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PACES MRCP > Abdomen > Flashcards

Abdomen Flashcards

1
Q

How does ADPKD present?

A 
Signs of acute or chronic kidney disease
Hypertension
Proteinuria
Abdominal pain
Haematuria
Recurrent UTIs
Extra renal manifestations: valvular abnormalities (MVP), cysts in liver/spleen, IC aneurysms (intracerebral/SAH), colonic diverticulae
Could present with screening
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2
Q

What is the inheritance of ADPKD?

A 
Autosomal dominant 
Chromosome 4 (PKD2, less severe, later onset, less cysts, later progression to renal failure) 
Chromosome 16 (PKD1) - 80%
No detectable genetic abnormality (small)

Infantile PKD - much less common, AR

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3
Q

What is the treatment for ADPKD?

A

MDT
Dietician - high fluid (suppress vasopressin), low salt diet
Lifestyle measures - stop smoking, reduce alcohol, weight loss
Medical - treat hypertension, ACEI to reduce proteinuria, statins to treat hyperlipidaemia
Surgical - renal transplant

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4
Q

Indication for nephrectomy in ADPKD

A

Ideally avoided
To make room for transplanted kidney if needed
Renal cell carcinoma
Chronic pain/infection

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5
Q

Present kidney disease

A

Diagnosis

Likely cause - HTN, diabetes (finger prick marks), GN, ADPKD
In ADPKD - presence/absence of HSP, 3rd nerve palsy (?IC aneurysm)

Presence of renal impairment - fluid status, uraemic
Evidence of RRT - fistula (working? used recently?), line scars, tunnelled lines

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6
Q

What is ESRF?

A

eGFR <15ml/min

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7
Q

Difference between modes of dialysis?

A

Haemodialysis

Peritoneal dialysis - may not be able to tolerate in PKD due to space needed, risk of cyst infection or peritonitis

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8
Q

Causes of CLD

A

In UK - alcoholic liver disease and NAFLD
Globally - viral hepatitis
Other - autoimmune (AI hepatitis), haemochromatosis, Wilsons disease, PBC, PSC, drug induced

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9
Q

Present liver disease

A

Diagnosis

Signs of CLD - palpable liver edge –cm below costal margin, spider nevae, bruising, palmar erythema, clubbing, gynaecomastia, loss of axiliary hair, dupytrens contracture
Signs of portal hypertension - splenomegaly, caput medusae, ascites
Signs of decompensation - encephalopathy (asterixis), ascites, jaundice
Nutritional status

Signs of causes - tattoos, xanthelasma (eye deposits), corneal arcus, diabetes (NAFLD)

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10
Q

Causes of CLD

A

In UK - alcoholic liver disease and NAFLD
Globally - viral hepatitis
Other - autoimmune (AI hepatitis), haemochromatosis, Wilsons disease, PBC, PSC, drug induced, HHT

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11
Q

Investigations in CLD

A 
Full history (comorbidities, drug, alcohol, travel and family history)
Bloods - FBC, LFTs, coag, U&Es, BB viral screen, autoantibodies (ANA, ANCA, AMA, anti SM, anti LKM), caeruloplasmin, ferritin, lipid screen, tumour markers (AFP for HCC)
Imaging - USS abdomen (liver appearance, focal lesions, doppler for flow/portal vein thrombosis, splenomegaly), CT or MRI 
Other - ascitic tap, biopsy
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12
Q

Investigations in CLD

A 
Full history (comorbidities, drug, alcohol, travel and family history)
Bloods - FBC, LFTs, coag, U&Es, BB viral screen, autoantibodies (ANA, ANCA, AMA, anti SM, anti LKM), caeruloplasmin, iron studies, lipid screen, tumour markers (AFP for HCC)
Imaging - USS abdomen (liver appearance, focal lesions, doppler for flow/portal vein thrombosis, splenomegaly), CT or MRI 
Other - ascitic tap, biopsy, OGD (varices, GAVE, portal hypertensive gastropathy)
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13
Q

Causes of jaundice

A

Pre-hepatic (unconjudes

Intrahepatic

Post-hepatic

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14
Q

Causes of jaundice

A

Pre-hepatic (unconjugated): haemolytic anaemia, Gilbert’s, Crggler Najar

Intrahepatic (mixed): viral hepatitis, alcoholic liver disease, drug induced, haemochromatosis, AIH, PBC/PSC, HCC

Post-hepatic:

  • Intraluminal: gall stones
  • Luminal: cholangiocarcinoma, strictures, drug induced cholestasis
  • Extra luminal: pancreatic cancer or other abdominal masses such as lymphoma
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15
Q

Present renal transplant

A

Functioning or not functioning
- describe scar and mass, ?tender ?bruit

Any ongoing RRT?
Any fistula? (thrill, needling?)
Other access for dialysis? PD scars?

Immunosuppression SE - gum hypertrophy, skin malignancy, thinning of skin, tremor

Cause - ?ADPKD, diabetes?

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16
Q

Management of varices and variceal bleeding

A

Need gastroscopy in cirrhosis to look for varices, GAVE, gastropathy
Banding if bleeding/red sign
Otherwise beta blockers and surveillance

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17
Q

Investigation/management of ascites

A

Ascitic tap - SAAG i.e. serum albumin - ascitic albumin (>1.1g/L = portal HTN i.e. cirrhosis, CCF, nephrotic syndrome, budd chiari), <1.1g/DL = not portal hypertension such as pancreatitis, cancer, TB), cytology, amylase/lipase (pancreatic ascites ?ductal leak), gram stain and MCS, WCC (?SBP neu >250)
USS, CT, fibroscan
Biopsy (transjugular in ascites)

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18
Q

Indications and contraindication to liver transplantation

A

Cirrhosis - alcoholic liver disease, NAFLD, AIH, chronic viral hepatitis, haemochromatosis, wilsons, alpha 1 antitrypsin
Acute hepatic failure (severe acute impairment of liver function with encephalopathy within 8 weeks of start of symptoms and no recognised underlying CLD) - paracetamol overdose
HCC
Variants - diuretic resistent ascites (not responsive to TIPS), intractable pruritus, polycystic liver

Assess via MDT approach.
Criteria such as UK End stage liver disease (UKELD) model to prognosticate (>49. Na, Cr, INR, bilirubin). Severe acute alcoholic hepatitis considered if survival in absence of transplant if less than that obtained with transplant. All electives must have predicted post transplant survival of >50%.

HCC - no extrahepatic spread, criteria surrounding size and number.

Acute - i.e. in paracetamol OD - pH<7.25 24hr post OD and fluid resus, PT>100s, INR>6.5, Cr >300, unuria, grade 3-4 encephalopathy

Contraindications - IVDU, alcohol excess (abstinence is mandatory), significant medical or psychiatric morbidities if likely to affect transplant longevity, prior malignancy with high risk of recurrence

Steroids weaned to small dose or completely.

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19
Q

Present renal transplant

A

Functioning (euvolaemic, no sign of RRT) or not functioning
- describe scar and mass, ?tender ?bruit

Any ongoing RRT?
Any fistula? (thrill, needling?)
Other access for dialysis? PD scars?

Immunosuppression SE - gum hypertrophy, skin malignancy, thinning or bruising of skin, tremor, NODAD (new onset diabetes after transplant)

Cause - ?ADPKD, diabetes? could also be post transplant

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20
Q

Causes of hepatomegaly and ascites without signs of CLD

A

Cirrhosis (alcohol, NAFLD, chronic viral hepatitis)
CCF (midline sternotomy, peripheral oedema)
Malignancy - cachectic, lymph nodes, nodular liver
ADPKD
Amyloid, MP disorder
Haemochromatosis
Budd chiari

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21
Q

Treatment in alcoholic liver disease

A 
MDT
Alcohol cessation
Dietician - low salt, high protein
Gastroscopy to assess/treat for varices
Heptaology input
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22
Q

Treatment of chronic pancreatitis

A

Check function with: Mg, lipase, albumin, glucose
Creon/enzyme replacement
PPI

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23
Q

Treatment of chronic pancreatitis (long standing alcoholics with abdominal pain)

A

Check function with: faecal elastase, Mg, albumin, vitamin D
Creon/enzyme replacement
PPI

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24
Q

Causes of hepatomegaly and ascites without signs of CLD

A

Cirrhosis (alcohol, NAFLD, chronic viral hepatitis)
Vascular - CCF (midline sternotomy, peripheral oedema), Budd chiari
Malignancy - cachectic, lymph nodes, nodular liver
ADPKD
Amyloid, MP disorder
Haemochromatosis

25
Q

Causes of moderate splenomegaly

A

4-8cm (to umbilicus)

Myelo- and lympho-proliferative disorders (CLL), lymphoma, infiltrative (i.e. gauchers, amyloidosis)

26
Q

Causes of massive splenomegaly

A

> 8cm
Myeloproliferative disorders, CML, AML, myelofibrosis
Malaria, visceral leishmaniasis
HIV

27
Q

General causes of splenomegaly (categories and examples)

A

In

28
Q

General causes of splenomegaly (categories and examples)

A

Infiltration - myeloproliferative, lymphoproliferative, lymphoma, amyloidosis, sarcoidosis, gauchers, thyrotoxicosis

Increased function - increased removal of RBC (HS, thalassaemia, nutritional anaemia, sickle cell), immune hyperplasia in response to infection (chronic malaria, visceral leishmaniasis, glandular fever, infectious hepatitis, subacute IE, brucellosis), disordered immunoregulation (feltys syndrome, SLE, sarcoidosis)

Abnormal flow - vascular (hepatic or portal vein obstruction)

29
Q

Causes of massive splenomegaly

A

> 8cm
Myeloproliferative disorders, CML, myelofibrosis
Malaria, visceral leishmaniasis
HIV

30
Q

General causes of splenomegaly - categories and examples

A

Most common for isolated splenomegaly - malaria, myelofibrosis and CML

Infiltration - myeloproliferative, lymphoproliferative, lymphoma, amyloidosis, sarcoidosis, gauchers, thyrotoxicosis

Increased function - increased removal of RBC (HS, thalassaemia, nutritional anaemia, sickle cell), immune hyperplasia in response to infection (chronic malaria, visceral leishmaniasis, glandular fever, infectious hepatitis, subacute IE, brucellosis), disordered immunoregulation (feltys syndrome, SLE, sarcoidosis)

Abnormal flow - vascular (hepatic or portal vein obstruction), portal hypertention

31
Q

Gauchers disease - definition and inheritance, types, signs/symptoms

A

AR inherited disorder fat storage disorder. Accumulates in liver, spleen, BM, lung, brain.

Type 1 - most common, Ashkenazi Jew
Type 2 and 3 not as common, more neuro effects

Signs/symptoms - fractures/bony pain, HSM, thrombocytopenia, anaemia, bruising

32
Q

Felty’s syndrome - definition, aetiology, complication

A

RA, splenomegaly, neutropenia.

Cause unknown. Risk of infection due to neutropenia.

Complications: infection, hypersplenism (causing anaemia and thrombocytopenia), skin hyperpigmentation, cutaneous ulceration

33
Q

Brucellosis - sentence summary

A

Zoonosis from infected animals, their mild or uncooked meat.
Undulant fevers and sweating, arthralgia and myalgia

34
Q

Malaria - types, presentation, complications, treatment

A

Types - plasmodium falciparum, vivax/ovale/malariae

Falciparum - most deaths, prodrome of flu symptoms, paroxysms of chills/fever/sweats and haemolysis, HSM, jaundice, confusion, seizure

Complications - intravascular haemolysis with haematuria (i.e. blackwater fever)

Transmitted by blood transfusion and transplacentally
Protective - sickle cell, HLA B53 positive

Diagnosis - 3 thick and thin blood films, rapid diagnostic test

Treatment of falciparum - quinine (PO) + doxycycline, IV quinine if severe, may need exchange transfusion (>30% RBC parasitized or >10% parasitaemia)
Treatment of non falciparum - chloroquine

35
Q

Hereditary spherocytosis and elliptocytosis summary

A

HS = AD (most common defect on chromosome 8).

  • Spherical rather than biconcave (defect within RBC membrane protein) causing haemolysis within the spleen
  • Triad of anaemia, jaundice and splenomegaly. Through screening programmes for first degree relatives or with neonatal jaundice.
  • Features - jaundice, chronic haemolysis (anaemia, splenomegaly, pigment gallstones, cholecystitis, leg ulceration), aplastic crises (parvovirus or folate def)
  • Diagnose with blood smear (small cells without central pallor, retics), osmotic fragility (RBC resistance to haemolysis whilst exposed to saline) or flow cytometry w/ EMI binding (lower fluorescence with sphrerocytes), haemolysis screen (split bilirubin - unconjugated high, LDH high, haptoglobin low), Coombs to exclude AIHA
  • Treat with folic acid, splenectomy in mod-severe disease (with prior vaccinations and then keep up to date after - influenza, pneumococcal, meningococcal), serial blood transfusions in anaemia

HE = AD, no anaemia or splenomegaly, mild haemolysis, no treatment needed if mild form.

36
Q

Extras in abdominal exam

A
  • check arms for AV fistulas
  • check gums for hypertrophy
  • axillary nodes
  • gynaecomastia
  • spleen when lying on side
  • to complete: obs, urinalysis, hernia orifices, external genitalia, DRE
37
Q

Presenting liver transplant

A

1- J shaped scar in right hypochondrium or mercedes benz, transplant may or may not be palpable. Other scars i.e. post op drain, tracheostomy,

2 - Evidence of transplant function - signs of CLD (gynaecomastia and dupytrens persist), portal hypertension (spleen may stay enlarged), decompensation etc.

3 - Signs of immunosuppression - infection, malignancy (skin), steroids (skin thinning, cushingoid, bruising, diabetes), ciclosporin (gum hypertrophy), tacrolimus (tremor), nephrotoxicity, HTN

4 - Signs of underlying disease - haemochromatosis (venesections), tattoos (viral hepatitis), xanthelasma (PBC)

38
Q

Haemochromatosis - inheritance, presentation, investigations, treatment

A

AR (HFE gene on ch 6 - variable penetrance), iron absorption disorder causing increased absorption and increased iron storage

Presentation - genetic screening programme, asymptomatic with raised ferritin, arthralgia (synovitis, pseudogout seen with chondrocalcinosis on XR, calcium pyrophosphate), tiredness, sexual dysfunction (testicular and pituitary iron deposition). Later - slate grey pigmentation of the skin, diabetes T1, cardiomyopathy, hepatomegaly

Ix - iron studies (raised ferritin, tsat), genetic testing in 1st degree relatives, ferritin >200 females >300 male, tsat >40% females >50% male, regular Hba1c, 6 monthly USS liver and AFP to look for hepatoma, baseline echo, liver biopsy not needed for diagnosis but for severity of fibrosis if present, fibroscan

Tx - abstain from alcohol, weekly venesection until ferritin 20-30mcg/L and tsat <50% then maintenence venesection (can improve fibrosis, LVF and portal hypertension), transplant

39
Q

Complications of liver transplant

A

Infection and malignancy (skin, PTLPD) due to immunosuppression

Metabolic syndrome

AKI, CKD by multitude of factors (HTN, diabetes, calcineurin inhibitors)

Hepatobiliary - rejection, leaks, strictures

Recurrence of liver disease - budd chiari, viral hepatitis, pbc

40
Q

Causes of ascites

A

Vascular - budd chiari, CCF, cirrhosis with portal hypertension

Low albumin - nephrotic syndrome, protein loosing enteropathy

Peritoneal disease - Meig’s (pleural eff, ascites, benign ovarian tumour), infection (TB, fungal), malignancy (ovarian, GI)

Misc - pancreatic leak, chylous ascites, PD associated, advanced hypothyroid

41
Q

Budd chiari

A

Thrombosis of hepatic vein

Abdo pain, ascites, hepatomegaly

42
Q

Abdominal causes of clubbing

A

Cirrhosis
GI lymphoma
IBD
Coeliac

43
Q

No abdominal signs

A

Coeliac - inflammation of small bowel due to abnormal immune response to gliadin of gluten in wheat.

  • Presentation: alternating bowel habit, N&V, abdominal pain and bloating, anaemia (iron/B12/folate def), tiredness, weight loss, other AI disease such as thyroid disease and diabetes, dermatitis herpetiformis
  • Ix: need gluten free diet for Ix, EMA, TTG, duodenal biopsy (subtotal villous atrophy and crypt hyperplasia, increased epithelial lymphocytes)
  • Tx: MDT i.e. dietician, gastro, gluten free diet (wheat, rye, barley), serological testing for 1st degree relatives
  • Complications: osteoporosis, intestinal lymphoma (T cell), hyposplenism (increased risk of infection from encapsulated bacteria)
44
Q

Combined kidney and pancreas transplant

A

One scar in each iliac fossa - palpable mass beneath each

Increasingly common in poorly controlled diabetes and related ESRF
Can cure both ESRF and diabetes (no new diabetic nephropathy, neuropathy static or improved, unclear effects on diabetic retinopathy)
T1DM (most common) or IDT2DM meeting certain
Pancreas - in pelvis, drained into small bowel or urinary bladder (urinary lipase monitoring to check rejection), old pancreas left in situ
Decision made through MDT and patient choice
Single deceased donor following brain death. Can involved live kidney and cadaveric pancreas
Improves 10 yr survival of cadaveric kidney only but equal to live kidney transplant at 10 yrs, better survival beyond this for combined

Sole pancreas transplant - acute rejection 60-80%
Combined - pancreas rejection lags behind kidney which means monitoring is easier. 5%.
Graft thrombosis and graft pancreatitis, infection

Islet cell transplant - less invasive

45
Q

Types of kidney transplant

A

Live - relatives or altruistic, can be bought to same hospital to minimise ischaemic time
Cadaveric - after circulatory death or after neurological death, more likely to have longer graft time if combined kidney-pancreas due to reduced effects of diabetes on the kidney

46
Q

Features of encephalopathy on examination

A

Cognitive impairment and lack of concentration
Euphoria or anxiety
Impaired addition/subtraction i.e. serial 7s test
Reversed sleep wake cycle
Agitation and aggression, acute confusion
Progressive stupor and coma
Asterixis

Tx - correct precipitating factors, careful protein, lactulose, probiotics, rifaximin

47
Q

Classification of HE

A

West Haven Criteria
Grade 4 - coma
Grade 4 - confusion, gross disorientation, sleepy to semi stupor but responsive to verbal stimuli
Grade 2 - lethargy, minimal disorientation, inappropriate behavior, impaired subtraction
Grade 1 - trivial lack of awareness, euphoria or anxiety, short attention span, impaired addition

48
Q

Prognostic scores for cirrhosis

A

Childs-Pugh - Bilirubin, refractory ascites, albumin, INR, eNcephalopathy. A/B/C, 5 year survival.
MELD - model for ES liver disease. Dialysis, creatinine, bili, INR, sodium

49
Q

Treatment of ascites

A

Diuretics
Drained is uncomfortable or cardioresp compromise
TIPS
Liver transplant

50
Q

Complications of TIPS

A

Coagulopathy

Encephalopathy

51
Q

Causes of gynaecomastia

A

Relative deficiency in androgens or excess oestrogen
Physiologically in puberty
Testicular atrophy or orchidectomy
Drugs - spironolactone, digoxin

52
Q

Complications of ETOH

A

CV - dilated cardiomyopathy, HTN
GI - peptic ulceration, pancreatitis, upper GI cancer
Neuro - cerebellar atrophy, polyneuropathy, wernickes and korsakoffs

53
Q

Chronic pancreatitis

A

Causes - alcohol, gallstones, trauma, ERCP, hypertriglycerideaemia, hypercalcaemia, drugs (steroids, azathioprine), CF, smoking, IGG4 disease, AI pancreatitis, cancer

Ix - PRSS1 (AD), CFTR (AR), SPINK1

Complications of pancreatitis:
Acute - multisystem disorder leading to SIRS, respiratory failure, death
Chronic - chronic pancreatis, splenic and portal vein thrombosis, pseudocysts (>6 weeks drained with cystogastrostomy AXIOS stent) with compression effects, biliary and duodenal obstruction, T3DM (increased hypoglycaemic episodes), pancreatic ductal stricturing (ERCP stenting)

Chronic pancreatitis:

  • chronic pain with flares may be associated with food (epigastric radiating to back, better sitting forwards), gnawing pain
  • exocrine and endocrine dysfunction

Treatment: eliminate smoking and alcohol, analgesia, creon (75-125000 pre meal and 50-75000 pre snacks) if signs of malabsorption (weight loss, steatorrhoea, hypomagnesaemia, low faecal elastase, low albumin and vit D) with PPI, balanced diet

54
Q

Presenting IBD

A

Young patient with no evidence of any peripheral stigmata of disease
Evidence of previous abdo surgery and stoma
Contents in stoma ? colostomy (LIF) or ileostomy (RIF, spout)

55
Q

Investigating IBD

A

Bloods - anaemia, malabsorption, CRP, LFTs (extra intestinal)
Stool - cultures
AXR - large or small bowel dilatation or toxic megacolon
Colonoscopy - biopsy
Dietician input

56
Q

UC Vs Crohns

A

UC - large bowel, mucosa effected, lead piping fibrosis

Crohns - any part of GIT, fissures and fistulas, transmural

57
Q

Indications for surgery in IBD

A

Symptoms in chronic active disease despite max medications
strictures and fistulas\toxic mc
haemorrhage
perforation

58
Q

Surgical procedures in IBD

A

subtotal colectomy with end ileostomy +/- mucus fistula

proctocolectomy w end ileostomy or ilelanal pouch (no stoma)

59
Q

Medical treatment in UC

A

5 ASA in mild and mod (oral and enema)
PO steroids in non responders or mod and severe dosease
High dose IV steroids (hydro 1–mg qds) in acute severe
Maintenance - 5 ASA -> aza or biologics if 2+ flares

PACES MRCP (6 decks)

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