Renal Flashcards
1
Q
Mannitol
A
- Proximal Tubule
- Mechanism
-
Osmotic diuretic
- increases tubular fluid osmolarity
- increases urine flow
- decreases intracranial/ intra-ocular pressure
- increases tubular fluid osmolarity
-
Osmotic diuretic
- Clinical Use
- drug overdose
- elevated intracranial pressure
- increased intraocular pressure
- glaucoma
- Toxicity
- pulmonary edema
- dehydration
- No sulfa allergy
- Contraindication
- CHF
- Anuria (no urination)
- Water expansion into ECF
- Hyponatremia before diuresis
- Hypernatremia + dehydration after diuresis
2
Q
Acetazolamide
A
- Proximal Tubule
- Mechanism
-
Carbonic anhydrase inhibitor
- Prevents H+ secretion in exchange for Na+
- Na+ excreted
- HCO3- excreted
- self limited diuresis
- reduction in total HCO3- stores
-
Carbonic anhydrase inhibitor
- Clinical Use
- Glaucoma
- Urinary alkalinization
- Metabolic alkalosis (lose HCO3-)
- Altitude sickness
- Pseudotumor cerebri
- Toxicity
- Hyperchloremic metabolic acidosis
- Paresthesias
- NH3 toxicity
- Sulfa allergy
3
Q
Furosamide
A
Loop Diuretic
- Most potent diuretics but shortest 1/2 life
- Sulfonamide
- Mechanism
-
Inhibits NKCC cotransporter
- thick asckending limb
- *Na+, K+, 2Cl- *in
- Prevents concentration of urine
- abolishes medulal hypertonicity
- **Stimulates PGE release **
- vasodilation of arterioles
- inhibited by NSAID
- Ca+ wasting
-
Inhibits NKCC cotransporter
- Use
- Edema states: CHF, cirrhosis, nephrotic syndrome, pulmonary edema
- HTN
- Hypercalcemia
- Toxicity
- OHH DANG
- Ototoxicity
- Hypokalemia
- Hypokalemic Metabolic Alkalosis
- Hypocalcemia
- Dehydration
- Allergy (sulfa)
- Nephirits (interstitial)
- Gout (hyperuricemia)
4
Q
Ethacrynic Acid
A
Loop Diuretic
- Most potentt diuretics but shortest 1/2 life
- Phenoxyacetic acid derivative
- Not sulfonamide
- Mechanism
-
Inhibits NKCC Cotransporter
- Na+, K+, 2Cl- in
- thick ascending limb
- Prevents concentration of urine
- abolishes hypertonicity of medulla
-
Stimulates PGE release
- vasodilation of arterioles
- Inhibited by NSAID
- **Increase Ca++ excretion **
-
Inhibits NKCC Cotransporter
-
Use
- Diuresis in patients allergic to sulfa drugs
- Toxicity
- Ototoxicity
- Hypokalemia
- Hypokalemic metabolic alkalosis
- Hypocalcemia
- Dehydration
- Nephritis (interstitial)
- Gout (hyperuricemia)
5
Q
Loop Diuretic Resistance
A
- Increase Na+ delivery to distal tubule by decreasing Na+ reabsorption in loop of henle
- increased Na+ reabsorption in distal tubule
- Prolonged diuretic use
- Distal tubule hypertrophy
- Due to increased activity
- Enhanced Na+ reabsorption
- Resembles resistance to loop diuretics
- Distal tubule hypertrophy
- Overcome by adding Thiazide diuretic
- works in distal tubule
6
Q
Hydrochlorothiazide
chloralidone
A
Thiazide Diuretic
- Distal tubule
- Mechanism
- **Inhibits NaCl reabsorption **
- Reduces diluting capacity of neuron
-
Ca+ sparing
- decrease Ca+ excretion
- **Inhibits NaCl reabsorption **
- Use
- HTN
- esp with loop diuretic if “Resistance” evolves
- 1st line for essential HTN in general population
- CHF
- Idiopathic hypercalciuria
- Nephrogenic diabetes insipidus
- Osteoporosis + one of above problems
- Calcium kidney stones
- HTN
- Toxicity
- Hypokalemic Metabolic alkalosis
- Hyponatremia
- Hyperglycemia
- Hyperlipidemia
- Hyperuricemia (gout)
- Hypercalcemia
- Sulfa allergy
7
Q
Spironolactone
A
K+ Sparing Diuretic
- Cortical collecting tubule
- Mechanism
- **Competitive aldosterone receptor antagonists **
- inhibit aldosterone = inhibit Na+ reabsorption and K+ excretion
- release Na+ and H20
- hold onto K+
- inhibit aldosterone = inhibit Na+ reabsorption and K+ excretion
-
Mild Androgen receptor antagonist
- Gynecomastia
- Switch to eplerenone if this occurs
- **Competitive aldosterone receptor antagonists **
- Use
- Hyperaldosteronism
- K+ depletion
- CHF
- PCOS
- Toxicity
- Hyperkalemia
- Arrhythmias
- Gynecomastia
- Hyperkalemia
8
Q
Eplerenone
A
K+ Sparing Diuretic
- Cortical collecting tubule
- Mechanism
-
Aldosterone receptor antagonist
- No aldosterone = no Na+ reabsorption and K+ excretion
- Na+ and H20 excreted
- K+ reabsorbed
- No aldosterone = no Na+ reabsorption and K+ excretion
-
Aldosterone receptor antagonist
- Use
- Hyperaldosteronism
- K+ depletion
- CHF
- Toxicity
- Hyperkalemia
- Arrhythmias
- Hyperkalemia
9
Q
Triamterene
A
K+ Sparing Diuretic
- Cortical Collecting Tubule
- Mechanism
- **Block Na+ channels **
- Na+ and water excretion
- **Block Na+ channels **
- Use
- Hyperaldosteronism
- K+ depletion
- CHF
- Toxicity
- Hyperkalemia
- arrhythmias
- kidney stones
- Hyperkalemia
10
Q
Amiloride
A
K+ Sparing Diuretic
- Cortical Collecting Tubule
- Mechanism
-
Block Na+ channels
- Na+ and H20 excretion
-
Block Na+ channels
- Use
- Hyperaldosteronism
- K+ depletion
- CHF
- Toxicity
- Hyperkalemia
- arrhythmias
- Hyperkalemia
11
Q
Urine NaCl with Diuretics
A
- All increase urine NaCl
- Serum NaCl may decrease as a result
12
Q
Urine K+ with diuretics
A
- K+ sparing decrease urine K+
- All others increase urine K+
- serum K+ may decrease as a result
13
Q
Acidemia and diuretics
A
- Acetazolamide- CA inhibitor
- decrease HCO3- reabsorption
- K+ sparing
- aldosterone blockade prevents K+ secretion and H+ secretion
- hyperkalemia causes K+ to enter cells and H+ is excreted in exchange
- H+/K+ exchanger
14
Q
Alkalemia and diuretics
A
- Furosemide + Ethacrynic acid (loop)
- Hydrochlorothiazide (thiazides)
- Volume contraction –> increased AT II –> increased Na+/H+ exchanger in proximal tubule –> increased HCO3- reabsorption
- Hypokalemia–> K+ exits cells and H+ enters cells via H+/K+ exchanger
- Hypokalemia –> H+ is exchanged for Na+ instead of K+, leading to paradoxical aciduria
15
Q
Urine Ca+ levels diuretics
A
- Furosemide + Ethacrynic acid (loops)
- increase urine Ca+ ==> hypocalcemia
- decrease paracellular Ca+ reabsorption
- increase urine Ca+ ==> hypocalcemia
- Hydrachlorothiazide (thiazides)
- decrease urine Ca+ ==> hypercalcemia
- enhance paracellular Ca+ reabsorption in proximal tubule and loop of henle
- decrease urine Ca+ ==> hypercalcemia
16
Q
Captopril
A
**ACE inhibitors **(-pril)
- Mechanism
-
Inhibits Angiotensin Converting Enzyme
- decrease angiotensin II –> decreases GFR by preventing constriction of efferent arterioles
- *decreased aldosterone *
- increased renin due to loss of feedback inhibition
-
Prevents inactivation of bradykinin
- vasodilator
-
Inhibits Angiotensin Converting Enzyme
- Use
- HTN
- CHF
- Proteinuria
- diabetic renal disease- prevent progression of diabey nephropathy
- Prevent unfavorable heart remodeling from chronic HTN
- Toxicity
- Bradykinin cough
- Angioedema
- rapid swelling of dermis, subQ tissue, mucosa, submucosa tissue
- Hives but under skin
- primarily: tongue, lips, eyelids
- due to bradykinin accumulation
- vasodialtion = increased vascular permeability
- rapid swelling of dermis, subQ tissue, mucosa, submucosa tissue
- Teratogen
- fetal renal malformation
- Creatinine increase
- decrease GFR
- Hypekalemia
- Hypotension
- first dose hypotension **
- predisposing factors: hyponatremia, hypovolemia (already using diuretic), low baseline blood pressure, high renin or aldosterone levels, rena impairment, heart dialure
- Contraindicated
- bilateral renal artery stenosis b/c will further decrease GFR by dilating efferent arteriole–> Renal fail
17
Q
Enalapril
A
ACE inhibitors (-pril)
- Mechanism
-
Inhibit Angiotensin converting enzyme
- Decrease angiotensin II –> Decrease GFR by preventing efferent arteriole constriction
- Decrease aldosterone
- Increase renin due to los of feedback inhibition
-
Prevent bradykinin inactivation
- vasodilator
-
Inhibit Angiotensin converting enzyme
- Use
- HTN
- CHF
- Proteinuria
- Diabetic renal disease- prevent progression of diabetic nephropathy
- Prevent unfavorable heart remodeling from chronic HTN
- Toxicity
- Bradykinin cough
- Angioedema (bradykinin)
- Teratogen (fetal renal malformation)
- Creatinine increase (decrease GFR)
- Hyperkalemia
- Hypotension
- first dose hypotension**
- predisposing factors: hyponatremia, hypovolemia (currently using diuretic), low baseline BP, high renin or aldoserone levels, renal impairment, heart failure
- Contraindications
- bilateral renal artery stenosis b/c will further decrease GFR by dilating efferent arteriole–> Renal failure
18
Q
Lisinopril
A
ACE Inhibitors (-pril)
- Mechanism
-
Inhibit angiotensin converting enzyme
- decrease angiotensin II –> decrease GFR by preventing efferent arteriole constriction
- decrease aldosterone
- increase renin due to loss of feedback inhibition
-
Prevents bradykinin inactivation
- vasodilator
-
Inhibit angiotensin converting enzyme
- Use
- HTN
- CHF
- Proteinuria
- Diabetic renal disease- prevent progression of diabetic nephropathy
- Prevent unfavorable heart remodeling from chronic HTN
- Toxicity
- Bradykinin cough
- Angioedema (bradykinin)
- Teratogen (fetal renal malformation)
- Creatinine increase (decrease GFR)
- Hyperkalemia
- Hypotension
- first dose hypotension
- predisposing factors: hyponatremia, hypovolemia (already on diuretic), low baseling BP, high renin or aldosterone, renal impairment, heart failure
- Contraindication
- bilateral renal artery stenosis b/c will further decrease GFR by dilating efferent arteriole–> Renal failure
19
Q
- Sartan
A
Angiotensin II Receptor Blocker
- Similar to ACE
- No increase in bradykinin
- no cough
- no angioedema
20
Q
Prazosin
Terazosin
Doxazosin
Tamsulosin
Class
MOA
Use Toxcity
A
selective alpha blocker
- prevents vasoconstriction