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Flashcards in endocrine Deck (180):
1

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

TSH - most important test clinically

2

what does TSH have a log-linear relationship with?

T4

3

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

false

4

which is the prohormone - T3 or T4?

T4

5

which has more in circulation, T3 or T4?

T4 (99%)

6

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

true

7

formula for free T4 index

total T4 x T3 resin uptake

8

mild hypo or hyperthyroidism; no obvious symptoms

subclinical disease

9

biochemical definition of subclinical disease

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

10

what is low T3 syndrome/sick euthyroid syndrome?

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

11

normal TSH

0.5-5.0

12

normal T4

0.8-1.8

13

tests to determine the etiology of the thyrotoxicosis

radioactive iodine uptake
radioactive iodine or technecium scan

14

tests to evaluate for structural thyroid disease

imaging the thyroid gland - US

15

what is I-123 uptake?

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

16

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

NO

17

when can the I-123 test not be done?

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

18

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

low thyroid gland activity = thyroiditis as cause of thyrotoxicosis

*uptake distinguishes between thyroiditis and the other diagnoses

19

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

favors active gland = Graves or "hot nodules"

20

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

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

21

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

NO - wasteful because nothing to look for on scan

22

how do you treat hypothyroidism?

**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

23

how do you treat hyperthyroidism?

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

radioactive iodine

surgery

24

Wolff-Chaikoff vs. Jod-Basedow effect

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

25

anti-thyroid drugs

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)

26

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

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

27

who is a candidate for thyroid surgery?

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

28

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

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

29

does mild thyroid functional disease require treatment?

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

30

subclinical thyrotoxicosis

low TSH, but T3 and T4 normal

31

subclinical hypothyroidism

High TSH, but T3 and T4 normal

32

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

risk of afib (3x increase)

33

are thyroid nodules common?

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

34

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

benign adenomatous nodule

35

how common is thyroid cancer?

5-15%

36

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

check TSH! (should be done before biopsy)

37

are overactive nodules usually cancerous?

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

38

when is a FNA required for a nodule?

if > 1.5 cm

39

most nodules are what kind?

hypofunctioning or "cold"

40

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

surgery!

41

is thyroid cancer common?

yes, but usually non-fatal
women to men 3:1

42

who are microcarcinomas (thyroid) most common in?

elderly (

43

most common type of thyroid cancer?

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

44

which thyroid cancer is almost uniformly fatal?

anaplastic (occurs in older people, very rapid)

45

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

poorly differentiated - much worse prognosis

46

what is medullary thyroid cancer?

very uncommon (

47

treatment of thyroid cancer

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

48

surveillance for follicular-derived cancers

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

49

surveillance for medullary thyroid cancer

calcitonin
CT scans

50

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

obesity

51

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

T

52

metabolic syndrome criteria

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

53

body shapes with increased risk

apple (android)
ovoid (fruit box

pear shaped/gynoid has no increased risk

54

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

adipose cells

55

what is leptin?

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

56

what is gherlin?

hormone that counteracts leptin, hunger signaling

57

what is adiponectin?

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

58

which fat is "good fat"

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

59

how many cormorbid conditions with obesity?

62

60

when should you consider anti-obesity medication?

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

61

absolute contraindication for obesity meds?

childbearing age

62

qualifiers for surgical treatment for obesity?

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.

63

deficiencies common in gastric bypass

vitamin B12 and K

64

what is the functional unit of the thyroid?

follicle (balls of cells)

65

what is the active ingredient in the thyroid hormone?

iodine

66

what is hypothyroxinemia?

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

67

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

hypothyroidism

68

when is the fetal thyroid gland operational by?

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

69

what is cretinism?

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

70

what happens with congenital hypothyroidism?

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

71

clinical manifestations of hypothyroidism in newborns/infants

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

72

biggest sign of hypothyroidism in children and adolescents

growth retardation

73

clinical manifestations of hypothyroidism in adults

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

biggest complication with hypothyroidism?

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

what happens with hyperthyroidism in utero?

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

76

Hyperthyroidism in Childhood

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

77

symptoms of hyperthyroidism

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

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

78

worst complication of hyperthyroidism

thyroid storm (usually patients have comorbidity like cardiac problems)

temperature, CNS changes, GI dysfunction, tachycardia, CHF

79

autoimmunce thyroid disease of hypothyroidism

hashimotos

80

autoimmunce thyroid disease of hyperthyroidism

graves disease

81

most common etiology of hypothyroidism in adults

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

less common etiologies of hypothyroidism in adults

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

central = pituitary proglem

83

what can thyroiditis cause

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

how long does thyroiditis last?

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

most common etiology of thyrotoxicosis?

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

what is graves disease?

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

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

include the eye, or else you're not thinking

88

what is nodular thyrotoxicosis?

"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

Simplified Ddx of Low TSH:

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

90

Simplified Ddx of High TSH

Hypothyroxinemia
Central Hyperthyroidism (rare)

91

which is more adrenal weight, the cortex or medulla?

cortex (90%), and has 3 different zones

92

what is made in the zona glomerulosa?

aldosterone ('salt')

93

what is made in the zona fasiculata?

cortisol ('sugar')

94

what is made in the zonal reticularis?

androgens ('sex')

95

what is made in the medulla?

catecholamines

96

what are adrenal hormones derived from?

common cholesterol

97

what are androgens precursors for?

dihydrotestosterone and estradiol

98

what can too much ACTH production do?

excess alpha MSH which can cause hyperpigmentation

99

what is excess cortisol's effect on bones?

suppresses osteoblast production and stimulates bones to be thinner

100

organs effected by cortisol

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

101

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

DHEA

102

adrenal androgens

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

103

what are female androgens important for?

axillary hair and pubic hair development

104

Adrenal Androgen Excess in prepubertal boys

isosexual precocious puberty - early puberty

105

Adrenal Androgen Excess in adult women

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

106

Adrenal Androgen Excess in pubertal girls

heterosexual precocious puberty

107

what are the catecholamines?

epinephrine, norepinephrine, dopamine

108

what is synthesized and stored in the adrenal medulla?

epi and NE (+ peripheral sympathetic nerves)

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

109

how does catecholamine action come about?

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

110

difference between cushing's syndrome and cushing's disease

disease is pituitary cause only, syndrome is all causes

111

signs and symptoms of cushing's

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

112

when are your ACT/cortisol levels highest and lowest?

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

113

ACTH independent cushing's syndrome causes

Adrenal adenoma (10-15%) and carcinoma (

114

ACTH-dependent cushing's syndrome

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

115

Pseudo-cushing’s syndrome

alchoholism, depression, obesity

116

how do you diagnose cushings?

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

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

pituitary (tumor maybe)

if ACTH is

118

most common sources of ectopic ACTH

small cell lung carcinoma, pancreatic tumors, lung carcinoids

119

treatment of cushings

surgical: pituitary resection, adrenalectomy, resection of ectopic ACTH source

medical: mitotane (for ACC), ketoconazole, metyropone, aminoglutethimide, trilostane

120

signs/symptoms of adrenal insufficiency

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

causes of primary adrenal insufficiency (Addison's disease)

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

Causes of Secondary Adrenal Insufficiency

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

problems with long-term glucocorticoid therapy

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

eval & treatment of adrenal insufficiency

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

adrenal insufficiency treatment

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

126

10% of all HTN patients present with what?

primary hyperaldosteronism

127

when should you suspect primary hyperaldosteronism?

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

hypokalemia

adrenal incidentaloma

128

what is the most common cause of hyperaldosteronism?

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

diagnosis of hyperaldosteronism

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

what is congenital adrenal hyperplasia (CAH)

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

which deficiency is the most common with congenital adrenal hyperplasia?

21-hydroxylase deficiency (95% of CAH)

132

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

pheochromocytomas

Paragangliomas or extra-adrenal pheochromocytomas – arise from sympathetic ganglia

133

symptoms of patients with pheo

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

134

when should you screen for pheo?

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

familial pheo forms

younger, usually bilateral, many with no HTN

136

what should you order in the management of pheo?

fractionated metanephrines
fractionated catecholamines
(urine/plasma)

137

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

biochemical testing

138

which organs play a major role in assuring calcium homeostasis?

the skeleton, the gut and the kidney

139

what accounts for 90% of cases of hypercalcemia?

PHPT (primary hyperparathyroidism) and malignancy

140

epidemiology of PHPT

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

141

etiology of PHPT

sporadic benign solitary adenoma - 80-85%
parathyroid hyperplasia 10-15%

142

What symptoms do most patients with PHPT present with?

none!

Incidentally discovered on routine biochemical screening test

143

Osteitis Fibrosa Cystica

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

what is th emost common overt complication of PHPT?

kidney stones (about 10-15% now)

145

which meds can cause increase calcium levels?

litium and thiazide (HCTZ)

146

what is the only curative therapy for PHPT?

parathyroidectomy

bone density improves, incidence of fractures and kidney stones reduces

147

Possible complications of PTx

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

148

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

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

should patients with asymptomatic PHPT limit calcium intake?

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

Cinacalcet

150

FHH - Familial Hypocalciuric Hypercalcemia

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

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

malignancy - negative prognostic factor

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

152

Pharmacologic Therapy for Hypercalcemia Associated with Cancer

fluids!!! and phosphonates

153

how should you treat Bisphosphonate-Refractory Hypercalcemia of Malignancy

denosumab

154

most common cause of hypocalcemia/vitamin D deficiency?

postsurgical (on thyroid gland)

155

hypoparathyroidism

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

Pseudohypoparathyroidism

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

Causes of Vitamin D deficiency

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

signs/symptoms of hypocalcemia

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

Diagnosis/Management of hypocalcemia

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

what is osteoporosis?

compromised bone strength (bone density, bone quality)

161

Risk Factors for Osteoporosis

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

adult bone mass is achieved until what age?

30

163

symptoms of osteoporosis

none! until you have a fracture

164

diagnosis of osteoporosis

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

what is a fragility fracture?

fall from a standing height or less

166

Osteoporosis Evaluation and Management

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

what is the most used pharmacologic treatment for osteoporosis?

bisphosphonates

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

168

what does teriparatide do?

physiologically moves calcium from bone

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

169

type 1 diabetes

Beta-cell destruction- complete lack of insulin

170

type 2 diabetes

Beta- cell dysfunction and insulin resistance

171

which DM is inheritable?

type 2 (type I is not, its autoimmune)

172

what percent of all cases of diabetes are type 1?

5%

173

two forms of DM I

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

what are the long-term complications of DM?

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

what is diagnostic for DM?

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

fasting glucose >/= 126

random >/= 200

176

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

PCOD

177

what is microalbuminuria an indicator of?

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

how can you reverse microalbuminuria?

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

what is the first sign of diabetic kidney failure?

proteinuria

180

microvascular and macrovascular complications are predicted by what in DM?

microvascular - duration of diabetes, A1C, BP

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