Exam 1 Flashcards

weeks 1-4 (132 cards)

1
Q

Tylenol MOA

A

inhibits synthesis of prostaglandins

dec pain and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tylenol Education

A

avoid alcohol
discontinue if rash forms
take exact dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tylenol adverse affects

A

Steven- Johnson Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aspirin MOA

A

produce analgesia

dec pain, fever and inflamation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aspirin Education

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

aspirin adverse affects

A

GI Bleed
DRESS
Hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

antihistamine

A

H1 antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

antihistamine education

A

sedation may occur

avoid alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

antihistamine adverse affects

A

anticholernegic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

insulin moa

A

dec blood glucose

stimulate uptake and inhibit liver production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

insulin education

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

insulin adverse affects

A

hypoglycemia
hypersensitivity
hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

glucocorticoids moa

A

modulate regulatory proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

glucocorticoids education

A

long term effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

glucocorticoid adverse affects

A

osteoporosis
infection
glucose intolerance
growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

vasopressin moa

A

identical to ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Vasopressin adverse affects

A

vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

desmopressin moa

A

analoug of ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

desmopressin adverse

A

no significant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

vasopression and desmopressin treat

A

hypothalamic and pituitary function (DI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

levothyroxine

A

T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Levothyroxine education

A

QD on empty stomach

Inc absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

levothyroxine adverse affects

A

tachycardia, angina, tremor, nervousness, insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

methimazole MOA

A

surpress TH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
methimazole Education
QD at the same time
26
methimazole adverse affects
agranulocytosis
27
hydrocortisone moa
provides adrenocorticoid
28
hydrocortisone education
follow prescribed schedule
29
hydrocortisone adverse affects | gluco- and mineralo-
thromboembolism peptic ulceration pheochromocytoma anaphylaxis
30
fludrocortisone MOA
mineralocorticoid
31
fludrocortisone education
follow prescribed schedule
32
fludrocortisone adverse affects
s/s of water and salt retention | hypokalemia
33
pharmacodynamics
drugs to the body - dose-response relationship - efficacy vs potency
34
single occupancy theory (p.dynamics)
respond proportionate to number of occupied receptors
35
modified occupancy
potency vs efficacy
36
affinity
strength of attraction b/w drug and receptor | - potency
37
intrinsic activity
ability of the drug to activate a receptor | -efficacy
38
agonist
activates receptors | - normal reg molecule response
39
antagonist
prevents receptors - stops reg molecule response * must have an agonist to produce effect
40
pharmacokinetics
body to the drugs - absorption - distribution - metabolism - excretion
41
absorption
drugs crossing the membrane into the blood
42
absorption factors (body)
route gastric emptying time surface area for absorption blood flow
43
absorption factors (drug)
``` solubility surface area dissolution structure pH ionization ```
44
solubility
channels and pores transport penetration
45
active transport
P-glycoprotein (PGP) | -multi drug transporter-OUT
46
LIVER ATS
into bile | -elimination
47
KIDNEY ATS
into urine | -excretin
48
metabolism
biotransformation
49
p450 system
inhibitor- blocks metabolic activity of enzyme | inducer- increases metabolic activity
50
1st pass effect
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
51
enterohepatic circulation
repeating cycle glucuronidation liver to bile bile to duodenum duodenum to intestine
52
excretion
removal of drug | - mainly in kidneys
53
passive tubular reabsorption
lipid soluble | H2O soluble
54
active tubular secretion
PGP
55
excretion factors
pH | polypharm
56
glomerular filtration
blood to urine | protein-bound drugs are not filtered
57
passive reabsorption
lipid-soluble drugs move back into the blood polar and ionized drugs remain in the urine
58
active transport
tubular pumps for organic acids and bases move drug to urine
59
nurse roles in drug admin
- pre-adim assesment - evaluate response - promote pt adherence - implement non-drug measures - minimize adverse effects and interractions - make PRN decisions - 5 R's
60
Drug routes
``` PO SC IM IV ID SL NGT R V ```
61
injection angles
IM-90 IV-25 SC-45 ID-10-15
62
5 Rights
``` PT ROUTE DRUG DOSE TIME ```
63
inflammation
``` INJURY: -chemokinase - vasodilation -neutrophil/macrophage binding PHAGOCYTOSIS ```
64
five signs of inflammation
``` redness swelling heat pain loss function ```
65
inflammatory response
a. vasodilation and inc vascular permeability b. recruitment of leukocytes c. phagocytosis of ANTIGEN
66
Immune Response
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
leukocytes
``` neutrophil lymphocyte monocyte eosinophils basophils ```
68
neutrophil
``` 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
mediators
complement kinins clotting factors cyto-, chemo-kinins
70
humoral immunity
- TH cell binds with self and non-self complex - displays MHC II on surface - TH releases interleukin to complete B cell activation
71
complement activation
- recruitment of inflammatory cels - opsonization of pathogen - killing of pathogen
72
IgA
1st life of defense | -secretions
73
IgM
target cell lysis | -miserable
74
IgD
surface of mature B cells
75
IgE
binds to mast cells- allergic response | - epi
76
IgG
PHAGOCYTOSIS | -gone
77
Cellular immunity
1- TH binds dendritic cell 2- TH cell stimulates dendritic cell to express co-stim molecules 3. dendritic cell can activate CD8
78
Hypersensitivity 1
IgE (anaphylaxis) | -Ag induces crosslink of IgE and Mast cells
79
Hypersensitivity II
IgG (blood transfusion) | -Ab directed against Ag mediated cell destruction
80
Hypersensitivity III
``` Immune Complex (artus Reaction) -Ab-Ag complex deposited in tissues ```
81
Hypersensitivity IV
Cell mediated | -mediate direct cellular damage
82
Insulin types
rapid, short. intermediate acting, long acting
83
rapid acting insulin used in patients with
hyperglycemic events in diabetic pt
84
short acting insulin is used with patients who
need more than 200 units a day
85
intermediate acting insulin MOA
protamine delays effect | -inc action time
86
long acting insulin
gives constant concentration for more than 24 hours
87
adverse effects of insulin
hypoglycemia hypersensitivity reactions hypokalemia
88
interventions
demonstrate technique and use of equipment | inform on s/s of hypo and hypergylcemic events
89
metaformin
increase insulin sensitivity | decrease glucose production
90
metaformin education
type II management not cure | take daily at the same time
91
sulfonylureas
decrease blood sugar-stimulate pancreas to receive insulin | increases receptor site sensitivity
92
sulfonyreas moa
pancreatic function needed
93
sulfonyreas education
daily at same time | type 2 treatment not a cure
94
hormone function
``` reproduction growth and development fluid homeostasis metabolism stress response ```
95
negative feedback loop
stimulus to sensor sensor to control mechanism mechanism to effector effector to stimulus
96
H2O soluble
``` ADH ACTH glucagon Insulin TSH ```
97
g-protein
2nd messenger
98
protein kinase
become kinase and associate with kinase
99
lipid soluble
T3 T4 Aldosterone Cortisol
100
lipid soluble process
mRNA transcription | no signaling cascade
101
lipid soluble receptors are in
nucleus and cytoplasm
102
Hormones are
``` synthesized -> primary location secretion-> cyclical feedback-> negative metabolize excretion ```
103
posterior pituitary
ADH- regulated by osmolality of plasma and detected in hypothalamus - act on kidney to reabsorb H20 when blood is too concentrated
104
oxytocin
similar to ADH | surpress diuresis
105
hypothalmic pituitary
SIADH | Diabetes insipidus
106
SIADH (hyper)
ectopic production from tumors and medically induced
107
s/s of SIADH
``` hypoatremia fatigue cramps vomitting anorexia postural BPchange ```
108
SIADH sequence
ADH - 2 aquaporin- permeable membrane to H2O reabsorbed in urine results in: inc plasma, inc concentration
109
Diabetes Insipidus (HYPO)
central and nephrogenic DI Idiopathic brain trauma/surgery/tumor chronic renal disease
110
Diabetes Insipidus s/s
polyuria polydyspia hyperatremia hyperosmolality
111
Diabetes Insipidus Treatment
replacement of ADH
112
Thyroid Hormone Synthesis
dietary iondine thyroglobulin protein tyrosine AA thyroid peroxide
113
TH secretion is stumalated by
TSH
114
Hypothyroidism
Thyroid gland dys. function
115
Hypothyroidism s/s
``` lethargy weakness dry-pale skin cold intolerance weight gain constipation bradycardia ```
116
graves disease
follicular cell hyper function | -leads to: destruction of cell
117
graves s/s
``` sleepiness inc appetite with weight loss heat intolerance tachycardia hyperreflex ```
118
graves treatment
radioactive iodine beta blocker surgical removal
119
DKA
diabetic ketoacidosis - more T1DM - <65 years old - decrease in glucose conc
120
NHHS
nonketoic hyperglycemia hyperosmolar syndrome - more T2DM - >65 years old - elevated ketones
121
Penicilin G- | Beta Lactams
MOA- bind to bacterial cell wall, resulting in cell death ED- notify professional if fever, diarrhea develop ADVERSE- seizures,anaphylaxis, serum sickness, urticaria
122
cephalosporin
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
vancomycin
MOA-binds to bacterial cell wall resulting in cell death ED- take as directed, contact professional if no improvement ADVERSE- hypersensitivity, nephrotoxicity, phlebitis
124
erythromyscin
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
gentamycin
MOA- inhibits protein synthesis at 30s ED-remain hydrated, report sines of hypersensitivity ADVERSE- ototoxicity, nephrotoxicity, ataxia, vertigo, hypersensitivity
126
sulfamethazole
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
NRTI
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
NNRRTI
MOA- inhibit RT, metabolized through cytochrome P450 ED- emphasize comliance to ensure efficacy ADVERSE- rash, dizziness, CNS effects, flu like
129
protease inhibitors
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
Integrase inhibitors
MOA- inhibits activity of integrate, blocks HIV-1 formation ED- caution pregnant women about rhabdomyolysis ADVERSE- CNS, Musculoskeletal rhabdomyolysis and myopathy
131
HIV Fusion inhibitors
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
CCR5 Antagonist
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