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Renal injury and disease Flashcards

1
Q

Where are glomeruli located?

A

Cortex

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2
Q

Where do you take a biopsy from?

A

Cortex only

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3
Q

Why is the proximal tubule much pinker?

A

Full of mitochondria - 90% of solute reabsorbed here

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4
Q

Kidney function

A
  • Formation of urine
  • Control of water balance
  • Control of electrolytes
  • Drug metabolism
  • Drug excretion
  • Hormone synthesis
  • Calcium/phosphate regulation
  • Acid-base regulation
  • BP control
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5
Q

Which membrane surrounds arteriole?

A

Glomerular

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6
Q

Function of Bowman’s space

A

Collects urine before concentration in tubules

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7
Q

Function of JGA

A

Recognises drop in perfusion/BP to release renin

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8
Q

Function of angiotensin ii

A

Vasoconstriction of efferent arteriole

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9
Q

GFR

A
  • Filtration happens in glomerulus
  • Driven by hydrostatic pressure of blood
  • RBCs and large molecules don’t pass through filter
  • To assess, look at urine output and serum creatinine - state creatinine is inversely proportional to GFR
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10
Q

CKD

A
  • Chronic kidney disease: long time, irreversible, often due to injury etc or due to diabetes/hypertension
  • CKD: damage over 3 months with decreased GFR, pathological abnormalities or markers of kidney damage, 2 blood tests
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11
Q

Acute kidney disease

A

Deterioration of kidney function over long period

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12
Q

Acute on chronic kidney disease

A

Acute injury with background of CKD

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13
Q

Stage 1 GFR

A

90+, normal kidney function but urine abnormalities - annual observation of BP

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14
Q

Stage 2 GFR

A

60-89, mildly reduced kidney function, BP, monitoring, find out why

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15
Q

Stage 3 GFR

A

30-59, moderately reduced function, probable diagnosis made

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16
Q

Stage 4 GFR

A

15-29, severely reduced kidney function, management of complications, plan for renal failure

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17
Q

Stage 5 GFR

A

<15, very severe/end stage, renal replacement therapy needed

18
Q

Acute kidney disease

A
  • Acute decline of function with risk of clinically significant toxicity which is potentially reversible and potentially requires RRT
  • Very common in hospitals
  • RIFLE: risk, injury, failure, loss, ESRD
  • Impacts: inflammatory response - activated leukocytes and ischemic kidney
19
Q

Causes of acute kidney disease

A

Pre-renal (diabetes, hypertension etc), intra-renal (ATN, glomerular, vascular, nephritis), post-renal

20
Q

Class I AKI

A

Increase of serum creatinine by 1.5-2x baseline

Low urine output (<0.5ml/hr)

21
Q

Class II AKI

A

Increase serum creatinine by 2-3x baseline

22
Q

Class III AKI

A

Increase of serum creating by 3x baseline

23
Q

AKI consequences on heart

A
  • Potassium increase because of no excretion
  • Look at heart
  • Hyperkalaemia: high t-waves, wide QRS complexes, bradycardia
  • Hypokalaemia: tachyarrythmias
24
Q

Hyperkalaemia

A
  • Assess: is pt passing urine (yes = medical therapy, no = dialysis)
  • How high is potassium? 5.5-6.5 (no risk of cardiac arrest), 6.5-7.5 (moderate risk, treatment needed), >7.5 (high risk, impending cardiac arrest
  • Antagonise K+ effect (IV calcium)
  • Shift K+ into cells (beta-antagonist e.g. salbutamol, insulin, acidosis with sodium bicarbonate)
  • Remove potassium from body - diet, drugs, dialysis
25
Q

Metabolic acidosis causes

A
  • Hypotension
  • Reduced cardiac output
  • Respiratory compromise
  • Cardiac arrythmias
26
Q

Indications for dialysis in ARF

A

Uremia (seizures, nausea, vomiting, pericarditis)
Hyperkalaemia
Fluid overload (resistant to diuretics, especially pulmonary oedema)
Metabolic acidosis (low pH , sodium bicarbonate therapy not tolerated)

27
Q

CKD

A
  • Hypokalaemia, secondary hyperparathyroidism, hyperphosphataemia
  • Give activated vit D because can’t do second hydroxylation step - increase calcium, decrease PTH
28
Q

Stimulus for erythropoietin production

A

Fall in oxygen to kidneys

29
Q

How do RBCs replicate

A
  • Response: kidney capillaries secrete erythropoeitin into blood
  • Acts on bone marrow to stimulate proliferation of precursors and differentiation into RBCs
30
Q

Treatment for reduced erythropoietin

A

IV iron and erythropoisis stimulating agents

31
Q

Small kidneys

32
Q

History of kidney disease

33
Q

Reversible

34
Q

Anaemia, metabolic acidosis, hyperkalaemia

35
Q

How does sodium change in renal failure?

36
Q

How doe potassium change in renal failure?

A

Normal/high

37
Q

How does bicarbonate change in renal failure

38
Q

How does pH change in renal failure

A

Normal or low

39
Q

How does calcium change in renal failure

A

Normal or low

40
Q

How does phosphate change in renal failure

41
Q

How does Hb change in renal failure

A

Normal or low

Renal (26 decks)

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