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55 Cards in this Set

  • Front
  • Back
bronchial asthma - pathology
Increased airway reactivity
increased bronchoconstrictor response to stimuli (allergens, pollen, chemicals, stress, cold, exercise, infection, unknown factors?)
trigger release of proinflammatory mediators (prostoglandins, histamine, leukotrienes)
irritation of respiratory epithelium leads to contraction of bronchiole smooth muscle and narrow airway
clinical features of asthma
wheezing, secretions

dyspnea, increased accessory muscle use

anxiety,tachycardia, tachypnea, hypoxemia with cyanosis

often see GERD with asthma (not sure which comes first)
Treatment of asthma
Inhaled steroids (Pulmicort) to reduce inflammation
May add-Leukotriene inhibitors (Singular) to decrease inflammation, helps lower the steroid dose needed
Short acting Beta 2 agonists MDIs(Albuterol) as rescue therapy
treatment of chronic asthma
If not responding to other treatments:

Long acting beta 2 agonists (Advair) may be used to supplement glucocorticoids

Xanthines (Theophylline) in lowest possible doses to supplement glucosteroids – watch for toxicity

Use meds cautiously if cardiovascular disease present – common side effect tachycardia
rehab goals for asthma
Patient Education: teach strategies to avoid triggers, breathing exercises

Encourage aerobic exercise (such as swimming) if exercise is not a trigger

Environmental modifications
COPD
COPD affects more than16 million in USA, increasing mortality and prevalence

Emphysema (pink puffers): destruction of alveolar walls, enlarged terminal air spaces, CO2 retention causes flushing)

Bronchitis (blue bloaters): cyanosis/ hypoxemia due to long standing bronchial tree inflammation with hypersecretion of mucus
COPD Pathology
Chronic airflow obstruction due to air trapped in lungs
Airways are narrowed (bronchial smooth muscle spasm), further narrowing when exhale
Lungs are hyperinflated which leads to barrel chest deformity
Diaphragm is flattened - disturbed length-tension relationship causes diaphragm to be less effective
Accessory muscle use increases
Determine stage by % air expired with forced exhalation (FEV1)
COPD classic symptoms
chronic cough, increased mucus production and viscosity
wheezing, dyspnea on exertion
hyperventilation (overbreathing)
causes decreased carbon dioxide levels-dizziness
COPD pt education
Pursed lip breathing
with trunk flexion/leaning forward: improves diaphragm length-tension relationship to help force air out
with weight on arms: stabilizes arms to allow more efficient accessory muscle use and improved rib movement

Pacing/Energy Conservation
COPD bronchiodilators
Anticholinergics (Spiriva, Atrovent inhalers)
Long acting Beta 2 agonists (Advair)
Theophylline (Theo-Dur) oral for acute exacerbations
Glucocorticoids (Pulmicort inhaler) for severe exacerbations
COPD oxygen therapy
COPD breathing is triggered by O2 levels, not CO2 as it is in “normals” ( they have grown accustomed to elevated CO2)

Goal of O2 therapy:
Reach PaO2 (oxygen level in blood) of 60mmHG

SaO2 (hemoglobin saturated with O2) of 89-92% (don’t want too high O2 levels as it suppresses urge
to breathe in COPD patients)
COPD oxygen therapy - treatment implications
rapid drop in O2 with activity-may need to increase oxygen only during activity.

delayed drop in O2 such as at the end of the 6 min walk test, problem is CO2 build up - focus on pursed lip breathing rather than increasing O2
GI disorders: a challenge to rehab
GI problems result from:
Damage caused by gastric acid secretion
Abnormal GI motility (constipation, diarrhea, emesis)

Goals of GI Meds:
decrease acid
help protect and heal the mucosal lining
restore normal motility
GI disorders: special concerns in rehab pts
PT routinely ordered for post op GI surgeries:
Goals:
Decrease pain
Increase peristalsis
Early foley removal
Decrease chances for pneumonia
Decrease length of stay

GI issues can decrease participation in therapy and lead to slow recovery:
Constipation is a significant problem for rehab patients due to bedrest, pain medications
Nausea is common with cancer patients, post-surgical patients due to pain meds
Exercise tends to increase gastric acid, may exacerbate symptoms
GI disorders: acid base diseases - GERD, gastritis, ulcer disease
GERD
Damage to lower esophageal sphincter from irritants, infection
Reflux of pepsin/bile into esophagus
Effects 20% of Americans

Gastritis
Inflammation of stomach mucosa
Intense pain, nausea

Ulcer Disease
Disruption of the gastric or duodenal mucosa
Causes bleeding, pain
Acid bases disorders - treatments (antacids)
Antacids (Tums, Rolaids)

Chemically neutralize stomach acids
Promote healing of gastric ulcers
Used to treat minor dyspepsia/heartburn

Side effects: depend on composition
constipation – aluminum based
diarrhea – magnesium based
Acid rebound (calcium based products - Tums, Rolaids)
Altered drug metabolism/excretion
Acid base disorders - treatments (H2 receptors)
H2 receptor blockers (Tagamet, Pepcid, Zantac)

Used for acute/ long term care of GERD, ulcers
Blocks H2 receptor (increase gastric acid secretion) on GI smooth muscle

Side effects: dizziness, diarrhea, headache, arthralgia, acid rebound, can cause B vitamin deficiencies
*Not as effective as proton pump inhibitors in acid control and healing
acid based disorders - treatments (2) NSAIDS
NSAID-Induced Ulcers (Cytocec- misoprostol)

Long-term NSAID use leads to gastritis and ulcerations
Inhibit gastric acid secretion, stimulate mucus secretion and mucosal blood flow.
Less effective than PPIs

Side Effects: diarrhea and abdominal cramping
acid base pump disorders - treatment 3 - proton pump inhibitors
Proton pump inhibitors (Prilosec, Nexium, Prevacid, Protonix)

Effective treatment of GERD and ulcers
Less risk of esophageal damage/cancer
Inhibits the proton pump on the parietal cell membrane of the gastric mucosa to completely block all gastric acid secretion*

Side Effects: dizziness, fatigue, may have acid rebound when discontinued, B vitamin deficiencies with long term use
*may lead to more GI infections
acid base disorders - treatments - proton pumps continued
Inhibition of gastric acid secretion by PPI’s may increase incidence of C-difficile infection
Vegetative form of C difficile can survive in gastric contents with a raised pH
Patients using PPIs may be prone to colonization with C difficile.
C diff colitis
Increasing incidence in young as well as old
Usually related to antibiotic use, PPIs may predispose
Infection releases toxins that damage the protective lining of the large intestine, this produces severe diarrhea, pain, fever
Treat with Flagyl for 10 days if mild, severe disease requires vancomycin and possible surgery consult for colon resection
Eating yogurt daily recommended
Florastor – probiotic in oral form (better than yogurt, OTC)
C diff colitis transmission prevention
Transmission Prevention
Fecal-oral transmission-spore remains for 30+days!
Alcohol waterless handwashes don’t break down the spore, must use soap and water
Keep on contact isolation until 2 negative stool cultures
acid base disorder treatments - H. Pylori
H. Pylori is a bacteria found in upper GI tract may cause or potentiate ulcers via mucosal breakdown leading to chronic gastritis, PUD, GERD and gastric CA-very undiagnosed
Triple therapy used: 2 antibiotics and one PPI, include bismuth with diarrhea
Successful eradication of this infection may eliminate need for antiulcer meds
acid base disorder treatments - Mucosal Protectors: Bismuth Chelate
Mucosal Protectors: Bismuth Chelate

Coats the base of the ulcer, increases gastric mucous epithelial cell growth
Offers protective properties against H. pylori

Side Effects: blackening of the tongue & feces, nausea, vomiting
acid base disorder treatments - Mucosal Protectors: Sucralfate (Sulcrate)
Forms a protective coating over an ulcer
Used for stress ulcers and chronic peptic ulcer disease
Stays local, does not interact with other drugs

Side effects: constipation, nausea, can decrease the absorption of other meds
abnormal GI motility - Antiemetic drugs
Prokinetic Drugs: Reglan (metoclopramide)
Stimulates peristalsis, facilitating gastric emptying
Moves contents away from esophagus which decreases GERD irritation
Used for chemotherapy-related vomiting

Side Effects: CNS/dopamine antagonist, motor restlessness, fatigue, diarrhea, weakness, parkinsonlike tremor (long term), hypotension, HTN, tachycardia
Abnormal GI motility - antiemetic drugs: anticholinergics, antihistamines, neuropleptics
Anticholinergics (Scopolamine)- motion sickness
Side effects: dizziness, drowsiness, blurred vision, dilated pupils, dry mouth, difficulty urinating
Antihistamines (Antivert, Benadryl, Dramamine)-motion sickness
Side effects: diziness and sedation
Neuroleptics (Compazine, Phenergan)- immediately post-op
Side effects: orthostatic hypotension, tachycardia, blurred vision, dry eyes, urinary retention
Abnormal GI motility - antiemetic drugs: serotonin blockers, cannabinoids, neurokinin 1 receptor agonists
Antiemetic Drugs - chemotherapy-related
Serotonin Blockers (Zofran)
Side effects: headache, dizziness, diarrhea
Cannabinoids (Marinol)
Side effects: ataxia, light-headedness, blurred vision, dry mouth, weakness, tachycardia or bradycardia, CNS effects, munchies
Neurokinin 1 receptor antagonists (Aprepitant) in combination w/corticosteroids and serotonin blockers
Side effects: Hiccups
Abnormal GI motility - antidiarrheal drugs
Slow GI mobility, enhance absorption of nutrients/water, provide bulk to stool
Prolonged diarrhea can cause dehydration, a common admitting diagnosis in the elderly
abnormal GI motility - antidiarrheal drugs: absorbents and opoid derivatives
Antidiarrheal Drugs
Adsorbents (Pepto-Bismol*, Kaopectate)
Coat GI tract wall, bind to bacteria & carry them out
Decrease effectiveness of many drugs (digoxin, hypoglycemic drugs, oral anticoagulants)
*Aspirin product

Opiod derivatives (Immodium)
decreases GI motility, increases absorption of electrolytes and water
Side effects: nausea, fatigue, addiction?
abnormal gi motility: laxatives
Promote bowel evacuation when there is decreased GI motility due to bed rest, medications, surgery, SC injuries

Frequently abused, dependence develops

Teach patients to focus on high fiber diet, hydration, exercise
abnormal GI motility: laxative meds: bulk forming & emollient/lubricant
Bulk forming (Metamucil, Citrucel)
Absorb water, increases bulk of intestinal contents, stretch stimulates BM
Emollient/Lubricant (Colace, mineral oil)
Side effects: decreased absorption of vitamins, cramps, nausea, electrolyte imbalances
Abnormal GI motility: laxative meds - hyperosmotics: saline & stimulants
Laxative Meds
Hyperosmotics (Milk of Magnesia)
Saline (Fleet Enema)
Enhance peristalsis by osmotically increasing the bowel fluid volume
Stimulants (Correctol, Dulcolax)
Irritate GI mucosa, nerve stimulus for BM
Anticholinergics - decrease bronchospasm
- Block acetylcholine receptors on airway smooth muscle; leading to bronchodilation. Max bronchodilation occurs in 30 minutes, duration up to 5 hours.

Atrovent (ipratropium)
Oxitropium
Spiriva (tiotropium)

*First choice for COPD because they also decrease mucous secretion. Effective in asthma when combined with beta 2 agonist
Corticosteroids - decrease inflammation
Inhibit production of pro-inflammatory products which trigger exaggerated response in respiratory passages

Also increase anti-inflammatory proteins

Inhalation preferred – goes directly to mucosa, fewer systemic side effects

Given by IV during severe attacks
Corticosteroids - Pulmocort & Flovent - decrease inflammation
Side Effects: Steroid catabolic effect on support tissues -
osteoporosis, weakening muscles, ligaments, skin tears
cataracts , glaucoma (with inhaler use)
hypergylcemia, hypertension, fluid retention
adrenal suppression
Oral thrush – rinse mouth after use
Cromones (inhaled non-steroids) - descrease inflammation (respiratory)
Intal, Tilade

Must be taken prior to the onset of bronchoconstriction

Prevents bronchospasm by inhibiting release of inflammatory mediators (histamine, leukotrienes)

Used with allergies and asthma to prevent response to pets etc- take before you go

Administered by MDI, nebulizer, or nonprescription nasal spray (Nasalcrom)
leukotriene inhibitors - decrease inflammation (respiratory)
Leukotriene Inhibitors - Blocks the inflammatory effects of leukotrienes which cause bronchial constriction and mucus production

Singular (montelukast) - blocks the respiratory tissue receptor for leukotrienes
Zyflo (zileuton) – inhibits the production of leukotrienes


Can be combined with beta agonists and steroids for optimal treatment for COPD and asthma

Side effects: Safer than other anti-inflammatory agents, low side effects
Durg Nomenclature
Trade name always capitalized (Tylenol)

Generic (non-proprietary) in lower case letters (acetaminophen)
pharmacokinetics: why imp. for PTs
So we can schedule our therapy for desired effect, therapists need to understand:

What the medication is used for
How it works
How it is absorbed, distributed and eliminated
Administration and Absorption: Enteral
Absorbed by GI tract

Oral (p.o.) - depending on med - take with food to buffer or no food for absorption.

Sublingual (sl.) - Large vein under tongue - fast to venous system

Rectal (p.r.) - unconscious or vomiting
Parenteral
Inhalation – rapid absorption due to large surface area of alveoli (respiratory MDI, nebs)
Injection - IV (reaches target quickly), IM (local or prolonged systemic release, subq (local response, slow systemically)
Transdermal - topical (skin or mucous problems)
Intrathecal - bypasses blood-brain barrier to reach CNS
pharmacokinetic Considerations
Age: metabolism slows with age

Medical History: liver, kidney, cardiac disease

Gender/Genetics: hormones may influence

Diet: foods/other meds may interact

Body Composition: fat cells may store meds

Mode of Delivery: IV=100%, Inhalation-blocked if congested, oral depends on stomach absorption, liver metabolism
distribution and Timing
How long before it starts working?

When is the peak effect? (ie: Ativan peaks 6 hours later)

How long will it last?

Generally it takes 5 half- lives to clear a drug
Example: Drug with 2 hour half- life takes 10 hours to clear.
metabolism and excretion
Metabolism occurs in the liver-the drug is chemically changed to a less active state

Excretion of drug is primarily by the kidneys:
Decreased drug clearance with kidney dysfunction- check creatine clearance labs, watch for toxicity
implications for PT
Physical activity and modalities may affect absorption and bioavailability of the drug:
Heat and exercise increase blood flow and speeds absorption and dispersion away from the site
Diabetics may become hypoglycemic if injected insulin is absorbed too fast
Cold decreases dispersion, slows distribution
Pulmonary system function review
Respiration is the exchange of O2 and CO2
Oxygen is needed to produce energy in cells
Alveoli act as a “sponge”
O2 exchanged between alveoli and capillaries
O2 binds to HgB, transported in blood
CO2 exchanged from blood to alveoli as bicarbonate (HCO3)
and exhaled as waste gas
Goal: maintain acid -base balance (kidneys,lungs)
Level of H+ ions (C02) stimulates inspiration
Excess retained CO2 leads to acidosis
Antitussives (Robitussin DM)
- help annoying dry coughs

Side Effects: sedation, dizziness, GI upset, constipation
Decongestants
Decongestants: Help thin AND clear secretions by drying up mucosal vasculature

Pseudo-epinephrine
Sudafed: oral
Afrin: spray (nasal sprays do not penetrate severe congestion)


Systemic side effects: increases sympathetic drive (i.e.: headache, nervousness, nausea, increased blood pressure, palpitations; dangerous with prolonged use
Mucolytics and expectorants (thin and clear secretions
- Used to prevent accumulation of thick secretions that can clog respiratory passages
Mucomyst or Mucosil (acetylcysteine): inhaled, decreases viscosity of secretions (may decrease free radical damage)
Antihistamines (thin and clear secrections)
- compete with H1 receptor sites, not allowing histamine to attach. Decreases nasal congestion, discharge, coughing and sneezing

Side effects: sedation, fatigue, nausea
non-sedating antihistamines
Zyrtec (cetirizine)
Claritin (loratadine)
Allegra (fexofenadine)
Clarinex (desloratidine)
Beta 2 Agonists - decrease bronchospasm
- Promotes bronchodilation by relaxing smooth muscles and increasing mucociliary clearance. Delivery by MDI, DPI, nebulizer or oral*

Albuterol: rescue inhaler – rapid onset, duration 4 - 6 hours
Advair: delayed onset, long acting – 12 – 15 hours

*Inhalation preferred – fewer side effects and more effective however oral form may be needed to reach more distal branches if bronchioles constricted
Beta 2 Agonist Side Effects
increases airway irritation and severity of attacks with prolonged use
May develop tolerance to drug
CNS/cardiac irregularities: tachycardia, tremor, hypokalemia, hyperglycemia, increased BP and cardiac contractility
Xanthine derivatives - decreased bronchospasm
Promotes respiratory smooth muscle relaxation
Increases contractility and endurance of the diaphragm
Found in coffee, tea, and chocolate in small amounts

Side effects: strong tachycardic and hypertensive effects, nausea, vomiting, headache, insomnia

* Serious problems with toxicity due to narrow therapeutic range