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NURS 5590 > Module 9 Quiz > Flashcards

Module 9 Quiz Flashcards

1
Q

Dietary sources of Ca

A

spinach, tofu, dairy, broccoli
-Many foods are fortified with Ca now as well..E.g. cereal and OJ

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2
Q

Where is Ca stored

A

95% stores in teeth and bones

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3
Q

Where is Ca regulated

A

Parathyroid hormone, Vitamin D, Calcatonin

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4
Q

Is ca protein bound?

A

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

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5
Q

what happens if serum Ca is low

A

the body will reabsorb it from the bone, even if compromise of structural integrity occurs

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6
Q

Ca Kinetics absorption vs. excretion

A

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

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7
Q

Hypercalcemia etiology, symptoms, treatment goals

A

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)

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8
Q

Calcatonin indications, action, and administration

A

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

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9
Q

Hypocalcemia etiology, symptoms, treatment, considerations

A

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

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10
Q

Hypovitaminosis D actions, indications, forms, treatment

A

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

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11
Q

Osteoporosis

A

-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

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12
Q

Bisphosphonates

A

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

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13
Q

current treatment for post menopausal osteoporosis

A

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

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14
Q

Allergic Rhinitis

A

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

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15
Q

Drugs for rhinitis

A

glucocorticoids, antihistamines, and sympathomimetics

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16
Q

Intranasal glucocorticoids

A

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

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17
Q

Antihistamines

A

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

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18
Q

Sympathomimetics/Decongestants action and adverse effects

A

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

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19
Q

Drugs for cough (3)

A

Expectorants, mucolytics, anti tussives

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20
Q

Anti Tussives

A

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)

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21
Q

Mucolytics

A

-hypertonic saline/acetylcysteine
-inhalation
-acts directly on mucous to make it more liquid
-can trigger bronchospasm (give with beta 2 agonist to prevent bronchospasm)

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22
Q

Expectorants

A

E.g. Guaifenesin
-increases productivity of cough
-stimulates the flow of respiratory secretions

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23
Q

Gout

A

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)

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24
Q

Goals

A
  1. short term symptom managemnt
  2. long term uric acid lowering

if < 3 flares (occasional) per year persue symptoms managemant with
NSAIDS (first line), then add glucocorticoids

25
Q

Pharmacotherapeutics

A

Agents that decrease uric acid production

agents that increase uric acid secretion

anti gout anti-inflammatory (colchicine)

26
Q

Urate lowering therapy

A

-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

27
Q

Uricosuric Agents

A

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

28
Q

Recombinant Uric Acid Oxidases

A

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

29
Q

Anti gout anti inflammatory

A

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

30
Q

RA

A

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)

31
Q

RA Pathophysiology

A

Synovial inflammation–> envelopment of joint in pannus
chemicals released=damage and degradation to articular cartilage
bone-bone contacts followed by fusion

32
Q

RA symptoms

A

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

33
Q

RA treatment

A

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)

34
Q

RA medication therapy NSAIDS, glucocorticoids

A

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)

35
Q

DMARDS (3)

A

-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)

36
Q

MTX

A

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

37
Q

Biologics: TNF inhibitors

A

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

38
Q

B lymphocyte depleting agents

A

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

39
Q

T-cell activation inhibitors

A

Activation of t cells in synovium play a key role in disease
-prevent t cell activation

40
Q

IL-6 antagonist

A

IL-6 amplifies immune attack on joints
-serious and fatal infections

41
Q

IL-1 antagonist

A

IL-1 is a proinflammatory cytokine in synovial inflammation and joint destruction
-receptor block reduces activity

42
Q

Janus Kinase Inhibitors

A

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

43
Q

Clinical pearls for DMARD therapy

A

-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

44
Q

Patient education

A

-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

45
Q

Inhalation medications and its advanatges

A

-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

46
Q

MDI

A

-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

47
Q

Dry powder inhalers

A

-micronized medication directly to the lungs; activated by breath; does not require hand/breath coordination
-more drug delievered (20%)

48
Q

Nebulizers

A

-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

49
Q

GINA

A

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

50
Q

Acute emergent treatment of asthma

A

O2 to relieve hypoxia
IV systemic glucocortocids
nebulized high dose SABA
nebulized ipratropium

51
Q

Drugs for asthma and COPD antiinflammatories and bronchodilators

A

anti-inflammatories
-glucocorticoids, mast cell stabilizers/leukotryine receptor antagonists, monoclonal antibodies, PDE-4 inhibitors

Bronchodilators: SABA, methylxanthines, anticholinergic drugs

52
Q

Glucocorticoids

A

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

53
Q

Leukotriene receptor antagonist

A

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

54
Q

Monoclonal Antibodies

A

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

55
Q

PDE4 inhibitors

A

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

56
Q

Beta 2 adrenergic agonists

A

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

57
Q

Methylxanthines

A

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

58
Q

Anticholinergic Drugs

A

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

NURS 5590 (11 decks)

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