Ch 46 Flashcards
1
Q
pituitary gland anterior lobe hormones
A
growth hormone
TSH
adrenocorticotropic hormone
2
Q
pituitary gland posterior lobe hormones
A
ADH
oxytocin
3
Q
thyroid gland hormones
A
thyroxine (T4)
triiodothyronine (T3)
4
Q
growth hormone target? effects there?
A
a. No specific target gland-Affects body tissue and bone
f. GH acts on newly forming bone> must be administered before epiphyses are fused
h. GH over several years may increase height by 1 foot
5
Q
drug therapy for growth hormone def
A
somatropin (Genotropin)
6
Q
growth hormone route?
A
c. NOT PO: inactivation by GI enzymes. Given subQ or IM
7
Q
growth hormone considerations?
A
e. Can be very expensive: extensive testing before therapy initiated
i. Not appropriate for athletes to build muscle due to extensive side effects
g. Prolonged therapy can antagonize insulin secretion > diabetes mellitus
8
Q
somatropin (Genotropin)
A
- Growth hormone used to treat growth failure in children due to pituitary GH deficiency
- Identical amino acid sequence as human growth hormone
9
Q
drug therapy for growth hormone excess
A
possibly prolactin release inhibitor bromocriptine
10
Q
gigantism
A
excessive growth during childhood (GH excess)
11
Q
acromegaly
A
excessive growth after puberty (GH excess)
12
Q
what are gigantism and acromegaly due to?
A
both are due to hypersecretion of GH, often caused by tumors.
-if tumor cannot be destroyed by radiation, prolactin-releasing inhibitor, bromocriptine, can inhibit release of GH from the pituitary.
13
Q
TSH
A
TRH from hypothalamus>TSH is released>TSH stimulates thyroid to release Thyroxine(T4) and triiodothyronine(T3)
14
Q
trh from where?
A
hypothalamus
15
Q
excess tsh
A
hyperthyroidism
16
Q
deficient TSH
A
hypothyroidism
17
Q
adrenocorticotropic hormone(ACTH)
A
CRF(corticotropin releasing factor) stimulates pituitary corticotrophs to secrete ACTH>ACTH stimulates release of glucocorticoids, mineralcorticoids, and androgen from adrenal cortex
18
Q
glucocorticoids
A
cortisol
from adrenal cortex
stimulated release by ACTH
19
Q
mineralcorticoids
A
aldosterone
from adrenal cortex
stimulated release by ACTH
20
Q
ACTH pattern
A
follows diurnal rhythm
i. Cortisol secretion is higher in the early morning, and decreases throughout the day
ii. Stress, and trauma override the diurnal rhythm, and can cause an increase in secretions of ACTH and cortisol
21
Q
pituitary gland posterior lobe aka
A
neuro-hypophysis
22
Q
ADH
A
promotes water reabsorption from renal tubules to maintain water balance
23
Q
ADH deficiency causes? can be caused by?
A
a. large amounts of water to be excreted by the kidneys
i. Can be caused by Diabetes Insipidus (DI), head trauma, brain tumors
1. Fluid and electrolyte imbalance must be closely monitored, and ADH replacement may be needed
24
Q
vasopressin(Pitressin)
A
given for DI intranasally, subq, or IV for ADH deficiency
25
desmopressin(DDAVP)
given for DI for ADH deficiency
26
ADH excess caused by?
a. Most common cause is small cell carcinoma of the lung
| i. Can also be due to medications, other malignancies, and stress
27
ADH excess causes?
b. Excess amount of water retention causes expansion of the intracellular volume >increased glomerular filtration, and decreased tubular sodium reabsorption > natriuresis (excretion of urinary sodium) > hyponatremia
c. Can cause SIADH (syndrome of inappropriate diuretic hormone)
28
tolvaptan(Samsca) PT/PD
PT: hyponatremia, SIADH
PD: remove excess fluid, promote natriuresis to balance sodium
29
tolvaptain(Samsca) NI/PT ed
NI: monitor neurologic status, intake/output, serum sodium
PT ed: take meds at specific intervals as prescribed, get serial labs esp for Na, no grapefruit juice(increases eff of med), careful of fluids (high levels will further hyponatremia, possibly fluid restriction)
30
thyroxine (T4) and triiodothyronine (T3)
from thyroid gland
regulate protein synthesis and enzyme activity to simulate mitochondrial oxidation
b. Feedback mechanisms regulate T4 and T3 secretion from the thyroid gland
31
feedback mechanisms to regulate T3/T4
hypothalamus-pituitary thyroid axis(HPT)
c. Hypothalamus releases TRH (thyrotropin-releasing hormone) > stimulates release of TSH from pituitary gland > TSH stimulates synthesis and release of T4 and T3
32
excess free T4 and T3?
i. Excess free T4 and T3 inhibit HPT axis > decreased TRH and TSH
33
decreased T4 and T3?
ii. Decreased T4 and T3 will increase the function of the HPT axis
34
hypothyroidism
decrease in thyroid secretion
| -primary or secondary
35
primary hypothyroidism
thyroid gland disorder
| a. Occurs more frequently than secondary
36
secondary hypothyroidism
lack of TSH secretion
37
levothyroxine sodium(Synthroid) PT/PD
PT: hypothyroid, myxedema, cretinism
PD: inc metabolic rate/o2 consumption and body growth
38
levothyroxine/synthroid CI
thyroxtoxicosis, MI, renal dx, adrenal insufficiency
39
levothyroxine/synthroid DFL
drugs: dec eff of antidiabetics (oral and insulin)
| increase risk of digitalis tox
40
levothyroxine/synthroid pt ed
take on empty stomach same time every morning, 30min-1hr before eating breakfast (food interferes w/absorption).
drug will be lifelong.
may take 2-4wks for PT.
report symps of hyperthyroidism>>>thyroid storm
wear medical alert card.
avoid foods that inhibit thyroid secretions: strawberries, peaches, pears, cabbage, turnips, spinach, kale, brussel sprouts, cauliflower, radish, peas
41
levothyroxine/synthroid prec
CV dx, HTN, angina, DM, osteoporosis
42
levothyroxine/synthroid adv rxn
tachycardia, HTN, palpitations, osteoporosis, seizures
| Life threatening: thyroid crisis, angina pectoris, dysrhythmias (A fib), cardiovascular collapse
43
levothyroxine/synthroid SE
n/v/d/anorexia (weight loss), cramps
tremors/nervous/irate/insomnia/headache
diaphoresis, amenorrhea
44
levothyroxine/synthroid NI
serum T3, 4, TSH
| monitor weight: weight gain common in hypothyroidism
45
hyperthyroidism cause
i. Due to an increase in circulating T4 and T3 resulting from an overactive thyroid or excessive output of thyroid hormones from thyroid nodules
46
hyperthyroidism symptoms may be?
| characterizations?
may be mild-severe.
characterized by weight loss, irritability, tachycardia, palpitations, nervousness,
intolerance to heat, excessive perspiration, exophthalmos (bulging eyes)
47
Grave's disease
iii. Graves’ disease or thyrotoxicosis is the most common type of hyperthyroidism caused by hyper-function of the thyroid gland
48
hyperthyroidism tx?
v. Treated by surgical removal of a portion of the thyroid, radioactive iodine, or antithyroid drugs
49
hyperthyroidism treatments can induce?
a. Hypothyroidism
| b. Thyroid crisis
50
thyroid crisis
i. Due to excess thyroid hormone released
ii. Characterized by fever, flushed skin, apathy/confusion/behavioral changes, tachycardia/heart failure/dysrhythmia, hypotension/vascular collapse
51
antithyroid drugs
1. Thirourea derivatives (thioamides)
a. Drugs of choice to decrease thyroid hormone production
b. Interfere with synthesis of thyroid hormone
c. Does not destroy thyroid tissues, but rather block thyroid hormone action
52
methimazole (Tapazole) PT/PD
```
antithyroid drug - thioamide
PT: hyperthyroidism
PD: 1. Inhibits thyroid synthesis
2. Does not inhibit peripheral conversion of T4 to T3
3. 10 times more potent then PTU
```
53
methimazole(tapazole) CI
preg cat D
54
propylthiouracil (PTU) PT/PD
PT: grave's dx
hyperthyroidism
before surgery or radioactive iodine tx
palliative control for toxic goiter
PD: inhibits conversion of T4 and T3
55
propylthiouracil (PTU) ci
Preg cat d
56
parathyroid gland hormone
PTH - parathyroid hormone.
stimulated by decrease in calcium.
regulates calcium levels in blood
57
hypoparathyroidism cause?
1. Caused by PTH deficiency, vitamin D deficiency, renal impairment, and diuretic therapy
58
calcitriol PT/PD
PT: Hypoparathyroidism, management of hypocalcemia in chronic renal failure
PD: Enhances calcium deposits in bones
59
calcitriol CI
a. Hypersensitivity, hypercalcemia, hypervitaminosis D, malabsorption syndrome
60
calcitriol prec
CV dx, renal calculi, renal failure, hyperphosphatemia, dehydration, excess sunlight exposure
61
calcitriol DFL
drug: increase dysrhythmias with digoxin/verapamil
decreased absorption with cholestyramine
lab: inc serum calcium with thiazide diuretics and calcium supps
62
calcitriol adv rxn
hypercalciuria, hypercalemia, hyperphosphatemia, hematuria
63
calcitriol SE
```
n/v/d/Anorexia/cramps
drowsiness/headache/dizziness/vertigo
metallic taste
lethargy
photophobia
```
64
calcitriol NI/PT ed
NI: Monitor calcium levels before treatment, and throughout
b. Assess for symptoms of tetany in hypocalcemia (Twitching of mouth, numbness and tingling of fingers, carpopedal spasms, spasmodic contractions, laryngeal spasms)
PT ed: pt must report s/s of tetany
65
hyperparathyroidism causes
i. Can be caused by malignancies of the parathyroid glands
| ii. Ectopic PTH hormone secretion from lung, cancer, hyperthyroidism, or prolonged immobility
66
calcitonin-salmon PT/PD
for hyperparathyroidism
PT: i. Prevent bone loss and fractures
ii. Increases bone density
iii. Alleviates pain due to fractures and bone metastasis
PD: Decreases serum calcium by binding at receptor sites on osteoclasts
67
calcitonin-salmon CI
allergies to fish
68
calcimimetics
for hyperparathyroidism
ex: cinacalcet
Mimics calcium, and increases sensitivity of calcium-sensing receptors in the parathyroid cells in turn reducing PTH release in turn decreasing the serum calcium slowing progression of bone disease
69
bisphosphonates
for hyperparathyroidism
a. ex: alendronate, etidronate, ibandronate, risedronate
b. Work by blocking osteoclast activity inhibiting mineralization and/or reabsorption of the bone
c. Must measure bone density before beginning treatment and throughout in addition to calcium levels
d. Also used in patients with osteoporosis and osteopenia
e. Patient Education: sit upright for a minimum of 30 mins after administration
70
adrenal glands structure
consists of adrenal cortex and adrenal medulla
71
adrenal cortex hormones
i. Produce two types of Corticosteroids (hormones)
1. Glucocorticoids (cortisol)
2. Mineralcorticoids (aldosterone)
72
corticosteroids promote?
sodium retention/potassium excretion
73
decreased corticosteroid secretion
from adrenal hyposecretion or adrenal insufficiency.
| -Addison's dx
74
increased corticosteroid secretion
adrenal hypersecretion.
| -cushing's syndrome
75
glucocorticoids mechanism
i. Decrease in cortisol increases CRF and ACTH secretions, stimulating the adrenal glands to secrete and release cortisol
ii. Increased cortisol exerts negative feedback mechanism from HPA axis causing inhibition, resulting in less cortisol being released
iii. Drugs are called cortisone drugs are synthetically produced with several routes of administration
76
glucocorticoids tx what?
1. Allergic
a. Asthma, drug reactions, contact dermatitis, anaphylaxis
2. Inflammatory
a. Autoimmune disorders
3. Debilitating conditions
a. Malignancies
77
prednisone PT/PD
PT: adrenocortical insufficiency, Addison's
PD: suppress inflammation/adrenal fx
78
prednisone CI/prec
CI: Hypersensitivity, psychosis, fungal infection, peptic ulcer disease
prec: DM, renal, HF, MI, HTN, osteoporosis, seizures, cataracts, glaucoma
79
prednisone SE/ADV
SE: n/d/abd distention, increased appetite, sweatings, headache, depression, flushing, mood change, cataract, amenorrhea
ADV: petechiae, ecchymosis, HTN, tachycardia, osteoporosis, muscle wasting, sodium/fluid retention
80
prednisone NI/pt ed
a. baseline VS: may be increase in BP and sodium and water retention
b. Monitor patients weight
c. Monitor serial labs, especially electrolytes (possible decrease) and blood glucose (possible increase)
d. Assess for side effects if drug therapy is lasting more than 10 days, and taken in high dosages
e. Monitor older patients, and those at risk for osteoporosis closely due to increased calcium loss from bone
8. Patient Teaching
a. Common side effects that can occur from high doses or prolonged usage
i. Cushing-like features:
1. Edema, muscle wasting, thin skin with purpura, weight gain, abnormal fat deposits in the face and trunk (moon face and buffalo-hump), decreased extremity size
b. Educate that long term use can cause adrenal atrophy
c. Cannot abruptly stop therapy due to high risk of adrenal crisis, must taper dose
d. Report weight gain of 5lbs in several days due to the risk of fluid retention
e. Notify healthcare provider if any muscle weakness, as glucocorticoids promote loss of muscle tone
f. Avoid people who are ill with active infections, as glucocorticoids suppress immune function
g. Wear a MedicAlert ID
h. If diabetic monitor blood sugar closely, as glucocorticoids may raise your blood sugar
i. Eat foods rich in potassium as prednisone promotes potassium loss
i. Fresh and dried fruits, vegetables, meats, and nuts
81
mineralcorticoids
i. Second type of corticosteroid that secretes Aldosterone
ii. Maintain fluid balance by promoting reabsorption of sodium from renal tubules
iii. If hypovolemia occurs more aldosterone is secreted to increase sodium and water retention to restore fluid balance
82
fludrocortisone(Florinef) PT/PD
PT: addisons, adrenocortical insufficiency
PD: promotes reabsorption of sodium from renal tubules
83
fludrocortisone(Florinef) adv
electrolyte derangement: hypokalemia
84
fludrocortisone(Florinef) NI
a. Monitor serum potassium
b. Monitor I&O
c. Monitor BP, baseline prior to initiation of medication
85
fludrocortisone(Florinef) Pt ED
a. Cannot abruptly stop > risk of adrenal crisis, must taper dose
b. Report weight gain of 5lbs in1-2 days > risk of fluid retention
c. Eat foods rich in potassium as florinef promotes potassium loss
i. Fresh and dried fruits, vegetables, meats, and nuts
d. Decreased salt intake to reduce risk of retention
e. Wear a MedicAlert ID
