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PathoPharm > Exam 1 > Flashcards

Exam 1 Flashcards

weeks 1-4

1
Q

Tylenol MOA

A

inhibits synthesis of prostaglandins

dec pain and fever

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2
Q

Tylenol Education

A

avoid alcohol
discontinue if rash forms
take exact dose

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3
Q

Tylenol adverse affects

A

Steven- Johnson Syndrome

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4
Q

Aspirin MOA

A

produce analgesia

dec pain, fever and inflamation

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5
Q

Aspirin Education

A

avoid alcohol use
take sitting up and with water
take exact dose

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6
Q

aspirin adverse affects

A

GI Bleed
DRESS
Hypersensitivity

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7
Q

antihistamine

A

H1 antagonist

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8
Q

antihistamine education

A

sedation may occur

avoid alcohol

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9
Q

antihistamine adverse affects

A

anticholernegic

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10
Q

insulin moa

A

dec blood glucose

stimulate uptake and inhibit liver production

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11
Q

insulin education

A

s/s of hypoglycemia (hyper)
inform on how to monitor glucose
display the technique and equipment

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12
Q

insulin adverse affects

A

hypoglycemia
hypersensitivity
hypokalemia

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13
Q

glucocorticoids moa

A

modulate regulatory proteins

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14
Q

glucocorticoids education

A

long term effects

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15
Q

glucocorticoid adverse affects

A

osteoporosis
infection
glucose intolerance
growth

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16
Q

vasopressin moa

A

identical to ADH

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17
Q

Vasopressin adverse affects

A

vasoconstriction

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18
Q

desmopressin moa

A

analoug of ADH

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19
Q

desmopressin adverse

A

no significant

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20
Q

vasopression and desmopressin treat

A

hypothalamic and pituitary function (DI)

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21
Q

levothyroxine

A

T4

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22
Q

Levothyroxine education

A

QD on empty stomach

Inc absorption

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23
Q

levothyroxine adverse affects

A

tachycardia, angina, tremor, nervousness, insomnia

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24
Q

methimazole MOA

A

surpress TH production

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25
Q

methimazole Education

A

QD at the same time

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26
Q

methimazole adverse affects

A

agranulocytosis

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27
Q

hydrocortisone moa

A

provides adrenocorticoid

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28
Q

hydrocortisone education

A

follow prescribed schedule

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29
Q

hydrocortisone adverse affects

gluco- and mineralo-

A

thromboembolism
peptic ulceration
pheochromocytoma
anaphylaxis

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30
Q

fludrocortisone MOA

A

mineralocorticoid

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31
Q

fludrocortisone education

A

follow prescribed schedule

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32
Q

fludrocortisone adverse affects

A

s/s of water and salt retention

hypokalemia

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33
Q

pharmacodynamics

A

drugs to the body

  • dose-response relationship
  • efficacy vs potency
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34
Q

single occupancy theory (p.dynamics)

A

respond proportionate to number of occupied receptors

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35
Q

modified occupancy

A

potency vs efficacy

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36
Q

affinity

A

strength of attraction b/w drug and receptor

- potency

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37
Q

intrinsic activity

A

ability of the drug to activate a receptor

-efficacy

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38
Q

agonist

A

activates receptors

- normal reg molecule response

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39
Q

antagonist

A

prevents receptors

  • stops reg molecule response
  • must have an agonist to produce effect
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40
Q

pharmacokinetics

A

body to the drugs

  • absorption
  • distribution
  • metabolism
  • excretion
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41
Q

absorption

A

drugs crossing the membrane into the blood

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42
Q

absorption factors (body)

A

route
gastric emptying time
surface area for absorption
blood flow

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43
Q

absorption factors (drug)

A 
solubility
surface area
dissolution
structure
pH
ionization
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44
Q

solubility

A

channels and pores
transport
penetration

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45
Q

active transport

A

P-glycoprotein (PGP)

-multi drug transporter-OUT

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46
Q

LIVER ATS

A

into bile

-elimination

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47
Q

KIDNEY ATS

A

into urine

-excretin

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48
Q

metabolism

A

biotransformation

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49
Q

p450 system

A

inhibitor- blocks metabolic activity of enzyme

inducer- increases metabolic activity

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50
Q

1st pass effect

A

rapid inactivation of oral drugs
PO meds from GI tract to portal
high metabolic rate- inactivated on 1st pass no effect
- high metabolism of PO med from Hi to liver and
inactivated drug

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51
Q

enterohepatic circulation

A

repeating cycle glucuronidation
liver to bile
bile to duodenum
duodenum to intestine

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52
Q

excretion

A

removal of drug

- mainly in kidneys

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53
Q

passive tubular reabsorption

A

lipid soluble

H2O soluble

54
Q

active tubular secretion

A

PGP

55
Q

excretion factors

A

pH

polypharm

56
Q

glomerular filtration

A

blood to urine

protein-bound drugs are not filtered

57
Q

passive reabsorption

A

lipid-soluble drugs move back into the blood polar and ionized drugs remain in the urine

58
Q

active transport

A

tubular pumps for organic acids and bases move drug to urine

59
Q

nurse roles in drug admin

A
  • pre-adim assesment
  • evaluate response
  • promote pt adherence
  • implement non-drug measures
  • minimize adverse effects and interractions
  • make PRN decisions
  • 5 R’s
60
Q

Drug routes

A 
PO
SC
IM
IV
ID
SL
NGT
R
V
61
Q

injection angles

A

IM-90
IV-25
SC-45
ID-10-15

62
Q

5 Rights

A 
PT
ROUTE
DRUG
DOSE
TIME
63
Q

inflammation

A 
INJURY:
    -chemokinase
    - vasodilation
    -neutrophil/macrophage binding
PHAGOCYTOSIS
64
Q

five signs of inflammation

A 
redness 
swelling 
heat 
pain
loss function
65
Q

inflammatory response

A

a. vasodilation and inc vascular permeability
b. recruitment of leukocytes
c. phagocytosis of ANTIGEN

66
Q

Immune Response

A

NK cells- non-specific and attack ALL foreign
B cells- specific, produce antibodies with antigens need
CD4
Cytolytic T cells- secrete cytokines to activate other cells
HELPER
Cytotoxic T cells- destroy foreign, require CD4
TOXIC
Macrophage- engulfs and process Ag
Dendritic- capture Ag and migrate to lymphoid

67
Q

leukocytes

A 
neutrophil
lymphocyte
monocyte 
eosinophils 
basophils
68
Q

neutrophil

A 
60-80% -neutrophil 1st responder
20-30%-lymphocyte- immune response
3-8% - monocyte- phagocytosis 
1-6%-eosinophils - allergic rxn
0-2%-basophil- histamine by IgE
69
Q

mediators

A

complement
kinins
clotting factors
cyto-, chemo-kinins

70
Q

humoral immunity

A
  • TH cell binds with self and non-self complex
    • displays MHC II on surface
  • TH releases interleukin to complete B cell activation
71
Q

complement activation

A
  • recruitment of inflammatory cels
  • opsonization of pathogen
  • killing of pathogen
72
Q

IgA

A

1st life of defense

-secretions

73
Q

IgM

A

target cell lysis

-miserable

74
Q

IgD

A

surface of mature B cells

75
Q

IgE

A

binds to mast cells- allergic response

- epi

76
Q

IgG

A

PHAGOCYTOSIS

-gone

77
Q

Cellular immunity

A

1- TH binds dendritic cell
2- TH cell stimulates dendritic cell to express co-stim molecules
3. dendritic cell can activate CD8

78
Q

Hypersensitivity 1

A

IgE (anaphylaxis)

-Ag induces crosslink of IgE and Mast cells

79
Q

Hypersensitivity II

A

IgG (blood transfusion)

-Ab directed against Ag mediated cell destruction

80
Q

Hypersensitivity III

A 
Immune Complex (artus Reaction)
-Ab-Ag complex deposited in tissues
81
Q

Hypersensitivity IV

A

Cell mediated

-mediate direct cellular damage

82
Q

Insulin types

A

rapid, short. intermediate acting, long acting

83
Q

rapid acting insulin used in patients with

A

hyperglycemic events in diabetic pt

84
Q

short acting insulin is used with patients who

A

need more than 200 units a day

85
Q

intermediate acting insulin MOA

A

protamine delays effect

-inc action time

86
Q

long acting insulin

A

gives constant concentration for more than 24 hours

87
Q

adverse effects of insulin

A

hypoglycemia
hypersensitivity reactions
hypokalemia

88
Q

interventions

A

demonstrate technique and use of equipment

inform on s/s of hypo and hypergylcemic events

89
Q

metaformin

A

increase insulin sensitivity

decrease glucose production

90
Q

metaformin education

A

type II management not cure

take daily at the same time

91
Q

sulfonylureas

A

decrease blood sugar-stimulate pancreas to receive insulin

increases receptor site sensitivity

92
Q

sulfonyreas moa

A

pancreatic function needed

93
Q

sulfonyreas education

A

daily at same time

type 2 treatment not a cure

94
Q

hormone function

A 
reproduction
growth and development
fluid homeostasis
metabolism
stress response
95
Q

negative feedback loop

A

stimulus to sensor
sensor to control mechanism
mechanism to effector
effector to stimulus

96
Q

H2O soluble

A 
ADH
ACTH
glucagon
Insulin 
TSH
97
Q

g-protein

A

2nd messenger

98
Q

protein kinase

A

become kinase and associate with kinase

99
Q

lipid soluble

A

T3
T4
Aldosterone
Cortisol

100
Q

lipid soluble process

A

mRNA transcription

no signaling cascade

101
Q

lipid soluble receptors are in

A

nucleus and cytoplasm

102
Q

Hormones are

A 
synthesized -> primary location
secretion-> cyclical
feedback-> negative 
metabolize
excretion
103
Q

posterior pituitary

A

ADH- regulated by osmolality of plasma and detected in hypothalamus
- act on kidney to reabsorb H20 when blood is too concentrated

104
Q

oxytocin

A

similar to ADH

surpress diuresis

105
Q

hypothalmic pituitary

A

SIADH

Diabetes insipidus

106
Q

SIADH (hyper)

A

ectopic production from tumors and medically induced

107
Q

s/s of SIADH

A 
hypoatremia 
fatigue
cramps
vomitting 
anorexia
postural BPchange
108
Q

SIADH sequence

A

ADH - 2 aquaporin- permeable membrane to H2O reabsorbed in urine

results in: inc plasma, inc concentration

109
Q

Diabetes Insipidus (HYPO)

A

central and nephrogenic DI
Idiopathic
brain trauma/surgery/tumor
chronic renal disease

110
Q

Diabetes Insipidus s/s

A

polyuria
polydyspia
hyperatremia
hyperosmolality

111
Q

Diabetes Insipidus Treatment

A

replacement of ADH

112
Q

Thyroid Hormone Synthesis

A

dietary iondine
thyroglobulin protein
tyrosine AA
thyroid peroxide

113
Q

TH secretion is stumalated by

A

TSH

114
Q

Hypothyroidism

A

Thyroid gland dys. function

115
Q

Hypothyroidism s/s

A 
lethargy
weakness
dry-pale skin
cold intolerance
weight gain
constipation
bradycardia
116
Q

graves disease

A

follicular cell hyper function

-leads to: destruction of cell

117
Q

graves s/s

A 
sleepiness
inc appetite with weight loss 
heat intolerance
tachycardia
hyperreflex
118
Q

graves treatment

A

radioactive iodine
beta blocker
surgical removal

119
Q

DKA

A

diabetic ketoacidosis

  • more T1DM
  • <65 years old
  • decrease in glucose conc
120
Q

NHHS

A

nonketoic hyperglycemia hyperosmolar syndrome

  • more T2DM
  • > 65 years old
  • elevated ketones
121
Q

Penicilin G-

Beta Lactams

A

MOA- bind to bacterial cell wall, resulting in cell death
ED- notify professional if fever, diarrhea develop
ADVERSE- seizures,anaphylaxis, serum sickness, urticaria

122
Q

cephalosporin

A

MOA- 1st gen target gram positive, 2nd gen target gram negative and 3rd gen penetrate cerebral spinal fluid
ED- may be allergic, if allergic to penicillin
ADVERSE- anaphylaxis, swelling, urticaria, seizures, inc bleeding

123
Q

vancomycin

A

MOA-binds to bacterial cell wall resulting in cell death
ED- take as directed, contact professional if no improvement
ADVERSE- hypersensitivity, nephrotoxicity, phlebitis

124
Q

erythromyscin

A

MOA- suppresses protein synthesis at level of 50S bacterial ribosome, bacteriostatic
ED- caution pt to notify if fever and diarrhea occur
ADVERSE- torsades se pointes, ventricular arrhythmia, CDIFF

125
Q

gentamycin

A

MOA- inhibits protein synthesis at 30s
ED-remain hydrated, report sines of hypersensitivity
ADVERSE- ototoxicity, nephrotoxicity, ataxia, vertigo, hypersensitivity

126
Q

sulfamethazole

A

MOA- inhibits folic acid metabolism
ED- double stress, notify prof if rash, fever, or diarrhea develop
ADVERSE- erythema multiform, SJ syndrome, toxic epiderrmal, necrolysis

127
Q

NRTI

A

MOA- prevents formation of 3’-5’ phosphodiester
ED- importance of compliance and to discontinue if rash forms
ADVERSE- mitochondrial toxicity, SJ syndrome, CNS effects

128
Q

NNRRTI

A

MOA- inhibit RT, metabolized through cytochrome P450
ED- emphasize comliance to ensure efficacy
ADVERSE- rash, dizziness, CNS effects, flu like

129
Q

protease inhibitors

A

MOA- inhibit and block protease activity, viruses unable to infuse and inject
ED- monitor blood glucose if diabetic, discontinue if rash forms
ADVERSE- diarrhea, nausea, anorexia, elevated cholesterol. SJ syndrome

130
Q

Integrase inhibitors

A

MOA- inhibits activity of integrate, blocks HIV-1 formation
ED- caution pregnant women about rhabdomyolysis
ADVERSE- CNS, Musculoskeletal rhabdomyolysis and myopathy

131
Q

HIV Fusion inhibitors

A

MOA- prevent fusion of virus with cell membrane, prevents entry of HIV-1
ED- site reaction may occur,
ADVERSE- diarrhea, pneumonia, Site reaction, insomnia, neuropathy

132
Q

CCR5 Antagonist

A

MOA- blocks receptor site on cell membrane, blocking HIV virus from interacting with the cell
ED- caution about change in effectiveness with drug interaction, possible renal impairment, hypersensitivity
ADVERSE- marviroc, hepatotoxicity, dizziness

PathoPharm (1 decks)

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