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Cardiologia (lilly) > 13- Hypertension > Flashcards

13- Hypertension Flashcards

1
Q

Primary or essential HTA?

A

The cause of blood pressure elevation is unknown. >90% HTA px

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2
Q

Secondary Hypertension

A

High blood pressure attributed to a definable cause

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3
Q

What pressure predicts more accurately cardiovascular complications?

A

Systolic

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4
Q

Stroke volume is determined by:

A
  1. Cardiac contractility
  2. Venous return to the heart
  3. The resistance the left ventricle must overcome to eject blood into the aorta (afterload)
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5
Q

What are the four systems responsible for blood pressure regulation?

A
  1. Heart
  2. Blood vessel tone
  3. Kidney
  4. Hormones
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6
Q

What is the normal sistolic/diastolic pressure?

A

<120/<80!

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7
Q

What are considered prehypertensive values?

A

120-139/80-89 mmHg

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8
Q

What is considered stage 1 hypertension?

A

140-159/90-99

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9
Q

What is considered stage 2 hypertension?

A

> 160/>100

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10
Q

In the presence of normally functioning kidneys, an increase in blood pressure leads to augmented urine volume and sodium excretion, which then returns blood pressure back to normal. This process is called:

A

Pressure natriuresis

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11
Q

What are the two possible reasons why pressure natriuresis is blunted in HTA patients?

A
  1. Microvascular and tubulointersticial injury within the kidneys which impairs sodium excretion
  2. Hormonal factors (RAA axis)
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12
Q

Which feedback mechanisms continuously monitor blood pressure?

A

Baroreceptors

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13
Q

Where can you find the baroreceptors?

A

Aortic arch and carotid sinus

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14
Q

How do baroreceptors monitor blood pressure?

A

By sensing stretch and deformation of arteries

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15
Q

How do baroreceptors regulate blood pressure?

A

They regulate bp by sending negative feedback via a Autonomic nervous system.

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16
Q

Signals of the carotid sinus are carried by:

A

Glosopharingeal nerve (IX)

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17
Q

Signals from the aortic arch are carried by:

A

Vagus nerve (X)

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18
Q

where do the glosopharingeal and vagus nerve converge?

A

Tractus solitarius

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19
Q

what do the baroreceptor impulses do in the tractus solitarius?

A
  1. inhibit sympathetic nervous system outflow

2. Excite parasympathetic effects

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20
Q

what is the net result of the baroreceptor impulses?

A
  1. decline in PVR (vasodilation)

2. reduction in CO (lower HR and reduced inotropism

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21
Q

what happens when baroreceptors sense a fall in systemic blood pressure?

A

fewer baroreceptor impulses are transmitted to the medulla leading to a reflexive increase in BP

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22
Q

why don’t baroreceptors prevent the development of chronic hypertension?

A

they regulate moment-by-moment variation of BP. After a day or two of exposure of higher than baseline pressure the baroreceptor firing rate slows back to its control value.

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23
Q

what is the most likely cause of EH?

A

a complex genetic disorder involving several loci.

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24
Q

what race is more frequently affected of EH?

A

blacks

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25
Q

how can the heart contribute to HTA?

A

through high CO-based HTA due to sympathetic over reactivity. (excessive HR acceleration in stressful conditions)

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26
Q

How can the blood vessels contribute to HTA?

A

they can by PVR based HTA by constricting in response to:

  1. increased sympathetic activity
  2. abnormal regulation of tone by NO, endothelin and natriuretic factors
  3. ion channel defects in contractile vascular smooth muscle
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27
Q

How can the kidney contribute to HTA?

A

it can induce volume based HTA by:

  1. failure to regulate renal blood flow
  2. ion channel defects
  3. inappropriate hormonal regulation
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28
Q

how are renin levels found in HT px?

A

25%: subnormal
60%: normal
10-15%: high

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29
Q

How should renin levels be in HT patients?

A

low

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30
Q

how does insulin play a role in the development of hypertension?

A
  1. increased sympathetic activation

2. vascular smooth muscle cell hypertrophy

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31
Q

How does obesity play a role in the development of hypertension?

A
  1. release of angiotensinogen from adipocytes
  2. augmented blood volume related to increased body mass
  3. increased blood viscosity caused by adipocyte release of pro fibrinogen and plasminogen activator inhibitor 1.
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32
Q

Where can the potential primary abnormalities in EH be found?

A
  1. blood vessels
  2. adrenal glands
  3. CNS
  4. Pressure and volume receptors
  5. Kidney
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33
Q

what functional and structural abnormalities of blood vessels could cause EH?

A

FUNCTIONAL

  1. less NO
  2. more Endothelin
  3. Ca++ or Na+/K+ channel defects
  4. Hyper-responsiveness to catecholamines

STRUCTURAL
-exaggerated medial hypertrophy

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34
Q

What abnormalities of Adrenal glands could be a cause of EH?

A

catecholamine leak or malregulation

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35
Q

What abnormalities of the CNS could be a cause of EH?

A
  1. Increased basal sympathetic tone
  2. abnormal stress response
  3. abnormal response to signals of baroreceptors and volume receptors
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36
Q

What abnormalities of the pressure/volume receptors could be a cause of EH?

A

Desensitization

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37
Q

What abnormalities of the kidney could be a cause of EH?

A
  1. RAA disfunction

2 Ion channel defects

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38
Q

at what age does the diastolic pressure begin to decline?

A

50

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39
Q

what is the hyperkinetic phase of EH?

A

high CO with normal PVR. Seen in younger px.

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40
Q

What abnormality is usually found in younger EH px?

A

elevated CO

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41
Q

What abnormality is usually found in older EH px?

A

elevated TPR

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42
Q

Why should we always screen for secondary HT?

A

1 they require different treatment
2 they can be cured often.
3 adaptative changes may cause chronic HT

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43
Q

What are the clues that a px may have a correctable condition (SHT)

A
  1. AGE: HT <20 or >50
  2. SEVERITY: often causes blood pressure to rise dramatically
  3. ONSET: presents abruptly in previously normotensive
  4. ASOCIATED SIGNS AND SYMPTOMS: eg Renal artery bruits
  5. FAMILY HISTORY: occurs sporadically
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44
Q

In the patient evaluation (history and physical) what clues should we look for to see if the pax has a secondary form of HT?

A
  1. recurrent UTI
  2. Excesive weight loss
  3. weight gain
  4. excesive acohol consumption
  5. medications
  6. obstructive sleep apnea
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45
Q

what lab tests should be performed in the initial evaluation of the HT patient?

A
  1. URINALISIS
  2. K+ serum levels
  3. blood glucose
  4. cholesterol
  5. EKG
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46
Q

HT px with recurrent UTI, you think of..?

A

chronic pielonefritis

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47
Q

HT px with excessive weight loss. you think of..?

A

pheochromocytoma

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48
Q

HT px with excessive weight gain, you think of..?

A

Cushing syndrome

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49
Q

What are the main causes of HT?

A
  1. essential
  2. Chronic renal disease
  3. primary aldosteronism
  4. Renovascular
  5. Pheochromocytoma
  6. Coartation of Aorta
  7. Cushing syndrome
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50
Q

what percentage of px are ESSENTIAL HT and what are the clues?

A

~90%

  1. age onset: 20-50 years
  2. family history of HT
  3. Normal serum K+, urinalisis
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51
Q

What % of HT patients are caused by CHRONIC RENAL DISEASE and what are the clinical clues?

A

2-4%

  1. rise in creatinine
  2. abnormal urinalisis
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52
Q

What % of HT px are caused by PRIMARY ALDOSTERONISM and what are the clinical clues?

A

<2-15%

-LOW SERUM K+

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53
Q

What % of HT px are caused by RENOVASCULAR DISEASE and what are the clinical clues?

A

1%

  1. abdominal bruit
  2. sudden onset (especially if <20 or >50)
  3. low serum K+
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54
Q

What % of HT px are caused by PHEOCROMOCYTOMA and what are the clinical clues?

A
  1. 2%
  2. paroxysms of palpitations, diaphoresis and headache
  3. weight loss
  4. episodic HT in 1/3 of px
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55
Q

What % of HT px are caused by COARCTATION OF THE AORTA and what are the clinical clues?

A
  1. 1%
  2. BP in arms> legs or right arm>left arm
  3. Midsystolic murmur between scapulae
  4. Chest X-ray: aortic indentation, rib-notching due to arterial collateral’s
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56
Q

What % of HT px are caused by CUSHING SYNDROME and what are the clinical clues?

A
  1. 1%

- “cushingoid” appearance (e.g. central obesity, hirsutism.)

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57
Q

What are the EXOGENOUS causes of HT?

A
  1. oral contraceptives
  2. glucocorticoids
  3. cyclosporine
  4. eryhtropoietin
  5. sympaticomimetic drugs
  6. NSAIDS
  7. Ethanol
  8. Cocaine
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58
Q

renal disease contributes to two important endogenous causes of secondary HT which are:

A
  1. renal parenchymal disease (2-4%)

2. renal arterial stenosis (1%)

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59
Q

How can renal parenchymal disease induce HT?

A
  1. increased Intravascular Volume

2. excessive elaboration of renin

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60
Q

What are the causes of renovascular HT?

A
  1. atheroesclerotic lesions
  2. fibromuscular lesions
  3. emboli
  4. vasculitis
  5. external compression of the renal arteries
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61
Q

RH ateroesclerotic lesions are most common in:

A

elder men

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62
Q

RH fibromuscular lesions are most common in:

A

young women

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63
Q

by what mechanism does RH evolve?

A

there is reduced renal blood flow therefore the kidney releases renin which raises blood pressure

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64
Q

what clinical findings suggests RH?

A

abdominal bruit or unexplained hipokalemia hypokalemia

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65
Q

what % of RH patients present abdominal bruit?

A

40-60%

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66
Q

where can we find ANG II receptors?

A
  1. arterial smooth muscle
  2. adrenal gland
  3. sympathetic nervous system
  4. kidney
  5. brain
  6. heart
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67
Q

what the function of ANG II receptors on arterial smooth muscle?

A

vasoconstriction

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68
Q

whats the function of ANG II receptors on the adrenal glands?

A

secretion of aldosterone (Na+ reabsorption in distal nephron, K excretion)

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69
Q

whats the function of ANG II receptors in the sympathetic nervous system?

A

facilitates release of norepinephrine (vasoconstrictor, raises TPR)

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70
Q

whats the function of ANG II receptors in the kidney?

A

raise renal tubular absorption of Na+

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71
Q

whats the function of ANG II receptors in the brain?

A

stimulates thirst and vasopresin secretion

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72
Q

whats the function of ANG II receptors in the heart?

A

ENHANCES CONTRACTILITY AND VENTRICULAR HYPERTROPHY

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73
Q

how can RH be corrected?

A
  1. percutaneus catheter intervention
  2. surgical reconstruction of a stenosed vessel
  3. Ace inhibitors (unilateral stenosis ONLY)
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74
Q

mechanical cause of HT?

A

Coarctation of the aorta

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75
Q

what could cause lower pressure in the left arm compared to the right arm?

A

coartation of the aorta that involves the origin of the left subclavian artery

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76
Q

by what mechanisms does coarctation of the aorta rise blood pressure?

A
  1. reduced blood flow to kidneys stimulates the renin angiotensin system
  2. high pressures proximal to the coarctation stiffen the aortic arch through medial hyperplasia and accelerated ateroesclerosis blunting the normal baroreceptor response to elevated intravascular pressure.
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77
Q

what are the clinical clues to the presence of coarctation?

A
  1. inadequate blood flow to legs or left arm
  2. claudication or fatigue
  3. weakened or absent femoral pulses
  4. midsystolic murmur
    5 RX: indentation of the aorta
  5. notched appearance of the ribs
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78
Q

treatment of coarctation of the aorta

A

angioplasty of surgery

*HT may not abate completely due to desensitisation of the baroreceptors

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79
Q

how can we evaluate endocrine causes of hypertension?

A
  1. HISTORY of characteristic signs and symptoms
  2. measurement of hormone levels
  3. Assessment of hormone secretion in response to stimulation inhibition
  4. imaging studies to identify tumours secreting the excessive hormone.
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80
Q

what are the endocrine causes of hypertension?

A
  1. pheocromocytoma
  2. Adrenocortical Hormone Excess
  3. Thyroid hormone abnormalities
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81
Q

what are pheocromocytomas?

A

Catecholamine secreting tumours of neuroendocrine cells (usually in the adrenal medulla)

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82
Q

what % of hypertension is caused by pheochromocytomas?

A

0.2%

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83
Q

what is the characteristic presentation of a pheochromocytoma?

A

paroxysmal rises in blood pressure with “autonomic attacks”

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84
Q

What are “autonomic attacks”?

A
  1. severe throbbing headaches
  2. profuse sweating
  3. palpitations
  4. tachycardia
    caused by the increased catecholamine levels in pheochromocytomas
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85
Q

what % of pheochromocytomas are malignant?

A

10%

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86
Q

what lab tests are used to determine pheochromocytomas?

A
  1. plasma cathecolamine levels

2. urine catecholamines and their metabolites (vanillylmandelic acid and metanephrine)

87
Q

What is the pharmacologic therapy of pheochromocytomas?

A

alpha receptor blocker + Beta blocker

once located= surgical resection

88
Q

what imaging techniques can be used to localise a pheochromocytoma?

A
  1. computed tomography
  2. magnetic resonance imaging
  3. angiography
89
Q

whats the treatment for inoperable pheochromocytomas?

A

alfa block, beta block and drugs that inhibit catecholamine biosynthesis

90
Q

What adrenocortical hormones can produce HT when found in excess?

A
  1. mineralocorticoids

2. glucocorticoids

91
Q

what is an important marker of mineralocorticoid excess?

A

HIPOKALEMIA

92
Q

what is the mechanism of hypertension due to mineralocorticoid excess?

A

aldosterone increases blood volume by stimulating reabsorption of Na+in exchange for K excretion.

93
Q

Primary Aldosteronism results from:

A
  1. adrenal adenoma (conn syndrome)

2. Bilateral hyperplasia of the adrenal glands

94
Q

what is Conn syndrome?

A

adrenal adenoma that results in primary aldosteronism

95
Q

whats the frequency of primary aldosteronism amongst hypertensives?

96
Q

the majority of hypertensives with primary aldosteronism have:

A

bilateral hyperplasia of the adrenal glands

97
Q

how can primary aldosteronism be diagnosed?

A

suspected by: hypokalemia

dx by: excessive plasma aldosterone levels + suppressed renin

98
Q

what is the treatment of primary aldosteronism?

A
  1. surgical removal of adenoma (if present)

2. aldosterone receptor antagonists

99
Q

what is Glucocorticoid remediable aldosteronism?

A

HAD form of primary aldosteronism where aldosterone synthesis comes under the regulatory control of ACTH.

100
Q

How does glucocorticoid remediable aldosteronism present?

A

severe hypertension in childhood or young adulthood

101
Q

non GRA primary aldosteronism is seen most commonly in what ages?

A

30-60 YRS OLD

102
Q

Tx of GRA?

A

glucocorticoids suppress ACTH release from the pituitary gland

103
Q

secondary aldosteronism can result from:

A
  1. rare renin secreting tumors
  2. oral contraceptives
  3. chronic liver disease
104
Q

mechanism of secondary aldosteronism HT by RENIN SECRETING TUMORS

A

increased ANG II

105
Q

mechanism of secondary aldosteronism HT by ORAL CONTRACEPTIVES

A

SECONDARY ELEVATION OF ALDOSTERONE AS A RESULT OF AUGMENTED CIRCULATING ANG II DUE TO HEPATIC STIMULATION TO PRODUCE ANGIOTENSINOGEN

106
Q

mechanism of secondary aldosteronism HT by CHRONIC LIVER DISEASE

A

impaired ANG II degradation

107
Q

what is the mechanism of HT due to glucocorticoid excess?

A

cortisol elevates blood pressure via blood volume expansion and stimulated synthesis of components of the renin-ang system.
Additionally the can activate renal tubules like mineralocorticoids

108
Q

what % of px with Cushing Syndrome present HT?

109
Q

What are the classic cushingoid features?

A
  1. rounded face
  2. central obesity
  3. proximal muscle weakness
  4. hirsutism
110
Q

What are the causes of cushing syndrome?

A
  1. pituitary ACTH secreting adenoma
  2. peripheral ACTH-secreting tumor
  3. Adrenal cortisol-secreting adenoma
111
Q

How is the diagnosis of cushing syndrome confirmed?

A

24 hour collection of urine or a dexamethasone test

112
Q

what proportion of Hyperthiroids present HT?

113
Q

WHAT % of hypothyroids have HT?

114
Q

How do Thyroid hormones exert their cardiovascular effect?

A
  1. inducing sodium potassium ATPases in the heart and vessels
  2. increasing blood volume
  3. stimulating tissue metabolism and oxygen demand w. secondary accumulation of metabolites that modulate local vascular tone.
115
Q

mechanism of HT in Hypothyroid px

A

they have predominantly diastolic HT + increase in TPVR (sympathetic + adrenal activation)

116
Q

what are the most common symptoms found in HT px?

A
  1. flushing
  2. sweating
  3. blurred vision
117
Q

HT complicated with atheroesclerosis can manifest through:

A

arterial bruits

118
Q

HT organ damage can be attributed to

A
  1. increased workload of the heart

2. arterial damage resulting from combined effects of the elevated pressure itself and accelerated atheroesclerosis

119
Q

what abnormalities of the vasculature can result from elevated blood pressure?

A
  1. smooth muscle hypertrophy
  2. endothelial cell disfunction
  3. fatigue of elastic fibers
120
Q

chronic HT trauma to the endothelium promotes atheroesclerosis by:

A

disrupting normal protective mechanisms ( secretion of NO)

121
Q

What organs are mainly targeted by Ht?

A
  1. heart
  2. cerebrovascular system
  3. the kidney
  4. the retina
122
Q

If left untreated HT px die of:

A
  1. 50% CAD or congestive heart failure
  2. 33% stroke
  3. 10-15% complications of renal failure
123
Q

what are the manifestations of organ damage in the HEART?

A
  1. left ventricular hypertrophy
  2. Heart failure
  3. myocardial isquemia and infarction
124
Q

What are the manifestations of HT organ damage of the cerebrovascular system?

125
Q

what are the manifestations of organ damage of HT in the AORTA AND PERIPHERAL VASCULAR SYSTEM?

A
  1. aortic aneurism

2. arterioesclerosis

126
Q

what are the manifestations of organ damage of HT in the KIDNEY?

A
  1. nephroesclerosis

2. renal failure

127
Q

what are the manifestations of organ damage in the RETINA?

A
  1. arterial narrowing

2. hemorrhages, exudates, papilledema

128
Q

what kind of heart hypertrophy is the normal pattern of compensation when high arterial pressure increases the wall tension?

A

concentric hypertrophy w/o dilatation

129
Q

what kind of heart hypertrophy is seen in conditions where increased circulating volume increases wall tension?

A

Eccentric hypertrophy with chamber dilatation

130
Q

left ventricle hypertrophy results in:

A
  1. increased LV stiffness
  2. diastolic disfunction
  3. elevated filling pressures (pulmonary congestion)
131
Q

what are the physical findings of left ventricular hypertrophy?

A
  1. heaving LV impulse on chest palpation

2. 4th heart sound (stiff LV)

132
Q

the degree of cardiac hypertrophy correlates with:

A
  1. congestive heart failure
  2. angina
  3. arrhythmia’s
  4. myocardial infarction
  5. sudden cardiac death
133
Q

what are the findings of systolic disfunction?

A
  1. reduced CO

2. pulmonary congestion

134
Q

systolic disfunction is provoked by:

A
  1. failure to balance high wall tension caused by the elevated pressure
  2. myocardial ischemia due to accelerated CAD
135
Q

What post infarct complications are present in HT px?

A
  1. rupture of the ventricular wall
  2. LV aneurysm formation
  3. congestive heart failure
136
Q

what % of px who die of transmural infarctions have history of HT?

137
Q

HT induced stokes can be:

A
  1. hemorragic

2. atherothrombotic (most common)

138
Q

what are lacunar infarctions?

A

< 3mm cavities

139
Q

Where are most lacunar infarctions found?

A

in the penetrating branches of the middle and posterior circulation of the brain

140
Q

mechanism of formation of “watershed” infarcts?

A

there is a generalised arterial narrowing due to HT which leads to hipoperfusion specially if there is a sudden BP drop.

141
Q

Where are abdominal aortic aneurisms (AAA) usually located?

A

below the renal arteries

142
Q

aneurisms greater than 6 cms have a very high likelihood of rupture within:

143
Q

what is the mortality of an aortic dissection?

144
Q

what do yo call hypertension induced kidney disease?

A

nephroesclerosis

145
Q

when vessel walls become infiltrated by a hyaline infiltrate it is known as:

A

hyaline arterioesclerosis

146
Q

what changes in HT lead to reduced vascular supply and ischemic atrophy of the renal tubules?

A
  1. smooth muscle hypertrophy
  2. necrosis of the capillary walls (fibrinoid necrosis)
  3. hyaline arterioesclerosis
147
Q

one of the consequences of HT renal failure is:

A

perpetuation of elevated blood pressure

148
Q

what is the only location where the arteries can be directly visualised by physical examination?

A

the retina

149
Q

hypertensive retinopathy serves as:

A

an asymptomatic clinical marker for the severity of HT and its duration

150
Q

ACUTE severe HT leads to what retinal findings?

A
  1. haemorrhages, exudation of plasma lipids
  2. areas of local infarction
  3. papiledema
151
Q

ischemia of the optic nerve leas to:

A

generalized blurred vision

152
Q

retinal ischemia due to hemorrage leads to :

A

patchy loss of vision

153
Q

CHRONIC svere HT has the following retinal findings:

A
  1. arterial narrowing (vasoconstriction)
  2. medial hypertrophy (arteries indent crossing veins)
  3. arterial sclerosis (copper or silver wiring)
154
Q

copper/silver wiring evidences:

A

arterial sclerosis

155
Q

indentation of veins of the retina evidence:

A

medial hypertrophy

156
Q

a Hypertensive crisis is usually caused by:

A

an acute hemodinamic insult (acute renal disease) superimposed on a chronic hypertensive state

157
Q

a px with severe HT + headache, blurred vision, confusion, somnolence or coma probably is developing:

A

hypertensive encefalopathy

158
Q

when hypertension results in acute damage of the retinal vessels the patient is said to be presenting:

A

accelerated malignant hypertension

159
Q

how can an acute hemodinamic insult like acute renal disease worsen a hypertensive state?

A

by increasing volume expansion and vasoconstriction because renal perfusion is dropping and serum renin and angiortensin levels rise`

160
Q

the increased load on the LV during a hypertensive crisis may precipitate:

A

an angina or pulmonary edema

161
Q

after a hypertensive crisis is treated correctly:

A

there is reversal of the acute pathologic changes (papiledema and retinal exudation)
renal damage often persists

162
Q

what is the additional risk of stroke in a person with stage 1 HT?

163
Q

what are the lifestyle modifications used as a nonpharmacologic treatment of HT?

A
  1. weight reduction
  2. exercise
  3. diet
  4. lower sodium intake
  5. higher potassium intake
  6. decrease chronic alcohol intake
  7. smoking cessation
  8. relaxation therapy
164
Q

blood pressure reduction follows weight loss in a rye portion of hypertensives who are more than what % above of their ideal weight?

165
Q

each 10kg of weight loss is associated with ___mmHg fall in systolic blood pressure

166
Q

normotensive sedentary people have ____ higher risk of developing HT.

167
Q

what kind of diet composition has been shown to beneficial for BP reduction

A

Diet high in fruits, vegetables and low fat diary products

168
Q

what % of EH px have been found to have BP that vary with Na+ intake?

169
Q

sensitivity to Na+ is more common in :

A

african american and elderly

170
Q

what is the current recommendation of sodium chloride intake?

A

<6gr per day

171
Q

what deficiencies have been found to be associated with higher BP?

A

Mg. K+ and Ca++

172
Q

chronic consumption of alcohol correlates to

A

resistance to antihypertensive medications

173
Q

Caffeine ingestion transiently increases BP as much as:

174
Q

Why does cigarette smoking transiently increase BP

A

nicotine effect un autonomic ganglia

175
Q

cigarettes atherogenic effect may contribute to the development of:

A

renovascular HT

176
Q

in what 4 classes do most antihypertensive medications fall in?

A
  1. Diuretics
  2. Sympaticolitics
  3. Vasodilators
  4. Drugs that interfere with the renin-angiotensin system
177
Q

how can diuretics help lower BP?

A

They reduce circulatory volume, CO and mean arterial pressure.

178
Q

Diuretics are most effective in what type of HT?

A

mild to moderate HT

179
Q

Diuretics are specially effective on what pxs?

A

AFRICAN AMERICAN AND ELDERLY(salt sensitivity)

180
Q

what are the most common diuretics use in HT?

181
Q

What diuretics are usually only used in renal insufficiency?

A

loop diuretics

182
Q

which diuretics promotes Na+ excretion through the distal nephron

A

thiazide and potassium sparing diuretics

183
Q

what are the side effects of thiazides?

A
  1. elevation of serum glucose
  2. cholesterol
  3. triglycerides
  4. hypokalemia
  5. hyperuricemia
  6. decreased sexual function
184
Q

what is the subclasification of sympaticolitic agents?

A
  1. B blockers
  2. central alfa adrenergic agonists
  3. systemic alfa adrenergic blocking drugs
185
Q

By what mechanisms do B blockers reduce BP?

A
  1. reducing CO (<hr>
186
Q

are B blockers less effective in elderly and african americans

187
Q

what are the side effects of B blockers?

A
  1. broncospasm
  2. fatigue
  3. impotence
  4. hyperglycemia
  5. > tryglicerides and
188
Q

what types of B blockers do not alter HDL levels?

A

combined alfa and beta blockers (labetalol)

189
Q

examples of centrally acting alfa 2 adrenergic agonists?

A

methyldopa and clonidine

190
Q

whats the mechanism of action of centrally acting alfa 2 adrenergic agonists to lower BP?

A

they reduce sympathetic outflow to the heart, blood vessels and kidneys

191
Q

why are centrally acting alfa 2 adrenergic agonists rarely used?

A

because of the high frequency of their side effects (dry mouth, sedation)

192
Q

examples of systemic alfa 1 antagonists

A

prazozin, terazosin and doxazosin

193
Q

how do systemic alfa 1 adrenergic antagonists lower BP?

194
Q

what type of sympatholitic agents are only useful in older men and why?

A

systemic alfa 1 antagonists, they also improve symptoms of prostatic enlargement.
(greater number of adverse cv effects)

195
Q

whats the subclasification of peripheral vasodilators?

A
  1. Ca++ channel blockers
  2. hydralazine
  3. minoxidil
196
Q

how do Ca++ channel blockers induce vasodilation?

A

they reduce the Ca++ influx responsible for cardiac and vascular smooth muscle contraction, reducing cardiac contractility and TPR.

197
Q

how do Hydralazine and Minoxidil work?

A

by directly relaxing vascular smooth muscle of pre capillary resistance vessels

198
Q

Why do Hydralazine and minoxidil have to be combined with B blockers?

A

because of the reflex increase in HR

199
Q

Name the three types of drugs that interfere with the renin-agiotensine aldosterone system

A
  1. ACE inhibitors
  2. ang II receptor blockers
  3. direct renin inhibitors.
200
Q

how do ACE inhibitors decrease BP?

A

by blocking conversion of ANG I to ANG II, therefore reducing vasopressor effect of ANG II and the secretion of aldosterone. bradikinin

201
Q

ACE inhibitors have been shown to reduce mortality of which px?

A
  1. acute MI
  2. chronic symptomatic systolic heart failure
  3. px at high risk of CV disease
202
Q

Can ACE inhibitors slow the deterioration of the renal function in px with diabetic nephropathy?

203
Q

which antiHT develop reversible dry cough and why?

A

ACE inhibitors, due to release of bradikinin

204
Q

what are the side effects of ACE inhibitors?

A

dry cough, hyperkalemia, azotemia

205
Q

How do ang II receptor blockers (ARBs) lower BP?

A

they block the binding of ANG II to its receptors in blood vessels and other targets

206
Q

In clinical trials what other antiHt medications are said to be similar to ARBs?

A

ACE inhibitors

207
Q

which is the most recent group of antiHT introduced?

A

oral direct renin inhibitors

208
Q

how does direct renin inhibitors work?

A

THEY INHIBIT THE BINDING OF ANGIOTENSINOGEN TO RENIN

209
Q

the JNC establishes which medication as a first line treatment for uncomplicated HT?

A

thiazide diuretics

210
Q

In the following px which HT medication would be suitable?

  1. heart failure
  2. diabetes
  3. LV disfunction following MI
A

ACE inhibitor

211
Q

what HT medication would be suitable for a paint with concurrent ischemic disease?

212
Q

what HT medication would be probably used in a young person?

213
Q

what type of HT medication would be probably used in a elder person?

A

vasodilator (long acting calcium inhibitor)

214
Q

why are direct vasodilators paired with a low dose diuretic?

A

because vasodilators can activate the RAA axis leading to volume retention

Cardiologia (lilly) (8 decks)

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