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PACES > Medical Abdomen > Flashcards

Medical Abdomen Flashcards

1
Q

Signs of Chronic Liver Disease on Examination

A

General

Jaundice

Ascites

Cachexia

Tattoos and track marks

Pigmentation

Hands

Clubbing (esp in Primary Biliary Cholangitis/Cirrhosis)

Leukonychia

Terry’s nails (white proximally, red distally)

Palmar erythema

Dupuytren’s contacture

Face

Pallor: anaemia of chronic disease

Xanthelasma: primary biliary cholangitis/cirrhosis

Keiser-Fleischer rings

Parotid enlargement (alcohol excess)

Trunk

Spider naevi (distribution of SVC)

Gynaecomastia

Loss of secondary secual hair

Ankle: peripheral oedema

Abdomen

Distension

Para/-umbilical hernia

Dilated veins

Drain scars

+/- hepatomegaly

+/- splenomegaly

Shifting dullness

Significant negatives: Jaundice, Encephalopathy, Feoter hepaticus, hypoabuminaemia, coagulopathy

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2
Q

Differential for Chronic Liver Disease

A

Common

Alcoholic liver disease

Viral Hep C liver disease

NASH

Rarer

Congenital: Hereditary haemochromatosis, Wilson’s, alpha-1-antitrypsin deficiency, Cystic fibrosis

Autoimmune: Autoimmune hepatitis, Primary sclerosing cholangitis, Primary biliary cholangitis/cirrhosis

Drugs: methotrexate, amiodarone, isoniazid

Neoplastic: HCC, metastatic

Vascular: Budd-Chiari, Right heart failure, Pericarditis

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3
Q

Investigations for Chronic Liver Disease

A

Urine: dip, MC+S ?UTI

Bloods

FBC, U+E, LFTs, INR, Glucose

Ascitic Tap

Chemistry

Cytology

MC+S

SAAG

PMN ?>250 –> SBP

USS + Duplex

Liver size and texture

Focal lesions

Ascites

Portal vein flow

Liver Screen

Alcohol: MCV, GGT, AST:ALT >2

Viral: Hep B and C serology

NASH: lipids

Auto-antibodies: SMA, AMA, pANCA, ANA

Ig: IgG - AIH, IgM- PBC

Genetic: caruloplasmin, ferritin, alpha1-antitrypsin

Cancer: AFP, Ca19-9

Liver biopsy

MRCP: PSC

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4
Q

Management of Chronic Liver Disease

A

MDT: hepatologist, GP, Dietician, Pallative care, family

Alcohol abstinence

Nutrition

Cholestyramine for pruritus

Screening: HCC and varices

Specific

HCV: interferon alpha and Ribavarin

PBC: Ursodeoxycholic acid

Wilson’s: penicillamine

Haemochromatosis: venesection and desferrioxamine

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5
Q

Complications of Chronic Liver Disease

A

Varices: beta blockers, banding

Ascites: fluid and salt restrict, spironolactone, fruse, daily weights, tap

Coagulopathy: Vitamin K, FFP, platelets

Encephalopathy: avoid sedatives, lactulose, rifaximin

Sepsis / SBP: tazocin or cefotaxime

Hypoglycaemia: dextrose

Hepatorenal syndrome: IV albumin and terlipressin

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6
Q

Child-Pugh Grading

A

Evaluates prognosis in liver cirrhosis

Graded A- C using 5 factors

A: 5-6

B: 7-9

C: 10-15 (50% 1 year mortality)

Albumin

Bilirubin

Clotting

Distension (ascites)

Encephalopathy

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7
Q

Causes of Decompensation in Chronic Liver Disease

A

HEPATICS

Constipation is the most common cause of decompensation

Haemorrhage: e.g. variceal bleed

Electrolytes: hypokalaemia, hyponatraemia

Poisons: sedatives, diuretics, anaesthetics

Alcohol

  • *T**umour: HCC
  • *I**nfection: SBP, pneumonia, UTI, Hep D virus

Constipation (COMMONEST CAUSE)

Sugar: hypoglycaemia

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8
Q

Management of Decompensation of Chronic Liver Disease

A

General Mx

HDU or ITU

Treat precipitant

NGT tube with high caloric intake- good nutrition

Thiamine supplementation

PPI to cover against stress ulcer

Monitoring

Fluid-balance: Urinary catheter, Central catheter

Daily bloods

Glucose every 1-4 hours: 10% dextrose IV

Mx Complications

Acites: daily weights, fluid and Na restrict, Diuretics, Tap

Coagulopathy: Vit K, FFP, platelets

Encephalopthy: avoid sedatives, lactulose, rifaximin

Sepsis/ SBP: tazocin or cefotaxime

Hypoglycaemia: 10% dextrose

Hepatorenal syndrome: IV albumin + terlipressin

Rifaximin is antibiotic with poor absorption when taken orally so wipes out intestinal bacteria

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9
Q

Path of Encephalopathy

A

Decreased hepatic metabolic function

Diversion of toxins into systemic circulation (protal shunting)

Ammonia accumulates and passes into brain

Converted into glutamine by astrocytes

Increased glutamine –> osmotic imbalance –> cerebral oedema

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10
Q

Presentation of Encephalopathy

A

Asterixis, Ataxia

Confusion

Dysarthria

Constructional apraxia: draw spiral, 5 point star

Seizures

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11
Q

Management of Encephalopathy

A

Conservative

Nurse in well-lit calm environment

Correct precipitants

Avoid sedatives

Medical

Lactulose

Rifaximin

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12
Q

Path of Hepatorenal syndrome

A

Renal failure in patients with advanced liver disease

Cirrhosis –> splanchnic arterial vasodilatation

–> Reduced circulating volume

–> Increased RAS activation

–> Afferent arteriolar vasoconstriction

–> Reduced renal perfusion

–> Renal failure

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13
Q

Classification of hepatorenal syndrome

A

Type I: Rapidly progressive (survival <2 weeks)

Type II: Steady deterioration (survival ~ 6 months)

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14
Q

Treatment of Hepatorenal Syndrome

A

IV albumin

Terlipressin (splanchnic vasoconstrictor)

Haemodialysis

Liver transplant

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15
Q

Spontaneous bacterial peritonitis

A

Patient with ascites and peritonitic abdomen

Complicated by hepatorenal syndorme in 30%

E.coli

Klebsiella

Strep

PMN > 250/mm3

MC+S

Mx: Tazocin or cefotaxime until sensitivities known

Prophylaxis: long-term ciprofloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved’

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16
Q

Signs of Ascites on Examination

A

Signs of cause:

CCF: increased JVP, bibasal crepitations, peripheral oedema

CLD: asterixis, juandice, gynaecomastia, spider naevi

Nephrotic: periorbital oedema

Budd-Chiari: abdo pain, hepatomegaly, jaundice

Abdomen

Shifting dullness

Splenomegaly - portal hypertension

Complete: CVS and resp for CCF, urine dip (proteinuria in nephrotic syndrome)

Significant negatives: CLD, acute liver failure, JVP, periorbital oedema

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17
Q

Causes of Ascites

A

Commonest: CCC

Cirrhosis

Congestive cardiac failure

Carcinomatosis

Can base on Serum Ascites Albumin Gradient (SAAG)

= serum albumin - ascites albumin

SAAG >1.1g/dL = portal HTN

Cirrhosis in 80%

Pre-hepatic(protal vein thrombosis), hepatic (cirrhosis) and post-hepatic (Budd Chiari) causes

SAAG <1.1g/dL (NI NI)

Neoplasia: peritoneal mets or ovarian cancer

Inflammation: pancreatitis

Nephrotic syndrome

Infection: TB peritonitis

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18
Q

Definition of Portal Hypertension

A

Portal pressure of >10mmHg

Normally 5-10mmHg

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19
Q

Causes of Portal Hypertension

A

Portal pressure of >10mmHg

Pre-hepatic

Portal vein thrombosis

  • Polycythaemia vera
  • Essential thrombocythaemia
  • Nephrotic syndrome
  • Paroxysmal nocturnal hemoglobinuria

Hepatic

Cirrhosis

Post-Hepatic

Cardiac: Right heart failure, Tricuspid regurgitation, constrictive pericarditis

Budd Chiari (hepatic vein thrombosis)

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20
Q

Management of Ascites

A

General

  • Alcohol abstinence
  • Daily weights: aim for <0.5kg / day reduction
  • Fluid restrict <1.5L/day
  • Low na diet

Diuretics

Spironolactone

Furosemide if needed

Therapeutic paracentesis

  • Temporary insertion of pig-tail drain or Bonnano catheter
  • Indicatons: respiratory compromise, pain, renal impairment
  • Risk: severe hypovolaemia, SBP
  • Need to replace albumin

Refractory Ascites: TIPSS, transplant

SBP: tazoxin or cefotaxime, ciprofloxacin prophylaxis

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21
Q

Signs of Medical Jaundice on Examination

A

Abdomen

Excoriations

Splenomegaly

Hepatomegaly

Palpable gallbladder: Ca head of pancreas

Urine dip: urobilinogen and Hb

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22
Q

Differential for Jaundice

A

Splenomegaly

Haemolysis

Chronic liver diease –> Portal HTN

Viral hepatitis: EBV

Hepatomegaly

Hepatitis

Early CLD

No organomegaly or CLD
Biliary obstruction

Haemolysis

Drugs: flucloxacillin, OCP

Gilbert’s

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23
Q

Causes of Jaundice

A

Commonest causes

Haemolysis

Chronic liver disease

Gallstones

Pre-Hepatic

  • Haemolysis
    • Autoimmune haemolytic anaemia
    • Hereditary spherocytosis
    • Sickle cell disease
    • Paroxysmal nocturnal haemoglobinuria
    • Microangiopathic haemolytic anaemia (MAHA)
    • Malaria
    • G6PD

Hepatic

  • Chronic liver disease
  • Hepatitis
    • Alcoholic
    • virla
  • Drugs
    • Paracetamol
    • Statins
    • Isoniazid
  • Congenital: HH, Wilson’s A1AT def,
  • Autoimmune: AIH,
  • Cancer: primary or metastatic
  • Vascular

Post-Hepatic

  • Gallstones
  • Cancer of head of pancreas
  • LNs at porta hepatis: Cancer or TB
  • PBS
  • PSC
  • Cholangiocarcinoma
  • Drugs
    • Flucloxacillin
    • Augmentin
    • OCP
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24
Q

Investigations for Jaundice

A

Urine Dip

Bilirubin: absence in pre-hepatic

Urobilinogen: absent in post-hepatic

Both present: Hepatic

Bloods

DAT and blood film - haemolysis

FBC, U+Es, LFTs, Clotting, Liver screen

Immunnoloy: ANA, AMA, etc.

Imaging

Abdo USS + portal vein duplex

MRCP, CT, MRI

Liver biopsy

Check clotting first

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25
Q

Signs of Liver Transplant on Examination

A

Inspection

Nystatin for oral thrush

Signs of CLD

Pigmentation - haemochromatosis

Tattoos and needle marks: Hep B/ Hep C

Immunosuppression stigmata

Cushingoid

Skin tumours: Actinic keratosis, Squamous cell carcinoma, basal cell carcinoma, melanocytic melanoma

Gingival hypertrophy: ciclosporin

Abdomen: mercedes-benz scar

Significant negatives: CLD, immunosuppression,

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26
Q

Differential for Mercedes Benz scar

A

Hepatobiliary surgery

Liver transplant

Segmental resection

Whipples: pancreaticoduodenectomy

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27
Q

Investigations for Liver Transplant patient

A

Bloods

FBC: infection

U+Es: ciclosporin can cause renal impairment

LFTs: assess graft function

Clotting

Fasting glucose: tacrolimus and steroids –> DM

Drug levels: tacrolimus and ciclosporin

Liver biopsy if signs of rejection

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28
Q

Common causes for Liver Transplant

A

Cirrhosis

Acute liver failure

Hep A, B

Paracetamol overdose

Malignancy

Prognosis: 70% 5 yrs

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29
Q

Immunosuppression regiment for Liver transplant

A

Tacrolimus / Ciclosporin

Azathioprine

Prednisolone

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30
Q

Signs of Hepatomegaly on Examination

A

Signs of cause:

CLD

Alcohol: Dupuytren’s, palmar erythema

Haemochromatosis: pigmentation

Cancer: cachexia

CCF: increased JVP, bibasal creps, peripheral oedema, ascites

Haematological: pallor, bruising, purpura, LNs

Hepatomegaly

Define size in fingerbreadths below costal margin

Moves inferiorly with inspiration

Can’t get above it

Dull percussion note

Edge: smooth, craggy, nodular

Pulsatile?

Tender?

Percuss above and below

Auscultate for liver bruit –> HCC

?Associated splenomegaly

Inguinal nodes

Ascites

Significant negatives: splenomegaly, acute liver failure

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31
Q

Causes of Hepatomegaly

A

Common Causes

Hepatitis:

Alcholic hepatitis

Viral hepatitis

NAFLD

Chronic Liver Disease

Congestion secondary to cardiac failure

Other Causes: MACHO

Malignancy: secondary

Anatomical: Reidel’s lobe, hyperexpanded chest

Congestion: Tricuspid regurg, Budd Chiari

Haematological: Leukaemia, Lymphoma, Myeloproliferative, SCD

Other: sarcoidosis, Amyloidosis, Gaucher’s, ADPKD

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32
Q

Micronodular cirrhosis

A

Alcoholic liver disease

Haemochromatosis

Wilson’s

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33
Q

Macronodular

A

Viral hepatitis

C

B

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34
Q

Rhodamine stain on liver biopsy

A

Wilson’s disease

Copper

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35
Q

Pearl’s stain on liver biopsy

A

Haemochromatosis

Stains iron

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36
Q

Granulomata on liver biopsy

A

Primary biliary cholangitis

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37
Q

Signs of Splenomegaly on Examination

A

Signs of cause:

Haematological: pallor, bruising, purpura, LNs, cachexia

Portal HTN: CLD

Infective endocarditis: splinter haemorrhages, clubbing

Felty’s syndorme: rheumatoid hands

Abdomen

Asymetrical appearance

Splenomegaly: can’t get above it, moves inferiorly towards RIF with inspiration, has notch, dull percussion note,

?hepatomegaly

?inguinal nodes

How big?

Completion: Cardio and resp –> infective endocarditis or sarcoidosis

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38
Q

Causes of Massive Splenomegaly

A

Myeloproliferative: chronic myeloid leukaemia, myelofibrosis

Lymphoproliferative: Chronic lymphocytic leukaemia, lymphoma

Infiltrative: amyloidosis, Gaucher’s

Infectious: malaria, visceral leishmaniasis

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39
Q

Causes of splenomegaly

A

Haematological: myeloproliferative, lymphoproliferative, haemolysis

Portal HTN: secondary to cirrhosis

Infection: EBV, herpes viruses, hepatitis viruses, infective endocarditis, malaria

Inflammation: Rheumatoid arthritis, SLE, Sjogren’s

Rare: sarcoidosis, amyloidosis, Gaucher’s CVID

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40
Q

Gaucher’s

A

Genetic disorder of deficiency of the enzyme glucocerebrosidase

Characterized by bruising, fatigue, anemia, low blood platelet count and enlargement of the liver and spleen

Glucocerebroside accumulates, particularly in white blood cells and especially in macrophages (mononuclear leukocytes)

Glucocerebroside can collect in the spleen, liver, kidneys, lungs, brain, and bone marrow.

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41
Q

Investigations for Splenomegaly

A

Bloods

FBC, U+Es, LFTs, …

Blood film

Leukoerythroblastic with teardrop poikiolcytes = myelofibrosis

Smear cells = CLL

Haemolysis = hereditary spherocytosis, reticulocytosis

DAT

Urate: malignancy –> uropathy

Imaging:

Abdo USS

CT chest and abdopelvis

Histology

BM aspirate

Genetics

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42
Q

Chronic Myeloid Leukaemia

A

Clonal proliferation of myeloid cells

15% of leukaemias

Presentation

  • Hypermetabolism: weight loss, fever, night sweats, lethargy
  • Massive hepatosplenomegaly –> ando discomfort
  • Bruising
  • Bleeding
  • Gout
  • Hyperviscosity

Invx

  • Increased White cell count
    • Myelocytes
    • PMN and basophils
  • Anaemia
  • Thrombocytopenia
  • Increase urate
  • BM cytogenetic analysis: Ph +ve t:(9,22)

Mx

Imatinib: tyrosine kinase inhibitor

Allogenic stem cell transplant

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43
Q

Philadelphia Chromosome

A

Reciprocal translocation t(9:22)

Formation of BCR-ABL fusion gene

—> Constitutive tyrosine kinase activity

Present in >80% of CML

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44
Q

Primary Myelofibrosis

A

Clonal proliferation of megakaryocytes –> Increased PDGF –> myelofibrosis

Extramedullary haematopoiesis: Liver and spleen

Presentation

Elderly

Massive hepatosplenomegaly

Hypermetabolism: weight loss, fever, night sweats

Bone marrow failure: anaemia, infections, bleeding

Invx

Blood film: leukoerythroblastic changes with teardrop poikilocytes

Cytopenias

Bone marrow: Dry tap

50% JAK2 +ve

Mx

Supportive: blood products

EPO, Allopurinol,

Ruxolitinib

Hydroxycarbamide:

Splenectomy

Allogenic BMT may be curative

5yr median survival

45
Q

Function of the spleen

A

Part of the mononuclear phagocytic system

Phagocytosis of:

Old RBCs, WBCs

Opsonised bugs esp. encapsulated

Sequestration of formed blood elements: platelets, lymphocytes, monocytes

Haematopoiesis

46
Q

Causes of Hyposplenism

A

Splenectomy

Coeliac disease

Inflammatory bowel disease

Sickle cell disease

47
Q

Signs of Hyposplenism on film

A

Howell-Jolly bodies

Pappenhemier bodies

Target cells

Increased platelets transiently after splenectomy

48
Q

Mx of a patient after splenectomy

A

Daily erythromycin as prophylaxis

Immunisations: pneumovax, HiB, Men C, Yearly Flu

Warning bracelet

Susceptible to encapsulated bacteria:

Haemophilus

Meningococcus

Pneumococcus

49
Q

Complications of Splenectomy

A

Early

Redistribution thrombocytosis –> early VTE (give temporary post-operative aspirin)

Gastric dilatation: transient ileus (use prophylactic NG tube after surgery)

Left lower lobe atelectasis

Pancreastitis, tail shares blood supply with spleen

Late

Increased susceptibility to encapsulated bacteria

HMS

Haemophilus

Meningococcus

Strep Pneumo

50
Q

Signs of Renal Disease on Examination

A

Renal impairment

Hypertension

Pallor

Renal Replacement Therapy

AV fistula (or scar)

Tunnelled dialysis lines (or scar)

Tenchkhoff catheter (or scar)

Immunosuppressant stigmata

Cushingoid

Skin tumours: Actinic keratosis, Squamous cell carcinoma, Basal cell carcinoma, Malignant melanoma

Gingival hypertrophy: ciclosporin

Abdomen

Nephrectomy scar

Rutherford Morrison scar

Tenchkhoff catheter

Palpable kidneys

Flank mass, able to get above it, ballotable, moves inferiorly with inspiration, resonant percussion note

Renal bruit

Completion: External genitalia (hydrocele secondary to RCC)

Urine drip (proteinuria and haematuria),

CVS: mitral valve prolpase (increased in ADPKD)

Significant negatives: unilateral enlargement, hepatomegaly, evidence of RRT, immunosupression

51
Q
A

Tenckhoff Catheter

indwelling peritoneal catheter

52
Q

Differential of Enlarged Kindey(s)

A

Bilateral (AABB)

ADPKD

Amyloidosis

Bilateral renal cell carcinoma (5%)

Bilateral cysts (in Von Hippel–Lindau disease)

Unilateral

Simple renal cyst

Renal cell carcinoma

Compensatory hypertrophy

+ contralteral necphrectomy: ADPKD

53
Q

ADPKD

A

PKD1 gene on chromosme 16: 85%

PKD2 gene on chromosome 14: 15%

Presentation

Age 30-50

Hypertension

Recurrent UTIs

Loin pain: cyst haemorrrhage or infection

Haematuria

Extra-Renal Involvement

Hepatic syst –> hepatomegaly

Intracranial berry aneurysms –> SAH

Mitral valve prolapse: mid-diastolic click and late systolic murmur

Mx

General

Increase water intake, decrease Na, decrease caffeine (may decrease cyst formation)

Monitor U+Es, BP

Genetic counselling

MRA for Berry aneurysm

Medical

Treat hypertension <130/80 aggressively

Treat infections

Surgical

Nephrectomy if recurrent bleeds or infections

If painful

Renal Replacement Therapy

54
Q

Autosomal Recessive PKD

A

Fibrocystin gene on chromosome 6 (PKHD1)

Presentation

Perinatal

Oligohydramnios may –> Potter sequence (clubbed feet, pulmonary hypoplasia, cranial abnormalities)

Bilateral abdominal masses

Hypertension

Chronic renal failure

Can lead to congenital hepatic fibrosis –> portal hypertension

ESRF by 20 years

55
Q

Simple Renal Cyst

A

1/3 of patients over 65 - Common

Renal mass

Haematuria

Contain fluid only, no solid elements

Differential: RCC

56
Q

Dialysis Associated Renal Cyst

A

Seen after prolonged dialysis use

Secondary to obstruction of renal tubules by oxalate crystals

Increased risk of RCC - 15% of patients on haemodialysis

57
Q

Tuberous Sclerosis

A

Autosomal dominant condition characterised by hamartomas in the skin, brain, eye and kdiney

Skin:

Nasolabial adenoma sebaceum

Ash-leaf macules

Peri-ungal fibromas

Neurological:

Astrocytoma

Epilepsy

Decreased IQ

Renal

Cysts

Angiomyolipomas

58
Q

Renal Cell Carcinoma

A

90% of renal cancer

Age: 55 yrs

Adenocarcinoma of proximal renal tubular epithelium

Clear cell subtype makes up 80%

Presentation

Triad: Haematuria, loin Pain and Loin Mass

50% incidental

Invasion of left renal vein –> varicocele

Cannonball mets –> SOB

Paraneoplastic features (polycythaemia etc.)

Spread: direct to renal vein, lymph, haematogenous (bone, liver and lung)

Invx

Blood: polycythaemia, ESR, U+Es, ALP, calcium

Urine: dip and cytology

Imaging:

CXR: cannonball mets

USS: Abdominal mass

IVU: filling defect

CT/MRI

Mx

Medical

Temsirolimus - pecific inhibitor of mTOR

(reserved for patients with poor prognosis)

Surgical

Radical nephrectomy

Consider partial if small or only 1 kidney

Prognosis 45% 5 year survival

59
Q

Risk Factors for RCC

A

Risk factors

Smoking

Obesity

Hypertension

Dialysis: 15% develop RCC

4% heritableL Von-Hippel Lindau

60
Q

Von Hippel-Lindau

A

Autosomal dominant genetic disorder characterised by multiple visceral cysts and benign tumors

(with potential for subsequent malignant transformation)

Type of phakomatosis that results from a mutation in the von Hippel–Lindau tumor suppressor gene on chromosome 3

Complications

Renal and pancreatic cysts

Bilateral renal cell carcinoma

Haemangioblastoma: often in cerebellum –> cerebellar signs

Phaeochromocytoma

Islet cell tumouts

61
Q

Signs of Renal Transplant on Examination

A

Renal impairment: anaemia, HTN

Renal replacement therpay

  • AV fistula
  • Tunnelled dialysis line
  • Tenckhoff catheter

Immunosuppressant stigmata

  • Cushingoid
  • Skin tumours: actinic keratosis, squamous cell carcinoma, basal cell caricnoma, malignant melanoma
  • Gingival hypertrophy: ciclosporin

Signs of cause:

DM - finger pricks from BM monitoring, lipodystrophy

Cystic kidney disease: nephrectomy

Connect tissue: SLE, Systemic slerosis, Rheumatoud arthritis

Abdomen

Rutherford Morrison scar in RIF

Nephrectomy scars

Tenchkoff catheter

Smooth oval mass under scar

Dull percussion

Can’t get below it

Doesn’t move with respiration

Renal bruit heard over transplant

Completion: urine dip (haem/proteinuria), drug chart review, BP (HTN common post-transplant)

62
Q

Paraneoplastic Features of RCC

A

EPO —> Polycythaemia

PTHrP —> Hypercalcaemia

Renin —> Hypertension

ACTH —> Cushing’s syndrome

Amyloidosis

63
Q

Differential for Gum Hypertrophy

A

Drugs:

Ciclosporin, Phenytoin, Nifedipine

Familial

AML

Scurvy

Pregnancy

64
Q

Investigations for post-transplant patient

A

Urine

Dip: haematuria, proteinuria

MC+S

Bloods

FBC (infection), U+Es (GFR)

LFTS: ciclosporin can cuase hepatic dysfunction

Fasting glucose: tacrolimus is diabetogenic

Drug levels: ciclosporin, tacrolimus

Renal biopsy: if rejection suspected

65
Q

Common indications for Renal Transplant

A

Diabetic nephropathy

Glomerulonephritis

Polycystic kidney disease

Hypertensive nephropathy

66
Q

Transplant Assessment

A

Virology: CMV, HIV, HZV, hepatitis

Co-morbities: Cardiovascular disease

ABO group

Anti-HLA antibodies

Halotype

Importance: HLA-DR > HLA-B > HLA-A

2 alleles at each locus, 6 possible mismatches

Pre-implantation x-match: recipient serum vs donor lymphocytes

67
Q

Contraindications to Renal Transplant

A

Active infection

Malignancy

Severe co-morbidity

Failed pre-implantation x-match

68
Q

Types of Graft

A

Cadaveric: brainstem death with CB support

Non-heart beating donor: no active circulation

Live-related

Live unrelated

69
Q

Immunosuppression for Renal Transplant

A

Pre-operative: Alemtuzumab (anti-CD52)

Post-operative

Short-term: prednisolone

Long-term: Basiliximab, when used as part of an immunosuppressive regimen that includes a calcineurin inhibitor (tacrolimus or ciclosporin)

70
Q

Complications of Renal Transplant

A

Post-operative:

Bleeding

Graft thrombosis

Infection

Urinary leak

Rejection

Drug toxicity

71
Q

Transplant Rejection

A

Hyperacute rejection: minutes

ABO incompatbility

–> thrombosis and systemic inflammatory response

Acute rejection

Cell-mediated rejection

Fever, graft pain, decreased urine putput, Increased creatinine

Mx: immunosuppression

Chronic rejection

>6 months

Gradual increase in creatinine and proetinuria

Interstitial fibrosis and tubular atrophy

Mx: supportive, not responsive to immunosuppression

72
Q

Ciclosporin toxicity

A

Calcineurin inhibitor: block IL-2 production

Nephrotoxic, may contribute to organ rejection

Gingival hypertrophy

Hypertrichosis

Hepatic dysfunction

73
Q

Tacrolimus toxicity

A

Calcineurin inhibitor: blocks IL-2 production

Less nephrotoxic vs ciclosporin

Diabetogenic

Cardiomyopathy

Neurotoxicity: peripheral neuropathy

74
Q

Steroid excess

A

Cushing’s syndrome

75
Q

Complications of reduced immune function due to immune modulation

A

Increase risk of infection

CMV

PCP

Fungi

Increased risk of malignancy

Skin: squamous cell carcinoma, basal cell carcinoma, malignant melanoma, kaposi’s

Post-transplant lymphoproliferative disease (secondary to EBV)

76
Q

Indications for Renal Replacemnt Therapy

A

GFR<15ml/min AND Symptoms

Psychlogical preparation necessary

Peritoneal vs haemodialysis is a multi-factor decision (med, social, psychological and personal factors)

77
Q

Complication of Dialysis

A

20% annual mortality

Cardiovascular disease

Malnutrition

Infection: uraemia –> granulocyte dysfunction –> increased risk of sepsis

Amyloidosis

Beta2-microglobulin accumulation

Carpal tunnel, arthralgia

Renal cysts –> RCC

78
Q

Mechanism of Haemodialysis

A

Counter-current flow

Blood flows on one side of a semi-permeable membrane

Dialysate flows in opposite direction on the other side of the semi-permeable membrane

Solute transfer by diffusion

Ultrafiltration

Fluid removal by creation of a negative transmembrane pressure by decreasing the hydrostatic pressure of the dialysate

79
Q

Complications of haemodialysis

A

Disequilibration syndrome

Usually only 1st dialysis

Rapid change in plasma osmolarity –> cerebral oedema

Nause, vomiting, headache, decrease GCS

Fluid balance

Hypotension

Pulmonary oedema

Electrolyte imbalance

Aluminium toxicity (in dialysate) –> dementia

Psychological trauma

80
Q

Haemofiltration

A

Usually only in ITU

Takes longer than haemodilaysis

Less haemodynamic instability

Uses Vas Cath

Blood filtered across a highly permeable membrane by hydrostatic pressure

Water and solutes are removed by convection

Ultrafiltrate replaced with isotonic fluid

81
Q

Mechanism of Peritoneal Dilaysis

A

Dialysate introduced into peritoneal cavity by Tenchkoff catheter

Uraemic solutes diffuse into fluid across peritoneum

Ultrafiltration: addition of osmotic agent e.g. Dextrose

3L 4/day with 4 h dwell times

Types:

Continuous ambulatory peritoneal dialsysi (CAPD): fluid exchanged duringthe day with long swell at night

Automated peritoneal dialsysis (APD): fluid exchanged throughout the night by machine with logn dwell during the day

82
Q

Advantages and complications of Peritoneal Dialysis

A

Advantages: simple, can do it at home

Less haemodynamic instability = great for patients with cardiovascular disease

Disadvantages

Inconvenience, Body image, Anorexia

Complications

Peritonitis

Exit site infection

Cathter malfunction

Obesity: glucose in dialysate

Mechanical: hernias and back pain

83
Q

Signs of Renal Access on Examination

A

AV fistula

Swelling with surgical scar over distal forearm or elbow

Evidence of needle marks (cannulation of fistula)

Evidence of infection

Check if painful

Check temperature

Palpable trhill

Audible bruit

Significant negatives: evidence of infection, stenosis, aneurysm

Tunnelled Cuffed Catheter

Tessio lines: two lines tunnelled under skin entering internal jugular vein

84
Q

Types of AV fistula

A

= Surgically created connected between artery and vein

Radio-cephalic at the wrist = Cimino-Brescia

Brachio-cephalic at the elbow

Brachial-basilic

85
Q

Advantages and Disadvantages of AV Fistula

A

Advantages

High flow rates: low recirculation

Low infection rates

Less chance of stenosis compared with grafts

Disadvantages

Takes 6 weeks to develop

Affects patients body images

Need to be careful of area e.g. shaving, taking BP

Complications:

Thrombosis

Stenosis

Infection

Bleeding

Aneurysm

Steal syndrome

86
Q

Complications of AV Fistula

A

Thrombosis

Stenosis

Aneurysm

Infection

Bleeding

Steal syndorme

87
Q

Steal Syndrome

A

Distal tissue ischaemia

Presenting as pallor, pain, and reduced pulses

May lead to necrosis

Decreased wrist: brachial pressure index

Mx: banding of fistula

88
Q
A

Tesio Line

89
Q

Advantages and Disadvanatges of Tunnelled Cuffed Cathter for Renal Replacement (Tessio Line)

A

Disadvantges

Increased risk of recirculation compared with AV fistula

Lower flow rates

Increased risk of infection

Increased risk of thrombosis

Complications

Adverse events at insertion: pneumothorax

Line or tunnel infection

Blockage

Retraction

90
Q

Claddification of Chronic Renal Failure

A

Stage I: eGFR >90

minus 30

Stage II: eGFR 60-89

minus 20

Stage III: eGFR 30-59

minus 15

Stage IV: eGFR 16-29

Stage V: eGFR <15

91
Q

Causes of Chronic Renal Failure

A

Common

Diabetes melitus nephropathy

Hypertensive nephropathy

Other

Renal artery stenosis

Glomerulonephritis

Connective tissue disease: rheumatoid, SLE, systemic sclerosis

Polycystic kidney disease

Drugs: analgesic nephropathy (aspirin, phenacetin, and paracetamol)

Pyelonephritis seconday to vesicoureteral reflux

Myeloma

Amyloidosis

92
Q

Definition of Chronic Renal Failure

A

Kidney damage for more than 3 months indicated by decline in renal function

93
Q

Investigations for Chronic Renal Failure

A

Urine

Dip: proteinuria, haematuria, glycosuria

Protein:creatinine ratio: normal <20, Nephrotic >300mg/mM

Bence Jones: Myeloma

Function

FBC (anaemia), U+E (eGFR), Bone (hypocalcaemia, phosphataemia, increased PTH, increased ALP)

Renal Screen

Fasting glucose, HbA1c: Diabetes

ESR

Immune:

SLE (ANA, C3, C4)

Goodpasture;s: Anti-GBM

Vasculitis: ANCA

Hepatitis: viral serology

Serum protein electrophoresis

Imaging

CXR: pulmonary oedema

Renal USS: usually small non-functioning, may be large of PCKD

Bone x-rays: renal osetodystrophy

CT KUD: Cortical scaring form pyelonephritis

Renal Biopsy

Histology

Amyloid: apple green bifringence with congo red

94
Q

Complications of Chronic Renal Failure

CRF HEALS

A

CRF HEALS

Cardiovascular disease

Renal osteodystrophy

Fluid: oedema

Hypertension

Electrolyte disturbance: hyperkalaemia and acidosis

Anaemia

Leg restlessness

Sensory neuropathy

95
Q

Renal Osteodystrophy

A

Freatures

Osteoporosis: decreased bone density

Osteomalacia: decreased mineralisation of osteoid (matrix)

Secondary an Tertiary hyperparathyroidism –> Osteitis fibrosa cystica

Subperiosteal bone resorption

Acral osteolysis: short stubby fingers

Pepperpot skull

Osteosclerosis of the spine –> Rugger Jersey spine (indicative of hyperparathyroidism)

Sclerotic vertebral end-plate with lucent centre

Extra-skeletal calcification e.g. band keratopathy

96
Q

Mechanism of Renal Osteodystrophy

A

Phosphate retention --> Increases PTH directly

Decreased 1 alpha hydroxylase –> reduced vit D activation –> Hypocalcaemia –> increased PTH

Increased PTH –> activation of osteoclasts and osteoblasts

Acidosis –> bone rresorption

97
Q

Management of Chronic Renal Failure

A

General Mx

Treat reversible causes

Stop nephrotoxic drugs

Na, K, fluid and phosphate restriction

Optimise CV risk factors

Smoking cessation

Exercise

Atorvastatin

Antiplatelet

Hypertension: aim <140/90 (130/80 if Diabetic)

If diabetic, give ACE-I

Oedema –> Frusemide

Bone disease

Phosphate binders: calcichew, sevelamar

Vitamin D anlogues: alfacalcidol (increased hydroxylated Vit D)

Ca supplements

Cinacalcet: Ca mimetic

Anaemia

Exclude IDA

EPO to raise Hb to 11

Restless legs: clozapine

98
Q

Diabetic Nephropathy

A

Commonest cause of ESRF >20%

Gloermulosclerosis and nephron loss

Nephron loss –> RAS activation –> hypertension

Presentation

Microalbuinaemia

albumin:creatinine ratio >3, strong risk factor for CV disease

Screen diabetics for microalbuminaemia every 6 months

Progresses to proteinuria

Mx

Good glycaemic control delays onset and progression (UK prospective Diabetes Study UKPDS, Diabetes control and complications trial DCCT)

Control BP: <130/80mmHg

ACE-inhibitor or ARB even if normotensive

Stop smoking

Combined kidney and pancreas transplant in selected patients

99
Q

Rheumatological Renal Disease

A

Rheumatoid arthritis

NSAIDs –> ATN

Penicillamine and gold –> membranous glomerulonephritis

AA amyloidosis occurs in 15%

SLE

Involvement of glomerulus –> ARF/CRF

Immune complexes deposition –> Type 3 hypersensitivity

Proteinuria and hypertension

Mx: ACE-inhibitor and immunosuppression

Systemic Sclerosis

Renal crisis: malignant HTN and acute renal failure = commonest cause of death

Mx: ACE-inhibitor

100
Q

Myeloma –> Chronic Renal Disease

A

Excess production of monoclonal antibodies and light chains

Light chains block tubules and have direct toxic effects –> Acute tubular necorsis

Associated with hypercalcaemia

Urinary Bence Jones protein

Drink at least 3L / day to reduced ATN

Dialysis may be required

101
Q

Renal artery stenosis

A

Causes

Atherosclerosis (80%)

Fibromuscular dysplasia

Thromboembolism

External mass compression

Presentation

Refractory hypertension

Renal bruits

Worsening renal function after ACE-inhibitor / ARB

Flash pulmonary oedema (with no LV impairment on echo)

Other signs of peripheral vascular disease

Invx: CT/ MR angio

Renal angiography

Mx: Treat CV risk factors

Angioplasty and stenting

Avoid ACE-inhibitors or ARB

102
Q

Signs of Inflammatory Bowel Disease on Examination

A

Ileostomy

Inspection

Often young female patient

Laparatomy scars

Malnutrition or weight loss

Cushingoid

Pallor

Hands

Clubbing

Leukonychia

Beau’s lines

Eyes

Pale conjunctivae

Iritis

Episcleritis

Mouth

Aothous ulcers

Ginigval hypertrophy (ciclosporin)

Legs

Erythema nodosum

Pyoderma gangrenosum

Abdomen

Scars: healed stoma sites, healed drains, midline laparatomy

Stomas

Enterocutaneous fistula

Tender palpation, RIF mass

+/- hepatomegaly

Completion: inspect perineum, examine for extra-intestinal features

Large joint monoarthritis

Sacroileitis

Bronchiectasis

DDx: Crohns, UC

Malabsorption: Coeliacs

Midline lap: FAP

103
Q

Investigations for Inflammatory Bowel Disease

A

Bloods

FBC, U+Es, LFTs, Clotting, Increased ESR, Increased CRP, Haematinics

Markers of activity

Hb

ESR

CRP

WCC

Albumin

Stool

Culture, MC+S

Exlcude infectious causes

Imaging

AXR: toxic megacolon in UC, bowel obstruction secondary to strictures in Crohn’s

Contrast studies: Ba or Gastrograffin enema in UC

MRI: peri-anal disease in Crohn’s

?Endoscopy

Ileocolonoscopy + regional biopsy

?Not safe in acute disease

Distinguishes UC from Crohn’s

Assess disease severity

Witeless capsule endoscopy

104
Q

Complications of UC

A

Toxic megacolon

Haemorrhage

Malignancy

Colorectal carcinoma

Cholangiocarcinoma

VTE

105
Q

Complications of Crohn’s

A

Fistulae

Perianal abscess

Strictures

Malabsorption

Toxic dilatation

106
Q

True-Love and Witts

A

Severity of Acute Flare of Inflammatory Bowel Disease

Symptoms

Bowel motions >6/day

Large PR bleed

Systemic Signs

HR >90

Pyrexia >37.8

Lab Values

Hb <10.5

ESR >30

107
Q

Extra-intestinal Features of Inflammatory Bowel Disease

A

Skin

Clubbing

Eyrthema nodosum

Pyoderma gangrenosum (esp. UC)

Mouth: Apthous ulcers

Eyes

Anterior uveitis

Episcleritis

Joints

Large joint arthritis

Sacroileitis

Hepatic

Fatty Liver

Chronic hepatitis –> cirrhosis

Gallstones (esp. Crohn’s)

Primary sclerosing cholangitis and cholangiocarcinoma (Esp. UC)

Other

Amyloidosis (AA)

Oxalate renal stones

108
Q
A

PACES (10 decks)

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