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Finals RP > Renal > Flashcards

Renal Flashcards

1
Q

Describe the RAAS system?

A

Angiotensinogen released by liver

RENIN enzyme secreted by kidneys converts Angiotensinogen to Angiotensin I

ACE enzyme secreted by the lungs conversts Angiotensin I to Angiotensin II

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2
Q

What does Angiotensin II do?

A
  • Vasoconstriction at arterioles - this increases calcium in cells
  • Noradrenaline release
  • Aldosterone release by adrenals –> Na reabsorption and K secretion in DCT and collecting ducts
  • ADH release –> increases water reabsorption at collecting ducts
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3
Q

In acute and chronic kidney patients, what should you use to measure function?

A

Acute - Serum creatinine

Chronic - eGFR

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4
Q

What are the three categories for AKI?

A

Pre-renal
Renal
Post-renal

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5
Q

What are the common pre-renal causes of AKI?

A

Anything that reduces blood flow to arteries:

  • Sepsis, Haemmorhage, Hypovolemia, heart failure
  • Renal Artery Stenosis
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6
Q

What are the common Renal causes of AKI?

A

Acute Tubular Necrosis (ATN)

      - Ischaemic ATN
      - Nephrotoxic - aminoglycoside ABs and cisplatin

Acute Intersititial Nephritis (AIN)
- Nephrotoxic - beta-lactam ABs, NSAIDs

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7
Q

what is DRESS syndrome?

A

Drug Rash with Eosinophilia and Systemic Symptoms

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8
Q

What drugs cause DRESS syndrome?

A

Anti-epileptics
Antibiotics - esp B-lactams
Allopurinol

NSAIDs
Captopril

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9
Q

Management of DRESS syndrome?

A

Stop offending drug and give steroids

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10
Q

What are some post-renal causes of AKI?

A

Anything that causes a blockage to outflow, such as tumours, clots, calculi –> causes cytokine release and leukocyte infiltration

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11
Q

Features of AKI?

A

Increased urea in blood causes:
general malaise, lethargy, pruritis, altered mental state, pericarditis

Hyperkalaemia causes:
palpitations, chest pain

Acidosis causes: kussmaul breathing, confusion

Fluid overload causes: oedema, breathless, raised JVP

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12
Q

What are the criteria for diagnosing AKI?

A

Rise in serum creatinine of 26.5 mmol/L or more within 48 hours

1.5x increase from baseline serum creatinine in the last 7 days

<0.5ml/kg/hour urine output for at least 6 hours

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13
Q

Management of AKI?

A

1) Fluid balance chart - consider catheter
2) Review medicines
3) Refer to Nephrologist if unresponsive or requires renal replacement therapy

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14
Q

When to refer for renal replacement therapy?

A

POAU

Potassium
Oedema
Acidosis
Uremia complications - pericarditis, encephalopathy

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15
Q

What is rhabdomyolosis?

A

When skeletal muscle breaks down and releases contents into bloodstream - particularly myoglobin, which is toxic to kidneys

Also causes high potassium and phosphatemia, and lower calcium in blood - as myoglobin binds to calcium and mops it up

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16
Q

Risk factors for rhabdomyolosis?

A

Anything that causes muscle death

Alcohol, DKA, trauma, long lie, compartment syndrome

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17
Q

Features of Rhabdomyolosis?

A

Red-brown urine
muscle pain and swelling
fever, nausea, vomiting

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18
Q

Electrolyte abnormalities in rhabdomyolosis?

A

high potassium and phosphate
low calcium
CK high (5x basline)

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19
Q

Treatment for rhabdomyolosis?

A

FLUIDS! - normal saline or lactated Ringer’s

Correct electrolytes if life-threatening hyperpotassium or hypocalcaemia

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20
Q

When to consider haemodialysis in rhabdomyolosis?

A

If not urinating at all or if no response to fluids first

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21
Q

What is the definition of CKD?

A

Kidney damage for 3 or more months, secondary to structural disorders

eGFR <60 on two separate occasions

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22
Q

Classify CKD based on eGFR

A

Stage 1) Normal/ high >=90

2) Mild reduction 60-90
3a) Mild/Moderate 45-59
3b) Moderate/severe 30-44
4) Severe 15-29

5) Kidney failure <=15 –> transplant or dialysis

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23
Q

KDIGO guidelines also include albumin in urine in CKD stratification.

Classify CKD based on Albuminuria

A

Mild <30 mg/g
Moderate 30 - 300 mg/g
Severe >300mg/g

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24
Q

Which patients should you be careful about eGFR rates as they may not be accurate?

A

Bodybuilders

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25
Q

Which two conditions go hand in hand with CKD?

A

Hypertension and T2DM

26
Q

Other causes of CKD?

A

GN, SLE!

Polycistic kidney disease

27
Q

Ix for CKD?

A

1) Kidney function assessment - eGFR
- no meat in 12 hours before eGFR measurement

2) Blood test and urine dipstick: will show normochromic normocytic anaemia
3) Renal ultrasound - espeically if chance of obstruction

28
Q

Mx of CKD?

A
  • Manage HTN - Ace inhibitors: <140/90
  • Manage cardiovascular risk - statins and antiplatelets
  • If eGFR <30, check for calcium, phosphate, PTH and Vit D levels
  • Manage Anaemia - erythopoetin if needed
  • Manage Oedema - loop dieuretics
29
Q

eGFR can be influenced by?

A

pregnancy, eating red meat, muscle mass

30
Q

What kind of CKD patients need a nephrologist referral?

A

If eGFR falls below 30 or by more than 15 in one year

OR
if ACR ratio >70

31
Q

What do you do with a Post-menopausal woman with iron deficiency anaemia?

A

Refer to gastro for colonoscopy in 2ww!

32
Q

How can CKD cause bone disease?

A

Normally, kidneys hydroxylate Vitamin D into calcitriol which helps absorb calcium

In CKD, kidneys can’t hydroxylate Vitamin D –> low Vit D and low Calcium.

In CKD, kidneys can’t excrete phosphate either –> high phosphate –> high phosphate drags calcium out of bones –> even lower calcium

33
Q

How does CKD affect calcium?

A

CKD –> kidneys can’t hydroxylate vitamin d –> lower calcium and vitamin D

kidneys cant excrete phosphate –> high phosphate and PTH

High PTH causes bone breakdown

= SECONDARY HYPERPARATHYROISISM

Which is the most common type of renal osteodystrophy

34
Q

Management of Renal osteodystrophy?

A

Reduce Phosphate and PTH, and increase calcium and Vit D

  • reduce phosphate in diet
  • phosphate binders - sevelamer or calcichew
  • Add calcium and Vitamin D supplement
  • maybe cinacalcet, calcium mime that reduces PTH levels
35
Q

What is tertiary Hyperparathyroidism?

A

After prolonged Secondary Hyperparathyroidism (and low calcium), adenoma forms in parathryroid gland releasing LOTS of PTH - even if kidney is treated, the PTH gland is autonomous –> surgery

36
Q

What are the two main types of glomerulonephritis?

A

NephrOtic and NephrItic

37
Q

What is Nephrotic syndrome?

A

Triad of:

- ProteinURIA:
        >3g in 24 hours
   or   PCR >300
   or ACR >250
- HypoAlbuminAEMIA: <25g / L
- Oedema

+ Hyperlipidaemia

38
Q

What are the common types of NephrOtic disease?

A
  • Minimal change nephropathy
  • Focal segmental Glomerulosclerosis
  • Membranous Nephropathy
39
Q

What is minimal change nephropathy?

A

Podocyte fusion on electron microscopy

Treat with prednisolone

Good prognosis

40
Q

What is FSGS?

A

Parts of glomerulus damaged

Associated with black people, HIV and heroin users

Treat with steroids and immunosuppressants

Half people go into remission, half progress

41
Q

What would an FSGS biopsy show?

A

IgM deposition

42
Q

What is membranous nephropathy?

A

Most common cause of nephrotic syndrome in adults - idiopathic damage to podocytes

43
Q

What would histology show in membranous nephropathy?

A

“spike and dome” pattern caused by igG deposits enveloped by basement membrane

44
Q

How many people with membranous nephropathy recover?

A

1/3 spontaneous remission
1/3 respond treatment
1/3 end stage disease

45
Q

What are the characteristics of NephrItic syndrome?

A

Haematuria
Hypertension
Proteinuria with oedema

46
Q

Types of NephrItic syndrome?

A

Thin basement membrane disease

IgA nephropathy, or Berger’s disease

Post-strep glomeulonephritis

Rapidly progressing glomerulonephritis

Granulomatosis w polyangiitis

47
Q

What is thin membrane disease?

A

Autosomal dominant, usually presents incidently w microscopic haematuria

  • Fine prognosis, reassure patient
48
Q

What is IgA nephropathy also known as?

A

Berger’s disease

49
Q

What is the classic Berger’s disease patient?

A

Frank haematuria days after a Respiratory or gastro infection

Associated with cirhossis, coeliac/ dermatitis herpetiformis, HSP

50
Q

First and Definitive Investigation for Berger’s?

A

Urinalysis is first

Renal biopsy showing mesangial IgA deposits is definitive

51
Q

What is Henoch Schonlein purpura a variant of?

A

IgA nephropathy

52
Q

What is Post-streptococcal glomerulonephritis (PSGN)?

A

Kidney damage caused by strep virus a week after strep infection

Ix with Anti-streptolysin O titre (ASOT) w low c3

Supportive treatment, good prognosis

53
Q

What is Rapidly Progressing Glomerulonephritis?

A

Aggressive decline in kidney function associated with epithelial crescents

54
Q

What antibody in Goodpastures?

A

Anti-GBM antibodies which bind to Type 4 collagen

55
Q

Investigation for Goodpastures?

A

Biopsy shows IgG deposits

56
Q

Treatment for Goodpastures?

A

Plasmapheresis to remove antibodies

- Steroids and Immunosuppressants

57
Q

Types of RPGNs?

A

Type 1 = goodpastures
Type 2 = Immune complex: SLE, PSGN
Type 3 = Pauci-immune: Microscopic pol, Churg- Strauss, Gran w Pol,

58
Q

What antibody in Gran w Pol?

A

cANCA

59
Q

What is Gran w Pol?

A

systemic vasculitis that causes inflammation of small and medium vessels

60
Q

Features of Gran w Pol?

A

Haemoptysis, otitis, nose-bleeds, rashes

Saddle shaped nose

Conjuctivitis, episcleritis

61
Q

Treatment for Gran w Pol?

A

Induce remission with steroids and
Cyclophosphamide or 2nd line rituximab (if fertility needed)

+ give ergocalciferol + alendronate/risendronate for osteoporosis prophylaxis cos of the steroids

Finals RP (11 decks)

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