrine dysfunction, increased risk of pancreatic Ca and type 3c diabetes**

Answer 68

-Gastroenterology team -IVF and analgesia -ITU if severe **-Manage electrolytes and glucose** -Manage complications e.g. drain collections or Axios stent for pseudocyst (EUS-guided drain) -Manage cause e.g. cholecystectomy when well or alcohol abstinence and withdrawal pathway **-Smoking cessation -Pancreatic enzyme supplements Creon (with PPI to prevent breakdown)**

Answer 69

Steatorrhea Weight loss Hypomagnesaemia **Low vitamin ADEK (particularly A and E)** Low faecal elastase

Answer 70

IBS IBD Coeliac Infective Other autoimmune conditions e.g. thyroid disease Pancreatitis

Answer 71

AI disease causing SB villous atrophy and malabsorption

Answer 72

-FBC, haematinics, U+Es, LFTs -TSH and CRP to rule out other causes -Stool culture -Anti-TTG (should be done on gluten-containing diet; seronegative CD can occur) -Quantitative IgA (IgA deficiency renders IgA-TTG insensitive) -OGD (scalloping of duodenal mucosa) biopsy from D2 villous atrophy (on gluten-containing diet) **-Consider biopsy of skin in dermatitis herpetiformis (IgA deposits in dermis**

Answer 73

-Gluten avoidance -Dietician input -Vitamin supplementation as required -Manage osteoporosis risk -Dapsone if DH -Follow-up biopsies considered as risk of lymphoma -Pneumococcus vaccination -GF prescriptions and CD support group

Answer 74

(N.B. Lower midline abdominal incision, with palpable kidney in iliac fossa but no overlying scar) For poorly-controlled DM (usually T1) with ESRD Decision made by MDT/patient choice Improves mortality and QOL (avoids BM monitoring, insulin, dialysis) Better glucose and lipid metabolism Affect on retinopathy not yet understood New nephropathy prevented Neuropathy may stay the same or improve Pancreas connected to bladder or bowel

Answer 75

Gynaecomastia Dupuytren's

Answer 76

Drugs: ciclosprin, phenytoin, nifedipine Scurvy AML Pregnancy Familial

Answer 77

Ileostomy: spouted, RLQ, semi-solid effluent Colostomy: flush to skin

Answer 78

To manage chronic active symptoms on maximal medical therapy To mange complications such as stricture or fistula In emergencies such as toxic megacolon, haemorrhage or perforation

Answer 79

-FBC (anaemia), B12, folate and iron studies -U+E, bone and Mg (electrolytes) -LFTs (PSC) -CRP (disease activity) -Stool for calprotectin, culture and C. difficile -AXR if acute abdomen (ileus, perforation, toxic megacolon) -Sigmoidoscopy with biopsy -Colonoscopy (if sigmoidoscopy suggests proximal extension; to rule out infection)

Answer 80

Maintain remission: In mild to moderate: 5-ASAs (rectal +/- oral) Those who do not respond to 5-ASAs: oral steroids In moderate to severe: Consider JAK inhibitors or biologics under specialist guidance --- Acute severe UC (Truelove and Witts criteria): -Gastroenterology, surgical and wider MDT input -High dose IV HC -Consider IV ciclosporin or infliximab if worsening or no improvement in 72 hours -Assess need for surgery -May need blood transfusion, fluids, and electrolyte replacement -If severe intractable symptoms OR if megacolon or perforation, colectomy -Nutrition -pLMWH --- To maintain remission: 5-ASAs **Consider thiopurine if remission not maintained by ASAs OR >2 steroid course in year OR ASUC** **Treatment with biologics (e.g. infliximab) or JAK inhibitors can be continued into maintenance phase** Also: psychological support and nutrition, manage bone disease, consider surveillance colonoscopy CAP BEN N.B. NO EVIDENCE FOR MTX

Answer 81

>6 stools/day With systemic disturbance as evidenced by fever, tachycardia, **anaemia** or ESR >30

Answer 82

-FBC (anaemia) and B12, folate and iron studies -U+E, bone profile and Mg (electrolytes) -LFTs (PSC) -CRP (disease activity) and blood cultures -Stool for calprotectin, culture and C. difficile (and Yersinia serology) -Consider AXR (dilatation, sacroiliitis) -MR abdomen is best imaging (skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae) -Segmental colonic and ileal **biopsies**

Answer 83

Managed by gastroenterology team with wider MDT input Induce remission: Conventional glucocorticosteroid (PO/IV) or budesonide +/- thiopurine or MTX Or TNF alpha inhibitor biologics (e.g. infliximab) (Consider ustekinumab and vedolizumab if TNF alpha therapy fails) Consider **antibiotics**, manage complications (abscess, fistula, stricture) and consider surgery Nutrition pLMWH --- Maintenance: **Thiopurines or MTX (+/- infliximab)** --- Also: smoking cessation, anti-diarrhoeal, anti-spasmodics, psychological support, nutrition, manage bone disease, manage extra-intestinal manifestations, consider surveillance colonoscopy "In addition these patients may need... CAPS BEN"

Answer 84

Abscess antibiotics and drainage Strictureplasty or **balloon dilatation** for strictures Fistulae medical control of inflammation and surgery

Answer 85

-Arthropathy* -Erythema nodosum* -Pyoderma gangrenosum **-Uveitis** -Episcleritis* -Apthous ulcers* -Metabolic bone disease* -Psoriasis **-Hepatobiliary complications** *Associated with disease activity (AAEEM)

Answer 86

HBV, HCV and HIV (and VZV if no history of chicken pox, shingles or varicella vaccination) For anti-TNF: screen for active or latent TB (history, IF-gamma assays and CXR) For thiopurines: TPMT

Answer 87

Crohn's: -Presents more commonly with abdominal pain, more gradual-onset **-Skip lesions, transmural inflammation** **-Non-caseating granulomas** -Whole GI tract (predilection for terminal ileum) -Smoking increases risk -Fistulae and stenosis common UC: -Presents with blood in stools -Continuous, superficial inflammation -Crypt abscesses -Large bowel (predilection for rectum), though can get 'backwash ileitis' -Fistulae and stenosis rare

Answer 88

CHIPS and MATHI but HIP MAI Also endocrine **(acromegaly and thyrotoxicosis)**

Answer 89

Caused by an autosomal recessive single gene defect in the beta chain of haemoglobin, which results in production of sickle cell haemoglobin (denoted HbS) Sickle cells can obstruct blood flow and break down prematurely, and are associated with varying degrees of anaemia Obstruction of small blood capillaries can cause painful (vaso-occlusive) crises, damage to major organs (bone, kidneys and lungs as in acute chest syndrome), and increased vulnerability to infection Crisis is often precipitated by viral illness, exercise or hypoxia Treatment goals include symptom control (including pain management), and prevention and management of complications (hydroxycarbamide) Worse prognosis for patients with triad of 1) leg ulcers 2) priapism 3) pulmonary HTN

Answer 90

Budd-Chiari syndrome (BCS) = hepatic venous outflow obstruction **Abdominal pain, ascites, and hepatomegaly (AHA!)** Colour and pulsed Doppler ultrasonography and testing for hypercoagulable states Radiological interventional procedures, surgical or medical (anticoagulation)

Answer 91

-Scar in L/R iliac fossa, overlying a smooth, firm, non-tender mass -Scars on the chest wall from previous site of vascular access for HD and there is a non-functioning fistula in L/R arm -No signs of uraemia and the patient is euvolaemic -There is gum hypertrophy and bruising -Aetiology (diabetes, PKD, SLE signs) These findings are in keeping with a functioning renal transplant with evidence of current or previous ciclosporin or steroid use I suspect the underlying aetiology is....

Answer 92

Investigate (FBC UE LFT CRP clotting electrolytes, blood cultures, urine culture, CXR, US, ascitic tap) Alcohol Infection (including SBP) AKI or hyponatraemia (IP/OP) GI bleed Encephalopathy (low threshold for CT head) Look for cause of decompensation if unclear pLMWH (unless bleeding or platelets below 50) Gastro review Escalate to critical care