unit 4 exam

Question 1

1. What are the two major types of hypertensions?

Answer 1

essential hypertension and secondary hypertension.

Question 2

2. What are the factors that affect blood pressure?

Answer 2

Factors include age, gender, family history, obesity, diet, physical inactivity, excessive alcohol consumption, smoking, stress, and certain medical conditions.

Question 3

What are the JNC guidelines for classifying and treating HTN?

Answer 3

The 2017 AHA/ACC guideline categorizes BP as:
* Normal: SBP<120 and DBP<80 mm Hg
* Elevated: SBP120-129 and DBP<80mm Hg
* Stage 1 HTN: SBP 130-139 or DBP 80-89 mm Hg
* Stage 2 HTN: SBP >140 or DBP >90 mm Hg.
* Note: If a person’s SBP and DBP are in 2 different
categories, the category with the higher BP should
be used.

Treatment:
Lifestyles should be implemented first.
* If these fail to adequately lower BP, drug therapy
should be started while continuing lifestyle
changes
Treatment often begins with single drug.
* If needed, another drug may be
* added (if initial drug well-tolerated or inadequate) or
* substituted (if initial drug poorly tolerated).
* Before adding another drug, assess possible
reasons for failure of initial drug:
* Nonadherence to drug regimen
* Insufficient dosage
* Excessive salt intake
* Presence of secondary HTN

Question 4

4. How do diuretics
   treatment HTN? What are the side common side effects of this drug category?

Answer 4

Diuretics:
Treatment:
Increase formation and excretion of urine
* Increase renal excretion of water and sodium,
decreasing volume of fluid within vascular system.
* Analogous to decrease in pressure inside balloon which
occurs if some of the air in balloon is left to leak out.
* Often first-line drugs to treat hypertension
Side effect:
Fluid depletion and electrolyte imbalance, Fluid depletion and electrolyte imbalance, Fluid depletion (decrease in blood volume) may cause
reflex increase in CO and PVR due to baroreflex
activation, Hyperlipidemia
Hyperglycemia
* Other
* GI disturbances
* Weakness/fatigue
* Orthostatic hypotension
* Changes in mood/confusion
* Hearing loss-loop diuretics

Question 5

How do beta blocker
treatment HTN? What are the side common side effects of this drug category?

Answer 5

Exert primary effect on heart (blocking beta-1receptors)
decreasing HR and force of myocardial contraction (SV).
* Lower BP by decreasing HR and CO
Usually well-tolerated, incidence side effects is low
* Nonselective beta-blockers (affinity for both beta-1
and beta-2 receptors) may produce
bronchoconstriction in asthma and COPD patients.
* C-V side effects
- Excessive depression of HR
- Depression of myocardial contractility (may worsen HF)
- Orthostatic hypotension
* Hyperglycemia
- Inhibit insulin secretion/generate insulin resistance
- Mask signs of and delay recovery of hypoglycemia in
diabetic patients on insulin
Hyperlipidemia
Others
* Depression
* Fatigue
* Decreased exercise tolerance
* GI disturbances
* Erectile dysfunction
* Vivid dreams and hallucinations
* Sudden withdrawal may lead to exacerbation of
angina and MI

Question 6

How do alpha blocker
treatment HTN? What are the side common side effects of this drug category?

Answer 6

Drugs that block alpha-1 adrenergic receptors on vascular
smooth muscle promote a decrease in vascular resistance.
* Since peripheral vascular resistance is often increased in
essential hypertension, these drugs have an antihypertensive
effect.
* Sometimes used in more severe cases of essential
hypertension

Side effects: reflex tachycardia, orthostatic hypotension

Question 7

How do ACE inhibitors
treatment HTN? What are the side common side effects of this drug category?

Answer 7

Renin-angiotensin-aldosterone system becomes overactive.
* By inhibiting angiotensin converting enzyme (ACE), these drugs
prevent conversion of angiotensin I to angiotensin II,
decreasing angiotensin II levels and activity.
* Results in decreased PVR, and decreased fluid retention by
kidneys (decreased aldosterone release), resulting in a
decreased BP
Adverse Effects–Well-tolerated in most patients
* Allergic reaction–skin rash, angioedema (swelling) of face and oral cavity.
* Persistent cough—due to increased bradykinin
* Alteration in taste sensation (captopril)
* Others–gastrointestinal discomfort, dizziness, chest pain

Question 8

How do ARBS
treatment HTN? What are the side common side effects of this drug category?

Answer 8

Mechanism of Action
* Block binding of angiotensin II to type I angiotensin II
(AT-1) receptors in blood vessels and other tissues.
* Produce vasodilation
* Inhibit aldosterone release from adrenal cortex.
* Like ACE inhibitors, are less effective in black patients.

Adverse Effects
* Low incidence of dizziness
* Cough is not a problem
* Angioedema has not been reported
* Hyperkalemia may occur, but not usually severe enough
to discontinue drug.

Question 9

How do vasodialators
treatment HTN? What are the side common side effects of this drug category?

Answer 9

Directly vasodilate the peripheral vasculature,
decreasing PVR.
* Other drugs (alpha-blockers) ultimately produce
vasodilation by interrupting adrenergic supply to
vasculature.
* Vasodilator drugs exert inhibitory effect directly on
vascular smooth muscle.
* Vasodilators inhibit smooth muscle contraction by
increasing intracellular production of “second
messenger” such as cyclic GMP.
* Increased amounts of cGMP inhibit function of contractile
process in vascular smooth muscle cell, leading to vasodilation
Adverse Effects
* Reflex tachycardia
Baroreflex responses attempting to compensate for fall in PVR
produced by these drugs.
Often used with beta-blocker to minimize
* Fluid retention
Often used with diuretic to minimize.
* Rheumatoid arthritis or systemic lupus erythematosus-
like syndrome with prolonged use of hydralazine
Others:
* dizziness
* postural hypotension
* weakness
* nausea
* headaches
* Minoxidil–increases hair growth on face, ears,
forehead, and other hairy body surfaces.
- cause for discontinued use in women
- marketed as hair-growth stimulus (Rogaine) to treat
baldness.

Question 10

How do calcium channel blocker
treatment HTN? What are the side common side effects of this drug category?

Answer 10

Selectively block calcium entry into vascular smooth
muscle cells
calcium plays role in activating contractile element in
smooth muscle in same way that calcium “activates“
actin-myosin interaction in skeletal muscle cells.
* Drugs inhibiting calcium entry into vascular smooth
muscle cells inhibit contractile process, leading to:
* Vasodilation
* Decreased vascular resistance
* Calcium channel blockers also tend to decrease HR and
force of myocardial contraction (non-dihydropyridine CCBs)
Adverse effect:
Dihydropyridines
* Dizziness
* HA,
* Peripheral edema (swelling in feet and ankles)—more common than
with nondihydropyridines.
* Flushing
* Reflex tachycardia (secondary to excessive vasodilation)
* Rash
* Gingival hyperplasia
Nondihydropyridines
* Dizziness
* HA,
* Edema
* Constipation (especially verapamil)
* AV block
* Bradycardia
* Lupus-like rash with diltiazem.
May have heart failure

Question 11

How do direct renin inhibitors
treatment HTN? What are the side common side effects of this drug category?

Answer 11

Aliskiren (Tektura)
* Binds renin, leading to reduced levels of angiotensin I,
angiotensin II, and aldosterone.
* Can be used alone in treatment of HTN or combined
with other hypertensive agents.
* Does not cause cough seen with ACEIs; low incidence of
angioedema in clinical trials.

Adverse effect:
* Nausea and vomiting
* Diarrhea
* Rash
* Cough
* Hyperkalemia (increase in potassium levels in the blood)
* Severe hypotension (low blood pressure)
* Dizziness
* Headache
* Angioedema (accumulation of fluid cause swelling of the area below the skin or mucosa)
* Tiredness
* Chest pain
* Rhabdomyolysis (muscle injury)
* Toxic epidermolysis (severe skin reaction)
* Hyponatremia (decreased sodium levels)
* Renal stones
* Increased serum creatinine
* Hyperuricemia (high uric acid levels in the blood)
* Anaphylaxis (life-threatening allergic reactions)

Question 12

What are common drugs used to treat angina pectoris and what are their mechanisms of
action?

Answer 12

Three families of antianginal agents
 Organic nitrates decrease –decrease myocardial O2
demand.
* Nitroglycerin
 Beta blockers–decrease myocardial O2 demand.
* Example: Metoprolol
 Calcium channel blockers—increase myocardial O2
supply.
* Example: Verapamil
 Ranolazine
 Newer drug with limited indications
 Can be combined with other drugs

Question 13

8. How is congestive heart failure defined?

Answer 13

Congestive heart failure is a condition where the heart is unable to pump blood effectively, leading to fluid buildup in the lungs and other tissues.

congestive heart failure
(CHF) due to the accumulation of fluid in lungs and peripheral that often accompanies this disorder.
however, many patients do not have signs of congestion—hence the name change.

Question 13

What is the etiology of coronary artery disease? What are common disease states
associated with coronary artery disease?

Answer 13

Coronary artery disease is often caused by atherosclerosis. Common disease states associated with it include angina pectoris, myocardial infarction (heart attack), and heart failure.
CAD happens when coronary arteries struggle to supply the heart with enough blood, oxygen, and nutrients. Cholesterol deposits, or plaques, are almost always to blame. These buildups narrow your arteries, decreasing blood flow to your heart. This can cause chest pain, shortness of breath or even a heart attack.

Question 14

6. How do nitrates work in the management of angina pectoris?

Answer 14

Organic nitrates decrease –decrease myocardial O2
demand.
* Nitroglycerin
Nitrates relax and dilate blood vessels, leading to increased blood flow to the heart muscle and decreased oxygen demand.

Question 15

What is the pathophysiology and corresponding signs/symptoms associated with heart
failure?

Answer 15

Pathophysiology: Mechanisms underlying HF are complex.
* Involve disturbances in myocardial pumping ability as well as systemic changes in nervous/endocrine
systems.
* Body’s compensatory mechanisms often lead to vicious cycle, which make condition progressively
worse.

Signs and symptoms:
* Shortness of breath with activity or when lying down.
* Fatigue and weakness.
* Swelling in the legs, ankles and feet.
* Rapid or irregular heartbeat.
* Reduced ability to exercise.
* Wheezing.
* A cough that doesn’t go away or a cough that brings up white or pink mucus with spots of blood.
* Swelling of the belly area.
* Very rapid weight gain from fluid buildup.
* Nausea and lack of appetite.
* Difficulty concentrating or decreased alertness.
* Chest pain if heart failure is caused by a heart attack.

Question 16

10. What are common drugs used to treat HF and how do they work?

Answer 16

• Drugs that inhibit the RAAS
  – ACE inhibitors/Angiotensin Receptor Blockers—
• Reduce Angiotensin II levels, resulting in vasodilation, reducing preload and afterload.
• Reduce aldosterone release, reducing extracellular fluid.
  – Angiotensin receptor neprilysin inhibitors (ARNIs) (Entresto)
• Same benefits as ACE inhibitors/ARBs plus inhibits breakdown of natriuretic peptides
• Mineralocorticoid Receptor Antagonists (MRAs) aka Aldosterone
  antagonists—reduce extracellular fluid and abnormal cardiac
  remodeling.
• Beta blockers—reduce excessive sympathetic stimulation of cardiac
  myocytes, allowing them to return to a normal level of functioning.
• Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors—reduce risk
  of hospitalization in HF patient.

Other agents, depending on patient specific factors:
– Diuretics—reduce extracellular fluid volume
– Inotopic Agents
* Digoxin—increases myocardial contractility
* Sympathomimetic Drugs
– Dopamine—increases myocardial contractility
– Dobutamine—increases myocardial contractility
* Phosphodiesterase Inhibitors
– Milrinone—increases myocardial contractility and promotes vasodilation
– Vasodilators (other than ACE inhibitors and ARBs)
* Isosorbide dinitrate plus hydralazine
– Ivabradine (Corlanor)—dose-dependent reduction in HR
– Soluble guanylyl cyclase (sGC) stimulators (e.g., vericiguat)—
produces smooth muscle relaxation and vasodilation.

Chatgpt: Common drugs include ACE inhibitors, beta-blockers, diuretics, and aldosterone antagonists. They work by reducing afterload, improving contractility, and managing fluid balance.

Question 17

To what receptors do the opioid analgesics bind, and what responses are produced?

Answer 17

Opioid analgesics primarily bind to mu-opioid receptors in the central and peripheral nervous system in an agonist manner to elicit analgesia. Activation of these receptors produces analgesia (pain relief), sedation, and a sense of euphoria.
Analgesics are drugs that relieve pain without causing the loss of consciousness.

Question 18

What is the role of cardiac glycosides (digitalis) in management of HF?

Answer 18

Cardiac glycosides inhibit enzyme adenosine triphosphatase
(ATPase), which energizes Na+/K+ pump.
* Leads to accumulation of Na+ ions inside heart muscle cells.

Basically: Cardiac glycosides, such as digoxin, are used in heart failure to increase the force of the heart’s contractions. They do this by inhibiting the sodium-potassium pump, leading to an** increase in intracellular sodium,** which, in turn, increases intracellular calcium. This increased calcium enhances cardiac contractility.

Question 19

What are symptoms of opioid withdrawal?

Answer 19

Defined as state in which an abstinence (withdrawal) syndrome will occur if drug use is abruptly
discontinued
* Expected consequence of chronic opioid use.
* Occurs more commonly when opioid has been used in
high doses over prolonged periods (>20 days)
* Adaptive biochemical changes occur in response To continuous use, and body requires continued
presence of opioids to function normally.
* Can be precipitated by administration of an opioid antagonist such as naloxone.

Abstence syndrome:
* For those highly dependent, can be very unpleasant
* Syndrome is rarely dangerous (in contrast to withdrawal from CNS
depressants e.g., barbiturates, alcohol which can be lethal).

• Onset usually occurs about 10 hours after last dose.
• Early symptoms:
• yawning
• rhinorrhea
• sweating
• Followed by:
• anorexia
• irritability
• tremor
• gooseflesh—”cold turkey
  Peak response occurs in 3 to 5 days
• violent sneezing
• nausea, vomiting, diarrhea, abdominal cramps
• bone and muscle pain, muscle spasm and kicking movements-“kicking the habit”
• Administration of opioids will rapidly reverse all signs and symptoms.
• Left untreated–syndrome runs course in 7 to 10 days

Question 20

. What drug is most commonly used to reverse opioid toxicity?

Answer 20

Naloxone is commonly used to reverse opioid toxicity by competitively binding to opioid receptors, blocking the effects of opioids. It is an opioid antagonist—meaning that it binds to opioid receptors and can reverse and block the effects of other opioids, such as heroin, morphine, and oxycodone.

Question 21

What are the uses of opioids other than pain management?

Answer 21

Cough suppression
* Morphine-like drugs act at opioid receptors in medulla to
suppress cough.
* Opioids are used as antitussives:
-Codeine
-Hydrocodone
-Dextromethorphan–low abuse potential, preparations containing are usually OTC.
* Antitussive doses considerably lower than analgesic doses.
* Diarrhea
* Opioid agonists decrease gastrointestinal motility
-Diphenoxylate + atropine sulfate (Lomotil)
-Loperamide (Immodium)
-Preoperatively–for sedation and reduction of anxiety.
* Adjunct in General Anesthesia
-Used in induction and maintenance of surgical anesthesia.
-Example–fentanyl [Sublimaze]

Dyspnea associated with left ventricular failure
* Morphine—no longer drug of choice
* Vasodilating effects reduces pulmonary edema
* Reduces feelings of intense panic and anxiety associated
with dyspnea.
* Patients feel they can breathe better.
* Myocardial Infarction
* Morphine—no longer drug of choice
* Reduces comfort without excessive resp.depression and
adverse CV effects.
* By reducing BP can decrease cardiac work

ChatGPT: Opioids are sometimes used in the treatment of severe cough, as antitussives, and in some cases of severe diarrhea.

Question 21

What are endorphins?

Answer 21

endorphins are endogenous (naturally occurring in the body) neurotransmitters that act as natural painkillers. They bind to opioid receptors and reduce the perception of pain.
Endorphin—derived from endogenous and morphine.
- Endorphins have been shown to be 4 times more potent than morphine.

Question 22

What are the therapeutic uses of NSAIDs?

Answer 22

NSAIDs Inhibit cyclooxygenase enzyme, and hence
decrease prostacyclin, prostaglandin, and
thromboxane synthesis.
- Aspirin irreversibly inhibits cyclooxygenase; all other
NSAIDs are reversible inhibitors of COX.
- By interfering with prostaglandin synthesis, the NSAIDs
reduce the inflammatory process, pain and fever.
* The three primary actions of NSAIDs, including ASA
are anti-inflammatory, analgesic, and antipyretic.
* ASA can be though of as a traditional NSAID, but it
exhibits anti-inflammatory activity only at relatively
high doses that are rarely used.** Used more
commonly today at lower doses for prevention of CV
events such as stroke and MI**

Google: Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used to manage the pain and inflammation (swelling and redness) associated with some types of arthritis (such as rheumatoid arthritis) and other musculoskeletal disorders.

Question 23

What is the central mechanism of action of the NSAIDs?

Answer 23

The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins.[9] The therapeutic effects of NSAIDs are attributed to the lack of these eicosanoids.

Chatgpt: NSAIDs work by inhibiting the enzyme cyclooxygenase (COX), which is involved in the synthesis of prostaglandins. Prostaglandins play a role in inflammation, pain, and fever.

Question 24

What are common adverse effects of aspirin and the NSAIDs?

Answer 24

NSAIDS:
dyspepsia
* epigastric pain
* nausea
* vomiting
* abdominal cramps
* peptic ulceration
* NSAID-induced gastropathy can lead to hemorrhage and perforation,
often without warning.
* Proposed as most frequent serious adverse drug effect in United
States.
* FDA requires black box warning for all NSAIDs regarding increased
risk of serious GI adverse events with use.

Aspirin:
GI disturbance

Chatgpt: heart burn, Adverse effects can include gastrointestinal irritation, peptic ulcers, increased bleeding risk, and impaired kidney function.

Question 25

How does acetaminophen differ from the NSAIDs in terms of therapeutic activity?

Answer 25

What is acetaminophen? This OTC medicine is not an NSAID; it can ease mild-to-moderate pain and bring down a fever, and it tends to cause fewer stomach problems than other OTC pain relievers. But, unlike NSAIDs, it does not treat inflammation.
Acetaminophen has analgesic (pain-relieving) and antipyretic (fever-reducing) properties but lacks significant anti-inflammatory effects, which are present in NSAIDs.

Question 26

What OTC drug is safest for management of pain in pediatric patients recovering from
the flu?

Answer 26

Acetaminophen (e.g., Tylenol) mainly. Or ibuprofen (Advil, Motrin IB)

Question 27

What are therapeutic effects of glucocorticoids (corticosteroids)?

Answer 27

Therapeutic use:
* Inflammatory disorders (e.g., rheumatoid arthritis, asthma)
* Certain cancers
* Suppression of immune responses in transplant patients.

Glucocorticoids can reduce how active immune cells are. This helps reduce the internal damage from these diseases. They suppress inflammation from autoimmune reactions. This can reduce pain, swelling, cramping, and itching.

anti-inflammatory, immunosuppressive, anti-proliferative, and vaso-constrictive effects

Question 28

What is a physiologic vs. a pharmacologic dose of a corticosteroid?

Answer 28

Physiologic effects
* Elicited by low doses
* Example: modulation of glucose metabolism
* Therapeutic use: treatment of endocrine disorders (e.g.,
adrenocortical insufficiency)
Pharmacologic effects
* Higher dosages
* Example: suppression of inflammation

Question 29

What are mineralocorticoid properties of corticosteroids?

Answer 29

Salt, water.
Some corticosteroids have mineralocorticoid activity, influencing salt and water balance.
The term “mineralocorticoid” is used to describe those actions of adrenal corticosteroids producing sodium and fluid retention and potassium excretion. The most important physiological mineralocorticoid is aldosterone, which, like other mineralocorticoids, acts on a specific mineralocorticoid receptor (MR).

Question 30

What is the mechanism of action of the corticosteroid anti-inflammatory drugs?

Answer 30

Corticosteroids exert their anti-inflammatory effects through influencing multiple signal transduction pathways. Their most important action is switching off multiple activated inflammatory genes through inhibition of HAT and recruitment of HDAC2 activity to the inflammatory gene transcriptional complex.

Inhibition of chemical mediators of inflammatory
process (prostaglandins and leukotrienes)
* Glucocorticoids promote synthesis of a protein that
inhibits phospholipase A2 enzyme.
* Phospholipase A2 liberates phospholipids from cell
membranes so that they can be transformed into
prostaglandins and leukotrienes.
* By inhibiting this enzyme, glucocorticoids prevent
production of prostaglandins and leukotrienes.
Inhibition of chemotaxis
* Suppress migration of macrophages such as neutrophils
and monocytes.
* Normally attracted to inflammatory sites by chemotactic
factors, released by various chemical cells.
* Glucocorticoids appear to inhibit release and function of
these chemotactic factors.
* Stabilization of lysosomes
* Glucocorticoids appear to stabilize lysosomal
membranes, making them less susceptible to rupture.
* Help prevent subsequent damage that contribute to
inflammatory response.

Glucocorticoids suppress inflammation by more
diverse mechanisms than the NSAIDs, which
primarily reduce inflammation by inhibition of
prostaglandin synthesis only; glucocorticoids share
this mechanism with NSAIDs plus others and hence
have a much more powerful anti-inflammatory
effects than NSAIDs.

Question 31

What are the most serious adverse effects of corticosteroids?

Answer 31

The most common adverse effects of corticosteroids include osteoporosis and fractures, suppression of the hypothalamic-pituitary-adrenal (HPA) axis, Cushingoid features, diabetes and hyperglycemia, myopathy, glaucoma and cataracts, psychiatric disturbances, immunosuppression, cardiovascular disease, gastrointestinal and dermatologic adverse effects.[2] In general, the synthetic corticosteroids (e.g., prednisone, methylprednisone, dexamethasone, and betamethasone) tend to have more Cushingoid and suppression of HPA axis function and little mineralocorticoid, androgenic or estrogenic effect.

Slides: adrenal insufficiency, peptic ulcer disease, glucose intolerance, myopathy, osteoporosis, infection, fluid and electrolyte disturbance, delayed growth, cataracts and glaucoma, cutaneous atrophy, psychologic disturbance, iatrogenic cushion syndrome, hirsutism,

Chatgpt: Serious adverse effects include immunosuppression, osteoporosis, and metabolic effects such as hyperglycemia.

Question 32

What effects do corticosteroids have on metabolism in the body?

Answer 32

Metabolic effects–Influence metabolism of
carbohydrates, proteins, and fats.
* Carbohydrate metabolism–principal effect
elevation of blood glucose levels.
- Promote synthesis of glucose from amino acids
(gluconeogenesis)
- Reduce peripheral glucose utilization (reduces glucose
uptake into muscle and fat cells) thereby allowing more
glucose to remain in the bloodstream.
- Promotes storage of glucose as glycogen
Protein metabolism–unfavorable impact
- Suppress synthesis of proteins from amino acids.
- Divert amino acids for production of glucose
* Results in:
Reduction in muscle mass
Thinning of the skin
Decrease in protein matrix of bone
Nitrogen balance becomes negative
* Fat metabolism
- Stimulation of lipolysis (fat breakdown)–principal effect.
- Fat redistribution occurs with long-term high dose therapy
(symptoms same as seen in Cushing’s disease).
Central obesity–pot belly
Rounded face–“moon face”
Fat-pad in cervical spine–“buffalo hump

Question 33

How does pattern of use relate to corticosteroid toxicity?

Answer 33

Determined by pattern of use
* Devoid of toxicity
- When used in physiologic doses
- When taken acutely, even when dosage is extremely large
* Pharmacologic doses for extended periods can produce
multiple, adverse effects.
* All glucocorticoid drugs can elicit same therapeutic
effects
- Differences primarily pertain to duration of action and
side effects.

Question 34

Define tolerance, abuse, pseudoaddiction, and addiction as they relate to opioid use.

Answer 34

Abuse:
Abuse
- Drug use that is inconsistent with medical or social norms
* Morphine and opioids subject to abuse, due to ability to
cause pleasurable experience
- Euphoria, sedation, sensation in lower abdomen resembling sexual
orgasm.
* Physical dependence contributes to abuse
-Once dependence exists, the ability of opioids to ward off withdrawal serves
to reinforce desirability by abuser.
* Abuse liability reflected in classification under Controlled
Substances Act.
-Morphine and all other strong opioids are classified under Schedule
II.
* Most of the moderate to strong opioids are classified as schedule III
or IV, especially when combined with aspirin or acetaminophen
(e.g., Tylenol with Codeine) since abuse potential is lower
Addiction:
defined as a constellation of behaviors surrounding
the use of opioids for purposes other than pain relief.
* Behavior pattern characterized by continued use of a
psychoactive substance despite physical, psychologic,
or social harm.
-loss of control over drug use (e.g., compulsive overuse and
craving).
- preoccupation with the drug (e.g., refusal to comply with
other therapeutic recommendations; insistence on use of
the drug).
- continued use despite consequences (e.g., oversedation)
* Addiction is a neurobiologic disease that is not a
natural consequence of chronic opioid use for pain
management.
* Development of addiction is influenced by genetic,
psychological, social and environmental factors, as
well as drug exposure
* Cravings result in repeated relapse to opioid use, even
in the presence of powerful consequences and strong
motivation.
* Often leads to significant emotional and behavioral
problems, including problems at home or work.
* Most pain experts believe addiction is very
uncommon among patients with no history of
substance abuse or addiction.
* To minimize physical dependence and abuse, opioid
analgesics should be administered in the lowest
effective doses for the shortest time needed
Pseudoaddiction
* Drug seeking behaviors that occur when pain is
undertreated and mimic addictive behaviors.
* Once pain is controlled, these patients use medications as
prescribed without addiction.
Tolerance:
Defined as a state in which a large dose is required to produce
the same response that could formerly be elicited by a small
dose.
* Natural state of adaptation; should be anticipated in patients on
chronic therapy.
* Tolerance develops to some, but not all effects of opioids.
* With prolonged treatment, tolerance develops to
-analgesia
- euphoria
- sedation
- respiratory depression
* Very little tolerance develops to:
- constipation
- urinary retention
- miosis
* Tolerance can be conferred from one opioid agonist to others (cross-
tolerance)

Question 35

If a patient has received a corticosteroid for a prolonged period of time (e.g. two
months), how should infection or trauma be managed? How should the drug be
discontinued?

Answer 35

Patient’s receiving long-term glucocorticoid therapy
must be given increased doses at times of stress (unless
dosage is already high)
Once glucocorticoid therapy has ceased, supplemental
doses are required whenever stress occurs until recovery
of adrenal function is complete.

Question 35

Patients with what disease state are most likely to experience an allergic reaction with
aspirin?

Answer 35

Aspirin sensitivity is most often manifested as rhinitis and asthma or urticaria/angioedema induced by cross-reacting nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase

Question 36

A patient with angina pectoris is prescribed sublingual
nitroglycerin. Which statement made by the patient
indicates understanding of the medication teaching?
A. “I may experience a headache as a side effect.”
B. “The chest pain should be relieved within 20 minutes.”
C. “I should swallow the tablet and drink a glass of water.”
D. “I should take this medication in the morning before
breakfast.

Answer 36

A

Question 37

A physician assistant teaches a patient diagnosed with chronic
stable angina about the mechanism of action of nitroglycerin.
The PA should include which instruction?
A. “Nitroglycerin reduces vasospasms of the heart’s arteries,
which improves blood supply.”
B. “Nitroglycerin opens the arteries to allow more oxygen to be
delivered to the heart muscle.”
C. “Nitroglycerin dilates veins, which decreases the amount of
oxygen needed by the heart.”
D. “Nitroglycerin improves blood flow to the heart muscle by
increasing blood pressure.”

Answer 37

C