Exam 2 Flashcards

1
Q

rapid acting insulin (lispro)

A

onset: 15 mins
peak: 1 hour
duration: 2-4 hours

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2
Q

regular insulin (short acting)

A

onset: 30-60 mins
peak: 2-6 hours
duration: 3-8 hours

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3
Q

intermediate insulin (NPH)

A

onset: 2-4 hours
peak: 4-10 hours
duration: 10-20 hours

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4
Q

long acting insulin (glargine)

A

onset: 70 mins
peak: NONE
duration: 24 hours

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5
Q

regulating glucose depends on the

A

liver
-extracts glucose
-synthesizes it into glycogen (energy storage)
-glycogenolysis (breakdown glycogen)

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6
Q

pancreas

A

controls body’s fuel supply (glucose/insulin)
2 major functions:
-exocrine: pancreatic cells secrete directly into ducts NOT bloodstream
-endocrine: cells secrete INSULIN directly into blood stream

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7
Q

islet of langerhans

A

pancreatic islets are small islands of cells within the pancreas that make up the endocrine function

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8
Q

alpha cells

A

secrete glucagon in response to low blood sugar
-glucagon stimulates the liver to release stored glucose into the blood

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9
Q

beta cells

A

produce insulin, which lowers glucose levels by stimulating the movement of glucose into body tissues

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10
Q

hormones that RAISE blood glucose levels

A

-glucagon (islet of langerhans)
-epinephrine (adrenal medulla and other chromafin tissues)
-glucocorticoids (adrenal cortex)
-growth hormone (anterior pituitary)

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11
Q

insulin

A

-hormone secreted by the pancreas (beta cells)
-stimulates uptake, utilization, and storage of glucose
-stimulates the liver to store glucose (as glycogen)

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12
Q

polyphagia

A

increased hunger
-catabolism of fat and protein and cellular starvation

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13
Q

polydipsia

A

excessive thirst
-increased serum osmolality

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14
Q

polyuria

A

excessive urination
-osmotic diuresis, excreting water, loss of electrolyte

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15
Q

somogyi effect

A

overdose of insulin causes hypoglycemia and counter regulatory mechanisms cause hyperglycemia and ketosis
-bc poor diabetes management, must talk about ways to fix it

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16
Q

dawn phenomenon

A

hyperglycemia in the morning due to natural hormonal release
-don’t do anything

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17
Q

glipizide and glyburide are what class of meds

A

sulfonylureas

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18
Q

adipose tissue

A

provides insulation and mechanical support for the body
-secretes hormone-like molecules=adipokines
-contributes to immune cell function

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19
Q

adipocytes

A

fat-storing cells
-store calories as triglycerides
-can increase in number and HYPERTROPHY to increase fat mass

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20
Q

adipokines

A

secreted by adipose tissue (ENDOCRINE organ)
-cell-signaling proteins
-help regulate: appetite, food intake, energy expenditure, lipid storage, insulin secretion/sensitivity, etc

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21
Q

adiponectin

A

good adipokine
-inverse relationship with fat content in the body
-increased fat content=less adiponectin produced

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22
Q

what does adiponectin do

A

-increase energy expenditure
-enhance cell sensitivity to insulin
-anti-inflammatory effects
-protects against arteriosclerosis

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23
Q

leptin

A

good adipokine
-more fat, more leptin
-obese ppl become leptin resistant
-normally tells body that you’ve had enough to eat (satiety)
-works with adiponectin to increase insulin sensitivity, reduce triglyceride levels, and inhibit fat accumulation

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24
Q

glipizide class

A

sulfonylureas

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25
Q

glyburide class

A

sulfonylureas

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26
Q

sulfonylureas (glipizide and glyburide) MOA

A

binding and closing K-ATP channels in the pancreatic beta cells thereby stimulating secretion of insulin
-increase body’s sensitivity or response to insulin
-reduces the release of glucose from the liver

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27
Q

sulfonylureas (glipizide and glyburide) side effects

A

hypoglycemia (in pts with liver or kidney dysfunction)

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28
Q

sulfonylureas (glipizide and glyburide) nursing considerations

A

-do not take during pregnancy
-teach patients to avoid or limit ETOH, NSAIDS, Tagamet, sulfa-based abx taking these makes it more likely to experience side effect of hypoglycemia

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29
Q

metformin class

A

biguanides

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30
Q

biguanides (metformin) MOA

A

-lowers blood glucose by decreasing production of glucose in the liver
-enhances glucose uptake and utilization by muscle
-does not promote insulin release from the pancreas
-does not cause hypoglycemia

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31
Q

biguanides (metformin) side effects

A

-abdominal bloating, N/V/D, risk for acidosis in patients with elevated creatinine, do not use in patients with elevated ALT levels

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32
Q

biguanides (metformin) nursing considerations

A

-monitor serum glucose levels, give 30 minutes before meals
-must be held for 48 hours post IV contrast usage

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33
Q

linagliptin class

A

DPP4 inhibitor

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34
Q

sazagliptin class

A

DPP4 inhibitor

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35
Q

sitagliptin class

A

DPP4 inhibitor

36
Q

DPP4 inhibitors (-gliptin) MOA

A

inhibits DPP4, an enzyme that inactivates the incretin hormone

37
Q

DPP4 inhibitors (-gliptin) side effects

A

GI problems, N/V, stomach pain, flu-like symptoms, skin reactions, increased risk of pancreatitis

38
Q

dulaglutide class

A

GLP-1 receptor agonist

39
Q

exenatide class

A

GLP-1 receptor agonist

40
Q

semaglutide class

A

GLP-1 receptor agonist

41
Q

GLP-1 receptor agonist (-tide) MOA

A

-enhances glucose dependent insulin secretion
-stimulates glucose-dependent release of insulin, inhibits postprandial release of glucagon, and suppresses appetite
-slowed gastric emptying

42
Q

GLP-1 receptor agonist (-tide) side effects

A

-N/V/D, injection site reactions, headache, upper respiratory infections, weight loss

43
Q

GLP-1 receptor agonist (-tide) nursing considerations

A

-do not use for pts with history of pancreatitis
-black box warning: risk of thyroid c-cell tumors
-not recommended for people with ESRD or severe renal disease
-subq

44
Q

dapagliflozin class

A

SLG-2 inhibitors

45
Q

SLG-2 inhibitors (dapagliflozin) MOA

A

-prevents kidneys from reabsorbing glucose back into the blood
-kidneys lower BG, excess BG removed via urine

46
Q

SLG-2 inhibitors (dapagliflozin) side effects

A

-increased UTI risk, genital mycotic infections
-hypotension, fainting, dizziness, fatigue

47
Q

SLG-2 inhibitors (dapagliflozin) nursing considerations

A

-oral
-do not give to someone with ESRD or severe kidney disease
-only type 2

48
Q

orlistat is

49
Q

orlistat MOA

A

binds to gastric and pancreatic enzymes and BLOCKS these enzymes; reduces fat absorption by 30%

50
Q

orlistat side effects

A

-black box: liver injury
-GI symptoms: oily spotting, flatulence, and fecal incontinence…reduce by reducing fat intake to less than 30%
-decreases vitamin concentrations…MUST TAKE multi-vitamin with this medication

51
Q

orlistat nursing considerations

A

-MUST TAKE FOR 3 MONTHS TO START SEEING EFFECT

52
Q

glucagon

A

hypoglycemia antidote

53
Q

glucagon MOA

A

activates hepatic glucagon receptors, stimulates glycogenolysis and release of glucose
-check finger stick 15 minutes post

54
Q

donepezil class

A

cholinesterase inhibitors

55
Q

cholinesterase inhibitors (donepezil) MOA

A

-works centrally in the brain to increase levels of acetylcholine by inhibiting acetylcholinesterase

56
Q

cholinesterase inhibitors (donepezil) side effects

A

-normally none to mild, resolve on their own
-GI upset, drowsy, dizzy, insomnia, muscle cramping
-bradycardia, reflex tachycardia, syncope
-PO at bedtime, best with food

57
Q

cholinesterase inhibitors (donepezil) nursing considerations

A

-patients forgetful, must have some way to ensure patient is taking medications

58
Q

memantine class

A

NMDA receptor antagonist

59
Q

NMDA receptor antagonist (memantine) MOA

A

-blocks stimulation of NMDA receptors believed to be associated with AD

60
Q

NMDA receptor antagonist (memantine) side effects

A

-uncommon
-confusion, hypotension, headache, dizziness, CONSTIPATION

61
Q

tramadol class

A

centrally acting analgesic

62
Q

centrally acting analgesic (tramadol) MOA

A

-binds weakly to mu opioid receptors
-inhibit reuptake of norepi and serotonin

63
Q

side effects of centrally acting analgesic (tramadol)

A

-usually none
-drowsy, dizzy, headache, nausea, constipation, respiratory depression
-rare: seizures when combined with other CNS depressants

64
Q

gabapentin class

A

anti-convulsants

65
Q

pregablin class

A

anti-convulsants

66
Q

anticonvulsants (gabapentin and pregablin) MOA

A

-unknown, but thought to spontaneously suppress neuronal firing-pain
-to complement effects of opioids
-used specifically for neuropathic pain

67
Q

anticonvulsants (gabapentin and pregablin) side effects

A

-drowsy, dizzy, visual problems
-can only be partially reversed with Naloxone
-NEUROPATHIC PAIN

68
Q

aspirin, ibuprofen, naproxen, ketolorac, celecoxib class

69
Q

NSAIDS MOA

A

-anti-prostaglandins
-decreased prostaglandins by blocking key enzyme cyclooxygenase (COX) (an enzyme crucial to production of prostaglandins)
-COX-1 & COX-2

70
Q

NSAIDS side effects

A

NON-SELECTIVE COX:
-GI upset, stomach ulcers, GI bleeding, rash, edema, kidney failure, increase in BP, inhibits platelet aggregation, SOA in asthma patients
SELECTIVE COX-2 INHIBITORS:
-GI mucosa still protected, and platelet function not impacted
-no impact/effect on platelets
-SERIOUS CARDIOVASCULAR THROMBOTIC EVENTS
-cardiovascular and GI risk black box warnings

71
Q

acetaminophen MOA

A

-unknown
-decreases prostaglandin synthesis in the CNS possibly

72
Q

acetaminophen side effects

A

-with normal doses hardly any
-large amounts hepatic necrosis (acute), LIVER FAILURE with chronic-long term use, and mild nephropathy
-potentially lethal when overdosed
-hepatotoxicity-ceiling effect
-NO-ANTI-INFLAMMATORY properties
-look for jaundice, elevated LFTs, creatinine levels
-adult dose restriction: 4 g/24 hrs

73
Q

morphine MOA

A

-mu agonist mimics the action of endogenous opioids at the mu receptors

74
Q

morphine side effects

A

-respiratory depression
-CNS depression
-constipation
-drowsiness/fatigue
-confusion, dry mouth, itching -assess LOC, BP, pulse, RR

75
Q

when to use hydromorphone

A

SEVERE PAIN

76
Q

when to use fentanyl

A

-moderate to severe pain
-surgical induction
-chronic pain
-EXTREMELY POTENT

77
Q

when to use merperidine

A

-moderate to severe pain
-weaker than morphine and shorter duration of action
-less respiratory depression
-LOTS of drug/drug interactions -CNS stimulations=seizures DO NOT USE WHEN MULTIPLE DOSES NEED TO BE GIVEN

78
Q

when to use codeine

A

-mild-moderate pain, reduce coughing
-not for children under 18 related to life threatening breaking problems

79
Q

oxycodone

A

-moderate to severe pain
-10x more potent than codeine

80
Q

hydrocodone

A

-mild-moderate pain and cough relief
-cough suppressant
-6x more potent than codeine

81
Q

methandone

A

-choice for detoxification treatment in opioid addiction
-longer half-life

82
Q

naloxone

A

-opioid antagonist
-antidote to reverse effects of morphine
-abrupt reversal of opioid effects with RECURRENT PAIN, increased BP

83
Q

phenytoin class

A

hydantoins

84
Q

phenytoin uses

A

tonic-clonic and partial seizures

85
Q

valproic acid

A

-absence, myoclonic, and tonic-clonic seizures
-highly protein bound
-contraindicated for liver disease and urea cycle disorders
-adverse effects: hepatotoxicity, pancreatitis

86
Q

topiramate

A

adjunct therapy for partial and secondary generalized seizures, tonic-clonic
-side effects: general CNS depression, GI upset, watch for visual changes
-can interact with contraceptives

87
Q

levetiracetam

A

indicated for adjunct therapy for partial seizures with and without generalization