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Nurs 711 Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is the function of the Autonomic nervous system?

A

Regulation of the heart, secretory glands and smooth muscles

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2
Q

What are the two components of the Autonomic nervous system?

A

The parasympathetic and sympathetic nervous systems

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3
Q

What does the parasympathetic nervous system do?

A

Slows Heart Rate
Increases Gastric Secretion
Emptying of the bladder
Emptying of bowels
Constricting the pupils
Contracting bronchial smooth muscle

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4
Q

What does the sympathetic nervous system do?

A

Increases heart rate
Increases blood pressure
Dilates bronchi
Vasoconstriction
Dilates pupils
Flight of fight
Shunting blood from skin to muscles

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5
Q

What is the baroreceptor reflex?

A

Feedback loop between spinal cord and brain that regulates BP and maintains homeostasis

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6
Q

What are molecules that activate receptors?

A

Agonists

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7
Q

An agonist’s action depends on the?

A

receptor

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8
Q

What is the method of action of an Agonist?

A

Agonists bind to the receptor and mimic the body’s own molecules

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9
Q

What are the two types of agonists?

A

There are full agonists and partial agonists

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10
Q

What are molecules that prevent or block receptors?

A

Antagonists

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11
Q

What kind of effect does an antagonist have on their own receptors?

A

Antagonists essentially have no effect on their own on receptors but their action is the prevention of receptor activation by agonists

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12
Q

What are the two types Adrenergic receptors?

A

Adrenergic and Cholenergic

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13
Q

What do adrenergic drugs mediate?

A

responses to epinephrine and norepinephrine

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14
Q

What locations are Alpha 1 receptors located?

A

Eye
Arterioles (skin, viscera, mucous membranes)
Veins
Penis
Prostate Capsule
Bladder

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15
Q

What is the response to receptor activation for the Alpha 1 receptor in the eye?

A

Contraction of iris muscle increases pupil diameter (mydriasis-pupil dilation)

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16
Q

What is the response to receptor activation for the Alpha 1 receptor in the arterioles and were are these arterioles located?

A

Vasoconstriction

Skin, viscera, mucous membranes

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17
Q

What is the response to receptor activation for the Alpha 1 receptor in the veins?

A

Constriction

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18
Q

What is the response to receptor activation for the Alpha 1 receptor in the penis?

A

Ejaculation

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19
Q

What is the response to receptor activation for the Alpha 1 receptor in the prostate capsule?

A

Contraction

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20
Q

What is the response to receptor activation for the Alpha 1 receptor in the bladder?

A

contraction of sphincter (prevents voiding)

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21
Q

Where are the alpha 2 receptors located?

A

The presynaptic nerve terminals

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22
Q

What is the response to receptor activation for the Alpha 2 receptors in the presynaptic nerve terminals?

A

inhibition of transmitter release

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23
Q

Where are the Beta 1 receptors located?

A

The heart and kidney

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24
Q

What is the response to receptor activation for the Beta 1 receptors in the heart?

A

Increased rate, contractile strength, conduction velocity over AV node

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25
Q

What is the response to receptor activation for the Beta 1 receptors in the Kidney?

A

Release of Renin

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26
Q

Where is the location of the Beta 2 receptors?

A

Arterioles (heart, lung, skeletal muscle)
Bronchi
Uterus
Liver
Skeletal muscle

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27
Q

Where is the location of the Beta 2 receptors?

A

Arterioles (heart, lung, skeletal muscle)
Bronchi
Uterus
Liver
Skeletal muscle

A Big Umbrella Leans Securely

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28
Q

Where are the location of dopamine receptors?

A

in the kidney

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29
Q

What is the response to receptor activation for the Beta 2 receptors in the arterioles and where are these arterioles located?

A

Dilation

Located in the heart, lung and skeletal muscles

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30
Q

What is the response to receptor activation for the Beta 2 receptors in the bronchi?

A

Dilation

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31
Q

What is the response to receptor activation for the Beta 2 receptors in the uterus?

A

relaxation

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32
Q

What is the response to receptor activation for the Beta 2 receptors in the liver?

A

Glycogenolysis

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33
Q

What is the response to receptor activation for the Beta 2 receptors in the skeletal muscle?

A

Enhanced contraction, glycogenolysis

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34
Q

What is the response to receptor activation for the Dopamine receptors in the kidney?

A

Dilation of kidney blood vessels

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35
Q

What is the span of receptor coverage of epinephrine?

A

Alpha 1
Alpha 2
Beta 1
Beta 2

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36
Q

What is the span of receptor coverage of Norepinephrine?

A

Alpha 1
Alpha 2
Beta1

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37
Q

What is the span of receptor coverage of Phenylephrine?

A

Alpha1

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38
Q

What is the span of receptor coverage of Dopamine?

A

Alpha1
Beta 2
Dopamine

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39
Q

What is the span of receptor coverage of Isoproterenol?

A

Beta 1
Beta 2

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40
Q

What is the span of receptor coverage of Dobutamine?

A

Beta 1

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41
Q

What is the span of receptor coverage of Albuterol?

A

Beta 2

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42
Q

The adrengergic agonists have what direct method of binding?

A

Direct receptor binding

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43
Q

The theraputic uses for Alpha 1 Activation are?

A

mostly based on vasoconstriction

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44
Q

What are the reasons to activate Alpha 1 receptors to promote vasoconstriction?

A

Nasal Decongestion
Hemostasis (topical application)
Adjunct to local anesthesis
Mydriasis (pupil dilation)
BP elevation

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45
Q

What are the adverse effects of Alpha 1 Agonists?

A

HTN (can be severe with IV administration)
Bradycardia (baroreceptor reflex)
Tissue necrosis

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46
Q

What occurs when an IV extravates?

A

Medicine is released from the IV site causing necrosis of the tissue

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47
Q

What are the therapeutic effects of Beta1 activation?

A

Heart Failure
Shock
AV heart blocks
Restarting heart after cardiac arrest

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48
Q

What are the adverse effects of Beta 1 activation?

A

Tachycardia
Dysrhymias
Agina Pectoris

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49
Q

What are the therapeutic effects of Beta 2 activation?

A

Occur in the lungs and uterus

Asthma
Delay of preterm labor

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50
Q

What are the adverse effects of Beta 2 Activation?

A

Hyperglycemia
Muscle tremors

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51
Q

If using an Beta 2 adrenergic agonist on a diabetic patient, what nursing interventions should be taken?

A

Blood sugar should be checked frequently

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52
Q

Dopamine has a special quality unlike the other receptors. What is it?

A

Dopamine is both the receptor and the drug

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53
Q

What are the pharmacokinetics of dopamine administration?

A

Given IV, weight based and very short half life

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54
Q

Dopamine is considered to be ‘dose dependent’. What does this mean?

A

Effects depend on how much of drug is given

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55
Q

What are the effects of dopamine in low doses?

A

Dilation of blood vessels
Improves GFR and urine output
Maintains kidney function

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56
Q

What is the effect of dopamine if given in high doses?

A

Beta 1 and Alpha 1 effects:
Vasoconstriction
Increased BP & HR
Improved cardiac output

Used for hemodynamic support:
Shock
Advanced Heart failure

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57
Q

What are the adverse effects of high doses of Dopamine Receptor activation?

A

Dysrhymias/tachycardia (activation of Beta 1)
Angina pectoris (activation of beta 1)
Tissue necrosis if IV extravastes

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58
Q

What type of receptors does epinephrine activate?

A

Activates all alpha and beta receptors

Treatment of Anaphylaxis/anaphylactic shock

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59
Q

What are the Alpha 1 activation effects of epinephrine?

A

Delays absorption of local anesthetic
Controls bleeding
Raises BP
Induces mydriasis

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60
Q

What are the Beta 1activation effects of epinephrine?

A

Reverses AV heart block
Restores rhythm during cardiac arrest

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61
Q

What are the Beta 2 activation effects of epinephrine?

A

Bronchodilation

(not the preferred drug)

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62
Q

How is epinephrine administered and how is concentration determined?

A

Absorption: Topically or by injection
Different concentrations for different routes

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63
Q

What are the Pharmocokinetics of epinephrine metabolism?

A

Metabolized in liver and intestine and has a very short half life

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64
Q

What are the adverse effects of epinephrine?

A

HTN crisis
Dysrhythmias/tachycardua
Angina Pectoris
Necrosis (if iv exravation)
Hyperglycemia
Interacts with A1 and Beta blockers

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65
Q

How is epinephrine concentration determined?

A

By the administration route

Oral inhalation = Highest
SC/IM
IV/intracardiac
Combined with local=Lowest

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66
Q

What must you do before administering epinephrine?

A

Must confirm the concentration and intended route before administering especially in emergency situations

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67
Q

What do adrenergic antagonists do?

A

These drugs block the activation of a and b receptors

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68
Q

What are the therapeutic uses for Alpha 1 blockers?

A

Essential HTN
Benign prostatic hypertrophy
Renal stones
Pheochromocytoma
Raynaud’s Disease
Reversal of overdose/toxicity of A1 agonists

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69
Q

What are the Adverse effects of Alpha 1 Blockers?

A

Orthostatic hypertension
Reflex tachycardia
Nasal Congestion
Inhibition of ejaculation
Na retention and increased blood volume

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70
Q

What is Pheochromocytoma?

A

Tumor in adrenal glands

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71
Q

What is Phentolamine?

A

A non selective alpha blocker (antagonist)

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72
Q

What are the therapeutic uses for Phentolamine?

A

Pheochromocytoma
Treatment of tissue necrosis (after extravasion of an a1 agonist, it’s the antidote)

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73
Q

What are the adverse effects of Phentolamine?

A

Same as the a1 antagonists
Significant reflex tachycardia (may need to be given a beta blocker)

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74
Q

What are the therapeutic uses for Beta 1 blockers?

A

Hypertension
Stable Angina
Tachycardia
Post-MI
Heart Failure
Migraines
Stage Fright/anxiety
Glaucoma

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75
Q

What are the adverse effects of Beta1 Blockers?

A

Bradycardia
Reduced cardiac output
Precipitation of heart failure
AV heart block
Rebound cardiac excitation
Fatigue/Depression
Can mask hypoglycemia

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76
Q

What are the therapeutic uses for Beta 2 blockers?

A

NONE

Some non-selective Beta blockers can block B2, but never give for a therapeutic use

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77
Q

What is the first generation beta blocker?

A

Propanolol

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78
Q

What is the method of action of propanolol?

A

Blocks both Beta 1 and Beta 2 receptors

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79
Q

What are the therapeutic uses of propanolol?

A

HTN
Angina Pectoris
Tachycardiac dysrythmias
Myocardial infarction
Stage Fright
Can cause depression

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80
Q

How can propanolol cause depression in some patients?

A

Because it is highly lipid soluble, it can cross the membrane to CNS causing depression

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81
Q

What are the adverse effects of propanolol?

A

Beta 1 and Beta 2 blocking adverse effects

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82
Q

What is the second generation Beta blocker?

A

Metoprolol

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83
Q

What is the method of action of metoprolol?

A

Cardioselective, blocking beta 1 receptors

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84
Q

What are the therapeutic uses for metoprolol?

A

HTN
Angina pectoris
Tachycardic dysrythmias
Myocardial infarction
Heart Failure
Crosses CNS

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85
Q

What are the therapeutic uses for metoprolol?

A

HTN
Angina pectoris
Tachycardic dysrythmias
Myocardial infarction
Heart Failure
Crosses CNS

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86
Q

What are the adverse effects of metoprolol?

A

Beta 1 only

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87
Q

What are the differences between propanolol and metoprolol?

A

Propanolol is a nonselective blockade, so it blocks both Beta 1 and 2 receptors
Propanolol is used to treat stage fright

Metoprolol is a Beta 1 blocker, and it is also used to treat Heart failure and not stage fright

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88
Q

What is the 3rd generation Beta Blocker?

A

Carvedilol

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89
Q

What is the method of action of Carvedilol?

A

Nonselective blockade of Beta 1 and 2 plus alpha 1 blockade

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90
Q

What are the therapeutic uses of carvedilol?

A

HTN
Angina Pectoris
Tachycardic dysrhythmias
Myocardial infarction
Heart failure

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91
Q

What are the adverse effects of carvedilol?

A

Beta 1 blockage effects
Beta 2 blockage effects
Alpha 1 blockage effects

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92
Q

Cholinergic drugs mediate responses to?

A

Acetylcholine

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93
Q

What is acetylcholine?

A

Aceytlcholine is the chief neurotransmitter of the Autonomic nervous system that:
Contracts smooth muscle
Dilates blood vessels
Increases bodily secretions
Slows heart rate

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94
Q

The response of a Cholinergic drug depends on?

A

The type of receptor that is activated or blocked

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95
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the eye

A

Contraction of the lens and iris to focus

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96
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the eye

A

Contraction of the lens and iris to focus

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97
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the eye

A

Contraction of the lens and iris to focus

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98
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the heart

A

Decreases heart rate

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99
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the lungs

A

Contraction of bronchi and promotion of secretions

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100
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the bladder

A

Contraction of detrusor muscle
Relaxation of sphincter
Coordination of these two actions

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101
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the GI Tract

A

Salivation
Gastric secretion increase
Intestinal tone, motility and defecation increase

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102
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the sweat glands

A

Generalized sweating

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103
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the sex organs

A

Erection

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104
Q

Cholinergic Drug Receptors:
Muscarinic receptors in the blood vessels

A

Vasodilation

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105
Q

What are the two subcategories of Cholinergic medications?

A

Agonists and Antagonists

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106
Q

What is Bethanechol?

A

A muscarinic agonist

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107
Q

What are the therapeutic uses for Bethanechol?

A

Non-obstructive urinary retention
Off label for GERD

108
Q

What are the pharmacokinetics of bethanechol?

A

Absorbed rapidly PO
Given on an empty stomach (food decreases absorption and can cause N/V)

109
Q

What is the metabolism of bethanechol?

A

A short T1/2
Metabolized by cholinesterase at the cholinergic sites in the plasma and liver

110
Q

What are the adverse effects of Bethanechol?

A

Cardiovascular: Bradycardia, hypotension

Respiratory: Shortness of breath (bronchioconstriction)

GI/GU: Increased salivation and GI motility

111
Q

What are the contraindications for muscarinic agonists?

A

Toxicology: Can OD on too much
Patients with gastric ulcers, asthma or heart failure

112
Q

What are the contraindications for muscarinic agonists?

A

Toxicology: Can OD on too much
Patients with gastric ulcers, asthma or heart failure

113
Q

What are the nursing considerations for muscarinic agonists?

A

Advise to take 1 Hr before or 2 hrs after meals

Monitor HR and BP

Watch for SLUDGE

114
Q

What does SLUDGE stand for?

A

It’s the signs of toxicity from muscarinic agonists

S-Salivation
L-Lacrimation
U-Urination
D-Defication
G-Gastric upset
E-Emesis (vomiting)

115
Q

What is overactive bladder?

A

Defined as urgency, frequency, nocturia and/or urge incontinence

116
Q

What causes overactive bladder?

A

It is usually due to involuntary contractions of detrusor muscle or bladder and is more common with increasing age and/or multiple pregnancies

117
Q

What are the non-pharmocological therapies for overactive bladder?

A

Scheduled voiding
Timing Fluid intake
Kegel Exercises
Avoid caffine

118
Q

An anticholinergic is?

A

A muscarinic antagonist

119
Q

What is the MOA of an anticholinergic?

A

Blocks acetylcholine at muscarinic receptors

120
Q

What is an anticholinergice used to treat?

A

Overactive bladder
Bradycardia (atropine)
Eye disorders/Eye exams
Intestinal hypertonicity and hypermotility disorders
Motion sickness
Asthma/COPD

121
Q

What is an easy way to remember what anticholinergics do?

A

Can’t think (confusion)
Can’t blink (dry eyes)
Can’t see (blurred vision)
Can’t pee (Urine retention)
Can’t spit (dry mouth)
Can’t shit (constipation)

122
Q

What is Oxybutynin?

A

A muscarinic antagonist that is the top therapy for overactive bladder

123
Q

What is the MOA of Oxybutynin?

A

Blocks the muscarinic receptors on the bladder detrusor muscle which inhibits bladder contraction which decreases the urge to void

124
Q

What are the pharmacokinetics of Ocybutynin?

A

PO (IR/ER), patch, gel
Crosses BBB
Metabolized by CYP enzymes
Short half life

125
Q

What are the adverse effects of Oxybutynin?

A

Causes typical anticholinergic effects
Contraindicated to be given with other anticholinergic drugs

126
Q

What is atropine?

A

A muscarinic antagonist that is a common drug given for diverticulitis, eye exams and is an antidote to muscarninic agonists

127
Q

What is the method of action of Atropine?

A

Prevents receptor activation from acetylcholine

128
Q

What are the uses for atropine?

A

Bradycardia (ACLS drug)
Eye Exams
Diverticulitis
Cholinergic overdose

129
Q

What are the pharmacokinetics of atropine?

A

PO, Eye drops or IM/IV/SC
If given IV, begins to work immediately and is metabolized by the liver and excreted by the kidneys

130
Q

What are the adverse effects of Atropine?

A

CNS: mild excitation at therapeutic doses

Eyes: Blurred vision/increase in intracellular pressure/photophobia

Cardiovascular:Tachycardia

GI: Decreased secretions/constipation

Misc: Decreased sweating

131
Q

What is Ipratropium bromide (Atrovent)?

A

A muscarinic antagonists that is an inhaler/nebulizer or nasal spray

132
Q

What are the two types of histamines?

A

H1-dilates small vessels, constriction of bronchi smooth muscle, CNS effects, itching, pain in nerves, secretion of mucus

H2: Increases in gastric acid

133
Q

An antihistamine is?

A

A H1 antagonist/blocker that relieves itching, sneezing or rhinorrhea

134
Q

What is the MOA of a antihistamine?

A

Selectively binds to H1 histamine receptors blocking their action

Does not bind to H2 receptors

Blocks some muscarinic receptors

135
Q

Can an antihistamine be used in pregnancy?

A

It is not advised, especially in the 3rd trimester because it crosses the blood brain barrier and could cause sedation and a decreased apgar score

136
Q

What are the differences between the first generation antihistamines and the second generation of antihistamines?

A

First Gen (Benadryl): Sedating effect, CNS effects, anticholinergic effects, paradoxical excitation in some

Second Gen (zyrtec): Not sedating, no anticholinergic effects

137
Q

What is allergic Rhinitis?

A

Approved medical diagnosis of seasonal allergies that is an inflammation of the eyes, upper and lower airways

138
Q

What are the symptoms of allergic Rhinitis?

A

Sneezing, rhinorrhea, pruritus, nasal congestion, conjunctivitis, possible asthma

139
Q

What are intranasal antihistamines?

A

They are part of the second gen. of antihistamines and in theory, have less systemic adverse effects

140
Q

What are the adverse effects of intranasal antihistamines?

A

Nasal dryness, epistaxis (nose bleed), headaches

141
Q

What type of medication is Aselastine and Olopatadine?

A

Intranasal antihistamines

142
Q

What are the most effective medications for allergic rhinitis due to their anti-inflammatory action?

A

Intranasal glucocorticoids

143
Q

What are the adverse effects of intranasal glucocorticoids?

A

Dry mucosa, epistaxis and headache

144
Q

Fluticasone and Mometasone are both what kind of drug?

A

Intranasal glucocorticoids

145
Q

What type of drugs are decongestants?

A

Sympathomimetics/Alpha 1 agonists

146
Q

What is the method of action of decongestants?

A

Reduces the swelling of the nasal mucosa

147
Q

What are the adverse effects of decongestants?

A

Nasal: Rebound congestion (wean with glucocorticoid)
Oral: Restlessness, anxiety, insomnia, vasoconstriction

148
Q

What are some examples of common decongestants?

A

Phenylephrine
Psuedoephedrine
Oxymetazoline

149
Q

How long should you take decongestants?

A

Do not take for longer than 3 days or just at bedtime 4x

150
Q

B2 agonists, methylxsnthines and anticholigergics all fit into what category of respiratory drugs?

A

Bronchodilators

151
Q

Glucocorticoids and leukotriene modifers and what type of respiratory drugs?

A

Anti-inflammatory medications

152
Q

Inhaled Corticosteroid is used for?

A

An Asthma controller

It is used prophalatically to prevent asthma attacks. NOT for PRN use

153
Q

What is the method of action of a inhaled corticosteroid?

A

It decreases:
Bronchial hyperactivity
Airway edema
Synthesis of inflammatory mediators

It increases:
# of Beta 2 receptors
Responsivness to Beta 2 agonists

154
Q

What are the pharmacokinetics of a glucocorticoid?

A

Usually inhaled, can be given PO in severe cases for a brief duration

155
Q

What are the adverse effects of a glucocorticoid?

A

Oropharyngeal candidiasis
Dysphonia (horseness)
Increase in glucose level
Adrenal suppression possible with long term use
Bone loss possible
Slowing of growth in children

156
Q

What is a SABA?

A

A short acting Beta 2 adrenergic Agonist that is used as a rescue inhaler PRN or before exercise

157
Q

What are the adverse effects of a SABA?

A

tachycardia
Angina
Tremor

158
Q

What kind of drugs are Albuterol and Levalbuterol?

A

SABA

159
Q

What is a LABA?

A

A long-acting Beta 2 Adrenergic Agonist that is used as a controller, not a rescue inhaler with fixed schedule dosing that must be combined with a ICS

160
Q

What drug must be combined with a inhaled corticosteroid?

A

A LABA

161
Q

Salmeterol and Aformoterol are what kinds of drugs?

A

LABAS

162
Q

Step 1 in the asthma treatment scale is?

A

The use of an inhaled short acting Beta 2 agonist PRN (SABA)

163
Q

Step 2 of the asthma treatment scale is?

A

A inhaled corticosteroid is added to the short acting B2 agonist (SABA

164
Q

Step 3 of the asthma treatment scale is?

A

An inhaled long acting B2 agonists (LABA) is added to SABA and inhaled corticosterioid

165
Q

Step 4 of the asthma treatment scale is?

A

Increasing the dosage of already administered drugs, or constider the addition of a fourth drug

166
Q

Step 5 in the asthma treatment scale is?

A

The use of a daily steroid tablet on top of LABA, SABA and inhaled corticosteroid

167
Q

Oral B2 agonists are used for?

A

Long term control of asthma, not an acute attack because they take a while to take effect if given orally but have significantly more adverse effects because they are absorbed systemically

168
Q

What are the pharmacokinetics of oral B2 agonists?

A

Short half life so multiple doses

169
Q

Dry-powder inhalers have?

A

no propellant and are breath activated

170
Q

What dose a nebulizer do?

A

Its a machine that converts medication into a mist

171
Q

With a spacer, a metered dose inhaler receives how much more medication to the mouth and throat and lungs?

A

With a spacer, the Mouth and throat get 22% of the medication while 21% reaches the lungs.

Comparitively, without a spacer the mouth and throught get 81% of the medication and the lungs only get 9%

172
Q

Budesonide (Pulmicort) and Fluticasone propionate (flovent) are both what type of drug?

A

Inhaled corticosteroids

173
Q

What type of drug is Montelukast (singulair)?

A

A leukotriene modifier

174
Q

What is the MOA of Montelukast?

A

Blocks the leukotriene receptors therefore decreasing both bronchioconstriction and inflammatory response

175
Q

What are the uses for Montelukast?

A

Asthma, EIB, Allergic Rhinitis

176
Q

Montelukast is not a _____________ ____________ ____________ but is used in combination with a glucocorticoid to lower steroid dose..

A

first line treatment

177
Q

Theophylline is what type of drug?

A

A Methylxanthine is a group of drugs derived from xanthine (Caffeine) that was the first line asthma drug before the development of inhaled glucocorticoids

178
Q

What does Theophylline cause?

A

CNS stimulation
Cardiac Stimulation
Bronchial dilation

179
Q

What are the pharmacokinetics of Theophylline?

A

Only available as sustained release
PO
Wide variation in half life, so indivual dosing is required
NTI Drug: Levels between 10-20 mcg/mL are therapeutic

180
Q

What are the NTI levels of Theophylline?

A

10-20 mcg/mL

181
Q

Ipratroprium (Atrovent) and Tiotropium (Spriva) are what types of drugs?

A

Anticholinergics that are used for COPD and off label for asthma by blocking muscarinic receptors in the bronchi and prevent bronchoconstriction

182
Q

In regards to insulin, what is the difference between Type 1 and Type 2 diabetes?

A

Type 1 diabetes requires insulin replacements
Type 2 will likely start with oral medication and may eventually need insulin replacement over time

183
Q

How is Diabetes monitored?

A

With Fasting blood glucose levels
Glycosylated hemoglobin
Continuous glucose monitoring

184
Q

What is an HbA1C?

A

The Glycosylated hemoglobin in the blood, it shows a 3 month average percent

185
Q

What is a goal number for an HbA1C?

A

Goal is <7% (150) but <8% if hypos or limited life expectancy

186
Q

A HbA1C of 12% would be?

A

300

187
Q

What is the goal range for continous glucose monitoring?

A

Over 70%

188
Q

All types of insulin are given _________________, why?

A

Parentally because of the first pass effect

189
Q

All insulins carry some risk of?
Which type has the most risk?

A

Hypoglycemia
Shorter acting insulins carry more risk

190
Q

The concentration of insulin is measured in?

A

Units

191
Q

Insulin is a high alert drug, what does this mean?

A

You may need two RN signatures before administering

192
Q

Insulin:
What is the onset, peak and duration of insulin lispro?

A

onset: 15-30 min
Peak: 0.5-2.5 hr
Duration: 3-6 hr

193
Q

Insulin:
What is the onset, peak and duration of regular insulin?

A

Onset: 30-60 min
Peak: 1-5hr
Duration: 6-10hr

194
Q

Insulin:
What is the onset, peak and duration of NPH insulin?

A

Onset: 60-120 min
Peak: 6-14 hr
Duration: 16-24ht

195
Q

Insulin:
What is the onset, peak and duration of insulin glargine (100)?

A

Onset: 70min
Peak: None
Duration: 18-24 hr

196
Q

Insulin:
What is the onset, peak and duration of insulin determir

A

Onset: 60-120min
Peak: None
Duration: 12-24hr

197
Q

Insulin:
What is the onset, peak and duration of insulin glargine (300)?

A

Onset: 360min
Peak: None
Duration: >24hr

198
Q

Insulin:
What is the onset, peak and duration of insulin degludec?

A

Onset: 30-90min
Peak: None
Duration: >24hr

199
Q

What insulin is NEVER given IV?

A

insulin lispro
insulin lantus
insulin levimir

200
Q

Why would a patient need a different concentration of insulin?

A

to reduce the volume of the injection

201
Q

Which insulin in considered the rapid prototype and can be used for both meals and basal control?

A

insulin lispro

202
Q

U-500 regular insulin is only available in which form?

A

pen form

203
Q

What is the only insulin given IV?

A

U-100 regular insulin

204
Q

Which insulin has a cloudy suspension?

A

NPH insulin

205
Q

How is NPH insulin mixed before drawing?

A

by gently rolling in hands

206
Q

When injecting a patient with a long acting insulin and a NPH, which insulin should be drawn first?

A

Clear before cloudy as to not contaminate the regular insulin with NPH insulin

207
Q

Which two insulins are both long acting, normally given once per day at night and are the best insulins for basal control?

A

Insulin Lantus
Insulin Levimir

208
Q

What are the major differences between insulin glargine and insulin degludec?

A

Both ultra long acting insulins but:
insulin glargine is available in U-300 prefilled pens, effects begin within 6 hrs

Insulin degludec is available in U-100 and U-200 prefilled pens and effects begin in under 90 minutes

209
Q

What are the major similarities between insulin glargine and insulin degludec?

A

Both are good for someone who is busy or inconsistent with administration
Both are used once daily
Both mimic basal control
Both have no significant peak and are steady all day
Both are only given subq

210
Q

Which site is the fastest for insulin administration?

A

The abdomen

211
Q

Which site is slowest for insulin administration?

A

The thigh

212
Q

What the the ‘magic number’ for blood sugar?

A

70

213
Q

What are the side effects from a rapid fall in BS?

A

increased HR, sweating, shakeness

214
Q

What are the side effects from a slow fall in BS?

A

HA, confusion, fatigue, drowsiness

215
Q

What are the interventions for hypoglycemia?

A

For a conscious patient:
glucose tabs, OJ, soda, candy

For an unconscious patient:
D50 or glucagon SQ/Iv

216
Q

What patients are at the highest risk of hypoglycemia?

A

Patients with:
Decreased food intake
vomiting/diarrhea
Increased exercise activity
Alcohol intake
Uncontrolled diabetes

217
Q

What are the oral medications for Type 2 diabetes?

A

Biguantide (metformin)
Sulfonylureas
Thiazolidinedones (glitazones)
Alpha-glucosidease inhibitors
SGLT-2 inhibitors
Gliptins (DPP-4 inhibitors)
GLP-1 receptor agonists

Big Green Snakes go through alot

218
Q

What is the first line oral therapy for diabetes and pre-diabetes?

A

Biguantide (Metformin)

219
Q

What are the pharmacokinetics of Biguantide (Metformin)?

A

Inhibits glucose production in the liver
Increases insulin sensitivity in the tissues
Lowers blood glucose but DOES NOT cause hypoglycemia**
Taken with meals 1-2 times a day

220
Q

What are the adverse effects of Biguantide (Metformin)?

A

GI effects (taken with food)
B12 deficency
Toxicity with lactic acidosis so no alcohol
Kidney excretion (so watch out for renal issues)

221
Q

What are the oldest class of oral anti-hypoglycemics?

A

Sulfonylureas

222
Q

What are the pharmacokinetics of Sulfonylureas?

A

Stimulates insulin secretion in pancreas
Increases insulin sensitivity
With means 1-2 times per day

223
Q

What are the adverse effects of Sulfonylureas?

A

Hypoglycemia (especially in hepatic or renal impairment)
No alcohol (flushing, palpitations, N.V)
Beta blockers (can mask effects of hypoglycemia)

224
Q

What are the pharmacokinetics of Thiazolidinediones/Glitazones?

A

Increases insulin sensitivity
Inhibits glucose production
Half life of 16-24hrs
Metabolized by CYP enzyme *

225
Q

What are the adverse effects of Thiazolidinediones/Glitazones?

A

Fluid rention (not for use in HF patients)
Drug interactions with CYP inhibitors/inducers
Risk of bladder cancer (watch for blood in urine)
Risk of fractures in women
Possibly hepatotoxic

226
Q

What are the pharmacokinetics of Alpha glucosidase inhibitors?

A

Delays carb absorption in the gut
With meals 3x per day

227
Q

What are the adverse effects of Alpha glucosidase inhibitors?

A

Frequent GI distress (gas, bloating, cramps, diarrhea, borborygmus)
Delayed iron absorption
Possible liver dysfunction

228
Q

What are the pharmacokinetics of Dipeptiyl Peptidase-4 (DPP-4) inhibitors such as sitagliptin?

A

They enhance incretin hormone that stimulates insulin secretion in the pancreas
Supress post-prandial release of glucagon

229
Q

What are the adverse effects of DPP-4 inhibitors?

A

RARE Pancretitis
Severe and persistant upper abdominal pain
Vomiting

230
Q

What are the pharmacokinetics of Sodium-Glucose co-transporter 2 (SGLT-2) inhibitors such as canaglifozin?

A

Inhibits SGLT-2 in the kidneys
Decreases reabsorption of glucose
Increases urinary glucose excretion
Glucosuria->caloric loss->modest weight loss
Half life of 12 hr
Shown to prevent CV events

Basically you pee out the glucose
CanaglifOZIN->helps urine flow!

231
Q

What is the non-insulin injectable?

A

Glucagon-like Peptide 1 (GLP-1)
Known as Ozempic

232
Q

There are two types of Glucagon-like Peptide 1 (GLP-1), what are they?

A

Short acting: Exenatide (Byetta) 1/2x per day
Long acting: Exentide (Bydureon) 1x per week

233
Q

What are the pharmacokinetics of Glucagon-like Peptide 1 (GLP-1)?

A

Mimics incretin hormones by:
Stimulating insulin secretion
Supresses post prandial release of glucagon
Slows gastric emptying
Supresses Appetite (promotes weight loss)

234
Q

What are the adverse effects of Glucagon-like Peptide 1 (GLP-1)?

A

GI effects (reflux, N/V, diarrhea)
Hypoglycemia
Pancreatitis (rare)
Renal impairment (rare)

235
Q

What is the treatment for diabetic ketoacidosis?

A

Replace fluids
Slow adjustment of plasma glucose
Potassium Issues (expect to give replacement)
Sodium Bicarb

236
Q

What is the treatment for Hyperosmolae Hyperglycemic (nonketotic state)

A

Replace fluids
Slow adjustment of plasma glucose
Potassium issues corrected

(the only difference is no bicarb)

237
Q

How does the hypothalamic-pituitary thyroid axis work?

A

On a negative feedback loop
Thyroid uses iodine in body to produce T3 and T4
Increase in T3 & T4 will decrease TSH and vice versa

238
Q

What are the fuctions of thyroid hormones?

A

Regulates metabolic rate
Regulates body heat production
Maintains Growth hormone and skeletal maturation
CNS development
Maintains cardiac rate, force and output
Maintains secretion of GI tract
Affects Respiratory rate and O2 use
Affects RBC production

Metabolism, Heat, Growth, Bones, Heart, GI, Lungs

239
Q

What occurs when there is not enough circulating T3 and T4, or any other issue with the negative feedback loop?

A

Hypothyroidism

240
Q

What are the causes of hypothyroidism?

A

Gland malfunction
Pituitary Tumor
Removal of gland
Iodine deficency

241
Q

What are some of the symptoms of hypothyrodism?

A

Everything is sluggish, tired, poor memory, dry skin, brittle hair and nails, bradycardia, constipation, heavy menses, cold intolerant, weight gain

242
Q

What drug is the mainstay treatment for hypothyroidism?

A

Levothyroxine (Synthroid)

243
Q

What is an important consideration in the prescribing of Levothyroxine (Synthroid)?

A

The brand name and the generic are not the same and therefore dosing must be made for the specific drug that the patient is using

244
Q

What is the MOA of Levothyroxine (Synthroid)?

A

Synthetic T4 is converted to T3

245
Q

What are the pharmacokinetics of Levothyroxine (Synthroid)?

A

Oral or IV
Food, especially calcium can interfere with absorption
Very highly protein bound (long half-life)
NTI drug (several strengths available)
SAFE IN PREGNANCY

246
Q

What hypothyroid drug is safe in pregnancy and why is if in fact good to take in pregnancy?

A

Levothyroxine (Synthroid)

Untreated hypothyroid can cause unintentional miscarrage, and therefore is necessary to take if pregnant to protect the pregnancy

247
Q

What are the adverse effects of Levothyroxine (Synthroid)?

A

Side effects are rare if within the therapeutic range->
Overdose is thyrotoxic crisis which involves:
Hyperthermia
Tachycardia
Restlessness
Tremor
Weight loss

248
Q

What is the patient education for Levothyroxine (Synthroid)?

A

It’s a ‘picky little pill’
-Needs to be taken on an empty stomach
-Generic/Brand consistancy
-Regular lab monitoring
-Report any thyrotoxic symptoms

249
Q

Hyperthyroidism occurs when?

A

There is excess T4 in the body

250
Q

What are the causes of hyperthyroidism?

A

Graves Disease
Toxic nodular goiter (pt develops nodules on thyroid gland that start to produce their own T4)

251
Q

What are the symptoms of hyperthyroidism?

A

Everything is revved up
Anxious, poor concentration, hungry, tachycardia, chest pain, hyper defication, irregular to no menses, heat intolerance, weight loss

252
Q

What are the drugs to treat hyperthyroidism?

A

Methimazole and Propylthiouracil (PTU)

253
Q

What is the MOA of Methimazole and Propylthiouracil (PTU)?

A

They are thionamides that
inhibit thyroid synthesis
PTU also supresses conversion of T4 to T3 in the body

254
Q

What are the pharmacokinetics of Methimazole and Propylthiouracil (PTU)?

A

PO
Slow onset (3-4 weeks)
Methimazole has longer half life
Short or long term use

255
Q

Out of Methimazole and Propylthiouracil (PTU), which is preferred in pregnancy and why?

A

PTU is preferred because it does not cross the placenta

256
Q

What are the adverse effects of Methimazole and Propylthiouracil (PTU)?

A

Methimazole is teratogenic
Too much can cause hypothyroidism
Frequent lab monitoring is required

257
Q

What is the main function of the Adrenal Cortex?

A

Maintain glucose availability (glucocorticoids)
Cortisol

258
Q

What are the prototypes for Corticosteroids/glucorticould/mineralocorticoid?

A

Hydrocorisone and Prednisone

259
Q

What are the pharmacokinetics fo hydrocorisone and prednisone?

A

PO/IV/IM/Rectal/Topical
Metabolized in liver
Excreted in urine

260
Q

What are the adverse effects of physiologic levels vs pharmcological levels of glucocorticoids?

A

Minimal adverse effects for physiological levels

Higher risk of adverse effects for pharmacological levels

261
Q

When would you use pharmacological levels of glucocorticoids?

A

Allergic reactions
Lung conditions
Inflammation
Dermatological conditions

262
Q

What is Addison’s Disease?

A

Chronic adrenocorticoid insuffciency

263
Q

What are some of the symptoms of Addison’s Disease?

A

Bronze pigmentation of the skin
Changes in body hair distribution
Hypoglycemia
Postural hypotension
Weight loss
GI disturbances
Weakness

264
Q

In an adrenal crisis, what occurs?

A

Profound fatigue
Dehydration
Vascular collapse
Renal shutdown
Decreased serum Na
Increase serum K

265
Q

What is the treatment for Addison’s Disease

A

Lifelong supplementation with glucocorticoid
Needs extra steroids during times of physical stress like fever, illness, surgery

266
Q

What is Cushing’s Syndrome?

A

It is a syndrome that can occur when someone is on a steroid med for a long time

267
Q

What are the symptoms of Cushing’s syndrome and how are they managed?

A

Hyperglycemia-focus effort of diet and exercise
Adrenal suppression-taper after long periods of time
Osteoporosis-Wt bearing exercise, Calcium & Vit D
Suseptibility to infection: screen and prevent
Psychological issues: Educate
Peptic ulcers and Hypertension: Avoid NSAIDS

Nurs 711 Pharmacology (6 decks)

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