You are on page 1of 36

ENDOCRINOLOGY

PATHOLOGY
1. PITUITARY GLAND
HORMONE
Adeno
GH

Neuro

HYPER
Acromegaly/Gigantism

Prolactin
ACTH
Gonadotrophs
(LH/FSH)
ADH
Oxytocin

Complete

HYPO

Hyperprolactinemia

SIADH

CDI/NDI

Pituitary adenomas

1. Pituitary apoplexy
2. Sheehans
3. Empty sella syndrome

2. THYROID GLAND
HYPER
HYPO
1. Toxic
1. Hashimoto
Multinodular
2. Congenital (cretinism)
goiter
3. Subacute (de-Quervain)
2. Graves disease
4. Riedels
3. Thyroid storm
5. Euthyroid Sick syndrome
6. Other (Iodine def.,
goitrogens, wolff-chakoff,
painless thyroiditis)

CANCERS
1. Papillary CA
2. Follicular CA
3. Anaplastic CA
4. Medullary CA

3. PARATHYROID
HYPER
Hypercalcemia
Hyperparathyroidism
(1, 2, 3)

Calcium
PTH

4. PANCREAS
HYPER
DM (type 1 and type 2)

HYPO
Hypocalcemia
1. Hypoparathyroidism
2. Pseudohypoparathyroidis
m
HYPO
Hypoglycemia

5. ADRENAL GLANDS
HYPER
Aldosterone
Hyperaldosteronism (1, 2)
Cortisol (ACTH)

Cushings

Sex hormones

Hyperadrogenism

catecholamines

1. neuroblastoma
2. pheochromocytoma

HYPO

1. Hypogonadism
2. Klinefelters
3. Post-pubertal
hypogonadism

ENDOCRINOLOGY
COMPLETE

Congenital adrenal hyperplasia

I.
II.

Addisons
Waterhouse Friderichsen
Sx

ENDOCRINOLOGY

PITUITARY GLAND
1. ACROMEGALY/GIGANTISM:
a. DEFINITION: Excessive secretion to GH
b. ETIOLOGY: Pituitary adenomas (macroadenoma)
c. PRESENTATION:
i. 30s and 50s years of age *
ii. Various skeletal and soft tissue changes
iii. Enlargement of hands and feet, coarsening of facial features and
thickened skin folds.
iv. Nose and mandible enlarges (separated teeth)
v. Deeper voice
vi. Increasing sweating
vii. OSA
viii. Menstrual problems (coz prolactin co-secreted)
ix. Cardiac abnormalities. (MC cause of DEATH)
x. Impaired glucose tolerance and diabetes
xi. Hypertension
xii. Articular cartilage proliferates and causes severe joint disease.
d. DIAGNOSIS:
i. BIT- IGF-1 level test

ENDOCRINOLOGY
ii. Confirmatory test measuring of GH after 100g of glucose orally taken.
Positive if GH>5 ng/ml (high). Normally glucose should suppress level
of GH.
iii. CT scanning and MRI localize the tumor
iv. Somatomedins
e. MANAGEMENT
i. Surgery Trans-sphenoidal surgery
ii. Somatostatin analog (octreotide and lanreotide) reduces GH values.
SE- cholecystitis
iii. Dopamine agonists (bromocriptine, cabergoline (less SE))
iv. Pegvisomant GH analog (antagonizes endogenic GH by blocking
peripheral GH binding to its receptor in the liver.
v. Radiotherapy
2. HYPERPROLACTINOMA
a. DEFINITION: excess prolactin secretion galatactorrhea-amenorrhea.
i. Inhibition of GnRH LH/FSH
ii. Prolactin inhibits LH surge no ovulation
b. ETIOLOGY:
i. Natural physiological states: Pregnancy, early nursing, hypoglycemia,
seizure, exercise, stress, sleep, cirrhosis, nipple stimulation and chronic
renal disease (PL clearance)
ii. Autonomous: pituitary adenomas (prolactinomas), micro in women and
macro in men block the stalkinhibiting DOPAincreasing PRL
iii. inhibitory actions of DOPA:
1. Drugs: phenithiazines, metoclopramide
2. Dopamine- depleting agents: alpha-methyldopa, reserpine
3. TCAs, narcotics, cocaine, SSRI, risperidone increase PRL
4. Stimuli that overcome the normal DOPA inhibition ( 1*
hypothyroidism Inc. TRH) inc PRL
c. PRESENTATION: Galactorrhea, menstrual abnormalities,
amenorrhea/oligomenorrhea, osteopenia, osteoporosis
d. DIAGNOSIS:
i. Exclude (pregnancy, lactation, hypothyroidism and medications before
starting workup. Prolactinomas co-secrete GH.
ii. Prolactin levels >100ng/ml
e. MANAGEMENT:
i. Initially treat with cabergoline and bromocriptine reduce PRL levels
ii. Surgery (for pts not responsive to treatment)
iii. Radiation
3. SIADH
a. ETIOLOGY:
i. CANCERS (small cell CA, carcinomas of the pancreas, ectopic ADH
secretion)
ii. Pulmonary diseases (TB, pneumonia, lung abscess

ENDOCRINOLOGY
iii. CNS disorders (head injury, CVAs, encephalitis)
iv. Drugs (chlorpropamide, clofibrate, vincristine, vinblastine,
cyclophosphamide, carbamazepine)
b. PRESENTATION:
i. Increased ADH water retention, ECF expansion w/o edema or HTN
owing to natriuresis hyponatremia
ii. HYPOnatremia + concentrated urine (>300mOsm)
iii. No signs of edema or dehydration.
iv. If its severe (<200mOsm) confusion, irritability, seizures and coma
c. DIAGNOSIS:
i. Hyponatremia <130 mEq/L
ii. Posm <270 mOsm/kg
iii. Urine Na 20mEq/L
iv. Maintained hypervolemia
v. Suppression of RAAS
vi. Equal conc of ANP
vii. Creatinine, BUN, uric acid and albumin LOW
d. MANAGEMENT
i. Treat the underlying cause,
ii. Fluid restriction (800-1000 ml/d increase serum Na
iii. Demeclocycline chronic situation if fluid restriction is not working
(inhibits ADH at V2)
iv. Conivaptan and tolvaptan are v2 blockers
v. Severe pts hypertonic saline (3%) 200-300ml IV q3 hours
vi. Rate of correction 0.1/hr of Na
4. DIABETES INSIPIDUS
CDI
ETIOLOGY
Pituitary tumor, autoimmune,
trauma, surgery, ischemic
encephalopathy, idiopathic (start
in childhood)
FINDINGS

ADH

NDI
Hereditary (ADH receptor
mutation), 2 to Hypercalcemia,
hypokalemia, SCD, amyloidosis,
myeloma, pyelonephritis or drugs
(lithium, demeclocycline or
colchicine)
NORMAL ADH

Urine specific gravity <1.006


Serum osmolarity >290 mOsm/L
Hyperosmotic volume contraction

Urine specific gravity <1.006


Serum osmolarity >290 mOsm/L
Hyperosmotic volume contraction

DIAGNOSIS Water deprivation test: >50%


increase in urine osmolarity

Water deprivation test: no change


in urine ormolarity

DD

Psychogenic polydipsia
Drug induced polydipsia
(chlorpromazine, anticholinergic ,

Psychogenic polydipsia
Drug induced polydipsia
(chlorpromazine, anticholinergic ,

ENDOCRINOLOGY
thioridazine)
Hypothalamic disease
TREATMEN
T

1. hormone replacement with


vasopressin SQ
desmopressin SQ,
oral, intranasa
2. drugs to increase release
ADH (chlorpropamide,
clofibrate, carbamazepine)

thioridazine)
Hypothalamic disease
HCTZ
Amiloride
Chlorthalidone

5. HYPOPITUITARISM
a. DEFINITION: partial or complete loss of anterior function that may result from
any lesion that destroys the pituitary or hypothalamus
i. Starts with GHGnRH
b. ETIOLOGY:
i. Large pituitary tumors/cysts , hypothalamic tumors
ii. Panhypopituitarism MC caused by pituitary adenomas
iii. Pituitary apoplexy :
1. Acute hemorrhagic infarction of pre-existing pituitary adenoma
2. Presents with headache, N/V, depressed consciousness
iv. Inflammatory diseases:
1. Granulomatous diseases (sarcoidosis, TB, sphyillis), eosinophillic
granuloma, autoimmune lymphocytic hypophysitis
v. Sheehan postpartum necrosis
1. Inability to lactate
c. FINDINGS
GnRH def
Womenamenorrhea, genital atrophy, infertility, libido, loss
(lh/fsh)
of axillary hair.
Men impotence, testicular atrophy, infertility, libido, loss
of axillary hair.
GH
Fine wrinkles, increased sensitivity to insulin (hypoglycemia)
Asymptomatic increase in lipid levels and in muscle bone
and heart mall,
CHILDREN growth failure and short stature
TSH
Hypothyroidism
ACTH
2 adrenal deficiency, cortisol
d. DIAGNOSIS:
i. Measure GH (insulin induced hypoglycemia, arginine infusion)), TSH,
LH, IGF-1
ii. Measure ACTH insulin tolerance test, cortisol >19, metyrapone test
(blocks cortisolincrease ACTH)
iii. Measure GnRH (LH, FSH and estrogen)
iv. TSH serum T4, free T3 which should be LOW with a normal to low TSH
e. MANAGEMENT
i. Treat the underlying cause
ii. Multiple hormones must be replaced, but most important is cortisol
replacement

ENDOCRINOLOGY

THYROID GLAND
1. HYPERTHYROIDISM:
a) ETIOLOGY:
a. Can result from excess production of TSH (rare), or abnormal thyroid
stimulators.
b. Amiodarone can induce thyrotoxicosis
c. Graves disease/toxic diffuse goiter hyperthyroidism +diffuse goiter
+exophthalmos+ dermopathy
i. MC cause <50 years. WOMEN>men
ii. Graves diffuse enlargement of thyroid and the formation of
autoantibodies that bind to the TSH receptors in thyroid cell
membranes and stimulate the gland to hyperfunction
iii. Dermopathy raised, pruritic and hyperpigmented
iv. Graves may be associated with other autoimmune diseases
pernicious , myasthenia and Diabetes.
v. Eye disease steroids/radiation

ENDOCRINOLOGY
vi. Skin steroids
d. Intrinsic thyroid autonomy
i. Result from hyperfunctioning adenoma (toxic).
ii. 2 to toxic Multinodular goiter (plummers disease)- non-autoimmune
disease of the ELDERLY, associated with arrhythmias and CHF
e. Transient hyperthyroidism
i. Results from Subacute thyroiditis (painful) or lymphocytic thyroiditis
(painless, postpartum)
f. Extrathyroid source of hormones
i. Thyrotoxicosis facticial
ii. Ectopic thyroid tissue (struma ovarii, functioning follicular carcinoma)
b) CLINICAL FINDINGS
a. CNS
i. Younger patients
ii. Emotional liability
iii. Inability to sleep
iv. Tremors
v. Frequent bowel movements
vi. Weight loss
b. CVS/ myopathies
i. Older patients
ii. Atrial fibrillation
iii. Dyspnea
iv. CHF
v. Palmar erythema
c. Ocular signs
i. Staring, infrequent blinking, and lid lag
d. Menstrual irregularities (oligomenorrhea)
e. Osteoporosis and HYPERCALCEMIA can occur from increases in osteoclastic
activity.
c) DIAGNOSIS:
a. H & P
b. LAB:
i. PRIMARY- TSH
ii. SECONDARY- inc TSH
iii. T3 and T4 elevated
c. RAIU increased
d. Anti-thyroglobulin and
antimicrosomal antibodies are
elevated in graves disease and
autoimmune thyroiditis
d) DD:
a.
b.
c.
d.

Anxiety, neurosis, mania


Pheochromocytoma
Acromegaly
Cardiac disease

ENDOCRINOLOGY
e. Myasthenia gravis and orbital tumors exophthalmos
e) MANAGEMENT:
a. Propranolol- to control adrenergic symptoms
b. Anti-thyroid drugs PTU (PREGOS) and Methimazole
i. Methimazole hepatotoxicity
ii. SE- Agranulocytosis
c. Ablative therapy RAIU
d. Subtotal thyroidectomy (PREGOS 2nd tri, and, children)
e. Hormone replacement after surgery

2. THYROID STORM
a) DEFINITION
a. Extreme form of thyrotoxicosis
b. Endocrine emergency
c. Precipitated by: stress, infection, surgery or trauma
b) CLINICAL FINDINGS
a. Extreme irritability, delirium, coma, tachycardia, restlessness, vomiting,
jaundice, diarrhea, hypotension, dehydration and high fever (>104)
c) MANAGEMENT
a. Supportive therapy
i. Saline and glucose hydration, glucocorticoids and oxygen cooling
blanket
b. Therapy for hyperthyroidism ANTI-THYROID agents
i. Should be stopped 1-2 weeks before and after RAIU treatment
ii. PTU blocks the uptake of radioactive iodine
c. Iodine to inhibit hormone release

ENDOCRINOLOGY
d. Adrenergic antagonists
e. Dexamethasone inhibit hormone release, impair peripheral generation of
T3 and provide adrenal support

3. HYPOTHYROIDISM
a) ETIOLOGY:
a. PRIMARY:
i. 2 to chronic thyroiditis (Hashimotos) - MC
ii. Post ablative surgery/ RAUI
iii. Heritable biosynthetic defects
iv. Iodine deficiency
v. Lithium, and, acetylsalicyclic acid, amiodarone, interferon and
sulfonamide
b. SECONDARY
i. Pituitary induced
c. TERTIARY
i. Hypothalamic induced
b) CLINICAL FINDINGS:
a. NEWBORN:

ENDOCRINOLOGY
i. Cretinism and juvenile hypothyroidism
ii. Persistent physiologic jaundice, hoarse cry, constipation, somnolence
and feeding problems delayed milestones, coarse features,
protruding tongue, broad flat nose, widely set eyes, sparse hair, dry
skin, protuberant abdomen, potbelly with umbilical hernia,
impaired mental development, retarded bone age, and delayed
dentition.
b. ADULT
i. Lethargy, constipation, cold tolerance carpel tunnel, menorrhagia,
deafness, slow DTR, prolonged relaxation phase, HIGH cholesterol,
myxedema (expressionless face), periorbital puffiness, large tongue,
HYPOnatremia, and , anemia
c) DIAGNOSIS
TSH
T4/ FT4
T3

1
Inc

in lesser extent

2/3
N/

Accompanied by secre
of other hormones

d) MANAGEMENT
a. Restore metabolic state gradually in the elderly and patient with CAD
b. Levothyroxine (T4) takes 6 weeks to stabilize
c. 2/3 gives hydrocortisone first and then replace thyroid.
d. Myxedema coma results in patients who have severe long-standing
hypothyroidism that is left untreated from hypothermic, stuporous state
i. Ass/w respiratory depression (CO2 retention).
ii. Precipitated by cold exposure, trauma, infections, and CNS
depressants.
iii. Tx- high doses of T4 and T3

4. THYROIDITIS
a. SUBACUTE:
Granulomatous, giant cell or de Quervain thyroiditis
40, 50 years old
Viral origin and follows URI symptoms including malaise, fever, pain over
the thyroid and referred to the lower jaw, ears, neck or arms.
Thyroid is enlarged and firm in settings.
LABS:
o ESR inc
o RAUI-
o T4, T3 initially inc (leaking of hormone from the gland)

ENDOCRINOLOGY
DD
o Graves
TREATMENT:
o NSAIDs, Prednisone and propranolol (it may smolder for months but
eventually subsides with return to normal function)
b. HASHIMOTO
Chronic inflammatory process of the thyroid with lymphocytic infiltration of
the gland/ autoimmune factors
ETIOLOGY:
o Middle-aged women, MCC of sporadic goiter in children
o Autoimmune factors are implicated as evidence by lymphocytic
infiltration, presence of increased IG and antibodies against
components of thyroid tissues (antithyroglobulin Abs)
CLINICAL FINDINGS
o Painless goiter, rubbery and not always symmetrical
o Hypothyroidism occurs
DIAGNOSIS
o Firm, non-toxic goiter on examination
o LABS
TSH- inc
T3/T4-
Antithyroid abs, antimicrosomal abs, anti-thyroperoxidase abs
o Needle biopsy
MANAGEMENT
o L-thyroxine
c. LYMPHOCYTIC (silent, painless or postpartum) THYROIDITIS
Self-limiting episode of thyrotoxicosis ass/w chronic lymphocytic thyroiditis
More common in women of any age
Non-tender, firm, symmetrical and slightly to moderately enlarged
T4/T3 elevated
RAIU- low
ESR- normal
Etiology and pathogenesis unclear
May last for 2-5 months and be recurrent (as in postpartum thyroiditis)
Treatment symptomatic w/ propranolol

d. REIDEL
Results from intense fibrosis of the thyroid and surrounding structures
Including mediastinal and retroperitoneal fibrosis
5. NEOPLASIA OF THYROID CANCER
a. PAPILLARY CA
MC, women>men
H/o radiation exposure
Bimodal frequency

ENDOCRINOLOGY
Tumor is slow growing and spreads via lymphatics
Treatment:
o Surgery large tumors
o TSH suppression therapy
Levothyroxine
b. FOLLICULAR CA
Elderly, women>men
More malignant
Spreads hematogenously with distant metastasis to lung and bone
Treatment: total thyroidectomy w/ post-operative radio-iodine ablation
c. ANAPLASTIC CA
ELDERLY (women>men)
Highly malignant with rapid and painful enlargement
Spreads by direct extension
d. MEDUALLARY CA
Sporadic form or familial
Parafollicular cells (c-cells) calcitonin
Ass/w MEN2a and 2b
Treatment: thyroidectomy
WHEN TO SUSPECT A THYROID CANCER?
When there is recent growth of thyroid or mass with no tenderness or hoarseness
Patient with a radiation therapy history of the head/neck or upper mediastinum in
childhood average 30 years to develop thyroid cancer.
Solitary nodule or the production of calcitonin
Calcifications (psammoma bodies), increased density in medullary carcinoma
Do thyroid function tests first CANCER is NEVER hyper functioning.
DIAGNOSIS OF NON-FUNCTIONING NODULE
FNA0 initial procedure of choice
5% malignant
first test TSHFNA
Ultrasound is useful to distinguish cysts from solid nodules.

ENDOCRINOLOGY

ENDOCRINOLOGY
PARATHYROID GLANDS
1. HYPERCALCEMIA:
a. DEFINITION:
i. increase in total or free Calcium level, 98% stored in the bone
ii. absorbed from duodenum
iii. 80% unabsorbed, 2% circulating in blood (F Ca 50%, protein bound
40%, citrate/phosphate bound 10%)
b. ETIOLOGY:
i. Primary hyperparathyroidism- MC
ii. Hypercalcemia of Malignancy PTHrP (SCC of lung)
iii. Granulomatous diseases (sarcoidosis, TB, berylliosis, histoplasmosis
and coccidiodomycosis)neutrophil have their own 25 V-D
hydroxylation active 1,25 V D
iv. Vitamin D intoxication, thiazine diuretics, lithium, Pagets, prolonged
immobilization
v. Acidosis from F Ca, because albumin buffers acidosis and increase H+
ions results in displacement of Calcium from albumin.
c. CLINICAL PRESENTATION:
i. Neurologic: mental activity (lethargy and confusion)
ii. GIT:
1. bowel activity (constipation, anorexia, N/V)
2. Pancreatitis (severe in hypocalcaemia coz calcium would bind to
malabsorbed fat in the intestines)
3. Ulcer disease
iii. RENAL
1. Polyuria, polydipsia (induces NDI)
2. Kidney stones,
3. Nephrolithiasis
iv. CVS:
1. Hypertension, SHORT QT
d. TREATMENT:
i. Severe vigorous fluid replacement w/ NS or NS loop diuretics
ii. IV bisphosphonates inhibits osteoclasts and promote blasts (2-3 days)
iii. Calcitonin inhibits osteoclasts (rapid )

ENDOCRINOLOGY

2.

ENDOCRINOLOGY
3. 1 HYERPARATHYROIDISM
a. ETIOLOGY:
i. MC from adenoma
ii. Hyperplasia of all 4 glands
iii. Parathyroid cancer (RARE)
iv. Can occur as a part of MEN type 1 and 2
b. CLINICAL PRESENTATION:
i. 1/3 asymptomatic
ii. Osteitis fibrosa cistica increased rate of osteoclastic activity pain,
fractures, deformities, and areas of demineralization, bone cysts and
brown tumors (salt and pepper)
iii. Genitourinary
1. Polyuria, polydipsia and stones (NDI)
iv. Neurological
1. Severe psyc disorders, mental obtundation, coma,
neuromuscular weakness and atrophy of muscles
v. GIT
1. Anorexia, weight less,
constipation, n/v, thirst,
abdominal pain with
pancreatitis and PUD
vi. CVS
1. HTN and arrhythmias
c. DIAGNOSIS:
i. Serum Ca >10.5
ii. PTH- elevated
iii. Urine Ca NORMAL, coz Ca
resorbing action of PTH, there
may be normal levels in 1/3rd
patients.
iv. Serum PO4 LOW
v. SESTAMIBI- a nuclear scan to localize the adenoma (+ US high
specificity)
d. TREATMENT
i. Surgical removal
1. Only if there is symptoms of hypercalcemia (>11.5), bone
disease (osteoporosis) or renal disease (nephrocalcinosis) or
PREGOs, age <50.
ii. Calcitonin (immediate)bisphosphonates (2-3 days)
iii. Dietary Ca <400 mg/d
iv. Oral hydration 2-3 L of fluid
v. Phosphate supplementation phospho- soda
vi. Estrogen (post-menopausal)
vii. HUNGRY- BONE syndrome: after surgical removal, due to increased
osteoblastic activity. Rapidly Ca, PO4, Mg (1-4 wks post)

ENDOCRINOLOGY
viii. Cinacalcet calcimimetic agent (shuts off parathyroid) increases
sensitivity of Ca sensing (basolateral membrane potential) on
Parathyroid.
1. Used for Tx of 2 hyperparathyroidism in HD pts. and parathyroid
in OA and in people unamenable to surgery
4. HYPOCALCEMIA
a. ETIOLOGY:
i. Hypoparathyroidism, renal failure, hyperphosphatemia, hypomagnesia
(alcoholics)
ii. Drugs (loop, phenytoin, alendronate and foscarnet)
iii. Alkalosis free Ca levels by binding to albumin
iv. PSEUDOHYPOCALCEMIA:
1. Low albumin levels ( F Ca N, total Ca- )
2. Massive blood transfusions (Ca binds to citrate)
b. CLINICAL PRESENTATION
i. Increased neural hyperexcitability (seizures, tetany, curcumoral
numbness, and tingling of extremities)
ii. Arrhythmias (prolonged QT)
iii. Cataracts
c. TREATMENT
i. IV/ORAL calcium replacement,
ii. Vitamin D replacement.

ENDOCRINOLOGY

5. HYPOPARATHYROIDISM
a. ETIOLOGY:
i. Surgical removal of THYROID MCC
ii. Low PTH-

ENDOCRINOLOGY
1. Hereditary hypoparathyroidism,
2. Acquired (surgical) and
3. Hypomagnesaemia: results from prevention of release of PTH
from the gland.
a. Occurs from decreased GI absorption or alcoholism
b. CLINICAL PRESENTATION:
i. Neuromuscular:
1. Tetany, laryngospasm, cramping, seizures and impaired memory
function, tingling of hands and feet
2. Chvostek sign +
3. Trousseau sign +
ii. Ocular signs: cataracts and soft tissue calcifications
iii. CVS
1. QT prolongation, refractory CHF and hypotension
iv. HYPERVENTILLATION from alkalosis
c. DIAGNOSIS
i. Serum calcium LOW (important to check albumin and use corrected
Ca)
1. 1.0 of albumin total Ca by 0.8 mg/dl
2. it is better to measure ionized Calcium
d. MANAGEMENT
i. Acute: calcium gluconate IV
ii. Chronic:
1. Oral calcium (2-4g/day)
2. Vitamin D
iii. Hyperphosphatemia diet restriction and phosphate binders (CaCO3 /
Al OH3)

GLUCOSE METABOLISM
1. DIABETES MELLITUS
a. OVERVIEW

ENDOCRINOLOGY

ENDOCRINOLOGY

ENDOCRINOLOGY
b. TREATMENT OF DIABETES MELLITUS

ENDOCRINOLOGY
c. COMPLICATIONS
i. DKA vs. HONK

ENDOCRINOLOGY
ii. NEUROPATHY

iii) RETINOPATHY

2. HYPOGLYCEMIA

ENDOCRINOLOGY

ENDOCRINOLOGY

ADRENAL GLAND
1. HYPERFUNCTIONING OF THE GLAND
a. CUSHING SYNDROME
i. DEFINITION: results from prolonged exposure to increased amounts of
cortisol or related corticosteroids
ii. ETIOLOGY:
1. Exogenous, iatrogenic MC (prolonged exposure to
glucocorticoids)
2. Adrenal hyperplasia
a. 2 to pituitary ACTH production which occurs in pituitaryhypothalmic dysfunction
b. Pituitary ACTH producing adenomas
c. ACTH/CRH producing tumors (bronchogenic carcinoma,
carcinoma of thymus, pancreatic CA, bronchial adenoma)
iii. CLINICAL FINDINGS
1. Moon facies, interscapular buffalo hump, mesenteric bed, truncal
obesity

ENDOCRINOLOGY
2. Hypertension
3. Muscle weakness, fatigability
4. Osteoporosis
5. Striae , easy bruisability
6. Women: hirsuitism, acne, oligomenorrhea
iv. DIAGNOSIS
v. MANAGEMENT
1. Depends on etiology
2. Surgical or medical
3. Unresectable tumors: ketoconazole and metyrapone

ENDOCRINOLOGY
2. HYPERALDOSTERONISM

ENDOCRINOLOGY
3. CONGENITAL ADRENAL HYPERPLASIA
i. DEFINITION: increased adrenal androgens because of enzymatic
defects
ii. ETIOLOGY:
1. Infancy and childhood
2. AR mutations
iii. COMMON DEFECTS
iv. DIAGNOSIS
1. Any infant exhibiting failure to
thrive, especially those with
episodes of acute adrenal
insuffieciency, salt wasting and
hypertension
2. Serum testosterone,
androstenedione, DHT, 17hydroxyprogesterone, urinary 17ketosteroid, and pregnanetriol
v. MANAGEMENT
1. Glucocorticoid (hydrocortisone) replacement+ fludrocortisone for
cortisol replacement

ENDOCRINOLOGY

4. HYPOFUNCTIONING OF THE GLAND


a. ADRENAL INSUFFIENCY
i. DEFINITION:
1. 1 adrenocorticoid insufficiency AKA Addisons slow and
progressive
2. 2 failure in the elaboration of ACTH
ii. ETIOLOGY:
Secondary to anatomic destruction from
Idiopathic atrophy,
Surgical removal,
Infection (TB, CMV), hemorrhagic,
Trauma
Metabolic failure
2 to CAH, enzyme inhibitors and MITOTANE
Autoimmune mechanisms (80%)

ENDOCRINOLOGY

iii. CLINICAL FINDINGS


1. Weakness, Paresthesias, cramping, Intolerance to stress and
Personality changes
2. Hyperpigmentation of skin
3. Arterial hypotension (orthostatic coz lack of effect of cortisol on
vascular tone)
4. GIT: n/v, diarrhea, abdominal pain
5. ACUTE Addisons: fever and hypotension, Na, high K and milk
acidosis
iv. DIAGNOSIS
1.
Cosyntroin/ACTH
stimulation test
2. LABS
a. Neutropenia,
lymphocytosis,
eosinophilia
b. High serum K/
BUN
c. Na, blood
glucose,
morning
plasma cortisol
v. MANAGEMENT
1. Glucocorticoid, mineralocorticoid and NaCl replacement
ADRENAL CRISIS:
Fever, vomiting and abdominal pain, AMS, vascular collapse

ENDOCRINOLOGY
Cortisol level rapid fluid and hydrocortisone
This may occur in
o Previously undiagnosed patients w/ adrenal insufficiency who has undergone
surgery, infection or major stress
o Bilateral adrenal infarction/hemorrhage
o Abrupt withdrawal from glucocorticoid therapy

b. PHEOCHROMOCYTOMA
i. DEFINITION:
1. Rare, usually benign tumor that arises from the chromaffin cells
of the sympathetic nervous system.
a. 10% rule
2. Autosomal Dominant
3. Ass/w MEN 2, MEN 3, Von Hipple Lindau retinal cerebellar
hemangioblastomatosis, von Recklinghausen neurofibromatosis
ii. CATECHOLAMINES
1. DOPA familial syndrome ass/w HTN
2. EPI- tachycardia, sweating, flushing, HTN
3. NE secreted by all extra-adrenal tumors
iii. CLINICAL FINDINGS:
1. Paroxysms or crises
2. Sudden onset, lasting from a few minutes to several hours.
3. Headaches, profuse setting, palpitations, chest pain, increase BP
4. Glucose intolerance, orthostatic hypotension
iv. DIAGNOSIS:
1. Catecholamine metabolites (24 hours urine collection) INC

ENDOCRINOLOGY
- (Urinary metanephrines, vanillymendelic acid, plasma
catecholamines)
2. Clonidine suppress the levels of epinephrine.
3. CT/MRI
4. MIBG scan to locate the Pheochromocytoma
v. DD
1.
2.
3.
4.
5.

Essential HTN,
Anxiety attacks
Factitious crises
Intracranial lesions
Autonomic epilepsy

vi. MANAGEMENT
1. Controlling BP alpha blockers ( phentolamine,
phenoxybenzamine)
2. Surgical removal

HYPOGONADISM
1. 1 HYPOGONADISM:
a. ETIOLOGY: hypergonadotropic; increased LH, FSH
b. Can result from
i. Klinefelter syndrome (small testes, eunuchoid, 47XXX)
ii. Anorchia
iii. Surgical
iv. Accidental castration
v. Radiotherapy
vi. Infections (mumps, TB, leprosy)
vii. Chemotherapy
2. SECONDARY HYPOGONADISM
a. ETIOLOGY: Hypogonadotropic, low LH/FSH
b. Can result from:
i. Hypopituitarism 2 to idiopathic causes or tumors
ii. Hypothalamic lesions

ENDOCRINOLOGY
iii. Kallmann syndrome (hypogonadotropic hypogonadism ass/w
sense of smell.
c. CLINICAL FINDINGS:
i. Prepubertal hypogonadism
1. External genetalis are under0developed
2. Voice is high pitched
3. Beard does not grow
4. Patient lacks libido and potency
ii. Adult
1. Youthful appearance
2. Obesity,
3. Disproportionately long extremities
4. Lack of temporal recession of the hairline
5. Small adams apple
iii. Bone age is retarded.
iv. Urinary 17-ketosteroid LOW to N
v. Testosterone LOW
d. TREATMENT:
i. Testosterone
3. POST-PUBERTAL HYPOGONADISM
a. ETIOLOGY: any pituitary lesion or testes that may be damaged by trauma,
radiation, infection or drugs.
b. PRESENTATION
i. Libido and potency are lost
ii. Hair growth is retarded
iii. Vasomotor symptoms (flushing, dizziness, chills)
iv. Lack of aggressiveness, sterility, muscle aches, back pain.
v. Skin on the face is thin and finely wrinkled
c. DIAGNOSIS
i. Urinary and plasma testosterone LOW
ii. Urinary and serum FSH/LH LOW with pituitary lesion and HIGH with
pituitary testicular failure
iii. PRL- ELEVATED
d. TREATMENT
i. Testosterone
4. KLINEFELTERS SYNDROME
a. ETIOLOGY: MC 1 developmental abnormality. Testicular damage
i. Caused by one or more supernumerary X-chromosomes
b. PRESENTATION
i. Sterility
ii. Lack of libido
iii. Mental retardation
iv. Small and thin testes
c. DIAGNOSIS
i. LH/FSH high
ii. Urinary 17-ketosteroids LOW/N
iii. Testosterone LOW/N

ENDOCRINOLOGY
iv. Serum estradiol HIGH
d. TREATMENT
i. Testosterone

You might also like