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GERR Semester 1 > AKI And CKD > Flashcards

AKI And CKD Flashcards

1
Q

Difference between AKI and CKD

A

AKI- decrease in GFR which usually occurs within hours to weeks and is usually reversible

CKD is chronic kidney disease in which GFR is decreased over the course of over 6months, and is usually irreversible

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2
Q

Renal function is measured by…

A

Serum creatinine (U+E test)
Urination rate per hour
GFR (estimated through the serum creatinine value)

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3
Q

Causes of acute kidney injury AKI (pre, renal and post)

A

Pre renal AKI- caused by impaired perfusion (Shock)

Renal AKI- injury to the glmoeruli and tubules

Post renal AKI- caused by obstruction to urine excretion

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4
Q

Causes of shock

A

Hypovolemia

Sepsis = vasodilation=hypotension

Cardiac failure= ↓ blood output= ↓ perfusion

Embolis (obstruction to renal artery)

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5
Q

Body’s response to ↓ GFR and perfusion

A

Macula densa cells sense ↓ perfusion

JG apparatus

Renin release

Angiotensin II release with aldosterone = vasoconstriction and retention of sodium and water

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6
Q

Effect of the afferent arteriole and efferent arteriole in AKI

A

Vasodilation due to prostaglandins (afferent)

Vasoconstriction due to Ang II (efferent)

↑ resistance = ↑ pressure = ↑ GFR

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7
Q

Aldosterone effect on the kidneys

A

Causes the ↑ uptake of sodium ions in the DCT, causing ↑ water retention as a result which ↑ blood volume and rectifies any ↓ in BP

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8
Q

Features in prerenal AKI

A

↑ Na+ and water reabsorbtion

↑ urine osmolality

↑ urine specific gravity

↓ urine production

↓ fractional excretion of Na+

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9
Q

Renal AKI definition (ATN- acute tubular necrosis)

A

Inability of tubular cells to reabsorb/filter due to cell death, as a result of poor perfusion or toxicity

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10
Q

What causes poor perfusion in ATN acute tubular necrosis

A

Surgery

Hypotension

Sepsis= vasodilation = ↓ perfusion

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11
Q

What does ATN result in

A

↓ Na+ H2O reabsorption = ↓ volume of ECF

↓ urine osmolality

↑ urine output (damage to tubular cells = ↓ reabsorbtion of H2O)

↑ fractional Na+ excretion

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12
Q

Signs of Acute Tubular necrosis

A

↑ sodium in urine
↑ urine due to lack of reabsorption

Hyperkalemia (no swapping g with Na+)

Metabolic acidosis (H+ rentention and no secretion of HCO3- ions)

↓ GFR = fluid overload (oedema, pulmonary oedema)

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13
Q

Causes of renal toxicity

A

Radiocontrast dye

DAMN drugs

Myoglobin from muscles, which results from crush injuries

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14
Q

Post renal AKI definition

A

Obstruction to urinary excretion due to stones, ↑ prostate size or ureter tumour

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15
Q

Treatment of post renal AKI

A

Check for catheter
Add catheter if necessary, check the obstruction isn’t above this

Treat underlying cause, stones, prostate enlargement or tumour

Treat UTI/ Prevent

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16
Q

What kills patients with AKI

A

Hyperkalemia - ATN, no excretion in urine= ventricular fibrillation

Metabolic acidosis - ↓ excretion of H+ and lack of HCO3- reabsorbed

Pulmonary oedema- ↓ homeostatic control of fluid

17
Q

Treatment of kidney failure

A

IV fluids

Avoid DAMN drugs

Treat hyperkalaemia

O2
Treat sepsis if there

18
Q

Chronic kidney disease definition

A

Decrease in GFR which occurs over months or years and is usually irreversible

19
Q

Measurement of renal function

A

Serum creatinine (u and e blood test)

GFR (estimated through the serum creatinine)

20
Q

Symptoms of chronic kidney disease (kidney functions and related systems)

A

Bone pain (vit d deficiency)

Nausea, anorexia, weight loss (toxins)

Itch (toxins)

Breathlessness (pulmonary oedema)

Leg swelling (fluid retention)

Fatigue (2° anaemia from ↓ EPO production)

21
Q

Signs of abnormal kidney function (anaemia, fluid retention)

A

Pallor (anaemia)

Hypertension (fluid retention)

Oedema (fluid retention)

Proteinurea

22
Q

Causes of CKD (infection, other diseases, damage to glmoeruli/tubular cells, inheritance)

A
  1. Diabetic kidney disease
  2. Hypertension/atherosclerosis
  3. Glomerulonephritis
  4. Poly cystic kidney disease (inherited renal disease)
  5. Pyelonephritis, reflux nephropathy
23
Q

Risk factors associated with CKD

A

Diabetes

Hypertension

Dyslipidemia

Family Hx

CARDIAC DISEASE

Smoking

Male

Age

24
Q

How does diabetes cause CKD (Basement membrane) diabetic nephropathy

A

Diabetes causes hyperglycaemia

Hyperglycaemia = thickening of the basement membrane of the glomeruli, and expansion of the mesangial cells

Diabetic hypertension = ↑ BP (vasodilation of the afferent and vasoconstriction of the efferent)

Albumins leak into the filtrate= proteinurea toxic to tubules… causing tubular atrophy and interstitial fibrosis

25
Q

Why does proteinurea cause tubular cell atrophy and interstitial fibrosis?

A

Albumins (proteinurea) are toxic to the tubular cells, causing death.

This can be caused due to diabetic nephropathy

26
Q

Treatment of diabetic nephropathy (hypertension and hyperglycaemia)

A

Better management of the diabetes, insulin injections/metformin

ACEi or ARB to ↓ the RAAS effects of ↑ blood pressure in glmoerulus (↓ vasoconstriction of the efferent arteriole)
Eg ramopril

27
Q

Consequences of ↓ GFR in chronic kidney disease

A

Fluid retention

  • heart failure
  • oedema (pulmonary, limbs and ascites)

Retention of metabolites

  • uraemia (additional metabolites in system)
  • urate in system causes gout
  • ↑ serum creatinine
  • prolonged drug half-life= easier drug toxicity
28
Q

Drug prescribing in CKD

A
  1. Prolonged drug half-life = possible toxicity
  2. ↓ dosage/↑ time between doses
  3. Stop DAMN drugs
29
Q

DAMN drugs

A

Diuretics
ACEi/ARB
Metformin
NSAIDs

30
Q

Consequences of reduced renal tubular function

A

↓ fluid reabsorbtion

  • polyurea
  • nocturia

↓ potassium excretion
- hyperkalaemia

↓ acid excretion and ↓ HCO3- formation
- metabolic acidosis

31
Q

How does renal bone disease form (osteomalacia)

A

Vitamin D is activated by thr kidneys

In CKD, this does not happen

↓ calcium abrogation in the gut

Leads to ↓ mineralisation of bone
OSTEOMALACIA

32
Q

Consequences of hyperparathyroidism in renal bone disease (calcium, vitamin D and osteoclasts)

A

With ↓ Ca2+ and ↓ activated Vit D, parathyroid is stimulated

This leads to osteoclasts stimulation by PTH and breakdown of bone to ↑ calcium levels

Osteoblasts don’t lay down calcium due to ↓ in activated vit D = osteomalacia

33
Q

Osteomalacia defiantion

A

The softening of bones due to inadequate mineralisation

34
Q

Management of CKD (hypertension, anaemia, CVD, hypers, kidney)

A

Dialysis (haemo, peritoneal)

Kidney transplant

Anti-hypertensives

ACEi/ARB

Statins (hyperlipidaemia)

EPO injections (anaemia)

Activated vit d (osteomalacia)

Phosphate binding drugs (hyperphosphataemia)

Restrict intake of potassium (hyperkalaemia)

35
Q

Therapies for end stage renal disease

A

Haemodialysis
- ateriovenous fistula/central venous catheter

Peritoneal dyalysis

  • Catheter into abdomen
  • incision below umbilicus

Kidney transplant (iliac fossa)

GERR Semester 1 (26 decks)

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