Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
146 Cards in this Set
- Front
- Back
|
Blood Pressure =
|
CO X PVR
|
|
|
CO=
|
SV X HR
|
|
|
Blood pressure is continually regulated by changes in
|
CO and PVR
|
|
|
What are peripheral sites of control
|
1. arterioles
2. veins 3. heart 4. kidneys |
|
|
Rapid adjustments in BP occur by CNS relexes--what
|
aterioles, veins and heart
|
|
|
Long term regulation of BP occurs via
|
kidney
|
|
|
Blood pressure in normotensive and hypertesnives is maintained by
|
sympathetic mechanisms
humoral mechanisms |
|
|
What are types of antihypertensive agents
|
1. sympathoylitic agents
2. vasodialators 3.vasopetidase inhibitors 4. Diuretics |
|
|
Often combination drugs are given, sympatheolytic agents decrease BP, what happens
|
decrease Renal blood flow, and increases renin secretion and increase angiotensin II, and increases aldosterone, fluid retention, increase BP so give diuretic
|
|
|
Often BP decreases with diretucs what happens
|
activates the baroreceptor reflex and increases sympatheic outflow and increase BP
|
|
|
How do sympahtolyic agents work (generally)
|
by inhibiting cardiovascular effect of the sympahtic nervous system
|
|
|
What mechanisms tend to counter the actions of sympatholytic agents
|
renal mechanisms
|
|
|
Sympatholytic agents are categorized according to locus of action which includes
|
1.centrally acting
2. gnaglion blocking 3. adrengegic neuron blocking 4.adrenoceptor antagoinst |
|
|
Where do Centrally acting drugs act
|
in CNS to influence sympathetic nervous system to control BP
|
|
|
What are centrally acting drugs
|
Clonidine, methyldopa, mononidine
|
|
|
What is clonidine
|
a2 adrenceptor AGOINST in CNS and periphery, so presynpatic inhibition of NE release, decrease BP
|
|
|
What is MOA of clonidine
|
decrease sympathetic outflow decrease BP, and increases parasymahteic which dcreases HR, and increases sensitivty of vasopressor centers to baroceptor control
|
|
|
Clondinie decrease NE release which does what
|
decreases HR, SV, and CO
dilates veins dialtes arterioles |
|
|
What is result of dilate veins
|
decrease venous return
|
|
|
What is result of dilate arterioles
|
decrease PVR
|
|
|
Clonidine also decrease renal vascular resistance which
|
lead to renal blood flow maintance which is good for pts with renal failure
|
|
|
What is benifit of Clondie increase bareceptor senstivity
|
decreases orthostatic hypotension
|
|
|
SE's of Clonidine
|
Xerostomia, sedation (decreases with continued therapy), rebound hypertension (nervousness, tachcardia, sweating HA
|
|
|
What causes the rebound hypertension with Clondiie
|
increased in sympathetic discahgne brakes are off
|
|
|
What is methyldopa
|
alpha 2 agonist in CNS
|
|
|
MOA of methyldopa
|
transformed into alpha-methly NE which is false transmistter and decrease sympathetic outflow
|
|
|
Does methyldopa have an effect on HR or CO
|
NO
|
|
|
Methyldopa also decreases vascular resistance and baroreceptor reflex inatct
|
YES
|
|
|
What are SEs of methlydopa (NOT GENERALLY USED b/c of THIS)
|
dry mouth sedation, hepatotoxcity, postivie Coombs test interferes with blood matching
|
|
|
What are MOA of Moxonidine or Rilmenidine
|
imiazoline I1 agoinsts, which decrease sympathetic outflow , also alpha 2 agoinsts in CNS and periphery
|
|
|
SEs of Mononidine and Rilmenidine
|
less dry mouth
sedation no REBOUND hypertension |
|
|
What are adrenergic neuron-blocking drugs
|
Reserpine
|
|
|
What is general action of Adrenergic neuron blocking drugs
|
decreases NE release from sympathetic neruons and PARIAL depletion of CCAs
|
|
|
What is MOA of reserpine
|
inhibits uptake and storage of NE, DA, 5-HT in synaptic vesicles
|
|
|
Low doses of Reserpine
|
Decrease CO
Decrease PVR |
|
|
IS sympatetic reflex inatct for resperpine
|
YES-less CA's released
|
|
|
SE's of Reserpine
|
diarrhea, GI, increase Gastric acid secretion (parasympathetic)
parkinsonian (derease DA) mental depression (decrease 5-HT |
|
|
What pts should avoid Reserpine
|
pts with history of depression or PUD
|
|
|
Problems with reserpine CNS occur after long duration, and effect persist long after drug removed why
|
have to make new vesicles
|
|
|
Arenoceptor blocking drugs decreases sympatthetic activation at receptors A1, A2, B1, B2
|
YES
|
|
|
What are Normal actions of A1 and A2
|
A1 cause vasoconstrion which increases PVR and VR
A2 decreae NE release |
|
|
What are effect of B1
|
heart-increae HR contractility,conduction
Increase JGA release of renein stimulate ANGII increase PVR aldosterone increase BV and VR |
|
|
What are effects of B2
|
vasodialte and decrease PVR
|
|
|
What are Alpha 1 adrenoceptor antagoinsts
|
Prazosin, terazosin, doxazosin,
|
|
|
MOA of Alpha-1 ANTAGOINSTS
|
results in vasodialtion of arterioes and vein, which Decrease PVR, and Decreases VR
|
|
|
Vasodilation of arterioles and veins does what
|
Decrease BP
|
|
|
How does sympathetic system respond to decrease BP in alpha-1 antagoinsts
|
increase HR, cardiac contractility
increase renin, increase fulid retention |
|
|
How do you combat increase HR and increase cardiac contractility
|
Beta blocker
|
|
|
How do you combat increased renin and increase fluid retention
|
diuretic
|
|
|
SE's of Alpha 1 ANTAGOINSTS
|
dizziness, HA fatigue, edema FIRST DOSE othrostatic hypotension
|
|
|
What are Alpha-1 ANTAGOINSTS effects on blood lipids
|
decreases TG's
decreases total and LDL Cholesterol and increases HDL |
|
|
What are Non-selective B-Antagoinsts (Block both B1 and B2)
|
Nadolol
Propranolol timolol |
|
|
What are the selective B anatgonist
|
B1
Atenolol betaxolol bisoprolol metroprolol |
|
|
What are Non-selective B-antagoinstis with ISA (less B2 blocking effect)
|
Cartelol
penbutolol pindolol |
|
|
What drug is selective B1 antagoinst and has ISA
|
acebutolol
|
|
|
What are properties of Carvediolol and labetolol
|
Non-selective Beta antagoinst and alpha 1 antagoinst
Labetolol has partial ISA |
|
|
What are properties of Nebivolol
|
Selective B1 blocker and NO dependent dialtes BV, and decreasess PVR
|
|
|
Initally NON-SELECTIVE Beta antagoinst blocks cardiac effect by
|
decreasing HR and contractility
|
|
|
Pts chronically on non-selective Beta blockers CO may return to normal why
|
b/c of Decreased PVR
|
|
|
Side effects of Beta antagoinsts
|
mental depression lassitude
abstince syndromw |
|
|
What is abstinence syndrome
|
nerouvs tachycardia and increase BP on abrupt discontinuation
|
|
|
Who should I use beta-blocker in care with
|
Asthma
HF Diabetes PVD |
|
|
What should I be careful in Asthma and HF, Diabetes and PVD
|
astham--B2 blocked triggers asthma (vasoconstion)
HF is supported on sympathetic Diabetes ,PVD vasoconstrion of B2 |
|
|
What are non-selective B-antagoinsts effect on lipids
|
Increase TG, Cholesterol, and decrease HDL
|
|
|
What do ISA effects on lipids
|
increases HDL
|
|
|
Name Ca+ Channel antagoinsts
|
Verapamil, diltiazem, amlodipine, felodipine DIPINES
|
|
|
What are the 2 main types of caclium channels
|
ROC (linked to receptors)
Voltage operated chanlles |
|
|
ROC's linked to receptor VOC's ----
|
open in response to membrane depolarization
|
|
|
What are 3 types of VOCs
|
Transient
Long lasting Neural |
|
|
Where are transients and fuction
|
oepne short time present in cardiac muscle
|
|
|
What are Long lasting VOCs
|
open long time in vascular smooth muscle/cardiac
|
|
|
What are neuronal VOCs
|
nerve terminal, involved in NT release
|
|
|
The Ca channels exits in one of 3 states
|
resting
active or inactive |
|
|
Resting is close, then goes to active, then to inactive, inactive must go back to
|
resting state to be stimulated again
|
|
|
What is MOA of dilitazem and verapamil
|
bind stronglt to inactive state, so slow recovery from inactive to RESTING
|
|
|
Verapamil and diltriazem bind strongly to inactive state ressults in prolognatio of recovery is most obvious at
|
high stimulation rate
|
|
|
Blocking openign of VOC results in what for vascular smooth muscle
|
dialtion of vascular smooth muscle greater in arteriole than in venous which decreases PVR and Decrease BP
|
|
|
By blocking opening of VOC this results in decrease Ca+ influx which
|
decrease intraceullar Ca+ conc and decreases contraction and results in relaxation
|
|
|
What are verapamil or diltizem affects on heart
|
SA node depression which decrease HR (inhibits reflex tachycardia)
|
|
|
The dihydropyridines (amlodipine, felodpine, nifedipine affects on heart
|
little cardic blocking activity so dialtes BVs decreases HR and see reflex tachycardia
|
|
|
Is ther fluid retention with Caclium Channel antagonists
|
NO
|
|
|
Memorize chart
|
YES
|
|
|
SE's of ca+ channel blockers
|
dizziness, hypotension HA flusion
constipation cardiac depression |
|
|
Why is constipation prevalent in verapamil
|
b/c L types channels on GI smooth muscle inbhitited
|
|
|
Verabpil and diltizem cause cardiac depression examples
|
SA or AV node abnormailites
|
|
|
Should Ca+ Channel antagonists be used in HF
|
no make wrose decrease HR and decrease contracilty even more
|
|
|
Verapamil and propranolol should not be co-administred why
|
both depres heart
|
|
|
Ca+ channel blockers are safe to use in HTN pts with daibetes mellitus, asthma or hyperlipiemia, which agents would you not use
|
non-selective beta blockers
|
|
|
What medications are the vasodialtors
|
Ca Channel blockers
Hydralzine minoxidil Na Nitroprusside |
|
|
Hydralazine is one the first orall active antihypertensive agents MOA
|
relax arteriole smooth msucle by:
endotherlium-dependent mechansim |
|
|
What is the endothelium dependent mechanism
|
NO dependent mehaism
|
|
|
What is the hyperpolarization of vascular smooth msucles
|
makes it harder to depolaries, decreases opening of voltage operated Ca+ channels and decreases contraction
|
|
|
Relaxation of smooth muscle results in Decreased PVR and Decrease BP, what are reflex
|
increase sympatehic reflex--increases CO
decrease BP increases fluid retention |
|
|
How do you treat hydralazine induced increased CO
|
used a beta blocker
|
|
|
SEs of Hydralazine
|
HA, Flushing dizzines
1st pass metabolism by N-acetlyation, drug induced lupus syndrome, and secondary tachphylxis |
|
|
What happens as result of 1st pass metabolism by N-acetlyation
|
low oral bioaailability (depends if you are fast or slow acetlator
|
|
|
Why should you NEVER use hydralazine as SOLE therapy for long term treatment of hypertension
|
scondary tachphylacis, and unable to keep BP low enough by itself
|
|
|
What should you use hydralazine in combination with
|
b-blockers and diuretics
|
|
|
WHat is MOA of minoXIDIL (not active in vitro--so what happens
|
converted to active compound by hepatic sulfotranserase
|
|
|
MOA of minoxidil
|
activates ATP K+, and opens K+ channels
|
|
|
Wha tis result of opening K+ channels
|
hyperpoliaztaion of cells and inhibit VOC, and reslt sin relaxes ATERIOLAR smooth smooth
|
|
|
Relaxtion of ateriolaor smooth muscle does what
|
decreases PVR and decrease BP
|
|
|
What is bodys response to decrease BP
|
increase sympatehtic reflexa and increase fluid retention
|
|
|
SE's of minoxidil
|
ptoentation stimulation fo renin secretion and Na+ and H20 retention which decreases renal perfusion
Hypertrichosis |
|
|
What happesn are sresul tof decreased renal perfusoin
|
increases symahtetic drive to to renal tubule alpha receptors, and increases PCT absroption of Na+ and H20
|
|
|
What caues hypertrichosis
|
Minoxidil icnrease cutaneous Blood flow which promotes hair growth on face, back, and arms
|
|
|
Sodium Nitroprusside has a nitrosos mietry necessary for activity, MOA
|
relaxation is mediated by release of NO
|
|
|
What does NO do in Sodium Nitroprusside
|
relaxes arterial and venous smooth muscle decrease PVR and VR which decreases BP
|
|
|
Does Sodim Nitropursside only cause modest increases in HR and does it decrease myocardial oxygen requirements
|
YES
|
|
|
Side effects/considerations of Sodium Nitroprusside
|
Not orally active
rapdi infusion results in accumulation of cynaide and thiocynate in blood |
|
|
SES of thiocyanate inblood
|
anorexia, nausea, fatigue, toxic pyshosis, and disorientation
|
|
|
What disease state should avoid Nodium nitroprusside
|
COPD, b/c it promotes ventilation/perfusion mismatching
|
|
|
What are examples of ACE inhibitors
|
PRIL
captropril lisinopril enalparil enaprilat moexpril |
|
|
MOA of Ace inbhitiors
|
inbhit the conversion of angiotension I to angiotensin II
|
|
|
What is the rate liminting enzyme in agiontensin II formation
|
renin
|
|
|
Anngiontensin II has greatest pharmacoligcal activites
|
1. Constrictr vascular smooth muscle (indirectly) directly constricts arterolies
2.Increases sympatehtic nervous system activyt 3. Aldosterone 4. Kidenys 5. Brain (CNS) |
|
|
What are angiotensin II effects on cardiac contractility=
|
direct (angio II receptors on heart)
indirect (increases sympatehtic effects |
|
|
What are angiontensin II efeect on aldosterone
|
increase Na+ retention, K+ loos and increases BP
|
|
|
ANgtiontensin II also stimualtes vascular and myocaridal hypertopry by induction of
|
protononcogens C-fos and c-jun
|
|
|
What does c-fos and c-jun do
|
causes cell proliferation/synthesis and hypertrophy
|
|
|
On a moelcular bases is angiotensin II 40x more potent than NE at Increased BP
|
YES
|
|
|
The antihypertensive effects of ACE inhbiitors relate to the inhibition of
|
angiotensin II foramtion mainly
|
|
|
Initially antihpertensive actions are direcly related to plasam renin conc. however conronically
|
NO relationsip exists
|
|
|
What are effets of ACE inbhitiors
|
Decrease PVR which Decrease BP
|
|
|
Why is there only a small compensatory increase in CO and HR
|
b/c ACE-I inhbit both renal and sympatehtic outflow
|
|
|
What are side effects of ACE-I
|
SAD H
severe hypotension in hypovolemic pts or pts who are Na+ depleter acute renal failure drycough/wheezing hyperkalemia |
|
|
Why can ACE-I cause acute renal failure
|
angiotensin II constricts efferent arteriles, inhbito results in vasodilation and increase GRP
|
|
|
What causes Hyperkalemia in ACE inhibtiors
|
decrease ANgII, decrease aldosterone and increase K+ RETNENTION
|
|
|
What are Angiotensin II Receptor Blockers
|
losartan
ibesartan canderstan valsartan |
|
|
MOA of ARB
|
inhibtion angiotensin II type 1 receptors, which decreases pressor effects of AII
|
|
|
Whta are SE/considerations for ARBs
|
SAD H
Severe hypotension Acture renal failure NO dry cough/wheezing diarrhea, dizziness insomina |
|
|
Should ARB's be adminsted to pregnant women
|
NO--losartan is passed in breast milk
|
|
|
Why dont ARB cause dry cough or wheezing
|
do not prevent the breakdown of bradykinin
|
|
|
What are the vasopeptiase inhibitors
|
omapratrilate (atrilat)q
|
|
|
MOA of vasopeptidase inhibitors
|
inhibition ACE and netural endopeptidase
|
|
|
SES of vasopeptidase inhibitors
|
dry cough/wheezing
facial redness severe agnioedema |
|
|
What are Renin inhibitors
|
Alikiren (KIREN)
|
|
|
WHat is MOA of Renin inhbitors
|
block formation of angiotensin I and and angiotensin II
|
|
|
SEs of alikiren
|
diarrhea, dyspepsia, cough, angioedema, poor absroption
|
|
|
Main problem of alikeren (kiren)
|
poor absorptionq
|
|
|
What are endothelin receptor antagoinsts
|
abrisentan
bosentan darusentan SENTAN |
|
|
What is MOA of noram endothelin-1
|
causes vasoconstriction, which increase PVR and increases BP
|
|
|
Blaock of ETa receptor does what
|
decreases PVR and BP
|
|
|
SES of endothelin receptor antagoinsts
|
Swelling of angles and legs facail fluusing
liver injury |
|
|
Is Endothelin receptor antagoinsts contraindiated in pregnancy
|
YES mAJORLY---women has to confirm no preganta nd 2 forms of contraception
|
|
|
What are endothelin receptor antagoinsts used in
|
pulmonary HTN and resitant hypertension
|
