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Pharmacology > Exam 2 Flashcards > Flashcards

Exam 2 Flashcards

1
Q

What type of drug is memantine?

A

An NMDA receptor blocker

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2
Q

What is the first and only drug in the NMDA drug class?

A

memantine

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3
Q

What is memantine used for?

A

moderate to severe Alzheimer’s disease

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4
Q

How does memantine work in the body?

A

It blocks NMDA receptors, which reduces high levels of glutamate that cause neuronal damage in Alzheimer’s

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5
Q

What are adverse effects on memantine?

A

CNS effects: dizziness, headache, increased confusion; constipation

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6
Q

What are some nursing considerations for NMDA drugs (memantine)?

A

Assist with ambulation (client can be dizzy), increase fluids and fiber, monitor adverse effects and include caregiver in instructions

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7
Q

When are cholinesterase inhibitors indicated?

A

For mild to moderate Alzheimer’s disease

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8
Q

T/F Cholinesterase inhibitors are effective in 1 of 12 patients.

A

True

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9
Q

How long do cholinesterase inhibitors delay or slow progression of AD?

A

A few months

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10
Q

How do cholinesterase inhibitors work?

A

They prevent the breakdown of ACh by cholinesterase and increase ACh levels in the brain

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11
Q

What are patients taking cholinesterase inhibitors at risk for?

A

Falls and safety issues

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12
Q

Cholinesterase drugs need to be tapered when discontinued. T/F

A

True

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13
Q

What are some cholinergic effects that may be shown in cholinesterase inhibitors?

A

They affect the GI system mostly; can cause N/V/D, increased salivation, involuntary defecation; Cardiovascular: bradycardia, hypotension, syncope

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14
Q

What drugs are contraindicated in cholinesterase inhibitors?

A

NSAIDS (cause GI bleed and ulcers) and anticholinergic drugs (reduce drug responses)

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15
Q

What drug is the prototype for cholinesterase inhibitors?

A

donepezil

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16
Q

What are nursing considerations for cholinesterase inhibitors (donepezil)?

A

Administer with food to decrease GI effects, assist with ambulation, monitor HR, weight loss, GI bleeding, CNS effects

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17
Q

T/F antipsychotics cause an increased risk of mortality in dementia.

A

True

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18
Q

What is the most prevalent neurologic disorder?

A

Epilepsy

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19
Q

What major risk is associated with seizure disorders?

A

Family planning risks (risk of abnormalities)

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20
Q

T/F Seizure meds need to be continued during pregnancy because of greater risk of seizures.

A

True

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21
Q

T/F Pregnant women and elderly have a higher frequency of seizures.

A

True

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22
Q

generalized onset seizures begin in ____ area of the brain and rapidly spread throughout ____ hemispheres of the brain

A

one, both

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23
Q

Tonic-clonic seizures may have an ____ and last ___ minutes.

A

aura, 1-2

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24
Q

T/F Absence seizures are more common in children starting at 3 years old, and go away in adolescence.

A

True

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25
Q

Absence seizures can be characterized by ‘staring into “space”. T/F

A

True

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26
Q

What is an atonic seizure?

A

A drop attack, lasting a few seconds.

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27
Q

What is the biggest concern for atonic seizures (drop attacks)?

A

Falls and injuries

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28
Q

What are myoclonic seizures?

A

Seizures involving the neck, shoulders and arms with 2 types of seizures.

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29
Q

What can status epilepticus (medical emergency) lead to?

A

hypoglycemia, acidosis, hypothermia, hypoxia, brain damage, death

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30
Q

What period of time must withdrawing antiepileptic drugs be done over?

A

6-12 weeks

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31
Q

What are problems associated with withdrawing antiepileptic drugs?

A

Physical dependence and risk for reoccurrence of seizures

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32
Q

What needs to be kept in consideration to antiepilectic drugs?

A

Family planning since this is a category D drug.

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33
Q

Which cultural groups metabolize antiseizure drugs differently and what needs to be done to achieve the same therapeutic effects as those of other cultural groups?

A

Arab Americans and Asian Americans; they may require lower doses and frequent dose adjustment

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34
Q

What drug type is for absence seizures?

A

Succinimides

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35
Q

What are the prototypes for barbiturates?

A

phenobarbital and primidone

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36
Q

How are barbiturates helpful as AED’s?

A

They reduce tonic-clonic, muscular and emotional responses to stimulation

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37
Q

What are disadvantages of barbiturates (phenobarbital and primidone)?

A

Low safety margin, profound CNS depression, respiratory depression, bradycardia, syncope and hypotension, and a high potential for drug abuse

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38
Q

What is the MOA of benzodiazepines?

A

Increases GABA

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39
Q

What do benzodiazepines end in?

A

-pam

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40
Q

What is the benzodiazepine prototype?

A

Diazepam

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41
Q

What should never be done and why regarding benzodiazepines?

A

Discontinuing abruptly can cause status epilepticus

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42
Q

What is the #1 treatment for status epilepticus?

A

benzodiazepines

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43
Q

What can benzodiazepines also be used for, besides seizures?

A

alcohol withdrawal

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44
Q

What is the only antidote for benzodiazepine toxicity?

A

flumazenil

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45
Q

What should be avoided with benzodiazepines (diazepam)?

A

Other CNS depressants/alcohol and grapefruit juice

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46
Q

What adverse effect is the most common with diazepam (benzos)?

A

CNS depression

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47
Q

What is the most serious adverse effect with diazepam?

A

Cardiovascular collapse; assess for bradycardia, tachycardia, hypotension and edema

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48
Q

What are hydantoins?

A

Antiepileptic drugs

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49
Q

What is the prototype for hydantoins?

A

Phenytoin

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50
Q

What is the use for phenytoin?

A

tonic-clonic and partial seizures

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51
Q

What do all hydantoins end in?

A

-toin

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52
Q

What is the most common adverse effect of phenytoin?

A

CNS effects–mild drowsiness and CNS depression

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53
Q

What are serious adverse effects of phenytoin?

A

Gingival hyperplasia, bone marrow suppression, and skin rash

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54
Q

What is gingival hyperplasia?

A

The swelling and overgrowth of gums

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55
Q

What is the black box warning for phenytoin?

A

If given too fast, it can cause hypotension and arrhythmias

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56
Q

How fast should phenytoin be given?

A

50mg/minute is the IV rate

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57
Q

What are signs of phenytoin toxicity?

A

nystagmus, ataxia, sedation, blurred/double vision

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58
Q

T/F IV phenytoin is incompatible with dextrose solutions.

A

True

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59
Q

T/F phenytoin decreases effects to oral contraceptives, warfarin and glucocorticoids.

A

True

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60
Q

What are some nursing considerations for hydantoins (phenytoin)?

A

Do not drive/perform hazardous activities if experiencing CNS effects, obtain regular dental checkups and brush teeth with a soft bristled toothbrush, do not abruptly stop medication

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61
Q

What is the only drug type used for absence seizures?

A

Succinimides

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62
Q

What is the prototype for succinimides?

A

ethosuximide

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63
Q

How long does it take ethosuximide to reach optimal effects?

A

4-7 days

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64
Q

ethosuximide, a succinimide, is ineffective at treating simple or complex partial and tonic clonic seizures. T/F

A

True

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65
Q

T/F ethosuximide cannot cause fatal pancytopenia and bone marrow suppression.

A

False

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66
Q

What drug can be used for all seizure types, migraines and mania?

A

valproic acid

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67
Q

What are serious adverse effects in valproic acid?

A

liver toxicity and neural tube defects

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68
Q

What is the serum drug level for valproic acid?

A

50-100 mcg/ml

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69
Q

What medication is used for valproic acid overdose?

A

naloxone

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70
Q

What are some nursing considerations for valproic acid?

A

Fall precautions and enteric coated tabs to minimize GI distress

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71
Q

What are goals of treatment for status epilepticus?

A

maintaining ventilation, correcting hypoglycemia and termination the seizure as well as initiating or continuing long term suppression drugs

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72
Q

What are two drugs that are used in status epilepticus?

A

lorazepam or diazepam

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73
Q

What drug is used alone or in combination for treating partial seizures?

A

carbamazepine

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74
Q

What drug can be used for neuropathy and partial seizures?

A

gabapentin

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75
Q

What drug should be taken into consideration with Asian ancestry and why?

A

carbamazepine, Asian ancestry has a high risk of Steven-Johnson syndrome

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76
Q

What are dermatologic adverse effects of carbamazepine?

A

rash, photosensitivity, alopecia, toxic epidermal necrosis and Stevens-Johnson syndrome

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77
Q

What is the black box warning for carbamazepine?

A

It can cause cytosis and aplastic anemia

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78
Q

What is something unique about carbamazepine?

A

It can decrease effectiveness of contraceptives and give false negatives on pregnancy tests

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79
Q

What are nursing considerations for carbamazepine?

A

Give at bedtime if possible (CNS effects), give with meals to reduce GI symptoms, use sunscreen, fall precautions

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80
Q

What pregnancy category is gabapentin?

A

C

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81
Q

What are adverse effects of gabapentin?

A

increased frequency of viral infections, weight gain and gastric upset

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82
Q

What two drugs should be avoided with gabapentin?

A

Morphine and hydrocodone

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83
Q

What are muscle spasms?

A

cramps or charlie horses

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84
Q

What is muscle spasticity?

A

a neurological condition where certain muscle groups remain in a continuous state of contraction

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85
Q

T/F Patients experiencing muscle spasticity are able to voluntarily relax their limbs.

A

False

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86
Q

What drug class is the 1st line for mild to moderate pain d/t muscle overexertion?

A

NSAIDS

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87
Q

How do centrally acting skeletal muscle relaxants work in the body?

A

They relieve actions in the CNS and do not work on the muscles themselves

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88
Q

What is the prototype for centrally acting muscle relaxants?

A

cyclobenzaprine

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89
Q

What is the MOA of cyclobenzaprine?

A

Enhances the inhibitory effects of GABA on receptors in the spinal cord

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90
Q

What are patients at risk for when coming off of cyclobenzaprine (a centrally acting muscle relaxant?)

A

physical dependence; abstinence syndrome, anxiety, restlessness, hallucinations and seizures

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91
Q

What age group should be cautioned with use of cyclobenzaprine?

A

65 and older; they are more likely to experience CNS effects

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92
Q

What are drugs used for spasticity?

A

baclofen, diazepam and dantrolene

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93
Q

T/F Baclofen has no direct effect on skeletal muscle, so it doesn’t decrease muscle strength.

A

True

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94
Q

How long of a period should baclofen be withdrawn over?

A

1-2 weeks d/t physical dependence

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95
Q

T/F PO Baclofen should be taken with food/milk.

A

True

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96
Q

What will nursing education of baclofen focus on?

A

Safety

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97
Q

What is the only benzo approved for spasticity?

A

diazepam

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98
Q

How does diazepam work in the body?

A

It acts in the CNS and mimics the actions of GABA

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99
Q

Which drug used for spasticity is direct acting on muscles and decreases muscle strength?

A

Dantrolene

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100
Q

T/F Dantrolene is also the treatment of malignant hyperthermia.

A

True

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101
Q

T/F Women taking estrogen and dantrolene are at a higher risk of hepatic toxicity.

A

True

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102
Q

What is the black box warning for dantrolene?

A

hepatotoxic death

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103
Q

higher virulence causes _____

A

more harm to the patient

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104
Q

What is pathogenicity?

A

The ability of an organism to cause disease

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105
Q

What is virulence?

A

A quantitative measure of an organism’s pathogenicity

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106
Q

What are exotoxins?

A

Proteins released by bacteria to surrounding tissues that can inactivate or kill host cells

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107
Q

What are endotoxins?

A

Harmful non-protein chemicals that are part of the outer layer of a normal cell and are released after a bacteria dies, causing inflammation, fever and chills.

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108
Q

T/F antibiotics may make a person feel worse before they feel better.

A

True

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109
Q

Describe gram positive bacteria.

A

Thick cell wall, retain violet color in stains

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110
Q

Describe gram negative bacteria.

A

Thin cell wall, lose violet color in stains

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111
Q

Which gram is harder to penetrate?

A

gram negative, because it has three layers.

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112
Q

Bactericidal drugs _____

A

kill bacteria

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113
Q

Bacteriostatic drugs ____

A

kill bacteria indirectly by slowing bacterial growth and allow natural defenses to eliminate the microorganism

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114
Q

Inhibition of bacterial cell wall synthesis works by ______

A

causing the cell wall to swell and burst

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115
Q

T/F in acquired resistance to antimicrobial drugs, the microbes become resistant, not the person.

A

True

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116
Q

Which antibiotics promote resistance?

A

Broad spectrum

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117
Q

How does antibiotic use promote resistance?

A

Antibiotics kill all of an infection besides one resistant organism, which rapidly divides

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118
Q

What is the most common site of HAIS (Healthcare Associated Infections)?

A

Catheters

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119
Q

What is important regarding cultures and antibiotics?

A

You must obtain the culture first and then start antibiotics.

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120
Q

What are indicators for success of antimicrobial therapy?

A

Fever reduction, resolution of s/s

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121
Q

What is a severe form of hypersensitivity reaction to abx?

A

Anaphylaxis

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122
Q

When do we see superinfections appear?

A

With broad spectrum abx use or long term abx

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123
Q

How can you prevent superinfections?

A

lactobacillus (probiotic) or yogurt

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124
Q

What are examples of superinfections?

A

C-diff, fungal infections in skin or oral mucous membranes

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125
Q

What are the drug classes that affect cell walls?

A

Penicillins, Cephalosporins, Carbapenems, Vancomycin

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126
Q

What is the MOA of penicillins (prototype PCN G (natural) and Ampicillin (broad spectrum)?

A

weaken and destroy cell wall, bactericidal

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127
Q

What is an enzyme that makes penicillin inactive?

A

penicillinase or anything ending in -ase

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128
Q

What penicillins can work against penicillinase?

A

Penicillinase-resistant PCNs

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129
Q

T/F allergies to penicillin may also happen in cephalosporins.

A

True

130
Q

T/F you cannot outgrow a penicillin allergy.

A

False

131
Q

T/F penicillin is effective against gram positive, gram negative and pseudimonas.

A

True

132
Q

PCN G (a natural penicillin) is ____ spectrum and includes most gram __ bacteria.

A

narrow, positive

133
Q

Ampicillin is a ___ spectrum and includes gram __ and some dram ___ bacteria.

A

broad, positive, negative

134
Q

What is the prototype for cephalosporins?

A

Cefazolin

135
Q

What is the prefix for all cephalosporins?

A

Cef- or Ceph-

136
Q

When is Cefazolin (a cephalosporin) used?

A

As a broad spectrum, against gram - infections and for those who are allergic to PCN or PCN resistant

137
Q

What happens when cefazolin is taken with alcohol?

A

A disulfiram like reaction (violent vomiting)

138
Q

Which generation of cephalosporins is only effective against gram +?

A

1st generation

139
Q

What is the prototype for carbapenems?

A

Imipenem

140
Q

When is imipenem used?

A

for more serious infections

141
Q

What class is imipenem in?

A

Carbapenem

142
Q

What drugs antagonize carbapenems (Imipenem)?

A

PCN, cephalosporins and aztreonam

143
Q

T/F you should take carbapenems (Imipenem) at the same time as PCN, cephalosporins and aztreonam.

A

False; should be at different times d/t cross sensitivity.

144
Q

What is the suffix for carbapenems?

A

-penem

145
Q

What is the most effective drug against MRSA and c diff?

A

Vancomycin

146
Q

T/F If a systemic infection is present, vancomycin has to be given via IV.

A

True

147
Q

T/F vancomycin has a low safety margin and peak and trough needs to be monitored.

A

True

148
Q

What are some serious adverse effects of vancomycin?

A

Renal failure, ototoxicity, red man syndrome

149
Q

What are signs of ototoxicity?

A

tinnitus, high tone hearing loss and deafness

150
Q

What are signs of red man syndrome?

A

hypotension, tachycardia, rash and flushing of the face and trunk

151
Q

How can a person get red man syndrome?

A

From a rapid Vanco IV infusion

152
Q

How can red man syndrome be prevented?

A

By infusing vanco over 60 mins or more.

153
Q

What are the three drug classes that affect bacterial protein synthesis?

A

Tetracyclines, macrolides and aminoglycosides

154
Q

When are tetracyclines used?

A

When an infection is resistant to first line abx

155
Q

What is the prototype for tetracyclines?

A

tetracycline

156
Q

How does tetracycline work in the body?

A

It inhibits protein synthesis

157
Q

How can GI irritation be treated with tetracycline?

A

It can be reduced if taken with food; food must be nondairy

158
Q

How soon must tetracycline be given before ingesting dairy?

A

1-2 hours

159
Q

What are some adverse effects of tetracycline?

A

photosensitivity (severe sunburn type reaction) and teeth discoloration

160
Q

Why should tetracycline be avoided for kids under 8 or pregnant/lactating women?

A

They are at higher risk for teeth discoloration and it can slow down growth rates in fetuses and children

161
Q

Why should patients taking tetracycline have their hepatic or renal function monitored?

A

It forms insoluble content in the body

162
Q

What is the prototype for macrolides?

A

Erythromycin

163
Q

What type of abx is erythromycin?

A

broad spectrum, most effective against gram + bacteria

164
Q

What is the first line drug for Legionnaires’ disease, whooping cough and diphtheria?

A

Erythromycin

165
Q

T/F erythromycin can increase effects of warfarin.

A

True

166
Q

T/F erythromycin is safe but in rare cases can kill you.

A

True

167
Q

What are important adverse effects of erythromycin?

A

ventricular dysrhythmias, cardiotoxicity and ototoxicity

168
Q

What is the prototype for aminoglycosides?

A

Gentamycin

169
Q

When would gentamycin be given?

A

As a second line abx, where there are no less toxic alternatives

170
Q

T/F gentamycin is a narrow spectrum abx and works against gram - bacteria.

A

True

171
Q

Which serious adverse effects are present in gentamycin?

A

ototoxicity and nephrotoxicity

172
Q

What should a nurse educate a patient on when taking gentamycin?

A

signs of hearing loss, tinnitus and vertigo

173
Q

What are things that should be monitored when taking gentamycin and why?

A

I/O’s, BUN & Creatinine; if irregularities are not caught early on, this medication can cause irreversible kidney damage

174
Q

What is the prototype for fluoroquinolones?

A

ciprofloxacin (2nd generation)

175
Q

What type of inhibitor is ciprofloxacin (a fluoroquinolone)?

A

bacterial DNA replication inhibitor

176
Q

Which medication can cause tendonitis as an adverse effect?

A

ciprofloxacin

177
Q

What are some adverse effects for ciprofloxacin?

A

tendon toxicity (Achilles tendon rupture), photosensitivity, cardiotoxicity, fatal dysrhythmias and prolonged QT intervals

178
Q

Who is at risk for tendon toxicity for ciprofloxacin?

A

children, older adults and those taking glucocorticoids

179
Q

What are contraindications for ciprofloxacin?

A

tendon pain, those under 18; also monitor patients with impaired renal function or CNS disorders

180
Q

T/F antacids or mineral supplements speed up absorption when taking ciprofloxacin.

A

False; they delay absorption

181
Q

What is the time period for taking antacids or mineral supplements when taking ciprofloxacin (fluoroquinolones)?

A

2 hours after or 6 hours before taking fluoroquinolones

182
Q

What is the suffix for fluoroquinolones?

A

-floxacin

183
Q

What medication is used for protozoal infections, peptic ulcer disease and infections caused by obligate anaerobic bacteria?

A

Metronidazole

184
Q

What is the black box warning for metronidazole?

A

it can cause cancer

185
Q

What are adverse effects of metronidazole?

A

It can cause violent vomiting with alcohol and causes harmless darkening of urine

186
Q

What are sulfonamides used for?

A

Broad spectrum abx (gram + and gram -), UTI prophylaxis and tx

187
Q

sulfonamides inhibit synthesis of folic acid T/F

A

True

188
Q

What are some adverse effects of sulfonamides?

A

Kernicterus (a fatal type of jaundice), crystalluria and renal damage

189
Q

How can crystalluria be prevented in sulfonamides?

A

by encouraging fluids

190
Q

How much fluid intake and output should be encouraged to prevent the development of crystals when taking sulfonamides?

A

3 liters of fluid a day with 1500 mL of urine output in 24 hours

191
Q

What are contraindications for sulfonamides?

A

pregnancy, nursing, children under the age of 2, folate deficiency anemia and severe renal impairment, hyperkalemia

192
Q

Oral anticoagulants ______ ______ when taken with sulfonamides

A

increase bleeding

193
Q

Potassium supplements and potassium sparing diuretics can _____ effectiveness when taken with sulfonamides.

A

Increase

194
Q

What are the prototypes for sulfonamides?

A

TMP-SMZ

195
Q

TMP-SMZ are used in ________ and when given ____ they ___ more bacteria.

A

combination, together, kill

196
Q

TMP-SMZ carries the risk of kernicterus, which is ___

A

a fatal type of jaundice

197
Q

What pregnancy category is TMP-SMZ?

A

Category D

198
Q

Why are mycobacterial infections difficult to treat?

A

They have a thick layer and are often resistant

199
Q

mycobacterial infections are ____ growing and require _____ treatment

A

slow, prolonged

200
Q

What are the 3 species (diseases) of mycobacteria?

A

tuberculosis, leprosy, and mycobacterium avum which is secondary to HIV and AIDS

201
Q

Primary tuberculosis is obtained through _______

A

inhaling particles from someone with TB

202
Q

postprimary TB is special because ______

A

dormant bacteria reactivates upon weakened immune system

203
Q

What is DOT therapy?

A

where each dose of TB needs to be taken in front of an observer

204
Q

T/F TB is always treated with 4 or more drugs.

A

False; 2 or more.

205
Q

What is the drug regimen for active or latent TB?

A

3-4 drugs for 6-12 months

206
Q

What is the drug regimen for multi-drug resistant TB?

A

Up to 7 drugs for up to 2 years

207
Q

What is the drug regimen for prophylactic treatment of TB?

A

2 drugs for 2 months

208
Q

What is the first line of drugs for tx for active TB?

A

RIPE (rifampin, isoniazid, pyraziniamide, ethambutol)

209
Q

What is the prototype for anti-tubercular drugs?

A

isoniazid

210
Q

What is special about the adverse effect of rifampin?

A

orange body fluids

211
Q

T/F Rifampin decreases effectiveness of oral contraceptives.

A

True

212
Q

what are some adverse effects of isoniazid (anti-tb drug)?

A

Visual defects, CNS effects such as dizziness, seizures and psychosis, peripheral neuropathies and hepatotoxicity/hepatitis

213
Q

How can peripheral neuropathies be treated when taking isoniazid (anti-tb drug)?

A

Vitamin B6

214
Q

How can hepatotoxicity/hepatitis be treated when taking isoniazid (anti-tb drug)?

A

Pyroxidine

215
Q

What are the viral infections that an be treated with antivirals?

A

influenza, herpes simplex virus, herpes zoster (shingles), RSV and HIV

216
Q

How do antiviral medications work?

A

They shorten the course of the virus by inhibiting DNA or RNA replication

217
Q

What is the most important molecule reabsorbed in the tubules?

A

Water

218
Q

Aldosterone stimulates _______ reabsorption in the distal nephron which promotes _______ excretion

A

sodium, potassium

219
Q

Antidiuretic hormone (ADH) increases _____ reabsorption by making the collecting ducts more ______ to water

A

water, permeable

220
Q

What are some dietary restrictions a person with renal failure may have?

A

potassium, phosphate and sodium

221
Q

T/F Loop diuretics prevent reabsorption of sodium in the renal tubules.

A

False; they promote reabsorption of sodium in the Loop of Henle.

222
Q

Which drug group of diuretics act by blocking sodium in the distal tubule?

A

Thiazides

223
Q

Which diuretic drug group have minimal effect of potassium ion excretion?

A

Potassium-sparing

224
Q

What type of diuretics are the most effective, and what is their suffix?

A

Loop diuretics, -mide or -nide

225
Q

T/F Loop diuretics (furosemide) are able to increase urine output even when blood flow to kidneys is diminished.

A

True

226
Q

What are some serious adverse effects when taking furosemide (loop diuretics)?

A

Dehydration, low bp and syncope, electrolyte imbalances, hypokalemia, hyperuricemia (can cause exacerbations of gout); tachycardia, dysrhythmias, n/v, ototoxicity (permanent)

227
Q

What is the black box warning referring to regarding furosemide (loop diuretics)?

A

diuresis, water and electrolyte depletion

228
Q

What are contraindications for furosemide?

A

Hypersensitivity, anuria, severe fluid or electrolyte depletion

229
Q

What is a nursing consideration for furosemide?

A

Check vitals before giving a loop diuretic

230
Q

What is one of the main differences between thiazide and loop diuretics?

A

You cannot use thiazide if you do not have enough renal function, but you can with loop diuretics.

231
Q

What is the most commonly prescribed class of diuretics?

A

Thiazide-like diuretics

232
Q

What is the prototype for thiazide like diuretics?

A

hydrochlorothiazide

233
Q

Which diuretics do not cause ototoxicity?

A

thiazide and thiazide like diuretics (hydrochlorothiazide)

234
Q

What are patients taking thiazide and thiazide like diuretics (hydrochlorothiazide) at risk for?

A

Falls, fluid and electrolyte imbalances, hypotension and orthostatic hypotension

235
Q

What causes dysrhythmias in hydrochlorothiazide or thiazide like diuretics?

A

hypokalemia

236
Q

What medication can have toxic effects if taken with thiazide and thiazide like diuretics?

A

Digoxin

237
Q

What is an advantage of potassium sparing diuretics?

A

They retain potassium not waste it

238
Q

What is the prototype for potassium sparing diuretics?

A

Spironolactone

239
Q

What patient population is potassium sparing diuretics useful for?

A

Those who are at high risk for hypokalemia

240
Q

What is an individual taking spironolactone (a potassium sparing diuretic) at risk for?

A

Hyperkalemia d/t retaining potassium; gynecomastia (man boobs), impotence, diminished libido in men; menstrual irregularities, hirsutism (excessive hair growth), breast tenderness, decreased fertility

241
Q

Can the adverse effects for taking spironolactone be reversed?

A

Yes, when the medication is stopped.

242
Q

what is the black box warning for spironolactone?

A

It produces tumors in lab animals

243
Q

What should be avoided when taking spironolactone?

A

Potassium supplements, ACE inhibitors, ARBs (can cause severe hyperkalemia) and foods high in potassium

244
Q

What class does spironolactone belong to?

A

potassium sparing diuretics

245
Q

What is stroke volume?

A

the amount of blood pumped out of ventricles with each heartbeat

246
Q

What are the 3 elements that control blood pressure?

A

Heart rate, stroke volume, and total peripheral resistance

247
Q

What is primary hypertension?

A

HTN with no underlying cause

248
Q

What is secondary hypertension?

A

HTN with an identifiable cause

249
Q

What is important to educate on regarding HTN?

A

routine screenings and risks if noncompliant with meds

250
Q

What are repercussions of uncontrolled HTN?

A

Damage to vessels, heart, brain, kidneys, eyes

251
Q

What does CCB stand for?

A

Calcium Channel Blockers

252
Q

What is important regarding ACE inhibitors or ARBs?

A

They can only be on one or the other.

253
Q

What is important to remember in black patients regarding HTN tx?

A

Thiazides or CCBs are given before ACE or ARBs

254
Q

T/F African Americans are most responsive to single drug therapy for HTN.

A

True

255
Q

What is the goal of medication for HTN?

A

To decrease morbidity and mortality

256
Q

What medications are the 1st line of treatment for mild to moderate HTN?

A

Thiazide diuretics

257
Q

Renin releases when blood pressure is ______ to ______ blood pressure

A

lower, increase

258
Q

Renin forms angiotensin I from angiotensinogen, which then converts to ________

A

angiotensin II.

259
Q

Angiotensin II ______ blood pressure.

A

raises

260
Q

ACE inhibitors ____ blood pressure from _____

A

blocks, increasing

261
Q

ARBs stands for ____

A

Angiotensin receptor blockers

262
Q

Aldosterone antagonists ________

A

prevent aldosterone induced blood pressure increase

263
Q

Direct renin inhibitors ______

A

inhibit renin so angiotensin I and its cascade does not occur

264
Q

What is the 1st line treatment for HTN?

A

ACE inhibitors–they reduce HTN related morbidity and mortality

265
Q

How do ACE inhibitors work?

A

They block the conversion of angiotensin I to angiotensin II.

266
Q

What is the suffix for ACE inhibitors?

A

-pril

267
Q

T/F ACE inhibitors are used with thiazide diuretics because effects are enhanced.

A

True

268
Q

What is the prototype for ACE inhibitors?

A

Lisinopril

269
Q

What are the most prominent adverse effects with lisinopril (an ACE inhibitor)?

A

Persistent dry cough, angioedema.

270
Q

What is the black box warning for lisinopril?

A

A risk for major congenital defects if taken during pregnancy

271
Q

Which medication class should not be taken with lisinopril due to decreasing antihypertensive activity and worsening renal disease?

A

NSAIDS

272
Q

What is the prototype for ARBS?

A

Losartan

273
Q

What is the suffix for ARBS?

A

-sartan

274
Q

What is the difference between losartan (ARBS) and lisinopril (ACE Inhibitor)?

A

They do not cause a cough and have a lower risk of angioedema

275
Q

T/F ARBS (losartan) have the lowest incidence of serious adverse effects of any of the antihypertensive classes.

A

True

276
Q

What forms are calcium channel blockers (CCBS) available in?

A

sustained or extended release

277
Q

What is the function of calcium channel blockers?

A

They decrease BP, cardiac workload and myocardial oxygen demand

278
Q

What is the suffix for calcium channel blockers?

A

-pine

279
Q

What is the prototype for calcium channel blockers?

A

Amlodipine

280
Q

What two medications are CCBs but not used for HTN?

A

Verapamil, diltiazem

281
Q

Regarding administration of CCBs, what is the biggest concern as an adverse effect?

A

Hypotension when taken with alcohol (will be on exam!)

282
Q

What are adverse effects of CCBs (amlodipine)?

A

hypotension, bradycardia, peripheral edema, heart block, flushing and skin rash

283
Q

What are alpha 1 antagonists used for?

A

BPH and hypertension

284
Q

T/F Caution must be used in nonspecific beta blockers w/ those who have COPD and asthma.

A

True

285
Q

What are Beta II agonists used for?

A

asthma and preterm labor

286
Q

What is the 2nd line of drugs for HTN?

A

Adrenergic antagonists

287
Q

What do adrenergic antagonists do?

A

They prevent symptoms of the fight or flight response

288
Q

What are adrenergic antagonists used for?

A

To treat HTN, angina pectoris, dysrhythmias and MI prophylaxis

289
Q

What is the suffix for Alpha 1-adrenergic antagonists?

A

-sin (think -sin and BPH)

290
Q

What is the prototype for Alpha 1-adrenergic antagonists?

A

Prazosin

291
Q

What is Prazosin used for?

A

HTN, BPH and Raynaud’s disease

292
Q

How does Prazosin (an alpha 1-adrenergic antagonist) help BPH?

A

it relaxes the bladder and prostate

293
Q

What is the first dose phenomenon with prazosin and other alpha 1 adrenergic antagonists?

A

pronounced orthostatic hypotension

294
Q

What are adverse effects caused by in prazosin (alpha 1 adrenergic antagonists)?

A

the increased parasympathetic activity

295
Q

Why is hypotension a risk in prazosin?

A

because of vasodilation

296
Q

What is the treatment for reflex tachycardia in alpha 1-adrenergic antagonists?

A

Beta blockers

297
Q

What are some adverse effects with alpha 1 adrenergic antagonists (prazosin)?

A

nasal congestion, decreased libido, erectile dysfunction or ability to ejaculate

298
Q

What is the most important nursing consideration with beta blockers?

A

HOLD medication if systolic BP is less than 100 or HR is less than 60

299
Q

What is the suffix for beta blockers?

A

-olol

300
Q

What is the nonselective prototype for beta blockers?

A

propranolol

301
Q

What is the selective (cardioselective) prototype for beta blockers?

A

metoprolol

302
Q

Why should a beta blocker be withdrawn gradually over several weeks?

A

abrupt withdrawal can cause rebound cardiac excitation

303
Q

What type of beta blockers are safe for those with COPD and asthma to take?

A

cardioselective

304
Q

How do you treat a beta blocker overdose?

A

with an anticholinergic (atropine) or beta adrenergic agonist (isoproterenol)

305
Q

Which drugs that are nonselective alpha 1 and beta adrenergic antagonists block alpha 1?

A

carvedilol and labetalol

306
Q

What is the prototype for direct acting vasodilators?

A

hydralazine

307
Q

When is hydralazine indicated?

A

When severe HTN has not responded to other therapy

308
Q

What are adverse effects of direct acting vasodilators?

A

hypotension, reflex tachycardia, sodium and water retention, and a lupus like syndrome

309
Q

When should hydralazine be discontinued gradually?

A

If there is an appearance of a lupus like syndrome: rash, hives, weakness, fatigue.

310
Q

How can reflex tachycardia be prevented?

A

By administration of a beta blocker

311
Q

How is a hypertensive emergency defined?

A

diastolic pressure is >120 mmHg with evidence of target organ system damage

312
Q

what causes a hypertensive emergency (HTN-E)?

A

untreated or poorly controlled essential HTN

313
Q

What are common symptoms of a hypertensive emergency (HTN-E)?

A

chest pain, dyspnea, headache

314
Q

What is the goal of management of hypertensive emergencies (HTN-E)?

A

To lower BP quickly but not too fast; lower BP progressively by 20-25% over 30-60 minutes and gradually reduce it further over 12-48 hrs until BP is in a normal range

315
Q

What is the 1st line drug for aggressive, life threatening HTN?

A

Nitroprusside Sodium

316
Q

Nitroprusside Sodium is limited to __ hours because ____

A

72, toxic thiocyanate and cyanide

317
Q

What is an adverse effect of nitroprusside sodium?

A

Thiocyanate toxicity

318
Q

What are s/s of thiocyanate toxicity?

A

hypotension, lethargy, blurred vision, metabolic acidosis, faint heart sounds, LOC

319
Q

T/F Nitroprusside sodium must be diluted prior to infusion.

A

True; if not diluted, it can cause irreversible ischemic injury and death d/t significant drops in BP.

320
Q

serum thiocyanate levels must be monitored and discontinued if it exceeds __ mg/dL

A

12

321
Q

What are other adverse effects of nitroprusside sodium?

A

inadequate cerebral circulation and kidney impairment.

Pharmacology (3 decks)

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