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NURS 3550 > Final Test Review > Flashcards

Final Test Review Flashcards

1
Q

What are the 5 elements of Poison Management?

A 
Supportive Care
ID poison
Prevent absorption
Poison Removal
Specific Antidotes
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2
Q

What is the MA for chelating agents?

A

Heavy metal antagonists. Forms chelates that are less toxic than free metals, which are easily excreted.

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3
Q

What ways can poisons be removed?

A 
Activated charcoal
Gastric Lavage
Whole-Bowel Irrigation
Surface Decontamination
Sodium Bicarb
Hemodialysis
Pharm Therapy
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4
Q

What are some drugs used for iron poisoning?

A

Deferoxamine, Deferasirox, Deferiprone.

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5
Q

What are some drugs for other heavy metals?

A

Dimercaprol, Edetate Calcium Disodium, Penicillamine, Succimer.

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6
Q

What is peptic ulcer disease?

A

Erosion of the gut wall and ulcers that can cause hemorrhage.

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7
Q

Why does peptic ulcer disease occur?

A

Imbalance of mucosal defensive factors and aggressive factors of mucus and bicarb.

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8
Q

How does gastric acid affect PUD?

A

Deteriorates stomach wall, leading to ulcers. Also activates pepsin, which injures unprotected cells.

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9
Q

What are the goals for PUD tx?

A

Alleviate symptoms, promote healing, prevent complications, prevent recurrence.

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10
Q

Name drugs that eradicate H. pylori, reduce gastric acidity, and enhance mucosal defenses.

A

Antibiotics, Proton pump inhibitors, mucosal protectants.

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11
Q

What are proton pump inhibitors?

A

Suppresses gastric acid secretion. Prefered over antihistamines. Chosen based on cost.

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12
Q

What are some PPIs?

A

-prazole drugs. Omeprazole, Esomeprazole, lansoprazole, pantoprazole.

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13
Q

How do antihistamine’s treat PUD?

A

Suppresses secretion of gastric acid.

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14
Q

What are the 4 types of antihistamines used in PUD?

A

Cimetidine,
Ranitidine,
Famotidine,
Nizatidine.

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15
Q

What are the 4 families of antacids?

A

Aluminum Hydroxide,
Magnesium Hydroxide,
Calcium Carbonate,
Sodium Bicarb.

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16
Q

How do antacids work?

A

Neuralize stomach acids using alkaline compounds.

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17
Q

What are the AE for antacids?

A

Constipation, diarrhea, sodium loading, interactions w/ other drugs.

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18
Q

How do antibiotics treat PUD?

A

Eradicate H. pylori.

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19
Q

What are some antibiotics that treat PUD?

A

Amoxicillin, bismuth, clarithrombycin, metroindazole, tetracycline, tinidazole.

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20
Q

What are some reason’s one antihistamine may be picked over another for PUD?

A
  • Cimetidine blocks hepatic drug enzymes, not chosen as often. Can cause CNS effects.
  • Ranitidine has little effect on drug metabolism.
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21
Q

How is an H. pylori infection managed?

A

2 antibiotics, and a PPI/antihistamine.

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22
Q

What are some other antiulcer drugs?

A

Sucralfate- creates barrier which promotes ulcer healing.

Misoprotosol- prostaglandin E1, prevents ulcers caused by NSAIDs. Don’t use in pregnancy.

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23
Q

What is selective toxicity?

A

Most antibiotics only affect bacterial organisms due to their structure. Not toxic to human cells.

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24
Q

Mechanisms for acquired resistance

A

Spontaneous mutation, conjugation (bacteria cocktail).

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25
Q

What is the MA of penicillin?

A

Weakens cell wall by causing bacteria to take up water. 2 actions- inhibit transpeptidases, disinhibition of autolysins. Only work on cells that are growing.

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26
Q

What are the differences between gram + bact and gram - bact?

A

Gram + have 2 wall layers,

gram - have 3 layers, making it harder for penecillins to penetrate.

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27
Q

What is the bata-lactam ring?

A

Beta-lactam rings determine:

1) affinity for PBPs on bacteria
2) resistance to Penicillinase
3) ability to penetrate the gram negative cell envelope
4) acid stability

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28
Q

What are the 4 classes of penicillians?

A

Narrow-spectrum penicillins: penicillinase sensitive
Narrow-spectrum penicillins: penicillinase resistant (antistaphylococcal penicillins)
Broad-spectrum penicillins (aminopenicillins)
Extended-spectrum penicillin (antipseudomonal penicillin)

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29
Q

Give an example of a narrow spectrum pen, that is pen sensitive?

A

Pen G.

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30
Q

Example of Narrow spectrum not pen sensitive penicillin.

A

Nafcillin

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31
Q

Give an example of a broad spectrum penicillin

A

Amoxicillin

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32
Q

Give an example of an extended class penicillin

A

Pipercillin

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33
Q

If someone is severely allergic to penicillin, what other class of antibiotics should NOT be given?

A

Cepha’s (due to potential cross allergy)

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34
Q

Run down of Pen G go.

A

First pen available, bacterialcidal to most gram + bact, first choice for pharyngitis, IE, syphillis. Available as 4 salts. All can be given IM, different absorption, K+ and Na salts can be given IV. Renal excretion.

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35
Q

Why are aminoglycides and penicillins given together, and how do they need to be administered?

A

Given for some infections cause pen weakens cell wall, allowing amino to get their faster. Must be given separately cause pen can deactivate amino.

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36
Q

What is the MA for cephalosporins?

A

Bind to PBP and disrupt wall synthesis. Activate autolysins. Effective when cells undergo growth and division.

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37
Q

How does resistance develop to cephalosporins?

A

Caused by beta-lactamase production which leave drug inactive. 2, 3, 4 and 5 gen highly resistant.

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38
Q

Example of 1st gen cepha

A

Cephalexin- active against gram +, modest gram -, no effective CSF concentrations.

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39
Q

2nd gen cepha

A

Cefoxitin- effective against gram-, poor CSF distribution, good resistance to beta-lactamase.

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40
Q

3rd gen Cepha

A

Cefdinir- good gram - response, good CSF distribution, resistant to beta-lactamase.

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41
Q

4th gen cepha

A

Cefepime- highest affinity for gram - bact, highest resistance to beta-lactamase, good distribution to CSF.

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42
Q

5th gen cepha

A

Ceftaroline- gram - bact, highest resistance to beta-lactamase, good distribution to CSF.

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43
Q

Talk about Imipenem

A

Broad antimicrobial specturm, used to treat mixed infections. Binds to PBP 1 and 2, weakening bact cell wall. Active against gram +/-. IV admin. Renal excretion. Penetrates CSF.

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44
Q

Talk about Vancomycin

A

Used for C. Diff, pts allergic to pen. Major renal and ototoxicity. Inhibits cell wall synthesis. Only active against gram +. Given IV.

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45
Q

What are the AE for vancomycin

A

Renal failure, trough serum levels important, rapid infusion can cause flushing, rash, pruritus, urticaria, tachy, hypo.

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46
Q

What other drugs affect the cell wall?

A

Fosfomycin
Aztreonam
Telavancin

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47
Q

Talk about oral tetracyclines and Ca, Fe, Mg, Al, and Zn.

A

Can form non-absorbable chelates which can be toxic. To avoid, administer separately which drugs containing those things.

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48
Q

What is tetracycline

A

Broad spectrum antibiotic, bacteriostatic at therapeutic concentrations, does not affect mammalian cells, not usually drug of choice. Used to treat acne, PUD, peridontal disease, do not admin with food. Percautions for pregant women, renal disease, kids under 8.

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49
Q

What are macrolides?

A

Broad-spectrum antibiotics that inhibit bacterial protein synthesis. Ie. Erythromycin.

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50
Q

What is erythromycin?

A

Macrolide, inhibits protein synthesis, spectrum similar to pen, first drug for many infections, used as alternative to pen. First choice for whooping cough, diptheria, chlamydia, pneumonia. PO, IV admin. Dont give with food. Hepatic excretion (inhibits CYP3A4).

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51
Q

What is clindamycin?

A

Macrolide, only indicated for certain anaerobic infections outside CNS, inhibits protein synthesis, used for severe strep A.

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52
Q

What is linezolid?

A

Used against MRSA and vanco-resistant bugs. Protein synthesis inhibitor.

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53
Q

What is dalfoprisitn/quinuprisitin?

A

Inhibits bacterial protein synthesis, used for vanco-resistant bug and MRSA, inhibits CYP 3A4.

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54
Q

What is tigecycline?

A

Bacteriostatic inhibitor of protein synthesis, broad spectrum antibiotic. Only approved for intra-abdo infections and complicated skin infections.

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55
Q

What is Retapamulin/ mupirocin?

A

drugs for impetigo

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56
Q

What drugs should you not combine erythromycin with?

A

Theophyline, carbamazepine, warfarin, verapamil, diltiazem, HIV protease inhibitors, -azole antifungal drugs.

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57
Q

What is a unique response to linezolid?

A

Can cause reversible myelosuppression (anemia, leukopenia, thrombocytopenia)

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58
Q

What are the main uses for fluoroquinolones?

A

Broad spectrum agents. Used for aerobic gram - and some gram +.

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59
Q

What are the AE of fluoroquinolones?

A

GI effects, CNS effects, candida infections, tendon rupture, phototoxicty, increased risk for C. Diff.

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60
Q

what populations should not use fluoroquinolones due to tendon rupture?

A

60+ pop, pts taking glucocorticoids, pts who undergo kidney, heart, lung transplant.

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61
Q

What is the MA of alkylating agents?

A

Transfer an alkyl group from the drug to DNA of cells, causes difficulty in replicating. Not phase specific.

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62
Q

What is the MA of platinum agents?

A

Create cross-links in the DNA, causing difficulty replicating. Non-phase specific.

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63
Q

What is the MA of antimetabolites?

A

S-phase specific, stops DNA from being made, causing problems with cell replication.

64
Q

What is the MA for hypomethylating agents?

A

Inhibits DNA methyltransferase, causes apoptosis.

65
Q

What is the MA for antitumour antibiotics?

A

Interact with DNA which causes cell injury. Only used to treat tumours, not infections.

66
Q

What is the MA for mitotic inhibitors?

A

M-phase specific, blocks mitosis, leading to inability to replicate.

67
Q

What is the MA of topoisomerase inhibitors?

A

Alter the shape of supercoiled DNA, causes cell death by disrupting DNA while drug is present.

68
Q

What are the main AE’s of cancer drugs?

A

Anemia, alopicia, thrombocytopenia, constipation, delirium, edema, fatigue, NV.

69
Q

What is the difference between cell-cycle phase specific and non-phase specific drugs?

A

Phase specific only affect cells during a particular phase, changes admin times and doses, and routes. Non phase specific can be given whenever and have more routes.

70
Q

What is antibody mediated

(humoral) immunity?

A

Branch of the immune system that is done by antibodies. Antibodies bind to antigens and have a specific role.

71
Q

What is cell-mediated immunity?

A

Targets are attacked by specific immune cells.

72
Q

What are cytolytic T-lymphocytes?

A

Attack and kill target cells directly. Attack determined by presence of antigen molecules on the surface of target cell and specific receptors for that antigen on the surface of the T cell. Also known as CD8 cells and cytotoxic T cells.

73
Q

What are macrophages?

A

begin in bone marrow, enter as monocytes, infiltrate tissues, evolve into macrophages.
o Primary function is phagocytosis.
o Specific acquired immunity- required for activation of T cells, final mediators of DTH, phagocytize cells that have been tagged with antibodies.

74
Q

What are helper T lymphocytes?

A

contribute to immune response by
o Essential role in antibody production by B cells.
o Release factors that promote type IV sensitivity reacttions (delayed-type hypersensitivity)
o Participate in activation of cytolytic T cells.
o Helper cells required for effective immune response. Attacked by HIV.

75
Q

What are B lymphocytes?

A
  • make antibodies. Mediate humoral immunity. Circulate in the blood and lymph. B cells produced in bone marrow.
76
Q

What does IgA do?

A

Found in mucous membranes in GI tract, lungs. First line of defence.

77
Q

What does IgD do?

A

Receptor for antigen recognition.

78
Q

What does IgE do?

A

Stimulates release of histamine, heparin, and mediators causing allergy symptoms.

79
Q

What does IgG do?

A

Promotes target cell lysis, enhances phagocytosis,

80
Q

What does IgM do?

A

Fixes complement, promoting cell lysis, serves as receptor for antigen recognition.

81
Q

What are major histocompatibility complexes?

A

Activate cyto T’s and helper T’s. Guide cyto T’s to target cells. Provide basis for distinguishing between self and non-self cells.

82
Q

How does the classical pathway cause cell death?

A

C1 gets activated by antibodies, which leads to a series of reactions that injures cells, which form membrane attack complexes, leading to death.

83
Q

What is active immunity?

A

Response to an infection or vaccine or toxoid.

84
Q

What is passive immunity?

A

Admin of antibodies. Immunity only lasts as long as antibodies are present.

85
Q

3 contradictions to Vaccines

A

a) Anaphylactic reaction to specific vaccine.
b) Anaphylactic reaction to component of vaccine.
c) Moderate to severe illness w/ or w/o fever.

86
Q

What is the difference between bactericidal and bacteriostatic drugs?

A

Bacteriostatic means the drug prevents growth of bacteria. Bactericidal means the drug kills the bacteria.

87
Q

What is the purpose of broth dilution and disk diffusion culturing?

A

To see what grows from a culture in order to know what antibiotics to use.

88
Q

Why is the misuse of antibiotics a problem?

A

Because resistance occurs due to things mutating and then drugs aren’t as effective and more people die.

89
Q

What are the 3 major symptoms of diabetes?

A

Polyphasia, polydipsia, polyuria.

90
Q

What are the 3 classes of steroid hormones produced by the adrenal cortex?

A

Glucocorticoids, Mineralocorticoids, androgens.

91
Q

What do mineralocorticoids do?

A

Modulate salt and water in body.

92
Q

What do androgens do?

A

Sex hormones. Testosterone, estrogen ya know.

93
Q

What do glucocorticoids do?

A

Influence carb metabolism, maintain CV system, and keep body alive.

94
Q

What are the therapeutic uses of glucocorticoids?

A

RA, systemic lupus erythematosus, IBD, allergic reactions, asthma, neoplasms, derm disorders, suppress allograft rejection.

95
Q

what is the MA of glucocorticoids?

A

Modulate the production of regulatory proteins.

96
Q

How do glucocorticoids affect metabolism of carbs, fats and proteins?

A

Promote synthesis of glucose by amino acids, which reduces glucose uptake. Suppress protein synthesis. Stimulates lipolysis.

97
Q

How do glucocorticoids affect the inflammatory process?

A
  • Inhibit creation of chemical mediatiors.
  • Suppress infiltration of phagocytes.
  • Suppress proliferation of lymphocytes, inhibiting immune process of inflammation.
98
Q

STRESSED Cushings Acronym

A

Skin is Fragile
Truncal Obesity in the Arms
Round face (like a moon),Reproductive issues (Amennorhea and Erectile Dysfunction)
Ecchymosis andElevated Blood Pressure
Striae in the abdomen and extremities (Purplish)
Sugar is High (Hyperglycemia)
Excessive body hair (Hirsutism),Electrolyte Imbalance (Hypokalemia)
Dorsocervical Fat Pad (Buffalo Hump) &Depression

99
Q

STEROID Acronym for Addison’s disease

A

STEROID
Sodium is low,Sugar is low andSalt Cravings
Tired all the time and muscle weakness
Electrolyte imbalance (high potassium and high calcium)
Reproductive difficulties (Irregular menstrual cycle and Erectile dysfunction)
LOw blood pressure
Increased skin pigmentation or hyperpigmentation of the skin
Diarrhea, nausea andDepression

100
Q

What are the 2 mineralcorticoid’s?

A

Aldosterone and Fludrocortisone

101
Q

What tests are used to diagnose Addison’s and Cushing’s disease?

A

ACTH stimulation test, insulin tolerance test, CT, antibody tests, 24 hr urine, saliva tests.

102
Q

Why do glucocorticoids have greater inflammatory effects than NSAIDs?

A

Cause they interfere with the creation of inflammatory producs.

103
Q

What phase of the menstrual cycle are estrogen and progesterone at their highest?

A

Estrogen spikes at ovulation, progesterone spikes in the luteal phase.

104
Q

What are the physiologic effects of estrogen?

A

Support development of sex characteristics in females, effect bone mass positively, decrease cholesterol levels, promote and suppress blood coagulation, protect neurons, maintain glucose levels.

105
Q

What are the therapeutic indications of estrogen?

A

Menopause hormone therapy, female hypogonadism, acne treatment, palliation in men w/ prostatic cancer.

106
Q

What are contraindications for estrogens?

A

Hx of DVT, PE, stroke, MI, liver problems, cancers.

107
Q

What does progesterone do?

A

Acts before gestation, prepares uterus for pregnancy,

108
Q

What are the therapeutic uses of progesterone?

A

Contraception, menopause hormone therapy, dysfunctional uterine bleeding.

109
Q

What does hormone therapy do for women going through menopause?

A

Treats hot flahses, night sweats, vaginal atrophy, prevents osteoporosis.

110
Q

What are some of the AE of estrogen?

A

Nausea, can cause endometrial hyperplasia, may be teratogenic.

111
Q

Why are progesterone and estrogen combined for hormone therapy?

A

Estrogen to manage symptoms of estrogen loss, progesterone to counteract the adverse effects of estrogen on the uterus.

112
Q

What are the risks for hormone therapy?

A

CHD, MI, DVT, PE, stroke, breast cancer, gallbladder disease, dementia.

113
Q

How do oral contraceptives work?

A

Inhibit ovulation by suppressing FSH, and suppressing LH. Also thickens cervical mucus, and alters endometrium.

114
Q

What are the risks associated with OCs?

A

Ovarian cancer, endometrial cancer, ovarian cysts, pelvic inflammatory disease, anemia, acne.

115
Q

What is PMS and what drugs help it?

A

SSRIs, NSAIDs, Diuretics, HCs.

116
Q

What are the uterine relaxants (tocolytics)?

A

Magnesium Sulfate
Indomethacin
Nifedipine
Turbutane

117
Q

What are the 2 reasons oxytocic’s are used?

A
  • Mom’s who are overdue.

- when the baby needs to come out for everyone’s safety.

118
Q

What are the risks of magnesium sulfate?

A

Doesn’t work. High risk of infant mortality, fetal bone changes, hypotension, flushing, headache etc, pulmonary edema.

119
Q

What are the 3 groups of uterine stimulants?

A

Oxytocics, Ergot alkaloids, prostaglandins.

120
Q

What does oxytocin do?

A

Used to cause contractions in uterus, gets baby out in a jiffy.

121
Q

What is ergot alkaloids used for?

A

Prevent and control bleeding.

122
Q

What are prostaglandins used for?

A

Used for postpartum bleeding.

123
Q

What are androgens?

A

Hormones produced by testes, ovaries, and adrenal cortex. Effect sex characteristics of both sexes.

124
Q

What are the benefits to hormone replacement in males w/ hypogonadism?

A

Restored libido, increased ejaculate volume, secondary sex characteristics.

125
Q

What are the AE of anabolic steroid abuse?

A

hypertension, suppressed release of LH, FSH, testicular shrinkage, sterility, gynecomastia, acne, kidney damage. All other AE of testosterone but worse due to high dosage.

126
Q

What potential psychological effects can anabolic abuse cause?

A

depression, manic episodes, aggressiveness, abuse syndrome.

127
Q

What factors contraindicate PDE5 in males?

A

Men taking nitrates, alpha blockers, CYP3A4 inhibitors.

128
Q

Why does viagra mess with nitrates?

A

Both cause hypotension, causing men to drop it like its hot.

129
Q

What happens when viagra is combined with CYP3A4 inhibitors?

A

CYP3A4 inhibitors suppress metabolism of sildenafil, leading to an increase of levels.

130
Q

What are some examples of CYP3A4 inhibitors?

A

Erythromycin, itraconazole, cimetidine, grapefruit juice.

131
Q

What are the guidelines for pts taking nitrates and PDE5 inhibitors?

A

Take at least 24 hours apart. Absolutely contraindicated so avoid use as much as possible.

132
Q

What is the patho of benign prostate hyperplasia?

A

Overgrowth leading to mechanical obstruction.

133
Q

How do 5-alpha-reductase inhibitors help BPH?

A

Slowly reduce prostate through drug ways.

134
Q

What are the 2 types of diabetes?

A

T1 and T2. T1 is an autoimmune disease. T2 is insulin resistance.

135
Q

Why is the Ac1 test used to monitor diabetes?

A

Reflects average blood glucose levels over 2 or 3 months.

136
Q

What are the main goals of therapy for diabetes?

A

Prevent long term complications and manage hyperglycaemia symptoms.

137
Q

What are the 3 types of insulin (time)?

A

Short acting (clear), intermediate acting (cloudy), long acting (clear).

138
Q

What are the peak times for the different types of insulin?

A

Rapid- peak 1-2 hrs.
Intermediate- 5-8 hrs.
Long-acting- no peak.

139
Q

What insulin can be given IV?

A

Regular insulin only!

140
Q

What factors contribute to insulin resistance?

A

Metabolic syndrome, race, sedentary lifestyle, family hx, hypertension.

141
Q

What does metformin do?

A

Decreases hepatic production of glucose and reduce insulin resistance.

142
Q

What are sulfonylureas and what do they do?

A

Stimulate insulin release, increase insulin sensitivity.

143
Q

What are the side effects of sulfonylureas?

A

Hypoglycemia, weight gain, GI distres.

144
Q

What are the side effects for metformin?

A

GI effects, headache, dizziness, anorexia, fatigue.

145
Q

What are alpha-glucosidase inhibitors and what are they used for?

A

Block enzymes that break down complex carbs.

146
Q

What are AEs for alpha-glucosidase inhibitors?

A

Abdo cramping, diarrhea, flatulance.

147
Q

What are meglitinides? MA and AE.

A

Stimulate insulin release from pancreatic islet cells. AE: hypoglycemia, weight gain, flu-like symptoms.

148
Q

What are thiazolidinediones. MA and AE.

A

MA: improve insulin sensitivity, transport and utilization.
AE: CV events, weight gain, edema.

149
Q

What are incretin enhancers. MA and AE.

A

MA: Signal pancreas to increase insulin and liver to stop glucagon production.
AE: Flu-like, URTI, nausea, fatigue, headache, diarrhea.

150
Q

What are the therapeutic indications for metformin?

A

Glycemic control, prevention, gestational diabetes, PCOS.

151
Q

What is an example of meglitinides?

A

Repaglinide and nateglinide.

152
Q

What is an example of a thiazolidinediones?

A

Pioglitazone.

153
Q

What is an example of AGIs?

A

acarbose.

154
Q

What drugs interact with insulin?

A

hypoglycaemic agents, hyperglycaemic agents, beta blockers.

155
Q

How can you manage hypoglycemia?

A

Sugary snacks on hand, IV fluids, sugar.

156
Q

How can uncontrolled diabetes affect mom and baby?

A

Infant mortality.

NURS 3550 (11 decks)

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