Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

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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?

Study These Flashcards
A
  1. Decreases Aldosterone reabsorption and thus decreases sodium and water retention
  2. Decreases TPR and vasodilation
25
RAAS pharmacology side effects and when is it exacerbated
Hyperkalaemia Esp when taken with Potassium sparring diuretics (Amiloride or Triamterene)
26
RAAS pharmacology CI?
-Pregnancy -Sever renal failure -Renal stenosis -Caution with spironolactone
27
Organic nitrates drugs and duration?
1. Isosorbide mononitrate (Long acting) 2. Isosorbide dinitrate (Short acting) 3. Glyceral trinitrate(Short acting)
28
Organic nitrates pathway
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
Organic nitrates S/E?
-Headache -Hypotension -Reflex tachycardia(to counter decreased BP and bradycardia)
30
Organic nitrates uses?
Angina
31
What regulates cGMP?
PDE(naturally occurring)
32
PDE?
PDE decreases cGMP levels
33
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
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
Glyceryl trinitrate 1. Admin types and why 2. First-pass metabolism
1. Sublingual admin( bypass first pass metabolism) & IV form for myocardial ischaemia 2. Bypass first metabolism
35
Isosorbide dinitrate Admin & Substantiate
In place of SL form of glycery; trinitrate because it bypasses first pass metabolism
36
Drug that inhibit PDE and which subtype
Sildenafil(viagra) ibhibit tha action of PDE-5 and thus increase cGMP and thus will increase venodilation PDE-5
37
Organic nitrates CI?
Sildenafil (PDE-5) As it potentiates the effect of organic nitrates
38
Direct vasodilators normal physiology pathway?
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
Direct vasodilators CI?
Sildenafil
40
Direct vasodilators drugs and duration?
1. Sodium nitroprusside-short acting 2. Hydralazine-long acting "How stretchy"-they cause vasodilation
41
Hydralazine systematic effects-two?
1. Vasodilation therefore decreases TPR 2. Venodilation and thus increases capacitance
42
Direct vasodilators drugs 1. Potency 2. Admin
1. Sodium nitroprusside 1. Potent vasodilator 2. IV 2. Hydralazine 1. Potent vasodilator 2.Oral
43
Sodium nitroprusside alkalinity effects?
Causes lactic acidosis
44
Hydralazine line of treatment?
Not first line
45
Hydralazine autoimmune effects?
Increases the risk of SLE
46
Direct vasodilators S/E?
-Tachycardia -Hypotension -Headache
47
Direct vasodilators treatment?
-Heart failure -Hypertension(with thiazide diuretics)
48
Calcium-Channel blockers normal physiology?
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
Types of calcium-channel blockers and drugs under that
1. Vascular selective -Nifedipine -Amlodipine 2. Cardiac & vascular selective -Verapamil -Diltiazem
50
Calcium-Channel blockers 3 systemic effects?
1. No renin release 2. No Na+ & H2O 3. No postural hypotension
51
Calcium-Channel blockers S/E?
1. Ankle oedema/Pedal oedema 2. Reflex tachycardia(counters decreased venous return) 3. Headache
52
Calcium-Channel blockers Indications?
-Angina -Hypertension
53
Overall Calcium-Channel blockers effects in pathway?
1. Decrease in MLC-P 2. Decreases MLC-P + Actin 3. Causes vasodilation
54
Cardiac & vascular selective S/E? SA node Oedema Aches
1. Decrease in SA node and AV node conduction=AV nodal block and bradycardia 2. Pedal Oedema 3. Headache
55
Cardiac & vascular selective treatments?
1. Supraventricular arrhythmias 2. Angina pectoris 3. Hypertension
56
What are classes of antihypertensies?
1. Resistance 2. Diuretics-Na+/Volume 3. Direct vasodilators 4. Calcium channel blockers 5. Angiotensin inhibitors -Resistance -Na/water
57
RAAS-ARB/ACE-1 systematic effects? 1. Preload 2. Filling pressure 3. Vasoconstriction 4. Symptoms 5. Afterload 6. Mortality
1. Reduces Preload 2. Reduces Filling pressure 3. Reduces Vasoconstriction 4. Improve Symptoms 5.Reduces Afterload 6. Reduces Mortality by 5%
58
ACE-1 and ARB association with bradykinin?
ACE-I: -Increase bradykinin -Dry Cough -Angiooedema ARBS: -No increase in bradykinin levels -No dry cough -No angiooedema
Pharmacology
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