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Pathophysiology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Hypertension?

A

Persistently elevated blood pressure (>140/90mmHg)

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2
Q

What is the formula for BP?

A

BP = CO x PR

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3
Q

At rest are CO & PR stable?

A

CO is stable however PR fluctuates for varying reasons (such as vasoconstriction & vasodilation occurring in the body)

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4
Q

Systole?

A

Pumping phase; usually around 120 mmHg

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5
Q

Diastole?

A

Filling phase; usually around 80 mmHg

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6
Q

What are the 4 mechanisms to monitor BP?

A
  1. Baroreceptors
  2. Vascular Autoregulation
  3. Renin Angiotensin Aldosterone System
  4. Fluid volume regulation by the kidneys
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7
Q

Baroreceptors?

A

Detect changes in pressure (feed information to the nervous system, homeostatic mechanisms engage to return pressure to original state)

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8
Q

“baro-“?

A

Pressure

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9
Q

Where are baroreceptors located on the blood vessel?

A

In the tunica external/adventitia

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10
Q

Explain the pathophysiology of baroreceptors.

A

Type of mechanoreceptor sensory neutron that is excited by stretch of the blood vessel -> creates an action potential -> CNS -> stimulation of vascular smooth muscle -> constrict/dilate -> alters PR -> alters BP

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11
Q

In the body, where are baroreceptors located and why?

A

Located in the aorta (BP going to the body) and located in the carotid arteries (BP going to the brain)

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12
Q

Vascular Autoregulation?

A

Blood vessels constrict and dilate

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13
Q

What does vascular auto regulation occur in response to?

A

Changes in the body (such as change in pH)

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14
Q

How should vascular autoregulation be controlled?

A

In a localized way so only the area perfused by that specific vessel is affected

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15
Q

What does RAAS stand for?

A

Renin Angiotensin Aldosterone System

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16
Q

What is RAAS?

A

A homeostatic mechanism triggered by a decrease in BP, with the end result of an increased BP to normal range.

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17
Q

In RAAS what detects the decrease in BP?

A

Juxtaglomerular cells (granular cells) detects a decrease in BP [less stretch ]

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18
Q

Explain in detail what occurs in RAAS.

A

Juxtaglomerular cells (or granular cells) in the kidneys release renin into the blood. The release of renin causes the precursor protein angiotensinogen to transform into angiotensin 1. Angiotensin 1 circulates until ACE is made by pulmonary capillaries. ACE converts angiotensin 1 into angiotensin 2. Angiotensin 2 has multiple functions to increase BP such as:

  1. Stimulates thirst by increasing plasma volumes which increases the venous return, stroke volume, and cardiac output which increases blood pressure.
  2. Constricts efferent arteriole to increase pressure within the glomerulus and restores GFR.
  3. Stimulates the release of 2 hormones [aldosterone and anti-diuretic hormone]
    - Aldosterone -> secreted from the adrenal cortex and promotes the insertion of Na+ channels-> reabsorption of Na+, following by H20, increases blood volume, increases blood pressure
  • ADH secreted by the posterior pituitary gland and promotes the insertion of H20 channels into distal convoluted tubule and collecting duct -> reabsorption of H20 -> increased blood volume -> increased blood pressure. [It also stimulates thirst which increases BP)
    4. Angiotensin 2 is a potent vasoconstrictor itself. It constricts arterioles throughout the body which increases PR -> increases BP
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19
Q

What is renin?

A

An enzyme

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20
Q

What releases renin?

A

Juxtaglomerular (or granular) cells from the kidneys

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21
Q

Where is angiotensinogen made?

A

In the liver

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22
Q

ACE?

A

Angiotensin converting enzyme

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23
Q

Where is ACE made?

A

Pulmonary capillaries

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24
Q

In a nutshell, what are the 4 main functions of angiotensin 2 that help it increase BP? (You don’t have to describe the 4)

A
  1. Stimulates thirst
  2. Constricts efferent arteriole to increase pressure within the glomerulus and restores GFR
  3. stimulates the release of aldosterone and antidiuretic hormone
  4. angiotensin 2 is a potent vasoconstrictor itself
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25
Q

One of the main functions of angiotensin 2 to increase blood pressure is that it stimulates thirst. Explain.

A

It increases plasma volume which increases venous return, CO and SV -> increases BP

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26
Q

One of the main functions of angiotensin 2 to increase blood pressure is it stimulates the hormone aldosterone. Explain.

A

Aldosterone is secreted from the adrenal cortex and it promotes insertion of Na+ channels -> Reabsorption of Na+, followed by H20 -> increase in BV -> increase in BP

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27
Q

One of the main functions of angiotensin 2 to increase blood pressure is it stimulates the antidiuretic hormone. Explain.

A

ADH is secreted from the posterior pituitary and promotes the insertion of water channels into distal convoluted tubule & collecting duct. -> Reabsorption of water -> increase in blood volume -> increase in BP

  • It also stimulates thirst -> increase in BP
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28
Q

Fluid volume regulation by the kidneys?

A

Kidneys excrete or retain fluid to maintain blood volume and BP

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29
Q

What does the fluid volume regulation work together with?

A

RAAS

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30
Q

Explain what occurs in the fluid volume regulation?

A 
Juxtaglomerular cells (granular cells) produce renin to start RAAS when low BP is detected. It reacts to aldosterone and ADH (released by angiotensin 2) by reabsorbing more sodium and water. 
- Constricts efferent arteriole so pressure builds up in the glomerulus [blood filtration continues despite the lowered kidney blood flow], less fluid in peritubular capillaries -> decrease in hydrostatic pressure in the peritubular capillaries and increase in osmotic pressure. -> decrease in filtration and increase in reabsorption -> increase blood volume -> increase blood pressure
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31
Q

In the fluid volume regulation, when the efferent arteriole is constricted, does the blood filtration continue?

A

Yes, it continues despite the lowered kidney blood flow.

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32
Q

In the fluid volume regulation, is RAAS still activated if the BP is high?

A

NO

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33
Q

What does BP vary based off?

A

The circadian rhythm (sleep-wake cycle)

34
Q

When is BP :

  1. Highest?
  2. Lowest?
A
  1. Highest in the morning, decreases throughout the day

2. Lowest between 2-5 am (highest after this period)

35
Q

What is the etiology of primary/essential hypertension?

A

Idiopathic (unknown cause) [we know that it is one of the 4 control mechanisms that is defective, but are not able to identify which one and it could be multifactorial]

36
Q

What is another name for primary HTN?

A

essential HTN

37
Q

Approximately how many HTN cases fall under primary HTN?

A

90%

38
Q

What is the mmHg of primary HTN?

A

> 140/90

39
Q

What is the systolic & diastolic BP of stage 1: Mild HTN?

A

S: 140-159 or D: 90-99

40
Q

What is the systolic & diastolic BP of stage 2: Moderate HTN?

A

S: 160-179 or D: 100-109

41
Q

What is the systolic & diastolic BP of stage 3: Severe HTN?

A

S: >180 or D:>110

42
Q

What is systolic HTN?

A

S: >140 but diastolic remains <90

43
Q

Which age group does systolic HTN occur in?

A

Mostly after age 50

44
Q

Why does systolic HTN usually occur after the age of 50?

A

In terms of aging, theres always degenerative change with tissues. For some tissues you can replenish them, but not for all. Vessels lose compliance which associated with elasticity. Pressure elevates due to weak compliance. Also d/t atherosclerosis, lumen is compromised. There is also an increase in CO as we age.

45
Q

Scenerio: The aorta has compliance. This means that when the heart contracts and a large amount of pressure is put on the vessel, it can stretch and accommodate for this change in pressure.

Q: What occurs in this scenario when someone has systolic HTN?

A

The aorta loses its compliance and remains at a set tone so pressure increases within the vessel due to decrease in elasticity.

46
Q

Why is diastolic pressure not effected in systolic HTN?

A

B/c compliance and elasticity is not needed when the pressure is lower (such as when the heart is relaxing or filling)

47
Q

Which system does “filling” happen in?

A

Venous system (NOT ARTERIAL SYSTEM)

48
Q

White coat HTN?

A

Patient is hypertensive in a clinical setting, but is normal outside the clinical setting.

49
Q

Malignant HTN?

A

Acute scenerio where diastolic pressure exceeds 120 (considered an emergency situation)

50
Q

Etiology of secondary HTN?

A

It is identifiable but cause is elusive

51
Q

What occurs with renal function and cardiac function as you age and why is this significant?

A

They both decrease and they contribute to HTN

52
Q

What is Secondary HTN mainly related to?

A

Renal disease

53
Q

Approximately how many cases are a result of secondary HTN?

A

5-10%

54
Q

What is HTN often called?

A

a “silent killer”

55
Q

What are the initial manifestations of HTN?

A

elevated BP (if it is not measured regularly the pt will not even know they have HTN)

56
Q

What are the manifestations/complications that can occur later?

A
  • Fatigue
  • Dizziness
  • Palpitations
  • Blurred vision because the small vessels of the retina burst
  • Morning headaches because BP is highest in the morning.
57
Q

Palpitations?

A

Sensations of a forceful heartbeat

58
Q

What can HTN result in?

A

Multi-organ failure

59
Q

List 3 of the main organs that would be effected and briefly explain.

A
  1. Kidneys -> Increased pressure damages capillaries easily so that glomerulus (which function is ultra filtration) would be damaged.
  2. Eyes -> Retina has tiny blood vessels. Increased pressure can cause vessels to rupture causing serious problems.
  3. Heart
60
Q

What should the first treatment be in treating HTN?

A

Addressing lifestyle modifications

61
Q

In a nutshell, which factors can a pt address when considering lifestyle modifications in treating HTN?

A
  • Diet
  • Exercise
  • Weight Control
  • Alcohol consumption
  • Smoking cessation
  • Sodium consumption
  • stress management
62
Q

What diet is recommended for pt’s with HTN?

A

DASH diet = Dietary approaches to stop hypertension

- low in cholesterol, saturated fat, salt

63
Q

How much exercise is recommended for pt with HTN?

A

30-60 mins of moderated intensity, dynamic activity 4-7x a week

64
Q

What is the target BMI for a pt with HTN?

A

18.5-24.9 kg/m^3

65
Q

How much alcohol is healthy for a person with HTN to consume?

A

2 or less drinks per day; men = less than 14 / week , women = less than 9 / week

66
Q

How much sodium would you recommend a pt with HTN to consume?

A

Less than 2000 mg/day

67
Q

In terms of pharmacologic treatment, what is the first line of treatment given to pt’s with HTN?

A

Diuretics

68
Q

Diuretics?

A

Drugs that act on the level of the kidney to enhance fluid excretion

69
Q

What do diuretics promote?

A

Promotes diuresis (increase voiding, excrete fluids and lower blood volume)

70
Q

If required, which pharmacological treatments can you add?

A
  1. Calcium channel blockers
  2. Angiotensin 2 Receptor block
  3. ACE inhibitor
71
Q

What is the role of calcium in the heart?

A

It aids in contraction of muscles (smooth & cardiac)

72
Q

What do calcium channel blockers do?

A

Block calcium channels, contraction of these muscles is decreased

73
Q

What is the result of calcium channel blockers?

A

Vasodilation + decreased HR = decreased total PR and decreased CO = decreased BP

74
Q

How does Angiotensin 2 Receptor Blocker work?

A

Angiotensin 2 must bind to its receptor to be activated (if it does not bind then vasoconstriction doesn’t occur). The drug blocks receptor causing vasodilation -> decrease in BP

75
Q

How does an ACE inhibitor work?

A

Angiotensin 1 cannot be converted into Angiotensin 2 so no vasoconstriction occurs = decrease in BP

76
Q

When vessels constrict, what happens to pressure?

A

Pressure increases (Increase in resistance) [VASOCONSTRICTION]

77
Q

When vessels dilate, what happens to pressure?

A

Pressure decreases (decrease in resistance) [VASODILATION]

78
Q

When blood volume increases, what happens to pressure?

A

Pressure increases

79
Q

When blood volume decreases, what happens to the pressure?

A

Pressure decreases

80
Q

What applies:

  1. hydrostatic pressure?
  2. osmotic pressure?
A
  1. blood

2. solutes

Pathophysiology (17 decks)

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