metabolic mc1

Question 1

define AKI

Answer 1

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

Question 2

what does KDIGO leave out for AKI

Answer 2

GFR (apart from in children)

Question 3

AKI stage 1

Answer 3

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.

Question 4

AKI stage 2

Answer 4

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.

Question 5

AKI stage 3

Answer 5

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.

Question 6

dehydrated AKI treatment/pre renal

Answer 6

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

Question 7

causes of hyperK

Answer 7

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

Question 8

spironolactone MOA

Answer 8

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.

Question 9

spironolactone active metabolite

Answer 9

canrenone

Question 10

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

Answer 10

spiro

eple

Question 11

what upregulates Enac

Answer 11

ALDOSTERONE

Question 12

what is required for spiro and epel to work

Answer 12

aldosterone

Question 13

what enhances the work of spiro and epel

Answer 13

hyperaldosterone

Question 14

spironolactone indications

Answer 14

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

Question 15

first line diuretic for ascites with liver failure

Answer 15

spironolactone

Question 16

would you use spironolactone in primary hyperaldosterone

Answer 16

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

Question 17

spironolactone adverse effects

Answer 17

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

Question 18

when not to use spironolactone

Answer 18

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

Question 19

why can you use spironolactone in addisons

Answer 19

no aldosterone

Question 20

why not to use spironolactone in pregos

Answer 20

crosses placenta and milk

Question 21

spironolactone interactions

Answer 21

ACEi and K supplement

Question 22

loop diuretics MOA

Answer 22

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

Question 23

what do loop diuretics cause the excretion of

Answer 23

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

Question 24

loop diuretics side effecs

Answer 24

Dehydration
Hypotension/Hyponatraemia/Hypokalaemia/Hypochloraemia/Hypocalcaemia/Hypomagnesaemia
Metabolic alkalosis
Gout
Deafness
Tinnitus

Question 25

why do you get tinnitus in loop diuretics

Answer 25

A similar Na+/K+/2Cl− co-transporter is responsible for regulating endolymph composition in the inner ear

Question 26

main use of loop diuretics

Answer 26

Management of oedema associated with heart failure and hepatic or renal disease; acute pulmonary oedema; treatment of resistant hypertension

Question 27

how does ramipril become active

Answer 27

saponification

Question 28

ramipril active metabolite

Answer 28

ramiprilat

Question 29

why does ramipril have a long duration of action

Answer 29

slow rate of dissociation of enzyme inhibition

Question 30

how can a CNS mech be involved in lowering BP with ACEi

Answer 30

angiotensin II increases adrenergic outflow from CNS; vasoactive kallikreins may be decreased in conversion to active hormones by ACE inhibitors

Question 31

indications for ACEi

Answer 31

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

Question 32

ACE adverse effects

Answer 32

Hypotension 
Hyperkalaemia
Cough
Worsening renal function
Angioedema
Anaphylactoid reactions

Question 33

ACEi interactiosn

Answer 33

ACE inhibitors and ARBs: hyperkalaemia
Potassium supplements and potassium sparing diuretics: hyperkalaemia
NSAIDs: acute kidney injury

Question 34

pharmacokinetic

Answer 34

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

Question 35

pharmacodynamic

Answer 35

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’.

Question 36

how can NSAIDs cause AKI

Answer 36

hemodynamically mediated acute kidney injury (AKI); electrolyte and acid-base disorders; acute interstitial nephritis (AIN)

Question 37

increase in PG syntheis

Answer 37

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

Question 38

gold standard filtration marker

Answer 38

inulin

Question 39

why is iulin good

Answer 39

freely filtered at the glomerulus, and is neither secreted, reabsorbed, synthesized, nor metabolized by the kidney

Question 40

bad things about inulin

Answer 40

short supply, expensive, and difficult to assay. continuous intravenous infusion, multiple blood samples, and bladder catheterization

Question 41

why is cockroft and gault more accurate

Answer 41

includes weight

Question 42

bad about cockroft and gault

Answer 42

overestimates by 10-14%

Question 43

what does the MDR formula use

Answer 43

serum creatinine, age, sex, and race

Question 44

how is renal function measured

Answer 44

eGFR calculated from ‘MDRD formula’

expressed as creatinine clearance

Question 45

information on dosage adjustment in the BNF is expressed in terms of

Answer 45

eGFR

Question 46

for txic drugs what should be used to calc dose

Answer 46

creatinine clearance (calculated from the Cockcroft and Gault formula)

Question 47

what happens to Drug excreted by the kidneys with CKD

Answer 47

Increased half life so longer to reach steady state

Question 48

how to prescrive with CKD and renal excretion of a drug

Answer 48

Loading dose if needed to reach steady state quickly but lower dose at more frequent intervals