Lec 5- Acute and Chronic Kidney disease Flashcards

1
Q

Chronic kidney disease (CKD)

A
  • Describes abnormal kidney function and or structure
  • Common, but frequently unrecognised and often exists together with other conditions
    • CVD and diabetes- most at risk
  • Risk increases with age due to less functioning nephrons
  • Usually asymptomatic but detectable
  • Treatment can
    • Prevent or delay progression
    • Reduce or prevent the development of complications
    • Reduce the risk of CVD
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2
Q

CKD causes

A
  • Diabetes- high glucose cause nephron death- sclerosis
  • HTN- increase thickening of blood vessels- increase renal BP- activate RAAS further increasing pressure= nephron damage and death
  • Hyperlipidaemia
  • Infections/inflammation-
  • Genetic/structural abnormalities- polycystic kidney syndrome
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3
Q

CKD complications

A
  • Renal bone disease
  • Renal anaemia
  • Hyperphosphateaemia
  • Worsening co-morbidities e.g. HTN, diabetes and CVD
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4
Q

Classification of CKD

A
  • ACR needs to be done to diagnose CKD
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5
Q

Signs and symptoms

A
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6
Q

Aims of CKD treatments

A
  • Reverse or stop the process responsible for CKD (Identify the cause and treatment)- main treatment is control of BP
  • Relive symptoms
  • Treat complications
  • Reduce CV morbidity and mortality
  • Prevent further renal damage
    • Control BP
    • Control proteinuria
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7
Q

Monitoring ACEI

A
  • Pre-therapy: Baseline creatinine and K+
  • Start low and titrate
  • Doubling the dose every 1–2weeks.
  • Monitor creatinine, potassium and BP after each upward titration
  • Do not increase the dose further if there is worsening renal
  • If Cr rise >30%, then repeat the test, rule out volume depletion or other nephrotoxic drugs. If K> 6 rule out causes before stopping
  • BP target:
    • HTN, CKD and an ACR less than 70mg/mmol:
    • Systolic blood pressure less than 145/90mmHg (target systolic range lower the better)
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8
Q

Management of CKD

Symptoms and complications of advanced CKD

A
  • Anaemia
  • Osteodustrophy (Hypocal/phosphaturia, Vit D deficiency and Hyperparathyroidism)
  • Fluid retention
  • Pruritus
  • Neurological problems (restless legs)
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9
Q

Anaemia

A
  • Damage of peritubular cells = inadequate secretion of erythropoietin
  • Erythropoeitinproduced mainly by the kidney
  • Regulator of red cell proliferation and differentiation
  • Shortened red cell survival
  • Marrow suppression by uraemic toxins
  • A major cause of:
    • Fatigue, breathlessness, lethargy and angina.
    • Patients complain of feeling cold,
    • poor concentration, reduced appetite and libido
  • Treat with erythropoietin stimulating agents
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10
Q

Anaemia (Erythropoetins)

A
  • Human recombinant erythropoietin.
  • Hormone to boost red blood cell production.
  • Different types
    • Biosimilars
  • Target Hb: 100 to 120g/L
  • Relieve symptoms, avoid the need for blood transfusions
  • Correct iron, B12 or folate deficiency
  • CAUTION
    • Overcorrection of Hb can increase risk of death and serious cardiovascular events
    • Cause HTN, hyperkalaemia and thromboses
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11
Q

Hyperphosphataemia

A
  • A decline in renal function reduces phosphate excretion
  • Typically asymptomatic.
    • Can cause bone and joint pain, rash, pruritus
  • Dietary advice
  • Phosphate binders- chelates phosphate, take with food
    • Reduce absorption of orally ingested phosphate in the gut
    • Form insoluble, non-absorbable complex
    • Take a few minutes before food or with a meal
    • Calcium acetate (calcification of heart and nephrons), Sevelamer Lanthanum
    • Tablet burden/GI side effects •Aim:–0.9-1.5mmol/l in CKD stage 3b, 4 or 5 not on renal replacement therapy (RRT)–<1.8mmol/L if on RRT
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12
Q

Bone disease (Renal Osteodystrophy)

A
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13
Q

Bone disease

A
  • Monitor Ca2+ levels
  • Treat with synthetic Vit D analogues
    • Vit D requires hydroxylation in the kidney to become active
    • Alfacalcidol (0.25mcg to 1mcg/day) or calcitriol (1-2mcg/day)
    • Calcium carbonate
    • Increase calcium absorption and suppresses parathyroid gland
    • Parathyroidectomy
    • Clinical- calcium mimetic
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14
Q

Other symptoms and treatment

A
  • ITCH- Excess urea in the blood
    • A common complaint, often worse at night
    • Antihistamines (Chlorphenamine) topical (crotamiton
    • Phosphate control
  • LEG CRAMPS/RESTLESS LEGS
    • Unpleasant (Burning, creeping, tugging or like insects crawling inside the legs)
    • Occurs at night
    • Clonazepam, haloperidol, carbamazepine, pramipexole, ropinirole, rotigotine•H2antagonists / PPIs
  • NAUSEA
    • Accumulation of urea and other toxins
    • Anti-emetics (cyclizine, metoclopramide, ondansetron and prochlorperazine or dialysis)
  • OEDEMA
    • High dose diuretics (furosemide, bumetanide)
    • Thiazides (metolazone)
    • Fluid restrict- help control oedema due to excess fluid
  • ACIDOSIS–Oral sodium bicarbonate (1-6g/day)
  • PPI- urea can cause GI bleeds
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15
Q

End-stage renal disease

A
  • When life can only be sustained by dialysis or transplantation
  • Options
    • Haemodialysis
    • Peritoneal dialysis
    • Transplant
    • Palliative care (Conservative management)
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16
Q

Renal replacement therapy

A
  • Remove uraemic toxins
  • Removes fluid resistant to diuretics
  • Correct acid-base imbalances and electroyltes
  • Two types
    • 1) Haemodialysis
  • Does what a kidney does: remove toxins and correct acid balance
17
Q

2) Peritoneal dialysis

A
  • Peritoneal membrane is the main membrane for diffusion
  • Max use (5 years)
  • Prone to infection by culturing peritoneal fluid
18
Q

Pain

A
  • Oxycodone 1.25-2.5mg six hourly
    • Start with low doses and extended dose interval and titrate according to response
    • Limited accumulation of metabolites in renal impairment vs morphine, codeine (accumulation)
  • Pethidine
  • AVOID!!!
  • Use less renally excreted options
    • Oxycodone
    • Fentany
    • Hydromorphone
  • NSAIDs–AVOID Unless (?? end stage)
19
Q

Drugs in renal replacement therapy

A
  • Is the drug removed by dialysis or hemofiltration
  • If drug removal is significant would you
    • Increase the dose
    • Decrease
  • Think about timing in relation to dialysis
  • What is the drug is not removed
  • Consider newly prescribed medicines and pre-admission medicines
20
Q

Summary AKI v CVD

A