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pharm final -new content Flashcards

1
Q

the nueromuscular junction

A
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2
Q

Centrally acting muscle relaxants

A

baclofen, cyclobenzaprine, tizanidine, benzodiazepine, diazepam

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3
Q

centrally acting muscle relaxant actions

A

work in upper levels of CNS to interfere with reflexes that are causing muscle spasms- enhances the effects of GABA

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4
Q

centrally acting muscle relaxants adverse effects

A

-CNS: drowsiness, fatigue, weakness, confusion
-hypotension, cardiac dysrythmias
- dont abruptly withdrawal, can cause anxiety, restlessness, hallucinations, and seizures

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5
Q

centrally acting relaxants drug drug

A

-CNS depressants and alcohol

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6
Q

direct acting relaxants

A

-peripherally acting skeletal muscle relaxants:
-dantrolene- also used for malignant syndrome and hyperthermia
-botulism (botox)

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7
Q

direct acting relaxants actions

A

-dantrolene: acts within skeletal muscle fibers, interfering with the release of calcium from the muscle tubules and prevents muscle contraction)
-Botulism: toxins bind directly to the receptor sites of nerve terminals and inhibit the relese of Ach- causing local muscle paralysis

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8
Q

Narcotic agonists

A

drugs that react with opiod receptors
-cause analgesia (inability to feel pain). sedation, and dysphoria
-controlled substances with the potential for physical dependence and a rising problem of addiction

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9
Q

opioid receptors

A

Mu receptors: pain blocking receptors- also account for respiratory depression, euphoric, decreased GI, pupil constriction, and development of physical dependence

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10
Q

Drug names of opioids

A

morphine, hydromorphone, oxycodone (oxycoton, percaset), hyrdocodone, fentanyl, meperidine, tramadol

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11
Q

indications of opioid agonists

A

-acute pain
-analgesia before, during, after surgery
-relief of nonproductive cough (codeine)

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12
Q

cautions of opioids

A

-pulmonary disorders, respiratory dysfunction
-pregnancy, lactation, labor

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13
Q

opioids adverse effects

A

-respiratory depression with apnea, cardiac arrest, shock
-orthostatic hypotensionn
-lightheaded and dizziness
-GI: nausea, vomiting, constipation
-hallucinations
-pupil constriction
-GU: urinary retention, urethral spasm
BLACK BOX: risk of addiction and misuse can lead to overdose and death

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14
Q

opioid antagonists

A

-drugs that bind strongly to opioid receptors but do not activate them
-block the effects of the opioid receptors and are often used to block the effects of too many opioids in the system (effects include: respiratory depression, sedation, hypotension)

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15
Q

opioid antagonists

A

-naloxone (narcan): -reversal of the adverse effects of narcotics, diagnoses suspects acute narcotic overdose
-naltrexone: adjunct treatment of alcohol or opoioid dependence in adults

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16
Q

opiod antagonists adverse effects

A

-acute narcotic abstinence syndrome: nausea, vomiting, sweating, tachycardia, hypertension, tremulousness, anxiety
-tachycardia, BP changes, dysrythmias

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17
Q

Ergot derivatives: migraine headaches

A

used in the mainstay of migraine headache treatment before the development of triptans

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18
Q

Ergot derivatives: action

A

block alpha-adrenergic and serotonin receptor sites in the brain to cause vasoconstriction of cranial vessels, a decrease in cranial artery pulsation, and decrease in the hyperperfusion of the basilar artery bed

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19
Q

ergot derivatives drug names

A

dihyrdoergotamine: treatment of acute migraines in adults
ergotamine: prevention and abortion of migraines in adults
* both have ergotamine in name*

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20
Q

ergot derivatives adverse effects

A

-numbness and tingling
-chest pain and MI
-cardiac dysrythmias and pulselessness - because trying to get rid of pulses that contribute to mirgraine
-ergotism!!!- a syndrome which causes nausea, vomiting, severe thirst, hypoperfusion, chest pain, blood pressure changes, confusion, drug dependency, and drug withdrawal syndrome

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21
Q

ergot derivatives drug drug

A

beta blockers (peripheral ischemia and gangrene)

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22
Q

triptans actions

A

bind to selective serotonin receptor sites (activate) to cause vasoconstriction of cranial vessels
-sumatriptan, almotriptan, eletriptan
-all have triptan in the name!!

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23
Q

triptans indications

A

-acute migraines
-not for prevention tho!!

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24
Q

triptans adverse effects

A

-blood pressure alterations
-angina–avoid in clients with coronary artery disease

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25
Q

triptains drug drug

A

-ergot derivatives increase risk of angina due to prolonged vasoconstriction

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26
Q

calcitonin gene related peptide (CGRP inhibitors)

A

-rimegepant and ubrogepant: treats acute migraine by blocking CGRP receptor (CRGP causes major vasodilation)
-erenumab-aooe: prevention of migraines in adults because it is a monoclonal antibody that targets the CGRP receptor or CGRP directly (ergotamine prevents as well)

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27
Q

anesthetic agents

A

-drugs that are used to cause complete or partial loss of sensations

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28
Q

general anesthetics

A

-general anesthetics: CNS depressants, produce loss of pain sensation and consiousness

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29
Q

local anesthetics

A

-local anesthetics: used to kill loss of pain sensation and feeling in a designated area of the body
- does NOT produce the systemic effects associated with severe CNS depression

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30
Q

Stages of anesthesia: 1

A

the analgesia stage: loss of pain sensation with the client still conscious and able to communicate

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31
Q

stages of anesthesia: 2

A

the excitement stage: period of excitement and often combative behavior with many signs of sympathetic stimulation (tachycardia, increased RR, BP changes)

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32
Q

stages of anesthesia: 3

A

surgical anesthesia: relaxation of skeletal muscles, return of regular respirations, and progressive loss of eye refluxes and pupil dilation

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33
Q

stages of anesthesia: 4

A

medulla paralysis: very deep CNS depression with loss of respiratory and vasomotor center stimuli in which death can occur rapidly (anesthesia has become too intense and the situation is critical)

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34
Q

adminstering general anesthesia: induction

A

period from the beginning of anesthesia until stage3 is reaches (NMJ blockers are used during induction to facilitate intubation)

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35
Q

administering gen anesthesia: maintenance

A

period from stage 3 until the surgical procedure is complete

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36
Q

administering gen anesthesia: recovery

A

-period from discontinuation of the anesthetic until the client has regained consiousness
-continuous monitoring for any adverse effects of the drus used while ensuring support of the clients vital functions as necessary is imperative during recovery

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37
Q

balanced anesthesia: preop meds

A

anticholinergics: decrease secretions and facilitate intubation and prevent bradycardia associated w neural depression (glycopyrrolate, atropine)

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38
Q

balanced anesthesia: preop meds

A

sedative-hypnotics:
-relax the client, facilitate amnesia, decrease sympathetic stimulation
-include barbituates and benzodiazepines that increase GABA

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39
Q

balanced anesthesia: preop meds

A

antiemetics: decrease nausea and vomitting associated with slowing of GI activity: ondansetron

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40
Q

balanced anesthesia: preop meds

A

antihistamines: to decrease the chance of allergic reaction and help dry secretions

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41
Q

balanced anesthesia: preop meds

A

opioids: aid in pain reductions and sedation

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42
Q

general anesthetics

A

barbituates: methohexital sodium
-induce rapid anesthesia and are then maintained w inhaled drug (volatile liquids and gas anesthetics)

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43
Q

general anesthetics

A

non-barbiturates: midazolam, ketamine, etomidate, propofol

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44
Q

general anesthetics

A

gas anesthetics: nitrous oxide
-anesthetic gases enter the bronchi and alveoli and rapidly pass into the capillary system– quickly pass into the brain and cause severe CNS depression

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45
Q

general anesthetics

A

Volatile Liquids: desflurane, enflurane, isoflurane (all end in flurane) sevoflurane!!- has the least side effects
-liquids that are unstable at room temperature and release gases that are inhaled by the client

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46
Q

ketamine (nonbarbiturate)

A

-30 second onset of action, 45 min recovery period
-crosses blood brain barrier
-associated with bizarre state of unconsciousness in which the client appears to be awake but is unconscious and cannot feel pain- may experience hallucinations, dreams, phsycosis
-casues sympathetic stimulations with increases in BP and HR

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47
Q

propofol (nonbarbiturate)

A

-used for short procedures
-short acting 25-100 min with rapid 30-60 sec onset
-produces less hangover effect and quicker recovery
-often causes local burning on injection
-can cause bradycardia and hypotension
-also used for sedation in clients receiving mechanica ventilation
-white liquid that looks like milk- milk of amnesia

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48
Q

local anesthetic agents

A

-lidocaine, bupivacaine, benzocaine, tetracaine
-actions: causes temporary interruption in the production and conduction of nerve impulses
-affects the permeability of nerve membranes to sodium ions and stops the nerve from depolarizing
-indications: infiltrations anesthesia, peripheral nerve block, spinal anethesia, relief of local pain

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49
Q

local anethestic agents

A

epinephrine: sometimes added to lidocaine in order to increase the length of time that the affected area is numb
-closely monitor the sites distal to the inject site for lack of circulations- can cause gangrene due to vasoconstrictive effects of the “caines”

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50
Q

hypothalamus

A

-“master gland” of the endocrine system
-coordinating center for the nervous and endocrine responses to internal and external stimuli
-regulates body temp, thirst, hunger, water retention, blood pressure, respirations, reproduction, and emotional reactions

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51
Q

hypothalamus releasing hormones

A

-growth-hormone releasing hormone (GHRH)
-thyrotropin releasing hormone (TRH)
-gonadotropin releasing hormone_GnRH)
-corticotropin releasing hormone (CRH)
-prolactin realeasing hormone (PRH)

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52
Q

hypothalamus inhibiting hormones

A

Growth hormone release-inhibiting factor (somatostatin)
-prolactin inhibiting factor (PIF)

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53
Q

posterior pituitary gland hormones

A

anti-diuretic hormone (ADH)- also reffered to as vasopressin and acts on the kidneys to increase retentions of water in order to decrease the osmolarity of the blood volume
OXYTOCIN: stimulates uterine smooth muscle contraction in late phases of pregnany and causes milk release or let down reflex in lactating women

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54
Q

anterior pituitary gland hormones

A

-growth hormones- cell growth
-adrenocorticotropic hormone (ACTH)
-follicle-stimulating hormone- estrogen/progesterone/ testosterone
-luteinizing hormone- estrogen/progesterone/testosterone
-prolactin- milk production
-thryroid stimulating hormone

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55
Q

diabetes insipidus

A

defiecency in the amount of posterior pituitary ADH and may result from pituitary disease or injury (trauma, surgery, tumor)
-two types: neurogenic and nephrogenic

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56
Q

diabetes insipidus

A

production of a large amount of dilute urine containing no glucose- blood become concentrated and blood glucose levels are higher than normal
-S/S polyuria, polydispia (thirst), dehyrdation

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57
Q

diabetes insipidus treatment

A

-desmopressin- neurogenic diabetes
-synthetic ADH

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58
Q

syndrome of inappropriate ADH

A

-excessive secretion of ADH causing fluid retention, dilution of the blood and al of the blood elements, and serious issues with water balance and fluid volume
-treated with drugs that block the ADH or vasopressin receptors, so water is no longer retained and urine is producted
-fluid balance needs to be closely monitored

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59
Q

syndrome of inappropriate ADH treatment

A

-conivaptan- IV loading dose followed by continous infusion- blocks ADH receptors
-tolvaptan- PO- blocks ADH receptors
-both vaptan

60
Q

vasopressin

A

-parental administration continuous- used in vasodilatory shock/hypotensions .01-.04
-directly stimulated V1 V2 receptors in the kidney resulting in vasoconstriction
-closely monitor the IV insertion site from extravasation (PICC line prefered)

61
Q

vasopressin adverse effects

A

water intoxication, hyponatremia, ischemic injury, MI

62
Q

vasopressin contraindications

A

-CAD, PVD

63
Q

adrenal insufficiency

A

-adrenal cortex produces hormones called corticosteroids (androgens, glucocorticoids, mineralocorticoids)

64
Q

causes of adrenal insufficiency

A
  • not enough ACTH production
    -adrenal glands are not able to respond to ACTH
    -adrenal gland is damaged (addison disease)
    -adrenal gland is removed
    -prolonged use of corticosteroids (most common)
65
Q

adrenal insufficiency: prolonged corticosteroid use

A

-when exoenous corticosteriofs are used, they act to negate the regular feedback systems
-the adrenal glands begin to atrophy because ACTH release is suppessed by the exogenous hormones, so the glands are no longer stimulated to produce or secrete the hormone
-taper corticosteroids gradually to avoid adrenal insufficiency or adrenal crisis

66
Q

adrenal crisis S/S

A

-physiological exhaustion
-hypotension
-fluid shift
-shock
-even death

67
Q

adrenal crisis treatment

A

-massive infusion of replacement steroids (usually IV hyrdocortisone)
-constant monitoring anad life support procedures

68
Q

corticosteroids: androgens

A

male and female sex hormones

69
Q

corticosteriods: glucocorticoids

A

actions: stimulate an increase in glucose levels for energy
-increase the rate of protein breakdown and decrease the rate of protein formation from amino acids(preserve energy)
-cause increase mobilization of fatty acids to be used as energy
-high levels can suppress the inflammatory response and immune system

70
Q

corticosteroids: mineralocorticoids

A

affect electrolyte levels and homeostasis

71
Q

adrenocortical agents

A

-some agents of both a glucocorticoids and a mineralocorticoid
-hydrocortisone
-cortisone
-prednisolone
-prednisone

72
Q

glucocorticoids: indications

A

-short term treatment of inflammatory disorders
-to relieve discomfort
-to give the body a chance to heal from effects of inflammation
-help manage allergic reactions
-used in conjunction with other immunosuppresant medications to inhibit transplant rejection
-when combined with mineralocorticoids, some can be used as replacement therapy for adrenal insuffiency

72
Q

glucocorticoid adverse effects

A

-related to the route of administration
-peptic ulcers, increased appetite, weight gain
-heart failure related to fluid retention
-hypernatremia, hypokalemia, hypocalcemia
-hyperglycemia, increased cholesterol
-osteoporosis, spontaneous fractures
-steroid myopathy, muscle weakness
-cataracts, glaucoma
-immunosuppression, aggravating or masking of infections
-delayed wound healing, frail skin
-oral fungal infections

73
Q

mineralcorticoids

A

cortisone: replacement therapy in adrenal insufficiency, treatment of allergic and inflammatory disorders
-fludrocortisone: primary and secondary adrenocorticoid insufficiency
-hyrdocortisone: replacement therapy, treatment of allergic and inflammatory disorders

74
Q

mineralocorticoids: actions

A

increase sodium reabsorption in renal tubules, leading to sodium and water retention, and increase potassium excretion

75
Q

dosing and adminstering adrenocorticoid

A

-adminster oral preparations in the morning with meals
-if dose is divided, administer 2/3 of the dose in the morning and 1/3 of the dose in the early afternoon to mimic the bodies natural cortisol secretion
-for clients NOT taking lifelong adrenocorticoid agents, taper, glucocorticoids gradually to prevent crisis

76
Q

Thyroid hormone

A

-regulates the rate of metabolism
-affects heat production and body temp, oxygen consumption and cardiac output, and metabolism of carbs, fats, and proteins
-an important regulator of growth and development

77
Q

thyroid hormone

A

production and release are regulated by the anterior pituitary hormone, thryoid-stimulating hormone
-TSH secretion is regulate by the hypothalamic regulating factor, thryotropin releaseing hormone

78
Q

the thyroid gland hormones

A

-produces 2 thyroid hormones using iodine found in the diet:
-tetraiodothyronine or levothyroxine (t4)- contains 4 iodine atoms -tetra4
-triiodothyronine or liothyronine (t3): contains 3 iodine atoms -tri3

79
Q

hypothyroidism

A

-lack of sufficient levels of thyroid hormone to maintain a normal metabolism

80
Q

hypothyroidism causes

A

-absense of thyroid gland
-lack of sufficient iodine in the diet to produce needed levels
-lack of sufficient functioning thyroid tissue due to tumor or autoimmune
-lack of TSH due to pituitary disease
-lack of TRH related to tumor or hypothalamus disorder

81
Q

treatment of hypothyroidism

A

-levothyroxine: synthetic salt of T4
-thryoid desicated: prepare from dried animal thryoid glands and contains both T3 and T4
-liothyronine: synthethic salt of t3

82
Q

treatment of hypothyroidism nursing interventions

A

-instruct the client to take on an empty stomach 30-60 minutes before breakfast (do not take w other meds)
-client with need of life long replacement of thyroid hormone

83
Q

hypothyroidism treatments adverse effects

A

-symtoms of hyperthyroidism
-cardiac stimulation: dysrythmias, and hypertension
-CNS effects: anxiety sleeplessnes, headache

84
Q

hyperthyroidism

A

-excessive amounts of thyroid hormones are produced and released into circulation

85
Q

hyperthyroidism cause

A

graves disease

86
Q

hyperthyroidism S/S

A

-increased body temp, intolerance to heat
-tachycardia
-thin skin
-palpitations
-hypertension
-flushing
-nervousness
-amenorrhea
-weight loss, increased appetite
-goiter (enlarged thyroid gland)

87
Q

hyperthyroidism treatment

A

-thioamides: propylthiouracil, methimazole,
-Iodine solutions: sodium iodine i 131, i 123 OR potassium iodine

88
Q

hyperthyroidism treatment actions

A

thioamides: prevent formation of thyroid hormone within the cells, lowe4ring the serum level, partially inhibit conversion of t4 to t3
iodine solutions: high doses cause the thyroid cells to become oversaturated with iodine and stop producing the hormones

89
Q

hypertyroidism treatment adverse effects

A

thioamides: drowsiness, lethargy, bradycardia
-PTU is associated with nausea, vomiting, GI, and severe liver toxicity
-methimazole is associated with bone marrow suppression CBC NEED OFTEN
iodine solutions: hypothyroidism (will need thyroid replacement for life)
-iodism is a metallic taste and burning in the mouth, sore teeth and gum, diarrhea, cold symtoms, and stomach upset
-development of goiter

90
Q

anti-hypercalcemic agents actions: bisophosphonates

A

-aledronate, pamidronate, ibadronate
-act on serum levels of calcium and not directly on the parathyroid gland or PTH
-act to slow or block bone reabsorption, thereby lower serum calcium levels
-used in prevention and treatment of postmenopausal osteroporosis and glucocorticoid osteoporosis

91
Q

anti-hypercalcemic agents actions: calcitonins

A

-hormone secreted by the thyroid gland to balance the effects of PTH, inhibits bone reabsorption
-increase the excretion of phosphate, calcium, and sodium from the kidneys
-used in emergency treatment of hypercalcemia, and Paget disease

92
Q

glucose regulation: insulin

A

-hormone produced by beta cells of the islets of Langerhans that is
released into circulation when levels of glucose around these cells rise and in response to incretins
-stimulates glycogen (glucose stored for immediate release during times of stress or low glucose) synthesis, conversion of proteins from amino acids
-released after meals in response to incretin release and when blood glucose levels rise, causing blood glucose levels to fall

93
Q

glucose regulation: glucagon

A

-released from alpha cells into islets of langerhans in response to low blood glucose levels
-caused immediate mobilization of glycogen stored in the liver and raised blood glucose levels

94
Q

classifications of diabetes mellitus

A

Type 1- insulin-dependent
-generally caused by autoimmune destruction of beta cells of the pancreas causing a lack of insulin requiring insulin replacement

95
Q

type 2 non-insulin dependent

A

-occurs in mature adults
-progressive loss of beta cell release of insulin as well as decreased insulin sensitivity in the peripheral cells (insulin resitance)

96
Q

gestational diabetes

A

-2-3rd trimester

97
Q

hyperglycemia S/S

A

-fatigue, lethargy, weakness, irritation, glycosuria, polyphagia, polydipsia, polyuria, itchy skin, can progress to diabetic ketoacidosis

98
Q

hypoglycemia S/S

A

-blood glucose less than 70
-fatigue and weakness
-blurred vision or diplopia
-tachycardia and palpitations
-rapid, shallow respirations
-nausea
-diaphoresis, cool and clammy skin

99
Q

insulin

A

-a hormone that promotes the storage of the bodys fuels
-stimulates the synthesis of glycogen from glucose
-reacts with specific receptor sites on the cells for glucose utilization

100
Q

insulin indications

A

-treatment of type 1
-treatment of type2 in pateints whose diabetes cannot be controlled by other things

101
Q

regular insulin

A

short acting with onset of action 30-60 min and duration of 6-12 hours (used in treatment of diabetic ketoacidosis, only insulin that can be put IV)

102
Q

lispro insulin

A

short acting with onset of action less than 15 min but duration of 2-5 hours

103
Q

aspart insulin

A

short acting with onset 10-20min and 2-5 hour duration

104
Q

NPH insulin

A

long acting with onset 1-1.5 hour and duration 24 hours
-can be mixed w regulat–clear to cloudy

105
Q

glargine insulin

A

long acting with onset of action 60-70minutes and duration 24hours only once daily

106
Q

detemir insulin

A

long acting with onset of action 1-2 hours and duration of 5.7-23.3 hours

107
Q

insulin admin and storage

A

-rotate injection sites at least 1 in
-premixed insulin can be stored at room temp for 30 days after opening
-refigerate unopened prefilled vials until using them or until they have passed their expiration
-insulin that is premixed may be kept for 1-2 if they are refrigerated and kept in vertical position
-allow refigerated insulin to warm to room temp before injection

108
Q

sulfonylureas: first gen

A

associated with increase risk of CVD

109
Q

sulfonylureas: second gen

A

glimepiride, glipizide, glyburide (start w g end with -ide)

110
Q

sulfonylureas: indications

A

adjunct to diet and exercise to lower blood glucose in type 2

111
Q

sulfonylureas: actions

A

stimulate insulin release from functioning beta cells in the pancreas
-may improve binding to insulin receptors

112
Q

sulfonylureas: adverse effects

A

-hypoglycemia: take 30 minutes before meals
-nausea, vomitting, epigastric discomfort, heartburn, anorexia

113
Q

drug-drug interactions sulfonylureas

A

beta blockers- may mask the signs and symptoms of hypoglycemia

114
Q

Biguanide: metformin actions

A

decreases the production and increased the uptake of glucose, decreased hepatic glucose production, decreases intestinal absorption of glucose, improves insulin sensitivity of peripheral cells

115
Q

buguanide: indications

A

first-line standard care for type 2
-can also treat polycystic ovarian syndrome

116
Q

biguanide adverse effects

A

lactic acidosis- renal disease
-GI upset
-does not cause hypoglycemia
-take drug with meals

117
Q

Dipeptidyl peptidase-4 inhibitors

A

-linagliptin, saxagliptin, sitagliptin
-liptin

118
Q

DPP4 inhibitors actions

A

slow the breakdown of glucagon-like peptide which leads to increased insulin release, decreased glucagon release and slowed GI

119
Q

DPP4 inhibitors adverse effects

A

-acute pancreatitis,hypoglycemia,oral antidiabetic agents

120
Q

glucagon-like peptide 1 agonists

A

-dulaglutide- SQ every week
-liraglutide- SQ daily
-semaglutide- SQ weekly

121
Q

GLP1 agonists actions

A

increase insulin release, decrease glucagon release, slow GI emptying to allow more absorption of nutrients that will soon be absorbed, stimulate the satiety center in the brain to decrease desire to eat

122
Q

GLP1 agonists adverse

A

-pancreatitis
-hypoglycemia
-some are used for weight loss

123
Q

glucose elevating agents

A

-instruct client to take 15 grams of fast acting concentrated source of carbs (2-3 glucose tablets, 1 tube glucose gel, 1/2 cup juice)

124
Q

glucose elavating agents

A

raise the blood level of glucose when severe hypoglycemia occurs
-less than 40
-glucaon: 1mg SQ or IM
-hormone produced by alpha cells of the pancrease that stimulate liver breakdown of glycogen
-may take 20 min to gain consciousness
-adverse effects: nausea vomitting, turn patient onto side if unconscious
-dextrose 50% in water- 25-50 grams IV

125
Q

estrogens

A

-utilized are hormone replacement therapy when ovarian activity is blocked or absent and during menopause, treatment of ovarian failure, part of contraceptives, palliation for certain cancers with know estrogen receptor sensitivity
-estra/o’s

126
Q

estrogens contraindications

A

-breast cancer and estrogen dependent cancers
-history of thromboembolic disease, there is an increase risk of thrombus and embolism with orals

127
Q

estroens adverse effects

A

breakthrough bleeding, menstrual irregularities, dysmenorrhea, amenorrhea, changes in libido

128
Q

estrogens drug drug

A

nicotine increases clot risk

129
Q

oxytocics

A

stimulate uterine contractions to assist labor
-stimulate lacteal glands in the breast to contract promoting milk ejection
-used to prevent and treat uterine atony atony after delivery
-oxytocin (pitocin)
-severe water intox

130
Q

Androgens

A

testosteron, danazol, methyltestosterone
-CLASS 3 controlled subs

131
Q

androgens action

A

responsible for the growth and development of the male sex organs:
-increaser retention of nitrogen, sodium, potassium, and phosphorus- decrease urinar exretion of calcium
-increase protein anabolism and decreaase protein catabolism
-increase production of RBC

132
Q

androgens drug lab test interferences

A

-thyroid functon studies
-creatinine
-effects can last up to 2 weeks after discontinuation of androgens

133
Q

androgens cautions and adverse

A

hepatic dysfunction and cardiovascular disease
-acne, oily skin, hirsutism, deeping of voice
-edema weight gain
-altered electrolytes
-hepatocellular cancer
-innapropriate use of testosterone: CVD events

134
Q

androgens black box warning

A

-virilization in children who touch clothes or skin of man using the drug
-danazol: thromboembolic events, fetal abnormalities, hepatitis, intracranial hypertension

135
Q

erectile dysfunction

A

: the corpus cavernosum does not fill with blood to allow for penile erection
-ed can result for the aging process and in vascular and some nuerological conditions
drugs: prostaglandin and the afils that can also treat PAH

136
Q

ED: prostaglandins action

A

injected directly into the cavernosum
-acts locally to relac the vascular smooth muscle and promote blood flow into corpus cavernosim causing erection

137
Q

ED: PDE5 receptor inhibitors (afils)

A

selectively inhibit pde5 receptors causing a release of nitrous oxide leading to prolonged relaxation of smooth muscle and allowing blood flow to create erection

138
Q

ED: PDE5 receptor inhibitors (afils) adverse

A

headache and flushing
-priapism- very long erection
-8th cranial nerve toxicity and loss of hearing
-vision loss

139
Q

PDE5 inhibitors drug drug

A

-nitrates CV effects
-alpha adrenergic blockers: orthostatic hypo
-ketoconazole, itraconazole, erythromycin: priapism
-grapefruit

140
Q

ginkgo biloba: complemetary therapy

A

vascular dilation, increases blood flow to brain to improve cognitive function, can be used with alzheimers
-can cause seizures and should not be taken with anticoagulants, nsaids, or aspirin

141
Q

ginseng: complementary

A

aphrodisiac, mood elevator, antihypertensive, decreases cholesterol, lowers blood glucose
-avoid use with anticoags, aspirin, nsaids

142
Q

glucosamine: complementary

A

treatment of OA

143
Q

Saw palmetto

A

-benign prostatic hyperplasia
-do not use with finasteride or estrogen replacement

144
Q

st johns wort

A

treatment of depression, anti-inflammatory, antiviral
-try not to eat tyramine foods
-can cause thrombocytopenia, photosensitivites, SSRIS MAOIS

pharm (5 decks)

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