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NURS 200 > Midterm #1 > Flashcards

Midterm #1 Flashcards

(66 cards)

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1
Q

pharmacokinetics
- 4 parts

A

1 ) absorption
2 ) distribution
3 ) metabolism
4 ) excretion

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2
Q

factors that affect drug absorption

A
  • food, stomach motility, lipid/water soluble
  • blood flow
  • grapefruit juice = ↑ absorption of drug
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3
Q

metabolism of drugs and its application to pharm

A

hepatic 1st pass effect
PO drugs > extensively metabolized by the liver before reaching the systemic circulation (high 1st pass effect) and its target organs

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4
Q

discuss how drugs are distributed throughout the body

A

blood flow:
rapid distribution > highly vascularized or w/ large blood volume
- heart, liver, kidneys, brain
slower distribution > less vascularized
- muscle, skin
slowest distribution > least vascularized
- bones, fat

drug solubility: H2O vs. lipid
- lipophilic drugs can readily cross cell membranes
- H2O soluble can only cross cell membranes by active transport

tissue storage

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5
Q

describe how plasma proteins affect drug distribution

A
  • not all drugs molecules in plasma will reach their target cells as they become bound to plasma protein especially albumin to form drug-protein complexes
  • drugs bound to proteins will circulate in plasma until they are released or displaced
  • a drug can only be freely distributed to extravascular tissue if it is not bound to protein
  • drug-drug interaction is when two drugs are administered that both are protein binding drugs—each will compete for albumin sites and the result will be difficult to predict and manage
    why?
  • don’t know how many will attach to the protein and not go to the target site
  • dosage changes
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6
Q

identify major process by which drugs are excreted

A

via kidneys, lungs, saliva, sweat, breastmilk, feces

  • pH of urine > ASA is excreted faster IF urine is basic (Na bicarb)
  • non-ionized and lipid soluble drugs cross renal tubule membranes easily and return to circulation
  • ionized and H2O-soluble drugs are easily filtered and excreted
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7
Q

enterohepatic recirculation

A
  • some drugs are secreted in bile
  • however, most bile is circulated back to the liver by enterohepatic recirculation
  • % of drug may be recirculated multiple x with the bile
  • recirculation and elimination of drugs through biliary excretion may continue for several wks after therapy has been discontinued
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8
Q

plasma half-life (T1/2)

A

the length of time required for a med to [decrease] in the plasma by 1/2 after administration

*short-acting drugs are excreted rapidly, the risk for long term adverse effects is reduced
short-acting drug > given more freq
long-acting > less freq

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9
Q

how a drug reaches and maintains its therapeutic range in plasma

A

drug administered is = to amount being eliminated
- 4-5 half lives to accomplish this equilibrium
- constant levels of the drug in the body to achieve desired therapeutic effect

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10
Q

loading dose vs. maintenance dose

A

loading dose: higher amount of drug is given only 1-2x and is administered to ‘prime’ the bloodstream w/ a level sufficient to quickly induce a therapeutic response

maintenance dose: given to keep the [plasma blood] in the therapeutic range

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11
Q

compare/contrast median lethal dose (LD50) and toxicity dose (LD50)

A

TD50 = more practical value in clinical setting
- TD50 the dose that will produce a given toxicity to 50% of the pts.

LD50 = the dose lethal to 50% of the animals

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12
Q

correlate a drugs therapeutic index to its margin of safety

A

the ratio of a drugs LD50 to its ED50
LD50/ED50 = TI

the larger the difference between the 2 doses the greater the therapeutic index

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13
Q

compare/contrast potency vs. efficacy

A

potency: a drug that is more potent will produce a therapeutic effect at a lower dose
- the ability for a drug to attach to a receptor

efficiency: the maximum response that can be produced from a drug
- a higher maximum response

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14
Q

agonist

A

a drug that produces the same type of response as the endogenous substance

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15
Q

partial agonist

A

a med. that produces a weaker or less effectivous response than an agonist

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16
Q

antagonist

A

a drug that occupies a receptor and prevents an endogenous chemical from acting
‘antidote’
protamine sulfate to heparin

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17
Q

adverse vs side effects

A

adverse effects: undesirable and potentially harmful action caused by the administration of the drug
- as the dose ↑ then the adverse effects also ↑

side effects: predictable and known
- these may occur at therapeutic doses
- less serious than adverse effects

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18
Q

plan to minimize/ prevent adverse rxns

A

1 ) obtain thorough medical hx
- allergies or conditions that contraindicate certain meds
- prescription drugs, OTC, herbs
2 ) thoroughly assess the pt. and all diagnostic data
- underlying hepatic/ renal issues
3 ) prevent med errors
4 ) monitor pharmacotherapy carefully
- baseline effects
5 ) know the drug
6 ) be prepared for the unusual
- anaphylaxis
- some adverse effects may be delayed
7 ) question unusual orders
8 ) teach pts. about adverse rxns
- good teaching should have good pt. adherence

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19
Q

carcinogenic and teratogenic drugs

A

risk-benefit ratio

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20
Q

organ specific toxicity
– nephrotoxicity

A

↓ urine production, ↓eGFR, ↑ BUN and creatinine
- proper hydration, lab values, adjusting doses

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21
Q

organ specific toxicity
– neurotoxicity

A

drowsiness, depression, mania, sedation, behavioral changes
- suicidal feelings, hallucinations, seizures
special sense: hearing, vision, loss of balance

tx: effective teaching, recognizing sx

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22
Q

organ specific toxicity
– hepatoxicity

A

S/S: RUQ pain. anorexia, bloating, fatigue, N/V, jaundice, itching, easy bruising
tx: lab values (LFT)

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23
Q

organ specific toxicity
– dermalogical toxicity

A

S/S: rash, pruritis. urticaria (hives), angioedema, phototoxicity, Steven-Johnson syndrome
tx: antihistamine or corticosteroid for itching

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24
Q

organ specific toxicity
– cardiotoxicity

A

S/S: bradycardia, tachycardia, HF, acute LV failure
tx: assess for excessive fatigue, cough, SOB, weight gain, peripheral edema
HR, BP

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25
organ specific toxicity -- skeletal muscle toxicity
S/S drug-induced myopathy > rhabdomyolysis tx: assess for unexplained muscle or joint soreness or pain during therapy test: creatine kinase
26
drug-food interactions
-grapefruit juice can significantly ↑ the absorption of some drugs - high fat meals can slow the absorption of oral meds - St. Johns Wort > depression
27
roles / responsibilities of the nurse in drug administration
three checks 1 ) when removing from storage 2 ) when drawing it up 3 ) prior to administering to pt - aseptic technique - check LFTs and KFTs - check for adverse effects >> assess, document, report, advocate
28
10 rights
1 ) right pt 2 ) right med 3 ) right dose 4 ) right time/frequency 5 ) right route 6 ) right reason / assessment 7 ) right education 8 ) right to refuse 9 ) right documentation 10 ) right evaluation
29
med adherence
- proper education - demonstrate proper administration of a drug - therapeutic use & outcomes - side effects and adverse rxns
30
enteral, topical, parenteral drugs
enteral: - GI system - hepatic 1st pass effect - less invasive, convenient, cheaper topical: - skin, eye, ear, nose, resp tract, GU, vagina, rectum - change sites parenteral: - most invasive - infection risk - rotate sites for SUBQ and IM
31
documentation
a legal record of pt. care - know who and when gave the med - documentation of late drugs
32
reporting and managing med errors
- factual and objective - include specific interventions - record all names of individuals notified or error - failure to document = negligence - follow agency specific policies and procedures
33
strategies for reducing med errors/ incidents
assessment planning - clarify orders - follow agency policies /procedures implementation - correct procedure and technique for all routes of administration evaluation - assess for expected outcome or adverse rxns pt education adherence/compliance
34
medication reconciliation
med hx - obtaining, verifying, documenting accurate list of current meds discrepancy complete transfer of information inadequate reconciliation in handoffs during administration, transfer, discharge
35
nurse reporting adverse drug reactions (ADRs)
report immediately / treat stop meds
36
'statins'
prototype drug: atorvastatin mech of action: HMG-CoA reductase therefore the liver makes less cholesterol, it responds by making more LDL receptors on liver surface - ↑ removal of LDL in bloodstream adverse effects: - GI complaints -> intestinal cramping, diarrhea, constipation - headaches, elevated liver enzymes
37
insulin overdose vs overdose
overdose: hypoglycemia S/S: pale, cool, moist skin, BG <4 underdose: hyperglycemia S/S: polyuria, polydipsia, polyphagia, weight loss, fatigue, blurred vision
38
somogyi phenomenon and morning hyperglycemia (dawn)
SP: rapid ↓ in BG at night - stimulates the release of hormones (E, cortisol, glucagon) result = ↑ BG in the morning - hyperglycemia caused by hypoglycemia MH: early-morning rise in BS - ↑ hormones in the morning
39
pharmacotherapy of T1 + T2 DM
T1DM: insulin T2DM: oral antihyperglycemics, insulin (temp) > usually for periods of stress
40
metformin - biguanides
↓ the hepatic production of glucose and ↓ insulin resistance S/S: common GI adverse effects; lactic acidosis; low risk for hypoglycemia
41
glyburide - sulfonylurea prototype drug
↓ BG by stimulating the release of insulin from pancreatic B cells ↑ sensitivity of peripheral tissues to insulin S/S: nausea, heartburn, dizziness, headache, drowsiness
42
stigliptin - incretin enhancer
slows the breakdown of insulin so it circulates longer S/S: N/V, diarrhea, headache, nervousness
43
Diuretics
1st drug given b/c least side effects - reduce blood volume by preventing the reabsorption of Na leading to fluid loss by peeing - lasix > loop of henle > HF - thiazides > distil convoluted tubule risk: dehydration and loss of electrolytes K > heart ↓ BP HF to ↓ fluid buildup - ↓ weight - ↓ edema
44
calcium channel blockers
- block Ca channels preventing Ca from entering limiting muscular contraction - certain ones block Ca channels on arterioles ↓BP by relaxing smooth muscle - some in the heart and some block both > ↓ HR contractility and rate
45
ACE inhibitors
- block angiotensin II - block aldosterone which stimulates the kidneys to reabsorb Na - block ADH and causes our kidneys to retain H2O and can cause vasoconstriction ↓BP lose Na -> lose H2O
46
angiotensin receptor blocker ('artens)
similar action but does not prevent the formation of Angiotensin II > just blocks it from attaching to receptors
47
Beta blockers
- selective/non-selective - block the beta-adrenergic receptor (SNS) Beta1> slow HR (- chrontropes) - ↓ contractility (-inotropes) they also block the production of RENIN which activates the renin angiotensin system - ↓ angiotensin II - aldosterone ↓BP
48
direct vasodilators
indications is HTN mechanism is it relax arterial smooth muscle directly causing ↓ in BP - LOTS OF SIDE EFFECTS SO NOT FIRST PICK - adverse effects: reflex tachycardia - only really in emergencies
49
direct vasodilator -- prototype
hydralazine (apresoline) mech of action: - direct vasodilation of vascular smooth muscle adverse effects: - reflex tachycardia
50
nursing considerations for planning and interventions w/ pts w/ hypertension
planning: - provide education regarding drug action - precautions - adverse effects interventions: - BP is critical - dizziness and altered LOC -> poor cerebral circulation
51
nursing management of pts who are receiving drugs for hypertension
monitor in and outs BP, P, HR education LFTs and KFTs hypotension
52
general principles guiding the pharmacotherapy of hypertension
- goal of therapy is to reduce morbidity and mortality - individualized to patient's risk factors, comorbid medical conditions, and degree of blood pressure elevation - if pt doesn't respond to monotherapy, more drugs may be added to the regiment including vasodilators, alpha2 agonists
53
how drugs modify functions of the ANS
drugs that stimulate SNS > adrenergic receptors - fight or flight drugs that stimulate the PNS > cholinergic receptors - rest and digest inhibition of the SNS > adrenergic antagonists, antiadrenergic or adrenergic blockers - opposite action inhibition of PNS > anticholinergics, parasympatholytic, or muscarinic blockers - oppose cholinergic
54
types of responses that occur when a drug activates alpha 1,2 or beta 1,2
alpha 1 primary location: all sympathetic target organs except the heart responses: constricted blood vessels; dilated pupils alpha 2 primary location: presynaptic adrenergic nerve terminals responses: inhibited release of NE beta 1 location: heart and kidneys responses: ↑ HR and force of contraction; release of renin beta 2 location: all sympathetic target organs except the heart response: inhibition of smooth muscle
55
physiological responses when a drug activates adrenergic receptor
fight or flight - dilates pupils - inhibits salivation - dilates bronchi - accelerates HR - inhibits peristalsis / secretions - stimulates release of glucose - relaxes the bladder - release NE and E - inhibits sex organsp
56
pharmacotherapy w/ adrenergic agonists
alpha 1- nasal congestion, hypotension, and mydriasis alpha 2- Hypertension Beta 1- cardiac arrest, HF & shock - sometimes called cardiotonic or inotropic because they increase the force of contraction of the heart Beta 2- Asthma - relaxation of bronchial smooth muscle (bronchodilators)
57
physiological responses produced when a drug blocks adrenergic receptors
alpha1 antagonist: vasodilation, ↓BP beta 1,2 antagonists: - effects on the CV system - ↓ rate and force of contraction
58
clinical applications (actions) of adrenergic agonists and antagonists
agonists: induce fight-or-flight response of the SNS - ↑HR (+chronotropic) - ↑ force of contraction (+inotropic) - ↑CO, ↑BP - bronchodilation antagonists: inhibit so many of the therapeutic effects mimic rest and digest of the PNS - tx of hypertension and angina
59
advantages for selective vs non-selective beta antagonists
they have little affect on non-cardiac tissue and exert fewer side effects than non-selective
60
non-pharmalogical management of angina pectoris
nutritional therapy - avoid large meals smoking cessation
61
pharmacological management of angina pectoris, MI, CVA
organic nitrates - dilates coronary arteries to decrease O2 needs Beta Blockers - prevent anginal episodes by decreasing cardiac workload and O2 demand Calcium channel blockers - reducing CO - dilating coronary arteries
62
drug classes for CVA -- thrombolytics
stimulates formation of plasmin, an enzyme that breaks down fibrin causing active clots to dissolve - coronary artery opens allowing perfusion of myocardium
63
other meds used in prevention of a CVA
anti platelets - ASA anticoagulants - heparin IV atropine - symptomatic bradyarrythmias dimenhydrinate - gravol lorazepam - antianxiety metoclopramide - nausea morphine - pain, ↓platelet, ↓preload nitrospray - pain, vasodilation
64
nutritional therapy for post CVA
aspiration risk dysphagia dexterity different tools SLP
65
nitroglycerin
trade name: - Nitro-dur mech. of action: - forms nitric oxide (NO), a vasodilator therapeutic effects: - acute angina - acute CHF - acute pulmonary edema - acute MI adverse effects
66
at home use of nitroglycerin
3 doses of nitro 5 minutes apart - call 911 after the 2nd dose

NURS 200 (3 decks)

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