pharm exam 1 Flashcards
Goal: to keep pH balanced due to continual production of acid as a result of cellular metabolism
pH is a expressed using a negative relationship
-Higher concentration of H+ = lower pH level
3 ways to regulate the pH level
Compensation can occur using one of these systems
Buffer system
-Change strong acids to weaker one
-Bind with strong acids to neutralize
Respiratory system
-Lungs excrete CO2 to decrease acidity
-Results in increased pH
Renal system
-Kidneys can reabsorb additional HCO3 and eliminate excess H+
-Results in increased pH
acid/base imbalance
Compensation will be attempted by the opposing system
- Buffers react immediately
- Respiratory system within minutes
- Renal system takes hours to days
- -Can compensate for an indefinite amount of time (chronic imbalance)
compensation for acid/base imbalance
also look at handout
Depends on the cause
Must try to correct underlying reason
Mild alterations usually do not require treatment
Compensation may or may not occur by the opposing system depending on need for treatment
-Compensation for respiratory alkalosis is rare
Metabolic acidosis: sodium bicarb is drug of choice
- other alkalinizing salts can be given for mild or chronic acidosis
Metabolic alkalosis: *chloride and bicarb have inverse relationship
- Most imbalance will respond to IVF (NaCl and KCl)
- Severe cases: may need to correct pH level - diluted hydrochloric acid or ammonium chloride via centra line
- Acetazolamide: rarely used and has diuretic effect
treatment for acid/base imbalance
Side effects
-increase plasma pH (alkalosis) if given too fast/much
-hypernatremia r/t increase sodium concentration
-hypokalemia r/t potassium shift
-hypocalcemia r/t calcium shift
-extracellular volume excess
-hypoventilation
–if overdose - go into alkalosis
NM: don’t correct imbalance rapidly, monitor Na, K, Ca, ABG’s, pH, monitor for s/s of high Na, low K, low Ca
indication:
PO: HCO3 <22
IV: for severe: pH <7.2 or HCO3 <12-14 (need to fix fast)
*chloride and bicarb have inverse relationship
sodium bicarbonate
other alkalinizing salts: sodium citrate (constipation) and sodium carbonate
for acid/base imbalance met acidosis
Side effects
-hyponatremia
-hypokalemia (s/s paresthesia)
-*increase ammonia reabsorption
-parasthesias
-tinnitus
NM: monitor electrolyte levels and pH closely, don’t use in pts with low fluid balance, *don’t use if kidney or liver dysfunction is present (severe cirrhosis can cause hepatic), don’t give if allergic to sulfonamides)
indication: metabolic alkalosis with fluid excess
given IV
carbonase inhibitor with diuretic properties so excretes extra bicarb - not used as much
acetazolamide
for acid/base imbalance met alkalosis
Also known as corticosteroids and nearly identical to steroids produced by the adrenal cortex
2 types of dosing/effects
1. Physiologic effects (give low doses)
-Trying to mimic what the body normally produces
-to replace hormones due to adrenocortical insufficiency
2. Pharmacologic effects (give high doses)
-Try to do something the -body doesn’t normally do
-Decrease inflammation
-Suppress immune response
Reasons for use
1. Anti-inflammatory effects
-Inhibit synthesis of chemical mediators that begin the process of inflammation resulting in reduction of swelling, warmth, redness, and pain
-Suppress infiltration of phagocytes which prevents tissue damage
-Much more effective than NSAIDS (only act on prostaglandins)
2. Immunosuppression
-Suppress proliferation of lymphocytes (B & T cells) that from antibodies and attack antigens
Glucocorticoid receptors are inside cell
Glucocorticoids modulate the production of regulatory proteins rather than signaling pathways
glucocorticoids
Suppress infiltration by phagocytes (WBC’s)
-Neutrophils are first responder
–Engulf bacteria, foreign material, or damaged cells
-Monocytes become macrophages
–Assist in cleaning up products of inflammation before healing can occur
Suppress proliferation of lymphocytes
-Provide humoral and cell-mediated immunity - Turn into…
–B cells produce antibodies
–T cells provide long-term immunity (Attack and destroy foreign cells)
mechanism of action: suppress immune respond
glucocorticoids
Short Acting: for adrenal insufficiency and not making enough aldosterone, etc. physiologic effects Cortisone Hydrocortisone Have increase mineralocorticoid properties (effects aldosterone release and decrease inflammation) individual glucorticoids differ in 3 ways: biologic half life, mineralocorticoid potency, glucocorticoid potency *we want immune suppression and decrease inflammation with this Short acting -cortisone -hydrocortisone Intermediate Acting -Prednisolone -Prednisone -Methylprednisolone -Triamcinolone Long Acting -Betamethasone -Dexamethasone increase ability to lower inflammation decease effect on aldosterone
-Do not take NSAIDS with glucocorticoids, Cannot receive live vaccines, Other vaccines cannot be given without approval from HCP
glucocorticoids
Clinical use of glucocorticoids stem from their ability to suppress immune responses and inflammation
Only decreases/minimize/help symptoms
*Don’t do anything to the disease (improve, cure, etc.)
Therapeutic uses (anything with chronic inflammation basically)
-Autoimmune Disorders
-Inflammatory Bowel Disease
-Chronic Respiratory
-Conditions
-Cancer
-Organ Transplant Rejection
-Miscellaneous Inflammatory Disorders
- Rheumatoid Arthritis
–Adjunctive treatment of acute exacerbations
–Prolonged use should be avoided
–Localized injections are effective and have a lower risk of side effects
-Systemic Lupus Erythematosus
–Usually requires chronic use of oral glucocorticoids
–Exacerbations are treated with high dose IV glucocorticoids
-Inflammatory Bowel Disease
–Ulcerative Colitis
–Crohn’s disease
-Allergic conditions (Type I reactions)
–Dosing is dependent on severity of reaction
–Anaphylaxis requires high doses given IV at the time of reaction
–Localized reactions can often be treated with short-term oral dosing or topical forms
-Asthma/COPD
–Glucocorticoids are given by inhalation for prevention of symptoms
-Neoplasms (Cancer)
–Glucocorticoids are used in combination with other anti-cancer agents
–Causes direct toxicity to malignant lymphocytes (abnormal cancerous cells)
-Organ Transplants
–Prevents rejection
–Used in combination with other immunosuppressive drugs
–Chronic dosing usually required in some form
–Sudden withdrawal will result in rejection
Side effects: Will always occur when given for pharmacologic effect Dependent on dose and duration Management of side effects -Put on lowest dose -Shortest duration -Alternate route of administration --To decrease systemic side effects: inhalation, topical and direct/local injections r/t only going into lungs --Systemic: PO and IV -Alternate day dosing
glucocorticoid clinical use and SE
Side effects:
-Suppression of glucocorticoids from adrenal glands
-Effects seen with severe stress and with glucocorticoid withdrawal
NM:
-Dosing during increase physiological stress
-Glucocorticoid withdrawal schedule
-Monitor for adrenal insufficiency (s/s: hypovolemic, dizzy, ortho BP, low BS, hyperkalemia, fatigue)
-Physiologic stress (for example, surgery, infection, trauma, hypovolemia): Adrenal glands secrete large quantities of glucocorticoids and epinephrine
-Result: Hormones help maintain blood pressure and blood glucose levels
Insufficient release of glucocorticoids: Hypotension and hypoglycemia occur
-Very severe stress: Glucocorticoid insufficiency can result in circulatory failure and death
-Can exert actions like those of aldosterone
-Can act on the kidney to promote retention of sodium and water while increasing urinary excretion of potassium
-Net result is hypernatremia, hypokalemia, and edema
-Most glucocorticoids used as drugs have very low mineralocorticoid activity
adrenal suppression of glucocorticoids
don’t see while taking the med, see when you suddenly stop
reaction: suppression of glucocorticoids from adrenal glands
Side effects:
-Suppression of bone formation by osteoblasts
-Accelerated bone resorption by osteoclasts
-Decreased intestinal absorption of calcium and increasing PTH synthesis (pulling Ca+ from bone to correct serum hypocalcemia)
-Osteoporosis & fractures
NM:
-Identify high risk patients: Older women, check bone density scan
-Consider other routes: COPD: inhalation route
-Supplements: Vitamin D and calcium (give both to increase absorption; Calcitonin that doesn’t go through intestinal absorption
-Medications: Bisphosphonates (can prevent bone loss or stimulate ore bone cells; Estrogen therapy
effects on bone for glucocorticoids
reaction: suppression of bone formation by osteoblasts and accelerated bone resorption by osteoclasts
Decreased intestinal absorption of calcium
side effects:
-Increase susceptibility
–New infections
–Reactivate latent infection
—TB, shingles, herpes, HPV can stay dormant can come reactivated
-Mask symptoms of infection
NM:
-Education: Good hand washing, avoid high populated areas, NO live vaccines (varicella, MMR)
-Stop or decrease dose: If condition allows
-Other medications
infection for glucocorticoid
reaction: suppression of immune response and phagocytic activity of neutrophils and macrophages
Increase susceptibility AND mask symptoms of infection
side effects
-Increased metabolism of carbs
-promotes synthesis of glucose
-reduces glucose use in the body
-reduces glucose uptake by muscle and adipose tissue
-Increased storage of glucose as glycogen
NM:
-Non-diabetic patients
-Pre-diabetic patients: Could induce diabetes
-Diabetic patients: Will cause very high BS levels, Use higher sliding scale insulin, schedule dose in addition to sliding scale, Harder to manage BS
-Can induce diabetes post-transplant (high doses given long term)
glucose intolerance of glucocorticoids
- will always occur with cortiocosteriods
reaction: promotes synthesis of glucose, reduces glucose use in the body, and reduces glucose uptake by muscle and adipose tissue
Side effects: Cushing syndrome: Hyperglycemia, glycosuria, fluid and electrolyte disturbances, osteoporosis, muscle weakness, cutaneous striations, lowered resistance to infection; redistribution of fat produces a “potbelly,” “moon face,” and “buffalo hump” -this is unavoidable while taking med -reduced muscle mass -glucose intolerance -thinning of skin -lipolysis and fat redistribution
metabolic effects of glucocorticoids
reaction: suppress synthesis of proteins resulting in decreased muscle mass, weakness, or myopathy
Stimulates fat breakdown which redistributes fat cells causing moon face, buffalo hump, and accumulation of fat in the abdomen
side effects
- increase secretion of gastric acid and pepsin
- decrease production of cytoprotective mucus
-reduce gastric mucosal blood flow
- decrease gastric pain –> perforation & hemorrhage
-Peptic Ulcer Disease: Can perforate and bleed without warning
NM
- Monitoring: Black/tarry stool, stool sample
-Education
-Prophylactic Medication: PPI (azoles) to decrease gastric acid section
- Do not use… NSAIDS – ASPRIN r/t increase risk of peptic ulcer disease/hemorrhage
GI effects on glucocorticoids
ex: peptic ulcer disease
reaction: inhibits prostaglandin synthesis which increases secretion of gastric acids, but also decrease gastric pain which can mask symptoms of ulcers
side effects
Mild reactions:
-Insomnia
-Anxiety
-Agitation
-Irritability: Resolves when stop taking
Severe reactions
-Delirium: more likely with high short term dose
-Hallucinations: more likely with high short term dose
-Depression: more likely: put on SSRI, etc.
-Euphoria
-Mania: on lower chronic dose
-Suicidal thoughts/behaviors: Resolves quick, within a week of when you stop taking
psychological disturbances
reaction: insomnia, anxiety, agitation, or irritability in about 60%
Severe reactions: delirium, hallucinations, depression, or mania in about 6%
Long-term low dose is most likely to cause depression
Short-term high doses are more likely to cause psychoses
side effects
-Cataracts: Common with long-term therapy - So make sure patient reports: blurry/cloudy vision, vision changes, eye exams q 6 months with long term therapy
- Open-angle glaucoma: Seen with oral therapy
NM:
-education
-monitoring
-withdrawal of meds
vision problems
Drug interactions
-Interactions related to potassium loss
–Careful with diuretics since they can cause K loss
–Digoxin can become toxic when potassium is low
-Nonsteroidal anti-inflammatory drugs (NSAIDS)
-Vaccines
Contraindications and precautions
-Systemic fungal infections should NOT but on corticosteroids until it resolves
-Live vaccines
Withdrawal Symptoms: -Severe fatigue & weakness -Body aches & joint pain -Headache -Nausea & vomiting -decrease appetite -Lightheadedness & hypotension -Mood swings - low Na+ and glucose -Adrenal crisis Prevention: -Slowly decrease dose: The longer they’ve been on it and higher the dose the slower you will withdraw -Alternate day therapy -Monitor for symptoms -Switch to hydrocortisone -Emergency med kit and ID bracelet if it’s truly an adrenal insufficiency
cautions and withdrawal from glucocorticoids
Most medications for COPD are given via inhalation (preferred route). Advantages of Inhalation Administration
1. Therapeutic effect is enhanced by delivering more drug to the site of action
2. Limited systemic effects
3. Rapid relief during acute attacks
Metered dose inhalers (MDIs)
-Delivers a measured dose of drug with each inhalation
-Even with correct use, only 10% of the drug reaches the lungs
-NM: wait 1 minute between doses, must begin to inhale before activating device, spacers can be used to increase delivery of drug to lungs
Dry powder inhalers (DPIs)
-Used to deliver drugs in the form of a dry powder directly to the lungs; no propellant is used
-Delivers more of the drug to the lungs, and less to the oropharynx
-NM: breath activated, easier for patients to use, no spacer needed
Nebulizers:
- Converts a drug solution into a fine mist which is inhaled and given over a longer time
-Increased drug delivery to the lungs
NM: most effective delivery, should be used during acute attacks
COPD
2 categories both used to reduce S/S and prevent/slow progression
- Anti-inflammatory Medications
- Glucocorticoids
- Leukotriene Modifiers - Bronchodilators
- Beta 2 Agonists
- -Short acting: given PRN for acute symptoms
- -Long acting: given scheduled for control and prevention
- Methylxanthines
- Anticholinergics
meds for COPD
Action: Suppress inflammation by Decrease production and release of inflammatory mediators (leukotrienes, histamine, prostaglandins), Decrease infiltration and activity of inflammatory cells, Decrease edema of the airway mucosa, Decrease mucous production
SE:
-Oropharyngeal candidiasis (yeast infection/thrush)
-Dysphonia (hoarseness, dry/scratchy throat, speaking difficulty)
–Rinse mouth out after using these and use spacer to help get med down into lungs
-Both are from local disposition of the drug into oropharynx
-Inhaled glucocorticoids may promote bone loss in premenopausal women
-Can slow growth in children and adolescents
-PO/IV glucocorticoids result in increased side effects and should only be used short-term
NM:
-To minimize effects of oropharyngeal candidiasis and dysphonia:
1. Gargle after each administration
2. Use a space device during administration which will help deliver more of the medication to the lungs
-To minimize effects of premenopausal bone loss:
1. Use the lowest dose possible
2. Ensure adequate intake of calcium/vitamin D
3. Participate in weight bearing exercises
Glucocorticoids
ICS have limited effectiveness for treating COPD-induced inflammation and should be given in combination with a bronchodilator (LABA) for COPD
Inhaled
Budesonide (Pulmicort)
Fluticasone (Flovent)
PO/IV (try to reserve for severe exacerbation)
Methylprednisolone
Prednisolone
Prednisone
Systemic (PO or IV) corticosteroids are recommended to treat COPD exacerbations
Beta2 Agonists provide symptomatic relief of symptoms (in COPD and just slows S/S and improves quality of life), but they do not alter the underlying disease process
-aka sympathomimetics because of the ability to mimic actions of the sympathetic nervous system. So they have the opposite effect Beta-Blockers
Beta2 Adrenergic Agonists: Stimulate beta2 receptors which promotes bronchodilation and relieves bronchospasms
Beta 2 = 2 lungs
Suppress histamine release in the lung
Increase ciliary motility
short acting: albuterol, levalbuterol Long acting (inhaled): formoterol, salmeterol, indacaterol given 1-2X/day and preferred for COPD
Methylaxanthines, aminophylline (for IV/COPD exacerbation)
bronchodilators short acting: albuterol, levalbuterol Long acting (inhaled): formoterol, salmeterol, indacaterol given 1-2X/day and preferred for COPD
Side effects
- Inhaled medications have lower occurrence of systemic effects than oral or IV dosing
-Tachycardia
-Increased BP
-Tremors
-Angina
(more likely with high dose)
Oral Beta2 Agonists: May produce activation of beta 1 receptors in the heart and produce angina or tachycardia/dysrhythmias, tremors may also occur by activating beta2 receptors in skeletal muscle
NM:
- Nebulizers may work better than MDI due to the slow delivery of the drug (as bronchi gradually dilate, the drug gains deep access to the lungs)
- *SABA should be initial treatment for COPD exacerbation because that’s when we want the quick action
- *LABA should never be used as only method of treatment in asthma patients, but can be used as monotherapy for stable COPD
Short-acting (inhalation only)
Albuterol
Levalbuterol
*Long-acting (inhaled) Formoterol Salmeterol Indacaterol Given 1-2x day Preferred for COPD
bronchodialator for COPD beta 2 adrenergic agonist
side effects
- Rapid Infusion can cause severe hypotension and death
- Toxicity results at levels >20mcg/mL
- Mild toxicity 20-25: nausea, vomiting, diarrhea, insomnia, restlessness
- -Important to recognize in mild to prevent it from going further
- Severe toxicity >30: dysrhythmias (v.fib), convulsions
- -Stop infusion at first sign of toxicity
- –V.fib: lidocaine
- –Seizures: diazepam
NM:
-Infusion must be slow (max rate of 25mg/min)
–Give big loading dose then put on maintenance drip
–Once loading dose is given, must monitor range
-Therapeutic range is 10-20 mcg/mL but most patients respond well at 5 mcg/mL
Drug interactions
-Caffeine can intensify adverse effects & increase serum levels
-Instruct patient to AVOID caffeine – no coffee/pop
-Some ABX (ciprofloxacin) can elevate serum levels
Methylaxanthines: cause CNS stimulation and relaxation of smooth muscle of bronchi
Theophylline
No longer recommended for use in COPD
Aminophylline
Preferred for IV use - Reserved for severe COPD exacerbation
Very narrow therapeutic range because below that you don’t have effectiveness and above you have toxic
Bronchodialtor used for COPD
