Renal Pharmacology

Front 1

MOA: Acetazolamide

Back 1

Carbonic anhydrase inhibitor: less conversion to water/H2O --> more HCO3- excretion --> diuretic, alkalizes urine, promotes serum acidemia.

Front 2

Which of the following laboratory results would you expect in a subject taking acetazolamide? (CA inhibitor)

a.Na 140, K 3.5, Cl 112, HCO3 18 Urine pH 4.5

b.Na 140, K 3.5, Cl 112, HCO3 18, Urine pH 7

c.Na 140, K 3.5, Cl 98, HCO3 18, Urine pH 7

d.Na 140, K 3.5, Cl 98, HCO3 18, Urine pH 4.5

e.Na 140, K 3.5, Cl 98, HCO3 24, Urine pH 7

Back 2

b.Na 140, K 3.5, Cl 112, HCO3 18, Urine pH 7

Na and K are the same in these questions

Serum chloride will increase (less bicarb reabsoprtion --> more chloride reabsorption) Serum HCO3- would be low because its being excreted Which would also make the urine pH basic

Front 3

Which of the following diuretic classes would most likely cause hyponatremia?
A.Loop diuretics
B.Thiazides

Back 3

Thiazides selectively impair urinary dilution (selective effects on DCT). This means ADH is still effective at concentrating urine, there is disproportionately more sodium loss in a given volume of urine, and hyponatremia ensues.

In contrast, the loop diuretics impair both urinary dilution and concentration. That is, it effects the corticopapillary gradient, so ADH is not effective at concentrating the urine, Na+ and water loss is proportional, and hyponatremia is less likely.

Front 4

Trimethoprim: renal AE

Back 4

ENAC inhibitor --> hypovolemia, hyperkalemia

Front 5

A 30-year old man is brought to the emergency department in a deep coma. Respiration is severely depressed and he had pinpoint pupils. His friends said he self-administered a large dose of morphine 6h earlier. An immediate blood analysis shows a morphine blood level of 0.25 mg/L. The Vd of morphine is 200L, and the half-life is 3h.

How much morphine did the patient inject 6 h earlier?

Back 5

[morphine]P at 6 hrs = 0.25 mg/L

Half-life = 3 hrs

At three hours: 0.5 mg/L

At T0: 1.0 mg/L

D = (C0)(VD) = (1.0mg/L) (200L) = 200 mg morphine

Front 6

A new antibiotic drug is actively secreted by the kidney; Vd is 35 L in a healthy adult. The total clearance Cltotal of this drug is 650 ml/min.

What is the elimination half-life for this drug?

Back 6

Cltotal = (kE) (VD)

KE = 0.693/T1/2

Cltotal = (0.693/T1/2)(VD)
T1/2 = (0.693) (VD)/(CLtotal)

T1/2 = (0.693) (35L) (0.65 L/min)

T1/2 = 37 minutes

Front 7

According to the manufacturer, after the antibiotic cephradine (Velosef), given by IV infusion at a rate of 5.3 mg/kg/h to 9 adult volunteers (average weight, 71.7 kg), a steady state serum concentration of 17 mg/ml was measured. Calculate the average total body clearance for this drug in adults.

Back 7

CSS = K0/CLtotal

Cltotal = K0/CSS = (5.3 mg/kg*hr) (17 mg/mL)

Cltotal = 0.311 mL/kg*hr = 22.35 mL/hr

Front 8

A male adult patient (65 yr, 70 kg) with hypertension and stage IV chronic kidney disease has a serum creatinine is 2.5 mg/dL. After sustaining a penetrating injury to his lower calf and developing an infection, he is placed on the antibiotic Tobramycin. The dose used for patients with normal renal and hepatic function is 200 mg twice a day by IV injection. Tobramycin is 90% excreted unchanged in the urine. Assume normal creatinine clearance is 100 ml/min.

What is the creatinine clearance of this patient?

Back 8

ClCr = [140-age] x body weight /(72x [Creatinine]P)

ClCr = (75)(70)/(72)(2.5)

ClCr = 29 mL/min

Front 9

A male adult patient (65 yr, 70 kg) with hypertension and stage IV chronic kidney disease has a serum creatinine is 2.5 mg/dL. After sustaining a penetrating injury to his lower calf and developing an infection, he is placed on the antibiotic Tobramycin. The dose used for patients with normal renal and hepatic function is 200 mg twice a day by IV injection. Tobramycin is 90% excreted unchanged in the urine. Assume normal creatinine clearance is 100 ml/min, and patient's creatinine clearance of 29 mL/min.

What is his adjusted dose and dosing interval?

Back 9

Adjustment factor:
ku/kn = 1-[fe(1-(CuCr/CnCr))]

ku/kn = 1-[0.9(1-0.29)]

ku/kn = 1-[0.9(0.71)

ku/kn = 1 - 0.639

ku/kn = 0.361

Dose: (0.361) (200mg) = 72.2 mg twice a day

Interval: (1/0.361)(12hrs) = 33 hours

Front 10

A female patient (35 years old, 65kg) with normal renal and hepatic function is to be given a drug by IV infusion. According to the literature, the elimination half-life (t1/2) of this drug is 7 hr (k = 0.099 h-1) and the apparent volume of distribution (Vd) is 15 L. The pharmacokinetics of this drug assumes a first order elimination process. The desired steady-state plasma concentration (Cpss) is 10ug/ml.

Assuming no loading dose, how long after starting the infusion will it take to attain most of the steady state plasma concentration (Cpss)?

What is the appropriate loading dose for this antibiotic?

What is the appropriate infusion rate for this antibiotic?

Back 10

1. It will take 4x(t1/2) = 28 hours

2. Loading dose = (VD) (Css)
LD = (15,000 mL) (10 ug/mL) = 150,000 ug = 150 mg

3. Steady-state infusion:
Css = K0 / Cltotal
Cltotal = (0.693)(VD)/(T1/2)

K0 = (Css) (0.693)(VD)/T1/2

K0 = (10 mg/L)(0.693)(15L)/7hr

K0 = 14.85mg/hr

Front 11

Determinations of drug absorption (4)

Back 11

1. Electrochemical gradient

2. Lipophilicity or passage through aqueous pores

3. Ionization: low pH for acidic drugs, high pH for basic drugs

4. Active transport or receptor-mediated endocytosis

Front 12

How is circulating drug protected from filtration

Back 12

Binding to albumin in plasmas

Front 13

Determining the volume of distribution?

Back 13

Vd = Dose/C0

Where C0 is the [drug] at t = 0, which can be extrapolated from the y-intercept of the ln[drug] vs time graph.

Can be normalized for patient's weight

Front 14

Calculating bioavailability

Back 14

By definition, bioavailabiltiy of an IV drug is 100%

The bioavailability of some other form of the drug is defined as:
AUC(drug formulation) / AUC (IV drug formulation) x 100

Front 15

Equation for total clearance

Back 15

CLtotal = (KE) (VD)

Where KE = slope of ln[drug] vs time
and
KE = 0.693 / T1/2

Front 16

How can you tell whether a drug is reabsorbed, secreted or freely filtered?

Back 16

Assume GFR is roughly 120 mL/min

Cdrug = VUdrug/Pdrug

If Cdrug>120, drug is secreted

If Cdrug<120, drug is reabsorbed (likely passively)

If Cdrug = 120, drug is simply filtered by the glomerulus

Front 17

Steady-state infusion equations (assume 100% bioavailability)

Back 17

CSS = k0/CLtotal

If there is no loading dose, it will take 4x(t1/2) to reach the steady-state concentration.

LD = (VD)(CSS)

Front 18

Steady-state dosing with non-IV medications

Back 18

With IV medications:
CSS = input/output = K0/CLtotal

Instead of K0, our input is going to be the dosing rate (D/t) times the absorption fraction, F.

So:

CSS = (D/t)(F)/Cltotal

LD = (CSS)(VD)/(F)

Front 19

What happens if you don't adjust for renal insufficiency in your infusion?

Back 19

The principal behind an infusion is that, to reach a steady-state concentration, your input must equal your output.

If you don't account for a decreased output, the drug will accumulate.

Front 20

Adjustment of loading dose for renal insufficiency

Back 20

Loading dose is not dependent on output - and is thus not adjusted for renal insufficiency!

LD = (CSS)(VD)

Front 21

Methods for calculating the renal dose adjustment factor

Back 21

1. (D)U = (D)N ClTU / CLTN

Where:
(D)U = uremic dose (D)N = normal dose

ClTU = total uremic clearance
ClTN = total normal clearance (usually assumed to be 100 mL/min)

2. Welling and Craig Normagram:

- Find which class the drug of question belongs to (this will depend on the reliance of its clearance on renal clearance)

- Find the patient's ClCr

- The point you land on will tell you the half-life (R axis) and the dose adjustment factor (L axis)

3. Giusti-Hayton: when urinary [drug] is known

Dose adjustment factor =
1 - [Fe[1-(ClUCr/ClNCr)]

Where:
Fe = fraction of drug excreted in urine

ClUCr/ClNCr = uremic creatinine clearance as a fraction of normal creatinine clearance

Front 22

500 mg of Amikamycin, a group F drug, is given every 6 hours to a normal 75 kg patient.

What is your plan for a 75 kg patient with ClCr = 10 mL/min

Back 22

Dose adjustment factor = 0.48

Give 240 mg every 6 hours or:
500 mg every 12.5 hours

Front 23

Calculate creatinine clearance based on age, weight and plasma creatinine

Back 23

Males:
ClCr = [(140-yrsAge) x body weight (Kg)] / (72 x [Cr]plasma)

Females: multiply by 0.85

Front 24

Biotransformation reactions

Back 24

Phase I reactions: redox, P450 metabolism and hydrolysis --> creation of a reactive intermediate, capable of being conjugated.

Phase II reactions: acetylation, methylation, gluconiration, glycine conjugation, etc.

Front 25

The PK properties of a new drug are being studied in normal volunteers during phase I clinical trials. The volume of distribution and clearance determined in the first subject are 80L and 4 L/hr, respectively. The half-life of the drug in this subject is approximately:
(A) 0.03 hours
(B) 14 hours
(C) 78 hours
(D) 139 hours
(E) 222 hours

Back 25

(B) 14 hours

Step 1 (calculate k) CL = k x Vd 4 L/h = k x 80 L k = 4/80 = 1/20 h-1

Step 2 (calculate t ½) t ½ = 0.7/k t ½ = 0.7 x 20 h t ½ = 14 hours

Front 26

A continuous IV infusion of lidocaine is given to a 70-kg patient with cardiac arrhythmias. The PK parameters for lidocaine are as follows: clearance (CL) = 9mL/min/kg, volume of distribution (Vd) = 70 L, half-life = 2 hours. How long will it take for drug levels to reach 87.5% of steady state?

(A) 1.75 hours
(B) 3.5 hours
(C) 5.5 hours
(D) 6.8 hours
(E) 8.4 hours

Back 26

(D) 6.8 hours

Front 27

A new antibiotic is being tested in clinical trials. The following PK parameters have previously been determined: Clearance = 100 mL/min Volume of distribution = 50 L Half-life = 3 hours Assuming that the drug is being administered IV, what loading dose should be given to a patient to quickly obtain a plasma concentration of 10mg/L?

(A) 5mg
(B) 25mg
(C) 100mg
(D) 500mg
(E) 1000mg

Back 27

(D) 500mg

LD = Vd x Cp

Loading dose = (volume of distribution) x (plasma concentration)

In this case, LD = 50 L x 10mg/L = 500mg

Front 28

A pharmacy resident is trying to determine the plasma concentration of an experimental anti-arrhythmic agent (Drug X) at steady-state. A continuous IV infusion of the agent began 6 hours earlier at a rate of 3mg/min. Drug X has a half-life of 3 hours, a volume of distribution of 120L, and a clearance of 0.6L/min. If the rate of infusion remains constant, what will the plasma concentration be at steady-state?
(A) 0.005 mg/L
(B) 0.4 mg/L
(C) 2 mg/L
(D) 5 mg/L
(E) 40 mg/L

Back 28

(D) 5 mg/L

What is needed to solve the problem? Patient given a constant IV infusion of a drug Clearance The equation need in this case is Css = k0 / CL Plasma concentration = infusion rate/clearance Css = 3mg/min / 0.6L/min = 5mg/L

Front 29

A new antibiotic is being tested in phase II clinical trials. The following PK parameters had been determined in earlier trials: Vd = 60 L, CL = 30 mL/min, t ½ = 23 hours F (bioavailability) = 50% This antibiotic is administered orally, and the target plasma concentration (Cp) is 2mg/L. What is the appropriate loading dose for this drug?

(A) 15mg
(B) 30mg
(C) 60mg
(D) 120mg
(E) 240mg

Back 29

(E) 240mg

What is needed to solve the problem? Volume of distribution Desired plasma concentration Bioavailability LD = Cp x Vd / F Loading dose = plasma concentration x volume of distribution / bioavailability In this case, 2 mg/L x 60 L x 0.5 = 240mg

Front 30

A patient with CHF, HTN, DM, and glaucoma is on several medications. During a routine urine and blood sample analysis, the following electrolyte disturbances are noted: ↓ sodium, ↑ chloride, and ↓ potassium in the blood, ↑ calcium phosphate and bicarbonate in the urine Which of the following drugs most likely caused these electrolyte disturbances?
(A) Captopril
(B) Furosemide
(C) Acetazolamide
(D) Spironolactone
(E) Hydrocholorthiazide

Back 30

(C) Acetazolamide

Front 31

Therapeutic effects of Aspirin (4)

Back 31

1. Analgesia

2. Antipyresis (though paradoxically, since it increases metabolic rate)

3. Anti-inflammatory

4. Anti-thrombosis

Front 32

Aspirin MOA

Back 32

Primary: irreversible COX acetylation and inactivation

Secondary: inhibition of NF-KB transcription factor of inflammatory mediators

Front 33

How does higher dosage of aspirin cause toxicity?

Back 33

High dose -->

1. Higher tissue concentration

2. More rapid tissue concentration

3. Slower clarance (saturation of patwhays for metabolism)

4. Slower clearance --> more accumulation

Front 34

Predict severity of Aspirin toxicity based on dosing.

How do you do prognostic estimates if initial dosage is not known?

Back 34

< 150 mg/Kg: no toxicity

150-300 mg/kg: mild/moderate toxicity

300-500 mg/kg: expect severe toxicity

>500 mg: high risk of death

If initial dosage is not known: plot current plasma concentration versus time that has elapsed since ingestion on a normogram!

Front 35

How does the volume of distribution of Aspirin play into its toxicity?

Back 35

High VD means that clearance is slower (half-life is longer). Additionally, aspirin takes awhile to fully distribute, meaning of poisoning was recent, symptoms of toxicity will likely worsen (up to 60 hours after ingestion!)

Front 36

How does serum protein binding play a role in aspirin toxicity?

Back 36

Protein binding sites are relatively saturable -> once you surpass protein binding ability, active form of aspirin will dramatically increase --> more able to distribute in tissues that are not the blood compartment --> less accessible by renal elimination mechanisms

Front 37

Clinical manifestations of aspirin toxicity

Back 37

1. Mild: tinnitus (most sensitive for toxicity), mild hyperpnea, vomiting

2. Moderate: severe hyperanpea, lethargy and/or excitation, fever

3. Severe: severe hyperapnea, acid/base disturbances, coma, convulsions

Front 38

Mechanisms of aspirin toxicity

Back 38

1. Uncoupling of oxidative phosphorylation --> pyrexia, lactate production

2. Acid-base disorder:

- Increased production of organic acids lactate --> anion-gap metabolic acidosis

- Stimulation of respiratory center --> respiratory alkalosis

Acidosis is most common in infants & toddlers; alkalosis most common in children

Front 39

Principles of management of aspirin toxicity

Back 39

1. Prevention of further aspirin absorption: cathartics (increase poop), induction of emesis, gastric lavage, activated charcoal

2. Gold standard: hemodialysis

3. Correct metabolic abnormalities: IV fluids, electrolytes, etc.

4. Alkalinization of urine: controversial since carbonic anhydrase inhibitors also alkalinize CHF fluids and thus trap aspirin in there.

Front 40

How does Aspirin's elimination mechanism contribute to toxicity?

Back 40

Major pathways of phase II reactions - glycine conjugation and Glucuronidationare - are saturable, forcing aspirin to be metabolized through less significant pathways during overdose --> slower clearance

Front 41

Indications for diuretics

Back 41

1. HTN

2. Heart failure (decrease preload)

3. Non-cardiogenic edematous states (nephrotic syndrome, cirrhosis, etc.)

4. Management of electrolyte abnormalities

Front 42

What is the breaking phenomenon?

Back 42

Initially w/diuretic administration, Na+ excretion > Na+ absorption. However, this negative sodium balance is incompatible with life, and after a few days sodium balance will equalize to zero.

Ameliorating the breaking phenomenon:

- Sodium restriction

- Multiple diuretics

- Multiple dosing intervals of diuretics

Front 43

Contraindicated drugs with diuretics?

Back 43

NSAIDs!

Front 44

Carbonic anhydrase inhibitors: examples

Back 44

Acetazolamide

Front 45

Carbonic anhydrase inhibitors: MOA

Back 45

Inhibition of PCT lumial brush border carbonic anhydrase --> less uptake of luminal H+ and HCO3-. This causes:

- Less sodium reabsorption (diuretic effect)

- Less HCO3- reabsorption (treats metabolic alkalosis)

- More Cl- reuptake in late PCT

Front 46

Carbonic anhydrase inhibitors: indications

Back 46

Hypervolemic metabolic alkalosis

Front 47

Carbonic anhydrase inhibitors: AEs

Back 47

Hypokalemia, metabolic acidosis

Front 48

Loop diuretics: examples

Back 48

Furosemide, Torsemide, Bumetanide, Ethacrynic acid

Front 49

Loop diuretics: MOA

Back 49

Inhibition of thick ascending limb Na+/K+/2CL- symporter:

- Decreased potassium reabsorption

- Decreased sodium reabsorption

- Although the symporter is electroneutral, K+ will diffuse back into the lumen and make it more positive. Thus, inhibition of the channel --> more negative lumen --> less calcium and magnesium reuptake

- Abolishment of corticopapillary gradient

Front 50

What is the most potent diuretic class?

Back 50

Loop diuretics

Front 51

Loop diuretics: AEs

Back 51

- Hypokalemia

- Hypocalcemia/hypomagnesia

- Volume depletion --> sodium avidity --> HCO3- reabsorption --> metabolic alkalosis

Front 52

Loop diuretics: therapeutic considerations

Back 52

Most prone to breaking due to compensatory reuptake of Na+ downstream

Front 53

Thiazide diuretics: examples

Back 53

Hydrochlorothiazide, Clorthalidone, Metolazone

Front 54

Thiazide diuretics: MOA

Back 54

Inhibition of DCT Na+/Cl- symporter

Front 55

Thiazide diuretics: AEs

Back 55

1. Hyponatremia (does not impair corticopapilalry gradient --> urine can be hyperosmotic if ADH is around)

2. Hypokalemia

3. Volume contraction --> increased PCT Na+ avidity --> increased HCO3- reabsorption --> metabolic alkalosis

4. Hypercalcemia

Front 56

Thiazide diuretics: indications

Back 56

First line agent for mild-moderate HTN

Front 57

K+-sparing diuretics: examples

Back 57

ENAC channel inhibitors: Amiloride, Triamterene

Aldosterone antagonists: Spironolactone, Eplerenone

ACEis: -prils

Front 58

K+-sparing diuretics: MOA

Back 58

ENAC channel inhibition --> less sodium reabsorption, less Na+/K+ ATPase --> less potassium excretion. Also inhibits H+ secretion due to actions on intercalated cells.

Front 59

K+-sparing diuretics: indications

Back 59

Weak diuretics; usually used to potentiate other diuretics or to correct hypokalemia

Front 60

K+-sparing diuretics: AEs

Back 60

Hyperkalemia, metabolic acidosis

Front 61

Osmotic diuretics: examples

Back 61

Mannitol

Front 62

Osmotic diuretics: MOA

Back 62

Increases osmolality of the urine --> drags water --> increased urinary flow

Front 63

Osmotic diuretics: indications

Back 63

Hypertensive emergencies (drug overdose, increased intracranial/intraoccular pressure, etc.)

Front 64

Therapeutic targets of antihypertensives

Back 64

1. Decrease volume status (preload)

2. Decrease peripheral vascular resistance (afterload)

3. Decrease HR

4. Decrease myocardial contractility

Front 65

Peripheral alpha-1 adrenergic antagonist antihypertensives: examples

Back 65

-zosins

Front 66

Peripheral alpha-1 adrenergic antagonist antihypertensives: MOA

Back 66

Alpha-1 blockade --> vasodilation --> decrease in PVR

Front 67

Peripheral alpha-1 adrenergic antagonist antihypertensives: AEs

Back 67

- Orthostatic hypotension

- Nausea

- Drowsiness

- Reflex sodium avidity (useful in conjunction w/diuretics)

Front 68

Peripheral alpha-1 adrenergic antagonist antihypertensives: therapeutic advantages

Back 68

1. No reflex tachycardia

2. No exercise intolerance

Front 69

Central alpha-2 adrengergic agonist antihypertensives: MOA

Back 69

Stimulation of medullary CV alpha-2 adrenergic center --> decreased CNS sympathetic discharge --> vasodilation --> decrease in PVR

Front 70

Central alpha-2 adrengergic agonist antihypertensives: examples

Back 70

Clonidine and Methyldopa

Front 71

Central alpha-2 adrengergic agonist antihypertensives: AEs

Back 71

- Dry mouth

- Sedation

- Impotence

- HTN on discontinuation

- Reflex sodium avidity (useful in conjunction with diuretics)

Front 72

Central alpha-2 adrengergic agonist antihypertensives: indications

Back 72

Clonidine: HTN w/drug overdose
Methyldopa: HTN w/pregnancy

Front 73

Name the different classes of antihypertensives (8)

Back 73

1. Diuretics

2. Peripheral alpha-1 adrenergic antagonists

3. Central alpha-2 adrenergic agonists

4. Beta adrenergic antagonists

5. Anti-angiotensin II agents

6. Direct renin inhibitors

7. Calcium channel blockers

8. Vasodilators

Front 74

Beta-adrenergic antagonist antihypertensives: examples

Back 74

-olols

Front 75

Beta-adrenergic antagonist antihypertensives: MOA

Back 75

Beta-2 antagonism: decreases myocardial contractility, HR and renin secretion

Beta-1 antagonism: promotes non-vascular smooth muscle constriction (i.e. bronchoconstriction - often side effect)

Front 76

Beta-adrenergic antagonist antihypertensives: indications

Back 76

Effective in treating chronic HTN (mechanism is poorly understood); not indicated for treatment of acute HTN

Front 77

Beta-adrenergic antagonist antihypertensives: AEs

Back 77

- Bronchoconstriction

- Masking of hyperglycemic symptoms in diabetics

Front 78

Anti-angiotensin II antihypertensives: examples

Back 78

ACEis: -prils

ARBs: -sartans

Front 79

Anti-angiotensin II antihypertensives: MOA

Back 79

Angiotensin II antagonism, which prevents:

- Direct peripheral vasoconstriction

- Aldosterone release

- Angiotensin II-mediated arterial remodeling

ACEIs: inhbiits angiotensin converting enzyme
ARBs: blocks angiotensin II receptor

Front 80

Anti-angiotensin II antihypertensives: AEs

Back 80

- Cough (ACEis but not ARBs)

- Angioedema

- Hyperkalemia

- Contraindicated in bilateral renal artery stenosis and pregnancy

Front 81

Anti-angiotensin II antihypertensives: therapeutic advantages

Back 81

- Renal protective in DM patients

- Useful for renal failure w/proteinuria

- Slows progression of LV hypertrophy after MI

Front 82

Calcium channel blockers: examples

Back 82

Diltiazem, Verapamil, Amlodipine, Nifedipine

Front 83

Calcium channel blockers: MOA

Back 83

Amlodipine, Nifedipine: vasodilation --> decreased PVR

Verapamil: decrease in HR & myocardial contractility

Diltiazem: both effects

Front 84

Calcium channel blockers: AEs

Back 84

- Verapamil: interaction w/cardiac glycosides

- Contraindicated in CHF & s/p MI

- Contraindicated in pregnancy and lactation

Front 85

Vasodilators: examples

Back 85

- Hydralazine

- Minoxidil
- Nitroprusside

- Diazoxide

- Fenlodopan

Front 86

Vasodilators: AEs

Back 86

- Reflex tachycardia

- Hydralazine: lupus

- Nitroprusside: cyanide toxicity

- Minoxidil: hypertrichosis

Front 87

Direct renin inhibitors: adverse effets

Back 87

- Very expensive

- Significant hypotension, esp. when used in conjunction with other antihypertensives

- Significant hyperkalemia, esp. when used in conjunction with other anti-hypertensives or in the context of renal failure

Front 88

Treatment algorithm for HTN

Back 88

In general: ACEis and ARBs are interchangeable, but should never be used together.

1. Stage 1, no comorbidies: single agent, either ACEi, calcium channel blocker or beta-blocker

2. Stage 2: combine ACEi with calcium-channel blocker or beta blocker

3. African-American: start with calcium-channel blocker or thiazide diuretic

4. CKD: treatment plan should include ACEi

5. Second-line: vasodilators, alpha-adrenergics, direct renin inhibitors, etc.

6. Triple therapy: time to refer to a HTN specialist

Front 89

What is Indapamide?

Back 89

A thiazide diuretic

Front 90

What is Oxybutynin?

Back 90

Anticholinergic that relaxes the detrusor muscle and treats overactive bladder/urge incontinence

Front 91

What is Aliskiren?

Back 91

Direct renin inhibitor

Front 92

What is Sorbitol?

Back 92

Laxative that promotes K+ excretion

Front 93

What is probenecid?

Back 93

Gout medication contraindicated w/history of calcium oxalate stones.