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Gen Med > Renal > Flashcards

Renal Flashcards

1
Q

Under microscopy muddy brown casts are found in a patients urine who has just fractured their right tibia and had a fasciotomy what is the diagnosis

A

Acute tubular necrosis

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2
Q

What type of injury to the kidney is likely to occur from drug toxicity

A

acute interstitial nephritis

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3
Q

When the anion gap is raised it suggests increased production or reduced excretion of acids what are the differentials

A

Lactate - sepsis, ischaemia
Urate - renal failure
Ketones - DKA
Drugs/toxins - salicylates, methanol, ethylene glycol

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4
Q

What are the causes of a metabolic acidosis with a normal anion gap

A

Due to increase Hydrogen ions or due to loss of bicarb

  • renal tubular acidosis
  • diarrhoea
  • Addisons disease
  • pancreatic fistula
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5
Q

How are the different stages of CKD classified

A

Stage 1: eGFR 90+ normal kidney function however urine findings, structural abnormalities, genetic trait
Stage 2: 60-89 - mildly reduced kidney function and other findings to point towards kidney disease
Stage 3A 45-59 - moderately reduced kidney function
Stage 3B 30-44
Stage 4 15-29 - severely reduced kidney function
Stage 5: <15 or on dialysis - very seveve/end stage kidney failure

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6
Q

When is albumin:creatinine ratio used

A

Assessed as a yearly marker of CKD

Useful in diabetic patients

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7
Q

What are some of the causes of CKD

A

Renal: automsomal dominant polycystic kidney disease
Glomerulonephritis - IgA, SLE, Vasculitis
Chronic Pylonephritis

infections: HIV

Drugs: NSAIDs, Tobacco

Systemic causes:

  • SLE
  • HTN
  • RA
  • Diabetes

Idiopathic
Rare: AKI that becomes chronic
Chronic interstitial nephritis

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8
Q

Why do patients with CKD get anaemia

A

Decreased production of erythropoietin which leads to a decreased production of RBC
so less oxygen being carried in the blood because less RBC –> anaemia

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9
Q

WHy do patients with CKD get hypocalcaemia

A

Kidney normally activates vitamin D when its damaged it is unable to do this
so less Calcium reabsorbed therefore less calcium in the blood causing HYPOCALCAEMIA
This then activates the Parathyroid gland to make more PTH
Calcium is then lost from the bone due to increased PTH
Causes bone to become weaker
RENAL OSTEODYSTROPHY

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10
Q

What are the symptoms of high urea

A

Nausea and loss of appetite
Encephalopathy - asterixis - tremor of hand - leads to coma and death
Pericarditis
Bleeding - platelets less likely to adhere to each other

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11
Q

How does hypertension lead to kidney damage

A

Hypertension causes damage to renal artery wall leading to thickening of the wall –> less blood flow
Therefore there is reduced blood flow and oxygen to the kidney causing ischaemic injury
Ischaemic injury then causes immune cells to be recruited and form extracellular matrix around the mesangial cells –> causes glomerulosclerosis which decreases eGFR further

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12
Q

Why is CKD does hypertension get worse

A

Less fluid enters the kidney, reduced perfusion so reduced pressures at juxtaglomerular apparatus causing an increase in Renin and activation of RAAS therefore increasing BP

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13
Q

How is CKD treated

A

Manage hypertension
Smoking cessation
Lifestyle changes - healthy diet, exercise
Stop nephrotoxic drugs - caution in use of NSAIDs
Treat underlying cause
Treat symptoms and complications
anaemia -> Fe, B12, folate, EPO replacement
Oedema -> furosemide, control fluid intake
Acidosis -> oral bicarb
Osteoporosis -> bisphosphonates, Vit D, calcium

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14
Q

What are the complications of Chronic Kidney disease

A 
Hyperkalaemia 
Hypocalcaemia 
Uraemia - pericarditis, encephalopathy, bleeding, nausea and vomiting 
Restless legs 
Osteoporosis 
Anaemia 
Acidosis 
Oedema - fluid not being excreted 
Hypertension
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15
Q

What are the indications for dialysis

A
  1. Hyperkalaemia not able to be medically managed
  2. Metabolic acidosis
  3. pulmonary oedema
  4. Uraemic encephalopathy
  5. Uraemic pericarditis

Also:
- toxins - methanol, lithium
other electrolyte abnormalities

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16
Q

What do patients need to be one when having haemodialysis

A

Anticoagulants

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17
Q

What do patients need in order to have haemodialysis

A

An AV fistula

18
Q

What is an AV fistula

A

fistula between a peripheral artery and vein
palpation = feel a thrill
Listen = bruit
in non-dominant arm

19
Q

What are the pros an cons of an AV fistula

A

Pros:

  • decreased infection
  • increased blood flow rates
  • decreased risk of thrombosis

Cons:

  • Aneurysm
  • wall of vein is weakened by repeated insertion of needles
  • can become blocked
  • excessive bleeding can occur due to high volume of blood
20
Q

What are the complications of haemodialysis

A

Hypotension
Nausea
Headaches
Cardiac arrhythmias/cardiovascular instability
Air embolism
Access related: local infection, endocarditis, osteomyelitis, creation of stenosis, thrombosis, aneurysm
Dialyser reactions: anaphylaxis to sterilising agents
Heparin induced thrombocytopenia

Also limits holidays, fluid and diet restrictions

21
Q

How is peritoneal dialysis done

A

Dialysate is infused into peritoneal cavity and blood flowing through acts as blood source
Ultrafiltration is controlled by altering the osmolality of dialysate solution - can be achieved by using glucose or other large molecules

22
Q

What are the contra indications for peritoneal dialysis

A 
Hernias
Respiratory disease 
intestinal disease e.g. Crohns and UC 
Obesity 
Abdominal wall stoma 
intra-abdominal adhesions
23
Q

What are some of the complications of peritoneal dialysis

A 
Peritonitis - strep epidermidis or staph aureus (coagulase negative staphylococci)
Sclerosing peritonitis 
Catheter problems 
Constipation
Fluid retention 
Hyperglycaemia 
Weight gain 
hernias 
Back pain 
Malnutrition 
Depression - reduced quality of life
24
Q

How would nephritic syndrome present

A

haematuria - due to RBC entering filtrate - cola coloured urine
hypertension - salt and water retention
Blurred vision, possible oedema as a result of hypertension

25
Q

How may CKD present

A

Renal colic - chronic stone may be the cause
Uraemic symptoms - nausea, vomiting, loss of appetite, restless legs, fatigue, pruritus
Bone pain
Difficulty breathing on lying down - nocturnal dyspneoa
May have diabetes symptoms
uraemic tinge to skin - slightly yellow
Purpura
Raised BP
Signs of diabetes
Signs of fluid overload - peripheral oedema, left ventricular dysfunction
Ballotable, polycystic kidneys

26
Q

How would you investigate for CKD

A 
Bedside: Urine dip, ECG (to rule out cardiac issues if presenting with peripheral oedema)
BP
Bloods 
- U+Es 
- eGFR and albumin:creatinine ratio 
- FBC - may show anaemia 
- Blood glucose and HbA1c 
- Bone profile - calcium and phosphate 
- PTH 
- LFTs for albumin - may be low in nephrotic syndrome

Imaging
- Ultrasound of kidneys - usually small in CKD

Consider biopsy if cause unknown

27
Q

What are the contra indications for renal transplantation

A

Cancer - may be considered if >5 years
Active infection
Comorbidities

28
Q

Which drugs are given in renal transplantation at induction and in maintenance

A

Induction: anti-Il2 monoclonal antibody - basiliximab
Alemtuzab
Maintenance therapy:
- calcineurin inhibitor –> Cyclosporin or tacrolimus
- Antimetabolite –> mycophenolate mofetil or azathioprine
- corticosteroid –> prednisolone

29
Q

What are some post op problems of renal tansplantation

A

ATN of graft
Thrombosis
urine leakage
UTI

30
Q

What is the pathophysiology behind nephritic syndrome

A

Inflammation of the glomeruli leading to podocyte damage allowing proteins and RBC to enter the filtrate

31
Q

How is nephritic syndrome investigated

A

Bedside: Urine dip
BP
MSU for urine culture - microscopy may show red cell casts

Bloods

  • FBC - anaemia, inflammatory markers
  • CRP
  • U+Es and eGFR for renal function
  • LFTs
  • blood glucose and HbA1c
  • Autoantibody testing

Kidney biopsy may be considered

32
Q

What are some of the autoimmune causes of nephritic syndrome and how would they be investigated

A

IgA nephropathy - immunoglobulins
Myeloma - light chains and Bence-Jones proteins (serum and urine electrophoresis)
Serum Complement
- low in SLE
- low in some primary glomerulonephritis
- low in cryobulinaemia
Autoantibodies
- ANA and Anti-dsDna in SLE
- pANCA - associated with Churg-Strauss
- cANCA - associated with granulomatosis with polyangiitis
- Anti glomerular basement membrane - Good pastures

Imaging

  • Renal ultrasound
  • CXR - churg-strauss and good pastures affects the lungs

Renal biopsy

33
Q

How is nephritic syndrome treated

A 
Restrict fluids and salts until levels are normal
Corticosteroids to reduce inflammation
Avoid NSAIDs - further damage 
Loop diuretics if oedema 
May need haemodialysis 
May need abx for infective cause 
Immunosuppression for autoimmune causes
34
Q

How does nephrotic syndrome present

A

Proteinuria - frothy urine
Hypoalbuminaemia - leukonycia
Oedema - reduced oncotic pressure
Hypercoagulability - more likely to get DVT
Recurrent infection, general fatigue - patients lose immunoglobulins in urine
Xanthoma and xanthalasma - dyslipidaemia

35
Q

What is the pathophysiology behind nephrotic syndrome

A

Inflammation of glomeruli leds to leaks or larger substance into filtrate such as proteins

36
Q

What are some causes of nephrotic syndrome

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy - most common cause in adults

Secondary causes 
Amyloidosis 
Diabetic Nephropathy 
Drugs: NSAIDs, pencillamine, Gold, Anti-TNF
HIV
Hep B or C
SLE
37
Q

How would you investigate nephrotic syndrome

A 
Bedside obs - Urine dip, BP, Urine sample for Microscopy, BM
Bloods 
- FBC 
- CRP
- U+Es and eGFR 
- LFTs - rule out liver damage due to low albumin
- Clotting - may have deranged clotting 
- Screen for Hep B, C and HIV 
- blood glucose and HbA1c

Imaging

  • USS abdo-renal
  • CXR –> amyloidosis also affects lungs, also to look for cardiomegaly

Renal biopsy - is diagnostic may affect treatment but not always necessary

38
Q

How is nephrotic syndrome treated

A

Monitor weight - for fluid loss
Salt and fluid restrictions with high dose diuretics to move the fluid
Steroids - most nephrotic syndromes are steroid responsive
ACE inhibitors or angiotensin
Anticoagulation may be relevant as prophylaxis for possible DVT or PE due to deranged clotting
Cyclophosphamide and ciclosporin in autoimmune cases such as SLE and RA

39
Q

What is glomerulonephritis

A

Group of disease which cause inflammation to the glomeruli causing it to become damaged allowing the leak or proteins and/or rbc out into the filtrate
May present with either Nephrotic or Nephritic syndrome

40
Q

What are the causes of a unilateral small kidney

A

Vascular: Renal artery stenosis with ischaemia
Infection: Chronic Pyelonephritis, TB
Obstructive renal atrophy
Congenital: Congenital hypoplastic kidney

41
Q

How is diabetic nephropathy managed

A

Optimise diabetes management
Smoking cessation
Check blood glucose and HbA1c
Control BP
ACE inhibitors - use with caution in pts with peripheral arterial disease, renovascualr disease and reduced eGFRs
Measure albumin and creatinine ratio more frequently e.g six monthly

Gen Med (10 decks)

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