NSG 511 exam 2 Questions with 100% accurate solutions+ rationales 2026

pathways to airflow limitation in asthma

airflow limitation in asthma is caused by bronchospasm and/or inflammation

- allergen > mast cell reaction > inflammatory mediators > bronchospasm

- allergen > mast cell reaction> infiltration of inflammatory mediators and inflammatory cells > inflammation

- bronchial hyperreactivity > triggers > bronchospasm

bronchitis (COPD) pathway to airflow limitation

- continuous irritation from smoke/pollution > inflammation > bronchial edema/hyper secretion of mucus > airway obstruction

emphysema (COPD) pathway to airflow limitation

- continuous irritation from smoke/pollution > inflammation > increased protease activity > destruction of alveolar walls > airway obstruction

considerations for metered dose inhalers (MDIs)

- most commonly prescribed

- must coordinate between activation and inhalation

- notorious for incorrect use: patient education necessary

- more drug reaches lungs with use of spacer (21% vs 9%)

considerations for dry powder inhaler (DPIs)

- activated by inhalation (no coordination/spacer necessary)

- improved medication delivery to lungs

considerations for nebulizers

- fine mist droplets

- no coordination necessary

- powered equipment (not portable, needs battery or plug)

considerations for respimats

- better than other drug inhalation delivery devices

- activated by inhalation (no coordination)

- fine mist droplets (better delivery to lower respiratory tract)

- portable

Uses for pulmonary glucocorticoids

asthma and COPD

routes for pulmonary glucocorticoids

- oral

- parenteral

- inhalation

mechanism of pulmonary glucocorticoids

- anti-inflammatory

- immunosuppressant

pulmonary glucocorticoid prototypes (and their routes)

- fluticasone/budesonide (inhalation)

- prednisone/prednisolone (oral)

- methylprednisolone (IV)

indications for pulmonary glucocorticoids

prophylaxis for obstructive airway diseases

- inhaled

- on a fixed schedule

- controller medication

temporary use for severe obstructive disease when unable to deliver drug via inhalation

- oral or parenteral

- ex: no airway movement during status asthmaticus finch

side effects for pulmonary glucocorticoids

- thrush (oral candidiasis): rinse mouth after usage of inhaled agents to prevent this

- hyperglycemia

- peptic ulcer disease

theoretical side effects

- immunosuppression

- skeletal muscle growth suppression in children

- bone loss

- adrenal suppression

why are side effects of inhaled glucocorticoids rare (other than thrush)?

These side effects are predictable for glucocorticoid use. However, the inhaled dose for asthma patients is typically too low to elicit any of these effects. They may be seen during long term oral use, which is also uncommon for asthma patients.

short acting beta agonists (SABA) prototype and route

- albuterol

- oral or inhaled

long acting beta agonists (LABA) prototype

Salmeterol

"-terol" mechanism of action

- beta 2 agonist

- epinephrine and "-terols"

Short acting beta agonist (SABA) indications

quick relief during asthma (or similar) exacerbation

long acting beta agonist (LABA) indications

- long term control of asthma

- must be combined with glucocorticoids

side effects of -terols

- tachycardia is most common

- activation of the sympathetic nervous system (cross over of beta 2 agonists to beta 1 receptors)

types of bronchodilators

- beta agonists (-terols)

- muscarinic antagonists

pulmonary muscarinic antagonist prototypes and route

- ipratropium

- tiotropium

- both inhaled

pulmonary muscarinic antagonist mechanism of action

antagonize muscarinic receptors in the lungs causing:

- drying of respiratory secretions (a significant component of bronchitis)

- permits the sympathetic nervous system (β2) to dominate resulting in bronchodilation (especially useful in COPD)

leukotriene modifiers for asthma prototype drug

- montelukast (singulair)

Montelukast mechanism of action

- inhibits leukotrienes, a single mediator of inflammation

- leukotrienes trigger bronchospasm and inflammation

indications and route for montelukast

- oral

- second line therapy as an adjunct for glucocorticoids

- NOT for acute attacks

montelukast side effects

neuropsychiatric problems:

- anxiety

- agitation

- aggression

- suicidal thoughts

cromolyn mechanism of action

- blocks mast cells, thus

- inhibits the release of inflammatory mediators

cromolyn indications and route

- inhaled

- regular use can reduce the frequency of chronic asthma attacks

- used prophylactically for exercise-induced asthma

phosphodiesterase inhibitor prototypes

- theophylline (methylxanthines)

- roflumilast

theophylline mechanism of action

non selectively inhibits phosphodiesterase

indications for theophylline

- management of obstructive pulmonary disease (especially COPD)

considerations for theophylline

- lots of drug interactions (including coffee)

- induction/inhibition of CYP hepatic enzymes

- variable half life makes dosing problematic

- thus is rarely used

theophylline drug levels

< 20 mcg/mL = therapeutic, no side effects

20 - 25 mcg/mL = GI (n/v/d) and CNS (stimulation) side effects

> 25 mcg/mL = dysrhythmias, convulsions, death

what is the normal half life for theophylline and what causes variability in this number?

- average is 8 hours

- half (4 hours) in smokers and youngins

- double (16 hours) in adults with heart/liver/kidney disease

Roflumilast mechanism of action

- selective phosphodiesterase type 4 (PD4) inhibitor

- PD4 normally converts cAMP to AMP

- inhibition increases cAMP levels

- increased cAMP reduces inflammation, mucus production, cough, and increases bronchodilation

indications for roflumilast

- management of obstructive pulmonary disease

- more selective/targeted than theophylline

considerations for roflumilast

much more expensive than theophylline

side effects of roflumilast

- headaches

- dizziness

- insomnia

- decreased appetite

- nausea

- diarrhea

- weight loss

- back pain

- flu-like symptoms

how is asthma classified?

- persistent or intermittent

- mild, moderate, or severe

what are the variables when examining degree of impairment with asthma

- frequency of symptoms

- nighttime awakenings

- SABA use

- normal activity

- lung function (FEV1 > 80%)

goals of asthma therapy

- symptoms < 2x per week

- nighttime awakenings < 2x per month

- SABA use < 2x per week

- normal activity not restricted

- lung function (FEV1) > 80%

considerations for asthma treatment

- age dependent

- follows a predictable stepwise pattern

- progression of medicines is pretty similar regardless of age

how often do you evaluate asthma therapy?

every 2-6 weeks until control is achieved

a patient requiring oral corticosteroids for asthma is considered:

high risk

what is the sole treatment for intermittent asthma?

albuterol

what is used for management of an acute asthma attack?

albuterol

what drug is used in every step of asthma treatment?

albuterol

what is the progression of drugs used for persistent asthma?

1) progressing doses of inhaled and then systemic corticosteroids (corticosteroids are controllers used on a fixed schedule)

2) addition of LABA

3) addition of alternative drugs (montelukast, cromolyn theophylline, etc)

when to step up asthma therapy?

if SABA use is > 2x/week

when to step down asthma therapy?

asthma is well controlled for at least 3 months

what does it mean if asthma is "well controlled"?

- symptoms ≤ 2 days/week

- no interference with normal activity

- SABA use ≤ 2 days/week

- FEV1 > 80%

- asthma exacerbations requiring corticosteroids 0-1x per year

(looks like an intermittent asthma patient)

true or false

a patient with well controlled persistent moderate asthma should stop using inhaled corticosteroids or LABA

false. persistent asthma patients should remain on stepped therapy even if their asthma is well controlled

COPD is (more/less?) complex than asthma

less

there are (more/less?) treatment options for COPD than asthma

less

why are long acting muscarinic antagonists (LAMAs) commonly used to treat COPD?

the anticholinergic effect dries the respiratory secretions of bronchitis AND bronchodilates

t/f

cough and cold medicines should not be used in children less than 6 years old

true. risks > benefits

t/f

home remedies for upper respiratory symptoms (common cold, viral illness, etc) are less effective than abx or cold and flu medicines

False

home remedies for upper respiratory symptoms

- drink lots of water

- cool mist vaporizer or saline nasal spray to relieve nasal congestion

- ice chips, sore throat spray, lozenges for sore throat

- use honey to relieve cough

do not give honey to infants under 1 year old

fun fact: the antidote (BabyBIG) for infant botulism caused by honey costs like $50,000 per dose

What is allergic rhinitis?

- inflammation of the nasal mucosa

- allergen > histamine release > mucosal swelling

drug treatments for allergic rhinitis

- antihistamines: relieve allergic symptoms. use regularly during allergy season

- cromolyn and glucocorticoid (flonase): nasal inhaler blocks mast cells and inhibits inflammation in nasal mucosa

- nasal decongestants: use as needed

prototype antihistamines

- loratidine

- diphenhydramine

- fexophenidine (2nd gen)

prototype nasal decongestant

pseudoephedrine

nasal decongestant mechanism of action

- sympathomimetics

- alpha 1 agonist constricts nasal blood vessels

- reduces swelling and stuffiness

considerations for nasal decongestants

- chronic use of these agents down regulates receptors requiring progressively higher doses for effect

- rebound symptoms when withdrawn

- do not use more than 3 days

side effects of pseudoephedrine

- increased HR (and BP)

- increased BG

- insomnia

what are antitussives?

cough suppressants

what are used as antitussives?

- opioids (not as much these days)

- dextromethorphan (non opioid)

what are tussives?

- expectorants: increase respiratory secretions to make phlegm more liquid

- mucolytics: literally break up mucus

antitussive prototype

dextromethorphan

expectorant prototype

Guaifenesin

mucolytic prototype

acetylcysteine

bonus effect of acetylcysteine

restores glutathione which protects the liver from the adverse effects of acetaminophen and the kidney from the adverse effects of dye

what cold/flu meds are prn?

- nasal decongestants

- cough meds (?)

what cold/flu meds should be taken on a regular schedule?

- antihistamines

- flonase

what cold/flu meds cause sedation?

- antihistamines

- dxm (all antitussives?)

what cold/flu meds are stimulants?

- pseudoephedrine

pathophysiology of Alzheimer's

- neurons degenerate in the hippocampus and cerebral cortex

- hippocampal degeneration impairs memory

- cerebral cortex degeneration impairs higher function

- advanced disease causes loss of memory, language, self care, and independence

- damaged neurons do not synthesize or respond to acetylcholine. ACh levels are below normal in advanced disease

main theories for neuronal degeneration in AD

- neuritic plaques with central beta amyloid core (dead neurons)

- neurofibrillary tangles caused by abnormal forms of tau protein that destroy the microtubules

Drugs to treat Alzheimer's Disease

- cholinesterase inhibitors

- donepezil

donepezil mechanism of action

- acetylcholinesterase inhibitor

- raises levels of ACh

- modest improvement of symptoms

- lasts a short time

considerations for donepezil

- only 1/12 patients benefit from the drug. discontinue if no benefit

- predictable side effects of parasympathetic nervous system (rest, digest secrete)

-

predictable side effects of donepezil

- muscarinic agonist

- GI (n/v/d)

- cardiovascular (bradycardia, risk of falls)

- bronchoconstriction and increased airway secretions

pathophysiology for parkinsons disease

- dopamine (DA) and acetylcholine (ACh) are needed in balance for controlled movements

- DA producing neurons degenerate and DA and ACh are out of balance

- disturbed movements occur

parkinsons disease presentation mneumonic

TRAP

- Tremors

- Rigidity

- Akinesia

- Postural instability

pharmacological therapy for parkinsons

- dopameinergic agents to increase dopamine levels and restore balance with ACh

- levadopa/carbidopa

t/f

levodopa/carbidopa does not cure parkinsons disease or delay disease progression

true

Why is carbidopa-levodopa preferred over levodopa alone?

- carbidopa prevents the metabolism of levodopa in the periphery

- thus more is available in the CNS

what is the efficacy of levodopa/carbidopa?

- very effective

- failure to respond to treatment with these drugs suggests an incorrect diagonsis

considerations for carbidopa/levodopa therapy

- increase dose as disease progresses

- loss of efficacy occurs at the end of the dosing period (give more often) or acutely (on/off effect occurs more frequently as the disease progresses)

- levodopa competes with dietary protein for absorption (avoid protein heavy meals)

side effects of carbidopa/levodopa

- n/v (take with food)

- orthostatic hypertension

- dyskinesias

- psychosis

nociceptive pain

- caused by injury

- responsive to opioids and non-opioid analgesics

- somatic (bones, muscles, joints) pain may be described as sharp, dull, localized

- visceral pain may be described as aching, diffuse

neruopathic pain

- caused by nerve pathology

- described with sensory terms: shooting, tearing, burning, numb, tingling

- like hitting funny bone or "falling asleep"

- responsive to adjuvants: antidepressants, anti-seizure drugs

who uses DVPRS pain scale?

those who can self report

who uses CPOT pain scale?

patients that are not reliable or cannot speak

how is the CPOT scale used?

- scale from 0-8

- scored by facial expression, body movements, compliance/vocalization, and muscle tension

- score ≥ 3 indicates pain

- goal is ≤ 2

considerations for pain interventions

- safety

- efficacy

- how to take (i.e. with food, etc)

- side effects

- getting ahead of the pain (i.e. dose 30 minutes before physical therapy)

prototype opioid agonist

- morphine

- agonizes kappa and mu receptors

prototype opioid agonist-antagonist

- pentazocine

- agonizes kappa receptors

- antagonizes mu receptors

Prototype opioid antagonist

- naloxone

- reversal agent/antidote for opioid overdose