Abdominal Flashcards
Signs of decompensation of liver disease? (BSG)
Deterioration in liver function in a patient with cirrhosis
“JAVE”
-Jaundice
-Ascites (increasing)
-Variceal bleeding (GI bleeding)
-Encephalopathy (asterixis, altered GCS, constructional apraxia)
Causes of decompensation in cirrhosis? (BSG)
-GI bleed
-Infection including SBP
-Alcoholic hepatitis
-Acute portal vein thrombosis/ischaemic liver injury
-Constipation
-Drugs including sedatives
-Dehydration
-Hypokalaemia
-HCC
Signs of chronic liver disease?*
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
Stages of encephalopathy? (BMJ)
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
How would you manage an UGIB? Scoring system? (BSG bundle)
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
Consider FFP, platelets and vitamin K
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
Scoring systems for UGIB? (MDCalc)
GBS 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)
How to assess for encephalopathy? (BMJ)
-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
Causes of jaundice? Drugs causing jaundice? (NICE)
Pre-hepatic jaundice:
-Haemolytic anaemias (hereditary spherocytosis, G6PD deficiency, B12 deficiency, sickle cell, thalassaemia, SLE)
-Gilbert’s 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)
How to treat encephalopathy? (BMJ)
-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
Hepatorenal syndrome? (Ox PP) (BMJ)
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
Things to remember to present in CLD patient?
Signs of uncomplicated CLD present
Portal HTN signs?
Decompensation signs?
Underlying cause?
Causes of CLD? (Ox)
Alcohol
NAFLD
Viral (hepatitis B and C)
Autoimmune (AIH, PSC, PBC)
Metabolic (haemochromatosis, Wilson’s, alpha-1 antitrypsin, CF)
Drugs (MTX, isoniazid, amiodarone, phenytoin)
Investigations in a patient with CLD? Autoantibodies in liver disease?*
FBC, clotting, U+E, LFTs, HbA1c (plus INR and albumin to check synthetic function)
Liver screen (autoantibodies (ANA, smooth muscule, AMA, LKM1) and immunoglobulins (IgG raised in AIH), hepatitis B (surface antigen) and C (antibody) serology, ferritin (and T-sats), caeruloplasmin (low in Wilson’s) (and copper), 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 (SAAG), differential WCC, gram stain and culture (+ AFB), cytology)
If decompensated, look for cause of decompensation and treat this e.g. infection screen
In addition:
-Fibroscan
-Liver biopsy e.g. if diagnostic uncertainty (or in AIH, pre-transplant, ?Wilson’s)
-Think about MRCP/ERCP to exclude PSC
-CT-TAP +/- bidirectional scopes if considering malignancy
Autoantibodies:
PBC: AMA, IgM
PSC: ANA, anti-SM
AIH: anti-SM, anti-LKM1
Complications of cirrhosis? (Ox)
Portal hypertension which can cause:
-Ascites (and SBP)
-Variceal haemorrhage
-Encephalopathy
-Hypersplenism (thrombocytopenia)
-Hepatorenal syndrome
-Hepatopulmonary disease/portopulmonary hypertension
Synthetic:
-Coagulopathy
-Hypoalbuminaemia
Patients are at higher risk of:
-HCC
-Malnutrition and osteoporosis
Signs of portal HTN? (Ox PP)
Caput medusae
Ascites
Splenomegaly
(Varices on OGD)
Causes of ascites?
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
Complications of TIPSS?
Encephalopathy (up to 30%)
N.B. Transvenous intrahepatic porto-systemic shunt that diverts blood from portal to systemic system to relieve refractory portal hypertension
How to interpret SAAG? (BSG)
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
-Perforation (bowel)
-Nephrotic syndrome (hypoalbuminaemia)
Investigations for ascites?
FBC, clotting, U+E, LFTs, HbA1c, TFTs, consider BNP and lipase
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 (SAAG), differential WCC, gram stain and culture (+ AFB), cytology)
CT-TAP if considering malignancy
CXR to look for features of heart failure
Possibly Fibroscan and liver biopsy
How to manage alcoholic hepatitis? (BSG)
-Managed by gastroenterology team
-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
Treatment of ascites in cirrhosis?
-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
Treat underlying cause for decompensation
If refractory ascites:
TIPSS
Consider liver transplantation
Consider palliation
In addition:
Treat SBP
What are the signs of chronic alcohol misuse? (Ox)
From end-of-bed to arms to face to neurology:
-Cachexia
-Tremor
-Dupuytren’s contracture
-Parotid enlargement
-Cerebellar syndrome
-Peripheral neuropathy
How do you assess the severity of cirrhosis? (Ox)
Childs-Pugh score takes into account bilirubin, ascites, encephalopathy, PT and albumin
MELD score also used
Management of cirrhosis?*
Managed by gastroenterology team
1) Treating underlying disease (antivirals, immunosuppression etc.) and preventing superimposed liver damage (abstinence, avoid hepatotoxic medications, immunisations, manage metabolic risk factors)
2) Preventing and managing complications:
-Ascites: with diuretics and prophylactic antibiotics if prior SBP
-Variceal haemorrhage: with propranolol or variceal banding
-Encephalopathy: with laxatives
-HCC: with surveillance imaging
-Osteoporosis
-Malnutrition: dietetics assessment
-Hepatorenal syndrome: treated with terlipressin
3) Liver transplant (6 months abstinence, <65 years), TIPS or consider palliative input
How would you manage SBP? (BSG)
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
Scoring system for alcoholic hepatitis? (BSG)
A Glasgow Score of >9 or a Maddrey’s score >32 defines severe AH and predicts worse outcomes
Alcohol abuse risks?
-Cardiac: alcoholic cardiomyopathy
-GI: cirrhosis, pancreatitis, peptic ulceration, UGI Ca
-Neurological: cerebellar atrophy, polyneuropathy, Wernicke’s/Korsakoff’s
What are the causes of hepatomegaly?*
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
Signs of hepatomegaly?*
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)?
Infective causes of acute hepatitis? (Ox)
-Hepatitis A, B, E (sometimes C)
-EBV and CMV
-Toxoplasmosis
-HSV
Causes of splenomegaly?*
“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
How to investigate malaria? (BMJ)
Thick and thin films
Also rapid diagnostic tests
ID team input needed!
How to investigate splenomegaly?
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
Splenomegaly sign?*
LUQ mass which moves infero-medially with respiration, has a notch, dull to percussion, cannot get above nor ballot
What are the significance of B symptoms in NHL? (Ox)
40% patients will have B-symptoms (fever, weight loss >10% over 6 months, night sweats)
If one present, staging is altered accordingly
Cytogenetics of CML? (Ox)
Philadelphia chromosome in 95%
Translocation between chromosome 9 and 22
Increased oncogene activity
Causes of hyposplenism? (Ox)
Splenic infarction/splenic artery thrombosis
Coeliac or other autoimmune disease
Sickle cell disease
Indication for splenectomy? Work-up?*
-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
What are the differential diagnoses for bilateral palpable kidneys? Versus single?*
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
Investigations for patient with renal enlargement?*
BP, urinalysis and urine cytology
U+Es
USS abdomen
CT if ?RCC
Genetic studies (ADPKD)
Echo (MV prolapse) and consider cerebral angiogram
What is PKD? Genetics of PKD?*
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
How would PKD present? Complications?*
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
Complications of PKD?
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
Management of ADPKD?*
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
How is HH inherited? (Ox)
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
How does HH present? (BSG)
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
Differential for HH? (180)
Secondary iron overload e.g. in repeated transfusions
How would you investigate a patient with suspected HH? (BSG)
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
How to management HH? (BSG)
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
Survival in HH? (BSG)
Survival equivalent to general population provided venesection started in a patient before cirrhosis and DM develops
What are the clinical features of PBC? (Ox)
1) Fatigue 2) Pruritus 3) Sicca
Liver disease occurs late and is rarely a presenting feature
How to diagnose PBC? (Ox)
-LFTs showing cholestasis
-AMA present in 95%
-Liver biopsy portal tract granuloma progressing to cirrhosis
-US and ERCP/MRCP to exclude extra-hepatic cholestasis
How is PBC managed? (Ox)
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
What other diseases are associated with PBC? (BSG)
Other autoimmune diseases (CSST):
-Coeliac
-Sjögren’s
-Scleroderma
-Thyroid disease
Diseases associated with PSC? (BSG)
Up to 83% have IBD
Associations including (CSSTT):
-Coeliac
-Sjögren’s
-Scleroderma
-Thyroid disease
-Type 1 diabetes mellitus
What are the major causes of chronic renal disease? (Ox)
Diabetes (34%)
GN (21%)
HTN (12%)
Also less commonly PKD, reflux nephropathy and analgesic nephropathy
Top causes for renal transplant?*
Diabetes
GN
ADPKD
Management of CKD? (Ox)
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
Indications for RRT? In AKI? In CKD? (Ox)
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
CI to renal transplant? (BMJ)
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
Complications of renal transplantation? (BMJ)
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
Renal transplant survival?
95% 1 year graft survival
50% 15 year graft survival
What are some of the side effects of IS? (BMJ)
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
How do you know the transplant is failing?
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)
Problems with dialysis? (Geekymedics)
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
Differences between HD and PD?
Ascites in cirrhosis pathophysiology? (M)
Splanchnic vasodilation
RAS activation
Na and H20 retention
When to start working up a patient for renal transplant?
As per KDIGO guidelines when eGFR <30
What are the manifestations of renal osteodystrophy? (Ox)
Probably not very relevant
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
What are some of the advantages and disadvantages of tunnelled line versus fistula?
Tunnelled CVC more prone to infection, thrombosis, shorter lifespan and lower blood flow rate
However, don’t need to wait to mature
How to work up AKI?
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
Define an AKI. (NICE)
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
Things to remember when presenting renal patient?
-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
Causes of palmar erythema?*
-Cirrhosis
-Hyperthyroidism
-RA
-Pregnancy
Abdominal causes of clubbing?*
Cirrhosis
IBD
Causes of gynaecomastia?*
-Physiological (puberty and senility)
-Cirrhosis
-Drugs (spironolactone or digoxin)
-Testicular tumour
-Klinefelter’s
-Endocrinopathy (hyperthyroidism, hypothyroidism, Addison’s)
Types of surgery in IBD? (M)
Subtotal colectomy with end ileostomy
End ileostomy with mucous fistula (usually emergency)
Proctocolectomy and end ileostomy
Proctocolectomy with ileo-anal pouch reconstruction
What are the indications for liver transplant? (BSG)
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
Differentials for a rooftop incision? (180)
Liver transplant
Hepatic resection for neoplastic disease
Gastrectomy
Oesopageal Ca
Whipple’s procedure
CI for LT? (BSG)
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
Scoring system for LT? (BSG)
UKELD (Na, creatinine, INR, bilirubin) >49 indicates survival advantage
King’s College criteria in paracetamol
When to discuss with LTU in paracetamol ALF? (BSG)
► 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
What is the definition of acute liver injury? Causes of ALI? (BSG)
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
Signs of a failing liver transplant?
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
Complications of liver transplant? (BSG)
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
Liver transplant survival?
Survival 90% at one year
80% at 5 years
Tell me about alpha-1 antitrypsin deficiency. (BMJ)
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
Tell me about tuberous sclerosis. (BMJ)
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
Von-Hippel-Lindau? (BMJ)
Autosomal dominant condition characterised by multiple vascularised tumours, particularly cerebellar, retinal or visceral
Tell me about hereditary spherocytosis. (BMJ)
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
Causes of acute/chronic pancreatitis? (BSG)
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)
Complications of pancreatitis? (BSG)
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
Treatment of pancreatitis? (BSG)
-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)
Pancreatic exocrine insufficiency indicators? (BMJ)
Steatorrhea
Weight loss
Hypomagnesaemia
Low vitamin ADEK (particularly A and E)
Low faecal elastase
Normal abdominal examination differentials? With abdominal pain or diarrhoea?
IBS
IBD
Coeliac
Infective
Other autoimmune conditions e.g. thyroid disease
Pancreatitis
Tell me about coeliac.*
AI disease causing SB villous atrophy and malabsorption
How would you investigate a patient with suspected coeliac disease?
-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
How would you manage a patient with coeliac disease? (BSG)
-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
Indications for SPK?
(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
What signs of CLD persist after liver transplant?
Gynaecomastia
Dupuytren’s
Causes of gum hypertrophy?*
Drugs: ciclosprin, phenytoin, nifedipine
Scurvy
AML
Pregnancy
Familial
How to tell ileostomy or colostomy?
Ileostomy: spouted, RLQ, semi-solid effluent
Colostomy: flush to skin
Indications for surgery in IBD?
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
Investigations for UC?*
-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)
Medical treatment for UC? (BMJ)
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
Truelove and Witts severe? (Ox PP)
> 6 stools/day
With systemic disturbance as evidenced by fever, tachycardia, anaemia or ESR >30
Crohn’s investigations? (BMJ)
-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
Crohn’s management? (NICE/BMJ)
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”
Complications of Crohn’s and management? (BMJ)
Abscess antibiotics and drainage
Strictureplasty or balloon dilatation for strictures
Fistulae medical control of inflammation and surgery
Extra-intestinal features of IBD? (NICE)
-Arthropathy*
-Erythema nodosum*
-Pyoderma gangrenosum
-Uveitis
-Episcleritis*
-Apthous ulcers*
-Metabolic bone disease*
-Psoriasis
-Hepatobiliary complications
*Associated with disease activity (AAEEM)
Screening prior to biologics (e.g. infliximab) or immunomodulators? (BSG)
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
Differences between UC and Crohn’s? (GeekyMedics)
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
Hepatosplenomegaly?
CHIPS and MATHI
but HIP MAI
Also endocrine (acromegaly and thyrotoxicosis)
Sickle cell disease? (BMJ)
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
Budd Chiari? (BMJ)
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)
Present CLD, hepato/splenomegaly, liver transplant, PKD, ascites, IBD.
Kidney transplant presentation
-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….
How to manage decompensated cirrhosis? (BSG bundle)
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
