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ACP Entrance Exam > Vascular Access Pharmacology exam > Flashcards

Vascular Access Pharmacology exam Flashcards

1
Q

Drug half-life is defined as?

A

The time it takes for the drug to reach half its therapeutic effect.

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2
Q

Define: agonist

A

stimulates the cell and provides the desired effect

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3
Q

Define: antagonist

A

attaches to the cell receptor and blocks anything from stimulating the cell

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4
Q

Define: Pharmacodynamics

A

what the body does to the drug

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5
Q

Define: Pharmacokinetics

A

what the drug does to the body

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6
Q

Alpha 1 receptor abilities are;

A

vasoconstriction

in the arteries and veins

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7
Q

Alpha 2 receptor abilities are;

A

vasodilation

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8
Q

Indications for vascular access?

A

10 year of age or older

fluid replacement

drug administration

reasonable belief the patient my deteriorate and require any of the above

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9
Q

Contraindications for vascular access?

A

age 0-9

if the extremity has any of the following;
massive edema
burns
infection like cellulitis
trauma
phlebitis
thrombosis
dialysis fistula - unless vital signs abscent (DCPO skill)

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10
Q

what are the two types of IV access?

A

central and pheripheral

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11
Q

central IV locations?

A

subclavian

internal jugular

femoral

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12
Q

peripheral IV locations?

A

arms * preferred site

legs * foot veins are a last resort because of the higher probability of complications

external jugular (not WFPS)

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13
Q

disadvantage of peripheral IV’s?

A

veins could collapse in shock or hypothermia

geriatrics, pediatrics, and vascular disease patients may have veins hard to cannulate

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14
Q

ACF stands for?

A

anterior cubital fossa

antecubital fossae (AC space)

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15
Q

7 patient rights?

A

D rug
D ose
D ocument
P atient
T ime
R oute
R esponce

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16
Q

IV access complication

what is circulatory overload?

A

when too much fluid is administered

generally occurs with heart or kidney failure patients

auscultated the lungs especially in CHF and dialysis patients

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17
Q

IV access complication

what is pyrogenic reaction?

A

abrupt onset

foreign material causes fever, N/V, and shock

remove IV

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18
Q

IV access complication

what is infiltration?

A

catheter is no longer in the vein

fluid collects in the interstitial space

swelling around the site

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19
Q

IV access complication

catheter sheer?

A

can occur if you pull the catheter back over the needle

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20
Q

IV access complication

thrombus formation?

A

blood clot that remains in place can become a thromboembolism.

aspirate clot if possible

remove IV if unable to asperate

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21
Q

IV access complication

air embolism?

A

most likely with central lines

ensure air is out of tubing

tamponade veins when attaching tubing

The volume of air that the venous bloodstream can tolerate is thought to be between 200 and 300 mL. The risk is the greatest when the IV is started in the central circulation where there are negative pressures and air can actually get pulled in.

Air can enter the circulation upon insertion or when the tubing is disconnected to replace the solution or to add new extension tubing.
Accidental disconnection of the IV tubing.

If enough air enters the heart, it can impede the flow of blood which can lead to shock. S/Sx hypotension, cyanosis, weak, rapid pulse, and LOC.

Tx close the tubing, turn the patient on the left side with the head down, check the tubing for leaks, administer O2, and notified medical direction.

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22
Q

IV access complication

arterial puncture?

A

S/Sx pulsating bright red blood in the catheter hub.

Tx catheter should be removed and direct pressure applied to the site for at least five minutes (ten if the patient is on an anticoagulant).

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23
Q

IV access complication

necrosis?

A

Sloughing (separation of tissues) and necrosis (tissue death) - infiltration of some IV medications (for example Dextrose, Sodium Bicarbonate, Epinephrine, Potassium, Digoxin, Calcium, Dopamine, and Promethazine).

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24
Q

OH- is the chemical abbreviation for what?

A

hydroxide ions

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25
Q

define

respiratory acidosis?

A

retention of CO2 (pCO2>45)

which causes decrease pH (see-saw)

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26
Q

define respiratory alkalosis?

A

increased elimination of CO2 (pCO2<35)

which causes an increase in pH (see-saw)

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27
Q

define metabolic acidosis?

A

when the arterial blood HCO3- level drops below 22

which causes the pH to drop (elevator)

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28
Q

define metabolic alkalosis?

A

when the arterial blood HCO3- level rises above 26

which increases the pH (elevator)

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29
Q

ABG normal values?

A

pH 7.35-7.45 mmHg

pCO2 35-45 mmHg

HCO3- 22-26 mEq/L

pO2 80-100 mmHg

30
Q

what are the three buffer systems the body uses to balance pH?

A

buffer system - quickest in minutes
- protein
- carbonic acid-bicarbonate buffer system
- phosphate buffer system

respiratory systems - happens in minutes

renal systems - happens in hours

31
Q

pH abnormal

CO2 abnormal

HCO3 abnormal

what level of compensation is this?

A

partially compensated

if CO2 is moving with HCO3 then it is compensating

if HCO3 is moving with CO2 then it is compensating

32
Q

pH abnormal

CO2 of HCO3 normal and the other is abnormal

what level of compensation is this?

A

uncompensated

33
Q

pH normal

CO2 abnormal

HCO3 abnormal

what level of compensation is this?

A

fully compensated

34
Q

pH normal

CO2 normal

HCO3 normal

what level of compensation is this?

A

compensated

35
Q

what is plasma?

A

proteins-salt solution that acts as a transport medium for blood components

straw colored

90% water

assists in clotting, fighting infection, maintenance of BP

contains minerals

36
Q

what are mild reactions to watch out for when a pt is receiving a blood transfusion?

A

restlessness

chills

headache

flushing

itching

seek advice from sending facility

37
Q

what are severe reactions to watch out for when a pt is receiving a blood transfusion?

A

dyspnea

CP

N/V

anaphylaxis

oozing of blood from puncture site or mucous membranes

38
Q

What will happen to a cell if it is placed into a hypertonic solution?

A

shrink

think ICP and mannitol

draws water from the cells into the vascular space

39
Q

What will happen to a cell if it is placed into a hypotonic solution?

A

swell

think hippo

used to hydrate pts or prevent dehydration

40
Q

Extracellular fluid can be broken down into interstitial and intravascular fluid

Define interstitial fluid

Define intravascular fluid

A

Interstitial Fluid: The extracellular fluid between the cells and outside the vascular bed (i.e., connective tissues, cartilage, and bone). (CSF and intraocular fluid)

intravascular fluid is found inside veins and arteries (blood plasma)

41
Q

define osmosis

A

water through a semi-permeable membrane from low to higher gradient

42
Q

define diffusion

A

movement of particles from area of higher concentration to low concentration

passive process

CO2 and O2 exchange is performed by diffusion

43
Q

what is the formula for calculating IV drip rates?

A

V to be infused * drip factor / minutes

44
Q

define shock?

A

inadequate tissue perfusion

45
Q

heparin is what class of drug?

A

anticoagulant - are used to prevent intravascular thrombosis. The therapy works by decreasing blood coagulability.

46
Q

tPa and TNK are what class of drug?

A

fibrinolytic - dissolve clots after their formation by promoting the digestion of fibrin.

47
Q

Aspirin, clopidogrel, and ticagrelor are what classes of dug?

A

platelet inhibitor - are drugs that interfere with platelet aggregation

48
Q

What are the classes of anti-arrythmics

A

Class I - sodium channel blockers, slow conduction.
Ia drug examples as quinidine, disopyramide (Norpace), and procainamide (Pronestyl).
Ib drug example lidocaine
Ic drug example flecainide (Tambocor)

Class II - beta-blocking agents. These reduce adrenergic stimulation of the heart; metoprolol.

Class III - potassium channel blockade, which increases the contractility. These do not affect automaticity and also have no effect on conduction velocity. These drugs are thought to cease dysrhythmias that result from the reentry of blocked impulses; amiodarone.

Class IV - calcium channel blockers. Thought to work by blocking the inflow of calcium through the cell membranes of the cardiac and smooth muscle cells; verapamil (Isoptin) and diltiazem (Cardizem, Tiazac).

49
Q

define action potential

A

a change in membrane potential in an excitable tissue that acts as an electrical signal and is propagated in an all-or-nothing fashion

50
Q

define biologic half-life

A

time required to metabolize or eliminate half the total amount of a drug in the body

51
Q

define acetylcoline

A

a neurotransmitter, widely distributed in body tissues, with the primary function of mediating the synaptic activity of the nervous system

52
Q

define cholinergic

A

of or pertaining to the effects produced by the parasympathetic nervous system or drugs that stimulate or antagonize the PNS.

53
Q

define first-pass metabolism

A

the initial biotransformation of a drug during passage through the liver from the portal vein that occurs before the drug reaches the general circulation

54
Q

define loading dose

A

a large quantity of drug that temporarily exceeds the capacity of the body to excrete the drug

55
Q

define maintenance dose

A

the amount of drug required to keep a desired steady states of drug concentration in tissues

56
Q

define neurotransmitters

A

chemicals that are released from neurons at the presynaptic nerve fiber

57
Q

define therapeutic action

A

the desired, intended action of a drug

58
Q

define therapeutic index

A

a measurement of the relative safety of a drug.

the closer to 1, the more dangerous example Digoxin

59
Q

describe how ACE inhibitors work as a antihypertensive medication

A

Angiotensin II is a strong vasoconstrictor and also causes the release of aldosterone. Aldosterone contributes to sodium and water retention. By inhibiting the conversion of the precursor angiotensin I to activate molecule angiotensin II (a process triggered by ACE), the RAAS is suppressed and blood pressure is lowered; captopril (Capoten), enalapril (Vasotec), benazepril (Lotensin), fosinopril (Monopril), lisinopril (Prinivil, Zestril), and quinapril (Accupril).

60
Q

describe how beta blockers work as a antihypertensive medication

A

Sympathetic-blocking agents may be classified as beta-blocking agents and adrenergic-inhibiting agents.

Beta-blocking works by decreasing cardiac output and inhibiting renin secretion from the kidneys. Beta-blocking drugs compete with epinephrine for available beta-receptor sites as well.

Adrenergic-inhibiting agents work by modifying the actions of the sympathetic nervous system. Arterial pressure is influenced by various mechanisms of the heart, blood vessels, and kidneys, blocking this sympathetic stimulation can reduce blood pressure. Classified as centrally acting or peripheral.

61
Q

describe how diuretic work as a antihypertensive medication

A

Diuretics which cause a loss of excess salt and water from the body by the kidneys, are the drugs of choice in managing hypertension.

Thiazides are diuretics that work well to lower blood pressure. Many agents cause retention of sodium and water; thiazides, such as hydrochlorothiazide, may be given concomitantly (along with other drugs) to help prevent this side effect.

Loop diuretics, such as furosemide, are potent, short-acting agents that inhibit sodium and chloride reabsorption in the loop of Henle and cause excessive loss of potassium. They also cause an increase in the exertion of sodium and water. Side effects are hypokalemia and profound dehydration.

Potassium-sparing agents, such as spironolactone (Aldactone), can be effective when they are used in combination with other diuretics because they prompt sodium and water loss without a loss of potassium.

62
Q

describe how calcium channel blockers work as a antihypertensive medication

A

Calcium Channel Blockers reduce peripheral vascular resistance by inhibiting the contractility of vascular smooth muscle. They dilate coronary vessels through the same mechanism, decreasing the oxygen requirements of the heart (through decreased afterload), and increasing oxygen supply (by abolishing coronary artery spasm). Examples; verapamil, amlodipine (Norvasc), felodipine (Plendil), and diltiazem.

63
Q

describe how proton pump inhibitors work

A

Proton Pump Inhibitors decrease hydrochloric acid secretion by inhibiting the actions of the parietal cells. In addition, the gastric pH of the stomach is altered. Examples are esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec), pantoprazole (Protonis), dexlansoproazole (Dexilant), and rabeprazole (Aciphex).

64
Q

describe how antacids work

A

Antacids buffer or neutralize hydrochloric acid in the stomach. Rx hyperacidity, including peptic ulcer, gastritis, esophagitis, heartburn, and hiatal hernia. Common OTCs are Alka-Seltzer, Gaviscon, and Rolaids.

65
Q

in the autonomic nervous system

the afferent and efferent nerves send signals which way?

A

afferent = arrive at the brain. stimulus to brain

efferent = exit the brain. brain to muscle

66
Q

beta 1 receptors abilities are

A

increased HR (chrono trophy)

increase contractility (dromoprophy)

located in the heart

67
Q

beta 2 receptor abilities are

A

bronchodilation
vasodilation
snow HR

location lungs

68
Q

what are the five major sources for drugs

A

plants
chemicals
microorganisms
animals
minerals

69
Q

according to the controlled substances act there are five schedule of drugs, what are they?

A

schedule 1 no medical use high risk of abuse = heroin

schedule 2 medical use but high abuse potential = opioids

schedule 3 low abuse potential, high likely hood of physical dependence = anabolic steroids

schedule 4 low abuse potential, may lead to dependence = benoz’s

schedule 5 low abuse potential, may lead to dependence = T3’s

70
Q
A

ACP Entrance Exam (17 decks)

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