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verbal exam #1 Flashcards

1
Q

what is the mechanism of action for acetaminophen?

A

central inhibition of prostaglandin synthesis

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2
Q

what is the drug class of acetaminophen?

A

antipyretic, analgesic

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3
Q

what is the drug class of ibuprofen?

A

antipyretic, analgesic, anti-inflammatory (NSAID) non-steroidal anti-inflammatory drug

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4
Q

What is the mechanism of action for ibuprofen?

A

Inhibits COX-1 and COX-2 centrally and peripherally to reduce prostaglandin synthesis

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5
Q

what are the side effects of acetaminophen related to its mechanism of action?

A

none

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6
Q

what are the side effects of ibuprofen related to its mechanism of action?

A

stomach upset, stomach ulcer/bleeding, bleeding, decreased kidney function, increased blood pressure, worsening of heart failure/fluid retention, increased risk of MI and stroke

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7
Q

what are the contraindications for ibuprofen?

A

3rd trimester of pregnancy, babies less than 6 mos. old, aspirin allergy

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8
Q

What are the signs & symptoms of myalgia?

A

dull, constant ache, sharp pain is relatively rare, weakness & fatigue of muscles

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9
Q

What are the characteristics of a tension headache?

A

bilateral, over the top of the head, extending to the base of the soul, gradual onset, can last minutes to days, may have scalp tenderness

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10
Q

What are the characteristics of a sinus headache?

A

pain in face, forehead or periorbital area, pressure behind eyes or face; dull, bilateral pain, worse in the morning. comes on with sinus symptoms, including purulent nasal discharge, lasts days (resolves with sinus symptoms), also can involve nasal congestion

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11
Q

What are the characteristics of a migraine headache?

A

usually unilateral, throbbing, may be preceded by an aura, sudden onset, can last hours to 2 days, may be accompanied by nausea

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12
Q

What are the exclusions for self-treatment of headache?

A

Severe head pain,
headaches that persist for 10 days with or without treatment,
last trimester of pregnancy,
less than 8 years old,
high fever or signs of serious infection
history of liver disease or consumption of 3 or more alcoholic drinks every day
Headache associated with underlying pathology except for minor sinus
symptoms consistent with migraine but no formal diagnosis of migraine headache

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13
Q

what are nonpharmacologic treatments for tension headache?

A

chronic tension headaches: relaxation exercises, stretching & strengthening of head & neck muscles

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14
Q

what are nonpharmacologic treatments for migraine?

A

take analgesic (NSAID) before predicted onset, look for food triggers, plenty of water

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15
Q

What is the dosage for APAP?

A

10-15 mg/kg, every 4-6 hours

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16
Q

What is the dosage for ibuprofen?

A

5-10 mg/kg every 6-8 hours

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17
Q

What ages can take naproxen

A

12 years and up

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18
Q

What ages can take aspirin?

A

15 years and up

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19
Q

what it the maximum dose of acetaminophen?

A

4000mg/day (more is potentially hepatotoxic)

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20
Q

what is the maximum dose of ibuprofen?

A

1200 mg

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21
Q

what its the dosage for naproxen?

A

220mg every 8-12 hours

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22
Q

What is the maximum dose of naproxen?

A

660 mg (440mg for over 65 yrs old)

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23
Q

what is the strength of children’s tylenol?

A

160mg/5mL

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24
Q

what is the strength of children’s motrin?

A

100mg/5mL

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25
Q

what are the drug-drug interactions with acetaminophen?

A

alcohol - increased risk of hepatotoxicity (avoid concurrent use, minimize alcohol intake when using acetaminophen)
warfarin - increased risk of bleeding (elevations in INR (measurement of blood clotting)

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26
Q

What are the drug-drug interactions with aspirin?

A 
valproic acid (displacement from protein-binding sites & inhibition of valprioc acid metabolism) - use naproxen instead
NSAIDs including COX-2 inhibitors - increased risk of gastroduodenal ulcers & bleeding - consider use of gastroprotective agents
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27
Q

What are the drug-drug interactions with ibuprofen?

A

aspirin - decreased anti platelet effect of aspirin - so take aspirin 30 min. before or 8 hrs after ibuprofen or use acetaminophen instead
phenytoin -displacement from protein-binding sites (monitor phenytoin levels, adjust dose as indicated)

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28
Q

What are the drug-drug interactions with NSAIDS?

A

bisphosphonates - increased risk of GI or esophageal ulceration
Digoxin - renal clearance of digoxin inhibited - monitor digoxin levels & adjust dose as indicated

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29
Q

what are the drug-drug interactions of salicylates and NSAIDs?

A

anticoagulants (increased risk of GI bleed)
alcohol (increased risk of GI bleed)
Methotrexate (decreased methotrexate clearance)
sulfonylureas (increased risk of hypoglycemia)

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30
Q

what is the mechanism of action for salicylates? (ASA)

A

inhibit prostaglandin synthesis from arachidonic acid by inhibiting COX-1 & COX-2 - mainly peripheral

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31
Q

What are some exogenous pyrogens and how do they cause fever?

A

toxins, microbes - do not independently increase the hypothalamic temperature set point - they stimulate the release of endogenous pyrogens. Endogenous pyrogens stimulate production of Prostaglandins E2 (PGE2) that elevate thermoregulatory set point in the hypothalamus.

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32
Q

What are endogenous pyrogens?

A

products released in response to or from damaged tissue: interleukins, interferons & tumor necrosis factor

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33
Q

What happens while body temperature set point is increasing?

A

patient experiences chills caused by peripheral vasoconstriction & muscle rigidity to maintain homeostasis.

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34
Q

What are the causes of fever?

A

infection, abnormal metabolism, drug induced

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35
Q

What are typical symptoms that accompany fever?

A

headache, diaphoresis

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36
Q

what is diaphoresis?

A

sweating profusely

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37
Q

what is the medical term for sweating profusely?

A

diaphoresis

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38
Q

What is considered a fever at each site of measurement?

A 
Rectal >100.4
Temporal>100.1 (0-2 mos. > 100.7, 3-47 mos. > 100.3)
Tympanic > 100
Oral > 99.7
Axillary > 99.3
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39
Q

What sites can electronic probe thermometers measure?

A

oral, rectal & axillary

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40
Q

What sites can infrared measure?

A

typmanic artery & temporal (detect heat from arterial blood supply - must be placed directly in the line of a blood supply)

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41
Q

What are the parameters for oral temp measurement?

A

should not engage in vigorous physical activity nor smoke nor drink hot or cold beverages at least 20 minutes prior to taking temp.

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42
Q

What is the age recommendation for tympanic temperature taking?

A

not for younger than 6 months, because ear canals are not developed fully - inaccurate readings

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43
Q

What are the major risks of fever?

A

seizures, dehydration & changes in mental status

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44
Q

What is the goal of treatment with fever?

A

to alleviate discomfort of fever by reducing body temp to a normal level

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45
Q

What are the exclusions for self-treatment of fever?

A

patients > 6 mos. w/rectal temp of >/= 104 (or equivalent)
Children < 6 mos. w/temp >/= 101
severe symptoms of infection that aren’t self-limiting
risk for hyperthermia
impaired oxygen utilization (COPD, respiratory distress, heart failure)
impaired immune function (cancer, HIV)
CNS damage (head trauma, stroke)
children w/history of febrile seizures
fevers that persist > 3 days
children who develop spots or rash
children who refuses to drink any fluids
children who are sleepy, irritable or hard to wake up
child who is vomiting & can’t keep down fluids

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46
Q

What are nonpharm therapy for fever?

A

fluid intake to prevent dehydration, body sponging w/tepid water (doesn’t reduce set point, so do it 1 hour after antipyretic therapy to permit appropriate reduction of set point & more sustained temp lowering response)
lightweight clothing
removing blankets
comfortable room temp (68)
increase fluid intake by 1-2 oz per hour for children & 3-4 oz per hour for adults

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47
Q

When does maximum fever reduction occur?

A

2 hours

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48
Q

For how many days can a person take fever reducing medication?

A

3 days - after that, see dr.

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49
Q

What is the pathophysiology of musculoskeletal pain?

A

pain impulses transmit from peripheral nociceptor to CNS by nerve fibers (commonly myofascial as in muscle strain or musculoskeletal as in arthritis). Trigger points cause reproducible referred pain pattern when pressure is applied.
mechanoreceptors and chemoreceptors mediate muscle pain
ischemic muscle pain caused by intramuscular pressure during activity that reduces blood supply to muscle (disappears w/in seconds of relaxing)
erythema (redness), edema & hyperalgesia (tenderness) - inflammatory response - histamine, bradykinin, serotonin, leukotrienes & prostaglandin E

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50
Q

What are the different types of muscle injuries?

A

strains, sprains, myalgia, tendonitis, bursitis, contusions caused by blunt trauma and delayed onset muscle soreness (overexertion)

51
Q

What is overexertion associated with

A

delayed-onset (8 hours or more) muscle soreness, can last for days, peaking at 24-48 hours.
reflects muscle damage initiated by force generated in the muscle fibers - induced by inflammation, acidosis, muscle spasms and/or microlesions.

52
Q

describe myalgia

A

possible swelling (rare), dull, constant ache (sharp pain rare), weakness & fatigue of muscles also common, acute onset if associated w/trauma, insidious (gradual, cumulative) w/drug-induced, hurts more when muscles contract,

53
Q

describe tendonitis

A

located in tendons around joint areas, warmth, swelling, erythema (redness), mild to severe pain generally occurring after use, loss of range of motion, often gradual onset, but can develop suddenly, hurts when you move affected joint

54
Q

describe bursitis

A

inflammation of the bursar within joints, commonly in knee, shoulder, big toe, warmth, edema, erythema, & possible crepitus (cracking), constant pain that worsens with movement or application of external pressure over the joint
onset is acute with injury; recurs with precipitant use of joint, hurts when you move affected joint

55
Q

describe sprain

A

stretching or tearing of a ligament within a joint, swelling, bruising, initially severe pain followed by pain, particularly with joint use; tenderness; reduction in joint stability and function, onset is acute with injury, hurts with movement of affected joint

56
Q

describe strain

A

hyperextension of a muscle or tendon, swelling, bruising, initial severe pain w/continued pain upon movement and at rest, muscle weakness, loss of some function, acute onset with injury, hurts with use of affected muscle or tendon

57
Q

describe osteoarthritis

A

affects weight bearing joints, knees, hip, low back, hands, noninflammatory joints, narrowing of joint space, restructuring of bone & cartilage (resulting in joint deformities), possible joint swelling, dull joint paint relieved by rest, joint stiffness, insidious development over years, exacerbating factors: obesity, lack of activity, heavy physical activity, repetitive movement, trauma

58
Q

What are modifying factors of myalgia?

A

elimination of cause, use of stretching, rest, heat, topical analgesics, system analgesics

59
Q

What are modifying factors of tendonitis?

A

elimination of cause; use of stretching, rest, ice, heat, topical analgesics, system analgesics

60
Q

What are modifying factors of bursitis?

A

joint rest, immobilization, topical analgesics, systemic analgesics

61
Q

What are modifying factors of sprain?

A

RICE; stretching, use of protective wraps, topical counterirritants, systemic analgesics

62
Q

What are modifying factors of strain?

A

RICE; stretching, use of protective wraps, topical counterirritants, systemic analgesics

63
Q

What are modifying factors of osteoarthritis?

A

continuous exercise (light to moderate activity), weight loss, analgesic medication, topical pain relievers

64
Q

What are exclusions for self-treatment of musculoskeletal injuries?

A

moderate to severe pain (greater than 6)
pain that lasts more than 10 days
pain that continues > 7 days after treatment w/topical analgesic
increased intensity or change in character of pain
pelvic or abdominal pain (other than dysmenorrhea (cramps))
accompanying nausea, vomiting, fever or other signs of systemic infection or disorder
visually deformed joint, abnormal movement, weakness in any limb, or suspected fracture
3rd trimester of pregnancy
< 2 years of age

65
Q

What are the treatment goals of musculoskeletal injuries?

A

decreasing pain, restoring function to affected areas, preventing re-injury & disability, improve activities of daily life, preventing acute pain from becoming chronic persistent pain

66
Q

describe RICE

A

rest, ice, compression, elevation
ice: 10-15 minute increments, 3-4 times/day for 1-3 days depending on severity of injury
elevate for 2-3 hours/day to reduce swelling relieve pain

67
Q

What is the limit for systemic analgesic therapy for musculoskeletal injuries?

A

10 days

usually scheduled dosing is good for 1-3 days followed by quick tapering of dose & interval as injury improves

68
Q

What is the recommended 1st line of treatment for osteoarthritis?

A

of hip & knee - APAP - based on safety rather than efficacy. Chronic NSAID use leads to more severe & prevalent side effects such as nephropathy (kidney disease), GI ulcerations & bleeding & potential for cardiac events.

69
Q

What are the four classes of counterirritants?

A

rubefacients, those producing cooling sensation, cause vasodilation, incite irritation without rubefaction

70
Q

What is the frequency & duration of use for counterirritants?

A

apply no more than 3-4 times/day for up to 7 days

71
Q

What are the products associated with each type of counterirritant?

A

rubefacients: methyl salicylate, turpentine oil, ammonia water, allyl isothiocynanate
Produce cooling sensation: camphor, menthol
cause vasodilation: histamine dihydrochloride, methyl nicotinate
incite irritation w/out rubefaction: capsicum, capsaicin

72
Q

How do counterirritants work?

A

pain relief results from nerve stimulation (rather than depression). paradoxical relieving of pain achieved by producing a less severe pain to counter a more intense one.

73
Q

where does methyl salicylate occur?

A

wintergreen oil or sweet birch oil (mountain tea)

74
Q

what is the MOA for methyl salicylate?

A

causes vasodilation of the cutaneous vasculature - reactive hyperemia (blood pooling responsible for hot feeling)

75
Q

What are the adverse affects of methyl salicylate?

A

skin irritation or rash (localized reaction) or systemic (salicylate toxicity). strong local reactions could be erythema, blistering, neurotoxicity, thermal hyperalgesia (increased sensitivity to pain)
heat exposure & exercise cause 3x increase in systemic absorption - increase in adverse systemic reactions
percutaneous absorption can occur, so avoid using with children, people who are sensitive to aspirin, have severe asthma or nasal polyps

76
Q

what is the MOA of camphor?

A

.1%-3% concentration depresses cutaneous receptors - used as topical analgesic, anesthetic & antipruritic (anti-itch),
concentrations > 3% stimulate nerve ending in skin & induce pain relief by masking moderate to severe deeper visceral pain w/milder pain arising from skin at level of innervation. Rubefacient if applied vigorously

77
Q

What are adverse reactions of camphor?

A

(high doses) nausea, vomiting, colic (spasmodic pain in abdomen), headache, dizziness, delirium, convulsion, coma & death.
camphor in infant nostrils can cause immediate respiratory collapse

78
Q

What is the MOA of menthol?

A

concentrations less than 1%, depresses cutaneous receptor response.
acts as counterirritant in concentrations > 1.25%
activates the TRPM8 receptor, triggering sensation of cold. Cold sensation travels along pathways similar to somatic pain sensations from the affected muscle or joint, which distracts from the sensation of pain. Initial feeling of coolness is soon followed by sensation of warmth.
also used as permeability enhancer to increase absorption of other topical medications
smaller concentrations used for upper respiratory congestion & rhinitis

79
Q

What are the CI of menthol?

A

hypersensitivity or sensitization to the agent. discontinue use if patient develops irritation, rash, burning stinging, swelling, or infection

80
Q

What is the MOA of methyl nicotinate?

A

inactive topically, readily penetrates cutaneous barrier. vasodilation and elevation of skin temperature with low concentrations. higher penetration rates achieved with gels (hydrophilic mediums)
ibuprofen & aspirin significantly depress skin’s vascular response, & b/c they suppress prostaglandin synthesis, the vasodilator response to methyl nicotinate is mediated, at least in part, by prostaglandin biosynthesis.

81
Q

What are side effects of methyl nicotinate?

A

generalized vascular dilation can occur when it passes through skin into circulatory system. –> drop in blood pressure, decrease in pulse rate, syncope (fainting)

82
Q

What is the MOA of capsicum (capsaicin, capsicum, and capsicum oleoresin)

A

capsicum contains 1.5% of an irritating oleoresin (.02% of that is capsaicin), Capsaicin is major pungent ingredient of hot (chili) pepper. capsaicin elicits a transient feeling of warmth through stimulation of TRPV1 receptor. More concentrated solutions produce sensation of burning pain, but that local sensation diminishes w/repeated applications due to tachyphylaxis. Do NOT cause blistering or reddening of skin b/c do not act on capillaries or other blood vessels.
MOA related to depletion of substance P - found in slow-conduction, unmyelinated type C neurons that innervate the dermis & epidermis. Substance P is released in the skin in response to endogenous (stress) and exogenous (trauma or injury) factors. pruritic (itching) stimuli along w/pain impulses are conveyed to central processing centers by type C fibers in skin, for which capsaicin has selective activity. Local application of capsaicin to peripheral axon depletes substance P from sensory neurons - occurs both peripherally and centrally. When substance P is released, burning pain occurs, but abates w/repeated applications.

83
Q

What is the dosing of capsaicin?

A

used to reduce pain but not inflammation of RA and OA. Efficacy decreases & local discomfort increases when capsaicin is applied less often. Duration of action is 4-6 hours, pain relief is usually noted w/in 14 days, but sometimes delayed by as much as 4-6 weeks. Once relief has been achieved, must continue to use it 3-4 times per day to keep pain from returning. use a glove and wash hands following use to reduce likelihood of capsaicin reaching topically sensitive areas like mucous membranes

84
Q

What are adverse reactions to capsaicin?

A

burning & stinging - diminishes w/use
causes burning in eyes
concentrations greater than .025% have been associated w/cough
CI w/hypersensitivity to capsaicin
discontinue w/broken skin (weeping, red, & presence of small ulcers)

85
Q

What’s the scoop on trolamine salicylate?

A 
category III (insufficient data to establish safety & efficacy), absorbed through skin & results in synovial fluid slicylate concentrations slightly below oral aspirin
recommended dosage for adults & children over 2 is 10-15% concentration applied not more than 3-4 times/day
most useful for patients who don't want counterirritant effects
some effectiveness in musicians playing time (hands, wrists, arms & fingers) & OA of the hands
86
Q

What are the age limits for external analgesics?

A

not for children younger than 2
most say older than 12
capsaicin say 18 and older b/c of potential for systemic absorption

87
Q

Glucosamine, in a nutshell

A

need glucosamine sulfate (not HCl), stimulates chondrocytes & synoviocytes to produce cartilage & synovial fluid, inhibits matrix metalloproteinase & modulates activities of collagenase & cytokines involved in stress reaction
1500mg/day - takes 6-8 weeks for pain relief, 4-6 months for full benefit
can cause nausea, stomach upset, constipation, diarrhea - alleviate by dividing dose & taking w/meals

88
Q

What are non drug measures for musculoskeletal?

A

RICE for muscle or joint injuries
periodic muscle cramps: stretch & massage affected area then rest or reduce activity to the muscle to allow it to loosen
Persistent cramps: apply heat
OA: heat or cold to affected areas, supporting area w/splints & range-of-motion & strength-maintenance exercises

89
Q

counseling tips for musculoskeletal

A

OTC analgesic for no longer than 10 days
don’t use counterirritants on damaged skin (abrasions, sunburns, etc)
wash hands after application
rub it in until you can’t see product (thin layer)
don’t put tight bandage or heat/warming devices on counterirritant
OA - consult Dr before treating
asthma - if you have wheezing or shortness of breath worsen while you use mentholated stuff, stop using it
don’t use any salicylates if you are receiving anticoagulation therapy or warfarin
nausea, vomiting, colic or other unusual symptoms while using camphor - seek med care

90
Q

what is a cold

A

viral infection of upper respiratory tract
nose has sensory, cholinergic & sympathetic nerves. Sensory fibers respond to mechanical & thermal stimuli & to mediators like histamine & bradykinin. Cholinergic & sympathetic nerves innervate glands & arteries that supply the glands. cholinergic stimulation dilates. sympathetic stimulation constricts arterial blood flow.

91
Q

What is the pathophysiology of a cold?

A

rhinovirus binds to intercellular adhesion molecule-1 receptors on respiratory epithelial cells in nose & nasopharynx. once inside epithelial cells, virus replicates & infection spreads to other cells. peak viral concentrations at 2-4 days - present for 16-18 days. infected cells release chemokines, then cytokines activate inflammatory mediators and neurogenic reflexes - result in recruitment of additional inflammatory mediators, vasodilation, transudation of plasma, glandular secretion & stimulation of pain nerve fibers & sneeze & cough reflexes. Inflammatory mediators & parasympathetic nervous system reflex mechanisms cause hyper secretion of water nasal fluid.

92
Q

what is the most common way to get a cold

A

self-innoculation of the nasal mucosa or conjunctiva after contact w/viral-laden secretions on animate or inanimate objects.

93
Q

when do cold symptoms appear?

A

1-3 days after infection. Sore throat is first, then nasal symptoms which dominate by day 2 or 3. Cough appears by day 4 or 5 (infrequent).
rarely have fever above 100F

94
Q

What is the treatment goal of cold?

A

prevent transmission of cold viruses & reduce bothersome symptoms

95
Q

What is the mainstay of cold treatment?

A

nonpharm therapy and hand washing

96
Q

What are the exclusions for self-treatment of cold

A

fever > 101.5
chest pain
shortness of breath
worsening of symptoms or development of additional symptoms during self-treatment
concurrent underlying chronic cardiopulmonary diseases (asthma, COPD, CHF)
AIDS or chronic immunosuppressant therapy
Frail patients of advanced age
infants < 9 mos.
hypersensitivity to recommended OTC medications

97
Q

What are nonpharm treatments for cold?

A

increase fluid intake
adequate rest
nutritious diet
increased humidification with steamy showers
humidifiers (cool mist)
vaporizers (steam)
saline nasal sprays or drops(moisten irritated mucosal membranes & loosen encrusted mucus)
saline gargles (sore throat)
infants: upright positioning, adequate fluid intake, irrigating nose w/saline drops, bulb syringe

98
Q

what is the MOA for decongestants?

A

adrenergic agonists (sympathomimetics) - stimulate alpha-adrenergic receptors which constricts blood vessels, thereby decreasing sinusoid vessel engorgement and mucosal edema

99
Q

what are the types of decongestants?

A

direct-acting (phenylephrine, oxymetazoline,& tetrahydrozoline)
Indirect-acting (ephedrine)
mixed (pseudoephedrine)

100
Q

What is the MOA for direct acting decongestants?

A

bind directly to adrenergic receptors

binds directly to adrenergic receptor site and acts as agonist to activate sympathetic nervous system

101
Q

What is the MOA for indirect acting decongestants?

A

displace norepinephrine from storage vesicles in pre junctional nerve terminals. have slowest onset & longest duration of action, but tachyphylaxis develops as stored neurotransmitter is depleted
increases the release of the neurotransmitter, norepinephrine at postganglionic nerve endings - activates the sympathetic nervous system

102
Q

What is the MOA for mixed decongestants?

A

bind directly to adrenergic receptors and displace norepinephrine from storage vesicles in pre junctional nerve terminals.

103
Q

What are the systemic decongestants

A

pseudo ephedrine and phenylephrine

104
Q

How are system decongestants metabolized?

A

rapidly metabolized by monamine oxidase (MAO) and catechol-O-methyltransferase in GI mucosa, liver & other tissues. short half-lives (Pseudoephdrine 6 hrs, phynyephrine, 2.5 hours) - peak concentrations at .5 - 2 hours.

105
Q

What are topical nasal decongestants?

A

ephedrine, naphazoline, oxymetazoline, phenylephrine, xylometazoline

106
Q

adverse effects w/decongestants

A 
cardiovascular stimulation (elevated blood pressure, tachycardia, palpitation, arrhythmias) CNS stimulation (restlessness, insomnia, anxiety, tremors, fear, hallucinations) children & adults more likely to experience adverse effects - more common w/systemic rather than topical
CI for patients receiving MAOinhibitors
may exacerbate diseases sensitive to adrenergic stimulation like HT, hyperthyroidism, diabetes mellitus, coronary heart disease, elevated intraocular pressure, BPH
107
Q

what are some complementary therapies for cold?

A

zinc - reducing cold symptoms or duration if started w/in 24 hours of symptom onset & taken every 2 hours while awake + prophylaxis for at least 5 mos.
high vitamin C prophylaxis w/marathon runners

108
Q

What is the MOA of 1st generation antihistamines

A

compete w/histamine at central and peripheral histamine 1 receptor sites - preventing histamine-receptor interaction & subsequent mediator release. nonselective - sedating - expose patients to risks of anticholinergic effects

109
Q

what are some of the 1st generation antihistamines?

A

diphenhydramine, doxylamine, brompheniramine (all of the -amines)

110
Q

what are the adverse reactions to antihistamines?

A

CNS effects (depression and stimulation) and anticholinergic effects (no see, no pee, no spit no shit).
CI in newborns, lactating women, patients w/narrow angle glaucoma
MAOIs
photosensitizing, so use sunscreen

111
Q

What is the pathophysiology of cough?

A

stimulated by chemically & mechanically sensitive, vaguely mediated sensory pathways in laryngeal, esophageal & tracheobronchial airway epithelium.

112
Q

What are the classifications of cough?

A

acute: less than 3 weeks
subacute: 3-8 weeks
chronic: more than 8 weeks

113
Q

What are the treatment goals of cough?

A

reduce number and severity of cough episodes and to prevent complications

114
Q

What are the exclusions for self-treatment of cough?

A

cough that lasts > 7 days or comes & goes & keeps coming back
high fever >/= 103 that does not resolve with usual self-care
cough accompanied by shortness of breath, chest pain, hemoptysis, chills, night sweats, tight-feeling throat, swollen legs/ankles, cyanosis, unintentional weight loss, rash, persistent heartache
cough that produces thick, yellow, tan, or green mucus or pus-like secretions
cough that suddenly worsens as cold or flu resolves
suspected drug-associated cough
history of symptoms of chronic disease associated w/cough (asthma, COPD, chronic bronchitis)
cough associated with inhalation of dust particles or objects, if irritant stays in the lungs

115
Q

what are nonpharm treatments for cough?

A

nonmedicated lozenges, humidification, hydration,
cautious hydration for those w/lower respiratory tract infections, heart failure, renal failure or other conditions potentially exacerbated by over hydration.

116
Q

what is the MOA of codeine

A

acts centrally on medulla to increase cough threshold. indicated for suppress of nonproductive cough caused by chemical or mechanical respiratory tract infection

117
Q

what are side effects of codeine?

A

nausea, vomiting, sedation, dizziness & constipation
additive CNS depression w/ depressants (barbiturates, sedatives or alchol)
CI for codeine hypersensitivity & during labor when premature birth is anticipated
impaired respiratory reserve (asthma, COPD), or preexisting respiratory depression, drug addicts, or individuals who take other respiratory depressants or sedatives, including alcohol - use codeine w/caution

118
Q

What is MOA of dextromethorphan?

A

nonopioid w/no analgesic, sedative, respiratory depressant or addictive properties. acts centrally in the medulla to increase cough threshold.

119
Q

what are side effects?

A

additive CNS depression w/alcohol, antihistimines, and psychotropic medications. combo w/MAOIs may cause serotonergic syndrom: increased blood pressure, hyperpyrexia, arrhythmia
should not be taken 14 days after MAOI is discontinued
can be abused for phencyclidine-like euphoric effect

120
Q

What is MOA of diphenhydramine?

A

acts centrally in medulla to increase cough threshold.

121
Q

what are side effects of diphenhydramine?

A

drowsiness, disturbed coordination, respiratory depression, blurred vision, urinary retention, dry mouth, dry respiratory secretions

122
Q

What is the MOA of guaifenesin?

A

loosens and thins lower respiratory tract secretions

123
Q

What are side effects of guifenesin?

A

nausea, vomiting, headache, rash, diarrhea, drowsiness, stomach pain.

PCC (2 decks)

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