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nephrology Flashcards

1
Q

3 nephron processes

A

filtration
reabsorption
secretion

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2
Q

What is filtration?

A

Passes from plasma into the renal tubule

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3
Q

What is reabsorption

A

Moves back up into the plasma from the tubule

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4
Q

What is secretion?

A

Moves into the tubule from the plasma

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5
Q

What are 6 uses for diuretics?

A 
Glaucoma
Metabolic Alkalosis
Acute Mountain Sickness
Acute Renal Failure (ARF)
Acute Kidney Injury (AKI)
Electrolyte imbalances
Hypertension
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6
Q

What are 5 ions effected by diuretics?

A 
Na+
Mg2+
Ca2+
Cl- 
HCO3-
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7
Q

What is the glomerulus?

A

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

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8
Q

proximal tubules reabsorb what?

A

65% of NaCl, K+, Ca2+, Mg2+
85% of NaHCO3
Close to 100% of glucose and amino acids

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9
Q

Proximal tubules secrete what?

Site of action?

A

Organic acid and bases

Site of action
Carbonic anhydrase inhibitors (CAI) proximal tubular
Adenosine antagonist

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10
Q

Carbonic anhydrase Inhibitors (CAI) 3 agents

A

Acetazolamide (Diamox)
Dorzolamide (Trusopt)*
Brinzolamide (Azopt)

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11
Q

Carbonic anhydrase Inhibitors (CAI) MOA

A

Inhibits enzyme responsible for dehydration of H2CO3

Reduces aqueous humor production in the eye

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12
Q

Carbonic anhydrase Inhibitors (CAI) indications

A

Glaucoma, urinary alkalization, metabolic alkalosis, acute mountain sickness

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13
Q

CAI kinetics

A

Absorbs well: oral and ocular
Increase urine pH; onset 30 min, duration 12 hr, peak 2 hr
Excretion: proximal tubular secretion

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14
Q

CAI contraindication and adverse reactions?

A

Adverse Reactions
Renal stones, potassium wasting, drowsiness, hypersensitivity reaction
Contraindication
Hepatic cirrhosis

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15
Q

Loop of henle reabsorption

A

15-25% NaCl, K+

Secondary: Ca2+, Mg2+

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16
Q

Secretion and site of action for loop of henle

A

Secretion
Some K+
Site of action
Loop diuretics

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17
Q

Loop diuretic agents

A

Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Dexadex)
Ethacrynic acid (Edecrin)

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18
Q

Loop diuretic MOA

A

Inhibits Na+/K+/2Cl- transporter

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19
Q

indication for loop diuretics

A

Edema, hypercalcemia, hyperkalemia, anion overdose

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20
Q

kinetics for loop diuretics

A

Orally well absorbed; duration of action
Torsemide 1 hour; 4-6 hours
Furosemide 2-3 hours; 2-3 hours

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21
Q

adverse effects for loop diuretics

A

Hypomagnesemia, hyperuricemia, ototoxicity, allergic reaction

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22
Q

Contraindications for loop diuretics

A

Overuse in hepatic cirrhosis, renal failure, or heart failure
Sulfonamide allergy*

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23
Q

what decreases the effectiveness of loop diuretics

A

NSAIDs – decrease effectiveness of loop

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24
Q

If your patient had an sulfa allergy related to furosemide, what other loop diuretic could you use

A

Ethacrynic acid

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25
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
26
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 ```
27
2 types of thiazide agents
Hydrochlorothiazide (Hydrodiuril) | Chlorothiazide (Diuril)
28
MOA of thiazides
Inhibits NaCl transporter | Enhances Ca+ reabsorption
29
indication of thiazides
Hypertension, heart failure, nephrogenic diabetes insipidus, nephrolithiasis
30
3 thiazide like diuretics
Metolazone (Zaroxolyn) Indapamide (Lozol) Chlorthalidone (Thalitone) a sulfonamide group and having same MOA
31
thiazide kinetics
Absorbed slowly | Chlorthalidone slowest but longer duration of action
32
adverse reaction for thiazide kinetics
Hyponatremia, hypokalemia, hyperuricemia, hyperlipidemia, allergic reaction, photosensitivity
33
contraindications for thiazide kinetics
Overuse in hepatic cirrhosis, renal failure, or heart failure
34
When are thiazide diuretics ineffective?
GFR less than 20 ml/min except metolazone | Chlorothiazide is the only thiazide in IV formulation
35
Cortical collecting tubule | reabsorption, secretion, site of action
``` Reabsorption 2-5% Na+ Secretion K+ and H+ Site of action Potassium sparing diuretics Adenosine antagonists ```
36
2 potassium sparing agents
Spironolactone (Aldactone) | Eplerenone (Inspra)
37
MOA of potassium sparing agents
Prevents K+ secretion by antagonizing mineralocorticoid receptors (preventing aldosterone from binding)
38
indications for potassium sparing agents
Hypokalemia (prevention and treatment), primary | Spironolactone: hyperaldosteronism, polycystic ovary disease, hirsutism
39
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
40
adverse reactions for potassium sparing agents
Hyperkalemia Triamterene – kidney stones Spironolactone only – gynecomastia, impotence, tumorgenic
41
contraindications for potassium sparing agents
Hyperkalemia, renal impairment, hepatic impairment | Spironolactone – Addison’s disease
42
drug interactions for potassium sparing agents
Eplerenone only: strong CYP3A4 agents: fluconazole, diltazem, grapefruit juice
43
Medullary collecting duct | reabsorption, secretion, site of action
``` Reabsorption Water Secretion None Site of action Vassopressin ```
44
ADH antagonist indirectly
Lithium (Lithobid) Demeclocycline (Declomycin) MOA – not known
45
ADH antagonist directly
Conivaptan (Vaprisol) Tolvaptan (Samsca) MOA – Inhibits vasopressin receptors *never seen in practice
46
Indications for ADH antagonists
Congestive heart failure, syndrome of inappropriate ADH secretion (SIADH)
47
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
48
Direct ADH Antagonist contraindications
Hypovolemia, hyponatermia
49
2 osmotic diuretics
Glycerol | Mannitol
50
MOA of osmotic diuretics
Increase osmotic pressure in the glomerulus, decreasing reabsorption of water and electrolytes
51
indications for osmotic diuretics
Cerebral edema, acute glaucoma, bronchial hyper-responsiveness
52
Adverse reactions for osmotic diuretics
Glycerol – nausea, vomiting, diarrhea | Mannitol – excessive volume expansion  heart failure, edema, pulmonary congestion
53
Kinetics and contraindications for osmotic diuretics
Kinetics Poorly absorbed, quickly excreted Contraindications Hypersensitivity
54
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
55
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 ```
56
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
57
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
58
4 types of renal disease
pre renal postrenal intrinsic functional
59
functional damage for renal disease
Hemodynamic changes without hypotension or structural damage
60
intrinsic damage for renal disease
Structural damage urine sediment- casts, cellular debris RBC + WBC in urine- 2-4 urine Na+ - >40
61
postrenal for renal disease
obstruction of urine flow | urine WBC 1+
62
Prerenal azotemia for renal disease
Decrease renal perfusion urine Na+ 20 urine/ SCr- > 40:1
63
Non-oliguria
Adults: > 400 mL/day or > 0.5 mL/kg/hr Pediatric: >1 mL/kg/hr
64
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
65
Anuria
< 50 mL/day (Adults and pediatrics) | Most severe patients because they are not making urine
66
Medication induced AKI-- Vasoconstriction into kidney
``` NSAIDS Cyclosporine Tacrolimus Amphotericin B Radiocontrast agents Vasopressors ```
67
Medication induced AKI-- Vasodilation out of the kidney
ACEIs, ARBs | Diltiazem, Verapamil
68
medication induced AKI-- Direct toxicity to renal tubules
Aminoglycosides Amphotericin B* Cisplatin and carboplatin Radiocontrast agents*
69
patient risk factors for AKI
``` History of chronic kidney disease Increased age Comorbid conditions: Diabetes Dehydration Patient already on AKI inducing medication ```
70
Treatment of AKI
evaluate fluid status identify cause supportive therapy

Pharm Renal & GU (2 decks)

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