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Pharmacology exam 3 study guide notes, Study Guides, Projects, Research of Pharmacology

Virginia State University (VSU)Pharmacology

Pharmacology exam 3 study guide notes

Typology: Study Guides, Projects, Research

2025/2026

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Pharmacology exam 3 study guide
notes
ASTHMA
1. Asthma is characterized by airway narrowing and inflammation
primarily in medium sized bronchi
2. Therapeutic treatment involves opening airways and reducing inflammation
3. Treatment goals include
a. Control of symptoms
b. Maintain normal or near normal pulmonary function
c. Maintain normal activity levels
d. Meet patient’s expectations of asthma care
e. Prevent acute attacks and hospitalization
f. Prevent loss of lung function
g. Provide effective medications with minimal side effects
h. Prevent death
4. Precipitating factors:
a. Obesity
b. Rhinosinusitis
c. Confirmed food allergy
d. Eosinophilia
e. Pregnancy
f. Psychological or socioeconomic problems
g. Frequent use of SABA
5. Factors of control: UNCONTROLLED ASTHMA HAS 3-4 OF THESE
a. Daytime asthma more than twice a week
b. Nighttime awakening
c. Reliever needed more than twice a week
d. Activity intolerance
6. Consider step down therapy once symptoms are controlled for three months
7. Symptoms less than 2 times a month: as needed low dose ICS-
formoterol, or as needed low dose ICS with SABA as rescue
8. Symptoms more than 2 times a month: daily low dose ICS with as needed
SABA/ or as needed
low dose ICS-formoterol
9. Symptoms most days of the week: SMART low dose ICS-formoterol and
reliever therapy/ or medium dose ICS with SABA
10.Daily symptoms: daily High dose ICS and as needed SABA/ or daily
medium dose ICS-formoterol and as needed oral steroid burst
11.Rescue medications:
a. Short acting beta agonists: reverse bronchoconstriction, duration of
action is 4-6 hours, 4-10 puffs every 20 minutes for up to an hour for
exacerbation
i. May cause tachycardia, tremor, hypokalemia
b. ICS-formoterol: budesonide and formoterol is the only medication in
this class
i. Do not exceed 72 mcg per day
ii. Often used for mild asthma
c. Short acting muscarinic antagonist: ipratropium bromide
i. Nebulizer
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Pharmacology exam 3 study guide

notes

ASTHMA

  1. Asthma is characterized by airway narrowing and inflammation primarily in medium sized bronchi
  2. Therapeutic treatment involves opening airways and reducing inflammation
  3. Treatment goals include a. Control of symptoms b. Maintain normal or near normal pulmonary function c. Maintain normal activity levels d. Meet patient’s expectations of asthma care e. Prevent acute attacks and hospitalization f. Prevent loss of lung function g. Provide effective medications with minimal side effects h. Prevent death
  4. Precipitating factors: a. Obesity b. Rhinosinusitis c. Confirmed food allergy d. Eosinophilia e. Pregnancy f. Psychological or socioeconomic problems g. Frequent use of SABA
  5. Factors of control: UNCONTROLLED ASTHMA HAS 3-4 OF THESE a. Daytime asthma more than twice a week b. Nighttime awakening c. Reliever needed more than twice a week d. Activity intolerance
  6. Consider step down therapy once symptoms are controlled for three months
  7. Symptoms less than 2 times a month: as needed low dose ICS- formoterol, or as needed low dose ICS with SABA as rescue
  8. Symptoms more than 2 times a month: daily low dose ICS with as needed SABA/ or as needed low dose ICS-formoterol
  9. Symptoms most days of the week: SMART low dose ICS-formoterol and reliever therapy/ or medium dose ICS with SABA 10.Daily symptoms: daily High dose ICS and as needed SABA/ or daily medium dose ICS-formoterol and as needed oral steroid burst 11.Rescue medications: a. Short acting beta agonists: reverse bronchoconstriction, duration of action is 4-6 hours, 4-10 puffs every 20 minutes for up to an hour for exacerbation i. May cause tachycardia, tremor, hypokalemia b. ICS-formoterol: budesonide and formoterol is the only medication in this class i. Do not exceed 72 mcg per day ii. Often used for mild asthma c. Short acting muscarinic antagonist: ipratropium bromide i. Nebulizer

ii. Onset is 15 minutes and lasts 4-8 hours iii. Used with SABA for moderate to severe asthma exacerbation iv. Only indicated in emergency room settings

13.Theophylline: bronchodilator with a narrow therapeutic range, difficult to titrate, wrong titration can cause death a. Not to be used with acute pulmonary edema, hypothyroidism, liver disease, reduced renal function, recent smoking cessation, pregnancy, antifungal agents, carbamazepine, rifampin, and special considerations with many other drugs b. In patients who smoke, doses may need to be higher and/or more frequent 14.Beta blockers contraindicated for asthma: nadolol, propranolol, timolol, sotalol COPD

  1. Inflammation in asthma is mediated through eosinophils and mast cells while COPD inflammation is mediated through neutrophils, macrophages, and CD8+ T lymphocytes
  2. Bronchodilators and ICS are better for patients with increased eosinophils, indicative of coexisting asthma
  3. Spirometry is required to make a clinical diagnosis of COPD. The presence of a post- bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and of COPD
  4. Risk factors of COPD: smoking, early childhood lung infections, preterm birth, maternal smoking, occupational exposure to air toxins, asthma, bronchial hyperresponsiveness
  5. Smoking cessation in active smokers with copd slows the risk of pulmonary decline and reduced incidences of exacerbations.
  6. GOLD classification a. A: few symptoms, low exposure risk : bronchodilator (SABA) b. B: more symptoms low exacerbation risk: LABA or LAMA c. C: few symptoms high exacerbation risk: LAMA d. D: more symptoms high exacerbation risk: LAMA or LAMA + LABA or ICS + LABA e. If these groups have any further exacerbations with eosinophils > 100 cells then use LAMA + LABA + ICS f. If further exacerbations with eosinophils less than 100 consider roflumilast, azithromycin, and discontinue ICS
  7. LAMAs may be more beneficial than LABAs in reducing symptoms and decreasing hospitalizations
  8. Patients using LAMAs should be prescribed a SABA for rescue therapy
  9. Methylxanthine: theophylline: nonselective phosphodiesterase inhibitor that increases intracellular cAMP within airways smooth muscle resulting in bronchodilation and improved inspiratory function a. Reserved for patients who cannot use inhaled medications, or remain symptomatic despite inhaled medications 10.ICS a. Only use ICS in stable COPD groups C and D, not controlled by inhaled bronchodilators b. Eosinophils greater than 220 will show improvement
  10. Roflumilast a. Oral phosphodiesterase-4 inhibitor b. Used in preventing moderate to severe exacerbations in severe COPD c. May cause weight loss and diarrhea and SI avoid in underweight patients or those with depression d. Considered in patients with chronic bronchitis, an FEV1 o less

than 50%, frequent exacerbations despite therapy, and recent hospitalization 12.Antibiotics indicated with purulent sputum production, increased sputum volume, or dyspnea

  1. Non-pharm treatment: lower salt intake, increased potassium intake, low fat diet, more plant based foods, weight loss, physical exercise, moderation of alcohol consumption
  2. Pharm should be initiated if: a. BP 130-140/80-90 AND at least one of the following i. History of CAD, DM, CKD ii. 10 yr risk of CVD greater than or equal to 10% iii. Age 65 or older and SBP over or equal to 130 b. BP greater than or equal to 140/
  3. Treat hypertension with a. Step 1: ACE inhibitor or ARB or CCB or thiazide diuretic b. Step 2: ACE inhibitor or ARB + CCB or thiazide diuretic c. Step 3: ACE inhibitor or ARB + CCB + thiazide diuretic d. Step 4: ACE inhibitor or ARB + CCB + thiazide diuretic + spironolactone
  4. Two weeks to see full effect
  5. In blacks: thiazide diuretic and CCB more effective
  6. Alternatives to spironol\ 9. 10.actone: eplerenone, amiloride, triamterene 11.AVOID ACE inhibitors and ARBs in pregnancy 12.Heart failure: avoid CCB 13.After MI: avoid ARB and CCB 14.CKD: use ACE inhibitor and ARB 15.STROKE prevention: use diuretic and ACE inhibitor 16.Thiazide diuretics increase uric acid 17.ACE inhibitors and ARBS increase potassium 18.Diuretics unless potassium sparing decrease potassium 19.Calcium Channel blockers a. Dihydropyridines: “dipine” i. Mainly act on the smooth muscle cells of the blood ii. Used for hypertension and preventing angina iii. Side effect: reflex tachycardia, flushing, dizziness, peripheral edema b. Non-dihydropyridines: “verapamil and diltiazem” i. Greater effect on the heart ii. Less effective for vasodilation iii. Verapamil: more cardio selective and effective for angina iv. Diltiazem: better at vasodilation v. Contraindicated in HF HEART FAILURE
  7. Neurohormonal players in HF a. Angiotensin II: increased SVR, vasoconstriction, and increased BP, increase in afterload b. Aldosterone: sodium and water retention, increase in preload, hypokalemia, hypomagnesemia c. Norepinephrine: increases HR and myocardial contractility d. Endothelin: vasoconstrictor e. Arginine vasopressin: vasoconstrictor, increases preload and afterload, hyponatremia f. Natriuretic peptides: decrease sodium reabsorption, vasodilation g. Bradykinin: elevated in HF

h. Nitric oxide: a vasodilatory hormone found in higher concentrations in HF patients i. Proinflammatory cytokines: increased in HF patients

  1. Compensatory mechanisms a. Increased preload and vasoconstriction (through sodium and water retention): increases stroke volume but also causes systemic congestion and edema formation b. Tachycardia and increased contractility: increase CO, shortened diastolic filling time, ventricular arrhythmias c. Ventricular hypertrophy and remodeling: increased risk of myocardial ischemia and arrythmia.
  2. Heart failure classification a. A: patients at risk for HF but are asymptomatic and have no structural changes b. I/B,C: structural disease, asymptomatic c. II/C: structural changes, slight limitations to physical activity d. III/C: structural heart disease, marked limitation of physical activity, comfortable at rest e. IV/C,D: structural heart disease, symptoms at rest and activity, D refers to as end stage HF
  3. Diuretics: relieve acute symptoms of congestion, maintenance of euvolemia in HF C and D a. Loop diuretics most common: ex. Furosemide i. Drugs that compete for active transport such as those used in gout will compete with loop diuretics b. Diuretics do not improve mortality
  4. Goals of treatment: preventing or reducing symptoms, hospitalizations, slowing disease progress, increasing quality of life, prolonging survival
  5. ACE inhibitors (“pril”) a. Reduces preload and afterload, increases vasodilation b. Adverse effects: angioedema, cough, hyperkalemia, hypotension, renal dysfunction c. Monitor: BP, electrolytes, BUN and CR d. Contraindications: bilateral renal artery stenosis, h/o angioedema, pregnancy
  6. Beta Blockers a. Adverse effects: bradycardia, heart block, bronchospasm, hypotension, worsening HF b. Monitor: BP, HR, ECG, signs of worsening HF, blood glucose c. Contraindicated in COPD and asthma d. Increase triglycerides e. Nonselective B1 and B2: propranolol, timolol, nadolol, sotalol, pindolol i. May cause hypoglycemia; watch out for diabetes f. SELECTIVE B-2: atenolol, metoprolol, bisoprolol, esmolol, acebutolol (weak b-1 affects) i. Safe with COPD and asthma and diabetes (in low doses) g. B1 and A1 receptor blockers: labetolol and carvediolol: best for hypertensive, pregnancy okay in labetolol h. Avoid in patients with edema or prizmental angina
  7. Aldosterone receptor antagonists a. Adverse effects: increase in estrogen, hyperkalemia, worsening renal function

11.ARBS: “Sartan” a. Similar to ACE inhibitors but don’t increase bradykinin levels b. Used if pt cannot have ACE inhibitors c. Do not use in pregnancy ISCHEMIC HEART DISEASE

  1. Cause of IHD: imbalance between myocardial oxygen supply and oxygen demand: chronic stable angina, unstable angina, ACS, NSTEMI, STEMI
  2. Most common symptom is angina.
  3. Primary prevention: co-morbid disease management, lifestyle changes, antiplatelet and statin therapy
  4. Secondary prevention: co-morbid disease management, lifestyle changes, antiplatelet and statin therapy, ACE inhibitors and anti-anginal therapy
  5. Beta blockers can be used to prevent angina however should be avoided in combination with digoxin, non-dihydropyridine CCBs (verapamil and diltiazem), severe bradycardia, AV conduction defects a. Beta blockers can mask the symptoms of hypoglycemia such as tachycardia and tremor so caution must be used with diabetics. Nonselective BB can alter glucose metabolism and should not be used in Type 1 diabetics. b. Beta blockers are negatively inotropic (reduce heart contractility) and may worsen HF in patients with LV dysfunction (EF less than 40%) c. Beta blockers should not be stopped abruptly as it can worsen angina
  6. Calcium channel blockers: inhibit calcium into the smooth muscle and cardiac muscle cells, inhibiting contraction, which leads to vasodilation a. Non dihydropyridines: have negative chronotropic effects and are more effective for antianginal therapy i. Verapamil and diltiazem b. Recommended as alternative to beta blockers or in combination with beta blockers if initial treatment is unsuccessful i. Use long acting dihydropyridine CCB c. Amlodipine and felodipine have less inotropic effects compared to other CCBs and are safe for patient with LV systolic dysfunction d. Short acting agents may cause cardiac events and should be avoided in management of SIHD DYSLIPIDEMIA
  7. Four statin benefit groups a. Secondary prevention: Patients with ASCVD b. Primary prevention: Patients with LDL-C > c. Primary prevention: Patients over 40 with diabetes and LDL-C from 70- 189 d. Primary prevention: Patients over 40 with 10-year ASCVD risk of >7.5% and LDL-C 70- 189
  1. If patients have ASCVD or have LDL over 190 they are indicated for high intensity statin therapy
  2. Low intensity (<30%) Moderate intensity (30-49%) High intensity (≥50%) Atorvastatin - - 10- 20 40- 80 Rosuvastatin - - 10 20- 40 simvastatin 10 20- 40 - - pravastatin - - 40- 80 - - lovastatin 20 40- 80 - - Fluvastatin 20- 40 80 - -

4. Target LDL: less than 100

5. If patient complains of SAMS, rule out any other causative factors

a. CK less than 10 times the upper limit- continue statin therapy

and monitor in one week

b. If CK is increasing, stop statin and see if symptoms resolve

c. If CK is over 10x the upper limit, stop statin and drink lots of

water

d. If Ck 40x the upper limit, go to the ER

6. If pt falls into statin benefit group but is over the age of 75, treat

with moderate to high intensity statin, then add ezetimibe if LDL is

greater than 70, add PCSK9-1 if still over 70

7. Ezetimibe: blocks dietary absorption of cholesterol

a. Better effect combined with statin

b. Contraindicated in liver disease

8. Bile acid sequestrants

a. Allows Loss of bile to produce compensatory mechanisms which

result in loss of cholesterol to make new bile.

b. Moderately lower LDL but not triglycerides

c. Enhanced effect with statins

d. Take 1 hour before or 4 hours after taking digoxin, warfarin,

thyroxine, thiazides, b-blockers, fat soluble vitamins, and folic

acid

e. Safe for pregnancy

9. Bempedoic acid: often combined with ezetimibe for increased effect

a. Increases uric acid

10. Niacin

a. Major adverse reactions are flushing and hepatotoxicity

11. Fibrates: most effective triglyceride lowering drugs

a. Fenofibrate preferred with statin

b. Can increase bile

12. PCSK9 Inhibitors

a. Alirocumab & evolocumab

b. Injectabl

es Antithrombotics

g. Used for stroke prevention, systemic embolism, VTE prevention

after surgery