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Renal > 05.20 - Drugs and Renal Fxn (Sweatman) > Flashcards

05.20 - Drugs and Renal Fxn (Sweatman) Flashcards

1
Q

2 peptide-like drugs

A

beta-lactams, ACEi’s

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1
Q

Though inward conductance is greater than outward, K efflux does not occur b/c

A

Vm is more positive than EK

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2
Q

What provides driving force for K excretion in DT epithelial cells

A

Na absorption –> Depolarizes membrane

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3
Q

Tx for hyperkalemia is required if

A

EKG changes

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4
Q

What mediates reabsorption of peptide-like drugs

A

Peptide Transporters (PEPT1, PEPT2)

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5
Q

Capacity rate limited

A

Extraction ratio is limited by the reversible binding of the drug to plasma proteins or its location in RBCs

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5
Q

NSAID use in CKD will cause

A

Acute reductions in renal bloodflow and GFR

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6
Q

PGI2/PGE2 preserve GFR by antagonizing arteriolar vasoconstrictors and

A

blunting mesangial and podocyte contraction

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7
Q

Drugs that antagonize ___ increase risk of AKI when NSAID is administered

A

Drugs that antagonize RAAS

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8
Q

Effect of PG’s on RAAS

A

Stimulate Renin secretion –> Enhance Na retention and K secretion

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8
Q

Effect of PG’s on ADH

A

Inhibit cAMP synthesis and oppose ADH –> Water excretion

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10
Q

What provides driving force for reabsorptio of drugs and drug metabolites

A

Extensive reabsorption of filtered water

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11
Q

Why doesn’t K efflux thru ROMK at physiological intracellular Mg

A

Intracellular Mg binds ROMK and blocks K efflux

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12
Q

T/F: PGs are a primary regulator of renal function

A

False, minimal importance in kidney of health individuals with normal volume status

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12
Q

What can be used to remove K+ in patients with renal failure

A

Dialysis

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12
Q

Low magnesium can exacerbate ___ by ___

A

K wasting by incr K secretion in DT

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13
Q

Most common cause of drug-induced hypokalemia

A

Anti-infective agents

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14
Q

Effect of PGI2 and PGE2 in kidney

A

Vasodilation of interlobular arteries, afferent and efferent arterioles, and glomeruli

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14
Q

Effects of PG’s on LOH and Distal Nephron

A

(1) Incr renal Na excretion, decr medullary tonicity; (2) Stimulate Renin secretion; (3) Inhibit cAMP and oppose ADH

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14
Q

Acute NSAID toxicity is manifest in terms of

A

Tubular Epithelial Necrosis secondary to altered renal hemodynamics

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15
Q

Anti-infective agents commonly cause what electrolyte abnormality

A

HypoKalemia

16
Q

Diureti-induced hypokalemia is associated with

A

Mild-Moderated Metabolic Alkalosis

18
Q

2 commonly used formulas that estimate GFR

A

Cockroft-Gault; MDRD

18
Q

Effect of PGE2 on cellular transport of NaCl

A

Decreases cellular transport of NaCl –> Increase Na excretion and decr in medullary tonicity

20
Q

Kidney PGs have their major role in

A

preservation of renal fxn when pathologic states supervene and compromise physiologic kidney processes

21
Q

3 steps in hyperkalemia tx

A

(1) Calcium Gluconate, (2) Shift to intracellular, (3) Removal of excess K+

23
Q

Risk of NSAID-associated AKI in health persons

A

Low, b/c PG production is low in healthy persons

24
Q

Second most common cause of drug-induced hypokalemia

A

Diuretics

26
Q

Net effect of PG actions on LOH and Distal Nephron is that chronic NSAID consumption can lead to

A

a mild, dose-dependent increase in BP

28
Q

Tubular secretion occurs primarily in

A

pT

28
Q

GFR > ___ is normal

A

80

29
Q

At physiological intracellular Mg concentration, ROMK conducts K in which direction

A

Inward

30
Q

Perfusion rate limited

A

extraction ratio is not limited to the unbound fraction of drug

30
Q

COX-2 inhibitor effects on kidneys

A

equivalent to other classes with respect to their nephrogenic potential

31
Q

NSAIDs are also associated with interstitial nephritis that is thought to be result of

A

Allergic reaction

32
Q

GFR < ___ is severe renal impairment

A

30

34
Q

3 conditions with increased prevalence that are exacerbated by GFR

A

HTN, CHF, Renal insufficiency

35
Q

Organic anion and cation transporter systems, w/ overlapping specificities, allow potential for

A

Drug-Drug interactions

35
Q

How does insulin lower hyperkalemia

A

Stimulates Na/H exchange –> Na in –> Stimulates Na/K –> Uptake of K into cell

36
Q

PG production is increased in ___ disease

A

chronic kidney disease

37
Q

Leading causes of drug-induced hyperkalemia

A

Aldosterone antagonist/k-sparing agents and ACEi/ARB

39
Q

___ locally mediate effects of both systemic and locally produced vasoconstrictor hormones

A

Eicosanoids

40
Q

K secretion in DT is under regulation of

A

intracellular Mg

42
Q

3 effects of Calcium in HyperKalemia

A

(1) Less neg resting Vm; (2) Shift upwards and right of Vm x Vmax curve; (3) Reverses depressed conduction

44
Q

Action of Albuterol tx of Hyperkalemia

A

Activates Na/K –> Na leaving forces K in

46
Q

2 “situations” when PG’s play role in preserving renal fxn

A

True intravascular volume depletion; Effective decrease in renal blood flow

47
Q

Surge in catecholamines is often associated with what electrolyte change

A

Hypokalemia

48
Q

With no Mg and normal K concentrations, the chemical gradient drives K in which direction?

A

Outward

49
Q

2 drugs commonly used to tx Hyperkalemia

A

B2 agonist (Albuterol) and Insulin

50
Q

Insulin stimulates what transporter

A

Na/H exchange (Na in, H out)

51
Q

PGI2/PGE2 antagonize

A

local effects (vasoconstriction) of circulating Ang2, Endothelin, Vasopressin, and Catecholamines (that would normally maintain systemic pressure at expense of renal circulation)

52
Q

What aspect of tubular secretion allows for drug-drug interactions

A

Transporters with overlapping substrae specificities

Renal (31 decks)

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