Quiz 2 Flashcards

1
Q

THYROID: levothyroxine [synthroid]

A

it is a synthetic form of T4 used to treat hypothyroidism which is then converted to T3 in the body
adverse effects: thyrotoxicosis, osteoporosis, atrial fibrillation
drug interactions: increases effects of warfarin, increases requirements of insulin or oral hypoglycemic agents, increases cardiovascular effects w/ adrenergics, increased thyroid replacement requirements w/ estrogen therapy, decreased absorption w/ bile acid sequestrants, decreased effect w/ Ca+ supplements, antacids, H2-receptor blockers, proton pump inhibitors
nursing implications: monitor height and development in infants and children, teach to take on empty stomach, frequent follow-up and lab monitoring [i.e. thyroid studies], educate pt. that they are going to be on these med.’s for the rest of their lives

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2
Q

THYROID: methimazole [tapazole]

A

action: used to treat hyperthyroidism by inhibits thyroid hormone synthesis [does not destroy existing stores of T.H.]
uses: first line drug for those w/ Graves’ diseases, ass an adjunct to radiation therapy, to suppress thyroid synthesis in prep. for thyroidectomy
adverse effects: agranulocytosis [reduction of granulocytes (WBC)]
nursing implications: educate pt. to report s/s of infections

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3
Q

THYROID: propylthiouracil [PTU]

A

action: used to treat hyperthyroidism by suppressing synthesis of thyroid hormones and blocking conversion of T4 to T3
uses: safe for preg. women in 1st trimester, safe for breast-feeding women, those experiencing thyroid storm, those w/ intolerance’s to methimazole

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4
Q

THYROID: beta blockers

A

action: used to treat hyperthyroidism by suppressing tachycardia and other sx’s of Graves’ disease
uses: those w/ thyrotoxic crisis
adverse effects: bronchodilation, decreases heart rate, increases force of heart contraction

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5
Q

DIABETES MELLITUS: type I diabetes

A

or absolute insulin deficiency
it is failure of the beta cells in the pancreas to produce insulin
5-10% of diabetics have type I and is usually seen in those under the age of 40 and over the age 20
causes: genetics [recessive], toxins, virus
s/s: DKA, polyuria, polyphagia, polydipsia
tx: requires exogenous insulin

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6
Q

DIABETES MELLITUS: type II diabetes

A

or relative insulin deficiency
it is a resistance to insulin that the body builds up despite the pancreas manufacturing insulin
- resistance can be caused by an insufficient # of receptors or receptor unresponsiveness t insulin
90-95% of diabetics have type II and is usuall seen in Nat. Ame.’s and Hispanics, those under the age of 35
causes: genetics [dominant], env’t., lifestyle, obesity, multi-factorial
s/s: HHNK, hyperglycemia, hyperinsulinemia, polyuria, polydipsia, fatigue, visual changes, prolonged healing times, metabolic syndrome

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7
Q

DIABETES MELLITUS: metabolic syndrome

A

it is a cluster of abnormalities working synergistically to greatly increase the risk for cardiovascular disease and diabetes which include:
- elevated insulin levels [insulin resistance]
- high triglycerides
decreased HDL, increased LDL
- hypertension
- obesity
- sedentary lifestyle
estimated 34% of American’s fit the criteria
tx: weight loss [via a healthy diet and exercise

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8
Q

DIABETES MELLITUS: sulfonylureas

A

it is a type of oral hypoglycemic drug
action: actively drives blood glucose down by promoting insulin release and by decreasing tissue response to insulin
prototype: glipizide [glucatrol]
adverse effects: hypoglycemia
drug interactions: sulfa allergies can cause cross rx’s, alcohol produces disulfiram-like rx [flushing, palpitations, nausea], beta blockers mask the sx’s of hypoglycemia

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9
Q

DIABETES MELLITUS: glinides

A

it is a type of oral hypoglycemic drug
action: actively drives blood glucose down by increasing the release of insulin from the pancreas
prototype: repaglinide [prandin]
adverse effects: hypoglycemia

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10
Q

DIABETES MELLITUS: thiazolidinediones

A

it is a type of oral hypoglycemic drug
action: actively drives blood glucose down by decreasing insulin resistance and by decreasing glucose production by liver
prototype: pioglitazone [actos]
adverse effects: fluid retention, elevation of lipid levels, hypoglycemia

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11
Q

DIABETES MELLITUS: biguanide

A

it is a type of oral hypoglycemic drug
action: effects the rise in glucose after a meal by inhibiting glucose production in the liver, by slightly reducing absorption in GI tract and by sensitizing insulin receptors in target tissues [increases the cells ability to take in glucose whenever insulin is present]
prototype: metformin [glucophage]
adverse effects: GI disturbance, vit. B12 and folic acid deficiency, weight loss, lactose acidosis [s/s: hyperventilation, myalgia, malaise, lethargy]
drug interactions: alcohol increases lactic acid, IV contrast dy containing iodine can cause acute renal failure [:. D/C ac exam and hold pc exam]

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12
Q

DIABETES MELLITUS: alpha-glucosidase inhibitors

A

it is a type of oral hypoglycemic drug
action: effects the rise in glucose pc a meal by delaying absorption of dietary CHO, by inhibiting enzyme alpha-glucosidase] that breaks down complex CHO to simple CHO, and by decreasing post-prandial rise in blood glucose
prototype: acarbose [precose]
adverse effects: flatulence, cramps, abdominal distention, diarrhea, liver dysfunction

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13
Q

DIABETES MELLITUS: gliptins

A

it is a type of oral hypoglycemic drug
action: enhances activity of increntin hormones [increases insulin release and decreases glucagon] and decreases hepatic glucose production
prototype: sitagliptin [januvia]
adverse effects: pancreatitis, hypersensitivity rx’s

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14
Q

DIABETES MELLITUS: glucagon

A

used as a tx for hypoglycemia
this hormone is produced by alpha cells of the pancreas that breaks down glycogen stores [opposite effects of insulin]
can be given as a substitute for IV glucose for pt.’s /o a access line as it can be given IM, SQ, and IV
it cannot correct hypoglycemia caused by starvation

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15
Q

THYROID: thyroid physiology

A

its function is the production, storage and release of T4 [thyroxine] and T3 [triiodothyronine]
- the pituitary gland releases TSH which prompts the thyroid gland to release its hormones
iodine is necessary for T4 and T3 hormone production
- too little or too much will cause the thyroid to not produce the hormones
T4 and T3 affects metabolic rate, growth and development, CHO and lipid metabolism
the thyroid gland also produces and releases calcitonin in response to high levels of Ca+ in the blood
- this is done by inhibiting resorption of bone out of the blood, increasing Ca+ in the bone, and increasing renal excretion of Ca+

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16
Q

THYROID: thyroid function tests

A
TSH
serum T4 and T3
ultrasound [for nodules]
thyroid scan
radioactive iodine uptake
- there is a tracer that is introduced and absorbed into a pt.'s blood; using a probe, this test show how much tracer is absorbed by the thyroid gland and if it is evenly spread in the gland
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17
Q

THYROID: hypothyroidism

A

causes: those w/ Hashimoto’s thyroiditis, tx for hyperthyroidism, thyroid surgery, radiation therapy, med.’s
s/s: weight gain, bradycardia, decreased B.P., fatigue, intolerance to cold, elevated TSH, decreased resp.’s
tx: mechanical ventilation, IV thyroid suplements, isotonic fluids [unless presenting w/ hyponatremia then give a hypertonic sol’n.], IV glucose

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18
Q

THYROID: hyperthyroidism

A

s/s: weight loss, increased appetite, diarrhea, fatigued, diaphoresis, tachycardia, hypertension, exopthalmia [protect the eyes]
tx: drug therapy [anti-thyroid drugs, iodine (forces T4 and T3 to leave the blood and go into storage), B-adrenergic blockers (decreases blood pressure and the heart rate), sedatives, insulin, O2], radioactive iodine therapy, surgical therapy

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19
Q

ANALGESICS: what is the diff. b/w analgesic and anesthetics?

A

analgesics are drugs that relieve pain W/O CAUSING LOSS OF CONSCIOUSNESS
anesthetics are drugs that PRODUCE UNCONSCIOUSNESS and insensitivity to painful stimuli

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20
Q

ANALGESICS: tolerance

A

a state in which a larger dose is required to produce the same response

21
Q

ANALGESICS: physical dependence

A

a state in which an abstinence syndrome will occur if drug use is abruptly D/C
the half-life of the opioid used and the degree of physical dependence will affect the intensity and duration of the abstinence syndrome

22
Q

ANALGESICS: addiction

A

a DISEASE PROCESS characterized by the continued use of a specific psychoactive substance despite physical, psychologic, or social harm
ADDICTION IS NOT EQUATED W/ PHYSICAL DEPENDENCE
physical dependence can contribute to addictive behavior, however, it is not necessary nor sufficient for addiction to occur

23
Q

ANALGESICS: drug schedules

A

schedule I: no accepted medical use
schedule II: drugs w/ high abuse risk but w/ medical purpose
- this is where opioids fall
schedule III, IV: abuse risk less dangerous than II
schedule V: considered least dangerous for abuse

24
Q

ANALGESICS: morphine

A

it is a strong opioid agonist
action: analgesia, SEDATION, EUPHORIA MENTAL CLOUDING, sense of well-being, miosis [pupil constriction], resp. depression, cough suppression, bowel motility suppression
uses: post-op. pain, pain of labor and delivery, chronic pain, M.I. [vasodilation to promote venous return to heart], pre-op. [sedation, reduction of anxiety]
adverse effects: constipation, urinary hesitancy/retention, RESP. COMPLICATIONS [i.e. cough suppressant; problematic w/ post-op. pt.’s b/c we want to encourage oxygenation via breathing], depression of fetal resp. and uterine contraction, elevation of intracranial pressure [decreased resp. -> CO2 narcosis -> cerebral vasculature dilation -> increased ICP], euphoria/dysphoria [usually seen in pt.’s given this drug for non-pain related conditions], miosis [pupil constriction], neurotoxicity [may lead to coma], orthostatic hypotension
drug interactions: CNS depressants cause resp. depression, anticholinergics causes constipation, urinary retention, hypotensive drugs cause hypotension, toxicity may cause coma

25
Q

ANALGESICS: methadone

A

it is a strong opioid agonist
uses: ease of withdrawal and prevents regression back to opioid-use
adverse effects: fatal dysrhythmias [b/c of prolongation of QT interval]
nursing interventions: combine w/ non-drug measures directed at altering drug-abuse patterns to boost effect of therapy

26
Q

ANALGESICS: other strong opioid agonists

A

fentanyl- more potent than morphine
meperidine [demerol]- should not be given for more than 48 hours and at a specific schedule to prevent development of toxic metabolite
hydromorphone [dilaudid]- causes less nausea than morphine
heroin -schedule I drug in U.S.

27
Q

ANALGESICS: codeine

A

it is a moderate to strong analgesic
action: produces less analgesia and resp. depression than morphine and has a lower potential for abuse
uses: cough suppressant
drug interactions: analgesia increases effects

28
Q

ANALGESICS: buprenorphine [subutex]

A

it is a partial analgesic agonist
action: alleviates craving, decreases resp. depression
uses: maintenance therapy, facilitates detox.
adverse effects: withdrawal
drug interactions: will decrease effect when taken w/ pure opioid agonist’s

29
Q

ANALGESICS: naloxone [narcan]

A

it is an opioid antagonist
action: acts as antagonists at mu and kappa receptors which block the opioids, does not cause analgesia
uses: reversal of resp. and CNS depression caused by overdose w/ opioid, reversal of post-op. opioid effects, management of opioid addiction, treats itching from PCA opioid analgesics
adverse effects: toxicity -> withdrawal

30
Q

ANALGESICS: tramadol [ultram]

A

it is a non-opioid analgesic
action: weak agonist activity at mu opioid receptors, blocks uptake of norepi. and serotonin
uses: for moderate to moderately severe pain
adverse effects: seizures

31
Q

ANALGESICS: opioid withdrawal

A

in highly dependent individuals, sx start 10 hr.’s after last dose and runs its course in 7-10 days
early response: yawning, rhinorrhea, sweating, anorexia, irritability, tremors, piloerection
peak responses: sneezing, weakness, N.V.D., abd. cramps, bone and muscle pain, muscle spasms, kicking movements
administration of opioids will abruptly arrest sx
physical dependence is rarely a complication when opioids are taken acutely [BID or TID for 2 weeks]

32
Q

ANALGESICS: PCA pumps

A

or patient controlled analgesia pumps
pt. self-administers opioids on “as needed basis”
most frequently used w/ post-op. pt.’s
they work by delivering a preset bolus dose to provide continuous basal infusion and it is time-controlled

33
Q

ANESTHETICS: principles of idealness

A

produce unconsciousness, analgesia, muscle relaxation, and amnesia
induction and emergence would be brief and pleasant
depth would be raised or lowered w/ ease
adverse effects would be minimal
large margin of safety

34
Q

ANESTHETICS: balanced anesthesia

A

use of a combo of drugs to accomplish what we cannot achieve w/ an inhalation anesthetic alone
compensates for lack of an ideal anesthetic
allows for full general anesthesia at lower [safer] doses

35
Q

ANESTHETICS: general anesthesia

A

produces unconsciousness and lack of responsiveness to all painful stimuli

36
Q

ANESTHETICS: local anesthesia

A

do not reduce consciousness

blunts sensation in a limited area

37
Q

ANESTHETICS: neuromuscular blocking agents [NMB]

A

interferes w/ nicotinicM receptor activation
causes muscle relaxation but does not reduce consciousness or pain
works either by:
- depolarizing: binds w/ nicotinicM receptor causing depolarization leading to a transient muscle contraction, remains bound and prevents end-plate from repolarizing which causes a state of constant depolarization [paralysis]
- competitive: blocks Ach from binding to nicotinic receptors

38
Q

ANESTHETICS: med.’s used for balanced anesthesia

A
propofol and short-acting barbituates [pentothal]
- for rapid induction
neuromuscular blocking agents
- for muscle relaxation
opioids and nitrous oxide
- provides analgesia
39
Q

ANESTHETICS: inhalant anesthesia [mechanism of action]

A

may work via selective alteration of synaptic transmission
nearly all agents used today [except nitrous oxide] enhance activation of receptors for GABA, the principle inhibitor transmitter in the CNS
drugs promote generalized inhibition of CNS function

40
Q

ANESTHETICS: inhalant anesthesia [adverse effects]

A

resp. depression
cardiac depression, dysrhythmias
- b/c some anesthetics can increase sensitivity of heart to stimulation of catecholamines [epi. and norepi.]
malignant hyperthermia
- fatal rx that causes muscle rigidity and an increase in body temp. to > 106o F
- there’s a genetic predisposition
- the greatest risk is when inhalation anesthetic is combined w/ succinylcholine
aspiration of gastric contents
- suppressed reflexes that prevent aspiration of gastric contents
hepatotoxicity, toxicity to operating room personnel

41
Q

ANESTHETICS: inhalant anesthesia [types]

A

volatile liquids or “-fluranes”
- liquid state, easily converted to vapor
- rapid induction time, easy to adjust, rapid emergent time
- can cause resp. depression, hypotension
nitrous oxide or “laughing gas”
- is used as an adjunct in balanced anesthesia [can be given w/ volatile liquid]
- cannot produce surgical anesthesia alone
– :. it is a powerful analgesic but a weak anesthetic
- blocks the action of NMDA, an excitatory neurotransmitter by binding w/ NMDA receptor and thereby prevents receptor activation by NMDA itself

42
Q

ANESTHETICS: adjuncts to inhalation anesthesia

A
benzodiazepines
- reduces anxiety and promotes amnesia
- given to induce anesthesia or for conscious sedation
- i.e. midazolam [versed]
opioids
- pain relief, cough suppressant
alpha-2 adrenergic agonist
- reduces anxiety and causes sedation
- i.e. clonidine [catapres]
anticholinergic drugs
- given to decrease risk of bradycardia during surgery 
- parasympathetic stimulation can occur w/ surgical manipulation resulting in severe bradycardia
- i.e. atropine
neuromuscular blocking agents
- i.e. succinylcholine
43
Q

ANESTHETICS: succinylcholine

A

it is a neuromuscular blocking agent
action: works by depolarization of nicotinicM receptor
uses: endotracheal intubation, endoscopy, short procedures
adverse effects: hyperkalemia [promote release of K+ from the tissues], malignant hyperthermia [when combined w/ other inhalation anesthetic]

44
Q

ANESTHETICS: propofol [diprivan]

A

it is an IV anesthetic
- may be used alone or to supplement the effects of inhalation agents
- when combined w/ inhalation agents they permit dosage of the inhalation agent to be reduced and they produce effects that cannot be achieved w/ an inhalation agent alone
action: rapid loss of consciousness
adverse effects: N/V, profound resp. depression, hypotension, high risk of bacterial infection [since it is a lipid-based drug]

45
Q

ANESTHETICS: lidocaine [xylocaine]

A

it is a local anesthetic
action: they suppress pain by blocking impulse conduction along axons located near the site of administration
uses: infiltration anesthesia, nerve blocks, spinal and epidural blocks, antidysrhythmic agent
adverse effects: CNS agitation followed by depression [seizures, lethargy, coma], suppression of excitability of the heart [bradycardia, heart block, decreased force of contraction cardiac arrest], vasodilation [hypotension], allergic rx’s, labor prolongation of labor and delivery
nursing implications: monitor for cardiovascular status, resp. function, and LOC; equip room w/ resuscitation equip’t., careful to not inject in artery or vein [causes toxicity]

46
Q

DIABETES MELLITUS: rapid acting insulin

A

i. e. lispro [humalog], aspart [novolog]
onset: 10-30 min.
peak: 30 min.-3 hr.
duration: 3-5 hr.

47
Q

DIABETES MELLITUS: short-acting insulin

A

i. e. regular [humalin R, novolin R]
onset: 30 min.-1 hr.
peak: 2-5 hr.
duration: 5-8 hr.

48
Q

DIABETES MELLITUS: intermediate-acting diabetes

A

i. e. NPH [humalin N, novolin N
onset: 1.5-4 hr.
peak: 4-12 hr.
duration: 12-18 hr.

49
Q

DIABETES MELLITUS: long-acting insulin

A
i.e. glargine [lantus], detemir [levemir
this can not be mixed w/ any other form of insulin
onset: 0.8 -4 hr.
peak: no pronounced peak
duration: 24+ hr.