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Pharmacology & Medical Chemistry II > Exam 1: Lecture 2 & 3: Diuretics > Flashcards

Exam 1: Lecture 2 & 3: Diuretics Flashcards

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1
Q

Diuretics that work in the PCT

A

Carbonic Anhydrase Inhibitors
SGLT2 Inhibitors
Osmotic diuretics (not main site)

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2
Q

Diuretics that work in the Thin Descending Limb

A

Osmotic Diuretics (Main site of action)

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3
Q

Diuretics that work in the Thick Ascending Limb

A

Loop Diuretics

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4
Q

Diuretics that work in the DCT

A

Thiazide Diuretics

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5
Q

Diuretics that work in the Collecting Duct

A

Vasopressin Receptor Antagonists
ENaC Inhibitors, K+ Sparing Diuretics
Aldosterone Antagonists, K+ Sparing Diuretics

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6
Q

Carbonic Anhydrase Inhibitors: Prototype

A

Acetazolamide

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7
Q

Carbonic Anhydrase Inhibitors: MOA

A

Inhibition of Carbonic Anhydrase, preventing Sodium Bicarbonate reabsorption, leading to increased Sodium and Water excretion

Sodium stays in the Lumen since less moves through NHE3 and water goes where Sodium goes

Occurs mostly PCT

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8
Q

Carbonic Anhydrase Inhibitors: Applications

A 
Glaucoma
Urinary alkalinization
Metabolic alkalosis
epilepsy
CSF leakage
Respiratory Stimulant
Acute mountain sickness
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9
Q

Carbonic Anhydrase Inhibitors: Notables

A

Ineffective as a diuretic mono therapy due to effect on renal excretion are self limiting. Tolerance develops after 2-3 days

Risks associated are hyperchloremic & hypokalemic metabolic acidosis from Net lose of base in plasma and gain of CL-

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10
Q

Where does most potassium wasting occur?

A

Most occurs at the level of the collecting tubule

This is due to the ENaC, which when their is high Na+ in Lumen, will drive Na into cell causing K+ to be driven out. (causing hypokalemia)

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11
Q

Carbonic Anhydrase Inhibitors: Drugs

A

Acetazolamide = Prototype

Dorzolamide, Brinzolamide = eye drops

Dichlorophenamide, Methazolamide = oral

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12
Q

Carbonic Anhydrase Inhibitors: Glaucoma application

A

Block carbonic anhydrase, decreasing sodium and bicarbonate entry into cell. This reduces aqueous humor production which causes excess pressure causing glaucoma

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13
Q

Carbonic Anhydrase Inhibitors: Acute Mountain Sickness

A

Due to exposure to low oxygen lvls at high elevation

Preventing release of bicarbonate into CSF, which causes decrease in pH, and increase ventilation/oxygen delivery and decreasing the symptoms of acute mountain sickness

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14
Q

SLGT2 Inhibitors: Prototype

A

Dapagliflozin

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15
Q

SLGT2 Inhibitors: General MOA

A

Inhibition of SGLT2, preventing reabsorption of glucose in the PCT

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16
Q

SLGT2 Inhibitors: Applications

A

Diabetes mellitus, Type II Diabetes

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17
Q

SLGT2 Inhibitors: Notables

A

Side effects associated with non-specificity (bind to other SGLT), genetic and epigenetic variations

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18
Q

SLGT2 Inhibitors: Drugs

A

Dapagliflozin = Prototype (Farxiga)

Canagliflozin (Invokana)
Empagliflozin (Jardiance)

3rd line for type II Diabetes

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19
Q

SGLT2 Inhibitors: Steps

A

1st: SGLT2 inhibition, leading to increased conc of tubular fluid (more Glucose and Na excretion), reduction in extracellular fluid volume

Sensing of increased tubular Na leads to vasoconstriction (afferent)

Sensing increased tubular Na leads to inhibition of renin release, causing vasodilation (efferent)

This combo causes reduction in GFR, and intraglomerular hydrostatic pressure

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20
Q

What is the renal protective effect of SGLT2 inhibitors?

A

Reducing of GFR

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21
Q

SGLT2 Inhibitor: Clinical Application

A

Diabetes Mellitus, 3rd line therapy

Occurs when excess blood glucose, SGLT2 inhibitors will not allow excess glucose to be reabsorbed and thus excreted

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22
Q

Osmotic Diuretic: Prototype

A

Mannitol (Must be given IV, orally it will cause diarrhea)

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23
Q

Osmotic Diuretic: MOA

A

Prevents absorption of water through osmotic force mainly in Thin Descending Limb, also PCT

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24
Q

Osmotic Diuretics: Applications

A

Reduction of intracranial and intraocular pressure

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25
Q

Osmotic Diuretics: Risks

A

Hyperkalemia, Hypernatremia, and Hyponatremia (if any renal failure)

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26
Q

Osmotic Diuretics: Drugs

A

Mannitol (Prototype)

Glycerin isn’t really used much

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27
Q

Osmosis

A

Movement of water (solvent) from low to high solute concentration through semipermeable membrane

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28
Q

Osmotic Diuretics: MOA at PCT

A

Mannitol will reduce water reabsorption

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29
Q

Osmotic Diuretics: MOA in Thin Descending Limb in loop of Henle

A

Decreased sodium reuptake and decreased water reabsorption leading to an indirect effect in DCT and Collecting duct.

Will have increased delivery in lumen space, increasing the rate which also lowers Na reabsorption in DCT and Collecting duct, thanks to rate of flow.

increase urinary excretion of just about all electrolytes

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30
Q

Osmotic Diuretics: Clinical applications

A

Reduction of Intracranial pressure and
Reduction of Intraocular Pressure.

sometimes in drug OD, to make you pee more

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31
Q

Osmotic Diuretics Notables

A

Mannitol should be given IV

Key risks is dehydration

Hyperkalemia, Hyperatremia and Hyponatremia are all risks depending on dose and pathology

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32
Q

Osmotic Diuretic: Hypernatremia

A

Due to ENaC

33
Q

Osmotic Diuretic: Hyponatremia

A

Can occur in patient with renal damage due to retaining mannitol in the blood

34
Q

Osmotic Diuretic: Hyperkalemia

A

Can occur in high dose, patient dependent.

due to expansion of ECF volume, pulls K+ into plasma

35
Q

Loop diuretics focus on which channel?

A

Inhibitors of NKCC2

Also known as “High Ceiling” diuretics

36
Q

Where do loop diuretics work?

A

Thick ascending limb.

37
Q

Loop Diuretic: Prototype

A

Furosemide

38
Q

Loop Diuretic: MOA

A

Inhibition of NKCC2 in the Thick Ascending Limb

By inhibiting NKCC2, will reduce ROMK activity which drives Mg,Ca moving back into interstitial space.

Can also cause potassium wasting

39
Q

Loop Diuretic: Applications

A

Mainly used for acute pulmonary edema and hypertension

Not first line of therapy for Hypertension,

40
Q

Loop Diuretics: Notables

A

High Ceiling = most effective at producing diuresis

Risk: Hypokalemic metabolic alkalosis, hyperuricemia, hypomagnesemia, ototoxicity

Allergic Reaction

41
Q

Potassium wasting

A

Happens at the level of the collecting duct

Increase in ions in lumen. The high conc of sodium taken up by principle cells (via ENaC) will cause potassium to move through the principle cell and back into the urine

42
Q

Loop Diuretics: Drugs

A

Prototype: Furosemide

Torsemide, Bumetanide, Ethacrynic acid

43
Q

Loop Diuretics: Acute Pulmonary edema

A

Very effective at removing water and treating edema

44
Q

Cardiogenic

A

Cardiac component, related to cardiac dysfunction

45
Q

Loop Diuretics: Hypertension and Hypercalcemia

A

Hypercalcemia = High plasma calcium levels

Works by reducing ROMK activity, reducing how much Ca it drives into cell

46
Q

Loop Diuretics: Hypertension and Hypercalcemia

A

Hypercalcemia = High plasma calcium levels

Works by reducing ROMK activity, reducing how much Ca it drives into cell

47
Q

Thiazides: Prototype

A

Hydrochlorothiazide

48
Q

Thiazide: MOA

A

Inhibition of NCC in the DCT

49
Q

Thiazide: Applications

A

Hypertension
Heart Failure
Nephrolithiasis due to idiopathic hypercalciuria (Kidney stone), and nephrogenic diabetes insidious (excessing urination)

50
Q

Thiazide: Notables

A

Preferred over loops due to longer duration of action

Potassium wasting, lesser extent than loop diuretics though

Hypokalemic metabolic alkalosis, impaired carbohydrate tolerance, hyperlipidemia, hyponatremia, *impaired uric acid metabolism and gout , allergy

51
Q

Thiazides: Drugs

A

HCTZ (prototype)
Metolazone
Chlorthiazide
Chlorthalidone

52
Q

Thiazide Detailed MOA

A

Inhibition of NCC in DCT

Will cause modest increase in Na excretion

Some K+ wasting

Will enhance Ca reabsorption, opposite of loop diuretics which will decrease Ca in urine

53
Q

Clinical Indications Thiazides

A

Hypertension
Edema in Heart failure
Kidney stones
Excessive peeing

54
Q

Where is ADH produced

A

Produced in the Hypothalamus

55
Q

Where is ADH stored

A

stored in the pituitary gland

56
Q

What do Vasopression Receptor Antagonists target (Vaptans)

A

Vasopressin receptors

57
Q

Quick facts about Aquaporins

A

6 Transmembrane regions

Create a pore, H2O moves in single file.

Selective binding for H2O

58
Q

How many monomers is an aquaporin made of?

A

Four

59
Q

Vaptans: Prototype

A

Canivaptan

60
Q

Vaptans: MOA

A

Inhibition of V1 and V2 receptors (Nonselective)

or

Inhibition of V2 receptors (Selective)

61
Q

Vaptans: Applications

A

Autosomal dominant polycystic kidney disease (try and slow progression)

Heartfailure

SIADH (Excessive release of ADH)

62
Q

Vaptans: Notables

A

Nephrogenic diabetes insipidus (excessive water in urine)

Renal failure (Lithium and demeclocycline)

Dry mouth
Thirst
Hypotension (Tolvaptan)

Lithium = a lot of side effects

63
Q

Vaptan: Drugs

A

Conivaptan (IV only, usually continuous)
Tolvaptan

  • Lithium
  • Demeclocylcine
64
Q

Vaptan: MOA Steps

A

Vaptan prevent binding to V2 receptor and prevents the following from occuring

V2 work by….

Activating Adenylyl cyclase 6, which activates cAMP, which activates Protein Kinase A

PKA phosphorylates AQUA-2, which gets placed in lumen and causes water to move from Lumen through cell and into capillary

65
Q

3 Main indications for vaptans

A

Polycystic Kidney Disease:(cAMP mediates cysts development, since cAMP is in cascade of V2 signaling….inhibiting V2 will slow cysts)

Heart failure:
Low blood volume triggers vasopressin release, so prevent cycle can help manage

SIADH: increase ADH leading to decreased plasma osmolality or increased arterial circulating volume

66
Q

What do Potassium Sparing Diuretics target?

A

ENaC

Work via ENaC inhibitors and Aldosterone Antagonists (slower reaction, days to weeks for maximal effect)

67
Q

Two kinds of K+ Sparing Diuretics?

A

ENac Inhibitors and Aldosterone Antagonists

68
Q

K+ Sparing Diuretics: Prototype

A

ENaC inhibitor: amiloride

Aldosterone Antagonists: spironolactone

69
Q

K+ Sparing Diuretics: MOA

A

Direct or indirect inhibition of ENaC

70
Q

K+ Sparing Diuretics: Applications

A

Edema
Hypertension
*Hyperaldosteronism for AAs

71
Q

K+ Sparing Diuretics: Notables

A

Weak diuretics but important for patients with hypokalemia

72
Q

K+ Sparing Diuretics: Risks

A

Hyperkalemia, hyperchloremic metabolic acidosis, Gynecomastia (Man Boobies…AAs), Acute renal failure and Kidney stones

73
Q

Direct ENaC inhibitors:

A

Amiloride (Prototype)

Triamterene

74
Q

Indirect ENaC inhibitors

A

Spironolactone (Prototype)

Epierenone

75
Q

K+ Sparing Diuretic MOA detailed

A

Direct: Blocking ENaC, preventing uptake of sodium so it stays in lumen (urine)

Indirect: Prevent signaling of aldosterone receptor, which is responsible for up regulating insertion of ENaC and Na/K+ ATPase

76
Q

K+ Sparing Diuretics: Drivers for side effects

A

Reduction in Na uptake, will decrease electrogenic exchange of Na for K/H, which can cause hyperkalemia and acidosis.

77
Q

Why are K+ Sparing Diuretics less effective?

A

Because the collecting duct only filters about 2-5% Na

78
Q

Why are Thiazides preferred over loop diuretics?

A

Longer half life

Pharmacology & Medical Chemistry II (43 decks)

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