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DEENT > Exam 2 Material > Flashcards

Exam 2 Material Flashcards

1
Q

locations of histamine

A

basophils and mast cells
CNS
enterochomaffin-like cells (ECLs)

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2
Q

antigen mediated release or degranulation

A

tissue mast cells and blood basophils-immediate hypersensitivity rxn
antigen causes the generation of IgE
antigen bridges the IgE and increase Ca2+ levels in the cell
exocytosis of contents (degranulation)

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3
Q

nonantigen mediated release of histamine

A

receptor mediated
any thermal mechanical stress
basic drugs and chemicals
some venoms

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4
Q

H1 receptor

A

expressed in smooth muscle, endothelium, and brain
structurally different from H2 rec, similar to muscarinic rec
higher affinity for histamine than H2 rec
some constitutive activity in some systems

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5
Q

histamine affects on the H1 receptor

A

mediates pain and itching
contraction of the bronchi, gut, uterus, and iris
relaxation of small blood vessels causing vasodilation
contraction of endothelial cells->edema
increases arachidonic acid (AA) release and prostaglandin release
increases the amount and viscosity of mucus from goblet cells
stimulates the cough reflex

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6
Q

during allergic responses and inflammation H1

A

increased adhesion molecules and chemotaxis

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7
Q

H2 receptor

A

expressed in gastric mucosa, cardiac muscle, and brain
structurally diff from H1 rec; similar to 5-HT receptors
some constitutive activity in some systems

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8
Q

histamine affects on H2 receptor

A

increases gastric acid secretions
autoreceptor for histamine release in mast cell and basophils
relaxation of airway, uterine, and vascular smooth muscle
positive inotropic and chronotropic effects

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9
Q

during allergic responses and inflammation H2 rec

A

decreased eosinophil and neutrophil chemotaxis
decreased cytokine production

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10
Q

H3 receptor

A

presynaptic autoreceptor in brain, myenteric, and other neurons
some constitutive activity in some systems

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11
Q

histamine affects on the H3 receptor

A

sleep/wake cycle, energy, and endocrine homeostasis
cognition and memory

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12
Q

during allergic rxns and inflammation H3 receptors

A

neurogenic inflammation
pro-inflammatory
prevents excessive bronchoconstriction

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13
Q

H4 receptor

A

expressed in eosinophils, neutrophils, and CD4 T cells
NOT similar to other H receptors
some constitutive activity in some systems

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14
Q

histamine affects on H4 receptor

A

causes differentiation of myeloblasts

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15
Q

during allergic rxns and inflammation H4 receptor

A

increases eosinophil chemotaxis

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16
Q

MOA of H1 antihistamines

A

inverse agonist at the H1 receptor
binds and stabilizes the inactive state of the receptor

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17
Q

1st generation of H1 antihistamines

A

strong sedative effects
more likely to block autonomic receptors

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18
Q

2nd generation H1 antihistamines

A

less sedating bc of reduced distribution into CNS
less affect on autonomic receptors
some metabolized by CYP3A4, so need to watch for DIs

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19
Q

pharmacodynamics of 1st generation antihistamines

A

some inhibit mast cell release of histamine
sedation
antinausea and antiemetic action
antiparkinsonism effects
antimuscarinic actions
adrenoreceptor-blocking actions
serotonin-blocking actions
local anesthesia

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20
Q

side effects of 1st generation antihistamines

A

sedation
paradoxical excitement in children
nervous system effects
anticholinergic effects
CV effects
sensitivity reactions

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21
Q

sedation of 1st generation antihistamines

A

may be a result of inverse agonism at the central H1 rec
readily cross the BBB and occupy 50-90% of the H1 receptors in the brain

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22
Q

paradoxical excitement in children 1st generation antihistamines

A

restlessness, tremors, euphoria, delirium, and seizures

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23
Q

nervous system effects 1st generation antihistamines

A

disturbed coordination
decreased cognition
increased appetite
abuse potential
peripheral sodium channel blockade

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24
Q

anticholinergic effects of 1st generation antihistamines

A

dryness of mouth, nose, eyes, and throat
urinary retention and impotence
blurred vision, loss of accommodation and mydriasis
thickening of bronchial secretion, wheezing, nasal stuffiness
decreased GI motility and constipation
tachycardia and chest tightness

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25
Q

CV effects of 1st generation antihistamines

A

tachycardia
prolongation of QT interval
hypotension or orthostatic hypotension

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26
Q

sensitivity rxns of 1st generation antihistamines

A

occurs most commonly with topically applied antihistamines
ethylenediamine
antihistamines act as haptens to cause IgE mediated type I reactions or T cell mediated type IV reactions

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27
Q

order of ability (1st generation antihistamines) to cross BBB

A

sedation
diphenhydramine=promethazine=hydroxyzine>chlorpheniramine=dexchlorpheniramine

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28
Q

anticholinergic order of 1st generation antihistamines

A

diphenyhydramine=promethazine>brompheniramine=chlorpheniramine=hydroxyzine> azelastine

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29
Q

side effects of 2nd generation antihistamines

A

no or low sedation

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30
Q

fexofenadine food DDI

A

orange, apple, or grapefruit juice reduces serum levels of fexofenadine
-reduces OATP activity=decreased oral bioavailability
separate by 2 hrs

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31
Q

anticholinergic/antimuscarinic medication

A

ipratropium

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32
Q

ipratropium

A

nasal spray
anticholinergic agent that has antisecretory prop when applied locally
provides symptomatic relief of rhinorrhea associated with allergic and other forms of chronic rhinitis
usually used in pts who fail or cannot tolerate other therapies
dose determined based on pts’ symptoms and response

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33
Q

adverse effects of ipratropium

A

headache, epistaxis, and nasal dryness

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34
Q

leukotriene receptor antagonist medication

A

montelukast

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35
Q

montelukast

A

inhibits cysteinyl leukotriene receptor (CysLT)
perennial AR: > 6 months
seasonal AR: > 2 years
PO once a day

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36
Q

adverse effects of montelukast

A

a lot of serious neuropsych effects (CNS effects)
GI effects as well

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37
Q

where are a2 receptors located

A

arterioles
mucosal membrane of vasculature of nasopharynx
vascular smooth muscle
pancreas
CNS/peripheral NS

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38
Q

where are a1 receptors located

A

venules
mucosal membrane of vasculature of nasopharynx
vascular smooth muscle
heart
NCS
bladder neck
piloerector muscle

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39
Q

secretory cells

A

epithelial cells, goblet cells, and basal cells
secretes: enzymes, IgA, mucus

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40
Q

cholinergic innervation of alpha receptors

A

vasodilation
increases mucus secretion

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41
Q

adrenergic innervation of alpha receptors

A

vasoconstriction
decreases mucus secretions

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42
Q

alpha receptor agonist pharm effect

A

constriction of nasal vasculature
reduced tissue swelling
increased nasal drainage
improved airflow through nasal passages
reduce mucus secretions by decreasing blood flow to mucus glands

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43
Q

pseudoephedrine (alpha 1 agonist) side effects

A

CNS effects
-nervousness, irritability, insomnia
-athletic performance enhancement
CV effects
-increase BP, HR
-HTN and ischemia
GI effects
-decrease appetite
piloerection

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44
Q

alpha2 agonists

A

oxymetazoline, xylometazoline, tetrahydrozoline
topically
-constricts dilated blood vessels in nasal mucosa
-depresses CNS

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45
Q

alpha2 agonists side effects

A

rhinitis medicamentosa
burning, stinging, nasal dryness, and sneezing
damage to nasal septum with long term use
CNS depression

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46
Q

cough reflex

A

central cough center coordinates the actions which produce a cough
1) deep inspiration
2) closure of glottis
3) forceful contraction of the muscles of the chest wall, abdomen, and diaphragm
can be voluntary or involuntary

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47
Q

where do drugs work in the cough reflex

A

sensory receptors
cough center

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48
Q

sensory receptors

A

send signals through vagal afferent fibers to the central cough center in the medulla

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49
Q

codeine and hydrocortisone MOA

A

PO antitussives
central MOA on mu opioid receptors in the medullary cough center
may have additional peripheral action on cough receptors in the proximal airways

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50
Q

dextromethorphan MOA

A

PO antitussives
NMDA receptor antagonist and agonist at delta opioid receptors

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51
Q

antihistamines PO antitussives MOA

A

H1 inverse agonist and muscarinic antagonist on medullary cough center and resp. tract

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52
Q

local anesthetic/Na+ channel blockers PO antitussives MOA

A

decreases Na+ permeability through reversible stabilization of the neuronal membrane
inhibits depolarization of the neuronal membrane which blocks the initiation and conduction of nerve impulses
anesthetizes stretch receptors in the resp. passages, lungs to reduce the cough reflex

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53
Q

codeine and hydrocortisone side effects

A

nausea, drowsiness to sedation, dizziness, and constipation

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54
Q

dextromethorphan side effects

A

nausea, drowsiness, dizziness, and constipation
extremely large doses do produce intoxication with hallucinations

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55
Q

local anesthetic/Na+ channel blockers PO antitussives side effects

A

drowsiness, dizziness, headache, nasal congestion, a vague “chilly” feeling

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56
Q

diphenhydramine and promethazine side effects

A

drowsiness and sedation
anticholinergic effects

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57
Q

local anesthetic/Na+ channel blockers topical antitussives MOA

A

decreases Na+ permeability through reversible stabilization of the neuronal membrane
inhibits depolarization of the neuronal membrane which blocks the initiation and conduction of nerve impulses

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58
Q

local anesthetic/Na+ channel blockers topical antitussives side effects

A

irritation, redness, or blistering of skin

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59
Q

toxicity of local anesthetic/Na+ channel blockers topical antitussives

A

2 g dose of menthol can be fatal
conc > 10% of camphor can produce seizures
4 teaspoons of 5% camphor can be lethal in children

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60
Q

demulcents

A

forms a soothing film over a mucous membrane, relieving minor pain and inflammation
effective for no more than 30 minutes usually

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61
Q

expectorants medication

A

guaifenesin

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62
Q

guaifenesin MOA

A

increase volume and reduce the viscosity of secretions in the trachea and bronchi; increase efficiency of the cough reflex and facilitate removal of the secretions

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63
Q

guaifenesin side effects

A

N/V, dizziness, headache, rash

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64
Q

mucolytic products

A

acetylcysteine
dornase alfa
water

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65
Q

dornase alfa

A

DNAase
purulent mucus is composed of highly polymerized DNA
selectively cleaves DNA

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66
Q

uses of mucolytics

A

cystic fibrosis
APAP antidote (acetylcysteine)

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67
Q

corticosteroids

A

endogenous are produced by adrenal cortex
have many physio effects
-affect carb, lipid, and protein metabolism
-maintain fluid and electrolyte balance
-preserve normal function of CV system, kidney, skeletal muscle, endocrine, NS, and immune systems
variety of therapeutic purposes

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68
Q

corticosteroids therapeutic uses

A

autoimmune diseases
used to limit allergic rxns to other immunosuppressants
treat graft-vs-host disease
used to block 1st dose cytokine stor,
combined with other immunosuppressants to prevent and treat transplant rejections

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69
Q

direct action corticosteroid MOA

A

drug-receptor complex binds to DNA (RE) to inhibit or promote transcription
requires 2 drug receptor complexes that bind to a response element

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70
Q

indirect action corticosteroid MOA

A

drug receptor complex binds to a transcription factor, preventing it from binding to DNA->inhibits the transcription of proteins
require only 1 drug-receptor complex to bind to transcription factor

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71
Q

corticosteroids side effects

A

growth inhibition in children
avascular necrosis of bone
osteopenia
increased risk of infection
poor wound healing
cataracts
hyperglycemia
HTN
masking of inflammation

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72
Q

NSAIDs general mechanism

A

anti-inflammatory mostly due to inhibition of prostaglandin biosynthesis
-inhibits chemotaxis, down regulation IL-1 production, decrease production of free radicals and superoxide, interfere with calcium-mediated intracellular events

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73
Q

aspirin MOA

A

irreversibly acetylates and blocks platelet COX

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74
Q

ibuprofen and other non-COX selective NSAIDs

A

reversibly inhibit COX

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75
Q

common adverse effects of NSAIDs

A

CNS
CV
GI
hematologic
hepatic
pulm
skin
renal

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76
Q

ibuprofen side effects

A

better tolerated than aspirin
may be tolerated in pts with history of GI intolerance to other NSAIDs
rashes, thrombocytopenia, headache, dizziness, blurred vision, toxic amblyopia, fluid retention, and edema
discontinue if ocular disturbances develop and have ophthalmic evaulation

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77
Q

drug interaction of ibuprofen

A

interferes with antiplatelet effects of aspirin

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78
Q

cautions of ibuprofen

A

can be used occasionally by pregnant women, but may have third trimester effects, including delay of parturition
excretion into breast milk is minimal

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79
Q

contraindications of ibuprofen

A

nasal polyps, angio-edema, pts that have bronchospasms with aspirin

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80
Q

acetaminophen MOA

A

nonselective, weak COX-1 and COX-2 inhibitor in peripheral tissues
inhibits COX by binding to the peroxide-binding site in the enzyme
no significant anti-inflammatory effects

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81
Q

acetaminophen pharmacodynamics

A

raises threshold of painful stimuli, therefore effective against various kinds of pain
analgesic and antipyretic effects similar to aspirin, but only weak anti-inflammatory effects
high conc of peroxides, which occurs with inflammation, reduces COX-inhibitory activity

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82
Q

acetaminophen PK

A

administered PO or rectally
peak blood conc reached in about 30-60 min
poorly bound to plasma proteins
t1/2=2-3 hrs
doses or liver disease may increase t1/2 twofold or more

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83
Q

symptoms of acetaminophen OD

A

nausea, vomiting, diarrhea, and abdominal pain

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84
Q

max daily dose is 4 g of acetaminophen

A

mild, reversible increased liver function tests
possible renal damage without hepatic damage
hemolytic anemia and methemoglobinemia, but v rare
caution in pts with any type of liver disease
CI with history of alcoholism

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85
Q

larger doses of acetaminophen side effects

A

dizziness, excitement, and disorientation

86
Q

15 g of acetaminophen side effects

A

severe hepatotoxicity with centrilobular necrosis, possible acute renal tubular necrosis

87
Q

acetaminophen OD management

A

normal supportive measures
decontamination by activated charcoal (not multiple dose)
NAC antidote 140 mg/kg LD followed by 17 doses of 70 mg/kg every 4 hrs

88
Q

elimination of acetaminophen OD

A

dialysis has been used to enhance APAP elimination
use has largely been abandoned
role in MASSIVE ODs where pts presents with coma, acidosis, and high levels

89
Q

biosynthesis of histamine

A

L-histidine to histamine via L-histidine decarboxylase

90
Q

1st generation antihistamines chem

A

ethanolamines
ethylenediamines
piperazines
propylamines
tricyclics

91
Q

ethanolamines

A

1st gen antihistamines
diphenhydramine, dimenhydrinate, doxylamine, carbinoxamine, clemastine
O_/N
undergoes N-demethylation, then 1)MAOs, 2) ALDH to form conjugates

92
Q

ethylenediamines chem

A

less potent-fewer SEs
tripelennamine, pyrilamine, antazoline
N_/N
undergoes N-demethylation, then 1)MAOs, 2) ALDH to form conjugates

93
Q

piperazines 1st gen chem

A

cyclized ethyenediamines
slow onset; long DoA
cyclizine, chlorcyclizine, meclizine, hydroxyzine
undergoes N-demethylation or CYPs/FMO

94
Q

propylamines chem

A

1st gen antihistamines
pheniramine, brompheniramine, dexbrompheniramine, chlorpheniramine, dexochlorpheniramine, triprolidine
_/-N
undergoes N-demethylation, then 1)MAOs, 2) ALDH then AA to make glycine conjugates

95
Q

tricyclic chem 1st gen

A

1st gen antihistamine
azatadine, cyproheptadine, phenindamine, olopatidine, promethazine
3 fused rings attached N; undergoes de-alkylation

96
Q

2nd generation antihistamine chem

A

piperidines
tricyclics
piperazines
multicyclics

97
Q

piperidines

A

2nd gen antihistamines
fexofenadine-active metabolite of terfenadine
1) CYP, 2) ADH, 3) ALDH

98
Q

tricyclics 2nd gen chem

A

loratadine, desloratadine (active metabolite of loratadine)
desloratadine-long DoA active metabolite
3 fused rings attached with N

99
Q

piperazines 2nd gen chem

A

cetirizine, levocetirizine
products of 1) ADH, 2) ALDH of hydroxyzine
cetirizine-racemic
levocetirizine-more active isomer

100
Q

multicyclics

A

2nd gen antihistamines
acrivastine, levocabastine, emadastine
multiple cyclic groups with a difference from amine
ionize at physio pH

101
Q

SAR antihistamine

A

terminal N is tertiary
AR-groups (free or fused)
linker: alkyl or alkene (branched or cyclic)
small to bulkier R-groups on N

102
Q

codiene

A

well-distributed, including into breast milk
O- and N-demethylations to morphine/O-glucuronidation/O-sulfation to glucs/sulfates metabolites

103
Q

opioid antitussives

A

morphine, dextromethoprhan, hydrocodone, codiene

104
Q

non-opioid antitussives

A

benzonatate
chlophedianol

105
Q

benzonatate chem

A

non-opioid antitussives
PABA derivative
v lipophilic ester
peripheral antitussive effects
15-20 min onset, t1/2=3 hrs

106
Q

chlophedianol

A

non-opioid antitussives
1/3 codeine’s activity
weak antihistamine/local anesthetic props
slow onset-prolonged antitussive activity

107
Q

SAR local anesthetics

A

basic amine
esters/amides/phenols/aromatic FG

108
Q

local antitussives metabolism

A

ester and amide hydrolysis; N-dealkylation; N-OH

109
Q

toxicity of local antitussives

A

benzocaine, benzocaine hydroxylamine, xylidine hydroxylamine

110
Q

decongestant metabolism

A

phenylephrine-poor PO bioavailability
pseudoephedrine-good PO bioavailability-slow MAO metabolism @ N

111
Q

SAR of decongestants

A

phenethylamine
OH increases activity
CH3 decreases activity but increases DoA (resistance to MAO)
2C spacer btwn Ar and N (optimal)

112
Q

adamantanes

A

older anti-influenza agents
embed a lipophilic cage
inhibits viral replication
CNS side effects

113
Q

sialic acid analogs

A

neuraminidase inhibitors are newer
mimic sialic acid and inhibit viral replication
oseltamivir, zanamivir, peramivir

114
Q

oseltamivir

A

prodrug via carboxyesterases and 1st oral NA inhibitor

115
Q

zanamivir and peramivir

A

contain guanine (basic group)
active drugs

116
Q

SAR of sialic acid analogs

A

COOH-drug activity
X (OH, NH2, guanidine) increases binding to NA

117
Q

dibenzothiepine(s)

A

carbonate prodrug activated by ester hydrolysis
selectively inhibits cap-endonucleases, which initiate mRNA synthesis in influenza virus

118
Q

acetaminophen chem

A

p-aminophenols
no anti-inflammatory effects bc it doesn’t have COOH
antipyretic and analgesic activities
no GI toxicity bc it doesn’t have COOH
useful in salicylate sensitive patients
antipyretic effects require CNS/BBB entry

119
Q

NSAIDs chem

A

non-steroidal
salicylates and arylalkanoic acids
antipyretic: only those which enter CNS
anti-inflammatory: agents w/o COOH lack this
MOA: COX-1 and 2 enzyme inhibition
achieve analgesia by decreasing PG levels and actions

120
Q

salicylates chem goals

A

minimize GI erosin
enhance potency
improve DoA

121
Q

salicylate prodrugs

A

reduced via azo-reductase enzymes

122
Q

salicylates metabolism

A

amino acid conjugation-major metabolit-salicyuric acid

123
Q

acetic acids NSAIDs

A

indomethacin
diclofenac
etodolac
sulindac

124
Q

propionic acids NSAIDs

A

ibuprofen
fenoprofen
ketoprofen
naproxen
oxaprozin

125
Q

ibuprofen chem

A

propionic acid
isomerase with w-oxidations via 2C9 and 2C19

126
Q

naproxen chem

A

propionic acid
sold as separate isomers
DoA: 12 hrs
metabolism: aromatic oxidation, P II glucuronidation

127
Q

phases of allergies

A

Phase I: sensitization phase (initial exposure)
phase II: early phase
phase III: cellular recruitment
phase IV: late phase (symptoms begin)

128
Q

risk factors of allergic rhinitis

A

fam history of allergic disorders in one or both parents
elevated serum IgE before 6 years old
higher socioeconomic level
eczema
positive rxn to allergy skin tests

129
Q

clinical presentation of allergic rhinitis

A

symptoms: nasal congestion, sneezing, rhinorrhea, itchy nose, watery eyes, postnasal drip, cough and throat clearing, malaise and fatigue (children)
Signs: allergic salute, allergic shiners, nasal crease, swelling of nasal mucosa

130
Q

allergic rhinitis (AR)

A

IgE mediated inflammatory response of nasal mucous membranes after exposure to inhaled allergens
may consider this if the allergen is unknown

130
Q

seasonal allergic rhinitis

A

IgE mediated inflammatory response to seasonal allergens
length of exposure varies on location and climate

131
Q

perennial allergic rhinitis

A

IgE mediated inflammatory response to year around environmental allergens (dust mites, mold, pet dander)
can be episodic or could be consistent and year around if they live in an environment with the allergens

132
Q

duration classification of AR

A

intermittent
persistent
episodic

133
Q

intermittent AR

A

symptoms occurs <4 days/week OR < 4 weeks

134
Q

persistent AR

A

symptoms occur > 4 days/week AND > 4 weeks

135
Q

episodic AR

A

symptoms occur on exposure to or contact with potential allergen that is not a part of the person’s environment

136
Q

mild symptoms of AR

A

do NOT impair sleep or daily activities

137
Q

moderate-severe symptoms AR

A

one or more of the following occurs:
impairment of daily activities or sleep

138
Q

common cold symptoms

A

sneezing +/-
sore throat (1st symptom)
fever +/-
cough +/-
muscle aches +/-

139
Q

influenza symptoms

A

cough
muscle aches
sore throat
fever
SOB

140
Q

allergic rhinitis symptoms

A

sneezing
no sore throat
no fever
itchy eyes

141
Q

COVID-19 symptoms

A

cough (mostly dry)
muscle aches
fever
SOB

142
Q

diagnosis of AR

A

patient history and assessment
allergy testing
assess presence of associated conditions such as asthma, atopic dermatitis, sleep disordered breathing, conjunctivitis, rhinosinusitis, and otitis media

143
Q

exclusions of AR

A

children under 12
pregnant or lactating women
symptoms of non-allergic rhinitis (bacterial infection, rhinitis medicamentosa)
symptoms of undiagnosed or uncontrolled asthma or COPD
severe or unacceptable side effects of treatment

144
Q

nonpharm therapy for AR

A

allergen avoidance
-dust mites
-pollen/environmental allergens
-pets
netipot
-nasal symptoms

145
Q

first lines of pharm therapy for AR

A

intranasal steroid (INS):
-moderate to severe
-nasal congestion and rhinitis
2nd generation Oral antihistamines
-mild symptoms with sneezing, itching, and rhinorrhea
-episodic or infrequent symptoms

146
Q

adjunctive therapy for AR

A

decongestants

147
Q

intranasal steroids for AR

A

may take 1-2 weeks
budesonide, fluticasone furoate, fluticasone propionate, mometasone, triamicolone

148
Q

intranasal steroids side effects

A

minor side effects: dryness, stinging, headache, epistaxis
systemic side effects: minimal

149
Q

intranasal steroids special pops

A

pediatrics:
-triamcinolone: > 2 years
-beclomethasone, fluticasone proprionate: > 4 years
-budesnoide, mometasone: > 6 years
elderly: safe
pregnancy: generally safe, but budesonide has most evidence
breastfeeding: minimal data, but likely safe

150
Q

2nd generation antihistamine Oral for AR

A

less sedating than 1st gen
mild-moderate symptoms
more severe symptoms in combo with INS when initially starting therapy
relieve itching, sneezing, and runny nose
side effects: minimal; headache, some drowsiness
cetirizine, levocetirizine, loratadine, fexofenadine

151
Q

2nd generation antihistamines: non-oral for AR

A

less systemic effects with topical meds
can be used in combo with INS if symptoms not controlled on INS alone
azelastine

152
Q

2nd generation antihistamines: special pops

A

pediatrics:
-can use products down to 2 year old
elderly:
-much safer than 1st gen
-NOT on Beers list
-still can cause some sedation, but the risk of confusion is v low
pregnancy:
-safe, loratadine and cetirizine are preferred
breastfeeding:
-generally safe, can cause some irritability and drowsiness in the infant

153
Q

decongestants for AR

A

PO: pseudoephedrine
intranasal: oxymetazoline
nasal congestion
short-term relief only (1 week for PO, 3 days for intranasal)->rebound congestion

154
Q

other agents for AR

A

intranasal cromolyn
intranasal ipratropium
oral epinephrine inhalation
montelukast
immunotherapy

155
Q

intranasal cromolyn for AR

A

not as effective as other agents->better if started BEFORE symptoms begin
good safety profile: pregnancy and children < 2

156
Q

intranasal ipratropium for AR

A

effective for rhinorrhea only
may be used in combo other products if rhinorrhea is a prominent symptom

157
Q

oral epinephrine inhalation for AR

A

not recommended for use in AR or asthma

158
Q

montelukast

A

adjunctive agent in pts with an inadequate response to or cannot tolerate all other AR therapies
for those with coexisting asthma
BBW: serious neuropsych events

159
Q

immunotherapy (allergy shots) for AR

A

severe allergic symptoms or if 1st line treatments are unsuccessful
sublingual admin or SQ injection
slowly increases tolerance to allergen
-IgE to IgG
-works similar to a vaccine

160
Q

monitor and evaluate for AR

A

own self-monitoring

161
Q

intranasal admin

A

1) blow nose
2) shake bottle
3) tilt head forward
4) close 1 nostril and place spray pump tip 1/4 to 1/2 inch
5) do not spray into the septum
6) keep bottle upright
7) repeat and clean

162
Q

common cold

A

viral infection of the upper resp tract
transmission: self-inoculation or airborne
self-limiting illness: symptomatic treatment only

163
Q

influenza

A

viral infection of the upper resp tract
transmission: self-inoculation or airborne
can be self-limiting illness but is more severe in certain pop: symptomatic and antiviral treatments available

164
Q

COVID-19

A

viral infection of the upper and/or lower resp tract
can be a self-limiting illness for some pts and severe in others: symptomatic and antiviral treatments available

165
Q

risk factors for common cold

A

environmental exposure
allergic disorders
less diversity in social network
weakened immune systems

166
Q

clinical presentation of cold

A

1st symptom: Sore throat
nasal symptoms day 2-3
cough by day 4-5

167
Q

acute cough

A

< 3 weeks
viral upper resp tract infection

168
Q

subacute cough

A

3-8 weeks
does NOT require antibiotic treatment

169
Q

chronic cough

A

> 8 weeks
common cause: smoking, postnasal drip, asthma, GERD
ask about ACE inhibitor use

170
Q

exclusions for common cold

A

Difficulty breathing, SOB, or chest pain; cyanosis or hemoptysis; concern for TB; symptoms improve after 7-10 days; children < 2 years old; temp > 100.4; barking cough; whooping cough; HIV or chronic immunosuppressant therapy; risk factors for HIV infection; chronic illness; signs/symptoms consistent with influenza and/or COVID-19

171
Q

nonpharm therapy for common cold

A

rest, hydration, lozenges or hard candies, honey, chicken soup, broths, tea, nasal strips, nasal irrigation, salt gargles, humidifier

172
Q

zinc sulfate for cold

A

if admin orally within 24 hrs of the onset of symptoms, can reduce the duration of cold symptoms by up to 1 day
proposed mechanism: preventing rhinovirus and attachment in mucous membranes
nasal spray formulation->NOT SAFE
side effects: bad taste, nausea

173
Q

vitamin C for cold

A

may reduce duration of cold symptoms
lack of data for it as a therapeutic agent for colds

174
Q

echinacea

A

hot drink for 10 days for reducing symptom severity and duration

175
Q

treatment of upper respiratory symptoms

A

NO cure for cold, antibiotics are ineffective
1st line: nonpharm treatment preferred for all patients
adjunctive therapy: OTC meds

176
Q

1st generation antihistamines for cold

A

anticholinergc
caution: narrow-angle glaucoma, BPH

177
Q

1st gen antihistamine special pops

A

pediatrics:
> 6 years: use weight based dose
2-6 years: use CAUTION due to paradoxical excitation
<2 years: AVOID use
elderly:
AVOID use due to anticholinergic effects
pregnancy:
chlorpheniramine, diphenhydramine, clemastine are safe
breastfeeding:
use CAUTION-decreases milk supply and cause irritability and drowsiness in baby (CI)

178
Q

oral decongestants for cough due to cold

A

pseudoephedrine
max 7 days
CV stimulation
CNS stimulation
CI: w MAOIs
Caution: uncontrolled HTN, BPH, glaucoma

179
Q

special pop alpha1 agonists

A

pediatrics: down to 2 years
elderly: use CAUTION
pregnancy: must avoid during 1st trimester
breastfeeding: can decrease milk supply

180
Q

topical (intranasal) decongestants for cough due to cold

A

oxymetazoline
minimal systemic absorption
local SEs: nasal stinging, burning, dryness
CI: do NOT use > 3 days

181
Q

topical (intranasal) decongestants special pops

A

can be safely in elderly, children > 6 years, pregnancy, and breastfeeding

182
Q

topical analgesics for cough due to cold

A

benzocaine, phenol
lozenges, troches, mouthwash, sprays
soothe sore throat, avoid benzocaine in patients with hypersensitivities to other anesthetics

183
Q

topical antitussives for cough due to cold

A

menthol, camphor
ointments, lozenges, inhalation
nasal congestion, soothe sore throat

184
Q

topical analgesics/antitussives for cough due to cold special pop

A

safe for use in elderly and breastfeeding women
pregnancy: AVOID phenol, other products safe
pediatrics:
-benzocaine: >2 years
-oral sprays, topical rubs: > 2 years
-oral lozenges: > 5 years

185
Q

oral antitussives

A

ONLY cough
codeine
dextromethorphan
benzonatate

186
Q

codeine

A

oral antitussive
effects come from metabolites->morphine
CYP polymorphisms->unpredictabilty
BBW: addiction, abuse, resp, and CNS depression
side effects: nausea, sedation, dizziness, constipation

187
Q

codeine special pops

A

pediatrics: CANNOT be used in < 18 years
elderly: use CAUTION-CNS depression
pregnancy and breastfeeding: AVOID

188
Q

dextromethorphan

A

side effects < codeine
should NOT be taken within 14 days after stopping MAOIs

189
Q

dextromethorphan special pop

A

safe in elderly, >2 years, preg and breastfeeding

190
Q

benzonatate MOA

A

suppresses cough peripherally by anesthetizing the stretch or cough receptor of vagal afferent fibers

191
Q

benzonatate side effects

A

sedation, nasal congestion, chills, chest numbness, bronchospasms

192
Q

benzonatate special pops

A

safe in elderly, children > 10 years
limited data on safety in preg and breastfeeding

193
Q

protussives (expectorants)

A

guaifenesin
lack of evidence to support in treatment of cough due to the common cold
with a glass of water
avoid combo with dextromethorphan
well tolerated

194
Q

protussives (expectorants) special pops

A

safe in elderly, children > 2 years, pregnancy, breastfeeding

195
Q

referral for cough due to cold

A

7-10 days

196
Q

clinical presentation of fever

A

headache, diaphoresis, generalized malaise, chills, tachycardia, myalgia, irritability, anorexia, loss of appetite

197
Q

febrile seizures

A

risk factors: fam history, day care attendance, developmental delay, neonatal hospital stay > 30 days
risk of recurrence: multiple febrile seizures, first febrile seizure < 1 year, and fam history of epilepsy
antipyretics alleviate discomfort but do not minimize risk of recurrence

198
Q

exclusions for self care of a fever

A

patients > 3 months with rectal temp > 104 or < 3 month with rectal temp > 100.4
severe symptoms of infection
comorbidities that impair oxygen utilization (COPD, resp distress, heart failure)
impaired immune function
CNS damage
children: history of febrile seizures, spots or rash, refuse to drink, lethargic, irritable, vomiting and cannot keep down fluids, stiff neck

198
Q

referral for fever

A

doesn’t resolve in 3 days for adults or within 24 hrs for children < 2 years

199
Q

nonpharm therapy for fever

A

wear light weight clothing
remove blankets
maintain room temp at 68
adequate fluid intake is essential: balanced electrolyte formulations
sponging or baths have limited utility
ice baths are dangerous and NOT recommended

200
Q

pharm treatment of fever

A

ibuprofen
acetaminophen
aspirin

201
Q

ibuprofen special pops

A

pediatrics: > 6 months
elderly: use with caution
pregnancy: avoid in the 3rd trimester
breastfeeding: safe

202
Q

acetaminophen special pop

A

> 3 months
safe in preg, elderly, breastfeeding

203
Q

aspirin special pops

A

> 16 years
use with caution in elderly
avoid in 3rd trimester
breastfeeding: other agents preferred

204
Q

biphasic reaction

A

initial symptoms develop rapidly, reaching peak severity within 3-30 min
may be quiescent perod of 1-8 hrs before a 2nd
protracted anaphylaxis may also occur-persisting for days

205
Q

treatment of anaphylaxis

A

A: adrenalin
B: benadryl
C: corticosteroids

206
Q

risk factors for motion sickness

A

females, children, previous episodes, preg and use of hormonal contraceptives, inflammation of the inner ear, migraine headaches, emotional stress, anxiety

207
Q

clinical presentation of motion

A

nausea, vomiting, irritability, fatigue and drowsiness, yawning and belching, paleness, sudden sweating, increased salivation

208
Q

nonpharm strategies for motion sickness

A

avoid travel in difficult conditions and locations
slow, intermittent exposure to the offending motion can reduce symptoms
position self at most stable part of the vehicle
view true horizon
sych body with motion
minimize and prevent upset stomach

209
Q

pharm prevention for motion sickness

A

1st line: scopolamine
2nd line: 1st gen antihistamines

210
Q

scopolamine

A

apply 4 hr before travel, then every 72 hrs as needed
not indicated in children
AVOID in elderly
dry mouth
AVOID alcohol

DEENT (4 decks)

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