Endocrinology

Hormones
• Major function of hormones: regulation of energy, adaptation to stress, facilitate growth/development, maturation & function of reproductive system
• 2 classes: act on nuclear receptors (steroids, TH, vit D), act on membrane receptors (peptide, amino acid)

PNS

Hormones:

Hormone Origin Target Action Release

Insulin Pancreatic beta Liver, muscle, fat Take up glucose from blood to store in liver & After a meal
cells muscle
Epinephrine Adrenal medulla Alpha 1, 2, B1, B2, D1, D2 Stimulate HR, BP, dilate pupils High-stress conditions,
excitement, fear
Cortisol Adrenal cortex Multiple tissues Breaks down fat & protein to glucose +anti- STRESS
inflammatory
Progesterone Ovary Uterus Control menstruation, pregnancy After follicular phase
Thyroxine Thyroid gland Most cells Control metabolic processes
PTH Parathyroid Calcium rec in bone, kidney,  calcium extracellular Ca is low
brain, intestine (Negative feedback)
Testosterone Testicles/adrenals Body-hair cells, muscle, Male sexual characteristics, females also Highest at puberty
reproductive structures produce small amounts
DIABETES
#1 cause of ESRD, non-traumatic LE amputations, & adult blindness
7th leading cause of death in US
Type 1 Diabetes Immune-mediated Beta cell destruction, leading to absolute insulin deficiency
Mellitus • Catabolic disorder in which circulating insulin is virtually absent, plasma glucagon is elevated, and the B cells fail to respond to insulinogenic stimuli.
• 2 peak ages of onset: 4-6 years old, 10-14 years old
Pathophysiology:
• Autoantibodies against B cells → islet cell ab (ICAs) are present in majority
• Catabolic state = breaking down or losing mass → look skinnier
• Many individuals with long-standing DM1 produce a small amount of insulin ➔ C-peptide
o … but… patients with T1DM ALWAYS require exogenous insulin therapy & glucose monitoring
• Genetics: HLA region on chromosome 6
Symptoms
 Polydipsia + polyuria (+glucose)
• Weight LOSS
• Blurred vision
• Paresthesias
• Altered LOC
ALARM SXS:
• DKA→ classic SXS + fruity breath + lethargy + vomiting
• Silent DM
Type II Diabetes Long term metabolic disorder characterized by insulin resistance & abnormal insulin secretion. Adult-onset
Mellitus Pathophysiology: In early stages of disorder, glucose tolerance remains near normal despite insulin resistance bc beta cells compensate by  insulin output. With
progression, pancreatic islet cells are unable to sustain hyperinsulinemic state and patients manifest with IGT.
• Insulin resistance:
o  ability of insulin to act effectively on target tissues, so it’s potency & efficacy  (more adipose tissue = more insulin receptors. Pumping out the
same amount of insulin, but for more receptors)
o  hepatic glucose output d/t body not utilizing glucose because of insulin resistance
▪  peripheral glucose utilization ➔ post-prandial hyperglycemia
o Insulin resistance in adipose tissue→ lipolysis →  cholesterol → dyslipidemia →  trigs,  HDL, LDL
• Impaired insulin secretion
o Initially, insulin  in response to resistance.
o Inflammation leads to defect in beta cell function & mass → “glucose toxicity”
• Don’t forget about insulin resistance syndromes: metabolic syndrome, PCOS (anovulation + hyperandrogenism), lipodystrophies
• Strong genetic component
RF: FH, ethnicity, obesity, sedentary lifestyle, smoking, diet, children of GDM pregnancy
SXS: polyuria + polydipsia + appetite
• Blurred vision, paresthesias/neuropathy, altered LOC, skin changes
• Skin: pruritus, vaginitis, candidiasis, cellulitis, diabetic wounds, acanthosis nigricans
Gestational • Glucose intolerance developing during the 2nd or 3rd trimester
Diabetes o Diabetes in 1st trimester = preexisting pregestational diabetes
• Cause: hormones released from placenta  insulin resistance,  insulin demands → IGT
• Many women revert to normal but have  risk of developing DM
SCREENING: ALL PREGNANT WOMEN SHOULD BE SCREENED AT 24-28 WEEKS GESTATION WITH ORAL GLUCOSE TOLERANCE TEST
• Screen those with RF (obese, FH, prior preg) @ first visit
• Screen again 4-12 weeks PP to ensure resolution, then q 3 years
TX
• Diet, exercise, blood glucose monitoring
• Tight control of blood glucose ➔ USE INSULIN
• Complications for baby: shoulder dystocia, hypoglycemia, jaundice, macrosomia
Diagnosis ADA CRITERIA: Confirmatory test: Screening:
• HbA1c >6.5% Antibodies PEDS: start @ 10 y/o or first signs of puberty
• FPG >126 mg/d Insulin level:  T2, T1 • Overweight (BMI>85%), weight >120% ideal for heigh PLUS 2 of the
• 2-hr glucose >200 mg/dL during OGTT C-peptide: following
• Random BG >200 + SXS • Reflects only insulin o FH, High risk race/ethnicity, signs of insulin resistance, maternal
Normal Pre DM being produced by hx of GDM
FPG <100 100-125 >126 body’s functioning B • Normal → Repeat q 3 years
OGTT <140 140-199 >200 cells Asymptomatic Adults:
HbA1c <5.7% 5.7-6.4 >6.5% • T2, T1 • Any age adult with BMI >25 and at least one risk factor
• Age 35 years if normal BMI and no RF
 • For normal result → q 3 years
Treatment T1DM T2DM
INSULIN!!! Drugs
Basal insulin regulates glycogen breakdown, gluconeogenesis, lipolysis, and
ketogenesis during fasting state—“Background insulin” Diabetes non - insulin meds .pdf
Prandial insulin replacement should be appropriate for the carbohydrate intake
(short-acting)
Typical requirement of 0.3-1.0 unit/kg/day with ½ given as dividend doses When to start insulin?
before meals as 1 unit for every 10-15 g of meal carbohydrate. • Evidence of ongoing catabolism (weight gain)
• HbA1c > 10%
Rapid: lispro, aspart, glulisine • Glucose >300
• Onset: 5-15 min, Peak: 1-1.5 hrs
• Uncontrolled on other meds
• Effective for 3-4 hrs
Short: regular Start on once daily injection of basal insulin 10 units
• Onset: 30-60 mins, Peak: 2-4 hours, Duration: 5-8 hours
Intermediate: NPH
• Onset: 2-4 hours, Peak: 6-7 hours
• Duration: 10-20 hours
Long acting:
Glargine: onset in 1 hr, duration ~24 hours
Detemir: onset in 1 hr, duration 17 hours
Degludec: onset in 2 hr, no peak, duration 42 hours

**Hypoglycemia as a side effect

• <70 + normal mental status → 15-20 g fast acting carbs
• <70 + AMS but with gag reflex → thickened liquid like honey or glucose
gel
• <70 + unconscious → IV dextrose or glucagon
Dawn Phenomenon:
• Early AM (3 am) liver dumping of glucose due to hormonal  overnight
• TX: nighttime basal insulin, avoiding late night snack, insulin in AM
• The sun rises at 3 am, and this is when glucose is high
Somogyi Effect:
• Reactive hyperglycemia after hypoglycemia
event overnight (going to bed with too much
insulin)
• If the 3 am dose is lOw (hypOglycemia =
sOmOgyi)
• TX: decrease nighttime basal insulin

DM Ocular Renal Neurologic Skin

Complications Diabetic Retinopathy Diabetic nephropathy manifests Diabetic neuropathy: • Acanthosis nigricans
as albuminuria • Stocking and glove • Charcot arthropathy: limb-
pattern threatening, presents as warm,
TX: ACEi/ARBs, SGLT2i • Distal symmetric swollen foot, which leads to bone
tingling/numbness destruction of midfoot
ASCVD
 Leading cause of M&M for pts • TX: gabapentin (if 
with T2DM renal function→
amitriptyline)
HTN Autonomic neuropathy:
Goal: <140/80 or <130/80 • Gastroparesis (T1)
• Bladder function
• ED

Premature cataracts
DKA Primarily affects T1DM but can affect T2DM Polyuria, polydipsia, nausea, Glucose >250 mg/dL SIPS
with sepsis or trauma. May be initial vomiting, mental stupor Arterial pH <7.3 • Saline: start NS, once glucose <250,
manifestation of T1DM. Bicarb <18 (elevated AGAP) switch to D5W
Dehydration, hypotension, Ketonuria • Insulin: 0.1 u/kg
*life-threatening Fruity breath odor of acetone o Once glucose reaches 200,
Kussmaul breathing Hyponatremia, beta- decrease insulin
hydroxybutyrate > 4 • Potassium
PCO2 LOW • Search for underlying cause

Resolving:
• AGAP <12
• Serum bicarb >15
• Venous pH >7.3
HHS Consequence of insulin deficiency and  in AMS, polyuria, polydipsia, Plasma glucose >600 SIPS
counterregulatory hormones (glucagon), polydipsia Arterial pH >7.3
leading to osmotic diuresis and dehydration Bicarb >15
Illness or other stress causes Serum osmolarity >320
MC in TII DM, higher mortality lack of fluid intake leading to
Causes: severe dehydration ultimately *Absence of acidosis*
Infection** (UTI, PNA, GI, pancreatitis) leading to hyperosmolality,
Infarction (MI) hyperglycemia, and Compared to DKA: higher
Iatrogenic hypokalemia. glucose, no acidosis/AGAP, high
Insulin deficiency serum osmolality
Intra-abd process
Ingestion (drugs)

Adrenal Disorders: Hypoaldosteronism, Hyperaldosteronism, Cushing’s Syndrome, masses, pheochromocytoma, MEN, ACC,
paraneoplastic syndrome
Disease Description Clinical Manifestations Diagnosis Treatment
Primary Adrenal Pathology directly affecting adrenal glands Skin changes: 8 am ACTH, cortisol, renin: HYDROCORTISONE 15-
Insufficiency Hyperpigmentation (esp of new scars • Cortisol <3 30 mg
Autoimmune (Addison’s) MCC** & palmar creases), longitudinal • ACTH > 200
Drugs (ketoconazole, rifampin) pigmented bands on nailbeds •  PRL (indicates need for Fludrocortisone
Destruction (trauma, hemorrhage- Waterhouse- fludrocortisone) -prevent loss of Na, K,
Friedrichsen syndrome) Orthostatic hypotension ACTH +  cortisol and vol depletion
Infection (TB, HIV, metastatic carcinoma, -replace
lymphoma) Fatigue, weight loss,  appetite, low ACTH Stimulation Cosynotropin Test: no mineralocorticoids
BP, n/d/v, muscle and joint pains, increase in cortisol
irritability, depression, salt craving DHEA 50 mg
aldosterone (mineralocorticoids)
Women: sexual dysfunction and hair DHEA <1000 Pt education:  dose in
loss stress (sick days, fever,
Hyponatremia acute illness, trauma,
surgery, emotion (+10),
Hyperkalemia get medical bracelet and
Metabolic acidosis emergency kit)
Hypoglycemia

Anti-adrenal ab

CT scan
Secondary Adrenal Pathology directly affecting the pituitary gland ^^ 8 am ACTH, cortisol, renin: HYDROCORTISONE 15-
Insufficiency • Cortisol <3 30 mg
Pituitary tumors Clinical SXS are like Addison’s, but NO ACTH +  cortisol
Pituitary hemorrhage/infarction (Sheehan HYPERPIGMENTATION OR VITILIGO. DHEA 50 mg
Syndrome) Because aldosterone is preserved, vol Cosynotropin Test:
Infectious disease (TB, head trauma, aneurysms) depletion, dehydration, hypotension, See an increase in cortisol Pt education:  dose in
Drugs- high dose progestins, chronic opiates and electrolyte disturbances do not stress (sick days, fever,
occur Preserved aldosterone (RAAS) acute illness, trauma,
DHEA <1000 surgery, emotion (+10),
get medical bracelet and
Hyponatremia emergency kit)
NORMAL K+

CT scan
Tertiary Adrenal Hypothalamic failure to stimulate pituitary ^^ 8 am ACTH, cortisol, renin: HYDROCORTISONE 15-
Insufficiency • Cortisol <3 30 mg
Abrupt cessation of high-dose glucocorticoid ACTH +  cortisol
therapy DHEA 50 mg
Cosynotropin Test: increase in cortisol
Cushing’s disease cure following removal of Pt education:  dose in
pituitary or non-pituitary ACTH-secreting or Preserved aldosterone (RAAS) stress (sick days, fever,
cortisol-secreting tumor because the chronically DHEA <1000 acute illness, trauma,
high serum cortisol concentration before surgery surgery, emotion (+10),
suppresses the HPA axis in the same manner as Hyponatremia get medical bracelet and
chronic administration of high-dose steroids NORMAL K+ emergency kit)
Acute Adrenal Crisis Life-threatening! Worsening of adrenal Shock NOT RESPONSIVE TO IVFs & Labs (but start tx ASAP even before ASAP!!!
insufficiency Pressors results(
-ACTH, cortisol, renin, DHEA, CBC, CMP Hydrocortisone 100 mg
Triggered by stressful event (lower resp, urinary, N/V acutely *** adult IV/IM followed by
GI infections) or abrupt withdrawal of Fever, AMS, reversible CT scan 200 mg over the next 24
glucocorticoids cardiomyopathy, HF hours (50 mg in child)

Presents like surgical abdomen Fluid resus: NS+

dextrose +/-abx
Cushing’s Syndrome Endogenous cause: Trunk obesity 24 hour urine free cortisol Exogenous → d/c
(hypercortisolism) • ACTH-dependent Moon face Nighttime salivary cortisol glucocorticoid with slow
o Ectopic ACTH-producing tumor Buffalo hump Low dose overnight dexamethasone taper
suppression test
(small cell lung cancer) Supraclavicular fat pads
• Give dexamethasone (1 mg)
o Cushing’s disease: pituitary Thin extremities before they go to bed. Test
Endogenous →
adenoma,  ACTH Oligomenorrhea, amenorrhea cortisol in morning to see if there resection
• ACTH-independent ED is an  or .
o Adrenal adenoma HTN • If cortisol → Cushing’s Cushing’s disease:
Exogenous cause: Osteoporosis Determine etiology: Baseline ACTH + High transsphenoidal
• **Long term corticosteroid use** MC Acne dose dexamethasone suppression test resection
• ACTH-independent Impaired wound healing • If Cushing DISEASE (pituitary
Purple striae tumor):
Acanthosis nigricans •  ACTH + suppression
Hirsutism of cortisol
• This is the only
etiology that
will suppress
with the high
dose
dexamethasone
suppression
test*********
• If ectopic-ACTH secreting tumor:
• ACTH + NO
suppression of cortisol
• The tumor is
secreting
ACTH!
▪ ACTH + NO suppression of
cortisol
▪ Tumor is secreting
cortisol, so there is an
excess of cortisol and a
ACTH to try to
compensate

Hyperaldosteronism Primary (MC): Plasma renin activity Unilateral: total

• Excessive production from adrenal gland
HTN + Hypokalemia + Aldosterone after 4 hour upright posture adrenalectomy +
(zona glomerulosa) Metabolic alkalosis spironolactone
• Renin-independent Ald:renin >20:25
• Conn syndrome: adrenal aldosteronoma Proximal muscle weakness Bilateral: spironolactone
 Secondary:
• Excessive stimulation of RAAS →  renin Often asymptomatic
→  aldosterone
• Tumor, renal artery stenosis, LVHF, preg,
cor pulmonale

Adrenal Most are benign but become more serious with Types:
Incidentaloma age. Usually is adrenal metastasis Adrenal medullary tumors:
pheochromocytoma

Adrenal cortical tumors: adenoma,

Cushing’s syndrome, Conn’s,
carcinoma
Plasma-fractionated metanephrines and Alpha → BB → Surgical
Pheochromocytoma Catecholamine-secreting tumors that arise from Triad= PHE→ Palpitations catecholamines (or urine)
chromaffin cells of medulla resection
(tachy) + Headache +
CT abd/pelvis first (MRI alternative)
Well vascularized tumors that arise from Excessive Sweating PET scans for metastatic disease
Prior to surgery:
sympathetic or parasympathetic paraganglia. Start alpha blockers
Symptoms caused by over secretion of NE, Epi, (doxazosin) 7-14 days
Sustained or paroxysmal HTN
and DA. prior to surgery. 3-4
is MC sign (paradoxical response to
days after alpha-blocker
antihypertensive drugs)
begins, add a beta-
blocker (atenolol,
6 P’s: Pressure, Palpitations, Pallor,
propranolol (to control
Perspiration, Pain, Polyuria
tachycardia.

Control the BP

following removal
Multiple Endocrine A group of heritable syndromes characterized by Surgical excision, pharm
Neoplasia growth of benign or malignant tumors in a management of
subset of endocrine tissues have been given the endocrinopathies
collective term MEN

Paraneoplastic Rare Produce autoantibodies, cytokines, DX of exclusion

Syndrome Seen in those with lung, breast, hematologic, hormones, or peptides that affect
medullary thyroid, gynecological, prostate cancer multiple organ systems.
PITUITARY DISORDERS: Adenoma, HyperPRL, Gigantism, acromegaly, hypopituitarism, central DI, SIADH
Pituitary Adenomas:
• Benign tumor of the anterior pituitary gland, functional or non-functional. Common in adults 35-60 y/o, sporadic.
• Size: <1 cm – microadenoma, >1 cm-macroadenoma
• Classification: PROLACTINOMA MC**
Somatotroph adenoma GH
Acromegaly, gigantism
Lactotroph, prolactinoma PRL
Galactorrhea, amenorrhea
Corticotrope adenoma ACTH
Cushing’s
Thyrotrope adenoma TSH
Gonadotroph adenoma LH, FSH
• Hypopituitarism: bitemporal hemianopsia, h/a, n/v
• DX: MRI of head
• TX: Transnasal, transsphenoidal
• Prolactinomas: med tx (bromocriptine)
• Acromegaly- TSS + Bromocriptine

Hyperprolactinemia PRL is highest during REM sleep, stimulates PREmenopause: infertility, PRL levels: Dopamine agonist: Cabergoline,
milk production, inhibits -elevated: exclude possibility of bromocriptine, pergolide
ovulation/spermatogenesis (GnRH). amenorrhea, pharm or other factors prior to MRI
Dopamine inhibits PRL. galactorrhea Transnasal, transsphenoidal
PRL>200 + macroadenoma = surgery if no response to meds
MCC: Prolactinoma POSTmenopause: h/a, impaired prolactinoma
Pregnancy, breast feeding, exercise, DA vision Pituitary radiation last option
antagonists, hypothyroidism, renal failure PRL <200 + macroadenoma =
Men: infertility,  libido, hyperprolactinemia 2/2
impotence, gynecomastia,  body hypothalamic compression
hair, osteoporosis
Gigantism and Too much GH stimulates IGF-1 release from Tall stature, abnormal growth of IGF-1 levels*** Pituitary transsphenoidal
Acromegaly liver → periosteal bone growth,  organ hands & feet. Obesity occurs after
-normal: acromegaly unlikely
microsurgery
size,  glucose intolerance  in height -elevated: further tests
Dopamine agonists ( release),
Gigantism: GH hypersecretion begins in Thick facial features, large tongue octreotide or lanreotide ( GH),
Oral glucose tolerance
CHILDHOOD, before closure of epiphyses (sleep apnea) raloxifene (breast ca), pegvisomant
testing***
(DM)
-failure to suppress GH to <1
Acromegaly: GH hypersecretion begins in Irregular menses in females
ng/mL = acromegaly
ADULTHOOD, causes lateral growth of bone Monitor OGTT 3 mo post surgery
& soft tissue Excessive sweating w/ minimal (GH<1, IGF-1 normal)
Glucose elevated; insulin elevated
activity
PRL, glucose, TSH, free T4, liver
Delayed puberty, double vision,
enzymes, kidney function, Ca, P
CHF, dilated cardiomyopathy*
Pituitary MRI
Hypopituitarism Pituitary dwarfism (children)- pituitary gland Children: slow or flat rate of GH stimulation: peak GH <7 ng/mL Kids: recombinant GH supplements
does not make enough growth hormone growth → GH deficiency
-delayed or absent puberty Adults: if onset in childhood, treat
GHD_ congenital or acquired -weight gain out of proportion to Bone age in children 2 years it. If onset in adulthood, probably
growth behind. leave it.

Adults:  lean body mass, increase Only eval adults who have RF
fat mass,  bone mineral density (known hypothalamic or pituitary
( risk of fx), usually have other disease)
endocrine disorders
Diabetes Insipidus Deficiency of ADH Polyuria, nocturia, and polydipsia Uosm < Posm (concentrated Central: ddAVP or carbamazepine
• Hypotonic polyuria <300 plasma, low vol urine)
Central DI: MC*** mOsm/kg Nephrogenic: Na/protein
• Inadequate ADH release from Symptomatic after  water intake Hypotonic urine <300 mOsm/kg restriction, Low Na diet, and
pituitary gland Serum Na , serum osm  thiazide diuretics
• Idiopathic, head trauma, stroke, Hypernatremic
brain tumor Dehydrated Water Deprivation Test with serum
Nephrogenic DI Hypotension copeptin—central/nephrogenic vs
• ADH levels are normal or , but the AMS, seizures primary polyuria
kidneys are less sensitive to the • Normal response:
effects progressive urine
• Lithium, Amp B, AKI, CKD, concentration
hypercalcemia, hypokalemia • there is persistent
excretion of hypotonic
urine

Desmopressin (ddAVP)
Stimulation Test
Peeing too much
• Central DI →  urine
output,  urine osmolality
• Nephrogenic DI →
continue to have dilute
urine
Syndrome of Disorder of impaired water excretion caused H/a, confusion, anorexia, n/v, Low BUN, Cr, uric acid, and Restrict fluid intake to 500 mL
Inappropriate ADH by inability to suppress the secretion of ADH coma, convulsions albumin <urinary output
(SIADH)
• WATER RETENTION + Not peeing at all Urine Na >20 () Severe: hypertonic (3%) saline
HYPONATREMIA Serum Na  <130 *caution of central pontine
Due to non-physiologic excess & Serum osm <270 myelinolysis
unsuppressed ADH release from pituitary
gland or ectopic Tolvaptan can be given orally
THYROID
TEST Description Clinical Utility
TSH Thyroid stimulating hormone •
Best thyroid function screening test
(Released from anterior pituitary) •
Initial test for suspected thyroid disease
TSH= hyperthyroidism or secondary hypothy
•
TSH = primary hypothyroidism
•
•
Used to follow patients on thyroid hormone tx
o low TSH →  dose of levo
o high TSH →  dose of levo
• Used with T4 to manage patients with Grave’s
Free T4 Free thyroxine levels (metabolically active Ordered when TSH is abnormal to determine thyroid hyperfunction or hypofunction
hormone) • If : hyperthyroidism
• If : hypothyroidism
Measure unbound T4 (what is able to enter tissues)
Total T4 Main form of thyroid hormone circulating in Measure the bound AND free hormone and can change when binding proteins differ (pregnancy, OCP)
blood
Thyroid Anti-thyroid peroxidase Ab (TPOAb) • Used to dx Hashimoto’s thyroiditis
antibodies Anti-thyroglobulin Ab (TGAb) OR
• Other autoimmune thyroiditis

Thyroid stimulating Ab (TSH receptor ab) • Specific for Grave’s disease

(TSI ab)
Free T3 Serum triiodothyronine • Useful to diagnose hyperthyroidism when TSH is low and T4 is still normal (T3 )
• Useful to determine severity of hyperthyroidism (not helpful in hypothyroidism)
FTI Free Thyroxine Index • Used in thyroid disease when the patient has protein abnormalities
Thyroglobulin Protein produced by normal thyroid cells • Monitor AFTER thyroidectomy for thyroid cancer
(Tg) and thyroid cancer cells

Goiter Enlarged thyroid gland Incidental swelling in neck Initial screening: TSH Small benign → no tx
Thyroid function may be normal (non- • If TSH is negative → No further Large and complicated → remove
toxic goiter), overactive (toxic goiter), Local compression → dysphagia, testing surgically
or underactive (hypothyroid goiter) dyspnea, stridor, hoarseness • TSH abnormal → FTI
• Look for ab, thyroglobulin, ESR, *if thyroid removed, need to
Pain d/t hemorrhage, inflammation, calcitonin supplement with levothyroxine*
necrosis, malignant transformation US is best imaging technique
Hyperthyroidism TSH T3 T4 Palpitations and tachycardia Check TSH, free T4, and total T3: BB’s for all!! Control SXS
MCC: Grave’s Disease
Heat intolerance or sweating TSH, T4/T3 →
Tremor • Check TSH ab 3 definitive treatments:
-Autoimmune disease with thyroid-
Weight loss • Normal → • Radioactive iodine ablation MC
stimulating ab that lead to production
Increased bowel movements-diarrhea • Thyroid uptake used, preferred for graves
and release of T4 and T3 + growth of 1. pt placed on lifelong
Irritability scan
thyroid gland by stimulating TSH rec. levothyroxine
Dyspnea, exertional intolerance • Elevated → GRAVES 2. obtain preg test before
Ab: • Antithyroid drugs (Methimazole,
Specific to Graves:
• Graves: anti-TPO, TSI ab Propylthiouracil)
 Toxic Multinodular Goiter (TMNG): EXOPTHALMOS • TMNG/toxic adenoma:  anti- 1. Monitor TSH
autonomous hyperfunctioning thyroid PRETIBIAL MYXDEMA TPO, - TSI ab • Thyroidectomy (total or subtotal)
1. Preferred for women
nodules
planning on becoming
preg in 6 mo, +Graves
Toxic Adenoma Thyroid uptake scan: orbitopathy, malignancy,
• High, diffuse uptake → graves compressive goiters,
coexisiting hyperPTH
• Patch uptake: TMNG 2. Side effects: hyper- or
• Focal uptake: toxic adenoma hypocalcemia, permanent
• Low uptake: thyroiditis hypothyroidism, recurrent
laryngeal nerve damage
Toxic Adenoma Result of focal/diffuse hyperplasia & Hx of long-standing, slow-growing neck  TSH , free T4 or T3 Surgery & radioiodine 131 ablation
hyperfunctioning of thyroid follicular lump → obstructive symptoms
cells whose capacity is independent of (dyspnea, dysphagia, stridor, Uptake scan: single or multiple areas of  BB for sxs
regulation by TSH, leading to hoarseness) iodine uptake (“hot nodules”)
thyrotoxicosis
Mild hyperthyroid sxs Thyroid US***
Toxic Multinodular thyroid gland develops Cardiac symptoms very prominent: TSH, free T4 or T3 Surgery or radioiodine
Multinodular autonomously functioning nodules palpitations, A-FIB, tachycardia
Goiter (Plummer over time Thyroid US** BB for sxs
disease) Palpable nodular goiter
MC>50 w/ hx of thyroid nodules Uptake scan- normal to  uptake with
focal areas of  uptake
Thyroid Storm Rare, potentially fatal complication of Exaggerated manifestation of Clinical ICU admit
thyrotoxicosis usually after a hyperthyroid symptoms and BB for cardiac symptoms
precipitating event hypermetabolic state: TSH, T4 or T3
PTU preferred to inhibit thyroid
Triggers: Fever >104 (hyperthermia) + hormone synthesis
-MC underlying condition in Graves diaphoresis
-Infection, trauma, burns, surgery, Tachycardia >140, HTN Potassium iodide to inhibit release of
acute illness Delirium/confusion/AMS thyroid hormone from gland
-DKA, HHS
-MI, CVA, PE Can progress to apathy, stupor, coma Iodinated radiocontrast agent to
-abrupt withdrawal of antithyroid inhibit the peripheral conversion of
meds, ingestion of TH, amiodarone, T3→ T4
salicylates
-eclampsia, L&D Acetaminophen for fever,
glucocorticoids to support tress on
body
Hypothyroidism TSH, T4 or T3 Fatigue TSH, T4 or T3 LEVOTHYROXINE
Weight gain—“doughy” • Tx when TSH >10
MCC: Hashimoto’s thyroiditis
Cold intolerance • Pts should receive same
•  women 30-50
Dry skin, course/brittle hair brand of medication
• Anti-thyroid peroxidase ab,
Goiter throughout tx
anti-thyroglobulin ab
Reflex delay- hyporeflexia + delayed • Take on empty stomach, in
Iodine deficiency or excess
relaxation response morning, 30-60 min prior to
Drugs: amiodarone, lithium,
Constipation (new onset) breakfast
immunotherapy
Memory issues and  concentration • 1.6 mcg/kg/day
Depression
 Irregular or heavy menses
Loss of outer 1/3 of eyebrow hair

•
• Re-check levels q 4-6 weeks
using free T4 to track
Myxedema Hypothyroid emergency, rare Decreased mental status, hypothermia, TSH, T4, T3 ICU admit, ventilation PRN, correct
Coma coma Cortisol level hypothermia, hypotension, metabolic
abnormalities
Hypotension, bradycardia,
hypoNa, hypoglycemia, hypotension IV T4 and T3
Glucocorticoids until coexisting
adrenal insufficiency is ruled out
Thyroiditis
Inflammation of the thyroid gland with transient hyperthyroidism due to release of preferred hormone from the colloid space. The inflammation of the thyroid leads to sequential
pathologic process that can result in SXS of hyperthyroidism followed by SXS of hypothyroidism. Treatment depends on underlying cause.
Hashimoto’s Autoimmune (anti-thyroid ab) Clinical hypothyroidism + thyroid ab present: thyroglobulin ab, Levothyroxine therapy
Thyroiditis Painless, enlarged thyroid TPO ab
May present in euthyroid state TSH, T3 and T4
radioactive iodine uptake
Subacute Autoimmune (anti-thyroid ab) Painless, enlarged thyroid +thyroid ab present Return to euthyroid state in 12-18 mo
thyroiditis without treatment
Thyrotoxicosis → hypothyroid TFTs
(depends on when they present) uptake Aspirin

No antithyroid meds***
Postpartum Autoimmune Painless, enlarged thyroid +thyroid ab present Return to euthyroid state in 12-18 mo
thyroiditis 1-6 months post delivery Thyrotoxicosis → hypothyroid without treatment
(depends on when they present) TFTs
uptake Aspirin, NSAIDs

No antithyroid meds***
deQuevain’s MC POST VIRAL* PAINFUL, tender neck/thyroid ESR (hallmark)*** Return to euthyroid state in 12-18 mo
thyroiditis without treatment
(granulomatous) HLA-B35 Clinical hyperthyroidism NO thyroid ab
Thyrotoxicosis → hypothyroid TFTs (TSH, T4) Aspirin
More on this below… (depends on when they present) radioactive uptake
No antithyroid meds***
Medication AMIODARONE, LITHIUM, alpha- Painless, enlarged thyroid Often returns to euthyroid states
induced interferon Clinical hyperthyroidism when med is stopped, corticosteroids
Thyrotoxicosis → hypothyroid
(depends on when they present)
Acute S. aureus MC May have PAINFUL, fluctuant thyroid WBC with left shift ABX, I&D
(suppurative)
thyroiditis Very ill, febrile Euthyroid
 SUBACUTE THYROIDITIS (De Quervain’s thyroiditis) aka granulomatous thyroiditis
She has dQuerPAINS:
Diffuse  uptake on radioactive uptake scan (also in Hashimoto & postpartum)
Painful thyroid hallmark! Diffusely tender thyroid on exam
After VIRAL illness, symptoms last wks to months
Increased ESR & CRP
Negative thyroid ab
Self-limiting. Salicylates or NSAIDs for pain. Prednisone if severe
Initial hyperthyroid → hypothyroid → euthroid
1. Hyperthyroid (thyrotoxic) phase: thyroid inflammation & attack by cytotoxic T lymphocytes damage thyroid follicles→ activate proteolysis of thyroglobulin stored in
follicles. This inflammation results in unregulated release of large amounts of preformed T4 and T3 into circulation from destroyed follicles, instead of synthesis of
new T3 and T4, resulting in biochemical hyperthyroidism. T3 & T4, TSH
2. Hypothyroid phase: usually a period of rapid evolution through euthyroidism and then into transient and asymptomatic hypothyroidism. Occurs d/t follicular cell
damage, leading to reduction of new hormone synthesis and the depletion of hormone stores. T3 & T4, TSH
3. Recovery phase: as inflammation subsides, thyroid follicles regenerate and thyroid hormone synthesis and secretion resume, with resolution & restoration of normal
thyroid function.

Malignancies
RF: hx of head/neck irradiation, FH
Type of Cancer Description Diagnosis Treatment
Papillary Thyroid • MC type of thyroid cancer, Differentiated Thyroid THYROID US: most sensitive test Thyroidectomy***
Carcinoma Carcinomas (DTCs)
“Papillary is popular” • More common in women, prognosis worse in men CT or MRI: relationship to adjacent Radioactive therapy (post-surgery)
• Least aggressive structures
• Metastasis = local cervical lymph nodes TSH suppression with high doses of
Radioactive iodine scanning: determine hot levothyroxine to  recurrence
Follicular Carcinoma • 2nd most common, DTC vs col
“Follicular= Far” • More aggressive than papillary, but also slow • COLD=CANCER (no uptake) External beam radiation (if advanced)
growing • HOT= uptake
• Distant mets more common than local METs PET: metastatic disease Chemo for metastatic
(hematogenous spread: lung MC)
Medullary Thyroid Neuroendocrine tumor derived from parafollicular C cells TSH- if normal → biopsy Surgery
Carcinoma 25% related to MEN2
Carcinoid syndrome, Cushing syndrome FNA: most accurate diagnostic test
Anaplastic thyroid Most aggressive, undifferentiated, fatal • >1 cm, hypoechoic on US, US finds Palliative
carcinoma Metastasizes early to surrounding nodes and distant sites lymph node spread, any hx of
Rock hard mass on PE irradiation or FH or thyroid surgery
PARATHYROID GLAND
Condition Description Clinical Manifestations Diagnosis Treatment
Hypoparathyroidism Most frequently occurs following thyroidectomy Hypoparathyroidism → PTH  Ca P Calcium supplementation
or head/neck surgery for hyperparathyroidism hypocalcemia
urinary calcium, Mg Vitamin D supplementation
Can be transient with removal of PTH adenoma Uncontrollable painful spasms of
→ “hungry bone syndrome” face, hands, arms, feet ECG: prolonged QT interval If acute
hypoparathyroidism/hypocalcemia:
DiGeorge Syndrome: “CATCH 22” Paresthesias in hands & around IV Calcium, Calcitriol, Mg
• Cardiac abnormalities (TOF) mouth
• Abnormal facies PREGNANCY:
• Thymic absence, T cell abnormality Chvostek’s sign: facial muscle -maternal hypoCa can adversely
• Cleft palate contraction when tapping facial affect skeletal development of fetus
• Hypocalcemia nerve 0maternal hypercalcemia can
• Chromosome 22 suppress fetal PT development
Trousseau phenomenon: carpal →neonatal hypocalcemia
Magnesium abnormality- suppress PTH spasm after application of BP cuff
secretion
Cataracts, thin hair, hyperactive
Malabsorption or chronic alcoholism reflex,

Primary HyperPTH MCC of hypercalcemia, more common in Most are asymptomatic PTH Ca P Parathyroidectomy
women >50 y/o
Signs of hypercalcemia: bones, EKG: prolonged PR interval Observation if asymptomatic
Etiologies: moans, stones, groans • DEXA every 1-2 hours
• Parathyroid adenoma MCC 24 h urine calcium excretion • Avoid thiazides or calcium-
• Lithium, thiazide therapy containing antacids
• MEN 1 DEXA scan • Bisphosphonates
• MEN 2A • Estrogen replacement in
PM women
Secondary hyperPTH  PTH by a physiologic response to Bones, moans, stones, groans PTH, 24 h urine calcium, Vit D Replace the cause (vit D or calcium
hypocalcemia or vitamin D deficiency supplementation)
Calcification in blood vessels and
Renal failure MCC: GFR → serum P → Ca soft tissues Calcitriol for dialysis patients or
→ Vit D → PTH *cinacalcet
Tertiary HyperPTH Occurs due to prolonged hypocalcemia Parathyroid gland hyperplasia, Ca, Phos, PTH, Vit D Cinacalcet, Calcitriol
oversecretin of PTH
Individuals who have had secondary hyperPTH
for many years develop primary hyperPTH. In
tertiary hyperPTH, parts of the parathyroid
gland start making PTH independently of blood
Ca levels → hypercalcemia

2/2 CKD
Review:
Serum Ca Serum Phos Serum PTH Vit D
Primary    
Secondary Normal or    
Tertiary    
Urine: hypERphosphaturia, hypercalciuria (this makes sense because all that calcium and phosphorus must go somewhere, so they go out through the kidneys into the urine)
Blood: PTH, calcium, phosphate (because PTH inhibits reabsorption of phosphate by the kidney. Therefore, with too much PTH there is less reabsorption of phosphate)

Osteoporosis
Osteopenia: T score -1 to -2.5
Osteoporosis: T score -2.5 or less

Etiology
• PRIMARY: related to aging process in conjunction with  sex hormones (PM + senile)
• RF: Caucasian, low BMI, steroid use, smoking, CKD, alcohol,  Ca & vit D intake, physical inactivity
• SECONDARY: due to chronic disease or meds
• Men more likely
• Glucocorticoids, antiepileptics, chemo, PPIs, glitazones
• Secondary hyperparathyroidism
Patho: imbalance of bone resorption and bone remodeling. Upregulation of RANKL and osteoclasts

SXS: asymptomatic.
• BONE FRACTURES- vertebral compression fx MC
• Loss in height, angular kyphosis→ restrictive lung disease
• Hip fx
• Distal radius fx 2nd MC
DX
Clinical criteria:
• Presence of fragility fracture
• FRAX: 10-yr risk of hip fx and major OP fx based on presence of RFs
• For untreated patients between 40-90 y/o
• DEXA:
• T-score: SDs difference between your bone density and avg bone density for healthy young adults of same sex
• OP: T-score <-2.5
• Osteopenia: T-score -1 - -2.5
• Z-score: your bone density to people of same age and gender
Treatment
• Lifestyle: weight bearing exercise, smoking cessation, fall prevention
• Vit D + Ca supplementation
#1: Bisphosphonates

SERMs, IN calcitonin, Denosumab, anabolic therapy