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endocrine Flashcards

1
Q

which test is the most sensitive for pathologic changes in the thyroid?

A

TSH - most important test clinically

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2
Q

what does TSH have a log-linear relationship with?

A

T4

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3
Q

T or F: TSH is trustworthy in central (pituitary) disease?

A

false

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4
Q

which is the prohormone - T3 or T4?

A

T4

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5
Q

which has more in circulation, T3 or T4?

A

T4 (99%)

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6
Q

T or F: T4 is less sensitive for disease than TSH

A

true

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7
Q

formula for free T4 index

A

total T4 x T3 resin uptake

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8
Q

mild hypo or hyperthyroidism; no obvious symptoms

A

subclinical disease

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9
Q

biochemical definition of subclinical disease

A

TSH abnormal but free T4 (T3) still within normal range

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10
Q

what is low T3 syndrome/sick euthyroid syndrome?

A

in any critical illness, thyroid tests decrease (except rT3) probably both central (CNS) and peripheral causes of this. data does NOT support replacement in the ICU

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11
Q

normal TSH

A

0.5-5.0

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12
Q

normal T4

A

0.8-1.8

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13
Q

tests to determine the etiology of the thyrotoxicosis

A

radioactive iodine uptake

radioactive iodine or technecium scan

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14
Q

tests to evaluate for structural thyroid disease

A

imaging the thyroid gland - US

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15
Q

what is I-123 uptake?

A

day 1 am: ive patient ~300 micro Curies of I-123

day 2 am: measure percent of I-123 that has been “taken up” by the thyroid gland (this is NOT a picture)

normal uptake is 15-35% @ 24 hours

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16
Q

is the I-123 test helpful in the evaluation of hypothyroidism?

A

NO

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17
Q

when can the I-123 test not be done?

A

when the patient has recently received a dose of iodinated IV contrast

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18
Q

what does “low uptake” in the I-123 test suggest?

A

low thyroid gland activity = thyroiditis as cause of thyrotoxicosis

*uptake distinguishes between thyroiditis and the other diagnoses

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19
Q

what does normal or High uptake in the I-123 test indicate?

A

favors active gland = Graves or “hot nodules”

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20
Q

what does nuclear imaging (scintigraphy) do for thyroid testing?

A

gives the pattern of uptake, answers the question of Graves’ vs. hot nodules

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21
Q

when the uptake is low in the I-123 test, should you order a scan?

A

NO - wasteful because nothing to look for on scan

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22
Q

how do you treat hypothyroidism?

A
  • *levothyroxine (L-T4)
  • can be dosed in terms of weekly dose; miss one, take 2 th enext day (pro-hormone)

can use L-T3 (cytomel) but short acting and requires multiple daily dosing

in primary hypothyroidism: monitor TSH levels (4-6 weeks after dose change)

in central hypothyroidism - monitor free T4 levels

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23
Q

how do you treat hyperthyroidism?

A

meds: beta blockade: propanol, metoprolol, etc
iodine (to block T3, T4 production)
thionamides (PTU or methimazole)
steroids (if thyroiditis is suspected)

radioactive iodine

surgery

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24
Q

Wolff-Chaikoff vs. Jod-Basedow effect

A

WC: “wolff choke off” –> sudden iodine load temporarily (few weeks) inhibits organification of iodinde, thus blocking synthesis, iodine is useful for acute treatment of severe hyperthyroidism (but be aware of jod-basedow)

JB: “jod blastoff effect” –> iodine induced thyrotoxicosis, may be delayed, caused by administration of iodine in setting of autonomous thyroid tissue and prior iodine deficiency; be careful giving iodine to patient with Graves’ who just arrived from a third world country

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25
Q

anti-thyroid drugs

A

thionamides :

propylthiouracil or PTU: now falling out of favor, but “safer” in pregnancy (3 times a day dosing)

methimazole: (tapazole) drug of choice

both rarely cause allergic reactions (neutropenia or even agranulocytosis)

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26
Q

what is the therapy of choice for graves’ or hot nodules?

A

radioactive iodine

  • takes 1-4 months to work
  • can cause transient exacerbation of hyperthyroidism, but usually mild
  • 85-90% of graves patients become permanently hypothyroid by 6-12 months
  • may worsen pre-existing
  • ophthalmopathy in graves’ patients, especially smokers

hot nodule patients - great treatment

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27
Q

who is a candidate for thyroid surgery?

A

mechanical complicaitons of goiter, or urgency for treatment (wants to get pregnant, doesn’t want to deal with radiation or thionamide risks)

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28
Q

maternal demand for thyroid hormone (increases or decreases) during pregnancy?

A

INCREASES - up to 50% by 2nd trimester: in patients requiring oral T4 replacement, must often increase the dose

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29
Q

does mild thyroid functional disease require treatment?

A

may not have to treat all cases since typically patients are asymptomatic, but even subclincial thyroid disease may have subtle physiologic sequelae

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30
Q

subclinical thyrotoxicosis

A

low TSH, but T3 and T4 normal

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31
Q

subclinical hypothyroidism

A

High TSH, but T3 and T4 normal

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32
Q

what is the most common reason to treat subclinical thyrotoxicosis/hyperthyroidism?

A

risk of afib (3x increase)

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33
Q

are thyroid nodules common?

A

yes! typically asymtomatic, often difficult to palpate; under-reporting of true incidence

woman more than men

cancer is uncommon but not rare. should get an US to better visualize nodules

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34
Q 
cold (non-functioning) nodules; the vast majority of nodules 
hot nodules (autonomous/TSH independent T4/T3 production) are almost never malignant
A

benign adenomatous nodule

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35
Q

how common is thyroid cancer?

A

5-15%

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36
Q

whats the first thing to do if you find a nodule?

A

check TSH! (should be done before biopsy)

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37
Q

are overactive nodules usually cancerous?

A

no! (so if TSH is low (hyperthyroidism), do a I-123 scan/uptake

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38
Q

when is a FNA required for a nodule?

A

if > 1.5 cm

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39
Q

most nodules are what kind?

A

hypofunctioning or “cold”

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40
Q

Management of Suspicious Nodules (suspicious FNA cytology result) or Big Goiters with Compressive Symptoms

A

surgery!

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41
Q

is thyroid cancer common?

A

yes, but usually non-fatal

women to men 3:1

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42
Q

who are microcarcinomas (thyroid) most common in?

A

elderly (

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43
Q

most common type of thyroid cancer?

A

papillary and follicular - well differentiated = still behave in some respects like normal thyroid tissue

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44
Q

which thyroid cancer is almost uniformly fatal?

A

anaplastic (occurs in older people, very rapid)

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45
Q

thyroid cancer where loses thyroid character, no longer takes up iodine

A

poorly differentiated - much worse prognosis

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46
Q

what is medullary thyroid cancer?

A

very uncommon (

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47
Q

treatment of thyroid cancer

A

surgical removal of all normal thyroid tissue and cancer (if possible)

follicular cell-derived tumors (papillary follicular): radioactive iodine 131 to destroy any of above that is left

medullary thyroid cancer: surgery only

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48
Q

surveillance for follicular-derived cancers

A

monitoring with US and serum thyroglobulin (TG - a high TG suggests cancer is present), radioactive iodine whole scans

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49
Q

surveillance for medullary thyroid cancer

A

calcitonin

CT scans

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50
Q

complex, multifactorial condition of increased fat stores with both genetic, behavioral and environmental causes

A

obesity

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51
Q

T or F; higher body weights are associated with an increase in all-cause mortality

A

T

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52
Q

metabolic syndrome criteria

A

at least 3 of the following 5:

waist cicrumference:
men > or equal to 102 cm/40 inches
women > or equal to 88 cm/ 35 inches

triglycerides greater or equal to 150

HDL men or equal to 130/85 or antihypertensive meds

fasting glucose greater than 100

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53
Q

body shapes with increased risk

A

apple (android)
ovoid (fruit box

pear shaped/gynoid has no increased risk

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54
Q

these are endocrine organs for the language of fat-inflammation and pro-coagulation

A

adipose cells

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55
Q

what is leptin?

A

pro-satiety hormone - signals to the brain how much fat the body has so it adjusts to eat less and keeps the fat stores in equilibirum

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56
Q

what is gherlin?

A

hormone that counteracts leptin, hunger signaling

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57
Q

what is adiponectin?

A

an “anti-inflammatory” hormone that makes the body more sensitive to insulin. this is decreased in obesity

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58
Q

which fat is “good fat”

A

brown fat - found in babies, more metabolically active. generates non-shivering heat

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59
Q

how many cormorbid conditions with obesity?

A

62

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60
Q

when should you consider anti-obesity medication?

A

BMI> 30 or >27 with a comorbid condition, have utilized lifestyle approaches of diet, physical activity and behavioral tools to the best of their ability, unable to control weight or reach target weight loss with a lifestyle treatment alone. has reasonable expectations and understanding of how meds work, no contraindications

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61
Q

absolute contraindication for obesity meds?

A

childbearing age

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62
Q

qualifiers for surgical treatment for obesity?

A

BMI> or equal to 40, and BMI of 35 or higher who have 2 other cardiovascular risk factors

The LAP-BAND System-patients with a BMI of ≥ 30 kg/m2 and one or more obesity related comorbid conditions.

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63
Q

deficiencies common in gastric bypass

A

vitamin B12 and K

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64
Q

what is the functional unit of the thyroid?

A

follicle (balls of cells)

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65
Q

what is the active ingredient in the thyroid hormone?

A

iodine

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66
Q

what is hypothyroxinemia?

A

low plasma levels of thyroid hormone, which leads to low saturation of nuclear thyroid hormone receptors

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67
Q

constellation of signs and symptoms caused most commonly by deficiency of thyroid hormone

A

hypothyroidism

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68
Q

when is the fetal thyroid gland operational by?

A

10-12th week- fetal thyroid economy includes a contribution from maternal thyroid hormones (T3, T4)

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69
Q

what is cretinism?

A

maternal iodine deficiency - hypothyroidism in utero. leads to impaired brain development, short stature, deaf mutism, spasticity, thyroid gland structural abnormalities (goiter)

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70
Q

what happens with congenital hypothyroidism?

A

can be compensated in utero (mostly) but must be treated after birth. MAJOR PREVENTABLE CAUSE OF MENTAL RETARDATION

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71
Q

clinical manifestations of hypothyroidism in newborns/infants

A 
birth weight >4 kg
gestation >42 weeks
jaundice
hypothermia
cyanosis
macroglossia
large posterior fontanelle
umbilical hernia
retardation of bone maturation
respiratory difficulties/distress
poor feeding/sucking ability
failure to gain weight
hoarse cry
decreased activity/lethargy
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72
Q

biggest sign of hypothyroidism in children and adolescents

A

growth retardation

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73
Q

clinical manifestations of hypothyroidism in adults

A 
fatigue, lethargy
depression
increased sensitivity to cold
mild weight gain (wont make you obese)
dry skin, brittle nails and hair
delayed ankle reflex (relaxation phase delayed)
hypercholesterolemia
hyponatremia
74
Q

biggest complication with hypothyroidism?

A

myxedema coma (severe hypothyroidism plus other medical condition)

decreased mental status, bradycardia, etc

usually people with another medical problem like pneumonia, or elderly patients who can’t communicate well

75
Q

what happens with hyperthyroidism in utero?

A 
spontaneous abortion
premature labor
low birth weight
stillbirth
preeclampsia (CHF)
76
Q

Hyperthyroidism in Childhood

A

Accelerated growth but early epiphyseal maturation (advanced bone age)
Delayed puberty
Tendency towards lower weight
Almost always Graves’ disease

77
Q

symptoms of hyperthyroidism

A 
heat intolerance/sweaty
palpitations
increased perspiration
sleep disturbance
tremor
irritability
fatigue
anxious

Hyperactivity
Hyperreflexia
tachycardia/atrial arrhythmia (increased risk of afib)

78
Q

worst complication of hyperthyroidism

A

thyroid storm (usually patients have comorbidity like cardiac problems)

temperature, CNS changes, GI dysfunction, tachycardia, CHF

79
Q

autoimmunce thyroid disease of hypothyroidism

A

hashimotos

80
Q

autoimmunce thyroid disease of hyperthyroidism

A

graves disease

81
Q

most common etiology of hypothyroidism in adults

A

acquired

  • autoimmune: ***hashimoto’s disease (90%)(and post-thyroiditis) –> chronic lyphocytic thyroiditis (common, painless, lymphocytic ilfiltrate, perhaps most common AI disease)
  • drug related (amiodarone, INF-alpha)
  • post surgical (thyroid cancer patients)
82
Q

less common etiologies of hypothyroidism in adults

A

congenital (rare)
central (uncommon) - TSH deficiency, or less commonly TRH deficiency (pituitary/hypothalamic tumors)

central = pituitary proglem

83
Q

what can thyroiditis cause

A

a spectrum, from hashimotos to graves (can be associated with hypo , hyper, or euthyroidism)

usually painless

common in first post-partum year!

Attempts to subtype = many unhelpful names
Painless = Hashimoto’s = Chronic
Painful = Subacute = Granulomatous = DeQuervain’s
Infectious (rare)
Reidel’s = sclerosing (destructive)

84
Q

how long does thyroiditis last?

A

NO LONGER THAN 6 MONTHS - if you have hyperthyroidism lasting longer than 6 months, not thyroiditis

thyroid hormone leaking into the blood, causes hyperthyroidism

very common in year after pregnancy

3 phase: hyperthyroidism, hypothyroid briefly, then should recover (self limiting)

85
Q

most common etiology of thyrotoxicosis?

A

graves disease, esp in younger patients

Single or multiple autonomously functioning “hot” nodule(s): more likely in older patients (toxic uni/multi-nodular goiter)

86
Q

what is graves disease?

A

A distinct autoimmune syndrome

TSH-receptor stimulating antibodies,cell-mediated as well..

Much more common in women

Thyrotoxicosis (goitrous), Opthalmopathy (widened, palpebral fissure, periorbital edema, proptosis, chemosis, conjuctival injection), pretibial myxedema (rash)

“stare” - can be associated with any kind of hyperthyroidism
“orbitopathy/opthalmopath” specific to graves disease

TSH receptors in the thyroid, so if you have an antibody that mistakenly turns on that receptor, its like you have TSH, so it makes more thyroid hormone

87
Q

what should you always include with you are giving report about a thyroid patient?

A

include the eye, or else you’re not thinking

88
Q

what is nodular thyrotoxicosis?

A

“hot nodule” = abnormal growth of follicular cell into a lump that produces thyroid hormone autonomously (regardless of TSH)

Can be one nodule, or many, i.e. toxic multinodular goiter

More prevalent in older patients than younger

89
Q

Simplified Ddx of Low TSH:

A

Thyrotoxicosis
Central Hypothyroidism
Pregnancy (hCG effect)
Non-thyroidal illness/low T3 syndrome (pressors, steroids, etc.)

90
Q

Simplified Ddx of High TSH

A 
Hypothyroxinemia
Central Hyperthyroidism (rare)
91
Q

which is more adrenal weight, the cortex or medulla?

A

cortex (90%), and has 3 different zones

92
Q

what is made in the zona glomerulosa?

A

aldosterone (‘salt’)

93
Q

what is made in the zona fasiculata?

A

cortisol (‘sugar’)

94
Q

what is made in the zonal reticularis?

A

androgens (‘sex’)

95
Q

what is made in the medulla?

A

catecholamines

96
Q

what are adrenal hormones derived from?

A

common cholesterol

97
Q

what are androgens precursors for?

A

dihydrotestosterone and estradiol

98
Q

what can too much ACTH production do?

A

excess alpha MSH which can cause hyperpigmentation

99
Q

what is excess cortisol’s effect on bones?

A

suppresses osteoblast production and stimulates bones to be thinner

100
Q

organs effected by cortisol

A

brain, bone, CVS, immune system, kidney, skin/connective tissue

101
Q

which can be converted to sex steroids? DHEA or DHEAS?

A

DHEA

102
Q

adrenal androgens

A

androstenedione, DHEA, DHEA sulfate - direct biologic activity minimal, act as precursors for peripheral conversion –> testosterone and dihydrotestosterone

103
Q

what are female androgens important for?

A

axillary hair and pubic hair development

104
Q

Adrenal Androgen Excess in prepubertal boys

A

isosexual precocious puberty - early puberty

105
Q

Adrenal Androgen Excess in adult women

A

cystic acne, hirsutism, male type baldness, menstrual irregularities, oligoovulation or anovulation, infertility and or frank virilization

106
Q

Adrenal Androgen Excess in pubertal girls

A

heterosexual precocious puberty

107
Q

what are the catecholamines?

A

epinephrine, norepinephrine, dopamine

108
Q

what is synthesized and stored in the adrenal medulla?

A

epi and NE (+ peripheral sympathetic nerves)

(dopamine - precursor for NE - is found in the adrenal medulla and peripheral sympathetic nerves

109
Q

how does catecholamine action come about?

A

stressful stimuli causes catecholamine production, which causes a “fight or flight” response (in creased HR, BP, myocardial contractility, and cardiac conduction velocity)

110
Q

difference between cushing’s syndrome and cushing’s disease

A

disease is pituitary cause only, syndrome is all causes

111
Q

signs and symptoms of cushing’s

A

weight gain, menstrual irregularity, hirsuitism, psychiatric dysfunction, back ache, obesity, plethora, moon face, HTN, bruising, purple striae

112
Q

when are your ACT/cortisol levels highest and lowest?

A

highest in the morning at 8:00 and lowest at midnight

113
Q

ACTH independent cushing’s syndrome causes

A

Adrenal adenoma (10-15%) and carcinoma (

114
Q

ACTH-dependent cushing’s syndrome

A 
Cushing's disease (pituitary-dependent)  - 70%
Ectopic ACTH syndrome - 15% 
Ectopic CRH syndrome 
Macronodular adrenal hyperplasia
Iatrogenic (treatment with ACTH 1-24)
115
Q

Pseudo-cushing’s syndrome

A

alchoholism, depression, obesity

116
Q

how do you diagnose cushings?

A

mightnight plasma or sailvary cortisol

24 hr urinary free cortisol

low-dose dexamethasone suppression test (1 mg x 1 at 11pm OR 0.5 mg q6hr x 48 hrs) (normal result

117
Q

if ACTH (>15) and cortisol are high, where is the source of the hypercortisolism?

A

pituitary (tumor maybe)

if ACTH is

118
Q

most common sources of ectopic ACTH

A

small cell lung carcinoma, pancreatic tumors, lung carcinoids

119
Q

treatment of cushings

A

surgical: pituitary resection, adrenalectomy, resection of ectopic ACTH source
medical: mitotane (for ACC), ketoconazole, metyropone, aminoglutethimide, trilostane

120
Q

signs/symptoms of adrenal insufficiency

A

Dehydration, hypotension, or shock out of proportion to severity of current illness
Nausea and vomiting with a history of weight lost and anorexia
Abdominal pain
Unexplained hypoglycemia
Unexplained fever
Hyperpigmentation or vitiligo
Other autoimmune endocrine deficiencies, such as hypothyroidism or gonadal failure
Fatigue, weakness
Hyponatremia, hyperkalemia, azotemia, hypercalcemia, or eosinophilia

121
Q

causes of primary adrenal insufficiency (Addison’s disease)

A

Autoimmune: Sporadic or Autoimmune polyendocrine syndrome
Infections: Tuberculosis, Fungal, Cytomegalovirus, HIV
Metastatic tumor
Infiltrations: Amyloid, Hemochromatosis
Intra-adrenal hemorrhage: (Waterhouse-Friderichsen syndrome) after meningococcal septicemia, anticoagulation
Adrenoleukodystrophies
Congenital adrenal hypoplasia: DAX-1 mutations, SF-1 mutations
ACTH resistance syndromes
Bilateral adrenalectomy
Medications: ketoconazole, metyrapone

Need to have 90% infiltration to get adrenal insufficiency, so even if you loose the function of one gland, still won’t really see effects

122
Q

Causes of Secondary Adrenal Insufficiency

A 
Exogenous glucocorticoid therapy
Pituitary surgery or irradiation
Pituitary apoplexy
Postpartum pituitary infarction (Sheehan’s syndrome)
Granulomatous disease (TB, sarcoid)
Isolated ACTH deficiency
Lymphocytic hypophysitis
Idiopathic
Metastatic disease to pituitary
123
Q

problems with long-term glucocorticoid therapy

A

Abrupt cessation –> suppress HPA axis –> adrenal insufficiency (can occur with synthetic progestogen, medroxyprogesterone acetate, megestrol acetate, have GC agonist activity)

Excessive longterm use –> Cushing’s syndrome

Duration

124
Q

eval & treatment of adrenal insufficiency

A 
Evaluation:
8am cortisol  10 : rules out AI
8am cortisol 3-10 : 250 mcg ACTH stim test -->  >18 at 30 min or 60 min rules out AI
ACTH high : primary AI
ACTH low/low normal : secondary AI
125
Q

adrenal insufficiency treatment

A

IVF
glucocorticoud replacement: hydrocortisone 15-30 mg divided BID - TID
mineralocorticoid in primary AI = florinef 0.1 mg/day

126
Q

10% of all HTN patients present with what?

A

primary hyperaldosteronism

127
Q

when should you suspect primary hyperaldosteronism?

A

when HTN is resistant to treatment ( on 3 drugs including diuretic)

hypokalemia

adrenal incidentaloma

128
Q

what is the most common cause of hyperaldosteronism?

A

aldosterone producing adenoma (APA)
-65%, more severe, increase in aldo secretion, tx-surgery

bilateral hyperplasia is less common and is idiopathic hyperaldo = IHA. - 30-40%, milder, less aldo secretion, tx is drugs

129
Q

diagnosis of hyperaldosteronism

A

PAC/PRA ( aldosterone/renin ratio) > 20 or 30 and PAC > 15

confirm with salt loading (2 1 g sodium chloride tablets TID x 3 days)- On day #3, collect a 24-hour urine for aldosterone, sodium, and creatinine
24-hour urine sodium should exceed 200 meq to confirm adequate sodium loading
Urine aldosterone excretion >12 mcg/24 hours confirms hyperaldosteronism

  • excess salt should normally suppress aldosterone secretion
  • abdominal CT to look for adrenal mass - if unilateral mass, then adrenalectomy**if patient is > 40 yo then must do bilateral adrenal vein sampling to distinguish unilateral source
130
Q

what is congenital adrenal hyperplasia (CAH)

A

caused by various genetic defects in the enzymes involved in cortisol biosynthesis

decrease in cortisol production –> increase ACTH

manifestations due to decreased production of cortisol and decrease or increased production of mineralcorticoids and androgens (depending on the site of enzyme defect)

131
Q

which deficiency is the most common with congenital adrenal hyperplasia?

A

21-hydroxylase deficiency (95% of CAH)

132
Q

what are catecholamine-secreting tumors that arise form chromaffin cells of the adrenal medulla?

A

pheochromocytomas

Paragangliomas or extra-adrenal pheochromocytomas – arise from sympathetic ganglia

133
Q

symptoms of patients with pheo

A

HTN (may or may not have)
sweating
palpitations
paroxysmal HA (abrupt, bilateral, diminishes in hour)

134
Q

when should you screen for pheo?

A 
When patients are having Hyperadrenergic spells (eg, self-limited episodes of nonexertional palpitations, diaphoresis, headache, tremor, or pallor) 
Adrenal incidentaloma
Idiopathic dilated CM (cardiomyopathy)
Resistant HTN 
Onset of HTN at a young age (eg,
135
Q

familial pheo forms

A

younger, usually bilateral, many with no HTN

136
Q

what should you order in the management of pheo?

A

fractionated metanephrines
fractionated catecholamines
(urine/plasma)

137
Q

with adrenal diseases, what should you order first- biochemical testing or imaging?

A

biochemical testing

138
Q

which organs play a major role in assuring calcium homeostasis?

A

the skeleton, the gut and the kidney

139
Q

what accounts for 90% of cases of hypercalcemia?

A

PHPT (primary hyperparathyroidism) and malignancy

140
Q

epidemiology of PHPT

A

incidence is 1 in 500-1 in 1000
women> men
postmenopausal women- first decade

141
Q

etiology of PHPT

A

sporadic benign solitary adenoma - 80-85%

parathyroid hyperplasia 10-15%

142
Q

What symptoms do most patients with PHPT present with?

A

none!

Incidentally discovered on routine biochemical screening test

143
Q

Osteitis Fibrosa Cystica

A

characterized by subperiostal resorption of the distal phalanges, tapering of the distal clavicles, a “salt and pepper” appearance of the skull, bone cysts, and brown tumors of the long bones. It is now seen in fewer that 5% of pts with PHPT.

144
Q

what is th emost common overt complication of PHPT?

A

kidney stones (about 10-15% now)

145
Q

which meds can cause increase calcium levels?

A

litium and thiazide (HCTZ)

146
Q

what is the only curative therapy for PHPT?

A

parathyroidectomy

bone density improves, incidence of fractures and kidney stones reduces

147
Q

Possible complications of PTx

A

Damage to the recurrent laryngeal nerve – hoarseness and reduced voice volume
Permanent hypoparathyroidism
Transient hypocalcemia

148
Q

Guidelines for Monitoring Patients with Asymptomatic PHPT Who Do Not Undergo Parathyroid Surgery

A

serum calcium - annually
skeletal - every 1-2 years (3 sites)
renal: eGFR annual, serum creatinine annually. If renal stones suspected, 24-h biochemical stone profile, renal imaging by x-ray, US, or CT

149
Q

should patients with asymptomatic PHPT limit calcium intake?

A

no (low Ca diet could lead to further PTH stimulation), should have vitamin D repletion though + adequate hydration and encourage ambulation

Cinacalcet

150
Q

FHH - Familial Hypocalciuric Hypercalcemia

A

autosomal dominant (2% of cases of PHPT)

Inactivating mutation of the CASR gene – impaired calcium suppression of PTH secretion

Patients usually have mild or no symptoms

Benign course, rarely need treatment

151
Q

what is the cause of 90% of hypercalcemia of hospitalized patients?

A

malignancy - negative prognostic factor

HHM (humoral hypercalcemia of malignancy): Most common mechanism hypercalcemia in cancer.

152
Q

Pharmacologic Therapy for Hypercalcemia Associated with Cancer

A

fluids!!! and phosphonates

153
Q

how should you treat Bisphosphonate-Refractory Hypercalcemia of Malignancy

A

denosumab

154
Q

most common cause of hypocalcemia/vitamin D deficiency?

A

postsurgical (on thyroid gland)

155
Q

hypoparathyroidism

A

low Ca, High Phos, low/nl PTH

gland destruction (postop), autoimmune, congenital (DiGeorge syndrome: dyspmorphic features, anomalies)

impaired parathyroid function (hypomagnesemia)

resistance to PTH (hypomagnesemia)

156
Q

Pseudohypoparathyroidism

A

genetic disorder of target-organ unresponsiveness to PTH (low Ca, low phos, but high PTH)

Type 1a is the most common form: Albright hereditary osteodystrophy – short stature, round face, short neck, obesity, brachydactily, subcutaneous ossifications, mental retardation.

157
Q

Causes of Vitamin D deficiency

A 
Inadequate exposure to sunlight
Winter
Pollution
Sunscreen
Increased skin pigmentation

Obesity
Malabsorption syndrome – fat soluble vit
Meds: anti-convulsants, glucocorticoids, medications HIV/AIDS
Granulomatous diseases, lymphomas, PHPT – increase metabolism of vitamin D

158
Q

signs/symptoms of hypocalcemia

A 
Tetany, Chvostek’s (Tap facial nerve 2 cm ant to earlobe – contraction facial muscles), Trousseau’s (Elicited by inflating blood pressure cuff to about 20 mmHg above SBP for 3 min – carpal spasm)
Muscle twitching/cramping
Circumoral/acral tingling
Abdominal cramps
Generalized weakness, fatigue, depression
Laryngospasm, bronchospasm, seizures
Basal ganglia calcifications on imaging
Long QT, Heart failure
159
Q

Diagnosis/Management of hypocalcemia

A

Io Ca2+, Mg, Phos, iPTH, 25(OH)D

Goals of treatment
Alleviate symptoms (Ca 8.5-9.0 mg/dl)
Heal demineralized bones
Maintain acceptable Ca and avoid hypercalciuria (>300/24h)

Calcium – IV, PO
Vitamin D
Thiazides
Mg replacement
Replacement Therapy with PTH
160
Q

what is osteoporosis?

A

compromised bone strength (bone density, bone quality)

161
Q

Risk Factors for Osteoporosis

A

Low peak bone mass
Anorexia, bulimia, athletic amenorrhea
Decline estrogen – menopause
Endocrine: hypogonadism, hyperthyroidism, primary hyperparathyroidism, acromegaly
Nutrition/lifestyle: vitamin D deficiency, malabsorption syndromes
Medications: Glucocorticoids, thyroid hormone excess, Pioglitazone, Anti-seizure meds
Other: Primary hypercalciuria

162
Q

adult bone mass is achieved until what age?

A

30

163
Q

symptoms of osteoporosis

A

none! until you have a fracture

164
Q

diagnosis of osteoporosis

A

DEXA scan

T-scores between —1.0 and —2.5 define osteopenia. T-scores less than or equal to —2.5 define osteoporosis
A T-score is the number of standard deviations an individual’s bone density result is from the mean of healthy, gender-matched young adult controls

165
Q

what is a fragility fracture?

A

fall from a standing height or less

166
Q

Osteoporosis Evaluation and Management

A

Address secondary causes, if any
Ensure adequate calcium and vitamin D intake
1000-1200 mg of elemental calcium daily are recommended
At least 800-1200 international units of vitamin D daily are recommended. However, it is best to measure 25(OH) vitamin D to ensure intake is adequate.
Encourage weight-bearing exercises
Address fall prevention
Avoid tobacco, limit alcohol intake
Pharmacologic therapy if indicated

167
Q

what is the most used pharmacologic treatment for osteoporosis?

A

bisphosphonates

then SERMS, estrogen (but increases risk for heart disease), denosumab, PTH

168
Q

what does teriparatide do?

A

physiologically moves calcium from bone

when given intermittently and @ low doses –> anabolic effect on blasts

169
Q

type 1 diabetes

A

Beta-cell destruction- complete lack of insulin

170
Q

type 2 diabetes

A

Beta- cell dysfunction and insulin resistance

171
Q

which DM is inheritable?

A

type 2 (type I is not, its autoimmune)

172
Q

what percent of all cases of diabetes are type 1?

A

5%

173
Q

two forms of DM I

A

immune mediated- beta cells destroyed by autoimmune process
- genetic predisposition, autoimmune reaction may be triggered by viral infection, toxins. Destroys beta cells in pancreas that produce insulin

idiopathic - cause of beta cell function loss is unknown

circulating autoantibodies (ICA, GAD65)

174
Q

what are the long-term complications of DM?

A

microvascular –> retinopathy, nephropathy (microalbuminuria, gross albuminuria) and end-stage renal disease (ESRD), neuropathy (peripheral or autonomic) –> can lead to amputation

macrovascular complications–> coronary heart disease cerebrovascular disease, peripheral vascular disease

175
Q

what is diagnostic for DM?

A

HgA1C > or equal to 6.5% (normal is 4-6)

fasting glucose >/= 126

random >/= 200

176
Q

what disease can lead to insulin resistance and they can develop DM later in life?

A

PCOD

177
Q

what is microalbuminuria an indicator of?

A

incipient nephropathy, especially in type 1 diabetics (over 80% of patients with persistent microalbuminuria develop nephropathy)

In type 2 diabetes, microalbuminuria is also an indicator of macrovascular disease, especially coronary artery disease

178
Q

how can you reverse microalbuminuria?

A

ACE inhibitor. if you dont reverse, and it progresses to gross albuminura, diabetic kidney disease is past the point of no return and they will need dialysis

179
Q

what is the first sign of diabetic kidney failure?

A

proteinuria

180
Q

microvascular and macrovascular complications are predicted by what in DM?

A

microvascular - duration of diabetes, A1C, BP

macrovascular complicatons: duration of diabetes, A1C, BP, lipids

clin med (12 decks)

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