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Pharmacology-School > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Captopril

A

Can cause ACE inhibitor induced cough

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2
Q

Chlorpheniramine and Diphenhydramine (First Generation Antihistamines)

A

M: Block H1 histamine receptor

  • crosses BB
  • antimuscarinic effects

CU: Allergic rhinitis

Prob: Sedation, antimuscarinic effects

*Avoid in elderly due to increased risk of confusion, constipation

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3
Q

Cetirizine, Loratadine, Fexofenadine (Second Generation Antihistamines)

A

M: Block H1 histamine receptor

  • does not cross BBB (non-sedating)
  • fewer antimuscuranic effects
  • ionized at pH 7.4 and highly bound to albumin

CU: Allergic rhinitis

Prob: few

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4
Q

Pseudoephedrine

A

Oral decongestant

M: indirect sympathomimetic: taken up via NET and VMAT, displaces NE, NE released via NET
-activates alpha 1

CU: Nasal congestion

Prob: Do not administer with MAO inhibitor

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5
Q

Benzonatate

A

M: Ester local anesthetic action on respiratory stretch receptors

CU: Relief of non-productive cough

Prob: Effectiveness is questionable
-Metabolized to para-aminobenzoic acid (PABA)

*Not approved in children <10 years of age

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6
Q

Guaifenesin

A

M: Stimulates respiratory secretions to increase respiratory fluid volumes and decease mucous viscosity

CU: Expectorant

Prob: Few

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7
Q

Effects of Nicotine

A

Low doses:

  • Stimulate reticular activating system (alerting)
  • Dopamine release (addictive)

Higher doses:
-CV effects (HTN, tachycardia)

Toxic doses:
-Seizures

Acute Toxicity:

  • HTN
  • Arrhythmias
  • Neuromuscular failure
  • Seizures
  • Coma
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8
Q

Gastroesophageal reflux (GERD)

A

Suppression of gastric acid with H2 receptor antagonist or proton pump inhibitor
-cause of cough

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9
Q

Codeine

A

Centrally acting (inhibit medullary cough center)

M: Metabolized to morphine via CYP2D6
-Antitussive mechanism not well understood

CU: Nasal congestion, pain management

Prob:

  • Increased risk of respiratory depression when combined with other CNS depressants
  • CYP2D6 ultra-rapid metabolizers may have enhanced opioid-mediated effects (including resp. depression) due to increased conversion to morphine
  • concerns in pediatrics
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10
Q

Dextromethorphan

A

Central acting (inhibit medullary cough center)

M:

  • No activity at opioid receptors
  • Glutamate receptor antagonist (NMDA receptor)
  • Exact mech for antitussive effect is unclear

CU: Antitussive-no analgesic or addictive properties

Prob: Relatively safe

  • At high doses (>2mg/kg), tachycardia, agitation, psychosis, seizure
  • Abuse (see slide)

*Prohibited in children younger than 6 years old

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11
Q

Roflumilast

A

M:

  • Decrease breakdown of cAMP leading to relaxation of smooth muscle
  • inhibitor of inflammatory cells

Delivery: oral

CU:

  • recurrent COPD exacerbations
  • chronic bronchitis

Prob: diarrhea, nausea, HA

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12
Q

N-acetylcysteine (NAC)

A

M:

  • Mucolytic agent used to decrease secretions in COPD via severing disulfide bonds of mucoproteins and DNA
  • Antioxidant
  • Replenish glutathione enabling detoxification of acetaminophen’s toxic metabolite (NAPQI)

CU:

  • Decrease COPD exacerbations
  • Acetaminophen OD (high doses)
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13
Q

Corticosteroids (Systemic)

-Dexamethasone, Prednisone

A

M: Activate nuclear glucocorticoid receptor to decrease transcription of certain pro-inflammatory cytokines

Delivery: oral

CU:

  • Asthma
  • Immunosuppressive effects

Prob:

  • Adrenal insufficiente upon abrupt cessation (taper)
  • many adv. effects (Cushing’s Syndrome-like sx., adrenal insufficiency, moon face, red face, bruises and petechiae, osteoporosis, edema)

** do not produce bronchodilation; decrease hyperactivity and reduce asthma exacerbations

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14
Q

Mepolizumab

A

M: Antibody to IL-5 which is involved in eosinophilic inflammation and eosinophil survival and priming

Delivery: subcutaneous injection every 4 weeks

CU: Add-on maintenance tx for severe asthma in patients with eosinophilic phenotype

Prob: Hypersensitivity runs
-rare reports of herpes zoster (vaccinate those at risk)

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15
Q

Barbiturates: Thiopental, Methohexital

A

M: Positive allosteric modulator at GABAa receptor

CU: Induction of anesthesia (gen. replaced with propofol)

  • anti-seizure activity
  • LOC
  • Amnesia
  • Poor analgesia
  • Poor muscle relaxation

Onset: rapid, higher induction doses for neonates and infants
*undergoes re-distribution

Context-sensitive half-time:

  • Long for thiopental,
  • methohexital rapidly cleared

CNS:
-Decreased cerebral metabolism and cerebral blood flow

Cardiovascular:
-Decreased systemic blood pressure

Respiratory:
-Respiratory depression worsened with co-administration with opioids

Contraindication:
- Patients with porphyria

Prob: Hiccups (esp. meth), paradoxical excitation (muscle tremors)

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16
Q

Sevoflurane

A

Analgesia: weak

Blood/gas partition coefficient: low, rapid onset, rapid emergence

Clinical Use: induction and maintenance – not irritating to airways

CNS: increased cerebral blood flow

Cardiovascular: decreased arterial blood pressure and cardiac output

Respiration: bronchodilation
Skeletal muscle: relaxant

Problems:
Malignant hyperthermia

17
Q

Desflurane

A

Analgesia: weak

Blood/gas partition coefficient: lowest, rapid onset, rapid emergence

Clinical Use: maintenance of anesthesia; not induction due to airway irritation

CNS: increase in cerebral blood flow with possible increase in intracranial pressure

Cardiovascular: tachycardia
Respiration: bronchodilation

Skeletal muscle: relaxant

Problems:

  • Malignant hyperthermia
  • Strong airway irritant leading to coughing, salivation, bronchospasm in awake patients
18
Q

Methoxyflurane (C3H4Cl2F2O)

A

Analgesia: good

Blood/gas partition coefficient: higher, slow onset and offset

Clinical Use: withdrawn in US but may be used in other countries

Problems:

  • An inhalation anesthetic used in the past, but withdrawn because of detrimental effects on the kidneys.
  • Extensive metabolism in the kidney (only 35% excreted unchanged by exhalation) results in the production of substantial amount of fluoride ions.

MAC = 0.2
Blood/gas partition coefficient = 13

19
Q

Non-Depolarizing NM Blockers:

Tubocurarine, Pancuronium, Vecuronium, Rocuronium, Cisatracurium, Mivacurium

A

M: Nicotinic receptor competitive antagonist

  • producing non-depolarizing blockade
  • producing flaccid paralysis

CU: Skeletal muscle relaxation during anesthesia – particularly useful for intubation

Interactions: Inhaled anesthetics can potentiate neuromuscular blockade by non-depolarizing muscle relaxants

Problems

Tubocurarine:

  • weak block of autonomic ganglia leading to decreased blood pressure
  • may cause histamine release leading to decreased blood pressure, bronchospasm, increased secretions

Mivacurium:
-may cause histamine release leading to decreased blood pressure, bronchospasm, increased secretions

Pancuronium:
-may block cardiac muscarinic receptors leading to tachycardia

20
Q

Non-Depolarizing NM Blockers:

Onset, Duration, Elimination

A

Onset:
2-6 min for most
Rocuronium: 1-2 min

Duration of action
Short: mivacurium (shortest at 15-20 min)
Intermediate (30-90 min): rocuronium, vecuronium, cisatracurium
Long: tubocurarine (3 hr)

Elimination:
Renal for most
Rocuronium and vecuronium: hepatic
Cisatracurium: spontaneous breakdown (Hofmann elimination)  
Mivacurium: plasma esterases
21
Q

Sugammadex

A

Action:
-Binds non-depolarizing neuromuscular blockers and encapsulates them
-Rapid reversal of blockade
Greatest affinity: rocuronium and vecuronium

Clinical Use:
Rapid reversal of neuromuscular blockade

Problems:
Few
-can cause hypersensitivity/allergic reactions (may cause anaphylaxis in 0.3% of patients)

22
Q

Neostigmine

A

Action:
-Substrate of acetylcholinesterase but hydrolyzed more slowly than acetylcholine leading to less availability of the enzyme for ACh degradation and increased levels of ACh at the NMJ

BBB?
-Does not cross blood-brain barrier

Clinical Use:

  • Used for MG
  • reversal of non-depolarizing neuromuscular blockade
  • post-op urinary retention

Problems:
Excessive cholinergic activation

23
Q

Atropine

A

Action:
Muscarinic receptor antagonist

Clinical Use:

  • Mydriasis (often for eye exam)
  • Antidote for muscarinic toxicity (mushroom poisoning, cholinesterase inhibitors)

Problems:
Systemic antimuscarinic effects

24
Q

Dantrolene

A

Action: NOT CENTRALLY ACTING!
-Binds to ryanodine receptor and blocks its opening thus decreasing release of calcium from sarcoplasmic reticulum in the muscle fiber

Clinical Use:

  • spasticity
  • malignant hyperthermia (reduces mortality from 80% to <10%)

Advantages: less sedation than diazepam or baclofen

Problems:

  • generalized muscle weakness,
  • sedation
  • potential serious hepatotoxicity (black box warning)
25
Q

Baclofen

A

Agonist at GABAb receptor (Gi)

26
Q

Cyclobenzaprine

A

Action:

  • Inhibits muscle stretch reflex in spinal cord by poorly understood mechanism.
  • Structurally related to tricyclic antidepressants, thought to act at brainstem.

Clinical Use: Treatment of ACUTE local muscle spasm due to local tissue trauma or muscle sprains

Problems:

  • strong antimuscarinic effect,
  • confusion
  • sedation
  • avoid in elderly

NOTE: does not treat muscle spasm due to cerebral palsy or spinal cord injuries

27
Q

Corticosteroids (Inhaled):

Fluticasone, Budesonide, Mometasone

A

Action: Activate the nuclear glucocorticoid receptor to decrease transcription of certain pro-inflammatory cytokines

Delivery: inhalation, formulations available combining with LABA

Clinical Use: Persistent asthma (mild to severe) or severe COPD (to reduce exacerbations)

Problems: local effects: oropharyngeal candidiasis, hoarseness, throat irritation and cough; systemic effects with chronic use: osteoporosis and cataracts and other systemic effects

NOTE: Concern of systemic absorption with daily use (swallowed: rinse mouth or use spacers in inhalers to minimize delivery of too much drug)

NOTE: Corticosteroids do not produce bronchodilation but decrease bronchial hyperreactivity and reduce asthma exacerbations

Pharmacology-School (2 decks)

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