Renal Flashcards

(23 cards)

1
Q

What is the main action of renin?

A

converts angiotensin (from liver) into angiotensin I

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2
Q

What is the main action of ACE (angiotensin converting enzyme)?

A

convert angiotensin I into angiotensin II in lungs

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3
Q

What is the main action of angiotensin II?

A

causes vasoconstriction -> increases BP
stimulates release of aldosterone from adrenal glands
promotes hypertrophy of heart muscle cells

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4
Q

What is aldosterone? Where is it released from?

A

mineralocorticoid, released by adrenal glands

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5
Q

What are the main actions of aldosterone?

A

Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts

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6
Q

What effect does higher sodium reabsorption have on blood pressure?

A

When sodium is reabsorbed in the kidneys, water follows it by osmosis. This leads to increased intravascular volume and, subsequently, blood pressure.

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7
Q

What are the main categories of AKI causes?

A

prerenal
intrinsic
postrenal

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8
Q

What are the prerenal causes of AKI?

A

ischaemia e.g. in
- renal artery stenosis
- hypovolaemia secondary to vomiting, diarrhoea

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9
Q

What are some intrinsic causes of AKI?

A

intrinsic damage to glomeruli, e.g. due to drugs, toxins, immune-mediated
- glomerulonephritis
- acute tubular necrosis
- acute interstitial nephritis
- rhabdomyolysis
- tumour lysis syndrome

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10
Q

What are some postrenal causes of AKI?

A

obstruction e.g.
- kidney stone in ureter, bladder
- BPH
- external compression of the ureter

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11
Q

Who is at an increased risk of AKI?

A

CKD
organ failure / chronic disease
Hx of AKI
use of nephrotoxic drugs - e.g. NSAIDs, ACEi, ARBs - within the past week
use of iodinated contrast agents in the past week
age 65+

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12
Q

What is oliguria?

A

reduced urine output
less than 0.5 ml/kg/hr

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13
Q

How can AKI be detected?

A

U&Es - rise in electrolytes normally excreted by the kidneys
urinalysis
imaging - renal USD - if no identifiable cause for deterioration or at higher risk of urinary tract obstruction

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14
Q

How is AKI managed?

A

supportive management
- fluid balance
- medication review

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15
Q

Which medications are safe to continue in AKI?

A

paracetamol
warfarin
statins
aspirin
clopidogrel
beta blockers

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16
Q

What treatments are available for hyperkalaemia?

A
  1. IV calcium gluconate - to stabilise the cardiac membrane
  2. insulin + dextrose infusion
    nebulised salbutamol
    -> to provide short term shift of K from outside into the cells
  3. loop diuretics
    dialysis
    -> to remove K from the body
17
Q

What is acute tubular necrosis?

A

most common intrinsic cause of AKI
necrosis of renal tubular epithelial cells
reversible in early stages if cause is removed

18
Q

What are the main causes of acute tubular necrosis?

A
  1. ischaemia - shock, sepsis
  2. nephrotoxins
    - rhabdomyolysis
    - radiocontrast agent
    - lead
19
Q

What are the features of acute tubular necrosis?

A

raised urea, creatinine, potassium
muddy brown casts in urine

20
Q

What are the phases of acute tubular necrosis?

A

oliguric
polyuric
recovery

21
Q

Why do patients with CKD have anaemia?

A

reduced erythropoietin production
reduced Fe absorption

22
Q

What are the most common causes of polyuria?

A

diuretics, caffeine, alcohol
DM
lithium
HF