NSG 304 quiz 2

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  1. Combining a beta-blocker
    along with a calcium channel blocker may cause hypotension
    • -because beta and calcium
    • channel blockers both suppress myocardial contractility, concurrent use may
    • lead to additive bradycardia.

    • Beta Blockers:
    • -pg 251, 253 “drug
    • interactions”
    • nonselective and selective

    • nonselective block beta 1 and beta 2
    • selective drug only blocks beta 1 (cardioselective agents)

    • -catelcholamines: class of
    • endogenous hormones involved in neurotransmission that include epinephrine
    • (adrenaline), norepinephrine, and dopamine.
    • -mechanism of action is to
    • antagonize the effects of catecholamines reducing heart rate, decrease force of
    • myocardial contraction, and slow conduction velocity through atrioventricular
    • node
    • Calcium Channel Blockers (CCBs)
    • pg518
    • -The influx of calcium ions into smooth muscle is essential for contraction
    • -CCBs prevent contraction of peripheral arterioles, resulting in vasodilation and fall in systemic blood
    • pressure.
    • -Under normal conditions, the SA
    • node automatically generates an action potential because of an inward movement
    • of CA 2+ ions through calcium channels.

    • Blocking calcium entry causes the SA
    • node to generate fewer action potentials, thus decreasing automaticity and slowing
    • heart rate.
    • -Calcium Channel blockers in the AV
    • node:

    • reducing conduction velocity through this region of the heart and further slowing the spread of the action potential across the myocardium.

  2. timing of sleeping

    • 3 types of therapy treating insomnia/anxiety:
    • 1)complementary and alternative
    • therapies
    • 2)non prescription drugs
    • 3) prescription drugs
    • -long term use of sleep medications
    • is likely to worsen insomnia and many of these meds cause psychological or physical dependence.
    • Sedative:
    • -Most often prescribed during the
    • day to induce a feeling of calm or relaxation without sleep
    • Hypnotic:
    • Used at night to induce sleep
    • All sleeping meds are CNS depressants
    • Benzo – used ¾ of time
    • Versed (midazolam) benzodiazepine:
    • Rapid onset time of 15-30 minutes
    • Halazepam (paxopam):
    • 1-3 hours onset time

  3. First and second-generation
    antihistamines (differences)

    • Pg712: histamine
    • interacts with two different receptors to elicit an inflammatory response.
    • pg. 711
    • H1 receptors:
    • -Present in the bronchial tree, and
    • the digestive tract.

    • -Their stimulation results in itching, pain, edema,
    • vasodilation, bronchoconstriction, and the characteristic symptoms of inflammation and allergy.
    • Pg 1265: H1 receptor antagonists:
    • -(Antihistamines), are used to treat
    • allergies and inflammation.

    • -These drugs block histamine from reaching its H1
    • receptors, thus alleviating allergic symptoms.

    • -Widely used as OTC remedies for
    • the relief of allergy symptoms, motion sickness, and insomnia.
    • H2 receptors:
    • -Present primarily in the stomach
    • and their stimulation results in the secretion of large amounts of hydrochloric acid.
    • H2 receptor antagonists
    • Are used to treat peptic ulcers.

    -H2 receptor antagonists reduce gastric acid secretion and are used to treat gastric ulcer disease and gastroesophageal reflux disease.

    • -This histamine receptor activity is not related to allergic responses.
    • Histamine:
    • Chemical released by mast cells in
    • response to an antigen that causes dilation of blood vessels, bronchoconstriction, tissue
    • swelling, and itching.
    • During inflammation:
    • Pathogens, chemicals, or physical
    • trauma cause the damaged tissue to release chemical mediators (histamine),
    • which act as alarms to notify the surrounding area of the injury.
    • Antihistamines may cause drowsiness

  4. Inhalers, broncodialators, albuterol, if using both broncodialator and steroid...
    • pg1241:
    • -Rationale: asthma pts should be taking long-term control meds along with quick relief PRN meds to treat symptoms
    • Pg 1242:

    • -Asthma drugs separated into two different classes (pg 1244 table 73.3)
    • 1) Quick relief / short acting medications

    • -(beta 2 adrenergic agonists) “rescue agents”
    • 2) Long term control medications (corticosteroids)
    • -FDA issued warning regarding an
    • increase in deaths among persons only taking the long acting beta2 agonists.

    • -Taking a long acting drug during an asthma attack could result in unrelieved
    • bronchospasm and subsequent death.
    • -The inhalation route works especially well because the respiratory system offers a rapid and efficient
    • mechanism for delivering drugs directly to their site of action.

    • -The enormous surface area of the bronchioles and alveoli and rich blood supply to these
    • areas result in an almost instantaneous onset of action for inhaled substances.

  5. Treatment of acute pain
    • pg.428:
    • Often self-limiting,

    -high doses of pain medication may be necessary, but therapy is usually limited to several weeks.

    • -There is little risk for chronic drug adverse effects or dependence because of the relatively short length of the treatment period.
    • Pain is classified by its duration and its source
    • Acute pain:
    • -Often brief duration, usually from
    • injury, subsides as healing takes place or the stimulus ceases.
    • Chronic pain:
    • -Persists longer then 6 months, can interfere with daily activities, and is associated with feelings of helplessness or hopelessness.

    • -May be further classified as malignant or non malignant

  6. Side effects of statins
    • pg.501:
    • Minor adverse effects:
    • -Include headache, abdominal cramping, diarrhea, muscle or joint pain, and heartburn.
    • Sever adverse effects:
    • Include severe myopathy and rhabdomyolysis.
    • -Myopathy:
    • -a muscular disease in which the muscle fibers do not function for any one of many reasons, resulting in muscular weakness.
    • -Rhabdomyolysis:
    • -Breakdown of muscle fibers usually due to muscle trauma or ischemia.

    • -Contents of muscle cells spill into the circulatory system causing potentially fatal acute renal failure.
    • Statins are the most effective drugs for reducing blood
    • lipid levels.
    • -They can reduce a dramatic 20-40% reduction of LDL cholesterol levels in the blood, also lower triglycerides and raise the HDL (good cholesterol).

    • -These events have shown to reduce the incidence of serious cardiovascular related events by 25-30%.
    • Note:
    • -Levels of creatine kinase (CK), an enzyme released during muscle injury, should be
    • obtained if myopathy or rhabdomyolysis are suspected.
    • Mechanism of action:
    • -Inhibit HMG-CoA reductase, resulting in less cholesterol biosynthesis.

    • -As the liver makes less cholesterol, it responds responds by making more LDL receptors on the surface of the liver cells removing more LDL from the blood.

  7. Meds to treat migraines, (better choices)
    • pg.449
    • Two types of drugs used to treat migraines:
    • 1) Analgesics

    • 2) Triptans
    • Two primary goals for migraine pharmacotherapy-
    • -1) Terminate an acute migraine in
    • progress
    • -2) And to prevent or reduce
    • frequency of the disorder.
    • Drug therapy is conducted in stages:
    • Mild migraine
    • -(Occasional headaches with no ther functional impairement)
    • -NSAIDs offer safest and least expensive therapy. Acetaminophen combined with caffeine
    • -Oral serotonin (5-HT) agonist (triptans or ergot alkaloids)
    • Moderate Migraine
    • -(Moderate headaches more than 3 times per month, marked nausea or vomiting, and functional impairement)
    • -Oral, intranasl, or subcutaneous serotonin (5-HT) agonists are the drugs of choice.

    • -If ineffective, administer dopamine agonists such as metoclopramide (reglan) or prochlorperazine (compazine)
    • Severe Migraine
    • -(Severe headaches more than 3 times per month, marked nausea or vomiting, and functional impairment)
    • -Subcutaneous, IM, or IV serotonin agonists maybe indicated.
    • -Secondary choice would be a parenteral dopamine agonist, either as monotherapy or in combination with a serotonin agonsit.
    • -Narcotic analgesics are effective at terminating pain from migraines that have proven to be refractory to other therapies.
    • Migraine Definition:
    • -Severe type of headache related to
    • a trigger.

    • -The most painful type of headache characterized by throbbing or pulsating pain, sometimes preceded by auras or sensory warnings of an imminent
    • migraine attack.
    • -When headaches are persistent, or manifest as migraines, drug therapy is warranted
    • -Although the skull and brain lack pain receptors, the muscles of the scalp, face, and neck are abundantly
    • supplied with nociceptors.

    • -These receptors may be stimulated by muscle tension,
    • dilated blood vessels, and other headache triggers.
    • -Tension headache the most common caused by the muscles of the head and neck becoming tight due to stress.

  8. Ch20- side effects of lopressor
    • Pg. 256
    • Therapeutic:
    • -Antihypertensive, selectivebeta1-andrenergic antagonist
    • Side effects:
    • -Nausea and vomiting are the most common adverse effects.
    • Other side effects include:
    • -Dizziness, fatigue, insomnia, bradycardia, heartburn, and dyspnea.
    • Serious adverse effects:
    • -agranulocytosis (an acute condition involving a severe and dangerous lowered white blood cell count), laryngospasm, complete heart block, thyroid storm in pts thyrotoxicosis.
    • -Adverse effects when a sudden withdrawal occurs from lopressor: Dysrythmias, severe HTN, MI

  9. African Americans and blood pressure treatment
    • Page 573
    • -Incidence in African Americans is significantly higher then in other ethnic groups
    • -Experience greater target organ damage then other groups
    • -Studies suggest that certain anti hypertensive drugs are less effective on blacks
    • Example:
    • -Monotherapy with ace inhibitors, angiotensin II receptor blockers, or beta adrenergic antagonists does not reduce blood pressure in
    • blacks like they do in other races.
    • Thiazide diuretics and Alcuin channel blockers:
    • -Seem to provide the greatest blood pressure reduction in black population.
    • -Some healthcare providers recommend initiating two classes of drugs to ensure an adequate response

  10. Treatment of angina:
    • Page: 591
    • Pharmacologic management:
    • -Includes beta-adrenergic blockers, organic nitrates, and calcium channel blockers
    • -Medications placed into two categories to treat angina:
    • -1) Those that terminate an acute angina episode in progress
    • -2) Those that decrease the frequency of episodes
    • -Antianginal medications work by reducing the myocardial demand for o2
    • Accomplished by:
    • -Slowing the heart rate
    • -Dilating veins so that the heart receives less blood
    • (reduced preload)
    • -Causing the heart to contract with less force (reduced
    • contractility)
    • -Lowering blood pressure
    • -Persistent angina requires use of from two or more classes such as beta blockers combined with long acting nitrates or a calcium channel blocker
    • Primary goal of treating angina:
    • Is to reduce frequency and intensity of episodes.
    • -Successful management should allow pt to more actively participate in daily activities.
    • Long term goals:
    • -Include extending the pts lifespan by preventing lifespan by preventing serious consequences of ischemic heart disease such as disrythmias,
    • heart failure, and MI.
    • -Pharmacology and therapeutic lifestyles necessary to promote a healthy heart

  11. Different kinds of pain and where they're located:
    • Page 429
    • -Pain transmission processes allow multiple targets for pharmacological interventions.
    • Two primary classes of anagesics act at different
    • locations:
    • -1)Nonsteroidal anti-inflammatory drugs (NSAIDS) act at the peripheral level
    • 2)Opioids act on the CNS
    • -Drugs that affect or mimic the inhibitory neurotransmitters are used as adjuvant anagelsics.
    • Pain physiology has four phases:
    • -Transduction, transmission, perception, modulation
    • -The 4 phases of pain physiology allow for multiple targets for the pharmacologic intervention of pain impulse transmission.
    • Transduction:
    • -Begins when nociceptor nerve endings in the peripheral nervous system are stimulated
    • This occurs with local tissue injury causes the release of chemical mediators of inflammation, including prostaglandins, leukotrienes,
    • histamine, bradykinin, and substance P.

    • -these substances sensitize peripheral
    • nociceptors making them easier to activate
    • Pain transmission:
    • -The nerve impulse signaling pain from the nociceptor to the spinal cord along two types of sensory neurons called A and C fibers.
    • A fibers-
    • -Wrapped in myelin, a lipid substance that speeds transmission and carries signals for intense well defined pain.
    • C fibers-
    • -Unmyelinated and this carry information more slowly and conduct poorly localized pain, which is often percieved as burning or a dull ache
    • Sensory nerve fibers:
    • -Enter the dorsal horn of the spinal Cord
    • and have adjacent synapses in an area called the substantia gelitinosa.
    • -Once a pain impulse reaches the spinal cord it relies on neurotransmitters for passing the message along to the next neuron.
    • Pain perception:
    • -The conscious perception of pain occurs in the brain.
    • -Numerous cortical structures and pathways are involved in perception including the reticular activating system, the somatosensory system,
    • and the limbic system.
    • -When pain impulses reach the brain, it may respond with a wide variety of actions ranging from signaling the skeletal muscles to contract
    • to mental depression in those suffering from chronic pain
    • Pain modulation:
    • -Involves descending nervous impulses traveling down spinal cord that inhibits afferent pain transmission is a feedback mechanism.
    • -Neurotransmitters such as serotonin, norenephrine, and endogenous opioids (endorphins and enkephalins) inhibit pain transmission.

  12. Opioid antagonists:
    • Page 435:
    • Used when respirations fall below 10 per minute:
    • -Opioids most Adverse effect is to cause a profound respiratory depression by activating the MU receptor.

  13. Cholysteramine, what do you want to teach pt about this med:
    • Page 507
    • Treats hypercholesterolemia, especially elevated LDL cholesterol
    • -Med should be mixed with 60-180 ml water

    • -no carbonated beverageshighly liquid soups, or pulpy fruits to prevent esophageal irritation.
    • -Pt should swallow medication immediately after stirring
    • -If taken with too small of a fluid volume, or if not
    • completely swallowed, the drug can swell in the throat or esophagus to cause an obstruction
    • -May take 30 or more days to produce its maximum effect
    • -Should not be taken at the same time as vitamins or other medications
    • Report symptoms such as:
    • -Severe gastric distress with nausea or vomiting,
    • unexplained weight loss, black stools, severe hemorrhoids, unusual bleeding, or
    • sudden back pain to health care provider
    • Do not omit doses:
    • -Sudden cessation can promote the absorption of other meds possibly leading to toxicity or overdose
    • -Consult with health care provider about taking vitamin supplements because this drug can reduce the absorption of vitamins
    • -Increase intake of oral fluids and maintain a high fiber diet to prevent constipation
    • Report constipation to health care provider
    • -GI symptoms usually subside after the first month of therapy

  14. Aldosterone:
    • Page 1169
    • -Primary hormone regulating sodium and potassium balance in the body
    • -Its actions on the kidneys include resorption of sodium and water
    • Regulation of aldosterone:
    • -Through activation of the renin angiotensin aldosterone system
    • -When plasma levels fall, the kidneys secrets renin which results in the production of angiotensin II. Angiotensin II then promotes
    • aldosterone secretion, which in turn acts on the renal tubule to promote sodium and water retention.

  15. Negative effects of hypertension pg. 568-569
    • Definition:
    • -Consistent elevation of systemic arterial blood pressure:
    • Primary Hypertension:
    • No identifiable cause
    • Secondary (aka idiopathic or essential) Hypertension:
    • When specific cause are identified
    • Negative effects:
    • The heart is the primary organ damaged
    • -Increases heart after load forcing the heart to work harder to pump blood to the tissues
    • -Heart subjected to chronic pressure
    • overload resulting in left ventricular hypertrophy
    • -If untreated excessive workload of heart causes heart failure and lungs to fill up with fluid (congestive heart
    • failure)
    • -Accelerates the deposition of atherosclerotic plaque placing pt at greater risk for dysrythmia, angina
    • pectoris, and myocardial infarction
    • -Occlusion of small blood vessels to the brain can cause transient ischemic attacks and cerebrovascular accident
    • (CVA)
    • -Chronic hypertension crates major stress on kidneys when the small arterioles supplying the kidney become
    • inflamed and atherosclerotic, the pts renal function gradually declines.
    • May cause kidney failure and end stage kidney disease
    • -Major cause of visual impairment, which occurs when vessels in the eye become atherosclerotic, small hemorrhages that effect vision may occur
    • -Symptoms of retinal damage range from subtle vision changes to blindness
    • -Risk for cardiovascular disease beginning at 115/75 doubles when BP doubles with each additional increment of
    • 20/10
    • Cushings disease
    • Hyperthyroidism
    • Chronic renal impairement
    • -Pheochromocytoma= a tumor, usually benign, arising from the adrenal medulla that is characterized by excessive secretion of catecholamines
    • Arteriosclerosis
    • -Damage to blood vessels (particulary small arteries and arterioles)
    • -Arteriole walls begin to thicken to compensate for the increased pressure
    • -Injured blood vessels become inflamed increasing permeability causing additional thickening.

    • -Eventually the lumen of the artery permanently narrows reducing blood flow to vital tissues
    • Accelerates atherosclerosis

  16. Angina and MI comparison pages 588-590
    • Angina:
    • Acute chest pain caused by myocardial ischemia
    • -Pain caused by the narrowing of the arteries restricting blood flow.
    • Rarely leads to death
    • -Usually immediately relieved by administering nitroglycerine
    • -Characterized by severe chest pain brought on by physical exertion or emotional distress
    • Myocardial Ischemia:
    • High mortality rate
    • -Pharmacologic intervention must be immediately initiated and systematically maintained
    • -Occurs when cardiac demands exceed the amount of oxygen that can be supplied through the narrowed, inelastic vessels characterized of coronary artery disease and atherosclerosis.
    • -A condition where the heart is receiving an insufficient amount of O2 to meet its metabolic needs.
    • -Occurs when there is an imbalance between oxygen supply and oxygen demand in myocardial cells
    • -Coronary Artery Disease (CAD) is the leading cause of MI and death in the US.
    • -Narrowing of coronary arteries from atherosclerosis or coronary artery disease deprives cells of needed oxygen and nutrients.

    -If the narrowing develops over a long period of time, the heart compensates for its inadequate blood supply and the pt may be asymptomatic.

    • -Coronary arteries may be occluded up to 50% and cause no symptoms.
    • -Pts with heart failure have a thickened myocardium (increased tension), which will require more work to
    • contract

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NSG 304 quiz 2
2011-12-04 03:38:06
nsg 304

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