endocrine Flashcards
which test is the most sensitive for pathologic changes in the thyroid?
TSH - most important test clinically
what does TSH have a log-linear relationship with?
T4
T or F: TSH is trustworthy in central (pituitary) disease?
false
which is the prohormone - T3 or T4?
T4
which has more in circulation, T3 or T4?
T4 (99%)
T or F: T4 is less sensitive for disease than TSH
true
formula for free T4 index
total T4 x T3 resin uptake
mild hypo or hyperthyroidism; no obvious symptoms
subclinical disease
biochemical definition of subclinical disease
TSH abnormal but free T4 (T3) still within normal range
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
normal TSH
0.5-5.0
normal T4
0.8-1.8
tests to determine the etiology of the thyrotoxicosis
radioactive iodine uptake
radioactive iodine or technecium scan
tests to evaluate for structural thyroid disease
imaging the thyroid gland - US
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
is the I-123 test helpful in the evaluation of hypothyroidism?
NO
when can the I-123 test not be done?
when the patient has recently received a dose of iodinated IV contrast
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
what does normal or High uptake in the I-123 test indicate?
favors active gland = Graves or “hot nodules”
what does nuclear imaging (scintigraphy) do for thyroid testing?
gives the pattern of uptake, answers the question of Graves’ vs. hot nodules
when the uptake is low in the I-123 test, should you order a scan?
NO - wasteful because nothing to look for on scan
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
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
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
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)
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
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)
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
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
subclinical thyrotoxicosis
low TSH, but T3 and T4 normal
subclinical hypothyroidism
High TSH, but T3 and T4 normal
what is the most common reason to treat subclinical thyrotoxicosis/hyperthyroidism?
risk of afib (3x increase)
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
cold (non-functioning) nodules; the vast majority of nodules hot nodules (autonomous/TSH independent T4/T3 production) are almost never malignant
benign adenomatous nodule
how common is thyroid cancer?
5-15%
whats the first thing to do if you find a nodule?
check TSH! (should be done before biopsy)
are overactive nodules usually cancerous?
no! (so if TSH is low (hyperthyroidism), do a I-123 scan/uptake
when is a FNA required for a nodule?
if > 1.5 cm
most nodules are what kind?
hypofunctioning or “cold”
Management of Suspicious Nodules (suspicious FNA cytology result) or Big Goiters with Compressive Symptoms
surgery!
is thyroid cancer common?
yes, but usually non-fatal
women to men 3:1
who are microcarcinomas (thyroid) most common in?
elderly (
most common type of thyroid cancer?
papillary and follicular - well differentiated = still behave in some respects like normal thyroid tissue
which thyroid cancer is almost uniformly fatal?
anaplastic (occurs in older people, very rapid)
thyroid cancer where loses thyroid character, no longer takes up iodine
poorly differentiated - much worse prognosis
what is medullary thyroid cancer?
very uncommon (
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
surveillance for follicular-derived cancers
monitoring with US and serum thyroglobulin (TG - a high TG suggests cancer is present), radioactive iodine whole scans
surveillance for medullary thyroid cancer
calcitonin
CT scans
complex, multifactorial condition of increased fat stores with both genetic, behavioral and environmental causes
obesity
T or F; higher body weights are associated with an increase in all-cause mortality
T
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
body shapes with increased risk
apple (android)
ovoid (fruit box
pear shaped/gynoid has no increased risk
these are endocrine organs for the language of fat-inflammation and pro-coagulation
adipose cells
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
what is gherlin?
hormone that counteracts leptin, hunger signaling
what is adiponectin?
an “anti-inflammatory” hormone that makes the body more sensitive to insulin. this is decreased in obesity
which fat is “good fat”
brown fat - found in babies, more metabolically active. generates non-shivering heat
how many cormorbid conditions with obesity?
62
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
absolute contraindication for obesity meds?
childbearing age
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.
deficiencies common in gastric bypass
vitamin B12 and K
what is the functional unit of the thyroid?
follicle (balls of cells)
what is the active ingredient in the thyroid hormone?
iodine
what is hypothyroxinemia?
low plasma levels of thyroid hormone, which leads to low saturation of nuclear thyroid hormone receptors
constellation of signs and symptoms caused most commonly by deficiency of thyroid hormone
hypothyroidism
when is the fetal thyroid gland operational by?
10-12th week- fetal thyroid economy includes a contribution from maternal thyroid hormones (T3, T4)
what is cretinism?
maternal iodine deficiency - hypothyroidism in utero. leads to impaired brain development, short stature, deaf mutism, spasticity, thyroid gland structural abnormalities (goiter)
what happens with congenital hypothyroidism?
can be compensated in utero (mostly) but must be treated after birth. MAJOR PREVENTABLE CAUSE OF MENTAL RETARDATION
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
biggest sign of hypothyroidism in children and adolescents
growth retardation
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
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
what happens with hyperthyroidism in utero?
spontaneous abortion premature labor low birth weight stillbirth preeclampsia (CHF)
Hyperthyroidism in Childhood
Accelerated growth but early epiphyseal maturation (advanced bone age)
Delayed puberty
Tendency towards lower weight
Almost always Graves’ disease
symptoms of hyperthyroidism
heat intolerance/sweaty palpitations increased perspiration sleep disturbance tremor irritability fatigue anxious
Hyperactivity
Hyperreflexia
tachycardia/atrial arrhythmia (increased risk of afib)
worst complication of hyperthyroidism
thyroid storm (usually patients have comorbidity like cardiac problems)
temperature, CNS changes, GI dysfunction, tachycardia, CHF
autoimmunce thyroid disease of hypothyroidism
hashimotos
autoimmunce thyroid disease of hyperthyroidism
graves disease
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)
less common etiologies of hypothyroidism in adults
congenital (rare)
central (uncommon) - TSH deficiency, or less commonly TRH deficiency (pituitary/hypothalamic tumors)
central = pituitary proglem
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)
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)
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)
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
what should you always include with you are giving report about a thyroid patient?
include the eye, or else you’re not thinking
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
Simplified Ddx of Low TSH:
Thyrotoxicosis
Central Hypothyroidism
Pregnancy (hCG effect)
Non-thyroidal illness/low T3 syndrome (pressors, steroids, etc.)
Simplified Ddx of High TSH
Hypothyroxinemia Central Hyperthyroidism (rare)
which is more adrenal weight, the cortex or medulla?
cortex (90%), and has 3 different zones
what is made in the zona glomerulosa?
aldosterone (‘salt’)
what is made in the zona fasiculata?
cortisol (‘sugar’)
what is made in the zonal reticularis?
androgens (‘sex’)
what is made in the medulla?
catecholamines
what are adrenal hormones derived from?
common cholesterol
what are androgens precursors for?
dihydrotestosterone and estradiol
what can too much ACTH production do?
excess alpha MSH which can cause hyperpigmentation
what is excess cortisol’s effect on bones?
suppresses osteoblast production and stimulates bones to be thinner
organs effected by cortisol
brain, bone, CVS, immune system, kidney, skin/connective tissue
which can be converted to sex steroids? DHEA or DHEAS?
DHEA
adrenal androgens
androstenedione, DHEA, DHEA sulfate - direct biologic activity minimal, act as precursors for peripheral conversion –> testosterone and dihydrotestosterone
what are female androgens important for?
axillary hair and pubic hair development
Adrenal Androgen Excess in prepubertal boys
isosexual precocious puberty - early puberty
Adrenal Androgen Excess in adult women
cystic acne, hirsutism, male type baldness, menstrual irregularities, oligoovulation or anovulation, infertility and or frank virilization
Adrenal Androgen Excess in pubertal girls
heterosexual precocious puberty
what are the catecholamines?
epinephrine, norepinephrine, dopamine
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
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)
difference between cushing’s syndrome and cushing’s disease
disease is pituitary cause only, syndrome is all causes
signs and symptoms of cushing’s
weight gain, menstrual irregularity, hirsuitism, psychiatric dysfunction, back ache, obesity, plethora, moon face, HTN, bruising, purple striae
when are your ACT/cortisol levels highest and lowest?
highest in the morning at 8:00 and lowest at midnight
ACTH independent cushing’s syndrome causes
Adrenal adenoma (10-15%) and carcinoma (
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)
Pseudo-cushing’s syndrome
alchoholism, depression, obesity
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
if ACTH (>15) and cortisol are high, where is the source of the hypercortisolism?
pituitary (tumor maybe)
if ACTH is
most common sources of ectopic ACTH
small cell lung carcinoma, pancreatic tumors, lung carcinoids
treatment of cushings
surgical: pituitary resection, adrenalectomy, resection of ectopic ACTH source
medical: mitotane (for ACC), ketoconazole, metyropone, aminoglutethimide, trilostane
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
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
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
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
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
adrenal insufficiency treatment
IVF
glucocorticoud replacement: hydrocortisone 15-30 mg divided BID - TID
mineralocorticoid in primary AI = florinef 0.1 mg/day
10% of all HTN patients present with what?
primary hyperaldosteronism
when should you suspect primary hyperaldosteronism?
when HTN is resistant to treatment ( on 3 drugs including diuretic)
hypokalemia
adrenal incidentaloma
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
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
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)
which deficiency is the most common with congenital adrenal hyperplasia?
21-hydroxylase deficiency (95% of CAH)
what are catecholamine-secreting tumors that arise form chromaffin cells of the adrenal medulla?
pheochromocytomas
Paragangliomas or extra-adrenal pheochromocytomas – arise from sympathetic ganglia
symptoms of patients with pheo
HTN (may or may not have)
sweating
palpitations
paroxysmal HA (abrupt, bilateral, diminishes in hour)
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,
familial pheo forms
younger, usually bilateral, many with no HTN
what should you order in the management of pheo?
fractionated metanephrines
fractionated catecholamines
(urine/plasma)
with adrenal diseases, what should you order first- biochemical testing or imaging?
biochemical testing
which organs play a major role in assuring calcium homeostasis?
the skeleton, the gut and the kidney
what accounts for 90% of cases of hypercalcemia?
PHPT (primary hyperparathyroidism) and malignancy
epidemiology of PHPT
incidence is 1 in 500-1 in 1000
women> men
postmenopausal women- first decade
etiology of PHPT
sporadic benign solitary adenoma - 80-85%
parathyroid hyperplasia 10-15%
What symptoms do most patients with PHPT present with?
none!
Incidentally discovered on routine biochemical screening test
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.
what is th emost common overt complication of PHPT?
kidney stones (about 10-15% now)
which meds can cause increase calcium levels?
litium and thiazide (HCTZ)
what is the only curative therapy for PHPT?
parathyroidectomy
bone density improves, incidence of fractures and kidney stones reduces
Possible complications of PTx
Damage to the recurrent laryngeal nerve – hoarseness and reduced voice volume
Permanent hypoparathyroidism
Transient hypocalcemia
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
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
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
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.
Pharmacologic Therapy for Hypercalcemia Associated with Cancer
fluids!!! and phosphonates
how should you treat Bisphosphonate-Refractory Hypercalcemia of Malignancy
denosumab
most common cause of hypocalcemia/vitamin D deficiency?
postsurgical (on thyroid gland)
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)
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.
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
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
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
what is osteoporosis?
compromised bone strength (bone density, bone quality)
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
adult bone mass is achieved until what age?
30
symptoms of osteoporosis
none! until you have a fracture
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
what is a fragility fracture?
fall from a standing height or less
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
what is the most used pharmacologic treatment for osteoporosis?
bisphosphonates
then SERMS, estrogen (but increases risk for heart disease), denosumab, PTH
what does teriparatide do?
physiologically moves calcium from bone
when given intermittently and @ low doses –> anabolic effect on blasts
type 1 diabetes
Beta-cell destruction- complete lack of insulin
type 2 diabetes
Beta- cell dysfunction and insulin resistance
which DM is inheritable?
type 2 (type I is not, its autoimmune)
what percent of all cases of diabetes are type 1?
5%
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)
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
what is diagnostic for DM?
HgA1C > or equal to 6.5% (normal is 4-6)
fasting glucose >/= 126
random >/= 200
what disease can lead to insulin resistance and they can develop DM later in life?
PCOD
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
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
what is the first sign of diabetic kidney failure?
proteinuria
microvascular and macrovascular complications are predicted by what in DM?
microvascular - duration of diabetes, A1C, BP
macrovascular complicatons: duration of diabetes, A1C, BP, lipids
