Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pulmonary > Pulmonary Pharmacology Hit List > Flashcards

Pulmonary Pharmacology Hit List Flashcards

1
Q

Asthma & COPD
Epinephrine
Class

A

Bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Asthma & COPD
Epinephrine
Mechanism

A

Adrenergic agonists – Non-specific
Increase cAMP, some inhibitory effect on mast cells, some inhibitory effect on microvascular permeability, promote a small degree of mucociliary transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Asthma & COPD
Epinephrine
Route/Time

A

30-90 min duration; mist form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Asthma & COPD
Epinephrine
Adverse Rxns:

A

N/V, headache, fall in BP, increase HR, cardiac arrhythmias, PaO2 may decrease, CNS toxicities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Asthma & COPD
Albuterol
Class

A

Bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Asthma & COPD
Albuterol
Mechanism

A

Adrenergic agonists – B2 specific, quick onset, short acting.
Rescue medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Asthma & COPD
Albuterol
Route/Time

A

Quick onset, 3-6 hour duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Asthma & COPD
Salmeterol
Class

A

Bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Asthma & COPD
Salmeterol
Mechanism

A

Adrenergic agonists – B2 specific, slow onset, long-acting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Asthma & COPD
Salmeterol
Route/Time

A

Long-acting used in combination w/ corticosteroids

12+ hour duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Asthma & COPD
Formoterol
Class

A

Bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Asthma & COPD
Formoterol
Mechanism

A

Adrenergic agonists – B2 specific, slow onset, long-acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Asthma & COPD
Formoterol
Route/Time

A

Long-acting used in combination w/ corticosteroids

12+ hour duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Asthma & COPD
Ipratropium
Class

A

Bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Asthma & COPD
Ipratropium
Mechanism

A

Cholinergic Antagonists / Anti-muscarinics
Reduces airway constriction, decrease in mucous secretion, enhance B2 mediated dilation, can cause pupillary dilation and cycloplegia on contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Asthma & COPD
Theophylline
Class

A

Bronchodilators & Anti-Inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Asthma & COPD
Theophylline
Mechanism

A

Methlxanthines (related to caffeine)
Increases cAMP, blocks muscle adenosine receptors, causes bronchodilation, anti-inflammatory; increases CNS activity, increases gastric acid secretion, has a weak diuretic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Asthma & COPD
Theophylline
Adverse Rxns:
Dose: 5-10ug/m

A

5-10ug/ml can cause N/V, nervousness, headache, insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Asthma & COPD
Theophylline
Adverse Rxns:
Dose: greater than 20 ug/mL

A

Serum levels greater than 20 ug/mL cause vomiting, hypokalemia, hyperglycemia, tachycardia, cardiac arrhythmias, tremor, neuromuscular irritability, seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Asthma & COPD
Cromolyn sodium
Class

A

Anti-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Asthma & COPD
Cromolyn sodium
Mechanism

A

May alter the activity of chloride channels, inhibit degranulation of mast cells in the lung, inhibit inflammatory response by acting on eosinophils, inhibit cough by action on airway nerve, reduce bronchial hyperactivity associated w/ exercise and antigen-inhaled asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Asthma & COPD
Cromolyn sodium
Adverse Rxns:

A

Unpleasant taste, no systemic toxicity, irritation of trachea, rarely – chest pain, restlessness, hypotension, arrhythmias, NV, CNS depression, seizures, anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Asthma & COPD
Beclomethasone
Class

A

Corticosteroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Asthma & COPD
Prednisolone
Class

A

Corticosteroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Asthma & COPD
Monteleukast
Class

A

Leukotriene Receptor Blocker – Anti-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Asthma & COPD
Monteleukast
Mechanism

A

LTD4 activation  bronchial hyper-reactivity, bronchoconstriction, mucosal edema, increased mucus secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Asthma & COPD
Monteleukast
Effective in some patients

A

To reduce aspirin-related asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Asthma & COPD
Monteleukast
Adverse Rxns:

A

GIT, laryngitis, pharyngitis, nausea, otitis, sinusitis, viral infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Asthma & COPD
Monteleukast
Unusual Adverse Rxn:

A

Possible association w/ suicide ideation

High doses tumorigenic in rodents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Asthma & COPD
Zileuton
Class

A

Leukotriene Synthesis Blocker – Anti-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Asthma & COPD
Zileuton
Mechanism

A

Inhibits leukotriene formation, decreases smooth muscle contraction and blood vessel permeability, reduces leukocytes migration to damaged areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Asthma & COPD
Zileuton
Adverse Rxn:

A

Causes hepatic enzyme elevation – LFTs required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Asthma & COPD
Zileuton
Interactions:

A

CYP1A2 interaction w/ theophylline; evaluation for other inflammation-related diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Asthma & COPD
Omalizumab
Class

A

Anti-IgE antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Asthma & COPD
Omalizumab
Mechanism

A

Binds to IgE and prevents release of inflammatory mediators  decreases allergic response
Reduces the frequency & severity of asthma attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Cyclophosphamide
Class

A

Alkylating agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Cyclophosphamide
Mechanism

A

Produces B & T cell lymphopenia, suppression of B cell activity and decreased Ig secretion; associated with neutron- thrombocytopenia, bladder cancer, myeloproliferative malignancie s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Cyclophosphamide
Adverse Rxn:

A

Hemorrhagic cystitis is a frequent complication, but this is prevented by adequate fluid intake and mesna.
Can cause diarrhea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Ambrisentan
Class

A

Endothlin-1 Receptor Antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Ambrisentan
Mechanism

A

Blocks smooth muscle proliferation and pulmonary artery vasoconstriction by binding to endothliun-1 type A (smooth muscle) and type B (endothelial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Ambrisentan
Route

A

Orally active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Ambrisentan
Black Box Warning

A

Teratogenic (category X)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Beractant
Class

A

Exogenous surfactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Beractant
Mechanism/Target

A

Administered to preterm (<30 weeks) infants to reduce pulmonary surface tension; purified animal-derived products rich in surfactant proteins B, and C, neutral lipids, surface active PLs, and DPPC (primary surface active component)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Epoprostenol
Class

A

Prostanoid for PAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Epoprostenol
Mechanism

A

Prostanoids induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Epoprostenol
Route/Time

A

Half life of 3-5 minutes, requires continuous IV infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Epoprostenol
Dose limiting

A

Hypotension, muscle pains, headache, flushing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Tadalafil
Class

A

Phosphodieterase type 5 inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Tadalafil
Treatment

A

Tx of benign prostatic hypertension and erectile dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Tadalafil
Side effect

A

Headache is most common side effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Tadalafil
Time

A

Halflife 17 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Tadalafil
Unusual Adverse Rxn

A

Change in color vision due to non-arteritic anterior ischemic optic neuropathy (NAION)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Methotrexate
Class

A

Immunosuppressent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Methotrexate
Mechanism

A

DHFR inhibition, additional actions that increase adenosine-mediated immunosuppression (increase in cAMP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Methotrexate
Treatment

A

Tx for sarcoidosis (non-caseating granulomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Methotrexate
Significant side effects

A

– NOT a front-line therapy

High-dose intravenous methotrexate chemotherapy acute kidney failure and severe and life-threatening CNS toxicity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Iloprost
Class

A

Prostanoid for PAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Iloprost
Mechanism

A

Prostanoids induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Iloprost
Time

A

Halflife of 25 minutes, requires 6-9 inhaled doses/ day (10 min per dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Iloprost
Side effects

A

Cough, flushing, headache are common, hypotension, muscle cramps, bleeding, reports of hemoptysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Diltiazem
Class

A

Calcium Channel Blocker (CCB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Diltiazem
Mechanism

A

CCB – prevent membrane depolarization, block the key mediator of smooth muscle contraction allowing vasodilation to endure; not all patients respond to these drugs, some develop hemodynamic decompensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Diltiazem
Time/Route

A

Halflife 3-6 h, PO TID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Diltiazem
Side effects

A

CYP3A4

Bradycardia, headache, edema, hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Rituximab
Class

A

mAb against CD20 on B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Rituximab
Mechanism

A

mAb that binds CD20 on M cell precursors and mature B cells) Depletion lasts 6-9 months (depletion via 2 mechanisms: ACDC, complement mediated  MAC, induction of apoptosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Rituximab
Can cause

A

HTN, asthenia, pruritis, urticarial, rhinitis, arthralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Rituximab
Treatment

A

tx for Wegener’s granulomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Treprostinil
Class

A

Prostanoid for PAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Treprostinil
Mechanism

A

Prostanoids induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Treprostinil
Route/Time

A

Halflife of 4 hours, continuous SC or IV infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Treprostinil
Injection site rxns;

A

Headache, nausea, diarrhea, vasodilation, jaw pain,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Treprostinil
Monitor

A

monitor for bleeding, decreased clearance w/ gemfibrozil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Azathioprine
Class

A

Facilitates apoptosis of T cell populations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Azathioprine
Mechanism

A

DNA, RNA synthesis inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Azathioprine
Associated

A

associated w/ neoplastic, mutagenic, and leukopenic & thrombocytopenic toxicity; increases the risk of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Bosentan
Class

A

Endothlin-1 Receptor Antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Bosentan
Mechanism

A

Blocks smooth muscle proliferation and pulmonary artery vasoconstriction by binding to endothliun-1 type A (smooth muscle) and type B (endothelial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Bosentan
Route/Time

A

Orally active

5-8 hours; PO BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Bosentan
BBW/Side effects

A

Teratogenic (category X)
Liver and blood toxicities
Significantly elevated LFTs, anemia, naopharyngitis, interactions w/ CYP2C9 and 3A4 substrates; leading cause of drug-drug interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Amlodipine
Class

A

Calcium Channel Blockers (CCB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Amlodipine
Mechanism

A

CCB – prevent membrane depolarization, block the key mediator of smooth muscle contraction allowing vasodilation to endure;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Amlodipine
Time

A

Halflife 35-50 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Amlodipine
Adverse Rxn

A

Not all patients respond to these drugs, some develop hemodynamic decompensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Amlodipine
Side effects

A

CYP3A4

Edema, fatigue, hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Verapamil
Class

A

Calcium Channel Blockers (CCB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Verapamil
Mechanism

A

CCB – prevent membrane depolarization, block the key mediator of smooth muscle contraction allowing vasodilation to endure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Drugs for Restrictive Lung Diseases
& Pulmonary Artery Hypertension
Verapamil
Side effects

A

Headaches, facial flushing, dizziness, lightheadedness, swelling, increased urination, fatigue, nausea, ecchymosis, galactorrhea, and constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Diphenhydramine

Class

A

Antihistamines
1st generation
Antitussive
Ether/ Ethanolamine derivative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Diphenhydramine

Mechanism

A

Based on structure of histamine – short lived, multiple dosing, H1 blockade.
Antihistamine-H1 antagonist, suppresses cough by action on the respiratory center due to its anticholinergic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Diphenhydramine

Side effects

A

Side Effects – drowsiness, respiratory distress, blurred vision, dry mouth, urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Diphenhydramine

Time

A

Duration 4-6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Dimenhydrinate

Class

A

Antihistamines
1st generation
Ether/ Ethanolamine derivative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Dimenhydrinate

Mechanism

A

Based on structure of histamine – short lived, multiple dosing, H1 blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Dimenhydrinate

Side effects

A 
Highly sedative, anticholinergic side effects
Sedative 
Anticholinergic 
GI
Can potentiate nasal congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Dimenhydrinate

Time

A

Duration 4-6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Chlorpheniramine

Class

A

Antihistamines
1st generation
Alklamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Chlorpheniramine

Mechanism

A

Based on structure of histamine – short lived, multiple dosing, H1 blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Chlorpheniramine

Side effects

A 
Highly sedative, anticholinergic side effects
Sedative 
Anticholinergic 
GI
Can potentiate nasal congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Chlorpheniramine

Time

A

Duration 4-6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Hydroxyzine

Class

A

Antihistamines
1st generation
Piperzine derivative – much longer duration: 4-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Hydroxyzine

Mechanism

A

Based on structure of histamine – short lived, multiple dosing, H1 blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Hydroxyzine

Side effects

A 
Highly sedative, anticholinergic side effects
Sedative 
Anticholinergic 
GI
Can potentiate nasal congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Hydroxyzine

Time

A

Much longer duration: 4-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Fexofenadine

Class

A

Antihistamines

2nd generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Fexofenadine

Mechanism

A

Divergent structures, different from histamine, longer therapeutic doses,interactions H1 blockade
Anti-asthmatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Fexofenadine

Side effects

A

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug
Has only mild cognitive disturbances
-adine
-stine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Fexofenadine

Time

A

Duration 8-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Desloratadine

Class

A

Antihistamines

2nd generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Desloratadine

Mechanism

A

14-7x greater binding to H1 receptors than loratadine

15-50 fold lower affinity for muscarinic receptors compared w/ H1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Desloratadine

Side effects

A

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug
Has only mild cognitive disturbances
-adine
-stine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Desloratadine

Time

A

Long elimination halflife = 27 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Cetirizine

Class

A

Antihistamines

2nd generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Cetirizine

Mechanism

A

Divergent structures, different from histamine, longer therapeutic doses,interactions H1 blockade
Anti-asthmatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Cetirizine

Side effects

A

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug
Has only mild cognitive disturbances
-adine
-stine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Cetirizine

Time

A

Duration 8-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Azelastine

Class

A

Antihistamines

2nd generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Azelastine

Mechanism

A

Divergent structures, different from histamine, longer therapeutic doses,interactions H1 blockade
Anti-asthmatic

120
Q

Azelastine

Side effects

A

Limited or nonsedating, enhanced safety profiles (cardiac arrhythmias, drug-drug
Has only mild cognitive disturbances
-adine
-stine

121
Q

Azelastine

Time

A

Duration 8-24 hours

122
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetaminophen
Class

A

Mild analgesic

123
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetaminophen
Mechanism

A

Inhibition of cyclooxygenase (COX), and recent findings suggest that it is highly selective for COX-2.

124
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetaminophen
Treatment

A

Fever, pain, myalgia, and headache.

125
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetaminophen
Adverse Rxns:

A

Metabolized by the liver and is hepatotoxic; side effects are multiplied when combined with alcoholic drinks.

126
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetaminophen
Time

A

The onset of analgesia is approximately 11–29.5 minutes after oral administration and its half-life is 1–4 hours.

127
Q

Diphenhydramine

Contraindicated

A

Prostate hypertrophy, urinary obstruction, asthma, COPD, peptic ulcer, MAOIs

128
Q

Cough Suppressants, Degongestants
& Mucolytics
Dextromethorphan
Class

A

Antitussive

129
Q

Cough Suppressants, Degongestants
& Mucolytics
Dextromethorphan
Mechanism

A

Suppresses cough reflex via direct action on the cough center in the medulla of the brain. Metabolized by CYP2D6 into active metabolite dextrorphan

130
Q

Cough Suppressants, Degongestants
& Mucolytics
Dextromethorphan
Contraindications:

A

MAOIs, antidepressants, respiratory insufficiency, HS White margin of safety (12-75x of TD to produce halllucinations.

131
Q

Cough Suppressants, Degongestants
& Mucolytics
Dextromethorphan
Time

A

Onset: 15-30 min, duration 3-6 hours

132
Q

Cough Suppressants, Degongestants
& Mucolytics
Codeine
Class

A

Opoid analgesic, Antitussive

3-methylmorphine

133
Q

Cough Suppressants, Degongestants
& Mucolytics
Codeine
Mechanism

A

Suppresses cough by action on the respiratory center

10% is converted to morphine

134
Q

Cough Suppressants, Degongestants
& Mucolytics
Codeine
Side effects

A

Constipation, sedation, histamine release, vasodilation, orthostatic hypotension, dizziness

135
Q

Cough Suppressants, Degongestants
& Mucolytics
Camphor
Class

A

Topical Agent = ointment, lozenges, inhalation

136
Q

Cough Suppressants, Degongestants
& Mucolytics
Camphor
Mechanism

A

Rub on throat and chest as a thick later, not used in nostrils or mouth

137
Q

Cough Suppressants, Degongestants
& Mucolytics
Menthol
Class

A

Topical Agent= ointment, lozenges, inhalation

138
Q

Cough Suppressants, Degongestants
& Mucolytics
Menthol
Mechanism

A

Rub on throat and chest as a thick later, not used in nostrils or mouth

139
Q

Cough Suppressants, Degongestants
& Mucolytics
Pseudoephedrine
Class

A

Nasal decongestant

140
Q

Cough Suppressants, Degongestants
& Mucolytics
Pseudoephedrine
Mechanism

A

Vasoconstricive drug that reduces nasal congestion, does not affect the release of histamine or other mediators in the allergic reaction, commonly formulated with antihistamines
Alpha-adrenergic agonist
Acts primarily by releasing NE from adrenergic nerves

141
Q

Cough Suppressants, Degongestants
& Mucolytics
Pseudoephedrine
Metabolized

A

Metabolized to a minor extent, 88% excreted unchanged in the urine

142
Q

Cough Suppressants, Degongestants
& Mucolytics
Pseudoephedrine
Time

A

Better bioavailability – but both have a short half-life, with a peak at 0.5-2 hours

143
Q

Cough Suppressants, Degongestants
& Mucolytics
Pseudoephedrine
Side effects:

A

Side effects: CV stimulation, CNS stimulation, rebound congestion (ischemic as a result of vasoconstriction of the drug or local irritation of the drug)
Behind the Counter OTC product to reduce use in meth

144
Q

Cough Suppressants, Degongestants
& Mucolytics
Phenylephrine
Class

A

Nasal decongestant

145
Q

Cough Suppressants, Degongestants
& Mucolytics
Phenylephrine
Mechanism

A

Acts by directly stimulating adrenergic receptors on postsynaptic sites

146
Q

Cough Suppressants, Degongestants
& Mucolytics
Phenylephrine
Metabolized

A

Rapidly metabolized by MOA and COMT in the GI mucosa, liver, and other tissues

147
Q

Cough Suppressants, Degongestants
& Mucolytics
Oxymetazoline
Class

A

Topical nasal decongestant

148
Q

Cough Suppressants, Degongestants
& Mucolytics
Oxymetazoline
Adverse Rxn

A

Do not use for more than 3-5 days because it can cause rhinitis medicamentosa

149
Q

Cough Suppressants, Degongestants
& Mucolytics
Oxymetazoline
Preferred Treatment

A

Preferred agent during pregnancy

150
Q

Cough Suppressants, Degongestants
& Mucolytics
Guaifenasin
Class

A

Expectorants

Mucinex

151
Q

Cough Suppressants, Degongestants
& Mucolytics
Guaifenasin
Mechanism

A

Symptomatic relief of ineffective productive coughs, not used for chronic coughs, loosens and thins lower respiratory tract secretions by increasing volume and reducing volume of secretions.

152
Q

Cough Suppressants, Degongestants
& Mucolytics
Guaifenasin
Trivia

A

In veterinary medicine, used to induce and maintain anesthesia in horses

153
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetyl cysteine
Class

154
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetyl cysteine
Mechanism

A

Use in diseases with increased mucus production – cystic fibrosis, COPD, Bronchiectasis, Respiratory infections, TB.
Break H bonds by substituting a sulfhydryl radical-HS

155
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetyl cysteine
Route

A

Given aerosol or by direct instillation into the ET tube

156
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetyl cysteine
Unique Treatment

A

Given orally to reduce liver injury w/ acetoaminophen (Tylenol) overdose

157
Q

Cough Suppressants, Degongestants
& Mucolytics
Acetyl cysteine
Side effects

A

Side effects – bronchospasm (asthma) – if used with asthma, use 10% with bronchodilator
Side Effects – increase mucus production (be prepared to suction a patient who cannot cough), do not mix with antibiotics in the same nebulizer, disagreeable odor due to the hydrogen sulfide, N/V

158
Q

Cough Suppressants, Degongestants
& Mucolytics
Amiloride
Class

A

Aersolized Diuretic/ sodium channel blocker

159
Q

Cough Suppressants, Degongestants
& Mucolytics
Amiloride
Mechanism

A

Diuretic that can be given by aerosol to patients w/ CF, sodium channel blocker.
In CF, sodium is absorbed into the epithelium along with water, leaving the mucus thick and dehydrated – but by blocking the absorption, dehydration of the mucus is prevented

160
Q

Cough Suppressants, Degongestants
& Mucolytics
Amiloride
Route

A

The drug is dissolved in 0.3% NaCl solution and nebulized

161
Q

Treatment of Tuberculosis
Rifampin
Class

162
Q

Treatment of Tuberculosis
Rifampin
Mechanism

A

Inhibition of RNA synthesis, binds the beta subunits of RNA polymerase
Bactericidal for IC and EC bacteria
Resistance – DNA dependent RNA polymerase does not bind drug
Never given as a single agent due to resistance

163
Q

Treatment of Tuberculosis
Rifampin
Route/Time

A

Abs – oral, impaired by food & para-aminosalicylic acid (admin 8-12 hours apart)

164
Q

Treatment of Tuberculosis
Rifampin
Tissues/Metabolized

A

Penetrates all tissues well including CSF (meningitis)
Metabolized – de-acetylated in liver (halflife increased by hepatic dysfunction/ de-acetylated rifampin still has full antibacterial activity but is not resorbed
Excreted primarily in bile, small amount renal tubular secretion, but no adjustment w/ renal failure

165
Q

Treatment of Tuberculosis
Rifampin
Adverse effects

A

Discolors body fluids – orange/red tears, urine, saliva), GI disturbances, CND complains, Hepatotoxic (more relevant in slow acetylators);

166
Q

Treatment of Tuberculosis
Rifampin
Drug interactions

A

Induces P450 (within 2 weeks of drug use), reduces the halflife of prednisone, BBs, suldonamides, dapsone, NNRTIs
Probenecid increases serum levels of rifampin
Rifabutin has less effect on the metabolism of HIV protease inhibitors

167
Q

Treatment of Tuberculosis
Rifampin
Other indications:

A

MRSA, MRSE, prophylaxis of household members exposed to memingococci or H. influenza, eradication of staph in nasal carriers

168
Q

Treatment of Tuberculosis
Isoniazid
Class

169
Q

Treatment of Tuberculosis
Isoniazid
Mechanism

A

Interferes w/ mycolic acid synthesis – disrupts cell wall synthesis; cidal for rapidly dividing bacilli; extracellular cavitary lesions; static for slowly growing lesions; penetrates host cells – effective for intracellular bacilli

170
Q

Treatment of Tuberculosis
Isoniazid
Resistance

A

Inability to take up the drug, alteration of target enzyme, overproduction of target enzyme, emerges rapidly (INH is never used as a single agent in active infections) – 1/10^6 will develop resistance, and the average cavitary lesion has 100 million bacteria

171
Q

Treatment of Tuberculosis
Isoniazid
Absorbed/Distributed

A

Absorbed rapidly from the GI tract with oral dose or can be given IM.
Distributed to all tissues/ fluids (including placenta, meninges in meningitis, breast milk)

172
Q

Treatment of Tuberculosis
Isoniazid
Metabolism

A

Acetylated via N-acetyl transferase (some people are fast metabolizers, some are slow – slow metabolizers have levels 2-3 times higher)- determines halflife of 1-5 hours

173
Q

Treatment of Tuberculosis
Isoniazid
Excretion

A

Drug and inactive metabolites excreted in the urine (~75%) – no adjustment w/ renal failure

174
Q

Treatment of Tuberculosis
Isoniazid
Adverse effects

A

Peripheral neuropathy due to competition w/ pyridoxical phosphate (corrected w/ B6 admin) – more frequent in malnourishment
Hepatotoxic (2% major toxic rxn to metabolite)

175
Q

Treatment of Tuberculosis
Isoniazid
Interactions w/:

A

Antacids w/ Al3+ salts decrease absorption; administer 1h before any antacids
Corticosteroids decrease efficacy
Inhibits P450 that metabolizes phenytoin, diazepam, fluoxentine, nelfinavir

176
Q

Treatment of Tuberculosis
Pyrazinamide
Class

177
Q

Treatment of Tuberculosis
Pyrazinamide
Mechanism

A

Bacilli convert pyrazinamide to pyrazinoic acid, decreasing pH and inhibiting growth; resistant strains may lack pyrazinamidase/ cidal or static depending onconcentration in infected site

178
Q

Treatment of Tuberculosis
Pyrazinamide
Active against

A

Active against tubercle bacilli in acid environment of lysosome & macrophage (most significant effect at intracellular sites where MTB replicates slowly)

179
Q

Treatment of Tuberculosis
Pyrazinamide
Route/Time

A

Well/ rapidly absorbed within 2 hours & widely distributed- including to CSF

180
Q

Treatment of Tuberculosis
Pyrazinamide
Metabolized

A

Metabolized in liver, excreted in urine via glomerular filtration

181
Q

Treatment of Tuberculosis
Pyrazinamide
Adverse effects

A

Dose related hepatotoxicity (most severe rxn), mild non gouty arthalgias, hyperuricemia is usually asymptomatic

182
Q

Treatment of Tuberculosis
Ethambutol
Class

183
Q

Treatment of Tuberculosis
Ethambutol
Mechanism

A

Inhibition of RNA synthesis. Disrupts cell wall synthesis – inhibits arabinosyl transferase, necessary for peptidoglycan units of cell wall resulting in increased cell wall permeability
Static, possibly cidal at high levels
Bacilli must be actively dividing

184
Q

Treatment of Tuberculosis
Ethambutol
Esistance

A

Slow development of resistance

No cross resistance

185
Q

Treatment of Tuberculosis
Ethambutol
Absorption/Elimination

A

Absorption of 75% dose, concentrates in kidneys, lungs, saliva, therapeutic levels in CSF with inflamed meninges , placenta, breast milk.
Elimination – partly metabolized in the liver, excreted in the urine, T1/2 of 3.5 hours

186
Q

Treatment of Tuberculosis
Ethambutol
Adverse Rxn:

A

Optic neuritis, dose related, decreased visual acuity, loss of color discrimination – monthly visual exams- reversible weeks to months after therapy, can cause allergic rxns, hyperuricemia, drug interactions (Al3+ containing antacids reduce absorption

187
Q

Treatment of Tuberculosis
Cycloserine
Class

A

Antiobiotic Second line drub TB

188
Q

Treatment of Tuberculosis
Cycloserine
Mechanism

A

Blocks cell wall synthesis; structural analog of D-alaninel can block enzymes, L-alanine racemase & D-alanine synthetase/ enzymes for D-alanine incorporation into pentapeptide or peptidoglycan strands
Depending on conc – cidal or static

189
Q

Treatment of Tuberculosis
Cycloserine
Effective

A

Effective in resistant organisms – no cross-resistance

Broad spectrum, second-line agent, active against pulmonary and extra-pulmonary TB

190
Q

Treatment of Tuberculosis
Cycloserine
Treatment

A

Only used when other treatments fail – MDR-TB (INH, RIF-R)
Used against mycobacterium avium
Used to treat UTIs

191
Q

Treatment of Tuberculosis
Cycloserine
Route

A

Administered orally w/ good absorption (70-90%)
Distributed widely & not protein bound
Lungs, pleura, synovial fluid, CSF more when inflamed/ excreted unchanged –renal – dose adjustment in renal failure

192
Q

Treatment of Tuberculosis
Cycloserine
Adverse effects

A

Adverse effects – involve CNS – reversible when therapy is discontinued- Headache, tremor, vertigo, confusion, psychotic states w/ suicidal tendencies, paranoia, seizures (not for use in epileptic pts) – risk of suicide increased w/ depression / manifest within first 2 weeks

193
Q

Treatment of Bacterial Infections
Amoxicillin
Class

A

Aminopenicillins

Cell wall

194
Q

Treatment of Bacterial Infections
Amoxicillin
Route/Dose considerations

A

Can be taken with food unlike other penicillins

=dose is affected by the state of the kidneys or admin of other organic acids

195
Q

Treatment of Bacterial Infections
Amoxicillin-clavulanate=Augmentin
Class

A

Aminopenicillins

Cell wall

196
Q

Treatment of Bacterial Infections
Amoxicillin-clavulanate=Augmentin
Treatment/Side effects

A

MSSA, anaerobes

Can cause N/V in children

197
Q

Treatment of Bacterial Infections
Ampicillin-sulbactam=Unasyn
Class

A

Aminopenicillins

Cell wall

198
Q

Treatment of Bacterial Infections
Ampicillin-sulbactam=Unasyn
Treatment

A

Amp-R H influenza, mixed gram positive and anaerobic infections (CAP)

199
Q

Treatment of Bacterial Infections
Carbapenem
Class

A

B-lactam

Cell wall

200
Q

Treatment of Bacterial Infections
Carbapenem
Mechanism

A

Small hydroxyethyl side chain makes it easier for B lactam to move through complex outer membrane of GN bacteria.

201
Q

Treatment of Bacterial Infections
Carbapenem
Resistance/Spectrum

A

High resistance to beta-lactamases

Broadest spectrum of the B-lactams

202
Q

Treatment of Bacterial Infections
Carbapenem
Route/Metabolized

A

Give IV
Excreted by glomerular filtration and secretion
Drug formulated w/ cilastatin to inhibit hydrolysis in brush border

203
Q

Treatment of Bacterial Infections
Carbapenem
Treatment

A

Active against GN and GP, not as a monotherapy for P aeruginosa/ resistant nosocomial gram-negative (Enterobacter) /
Combine w/ aminoglycoside to tx actinobacter

204
Q

Treatment of Bacterial Infections
Carbapenem
Contra-indicated

A

Contra-indicated in patients w/ CNS seizures/ expensive

205
Q

Treatment of Bacterial Infections
Ceftriaxone
Class

A

(Cell wall)
B-lactam
3rd generation cephalopsporin

206
Q

Treatment of Bacterial Infections
Ceftriaxone
Mechanism

A

Same 4 membered B-lactam ring as penicillins w/ a 6 membered dihydrothizide ring – more chemical binding sites
More resistant to B-lactamases
Broader spectrum

207
Q

Treatment of Bacterial Infections
Ceftriaxone
Penicillin Allergies

A

Effective in pts allergic to penicillin

208
Q

Treatment of Bacterial Infections
Ceftriaxone
3rd Generation Benifits

A

1st  3rd = greater GN less GP / more resistance to B-lactamases / increased ability to enter CSF

209
Q

Treatment of Bacterial Infections
Ceftriaxone
Treatment

A

Used for active infections – bacteremia, severe pulmonary infections use w/ aminoglycosidases, do not work against enterococci

210
Q

Treatment of Bacterial Infections
Ceftriaxone
Route/Metabolized

A

Mostly IV/ IM (can be oral)

Renal Excretion

211
Q

Treatment of Bacterial Infections
Clarithromycin
Class

212
Q

Treatment of Bacterial Infections
Clarithromycin
Mechanism

A

Binds to 50S ribosomal subunit / Static

213
Q

Treatment of Bacterial Infections
Clarithromycin
Route/Metabolized

A

More acid stable, rapid first pass metabolism (primary metabolite is still active), eliminated by kidney & liver
Absorption increases w/ food
Inhibits CYP P450 but not as much as erythromycin

214
Q

Treatment of Bacterial Infections

Clarithromycin

A 
Legionnaire’s disease 
Mycoplasma pneumonia
Chlamydia pneumonia 
H influenza
Strep pneumo & GAS
Moraxella
215
Q

Treatment of Bacterial Infections
Doxycycline
Class

A

Tetracycline

30S – protein synthesis

216
Q

Treatment of Bacterial Infections
Doxycycline
Mechanism

A

First broad spectrum (GN & GP)
Bacteriostatic – binding to the ribosome 30s is reversible
Enters cell through porin channels

217
Q

Treatment of Bacterial Infections
Doxycycline
Resistance

A

Resistance occurs slowly – can develop if the efflux pump is induced
Inhibited by di & tri-valent cations

218
Q

Treatment of Bacterial Infections
Doxycycline
Route/Metabolized

A

Best absorbed in acidic conditions of the stomach

Hepatic elimination

219
Q

Treatment of Bacterial Infections
Doxycycline
Adverse effects

A

Adverse – N/V – less w/ doxy
Superinfections, chelation of calcium (teeth discoloration/ depression of bone growth)
Some vestibular toxicity (minoclycine), photosensitivity (doxy)

220
Q

Treatment of Bacterial Infections
Doxycycline
Treatment

A

Used for Atypical pneumonia (Mycoplasma, Legionells, Chlamydia), Lyme disease, acne, periodontal disease

221
Q

Treatment of Bacterial Infections
Erythromycin
Class

222
Q

Treatment of Bacterial Infections
Erythromycin
Mechanism

A

Binds to 50S ribosomal subunit / Static

Narrow spectrum

223
Q

Treatment of Bacterial Infections
Erythromycin
Route/Metabolized

A

Admin orally, but increased acidity may inactivate
Well –distributed but not to CSF
Concentrates in liver (check liver functions)
Excreted in bile/ feces
Placenta/ breast milk

224
Q

Treatment of Bacterial Infections
Erythromycin
One of few drugs that can?
Also crosses into?

A

One of few drugs to cross into prostatic fluid and accumulates in macrophages

225
Q

Treatment of Bacterial Infections
Erythromycin
Treatment

A 
Legionnaire’s disease 
Mycoplasma pneumonia
Chlamydia pneumonia 
GP & GN atypical organisms 
Can be used to eliminate the carrier state w/ corynebacterium diphtheria
226
Q

Treatment of Bacterial Infections
Erythromycin
Side effects

A

Epigastric distress is the most common side effect
Transient deafness
Big time inhibitor of CYP P450
Cholestatic hepatitis

227
Q

Treatment of Bacterial Infections
Imipenem
Class

A

B-lactam

Cell wall

228
Q

Treatment of Bacterial Infections
Imipenem
Contrindication
Advantage

A

Not used in patients w/ seizures

Does not need co-admin of cilastatin

229
Q

Treatment of Bacterial Infections
Imipenem
Treatment

A

Best outcomes for Extended Spectrum Beta-lactam (ESBL) E coli & Klebsiella

230
Q

Treatment of Bacterial Infections
Levofloxacin
Class

A

Newer Fluoroquinolone

231
Q

Treatment of Bacterial Infections
Levofloxacin
Mechanism

A

Analog of quinolone nalidixic acid
Inhibition of bacterial DNA gyrase
Bactericidal

232
Q

Treatment of Bacterial Infections
Levofloxacin
Resistance

A

Resistance via alterations in DNA gyrase enzyme (increases in SA and PA) = quinolone resistance-determining region (QRDR)
Resistance – not plasmid mediated – decreased porins, energy-dependent efflux

233
Q

Treatment of Bacterial Infections
Levofloxacin
Route/Metabolized

A

Good oral absorption, wide distribution, decreased abs w/ antacids, poor CSF penetration, renal & liver excretion

234
Q

Treatment of Bacterial Infections

Levofloxacin

A

Strep pneumo, Legionella, GN coverage similar to aminoglycosides – synergism w/ B-lactams

235
Q

Treatment of Bacterial Infections
Meropenem
Class

A

(Cell wall)

B-lactam

236
Q

Treatment of Bacterial Infections
Meropenem
Activity

A

Does not need co-admin of cilastatin
Less G+ activity
Less CNS px

237
Q

Treatment of Bacterial Infections
Meropenem
Treatment

A

Best outcomes for Extended Spectrum Beta-lactam (ESBL) E coli & Klebsiella

238
Q

Treatment of Bacterial Infections
Moxifloxicin
Class

A

Newer Fluoroquinolone

239
Q

Treatment of Bacterial Infections
Moxifloxicin
Mechanism

A

Analog of quinolone nalidixic acid
Inhibition of bacterial DNA gyrase
Bactericidal

240
Q

Treatment of Bacterial Infections
Moxifloxicin
Metabolism

A

Mostly hepatic clearance
Not used for UTIs
Hepatic elimination

241
Q

Treatment of Bacterial Infections
Penicillin
Class

A

(Cell wall)

B-lactam

242
Q

Treatment of Bacterial Infections
Penicillin
Metabolism

A

An acid administered as a salt w/ high doses – evaluate pt w/ HTN CHF exists as a non-absorble anion, K+ moves into the tubule in exchange for H+  hypokalemic alkylosis

243
Q

Treatment of Bacterial Infections
Penicillin
Adverse Rxns

A

Can cause HS rxns, delayed allergic rxns, >2 days rash, more common with ampicillin & amoxicillin
Hives/ uticaria
Most life-threatening responses are caused by peritoneal drug admin

244
Q

Drugs to Treat Lung Cancer
Bevacizumab
Treatment

A

Adenocarcinoma

Non-squamous NSCLC

245
Q

Drugs to Treat Lung Cancer
Bevacizumab
Mechanism

A

Humanized antibody, binds VEGF, given IV
Inhibition promotes non-physiologic apoptosis of endothelial cells and decreases deposition of subendothelial matric making the vasculature more susceptible to severe bleeding

246
Q

Drugs to Treat Lung Cancer
Bevacizumab
Contraindicated/Side effect

A

Risk of bleeding in squamous lung cancers – not approved

Can cause HTN

247
Q

Drugs to Treat Lung Cancer
Carboplatin
Treatment

248
Q

Drugs to Treat Lung Cancer
Carboplatin
Mechanism

A

Forms DNA intra-strand cross-links and adducts

249
Q

Drugs to Treat Lung Cancer
Carboplatin
Adverse Rxns

A

Allergic (platinum rxns)
Dose-related myelosuppression; cumulative anemia
Dose-related N/V
Blood chemistry dyscrasia, increase in hepatic enzymes, BUN & creatinine

250
Q

Drugs to Treat Lung Cancer
Cisplatin
Treatment

A

SCLC/ NSCLC

251
Q

Drugs to Treat Lung Cancer
Cisplatin
Mechanism

A

Forms DNA intra-strand cross-links and adducts

252
Q

Drugs to Treat Lung Cancer
Cisplatin
Adverse Rxns

A

Dose-related severe nephrotoxicity, myelosuppression, N/V

Significant ototoxicity

253
Q

Drugs to Treat Lung Cancer
Crizotinib
Treatment

A

Adenocarcinoma

254
Q

Drugs to Treat Lung Cancer
Crizotinib
Mechanism

A

Reversible multi-kinase inhibitor, ALK

CYP3A4 inhibitor

255
Q

Drugs to Treat Lung Cancer
Crizotinib
Route

A

Oral on empty stomach

256
Q

Drugs to Treat Lung Cancer
Crizotinib
Adverse Rxn

A

Visual disorders are common

257
Q

Drugs to Treat Lung Cancer
Cyclophosphamide
Treatment

258
Q

Drugs to Treat Lung Cancer
Cyclophosphamide
Mechanism

A

Pro-drug of active alkylating moiety

259
Q

Drugs to Treat Lung Cancer
Cyclophosphamid
Adverse Rxns

A 
Blood dyscrasias  anemia 
Hemorrhagic cystitis (mesna)
Infertility 
Monitor for 2ndary malignancies
Pulmonary fibrosis
260
Q

Drugs to Treat Lung Cancer
Doxorubicin
Treatment

261
Q

Drugs to Treat Lung Cancer
Doxorubicin
Mechanism

A

Intercalator, free radical generator, topo II inhibitor (DNA STRUCTURE)

262
Q

Drugs to Treat Lung Cancer
Doxorubicin
Adverse Rxns

A 
Myelosuppresion, 
Cumulative dose cause CHF
Hepatic disease 
2ndary malignancies 
Extravasational necrosis
N/V
263
Q

Drugs to Treat Lung Cancer
Erlotinib
Treatment

A

Adenocarcinoma

264
Q

Drugs to Treat Lung Cancer
Erlotinib
Mechanism/Epidemiology

A

EGFR kinase inhibition
(lung cx) – most never smokers
Mutations high in Asian populations

265
Q

Drugs to Treat Lung Cancer
Erlotinib
Route/Side effects

A

Oral, few side effects

266
Q

Drugs to Treat Lung Cancer
Etoposide
Treatment

267
Q

Drugs to Treat Lung Cancer
Etoposide
Mechanism

A

DNA-topo II complex stabilizer

268
Q

Drugs to Treat Lung Cancer
Etoposide
Side effects

A

Myelosuppression, infection
N/V
Diarrhea, alopecia

269
Q

Drugs to Treat Lung Cancer
Gemcitabine
Treatment

270
Q

Drugs to Treat Lung Cancer
Gemcitabine
Mechanism

A

DNA polymerase inhibitor via incorpotation of triphosphate form during DNA synthesis (DNA SYNTHESIS)

271
Q

Drugs to Treat Lung Cancer
Gemcitabine
Adverse Rxns

A

Myelosuppression, arthralgia, sensory peripheral neuropathy

272
Q

Drugs to Treat Lung Cancer
Ifosfamide
Treatment

273
Q

Drugs to Treat Lung Cancer
Ifosfamide
Mechanism

A

Intra- and Inter- strand cross-linker

274
Q

Drugs to Treat Lung Cancer
Ifosfamide
Side effcts

A

Alopecia, N/V, blood dyscrasia  infection

275
Q

Drugs to Treat Lung Cancer
Ifosfamide
Adverse Rxn

A

Hemorrhagic cystitis is rare when ifosfamide is given together with mesna.
Dose-limiting side effect is encephalopathy

276
Q

Drugs to Treat Lung Cancer
Irinotecan
Treatment

A

SCLC Myelosuppression and GI toxicity

Elevated liver functions and serum creatinine

277
Q

Drugs to Treat Lung Cancer
Irinotecan
Mechanism

A

Prevents DNA from unwinding by inhibition of topoisomerase 1.

278
Q

Drugs to Treat Lung Cancer
Irinotecan
Side effects

A

Myelosuppression and GI toxicity

Elevated liver functions and serum creatinine

279
Q

Drugs to Treat Lung Cancer
Methotrexate
Treatment

280
Q

Drugs to Treat Lung Cancer
Methotrexate
Mechanism

A

Folic Acid analog
Dihydrofolate reductase inhibition (universal)
Folic acid essential dietary factor
Polyglutamation (which traps drug) also inhibits thymidylate synthase (TS) and 2 early enzymes in purine biosynthesis
Rescue other cells with Leucovorin

281
Q

Drugs to Treat Lung Cancer
Methotrexate
Toxicity

A

Methotrexate is a highly teratogenic drug and categorized in pregnancy category X

282
Q

Drugs to Treat Lung Cancer
Paclitaxel
Treatment

283
Q

Drugs to Treat Lung Cancer
Paclitaxel
Mechanism

A

Micro tubule (MT) stabilizer inhibiting depolymerization (MT)

284
Q

Drugs to Treat Lung Cancer
Pemetrexed
Treatment

285
Q

Drugs to Treat Lung Cancer
Pemetrexed
Mechanism

A 
Inhibiting dihydrofolate reductase (DHFR)
DHFR inhibitor (DNA SYNTHESIS)
286
Q

Drugs to Treat Lung Cancer
Pemetrexed
Dose limiting toxicity

A

Low blood cell counts, as measured by a Complete Blood Count. This is a dose-limiting toxicity.

287
Q

Drugs to Treat Lung Cancer
Topotecan
Treatment

288
Q

Drugs to Treat Lung Cancer
Topotecan
Mechanism

A

DNA topo I complex stabilizer

289
Q

Drugs to Treat Lung Cancer
Topotecan
Side effects

A

Myelosuppression and GI toxicity

Hyperbilirubinemia

290
Q

Drugs to Treat Lung Cancer
Vincristine
Treatment

291
Q

Drugs to Treat Lung Cancer
Vincristine
Mechanism

A

MT inhibitor, tubules disintegrate into spiral aggregates/ protofilaments

292
Q

Drugs to Treat Lung Cancer
Vincristine
Side effects

A

Peripheral neuropathy, hyponatremia, constipation, and hair loss.
First symptoms of peripheral neuropathy is foot drop:

293
Q

Drugs to Treat Lung Cancer
Vinorelbine
Treatment

294
Q

Drugs to Treat Lung Cancer
Vinorelbine
Mechanism

A

MT inhibitor, tubules disintegrate into spiral aggregates/ protofilaments

295
Q

Drugs to Treat Lung Cancer
Vinorelbine
Side effects

A

Neutropenia, (peripheral neuropathy)

Pulmonary (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions