Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal/Skeletal > Renal/Uro pharm > Flashcards

Renal/Uro pharm Flashcards

1
Q

Diuretic

A

Any substance that increases urine volume

  • Inhibitors of renal ion transporters
  • Decreases the reabsorption of sodium at different sites of the nephron
  • Increase in urine flow is secondary to increase in sodium excretion
  • Kidneys adjust the excretion of sodium and water to maintain extracellular fluid (ECF)
  • In pathophysiologic states, this balance is altered

Used for:

  1. Diseases causing edema: CHF, Cirrhosis, nephrotic syndrome, renal failure
  2. HTN
  3. Nephrolithiasis
  4. Hypercalcemia (loop diuretics)
  5. Diabetes insipidus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Natriuretic

A

Any substance increasing renal sodium excretion (same function as diuretci)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acetazolamide

A

Carbonic anhydrase inhibitor

Site of action: proximal tubule

MOA:

  • Inhibits carbonic anhydrase
  • Decreases sodium bicarbonate reabsorption
  • Cause bicarbonate diuresis (up to 85%) that may lead to metabolic acidosis
  • Over time (several days), effectiveness decreases–> soon increase Na reabsorption (thus reversing diuresis)

Use: metabolic alkalosis (alkalinizes urine)

  • Induces hyperchloremic metabolic acidosis after excessive use of other diuretics
  • Prophylax acute mountain sickness (decreases CSF formation, pH–> increase minute ventilation–> decrease symptoms)
  • Glaucoma (decreases rate of aqueous humor formation–> decreased IOP)

AEs:

  • Metabolic acidosis
  • Phosphaturia, hypercalciuria (can cause calcium stone formation)
  • Potassium wasting
  • Toxicity: drowsiness/fatigue (CNS carbonic anhydrase inhibition), parasthesis, avoid in liver disease (increases ammonia–> hepatic encephalopathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dichlorphenamide

A

Carbonic anhydrase inhibitor

Site of action: proximal tubule

MOA:

  • Inhibits carbonic anhydrase
  • Decreases sodium bicarbonate reabsorption
  • Cause bicarbonate diuresis (up to 85%) that may lead to metabolic acidosis
  • Over time (several days), effectiveness decreases–> soon increase Na reabsorption (thus reversing diuresis)

Use: metabolic alkalosis (alkalinizes urine)

  • Induces hyperchloremic metabolic acidosis after excessive use of other diuretics
  • Prophylax acute mountain sickness (decreases CSF formation, pH–> increase minute ventilation–> decrease symptoms)
  • Glaucoma- topical use (decreases rate of aqueous humor formation–> decreased IOP)

AEs:

  • Metabolic acidosis
  • Phosphaturia, hypercalciuria (can cause calcium stone formation)
  • Potassium wasting
  • Toxicity: drowsiness/fatigue (CNS carbonic anhydrase inhibition), parasthesis, avoid in liver disease (increases ammonia–> hepatic encephalopathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Methazolamide

A

Carbonic anhydrase inhibitor

Site of action: proximal tubule

MOA:

  • Inhibits carbonic anhydrase
  • Decreases sodium bicarbonate reabsorption
  • Cause bicarbonate diuresis (up to 85%) that may lead to metabolic acidosis
  • Over time (several days), effectiveness decreases–> soon increase Na reabsorption (thus reversing diuresis)

Use: metabolic alkalosis (alkalinizes urine)

  • Induces hyperchloremic metabolic acidosis after excessive use of other diuretics
  • Prophylax acute mountain sickness (decreases CSF formation, pH–> increase minute ventilation–> decrease symptoms)
  • Glaucoma (decreases rate of aqueous humor formation–> decreased IOP)

AEs:

  • Metabolic acidosis
  • Phosphaturia, hypercalciuria (can cause calcium stone formation)
  • Potassium wasting
  • Toxicity: drowsiness/fatigue (CNS carbonic anhydrase inhibition), parasthesis, avoid in liver disease (increases ammonia–> hepatic encephalopathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Furosemide

A

Loop diuretic

Site of action: cortical and medullary TAL of loop of Henle

MOA: inhibits Na+-K+-2Cl- transporter

Clinical:

  • Rapid onset of action (first line in pulmonary edema)
  • Stimulates prostaglandin synthesis in lung, kidneys (NSAIDs–> decreased prostaglandins–> decreased diuresis)
  • CHF (decrease ECF volume)
  • Excretion of: K+, Mg+2 and Ca+2 (Ca reabsorbed later in DCT, but can be used in hypercalcemia)
  • Blocks reabsorption of bromide, fluoride, iodide (poisoning)
  • Used 2nd line or with thiazide diuretics for HTN
  • Edema of nephrotic syndrome (refractory to other diuretics)

Side effects:

  • hypokalemia, hypomagnesemia
  • hyperuricemia (gouty attack)
  • hypochloremic metabolic alkalosis (increased excretion of H+)
  • Dose-related irreversible hearing loss (alters membranous labyrinth in inner ear)
  • Cross-reactivity with sulfonamide allergy
  • Dehydration
  • Increased LDL, triglycerides, decreased HDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bumetanide

A

Loop diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Torsemide

A

Loop diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ethacrynic acid

A

Loop diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hydrochlorothiazide

A

Thiazide diuretics

Site of action: distal convoluted tubule

MOA: inhibits luminal co-transport of Na, Cl
- Contraction of ECF volume–> decrease in CO–> decrease peripheral vascular resistance

Clinical use:

  • Augment production of vasodilatory prostaglandins (NSAID interaction)
  • Use in HTN, mild CHF
  • Edema due to liver/renal disease
  • Only moderately efficacious in decreasing Na+ reabsorption (most reabsorbed before DCT)
  • Increased K, H excretion
  • Decreased renal Ca+2 excretion (good with urinary stone treatment)

Conditions:
- Nephrogenic DI: paradoxical decrease in urine output

AEs:

  • Avoid in low GFR
  • “Ceiling diuretics”: increasing dose does not promote further diuresis
  • hypokalemia, hypomagnesemia
  • hyperuricemia (gouty attack)
  • hypochloremic metabolic alkalosis
  • Sulfa allergy interaction: photosensitivity, generalized dermatitis (rare)
  • Hyperglycemia (impair pancreatic insulin release, tissue utilization of glucose)
  • Hyperlipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Chlorothalidone

A

Thiazide diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Metolazone

A

Thiazide diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Spironolactone, eplerenone

A

Potassium-sparing diuretic

MOA: competitive antagonist of aldosterone receptors on collecting tubule (Na-H exchanger)

SIte of action:
- Cortical collecting tubule

Clinical:

  • Most effective in primary/secondary hyperaldosteronism (Conn syndrome) - prevents binding of aldosterone to its receptor
  • Secondary hyperaldosteronism seen in: CHF, hepatic cirrhosis, nephrotic syndrome
  • Ascites
  • HTN
  • Loop/thiazide-induced hypokalemia

AEs:

  • Hyperkalemia (if not on another diuretic)
  • Hyperchloremic metabolic acidosis= blocks collecting duct Na-H exchange (aldosterone receptor)–> can’t excrete H+
  • Endocrine abnormalities: gynecomastia, hirsutism, impotence, benign prostatic hyperplasia, menstrual irregularities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Triamterene, amiloride

A

Postassium-sparing diuretic

MOA: interferes with Na+ influx thru epithelial Na ion channels in luminal membrane (Na-H exchanger in collecting duct)
- K+ secretion coupled with Na+ entry (therefore spare K+ secretion by blocking Na entry)

Clinical use:

  • HTN
  • Loop/thiazide-induced hypokalemia

AEs:

  • Hyperkalemia (if not on another diuretic)
  • Hyperchloremic metabolic acidosis= blocks collecting duct Na-H exchange (aldosterone receptor)–> can’t excrete H+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Eplerenone

A

Spironolactone with greater selectivity to mineralocorticoid receptor

  • Less activity on androgen, progesterone receptors (decreased side effects)
  • Blocks fibrosis/inflammation caused by aldosterone–> slows albuminuria in diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mannitol

A

Osmotic diuretic

Not reabsorbed, causing water to be retained initially, then diuresis

Site of action:

  • Proximal tubule: decreased Na reabsorption by osmotic gradient–> increased urine volume
  • Descending loop of Henle: increased medullary blood flow, inhibit reabsorption of water
  • Collecting duct: opposes action of ADH

Clinical:

  • Prevents acute renal failure after severe trauma, complicated surgical procedures (hemolysis, rhabdomyolysis)
  • Toxin excretion
  • Reduces intracranial, intraocular pressure–> fluid (not Na) leaves cells
  • Does not increase Na excretion (only water)
  • Must be given IV (only effects colon if given orally)

AEs:

  • Rapidly distributes to ECF–> extracts water from cells
  • Causes acute increase in ECF/hyponatremia (can’t use in CHF, pulmonary edema)
  • N/V, headache
  • Severe dehydration, hypernatremia
  • Hyperkalemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Conivaptan

A

Antidiuretic hormone antagonist

MOA: inhibits effects of ADH

Site of action: collecting duct

Clinical use:

  • Hypervolemic, euvolemic hyponatremia not corrected by fluid restriction
  • SIADH (with failure of water restriction)
  • CHF, cirrhosis (diminished circulating blood volume)–> increased ADH
  • Conivaptan= IV

AEs:

  • Severe hypernatremia
  • Too rapid correction can cause seizures/death
18
Q

Tolvaptan

A

Antidiuretic hormone antagonist

Can be administered PO

19
Q

Edema and diuretics

A

NaCl reabsorption too high in many disease states leading to:

  • Water retention
  • increased blood volume
  • Expansion of ECF compartment
20
Q

CHF and diuretics

A

Diuretic of choice: Loop diuretic

CO continues to deteriorate–> kidney retains sodium, water
- Water leaks from vasculature–> interstitial–> pulmonary edema

Diuretics:

  • Improve exercise tolerance, quality of life
  • Reduce fluid retention symptoms
  • Reduce hospitalizations

Do not:
- alter disease progression

Clinical:
- Change in body weight is sensitive marker of fluid retention due to CHF

21
Q

Kidney disease and diuretics

A

Cause retention of sodium, water

  • Milder renal insufficiency, diuretics beneficial
  • Need larger doses as GFR declines (risk hearing loss)
  • Continuous infusion dosing best

Does not:

  • reverse clinical disease, help with renal function
  • minimally beneficial in severe insufficiency
  • avoid acetazolamide (worsening acidosis) and potassium-sparing diuretics (hyperkalemia)
22
Q

Diuretic resistance in renal failure

A
  1. Excessive sodium intake
  2. Inadequate diuretic dose
  3. Reduced oral bioavailability (double dose IV to oral)
  4. Nephrotic syndrome: glomerulus allows plasma protein loss–> decreased osmotic pressure and increased aldosterone–> edema/Na/water retention
  5. Reduced renal blood flow:
    - NSAIDs, ACE-I, Vasodilators
    - Hypotension (Intravascular volume expansion, vasopressors)
    - Intravascular depletion (volume expansion)
  6. Heart failure
  7. Nephrotic adaptation
  8. Cirrhosis (tx: paracentesis)
  9. Acute tubular necrosis
  10. Some patients with resistance respond to continuous infusions
23
Q

Cirrhosis and diuretics

A

Liver disease–> obstructed portal blood flow–> increased portal pressure

  • Decreased plasma protein synthesis–> decreased oncotic pressure
  • Both cause fluid to leave portal vascular system–> collects in abdomen

Mechanism for Na retention:

  • diminished renal perfusion
  • Diminished plasma volume (+ ascites)
  • Diminished oncotic pressure (low albumin)
  • Primary sodium retention (elevated aldosterone)
24
Q

HTN and diuretics

A

Thiazide= first line

Enhance other anti-hypertensives

25
Q

Nephrolithiasis and diuretics

A

Thiazide diuretics: enhance calcium reabsorption (decrease urinary calcium concentration)

2/3 kidney stones have calcium phosphate or oxalate crystals (hypercalcuria)

26
Q

Drug treatments for BPH

A
  1. Alpha antagonists (-zosin)
    - Old= terazosin, dexazosin (need to be titrated to avoid hypotension)
    - Newer formulas target Alpha-1 receptors
    - Decreased risk of postural hypotension
  2. 5-alpha reductase inhibitors
    - May take 6-12 months for maximal effect
27
Q

Alpha-1 antagonists: AEs

A
  • Postural hypotension (dizziness)
  • Nasal congestion
  • Headache
  • Asthenia (weakness)
  • Abnormal (retrograde) ejaculation)
  • Erectile dysfunction (can cause or improve)
  • Avoid with planned cataract surgery (Floppy Iris Syndrome)
28
Q

5-alpha reductase inhibitors

A

Testosterone converted to 5-DHT in prostate by 5-alpha reductase

  • 5DHT contributes to BPH
  • Blocking 5-alpha reductase–> decreased DHT–> decreased BPH

Type 2= seen primarily in genitals vs Type 1 (liver and skin)

29
Q

Finasteride

A

Inhibits Type II 5-AR

Side effects:

  • Decreased libido
  • Ejaculatory disorder
  • Erectile dysfunction
  • Breast tenderness
  • Gynecomastia
30
Q

Dutasteride

A

Inhibits Type I and II 5-AR

Side effects:

  • Decreased libido
  • Ejaculatory disorder
  • Erectile dysfunction
  • Breast tenderness
  • Gynecomastia
31
Q

Comparison of 5-alpha reductase inhibitors vs alpha-1 blockers

A

5-AR inhibitors:

  • Symptom improvement from ~6 months
  • increased flow from 1 month
  • Effects on symptoms and flow demonstrated to 10 yr
  • Reduce prostate volume
  • Reduce the risk of AUR (acute urinary retention)
  • Reduce the risk of surgery
  • Decrease PSA (< 1 month

Alpha-1 blockers;

  • increased flow from < 1 month
  • Effect on symptoms and flow > 12 months not well established
  • Do not reduce prostate volume
  • Do not prevent AUR and surgery (Delay??)
32
Q

Treatment of Erectile Dysfunction

A

Phosphodiesterase-5 inhibitors:
- Prevent break down of cGMP

Lifestyle modifications:

  • Smoking cessation
  • Limit/avoid EtOH
  • Diet
  • Exercise

Medication-induced

  • Anti-HTN
  • SSRIs
  • Hormonal agents
  • H2-receptor antagonists
33
Q

Oral PDE5 inhibitors

A

Sildenafil
Tadalafil
Vardenafil

AEs:

  1. Contraindicated with nitrates
    - Can potentiate vasodilation and hypotension associated with NO
    - Several early deaths in elderly men with concomittant heart disease on nitrates
  2. Caution in vascular disease, coronary disease, vascular risk factors (cardiac eval)
  3. Any recent MI, arrhytmias, obstructive hypertrophic cardiomyopathy
34
Q

Second-line therapy for ED

A
  1. MUSE: Medicated uretheral suppository for erection
    - Administers local alprostadil (PGE-1) to enhance erection
    - Useful in non-responsive patients or patients on nitrates
    * * PGE-1= stimulates adenylyl cyclase–> increased cGMP
  2. Intracavernosal injection (PDE-inhibitors: alprostadil, papaverine)
    - More reliable, instant predictable erection
    - Fewer AEs, contraindications
    * Phentolamine= alpha-blocker
35
Q

Muscarinic receptors in bladder

A

Normal contraction mediated by activation of muscarinic receptors in detrusor muscles (Ach binding):

  • M3 receptor= primary mediator of bladder contraction
  • M2= more prevalent
36
Q

Fesoterodine
Derofenisine
Tolteradine
Solifenacin

A

MOA:

  1. Antimuscarinic action
    - Inhibits binding of acetylcholine to cholinergic receptor and suppresses bladder contractions
  2. Antispasmodic
    - Allows detrusor smooth-muscle relaxation to control overactive bladder and urge urinary incontinence

Effects on Urinary Bladder= Motor and sensory

  • Increase bladder capacity
  • Reduce urinary frequency
  • Diminsh urinary incontinence episodes resulting from involuntary bladder contractions

AEs:

  • Dry mouth
  • Headache
  • Constipation
  • Diarrhea
  • Pain
  • Dyspepsia
37
Q

Oxybutynin

A

Tertiary amine, antimuscarinic agent

HIgher rates of AEs than tropsium

38
Q

Tropsium

A

Quarternary amine

Less likely to cross BBB- better for use in older patients with concern of interfering with cognitive function

39
Q

Mirabegron

A

Beta-3 adrenergic agonist

- Relaxes bladder detrusor muscle

40
Q

Testosterone replacement

A 
ROA:
Oral androgens not used in US
- Difficulty with achieving consistent levels
- Hepatotoxicity
Injectable agents
Transdermal/topical agents
Buccal preparations
Long acting implants

Used to treat symptoms of hypogonadism:
- ED, low libido, depression, fatigue, anemia

Diagnosis both clinical and serological

  • Should have endocrine eval before T replacement
    • Need to be careful in prostate cancer

Renal/Skeletal (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions