HTN - Hockerman Flashcards
Vasoconstriction:
________ receptors are main cause
alpha (1) adrenergic
Vasoconstriction:
pathway from receptor to cell to potentiate constriction (@ alpha 1 receptor)
Gq –> PIP(3) –> Diacyglycerol and IP3 –> IP3 will cause increase in calcium…
How does Calcium lead to contraction?
Ca2+ + Calmodulin –> stimulates myosin light chain kinase which will phosphorylate myosin LC –> Myosin LC-PO(4) + actin - CAUSE CONTRACTION
2 main mechanisms for controlling smooth muscle tone
voltage gated Ca2+ channels
&
pharmaco mechanical coupling (Gq to IP3 to Ca2+ etc..)
what are the endogenous peptide vasoconstrictors?
angiotensin, vasopressin, endothelin, urotensin
which endogenous peptide vasocontstrictor is elevated in diabetes?
Urotensin
which endogenous peptide vasocontstrictor is elevated in PAH (pulmonary arterial hypertension)?
Endothelin
Urotensin (an endogenous vasoconstrictor) binds to ______ in ______ & _______
GPCRs; VSM (vascular smooth muscle); cardiac muscle
Urotensin is produced where?
heart, liver, kidney
Endothelin is produced where?
vascular endothelium…
Endothelin binds to ______ in _____ and contracts ______
GPCRs; VSM; VSM
3 main reasons we would want to modulate vascular smooth muscle?
resistance vessels; controlling blood flow, cerebral arteries
What are therapeutic uses of vasoconstrictors?
TREATING HYPOTENSION:
b/c shock, anesthesia, or chronic orthostatic hypotension
For treating hypotension - what receptor agonists are used?
alpha 1 adrenergic
what are examples of drugs that treat hypotension (aka what are some alpha 1 adrenergic drugs)
epinephrine, ephedrine, midodrine
what types of shock can be treated with vasoconstrictors
anaphylactic shock, brain trauma, hemorrhagic
Using Vasoconstrictors for controlling of blood flow: what are reasons to do this?
- using with anesthetics b/c it will reduce blood flow to site of injection
- Hemostasis during surgery
- Nasal/Opthalmic Decongestants
what type of vasoconstrictor is used adjunctively with anesthetics
epinephrine
what type of vasoconstrictors are used for hemostasis during surgery
epinephrine, cocaine
What is a direct acting vasoconstrictor used as a decongestant
phenylephrine
What is a indirect acting vasoconstrictor used as a decongestant
pseudoepedrine, ephedrine, phenylpropanolamine
What is a partial acting vasoconstrictor agonist used as a decongestant
naphazoline, tetrahydrolozine, oxymetazoline
what are the 4 main groups of vasodilators talked about?
- ________ modulators
- _______ Agonists
- _______ Antagonists
- _______ Analogs
- Cyclic GMP modulators
- K+ Channel Agonists
- Endothelin Antagonists
- PGI2 Analogs
what are the 3 group/subsets of cyclic GMP modulators
- organic nitrates/nitrites
- PDE inhibitor
- Natriuretic peptide
Nitric Oxide Synthase has __(#)___ of isoforms and there names are….
3!
nNOS; iNOS; eNOS
which isoform of NOS (nitric oxide synthase) is most important to us?
eNOS (endothelial)
NOS (nitric oxide synthase) is found in the _________
vascular endothelium
What is the pathway/process of Nitric Oxide Synthase?
L-Arginine –? L-Citruline + NO
eNOS is found in ________ and gets activated by ______
vascular endothelium/ Ca2+-CAM
where is Guanylate Cyclase found? (talking about Nitric Oxide-Cyclic GMP Pathway)
vascular smooth muscle
______ is an activator of guanlyl cyclase
NO
Why/How does Ach (acetylcholine) lead to Smooth Muscle Relaxation
Ach will increase Ca2+ in endothelium which will stimulate eNOS –> eNOS makes NO –> NO causes smooth muscle relaxation
NO stimulates Guanlyl cyclase –> what does guanlyl cyclase do?
it will take GTP and make it into cGMP
GTP –> cGMP
Nitric Oxide binds to ___________ in guanylate cyclase
heme iron prosthetic group
NO binds to Guanlyate cyclase and will stimulate production of ______ and will activate _______
cGMP; cGKI (aka PROTEIN KINASE G aka PKG)
how does cGMP lead to relaxation (talking about Nitric Oxide-Cyclic GMP Pathway)
cGMP will cleave the PO(4) group from Myosin-LC (this leads to relaxation)
Myosin-LC will cause ________
vs
Myosin-LC-PO(4) will cause ______
relaxation; contraction
how does PKG (cGKI) cause relaxation in smooth muscle (talking about Nitric Oxide-Cyclic GMP Pathway)
- ________ of L-Type Ca2+ Channels
- ________ of Ca2+-activated K+ channels
- ________ MLC phosphorylation
- ________ Ca2+ uptake in to ER
inhibit (Ca2+ channels)
Stimulate (Ca2+ activated K+ channels)
decrease (MLC phosphorylation)
enhance (Ca2+ into ER)
how does PKG (cGKI) cause relaxation in smooth muscle (talking about Nitric Oxide-Cyclic GMP Pathway)
inhibit (Ca2+ channels)
Stimulate (Ca2+ activated K+ channels)
decrease (MLC phosphorylation)
enhance (Ca2+ into ER)
PKG will _______ L-Type Ca2+ Channels - why does this cause relaxation of smooth muscle?
inhibit ;less Ca2+ influx = less contraction
PKG will _______ Ca2+ activated K+ Channels - why does this cause relaxation of smooth muscle?
STIMULATE (because it will cause repolarizaiton of the membrane potential)
PKG will _______ myosin phosphorylation -
why does this cause relaxation of smooth muscle?
decrease (because when there is NOT a PO4 group on myosin head dettaches from myosin and no contraction can happen aka relaxation…)
PKG will _______ Ca2+ uptake in to ER -
why does this cause relaxation of smooth muscle?
enhanced (b/c less Ca2+ available = less contraction)
what channel does PKG inhibit?
Ca(v1.2)
what channel does PKG stimulate
BK(Ca)
what is used by PKG to enhanceCa2+ uptake in the ER
phospholamban (it gets phosphorylated and then will increase the reuptake of Ca2+)
Organic Nitrates cause vaso________
dilation
Organic Nitrates are (selective or non-selective) vasodilators
NON-selective
Organic Nitrates (do or do not) require a functional endothelium
DO NOT
Organic nitrates can be used (acutely, chronically, or both)
BOTH!
Organic nitrates require ________ to get broken down to _____
bioactivation; Nitric Oxide
Organic Nitrates can be by what routes for prolonged prophylaxis
Transdermal/Orally
Organic Nitrates can be by what routes for acute attacks of angina
give sublingually
T or F: Organic Nitrates cannot develop tolerance
FALSE
Which of the following Organic Nitrates has the greatest oral bioavailability?
GTN, ISDN, 5-ISMN
5-ISMN (isosorbide mononitrate)
Which of the following Organic Nitrates has the lowest oral bioavailability?
GTN, ISDN, 5-ISMN
GTN ( super freaking low)
Which of the following Organic Nitrates has the longest half life?
GTN, ISDN, 5-ISMN
5-ISMN
which organic nitrate is commonly known to not be efficacious in the Asian Population
GTN (Glycerol Trinitrate)
what is the polymorphism known to decrease the efficacy of GTN
GLU 504 –> LYS 504 (in ALDH-2)
what enzyme is needed to activate GTN
ALDH-2
The ______ allele is the reason for decreased efficacy of GTN AND it can cause _____
LYS 504; Alcohol intolerance (aka “Asian Glow”)
what is the idea behind organic nitrate tolerance? (Example given in class is GTN bc it is the most understood)
GTN gets metabolized by ALDH-2 into a thionitrate intermediate. ALDH-2 needs to be regenerated and a reduced form of LIPOIC ACID is needed (can eventually deplete lipoic acid store!)
Explain the differences in GTN vs ISMN/ISDN activation
GTN - needs lipoic acid/needs ALDH-2!!
ISMN/ISDN = uses enzymes outside of mitochondria to be metabolized (P450 and others…)
which organic nitrate is used for acute management of HTN crisis/severe decompensated heart failure
Sodium Nitroprusside (SNP) (GIVEN IV)
SNP - Sodium Nitrodpursside will ______ veins and arterioles
Dilate
SNP - Sodium Nitrodpursside gets metabolized by _______
erythrocytes
SNP - Sodium Nitrodpursside is metabolized and made into what things?
NO (duh), 4 CN (obvs not good to have hella cyanide in your body), and Cyanmethemoglobin
SNP - Sodium Nitrodpursside: Its metabolite (CN-) can inhibit \_\_\_\_\_\_\_ metabolism/ \_\_\_\_\_\_\_ accumulation
oxidative; lactic acid
SNP - Sodium Nitrodpursside:
CN- gets converted to _______ by ______ (bc it is less toxic in this form) and then is excreted by ______
SCN (thiocyanate); rhodanase; kidney
what 2 things can be used for detoxification (of CN-) after using SNP - Sodium Nitrodpursside
Sodium thiosulfate OR hydroxocobalamin
what class of drug is Hydralazine apart of? (Organic nitrate? Natriuretic Peptide? PDE Inhibitor? K+ Channel Agonist?)
Organic Nitrate!
Hydralazaine causes vaso______
dilation (its a nitrate!) of ARTERIOLES
Predicted mechanism of Hydralazine
interferes w/ release of Ca2+ from the ER
Hydralazine can induce a _______ syndrome
lupus-like
Hydralazine dilates what?
ARTERIOLES! (not veins like other organic nitrates)
what is drug called that is a combo of ISDN and Hydralazine?
BiDil
why is hydralazine and ISDN in a combo pill together?
the antioxidant activity of Hydralazine will potentiate vasodilatory activity of ISDN
What is Natrecor (Nesiritide)?
a vasodilator;
a natriuretic peptide
Natrecor (Nesiritide) is given by what route?
IV
Natrecor (Nesiritide) is given IV for what?
acutely decompensated HF
how does Natrecor (Nesiritide) work?
it BINDS to and ACTIVATES membrane bound guanylate cyclase in vascular smooth muscle and endothelial cells
ALSO
causes you to lose fluid = less blood volume = less work load on the heart
Natrecor (Nesiritide) is synthesized and secreted from where?
heart muscle
Natrecor (Nesiritide) is released from the heart in response to what?
response to INCREASED blood volume
PDE Inhibitors cause vaso_______
dilation
What are the 2 groups of PDE inhibitors we learned about?
PDE3 inhibitor/ PDE5 inhibitor
PDE3 inhibitors prevent the breakdown of c____ and PDE5 inhibitors prevent the breakdown c____
AMP; GMP
How do PDE3 inhibitors work?
NORMALLY PDE3 will breakdown cAMP into AMP; but if that is inhibited you have more cAMP –> more MLCK-PO(4) –> Relaxation
a part of what drug class is Amrinone?
PDE3 inhibitor (cAMP modulator - Vasodilator)
a part of what drug class is Milrinone?
PDE3 inhibitor (cAMP modulator - Vasodilator)
a part of what drug class is Dipyridamole?
PDE5 inhibitor (cGMP modulator - Vasodilator)
a part of what drug class is sildenafil?
SELECTIVE PDE5 inhibitor (cGMP modulator -
Vasodilator)
a part of what drug class is Hydralazine?
Organic Nitrate (cGMP modulator - Vasodilator)
a part of what drug class is Tadalafil?
SELECTIVE PDE5 inhibitor (cGMP modulator -
Vasodilator)
a part of what drug class is Vardenafil?
SELECTIVE PDE5 inhibitor (cGMP modulator -
Vasodilator)
Amrinone/Milrinone (cAMP PDE3 inhbitors)
Are given by _____ route
IV
Amrinone/Milrinone (cAMP PDE3 inhbitors)
have a direct ________ effect on the ______
positive inotropic; Myocardium
Amrinone/Milrinone (cAMP PDE3 inhbitors):
has (minimal or maximal) chronotropic effect
MINIMAL
Amrinone/Milrinone (cAMP PDE3 inhbitors) has a direct vasodilatory effect on _________
vascular smooth muscle
Amrinone/Milrinone (cAMP PDE3 inhbitors)
is used mainly in _____ (acute treatment)
CHF
PDE 5 is predominant in _______ (what area of the body)
corpus cavernosum (why ED meds work where they do)
Sildenafils effect on the blood flow of the penis:
_______ artery dialtes + ______ smooth muscle –> increased _______ space
Helicine (artery); relaxaed; Sinusoidal
Brand for Tadalafil
Cialis
Brand for Vardenafil
Levitra
Brand for Sildenafil
Viagra
which ED med…
has a shorter time to onset than Viagra
AND
is more selective for PDE5 than viagra
Levitra (Vardenafi)
which ED med…
is more selctive for PDE5 than viagra
AND
has a longer duration of action than the other drugs in its class
Cialis (Tadalfil)
K+ channel agonists/openers cause vaso______
dilation
why do K+channels cause vasodilation?
when the K+ channel is open - the membrane potential gets closer and closer to K+ equilibrium potential —–> makes it harder to depolarize the membrane enough to open the voltage gated Ca2+ channels (and Ca2+ channels normally cause vasoconstriction)
what drug class is Minoxidil apart of ?
K+ channel agonists/openers (Vasodilator)
what drug class is diazoxide apart of?
K+ channel agonists/openers (vasodilator)
what are the K+ Channel agonists/openers we learned about
Minoxidil; Diazoxide
Minoxidil: activated by ________
sulfonotransferase 1A1
Minoxidil: used with what 2 medications
loop diuretics and beta blockers (why? idfk)
Minoxidil: is a very potent vaso______
dilator!! (used for severe/drug resistant forms of HTN)
Minoxidil: is given by what route?
orally
Minoxidil: __________ may contribute to its efficacy
cAMP PDE inhibition
Diazoxide: used by what route for acute HTN
IV
Diazoxide: very potent vaso_______
dilator!! (used for severe/drug resistant forms of HTN)
Diazoxide: inhibits the release of _________ from _______
insulin; pancreatic Beta-cells
Diazoxide: used orally for ___________
hypoglycemia secondary to hyperinsulinemia
Adenosine is a vaso______
dilator
adenosine binds to __________
A1 receptor GPCR
Adenosine increases conductance of a ________ which causes _____ polarization and relaxation of vascular smooth muscle
K+ channel; hyper
A1 receptor causes hyperpolarization - via the ______ channel
GIRK
Adenosine uses what type of GPCR/works how
G(beta/gamma) binds to GIRK to conduct K+ and causing membrane hyperpolarization
What classes of drugs can be used for PAH (Pulmonary Arterial HTN)
Vasoconstrictor Antagonists; Prostacyclin Analogs
what drug class is Bosentan in?
Vasoconstrictor antagonist for PAH (aka a vasodilator)
what drug class is Macitentan?
Vasoconstrictor antagonist for PAH (aka a vasodilator)
what drug class ambrisentan?
Vasoconstrictor antagonist for PAH (aka a vasodilator)
how do vasoconstrictor antagonists work?
they are antagonists to endothelin receptors
which vasoconstrictor antagonist(s) (-entans) block both ET(A) and ET(B)
Bosentan; Macitentan
which vasoconstrictor antagonist(s) (-entans) block only ET(A)
Ambrisentan
T or F: Vasoconstrictor antagonists can be used in pregnancy
FALSE!!
Which (entan) drug can cause hepatotoxicity
bosentan
Prostacyclin analogs can be used to cause vaso_____
dilation
Prostacyclin analogs can be used to treat ___________
PAH (pulmonary arterial HTN)
what are the possible prostacyclin analogs?
PGI2; Trepostinil; Iloprost; Selexipag
What are the 4 different classes of drugs that can be used for PAH
- Vasoconstrictor antagonists (endothelin antagonist)
- Prostacyclin analogs (vasodilator)
- Allosteric Activator of sGC
- Selective PDE5 inhibitors (Cialis/Viagra)
what is the drug used for PAH that is known as an allosteric activator of sGC
Riociguat (Adempas)
how does the Riociguat (Adempas) work?
it is an allosteric activator of sGC; it potentiates the effect of NO; will increase cGMP concentration in VSM
Riociguat (Adempas)
- Not combined with _______ or ______
- Contraindicated in _________
- Risk of ________
Nitrates or PDE 5 inhibitors; Pregnancy; Hemorrhage
What two things that determine the direction of flow of ions?
Concentration gradient and Electrical
Ion Channels are ______ that form ______ in the plasma membrane
proteins; pores
Ion Channels can be categorized by what 3 main things
Gating mechanism; Ion selectivity, Pharmacology (Passive-ness?)
Membrane Potential:
Excitable cells have a ______ inward potential across the membrane due to the selective permeability of the resting membrane to ______
negative; K+
K+ is ____ inside of the cell and ____ outside
HIGH INSIDE; LOW OUTSIDE
Na+ is ____ inside of the cell and ____ outside
LOW INSIDE; HIGH OUTSIDE
Ca2+ is ____ inside of the cell and ____ outside
HIGH OUTSIDE; VERRRRRY LOW OUTSIDE
Ca2+/Na+/K+ - which one has the highest gradient (difference between outside and inside of the cell)
Ca2+!!
Ca2+ channel - open slow or fast?
V slow
Structure of Voltage Gated-Channels:
There is a _______ filter to allow the ion to come in and a _____ of ______ to block the ion
selectivity; bundle of helicies
______ is a H+ gated K+ channel from bacteria
Kcsa
______ is a Ca2+ gated K+ channel from bacteria
MthK
what are the possible types of Calcium Channels
L-Type; P/Q type; N-type; R-type
What Calcium channel do we care the most about for Ca2+ blockers for HTN
Cav1.2
where is Cav1.2 calcium channels found
Cardiac & Smooth Muscle
Ca2+ entry triggers contraction
The following are the responses that come from Calcium Channel Blockers:
Decrease in ________
Relief of _________
Anti________
Decrease in BLOOD PRESSURE;
Relief of ANGINA PECTORIS
AntiARRHYTHMIC
Vasc. Smoot Muscle Contraction (related to Calcium)
(_ _ _ _) - a four letter acronym and what does it stand for
CICR; Ca2+ induced Ca2+ release
[Vasc. Smoot Muscle Contraction - CICR]
How does it work?
Ca2+ comes into cell (influx) via Cav1.2 which induces Ca2+ from intracellular stores via RYR2 in the SR
[Vasc. Smoot Muscle Contraction - CICR]
Ca2+ comes into cell (influx) via Cav1.2 which induces Ca2+ from _____cellular stores via ______ (_________) in the _____
INTRAcellular; via RYR2 (ryanodine receptor 2); in the SR
Beta-adrenergic Modulation via Ca2+ Channels: (aka epinephrines effect on Ca2+/vasc. smooth muscle)
The adrenergic receptor will cause ___________ of _____ and increase Ca2+ influx
PKA phosphorylation; Cav1.2
Beta-adrenergic Modulation via Ca2+ Channels: (aka epinephrines effect on Ca2+/vasc. smooth muscle)
This will cause the increase in what two things?
Increase in contractility/force of contraction
Increase AV nodal action potential conduction rate
T or F: Extracellular calcium is NOT required for contraction of cardiac and vascular smooth muscle
FALSE! it is required
Myosin LC-PO4 is needed to work with _____ to cause contraction
ACTIN
T or F: Myosin LC-PO4 is INACTIVE and will not cause contraction
FALSE! Myosin LC has to be phosphorylated to work with actin and cause contraction
T or F: Myosin LC kinase - PO4 is INACTIVE and will not cause contraction
True! if the KINASE is phosphorylated then no contraction…(opposite of just straight up myosin LC)
[Cardiac Muscle Contraction]
the Ca2+ ion gets released from _________ and binds to _________
sarcoplasmic reticulum; Troponin C
[Cardiac Muscle Contraction]
When Ca2+ binds to ________ it causes the displacement of _________
troponin C; Tropomyosin
[Cardiac Muscle Contraction]
When Tropomyosin is displaced it allows ______ to bind to _____ which causes ________
myosin; actin; contraction! (duh)
What calcium channel and receptor is used in skeletal muscle? (close to cardiac and smooth but different…)
Cav1.1 and RYR1
aka 1’s instead of 2’s
T or F: Extracellular Ca2+ is NOT required for contraction in skeletal muscle
TRUE! (opposite of cardiac/smooth)
CCBs (calcium channel blockers) work at which location(s)?
Cardiac
Skeletal
Smooth
Cardiac and Smooth! (NOT skeletal)
what are the 3 main classes of CCBs
Dihydropyridines
Phenylalkylamines
Benzothiazepines
What are the clinical applications of CCBs (per Hockerman)
Angina Pectoris
Arrhythmia
HTN
what class of CCB is the drug a part of? Nifedipine
DHP
what class of CCB is the drug a part of? Felodipine
DHP
what class of CCB is the drug a part of? Isradipine
DHP
what class of CCB is the drug a part of? Amlodipine
DHP
what class of CCB is the drug a part of? Nisoldipine
DHP
what class of CCB is the drug a part of?Nicardipine
DHP
what class of CCB is the drug a part of? Nimodipine
DHP
what class of CCB is the drug a part of? Clevidipine
DHP
what class of CCB is the drug a part of? Dilitiazem
Benzothiazepine
what class of CCB is the drug a part of? Verapamil
Phenylalkylamine
List the Structural Qualities of DHPs
Dihydropyridine Ring….
Aryl group
Chrial Center!! (@ pos 4)
Ester linked side chains
which CCB is formulated w/ lipids from soy and egg
Clevidipine
which CCB is known as a short acting DHP & why is it short acting
Clevidipine; fast metabolism by esterases!
DHP’s blocking mechanism: stems form clues seen from _________
enatiomers
DHP’s Enantiomer:
a (+) enantiomer will _____ current
BLOCK
DHP’s Enantiomer:
a (-) enantiomer will _____ current
POTENTIATE
DHP’s Enantiomer:
Mechanism involves interference with _______
gating
DHP’s Enantiomer:
(+) enantiomer will interfere with (opening or closing?
opening!
DHP’s Enantiomer:
(-) enantiomer will interfere with (opening or closing?
closing!
DHP Enantiomer:
(+) enantiomer - what is its effect on gating and current?
it BLOCKS current by OPENING the gate (opening a gate will stop voltage)
DHP Enantiomer:
(-) enantiomer - what is its effect on gating and current?
it POTENTIATES current by CLOSING the gate
T or F: DHPs are not selective for vasculature
FALSE! they are dope bc they are selective for vasculature –
T or F: DHPs are NOT antiarrhythmics
True! - they do not compromise cardiac function
How do DHP drugs work at their binding site/in what “state” must the channel be in for the drug to bind
channel must be CLOSED!
this is known as TONIC BLOCK/Voltage Dependence
Explain Voltage Dependence (related to DHP block)
The affinity of the drug is dependent on the voltage. If the voltage is more positive - there is greater binding/blockage. this is because if it is MORE (+) of a voltage - channel more likely to be closed and DHPs need the channel to be closed to bind!
which DHP exhibits selectivity for cerebral arteries
Nimodipine (aka good for brain bleeds)
Do DHPs have reflex tachycardia/cause an increase in Heart rate?
Yes
Which DHP has LESS vascular specificity
Nifedipine
Why do DHPs have efficacy in angina?
the reduce oxygen demand in the heart
DHPs reduce the _______ demand in the heart
Oxygen
DHPs (except ________) do or do not depress cardiac function
Nifedipine; DO NOT
most DHPs do NOT depress cardiac function
DHPs - what is their binding to serum proteins like? (low or high binding?)
HIGH protein binding
DHPs - do they undergo 1st metabolism in the liver? yes or no?
yes they do - extensive 1st pass
which DHP has a slow onset and long duration of action
amlodipine
DHPs have VASCULAR SELCTIVITY: This means that they have - Marked decrease in \_\_\_\_\_\_\_\_\_\_ - Decreased \_\_\_\_\_\_\_\_\_ - Have little effect on \_\_\_\_\_\_\_\_\_
Decrease in Peripheral resistance;
Decreased afterload
Little effect on heart rate/force of contraction
DHPs have VASCULAR SELCTIVITY:
This means that they dilate ______ but have little effect on ______
(fill the blanks with arterioles or venules)
dilate arterioles
little effect on venules
which DHP had increased risk of subsequent of MI?
Nifedipine
The fast/prompt release formulations could increase risk of subsequent MI
Why could Nifedipine cause a subsequent MI?
the prompt release formulations - can cause rapid decrease in BP may lead to reflex sympathetic response (Tachycardia)
Phenylalkylamine - Verapamil:
Is it more or less potent at vasodilation compared to DHPs
LESS potent
Phenylalkylamine - Verapamil:
Reduces HR/Force of Contraction via what mechanism?
it slows conduction through SA and AV nodes
Phenylalkylamine - Verapamil:
Tachycardia reflex present ?
no! the tachycardia is blunted
Phenylalkylamine - Verapamil:
Has an inhibitory effect on the heart - this is due to ________ block
frequency dependent
Phenylalkylamine - Verapamil:
Binds to the channel when it is ______ aka _______ block
OPEN! (drug has to enter the pore); frequency dependent block
Explain Frequency dependent block
the drug (Verapamil) has to bind to the channel when it is OPEN - therefore higher frequency of the channel opening = higher potency.
DHP or Phenylalkylamine:
has NO effect on the heart
DHP (its not like 0 effect but it is much lower than Phenylakylamine)
DHP or Phenylalkylamine:
will reduce HR and force of contraction via slowing conduction through SA/AV nodes
phenylalkylamine
DHP or Phenylalkylamine:
which one has LESS vasodilation
Phenylalkylamine:
DHP or Phenylalkylamine:
which one has greater vasodilation
DHP
DHP or Phenylalkylamine:
which one has reflex tachycardia
DHP
DHP or Phenylalkylamine:
Which one does NOT have reflex tachycardia
Phenylalkylamine:
DHP or Phenylalkylamine:
which one uses frequency dependent block
Phenylalkylamine:
DHP or Phenylalkylamine:
which one uses tonic block?
DHP (voltage dependence)
which drug is apart of the benzothiazepine class?
diltiazem
Benzothiaxepine - Diltiazem
Causes vasodilation but is less potent than ______
DHPs
Benzothiaxepine - Diltiazem
will directly inhibit the heart but is less potent than ______ but more than _____
verapamil; DHPs
which CCB causes constipation?
Verapamil
which CCB causes ankle edema and why?
all of them do!! because they are dilating vessels
which CCB causes facial flushing
DHPs
which which CCB causes tachycardia
DHPs (not amlodipine)
which CCB has a greater decrease in heart rate?
Verapamil (diltiazem also decrease HR but not as much as verapamil)
which CCB has the greatest vasodilation effect
DHPs (all cause vasodilation tho)
which CCB has the greastest effect/decrease in AV conduction and myocardial contraction?
Verapamil (Diltiazem does it too but not as much as Verapamil)
