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NUR311 > Exam II > Flashcards

Exam II Flashcards

1
Q

List and explain the 4 defensive factors which protect the stomach and duodenum from self-digestion.

A

Mucus – forms a barrier to protect underlying cells from gastric acid and pepsin.
Bicarbonate – neutralizes any acid which penetrates the mucus.
Blood flow – maintains integrity or health of the mucosa
Prostaglandins – Stimulates mucus and bicarbonate, vasodilates blood vessels, suppresses gastric secretion

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2
Q

List and explain 5 aggressive factors which predispose the stomach and duodenum to ulcerations.

A

Helicobacter pylori (H. pylori) – gram-negative bacillus which lives between the mucus layer and the mucosa. Produces CO2 and ammonia from urea which damages the mucosa.
NSAIDs – decreases the production of prostaglandins which decreases blood flow, decreases bicarbonate and mucus secretion, and increases gastric acid.
Gastric Acid – injures cells of the mucosa and activates pepsin.
Pepsin – breaks down protein of the gut wall.
Smoking – delays healing of ulcers and increases risk of recurrence.

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3
Q

What are three mechanisms of action for antacids?

A

Binds gastric acid and forms a neutral salt, decreases pepsin if pH > 5, and stimulates prostaglandins.

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4
Q

How are antacids administered in relation to meals, sleep, or other drugs? If not eating, how often are they given?

A

1 and 3 hrs after meals and at bedtime, 1 hour before another drug, or every 2 hours if not eating

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5
Q

Which antacids can cause complications in heart failure and renal disease?

A

Aluminum hydroxide and sodium bicarbonate – heart failure, magnesium hydroxide – CNS toxicity in renal patients

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6
Q

How do histamine2 receptor antagonists work?

A

Block H2 receptors on parietal cells which suppress gastric acid secretion and decrease the hydrogen ion concentration in gastric acid.

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7
Q

How are histamine2 receptor antagonists administered in relation to meals?

A

May be taken without regard to meals, except take Tagamet with food

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8
Q

Which histamine2 receptor antagonist is noted for drug-drug interactions caused by inhibition of hepatic drug-metabolizing enzymes?

A

cimetidine (Tagamet)

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9
Q

Which histamine2 receptor antagonist is known for its ability to block androgen effects?

A

cimetidine (Tagamet)

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10
Q

Proton-pump inhibitors may decrease the absorption of antifungals by what action?

A

Decreased gastric acid production

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11
Q

When is esomeprazole/nexium given?

A

Esomeprazole (Nexium) is given one hour before a meal

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12
Q

How long does it take for full recovery of the H+, K+-ATPase pump after stopping a proton pump inhibitor?
Why? How long for partial recovery?

A

Weeks due to irreversible inhibition. 3-5 days.

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13
Q

Why is misoprostol (Cytotec) used?

What are the mechanisms of action?

A

Prevention of NSAID-caused gastric ulcers. Stimulates the secretion of mucus and bicarbonate, vasodilates blood vessels, suppress gastric acid secretion. Replaces prostaglandins.

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14
Q

Why is misoprostol (Cytotec) not given during pregnancy?

A

Stimulates uterine contractions.

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15
Q

How does sucralfate (Carafate) work? When should it be given?

A

Polymerization and cross-linking occurs when the pH is < 4. It adheres to the crater for 6 hours. Given on an empty stomach.

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16
Q

How many hours must elapse between an antacid and sucralfate (Carafate)? Between other drugs and sucralfate (Carafate)?

A

1 hour between an antacid and sucralfate.

2 hours between drugs and sucralfate.

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17
Q

In order to kill Helicobacter pylori, what combination of drugs is given?

A

2-3 antibiotics with a proton pump inhibitor or histamine-2 receptor antagonist

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18
Q

How does bismuth (Pepto-Bismol) work? What are two common side effects?

A

Disrupts the cell wall of H. pylori, inhibits urease, and keeps H. pylori from adhering to the mucosa. Black tongue and stools.

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19
Q

At what pH will pepsin be decreased?

A

> pH 5

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20
Q

What is the preferred drug category for the prevention of NSAID-induced ulcers?

A

Proton Pump Inhibitors

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21
Q

What are two signs of gastrointestinal bleeding?

A

Black, tarry stools and coffee-ground vomitus.

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22
Q

What is the acid-neutralizing capacity (ANC)?

A

The number of mEq of hydrochloric acid that is neutralized by a given amount of the antacid.

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23
Q

What are MDIs and how should they be used?

A

Metered-dose inhalers. Small, hand-held, pressurized devices. Begin slow inhalation before activation, hold medicine in lungs for 10 seconds, and wait 1 minute between activations.

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24
Q

What are SMIs and how should they be used?

A

Soft mist inhalers. Begin slow inhalation, hold medicine in lungs for 10 seconds, and wait 1 minute between activations.

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25
Q

What is the advantage of DPIs?

Disadvantage? How fast should the patient inhale?

A

No hand-lung coordination needed, breath-activated. Must have adequate inspiratory flow to inhale powder. Inhale rapidly.

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26
Q

What are SVNs and how are they used? What are the advantages?

A

Small volume nebulizers. Converts a solution into a mist. Does not require timing of dose with inhalation, rapid deep inspiration, or hand strength.

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27
Q

List three ways glucocorticoids treat asthma.

A

Suppress inflammation and bronchial reactivity, decrease mucus production, increase number and responsiveness of beta-adrenergic receptors.

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28
Q

What is the first-line treatment for moderate to severe persistent asthma?

A

Inhaled glucocorticoids

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29
Q

Discuss the proper way to administer inhaled glucocorticoids. Why?

A

Gargle & spit after use. Use the beta-adrenergic inhaler first if one is used. The beta-adrenergic inhaler opens the airways so that the glucocorticoid can penetrate deeper into the lungs. Gargling and spitting decreases the chance of an oropharyngeal infection.

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30
Q

Why might oral glucocorticoids be necessary during stress even if asthma symptoms are controlled?

A

May need to supplement because stressful events require bursts of steroids. The patient may develop adrenal crisis without supplementation.

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31
Q

How does montelukast (Singular), a leukotriene modifier, work?

A

Blocks leukotriene receptors.

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32
Q

What are four mechanisms of action for leukotriene modifiers?

A

Bronchodilation, decreased mucus, decreased edema, and decreased eosinophilic infiltration

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33
Q

How does Cromolyn, a mast cell stabilizer, work?

A

Prevents mast cells from lysing and releasing histamine and other mediators.

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34
Q

How long must mast cell stabilizers be used to obtain a therapeutic effect?

A

May take several weeks.

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35
Q

How does omalizumab (Xolair) work? Why are patients asked to stay in the clinic after injections?

A

Myoclonal antibody binds free IgE so that it cannot bind to mast cells and cause their lysis. Risk for anaphylaxis.

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36
Q

Why are beta2-adrenergic agonists used?

A

Relieve bronchospasm and prevent exercise-induced bronchospasm.

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37
Q

What are the three mechanisms of action for beta2-adrenergic agonists?

A

Bronchodilation, suppression of histamine release, increased ciliary motility.

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38
Q

What is the difference between short-acting and long-acting beta2-adrenergic agonists?

A

Short-acting: lasts 3-5 hrs, immediate effect, used for relief of bronchospasm and before exercise.
Long-acting: given every 12 hrs, used to prevent bronchospasm.

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39
Q

Discuss the adverse effects of beta2-adrenergic agonists.

A

Tachycardia, angina, tremor, hypokalemia, nervousness, insomnia, seizures, paradoxical bronchospasm.

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40
Q

Discuss three drug-drug interactions of beta2-adrenergic agonists.

A

Decreased potassium levels with diuretics, glucocorticoids, and methylxanthines. Beta-blockers block their therapeutic effects. Use of long-acting inhaled glucocorticoids may protect against increase in asthma-related deaths with inhaled long-acting beta2-adrenergic agonists.

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41
Q

Explain how anticholinergic inhalers work. List three anticholinergic inhalers.

A

Interrupt parasympathetic response causing bronchodilation and decreased mucus.
Atrovent (ipratropium)
Spiriva (tiotropium)
Tudorza Pressair (aclidinium)

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42
Q

How many minutes should elapse between 2 inhalations of a beta-adrenergic agonist? How long should the patient hold his breath? In what order should you have the patient take two inhalations of an inhaled steroid and 2 inhalations of a beta-adrenergic agonist inhaler?

A

1 minute
Hold breath for 10 seconds
2 inhalations of beta-agonist, then 2 inhalations of inhaled steroid.

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43
Q

How many times per week can a patient have symptoms and still be classified as mild intermittent asthma? How many night-time symptoms in a month?

A

< 2 /week

< 2/month

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44
Q

A patient with daily asthma symptoms is classified as having what type of asthma?

A

Moderate persistent

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45
Q

Explain the PEF zone system. If a patient’s personal best is 1000 and the PEF drops to 600, what zone is he in? What drug should he use?

A

Yellow 50-80%.

Use short-acting beta agonist.

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46
Q

In conscious persons with severe asthmas exacerbations, which drugs should be administered first?

A

Beta-agonist and ipratropium (Atrovent) inhalations in a SVN

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47
Q

What drug categories are used to maintain patients who have COPD?

A

Long-acting beta2-adrenergic agonists or anticholinergic inhalers.

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48
Q

What drugs categories are used initially for acute exacerbations of COPD?

A

Short-acting beta2-adrenergic agonists alone or with an anticholinergic inhaler.

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49
Q

What two drugs may be added for control of severe COPD?

A

Longterm inhaled glucocorticoids and Roflumilast (Daliresp)

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50
Q

What fasting and casual plasma glucose levels suggest diabetes mellitus?

A

Fasting: > 126 mg/dL
Casual: > 200 mg/dL

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51
Q

What are the preprandial and postprandial targets for patients with DM/ What is the target for A1c?

A

Preprandial: 70-130 mg/dL
Postprandial: < 180 mg/dL
A1c: < 7% (154 mg/dL)

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52
Q

What is an electrolyte indication for insulin?

A

Hyperkalemia

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53
Q

How are insulin durations changed?

A

Change amino acid sequence or add a protein.

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54
Q

What are the mechanisms of action of insulin?

A

Transports glucose, amino acids, nucleotides, and potassium into cells. Promotes synthesis of glycogen, proteins, and triglycerides.

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55
Q

What are two contraindications for insulin?

A

Hypoglycemia and hypokalemia.

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56
Q

How long may opened insulin vials be stored at room temperature?

A

1 month.

57
Q

When drawing up a short-acting insulin and NPH insulin in the same syringe, which is drawn first? Which short-acting insulins may be mixed with NPH insulin?

A

Short-acting insulin.

Regular insulin and the rapid-acting insulin analogs – insulin lispro, insulin aspart, & insulin glulisine

58
Q

Are all clear insulins short-acting? Explain.

A

No. Insulin detemir (Levemir) and insulin glargine (Lantus) are long-acting insulins respectively and are clear.

59
Q

How can you minimize lipohypertrophy with insulin injections?

A

Use the same site only one time per month and keep the sites one inch apart.

60
Q

Which of the insulins may be given IV?

A

Insulin lispro (Humalog), insulin aspart (Novolog), insulin glulisine (Apidra), regular insulin (Humulin R or Novolin R).

61
Q

When should short, rapid-acting insulin analogs be given?

A

5-15 minutes before meals

62
Q

When should regular insulin be given?

A

30 minutes before meals

63
Q

When is NPH insulin given when given mixed with regular insulin?

A

30 minutes before breakfast and dinner

64
Q

How often is insulin glargine (Lantus) given? When is the drug usually dosed?

A

Once per day. Same time each day.

65
Q

Why are beta-blockers not recommended to be given to patients with diabetes?

A

Beta-blockers mask the signs of hypoglycemia and also prevent glycogenolysis, which allows glycogen to breakdown into glucose (necessary to prevent hypoglycemia).

66
Q

What are the symptoms of hypoglycemia?

A

Tachycardia, palpitations, sweating, nervousness, headache, confusion, drowsiness, fatigue. Also convulsions, coma, death.

67
Q

What is the treatment for hypoglycemia in alert patients? What about those taking alpha-glycosidase inhibitors?

A

Glucose tablet, orange juice, sugar cubes, honey, corn syrup, nondiet soda. Must use glucose tablets if take alpha-glycosidase inhibitors that prevent the breakdown of sugars into monosaccharides.

68
Q

What drug is administered to unconscious patients with hypoglycemia? How does it work? What works faster?

A

Glucagon. Breaks down glycogen into glucose and accelerates hepatic gluconeogenesis. IV glucose.

69
Q

What are the mechanisms of action of metformin (Glucophage), a biguanide?

A

Sensitizes cells to insulin and decreases liver glucose production. Also slightly inhibits intestinal absorption of glucose.

70
Q

What procedure is used for patients who use metformin (Glucophage) who are undergoing tests with radiocontrast dye?

A

Stop drug 1-2 days before procedure, drink lots of fluids, restart drug if BUN, Cr have normalized 48 hours after the procedure.

71
Q

What are the mechanisms of action of second-generation sulfonylureas? What occurs over time?

A

Stimulates the release of insulin from pancreatic beta cells. Lose effectiveness over time.

72
Q

What allergic contraindication do sulfonylureas have?

A

Sulfa

73
Q

What is adverse effect occurs with sulfonylureas and alcohol?

A

Dilsulfiram-like reaction

74
Q

What is the difference in mechanisms of action between sulfonylureas and glinides?

A

Glinides must be given immediately before meals, because their action is much faster than sulfonylureas.

75
Q

What is the mechanism of action of thiazolidinediones?

A

Sensitizes cells to insulin and decreases liver glucose production.

76
Q

What is the black box warning for thiazolidinediones? Signs to look for?

A

Avoid with severe heart failure due to water retention. Shortness of breath with exertion, crackles, chest pain, restlessness, changes in level of consciousness, increasing weight.

77
Q

What is the mechanism of action of alpha-glycosidase inhibitors?

A

Prevents breakdown of carbohydrates into monosaccharides.

78
Q

What adverse effect may occur with gliptins, incretin mimetics, and amylin mimetics?

A

Pancreatitis.

79
Q

What drug interactions may occur with gliptins, incretin mimetics, and amylin mimetics?

A

Hypoglycemia if taken with other antidiabetic drugs. Slows absorption of other drugs.

80
Q

How does canagliflozin (Invokana), a sodium-glucose co-transporter 2 inhibitor, work?

A

Blocks the reabsorption of glucose from the tubular urine back into the kidney’s bloodstream.

81
Q

What is selective toxicity? Why is it important?

A

Injuring a target cell or organism without injuring other cells or organisms in intimate contact with the target. Makes antibiotics safer.

82
Q

What is the difference between bactericidal and bacteriostatic?

A

Bactericidal – kills bacteria

Bacteriostatic – slows growth, phagocytes eliminate bacteria

83
Q

What are ranges and chances of drug resistance with narrow-spectrum and broad-spectrum antibiotics?

A

Narrow: smaller range
less resistance
Broad: larger range
more resistance

84
Q

What is acquired resistance? What are four ways bacteria become resistant to antibiotics? How do we lessen the chance for resistance?

A

Bacteria become less susceptible or lose sensitivity to drug.
1) Reduce drug concentration at sites, 2) Alter drug receptors, 3) Synthesize an antagonist, & 4) Produce drug-metabolizing enzymes.
Treat infection, not colonization, and use correct drug in correct concentration for entire course of therapy.

85
Q

What is the difference between the MIC and MBC?

A

MIC – amount of drug required to halt growth

MBC – amount of drug required to kill 99.9%

86
Q

Explain the importance of conjugation. What bacteria are most affected?

A

Conjugation allows the DNA code for drug resistance to be passed to other bacteria. Gram negative bacteria.

87
Q

What are two examples of suprainfections?

A

Candidiasis (yeast infection), Clostridium difficile infection (CDI) – 3 or more unformed stools in 24 hours with C. difficile or toxin from C. difficile in stools.

88
Q

What is the difference between an additive and potentiative effect?

A

Additive – sum of the effect

Potentiative – greater than the sum of the effects

89
Q

How do penicillins kill bacteria?

A

Disrupts cell wall (inhibits cross-linkages between peptidoglycan strands and lyses cell wall bonds)

90
Q

What is the major adverse effect of penicillins?

A

Allergic reactions

91
Q

What are some common signs and symptoms of anaphylaxis and serum sickness to penicillins?

A

Laryngeal edema, bronchoconstriction, severe hypotension, nausea and vomiting, tachycardia
Rash, hives, pruritis, arthralgias, fever

92
Q

Which three penicillins can be taken with food?

A

Penicillin V or VK, Amoxicillin, Augmentin

93
Q

Why is Penicillin G given IM?

A

Destroyed by gastric acid

94
Q

What lab abnormality can occur with Penicillin G or V when administered with potassium supplements?

A

Hyperkalemia

95
Q

What types of enzymes can destroy the penicillin molecule?

A

General beta-lactamases and penicillinases. Cephalosporinases deactivate cephalosporins.

96
Q

What is the advantage of Nafcillin over other penicillins?

A

Penicillinase-resistant

97
Q

Amoxicillin has what kind of bacterial spectrum?

A

Broad-spectrum

98
Q

How does clavulanic acid prevent amoxicillin from being deactivated?

A

Clavulanic acid inhibits beta-lactamase

99
Q

What are other beta-lactam antibiotic groups that have cross-allergenicities with penicillins?

A

Cephalosporins, carbapenems

100
Q

How do cephalosporins kill bacteria?

A

Inhibits cell wall synthesis

101
Q

Each subsequent generation of cephalosporins show more activity against what type of bacteria? How does each subsequent generation penetrate into the cerebral spinal fluid?

A

Gram negative bacteria and anaerobes, more resistant to beta-lactamases.
Each subsequent generation is more likely to reach the cerebral spinal fluid.

102
Q

What percentage of penicillin-allergic patients will have an allergic reaction to a cephalosporin?

A

< 1%

103
Q

What is the adverse effect seen with some cephalosporins and alcohol?

A

Antabuse-like effects: weakness, pulsating headache, chest pain, abdominal cramps

104
Q

What is the drug interaction is seen between IV calcium and IV cephalosporins in neonates?

A

Lung and renal precipitates.

105
Q

How does vancomycin kill bacteria? What bacteria does it kill?

A

Inhibits cell wall synthesis. Gram-positive bacteria.

106
Q

For what types of infection is vancomycin reserved? How is it given for CDI?

A

Severe C. difficile infections (CDIs), MRSA, & Staph. Epidermidis. Must be given PO for CDI, because cannot cross between GI tract and bloodstream.

107
Q

What are the signs and symptoms of Red Man Syndrome seen with the rapid infusion of vancomycin?

A

Red rash, hives, flushing, and pruritis on face & upper body. Hypotension, tachycardia. From histamine release, NOT an allergic reaction.

108
Q

Creatinine (Cr) is monitored with vancomycin therapy to avoid what? What is an indication for stopping vancomycin?

A

Renal failure. Stop if Cr rises 50%.

109
Q

Aztreonam is used to treat what type of infection? Why?

A

Gram-negative aerobic bacteria. Only attaches to PBPs on gram-negative aerobic bacteria.

110
Q

How do tetracyclines inhibit the replication of bacteria?

A

Inhibits protein synthesis at ribosomes

111
Q

How long should a patient wait after taking tetracycline before he has a glass of milk?

A

2 hours

112
Q

Why are tetracyclines avoided in children younger than 8 years of age?

A

Discoloration and hypoplasia of teeth

113
Q

What precautions should patients take with tetracycline?

A

Sun protection for photosensitivity. Take with a full glass of water to prevent esophageal ulcerations.

114
Q

How does erythromycin increase the chance of drug interactions?

A

Inhibits hepatic drug metabolism by P450 system.

115
Q

What is the major risk of drug interactions with erythromycin?

A

QT prolongation, which places person at risk for Torsades de Pointes,

116
Q

How does erythromycin inhibit the replication of bacteria?

A

Inhibits protein synthesis at ribosomes

117
Q

What are common adverse effects of erythromycin? How can this be mitigated?

A

Nausea, vomiting, diarrhea, epigastric pain. Give ethylsuccinate or enteric-coated tablets with food.

118
Q

How does clarithromycin (Biaxin) inhibit the replication of bacteria?

A

Inhibits protein synthesis at ribosomes

119
Q

Which macrolide does not inhibit hepatic enzymes? What drug interaction is still significant with this drug?

A

Azithromycin (Zithromax). Raises warfarin (Coumadin) levels.

120
Q

Linezolid is used primarily for what 2 bacteria?

A

Vancomycin-resistant enterococci (VRE) and methicillin-resistant Staphylococcus aureus (MRSA)

121
Q

How do sulfonamides inhibit replication of bacteria?

A

Competes with PABA in synthesizing folic acid and inhibits enzyme (dihydrofolate reductase) used to synthesize folic acid

122
Q

Why are sulfonamides contraindicated for infants less than 2 months old?

A

Kernicterus

123
Q

Which antibiotic drug class is avoided in patients with G6PD deficiency? Why?

A

Sulfonamides may cause hemolytic anemia.

124
Q

What drugs should be used with caution if the person in allergic to sulfonamides? Should a person with anaphylaxis try these drugs?

A

Sulfonylureas (oral antidiabetic drugs), loop diuretics, thiazide diuretics, and Celebrex (COX-2 inhibitor). Absolutely not due to a higher risk of hypersensitivity.

125
Q

Why should a patient stop using a sulfonamide with a blistering, sunburn-like rash? What other skin reaction may occur

A

Risk for Stevens-Johnson Syndrome. Photosensitivity.

126
Q

How do fluoroquinolones kill bacteria?

A

Inhibit synthesis of nucleic acids

127
Q

Why should fluoroquinolones not be used in patients under the age of 18?

A

Tendon injury

128
Q

For what type of bacteria are aminoglycosides given?

A

Aerobic gram negative bacilli

129
Q

Fluoroquinolones are ordered to be given in the morning with a multivitamin with minerals. Why is this contraindicated?

A

Calcium, aluminum, magnesium, iron, zinc may combine with the fluoroquinolone and prevent its absorption. Give fluoroquinolones 2 hours before or 6 hours after minerals. Give fluoroquinolones on an empty stomach.

130
Q

Ciprofloxacin (Cipro) is given for what common disease processes?

A

UTIs, enteric organisms.

131
Q

What are the two mechanisms of action for aminoglycosides?

A

Inhibit protein synthesis at ribosomes and insert abnormal proteins into the cell wall.

132
Q

Instead of keeping the serum drug levels above the MIC (minimum inhibitory concentration), how do aminoglycosides kill bacteria?

A

Concentration-dependent kill with post-antibiotic effect.

133
Q

Discuss the distribution of aminoglycosides.

A

Unable to cross cell membranes. Not absorbed orally and does not cross blood-brain barrier.

134
Q

What two organs can be damaged by aminoglycosides?

A

Ears, kidneys

135
Q

When are gentamicin peak and trough levels drawn?

A

Multiple doses: Peak level 30 min after IM or after 30-min IV infusion. Trough level immediately before next dose.
Daily dose: Trough level 1 hr before next dose. No need for peak level.

136
Q

What two antibiotics are reserved mainly for anaerobic bacteria?

A

Clindamycin (Cleocin) and metronizadole (Flagyl).

137
Q

What viruses does acyclovir (Zorivax) treat? Does it cure the disease?

A

Herpes simplex viruses (HSVs) – cold sores and genital infections, varicella-zoster virus (VZV) – chickenpox and shingles. The drug manages the symptoms, but does not cure or prevent transmission.

138
Q

When are omeprazole/Prilosec and iansoprazole/Prevacid given?

A

Directly before a meal

139
Q

When are proton pump inhibitors given?

A

Other than nexium, Prilosec, and Prevacid, given at any time

NUR311 (7 decks)

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