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PHARMACOLOGY - Renal > Diuretics and Aquaretics > Flashcards

Diuretics and Aquaretics Flashcards

1
Q

What drug acts as a carbonic anhydrase inhibitor?

A

Acetazolamide

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2
Q

What drug acts an osmotic diuretic?

A

Mannitol

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3
Q

What drugs act as loop diuretics?

A
  • Furosemide
  • Torsemide
  • Bumetanide
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4
Q

What diuretics act predominantly in the distal convoluted tubule?

A
  • Hydrochlorothiazide*
  • Metolazone
  • Spironolactone*
  • Amiloride*
  • Chlorthaliodone*
  • Eplenerone
  • Triamterene*
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5
Q

What drugs act on the collecting ducts by V2R agonism?

A
  • Arginine Vasopressin

* Desmorpressin [DDAVP]

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6
Q

What drugs act on the collecting ducts by V2R antagonism?

A
  • Conivaptan

* Tolvaptan

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7
Q

What diuretic is known to cause acidosis?
• describe how this happens?
• how does this drug have a diuretic effect?

A

Acetazolamide
• Inhibits Carbonic Anhydrase which results in more Na+ HCO3- being lost in the urine
• Cl- gets reabsorbed instead and combines with H+ in the blood to make HCl =>

Diuretic Effect:
• Increases Solute concentration and thus leads to more fluid being in the tubule

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8
Q

Why does acetazolamide only have a weak diuretic effect?

A

• We don’t have that much HCO3- in the blood

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9
Q

What are the Clinical Uses of Anhydrase Inhibitors?

• name them.

A 
Clinical Uses: 
• Alkalinize Urine (cystinuria) 
• Reduce intra ocular pressure 
• Given Prophylactically for Mountain Sickness 
• LIMITED USE as Diuretic

Acetazolamide

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10
Q

What are the Side Effects of the Carbonic Anhydrase Inhibitors?
• Name them

A

Acetazolamide

  • Metabolic Acidosis
  • Markedly increase K+ loss in the urine (ACUTE EFFECT ONLY)
  • AVOID in Advanced renal failure
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11
Q

What is the key chemical characteristics of osmotic diuretics?

A

•Small molecules that are filtered (make it through glomerulus) but NOT reabsorbed by the kidney

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12
Q

Osmotic Diuretics
• MOA (minor, major)
• Location of Action

A

MOA:
Minor Effect = PROXIMAL CONVOLUTED TUB.
• Osmotically inhibits Na+ and H2O reabsorption

MAJOR EFFECT = Loop of HENLE:
• Extracts Water from peripheral tissues and decreases blood viscosity

  • Increases Medullary Renal Blood Flow and Reduces its Tonicity
  • Impairs water reabsorption by THIN DESCENDING Limb of LOH
  • Impairs NaCl and urea extraction by THIN ASCENDING limb of LOH
  • Interfere with transport processes in the TALH
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13
Q

What is the Net effect and Clinical use of Osmotic Diuretics?
• name one.

A

Net Effect:
• Significantly Increase Urine with Small increments of NaCl and other ions

Clincial uses:
• Treatment of Dialysis disequilibrium syndrome
• Reduce intra cranial pressure*MAIN USE
• Reduce Intraocular pressure

MANNITOL

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14
Q

What are some side effects of osmotic diuretics?

• name one

A

Side Effects:
• Volume Overload
• High Doses are Toxic in Renal Failure
• Contraindicated in Cardiac Failure

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15
Q

What group of diuretic drugs works to inhibit NK2C symporters?
• where does this inhibition occur?
• Why does this work?

A

LOOP DIURETICS block Cl- channel in NK2C

Where:
• Thick Ascending Loop of Henle

Why does it work?
• Prevents Macula Densa (which is present right after the LOH) from sensing NaCl

  • Stimulates biosynthesis of prostaglandins (by macula densa) which REDUCE Na+ reabsorption in the distal nephron and ANTAGONIZE ADH; also Redistributes blood flow from cortex to juxtaglomerulus
  • Increase Total Renal Blood Flow
  • Maintains GFR by increasing % of the filtration fraction
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16
Q

What is the Effect of Loop Diuretics on Total Renal Blood Flow?
• GFR?
• name them.

A

Furosemide, Bumetanide, Torsemide

  • Increases Total Renal Blood Flow
  • Maintain the GFR by increasing the % of the FILTRATION FRACTION
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17
Q

What is the Effect of Loop Diuretics on Renin Release?
• intra-renal and extra-renal effects?
• Name them.

A

Furosemide, Bumetanide, Torsemide

Renin Intra-Renal:
•Inhibits the Macula Densa

Renin Exta-Renal:
• Reflexely activates sympathetic Nervous System

• Stimulates Intrarenal Baroreceptor Mechanisms

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18
Q

What is the NET EFFECT of the loop Diruretics?

• Name them.

A

Furosemide, Bumetanide, Torsemide

  • Cause COPIOUS DIURESIS and SIGNIFICANT NaCl loss - Most potent diuretics at mobilizing NaCl
  • Increased Urinary Excretion of K+/H+
  • Increased excretion of Ca2+ and Mg2+
  • OVERALL THESE IMPAIR THE ABILITY OF THE KIDNEY TO CONCENTRATE URINE
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19
Q

At what GFR do you consider using Loop Diuretics?

• why?

A

• People with a GFR lower than 30 mL/min should be on loop diuretics

why:
• Loop Diruretics are SECRETED into the PROXIMAL CONVOLUTED tubule rather than filtered through the glomerulus

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20
Q

What are some of the principle uses of Loop Diuretics?

• name them

A

Furosemide, Bumetanide, Torsemide

EDEMA: cadiac/hepatic/renal/pulmonary
HYPERCALCEMIA: mobilizes Ca2+
WASHOUT: increases urine flow
ANTIHYPERTENSIVE

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21
Q

How do Loop Diuretics help treat pulmonary edema?

• Name them

A

Furosemide, Bumetanide, Torsemide

  • Relaxes Pulmonary Veins - decreased pulmonary wedge pressure
  • Increase Compliance of Pulmonary Vessels
  • Increase Peripheral Venous Capacitance
  • REDUCES PRELOAD (aka LV Filling Pressure)
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22
Q

If you were giving a loop diuretic to treat someone for hypercalcemia, how would you administer it?

A

• Give it in NORMAL SALINE

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23
Q

Furosemide:
• Methods of Administration
• Therapeutic window?
• Dosing Problems

A

Loop Diuretic that’s given Orally, IV, or IM

Method of Administation:
• PO, IV, IM

Therapeutic Window:
• Large Margin of Safety

Dosing Problems:
• Requires Delivery to the Luminal Symporter
• In RENAL DISEASE there is IMPAIRED secretion and consequently the Dose-Response curve is shifted RIGHT

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24
Q

Why is Furosemide contraindicated with Warfarin?

A

• Both Drugs are protein bound

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25
How long does it take Furosemide to kick in? • how long until its effects are gone? • MOA
~30 min to kick in and lasts ~8 hours with a 1.5 hour half life MOA: • Loop Diuretic so it blocks NK2C channels • Prevents Urine Concentration
26
What are drugs that Furosemide is contraindicated with and why?
* Interactions with Li+ - it deceases Li+ excretion, MUST REDUCE Li+ dose in this case * Indomethacin - this inhibits prostaglandins that are vital for Macula Densa sensing (NSAIDs will do the same thing) * Probenecid - drug used in gout * Warfarin - 99% bound to protein bound
27
What are some side effects of furosemide?
* Volume and Na+ Depletion * HYPOKALEMIA and METABOLIC ALKALOSIS * REQUIRES INITIAL MONITORING * Elevates BUN (via effects on distal convoluted tubule) * Hyperglycemia and Hyperuricemia • Ototoxicity and Sialadenitis (inflammation of Salivary Glands)
28
Compare the Potency of Furosemide and Bumetanide?
Bumetanide = 40x as potent than furosemide • only 1 mg once daily needed ***Not protein bound so GOOD SUBSTITUTE FOR FUROSEMIDE in patients recieving Warfarin***
29
What make Torsemide differenent from other loop diuretics?
* LOWERS BLOOD PRESSURE | * Only needs 1 daily dosing rather than 2x a day dosing like Furosemide and Bumetanide
30
Distal Convoluted Tubule and Collecting Ducts • Amount of Sodium Reabsorbed • Types of Sodium Channels?
Up to 5% of Na+ filtered at the glomerulus may be reabsorbed here 3 types of Na+ channels: 1. Na+-Cl- Symporter in the Na+-K+ aldosterone-independent Segment 2 types of ENaC: 1. Amiloride-Sensitive, cyclic nucleoside gated cation (CNG) channel - --> aka Aldosterone Sensitive 2. Low-conductance highly-selective Na+ ENaC channel
31
What group of diuretics is most often used chronically?
Benzothiadiazides (Thiazide Diuretics)
32
What is the MOA of the Thiazide Diuretics? | • Location of Action
• Bind to the CHLORIDE site of the NaCl Symporter in the Na+-K+ ALDOSTERONE-INDEPENDENT segment of the Distal Tubule
33
What are the Pharmacological Effects of Thiazide Diuretics?
Pharm. Effects: • Moderate Loss of Na+, K+ (HYPOKALEMIA), Cl- • Elevation of Excreted Urinary Potassium • Increased Excretion of Titratable acid b/c of increased delivery of Na+ to the distal tubule • DECREASED Ca2+ excretion, INCREASED Mg2+ excretion
34
What side effects of Thiazide Diuretics are associated with chronic Thiazide use?
Sodium Loss and VOLUME CONTRACTION with REDUCED GFR
35
Why do Thiazide Diuretics cause reduced urinary excretion of Ca2+?
Proximal Convoluted Tubule is acted on in a way that leads to more Ca2+ getting taken up by the body
36
What are the Therapeutic Effects of Benzothiadiazides?
* Diuretic - less edema in CHF, Cirrhosis, and nephrotic syndrome * Hypercalcuria (Osteoporosis) and Renal Calcium Stones * Antihypertenssive or to AUGEMENT action of other antihypertensives * NEPHROTIC Diabetes Insipidus
37
T or F: like loop diuretics, thiazides require secretion into the tubular fluid to exert their effect.
True
38
At what GFR do most Thiazides become ineffective? | • Exceptions?
GFR less than 30 or 40 mL/min Exceptions: METOLAZONE and Indapamide
39
What are the Class I and Class II thiazide diuretics? | • what is the difference in their utility?
Class I: • Hydrochlorothiazide • Chlorthalidone ****Good if GFR is above 50 mL/min Class II: • Metolazone (10X as potent as HCTZ) • Indapamide (20x as potent as HCTZ) *****Good if GFR is between 30 and 50 mL/min Below 30 you'll have to go to a loop diuretic
40
Why can't you just up the dose on someone's Chlorthalidone if they start become edematous?
* Therapeutic effects of Thiazides maxes out at 25mg | * anything above 25mg will just cause more side effects
41
What are the 4 general Adverse effects of Thiazides?
``` Depletion of Phenomena • (K+) Hypokalemia • (Cl-) Hypochloremic Alkalosis • (Na+) Dilutional Hyponatremia • (Mg2+) Hypomagensemia ``` Retention Phenomena • Hyperuricemia • Hypercalcemia Metabolic Changes • Hyperglycemia • Hyperlipidemia • Hypersecretion of renin and aldosterone ``` Hypersensitivity and Other • Pancreatitis • Withdrawal Edema • Sialadenitis • Fever, Rash, Pupurea ```
42
What metabolic changes can be prevented by controlling Hypokalemia associated with Thiazide use?
K+ is needed in the conversion of Proinsulin to Insulin
43
What are the physiological actions of aldosterone? | • where does it act?
• Aldosterone - binds to INTRACELLULAR mineralcorticoid receptor in DISTAL CONVOLUTED TUBULE Gene Expression Upregulated: • ENaC Na+ channels (aka aldosterone induced channels) Other Effects: • Lumen-Negative Transepithelial NaCl transport is increased • INCREASES K+ and H+ excretion
44
What is the MOA of Aldosterone antagonists? • Net Effect. • name them.
Spironolactone and Eplenerone MOA: • Binds to Aldosterone receptor in the cytoplasm to prevent its translocation to the nucleus • Reduces ENaC expression (less Na+ reabsorption) Net Effect: • Increased Urinary Excretion of Na+ • INHIBITION of K+ and H+
45
Spironolactone • Metabolism • Side Effects
EXTENSIVE metabolism until CANRENONE (biologically active derivative) is made Side Effects: • Hyperkalemia • Gynecomastia (man boobs), Hirsuitism, Uterine Bleeding
46
Compare the side effects of Eplenerone and Spironolactone.
Eplenerone has much few side effects because it binds more specifically to ALDOSTERONE receptor and less on Androgen receptors than spironolactone
47
What drug combination is typically used with the aldosterone inhibitors?
Spironolactone or Eplenerone are typically combined with THIAZIDE diuretics to balance the Hyper and Hypokalemic effects of each drug respectively
48
What are the clinical uses of the aldosterone inhibitors?
* Diuretics, tyically in combination with HCTZ * Treatement of CHF * Management of Cirrhosis
49
What are the two TRUE potassium Sparing Diuretics? | • MOA
Triametrene and Amiloride MOA: • Blockage of ENaC sodium channels to inhibit Na reabsorption in the late distal tubule
50
How do Aldosterone blockers and Potassium Sparing diuretics differ in their effects of sodium depletion?
Aldosterone Receptor Blockers tend to INCREASE URINARY Na+ excretion True Potassium Sparing Diuretics (Triametrene and Amiloride) have much less of a Na+ depleting effect
51
What are the clinical uses of the Triametrene and Amiloride? • side effects.
• Combined with Thiazides to increase Thiazide effectiveness and reduce HCTZ K+ excretion Side Effects: • Hyperkalemia (if given alone) • Megaloblastic Anemia in pts. with Cirrhosis • Trimterene sometime forms Kidney Stones
52
T or F: Diuretics can be used as monotherapy.
True
53
What drugs are ACE I's certainly contrainidcated with?
DON'T GIVE WITH K+ Sparing Diuretics!!! | • this is because ACE Is are potassium sparing too
54
What is the best monotherapy of HTN?
• Low Dose Diuretics or ACE Inhibitors
55
In what patients are diuretics required to treat HTN?
* Low Renin/Volume Dependent HTN * Typically seen in African Americans and the Elderly ****Thiazides are good to use because they're cheap****
56
What is the most popular drug prescribed for treatment of mild or moderate HTN? • what about its dosing makes it easy?
* Thiazide Diuretics * you can take one morning dose and it will provide a sustained effect and reduce K+ wastage during Nighttime ***Remember never need to give more than 25mg***
57
Someone starts taking a thiazide diuretic and their blood pressure does not decrease. What are some possible explanations?
* Overwhelming Dietary Sodium Intake | * Impaired Renal Capacity to Excrete Sodium
58
What are some of the Clinical Uses of Loop Diuretics?
* Used in patients with Severe HTN that are unresponsive to thiazides - often ppl. with RENAL INSUFFICIENCY, CARDIAC FAILURE, or CIRRHOSIS * IV administration in Acute Pulmonary Edema
59
What drug-drug interaction commonly occurs with loop diuretics?
• NSAIDS with loop diuretics is the MOST COMMON CAUSE of diuretic resistance (because it relies on prostaglandins synsthesized by macula densa)
60
T or F: K+ sparing diuretics are particularly useful in patients with hyperuricemia.
True
61
What is the Drug of Choice in liver Cirrhosis? why?
Spironolactone - it can be titrated up to 400 mg/day
62
T or F: K+ diuretics are one of the drugs of choice in renal insufficiency.
FALSE, K+ sparing diuretics are CONTRAINDICATED in Renal Insuffiency with GFR below 75 mL
63
Where is ADH synthesized?
• Paraventricular and Supraoptic nuclei of the Hypothalmus
64
When is ADH released?
* Elevated Plasma Osmolarity >280 mOsm/Kg * Depletion of Extracellular Volume * Pain, nausea, hypoxia
65
Where is the V1 receptor found? • what pathway does it act through? • End result of pathway activation?
V1 = Vascular Smooth Muscle Pathway: Gq-PLC-IP3 pathway leading to Ca2+ mobilization End Result: More Ca2+ in the cytoplasm = VASOCONSTRICTION
66
Where is the V2 receptor found? • what pathway does it act through? • End result(s) of pathway activation?
V2 = principal cell in renal collecting ducts Pathway: Gs-cAMP, PKA PKA phosphorylates: • Aquaporin-2 vesicles and targets to membrane • Urea Transporter - VRUT/UT1 End Result: • Increased permeability of H2O and Urea
67
What is the point of increasing CD permeability to urea?
It allows for 4 times the osmolarity of plasma in the TALH
68
What are some drugs that cause nephrogenic diabetes insipidus? • how common is this?
LITHIUM!!!!, clozapine • 50% of pts. on lithium will have IMPAIRED Renal function
69
What is the most effective treatment for central diabetes insipidus? • MOA • how is it administered?
Desmopressin [DDAVP] • Mimicks AVP/ADH effects Administration: • Nasally • IV • Oral Tablet
70
What are some uses of Desmopressin [DDAVP] other than treatment of Diabetes Incipidis? • explain why these can be used?
* BLEEDING disorders (IV or nasal) increases circulating levels of Factor VIII and vWF via extrarenal V2 receptors *  Nocturnal Enurisis (bed wetting in children )
71
What other drugs besides DDAVP are used in treatment of Nephrogenic DI? • side effects? • Rational for using this treatment?
• Thiazide Diuretics - might reduce polyuria by 50% Side Effects: • Depletion of Extracellular Volume and Na+ (b/c you're blocking the NC cotransporter) Rational: • Increased Na+ in the tubule lumen caused by thiazide blocking increases the resorptive capacities of the PCT reducing the vol. of H2O
72
What are V1 Receptor Agonists used to treat? | • Rationale
Treatment: • Post Operative Ileus • Reduce bleeding in esophageal varices • REDUCE BLEEDING DURING ACUTE HEMORRHAGIC GASTRITIS Rational: Activation of V1R causes GI and Vascular Smooth muscle contraction
73
What drugs are V1 Receptor Agonists? | • Administration
Terlipressin Administration: • IV ***NOTE: the use of this drug is super restricted***
74
What is the Etiology of Syndrome of Inappropriate Secretion of ADH (SIADH)?
• Excessive production of ADH | ***results in impaired H2O excretion and plasma HYPOosmolarity (hyponatremia)
75
What are 3 drugs groups known to cause SIADH?
* Psychotropics: SSRI, haloperidol and Tricyclic Anti-depressants * Sulfonylureas: Chloropropamide * Vinca Alkaloids: Vincristine and Vinblastine
76
How are patients with SIADH treated?
* Water Restriction * if SEVERE pts. may be treated with IV hypertonic saline * Loop Diuretics * Demeclocycline * Vaptans
77
What does Demeclocycline do?
• Antagonizes AHD at V2 receptors
78
What is the point of giving someone with SIADH loop diuretics?
• NO FUCKING CLUE
79
Tolvaptan • MOA • indications for use • Side Effects
MOA: • V2 Receptor Antagonist Indications: • SIGNIFICANT hypervolemia and euvolemic hyponatremia • Symptomatic Hyponatremia that has resisted correction with fluid restriction **TO BE USED ONLY IN THE HOSPITAL SETTING*** Side Effects: • Hyperglycemia, GI disturbances, Clotting probs.
80
What other drug shares the same MOA as Torvaptan? • compare selectivity • side effects that differ from torivaptan
• Conivaptan * Less Selective for V2R * May cause infusion Rxn

PHARMACOLOGY - Renal (2 decks)

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