Nur 218 - Pharm Final - Lecture notes 1-27 PDF

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This is material consisting of the 3 tests to prepare me for the final exam. You can find information for the other exams by searching through this document. Topics include: Intro to pharmacology policies, drug development, safety, pharmacokinetics, pharmacodynamics, autonomic nervous system, cholin...

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Pharmacology Final ● ●

FDA Drug schedules ○ Potential for abuse ■ Schedule I is highest potential for abuse (little medical use at this time) ■ Schedule V is lowest potential for abuse ○ Opioids, benzodiazepines, anabolic steroids, barbiturates ○ Controlled substances ■ Restricted prescribing procedures, ie schedule II PHARMACOKINETICS Pharmaceutics ● Oral drugs become liquid/ solution to cross plasma membrane and be absorbed Disintegration: break down of tablet into smaller particles

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Dissolution: is smaller particles dissolve in the GI fluid

Rate of absorption: Time until drug is available to the body after disintegration and dissolution

Enteric coated drugs resist disintegration in the gastric acid and wait to be absorbed in alkaline environment-therefore do not crush Food can increase or decrease absorption Never crush coated capsules--go further into GI tract

Pharmacokinetics ● ● ●

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Movement of drug to achieve action of drug Obstacles: fewer with IV meds than PO PO meds: stomach acid break down drug molecules ○ Liver chemical changes make a drug less active ○ GI plasma membrane may prevent entrance into the bloodstream ○ Drugs go from GI tract to the liver Drugs need to cross plasma membranes to enter cells to produce effect Diffusion Passive, high to low concentration (blood to tissues) Small, nonionized and lipid soluble drugs will pass through most easily. Weak acidic drugs are less ionized, so they pass through more quickly, easily Large, ionized (no charge) water soluble drugs cannot pass easily

Active transport Carrier protein or enzyme Proteins are specific for what they will carry (sodium potassium pumps) Low concentration to high concentration Needs energy

● 4 phases: absorption, distribution, metabolism, excretion Absorption ● Process of movement of drug particles to body fluids. Movement happens in small intestines ● Absorption doesn't happen for IV meds (already in blood stream) ● Determines onset action and intensity of drugs ● Absorption rate 0-100%. Higher rate= greater effect

Passive absorption of drugs Facilitated diffusion Carrier protein moves drug from higher to lower

Active absorption Need carrier protein against concentration gradient

Pinocytosis Cells carry drugs across membrane by engulfing drug

Factors of absorption ● Concentration: higher dose= faster and greater response ○ Greater concentration gradient for diffusion ● GI membrane composed of lipids and fats. Lipid soluble drugs pass through faster. Water soluble drugs need carrier to pass membrane ● Blood flow, pain, stress (slow gastric emptying time) ● Exercise, hunger pH ● IM in areas of increased blood flow ● Subcutaneous: decreased blood flow than muscle Drug Ionization ● Large particles can pass through mucus membrane if nonionized ● charged/ionized particles don’t pass through easily ● Charge depends on environment ● Acidic drugs are absorbed in acidic environments since they are nonionized ● basic/alkaline drugs are absorbed in bases/basic environments since they are nonionized ● Drugs are absorbed better in a matched environment First pass effect, first pass mechanism, hepatic first pass ● Drugs metabolized in liver after GI absorption ○ Intestinal lumen to portal vein to liver ○ Becomes inactive and is then excreted ● Most drugs affected by first pass ● Decrease in liver function= decrease in metabolism=decrease breakdown= a need for a decrease in pt dose Bioavailability ● Percent of drug that reaches systemic circulation and causes effect ● Oral drugs are never 100% Iv are usually 100% (IV dose is lower than oral) ● Factors affecting bioavailability ○ Form of drug, route, food, other drugs ○ Liver status ○ Liver disorders cause less of drug to be available Distribution ● Process of which drug become available to body fluids and tissues ● Influenced by blood flow, drugs affinity to tissues, and protein binding effect ● Areas with highest blood flow have highest exposure to absorbed drugs ○ Heart, kidney, and liver have high exposure ○ Skin, bones, and cells have low exposure ○ Damaged blood cells have lower distribution (necrotic areas or broken bones) Solubility ● Lipid solubility- increased distribution since plasma membranes allow them, pass more easily

● Only unbound or free drugs can reach target cells ● Bound drugs do not have an affect ● Higher protein binding, the less the effect of the drug Drug protein complexes ● Protein binding effect (albumin, AGP-alpha glycoprotein) ● Some drugs bind to proteins too big to distribute across capillary membranes ○ Bind with protein no longer available to tissues ○ Only unbound free drugs can make an effect ● Can compete for binding sites on proteins ○ Drug with higher protein binding effect binds first. The other drug is more free ○ Drug that is less protein bound has a greater effect ○ Watch for toxicity ○ Higher protein bound have less effect. Free drug causes an effect Other factors of distribution ● Blood brain barrier- can prevent certain drugs from getting into the brain. Good or bad ● Capillaries packed tightly do not let substances in easily ○ Lipid soluble and glucose can pass through ○ Large, water soluble can’t pass through ● Harmful cannot get in/out of the brain ● Some meds cannot get into the brain Metabolism ● Biotransformation = chemical change of the drug ● Occurs in liver mostly. Sometimes GI tract and kidneys ● Metabolic changes of drugs in the liver allow for it to be excreted ● Active metabolites have greater effect than original form of the drug ● Liver disease can impact metabolism Liver hepatic first pass ● Drugs not absorbed in intestines go to the liver ● Some of the drug is metabolized in the liver, inactivated or excreted before effect of drug occurs ● Some drugs cannot be given orally b/c of the first pass, so it is destroyed and unable to use

Four processes within the pharmacokinetic stage 1. Absorption ● Process of movement of drug particles to body fluids, mostly in the small intestine. ● Determines the onset of action for the drug ● Determines the intensity of drug action - 0-100% absorption (oral meds cannot be 100%) - Higher absorption=greater effect ● Enteric coating: protects against acid in stomach, allows absorption in small intestine (no absorption in stomach) ● Extended release formula: absorption over long period ● Absorption of drugs - Diffusion

- Facilitated diffusion - Active absorption - Pinocytosis ● Other effects on absorption ● Blood flow, pain, stress (slow gastric emptying time), Exercise (shunts blood flow to muscles, decreased blood flow to GI tract), hunger, pH 2. Distribution ● Those areas with highest blood flow have the highest exposure to absorbed drugs ● Lipid solubility increases distribution; tissue storages decreases distribution with increased affinity; drug protein complexes Solubility o Only unbound or free drugs, can reach target cells; bound drugs do not have an effect; the higher the protein binding the less the effect of the drug o Drugs can have different binding effects - Highly protein bound: (>89% of drug is bound); 11% is causing an effect - Moderately protein bound:(30-60% of drug is bound) - Low protein bound: ( increase in cardiac output - Sympathetic stimulation of the heart goes down - Increase the force of contraction - Improves symptoms, does not improve mortality - Stabilizes cardiac conduction issues (negative dromotropic) - Digitalization: taper dose up to decrease HF symptoms - Need to give loading dose in order to get a minimum effective concentration - Side effects: bradycardia (negative chronotropic) **hold at 60 bpm, cardiac dysrhythmias (PVCs abnormal beat in the ventricles), anorexia, N/V/D, headache, blurred vision, “yellow vision” - Toxicity effects: same as side effects and premature ventricular contractions - Need to watch levels closely - Antidote - Digi bind: binds and inactivates Digoxin - Interactions: Diuretics (related to hypokalemia), Cortisone (related to sodium retention), Antacids (decrease the absorption of Digoxin) - Nurse Responsibilities: - Take apical pulse 1 minute before admin (withhold if below parameters) - Monitor labs, monitor for toxicity, and monitor I&O ACE Inhibitors ARBs (angiotensin receptor blockers) Diuretics - Reduce blood volume, lower BP, reduce workload, increase CO - Used only for fluid overload (loop diuretics are best with thiazide added) Phosphodiesterase Inhibitor: Primicor (other positive inotropic agents) - Action: inhibits Phosphodiesterase III in cardiac and vascular smooth muscle. Rise in cAMP increases intracellular calcium, resulting in greater contractility -

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Increases contractility, decreased pulmonary vascular resistance Vasodilator, so afterload is decreased and increased effectiveness of the contraction - Contractions/precautions: valvular heart disease, preexisting dysrhythmias, hypovolemia, electrolyte imbalances, renal impairment - Cascade: related to increased calcium reflux=increased contractility - Multiple toxicities with other drugs - Additive cardiac effects with inotropic drugs - Additive hypotension with antihypertensive drugs - For patients with HF who do not respond to ACE inhibitors, digoxin, or others. - Made for resistant HF (HF we cannot get a hold of) - Spironolactone (Aldactone) - Aldosterone antagonist (not a diuretic) - Prevents cardiac remodeling - Beta Adrenergic Antagonists - Blocks the catecholamines, slows HR, reduces contractility - prevents tachydysrhythmias, prevents MI damage - May produce remodeling of the heart - May worsen failure, taper dose up Antihypertensives - Regulators of BP - kidneys via RAAS - Baroreceptors in the aorta and carotid (feel the pressure and the need for pressure change) - Vasomotor center in the medulla - Hormones: ADH, ANP, BNP - Physiologic Risk Factors - Excess saturated fat and simple carbs, alcohol increases renin secretions, obesity increase CO, SV, and left ventricular filling - Race factors - African Americans have lower renin levels - Asian Americans tend to be more responsive to drugs - Native Americans are less responsive to beta blockers - Older adults have a higher baseline BP -

Category

Systolic pressure

Diastolic pressure

Normal

Less than 120

Less than 80

prehypertension

120-139

80-80

Stage 1 HTN

140-159

90-99

Stage 2 HTN -

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Greater than 160

Greater than 100

Antihypertensive drugs - Diuretics - Thiazides - Loop diuretics - Combo of thiazide with K-sparing diuretics - Combine K-sparing with K-wasting to even out potassium - Combo of thiazide with other antihypertensive (ACE inhibitors, beta blockers, ARBs) Sympatholytic - Slows down BP by stopping sympathetic system - Beta-adrenergic blockers - Nonselective - Inhibit beta1 and beta2 receptors - Propranolol - Cardio selective - Block beta1 receptors - Metoprolol (prototype) - SE: hypotension, dizziness, fatigue, insomnia, nightmares, depression, sexual dysfunction, decrease BP, decreased HR, bronchoconstriction (if possibly non-selective) - Centrally acting alpha2 agonists - Action: stimulate alpha2 receptors, decrease CO, decrease epinephrine, norepinephrine, and renin release - Contradictions: impaired liver function - SE: Na and water retention, dry mouth, bradycardia - Rebound HTN is stopped abruptly - Alpha-adrenergic blockers - Action: block the alpha-adrenergic receptors results in vasodilation and decreased blood pressure - SE: ortho hypotension, headache, dizziness, drowsiness, nausea. Nasal congestion, edema, weight gain - Adrenergic neuron blockers - Action: block norepinephrine release from the sympathetic nerve endings, decrease in norepinephrine release, results in a lower BP - SE: ortho hypotension, tachycardia, dizziness, drowsiness, headache, nasal congestion, edema, weight gain - Alpha1- adrenergic blockers - Action: blocks alpha1 receptors - SE: hypotension, bradycardia

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Direct acting arteriolar vasodilators - Action: relax smooth muscles of blood vessels, especially causing vasodilation - SE: tachycardia, palpitations, edema, headache, dizziness, nasal congestion, GI bleeding, lupus like symptoms - ACE inhibitors - Action: inhibits formation of angiotensin II, interrupts cascade - SE: Nonproductive cough, fatigue, insomnia, N/V/D, hyperkalemia, dizziness, tachycardia, hypotension, angioedema - African American adults and older adults do not respond to ACEI monotherapy - Contradictions: pregnancy, k-sparing diuretics, salt substitutes - Angiotensin II receptor Blockers (ARBs) - Action: prevent release of aldosterone, act on RAAS, block angiotensin II from angiotensin I receptors - SE: dizziness, hypotension, headache, hyperkalemia, hyperglycemia, GI distress, diarrhea, pyrosis - Direct Renin Inhibitor - Action: bind with renin causing a reduction of angiotensin I, angiotensin II, and aldosterone levels - Decreases BP - SE: Hypotension, peripheral edema, hyperkalemia, diarrhea, renal failure, Steven-Johnson Syndrome - Calcium Channel Blockers - Action: slow calcium channels in myocardium and vascular smooth muscle cells promoting vasodilation - SE/AE: flushing, headache, dizziness, peripheral edema, fatigue, GI distress, constipation, bradycardia, hypotension, palpitations Pharmacotherapy of Hyperlipidemia - Lipids - Triglycerides, phospholipids, steroids (cholesterol) - Lipoproteins - HDLs high density lipoproteins (good cholesterol) >45 - LDLs low density lipoproteins (bad cholesterol) causes ischemia - Pharmacologic treatment - Statins (most effective) - Blood lipid profiles Drugs for Dyslipidemia Statins - Can reduce LDL levels by 20-40% - Also, lower triglycerides and VLDL levels - Can raise HDL levels - More commonly used - Action: inhibits HMG CoA reductase which manufactures cholesterol - Basically makes cholesterol not form - SE: Headache, abdominal cramping, diarrhea, muscle/joint pain, heartburn - Serious SE: Rhabdomyolysis (breakdown of muscle fibers) Bile Acid Sequestrants - Complex formed with bile acid and the drug - Binds with bile acids to inhibit cholesterol formation - Interacts with Warfarin - Has to be separately given an hour after other drugs are given - More adverse events than other statins - GI problems are the most concerning - Can have an increase in triglycerides Niacin (Nicotinic Acid) - Action: decrease production of VLDL, lower serum triglycerides levels, also lowers LDL levels because it synthesis the same way as VLDLs - SE: warmth, flushing, itching, numbness, tingling, hypotension, dizziness, headache, cough

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- Can give aspirin to mediate the flushing - Cannot be used with diabetes patient because it can increase glucose levels Fibric Acid - Action: activates enzymes which increase breakdown of triglycerides - AE: GI problems - Take with food - Example: Gemfibrozil - Highly protein bound - Peripheral Vasodilators - Used in PVD - Causes increased ability for blood flow - Action: vasodilator - Increases O2 in blood - Treat pain with activity - intermittent claudication - Ischemia = pain

Renal and Urologic Drugs Urinary antiseptics/anti-infectives and antibiotics - Limited to the treatment of UTIs. - Action: occurs in the renal tubule and bladder - As bactericidal agents, they risk potential superinfections. - Fluoroquinolones - SE: tendon rupture, peripheral neuropathy, CNS effects, and exacerbation of myasthenia gravis, headaches, photosensitivity, dizziness, N/V/D, visual impairment, rash, and pruritus. Urinary analgesics - Used to relieve pain, burning, frequency, and urgency. - SE: GI disturbances, abd cramps, hemolytic anemia, and renal and hepatic dysfunction - Urine become harmless red/orange - Monitor blood glucose carefully Urinary Stimulants - When bladder function is lost by 1. A neurogenic bladder (a dysfunction caused by a lesion of the nervous system) or 2. A spinal cord injury or 3. A severe head injury, a parasympathomimetic may be used to stimulate micturition (urination). - Direct-acting parasympathomimetic - Action: increase bladder tone by increasing tone of the detrusor urinal muscle, which produces a contraction strong enough to stimulate urination Urinary antispasmodics/antimuscarinics/anticholinergics - Spasms result from infection or injury can be relieved by antispasmodics that have direct action of the smooth muscles or the urinary tract

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- Contraindicated for those with a GI obstruction or glaucoma Antimuscarinics - Have the same effect as antispasmodics - Action: block parasympathetic nerve impulses, parasympatholytics, and anticholinergics - Use: to control overactive bladder, decrease urgency and urinary incontinence - SE: blurred vision, headache, dizziness, dry mouth, constipation and tachycardia - Patient's should report urinary retention, severe dizziness, blurred vision, palpitations, and confusion.

Respiratory Drugs Allergic rhinitis vs. Acute rhinitis - Allergic rhinitis is the inflammation of nasal mucosa, throat, and airways related to allergens - S/S: tearing, burning, red, swollen, itchy eyes, sneezing, nasal itching, congestion, post nasal drip, cough, scratchy throat, chronic loss of taste/smell, sinusitis, hoarseness, plugged ears Pharm - Antihistamines - H1 blockers, Histamine1 Antagonists - Action: block H1 receptors to decrease nasopharyngeal secretion - H1 receptor stimulation causes the constriction of extravascular smooth muscle - First Generation Antihistamines (Benadryl) - SE: drowsiness, dry mouth, decreased secretions (anticholinergic effects) - Second Generation Antihistamines (fewer side effects) - Fewer anticholinergic effects, less drowsiness, longer half life - Ex. Claritin - Nasal Decongestants - Sympathomimetics stimulate alpha and beta receptors - Vasoconstriction in capillaries which leads to decreased swelling - Issues: can cause tolerance and rebound congestion - Only used 3-5 days - Anticholinergic effect (parasympathetic but acts sympathetic): drying of mucous membranes - Systemic Decongestants (Ex. Sudafed) - Alpha-adrenergic agonists - Used for allergic rhinitis - Slower effect, but generally a longer response than nasal decongestants - More SE than nasal decongestants: can increase BP, and HR - Interactions: beta blockers (can cancel each other out), MAOIs

Intranasal Glucocorticoids (Ex. Flonase) - Treats allergic rhinitis - Anti-inflammatory actions - Decrease in sneezing and coughing - Can increase blood sugar and should caution with diabetes - Antitussives - Act on cough control center in the medulla, Use it to get some sleep - Suppresses cough reflex - Problems: you want to cough out junk, if not it can cause pneumonia; a cough is there for a reason - Types: OTC, narcotic (codeine), and non-narcotic - Expectorants (Robitussin) - Loosen bronchial secretions to be coughed out - Mucolytics - Loosen thick, viscous bronchial secretions - Breaks down the chemical structure of mucous molecules - The mucous become thin, and can be removed out by coughing Sinusitis - Inflammation of the mucous membranes of the sinuses Acute Pharyngitis - Sore throat caused by virus, bacteria - S/S: sore throat, pain, fever, cough Lower Respiratory Tract - Respiration: gases exchange - Ventilation: moving air in and out of lungs (controlled by size and diameter of airways - Pulmonary Perfusion: blood flow through the lungs (alveoli inflate during inspiration) - Capillaries with thin membrane, gases move to/from the blood - Bronchoconstriction - Increase airway resistance = less air flow - Bronchodilation - Allows air to enter alveoli more easily = more O2 to tissues - Sympathetic = smooth muscle relaxation = bronchodilation - Bronchospasm - Sudden contraction of smooth muscles surrounding airway= acute dyspnea - Asthma - Chronic, inflammatory or obstructive - Mast cell lining bronchial passageways release mediators of immune and inflammation - Histamine, leukotrienes, prostaglandins, interleukins - Increased airway edema and secretions which narrows/o...