Transcript Endocrine Blueprint Lecture Slides PPT

Endocrine Blueprint
PANCE Blueprint
Diseases of Thyroid
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Hyperparathyroidism-
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Should be suspected when high
serum calcium levels are detected
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Primary hyperthyroidism occurs due
to PTH activation of osteoclasts
leading to more bone reabsorption
causing elevated calcium levels
•
This also causes increased intestinal
absorption of calcium
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Most common cause of primary
hyperthyroidism is due to parathyroid
adenoma
Hyperparathyroidism
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Diagnosis of primary
hyperparathyroidism is made with a
high PTH or one that is in the normal
range but elevated inappropriately
given the elevated given the patients
hypercalcemia
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Patients with primary
hyperparathyroidism are usually
asymptomatic
•
Elevated isolated serum calcium level
should be repeated.
•
Malignancy is another cause for
hypercalcemia. Malignancy and
Primary Hyperparathyroidism account
90 percent of cases of hypercalcemia
Hyperparathyroidism
•
If malignancy is present, the PTH level is usually normal or low, where
as in primary hyperparathyroidism the levels are usually high
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Familial hypocalciuric hypercalcium (FHH) is due to an inactivating
mutation of the calcium sensing receptor in the kidneys. See a
hypercalcemia with a mildly elevated PTH concentration
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Family history of hypercalcemia that is symptomatic is helpful for
coming up with the diagnosis
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Thiazide diuretics reduce calcium urine excretion and can cause mild
hypercalcemia
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Lithium decreases parathyroid gland sensitivity to calcium, and
decreases urinary excretion.
Hyperparathyroidism
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Secondary Hyperparathyroidism is
when the parathyroid appropriately
responds to a reduced level of
calcium. This causes elevated PTH,
the calcium absorption from the
intestines to increase and increase
bone reabsorption.
•
Secondary Hyperparathyroidism has
an elevated PTH and a low or
normal calcium
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Secondary hyperparathyroid may
come from renal failure and impaired
calcitrol production and inadequate
calcium uptake. Vitamin D
Deficiency can cause.
Hyperparathyroidism
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Normocalcemic Primary
Hyperparathyroidism-secondary
hyperparathyroid causes need to be
ruled out. Normal calcium and
elevated PTH. Vitamin D deficiency
can cause
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Clinically most the time
hyperparathyroidism can be
asymptomatic
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Classic symptoms if present "bones,
stones, abdominal moans, and
psychic groans." Anorexia, nausea,
constipation, polydipsia, bone pain,
kidney stone, muscle weakness,
polyuria, and psychiatric psychosis.
Hypoparathyroidism
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Most common cause is neck surgery on the
thyroid or parathyroid
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After surgery hypoparathyroidism may be
transient or may be permanent
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Clinically will see a low PTH and low serum
calcium
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Calcium and vitamin D supplementation are the
mainstays of hypoparathyroidism treatment
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Symptoms of hypoparathyroidism
include: tingling in hands and feet, involuntary
muscle movements, muscle cramps, fatigue,
irritability, anxiety, and depression
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Long term hypoparathyroidism can cause
cataracts, dry skin, coarse hair, and brittle
fingernails
Hyperthyroidism
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Many disorders can cause
hyperthyroidism: Graves Disease,
Hashiomotos Thyrotoxicosis, Toxic
Adenoma, Toxic Multiple Nodular Goiter,
Iodine Induced Hyperthyroidism,
Trophoblastic Disease from Germ Cell
Tumors, TSH mediated hyperthyroidism,
Thyroiditis, and exogenous and ectopic
hyperthyroidism
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Graves Disease is the most common
cause of hyperthyroidism.
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Graves Disease is an autoimmune
disorder that causes thyrotropin (TSH)
receptor antibodies, which stimulate
thyroid gland growth and thyroid hormone
synthesis and release.
Hyperthyroidism
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Hashimoto's Thyroiditis is an autoimmune disease that causes patients initially to
present with hyperparathyroidism and high radio iodine uptake similar to Graves
disease but eventually go hypothyroid
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Hypothyroid develops because of the infiltration of the thyroid gland with lymphocytes
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Toxic adenoma and multinodular goiter result from focal or diffuse hyperplasia of the
thyroid follicular cells whose functional capacity is independent regulation of TSH.
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Toxic multinodular goiter tends to be more common in areas where iodine uptake is
low
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Thyroid adenomas are not related to iodine uptake
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Iodine Induced Hyperthyroidism can occur after an iodine load such as IV contrast for
CT scan, or amiodarone administration.
Hyperthyroidism
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Iodine Induced Hyperthyroidism is rare
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Trophoblastic or germ cell tumors can be rare causes of
hyperthyroidism
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Can occur as a hydatidiform mole in women
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Can occur in Choriocarcinoma in men with testicular germ cell
tumors via direct stimulation of the TSH receptors
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TSH mediated hyperthyroidism is when there is a pituitary
adenoma producing TSH. Therapy is directed at removing the
tumor
Hyperthyroidism
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Thyroiditis is a group of heterogenous
disorders that result from inflammation
of thyroid tissue with transient
hyperthyroidism
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Thyroiditis has hyperthyroid phase,
then hypothyroid phase and then a
recovery of thyroid function
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Exogenous and ectopic
hyperthyroidism occurs from taking
too much thyroid hormone or it being
produced by other parts of the body.
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Exogenous thyroid hormone can be
produced by struma ovarii, which is
from a functioning ovarian neoplasm.
Hyperthyroidism
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Thyroid hormone effects almost every
organ system in the body.
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Skin-hyperthyroidism causes increased
sweating due to increased caloric burning
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Hyperthyroidism causing softening of nails,
thinning of hair, and can cause
hyperpigmentation
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Stare and lid lag occur in patients with
hyperthyroidism because of sympathetic
overactivity
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Patients with graves disease can get
exophthalmus because of inflammation of
the extraocular muscles and orbital fat and
connective tissue.
Hyperthyroidism
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Hyperthyroid patients have lower serum total and HDL cholesterol
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Hyperthyroid patient can have impaired glucose tolerance if
untreated
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Hyperthyroidism can result in lower serum cortisol concentrations
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Dyspnea can occur with hyperthyroidism because oxygen
consumption and CO2 production increase
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Can be tracheal obstruction due to large goiter
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Respiratory muscle weakness can cause dyspnea with
hyperthyroidism
Hyperthyroidism
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Weight loss with hyperthyroidism is due to
increased metabolic rate and increased gut
motility.
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Dysphagia may occur because of goiter
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RBC mass index is increase with
hyperthyroidism
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May have a normochromic normocytic
anemia
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Hyperthyroidism can be associated with ITP
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Urinary frequency and nocturia are common
with hyperthyroidism
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Woman with hyperthyroid may see high
serum estradiol, high LH, and may get
oligomenorrhea and anovulatory infertility
Hyperthyroidism
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Thyroid hormone stimulaters bone reabsorption, bone loss
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May see increased urinary calcium excretion
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Hyperthyroidism can cause psychosis, agitation and depression
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Treatment of hyperthyroidism includes beta blockers, PTU or methimazole,
or radioactive iodine
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Beta Blockers are for symptomatic treatment of hyperthyroidism
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PTU or methimazole are thyroid hormone antagonists
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Radioactive iodine is indicated for graves disease
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Surgical removal of thyroid gland is an option if necessary
Hypothyroidism
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Several different causes of
hypothyroidism
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Primary hypothyroidism is when there
is decreased secretion of T3 and T4
which results in a increase int TSH
secretion
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Chronic autoimmune (Hashimoto's)
Thyroiditis- most common cause of
hypothyroidism. When there is cell and
antibody mediated destruction of
thyroid tissue
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Iatrogenic Hypothyroidism-caused by
thyroidectomy radio iodine treatment,
or external radiation and there is less
secretion of T3 and T4 as a result of it
Hypothyroidism
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Iodine related hypothyroidism-excess or iodine deficiency can cause
hypothyroidism. Iodine excess causes the inhibition of iodide
organification from T4 to T3 synthesis. Iodine deficiency causes the
inability to synthesize thyroid hormone.
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Drugs such as PTU and methimazole can cause hypothyroidism.
Lithium, Amiodarone and Ethionamide have been known to cause
hypothyroidism.
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Infiltrative disease such as fibrous thyroiditis, hemochromatosis,
scleroderma, leukemia, and cystinosis are rare causes of
hypothyroidism
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Hypothyroidism in infants and children are caused by agenesis and
dysgenesis of the thyroid
Hypothyroidism
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Transient hypothyroidism can be
caused by post partum thyroiditis,
subtotal thyroidectomy, or patients
post radioactive iodine therapy with
Graves disease
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Secondary Hypothyroidism is
caused by lack of TSH secretion
from the anterior pituitary gland
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Tertiary (Central) is caused by lack
of TRH secretion form the
hypothalamus
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Hypothyroidism affects essentially
every organ system
Hypothyroidism
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Hypothyroidism causes decreased sweating, skin
discoloration, hair to be coarse, non pitting edema
(myxedema), vitiligo, and alopecia
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Hypothyroidism cans cause periorbital edema
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Hypothyroidism can cause normochromic normocytic anemia
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Hypothyroidism causes decrease cardiac output and reduction
of heart rate and cardiac contractility. Hypertension can be
caused from an increased in peripheral vascular
resistance. Increased cholesterol can be seen from
decreased cholesterol metabolism
Hypothyroidism
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Fatigue, shortness of breath on exertion
and rhinitis can be caused by respiratory
muscle weakness with hypothyroidism
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Hypothyroidism causes decreased gut
motility, constipation, and decreased taste
sensation, and gastric atrophy
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Hypothyroidism can cause
oligomenorrhea, amenorrhea, or
hypermenorrhea. This can lead to
infertility. Decreased libido, erectile
dysfunction, and delayed ejaculation are
possible in hypothyroidism
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Hypothyroidism left untreated can cause
hashimotos encephalopathy, myxedema
coma, and carpal tunnel syndrome
Hypothyroidism
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Hypothyroidism can also cause
joint pain, aches, and
stiffness. There is an increased
incidence of gout with
hypothyroid patients.
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Hypothyroidism can cause
hyponatremia
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Standard treatment of
hypothyroidism is replacement
therapy. Synthetic thyroxine
(T4) or combination T3 and T4
therapy. There is also T3 alone
therapy
Neoplastic Disease
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Thyroid Cancer is divided into 4
categories: papillary follicular,
medullary, and anaplastic
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Papillary and follicular cancers are
differentiated tumors and are
basically treated the sam
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Anaplastic cancer appear to arise
from other cancers
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Other cancers include primary
thyroid lymphoma, multiple
endocrine neoplasia type 2, familial
medullary cancer, or mets from
breast, colon, renal cancer, or
melanoma
Neoplastic Disease
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Initial staging is done with TMN
(Tumor Node Metastasis)
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Surgery is the initial treatment for
differentiated thyroid cancer. It is
recommended if the primary tumor
is at least 1-2 cm in diameter or if
mets are present
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Radioiodine therapy is used post
thyroidectomy for adjuvant ablation
on residual thyroid tissue and
possible microscopic residual
cancer, treatment of residual or
metastatic thyroid cancer, and
distant metastasis
Neoplastic Disease
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After thyroidectomy levothyroxine is need
in all patients to prevent hypothyroidism.
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Radiation therapy may be needed for
patients with differentiated thyroid cancer
who have metastatic disease that is not
responsive to radioiodine or patients with
tumors that do not concentrate radioiodine
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Diagnosis is made by biopsy usually on
fine need aspirate.
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This is done after Iodine 129 scan nuclear
scan
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Serum thyroglobulin is used to monitor
patients with differentiated thyroid cancer
Parathyroid Cancer
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It is rare cause of
hyperparathyroidism
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Most patients have hypercalcemia or
normal calcium and present with a
neck mass
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Multiple glands being affected are
extremely rare
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Surgery is the mainstay in treatment
of parathyroid carcinoma
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Radiation and Chemotherapy have
poor results and should only be
considered when patient not a
candidate for surgery
Thyroiditis
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Thyroiditis refers to a group of disorders
that cause thyroid inflammation
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Subacute thyroiditis is characterized by
neck pain, tender goiter, and elevated T3
and T4. Usually has hyperthyroidism
followed by hypothyroidism
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Infectious Thyroiditis can be acute or
chronic. Acute infections may cause
abscess formation. Staph or strep may
cause.
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Radiation Thyroiditis happens when a
patient with Graves Disease develops
thyroid pain and tenderness 5-10 days
after radiation therapy
Thyroiditis
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Palpation or trauma induced thyroiditis
can happen from a vigorous exam or
manipulation of the thyroid during
biopsy or neck surgery. Can also be
from seat belt during auto accident
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Post Partum Thyroiditis occurs within a
year after childbirth. It is usually
painless
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Drug Induced Thyroiditis can occur with
patients taking interferon alpha,
amiodarone, lithium, or intraleukin 2.
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Fibrous Thyroiditis is when there is
fibrous from macrophage or eosinophil
infiltration and extends to adjacent
tissues
Diseases of the
Adrenal Glands
Corticoadrenal
Insufficiency
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The symptoms of adrenal
insufficiency depend on the
amount of adrenal function loss
and the rate of which it is lost
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Common symptoms of adrenal
insufficiency are malaise,
lassitude, fatigue, generalized
weakness, anorexia, abdominal
pain, nausea, vomiting,
diarrhea, and weight loss
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May have postural hypotension
or syncope
Corticoadrenal
Insufficiency
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Hyponatremia is common, hyperkalemia and hypoglycemia
are common
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Hyperpigmentation is seen in almost all patients
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Decreased axillary and pubic hair loss, loss of libido are
common in women. Amenorrhea may be present
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May have psychosis, depression, impairment of memory, or
mild organic brain syndrome
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Can come from prolonged administration of
glucocorticoids. This is the most common causes of adrenal
insufficiency
Corticoadrenal
Insufficiency
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Initial workup should include CBC, Chem
7, ACTH, renin, cortisol, aldosterone
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ACTH stimulation test is good for helping
establishing the diagnosis
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Abdominal CT scan may show enlarged
adrenal glands or adrenal calcification
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Causes of adrenal insufficiency include:
destruction of adrenal cortex (from
autoimmune adrenalitis), polyglandular
autoimmune syndrome type 1 and 2,
infectious, tuberculosis, fungal infections,
HIV, hemorrhagic infarction of the
adrenal gland, metastatic disease, and
drugs
Corticoadrenal
Insufficiency
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Adrenal Insufficiency can come from 3 different mechanisms-
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Primary Adrenal Insufficiency (Addison's Disease)-an inadequate
serum cortisol response to ACTH stimulation shows adrenal
insufficiency but does not show if primary, secondary or tertiary.
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A Pituitary Disorder resulting from deficiency of ACTH
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A Hypothalamic Disorder resulting from CRH deficiency and leads
to low ACTH
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Treatment of Chronic Primary Adrenal Insufficiency includes
supplement of dexamethasone or prednisone, fludicortisone,
liberal salt intake, androgen replacement and patient medication
Corticoadrenal
Insufficiency
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Fever should be examined for
etiology and treated
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Adrenal crisis usually presents as
shock. Abdominal tenderness and
fever may be present. Fever would
be do to infection and needs to be
treated.
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Treatment of adrenal crisis includes
IV fluids 1-3 liters of NS or D5 NS
within the first 12-24
hours. Hypotonic saline could make
the hyponatremia worse
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Dexamethasone 4 mg IV should be
given
Cushing Syndrome
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Cushing Syndrome may be either
ACTH dependent or independent
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The most common cause of Cushing
Syndrome is from administration of
glucocorticoids
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If the cause is ACTH dependent will
see adrenal cortical hyperplasia on
imaging studies
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If the cause is ACTH independent, it is
most commonly iatrogenic. Can see it
also from adrenal adenomas or
carcinomas
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Most patients with Cushing Disease will
have a pituitary adenoma
Cushing Syndrome
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There may be ectopic ACTH from benign neuroendocrine tumors
(carcinoid) or from malignant sources like Oat Cell carcinoma
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There may ectopic CRH where the tumor causes hyperplasia and
hyper secretion of pituitary corticotrophs
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To establish the diagnosis of Cushing Syndrome want to exclude the
presence of exogenous steroid ingestion
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Patients with other disorders may have high cortisol levels and not
have Cushing Syndrome, these disorders are: physical stress, severe
bacterial infection, severe obesity, polycystic ovarian syndrome, major
depression, and chronic alcoholism. These patients are sometimes
referred to as having pseudo Cushing Syndrome.
Cushing Syndrome
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Need two first line tests to confirm
the presence of Cushing Syndrome
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Should use late night salivary
cortisol, urinary cortisol, and low
dose dexamethasone suppression
test as the first line tests
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Urine and saliva cortisol tests
should be obtained twice
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Urine cortisol excretion should be 3
times the upper limit of normal to
rule in Cushing Syndrome
Cushing Syndrome
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Treatment of Cushing Syndrome includes reveres clinical
manifestations by normalizing cortisol levels, remove any tumors
causing, avoid permanent dependence on medications, and avoid
hormone deficiency
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Need to discontinue exogenous glucocorticoids
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Need to treat pituitary adenomas with transsphenoidal
microadenomectomy
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Adrenal enzyme inhibitors can be used if surgery is delayed or
contraindicated
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Pituitary irradiation can be done on patients where fertility is a concern
Cushing Syndrome
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Bilateral adrenalectomy with
lifelong glucocorticoid and
mineralocorticoid replacement
is a final definitive cure
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Patients with ectopic ACTH or
CRH syndromes the tumor
should be removed
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Somatostatin Analogues rapidly
reduces ACTH secretion by
non pituitary tumors
Neoplastic Disease
•
Unilateral tumors or masses of the Adrenal
Gland are considered functional (hormone
secreting) or silent
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Adrenal tumors are also classified as either
benign or malignant
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Most adrenal tumors are benign, silent
tumors known as adrenal incidentalomas
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There are other benign functional tumors
that cause Cushing Syndrome, Primary
Hyperadosteronism, and virlization
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Adrenocortical Carcinomas are aggressive
tumors that can be functional and cause
Cushing Syndrome or can be non
functional and just present as an
abdominal mass
Neoplastic Disease
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Pheochromocytomas are catecholamine
producing tumors that arise from the
adrenal medulla. They can be benign or
malignant. They cause high blood
pressure and catecholamine related
physiologic changes
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Adrenocortical Adenomas are begin
neoplasms that can secrete steroids
independently from ACTH or the renin
angiotensin mechanism
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Aldosteronemas are adrenal
incidentalomas that can cause primary
aldosteronism
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The maximum diameter is predictive of
malignancy, most adrenal adenomas are
less than 4 cm in diameter
Diseases of the
Pituitary Gland
Acromegaly/Gigantism
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Acromegaly is caused from excessive
secretion of growth hormone (GH)
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Most common cause of acromegaly is a
somatotroph (GH) adenoma
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This causes fusion of the epiphyseal
growth plates n a child or adolescent called
pituitary gigantism
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Metabolic effects include nitrogen
retention, insulin antagonism, and lipolysis
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May get headache and/or vision loss
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If the macroademona is large, may get
decreased secretion of other pituitary
hormones
Acromegaly/Gigantism
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May get skin overgrowth and skin
thickening
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May get macroglossia
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Many organs can become enlarged
including thyroid, heart, liver,
lungs, and kidneys. Prostate
enlargement may occur
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Patients may get HTN, left
ventricular hypertrophy, and
cardiomyopathy
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Patients with acromegaly have an
increased risk of colon cancer
Diabetes Insipidus
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Polyuria is urinary output greater
than 3 liters per day
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Types of Diabetes Insipidus:
Central diabetes insipidus,
nephrogenic diabetes insipidus
•
Can also have primary
polydipsia where it is
characterized by increased
water intake, usually seen in
those with psychiatric illness.
Can be seen ion those taking
phenothiazine therapy which has
a side effect of dry mouth
Diabetes Insipidus
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Central Diabetes Insipidus-is characterized by deficient secretion of antidiuretic
hormone (ADH). Common causes include trauma, pituitary surgery, and
hypoxic or ischemic encephalopathy
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Nephrogenic Diabetes Insipidus-has normal ADH but the kidney has varying
degrees of resistance to its renal retaining effects. If seen during childhood is
due to inherited defects. Adults is usually acquired and secondary to lithium
use and hypercalcemia
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Low plasma sodium concentration an low urine osmolality is due to overload
from primary polydipsia
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A high to normal plasma sodium concentration and low urine osmolality is less
than plasma, points to diagnosis of diabetes insipidus
•
A normal plasma sodium concentration with a urine osmolality more than 600
excludes the diagnosis of diabetes insipidus
Diabetes Insipidus
•
Water restriction test is raising the plasma osmolality by either water
restriction or administration of hypertonic saline (0.05 mL/kg/min) for no
more than 2 hours.
•
Raising plasma osmolality leads to progressive ADH release and increase
in urine osmolality in normal patients
•
Once the plasma osmolality reaches 295-300 or the plasma sodium is 145
or higher, the effect of endogenous ADH is maximal. Administering ADH at
this point will not elevate urine osmolality unless ADH release is impaired
(except patients with central diabetes insipidus)
•
The water restriction tests involves measurement of the urine volume and
osmolality every hour and the plasma sodium concentration and osmolality
every 2 hours. The patient should not drink 2-3 hours before the test
Diabetes Insipidus
•
End point for the water restriction test is
when the urine osmolality reaches
normal value above 600 (means normal
ADH release)
•
Also when the urine osmolality is stable
on 2 or 3 consecutive measurements,
with a rising plasma osmolality
•
Also when the plasma osmolality
exceeds 295-300 or the plasma sodium
is over 145.
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Desmopressin is administered
•
Plasma and urine ADH levels should be
measured if the response to the water
restriction test is equivocal
Diabetes Insipidus
•
Central DI-ADH release and urine and plasma osmolality may rise
submaximally. Desmopressin will rise urine osmolality
•
Nephrogenic DI-has a submaximal rise in urine osmolality in response to
water restriction. The plasma osmolality stimulates ADH release. This will
produce a modest increase in urine osmolality due to resistance to ADH
•
Patients with Central DI or Nephrogenic DI present with polyuria,
polydipsia, and nocturia
•
Treatment of Central Diabetes Insipidus involves Desmopressin which is
the preferred medication
•
A low solute and sodium diet should be instituted
•
Desmopressin has little effect on nephrogenic diabetes insipidus
Dwarfism
•
Dwarfism is defined as usually a height
less than 4 feet 10 inches
•
It is caused by multiple medical condition
•
Achondroplasia accounts for 70-80 percent
of the cases
•
Turner syndrome and growth hormone
deficiency can be traced to some of the
cases of dwarfism
•
Three to thirty percent of children with
growth hormone deficiency have a parent,
sibling or child affected
•
Short stature is a term applied to child who
is two standard deviation below the mean
Dwarfism
•
Idiopathic short stature is when there is
no endocrine, metabolic, or other
diagnostic cause
•
Intrinsic short stature is a normal family
variant
•
Delayed growth and puberty usually is
due to under nutrition
•
Attenuated growth usually results from
metabolic or endocrine disorders or
severe systemic illness
•
Endocrine causes include Vitamin D
deficiency or resistance, growth
hormone deficiency, growth hormone
insensitivity, and hypothyroidism
Dwarfism
•
Glucocorticoid therapy long term
effects endogenous growth
hormone secretion
•
Autoimmune Diabetes Mellitus can
cause attenuated growth
•
Growth hormone deficiency results
from deficiency of the growth
hormone releasing hormone
(GHRH) but can be because of
sellar and presellar tumors
•
Treatment is targeted at finding the
cause and reversing what can be
reversed
Neoplastic Disease
•
There are other sellar lesions that
are not adenomas, but cannot be
differentiated from other adenomas
until biopsy.
•
Craniopharyngiomas are mixed solid
and cystic lesions that arise from
remnants of Rathke's pouch. It is a
benign lesion
•
Meningioma-usually benign lesion
that comes from the meninges and
can be anywhere in the head
•
Pituicytoma- uncommon glioma that
arises from the posterior
pituitary. Has no known hormonal
function.
Neoplastic Disease
•
Germ Cell Pituitary Tumors-they are also ectopic pinealomas that are
malignant and present with headache, nausea, vomiting, and lethargy,
diplopia, and can have diabetes insipidus. These usually respond well to
radiation. Human Beta HCG and alpha fetal protein can be increased.
•
Chordomas- locally aggressive tumors that metastasize from the Pituitary
gland. They present with headaches, vision disturbances, and anterior
pituitary hormone abnormalities. It is a malignant tumor
•
Primary Central Nervous System Lymphoma-sometimes involves both the
pituitary any hypothalamus. It is a malignant tumor
•
One to two percent of sellar masses involve metastasis from a distant
site. Most commonly it occurs with breast cancer in women and lung
cancer in men.
Adenomas
•
Lactotroph Pituitary Adenoma- dopamine
agonist should be used for decreasing adenoma
size. These can be very large and cause visual
defects
•
Somatotroph Pituitary Adenomas-cause
acromegaly. They are confined to the sella. If
these tumors impair vision, surgical removal is
recommended. Surgery offers a rapid cure of
acromegaly.
•
Corticotroph Pituitary Adenomas-no matter if
they are micro or macro adenomas surgery is
recommended first line. Before surgery you
want to confirm Cushing Syndrome and
demonstrate the adenoma is the source of the
excessive ACTH secretion
•
Thyrotrph Pituitary Hyperplasia-can be do to
long standing hypothyroidism and primary
hypogonadism
Diabetes Mellitus
Diabetes Mellitus Type I
•
DM Type IA is caused by autoimmune
destruction of the insulin producing
beta cells of the Islet of Langerhans
•
DM Type IIB is just non autoimmune
destruction of the insulin producing
beta cells of the Islet of Langerhans
•
It is a matter of insulin not being
produced instead of our bodies not
being able to utilize the insulin the body
produces
•
DM Type I is best managed with a long
acting insulin such as Lantus to take
manage basal needs and immediate
acting to manage short term needs
Diabetes Mellitus Type I
•
Typically presents with polydipsia, polyuria, and weightless with hyperglycemia and
ketonuria
•
May be asymptomatic
•
Can present with Diabetic Ketoacidosis. Present with similar symptoms but with
drowsiness, fruity smelling breath, and tachypnea, with vomiting.
•
To diagnosis Diabetes, fasting glucose of >126, random glucose >200, post prandial
glucose of >200 after two hours, or a Hgb A1C of >6.5%.
•
Other causes of hyperglycemia include: critically ill patients (shock or sepsis),
medications, and neonatal hyperglycemia (from stress, sepsis and drugs)
•
Patients with diabetes need to be screened for complications-
•
Patients need annual eye exams to screen for refractive errors, cataracts, glaucoma,
and retinopathy
Diabetes Mellitus Type I
•
Foot examination should be inspected at
each routine visit to identify problems with
nail care, poor fitting footwear, fungal
infections, and to screen for neurologic and
vascular disease
•
Neuropathy and vascular complications put
the patient at risk for ulcers which can
cause infections and lead to amputations
•
Measurement of urinary albumin
excretion. Abnormal results should be
repeated at least 2-3 times over a 3-6
month period because of high rate of false
positives. ACE inhibitors or ARB's help
this. The need for further monitoring after
instituting these therapies are not certain
Diabetes Mellitus Type I
•
Screening for coronary heart
disease. Clinicians obtain a fasting
lipid profile, blood pressure, and
smoking history to decrease risk
factors. It is not recommended to
perform routine stress tests on
asymptomatic diabetic patients.
•
patients over 50 staring an exercise
program, a resting 12 lead EKG is
recommended for screening.
•
Goal Hgb A1C is less than 7. It is
obtained with every routine office
visit lab screen
Diabetes Mellitus Type II
•
Patients with type 2 diabetes have
different degrees of insulin
resistance
•
Hyperglycemia can impair
pancreatic beta cell function and
make insulin resistance worse
•
Majority of therapies are targeted
at either increasing pancreatic beta
cell activity or to better utilize the
insulin in the body
•
Recommended routine screening
tests for type 2 diabetics is the
same as type 1 diabetes
Diabetes Mellitus Type II
•
Therapy for Type 2 Diabetes includes:
dietary modification, exercise, weight
reduction and medications
•
Lifestyle modifications are the first line
in treatment
•
Metformin should be the initial anti
glycemic agent
•
Next step should include an oral
sulfonylurea or basal insulin
•
If this therapy fails intensive insulin
should be used
•
Less well validated therapies include
pioglitazone or a GLP agonist
Diabetes Mellitus Type II
•
Sulfonylureas can lower glucose by
20 percent but lose their
effectiveness over time
•
Meglitinides are short acting glucose
lowering drugs that act like
sulfonylureas but are less effective
•
Thiazolidinediones (Actos and
Avandia) lower glucose by
decreasing insulin sensitivity
•
DPP Inhibitors-are common second
line treatments who patients that do
not respond to a sulfonylurea
Diabetes Mellitus Type II
•
Glucagon Like Peptide
Agonists (GLP-1)-these are
administer subcutaneously.
These are add on drugs to
patients that are poorly
controlled on maximal dose of
one or two agents
•
Alpha Glucosidase Inhibitorshave additive hypoglycemic
effects in the patients receiving
diet and already on
sulfonylureas, metformin, or
insulin therapy
Lipid Disorders
Hypercholesterolemia
•
Lipid disorders occur either as a result
of one or more genetic abnormalities or
secondary to underlying disease
•
Family history of hypercholesterolemia
is a major risk factor
•
High levels of cholesterol have been
shown to lead to atherosclerosis and
lead to coronary heart disease
•
The first line recommendation in the
treatment of hypercholesterolemia is
diet modification and exercise
•
Low HDL is also an indication for
instituting therapy
Hypercholesterolemia
•
Weight loss has been shown to lower LDL levels by 5-7 percent
•
Statins can reduce the cardiovascular risk by 20-30 percent regardless of the baseline
LDL
•
Patients that are given a medication to lower LDL should be given a statin
•
If patients have known coronary heart disease or have a similar risk should be treated
with a higher dose of the statin (ex Lipitor 40-80 mg or Crestor 20-40 mg) regardless of
the baseline LDL
•
Patients with acute coronary syndrome and those with similar risk Crestor 80 mg daily
•
Patients with stable cardiovascular disease should get at least a 50 percent reduction
of the LDL or a LDL level of less than 100 or have their dose increased
•
If patients are on the high statin dose, a second LDL lowering medicine should be
added
Hypertriglyceridemia
•
Lipid disorders occur either as a result
of one or more genetic abnormalities or
secondary to underlying disease
•
The primary dyslipidemias are
associated with an overproduction or
impaired removal of lipoproteins
•
Normal triglycerides is less than 150
•
Borderline high is 150-199
•
High 200-499
•
Very High over 500
Hypertriglyceridemia
•
Elevated triglyceride levels are independently associated with
cardiovascular risk
•
There is an association between elevated triglycerides and
coronary heart disease
•
Non fasting triglyceride elevations have been showed to show
increase risk for ischemic stroke
•
Many acquired disorders, conditions, and therapies raise serum
triglycerides: obesity, diabetes mellitus, nephrotic syndrome,
hypothyroidism, pregnancy, tamoxifen, beta blockers,
immunosuppressive medications, HIV medications, retinoids,
and estrogen replacement
Hypertriglyceridemia
•
Family history is a strong risk
factor for development of
hypertriglyceridemia
•
Mild to Moderate
Hypertriglyceridemia (150-500)
should be treated with lifestyle
modifications. Cardiovascular
risk reduction with statins is best
accomplished when instituting
medications
•
Gemfibrozil has been shown to
reduce triglyceride levels by 31
percent and raise HDL
Hypertriglyceridemia
•
Severe Hypertriglyceridemia
(>500) are at increased risk for
pancreatitis. It is
recommended to decrease
level so there is no
development of pancreatitis.
This can be done with statins or
Gemfibrozil
•
Fibrates (Fenofibrate or
Gemfibrozil) , Nicotinic Acid,
and fish oil can also be used to
help lower triglyceride levels
References
•
J. Tintinalli et al, Emergency Medicine: A Comprehensive Study
Guide, 6th Ed.2014
•
Currrent Medical: Diagnosis and Treatment 2013, 44th ed.
•
Essentials of Musculoskeletal Care, Greene, 2nd Ed.
•
www.medscape.com
•
Nelson's Essentials of Pediatrics, 5th ed.
•
www.uptodate.com
•
Current Pediatric Diagnosis & Treatment, 16th ed.
•
Current Obstetric & Gynecologic Diagnosis &
Treatment, 9th Ed.
•
Schwartz’s Schwartz’s Principles of Surgery, 2005
•
Habif, Clinical Dermatology, 4th ed.
•
2014CURRENT Medical Diagnosis and Treatment