Chapter 36 - Hypertension - Exam 2 Flashcards

1
Q

alright here we go, what is hypertension

A

high blood pressure

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2
Q

as bp increases so does the risk for

A

MI, HF, stroke, renal disease, and vision loss

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3
Q

what is bp

A

the force exerted by the blood against the walls of the blood vessell

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4
Q

BP is mainly a function of

A

cardiac output and systemic vascular resistance

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5
Q

Cardiac output or CO is

A

total blood flow thru the systemic or pulmonary circulation per minute

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6
Q

CO is determined by..

A

SV x HR

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7
Q

systemic vascular resistance or SVR is

A

the force opposing the movement of blood w/in the blood vessels

as we already know, as arteries narrow resistance to blood flow increases.

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8
Q

HTN often accompanies a ______disease

A

lipid

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9
Q

how do baroreceptors help regulate bp

A

vital role in maintaining bp stability, sensitive to stretching.

when stimulated by an increase in BP, they send INHIBITORY impulses to the sympathetic vasomotor center.

sym NS inhibition results in decreased HR, decreased force of contraction, and vasodilation in peripheral arteries

vice versa when barorecepters sense a fall in bp

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10
Q

how does the vascular endothelium help regulate bp

A

the vascular endothelium is a single cell layer that lines the blood vessels
Responsibilities include:
platelet adhesion, coagulation regulation, immune function, and regulating fluidcontrol within the vessel and extra vascular space.

the endothelium is essential to the regulation and maintanence of vasodilating/constricting substances such as nitric oxide and prostacyclin, endothelin

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11
Q

how does the renal system help regulate bp

A

control sodium excretion and extracellular fluid volume

eg sodium retention results in water retention, which increases ECF volume

prostaglandins secreted by the renal medulla have a vasodilator effect on the systemic circulation this results in decreased systemic vascular resistance and lower bp

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12
Q

what the fuck is the renin-angiotensin-aldosterone system or RAAS

A

essential role in bp regulation

okay, the kidney secretes RENIN in response to either:
- sympathetic nervous system stimulation
- decreased blood flow through the kidneys
- decreased serum sodium concentration

RENIN is an ENZYME that CONVERTS angiotensinsinogen to angiotensin 1

angiotensin 1 is then converted to angiotensin 2 by angiotensin-converting enzyme (ACE).

angiotensin 2 increases BP by 2 different mechanisims:
1. A2 is a potent vasoconstrictor and incresases systemic vascular resistance. This results in an immediate increase in bp
2. over the period of hours or days, A2 increases bp indirectly by stimulating the adrenal cortex to secrete aldosterone

aldosterone stimulates the kidneys to retain sodium and water which increased blood volume and cardiac output

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13
Q

what is primary hypertension

A

(essential or idopathic) is elevated bp without an identifiable cause
contributing factors: damaged vessels, overactive SNS, increased sodium intake

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14
Q

what is secondary hypertension

A

elevated bp with a specific cause that can be identified and corrected

eg, renal disease, obstructive sleep apnea, cirrhosis, drug related, pregnancy,

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15
Q

excess _______intake is linked to the development of hypertension

A

sodium

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16
Q

complications:
coronary artery disease

A

hypertension disrupts the coronary artery endothelium, rigid arterial wall with a narrowed lumen

17
Q

complications:
left ventricular hypertrophy

A

sustained high bp increases the cardiac workload and causes left ventricular hypertropy

18
Q

complications:
heart failure

A

Heart is overwhelmed and can no longer pump enough blood to meet body’s demands

19
Q

mechanism of action:
a1-adrenergic blockers

A

block a1-adrenergic effects, producing peripheral vasodilation

eg doxazosin, prazosin

20
Q

mechanisim of action:
angiotensin-converting enyzme ACE inhibitors

A

inhibit ACE

eg benazepil, lisionopril

21
Q

mechanisim of action:
Calcium channel blockers - non-dihydropyridines

A

inhibit movement of Ca++ across cell membrane, resulting in vasodilation

eg diltiazem extended release

22
Q

mechanism of action:
calcium channel blockers - dihydropyridines

A

cause vascular smooth muscle relaxation resulting in decreased systemic vascular resistance and arterial bp

eg amlodipine

23
Q

mechanisim of action:
hydralazine

A

decrease systemic vascular resistance and bp by direct arterial vasodilation

24
Q

mechanism of action: nitroglycerin

A

relaxes arterial and venous smooth muscle, reducin preload and systemic vascular resistance

25
Q

mechanism of action:
loop diuretics

A

inhibit NaCl reabsorption in the ascending limb of the loop of henle

increased excretion of na+ and cl-

26
Q

the patho of HTN in the older adult involves:

A
  1. loss of elasticity in large arteries from atherosclerosis
  2. increased collagen content and stiffness of myocardium
  3. increased peripheral resistance
  4. decreased adrenergic receptor sensitivity
  5. blunting of baroreceptors
  6. decreased renal function
  7. decreased renin response to sodium and water depletion
27
Q

the systolic and diastolic values that categorize hypertension are

A

> or equal to 140
or equal to 90

140/90

28
Q

what do beta blocker drugs do?

A

Beta blockers, also known as beta-adrenergic blocking agents, work by blocking the action of adrenaline (epinephrine) and other stress hormones at beta receptors in the body. These receptors are found in various tissues, including the heart, blood vessels, and kidneys.

In the heart, beta blockers primarily block beta-1 receptors, which are responsible for regulating heart rate and the force of heart contractions. By blocking these receptors, beta blockers slow down the heart rate, decrease the force of contraction, and reduce the workload on the heart. This can be beneficial in conditions such as hypertension (high blood pressure), angina (chest pain), and heart failure, where reducing the heart’s workload can improve symptoms and outcomes.

Beta blockers also have effects outside the heart. For example, they can block beta-2 receptors in the blood vessels, leading to vasodilation (widening of blood vessels), which helps lower blood pressure. In addition, beta blockers can reduce the release of renin, a hormone involved in blood pressure regulation, from the kidneys.

Overall, beta blockers help to reduce the effects of adrenaline and other stress hormones on the body, leading to decreased heart rate, reduced blood pressure, and decreased workload on the heart, which can be beneficial in various cardiovascular conditions.

29
Q

how do ace inhibitors work

A

CE (angiotensin-converting enzyme) inhibitors work by blocking the action of ACE, an enzyme responsible for converting angiotensin I into angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it causes blood vessels to narrow, leading to an increase in blood pressure.

By inhibiting ACE, ACE inhibitors prevent the formation of angiotensin II, resulting in vasodilation (widening of blood vessels) and a decrease in blood pressure. This helps to reduce the workload on the heart and improve blood flow to the heart and other organs.

Additionally, ACE inhibitors can also inhibit the breakdown of bradykinin, a substance that promotes vasodilation and reduces blood pressure. By increasing bradykinin levels, ACE inhibitors further contribute to their blood pressure-lowering effects.

Overall, ACE inhibitors are commonly used to treat hypertension (high blood pressure), heart failure, and other cardiovascular conditions by lowering blood pressure and reducing the workload on the heart. They are also beneficial in protecting the heart and kidneys in certain conditions.