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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What type of diuretics do we have?

A
  1. Loop diuretics
  2. Thiazide diuretics
  3. Potassium sparring diuretics(Aldosterone in/dependent)
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2
Q

Furesemide

  1. MOA
  2. Site
  3. DI
  4. Admin
  5. Therapeutic index
A
  1. Blocks the reabsorption Na+, K+ and Cl-
    Below that it blocks the reabsorption of Mg+ and Ca2+
  2. In the ascending loop of Henle
  3. NSAIDs: Inhibit the natriuretic response to diuretics and increase the risk of NSAID-associated renal adverse effects
  4. IV or Oral
  5. -Rt/Lt-sided heart failure
    -Congestive heart failure
    -Acute pulmonary oedema
    -Hypertension
    -Hypercalcaemia
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3
Q

Furosemide ADR

A
  1. Hypokalaemia
  2. Hyponatraemia
  3. Hypomagnesia
  4. Hyperuricaemia
  5. Hyperglycaemia
  6. Alkalosis
  7. Ototoixic DI
  8. Hypotension
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4
Q

Furosemide antidote for hypokalemia?

A

Potassium supplements

NOT Potassium sparring diuretics

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5
Q

Furosemide and the treatment of cancer-induced ailments?

A

Furosemide is used in the treatment of cancer-induced hypercalcaemia

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6
Q

Furosemide

  1. Potency
  2. Ceiling
  3. OOA
A

1.Highly potent
2. High ceiling
3. Rapid acting

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7
Q

Furosemide usage with thiazide diuretics

A

Used with thiazide diuretics

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8
Q

Thiazide diuretics drugs?

A

Hydrochlorothiazide
Indapamide

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9
Q

Thiazide diuretics uses?

A
  1. Hypertension
  2. Mild heart failure
  3. Diabetes insipious(paradoxical effect)
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10
Q

Thiazide diuretics:

  1. Site
    2.MOA
  2. S/E
  3. Ceiling
  4. Type of therapy
A
  1. Distal convoluted tubules
  2. Blocks reabsorption Sodium channels in the distal convoluted tubule
  3. Hypokalaemia
    - Hyperuricaemia
    - Hyperglycaemia
    -Increased skin cancer(melanoma)
    -CNS Disturbances
  4. Low ceiling
  5. Monotherapy
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11
Q

Thiazide diuretic effects on blood

A

Little effect on blood volume

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12
Q

Thiazide antidote for hypokalemia

A

Potassium sparring diuretics

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13
Q

Thiazide diuretic effect on collecting duct

A

Even though thiazide diuretic block the reabsorption of sodium in the distal convutuble , at the collecting duct, the Na+/K pump will be activated and reabsorp Na+ and excretes K+(thus the hypokalemia)

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14
Q

Potassium-sparring diuretics drugs?

A
  1. Amiloride
  2. Triamterene
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15
Q

Potassium-sparring diuretics MOA

A

Blocks the Na+/K+ exchange in the collecting duct

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16
Q

Thiazide diuretics relationship with aldosterone

A

independent of aldosterone

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17
Q

Potassium-sparring diuretics DI?

A

ACE-1

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18
Q

Which thiazide diuretic is used with Potassium-sparring diuretics?

A

Hydrochlorothiazde(HCTZ) to prevent hyokalamia

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19
Q

Spirinolactone MOA?

A

Aldosterone antagonist

Blocks the Na+/K+ exchange in the collecting duct

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20
Q

Spironolactone indications and combined drugs?

A

Hypertension(with HCTZ)

Heart failure(with Ace-Ibhibitors)

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21
Q

Spirinolactone side effects?

A

-Hyperkalaemia
-Gynaecomastia
-Acidosis

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22
Q

Describe the RAAS system

A
  1. Angiotensinogen is converted into angiotensin I by renin
  2. Angiotensin I is converted into Angiotensin II by ACE
  3. Angiotensin II binds to AT1 receptor
  4. The are two consequences of this:
    - Increased Aldosterone and increased sodium and water retention
    -Vasoconstriction and an increase in TPR
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23
Q

What are the RAAS pharmacology drugs and where do they act?

A
  1. ACE inhibitors
    Ramipril
    Enalapril
    Captopril
  2. ARBS
    (Prevent binding of ANGII to AT-1 receptor)
    Lorsartan
    Valsartan
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24
Q

Results of RAAS pharmacology?

A
  1. Decreases Aldosterone reabsorption and thus decreases sodium and water retention
  2. Decreases TPR and vasodilation
25
Q

RAAS pharmacology side effects and when is it exacerbated

A

Hyperkalaemia

Esp when taken with Potassium sparring diuretics (Amiloride or Triamterene)

26
Q

RAAS pharmacology CI?

A

-Pregnancy
-Sever renal failure
-Renal stenosis
-Caution with spironolactone

27
Q

Organic nitrates drugs and duration?

A
  1. Isosorbide mononitrate (Long acting)
  2. Isosorbide dinitrate (Short acting)
  3. Glyceral trinitrate(Short acting)
28
Q

Organic nitrates pathway

A
  1. Organic nitrate donates NO
  2. Guanylate cyclase is converts GTP and cGMP
  3. cGMP is then converted into MLC and causes venodilation/vasodilation with increased capaciatance
29
Q

Organic nitrates S/E?

A

-Headache
-Hypotension
-Reflex tachycardia(to counter decreased BP and bradycardia)

30
Q

Organic nitrates uses?

31
Q

What regulates cGMP?

A

PDE(naturally occurring)

32
Q

PDE?

A

PDE decreases cGMP levels

33
Q

Isosorbide mononitrate

  1. Admin
  2. First pass metabolism
  3. Bioavailability
  4. Usuage with which drugs
  5. Which drug do we use with for heart failure
A
  1. Admin: Oral
  2. First pass metabolism: No first metabolism
  3. Bioavailability: 100%
  4. Usage with which drugs: B-blockers and Ca2+ channel blockers
  5. Which drug do we use with for heart failure: Use with hydralazine
34
Q

Glyceryl trinitrate

  1. Admin types and why
  2. First-pass metabolism
A
  1. Sublingual admin( bypass first pass metabolism) & IV form for myocardial ischaemia
  2. Bypass first metabolism
35
Q

Isosorbide dinitrate

Admin & Substantiate

A

In place of SL form of glycery; trinitrate because it bypasses first pass metabolism

36
Q

Drug that inhibit PDE and which subtype

A

Sildenafil(viagra) ibhibit tha action of PDE-5 and thus increase cGMP and thus will increase venodilation

PDE-5

37
Q

Organic nitrates CI?

A

Sildenafil (PDE-5)

As it potentiates the effect of organic nitrates

38
Q

Direct vasodilators normal physiology pathway?

A
  1. Direct donates NO
  2. Guanylate cyclase is converts GTP and cGMP
  3. cGMP is that dephosphorilates MLC and causes vasodilation with increased capaciatance
39
Q

Direct vasodilators CI?

A

Sildenafil

40
Q

Direct vasodilators drugs and duration?

A
  1. Sodium nitroprusside-short acting
  2. Hydralazine-long acting

“How stretchy”-they cause vasodilation

41
Q

Hydralazine systematic effects-two?

A
  1. Vasodilation therefore decreases TPR
  2. Venodilation and thus increases capacitance
42
Q

Direct vasodilators drugs

  1. Potency
  2. Admin
A
  1. Sodium nitroprusside
  2. Potent vasodilator
  3. IV
  4. Hydralazine
  5. Potent vasodilator
    2.Oral
43
Q

Sodium nitroprusside alkalinity effects?

A

Causes lactic acidosis

44
Q

Hydralazine line of treatment?

A

Not first line

45
Q

Hydralazine autoimmune effects?

A

Increases the risk of SLE

46
Q

Direct vasodilators S/E?

A

-Tachycardia
-Hypotension
-Headache

47
Q

Direct vasodilators treatment?

A

-Heart failure
-Hypertension(with thiazide diuretics)

48
Q

Calcium-Channel blockers normal physiology?

A
  1. Ca2+ion influx in L-type tubules
  2. Calcium binds to calmodulin. Ca2+ + Calmodulin=Ca2+-Calmodulin complex
  3. MLC is converted into MLC-P by myosin-like chain kinase
  4. MLC-P is then bound by actin and that causes vasoconstriction
49
Q

Types of calcium-channel blockers and drugs under that

A
  1. Vascular selective
    -Nifedipine
    -Amlodipine
  2. Cardiac & vascular selective
    -Verapamil
    -Diltiazem
50
Q

Calcium-Channel blockers 3 systemic effects?

A
  1. No renin release
  2. No Na+ & H2O
  3. No postural hypotension
51
Q

Calcium-Channel blockers S/E?

A
  1. Ankle oedema/Pedal oedema
  2. Reflex tachycardia(counters decreased venous return)
  3. Headache
52
Q

Calcium-Channel blockers Indications?

A

-Angina
-Hypertension

53
Q

Overall Calcium-Channel blockers effects in pathway?

A
  1. Decrease in MLC-P
  2. Decreases MLC-P + Actin
  3. Causes vasodilation
54
Q

Cardiac & vascular selective S/E?

SA node

Oedema

Aches

A
  1. Decrease in SA node and AV node conduction=AV nodal block and bradycardia
  2. Pedal Oedema
  3. Headache
55
Q

Cardiac & vascular selective treatments?

A
  1. Supraventricular arrhythmias
  2. Angina pectoris
  3. Hypertension
56
Q

What are classes of antihypertensies?

A
  1. Resistance
  2. Diuretics-Na+/Volume
  3. Direct vasodilators
  4. Calcium channel blockers
  5. Angiotensin inhibitors
    -Resistance
    -Na/water
57
Q

RAAS-ARB/ACE-1 systematic effects?

  1. Preload
  2. Filling pressure
  3. Vasoconstriction
  4. Symptoms
  5. Afterload
  6. Mortality
A
  1. Reduces Preload
  2. Reduces Filling pressure
  3. Reduces Vasoconstriction
  4. Improve Symptoms
    5.Reduces Afterload
  5. Reduces Mortality by 5%
58
Q

ACE-1 and ARB association with bradykinin?

A

ACE-I:
-Increase bradykinin
-Dry Cough
-Angiooedema

ARBS:
-No increase in bradykinin levels
-No dry cough
-No angiooedema

Pharmacology (44 decks)

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