ENDOCRINE DISORDERS

ADRENAL GLAND DISORDERS

Adrenal Gland A&P ● 2 glands on top of each kidney w/ 2 parts:
o adrenal cortex = produces steroid hormones (glucocorticoids, mineralcorticoids, adrenal androgens)
o adrenal medulla = produces E/NE
● ACTH/ cortisol are released in pulsatile pattern in response to stress, exercise, surgery, hypoglycemia
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● Autoimmune adrenalitis – ● Weakness, fatigue, anorexia, wt ● Low AM cortisol level < 3 ● Life long glucocorticoid
Addision’s Disease M/C loss mcg/dL @ 8 am = diagnostic therapy
(Hypocortisolism) ● Adrenal hemorrhage ● Hyperpigmentation= diffuse ● Hyponatremia ● Hydrocortisone BID
● Metastatic malignancy/ tanning over non- ● Hyperkalemia ● Fludrocortisone AM to
lymphoma exposed/exposed areas, ● Normocytic normochromic replace mineralcorticoid
Primary Adrenal ● Infection: TB, CMV, fungi most prominent over jts/ anemia component
Insufficiency ● Amyloidosis posterior neck ● Azotemia ● Pt should wear alert
● Hemochromatosis ● Dizziness, orthostatic ● DX = ACTH stimulation test medical bracelet
● Dysfxn/ absence of ● Congenital Adrenal hypotension →no change in cortisol level
adrenal cortices Hyperplasia (CAH) ● N/V from baseline ** double/ triple steroid doses
● 2.6:1 F:M ratio ● Familial glucocorticoid def & ● Salt craving ● CT scan of abd →evaluate during stressful situations
hypoplasia ● Amenorrhea adrenal glands (cold/fever), trauma, surgery
● onset = 3050 y/o
● Drugs – ketoconazole; steroid ● Loss of axillary/ pubic hair ● Decreased DHEA levels
● Plasma ACTH level high
(usually >200)
● Exogenous glucocorticoid ● Usually chronic & nonspecific ● Hyponatermia ● Life long glucocorticoid
Secondary Adrenal therapy= M/C/C manifestations ● Normocytic normochromic steroid therapy
Insufficiency ● Defect in hypothalamus- ● Weakness, lethargy, easy anemia ● Hydrocortisone oral only
pituitary axis fatigability, anorexia, nausea, ● ACTH provocation test
→ACTH def myalgia, menstrual disturbances, ● Plasma ACTH will be ** double/ triple steroid doses
wt loss, hypotension, skin normal/ low during stressful situations
changes (cold/fever), trauma, surgery
● Hx of steroid therapy
● Occurs in pts w/ Addison’s ● Hypotension ● Eosinophil count usually ● IV hydrocortisone
Acute Adrenal Disease precipitated by: ● Fever high ● IVF
Insufficiency o Infection ● Dehydration ● Hyponatremia/ hyperkalemia ● Correction of
o Surgery ● Abd pain or both present hypoglycemia w/ glucose
(Adrenal Crisis)
o Dehydration to due salt ● N/V/ anorexia ● Dx made by ACTH IV
deprivation, vomiting, ● Weakness stimulation test → ● Broad spectrum ABx
diarrhea ● Depressed mental status markedly elevated ACTH >
● Hypoglycemia 200
● Shock/ coma →death in
untreated patients
● Autosomal recessive trait → ● @ birth →female w/ ambiguous ● increased levels of ACTH ● prednisone replacement
Congenital Adrenal deficiency in enzymes external genitalia ● adrenal hyperplasia life long
Hyperplasia (CAH) necessary for synthesis of ● primary amenorrhea ● high level of AM 17
cortisol = dec cortisol level hydroxyprogesterone
● Common in infancy/
childhood
Cushing’s Syndrome
(Hypercortisolism)
(consideredCushing’s
Diseasewhen specific type
of Cushing’s syndrome is
due to excessive pituitary
ACTH secretion from
pituitary adenoma)
Hirsutism/ Virilism
● Hirsutism:excessive
terminal hair growth that
appears in male pattern in a
female
● Virilism:increased
muscularity, deepening of
voice, clitoromegaly
Hyperaldosteronism
● Excessive secretion of
aldosterone → inc Na
reabsorption/ loss of K+/
H+
● M/C = 21hydroxylase
● Pituitary adenoma (Cushing’s
Disease)= M/C; 70%
● non pituitary neoplasm
(ectopic ACTH); 1520%;
M/C seen in pts w/ SCC of
lung
● iatrogenic overuse of steroids
● adrenal neoplasm
(adenoma/carcinoma)
● nodular adrenal hyperplasia
● tertiary hypercortisolism
● Excessive adrenal/ ovarian sex
hormones
● High levels of DHEA,
DHEAS, testosterone
● Idiopathic – familial
● PCOS, menopause, androgen
producing ovarian tumors
● Cushing’s syndrome
● Adrenal carcinoma/ tumors/
CAH
● Anabolic steroids, danazol,
minoxidil, progesterone
● Severe insulin resistance,
hypothyroidism, acromegaly
● Primary→adenoma of
hyperplasia of adrenal gland
o Adenoma – 40%
o Idiopathic 60%
● Secondary
o Stimulation is
extraadrenal
● lack of development of
secondary sexual characteristics
● central obesity → effecting
face, neck, trunk, abd
● “moon faces”/ “buffalo hump”
● easy to bruise, facial plethora,
red purple striae, acne
● hirsutism
● HTN
● Hyperglycemia
● Gonadal dysfxn – inc androgens,
amenorrhea, infertility, dec
libido
● Poor concentration/ depression
● Muscle weakness
● Osteoporosis
● Renal calculi from steroid
induced hypercalcemia
● Increased hair on face, chin,
chest, abd
● Acne
● Alopecia
● Anovulation/ infertility,
amenorrhea
● Decrease in breast size/ adipose
tissue
● Increase muscle mass
● Male pattern baldness,
deepening of voice, enlarged
clitoris
● Primary
o HTN (>140/90)
o Hypokalemia
o Fatigue, weakness
o HA
o Polydipsia/ polyuria
o Facial flushing
● Elevated cortisol
● CBC →elevated H&H, RBC
● Low potassium
● Fasting hyperglycemia
● TO DIAGNOS
o Elevated AM cortisol
o Dexamethasone
suppression test →
cortisol > 5 mcg/dL
o 24 hour urine collection
for free cortisol = high
o Midnight salivary
cortisol test; elevated =
diagnostic
● Pituitary MRI
● Chest CT to r/o SCC
● Abd/ pelvic CT to r/o adrenal
tumor
● Increased serum testosterone,
DHEA, DHEAS
● Pelvic sonogram →r/o
PCOS/ ovarian tumor
● CT of drenal → r/o
adrenal mass
● FSH: LH ratio > 2 (high in
PCOS)
● 17 hydroxyprogesterone →
r/o CAH
● 24 hour urine for free
cortisol → r/o
Cushing’s syndrome
PRIMARY
● EKG →LVH due to
uncontrolled BP
● High plasma aldosterone &
low plasmia renin activity
● Persistent hypokalemia
● HTN w/o edema
● Cushing’s disease→
removal of pituitary
adenoma
● Ectopic ACTH syndrome
→spironolactone,
ketoconazole, metyrapone,
aminoglutethimiate
● Adrenal adenoma→
unilateral adrenalectomy or
laparoscopic adrenal
surgery
● Adrenal carcinoma
→mitotane, ketoconazole,
metyrapone &
aminoglutethimiate; RAD/
chemo not successful; poor
prognosis
** untreated Cushing’s is
frequently fatal
● tx underlying cause
● oophorectomy (for ovarian
tumor)
● spironolactone/ vanique
cream (for hirsutism)
● finasteride
● OCP’s
● Metformin (PCOS)
● Clomiphene (infertility)
● Laser therapy, waxing,
bleaching excess hair
● Adrenolectomy (unilateral)
if adenoma found
● Spironolactone (treatment
of choice) = correct
hypokalemia/ control BP
prior to surgery
● Cure rate is > 70%

● Mechanism unknown
Pheochromocytomas ● 10% hereditary
= Adrenal Tumor ● usually tumor located in
adrenals
● associated w/ vonhippel-
● Rare; produces/ Lindau (VHL) syndrome,
secretes multiple endocrine Neoplasia
catecholamines type 2 (MEN2),
● Female = males neurofibromatosis type 1
● All ages (mostly in
youngmid adult life)
● Adrenal mass discovered
Adrenal Incidentalomas incidentally
● triad= palpitation, HA, episodic
diaphoresis
● RULE OF 10 →10% not
associated w/ HTN, 10% extra-
adrenal, 10% occur in children,
10% involves both adrenals,
10% have mets disease
● Paroxysmal sx which may last
minutes to hour
● “adrenal rush” → fight/flight
response
● tremors, anxiety, paresthesia
● abd pain & vomiting, secondary
to ischemic enterocolitis
● Asymptomatic
● Aldosterone renin ratio →
>30 in upright position =
diagnostic of primary
● CT of abd/ pelvic →check
for adrenal mass
● Adrenal vein sampling =
GOLD STANDARDto dx;
usually performed if CT neg
SECONDARY
● High PRA
● HTN > 140/90
● LVH w/ dilated
cardiomyopathy
● Facial flushing
● EKG = sinus tachycardia
● plasma catecholamines &
metanephrines
● 24 hour urine collection for
catecholamines,
metanephrines,
vanillylmandelic acid
(VMA)
● serum chromagranin A
(CgA) = elevated; normal =
low @ 8 am/ high in
afternoon & 11 pm
● CT/ MRI abd/ pelvic →r/o
adrenal mass
● MIBG I131 or I123 scan →
useful to determine if mass is
pheo or exraadrenal mass
● Focused work up needed
● Laparoscopic
adrenalectomy
● Oral antihypertensive
started1014 days before
surgery
o CCB – preferred
o Phenoxybenzamine
(C/I in pregnancy)
o ACE (2ndline/ comb
w/ previous) or BB
● Lifetime surveillance
required
o Recheck plasma
metanephrines 2 wks
post up/ then yearly
for 10 years
o Monitor BP
● tx based on cause
● if no surgery warranted →
monitor w/ CT scan q 612
months x 5 years

ANTERIOR PITUITARY
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● congenital defect on pituitary ● Children– growth failure, ● Low GH/ IGF1 ● Consult w/ peds/ adult
Growth Hormone development, empty sella, short stature, low growth ● GH stimulation test (4 types, endo & neurosurgeon
Deficiency encephalocele, velocity for age, pubertal must do 2 to confirm dx) ● Surgical resection of
panhypopituitarism, genetic stage ● Xray to assess bone age in pituitary tumors
abnormalities ● Adults– non specific sx = children ● GH recombinant
● 1 in 4,000 ● Achrondoplasia fatigue, dec strength/ exercise ● DEXA scan for osteoporosis replacement therapy (SQ
● Craniopharyngioma intolerance, increase wt/
● ~600 adults dx each ● Cranial radiation difficulty losing wt, anxiety, ● EKG to look for reduced EF at weekly): Humatropin,
year ● Sarcoidosis social isolation, dec libido, rest/ exercise Genetropin
● M>F ● Laron’s syndrome impaired sleep ● MRI (or CT) of pituitary to r/o
● Tumor, surgery ● Some are asymptomatic tumor ● Close monitor by endo,
● head trauma assess ht/ wt/ growth
velocity

● Increased CV mortality/
metabolic syndrome →
cardiac/ lipid monitoring

THYROID DISORDERS
● Located in neck: 2 lateral lobes connected by thin isthmus
● Size: 1020 g in normal adults
Anatomy & Histology of Thyroid Gland ● Rich in blood supply
● 4 PTH glands that lie behind & recurrent laryngeal nerve
● develops during 3rdweek of gestations & hormone synthesis beings at ~11 wks of
gestation
o hormone promotes growth, development, regulates # of homestatic fxn (energy
& heat)
● produces T3/ T4
● contains 5965% of element iodine
o cretinism– severe mental retardation that occurs in children who live in
iodinedef regions that are left untreated during early childhood
Control of Thyroid Fxn ● Hypothalamic – pituitarythyroid axis
o Hypothalamus = command center for endocrine system →receives input from
cerebral cortex, from environment (EX = increased cortisol at night) & FB from
organ it controls
▪ Releases TRH(thyrotopin releasing hormone) which regulates pituitary
TSHsecretion
o Anterior pituitary– releases TSH(thyroid stimulating hormone or thyrotopin)
in response to TRH
o Thyroid gland– releases T 3/T4in response to TSH
▪ T3 is more potent/ active hormone, T4 must be converted to T3 in
periphery
● (+) FB = low levels of T3/T4 is sensed by hypothalamus →increased secretion of
TRH from hypothalamus
● () FB = increased levels of T3/T4 inhibit secretion of TRH form hypothalamus &
TSH from anterior pituitary
Fxn of Thyroid Hormone ● Increased metabolism of all body tissues (excluding retina, spleen, testes, lung) →
increased rate of use of glucose, fat, protein
o High cholesterol in hypothyroidism/ low cholesterol in hyperthyroidism
● Increase in O2 consumption →increased vasodilation →changes in skin temp, HR,
BP
● Increase GI motility/ production of GI secretion →diarrhea

THYROID FXN TESTS
THYROID FXN TESTS
DISEASE
Hypothyroidism
● Slowing down of
metabolic processes
● 23% prevalence
● mean age = 50
● 10:1 F to M ratio
● PRIMARY= thyroid
failure
● SECONDARY=
pituitary TSH deficiency
● TERTIARY=
hypothalamic deficiency
of TRH
Myxedema Coma
● End stage of untreated
hypothyroidism
● Tremors
TSH ● BEST THYROID FXN SCREENING TEST
● Clinical uses = Initial test for suspected thyroid ds, follow pts on hormones, used w/ T4 to
manage pts w/ graves
● HIGH→increased dose of levothyroxing
● LOW →decreased levothyroxin
Free T4 (FT4) ● METABOLICALLY ACTIVE HORMONE
● Ordered when TSH is abn to determine the thyroid hyper or hypo fxn
Antithyroid ● Used to dx Hashimotosin hypothyroidism or autoimmune thyroiditis
peroxidase Ab
Anti
thyroglobulin Ab
Thyroid ● Specific for Graves dsin hyperthyroid
Stimulating Ab
T3 ● Used to dx hyperthyroidwhen T SH is low & T4 is still normal
FTI ● Used in thyroid ds when pt has protein abnormalities
CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● In US → ● Fatigue ● On PE – delayed reflexes, ● Start tx if TSH >10, TSH>5
Hasimoto’s ● Cold intolerance bradycardia, coarse hair, + (+) TPO Ab, or TSH > 2.5
thyroiditis ● Dry skin, brittle nails, hair periorbital swelling, CTS, ● Levothyroxine (LT4) –
● Worldwide → loss Goiter gold standard/ standard of
Iodine Deficiency ● Weight gain ● Primary care
● Drugs that block thyroid ● Weakness o Labs = high TSH/ low o Once daily, in AM on
hormone synthesis (lithium, ● Hoarse voice Free T4, T3 variable empty stomach & wait
amiodarone, PTU, interferon) ● Joint aches ● Secondary 12 hrs before eating/
● RAI therapy → iatrogenic ● Constipation o TSH normal/ low, free taking other meds
34 months after tx ● Puffy face/ hands; non pitting T4 low, TRH high o Start dose = 1.1.6
● Totally thyroidectomy edema ● Tertiary– all three are low mcg/kg in adults
● Excessive iodine intake ● Menstrual irregularities ● (+) thyroid peroxidase Ab +/ o Elderly = start w/ low
● Neck radiation (amenorrhea/ thyroglobulin Ab → dose if CV risk present
● Postpartum thyroiditis oligomenorrhea) Hashimoto’s ● Recheck TSH in 46 wks &
● Sub acute thyroiditis ● Decrease libido/ infertility ● Hypercholesterolemia adjust dose appropriately
● Side effects of med= allergy
● Congenital ● Depression, impaired
memory/ concentration to coloring dye, overdosing
→hyperthyroidism →
arrhythmia (afib),
osteoporosis
● Cytomel (synthetic T3)
● Precipitated by sepsis, ● AMS = hallmark ● Markedly elevated TSH & ●
● Armour
ACUTE Thyroid
cardiac ds, respiratory ● Progressive weakness FT4/Te MEDICAL
distress, CNS ds, cold ● Stupor ● Hypoglycemia EMERGENCY
exposure, drug use, ● Hypothermia ● Hyponatremia ● Tx in ICU
noncompliance w/ tx ● Hypoventilation ● LT4 IV, warm blankets, lyte
replacement
● Shock
● Death
 ● High mortality in elderly w/
underlying pulmonary/ CV
ds
● Fetla thyroid develop at 1113 wks gestation
Hypothyroidism in ● 1sttrimester TSH = 12,5, 2ndtrimester = 0.2 3.0, 3rdtrimester = 0.33.0
Pregnancy ● check labs – TSH, free T4, Free T3, TPO AB, thyroglobulin AB to r/o hypothyroidism
● TX = Levothyroxine
● Check TSH every 4 wks during first half of pregnancy
● If planning pregnancy →need to adjust LT4 w/ a TSH <2.5
● If pt becomes pregnant →increase LT4 by 2530% as soon as they miss a period/ have (+) pregnancy test
● Fetal risks if untreated = premature birth, low birthweight, miscarriage, low IQ babies
● Hyperactivity of thyroid gland (excess thyroid fxn)
HYPERTHYROIDISM ● CAUSES
o Graves ds (diffuse toxic goiter)= M/C o
Toxic adenoma (Plummer’s disease) o
Toxic multinodular goiter
o Sub acute Thyroiditis
● Primary– Increased T4/T3, decreased TSH/TRH
● Secondary– increased T4/T3, TSH, decreased TRH
● Tertiary– increased T4/T3, TSH, TRH
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● Cause unknown ● Hyperactivity, irritability ● Elevated FT4 ● Antithyroid drug therapy
Graves Disease ● Thought to be autoimmune ● Heat intolerance/ sweating ● Elevated T3/T4 o PTU/ Methimazole
o Tlymphocytes become ● Palpitations ● Suppressed/ low TSH o +/ propranolol to
● F>M sensitized to Ag w/in the ● Fatigue ● Elevated thyroid uptake control tachy/ HTN
thyroid gland & ● Wt loss w/ increase appetite scan→shows hyperactivity ● SubTotal Thyroidectomy
● Mean age = 2040 y/o
stimulate Blymphocytes ● Diarrhea ● TPO AB might be elevated o Pretreat pt w/ anti-
● M/C/C primary
to synthesize Ab to these ● Insomnia ● Elevated TSHreceptor Ab & thyroid meds until
hyperthyroidism
Ag ● Oligomenorrhea/ loss of TSI = specific euthyroid to avoid
● Stress is thought to be a libido ● MRI/ CT of head/ neck → thyrotoxic crisis
trigger ● Tachycardia/ Afib check for ophthalmic o Thyroid
● 15% have strong familial ● Tremors involvement supplementaiotn
predisposition ● Goiter following w/ LT4
● Warm, moist skin ● Radioactive Iodine
● Muscle weakness Therapy (RAI) I 131 →
● Lid lag causes progressive
● Eyes bulging outwards destruction thyroid
● Graves Ophthalmopathy– o Pretreat pt w/
sensation of grittiness, eye methimazole & d/c 35
discomfort, excessive days prior
tearing, diplopia possible o C/I in pregnancy/
o Tx= refer to endo, breastfeeding
artificial tear drops, o Repeat 2nddose in 6
subtotal months if needed
 thyroidectomy/RAI if ● Some pts will spontaneous
severe relapse
● Graves Dermopathy– ● Rare to fluctuate btwn
thyroid acropathy (form of hypo/hyperthyroidism due to
clubbing), preitibial changes in fxn of activity of
myxedema TSHR AB

Precipitating Factors: ● Fever/ flushing/ sweating ● Labs usually consistent w/ ● High mortality/ 20% enter
Thyrotoxic Crisis ● Stressful acute illness ● Marked tachy (afib) hyperthyroidism (& only coma
“Thyroid storm” ● Thyroid surgery ● Agitation/ restlessness/ useful if not previously dx) ● PTU in large dose (PO/
● Infection delirium o Elevated T3/T4 & FT4, NGT)
● Childbirth ● N/V/D dec TSH ● Potassium iodine
● Acute exacerbation of all sx
● trauma ● Jaundice ● CBC might show mild ● IV corticosteroids
of thyrotoxicosis
leukocytosis w/ left shift ● Propranolol IV/ PO to
● May be life threatening
● Non specific LFT abn control tachy
● Possible hypercalcemia ● Cooling blanket/
acetaminophen to control
fever
● Most likely due to viral ● Fever ● On PE = exquisitely tender ● Acetaminophen
Subacute Thyroiditis infection → mumps, ● Sore throat thyroid gland ● Prednisone
coxsackie virus, influenza, ● Enlarged thyroid w/ neck ● High T4& T3 ● Monitor TSH/ Free T4 q 24
● Acute inflammation of the adenovirus soreness ● Low TSH wks
thyroid ● Initial sx of hyperthyroidism: ● Low thyroid uptake scan ● Sx usually improve
● Age 3050 palpitation, sweating, ● Elevated ESR >100 spontaneously
● M/C women agitation ● LT4 if become hypothyroid
● 3 phases: hyperthyroid,
hypothyroid, recovery
● OTHER FORMS OF THYROIDITIS
o Hashimoto’s thyroiditis(chronic autoimmune): (+) thyroglobulin AB, (+) TPO AB & can progress to hypothyroidism
▪ Associated w/ virtiligo, RA, Addison’s ds, DM type 1, hypoparathyroidism, pernicious anemia
o Silent Thyroiditis/ Postpartum thyroiditis:5% of women 36 months postpartum
o Drug induced:IFN alpha, interleukin 2, amiodarone
o Acute thyroiditis:due to acute bacteria/ fungal infection & radioactive thyroiditis after RAI I131 tx

● Acute & severe illness can ● Consider in pts w/ low T4 & ● Tx controversial
Sick Euthyroid Syndrome cause abnormalities in TSH/ low FT4 w/o thyroid ds ● Observation unless there is
thyroid hormone levels, in ● Free T3 is low = LOW T3 historic/ clinical evidence
the absence of underlying SYNDROME suggestive of hypothyroidism
thyroid disease ●
● Major cause = release of
cytokines
● Severe illness, caloric
deprivation, major surgery

Thyroid Nodules
● Present in 47% of adults in
US
● 4:1 F:M
● thyroid CA rare
THYROID CA
DISEASE
Papillary Throid CA (PTC)
– M/C
Follicular Thyroid CA
(FTC)
Medullary Thyroid CA
(MTC)
Undifferentiated
(anaplastic) carcinoma
● Chronic thyroiditis:
Hasimoto’s
● Dominant portion of MNG
● Thyroid, parathyroid,
thyroglossal cyst
● Agenesis of thyroid lobe
usually left
● Postsurgical reminiance
hyperplasia/ scarring
● Post RAI hyperplasia
● Benign adenoma (Hurthle
cells)
● Exposure to neck/ head radiation
● Fhx of medullary thyroid CA
● Children, young, adults, male
● RF: hx of head/neck radiation, <20/ > 70 y/o, male, increased nodule size (>4cm), new/ enlarged neck mass, vocal cord paralysis, iodine
deficiency, fhx of MEN2/ thyroid CA
● c/o hoarseness/ dysphagia, exposure of head/ neck radiation, fhx of medullary thyroid CA, children, young adults, males →suggestive
CAUSE
● PTC= 7090% of all thyroid
CA
● Not associated w/ radiation
exposure
● Disease of parafollicular
ccells →production of
calcitonin
● More aggressive than PTC/
FTC
● Extends to cervical lymph
nodes early & distance mets
later (bone, brain, liver,
adrenal medulla)
● Familial – can be associated
w/ MEN 2 A & MEN 2B
● Older pts
● Least common
● 95% present as thyroid lump/ ● Thyroid sonogram →
nodule distinguish btwn cyst vs.
● most benign / asymptomatic solid
● ● Radionuclide scan →
identify “hot” vs “cold”
o Hot= absorb iodine/
non cancerous
o Cold= non fxn (no
absorption) 5% CA
● Needle bx/ FNA for nodules
> 10 mm
SIGNS/SYMPTOMS LAB/DX
● FTC = mets common to neck ● PTC – thyroglobulin (used as
nodes, bone, lung marker for recurrence/ mets)
● Flushing ● MRI of neck to r/o mets
● Diarrhea
● Fatigue
● Cushings syndrome
● s/sx of pressure/ invasion =
recurrent laryngeal nerve
palsy (hoarseness)
● Results of bx/ FNA depict tx:
o Malignant = refer to
surgery
o Unsatisfactory FNA =
repeat bx
o Benign = monitor w/
thyroid US
o Follicular neoplasm =
radioanuclide scan to
check hot vs. cold
● Benign nodules may regress
spontaneously
TREATMENT
● Total/ near total
thyroidectomy
● High risk pts →RAI of
residual thyroid remnant
● LT4 replacement w/ TSH
btwn 0.10.5
● F/U – whole body scan,
monitor thyroglobulin Ab q 6
months initially then yearly
for recurrence/ mets
● Total thyroidectomy
● (RAI & chemo not effective)
● calcitonin levels used to
monitor if residual disease is
present after tx of detection
of recurrence
● Very resistant to therapy
 ● MOST AGGRESSIVE → ● Poor prognosis/ death
rapid growth w/ compressive anticipated w/in 612 months
sx of dx
● Total thyroidectomy

DISEASES OF PARATHYROIDS
Calcium ● Critical to our survival →important role intracellular/ extracellular metabolism
● Serum total Ca = ~9.5 (4.5 is bound to serum protein, 0.5 circulated as insoluble
complexes, 4.5 circulates as free/unbound/ionized calcium)
● Total serum Ca2+ can change w/o a change in ionized Ca2+ →serum must be
adjusted for abnormal albumin levels
● ALWAYS CORRECT FOR ALBUMIN
● Regulated by Intestine, Kidney, Skeleton & PTH, calcitriol, calcitonin
Parathyroid Hormone ● Produced by 4 parathyroid glands (behind both thyroid glands)
● Serum ionized Ca2+ concentration is continuously monitored by PTH glands
● Targets Kidneys →inhibits renal Ca2+ excretion, phosphate/ bicarb reabsorption,
PCT production of active vitamin D
● Targets skeleton → immediately mobilizes Ca2+ from skeleton via activation of
osteoclasts (overtime osteoblasts stimulated)
● Targets gut →increasing intestinal absorption of Ca2+ through its ability to inc renal
synthesis of vitamin D
Vitamin D ● Inactive form is made to active form (calcitriol) in kidney
● Regulated by PTH → increases in PTH stimulate calcitriol production
● Primary action of calcitriol = regulate intestinal Ca2+ absroption
Calcitonin ● Produced by thyroid gland in response to hypercalcemia
● Directly inhibits osteoclast fxn
● Overall not important to human phys
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
Hypercalcemia ● Results from excessive Ca2+ ● Usually asymptomatic unless ● Usually found on routine labs ● Initial tx may be started w/o
finlux into ECF severe →CNS, renal, GI, ● Next look at PTH level specific dx
● Hyperparathyroidism/ cardiac ● GOALS →correct
malignancy = 90% dehydration (fluds), enhance
o Malignancy = M/C/C in **stones, bones, abd moans, & renal calcium excretion,
hospitalized pts psychic groans** inhibit accelerated bone
o Occurs w/ far ● Stones = renal, polyuria, resorption
advancement polydipsia, uremia ● Tx underlying disorder →
● Various vit d related ● Abd gorans = parathyroidectomy, low
problems constipation, Ca2+, d/c certain meds,
● Disorders associated w/ rapid indigestion, peptic ulcer, chemotherapy, tx of sarcoid,
bone turnover pancreatitis avoid vit d, bisphosphates
● Thiazides ● Bones = osteitis, bone
● Renal failure pain, fx
● Familial causes (rare) ● Psychic moans =
lethargy, fatigue,
depression

Hyperparathyroidism
● Age at dx = 5256 y/o
● 3:1 F:M ratio
● 21 in 100,000
Renal Osteodystrophy
● affects 90% of dialysis pts
Hypoparathyroidism
PITUITARY ADENOMAS
● primary–
o 85% from single
parathyroid adenoma →
() FB on parathyroid is
lost
o 15% from multiple
gland hyperplasia →
increase in cells
o <1% from parathyroid
carcinoma
● secondary– initiated by
another organ (M/C kidney)
● Tertiary– bone disease
● renal ds→ reduced
circulating vit d levels due to
decreased nephron mass
● deficient PTH activity which
causes dec ionized Ca2+
● M/C/C = thyroidectomy
● Autoimmune
● Congenital
● Metal overload
● Asymptomatic
● Possible non specific sxs
● most will have osteitis
fibrosa
● Increased neuromuscular
excitability
● Chvostek’s sign– twitching
of upper lip after tapping on
facial nerve below zygomatic
arch
● Trousseau’s signcarpal
spasm after inflating a cuff
on upper arm above SBP for
23 min
● Often discovered incidentally
on labs w/ hypercalecemia
noted
● PE – noncontributory
● Labs– total/ ionized Ca2+,
albumin levels, PTH
● Imaging studies used to
guide surgeon once surgical
therapy decided
o Sestamibi scan
o U/S of neck
o CT/MRI
● decreased vitamin d/
hypocalcemia →
persistent
hyperparathyroidism
● Hypocalcemia
● Labs– PTH, vit D, calcium,
magnesium, phosphorus
● Primary
o Mild = observe
o Parathyroidectomy for
sx/ severe
● Secondary
o Medical management
o Correct vit d deficiency
● For underlying CKD →
reduce PTH levels = dietary
phosphate restriction,
phosphate binders, calcium
supplementation limited,
calcitriol
● Indications for surgery=
bone pain/ fx, pruritus,
calciphylaxis, extraskeletal
nonvascular calcifications,
elevated PTH despite med
therapy, refractory
hypercalcemia/
hyperphosphatemia
● f/u calcium labs x several
months after surgery
● calcitriol 0.51 mcg daily
● calcium carbonate
supplementation 13 grams
daily
● phosphate restriction
● Calcium + vit d
supplementation/ diet rich in
calcium containing foods
● Parathyroidectomy/ perform
auto transplantation
● Treat underlying cause if
possible
● Necessary to wear bracelet
that ID them as having
disorder
 ● NonFunctional Adenoma= 10% of all pituitary adenomas
o Can be w/ or w/o sx, but all labs are normal
o If no sx = monitor q 612 months & repeat MRI yearly
● Microadenomas = < 1 cm
● Macroadenomas = > 1 cm
● Clinical manifestations= temporal field defects (unilateral/ bilateral), decrease visual activity, diplopia, ptosis, HA
● Labs= Prolactin, GH, IGF1, AM cortisol, ACTH, 24 hr urine for free cortisol, FSH,LH,TSH, FT4, testosterone
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● Pregnancy/ lactation ● Women= amenorrhea/ ● Visual exam/ visual fields by ● Long life management/ f/u
Prolactenoma oligomenorrhea, confrontation ● Dopamine Agonists
galactorrhea, infertility, dec ● Breast exam →glactorrhea/ o Cabergoline
libido, wt gain, mild gynecomastia o Bromocriptine
● Prolactin hypersecretion
hirsutism ● Beta hCG →r/o pregnancy (FIRST LINE)
● M/C/C of microadenomas in
brain ● Men= dec libido, low ● Prolactin (PRL) > 100 ● Repeat PRL x 1 month after
testosterone, impotence, ng/mL(normal is <20 med initiation & MRI in 612
● F>M
infertility, dec muscle mass, ng/mL) months
● 85% have long term
visual changes, ● Labs= PRL, TSH, ● Transsphenoidal pituitary
remission, 15% have testosterone, LH/FSH, LFT,
recurrence gynecomastia, dec energy, adenomectomy – 2ndline/ pts
osteoporos BUN/ Cr intolerable to meds, mass too
● MRIof pituitary w/ & w/o large
** Prolactin→maintains
contrast → confirm dx ● Radiation therapy – 3rdline
lactation, decreases reproduction
fxn, suppresses sexual drive
● almost always due to ● Extremity enlargement, ● Elevated GH/ IGF1 ● Transsphenodial
Somatotropinoma pituitary adenoma hands bulky w/ moist elevated(best test) microsurgery = FIRST
● 40% due to mutation of alpha handshake, prominent o Not dx b/c of episodic LINE
(GH Secreting Adenomas)
subunit of stimulatory mandible secretion & short ½ life ● Dopamine antagomist –
guanosine triphosphate ● Carpal tunnel syndrome ● Abnormal 2 hr GTT cabergoline/ bromocriptine
● Leads to excessive IGF1 ● Somatostatin analogs
binding protein ● Arthralgia/ degenerative ● High serum insulin
● 2ndM/C pituitary tumor (Ocetreotide LAR/
● Gigantism –prepubescent arthritis ● Glucose Suppression test –
● Mean age – 4050 y/o Lanreotide)
adolescent before fusion of ● Hypertrophic most specific
● M=F ● Radiation – 3rdline; need to
epiphyses of long bones cardiomyopathy o GH > 2ng/mL =
● Uncommon be followed q 6 months for
● Acromegaly(adults only) ● Glucose intolerance/ diagnostic (in healthy
● 15% GH/ another anterior
hyperinsulinema pts GH is suppressed
● HA, visual loss (bitemporal below 2) pituitary fxn
hemianopsia) ● MRI of pituitary – r/o tumor ● Recheck GH/ IGF1 levels
● Dec libido, impotence, 46 wks after surgery (add
irregular menses, amenorrhea drug if still high)
● Obstructive sleep apnea o GH < 2 →f/u GH &
● Sx develop insidiously IGF1 q 6 months to 2
~510 yrs yrs q yearly
● At risk fro colon CA – early
colonoscopy
● Benign microadenomas (<10 ● Insidious onset ● AM cortisol/ ACTH ● Transsphenoidal resection
Cushing’s Disease mm or 1 cm) ● Central obesity ● 24 hr urine collection for of pituitary adenoma –
● Moon faces free cortisol→high FIRST LINE

● More common in F
● Onset age = 2040
● Accounts for 70% of
cushing’s syndrome
Thyrotropin – Secreting
Pituitary Adenoma
Gonadotropin Secreting
Pituitary adenomas
Androgen Secreting
Tumors
(Ovaries or adrenal)
● Excess ACTH by tumor from
anterior pituitary tumor
● rare
● Very rare
● Adrenal cause of amenorrhea
● Plethora
● Thin extremeties
● Easy bruising/ purple striae/
hyperpigmentation
● Acne, hirsutism
● Supraclavicular fat pads
● Myopathy
● HTN, IGT, depression
● Sx of hyperthyroidism w/
goiter
● DOES NOT have systemic
manifestaitons of Grave’s ds
(ophthalmopathy or
dermopathy)
● Visual changes (w/ large)
● Sx of hypogonadism
● Wt loss
● Anorexia
● Bloating
● Back pain
o > 125 mg/dL in 24 hr – ● Radiation Therapy
diagnoistic o Pt w/ persistent/
● Low doseover night 1 mg recurrent after surgery
dexamethasone suppression ● Ketaconazole or Metyropone
test; > 5 ng/mL is diagnostic o Block adrenal steroid
● Highdose dexamethasone synthesis
suppression test o Used if surgery is not an
o Differentiate btwn option
cushing’s ds & ectopic
ACTH or adrenal tumor
o > 50% = pituitary (need
MRI)
o <50% = ectopic ACTH
(CT chest/ abd rec)
● Midnight salivary cortisol
test
● MRI of pituitary to r/o
pituitary adenoma
● High TSH, FT4, FT3 ● Transsphenoidal Surgery
● MRI to look for tumor ● Somatostatin agonist –
normalize TSH/ FT4
● Radiation therapy
● Radioactive iodone therapy
or thyroidectomy
● Increased FSH & normal/ ● Surgery
high LH ● Radiation (if needed)
● Increased alpha subunit
● Elevated serum estradiol
● High testosterone > 200 ● Surgical resection
ng/dL & DHEAS > 700
ng/dL
● Ct scan to confirm dx

DIABETES INSIPIDUS (DI)

● “excretion of tasteless urine”
● Inability of kidneys to produce concentrated urine b/c lack of hormone vasopressin/ lack of response to hormone
● Deficient ADH action →passage of large amounts of very diluted water
● Two kinds: C entral/ Neurologic & Nephrogenic
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● Autoimmune ● polyuria, polydipsia, nocturia ● History – water drinking ● Desmopressin (synthetic
Central/ Neurologic DI ● Hypophysectomy colorless urine, dehydration patterns, urinary behavior, vasopressin)
● Surgery ● infants– irritability, crying, family hx ● Monitor q 612 months
● Idiopathic growth retardation, ● Exam is usually normal ● Pt edu – avoid dehydration/
● Failure of pituitary to secrete
● Familial hyperthermia, wt loss ● Labs– CMP, UA, urine water intoxication
ADH
● Tumors/ cysts sodium, serum/ urine
 ● Interruption to blood supply ● children– enuresis, osmolality (SG < 1.005,
from head trauma anorexia, linear growth urine osmolality < 300)
● 3rdtrimester pregnancy defect ● Water Deprivation Test
● chronic renal disease ● high volume of daily urine ● Vasopressin Test ● Tx underlying cause if
● hypokalemia ● MRI of pituitary w/ & w/o possible
● hypercalcemia contrast – r/o tumors ● Diuretic/ salt restriction
Nephrogenic DI
● protein starvation ● Monitor q 612 months
● sickle cell ● Pt edu – avoid dehydration/
● kidneys failure to response to
● Sjogren water intoxication
circulating ADH
● Lithium toxicity
● Other meds
● Congenital defect

METABOLIC BONE DISEASE

Osteoblasts ● Located on surface of bone/ osteoid
● Synthesize/ secrete components of bone matrix
● Can give rise to osteocytes→when cell is encased by osteoid matrix that
it synthesizes itself
o Actively involved w/ maintenance of bony matrix
Osteoclasts ● Responsible for bone resorption
o Lie in resorption craters (Howship lacunae) on
bone surfaces/ in deep cavities (cutting cones)
o Secrete protons, proteases, proteoglycandigesting
enzymes →acid hydroxyapatite crystals releasing Ca2+
● Derived from macrophages
Fxn of bone ● Provides rigid support to extremities & protects vital organs
● Assure normal locomotion & strong site attachments for muscle
● Provide large reservoir of ions such as Ca2+, Mg+, Phosphorus
● Houses hematopoietic elements
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● M/C/C = aging, high dose ● Usually asymptomatic until ● PE →low body wt (BMI ● Prevention= adequate
Osteoporosis corticosteroid admin, fractures occur <19) + signs Ca2+/ vitamin D intake,
alcoholism, smoking, sex ● Loss of height ● Labs– calcium, phosphate exercise, tobacco use, ID/ tx
hormone deficiency PTH normal; alk phos alcoholism, d/c steroids asap
● “silent thief”
● RF:white, female, early normal unless fx or use at minimal dose
● skeletal disorder
menopause/ late menarche, ● Osteonecrosis of the jaw→ ● xray ● Estrogen Treatment– used
characterized by ● DXA scan→determines bone
amenorrhea, postmenopausal possible complication of for prevention; available
compromised bone strength, density of lumbar spine/ hip
state, thin build/ small bisphosphate usage PO/transdermal
predisposing to inc risk of fx o Est/ confirm dx, predict
● M/C metabolic bone ds in US stature, smoker, ETOH,
immobility, family hx, use of future fx risk, assess ● Weight bearing exercise
● Primary= reduced bone
systemic steroids, heparin, changes in bone mass ● Endocrine consult
mass/ fx in postmenopausal
● Vertebroplasty/ kyphoplasty
 or older men/ women
(Senile)
● Secondary= bone loss
resulting form specific
disorder (hyperthyroidism,
immobilizaitons,
hypervitaminosis A)
Paget’s Disease
● 2ndM/C bone ds
● focal disorder of bone
remodeling characterized by:
o accelerated rate
bone turnover
o disruption of normal
architecture of bone
o gross deformity of
bones
● unusual < 40 y/o
● rare < 25 y/o
● M:F = 3:2 ratio
Vitamin D Deficiency
● Absorbed via diet/ sun →
liver →kidney to become
active vitamin D
● Fxn →increase Ca2+
absorption in SI/ kidney,
insulin secretion,
immunomodulation, bone
resorption/ remodeling
thyroxine, anticonvulsants,
chemo, lithium
● chronic slow viral infection
of bone
● paramyxovirus/ measles
● familial clusters of disease
● Inadequate sun exposure
● Poor vitamin d intake
● Malabsorption
● Darker skin →interferes w/
cutaneous synthesis
● Synthesis in skin declines w/
age
● Medications
(anticonvulsants,
glucocorticoids)
● asymptomatic – 7090%
● bone pain = M/C compliant if
they do complain
● skeletal deformity
● fx
● hat size increases
● bones near to surface may
feel hot
● complications
o CNS: compression of
nerves, deafness, HA
o Rheum: OA, gout
o Cardiac: CHF
o Metabolic:
hyperuricemia, gout
o Neoplastic:
osteosarcoma,
fibrosarcoma,
chondrosarcoma
● Often silent
● Children = bowing of legs
● Adults = chronic muscle
aches/ pains
o Measure in women > 65,
men > 70, F/M 5070
w/ known RF
o T 1 to 2.4 = osteopenia
o T < 2.5 =
osteoporosis o T<-
2.5 + fx = severe
** repeated q 23 years w/
normal levels, or 12 yrs in
those undergoing tx
● increase alk phos level →
bone turnover
● incidental finding on routine
xray
o pelvis, femur, skull,
vertebrae = M/C
involved
● Low vitamin D levels (25
OH)D
● Elevated PTH levels
● Meds for bone formation
→vitamin D, bisphosphates,
PTH
● Meds to reduce resorption
→bisphophates, SERM
(raloxifene), calcitonin,
Forteo
● Prognosis= good if detected
early; fx may lead to chronic
pain, disability, death
● pt edu→prevention, RF,
DXA scan, benefits of
exercise, no smoking, limit
EToh
● GOALS→ relieve sx/
prevent complications
● Physical therapy
● Bisphosphates
● Acetaminophen/ NSAIDs
● Calcitonin (only if
bisphophates C/I)
● Various methods
● No standard tx regimen
exists
● Ergocalciferol (vitamin d2)
= most widely used form of
vitamin d
o Stimulates calcium/
phosphate absorption
from SI
 (activates osteoclasts &
induction of osteoblasts)
Rickets
Osteomalacia
REPRODUCTIVE & GONADAL DISORDERS (MALE/FEMALE)
Gonadal Hormone production
Evaluation of Male Gonadal Fxn
● Minimal amts of vit d in
human breast milk
● Occurs in children w/ open
growth plates
● Vitamin d deficiency –
M/C/C
● Hereditary= x linked
hypophosphatemia
● Lack of sun exposure
● Occurs in adults w/ closed
epiphyses
● Lack of sun exposure
● Lack of vitamin D intake
● Certain surgeries
● Celiac sprue
● Chronic pancreatitis
o Promotes calcium
release form bone into
blood
● Bulbous knobby ● prevention
deformities of knees, ankles, o breast feeding
costochondral jxn (rachitic ● vitamin d supplementation
rosary)
● Dental abnormalities
● Impaired/ poor linear growth
● fractures
● Bone pain ● Prevention
● Muscle weakness o Inadequate sun
● Looser’s zones/ Milkman’s exposure/ aging,
pseudofractures pregnant, lactating =
8001000 IU daily + sun
o Malabsorption = 50000
IU vit D2 q weekly
o Interactive meds =
50000 IU vit D2 q 1,2,or
4 weeks
● Vitamin d supplementation
+/ UVB radiation (tanning
bed or portable UVB device)
● Braces
● surgery
● Hypothalamus releases GnRH is secreted in pulses q 90120 min →stimulates
LH & FSH
o In men– LH stimulates testosterone production & FSH
spermatogenesis
▪ Testosterone, DHT, DHEA, estradiol produced by testes
▪ 95% of testosterone is produced by leydig cells (the rest is
produced in adrenal/ peripheral tissues)
▪ 60% is bound to sex hormone binding globulin (SHBG)
▪ 2% is not bound to protein
▪ total testosterone →DHT via 5 alpha reductase enzyme
● DHT induces formation of prostate & external male
genitalia, pubic hair
o In women– LH causes ovulation & FSH stimulates ovarian follicle
maturation
● DHT reduces LH pulse frequency
● Estradiol reduces LH pulse amplitude
● Androgen deficiency during 23 months of fetal development →ambiguous
genitalia

General labs to evaluate testicular fxn
TX of Hypogonadism
Female Reproductive Endo/ Infertility
DISEASE CAUSE
● Accumulation of
Polycystic Ovarian incompletely developed
Syndrome (PCOS) follicles in ovaries due to
anovulation
● M/C/C of chronic
anovulation ● Associated w/ increased
ovarian androgen production
→LH > FSH = testosterone
production
● Genetic link
o Leydig cell aplasia= defective development of testicular Leydig cells
caused by mutation of LH receptor
● Prepubertal androgen deficiency → poor secondary sexual development
o Fail of penis to enlarge, small testes, failure of marked rugae
characteristics of puberty due to failure of scrotum to develop
o Voice remains high pitch, decrease muscle mass, decrease axillary/
pubic hair
o Absent/ sparse facial, chest, upper abd, back hair
● Deficiency after puberty →dec libido, ED, low energy/ decrease facial & body
hair growth
● Semen Analysis – 3 samples over 23 month pd
● Check AM total & free testosterone
● Sex hormone binding protein/ globulin
● Check LH & FSH & Prolactin
** low testosterone w/ low/ normal LH & FSH →hypothalamic or pituitary
hypogonadism
** low/ normal testosterone w/ high LH & FSH →gonadal failure (primary)
● Testosterone Therapy– IM testosterone enanthate, androderm patch, testim,
androgel, axiron
o Check CBC, LFT, PSA before starting therapy
o w/o tx until male reaches 13
o C/I w/ prostatic carcinoma
o Adverse rxn: erythrocytosis (polycythemia), gynecomastia, priaprism,
acne, aggressive behavior, worsening sleep apnea, CV risks
o Monitor PSA/ DRE initially & then yearly due to increase risk for
prostate CA
● LH cause ovulation & FSH stimulates ovarian follicle maturation
● Follicular phase→release of GnRH stimulates secretion of FSH →binds to
ovarian granulosa cells →thecal androgen to estrogen conversion & follicular
maturation →secretion of estradiol →pituitary LH surge
● Luteal phase→LH surge →release of mature oocyte →corpus luteum
secretes progesterone, estradiol, & inhibits androgen →suppression of GnRH/
FSH →corpus luteum dissolves & menstruation occurs
SIGNS/SYMPTOMS LAB/DX TREATMENT
● Menstrual abnormalities ● High total testosterone ● Life style modifications –
oligomenorrhea or ● High DHEA/DHEAS appropriate diet/ exercise
amenorrhea ● High total insulin ● COCPS
● Hyperandrogenism – acne, ● Low SHBG ● Spironolactone
hirsutism, male pattern ● High LH/FSH ratio ● Metformin for insulin
baldness/alopecia ● US – polycystic ovaries resistance
● Infertility ● Clomiphene citrate/ low dose
● Insulin resistant gonadotropins
● Central obesity ● Complications:infertility,
● Metabolic syndrome risk for endometrial CA, risk
● DM type 2 for type 2 DM/ gestational

Primary Amenorrhea ● Gonadal gysgenesis (turner’s
syndrome)
● Hypothalamic pituitary
insufficiency
● Androgen insufficiency
● Imperforate hymen
● Outflow tract disorders
● Anorexia
Secondary Amenorrhea ● Pregnancy – M/C/C
● PCOS
● Premature ovarian failure
● Wt related amenorrhea
● Hyperprolactinemia
● Exercise related
● hypopituitarism
● Outflow obstruction of
menstrual blood flow
● Imperforate hymen
Cryptomenorrhea
● Transversevaginal septum w/
functioning uterus
● Isolated vaginal agenesis w/
functioning uterus
● Isolated cervical agenesis w/
functioning uterus
HYPOTHALAMIC ● Genetic, endocrine, anatomical causes (developmental defects, brain tumors, infiltrative ds I.E = Sarcoidosis, hemochromatosis, lymphoma)
AMENORRHEA ● Check serum estradiol or progesterone withdraw test →
o (+) = use it q 3 months to avoid endometrial hyperplase
o () = may need HRT
Functional Hypothalamic ● Malnutrition
Amenorrhea ● Excessive exercise
● Sleep apnea DM, CV disease,
dyslipidemia, hepatic
steatosis, obstructive sleep
apnea, HTN
● No menses by age 16 but ● History ● Treat medical condition
normal growth/ secondary ● Physical exam ● OCPs
sex characteristics OR ● TSV sonogram ● Progesterone alone
● No menses & no onset of ● REFERALLS ESP > 30
puberty by age 14 GENERAL WORK UP Y/O
● FIRST R/O PREGNANCY ● Reassurance
● Progesterone w/draw test
(Provera 10 mg x 510 days) ● Those who desire pregnancy
● No menses for more than 3 o (+) = anovulation
cycyles in a women who has o () = estrogen deficiency/ o Bromocriptine –
previously cyclic menses OR outflow tract abn suppress secretions of
● No menses for 6 months if ▪ inc FSH/ LH = prolactin
previous cycles irregular ovarian failure o Clomid induces
▪ low/ normal ovulation
FSH/LH = CNS o Gonadotropins –
pituitary dysfxn FSH/LSH
● Intermittent abd pain ▪ now W/D bleeding ● Surgical intervention needed
● Possible difficulty w/ w/ E & P test =
urination outflow tract
infection
● Possible lower abd swelling
● Bulging bluish membrane at ● Check TSH, FT4
introitus ● Check LH/FSH
● Measure prolactin
o High prolactin, normal
TSH/FT4 = MRI of
brain to r/o pituitary
adenoma
o High/ NL prolactin w/
high TSH/ low FT4=
primary hypo
● Check DHEA, DHEAS &
total testosterone
o High = PCOS, androgen
–secreting tumor
● Low/ low normal FSH/ LH ● Reversible
→anovulation
● M/C/C of amenorrhea ● Psychological stress
● Dysfxnal release of GnRH
Exercise Induced ● women who participate in ● TRIAD = eating disorder, ● Exercise → severe
Amenorrhea competitive sports: amenorrhea, osteoporosis depression of GnRH →low
gymnastics, ballet, estradiol level
marathons, running,
swimming/diving
Amenorrhea associated w/ ● Anorexia Nervosa; mean age ● A.N = body wt < 85% ● Hypothalamic suppression → ● Psychiatric referral
eating disorders = 1314 normal age/ ht severe dec in GnRH →low ● Need to gain weight
● Could be primary or ● Bulimia ● Usually normal body wt w/ LH/FSH →low estradiol
secondary bulimia
PITUITARY ● Genetic Causes: GnRH receptor gene mutation →LH/FSH def
AMENORRHEA ● Endocrine causes:
o hyperprolactemia →high PRL suppresses GnRH secretion; 50% w/ pituitary tumor
o Craniopharyngioma
● Anatomic causes: Autoimmune disease (lymphocytic hypophysitis), pituitary necrosis, heehan’s syndrome
● Pituitary inability to secrete ● Inability to breast feed ● labs– FSH/LH, PRL, TSH, ● Replacement of deficient
gonadotropins ● Fatigue AM cortisol, ACTH, hormones
● Postpartum pituitary ● Wt loss GH/IGF1 ● Watch for minor illnesses →
Sheehan Syndrome
ischemia/ necrosis ● Lack of menstrual bleeding *** all hormones are low = can lead to crisis & may
(postpartum ● Severe HTN ● Loss of pubic hair/ axillary panhypopituitarism require adjustment of
hypopituitarism) hair ● CT/ MRI of pituitary– r/o hormones
● Low BP tumors
● Hypothyroidism
● hypocortisolism **Dx based off clinical evidence
of hypopituitarism w/ hx of
postpartum hemorrhage
OVARIAN ● Ovarian failure cause by depletion of ovarian follicles
AMENORRHEA ● Clinical picture of amenorrhea & FSH > 40 IU/L
● Causes: Premature ovarian failure, menopause, autoimmune destruction, iatrogenic ovarian injury causing POF (chemo, radiation, torsion w/
surgery)
● Possible genetic ● Irregular periods/ skipping ● low estradiol < 50 pg/mL ● Hormone replacement
● Depletion of ovarian follicles periods, amenorrhea ● FSH > 40 therapy
● RF: age, family hx ● Hot flashes ● Support
Premature Ovarian Failure
● Night sweats ● Complications= infertility,
(before age 40) osteoporosis, psych:
● Vaginal dryness
● Irritability/ mood swings depression/ anxiety
● Dec libido
OTHER CAUSES ● Thyroid Disorders– Hyper/Hypothyroidism
AMENORRHEA ● Outflow Tract Disorders–, Asherman’s syndrome
o Mullerian agenesis– M/C/C of primary amenorrhea; normal ovaries & female sexual charactertistics; shortened or absent vagina & NO
UTERUS
o androgen insensitivity syndrome (AIS) – minimal sexual hair, male karyotype w/ mutation of androgen receptor on x chromosome,
normal testicular development (but not external male sexual structure= female phenotype)

Precocious Puberty
Kallmann’s Syndrome
● 1 in 10,000 – 86,000 ppl
● M>F
o congenital outflow obstruction– Transvaginal septum & imperforated hymen, present of cyclic lower abd pain/ amenorrhea, presence
of uterus; needs to be surgically corrected
o Asherman’s Syndrome– intrauterine adhesions (from uterine surgery) →menstrual disturbances, infertility, recurrent spontaneous
abortions
▪ Dx via hysteroscopy & () w/draw bleeding w/ estrogen & progesterone test
▪ OBGYN ovulation needed & tx w/ lysis of adhesions & HRT
● Post infection (mumps), Post radiation, Post chemo
● Contraceptive related–
o Post pill amenorrhea failure to resume menstruation w/in 6 months after d/c of OCP due to disruption of hypothalamic pituitary
ovarian mechanism
o Mirena IUD
o Depo Provera– amenorrhea after 1styear of use; this is reversible
● Puberty onset before age 8 in girls/ 9 in boys
● Develop tall stature during childhood but become short as adults due to early epiphyseal fusion of long bones
● Central/ complete/ true precocious puberty (CPP)– early/ premature activation of maturation of hypothalamic GnRH production
o M/C idiopathic
o CNS tumors
● Incomplete isosexual precocious puberty/ precocious pseudopuberty/ peripheral precocious (PPP)– ectopic gonadotropic secretion
(nonGnRH produced)
o Less common
o Presence of sex steroids is independent of pituitary gonadotropin release & w/o involvement of GnRH
CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● GIRLS ● GIRLS ● High early morning ● CPP
o Follicular cysts o Breast/clitoris testosterone in boys o GnRH analog – only tx
o Granulosa/ theca cell enlargement ● High estradiol levels in girls (Lupron, Histrelin,
tumors o pubic/ axillary hair ● High DHEA/DHEAS Nafarelin acetate)
o Adrenal rest trissue o menarch – 23 yrs after ● Low LH/FSH ● PPP(depends on cause)
o Exogenous estrogen breast enlargement ● 17OH serum progesterone – o Medical
admin o pubertal growth spurt r/o CAH o Surgical
o Hypothyroidism ● BOYS ● TSH – r/o hypothyroidism ● GOAL= suppress episodic
o McCuneAlbrigth o Testicular enlargement ● Beta hCG secretion of gonadotropins
Syndrome o Growth of penis/ ● GnRH stimulation test w/ ● Refer to peds endo
● BOYS scrotum leuprolide (LH/FSH will be ● f/u q 46 months to ensure
o Gonadotropin secreting o Appearance of pubic elevated in CPP) progression of puberty has
tumor hair ● Xray of hand to determine been arrested
o Autonomous androgen o Pubertal growth spurt bone age ● GnRH agonist can be
secretion ● MRI of brain – r/o pituitary stopped once age appropriate
tumors puberty is reached
● Pelvic sonogram, US testes,
CT pituitary – r/o tumors
● Congenital ● Decreased sense of smell ● Low GnRH ●
● Idiopathic ● Men= decreased libido, ED, ● Low testosterone
dec muscle strength ● Low FSH
● Women= amenorrhea

Klinefelter’s Syndrome
● M/C cause of genetic
hypogonadism
● 1 in 5000 male births
Noonan’s Syndrome
Bilateral Anorchia
(Vanishing Testes
Syndrome)
● 1 in 20,000 males
● 3% of phenotypic boys that
undergo surgery to correct
uni or B/L cryptorchidism
are found to have absence of
1 or both testes
Cryptorchidism
Myotonic Muscular
Dystrophy
● One extra X chromosome –
mostly XXY
● Abnormal development of
seminiferous tubules,
azoospermia, abnormal
leydig cells
● Inherited autosomal
dominant
● ½ have mutation in PTPN11
gene on chromosome 12
● associated w/ seminiferous
tubular size w/ or w/o
sclerosis, diminished or
absent germ cells & leydig
cell hyperplasia
● embryonic development
● testosterone deficiency
during 3rdtrimester of
pregnancy
● failure of testes (one or both)
to descent in scrotum
● spontaneous descent occurs
during 1styear of life
● familiar form of muscular
dystrophy
● Type 1 – 80% affected males
are associated w/ primary
testicular failure
● Diminished facial/ body hair
● Persistent gynecomastia
● Small/ firm testes
● Insufficient libido/ infertility
● Abnmoral skeletal
proportions
● Intellectual impairment/
lower IQ
● Dyssocial behavior
● Inc risk for COPD,
extragonadal germ cell
tumors, CVA, glucose
intolerance, primary
hypothyroidism, breast CA
● short statue
● webbed neck, hypertolerism,
cubitul valgus, unusual chest
shape (usually sunken chest
→pectus excavatum)
● congenital cardiac anomalies
● cryptorchidism
● appear during puberty
● small penis
● decreased axillary/ pubic hair
● empty scrotum
● unable to palpate testis in
scrotal sack
● unilateral M/C
● Progressive muscle weakness
& atrophy of face, neck,
hands, LE muscles
● Testicular atrophy noted in
adult hood
● Normal/ low testosterone
● High LH/FSH
● High estradiol
● Azoospermia
● Chromosomal analysis →47,
XXY
● low/ normal testosterone
● high LH/FSH
● 46 XY karyotype
● very low testosterone
● markedly high LH/FSH
● 46 XY karyotype on
chromosome analysis
● found on PE
● Testosterone replacement
therapy: 200 mg IM q 24
wks
● Prognosis
o Pt feel better w/
androgen replacement
o Personality defects do
no improve & they
require long term
psychiatric counseling
● testosterone replacement
therapy
● testosterone replacement
therapy
● implantation of testicular
prostheses for cosmetic
purposes
● surgery by age 2
● complications– inc risk of
inguinal hernia, torsion,
testicular CA, infertility
● No therapy to prevent
progressive muscular atrophy
● Testosterone therapy
indicated only if testosterone
low
 ● Autosomal dominant
● mutation of androgen
Androgen insensitivity receptor
● gonadal tumor
● Initially testosterone
secretion is normal &
secondary sexual
characteristics develop
● After puberty the
seminiferous tubular atrophy
results in dec in testicular
size →infertility
● completeMale, XY w/ testes, ● high LH ● peds endo referall
full breasts but primary ● variable FSH ● surgery
amenorrhea (mix of male/ ● high testosterone level ● psychiatric counseling
female characteristics)
● incomplete– vary; isolated
infertility to ambiguous
genitalia & hypospadias

LIPID DISORDERS
● Cholesterol ● soft, waxy substance found among lipids in bloodstream
● used to form cell membranes + hormones
● high levels in blood →major risk factor for CHD
● LDL ● “bad cholesterol”
● major cholesterol carrier in blood
● high levels →slow build up of plaques in the walls of arteries → restricted blood
flow →MI/ stroke
● HDL ● “good cholesterol”
● carries cholesterol away from arteries & back to liver
● may remove excess cholesterol from fatty plaques/ slow their growth
● high levels → protective
● CAUSES OF DECREASED LEVELS:physical inactivity, smoking, DM,
obesity, anabolic steroids, BB, retinoids
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
Hyperlipidemia ● familial (primary) caused by ● most are asymptomatic ● evidence of CVD/ CHD risk ● USPSTF recommends
genetic abnormalties ● xanthoma – usually indicate equivalent = screened w/ screening those w/ no
● acquired (secondary) – from genetic cause fasting complete lipid profile evidence of CVD at age 35 &
DM, alcohol use, o M/C = xanthelasmas = ● those w/o RF = screened w/ NCEP says 20
hypothyroidism, obesity, affecting eyelids; in 2/3 total cholesterol ● Life style modifications =
sedentary lifestyle, renal/liver ● tendenous xanthoma FIRST LINE
ds, drugs (estrogen, thiazides, ● corneal arcus o Reduce total fat intake to
BB) 2530% of diet,
Hypercholesterolemia ● lifestyle ● Premature arcus senilis ● Increased total cholesterol saturated fat to 7%,
● genetic ● Lipemia retinalis – cream >240 dietary cholesterol < 200
colored retinal vessels mg/day, Mediterranean
diet
o 30 mins exercise daily
 o increase antioxidants via
fruits & veggies; inc
fiber
o CAD prophylaxis w/
low dose aspirin
o Smoking cessation
● Statins = first line pharm tx
● Niacin, bile acid sequestrate,
fibric acid derivatives,
ezetimibe

OBESITY DISORDERS
● Obesity ● Significant increase above ideal body wt due to accumulation of excess body fat,
adversely affecting life expetancy
● BMI ● Wt in kilograms divided by the ht in meters squared
● Wt in pts multiplied by 704, divided by ht in inches squared
● Widely used in epidemiologic research & clinical practice to assess adiposity
● Normal= 18.524.9
● Overweight= 25.0=29.8
● Class I Obesity= 30.0 34.9
● Class II Obesity= 35.039.9
● Class III obesity= > 40
● Waist Circumference (measuring abdominal obesity) ● Males= > 40 inches
● Women= > 35
● Assessment of Obesity ● Measurement of % fat by DEXA →GOLD STANDARD; but its expensive/
used primarily in research
● Bioimpedance →inexpensive & widely used tool; useful in following tx
response
● CT / MRI →measure distribution of body fat; subQ vs. intraabd; useful in
research
● Waist circumference/ skinfold thickness →simple assessment tools; useful in
assessment of body fat distribution
● Thrifty gene hypothesis ● Constant abundance of food in those w/ genotype efficiently prepares individuals
for a famine that never comes
● Leptin ● Mediator of long term regulation of energy balance →suppressing food intake
→inducing wt loss
● In obese →high circulating levels BUT they are leptinresistant
● Ghrelin ● Fast acting hormone
● Plays role in meal initiation
● In obese →decreased levels
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● Small excess caloric intake in ● ● Measure BMI ● Initially reduce caloric intake
Obesity relation to energy ● Measure waist circumference by 5001000 kcal/day
 expenditure over long pd of ● Portion control, split entrée,
time set regular times to eat
● Genetic factors/ ● Limit saturated/ trans fats
susceptibility genes ● Increase daily intake of
● Environmental factors – fetal fruits/ vegs
undernutrition, food intake, ● Increase fiber
physical activity, culture, ● Limit sweetened beverages;
medications, classic drink more water
endocrinopathy ● Physical activity that is
equivalent to weekly
expenditure of 2,500 kcal
● Behavioral modification
therapy
● Bariatric surgery

DIABETES
● RF→physical inactivity, first degree relative w/ DM, high risk race/ ethnicity, women who delivered baby > 9 lbs, HDL < 35, hypertension >140/90, A1c >5.7, conditions
associated w/ insulin resistance (severe obesity, acanthosis nigricans, PCOS), CVD history
● TO DIAGNOSE DM:
o A1c > 6.5%, FBG > 126 or 2 hr >200 during OGTT or random PG > 200
● Type 2 DM testing→ all individuals overweight/ obese w/ > 1 DM risk factor, testing starting at 45, if normal results →3 year interval repeat testing
● Pre – DM testing→A1c, FPG, 2 hr PG after 75 g OGTT, identify/ treat other CVD risk factors, consider testing in children/ adolescents who are overwt & have > 2 DM risk
factors
● Gestational DM→screen at 2428 wks
DISEASE CAUSE SIGNS/SYMPTOMS LAB/DX TREATMENT
● Abnormalities in ● Begin w/ FPG < 60 ● Depend on suspected cause ● Tx underlying cause
Hypoglycemia mechanisms involving ● AMS @ < 50 ● Counter regulatory hormones ● Glucose 1520 g
glucose homeostasis o Glucose = predominant →inc in E/ NE, glucagon, ● Glucagon w/ risk of severe
● Secondary to endocrine metabolic fuel of brain cortisol, GH
● Reduction in plasma glucose
disorders →survival dependent
concentration to a level that
● Liver malfunction/ renal on cont. supply of
may induce s/sx
failure glucose from peripheral
● GI surgery/ dumping circulation
syndrome
● Functional B cell dysfunction
● Alcohol related
● Drug induced
Hypoglycemia w/o DM ● Adenoma of islets of ● WHIPPLE TRIAD→ hx of ● Serum insulin + Cpeptide ● Surgical resection
langerhans → hypoglycemia, confirmed BG (for endogenous insulin)+ ● Diazoxide until surgery
insulinoma of 45 or <, immediate proinsulin levels in presence ● AE = sodium retention, CHF,
● 90% benign recovery w/ glucose admin of hypoglycemia hirsutism
● rare ● Sulfonylurea screen ()
● can be associated w/ MEN ● Ketone levels low
● type
25% 1of general non obese, ● insulin resistance similar to ● TRI > 150 ● Much higher risk of
non diabetic population DM type II ● HDL < 40 developing DM type II,
 Metabolic Syndrome
(PreDiabetes/ Syndrome
X)
Type I DM ● Autoimmune 90%
● Little to no endogenous
insulin secretion
● Plasma glucagon elevated
● Pancreatic B cells fail to
respond to stimuli→
destruction
● Mumps, coxsackie B4 virus
infection
● Toxic chemicals
● Young age
Type II DM ● Genetic
● Ethnicity: American Indians/
Alaskan Natives w/ highest
risk
● Middle to older age
● Overweight/ obesity
● Infections – 3050%
● Inadequate Insulin tx
2040%
● MI, Ischemia, infarct (silent
Diabetic Ketoacidosis
in DM) – 36%
● CVA
● M/C W/ DM TYPE 1
● 3 Ps →polyuria, polydipsia,
polyphagia
● rapid weight loss despite
normal appetitive
● blurred vision
● pruritis
● weakness
● postural hypotension
● paresthesias
● vulvovaginitis
● untreated can lead to DKA
(see sx above)
● Polyuria, polydipsia
● Ketonuria/ wt loss RARE
● Fatigue
● Pruritus
● Recurrent candida vaginitis
● Chronic skin infections
● Blurred vision
● Poor wound healing
● 3 Ps →polyuria,
polydipsia, polyphagia
● Wt loss
● Vomiting
● Abd pain (mimics
appendicitis)
● HTN
● IFG > 100 125
● Waist circumference > 40 for
M/ > 35 for W
● A1c – 5.76.4
● random PG > 200 w/ classic
sx or FPG > 126
● A1c
● limited to 33 mg/day, high
● FPG 100125
● Diabetic dyslipidemia w/
high TRI, low HDL,
alterations in LDL
● pH < 7.30 to <7.00 if severe
● plasma glucose > 250
● serum bicarb 1018
● urine ketones ++
● serum ketones ++
● anion gap > 10
increased risk for elevated
plasma TRIs, lower HD,
higher BP
● Diet →well balanced; 45-
65% carbs, 1035%
protein, 2535% fat, chol
fiber
● Multiple dose
insulin injections or
continuous subQ
infusion
● Exercise
● Flu, penumococcla, Hep B
vaccine
● Continuous glucose
monitoring
● Low dose ASA
Diet
● Exercise
● Oral hypoglycemic agents
o M/C sulfonylureas
● Metformin = DOC
● Thiazolidinediones
● Insulin
● Careful foot care, meticulous
personal hygiene, promote tx
of infections
● Daily ASA (81 mg)
● HTN therapy for BP 130/80
● HDL < 100
● Annual ophthalmologic
exams, urine albumin, serum
creatinine
● Flu, pneumococcal, Hep B
vaccine
● Bariatric surgery for those w/
BMI > 35
● 5% death w/ treatment
● IVF – large bore catheter (1L
w/in first hour)
● Insulin Bolus (will correct
high extracellular K+)
 ● PE ● Dehydration – tenting of ● elevated serum K+ ● Electrolyte Replacement →
● Obstruction skin, dry mucosa, no tear Na, K, Phosphate, Mg,
● RF production in children Bicarb (don’t treat K+ w/
● Burns ● Clouded sensoria replacement until neutralize
● Prescription ● PE→poor skin turgor, insulin)
● Drug related hypotension, AMS, shock,
KUSSMAUL respirations
● Stupor ● pH > 7.30 ● fluid replacement
Hyperosmolar ● Coma ● plasma glucose > ● Insulin 0.1 unit/kg followed
Hyperglycemic State (HHS) 600 (8002400) by insulin infusion of 0.1
● serum osmolarity > 320 unit/kg/hr then subQ w/
● ~15% mortality
● serum bicarb > 15 levels around 250
● M/C w/ DM type II ● urine ketones – small ● Potassium may be indicated
● serum ketones – small ● Phosphate if severe
● anion gap > 12 hypophosphatemia develops
● during insulin therapy
DM COMPLICATIONS
● DM Neuropathy ● M/C form; consequence of chronic hyperglycemia, affects up to 50%
● Sensory deficits
o Small fibers→loss of temp, pins/ needles, numb, cold, swelling, contact pain
o Large fibers→loss of balance/ position sense, unable to feel feet when walking
o Motor nerve damage→loss of muscle tone in hands/ feet
o Foot deformities→ callus, charcot joint, deformation of toes/ feet, open sores/
ulcers on feet
● Motor neuropathy:leads to muscle atrophy →weakness/ changes in foot shape;
allows flexors to predominate
o Foot takes on a pes cavus shape w/ high arch/ prominent metatarsal head
o Toes become deformed in hammer/ claw shape →irregular wt bearing/ areas of
high plantar pressure
o May lead to subtle changes in posture/ gain →changes in wt bearing/ plantar
pressure
● Charcot Foot→partly related to autonomic neuropathy w/ vasodilation & shunting
of blood flow → bone demineralization/ oosteolysis
o Acute stage= foot warm, swollen, erythematous; BOUNDING PEDAL PULSES
o Pain/ tenderness may be present
o Changes occur in forefoot, midfoot, hindfoot; M/C = collapse of longitudinal
arch
*** pts should check their own feet every day
● Autonomic Neuropathy ● Neurogenic bladder→diminished urinary frequency, incomplete emptying,
frequent UTIs, hydronephrosis, renal calculi, post void residual > 150 mL
● Gastroparesis→delayed gastric emptying, early satiety/ reflux, anorexia, wt loss,
erratic blood glucose levels, hypoglycemia, dumping syndrome
● DM Enteropathy→fecal incontinence, diarrhea (nocturnal)
● CV→orthostatic hypotension, fixed HR, painless MI, sudden death, hypotension w/
exercise
 ● Sudomotor→areas of symmetrical anhidrosis, gustatory sweating
● Pupillary→decreased/ absent response to light, decreased pupil size
● Erectile Dysfxn
o Males= retrograde ejaculation, impotence
o Females= diminished vaginal lubrication, dec frequency of orgasm
● CAD, PVD, CVA ● CVD death rates = 1.7% higher
● MI = 1.8% higher
● Stroke = 1.5% higher
● Blood Pressure ● GOAL = 140/90 or lower
● Tx w/ ACE or ARB
● Dyslipidemias ● Lifestyle modifications
● Reducing Fats
● Wt loss
● Exercise
● Statins
● Nephropathy ● Kidney disease →screen for microalbuminuria at dx for type II, after 5 years of ds w/
type I; serum Cr should be measured annually to measure for GFR in all adults w/
DM
● TX: lifestyle, wt loss DASH diet, EToH, exercise, control HTN w/ ACE or ARB,
monitor serum K+, correct LDL, protein restriction, refer to specialist
● Retinopathy ● RF= duration of DM, age, pregnancy, puberty, genetic predisposition, renal disease,
HTN, smoking, HLD, control of DM
● after 20 years →90% of DM type I/ 80% of DM type II on insulin
● 25% of type II have it by the time they are dx
● Non proliferative Mild→may be reversible, usually asymptomatic, on exam →
vascular microaneurysms, dot/ flame hemorrhages, cotton wool spots, hard exudates
● Non Proliferative modsevere→venous caliber changes/ beading, IRMA, capillary
loss, retinal ischemia, extensive intraretinal hemorrhages/ microaneurysms
● Proliferative→neovascularization
● Other eye disorders ● Common Senile cataracts→occur at younger age/ progress more rapidly
● DM cataracts→rare; associated w/ osmotic abnormalities, can mature in days/
progress rapidly
● Ocular Palsies→diplopia/ strabismus from impairment of extraocular muscles due
to ischemia of CN 3,4,6
● Open Angled glaucoma
● Blurred Vision
● Hypoglycemia visual changes→temporary diplopia, flashing lights, dimming of
vision
● Skin, Teeth ● Skin: Higher risk of infections → furuncolosis/ carbuncles, candida (genitalia, upper
thighs, under breast), cellulitis w/ vascular ulcerations
● Periodontal disease→changes in gum membrane/ microflora, impaired collagen
metabolism, altered leukocyte fxn
● Caries →increased
● Dental exam q 6 months
● Vaccination ● Altered immune fxn
 ● IMMUNIZATIONS = EFFECT/ REDUCE HOSPITALIZATION
o Flu
o Pneumococcal
o Hep B Series
● Clotting Risks ● Increased production of thromboxane
● ASA given to block thromboxane release in type II by acetylating platelet
cyclooxygenase