pharm GRM week #14...LAST ONE!!! (brief)

Chapter 37

1. What are gram negative infections more difficult to treat than gram positive?
a. their cells walls are more complex making it more difficult to penetrate

2. What is empiric therapy?
a. a broad spectrum antibiotic known to treat symptoms the patient is experiencing without identifying the specific specimen

3. Why should culture specimens be drawn before antibiotic therapy is begun?
a. it yields the most accurate specimen in the infection

4. What is prophylactic antibiotic therapy?
a. infection prevention in circumstances where infections are likely to occur

5. Under what circumstances do superinfections occur?
a. when antibiotics reduce or completely eliminate normal flora

6. What are the causes of strains of bacteria that are resistant to antibiotics?
a. over or inappropriate antibiotic prescribing and patients not finishing their antibiotic regimen

7. What does it mean for an antibiotic to be bacteriostatic?
a. inhibits bacterial growth

8. Why are antibiotics given using the “around the clock” method?
a. maintain therapeutic levels

9. What are the common manifestations to a hypersensitive reaction of an antibiotic?
a. wheezing, shortness of breath, swelling of face, tongue or hands, itching, or rash

Chapter 38

10. What is the benefit of once-daily aminoglycoside dosing?
a. reduces nursing care time and allows for outpatient or home-based therapy

11. Why are trough levels drawn on aminoglycosides?
a. ensure adequate renal clearance and avoid toxicity

12. When should aminoglycoside trough levels be drawn?
a. at least 18 hours after completion of the dose

13. What is the therapeutic goal for trough concentration of aminoglycosides?
a. at or below 1 mcg/mL

14. What is the risk when trough levels are above 2 mcg / mL?
a. toxicity to the ears and toxicity to the kidneys

15. How often are aminoglycoside trough levels monitored?
a. once every 3 days

Chapter 39

16. Viruses are particles that do what inside a cell?
a. replicate

17. How do antiviral drugs work?
a. destory virions or inhibit replication

18. How do the current antiviral drugs that are synthetic compounds work?
a. inhibit viral replication

19. Where must antiviral drugs go to disrupt viral replication?
a. enter the cells the same way the virion does

20. What are antiretroviral drugs specifically used for?
a. treatment of infections caused by HIV

21. What is the mechanism of action of non-retroviral antiviral drugs?
a. block activity of polymerase enzyme, impairing viral replication

Chapter 41

22. What is an infection cause by a fungus called?
a. mycosis

23. Generally, who is affected by systemic fungal infections?
a. hosts with compromised immune defenses

24. Why is it so difficult to produce systemic antifungals for human use?
a. drug concentrations cannot be tolerated by human beings

25. What are the side effects that nearly all patients who receive amphotericin B intravenously experience?
a. fever, chills, hypotension, tachycardia, malaise, muscle and joint pain, anorexia, nausea and vomiting, and headache

26. What drug classes are given to decrease the severity of reaction to amphotericin B?
a. anti-pyretics, anti-histamines, and anti-emetics

a ridiculous amount of pharm questions for exam #4...kind of

*Can sustained release capsules be crushed for administration?

*A patient is concerned about damage to her liver because of the 81 mg dose of aspirin she is getting. What can you tell this patient about the mechanism of action and why it is safe for her to get this daily dose?

*What is a safety issue for a Parkinson’s Disease patient?

*What are typical treatments for EPSs?

*Describe oxyhemoglobin-dissociation and factors affecting it.

*A patient on a statin is complaining of muscle pain and hemutria. What is the nurse’s concern?

*What tames heparin?

*Is it safe for a patient to be on coumadin and heparin IV?

*What is the treatment for status asthmaticus?

*How does Lopid lower LDLs?

*What else is Serevent useful in treating

*In what way is heparin and insulin similar, regarding medication administration?

*What is the normal range for PaO2 and PaCO2?

*What are the benefits of Clariton?

*What is the correct procedure for using Advair?

*What are the five things that can be done for a hypoxemic patient?

*What labs should be monitored for patients on lithium? Why?

*What is the relation between Sinemet and B6?

*A patient is receiving Plavix and is scheduled for surgery in a week and the nurse calls the
physician to discontinue the medication. What does the physician tell the nurse?

*Is it okay for a patient to be receiving 18-21% FIO2?

*What is warfarin’s mechanism of action?

*What is the nursing care of a patient on Plavix after coming back from surgery?

*How does adrenergics work as a decongestant?

*How can you test if a rescue inhaler is empty?

*Why should a patient on Albuterol or Serevent avoid caffeine?

*What labs should be checked for a patient on Lipitor or Zocor?

*What can result in pleural effusion and can it be solved?

*What is ordered for a person undergoing a percutaneous coronary intervention and what is the route of administration?

*What should a nurse always watch for when a patient is taking Tegretol and Depakote?

*What are the signs of a hypoxemic patient?

*How are mucolytics useful?

*What is another anti-hyperlipidemic drug that is best combined with Lipitor or Zocor?

*What are the two types of lung disorders and how do they differ?

*Why is warfarin’s therapeutic range for a prosthetic valve patient different from a patient
without a prosthetic valve?

*In general, how does an anti-hyperlipidemic work?

*What does a PaO2 less than 80 mm Hg indicate and what can it lead to?

*What labs should a nurse know about a patient before administering heparin?

*A patient is about to receive a tissue plasminogen activator to prevent clots. Is this correct?

*What type of lung disorder is pulmonary tuberculosis? Why?

*What are the routes of administration of heparin?

*What is the significance of high CYP3A4 enzyme levels of a patient on Lipitor or Zocor?

*What is the significance of monitoring the baseline platelet count?

*What is the right procedure for using a rescue inhaler? A MDI?

*What is the therapeutic range for theophylline?

*What are 4 types of respiratory units?

*What is the most common treatment of Parkinson’s Disease?

*Describe safety precautions for a patient prone to hypoxia of the brain.

*Compare and contrast Intal and Singulair.

*How should Dilantin be administered orally? IV?

*How are opiods and Robitussin DM similar?

*What can consolidation be a result of?

*What is the difference between a lipoprotein high in lipids and a lipoprotein low in lipids?

*What labs should be taken for a person on Rifampin?

*What is the mechanism of action of Atrovert?

*What is the patient suffering from acidemia prone to? Why?

*What is Zetia’s mechanism of action?

*A newly admitted patient has a platelet count of 650,000. What is this referred to as and
should the nurse be concerned about the count?

*What is the significance of PaCO2 that is out of normal range?

*What fluids can Dilantin IV be mixed with?

*How is tuberculosis spread?

*For every liter of O2, ___ increases by __%.

*What is the significance of administering heparin SubQ and administering heparin IV?

*What actions should be taken for a patient experiencing status epilepticus?

*Why is Benadryl discouraged in the elderly?

*What specific questions should a nurse ask a patient on Isoniazid?

*What is normal range for a platelet count?

*What are the three routes of administration of corticosteriods and an example of each?

*Why do anemic patients have a decreased circulation of gas?

*What should a patient know before beginning to take MAOIs?

*What are the adverse effects of lipoprotein removal drugs?

*What is the biochemical reason for mental illnesses?

*What is safe administration for a dose of heparin to prevent a clot?

*What drug class is aminophylline?

*What is the relation between carbon monoxide poisoning and oxygen affinity?

*What are the adverse effects of beta-2 agonists?

*What is offered to treat neurological symptoms of a patient on Isoniazid?

*What are examples of SSRIs and what do they improve?

*Describe three problems associated with corticosteroids.

*What are the side effects of niacin?

*What are specific signs and symptoms of bleeding?

*How does Sinemet work?

*A patient on warfarin is exhibiting unexplained swelling, chest pain, and weak pulses. What is
the nurse’s interpretation of these symptoms and what can be done?

*What is the duration of drug therapy for the schizophrenic patient?

*What is a side effect of Atrovert?

*What is patient education needed for a patient on drugs altering the clotting mechanism?

*What are the adverse effects of TCAs and MAOIs?

*What should a nurse expect to see after administering a methylxanthine and what might be a
side effect?

*What should a patient on TB treatment avoid?

*What is Robitussin useful for?

*What is the mechanism of action of unfractionated heparin?

*Can heparin be used on an emergency patient experiencing a stroke?

pharm GRM week #12 (brief)

Week 12-Chapter 15

1. How is the effectiveness of a psychotropic drug therapy often measured?
a. verbal reports from patients regarding improvements in social and occupational functioning

2. What factors constitute ideal mental health?
a. emotional, psychosocial, and spiritual factors

3. What is psychosis and what is its hallmark?
a. severe emotional disorder impairing mental functioning impairing ADLs; hallmark is loss of contact with reality

4. What is another name for affective disorders?
a. mood disorders

5. What is the biochemical concept of mental illness?
a. abnormal levels of neurotransmitters

6. Which neurotransmitters play a role in maintaining mental health?
a. dopamine, norepinepherine, serotonine, and histamine

7. What advantages do newer antidepressants have over TCAs and MAOIs?
a. fewer and less severe systemic adverse effects and less drug-drug and drug-food interactions

8. How long does it typically take antidepressants to reach their maximum clinical effectiveness?
a. 4-6 weeks

9. How do TCAs work?
a. block reuptake of neurotransmitters to correct imbalance of concentrations

10. In general, how do antipsychotics work?
a. produce state of transquility and work on abnormally functioning nerves

11. What are the positive symptoms of schizophrenia?
a. hallucinations, delusions, and conceptual disorganizations

12. What are the negative symptoms of schizophrenia?
a. apathy, social withdrawal, blunted effect, poverty of speech, and catatonia

pharm GRM week #11 (brief)

Week 11-Chapter 35

1. What causes the excessive mucus production in a URI?
a. inflammatory response by viral invasion

2. What causes nasal congestion in URI?
a. irritation of nasal mucosa resulting in dilated small blood vessels of the nasal sinuses

3. What 4 classes of drugs are used to treat URI?
a. antihistamines, decongestants, antitussives, and expectorants

4. What do histamine-1 receptors mediate?
a. smooth muscle contraction and dilatio of capillaries

5. What do histamine-2 receptors mediate?
a. acceleration of heart rate and gastric acid secretion

6. How does excessive histamine release cause a drop in blood pressure and edema?
a. vasodilation and increased capillary permeability, moving fluids from blood vessels into tissues

7. How do antihistamines work?
a. directly compete with histamine for specific receptor sites

8. What is the other term for antihistamines?
a. histamine antagonists or blockers

9. Which specific smooth muscle are histamine-1 antagonist particularly focused on?
a. smooth muscles surrounding blood vessels and bronchioles

10. What are the primary anticholinergic effects of antihistamines?
a. secretions of lacrimal, salivary, and respiratory mucosal glands

11. How does histamine cause pruritis?
a. stimulates nerve endings

12. What are the two main cells that release histamine?
a. basophils and mast cells

13. What do antihistamines do to smooth muscle in the bronchial tree?
a. cause extravascular muscle to contrict

14. Why is it most beneficial to give antihistamines early in a histamine-mediated reaction?
a. compete with histamine to occupy the unoccupied receptors

15. What are the consequences of histamine binding?
a. prevent consequences like vasodilation, increased secretions, and edema

16. What is the chief adverse effect of antihistamines?
a. drowsiness

17. How do the non-sedating antihistamines avoid causing drowsiness?
a. work peripherally without affecting the CNS

18. What is another name for non-sedating antihistamines?
a. peripherally acting antihistamines

19. What class of drug is loratadine (Claritin)?
a. non-sedating antihistamine

20. What class of drug is diphenhydramine?
a. antihistamine

21. Why is the use of diphenhydramine discouraged in the elderly?
a. hangover effect and increased risk of fall

22. What are the three classes of drugs used as decongestants?
a. adrenergics (sympathomimetics), anticholinergics (parasympatholytics), and corticosteroids

23. How do sympathomimetics produce decongestion?
a. constrict blood vessels to better drain nasal secretions

24. How do opioids reduce coughing?
a. suppress cough reflex

25. What are the two mechanisms of action for expectorants?
a. loosening and thinning of RT secretions and direct stimulation of secretory glands

Week 11-Chapter 36

26. Where does the oxygen-carbon dioxide exchange take place?
a. alveoli

27. What is the common feature of asthma, emphysema and chronic bronchitis?
a. obstruction of airflow through the airways

28. What is it that narrows bronchioles in asthma?
a. bronchospasm, inflammation, and edema of bronchial mucosa

29. What is the collective term for such substances as the histamines and leukotrienes?
a. inflammatory mediators

30. In asthma, what antibody sensitizes the patient to the offending allergen?
a. immunoglobulin E

31. How do bronchodilators work?
a. relax bronchial smooth muscle to dilate bronchi and bronchioles

32. What are the three classes of bronchodilators?
a. Beta-agonists, anticholinergics, and xanthine derivatives

33. How do each of the subtype beta adrenergic agonists work?
a. non-selective adrenergic drugs: stimulate alpha 1, beta 1, and beta 2 receptors
b. non-selective beta adrenergic drugs: stimulate beta 1 and beta 2 receptors
c. selective beta 2 drugs: stimulate beta 2 receptors

34. When a nonselective adrenergic agonist is given, what are the cardiovascular adverse effects?
a. increased HR, contractility, and BP

35. How are beta 2 agonists useful in treating hyperkalemia?
a. shifts potassium from blood stream to cells temporarily

36. List the adverse effects of alpha-beta agonists.
a. insomnia, restlessness, anorexia, cardiac stimulation, hyperglycemia, tremor, and vascular headache

37. How does the parasympathetic autonomic nervous system bring about bronchoconstriction? a. releases Ach which binds to bronchial trees to constrict airways

38. How do anticholinergic drugs indirectly cause airway dilation?
a. blocks Ach which causes constriction

39. What is the therapeutic range for theophylline?
a. below 20 mcg/ml

40. What do leukotrienes cause in asthmatics?
a. inflammation, bronchoconstriction, and mucus production

41. How do antileukotriene drugs work?
a. prevent leukotrienes from attaching to receptors on circulating and local immune cells

42. How are inhaled corticosteroids used?
a. control inflammatory response believed to cause bronchospastic disorders

43. How is fluticasone administered?
a. intranasally

44. Is it safe to crush a sustained-release capsule for administration?
a. no

45. What is the relationship of caffeine and beta agonist drugs?
a. increase in adverse effects like tachycardia, hypertension, headaches, nervousness, and tremors

Week 11-Chapter 40

46. Describe MTB.
a. a rod shaped bacterium thriving in highly oxygenated sites like the lungs

47. How is TB spread?
a. inhaled droplets from infected hosts to new host

48. Why is MTB more difficult to treat than most bacterial infections?
a. slow growing organism

49. Why are slow growing microorganisms difficult to kill?
a. cells are not as metabolically active compared to faster growing organisms

50. What is the most widely used antitubercular drug?
a. isoniazid (INH)

51. What it the major effect of drug therapy with antitubercular drugs?
a. reduction of cough, and therefore infectiousness

pharm GRM week #10 (brief)

Week 10-Chapter 13

1. What are seizures, convulsions and epilepsy?
a. seizures: brief episodes of abnormal electrical activity in the nerve cells of the brain
b. convulsions: involuntary spasmodic contractions of any or all voluntary muscles throughout the body, including skeletal and facial muscles
c. epilepsy: chronic, recurrent pattern of seizures

2. What is accurate diagnosis of seizure disorder based upon?
a. electroencephalogram (EEG)

3. What is an AED?
a. antiepileptic drugs

4. What other types of illnesses are AEDs used for besides seizures?
a. psychiatric disorders, migraine headaches, and neuropathic pain syndromes

5. Under what circumstances should an AED be abruptly stopped?
a. a severe adverse effect occurs

6. Under what circumstances would a patient with a seizure disorder be maintained on a subtherapeutic drug level?
a. decreases the risk for medication-induced adverse effects and interactions

7. What are the three pharmacologic effects of AEDs?
a. make it difficult for a nerve to be excited or reduce the nerves response to incoming electrical or chemical stimulation
b. limit the spread of seizure discharge from its origin
c. decrease the speed of nerve impulse conduction within a given neuron

8. At what time of day are AEDs typically given?
a. >?

9. Why should carbamazepine not be given with grapefruit?
a. >?

10. Why does IV phenytoin have to be given with normal saline?
a. avoid local venous irritation

11. Why does phenytoin IV have to be given slowly?
a. possible cardiovascular/respiratory collapse

12. What is the most common adverse effect of AEDs?
a. sedation, confusion, CNS depression

Week 10-Chapter 14

13. What does PD result from?
a. imbalance of dopamine and acetylcholine

14. What do dopamine and acetylcholine regulate?
a. proper regulation of posture, muscle tone, and voluntary movement

15. What are the classic PD symptoms?
a. slowness of movement (bradykinesia), rigidity, tremor, and danger of falling

16. What is the primary role of MAOs?
a. breakdown of catecholamines

17. What does selegiline do?
a. decrease amount of levodopa needed

18. What does levodopa do?
a. precursor for dopamine synthesis by the brain

19. How does amantadine (Symmetrel) exert its antiparkinsonian effect?
a. elicits release of dopamine from nerve endings

20. In PD, what are anticholinergic drugs useful in?
a. treat the muscle remors and muscle rigidity

21. What is the relationship of pyridoxine and levodopa?
a. B6: promotes levodopa breakdown and possibly reverse effects

22. Explain the concept of a drug holiday.
a. obtain more therapeutic effectiveness; allow patient to respond to lower doses of drug

pharm GRM week #9 (brief)

Week 9-Chapter 27

1. What are anticoagulants?
a. inhibits the action or formation of clotting factors thus preventing clots from forming

2. What are antiplatelet drugs?
a. prevent platelet plugs from forming by inhibiting platelet aggregation which is beneficial for preventing heart attacks and strokes

3. What do thrombolytic drugs do?
a. break down clots which have already formed

4. Why is frequent monitoring not necessary with LMWH?
a. low molecular weight heparins have a predictable anticoagulant response

5. How does warfarin work?
a. inhibits the four vitamin K-dependent clotting factors to prevent clot formation

Week 9-Chapter 28

1. How is cholesterol used in the body?
a. used to make steroid hormones, cell membranes, and bile acids

2. How doe statins lower serum cholesterol levels?
a. decrease rate of cholesterol production

3. What is rhabdomyolysis?
a. breakdown of muscle protein leading to myoglobinuria (urinary elimination of the muscle protein myoglobin

4. When assessing liver enzymes, which are it most important to assess when a patient is on statins?
a. activity of CYP3A4 in the liver to metabolize statins

pharmacology GRM week #9 (brief)

Week 9-Chapter 21

1. What do inotropic drugs do
a. change the force of myocardial contraction

2. What do positive chronotropic drugs do?
a. increase the rate at which the heart beats

3. What are the two main classes of positive inotropic drugs?
a. cardiac glycosides and phosphodiesterase inhibitors

4. What is the definition of heart failure?
a. abnormal condition in which cardiac pumping is impaired as a result of myocardial infarction

5. What is ejection fraction and what is the normal value?
a. amount of blood ejected with each contraction, normally 65% of the blood volume in the ventricle

6. When a person is in heart failure, which of their organs are the last to be deprived of blood?
a. those most dependent on blood, the brain and heart

7. What is the relationship of sodium and potassium to heart function?
a. depolarize the heart

8. Define systolic dysfunction and diastolic dysfunction.
a. systolic dysfunction: inadequate ventricular contractions during pumping of the heart
b. diastolic dysfunction: inadequate ventricular filling during ventricular relaxation

9. How does a cardiac glycoside improve myocardial contractility?
a. inhibits the ATPase pump, increasing calcium concentration

10. What are the inotropic, chronotropic, dromotropic and other cardiac effects of digoxin?
a. positive inotropic effect: increase in force and velocity of contractions without increasing oxygen consumption
b. negative chronotropic effect: lowers HR
c. negative dromotropic effect: decreases automaticity at SA node, decreases AV node conduction, reduces conductivity at the bundle of His, and prolongs the atrial and ventricular refractory periods
d. other cardiac effects: increase in stroke volume, reduction in heart size during diastole, decrease in venous BP and engorgement, and increase in coronary circulation

11. What are the primary indications for cardiac glycosides?
a. heart failure and supraventricular dysrhythmias

12. What is the normal therapeutic drug level for digoxin?
a. 0.5-2 ng/ml

13. How do low serum potassium levels affect digoxin therapy?
a. increase potential for toxicity

14. What are the common adverse effects of cardiac glycosides?
a. dysrhythmias, headache, fatigue, malaise, confusion, convulsions, colored vision, halo vision, flickering lights, anorexia, nausea, vomiting, and diarrhea

15. What is the step-by-step management of digoxin toxicity?
a. discontinue administration of the drug
b. begin continuous ECG monitoring for cardiac dysrhythmias, administering appropriate drugs as ordered
c. determine serum digoxin and electrolyte levels
d. administer potassium supplements for hypokalemia if indicated, as ordered
e. institute supportive therapy for GI symptoms like nausea, vomiting, or diarrhea
f. administer digoxin antidote if indicated, as ordered

16. How does digoxin immune Fab (Digibind) work?
a. binds to unbound digoxin to reverse effects and symptoms of toxicity

17. What are the results of inhibition of phosphodiesterase?
a. positive inotrophic response and vasodilation

18. What is an inodilator?
a. a drug producing positive inotrophic response and vasodilation

19. What is the effect of inhibition of phosphodiesterase on the
availability of calcium, systemic and pulmonary vessels and cardiac workload?
a. increases availability of calcium for heart to use for muscle contraction, dilates systemic and pulmonary vessels which decreases cardiac workload

20. How do PDI’s reduce afterload?
a. dilate blood vessels

21. What are the two most common PDI’s?
a. inamrinone and milrinone

22. What serum lab values should the nurse investigate before giving a cardiac glycoside?
a. serum potassium

23. What heart rates in the adult should cause the nurse to withholding a cardiac glycoside?
>?

24. What is the relationship between bran and digoxin?
a. bran in large amounts may decrease the absorption of digoxin

25. What is the safe infusion rate for IV digoxin?
a. usual digitalizing dose: 1-1.5mg/day
b. usual maintenance dose: 0.125-0.5 mg/day

Week 9-Chapter 23

26. How is the heart’s oxygen supply met?
a. delivered by coronary arteries

27. What is angina pectoris?
a. chest pain

28. Define coronary artery disease, myocardial infarction, chronic stable angina, unstable angina, and vasospastic angina.
a. coronary artery disease: supply of oxygen and energy-rich nutrients needed for the heart to meet its demands is decreased due to atherosclerosis
b. myocardial infarction: heart attack; blood flow through the coronary arteries to the myocardium is completely blocked so that part of the heart cannot receive oxygen from blood-borne nutrients
c. chronic stable angina: triggered by exertion or stress causing intense pain for 15 minutes and usually subsides
d. unstable angina: pain episodes increase in severity and frequency
e. vasospastic angina: spasms of the smooth muscle surrounding atherosclerotic coronary arteries often happening during rest

29. Which are two example classes of drugs that aim to correct the imbalance between myocardial oxygen supply and demand and how do they do it?
a. nitrates and nitrites: dilate all blood vessels
b. beta blockers: slow heart rate and reduce blood pressure

30. Explain the process that results in angina.
a. oxygen deprivation of the myocardium under ischemic conditions cause the heart to work anaerobically producing lactic acid and stimulating pain receptors surrounding the heart

31. What is it that actually causes the heart pain called angina?
a. lactic acid causes pain receptors to be stimulated

32. How do nitrates and nitrites vasodilate?
a. relaxes the smooth muscle cells of venous and arterial wall structure

33. What does dilation of coronary arteries by nitrates result in?
a. reverses or prevent exercise induced spasms, encouraging healthy physical activity in patients
34. Explain the way in which nitrates/nitrites reduce preload.
a. cause venous dilation and reduces venous return

35. Why are nitrates/nitrites contraindicated in persons with severe anemia, closed-angle glaucoma, hypotension and severe head injury?
a. conditions can be worsened

36. Why specifically is it risky to give nitrates/nitrites to a person with severe anemia?
a. cause drug-induced hypotensive episode

37. What is reflex tachycardia?
a. cardiovascular overcompensation marked by increased heart rate

38. What is the purpose of the regimen of removing transdermal patches at night for 8 hours and then applying a new patch in the morning?
a. prevent tolerance to nitrates

39. How do beta blockers improve the chances of survival in patients following an MI?
a. block harmful effects of the high levels of circulating catecholamines from irritating the heart

40. How do calcium channel blockers work?
a. promotes muscle relaxation causing coronary artery dilation increasing blood flow and oxygen supply

41. What is the primary beneficial antianginal effect of amlodipine and nifedipine?
a. indicated for angina and hypertension

42. What is the onset time for sublingual nitroglycerine?
a. 2-3 minutes

43. What systolic BP should be reported before giving a nitrate?
a. less than 60 mm Hg

44. Why is it unsafe to take nitrates when taking erectile dysfunction drugs?
a. worsens hypotensive response, paradoxical bradycardia, and increased angina with risk of cardiac or cerebrovascular complications from decreased perfusion

45. When receiving a nitrate, what position should the person be in?
a. seated to avoid falls

46. Where should nitroglycerine ointment be placed?
a. upper arms or body

47. Should nitroglycerine ointment be rubbed in and what is done with it when the dose is changed?
a. it should not be rubbed in and should be cleaned with soap and water and patted dry before applying the changing the dose

pharmacology GRM week #8 (brief)

Week 8-Chapter 22
1. What is it that results in disturbances in cardiac rhythm?
a. abnormally functioning cardiac cells

2. What is the term for spontaneous electrical excitability found in cardiac cells?
a. automaticity
3. What are the three main ions involved that move across the cell membrane causing cardiac electrical activity?
a. calcium, sodium, and potassium
4. What mechanism maintains the polarized distribution of ions in the myocardium?
a. sodium-potassium adenosine triphosphatase (ATPase) pump
5. How are antidysrhythmic drugs categorized?
a. Class 1, 1a, 1b, 1c, class II, class III, class IV
6. In general, how do antidysrhythmic drugs work?
a. affect the resting membrane potential (RMP) and sodium channels, in turn influencing the rate of impulse conduction
7. Be able to recognize from the pictures on pages 335 – 337 and defined on page 338, the following dysrhythmias:
a. atrial fibrillation: supraventricular dysrhythmia characterized by rapid atrial contractions that only incompletely pump blood into the ventricles

-rapid, ineffective atrial contractions: QRS complex separated by squiggly lines

b. ventricular tachycardia: rapid heartbeat from impulses originating in ventricles

-photo of sustained VT: uniform mounds

c. ventricular fibrillation: worsened ventricular tachycardia which can be fatal if not reversed

-rapid, ineffective ventricular contraction: small, irregular, bumpy hills

*photos from learntheecg.com

8. What are the therapeutic responses to antidysrhythmic drugs that the nurse should see in the patient?
a. improved cardiac output, decreased chest discomfort, decreased fatigue, improved vital signs, skin color, and urinary output

Week 8-Chapter 24
1. List all of the drug categories that are used to lower the blood pressure in those with hypertension.
a. Loop diuretics, potassium sparing diuretics, beta blockers, ACE inhibitors, alpha 1 antagonists, ARBs, CCBs and vasodilators

2. In Figure 24-1 on page 369, be familiar with the values that represent normal as well as the different classifications of hypertension. Know columns 1, 2 & 3 of the table.
BP Classification: SBP (mm Hg) / DBP (mm Hg)
a. normal: less than 120/less than 80
b. prehypertension: 120-139/80-89
c. stage 1 hypertension: 140-159/90-99
d. stage 2 hypertension: 160 or higher/100 or higher
3. Know Figure 24-3 on page 372 you need to know only the classes of antihypertensives, not the drugs that represent each class. Essentially, what I want you to know is where each anti-hypertensive class works in the body.
a. centrally-acting alpha 2-receptor agonists: vasomotor center
b. centrally and peripherally acting allergenic neuron blocker: vasomotor center and sympathetic ganglion --> blood vessel
c. peripherally acting alpha 1-receptor antagonists: blood vessel
d. direct-acting arteriolar dilators: blood vessel
e. direct-acting arteriolar and venous dilator: blood vessel
f. diuretics: kidney
g. angiotensin II receptor blockers (ARBs): angiotensin II
h. angiotensin-converting enzyme (ACE) inhibitors: angiotensin-converting enzyme
i: beta-adrenergic blocking drugs: heart

Week 8-Chapter 25
1. What do diuretics remove from the body?
a. sodium and water
2. What are the mechanisms that make diuretics hypotensive drugs?
a. direct arteriolar dilation which decreases peripheral vascular resistance
b. reduce extracellular fluid volume, plasma volume, and cardiac output
3. What is the main problem with diuretic use?
a. excessive fluid and electrolyte loss

4. How are diuretics classified?
a. carbonic anhydrase inhibitors, loop diuretics, osmotic diuretics, potassium-sparing diuretics, and thiazide and thiazide-like diuretics
5. List the diuretic subclasses according to their potency in the order of most potent to least potent.
a. loop diuretics, osmotic, thiazide-like diuretics, thiazides, and potassium sparing
6. Fill in the blanks. The more sodium and water diuretics inhibit from resorption, the greater the amount of diuresis.

7. What are the beneficial hemodynamic effects of loop diuretics?
a. reduction of preload and central venous pressures
8. What are the cardiovascular effects of loop diuretics?
a. reduces blood pressure, pulumonary vascular resistance, systemic vascular resistance, central venous pressure, and left ventricular end-diastolic pressure
9. What are the electrolyte losses associated with diuretic administration?
a. loss of sodium, potassium and some calcium
10. How do osmotic diuretics work?
a. produces osmotic pressure in the glomerular filtrate which pulls fluid (mostly water) into renal tubules from surrounding tissue
b. inhibits tubular resorption of water and solutes producing rapid diuresis
11. How does spironolactone lead to diuresis?
a. competitively binds to aldosterone receptors thus blocking the resorption of sodium and water induced by aldosterone secretion
12. How do thiazide diuretics work?
a. inhibit resorption of sodium, potassium, and chloride resulting in osmotic loss

pharmacology GRM week #7 (brief)

Week 7-Chapter 51

1. What are the functions of HCl, bicarbonate, pepsinogen, intrinsic factor, mucus and prostaglandins in the stomach?
a. HCl: aids in digestion and barrier to infection,
b. bicarbonate: natural mechanism to prevent hyperactivity
c. pepsinogen: precursor to pepsin which digests protein
d. intrinsic factor: facilitates absorption of B12,
e. mucus: protection from HCl and digestive enzymes
f. prostaglandins: antiinflammatory and protective functions

2. Which cells produce HCl?
a. parietal cells

3. What usually causes hyperacidity in the stomach?
a. food, caffeine, chocolate, alcohol or emotional stress

4. What is the typical pH of the stomach?
a. 1-4

5. What is the primary target of the drugs that treat acid-related disorders?
a. parietal cells

6. What are the three types of receptors on the parietal cells?
a. acetylcholine (Ach), histamine, and gastrin

7. What is the name of the mechanism which transports HCl from the parietal cells to the stomach?
a. proton pump

8. How do anticholinergics reduce HCl production?
a. block Ach receptors which also decrease hydrogen ion secretion from parietal cells

9. Why do aluminum and calcium based antacids also contain magnesium?
a. contributes to acid-neutralizing capacity and conteracts constipating effects of calcium and aluminum

10. To what degree do antacid dosages raise the gastric pH?
a. 0.3 points, reducing it by 50%
b. 1 point, reducing it by 90%

11. How do H2 receptor blockers raise the gastric pH?
a. competitively block H2 receptor of acid-producing parietal cells and reduces responsiveness to histamin and stimulation of Ach and gastrin

12. How do PPI’s raise the gastric pH?
a. bind to proton pump preventing movement of hydrogen ions and blocks gastric acid secretion

13. When both antacids and H2 blockers are given, what is the proper practice?
a. Do not administer simultaneously.

14. Why are antacids to be given with water?
a. enhance absorption in stomach

15. In relation to other medications, how should antacids be given?
a. 1-2 hours before other medications are taken

16. What may happen if ranitidine is given rapidly IV?
a. hypotension


Week 7-Chapter 52

17. What is the definition of diarrhea?
a. abnormal passage of stools with increased frequency, fluidity, weight, or with increased stool water excretion

18. How do adsorbents work in treating diarrhea?
a. coat the wall of the GI tract, binding to causative bacteria or toxin to their surface to be eliminated from the body through stool

19. How do anticholinergic drugs reduce diarrhea?
a. slow peristalsis by reducing the rhythmic contractions and smooth muscle tone of the GI tract

20. How do opioids treat diarrhea?
a. reduce bowel motility

21. How do opiods affect absorption?
a. increases the absorption of water, electrolytes, and nutrients

22. Why might someone who takes oral anticoagulants with absorbants be at higher risk for bleeding?
a. may bind to vitamin K which is needed for clotting

23. Why does Lomotil contain atropine?
a. discourages recreational opiate use

24. What is the definition of constipation?
a. abnormally infrequent and difficult passage of feces through the lower GI tract

25. What problems can chronic laxative use cause?
a. laxative dependence, damage to bowel or intestinal problems

26. What are the three ways in which laxatives work?
a. affecting fecal consistency, increasing fecal movement through colon and facilitate defecation through the rectum

27. Describe the way in which the 5 categories of laxatives work. Know drug examples from each laxative category. Table 52-4
Laxatives: Drug Effects
*Bulk: Psyllium
Increase peristalsis, causes increased secretion of water and electrolytes in small bowel, inhibits absorption of water in small bowel, increases water in fecal mass, softens fecal mass

*Emollient: Mineral oil
Increase peristalsis, causes increased secretion of water and electrolytes in small bowel, inhibits absorption of water in small bowel, increases wall permeability in small bowel, increases water in fecal mass, softens fecal mass

*Hyperosmatic: Glycerin
Increase peristalsis, acts only in large bowel, increases water in fecal mass, softens fecal mass

*Saline: Magnesium hydroxide
Increase peristalsis, causes increased secretion of water and electrolytes in small bowel, inhibits absorption of water in small bowel, increases water in fecal mass, softens fecal mass

*Stimulant: Senna
Increase peristalsis, causes increased secretion of water and electrolytes in small bowel, inhibits absorption of water in small bowel, increases wall permeability in small bowel, increases water in fecal mass, softens fecal mass

28. How does lactulose reduce serum ammonia levels in patients with hepatic encephalopathy?
a. converts ammonia to ammonium which cannot be reabsorbed in the small intestine

29. How long does it take polyethylene glycol 3350 to cleanse the bowel if it is taken properly?
a. 4 hours

30. What color does bismuth subsalicylate turn the stool?
a. black or grey

pharmacology GRM week #6 (brief)

Week 6-Chapter 26

1. What are the three main body fluid compartments?
a. intracellular fluid, interstitial fluid, and plasma volume

2. Know the terms extracellular fluid, extravascular fluid, interstitial fluid, intracellular fluid and intravascular fluid.
a. extracellular fluid: fluid outside the cells
b. extravascular fluid: fluid outside blood vessels
c. interstitial fluid: fluid between cells
d. intracellular fluid: fluid within a cell
e. intravascular fluid: fluid within blood vessels

3. What does isotonic mean?
a. equal concentration of solutes across a membrane

4. There are two forces within the capillaries that bring about the movement of water. Hydrostatic pressure pushes water out of the capillaries and oncotic or colloidal oncotic pressure pulls or retains water within the vessels. The arterial blood pressure is what provides for the hydrostatic pressure. It is a person’s arterial blood pressure that promotes the movement of fluid from within the capillaries to outside the capillaries (tissues and cells). Serum protein (albumin) is what causes a person to have oncotic pressure so it is actually the albumin that pulls water into the capillaries. So, hydrostatic pushes and oncotic pulls.

5. What is the principle extracellular electrolyte?
a. albumin

6. What are the three categories of agents used to replace lost fluids?
a. crystalloids, colloids, and blood products

7. What are the constituents of crystalloids?
a. fluids and electrolytes normally found in the body

8. How do colloids move fluid from the interstitial compartment to the plasma compartment? a. pull fluid from blood vessels

9. What are the indications for the following blood products?
a. Cryoprecipitate: 1, FFP: 1.7x, PRBCs: 2.2x, whole blood: 3.33


Week 6-Chapter 53

1. What are the two areas of the brain responsible for vomiting?
a. vomiting center and chemoreceptor trigger zone

2. What are parents advised to do when a child ingests a toxin?
>?

3. How do most antiemetics work?
a. block one of 6 vomit pathways and in doing so block the neurologic stimulus that induces vomiting

4. Know the ways in which categories of antiemetics work by studying

Antiemetic Drugs: Mechanisms of Action
*Anticholinergics: scopolamine
Block Ach receptors in the vestibular nuclei and reticular formation

*Antihistamines: diphenhydramine
Block H1 receptors, thereby preventing Ach from binding to receptors in the vestibular nuclei

*Neuroleptics: prochlorperazine
Block dopamine in the CTZ and may also block Ach

*Prokinetics: metoclopramide
Block dopamine in the CTZ or stimulate Ach receptors in the GI tract

*Serotonin blockers: ondansetron
Block serotonin receptors in the GI tract, CTZ, and VC

*Tetrahydrocannabinoids
Have inhibitory effects on the reticular formation, thalamus, and cerebral cortexcerebral cortex

pharmacology GRM week #5 (brief)

Week 5-Chapter 12

1. Compare sedatives and hypnotics.
a. sedatives reduce nervousness, excitability, and irritability without causing sleep in small amounts. Hypnotics have a more potent effect on the CNS and cause sleep.

2. In terms for barbiturates, what is meant by a “low therapeutic index?”
a. there is only a narrow margin where the drug is effective and beyond that margin the drug is rapidly toxic

3. Since GABA is an inhibitory amino acid, what happens to the CNS when it is potentiated?
a. inhibit nerve impulse transmission

4. What does it mean to raise the convulsive or seizure threshold?
a. decreases the threshold a patient has to convulse or have a seizure

5. What do barbiturates do to the respiratory rate?
a. decrease repiratory rate

6. By stimulating the action of enzymes that are responsible for the metabolism of many drugs, how do barbiturates affect the duration of action of these other drugs?
a. shortens their duration time

7. What are the 4 indications of barbiturates?
a. ultra-short acting, short acting, intermediate acting, and long acting

8. Which bodily system is most affected by barbiturates?
a. the CNS

9. What is the most frequent response to barbiturate overdose?
a. respiratory depression leading to respiratory arrest

10. What are the mainstays of treatment of barbiturate overdose?
a. maintenance of adequate airway, assisted respiration, and oxygen administration if needed

11. What is meant by “pressor support?”
a. drugs that cause vasoconstriction and therefore, raise the blood pressure.

12. How does activated charcoal cause the elimination of a drug from the body?
a. assists in pulling the drug from circulation then eliminating it through the GI tract

13. Know that Phenobarbital (Luminal) is the prototype barbiturate.
a. Luminal is the prototype barbiturate

14. What is the most commonly prescribed class of sedative-hypnotics?
a. benzodiazepines because they have favorable adverse effect profiles, efficacy and safety

15. What are the two classifications of benzodiazepines?
a. anxiolytics and sedative-hypnotics

16. How do benzodiazepines depress the CNS?
a. inhibit stimulation of the brain

17. Why are benzodiazepines used to prevent the symptoms of alcohol withdrawal?
a. their receptors in the CNS is the same area or alchohol addiction

18. What are the 4 most common uses of benzodiazepines
a. sedation, sleep induction, anxiety relief, and musculo-skeletal relaxation

19. What are the most commonly reported undesirable effects of benzodiazepines?
a. headaches, dizziness, paradoxical excitement or nervousness, drowsiness, vertigo, lethargy, and cognitive impairment

20. Why should benzodiazepines be avoided in the elderly?
a. create a significant fall hazard

21. What are the manifestations of a benzodiazepine overdose?
a. somnelence, confusion, coma, and diminished reflexes

22. What two substances should benzodiazepines not be combined with?
a. alcohol and analgesics

23. What is the reason for not inducing vomiting in an unconscious patient?
>?

24. How does flumazenil work as a benzodiazepine reversal agent?
>?

25. What are the pharmacologic properties of the nonbenzodiazepine hypnotics such as zolpidem (Ambien) and eszoplicone (Lunesta)?
a. anxiolytic, sedative, muscle relaxant, and anticonvulsive effects

26. How long should the nonbenzodiazepine drugs be used to treat insomnia?
a. 7-10 days

27. Which class of hypnotics has the shortest half-life, benzodiazepines or nonbenzodiazepines?
a. benzodiazepines

28. Which would you guess would have the greater “hangover” effect?
a. nonbenzodiazepines

29. How does the group of muscle relaxants act?
a. act within the CNS to relieve pain associated with skeletal muscle spasms

30. What are the two classes of muscle relaxants
a. central acting skeletal muscle relaxants and direct acting skeletal muscle relaxants

31. What is the antidote or reversal drug for muscle relaxant overdose?
a. no specific antidote

32. What may barbiturates undesirably cause in children and the elderly?
>?

33. What happens if a barbiturate is given too rapidly IV?
a. profound hypotension and marked respiratory depression

34. What is the normal blood level for phenobarbital?
>?

35. What standard safety precautions should be used on someone taking hypnotics?
>?

36. Should zolpiedem (Ambien) be taken with a mealtime snack or on an empty stomach?
a. empty stomach


Week 5-Chapter 16

37. How do most CNS stimulant drugs act?
a. stimulate the excitatory neurons in the brain

38. What are the 3 excitatory neurotransmitters?
a. dopamine, norepinepherine, and epinepherine

39. What do amphetamines stimulate?
a. areas of the brain associated with mental alertness like the cerebral cortex and thalamus

40. What is the pharmacologic action of amphetamines?
a. mood elevation or eupohoria, increased mental alertness and capacity for work, decreased fatigue and drowsiness, prolonged wakefulness, relaxation of bronchial smooth muscle, increased respiration, and dilation of pulmonary arteries

41. How do serotonin receptor agonists reduce migrane headache pain?
a. stimulate serotonin receptors in cerebral arteries and cause vasoconstriction

42. What is the original prototype SSRA?
a. sumatriptan (Imitirex)

Week 5-Chapter 17

43. What are adrenergics?
a. synthetic and naturally occurring substances

44. Why are adrenergics also called sympathomimetics?
a. mimic the effects of the SNS neurotransmitters of norepinepherine, epinepherine, and dopamine

45. You must know Table 17-1 on page 270 and what happens when alpha 1, beta 1 and beta 2 receptors are stimulated.
Adrenergic Receptor Responses to Stimulation

Body System --> Location --> Receptor --> Response

Cardiovascular:
*Blood Vessels
Alpha 1: Constriction
Beta 2: Dilation

*Cardiac Muscle
Beta 1: Increased Contractility

*Atrioventricular Node
Beta 1: Increased Heart Rate

*Sinoatrial Node
Beta 1: Increased Heart Rate

Endocrine
*Pancreas
Beta 1: Decreased Insulin Release

*Liver
Beta 2: Glycogenolysis

*Kidney
Beta 2: Increased Renin Secretion

Gastrointestinal
*Muscle
Beta 2: Decreased Motility

*Spinchters
Alpha 1: Constriction

Genitourital
*Bladder Spinchter
Alpha 1: Constriction

*Penis
Alpha 1: Ejaculation

*Uterus
Alpha 1: Contraction
Beta 2: Relaxation

Respiratory
*Bronchial Muscles
Beta 2: Dilation

Ocular
*Puppilary Muscles of Iris
Alpha 1: Mydriasis

46. What happens when a dopaminergic receptor is stimulated by dopamine?
a. cause vessels of renal, mesenteric, coronary, and cerebral arteries to dilate, increasing blood flow to these tissues

47. What happens when adrenergic drugs stimulate alpha 1 receptors?
a. vasoconstriction occurs on sites located on smooth muscle

48. What happens when adrenergic drugs stimulate beta 1 receptors?
a. increase force of contraction, increase in heart rate, and increase in the conduction of cardiac electrical nerve impulses through atrioventricular node

49. What happens when adrenergic drugs stimulate beta 2 receptors?
a. relaxation of bronchii, increased glycogenolysis, and increased renin secretion

Week 5-Chapter18

50. What is another name for an adrenergic blocker?
a. sympatholytic or adrenergic antagonist

51. What does alpha 1 adrenergic blockade lead to?
a. vasoconstiction of arterioles

52. What do ergot alkaloids cause?
a. peripheral and cerebral vasoconstriction as well as constriction of dilated arteries

53. What is an ergot alkaloid such as ergotamine (Ergostat) used for?
a. migraines and cluster headaches

54. What are the alpha blockers doxazosin, prazosin, terazosin, and tamsulosin used for?
a. venous and arterial vasodilation which lowers blood pressure

55. What are the two reasons prazosin is used?
a. treat hypertension and reduce urinary obstruction in men

56. What do beta adrenergic blocking drugs do?
a. lower HR, lower heart contractility, vasocontriction in the heart, and bronchoconstriction

57. Where are beta 1 receptors primarily located?
a. heart

58. Where are beta 2 receptors primarily located?
a. bronchioles

59. Distinguish cardioselective from nonselective beta blockers.
a. cardioselective beta blockers only block the beta receptors on the heart and nonselective beta blockers block receptors on the heart, bronchioles, and blood vessels

60. What is the effect of cardioselective beta blockade?
a. lowers HR, vasoconstriction, and lowers heart contractility

61. What happens to the bronchioles when beta 2 receptors are blocked?
a. bronchoconstriction

62. What happens to blood vessels when beta 2 receptors are blocked?
a. vasoconstriction

63. How might beta 2 blockade cause elevation of blood glucose?
a. impairs glycogenolysis

64. How does beta blockade raise blood triglyceride levels?
a. release free fatty acids from adipose tissue

65. How are some beta blockers useful in the treatment of angina?
a. lowers HR and contractility which leads to less oxygen consumption and relieves angina pain related to lack of oxygen

66. What is the mechanism for some beta blockers being cardioprotective?
a. inhibit stimulation of the heart muscles by circulating catecholamines

67. How might a beta blocker reduce the blood pressure?
a. lowers heart rate, contractility, and vasoconstriction

68. Page 291, right column under Assessment, the dotted bullets are very important information.
a. alpha blocking: cause block of the sympathetic stimulation of blood vessels which results in vasodilation and decrease in blood pressure
b. beta 1 blocking: cause block in sympathetic effects leading to lower HR, contractility and conduction which helpts treat dysfunctional irregularities in heart rate
c. beta 2 blocking: cause block in sympathetic effects on bronchial smooth muscle resulting in bronchoconstriction

69. When giving beta blockers, what SBP and HR measurements should the nurse use in determining when to notify the provider?
a. lower than 100 mm Hg or 60 bpm


Week 5-Chapter 19

70. What are the other terms for cholinergics?
a. cholinergic agonists and parasympathomimetics

71. What is the neurotransmitter responsible for transmission of effector cells in the PSNS?
a. acetycholine (Ach)

72. What are the two types of cholinergic receptors and what is it that stimulates them?
a. nicotinic receptors are stimulated by alkaloid nicatine and muscarinic receptors are stimulated by alkaloid muscarine

73. What does cholinesterase do?
a. enzyme responsible for breaking down acetylcholinesterase (AchE)

74. When cholinergic receptors are stimulated, what happens in the body?
a. permeability of cells changes and calcium and sodium are permitted to flow into the cell depolarizing the cell membrane to stimulate the effector organ

75. What are the indications or uses of cholinergic drugs?
a. reduce intraocular pressure for glaucoma patients or ocular surgery, treat various GI and bladder disorders, diagnose and treat myasthenia gravis, treat Alzheimer’s disease, and treat excessively dry mouth from Sjogren’s syndrome

76. How might cholinergics improve patient performance in Alzheimer’s?
a. replenish the brain of Ach for normal brain function

77. Page 302, right column under Assessment, the dotted bullets are very important information.
a. effects of cholinergic drugs:
-decrease in heart rate
-increase in GI and GU tone through increased contractility of the smooth muscle
-increase in the contractility and tone of bronchial smooth muscle
-increased respiratory secretions
-miosis (pupillary constriction)

Week 5-Chapter 20

78. What are the other terms for cholinergic blockers?
a. anticholinergics, parasympatholytics, and antimuscarine drugs

79. What do cholinergic blockers do?
a. block or inhibit actions of acetylcholine in the PSNS

80. What other class of ANS drugs do cholinergic drugs share the same effects with?
a. adrenergics

81. What are the major sites of action for anticholinergics?
a. heart, respiratory tract, GI tract, urinary bladder, eye, and exocrine glands

82. What do cholinergic blockers do to the eye?
a. causes pupil dilation and increased intraocular pressure
-Remember, cholinergic blockers might be detrimental to persons with glaucoma (abnormally high IOP) because they increase the IOP.

83. What is the effect of cholinergic blockers on the GI tract?
a. decreased GI motility, secretions, and salivation

84. What do cholinergic blockers do to the HR?
a. increase heart rate

85. What do they do to the bladder?
a. decrease bladder contraction leading to urine retention

86. What do they do to the skin?
a. reduce sweating

87. What do they do to the respiratory system?
a. dry mucous membranes and cause bronchial dilation

88. How do low doses of cholinergic blockers slow the HR?
a. effects cardiac center in the medulla

89. Table 20-1 on page 307 is important.
Cholinergic Blockers: Drug Effects

*Cardiovascular
Small Dose: decrease HR
Large Dose: increase HR

*Central Nervous
Small Dose: decrease muscle rigidity and tremors
Large Dose: cause drowsiness, disorientation, and hallucinations

*Eye
Dilate pupils, decrease accomodation by paralyzing ciliary muscles

*Gastrointestinal
Relax muscle tone, decrease intestinal and gastric secretions, decrease motility and peristalsis

*Genitourinary
Relax detrusor muscle of bladder, increase constriction of internal spinchter; may result in urine retention

*Glandular
Decrease broncial secretions, salivation, sweating

*Respiratory
Decrease bronchial secretions, dilate bronchial airways

pharmacology GRM week #4 (brief)

Week 4-Chapter 29

1. Which part of the CNS controls the pituitary?
a. hypothalamus

2. Know the functions of the hormones of the pituitary glands.
Anterior Pituitary:
Adrenocorticotropic Hormone (ACTH)
-Supports physical and emotional stress and starvation, redistributes body nutrients
Follicle-Stimulating Hormone (FSH)
-Stimulates egg and sperm growth/ production
Growth Hormone (GH)
-Promotes skeletal and muscular growth
Luteinizing Hormone (LH)
-Promotes secretions of sex specific hormones
Prolactin (PH)
-Stimulates mammary glands for lactation
Thyroid-Stimulating Hormone (TSH)
-Increases production and secretion of thyroid hormones

Posterior Pituitary:
Antidiuretic Hormone (ADH)
-Increases water retention and concentration of urine
Oxytocin
-Stimulates ejection of milk and contraction of uterine smooth muscle


Week4-Chapter 30

3. What is required in the diet in order to produce thyroid hormones?
a. iodide

4. What triggers the release of thyroid hormones?
a. thyroid stimulating hormone or thyrotropin

5. What is the most significant adverse effect of thyroid medications?
a. cardiac dysrhythmia with the risk for life-threatening or fatal irregularities caused by overdose

6. What might the effect of thyroid medications be on anticoagulants?
a. it may increase the activity of oral anticoagulants

7. What effect do thyroid medications have on digitalis levels?
a. increases potassium levels

8. When a patient is on thyroid medications and antidiabetic agents, how might this affect their antidiabetic medication dosing?
a. may need to increase dosing

Week 4-Chapter 32

9. What two hormones does the adrenal medulla secrete?
a. norepinepherine and epinepherine

10. What are the other names for epinephrine and norepinephrine?
a. adrenaline and noreadrenaline

11. What are the two types of hormones secreted from the adrenal cortex (corticosteroids)?
a. glucocorticoids and mineralocorticoids

12. What affect does aldosterone have on serum sodium?
a. it maintains sodium homeostasis by reabsorbing it

13. What affect does aldosterone have on serum potassium?
a. in affect, serum potassium is decreased

14. How does ACTH affect the adrenal cortex?
a. stimulates the production of corticosteroids

15. What is the disorder in which there is an oversecretion of adrenocortical hormones?
a. Cushing’s syndrome: redistribution of fat from the arms and legs to face, shoulders, trunk; retention of water and loss of potassium

16. What is the disorder in which there is an undersecretion of adrenocortical hormones?
a. Addison’s disease: low blood sodium and glucose levels, high potassium levels, dehydration and weight loss

17. Which is the only corticosteroid drug with exclusive mineralocorticoid activity?
a. fludrocortisone

18. What is the main effect of cortisol?
a. inhibition of inflammatory and immune responses

19. In what specific ways do glucocorticoid inhibit or help control the inflammatory response?
a. stabilize cell membranes of inflammatory cells called lysosomes, decreasing capillary permeability to inflammatory cells, and decrease the migration of white blood cells into already inflamed areas

20. What is the effect of glucocorticoids on protein metabolism?
a. loss of muscle mass and muscle weakness

21. What is the effect of glucocorticoids on glucose?
a. weight gain

22. What is the effect of glucocorticoids on fat distribution?
a. redistributes fat to face, shoulders, and trunk

23. Why is it best to give exogenous glucocorticoids early in the morning?
a. leads to the least amount of adrenal suppression; from 0600-0900

24. How does the nurse minimize the patient’s gastric upset when giving oral glucocorticoids?
a. administer with milk, food, or non-systemic antacids

25. What should the patient be advised to avoid when taking corticosteroids?
a. avoid alcohol, NSAIDS, and aspirin

26. Why should abrupt withdrawal of glucocorticoid hormones be avoided?
a. could lead to life threatening Addisonian crisis marked by fatigue, nausea, vomiting, and hypotension

27. What are the instructions that should be given to a patient using nasally instilled glucocoricosteroids?
a. rinse mouth with luke warm water

28. Why should the patient rinse his mouth after using an orally inhaled glucocorticoid?
a. prevent fungal overgrowth

29. What effect does long-term glucocorticoid therapy have on post-surgical healing?
a. increased healing time