Diabetes/Endocrine (Module 3) Flashcards

1
Q

Type 1 Diabetes

A

AUTOIMMUNE

pancreas doesn’t secrete insulin by beta cells
w/o insulin, DKA and severe metabolic disturbances can develop

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2
Q

Type 2 Diabetes

A

insulin resistance/secretory deficit with insulin deficiency

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3
Q

Polydipsia Symptoms

A

loss of skin turgor, skin warm and dry
dry mucous membranes
weakness/malaise
rapid weak pulse and hypotension

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4
Q

Polyphagia

A

excessive hunger and eating caused by inability of cells to receive glucose because of lack of insulin or cellular resistance to insulin and body use of protein and fat for energy (causes ketosis)

weight loss
ketones in blood due to breakdown of fatty acids when insulin isn’t available, metabolic acidosis

kussmauls respirations

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5
Q

Kussmauls Respirations

A

increased RR and depth in an attempt to excrete CO2 and acid due to metabolic acidosis (r/t ketones; see also protein in urine)

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6
Q

Diabetes Risk Factors

A

insulin resistance
metabolic syndrome (Syndrome X, Insulin-resistance syndrome) obesity, sedentary lifestyle, HTN, elevated cholesterol and triglycerides, cardiovascular disease

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7
Q

Fasting Blood Glucose Test

A

levels >100 mg/dL but less than <126 indicate impaired fasting glucose (IFG)

levels >126 mg/dL obtained in at least 2 occasions

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8
Q

Glucose Tolerance Test (2hr postload result)

A

levels >140 mg/dL (7.8 mmol/L) and <200 mg/dL indicate impaired glucose tolerance

levels >200 mg/dL (11.1 mmol/L) indicate diagnosis

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9
Q

Glycosylated Hemoglobin (A1C) Test

A

levels of 5.7-6.4% indicate prediabetes

levels >6.5% indicate diabetes
levels >8% indicate poor diabetes control and need for changes in therapy

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10
Q

Labs and Diagnostics

A

blood glucose
gylcosated hemoglobin A1C (HgbA1C)
urine ketones

duloxetine for peripheral neuropathy

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11
Q

Lispro, Aspart and Glulisine

A

RAPID INSULIN; SQ WITHIN 15 MIN OF MEALTIME

15 min onset
1-2 hr peak
half life 80 min.; duration 3-5 hrs

can give with NPH, draw lispro up first, give inmed

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12
Q

Isophane (NPH)

A

INTERMEDIATE; SQ MIX CLOUDY

1-2 hr onset
4-8 hr peak
10-18 hr duration (monitor for issues 9hr after admin)

can mix with aspart, lispro, reg.; DONT MIX WITH GLARGINE

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13
Q

Regular (Humulin R, Novolin R)

A

SHORT ACTING; SQ 30-60 MIN BEFORE MEAL; IV

30-60 min onset
2.5 hr peak
6-10 hr duration

CAN MIX WITH NPH, sterile water, NS; DO NOT MIX WITH GLARGINE

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14
Q

Detemir (Levemir)

A

LONG ACTING INSULIN; SQ (1/day or 2/day, same time each day)

gradual onset
6-8 hr pear
up to 24 hr duration

DONT MIX WITH ANY OTHER INSULIN

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15
Q

Glargine (Lantus)

A

LONG ACTING INSULIN; SQ, 1/day or 2/day, same time each day

1-2 hr onset
no peak
24 hr duration

DONT MIX WITH OTHER INSULIN

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16
Q

Lipoatrophy

A

loss of subQ fat around the site of repeated insulin injections, a rare complication of insulin therapy causing erratic insulin absorption

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17
Q

Insulin Patient Education

A

refrigerate insulin not in use; may be kept at room temp for up to 28 days to reduce injection site irritation from cold insulin; DONT FREEZE

store prefilled syringes in upright position, needle pointing upward

roll prefilled syringes between hands before using

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18
Q

Oral Hypoglycemics (Biguanides/Glucophage (metformin))

A

reduces insulin resistance, decreases sugar production in liver and should be taken with meals for best absorption and effect; decreasing intestinal absorption of glucose

DONT DRINK ALCOHOL TO REDUCE RISK FOR LACTIC ACIDOSIS
MUST BE DISCONTINUED 48 HRS BEFORE AND AFTER CONTRAST TESTING DUE TO INCREASED RISK OF KIDNEY DAMAGE AND LACTIC ACIDOSIS

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19
Q

DM Nursing Care

A

diet (AVOID ALCOHOL; CAN POTENTIATE HYPOGLYCEMIA)
WATER exercise
foot care
sick days

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20
Q

DM Complications

A

cardiovascular and cerebrovascular disease (HTN)
diabetic retinopathy (impaired vision and blindness)
diabetic neuropathy and nephropathy
sexual dysfunction
hyper/hypoglycemia
dawn phenomenon
somogyi phenomenon

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21
Q

Dawn Phenomenon

A

hyperglycemia in the AM (2-3 am)

caused by nighttime release of adrenal hormones because pt doesn’t have nighttime insulin prescribed or not enough

treated by adding intermediate insulin at 10pm or raise dose

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22
Q

Somogyi Phenomenon

A

nocturnal hypoglycemia followed by a marked increase in glucose and increase in ketones

hyperglycemia in the AM caused by rebound effect of nighttime hypoglycemia

treated by lower 10 pm dose or ensure adequate snack with 10 pm dose or evaluate exercise program

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23
Q

Hypopituitarism

A

deficiency of 1+ more anterior pituitary hormones resulting in metabolic problems, sexual dysfunction

selective hypopituitarism is most common where only one hormone is deficient, opposite of panhypopituitarism

deficiency of gonadotropins (sexual characteristics); GH stimulates liver to produce somatomedins that enhance growth activity

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24
Q

Life-Threatening Deficiencies

A

adrenicorticotropic hormone (ACTH) and TSH
because both deficiencies effect hormones vital for balanced metabolism

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25
Q

Gonadotropin (LH and FSH)

A

loss of sexual characteristics (facial hair, decreased libido, impotence, amenorrhea, infertility, breast atrophy, painful intercourse, decrease of axillary/pubic hair)

neurologic changes (loss of visual acuity esp. peripheral vision, temporal headaches, diplopia, ocular muscle paralysis, limiting eye movement)

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26
Q

Hypopituitarism Diagnostics Testing

A

blood levels of pituitary hormones
hormone stimulation testing
CT scan of head
MRI of head
angiography of brain

lab assessment measures effects of hormones rather than actual hormone levels (ex. T3 and T4 for thyroid function)

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27
Q

Hypopituitarism Management

A

lifelong replacement of deficient hormones; human growth hormone injections SQ

Gonadotropin: androgen therapy for virilization (gynecomastia, acne, baldness, prostate enlargement SE)..contraindicated w/prostrate cancer; HRT (DVT and HTN SE)

TSH AND ACTH are replaced with thyroid hormone and cortisol

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28
Q

Hyperpituitarism

A

pituitary tumors or tissue hyperplasia; GH, prolactin, ACTH

pituitary adenoma (prolactin secreting benign tumors) most common (decreases in normal lvl of sex hormones, loss of libido, infertility and spontaneous milk flow, HA, visual changes, increased ICP)

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29
Q

Gigantism

A

GH; BEFORE PUBERTY

continues in adulthood resulting in abnormal height

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30
Q

Acromegaly

A

GH; AFTER PUBERTY

changes are seen in face, hands, feet and ears

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31
Q

Hyperpituitarism Patient Assessment

A

age
sex
family history of endocrine issues
change in appearance (lip/nose size, clothing size changes)
fatigue and lethargy
backache
arthralgias
HA and vision changes
menstrual changes
changes in sexual functioning

32
Q

Hyperpituitarism Diagnostic Testing

A

hormone lvls in blood and urine
CT or MRI

suppression testing (high glucose lvls should normally suppress release of GH; give 100g of oral glucose or 0.5 g/kg followed by serial GH measurements..GH LVLS DONT FALL BELOW 5 ng/mL

33
Q

Hyperpituitarism Non Surgical Management

A

encourage pt to express concerns and fears about altered appearance or sexual function
help identify personal strengths and positive characteristics
drug therapy may be used alone or in combo with surgery and radiation (take long time to complete and many years may pass before an effect is seen, not recommended for acromegaly; SE: hypopituitarism, optic nerve damage, other vision problems)
gamma knife procedure

34
Q

Hyperpituitarism Drug Management

A

dopamine agonists to stimulate dopamine receptors in brain and inhibit release of certain pituitary hormones (prolactin and GH) (Bromocriptine (Parlodel) and Cabergoline (Dostinex))

somatostatin analogs (Ocreotide (Sandostatin) and lanreotide)

GH receptor blockers (Pegvisomant)

35
Q

Hypophysectomy

A

most common treatment (removal of pituitary gland along with tumor; minimally invasive trans-nasal or trans-sphenoidal vs craniotomy)

decrease abnormal hormone lvls, relieve HAs, possible reversal of sexual dysfunction

36
Q

Hyperpituitarism Pre-Op Care

A

explain the procedure, that body changes, organ enlargement and visual changes are usually not reversible
explain post-op wound management: nasal packing for 2-3 days after surgery, and mustache dressing placed under nose (breath through mouth)
instruct not to brush teeth, blow nose, cough sneeze or bend forward after surgery (increased ICP and delays healing)

decreases sense of smell may persist 3-4 mths after

37
Q

Hyperpituitarism Post Op Care

A

monitor neurological symptoms hourly for 24 hrs then every 4 hrs and document any changes in vision, mental status, LOC, decreased strength in extremities

observe for complications such as DI, CSF leakage, infection and increased ICP

keep HOB elevated
avoid coughing, perform deep breathing exercises hourly
avoid bending forward
perform oral rinses and apply moisturizer over lips
assess for manifestations of meningitis
teach pt self administration of prescribed hormones

38
Q

CSF Leak (Hyperpituitarism Post Op Complication)

A

assess nasal drainage for presence of glucose
halo signs
report persistent, severe HAs
most CSF leaks may heal themselves, repair surgery may be needed
provider must be notified

39
Q

Diabetes Insipidus

A

water metabolism problem caused by ADH deficiency or inability of kidneys to respond to ADH; excretion of large amount of dilute urine

40
Q

Nephrogenic DI

A

renal tubules don’t respond to ADH (severe kidney injury)

41
Q

Primary Neurogenic DI

A

problem in hypothalamus or pituitary gland; lack of ADH production/release

42
Q

Secondary Neurogenic DI

A

tumors, head trauma, infections, surgeries

43
Q

Drug-Related DI

A

lithium and demeclocycline interfere with kidney response to ADH

44
Q

DI Assessment

A

large amount of very dilute urine (causes dehydration and hypovolemia)
increased thirst but often not enough to compensate for volume less, can lead to hypovolemic shock
causes may include brain tumors and head trauma

24 hr fluid I/O: consider if urine output is more than 4L
dilute with low specific gravity and low osmolarity or osmolality

45
Q

DI Cardiac Symptoms

A

hypotension
tachycardia
weak pulses
hemoconcentration

46
Q

DI Skin Symptoms

A

poor skin turgor
dry mucous membranes

47
Q

DI Neurologic Symptoms

A

decreased cognition
ataxia
increased thirst
irritability

48
Q

DI Drug Therapy

A

desmopressin (DDAVP; FIRST LINE AGENT), a synthetic form of vasopressin given intranasally in a metered spray or oral tab

aqueous vasopressin (IV, IM, SQ) for short term therapy or when dosage must be changed often (may be required in acute care for dosage titration)

chlorpropamide (oral)

hydration with hypotonic IV fluids in acute care (lifelong vasopressin therapy with permanent condition, teach pt to weight themselves daily)

49
Q

DI Nursing Interventions

A

replace fluids by encouraging pt to drink fluids equal to urinary output

monitor I/O, daily weights, report weight changes in a timely manner (1kg=1L of fluid)

monitor for s/s of dehydration

monitor serum and urine lab results

50
Q

Fluid Deprivation Test

A

best test to diagnose central DI; urine production, blood electrolyte lvls and weight are measured regularly for a period of 24 hrs during which the person isn’t allowed to drink

51
Q

DI Patient Education

A

teaching pt that polyuria and thirst are signals for need for another dose
use daily weights to estimate dehydration/overhydration
SE of nasal sprays, including ulceration of mucous membranes, allergy sensation of chest tightness, inhalation of spray into lungs which precipitates pulmonary issues
how to self inject drug
always wear a self-ID bracelet

52
Q

SIADH

A

failure of negative feedback system; ADH (Vasopressin) secretes even when plasma osmolarity is low/normal

caused by shock, trauma, stress, malignancies

water retention>fluid overload

53
Q

SIADH Assessment

A

dilutional hyponatremia
neurological symptoms r/t hyponatremia
GI disturbances, n/v, loss of appetite
weight gain
bounding pulse, hypothermia
decreased urine volume and increased urine osmolarity

54
Q

SIADH Interventions

A

fluid restriction 500-1000 mL/24 hrs to monitor fluid overload
drug therapy with vasopressin receptor antagonists (vaptans), diuretics
treat/manage underlying cause
hypertonic saline (3% NaCl)
tube feedings and GI tube med admin (use saline instead of water)

55
Q

SIADH Nursing Considerations

A

frequent neurologic checks
patient safety needs (fall risks, seizure precautions)
measure I and O
treat hyponatremia
assess for signs of volume overload (esp. cardiac and respiratory complications)

56
Q

Adrenal Gland Hypofunction

A

adrenal cortex production of steroid hormone may decrease due to inadequate secretion of ACTH, dysfunction of hypothalamic-pituitary control mechanism or direct problems of adrenal gland tissue

acute adrenocorticol insufficiency (adrenal crisis) is life threatening

loss of aldosterone and cortisol action (hypoglycemia, potassium excretion decreased BUT Na and H2O excretion increased)

57
Q

Primary Adrenal Gland Hypofunction

A

Addisons Disease (autoimmune, dx, metabolic dx, AIDS, adrenalectomy)

58
Q

Secondary Adrenal Gland Hypofunction

A

pituitary tumors
hypophysectomy
sudden cessation of long term high dose glucocorticoid therapy

59
Q

Adrenal Gland Hypofunction Assessment

A

ask about factors that may cause (radiation activity, drug use?)
changes in activity level (lethargy, fatigue, muscle weakness)
GI problems (anorexia, n/v, diarrhea, abdominal pain)
assess for hypoglycemia (decreased cortisol) and fluid depletion (sweating, HA, tachycardia, changes in neuro status, dehydration)
hyperkalemia (risk for dysrhythmias)
hyponatremia (decreased cognition)

60
Q

Adrenal Gland Hypofunction Interventions

A

promote fluid balance
monitor for fluid deficit (weight pt daily, strict I/Os, monitor lab values for hemp concentration and electrolyte disturbances)
prevent hypoglycemia (steroids, -sone for fluid and electrolyte balance; glucose monitoring)
assess cardiac function (monitoring and vitals every 1-4 hrs)

61
Q

Addisonian Crisis

A

life threatening event, need for cortisol and aldosterone is greater than available supply

usually occurs in response to stressful event like surgery, trauma, severe infections

loss of aldosterone leads to severe hypotension r/t blood volume depletion

62
Q

Hypercorticolism (Cushing’s Syndrome/Disease)

A

syndrome (surplus of cortisol) disease (ACTH tumor)
can be caused by drug therapy (steroids)
most common non drug cause is ACTH-producing pituitary adenoma

63
Q

Cushing’s Syndrome History Assessment

A

other health problems and glucocorticoid therapy
weight gain, increased appetite
sleep disturbances common
emotional instability

64
Q

Cushing’s Syndrome S/S

A

changes in fat distribution (trunkal obesity, moon face, buffalo hump)
skin, cardiac, MSK, immune changes
glucose metabolism (fasting glucose high)
increased androgen production (acne, body hair, oligomenorrhea)

65
Q

Hypercorticolism Lab Assessment

A

blood, salivary, urine cortisol lvls
dexamethasone testing (either 24 hr or 3 day period of time; set doses are given with a 24-hr urine collection after administering, urine corticosteroid excretion and cortisol lvls are suppressed in healthy pts with med)

CT
MRI
arteriography

66
Q

Priority Problems for Hypercorticolism

A

fluid overload due to hormone induced water and sodium retention
potential for injury due to skin thinning, poor wound healing, bone density loss
potential for infection due to hormone-induced reduced immunity
potential for acute adrenal insufficiency

67
Q

Hypercorticolism Nursing Considerations

A

HTN due to increased aldosterone
increased hepatic gluconeogenesis and insulin resistance
can lead to cardiovascular disease and frequent/poor wound healing

68
Q

Pheochromocytoma

A

nonmalignant catecholamine-producing tumors of adrenal medulla
tumors produce, store and release epinephrine and norepinephrine (overproduction, hypertensive crisis!!)

69
Q

Pheochromocytoma S/S

A

high BP
HA
sweating
flushing
anxiety/panic
palpitations
abdominal pain
dizziness
blurry vision
diabetes symptoms
tachycardia
heart failure

70
Q

Pheochromocytoma Nursing Management

A

assess for and manage symptoms of HTN or HTN crisis
prevent additional injury and complications
perioperative care includes pt education, informed consent, post op management

alpha-adrenergic blockers (doxazosin, tolazoline) or removal of tumor

71
Q

Hypoparathyroidism

A

decreased function of parathyroid gland; serum Ca lvls cannot be maintained

occurs post surgically after thyroid/parathyroid removal or after surgery for head and neck cancer

72
Q

Hyperparathyroidism

A

increase in parathyroid hormone; hypercalcemia and hypophosphatemia

kidney stones, Ca deposits, bone lesions

73
Q

Parathyroidism Diagnostics

A

Ca lvl
parathyroid US
scintigraphy (radioisotope use with imaging)
CT/MRI

74
Q

Hypoparathyroidism Treatment

A

correct hypocalcemia
prevent kidney stones
calcium gluconate IV, oral calcitrol, oral Ca carbonate
oral vitamin D supplements

75
Q

Hyperparathyroidism Treatment

A

drug therapy via cinacalcet, bisphosphonates

parathyroidectomy

76
Q

DM Foot Care

A

NO SOAKING FEET or heat pads
moisturize (not between toes)
wear socks
don’t cross legs
cut nails straight across

77
Q

DM Sick Days

A

monitor BG Q4H
drink 8-12 oz of water
call doctor if n/v, large ketones, fever for more than 24 hrs or high BG after 2 doses of insulin