nephrology Flashcards
3 nephron processes
filtration
reabsorption
secretion
What is filtration?
Passes from plasma into the renal tubule
What is reabsorption
Moves back up into the plasma from the tubule
What is secretion?
Moves into the tubule from the plasma
What are 6 uses for diuretics?
Glaucoma Metabolic Alkalosis Acute Mountain Sickness Acute Renal Failure (ARF) Acute Kidney Injury (AKI) Electrolyte imbalances Hypertension
What are 5 ions effected by diuretics?
Na+ Mg2+ Ca2+ Cl- HCO3-
What is the glomerulus?
First stop in the nephron
Blood pressure – controls filtrate formation
No medication sites of action
Filter allows small particles and ions to pass and form the ultrafiltrate
proximal tubules reabsorb what?
65% of NaCl, K+, Ca2+, Mg2+
85% of NaHCO3
Close to 100% of glucose and amino acids
Proximal tubules secrete what?
Site of action?
Organic acid and bases
Site of action
Carbonic anhydrase inhibitors (CAI) proximal tubular
Adenosine antagonist
Carbonic anhydrase Inhibitors (CAI) 3 agents
Acetazolamide (Diamox)
Dorzolamide (Trusopt)*
Brinzolamide (Azopt)
Carbonic anhydrase Inhibitors (CAI) MOA
Inhibits enzyme responsible for dehydration of H2CO3
Reduces aqueous humor production in the eye
Carbonic anhydrase Inhibitors (CAI) indications
Glaucoma, urinary alkalization, metabolic alkalosis, acute mountain sickness
CAI kinetics
Absorbs well: oral and ocular
Increase urine pH; onset 30 min, duration 12 hr, peak 2 hr
Excretion: proximal tubular secretion
CAI contraindication and adverse reactions?
Adverse Reactions
Renal stones, potassium wasting, drowsiness, hypersensitivity reaction
Contraindication
Hepatic cirrhosis
Loop of henle reabsorption
15-25% NaCl, K+
Secondary: Ca2+, Mg2+
Secretion and site of action for loop of henle
Secretion
Some K+
Site of action
Loop diuretics
Loop diuretic agents
Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Dexadex)
Ethacrynic acid (Edecrin)
Loop diuretic MOA
Inhibits Na+/K+/2Cl- transporter
indication for loop diuretics
Edema, hypercalcemia, hyperkalemia, anion overdose
kinetics for loop diuretics
Orally well absorbed; duration of action
Torsemide 1 hour; 4-6 hours
Furosemide 2-3 hours; 2-3 hours
adverse effects for loop diuretics
Hypomagnesemia, hyperuricemia, ototoxicity, allergic reaction
Contraindications for loop diuretics
Overuse in hepatic cirrhosis, renal failure, or heart failure
Sulfonamide allergy*
what decreases the effectiveness of loop diuretics
NSAIDs – decrease effectiveness of loop
If your patient had an sulfa allergy related to furosemide, what other loop diuretic could you use
Ethacrynic acid
Conversion of loop diuretics
PO to IV conversion
Furosemide 2:1 (40 mg PO = 20 mg IV)
Torsemide and Bumetanide 1:1
Conversion between agents
Furosemide 40 mg = Torsemide 20 mg = Bumetanide 1 mg
Distal Convoluted Tubule
reabsorption, secretion and site of action
Reabsorption 4-8% of Na+, Cl- Secretion Ca+ by parathyroid control Site of action Thiazide diuretics
2 types of thiazide agents
Hydrochlorothiazide (Hydrodiuril)
Chlorothiazide (Diuril)
MOA of thiazides
Inhibits NaCl transporter
Enhances Ca+ reabsorption
indication of thiazides
Hypertension, heart failure, nephrogenic diabetes insipidus, nephrolithiasis
3 thiazide like diuretics
Metolazone (Zaroxolyn)
Indapamide (Lozol)
Chlorthalidone (Thalitone)
a sulfonamide group and having same MOA
thiazide kinetics
Absorbed slowly
Chlorthalidone slowest but longer duration of action
adverse reaction for thiazide kinetics
Hyponatremia, hypokalemia, hyperuricemia, hyperlipidemia, allergic reaction, photosensitivity
contraindications for thiazide kinetics
Overuse in hepatic cirrhosis, renal failure, or heart failure
When are thiazide diuretics ineffective?
GFR less than 20 ml/min except metolazone
Chlorothiazide is the only thiazide in IV formulation
Cortical collecting tubule
reabsorption, secretion, site of action
Reabsorption 2-5% Na+ Secretion K+ and H+ Site of action Potassium sparing diuretics Adenosine antagonists
2 potassium sparing agents
Spironolactone (Aldactone)
Eplerenone (Inspra)
MOA of potassium sparing agents
Prevents K+ secretion by antagonizing mineralocorticoid receptors (preventing aldosterone from binding)
indications for potassium sparing agents
Hypokalemia (prevention and treatment), primary
Spironolactone: hyperaldosteronism, polycystic ovary disease, hirsutism
kinetics for potassium sparing agents
Spironolactone: onset, duration, and peak – slow – several days to reach therapeutic levels
Triamterene: onset 2-3 hours, duration 7-9 hours
adverse reactions for potassium sparing agents
Hyperkalemia
Triamterene – kidney stones
Spironolactone only – gynecomastia, impotence, tumorgenic
contraindications for potassium sparing agents
Hyperkalemia, renal impairment, hepatic impairment
Spironolactone – Addison’s disease
drug interactions for potassium sparing agents
Eplerenone only: strong CYP3A4 agents: fluconazole, diltazem, grapefruit juice
Medullary collecting duct
reabsorption, secretion, site of action
Reabsorption Water Secretion None Site of action Vassopressin
ADH antagonist indirectly
Lithium (Lithobid)
Demeclocycline (Declomycin)
MOA – not known
ADH antagonist directly
Conivaptan (Vaprisol)
Tolvaptan (Samsca)
MOA – Inhibits vasopressin receptors
*never seen in practice
Indications for ADH antagonists
Congestive heart failure, syndrome of inappropriate ADH secretion (SIADH)
Direct ADH Antagonist kinetics and adverse reactions
Kinetics
Onset 2-4 hrs, peak 4-8 hrs, duration ~24 hrs
Adverse reactions
Nausea, dry mouth, thirst
Direct ADH Antagonist contraindications
Hypovolemia, hyponatermia
2 osmotic diuretics
Glycerol
Mannitol
MOA of osmotic diuretics
Increase osmotic pressure in the glomerulus, decreasing reabsorption of water and electrolytes
indications for osmotic diuretics
Cerebral edema, acute glaucoma, bronchial hyper-responsiveness
Adverse reactions for osmotic diuretics
Glycerol – nausea, vomiting, diarrhea
Mannitol – excessive volume expansion heart failure, edema, pulmonary congestion
Kinetics and contraindications for osmotic diuretics
Kinetics
Poorly absorbed, quickly excreted
Contraindications
Hypersensitivity
Glomerular Filtration Rate (GFR)
Most common method for measuring kidney function
Volume of plasma filtered across the glomerulus per unit of time
Normal GFR range: 90-120 mL/min
Difficult to measure directly
Serum Creatinine (SCr)
Endogenous substance – by product of muscle metabolism 100% cleared by kidneys 90% glomerular filtration 10% through tubular secretion Direct measure 24 hr urine collection Indirect measure Calculation based on SCr
Ideal Body Weights calculation
Males: 50 kg + (2.3 kg x inches over 5 ft)
Females: 45.5 kg + (2.3 kg x inches over 5 ft
Clinical Presentation for acute kidney infection
Increase in serum creatinine (Scr)
Decrease in glomerular filtration rate (GFR)
Accumulation of nitrogenous waste
Inability to regulate fluid, electrolytes, and acid-base balance
Weight gain (edema)
Foamy urine
Changes in urinary habits
4 types of renal disease
pre renal
postrenal
intrinsic
functional
functional damage for renal disease
Hemodynamic changes without hypotension or structural damage
intrinsic damage for renal disease
Structural damage
urine sediment- casts, cellular debris
RBC + WBC in urine- 2-4
urine Na+ - >40
postrenal for renal disease
obstruction of urine flow
urine WBC 1+
Prerenal azotemia for renal disease
Decrease renal perfusion
urine Na+ 20
urine/ SCr- > 40:1
Non-oliguria
Adults: > 400 mL/day or > 0.5 mL/kg/hr
Pediatric: >1 mL/kg/hr
Oliguria
Adults: < 400 mL/day or < 0.5 mL/kg/hr for > 6 hrs
Pediatric:
Infants: 0.5 mL/kg/hr for 24 hours
Older: <500 mL/1.73 m2
Anuria
< 50 mL/day (Adults and pediatrics)
Most severe patients because they are not making urine
Medication induced AKI– Vasoconstriction into kidney
NSAIDS Cyclosporine Tacrolimus Amphotericin B Radiocontrast agents Vasopressors
Medication induced AKI– Vasodilation out of the kidney
ACEIs, ARBs
Diltiazem, Verapamil
medication induced AKI– Direct toxicity to renal tubules
Aminoglycosides
Amphotericin B*
Cisplatin and carboplatin
Radiocontrast agents*
patient risk factors for AKI
History of chronic kidney disease Increased age Comorbid conditions: Diabetes Dehydration Patient already on AKI inducing medication
Treatment of AKI
evaluate fluid status
identify cause
supportive therapy