Renal Flashcards

1
Q

Mannitol

A
  • Proximal Tubule
  • Mechanism
    • Osmotic diuretic
      • increases tubular fluid osmolarity
        • increases urine flow
        • decreases intracranial/ intra-ocular pressure
  • 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
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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
  • Clinical Use
    • Glaucoma
    • Urinary alkalinization
    • Metabolic alkalosis (lose HCO3-)
    • Altitude sickness
    • Pseudotumor cerebri
  • Toxicity
    • Hyperchloremic metabolic acidosis
    • Paresthesias
    • NH3 toxicity
    • Sulfa allergy
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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
  • 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)
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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 **
  • Use
    • Diuresis in patients allergic to sulfa drugs
  • Toxicity
    • Ototoxicity
    • Hypokalemia
      • Hypokalemic metabolic alkalosis
    • Hypocalcemia
    • Dehydration
    • Nephritis (interstitial)
    • Gout (hyperuricemia)
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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
  • Overcome by adding Thiazide diuretic
    • works in distal tubule
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6
Q

Hydrochlorothiazide

chloralidone

A

Thiazide Diuretic

  • Distal tubule
  • Mechanism
    • **Inhibits NaCl reabsorption **
      • Reduces diluting capacity of neuron
    • Ca+ sparing
      • decrease Ca+ excretion
  • 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
  • Toxicity
    • Hypokalemic Metabolic alkalosis
    • Hyponatremia
    • Hyperglycemia
    • Hyperlipidemia
    • Hyperuricemia (gout)
    • Hypercalcemia
    • Sulfa allergy
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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+
    • Mild Androgen receptor antagonist
      • Gynecomastia
      • Switch to eplerenone if this occurs
  • Use
    • Hyperaldosteronism
    • K+ depletion
    • CHF
    • PCOS
  • Toxicity
    • Hyperkalemia
      • Arrhythmias
    • Gynecomastia
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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
  • Use
    • Hyperaldosteronism
    • K+ depletion
    • CHF
  • Toxicity
    • Hyperkalemia
      • Arrhythmias
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9
Q

Triamterene

A

K+ Sparing Diuretic

  • Cortical Collecting Tubule
  • Mechanism
    • **Block Na+ channels **
      • Na+ and water excretion
  • Use
    • Hyperaldosteronism
    • K+ depletion
    • CHF
  • Toxicity
    • Hyperkalemia
      • arrhythmias
    • kidney stones
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10
Q

Amiloride

A

K+ Sparing Diuretic

  • Cortical Collecting Tubule
  • Mechanism
    • Block Na+ channels
      • Na+ and H20 excretion
  • Use
    • Hyperaldosteronism
    • K+ depletion
    • CHF
  • Toxicity
    • Hyperkalemia
      • arrhythmias
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11
Q

Urine NaCl with Diuretics

A
  • All increase urine NaCl
  • Serum NaCl may decrease as a result
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12
Q

Urine K+ with diuretics

A
  • K+ sparing decrease urine K+
  • All others increase urine K+
    • serum K+ may decrease as a result
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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
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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
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15
Q

Urine Ca+ levels diuretics

A
  • Furosemide + Ethacrynic acid (loops)
    • increase urine Ca+ ==> hypocalcemia
      • decrease paracellular Ca+ reabsorption
  • Hydrachlorothiazide (thiazides)
    • decrease urine Ca+ ==> hypercalcemia
      • enhance paracellular Ca+ reabsorption in proximal tubule and loop of henle
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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
  • 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
    • 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
  • 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
  • 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