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Cardiology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What equation tells you what arterial pressure is?

A

cardiac output times total peripheral resistance

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2
Q

What is the role of the reticular substance in regulation of circulation?

A

lateral and superior portions involved in excitation

medial and inferior portions are involved in inhibtion

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3
Q

What is the role of the hypothalamus in circulation?

A

posterior lateral portions cause mainly excitation

anterior portion can cause excitations or inhbition

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4
Q

What is the role of the motor cortex on nervous regulation of circulation?

A

exciation or inhibition

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5
Q

what threee areas of the brain are involved in the regulation of the circulation?

A

reticular substance
hypothalamus
motor cortex

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6
Q

What is the vasomotor center?

A

located bilaterally in the reticular substance of the medulla and lower third of the pons

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7
Q

What is the vasoconstrictor area “C-1” anterolateral upper medulla do?

A

sympathetic discharge

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8
Q

What is the role of vasodilator area “A-1” anterolateral lower medulla?

A

inhibits C-1 area

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9
Q

What is the role of sensory area “A-2” bilateral in nucleus tractus solitarii: receive sensory signal from vagus and glossopharyngeal from barorecepotrs. ?

A

C-1 and A-1 areas

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10
Q

What is the cardiac center do?

A

heart rate and contractility

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11
Q

What are innervated by sympathetic system?

A

sympathetic nerve fibers innervates all vessels except capillaries and precapillary sphincters and some meta arteriorles

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12
Q

What is mainly controled by parasympathetic nervous system?

A

mainly important in control of heart rate via the vagus nerve

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13
Q

What is the effect of total spinal anesthesia on blood pressure?

A

drops it significantly

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14
Q

What does alpha 2 sympathetic activation do on a sympathetic never?

A

ihibit norepinephrine release

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15
Q

What does activation of alpha 1 sympathetic receptors sdo?

A

vasoconstriction

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16
Q

What type of system is a baroreceptor pressure control system?

A

negative feedback control system?

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17
Q

What is the equation for G the strength of feedback

A

G=correction of error signal/error(abnormalilty still remianing)

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18
Q

What is hte range of hte effect of carotid sinus barorecptors?

A

pressures between 60 and 180 mmHg

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19
Q

Where is hte baroreceptor reflex most sensitive?

A

100 mmHg

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20
Q

What occurs as the pressure increases in the carotid baroreceptor as far as nerve impules goes?

A

increase in number of impulees form carotid sinus resulting in inhibtion of vasoconstrictor and activation of vagal center

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21
Q

What occurs at the resetting of baroreceptors?

A

thought to prevent refelx from controling as a control system for changes in pressure that last more than a day

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22
Q

What splits angiotensinogen?

A

renin and splits it to angiotensin I

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23
Q

What splits angiotensin I?

A

ACE to angiotensin II; leading to aldosterone release and sodium retention

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24
Q

What splits kininogen?

A

kallikrein to bradykinin

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25
Q

What does bradykinin do?

A

cause nitric oxcde release; prostaglandin synthesis and vasodilation sodium excretion

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26
Q

What splits active bradykinin?

A

ACE inactivates bradykinin

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27
Q

How is hypertension diagnosed?

A

average of at least 2 readings per visit obtaned at 3 seperate visits each 2 to 4 weeks apart

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28
Q

What is the second leading cause of end stage renal disease?

A

hypertension

with high normal being associated with a 3 times risk of future development of ESRD

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29
Q

What are some exogenous causes of hypertension?

A 
oral contraceptives
NSAIDs
Cocaine,ethanol, amphetamines, decongestants
glucocorticoids
cyclopsporin
erythropoietin
30
Q

What are the causes of hypertension for most people

A 
primary genetic ~90%
secondary
Chronic kidney disease 2-4%
primary aldoseronism
pheochromocytoma
cushing
31
Q

What is the morphology of large/medium arteries?

A

accelerated atherogenesis
degenerative changes in vascular walls
increase risk of aortic dissection and cerebovascular hemorrhage

32
Q

What is the hypertension morphology of small arteries/arterioles?

A

hyaline arteriolosclerosis

hyperplastic arteriolosclerosis

33
Q

What is hyaline arteriolosclerosis pathology?

A

elderly pts
similar changes in diabetics
benign nephrosclerosis
homogenus pink thickening of vessels with narrow lumen
leakage of plasma across endothelium due to HTN
excess matrix production by smooth cells occurs secondarily

34
Q

What are the histology of hyperplastic arteries?

A

characteristic of malignant htn
onion skinning laminated wall with luminal narrowing
-replication basement membrane and smooth muscle cells

35
Q

What is necrotoizing arteriolitis?

A

malignant HTN; term used when these changes are associated with fibrinoid necrosis

36
Q

What is the systemic HTN heart disease: morpoholgy?

A

cardiomegaly: concentric hypertrophhy without dilation
thickness of left ventricular wall impairs diastolic filling and causes left atrial enalrgment
myoccyte hypertrophy– increased myocyte and nuclear enlargement

37
Q

What are the direct arterial vasodilators?

A 
hydralazine
minoxidil
diazoxide
nitroprusside
fenoldopam
38
Q

What is the compensatory mechanism that reduces effectiveness of direct arterial vasodilators?

A

baroreceptor activation: compensatory increase in sympathetic outflow; tachyphylaxis can cause loss of antihyptertensive as well as reflex rellease ofrenin

39
Q

What can be given with direct arterial vasodilators to counteract compensatory baroreceptor activation?

A

beta blocker

and diuretic for water retention

40
Q

What is hypertensive urgency?

A

elevated Bp but no acute or progressing target organ injury

41
Q

What is a hypertesnive emergency?

A

acute or progressing target organ damage from elevated BP

42
Q

What are adverse effects of hydralazine?

A

lupus like syndrome

43
Q

What are the general adverse effects of arterial vasodilators?

A

sodium/water retention

tachycardia/angina

44
Q

what is an adverse effect of minoxidil?

A

hair growth

45
Q

What are teh calcium channel blockers?

A

nifedipine
diltiazem
verapamil
amlodidpine

46
Q

What are two alpha blockers?

A

phenoxybenzamine and phentolamine

47
Q

What are teh effect of alpha blockers?

A

inhibit smooth muscle catecholamine uptake: vasodilation and BP lowering

48
Q

What are the benefits of alpha1 selective blockers?

A

allow activation of alpha 2 and inhiiton of NE release; and don’t stim renin release
and smaller increase in heart rate

49
Q

What are the alpha 1 selective blockers?

A

prazozin
terazosin
doxazosin

50
Q

What are the addverse effects of alpha1 blockers?

A

first dose effect
-orhtostatic hypotension
transient dizziness, faintness, palpitations, syncope
reflex tachy

51
Q

Where are hte Beta 1 receptors located?

A

heart and kidney, stimulate incrased HR, contractility and renin release

52
Q

Where are beta 2 receptors located and what do they do?

A

lung, liver, pancrease, arteriolar smooth muscle
stim bronchodilation and vasodilation
mediate insulin secretion and glycogenolysis

53
Q

What are the potential beta blockers adverse effects?

A 
glucose intolerance, masked hypoglycemia
bradycardia, dizziness
bronchospasm
up TG and decrease HDL
CNS depression, fatigue, sleep disturbance
reduce CO, exacerbattion of herat failure
impotence
exercise intolerance
54
Q

What are the central alpha2 agaonists?

A

clonidine
guanabenz
alpha-methyldopa

55
Q

What is tehmechansim of action of clonidine?

A

central alpha 2 agonist

  • reduces sympathetic outflow from braint o vasomotor sensor
  • increase vagal tone.
56
Q

What are the adverse effects of cnetral alpha2 agaonists?

A 
sodium retention
rebound HTN
depression
orthostatic hypotension
dizziness
57
Q

What is an adverse effect of clonididne?

A

anticholinergic side effects

58
Q

What is an adverse effect of methyldopa

A

hepitisi or rarely hemolytic anemia

59
Q

What are neuronal and ganglionic blockers used to treat HTN??

A

guanethidine
guanadrel
resperine
trimethaphan–ganglionic

60
Q

What are the adverse effects of reserpine and guanethidine?

A 
sedation(reserpine)
depression (reserpine0
decreased CO
sodium/water
increased gastric acid secretion (reserpine)
diarrhea
bradycardia
61
Q

What do you use with reserpine and guanethdine to avoid fluid retention?

A

a diuretic pref a thiazide

62
Q

What are the potential adverse effects of diuretics?

A 
electrolyte disturbance
hyperglycemia
hypotension
lipid abnormalities
photosensitvity
ototoxicity
hyperuricemia
63
Q

What are two aldosterone antagonists?

A

spironolactone

eplerenone

64
Q

What are the mechanism of ACE inhibtitors?

A

block bradykinin degradation which stimulate syntehsis of other vasodilating substances like PGE2 and prostacyclin

blocks conversion of angiotensin I to angiotensin II

65
Q

What disease can ACE inhibitiors it prevent or regress?

A

left ventricular hypertrophy

66
Q

What are the adverse effects associated with ACE inhibitors?

A

cough
angioedema
hyperkalemia
neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure

67
Q

What is the angiotensin II receptor blocker?

A

ARB, don’t block bradykinin breakdown

less cough than ACE inhibitor

68
Q

What is the renin inhibitor?

A

aliskiren; angiotensinogen to angiotensin I inhibitor

69
Q

What are the precautions needed to be taken with ACE inhibitor or arbs?

A

can cause kidney failure
in pts with severe bilateral renal artery steoniss
pregnancy

70
Q

What drug should you use in hypertensive emergency?

A 
sodium nitroprusside
or
-nicardipine
-clevidipine
-fenoldopam
-nitro
-hydralazine
-labetalol
-esmolol
71
Q

Combination therapy usually involves what?

A

two or more agents to control HTN

one should be a thiazide unelss contraindicated

72
Q

What is resistant HTN?

A

fialure to achieve BP goal on 3 drug regimen

Cardiology (12 decks)

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