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Phase 2a > Renal > Flashcards

Renal Flashcards

1
Q

What is acute kidney injury?

A

A significant deterioration in renal function

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2
Q

What causes AKI?

A

Pre-renal: hypoperfusion (severe drop in BP) - ischaemia, sepsis, drugs, cardiogenic shock
Renal: intrinsic renal disease - glomerulonephritis, infection, drugs
Post-renal: obstruction to urine flow - benign prostatic hyperplasia

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3
Q

How does AKI present?

A

Oliguria, pulmonary oedema, fatigue, shortness of breath

Hyperkalaemia - medical emergency

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4
Q

How is AKI diagnosed?

A

Blood: elevated serum urea an creatinine (>50%)
Decrease in urine output
Imaging

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5
Q

How is AKI managed?

A

Hypovolaemia - give crystalloid for volume replacement
Hypervoleaemia - fluid restriction and diuretics
Treat sepsis, stop NSAIDs, ACEi
Consider gastroprotection (H2 antagonist and PPI)

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6
Q

What is chronic kidney disease?

A

Irreversible loss of nephrons

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7
Q

What classifies CKD?

A

GFR <15 is kidney failure

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8
Q

What are some abnormalities of kidney function/structure?

A

Decreased glomerular filtration rate (GFR)
Increased albuminuria
Urinary sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders

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9
Q

What are some causes of CKD?

A

Acute renal failure, hypertension, diabetes, kidney disease e.g. PKD

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10
Q

Describe the pathology of CKD

A

Injury may primarily affect glomeruli or vessels but eventually it leads to reduction in nephron mass with reduction in renal function.
The reduction in nephron mass then causes haemodynamic stress in remaining nephrons, leading to further nephron loss.

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11
Q

How does CKD present?

A

Early disease is asymptomatic
Loss of appetite, fatigue, bone pain
End-stage renal failure - fluid overload and metabolic derangement (vomiting and diarrhoea)

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12
Q

How is CKD diagnosed?

A

Bloods - glucose, increased PTH, low calcium
Urine dipstick - albumin:creatinine ratio
Imaging - US for size and to exclude obstruction

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13
Q

How is CKD renal disease progression slowed?

A

Target to lower blood pressure, offer treatment with renin-angiotensin system antagonist (ACEi)

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14
Q

How are renal complications of CKD managed?

A

Anaemia: treat underlying cause
Acidosis: consider sodium bicarbonate supplements
Oedema: restrict fluid and sodium intake
CKD bone mineral disorders: give vitamin D supplements

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15
Q

What are the 2 biggest complications of CKD?

A

CVD due to hypertension, vascular calcification and hyperlipidaemia - patients more likely to die of CVD than need RRT
Renal bone disease (hyper-parathyroid bone disease, osteomalacia and osteoporosis)

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16
Q

What is renal replacement therapy?

A

Haemodialysis, peritoneal dialysis, haemofiltration

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17
Q

What symptoms of renal failure indicate the need for long-term dialysis?

A

Inability to control volume status or blood pressure
Acid-base or electrolyte abnormalities
Cognitive impairment

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18
Q

What is haemodialysis?

A

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction.
Access if via an AV fistula
3+ times a week

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19
Q

What is peritoneal dialysis?

A

Uses the peritoneum as a semi-permeable membrane. Catheter is inserted into the peritoneal cavity and fluid infused. Solutes diffuse slowly across.
Continuous process with intermittent drainage and refilling at home

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20
Q

What is haemofiltration?

A

Water cleared by positive pressure, dragging solutes into the waste by convention. The ultra filtrate is replaced with an appropriate volume of clean fluid

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21
Q

What are the complications of RRT?

A

CVD: increased BP, calcium/phosphate disregulation

Renal bone disease, infection

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22
Q

What immunosuppression is provided at the time of a kidney transplant?

A

Monoclonal antibodies e.g. daclizumab

23
Q

What is polycystic kidney disease?

A

An inherited disorder in which clusters of cysts develop primarily within your kidneys, causing your kidneys to enlarge and lose function over time

24
Q

What causes polycystic kidney disease?

A

Inherited mutation in PKD1 gene. Defects in the function of the PKD1 protein lead to cystic change in renal tubules and loss of normal renal tissue

25
Q

How does polycystic kidney disease present?

A

Hypertension, flank pain, haematuria, renal calculi

26
Q

How is polycystic kidney disease diagnosed?

A

USS, genetic testing, CT for renal colic as cysts obscure view on ultrasound

27
Q

How is polycystic kidney disease managed?

A

Water intake 3-4L/day suppresses cyst growth, treat high BP (ACEi), severe pain - cyst decompression

28
Q

What is renal colic?

A

A type of pain you get when urinary stones block part of your urinary tract

29
Q

What are the features of renal colic?

A

Rapid onset - woken from sleep
Pain from upper UT obstruction from loin to groin
Associated with nausea and vomiting
Often cannot lie still - patient writhing in pain from excruciating ureteric spasms

30
Q

What is glomerulonephritis?

A

Inflammation and damage to the glomeruli that allows protein +/- blood to leak out into the urine

31
Q

What are the features of glomerular disease?

A 
Caused by pathology in the glomerulus
Present with proteinuria, haematuria
Diagnosed on a renal biopsy
Cause CKD
Can progress to kidney failure
32
Q

How does glomerulonephritis present?

A

Acute nephritis syndrome, nephrotic syndrome, chronic kidney disease

33
Q

How is glomerulonephritis diagnosed?

A

Renal biopsy is required for diagnosis

34
Q

What is IgA nephropathy?

A

Immune complex GN related to glomerular deposition of immune complexes containing IgA
Causes acute nephritis syndrome

35
Q

What causes IgA nephropathy?

A

Primary - abnormal mucosal immune system

Secondary - IgA deposited in glomeruli, associated with liver/ bowel disease

36
Q

How does IgA nephropathy present?

A

Asymptomatic non-visible haematuria, episodic visible haematuria, high BP

37
Q

How is IgA nephropathy diagnosed?

A

Renal biopsy - IgA deposition in mesangium

38
Q

How is IgA nephropathy treated?

A

ACE inhibitors - reduce BP and protein in the urine

39
Q

What is nephrotic syndrome?

A

Proteinuria due to podocyte pathology

40
Q

What is the classic triad of nephrotic syndrome?

A

Proteinuria >3.5g/24 hours
Hypoalbuminemia
Oedema

41
Q

What causes nephrotic syndrome?

A

Primary renal disease e.g. membranous nephropathy, or secondary causes e.g. DM, lipid nephritis

42
Q

How does nephrotic syndrome present?

A

Oedema of ankles, genital, abdominal wall

Hypoalbuminaemia, frothy urine, systemic symptoms

43
Q

How is nephrotic syndrome diagnosed?

A

Establish cause via renal biopsy, urine dipstick shows high protein, serum albumin is low

44
Q

How is nephrotic syndrome managed?

A

Reduce oedema - fluid and salt restriction, loop diuretics
Reduce proteinuria - ACEi / ARB
Treat underlying cause and complications

45
Q

What are the features of minimal change disease?

A

Loss of podocyte foot processes, vacuolation and appearance of microvilli in the glomerulus
Does not progress to renal failure

46
Q

How is minimal change disease diagnosed and managed?

A

Electron microscopy shows abnormal podocytes (biopsy)

Steroids (prednisolone), second line is cyclophosphamide

47
Q

What is acute nephritic syndrome?

A

Loss of blood in the urine due to damage of the glomeruli in the kidney

48
Q

What is nephritic syndrome characterised by?

A

Haematuria, proteinuria, hypertension and oedema.

Low volume of urine

49
Q

What are the features of focal segmental glomerulosclerosis?

A

Nephrotic syndrome. Primary (genetic) or secondary (HIV)

Diagnosis: Ab tests all -ve. Glomeruli develop sclerosed lesions.

50
Q

How is focal segmental glomerulosclerosis managed?

A

Salt restriction and diuretics to reduce oedema
Antihypertensives
Statins - treat hyperlipidaemia
Transplant

51
Q

What are the features of Membranous glomerulonephritis?

A

Nephrotic syndrome. Slowly progressive. Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins.

52
Q

How is Membranous glomerulonephritis diagnosed?

A

Microscopic analysis shows thickened glomerular basement membrane
Immunofluorescence shows diffuse uptake of IgG

53
Q

How is membranous glomerulonephritis managed?

A

Steroids if disease progresses

Phase 2a (16 decks)

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