Exam 2 Material Flashcards
1
Q
locations of histamine
A
basophils and mast cells
CNS
enterochomaffin-like cells (ECLs)
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)
3
Q
nonantigen mediated release of histamine
A
receptor mediated
any thermal mechanical stress
basic drugs and chemicals
some venoms
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
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
6
Q
during allergic responses and inflammation H1
A
increased adhesion molecules and chemotaxis
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
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
9
Q
during allergic responses and inflammation H2 rec
A
decreased eosinophil and neutrophil chemotaxis
decreased cytokine production
10
Q
H3 receptor
A
presynaptic autoreceptor in brain, myenteric, and other neurons
some constitutive activity in some systems
11
Q
histamine affects on the H3 receptor
A
sleep/wake cycle, energy, and endocrine homeostasis
cognition and memory
12
Q
during allergic rxns and inflammation H3 receptors
A
neurogenic inflammation
pro-inflammatory
prevents excessive bronchoconstriction
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
14
Q
histamine affects on H4 receptor
A
causes differentiation of myeloblasts
15
Q
during allergic rxns and inflammation H4 receptor
A
increases eosinophil chemotaxis
16
Q
MOA of H1 antihistamines
A
inverse agonist at the H1 receptor
binds and stabilizes the inactive state of the receptor
17
Q
1st generation of H1 antihistamines
A
strong sedative effects
more likely to block autonomic receptors
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
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
20
Q
side effects of 1st generation antihistamines
A
sedation
paradoxical excitement in children
nervous system effects
anticholinergic effects
CV effects
sensitivity reactions
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
22
Q
paradoxical excitement in children 1st generation antihistamines
A
restlessness, tremors, euphoria, delirium, and seizures
23
Q
nervous system effects 1st generation antihistamines
A
disturbed coordination
decreased cognition
increased appetite
abuse potential
peripheral sodium channel blockade
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
25
CV effects of 1st generation antihistamines
tachycardia
prolongation of QT interval
hypotension or orthostatic hypotension
26
sensitivity rxns of 1st generation antihistamines
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
27
order of ability (1st generation antihistamines) to cross BBB
sedation
diphenhydramine=promethazine=hydroxyzine>chlorpheniramine=dexchlorpheniramine
28
anticholinergic order of 1st generation antihistamines
diphenyhydramine=promethazine>brompheniramine=chlorpheniramine=hydroxyzine> azelastine
29
side effects of 2nd generation antihistamines
no or low sedation
30
fexofenadine food DDI
orange, apple, or grapefruit juice reduces serum levels of fexofenadine
-reduces OATP activity=decreased oral bioavailability
separate by 2 hrs
31
anticholinergic/antimuscarinic medication
ipratropium
32
ipratropium
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
33
adverse effects of ipratropium
headache, epistaxis, and nasal dryness
34
leukotriene receptor antagonist medication
montelukast
35
montelukast
inhibits cysteinyl leukotriene receptor (CysLT)
perennial AR: > 6 months
seasonal AR: > 2 years
PO once a day
36
adverse effects of montelukast
a lot of serious neuropsych effects (CNS effects)
GI effects as well
37
where are a2 receptors located
arterioles
mucosal membrane of vasculature of nasopharynx
vascular smooth muscle
pancreas
CNS/peripheral NS
38
where are a1 receptors located
venules
mucosal membrane of vasculature of nasopharynx
vascular smooth muscle
heart
NCS
bladder neck
piloerector muscle
39
secretory cells
epithelial cells, goblet cells, and basal cells
secretes: enzymes, IgA, mucus
40
cholinergic innervation of alpha receptors
vasodilation
increases mucus secretion
41
adrenergic innervation of alpha receptors
vasoconstriction
decreases mucus secretions
42
alpha receptor agonist pharm effect
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
43
pseudoephedrine (alpha 1 agonist) side effects
CNS effects
-nervousness, irritability, insomnia
-athletic performance enhancement
CV effects
-increase BP, HR
-HTN and ischemia
GI effects
-decrease appetite
piloerection
44
alpha2 agonists
oxymetazoline, xylometazoline, tetrahydrozoline
topically
-constricts dilated blood vessels in nasal mucosa
-depresses CNS
45
alpha2 agonists side effects
rhinitis medicamentosa
burning, stinging, nasal dryness, and sneezing
damage to nasal septum with long term use
CNS depression
46
cough reflex
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
47
where do drugs work in the cough reflex
sensory receptors
cough center
48
sensory receptors
send signals through vagal afferent fibers to the central cough center in the medulla
49
codeine and hydrocortisone MOA
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
50
dextromethorphan MOA
PO antitussives
NMDA receptor antagonist and agonist at delta opioid receptors
51
antihistamines PO antitussives MOA
H1 inverse agonist and muscarinic antagonist on medullary cough center and resp. tract
52
local anesthetic/Na+ channel blockers PO antitussives MOA
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
53
codeine and hydrocortisone side effects
nausea, drowsiness to sedation, dizziness, and constipation
54
dextromethorphan side effects
nausea, drowsiness, dizziness, and constipation
extremely large doses do produce intoxication with hallucinations
55
local anesthetic/Na+ channel blockers PO antitussives side effects
drowsiness, dizziness, headache, nasal congestion, a vague "chilly" feeling
56
diphenhydramine and promethazine side effects
drowsiness and sedation
anticholinergic effects
57
local anesthetic/Na+ channel blockers topical antitussives MOA
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
58
local anesthetic/Na+ channel blockers topical antitussives side effects
irritation, redness, or blistering of skin
59
toxicity of local anesthetic/Na+ channel blockers topical antitussives
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
60
demulcents
forms a soothing film over a mucous membrane, relieving minor pain and inflammation
effective for no more than 30 minutes usually
61
expectorants medication
guaifenesin
62
guaifenesin MOA
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
63
guaifenesin side effects
N/V, dizziness, headache, rash
64
mucolytic products
acetylcysteine
dornase alfa
water
65
dornase alfa
DNAase
purulent mucus is composed of highly polymerized DNA
selectively cleaves DNA
66
uses of mucolytics
cystic fibrosis
APAP antidote (acetylcysteine)
67
corticosteroids
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
68
corticosteroids therapeutic uses
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
69
direct action corticosteroid MOA
drug-receptor complex binds to DNA (RE) to inhibit or promote transcription
requires 2 drug receptor complexes that bind to a response element
70
indirect action corticosteroid MOA
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
71
corticosteroids side effects
growth inhibition in children
avascular necrosis of bone
osteopenia
increased risk of infection
poor wound healing
cataracts
hyperglycemia
HTN
masking of inflammation
72
NSAIDs general mechanism
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
73
aspirin MOA
irreversibly acetylates and blocks platelet COX
74
ibuprofen and other non-COX selective NSAIDs
reversibly inhibit COX
75
common adverse effects of NSAIDs
CNS
CV
GI
hematologic
hepatic
pulm
skin
renal
76
ibuprofen side effects
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
77
drug interaction of ibuprofen
interferes with antiplatelet effects of aspirin
78
cautions of ibuprofen
can be used occasionally by pregnant women, but may have third trimester effects, including delay of parturition
excretion into breast milk is minimal
79
contraindications of ibuprofen
nasal polyps, angio-edema, pts that have bronchospasms with aspirin
80
acetaminophen MOA
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
81
acetaminophen pharmacodynamics
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
82
acetaminophen PK
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
83
symptoms of acetaminophen OD
nausea, vomiting, diarrhea, and abdominal pain
84
max daily dose is 4 g of acetaminophen
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
85
larger doses of acetaminophen side effects
dizziness, excitement, and disorientation
86
15 g of acetaminophen side effects
severe hepatotoxicity with centrilobular necrosis, possible acute renal tubular necrosis
87
acetaminophen OD management
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
elimination of acetaminophen OD
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
biosynthesis of histamine
L-histidine to histamine via L-histidine decarboxylase
90
1st generation antihistamines chem
ethanolamines
ethylenediamines
piperazines
propylamines
tricyclics
91
ethanolamines
1st gen antihistamines
diphenhydramine, dimenhydrinate, doxylamine, carbinoxamine, clemastine
O\_/N
undergoes N-demethylation, then 1)MAOs, 2) ALDH to form conjugates
92
ethylenediamines chem
less potent-fewer SEs
tripelennamine, pyrilamine, antazoline
N\_/N
undergoes N-demethylation, then 1)MAOs, 2) ALDH to form conjugates
93
piperazines 1st gen chem
cyclized ethyenediamines
slow onset; long DoA
cyclizine, chlorcyclizine, meclizine, hydroxyzine
undergoes N-demethylation or CYPs/FMO
94
propylamines chem
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
tricyclic chem 1st gen
1st gen antihistamine
azatadine, cyproheptadine, phenindamine, olopatidine, promethazine
3 fused rings attached N; undergoes de-alkylation
96
2nd generation antihistamine chem
piperidines
tricyclics
piperazines
multicyclics
97
piperidines
2nd gen antihistamines
fexofenadine-active metabolite of terfenadine
1) CYP, 2) ADH, 3) ALDH
98
tricyclics 2nd gen chem
loratadine, desloratadine (active metabolite of loratadine)
desloratadine-long DoA active metabolite
3 fused rings attached with N
99
piperazines 2nd gen chem
cetirizine, levocetirizine
products of 1) ADH, 2) ALDH of hydroxyzine
cetirizine-racemic
levocetirizine-more active isomer
100
multicyclics
2nd gen antihistamines
acrivastine, levocabastine, emadastine
multiple cyclic groups with a difference from amine
ionize at physio pH
101
SAR antihistamine
terminal N is tertiary
AR-groups (free or fused)
linker: alkyl or alkene (branched or cyclic)
small to bulkier R-groups on N
102
codiene
well-distributed, including into breast milk
O- and N-demethylations to morphine/O-glucuronidation/O-sulfation to glucs/sulfates metabolites
103
opioid antitussives
morphine, dextromethoprhan, hydrocodone, codiene
104
non-opioid antitussives
benzonatate
chlophedianol
105
benzonatate chem
non-opioid antitussives
PABA derivative
v lipophilic ester
peripheral antitussive effects
15-20 min onset, t1/2=3 hrs
106
chlophedianol
non-opioid antitussives
1/3 codeine's activity
weak antihistamine/local anesthetic props
slow onset-prolonged antitussive activity
107
SAR local anesthetics
basic amine
esters/amides/phenols/aromatic FG
108
local antitussives metabolism
ester and amide hydrolysis; N-dealkylation; N-OH
109
toxicity of local antitussives
benzocaine, benzocaine hydroxylamine, xylidine hydroxylamine
110
decongestant metabolism
phenylephrine-poor PO bioavailability
pseudoephedrine-good PO bioavailability-slow MAO metabolism @ N
111
SAR of decongestants
phenethylamine
OH increases activity
CH3 decreases activity but increases DoA (resistance to MAO)
2C spacer btwn Ar and N (optimal)
112
adamantanes
older anti-influenza agents
embed a lipophilic cage
inhibits viral replication
CNS side effects
113
sialic acid analogs
neuraminidase inhibitors are newer
mimic sialic acid and inhibit viral replication
oseltamivir, zanamivir, peramivir
114
oseltamivir
prodrug via carboxyesterases and 1st oral NA inhibitor
115
zanamivir and peramivir
contain guanine (basic group)
active drugs
116
SAR of sialic acid analogs
COOH-drug activity
X (OH, NH2, guanidine) increases binding to NA
117
dibenzothiepine(s)
carbonate prodrug activated by ester hydrolysis
selectively inhibits cap-endonucleases, which initiate mRNA synthesis in influenza virus
118
acetaminophen chem
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
NSAIDs chem
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
salicylates chem goals
minimize GI erosin
enhance potency
improve DoA
121
salicylate prodrugs
reduced via azo-reductase enzymes
122
salicylates metabolism
amino acid conjugation-major metabolit-salicyuric acid
123
acetic acids NSAIDs
indomethacin
diclofenac
etodolac
sulindac
124
propionic acids NSAIDs
ibuprofen
fenoprofen
ketoprofen
naproxen
oxaprozin
125
ibuprofen chem
propionic acid
isomerase with w-oxidations via 2C9 and 2C19
126
naproxen chem
propionic acid
sold as separate isomers
DoA: 12 hrs
metabolism: aromatic oxidation, P II glucuronidation
127
phases of allergies
Phase I: sensitization phase (initial exposure)
phase II: early phase
phase III: cellular recruitment
phase IV: late phase (symptoms begin)
128
risk factors of allergic rhinitis
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
clinical presentation of allergic rhinitis
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
allergic rhinitis (AR)
IgE mediated inflammatory response of nasal mucous membranes after exposure to inhaled allergens
may consider this if the allergen is unknown
130
seasonal allergic rhinitis
IgE mediated inflammatory response to seasonal allergens
length of exposure varies on location and climate
131
perennial allergic rhinitis
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
duration classification of AR
intermittent
persistent
episodic
133
intermittent AR
symptoms occurs <4 days/week OR < 4 weeks
134
persistent AR
symptoms occur > 4 days/week AND > 4 weeks
135
episodic AR
symptoms occur on exposure to or contact with potential allergen that is not a part of the person's environment
136
mild symptoms of AR
do NOT impair sleep or daily activities
137
moderate-severe symptoms AR
one or more of the following occurs:
impairment of daily activities or sleep
138
common cold symptoms
sneezing +/-
sore throat (1st symptom)
fever +/-
cough +/-
muscle aches +/-
139
influenza symptoms
cough
muscle aches
sore throat
fever
SOB
140
allergic rhinitis symptoms
sneezing
no sore throat
no fever
itchy eyes
141
COVID-19 symptoms
cough (mostly dry)
muscle aches
fever
SOB
142
diagnosis of AR
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
exclusions of AR
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
nonpharm therapy for AR
allergen avoidance
-dust mites
-pollen/environmental allergens
-pets
netipot
-nasal symptoms
145
first lines of pharm therapy for AR
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
adjunctive therapy for AR
decongestants
147
intranasal steroids for AR
may take 1-2 weeks
budesonide, fluticasone furoate, fluticasone propionate, mometasone, triamicolone
148
intranasal steroids side effects
minor side effects: dryness, stinging, headache, epistaxis
systemic side effects: minimal
149
intranasal steroids special pops
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
2nd generation antihistamine Oral for AR
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
2nd generation antihistamines: non-oral for AR
less systemic effects with topical meds
can be used in combo with INS if symptoms not controlled on INS alone
azelastine
152
2nd generation antihistamines: special pops
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
decongestants for AR
PO: pseudoephedrine
intranasal: oxymetazoline
nasal congestion
short-term relief only (1 week for PO, 3 days for intranasal)->rebound congestion
154
other agents for AR
intranasal cromolyn
intranasal ipratropium
oral epinephrine inhalation
montelukast
immunotherapy
155
intranasal cromolyn for AR
not as effective as other agents->better if started BEFORE symptoms begin
good safety profile: pregnancy and children < 2
156
intranasal ipratropium for AR
effective for rhinorrhea only
may be used in combo other products if rhinorrhea is a prominent symptom
157
oral epinephrine inhalation for AR
not recommended for use in AR or asthma
158
montelukast
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
immunotherapy (allergy shots) for AR
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
monitor and evaluate for AR
own self-monitoring
161
intranasal admin
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
common cold
viral infection of the upper resp tract
transmission: self-inoculation or airborne
self-limiting illness: symptomatic treatment only
163
influenza
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
COVID-19
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
risk factors for common cold
environmental exposure
allergic disorders
less diversity in social network
weakened immune systems
166
clinical presentation of cold
1st symptom: Sore throat
nasal symptoms day 2-3
cough by day 4-5
167
acute cough
< 3 weeks
viral upper resp tract infection
168
subacute cough
3-8 weeks
does NOT require antibiotic treatment
169
chronic cough
> 8 weeks
common cause: smoking, postnasal drip, asthma, GERD
ask about ACE inhibitor use
170
exclusions for common cold
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
nonpharm therapy for common cold
rest, hydration, lozenges or hard candies, honey, chicken soup, broths, tea, nasal strips, nasal irrigation, salt gargles, humidifier
172
zinc sulfate for cold
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
vitamin C for cold
may reduce duration of cold symptoms
lack of data for it as a therapeutic agent for colds
174
echinacea
hot drink for 10 days for reducing symptom severity and duration
175
treatment of upper respiratory symptoms
NO cure for cold, antibiotics are ineffective
1st line: nonpharm treatment preferred for all patients
adjunctive therapy: OTC meds
176
1st generation antihistamines for cold
anticholinergc
caution: narrow-angle glaucoma, BPH
177
1st gen antihistamine special pops
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
oral decongestants for cough due to cold
pseudoephedrine
max 7 days
CV stimulation
CNS stimulation
CI: w MAOIs
Caution: uncontrolled HTN, BPH, glaucoma
179
special pop alpha1 agonists
pediatrics: down to 2 years
elderly: use CAUTION
pregnancy: must avoid during 1st trimester
breastfeeding: can decrease milk supply
180
topical (intranasal) decongestants for cough due to cold
oxymetazoline
minimal systemic absorption
local SEs: nasal stinging, burning, dryness
CI: do NOT use > 3 days
181
topical (intranasal) decongestants special pops
can be safely in elderly, children > 6 years, pregnancy, and breastfeeding
182
topical analgesics for cough due to cold
benzocaine, phenol
lozenges, troches, mouthwash, sprays
soothe sore throat, avoid benzocaine in patients with hypersensitivities to other anesthetics
183
topical antitussives for cough due to cold
menthol, camphor
ointments, lozenges, inhalation
nasal congestion, soothe sore throat
184
topical analgesics/antitussives for cough due to cold special pop
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
oral antitussives
ONLY cough
codeine
dextromethorphan
benzonatate
186
codeine
oral antitussive
effects come from metabolites->morphine
CYP polymorphisms->unpredictabilty
BBW: addiction, abuse, resp, and CNS depression
side effects: nausea, sedation, dizziness, constipation
187
codeine special pops
pediatrics: CANNOT be used in < 18 years
elderly: use CAUTION-CNS depression
pregnancy and breastfeeding: AVOID
188
dextromethorphan
side effects < codeine
should NOT be taken within 14 days after stopping MAOIs
189
dextromethorphan special pop
safe in elderly, >2 years, preg and breastfeeding
190
benzonatate MOA
suppresses cough peripherally by anesthetizing the stretch or cough receptor of vagal afferent fibers
191
benzonatate side effects
sedation, nasal congestion, chills, chest numbness, bronchospasms
192
benzonatate special pops
safe in elderly, children > 10 years
limited data on safety in preg and breastfeeding
193
protussives (expectorants)
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
protussives (expectorants) special pops
safe in elderly, children > 2 years, pregnancy, breastfeeding
195
referral for cough due to cold
7-10 days
196
clinical presentation of fever
headache, diaphoresis, generalized malaise, chills, tachycardia, myalgia, irritability, anorexia, loss of appetite
197
febrile seizures
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
exclusions for self care of a fever
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
referral for fever
doesn't resolve in 3 days for adults or within 24 hrs for children < 2 years
199
nonpharm therapy for fever
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
pharm treatment of fever
ibuprofen
acetaminophen
aspirin
201
ibuprofen special pops
pediatrics: > 6 months
elderly: use with caution
pregnancy: avoid in the 3rd trimester
breastfeeding: safe
202
acetaminophen special pop
> 3 months
safe in preg, elderly, breastfeeding
203
aspirin special pops
> 16 years
use with caution in elderly
avoid in 3rd trimester
breastfeeding: other agents preferred
204
biphasic reaction
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
treatment of anaphylaxis
A: adrenalin
B: benadryl
C: corticosteroids
206
risk factors for motion sickness
females, children, previous episodes, preg and use of hormonal contraceptives, inflammation of the inner ear, migraine headaches, emotional stress, anxiety
207
clinical presentation of motion
nausea, vomiting, irritability, fatigue and drowsiness, yawning and belching, paleness, sudden sweating, increased salivation
208
nonpharm strategies for motion sickness
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
pharm prevention for motion sickness
1st line: scopolamine
2nd line: 1st gen antihistamines
210
scopolamine
apply 4 hr before travel, then every 72 hrs as needed
not indicated in children
AVOID in elderly
dry mouth
AVOID alcohol
