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SBOMS > Kidney disease > Flashcards

Kidney disease Flashcards

1
Q

Most common cause of CKD?

A

Diabetes

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2
Q

Main key functions of the kidneys?

A 
Waste excretion
Acid/base balance
Salt/water homeostasis
BP control
Glycaemic control
Secretion of hormones (e.g. EPO)
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3
Q

Organs that undergo gluconeogenesis?

A

Liver

Kidneys

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4
Q

Most common cause of AKI?

A

Ischaemia

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5
Q

Different pathogenic factors leading up to CKD?

A 
Glomerulosclerosis
Tubular Atrophy
Interstitial fibrosis
Loss of renal mass
Loss of renal function?
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6
Q

What is one of the most important factors that determines kidney damage when ultrasounding the kidneys?

A

Kidney size

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7
Q

Mechanisms of CKD progression?

A

Haemodynamic:

  • RAAS pathway
  • Hypertensive vascular damage

Inflammatory:

  • Pro-fibrotic cytokines
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8
Q

Mode of action of CKD in terms of glomerular function? How do ACE inhibitors and AR antagonists work to prevent this?

A

Glomerulosclerosis leads to loss of number of functioning glomeruli, leads to increased blood flow to remaining nephrons, this then leads to intraglomerular hypertension and more glomerulosclerosis.

ACE inhibitors prevent the increased intraglomerlar hypertension

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9
Q

Risks of using a ACE inhibitor in someone with hypertension caused by disseminated atheroma?

A

Will decrease renal perfusion to the point of AKI

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10
Q

one important molecule associated with the inflammatory pathway in CKD?

A

TGF-β

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11
Q

Process of inflammation in CKD?

A

Mechanical vascular stretching and Angiotensin II lead to increased TGF-β

Plasminogen activator inhibitor 1 expression that leads to:

  1. abnormal matrix deposition
  2. decreased NO

Decreased NO leads to hypertension, Proteinuria and interstitial fibrosis.

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12
Q

Effects of CKD?

A

Reduced GFR

  • Retention of nitrogenous waste products
  • Hyperphosphataemia
  • Salt/Water retention (oliguria)

Impaired Tubular function

  • Disturbed fluid balance (polyuria)
  • Acidosis and hyperkalaemia

Hormonal deficiency

  • Anaemia (EPO)
  • Vit D deficiency, hyperparathyroidism (calcitriol)
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13
Q

As pH goes up what does potassium do?

A

Goes down

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14
Q

Why do CKD patients have anaemia?

A

Iron deficient:

  • Diet
  • Occult GI loss

Chronic disease:

  • EPO deficiency
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15
Q

Treatment of anaemia in CKD?

A

Parenteral iron
recombinant EPO replacement
HIF stabilisers

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16
Q

Examples of features of chronic kidney disease mineral bone disorder (CKD MBD)?

A

Periosteal reabsorption
Browns tumour
Tumoral Calcinosis

17
Q

What causes CKD MBD?

A

Failure of the phosphate and calcium regulation system, regulated in the kidneys in part by calcitriol.

18
Q

Pathogenesis of CKD MBD?

A

on diagram

Decreased calcitriol causes decreased GI calcium absorption. (and increased PTH itself)

This leads to a reduction in serum calcium and this increases the production of PTH:

Increased PTH:

  1. causes an increase in calcitriol production (leading to increased serum calcium and decreased potassium)
  2. Causes the resportion of calcium and phosphate from bone to release it into the bloodstream

Leads to increased serum Ca++ and increased serum phosphate.

With the passage of time the parathyroid gland becomes hyperplastic and pathogenically releases PTH irregardless of the calcium levels in the bloodstream

19
Q

Management of CKD MBD?

A

Vit D replacement

Dietary Phosphate restriction

Phosphate binders

Calcimimetics

Parathyroidectomy

20
Q

GFR of end-satge renal disease?

A

About 5

21
Q

Management of end-stage renal disease?

A

Conservative management
Dialysis (replacement therapy)
Transplantation

22
Q

Types of renal replacement therapy?

A

Haemodialysis

Peritoneal dialysis

23
Q

What are the aims of haemodialysis

A

Remove nitrogenous waste

Correct imbalances in:

  • Serum electrolytes
  • Hydration status
  • Acid/Base
24
Q

What does haemodialysis not do?

A

Correct hormonal imbalances

Avoid cardiovascular risk associated with CKD

25
Q

Two factors that cause movement of waste products in dialysis?

A

DIffusion from blood to diasylate

Ultrafiltration: H2O essentially being pumped through the semi permeable membrane dragging other waste products with it.

26
Q

Risks of peritoneal dialysis?

A

The two fluids can equilibrate and the body can absorb teh waste products it was previously excreting.

27
Q

Advantages of peritoneal dialysis?

A

User friendly

Can be done anywhere by someone who knows how to

28
Q

Genes responsible for Polycystic kidney disease?

A

Pkd 1 and 2

29
Q

Who is eligible for kidney transplantation?

A

Progressive irreversible kidney failure

No current infection

No current malignancy

Proof of compliance with treatment

Life expectancy without a transplant of

30
Q

What do you assess for when seeing someone for renal transplant?

A

Vessel quality

Space

History and examination - fit enough

31
Q

Types of Renal donors?

A

Cadaveric organ:

  • Brainstem death (heart beating)
  • Cardiac death donor (non-heart beating)

Live donation

32
Q

If a potential donor is ABO incompatible, what are the options?

A
  1. Do a ABO incompatible transplant (push receivers immune system so that it will not reject organ) - remove antibodies etc
  2. paired/sharing scheme, gives to someone else who has a compatible kidney.
33
Q

If a donor has several renal arteries does this make them less suitable for a transplant, why?

A

Yes it does, will increase risk for patient as have to do more ‘plumbing’ in surgery

34
Q

Risks to surgery?

A

Excess bleeding

Thrombosis

Collections - form around kidney, lymphatic leakage.

Infection

Ureteric complications (leak, stenosis)

Kidney may not work

35
Q

How is immunosuppression obtained following transplant?

A

Steroids

Calcineurin inhibitors - inhibit IL2

Antiproliferative agent - MMF

Sometimes an induction agent

SBOMS (18 decks)

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