Endocrinology

TABLE OF CONTENTS
1. Fundamental Principles of Endocrinology

Endocrinology 2. Hypothalamus
3. Anterior and Posterior Pituitary
4. Thyroid
5. Parathyroids
REVIEW OUTLINE
1. General Principles
Endocrinology: A. Autocrine, Paracrine, Endocrine signaling

B. Hormone Classifications
2. Endocrine Glands
An Introduction 3.
A. Location and function
Feedback Loops
A. Negative Feedback Loops
B. Positive Feedback Loops
Endocrinology: An Introduction Bootcamp.com
General Principles
Autocrine, Paracrine, and Endocrine Signaling:
● Autocrine signaling: Cells signals themselves
● Paracrine signaling: Cells signal nearby cells
● Endocrine signaling: Cells signal other cells that are far away
- Signaling molecules (usually hormones) often enter the bloodstream to travel to distant organs
● Exocrine glands: Glands that produce substances for secretion outside the body (Ex. sweat, milk, saliva)
Hormone Classifications:
● Hormone: Signaling molecule that travels through the body to target distant cells
● Proteins/Peptides: Made from amino acids
- Often packaged in hydrophilic vesicles to travel through the bloodstream
- Hydrophilicity → ↓ Ability traverse cell membrane → ↑ Membrane bound receptor signaling
- Ex. Insulin, oxytocin
● Amino Acid Derivatives: Derived from single amino acids
- Ex. Thyroxine, melatonin (both derived from tyrosine)
● Steroids: Derived from cholesterol, lipophilic
- Lipophilicity → ↑ Ability traverse cell membrane → ↑ Binding intracellular nuclear receptors
- Ex. Estradiol, testosterone, cortisol
● Eicosanoids: Derived from fatty acids, most often arachidonic acid
- Bind to membrane bound receptors
- Ex. Prostaglandin, thromboxane
● Gases: Small molecules that often diffuse across membranes
- Ex. NO, Ethylene
Endocrine Gland Overview

Pineal Gland:
● Located behind third ventricle, secretes melatonin, regulates sleep/wake cycle
Hypothalamus:
● Located between thalamus and pituitary gland, connects nervous and endocrine system via pituitary gland
- Produces ADH, oxytocin which are stored in the posterior pituitary
- Regulates release of hormones from anterior pituitary
Pituitary Gland:
● Pea-sized gland resting on the sella turcica in the sphenoid bone
- Anterior pituitary: Releases hormones that regulate growth, thyroid hormone release
- Anterior pituitary hormones: GH, ACTH, FSH, LH, TSH, Prolactin
- Posterior pituitary: Stores and releases ADH, oxytocin
Thyroid Gland:
● Located on anterior neck, inferior to thyroid cartilage
- Produces T4, T3
- Regulates temperature, metabolism, heart rate
Parathyroid Glands:
● Located throughout thyroid gland
- Produce PTH → Regulates calcium levels
Adrenal Glands:
● Located above each kidney (suprarenal)
- Produce steroid hormones (cortisol, aldosterone, androgens)
Pancreas:
● Located in epigastric region, produces insulin and glucagon
Ovaries/Testes:
● Produce estrogen or testosterone, respectively
Adipose cells:
● Contain aromatase → Converts androgens to estrogen
Feedback Loops
Negative Feedback Loops: Positive Feedback Loops:
● End products downregulate production ● End products upregulate production
● Ex. CRH/ACTH/Cortisol feedback loop ● Ex. Stretching of the uterus during childbirth
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REVIEW OUTLINE
1. Hypothalamus
Endocrinology: A. Embryology
B. Function
2. Rapid Review: RAAS and ADH
Hypothalamus A. Renin-Angiotensin-Aldosterone System
B. Vasopressin/ADH
3. SIADH
A. Pathology
B. Presentation
C. Treatment
4. Diabetes Insipidus
A. Pathology
B. Presentation
C. Diagnostics
D. Treatment
E. Complications
5. Hyponatremia
A. How to Differentiate Causes of Hyponatremia
B. Evaluating Hypotonic Hyponatremia
C. Treatment
Endocrinology: Hypothalamus Bootcamp.com
Hypothalamus
Embryology:
● Forebrain → Diencephalon → Thalamus, Hypothalamus
Function:
● Connects CNS and endocrine system, parts not protected by BBB
● Regulates thirst, hunger, temperature, sexual urges, circadian rhythm
● Regulates anterior/posterior pituitary
● Hormones: TRH, GnRH, GHRH, CRH, Somatostatin, Dopamine, Oxytocin, ADH
- TRH → Anterior pituitary TSH → Thyroid releases T3, T4
- GnRH → Anterior pituitary LH, FSH → Testosterone/Estrogen release
- CRH → Anterior pituitary ACTH → Adrenals release cortisol
- GHRH → Anterior pituitary GH → Liver IGF1 → Growth mucle/bone/fat
- Somatostatin inhibits GI, endocrine, pancreatic, pituitary secretions
- Dopamine regulates movement, memory, reward motivation
- Oxytocin → Contraction of uterus, mammary glands for lactation
- ADH → Increased H2O reabsorption distal convoluted tubule
● Suprachiasmatic nucleus (SCN): Regulates sleep
- Norepinephrine release → Pineal gland → Melatonin
● Supraoptic Nucleus: Synthesizes oxytocin, ADH
● Paraventricular Nucleus: Produces oxytocin, ADH, TRH, CRH, somatostatin
● Lateral Nucleus: Hunger
● Ventromedial Nucleus: Satiety
● Anterior Nucleus: Cooling (Parasympathetic)
● Posterior Nucleus: Heating (Sympathetic)
● Preoptic Nuclei: Produces GnRH, thermoregulation, sleep regulation
● Arcuate Nucleus: Mediates metabolic signals (leptin, ghrelin, insulin)
● Dorsomedial Nucleus: Feeding, drinking, body weight, circadian rhythm
● Mammillary Bodies: Part of limbic system
- Relay information from amygdala/hippocampus to thalamus, important for recollective memory
Rapid Review: RAAS and ADH

Renin-Angiotensin-Aldosterone System:
● Function: Maintain renal perfusion and blood pressure
● RAAS Activators: ↓ BP, ↓ NaCl delivery macula densa cells, ↑ Sympathetic tone
● RAAS activated → JG cells → Renin → Renin converts angiotensinogen → Angiotensin I → ACE in lungs angiotensin I → Angiotensin II → Organ Effects
● Vascular smooth muscle → Vasoconstriction
● Posterior pituitary → Vasopressin/ADH release
● Adrenal cortex → Aldosterone release
● Kidney → ↑ Na+ reabsorption, ↑ K+ secretion (RAAS on → UNa < 30)
● RAAS Inhibitors: ↑ Volume → ANP, BNP released from atria and ventricles → RAAS off
- ↑ cGMP → Relax vascular smooth muscle → ↑ GFR → ↓ Renin
Vasopressin/ADH:
● Synthesized in hypothalamus, stored in posterior pituitary
● Angiotensin II → Posterior pituitary → ↑ ADH release → ↑ Aquaporins Collecting Duct, DCT → ↑ H2O reabsorption
● ADH → ↑ H2O reabsorption → ↑ Urine concentration → UOsm > 100
SIADH
Pathology: *correction - ADH exerts its effects on DCT and collecting duct
● SIADH: Syndrome of inappropriate antidiuretic hormone (vasopressin) secretion
● ↑ ADH → ↑ H2O reabsorption → Hemodilution → Euvolemic hyponatremia (↓ Na)
● ↑ H2O reabsorption → ↑ Blood volume → ↑ BP → ↑ ANP/BNP → RAAS off
● Causes: Ectopic (small cell lung cancer), CNS disorders/head trauma
- Drugs: Cyclophosphamide, SSRI, carbamazepine
Presentation:
● Clinical features of hyponatremia: Nausea, emesis, lethargy, confusion, AMS, seizures
● No hypotension, tachycardia, or edema
Diagnostics:
● Hypotonic euvolemic hyponatremia
● Osmolality: mOsm/Kg
- High osmolality = ↑ Particles/Kg = Concentrated
- Low osmolality = ↓ Particles/Kg = Dilute
● SIADH: ↑ Urine osmolality, ↓ Serum osmolality
● RAAS off → UNa > 30
● ↑↑ Serum ADH
Treatment:
● Fluid restriction, IV hypertonic saline (NS 0.9%, Hypertonic 3%)
● ADH antagonists: -vaptans (conivaptan, tolvaptan, demeclocycline)
Complications:
● Osmotic Demyelination Syndrome - Overly rapid correction hyponatremia → Rapid shrinking of neurons → Demyelination
- Chronic hyponatremia → Fewer brain osmolytes → Less resistance to shrinking when hyponatremia corrected
- Chronic hyponatremia more dangerous to correct than acute
- Demyelination → Dysphagia, quadriparesis, lethargy, coma, behavioral disturbances, seizures, confusion
Diabetes Insipidus
Pathophysiology:
● Central: No ADH production → ↓ H2O Reabsorption → ↑ H2O loss, dilute urine
- Posterior pituitary pathology, malignancy, TBI, subarachnoid hemorrhage, meningitis, surgical trauma, ischemia (Sheehan Syndrome)
- Langerhans cell histiocytosis, autoimmune diseases
● Peripheral/Nephrogenic: Insensitivity to ADH (collecting duct) → ↓ H2O Reabsorption → ↑ H2O loss, dilute urine
- Drugs: Lithium, Amphotericin B, demeclocycline
- Electrolyte abnormalities
Presentation:
Central Peripheral
● Polydipsia, polyuria, nocturia, dehydration/poor skin turgor (Nephrogenic)
● ↑ Na, ↑ Electrolytes → Muscle weakness, extreme thirst, confusion, lethargy, irritability, seizures, LOC
Diagnostics: Causes Malignancy, TBI, Lithium,
● Osmolality: mOsm/Kg trauma, ischemia, Amphotericin B,
- High osmolality = ↑ Particles/Kg = Concentrated autoimmune demeclocycline
- Low osmolality = ↓ Particles/Kg = Dilute
● DI: ↓ Urine osmolality, ↑ Serum osmolality, Hypernatremia, ↑ Electrolytes Pathology No ADH → ADH insensitivity →
● Central: ↓ ADH, Vasopressin challenge → ↓ Urine volume and ↑ Urine osmolality Dilute urine Dilute urine
● Peripheral/Nephrogenic: ↑ ADH, Vasopressin challenge → No change in urine volume/osmolality
● Primary Polydipsia: Vasopressin challenge → Hyponatremia ADH ↓↓ ↑/Normal
- Water deprivation test → ↑ Urine osmolality
Treatment: Vasopressin ↓ Urine volume No change
● Central: Vasopressin, desmopressin (DDAVP) Challenge ↑ Urine osmolality
● Peripheral/Nephrogenic: Hydrochlorothiazide, amiloride, indomethacin
Treatment Vasopressin, HCTZ, amiloride,
desmopressin indomethacin
How to Differentiate Causes of Hyponatremia:

1. Order serum osmolality. Is this hypotonic, isotonic, or hypertonic?
2. If hypotonic, obtain volume status, UNa, Urine Osmolality
RAAS: Controls UNa, volume status
- RAAS on → ↑ Volume
ADH: Controls Urine Osmolality (NOT volume!)
ADH Present ADH Absent

UOsm > 100 UOsm <100
RAAS Off 1.SIADH 1.Renal losses

UNa > 30 2. Renal sodium losses (AKI)
(Diuretics,
↓ Mineralocorticoids)
3.Hypothyroidism,
Adrenal Insufficiency
4. Cerebral Salt Wasting
RAAS On 1.Hypovolemia 1.↑ H2O intake

Treatment: UNa < 30 2.Hypervolemia with (Psychogenic
- Treat underlying cause if present poor renal perfusion Polydipsia)
- If repleting with hypertonic saline, start low, go slow (Heart failure, 2. ↓ Solute intake
cirrhosis, nephrotic (Beer Potomania)
- Osmotic Demyelination Syndrome - Rapid correction syndrome)
hyponatremia → Loss of motor function, dysphagia, catatonia
≣ Item 1 of 1 Test Your Knowledge
Difficulty Rating: ✪✪✪ Bootcamp.com
Question ID: 3001
A 49-year-old female presents to her primary care physician for difficulty sleeping at night due to leg cramps. She states that she has become
increasingly fatigued and has begun to experience frequent afternoon headaches since her symptoms started three months ago. She has also had
numerous episodes of intractable coughing resulting in hemoptysis. The patient has a 20-pack year smoking history and her other medications include
lisinopril for hypertension and dapagliflozin for type 2 diabetes mellitus. Medical records reveal a visit to a neurologist one week ago for a seizure of
unknown etiology. On examination, the patient has a JVP of 7 at 45 degrees, mucous membranes are moist, and there is no pitting edema. Chest
X-ray is shown below. What are the most likely diagnostic urinary findings in this patient?
Urine Na Urine Osmolality Serum Osmolality

⚪ A. ↓ ↓ ↑
⚪ B. ↓ ↓ ↓
⚪ C. ↓ ↑ ↓
⚪ D. ↓ ↑ ↑
⚪ E. ↑ ↑ ↓
⚪ F. ↑ ↑ ↑
Question ID: 3002
A 79-year-old male presents to the emergency department for increased confusion and irritability. His wife states that the patient has “not been acting
like himself” for the past several days and this morning was unable to carry on a simple conversation with her. She notes that the patient has had
increased watery, foul-smelling diarrhea requiring him to be near a toilet at all times. The patient’s wife states that these symptoms started after their
recent travel to Iowa to visit the patient’s grandchildren, but denies him having additional symptoms or ill contacts. The patient’s medications include
simvastatin and aspirin. His wife reports that he completed a course of ciprofloxacin and azithromycin approximately one month ago to treat
pneumonia. In the emergency department the patient is started on intravenous fluids and his condition initially improves. Two hours later he
experiences acute onset dysphagia and new weakness in his lower extremities. Deep tendon reflexes are noted to be increased at this time. What is
the most likely cause of this patient’s worsening condition?
⚪ A. Avulsion of nerve roots from the spinal cord
⚪ B. Autoimmune destruction of the myelin sheath
⚪ C. Accumulation of amyloid β-protein deposits
⚪ D. Cerebral apoptosis and shrinkage of oligodendrocytes
⚪ E. Antibodies against postsynaptic Ach receptors

Question ID: 3003
A 12-year-old girl is brought to her pediatrician by her mother for three weeks of diarrhea. The patient’s mother reports that she has been passing
frequent, loose stools ever since she returned from a family vacation to Mexico one month ago. No sick contacts have been reported in the family.
During this time the patient has also experienced frequent headaches and increased fatigue. She denies abdominal pain and dysuria. On examination
the patient’s abdomen is soft and non-tender, bowel sounds are present, and there are several small abrasions on her right knuckles. The patient
reports she scraped her hand while attempting to catch a softball at practice. Examination is otherwise unremarkable. Results of serum analysis are
shown below. What diagnostic urine studies would be most consistent with this patient’s underlying presentation?
Na 121 mEq/L
Vasopressin Aldosterone Serum Osmolality
⚪ A. ↓ ↓ ↑
K 2.8 mEq/L
⚪ B. ↓ ↓ ↓
Cl 111 mEq/L
⚪ C. ↓ ↑ ↓
HCO3- 16 mEq/L
⚪ D. ↑ ↑ ↓
BUN 4 mg/dL
⚪ E. ↑ ↓ ↓
Creatinine 0.4 mg/dL
⚪ F. ↑ ↑ ↑
Glucose 72 mg/dL
Serum pH 7.31
PaCO2 37 mm Hg
𝛼-amylase 93 U/L
REVIEW OUTLINE
1. Pituitary: Embryology 6. Hyperprolactinemia
Endocrinology: A. Embryology
B. Anatomy
A. Pathophysiology
B. Presentation
2. Anterior Pituitary: Function
Anterior and 3.
A. Function
Posterior Pituitary: Function
C. Diagnostics
D. Treatment
7. Hypopituitarism
Posterior Pituitary 4.
A. Function
Gigantism and Acromegaly
A. Sheehan Syndrome
B. Empty Sella Syndrome
A. Pathophysiology C. Pituitary Apoplexy
B. Presentation D. Craniopharyngioma
C. Diagnostics
D. Treatment
5. Growth Hormone Deficiency
A. Pathophysiology
B. Presentation
C. Diagnostics
D. Treatment
Endocrinology: Anterior and Posterior Pituitary Bootcamp.com
Pituitary: Embryology
Embryology:
● Anterior Pituitary/Adenohypophysis: From Rathke’s pouch, evagination of foregut, oral ectoderm
- Ectodermal cells in third ventricle → Hormone producing cells
● Posterior Pituitary/Neurohypophysis: Downgrowth neuroectoderm in diencephalon
- Unmyelinated axons with cell bodies in hypothalamus
● Infundibulum/pituitary stalk: Connection between hypothalamus and pituitary gland
- Develops and elongates, pituitary dangles on the end of this stalk
Anatomy:
● Portal circulation: Between hypothalamus and anterior pituitary
- Hypothalamus → Neuropeptides → Portal circulation → Pituitary stalk → Anterior pituitary
● Neurons from hypothalamus → Pituitary stalk → Neurotransmitters to posterior pituitary
● Rests in sella turcica of sphenoid bone, beneath optic chiasm (CN II)
● Bilateral Hemianopia: Can result due to pituitary mass, malignancy
Anterior Pituitary: Function

Function:
● Releases FSH, LH, ACTH, TSH, Prolactin, GH (FLAT PiG)
● Hypothalamus → GnRH → AP → LH, FSH → Ovaries/Testes
● Hypothalamus → CRH → AP → ACTH → Adrenal Cortex → Cortisol
- CRH also stimulates β-endorphins and MSH
- POMC gene → POMC protein → Cleaved → MSH, ACTH
● Hypothalamus → TRH → AP → TSH → Thyroid → T3, T4
● Hypothalamus → Dopamine, TRH → AP → Prolactin → Breast → Milk
● Hypothalamus → GHRH → AP → GH → Liver → IGF-1 → Tissue growth
Posterior Pituitary: Function

Function:
● Releases oxytocin, vasopressin (ADH)
● ↓ Volume, Angiotensin II, ↑ Osmolality → ↑ ADH release → ↑ Aquaporins collecting duct → ↑ H2O reabsorption
● Suckling → ↑ Oxytocin release → Milk let down
● Uterine stretch → ↑ Oxytocin release → ↑ Uterine contractions → Uterine stretch
Gigantism and Acromegaly

Pathophysiology:
● Usually benign pituitary adenoma → Excess GH release → ↑ IGF-1 release → Excess growth
- MEN-1, McCune Albright syndrome, familial isolated pituitary adenomas, GNAS associated
● Gigantism: Occurs before fusion of epiphyseal plates → ↑ Linear bone growth
● Acromegaly: Occurs after skeletal epiphyseal closure → Disproportionate growth
● Pseudoacromegaly: Medication-induced insulin resistance, minoxidil, phenytoin, hypothyroid
Presentation:
● Gigantism: Present from childhood → Increased stature
- Heart failure most common cause of death
● Acromegaly: Occurs in adulthood → Disproportionate skeletal, tissue, organ growth
- Frontal bossing → Increased hat size, headaches in the morning
- Jaw enlargement → Prominent jaw with spaces between the teeth
- Large hands and feet, carpal tunnel syndrome, muscle weakness, HTN
- Coarse facies, deep voice, diaphoresis
- ↑ Risk colorectal polyps, cancer
Diagnostics:
● ↑ IGF-1, hyperglycemia (excess GH → Insulin resistance)
● Glucose challenge → ↑ GH levels (not suppressed)
● Pituitary mass, enlargement of sella turcica on Brain MRI/CT
● Cardiomegaly on CXR
● Acromegaly: Old photo doesn’t look like same person
● Pseudoacromegaly: No change GH, IGF-1 axis
Treatment:
● Surgical resection of pituitary adenoma
● Octreotide (Somatostatin analog → ↓ GH release)
● Pegvisomant (GH receptor antagonist)
● Cabergoline (Dopamine analog, second line, suppress GH release)
Growth Hormone Deficiency:

Pathophysiology:
● Congenital: Usually from genetic mutation, also called “pituitary dwarfism”
● Acquired: Brain tumor, surgery, TBI, radiation to the pituitary
Presentation:
● Congenital: Short stature with proportional measurements
- Often associated with midface hypoplasia
● Acquired: Short stature with proportional measurements
Diagnostics:
● ↓ IGF-1, <10th percentile on growth curves
● GH stimulation test: IV Arginine → ↑ GH Release (benign physiology)
● Congenital GH deficiency → Possible deficiency other pituitary hormones
Treatment:
● Human GH injections
● GH administered patients with Turner Syndrome as well
- These patients are not GH deficient
Question:
A 5 y.o. girl is brought to your clinic by her father due to concern for short stature. Dad reports that
she is the shortest child in her class, and her growth chart reveals she is below the first percentile for
growth for her age. The patient’s parents are both average height, and her older brother plays for the
Portland Trail Blazers. She is otherwise well. The patient is short with proportional measurements, and
exam is otherwise unremarkable. Which of the following is most likely to confirm her diagnosis?
A. Karyotype
B. PCR
C. GH stimulation test
D. 24-hour urine cortisol
Hyperprolactinemia:
Pathophysiology:
● ↑ Prolactin → ↑ Lactotroph activity
● ↑ Prolactin → ↓ GnRH → ↓ FSH, ↓ LH → ↓ Estrogen, ↓ Testosterone → Hypogonadotropic hypogonadism
● Stimulation of prolactin secretion: Primary hypothyroidism, pregnancy, breastfeeding, sleep, stress, dopamine antagonists
● Benign pituitary adenoma → ↑ Lactotrophs → ↑ Prolactin secretion
● Non-secreting pituitary adenoma → Compression infundibular stalk → ↓ Dopamine → ↓ Inhibition of lactotrophs → ↑ Prolactin
● Dopamine antagonists → ↓ Inhibition of lactotrophs → ↑ Prolactin secretion
- Risperidone, haloperidol, fluphenazine, metoclopramide
Presentation:
● Lack of ovulation, vaginal atrophy in females, infertility/amenorrhea in women, ↓ spermatogenesis in males, osteoporosis
● Galactorrhea (nipple discharge), gynecomastia in men
● Bitemporal hemianopia: Loss of bitemporal peripheral vision due to compression of optic chiasm
Diagnostics:
● Prolactin level, TSH, T4, T3
● Brain MRI with contrast: Pituitary mass, enlargement of sella turcica
Treatment:
● Surgical resection if pituitary adenoma present
● Dopamine agonists (bromocriptine, cabergoline)
Hypopituitarism:
Sheehan Syndrome:
● Pathophysiology: Pituitary swells during pregnancy → Postpartum hemorrhage → Ischemia → Pituitary infarct
● Presentation: Prolactin deficiency → Lactation failure, amenorrhea
- ↓ TSH → Hypothyroid symptoms (cold intolerance, weight gain, bradycardia)
- ↓ ADH → Diabetes insipidus
● Diagnostics: Infarction of pituitary on head MRI, empty sella turcica
- ↓ ACTH, ↓ TSH, ↓ FSH/LH, ↓ GH, ↓ Prolactin, +/- ↓ ADH
● Treatment: Irreversible, treat with hormone replacement
Empty Sella Syndrome:
● Pathophysiology: Enlargement sella turcica → CSF leaks in → Atrophy/compression of pituitary
- Associated idiopathic intracranial HTN
● Diagnostics: Pituitary fossa replaced by CSF, “empty” sella turcica
● Treatment: No treatment if asymptomatic
Pituitary Apoplexy:
● Pathophysiology: Hemorrhage or infarction of pituitary
- Often with existing pituitary adenoma
● Presentation: Sudden-onset severe headache, bitemporal hemianopia, AMS
● Diagnostics: Head CT, intrasellar mass with hemorrhage
● Treatment: Corticosteroids, possible surgery
Craniopharyngioma:
● Pathophysiology: Benign tumor of Rathke’s pouch (derived from oral ectoderm)
- Most common childhood supratentorial tumor, age 5-14
● Presentation: Headaches, bitemporal hemianopia, can compress pituitary → Hypopituitarism
- ↓ TSH → Hypothyroid, ↓ ACTH → ↓ Cortisol, ↓ ADH → Diabetes insipidus
- Can compress infundibular stalk → ↓ Feedback hypothalamus → Hyperprolactinemia
● Diagnostics: Head CT, suprasellar calcified cyst, electrolyte abnormalities, ↓ ACTH, ↓ TSH, ↓ FSH/LH, ↓ GH, ↓/↑ Prolactin, +/- ↓ ADH
● Treatment: Surgical resection
REVIEW OUTLINE
1. Thyroid and Parathyroid Development 7. Hypothyroidism: Other Causes
A. Embryology A. General Findings of Hypothyroidism
Endocrinology: 2.
B. Pathology
Thyroid Anatomy and Function
A. Anatomy
B. Iodine deficiency
C. Congenital hypothyroidism
D. Radiation-induced damage
Thyroid
B. Function E. Euthyroid sick syndrome
3. T3, T4 Synthesis and Pharmacology F. Pharmaceutical agents
A. Synthesis 8. Thyroid Neoplasms
B. Pharmacology A. Thyroid adenoma
C. Wolff-Chaikoff Effect B. Papillary carcinoma
D. Jod Basedow Phenomenon C. Follicular carcinoma
4. Hyperthyroidism: Graves Disease D. Medullary carcinoma
A. Hyperthyroidism E. Undifferentiated/Anaplastic carcinoma
B. Graves Disease
5. Hyperthyroidism: Other Causes
A. General Findings of Hyperthyroidism
B. Toxic multinodular goiter
C. Extrinsic ingestion
D. Amiodarone
E. Pregnancy
6. Hyper/Hypothyroidism: Thyroiditis
A. General Findings of Hyperthyroidism and Hypothyroidism
B. Hashimoto’s Thyroiditis
C. Postpartum Thyroiditis
D. Subacute (de Quervain) Thyroiditis
E. Riedel Thyroiditis
Endocrinology: Thyroid Bootcamp.com
Thyroid and Parathyroid Development

Embryology:
● Endoderm between first, second pharyngeal pouches near base of tongue
● Diverticulum formation week 3 → Caudal migration anterior to hyoid, laryngeal cartilage → Separation right and left lobes week 5
● Thyroglossal duct: Connects thyroid and tongue during caudal migration from foramen cecum, obliterates week 8-10
● Dorsal wings third pharyngeal pouch → Inferior parathyroid glands (week 5)
● Dorsal wings fourth pharyngeal pouch → Superior parathyroid glands
● Ventral wing of fourth pharyngeal pouch → Parafollicular C cells
● 4th and 6th pharyngeal arches → Thyroid cartilage
Pathology:
● Ectopic thyroid tissue: Thyroid tissue located outside of normal position in anterior neck, most commonly at base of tongue
- Most commonly secondary to failure of embryological descent
- Most commonly at base of tongue, can occur anywhere along thyroglossal duct pathway
- Presentation: Asymptomatic unless physical obstruction → Cough, difficulty swallowing, snore
- Diagnostics: Thyroid scintigraphy, US
- Management: Usually surgical resection, radioiodine ablation
- Can cause hypothyroidism if this is the only thyroid tissue present
● Thyroglossal duct cyst: Portion of thyroglossal duct fails to involute
- Presentation: Anterior midline neck mass that moves with swallowing
- Differentiate from branchial cleft cysts and cystic hygroma (does not move with swallowing)
- Management: Surgical removal
Thyroid Anatomy and Function

Anatomy:
● Butterfly gland anterior to trachea inferior to cricoid cartilage
● Common carotid artery → External carotid artery → Superior thyroid artery
● Subclavian artery → Inferior thyroid arteries
● Recurrent laryngeal nerve: Runs near inferior thyroid artery
- Supplies all intrinsic muscles of larynx except cricothyroid (superior laryngeal n.)
Function:
● Combine iodine, tyrosine → Thyroxine (T4) → Triiodothyronine (T3)
- Iodine deficiency → Thyroid enlargement → Goiter
● Hypothalamus → TRH → Anterior pituitary → TSH → Thyroid → T3, T4
● T3: Regulates metabolism, temperature, weight, muscle strength, nervous system
● Hyperthyroidism: Increased T3, T4
- Heat intolerance, diaphoresis, weight loss, diarrhea, increased fracture risk
- Hyperactivity, restlessness, insomnia, anxiety, fine tremors, palpitations, hypertension
- Gynecomastia or abnormal uterine bleeding
● Hypothyroidism: Decreased T3, T4
- Cold intolerance, weight gain, dry skin, coarse, brittle hair, brittle nails, constipation
- Fatigue, weakness, lethargy, decreased reflexes, bradycardia
T3, T4 Synthesis and Pharmacology

Synthesis:
● In follicles of thyroid, iodine + tyrosine → T3, T4 → Some T4 converted to T3 (potent form) peripherally
- 2 Diiodotyrosine (DIT) = T4
- 1 DIT + 1 Monoiodotyrosine (MIT) = T3
● Thyroid peroxidase: Oxidation, organification of iodide, coupling of monoiodotyrosine (MIT) and diiodotyrosine (DIT)
● Thyroglobulin: Thyroid hormone substrate, Tyrosine → Iodination → Coupling → Cleavage → T3, T4 release
● Thyroid binding globulin: Produced by liver → Binds T3, T4 in serum preventing destruction
● 5’-Deiodinase: Converts T4 → T3 in peripheral tissues
Pharmacology:
● Thyroid peroxidase inhibitors: Propylthiouracil (PTU), methimazole
- PTU: Agranulocytosis, aplastic anemia, hepatotoxicity
- Methimazole: Aplasia cutis (first trimester), present in breast milk
● 5’-Deiodinase inhibitors: Glucocorticoids, β-Blockers, PTU, Amiodarone
● Lithium: Inhibits iodine uptake, TPO, and T3, T4 release
● Perchlorate/Pertechnetate: Inhibit iodine uptake
Wolff-Chaikoff Effect:
● Excess iodine administration inhibits T3, T4 synthesis for several days
● Mechanism: Iodopeptides form → Inhibit TPO synthesis
● Clinical Applications: Hyperthyroidism treatment (prior to thionamides)
- KI (Lugol’s iodine) for treatment of acute radiation exposure
Jod-Basedow Phenomenon:
● Hyperthyroidism following iodine administration
● Usually occurs in patients with dysregulated thyroid hormone synthesis
- Ex. Graves disease, toxic multinodular goiter, thyroid adenoma
● Mechanism: ↑ Iodine → Uncontrolled T3, T4 synthesis
Hyperthyroidism: Graves Disease

General Findings of Hyperthyroidism:
● Heat intolerance, diaphoresis, weight loss, diarrhea, hyperactivity, restlessness, insomnia, anxiety, fine tremors, palpitations, hypertension
Histopathology:
● Thyroid stimulating immunoglobulin (IgG) → Binds TSH receptors → ↑ T3, T4
● Type II hypersensitivity reaction, associated HLA-DR3, HLA-B8
● T cell activation → Lymphocyte infiltration retro-orbital space → ↑ Cytokines (TNF-⍺, IFN-𝛾) → ↑ Fibroblast secretion hydrophilic GAG’s →
↑ Muscle inflammation, osmotic muscle swelling → Exophthalmos
● Histology: Tall, crowded columnar follicular epithelial cells, scalloping
Presentation:
● Most common cause of hyperthyroidism in U.S., common females 20-40 y.o.
● Hyperthyroidism symptoms, goiter, pretibial myxedema, graves ophthalmopathy: Exophthalmos, lid retraction
Diagnostics:
● ↑ T3, T4, ↓ TSH, ↑ Anti-TSH receptor Ab (diagnostic), diffuse uptake on thyroid scintigraphy
● Lipid panel ↓ Cholesterol, ↓ Triglycerides, CBC normocytic anemia
Complications:
● Associated with diabetes, vitiligo, pernicious anemia
● Thyroid storm: Uncommon, life-threatening complication of untreated hyperthyroidism
- Usually exacerbated by acute stress (infection, trauma, etc.)
- Agitation, fever, delirium, coma, diarrhea, tachyarrhythmia (cause of death)
- Treat with 4P’s: Propranolol (β-Blockers), Propylthiouracil, Prednisolone (steroids), Potassium iodide
● Fetal hyperthyroidism: TSI IgG crosses placenta → Hyperthyroidism in utero
- β-hCG can also bind TSH receptor, ↑ Binding first trimester, ↓ Binding second trimester due to progesterone
- Symptoms of hyperthyroidism, low birth weight, prematurity, death
- Treat hyperthyroidism in the mother (PTU first trimester, methimazole after first trimester)
Management:
● Propranolol for acute sympathetic symptoms (palpitations, muscle weakness, etc.)
● Thionamides/TPO Inhibitors: Propylthiouracil, methimazole, inhibit thyroid hormone synthesis
● Radioiodine ablation (contraindicated in pregnancy), surgical thyroidectomy
Hyperthyroidism: Other Causes

General Findings of Hyperthyroidism:
● Heat intolerance, diaphoresis, weight loss, diarrhea, restlessness, insomnia, anxiety, fine tremors, palpitations, hypertension
● Increased fracture risk, gynecomastia or abnormal uterine bleeding
Toxic Multinodular Goiter:
● Pathophysiology: Focal patches hyperfunctioning follicular cells working independently TSH → ↑ T3, T4
- Commonly due to TSH receptor mutation
● Presentation: Hyperthyroid symptoms, possible goiter with multiple nodules (not smooth like in Grave’s)
● Diagnostics: Thyroid scintigraphy, “hot” nodules with increased iodine uptake (rarely malignant)
- ↑ T3, T4, ↓ TSH
● Management: Radioactive iodine ablation, surgical removal, thionamides (PTU, methimazole)
Extrinsic Ingestion:
● Presentation: Often patients seeking rapid weight loss with access to exogenous thyroid hormones, symptoms of hyperthyroidism
● Diagnostics: ↑ T3, T4, ↓ TSH, ↓ Thyroglobulin levels (or normal), low/undetectable 24-hour radioiodine uptake
● Management: Cease extrinsic ingestion, treat for thyrotoxicosis if necessary
Amiodarone:
● Contains iodine, can cause hyperthyroidism or hypothyroidism
● Wolff-Chaikoff effect: Failure to escape → Hypothyroid state
- More common in Hashimoto’s thyroiditis
● Jod-Basedow phenomenon: Autonomous thyroid hormone synthesis → Hyperthyroidism
- More common in Graves, toxic multinodular goiter
Thyroiditis:
● Hashimoto’s, subacute (de Quervain’s), acute infectious thyroiditis, drug-induced
- Usually cause hypothyroidism, may cause transient hyperthyroidism at onset
Pregnancy:
● ↑ Estrogen → ↑ Thyroid binding globulin in pregnancy → ↑ Circulating T3, T4 bound to thyroid binding globulin
● Free T3, T4 levels remain relatively unchanged (not clinically significant hyperthyroidism!)
Hyper/Hypothyroidism: Thyroiditis
General Findings of Hyperthyroidism and Hypothyroidism:
● Hyperthyroidism: Heat intolerance, diaphoresis, weight loss, diarrhea, restlessness, insomnia, anxiety, fine tremors, palpitations, hypertension
● Hypothyroidism: Cold intolerance, weight gain, dry skin, brittle hair, brittle nails, constipation, fatigue, weakness, lethargy, decreased reflexes, bradycardia
- Myxedema coma: Severe hypothyroidism → ↓ Mental status, hypothermia, slowing/failure of multiple organs, life threatening
Hashimoto’s Thyroiditis:
● Chronic lymphocytic thyroiditis, most common cause of hypothyroidism in iodine sufficient countries
● Pathophysiology: Autoimmune thyroiditis, auto-antibodies against thyroid peroxidase, thyroglobulin
- CD8+ cytotoxic T cells attack thyroid (Type IV HS) → Release TPO, thyroglobulin → Ab formation (Type II HS) → Further thyroid destruction
- HLA-DR3, HLA-DR5, associated SLE, T1DM, Grave’s Disease
● Presentation: Transient hyperthyroidism, “hashitoxicosis” → Hypothyroidism, nontender, enlarged, symmetrical, “rubbery” thyroid
● Diagnostics: Anti-TPO Ab’s, transient hyperthyroidism: ↓TSH, ↑ T3, ↑ T4 ↑ Thyroglobulin → Hypothyroidism: ↑TSH, normal T3 and T4 → ↑TSH, ↓T3, ↓T4
- Histopathology: Hurthlë cells, lymphoid aggregates with germinal centers
● Management: Levothyroxine (thyroid hormone replacement)
Postpartum Thyroiditis:
● Subacute lymphocytic thyroiditis
● Pathophysiology: Thyroid peroxidase Ab → Damage thyroid follicles → Release pre-formed T4, T3 → Stores T4, T3 exhausted → Hypothyroidism
● Presentation: Associated T1DM, up to one year after delivery, transient hyperthyroidism → Hypothyroidism, thyroid normal size and nontender
● Diagnostics: ↓ T4, ↓ T3, ↑ TSH, ↑ Thyroglobulin, ↑ Anti-thyroid peroxidase Ab’s
- Histopathology: Lymphoid aggregates with germinal centers, no Hurthlë cells or fibrosis
● Management: Usually self-limiting, no treatment required unless symptomatic
Subacute Granulomatous (De Quervain) Thyroiditis:
● Pathophysiology: Viral infection/flu-like illness → Inflammatory damage to thyroid follicles → Release T4, T3
● Presentation: Recent viral illness, transient hyperthyroidism → Hypothyroidism, very tender thyroid, jaw pain
● Diagnostics: ↓ T4, T3, ↑ TSH, ↑ Thyroglobulin, ↑ ESR, ↑ CRP
- Histopathology: Granulomatous inflammation, multinucleated giant cells, foamy histiocytes
● Management: Usually self-limiting, no treatment required unless symptomatic (consider propranolol, methimazole)
Riedel Thyroiditis:
● Pathophysiology: Thyroid replaced by fibrous tissue with inflammatory infiltrates, IgG4 related systemic disease
● Presentation: Fixed, “rock-like,” painless goiter, dysphagia, hoarseness, dyspnea, hypothyroidism
● Complications: ↑ Risk thyroid lymphoma
● Diagnostics: ↓ T4, T3, ↑ TSH, ↑ Thyroglobulin, fibrous tissue with inflammatory infiltrate on histology
● Management: Levothyroxine, thyroidectomy
Hyper/Hypothyroidism: Thyroiditis
General Findings of Hyperthyroidism and Hypothyroidism:
● Hyperthyroidism: Heat intolerance, diaphoresis, weight loss, diarrhea, restlessness, insomnia, anxiety, fine tremors, palpitations, hypertension
● Hypothyroidism: Cold intolerance, weight gain, dry skin, brittle hair, brittle nails, constipation, fatigue, weakness, lethargy, decreased reflexes, bradycardia
- Myxedema coma: Severe hypothyroidism → ↓ Mental status, hypothermia, slowing/failure of multiple organs, life threatening
Hashimoto’s Thyroiditis:
● Chronic lymphocytic thyroiditis, most common cause of hypothyroidism in iodine sufficient countries
● Pathophysiology: Autoimmune thyroiditis, auto-antibodies against thyroid peroxidase, thyroglobulin
- CD8+ cytotoxic T cells attack thyroid (Type IV HS) → Release TPO, thyroglobulin → Ab formation (Type II HS) → Further thyroid destruction
- HLA-DR3, HLA-DR5, associated SLE, T1DM, Grave’s Disease
● Presentation: Transient hyperthyroidism, “hashitoxicosis” → Hypothyroidism, nontender, enlarged, symmetrical, “rubbery” thyroid
● Diagnostics: Anti-TPO Ab’s, transient hyperthyroidism: ↓TSH, ↑ T3, ↑ T4 ↑ Thyroglobulin → Hypothyroidism: ↑TSH, normal T3 and T4 → ↑TSH, ↓T3, ↓T4
- Histopathology: Hurthlë cells, lymphoid aggregates with germinal centers
● Management: Levothyroxine (thyroid hormone replacement)
Postpartum Thyroiditis:
● Subacute lymphocytic thyroiditis
● Pathophysiology: Thyroid peroxidase Ab → Damage thyroid follicles → Release pre-formed T4, T3 → Stores T4, T3 exhausted → Hypothyroidism
● Presentation: Associated T1DM, up to one year after delivery, transient hyperthyroidism → Hypothyroidism, thyroid normal size and nontender
● Diagnostics: ↓ T4, ↓ T3, ↑ TSH, ↑ Thyroglobulin, ↑ Anti-thyroid peroxidase Ab’s
- Histopathology: Lymphoid aggregates with germinal centers, no Hurthlë cells or fibrosis Hashimoto Anti-TPO Ab’s
● Management: Usually self-limiting, no treatment required unless symptomatic Symmetrical, rubbery,
Subacute Granulomatous (De Quervain) Thyroiditis: enlarged thyroid
● Pathophysiology: Viral infection/flu-like illness → Inflammatory damage to thyroid follicles → Release T4, T3
● Presentation: Recent viral illness, transient hyperthyroidism → Hypothyroidism, very tender thyroid, jaw pain
Postpartum Pregnancy in stem,
● Diagnostics: ↓ T4, T3, ↑ TSH, ↑ Thyroglobulin, ↑ ESR, ↑ CRP
Normal size thyroid,
- Histopathology: Granulomatous inflammation, multinucleated giant cells, foamy histiocytes Nontender thyroid
● Management: Usually self-limiting, no treatment required unless symptomatic (consider corticosteroids)
Riedel Thyroiditis:
● Pathophysiology: Thyroid replaced by fibrous tissue with inflammatory infiltrates, IgG4 related systemic disease De Recent illness
Quervain Painful thyroid
● Presentation: Fixed, “rock-like,” painless goiter, dysphagia, hoarseness, dyspnea, hypothyroidism
● Complications: ↑ Risk thyroid lymphoma
● Diagnostics: ↓ T4, T3, ↑ TSH, ↑ Thyroglobulin, fibrous tissue with inflammatory infiltrate on histology Riedel Hard, immobile
● Management: Levothyroxine, thyroidectomy thyroid
Hypothyroidism: Other Causes

General Findings of Hypothyroidism:
● Cold intolerance, weight gain, dry skin, coarse brittle hair, brittle nails, constipation, fatigue, weakness, lethargy, decreased reflexes, bradycardia
Iodine Deficiency:
● Pathophysiology: ↓ Iodine → ↓ T3, T4 production → Hypothyroidism
● Presentation: Hypothyroidism symptoms, goiter, often patients in resource-limited countries
● Management: Iodine (potential for Wolff-Chaikoff effect)
Congenital Hypothyroidism:
● One of most common causes cognitive disability (preventable) in U.S.
● Etiology: Ab-mediated maternal hypothyroidism → IgG crosses placenta → Fetal thyroid dysgenesis
● Presentation: Pot-bellied, pale, puffy face, protruding umbilicus, protruding tongue, poor brain development, hoarse cry, hypotonia
- Often presents weeks, months after birth (maternal T4 crosses placenta)
● Management: Levothyroxine (thyroid hormone replacement therapy), screen pregnant women for hypothyroidism, thyroiditis
Radiation-Induced Damage:
● Nuclear accidents, palliative radiation, or radiofrequency ablation
● Pathophysiology: Radiation destroys thyroid tissue → No functional thyroid tissue left to produce T3, T4
● Management: Levothyroxine (thyroid hormone replacement therapy)
- Prevent nuclear accident damage with KI → Wolff-Chaikoff effect
Euthyroid Sick Syndrome:
● Pathophysiology: Non-thyroidal illness → ↑ Cytokines (IL-6) → ↓ T4 → T3 conversion in liver
- Potentially adaptive mechanism allowing body to preserve energy during illness
● Presentation: Non-thyroidal illness, hypothyroidism symptoms
● Diagnostics: ↓ T3, T4 may be within normal limits, sometimes ↑ TSH
● Management: None, self-resolving
Pharmaceutical Agents:
● Lithium, amiodarone
Thyroid Neoplasms:
Thyroid Adenoma:
● Histopathology: Benign, solitary growth of thyroid, “cold” nodules (usually, exceptions exist) → Hyperthyroidism, thyrotoxicosis
- Follicular, no capsular or vascular invasion
● Presentation: Most frequently asymptomatic
● Management: Surgical resection if necessary
Papillary Carcinoma:
● Most common form of thyroid cancer
● Histopathology: Orphan Annie nuclei: Empty appearing nuclei with central clearing, psammoma bodies
- Well-differentiated, risk factors: RET/PTC rearrangements, BRAF mutations, childhood irradiation
● Presentation: Usually asymptomatic
● Diagnosis: Fine needle aspiration
● Management: Excellent prognosis, treat with thyroidectomy
Follicular Carcinoma:
● Histopathology: Invasion of thyroid capsule and vasculature → Hematogenous spread → Bone, Lungs
- Well-differentiated, uniform follicles, associated with RAS mutation, PAX8-PPAR-𝛾 translocations
● Diagnosis: Fine needle aspiration
● Management: Good prognosis, treat with thyroidectomy
Medullary Carcinoma:
● Histopathology: Parafollicular C cells → Release calcitonin
- Well-differentiated, sheets of cells in amyloid stroma, stains Congo red, associated with RET mutations, MEN2A, MEN2B
● Diagnosis: Fine needle aspiration, staining with Congo red
● Management: Thyroidectomy
Undifferentiated/Anaplastic Carcinoma:
● Histopathology: Poorly differentiated, areas of necrosis, hemorrhaging, and giant cells
● Presentation: Usually older patients, rapidly enlarging neck mass → Compression of surrounding structures → Dysphagia, dyspnea
- Associated with TP53 mutation
● Management: Very poor prognosis even with thyroidectomy
Video Vignettes
Video 4.1: Thyroid and Parathyroid Development
○ A patient presents to clinic with a midline neck mass. The mass is firm, contender, and does move with swallowing. This patient’s pathology is the result of the failure of
which structure to form properly?
Video 4.2: Thyroid Anatomy and Function

○ A 15 year old patient is brought to the physician by her parents for unintentional weight loss, diarrhea, palpitations, and increased sweating over the past month. Her
father is concerned that the patient is taking drugs and requests a urine drug screen. Urine drug screen is negative but T3 and T4 are elevated. the patient undergoes
thyroidectomy to treat her underlying condition and you see her at her follow up appointment. At her follow up appointment the patient has been doing well, but she has
been having hoarseness and difficulty swallowing. The nerve most likely responsible for her symptoms innervates all of the following muscles except which one?
Video 4.3: T3, T4 Synthesis and Pharmacology

○ A patient presents to the emergency department after accidental exposure to radioactive waste at a job site. In the ED the patient is administered a high dose of
potassium iodide. What is the mechanism by which this medication prevents continued radiation damage?
Video 4.4: Hyperthyroidism: Graves Disease

○ You’re called to the bedside of a 1 day old female for poor feeding and irritability. Mom states the patient has been inconsolable, frequently crying, and disinterested in
breastfeeding. On exam, the patient is febrile and tachycardic and she is in the sixth percentile for weight. Pregnancy was uncomplicated and Mom was group B strep
negative. Mom does have a history of Grave’s disease and radioiodine ablation at 19. No history of substance abuse and no other medical problems. What are the most
likely values of T3, T4, and TSH in this infant now and at 3 months?
Video 4.5: Hyperthyroidism: Other Causes

○ A 15 year old patient is brought to the pediatrician by his mother. Mom states the patient has been increasingly irritable, hyper, and has been sleeping no more than
2-3 hours per night. Yesterday the patient complained of heart palpitations during wrestling practice and had to sit out. On interview, the patient is animated, speaks
loudly and enthusiastically about his upcoming wrestling match, for which he has been trying to drop a weight class. Laboratory tests reveal elevated T3 and T4 and
elevated thyroglobulin. Thyroid scintigraphy reveals scattered areas of increased iodine uptake. What is the most likely cause of this patient’s presentation?
Video Vignettes
Video 4.6: Hyper/Hypothyroidism: Hashimoto’s and Postpartum Thyroiditis
○ A woman presents to clinic 3 months postpartum for increased weakness, lethargy, and weight gain since delivery. T3 and T4 levels are decreased, anti-TPO Ab is
elevated, and the patient’s thyroid is enlarged and nontender on exam. What are the most likely histology findings of this patient’s thyroid?
Video 4.7: Hyper/Hypothyroidism: De Quervain and Riedel Thyroiditis

○ A patient presents for three weeks of heart palpitations, sweating, and difficulty sleeping. On exam, the patient has a hard, immobile mass on their midline neck. What is
the appropriate treatment for this patient?
Video 4.8: Hypothyroidism: Other Causes

○ A 3 week old female is brought to the pediatrician for paleness, abnormal cry sounds, and poor tone. Labs reveal decreased T3, T4, and increased TSH. What is the
embryological origin of the organ responsible for this patient’s symptoms?
Video 4.9: Thyroid Malignancies

○ A 56 year old patient is referred for a concerning thyroid nodule. He receives a fine needle aspiration which revealed orphan annie nuclei and psammoma bodies. What
is a risk factor for this particular form of thyroid cancer?
REVIEW OUTLINE
1. Parathyroid Physiology
A. Location
Endocrinology: 2.
B. Function
Vitamin D Deficiency
A. Causes of Vitamin D Deficiency
Parathyroids
B. Rickets
C. Osteomalacia
3. Hypoparathyroidism
A. Hypoparathyroidism
B. Pseudohypoparathyroidism
C. Pseudopseudohypoparathyroidism
4. Hyperparathyroidism
A. Primary
B. Secondary
C. Tertiary
D. Complications
5. Familial Hypocalciuric Hypercalcemia
A. Familial Hypocalciuric Hypercalcemia
Endocrinology: Parathyroids Bootcamp.com
Parathyroid Location and Function

Location:
● Two pairs of small, oval shaped glands on the posterior aspect of the thyroid
● Fourth pharyngeal pouch → Superior parathyroids
● Third pharyngeal pouch → Inferior parathyroids
Function:
● Parathyroid hormone maintains calcium homeostasis
● Hypercalcemia: Calcium oxalate kidney stones, constipation, bone pain, psychosis, arrhythmias
● Hypocalcemia: Tetany, prolonged QT interval, seizures
- Chvostek sign, Trousseau’s sign
● PTH: Peptide hormone, ↓ Ca2+ → Chief cells → ↑ PTH
- PTH → Bone → ↑ Ca2+ release, ↑ P release
- ↑ Osteoblast activity → ↑ Osteoclast activity
- PTH → Kidneys → ↑ Ca2+ absorption, ↑ PO43- excretion
- PTH → Kidneys → ↑ 1-ɑ-hydroxylase activity
● 1-ɑ-hydroxylase: Forms 1,25-Dihydroxyvitamin D
- PTH → ↑ 1-ɑ-hydroxylase activity → ↑ Calcitriol
● 1,25-Dihydroxyvitamin D: Calcitriol, active vitamin D, D3
- ↑ Calcitriol → GI → ↑ Ca2+ absorption, ↑ PO43- absorption
- ↑ Calcitriol → Bone → ↑ Ca2+ release, ↑ PO43- release
● Fibroblast Growth Factor 23: Phosphorus homeostasis
- Secreted by osteocytes, osteoblasts
- ↑ PO43-, ↑ Calcitriol → ↑ FGF23
- ↑ FGF23 → ↓ Calcitriol, ↑ PO43- excretion, ↓ PTH
● Calcitonin: Secreted by parafollicular C cells
- Opposes PTH
- ↓ Osteoclast activity, ↓ Renal Ca2+ resorption
Vitamin D Deficiency
Causes of Vitamin D Deficiency:
● Poor dietary intake, ↓ Sun exposure
● Malabsorption (IBD, gastric bypass), fat-soluble vitamin deficiencies (celiac disease, CF)
Rickets:
● Pathophysiology: Vitamin D deficiency → ↑ PTH
- Defective cartilage mineralization epiphyseal growth plates
● Presentation: Children with bowed legs, kyphosis, scoliosis
- Fractures, poor growth, bone tenderness to palpation
- Muscle weakness, joint pain, difficulty walking
● Diagnostics: ↓ 1,25-Dihydroxyvitamin D, ↑ PTH
- ↑ Alkaline phosphatase
- Normal or ↓ Ca2, normal or ↓ PO43-
● Management: Vitamin D replacement
Osteomalacia:
● Pathophysiology: Vitamin D deficiency → ↑ PTH
- Defective cartilage mineralization osteoid
● Presentation: Children or adults with bone pain, joint pain
- Muscle weakness, difficulty walking, fractures
● Diagnostics: ↓ 1,25-Dihydroxyvitamin D, ↑ PTH
- ↑ Alkaline phosphatase
- Normal or ↓ Ca2, normal or ↓ PO43-
● Management: Vitamin D replacement
Hypoparathyroidism:
Hypoparathyroidism:
● Pathophysiology: Surgical damage, damage to blood supply, DiGeorge syndrome, autoimmune destruction, hypomagnesemia
- ↓ PTH → Ca2+, PO43- dysregulation → ↓ Ca2+, ↑ PO43-
● Presentation: Hypocalcemia (Chvostek sign, Trousseau sign), hyperphosphatemia, tetany
● Diagnostics: ↓ PTH, ↓ Ca2+, ↑ PO43-, normal 25-hydroxyvitamin D, normal/↓ 1-25-dihydroxyvitamin D
● Management: Oral calcium, vitamin D, magnesium, thiazide diuretics, PTH replacement
Pseudohypoparathyroidism:
● Pathophysiology: Autosomal dominant mutation in GNAS1 gene, encodes Gs ɑ-subunit → ↓ End organ sensitivity PTH
- Type 1A: Paternal imprinting, maternally inherited mutation GNAS1 → Diffuse end organ insensitivity (most common type)
- Type 1B: Insensitivity to PTH, TSH confined to kidney
- Type 1C: Normal Gs activity
- ↓ PTH sensitivity → Ca2+, PO43- dysregulation → ↓ Ca2+, ↑ PO43-
● Presentation: Hypocalcemia (Chvostek sign, Trousseau sign), hyperphosphatemia, tetany
- Albright hereditary osteodystrophy: Short 4th/5th digits, short stature, developmental delay
● Diagnostics: ↑ PTH, ↓ Ca2+, ↑ PO43-
● Management: IV calcium, oral calcium, calcitriol
Pseudopseudohypoparathyroidism:
● Pathophysiology: Autosomal dominant mutation in GNAS1 gene
- Transmitted in imprinted form to offspring of males with pseudohypothyroidism
- Active maternal allele without mutation → Kidney responsive to PTH → No end organ PTH resistance
● Presentation: Albright hereditary osteodystrophy: Shortened 4th/5th digits, short stature, developmental delay
● Diagnostics: Normal PTH, normal Ca2+, normal PO43-
● Management: Symptomatic treatment
Hyperparathyroidism:
Primary:
● Pathophysiology: Parathyroid adenoma, hyperplasia
- ↑ PTH → Ca2+, PO43- dysregulation → ↑ Ca2+, ↓ PO43-
● Presentation: Hypercalcemia
- Calcium oxalate kidney stones, constipation, bone pain, psychosis
- Osteitis fibrosa cystica, bone pain, fracture
● Diagnostics: ↑ PTH, ↑ Ca2+, ↓ PO43-, ↑ Alkaline phosphatase
● Management: Calcimimetics (cinacalcet), bisphosphonates (alendronate), parathyroidectomy
Secondary:
● Pathophysiology: ↓ PO43- excretion, ↓ Vitamin D → Secondary hyperplasia
- CKD → ↓ 1-ɑ-hydroxylase activity (↓ 1,25-dihydroxyvitamin D), ↑ PO43- retention → ↑ PTH
- PTH fails to correct hypocalcemia due to ↓ 1-ɑ-hydroxylase activity, ↑ PO43- binding to Ca2+
- ↓ Vitamin D → ↓ Ca2+ absorption, ↓ 1,25-dihydroxyvitamin D → ↑ PTH
● Presentation: Hypocalcemia (Tetany, prolonged QT interval, seizures, Chvostek sign, Trousseau’s sign)
● Diagnostics: ↑ PTH, ↓ Ca2+ ↑ Alkaline phosphatase, ↑ PO43- (CKD)
● Management: Phosphate binders (sevelamer), calcimimetics (cinacalcet), bisphosphonates (alendronate), calcitriol, parathyroidectomy
Tertiary:
● Pathophysiology: Often post-transplant in CKD patients, autonomous hyperparathyroidism
- Long periods of ↑ PO43- retention in CKD → Continued stimulation of parathyroid → Parathyroid desensitization → Autonomous parathyroid activity
● Presentation: Hypercalcemia (Calcium oxalate kidney stones, constipation, bone pain, psychosis)
● Diagnostics: ↑ PTH, ↑ Ca2+, ↓ PO43-
● Management: Parathyroidectomy
Complications:
● Pseudogout, pancreatitis, polyuria (usually primary)
● Osteitis fibrosa cystica: Usually associated primary hyperparathyroidism, can associate with secondary
- ↑ PTH → ↑ Osteoclast activity → Cystic bone spaces with osteoclasts and hemosiderin from hemorrhage (“brown tumor”) → Bone pain
● Renal osteodystrophy: Usually associated with secondary, tertiary hyperparathyroidism from CKD
- CKD → ↓ 1-ɑ-hydroxylase activity (↓ 1,25-dihydroxyvitamin D), ↑ PO43- retention → ↑ PTH → ↑ Bone turnover → Weak bones, pain
Familial Hypocalciuric Hypercalcemia:

Familial Hypocalciuric Hypercalcemia:
● Pathophysiology: AD mutation CaSR gene → Defective G-coupled Ca2+ receptors in kidneys, parathyroids
- ↑ Ca2+ required suppress PTH → ↑ PTH → ↑ Ca2+
● Presentation: Hypercalcemia, usually asymptomatic
● Diagnostics: ↑ PTH, ↑ Ca2+, ↓ 24-hour urine Ca2+
● Management: None required, avoid parathyroidectomy
Practice Questions
Video 5.1: Parathyroid Location and Function
○ A 14 year old girl presents for three months of increased joint and muscle tenderness. She has a history of Crohn’s disease and has been taking
6-mercaptopurine to control her frequent flares. DEXA scan reveals evidence of increased bone remodeling. What would be the expected laboratory
values of PTH, 1,25-dihydroxyvitamin D, and Calcium in this patient?
Video 5.2: Vitamin D Deficiency
○ A 35 year old woman presents for evaluation of back pain after a ground level fall. XR reveals L3-L4 fractures. On interview, the patient endorses three
months of worsening diarrhea in the amount of 4-5 foul smelling bowel movements per day with associated abdominal cramping but no blood in her
stools. She notes an itchy, painful rash on her back. Labs reveal normal Calcium levels but increased PTH. What is the most appropriate treatment for
this patient?
Video 5.3: Hypoparathyroidism
○ A 5 year old boy is brought to the physician for his annual check up. On exam, the patient is unable to hop on one foot but can hop with both feet, and
can draw a square but not a triangle. Blood work reveals increased PTH and decreased Ca2+. What is the receptor most likely affected by this
patient’s genetic mutation?
Video 5.4: Hyperparathyroidism
○ A 65 year old woman presents after a ground level fall. Medical history is remarkable for CKD, for which the patient receives dialysis M/W/F. XR
reveals L4 and L5 fractures. In addition to treatment of her fracture, the physician recommends initiation of a medication which will directly inhibit
continued bone breakdown. What is the mechanism of action of this medication?
Video 5.5: Familial Hypocalciuric Hypercalcemia
○ A 26 year old woman presents for her annual physical. Routine blood work reveals elevated calcium. Further testing reveals increased PTH and
decreased 24-hour urine calcium. What is the most appropriate therapy for this patient’s underlying condition?
References:
Slide 1: Eicosanoids <a href="https://commons.wikimedia.org/wiki/File:Tipus_de_prostaglandines.jpg">BQUB14-Msanjose</a>, <a
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Slide 1: Cholesterol <a href="https://commons.wikimedia.org/wiki/File:Sterols.svg">Vaccinationist</a>, <a
Slide 1: Types of signaling, created with Biorender.com
Slide 1: Nuclear receptor signaling, created with Biorender.com
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& umimeto.org</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia Commons
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<a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia Commons
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Slide 3: Factory <a href="https://commons.wikimedia.org/wiki/File:Industry5.svg">Tsaoja</a>, CC0, via Wikimedia Commons
Slide 3: Jordans <a href="https://commons.wikimedia.org/wiki/File:Nike_Air_Jordan_X_Steel.jpg">2Pacalyp</a>, <a
Slide 3: Trader Joe’s <a href="https://commons.wikimedia.org/wiki/File:Trader_Joe%27s.JPG">Anthony92931</a>, <a
Slide 3: Pumpkins <a href="https://commons.wikimedia.org/wiki/File:FrenchMarketPumpkinsB.jpg">Infrogmation of New Orleans</a>, <a
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Commons
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Slide 1: Pituitary gland <a href="https://commons.wikimedia.org/wiki/File:1614_Pituitary_Tumor-02.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia
Commons
Slide 1: <a href="https://commons.wikimedia.org/wiki/File:Visual_field_bitemporal_hemianopia.png">RobertB3009</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia
Commons
Slide 1: <a href="https://commons.wikimedia.org/wiki/File:1808_The_Anterior_Pituitary_Complex.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia
Commons
Slide 2: Thyroid Hormone Feedback, created with BioRender.com.
Slide 2: GnRH, <ahref="https://commons.wikimedia.org/wiki/File:Hypothalamic%E2%80%93pituitary%E2%80%93gonadal_axis_in_females.png">Lu Kong, Ting Zhang, Meng Tang and Dayong Wang</a>, <a
Slide 2: CRH, <a href="https://commons.wikimedia.org/wiki/File:Hypothalamic-pituitary-adrenal_axis_diagram.jpg">Ross AP, Ben-Zacharia A, Harris C and Smrtka J</a>, <a
Slide 2: Growth hormone <a href="https://commons.wikimedia.org/wiki/File:1809_Hormonal_Regulation_of_Growth.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via
Wikimedia Commons
Slide 2: Prolactin <a href="https://commons.wikimedia.org/wiki/File:Prolactin_regulation.png">Procedureready</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
Slide 3: Oxytocin <a href="https://commons.wikimedia.org/wiki/File:2922_Let_Down_Reflex.jpg">OpenStax Anatomy and PhysiologyOpenStax</a>, <a href="https://creativecommons.org/licenses/by/4.0">CC BY 4.0</a>,
via Wikimedia Commons
Slide 3: ADH <a href="https://commons.wikimedia.org/wiki/File:Renin-angiotensin_system_in_man_shadow.png">Mikael Häggström</a>, Public domain, via Wikimedia Commons
Slide 4: Pituitary adenoma <a href="https://commons.wikimedia.org/wiki/File:Acromegaly.jpg">Elgee</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
Slide 4: Acromegaly face <a href="https://commons.wikimedia.org/wiki/File:Acromegaly_prognathism.JPEG">Philippe Chanson and Sylvie Salenave</a>, <a href="https://creativecommons.org/licenses/by/2.0">CC BY 2.0</a>, via Wikimedia Commons
Slide 4: Andre Giant <a href="https://commons.wikimedia.org/wiki/File:%C3%89douard_Carpentier,_Andre_the_Giant_and_Yvon_Robert.jpg">Unknown authorUnknown author</a>, Public domain, via Wikimedia Commons
Slide 9: Empty Sella <a href="https://commons.wikimedia.org/wiki/File:Empty_Sella_als_zufaelliger_Nebenbefund_88W_-_MR_FLAIR_sag_und_T1_KM_cor_-_001.jpg">Hellerhoff</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA
4.0</a>, via Wikimedia Commons
Slide 9: Craniopharyngioma <a href="https://commons.wikimedia.org/wiki/File:Craniopharyngioma-t1sagkm-005.jpg">Hellerhoff</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
References:
Slide 1:Pituitary Apoplexy CT <a href="https://commons.wikimedia.org/wiki/File:Pituitary_apoplexy.jpg">Dr. Frank Gaillard</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
Slide 1: Pituitary gland <a href="https://commons.wikimedia.org/wiki/File:1614_Pituitary_Tumor-02.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia
Commons
Slide 1: <a href="https://commons.wikimedia.org/wiki/File:Visual_field_bitemporal_hemianopia.png">RobertB3009</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via Wikimedia
Commons
Slide 1: <a href="https://commons.wikimedia.org/wiki/File:1808_The_Anterior_Pituitary_Complex.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia
Commons
Slide 2: Thyroid Hormone Feedback, created with BioRender.com.
Slide 2: GnRH, <ahref="https://commons.wikimedia.org/wiki/File:Hypothalamic%E2%80%93pituitary%E2%80%93gonadal_axis_in_females.png">Lu Kong, Ting Zhang, Meng Tang and Dayong Wang</a>, <a
Slide 2: CRH, <a href="https://commons.wikimedia.org/wiki/File:Hypothalamic-pituitary-adrenal_axis_diagram.jpg">Ross AP, Ben-Zacharia A, Harris C and Smrtka J</a>, <a
Slide 2: Growth hormone <a href="https://commons.wikimedia.org/wiki/File:1809_Hormonal_Regulation_of_Growth.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via
Wikimedia Commons
Slide 2: Prolactin <a href="https://commons.wikimedia.org/wiki/File:Prolactin_regulation.png">Procedureready</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via Wikimedia Commons
Slide 3: Oxytocin <a href="https://commons.wikimedia.org/wiki/File:2922_Let_Down_Reflex.jpg">OpenStax Anatomy and PhysiologyOpenStax</a>, <a href="https://creativecommons.org/licenses/by/4.0">CC BY 4.0</a>,
via Wikimedia Commons
Slide 3: ADH <a href="https://commons.wikimedia.org/wiki/File:Renin-angiotensin_system_in_man_shadow.png">Mikael Häggström</a>, Public domain, via Wikimedia Commons
Slide 4: Pituitary adenoma <a href="https://commons.wikimedia.org/wiki/File:Acromegaly.jpg">Elgee</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
Slide 4: Acromegaly face <a href="https://commons.wikimedia.org/wiki/File:Acromegaly_prognathism.JPEG">Philippe Chanson and Sylvie Salenave</a>, <a href="https://creativecommons.org/licenses/by/2.0">CC BY 2.0</a>, via Wikimedia Commons
Slide 4: Andre Giant <a href="https://commons.wikimedia.org/wiki/File:%C3%89douard_Carpentier,_Andre_the_Giant_and_Yvon_Robert.jpg">Unknown authorUnknown author</a>, Public domain, via Wikimedia Commons
Slide 9: Empty Sella <a href="https://commons.wikimedia.org/wiki/File:Empty_Sella_als_zufaelliger_Nebenbefund_88W_-_MR_FLAIR_sag_und_T1_KM_cor_-_001.jpg">Hellerhoff</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA
4.0</a>, via Wikimedia Commons
Slide 9: Craniopharyngioma <a href="https://commons.wikimedia.org/wiki/File:Craniopharyngioma-t1sagkm-005.jpg">Hellerhoff</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
References:
Slide 1: Thyroglossal Duct Cyst <a href="https://commons.wikimedia.org/wiki/File:Thyreoglossal_duct_cyst.jpg">Klaus D. Peter, Gummersbach, Germany</a>, <a
href="https://creativecommons.org/licenses/by/3.0/de/deed.en">CC BY 3.0 DE</a>, via Wikimedia Commons
Slide 2: Thyroid Gland <a href="https://commons.wikimedia.org/wiki/File:1811_The_Thyroid_Gland.jpg">OpenStax College</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
Slide 2, 4: Thyroid Hormone Release and Feedback, created with BioRender.com.
Slide 2: Goiter <a href="https://commons.wikimedia.org/wiki/File:Kone_med_stor_struma.jpg">Martin Finborud</a>, Public domain, via Wikimedia Commons.
Slide 3,4,7,9: Wolf <a href="https://commons.wikimedia.org/wiki/File:Kolm%C3%A5rden_Wolf.jpg">Wolf_Kolmården.jpg: Daniel Mott from Stockholm, Swedenderivative work: Mariomassone</a>, <a
Slide 3: Radiation symbol <a href="https://commons.wikimedia.org/wiki/File:Radiation_warning_symbol2.svg">No machine-readable author provided. Rfc1394 assumed (based on copyright claims).</a>, Public domain, via
Wikimedia Commons
Slide 4: Graves thyroid histology <a href="https://commons.wikimedia.org/wiki/File:Histopathology_of_Graves%27_disease_-_medium_mag.jpg">LiVolsi VA and Baloch ZW</a>, <a
Slide 4: Exopthalmos <a href="https://commons.wikimedia.org/wiki/File:Proptosis_and_lid_retraction_from_Graves%27_Disease.jpg">Jonathan Trobe, M.D. - University of Michigan Kellogg Eye Center</a>, <a
Slide 5: Iodine scan <a href="https://commons.wikimedia.org/wiki/File:Thyroid_scan.jpg">Myohan at en.wikipedia</a>, <a href="https://creativecommons.org/licenses/by/3.0">CC BY 3.0</a>, via Wikimedia Commons
Slide 6: Lymphoid follicle with germinal centers. Contributed by Andrey Bychkov, M.D., Ph.D.
https://www.pathologyoutlines.com/topic/thyroidhashimotosthyroiditis.html
Slide 6: Hurthle cells <a href="https://commons.wikimedia.org/wiki/File:Hurthle_cells_-_thyroid_FNA_--_very_high_mag.jpg">Librepath</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via
Wikimedia Commons
Slide 6: Granuloma Subacute thyroiditis: inflammatory infiltrate composed of lymphocytes, plasma cells, foamy histiocytes, epithelioid histiocytes, multinucleated giant cells and neutrophils. Variable background of fibrosis.
Contributed by Truong Phan Xuan Nguyen, M.D. https://www.pathologyoutlines.com/topic/thyroidgranuloma.html
Slide 7: Goiter <a href="https://commons.wikimedia.org/wiki/File:Kone_med_stor_struma.jpg">Martin Finborud</a>, Public domain, via Wikimedia Commons.
Slide 7: Congenital hypothyroidism <a href="https://commons.wikimedia.org/wiki/File:Treated_typical_cretin_(2).jpg">Alfred Loomis & William Thompson</a>, Public domain, via Wikimedia Commons
Slide 7: Wolf <a href="https://commons.wikimedia.org/wiki/File:Kolm%C3%A5rden_Wolf.jpg">Wolf_Kolmården.jpg: Daniel Mott from Stockholm, Swedenderivative work: Mariomassone</a>, <a
Slide 7: Radiation symbol <a href="https://commons.wikimedia.org/wiki/File:Radiation_warning_symbol2.svg">No machine-readable author provided. Rfc1394 assumed (based on copyright claims).</a>, Public domain, via
Wikimedia Commons
Slide 8: Psammoma bodies. <a href="https://commons.wikimedia.org/wiki/File:Psammoma_bodies.jpg">Dr. Roshan Nasimudeen</a>, <a href="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0</a>, via
Wikimedia Commons
Slide 8: Orphan Annie Nuclei. Contributed by Andrey Bychkov, M.D., Ph.D. https://www.pathologyoutlines.com/topic/thyroidpapillary.html.
Slide 8: Follicular Carcinoma <a href="https://commons.wikimedia.org/wiki/File:Follicular_thyroid_carcinoma_--_low_mag.jpg">Nephron</a>, <a href="https://creativecommons.org/licenses/by-sa/4.0">CC BY-SA 4.0</a>, via
Wikimedia Commons
Slide 8: Background of amyloid (x200). Contributed by Shuanzeng Wei, M.D., Ph.D. https://www.pathologyoutlines.com/topic/thyroidmedullary.html.
Slide 8: he turquoise of collagen (black arrows) must not be confused with the lime green of amyloid (open arrows). Contributed by Kenneth A. Iczkowski, M.D. https://www.pathologyoutlines.com/topic/stainscongored.html
Slide 8: High power of anaplastic carcinoma: pleomorphic tumor cells and necrosis. Contributed by Shuanzeng Wei, M.D., Ph.D. https://www.pathologyoutlines.com/topic/thyroidundiff.html.
References:
Slide 1: Calcium homeostasis, created with BioRender.com.
Slide 2: Richets <ahref="https://commons.wikimedia.org/wiki/File:Photo_of_young_girl_with_Rickets,_Scoliosis,_deformed_spine_Wellcome_L0034949.jpg">See
page for author</a>, <a href="https://creativecommons.org/licenses/by/4.0">CC BY 4.0</a>, via Wikimedia Commons
Slide 3: Pseudohypothyroidism, created with BioRender.com
Slide 4: Osteitis fibrosa cystica <a href="https://commons.wikimedia.org/wiki/File:Xray_OFC1.jpg">Scott Ngyuen</a>, <a
href="http://www.gnu.org/copyleft/fdl.html">GFDL</a>, via Wikimedia Commons.
Slide 4: Calcium in chronic kidney disease, created with BioRender.com.

Endocrinology

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Endocrinology

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TABLE OF CONTENTS

1. Fundamental Principles of Endocrinology

Endocrinology: A. Autocrine, Paracrine, Endocrine signaling

Endocrine Gland Overview

Rapid Review: RAAS and ADH

How to Differentiate Causes of Hyponatremia:

ADH Present ADH Absent

RAAS Off 1.SIADH 1.Renal losses

RAAS On 1.Hypovolemia 1.↑ H2O intake

Urine Na Urine Osmolality Serum Osmolality

⚪ A. Avulsion of nerve roots from the spinal cord

⚪ B. Autoimmune destruction of the myelin sheath

⚪ C. Accumulation of amyloid β-protein deposits

⚪ D. Cerebral apoptosis and shrinkage of oligodendrocytes

⚪ E. Antibodies against postsynaptic Ach receptors

1. Pituitary: Embryology 6. Hyperprolactinemia

Anterior Pituitary: Function

Posterior Pituitary: Function

Gigantism and Acromegaly

Growth Hormone Deficiency:

Thyroid and Parathyroid Development

Thyroid Anatomy and Function

T3, T4 Synthesis and Pharmacology

Hyperthyroidism: Graves Disease

Hyperthyroidism: Other Causes

Hypothyroidism: Other Causes

Video 4.2: Thyroid Anatomy and Function

Video 4.3: T3, T4 Synthesis and Pharmacology

Video 4.4: Hyperthyroidism: Graves Disease

Video 4.5: Hyperthyroidism: Other Causes

Video 4.7: Hyper/Hypothyroidism: De Quervain and Riedel Thyroiditis

Video 4.8: Hypothyroidism: Other Causes

Video 4.9: Thyroid Malignancies

Parathyroid Location and Function

Familial Hypocalciuric Hypercalcemia:

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