Module 9 Quiz Flashcards
Dietary sources of Ca
spinach, tofu, dairy, broccoli
-Many foods are fortified with Ca now as well..E.g. cereal and OJ
Where is Ca stored
95% stores in teeth and bones
Where is Ca regulated
Parathyroid hormone, Vitamin D, Calcatonin
Is ca protein bound?
yes, it is highly protein bound. 50% unavaliable, 50% free (ionized).
Ca is highly bound to albumin. when you are acutley ill you albumin decreases, there is now more free Ca avaliable for binding. Serum ca will not be accurate, check ionized Ca
what happens if serum Ca is low
the body will reabsorb it from the bone, even if compromise of structural integrity occurs
Ca Kinetics absorption vs. excretion
Absorption: dietary Ca absorbed in small intestine. decreased with glucocorticoids and increased absorption with Vit D and PTH
Excretion: renally cleared. decreased by Vit D, PTH and thiazide diuretics. Increased with loop diuretics, calcatonin, sodium, breast milk
Hypercalcemia etiology, symptoms, treatment goals
Etiology: Malignancy, hyperparathyroidism, thiazide diuretics (decrease excretionof Ca)
Symptoms: may be assymptomatic if mild. High levels of Ca=weakness, fatgue, nausea, cramping, constipation, anorexia
severe hypercalcemia: polyuria, confusion, ataxia
Treatment goals: increase urinary excreption (loop diuretics) decrease mobilization from bone, decrease intestinal absorption, bind free ca in serum
IV fluids + Diuretics (loop/furosemide) + other (calcatonin)
Calcatonin indications, action, and administration
Indications: hypercalcemia, postmenopausal osteoporosis, pagets disease
Action: inhibit osteoclast activity, decrease bone reabsorption, inhibits tubular reabsorption of Ca
Admin: nasal spray or injection (nasal dryness can occur)
Not drug of choice. will use bisphosphonates over calcatonin to decrease Ca levels
Hypocalcemia etiology, symptoms, treatment, considerations
Etiology: deficiency of PTH, dietary Ca, chronic renal failure, Vit D, SE of some medications (Mg)
symptoms: increased neuromuscular excitability, tetany, convulsions, spasms of pharynx and other muscles
treatment: IV Ca gluconate
maintenance calcium citrate
considerations: Ca salts absorption decrease with glucocorticoids
bind many other drugs=decreased absorption
food interactions=spinch, rubarb, whole grains
chewable tabs=better bioavaliability, take with a glass of water and wither before or after a meal to improve absoprtion of Ca
Hypovitaminosis D actions, indications, forms, treatment
Actions: Vit D regulates Ca and phosphorus homeostasis. increases intestinal absorption of Ca and promotes bone reabsorption
Indications: Vit D deficiency, ricketts, osteomalacia, hypoparathyroidism
Forms: Ergocalciferol (D2)
Cholecalciferol (D3)
Treatment: Difficult to get enough Vit D from foods ( oily fish, shitake mushrooms)
-Vit D3 preferred as it is more effective than D2 at raising levels of active vit d in the body
Osteoporosis
-Mainly effects women, most common bone disease in the US
Focus is on primary prevention
-ensure adequate intake of Ca and Vit D
-lifestyle promoting bone health
-abundant food sources of Ca (spinach, tofu, dairy, brocolli)
-Avoid smoking and etoh
-Weight bearing exercise (walking, yoga)
Secondary prevention
-Drugs that decrease bone reabsorption and promote bone formation e.g. bisphosphonates: alendronate
Bisphosphonates
Action: incorporated into bone and inhibit bone reabsorption by decreasing osteoclast activity
Indications: prevention and treatment of osteoporosis, treatment of bone metastatic disease
Prototype: Alendronate
well tolerated, esophagitis principle concern
-absorption dramatically reduced when taken with food (almost 0).
-fluids (coffee or juice) reduced absorption by 60%
-take in the AM before breakfast/empty stomach
-no food or drink 30 mins after
-wait 2 hours before taking Ca containing products, mineral supplements, or antacids
current treatment for post menopausal osteoporosis
Goal: reduce Fx and increase bone strength, two types of drugs can be used (a) agents that decrease bone reabsorption (B) agents that promote formation of bone
e.g. estrogen, raloxifene, bisphophonates, calcatonin, and denusumab
-need sufficient Vit D and Ca
-better if started early
Allergic Rhinitis
Inflammatory disorder of the upper airway
symptoms: sneezing, rhinitis, puritis, congestion
Etiology: triggered by allergens, IgE mediated. 1. seasonal/hay fever: spring and fall, reaction to outdoor allergens
2. Perennial/nonseasonal: triggered by indoor allergens
Drugs for rhinitis
glucocorticoids, antihistamines, and sympathomimetics
Intranasal glucocorticoids
Most effective drugs for prevention and treatment. antiinflammatory actions supress: congestion, rhinnorrhea, sneezing, nasal itching in 90%
-Most common SE: nasal dryness/burning, itching, epistaxis, HA
Systemic effects: effects are rare
Antihistamines
HI receptor antagonist=first line drug for mild/mod
Admin on regular bases throughout allergy season
histamine does not contribute to symptoms of infectious rhinitis=ineffective against the common cold
SEs: anticholinergic effects: dry mouth, dry nasal secretions, constipation, urinary hesitancy
Sympathomimetics/Decongestants action and adverse effects
Reduce nasal congestion via Alpha 1 activation on nasal vessels=results in vasoconstriction, shrinkage of swollen membranes–> decreased nasal congestion
-do not reduce rhinnorhea, sneezing, itching
-AE: CNS stimulations–> subjective feelings like those of amphetamine, alpha 1 activation in vessels=vasoconstriction=HTN
Rebound congestions: with prolonged use of topical agents=cycle of congestion and increased drug use. Can be stopped by abrupt withdrawal prevent by limiting use to 2-3 days
-can be uncomfortable
-consider discontinuation one nare at at time
Drugs for cough (3)
Expectorants, mucolytics, anti tussives
Anti Tussives
ask: should you treat this cough?
opioid: codeine/hydrocodone
-work by elevating cough threshhold in CNS
-minimal risk of dependance (schedule iv)
-cautious use in those with minimal respiratory reserve
Nonopioid: Dextromethorphan
-OTC drug
-Acts in CNS
-Euphoria in high doses (abuse potential)
Mucolytics
-hypertonic saline/acetylcysteine
-inhalation
-acts directly on mucous to make it more liquid
-can trigger bronchospasm (give with beta 2 agonist to prevent bronchospasm)
Expectorants
E.g. Guaifenesin
-increases productivity of cough
-stimulates the flow of respiratory secretions
Gout
painful inflammatory rheumatic disease r/t uric acid crystal formation
men most often affected
illness r/t hyperurecemia with episodes of severe joint pain (toe)
Hyperurecemia: excessive production or ineffective clearance
Accumulation of sodium urate=inflammation–> infiitration of leukocytes= phagocytization of urate crystals–>breakdown releasing lysosomal enzymes that are destructive to the joint
over time tophi develop (crystal deposits)
Goals
- short term symptom managemnt
- long term uric acid lowering
if < 3 flares (occasional) per year persue symptoms managemant with
NSAIDS (first line), then add glucocorticoids
Pharmacotherapeutics
Agents that decrease uric acid production
agents that increase uric acid secretion
anti gout anti-inflammatory (colchicine)
Urate lowering therapy
-weeks to months to work/life long therapy
-indicated for frequent attacks
-Goal: dissolve urate crystals, prevent new formation and disease progression, reduce frequency of attacks and improve QOL
-want uric acid level < 6 mg/dl
-risk of kidney stones: counsel patients to drink 2.5-3 L of water daily
E.g. Xanthine Oxidase inhibitors: Allopurinol
-inhibits uric acid formation
-no anti-inflammatory/analgesic affect
-regression of tophi, joint function improvement, reduces risk of nephropathy
SE: mild GI side effects, cataract development
Uricosuric Agents
protoype: probenecid
increases excretion of uric acid
-works at renal tubules to inhibit reabsorption
-SE: Mild GI effects can be reduced by taking with food
Recombinant Uric Acid Oxidases
IV therapy for those with chronic gout (non responders to uric acid lowering therapy) e.g. rasburicase
-$22,000 for a single dose
-significant risks of AE
-Approved only for hyperurecemia r/t malignancy
Anti gout anti inflammatory
Colchicine (no longer first line d/t GI toxicity)
-anti inflammatory with gout specific effects
-used short term to treat acute attack
-dramatic results w/in hours
-cessation of inflammation w/in days
-used long term to prevent attacks
-also prophylaxis when initiating ULT
The bad:
-narrow therapeutic window
-toxic to rapidly proliferating cells
-gi toxicity 2ndry to results from gastric epithelium (N//V, diarrhea, abd pain)
-myelosuppression/myopathy (rhabdo)
-significant drug-drug interactions (statins)
-problematic in older patients, cardiac, and gi issues
RA
autoimmune disease of the bones and joints
-most often present in 30-40s
-women> men before age 6 then =
-chronic progressive illness–>joint deformity + functional limitations
-drugs are not currative
immune response against synovial tissue mediatied by cytokines (TNF, IL-1, IL-6, Interferon Y, among others)
RA Pathophysiology
Synovial inflammation–> envelopment of joint in pannus
chemicals released=damage and degradation to articular cartilage
bone-bone contacts followed by fusion
RA symptoms
initial: joint stiffness and pain, more intense in AM improves throughout day. Tender, swollen, warm joints
Systemic: fever, fatigue, weight loss, weakness, thinning skin, scleritis, corneal ulcers, vasculitis, skin nodules
RA treatment
Goal: symptoms relief, maintinence of function, minimizing systemic effects, delaying progression
Drug therapy (NSAIDS, glucocorticoids, DMARDS)
Non drug therapy (PT, exercise with rest, orthopedic surgery)
RA medication therapy NSAIDS, glucocorticoids
NSAIDS (safest)
-inhibition of COX
-Rapid relief of symptoms
-Does NOT slow disease progression or confer joint protection
Glucocorticoids (LONG term toxicity)
-rapid relief of symptoms
-can delay progression
-Adj: flares and with DMARDS
-Limit to short term courses
NSAIDS + GLUCOCORTICOIDS= 4X risk for GI ulceration (DC NSAIDS)
DMARDS (3)
-reduce joint destruction and slow disease progression
- conventional/traditional (MTX), biologics (TNF, B lymphocyte depleting agents, t cell activation inhibitors, IL-1, IL-6 antagonist) , and targeted therapy (Janus Kinase inhibitors)
MTX
drug of choice, low cost, high safety and efficacy 80% will improve
-Adverse: hepatic fibrosis, bone marrow suppression, ulcers, pneumonitis
-take 3-6 weeks to work
Contraindicated in pregnancy or nursing
reduced life expectancy 2ndry to CVD, infection, cancer, reduced response to vaccine, liver damage when combined with ETOH
Biologics: TNF inhibitors
Action: immune suppresants that target specific components of inflammatory process
Other: combined w/ MTX, risk of serious infection/cancer
-$$$$$
TNF inhibitor: prototype: Etanercept
-disease and symptom suppression
-add on to MTX
-mod to severe RA
-Promotes severe infection (sepsis, fungai, hep a, b, TB), malignancy in adolecents
-severe allergic reactions: SJS and others
B lymphocyte depleting agents
Action: reduce b lymphocyte numbers=slow progression/reduce symptoms
prototype: Rituximab
-monoclonal antibody
-mod to severe RA
-promotion of severe hypersensitivity reaction
-30-120 mins
-hypotension, bronchospasm, angioedema, hypoxia, MI, cardiogenic shock
-post infusion renal toxicity=death w/in 24 hours
Pre medicate w. APAP, antihistamine, glucocortcoid
T-cell activation inhibitors
Activation of t cells in synovium play a key role in disease
-prevent t cell activation
IL-6 antagonist
IL-6 amplifies immune attack on joints
-serious and fatal infections
IL-1 antagonist
IL-1 is a proinflammatory cytokine in synovial inflammation and joint destruction
-receptor block reduces activity
Janus Kinase Inhibitors
Block specific immune pathways w/in the cell that are mediated by JAK
-reduce immune and inflammatory processes
-Last line, use when MTX and TNF inhibitors not effective
-bone marrow suppression and infections (check CBC)
-20% develop nasopharyngitis
-malignancies
-bradycardia
-DILI
Clinical pearls for DMARD therapy
-Early and aggressive therapy
-weeks to months to show effects
-begin w/ NSAIDS then DC
-glucocorticoids for short term flares
-Start with MTX then add if needed
Patient education
-risk for infection/myelosupression
-know the signs (M: bruising, bleeding, pallor, fatigue, fever/ CHF: edema, weight gain, sob/ liver failure jaundice, RUG pain, anorexia
-avoid those with communicable disease
-up to date on vaccines prior to therapy
-NO LIVE VACCINES
Inhalation medications and its advanatges
-metered dose inhaler, dry powders, nebulizers
Advantages
1. effects are enhanced as the drug is directly delivered to the lungs
2. can minimize systemic effects
3. rapid relief of acute attacks
MDI
-requires hand/breath coordination; need to inhale before activating, 10% med reaches the lungs but more will reach w/ use of spacer–>consider spacer and verbal/written instructions/lots of teaching
Dry powder inhalers
-micronized medication directly to the lungs; activated by breath; does not require hand/breath coordination
-more drug delievered (20%)
Nebulizers
-converted to mist
-can be used in the acute care setting and home setting
-increased delivery of medication to the site of action (lungs)
-takes longer to deliver medication compared to other inhalation methods–> goes over a few minutes compared to one single breath
-enables continuous administration if needed
GINA
global initiative for asthma
-EB guideline/recommendation for treatment
-step up and step down
-goal of drug therapy is to abort acute attacks and to establish long term control
Acute emergent treatment of asthma
O2 to relieve hypoxia
IV systemic glucocortocids
nebulized high dose SABA
nebulized ipratropium
Drugs for asthma and COPD antiinflammatories and bronchodilators
anti-inflammatories
-glucocorticoids, mast cell stabilizers/leukotryine receptor antagonists, monoclonal antibodies, PDE-4 inhibitors
Bronchodilators: SABA, methylxanthines, anticholinergic drugs
Glucocorticoids
Indications: daily therapy in asthma, used for exacerbation in COPD preventative therapy not abortive
-most effective for long term control
-start with high doses initially
standard is inhalation (can be given oral and IV)
-minimal adverse actions w/ inhaled therapies
-oral candida/dysphonia can develop
-Give SABA 5 min prior to increase absorption
Leukotriene receptor antagonist
Montelukast
-add on therapy/second agent, prevention of exercise bronchospasms, relief of allergic rhinits, prophylaxis and maintence therapy in asthma
-Does not provide quick relief, use for prophy/maintence
-Neuropsychiatric effects (depression, si) Should be included in ROS
Monoclonal Antibodies
Omalizumab
-add on therapy/second agent
-only effective in those whose asthma is allergen triggered
Black box warning: anaphylaxis. only used when others have failed
worry about cancers
given in healthcare facility subcutaneously
PDE4 inhibitors
Roflumilast
-severe chronic COPD w. component chronic bronchitism, may reduce exacerbations. ONLY COPD
-Inactivates CAMP, increased CAMP=less inflammation and less pulm infiltration
AE: diarrhea, weight loss, reduced appetite, nausea, HA
Beta 2 adrenergic agonists
Albuterol
first line drugs for asthma, most effective avaliable
-sympathomimetics that activate B2 receptors=bronchodilaition
Considerations: relative selectivity od B2
Oral: LABA (Can cause tachycardia, agina b/c works also on beta 1) or inhalation (SABA)
SABA can abort attack, not preventative
LABA can prevent attacks, no good at aborting
LABA carry black box warning, do not use alone. increased risk of asthma related death. Always in combo with glucocorticoid
Methylxanthines
Theophylline
-first line drugs for chronic stable asthma. decrease frequency/severity of asthma attacks
Actions: CNS stimulation and bronchodilation: relaxes smooth muscle of bronchi
Considerations: Do not use caffeine containing products=intensify adverse effects and prevents breakdown fo med leading to accumulation
Theophylline toxicity: N/V, abd discomfort, diarrhea, insomnia, palps, restlessness-dysrhythmias. VF, death
-smoking/marijuana
-contraindications: seizure disorder and PUD
Anticholinergic Drugs
Ipraptropium (1st inhaled, also have 3 LAMAs)
Indications:Block muscarinic receptors in the bronchi-relief of bronchoconstriction
-FDA improved only for COPD, but expert reccomended for asthma too)
Considerations
-prevention of bronchoconstriction via different effect than B2 agonist (addedd benefits when used together)
-minimal adverse effects
