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KLowe Pharm 2 > Final Exam Review > Flashcards

Final Exam Review Flashcards

1
Q

Issues with inhalation technique–___% delivered to the lungs, the rest to the mouth, pharynx, and larynx

A

12% delivered to the lungs

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2
Q

Issues with inhalation technique–presence of an ETT decreases the amount of drug delivered by a MDI to the trachea by ___-___%

A

presence of an ETT decreases the amount of drug delivered by a MDI to the trachea by 50-70%

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3
Q

Dose delivered by a nebulizer requires ___-___x that of a MDI dose to produce the same degree of bronchodilation

A

Dose delivered by a nebulizer requires 6-10x that of a MDI dose to produce the same degree of bronchodilation

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4
Q

What should be administered first, bronchodilators or corticosteroids?

A

Bronchodilators should be administered before corticosteroids

^ because the bronchodilator will open up the lungs and increase the surface area that the corticosteroid can work on

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5
Q

What are the (6) classes of respiratory medications?–anti___; ___ agonists; membrane ___; ___thines; ___lytics; cortico___

A
  • Anticholinergics
  • Adrenergic agonists
  • Membrane stabilizers
  • Xanthines
  • Tocolytics (related drug)
  • Corticosteroids
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6
Q

What (3) muscarinic receptors are stimulatory?

A

M1, M3, M5

Odd = stimulatory

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7
Q

What (2) muscarinic receptors are inhibitory?

A

M2, M4

Even = inhibitory

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8
Q

Antimuscarinic = anti___

A

anticholinergic

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9
Q

Antimuscarinic/anticholinergic both mean that we are blocking ___ from binding to ___ receptors

A

we are blocking ACH from binding to muscarinic receptors

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10
Q

Atropine antagonizes ___ effects on airway smooth muscle in large and medium sized airways; it affects airways that respond to vagal stimulation; it ___ (increases/decreases) airway resistance; ___ (increases/decreases) dead space

A

Atropine antagonizes ACH effects on airway smooth muscle in large and medium sized airways; it affects airways that respond to vagal stimulation; it decreases airway resistance; increases dead space

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11
Q

What is the main issue with nebulized atropine?–a lot of ___ complications, ___arrhythmias

A

A lot of CV complications, tachyarrhythmias

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12
Q

Atropine is ___ (more/less) lipophilic than glycopyrrolate

A

atropine is more lipophilic than glyocpyrrolate

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13
Q

Atropine is a ___ amine

A

tertiary amine

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14
Q

Atropine ___ (can/cannot) cross the BBB

A

can cross the BBB (because it’s a tertiary amine and more lipophilic)

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15
Q

Glycopyrrolate is a ___ ammonium; it ___ (does/does not) absorb systemically as much as atropine

A

glycopyrrolate is a quaternary ammonium; it does not absorb systemically as much as atropine

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16
Q

Ipratropium is most effective in treating bronchospasm due to ___

A

treating bronchospasm due to beta antagonists (i.e.: propranolol which has non-selective beta blockade)

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17
Q

Compared to beta agonists, ipratropium has a ___ (slower/faster) onset and is ___ (more/less) effective in treating bronchial asthma

A

ipratropium has a slower onset (30-90 minutes) and is less effective in treating bronchial asthma than beta agonists

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18
Q

Albuterol is better than ipratropium for acute asthma attacks because it has a faster onset of action–T/F?

A

True

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19
Q

Tiotropium (Spiriva) is a ___ (short/long) acting anticholinergic bronchodilator

A

long-acting anticholinergic bronchodilator

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20
Q

Tiotropium (Spiriva) is used as maintenance treatment of bronchospasm associated with COPD, including chronic ___ and ___

A

chronic bronchitis and emphysema

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21
Q

Long-acting bronchodilators ___ (should/should not) be used to treat acute anything

A

should NOT be used to treat acute anything

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22
Q

Warnings for inhaled anticholinergics–can cause ___ and severe ___

A

narrow angle glaucoma and severe urinary retention

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23
Q

Beta 2 agonists ___ (relax/contract) bronchial smooth muscle

A

relax bronchial smooth muscle

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24
Q

Newer beta 2 agonists lack stimulating effects on the heart at therapeutic doses–T/F?

A

True

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25
Q

Beta 2 agonists ___ (do/do not) have a catecholamine structure

A

do NOT have a catecholamine structure

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26
Q

The non-catecholamine structure of beta 2 agonists makes them resistant to what enzyme? What effect does this have on their duration of action?

A

Beta 2 agonists are resistant to COMT (because they are non-catecholamines); this contributes to their LONGER duration of action

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27
Q

Beta 2 agonists have a longer duration of action because they are __, NOT ___…do NOT have a ___ structure

A

Beta 2 agonists have a longer duration of action because they are sympathomimetics, NOT catecholamines…do NOT have a catecholamine structure

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28
Q

Uses of beta 2 agonists–preferred treatment for ___ (acute/chronic) episodes of asthma; prevention of ___-induced asthma; improve airflow and exercise tolerance in patients with ___; tocolytic to stop premature ___ contractions; treatment of ___kalemia

A

preferred treatment for acute episodes of asthma; prevention of exercise-induced asthma; improve airflow and exercise tolerance in patients with COPD; tocolytic to stop premature uterine contractions; treatment of hyperkalemia

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29
Q

Classes of beta 2 agonists–short acting = ___-___ hours; long acting = > ___ hours

A

short acting = 3-6 hours; long acting = > 12 hours

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30
Q

In spite of their non-respiratory side effects, ephedrine and epinephrine do have ___ effects from activation of beta 2 receptors

A

bronchodilating effects from activation of beta 2 receptors

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31
Q

Isoproterenol is a ___ (selective/non-selective) sympathomimetic that acts at ___ and ___ receptors

A

non-selective sympathomimetic that acts at beta 1 and beta 2 receptors

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32
Q

Isoproterenol is highly pro-

A

pro-arrhythmic

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33
Q

What medication is the preferred beta 2 agonist for acute bronchospasm?

A

Albuterol

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34
Q

Albuterol is a ___ (short/long) acting beta agonist

A

short acting beta agonist

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35
Q

Levoalbuterol (Xopenex) is the (___)-enantiomer of racemic albuterol

A

(R)-enantiomer of racemic albuterol

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36
Q

What was the main point of levoalbuterol (xopenex) for being marketed?

A

Because it is an (R)-enantiomer, it was expected to have little to no cardiac effects

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37
Q

Studies have shown that there is little or no clinically significant difference in adverse effects of levoalbuterol (xopenex) compared to albuterol–T/F?

A

True

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38
Q

Beta 2 ___ (relaxes/contracts) the uterus

A

Beta 2 relaxes the uterus

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39
Q

Ritodrine was removed from the market d/t ___ complications and 24 maternal ___

A

d/t CV complications and 24 maternal deaths

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40
Q

Side effects of ritodrine–crosses the ___; causes ___ and ___ effects in both the mother and fetus; dose-related ___cardia (because it’s slightly non-selective, beta1 and beta 2 agonism), ___ (increased/decreased) cardiac output; increased ___ secretion d/t beta1 stimulation; exaggerated systemic BP ___ (increase/decrease); ___glycemia in the mother (from beta2 effects) may cause reactive ___glycemia in the fetus

A

crosses the placenta; causes CV and metabolic effects in both the mother and fetus; dose-related tachycardia (because it’s slightly non-selective, beta1 and beta2 agonism), increased cardiac output; increased renin secretion d/t beta1 stimulation; exaggerated systemic BP decrease; hyperglycemia in the mother (from beta2 effects) may cause reactive hypoglycemia in the fetus

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41
Q

Side effects of ritodrine–increased renin secretion from beta1 stimulation causes ___ (increased/decreased) sodium; water ___ (reabsorption/secretion); ___ (increased/decreased) K+ and H+; pulmonary ___ may occur

A

increased renin secretion from beta1 stimulation causes increased sodium; water reabsorption; decreased K+ and H+; pulmonary edema may occur

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42
Q

Long acting beta agonists ___ (are/are not) used for acute effect

A

are NOT used for acute effect–used for long-term management

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43
Q

Salmeterol (serevent) and vilanterol are both ___ (short/long) acting beta agonists

A

long acting beta agonists

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44
Q

Formoterol and aformoterol are two other ___ (short/long) acting beta agonists

A

long acting beta agonists

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45
Q

Side effects of beta 2 agonists–___ usually occurs with overdose/systemic absorption due to stimulation of beta 2 receptors on ___ muscle; ___cardia from direct stimulation of receptors on the heart; metabolic response–___glycemia, ___kalemia, ___magnesemia

A

tremor usually occurs with overdose/systemic absorption due to stimulation of beta 2 receptors on skeletal muscle; tachycardia from direct stimulation of receptors on the heart; metabolic response–hyperglycemia, hypokalemia, hypomagnesemia

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46
Q

Why do you see hypokalemia/hypomagnesemia with beta 2 agonists?

A

When you give a beta 2 agonist, potassium is pulled into the cell in exchange for sodium; magnesium follows potassium into the cell

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47
Q

Black box warning for LABAs–increased risk of ___; ___ (should/should not) be used alone

A

increased risk of asthma related death; should not be used alone

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48
Q

How can LABAs (when used alone) lead to asthma related death?–LABAs have no ___ action

A

LABAs have no anti-inflammatory action–so if someone is having an asthma attack and you only give them an LABA, their lungs won’t react to the inflammatory response that is going on, leading to death

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49
Q

Cromolyn sodium is a ___; it inhibits antigen-induced release of ___ and other mediators from pulmonary mast cells during antibody mediated allergic responses

A

membrane stabilizer; it inhibits antigen-induced release of histamine and other mediators from pulmonary mast cells during antibody mediated allergic responses

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50
Q

Cromolyn sodium ___ (does/does not) relax bronchial or vascular smooth muscle

A

does NOT relax bronchial or vascular smooth muscle

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51
Q

Cromolyn sodium is used for ___ (acute/chronic) management; has no use in ___

A

used for chronic management; has no use in an acute asthma attack

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52
Q

What are (3) types of methylxanthines?

A
  • Theophylline/aminophylline
  • Caffeine
  • Theobromine
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53
Q

Methylxanthines ___ (stimulate/inhibit) the CNS; ___ (increase/decrease) BP; ___ (increase/decrease) myocardial contractility and heart rate; ___ (contract/relax) smooth muscle in the airways

A

stimulate the CNS; increase BP; increase myocardial contractility and heart rate; relax smooth muscle in the airways

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54
Q

Methylxanthines are non-selective ___ inhibitors

A

non-selective phosphodiesterase inhibitors–inhibit all fractions of PDE isoenzymes [PDE breaks down cAMP/cGMP]

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55
Q

Methylxanthines are also competitive antagonists of ___ receptors

A

competitive antagonists of adenosine receptors

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56
Q

Theophylline has more competitive antagonism for adenosine receptors than caffeine and theobromine–T/F?

A

True

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57
Q

Theophylline is used to treat ___ in infants

A

apnea of prematurity in infants (because it is a CNS stimulant)

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58
Q

Theophylline toxicities–___-___ mcg/ml = GI upset, nausea/vomiting, tremor

A

15-25 mcg/ml = GI upset, nausea/vomiting, tremor

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59
Q

Theophylline toxicities–___-___ mcg/ml = tachycardia, PVCs

A

25-35 mcg/ml = tachycardia, PVCs

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60
Q

Theophylline toxicities– >___ mcg/ml = fatal VTach, seizures

A

> 35 mcg/ml = fatal VTach, seizures

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61
Q

Caffeine effects–CNS ___ (stimulant/inhibitor); cerebral vaso___ (dilator/constrictor); secretion of ___

A

CNS stimulant; cerebral vasoconstrictor; secretion of gastric acid

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62
Q

Caffeine uses–apnea of ___; ___ headache; ___ remedies (to offset sedation from antihistamines)

A

apnea of prematurity; post-dural puncture headache; cold remedies (to offset sedation from antihistamines)

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63
Q

Histamine ___ (does/does not) easily cross the blood-brain barrier

A

does not easily cross the blood-brain barrier

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64
Q

Through H1 and H2 receptors, histamine causes ___ (increased/decreased) capillary permeability; ___tension; ___cardia; ___ing; ___ache

A

increased capillary permeability; hypotension; tachycardia; flushing; headache

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65
Q

What receptor(s) need to be blocked in order to completely block the vasodilatory effects of histamine release?

A

Both H1 and H2 receptors need to be blocked in order to completely block the vasodilatory effects of histamine release

So–if someone is having a severe allergic reaction, give Benadryl and pepcid to block H1 and H2 receptors

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66
Q

H1 = broncho___ (constriction/dilation)

A

H1 = bronchoconstriction

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67
Q

H2 = broncho___ (constriction/dilation)

A

H2 = bronchodilation

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68
Q

Histamine triple response (wheal and flare)–___ due to increased permeability; ___ (dilated/constricted) arteries around the edema (flare); ___ due to histamine in the superficial layers of the skin

A

edema due to increased permeability; dilated arteries around the edema (flare); pruritus due to histamine in the superficial layers of the skin

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69
Q

Histamine stimulates gastric ___ ion secretion (d/t H__ receptor stimulation)

A

Histamine stimulates gastric hydrogen ion secretion (d/t H2 receptor stimulation)

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70
Q

Histamine receptor antagonists are ___ (competitive/noncompetitive) and ___ (reversible/irreversible) antagonists of histamine receptors

A

competitive and reversible antagonists of histamine receptors

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71
Q

Histamine receptor antagonists ___ (do/do not) inhibit the release of histamine

A

do NOT inhibit the release of histamine–histamine is still released from the mast cells, but it is unable to bind to its receptor

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72
Q

Histamine receptor antagonists attach to receptors and prevent the responses mediated by histamine–T/F?

A

True–competitive antagonism

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73
Q

Histamine receptor antagonists stabilize the receptor in the ___ (active/inactive) form, making them ___ agonists

A

stabilize the receptor in the inactive form, making them inverse agonists

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74
Q

Two generations of H1 receptor antagonists–first generation = ___; second generation = ___

A

first generation = sedating; second generation = non-sedating

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75
Q

First generation H1 receptor antagonists are ___; they may also activate ___ or ___-adrenergic receptors; they block ___ receptors

A

First generation H1 receptor antagonists are sedating; they may also activate serotonin or alpha-adrenergic receptors; they block muscarinic receptors

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76
Q

Benadryl is a ___ (1st/2nd) generation H1 receptor antagonist; can cause ___/___ in the very young and very old; used as a ___ative, anti___, anti___, and used to treat type ___ allergic reactions (___)

A

Benadryl is a 1st generation H1 receptor antagonist; can cause agitation/restlessness in the very young and very old; used as a sedative, antipruritic, antiemetic, and used to treat type 1 allergic reactions (anaphylaxis)

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77
Q

Second generation H1 antagonists are unlikely to produce CNS side effects unless recommended doses are exceeded–T/F?

A

True

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78
Q

(3) second generation H1 antagonists

A
  • Zyrtec (cetirizine)
  • Claritin (loratidine)
  • Allegra (fexofenadine)
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79
Q

HPA axis–hypothalamus releases ___, anterior pituitary releases ___, adrenal cortex releases ___

A

hypothalamus releases corticotropin releasing hormone (CRH), anterior pituitary releases adrenocorticotropic hormone (ACTH), adrenal cortex releases cortisol

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80
Q

Adrenal cortex–zona glomerulosa = ___ layer; releases ___

A

outer layer; releases mineralocorticoids

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81
Q

Adrenal cortex–zona fasciculata = ___ layer; releases ___

A

middle layer; releases glucocorticoids

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82
Q

Adrenal cortex–zona reticularis = ___ layer; releases ___

A

inner layer; releases weak androgens

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83
Q

What hormone is produced in the adrenal cortex in response to stress?

A

Cortisol (hydrocortisone)

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84
Q

What is the major mineralocorticoid?

A

Aldosterone

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85
Q

Aldosterone is secreted secondary to ___ (increased/decreased) K+; ___ (increased/decreased) sodium; ___ (increased/decreased) BP/fluid volume

A

aldosterone is secreted secondary to increased K+; decreased sodium; decreased BP/fluid volume

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86
Q

Review of RAAS

A

renin is released by the kidneys in response to low BP –> angiotensinogen (released by the liver) converts renin to angiotensin I –> angiotensin I is converted to angiotensin II by ACE (released from the lungs) –> angiotensin II is potent vasoconstrictor, stimulates release of aldosterone from the adrenal cortex

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87
Q

Aldosterone ___ (increases/decreases) K+ excretion; ___ (increases/decreases) Na+ retention; ___ (increases/decreases) water retention; ___ (increases/decreases) blood volume

A

Aldosterone increases K+ excretion; increases Na+ retention; increases water retention; increases blood volume

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88
Q

Circadian rhythm–secretory rates of CRH, ACTH, and cortisol are ___ (low/high) in the early morning; ___ (low/high) in the late evening

A

high in the early morning; low in the late evening

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89
Q

Primary adrenocortical insufficiency is AKA ___ disease

A

Addison’s disease

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90
Q

Addison’s disease–the adrenals do not secrete ___ or ___; replacement therapy must include ___corticoid and ___corticoid

A

the adrenals do not secrete cortisol or aldosterone; replacement therapy must include glucocorticoid and mineralocorticoid

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91
Q

Secondary adrenocortical insufficiency is due to chronic ___ use and suppression of the ___ axis

A

due to chronic steroid use and suppression of the HPA axis

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92
Q

In secondary adrenocortical insufficiency, ___ secretion is maintained

A

aldosterone secretion is maintained

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93
Q

Replacement therapy for secondary adrenocortical insufficiency usually requires only ___corticoid

A

glucocorticoid

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94
Q

Glucocorticoid effect = anti-___ response

A

glucocorticoid effect = anti-inflammatory response

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95
Q

Mineralocorticoid effect = evoke distal renal tubular reabsorption of ___ in exchange for ___

A

mineralocorticoid effect = evoke distal renal tubular reabsorption of Na+ in exchange for K+

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96
Q

Which (2) corticosteroid medications have the greatest anti-inflammatory potency?

A
  • Betamethasone
  • Dexamethasone

^ Both are synthetic glucocorticoids

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97
Q

What corticosteroid medication has the greatest sodium-retaining potency?

A

Fludrocortisone–synthetic mineralocorticoid

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98
Q

Corticosteroids ___ (are/are not) able to cross the placenta

A

Corticosteroids are able to cross the placenta

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99
Q

Corticosteroid use can lead to ___kalemic metabolic ___osis due to ___corticoid effect of cortisol on distal renal tubules, leading to enhanced absorption of ___ and loss of ___; also leads to ___ and weight ___

A

corticosteroid use can lead to hypokalemic metabolic alkalosis due to mineralocorticoid effect of cortisol on distal renal tubules, leading to enhanced absorption of Na+ and loss of K+; also leads to edema and weight gain

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100
Q

Aldosterone secretion remains intact in ___ (primary/secondary) adrenal insufficiency

A

secondary adrenal insufficiency

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101
Q

Prednisone 5 mg/day or less or 10 mg every other day is ___ (likely/unlikely) to suppress the HPA axis

A

unlikely to suppress the HPA axis

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102
Q

Glucocorticoids any dose < ___ weeks does not clinically suppress the HPA axis

A

any dose < 3 weeks

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103
Q

Prednisone or dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated more commonly with HPA axis suppression–T/F?

A

True

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104
Q

Therapies assumed to suppress HPA axis–prednisone 20 mg/day (or equivalent) for > ___ weeks within the previous year; patient with clinical signs of ___ syndrome from any steroid dose

A

> 3 weeks; patient with clinical signs of Cushing syndrome

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105
Q

After cessation of steroid therapy, recovery of the HPA function can take ___ months or longer

A

12 months or longer

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106
Q

Patients at high risk of HPA suppression, including those treated with at least 20mg/day of prednisone for > 3 weeks or who have signs and symptoms of Cushings–unless data states otherwise, supplementation ___ (is/is not) recommended

A

supplementation is recommended

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107
Q

Patients at low risk of HPA suppression–any dose of steroid for < 3 weeks, less than 5 mg/day of prednisone (or 10 mg every other day)–steroids ___ (are/are not) required unless signs and symptoms of HPA suppression are observed

A

are not required unless signs and symptoms of HPA suppression are observed

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108
Q

What two conditions could exaggerate the need for exogenous corticosteroid supplementation?

A

Burns or sepsis

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109
Q

Signs and symptoms of acute adrenal crisis–___tension unresponsive to ___; ___dynamic circulation; ___glycemia; ___kalemia; ___natremia; ___volemia; metabolic ___osis; ___ (increased/decreased) level of consciousness

A

hypotension unresponsive to vasopressors; hyper dynamic circulation; hypoglycemia; hyperkalemia; hyponatremia; hypovolemia; metabolic acidosis; decreased level of consciousness

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110
Q

(4) medication classes that can cause hyperglycemia–gluco___; anti___; ___ medications; ___

A

glucocorticoids; antipsychotics; HIV medications; octreotide

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111
Q

Diagnosis of diabetes–fasting blood glucose ___ mg/dl or greater; random blood glucose > ___ mg/dl

A

fasting blood glucose 126 mg/dl or greater; random blood glucose > 200 mg/dl

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112
Q

Normal HgA1C = ___-___%

A

4-6%

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113
Q

ADA recommends HgA1C < ___-___%, depending on the age of the diabetic patient

A

< 7-8.5%

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114
Q

HgA1C gives an idea of the degree of control of blood glucose levels over the past ___ months

A

3 months

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115
Q

What does PI-3K do?–It moves a ___ into the cell wall of cells

A

It moves a glucose transporter into the cell wall of cells

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116
Q

Insulin MOA–binds to plasma membrane ___ receptors; translocation of ___ to plasma membranes

A

binds to plasma membrane insulin receptors; translocation of glucose transporters to plasma membranes

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117
Q

Glucose transporters facilitate ___ diffusion into cells; shift intracellular glucose metabolism toward ___ (glyco___); stimulate cellular uptake of ___ acids, ___ate, ___ium, and ___ium; stimulate protein ___ and inhibit proteo___; regulate ___ expression via insulin regulatory elements in target DNA

A

Glucose transporters facilitate glucose diffusion into cells; shift intracellular glucose metabolism toward storage (glycogenesis); stimulate cellular uptake of amino acids, phosphate, potassium, and magnesium; stimulate protein synthesis and inhibit proteolysis; regulate gene expression via insulin regulatory elements in target DNA

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118
Q

___ occurs when there is an impaired intracellular insulin signal that results in decreased recruitment of glucose transport proteins to the plasma membrane and subsequent decreased glucose uptake

A

Insulin resistance

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119
Q

Compensatory ___insulinemia occurs to overcome insulin resistance

A

Compensatory hyperinsulinemia occurs to overcome insulin resistance

Cells send signals to the CNS that they’re starving (because insulin signal is messed up and isn’t bringing glucose into the cells); body sends signals to the pancreas to make more glucose/release more insulin, resulting in hyperinsulinemia; hyperinsulinemia leads to eventual burnout of the pancreas and worsening of diabetes

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120
Q

Insulin receptor saturation occurs with ___ (low/high) circulating concentrations of insulin; ___ (more/less) insulin receptors are popped into the cell walls as a result

A

Insulin receptor saturation occurs with low circulating concentrations of insulin; more insulin receptors are popped into the cell walls as a result

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121
Q

The number of insulin receptors in a cell wall is ___ (inversely/directly) related to the plasma concentration of insulin

A

The number of insulin receptors in a cell wall is inversely related to the plasma concentration of insulin

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122
Q

The higher the plasma concentration of insulin, the ___ (less/more) insulin receptors in the cell wall

A

The higher the plasma concentration of insulin, the less insulin receptors in the cell wall

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123
Q

The lower the plasma concentration of insulin, the ___ (less/more) insulin receptors in the cell wall

A

The lower the plasma concentration of insulin, the more insulin receptors in the cell wall

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124
Q

Elimination half-life of insulin is ___-___ minutes

A

5-10 minutes

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125
Q

Insulin is metabolized by the ___ and ___

A

kidneys and liver

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126
Q

What prolongs the elimination half-life of insulin more–kidney or liver disease?

A

Kidney disease prolongs the elimination half-life of insulin more than liver disease

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127
Q

Despite rapid clearance from the plasma, there is a sustained pharmacologic effect of insulin for ___-___ minutes because insulin is tightly bound to ___ receptors

A

Despite rapid clearance from the plasma, there is a sustained pharmacologic effect of insulin for 30-90 minutes because insulin is tightly bound to tissue receptors

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128
Q

Basal rate of insulin secretion by the pancreas is ___ unit/hr

A

Basal rate of insulin secretion by the pancreas is 1 unit/hr

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129
Q

Food prompts a ___-___ fold increase in insulin secretion

A

Food prompts a 5-10 fold increase in insulin secretion

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130
Q

Total daily secretion of insulin is approximately ___ units/day

A

Total daily secretion of insulin is approximately 40 units/day

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131
Q

Insulin response to glucose is greater for IV infusion than oral ingestion–T/F?

A

FALSE–insulin response to glucose is greater for oral ingestion than IV infusion

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132
Q

Long acting insulins should be used for acute diabetic attacks–T/F?

A

FALSE–long acting insulins should NOT be used for acute diabetic attacks

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133
Q

What long acting insulin acts just like basal rate insulin; is sgiven once a day; good for people who have very brittle diabetes/lots of swings in glucose levels; also good for patients who are not good at keeping a schedule for giving themselves insulin?

A

Degludec (Tresiba)

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134
Q

What insulin is given at bedtime and helps to counteract the morning burst of hormones?

A

Glargine (Lantus)

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135
Q

Side effects of insulin–___glycemia; ___kalemia; ___magnesemia; ___phosphatemia; ___ reactions; ___dystrophy; insulin ___; drug ___

A

hypoglycemia; hypokalemia; hypomagnesemia; hypophosphatemia; allergic reactions; lipodystrophy; insulin resistance; drug interactions

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136
Q

Hypokalemia/hypomagnesemia that may occur with insulin administration puts patients at risk for ___

A

arrhythmias

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137
Q

Hypophosphatemia that may occur with insulin administration puts patients at risk for respiratory ___

A

respiratory depression

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138
Q

___ syndrome can occur in patients who have been NPO for awhile; get ___ (up/down) regulation of insulin receptors because the cells are hungry and waiting for more glucose to be introduced into the body

A

Refeeding syndrome can occur in patients who have been NPO for awhile; get up regulation of insulin receptors because the cells are hungry and waiting for more glucose to be introduced into the body

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139
Q

What happens if you give someone who has been NPO for so long 100% of their caloric requirements for the day?

A

Refeeding syndrome–they will get massive rush of insulin release from the pancreas; insulin will bind to all of the up regulated receptors; and there will be a rush of potassium, magnesium, and phosphate into the cells

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140
Q

Symptoms of hypoglycemia reflect the compensatory effects of increased ___–___esis, ___cardia, ___tension

A

increased epinephrine–diaphoresis, tachycardia, hypertension

Epi is released in response to hypoglycemia because it kickstarts gluconeogenesis/glycogenolysis to increase blood glucose levels

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141
Q

Rebound ___glycemia caused by ___ (sympathetic/parasympathetic) nervous system activity in response to hypoglycemia may mask the correct diagnosis–this is known as the ___ Effect

A

Rebound hyperglycemia caused by sympathetic nervous system activity in response to hypoglycemia may mask the correct diagnosis–this is known as the Somogyi Effect

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142
Q

Chronic NPH administration may lead to the development of antibodies to ___

A

protamine

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143
Q

Insulin resistance occurs in patients requiring > ___ units/day (remember avg daily insulin release from the body is ~___ units/day)

A

Insulin resistance occurs in patients requiring > 100 units/day (remember the avg daily insulin release from the body is ~40 units/day)

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144
Q

Insulin drug interactions–epinephrine ___ (inhibits/stimulates) the secretion of insulin; ___ (inhibits/stimulates) glycogenolysis

A

epinephrine inhibits the secretion of insulin; stimulates glycogenolysis

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145
Q

Perioperative management of blood glucose–optimal blood glucose levels ___-___ mg/dl; < ___ mg/dl for total joints; glucose infusion if blood glucose decreases to < ___ mg/dl

A

optimal blood glucose levels 110-180 mg/dl; < 150 mg/dl for total joints; glucose infusion if blood glucose decreases to < 80 mg/dl

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146
Q

What are the (8) classes of oral hypoglycemics?–___ureas; ___ inhibitors; ___nides; ___nides; ___diones; ___ inhibitors; ___ mimetics; ___inhibitor

A
  • Sulfonylureas
  • Alpha-glucosidase inhibitors
  • Meglitanides
  • Biguanides
  • Thiazolidinediones
  • DPP4 inhibitors
  • Incretin mimetics
  • SLGT2 inhibitor
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147
Q

Sulfonylureas MOA–act at ___ cells to stimulate release of ___

A

act at pancreatic beta cells to stimulate release of insulin

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148
Q

In order for sulfonylureas to work, you need to have a functioning ___

A

pancreas

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149
Q

Sulfonylureas have high ___ rates

A

high failure rates

20% primary failures (1 in 5 patients they won’t work for at all); each year 10-15% secondary failures

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150
Q

Sulfonylureas should be avoided in patients with allergy to ___ drugs

A

sulfa drugs

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151
Q

If patient took their sulfonylurea the morning of surgery, he/she will be at high risk for ___glycemia; have ___ or ___ available

A

he/she will be at high risk for hypoglycemia; have D50 or glucagon available

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152
Q

___ patients are at high risk of hypoglycemia from sulfonylureas

A

Renal failure patients are at high risk of hypoglycemia from sulfonylureas (because they are renally eliminated…renal failure prolongs their duration of action)

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153
Q

Most common severe complication of sulfonylureas is ___

A

hypoglycemia

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154
Q

Risk of hypoglycemia from sulfonylureas is highest with ___ and ___

A

glyburide and chlorpropamide (because they have the longest elimination half-life)

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155
Q

Duration of action of a sulfonylurea is up to ___ days

A

up to 7 days

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156
Q

Hypoglycemia from sulfonylureas is ___ (more/less) frequent than with insulin; it is often ___ and more ___ than hypoglycemia due to insulin

A

Hypoglycemia from sulfonlyureas is less frequent than with insulin; it is often prolonged and more dangerous than hypoglycemia due to insulin

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157
Q

Do sulfonylureas cross the placenta?

A

Yes–can cause fetal hypoglycemia

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158
Q

Contraindications/precautions for sulfonylurea use–hypersensitivity to ___; patients with ___glycemic unawareness; poor ___ function

A

hypersensitivity to sulfonamides; patients with hypoglycemic unawareness; poor renal function

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159
Q

What sulfonylurea is safest to use in patients with poor kidney function?

A

Glipizide (Glucotrol)

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160
Q

If CrCl is above 10, it ___ (is/is not) safe for the patient to take glipizide

A

it is safe for the patient to take glipizide

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161
Q

If someone took a sulfonylurea the morning of surgery, they are at risk for ___, especially if they took ___

A

they are at risk for hypoglycemia, especially if they took glyburide

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162
Q

Which 1st generation sulfonylurea is the longest acting?

A

Chlorpropamide (Diabinese)

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163
Q

Chlorpropamide (Diabinese) duration of action may approach ___ hours; 20% of the drug is excreted unchanged by the ___; it is associated with ___-like reactions; can cause severe ___natremia

A

duration of action may approach 72 hours; 20% of the drug is excreted unchanged by the kidneys; it is associated with disulfiram-like reactions; can cause severe hyponatremia (< 129)

Disulfiram = drug that causes an adverse reaction to alcohol, leading to nausea, vomiting, flushing, dizziness, throbbing headache, chest/abdominal discomfort, and general hangover-like symptoms

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164
Q

(2) meglitinides = ___ and ___

A

Repaglinide (Prandin) Nateglinide (Starlix)

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165
Q

Meglitinides MOA–increase ___ secretion from islet cells like ___ (what other drug class?)

A

increase insulin secretion from islet cells like sulfonylureas

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166
Q

Meglitinides have a ___ (slower/faster) onset and ___ (shorter/longer) duration of action than sulfonylureas

A

faster onset (1 hour) and shorter duration of action (4 hours)

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167
Q

Meglitinides can be administered while fasting–T/F?

A

FALSE–NEVER administer while fasting

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168
Q

Meglitinides are active only in the presence of ___; this decreases the risk of prolonged ___glycemic episodes

A

active only in the presence of glucose; this decreases the risk of prolonged hypoglycemic episodes

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169
Q

What is the name of (1) biguanide that is the #1 medication in type 2 diabetes treatment guidelines?

A

Metformin (Glucophage)

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170
Q

Metformin (Glucophage) decreases blood glucose concentrations with a very ___ (low/high) risk of hypoglycemia; has a positive effect on ___ concentrations; and leads to mild weight ___ in obese patients

A

very low risk of hypoglycemia; has a positive effect on lipid concentrations; and leads to mild weight loss in obese patients (unlike sulfonlyureas and meglitinides, which both cause weight gain)

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171
Q

Metformin MOA–___ (increased/decreased) hepatic glucose production [gluconeogenesis]; ___ (increases/decreases) glucose absorption from the intestine [similar to acarbose]; and ___ (increases/decreases) insulin sensitivity at the skeletal muscle cells

A

decreased hepatic glucose production [gluconeogenesis]; decreases glucose absorption from the intestine [similar to acarbose]; and increases insulin sensitivity at the skeletal muscle cells

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172
Q

Why should type 2 diabetics continue their metformin even if they are started on insulin?

A

Because metformin enhances the action of insulin at skeletal muscle cells

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173
Q

Rare side effect of metformin/black box warning for metformin = ___

A

lactic acidosis

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174
Q

Signs of lactic acidosis from metformin–___/___; ___ (increased/decreased) RR, HR; ___ pain; ___

A

nausea/vomiting; increased RR, HR; abdominal pain; shock

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175
Q

Metformin can exaggerate post-op nausea/vomiting–T/F?

A

True

Starting regular dose of metformin post-op can make patient very sick after surgery

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176
Q

Discontinue metformin ___ hours prior to elective surgery d/t risk of lactic acidosis in the intraoperative period

A

48 hours prior to elective surgery

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177
Q

Metformin and IV contrast = increased risk of ___toxicity; hold ___ hours prior to and after dye, check ___ levels

A

increased risk of nephrotoxicity; hold 48 hours prior to and after dye, check creatinine levels

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178
Q

Metformin contraindications/precautions–new recommendations for renal impairment–contraindicated in patients with eGFR < ___ ml/min; do not initiate or re-evaluate patients with eGFR < ___ ml/min

A

contraindicated in patients with eGFR < 30 ml/min; do not initiate or re-evaluate patients with eGFR < 45 ml/min

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179
Q

Metformin contraindications/precautions–age > ___ years old; ___ impairment; ___

A

age > 80 years old; hepatic impairment; CHF

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180
Q

(2) thiazolidinediones–___ and ___

A

rosiglitazone (Avandia) and pioglitazone (actos)

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181
Q

Thiazolidinediones MOA–___ (increase/decrease) insulin resistance; ___ (increase/decrease) hepatic glucose output

A

decrease insulin resistance; decrease hepatic glucose output

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182
Q

Thiazolidinediones require the presence of ___ and are especially effective in ___ patients

A

require the presence of insulin and are especially effective in obese patients

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183
Q

Thiazolidinediones side effects–weight ___ (loss/gain); ___toxicity; peripheral ___; ___ exacerbations; risk of ___

A

weight gain; hepatotoxicity; peripheral edema; CHF exacerbations; risk of bone fractures

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184
Q

Why was rosiglitazone (avandia) pulled from the market?

A

Controversial increase in MI and CV death

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185
Q

(4) DPP4 inhibitors

A
  • Sitagliptin (Januvia)
  • Saxagliptin (Onglyza)
  • Linagliptin (Tradjenta)
  • Alogliptin (Nesina)
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186
Q

DPP4 inhibitors MOA–___ (increase/decrease) pancreatic insulin secretion; ___ (limit/enhance) glucagon secretion; ___ (slow/speed up) gastric emptying; ___ (promote/inhibit) satiety

A

increase pancreatic insulin secretion; limit glucagon secretion; slow gastric emptying; promote satiety

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187
Q

How do DPP4 inhibitors specifically work though? They slow down metabolism of what protein?

A

slow down metabolism of GLP-1

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188
Q

Post-marketing, DPP4 inhibitors were found to cause ___titis, ___edema, ___ syndrome, ___laxis

A

pancreatitis, angioedema, Stevens Johnson syndrome, anaphylaxis

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189
Q

DPP4 inhibitors 08/2015 FDA safety warning for ___

A

joint pain

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190
Q

Incretin mimetics are also known as ___ analogs and ___ analogs

A

GLP-1 analogs and amylin analogs

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191
Q

(4) incretin mimetics–GLP-1 analogs

A
  • Exanatide (Byetta, Bydureon)
  • Liraglutide (Victoza)
  • Albiglutide (Tanzeum)
  • Dulaglutide (Trulicity)

^ These are injectables

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192
Q

GLP-1 analogs ___ (slow/speed up) gastric emptying; ___ (reduce/enhance) postprandial glucagon secretion

A

slow gastric emptying; reduce postprandial glucagon secretion

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193
Q

Amylin analogs ___ (increase/decrease) insulin secretion; ___ (slow/speed up) gastric emptying; ___ (increase/decrease) beta cell growth; ___ (suppress/stimulate) central appetite

A

increase insulin secretion; slow gastric emptying; increase beta cell growth; suppress central appetite

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194
Q

What is a risk postoperatively if the patient takes a GLP-1 analog?

A

Postop nausea/vomiting because GLP-1 analogs slow down the GI tract

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195
Q

Specific GLP-1 analog precautions–avoid Byetta in ___ failure; avoid Victoza in ___ carcinoma

A

avoid Byetta in renal failure; avoid Victoza in thyroid carcinoma

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196
Q

Side effects of amylin analogs–black box warning: ___glycemia, especially in type ___ diabetics; ___/___; ___rexia; ___ache; gastro___

A

black box warning: hypoglycemia, especially in type I diabetics; nausea/vomiting; anorexia; headache; gastroparesis

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197
Q

(3) SGLT2 inhibitors

A
  • Canagliflozin (Invokana)
  • Dapagliflozin (Farxiga)
  • Empagliflozin (Jardiance)
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198
Q

SGLT2 inhibitors MOA–___ (increased/decreased) urinary glucose excretion from the ___ tubule

A

increased urinary glucose excretion from the proximal tubule

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199
Q

Contraindications for SGLT2 inhibitors–CrCl < ___ ml/min, end stage ___ disease, patients on hemo___

A

CrCl < 30 ml/min, end stage renal disease, patients on hemodialysis

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200
Q

Warnings for SGLT2 inhibitors–___tension, ___ side effects

A

hypotension, urinary side effects

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201
Q

Increased risk of ___ and ___ with SGLT2 inhibitors

A

gangrene and amputations, primarily toe

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202
Q

What does SGLT2 inhibitor mean?

A

sodium glucose transporter 2 inhibitor

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203
Q

SGLT2 inhibitors–increased risk of perioperative ___glycemic keto___

A

euglycemic ketoacidosis

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204
Q

Thyroid gland hormones review–hypothalamus releases ___; pituitary releases ___; thyroid releases ___ and ___

A

hypothalamus releases thyroid releasing hormone (TRH); pituitary releases thyroid stimulating hormone (TSH); thyroid releases T3 ad T4

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205
Q

Clinical presentation of HYPOthyroid (Hashimoto disease)–___ (cold/heat) intolerance; ___ (moist/dry) skin; ___ness; weight ___ (loss/gain); ___cardia; ___ (slow/fast) reflexes; ___ (coarse/fine) skin and hair; periorbital ___; painful/heavy ___; ___ coma

A

cold intolerance; dry skin; weakness; weight gain; bradycardia; slow reflexes; coarse skin and hair; periorbital swelling; painful/heavy menstruation; myxedema coma

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206
Q

Clinical presentation of HYPERthyroid (Graves disease)–weight ___ (loss/gain); ___ (increased/decreased) appetite; ___ (cold/heat) intolerance; ___er; ___ (coarse/fine) hair; ___cardia; ___iety; ___nia; ___ (lighter/heavier) periods/___menorrhea; ___ (cold/warm) skin; ___thalmos; ___ storm

A

weight loss; increased appetite; heat intolerance; goiter; fine hair; tachycardia; anxiety; insomnia; lighter periods/amenorrhea; warm skin; exophthalmos; thyroid storm

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207
Q

Armour thyroid composition ratio of T4 to T3 is ___:___

A

4:1

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208
Q

T4 = ___ (active/inactive)

A

T4 = inactive

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209
Q

T3 = ___ (active/inactive)

A

T3 = active

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210
Q

What is the most frequently administered drug for the treatment of diseases requiring thyroid hormone replacement (i.e.: hypothyroidism)?

A

Levothyroxine (T4) (Synthroid)

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211
Q

If a patient is on PO Synthroid and is unable to take oral meds for several days, do they need immediate IV replacement of Synthroid? Why?

A

No because Synthroid has a long elimination half-life (7 days)

After 7 days, if patient is still not able to take PO, you can administer half the oral dose IV

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212
Q

The elimination half-life of Synthroid is ___ days

A

7 days

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213
Q

In the body, Synthroid is deiodinated and converted to ___

A

T3

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214
Q

Liothyronine (Cytomel) is a levorotatory isomer of ___

A

T3

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215
Q

Liothyronine (T3) (Cytomel) is __-__x as potent as levothyroxine

A

2.5-3x as potent as levothyroxine

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216
Q

Liothyronine (T3) (Cytomel) is usually added on if someone is on a max dose of Synthroid and their body isn’t responding appropriately to it–T/F?

A

True

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217
Q

Hypothyroidism anesthetic implications–___ (increased/decreased) sensitivity to depressant drugs, including inhaled anesthetics; ___dynamic (hyper/hypo) CV system; ___ (increased/decreased) CO d/t ___ (increased/decreased) HR and SV; ___ (slow/fast) metabolism of drugs, particularly opioids; unresponsive ___ reflexes; ___ (increased/decreased) intravascular fluid volume; impaired ventilatory response to ___ (low/high) PaO2 and/or ___ (increased/decreased) PaCO2; ___ (delayed/enhanced) gastric emptying; ___natremic; ___thermic; ___nemic; ___glycemic; primary ___ insufficiency

A

increased sensitivity to depressant drugs, including inhaled anesthetics; hypodynamic CV system; decreased CO d/t decreased HR and SV; slow metabolism of drugs, particularly opioids; unresponsive baroreceptor reflexes; decreased intravascular fluid volume; impaired ventilatory response to low PaO2 and/or increased PaCO2; delayed gastric emptying; hyponatremic; hypothermic; anemic; hypoglycemic; primary adrenal insufficiency

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218
Q

Two antithyroid drugs to treat hyperthyroidism–___ and ___

A

propylthiouracil (PTU) and methimazole (tapazole)

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219
Q

Methimazole MOA–inhibit the formation of ___ hormone

A

thyroid hormone

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220
Q

PTU blocks the peripheral deiodination of ___ to ___

A

T4 to T3

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221
Q

PTU and methimazole are useful in treating ___thyroidism (including thyroid ___) before elective ___

A

useful in treating hyperthyroidism (including thyroid storm) before elective thyroidectomy

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222
Q

PTU and methimazole are only available ___

A

orally

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223
Q

PTU and methimazole require several days for full effect because pre-formed hormone must be depleted–T/F?

A

True

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224
Q

What is the oldest effective treatment for hyperthyroidism?

A

Iodines–Lugol’s solution, saturated KI (potassium iodide) solution

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225
Q

Iodines inhibit the release of ___ hormone into the circulation

A

inhibit the release of thyroid hormone into the circulation

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226
Q

Iodines are combined with ___olol to treat hyperthyroidism before thyroidectomy

A

propranolol

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227
Q

Signs of thyroid storm–___thermia, ___cardia, ___, ___hydration, and ___

A

hyperthermia, tachycardia, CHF, dehydration, and shock

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228
Q

Thyroid storm resembles ___

A

malignant hyperthermia

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229
Q

Thyroid storm is more likely to occur in the first ___-___ hours postop than intraop

A

first 6-19 hours postop

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230
Q

Treatment of thyroid storm–IV infusion of ___ (warm/cold) crystalloid solutions; sodium ___ IV to reduce the release of active hormones from the thyroid gland; ___ IV to treat acute primary adrenal insufficiency from increased metabolism and use of corticosteroids; ___ IV to alleviate the CV effects of thyroid hormones; ___ PO to reduce synthesis of new thyroid hormone

A

IV infusion of cold crystalloid solutions; sodium iodide IV to reduce the release of active hormones from the thyroid gland; cortisol IV to treat acute primary adrenal insufficiency from increased metabolism and use of corticosteroids; propranolol IV to alleviate the CV effects of thyroid hormones; PTU PO to reduce synthesis of new thyroid hormone

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231
Q

Avoid ___ for elevated temperature because it may displace thyroxine from carrier proteins

A

Avoid aspirin for elevated temperature because it may displace thyroxine from carrier proteins (so then there will be more circulating thyroxine)

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232
Q

The lowest concentration of antibiotic required to prevent growth is the ___

A

minimum inhibitory concentration (MIC)

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233
Q

The lowest concentration of antibiotic required to kill bacteria is the ___

A

minimum bactericidal concentration (MBC)

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234
Q

You can compare MICs of different antibiotics to each other–T/F?

A

False–cannot compare MICs of different antibiotics to each other

You can, however, compare MIC of one single antibiotic to different organisms (i.e.: MIC of cipro for klebsiella vs. pseudomonas)

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235
Q

What is the difference between bactericidal and bacteriostatic?

A

Bactericidal = kills the bacteria

Bacteriostatic = stops the bacteria from replicating (but does not kill the existing bacteria)

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236
Q

Penicillins, cephalosporins, aminoglycosides, vancomycin, quinolone, aztreonam, imipenem, bacitracin, and polymyxins are all bacteri___

A

bactericidal

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237
Q

Tetracyclines, chloramphenicol, eryrthromycin, clindamycin, sulfonamides, and trimethoprim are all bacteri___

A

bacteriostatic

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238
Q

Time-dependent killing–greater concentrations ___ (do/do not) kill bacteria faster or in greater numbers

A

greater concentrations do NOT kill bacteria faster or in greater numbers

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239
Q

Time-dependent killing–clinical efficacy is related to the duration for which these levels are maintained–T/F?

A

True

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240
Q

What (3) antibiotic classes demonstrate time-dependent killing?

A
  • Beta-lactams
  • Monobactams (aztreonam)
  • Macrolides (erythromycin, clindamycin)
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241
Q

Continuous infusion of time-dependent killing antibiotics ___ (has/has not) shown to be more effective than intermittent boluses

A

continuous infusion of time-dependent killing antibiotics has NOT shown to be more effective than intermittent boluses

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242
Q

What term describes the following?–some antibiotics continue to suppress the growth of bacteria even after the antibiotic is no longer detectable

A

Post Antibiotic Effect (PAE)

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243
Q

PAE is demonstrated virtually for all antimicrobials–T/F?

A

True

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244
Q

PAE can be ___ (increased/decreased) in acidic, infected media

A

decreased

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245
Q

During the PAE phase, bacteria are ___ (more/less) susceptible to killing by leukocytes–this is known as what?

A

During the PAE phase, bacteria are MORE susceptible to killing by leukocytes–this is known post antibiotic leukocyte effect

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246
Q

(2) types of antibiotic resistance–___ and ___

A

intrinsic and acquired

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247
Q

___ (intrinsic/acquired) resistance is natural resistance to the antimicrobial

A

Intrinsic resistance is natural resistance to the antimicrobial

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248
Q

___ (intrinsic/acquired) resistance reflects a genetic alteration in the bacteria that renders a once effective antimicrobial ineffective

A

Acquired resistance reflects a genetic alteration in the bacteria that renders a once effective antimicrobial ineffective

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249
Q

The majority of nosocomial (hospital-acquired) infections are ___, ___, and ___ infections

A

urinary, respiratory, and blood infections

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250
Q

Rate of central line related infections (from highest risk location to lowest risk location)

A

Femoral > IJ > Subclavian

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251
Q

Clostridium difficile is now known as ___

A

Clostridioides difficile

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252
Q

What provokes C. difficile disease? How?

A

Antibiotic therapy, including prophylaxis…it alters normal bowel flora

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253
Q

Pathogenesis of C. diff–typically ___-mediated; bacteremia with C. diff is extremely ___ (rare/common)

A

toxin-mediated–enterotoxin A, cytotoxin B; bacteremia with C. diff is extremely rare

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254
Q

Diagnosis of C. diff is confirmed by detection of one of the ___

A

toxins

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255
Q

C. diff spores are extremely hearty and impervious to antibiotic therapy, resulting in a 10% relapse rate in successfully treated patients–T/F?

A

True

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256
Q

Treatment of C. diff = oral ___

A

oral vancomycin

257
Q

Dificid (fidaxomicin) is another antibiotic that can be used to treat C. diff with similar cure rates as Vancomycin and reduced recurrence for moderate to severe infection–T/F?

A

True

258
Q

In patients with ongoing original infection [the infection that they had before getting C. diff]…treat the infection with appropriate ___-spectrum antibiotics; continue C. diff therapy also and extend the C. diff therapy course for ___ to ___ days after the completion of the other antibiotics

A

In patients with ongoing original infection [the infection that they had before getting C. diff]…treat the infection with appropriate broad-spectrum antibiotics; continue C. diff therapy also and extend the C. diff therapy course for 5 to 10 days after the completion of the other antibiotics

259
Q

Treatment course of C. diff is usually ___ to ___ days

A

Treatment course of C. diff is usually 10 to 14 days

260
Q

In the future, C. diff ___ (can/cannot) be provoked with subsequent antibiotic courses because of the presence of latent ___

A

In the future, C. diff can be provoked with subsequent antibiotic courses because of the presence of latent spores

261
Q

Surgical antibiotic prophylaxis ___ (is/is not) usually necessary to continue past the 1st post-op day

A

Surgical antibiotic prophylaxis is NOT usually necessary to continue past the 1st post-op day

262
Q

For surgical antibiotic prophylaxis, usually use what antibiotic class?

A

1st generation cephalosporin–cefazolin

Low cost, broad spectrum, low incidence of allergic reactions

263
Q

Wound classification–classes __-__

A

classes I-IV

264
Q

Class I = ___; ___traumatic, no break in ___ technique; ___, ___, and ___ tracts not entered

A

Class I = clean

  • atraumatic
  • no break in sterile technique
  • respiratory, GI, and GU tracts not entered
265
Q

Class II = ___; surgery in areas known to harbor ___; ___ spillage of contents

A

Class II = clean-contaminated

  • surgery in areas known to harbor bacteria
  • no spillage of contents
266
Q

Class III = ___; major break in ___ technique; surgery on ___ wounds; gross ___ spillage; entrance into an infected ___ or ___ tract

A

Class III = contaminated

  • major break in sterile technique
  • surgery on traumatic wounds
  • gross GI spillage
  • entrance into an infected biliary or GU tract
267
Q

Class IV = ___; infection existed ___ the surgery, i.e.: old wound with devitalized tissue, perforated viscera

A

Class IV = dirty-infected; infection existed before the surgery, i.e.: old wound with devitalized tissue, perforated viscera

268
Q

Prophylactic antibiotic administration is initiated within ___ minutes prior to the surgical incision

A

120 minutes prior to the surgical incision

269
Q

Ancef is initiated within ___ minutes prior to the surgical incision

A

Ancef is initiated within 60 minutes prior to the surgical incision

270
Q

Vanco is initiated within ___ minutes prior to the surgical incision

A

Vanco is initiated within 120 minutes prior to the surgical incision

271
Q

JAMA surgery 2019–increasing duration of antimicrobial prophylaxis was associated with higher odds of acute ___ injury and ___ infection in a duration-dependent fashion

A

increasing duration of antimicrobial prophylaxis was associated with higher odds of acute kidney injury and C. diff infection in a duration-dependent fashion

272
Q

JAMA surgery 2019–extended duration of antibiotic prophylaxis (3 days, 5 days post-op) ___ (did/did not) lead to additional SSI reduction

A

extended duration (3 days, 5 days post-op) did NOT lead to additional SSI reduction

273
Q

Antibiotic medications by class–beta-___; ___sporins; ___bactams, ___penems; ___lides; ___quinolones; ___cyclines; ___glycosides

A
  • beta-lactams
  • cephalosporins
  • monobactams, carbapenems
  • macrolides
  • fluoroquinolones
  • tetracyclines
  • aminoglycosides
274
Q

What (4) antibiotic classes are beta-lactams?

A
  • Penicillin
  • Cephalosporins
  • Carbapenem
  • Monobactam
275
Q

Beta-lactams bind to the ___; they are ___ inhibitors

A

Beta-lactams bind to the penicillin binding protein (PBP); they are cell wall synthesis inhibitors

276
Q

What enzyme causes penicillin resistance?

A

B-lactamase–breaks a bond in the B-lactam ring of penicillin to disable the molecule

277
Q

Bacteria with B-lactamase can resist the effects of ___ and other ___ antibiotics

A

can resist the effects of penicillin and other B-lactam antibiotics (cephalosporins, carbapenem, monobactam)

278
Q

What can be added to penicillin antibiotics to prevent resistance?

A

A beta-lactamase inhibitor

279
Q

(3) beta-lactamase inhibitors = ___bactam, ___bactam, ___ acid

A

sulbactam, tazobactam, clavulanic acid

280
Q

Penicillins end in -___

A

-cillin

Examples = penicillin ampicillin, amoxicillin, piperacillin, ticarcillin, oxacillin, nafcillin, dicloxacillin, methicillin

281
Q

Zosyn = ___ + ___

A

piperacillin + tazobactam

282
Q

Penicillin ___ (is/is not) stable to beta lactamase

A

Penicillin is NOT stable to beta lactamase (have to add a beta-lactamase inhibitor to it)

283
Q

What is Jarisch-Herxheimer reaction? What antibiotic may cause it?

A

high fevers, rash, similar to Rocky Mountain spotted fever; penicillin may cause it

284
Q

If someone has a penicillin allergy, what are the next antibiotic choices? ___ or ___

A

vancomycin or cleocin

285
Q

Clinical Infectious Diseases October 2017–patients with a reported penicillin allergy had a 50% increased odds of SSI, attributable to the receipt of ___-line perioperative antibiotics

A

attributable to the receipt of second-line perioperative antibiotics

Because people with penicillin allergy will often receive vancomycin or cleocin instead–vanco only covers gram positive infections (staph, strep); cleocin has some broad spectrum coverage but doesn’t really cover some of the common bacteria that cause SSIs

286
Q

MRSA and C. diff rates are ___ (lower/higher) in patients with a reported penicillin allergy because they have higher use of ___-spectrum antibiotics

A

MRSA and C. diff rates are higher in patients with a reported penicillin allergy because they have higher use of broad spectrum antibiotics

287
Q

What antibiotic has the highest rates of resultant C. Diff infection?

A

Cleocin

288
Q

Pencillins, when given alone, ___ (are/are not) stable to beta-lactamase

A

Penicillins, when given alone, are NOT stable to beta-lactamase

289
Q

Penicillins with beta lactamase inhibitors ___ (do/do not) cover MRSA

A

Penicillins with beta lactamase inhibitors do NOT cover MRSA

290
Q

Ticarcillin +/- Clavulanate (Timentin) causes what electrolyte abnormalities?–___natremia, ___kalemia

A

hypernatremia, hypokalemia

291
Q

Piperacillin +/- Tazobactam (Zosyn) side effects–prolonged ___ time; ___kalemia; ___penia at high doses

A

prolonged bleeding time; hypokalemia; neutropenia at high doses

292
Q

Spectrum of action of cephalosporins is based on ___

A

generation

293
Q

As you go up in generation of cephalosporins, you lose gram ___ coverage and gain gram ___ coverage

A

As you go up in generation of cephalosporins, you lose gram positive coverage and gain gram negative coverage

294
Q

___ generation cephalosporins = cefazolin, cephalexin

A

1st generation

295
Q

Half-life of ancef is ___ hours

A

1.8 hours

296
Q

If procedure is going beyond ___ hours, need to redose ancef

A

If procedure is going beyond 4 hours, need to redose ancef

297
Q

Cephalexin (keflex) and cefazolin (ancef) are both ___ eliminated

A

renally eliminated

298
Q

Which 3rd generation cephalosporins cross the BBB and can be used to treat meningitis?

A

Ceftriaxone (rocephin); cefotaxime (claforan)

299
Q

Ceftazidime (Fortaz) is a ___ generation cephalosporin; it covers most gram ___ with good ___ coverage

A

Ceftazidime (Fortaz) is a 3rd generation cephalosporin; it covers most gram negatives with good pseudomonas coverage

300
Q

Ceftazidime (Fortaz) [3rd gen cephalosporin] + avibactam (beta lactamase inhibitor) offers significant gram ___ coverage and is usually reserved to treat ___

A

Ceftazidime (Fortaz) + avibactam offers significant gram negative coverage and is usually reserved to treat MDROs–multidrug resistant organisms

301
Q

Ceftriaxone (Rocephin) is a ___ generation cephalosporin; it covers ___ better than most 3rd gens and most ___; covers most gram ___; ___ (does/does not) cover pseudomonas

A

Ceftriaxone (Rocephin) is a 3rd generation cephalosporin; it covers staph better than most 3rd gens and most strep; covers most gram negatives; does NOT cover pseudomonas

302
Q

Side effects of ceftriaxone (rocephin) = ___ and biliary ___, particularly in young children; precipitates with ___ if running in the same IV line

A

diarrhea and biliary sludging, particularly in young children; precipitates with calcium if running in the same IV line

303
Q

Main differences between ceftazidime (fortaz) and ceftriaxone (rocephin)–fortaz covers more gram ___, better ___ coverage; rocephin has more gram ___ coverage (not as good as 1st and 2nd generation cephalosporins), ___ (does/does not) cover pseudomonas

A

fortaz covers more gram negatives, better pseudomonas coverage; rocephin has more gram positive coverage (not as good as 1st and 2nd generation cephalosporins), does not cover pseudomonas

304
Q

Ceftaroline (Teflaro) is a ___ generation cephalosporin; covers ___; gram ___ bacteria; has broad-spectrum activity against gram ___ bacteria

A

Ceftaroline (Teflaro) is a 5th generation cephalosporin; covers MRSA; gram positive bacteria; has broad-spectrum activity against gram negative bacteria

305
Q

Cefiderocol (Fetroja) is a ___ generation cephalosporin; it is the first cephalosporin to cover ___

A

Cefiderocol (Fetroja) is a 5th generation cephalosporin (just came out in 2020); it is the first cephalosporin to cover Acinetobacter baumannii complex

306
Q

Carbapenems–imipenem/cilastatin (primaxin) … cilastatin ___ (is/is not) a beta-lactamase inhibitor

A

cilastatin is NOT a beta-lactamase inhibitor

307
Q

What does cilastatin do?–it inhibits ___ enzyme from breaking down imipenem

A

Cilastatin inhibits dihydropeptidase enzyme from breaking down imipenem

308
Q

Imipenem/cilastatin (primaxin) has a high risk of ___

A

seizures

309
Q

Primaxin [imipenem/cilastatin] + relebactam = ___, reserved for ___ gram negative infections in the ___ and ___

A

Primaxin [imipenem/cilastatin] + relebactam = recarbrio, reserved for MDRO gram negative infections in the urine and abdomen

310
Q

Meropenem is a ___; it has a ___ (lower/higher) incidence of seizures than imipenem

A

Meropenem is a carbapenem; it has a lower incidence of seizures than imipenem

311
Q

Primaxin vs. meropenem–primaxin has ___ (better/worse) coverage, ___ (lower/higher) risk of seizures; meropenem has (better/worse) coverage, ___ (lower/higher) risk of seizures

A

Primaxin has better coverage, higher risk of seizures; meropenem has worse coverage, lower risk of seizures

312
Q

Ertapenem (Invanz) has a ___ (low/high) seizure risk

A

low seizure risk

313
Q

Vancomycin inhibits ___ formation; disrupts cell wall ___; bacteri___; ___ (concentration/time) dependent

A

Vancomycin inhibits peptidoglycan formation; disrupts cell wall synthesis; bactericidal; concentration dependent

314
Q

Vanco is given PO to treat ___ only; usually is given IV for treatment of other infections

A

Vanco is given PO to treat C. diff only; usually is given IV for treatment of other infections

315
Q

If you take vanco orally, it does not leave the GI tract–T/F?

A

True

316
Q

Vancomycin ___ (is/is not) a beta lactam

A

Vancomycin is not a beta lactam

317
Q

Beta lactams are ___ (time/concentration) dependent

A

Beta lactams are time dependent

318
Q

Vancomycin is ___ (time/concentration) dependent

A

Vancomycin is concentration dependent

319
Q

Vancomycin offers ___ (broad/narrow) spectrum gram ___ (positive/negative) coverage

A

Vancomycin offers broad spectrum gram positive coverage

Treats staph, strep, enterococci, C. diff

320
Q

Side effects of vanco = ___ syndrome; ___toxicity; ___toxicity; ___penia

A

Red-Man syndrome; nephrotoxicity; ototoxicity; thrombocytopenia

321
Q

Vanco weight based dosing–___mg/kg

A

15 mg/kg

1 g usually does not cut it as a loading dose

322
Q

Linezolid (Zyvox) inhibits protein synthesis by binding ___S ribosomal subunit of the ___S ribosome to prevent the formation of a functional ___S initiation complex

A

Linezolid (Zyvox) inhibits protein synthesis by binding 23S ribosomal subunit of the 50S ribosome to prevent the formation of a functional 70S initiation complex

323
Q

Side effects of linezolid (Zyvox)–___suppression–___emia, ___penia, ___penia, ___penia…check CBC; drug interaction with ___, potential for ___ syndrome

A

myelosuppression–anemia, leukopenia, pancytopenia, thrombocytopenia…check CBC; drug interaction with MAO (monoamine oxidase), potential for serotonin syndrome

324
Q

What should you do if a person is on an SSRI and is going to be started on linezolid (Zyvox)?

A

Hold SSRI to prevent the development of serotonin syndrome because linezolid is a MAOI

325
Q

Azithromycin (Zithromax) is a ___; half-life is ___ hours, only dose ___ per day; may prolong ___ interval

A

Azithromycin (Zithromax) is a macrolide; half-life is 68 hours, only dose once per day; may prolong QT interval

326
Q

Azithromycin (Zithromax) has drug interactions with ___phylline, ___sporine, ___toin, ___mazepine, ___vudine; interactions ___ (are/are not) a CYP3A4 mechanism

A

theophylline, ciclosporine, phenytoin, carbamazepine, zidovudine (AZT–azidothymidine…drug used to prevent/treat HIV/AIDS); interactions are NOT a CYP3A4 mechanism (so it’s not an inhibitor or inducer of these medications)

327
Q

Macrolides end in -___

A

-thromycin

328
Q

Clarithromycin (Biaxin) may prolong ___ interval, has significant ___ toxicity, same drug interactions as azithromycin but is a potent ___ (inhibitor/inducer) of CYP3A4

A

Clarithromycin (Biaxin) may prolong QT interval, has significant GI toxicity, same drug interactions as azithromycin but is a potent inhibitor of CYP3A4

329
Q

Erythromycin is the drug of choice for ___ disease; also used to treat gastro___, alternative to reglan

A

drug of choice for Legionnaires’ disease; also used to treat gastroparesis, alternative to reglan (because reglan has extrapyramidal side effects)

330
Q

Which macrolide has the most drug interactions?

A

Clarithromycin (Biaxin) because it is a CYP3A4 inhibitor

But all macrolides have CYP3A4 drug interactions

331
Q

Fluoroquinolones have many drug interactions–___s, ___, ant___, ___, pro___

A

NSAIDs, warfarin, antacids, amiodarone, probenecid–used to treat gout

332
Q

How do fluoroquinolone work?–inhibit ___ synthesis

A

inhibit DNA synthesis

333
Q

FDA safety communication for fluoroquinolones–black box warning for patients > ___ years

A

black box warning for patients > 65 years

Avoid in elderly patients > 65 years when other antibiotics are appropriate

334
Q

High risk of side effects with fluoroquinolones–___itis/___ tendon rupture; ___logic effects; ___glycemia (fatal); ___idity/___ality; ___ prolongation

A

tendonitis/Achilles tendon rupture; neurologic effects; hypoglycemia (fatal); morbidity/mortality; QT prolongation

335
Q

Fluoroquinolones end in -___

A

-floxacin

Examples = ciprofloxacin, levofloxacin, ofloxacin, moxifloxacin

336
Q

Main things to know for FQ antibiotics–they can cause ___ prolongation; they cover a lot of gram ___; black box warning for elderly > age ___

A

they can cause QT prolongation; they cover a lot of gram negatives; black box warning for elderly > age 65

337
Q

Delafloxacin (Baxdela) is the first fluoroquinolone antibiotic with activity against ___; unlike other FQs, it is not associated with ___ prolongation or ___sensitivity

A

Delafloxacin (Baxdela) is the first fluoroquinolone antibiotic with activity against MRSA; unlike other FQs, it is not associated with QT prolongation or photosensitivity

338
Q

Side effects of tetracycline antibiotics–___ upset; ___sensitivity; inhibition of ___ growth; ___toxicity; tooth dis___ and enamel ___plasia

A

Side effects of tetracycline antibiotics–GI upset, photosensitivity; inhibition of bone growth; hepatotoxicity; tooth discoloration (yellow teeth) and enamel hypoplasia

339
Q

Tetracycline antibiotics inhibit bone growth during ___ and ___ trimesters through the age of ___

A

inhibit bone growth during 2nd and 3rd trimesters through the age of 8

340
Q

Doxycycline (Vibramycin) has excellent tissue ___, including into the ___; causes permanent tooth ___; rare but fatal ___toxicity; drug interactions with ___farin, ___toin, ___pine, oral ___

A

Doxycycline (Vibramycin) has excellent tissue distribution, including into the CNS; causes permanent tooth discoloration; rare but fatal hepatotoxicity; drug interactions with warfarin, phenytoin, carbamazepine, oral contraceptives

341
Q

Aminoglycosides are ___ and ___toxic, prolong ___ blockade

A

Aminoglycosides are oto and nephrotoxic, prolong neuromuscular blockade

342
Q

Amikacin is an aminoglycoside used to treat ___

A

tuberculosis

343
Q

Need to check ___ of aminoglycosides; want to prevent ___toxicity and ___toxicity

A

Need to check levels of aminoglycosides; want to prevent nephrotoxicity and ototoxicity

344
Q

Bactrim affects ___ synthesis to starve out bacteria so that it can’t create new DNA

A

Bactrim affects folic acid synthesis to starve out bacteria so that it can’t create new DNA

345
Q

Side effects of Bactrim–___cytopenia, ___penia, ___penia, ___ syndrome

A

pancytopenia, neutropenia, thrombocytopenia, Stevens Johnson Syndrome

346
Q

Bactrim is a ___ antibiotic, so take ___ allergies seriously

A

Bactrim is a sulfonamide antibiotic, so take sulfa allergies seriously

347
Q

Nitrofurantoin (Macrobid, Macrodantin) is used to treat ___ pathogens

A

urinary pathogens

348
Q

Clindamycin (Cleocin) is used to treat ___ (aerobes/anaerobes), specifically ___ bacteria

A

Clindamycin (Cleocin) is used to treat anaerobes, specifically gut bacteria

349
Q

Clindamycin (Cleocin) has the highest ___ risk; and can cause prolonged ___ blockade

A

Clindamycin (Cleocin) has the highest C. diff risk; and can cause prolonged neuromuscular blockade

350
Q

What happens if you drink alcohol while taking flagyl?

A

Disulfiram like reaction–alcohol withdrawal symptoms

351
Q

Flagyl interacts with what blood thinner?

A

Coumadin

352
Q

Quinupristin/Dalfopristin (Synercid) (30/70) should be given via ___ due to significant phlebitis

A

should be given via central line due to significant phlebitis

353
Q

Rifampin and Rifabutin are potent ___ (inhibitors/inducers) of the CYP 450 system with significant interactions

A

Rifampin and Rifabutin are potent inducers of the CYP 450 system with significant interactions

354
Q

Rifampin and Rifabutin can rarely cause ___toxicity, ___ body fluids

A

Rifampin and Rifabutin can rarely cause hepatotoxicity, orange-red body fluids

355
Q

What (3) antibiotics are OK to use in pregnant patients?

A
  • Penicillins
  • Cephalosporins
  • Erythromycin
356
Q

What (2) antibiotics should only be used in pregnancy if necessary?

A
  • Aminoglycosides

- Isoniazid–usually only used to prevent or treat TB

357
Q

What antibiotics should be avoided completely in pregnancy?–___dazole, ___cillin, ___fampin, ___prim, ___lones, ___cyclines

A

metronidazole, ticarcillin, rifampin, trimethoprim, fluoroquinolones, tetracyclines

358
Q

Tetracycline in pregnant women is associated with acute ___ of the liver, ___titis, and possible ___ injury

A

Tetracycline in pregnant women is associated with acute fatty necrosis of the liver, pancreatitis, and possible renal injury

359
Q

Canadian Population Study 11/2017–cleocin, doxycycline, FQs, macrolides, phenyoxymetylPCN = ___ (increased/decreased) risk of congenital malformations, risk of organ specific malfunctions; ___ (higher/lower) risk if used first trimester

A

increased risk of congenital malformations, risk of organ specific malfunctions; higher risk if used first trimester

360
Q

Canadian Population Study 11/2017–___cillin, ___sporins, ___bid = no increased risk of congenital malformations/organ specific malfunctions

A

amoxicillin, cephalosporins, Macrobid = no increased risk of congenital malformations/organ specific malfunctions

361
Q

Besides amphoteracin B, what other antibiotics cause hypokalemia?

A

penicillins–Piperacillin +/- tazobactam (zosyn), Ticarcillin +/- Clavulanate (Timentin)

362
Q

First line treatment for status epilepticus = ___

A

benzos

363
Q

Anticonvulsants MOA–___ channel blockade, ___ channel blockade

A

sodium channel blockade, calcium channel blockade

364
Q

Anticonvulsants calcium channel blockade–particularly the ___-type channels located in the ___ which act as ‘pacemakers’ of normal rhythmic brain function

A

Anticonvulsants calcium channel blockade–particularly the T-type channels located in the thalamus which act as ‘pacemakers’ of normal rhythmic brain function

365
Q

Anticonvulsants other MOAs–GABA ___ (enhancers/inhibitors); glutamate ___ (enhancers/blockers); carbonic anhydrase ___ (enhancers/inhibitors); ___ hormones; synaptic vesicle protein ___

A

GABA enhancers [remember GABA is inhibitory]; glutamate blockers [remember glutamate is excitatory]; carbonic anhydrase inhibitors; sex hormones; synaptic vesicle protein 2A (SV2A)

366
Q

Carbamazepine is a ___ channel blocker

A

Carbamazepine is a sodium channel blocker

367
Q

Carbamazepine ___ (induces/inhibits) its own metabolism

A

Carbamazepine induces its own metabolism

368
Q

Carbamazepine is a CYP3A4 ___ (inducer/inhibitor)

A

Carbamazepine is a CYP3A4 inducer

369
Q

What is the most important thing to consider about carbamazepine?

A

Drug interactions–because it is a CYP inducer/substrate, it ramps up the metabolism of other drugs and itself, clears medications from the bloodstream faster, and shortens the duration of action of other drugs

370
Q

If patient is on carbamazepine, check ___ levels

A

sodium levels

371
Q

Why was oxcarbazepine created?–to eliminate the auto-___ of carbamazepine

A

to eliminate the auto-induction of carbamazepine

372
Q

As a person takes carbamazepine for a longer period of time, it loses its effectiveness because it’s an inducer and substrate–T/F?

A

True

373
Q

Main concerns for the -carbazepine anticonvulsants–check ___ levels, check for drug ___, check ___/___s

A

check sodium levels, check for drug interactions, check CBC/LFTs

374
Q

Phenytoin is a ___ channel blocker; has ___ (linear/non-linear) pharmacokinetics; CYP enzyme ___ and ___

A

Phenytoin is a sodium channel blocker; has non-linear pharmacokinetics; CYP inducer and substrate

375
Q

What is the therapeutic range for phenytoin?

A

10-20

376
Q

Dose adjustments for phenytoin are ___ (small/large)

A

Small because it has non-linear pharmacokinetics

Example: Patient is on 300 mg phenytoin. You check a level and it comes back at 5. You increase the dose to 300 mg bid. You re-check the level and it is 28, and patient is dizzy, nauseous, and having vision changes. You may just add 30-50 mg at a time to get to desired therapeutic levels for phenytoin.

377
Q

Fosphenytoin = ___drug for ___ (oral/parenteral) administration

A

prodrug for parenteral administration

378
Q

Side effects of phenytoin/fosphenytoin–gingival ___plasia; ___mias, CV ___, ___tension mostly at toxic levels; ___mus; vitamin ___ and ___ deficiencies; if given during pregnancy–cleft ___/___, congenital ___ disease, slowed ___ rate, mental ___

A

Side effects of phenytoin/fosphenytoin–gingival hyperplasia; arrhythmias, CV depression, hypotension mostly at toxic levels; nystagmus; vitamin K and folate deficiencies; if given during pregnancy–cleft lip/palate, congenital heart disease, slowed growth rate, mental deficiency

379
Q

Lamotrigine is a ___ channel blocker

A

sodium channel blocker

380
Q

If patient is on depakote/lamictal and stops taking both prior to surgery, if they are both not restarted in 3-4 days and you have to reinitiate, there is a long cross-taper period of 4-8 weeks where you can only make minor incremental increases in the dosages–T/F?

A

True

381
Q

What happens if you reinitiate a person’s regular doses of depakote/lamictal after having stopped both drugs for 3-4 days or more?What happens if you reinitiate a person’s regular doses of depakote/lamictal after having stopped both drugs for 3-4 days or more?

A

Steven Johnsons syndrome–very high rates, can cause devastating skin reactions

382
Q

Lamotrigine drug interaction with depakote = high risk of ___

A

high risk of SJS

383
Q

Zonisamide side effects–can cause renal ___ in 1.5% of patients

A

can cause renal stones in 1.5% of patients

384
Q

Lacosamide (Vimpat) has a ___ (low/high) side effect profile; pregnancy category ___

A

Lacosamide has a low side effect profile; pregnancy category C–still unsure of what the true risk is in pregnancy

385
Q

Benzodiazepines should be restarted as soon as possible if held before/after a surgical procedure to avoid withdrawal–T/F?

A

True–continue Benzos as long as possible, restart ASAP

386
Q

Higher lipophilicity for benzos = ___ (slower/faster) onset of action, ___ (shorter/longer) duration of action

A

higher lipophilicity for benzos = faster onset of action, longer duration of action

i.e.: diazepam (Valium), clonazepam (Klonopin)

387
Q

Lower lipophilicity for benzos = ___ (slower/faster) onset of action, ___ (shorter/longer) duration of action

A

lower lipophilicity for benzos = slower onset of action, shorter duration of action

i.e.: alprazolam (xanax), temazepam (restoril)

388
Q

Which benzodiazepine is only used for seizures and is not appropriate to use for anxiety/sleep? If this medication is discontinued, it needs to be restarted ASAP otherwise patient will experience wild withdrawal symptoms and will start seizing really quick. This medication has a long taper if you want to get a person off of it.

A

Clobazam (Onfi)

389
Q

Vigabatrin has a risk of permanent ___, and for this reason is only available through a very specific program with REMS monitoring

A

Vigabatrin has a risk of permanent vision loss, and for this reason is only available through a very specific program with REMS monitoring

390
Q

Gabapentin is more often used for ___ than ___ control

A

Gabapentin is more often used for neuropathic pain than seizure control

391
Q

Gabapentin ___ (is/is not) protein bound, ___ (is/is not) metabolized, is excreted completely ___ (changed/unchanged) by the ___, ___ (has/has no) PK drug interactions

A

Gabapentin is not protein bound, is not metabolized, is excreted completely unchanged by the kidneys, has no PK drug interactions

392
Q

A meta analysis of RCTs suggests that gabapentin given 1x 30 minutes pre-operatively in regional anesthesia for multiple procedures ___ (improves/worsens) post-op pain and ___ (increases/reduces) opiate requirements with increased post op ___ being the highest safety risk

A

A meta analysis of RCTs suggests that gabapentin given 1x 30 minutes pre-operatively in regional anesthesia for multiple procedures improves post-op pain and reduces opiate requirements with increased post op sedation being the highest safety risk

393
Q

You may see increased side effects of gabapentin in patients with poor kidney function–T/F?

A

True–because it is completely eliminated by the kidneys

394
Q

Gabapentin is very well tolerated–T/F?

A

True

395
Q

December 2019 FDA safety communication–gabapentinoids in combo with opiates may lead to severe ___ distress

A

gabapentinoids in combo with opiates may lead to severe respiratory distress

396
Q

Lots of people taking pregabalin complain of difficulty ___

A

Lots of people taking pregabalin complain of difficulty walking

397
Q

Valproic acid drug interactions occur through ___ (stimulation/inhibition) of oxidation and glucuronidation pathways

A

Valproic acid drug interactions occur through inhibition of oxidation and glucuronidation pathways

398
Q

In utero exposure to valproic acid leads to lower ___ in children compared to other anti-epileptics

A

In utero exposure to valproic acid leads to lower IQ in children compared to other anti-epileptics

399
Q

Valproic acid is pregnancy category ___-___

A

Valproic acid is pregnancy category D-X

400
Q

Valproic acid may cause ___penia

A

thrombocytopenia–just like carbamazepine family, heparin, H2 receptor antagonists, SSRIs

401
Q

Valproic acid may cause ___ammonemia

A

Valproic acid may cause hyperammonemia

402
Q

If someone is on depakote and becomes confused, what should you do?

A

Check ammonia level because depakote increases ammonia levels

403
Q

What labs should be routinely checked if patient is on valproic acid?

A

Ammonia, LFTs, CBC

404
Q

If patient is pregnant and in status epilepticus, you can give valproic acid–T/F?

A

False–never use depakote in pregnancy, even if patient is in status epilepticus

405
Q

What are (3) glutamate blockers?–___bamate, ___ramate, ___ampanel

A

Felbamate (felbatol), topiramate (topamax), perampanel (fycompa)

406
Q

Felbamate (felbatol) is very rarely used in the US because it has high risk of ___ anemia and fatal ___ failure

A

Felbamate (felbatol) is very rarely used in the US because it has high risk of aplastic anemia and fatal hepatic failure

407
Q

What is one common side effect of topiramate (topamax)? ___ slowing

A

Psychomotor slowing–want to do something, but can’t make it happen

408
Q

Perampanel black box warning–serious or life threatening ___ and ___ adverse effects

A

Perampanel black box warning–serious or life threatening psychiatric and behavioral adverse effects–aggression, hostility, irritability, anger, homicidal ideation, threats

409
Q

Common side effect of perampanel (in 43% of patients) = ___

A

dizziness

410
Q

Levetiracetam MOA is possibly related to synaptic vesicle protein ___, which appears to be important for the availability of __-dependent neurotransmitter vesicles ready to release their content

A

Levetiracetam MOA is possibly related to synaptic vesicle protein 2A, which appears to be important for the availability of calcium-dependent neurotransmitter vesicles ready to release their content

411
Q

Keppra–without SV2A, reduced action potential-___ (independent/dependent) neurotransmission, while action potential-___ (independent/dependent) neurotransmission remains normal

A

Keppra–without SV2A, reduced action-potential dependent neurotransmission, while action potential-independent neurotransmission remains normal

412
Q

Keppra also inhibits ___ release from IP3-sensitive stores

A

Keppra also inhibits calcium release from IP3-sensitive stores

413
Q

A significant side effect of keppra is ___ impairment

A

A significant side effect of keppra is cognitive impairment–have a convo and don’t even remember having it

414
Q

Baclofen is a ___ analog

A

Baclofen is a GABA analog

415
Q

Substance ___ is released in response to pain impulses

A

Substance P is released in response to pain impulses

416
Q

How does baclofen work?–it inhibits substance ___ release into the spinal cord to reduce pain

A

Baclofen inhibits substance P release into the spinal cord to reduce pain

417
Q

If baclofen is abruptly discontinued, patients will experience ___ symptoms–i.e.: ___nations, ___er, ___tation, ___or, ___cardia, ___ure

A

If baclofen is abruptly discontinued, patients will experience withdrawal symptoms–i.e.: hallucinations, fever, agitation, tremor, tachycardia, seizure

418
Q

Tizanidine is a centrally acting alpha ___–slows down ___ release using negative feedback

A

Tizanidine is a centrally acting alpha 2 agonist–slows down NE release using negative feedback

419
Q

Withdrawal is possible with abrupt discontinuation of tizanidine–T/F?

A

True

420
Q

Side effects of tizanidine–___ mouth, ___ation, anti___ effects

A

Side effects of tizanidine–dry mouth, sedation, anticholinergic effects

421
Q

Dantrolene blocks ___ channel, reduces ___ release from the ___

A

Dantrolene blocks ryanodine channel, reduces calcium release from the sarcoplasmic reticulum

422
Q

___ mutations are associated with malignant hyperthermia

A

RyR1 mutations are associated with malignant hyperthermia

423
Q

Dantrolene has dose dependent ___rrhea and ___toxicity (BB warning > ___mg/day with long term use)

A

Dantrolene has dose dependent diarrhea and hepatotoxicity (BB warning > 800 mg/day with long term use)

424
Q

Other side effects of dantrolene–___nea, ___phagia, ___lence

A

Other side effects of dantrolene–dyspnea, dysphagia, somnolence

425
Q

Skeletal muscle relaxants have risks of ___ sedation and ___

A

Skeletal muscle relaxants have risks of over sedation and withdrawal

426
Q

Zolpidem (Ambien), Zaleplon (Sonata), and Eszopiclone (Lunesta) are all ___, AKA ___-drugs

A

Zolpidem (Ambien), Zaleplon (Sonata), and Eszopiclone (Lunesta) are all sedative hypnotics, AKA Z-drugs

427
Q

Ramelteon (Rozerem) is a ___ receptor agonist

A

Ramelteon (Rozarem) is a melatonin receptor agonist

428
Q

Suvorexant (Belsomra) is a ___ antagonist; is associated with significant sleep ___

A

Suvorexant (Belsomra) is a norexin 2 antagonist; is associated with significant sleep activities

429
Q

Sedative hypnotics ___ (should/should not) be used regularly in the hospital to help patients sleep

A

Sedative hypnotics should NOT be used regularly in the hospital to help patients sleep

430
Q

Sedative hypnotics like Zolpidem (Ambien) are benzodiazepine like drugs–T/F?

A

True

431
Q

Patients can go through withdrawal when they stop taking sedative hypnotics like ambien, sonata, and Lunesta–T/F?

A

True–withdrawal symptoms include insomnia and anxiety

432
Q

Sedative hypnotics help people fall asleep and provide restorative REM sleep–T/F?

A

FALSE–sedative hypnotics DO help people fall asleep, but they DO NOT provide restorative REM sleep

433
Q

“Sleep behaviors” are very common with Z drugs, i.e.: sleep eating, sleep fighting, sleep walking; patients can hurt themselves when they take these medications–T/F?

A

True

434
Q

Ramelteon and melatonin help you fall asleep–T/F?

A

True

435
Q

Ramelteon and melatonin will help if you have difficulty staying asleep–T/F?

A

False–do not help you stay asleep, just help you fall asleep

436
Q

(6) classes of antidepressant medications

A
  • TCAs
  • SSRIs
  • SNRIs
  • DNRIs
  • 5HT2A antagonists
  • Nuedexta
437
Q

TCAs MOA–___ and ___ reuptake inhibition, anti___, ___ antiarrhythmic

A

TCAs MOA–serotonin and norepinephrine reuptake inhibition, anticholinergic, 1A antiarrhythmic

438
Q

TCAs are not typically used to treat depression anymore, but may still be used to treat neuropathic pain/migraines–T/F?

A

True–have fallen out of favor to treat depression since prozac came out

439
Q

Side effects of TCAs–anticholinergic side effects–___pation, ___fusion, ___tation in elderly/children, urinary ___, ___ vision, ___ mouth; CV effects–QT ___, ___mias

A

Side effects of TCAs–anticholinergic side effects–constipation, confusion, agitation in elderly/children, urinary retention, blurred vision, dry mouth; CV–QT prolongation, arrhythmias

440
Q

TCA overdose–administer ___ d/t metabolic ___osis, supportive therapy

A

TCA overdose–administer NaHCO3 d/t metabolic acidosis, supportive therapy

441
Q

Serotonin excitatory receptors

A

2, 3, 4, 6, 7

Increase cAMP

442
Q

Serotonin inhibitory receptors

A

1, 5

Decrease cAMP

443
Q

Side effects of SSRIs–___natremia, ___cytopenia, ___ality, ___mias, ___ syndrome, ___/___/___, weight ___

A

Side effects of SSRIs–hyponatremia, thrombocytopenia, suicidality, arrhythmias, serotonin syndrome, nausea/vomiting/diarrhea, weight fluctuations

444
Q

All antidepressants, most anticonvulsant mood stabilizers, and most psychiatric medications have a black box warning for ___

A

suicidality

445
Q

Neuroleptic malignant syndrome is precipitated by ___ antagonists; onset is ___-___ days

A

Neuroleptic malignant syndrome is precipitated by dopamine antagonists; onset is 1-3 days

446
Q

Serotonin syndrome is precipitated by ___ agents; onset is < ___ hours

A

Serotonin syndrome is precipitated by serotonergic agents; onset is < 12 hours

447
Q

NMS and SS identical features–___tension, ___cardia, ___pnea, ___thermia, ___salivation, ___phoresis

A

NMS and SS identical features–hypertension, tachycardia, tachypnea, hyperthermia (> 40 C), hypersalivation, diaphoresis

448
Q

NMS demonstrates ‘___’ rigidity in all muscle groups

A

NMS demonstrates ‘lead-pipe’ rigidity in all muscle groups

449
Q

SS has ___ (increased/decreased) muscle tone, especially in ___ (upper/lower) extremities

A

SS has increased muscle tone, especially in lower extremities

450
Q

NMS distinct features–___reflexia, pupils ___ (normal/dilated), bowel sounds ___ (normal/increased/decreased)

A

NMS distinct features–hyporeflexia, pupils normal, normal bowel sounds

451
Q

SS distinct features–___reflexia, ___ unless masked by increased muscle tone, pupils ___ (normal/dilated), bowel sounds ___active

A

SS distinct features–hyperreflexia, clonus unless masked by increased muscle tone, pupils dilated, bowel sounds hyperractive

452
Q

What antibiotic can cause serotonin syndrome?

A

Linezolid (because it is an MAOI)

453
Q

Opioids can cause serotonin syndrome–T/F?

A

True

454
Q

Serotonin syndrome has a slower onset than neuroleptic malignant syndrome–T/F?

A

False–serotonin syndrome has a faster onset (<12 hours) than neuroleptic malignant syndrome (1-3 days)

455
Q

Neuroleptic malignant syndrome has ___reflexia, whereas serotonin syndrome has ___reflexia

A

Neuroleptic malignant syndrome has hyporeflexia, whereas serotonin syndrome has hyperreflexia

456
Q

Neuroleptic malignant syndrome pupils are ___, serotonin syndrome pupils are ___

A

Neuroleptic malignant syndrome pupils are normal, serotonin syndrome pupils are dilated

457
Q

How do SNRIs like duloxetine, venlafaxine, desvenlafaxine, and levomilnacipran work?–___ and ___ reuptake inhibition

A

serotonin and norepinephrine reuptake inhibition

458
Q

SRNIs side effects–___ syndrome, ___toxicity, ___tension, ___nia, abnormal ___, ___somnolence throughout the day d/t sleep interruptions throughout the night, ___/___/___, weight ___ (loss/gain), ___or, ___tation

A

SNRIs side effects–serotonin syndrome, hepatotoxicity, hypertension, insomnia, abnormal dreams, hypersomnolence throughout the day d/t sleep interruptions throughout the night, nausea/vomiting/diarrhea, weight loss, tremor, agitation

459
Q

SNRIs can also cause ___natremia and ___cytopenia just like SSRIs

A

SNRIs can also cause hyponatremia and thrombocytopenia just like SSRIs

460
Q

Mirtazepine (Remeron) and Trazodone (Desryl) are ___ antagonists

A

Mirtazepine (Remeron) and Trazodone (Desryl) are 5HT2A antagonists

461
Q

Think ___ with mirtazepine (remeron) and trazodone (desryl)

A

sedation

462
Q

Nuedexta is a combination of ___ and ___

A

Nuedexta is a combination of dextromethorphan and quinidine

463
Q

Nuedexta is the only medication approved by the FDA to treat ___

A

Nuedexta is the only medication approved by the FDA to treat pseudobulbar affect

464
Q

Pseudobulbar affect is inappropriate ___ or ___, seen in patients with ___

A

Pseudobulbar affect is inappropriate crying or laughing, seen in patients with TBI

465
Q

Check ___ if someone is on a neuropsychiatric medication

A

platelets…many of these meds cause thrombocytopenia

466
Q

Lithium is a mood ___

A

Lithium is a mood stabilizer

467
Q

Side effects of lithium–diabetes ___, ___uria, ___dipsia

A

diabetes insipidus, polyuria, polydipsia

468
Q

It is important to check ___ levels and ___ levels in patients on lithium

A

It is important to check sodium levels and lithium levels in patients on lithium

469
Q

What is the difference between first and second generation antipsychotics?

A

First generation = mostly dopamine (D2) blockers; second generation = S2, D2 blockers

470
Q

Chlorpromazine (thorazine); prochlorperazine (compazine); and haloperidol (haldol) are all ___ (first/second) generation antipsychotics

A

first generation antipsychotics

471
Q

Aripiprazole (Abilify); clozapine (clozaril); olanzapine (zyprexa); quetiapine (Seroquel); risperidone (risperdal) are all ___ (first/second) generation antipsychotics

A

second generation antipsychotics

472
Q

Dopamine pathways in the CNS–meso___ = positive symptoms of schizophrenia and psychosis

A

Dopamine pathways in the CNS–mesolimbic = positive symptoms of schizophrenia and psychosis

473
Q

Dopamine pathways in the CNS–meso___ = negative symptoms, cognitive and affective symptoms

A

Dopamine pathways in the CNS–mesocortical = negative symptoms, cognitive and affective symptoms

474
Q

Dopamine pathways in the CNS–___ = Parkinsonian effects, i.e.: extrapyramidal symptoms, tardive dyskinesias

A

Dopamine pathways in the CNS–nigrostriatal = Parkinsonian effects, i.e.: extrapyramidal symptoms, tardive dyskinesias

475
Q

Dopamine pathways in the CNS–___ = hyperprolactinemia

A

Dopamine pathways in the CNS–tuberohypophyseal = hyperprolactinemia

476
Q

Side effects of antipsychotics–___ symptoms, ___ dyskinesias; metabolic side effects–weight ___ (gain/loss), ___glycemia; CNS side effects–___gy, ___ation, ___fusion; CV–QT ___, especially with ___

A

Side effects of antipsychotics–extrapyramidal symptoms, tardive dyskinesias; metabolic side effects–weight gain, hyperglycemia; CNS side effects–lethargy, sedation, confusion; CV–QT prolongation, especially with haldol

477
Q

Black box warning for clozaril 2008–___ related death, ___cytosis

A

Black box warning for clozaril 2008–dementia (CV/stroke) related death, agranulocytosis

478
Q

Antipsychotics should be used as a last resort when a patient is a risk to others and/or themselves–T/F?

A

True

479
Q

Carbidopa/Levodopa (Sinemet) and Carbidopa/Levodopa/Entacapone (Stalevo) are ___ analogs

A

dopamine analogs

480
Q

___ = dopamine precursor, looks and acts like dopamine

A

Levodopa = dopamine precursor, looks and acts like dopamine

481
Q

___ = false dopamine; confuses the enzymes MAO and COMT to prevent breakdown of levodopa

A

Carbidopa = false dopamine; confuses the enzymes MAO and COMT to prevent breakdown of levodopa

482
Q

___ = COMT inhibitor, has no effect on dopamine

A

Entacapone (Comtan) = COMT inhibitor, has no effect on dopamine

483
Q

Benztropine (Cogentin) and trihexyphenidyl (Artane) are anti___ used to treat ___ associated with antipsychotic administration

A

Benztropine (Cogentin) and trihexyphenidyl (Artane) are anticholinergics used to treat EPS associated with antipsychotic administration

484
Q

MAOB inhibitors rasaligine (azilect) and selegiline (eldepryl) ___ (increase/decrease) dopamine availability via enzyme inhibition

A

MAOB inhibitors rasaligine (azilect) and selegiline (eldepryl) increase dopamine availability via enzyme inhibition

485
Q

If you have a patient on MAOB inhibitors, you may see exaggerated effects of epi, NE, or ephedrine–T/F?

A

True

486
Q

Two classes of Alzheimer’s medications–___ inhibitors, ___ receptor antagonist

A

acetylcholinesterase inhibitors, NMDA receptor antagonist

487
Q

Side effects of acetylcholinesterase inhibitors–‘___’ side effects–___cardia, ___ stools, ___ bladder

A

‘rest and digest’ side effects–bradycardia, loose stools, overactive bladder

488
Q

Acetylcholinesterase inhibitors drug interactions–anti___, ___choline, ___ neuromuscular blockers

A

anticholinergics, succinylcholine, non depolarizing neuromuscular blockers

489
Q

Acetylcholinesterase inhibitors ___ (potentiate/reduce) the effects of succinylcholine

A

Acetylcholinesterase inhibitors potentiate the effects of succinylcholine (because you’re flooding the receptors with acetylcholine)

490
Q

Acetylcholinesterase inhibitors ___ (potentiate/reduce) the effects of nondepolarizing neuromuscular blockers

A

Acetylcholinesterase inhibitors reduce the effects of nondepolarizing neuromuscular blockers

491
Q

What benzodiazepine has risk of wild withdrawal when stopped abruptly?

A

ONFI

492
Q

Delirium and dementia are two different things–T/F?

A

True

493
Q

Post op delirium may be fatal and is preventable in up to 40% of cases–T/F?

A

True

494
Q

Almost 50% of cases of delirium are not reported–T/F?

A

True

495
Q

Post op delirium may occur in up to 75% of cases–T/F?

A

True

496
Q

JAMA Surgery 2018 STRIDE Trial–hip fracture repair, reducing sedation levels to reduce post op delirium–in the primary analysis, limiting the level of sedation provided no significant benefit in reducing incident delirium–T/F?

A

True

497
Q

JAMA Surgery 2018 STRIDE Trial–hip fracture repair, reducing sedation levels to reduce post op delirium–in a prespecified subgroup analysis, lighter sedation levels reduced postoperative delirium for persons with a Charlson Comorbidity Index of 0 (less sick patients)–T/F?

A

True

498
Q

Antipsychotics should not be used unless patient is at risk of harm to self or others–T/F?

A

True

499
Q

If using antipsychotics, use the ___ (lowest/highest) dose for the ___ (shortest/longest) duration

A

If using antipsychotics, use the lowest dose for the shortest duration

500
Q

Prophylactic low dose PO haloperidol did reduce delirium incidence in acutely hospitalized older patients–T/F?

A

FALSE–DID NOT reduce delirium incidence in acutely hospitalized older patients

501
Q

Prophylactic haldol reduces mortality in critically ill adults at high risk of delirium–T/F?

A

FALSE–prophylactic haldol DOES NOT reduce mortality in critically ill adults at high risk of delirium

502
Q

Benzos exacerbate delirium–T/F?

A

True

503
Q

The ___ sets up the final concentration of urine

A

The nephron sets up the final concentration of urine

504
Q

___ inside Bowman’s capsule is responsible for filtration; ___% of plasma that arrives here passes through the filtration barrier to become filtrate

A

Glomerulus inside Bowman’s capsule is responsible for filtration; 25% of plasma that arrives here passes through the filtration barrier to become filtrate

505
Q

Carbonic anhydrase inhibitors and osmotic diuretics work on the ___ tubule

A

Carbonic anhydrase inhibitors and osmotic diuretics work on the PROXIMAL tubule

506
Q

Loop diuretics work on the ___

A

Loop diuretics work on the LOOP OF HENLE

507
Q

___ (ascending/descending) loop of Henle is responsible for water reabsorption, sodium diffuses in

A

Descending loop of Henle is responsible for water reabsorption, sodium diffuses in

508
Q

___ (ascending/descending) loop of Henle is responsible for active reabsorption of sodium, water stays in

A

Ascending loop of Henle is responsible for active reabsorption of sodium, water stays in

509
Q

Thiazide diuretics work on the ___ (proximal/distal) tubule

A

Thiazide diuretics work on the DISTAL tubule

510
Q

Reabsorption of water in the distal tubule requires ___

A

ADH

511
Q

Reabsorption of water in the collecting duct requires ___

A

ADH

512
Q

The final concentration of urine is determined in the ___

A

collecting duct

513
Q

Chronic kidney disease = kidney damage for > ___ months defined by structural or functional abnormalities with or without decreased GFR

A

kidney damage for > 3 months defined by structural or functional abnormalities with or without decreased GFR

514
Q

Chronic kidney disease = GFR < ___ ml/min for > ___ months with or without structural kidney damage

A

Chronic kidney disease = GFR < 60 ml/min for > 3 months with or without structural kidney damage

515
Q

Stages of chronic kidney disease = stages ___-___

A

Stages 1-6

516
Q

Stage 1 CKD = damage with normal or increased GFR–GFR > ___ ml/min

A

GFR > 90 ml/min

517
Q

Stage 2 CKD = damage with mildly deceased GFR–GFR __-__ ml/min

A

GFR 60-89 ml/min

518
Q

Stage 3 CKD = moderately deceased GFR–GFR __-__ ml/min

A

GFR 30-59 ml/min

519
Q

Stage 4 CKD = severely deceased GFR–GFR __-__ ml/min

A

GFR 15-29 ml/min

520
Q

Stage 5 CKD = kidney failure–GFR < ___ ml/min

A

GFR < 15 ml/min

521
Q

Stage 6 CKD = ___

A

dialysis

522
Q

Acute kidney disease is kidney damage for < ___ months

A

< 3 months

523
Q

RIFLE criteria for acute kidney disease stands for ___

A
  • Risk
  • Injury
  • Failure
  • Loss of kidney function
  • ESRD
524
Q

Risk = increased Cr x ___ or decreased GFR by ___%; UO < 0.5 ml/kg/hr for ___ hours

A

Risk = increased Cr x 1.5 or decreased GFR by 25%; UO < 0.5 ml/kg/hr for 6 hours

525
Q

Injury = increased Cr x ___ or decreased GFR by ___%; UO < 0.5 ml/kg/hr for ___ hours

A

Injury = increased Cr x 2 or decreased GFR by 50%; UO < 0.5 ml/kg/hr for 12 hours

526
Q

Failure = increased Cr x ___ OR Cr > ___ mg/dl or decreased GFR by ___%; UO < 0.5 ml/kg/hr for ___ hours

A

Failure = increased Cr x 3 OR Cr > 4 mg/dl or decreased GFR by 75%; UO < 0.5 ml/kg/hr for 24 hours

527
Q

Loss of kidney function = persistent acute kidney disease, complete loss of kidney function > ___ weeks

A

Loss of kidney function = persistent acute kidney disease, complete loss of kidney function > 4 weeks

528
Q

ESRD = end stage > ___ months

A

ESRD = end stage > 3 months

529
Q

Pre-renal kidney disease = ___

A

dehydration

530
Q

Intrinsic kidney disease = ___

A

drug damage, i.e.: NSAIDs

531
Q

Post-renal kidney disease = ___

A

blockage preventing urine from freely flowing, causing a back up

532
Q

What are (6) classes of diuretics?

A
  • Carbonic anhydrase inhibitors
  • Osmotic diuretics
  • Loop diuretics
  • Thiazide diuretics
  • Potassium sparing diuretics
  • Aldosterone antagonists
533
Q

What is most commonly used carbonic anhydrase inhibitor?

A

Acetazolamide (Diamox)

534
Q

How do carbonic anhydrase inhibitors work?–inhibit ___, which inhibits ___ secretion in the ___ (proximal/distal) tubule; ___ and ___ are blocked from reabsorption

A

inhibit carbonic anhydrase, which inhibits H+ secretion in the proximal tubule; bicarb and sodium are blocked from reabsorption

535
Q

Carbonic anhydrase inhibitors cause ___ to be lost in the urine

A

Carbonic anhydrase inhibitors cause bicarb to be lost in the urine [water follows into the urine]

536
Q

Carbonic anhydrase inhibitors cause ___kalemic metabolic ___osis as an effect

A

Carbonic anhydrase inhibitors cause hypokalemic metabolic acidosis as an effect

537
Q

Tolerance to carbonic anhydrase inhibitors may develop after ___-___ days; why?

A

Tolerance to carbonic anhydrase inhibitors may develop after 2-3 days

Because they work very early on in the nephron (at the proximal tubule)–there is still a lot of time/traveling left in the nephron, still a lot of opportunities for water to be reabsorbed; even though we are holding water in the urine at the front of the nephron, it can still be reabsorbed later

538
Q

REVIEW–carbonic anhydrase inhibitors work at the ___ tubule; cause a loss of ___ to the urine; can lead to ___kalemic metabolic ___osis; tolerance may develop after __-__ days

A

carbonic anhydrase inhibitors work at the proximal tubule; cause a loss of bicarb to the urine; can lead to hypokalemic metabolic acidosis; tolerance may develop after 2-3 days

539
Q

Common side effects of carbonic anhydrase inhibitors–___ vision; changes in ___; ___/___/___/___ [all GI effects]; ___siness; frequent ___; loss of ___

A

blurred vision; changes in taste; nausea/vomiting/constipation/diarrhea; drowsiness; frequent urination; loss of appetite

540
Q

Two osmotic diuretics = ___ and ___

A

Two osmotic diuretics = mannitol and urea

541
Q

Where do osmotic diuretics work?

A

Proximal tubule

542
Q

How do osmotic diuretics work?–increase the ___ gradient in the ___ (proximal/distal) tubule

A

increase the osmotic gradient in the proximal tubule

Basically create a big bulky molecule [a concentration gradient] that begins to pull water in through osmosis

543
Q

Mannitol results in a significant loss of ___; reduced ___ (intra/extra)cellular volume; ___natremia risk

A

Mannitol results in a significant loss of water; reduced intracellular volume; hypernatremia risk

544
Q

Why is hypernatremia a risk with mannitol?

A

Because the sodium reabsorption cannot keep up with the loss of water

545
Q

Mannitol has an osmotic diuretic effect in the renal tubules that results in the urinary excretion of ___, ___, ___, and ___

A

urinary excretion of water, sodium, chloride, and bicarbonate ion

546
Q

Urinary pH ___ (is/is not) altered by mannitol-induced osmotic diuresis

A

Urinary pH is NOT altered by mannitol-induced osmotic diuresis

547
Q

IV mannitol ___ (increases/decreases) the plasma osmolarity; it draws fluid from ___cellular to ___cellular spaces; it acutely expands the ___ fluid volume

A

IV mannitol increases the plasma osmolarity; it draws fluid from intracellular to extracellular spaces; it acutely expands the intravascular fluid volume

548
Q

Detrimental effects of redistribution from mannitol = ___ in patients with poor myocardial function

A

Detrimental effects of redistribution from mannitol = CHF in patients with poor myocardial function

549
Q

Clinical uses of mannitol–prophylaxis against acute ___ failure; differential diagnosis of acute ___ria; treatment of increase in ___; decreasing ___ pressure

A

Clinical uses of mannitol–prophylaxis against acute renal failure; differential diagnosis of acute oliguria; treatment of increase in ICP; decreasing intraocular pressure

550
Q

Mannitol ARF prophylaxis–there ___ (is/is not) true evidence that mannitol is nephroprotective

A

There is NOT true evidence that mannitol is nephroprotective

551
Q

Mannitol ARF prophylaxis–mannitol ___ (is/is not) better than plain saline pre-radiocontrast dye

A

Mannitol is NOT better than plain saline pre-radiocontrast dye

552
Q

Mannitol ARF prophylaxis–mannitol is only shown to be nephroprotective in what type of surgery?

A

Mannitol is only shown to be nephroprotective in renal transplant surgery–less incidence of ARF

553
Q

Mannitol will increase urine output when the cause of acute oliguria is decreased intravascular fluid volume–T/F?

A

True

554
Q

If glomerular or renal tubular function is severely compromised, mannitol will increase urine output–T/F?

A

FALSE–mannitol will NOT increase urine output if glomerular or renal tubular function is severely compromised

555
Q

If mannitol is being used to treat increased ICP, it is important that the person has an intact blood-brain barrier–T/F?

A

True

Without intact blood-brain barrier, osmosis won’t be able to occur and you won’t get any benefit from using mannitol. Can lead to cerebral edema if BBB is not intact.

556
Q

Mannitol ___ (increases/decreases) plasma osmolarity; ___ (increases/decreases) CSF volume by ___ (increasing/decreasing) the rate of CSF formation

A

Mannitol increases plasma osmolarity; decreases CSF volume by decreasing the rate of CSF formation

557
Q

Chronic mannitol use reduces its effectiveness-T/F?

A

True

558
Q

Mannitol can cause vaso___ (dilation/constriction) of vascular smooth muscle; this can ___ (increase/decrease) cerebral blood volume and ICP, ___ (increase/decrease) systemic blood pressure

A

Mannitol can cause vasodilation of vascular smooth muscle; this can increase cerebral blood volume and ICP, decrease systemic blood pressure

559
Q

Because mannitol may initially increase ICP, you should infuse the selected dose over about ___ minutes; administer the dose in conjunction with treatments that decrease ICP, i.e.: ___ and ___ventilation

A

Because mannitol may initially increase ICP, you should infuse the selected dose over about 10 minutes; administer the dose in conjunction with treatments that decrease ICP, i.e.: corticosteroids and hyperventilation

560
Q

Side effects of mannitol–may precipitate pulmonary ___; ___volemia; electrolyte ___; plasma ___osmolarity d/t water and NaCl secretion

A

may precipitate pulmonary edema; hypovolemia; electrolyte disturbances; plasma hyperosmolarity d/t water and NaCl secretion

561
Q

Urea is another osmotic diuretic that has fallen out of favor because it has greater rebound increase in ___ than mannitol

A

Urea is another osmotic diuretic that has fallen out of favor because it has greater rebound increase in ICP than mannitol

562
Q

Urea also has high incidence of venous ___ and tissue ___ after extravasation

A

Urea also has high incidence of venous thrombosis and tissue necrosis after extravasation (not seen with mannitol)

563
Q

(3) loop diuretics =

A
  • Furosemide (Lasix)
  • Bumetanide (Bumex)
  • Torsemide (Demedex)
564
Q

What is (1) non-sulfa loop diuretic?

A

Ethacrynic acid (Edecrin)

565
Q

Caution using lasix, bumex, and demedex in patients with ___ allergy

A

sulfa allergy

566
Q

How do loop diuretics work?–inhibit ___ and ___ reabsorption in the ___ (ascending/descending) loop

A

Inhibit Na and Cl reabsorption in the ascending loop [and to a lesser extent in the proximal tubule]

567
Q

You get more significant and sustained diuretic effects with loop diuretics than with CAIs or osmotic diuretics–T/F?

A

True

568
Q

Loop diuretics block reabsorption of ___, ___, and 2 ___ in the ___; also lose ___ and ___ secondarily

A

Loop diuretics block reabsorption of sodium, potassium, and 2 chloride in the loop of Henle; also lose calcium and magnesium secondarily

569
Q

Loop diuretics as a class have the most significant electrolyte loss out of all other diuretics–T/F?

A

True

570
Q

Loop diuretics may cause ___kalemic metabolic ___osis

A

Loop diuretics may cause hypokalemic metabolic alkalosis

571
Q

CAIs may cause ___kalemic metabolic ___osis; loops may cause ___kalemic metabolic ___osis

A

CAIs may cause hypokalemic metabolic acidosis; loops may cause hypokalemic metabolic alkalosis

572
Q

What labs should be checked frequently in patients on a loop diuretic?

A

BMP + Mg

573
Q

Furosemide renovascular effect–furosemide induced production of prostaglandins results in renal vaso___ and ___ (increased/decreased) renal blood flow

A

Furosemide renovascular effect–furosemide induced production of prostaglandins results in renal vasodilation and increased renal blood flow

574
Q

Furosemide induced increases in RBF are inhibited by ___ (what medication class?), resulting in an attenuated (lessened) diuretic effect

A

Furosemide induced increases in RBF are inhibited by NSAIDs, resulting in an attenuated (lessened) diuretic effect

575
Q

Furosemide induced production of prostaglandins also leads to ___tension by causing vaso___

A

Furosemide induced production of prostaglandins also leads to hypotension by causing vasodilation

576
Q

Clinical uses of loop diuretics = mobilization of ___ d/t renal, hepatic, or cardiac dysfunction; treatment of increased ___; treatment of ___calcemia; differential diagnosis of acute ___

A

mobilization of fluid d/t renal, hepatic, or cardiac dysfunction; treatment of increased ICP; treatment of hypercalcemia; differential diagnosis of acute oliguria

577
Q

Combination of mannitol + lasix is greater than either drug alone–T/F?

A

True, synergistic effect when used together

Mannitol pulls as much fluid out of the extravascular space into the intravascular space; lasix keeps the fluid within the nephron through the movement of electrolytes and then all are excreted in the urine

578
Q

Peripheral vasodilation precedes the onset of diuresis when lasix is given–T/F?

A

True

579
Q

Decreased venous return from lasix administration provides prompt effects in the management of acute pulmonary ___

A

Decreased venous return from lasix administration provides prompt effects in the management of acute pulmonary edema

580
Q

Lasix increases lymph flow through the ___ duct

A

Lasix increases lymph flow through the thoracic duct

581
Q

Decreased ICP d/t lasix is NOT accompanied by changes in ___ blood flow or changes in plasma ___

A

Decreased ICP d/t lasix is NOT accompanied by changes in cerebral blood flow or changes in plasma osmolarity

Unlike mannitol–which causes [initially] increased cerebral blood volume/ICP and increases plasma osmolarity

582
Q

Compared to mannitol, furosemide ___ (is/is not) as effective in decreasing ICP

A

Compared to mannitol, furosemide is NOT as effective in decreasing ICP

583
Q

Mannitol may produce rebound intracranial ___tension if a disrupted BBB allows mannitol to enter the CNS

A

Mannitol may produce rebound intracranial hypertension if a disrupted BBB allows mannitol to enter the CNS

584
Q

Combination of furosemide and mannitol is ___ (more/less) effective in decreasing ICP than either drug alone

A

Combination of furosemide and mannitol is more effective in decreasing ICP than either drug alone

585
Q

Risk of severe dehydration and electrolyte imbalance is ___ (increased/decreased) when a combination of furosemide and mannitol is used

A

Risk of severe dehydration and electrolyte imbalance is increased when a combination of furosemide and mannitol is used

586
Q

Side effects of loop diuretics–___kalemia, ___chloremia, ___natremia, ___magnesemia, ___calcemia, metabolic ___osis

A

hypokalemia, hypochloremia, hyponatremia, hypomagnesemia, hypocalcemia, metabolic alkalosis

587
Q

What is this side effect of loop diuretics known as?–if someone is on a loop diuretic and does not have electrolytes replaced, the body won’t be able to maintain a gradient of electrolytes; as such, there is not enough electrolytes for water to follow anymore, so the loop diuretic loses its effectiveness

A

Acute Tolerance (Braking Phenomenon)

588
Q

Loop diuretics + aminoglycoside given together can cause ___toxicity

A

ototoxicity

589
Q

Allergic reaction cross-sensitivity may exist between loop diuretics and ___ drugs

A

Allergic reaction cross-sensitivity may exist between loop diuretics and sulfa drugs (i.e.: sulfa abx, sulfonylureas, thiazide diuretics)

590
Q

Risks of nephrotoxicity may be increased when loop diuretics are administered with what (3) antibiotic classes?

A
  • Aminoglycosides
  • Cephalosporins
  • Penicillin
591
Q

(2) thiazide diuretics = ___ and ___

A

hydrochlorothiazide (hydrodiuril) and metolazone (zaroxolyn)

592
Q

Thiazide diuretics work on the ___ (proximal/distal) convoluted tubule; they compete for the ___-___ cotransporter to inhibit reabsorption

A

Thiazide diuretics work on the distal convoluted tubule; they compete for the Na-Cl cotransporter to inhibit reabsorption

593
Q

Thiazide diuretics cause loss of ___ and ___; ___kalemic metabolic ___osis; increased ___ reabsorption

A

Thiazide diuretics cause loss of sodium and water; hypokalemic metabolic alkalosis; increased Ca reabsorption

594
Q

Loop diuretics cause ___ (loss/reabsorption) of calcium; thiazide diuretics cause ___ (loss/reabsorption) of calcium)

A

Loop diuretics cause loss of calcium; thiazide diuretics cause reabsorption of calcium

595
Q

Loops = ___calcemia; thiazides = ___calcemia

A

Loops = hypocalcemia; thiazides = hypercalcemia

596
Q

For patients without comorbidities, thiazides are recommended as first line treatment of ___

A

For patients without comorbidities, thiazides are recommended as first line treatment of hypertension

597
Q

Side effects of thiazide diuretics–___kalemia, ___chloremia, ___calcemia, metabolic ___osis with chronic administration; ___ and ___ depletion may accompany kaliuresis; ___ may occur as a result of diuretic-induced hypokalemia or hypomagnesemia; increased likelihood of developing ___ toxicity (d/t hypokalemia); ___ (potentiation/inhibition) of non depolarizing neuromuscular blockers

A

Side effects of thiazide diuretics–hypokalemia, hypochloremia, HYPERcalcemia, metabolic alkalosis with chronic administration; sodium and magnesium depletion may accompany kaliuresis; dysrhythmias may occur as a result of diuretic-induced hypokalemia or hypomagnesemia; increased likelihood of developing digoxin toxicity (d/t hypokalemia); potentiation of non depolarizing neuromuscular blockers

598
Q

Thiazide diuretics may also cause ___glycemia and ___uricemia, caution in patients with ___

A

Thiazide diuretics may also cause hyperglycemia and hyperuricemia, caution in patients with gout

599
Q

Potassium sparing diuretics–amiloride and triamterene inhibit ___ reabsorption induced by ___; inhibit active counter transport of ___ and ___ in the collecting duct

A

Amiloride and triamterene inhibit sodium reabsorption induced by aldosterone; inhibit active counter transport of Na and K in the collecting duct

600
Q

Potassium sparing diuretics–spironolactone and eplerenone compete for ___ receptor sites in the distal tubule to block ___ reabsorption and ___ secretion; they are also known as ___

A

Spironolactone and eplerenone compete for aldosterone receptor sites in the distal tubule to block sodium reabsorption and potassium secretion; they are also known as aldosterone receptor antagonists

601
Q

Aldosterone antagonists cause loss of ___ and ___; ___kalemia; and some risk of ___osis

A

Aldosterone antagonists cause loss of sodium and water; hyperkalemia; and some risk of acidosis

602
Q

K sparing diuretics have ___ (more/less) effective diuresis

A

K sparing diuretics have less effective diuresis, often used in combo with other diuretics

603
Q

K sparing diuretics may be used for treatment of refractory edematous states due to ___ or ___ of the liver

A

K sparing diuretics may be used for treatment of refractory edematous states due to CHF or cirrhosis of the liver

604
Q

Why are K sparing diuretics good to use in CHF and cirrhosis of the liver?–because decreased hepatic function and metabolism lead to increased plasma concentration of ___

A

Because decreased hepatic function and metabolism lead to increased plasma concentration of aldosterone

605
Q

What is the principle side effect of K sparing diuretics?

A

HYPERKALEMIA

606
Q

Patients are at increased risk of hyperkalemia if they are taking K sparing diuretic + ___s, ___s, and ___ blockers

A

NSAIDs, ACEIs, and beta blockers

607
Q

K sparing diuretics ___ (do/do not) produce hyperuricemia or hyperglycemia

A

K sparing diuretics do NOT produce hyperuricemia or hyperglycemia (unlike thiazides)

608
Q

Review–thiazide diuretics cause ___kalemic metabolic ___osis; ___glycemia; ___uricemia

A

Thiazide diuretics cause hypokalemic metabolic alkalosis; hyperglycemia; hyperuricemia

609
Q

Review–loop diuretics cause ___kalemic metabolic ___osis

A

Loop diuretics cause hypokalemic metabolic alkalosis

610
Q

Review–potassium-sparing diuretics cause ___kalemia

A

Potassium-sparing diuretics cause hyperkalemia

611
Q

Hypoaldosteronism causes ___kalemia; hyperaldosteronism causes ___kalemia

A

Hypoaldosteronism causes hyperkalemia; hyperaldosteronism causes hypokalemia

612
Q

ACEIs/ARBs cause ___kalemia

A

ACEIs/ARBs cause hyperkalemia

613
Q

Digoxin causes ___kalemia

A

Digoxin causes hyperkalemia

614
Q

Mineralocorticoids (i.e.: aldosterone) causes ___kalemia

A

Mineralocorticoids (i.e.: aldosterone) causes hypokalemia

615
Q

EKG changes with hyperkalemia that warrant emergent treatment–___, ___ T waves; loss of ___ wave; ___ (wide/narrow) QRS with ___ (tall/short) T wave

A

tall, peaked T waves; loss of P wave; wide QRS with tall T wave

616
Q

Why is IV calcium given to treat hyperkalemia?

A

Calcium is given to reduce EKG changes–causes membrane stabilization of the myocardium and slows down the rate of arrhythmia development

617
Q

IV calcium reduces potassium levels–T/F?

A

FALSE–calcium does NOT reduce potassium levels, it reduces EKG changes associated with high potassium levels

618
Q

Caution giving IV calcium to patients who are on ___; calcium has been reported to worsen the myocardial effects of ___ toxicity; use ___ as an alternative to stabilize the myocardium

A

Caution giving IV calcium to patients who are on digoxin; calcium has been reported to worsen the myocardial effects of digoxin toxicity; use magnesium as an alternative to stabilize the myocardium

619
Q

Calcium ___ is preferred, but calcium ___ is an option if central line is in place

A

Calcium gluconate is preferred, but calcium chloride is an option if central line is in place

620
Q

Can give ___ and ___ to treat hyperkalemia

A

Insulin and dextrose to treat hyperkalemia

10 units regular insulin IV + 50 ml of 50% dextrose (if BG < 250)

621
Q

What inhaled beta 2 agonist can be used to treat hyperkalemia because it helps with movement of K into cells?

A

Albuterol

622
Q

Sodium bicarbonate is not recommended to lower potassium levels–T/F?

A

True–super unpredictable, may take several hours to work

623
Q

Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are oral potassium binders that lower potassium levels through ___ elimination

A

Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are oral potassium binders that lower potassium levels through fecal elimination

624
Q

Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) should NOT be used for acute management of potassium levels–T/F?

A

True–should be used to manage potassium levels long-term

625
Q

Osmotic diuretics can cause ___natremia

A

hypernatremia

626
Q

Thiazides, loops, CHF, carbamazepine, lithium, SSRIs, and liver disease can all cause ___natremia

A

hyponatremia

627
Q

If you correct sodium levels too quickly, it can cause ___

A

permanent brain damage–central pontine myelinolysis

628
Q

Sodium correction rates–severe symptomatic hyponatremia–__-__ meq/L in the first 24 hours, __ meq/L or less in 48 hours

A

Severe symptomatic hyponatremia–6-12 meq/L in the first 24 hours, 18 meq/L or less in 48 hours

629
Q

Sodium correction rates–chronic hyponatremia–__ meq/L/hr with max change of __-__ meq/L in a 24 hour period

A

Chronic hyponatremia–0.5 meq/L/hr with max change of 8-10 meq/L in a 24 hour period

630
Q

You can correct sodium levels a little faster in patients with chronic vs. acute hyponatremia–T/F?

A

True

631
Q

What are VAPTANS?–___ receptor blockers

A

Vasopressin receptor blockers

632
Q

VAPTANS are used to treat ___volemic and ___volemic ___natremia

A

euvolemic and hypervolemic hyponatremia

Get rid of fluid to correct sodium levels

633
Q

VAPTANS can be used in hypovolemic hyponatremia–T/F?

A

FALSE–cannot use VAPTANS in people who are hypovolemic because they will cause even further loss of fluid, leading to CV collapse

634
Q

Calcium levels are dependent upon ___

A

albumin

635
Q

Hypercalcemia may be caused by ___parathyroidism, ___ diuretics

A

Hypercalcemia may be caused by hyperparathyroidism, thiazide diuretics

636
Q

Hypocalcemia may be caused by ___parathyroidism, ___ disease, ___ diuretics

A

Hypocalcemia may be cause by hyperparathyroidism, renal disease, loop diuretics

637
Q

Can give ___ to correct hypercalcemia

A

NS–dilute high calcium levels

638
Q

Can give ___ diuretics to treat hypercalcemia

A

LOOP, NOT thiazide!

639
Q

Pamidronate, zoledronic acid, denosumab, and calcitonin are medications used to treat ___; they can also treat ___calcemia

A

osteoporosis; they can also treat hypercalcemia–slow down bone resorption/breakdown to reduce calcium coming into the circulation

KLowe Pharm 2 (10 decks)

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