Sympathomimetic=producing physiological effects characteristic of the sympathetic
nervous system by promoting the stimulation of sympathetic nerves. Only relieve nasal
congestion.
1 What happens to the nose when the sympathetic nervous system is activated?
2 What happens to the nose when the parapsympathetic nervous system is activated?
3 why do the above 2 considerations matter?
4 why is nasal mucosa important?
5 what is the fundamental pathophysiology responsible for allergic rhinitis?
6 what causes the sneezing, itchy nose, and watery eyes?
7 what are the 2 categories of drugs used to tx allergic rhinitis?
8 what are the 2 therapeutic goals of tx allergic rhinitis? How are these goals met?
9 what is histamine?
10 which receptors are responsible for allergic symptoms?
11 what drugs are often combined with antihistamines?
12 how do intranasal corticosteroids work?
13 do intranasal corticosteroids have immediate benefits?
14 how does a mast cell stabilizer work?
15 example of a mast cell stabilizer?
16 additional alternative to intranasal corticosterpods in tx allergies?
17 what is the role of the decongestant? What is its most limiting side effect?
18 what is the prototype nasal decongestant?
19 why is there such a minimal potential for dependence with opoid-based antitussives?
20 most frequently used non-opiod antitussive for cough?
21 how does antitussive benzonatate (Tessalon) work?
22 what is the difference btw an expectorant and a mucolytic?
23 what is the most common mucolytic? Route? Best indicated for?
24 ventilation vs perfussion?
25 how does the ANS regulate the bronchioles?
26 what are drugs that stimulate beta2adrenergic receptors called?
27 How much of a drug actually reaches the LRT under optimal conditions? Precaution?
28 what contributes to airway obstruction in asthma?
29 what is status asthmaticus?
30 who are anticholinergics indicated for? How do they work?
31 most common SABA?
32 when are methylxanthines used?
33 aside from reducing inflammation, what else do corticosteroids do for the airways?
34 what is a corticosteroid?
35 how do leukotriene modifiers work? who appropriate for?
36 what are mast cell stablizers?
37 what happens with COPD?
38 what is emphysema?
39 why are diuretics given?
40 why do meds require significant dosage reduction in pt w/ mod/signif renal failure?
41 Most common mechanism by which diuretics work?
42 what are the 3 major groups of diuretics?
43 what do kidneys regulate? What do kidneys secrete?
44 why are 2+ drugs combined to tx HTN and fluid retention disorders? Decrease adverse
effects and enhance pharmacological effects.
45 which group is the most effective diuretic? What used for? Prototype?
46 what is the most commonly px loop diuretic? Benefit? Side effects? How do you care for pt
taking?
47 what is the most px diuretic overall? Indications? Prototype? Side effects?
48 what compounds are reabsorbed from filtrate? Secreted?
49 most serious adverse effect of thiazide and loop diuretics?
50 how strong of diuresis are protein-sparing diuretics? Why?
51 prototype potassium-sparing diuretic?
52 pt education loop diuretics?
53 pt education thiazide?
54 what are the 3 factors responsible for BP? Blood volume, peripheral resistance, cardiac
resistance .
55 what structure regulates blood pressure?
56 what factors influence BP?
57 primary vs secondary HTN?
58 what are the drugs in 1st line hypertension classes? 2nd line?
59 name the prototypes for the following drugs: ACE inhibitor; CCB; adrenergic antagonist;
direct vasodilators
60 what is the risk of using spironolactone and ACE inhibitors at the same time?
61 adverse effect of ACE inhibitors?
62 how does angiotensin II increase BP?
63 what do ACE inibitors end in? protype?
64 what do angiotensin II receptor blockers (ARBs) end in? how do they work?
65 what type of HTN med blocks receptors in kidney for aldosterone? Prototype?
66 which HTN drug works particularly well for A-A? how does this class work? Prototype? 2
Types?
67 what do CCBs end in?
68 how do beta-blockers work? Prototype? Why impt? What end in? What major side effect?
69 how do alpha1-adrenergic blockers work? Ending? Prototype?
70 how do alpha2-adrenergic agonists work?
71 how do direct vasodilators work? Why not used often? Prototype? Contraindicated?
72 what is the one recommended direct vasodilator? Why?
1 the arterioles in the nose constrict. The thickness of the mucosal layer is decreased. As a
result, the airway is widened and more air flows in. (fight or flight. More air to help you fight!)
2 the arterioles dialate. More mucus produced.
3 drug therapy considerations. Sympathomeimetics shrink nasal mucosa, relieving nasal
stuffiness of a cold.
4 first line defence. Fluid has ++ immunoglobins that neutralize airborne pathogens. Has
defense cells that engulf microbes. Mast cells line the mucosa.
5 the inflammation of of the mucous membranes in the nose, throat and airways
6 the release of histamine and other inflammatory mediators mast cells and basophils that line
the nasal mucosa. Can be immediate or delayed (4-8 hrs=conitual inflammation-chronic nasal
congestion)
7 preventers and relievers. Preventers=antihistamines, intranasal corticosteroids, and mast cell
stabilizers. Relievers=oral and nasal decongestants (simpatomimetics)
8 to (1) prevent its occurrence and to (2) relieve symptoms. Use preventers (antihistamines,
intranasal cortitcosteroids and mast cell stabilizers) and relievers (oral and intranasal
decongestants)
9 a chemical mediator of inflammation that is responsible for many of ar symptoms. Histamine
reaches receptors to cause trad’l symptom along with bronchoconstriction in severe cases.
10 H1 receptors
11 decongestants and analgesics
12 decrease secretion of inflammatory mediators (histamine), reduce tissue edema, and cause
mild vasoconstriction
13 no. they take 1-3 weeks for peak response.
14 inhibits release of histamine from mast cells
15 intranasal cromolyn. NassalCrom
16 montelukast (Singulair) and ipratropium (Atrovent).
17 sympathommimetics. To reduce nasal congestion. Rebound congestion=hypersecretion of
mucus and worsening nasal congestion. So use these no longer than 3-5 days.
18 oxymetazoline (Afrin 12 hr)
19 bc there is sol little does needed to suppress cough reflex. Reseserved for serious cough
conditions, Schedule 3, 4, or 5.
20 dextromethorphan (Delsym, Robitussin)
21 it anesthetizes the stretch receptors in the lungs .
22 expectorants create extra mucous to thin viscous secretions; mucolytics chemically dissolve
mucus
23 acetylcysteine (mucomyst). Inhalation. Patients with diseases that create++mucus. Like
cystic fibrosis. Sometimes IV
24 vent=air in and out of lungs. Perfusion=blood flow thru lungs
25 sympathetic activates beta2-andrenergic receptors-bronchiolar smooth muscle to relax,
airway diameter to increase and bronchodilation to occur. Parasympathetic activates
bronchoconstriction.
26 bronchodilators. Used first, THEN corticosteroids
27 10-50%. Rinse mouth to reduce potential for absorption.
28 bronchospasms and inflammation (infl contributes the mucus from histamine response)
29 severe, prolonged asthma that doesn’t respond to drugs. Can lead to respiratory failure.
30 people with pulmonary disease and/or chronic asthma. These block parasympathetic NS.
Work best in combination with beta antagonist
31 albuterol. Last only 2-6hrs. rescue drug.
32 when long-term oral preventative asthma meds don’t work (beta-agonists or inhaled
corticosteroids)
33 sensitize bronchial smooth muscle to be more responsive to beta-agonist stimulation.
Reduce bronchial hyper-responsiveness
34 the most potent natural anti-inflammatory substance known
35 they block leukotriene receptors (Singulair). Leukotrienes are inflammatory mediators like
mast cells. Don’t use for people with liver conditions.
36 reduce inflammation by inhibiting mast cells from releasing histamine. Preventer. Less
effective at prevention than inhaled corticosteroids. Takes several weeks for max effectiveness.
37 chronic bronchitis develops=excess mucus in LRT from smoking/irritation. This
obstructioncoughing and dyspnea. Often have comorbid cardiovascular conditions.
38 =terminal stage of copd. Bronchioles lose all elasticity; alveoli expand to max size for more
air—extreme dyspnea.
39 increase urine output to reverse abnormal fluid retention in body. HTN, heart/kidney/liver
failure,
40 bc kidneys excrete most drugs (or their metabolites). An avg dose can kill someone in severe
renal failure, pulmonary edema
41 blocking sodium reabsorption in nephron=more Na+ to urine (water follows)
42 loop, thiazides, potassium sparing
43 Regulate: Fluid volume, electrolytes, acid-base balance. Secrete: renin to regulate BP
production, erythropoietin to stimulate RBC production, and calcitrol (vit D)
44 Decrease adverse effects and enhance pharmacological effects.
45 Loop/high-ceiling. Used to reduce edema assoctd w/ heart failure. Get lots of water out of
body very quickly.
46 Furosemide (Lasix). Mod/severe fluid retention. Increase urine output even when blood flow
to kidneys is diminished. Dehydration, electrolyte imbalances (K+-dysrhythmias, bad for px on
digoxin). Ototoxic (deafness) Get baselines and monitor. Lab values, weight, urine output.
Labs=electrolytes. Creatinine, BUN, uric acid, blood glucose
47 Thiazide. Mild/moderate HTN. Edema (mild/mod heart failure). Don’t help renal failure.
Hydrochlorothiazide. Same as loop—dehydration, e-lyte loss. *diabetes pt—glucose levels can
rise.
48 Reabsorbed: Water, glucose, amino acids, Na+, chloride, Ca+, bicarbonate, some drugs.
Secreted: K+, phosphate, hydrogen, ammonium ions, some drugs.
49 hypokalemia
50 mild diuresis bc in distal tubule. Used in combo w/ other diuretics to minimize K+ loss.
51 spironolactone. Block Na+ reabsorption AND Inhibit aldosterone (secreted by adrenal
cortex)increase water excretion while K+ levels stay high. Enhances excretion of Na and
retention of K. significantly reduces mortality in heart failure pt.
52 take in am. Orthostatic hypotension so get up slowly, ++ potassium, weigh daily
53 tell dr if pregnant (Cat D), if joint pain, increased chance lithium toxicity, use sunscreen, eat
potassium rich foods
54 don’t eat too much potassium. No salt substitutes. Use sunscreen; no mentally rigorous
activities until used to. CONTRAINDICATED FOR PREGNANT/LACTATING WOMEN. Risk of
toxicity if taking lithium or digoxin. Can decrease effectiveness of anticoagulants.
55 vasomotor center in medulla oblongata of brain.
56 emotional state, hormones (ADH=vasoconstrictor that raises blood volume thus BP. Aka
vasopressin). (RAAS)
57 primary(=idiopathic/essential) 90%, no specific cause. Secondary, caused by certain diseases
or meds. Goal=remove underlying condition causing HTN. Cure comorbidity=cure HTN.
58 1st line=ACE, ARBs, CCBs, thiazide diuretics. 2nd line=alpha2-adrenergic agonists, alpha1adrenergic blockers, beta-adrenergic blockers, centrally acting alpha and beta blockers, directacting vasodilators, direct renin inhibitors, peripherally acting adrenergic neuron blockers.
59 ACE inhibitor=enalapril; CCB=nifedipine; adrenergic antagonist=doxazosin; direct
vasodilators=hydralazine.
60 retention of too much K+
61 persistent dry cough, hyperkalemia and postural hypotension. ANGIOEDEMA (swelling
around lips, eyes, throat, neck…can close airway)
62 direct vasoconstriction and increased water retention. So stopping those things lowers BP
63 -pril (enalapril)
64 -sartan (losartan). Block receptors for angiotensin II
65 potassium-sparing diuretics. Spironolactone.
66 CCBs. Block calcium ion channels, which limits muscular contraction of blood vessels.
Nifedipine. Selective (arterioles only) and nonselective (arterioles AND cardiac muscles)
67 -pine
68 only 2nd line drug considered impt for pharmacology HTN. Inhibit fight or flight= Decreases
heart rate and contractilityreduce cardiac output/workload and lower systemic BP. -olol
REBOUND HYPERTENSION
69 block sympathetic receptors which creates vasodilation. -zosin (doxazosin)
70 decrease the outward-bound nerve impulses from CNS to heart and arterioles. Dilation.
Slows heart rate. Can be a preferred drug in pregnancy
71 work like its name. can cause reflex tachycardia, which counteracts effect of HTN drug.
Hydralazine. No for lupus pt. medicate for the side effects of tachycardia using beta blocker
propranolol and by cautiously giving a diuretic (very cautiously bc EXCESSIVE DIURESIS AND
LOWERED BLOOD VOLUME MAY LEAD TO EXCESSIVE HYPOTENSION AND CIRCULATORY
COLLAPSE.
72 BiDil—hydralazine with isosorbide dinitrate. Good for heart failure in Afr-Amer