Pharmacology Test 2 Flashcards
1
Q
the nervous system can be divided into what two minor systems?
A
CNS and PNS
2
Q
two subsystems of the PNS
A
1). Autonomic Nervous System 2). Somatic Nervous System
3
Q
two subsystems of the Somatic Nervous System
A
Sensory (afferent), Motor (efferent)
4
Q
two divisions of the Autonomic Nervous System
A
Sympathetic and Parasympathetic
5
Q
what type of receptors does the sympathetic nervous system utilize?
A
Adrenergic
6
Q
what type of receptors does the parasympathetic nervous system utilize?
A
cholinergic receptors
7
Q
what are the types of adrenergic receptors?
A
alpha-1, alpha-2, beta-1, and beta-2
8
Q
what are the types of cholinergic receptors?
A
muscrainic (1, 2, and 3) and nicotinic (neural and muscular)
9
Q
cholinergic drugs mimic _______
A
the PNS
10
Q
anticholinergic drugs suppress ______
A
the PNS
11
Q
adrenergic drugs mimic ______
A
the SNS
12
Q
alpha and beta-blockers supress _____
A
the SNS
13
Q
T/F: within the ANS, two neurons link the CNS to the effector organ
A
True
14
Q
Pre/postganglionic fiber length comparision between SNS and PNS
A
PNS: long mylinated pre and short post
SNS: short mylinated pre and long post
15
Q
T/F: the synapse between the preganglionic and postganglionic fiber within the ANS is always nicotinic?
A
True
16
Q
the sympathetic division can be found exiting which region of the spinal cord?
A
thoracolumbar (T1-L2)
17
Q
the parasympathetic division can be found exiting which regions of the spinal cord?
A
carniosacral (CN 3, 7, 9 and 10; S2-4)
18
Q
what is the only exception to the 2 neuron rule within the ANS?
A
adrenal gland within the sympathetic division
19
Q
which division of the ANS will have more extensive branching?
A
sympathetic
20
Q
which division of the ANS tends to create/cause more discrete reactions affecting only 1 organ/tissue?
A
parasympathetic
21
Q
effect of SNS on heart?
A
increased HR (beta-1 and beta2),
increased contractility (beta-1 and beta-2)
22
Q
effect of PNS on heart
A
decreased HR (M2)
23
Q
SNS effect on lung airway muscles
A
bronchodilation (beta-2)
24
Q
effect of SNS on lung bronchial secretions
A
increased secretion (beta-2)
decreased secretion (beta-1)
25
effect of PNS on lung airway smooth muscles
bronchoconstriction (M3)
26
effect of PNS on lung bronchial secretions
increased secretion (M3)
27
effect of SNS on arterioles
vasoconstriction of skin and visera (alpha-1, alpha-2)
vasodilation of skeletal muscle and liver (beta-2)
28
effect of SNS on liver
glycogenolysis, gluconeogensis (alpha and beta-2)
29
effect of PNS on liver
glycogen synthesis (M)
30
catecholamine neurotransmitters
dopamine, epinephrine, norepinephrine
31
if activated an excitatory ligand-gated ion channel would cause \_\_\_\_\_\_
Na+ or Ca2+ to flow into cell;
K- to flow out
32
if activated an inhibitory ligand-gated ion channel would cause \_\_\_\_\_\_
Cl- to flow into cell
33
Additional neurotransmitters
Glutamate, GABA, Dopamine, Serotonin, and Histamine
34
cholinergic muscarnic receptor primary locations
1) . visceral and bronchiole smooth muscle,
2) . Cardiac muscle,
3) . Exocrine glands, salivary,intestinal, lacrimal,
4) . sweat glands
35
cholinergic muscurinic response to stimulation
1) . viseral/bronchiole smooth muscle - contraction
2) . cardiac - decreased HR
3) . glands - increased secretions
36
alpha-1 receptor locations
1) . vascular smooth muscle
2) . intestinal smooth muscle
3) . radial muscle iris
4) . Urinary sphincter
5) . Spleen capsule
37
stimulation of alpha-1 receptors results in ______ everywhere except \_\_\_\_\_\_
contraction;
intestinal smooth muscle (relaxation)
38
location of alpha-2 receptors
CNS inhibitory neurons
39
response of alpha-2 receptors
decreased sympathetic discharge from CNS
40
location of beta-1 receptors?
cardiac muscle, kidneys, and fat cells
41
respones of beta-1 receptors
1) . cardiac muscle - increased HR and contractility
2) . kidney - increased renin secretion
3) . fat cells - increased lipolysis
42
location of beta-2 receptors
bronchiole smooth muscles, liver and skeletal muscle arterioles and cell, GI smooth muscle, uterus, gallbladder
43
response of beta-2 receptors in gallbladder and uterus
relaxation
44
response of beta-2 receptors in skeletal muscle and liver
arterioles - vasodilation
cells - increased metabolism and mass
45
other responses of beta-2 receptors
bronchiole smooth muscle - bronchodilation
GI smooth muscle - decreased motility
46
broad function of anticholinergic drugs?
suppress PNS
47
Key AE of anticholinergic drugs
ABCDs
48
what does ABCDs stand for?
agitation, blurred vision, constipation/confusion, dry mouth, stasis or urine and sweat
49
when should an anticholinergic drug be avoided?
1). history of urinary retention, 2). narrow angle closure glaucoma
50
what are some indications for anticholinergic drugs?
COPD, asthma, Parkinson's, OAB, motion sickness, decreasing saliva/secretions pre-surgery, treating poisoning, opthalmic exams
51
Atropine indications
1). decrease saliva/secretions pre-surgery, 2). treat poisoning
52
MOA of anticholinergic drugs that treat OAB
antagonize muscarinic receptors on bladder smooth muscle =\> decrease contractions
53
general MOA of 1st gen antihistamines
bind histamine receptors in periphery and CNS = more sedation
54
general MOA of 2nd gen antihistamines
less muscarinic receptor binding = less anticholinergic effects
55
general MOA of antidepressants
primarily increases serotonin and NE; H1 antagonists (sedating) and muscarinic antagonists
56
anticholinergic drug that is an antidepressant
TCA (tricyclic antidepressants)
57
What is the Beers List?
list of potentially inappropriate meds on older adults
58
drugs on Beers list may worsen what symptoms?
delirium, CNS-effect (confusion), urinary retention
59
two general types of Cholinergic Drugs?
Direct Acting, Indirect Acting
60
Direct Acting cholinergic drugs do what?
act directly on muscarinic receptors
61
Indirect Acting cholinergic drugs do what?
inhibit Acetylcholinesterase (AChE)
62
indications for Cholinergic Drugs
glaucoma, GI disorders (paralytic ileus), urinary retention, Alzheimer's, diagnosis of myasthenia gravis
63
what is Alzheimer's Disease associated with?
decreased levels of Ach
64
general MOA of Alzheimer's drugs
reversibly bind AChE so it does not break down ACh (indirect acting)
65
AE of Alzheimer's drugs
varies but mostly GI (N/V/D)
66
Cholinergic drugs will do what?
enhance the PNS (increase secretions)
67
Cholingeric AE
SLUDGE or DUMBELLS
68
what does SLUDGE stand for?
Sweating, Lacrimation, Urination, Diarrhea, GI cramping, Emesis (vomiting)
69
What does DUMBELLS stand for?
Diarrhea, Urination, Miosis, Bradycardia, Emesis, Lacrimation, Lethargy, Salivation/Sweating
70
who should avoid Cholinergic drugs?
ppl w/history of COPD or asthma, urinary tract obstruction, Parkinson's, Peptic ulcer disease (PUD)
71
Therapeutic Concerns for Direct/Indirect acting muscarinic agents?
CV effects (bradycardia, decreased CO, syncope, hypotension), GI issues, bronchoconstriction, frequent urination, increased secretions
72
Atropine AE
low doses: dry mouth, high doses: blurred vision, hallucinations, confusion, coma
73
other Atropine AE
tachycardia, decreased bronchial secretions, constipation, urinary retention
74
where are alpha-1 receptors?
vascular smooth muscle
75
where are alpha-2 receptors?
presynaptic junction
76
where are beta-1 receptors?
heart, kidneys
77
where are beta-2 receptors?
Lungs, skeletal muscle blood vessels
78
where are beta-3 receptors
adipose tissue
79
stimulation of alpha-1 receptors results in what response?
vasoconstriction/vasodilation
80
stimulation of alpha-2 receptors results in what responses?
influence of NE release
81
stimulation of beta-1 receptors results in what responses?
HR, contractility, renin secretion
82
stimulation of beta-2 receptors results in what respones?
vasoconstriction/vasodilation, bronchoconstriction/bronchodilation
83
stimulation of beta-3 results in what?
impacts lipolysis
84
a positive iontropic effect does what?
increase stroke volume
85
a positive chronotropic effect does what?
increase heart rate
86
what are the general effects of catecholamines?
sympathommetic - they mimic the SNS
87
vascular effects of cataecholamines
EPI: peripheral vascular resistance (low = reduced; high = increased) NE: elevates BP
88
CNS effects of catecholamines
anxiety, tremors, headache
89
non-vascular smooth muscle effects of catecholamines
relax smooth muscles of GI tract, urinary retention, bronchodilation
90
metabolic effects of catecholamines
increase blood glucose, fatty acid levels, insulin secretion inhibition, increase glycogenolysis/glycuneogensis
91
net effect of epinephrine on all alpha and beta receptors
vasoconstriction & cardiac stimulation
92
what would epinephrine be used to treat?
anaphylactic shock, cardiogenic shock
93
how does epinephrine effect alpha receptors?
alpha-1: smooth muscle vasoconstriction alpha-2: presynaptic receptor
94
how does epinephrine effect beta-1 receptors?
increase strength/rate of cardiac contractions
95
how does epinephrine effect beta-2 receptors?
relaxes bronchial smooth muscle, activates glycogenolysis, dilates skeletal muscle blood vessels
96
how does epinephrine effect beta-3 receptors
activates lipolysis
97
NE mainly effects which receptors?
mainly alpha-1 but will also effect alpha-2 and beta-1
98
NE has little effect on which receptor?
beta-2
99
main effect of NE
increases BP, increases peripheral resistance, minimally increased HR
100
NE used to treat \_\_\_
severe hypotension septic shock
101
Dopamine is a precursor to \_\_\_\_
NE
102
Dopamine mainly activates \_\_\_\_\_\_
alpha-1 and beta-1 receptors
103
T/F: catecholamines can be used as vasopressors?
true
104
main effect of vasopressors
increase vasoconstriction --\> increases BP and MAP
105
MOA of direct acting adrenergic drugs (DAADs)
directly stimulate the alpha or beta receptors
106
DAADs suffix
end in -rine
107
MOA of indirect acting adrenergic drugs (IAADs)
enhance effect of NE or Epi by inhibiting their reuptake or degradation; or increasing the release of NE
108
IAADs are sympatho\_\_\_\_\_
mimetic --\> sympathomimetic --\> they mimic the SNS
109
examples of IAADs
1). adderall (amphetamine) 2). Focalin 3). Vyvanse 4). cocaine 5). ephedrine
110
How does Cocaine work?
inhibits re-uptake of NE, significant vasoconstriction = hypertensive crisis, MI, stroke
111
how do mixed acting adrenergic drugs (MAADs) work?
work on direct and indirect pathways
112
rehab concerns for sympathomimetics
1). OTC cold remedies may contain phenylephrine 2). may induce: HTN, cardiac arrhythmias, angina 3). ephedra (weight loss products): cerebral hemorrhage, seizures, and death
113
effect of SNS on HR and SV
increase
114
mean arterial pressure (MAP) = \_\_\_\_\_\_\_\_\_
CO \* peripheral resistance
115
General MOAs for antiHTN meds
affect variables in CO and MAP to alter BP
116
AntiHTN meds effect on variables of CO and MAP
1). reduce HR --\> decrease CO and AP 2). decrease contractility --\> decrease SV --\> decrease BP 3). increase vasodilation --\> lower peripheral vascular resistance --\> decrease BP 4). reduce plasma volume --\> decrease SV --\> decrease bP
117
Classes of AntiHTN meds
1). diuretics 2). direct vasodilators 3). calcium-channel blocking vasodilators 4). beta-blockers 5). α1-Adrenoceptor Blockers6). Dual α- & β- blockers7). alpha agonists 8). RAAS inhibitors
118
what is the recommended initial therapy for all HTN patients?
Diuretics
119
Types of Diuretics
1). Loop 2). Thiazide 3). K+ sparring
120
which diuretic is the most frequently used?
Thiazide
121
MOA of loop diuretics
inhibits reabsorption of Na+, K+, chlorine -- prevents reabsorption of water
122
AE of Loop Diuretics
dehydration, hypokalemia, hyponatremia, hypocalcemia, ototoxicity, hyperglycemia, increased LDLs
123
PK/PD considerations for Loop Diuretics
may be taken along with supplemental K+ or K+ sparing diuretics to reduce risk of hypokalemia and metabolic alkalosis
124
Loop diuretics suffix
-ide
125
MOA for Thiazide diuretics
inhibits mechanism that favors Na+ reabsorption --\> result in Na+ and K+ excretion and reabsorption of Ca2+
126
AE of Thiazide diuretics
similar to loop diuretics, may cause hypercalcemia and significant loss of K+
127
PK/PD considerations for Thiazide Diuretics
1). may be given along w/loop diuretics in cases of CHF, severe edema 2). favored for older adults to reduce Ca+ loss and maintain bone loss
128
which Diuretic is better choice for individuals prone to renal calculi?
Thiazide Diuretics
129
Thiazide Diuretic suffix
-azide
130
MOA for K+ sparring diuretics
inhibits the Na+/K+ exchange mechanism and limits the reabsorption of Na+ and excretion of K+. Limits osmotic gradient which drives reabsorption of water from tubule
131
AE of K+ sparring diuretics
hyperkalemia, nausea, lethargy, mental confusion
132
PK/PD considerations for K+ sparring diuretics
1). less effective at producing diuresis but are K+ sparring 2). Prevents hypokalemia (good for arrythmias)
133
Therapeutic Concerns with Diuretics
1). look for signs of hypokalemia or hyperkalemia 2). hyperglycemia and abnormal lipid levels 3). dehydration 4). DDIs with NSAIDs
134
T/F: there is a fall risk with diuretics
True: mental status can change due to hypo/hyperkalemia, dehydration
135
T/F: risk of orthostatic hypotension with diuretics
True, increased TPR
136
effect of NSAIDs in DDIs with diuretics
NSAIDs cause Na+ retention and decreases in renal perfusion --\> cause diuretics to be less effective
137
MOA of direct vasodilators
inhibit smooth muscle contraction in arterioles to directly vasodilate the peripheral vasculature
138
AE of direct vasodilators
dizziness, orthostatic hypotension (reflex tachycardia - to compensate for fall in BP)
139
examples of direct vasodilators
apresoline and Loniten
140
T/F: direct vasodilators are commonly used
FALSE
141
MOA of Calcium-channel blocking vasodilators
block Ca2+ entrance into vascular smooth muscle, reducing smooth muscle tone and allowing for vasodilation
142
Classes of Ca-channel blocking vasodilators
1). dihydropyridines 2). phenylakylamines 3). benzothiazepines
143
effect of dihydropyridines
reduce arteriole tone
144
effect of phenylalkylamines
affect the heart
145
effect of benzothiazepines
affect heart and vasculature
146
AE of Ca-channel blocking vasodilators
HA, dizziness, hypotension, bradycardia, reflex tachycardia, sweating, tremor, flushing, constipation
147
PK/PD considerations for Ca-Channel blocking vasodilators
1). useful when beta-blockers are contraindicated (asthma, DM, PVD) 2). originally developed for treating cardiac disease
148
MOA for beta-blockers
competitive antagonist, binds to beta receptors and prevents NE from binding, results in decrease HR, contractility and conduction
149
types of beta-blockers
1). non-selective 2). cardioselective
150
AE of Non-selective beta-blockers
contribution to peripheral vasoconstriction, bronchoconstriction, bradycardia, reduced exercise tolerance, dizziness, OH, depression, fatigue, sexual dysfunction
151
abrupt withdrawl of Non-selective Beta-blockers results in \_\_\_\_\_\_
arrhythmia, angina, MI
152
Non-selective beta-blockers suffix
-lol
153
MOA of cardioselective beta-blockers
selectively block beta-1 receptors without causing bronchoconstriction
154
AE of cardioselective beta-blockers
same as non-selective but no pulmonary effects
155
therapeutic concerns for beta-blockers
1). depresses HR and CO during exercise 2). may contribute to orthostatic hypotension 3). may cause CHF 4). masks symptoms of hypoglycemia in diabetic pts.
156
MOA of alpha-1 adrenoceptor blockers
reduces sympathetic tone of blood vessels causing VD and decreased peripheral vascular resistance
157
AE of alpha-1 adrenoceptor blockers
orthostatic hypotension, nasal stuffiness, reflex tachycardia, arrhythmia
158
seletive alpha-1 blockers suffix
-azosin
159
therapeutic concerns for alpha-1 adrenoceptor blockers
fall risk increased risk of CHF
160
types of alpha agonists
alpha-1 receptor agonists alpha-2 receptor agonists
161
alpha-2 receptor agonists indications
HTN, anxiety/PTSD, spasticity
162
central-acting alpha-2 agonist for HTN MOA
decrease sympathetic output from CNS (decrease NE) by binding to presynaptic
163
AE of central-acting alpha-2 agonists
dizziness, drowsiness, fatigue, headache
164
PT concerns for central-acting alpha-2 agonists
orthostatic hypotension, rebound hypertension
165
central-acting alpha-2 agonist that is in the form of a weekly patch
clonidine
166
clonidine indication
reserved for resistance HTN, ADHD, adjunct pain control
167
AE of clonidine
dry mouth, rash
168
what centrally acting alpha-2 agonist will be used with pregnant women w/HTN?
methyldopa
169
AE of methyldopa
sexual dysfunction, sodium/water retention with long-term use
170
Types of RAAS inhibitors
1). Direct renin inhibitor (DRI) 2). Angiotension 1 converting inhibitor (ACEi)3). Angiotensin II receptor blocker (ARB)
171
DRI MOA
block conversion of angiotensinogen to angiotensin I
172
AE of DRI
similar to ACEi and ARB
173
ACEi MOA
blocks conversion of angiotensin I and angiotensin II
174
downstream effects of ACEi
1). increases blood vessel VD, bradykinin \>\> increases VD 2). decreases aldosterone secretion \>\> decreases Na+ and H20 retention
175
ACEi indications
HTN, reduced ejection fraction heart failure, post-MI, post-stroke, kidney disease
176
Common ACEi AE
dry cough, hypotension/dizziness, hyperkalemia
177
rare ACEi AE
acute renal failure, angioedmea
178
PT concerns with ACEi
coughing, DDI with NSAIDs
179
ACEi suffix
-pril
180
ARB MOA
antagonist at receptor which blocks the binding of angiotensin II from the RAAS and other pathways
181
ARB indications
alternative if ACEi intolerant in HTN, kidney disease, HF
182
Common AE of ARB
hypotension/dizziness, hyperkalemia
183
Rare AE of ARB
acute renal failure, angioedema
184
ARB suffix
-sartan
185
which RAAS inhibitor is the best tolerated?
ARB
186
Therapeutic concerns about ACEi
cough (instant referral), NSAIDs are contraindicated
187
General therapeutic concerns for hypertensive agents
1). orthostatic hypotension 2). dehydration 3). caution w/heat 4). cannot use HR as exercise tolerance determinant 5). depletion of electrolytes 6). poly pharmacy
188
What are the 3 types of ischemic heart disease?
1). Arteriosclerosis 2). Angina3). MI
189
3 major forms of angina
1). exertional (stable) 2). Variant (Prinzmetal's) 3). Unstable
190
Which type of of angina occurs prior to an MI?
Unstable, pain will increase with frequency, severity, and/or duration
191
Two common drug types used to treat angina pectoris?
Vasodilators and Cardiac Depressants
192
what are the subtypes of vasodilators?
Nitrates and Ca2+ blockers
193
what are the subtypes of cardiac depressants?
Beta-blockers and Ca2+ blockers
194
general goal of drugs treating angina pectoris?
relieve vasoconstriction and workload of the heart (reduce the O2 requirement)
195
where do nitrates work?
directly on vascular smooth muscle (not a receptor!)
196
general result of Nitrates
decrease preload/afterload --\> reduce workload of heart -\> reduce O2 demand
197
T/F: nitrates are DOC for acute angina attacks?
True, especially sublingual
198
Important patient education concerning Nitrates
proper storage and dosing
199
AE Nitrates
1). reflex tachycardia 2). dizziness 3). OH4). weakness
200
what type of angina requires beta-blockers to treat?
stable angina along with short-acting nitrates
201
how do Ca2+ blockers work?
block Ca2+ channels resulting in decreased smooth muscle contractility
202
what are the zones injury MI?
1). zone of ischemia 2). zone of hypoxic injury 3). zone of infarction
203
two types of MI based on ECG interpretation?
STEMI and NSTEMI
204
how is STEMI treated?
thrombolytic agent, aspirin, nitrates, beta-blockers
205
how is NSTEMI treated?
heparin
206
Peripheral vascular disease (PVD) can result in what?
development of venous thrombosis (VT)
207
a VT can result in what?
pulmonary embolism (PE)
208
what is a VT?
partial/complete occlusion of a vein by a thrombus
209
two types of VTs
superficial and deep
210
a DVT can result in what?
pulmonary embolism
211
Signs and symptoms of a pulmonary embolism?
1). possible sudden death 2). chest pain 3). tachypnea 4). hemoptysis 5). anxiety, restlessness, apprehension 6). dyspnesa 7). persistent cough
212
Vascular injury results in what 2 immediate things?
1). exposure of collagen and VWF 2). Tissue factor exposure
213
exposure of collagen and VWF results in what?
platelets adhesion and release of ADP and thromboxane A2
214
once platelets adhere and release what happens?
more plates are recruited and activated
215
as more platelets are recruited and activated what results
platelet aggregation and ultimately platelet-fibrin thrombus formation
216
when tissue factors are exposed due to a tissue injury what is triggered?
coagulation pathways and thrombin generation
217
what does thrombin do?
recruit more platelets and convert fibrinogen to fibrin
218
how is fibrin important?
it binds platelets together to form a thrombus
219
primary hemostasis results in what?
platelet plug formation
220
secondary hemostasis results in what?
fibrin formation which is used to stabilize the platelet plug
221
What is artherosclerosis?
narrowing and hardening of the arteries
222
basic mechanism of artherosclerosis
injury occurs to arterial wall -\> cholesterol begins to build up in the wall
223
what can atherosclerosis eventually cause?
thrombus formation -\> MI, stroke, or other ischemic issues
224
what type of cholesterol is "good"?
High-density HDL
225
what are the 3 basic classes of drugs used to treat Artheroscerlosis?
1). Statins 2). PCSK9 inhibitors 3). Cholesterol Absorption Inhibitor
226
true name of statins?
HMG-CoA reductase inhibitors
227
T/F: even with low LDL some populations must take a statin to reduce risk of stroke
TRUE
228
basic MOA statins
block cholesterol synthesis
229
statins common AE
myalgia
230
other Statins AE
dyspepsia, headache, increased liver enzymes, tendinopathy and tendon rupture?
231
Rare AE of Statins
rhabdo and myopathy
232
T/F: statins have a decreased risk of drug-drug interactions?
FALSE, increased risk (especially fibrates)
233
how does grapefruit juice effect statins?
inhibits CYP enzymes - linked to statin rhabdo -\> increased 6x hosptialization rate
234
what are the 3 types of antithrombotic drugs classes?
1). Antiplatelets 2). anticoagulants 3). fibrinolytics
235
general concerns with antithrombotics as a whole?
bleeding or clotting
236
what do antiplatelets do?
prevent thrombus
237
basic MOA of antiplatelets
decrease platelet secretion and adhesion
238
which antithrombotic class has boxed warnings?
antiplatelets, warning against CYP interaction, increase risk of bleeding
239
suffix for antiplatelets
-gel/-grelor
240
what do anticoagulants do?
prevents thrombus & thrombus growth
241
LMWH and Heparin basic MOA
increase antithrombin to decrease thrombin
242
Heparin and Direct thrombin inhibitor basic MOA
prevents conversion of fibrinogen -\> fibrin
243
Arixtra basic MOA
selectively inhibits factor Xa
244
Anticoagulants that are administered via IV
LMWH, Heparin, Direct thrombin inhibitor, Arixtra
245
Anticoagulants that are administered via PO
Direct thrombin inhibitor, Factor Xa inhibitor, and Warfarin (VKa)
246
Direct thrombin inhibitor and Factor Xa are further classified as what?
DOAC
247
DOAC has less of a risk of what?
intercranial bleeding
248
Warfarin basic MOA
inhibits vitamin K - inhibits coagulation cascade indirectly (reduces factor formation)
249
Atrixtra is what type of anticoagulant?
factor Xa inhibitor
250
AE of Warfarin
intercranial bleeding , rare: skin necrosis, DDI with leafy green
251
Fibrinolytics generally do what?
lyse active thrombus
252
Fibrinolytics basic MOA
breaks fibrin links in active thrombus
253
when are Fibrinolytics prescribed?
immediately following stroke, MI, and PE
254
Fibrinolytics suffix
-kinase/-plase
255
what is the continuum from least to most risk of HIT(heparin induced thrombocytopenia) (for anticoagulants)
Atrixtra - direct thrombin inhibitor - LMWH - Heparin
256
Cholesterol Absorption Inhibitor MOA
inhibits absorption of cholesterol in small intestine
257
When might a cholesterol absorption inhibitor be used?
if a pt. is experiencing a lot of myalgia from statins
258
Cholesterol absorption inhibitors DDI
not metabolized by CYP enzymes, less DDI
259
basic MOA for PCSK9 Inhibitors
increase LDL uptake for degradation
260
PCSK9 common AE
injection site reactions
261
what is CHF?
heart is unable to pump sufficient blood to supply the needs of the body
262
How is CHF progressive?
structural changes over time lead to reduced cardiac contractility
263
Conditions that can lead to CHF
ischemic and hypertensive heart disease, cardiomyopathy, valve disease
264
What is compensated CHF?
pt is med stable. Combined efforts of 3 compensatory phases achieve a normal CO
265
what is decompensated CHF?
unable to maintain adequate circulation. Life-threatening: fluid overload and total heart failure
266
clinical manifestation of L ven CHF
1). dyspnea 2). fatigue and muscular weakness 3). renal changes 4). nocturia
267
in general R ven CHF deals with what?
fluid build up in the periphery
268
in general L ven CHF deals with what?
fluid build up in the lungs
269
which ventricular failure can result in pulmonary edema?
Left ventricle heart failure
270
HF with preserved ejection fraction results from what?
diastolic heart failure, cardiac hypertrophy -\> reduced volume capacity in L ven
271
HF with reduced ejection fraction is caused by what?
systolic heart failure, heart unable to adequately contract
272
which HF is more often related to aging and cardiac hypertrophy?
HFpEF (preserved heart failure)
273
goals of HFpEF
1). treat underlying comorbidities 2). give diuretics 3). may add aldosterone antagonist
274
general goal of HFpEF?
get rid of fluid, can't fix just treat symptoms
275
Goals of HFrEF
improve QOL and prolong survival
276
corresponding meds for HFrEF
diruretics, + inotropic drugs (digoxin), vasodilators
277
Entresto is what?
a type of ARB (higher risk of angioedema than other ARBS)
278
T/F: Digoxin reduces mortality?
FALSE
279
T/F: Digoxin is an NTI
TRUE
280
rEF Baseline Trx
ACEi or ARB, + beta-blocker, + diuretic (prn)
281
when is digoxin prescribed?
as a last resort if sympotoms not controlled on other therapy
282
what is an arrhythmia?
disturbance of HR due to SA node irregularities (origin, pattern, speed/rate)
283
Overall symptoms of arrhythmias
increase/decrease in HR palpitations
284
general symptoms of arrhythmias
fatigue, dyspnea, syncope, dizziness, angina, diaphoreseis (profuse sweating)
285
Anti-arrhythmic drug therapeutic concerns
also causes arrhythmia, take HR for 60s, decreases exercise tolerance, 30-60% efficacy
286
Amiodarone MOA
prolong duration of AP by blocking ion channels (K+, Na+, Ca2+)
287
Amiodrone indication
ventricular arrhytmia
288
Amiodarone AEs
LFTs, TFT, PFTs, bluish discoloration
289
considerations for Amiodrone
50 day half life
290
Digoxin MOA
increase contractility (Na+/K+ ATPase)
291
Digoxin indication
arrhythmia & CHF (last resort)
292
Digoxin AE
GI (Beer's list)CNS - blurred vision, confusion, lethargy Arrhythmia
293
Digoxin considerations
avoid pt who has kidney dysfunction (metabolized by kidneys) \*medical emergency if given to them
294
what controls respiration?
1). medullary rhythmic center 2). Vagal input from lungs 3). ABGs
295
effect of PNS on respiration?
produces mainly bronchoconstriction and mucus secretion
296
effect of SNS on respiration?
beta-2 receptors relax smooth muscles, increase mucocilliary clearance
297
what is a healthy V/Q ratio?
0.8(Ventilation to perfusion ratio)
298
difference between volumes and capacities in the lungs?
capacities are when you add volumes up/together
299
drugs that can be used to treat respiratory tract irritation & control of secretions
1). Decongestants 2). Antitussives 3). Antihistamines 4). Mucolytics 5). Expectorants
300
what do decongestants do?
counter mucous discharge from upper respiratory tract (nasal stiffness)
301
decongestants MOA
usually alpha-1 adrenergic agonist --\> causes vasoconstriction --\> reduces blood flow = "dry up" mucosal tracts
302
what do antitussives do?
used to suppress cough (dry unproductive cough)
303
Antitussives MOA
decrease afferent nerve activity or decrease cough center sensitivity
304
Antitussive drugs can include what?
Codeine and antihistamines
305
What are antihistamines used for?
to manage respiratory allergic responses to seasonal allergies
306
general MOA for antihistamines
act on nasal mucosa H1 receptor
307
what do H1 receptors blockers do?
reduce nasal congestion, mucosal irritation, and cough by reducing secretions
308
difference between 1st and 2nd generation antihistamines
1st generation cross the BBB which results in more drowsiness
309
general AEs for antihistamines
dry mouth, sore throat, cough, nausea, HA, diarrhea, and nervousness
310
Mucolytics MOA
split disulfide bonds --\> decreases viscosity of respiratory secretions making it easier to clear mucus from the airway
311
what do expectorants do?
facilitate the production and ejection of mucus.
312
issues with cold remedies and hypertension
decongestants can mimic effects of increased sympathetic activity, thus hypertensive individuals should avoid them
313
COPD is an umbrella term for what conditions?
1). emphysema 2). chronic bronchitis 3). asthma
314
what is emphysema?
pathologic accumulation of air in the tissues, particularly in the lungs
315
pathophysiology of emphysema?
alveoli are damaged and create large air spaces which reduce the SA for gas exchange.
316
clinical manifestations of emphysema
1). barrel chests 2). clubbed fingers 3). tachypnea 4). marked exertional dyspnea 5). hypertrophied neck muscles 6). anxiety related to dyspnea or fear of dyspnea
317
what is chronic bronchitis?
inflammation of airway and irritation that results in excess mucus production
318
hallmark of chronic bronchitis?
very productive cough that lasts for at least 3 months for 2 consecutive years
319
clinical manifestations of chronic bronchitis
1). SOB 2). persistent cough 3). prolonged expiration 4). recurrent infection due to increased mucus in airways 5). late effects include pulmonary hypertension
320
goals of trx for COPD
reduce airway edema secondary to inflammation and bronchospasm
321
how to achieve trx goals for COPD
1). facilitate the elimination of bronchial secretions 2). prevent and treat respiratory infections 3). increase exercise tolerance
322
Drug classes used to treat COPD
1). Bronchodilators 2). Anti-inflammatory 3). Antibiotics
323
Types of Bronchodilators
1). inhaled beta agonists 2). inhaled antimuscarinics
324
MOA of inhaled beta-agonists
agonize beta-2 receptors --\> increase bronchodilation
325
suffix for inhaled beta-agonists
-terol
326
what are SABAs?
short acting beta-agonists
327
what are SABAs used for?
acute exacerbations, works within 5 minutes and lasts 4-6 hours
328
what are LABAs?
long acting beta-agonists
329
what are LABAs used for?
chronic managements, 12-24 hour duration, must be dosed once or twice daily
330
AE for inhaled beta-agonists
generally well tolerated. AE can include: tachycardia, tremor, hypokalemia
331
MOA for Inhaled antimuscarinics
primarily bind M3 in airway smooth muscle which antagonizes ACh actions at those sites resulting in bronchodilation
332
what are SAMA/LAMAs?
short/long acting antimuscarinics
333
AE for inhaled antimuscarinics?
generally well tolerated other than dry mouth
334
Anti-inflammatory drugs used to treat COPD
1). inhaled corticosteriods (-asone or -sonide) 2). PDE-3 inhibitor
335
typical use for ICS?
acute exacerbation of COPD or more severe disease
336
ICS AEs?
oral candidiasis (prevent by rinsing mouth)
337
MOA for PDE-3 inhibitor
decrease breakdown of intracellular cyclic AMP --\> decreases inflammation
338
when would PDE-3 inhibitors be used?
when a pt has a more severe COPD case, this drug is used in to the hopes to decrease the amount of exacerbations
339
what is asthma?
reversible obstructive lung disease characterized by inflammation and increased smooth muscle reaction of the airways to various stimuli
340
types of asthma?
1). extrinsic 2). intrinsic 3). exercise-induced 4). asthma associated with COPD
341
Asthma Pathogenesis?
1). abnormal airway response 2). mediators cause thickening of airway walls and increased contractile response of bronchial smooth muscle 3). mucous plug can become significant and block up the airways that are in spasm and swollen (traps air distally)
342
Clinical manifestations of Asthma
1). sensation of chest constriction 2). inspiratory and expiratory wheezing 3). nonproductive cough 4). prolonged expiration 5). tachycardia and tachypnea
343
Goals for Asthma trx?
1). decrease impairments 2). decrease risk (prevent exacerbations, need for emergency care, prevent loss of lung function, decrease AE for therapy)
344
1st line (maintenance trx) for Asthma
1). ICS solo 2). LABAs only in combo with ICS
345
1st line trx for acute exacerbations of Asthma
PO ICS
346
Alternative trx for Asthma
1). Leukotriene Modifiers 2). Immunomodulators 3). Cromolyn Sodium 4). Methylxanthines
347
what are Leukotrienes?
released from mast cells eosinphils, they play a role in airway edema, smooth muscle contraction and inflammatory process
348
types of Leukotriene modifiers
1). Leukotriene receptor antagonist (LTRA) 2). 5-lipoxygenase inhibitor
349
MOA for LTRA
competitively antagonize leukotriene receptors
350
Types of Immunomodulators
1). Anti-IgE 2). Interleukin Antagonist
351
MOA of Anti-IgE?
binds IgE antibody --\> prevents IgE binding to receptors on mast cells and basophils --\> limits activation and release of allergic response mediators
352
AE of Anti-IgE
HA, injection site reactions; very rare anaphylactic allergic reactions
353
Interleukin antagonist MOA
monoclonal antibodies that binds interleukins results in decrease inflammatory response
354
Common interleukin antagonist AE
injection site reactions, HA, increase creatine kinase
355
What drugs are used for acute symptom relief and exacerbations of Asthma?
1). SABAs2). SAMAs 3). PO steroids
356
what is used for acute symptom relief and EIB?
SABAs. typically used up to 3 trx at 20 min intervals
357
when would SAMAs be used?
in combo with SABA in emergency care setting or as monotherapy if SABA not tolerated
358
when would PO steroids be used to treat Asthma?
moderate to severe exacerbations
359
what is a BPTs?
bronchial provocation test. Used to diagnose asthma in atheltes
360
What is cystic fibrosis?
gene defect that doesn't allow Cl- to pass in and out of the plasma membrane of epithelial cells. More commonly known for its copious amounts of mucus but is a multi-system disease
361
CF complications
1). CFRD 2). bone disease 3). liver disease 4). lung transplants
362
CF trxs
1). Bronchodilators 2). CFTR modulators 3). Mucolytics 4). Anti-inflammatory 5). Inhaled Antibiotics 6). PO Antibiotics 7). Nutritional support
363
Bronchodilators used in CF trx
may use LABAs for maintenance; SABAs used prior to chest physiotherapy
364
what is a CF trans-membrane regulator?
membrane protein and Cl- channel --\> regulates sodium and water which helps keep mucous thin
365
how does CF effect CFTRs?
genetic mutations cause closing and/or narrowing of CFTR or prevents CFTR from getting to the cell surface
366
purpose of CFTR modulators
decrease risk of exacerbation, increase lung function and QOL
367
common AE for CFTR modulators
HA, GI issues, respiratory issue
368
less common AE of CFTR modulators
dizziness and hypertension
369
why are mucolytics used in trx of CF?
decrease risk of exacerbations, improve lung function and QOL
370
type of mucolytic used ideally?
hypertonic saline and dornase alfa
371
MOA of hypertonic saline?
increase salt in airways which draws more water into airways -\> increases hydration of airway mucus secretions, increases mucucillary functions
372
MOA of dornase alfa (Pulmozyme)
cleaves DNA --\> decrease mucus viscosity --\> improved airflow
373
what is a red flag for a pt on dornase alfa?
chest pain -\> merits an automatic referral to a physician
374
what is a red flag for a pt on dornase alfa?
chest pain -\> merits an automatic referral to a physician
375
Anti-inflammatory used to trx CF
Chronic high dose ibuprofen if \<18 years old - has been proven to slow the loss of lung function
376
Inhaled Antibiotics used to trx CF
1). Tobramycin (Tobi) 2). Aztreonam
377
when would an inhaled antibiotic be used chronically for CF trx?
if P. aeruginosa persistently present in cultures
378
prescription instructions for Tobramycin
nebulized 2-3x daily for 28 days on and then 28 days off
379
AE of Tobramycin (9)
voice disorder, HA, fever, respiratory issue, ototoxicity, pharyngolarngeal pain, cough, nasal congestion, wheezing
380
additional AE for aztreonam
fever
381
supplemental vitamins used for nutritional support in pts with CF?
Vitamins A, D, E, and K
382
what is PERT?
pancreatic enzyme replacement therapy
383
Therapeutic concerns with Anti-cholinergic drugs used to trx respiratory conditions?
dry mouth, HTN and tachycardia
384
Therapeutic concerns with steroids used to trx respiratory conditions?
1). inhaled: oral candidiasis and thrush 2). increased infection risk, HTN, Osteoporosis (muscle weakness, skin atrophy)
385
Therapeutic concerns with Beta-2 agonists used to trx respiratory conditions
tremor, trachycardia, hypokalemia, hyperglycemia, reduced exercise capacity
386
what are the phases of digestion?
cephalic phase
gastric phase
intestinal phase
387
what occurs during the intestinal phase of digestion?
chyme enters the duodenum release of bicarbonate solution and pancreatic enzymes
388
T/F: the neuronal control of digestions is mostly cholinergic and excitatory?
True
389
what is peptic ulcer disease (PUD)?
ulcerations of the mucosal lining of the esophagus, stomach and/or duodenum
390
T/F: H pylori infection can cause chronic gastritis, PUD, GERD, and gastric cancer?
TRUE
391
how is H pylori infection treated?
antacid + antibiotic
392
T/F: one should discontinue use of NSAIDs during H. pylori infection if possible
TRUE
393
what regulates vomiting?
chemoreceptor trigger zone (CTZ) and the Vomiting center
394
where is the CTZ?
floor of the 4thh ventricle in cerebrum
395
what does the CTZ respond to?
toxins/drugs in blood and CSF
396
what does the vomiting center do?
integrates signals from multiple places including: CTZ, GI tract, pharynx, vestibular system
397
what is the typical cause of diarrhea?
from water and electrolyte imbalance in intestinal tract
398
common pathologies that can lead to diarrhea?
1. IBS
2. Crohn’s disease
3. Ulcerative colitis
4. Bowel impaction with overflow
5. Bacterial overgrowth
6. Bile acid malabsorption
7. Celiac disease
8. Short bowel syndrome
9. Laxative abuse can lead to diarrhea
399
what is constipation?
movement disorder of the colon; infrequent/painful defecation, hard stools, incomplete evacuation
400
what are some causes of constipation?
1. Bowel impaction
2. Endocrine or neurogenic condition
3. Sedentary lifestyle
4. Poor diet (limited roughage, dehydration)
5. Medications
401
drug classes indicated for acid reflux
1. antacid
2. H2 receptor antagonist
3. proton pump inhibitors (PPI)
402
Drug classes that heal/treat ulcers that form from gastric acid
1. H2 receptor antagonists
2. PPI
3. Mucuosal protectors
403
which drug classes that treat acid reflux also help heal ulcers?
1. H2 receptor blocker
2. PPI (more effective of the two)
404
MOA of antacids
neutralizes stomach acidity by increasing stomach pH
405
AE of antacids
1. Effervescent types (i.e. Alka-Seltzer) have high Na+ content – if pt has hypertension they should probably avoid this one
2. Magnesium products à diarrhea
3. Aluminum and calcium à constipation
4. Drug-Drug interactions
5. Alters absorption of electrolytes from GI tract à electrolyte imbalance
6. Avoid taking within 2 hours of other oral medications
406
how do antacids have DDIs?
↑ absorption of basic drugs and ↓ absorption of acidic drugs
407
MOA of H2 receptor anatagonists
reduce secretion of stimulated acid
408
T/F: H2 receptor antagonists are best taken HS (at bedtime)
TRUE
409
H2 receptor antagonist AE
1. diarrhea
2. muscle pain
3. rashes
410
PPI MOA
irreversibly inhibit H+/K+ ATPase pump on parietal cell membrane which blocks final step in acid secretion into lumen of stomach
411
PPI AE
generally well tolerated
long term: gastric polyps, altered Ca2+ metabolism (↓ bone mineralization), some cardiovascular abnormalities.
412
what are the types of mucosal protectors?
1. Bismuth chelate
2. Sucralafate
3. Misoprostol
413
how do bismuth protectors works?
coats ulcer, enhances prostaglandin synthesis, ↑ gastric mucous epithelial cell growth to protect against H. pylori-induced ulcers
414
how do sucralfates work?
an Al salt of sucrose that forms a protective coating over the ulcer; used for high-risk causes (trauma, burns, ARDS, major surgery, etc.)
415
How does misprostol work?
synthetic prostaglandin analog (PGE2) that inhibits acid secretion; used to prevent NSAID-induced ulcers.
416
Types of Antiemitic drugs
1. Anticholinergics
2. Antihistamines
3. Neuroleptic drugs
4. Prokinetic drugs
5. Serotonin blockers
6. Neurokinin-1 receptor blockers
7. Cannabinoids
417
MOA for anticholinergic antiemetics
binds to ACh receptors on vestibular nuclei, blocks communication
418
Anticholinergic antiemetics AE
1. dizziness,
2. drowsiness
3. dry mouth
4. blurred vision
5. dilated pupils
6. difficulty with urination
419
Antihistamine antiemetic MOA
inhibit vestibular input to the CTZ
420
Neuroleptic antiemetic drugs MOA
block dopamine receptors in CTZ
421
most important AE for neuroleptic antiemetic drugs
tardive dyskinesia
422
Prokinetic antiemetic drugs MOA
block dopamine in CTZ
423
Prokinetic antiemetic drugs AE
1. sedation
2. diarrhea
3. weakness
4. prolactin release
5. prolonged use causes extrapyramidal signs, motor restlessness
424
Serotonin blockers antiemetic drug MOA
block serotonin receptors in the GI tract, CTZ, and vomiting center
425
Neurokinin-1 receptor blocker antimetic drug MOA
blocks substance P from binding to NK-1 receptor, prevents both central and peripheral stimulation of vomiting centers
426
Which antiemetic drugs are used to prevent vomiting from motion sickness?
1. Anticholinergics
2. Antihistamines
427
Which antiemetic drugs are antipsychotic agents, some have anticholinergic actions and are good for postop vomiting?
Neuroleptic antiemetics
428
Which antiemetic drugs are used to treat vomiting resulting from chemotherapy?
1. Neurokinin-1 receptor blockers
2. Cannabinoids
429
Which antiemetic drug can cause Steven-Johnsons syndrome?
Neurokinin-1 receptor blockers
430
Types of antidirraheal drugs
1. Absorbents
2. Anticholinergics
3. Intestinal flora modifiers
4. Opiates
431
Absorbents MOA
binds to bacteria causing diarrhea and carry them out with feces
432
Absorbents AE
\*aspirin product: use with caution in children recovering from flu/chickenpox, increased bleeding time, GI bleed, tinnitus
\*decrease effectiveness of many drugs (digoxin, hypoglycemic drugs, anticoagulants)
433
Anticholinergic Antidirrheal MOA
reduce peristalsis of GI tract
434
Opiates Antidirrheal MOA
decrease GI motility and propulsion (in small doses)
Slowing transit time in intestines = absorption of water and electrolytes
435
Opiates antidirrheal AE
1. sedation
2. dizziness
3. constipation
4. nausea
5. vomiting
6. respiratory depression
7. bradycardia
8. hypotension
9. urinary retention
436
Types of Laxatives
1. Bulk-forming
2. Hyperosmotic
3. Saline
4. Emollient
5. Stimulant
437
Bulk forming laxatives MOA
increase water absorption à softens and increases bulk of intestinal contents
Distention of colon increases peristalsis
438
hyperosmotic laxatives MOA
creates gradient that draws fluid into colon to increase stool fluid content and stimulate peristalsis
439
Hyperosmotic laxatives AE
1. abdominal bloating
2. rectal irritation
3. electrolyte imbalance
440
Concerns with hyperosmotic laxatives
do not take if a pt is on diuretics or is at CV risk.
The electrolyte imbalance puts them at risk for cardiac arrhythmias
441
Saline laxatives MOA
similar to hyperosmotic – osmotic pressure pushed water/electrolytes into intestines
442
Saline Laxatives AE
salts may cause issues with individual with diminished cardiac or renal function
443
Emollient laxatives MOA
facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall
444
what are emollient laxatives also known as?
stool (fecal) softeners or lubricant laxatives
445
Emollient laxatives AE
\*generally well tolerated
1. skin rash
2. decrease vitamin absorption
3. electrolyte imbalance
446
Stimulant laxatives MOA
stimulates peristalsis through enteric nervous system
447
Important consideration with stimulant laxatives
Danger of long-term use:
dependence and damage to intestinal cells/loss of colon function
448
Therapeutic concerns with GI agents
1. patient positioning
2. Dehydration
3. Constipation
4. Drug interactions
449
T/F: exercise can facilitate bowel movements and improve gastric emptying?
TRUE
450
T/F: smoking can decrease effectiveness of H2 receptor blockers?
TRUE
451
DDI for Climetidine (tagemet)
Climetidine (tagemet) inhbits CYP450 enzymes
452
Antihypertensive Drug classes
1. Diuretics
2. Calcium channel blockers
3. Beta-blockers (-lol)
4. ACE Inhibitors (-pril)
5. ARB (-sartan)
6. Central acting alpha agonist
7. Nitrates
453
Diuretic Drugs
1. Furosemide (Lasix) - loop diuretic
2. Hydrochlorothiazide (HCTZ) - thiazide diuretic
3. Spironolactone - k+ sparring diuretic
454
Furosemide (Lasix) is what type of diuretic?
loop diuretic
455
what type of diuretic is Hydrochlorothiazide (HCTZ)?
Thiazide diuretic
456
what type of diuretic is Spironolactone?
K+ sparring diuretic
457
Calcium channel blocking diuretics
1. Amlodipin
2. Diltiazem
458
Beta blockers (-lol)
1. Metoprolol
2. Propanolol
3. Carvedilol
459
ACE inhibitors (-pril)
1. Lisinopril
2. Enalapril
3. Ramipril
460
ARBs (-sartan)
1. Losartan
2. Valsartan
461
Central acting alpha agonist
Clonidine
462
Nitrates
1. Nitroglycerin
2. Isosorbide mononitrate
463
What are the 3 types of antithrombotics (drug classes)
1. Antiplatelets
2. Anticoagulants
3. Fibrinolytics
464
Antiplatelet drugs
1. Aspirin
2. Clopidogrel (Plavix)
465
Anticoagulants drugs
1. Enoxaparin (Lovenox)
2. Apixaban (Eliquis)
3. Rivaroxaban (Xarelto)
4. Warfarin
466
Factor Xa inhibitors (-xaban)
1. Apixaban (Eliquis)
2. Rivaroxaban (Xarelto)
467
Statins are also called what?
HMG CoA Reductase Inhibitors
468
Statins
1. Atorvastatin (Lipitor)
2. Rosuvastatin (Crestor)
3. Simvastatin
4. Pravastatin
469
Other Cardiac Meds
1. Sacubitril/valsartan (Entresto)
2. Digoxin
3. Amiodarone
470
what type of drug is Sacubitril/valsartan (Entresto)?
ARNI
471
comparison of ARBs with ARNI
ARNI have a higher risk of angioedema
472
Inhaled medication classes
1. Inhaled beta agonist
2. Inhaled antimuscarinic
3. Inhaled corticosteroids
4. Combination inhaled meds
5. Inhaled mucolytics
473
Bronchodilators
1. Inhaled beta agonists
2. Inhaled antimuscarinics
474
Inhaled beta agonsits (-terol)
1. Albuterol (ProAir, Ventolin)
475
Inhaled Antimuscarinics
1. Tiotropium (Spiriva)
476
Inhaled Corticosteroids
1. Fluticasone (Flovent)
477
Combo inhaled medications
1. Fluticason + salmeterol (**Adavir**) -- (ICS with an LABA
2. Formoterol + budesonide (**Symbicort**) -- (LABA with an ICS)
3. Albuterol + ipratropium (**Combivent**) -- (SABA with a SAMA)
478
Inhaled Mucolytics
1. Hypertonic saline
2. Dornase alfa (Pulmozyme)
479
Other Pulmonary Drugs
1. Leukotriene modifiers
2. Immunomodulators
3. CFTR modulators
480
Leukotriene Modifiers
1. Montelukast (Singulair)
481
Immunomodulator (Anti-IgE)
1. Omalizumab (Xolair)
482
CFTR Modulators
1. Orkambi
2. Symdeco
483
Drug classes that treat gastric reflux
1. Antacids
2. H2 receptor blockers
3. Proton pump inhibitors (PPI)
484
Antacid Drugs
1. Calcium Carbonate (Tums)
485
H2 Blocker
1. Ranitidine (Zantac)
2. Famotidine (Pepcid)
486
Proton Pump Inhibitor (PPI)
1. Omeprazlone (Prilosec)
2. Esomeprazolone (Nexium)
487
Antiemetic Drug Classes
1. Anticholinergics
2. Antihistamines
3. Neuroleptic drugs
4. Prokinetic drugs
5. Serotonin blockers
6. Neurokinin-1 receptor blockers
7. Cannabinoids
488
Antiemetic Drugs
1. Scopolamine (Transderm Scop patch)
2. Meclizine
3. Ondansetron (Zofran)
4. Metoclopramide
489
Anticholinergic antiemetics
1. Scopolamine (Transderm Scop Patch)
490
Antihistamine antiemetics
1. Meclizine
491
Serotonin blocker antiemetic
1. Ondansetron (Zofran)
492
Prokinetic antiemetic
1. Metoclopramide
493
Antidirrheal drugs
1. Bismuth subsalicylate (Pepto-Bismol)
2. Diphenoxylate (**opiate**)/atropine (Lomotil)
494
Antidirrheal drug classes
1. Absorbents
2. Anticholinergics
3. Intestinal flora modifiers
4. Opiates
495
Absorbent antidirrheal drugs
1. Bismuth subsalicylate (Pepto-Bismol)
496
Types of Laxative drugs
1. Bulk-forming
2. Hyperosmotic
3. Saline
4. Emollient
5. Stimulant
497
Hyperosmotic laxatives
1. Polyethylene glycol 3350 (Miralax)
2. Lactulose
498
Emollient Laxative
1. Docusate sodium (Colace)
499
Bulk forming laxative
1. Methycellulose (Citrucel)
500
Stimulant Laxative
1. Senna glycoside (Senna)
