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Pharm II > Lecture 12 (endocrine)- Exam 6 > Flashcards

Lecture 12 (endocrine)- Exam 6 Flashcards

1
Q

Insulin with CKD – follow-up

A
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2
Q

Parathyroid gland
* Located where?
* What does is detect and regulate?

A
  • Located within the thyroid gland
  • Detect changes in calcium levels and regulates the release of parathyroid hormone (PTH)
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3
Q

Parathyroid disorders
* What does PTH release trigger? (3)

A
  • Bones to release Ca++
  • Kidneys to reabsorb Ca++
  • Synthesizes active vitamin D – increases GI Ca++ absorption
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4
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6
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7
Q

Hyperparathyroidism: Secondary
* Increased what? In response to what?
* MC in the setting of what?
* Kidneys not producing what? Not filtering out what?

A
  • Increased PTH in response to low calcium
  • MC in the setting of CKD
  • Kidneys not producing calcitriol; not filtering out phosphorus
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8
Q

What are the hypercalemia sxs? What about the EKG?

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9
Q

Treatment – Primary hyperparathyroidism
* What is definitive therapy?

A

Surgical removal as definitive therapy

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10
Q

Treatment – Primary hyperparathyroidism
* All symptomatic patients and asymptomatic patients who meet the following criteria (7)

A
  • ≤ 50 years of age
  • Serum calcium levels > 1mg/dL above upper limit of normal
  • Calcinuria (urine calcium levels >250 – 300 mg/24h)
  • Creatinine clearance < 60 ml/min/1.73m2
  • Osteoporosis (T-score < -2.5)
  • Nephrolithiasis / nephrocalcinosis
  • Desire for surgery
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11
Q

Treatment – Primary hyperparathyroidism
* Non-surgical candidates with symptoms of hypercalemia: What are the goals?

A

Goals: reduce serum calcium levels and/or improve bone mineral density

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12
Q

Treatment – Primary hyperparathyroidism
* What do you give for Patients with hypercalcemia and normal bone mineral density?

A

Calcimimetics (Cinacalcet)

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13
Q

Calcimimetics (Cinacalcet)
* How does Calcimietics work? (What does it bind, increase, decreade and what does it not impact)?

A
  • Bind calcium-sensing receptor in the parathyroid gland
  • Increase the sensitivity to calcium
  • Decreased secretion of PTH
  • Decreased serum calcium levels
  • Does not impact bone density
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14
Q

Treatment – Primary hyperparathyroidism
* What do you give to Patients with osteoporosis at risk of fracture?

A

Bisphosphonates

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15
Q

Osteoporosis treatment – 1st line therapy: Bisphosphonates
* What is the MOA?

A

Reduce bone resorption by:
* Stimulating osteoclast apoptosis
* Decrease cholesterol synthetic pathway – decreases osteoclast function

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16
Q

Bisphosphonates
* Bioavailability? Worse with what?
* Amount absorbed

A

Bioavailability poor - < 1%
* Worse with concomitant food intake

Amount absorbed
* 50% eliminated renally
* 50% remains for months to years

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17
Q

Bisphosphonate side effects
* What are the SE?

A
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18
Q

Bisphosphonates: Oral (alendronate, risedronate)
* Take on what?
* Full what?
* Remain what?

A
  • Take on empty stomach in the morning – increases poor bioavailability
  • Full glass of water
  • Remain upright for at least 30 minutes
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19
Q

Bisphosphonates
* IV verison?

A

Zoledronic acid

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20
Q

Bisphosphonates
* Not recommended for who?

A

Not recommended for creatinine clearance < 30 ml/min/1.73 m2

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21
Q

Secondary Hyperparathyroidism causing hyperphosphatemia

Treatment-secondary hyperphosphatemia
* What is first line?

A

Dietary phosphate restriction – 900mg phosphate/day

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22
Q

Treatment-secondary hyperphosphatemia
* What is second line? Who is this for?

A

Persistent phosphate > 5.5 mg/dL with dietary restriction
* Phosphate binders
* Calcium carbonate / calcium acetate
* Sevelamer (Renagel): Bind phosphate through Ion exchange

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23
Q

Hypoparathyroidism
* What is the MCC?
* What are some other causes?

A
  • MCC is surgical: Thyroid, parathyroid, or neck surgery
  • Immune-mediated destruction of parathyroid glands
  • Genetic disorders – DiGeorge syndrome
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24
Q

Hypoparathyroidism
* What are the levels of calcium, PTH, phosphorus and magnesium?

A

Low calcium
* Low or inappropriately normal parathyroid hormone (PTH)
* High phosphorus
* Normal magnesium

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25
What are the Signs & Symptoms due to hypocalcemia?
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Acute hypoparathyroid treatment * What do you do for Hypoparathyroidism with acute symptoms and corrected serum calcium of ≤ 7.5mg/dl? (4)
* Intravenous calcium gluconate 1 to 2 grams IV over 10 minutes * Repeat dose every 60 minutes until symptoms resolve * Followed by calcium gluconate continuous infusion (5 to 20 mg/kg/hr) * Obtain calcium levels every 6 to 12 hours until patient is stable
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Acute hypoparathyroid treatment * What should you start as soon as possible? * What is the dose of both? * Taper what?
Start oral vitamin D and oral calcium as soon as possible * 1, 25-dihydroxyvitamin D (calcitriol) – 0.5 mcg po BID * Calcium carbonate 1 to 4 grams elemental calcium/day * Taper IV calcium gluconate
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Acute hypoparathyroid treatment * how do you treat Hypoparathyroidism mild acute symptoms and corrected serum calcium of >7.5 mg/dL?
Initial treatment with oral vitamin D and calcium carbonate is sufficient
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Acute hypoparathyroid treatment * Postsurgical hypoparathyroidism is what? * Close monitoring of what? * What can be tapered?
Postsurgical hypoparathyroidism is usually transient (3 to 6 weeks) * Close monitoring of calcium * Calcium and vitamin D can be tapered
30
What are the six goals of chronic hypoparathyroid?
* Prevent signs and symptoms of hypocalcemia * Maintain serum calcium just below normal * Maintain calcium-phosphate product below 55mg2/dL2 * Avoid hypercalciuria * Avoid hypocalcemia * Avoid renal and other extra skeletal calcifications
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Calcium replacement * What are the two mainstays of treatment?
* Calcium carbonate (40% elemental) * Calcium citrate (20% elemental)
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Calcium replacement: Calcium carbonate * Absorption better when? * Binds what? * Decreased absorption with what?
* Absorption better when taken with meals * Binds phosphorus * Decreased absorption with achlorhydria
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Calcium replacement: Calcium citrate * Take with or without what? * Better alternative for what? * Dose what? Titrate to what?
* Take with or without meals * Better alternative for achlorhydria or constipation from calcium carbonate * Dose variable; titrate to calcium level
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Vitamin D replacement * What is the mainstay of treatment?
Active vitamin D (1, 25-dihydroxy vitamin D) * Calcitriol
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Vitamin D replacement * What impairs conversion of 25-hydroxy vitamin D to active form? (2) * Calcitriol: What is the onset and duration? * May cause what?
* Lack of PTH and hypophosphatemia impairs conversion of 25-hydroxy vitamin D to active form * Rapid onset, short duration of action * May cause hypercalcemia
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Adverse Effects and monitoring (Vit D / Ca++) * What are the SE?(5)
* Constipation * Hypercalcemia * Hypercalciuria * Nephrocalcinosis * Renal failure
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SE of Hypercalciuria with Ca/Vit D supplement * MC with what? * Lack of what? * Calcium replacement goal =
* MC with decreased PTH * Lack calcium reabsorption effect of PTH * Calcium replacement goal = low normal
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Adverse Effects and monitoring (Vit D / Ca++) * What do you monitor and how do you monitor?
Monitoring * Serum calcium * Urinary calcium Weekly until serum calcium stable, then every 3 to 6 months
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Hypercalciuria * MC with what? * Lack of what? * What is the calcium replacement goal?
MC with decreased PTH * Lack calcium reabsorption effect of PTH * Calcium replacement goal = low normal
42
Hypercalciuria * What is the txt?
* Decrease dose of calcium and vitamin D * Hydrochlorothiazide 12.5 to 50 mg PO daily
43
Recombinant PTH (Natpara) * Second line for who? * What type of therapy? * Vit D dose decreased by what? * Calcium dose maintained initially with what? * Daily what?
Second-line for patients who cannot maintain stable calcium levels * Add-on therapy * Vitamin D dose decreased by 50% with gradual taper off * Calcium dose maintained initially with gradual decrease * Daily subcutaneous injection
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Recombinant PTH (Natpara) * What are the SE? * What is the BBW?
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Primary hyperthyroidism * Excessive production of what? What is this caused by?
Excessive production of T3/T4 by the thyroid gland secondary to pathology within the thyroid gland
48
Primary hyperthyroidism * How you do dx it?
* Raised T3/T4 (due to excessive production) * Low TSH (due to negative feedback on the pituitary/hypothalamus)
49
Primary hyperthyroidism * What are the causes?
* Graves’ disease (75% of all cases) * Toxic multinodular goiter * Toxic adenoma
50
Graves hyperthyroidism * What do you give for symptom control? * Decrease sxs caused by what? * What sxs improve? * What is the medication? * Dose to what?
Beta-blockers * Decrease symptoms caused by increased beta-adrenergic tone * Palpitations, tachycardia, tremors, anxiety, heat intolerance * Atenolol 25 to 50 mg PO daily – beta-1 selective * Dose to HR < 90 BPM
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Graves hyperthyroidism: Decrease thyroid hormone synthesis * What is the initial therapy? What can you add to it?
Antithyroid medications (thioamides) * Initial therapy in most cases ± radioiodine or surgery * Monotherapy in mild cases
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Graves: Decrease thyroid hormone synthesis * Radioiodine is not recomended for who? (3)
Not recommended for * Severe orbitopathy * Inability to follow radiation precautions * CI in pregnancy or during lactation
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Graves hyperthyroidism: Decrease thyroid hormone synthesis * What is the treatment for severe goiter?
Surgery
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Thioamides * What are the examples? * What is the MOA? * PTU blocks what?
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thioamides * Who gets this? * Achieves what? * Used as what? * May induce what? What is the percentage?
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thioamides * What are the se?
* Pruritis/urticaria/rash * Paresthesias * Hair loss * Taste changes * Arthralgias * Lupus-like syndrome * Fever * Nausea / vomiting
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thioamides * What is the baseline and follow up labs?
* CBC with differential * CMP (includes LFTs)
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Thioamides and pregnancy
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Radioiodine ablation * _ Therapy * Lower complications than what? * Who is it indicated for? (2) * Pretreated with what?
* Definitive therapy * Lower complications than surgery * Indicated for * Patients with significant symptoms * Older patients with heart disease or other comorbidities * Pretreat with beta-blockers and thioamides prior to procedure (help sxs before hand)
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Radioiodine ablation * What is the medication? * What is the MOA? (3)
Oral capsule – sodium iodine 131 (I-131) MOA: * Concentrates in thyroid, omits beta radiation causing tissue ablation in 6 to 18 weeks * Results in hypothyroidism – thyroid replacement therapy will be required * May worsen Graves orbitopathy (GO)
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Radioiodine ablation * CI in who? * What are the SE?
CI: pregnancy or breastfeeding; noncompliance with radiation protocol Adverse effects * Infertility * Thyroiditis * Radiation toxicity – neoplasms, hematopoietic suppression, salivary and lacrimal toxicity
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# Graves Surgery * What are the benefits? What are the disadvantages?
Benefits * Near 100% cure rates * Rapid achievement of euthyroid or hypothyroid state * Identification of incidental cancers Disadvantages * Risks of surgery * Hypocalcemia * Hypothyroidism
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# Graves What are the indications for Surgery
* Resistant hyperthyroidism * Suspicion of cancer * Large goiter * Concomitant hyperparathyroidism * Pregnancy planning * Graves disease with GO (Graves' ophthalmopathy)
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Thyroid storm * magnified effects of what? * Exaggerated what? * _ intolerance? * What are other sxs? * What happens to the heart?
* Magnified effects of excess thyroid hormone * Exaggerated signs and symptoms of hyperthyroidism * Heat intolerance – fever * Hyperactivity and anxiety – agitation, confusion, coma seizures * Tachycardia – cardiac arrhythmias and high output failure
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Thyroid storm treatment * What are the goals? (4)
* Suppress thyroid hormone formation and secretion * Suppress sympathetic nervous system – beta blockers * Treat associated complications and coexisting factors * Prevent mortality
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Thyroid storm treatment * What medications do you need to give?
* BB: Esmolol, propranolol * PTU/methimazole * Iodine soultion * Steriod: hydrocortisone | Give in this order
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Hypothyroidism * Primary- _ problem * What the MCC in developing and developed countries?
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Hypothyroidism * What are some other causes?
* Thyroid ablation or surgical removal * Drug induced – lithium, amiodarone, antithyroid medications * Secondary – pituitary problem (adenoma MC)
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What are the sxs of hypothyroidism?
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Hypothyroidism - treatment * What are the goals? (4)
* TSH level within normal range (0.5 to 5mU/L) * Symptom resolution * Avoid hyperthyroidism * Reduce goiter size if present
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Hypothyroidism - treatment * What is first line treatment? * T4 is what?
* Thyroid replacement therapy with T4 (levothyroxine) * T4 is prohormone deiodinated to active T3
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Hypothyroidism - treatment (T4) * What is the dose for Healthy patients ≤60 without heart disease? * Dosing based on what?
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Hypothyroidism - treatment (T4) * What is the dose for Patients > 60 or with heart disease ?
12.5 to 50 mcg PO daily
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Hypothyroidism - treatment (T4) -ALL PATIENTS * Monitor what? * Adjust dose by what? * Repeat what?
* Repeat TSH and free T4 levels in six weeks * Adjust dose by 12.5 to 25 mcg/day every 4 to 6 weeks until stable * Repeat TSH and free T4 every 6 months
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Hypothyroidism treatment: Levothryoxine * What is not created equal? * Re-evaluated thyroid levels after what? * Take the medication how?
* All generic products are not created equal * Re-evaluated thyroid levels after 4 to 6 weeks with any brand changes * Take the medication on empty stomach * 30 to 60 minutes before or 2 hours after eating
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Hypothyroidism treatment: Levothyroxine * Nighttime administration may result in what? * Do not take with what? * Most important? * NOT indicated for what?
* Nighttime administration may result in insomnia for some patients * Do not take with calcium or aluminum containing antacids, iron supplements or fiber * Most important – be consistent * NOT indicated for the treatment of obesity or for weight loss
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Hypothyroidism – change in dose * Decrease requirements? (2)
Weight loss / increased age
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Hypothyroidism – change in dose * Increased requirements?
* Weight gain (> 10%) * Decreased absorption * Increase thyroid excretion – nephrotic syndrome * Pregnant women require larger replacement to maintain euthyroidism
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Hypothyroidism – change in dose * Pregnant women require larger replacement to maintain euthyroidism: Goal changes with what? Women with what? * Increase and decrease when?
* Goals change with trimester – see guidelines for details * Women with preexisting hypothyroidism * Increase current levothyroxine dose by 20 to 30% immediately and titrate to euthyroid * Decrease the dose back to baseline after delivery
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Hypothyroidism – T4-T3 products * What is not required? * What can still happen? * May benefit from what?
* Most literature suggests T3 not required * Subset of patients who achieve normal TSH / T4 and still feel poorly * May benefit from trial of T4-T3 product
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Toxic multinodular goiter / toxic adenoma * What is toxic adenoma?
Hyperthyroidism plus palpable nodule corresponding to increasing RAIU on scintigraphy
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Toxic multinodular goiter / toxic adenoma * What is a toxic multinodular goiter? * Multiple areas of what? * -/+ what?
* Hyperthyroidism plus palpable nodular goiter or ultrasound showing multiple nodules * Multiple areas of uptake on RAIU * ± obstructive symptoms (cough, dyspnea, dysphagia)
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Toxic multinodular goiter / toxic adenoma * What do you give for sxs control?
Beta-blockers (atenolol, propranolol) Thioamides * Do not induce remission, only symptom control * MC used before definitive therapy
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Toxic multinodular goiter / toxic adenoma * What is the only definitive therapy?
Surgery or radioiodine only definitive therapy
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Toxic multinodular goiter / toxic adenoma-Surgery * MC used for what? * Large what? * Suspicion of what? * Patients needing what?
* MC used for TMNG or TA * Large goiters * Suspicion of concomitant thyroid cancer * Patients needing rapid symptomatic relief
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Toxic multinodular goiter / toxic adenoma * Who gets radioiodine?
Radioiodine – patients not meeting surgical criteria
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Myxedema coma * Severe what? * Decreased what? Body temp? Slowing what?
Severe hypothyroidism * Decreased mental status, hypothermia, slowing organ function (bradycardia, hypoglycemia, hypoventilation)
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Myxedema coma * Patient with poorly controlled what? * Precipiated by what?
Patient with poorly controlled hypothyroidism * Precipitated by an acute event – surgery, infection, administration of sedating medications
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Myxedema coma * Edema of what? * Mortability rate?
* Edema of hands, face, tongue; pretibial edema * Mortality rate 30 to 50 %
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Myxedema coma * How do you dx it?
* History / physical exam * T4 very low * TSH depends on primary or secondary cause * Cortisol – looking for secondary causes
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Myxedema coma * What is the txt? What is the supportive care?
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Thyroiditis
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acromegaly-pathophysiology * Hypothalamus releases what? * Stomach releases what? * Both of these do what?
* Hypothalamus releases GHRH * Stomach releases ghrelin * Both stimulate the pituitary to produce GH * GH stimulates the liver to release IGF-1 * IGF-1 stimulates growth of various tissues
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Acromegaly * Excess what? * What is the MCC? * Vary in what? * What type of vision change?
Excess growth hormone (GH) MCC pituitary adenoma * Vary in size – large tumors can press on optic chiasm * Bitemporal hemianopia
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Acromegaly * How do you dx?
* IGF-1 * GH * OGTT * MRI
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Acromegaly: * What is the presentation?
102
Acromegaly Treatment * What is the preferred therapy?
Preferred - transsphenoidal resection
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Acromegaly Treatment * When is medical therapy an option? (2) * What are the examples? (3)
If not a surgical candidate (unresectable, patient preference or medical comorbidities) Persistent disease following surgery * Somatostatin analogs (SRL) * Dopamine agonists (DA) * Pegvisomant
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Acromegaly Treatment * What is last line?
Radiation therapy
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Acromegaly – medical treatment * Who is it for? (2) * What type of analogs?
* Patients not surgical candidates * Surgery not success * Somatostatin analogs (somatostatin = GH inhibiting hormone)
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MOA of pegvisomant?
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Adrenal gland * Where is it? * Adrenal Medulla activated by what?
* Sits on top of the kidneys * Adrenal Medulla – sympathetic nervous system activation stimulates the release of epinephrine and norepinephrine in response to acute stress->Fight or flight
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Adrenal gland-Adrenal Cortex * Releases what? * What does zona glomerulosa release? What does that cause?
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Adrenal gland-Zona Fasciculata * Releases what? What does that cause?
Zona Fasciculata = releases cortisol (glucocorticoids) * Increases blood pressure * Immune suppression * Hyperglycemia - gluconeogenesis * Osteopenia – increases osteoclast activity
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Adrenal gland-Zona reticularis * What is released? What does that cause?
Zona reticularis = releases androgens * No response to stress * Increases secondary sexual characteristics and prostate size in men * Increases libido in women
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What is the Normal cortisol control mechanism?
* Hypothalamus releases corticotropin releasing hormone (CRH) in response to everyday stressors * CRH stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH) * ACTH stimulates adrenal cortex to release cortisol (glucocorticoids) * Rising cortisol serves as negative feedback to control CRH and ACTH release
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Adrenal insufficiency diagnosis * What are the steps for dx?
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Primary adrenal insufficiency * What is the cortisol level before and after ATCH?
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Secondary adrenal insufficiency * What is the cortisol level before and after ATCH?
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Addison’s diagnosis (primary) * WHat is low, high, no increase in what after ACTH?
* Low cortisol * High ACTH * No cortisol increase after ACTH stimulation test
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Addison’s diagnosis (primary) * What else should be measured? What are the levels?
Serum aldosterone and renin activity should also be obtained * Low aldosterone * High renin activity
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Addison’s diagnosis- Secondary * What is low, Increase in what after acth?
* Low cortisol * Low ACTH * Increase in cortisol after ACTH administration * Further studies to differentiate between secondary and tertiary causes
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Primary Adrenal insufficiency: Adrenal gland problem * Acute?
Acute – less common * Sepsis, trauma, hemorrhage, adrenal thrombosis
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Primary Adrenal insufficiency: Adrenal gland problem * What are the MCC causes of chronic?
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Addison’s disease
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Addison’s Disease * What are the sxs of chronic disease?
* Hyperpigmentation – MC->Palmar creases, knuckles, oral mucosa * Weakness, fatigue * Anorexia, weight loss * Salt craving * Hypotension – hyponatremia * Hyperkalemia * Muscle and joint pain
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Addison disease treatment * What type of replacement? * What is first line? * What is the dosing? * Largest dose when? Smaller when? * Mimics what?
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Addison disease treatment * What are alternatives? * Monitoring: Lowest dose to do what? Monitor what? What is MC SE?
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Addison disease treatment * What other replacement? * Prevents what?
Mineralocorticoid replacement * Prevents sodium loss, hypovolemia, and hyperkalemia
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Addison disease treatment * Mineralocorticoid-What is the example? * Higher doses when? * Liberal what? * Monitor what?
Fludrocortisone 0.1 mg PO daily (0.05 to 0.2mg) * Higher doses needed in summer with increased perspiration * Liberal salt intake * Monitor orthostatic hypotension, serum sodium, potassium levels, and plasma renin activity
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Addison disease treatment-Androgen replacement * MC in who? * What are the sxs? * What is the drug?
135
Addison disease treatment-Androgen replacement * What are the SE?
* Oily skin / acne * Sweating * Hirsutism
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Adrenal Crisis/Addisonian Crisis * What happens to cause this?
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Adrenal Crisis/Addisonian Crisis * Rapid withdrawl of what? Treatment of what? * Body unable to do what?
Rapid withdrawal of prolonged glucocorticoid administration * Treatment of Cushing’s syndrome Body unable to release extra cortisol in response to stress
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Adrenal Crisis/Addisonian Crisis * What are the sxs?
140
Adrenal crisis treatment * What do you need access, obtain? What is high and low?
Emergent * IV access * Obtain cortisol, ACTH, electrolytes, cortisol, renin, blood glucose, electrolytes * Hyponatremia, hyperkalemia common
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Adrenal crisis treatment * What fluids and meds do you give? * What is not necessary? * Taper what?
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Adrenal crisis treatment- Patient education * Management of what? * Increase what? * Emergency what? * Contact who?
* Management of illness or stress * Increase glucocorticoid dose (2-3x) * Emergency hydrocortisone or dexamethasone * Contact provided if not improved
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Adrenal crisis treatment- Patient education * What type of bracelet? * What may require replacement? No need for what?
Medical alert bracelet Surgical procedures may require replacement * Supplemental hydrocortisone replacement recommendations vary with surgery type * Not needed for uncomplicated dental procedures
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Cushing syndrome (hypercortisolism) * What is the MCC of exogenous? What are the reasons for taking this?
MCC prolonged administration of exogenous glucocorticoids * Autoimmune diseases, asthma, leukemia induction * Mimic the effects of endogenous cortisol
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Cushing syndrome (hypercortisolism) * MCC of endogenous reason? What does it cause?
MCC of endogenous cortisol elevation is Cushing Disease * Pituitary adenoma increasing release of ACTH * Adrenal adenomas or carcinomas
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Cushing syndrome (hypercortisolism) * What is less common cause?
Less common – ectopic sources of ACTH secretion * Metastatic small cell lung cancer, bronchial carcinoids
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Cushing’s symptoms * What are the sxs due to? * What are the sxs?
Symptoms directly due to excess cortisol
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Treatment of cushing disease: * What is the txt? What is the MC complication?
* Transsphenoidal tumor resection * MC complication = Diabetes insipidus (15%)
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Treatment of cushing syndrome: * Control what? * Prepare for what? * Recurrent after what? * Waiting what? * What type of syndrome?
Cushing syndrome – control hypercortisolism * Preparation for surgery or if surgery contraindicated * Recurrent after initial surgery * Awaiting radiation therapy effects * Ectopic ACTH syndrome
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Cushing’s pharmacotherapy: Recurrent / remnant tumor following resection * What are the different drug therapies?
* Inhibits ACTH secretion – cabergoline, pasireotide * Adrenal inhibition of steroidogenesis – osilodrostat, ketoconazole, mitotane * Glucocorticoid receptor blockade
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Cushing’s pharmacotherapy * What is ketoconazole limied by?
Use limited by hepatotoxicity
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Ketoconazole * MOA?
* Inhibits first step in cortisol biosynthesis (side chain cleavage) * Decrease free cortisol levels to normal or by 50 to 75% of patients
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Ketoconazole * What are the SE? How do you monitor it?
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prolactinoma * What is the MCC? Gender? * What is are the sxs? (women, men, large tumors sxs)
MC hormone-secreting pituitary tumor * MC women Hypogonadotropic hypogonadism * Women – amenorrhea, galactorrhea, decreased libido, dyspareunia, osteoporosis * Men – decreased libido, erectile dysfunction, infertility * Large tumors – headaches, visual field deficits
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prolactinoma * How do dx? * How do you txt microadenomas and macroadenomas?
* Diagnosis – prolactin > 200 ng/mL, MRI * Microadenomas (< 1cm): medical therapy with dopamine agonist (cabergoline) * Macroadenomas (> 1 cm): surgical
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Cabergoline / bromocriptine * What is the MOA?
Dopamine agonists – inhibit prolactin secretion
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Cabergoline / bromocriptine * What is the preferred agent? Why?
Cabergoline preferred agent * More specifically binds to dopamine receptor * Lower incidence of adverse effects * Once weekly dosing
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Cabergoline / bromocriptine * What are the MC SE?
* Nausea, vomiting, headaches, dizziness * Improve over time
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Multiple endocrine neoplasia * What is the txt?
Surgeries are usually the treatments!
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Diabetes insipidus * Osmo receptors in what? What do they sense? * Osmolality= * What is it primarily made up of? * What is osmolatlity?
Osmo receptors in the hypothalamus sense changes in osmolality of blood * Osmolality = concentration of dissolved particles in the blood * Primarily Na, glucose, BUN * Normal = 285 to 295 mOsm/kg
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Normal response to dehydration * Increased what (2) * Osmo receptors in hypothalamus detect what? What does that cause? * What is the net effect?
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Diabetes insipidus * Large amounts of what? * Kidneys reabsorb too little water from renal tubule. What does that cause?
Large amounts of dilute urine Kidneys reabsorb too little water from renal tubule * Increased urine output * Serum osmolality increase * Increased thirst
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Diabetes insipidus * What are the four types?
* Central * Nephrogenic * Gestational * Dipsogenic – psychologic polydispsia
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Central Diabetes insipidus * What is the cause? * What happens with the vasopressin challenge?
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Central Diabetes insipidus * What is the txt?
Treatment * First-line: vasopressin * Low solute (sodium/protein) diet * Thiazide diuretics
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Nephrogenic Diabetes insipidus * What is the cause? * What happens in the vasopressin challenge?
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Nephrogenic Diabetes insipidus * What is the txt?
* Thiazide diuretics: Reduces serum Na – reduces blood osmolality – reduces thirst * Na restriction
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Central vs Nephrogenic Diabetes insipidus * Both have what?
Both = plasma osmolality high >300 mOsm/kg; urine osmolality low < 300 mOsm/kg; high volume, dilute urine
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Desmopressin - DDAVP * What is the MOA ? * What age group? * How should it be dosed?
MOA * Replace missing ADH * Children ≥ 6 years and adolescents Dose: * Dose should be titrated based on symptom control, urine and serum electrolytes / osmolality * Lifelong therapy may be required
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Desmopressin - DDAVP * What are the SE? * Black box warning?

Pharm II (14 decks)

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