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Pharm 1 - SP19 > 28 - hypertension > Flashcards

28 - hypertension Flashcards

1
Q

Systolic vs Diastolic

A

Systolic - moment when heart is contracting , BP raise as blood moving

Diastolic - heart is relax and BP falls and the heart fills

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2
Q

blood pressure categories

systolic/diastolic 
norm
elevated
hypertension 1
hyper2
A

normal - <120/<80

elevated 120-129/<80

hypertension stage 1 130-139/80-90

hyper 2 140/90 or higher

hypercrisis higher 180/120

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3
Q

CO x TPR = _

A

MAP - mean arterial blood pressure

CO drops, BP drops
TPR increases, BP increases

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4
Q

BP regulatory systems
sympathetic nervous system and norepinephrine

and the renal system

which was is short term regulation, which one long term reg

A

short term - norepi and sympathetic nervous system

long term - kidneys/renal system - can lead to problems

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5
Q

sympathetic regulation
Baroreflex regulation of blood pressure

  1. _ send blood pressure information to the medulla
  2. Sympathetic nerves adjust _ to regulate
    vasoconstriction, heart beat, and cardiac output.
A

Baroreceptors (carotid, aortic arch, arteriole, heart)

catacholamines(norepi, but also epi and DA)

Not first thing we try or best thing
Alpha 1 - SM
Beta 1 - heart beat and CO

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6
Q

renal regulation of BP

Juxtaglomerular cells have baroreceptors. Sense low renal blood
flow and secrete _ (need decent blood flow to get filtration).

A

renin

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7
Q

3 things that cause release of renin from juxtaglomerular
apparatus into plasma

BP
Na
_Stimulation

A

Blood pressure decrease
Na decrease in filtrate
Sympathetic stimulation

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8
Q

renin once released by the JG cells acts on _ converting it into _

A

Angiotensinogen
(secreted from liver
into plasma) + renin = angiotensin I

angiotensin 1 + ACE in lung capillaries = angiotensin II

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9
Q

what does angiotensin II do to BP

A

raise BP

adrenal cortex - aldosterone - renal Na retention and K secretion inhib
pituitary - ADH - same
Thirst - increased blood volume
systemic vasoconstriction
cardiac and vascular hypertrophy
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10
Q

Angiotensinogen is produced

constitutively by the_

A

liver

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11
Q

Angiotensinogen is
converted to angiotensin I
by _

Angiotensin I is converted
to _ by
angiotensin converting
enzyme (ACE) (synthesized
and secreted by vascular
endothelial cells of lungs and
kidneys).
A

renin from kidney

angiotensin II

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12
Q 
Working through
angiotensin II
receptor(s), angiotensin
II mediates direct and
indirect _,
sodium resorption and
water retention, and
can produce structural
remodeling
A

direct/indirect vasoconstriction

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13
Q

angiotension II has Two G protein coupled receptors, only one of
which is the site of drugs to treat hypertension

which once is for controlling BP

A

AT1 receptor - vasoconstricti, symatpthetic activation, cell growth, ADH release, Renal Na reabs

AT2 - vasodilation, inhib cell growth, apoptosis

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14
Q

Drugs to treat hypertension

  1. Lower blood pressure by depleting body of Na+ and reducing blood volume
  2. Lower blood pressure by reducing peripheral vascular resistance and
    diminishing cardiac output
  3. Lower blood pressure by relaxing vascular smooth muscle
  4. Lower blood pressure reducing vascular resistance and blood
    volume
A
  1. Diuretics
  2. Sympathoplegic agents
  3. direct vasodilators
  4. block angiotensin II production/activity
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15
Q

notes on diuretics and hypertension

_ diuretics favored for patients with mild to moderate
hypertension and normal renal and cardiac function.

More powerful (i.e. _) diuretics used 
(i) more severe
hypertension,
 (ii) when other drugs producing Na+ retention
are used, 
(iii) renal insufficiency, 
(iv) cardiac failure or liver
cirrhossis (both characterized by Na+ retention).

Potassium sparing diuretics: if one needs to avoid K+ depletion
(Aldosterone antagonists have favorable effects in patients with
heart failure).
Potassium depletion the most common side
effect.

A

Thiazide

loop- more powerful

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16
Q

Diuretics we start for high BP - usually start with combo of _ and _ at first

A

combo of thiazide and ACE inhib initially

17
Q

Sympathoplegic agents to treat hypertension

act on CNS

reduce the release of _ from sympathetictic nerve endings

block selective adrenoreceptors - Block _receptors - diminish CO and renin production - no longer most popular way to tx

A

norepineprine ( may cause static hypotension)

block β1 - diminish CO and renin production

All can elicit compensatory effects leading to sodium
retention (use diuretics).

18
Q

Sympathoplegic agents to treat hypertension acting on CNS which activate _ receptors

Diminish central sympathetic
outflow, reduced cardiac
output

A

Activate α2 receptors in CNS

Alpha 2 - presynatpic feedback - so if stimulating this we are acting feedback loop - diminishing effect

19
Q

Sympathoplegic agents to treat hypertension acting on CNS which block _receptors

block vasoconstriction - can cause Na and water retention

A

block alpha 1 receptors

alpha1 selevtive - still get negative feedback by catacholamines

20
Q

drugs to tx hypertension

_ - lower BP by relaxing vascular smooth muscle

NO pro-drugs that release NO from endothelium

reduce Ca influx into vascular SM - block L type (voltage) Ca channels

hyperpolarization of Vascular SM (opening K channels)

activation of dopamine receptors - D1 receptors - produce similar effects of Beta 2 adrenergic - bronchiole SM

A

direct vasodilators

Decreased mean arterial blood pressure elicits
compensatory sympathetic responses (orthostatic
hypotension less likely because of this)
Work best in combination with other drugs
that oppose compensatory cardiovascular
responses.

21
Q

direct vasodilators
Sodium nitroprusside, a _ prodrug. Relaxes arterioles
and venules. Emergency treatment of hypertension.

A

Nitric oxide

Directly relax SM in vessels – NO gas that doesn’t stay long - can’t give NO - so give a drug that turns into NO

22
Q

drugs to tx hypertension

block _ production or activity

(i) Angiotensin converting enzyme inhibitors - ACE inhibitors
(ii) Competitive antagonists of angiotensin receptors
(iii) Renin inhibitors
(iv) Aldosterone inhibitors

A

angiotensin II production

23
Q

ACE also degrades _, which is a vasodilator, so ACE

inhibitors also promote vasodilation this way.

A

bradykinin

increase bradykinin (by inhibiting its degradation), further lowering blood pressure.

24
Q

_ drugs lower blood
pressure by decreasing peripheral
vascular resistance.

 Cardiac
output and heart rate not
affected. Stabilize kidney function
(useful in kidney compromised).
Useful in treating heart failure.
A

ACE inhibitors

25
Q

drugs to tx hypertension

Don’t affect bradykinin metabolism so
more selective than ACE inhibitors.
Block AT1 receptor.

A

competitive antagonists of angiotensin receptors

26
Q

which direct vasodilators are rapid and better at tx of Angina?

A

drugs the reduce Ca influx into vascular SM

Systemic effects though too - a lot of L type Ca channels

27
Q

which hypertension drugs have no effect on heart

A

ACE inhibitors

Pharm 1 - SP19 (26 decks)

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