Drugs Affecting the Endocrine System Flashcards

1
Q

A chemical substance that’s secreted into the body by one of a group of cells and exert a physiological effect on other cells is defined as:

A

Hormones

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2
Q

What are the 4 general function of hormones:

A
  1. synthesizes/secretes hormones
  2. coordinate/maintain homeostasis
  3. Tells tatget organs/cells/tissue when to increase/decrease work
  4. Regulates basic metabolic activities essential for growth/development/reproduction
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3
Q

What is the hypophysis:

A

The pituitary gland with the anterior and posterior lobe

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4
Q

What does the adenohypophysis secrete (anterior pituitary gland secretes 7):

A
  1. GH: growth hormone stimulates growth in tissue and bone
  2. TSH: thyroid-stimulating hormone which acts on the thyroid gland
  3. ACTH: adrenocorticotropic hormone which stimulates the adrenal gland
  4. MSH: melanocyte stimulating hormone
  5. ICSH: interstitial cell stimulating hormone
  6. Gonadotropins: FSH (follicle-stimulating hormone), LH (luteinizing hormone)
  7. Prolactin: ?
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5
Q

What does the neurohypophysis (posterior pituitary lobe secretes 2) secrete:

A
  1. ADH: antidiuretic hormone/vasopressin
  2. oxytocin
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6
Q

The adrenocorticotropic hormone is secreted from where and acts on what:

A
  • Adrenocorticotropic hormone (ACTH) is secreted from the adenohypophesis/anterior pituitary
  • acts directly on the adrenal gland/cortex to increase bld sugar, decreases inflammation/protein stores, and increases catacholamines when stressed
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7
Q

The growth hormone (GH) is secreted from where and what does it act on:

A
  • Growth hormone (GH) is secreted from the adenohypophesis/anterior pituitary
  • GH directly acts on cells/tissue/bone tissue for increase growth/bld sugar/protein stores
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8
Q

The melanocyte stimulating hormone (MSH) is secreted from where and what does it directly act on:

A
  • Melanocyte stimulating hormone is secreted from the adenohypophesis/anterior pituitary
  • **MSH directly acts on cells/tissue to increase skin pigmentation **
  • side note: skin pigmentation may be increased if ACTH (adrenocorticotropic hormone) is secreted in addisons disease
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9
Q

The thyroid stimulating hormone is secreted from where and what does it act directly on:

A
  • Thyroid stimulating hormone (TSH) is secreted from the adenohypophysis/anterior pituitary
  • TSH directly acts on the thyroid gland to increase metabolism
  • side note: increase w/stress or cold
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10
Q

The antidiuretic hormone (ADH) is secreted from where and acts directly on what?

A
  • Antidiuretic Hormone (ADH) is secreted from the hypothalamus when stimulated by the neurohypophysis/posterior pituitary
  • ADH acts directly on the renal collecting ducts to increase reabsorption of H2O
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11
Q

Oxytocin is secreted from where and acts directly on what?

A
  • Oxytocin is secreted from the neurohypophysis/posterior pituitary
  • Acts directly:???
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12
Q

What drugs are used for a pt w/a growth deficiency and what are the routes/action, and contraindication:

A
  • somatrem (Protropin)

treats dwarfism via IM/subQ by affecting all tissue and bone growth

  • somatropin (Genotropin)

Treats growth deficiency via IM/subQ by affecting bone growth at epiphyseal plates

  • The somatropin/somatrem are contraindicated in peds w/Praderwilli syndrome/obesity/RR distress d/t fatalities
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13
Q

What suppressant drugs are used for a pt with GH excess, and what are the routes, action, and contraindications:

A
  • bromocriptine (parlodel):

A prolactin-release inhibitor that inhibits the relase of GH from the hypopphysis via PO in pts w/acromegaly (excessive growth post puberty); can be used in conjuction w/hypophysis radiation; will decrease lactation

  • octreotide (Sandostatin)

Suppresses GH release in acromegaly (excessive growth post puberty) via subQ;

  • GI S/S are common
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14
Q

What hormonal drug is given to a pt to dx w/hypothyroidism as a primary or secondary cause and what is the route/side effects:

A
  • Thyrotropin (Thytropar) is given to see if hypothyroidism is caused from either a thyroid gland disorder or from a pituitary disorder in the secretion of TSH
  • IM
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15
Q

What drug is given to Dx/Tx adrenal gland insufficiency, and as an antiinflammatory drug in the Tx (MS) of allergic response:

A
  • (a_C(contrainindications)_thar) Corticotropin stimulates the adrenal gland/cortex to secrete cortisol/corticosteroids which supresses the immune response/antiinflammatory/Tx MS
  • IV/IM/subQ
  • Side note: DM pt may need insulin d/t drug increasing bld glucose
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16
Q

What are the contrainindications/interactions of the hormonal drug Acthar?

A
  • contrainindicated in HF, peptic ulcer, severe fungal infections
  • Interactions: increase risk of ulcers w/ASA/Nsaids; increase effect of thiazide/loop diuretics (hypokalemia d/t potassium-wasting)
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17
Q

What are the side effects of Acthar/ACTH:

A
  • S/S: hypo-kalemia/calcemia, growth retardation, edema (Na retention), GI distress, petechiae, mood swings, glaucoma
  • Adverse S/S: osteoporosis, muscle atrophy, decreased wound healing, edema, ulcer perforation/pancreatitis (life-threatening), ecchymosis
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18
Q

What are the Nsg responsibilities for pts taking Acthar/ACTH:

A

Monitor: G&D in children, weight (d/t edema S/S if weight gain is present), doses should be TAPERED; teach pt to decrease Na intake (d/t edema S/S), electrolytes, GI distress, DM

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19
Q

What are the two hypothalamic hormones that regulate the GH:

A

GH-RH (releasing hormone) and GH-IH (inhibiting hormone/somastatin) which causes the andenohypophysis to relase/not release GH which stimulate bone/cell/tissue growth

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20
Q

Can you administer GH drugs post fusion of the epiphyses?

A

No, GH drugs must be administerd subQ/IM before the epiphysss of bones are fused as GH drugs only work on growing bones

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21
Q

What type of GH drug is given to peds w/a pituitary GH deficiency or adults suffering from SDS or HIV catabolism:

A

Peds: somatrem or somatropin IM/subQ

Adults w/SDS (somatropin deficiency syndrome)/HIV: somatropin IM/subQ

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22
Q

When is somatropin contraindicated in peds:

A

GH deficency d/t Prader-Willi syndrome, severe obesity, RR impairment (asthma)

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23
Q

What is the difference between Gigantism vs. acromegaly:

A
  • gigantism: excessive growth during childhood
  • acromegaly: excessive growth after puberty
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24
Q

What is the drug therapy for either gigantism or acromegaly:

A
  • bromocriptine (Parlodel) PO
  • octreotide (Sandostatin) subQ (GI s/s common)
  • Adverse effects: joint/back pain, muscle aches, HTN, rhinitis, hypothyroidism, hyperglycemia, HA
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25
Q

What are the nsg interventions/responsibilities/teaching when a pt’s on GH:

A
  • G&D and height and weight measurments; GH levels/thyroid/glucose tests/hip x-rays; funduscopic examination (d/t intracranial HTN/HA in children)
  • Teach that GH is not for building muscles, can cause DM, how to evaluate effectiveness of GH drug (G&D, H/W)
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26
Q

What are the hormones released by the neuropophysis:

A

ADH (antidiuretic hormone)/vasopressin and oxytocin

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27
Q

What drug thearpy is given to pts w/ DI diabetes insipidus (lrg amounts of water is secreted by kidneys d/t deficiency of ADH or brain truama/tumor on hypo/pituitary glands)/ nocturnal enuresis/ maintenance of homeostasis in hemophilia A or von willebrand disease:

A

ADH Meds:

  • Desmopressin (DDAVP): intranasal for DI, hemophilia A, Von Willebrand disease which promotes reabsorption of water from renal tubules
  • Vasopressin (Pitressin): subQ/IM for DI promotes water reabsorption from the renal tubules
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28
Q

What are the potential adverse effects when taking ADH meds (Desmopressin acetate DDAVP or Vasopressin):

A

Water intoxication (peds/adults will be extremely thirsty, have them drink enough only to quench their thirst); rhinitis, GI, HA,

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29
Q

What are the nsg responsibilities and interventions for ADH medications:

A
  • Monitor V/S and and Record UO: (increased heart rate and decrease systolic pressure can indicate hypovolemia resulting from decreased ADH production)
  • monitor weight, Serum and urine osmolality, electrolytes, especially Na
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30
Q

What hormones are secreted by the thyroid gland when stimulated by the TSH hormones from the adenohypophesis:

A

Thyroxine (T4) and Triiodothyronine (T3)

  • Regulates protein synthesis an enzyme activity and stimulates mitochondrial oxidation
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31
Q

What are the three types of thyroid drugs given to pts w/ hypothyroidism or Thyroidectomy:

A

T4, T3, T3/T4

  • T4: (synthroid) (Levothroid)=drug of choice
  • T3: (Cytomel)
  • T3/T4: Thyrolar
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32
Q

What are the two causes of hypothyroidism:

A

Primary:

  • thyroid gland disorder, more common (d/t thyroid gland inflammation, excess intake of antithyroid drugs, thyroidectomy surgery)
  • myxedema (edema of eyelids/face) severe hypothyroidism in adults
  • cretinism congenital hypothyroidism
  • *Secondary**:
  • lack of TSH hormones from adenohypophesis
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33
Q

What is the main drug of choice for Tx hypothyroidism and what it is the action, uses, and contraindications:

A

Levothyroxine (T4, Synthroid) PO, IM

  • T4, Synthroid treats hypothyroidism, myxedema, cretinism by increasing metabolic rate, cardiac output, protein synthesis, and glycogen use
  • contraindications: thyrotoxicosis, MI, severe renal disease
  • sidenote: usually lifelong treatment
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34
Q

What are the drug interactions when taking T4, Synthroid :

A
  • Increased effects of: cardiac insufficiency with epinephrine, anticoagulants, TCAs, vasopressor, decongestants
  • ** decreased effects of**: antidiabetics, digitalis, decrease dabsorption w/cholesterol pills
  • Side note: monitor cardiac and kidney function
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35
Q

What are the common side effects or adverse reactions when taking T4, Synthroid given PO/IM:

A
  • Common S/S: Nervousness, insomnia, GI distress/weight loss, tremors, headache,
  • Adverse reaction: tachycardia, palpitations, HTN, dysrhythmias, angina, thyroid crisis
  • Contrainindicated: MI, severe renal disease
  • sidenote: if S/S of hypothyroidism occurs, the dose is insufficient and should be increased.
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36
Q

Why isn’t T3, Cytomel not used for long-term maintenance therapy for hypothyroidism and when is it best used:

A

T3, Cytomel (given PO)

  • Not use as long-term therapy maintenance for hypothyroidism d/t short half-life duration of T3, Cytomel
  • ** instead T3, Cytomel is used as initial therapy for treatment of myxedema due to rapid onset of action **
  • sidenote: cardiac side effects (C in cytomel = cardiac)
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37
Q

What other type of drug therapy is used to Tx hypothyroidism that is not T4, Synthroid:

A

Thyrolar (T4, Synthroid and T3, Cytomel a 4:1 ratio)

  • Given PO
  • No significant advantage to using Thyrolar over Synthroid alone
  • Side effects: irritability, nervousness, insomnia, tachycardia, weight loss
38
Q

What are the nsg responsibilites in pts w/hypothyroidism:

A
  • Thyroid tests (T3, T4, TSH levels), muscle tone, Weight gain, HR (hold if >100BPM)/BP are decreased, Everything is much SLOWER: speech, lethargy, myexedema, lack of presperation, they feel COLDER
  • Synthroid/cytomel/thyrolar causes insomnia
  • avoid foods that inhibit thyroid secretion: strawberries/peaches/kales/brussel sprouts/ cauliflower
  • Take a single dose before breakfast d/t insomnia and meals affect absorption
  • **wear medic alert **
39
Q

N.E, 48 yo, has been dx as having hypothyroidism. She’s taking Cytomel 50 mcg/day. Which of the following is most likely to occur?

  1. Angina
  2. Fatigue
  3. Rash
  4. gastritis
A

1: angina

40
Q

What are the most common S/S of taking hypothyroidism drugs, and what are the common things to have pts do/look out for when taking them:

A
  • Hyperthyroidism side effects from excessive hypothyroid meds: HEART, insomnia/jitteriness/insomnia (nervousness/tremors)/weight loss
  • Have pts take early in the morning before meals d/t insomnia and meals affecting absorption of food; avoid foods that inhibit tyroid secretion strawberries/peaches/kale/brussel sprouts/cauliflower
  • have pts look out for S/S of hypothyroidism which means that the dose that they are currently on needs to be up-ed: hypothyroisism S/S makes everything SLOW (speech/memory loss/moods/apathy); myxedema; COLD intolerance, rough/thick/dry skin/weight gain/ lack of sweat
41
Q

What is hyperthyroidism:

A

Increase circulating levels of T4/3 d/t over active thyroid gland or excessive secretions of the T3/4 hormones.

Can cause Graves disease/thyroitoxicosis. If left untreated, thyroid storm may occur (vascular collapse which is fatal).

42
Q

How is hyperthyroidism (Grave’s disease/Thyroitoxicosis) characterized and what is the therapy used to Tx it:

A
  • Characteristics: hot intolerance, excessive prespirations, tacycardia/palpitations, expothalamus/jitters (nervousness, irritability)
  • Tx: subpartial thyroidectomy, radioactive Iodine Tx; antityroid drugs (Thiamides inhibit thyroid secretion of T3/4)
43
Q

What are the most common drugs given to treat thyrotoxic crisis, Graves disease, or before going to have partial thyroidectomy/radioactive iodine thearpy:

A
  • The thiamides: PTU/Tap (propylthiuracil and the tapazole) both are PO meds
  • Side note: Tapazole is much more potent than PTU and excessive amounts (of both drugs, but mostly Tapazole) can cause goiter.
44
Q

What are the common drug interactions when taking thiamides (PTU/Tap):

A
  • Dilantin increases serum T3 levels
  • Increases effect of oral anticoagulants
  • Derease effects of insulin/antidiabetic meds
  • Have pts take with food to limit GI distress
  • Sidenote: if prengnant or breastfeeding: may cause baby to have hypothyroidism
45
Q

What should I know about PTU:

A
  • PTU is a thiamide PO med given to tx hyperthyroidism,(Grave’s/Thyrotoxicosis), to control thyrotoxic crisis, and given in preparation of either partial thyroidectomy/radioactive Iodine therapy.
    *
46
Q

What should I know when giving Tapazole:

A
  • Tapazole is a thiamide PO med (more potent than PTU) given to treat hyperthyroidism
  • Less GI effects than PTU; hematologic effects are very common (Check CBC levels and WBCs as agranulocytosis occurs)
  • Adverse effects: cholestatic jaundice and agranulocytosis: stop med
47
Q

What do I need to know about Iodine-131:

A
  • Iodine-131 is a radioactive liquid drinked thru a star to treat hyperthyroidism; only effects the thyroid; allows for outpt tx
  • Common S/S:** assess mouth for metalic taste, burning sensation; induces hypothyroidism; GI distress;**
  • Teach pt to follow radioactive protoclol: diluting before throwing away
48
Q

What are the adverse effects when taking iodine131:

A
  • Most common S/S when taking Iodine-131: vertigo, paresthesia, prurtic skin rash, fatigue, GI distress, hypoprothrombinemia (risk of bleeding)
  • Adverse S/S: transient increase in liver transaminase (AST/ALT), jaundice, HEPATITS, AGRANULOYCYTOSIS
49
Q

What types of foods should be avoided when on Iodine-131 and why shouldn’t antihyperthyroid meds be stopped cold turkey:

A
  • shellfish, coughmeds have salt, seafood
  • stopping antithyroid meds can bring about thyroid crisis ot thyroid storm (both are the same)
50
Q

What does the parathyroid secrete and what’s the action:

A

The parathyroid gland secretes parathyroid hormone (PTH) to promote Ca reabsorption from the GI or from the renal tubules and activates vitamin D

51
Q

What antihypercalcemic med is given to treat hyperparathyroidism/hypercalcemia:

A
  • Plicamycin (mithracin) is a antihypercalcemic PO antineoplastic abx given to renal failure pts, testicular CA, and hypercalcemia
  • Check for S/S of hypocalcemia (letwitching of the mouth, tetany, tingling/numbness of the fingers, carpopedal spasm, spasmodic contractions, laryngeal spasms)
52
Q

What type of antihypocalcemic med is given to increase Ca levels:

A
  • Calcitriol (Rocaltrol) is given PO to increase Ca levels by promoting Ca absorption from GI/Renal tubules when treating hypoparathyroidism/hypocalcemia
  • Contrainindicated: hypercalcemia/hyperphosphatemia/excess Vitamin D/malabsorption issues
53
Q

What are the side effects/adverse reactions when taking Calcitriol (Rocaltrol):

A
  • Hypercalcemia/hyperparathyroid S/S when taking Calcitriol (Rocaltrol): bone pain, GI distress, polyuria, hyperphoshatemia, dry mouth, metalic taste, lethargy
  • Adverse reaction when taking Calcitriol (Rocaltrol): EKG will show short QT intervals signalling Bradycardia, avoid vitamin D
54
Q

What are the nsg responsibilities when giving Calcitrol (Rocaltrol):

A
  • Labs: Ca/phos/mg/alkaline phosphate levels
  • Have pt report S/S of hypocalcemia (drug is not working): lethargy, facial flushing, GI distress, Twitiching of cheek and BP cuff
  • Have pts report S/S of hypercalcemia: Polyuria, nocturia, muscle/boin pain, cold symptoms; GI disturbances
  • Potentially dangerous: Cardiac arrhythmias/HTN
55
Q

What are the three hormones produced by the adrenal gland:

A

THe 3 Ss:

  1. Sugar: (glucocorticoids) Metabolism of sugar, protein, and used as an antiflammatory
  2. Salt: (Mineralocorticoids) Water and electrolyte; retention of Na & H2O; excretetion of K all stimulated by the RAAS (renin-angiotensin-aldosterone system)
  3. Sex: (androgens & Estrogens)
56
Q

What does the adrenal medulla secrete that induces the adrenal cortex to produce glucocorticoids (cortisol):

A

Stress causes the adrenal medulla to secrete epinephrine (adrenalin)/Norepei (the catacholamines) which stimulates the adrenal cortex to secrete glucocorticoids (cortisol)

57
Q

If there’s a increased level of CRF (corticotropin Releasing Hormone from hypo) or ACTH/Acthar (from adenohypophysis) in the blood, what is the negative feedback system do:

A

The HPA (hypothalamus/pituitary/adrenal gland) causes less cortisol from being released into the bloodstream

58
Q

What’s the difference between Addison’s disease and Cushing syndrome:

A
  • Addison’s Disease: decrease in corticosteroid serum levels
  • Cushing Syndrome: increase in corticosteroid serum levels
59
Q

What are the S/S of adrenal hypersecretion:

A
  • Common S/S: hyperglycemic, muscle wasting, poor wound healing, buffalo hump, moon face; peptic ulcers, cateracts
  • Adverse Effects: HF, Edema, HTN; hypervolemia
  • Labs: hyperNA, hypoK
60
Q

What are the S/S of adrenal hyposecretion

A
  • hypoglycemia, muscle weakness, apathy, depression, fatigue, GI distress, anemia
  • Severe S/S: cardiovascular collapse, tachycardia, hypotension, hypovolemia
  • Labs: hypoNa/hyperK
61
Q

What glucocorticoid is given to treat hypoadrenal secretion:

A

Prednisone is a po intermediate acting glucocorticoid that txs adrenal hyposecretion by supressing inflammation and imminosuppression (MS) and antiflammatory (Asthma)

62
Q

What are the S/S of taking predinsone:

A
  • Cushing syndrome S/S: hyperglycemia, abnormal fat deposits, buffalo hump
  • increased appetite, muscle wasting, flushing
  • Adverse: Skeletal: osteoporosis, muscle atrophy, growth retardation, CHF, Caution in DM d/t hyperglycemia
63
Q

What can happen if a pt suddenly stops taking their prednisone:

A

**Sudden withdraway of glucorticosteroids can cause acute adrenal insufficiency **

  • Look for increased temp, decreased BP, decreased heart sounds, fluid electrolyte imbalance, dereased sexual drive, Gi distress
64
Q

Long term therapy of prednisone may cause what:

A

Cushing (moon face, buffalo hump, edema in feet, increased brusing, hyperglycemia, muscle atrophy),, peptic ulcers

65
Q

What are the NSG responsibilities in pts taking prednisone:

A
  • taper doses to prevent adrenal crisis, icrease dose if pt’s stress often to prevent drug-induced adrenal insufficiency; monitor wounds as they heal slowly/signs of infection; have pt wear medic alert bracelet
66
Q

What is the only mineralcorticoid given to treat Addison’s disease or adrenal deficiency and what are the adverse effects:

A

Fludrocortisone (Florinef) in small PO doses will replace adrenocortial deficiency; large PO doses will result as a glucocorticoid effect of decreaseing cortisol in the blood

  • High doses: Edema, HTN, CHF, cardiomegaly, hypokalemic alkalosis d/t pH being high but K is low
67
Q

If you have a asthmatic pt, would you administer short/intermediate/long acting glucocorticoid steroid:

A

Long-acting

68
Q

The patient is receiving the growth hormone somatrem to mention. Nsg understands the action of this drug is to do what?

  1. To act as an anti-inflammatory agent
  2. to increase metabolic rate and oxygen consumption
  3. to stimulate growth in long bones
  4. to promote water reabsorption from the renal tubules
A

3: stimulate growth in long bones

69
Q

The patient is given desmopressin acetate (DDAVP). The nsg knows that this drug is to treat which condition?

  1. Gigantism
  2. Diabetes mellitus
  3. diabetes insipidus
  4. adrenal insufficiency
A

3: diabetes insipidus

70
Q

A patient taking Synthroid. Which adverse effect will the nsg monitor in the pt?

  1. Tachycardia
  2. drowsiness
  3. constipation
  4. weight gain
A

1: tachycardia

71
Q

A patient is giving Acthar. Nsg knows to monitor the patient for which condition?

  1. weight gain
  2. hyperkalemia
  3. hypoglycemia
  4. hypercalcemia
A

1: weight gain
* Acthar causes hypokalemia, hypocalcemia, hyperglycemia.

72
Q

The NSG is administering prednisone to patient who’s newly admittied to the hospital was taking multiple other drugs. The nsg should consider which drug interactions with prednisone? (Select all that apply)

  1. The cardiac and CNS actions are increased when taking an adrenergic agent.
  2. Potassium wasting diuretics increase potassium loss resulting in hypokalemia
  3. the risk of G.I. bleeding and ulceration increases when taking with ASA and other NSAIDs
  4. the action of prednisone is decrease when taking Dilantin as they increase glucocorticoid metabolism
  5. the risk of dysrhythmias and digitalis toxicity increases when taken with cardiac glycoside
  6. the dosage of antidiabetic agents may need to be increased when taken concurrently with glucocorticoids
A

2,3,4,5,6

73
Q

The nsg administers vasopressing to a pt. What should the nsg monitor for? Select all that applies:

  1. record urinary output
  2. observe weight and note edema
  3. monitor for decreased BP
  4. monitor pt’s bld glucose
  5. monitor for increased pulse
  6. record daily Ca levels
A

3, 5 decreased BP and increased HR

74
Q

What is the cultural consideration when understanding Cushing Syndrome:

A
  • Family member is not “dumb” or disintterested
  • S/S do not just go away and progressed if Rx therapy is not followed correctly
  • Long term use of glucorticosteroid can cause Cushing syndrome
75
Q

When would you prescribe a short acting glucocorticoid steroid:

A

Hydrocortisone or cortisone, a short acting glucocorticoid steroid, is used for adrenocortical insufficiency and inflammation

76
Q

When would you prescribe an intermediate acting glucocorticoid steroid:

A

Prednisone, an intermediate acting glucocorticoid steroid, is used for anti-inflammatory or immunosuppressive effect arthritis bronchial asthma allergic reactions

77
Q

When would you prescribed a long acting the corticoid steroids:

A

Betamethasone, is a long acting glucocorticoid steroid use to treat Cushing’s syndrome and bronchial asthma

78
Q

What would you prescribe to a patient for Addison’s disease:

A

Florinef, a mineralocorticoid

79
Q

What are the signs and symptoms of adrenal hyposecretion, Addison’s disease:

A

Hypoglycemia, muscle weakness, tachycardia, hypertension, cardiovascular collapse, hypovolemia=hyponatremia, hyperkalemia, anemia

80
Q

What are the signs and symptoms of adrenal paper situation, Cushing’s syndrome:

A

Hyperglycemia, muscle wasting, osteoporosis, moonphase, Buffalo come, peptic ulcers, HTN, edema, hypervolemia=hypernatremia, hypokalemia, increase red blood cell count and neutrophils,

81
Q

Explain the cycle of how the hypothalamus causes production of cortisol and it’s action on the body:

A

The hypothalamus secretes corticotropin releasing hormone (CRF)–> adenohypophysis secretes adrenocorticotropic (ACTH/Acthar)–> adrenal cortex secretes glucocorticoid (cortisol)= increase blood sugar, decrease inflammation, decreased protein stores, increases action of epinephrine/Noriepinephrine when stressed

82
Q

Explains how the hypothalamus has a role in the growth hormone and what it does to the body:

A

Hypothalamus secretes (GH – RH or GH – IH)–> adenohypophysis secretes growth hormone–> Target cells/tissue/bones to increase growth/blood sugar/protein stores

83
Q

Explain the hypothalamus role in stimulating the thyroid gland and what it does to the body:

A

The hypothalamus secretes thyrotropin releasing hormone (TRH)–> the adenohypophysis secretes thyroid stimulating hormone (TSH)–> thyroid secretes T3/T4 to produce increase metabolism/with stress and cold

84
Q

explain the role of hypothalamus in the stimulation of the posterior pituitary (neurohypophysis) and it’s effect on the body:

A

The hypothalamus secretes antidiuretic hormone (ADH)–> aDH is stored in the posterior pituitary–> when there’s increase osmolarity or hypovolemia, ADH causes the reabsorption of water in the renal collecting ducts

85
Q

What are the side effects or adverse reactions when taking high dose or prolong use of glucocorticoids

A
  • HIGH Doses of glucocorticoids: can cause increased blood sugar, Cushing’s syndrome, decrease extremity size, muscle wasting, sodium and water retention, HTN, glaucoma, peptic ulcers
  • prolonged use of glucocorticoid: adrenal atrophy (loss of adrenal gland function, Should be tapered)
86
Q

Symptoms of Cushing’s syndrome:

A

Moonphase, puffy eyelids, edema in the feet, increased bruising, dizziness, bleeding

87
Q

Explain the role of the adrenal cortex and it’s production of mineralocorticoids (aldosterone):

A

The adrenal cortex secretes a mineralocorticoid called aldosterone which maintains blood pressure by the retention of sodium and H2O, and excretion of potassium aall of which stimulated by the renin-angiotensin system

88
Q

If a patient is not prescribed a mineralocorticoid such as Florinef, what could happen if the patient’s Addison’s disease is left untreated?

A
  • A decrease decrease in aldosterone, if not treated by Florinef, will cause hypotension and vascular collapse.
  • When on Florinef, a patient should be on a high-protein diet
89
Q

Some nursing interventions about glucocorticoids to know:

A

Glucocorticoids can increase blood pressure/sodium/water, a weight gain of 5 pounds in several days means water retention/edema, hypokalemia, hyperglycemia, hypocalcemia can cause osteoporosis, loss of muscle tone/Growth retardation, adrenal crisis can occur if glucocorticoid preparations are abruptly stopped, medic alert card, herbal laxatives and diuretics may increase the severity of hypokalemia

  • If a diabetic patient is taking glucocorticoids assess for cataracts, glaucoma, an increase of blood glucose which means a patient should be taking insulin
90
Q

The nsg is administrating vasopressin to a patient. The nsg realizes that the nsg applications for this drug would indicate which implications? (Select all that apply)

  1. Record urinary output
  2. observed the clients wait and note the adema
  3. monitor the patient for decrease blood pressure
  4. closely monitor the patient’s blood glucose levels
  5. Monitor the patient’s pulse for increased heart rate
  6. record the patient’s daily calcium levels
A

3 and 5 monitor the client for deep decrease blood pressure, monitor pulse/heart rate

91
Q
A