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Abdo Flashcards

1
Q

What are the genes in APKD?

A

AD. Polycystin 1 on Chromosome 16, and Polycystin 2 and Chromosome 4. 4 is less severe and presents later. Some patients with a positive family history do not have an identified mutation. A small percent develop a sporadic mutation that is then passed on in an AD pattern.

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2
Q

Complications of APKD?

A

Renal:
1. Pain
2. Haematuria
3. Stones
4. CKD
5. Infection

Extra-renal
1. HTN
2. Berry aneurysms
3. Liver/pancreatic cysts
4. MV prolapse, AR

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3
Q

APKD - indications for nephrectomy?

A
  1. Recurrent infection
  2. Uncontrolled bleeding
  3. Suspected RCC
  4. Uncontrolled pain
  5. Extension into transplanted kidney
  6. To make room for a transplanted kidney
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4
Q

What are the causes of renal osteodystrophy in CKD?

A
  1. Low Vitamin D leading to osteomalacia
  2. High phosphate
  3. Low calcium due to both above
  4. Secondary hyperparathyroidism (leading to bone cysts - hyperparathyroid bone disease)
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5
Q

What are the principles of managing CKD?

A
  1. Underlying cause
  2. HTN (ACEi)
  3. CV risk (QRISK)
  4. Volume overload
  5. Hyperkalemia
  6. Hyperphosphatemia (diet, non-calcium phosphate binders like Serelamer)
  7. Renal osteodystrophy (Address hyperphos, Vit D, consider parathyroidectomy)
  8. Anaemia (replete iron, then give EPO)
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6
Q

What are the indications for RRT?

A
  1. Refer when GFR <30
  2. Uraemic complications (pericarditis, encephalopathy, bleeding)
  3. Refractory acidosis
  4. Refractory fluid overload
  5. Refractory hyperkalaemia
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7
Q

What are the complications of haemodialysis?

A
  1. Dialysis washout - hypotension, fatigue, cramps, chest pain, headaches
  2. Infection
  3. Bleeding (heparin as anticoagulant)
  4. Amyloidosis
  5. Decreased bone turnover
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8
Q

What are the complications of peritoneal dialysis

A
  1. Peritonitis
  2. Peritoneal sclerosis
  3. DM due to systemic absorption of glucose
  4. Local complications: hernias, fluid leakage, catheter exit site infection,
  5. Decreased bone turnover
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9
Q

How do you clinically assess adequacy of RRT?

A
  1. Fluid status
  2. Asterixis
  3. Pericardial rub
  4. Tachypnoea
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10
Q

Name some causes of renal disease

A
  1. Diabetes
  2. Hypertension
  3. Glomerulonephritis
  4. Vasculitis
  5. PKD
  6. Alports
  7. Tuberous Sclerosis
  8. Lipodystrophy
  9. SLE

In PACES
1. Diabetes
2. HTN
3. Chronic GN
4. ADPKD

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11
Q

What are some of the complications of immunosuppression in renal transplant?

A
  1. Infection
  2. Skin lesions - BCC, SCC, melanoma
  3. Cyclosporin (calcineurin inhibitor) - hirsuitism, gum hypertrophy, hypertension
  4. Steroids - purpura, diabetes, HTN, cushingoid features
  5. Tacrolimus (calcineurin inhibitor) - DM, tremor (especially in toxicity)
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12
Q

Common causes of CLD

A

Cirrhosis
Carcinoma
Congestive heart failure
Infectious (HBV, HCV)

Immune (PBC, PSC, AIH)

Infiltrative (amyloid, myeloproliferative)

Other
Hereditary haemochromatosis, AIAT, Wilson’s

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13
Q

Tell me about alpha 1 anti-trypsin disease

A
  1. Variable phenotype based on amount of residual AIAT produced
  2. Lack of protease inhibitor A1AT
    PI MM - normal
    PI MZ - carrier
    PI SS - 50% normal AIAT
    PI ZZ - 10% normal AIAT (usually the ones that manifest disease)
    Lungs: lower lobe pan-acinar emphysema
    Liver: cirrhosis and HCC in adults; cholestasis in children
    Ix: AIAT levels, spirometry
    Rx: AIAT infusion, supportive, volume reduction surgery
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14
Q

How do you grade liver cirrhosis?

A

Child Pugh
based on
1. Excretion (bilirubin and ammonia)
2. Synthesis (albumin, PT)
3. Portal (portal hypertension and ascites)

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15
Q

Pathophys of ascites in cirrhosis?

A

Disruption of portal blood flow within liver that leads to splanchnic vasoDILATION
Self-propogating as this reduces renal blood flow that actives the RAS system. Net result is sodium and water retention that propagates the ascites and oedema

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16
Q

Hepatomegaly

A
  1. Liver problem
  2. Cancer
  3. Benign lesions
  4. Heart - CHF
  5. Infection
  6. Infiltration - amyloid etc.
  7. Vascular - Budd-Chiari, Sickle
  8. Cysts
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17
Q

Causes of Splenomegaly

A

In F iltration
-Malignant (AML, lymphoma, myelofibrosis)
-Benign (amyloid, sarcoid, gylcogen storage, Gaucher’s (Ashkenazi Jew), thyrotoxicosis)

F unctional
-Increased removal of blood cells (thalasemia, spherocytes, sickle cell)
-Immune hyperplasia (viral, malaria, bacterial, fungal, parasitic, infectious mononucleosis, Brucellosis, endocarditis)
-Disordered immune regulation (RA, Felty, SLE, sarcoid)

F low
-Cirrhosis
-Vascular problem - hepatic/portal vein obstruction

F*cking MASSIVE
-CML
-Myelofibrosis
-Gaucher’s storage
-Malaria
-Kala Azar

Ix
-FBC with film
-CT Neck TAP
-Bone marrow with trephine
-LN biopsy
-Sickle screen, x3 thick/thin films

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18
Q

What autoantibodies would you test for in CLD?

A

ANA
AMA (PBC)
Anti-smooth muscle (AIH)
Anti-LKM (AIH)

Also check Immunoglobulins

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19
Q

How does PBC present?

A

Early: fatigue, pruritis, hyperpigmentation, xanthelasma, anaemia, coagulopathy (malabsorption), RUQ pain

Late: Fullminant liver disease

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20
Q

What are the autoantibodies in PBC?

A

anti-mitochondiral antibodies
Raised IgM

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21
Q

What is the pathophsiology of PBC?

A

Autoimmune destruction of inter-lobar bile ducts leading to progressive cholestasis and eventually cirrhosis

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22
Q

Is PBC associated with other auto-immune conditions?

A
  1. Sjogren’s
  2. RA
  3. Systemic Sclerosis
  4. Thyroid disease
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23
Q

Rx for PBC?

A
  1. Ursodeoxycholic acid (improves prognosis)
  2. Liver transplant
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24
Q

Structuring presentation for CLD

A
  1. Peripheral signs of CLD and alcohol use (parotid swelling)
  2. Signs of portal hypertension
  3. Signs of decompensation (if present)
  4. Nutritional status
  5. Points to underlying cause
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25
Q

Initial investigations for CLD?

A
  1. Full history (including travel, drug use, alcohol, and family history)
  2. Bloods (UE FBC Liver profile, coagulation)
  3. Autoimmune screen (Anti-LKM, AntiSM, Anti-mitochondrial, immunoglobulins)
  4. Iron studies, caeruloplasmin, alpha 1 antitripsin levels
  5. Liver USS +/- biopsy
  6. AFP
  7. Cross sectional imaging if indicated
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26
Q

What are the causes of jaundice?

A

Pre-hepatic
Haemolysis
Gilbert’s
Criggler Najar (UDP glucoronyl transferase)

Hepatocellular
AIH
CLD
Viral hepatitis
Drugs

Hepatic ducts
PBC, PSC, drugs, obstetric cholestasis

Extra-hepatic
Biliary structures, gallstones, pancreatic mass

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27
Q

Define acute liver failure

A

Multi-system disorder in which severe impairment of liver function with hepatic encephalopathy occurs within 8 weeks of onset of symptoms and no underlying chronic liver disease.

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28
Q

Management of varices and variceal bleeding

A
  1. Stabilise airway
  2. Correct clotting
  3. Transfuse
  4. Terlipressin
  5. Antibiotics
  6. Urgent OGD for banding
  7. Sengstaken-Blakemore if uncontrollable haemorrhage
  8. TIPPS if above fail
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29
Q

What is the Rockall score?

A

Estimates mortality and re-bleed risk

Modified Rockall - pre-endoscopy (age, comorbidities, haemodynamics)

Rockall (Complete)
1. Age
2. Haemodyanimics
3. Co-morbidities
4. Diagnosis
5. Signs of recent/ongoing haemorrhage

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30
Q

Management of ascites

A

Identify cause
Na and fluid restrict
Diuretics
Therapeutic paracentesis with volume expansion
TIPS
Consider liver transplant (40% 1 year mortality)

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31
Q

What scoring criteria is used to assess liver transplant eligibility?

A

UKELD (UK model of end-stage liver disease) score
Predicts 1 year mortality
>=49 = survival advantage from transplant

UKELD score is based on:
1. INR
2. Cr
3. Bilirubin
4. Sodium

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32
Q

Drugs causing jaundice

A

Hepatocellular
Valproate
Isoniazid
Rifampicin
Amiodarone
Methotrexate

Cholestatic
Co-amox
Carbamazapine
Contraceptive pill (OCP)

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33
Q

What are the causes of acute liver failure?

A
  1. Paracetamol
  2. Alcohol
  3. Viral (Hep A,B,CMV)
  4. Drugs (valproate, isoniazid, nitrofurantoin, co-amox, sulfonamides)
  5. Metabolic: Wilson’s, Reye’s
  6. Vascular: Ischaemic hepatitis, Budd-Chiari
  7. Pregnancy - Fatty liver of pregnancy, HELLP
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34
Q

Variceal prophylaxis?

A

Propanolol
Endoscopic variceal band ligation
TIPPS

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35
Q

Indications for transplant in paracetamol OD

A
  1. Arterial pH <7.30 24-hours after ingestion
  2. PT >100s (INR 6.5)
  3. Creat >300 umol/L
  4. Grade III, IV encephalopathy
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36
Q

What are the indications for liver transplant?

A
  1. Acute Fulminant Liver failure including paracetamol and alcohol overdose
  2. HCC
  3. Cirrhosis (ALD, NASH, AI liver disease, Haemachromotosis, Wilson’s, A1AT)
  4. Other: Diuretic resistant ascites, chronic hep enceph, refractory pruritis, hepato-pulmonary syndrome, polycystic liver disease, recurrent cholangitis)
37
Q

What are the contra-indications for liver transplant?

A

Absolute
1. Untreated HIV
2. Other disease with >50% mortality at 5 years
3. Irreversible lung disease
4. Ongoing alcohol/drug misuse
5. Current or previous other cancer (HCC eligible)

Relative
1. Smoking
2. Poor social support
3. Extensive prev abdominal surgery
4. BMI >40
5. Poor clinical attendance

38
Q

How will you structure your presentation of a renal transplant case?

A
  1. The diagnosis of ESRF
  2. What is the fluid status
  3. Is there a renal transplant
  4. What is the mode of renal replacement therapy
  5. What are previous modes of renal replacement?
  6. Are there side effects of immunospresion
  7. Are there side effects of ESRF (IHD, Anaemia, hypercalcaemia/parathyroidectomy)
  8. Are there any clues to cause (DM, PKD, HTN, Chronic GN)
39
Q

Commonest causes for ESRF

A
  1. HTN
  2. DM
  3. GN
40
Q

When would you start discussing transplant?

A

As they approach end stage renal disease, but before they require dialysis
eGFR 30

41
Q

How do you define ESRF?

A

eGFR <15ml/min

42
Q

Barriers to renal transplant?

A
  1. Availability of donor
  2. Malignancy
  3. Ongoing infection/vasculitis
  4. Severe obesity
43
Q

Define the SAAG

A

Serum to Ascites albumin gradient. g / dL.
>1.1g/L = high SAAG
<1.1g/L = low SAAG

44
Q

Diagnosis of Hereditary Spherocytosis?

A

Can be clinical
EMA binding test and the cryohaemolysis test to confirm

45
Q

Structure for presenting a liver transplant case

A
  1. Identify the scar
  2. Adequacy of function: signs of CLD, PHTN (caput medussae, splenomegaly), hepatic decomp (asterixis, jaundice)
  3. Complications of immunosuppression (skin lesions - check sun exposed areas carefully, steroid side effects, tremor (Tac), gum hypertrophy (ciclosporin)
  4. Any evidence of underlying aetiology / differential
46
Q

How do you prognosticate acute alcoholic hepatitis?

A

Madrey Discriminant Function for alcoholic hepatitis
1. PT
2. Total biliruin

Glasgow Alcoholic Hepatitis Score
1. Age
2. Bil
3. Urea
4. INR
5. WCC

47
Q

What are the indications for super-urgent transplant in paracetamol poisoning?

A
  1. pH <7.25 24 hours after poisoning
  2. PT > 100 or INR >6.5
  3. SCr >300
  4. Grade 3-4 encephalopathy
48
Q

Surgical scars for liver transplant?

A

Bilateral roof-top with sternal incision (Mercedez Benz) or inverted J scar (Makuuchi)

49
Q

What are the common complications following liver transplant?

A

Surgical
1. Strictures
2. Leaks

Immunosuppression
1. Rejection
2. Infection
3. Malignancies
4. Metabolic Syndrome

ALD/CLD
1. Due to calcineurin inhibitors
2. DM
3. HTN

Underlying
1. Viral Hepatitis
2. Budd-Chiari
3. PBC

50
Q

Surgical scar for renal transplant?

A

Rutherford Morrison (backwards Nike)

51
Q

What causes a high SAAG?

A
  1. Portal Hypertension
  2. CHF
  3. Budd Chiari
  4. Nephrotic Syndrome
  5. Meig’s Syndrome
52
Q

What causes a low SAAG?

A
  1. TB
  2. Malignancy
  3. Pancreatitis
  4. SBP
53
Q

What is Meig Syndrome?

A

Benign ovarian tumour presents with high SAAG ascites and transudative (low protein) pleural effusion. A similar presentation can be seen in many metastatic malignancies

54
Q

What are the causes of ascites?

A
  1. Liver Cirrhosis
  2. Vascular: Budd Chiari, CCF, constrictive pericarditis
  3. Low albumin: nephrotic syndrome
  4. Peritoneal disease: Meig syndrome, infectious, malignancy
  5. Misc: Pancreatic leak, chylous leak, peritoneal dialysis, advanced hypothyroidism
55
Q

How is Hereditary haemochromatosis inherited?

A

Autosomal recessive

56
Q

What is the gene affected in Hereditary Haemochromatosis?

A

HFE gene on chromosome 6

57
Q

How does Hereditary Haemachromatosis usually present?

A
  1. Screening
  2. Raised ferritin
  3. Arthralgia, lethargy, sexual dysfunction
  4. DM, cardiomyopathy, bronze pigmentation of skin
58
Q

How do you diagnose HH?

A
  1. Raised ferritin (200 mcg/L in females, 300 mcg/L in males)
  2. Raised transferrin saturation (>40% in females, and 50% in males)
  3. Positive HFE gene defect (note there is variable penetrance)
59
Q

How do you assess for HH complications?

A
  1. Regular HbA1c
  2. 6-monthly liver USS and AFP
  3. Baseline echo

200x risk of HCC if cirrhotic
Reduced life expectancy if cirrhotic, norma life expectancy without cirrhosis + effective treatment

60
Q

How do you treat HH?

A
  1. Weekly venesection until ferritin is 20-30 mcg/L and TSAT <50% followed by maintenance venesection.
  2. Treat complications
61
Q

Which organs are typically affected in HH?

A

Liver, heart, pancreas, anterior pituitary

62
Q

What are the typical joint features in HH?

A
  1. Chondrocalcinosis
  2. 2+3 MCP arthropathy
  3. Squared off bone ends
  4. Hook like osteophytes
63
Q

How is Hereditary Spherocyteosis inherited?

A

AD - Chromosome 8
5 different genes coding for the structure of red blood cells

64
Q

Ix for Hereditary Spherocytosis?

A
  1. FBC
  2. Haemolysis screen (LDH, split bilirubin, haptoglobin, reticulocyte level)
  3. Coombs (negative)
  4. EMA binding/osmotic fragility test
65
Q

Rx for Hereditary Spherocytosis?

A

Folic acid (to keep up with RBC turnover)
Bood transfusions
Splenectomy (will need vaccination for encapsulated organisms particularly meningococcal, pneumococcal, and influenza, and prophylactic antibiotics)
Cholecystectomy

66
Q

What causes haemolysis in Hereditary Spherocytosis?

A

Spherocyte shaped RBCs undergo haemolysis in spleen - splenectomy virtually eliminates haemolysis

67
Q

How do you diagnose coeliac disease?

A

Anti-TTG.
If equivocal - OGD + D2 biopsy looking for total or sub-total villous atrophy

68
Q

How do you manage coeliac disease?

A

Wheat, rye, barley all have gluten.
Need dietitian consult

69
Q

What are the causes of gynaecomastia?

A

Liver disease
Testicular failure
Ectopic tumour secretion
Hyperthyroidism
Haemodialysis
Drugs: spironolactone, digoxin, GnRH analogues, finasteride

70
Q

What potential reasons might a patient have a surgical scar in both iliac fossa?

A

SPK transplant
One failed renal transplant

71
Q

Indications for SPK transplant?

A

Cure both patients diabetes and ESRF with potential that patient would be free of haemodialysis and insulin therapy, and vascular complications of diabetes (however unclear benefit in diabetic retinopathy where the damage may be irreversible)

72
Q

What is the drainage of a transplanted pancreas?

A

Into the small bowel (used to be into the bladder but caused UTIs)

73
Q

How do you assess for encephalopathy?

A
  1. Astrexisis and contructional apraxia.

Grade I = altered behaviour, constructional apraxia
Grade II = drowsiness
Grade III = marked confusion
Grade IV = coma

74
Q

What is your differential for gynaecomastia?

A

Gynaecomastia is due to imbalance in androgen:oestrogen ratio. It can be physiological

  1. Liver problem (reduced androgens)
  2. HypERthyroidism
  3. Syndromic (Klienfelters)
  4. HCG secreting testicular cancers
  5. Drugs (spironolactone, digoxin, finasteride, cimetidine)
75
Q

TIPS

A

Transvenous intrahepatic porto-systemic shunt that diverts blood from portal to systemic system to relieve refractory portal hypertension. 10% will subsequently become encephalopathic.

76
Q

What is hepatorenal/hepatopulmonary syndrome?

A

Due to splanchnic vasodilation = underfilling of kidneys

Type 1
Rapidly progressive and very poor prognosis

Type 2
Slowly progressive but poor prognosis

Rx: Terlipressin, albumin, TIPS, transplant

77
Q

What are the causes of chronic pancreatitis?

A

Alcohol
Gallstones
Hypercalcaemia
Hypertriglyceridaemia
Smoking
ERCP
Pancreatitic divisium
Pancreatic cancer
Idiopathic
Genetic (PRSS1, CFTR, SPNK1)

78
Q

What are the complications of chronic pancreatitis?

A

Pancreatogenic diabetes
Pancreatic ductal strictures
BIliary obstruction
Duodenal obstruction
Pseudocysts
Pancreatic malignancy

79
Q

What are the histological features of crohns vs. UC?

A

Crohns:
Transmural
Skip lesions
Mucosal ulcers
Fissures
Strictures

UC
Superficial mucosal and submucosal
start at anus and spread proximally
Crypt abscesses

80
Q

What are the extra-intestinal manifestations of Crohn’s disease?

A
  1. Skin: pyoderma, erythema nodosum
  2. Joints - arthritis
  3. Eyes - episcleritis/uveitis
  4. Gallstones
  5. PSC (more common in UC)
81
Q

What are the key differences in the treatment of Crohn’s and UC?

A

5-ASA are less effective in Crohn’s

5-ASA used as maintenance in UC (oral + topical); aza/merca can be added if >2 flares

Azathioprine/Mercaptopurine (need to check TPMT levels first) are used as maintenance in Crohn’s

82
Q

What immunosuppressive agents are used for renal transplants?

A
  1. Tacrolimus and Ciclosporin (calcineurin inhibitor - blocks IL2)
  2. MMF (blocks purine synthesis)
  3. Steroids (suppress immune response)
83
Q

What side effects do you know of with immunosuppression?

A

All - infection due to myelosupression
Tac - tremor, impaired glucose tolerance, HTN, lymphoma, skin cancer
Cic - less potent than Tac, lymphoma, skin cancer
MMF - rarely associated with GI bleeding and lung fibrosis

84
Q

Causes of palmar erythema?

A

Cirrhosis
Hyperthyroidism
RA
Polycythaemia
Pregnancy

85
Q

What vaccinations need to be provided in patients with a splenectomy, and when?

A

Ideally 2 weeks before if planned. Need to vaccinate against encapsulated bacteria including Pneumococcus, Meningococcus, HiB. Then lifelong prophylactic penicillin

86
Q

What are common indications for a splenectomy?

A

Haematological: haemolytic anaemia, thalasemia, haem malignancy, myeloproliferative disorders, ITP

Trauma

Infectious complications (hydatid, malaria)

Congestive disorders

Metabolic storage disorders

87
Q

What is a specific sign of ALCOHOLIC liver disease?

A

Parotid swelling
Dupuytren’s contracture (can be deforming of tendons and lead to fixed flexion/extension of digits!)

88
Q

End of the bed signs of CLD?

A

Cachecia and Loss of tricep bulk
Palmar erythema
Dupuytrens
Asterixis
Spider naevi
Gynaecomastia
Loss of central chest hair

PACES (6 decks)

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