Pharm Final Exam - From Review Session Flashcards
(423 cards)
1
Q
3 concerns with decreasing acid (with PPIS, etc)
A
decrease gastric emptying time, decrease drug absorption, increase in gastric ph can allow bacterial growth
2
Q
why use antacids w/ caution in HF and HTN patients
A
all contain a lot Na+
3
Q
which drug creates a sticky gel that provides a barrier over ulcer
A
sucrafalte
last 6 hours
4
Q
which drug is Direct replacement for NSAIDS that inhibit PG
A
misoprostol
don’t give in pregnancy!
5
Q
bulk forming laxative example and MOA
A
Psyllium
Act like dietary fiber
Absorb water→ soften and enlarge fecal mass → promotes peristalsis
6
Q
surfactant laxative
A
Factilates water penetration
Secretion of H2O/ e-lytes into intestine
Lowers surface tension of stool = facilitation of H2O entry
ex: docusate
7
Q
stimulant laxatives
A
Stimulates peristalsis
Secretion of H2O/ e-lytes into intestine
ex: Bisacodyl, Senna, Castor oil*
8
Q
Castor oil
A
only laxative that works in small intestine (very rapid and powerful)
type 1, very rapid
9
Q
osmotic laxative
A
retains water in the intestinal lumen & thereby soften & enlarges feces → promotes peristalsis
ex: Mag hydroxide* Mag sulfate* Mag citrate* Polyethylene glycol* Lactulose*
10
Q
methylnatrexone
A
Blocks mu receptors on GI tract → increases peristalsis
Selective mu antagonists
11
Q
two pathways for anti-emetics
A
Drugs either alter receptor agonizing in CTZ
OR neuronal transmission from inner ear to vomiting center
12
Q
anti-emetics that block CTZ
A
serotonin antagonists
substance P/NK 1 antagonists
dopamine antagonists
benzos
13
Q
antiemetics that work on inner ear
A
anti-cholinergics (scopolamine)
antihistamines (meclizine)
14
Q
AE of ondansetron
A
HA, dizziness
diarrhea
QT prolongation
15
Q
AE of aprepitant
A
can increase metabolism of warfarin and OCs
-teach pt to use alternative form of BC
16
Q
AEs of butyrophenones (dopamine antagonists)
A
hypotension, sedation, resp depression, EPS
-contraindicated in <2 years
-tissue injury w/ extravasation!
QT prolongation
17
Q
AEs of scopolamine
A
Dry mouth Blurred vision Drowsiness/sedation Less common Urinary retention Constipation Disorientation
18
Q
when is scopolamine most effective
A
prophylatically
19
Q
what is midazolam used for
A
Sedation, suppression of anticipatory emesis
More used for patients that get nausea after chemo
20
Q
which glucocorticoid can be used for N/V
A
dexmethasone
short term, low dose therapy
can lead to hyperglycemia
IV!
21
Q
which drug do you use for IBS in women
A
Alosetron
22
Q
MOA of alosetron
A
5-HT3 specific block→ ↓ abdominal pain, increased colonic transit time, increase absorption of water and sodium
23
Q
MOA of sulfasalazine (5-aminosalicylates)
A
Metabolized by intestinal bacteria → to 5-ASA and sulfapyridine = suppression of PG synthesis and migration of inflammatory cells
5ASA - suppression of PG synthesis and local inflammation
Sulfapyridine = leads to AE
24
Q
AE of sulfasalazine*
A
-N/V, rash, arthralgia
Rare: agranulocytosis, hemolytic anemia
25
what does metoclopramide do and what is it used for
Increase tone and motility of GI tract
DA & 5HT receptor block in CTZ
Increases upper GI motility via ACh enhancing
Used for N/V
26
when don't we give antibiotics
Viral infection
Fever of unknown origin
Before we know enough information and not life threatening
w/o surgically draining abscesses (abx will have limited efficacy)
27
bacteriostatic drugs
Tetracyclines
Macrolides
Clindamycin
Linezolid
28
bactericidal drugs
```
Penicillins (PCNs)
Cephalosporins
Vancomycin
Lipoglycoproteins
Daptomycin
Imipenem
```
29
The function of penicillin binding proteins (PBPs)
bind antbiotic and drug disrupts cell wall
30
pencillin binding proteins
expressed by bacteria during growth and division
| have to be present for pencillins to work
31
beta lactam ring
essential for antibacterial property of antibiotic
32
major concern with pencillin
```
allergic reactions (10% mortality)
watch for 30 mins after
```
33
MOA of pencillins
- bactericidal
- bind penicillin binding proteins (PBPs) on bacterial cell
- Weaken bacterial cell wall → H2O is absorbed d/t high intracellular osmotic pressure → cell bursts
34
AE of cephalosporins
1% cross sensitivity w/ PCN
Cefotetan, ceftriaxone, cefazolin: Can interfere with vit K. metabolism → Can increase bleeding time (w/ prolonged tx), caution with other drugs that cause bleeding
Cefazolin, cefotetan: Disulfiram like reaction → avoid alcohol
35
MOA of carbapenem
MOA: same as PCN but
Resistance to beta lactamase
Gram - penetration ability
Reserved for resistant to mixed type infections
ex: imipenem
36
MRSA
staph aureus infection that is resistance to all beta lactam antibiotics
Production of a PBP that has a low affinity for antibiotics
37
vancomycin MOA
no beta lactam ring
Inhibits cell wall synthesis
Doesn’t PBPS
Only gram +!
38
how to give vanco
IV/PO
| GIVE SLOWLY MAX 1G/HR
39
AE of vanco
- dose related renal failure
- ototoxicity
- rapid infusion leads to histamine release —> hypotension
- red man syndrome = anaphylactoid rxn
40
daptomycin MOA
Insert self into bacterial cell membrane → form channels to allow for K+ efflux → inhibition of DNA/RNA/proteins → cell death
41
Aminoglycosides MOA
Bactericidal
Binds 30S subunit = inhibition of protein synthesis + production of abnormal proteins
Gram - aerobic
42
AEs of aminoglycosides
Ototoxicity - drug accumulation occurs in inner ears
Make sure trough levels are low enough so drug diffuses out
First sign = tinnitus or HA
Irreversible
Nephrotoxicity - drug is taken up by tubular cells
Correlates with high trough levels also
s/s = ATN, proteinuria, casts, dilute UOP, BUN/cr elevation
Risks: elderly, CKD, other nephrotoxic drugs
Usually reversible
43
tetracycline MOA
Gram + and gram - = broad spectrum
Binds 30S subunit of ribosome → tRNA to mRNA cannot occur → amino acids cannot be added
44
AEs of tetracyclines
GI irritation
Bind Ca++ in developing teeth → discoloration --> Avoid > 4th month gestation to 8 yr old****
Superinfection (d/t broad spectrum)
C. diff
Hepatotoxicity d/t fatty infiltration of liver
Biggest risk with preg/postpartum and CKD
Renal toxicity (caution w/ CKD)
Photosensitivity
45
macroslides MOA
Bind 50S ribosomal subunit → block addition of new amino acids to peptide chain → proteins can’t be synthesized
46
can you give macroslides during pregnancy
yes
47
fluoroquinolones MOA
Inhibits 2 enzymes (DNA gyrase & topoisomerase IV)
48
AE of Fluoroquinolones
GI effects
CNS effects - seizures
Phototoxicity
Tendon rupture - black box warning!
49
how to avoid development of resistance w/ TB
Always treat 2+ (up to 7) drugs
| Treat x6-24 months (longer for HIV patients)
50
TB drugs (4)
isoniazid*
Rifampin*
pyrazinamide*
ethambutol*
51
AEs of isoniazid, rifampin, pyrazinamide
hepatotoxicity
52
Major AE of ethambutol
Optic neuritis (most sig)
s/s = blurred vision, change in virtual field and color
Usually resolves, not always
Assess pre-tx and monthly, educate pts
53
Amphotericin B MOA
Binds fungal cell membrane → increased permeability & leakage of electrolytes → cell death
54
how long an amphotericin B be detected in body for
up to 1 year
55
AEs of amphotericin B
```
Infusion reactions (fever, chills, rigors)
Phlebitis
Nephrotoxicity (dose related)
hypoK+ (d/t kidney damage)
Bone marrow suppression
```
56
what drug to use for malaria
Chloroquine - use for erythocytic phase
57
can malaria be cured?
yes
58
drug for cytomegalovirus
ganciclovir
59
ganciclovir MOA
Converted to active form inside infected cells
Suppresses replication of viral DNA - inhibits DNA polymerase
Incorporates into viral DNA chain → chain termination
60
Ganciclovir AEs
Teratogenic
Bone marrow suppression (thrombocytopenia, granulocytopenia)
Usually reversible
Monitor blood counts (hold for ANC < 500 and plts < 25k)
61
general principles of drugs for HIV (4)
1. high/nearly universal rate of relapse if medications are stopped
2. Drug resistance is common due to rapid viral replication
3. Most components of ART/HAART are cyp450 inhibitors, increasing chance of drug-drug interactions
4. Expensive
62
3 drugs for Hep C.
PEG Interferon A
ribavirin
sofosbuvir
63
is ribavirin effective alone
No - need to take with PEG IFA
64
PEG IFA MOA
Binds to host receptors blocks viral entry into cells
| Blocks viral synthesis of mRNA and proteins
65
administration of PEG IFA
SQ weekly
66
AE of PEG IFA
- Flulike sx in 50% (decreases over time)
- Neuropsych effects (depression, SI)
- Organ dysfunction: thyroid, heart, bone marrow
67
MOA of sofosbuvir
- Nucleotide analog inhibitor
- Direct antiviral activity - blocks transcription of HCV RNA
- Effective against resistance - can be used with other agents if needed
- Can cure HCV in 12 weeks but expensive
68
methotrexate MOA (DMARD)
Folate antagonist
| Results in ↓ B and T cell production
69
AEs of methotrexate
Hepatic fibrosis
Bone marrow suppression
GI ulceration
Pneumonitis
70
when is methotrexate contraindicated
blood dyscrasias, immunodeficiency, liver disease, pregnancy
*Vaccine risks - decreased efficacy, infection risk w/ live vaccines
71
how to treat RA
NSAIDs - do not alter disease progression!
glucocorticoids
DMARDS
72
tx for gout
NSAIDs: to treat symptoms
Glucocorticoids: PO or IM in those who can’t use NSAIDs
Colchicine: anti inflammatory agent specific for gout
73
what is long term therapy for gout?
1. Inhibit uric acid formation (xanthine oxidase inhibitors)
2. Accelerate uric acid excretion (probenecid)
3. Convert uric acid to metabolite allantoin - renally excreted (pegloticase and rasburicase)
*all are not anti-inflammatory
74
MOA of xanthine oxidase inhibitors
Inhibition of XO (enzyme required for uric acid formation) → decreased uric acid levels, prevention of tophi formation
75
when can you use colchicine?
Short term use for gout flare up OR long term use to prevent attacks
76
MOA of colchicine
Unknown - might inhibit WBC infiltration via disruption of cellular microtubules
77
MOA of bisphosphonates
Structural analogs of pyrophosphate (normal constituent of bone)
Drugs is incorporated into bone and remains active for years
Decreases osteoclast activity → decreased bone resorption
78
Bisphosphonates: AE
Esophagitis - Avoid by taking w/ fully glass of water and remain upright x30-60 mins
```
Serious AE:
Ocular inflammation
Osteonecrosis of jaw
Atypical femur fractures
New onset a fibrillation
```
79
AE calcium salts (IV)
```
Highly irritating (avoid extravasation)
Give slowly, severe HTN w/ rapid injection
```
80
AEs of traditional chemo
```
Bone marrow suppression
GI tract damage
N/V
Alopecia
Infertility, teratogenic effects
Urinary stones (uric acid crystals)
Extravasation: local injury- worry about IV moving out of vein --Refers to escape of a chemotherapy drug into extravascular space - leakage from a vessel or by direct infiltration
promo of secondary cancer
```
81
Anthracyclines (doxorubicin) AE
-Cardiac toxicity: may be more sensitive to cardiac depressive side effects of medications even if normal resting echo
free radical production causes myocardial damage
-bone marrow suppression
-red/orange color urine and sweat
82
anthracyclines (doxorubicin) AE: acute cardiac toxicity
acute (10%): tachycardia, arrhythmia, transient and rare
ECG changes and acute EF reduction
usually lasts < 1-2 months
83
anthracyclines (doxorubicin): AE: chronic cardiac toxicity
(2% w/ 60% fatality): severe cardiomyopathy/CHF
related to cumulative dose
protective therapies: dexrazoxane (prevents free radical formation), ACE inhibitors
84
non-anthracyclines (bleomycin) AE
- pulmonary toxicity
- -skin reactions
- hypersensitivity in lymphoma pts → fever, chlls, confusion, hypotension and wheezing (use test dose first)
- myelosuppression rarely seen
85
nonanthracyclines (belomycine) pulmonary toxicity AE
Lungs take up high concentrations of drug and lack hydrolase enzyme to inactivate bleomycin
↑ risk / ↑ cumulative dosing, age, chest radiation, pulmonary co-morbidity, o2 exposure, other chemo drugs, genetics
*d/c w/ signs of dry cough, dyspnea, tachypnea, and infiltrates on CXR
*Can lead to pulmonary fibrosis → severe fibrosis → death
↓ diffusion capacity
*Keep FIO2 concentrations at or below 30% during anesthesia if possible
86
vincristine AE
little bone marrow suppression!
Peripheral neuropathy via damage to neurotubules in almost 100% of patients (sensory loss, weakness, autonomic dysfunction)
fatal if given intrathecally
87
chemo handling/admin guidelines
Drugs are mutagenic, carcinogenic and teratogenic
Protect yourself!
Handle with gloves
Do not break, crush or chew
Patient should use an effective form of birth control and shouldn’t breastfeed
88
methotrexate AE (cancer)
- pulmonary fibrosis (8%) and/or noncardiogenic pulmonary edema
- neutropenia and thrombocytopenia
- mucositis & GI ulceration
- renal toxicity (10%) - tx:alkalinize urine and hydrate
- Hepatic toxicity
89
coenzyme Q10 AE
AE: GI upset, elevated LFTs
No safe dose in pregnancy
May antagonize warfarin
90
what is coenzyme Q10 used for
Correct of deficiency
Mitochondrial disease
To decrease statin related myopathy (theoretical)
91
what is flaxseed used for
- Constipation
- high cholesterol: can ↓ LDL and total cholesterol; no effects on HDL or triglycerides
- menopausal sx
92
AE of flaxseed
GI effects
93
what are glucosamine and chondroitin used for
osteoarthritis (w/ mixed results)
94
AE.of glucosamine and chondroitin
Nausea
Heartburn
Possible increased bleeding risk
95
what is saw palmetto used for
Symptom relief with BPH (does not decrease size of prostate or affect PSA)
96
when to use saw palmetto w/ caution
with antiplatelets and anticoagulants due to antiplatelet effects and increased bleeding risk
97
which vitamins are fat soluble
A, D, E, K
98
What is minimum effective concentration?
How much dose is needed for drug to work
99
What electrolyte should be monitored when giving digoxin?
Calcium
100
What is unique about the therapeutic index of digoxin and lithium?
Narrow therapeutic index
101
Opioid agonists have a stronger (efficacy/potency) than opioid agonist-antagonist.
Efficacy
102
How is the starting dose for new medications determined?
ED50
103
What is the definition of a black box warning?
Strongest safety warning available
104
Which anti-seizure drug should not be given during pregnancy?
Valproate
105
What are characteristics of a molecule that can pass through the BBB?
small, lipid-soluble, transport system, nonpolar
106
What characteristics of neonates affect their medication dosing?
Neonates have immature BBB, kidneys, and CYP450 systems
107
What receptor is located at the neuromuscular junction of the somatic nervous system?
Nm (N1)
108
What receptor is located at all autonomic ganglion (PSNS and SNS)?
Nn (N2)
109
What receptor does epinephrine agonize that norepinephrine does not?
Beta 2
110
What effect does baroreceptors have on the heart rate during severe vasoconstriction?
reflex bradycardia
111
What drug is an A1 receptor agonist that causes reflex bradycardia?
Phenylephrine
112
Are A2 agonist drugs catecholamines?
No. They are NOT catecholamines, so they CAN cross the BBB, causing decreased CNS effects.
113
What are alpha antagonists primarily used for?
BPH and HTN
| Phenoxybenzamine (noncompetitive, causes reflex tachy and congestion)
114
What class of drug is isoproterenol?
B agonist, nonselective
115
What is the role of isoproterenol?
Chemical pacemaker
116
What are major AEs of alpha blockers?
orthostatic hypotension, reflex tachycardia
117
What are common AEs of beta blockers?
bradycardia, decrease contractility
118
What are contraindications for beta blockers?
heart block, severe asthma
119
What are the effects of atropine?
increased HR, decrease secretions, decreased peristalsis, tachycardia
will promote SNS
120
What class of drug is neostigmine?
Acetylcholinesterase inhibitor
121
What are contraindications for using acetylcholinesterase inhibitors?
obstructions, bradycardia
i.e. neostigmine
will cause increase in Ach build up --> increase GI motility
122
Where is erythropoietin produced?
Kidneys
123
What population do you NOT want to give erythropoietin to?
Ppl with HTN
124
What clotting factor affects Hemophilia A?
```
Factor VIII (8)
Use Desmopressin
```
125
High dose use of glucocorticoids to prevent transplant rejection can cause what?
neoplasms, high risk for infections
126
Is the onset and duration of action of glucocorticoids long or short?
long
127
Long term use of glucocorticoids have what AEs?
osteroporosis, hyperglycemia
128
Which class of histamine receptors can cross the BBB?
1st Gen.
| 2nd Gen does not cross BBB, does not cause sedation
129
What should histamine receptor drugs not be taken with?
CNS depressants (i.e. alcohol)
130
What is the lifespan of a platelet?
8 days
131
Which COX inhibitor has a black box warning?
Celecoxib, d/t increase in CV events
132
What drug class does Celecoxib fall under?
COX2 selective inhibitor
133
What is the antidote for Tylenol overdose?
acetylcysteine
134
Does Tylenol cause suppress platelet aggregation?
No silly. Tylenol does not suppress platelet aggregation.
135
What are the effects of long-term, high dose use of COX inhibitors?
ulcers, bleeding
136
What is the drug for T4?
Levothyroxine
137
What are the signs of hypothyroidism?
sensitive to cold, bradycardia, fatigue, weight gain
138
What are the signs of hyperthyroidism?
sensitive to heat, tachycardia
139
If TSH is high, what changes must be made to the medication dose?
TSH is high, T4/T3 is low --> need to give higher dose
140
If you have hyperthyroidism, what medication would you give?
PTU
141
If you have hypothyroidism, what medication would you give?
T4
142
What is the difference between vasopressin and desmopressin?
Vasopressin causes vasoconstriction. Desmopressin also used for Hemophilia A.
143
When would you prescribe progestin only OCs?
If pt has high risk of thromboembolic events, if pt is breastfeeding
144
What are CI for OCs?
```
Acute liver disease
Hypertension
CVA
PE
MI
Uterine bleeding with unknown cause
Breast/endometrial cancer
```
145
What are drugs to halt labor?
Terbutaline
Indomethacin
Nifedipine
Magnesium sulfate
146
What drug is used to develop fetal lung maturity?
Betamethasone
147
What drug is used for cervical ripening?
Prostaglandins
148
What conditions need to be met before giving pitocin?
Cervical ripening is complete, and baby’s lungs have to be mature
149
What drugs are given for PP hemorrhage?
Pitocin
Hemabate (not to someone with asthma)
Methergine (not for ppl with HTN)
Cytotec (given PR)
150
What drug is PDE5 contraindicated with?
Nitroglycerin
151
What route of testosterone replacement therapy are hepatotoxic?
PO
152
What are the ultrashort acting insulin drugs?
apart, lispro, glulisine
153
What are the routes of administration for insulin?
SQ, IV
154
What is the name of the short acting insulin?
Regular insulin
155
Which insulin has a DOA of 4 hours and is considered intermediate acting?
NPH
156
Which insulin has no peak and lasts for 24 hours?
Glargine
157
Which oral anti-diabetic drugs have hypoglycemic risks?
Sulfonylureas (three Gs) and meglitinides
158
What are the AEs of HMG-CoA inhibitors?
rhabdo, myopathies
159
What is the best time to take HMG-CoA inhibitors?
At night
160
What lab values should be monitored when taking statins?
Creatinine kinase serum
161
What drug class lowers VLDLs rather than LDLs?
Fibrates
162
What clotting factors does Vitamin K affect?
2, 7, 9, 10
163
What lab value needs to be monitored when giving warfarin?
PT-INR
164
What are AEs caused by heparin infusions?
Bleed risk, heparin induced thrombocytopenia (watch for drop in platelets)
165
What are the four types of diuretics?
osmotic, loop, thiazides, potassium-sparing
166
What type of diuretic is mannitol?
Osmotic, usually for volume overload
167
What are the AEs of loop diuretics?
Hypokalemia, hyponatremia (all goes down), ototoxicity, HTN, dehydration
168
In the event of edema, what type of fluid would be infused?
hypertonic
169
In the event of ketoacidosis or hyperglycemia, what type of fluid would you infuse?
hypotonic
170
Out of all the RAAS drugs, which has the greatest amount of mortality/morbidity improvement?
ACE inhibitors
171
What kind of drugs are the "prils?"
ACE inhibitors
172
What kind of drugs are the "sartans?"
ARBs
173
If your patient develops a dry cough with ACE inhibitors, what do you do?
prescribe them ARBs instead
174
What are AEs of ACE inhibitors?
dry cough, angioedema, hyperkalemia
175
What are standard practices when taking nitroglycerin daily?
Change site
Wash hands immediately
Drug free time (take it off at night)
Don't take with PDE5
176
Absorption
drug’s movement from site of administration into the blood
177
What factors affect absorption?
```
Rate of dissolution
Surface area (i.e. how big a transdermal patch is)
Lipid solubility
Route Administration
Blood flow
```
178
what impacts PO meds
Increased or slower motility time
Gastric acids
Other foods, medications, empty stomach
179
Small vd
drug is mostly in vasculature → it is not widely distributed!
180
Large vd
drug is distributed outside of the vasculature
181
what impacts vd?
```
CO
Perfusion of tissues
Capillary system
Polarity of drug molecules - can they move through membranes
Protein binding
```
182
BBB
can make it hard to treat CNS pathologies
Made up of tight junctions and PGP
Drugs need to be Lipid soluble, non polar, has transport system
Catecholamines can’t cross
PGP works against us
183
If protein levels are too low...
it can lead to drug toxicity
184
cyp450 Inducers
increase enzyme concentration → increase drug metabolism → decrease therapeutic response of all drugs in the body
185
cyp450 inhibitors
decrease enzyme concentration → decrease drug metabolism → increases drug effects, risk for toxicity
I.e. grapefruit juice
186
Zero order kinetics
same amount of drug will be metabolized/hour no matter how much drug is present
*similar to alcohol
187
First order kinetics
% of drug metabolized depends on the dose - a larger dose will have a larger amount metabolized
*most drugs
188
older adults have...
increased body fat, decreased skeletal muscle mass, decreased renal blood flow
189
MEC
plasma drug level below which therapeutic effects will not occur
First dose is usually here
190
toxic concentration
plasma levels at which toxic effects begin
191
TI
b/w MEC and toxic concentration
Usually takes 4 half lives to get here
If we don't have time → bolus dose
192
Affinity (potency)
how much drug must be administered to elicit a desired response
193
Intrinsic activity (efficacy)
intensity of effect that the drug produces
194
criteria to cross placenta
```
Lipid soluble
Unionized
Not protein bound
Non polar
small
```
195
how to dose for pediatrics
by weight
Peds have greater variability in response
In very young - immature organ system
196
neonates and infants: BBB
is not fully developed
| Less Exclusion of drugs from CNS by BBB → risk of CNS effects
197
neonates and infants: hepatic drug metabolism
immature CYP450 → decreased metabolism→ increased drug accumulation
198
neonates and infants: renal drug excretion
low renal blood flow, GFR and active tubular secretion → reduced excretion
199
most common cause of ADRs in older adults?
Decreased renal blood flow, decreased GFR, decreased tubular section, decreased # of nephrons
200
what receptor does NE not agonize
B2 so NE won't cause hyperglycemia (d/t no glycogenolysis) and doesn't cause calcium release from muscles
201
baroreceptor reflex: when BP falls...
vasoconstriction and increase CO
202
baroreceptor reflex: when BP is too high
vasodilation + decreased CO
203
phenylephrine
a1 agonist
| leads to severe vasoconstriction
204
indirect agonists
drug doesn’t do it itself
| examples: increases NT concentration release from presynaptic, Blocks NE reuptake, Block NE breakdown (MAO)
205
which receptors does epi agonize
A1, a2, b1, b2
206
epi effects
- increased HR, contractility, AV node conduction rate (b1)
- vasoconstriction (a1) + vasodilation (a2, b2) → leads to increase in systolic BP
- other fight or flight effects!
207
indications for epi
- Anaphylactic shock
- bronchoconstriction from asthma
- cardiac arrest
208
cautions for epi
- Hypertensive crisis → dramatic increase in BP because of vasoconstriction
- Dysrhythmias
- Angina pectoris
- Necrosis after extravasation
- Hyperglycemia
209
AE of norepi
- Tachydysrhythmias - reflex brady and then increased HR so it doesn’t go too out of wack
- Angina
- Hypertension
- Local necrosis upon extravasation
- metabolic acidosis
210
what are the effects of agonizing alpha 2 receptors
- Suppresses firing of sympathetic nerves to the heart → can cause bradycardia and a decrease in CO
- Promotes vasodilation
- Decrease BP
211
effects of alpha antagonists
vascular vasodilation
212
AE of alpha antagonists
```
orthostatic hypotension
Reflex tachycardia
Nasal congestion
Inhibition of ejaculation
Decreased renal blood flow
```
213
what type of drug is phenoxybenzamine
alpha antagonist
214
phenoxybenzamine effect and indications
very long acting - permanently bindings
| indicated for: Long term HTN crisis - pheochromocytoma, BPH
215
location and effects of beta 1 receptors
Heart → contractility, increased HR, increased AV node conduction velocity
*does not vasodilate or constrict
Kidneys → stimulation of renin release
216
beta 2 receptors location and effects
Smooth muscle in the uterus, bronchioles, GI, GU, vascular system
Bronchodilation
Decreased uterine contractions
Vasodilation of the coronary arteries
GI/GU motility
Skeletal muscle → increased contraction, speed, glycogenolysis, tremor, increased K+uptake
Liver → glycogenolysis
217
beta agonists
isoproterenol
dobutamine
terbutaline
albuterol
218
isorproterenol effect
“Chemical pacemaker”
- increased HR
- increased contractility
- bronchodilation
219
beta antagonists effects
```
Cardiac - decrease HR/contractility
Bronchospasm
Vasoconstriction in skeletal muscles
Decreased renin release → decreases BP
Decreases K+ uptake → hyperkalemia = risk
Decreased glycogenolysis
```
220
CIs for beta blockers
```
Preexisting AV block or cardiac failure
Severe asthma
Reactive airway disease
Uncontrolled diabetes
Hypovolemia
```
221
when to use atropine?
- bradycardia
- reduce frequency of bowel movements
- reverse muscarinic poisoning
- can treat peptic ulcer disease
- asthma (rarely used because it could dry and thicken secretions)
222
effects of atropine
- increased HR
- decreased secretions
- bronchodilation
- mydriasis
- cycloplegia (paralysis of ciliary muscle)
223
when is pyridostigmine indicated
- glaucoma
- myasthenia gravis
- NMB reversal
224
pyridostigmine MOA
Pyridostigmine binds to cholinesterase → takes a while → less available to break down Ach → more Ach is available
225
how do you treat hemophilia A pts?
desmopressin --> Releases stored factor VIII from vascular endothelium
226
what is epoetin alfa and how is it administered?
EPO
| administered IV or SQ
227
glucocorticoid MOA
Diffuse into the cell → bind to receptor steroid complexes in the cytoplasm → migrates to nucleus and binds to to DNA → results in alteration of mRNA transcription → modulate production of regulatory proteins
*this is a slower process → DOA is long too
228
short acting glucocorticoids
8-12 hours
| cortisone, hydrocortisone
229
medium acting glucocorticoids
18-36 hours
| prednisone, triamcinolone
230
long acting glucocorticoids
36-54 hours
| dexamethasone (no sodium retaining potency!)
231
when do adverse effects of glucocorticoids happen
at higher pharmacologic doses
232
AEs of glucocorticoids at higher doses
```
anti inflammatory --> risk for infection
adrenal insufficiency
osteoporosis
hyperglycemia
growth delay in children
fluid/electrolyte disturbances (mineralcorticoids)
neoplasms w/ really high doses
```
233
stress dosing
adrenal cortex can’t muster up necessary extra glucocorticoid secretion d/t long term suppression
Might need extra dose with trauma, surgery and other stressors on the body
234
risks associated with immunosuppressants
infection and neoplasms
235
which H1 antagonists cross the BBB
first generation = small and highly lipid soluble
236
H1 antagonists
Diphenhydramine (benadryl)
| Promethazine (phenergan)
237
second generation H1 antagonists
large, polar
| Fexofenadine (allegra)
238
harmful effects of inhibiting Cox 1
Gastric erosion and ulceration - decreased prostaglandins → decreased vasodilation
Bleeding tendencies (decreases platelet aggregation)
Renal impairment - decreased prostaglandins → decreased vasodilation → decreased RBF
239
beneficial effects of cox1 inhibition
Protection against MI and stroke secondary to reduced platelet aggregation
240
beneficial effects of inhibiting cox 2
Suppression of inflammation
Alleviation of pain
Reduction of fever
Protection against colorectal cancer
241
harmful effects of inhibiting cox 2
Promotion of MI and stroke secondary to suppressing vasodilation
Renal impairment
242
nonselective COX inhibitor prototype
aspirin
243
second generation cox 2 selective inhibitor
celecoxib
244
AE of celecoxib
*does not inhibit cox 1 platelet aggregation → does not provide CV benefits like aspirin does → black box warning
GI ulceration - should be low b/c cox 1 produces protective gastric mucosa
Renal impairment
245
acetaminophen
cox 2 inhibitor
246
what effects does acetaminophen have
not anti-inflammatory
Inhibition is limited to the CNS - cox 2
Reduces prostaglandin in the CNS to reduce fever and pain
247
antidote to acetaminophen?
acetylcysteine
| 100% effective if given within 8-10 hours of overdose
248
hypothyroidism: TSH and T3 T4 levels
TSH↑
| T3T4↓
249
hyperthyroidism: TSH and T3T4 levels
TSH ↓
| T3t4↑
250
MOA of levothyroxine
synthetic T4
| long 1/2 life - can take 1 month to plateau
251
which hyperthryoidism drug is preferred in the first trimester
Propylthiouracil (PTU) (thioamide)
| less placental crossing
252
absolute CIs for hormone therapy or OCs (7)
```
Pregnancy
Breast or endometrial CA
Acute liver disease
Uncontrolled HTN
Thrombosis
Undiagnosed vaginal bleeding
Acute DVT
```
253
minipills
progestin only
Less effective
Change the cervical secretion/mucus
Recommended for new moms because they do not go into breastmilk
254
when can oxytocin be used
can only be used if cervix is ripe and fetal lungs are mature
IV infusion only
255
4 drugs for postpartum hemorrhage
Oxytocin (pitocin)
Misoprostol (PG) (cytotec)
Carboprost tromethamine (PG) (hemabate)
ergot alkaloids (Methylergonovine) (Methergine)
256
how is testosterone prepared
PO (both are 17 alpha = hepatotoxic)
Transdermal - can be transferred w/ skin to skin contact! - more consistent level
Nasal gel
Implantable pellets - 3-6 months
Buccal tablets
IM (T cypionate and T enanthate) - long acting - more consistent level
257
MOA of tamulosin
alpha 1 antagonist
- relaxes smooth muscle in bladder neck and prostate capsule to decrease dynamic obstruction
- does not decrease PSA
258
which drugs target mechanical obstruction of BPH
5 alpha reductase inhibitors
- finteraride
- dutasteride (longer ½ life)
decreases serum PSA
259
can insulin be given PO or IM?
no
260
which 2 diabetes drugs cause weight gain and hypoglycemia
Sulfonylureas (3Gs!)
- glimepiride
- glipizide
- glyburide
Meglitinides (Glinides)
- nateglinide (shorter acting)
- repaglinide
both need a working pancreas to release insulin!!
261
what drugs work best for lowering LDL?
first, Monoclonal antibody PCSK9 inhibitors
second, HMG COA inhibitors (statins)
262
AEs of statins
- myopathies (aches, tenderness, weakness) → can lead to CK + K+ increase which can lead to renal injury
* should measure CK at start
- rhabdo = skeletal muscle breakdown
- hepatotoxicity
263
fibric acid derivatives: MOA
Inhibit hepatic extraction of free fatty acids so the liver cannot synthesize as many TGs
lowervs VLDL by 40-55%
264
heparin MOA
- suppress thrombin and factor Xa
- hepatic metabolism/renal excretion
- cannot cross the placenta
- ½ life =1.5 hours
- large and polar
265
AEs of heparin
hemorrhage
- spinal/epidural hematoma with LP/epidural anesthesia
- HIT → drop in platelets will be the sign
- hypersensitivity reactions
266
heparin antidote
protamine sulfate
267
what factors does warfarin impact
decreases production of factors II, VII, IX, X to decrease fibrin production
*doesn’t impact existing factors
268
does warfarin cross the placenta and breastmilk
yes - CI in pregnancy
269
Direct Xa Inhibitor
Rivaroxaban
270
rivaroxaban MOA
- selective binding and inhibition of factor Xa → decreased production of thrombin → inhibition of fibrin mesh
- rapid onset
- PO
- CYP450
271
HIT
potentially fatal immune mediated disorder characterized by reduced platelet counts and paradoxical increase in thrombotic events
Development of antibodies against heparin platelet protein complexes
Antibodies activate platelets and damage endothelium → promote thrombosis and loss of circulating platelets
Can lead to DVT, PE, MI
272
abciximab
GP IIb/IIIa Receptor antagonist --> block IIb/IIIa receptors on platelets → inhibit the final step in platelet aggregation from all factors
273
MOA of alteplase
binds with plasminogen to form an active complex → catalyzes the conversion of other plasminogen molecules into plasmin = enzyme that digests the fibrin network of clots + degrades fibrinogen and other clotting factors
1/2 life = 5 minutes
274
indications for alteplase
Remove thrombi that ALREADY exist
Acute MI
Acute ischemic stroke
Acute massive PE
Not for hemorrhagic stroke
275
how to decrease risk of acute bleeding episodes
Minimizing physical manipulation of patient
Avoid SQ or IM injections
Minimize invasive procedures
Minimized concurrent use of anticoags
Minimize concurrent use of antiplatelet drugs
Fall risk
Can’t give after epidural → risk for spinal cord hemorrhage
276
which diuretic causes the most diuresis
loop diuretics (ex: furosemide)
277
AE of loop diuretics
Hyponatremia, Hypochloremia
Dehydration
Hypokalemia
ototoxicity
278
where do thiazide diuretics act
Blocks NaCl & K+ reabsorption in early DCT so blocks water absorption
279
AE of thiazide diuretics
-Hyponatremia, Hypochloremia
Dehydration
-Hypokalemia
-increase in uric acid levels
280
where do potassium sparing diuretics work
Act on late DCT and collecting ducts
| *least amount of diuresis
281
MOA for spironolactone
Blocks aldosterone which stops production of Na+/K+ exchange protein
K+ retention, Na+/H2O excretion
282
MOA for non aldosterone antagonists
Directly inhibits Na+/K+ exchange in DCT
| Leads to K+ retention, Na+/H2O excretion
283
when are osmotic diuretics used
Only used in certain situations like severely increased ICP or Intraocular pressure
284
AEs/cautions of mannitol (osmotic diuretic)
Edema since it can exist capillary beds (not BBB)
| Caution with HF and pulmonary edema risk
285
how should IV potassium be given
diluted and infused slowly (10 mEq/hour)
286
which drugs prevent CV remodeling the best
ACE inhibitors
| first line of defense = the strongest
287
AEs of the ACE inhibitors
```
First dose hypotension
Dry Cough
Hyper K+ b/c aldosterone is inhibited
Toxic to fetus
Renal failure
```
Rare:Angioedema, Neutropenia
288
MOA of ARBs
block effects of ang II at receptor
289
why do ACE inhibitors cause coughing?
ACE is also called Kinase II in some cells → by blocking Kinase II → build up of bradykinin → vasodilation, cough, angioedema (side effects)
290
MOA of aliskiren
inhibit release of renin → block entire RAAS
291
where do dihydropyridines (nifedipine) act?
on vascular smooth muscle leading to
arteriole vasodilation → decreases afterload, lowers arterial pressure
-reflex tachycardia/contractility increase
292
where do nondihyrdopyridines act and what is the effect
vascular smooth muscle and heart leading to:
- arteriole vasodilation
- ↓ HR, ↓ AV node conductivity, ↓ contractility
- decrease afterload, increase coronary perfusion
293
2 nondihyrdopyridines
- verapamil
| - diltiazem
294
which vasodilator acts on the arterioles
hydralazine
| will lead to reflex tachy and contractility
295
venous dilator
nitroglycerin
296
if you have active chest pain...
- take sublingual tab asap
- if there is no relief after 5 mins → call 911
- 3 doses in 15 minutes
- don’t chew or swallow
297
what is contraindicated with nitroglycerin
PDE5 (ED drug) inhibit cGMP breakdown - also results in vascular smooth muscle relaxation → orthostatic hypotension, major vasodilation
298
nitroglycerin patient instructions
* use lowest effective dose because tolerance can develop rapidly
* at least 8 drug free hours a day - at night
* avoid abrupt withdrawl to avoid coronary vasospasm
299
MOA of digoxin
- selectively inhibits Na+/K+/ATPase pump
- Build up Ca++ intracellularly (increased actin/myosin interactions) → increases contractility (inotropy) → increased workload
300
class I antiarrhythmic drugs
Na+ channel blockers
301
class II Antiarrhythmic drugs
Beta blockers
302
class III Antiarrhythmic drugs
K+ channel blockers
303
class IV Antiarrhythmic drugs
Ca++ channel blockers
304
how do beta blockers affect the heart
Block binding of epi and norepi in nodal and non nodal tissue
Decrease SA node automaticity
Inhibit AV response by prolonging refractory period and slowing conduction
decreased myocardial contractility
305
AEs of beta blockers
bradycardia, hypotension, fatigue
306
how to CCBs affect the heart
Decrease APs generate by SA node and can block AV nod, decrease HR, and block calcium entry into myocardial cells to decrease contractility
act mainly on AV node
307
AEs of CCBs
bradycardia
| decreased contractility
308
amiodarone
K+ channel blocker
| used emergently for someone in v tach
309
amiodarone AE
Torsades
Long term use: need to look out for:
Liver toxicity
Pulmonary toxicity
Thyroid toxicity
310
do CCBs and beta blockers have the same effect on the heart?
yes
311
MOA of adenosine
Binds to A1 receptors → activates opening of K+ channels → hyperpolarization, inhibition of pacemaker cells
half life = 10 seconds
312
What drug class is indomethacin and what is it used for?
COX inhibitor, tocolytic
313
What are the two classes of calcium channel blockers?
Nondihydropyridines (verapamil and diltiazem)
| Dihydropyridines (nifedipine)
314
What drug class does nifedipine fall under?
Dihydropyridines (calcium channel blocker)
315
What are the classes of RAAS drugs?
ACEs (prils)
ARBs (sartans)
Direct Renin Inhibitors (DRIs; aliskiren)
Aldosterone antagonists (spironolactone, eplerenone)
316
What are the effects of dihydropyridines?
- Decreased afterload
- Decreased coronary artery vasoconstriction
- Reflex tachycardia & increased contractility
317
What are the effects of nondihydropyridines?
- Decreased afterload & increased coronary perfusion
- Decreased HR (SA node) decreased nodal conduction (AV node)
- Decreased myocardial contractility
318
What is the main AEs of concern with vasodilation of venous vessels?
orthostatic hypotension
319
What is the main AEs of concern with vasodilation of arterial vessels?
Reflex tachycardia
320
Does hydralazine vasodilate arteries or veins?
Direct arteriole vasodilation, causes reflex tachycardia and contractility
321
What is the drug of choice for HTN emergencies?
Sodium nitroprusside (venous and arteriolar vasodilator)
322
Does nitroglycerine vasodilate venous or arteriole vessels?
Venous vasodilation
323
What is the indication for nitroglycerin?
Angina (active chest pain):
- Administer sublingual asap
- No relief after 5mins: call 911
- Take up to 3 doses Q5mins
324
What is the MOA of digoxin?
Mechanism: selectively inhibits Na+/K+/ATPase pump
- Build up of Ca++ intracellularly (increased actin/myosin interactions)
- Increased contractility
325
What is digoxin's electrical effects on the heart?
- Decreased SA node automaticity
- Decreased AV node conduction velocity & increased refractory period
- Increased automaticity in Purkinje Fibers (can lead to ectopic foci --> ventricular dysrhythmias)
326
What are the classes of antidysrhythmics?
Class I: Na+ channel blockers (Phenytoin, lidocaine)
Class II: beta blockers (propanolol, esmolol)
Class III: K+ channel blockers (amiodarone)
Class IV: Ca+ channel blockers (verapamil, diltiazem)
327
What are AEs of beta blockers as antiarrhythmic drugs?
bradycardia, hypotension, fatigue
328
Which antiarrhythmic drug has "torsades" as an AE?
Class III: K+ channel blocker (amiodarone)
329
What should be monitored when giving Class III channel blockers?
Blocking K+ channels, can lead to prolonged QT interval.
AE: torsades
330
What are AEs of class IV antiarrhythmics?
bradycardia, decreased contractility
331
What are CIs of class IV antiarrhythmics?
high grade heart blocks, heart failure
332
What is the route of administration and half life of adenosine?
IV, 10 seconds
333
What are the CIs of adenosine?
high-grade heart blocks
334
What are the AEs of digoxin?
AEs: arrhythmias, AV block, toxicity (Digibind)
335
Between esters and amides, which has higher allergic reaction rates?
esters
336
How are esters and amides metabolized?
Esters are metabolized by plasma esterases.
| Amides are metabolized by hepatic enzymes.
337
What is Methemoglobinemia?
AE from topical benzocaine.
- Converts Hgb --> metHgb (form that cannot release O2 to tissues).
- Most common in <2yrs (contraindicated)
338
What are drug examples of esters?
Cocaine
Chloroprocaine
Benzocaine
339
What class of drug is lidocaine?
Amide
340
Is there cross sensitivity between esters and amides? What does this mean?
No, there is no cross sensitivity. If you're allergic to esters, you can give amides instead.
341
What is a rare but fatal reaction of inhaled anesthetics?
Malignant hyperthermia
342
What is the MOA of most IV anesthetics?
+GABA transmission
Barbiturates, benzodiazepines, propofol, etomidate
343
What are the CNS effects of local anesthetics?
CNS excitation (seizures) --> CNS depression (coma, sedation, death)
344
What are the CV effects of local anesthetics?
Na+ block = decreased myocardial excitability
- bradycardia, heart block, decreased contractility, cardiac arrest
- vasodilation
345
What are the AEs of propofol?
Hypotension, bradycardia, respiratory depression, no muscle paralysis, CNS depression
346
What are s/s of propofol infusion syndrome?
- Metabolic acidosis
- Cardiac failure
- Renal failure
- Rhabdomyolysis
- Can be fatal
347
What should be monitored during propofol infusion syndrome?
CPK (marker of muscle injury)
348
Opioid tolerance develops to all effects except which ones?
Constipation and miosis
349
What drug is used to reverse the effects of opioids?
Naloxone (Narcan)
| ***reversal of opioid OD
350
What is the purpose of Naltrexone?
Block euphoric effects of opioids
351
What should be monitored when giving methadone?
AE: prolongation of QTc --> torsades
| - EKG prior to administration
352
Which strong opioid creates a toxic metabolite with metabolism?
Meperidine
353
Because meperidine creates a toxic metabolite when metabolized, what is the standard practice when prescribing this drug?
Keep use <48 hours
| Keep dose < 600mg/24hrs
354
In the liver, what is codeine converted to?
10% of dose is converted to morphine in liver
355
What is unique about codeine?
10% of dose is converted to morphine in liver
- Some people lack gene = cannot gain analgesic effects
- Some people are “ultrarapid metabolizers”
356
What is an AE of Buprenorphine?
Block kappa, partially agonize mu
| AE: Prolongs QTc
357
Which neurotransmitters are modulated in drugs for Parkinson's/AD/MS?
Dopamine and ACh
358
When administering Levadopa, what concurrent medication should you avoid?
MAO inhibitor (risk for severe HTN)
359
What is a key AE of Levodopa?
Dyskinesias
360
Which vaccines are live?
MMR, varicella, rotavirus, poliovirus (if oral)
361
Between benzodiazepines and barbiturates, which one has a ceiling effect on GABA?
Benzodiazepines only potentiate GABA.
| Barbiturates agonize GABA receptor directly, no ceiling effect to sedation/respiration depression.
362
What are differences between 1st and 2nd generation anti-psychotics?
1st gen: extrapyramidal symptoms, cheaper, more drug interaction d/t CYP450 metabolism
2nd gen: metabolic effects (weight gain, DM, dyslipidemia), risk for CV events, more expensive
363
What are the s/s of neuroleptic malignant syndrome?
rigidity, decrease bowel activity, normal pupils, gradual onset
364
What are the s/s of serotonin syndrome?
tremor, hyperreflexia, dilated pupils, hyperactive bowel activity, rapid onset
365
What class of drug does Chlorpromazaine belong to?
Conventional antipsychotics
Prolongs QT interval
AE = sedation, orthostatic hypotension, anticholinergic side effects
366
What class of drug does Haloperidol belong to?
Conventional antipsychotics
Prolongs QT interval, cheaper, EPS symptoms early
367
What is the SSRI prototype?
Fluoxetine
368
Between FGAs and SGAs, which is safer in pregnancy?
SGAs
369
What is the antidote for Tylenol?
acetylcysteine
370
What is the antidote for opioid reversal?
Naloxone (Narcan)
371
What class of drug does bupropion fall under?
Atypical antidepressant.
372
What are the uses of lithium?
Antiepileptic, bipolar disorder/mood stabilizer
373
What are other uses for valproate and carbamazepine, other than epilepsy?
Mood stabilizers, bipolar disorder
374
What are the classes of drugs used for depression?
```
SSRIs (Fluoxetine)
SNRIs (Venlafaxine)
TCAs (amitriptyline)
MAOIs (Nonselective, MAO-B selective)
Atypical antidepressants (Bupropion)
```
375
What depression drug classes should you avoid tyramine-rich foods?
MAOs and TCAs
376
How does tyramine and MAOIs lead to excessive NE?
MAO-A --> decreased NE breakdown
High concentration of NE in nerve terminals
Tyramine stimulates NE release
Excessive NE occurs
s/s = severe HA, tachycardia, HTN, N/V
377
What are effects of lithium toxicity?
Tremor, vision changes, agitation, slurred speech, thirst, polyuria (bc block of ADH), renal toxicity (monitor BUN/Cr)
378
How does hypernatremia affect lithium administration?
Decreases lithium in the body, causing subtherapeutic effects
379
Which vaccines are given PO?
Poliovirus (if given live, attenuated)
| Rotovirus
380
What two drugs augment levodopa
Carbidopa (decarboyxlase inhibitors)
| Entacopone (COMT inhibitor)
381
What are the AEs of Phenytoin?
- CNS = sedation, nystagmus, ataxia, diplopia
- Gingival hyperplasia = swelling, tenderness, bleeding
- Dermatologic effects = measles-like rash or worse (SJS, TEN)
- Teratogenic
- CV = dysrhythmias & hypotension w/ IV injection --> DILUTE, INFUSE SLOWLY
- Necrosis w/ IV extravasation
382
What schedule is ketamine
III
383
Benzo antidote
Flumazenil
384
What schedule is most benzodiazepines?
IV
385
What is the main difference between 1st and 2nd generation anti-psychotics?
1st: extrapyrimidal symptoms
2nd:
386
What is notable about varenicline?
Most effective for secession of nicotine.
387
Which anti-depressant class have cardiotoxicity as an AE?
TCAs
388
What drug classes should you avoid with MAOs?
TCAs, Levodopa
389
What drug do you use for anxiety?
Buspirone
390
What are the three classes of bronchodilators?
beta2 agonists, methylxanthines, anticholinergics
391
What is notable about inhaled bronchodilators?
Local, no systemic effects (Quantrenarymonium)
392
What drug is most effective for acute bronchospasms?
Short acting beta agonist (albuterol)
393
What are the names of the long acting beta2 agonists?
- Salmeterol
| - Formoterol
394
What class of drug is theophylline?
Methylxanthines, used for bronchodilation and ADHD
Low TI, variable metabolism
395
What are drug examples of short and long acting anticholinergic drugs?
Short acting: ipratropium
| Long acting: tiotropium
396
What are three ways glucocorticoids suppress inflammation?
Decrease inflammatory mediators, decrease edema of airway mucosa, decrease infiltration of inflammatory cell
397
What drug is used for allergic rhinitis?
Intranasal phenylephrine (Decrease nasal congestion via nasal vasoconstriction)
398
Which anti-inflammatory drug is safest?
Cromolyn, has rare AEs
| MOA: stabilizes membrane of mass cells to decrease histamine release
399
What is the MOA of glaucoma drugs?
- Alpha2 agonists: decrease aqueous humor
- Beta blockers: decrease aqueous humor
- Carbonic anhydrase inhibitors: decrease aqueous humor
- Prostaglandin analogues: increases outflow of aqueous humor
400
What are the four classes of glaucoma drugs?
- Beta blockers: timolol
- Prostaglandin analogues: latanoprost
- Alpha2 agonists: brimonidine
- Carbonic anhydrase inhibitors: dorzolamide
401
What are the AEs of glucocorticoids when used topically?
AE: local reactions, thinning of skin with long -term use (increased with higher potency, dressing, large area)
402
What are the AEs of keratolytics when used topically?
i.e. salicylic acid
| AE: rarely, toxicity with long -term, high-dose use
403
What are the AEs of Azelaic acid?
itching, burning, pigment reduction
404
What are the AEs of topical antibiotics?
i.e. benzoyl peroxide
| AE: peeling, drying
405
For ezcema, what are the first and second line treatments?
First line: Moisturizers, Topical glucocorticoids
| Second line: Topical immunosuppressants: tacrolimus (AE: erythema, pruritis)
406
What are the defensive factors against peptic ulcer disease?
Mucous, bicarbonate, prostaglandins, blood flow
407
What drugs decrease the aggressive factors of peptic ulcer disease?
PPIs, H2RAs, antacids, antibiotics
408
What drugs increase the defensive factors of peptic ulcer disease?
Misoprostol, Suprolafate
409
What are the concerns with decreasing aggressive factors?
Increase gastric pH causing bacterial growth, absorption affected, delayed gastric emptying time
410
What is notable about famotidine?
Large volume of distribution, can cross BBB
411
What are the two classes of antisecretory agents?
Histamine 2 receptor blockers, proton pump inhibitors
412
What population do you not use misoprostol in?
Pregnant
413
What are the 5 classes of laxatives?
Bulk forming laxatives, surfactant laxatives, stimulant laxatives, osmotic laxatives, selective mu antagonist
414
What class of drug has the fastest effect on constipation?
Stimulant laxatives (castor oil)
415
What is a risk with all laxatives?
Dehydration
416
What class of drug does docusate fall under?
Surfactant laxatives
417
What class of drug does Senna fall under?
Stimulant laxatives
418
Which pathway does ondansetron affect?
CTZ pathway
419
What neurotransmitter does Haloperidol antagonize?
Dopamine —> CTZ pathway
420
Which antiemetics affect the CTZ pathway?
Serotonin antagonists
Substance P/neurokinin 1 antagonists
Dopamine antagonists
421
How is amphotericin B given
IV only
422
what kind of drug is allopurinol
xanthine oxidase inhibitor
423
what drug is used for hyperparathyroidism
Cinacalcet
