MIDTERM Flashcards
(321 cards)
1
Q
magic charm for treating disease
remedy or drug
A
pharmacology
2
Q
a book containing an official list of medicinal drugs together with articles on their preparation and use
A
pharmacopeia (drug making)
3
Q
2 major subdivisions of pharmacology
A
pharmacokinetics and pharmacodynamics
4
Q
what the body does to the drug
A
pharmacokinetics
5
Q
what the drug does to the body
A
pharmacodynamics
6
Q
an adverse effect or complication caused by a physician (resulting from medical treatment or device)
A
iatrogenic effect
7
Q
a macromolecule whose biological function changes when a drug binds to it
A
receptor
8
Q
the measure of propensity of a drug to bind receptor; the force of attraction between drug and receptor
A
affinity
9
Q
dose or conc of a drug that produces 50% of maximal response
A
EC50
10
Q
some receptors have intrinsic activity even when no ligand is bound to them
A
inverse agonist
-when a ligand binds to them, their basal activity is reduced
11
Q
max effect produced by a drug; a measure of efficacy
A
Emax
12
Q
ability of a bound drug to change the receptor in a way that produces an effect
A
efficacy (intrinsic activity)
-some drugs posses affinity but no efficacy
13
Q
drugs that possess affinity and no efficacy
A
still have clinical use
14
Q
relative position of the dose-effect curve along the dose axis
A
potency of a drug
-need 2 drugs that act by the same mechanism to compare
15
Q
a drug which binds to the receptor and produces an effect
A
agonist
-has affinity and efficacy
16
Q
has affinity for a receptor, but less efficacy activity
A
partial agonist
17
Q
a drug which binds (competes for binding against other ligands), but does not activate the receptor
A
antagonist
-has affinity, but no intrinsic activity
18
Q
a higher dose of agonist is required to produce the same effect
A
competitive antagonism
-same Emax, but shifted right
19
Q
even a higher dose of agonist cannot produce maximal effect
A
non-competitive antagonism
-Emax will be lower
20
Q
info that can be derived from dose response curves
A
Emax EC50 agonist partial agonist competitive antagonism non-competitive antagonism
21
Q
the difference between the minimum effective concs for a desired response and an adverse response
A
therapeutic window
22
Q
quantal means
A
present or absent
-no degree of variation
23
Q
info derived from quantal dose response curves
A
therapeutic index
therapeutic window
sensitivity
24
Q
dose response curves shows graded response in a
A
single individual
25
quantal dose response curves show a specific response in a
group of individuals (population)
26
partial agonist produce
less than full effect when given alone
27
partial agonists act as ________ in the presence of a full agonist
antagonist
| -it blocks the full effect
28
has lower abuse potential
| less addictive than full agonists
partial agonists
29
provides some agonist activity and at the same time, blocks the full agonists
partial agonists
| ex) Pindolol for high BP and abnormal heart rhythms
30
the binding sites for the agonist and the antagonist are different on the recpetor
allosteric interaction
| -can produce inhibition or potentiation of the agonist response
31
example of allosteric interaction
receptor for benzodiazepines and GABA
32
4 signal transduction mechanisms
G-protein couples receptor systems
ion-channel receptors
enzymes as receptors
nuclear receptors
33
G-coupled receptor systems
- 2nd fastest
- uses energy obtained from GDP
- half of all drugs work through this system
- GPCRs, metabotropic receptors
34
ion channel receptors
- fastest
| - ionotropic receptors, GABA
35
enzymes as receptors
- 3rd fastest
- the interaction phosphorylates tyrosines in the intracellular region of the receptor, and the receptor becomes an active enzyme
- tyrosine kinase, serine/threonine kinase
36
nuclear receptors
- very slow, not common
- inside cytosol of the cell
- receptors for steroids, retinoids, and thyroid hormones
37
a drug that does not go through any of the 4 signal transduction mechanisms?
anti-acids
38
signal transduction
drug binds to receptor
39
____________ tend to desensitize receptors (down-regulate)
agonists
- frequent stimulation results in a decreased response
ex) decrease in receptor number or decrease in signal transduction
40
__________ tend to up-regulate receptors
antagonists
- causes a withdrawal rebound effect
- receptor number has increased, more receptors available to agonist
- gradually decrease dose when stopping
- ex) beta receptor antagonist
41
the pH at which half of the drug is ionized
pKa
42
the fraction of an orally given drug that reaches the circulation
bioavailability
43
the fluid volume that is required to contain the entire drug in the body at the same conc as measured in the plasma
volume of distribution
| =dose/Cp
44
the volume of blood from which a drug is irreversibly removed per unit of time
clearance
| -rate of administration = rate of elimination
45
the time required for the blood (or plasma) conc of a drug to be reached by 50%
half-life
46
a dose of a drug sufficient to produce a plasma conc of drug that would fall within the therapeutic window after only 1 or very few doses over a short interal
loading dose
| =Cp * Vd/F
47
the dose needed to maintain the conc within the therapeutic window when given repeatedly at a constant interval
maintenance dose
| =Cl * Css
48
affects all process of ADME
lipid solubility
49
high absorption factors
nonionized
small
lipid soluble
nonpolar
50
factors affectting distribution
ionization
capillary permeability
blood flow
PLASMA PROTEIN BINDING
51
in acidic medium, like the stomach
weak acid will be
weak base will be
acid will be unionized, better absorbed
| base will be ionized, less absorbed
52
ion trapping at steady state
acidic drug would accumulate on the more basic side, and
| a basic drug on the more acidic side
53
clinical significance of ion trapping
- breast milk
- to increase excretion of acidic drugs (ASA), give IV sodium bicarbonate
- to increase excretion of basic drugs, give ammonium chloride or ascorbic acid
54
if most the drug is extravascular, a change in free plasma drug conc caused by displacement from plasma protein binding would be
minimal
55
if most the drug is intravascular, a change in free plasma drug conc caused by displacement from plasma protein binding would be
very significant on the effect
| ex) warfarin
56
liver and spleen have
leaky capillaries
57
brain capillaries have
tight junctions
58
high capillary permeability in
liver
59
low capillary permeability in
the brain
| -exception is CTZ
60
only ________ drugs diffuse across brain capillaries
lipophilic
61
tight junctions between
endothelial cells in brain capillaries
62
to tx parkinson's, in regards to BBB
it is better to give dopa than dopamine
63
high Vd
highly lipid soluble
| -most of the drug is in the extravascular compartment
64
low Vd
not very lipid soluble OR highly plasma protein bound
- most of the drug is in the vascular compartement
ex) warfarin
65
phase 1 rxns of drug metabolism
functionalization: makes the drug more polar, but not necessarily inactive
- oxidation
- reduction
- hydrolytic rxns
66
phase 2 rxns in drug metabolism
conjugation: mostly result in drug inactivation
- glucoronidation
- sulfation
- acetylation
67
cap permeability determines
distribution
68
P450 monooxygenase family wich transfer electrons from
NADPH to an oxygen molecules and thus oxidize drugs
69
P450 enzyme characteristics
- not substrate specific
- located in ER
- require NADPH and oxygen
- mostly inactive drugs
- many subfamilies -CYP3 is most common
70
the primary enzyme for metabolism
CYP3A4
71
increase elimination of drugs
inducers
72
decrease elimination of drugs
inhibitors
73
most common polymorphism in caucasians is
CYP2D6
| -codeine must be metabolized by this enzyme to morphine to work
74
example of a prodrug
codeine
75
p-glycoprotein is an
efflux pump: removes drug from cell
- broad substrate specificity
- cancer tissue (resistance)
- high expression by st johns wort
- in the BBB, protects the CNS
- CCB inhibit the pump and reverse resistance
76
enterohepatic recirculation effect
a compound is conjugated in the liver, excreted in the bile, deconjugated in the intestine, and is reabsorbed into circulation
- this prolongs the duration of action (half-life)
ex) bilirubin
77
95% of bile salts are reabsorbed and used in
cholesterol synthesis
78
antibiotics and CYP enzymes
antibiotics induce CYP enzymes that metabolize the contraceptive hormones and thus reduce their effectiveness
-they kill the bacteria that reabsorbs the estrogen
79
Cl =
maintenance dose (steady state)
80
creatinine Cl is used to estimate
GFR
| -kidney function is assessed by GFR
81
when GFR is low, excretion is
low
82
creatinine clearance =
urine conc* (urine flow rate/plasma conc)
83
net removal of a drug by the kidney =
filtered + secreted - reabsorbed
84
filtration
passive
| -only free drug
85
secretion
active
| -mainly in the proximal tubule
86
reabsorbed
passive and active
| -happens unless the drug is very polar
87
1st order rate of elimination
a constant fraction of drug is eliminated per unit of time
| -metabolizing enzyme is not saturated
88
zero order rate of elimination
a constant amount of drug is eliminated per unit of time
- depends on metabolism
- the metabolic mechanism for most drugs will be saturated only at high concs
89
it takes about ________ half-lives for more than 90% of a drug to be effectively eliminated
5
90
any chemical agent that affects living processes
drug
91
3 different types of drug interactions
drug-drug
drug-food
drug-herb
92
drug-drug interaction example
NSAIDs and warfarin
93
drug-food example
grapefruit juice
94
2 drugs affecting the same system
pharmacodynamic interaction
| ex) 2 sedative drugs producing more sedation
95
one drug changing the ADME of another
pharmacokinetic interaction
| ex) Ca supplements reduce absorption of thyroxine metabolism
96
one drug affecting the ___________ of another drug is the most common form of drug-drug interactions
metabolism
97
almost always involved in drug-drug interactions
CYPs
| -CYP3A4
98
4 mechanisms involved in DDIs between NSAIDs and warfarin
1. protein bound warfarin is displaced by warfarin (pharmacokinetics)
2. NSAIDs suppress platelet formation, which adds to anticoagulation effect (pharmacodynamics)
3. NSAIDs prevent metabolism of warfarin by competition for metabolizing enzyme (pharmacokinetics)
4. NSAIDs cause gastric injury and warfarin can cause gastric bleeding (pharmacodynamics)
99
mechanisms of other drugs interacting with warfarin
- altered platelet formation
- GI injury
- vit K synthesis altered
- warfarin metabolism altered
100
during which trimester of pregnancy causes the most damage from drug use
first
101
factors that affect drug transfer across the placenta
```
MW
pKa
protein binding
degree of ionization
placental drug transporters
```
102
where is p-glycoprotein located
on the apical membrane
103
role of p-glycoprotein in placental drug transport
placental expression of drug transporters, like p-glycoprotein, protects the fetus by efflux of drug from the fetal to maternal circulation
104
risk levels of drugs for use during pregnancy
```
A = safe
B = likely safe
C = uncertain
D = likely unsafe
X = unsafe
```
105
parasympathetic nerves originate from the
adrenal medulla and sacral spinal cord
| -craniosacral outflow
106
sympathetic nerves originate from the
thoracic and lumbar spinal cord
| -thoracolumbar outflow
107
what is released at preganglionic parasymp nerves at their ganglia
Ach
108
what is released at preganglionic symp nerves at their ganglia and at their synapses in adrenal medulla
Ach
109
what is released from postganglionic parasymp nerves at their organs/tissue receptors
Ach
110
what is released from somatic motor nerves at the neuromuscular junction in the skeletal muscle
Ach
111
what is released from postganglionic symp nerves at their organ/tissue
NE
112
postganglionic symp fibers innervat all sweat glands, except
in the palms and skeletal blood vessels
| -release Ach
113
adrenal medulla releases 80% ______ into circulation when stimulated by pregang symp nerves
epi (adrenaline)
114
adrenal medulla releases 20% ______ into circulation when stimulated by pregang symp nerves
NE
115
phaeochromocytoma
a tumor of the adrenal medulla that releases large amounts of epi and NE into circulation
-the BP and HR are increased
116
2 clinical conditions where alpha blockers are used
hypertension and BPH
117
urinary bladder: dominant tone
parasympathetic
118
urinary bladder: parasymp agonists
muscarinic agonists will contract the detruser muscle and relax the sphincter to empty the bladder
ex) methacholine, cholinesterase inhibitors
119
urinary bladder: symp agonists
alpha1 agonists will contract the sphincter to prevent bladder emptying
120
urinary bladder: clinical relevance
urinary incontinence - want to reduce activity so give muscarinic blocker
urinary retention - use muscarinic agonist
121
tracheal & bronchial smooth muscle: parasymp
muscarinic agonists will contract the bronchial smooth mucles and increase bronchial secretions
122
tracheal & bronchial smooth muscle: symp
beta2 agonists will relax the bronchial muscle
| ex) albuterol or epi
123
tracheal & bronchial smooth muscle: clinical relevance
asthma, COPD
124
tracheal & bronchial smooth muscle: notes
non-selective beta blockers to tx hypertension, will contract bronchial muscle
-not used in asthma pts
125
GI tract smooth muscle: dominant tone
parasymp
126
GI tract smooth muscle: parasymp
muscarinic agonists will contract the GI muscle (stimulate peristalsis), relax sphincters, and increase secretions
127
GI tract smooth muscle: symp
beta and alpha agonists will relax the GI muscle (inhibit peristalsis), and inhibit secretions
128
GI tract smooth muscle: clinical significance
diarrhea and IBS - give muscarinic blocker
| gastric atony and paralytic ileus - give muscarinic agonist
129
salivary & parotid glands: dominant tone
parasymp
130
salivary & parotid glands: parasymp
muscarinic agonists will stimulate salivary gland secretions
131
salivary & parotid glands: symp
alpha1 agonists will stimulate salivary secreation
132
salivary & parotid glands: clinical relevance
muscarinic blockers are used for intubation
133
liver: dominant tone
symp
134
liver: symp
beta2 agonist will cause glycogenolysis and gluconeogenesis
| -increase plasma glucose
135
liver; clinical relevance
type 1 DM
| -do not give a DM pt a non-selective beta-blocker
136
uterus: dominant tone
symp
137
uterus: symp
beta2 agonist will cause relaxation of uterine smooth muscle
138
uterus: clinical relevance
prevent premature labor
139
eyes: dominant tone
parasymp
140
eyes: parasymp
muscarinic agonists will cause contraction of circular fibers of the iris and miosis (narrowing of the pupil)
M3, M2
141
eyes: symp
alpha1 agonists will cause mydriasis (dilation of pupil)
142
eyes: clinical relevance
glaucoma
| -muscarinic blockers will cause mydriasis (dilation)
143
glaucoma definition
increase in intraocular pressure
- increased of aqueous humor
- decreased outflow (drainage) of aqueous humor
144
skeletal muscle: dominant
motor neurons
145
skeletal muscle: stimulation of motor neurons
nicotinic agonists will stimulate contraction of the muscle
146
skeletal muscle: 2 types of neuromuscular blockers
competitive - tubocurarinel
| depolarizing - succinylcholine
147
succinylcholine causes
persistant stimulation and depolarization, so the muscle cannot recover and becomes paralyzed
148
brain: receptors
cholinergic & adrenergic
149
brain: stimulation of muscarinic receptors
plays a role in memory and control of muscle contraction
150
brain: tx Alzhiemer's
indirect cholinergic agonists (ChE inhibitors)
151
brain: tx Parkinson's
muscarinic antagonists (Ach blocker/antagonists)
152
parasymp effects can be mimicked by
muscarinic receptor agonists
| acteylcholinesterase inhibitors
153
parasymp effects can be blocked by
muscarinic receptor antagonists
| skeletal neuromuscular junction blockers
154
4 therapeutic uses of parasympathomimetics
1. reduce intraocular pressure in glaucoma
2. increase the motility (peristalsis) of the GI tract
3. increase the motility of urinary tract
4. increase salivary secretions
155
2 types of cholinesterase
AchE and BuChE
156
BuChE metabolizes
succinylcholine
157
compounds that bind to cholinesterase can produce one of 3 types of chemical rxns
1. acetylation - recovers rapidly
2. carbamylation - recovers more slowly
3. phosphorylation - poisons the enzyme
158
botylinum toxin
- used to paralyze skeletal muscle in cases of excessive involuntary skeletal muscle
- blocks Ach release
159
belladonna alkaloids
atropine and scopolamine
160
semisynthetic and synthetic
oxybutynin and glycopyrrolate
161
scopolamine
great fraction present in an unionized form at physiological pH
-duration of 3 days
162
glycopyrrolate
given preoperatively to inhibit excessive salivary secretions
163
pirenzepine
selective for M1 receptors
| -used to reduce gastric acid secretions in pts with peptic ulcers
164
parkinson's tx
muscarinic receptor antagonists
| ex) trihexyphenidyl and benztropine
165
muscarinic receptor antagonist side effects
- urinary retention
- constipation
- mydriasis
- blurred vision
- tachycardia
- inhibition of sweating
166
neuromuscular junction blockers: competitive
curare
| -no intrinsic activity
167
partially imparied when __________ receptors are occupied
75-80%
168
inhibited totally when __________ receptors are occupied
90-95%
169
competitive neuromuscular blockers side effects
- ganglionic blockade (low BP, high HR)
- block of vagal responses
- histamine release (bronchospasm)
170
depolarizing neuromuscular blocker side effects
- hyperkalemia
| - malignant hyperthermia
171
therapeutic uses of neuromuscular blockers
in surgical anesthesia to obtain relaxation of skeletal muscle
172
sympathetic effects can be mimicked byb
- adrenergic receptor agonists
- NE uptake blockers
- monoamine oxidase and COMT inhibitors
- NE releasing agents
173
monoamine oxidase and COMT inhibitors cause an ________ in N E conc
increase
174
sympathetic effects can be blocked by
-adrenergic receptor antagonists
175
NE can activate
alpha and beta1 receptors
| -very little effect on beta2
176
when treating asthma, epi vs NE
very little bronchodilation when NE is used
| -use epi when treating asthma
177
epi: alpha1 and beta2
alpha1 is vasoconstrictor
| beta2 is vasodilator
178
clinical uses of agrenergic drugs
- allergic rnxs (epi)
- bronchodilators (albuterol)
- as pressor agents - hypotension (epi or NE)
179
clinical uses of adrenergic receptors blockers
-hypertension
-glaucoma
-MI
-HAs
(metoprolol, propranolol)
180
main difference between beta blocker and choinesterase inhibitor?
- cholinesterase increases drainage (outflow)
| - beta blocker reduces production
181
autocoids
local hormones
| -have a brief lifetime and act near their site
182
autocrine
histamine, prostaglandins, serotonin, leukotrienes
183
paracrine
NO, ET-1
184
endocrine
hormones
| -insulin, thyroxine, estradiol
185
where is histamine stored in the body
mast cells and basophils
186
mast cells
gut and lungs
187
histamine works on two receptors
in neurons (CNS) and in peripheral nerves (H1)(minor allergies)
188
directly released by certain drugs that displace histamine in mast cells
morphine and d-curarine
189
agents that inhibit the release of histamine from mast cells are
cromolyn
theophylline/aminophylline
beta agonists
190
3 types of histamine receptors
H1, H2, H3
191
H1 receptors
contribute to rhinitis, urticaria
| -contribute to minor allergic rxns - hay fever
192
H2 receptors
gastric acid secretions
| -activation causes increase gastric acid secretion
193
H3 receptors
central neurotransmitter role
| -G-protein coupled
194
histamine will contribute to bronchial _____
constriction
195
4 types of antihistaminics
1. dimenhydrinate (gravol) sedative and has anticholinergic fx
2. diphenhydramine (benadryl) same
3. cyclizine (motion sickness) same
4. loratadine (claritin) nonsedative and no anticholinergic fx
196
main use of antihistaminics
to tx allergy rxn sx
| -hay fever, urticaria, rhinitis, cold and drug rxns
197
2nd generation agents
loratadine
- do not cross BBB
- no sedation
- more potent
- less side fx
- no anticholinergic fx
198
H2 blockers are given to reduce
gastric acid secretion
| ex) ranitidine
199
NSAIDs inhibit ______
COX enzyme
200
serotonin distribution
GIT, platelets, brain
201
distribution of serotonin in GIT
enterochromaffin cells
- carcinoid syndrome
- 90% of 5-HT is found here
202
distribution of serotonin in platelets
5-HT found here contribute to platelet aggregation
| 5-HT released from platelets contribute to vasoconstriction and increase BP
203
distribution of serotonin in brain
5-HT is one of the major neutrotransmitters in the brain
| -regulates sleep, temp, depression, and anxiety
204
serotonin agonists
buspirone (5-HT1a) - tx anxiety, depression
| sumatriptan (5-HT1b/1d) - tx HAs and migraines
205
serotonin antagonists
cyrproheptadine (blocks histamine, H1, and serotonin, 5-HT) - tx carcinoid syndrome, urticaria, pruritus
ondansetron (5-HT3) - tx nausea and vomiting (anti-emetic)
ketanserin (5-HT2) - antihypertensive
206
arachidonic acid
```
also called eicosanoids
-class of autocoids is derived from cell membrane phospholipids
```
207
eicosanoids types
- prostaglandins (PGs): uterine/gastric motility
- prostacyclin (PGI2): vasodilator, platelet disaggregation
- thromboxane (TXA2): vasoconstrictor, platelet aggregation
- leukotrienes (LTs): bronchoconstrictor
208
PGF2alpha
increase uterine contraction labor
| -potent abortificant
209
leukotrienes
produced from arachodonic acid and potent mediators of inflammation and allergy
210
montelukast blocks
CysLT1 receptors
211
Zileuton blocks
5-LO
| -decreases LT production
212
potent bronchodilators
LTC4, LTD4, LTE4 (CysLTs)
213
LT antagonists, CysLT1 antagonists manage
(montelukast and zafirlukast)
| manage bronchial asthma by decreasing CysLT mediated inflammation and mucus secretion
214
Zileuton inhibits the synthesis of
leukotrienes by inhibiting 5-LO
| -decreasing the production of inflammatory mediator leukotrienes
215
CysLT1 blocker (montelukast) blocks
leukotriene receptors
216
montelukast and zileuton both promote
bronchodilation and are helpful in ASA-induced asthma
217
st johns wort tx
depression
218
saw palmetto tx
BPH
| -benign prostatic hypertrophy
219
ginkgo biloba tx
alzheimer's disease and dementia
220
3 herbals that are comparable in efficacy to respective allopathic meds
st johns wort
saw palmetto
ginkgo biloba
221
kava kava root tx
anti-anxiety agent
222
black cohosh tx
postmenopausal sx
223
cinnamon bark (cinnulin) tx
type 2 DM
224
vanadium & chromium tx
type 2 DM
225
echinacea tx
cold and flu sx
226
ephedrine tx
asthma, weight loss, nasal congestion
227
st johns wort root extract comparable to
tricyclic antidepressant 75mg
228
highest herbal sales in germany and france
ginkgo biloba
229
ginkgo biloba comes from
1000 yr old trees, 10m circumference
230
extract from ginkgo
Egb761
| -shows improvement on ADAS-Cog scale
231
JAMA article
- shows ginkgo is effective in tx of both alzheimer's disease and vascular dementia
- fewer side fx than placebo
- 2 outcome measures ADAS (cog) and GERRI (social) showed improvement
232
saw paletto is comparable to
finasteride
233
saw palmetto: 5-a-reductase converts
testosterone to active androgen, dihydrotestosterone
234
finasteride is 5-a-reductase ___________
inhibitor
235
both saw palmetto and finasteride _____ IPSS
decrease
| -urgency, frequency, sensation of incomplete voiding
236
kava kava is comparable with
benzodiazepines
237
6 classes of drugs for asthma and COPD
1. beta2-selective adrenergic agonists
2. adenosine antagonist and PDE inhibitor
3. muscarinic antagonist
4. mast cells stabilizers
5. corticosteriod
6. leukotriene synthesis and LT antagonist
238
examples of beta2-selective adrenergic agonists
albuterol (salbutamol)
| salmaterol (LABA)
239
examples adenosine antagonist + PDE inhibitor
theophylline
240
examples of muscarinic antagonist
ipratropium and tiotropium
241
examples of mast cell stabilizers
cromolyn, nedocromil, omalizumab
242
examples of corticosteriods
beclomethasone, fluticasone, dexamethosone
243
examples of leukotrienes synthesis inhibitors and LT antagonsits
zileuton and montelukast
244
beta2 agonists _______ bronchioles
dilate
245
division of anti-asthmatic drugs
bronchodilators
| decrease inflammation and reduce bronchial hyperresponsiveness
246
bronchodilators
- beta selective agonists
- phosphodiesterase inhibitor + and Adenosine antagonist
- muscarinic antagonist
247
reduce inflammation and reduce bronchial hyperresponsiveness
- mast cell stabilizer
- leukotrienes
- corticosteriods
248
phosphdiesterase inhibitor - theophylline side fx
seizures and cardiac arrhythmias
249
antimuscarinic agents
inhaled increases their selectivity at localized site (bronchioles)
-minimal side fx
250
mast cell stabilizer: cromolyn
- given as prophylactic prior to onset
- not given orally
- inhibits the secretion of mediators from mast cells
- inhibits the release of inflammatory mediatorrs from mast cells in response to noxious stimuli
251
corticosteroids
- slow mechanism of action
- acts by blocking inflammatory mediators
- long term use is bad
252
management of COPD- stages
1. comb of inhalation agents: iprapropium+LABA+occasional use of ICS
2. beclamethasone+ iprapropium+combo of all diff bronchodilators
3. oral corticosteriod+iprapropium, consider giving vaccine
4. all drugs and tx stated in 3 + oxygen tent/ventilation
253
etanercept
new drugs for refractory asthma
- tumor necrosis factor alpha receptor antibody neutralizers inflammation
- it sits on TNF-alpha receptor so that TNF cannot sit on the receptor and act
254
anti-tussives: cough suppressants
dextromethorphan>codeine>noscapine>benzonatate>guaifenesin
255
proximal convoluted tubule
carbonic anhydrous inhibitors
| 40% Na reabsorbed (bicarbonate)
256
thin descending limb
osmotic diuretic
257
thick ascending limn
35% Na reabsorbed
| loop diuretics
258
distal convoluted tubule
10% Na reabsorbed
| thiazides
259
cortical collecting tubules
2-5% Na reabsorbed
| K+ sparing diuretics
260
examples of carbonic anhydrase inhibitors
acetazolamide
261
examples of osmotic diuretic
mannitol
262
examples of loop diuretics
furosemide, ethacrynic acid
263
examples of K+ sparing diuretics
spironolactone, triamterene
264
hydrochlorothiazide AEs
```
hypokalemia
alkalosis
hypercalcemia
hyperuricemia
imparied glucose tolerance
```
265
K+ sparing diuretics AEs
hyperkalemia
acidosis
gynecomastia
266
how tolerance develops to diuretics
excretion of Na leads to COMPENSATORY intake of Na
| -macula densa cells sense reduction in total body Na and stimulate renin release, which increases aldosterone
267
how to deal with tolerance to diuretics
furosemide, increase its dose
| and lower intake of Na and water
268
combos: thiazides/loop diuretics/K+ sparing
HCTZ+spironolactone
HCTZ+triamterene
HCTZ+amiloride
furosemide+spironolactone
269
combos: thiazides+ACEi or beta1 blockers
| - for hypertension
HCTZ+enalapril -ACE
| HCTZ+atenolol -beta1 blocker
270
carbonic anhydrase inhibitor uses
glaucoma, petitmal seizures
- acute motion sickness
- edema w/ severe metabolic alkalosis
271
therapeutic uses of mannitol
cerebral edema - decreases ICP
| in actute renal failure- maintain high urine flow
272
loop diuretic AEs
```
hypokalemia
hyponatremia
hypovolemia
alkalosis
hypotension
hyperuricemia
```
273
loop diuretics actions
block Na-K-Cl transport
274
alkalosis vs acidosis diuretics
CAIs and K+ sparing = acidosis
| Loop and thiazide =alkalosis
275
dont use beta2 agonists in
hypovolemia and hyponatremia
276
5 things that result from NE release from symp nerve endings
1. vasoconstriction of resistance type arterioles - direct effect
2. reabsorption of tissue fluid as a result of a decrease in cap pressure
3. increase in venoconstriction - cap vessels
4. release of renin and increase in renin-ang2-ald activity
5. increase in HR and increase in cardiac contractility
277
major effects following RAAS blockade
```
-ACE inhibitors decrease ang2 level and cause a fall in BP
decrease output of symp nervous systm
increase vasodilation
decrease in retention of Na and water
increase levels of bradykinin
```
278
vasopressin system restores
plasma volume
| -reabsorption of water from collecting ducts
279
bosentan is a
nonselective ET antagonist
280
ambrisentan is a
selective ETa antagonist
281
vascular ETa and ETb contributes to
vasoconstriction
282
release of NO
decreases Ca and promotes vasodilation
283
3 local (intrinsic) control systems: autocoids
histamines, serotonin, PGs
284
nitrates examples
nitroglycerin
isosorbide
dinitrate
285
beta-adrenergic blocker examples
metoprolol
| atenolol
286
CCBs examples
diltiziam
verapamil
amlodipine
nifedipine
287
2 goals of therapy for coronary ischemia
1. reduce oxygen demand and decrease workload on heart: give nitrates, beta-blockers, and CCBs
2. increase oxygen supply to the heart: give nitrates and CCBs (coronary vasodilation)
288
nitrates action
- increase cGMP levels
- vasodilator
- rapid onset
- best for acute angine
- tolerance develops
289
beta-blockers action
-decrease the oxygen demand to the heart
-decrease HR
-decrease contractility
-long term management of stable angine
USE WITH CAUTION IN UNSTABLE/VASOSPASTIC ANGINA
290
CCBs action
- inhibit Ca influx
- vasodilation
- decrease load on heart
- effective in both typical and atypical angine
291
sodium nitroprusside given for
hypertensive crisis
| -cyanide release from plasma NOT GOOD
292
rapid relief of acute angina by nitrates is due to
increase venodilation causes decreases venous return to the heart
decrease preload, decrease workload on the heart, resulting in decrease oxygen consumption
293
best example of drug causing tolerance
nitrates
| -need to give "drug holidays"
294
beta-adrenergic antagonists AEs
```
lots!
-bronchospasms
-decrease in max exercise tolerance
-asthma
-erectile dysfunction
decrease HR, decrease CO, decrease RAS
```
295
CCBs action
decrease HR, decrease afterload
| -higher affinity for smooth muscle than cardiac muscle
296
CCBs AEs
in smooth muscle
- constipation
- urinary retention
- HA
297
Dihydropyridines
amlodipine and nifedipine
| -used as antihypertensive agents
298
diltiazem use
angina
299
verapamil use
decrease AV conduction, decrease contractility
| -tx arrhythmias
300
features of CCBs and AEs
decreases workload, causes vasodilation
| -AEs = cardiac depression, ankle edema, constipation
301
preferred tx for both types of angina
diltiazem and verapamil
302
tx more effective as antihypertensive
amlodipine
| -cause a reflex increase in HR
303
pentoxifylline
PDE inhibitor, TNFalpha inhibitor, adenosine antagonist
- promotes red cell deformability
- helpful in vascular dementia
304
diuretics AEs
```
hypokalemia
hypovolemia
hyperuricemia
hypercalcemia
hyperglycemia
```
305
beta-blockers contraindications
lipid hostile and precipitates hypoglycemia
| COPD and asthma
306
CCBs AEs
constipation
HAs
flushing
307
direct renin inhibitor (DRIs)
shuts off ang1 and ang2
308
diff between DRI, ACE, ARB
ACE: increased renin, increased ang1, decreased ang2, decreased aldo, increased BK
ARB: increased renin, increased ang1, increased ang2, decreased aldo
DRI: decreased everything
309
Group A: ACE/ARB, beta-blocker, DRI
| Group B: CCB, diuretic
choose 1 from each group and combine for hypertension management
310
carvedilol/labetolol, non-selective alpha/beta blocker used for
CHF
311
phentolamine/phenoxybenzamine for
pheochromocytoma
312
8 classes of drugs for CHF
1. ACE inhibitors
2. beta1-blockers
3. ang2 blocker (ARB)
4. alpha/beta adrenergic blocker
5. tailored diuretics (lower edema)
6. digoxin
7. vasodilators
8. dobutamine
313
CHF: ACE inhibitors examples
enalapril
| lisinopril
314
CHF: beta1-blocker examples
atenolol
| metoprolol
315
CHF: ang2 blocker (ARB) example
losartan
316
CHF: alpha/beta adrenergic blocker example
carvedilol
| -has antioxidant properties
317
CHF: digoxin use
inhibits Na pump
| -narrow therapeutic window
318
CHF: vasodilators examples
hydralazine
| nitrates
319
CHF: dobutamine use
last ditch
320
goals of CHF drugs
| -overall decreasing CO
decreasing afterload - decreasing arteriolar resistance
decreasing preload - decreasing load coming to the heart
increasing cardiac contractility
321
CO =
HR*SV
| increased preload = increased SV
