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PACES > Abdominal > Flashcards

Abdominal Flashcards

1
Q

Signs of decompensation of liver disease? (BSG)

A

Deterioration in liver function in a patient with cirrhosis

“JAVE”
-Jaundice
-Ascites (increasing)
-Variceal bleeding (GI bleeding)
-Encephalopathy

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2
Q

Causes of decompensation in cirrhosis? (BSG)

A

-GI bleed
-Infection including SBP
-Alcoholic hepatitis
-Constipation
-Acute portal vein thrombosis/ischaemic liver injury
-Drugs including sedatives
-Dehydration
-Hypokalaemia
-HCC

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3
Q

Signs of chronic liver disease?*

A

General: cachexia, icterus, excoriation, bruising

Hands: Dupuytren’s, leuconychia, clubbing, palmar erythema

Face: xanthelasma, parotid swelling, fetor hepaticus

Chest and abdomen: spider naevi, caput medusae, reduced body hair, gynaecomastia, testicular atrophy

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4
Q

Stages of encephalopathy? (BMJ)

A

Grade 1 (covert): sleep rhythm alterations, shortened attention span

Grade 2 (overt): lethargy, disorientation, obvious personality change

Grade 3 (overt): somnolence, confused, gross disorientation

Grade 4 (overt): coma

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5
Q

How would you manage an UGIB? Scoring system? (BSG bundle)

A

A to E approach
Consider ITU if unstable +/- major haemorrhage protocol

IV fluids if haemodynamically unstable
Transfuse if Hb <70 aim for 70-100g/L

Calculate GBS (consider OP management if GBS 0 or 1)

If cirrhosis or suspected variceal, terlipressin 2mg QDS and antibiotics

N.B. Continue aspirin and suspend other antithrombotics

NBM
Refer for endoscopy and to gastroenterology team
IV PPI if high risk ulcer on scope

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6
Q

How to assess for encephalopathy? (BMJ)

A

-History (sleep or mood disturbances)

On examination 3As:

-Altered GCS or mental state alteration
-Asterixis or motor disturbances
-Constructional Apraxia (inability to draw a 5-pointed star)

-Look for precipitating factors and other causes of mental state alteration
-Bloods and CT head

-Raised Ammonia level (not commonly measured anymore)
-Triphasic slow waves on EEG

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7
Q

Causes of jaundice? Drugs causing jaundice? (NICE)

A

Pre-hepatic jaundice:
-Haemolytic anaemias (hereditary spherocytosis, G6PD deficiency, B12 deficiency, sickle cell, thalassaemia, SLE)
-Gilbert’s syndrome (unconjugated) and Crigler-Najjar syndrome (unconjugated)

Intrahepatic jaundice:
-Decompensated cirrhosis
-Viral hepatitis (hepatitis A to E, EBV and HIV)
-Alcoholic hepatitis
-Autoimmune liver disease (AIH, PBC, PSC)
-Drug-induced hepatitis (paracetamol, TB drugs) and drugs causing cholestasis (co-amoxiclav, flucloxacillin, COCP, steroids)
-Malignancy (HCC, cholangiocarcinoma and gallbladder)

Extrahepatic jaundice:
-Cholelithiasis
-Bile duct strictures
-Pancreatitis
-Malignancy (pancreatic cancer)

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8
Q

How to treat encephalopathy? (BMJ)

A

-Lactulose 25 mL every 12 h until at least two soft bowel motions are produced per day
-Rifaximin

-Supportive care (ITU if GCS <8)
-Reversal of precipitating factors -Investigation of alternative causes of altered mental status

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9
Q

Causes of CLD? (Ox)

A

Alcohol
NAFLD
Viral (hepatitis B and C)

Autoimmune (AIH, PSC, PBC)

Metabolic (haemochromatosis, Wilson’s, alpha-1 antitrypsin, CF)

Drugs (MTX, isoniazid, amiodarone, phenytoin)

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10
Q

Investigations in a patient with CLD? Autoantibodies in liver disease?*

A

FBC, clotting, U+E, LFTs, HbA1c (plus INR and albumin to check synthetic function)

Liver screen (autoantibodies and immunoglobulins, hepatitis B and C serology, ferritin, caeruloplasmin, alpha-1 antitrypsin, AFP)

USS of abdomen (to assess echotexture, exclude malignancy, splenomegaly would suggest portal HTN, hepatic and portal vein doppler to exclude thrombosis)

Diagnostic paracentesis (albumin, differential WCC, gram stain and culture (+ AFB), cytology) and to calculate SAAG

-Think about MRCP/ERCP to exclude PSC
-CT-TAP +/- bidirectional scopes if considering malignancy
-Possible Fibroscan and liver biopsy

PBC: AMA, IgM
PSC: ANA, anti-SM
AIH: anti-SM, anti-LKM1

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11
Q

Complications of cirrhosis? (Ox)

A

“JAVE”
-Jaundice
-Ascites and SBP
-Variceal haemorrhage due to portal hypertension
-Encephalopathy

More in MRCP book (4Hs):
Hypersplenism/thrombocytopenia/coagulopathy
Hypoalbuminaemia
Hepatorenal syndrome
HCC

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12
Q

Causes of ascites?

A

Most commonly (3Cs):
-Cirrhosis (80%)
-Cancer
-CCF

Less commonly (think about SAAG):
-Portal vein thrombosis
-Hypothyroidism
-Peritoneal TB
-Pancreatitis
-Bowel perforation
-Nephrotic syndrome (hypoalbuminaemia)

-Meig’s syndrome
-Chylous ascites
-PD-related

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13
Q

Complications of TIPSS?

A

Encephalopathy

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14
Q

How to interpret SAAG? (BSG)

A

SAAG = serum albumin - ascitic albumin

A high SAAG >11 (i.e. transudate):
-Portal hypertension
-Portal vein thrombosis
-Cardiac failure
-Hypothyroidism

Low SAAG <11 (i.e. exudate):
-Peritoneal carcinomatosis
-Peritoneal TB
-Pancreatitis
-Bowel perforation
-Nephrotic syndrome (hypoalbuminaemia)

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15
Q

Investigations for ascites?

A

FBC (thrombocytopenia suggests hypersplenism and portal HTN), clotting, U+E, LFTs, HbA1c (plus INR and albumin to check synthetic function)

Liver screen (autoantibodies and immunoglobulins, hepatitis screen, ferritin, caeruloplasmin, alpha-1 antitrypsin, AFP)

USS abdomen (to assess echotexture, exclude malignancy, splenomegaly would suggest portal HTN, hepatic and portal vein doppler to exclude thrombosis)

Diagnostic paracentesis (albumin, differential WCC, gram stain and culture (+ AFB), cytology) and to calculate SAAG

CT-TAP if considering malignancy

CXR to look for features of heart failure

Possibly Fibroscan and liver biopsy

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16
Q

How to manage alcoholic hepatitis? (BSG)

A

-Alcohol cessation
-Alcohol withdrawal pathway (Librium and IV Pabrinex)
-Nutrition
-Treat infections
-Steroids if severe AH (MELD score to help predict response to steroids)
-In addition, NAC has been shown to improve mortality at one month but is currently optional in current guidelines

In addition:

-ITU if needs support
-Consideration of liver transplant

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17
Q

Treatment of ascites in cirrhosis?

A

-Abstinence
-Na and fluid restriction
-Diuresis with aldosterone antagonist +/- loop (1kg/day)

In a tense abdomen:
Consider therapeutic drain with albumin cover

If refractory ascites:
TIPSS
Consider liver transplantation
Consider palliation

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18
Q

What are the signs of chronic alcohol misuse? (Ox)

A

From end-of-bed to arms to face to neurology:

-Cachexia
-Tremor
-Dupuytren’s contracture
-Parotid enlargement
-Cerebellar syndrome
-Peripheral neuropathy

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19
Q

How do you assess the severity of cirrhosis? (Ox)

A

Childs-Pugh score takes into account bilirubin, ascites, encephalopathy, PT and albumin

MELD score also used

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20
Q

Management of cirrhosis?*

A

1) Slowing or reversing underlying disease (abstinence, antivirals, immunosuppression etc.)

2) Preventing superimposed liver damage (abstinence, immunisation against hepatitis and pneumococcal or influenza)

3) Preventing complications (abdominal US and AFP, endoscopy, beta blockers, propylactic antibiotics if SBP)

Nutrition

Liver transplant (6 months abstinence, <65 years)

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21
Q

How would you manage SBP? (BSG)

A

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

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22
Q

Scoring system for alcoholic hepatitis? (BSG)

A

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

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23
Q

Alcohol abuse risks?

A

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

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24
Q

What are the causes of hepatomegaly?*

A

3Cs (as in ascites):
-Cirrhosis
-Cancer (primary or secondary usually colorectal)*
-Hepatic congestion (as in heart failure)*

Less commonly:
-Infectious (viral hepatitis B and C)*
-Immune (PBC)
-Infiltration (amyloid)
-Alcoholic hepatitis*
-Vascular*
-Polycystic liver disease

*may cause tender hepatomegaly

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25
Q

Infective causes of acute hepatitis? (Ox)

A

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

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26
Q

Causes of splenomegaly?*

A

“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):
-CMV
-Myelofibrosis
-Malaria
-Visceral leishmaniasis

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27
Q

How would you investigate a patient with splenomegaly?*

A

FBC, blood film, LFTs, LDH, beta-2 microglobulin, immunology screen

Viral serology/HIV testing/thick and thin films/malaria antigen test

CXR

Imaging (USS to evaluate but also CT/PET if haematological malignancy)

LN excision biopsy/bone marrow biopsy

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28
Q

What are the significance of B symptoms in NHL? (Ox)

A

40% patients will have B-symptoms (fever, weight loss >10% over 6 months, night sweats)

If one present, staging is altered accordingly

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29
Q

Cytogenetics of CML? (Ox)

A

Philadelphia chromosome in 95%

Translocation between chromosome 9 and 22

Increased oncogene activity

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30
Q

Causes of hyposplenism? (Ox)

A

Splenic infarction/splenic artery thrombosis

Coeliac/autoimmune disease

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31
Q

Indication for splenectomy? Work-up?*

A

-Rupture

-Haematological malignancy (ITP, hereditary spherocytosis)

Vaccination (2/52 prior to proect against encapsulated organisms): pneumococcus, meningococcus, Haemophilus influenzae

Prophylactic antibiotics (lifelong)

Medic alert bracelet

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32
Q

What does a spleen feel like on palpation? (Ox)

Versus a liver/kidney?

A

Enlarged towards RIF
Medial notch
Dull to percussion
Cannot palpate above
Cannot be balloted

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33
Q

What are the differential diagnoses for bilateral palpable kidneys? Versus single?*

A

N.B. First three are the same

Bilateral:
-PKD
-Bilateral RCC
-Bilateral HN
-Tuberous sclerosis (renal angiomyolipomata and cysts)
-Amyloidosis

Single:
-PKD (contralateral nephrectomy or other kidney not palpable)
-RCC
-HN due to ureteric obstruction
-Simple cysts
-Hypertrophy of single functioning kidney

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34
Q

Investigations for patient with renal enlargement?*

A

BP

U+Es

Urinalysis and urine cytology

USS abdomen

CT if ?RCC

Genetic studies (ADPKD)

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35
Q

What is PKD? Genetics of PKD?*

A

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

ARPKD is rare presents in infancy

36
Q

Features of PKD? Complications?*

A

Presents as part of familial screening or with:

HTN

Recurrent UTI

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

Macroscopic haematuria if bleeding into cysts

Complications:

ESRD by 40-60 years

Hepatic cysts in 70% or cysts elsewhere

Intracranial Berry aneurysms causing SAH

MV prolapse

37
Q

Management of ADPKD?*

A

Control HTN

Genetic counselling and family screening

Tolvaptan to slow progression

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

38
Q

How is HH inherited? (Ox)

A

Autosomal recessive fashion

Usually due to HFE gene mutation on chromosome 6 (most homozygous for C282Y, some H63D)

Males affected at earlier age as women protected by menstrual loss

39
Q

How does HH present? (BSG)

A

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

40
Q

How would you investigate a patient with suspected HH? (BSG)

A

Ferritin and transferrin (ferritin is less specific >200 females >300 males, TSATS >40% women >50% in men)

FBC (polycythaemia)

LFTs (can be normal), liver US, liver biopsy

Genetic testing for C282Y and H63D (variable penetrance)

-Blood glucose/HbA1C
-ECG/CXR/echo (can cause restricted or dilated cardiomyopathy, MRI is most sensitive)
-Plain films of joints
-Liver USS/AFP 6 monthly if cirrhotic

Liver biopsy not required for diagnosis but may help evaluate degree of fibrosis

41
Q

How to management HH? (BSG)

A

Phlebotomy (1 unit twice weekly initially, then once every 3 months when transferrin falls <50%)

Avoid alcohol

Management of complications e.g. DM, CM, joints
Surveillance for HCC (200x risk if cirrhotic, 6 monthly USS and AFP)

Screening for first degree relatives

N.B. Desferrioxamine second line

42
Q

Survival in HH? (BSG)

A

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

43
Q

What are the clinical features of PBC? (Ox) How is it diagnosed? (Ox)

A

1) Fatigue 2) Pruritus 3) Sicca

Liver disease occurs late and is rarely a presenting feature

44
Q

How to diagnose PBC? (Ox)

A

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

45
Q

How is PBC managed? (Ox)

A

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 6/12ly
If portal hypertension: variceal screening
If bilirubin >50 or decompensation: transplant

46
Q

What other diseases are associated with PBC? (BSG)

A

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

47
Q

Diseases associated with PSC? (BSG)

A

Up to 83% have IBD

Associations including (CSSTT):
-Coeliac
-Sjögren’s
-Scleroderma
-Thyroid disease
-Type 1 diabetes mellitus

48
Q

What are the major causes of chronic renal disease? (Ox)

A

Diabetes (34%)
GN (21%)
HTN (12%)

Also less commonly PKD, reflux nephropathy and analgesic nephropathy

49
Q

Top causes for transplant?*

A

Diabetes
GN
ADPKD

50
Q

Management of CKD? (Ox)

A

MDT approach and holistic manner

Treatment of reversible causes:
-Diagnosis of treatment glomerular disease (with biopsy)
-Cessation of nephrotoxic drugs
-Exclusion of obstructive uropathy and renovascular disease (with imaging)

Slowing disease progression:
-Manage HTN with drugs and minimising salt intake, blood sugar also dyslipidaemia (with statins)
-ACEi and SGLT-2 inhibitors (slow progression independent of BP and glucose)
-If diabetic kidney disease, Finerenone can slow progression
-Smoking cessation

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

51
Q

Indications for RRT? (Ox)

A

Preparation should begin when GFR falls become 30ml/min

Indications are (AEIOU):
-Refractory acidosis
-Refractory hyperkalaemia
-Removal of toxins e.g. lithium, salicylates
-Volume overload refractory to diuretics
-Pericarditis/pleuritis/encephalopathy due to uraemia

52
Q

CI to renal transplant? (BMJ)

A

Absolute:
-Untreated malignancy
-Active infection, untreated
-Untreated HIV infection or AIDS
-Life expectancy is <2 years

Relative:
-Comorbid condition
-Age >65 years
-Untreated coronary artery disease
-Obesity
-Previous malignancy
-Chronic hepatitis B or C
-HIV infection

53
Q

Problems following renal transplantation? (BMJ)

A

Early surgical:
* Haemorrhage
* Thrombosis
* Recipient vasculature injury
* Urine leak
* Wound complications

Late surgical:
* Ureteral obstruction
* Transplant renal artery stenosis

Early medical:
* Acute rejection
* Infection: bacterial, viral (CMV), fungal (PCP)

Late medical:
* Immunosuppression related (including malignancy and chronic alloimmune injury)
* Recurrent disease
* Cardiovascular disease
* Infections (polyoma virus)

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

https://geekymedics.com/renal-transplantation/

https://www.bmj.com/bmj/section-pdf/187380?path=/bmj/343/7832/Clinical_Review.full.pdf

54
Q

What are some of the side effects of IS? (BMJ)

A

Infections (bacterial, fungal, viral)
Malignancy including skin Ca

-Steroids: DM, hypertension, weight gain, osteoporosis
-Tacrolimus: DM, tremor, nephrotoxicity
-Ciclosporin: DM, hypertension, gum hypertrophy, hirsutism, nephrotoxicity

55
Q

What are some of the signs of a failing renal transplant?

A
56
Q

Problems with dialysis? (Geekymedics)

A

In HD:
-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)
-Acute intravascular haemolysis (can be from reactions to contaminants in the dialysate or from mechanical forces)
-Air embolism
-Haemorrhage from vascular access
-Hypotension
-Cardiovascular disease (the leading cause of death)
-Catheter-related bacteraemia
-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
-PD-associated peritonitis/fibrosis

57
Q

What are the manifestations of renal osteodystrophy? (Ox)

Probably not very relevant

A

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

58
Q

What are some of the advantages and disadvantages of tunnelled line versus fistula?

A
59
Q

How to work up AKI?

A

History (decreased intake, increased output, infective symptoms, medication history)

Examination (volume assessment, evidence of obstruction)

Urinalysis, culture, osmolality and Na
Bloods
CXR
Renal tract US
Renal immunology screen
Consider renal biopsy

60
Q

Causes of palmar erythema?*

A

-Cirrhosis
-Hyperthyroidism
-RA
-Pregnancy

61
Q

Abdominal causes of clubbing?*

A

Cirrhosis
IBD

62
Q

Causes of gynaecomastia?*

A

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

63
Q

What are the indications for liver transplant? (BSG)

A

Cirrhosis (ALD, NAFLD, viral, AIH, 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

64
Q

CI for LT? (BSG)

A

Absolute CI:
-Untreated HIV
-Severe extrahepatic disease with
predicted mortality >50% at 5 years
including psychiatric disorder
-Severe irreversible pulmonary disease
-Ongoing alcohol misuse
-Active illicit drug use
-Certain anatomic variants
-Ongoing extra-hepatic sepsis
-Active or previous extra-hepatic
malignancy
-Liver cancer outside criteria

Relative CI:
-Inadequate social support
-Smoking
-Certain anatomical variants
-Extensive previous abdominal
surgery
-BMI >40 kg/m2
-Poor clinic attendance and/or
adherence

65
Q

Scoring system for LT? (BSG)

A

UKELD (Na, creatinine, INR, bilirubin) >49 indicates survival advantage

66
Q

When to discuss with LTU in paracetamol ALF? (BSG)

A

► 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

67
Q

What is the definition of acute liver injury? Causes of ALI? (BSG)

A

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

68
Q

Signs of a failing liver transplant?

A

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

69
Q

Complications of liver transplant?

A

Survival 90% at one year
80% at 5 years

Rejection
Infection secondary to IS
Malignancy
Post-transplant lymphoproliferative disorder
Acute on chronic kidney disease
Metabolic syndrome
Recurrence of primary liver disease

70
Q

Tell me about alpha-1 antitrypsin deficiency.

A
71
Q

Tell me about tuberous sclerosis.

A
72
Q

Tell me about hereditary spherocytosis.

A

Autosomal dominant condition, most common defect on chromosome 8

Results from genetic alteration form one of 5 genes that encode for RC membrane proteins leading to spherocyte shape

Change affects change of lifespan as more prone to haemolysis

Presentation occurs at variable age and may be asymptomatic for many years

Presentation:
Fatigue (anaemia)
Jaundice
RUQ pain (pigment gallstones)

Anaemia may worsen with infections e.g. EBV which increases spleen size and in pregnancy
Parvovirus can also cause haemolytic crises

Investigates:
FBC and blood count
LDH unconjugated bilirubin reticulocytes high
Haptoglobin decreased
Coombs to rule out immune mediated
EMA binding test (previously osmotic fragility test)

Treatment:
Folic acid supplementation
Splenectomy virtually eliminates haemolysis, sometimes combined with cholecystectomy
Will need vaccinations for encapsulated organisms

73
Q

Causes and management of acute/chronic pancreatitis?

A

ETOH
Gallstones

ERCP
Hypertriglyceridemia
Hypercalcaemia
Drug-related
Trauma-related
Autoimmune pancreatitis
Genetic (cystic fibrosis, haemochromatosis)
Ductal obstruction e.g. tumours

74
Q

Complications of pancreatitis? Treatment of chronic pancreatitis?

A

Acute:
SIRS
ARDS
Pseudocyst
Type 3 diabetes
Pancreatic stricture

Analgesia
Alcohol abstinence
Smoking cessation
Pancreatic enzyme supplements Creon (with PPI to prevent breakdown)

75
Q

How would you investigate a patient with suspected IBD?

A
76
Q

How would you manage a patient with IBD?

A
77
Q

How would you investigate a patient with suspected coeliac disease?

A

FBC
Haematinics
Anti-TTG
TSH
OGD biopsy from D2 villous atrophy

78
Q

How would you manage a patient with coeliac disease?

A

Gluten avoidance
Dietician

79
Q

Indications for SPK?

A

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

80
Q

What signs of CLD persist after liver transplant?

A

Gynaecomastia
Dupuytren’s

81
Q

Causes of gum hypertrophy?*

A

Drugs: ciclosprin, phenytoin, nifedipine
Scurvy
AML
Pregnancy
Familial

82
Q

How to tell ileostomy or colostomy?

A

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

83
Q

Indications for surgery in IBD?

A

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

84
Q

Surgeries for UC? Medical treatment for UC?

A

Subtotal colectomy with end ileostomy

Or if emergency and end ileostomy with mucus fistula

Proctectomy with end ileostomy

Proctocolectomy with ileoanal pouch reconstruction (no stoma)

5-ASAs with mild to moderate disease

Oral steroids in those who do not respond to 5-ASAs/moderate to severe disease

Acute severe UC need high dose IV HC

To maintain remission: 5-ASAs

2 or more flares requiring steroids: escalate to azathioprine or biologics (such as infliximab)

85
Q

Abdominal mass

A
86
Q

Sickle cell disease

A
87
Q

Budd Chiari

A

PACES (4 decks)

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