Medical Abdomen Flashcards
Signs of Chronic Liver Disease on Examination
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
Differential for Chronic Liver Disease
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
Investigations for Chronic Liver Disease
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
Management of Chronic Liver Disease
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
Complications of Chronic Liver Disease
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
Child-Pugh Grading
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
Causes of Decompensation in Chronic Liver Disease
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
Management of Decompensation of Chronic Liver Disease
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
Path of Encephalopathy
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
Presentation of Encephalopathy
Asterixis, Ataxia
Confusion
Dysarthria
Constructional apraxia: draw spiral, 5 point star
Seizures
Management of Encephalopathy
Conservative
Nurse in well-lit calm environment
Correct precipitants
Avoid sedatives
Medical
Lactulose
Rifaximin
Path of Hepatorenal syndrome
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
Classification of hepatorenal syndrome
Type I: Rapidly progressive (survival <2 weeks)
Type II: Steady deterioration (survival ~ 6 months)
Treatment of Hepatorenal Syndrome
IV albumin
Terlipressin (splanchnic vasoconstrictor)
Haemodialysis
Liver transplant
Spontaneous bacterial peritonitis
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’
Signs of Ascites on Examination
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
Causes of Ascites
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
Definition of Portal Hypertension
Portal pressure of >10mmHg
Normally 5-10mmHg
Causes of Portal Hypertension
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)
Management of Ascites
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
Signs of Medical Jaundice on Examination
Abdomen
Excoriations
Splenomegaly
Hepatomegaly
Palpable gallbladder: Ca head of pancreas
Urine dip: urobilinogen and Hb
Differential for Jaundice
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
Causes of Jaundice
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
Investigations for Jaundice
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
Signs of Liver Transplant on Examination
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,
Differential for Mercedes Benz scar
Hepatobiliary surgery
Liver transplant
Segmental resection
Whipples: pancreaticoduodenectomy
Investigations for Liver Transplant patient
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
Common causes for Liver Transplant
Cirrhosis
Acute liver failure
Hep A, B
Paracetamol overdose
Malignancy
Prognosis: 70% 5 yrs
Immunosuppression regiment for Liver transplant
Tacrolimus / Ciclosporin
Azathioprine
Prednisolone
Signs of Hepatomegaly on Examination
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
Causes of Hepatomegaly
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
Micronodular cirrhosis
Alcoholic liver disease
Haemochromatosis
Wilson’s
Macronodular
Viral hepatitis
C
B
Rhodamine stain on liver biopsy
Wilson’s disease
Copper
Pearl’s stain on liver biopsy
Haemochromatosis
Stains iron
Granulomata on liver biopsy
Primary biliary cholangitis
Signs of Splenomegaly on Examination
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
Causes of Massive Splenomegaly
Myeloproliferative: chronic myeloid leukaemia, myelofibrosis
Lymphoproliferative: Chronic lymphocytic leukaemia, lymphoma
Infiltrative: amyloidosis, Gaucher’s
Infectious: malaria, visceral leishmaniasis
Causes of splenomegaly
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
Gaucher’s
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.
Investigations for Splenomegaly
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
Chronic Myeloid Leukaemia
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
Philadelphia Chromosome
Reciprocal translocation t(9:22)
Formation of BCR-ABL fusion gene
—> Constitutive tyrosine kinase activity
Present in >80% of CML
Primary Myelofibrosis
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
Function of the spleen
Part of the mononuclear phagocytic system
Phagocytosis of:
Old RBCs, WBCs
Opsonised bugs esp. encapsulated
Sequestration of formed blood elements: platelets, lymphocytes, monocytes
Haematopoiesis
Causes of Hyposplenism
Splenectomy
Coeliac disease
Inflammatory bowel disease
Sickle cell disease
Signs of Hyposplenism on film
Howell-Jolly bodies
Pappenhemier bodies
Target cells
Increased platelets transiently after splenectomy
Mx of a patient after splenectomy
Daily erythromycin as prophylaxis
Immunisations: pneumovax, HiB, Men C, Yearly Flu
Warning bracelet
Susceptible to encapsulated bacteria:
Haemophilus
Meningococcus
Pneumococcus
Complications of Splenectomy
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
Signs of Renal Disease on Examination
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
Tenckhoff Catheter
indwelling peritoneal catheter
Differential of Enlarged Kindey(s)
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
ADPKD
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
Autosomal Recessive PKD
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
Simple Renal Cyst
1/3 of patients over 65 - Common
Renal mass
Haematuria
Contain fluid only, no solid elements
Differential: RCC
Dialysis Associated Renal Cyst
Seen after prolonged dialysis use
Secondary to obstruction of renal tubules by oxalate crystals
Increased risk of RCC - 15% of patients on haemodialysis
Tuberous Sclerosis
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
Renal Cell Carcinoma
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
Risk Factors for RCC
Risk factors
Smoking
Obesity
Hypertension
Dialysis: 15% develop RCC
4% heritableL Von-Hippel Lindau
Von Hippel-Lindau
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
Signs of Renal Transplant on Examination
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)
Paraneoplastic Features of RCC
EPO —> Polycythaemia
PTHrP —> Hypercalcaemia
Renin —> Hypertension
ACTH —> Cushing’s syndrome
Amyloidosis
Differential for Gum Hypertrophy
Drugs:
Ciclosporin, Phenytoin, Nifedipine
Familial
AML
Scurvy
Pregnancy
Investigations for post-transplant patient
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
Common indications for Renal Transplant
Diabetic nephropathy
Glomerulonephritis
Polycystic kidney disease
Hypertensive nephropathy
Transplant Assessment
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
Contraindications to Renal Transplant
Active infection
Malignancy
Severe co-morbidity
Failed pre-implantation x-match
Types of Graft
Cadaveric: brainstem death with CB support
Non-heart beating donor: no active circulation
Live-related
Live unrelated
Immunosuppression for Renal Transplant
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)
Complications of Renal Transplant
Post-operative:
Bleeding
Graft thrombosis
Infection
Urinary leak
Rejection
Drug toxicity
Transplant Rejection
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
Ciclosporin toxicity
Calcineurin inhibitor: block IL-2 production
Nephrotoxic, may contribute to organ rejection
Gingival hypertrophy
Hypertrichosis
Hepatic dysfunction
Tacrolimus toxicity
Calcineurin inhibitor: blocks IL-2 production
Less nephrotoxic vs ciclosporin
Diabetogenic
Cardiomyopathy
Neurotoxicity: peripheral neuropathy
Steroid excess
Cushing’s syndrome
Complications of reduced immune function due to immune modulation
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)
Indications for Renal Replacemnt Therapy
GFR<15ml/min AND Symptoms
Psychlogical preparation necessary
Peritoneal vs haemodialysis is a multi-factor decision (med, social, psychological and personal factors)
Complication of Dialysis
20% annual mortality
Cardiovascular disease
Malnutrition
Infection: uraemia –> granulocyte dysfunction –> increased risk of sepsis
Amyloidosis
Beta2-microglobulin accumulation
Carpal tunnel, arthralgia
Renal cysts –> RCC
Mechanism of Haemodialysis
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
Complications of haemodialysis
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
Haemofiltration
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
Mechanism of Peritoneal Dilaysis
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
Advantages and complications of Peritoneal Dialysis
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
Signs of Renal Access on Examination
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
Types of AV fistula
= Surgically created connected between artery and vein
Radio-cephalic at the wrist = Cimino-Brescia
Brachio-cephalic at the elbow
Brachial-basilic
Advantages and Disadvantages of AV Fistula
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
Complications of AV Fistula
Thrombosis
Stenosis
Aneurysm
Infection
Bleeding
Steal syndorme
Steal Syndrome
Distal tissue ischaemia
Presenting as pallor, pain, and reduced pulses
May lead to necrosis
Decreased wrist: brachial pressure index
Mx: banding of fistula
Tesio Line
Advantages and Disadvanatges of Tunnelled Cuffed Cathter for Renal Replacement (Tessio Line)
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
Claddification of Chronic Renal Failure
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
Causes of Chronic Renal Failure
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
Definition of Chronic Renal Failure
Kidney damage for more than 3 months indicated by decline in renal function
Investigations for Chronic Renal Failure
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
Complications of Chronic Renal Failure
CRF HEALS
CRF HEALS
Cardiovascular disease
Renal osteodystrophy
Fluid: oedema
Hypertension
Electrolyte disturbance: hyperkalaemia and acidosis
Anaemia
Leg restlessness
Sensory neuropathy
Renal Osteodystrophy
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
Mechanism of Renal Osteodystrophy
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
Management of Chronic Renal Failure
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
Diabetic Nephropathy
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
Rheumatological Renal Disease
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
Myeloma –> Chronic Renal Disease
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
Renal artery stenosis
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
Signs of Inflammatory Bowel Disease on Examination
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
Investigations for Inflammatory Bowel Disease
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
Complications of UC
Toxic megacolon
Haemorrhage
Malignancy
Colorectal carcinoma
Cholangiocarcinoma
VTE
Complications of Crohn’s
Fistulae
Perianal abscess
Strictures
Malabsorption
Toxic dilatation
True-Love and Witts
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
Extra-intestinal Features of Inflammatory Bowel Disease
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
