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OU Pt Assessment Spring 2018 > Physical Effects of Meds > Flashcards

Physical Effects of Meds Flashcards

1
Q

mechanism of drug-induced urticaria, rash, or allergy

A
  • IgE-mediated, Type I reaction

- Hypersensitivity

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2
Q

Which medications can cause drug-induced urticaria, rash, or allergy?

A
  • Penicillin, ampicillin, amoxicillin, and related antibiotics
  • Sulfonamides
  • Carbamazepine and several antiepilelptic drugs (AEDs)
  • Allopurinol
  • Monoclonal antibodies
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3
Q

characteristics of drug-induced rash / allergy

A

Morbilliform (AKA exanthematous; appears maculopapular)

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4
Q

Warning signs (red flags) for a more severe reaction of a drug-induced urticaria, rash, or allergy

A
  • Pain
  • Facial edema
  • Blisters or epidermal detachment
  • Fever
  • Involvement of the mucous membranes
  • Painful erythema
  • Shortness of breath or wheezing
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5
Q

What does DRESS stand for?

A

Drug Rash with Eosinophilia and Systemic Symptoms

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6
Q

DRESS characteristics

A
  • Morbilliform rash with red flag symptoms

- need immediate evaluation -> ER

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7
Q

common medications that cause DRESS

A
  • AEDs – carbamazepine, lamotrigine, phenytoin
  • Sulfonamides – sulfamethoxazole, sulfasalazine
  • Other antibiotics – vancomycin, minocycline, dapsone
  • Allopurinol
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8
Q

timing of DRESS to occur

A

2-6 weeks of drug initiation

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9
Q

mortality rate of DRESS

A

5-10%

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10
Q

management of DRESS

A
  • Stop medication and avoid it in the future (further administration can cause a more severe reaction)
  • Antihistamines +/- corticosteroids often used to help symptoms resolve
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11
Q

What are conditions that consists of a series of mucocutaneous reactions with extensive necrosis and epidermal attachment?

A
  • Erythema multiforme (EM)
  • Stevens-Johnson Syndrome (SJS)
  • Toxic Epidermal Necrolysis Syndrome (TENS)
  • TENS/EM/SJS
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12
Q

What is the mechanism of TENS/EM/SJS?

A
  • T-lymphocyte-mediated immune reaction
  • Leads to widespread apoptosis of keratinocytes
  • Considered a type IV extreme cutaneous reaction
  • Primarily caused by medications
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13
Q

EM

A
  • Maculopapular rash +/- vesicles occurring on the trunk
  • Accompanied by target lesions on hands or forearms; presence of the target lesions puts pt at higher risk for SJS and TENS
  • Typically has an infectious cause but can be medication-related
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14
Q

SJS

A
  • Also known as EM major

- Vesicular and bullous lesions of mucous membranes (e.g. mouth, eyes, GI tract)

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15
Q

TENS

A
  • Widespread epidermal necrosis
  • Resembles 3rd degree burns
  • 20-30% mortality rate
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16
Q

common medications that cause EM

A
  • NSAIDs
  • AEDs
  • Antibiotics Sulfonamides
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17
Q

common medications that cause SJS

A
  • Allopurinol
  • AEDs
  • Antibiotics Sulfonamides
  • Oxicam NSADs (meloxicam, piroxicam)
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18
Q

common medications that cause TENS

A
  • Allopurinol
  • AEDs
  • Antibiotics Sulfonamides
  • Oxicam NSADs (meloxicam, piroxicam)
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19
Q

triage considerations of TENS/EM/SJS

A
  • Immediate evaluation – ED
  • Early diagnosis, withdrawal of offending agent, supportive care offer best chance at recovery
  • Any of the three manifestations indicates the medication should never be used again
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20
Q

What does skin color blue-gray indicate?

A

possible cause of amiodarone or tricyclic antidepressants

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21
Q

What does hyperpigmentation indication?

A
  • melanin sensitivity

- possible cause of chemotherapeutic agents, hormones, prostaglandin agonists (bimatoprost, latanaprost)

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22
Q

What does jaundice indicate/

A
  • Hyperbilirubinemia

- possible cause of Atazanavir

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23
Q

Triage considerations of skin pigmentation changes

A
  • Refer to prescribing provider
  • Not life-threatening, more of a cosmetic issue
  • Adherence can be affected
  • Reversal of pigment changes can take months
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24
Q

characteristics of tardive dyskinesia

A
  • Intermittent hyperkinetic involuntary movements
  • Typically involve face, tongue, eyelids, or limbs
  • Difficult to define temporal relationship as timing often delayed
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25
mechanism of tardive dyskinesia
Acetylcholine deficiency combined with dopamine receptor sensitivity
26
common medications that cause tardive dyskinesia
- Antipsychotics: Typical (e.g. haloperidol) > atypicals (e.g. risperidone) - Metoclopramide
27
triage considerations for tardive dyskinesia
- Occurs at a rate of about 20-40% - Difficult for patients to have to live with - Direct patient to prescribing provider; can provide recommendations
28
recommendations for drug-induced tardive dyskinesia
- Dose reduction - Addition of a benzodiazepine - Switch to an agent with less risk (e.g. atypical antipsychotic)
29
characteristics of pulmonary symptoms
most common are - SOB - cough
30
mechanism of pulmonary symptoms
- Oxidant injury - Immune-mediated - Drug mechanism-mediated
31
common medications that cause pulmonary symptoms
- Beta blockers – drug induced bronchiole constriction - ACEI or ARB – cough only - Cytotoxic agents typically cause the most severe effects
32
triage considerations for pulmonary symptoms
- Refer to PCP if non-severe symptoms; ED if severe (assess the patient) - Often a diagnosis of exclusion – everything else is ruled out before meds are suspected - Assess via dose reduction or drug discontinuation
33
characteristics of angioedema
- Swelling of dermis and subcutaneous tissue, development of wheals; typically non-pruritic - Wheals forming in mouth and pharynx can cause airway obstruction
34
mechanism and common causes of angioedema
- Most commonly IgE-mediated mast cell activation – opioids, NSAIDs, aspirin - ACEI – inhibition of kinin metabolism - CCBs – histamine-release
35
triage considerations of angioedema
immediate attention -> ER
36
characteristics of peripheral edema
swelling of lower extremities
37
mechanism of peripheral edema
- Increased hydrostatic pressure from pre-capillary dilation (CCBs cause arterial vasodilation) and post capillary constriction - Thiazolidinediones and NSAIDs – increased sodium reabsorption in kidneys; more commonly an issue in those with pre-existing heart disease
38
common medications that cause peripheral edema
- DHP CCBs - Vasodilators – hydralazine, minoxidil - Thiazolidinediones – pioglitazone, rosiglitazone - NSAIDs
39
triage considerations of peripheral edema
- A benign effect; cosmetically an issue but not an indicator of a systemic danger - Diuretics not needed - Be sure to assess the whole patient • Other symptoms of fluid retention (e.g. weight gain, SOB, orthopnea) indicates another process is going on • Often drug-induced edema is a diagnosis of exclusion
40
Gynecomastia characteristics
breast enlargement in males
41
mechanism of Gynecomastia
- Enhanced estrogen activity | - Inhibition of testosterone action or production
42
common medications of Gynecomastia
- Most have either an effect on sex hormones or a steroid-like structure - Enhanced estrogen activity – estrogens, anabolic steroids - Inhibition of testosterone – spironolactone, megestrol, efavirenz, ketoconazole, phenytoin
43
triage considerations for Gynecomastia
- Refer to prescribing provider - Not systemically harmful - Patient can report chest pain; use patient assessment skills to discern - Typically resolves a few days after treatment discontinuation
44
alopecia characteristics
hair loss
45
common medications that cause alopecia
``` - variable mechanisms handout. - Chemotherapeutic agents - AEDs - Hormones - Statins ```
46
triage considerations for alopecia
Can be reversible with treatment discontinuation
47
hair growth mechanism
- Hirsutism – often related to androgenic stimulation of hormone sensitive hair follicles - Hypertrichosis – a specific pattern of hair growth along the temporal regions and forehead
48
common medications that cause hair growth
- Hirsutism: anabolic steroids, contraceptives, testosterone | - Hypertrichosis: Minoxidil (aka Rogaine®), Phenytoin, Cyclosporine
49
common medications (and mechanisms) that cause musculoskeletal effects
- Diuretics – cramping can result from electrolyte imbalances - Statins – typically affects larger muscles (e.g. back, leg muscles) - Fluoroquinolones – can lead to tendon rupture; typically Achilles tendon
50
triage considerations for musculoskeletal effects
- Diuretics – check BMP, treat as needed - Statins – assess whether myalgia, myositis, or rhabdomyolysis; will need prescribing provider intervention - Fluoroquinolones – discontinue
51
characteristics of Gingival hyperplasia
overgrowth of gum tissue
52
common medications that cause Gingival hyperplasia
- CCBs - Phenytoin - Cyclosporine
53
triage considerations for Gingival hyperplasia
- Prevention and reduction can be accomplished with good oral hygiene - Cosmetic issue but can also lead to increased risk of infection - Not reflective of systemic disease
54
mechanism of Gingival hyperplasia
proliferation of epithelial keratinocytes, fibroblasts, and collagen
55
characteristics of skin necrosis
Cutaneous infarction
56
mechanism of skin necrosis
- Precipitous fall in protein C (anticoagulant) - Promotion of hypercoagulable state - Thrombosis occurs in the cutaneous microvasculature
57
common medications that cause skin necrosis
- Warfarin | - Injection site reactions: Heparin, Interferon
58
triage considerations of skin necrosis
immediate treatment -> ER
59
skin necrosis: warfarin
- Usually starts between 3 and 5 days after initiation | - Tends to occur in higher-fat areas (breasts, buttocks, abdomen)
60
characteristics of Petechiae
Small red/purple spots caused by bleeding under the skin; typically do not blanche
61
mechanism of Petechiae
- Usually indicates a hemotologic abnormality (often thrombycytopenia) - Caused by a medication or underlying disease process - Must evaluate both possibilities
62
common medications that cause Petechiae
- Heparin - Antiplatelet medications - NSAIDs - Chemotherapeutic agents - Beta lactam antibiotics, linezolid - AEDs
63
triage considerations for Petechiae
Not immediately life-threatening but warrants quick workup – immediate PCP or urgent care/ED if unavailable

OU Pt Assessment Spring 2018 (10 decks)

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