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Endocrine Exam 2 > Let's try this again > Flashcards

Let's try this again Flashcards

1
Q

Adrenal Gland destruction (lack of cortisol AND aldosterone)

A

primary adrenocortical insufficiency (addison’s disease)

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2
Q

Pituitary failure of ACTH secretion (lack of cortisol only)
*isolated glucocorticoid insuffiency (aka aldosterone is working, just cortisol effected)

A

Secondary adrenocortical insufficiency

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3
Q

etiologies of primary adrenocortical insufficency? What diseases is it frequently assoicated with?

A

Autoimmune- Most common cause in US
Infection- (most common in developing countries- tuberculosis, HIV)
Vascular: thrombosis or hemorrhage in adrenal gland
others: medications (e.g, Ketoconazole, rifampin)
Frequently assoicated with: Vitiligo, Type 1 DM, hashimoto’s thyroiditis, pernicious anemia

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4
Q

etiologies of secondary adrenocortical insufficiency?

A

History of exogenous glucorticoid use
hypopituitarism
pituitary lesions, metastatic breast, prostate, lung cancer, LT glucocortiocoid tx

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5
Q

what symptoms would you see with (primary) Addison’s disease? Lab findings?

A

symptoms due to lack of sex hormones (women may have loss of libido, amenorrhera & loss of axillary pubic hair)
Hyperpigmentation
orthostatic hypotension

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6
Q

What labs can be used as baseline labs for adrenal insufficiency? What levels would you expect?

A

8am ACTH, cortisol and renin levels obtained (increased renin, especially with primary)
* elevated ACTH in primary, decreased in secondary
* hypoglycemia in
* Primary- HYPOnatremia, HYPERkalemia, & non-anion gap metabolic acidosis (due to decreased aldosterone)

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7
Q

ways to screen for adrenal insufficiency? What result confirms adrenal insufficiency

A

High dose ACTH (cosyntropin) stimulation test
adrenal insufficiency if insufficient or absent rise in serum cortisol after ACTH administration
*normal response is rise in serum cortisol after ACTH administration

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8
Q

Precipitated by “stressful” event (eg illness, surgery, trauma, volume loss, hypothermia, MI, fever, sepsis, hypoglycemia, steroid withdrawl)

A

Adrenal Addisonian crisis

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9
Q

Etiologies of adrenal crisis?

A

Abrupt withdrawal of glucocortioids (especially without tapering)- most common cause

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10
Q

Clinical Manifestation Adrenal crisis

A

Shock is the primary manifestation- hypotension, hypovolemia (nonspecific symptoms)

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10
Q

Clinical Manifestation Adrenal crisis

A

Shock is the primary manifestation- hypotension, hypovolemia (nonspecific symptoms)
dehydration

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11
Q

Diagnosis of adrenal crisis has what significant features?

A

Hyponatremia, HYPERkalemia, hypoglycemia, HYPOtension

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12
Q

Cushing’s disease vs Cushing’s syndrome

A
  • Cushing’s disease: is when the pituitary gland causes ACTH production (about 2/3 of cases of endogenous cushing’s syndrome)
  • Cushing’s syndrome is excess glucocorticoids
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13
Q

Causes of Cushing’s syndrome

A
  • long-term high dose glucocorticoid therapy most common cause overall
  • ectopic ACTH-producing tumor (eg, small cell lung cancer, medullary thyroid cancer
  • adrenal tumor (adenoma)- secretion of excess cortisol
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14
Q

common signs of cushing’s syndrome

A

moon facies, obesity, buffalo hump, supraclavicular fat pads, thin extremities
Acanthosis nigricans
hypertension
hirtuisim

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15
Q

Three screening tests for cushing’s? What happens if the screening is positive?

A

24 hour urinary free cortisol (most specific) (at least 2 tests)
salivary cortisol (2-3 times)
low-dose overnight dexmethasone suppression test
*ALL tests likely needs a second confirmatory test

If test is positive, determine if ACTH independent or ACTH dependent
*THEN (and only then) order appropriate imaging

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16
Q

hyperpigmentation can be seen in?

A

Priamry adrenal insufficiency
ACTH-dependent Cushing’s syndrome (pituitary adenoma, ectopic ACTH, medullary cancer of thyroid, pheochromocytoma)

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17
Q

what disease are considered ACTH-dependent Cushing’s?

A

Pituitary adenoma (Cushing’s disease)
ectopic ACTH syndrome (oat cell ca, carinoid tumor, medullary ca of the thyroid, pheochromocytomas)

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18
Q

what diseases are considered ACTH independent cushing’s (much in higher in kids)

A

Iatrogenic- exogenous glucocorticoids
adrenal adenomas
adrenal cancers
micro and macronodular hyperplasia (rare)

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19
Q

Test that measures total cortisol(so not for women on OCPs)
substance should turn off CRH and ACTH production (and turn off signal for cortisol)

A

Dexmethasone suppresion test

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20
Q

After diagnosis of 1-2 postives with one of the three tests, what should you do to determine if cushing’s is ACTH independent or dependent? what distinguishes them?

A

Order an AM plasma ACTH
* if plasma ACTH is undetectable- ACTH Independent
* if plasma ACTH is detectable (normal or elevated)- ACTH dependent

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21
Q

what imaging would you order for ACTH dependent cushings? ACTH independent? what would you do if the ACTH dependent imaging is negative?

A

ACTH dependent: Pituitary MRI (cushing’s disease)
ACTH Independent: CT of adrenal glands (Cortisol producing tumor)
*If MRI is negative look for ectopic producing tumor- such as OAT cell carcinoma, carcinoid tumor, medullary CA, pheochromocytoma

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22
Q

why shouldn’t you do imaging without a clear diagnosis of cushing’s?

A

high number of incidentalomas- must have clear biochemical diagnosis and localization of where the problem is

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23
Q

when determining between cushing’s disease and ectopic ACTH production (both have high ACTH results from checking ACTH plasma levels) how could you determine which is which?

A

Give a high dose dexamethasone suppresion test.
* If there is NO suppresion: Ectopic ACTH producing tumor
* * if there is suppression: Cushing’s disease

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24
Q

treatment of cushing’s syndrome?

A

Surgical: Pituitary surgery is first line tx for cushing’s disease, adrenalectomy for cushing’s due to adreanal dx, ectopic ACTH syndrome, bilateral adrenalectomy for pituitary disease that is refractory to pituitary intervention

pharmacological: ketoconazole, miotane, metyrapone

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25
Q

stimuli for release of aldosterone?

A

Decrease in vascular volume, sympathetic nervous system stimulation of renin secretion, rise in serum potassium concentration will stimulate aldosterone synthesis by acting directly on the adrenal zona glomerulosa cells

excess aldosteron results in HYPOkalemic alkalosis
helps Na+ retention

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26
Q

Associated with increased aldosterone and decreased renin (often asymptomatic)- major hormone with mineralcorticoid activity

A

primary aldosteronism

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27
Q

Triad of symptoms for primary Hyperaldosteronism? what other symptoms should you be aware of?

A

HYPERtension, HYPOkalemia, metabolic alkalosis
* palpatations, polyuria, glucose intolerance, parasthesias, HA, muscle weakness, can sometimes see changes on EKG

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28
Q

Causes of primary aldosteronism?

A
  • Aldosterone producing adrenal adenoma most common cause
  • bilateral hyperplasion of the Zona Glomerulosa (idiopathic hyperaldosteronism) second most common cause
  • primary adrenal hyperplasia
  • adrenal carcinoma
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29
Q

HYPERtension, HYPOkalemia, HYPERnatremia, adrenal adenoma
* excess mineralcorticoid

A

Primary adosteronism (Conn’s syndrome) due to a benign adrenal tumor

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30
Q

Diagnosis of primary aldosteronism? what are precautions? expected levels?

A
  1. Plasma aldosterone/renin ratio (must be off spironolactone or epelerone for 6 weeks- other HTN meds ok; replace K+ if low or it will inhibit aldosterone; ratio >30 aldosteronism likely
  2. Expected levels: Increased aldosterone, decreased renin (if renin is normal than primary is excluded)
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31
Q

How do you CONFIRM the diagnosis of primary aldosteronism?

A

IV NS suppression test- caution with CHF
* 2-3L infused over 4-6 hours
* Hyperaldosteronism confirmed if PA> 10ng/dl

oral salt loading and also be done
* pts loaded with salt tablets and high salt diet- collect 24 hour urine- if aldosterone not supressed (>14ug/dl) primary aldosteronism
MRI/CT to confirm

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32
Q

results from the renin and aldosterone ratio tests can be altered by hypertensives- how so?

A

false positives: B-blockers
false negatives: ACE-inhibitors, ARBs, calcium channel blockers

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33
Q

Treatment for Hyperaldosteronism?

A
  1. Surgery- indicated for APA and Adrenal carcinoma
  2. medication for bilateral adrenal hyperplasia- Decrease HTN and increase K+ with spironolactione & eplernone

PANCE states ACE inhibitors as well for #2

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34
Q

what medications are mineralcorticoid antagonists?

A

spironolactone & eplerenone

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35
Q

chatecholemine secreting tumor from adrenal medulla

A

pheochromocytoma

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36
Q

symptoms of pheochromocytoma?

A

paraoxysmal symptoms (spells) or chronic- precipitated by postureal changes, exercise, inceased abdominal pressure
* severe and resistant HTN
* diaphoresis (sweating)
* tachycardia
* palpitations
* n/v
* pallor - cold hands and feet
* syncope
* tremor

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37
Q

Work-up for pheochromocytoma includes?

A
  1. 24 hour urine collection to measure catecholamines and metanephrines (Vanillymandic acid is a byproduct of epi and norepi)
  2. plasma -measure fractioned metanephrines
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38
Q

Diagnosis of pheochromocytoma? Treatment?

A
  • > 2 fold elevation above upper limit/ repeat if borderline
  • image with abdominal CT/ MRI

Treatment: Adrenalectomy (premedicate with alpha and beta blocker to avoid adrenal crisis)
* Alpha andrenergic: Phenoxybenzamine, prazocin, terazocin, doxazocin
* beta andrenergic: propranolol, metoprolol etc.

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39
Q

adrenal lesion seen on abdominal imaging orderd for another indication

A

adrenal incidentaloma

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40
Q

What should happen if an incidentaloma is found?

A
  • require hormonal work up

<4cm:
* 1mg dexmethasone supression test
* plasma aldosterone/renin ration
* plasma metanephrines (can be skipped based on imaging)

>4cm
* surgical removal AFTER pheochromocytoma is ruled out. if you don’t you can precipitate an adrenal crisis

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41
Q

what levels for ACTH and cortisol do you expect in primary adrenal insufficiency?

A

ACTH: high
Cortisol: low

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42
Q

what levels of ACTH and cortisol do you expect to see in seconday adrenal insufficiency

A

ACTH: Low
Cortisol: Low

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43
Q

when the CRH stimulation test is done in adrenal insufficency, what is the result expected in primary? in secondary?

A

primary: ACTH is increased/high
sencondary: ACTH is absent/low

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44
Q

symptoms of secondary adrenal sufficiency

A

*less pronounced
NO hyperpigmentation
NO hyperkalemia (mineral corticoid activity is NORMAL)
NO vitiligo
ISOLATED glucocorticoid insuffiency *
Symptoms can include: weakness, weight loss, hypotension, postural symptoms, GI symptoms, salt craving

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45
Q

treatment for adrenal insufficency?

A

Primary: Hydrocortisone & fludrocortisone
Secondary: Hydrocortisone only

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46
Q

treatment of adrenal crisis?

A

Hydrocortisone 100mg IV every 8 hours
IVF for hypotension and shock

To avoid adrenal crisis: Surgical patients chronically treated with prednisone,
*PREOPERATIVELY require 100mg IV hydrocortisone on call to OR and every 8 hours post op to avoid adrenal crisis

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47
Q

Inflammatory comparison of corticosteroids from lowest to highest?

A

Lowest: Cortisone
hydrocortisone
prednisone
triamcinolone
Highest: dexamethasone

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48
Q

Causes of HYPOthyroidism?

A

iodine deficiency
Hashimoto’s thyroiditis
postpartum thyroiditis
medications: Lithium, amiodarone, alpha interferon

49
Q

Common labs associated with thyroid

A
  • TSH: biotin effects, hold 2-3 days prior to lab
  • free T4, T3 if TSH is abnormal (reverse T3 only in critical illness; Total T4 monitored in pregnancy)

TPO antibodies, TSI levels, TG antibodies, TRab
* TPO and TG antibodies in hypothyroidism
* TSI and TRab in hyperthyroidism

thyroglobulin level used as a tumor marker for thyroid cancers
calcitonin used to monitor medullary thyroid cancer

50
Q

TSH elevated
free T4 is normal or low
free T3 often remains low until late in disease course

A

Primary hypothyroidism

51
Q

seen in hypothalmic/pituitary failure, pituitary gland abnormality
TSH is low-normal or low; free T4 is low

A

central hypothyroidism

52
Q

TSH is low
Free T4, T3 high

A

hyperthyroidism (thyrotoxicosis)

53
Q

TSH is normal or high
Free T4 elevated
Free T3 elevated

A

TSH secreting tumor or central thyroid hormone resistance syndrome

54
Q

what should you be aware of when measuring total thyroid hormone measurements?

A
  • Estrogen increases total T4 and T3 due to increased TBG
  • Illness decreases total T4 and T3 due to decreased protein levels
55
Q

what are etiologies of hyperthyroidism?

A

high iodine intake: Grave’s disease, Toxic multinodular goiter,
low iodine intake: thryoiditis (subacute,postpartum) and drug induced (iodine, amiodarone, thyroid hormone)

56
Q

Autoimmune disease: TSH-receptor antibodies target and stimulate the TSH receptor on the thyroid gland leading to increased thyroid hormone production, thyroid galnd enlargement and hyperthyroidism

A

Grave’s disease

57
Q

symptoms of grave’s disease

A
  • SX of hyperthyroidism: palpitations, heat intolerance, tremors, weight loss, atrial fibrillation
  • Orbitopathy: proptosis, exophthalmos, lid lag, diplpia vision change
  • pretibial myxedema: swollen or red brown patches on legs with non-pitting edema
58
Q

what lab levels would you expect to seen in Grave’s disease?

A

Decreased TSH, Increased free T4, T3
Thyroid stimulating immunoglobulins present

59
Q

more commonly seen in older individuals
type of hyperthyroidism
on nuclear imaging studies, one sees “hot” and “cold” areas
* Patchy areas of both increased and decreased uptake)

What lab levels would you expect to see in this?

A

Toxic multinodular goiter
Labs: decreased TSH, Increased T4/T3

60
Q

Often presents after upper respiratory infection
has thyrotoxic symptoms
anterior neck pain, thyroid tenderness
results from inflammation of gland
usually self-limited

A

Subactue thyroiditis

often treated with NSAIDs +/- steroids
use beta blockers for HR control

61
Q

similar to subacute thryoiditis but WITHOUT pain
often a diagnosis of exclusion
monitor for improvement
treat excess hormone or deficiency as needed

A

silent thyroiditis

62
Q
  • patient may experience hyperthyroid phase followed by hypothyroid phase before returning to euthyroid state
  • often misdiagnosed as post partum anxiety and depression
  • usually occurs within 6 months following delivery
  • tends to recur
A

postpartum thyroiditis

63
Q

amiodarone use and hyperthyroidism- what are the two types? how do you treat it?

A
  1. Type one: excess synthesis of homone- treat with thionamides or potassium/sodium perchlorate
  2. Type Two: result of damage to thyroid cells from amiodarone, its metabolite or iodine- treat with corticosteroides
64
Q

MOA: inhibit intrathyroidal peroxidase
do not affect iodine trapping or release of thyroid hormone

A

thicarbamides (PTU & methimazole)

65
Q

inhibits conversion of T4 to T3
drug of choice for Grave’s disease in 1st trimester of pregnancy
preferred treatment in thyroid storm

A

PTU

66
Q

Generally preferred agent due to less incidence of hepatotoxicity
less adverse effects but teratogenic in first trimester

A

Methimazole

67
Q

Side effects of anti-thyroid drugs such as thiocarbamides

A

rash, agranulocytosis, toxic hepatitis, risk of fulminant liver, lupus like syndrome, arthralgia, fever, apalsia cutis with methimazole used in 1st trimester of pregnancy

68
Q

usually results in permanent hypothyroidism
indication: grave’s disease, multinodular goiter, toxic adenoma
also used in treatment of thyroid cancer
may be used in diagnostic thyroid uptake and scan

A

Radioactive iodine (I-131)

69
Q

MOA: taken up and stores the same as iodide- incorporated into Tg
*generally max effect by 4-6 months

A

radioactive iodine (I-131)

70
Q

What are side effects of radioactive iodine? contraindications

A
  • AE: dry mouth, dry eyes, may need to repeat
  • Contraindicated: children and pregnant women; women should not conceive for 6 months; discontinue antithyroid durgs for at least 3 days; low iodine diet recommended for 1-2 weeks
71
Q

treatments for hyperthyroidism

A

anti-thyroid drugs
radioactive iodine (I-131)
surgery

72
Q

Etiologies of hypothyroidism

A

Hashimoto’s thyroiditis
congenital
infmmatory (thyroiditis)
iron deficiency
neoplatic
pharmacologic: Lithium- impairs release of T4 and T3; amiodarone, PTU, methimazole, interferon, rifampin

73
Q

treatment of hypothyroidism

A

Levothyroxine- synthetic but essential to endogenous T4 (drug of choice)
Liothyronine- short half life, may use for faster onset or bridge
dessicated thryroid- “natural” derived from bovine or porcine thyroid glands- contains T4 and T3 (contraindicated in pregnancy)

74
Q

severe hypothyroidism with mental status changes, hypothermia and respirtory failure
most common in older women
may have history of lithium or amiodarone treatment

A

myexdema coma

75
Q

treatment of myexedma coma?

A

Hydrocortisone 50-100mg IV q 8 hours
levothyroxine IV

76
Q

when should you treat subclinical disease?

A

TSH >10
consider treatment with TSH 5-10 with (family history, goiter, +TPO antibodies, hypercholesterolemia, desires pregnancy)

77
Q

most common- accounts for most throid cancers
excellent prognons
treatment: thyroidectomy (may be curative); radioactive iodine (specific cases); +/- TSH supression
**metastasizes via lymphatics **
monitor with neck ultrasound, follow thyroglobulin levels, I-131, metastatic surveys, PET scans

A

Papillary carcinoma

78
Q

10-15% of thyroid cancers
good prognosis depending on extra-thyroidal extension and vascular invasion
treatment: thyroidectomy, RAI with I-131, TSH supression
metastasizes hematogenously
hurthle cell varient may be more aggressive

A

Follicular carcinoma

79
Q

5-10% of cases
sporadic (75%) or familial (25%)
arises from parafollicular cells of thyroid
prognosis varies depending on extent od disease
tends to metastasize early- even before tumor is palpable
calcitonin is a serum marker and can be dx with FNA
treatment: Thyroidectomy, neck dissection, No I-131

A

medullary carcinoma

80
Q

rare < 5% of cases
more common in elderly
very poor prognosis 100% mortality
treatment: palliative
present as rapidly expanding, fixed hard thryoid mass
may be seen as a late diffentiation of papillary TCA

A

anaplastic carcinoma

81
Q

when should PTH be secreted? when should it not be secreted?

A

Secreted when calcium is low
not secreted when calcium is high

82
Q

calcium sensing in the kidneys

A

with increased calcium, calcium is excreted
with decreased calcium, calcium is retained

83
Q

what is PTH action at bone?

A
  • binds to receptors on osteoblasts, which in turn activate osteoclasts
  • increased bone turnover leads to release of calcium and phosphate
84
Q

PTH action at the kidneys?

A

PTH increases calcium reabsorption
PTH inhibits phosphate reabosorption (ie increase urinary phos loss)
PTH increases activation of Vitamin D by 1alpha hydroxylase

PTH is stim. by high phos-> loss in urine
high vit D-> suppress PTH

85
Q

Actions of Vitamin D in the GI tract? Parathyroid? Bone?

A

Works with PTH to raise calcium–> but counterbalances PTH by raising phosphate levels
In the GI tract: stimulates calcium (and phosphate) absorption
Parathyroid gland: decreases transcription of PTH and supresses cell proliferation
bone- some direct bone effects, but the main job is maintaing adequate minerals for bone health

86
Q

Best marker to measure to evaluate vitamin D status?

A

25(OH) Vit D (25-D)
this step is unregulated, so 25-d levels reflect total vitamin D entering the system

87
Q

what induces and what inhibits the activity of 1alpha hydroxylase

A

induced by PTH (to help raise caclium levels)
induced by low phosphate(because vitamin D raises phos levels)
inhibited by high calcium
inhibited by its product- 1, 25-D

88
Q
  • caused by abnormal regulation of PTH by calcium leading to excess PTH secretion: Increases calcium resorption from bone, increases calcium retention at kidney, activates vitamin D- increaseing GI calcium absorption
  • elevated calcium levels and high or inappropriately normal PTH levles
  • usually caused by single parathyroid adenoma
A

primary hyperparathyroidism

89
Q

symptoms of primary hyperparathyroidism?

A

Bones, stones, abdominal groans, psychic moans
Bone pain, kidney stones, nausea, vomiting, constipation, confusion, memory difficulties, difficulty concentrating

90
Q

treatment of hyperparathyroidism

A

surgical removal of the involved gland

91
Q
  • loss-of-function mutation in the CaSR (less sensitive calcium)
  • needs higher Ca before PTH is suppressed; needs higher Ca before calciuria is induced
  • mildly high Ca, high-nml/mildly high PTH, Low urinary Ca + family history
  • is benign
A

Familial hypocalciuric hypercalcemia

92
Q

what could cause hypercalcemia with a normal parathyroid gland

A

hypercalcemia of malignancy
vitamin D intoxication
sacoidosis/ granulomatous disease
hyperthyroidism
milk-alkali syndrome
prolonged immobilization

93
Q

symptoms of hypocalcemia?

A

perioral or digital parasthesias, muscle cramping, tetany, seizures

94
Q

Disorder of inadequate PTH secretion
low ca and low (or inappropriately normal) PTH
usually due to absent or damaged parathyroid glands

A

Primary hypoparathyroidism

95
Q
  • These conditions lead to an appropriate elevation of PTH
  • frequently the compensatory rise in PTH is able to correct the calcium level back into the normal range
  • thus, can present with either low or normal calcium and high PTH
A

secondary hyperparathyroidism

96
Q

how does vitamin D deficency lead to secondary hyperparathyroidism?

A

leads to poor intestinal absorption of calcium
decreases availability of calcium for bone mineralization
declining calcium levels trigger appropriate PTH secretion

97
Q

how does chronic kidney disease lead to secondary hyperparathyroidism?

A

renal clearance of phosphate is impaired
renal 1alpha-hydroxylase activity is impaired
*both are triggers for PTH secretion
*active vitamin D (calcitriol) or analogs are used to suppress this PTH to protect bones

98
Q

risk factors for osteoporosis

A

Previous history of fragility fractures
female gender(men get it later)
increasing age
postmenopausal status (or testosterone deficiency in men)
low weight
smoking
famiy history of osteoporosis

99
Q

the most common osteoporotic fracture? Highest mortality fracture? most common fracture in young women?

A
  1. vertebral compression fracture
  2. hip fractures have high morbidity
  3. distal radius fractures for younger women
100
Q

causes of secondary osteoporosis

A

Glucocorticoid induced- meds or endogenous cushings
endocrine: low testosterone, hyperthyroidism, hyperparathyroidism
malignancies: multiple myeloma, other lymphoproliferative malignancies

101
Q

ways that steroids are bad for bone?

A

decrease intestinal calcium absorption
increase expression of RANKL on osteoblasts
suppress maturaion and increase apoptosis of osteoblasts
increase renal Ca and Phos losses

102
Q

automatic diagnosis of osteoporosis?

A

the occurance of low-trauma fracture without alternative explanaion is diagnostic of osteoporosis

103
Q

score states how many standard deviation that a pts BMD is from the mean of a population of sex matched, young healthy controls
score of zero= an average healthy young control
Positive= above average
negative= below average

A

T- score

104
Q

exact thing as a T-score except the reference population is a sex-match, age-matched population

A

Z score

105
Q

when diagnosing what side is used for diagnosis?
when are T scores most useful?
what T score is osteoporosis? what score is osteopenia?

A
  1. the site with the lowest score is used for dx
  2. T scores are most useful in POSTmenopausal women, also in men over the age of 50
  3. A T-score of <-2.5 or lower =osteoporosis
  4. A T- score of -1.0-2.4=osteopenia
106
Q

when are Z score used? What does a score of -2.0mean? What are important things to think about with diagnosis?

A
  1. Z scores are used in PREmenopausal women and in young men
  2. scores less than -2.0 defines “lower than expected bone density for age”
  3. osteopenia should never be diagnosed in the young and healthy population
  4. in this group the diagnosis of osteoporosis should usually be reserved for those with fragility fractures and should not be made on DXA results alone
107
Q

disease of abnormal bone mineralization
Vitamin D deficiency is most common cause

A

rickets- occurs in growing bone
osteomalacia- in mature pone

sx include bone pain, tenderness, muscle weakness, inc. fracture risk

108
Q

a CaSR agonist- can be used to suppress abnormal/unwanted PTH secretion
-suppresses PTH in setthing of parathyroid carcinoma
-suppresses PTH in setting of secondary hyperparathyroidism due to ESRD/HD

A

Cinacalcet

109
Q

Clinical uses of Vitamin D?

A
  • Cholecalciferol supplements for vitamin D deficiency
  • Calcitriol or other active form for CKD with secondary hyperparathyroidism
  • calcium and calcitriol for hypoparathyroidism
110
Q

antiresorptive medications

A

Estrogen
SERMs
Bisphosphonates
calcitonin
denosumab

antiresoptives= decrease bone resorption- inhibit osteoclasts

111
Q

binds to the estrogen receptor but has differential effects depending on the tissue
* estrogen like at bone- small improvement in bond density, prevent further loss
* anti-estrogen at breast (decreases breast cancer ris)
* INCREASED risk of hot flashes and risk of thromboembolic disease
* decreaes risk of vertebral fracture

A

raloxifene (selective estrogen receptor modifiers)

112
Q
  • incorporated into bone matrix. When reabsorbed by osteoclasts, they impair their function and induce apoptosis
  • induce a small improvement in bone density, prevent further bone loss
  • only 4 agents used
A

Bisphosphonates
1. alendronate
2. risedronate
3. ibandronate
4. zoledronic acid

113
Q

side effects of bisphosphonates?

A

Upper GI symptoms/heart burn (oral only)
osteonecrosis of the jaw
atypical femoral fractures

114
Q

oral, dosed weekly for osteoporosis

A

alendronate

115
Q

dosed weekly or monthly- similar to alendronate

A

risedronate

116
Q

dosed orally monthly or IV every 3 months
antifracture efficacy demonstrated only for vertebral fracture (second line for this reason)

A

ibandronate

117
Q

IV, dosed yearly for osteoporsis (every 2 years for prevention of osteoporosis)
NO GI side effects
up to 1/3 of pts will have an acute phase reactionto 1st infusion
most potent bisphosphonate
antifracture efficacy at all sites

A

zoldronic acid

118
Q

give intranasally or subcutaneously
can be used to decrease calcium levels acutely in treatment of severe hypercalcemia (short lived)
has some data in pain control in acute vertebral compression fracture

A

calcitonin

119
Q

monoclonal antibody to RANK-L
decreases activation of osteoclasts
subcutaneous injection, dosed every 6 months
antifracture efficacy at all sites, vertebral fracture efficacy at all sites

A

denosumab

120
Q

Given as a daily injection
approved for use for x 2 years
can lead to significant gain in BMD
shown to decrease vertebral fractures by 65% and nonvertebral by 50%
pulsatile PTH induces osteoblastic activity leading to net gains in bone density

A

The anabolics: Teriparatide (short acting recombinant of PTH
abaloparatide is similar but (PTHrP analog)

121
Q

siede effects of anabolics?

A

side effects are mild
nausea
dizziness
weakness
*bone gains achieved are quickly lost when the drug is stopped. Teriparatide treatement must be follwed by an antiresorptive to maintain these improvements.

Endocrine Exam 2 (4 decks)

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