Exam Three Flashcards
1
Q
Does all pain serve as a protective function?
A
NO
2
Q
What are some factors that influence pain?
A
Age
Gender
Culture
3
Q
What is the number one reason ppl seek medical treatment?
A
Pain
4
Q
Does chronic and acute pain serve as a protection mechanism?
A
no just acute
5
Q
Explain the pain pathway.
A
Nociceptors are activated sending a sensory impulse to the SC and onto the spinothalamic tract followed by a release of neurotransmitters.
6
Q
How are analgesics used?
A
It can alter nerve conduction as a local anesthetic and modify CNS transmission as an opioid, and as an NSAID to decrease pain with inflammation.
7
Q
Define opium.
A
fluid from the poppy plant
8
Q
Define opiate.
A
a substance derived from the poppy plant.
9
Q
Define opioid.
A
a substance with morphine-like actions but not directly from the poppy plant.
10
Q
What are the most effective analgesics that can block emotional and subjective pain?
A
opioids
11
Q
Why are opioids so desirable?
A
sedation
antitussive effects
antidiarrheal effects
12
Q
What are some undesirable effects of opioids?
A
sedation
constipation
respiratory depression
cough reflex depression
miosis
physical dependence
tolerance
13
Q
What are the three opioid receptors?
A
Mu
Kappa
delta
14
Q
What did Henry Beecher observe during WW2?
A
Soldiers in Italy reported far less pain than civilians in the States, why? Under high stress, the body releases endogenous opioids.
15
Q
Explain the mu receptor.
A
Binds with beta-endorphin ligand
analgesia
euphoria
physical dependence
respiratory depression
bradycardia
GI effects
16
Q
Explain the kappa receptor.
A
Binds with dynorphin ligand
miosis
sedation
spinal analgesia
17
Q
Explain the delta receptor.
A
Binds to enkephalins ligands
analgesia
respiratory rate
18
Q
What superfamily are opioid receptors apart of?
A
GPCR’s
19
Q
What is happening in the presynaptic receptor during the opioid MOA?
A
Decreased calcium influx coupled with increased potassium efflux leading to decreased nt release.
20
Q
What is happening in the postsynaptic receptor during the opioid MOA?
A
Increased potassium efflux leading to hyperpolarization and decreased excitability.
21
Q
explain metabolic tolerance.
A
increased ability to metabolize the drug leading to less drug in the bloodstream.
22
Q
Explain cellular tolerance.
A
A given blood level of drug produces a weaker cellular response. Down regulation and desensitization of receptors
23
Q
Explain conditioned tolerance.
A
The bodys response to the drug is linked to the enviornment.
24
Q
is cellular tolerance pharmacokinetic?
A
no
25
Heroin binds to which opioid receptor?
mu
26
Do people develop a tolerance to miosis?
no
27
Explain the rate of tolerance for opioids.
first tolerance is sedation followed by analgesia and lastly constipation.
28
Explain physiological vs psychological dependence.
lack of drug causes a withdrawl episode while psychological state would include depression and cravings.
29
Which dependence do stimulants lead to?
psychological
30
Can the environment precipitate withdrawal?
yes
31
Do long-acting drugs cause more intense withdrawal?
no but short acting does
32
Do withdrawal sign tend to be opposite of what the drug causes?
yes
33
Are opioid withdrawals lethal?
no
34
explain drug dependence vs addiction.
a patient can be dependent for the pain while an abuser will ignore the negative outcome of consumption.
35
What are the signs of an opiate abuser?
early refills
opiate motived behavior in clinical visits of three or more
multiple providers of opiate.
36
Which substance is used during substitution therapy?
methadone and buprenorphine
37
Which substance is an opioid antagonist?
Naltrexone
38
Which substance is a symptomatic treatment for withdrawl?
Clonidine
39
Why is morphine sulfate so important?
the gold standard for analgesia
primarily works through mu receptors
produces both spinal and supraspinal analgesia
HEPATIC METABOLISM
40
Explain codeine
1/10 th potency of morphine
A prodrug where only 10% of codeine is metabolized into morphine by CYP450 and 2D6
used as an antitussive
41
Which substances are a mixture of codeine?
acetamenophen and NSAID's
42
Percodan aka oxycotin aka???
oxycodone
43
explain percodan.
semi-synthetic
slightly more potent than morphine
controlled release
CYP450 and 2D6
44
What are some synthetic compounds?
fentanyl
methadone
buprenorphine
45
explain fentanyl.
80x morphine
carfent is more potent
causes wooden chest syndrome
46
what is wooden chest?
could be due to NE causing vocal cord spasms leading to rapid death.
47
Explain methadone.
long half life
potency is simlar to morphine for IV admin
48
Explain loperamide.
Imodium is an OTC opioid with low abuse liability. used as an antidiarreal
activates mu receptors
49
What is the poor mans methadone? Why is it dangerous?
loperamide high lvls can lead to cardiotoxicity.
50
Explain Buprenorphine.
Potent with low efficacy
abused for its analgesia effects
schedule three with a decrease abuse liability
partial agonist at the mu receptor while acting as an antagonist for kappa/delta
sublingual, paranteral, and transdermal
ORAL = LOW BIOAVAILABILITY
51
What is the difference bn Naloxone and Naltrexone?
Naloxone: short half life, orally not effective, used for opioid reversal and combined for decreased abuse potential.
Naltrexone: long half life, effective orally or by injection, used for dependence Tx.
52
Which organ produces steroids?
the adrenal cortex of the kidneys
53
What are the three classes of steroids?
glucocorticoids
mineralocorticoids
androgens and estrogens
54
Which system regulates cortisol release?
CNS
55
Which class of steroids is the most predominant in the body?
glucocorticoids
56
What are some functions of glucocorticoids?
growth
cardiovascular function
immunity
intermediate metabolism regulation
57
How does glucocorticoids interact with inflammation?
by reducing peripheral leukocytes
blocking the arachodonic acid cascade leading to less chemokines and cytokines
58
Can NSAIDS block leukotrienes?
no
59
Can NSAIDS block leukotrienes, prostaglandins, thromboxanes, and prostacyclins?
yes except leukotrienes!
60
What are the two pathways of the arachidonic acid pathway?
lipooxygenase and cyclo-oxygenase
61
Which arachodonic pathway do NSAIDS block?
cyclo-oxygenase
62
Which arachodonic pathways leads to inflammation?
Both
63
Which arachadonic pathways leads to WBC modulation?
cyclo-oxygenase
64
Explain drug-induced Crushing's syndrome.
A result of glucocorticoid toxicity. A redistribution of fat around the face aka moon face. Supressed immune function, increased appetite, and body hair
65
What are the therapeutic uses for NSAIDS?
Antipyretic
Analgesic
Anti-inflammatory
66
What are the inflammatory effects of prostaglandins?
vasodilation
erythema
hyperalgesia (increased pain sensitivity)
67
Explain leukotrienes.
inflammatory cells
hyperalgesia
important role in asthma
not blocked by NSAIDS
68
Which cyclooxygenase is constitutively active IN MOST TISSUES?
COX-1
69
Which cyclooxygenase is constitutively active is the brain and kidney?
COX-2
70
Can NSAIDS inhibit both COX-1&2?
yes but its relative
71
Are ibuprofen and aspirin more COX-1 or COX-2 selective?
COX-1
72
When NSAIDS inhibit COX-1, is it due to a side effect or therapeutic effect?
side effect
73
How do NSAIDS work as an analgesic?
Blocks PGE pathways that sensitize nerve endings dealing with inflammation. Reduces mild to moderate pain
74
Which opioid effects do NSAIDS lack?
respiratory depression
tolerance development
75
Can NSAIDS help with cancer pain?
no
76
How do NSAIDS work as an antipyretic (reduces fever)?
NSAIDS block PGE 2 AND IL-1 effects on the brain. Reduces elevated temp and dissipates heat.
77
Explain Aspirin.
Aspirin is a prototypic NSAID. The acetyl group covalently binds to the thromboxane causing irreversible lack of platelet aggregation.
78
What if a patient is on aspirin and we need them to clot more?
we need them to turn over new platelets which takes 8 days.
79
How does Aspirin work as a anticoag and NSAID?
the acetyl group covalently binds to the prostaglandin enzyme and the remaining salicylic acid reduces pain and fever.
80
Where is aspirin absorbed?
small intestines
81
does aspirin irreversibly block cyclooxygenase?
yes
82
Does aspirin inhibit both thromboxanes and PG but not leukotrienes?
yes
83
What can happen if a patient is taking coumadin and aspirin?
The anticoag effects will go down a lot due to the high plasma protein binding of both drugs leading to excess competition and toxicity.
84
Symptoms of Salicyism?
can be lethal
headache
confusion
RINGING IN THE EARS
85
Why isnt apsirin used as much?
known for casuing stomach ulcers. NSAIDS are designed to replace aspirin. NSAIDS will REVERSIBLY inhibit COX 1&2
86
What are the side effects of aspirin and NSAIDS?
GI upset due to COX-1 inhibition (reduced mucosal lining)
reyes syndrome
hepatotoxicity
salicylism
decreased platelet aggregation
87
What are the advantages of COX-2 inhibitors?
les GI upset
approved for osteoarthritis and dysmenorrhea
88
What is Celebrex aka celecoxib?
the only COX-2 inhibitor on the market
89
Why were COX-2 inhibitors taken off the market?
cardiotoxicity and stroke
90
What is thromboxane?
COX-1 mediated prothrombotic
91
What is prostacyclin?
COX-2 MEDIATED ANTITHROMBOTIC
92
Does acetaminophen reduce inflammation?
no
93
Is acetaminophen used for its antipyretic and analgesia effecs?
yes
94
Is 15mg of tylenol fatal?
yes
95
How can tylenol be fatal?
your body runs out of ways to break down NAQPI.
96
How long do rbc live?
120 days
97
How many WBC do humans produce per day?
1 billion
98
Why is EPO (erythropoietin) used?
to tx anemia and often abused by endurance athletes.
99
Why is Neulesta used?
Myeloid growth factor to treat neutropenia a lack of wbc due to cancer mostly.
100
What is vit B for?
dna synthesis and repair.
101
What are the two different autonomic nervous systems?
Parasympathetic and sympathetic
102
Which system is responsible for fight or flight?
sympathetic
103
What are some features of the parasympathetic?
SLUDE
miosis
slowed HR
104
Is a contracted bladder apart of the parasympathetic system?
YES
105
What are the features of the sympathetic system?
mydriasis
increased HR
relaxed airway
relaxed bladder
106
How does the Sympathetic system raise the HR?
By utilizing both Ach and NE.
acetylcholine is released dfirst and binds to nicotinic receptors. Postganglionic neurons release NE that bind to beta-adrenergic receptors in the heart.
107
How does the parasympathetic system slow the HR?
By using only ach
108
Which receptors are expressed in the target organs of the parasympathetic system?
Muscarinic ACh receptors
109
Are the ganglions close to the target organ in the Sympathetic system? Why?
no bc in the sympathetic system the reactions have to be close to the spinal cord.
110
Which receptors do the postganglionic neurons express in the parasympathetic?
nicotinic ACh receptors
111
What does AChE do to ACh?
break ACh into choline and acetate
112
Which muscarinic GPCR is found in the heart?
M2
113
Which muscarinic GPCR is found in the CNS?
M1
114
Which muscarinic GPCR is found in the sweat glands?
M3
115
Tell me about the Nicotonic ion channel?
a pentamer made of Nn(N1) in the ganglion and afrenal medulla.
Nm(N2) found in the skeletal muscle.
116
What are the two types of cholinergic receptors?
muscarinic and nicotinic
117
Is the muscarinic receptor excititory?
no
118
what does the msucarinic receptor do to the gi-tract?
slow it down
119
does the muscarnic cause increased sweat production?
yes
120
Does a parasympathomimetic activate or inhibit the Para system?
activate
121
Which drug is a DIRECT and muscarinic parasympathomimetic?
Bethanechol
122
Bethanechol is resistant to AChE, what does this mean?
its long lasting
123
Bethanechol activates the muscarinic receptors in the GI system. Which form of admin is valid for this therapeutic effect?
Oral and SC only
124
What are the adverse effect of bethanechol?
bradycardia and hypotension
125
What happens if we admin bethanechol via IM or IV?
cardiac arrest and and death
126
What are the adverse effects of cholinergics?
Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Emesis
Lacrimation
Salivation
127
Which two ligands bind to nicotinic receptors as a direct parasympathomimetic?
ACh and nicotine
128
What does excessive receptor activation cause?
receptor inactivation
129
What are the symptoms of excess nicotinic activation?
Mydriasis
Tachycardia
Weakness (muscle paralysis)
Th Hypothermia
Fasciculations (muscle twitching)
all leads to seizures
130
What are the two REVERSIBLE and indirect parasympathomimetics?
Neostigmine and Physostigmine
131
What are the two IRREVERSIBLE and indirect PARASYMPATHOMIMETICS?
Insecticides and nerve gas
132
How do all of these indirect parasympathomimetics work?
By inhibiting ACh degradation.
133
If I need to have more ACh in the CNS to treat anticholinergic poisoning then would I use a lipid soluble or water-soluble drug? Which -stigmine?
Lipid soluble, Physostigmine
134
When would I use Neostigmine?
To treat myasthenia gravis
135
What are the differences b/n physostigmine and neostigmine?
neostigmine is water soluble and causes no ACh increase in the brain while physostigmine is lipid soluble.
136
What does the toxicity look like for AChE inhibition?
DUMBBELS (muscarinic) and MTWThF (nicotinic)
137
What is myasthenia gravis?
An autoimmune disease when the antibodies attack the nicotinic receptors of the NMJ causing a loss of receptors
138
What are some examples of the very toxic irreversible and indirect parasympathomimetics?
sarin
novichok
and insectacides
139
What causes nerve gasses to be so lethal?
NMJ paralysis and CNS induced convulsions.
140
How can we treat AChE inhibitor exposure?
Atropine (muscarinic antagonist) and Pralidoxime aka 2-PAM.
141
What are some of the effects of an antimuscarinic drug?
opposite of slude
142
What do some elderly patients experience with antimuscarinic drugs?
delirium
agitation
confusion
143
Name an anticholinergic drug?
Atropine
144
What does Atropine cause?
elevated HR
bronchodilation
decreased secretions
145
Name two competitive muscarinic antagonists?
atropine and scopolamine
146
Can atropine reduce life-threatening bradycardia?
yes if administered via IV
147
What is scopolamine used for?
as an antiemetic for motion sickness
also a drug of abuse
148
Which muscarinic antagonist is derived from belladonna the deadly nightshade?
Atropine
149
Which muscarinic antagonist is derived from datura and eadly nightshade?
Scopolamine
150
What are the symptoms of antimuscarinic toxicity?
mad hatter: CNS delirium
blind as a bat: cycloplegia
hot as hell: no sweating and lethal hyperthermia
151
How can we treat antimuscarinic toxicity?
neostigmine and physostigmine
152
What do the preganglionic neuros in the sympathetic nervous system release?
ACh
153
What do the postganglionic neurns in the sympathetic nervous system release?
NorEPI and EPI
154
What kind of receptors do the target organs have in the sympathetic nervous system?
Alpha and Beta-adrenergic receptors
155
cells in the adrenal medulla release which nt?
epinephrine primarily and norepi a little bit
156
Noradrenergic neurons are the primary source for which nt?.
norepi
157
Are both alpha and beta GPCR'S?
yes
158
Where is alpha-1 receptors found? Why?
In the smooth muscle of blood vessels to tightly control blood pressure. causes vasocontriction and elevated BP.
159
Where is alpha-2 found? why?
Found on the pre-synaptic neuron to control norepi release.
160
Where is beta-1 found? why?
In the heart for muscle contraction
161
Where is beta-2 found? Why?
Lungs, causes relaxation and dilation.
gi-tract
uterus
162
Does nor epi and epi have any selectivity against alpha and beta receptors?
NO
163
Name a nt sympathetic nervous system agonist?
Epinephrine
164
What are the therapeutic effects of epinephrine?
cardiac shock via IV and anaphylaxis
165
What does the epipen do?
vasoconstriction
elevate HR
bronchodilation
166
Name an alpha-1 agonist?
pseudoephedrine
167
What does pseudoephedrine do?
used for allergies due to vasoconstriction
decrease mucosa and swelling
168
What are the adverse effects of pseudoepherine? Why do hypertensive patients have to beware?
causes elevated blood pressure
169
Name an alpha-2 agonist?
Clonidine
170
What does clonidine do?
binds to negative feedback mechanism of the alpha-2. shuts down sympathetic nervous system and norepi release leading to:
lowered bp
lowered HR
VASODILATION
171
What are some adverse effects of clonidine?
sedation
bradycardia
hypotension
172
Name a beta-1 agonist?
Dobutamine
173
What is dobutamine used for?
cardiac arrest and acute heart failure
174
Name a selective beta-2 agonist.
Albeuterol
175
What does albuterol do?
relaxes smooth muscle and elevates bronchial dilation.
176
Name an alpha-1 antagonist.
Prazocin
177
What does prazocin do? Why is it used?
decreases BP used to treat hypertensive crisis
178
What are some adverse effects of prazocin?
orthostatic hypotension
nasal congestion
179
Name a nonselective beta blocker used for angina and hypertension?
Propranolol
180
Propranolol is a competitive antagonist for which nt?
NE
181
Name a selective beta-1 antagonist?
Metoprolol
182
T or F: The renal system produces hormones.
True
183
T or F: The renal system removes metabolic end products and toxins via fecal matter.
False its via urine
184
Does the renal system maintain homeostasis and the body fluids?
yes
185
What is the functional unit of the kidney?
Nephron
186
What are the two structures that make up the nephron?
Glomerulus and tubule
187
What are the three layers of the glomerulus?
podocytes
endothelium
basement membrane
188
What are the landmarks of the tubule?
proximal tubule
loop of henle
distal tubule
collecting duct
189
Describe the flow of the loop of Henle.
The descending limb goes from thin to thick followed by the ascending limb going from thin to thick. Ends with distal tubule and collecting duct.
190
What are the three steps to urine formation?
filtration
reabsorption
secretion followed by excretion
191
What is the filtrate composed of?
plasma
blood
protein
192
What are the most absorbed molecules in the kidney?
water
sodium
chloride etc
193
What are some of the least absorbed molecules in the kidney?
urea
potassium
194
What are the three main hormones produced in the kidney?
renin
vitamin D
Erythropoietin
195
What are the three major ways in which drugs interact with the kidney?
renal excretion of drugs
alteration of kidney function
nephrotoxicity
196
How do we get kidney excretion?
glomerular filtration
tubular reabsorption
tubular secreation
197
Which drugs do not get filtered?
protein bound drugs
198
How can a protein bound drug still be excreted?
via secretory transport
199
What is the purpose of using diuretics?
increase the excretion of sodium leading to less extracellular fluid volume.
200
Can diuretics help with hypertension and edema?
yes
201
How can a diuretics help with urine and sodium excretion?
by increasing glomerular filtration rate and inhibiting tubular reabsorption.
202
What is the most popular mechanism for diuretics?
inhibiting tubular reabsorption
203
Why would inhibiting tubular reabsorption be more effective?
because a 0.7% change in reabsorption yields double the amount of urine.
204
When refering to diuretics which MOA can be assumed?
tubular reabsorption inhibition
205
Where is most of the sodium and water reabsorption is happening?
proximal tubular and loop of henle
206
Where is the site of action for osmotic and carbonic anhydrase diuretics?
In the proximal tubule
207
Where is the site of action for the loop diuretics?
ascending loop
208
Where is the site of action for the thiazide diuretics?
distal tubule
209
Where is the site of action for the potassium sparing diuretics?
collecting duct
210
How are osmotic agents unqiue?
Due to having no specific target instead, they change the concentration of the target fluid, usually leading to fluid being drawn out of tissue and blood flow to the kidneys.
211
Give an example of osmotic diuretic?
Mannitol
212
What can osmotic diuretics be used for?
acute renal failure
decrease intracranial pressure during neurosurgery
213
During excretion how does mannitol keep acting as a potent diuretic?
by increasing the concentration of urine so that water doesnt follow sodium out of the proximal tubule
214
What is the MOA of Carbonic anhydrase inhibitors?
Block carbonic acid from breaking down filtered bicarbonate into water and carbon dioxide.
215
Which molecules are we losing on carbonic anhydrase inhibitors?
K+
HCO3
Na+
216
Name a carbonic anhydrase inhibitor?
Acetazolamide
217
Acetazolamide is a weak diuretic so why do we use it?
glaucoma and mountain sickness/high altitude sickness
218
What is the adverse effect of a carbonic anhydride inhibitor?
metabolic acidosis
219
Which class of diuretics are the most potent?
loop of henle diuretics
220
What is the MOA for loop of henle diuretics?
they block the symporters of Na+
K+
Cl- keeping these molecules on the lumen of thick ascending limb.
221
Name a loop of henle diuretic?
Furosemide
222
What is an unconventional ion that gets excreted under loop diuretics?
calcium and excessive potassium
223
What is an adverse effect of loop of henle diuretics?
dehydration and decreased blood volume
224
Why would we use loop of henle diuretics?
life-threatening edema
CHF
acute pulmonary edema
hypercalcemia
225
What is the MOA of early distal tubule diuretics?
These diuretics can block the cotransporters of calcium and sodium.
226
Name an early distal tubule diuretic?
Thiazide and thiazide-like diuretics.
227
Why are thiazides less potent than furosemide loop of henle diuretics?
due to the location of thiazide site of action, the distal tubule only absorbs 5% of ions.
228
How can thiazide help with decreasing the chances of forming kidney stones?
by decreasing the amount of calcium excreted and increasing reabsorption.
229
What are some adverse effects of thiazide diuretics?
hypokalemia
230
Thiazide is a first line treatment for what?
1. HTN by acting as a direct
2. Vasodilator management of long term low risk edema
3. Renal stone prevention
231
What is the MOA of potassium-sparing diuretics?
Inhibit sodium reabsorption in the late distal tubule and collecting duct by blocking sodium channels in the luminal membrane. Inhibits Na+/K+ exchange.
232
Are late distal tubule sodium channel blocking considered to be potent diuretics?
NO
233
Name a sodium channel blocker diuretic?
Amiloride
234
How can these late distal tubule diuretics be helpful since they are so weak?
Often used in combination with loop of henle diuretics that cause excessive potassium excretion.
235
Can Amiloride cause hyperkalemia?why is that dangerous?
yes, arrthymia
236
Name an aldosterone antagonist?
Spironolactone
237
What does aldosterone do?
a hormone that goes into the nucleus and transcribes sodium channels and sodium/potassium pumps.
238
What are the adverse effects of aldosterone antagonists?
estrogen-like effects in mael and females. Gynecomastia
239
Define stroke volume.
Volume of blood pumped from the left ventricle with each beat.
240
How to calculate the cardiac output?
stroke volume x heart rate
241
What is the base line cardiac output volume?
5L/min
242
What makes pace maker cells a pace maker?
they can spontaneously depolarize
243
What is the main pace maker cell?
Sinoatrial node
244
What is the latent pacemaker?
Atrioventricular node bundle of his and purkinje fibers
245
How does the cardiac action potential differ from the neuron action potential?
the use of calcium influx during the efflux of potassium.
246
What is happening in phase three of the cardiac action potential?
the calcium channels have closed while the potassium ions are still in efflux leading to -90mv membrane.
247
The sarcoplasmic reticulum releases which ion causing troponin and tropomyosin to allow actin to slide on myosin?
Ca2++
248
What are the two basic cardiac pathophysiologies?
arrhythmias (electrical) and heart failure ( pump malfunction)
249
What are the three mechanisms of arrythmias?
1.) non pacemaker cells overtaking SA and AV nodes
2.) abnormal impulse conduction
3.) re-entry of conducting loop
250
What causes re-entry of conducting loop? Which arrhythmia does this cause?
tissue injury and tachycardia
251
which category is 100+ bbm at rest?
tachycardia
252
Which category is <60 bbm at rest?
bradycardia
253
What is ventricular fibrillation?
absence of organized electrical activity and mechanical pumping.
254
What are some condition associated with arrhythmias?
ischemia ( acute myocardial infarction due to lack of blood flow)
electrolyte abnormalities
255
How can we pharmacologically treat arrhythmias?
suppress ectopic pacemaker activity
increase conduction
increase refractory period
256
Which cardiac class are sodium channel blockers in?
Class 1
257
Name two class one sodium channel blocker medications for arrhythmias.
Quinidine and Lidocaine
258
How are Quinidine and Lidocaine administered?
orally (Quinidine) and for Lidocaine I.V. and I.M.
259
Which class one drug has more GI adverse effects and which one has more CNS adverse effects?
lidocaine for CNS and quinidine for GI effects
260
Which cardiac class is propanolol found in?
Class two beta blockers
261
What are the therapeutic uses of class two beta blockers?
to increase the refractory period and increase action potential. Decreases automaticity of AV node
262
What is the adverse effect of class two cardiac meds?
AV block in pt with ventricular failure.
263
Which class can Bretylium be found in?
Class three potassium channel blockers
264
What are the effects of the class three medications like Bretylium?
Increase refractory period and decrease automaticity.
265
When is it appropriate to give class three potassium blockers?
During emergencies when lidocaine fails.
266
Which category is Verapamil found in?
class four calcium channel blockers
267
How is verapamil usually used as?
an antihypertensive
268
What are some adverse effects of a class four medication like Verapamil?
full AV block
269
What are the major effects of verapamil on cardiac tissue?
prevents calcium re-entry on SA and AV nodes
270
Define Congestive Heart Failure.
Inability for the heart to pump enough blood to meet the demands of the body.
271
What can cause CHF?
HTN
CAD
Ischemic heart disease
272
What are some ways the body will try to compensate for CHF?
Augmented sympathetic activity
sodium and water retention
273
What are the primary signs of CHF?
Tachycardia
fatigue
cardiomegaly
274
When a pt has CFH what are the therapeutic goals to increase CO2 in the body?
Reduce preload
Reduce afterload
Increase contractility
275
What is the preload all about?
decreasing heart size and increasing contractility
276
What is the afterload all about?
reducing blood pressure
277
Which type of drugs reduce fluid retention? Name one of each.
diuretics and ACE inhibitors
Lasix and Captopril
278
Which type of drugs inhibit ACE? Name one.
ACE inhibitors
Captopril
lisinopril
279
Can Angiotensin receptor blockers also reduce fluid volume?
Yes
280
Name an Angiotensin Receptor Blocker aka ARB?
Losartan
telmisartan
281
Can we also use vasodilators, cardiac stimulants to treat CHF?
Yes
282
Some cardiac drugs act on the kidneys as a way to reduce the preload. What are these drug classes?
diuretics
ACE inhibitors
ARB's
283
Which kind of drugs can reduce preload and afterload?
ACE inhibitors and ARB's like losartan
284
Which adverse side effect causes pt to switch from ACEI to ARB?
Cough
285
What category is Digoxin found in?
cardiac stimulants
286
What are the major effects of cardiac stimulants?
increased force of contraction and decreased heart rate.
287
How can dopamine be used as a cardiac sympathomimetics?
stimulates the beta-1 receptor leading to vasodilation
288
Chronic SNS activation in heart failure can be harmful long term. Beta blockers can help with the cardiac load. Which SELECTIVE beta antagonist can help with this?
Metoprolol
289
Do beta blockers refer to Beta -1 or beta-2?
Beta -1
290
What are the two factors of blood pressure?
cardiac output and resistance
291
What are the two components of blood pressure regulation?
kidneys
sodium
292
is 120/80 considered elevated HR?
YES
293
What is considered htn lvl's?
140/90
294
Why is htn called the silent killer?
due to damage of the blood vessels
295
Are most HTN cases primary and uncurable?
yes
296
What are the treatment strategies for htn?
reduce resistance and cardiac output
297
Which drugs are commonly used for htn?
diuretics
calcium channel blockers
ACE inhibitors
beta blockers
298
Which diuretics are used for htn?
chlorothiazide and amiloride
299
Why is the amiloride coupled with thiazide?
to counteract the hypokalemia
300
Calcium channel blockers like Nifedipine and cardizem reduce resistance by doing what?
VASODILATION
301
Sodium nitroprusside can also vasodilate by....?
releasing nitric oxide to dilate the veins and arteries.
302
What is atherosclerosis?
a formation of clots in the blood vessels during htn causing an inflammatory response.
303
Why can atherosclerosis be deadly?
bc the tissue is not getting enough oxygen and blood flow.
304
What drugs are used for atherosclerosis?
anti-platelet
anti-coagulant
thrombolytic agent
lipid-lowering drugs
305
Name an antiplatelet?
Aspirin
306
what is the moa of aspirin?
irreversibly blocks COX-1
307
Is aspirin used as a secondary or primary prevention?
secondary
308
Name a anticoag.
Heparin
309
Heparin MOA?
Inhibits thrombin factor IXa and Xa which converts fibrinogen to fibrin
310
Is herarin only given via I.V.?
YES
311
How does tPA work as an anti-thrombolytic agent?
by activating the thrombolytic system to break down fibrin.
312
Name an oral vitamin K antagonist anticoag?
warfarin
313
How does warfarin affect vitamin K?
Blocks VKORC 1 so vitamin K is recycled by vitamin K reductase.
314
What are the major differences of Heparin and Warfarin?
warfarin has a delayed onset and longer duration.
315
Is warfarin often used as a bridge for heparin?
yes
316
What are the new oral anticoags called?
Pradaxa and eliquis
317
Why are the new oral anticoag going to replace warfarin?
fewer drug interactions and a rapid onset. Used for long term prevention of thrombus formation.
318
Which organ synthesizes cholesterol?
liver
319
Does a healthy person have a high level of HDL and low levels of LDL?
YES
320
Why are LDL's bad for the body?
They transport cholesterol from the liver into the tissues.
321
What is the range for high LDL cholesterol?
>160 mg/dl
322
What would be a normal cholesterol level?
<130 mg/dl
323
How can we treat hyperlipidemia pharmacologically?
-statins as a first line treatment
fluvastatin
lovastatin
324
Moa of -statins.
blocks the synthesis of cholesterol by inhibiting HMG-CoA reductase.
325
What is the a major adverse CNS effect from -statins?
forgetfulness and confusion across all age groups.
326
Drug interactions with -statins can increase the risk of what?
myopathy
327
What is the primary symptom of ischemic heart disease?
angina pertoris
328
Strangling of the chest and pain radiating down the left arm indicates what?
angina pectoris
329
What causes angina pectoris?
lack of oxygen going to the heart muscles to meet the demands of cardiac output.
330
Define stable angina?
angina that occurs with exertion and is usually relieved at rest. increase O2 demand with unchanged supply.
331
Define unstable angina?
episodes at rest, crescendo pattern decreased O2 supply with unchanged demand.
332
define Variant angina.
caused by spasms of the coronary arteries.
333
What is the main method of improving angina?
decreasing cardiac workload.
334
What is the outdated concept of improving angina?
dilate the coronary arteries
335
What is the modern concept of improving angina?
Decreasing the cardiac workload and O2 demand
336
Why would dilating unobstructed arterioles be a harmful thing during angina?
it would divert more blood away from the obstructed arterioles and worsen angina. steel effect.
337
What are the three main mechanisms of altering supply and demand ratio?
reduction of afterload
decreased in preload
block sympathetic influence on the heart
338
Which drugs are used to decreased SNS?
Beta blockers
339
Name the three major classes of antianginal agents?
calcium channel blockers
beta blockers
nitrite/nitrate
340
Which antianginal agent will dilate arterial smooth muscle an reduce blood pressure?
calcium channel blockers
341
Which antianginal agents will decrease heart rate and myocardial contractility?
beta blockers
342
Which antianginal agent will return the blood to the heart?
nitrites and nitrates
343
Name a nitrate.
nitroglycerin
344
During an acute angina episode, how is nitroglycerin administered?
sublingual tablet
345
Which two calcium channel blockers are more wellrounded?
verapamil and diltiazem
