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Cardio Exam 1 > Diuretics HTN > Flashcards

Diuretics HTN Flashcards

1
Q

Arterial BP =

A

Cardiac output + peripheral vascular resistance

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2
Q

Cardiac output depends on?

A

Myocardial contractility

Ventricular filling pressure

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3
Q

Ventricular filling pressure is composed of?

A

Blood volume and venous tone

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4
Q

Vascular resistance depends on?

A

State of smooth muscle cells (contracted/relaxed)

Activity of the systems (controlling the diameter of resistance vessels)

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5
Q

Define Myocardial contractility

A

How the heart is contracting

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6
Q

Define ventricular filling pressure

A

How much blood if filling into the heart

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7
Q

What is the main function of the kidneys?

A

Maintain normal body fluid volume and electrolyte balance

- Filtration, reabsorption, secretion and excretion

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8
Q

Reabsorption of what?

A

Ions, amino acids, glucose, water,

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9
Q

Normal filtration rate?

A

120 mL/min

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10
Q

How much of fluid and electrolytes are reabsorbed?

A

99.9%

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11
Q

Rate if urine production?

A

1 mL/min

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12
Q

Nephron (urine forming unit) =

A

Glomerulus (filtration) + Tubule (reabsorption and conditioning)

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13
Q

What does the afferent arteriole do?

A

Brings the blood to the glomerulus

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14
Q

What does the efferent arteriole do?

A

Removes left over blood from the glomerulus

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15
Q

What is different about the glomerulus than other places in the body?

A

Endothelial cells are not tightly connected to each other leading to easier permeabilty

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16
Q

What holds filtered blood?

A

Bowman’s capsule

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17
Q

Where is reabsorption the greatest?

A

Proximal tubule and it declines distally towards the collecting ducts

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18
Q

Proximal tubules reabsorbs?

A

65% of sodium and highly permeable for water

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19
Q

Loop of Henle reabsorbs?

A

25% of sodium

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20
Q

Thin descending limb reabsorbs

A

Water but not sodium

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21
Q

Early distal tubule and distal convoluted tubules reabsorb?

A

5% of sodium

NO water or urea

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22
Q

Sodium reabsorption is controlled by?

A

Aldosterone

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23
Q

Water reabsorption is controlled by?

A

ADH

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24
Q

What is a major determinant of extracellular fluid volume?

A

NaCl

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25
Q

What do diuretics do?

A

Increase the rate of urine flow and sodium and chloride excretion

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26
Q

Diuretics –>

A

Increase Na and Cl excretion –> Decreased ECF volume –> decreased venous return –> Decreased cardiac output –> Decreased BP

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27
Q

Continued administration of diuretics cause?

A

Sustained net deficit of sodium & decreased ECF volume and BP

28
Q

Compensatory mechanisms mean what?

A

Balance between sodium intake and excretion

29
Q

Chronic effects of diuretics –>

A

Increased excretion and decreased fluid –> compensatory mechanisms –> decreased excretion & extracellular volume returns to normal –> decreased peripheral resistance –> BP remains low

30
Q

Initial BP lower effects of diuretics is due to?

A

Sodium excretion and ECF volume decrease

31
Q

Chronic BP lowering effect of diuretics is due to?

A

Reduction of peripheral resistance

32
Q

Loop diuretics drugs?

A

Bumetanide (Bumex)
Furosemide (Lasix)
Torsemide (Demadex)

33
Q

Loop diuretics site of action

A

Thick ascending limb of the Henle Loop where 25% of sodium reabsorption occurs

34
Q

Loop diuretics MOA

A

Inhibition of Na/K/Cl symporters

Inhibit the reabsorption of Na, K, Cl and indirectly inhibits reabsorption of Ca and Mg

35
Q

Loop diuretics urinary and hemodynamic effects?

A

Increased urine flow: excretion of Na, K, Cl, Ca, and Mg

Volume depletion and decrease of BP via renin release and SNS activity

36
Q

With acute use of loop diuretics what can you see that is lost during chronic use?

A

Increased excretion of uric acid

37
Q

What are Loop Diuretics main therapeutic uses?

A 
Acute pulmonary edema
HTN and HF
Edema and scites
Drug overdose
Hypercalcemia
38
Q

Define ascites

A

Accumulation of fluid in the peritoneal cavity

39
Q

What are the main adverse effects of loop diuretics due to fluid changes?

A

HYPOnaemia, hypotonia, circulatory collapse, thromboembolic episodes
Hypochloremic
Hypokalemia
Hypomagnesemia and hypocalcemia

40
Q

Hypokalmeia and hypomagnesmia are risk factors for?

A

Cardiac arrhythmias

41
Q

What are other main adverse effects of loop diuretics NOT due to fluid changes?

A

Ototoxicity
Hyperuricemia
Increased LDL cholesterol and decreased HDL

42
Q

What is the strongest diuretic?

A

Bumetanide

43
Q

Thiazide Diuretics

A

Chlorthalidone (Hygroton)
Hydrochlorithiazide (Microzide)
Indapamide (Lozol)
Metolazone (Zaroxolyn)

44
Q

Thiazide Diuretics Site of Action

A

Distal convoluted tubule

where 5% of Na reabsorption occurs

45
Q

Thiazide Diuretics MOA

A

Inhibition of Na/Cl symporters

No reabsorptions of Na or Cl

46
Q

What are the main effects of thiazide diuretics?

A

Increased excretion of Na, Cl, K (indirectly) and water

Lower BP bc of increased Na excretion

47
Q

What are the main effects of chronic thiazide diuretics uses?

A

Decreased excretion of Calcium and uric acid

48
Q

Main therapeutic uses of Thiazide diuretics?

A

HTN
Edema
Nephrogenic diabetes insipidus
Calcium nephrolithiasis & osteoporosis

49
Q

Define Nephrogenic diabetes insipidus?

A

Kidney is unable to conserve water

50
Q

What are other main adverse effects of thiazide diuretics due to fluid changes?

A 
Extracellular volume depletion, HYPOtension
HYPOnaemia, HYPOclemia
HYPOkemia
HYPERcaemia
HYPERuricemia
51
Q

Hyperuricemia leads to a risk of?

A

Gout

52
Q

What are other main adverse effects of thiazide diuretics NOT due to fluid changes?

A

Reduction of glucose tolerance due to reduced insulin secretion or K depletion
Increased risk for sexual impotency
Increase levels of LDL, total cholesterol and TGs

53
Q

Is chlorathalidone or hydrochlorthiazide more potent with a longer half life?

A

Chlorthalidone is 50% more potent and a MUCH longer halflife

54
Q

What is THE most potent thiazide diuretic?

A

Indapamide

55
Q

Inhibitors of renal epithelial Na Channels Potassium Sparing Diuretics

A

Amiloride (Midamor)

Triamterene (Dyrenium)

56
Q

Potassium-Sparing Diuretics Site of Action

A

Late distal tubule and collecting duct where ~2% of Na reabsorption occurs

57
Q

Inhibitors of renal epithelial Na Channels MOA

A

Inhibition of renal epithelial Na channels
Decreased reabsorption of Na and increased reabsorption of K
Involves principal cells collecting as much sodium as they can but not potassium

58
Q

Inhibitors of renal epithelial Na Channels main adverse effects

A

HYPERkalemia
N/V/D
Headache

59
Q

Triamterene can cause?

A

Glucose tolerance and photosensitization

60
Q

Aldosterone Antagonists Potassium Sparing diuretics

A

Eplerenone (Inspra)

Spironolactone (Aldactone)

61
Q

Aldosterone Antagonists site of action

A

Late distal tubule and collecting duct where ~2% of Na reabsorption occurs

62
Q

Aldosterone cascade

A

Aldosterone binds to its receptors in the cytoplasm –> translocates into the nucleus and binds to DNA where is stimulates expression of aldosterone-induced proteins and causes the retention of Na and the excretion of potassium

63
Q

Aldosterone antagonists bind?

A

At the receptor and block the effects of aldosterone causing the increased excretion of sodium and increased reabsorption of K

64
Q

Potassium sparing diuretics main therapeutic uses?

A

Used with other diuretics to spare K

Heart failure

65
Q

Spironolactone therapeutic uses are helpful in?

A

Primary (adrenal adenoma) and Secondary (overactivity of RAS) hyperaldosteronism
In pts with hepatic cirrhosis

66
Q

Potassium diuretics adverse effects?

A

HYPERkalemia

Spironolactone: gynecomastia, sexual impotency, decreased libido and altered clearance of digitalis glycosides

Cardio Exam 1 (7 decks)

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