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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 (asterixis, altered GCS, constructional apraxia)

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2
Q

Causes of decompensation in cirrhosis? (BSG)

A

-GI bleed
-Infection including SBP
-Alcoholic hepatitis
-Acute portal vein thrombosis/ischaemic liver injury
-Constipation
-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, obvious personality change

Grade 3 (overt): somnolence, confusion

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

Once patient has been managed, consider TIPSS and propranolol (if variceal)

If peptic ulceration, switch to oral PPI at 72 hours +/- H. Pylori eradication

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6
Q

Scoring systems for UGIB? (MDCalc)

A

GCS used to assess risk and likelihood of needing intervention

Rockall score used post-scope and determines severity of GI bleeding (gives percentage risks for re-bleed and mortality)

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7
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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8
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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9
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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10
Q

Hepatorenal syndrome? (Ox PP) (BMJ)

A

Inadequate hepatic breakdown of vasoactive substances
Leads to excessive renal vasoconstriction
Can happen fast (type I) or slowly (type II)
Mimic pre-renal renal failure
Diagnosis of exclusion

Treat with terlipressin, albumin and consider transplant

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11
Q

Things to remember to present in CLD patient?

A

Signs of uncomplicated CLD present
Portal HTN signs?
Decompensation signs?
Underlying cause?

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12
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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13
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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14
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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15
Q

Signs of portal HTN? (Ox PP)

A

Caput medusae
Ascites
Splenomegaly

(Varices on OGD)

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16
Q

Causes of ascites?

A

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

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

Even less commonly:
-Meig’s syndrome
-Chylous ascites
-PD-related

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17
Q

Complications of TIPSS?

A

Encephalopathy (up to 30%)

N.B. Transvenous intrahepatic porto-systemic shunt that diverts blood from portal to systemic system to relieve refractory portal hypertension

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18
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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19
Q

Investigations for ascites?

A

FBC (thrombocytopenia suggests hypersplenism and portal HTN), clotting, U+E, LFTs, HbA1c, BNP

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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20
Q

How to manage alcoholic hepatitis? (BSG)

A

-Alcohol cessation
-Alcohol withdrawal pathway (Librium and IV Pabrinex)
-Nutrition
-Treat infections
-Steroids if severe AH as defined by Maddrey and Glasgow score (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 guidelines

In addition:

-ITU if needs support
-Consideration of liver transplant

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21
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 100ml of human albumin solution 20% (HAS) for every 2-3 litres of ascitic fluid drained

If refractory ascites:
TIPSS
Consider liver transplantation
Consider palliation

In addition:
Treat SBP

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22
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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23
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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24
Q

Management of cirrhosis?*

A

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

2) Preventing superimposed liver damage (abstinence)

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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25
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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26
Q

Scoring system for alcoholic hepatitis? (BSG)

A

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

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27
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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28
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 (IIIVAP):
-Infectious (viral hepatitis B and C)*
-Immune (PBC)
-Infiltration (amyloid)
-Alcoholic hepatitis*
-Vascular*
-Polycystic liver disease

*may cause tender hepatomegaly

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29
Q

Signs of hepatomegaly?*

A

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)?

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30
Q

Infective causes of acute hepatitis? (Ox)

A

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

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31
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)

-CML
-Myelofibrosis
-Malaria
-Visceral leishmaniasis

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32
Q

How to investigate malaria? (BMJ)

A

Thick and thin films
Also rapid diagnostic tests

ID team input needed!

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33
Q

How to investigate splenomegaly?

A

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

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34
Q

Splenomegaly sign?*

A

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

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35
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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36
Q

Cytogenetics of CML? (Ox)

A

Philadelphia chromosome in 95%

Translocation between chromosome 9 and 22

Increased oncogene activity

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37
Q

Causes of hyposplenism? (Ox)

A

Splenic infarction/splenic artery thrombosis

Coeliac/autoimmune disease

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38
Q

Indication for splenectomy? Work-up?*

A

-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

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39
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)
-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

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40
Q

Investigations for patient with renal enlargement?*

A

BP

U+Es

Urinalysis and urine cytology

USS abdomen

CT if ?RCC

Genetic studies (ADPKD)

Echo (MV prolapse)

Consider cerebral angiogram

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41
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 (later onset, fewer cysts)

ARPKD is rare presents in infancy

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42
Q

How would PKD present? Complications?*

A

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

Other complications:

Polycythaemia

ESRD by 40-60 years

Hepatic cysts in 70% or cysts elsewhere

Intracranial Berry aneurysms causing SAH

MV prolapse

Diverticular disease

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43
Q

Management of ADPKD?*

A

Control HTN

Control other CV risk factors (e.g. statins)

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

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44
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

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45
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

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46
Q

Differential for HH? (180)

A

Secondary iron overload e.g. in repeated transfusions

47
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), HbA1c

HFE gene testing for C282Y and H63D (variable penetrance)

Liver US

-Liver USS/AFP 6 monthly if cirrhotic
-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

48
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

49
Q

Survival in HH? (BSG)

A

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

50
Q

What are the clinical features of PBC? (Ox)

A

1) Fatigue 2) Pruritus 3) Sicca

Liver disease occurs late and is rarely a presenting feature

51
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

52
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

53
Q

What other diseases are associated with PBC? (BSG)

A

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

54
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

55
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

56
Q

Top causes for renal transplant?*

A

Diabetes
GN
ADPKD

57
Q

Management of CKD? (Ox)

A

Treatment of underlying or 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, blood sugar also dyslipidaemia
-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
MDT approach and holistic manner

58
Q

Indications for RRT? In AKI? In CKD? (Ox)

A

Preparation should begin when GFR falls below 30ml/min

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

59
Q

CI to renal transplant? (BMJ)

A

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

60
Q

Complications of renal transplantation? (BMJ)

A

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

61
Q

Renal transplant survival?

A

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

62
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

63
Q

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

A

Fluid overload
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)

64
Q

Problems with dialysis? (Geekymedics)

A

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

65
Q

Differences between HD and PD?

A
66
Q

Ascites in cirrhosis pathophysiology? (M)

A

Splanchnic vasodilation
RAS activation
Na and H20 retention

67
Q

When to start working up a patient for renal transplant?

A

As per KDIGO guidelines when eGFR <30

68
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

69
Q

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

A

Tunnelled CVC more prone to infection, shorter lifespan and lower blood flow rate

However, don’t need to wait to mature

70
Q

How to work up AKI?

A

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

71
Q

Define an AKI. (NICE)

A

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

72
Q

Things to remember when presenting renal patient?

A

-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

73
Q

Causes of palmar erythema?*

A

-Cirrhosis
-Hyperthyroidism
-RA
-Pregnancy

74
Q

Abdominal causes of clubbing?*

A

Cirrhosis
IBD

75
Q

Causes of gynaecomastia?*

A

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

76
Q

Types of surgery in IBD? (M)

A

Subtotal colectomy with end ileostomy

End ileostomy with mucous fistula (usually emergency)

Proctocolectomy and end ileostomy

Proctocolectomy with ileo-anal pouch reconstruction

77
Q

What are the indications for liver transplant? (BSG)

A

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

78
Q

Differentials for a rooftop incision? (180)

A

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

79
Q

CI for LT? (BSG)

A

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

80
Q

Scoring system for LT? (BSG)

A

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

81
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

82
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

83
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

N.B. Jaundice post-transplant raises question of graft dysfunction versus extra-hepatic causes

84
Q

Complications of liver transplant? (BSG)

A

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

85
Q

Liver transplant survival?

A

Survival 90% at one year
80% at 5 years

86
Q

Tell me about alpha-1 antitrypsin deficiency. (BMJ)

A

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

87
Q

Tell me about tuberous sclerosis. (BMJ)

A

Autosomal-dominant, neurocutaneous, multi-system disorder characterised by cellular hyperplasia, tissue dysplasia, and multiple organ hamartomas

Presentations are epilepsy, cognitive impairment, ash leaf spots, facial angiofibromas, renal angiomyolipomas and giant cell astrocytomas

88
Q

Tell me about hereditary spherocytosis. (BMJ)

A

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 count
-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

89
Q

Causes and management of acute/chronic pancreatitis? (BSG)

A

G: gallstones
E: ETOH

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

90
Q

Complications of pancreatitis? (BSG)

A

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

91
Q

Treatment of pancreatitis? (BSG)

A

-IVF and analgesia
-NBM (if nausea, vomiting, abdominal pain)
-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

-Alcohol abstinence and withdrawal pathway
-Smoking cessation
-Pancreatic enzyme supplements Creon (with PPI to prevent breakdown)

92
Q

Pancreatic exocrine insufficiency indicators? (BMJ)

A

Steatorrhea
Weight loss

Hypomagnesaemia
Low vitamin ADEK (particularly A and E)

Low faecal elastase

93
Q

Normal abdominal examination differentials? With abdominal pain or diarrhoea?

A

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

94
Q

How would you investigate a patient with suspected coeliac disease?

A

-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 biopsy from D2 villous atrophy (on gluten-containing diet)

95
Q

How would you manage a patient with coeliac disease? (BSG)

A

-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

96
Q

Indications for SPK?

A

(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

97
Q

What signs of CLD persist after liver transplant?

A

Gynaecomastia
Dupuytren’s

98
Q

Causes of gum hypertrophy?*

A

Drugs: ciclosprin, phenytoin, nifedipine
Scurvy
AML
Pregnancy
Familial

99
Q

How to tell ileostomy or colostomy?

A

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

100
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

101
Q

Investigations for UC?*

A

-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)

102
Q

Medical treatment for UC? (BMJ)

A

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 and
-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

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

N.B. NO EVIDENCE FOR MTX

103
Q

Truelove and Witts severe? (Ox PP)

A

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

104
Q

Crohn’s investigations? (BMJ)

A

-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

105
Q

Crohn’s management? (NICE/BMJ)

A

Managed by gastroenterology team with wider MDT input

Induce remission:

Conventional glucocorticosteroid (PO/IV) or budesonide

+/- immunomodulator (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

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”

106
Q

Complications of Crohn’s and management? (BMJ)

A

Abscess antibiotics and drainage

Strictureplasty or balloon dilatation for strictures

Fistulae medical control of inflammation and surgery

107
Q

Extra-intestinal features of IBD? (NICE)

A

-Arthropathy*
-Erythema nodosum*
-Pyoderma gangrenosum
-Uveitis
-Episcleritis*
-Apthous ulcers*
-Metabolic bone disease*
-Psoriasis
-Hepatobiliary complications

*Associated with disease activity (AAEEM)

108
Q

Screening prior to biologics (e.g. infliximab) or immunomodulators? (BSG)

A

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

109
Q

Differences between UC and Crohn’s? (GeekyMedics)

A

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

110
Q

Sickle cell disease? (BMJ)

A

Caused by an autosomal recessive single gene defect in the beta chain of haemoglobin, which results in production of sickle cell haemoglobin (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 (acute chest syndrome), and increased vulnerability to infection

Treatment goals include symptom control (including pain management), and prevention and management of complications (hydroxycarbamide)

111
Q

Budd Chiari? (BMJ)

A

Budd-Chiari syndrome (BCS) includes hepatic venous outflow obstruction

Abdominal pain, ascites, and hepatomegaly

Colour and pulsed Doppler ultrasonography and testing for hypercoagulable states

Radiological interventional procedures, surgical or medical (anticoagulation)

112
Q

Hepatosplenomegaly?

A

CHIPS and MATHI
but HIP MAI

113
Q

Causes of non-cirrhotic portal HTN? (180)

A

Schistosomiasis and HIV
Resistance to RV filling
Vascular e.g. Budd-Chiari

114
Q

Present kidney transplant, CLD, hepato/splenomegaly, liver transplant, PKD, ascites, IBD.

A

PACES (4 decks)

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