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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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A
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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?

A
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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
Q

What are the Signs & Symptoms due to hypocalcemia?

A
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26
Q

Acute hypoparathyroid treatment
* What do you do for Hypoparathyroidism with acute symptoms and corrected serum calcium of ≤ 7.5mg/dl? (4)

A
  • 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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27
Q

Acute hypoparathyroid treatment
* What should you start as soon as possible?
* What is the dose of both?
* Taper what?

A

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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28
Q

Acute hypoparathyroid treatment
* how do you treat Hypoparathyroidism mild acute symptoms and corrected serum calcium of >7.5 mg/dL?

A

Initial treatment with oral vitamin D and calcium carbonate is sufficient

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29
Q

Acute hypoparathyroid treatment
* Postsurgical hypoparathyroidism is what?
* Close monitoring of what?
* What can be tapered?

A

Postsurgical hypoparathyroidism is usually transient (3 to 6 weeks)
* Close monitoring of calcium
* Calcium and vitamin D can be tapered

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30
Q

What are the six goals of chronic hypoparathyroid?

A
  • 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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31
Q

Calcium replacement
* What are the two mainstays of treatment?

A
  • Calcium carbonate (40% elemental)
  • Calcium citrate (20% elemental)
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32
Q

Calcium replacement: Calcium carbonate
* Absorption better when?
* Binds what?
* Decreased absorption with what?

A
  • Absorption better when taken with meals
  • Binds phosphorus
  • Decreased absorption with achlorhydria
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33
Q

Calcium replacement: Calcium citrate
* Take with or without what?
* Better alternative for what?
* Dose what? Titrate to what?

A
  • Take with or without meals
  • Better alternative for achlorhydria or constipation from calcium carbonate
  • Dose variable; titrate to calcium level
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34
Q
A
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35
Q

Vitamin D replacement
* What is the mainstay of treatment?

A

Active vitamin D (1, 25-dihydroxy vitamin D)
* Calcitriol

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36
Q

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?

A
  • 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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37
Q
A
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38
Q

Adverse Effects and monitoring (Vit D / Ca++)
* What are the SE?(5)

A
  • Constipation
  • Hypercalcemia
  • Hypercalciuria
  • Nephrocalcinosis
  • Renal failure
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39
Q

SE of Hypercalciuria with Ca/Vit D supplement
* MC with what?
* Lack of what?
* Calcium replacement goal =

A
  • MC with decreased PTH
  • Lack calcium reabsorption effect of PTH
  • Calcium replacement goal = low normal
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40
Q

Adverse Effects and monitoring (Vit D / Ca++)
* What do you monitor and how do you monitor?

A

Monitoring
* Serum calcium
* Urinary calcium

Weekly until serum calcium stable, then every 3 to 6 months

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41
Q

Hypercalciuria
* MC with what?
* Lack of what?
* What is the calcium replacement goal?

A

MC with decreased PTH
* Lack calcium reabsorption effect of PTH
* Calcium replacement goal = low normal

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42
Q

Hypercalciuria
* What is the txt?

A
  • Decrease dose of calcium and vitamin D
  • Hydrochlorothiazide 12.5 to 50 mg PO daily
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43
Q

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?

A

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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44
Q

Recombinant PTH (Natpara)
* What are the SE?
* What is the BBW?

A
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45
Q
A
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46
Q
A
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47
Q

Primary hyperthyroidism
* Excessive production of what? What is this caused by?

A

Excessive production of T3/T4 by the thyroid gland secondary to pathology within the thyroid gland

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48
Q

Primary hyperthyroidism
* How you do dx it?

A
  • Raised T3/T4(due to excessive production)
  • Low TSH(due to negative feedback on the pituitary/hypothalamus)
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49
Q

Primary hyperthyroidism
* What are the causes?

A
  • Graves’ disease (75% of all cases)
  • Toxic multinodular goiter
  • Toxic adenoma
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50
Q

Graves hyperthyroidism
* What do you give for symptom control?
* Decrease sxs caused by what?
* What sxs improve?
* What is the medication?
* Dose to what?

A

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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51
Q

Graves hyperthyroidism: Decrease thyroid hormone synthesis
* What is the initial therapy? What can you add to it?

A

Antithyroid medications (thioamides)
* Initial therapy in most cases ± radioiodine or surgery
* Monotherapy in mild cases

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52
Q

Graves: Decrease thyroid hormone synthesis
* Radioiodine is not recomended for who? (3)

A

Not recommended for
* Severe orbitopathy
* Inability to follow radiation precautions
* CI in pregnancy or during lactation

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53
Q

Graves hyperthyroidism: Decrease thyroid hormone synthesis
* What is the treatment for severe goiter?

A

Surgery

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54
Q

Thioamides
* What are the examples?
* What is the MOA?
* PTU blocks what?

A
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55
Q

thioamides
* Who gets this?
* Achieves what?
* Used as what?
* May induce what? What is the percentage?

A
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56
Q
A
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57
Q
A
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58
Q

thioamides
* What are the se?

A
  • Pruritis/urticaria/rash
  • Paresthesias
  • Hair loss
  • Taste changes
  • Arthralgias
  • Lupus-like syndrome
  • Fever
  • Nausea / vomiting
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59
Q

thioamides
* What is the baseline and follow up labs?

A
  • CBC with differential
  • CMP (includes LFTs)
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60
Q

Thioamides and pregnancy

A
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61
Q

Radioiodine ablation
* _ Therapy
* Lower complications than what?
* Who is it indicated for? (2)
* Pretreated with what?

A
  • 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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62
Q

Radioiodine ablation
* What is the medication?
* What is the MOA? (3)

A

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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63
Q

Radioiodine ablation
* CI in who?
* What are the SE?

A

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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64
Q

Graves

Surgery
* What are the benefits? What are the disadvantages?

A

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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65
Q

Graves

What are the indications for Surgery

A
  • Resistant hyperthyroidism
  • Suspicion of cancer
  • Large goiter
  • Concomitant hyperparathyroidism
  • Pregnancy planning
  • Graves disease with GO (Graves’ ophthalmopathy)
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66
Q

Thyroid storm
* magnified effects of what?
* Exaggerated what?
* _ intolerance?
* What are other sxs?
* What happens to the heart?

A
  • 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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67
Q

Thyroid storm treatment
* What are the goals? (4)

A
  • Suppress thyroid hormone formation and secretion
  • Suppress sympathetic nervous system – beta blockers
  • Treat associated complications and coexisting factors
  • Prevent mortality
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68
Q

Thyroid storm treatment
* What medications do you need to give?

A
  • BB: Esmolol, propranolol
  • PTU/methimazole
  • Iodine soultion
  • Steriod: hydrocortisone

Give in this order

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69
Q
A
70
Q

Hypothyroidism
* Primary- _ problem
* What the MCC in developing and developed countries?

A
71
Q

Hypothyroidism
* What are some other causes?

A
  • Thyroid ablation or surgical removal
  • Drug induced – lithium, amiodarone, antithyroid medications
  • Secondary – pituitary problem (adenoma MC)
72
Q

What are the sxs of hypothyroidism?

A
73
Q

Hypothyroidism - treatment
* What are the goals? (4)

A
  • TSH level within normal range (0.5 to 5mU/L)
  • Symptom resolution
  • Avoid hyperthyroidism
  • Reduce goiter size if present
74
Q

Hypothyroidism - treatment
* What is first line treatment?
* T4 is what?

A
  • Thyroid replacement therapy with T4 (levothyroxine)
  • T4 is prohormone deiodinated to active T3
75
Q

Hypothyroidism - treatment (T4)
* What is the dose for Healthy patients ≤60 without heart disease?
* Dosing based on what?

A
76
Q

Hypothyroidism - treatment (T4)
* What is the dose for Patients > 60 or with heart disease ?

A

12.5 to 50 mcg PO daily

77
Q

Hypothyroidism - treatment (T4) -ALL PATIENTS
* Monitor what?
* Adjust dose by what?
* Repeat what?

A
  • 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
78
Q

Hypothyroidism treatment: Levothryoxine
* What is not created equal?
* Re-evaluated thyroid levels after what?
* Take the medication how?

A
  • 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
79
Q

Hypothyroidism treatment: Levothyroxine
* Nighttime administration may result in what?
* Do not take with what?
* Most important?
* NOT indicated for what?

A
  • 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
80
Q

Hypothyroidism – change in dose
* Decrease requirements? (2)

A

Weight loss / increased age

81
Q

Hypothyroidism – change in dose
* Increased requirements?

A
  • Weight gain (> 10%)
  • Decreased absorption
  • Increase thyroid excretion – nephrotic syndrome
  • Pregnant women require larger replacement to maintain euthyroidism
82
Q

Hypothyroidism – change in dose
* Pregnant women require larger replacement to maintain euthyroidism: Goal changes with what? Women with what?
* Increase and decrease when?

A
  • 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
83
Q

Hypothyroidism – T4-T3 products
* What is not required?
* What can still happen?
* May benefit from what?

A
  • 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
84
Q
A
85
Q

Toxic multinodular goiter / toxic adenoma
* What is toxic adenoma?

A

Hyperthyroidism plus palpable nodule corresponding to increasing RAIU on scintigraphy

86
Q

Toxic multinodular goiter / toxic adenoma
* What is a toxic multinodular goiter?
* Multiple areas of what?
* -/+ what?

A
  • Hyperthyroidism plus palpable nodular goiter or ultrasound showing multiple nodules
  • Multiple areas of uptake on RAIU
  • ± obstructive symptoms (cough, dyspnea, dysphagia)
87
Q

Toxic multinodular goiter / toxic adenoma
* What do you give for sxs control?

A

Beta-blockers (atenolol, propranolol)

Thioamides
* Do not induce remission, only symptom control
* MC used before definitive therapy

88
Q

Toxic multinodular goiter / toxic adenoma
* What is the only definitive therapy?

A

Surgery or radioiodine only definitive therapy

89
Q

Toxic multinodular goiter / toxic adenoma-Surgery
* MC used for what?
* Large what?
* Suspicion of what?
* Patients needing what?

A
  • MC used for TMNG or TA
  • Large goiters
  • Suspicion of concomitant thyroid cancer
  • Patients needing rapid symptomatic relief
90
Q

Toxic multinodular goiter / toxic adenoma
* Who gets radioiodine?

A

Radioiodine – patients not meeting surgical criteria

91
Q

Myxedema coma
* Severe what?
* Decreased what? Body temp? Slowing what?

A

Severe hypothyroidism
* Decreased mental status, hypothermia, slowing organ function (bradycardia, hypoglycemia, hypoventilation)

92
Q

Myxedema coma
* Patient with poorly controlled what?
* Precipiated by what?

A

Patient with poorly controlled hypothyroidism
* Precipitated by an acute event – surgery, infection, administration of sedating medications

93
Q

Myxedema coma
* Edema of what?
* Mortability rate?

A
  • Edema of hands, face, tongue; pretibial edema
  • Mortality rate 30 to 50 %
94
Q
A
95
Q

Myxedema coma
* How do you dx it?

A
  • History / physical exam
  • T4 very low
  • TSH depends on primary or secondary cause
  • Cortisol – looking for secondary causes
96
Q

Myxedema coma
* What is the txt? What is the supportive care?

A
97
Q

Thyroiditis

A
98
Q
A
99
Q

acromegaly-pathophysiology
* Hypothalamus releases what?
* Stomach releases what?
* Both of these do what?

A
  • 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
99
Q

Acromegaly
* Excess what?
* What is the MCC?
* Vary in what?
* What type of vision change?

A

Excess growth hormone (GH)

MCC pituitary adenoma
* Vary in size – large tumors can press on optic chiasm
* Bitemporal hemianopia

100
Q

Acromegaly
* How do you dx?

A
  • IGF-1
  • GH
  • OGTT
  • MRI
101
Q

Acromegaly:
* What is the presentation?

A
102
Q

Acromegaly Treatment
* What is the preferred therapy?

A

Preferred - transsphenoidal resection

103
Q

Acromegaly Treatment
* When is medical therapy an option? (2)
* What are the examples? (3)

A

If not a surgical candidate (unresectable, patient preference or medical comorbidities)

Persistent disease following surgery
* Somatostatin analogs (SRL)
* Dopamine agonists (DA)
* Pegvisomant

104
Q

Acromegaly Treatment
* What is last line?

A

Radiation therapy

105
Q
A
106
Q
A
107
Q

Acromegaly – medical treatment
* Who is it for? (2)
* What type of analogs?

A
  • Patients not surgical candidates
  • Surgery not success
  • Somatostatin analogs (somatostatin = GH inhibiting hormone)
108
Q
A
109
Q
A
110
Q
A
111
Q
A
112
Q

MOA of pegvisomant?

A
113
Q

Adrenal gland
* Where is it?
* Adrenal Medulla activated by what?

A
  • 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
114
Q

Adrenal gland-Adrenal Cortex
* Releases what?
* What does zona glomerulosa release? What does that cause?

A
115
Q

Adrenal gland-Zona Fasciculata
* Releases what? What does that cause?

A

Zona Fasciculata = releases cortisol (glucocorticoids)
* Increases blood pressure
* Immune suppression
* Hyperglycemia - gluconeogenesis
* Osteopenia – increases osteoclast activity

116
Q

Adrenal gland-Zona reticularis
* What is released? What does that cause?

A

Zona reticularis = releases androgens
* No response to stress
* Increases secondary sexual characteristics and prostate size in men
* Increases libido in women

117
Q

What is the Normal cortisol control mechanism?

A
  • 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
118
Q

Adrenal insufficiency diagnosis
* What are the steps for dx?

A
119
Q

Primary adrenal insufficiency
* What is the cortisol level before and after ATCH?

A
120
Q

Secondary adrenal insufficiency
* What is the cortisol level before and after ATCH?

A
121
Q

Addison’s diagnosis (primary)
* WHat is low, high, no increase in what after ACTH?

A
  • Low cortisol
  • High ACTH
  • No cortisol increase after ACTH stimulation test
122
Q

Addison’s diagnosis (primary)
* What else should be measured? What are the levels?

A

Serum aldosterone and renin activity
should also be obtained
* Low aldosterone
* High renin activity

123
Q

Addison’s diagnosis- Secondary
* What is low, Increase in what after acth?

A
  • Low cortisol
  • Low ACTH
  • Increase in cortisol after ACTH administration
  • Further studies to differentiate between secondary and tertiary causes
124
Q

Primary Adrenal insufficiency: Adrenal gland problem
* Acute?

A

Acute – less common
* Sepsis, trauma, hemorrhage, adrenal thrombosis

125
Q

Primary Adrenal insufficiency: Adrenal gland problem
* What are the MCC causes of chronic?

A
126
Q

Addison’s disease

A
127
Q
A
128
Q
A
129
Q

Addison’s Disease
* What are the sxs of chronic disease?

A
  • Hyperpigmentation – MC->Palmar creases, knuckles, oral mucosa
  • Weakness, fatigue
  • Anorexia, weight loss
  • Salt craving
  • Hypotension – hyponatremia
  • Hyperkalemia
  • Muscle and joint pain
130
Q

Addison disease treatment
* What type of replacement?
* What is first line?
* What is the dosing?
* Largest dose when? Smaller when?
* Mimics what?

A
131
Q

Addison disease treatment
* What are alternatives?
* Monitoring: Lowest dose to do what? Monitor what? What is MC SE?

A
132
Q

Addison disease treatment
* What other replacement?
* Prevents what?

A

Mineralocorticoid replacement
* Prevents sodium loss, hypovolemia, and hyperkalemia

133
Q

Addison disease treatment
* Mineralocorticoid-What is the example?
* Higher doses when?
* Liberal what?
* Monitor what?

A

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

134
Q

Addison disease treatment-Androgen replacement
* MC in who?
* What are the sxs?
* What is the drug?

A
135
Q

Addison disease treatment-Androgen replacement
* What are the SE?

A
  • Oily skin / acne
  • Sweating
  • Hirsutism
136
Q
A
137
Q

Adrenal Crisis/Addisonian Crisis
* What happens to cause this?

A
138
Q

Adrenal Crisis/Addisonian Crisis
* Rapid withdrawl of what? Treatment of what?
* Body unable to do what?

A

Rapid withdrawal of prolonged glucocorticoid administration
* Treatment of Cushing’s syndrome

Body unable to release extra cortisol in response to stress

139
Q

Adrenal Crisis/Addisonian Crisis
* What are the sxs?

A
140
Q

Adrenal crisis treatment
* What do you need access, obtain? What is high and low?

A

Emergent
* IV access
* Obtain cortisol, ACTH, electrolytes, cortisol, renin, blood glucose, electrolytes
* Hyponatremia, hyperkalemia common

141
Q

Adrenal crisis treatment
* What fluids and meds do you give?
* What is not necessary?
* Taper what?

A
142
Q

Adrenal crisis treatment- Patient education
* Management of what?
* Increase what?
* Emergency what?
* Contact who?

A
  • Management of illness or stress
  • Increase glucocorticoid dose (2-3x)
  • Emergency hydrocortisone or dexamethasone
  • Contact provided if not improved
143
Q

Adrenal crisis treatment- Patient education
* What type of bracelet?
* What may require replacement? No need for what?

A

Medical alert bracelet

Surgical procedures may require replacement
* Supplemental hydrocortisone replacement recommendations vary with surgery type
* Not needed for uncomplicated dental procedures

144
Q

Cushing syndrome (hypercortisolism)
* What is the MCC of exogenous? What are the reasons for taking this?

A

MCC prolonged administration of exogenous glucocorticoids
* Autoimmune diseases, asthma, leukemia induction
* Mimic the effects of endogenous cortisol

145
Q

Cushing syndrome (hypercortisolism)
* MCC of endogenous reason? What does it cause?

A

MCC of endogenous cortisol elevation is Cushing Disease
* Pituitary adenoma increasing release of ACTH
* Adrenal adenomas or carcinomas

146
Q

Cushing syndrome (hypercortisolism)
* What is less common cause?

A

Less common – ectopic sources of ACTH secretion
* Metastatic small cell lung cancer, bronchial carcinoids

147
Q

Cushing’s symptoms
* What are the sxs due to?
* What are the sxs?

A

Symptoms directly due to excess cortisol

148
Q

Treatment of cushing disease:
* What is the txt? What is the MC complication?

A
  • Transsphenoidal tumor resection
  • MC complication = Diabetes insipidus (15%)
149
Q

Treatment of cushing syndrome:
* Control what?
* Prepare for what?
* Recurrent after what?
* Waiting what?
* What type of syndrome?

A

Cushing syndrome – control hypercortisolism
* Preparation for surgery or if surgery contraindicated
* Recurrent after initial surgery
* Awaiting radiation therapy effects
* Ectopic ACTH syndrome

150
Q

Cushing’s pharmacotherapy: Recurrent / remnant tumor following resection
* What are the different drug therapies?

A
  • Inhibits ACTH secretion – cabergoline, pasireotide
  • Adrenal inhibition of steroidogenesis – osilodrostat, ketoconazole, mitotane
  • Glucocorticoid receptor blockade
151
Q

Cushing’s pharmacotherapy
* What is ketoconazole limied by?

A

Use limited by hepatotoxicity

152
Q

Ketoconazole
* MOA?

A
  • Inhibits first step in cortisol biosynthesis (side chain cleavage)
  • Decrease free cortisol levels to normal or by 50 to 75% of patients
153
Q

Ketoconazole
* What are the SE? How do you monitor it?

A
154
Q

prolactinoma
* What is the MCC? Gender?
* What is are the sxs? (women, men, large tumors sxs)

A

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

155
Q

prolactinoma
* How do dx?
* How do you txt microadenomas and macroadenomas?

A
  • Diagnosis – prolactin > 200 ng/mL, MRI
  • Microadenomas (< 1cm): medical therapy with dopamine agonist (cabergoline)
  • Macroadenomas (> 1 cm): surgical
156
Q

Cabergoline / bromocriptine
* What is the MOA?

A

Dopamine agonists – inhibit prolactin secretion

157
Q

Cabergoline / bromocriptine
* What is the preferred agent? Why?

A

Cabergoline preferred agent
* More specifically binds to dopamine receptor
* Lower incidence of adverse effects
* Once weekly dosing

158
Q

Cabergoline / bromocriptine
* What are the MC SE?

A
  • Nausea, vomiting, headaches, dizziness
  • Improve over time
159
Q

Multiple endocrine neoplasia
* What is the txt?

A

Surgeries are usually the treatments!

160
Q

Diabetes insipidus
* Osmo receptors in what? What do they sense?
* Osmolality=
* What is it primarily made up of?
* What is osmolatlity?

A

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

161
Q

Normal response to dehydration
* Increased what (2)
* Osmo receptors in hypothalamus detect what? What does that cause?
* What is the net effect?

A
162
Q

Diabetes insipidus
* Large amounts of what?
* Kidneys reabsorb too little water from renal tubule. What does that cause?

A

Large amounts of dilute urine

Kidneys reabsorb too little water from renal tubule
* Increased urine output
* Serum osmolality increase
* Increased thirst

163
Q

Diabetes insipidus
* What are the four types?

A
  • Central
  • Nephrogenic
  • Gestational
  • Dipsogenic – psychologic polydispsia
164
Q

Central Diabetes insipidus
* What is the cause?
* What happens with the vasopressin challenge?

A
165
Q

Central Diabetes insipidus
* What is the txt?

A

Treatment
* First-line: vasopressin
* Low solute (sodium/protein) diet
* Thiazide diuretics

166
Q

Nephrogenic Diabetes insipidus
* What is the cause?
* What happens in the vasopressin challenge?

A
167
Q

Nephrogenic Diabetes insipidus
* What is the txt?

A
  • Thiazide diuretics: Reduces serum Na – reduces blood osmolality – reduces thirst
  • Na restriction
168
Q

Central vs Nephrogenic Diabetes insipidus
* Both have what?

A

Both = plasma osmolality high >300 mOsm/kg; urine osmolality low < 300 mOsm/kg; high volume, dilute urine

169
Q

Desmopressin - DDAVP
* What is the MOA ?
* What age group?
* How should it be dosed?

A

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

170
Q

Desmopressin - DDAVP
* What are the SE?
* Black box warning?

A

Pharm II (14 decks)

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