Pharm Exam1 Flashcards

1
Q

S/S of Stress (↑3 ↓2)

A

↑ HR, BP, Pupil dilation, ↓ secretions, GI mobility

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2
Q

How does stress cause cell damage (4)

A

free radicals, hypoxia, ATP depletion, !intracellular calcium homeostasis

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3
Q

Stress phase 1: Alarm (2, 4 released)

A

SNS and HPA on, fight v flight initiated

Cortisol, adrenaline, noadrenaline released

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4
Q

Stress phase 2: Resistance (4)

A

Selective defenses.
Homeostasis restores balance for period of recovery. Hormones normalize.
If condition persists body adapts to continued effort.

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5
Q

Stress phase 3: Exhaustion (4, 4 AKA)

A

Stress levels stay high, very hazardous for health
Resources depleted, results in systemic damage
AKA: Overload/burnout/adrenal fatigue/
maladaption/dysfx

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6
Q

Increase of cell numbers?

A

Hyperplasia

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7
Q

Adaptations to Stress (10)

A
Physiologic/Anatomic reserve
Time
Genetic Endowment
Age
Gender
Health Status
Nutrition
Sleep-wake cycles
Hardiness
Coping
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8
Q

Increased capacity to adapt to stress

A

Coping

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9
Q

Types of Stress (3)

A

Acute (time limited), Chronic (intermittent), PTSD (sustained)

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10
Q

Which type of stress if fight v. flight?

A

Acute

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11
Q

Which system manifested first w/ stress response?

A

Autonomic Nervous System

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12
Q

Wheezing/SOB w/ acute bronchial asthma is caused by? (2)

A

Inflammatory response and swelling

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13
Q

States of PTSD (1 description, 3 phases)

A

PTSD is chronic activation of stress related to an event (SNS is activated, cortisol levels ↓)
Intrusion
Avoidance (numbing)
Hyperarousal (irritability, startle reflex)

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14
Q

Definition of “Intrusion State”

A

“Flashbacks” and nightmares of event in detail

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15
Q

Sections of CNS? (2)

A

Brain and spinal cord

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16
Q

Where do SNS impulses come from? (3)

A

Hypothalamus, adrenal medulla, spinal cord

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17
Q

S/S of Fight v. Flight (6)

A

↑ RR, diaphoresis, dilated pupils, ↓ secretions, GI motility, constriction of sphincters

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18
Q

How does heat cause cell injury?

A

Coagulation of blood vessels and tissue proteins

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19
Q

How does cold cause cell injury?

A

Viscosity induces vasoconstriction through SNS reflex.
↓ blood results in hypoxia -> tissue injury
also… frost bite.

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20
Q

Types of Adrenergic Receptor sites (4)

A

A1 - bladder/vasoconstriction, iris dilation
A2 - ↑ insulin release from pancreas
B1 - cardiac and contractility
B2 - bronchi,vasodilation, relaxation of uterus

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21
Q

Which site when stimulated results in myocardial activity and an increased HR?

A

Beta 1

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22
Q

What does PNS do?

A

Opposite of SNS. Begins energy storage and conservation

“Rest of Digest”

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23
Q

Adrenergic blockers fx? (↑1 ↓3)

Treatment similar to?

A

↓ BP, pulse, renin levels ↑ renal perfusion

Treatment for HTN

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24
Q

When receiving adrenergic blockades. Priority assessment?

A

Monitor HR

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25
Q

Areas of Pharmacology (5)

A

Pharmaco…
Dynamics - org to chemi
Kinetics - drug action, HL, peak, duration, metabolism
Therapeutics - therapeutic fx of drugs + admin
Economics - value of therapy vs another
Genomics - drug fx vs. individual genetics

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26
Q

Area of pharmacology involved in exploring unique differences in drug responses due to genetic makeup?

A

Pharmacogenomics

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27
Q

Phases of Pharmacokinetics (4)

A

Absorption, Distribution, Metabolism/Biotransformation, Excretion

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28
Q

Labs to administer if giving nephrotoxic antibiotics

A

Creatinine and BUN

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29
Q

FDA Category where fetal abnormalities > beneficial fx of drugs

A

Category X substances.

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30
Q

Concerns when administering to older pts? (3)

A

↑ susceptible to AdFx
Monitor hydration, nutrition, hepatic renal fx
Ensure compliance (alarms/reminders)

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31
Q

More effective method of antibiotic therapy?

Broad vs Selective

A

Selective targets infections
(IV is quickest)
Broad used when C&S not available or pt is too sick to wait for results

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32
Q

Preventing drug resistance (4)

A

Only use if C&S identifies
↓ dis/misuse
Complete full round
!save for self-medication in future

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33
Q

How do penicillins fight bactera?

A

Interfere w/ cell wall building

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34
Q

What antibiotic is used to prophylactically treat family members living w/ a pt with tb?

A

Isoniazid

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35
Q

When does antibiotic therapy stop?

A

When full round is complete

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36
Q

How do organisms develop resistance?

A

alter cell walls/enzymes to become resistant to unfavorable conditions/situations

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37
Q

How to prevent accumulation of anti-infective in kidneys?

A

Hydration throughout drug therapy

38
Q

Lab values to monitor when administering aminoglycosides?

A

BUN and creatinine monitor renal system

39
Q

When is Flagyl (metronidazole) used prophylactically

A

For pts undergoing vaginal, abdominal, or colorectal surgery (pre/post op)

40
Q

Flagyl

Type of antiinfective?

A

Antiprotozoal

41
Q

Ketoconazole (Nizoral) and Lotrimin

Type of antiinfectives?

A

Antifungals?

42
Q

How are Nizoral/Lotrimin applied?

A

Topically. Nizoral also can be taken orally

43
Q

Nizoral/Lotrimin Contraindications? (6)

A
Hepatic dysfx
Renal dysfx
Endocrine/Fertility probs
Pregnant/Lactating
Known allergy/hypersensitivity reaction
Open lesions
44
Q

Where can Candidiasis infx occur? (2)

A

mouth and vagina (vaginitis)

45
Q

What is oral Candidiasis called?

A

Thrush

46
Q

Sidefx to warn pt when giving antifungals (5)

A

Systemic - bruising/bleeding, yellowing eyes/skin (hepatic toxicity)
Topical - serious irritation, burining, pain
STOP IF ANY OCCUR

47
Q

What should nurse monitor if administering antifungals? (!, 4)

A

They’re very toxic!

Monitor renal, hepatic fx, CBC (%blood, platlet b/c excessive bruising)

48
Q

Pressure generated through semipermeable membrane?

A

Osmotic

49
Q

Diffusion?

A

Movement of un/charged particles from [High] to [Low]

50
Q

What is tonicity if ECF > ICF

A

Hypertonic. Stronger forces draw H2O.

51
Q

Causes of interstitial edema (4)

A

↑ capillary filtration pressure, permeability ↓ capillary colloidal osmotic pressure, lymphatic flow

52
Q

Most effective method to measure body fluid volume (do this every day)

A

Urine output

53
Q

What condition can occur w/ rapid infusion of hypertonic solution

A

Edema

54
Q

How do electrolyes fx a cell

A

Electrolyes form ions.

Ions help determine osmotic pressure of body fluids

55
Q

Normal values of electrolyes (5)

A
Na 135-145
K 3.5-5
Mg 1.2-2
Ca 9-10.5
P 3-4,5
56
Q

Hyponatremia fx on cell?

A

Cell swells

57
Q

What electrolytes is inversely related to calcium?

A

Phosphorus

58
Q

Isotonic fluid body deficit results in? (what travels w/ h2o?)

A

Hyponatremia

59
Q

Causes of hyponatremia (4)

Manifestations (4)

A

↓ renal fx, sweating, GI losses, SIADH

Edema, cramps, weakness, fatigue

60
Q

What to administer to counter hypermagnesemia

A

IV Ca

61
Q

What to monitor when administering NSS? (5)

A

Hypervolemia, edema, crackles, HR, BP

62
Q

PSNS neurotransmitter and fx (3)

A

Acetylcholine.

Fx pre/postganglionic neurons to ↑ digestion, nutrient absorption, and protein building to conserve energy

63
Q

What are Cholinergic Agents? (Parasympathomimetics) and !?

A

Imitate AChs to make PSNS fx

!? cannot be limited to specific site, often cause fx on whole body and cause undesirable adfx

64
Q

What is Duvoid (bethanchol)

A

Cholinergic agonist, used for non-obstructive post/operative/partum UTR, also reflux esophagitis

65
Q

What are cholinergic agonists used to treat? (4+1)

A

↑ bladder tone, excretions, GI secretions, mouth secretions for dry mouth (Sjogren)
relieve intraocular pressure

66
Q

Fx of anti-cholinergics?

A

Depresses PSNS and lets SNS dominate

Fight v Flight S/S

67
Q

Most common anti-cholinergic and fx on vitals?

A

Atropine.
↑ HR.
Found in natural produces (belladona) and in herbal therapy which can cause toxciity

68
Q

Anti-cholinergic Adfx? (7)

A

dry mouth, constipation, UTR, ↑ HR. ↓ sweating, blurred vision, dilated pupils

69
Q

Conditions worsened w/ anti-cholinergics? (8)

A

Narrow angle laucoma, GI/GU obstruction, prostatic hypertrophy, HTN, tachycardia, renal/liver dysfx

70
Q

ARF vs CRF

A

Acute Renal Failure - seriously ill. rapid decline in fx due to poor balance/excretion
Chronic - permanent loss of nephrons.

71
Q

Fx lost in CRF

A

fx kidney nephrons and GFS. Remainders have to work harder

72
Q

Common indicator of ACF?

A

Azotemia, accumulation of nitrogenous wastes

73
Q

What does kidney activate to maintain Ca levels in body?

A

Vit K b/c it promotes Ca absorption

!P, it cannot excrete P

74
Q

Signs of recovery from ARF? (↑,↓, possibility?)

A

↑ urine output, ↓ creatinine

Possible BUN, Creatinine, K, and P levels remain elevated but eventually will normalize

75
Q

Pre/Intrinsic/Post Renal? (3,3,2)

A

Pre - ↓ blood flow b/c hemorrhage, CHF, dehydration
Intrin - injury to kidney, ischemia, obstruction, etc.
Post - urine outflow obstruction (prostatic hyperplasia)

76
Q

Renal failure caused by acute dehydration?

Urinary obstruction?

A

dehy - pre

obs - post

77
Q

Prototype Diuretics. (5)

A

Thiazide (Hydrochlorotiazide), blocks Cl pump results in ↓Na, K, Cl
Loop (Furosemia), fx loop of Henle, results in ↓h2o, Na, K
Carbonic Anhydrase inhibitors (Acetazolamid), inhibits carbonic anhydrase, resulting in basic urine (treats glaucoma)
Potassium sparing (Spironolactone), sparts K in exchange of ↓Na and H2o
Osmotic (Mannitol), ↑ osmalrity of GFR, ↓h2o, Na, Cl

78
Q

Lab to monitor when giving Furosemide? (4)

A

HypoK, HypopH, HypoCa, hyperGlycemia

79
Q

Diuretic for glaucoma?

A

Acetazolamid (Diamox)

80
Q

Class of diuretics most commonly used for out/inpt conditions?

A

Loops

81
Q

What does Chlorothiazide do? (treats what caused by 4)

A

treat edema caused by HF, liver dz, and renal dz.

Also HTN

82
Q

What imbalance if pt has leg cramps, fatigue when taking thiazide?

A

Hypokalemia

83
Q

Which tubules are fx’d by thiazide? (and 2 electros)

A

Distal, Cl and Na

84
Q

MOST important instruction when giving pt diuretic therapy

A

Maintain fluid intake to avoid rebound

85
Q

Diamox is a…?

A

Carbonic Anhydrase Inhibitor

86
Q

Drug interactions to watch w/ Diamox? (2)

A

Lithium and Salicylate levels

87
Q

Nephritis v. Nephrosis

A

Nephritic - inflammatory response w/ ↓ GFR, results in retention and accumulation
Nephrotic - ↑ GFR, proteins in urine yo

88
Q

What causes edema in pt with nephritic syndrome and glomerulonephritis?

A

nephritis causes Na and H2o retention, glomerulo - ↓ plasma pressure (↓ GFR) and protein loss

89
Q

Bladder/UT dz (3)

A

Lower UTObs/Stasis - kidney ok but retained (can cause kidney dmg)
Spastic - failure to store b/c spasms/neural dmg
Flaccid - failture to empty b/c muscle/neuropathy

90
Q

Types of incontinence (3)

A

Stress - involuntary loss b/c coughing
Overactive - urgency b/c hyperdetrusor muscle
Overflow - loss b/c increase pressure w/out muscle activity

91
Q

Which incontinence includes dysfx detrusor?

A

Overflow

92
Q

Most common Bacteria w/ uncomplicated UTIs?

A

Ecoli