MIDTERM EXAM Flashcards

1
Q

Define Pharmacokinetics

A

Describes the process of drug absorption, drug distribution, drug metabolism, and drug execration

Study of metabolism an action of drugs within the body including absorption, duration of action, distribution of drug in the body and method of excretion.

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2
Q

Know the difference between antagonists and agonists

A

Antagonist – drug that binds to a receptor and interferes (blocks) with other drugs or substances from producing a drug effect

Agonist - Drug that binds to a receptor and activates a physiologic response or drug action

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3
Q

Know the difference between the generic name and brand name of drugs

A

Generic Name- the official established Nonproprietary name of a drug and is descriptive of its chemical structure.

(Nonproprietary -not registered or protected as a trademark or brand name; generic.)

Brand Name (Trade Name)- Patented proprietary name of a drug sold by a specific drug manufacturer; also referred to as the brand name

(Proprietary- trade name and is protected by a patent)

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4
Q

Know which Act was designed to regulate the dispensing of drugs that have the potential to be misuse

A

Federal Comprehensive Drug Abuse Prevention and Control act. This act, commonly referred to as the CONTROLLED SUBSTANCES ACT, was started in 1970-amdended in 1990.

This act is designed to regulate the dispensing of drugs called controlled substances that have a potential for abuse. The controlled drugs are assigned to one of 5 schedules, depending on their medical usefulness and potential for abuse. This act is enforced by the DEA.

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5
Q

Define teratogens

A

Cause birth defects // an agent or factor which causes malformation of an embryo

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6
Q

Define the different pharmacokinetic processes: drug absorption, drug distribution, drug metabolism, and drug excretion

A

Drug absorption- entrance of a drug into the blood stream from its site of administration

Drug distribution-passage of a drug from the blood to the tissues and organs of the body// moving from the blood to the organ

Drug metabolism-the enzymatic biotransformation of a drug into metabolites// conversation of the drug into its metabolites (metabolites cause action)

Drug excretion- elimination of the drug from the body

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7
Q

Understand that the factor that plays the biggest role in drug distribution to overcome the blood-brain barrier is lipid solubility of the drug

A

Because the brain is composed of a large amount of lipid (nerve membranes and myelin) Lipid soluble drugs easily cross the blood brain burrier. As a general rule- then, a drug must have a certain degree of lipid solubility if it is to penetrate this barriers and gain access to the brain

  • Cell membranes are composed of a significant amount of lipid material
  • In general, the more lipid soluble a drug is, the faster it will pass through a lipid substance like the cell membrane.
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8
Q

What is the difference between a loading dose and maintenance dose

A

Loading dose- initial drug dose administered to rapidly achieve therapeutic drug concentrations

Maintenance dose-dose administered to maintain drug levels in the blood in the therapeutic range

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9
Q

Identify the different routes of drug administration

A

Nonparental administration- oral medications, liquid, ophthalmic, inhalation, supposit rectally, nasal, transdermal (patch), (everything other than a needle)

Parenteral Administration- (injection) Intramuscular (IM), Intravenous (IV), Subcutaneous, Intradermal, Subdermal

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10
Q

Determine the main effect aging has on drug distribution

A
  • Because cardiac output decreases by 1% each year after turning 25 or 30 years of age. This means by the age of 65 the liver and kidneys for example are receiving significantly less blood per minute than they did 40 years ago at age 25.
  • the percentage of lean body mass (muscle) and the percentage of total body water decrease with age. As the percentage of water decreases the same dose will produce higher concentration of drug in the body. As one becomes older the same dosage of drug given to a younger adult will produce a higher drug concentration in elderly
  • the percentage of body fact increases with age, causing lipid-soluble drugs to be more widely distributed to the body organs that have a high fat content, such as adipose tissue and muscle and away from the liver and kidneys. – since the liver and the kidneys are responsible for the drug metabolism and execration of the drug from the body. The drug will have a longer half life and duration of action
  • overall effects of aging on drug distribution is to generally make any adult drug dosage produce greater pharmacological effects in the elderly if the drug is given in the same dosage so a smaller dosage is required for elderly.
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11
Q

Define the following – drug tolerance, drug dependence

A

Drug Tolerance- decreased drug effect occurring after repeated drug administration

Drug Dependence- condition of reliance on the use of a particular drug characterized as physical and/or psychological dependence

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12
Q

Know the difference between the sympathetic and parasympathetic nervous system- what occurs in the body with each

A

Sympathetic Nervous system- part of the autonomic nervous system causing increased heart rate, increased blood pressure, increased breathing rate, and will decrease digestion. All in which help us run away from a tiger. Coined as fight or flight.

Parasympathetic Nervous system- is part of the autonomic nervous system coined as rest and digest. Decreases heart rate, decreases blood pressure, decreased breathing rate, increases digestion

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13
Q

Know which muscles are affected by norepinephrine

A

Smooth Muscle (vasoconstrict- decrease the lumen)

(Lumen- lumen is the inside space of a tubular structure, such as an artery or intestine. It comes from Latin lumen ‘an opening’. It can refer to: The interior of a vessel, such as the central space in an artery, vein or capillary through which blood flows.)

Cardiac Muscles(increase contraction)

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14
Q

Know the correct use of and EpiPen auto injector

A

Orange tip against the middle of the outer thigh at a right angle push auto injector firmly until it clicks and hold in place for three seconds and then massage injection sight for 10 seconds.

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15
Q

Most common side effect of decongestants

A

Irritation of the nasal sinuses or eyes due to excessive dryness caused by the vasoconstrictive decrease in blood flow.

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16
Q

Understand the difference between the neurotransmitter of the parasympathetic system and the neurotransmitter of the sympathetic system

A

Norepinephrine (NE)- neurotransmitter of sympathetic (adrenergic) nerves that stimulates the adrenergic receptor.

Acetylcholine (ACH)- neurotransmitter of parasympathetic (cholinergic) nerves; stimulates the cholinergic receptor.

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17
Q

Acetylcholine is stored in nerve endings, what causes it to be released

A

Stimulation of the preganglionic nerve fibers cause ACH to be released

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18
Q

What can excessive CNS depression produce in an individual

A

Slow speech, Lethargy, uncoordinated movements, but extreme would be death.

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19
Q

Advantages of benzodiazepines over barbiturates

A

Benzodiazepines Don’t interfere with rem sleep, they produce less tolerance, therefore are effective for a few weeks longer, less physical dependence.

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20
Q

Define automatism

A

Drug induced confusion that can cause increased drug consumption

an action performed unconsciously or involuntarily.

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21
Q

What are some patient instructions for antianxiety drugs

A

Don’t drive, drink alcohol, no cns depressants, no barbiturates,

Instruct patient to report excessive sedation, mental disturbances, or loss of memory

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22
Q

What effect do benzodiazepines have on patients

A

Produce skeletal muscle relaxation in various musculoskeletal disturbances, as anti convulsant and antiepileptic drugs, and as sedatives and hypnotics// feel calm and relaxed without excessive sedation

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23
Q

Name the 4 classes of antipsychotic drugs

A
  1. Phenothiazines (typical)
  2. Butyrophenones(typical)
  3. Thioxanthene’s (typical)
  4. atypical
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24
Q

What has been found to be the cause of mental depression

A

Deficiencies of Norepinephrine (NE) and Serotonin in the brain are the cause of mental depression

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25
Q

What kind of foods should be avoided while taking MAOIs and why

A

Foods that normally contain thyramine, including wine, beer, herring, and certain cheeses

-can cause dangerously high blood pressure in people taking a monoamine oxidase inhibitor.

26
Q

What disorders are SSRIs indicated

SSRIs - Selective Serotonin Reuptake Inhibitors

A

Anxiety disorder, depression disorders, Obsessive compulsive disorder, panic disorder, chronic pain disorder, and fibro myalgia

27
Q

What does patient monitoring include for Lithium?
What patient instructions need to be given?
(Side effects? onset of action? ect.)
Can pregnant patients take Lithium?

A

Explain to the patient that the therapeutic effects of lithium may require 1-2 weeks of treatment

Explain to the patient that side effects are common and usually include nausea or vomiting

Explain to the patient that lithium is a salt and that increased thirst and frequency of urination are common

Instruct patient on the importance of adequate fluid and sodium intake

Instruct patient to report excessive nausea and vomiting excessive CNS stimulation, dizziness, abnormal muscle movements, low blood pressure

Explain to the patient that periodic drug blood levels may be required

Lithium is pregnancy category D- DO NOT TAKE DURING PREGNANCY

28
Q

Define dependency, designer drug, and drug tolerance

A

Drug Dependence- condition of reliance on the use of a particular drug characterized as physical and/or psychological dependence

Designer Drug – chemically altered form of an approved drug that produces similar effects and that is sold illegally

Drug Tolerance- decreased drug effect occurring after repeated drug administration

29
Q

State pharmacological effects of marijuana

A

Reddening of the eyes and increased heart rate, mental relaxation, euphoria, increased sociability

Moderate intoxication is drowsiness, impairment of
memory, lapses in attention

Low doses- slight bronchodilation

High doses- reflexes are slowed muscle coordination decreases, ataxia is evident and speech and ability to concentrate become more difficult. Psychic effects also may include dysphoria acute panic-anxiety reactions, and psychotic episodes. Marijuana psychosis may in part be caused by unmasking of latent psychiatric disorders

30
Q

State the difference between anticonvulsant drugs and antiepileptic drugs

A

Anticonvulsant Drug- usually administered IM or IV that stops a convulsive seizure. // they have a selected effect at lower doses to prevent seizures
(sedation and hypnosis are common pharmacological effects produced by barbiturates. However, in the treatment of epilepsy, excessive sedation or hypnosis is an unwanted side effect).

Antiepileptic Drugs- usually administered orally, can be used prophylactically to reduce or prevent epileptic seizures.//decrease the excitability of brain cells and, consequently, reduce the incidence and severity for seizures.

(Prophylactically- Intend to prevent disease)

31
Q

Common adverse effects of phenytoin (Dilantin)

A Seizure Medication

A

The most common adverse effects involve the cerebellum.

Symptoms are

dizziness
ataxia
visual disturbances
postural imbalance
skin rashes
hirsutism
gingival hyperplasia

It’s been associated with birth defects referred to as the fetal hydantoin syndrome-defects include craniofacial abnormalities, growth retardation, cardiac defects, learning and developmental problem

32
Q

If a person has a grand mal seizure, what do they experience

A

Grand Mal Seizure (aka Tonic-clonic)- most dramatic in appearance and involve loss of consciousness.

begin with tonic followed by clonic muscle contractions.
Individual appears to jerk around due to the alternating muscle contractions and relaxations.

Increases in blood pressure and heart rate
urination
defecation
tongue biting are common

Usually lasts several minutes.

Following the seizure is
confusion
fatigue
muscle soreness.

33
Q

While taking levodopa, why would a patient experience orthostatic hypotension

(AKA- L-DOPA - is a Parkinson’s/seizure medication)

A

In the brain, HIGH LEVELS OF DOPAMINE interfere with cardiovascular reflexes that maintain blood pressure. Consequently some patients experience orthostatic hypotension or fainting.

34
Q

Since injecting dopamine in Parkinson’s patients does not help to increase dopamine levels, what drug can be converted to dopamine

A

In the dopaminergic neurons of the substantia nigra, levodopa is converted to dopamine

35
Q

Name drug interactions of levodopa

Parkinson’s/seizure medication

A

A Number of drugs interfere with the action of levodopa.

  • Antipsychotic drugs
  • MAO-A inhibitors
  • Vitamin B6 or pyridoxine
36
Q

Which drug aids levodopa from converting to dopamine too soon? What is the trade name?

(Parkinson’s/seizure medication)

A

In order to minimize this premature conversion, levodopa is usually given along with another drug- Carbidopa (Lodosyn) inhibits the enzyme DOPA decarboxylase that converts levodopa to dopamine peripherally so that more levodopa passes into the brain before being converted to dopamine.

A combination of levodopa and Carbidopa is available under the trade name of Sinemet, and is the most widely used drug preparation.

37
Q

State the difference between induction of general anesthesia and maintenance of general anesthesia

A

Induction of General Anesthesia- is the time required to take a patient from consciousness to Stage III

Maintenance of General Anesthesia- is the ability to keep a patient safely in Stage III.

38
Q

State the objective of using anesthesia during surgical procedures

A

The ideal general anesthetic would produce rapid induction (from stage I to stage III) and slow maintenance (stage III) without entering Stage IV anesthesia. In addition recovery from the ideal general anesthesia would occur rapidly without side effects.

39
Q

Opioid analgesics are primarily used for what kinds of pain

A

Opioid analgesics are first-line therapy for pain associated with procedures (bone marrow biopsy), pain due to trauma (burns, vehicular accident), cancer, or visceral pain (internal organs including pancreatitis, appendicitis).

  • can relieve virtually any type of pain.
  • relieve moderate to severe acute and chronic pain- such as pain often associated with myocardial infraction, post-trauma injury’s, and cancer.
  • drug of choice in treating acute postoperative pain, including dental pain because there is no increased risk of bleeding as with (NSAIDs)
40
Q

Why would fentanyl be given to a patient prior to surgery

A

Opioids (such as fentanyl) are frequently used during MAC (monitored anesthesia care) because they are able to suppress transmission of sensory information associated with moderate to severe pain of any origin. They depress transmission in the spinal cord by interacting with mu opioid receptors. // they block pain associated with the procedure and or condition during surgery

-opiates are not anesthetics at any dose// do not produce amnesia even at doses that create sedation. Sedation is more of a liability than a clinical benefit with opioid analgesics because the dose to produce sedation usually requires some degree of CNS and respiratory depression. For this reason and because they produce nausea and vomiting, opioid analgesics are seldom used alone in MAC

41
Q

Codeine, hydrocodone, morphine, oxycodone, fentanyl, along with others, are all schedule ????? Controlled Substances (I, II, III, IV, or V)

A

Schedule II – because of their high abuse potential, most opioids used as analgesics or adjuncts to anesthesia are restricted to Schedule II. Schedule II requires that listed drugs must have a new prescription written for each refill.

Except for- Heroin (I) Buprenophine(III) Butorphanol (III) Butophanol nasal spray (IV) Nalbuphine (***) Pentazocine (IV)

42
Q

Opioid analgesics are called central analgesics. Why?

A

Because they selectively act within the CNS to reduce the reaction to pain. Opioid

43
Q

List the cardinal signs of inflammation

A

Redness, swelling (edema), warmth, pain, and loss of function

44
Q

Why would a patient be told to take acetaminophen instead of aspirin or an NSAID?

A

If the patient has a fever, headache, minor musculoskeletal pain, and discomfort associated with the common cold and flu in adults and children.

  • the drug of choice (not aspirin) for reducing fever and aches (minor pain) in children.
  • particularly indicated for use in patients allergic to aspirin- those receiving anti-coagulant therapy for coagulation disorders, or patients who have upper GI disease and for whom aspirin therapy is not an option.
  • its recommended for patients who experience GI upset from aspirin or non steroidal anti-inflammatory drugs (NSAIDs) however it is not interchangeable with these products for chronic therapy of inflammatory conditions such as osteoarthritis.
45
Q

What can excessive use of acetaminophen cause

A

Toxicity may develop from chronic use of large doses of acetaminophen as well as acute overdose from a single episode of ingestion of a large dose.

46
Q

What does aspirin inhibit, giving anticoagulant benefits

A

Aspirin permanently hinders the access of achidonic acid to the active site on the COX-1 enzyme. Aspirin irreversibly blocks COX-1, THROMBOXANE is not generated and clotting is suppressed (anti-coagulant). This effect continues until new COX enzymes are synthesized. As a result, even low doses of aspirin increase bleeding time. In large doses, salicylates may depress the formation of other coagulation factors (prothrombin), thus increasing bleeding time

47
Q

Determine the main therapeutic effect of diuretics

ELMINATE?
(CHF)

A

The main therapeutic effect produced by diuretics is the elimination of excess sodium and water by the kidneys. Sodium and water retention are the main causes of edema and congestion in CHF.

48
Q

What are ACE inhibitors mechanisms of action

ACEI- angiotensin-converting enzyme inhibitor

A

ACEIs inhibit the formation of angiotensin II and decrease the release of aldosterone and antidiuretic hormone.

These actions LOWER BLOOD PRESSURE by causing a BALANCED VASODILATION of both ARTERIES AND VEINS.

In addition, ACEIs also INHIBIT INACTIVATION OF BRADYKININ, which also PRODUCES VASODILATION

(Aldosterone- causes the retention of sodium ions and excretion of potassium ions)

(Bradykinin- endogenous vasodilator)

49
Q

What are the therapeutic action of beta blockers

A

Beta Blockers antagonize the effects of norepinephrine and epinephrine at the beta-1 receptors, beta blockers decrease heart rate, AV conduction, and automaticity of SA and AV nodes, and of atrial and ventricular muscle.

-are mainly indicated for supraventricular arrhythmias and for prevention of recurrent myocardial infraction.

50
Q

CHF can be treated with beta blockers – name the preferred beta blockers

A

Metoprolol (lopressor), bisoprolol (zebeta), nebivolol (Bystolic) and carvedilol (Coreg) are usually the preferred treatment of CHF.

51
Q

Diuretics work on different parts of the nephron within the kidney. State what part of the nephron the thiazide diuretics, loop diuretics, and aldosterone antagonists act on

A

Thiazide diuretics- Thiazide and thiazide-like diuretics are similarly acting drugs that block the reabsorption of sodium in the DISTAL TUBULES of the kidney nephrons

Loop diuretics- The organic acids are commonly referred to as the loop diuretics because the site of diuretic action in the kidney nephrons is the THICK ASSENDING LIMB OF THE LOOP HENLE

Aldosterone antagonist- are weak diuretics that act on the COLLECTING DUCTS of the nephron.

52
Q

In general, how do anti-arrhythmic work

What affect do they have?

A

Most anti-arrhythmic drugs affect the movement of one or more specific ions and exert their major antiarrhythmic action on a specific phase of the action potential.

53
Q

How do calcium channel blockers work as anti-arrhythmics

A

They decrease the entry of calcium into cells whose electrophysiologic actions depend on the influx of calcium through the slow-type calcium channels.

In the heart, the depolarization (contraction) of SA (Sinoatrial)and AV (atrioventricular) nodal cells is highly dependent on the influx of calcium ions.

The effect of calcium channel blockers on the SA node is to SLOW DEPOLORIZATION AND DECREASE HEART RATE. The effect on the AV node is to SLOW CONDUCTION. These actions REDUCE the ventricular rate during fast supraventricular arrhythmias.

-Calcium channel blockers also affect the contraction of cardiac and smooth muscle. Entry of calcium during Phase 2 of the action potential is important for regulating the force of myocardial contractions.
INTERFERENCE WITH CALCIUM ENTRY into the CARDIAC MUSCLE REDUCES MYOCARDIAL CONTRACTILITY. This is usually not a desired therapeutic action and may precipitate heart failure in patients with CHF. The calcium channel blockers also DECREASE THE ENTRY OF SMOOTH MUSCLE to RELAX smooth muscle and cause VASODILATION, which is useful in the treatment of angina pectoris and hypertension.

They are divided into two groups:

-Dihydropyridines/ nondihydropyridines -
only block calcium in smooth muscle to cause arterial vasodilation. They do not have direct effects on the heart and are mainly used in the treatment of angina pectoris and hypertension.

-miscellaneous drugs – 
include verapamil (calan) and diltiazem (Cardizem) These two drugs are also arterial vasodilators and in addition have direct antiarrhythmic effects on the heart to slow heart rate (SA node) and slow AV conduction (AV node). Consequently, verapamil and diltiazem are the only calcium channel blockers used for their antiarrhythmic.
54
Q

Name side effects of nitroglycerin. What is the most serious adverse side effect?

A

Related to vasodilating action

Cutaneous flushing
dizziness
headache
weakness
fainting

Sudden or excessive drops in blood pressure can cause

reflex tachycardia.

55
Q

Define angina

A

Angina- Chest pain or discomfort that occurs when the heart muscle does not get enough blood and oxygen.

56
Q

How do beta blockers help patients with angina

A

The therapeutic action of beta- blockers in the treatment of angina lies in the ability of these drugs to
decrease heart rate and force of contractions. These changes decrease cardiac work and therefore oxygen consumption. Decreasing oxygen consumption often prevents development of myocardial ischemia and pain.

57
Q

Does cardiac work increase or decrease with the use of nitrates

A

The main effect of the nitrates is to produce a general vasodilation of systemic veins and arteries. This reduces venous return, cardiac work and oxygen consumption. Reduction of cardiac work and oxygen consumption provides relief of ischemia and pain.

58
Q

If a patient has a sudden attack of angina, which route of administration of nitrates would work faster, and is the most common route

A

Fastest route of administration for Angina- Sublingual 1-3 Minutes-peak effect in about 5 minutes. The duration of action is approximately 30 Minutes.

Most common route of administration for Angina- Sublingual

59
Q

Know patient instructions that should be given to a patient about nitroglycerin

A
  • it is important for paitents to carry the prescribed medication at all times
  • Nitroglycerin is volatile, and tablets lose potency if exposed to air or light. Therefore, it is important that tablets be carried in light- resistant, airtight containers.
  • standard practice is not to use nitroglycerin tablets that are more than 6 months old since there may be significant loss of potency
  • when patients experience angina they should be instructed to sit down, place a nitroglycerin tablet under the tongue, and allow it to dissolve without swallowing. Relief should occur within 5 minutes. If it does not they should repeat the process with another tablet. If there is no relief after three tablets, patients should notify the physician or seek medical assistance.
  • side effects cutaneous flushing, headache, dizziness- should be advised to lay down if they feel faint. These effects are expected and only last a few minutes
  • patients should become aware of the activities that cause angina (overexertion, emotional upset, or overeating) and try to avoid these situations if possible.
60
Q

Name drug interaction of levodopa and Anti Psychotic Drugs

Parkinson’s/Seizure Drug

A

(phenothiazines, haloperidol, drugs that block DA) decrease the effectiveness of levodopa because they block dopamine receptors. This may cause symptoms of Parkinson’s disease, referred to as parkinsonism.

61
Q

Name drug interaction of levodopa and MAO-A Inhibitors

Parkinson’s/Seizure Drug

A

used in treating mental depression also should not be taken with levodopa. They can produce high levels of norepinephrine and may cause a hypertensive crisis and other adverse effects.

62
Q

Name drug interaction of levodopa and Vitamin B6 or pyridoxine

(Parkinson’s/Seizure Drug)

A

may increase the rate of metabolism of levodopa if the patient is not also taking carbidopa. When used as a vitamin supplement, vitamin B6 may decrease the effectiveness of levodopa.