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Pathophysiology 1 > Jan 16 - Hypertension > Flashcards

Jan 16 - Hypertension Flashcards

1
Q

Why is hypertension dangerous?

A

High blood pressure (and high cholesterol) contribute to the risk of ACS

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2
Q

What is arterial blood pressure?

A

The pressure exerted on the artery walls

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3
Q

What are the two 2 measures of blood pressure?

A

Systolic: the pressure in the arteries during systole (contraction)
Diastolic: the pressure in the arteries during diastole (rest/filling)

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4
Q

What is the mean arterial pressure (MAP)?

A

The average pressure throughout the cardiac cycle (one heartbeat)

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5
Q

How is the MAP measured?

A

2/3 diastolic blood pressure (time spent in diastole) + 1/3 systolic blood pressure (time spent in systole)

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6
Q

What is good blood pressure?

A

120/80; MAP = 93 (normal = 70 to 110)

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7
Q

What happens when MAP drops below 65?

A

It’s an emergency because the person’s organs (brain, liver, kidneys, etc.) are not being perfused with enough blood (adequately)

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8
Q

What is blood pressure (mathematically)?

A

Blood pressure = total peripheral resistance x cardiac output

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9
Q

What is the definition of peripheral resistance?

A

The “squeeze” of the blood vessels outside the heart resisting blood flow

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10
Q

What is the definition of cardiac output?

A

A measure of how much blood is flowing through the heart

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11
Q

What is cardiac output (mathematically)?

A

Heart rate x stroke volume

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12
Q

What is stroke volume?

A

The amount of blood ejected with each beat of the heart

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13
Q

What happens to blood pressure if you give the patient a drug that increases heart rate?

A

Blood pressure will increase

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14
Q

What happens to blood pressure if you give a drug that decreases total peripheral resistance?

A

It will decrease blood pressure

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15
Q

What is the difference between essential and secondary hypertension?

A

About 90% of the time, we don’t know the actual cause of hypertension (essential). Secondary hypertension is caused by a drug or another disease

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16
Q

What are the short-term mechanisms of blood pressure regulation?

A

Humoral, neuronal, hormonal and vascular. These mechanisms kick in right away (e.g. if you start bleeding)

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17
Q

What is a long-term (within a few days) mechanisms of blood pressure regulation?

A

Renal

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18
Q

What is a third mechanism of blood pressure regulation?

A

Electrolytes

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19
Q

What makes up the humoral mechanism of blood pressure regulation?

A

The renin-angiotensin-aldosterone system (RAAS)

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20
Q

What does the RAAS regulate?

A

It regulates sodium ions, potassium ions and blood volume

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21
Q

How does the RAAS monitor blood pressure?

A

The kidneys have juxtaglomerular cells. These have cells have baroreceptors, which can detect changes in pressure. Renin is an enzyme that is synthesized, stored, and released by the kidneys in response to an increase in sympathetic activity or a decrease in blood pressure, extracellular volume, or extracellular sodium concentration

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22
Q

What is renin? How does it work?

A

It’s an enzyme that converts angiotensinogen into angiotensin I

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23
Q

What are ACE? How do they work?

A

Angiotensin converting enzymes that convert angiotensin I into angiotensin II

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24
Q

What are the different parts of the body that angiotensin II affects?

A

The adrenal cortex, the kidneys, the intestines, the CNS, the PNS, vascular smooth muscles, and the heart. All of the different affects work to raise blood pressure

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25
Q

How does angiotensin II affect the heart?

A

It raises contractility, which increases cardiac output (increase in blood pressure)

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26
Q

How does angiotensin II affect vascular smooth muscle?

A

It causes vasoconstriction, which increases total peripheral resistance (increase in blood pressure)

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27
Q

How does angiotensin II affect the PNS?

A

It causes sympathetic discharge, which increases total peripheral resistance (increase in blood pressure)

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28
Q

How does angiotensin II affect the CNS?

A

It causes sympathetic discharge, which increases total peripheral resistance. It also causes the secretion of vasopressin, which increases blood volume, which increase total peripheral resistance (increase in blood pressure)

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29
Q

How does angiotensin II affect the kidneys and the intestines

A

It causes sodium and water reabsorption, which increases blood volume, which increase total peripheral resistance (increase in blood pressure)

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30
Q

How does angiotensin II affect the adrenal cortex?

A

It causes an increase in aldosterone synthesis, which causes sodium and water reabsorption, which increases blood volume, which increase total peripheral resistance (increase in blood pressure)

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31
Q

Why is the RAAS so important?

A

Because the drugs we use to lower blood pressure affect this system

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32
Q

How does neuronal regulation of blood pressure work?

A

Extrinsic reflexes, intrinsic reflexes and higher centre reflexes affect the autonomic nervous system (ANS), which is the cardiovascular centre of the brain

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33
Q

What are extrinsic reflexes?

A

They are outside the circulatory system; through the hypothalamus e.g. pain, cold temperature

34
Q

What are intrinsic reflexes?

A

They are within the circulatory system; baroreceptors/chemoreceptors

35
Q

What are high centre reflexes?

A

Mood, emotion

36
Q

How does the ANS affect parasympathetics with regards to blood pressure?

A

Parasympathetics affect the heart via the vagus nerve and decrease heart rate (decrease in blood pressure)

37
Q

How does the ANS affect sympathetics with regards to blood pressure?

A

Sympathetics affect the heart (post-synaptic beta-1-adrenergic receptors) via the spinal cord and peripheral sympathetic nerves, which increases heart rate and contractility. Sympathetics also affect the blood vessels (post-synaptic alpha-1-adrenergic receptors) via the spinal cord and peripheral sympathetic nerves, which cause vasoconstriction. All this causes an increase in blood pressure

38
Q

Where are alpha-1 receptors found? How do they work?

A

Alpha-1 receptors are found in the peripheral arteries and veins. Agonists of alpha-1 receptors cause vasoconstriction (increase in blood pressure)

39
Q

Where are alpha-2 receptors found? How do they work?

A

Alpha-2 receptors are found in the brain (within the medulla). Activation of alpha-2 receptors stops norepinephrine secretion (angiotensin II causes the secretion of norepinephrine) (decrease in blood pressure)

40
Q

Where are beta-1 receptors found? How do they work?

A

Beta-1 receptors are found in the heart. Activation of beta-1 receptors increases heart rate (beta-blockers decrease heart rate)

41
Q

Where are beta-2 receptors found? How do they work?

A

Beta-2 receptors are found in the arteries (and veins) and the lungs. Activation of beta-2 receptors causes vasodilation and bronchodilation

42
Q

Why is it important to understand alpha and beta receptors?

A

Pharmacists can use different drugs to manipulate these receptors

43
Q

How does hormonal regulation of blood pressure work?

A

Via the natriuretic hormone and hyperinsulinemia

44
Q

How does the natriuretic hormone work?

A

It inhibits Na/K-ATPase which blocks active Na out of vascular smooth muscle cells. The end result is increased vascular tone (vasoconstriction)

45
Q

How does hyperinsulinemia work?

A

Hyperinsulinemia is when there is too much insulin in the bloodstream. It increases renal sodium ion retention. It acts as a growth hormone, leading vascular smooth muscle cells to grow (hypertrophy). It increases calcium ions in the vascular smooth muscles, leading to constriction. It increases sympatehtic nerve activity

46
Q

How does vascular regulation of blood pressure work?

A

The endothelium secretes factors that promote vasorelaxation or vasoconstriction

47
Q

What does the endothelium secrete to promote vasoconstriction?

A

Angiotensin II, vasopressin, enothelin. These factors promote vasoconstriction (increase in vascular resistance) and promote hypertrophy

48
Q

What does the endothelium secrete to promote vasorelaxation?

A

Prostacyclin, nitric oxide, bradykinin. These factors promote vasorelaxation (vasodilation) and decrease vascular resistance. Usually in hypertension, there aren’t enough of these factors

49
Q

How does renal regulation of blood pressure work?

A

The kidney can sense, via extracellular fluid in the body, if the blood pressure is too high or too low. When the blood pressure is too high, the kidneys excrete sodium ions and water to lower blood volume. When the blood pressure is too low, the kidneys retain sodium ions and water to increase blood volume

50
Q

How does chronic hypertension affect the kidneys?

A

Constantly having high blood pressure overworks the kidneys and they can give up (kidney failure)

51
Q

How does a sodium imbalance affect blood pressure?

A

Excess sodium intake (diets high in sodium) have been associated with hypertension. The exact mechanism is not known (however, we know in heart failure, excess sodium leads to water retention). Where sodium goes, water goes

52
Q

How does a calcium imbalance affect blood pressure?

A

Low calcium diets can disturb calcium balance, resulting in an increased intracellular calcium concentration. This can result in increased peripheral resistance (remember: blood pressure = TPR x CO)

53
Q

How does a potassium imbalance affect blood pressure?

A

Low potassium may increase peripheral vascular resistance (remember: blood pressure = TPR x CO). Patients with low potassium (or low calcium) don’t have enough to make the heart contract and to make a cardiac action potential (cardiac output is affected)

54
Q

How is blood pressure classified?

A

Normal: 120 and 80
Prehypertension: 120-139 or 80-89
Stage I hypertension: 140-159 or 90-99
Stage II hypertension: 160-179 or 100-109
Hypertensive crisis: 180-over or 110-over

55
Q

What is required for the diagnosis of hypertension?

A

Patients must have at least 2 physician office visits (up to five) with at least 2 averaged blood pressure readings at each visit for a hypertension diagnosis

56
Q

What is JNC7?

A

Seventh report of the Joint National Committee on the detection, evaluation, and treatment of high blood pressure

57
Q

What are some risk factors for the development of hypertension?

A

Age (55+ for men, 65+ for women)
Hyperinsulemia
Microalbuminuria
Family history of hypertension
Race (e.g., Africain Americans vs. Caucasians)
Obesity (BMI 30+ kg/m2)
Dyslipidemia (high LDL, low HDL or high triglycerides)
Hyperuricemia (too much uric acid in the blood)

58
Q

What are lifestyle factors that put a patient at risk for hypertension?

A

High sodium diet/poor diet
Excessive alcohol intake
Lack of exercise
Smoking

59
Q

What is microalbuminuria?

A

Small amounts of albumin in the urine (not a good thing; there’s also macroalbuminuria, which is worse)

60
Q

What is the only “currative” way to manage hypertension?

A

Changing your lifestyle

61
Q

What factors raise blood pressure?

A

Nicotine/smoking, stimulants (caffeine), steroids (legal and not legal), decongestants (i.e. sudafed), oral contreceptives (estrogen), NSAIDS, SNRIs (i.e. venlafaxine), illicit drugs (cocaine, ecstasy), exercise, emotions/stress, “white coat hypertension”

62
Q

What factors lower blood pressure?

A

Fasting, depressants (alcohol), resting, anti-hypertensives

63
Q

What are examples of diseases that cause secondary hypertension?

A

Chronic kidney disease, cushing syndrome, obstructive sleep apnea, thyroid/parathyroid disease, coarctation (narrowing) of the aorta

64
Q

What are examples of drugs that can cause secondary hypertension?

A

Stimulants, steroids, decongestants, oral contraceptives, NSAIDS, SNRIs, illicit drugs, anabolic steroids

65
Q

What are the symptoms of hypertension?

A

There are usually none (it’s the silent killer). Sometimes patients experience headaches (really high blood pressure)

66
Q

What happens when hypertension is left untreated?

A

Cerebrovascular disease (stroke/TIA/vascular dementia).
Retinopathy (high blood pressure causes the retinas to break and the patient could lose their site)
Left ventricular dysfunction/hypertrophy or heart failure
Coronary artery disease (MI, angina)
Renal disease (micro/macroalbuminuria, nephropathy)
Peripheral artery disease

In short, it affects the brain, the heart, the kidneys, the eyes and the blood vessels

67
Q

How much will weight reduction decrease blood pressure (systolic/diastolic)?

A

-7.2/-5.9 mmHg for every 4.5 kg of weight loss

68
Q

How much will adopting a DASH diet eating plan decrease blood pressure (systolic/diastolic)?

A

-11.4/-5.5 mmHg

69
Q

How much will restricting dietary sodium to less than 1500 mg/day decrease blood pressure (systolic/diastolic)?

A

-5.8/-2.5 mmHg

70
Q

How much will 30 minutes of physical activity a day decrease blood pressure (systolic/diastolic)?

A

-10.3/-7.5 mmHg

71
Q

How much will moderating alcohol intake to less than 2.7 drinks per day decrease blood pressure?

A

-4.6/-0.23 mmHg (males can drink 2 drinks/day, women can drink 1.5 drinks/day - drinking red wine can lower blood pressure)

72
Q

What are pharmacological treatments available for decreasing hypertension?

A

Diuretics, beta-blockers, ACEIs, ARBs, NDP-CCBs, DP-CCBs, Aldosterone antagonists, alpha-1 adrenergic antagonists

73
Q

How do diuretics work?

A

Diuretics lower total peripheral resistance and cause sodium and water excretion (they make you pee)

74
Q

How do ACEIs work?

A

ACE inhibitors inhibit angiotensin converting enzyme, the enzyme responsible for converting angiotensin I into angiotensin II (“prils”)

75
Q

How do ARBs work?

A

Angiotensin receptor blockers block the receptor activated by angiotensin II

76
Q

How do DP-CCBs work?

A

Dihydropyridine calcium channel blockers cause vasodilation

77
Q

How do NDP-CCBs work?

A

Non-dihydropyridine calcium channel blockers decrease contractility of the heart

78
Q

How do aldosterone antagonists work?

A

Aldosterone antagonist antagonize the action of aldosterone at mineralocorticoid receptors, causing the inhibition of sodium and water reabsorption

79
Q

Where are the three places that diuretics work?

A

The proximal tubule, the loope of henle and the distal tubule of the nephron (functional unit of the kidneys)

80
Q

How do thiazides and metolazones work? What are examples of thiazides?

A

They work in the distal tubule of the nephron and cause it to dump sodium so it gets peed out (where sodium goes, water follows). Examples: hydrochlorothiazide, indapamide, chlorthalidone

81
Q

How do loop diuretics work? What is an example of a loop diuretic?

A

They act on the loop of henle. They cause more sodium chloride to be excreted. They stop the NaCl to be reabsorbed in the blood (Furosemide)

82
Q

How do potassium sparing drugs work? What are examples of potassium sparing drugs?

A

They inhibit aldosterone from activating the Na/K pump, causing sodium to be dumped (water follows) and potassium is no longer dumped into the urine (blood potassium increases). Examples: spironolactone, eplerenone, triamterene

Pathophysiology 1 (11 decks)

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