metabolic mc1 Flashcards

1
Q

define AKI

A

Increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L) within 48 hours; or
Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days; or
Urine volume <0.5 mL/kg/h for six hours

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2
Q

what does KDIGO leave out for AKI

A

GFR (apart from in children)

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3
Q

AKI stage 1

A

Increase in serum creatinine to 1.5 to 1.9 times baseline, or increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L), or reduction in urine output to <0.5 mL/kg per hour for 6 to 12 hours.

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4
Q

AKI stage 2

A

Increase in serum creatinine to 2.0 to 2.9 times baseline, or reduction in urine output to <0.5 mL/kg per hour for ≥12 hours.

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5
Q

AKI stage 3

A

Increase in serum creatinine to 3.0 times baseline, or increase in serum creatinine to ≥4.0 mg/dL (≥353.6 micromol/L), or reduction in urine output to <0.3 mL/kg per hour for ≥24 hours, or anuria for ≥12 hours, or the initiation of renal replacement therapy, or, in patients <18 years, decrease in eGFR to <35 mL/min per 1.73 m2.

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6
Q

dehydrated AKI treatment/pre renal

A

IV fluid therapy – fluid challenge = 500 mL 0.9% NaCl over fifteen minutes
Withdrawal of nephrotoxins
Withholding of hypotensive agents and diuretics
Withhold atorvastatin

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7
Q

causes of hyperK

A

Reduced aldosterone secretion
aldosterone resistance
Reduced distal sodium and water delivery as occurs in effective arterial blood volume depletion
Acute and chronic kidney disease in which one or more of the above factors are present

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8
Q

spironolactone MOA

A

It competes with aldosterone for receptor sites in the distal renal tubules, increasing sodium chloride and water excretion while conserving potassium and hydrogen ions; may block the effect of aldosterone on arteriolar smooth muscle as well.

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9
Q

spironolactone active metabolite

A

canrenone

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10
Q

only diuretics that do not act at the luminal membrane of the tubular cells

A

spiro

eple

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11
Q

what upregulates Enac

A

ALDOSTERONE

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12
Q

what is required for spiro and epel to work

A

aldosterone

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13
Q

what enhances the work of spiro and epel

A

hyperaldosterone

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14
Q

spironolactone indications

A

Systolic heart failure
Resistant hypertension
Temporary treatment of Conn’s syndrome
Liver failure (oedema)

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15
Q

first line diuretic for ascites with liver failure

A

spironolactone

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16
Q

would you use spironolactone in primary hyperaldosterone

A

ye while waiting for surgery/cant have surgery/establishing diagnosis

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17
Q

spironolactone adverse effects

A
Hyperkalaemia
Gynaecomastia
Liver impairment
Jaundice
Stevens–Johnson syndrome (a T cell-mediated hypersensitivity reaction)
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18
Q

when not to use spironolactone

A

Severe renal impairment
Hyperkalaemia
Addison’s disease
Pregnant or lactating women

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19
Q

why can you use spironolactone in addisons

A

no aldosterone

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20
Q

why not to use spironolactone in pregos

A

crosses placenta and milk

21
Q

spironolactone interactions

A

ACEi and K supplement

22
Q

loop diuretics MOA

A

Inhibits reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule, interfering with the chloride-binding co-transport system

23
Q

what do loop diuretics cause the excretion of

A

excretion of water, sodium, chloride, magnesium, and calcium.

24
Q

loop diuretics side effecs

A
Dehydration
Hypotension/Hyponatraemia/Hypokalaemia/Hypochloraemia/Hypocalcaemia/Hypomagnesaemia
Metabolic alkalosis
Gout
Deafness
Tinnitus
25
why do you get tinnitus in loop diuretics
A similar Na+/K+/2Cl− co-transporter is responsible for regulating endolymph composition in the inner ear
26
main use of loop diuretics
Management of oedema associated with heart failure and hepatic or renal disease; acute pulmonary oedema; treatment of resistant hypertension
27
how does ramipril become active
saponification
28
ramipril active metabolite
ramiprilat
29
why does ramipril have a long duration of action
slow rate of dissociation of enzyme inhibition
30
how can a CNS mech be involved in lowering BP with ACEi
angiotensin II increases adrenergic outflow from CNS; vasoactive kallikreins may be decreased in conversion to active hormones by ACE inhibitors
31
indications for ACEi
Hypertension Symptomatic heart failure Prophylaxis after myocardial infarction in patients with clinical evidence of heart failure Prevention of cardiovascular events in patients with atherosclerotic cardiovascular disease or with diabetes mellitus and at least one additional risk factor for cardiovascular disease
32
ACE adverse effects
``` Hypotension Hyperkalaemia Cough Worsening renal function Angioedema Anaphylactoid reactions ```
33
ACEi interactiosn
ACE inhibitors and ARBs: hyperkalaemia Potassium supplements and potassium sparing diuretics: hyperkalaemia NSAIDs: acute kidney injury
34
pharmacokinetic
drug interactions occur when one drug changes the systemic concentration of another drug, altering ‘how much’ and for ‘how long’ it is present at the site of action
35
pharmacodynamic
drug interactions occur when interacting drugs have either additive effects, in which case the overall effect is increased, or opposing effects, in which case the overall effect is decreased or even ‘cancelled out’.
36
how can NSAIDs cause AKI
hemodynamically mediated acute kidney injury (AKI); electrolyte and acid-base disorders; acute interstitial nephritis (AIN)
37
increase in PG syntheis
Chronic kidney disease Volume depletion from aggressive diuresis, vomiting, or diarrhoea Effective arterial volume depletion due to heart failure, nephrotic syndrome, or cirrhosis Older age Severe hypercalcaemia with associated renal arteriolar vasoconstriction
38
gold standard filtration marker
inulin
39
why is iulin good
freely filtered at the glomerulus, and is neither secreted, reabsorbed, synthesized, nor metabolized by the kidney
40
bad things about inulin
short supply, expensive, and difficult to assay. continuous intravenous infusion, multiple blood samples, and bladder catheterization
41
why is cockroft and gault more accurate
includes weight
42
bad about cockroft and gault
overestimates by 10-14%
43
what does the MDR formula use
serum creatinine, age, sex, and race
44
how is renal function measured
eGFR calculated from ‘MDRD formula’ | expressed as creatinine clearance
45
information on dosage adjustment in the BNF is expressed in terms of
eGFR
46
for txic drugs what should be used to calc dose
creatinine clearance (calculated from the Cockcroft and Gault formula)
47
what happens to Drug excreted by the kidneys with CKD
Increased half life so longer to reach steady state
48
how to prescrive with CKD and renal excretion of a drug
Loading dose if needed to reach steady state quickly but lower dose at more frequent intervals