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chapter 7 onward
for final
| Question | Answer |
|---|---|
| allergic rhinitis | inflammatory disorder of the upper airway; triggered by airborne allergens; IgE Abs bind to mast cells --> release inflammatory mediators |
| season/hay fever | outdoor; fungi and pollen from weeds, grass trees |
| persistent (perennial/nonseasonal) | indoor; dust mites, pet dander, mold, roaches |
| histamine (H1) | a chemical mediator released during allergic reactions; released by mast cells |
| physiological effects of histamine | vasodilation, increased capillary permeability, bronchoconstiction, itching and pain, mucus secretion, sleep/wake cycle |
| glucocorticoids (intranasal) | prevent inflammatory response; more effective than antihistamines |
| antihistamines (oral, intranasal, opthalmic) | blocks H1 receptors, first and second generation, sedation and anticholinergic effects (FG>SG) |
| cromolyn (intranasal) | suppresses mast cells |
| sympathomimetics/"decongestants" (PO, intranasal) | alpha-1 agonist to reduce nasal congestion = vasoconstriction; PO may cause restlessness; cardiovascular effects and stroke more likely with PO |
| anticholinergics (intranasal) | block nasal muscarinic receptors; inhibits secretions from serous/seromucous glands |
| anti-leukotrienes (PO) | block LT receptor for congestion relief |
| oral antihistamines | for allergic rhinitis and mild allergies; CNS effects vary; dry effects from blocking muscarinic receptors (anti-SLUD, anti-parasympathetic rest and digest response); most effective if taken prophylactically |
| first generation (FG) | sedating; bind strongly to H1 receptors; crosses BBB; stronger anti-itch effect |
| second generation (SG) | non-sedating |
| intranasal glucocorticoids | first choice for rhinitis; works best when taken daily; may take 7 days for max effect for seasonal and 2-3 weeks for perennial; nasal decongestant should be used before if needed |
| intranasal cromolyn | reduces symptoms by suppressing release of H1 and other inflammatory mediators from mast cells; response may take 1-2 weeks |
| intranasal ipratropium | cholinergic blockade lowers nasal secretions from nasal mucosa |
| montelukast | leukotriene antagonist; can rarely have neuropsychiatric ADEs |
| opioid antitussives | act upon CNS to suppress cough; schedule V; can be abused and cause respiratory depression |
| codeine | member of opioid family, most effective cough suppressant; doses are 1/10 those used for analgesia; alone is schedule II |
| promethazine/codeine | antihistamine + opioid cough suppressant |
| guaifenesin/codeien | expectorant + opioid cough suppressant |
| non-opioid antitussives | dextromethorphan and benzonatate |
| dextromethorphan | most effective non-opioid cough suppressant; acts in CNS; OTC; abuse potential; not to be combined w/ opioids |
| benzonatate | Rx only; suppresses cough by decreasing sensitivity of stretch receptors in respiratory tract; can inhibit chewing and sucking |
| expectorants & mucolytics | stimulate flow of respiratory tract secretions; increasing productive cough; ex: mucinex, acetylcysteine and hypertonic saline |
| combination preparations | not cured with antibiotics, vitamin C, zinc; combo meds should be reserved for pts w/ multiple sx and should contain appropriate agents |
| OTC cold remedies | combo should contain two or more of: nasal decongestant, antitussive, analgesic, antihistamine, caffeine |
| pediatric OTC cold remedies | use w/ caution; avoid if younger than 4 to 6 yo |
| osmosis | movement of water across a semi-permeable cell membrane toward a high solute concentration; there must be an unequal concentration of a solute and the membrane must be more permeable to water than to solutes |
| diffusion | occurs w/ osmosis unless pores of membrane are too small |
| filtration | passage of a fluid such as water, through a cell or blood vessel membrane because of hydrostatic pressure differences on both sides of the membrane |
| when pressure gradient exists | water moves down through the membrane until the hydrostatic pressure is the same on both sides of the membrane |
| maintenance of extracellular and intracellular fluids | solutes; solvent; osmolarity - solute concentration in a liter; tonicity - concentration of IV fluids |
| fluid compartments & distribution | intracellular fluid - within the cells, comprises about 2/3 of TBW; extracellular fluid - outside the cells, comprises about 1/2 of TBW, includes interstitial fluid, intravascular fluid, and transcellular fluid (1% of body fluids) |
| total body water (TBW) | 60% of body weight in adults (40% intracellular, 20% extracellular (15% ISF, 5% intravascular, 1-2 L transcellular) |
| pediatric fluid distribution | TBW is 75-80% body weight |
| fluid distribution in aging | decreased percent of TBW (about 40%) |
| capillary hydrostatic pressure | pushes water out of capillaries into interstitial space at the arteriolar end |
| capillary osmotic/oncotic pressure | pulls water into capillaries from interstitial space at the venous end from plasma proteins |
| interstitial hydrostatic pressure | water movement from the interstitial space to capillary |
| interstitial osmotic pressure | attracts water from capillary to interstitial space |
| edema | accumulation of fluid within interstitial spaces, resulting from shift of fluid from intravascular fluid or lymphatic vessels to tissue |
| causes of edema | increased is capillary hydrostatic pressure, decreased in plasma oncotic pressure, increase in capillary permeability, lymph channel obstruction (lymphedema) |
| pitting edema | indentation |
| localized edema | single body region |
| effusion edema | fluid accumulation in body cavity r space |
| generalized edema | uniform throughout body within interstitial spaces; severe is called anasarca |
| dependent edema | gravity dependent areas |
| third space edema | a region where fluid acuumulates |
| most susceptible to fluid imbalances | obese people, women, pediatrics, elderly, comatose people, pts on diuretics, those with systemic conditions, post-surgery |
| antidiuretic hormone (ADH) secretion | responds to dehydration, vomiting, diarrhea, excessive seating; increases water reabsorption from kidney into the plasma; produced in posterior pituitary; secreted when plasma osmolality increases, decrease in BP, circulating blood volume decreases |
| thirst perception | hypothalamic osmoreceptors stimulated by increased osmolality because ECF is hypertonic; comatose patients at big risk as thirst reflex can't respond |
| assessment of alteration in Na+, Cl-, and water balance | weight, skin turgor, urinary output, mucus membranes, vital signs, breath sounds, labs (BUN/creatinine ratio), cap refill |
| fluid volume deficit (FVD)/hypovolemia | may occur alone but most often in combination with electrolyte imbalances; reduction in circulating blood volume, leading to a decreased perfusion of organs and tissues; primarily extracellular compartment affected |
| causes of FVD | loss of GI fluids, polyuria, diabetes insipidus, fever and sweating, anorexia |
| FVD manifestations | weight loss, orthostatic hypotension, decreased cap refill, decreased skin turgor, weak pulses, thirst, dry mucus membranes, longitudinal tongue furrows, decreased urine output, high BUN and Hct, high urine specific gravity |
| tx of FVD | oral rehydration w/ electrolytes and glucose, isotnic IV fluid to re-expand plasma and increased BP, hypotonic 1/2 NS to provide free water and lytes to make urine |
| hypertonic | causes fluid to shift out of cells; more solutes and less solvent |
| isotonic | causes no fluid shift; same concentration of solutes and solvent |
| hypotonic | causes fluid to shift into cells and interstitial compartments; fewer solutes and more solvent |
| hypovolemic shock | life-threatening when compensation is overwhelmed by continued intravascular volume loss; brief initial rise in BP, liver and spleen add volume by letting out RBCs and plasma; improper compensation can lead to decreased perfusion to tissues and organs |
| tx of hypovolemic shock | rapid fluid replacement, blood products, oxygen |
| fluid volume excess (FVE)/hypervolemia | abnormal retention of Na and H2O in same proportions |
| causes of FVE | HF, renal failure, cirrhosis, over-admin of isotonic fluids |
| FVE s/sx | hypertension, bounding pulse, jugular venous distension, dyspnea, orthopnea, lung crackles, edema, irritability, weight gain |
| tx of FVE | loop and thiazide diuretics, dialysis, monitor daily weight and edema, assess resp status, sodium-restricted diets, monitor for electrolyte losses and metabolic alkalosis from diuretics |
| isotonic IV fluid - 0.9% normal saline (NS) | no shrinking or swelling of cells; used to increase circulating volume; used in hypovolemia and dehydration; watch for fluid overload and hypokalemia/hypernatremia; maintains sodium levels without causing additional fluid shifts |
| isotonic IV fluid - lactated ringer's (LR) | liver converts lactate to bicarbonate; pts w/ liver disease cannot metabolize lactate well; not good for alkalosis |
| isotonic IV fluid - dextrose 5% in water (D5W) | can be used for fluid loss and dehydration to provide free water or hypernatremia; starts as isotonic then changes to hypotonic when dextrose is metabolized; should not be used for fluid resuscitation since it can cause brain swelling |
| hypotonic IV fluid - 1/2 (0.45%) NS | cells swell in hypotonic solution; used to treat intracellular dehydration and hypernatremia and to provide fluid for renal excretion of solutes; water is pulled from intravascular space to the cell; can cause water intoxication |
| hypertonic IV fluid - 3% NS, D5 1/2 NS, D5 0.9% NS | cells shrink in hypertonic solution; shift fluid from cells and interstitial spaces into intravascular space; used for hypotonic dehydration; not to be used w/ HF or renal failure |
| major electrolytes | sodium, potassium, magnesium, calcium |
| cations | positively charged electrolytes |
| anions | negatively charged electrolytes |
| electrolyte roles | acid-base and fluid balance, nutritional function, regulatory function, fluid balance |
| sodium (Na) | normal range 135-145 mEq/L; most significant and abundant ECF cation and prevalent electrolyte of extracellular fluid; main source is dietary intake; excretion by kidneys and GI tract; chloride and H2) follow Na |
| hypertonic alterations | increased osmolality in ECF; caused by hypernatremia or water deficit in ECF; water shifts out of cells into intravascular space; tx is hypotonic fluids |
| dehydration s/sx | hypernatremia, thirst, weakness, agitation, headache, oliguria, hard stool, poor skin turgor, dry and sticky mucous membranes, elevated temp, sunken fontanels in infants, weak pulse, low BP |
| hypernatremia | serum sodium > 145 mEq/L; brain cells shrink as fluid shifts out of cells to dilute blood and equalize concentrations; hypertonicity |
| causes of hypernatremia | water deprivation, hypertonic tube feedings w/o H2O supplements, extensive burns, watery diarrhea, lack of ADH, heatstroke |
| hypernatremia s/sx | dry sticky mucous membranes, lethargy, convulsions, seizures, flushed skin, low-grade fever |
| evaluation of hypernatremia | serum sodium > 145 mEq/L, urine specific gravity high > 1.030, high serum osmolality |
| tx of hypernatremia | oral water or hypotonic fluids (0.45% NS safest), replace fluids slowly to prevent cerebral edema |
| hypotonic alterations | decreased osmolality in ECF; caused by hyponatremia; loss of sodium exceeds loss of water; intracellular overhydration; ADH release suppressed |
| tx of hypotonic alterations | mild: infusing isotonic sodium chloride (o.9% NS), fluid restrictions; severe: hypertonic solution (3%) NaCl, cautious replacement |
| hyponatremia | serum sodium level < 135 mEq/L; related to sodium loss or water gain; triggers released of aldosterone to increase renal reabsorption; can signal an underlying disease; can cause neuro damage |
| causes of hyponatremia | inadequate Na+ intake, excessive/rapid plasma dilution by admin of hypotonic IV fluid, increased Na+ loss, diuretic use or HF, syndrome of inappropriate antidiuretic hormone (SIADH), Na movement intracellularly as in K+ deficiency, H2O intoxication |
| hyponatremia x/sx | primarily neurologic; nausea, malaise, abdominal cramps, headache, lethargy, coma, seizures |
| SALTLOSS | stupor/coma, anorexia, lethargy, tendon reflexes, limp muscles, orthostatic hypotension, seizures/headaches, stomach cramping |
| evaluation of hyponatremia | serum sodium < 135 mEq/L, low serum osmolality, low urine Na+ as kidneys attempt to retain Na+, urine specific gravity low < 1.010 |
| tx of hyponatremia | small amounts of IV hypertonic solution (3% NS) if neuro s/sx severe or Na < 110 mEq/L, salt tablets, fluid restrictions, neuro assessments, seizure precautions |
| potassium | major intracellular cation; 98% is intracellular; 3.5 - 5 mEq/L; most excreted by kidneys, some in sweat and bowel; must be replaced daily; concentration maintained by Na+/K+ ATPase pump |
| alterations in potassium levels | changes in pH affects K+ balance; kidney is most efficient regulator to excrete K+; insulin facilitate insulin into the cells; diuretics cause hypokalemia; ace-I, BBs cause hyperkalemia |
| potassium's role in acid-base balance: normal conditions | K+ content in the ICF is much greater than the ECF; H+ is low in both the ICF and ECF |
| potassium's role in acid-base balance: acidosis | H+ content increases in the ECF and H+ moves into the ICF; to keep the ICF neutral, an equal number of K+ ions leave the cell = hyperkalemia |
| potassium's role in acid-base balance: alkalosis | more H+ ions are present in ICF than ECF, therefore H+ ions moves from ICF to ECF; to keep ICF neutral K+ moves from ECF into ICF = hypokalemia |
| hyperkalemia | potassium level > 5 mEq/L; seldom occurs in pts with normal kidney function; cardiac arrest occurs more often with hypokalemia |
| causes of hyperkalemia | decreased renal excretion, hypoaldosteronism, drugs, high Ka+ intake, starvation, insulin deficiency |
| hyperkalemia s/sx | peaked T waves, widened QRS, disappearance of P waves leading to cardiac arrest, hypo tension, bradycardia; muscle weakness of lower exts, n/v/d, abdominal cramping, oliguria, kidney damage |
| evaluation of hyperkalemia | serum K+ level > 5 mEq/L; decreased arterial pH/acidosis; abnormal ECG |
| tx of hyperkalemia | treat underlying cause, stop contributing drugs, restrict dietary intake |
| hypokalemia | potassium level < 3.5 mEq/L |
| causes of hypokalemia | most commonly due to vomiting and GI suction, diarrhea, laxative abuse; hyperaldosteronism |
| hypokalemia s/sx | mild causes no symptoms; dysthymias, cardiac arrest, weak irregular pulse, EKG changes, leg cramps, muscle weakness in lower exts, resp arrest, paresthesias, n/v, decreased motility, paralytic ileus, decreased bowel sounds, inability to concentrate urine |
| tx of hypokalemia | prevent those at risk, fix underlying cause, eat K+ rich food, salt substitutes, KCl supplements, IV replacement 10-20 mEq/h NO IV PUSH, replace and treat acid-base |
| calcium | 99% in the bone, remainder in plasma and body cells; positively charged cation found in ECF and ICF; normal value 8.8 to 10.5 mg/dl; major role in nerve impulses |
| hypercalcemia | serum concentration > 10 - 12 mg/dl |
| causes of hypercalcemia | hyperparathyroidism, cancer, immobility, acidosis, drugs |
| hypercalcemia s/sx | muscle weakness, hyporeflexia, decreased muscle tone from excess sedative effect, fatigue, decreased or hypoactive DTRs, confusion, behavioral changes |
| tx of hypercalcemia | high fluid intake, fluid replacement with NS, loop diuretics, calcitonin, hemodialysis |
| causes of hypocalcemia | inadequate intake/vitamin D, parathyroidectomy, hyperphosphatemia, renal failure, hypomagnesemia, malabsorption syndrome, acute pancreatitis, loop diuretics, low serum albumin, alkalosis, massive blood transfusions |
| hypocalcemia s/sx | tetany, circumoral tingling of hands and feet, muscle spasms, Trousseau's sign, Chvostek's sign, confusion, anxiety, depression, psychosis, irritability, hyperactive DTRs, dysrhythmias, EKG changes |
| tx of hypocalcemia | seizure precautions, airway patency, confusion precutions, high calcium idet education, IV calcium, magnesium replacement, vit D supplement, oral calcium supplement |
| magnesium | intracellular cation, mostly stored in bone and muscle; normal range 1.8 - 3.0 mEq/L; main source is dietary intake; excreted through kidneys |
| hypermagnesium | serum concentration > 3.0 mEq/L |
| causes of hypermagnesemia | renal insufficiency, excessive intake of magnesium-containing antacids, IV Mg therapy |
| hypermagnesemia s/sx | skeletal smooth muscle contraction, loss of deep tendon reflexes, weak resp muscles, n/v, excess nerve function, hypotension |
| tx of hypermagnesemia | increased fluids, calcium gluconate, hemodialysis, avoid meds with Mg in renal failure, mechanical ventilation |
| hypomagnesemia | serum Mg concentration < 1.5 mEq/L |
| causes of hypomagnesemia | malnutrition, malabsorption syndrome, alcoholism, urinary losses, laxative abuse |
| hypomagnesemia s/sx | increased reflexes, tachycardia, hypotension, torsades de points, myocardial cells become more excitable, Chvostek's, Trousseau's |
| relationship between magnesium and calcium | calcium needed for muscle contraction, magnesium for muscle relaxation; magnesium converts vitamin D to its active form; vitamin D increases the body's ability to absorb calcium |
| relationship between magnesium and phosphorous | kidneys reabsorb more magnesium as they excrete more phosphorous, also raising levels of calcium |
| oncotic pressure | pulls fluid in |
| tuberculosis | infection by mycobacterium tuberculosis; highly contagious, acid-fast bacteria; airborne/droplets; can travel to lymph nodes, lungs, sprine; immune system traps TB bacteria in tubercle forms |
| latent TB | immunity usually develops within a few weeks; 90% w/ normal immune systems never develop clinical or radiologic evidence of TB; can harbor tubercle bacilli lifelong unless drugs given |
| primary infection of TB | bacilli enter lungs through inhalation; macrophage immune response activity |
| caseous necrosis | infected tissues and die within tubercle |
| dx of TB | persistent cough (often with sputum and/or blood), fever, night sweats, weight loss, fatigue |
| testing for TB | intradermal TB skin test: read 48-72 hours after injection quantiferon-TB gold blood test sputum and stain culture |
| tx of TB | thick layer of mycobacterium is resistant to drug penetration so treatment can take 6-9 months; minimum of 2 drugs, preferably 4, used; effective when no mycobacteria observed |
| causes of rx resistance with TB | some bacilli are inherently resistant or become resistant; usually to isoniazid and rifampin |
| tx regimens of TB: two phases | intensive phase: eliminate actively dividing tubercle bacilli and rapidly reduce the bacterial load; continuation phase: eliminate intracellular "persisters" and remaining bacteria and prevent relapse |
| isoniazid (INH) | standard tx for active TB and prophylaxis for latent TB |
| INH MOA | inhibit synthesis of mycolic acid in bacterial cell well; selective for TB |
| INH kinetics | widely distributed, crosses BBB; take w or w/o food; metabolized by liver; excreted in urine |
| INH ADEs | hepatotoxicity, peripheral neuropathy, CNS effects, GI distress |
| INH interactions | alcohol (since it is CYP450 inhibitor) |
| rifampin | most rx'd w/ INH; broad spectrum bactericidal antibiotic; active against gram+ and gram- |
| rifampin MOA | suppresses bacterial RNA synthesis and protein synthesis |
| rifampin kinetics | lipid soluble; selectively toxic to microbes |
| rifampin ADRs | hepatotoxicity, body fluid discoloration, GI effects, flu-like sx |
| rifampin interactions | CYP450 inducer of oral contraceptives, warfarin, HIV drugs (reduces effects of drugs) |
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