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8/11/2019 Endocrine Reviews Undana
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Endocrine Review
A. Makbul Aman Mansyur
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Organs of the Endocrine
1.Pituitary gland2. Hypothalamus
(neuroendocrine)
3. Pineal gland
4. Thyroid gland5. Parathyroid gland
6. Thymus gland
7. Adrenal gland
8. Pancreas (also hasexocrine function)
9. Gonads (testes orovaries - also haveexocrine functions)
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PITUITARY GLAND
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What is a pituitary?
Pituita: Mucus
Former Belief That Pituitary Gland
Secretes Mucus
TWO PARTS :ANTERIOR---ADENOHYPOPHYSIS
POSTERIOR--NEUROHYPOPHYSIS
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Pituitary Hormones
Anterior Pituitary
Testosterone
Estradiol
FSH & LHGrowth
HormoneACTH
Cortisol
TSH
T3T4
Prolac
tin
Posterior Pituitary
IGF-1
Oxytocin ADH
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Hypothalamic Releasing
Hormone
Corresponding Anterior
Pituitary Hormone(s)
Gonadotropin ReleasingHormone (GnRH)
Luteinizing Hormone (LH)Follicular Stimulating
Hormone (FSH)
Growth HormoneReleasing Hormone (GRH) Growth Hormone (GH)
Corticotropin Releasing
Hormone (CRH)
Adrenocorticotropic
Hormone (ACTH)
Thyrotropin ReleasingHormone (TRH)
Thyroid StimulatingHormone (TSH)
Dopamine Prolactin (PRL)
Green = stimulatoryRed = inhibitory
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Diseases of the Posterior
PituitarySyndrome of inappropriate antidiuretic
hormone secretion (SIADH) Hypersecretion of ADH
Clinical manifestations are related to enhanced renal water retention,hyponatremia, and hypoosmolarity
Diabetes insipidus Insufficiency of ADH
Polyuria and polydipsia
Partial or total inability to concentrate the urine
Neurogenic
Insufficient amounts of ADH
Nephrogenic
Inadequate response to ADH
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Vasopressin ( ADH)
Control
Increased plasmaosmolality
Decreased bloodpressure(Baroreceptors)
PaO2PaCO2
(cortisol Sex steroidsangiotensin II)
Action
Collecting ducts
permeability for
H2Oreabsorbtion of freewater
Vasoconstriction
Oversecretion of ADH even with low osmolalities
(Schwartz-Bartter Syndrome)
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ADH Syndromes -
Overproduction
Syndrome ofInappropriate
ADH (SIADH) Na+
(20mmol/l)
Brain injury/infection
Guillian Barre
Lung cancer/infection
Drugs
HypothyroidismPorphyria
Test Plasma and urine
osmolality Plasma and urine
electrolytes
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Syndrome of Inappropriate
Antidiuretic Hormone(SIADH)
Etiology: Bronchogenic carcinoma
Severe pneumonia
Pneumothorax
Head injury
Brain surgery
Brain tumor
Meningitis
Pituitary-stimulating drugs
Vincristine
Phenothiazines
Tricyclic antidepressants
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Signs & Symptoms of SIADHConfusion
Muscle weaknesslethargy
Decreased urine output
Increasing urine concentration
Weight gain
Seizures
Clinical Features SIADH
Confusion, nausea, irritable - progressing to seizures and coma
Dilution effect leads to Hyponatraemia (usually
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Management of SIADH
Eliminate underlying cause
Restrict fluids (500-1000 mls/day )
Strict intake & output
Diuretics
Daily weights
Frequent serum & urine chemistries
Frequent neurological checks
Demeclocycline (Demethylchlortetracycline -
tetracycline antibiotic) administered - inhibits ADH
action on renal tubules
Severe cases - Hypertonic saline
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ADH Syndromes -
Underproduction
Diabetes InsipidusPolyuria
Polydipsia
Na+
Plasma osmolality>295mOs/l
Urine osmolality3 l/day)
Cranial Genetic
Surgery
Injury infection
DrugsNephrogenic Genetic (X)
Infection
Drugs
Test Water deprivation test
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Hyposecretion Posterior Lobe-
DIABETES INSIPIDUS
Causes: hyposecretion of ADH
Pituitary tumours
Infection
Trauma
intracranial surgery
Renal Disease
Some drugs
Hypotonic Polyuria (10-15+ litres/day), nocturia, and
compensatory polydipsia - severe dehydrationstroke (CVA)
Hodgkins disease
tuberculosis
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CLASSIFICATIONS OF DI
NEPHROGENIC: Inherited disorder where kidneys do not respond to ADH; no deficiency
in hormone
CRANIAL ( CENTRAL )
PRIMARY:
Defect in pituitary or hypothalamus; lack of ADH production or secretionSECONDARY: Tumors of pituitary or hypothalamus; trauma, infection, surgery,
metastasis of oat cell cancer in lung or breast
DRUGS: Any drug that might interfere with kidneys response to ADH; lithium
carbonate (psych- manic/depressive)PSYCHOGENIC: Client ingests large quantities of water, usually 5 liters or more which in
turn depresses ADH production/secretion
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Investigations:
Diabetes Insipidus
Urine (low/dilute - 100 mosmol/kg)/plasma
Specific Gravity of Urine : 1.003 or less
Serum sodium: moderate increase upto 150
mmol/l when individual has free access to waterIf no free access to water there is an increase in
the plasma osmolality and sodium concentration
(160-170 mmol/l)
8 Hour Water depletion test (Dashe test )Prolonged water depletion test
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Treatment for Diabetes
InsipidusFluid replacement
Accurate intake & output
DDAVP (Desamino-D-Arginine Vasopressin)-
- 10-20 micrograms 1-3 times/day via intranasalroute for maintenance or 1-2 mcg post-operative.
or IM/SC route at 1/10th of dose.
Correct underlying intracranial problem
Wear Medic Alert braceletChlorpropamide (Diabinese), thiazide diuretics formild neurogenic DI
Clofibrateantidiuretic effect
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Diseases of the Anterior
Pituitary- function: Hyperpituitarism
- function: Hypopituitarism
Hypopituitarism Pituitary infarction
Sheehan syndrome
Hemorrhage
Shock
Others: head trauma, infections, and tumors
PanhypopituitarismACTH deficiency, TSH deficiency, FSH and LH deficiency, GH
deficiency
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Sheehans SyndromePituitary infarction associated with uterine hemorrhage at time of delivery
Symptoms: absence of lactation, amenorrhea, fatigue, cold intolerance
Empty Sella SyndromeAn intrasellar extension of the subarachnoid space resulting
in compression of the pituitary gland and an enlarged sella
turcicathat may be associated with galactorrhea and
hyperprolactinemia.
Radiologic finding of decreased pituitary gland volume
Only 10% of patients have hypopituitarism
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Dwarfism
Insufficient secretion of growth hormone (GH)
during childhood that limits growth
Body parts usually correctly proportioned, normal
mental developmentUsually accompanied by deficient secretion of
other anterior pituitary hormonesadditional
symptoms
Treatment with hormone therapy
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hipopituarisme
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Deficiency of growth hormone early in life leads to pronounced
inhibition of longitudinal growth, resulting in dwarfism. The
interrelationship between the pituitary and the thyroid is demonstrated
by the concomitant hypothyroidism secondary to deficiency of
thyrotropic hormone. Therefore, growth is not only stunted but the
development of secondary ossification centers is noticeably delayed,
and the epiphysial and apophysial growth plates remain open late in
adult life, although they do ultimately close in old age. The cranial
sutures remain widely open into adult age. The sella turcica may show
widening, if the tumor was intersellar, or an aperture may remain on the
floor of the endocranial bones. The skeleton is gracile in dimensions,
the cortices are thin, and the spongiosa porotic and sparse. Although
growth plates may remain, the metaphysial surface is usually closed bya thin layer of bone, an indication of arrested growth.
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Diseases of the Anterior
PituitaryHyperpituitarism Commonly due to a benign, slow-growing pituitary adenoma
Manifestations
Headache and fatigue
Visual changes
Hyposecretion of neighboring anterior pituitary hormones
Hypersecretion of growth hormone (GH)
AcromegalyHypersecretion of GH during adulthood
Gigantism
Hypersecretion of GH in children and adolescents
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Hypersecretion of Growth
Hormone (GH)
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Acromegaly
Rare diseaseIncreased morbidity/mortality
Gradual development; 5-15 year delay in diagnosis
Symptoms: acral overgrowth, sweating, diabetes,
HTN, headache, etc.Diagnosis: elevated IGF-1 on two occasions, MRI
brain
Treatment: surgery
Causes of Death Cardiovascular- 38 to 62 percent
Respiratory- 0 to 25 percent
Malignancy- 9 to 25 percent
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Acromegali
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Systemic effects of GH/IGF-I excess
Acral enlargement spade like hands rings too small
Inc shoe size
macroglossia
carpal tunnel syndrome
Increased skin thickness
Increased sweating
Skin tags and acanthosis nigricansChange appearance inter-dental spacing
Visceral enlargement
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Acromegaly - Signs and
SymptomsGH Excess Enlargement of hands and feet
Thick skin
Skin tags
Sweating Sleep Apnea
Carpal Tunnel Syndrome
Glucose intolerance
Osteoarthritis
Colonic Polyps
Tumor-related Headache
Visual field defect
Loss of pituitary function
Gonadotrophins
TRH - hypothyroid
ACTH -Addisons
Impaired fasting glucose, Impaired glucose tolerance, Diabetes mellitus
Insulin resistance, Reduced total cholesterol and increased triglycerides
Increased nitrogen retention
Metabolic features :
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Clinical Findings of Acromegaly
http://www.endotext.com/neuroendo/neuroendo5e/neuroendoframe5e.htm
Symptoms and signs atpresentation
Overall prevalence (%)
Facial change, acral enlargement, and soft-tissueswelling
100
Excessive sweating 83
Acroparesthesiae/ carpal tunnel syndrome 68
Tiredness and lethargy 53
Headaches 53
Oligo- or amenorrhea, infertility 55*
Erectile dysfunction and/or decreased libido 42#
Arthropathy 37
Impaired glucose tolerance/ diabetes 37
Goiter 35
Ear, nose throat and dental problems 32
Congestive cardiac failure/ arrythmia 25
Hypertension 23
Visual field defects 17
* percentage of female patients
# percentage of male patients
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Complications of Acromegaly
Cardiovascular
Ischemic heart disease
Cardiomyopathy
Congestive heart failure
ArrhythmiasHypertension
Respiratory
Kyphosis
Obstructive sleep apnea
Metabolic
Diabetes mellitus/IGT
Hyperlipidemia
NeurologicCarpal Tunnel syndrome
Stroke
Neoplastic
Colorectal
(Breast and prostate - uncertain)
Musculoskeletal
Degenerative arthropathy
Calcific discopathy, pyrophosphate
arthropathy
http://www.endotext.com/neuroendo/neuroendo5e/neuroendoframe5e.htm
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Diagnosis of Acromegaly
Random GHnot useful
Insulin like growth factor 1 (IGF-1)best for screening
Oral glucose GH suppression testing
gold standard to confirm diagnosis
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Skin Tags
Acromegaly
Frontal Bossing
Chin Protrusion
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Bone and Soft Tissue Manifestations
of Acromegaly
Acromegaly: Large Hands
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Gigantism
Oversecretion of GH during childhood
Height may exceed 2 M
Rare. Results of a pituitary gland tumor.
May have over-secretion of other pituitaryhormones.
Often have several metabolic
disturbances.
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Diseases of the Anterior
PituitaryHypersecretion of prolactin
Caused by prolactinomas
Most common of functional pituitary adenomas
(25-30% of all pituitary adenomas)In females, increased levels of prolactin cause
amenorrhea, galactorrhea, hirsutism, and
osteopenia
In males, increased levels of prolactin causehypogonadism, erectile dysfunction, impaired
libido, oligospermia, and diminished ejaculate
volume
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Hyperprolactinemia: Clinical
Presentation
Women:Amenorhea 57-90 %
Oligomenorrhea
10-28 %
Regular menses
9-15 %
Galactorrhea 30-80 %
Headache 40 %
Visual field defect
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Remember that there are four main known causes of
hyperprolactinemia
1. Pregnancy2. Drug use
3. Hypothyroidism
4. Pituitary tumors
Remember that it is not essential to treat asymptomatichyperprolactinemic women but follow-up is a must.
Remember that the problem is never overonce pregnancy occurs
REMEMBER:Not all hyperprolactinemia is due to a prolactinoma
About 3% to 5%of individuals with hyperprolactinemia have
hypothyroidism, and thusTSH, the most sensitive indicatorof hypothyroidism, should be measured in all individuals with
hyperprolactinemia.
Management
M di l t t t
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Indications for treatment include the presence
of significant symptoms such as :
1. Disabling galactorrhea,
2. Amenorrhea, and infertility;
3. Presence of visual field defect and cranial
nerve palsy; and
4. Abnormal test results such as detection of a
pituitary tumor,
5. Diminished libido,
6. Osteopenia, or osteoporesis.
Medical treatment
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1. Suppressing prolactin secretionand its clinical
and biochemical consequences,
2. Reducing the sizeof the prolactinoma, and
3. Preventing its progression or recurrence.
Pharmacotherapy of Prolactinomas :
Dopamine agonists are treatment of choice for most
prolactinomas
Choices include Bromocriptine, Pergolide and Cabergoline
Side effects include: postural hypotension, dizziness,
nasal stuffiness, GI side effects.
Medical treatment goals
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THYROID GLAND
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Evaluation of Thyroid FunctionTSHvery sensitive and specific marker of
thyroid functionTSH + T4 = hyperthyroidism
TSH + T4 = hypothyroidism
Radionuclide scans 123I (RAI)Nonfunctional areacold noduleHyperfunctional areahot nodule
If hyperthyroidism present then
uptake Graves Disease
Uptakeexogenous thyroid usage
Thyroiditis
A nodule which concentrates iodine hot is very unlikely to be
malignant
Nodule can be detected and classified as cystic, solid or mixed
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Hyperthyroidism= a hypermetabolic state, caused by increased levels of T3 & T4.
Signs and symptoms: thyrotoxicosis
Stimulates heart, protein synthesis, breakdown>build up leadingto negative nitrogen balance (degradation); hyperglycemia;increased fat metabolism
Effects: nervousness, warm moist skin, fine tremors, palpitations,
exophthalmos, weight loss,heat intolerance, muscle atrophy & weakness,osteoporosis, amenorrhea, tachycardia, lid lag or stare, goiter(Graves disease), atrial fibrillation
Most Common Causes: Graves disease, toxic multinodular goiter, toxicadenoma
Less Common Causes:- thyroiditis, struma ovarii, toxic carcinoma
- TSH-secreting pituitary adenoma
- overtreatment with thyroid hormone tablets (factitious hyperthyroidism)
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Thyroid - Hyperthyoidism
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Graves disease: toxic diffuse goiter
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Grave s disease: toxic diffuse goiterMost common cause hyperthyroidism
Strikes women, 20-30.
Multisystem syndrome, affecting eyes, skin, bones
No sure cause: autoimmune disorderGenerally emotional upset precedes symptoms
Has heredity component
Assessment: Increase appetite but slight wt loss
Dyspnea
Decreased heat tolerance
Menstruation may decrease or stop
Increased bowel movements or diarrhea
Nervous, irritable, restless
Speak rapidly; laugh inappropriately
Exopthalamus (BUG-EYE) Moist skin, thinning hair, elbows red; clubbing of nails (Plummers nails),hyperpigmentation (vitiligo- milk-white patches)
Tremors, weakness
Tachycardia, atrial fibrillation; widened pulse pressure
Fine, soft hair; moist skin
Hyperactive deep tendon reflexes
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Thyrotoxicosis (Graves Disease)
Abnormal protrusion of the eyes.
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HYPOTHYROIDISM- Deficiency in thyroid hormone = a hypometabolic state caused by deficiency
of T3 & T4.
- Goitre: iodine deficiency. No goitre: TSH deficiency
Leads to low metabolism with build-up of metabolites
Metabolites with water accumulate within cells, cause edema, called
myxedema
Myxedema coma: rare but can occur; heart becomes flabby, chambersincrease in size, CO decreases; life threatening; high mortality rate
3 TYPES: HYPOTHYROIDISM:adult onset; tissue destruction is most probable cause
CRETINISM:Profound hypothyroidism in infants, all developmental aspects are retarded,severe brain damage can occur
JUVENILE HYPOTHYROIDISM:
Begins during childhood, Hashimotos disease, caused by drugs,autoimmune
Affects growth and sexual maturation
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HYPOTHYROIDISM
SIGN AND SYMPTOMS :Changed sleeping habits (increased), Lethargy, wt gain, Coldintolerance, Dyspnea, Constipation, Menorrhagia, Muscle aches,
Anorexia, Lack of expression, Cool, dry, skin rough and thick,dry hair, coarse, enlarged tongue, Speech slow and deliberatewith hoarse voice, Impotence and infertility, decreased blood
pressure; bradycardia; dysrhythmias; decreased urinary output
Diagnostic tests:
Below-normal T3& T4
Above-normal TSH
Above-normal TRF
Above-normal creatinine phosphokinase
Anemia
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Thyroid - Hypofunction
HASHIMOTOS THYROIDITIS
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HASHIMOTOS THYROIDITIS
- MCC of hypothyroidism in areas where iodine intake is adequate
Clinically:- seen predominately in middle-aged women
- hypothyroidismwith painless enlargement of the gland
- may have transient thyrotoxicosis early on
- familial predisposition, associated with HLA-DR3 or HLA-DR5Pathogenesis:
- defective function of thyroid-specific suppressor T cells
emergence of helper T cells reactive with thyroid antigens
- helper T cells stimulate B cells to secrete antithyroid antibodies,directed against: thyroid peroxidase, TSH-receptors, iodinetransporter, & thyroglobulin, etc.
- thyroid injury is mediated by complement fixing cytotoxicantibodies, ADCC & CD8+ cytotoxic cells
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HYPOTHYROIDISM
Interventions: Requires life-long replacement hormone
Synthetic usually used T4(Levothyroxin, euthyrox )
Start with lowest dose possible and work way up
every 1-3 weeks With known cardiac problems, always use lowestdose possible
T3 (Cytomel) has more rapid effect.
Make sure client knows to continue with meds even if
he feels better Avoid sedation if possible
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THYROIDITIS
Inflammation of thyroidThree types: Acute: bacterial; pain, malaise, fever, dysphagia;treat with antibiotics
Subacute: viral infection; fever, chills, dysphagia, pain, hard &enlarged gland; treat symptoms; antivirals
Chronic:(Hashimotos)- auto immune, invade thyroid with antibodiesand lymphocytes causing tissue destruction; treat with thyroidhormone
Administer thyroid hormones; surgery; promote comfort and teaching
Acut Thyroiditis
Self-limited B-blockers for adrenergic Sign
PARATHYROIDS
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PARATHYROIDS
The parathyroid glands are embedded in the posterior surface of the thyroid gland.
Usually 4 parathyroid glandsa superior and inferior on each of the thyroids
lateral lobes.
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PARATHYROIDS
Parathyroid hormone corrects calcium deficiency by promotingcalcium conservation by kidneys, stimulating calcium release bybone, enhance calcium absorption from GI, & reduce serumphosphate levels.
Works on negative feedback control
Affects bones, kidneys, and intestine
In Bones: inhibits osteoblast (build bone) and stimulates osteocytesand osteoclasts to resorb bone and release calcium and phosphateions into the blood.
In kidneys, causes calcium to be reabsorbed with release ofphosphorus
Stimulates kidneys to convert Vit D to a metabolite that allows for
PTH to work on boneCalcitonin from thyroid causes inhibition of Ca++ release from bones
Increases blood calcium concentration and decreases bloodphosphate ion concentration
Intestine: stimulates calcium absorption from food in the intestine,increasing blood calcium concentration
Hyperparathyroidism
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Hyperparathyroidism
3 Type :
Primary:Faulty PTH regulation; adenoma, genetics, CA, radiation,
hyperplasia; occurs more commonly in women, 35-65
Secondary:
Compensatory response to defective homeostasis, chronic
renal failure, malabsorption disorders
Tertiary:
Compensates for secondary malfunction to primary, leading
to overgrowth of gland and overproduction and secretion
All three lead to increased calcium and
decreased phosphorus
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HYPERPARATHYROIDISMSign and Symptoms :
Urine calcium increase and kidneys fail to concentrate urine Phosphorus excretion increases
Enhances sodium, potassium, amino acids, bicarbonate(acidosis leading to excretion of Ca++ )
Polyuria
Renal calculi
Bone demineralization (breakdown):Bone pain, Pathologicfractures, Cystic bone disease
Others Sign : Weakness, wt. loss, fatigue, depression, Renal colicpain, back pain, Hematuria, renal calculi, cholelithiasis, Anorexia,vomiting, constipation, Peptic ulcer (stimulates gastric HCL),
Increase heart contractility; decreased automaticity, Hypertension,Depressed reflexes- hyporeflexia, Confusion, irritability, moodswings
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Hyperparathyroidism : Diagnostic Test
Serum PTH: elevated
Calcium: elevated (>10.5mg/dl; 5.2mEq/L
Kidney stones
Phosphorus: decreased
X-rays; CT; MRI: look at bone density anddemineralization
PTH infusion test: (Ellsworth-Howard excretion test);give IV PTH, hourly urine samples looking forphosphorus
Calcitonin stimulation test: if cancer suspected; usecalcium gluconate
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Hyperparathyroidism : Intervention
- Surgery
- Stabilize calcium levels prior to surgery Medical treatment:
Rehydration with isotonic fluids
Diuresis
Restrict intake of calcium (thyazides and Vit D.
Monitor EKG
Drugs: Phosphates: Neutra-phos
Calcitonin: IV; IM- decrease release from skeletal areas; increasedexcretion by kidneys
Calcium chelators ( bind calcium) Plicamycin: mithramycin; cytotoxicagents; watch for thrombocytopenia
Steroids: inhibit Vit D
Estrogen Alpha & beta blockers
cimetidine
Hypoparathyroidism
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Hypoparathyroidism Too little PTH leading to decreased calcium and
increase phosphorus
3 typesIatrogenic:
Most common, resulting from surgery of neck removing glands,radiation, or other trauma
Idiopathic:
Early onset and late onset; autoimmune; genetic causes ofabsent glands, pernicious anemia, ovarian failure
Functional:
Long term hypomagnesemia causes this (alcohol,malabsorption)
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Hypoparathyroidism
Sign and Symptoms : Neuromuscular problems, increased excitability, tetany, muscle
cramps, tingling, numbness, hyperreflexia
Tetany leads to anxiety; leads to hyperventilation; leads tohypocapnia and alkalosis, which worsens hypocalcemia
Seizures, laryngeal spasms
Personality changes
Nausea, vomiting
Dysrhythmias, decreased contractility, reduced CO
Cataracts, dry skin, scaly, coarse
Alopecia
Bands or pits on teeth
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PARATHYROID
Interventions: Treatment focuses on preventing tetany and
correcting hypocalcemiaIV calcium gluconate or calcium gluconate
Do not use saline, promotes calcium and sodium excretion
Avoid bicarbonate, cause precipitationVit D and calcium supplements
Ergocalciferol (Vit D2 ); Rocaltrol; may use combined therapy oforal and IV initially
Need 1 gram of calcium daily if using Vit D
Life-long therapy
Emergency airway if laryngeal spasms occur Foods high in calcium but low in phosphorus- milk, yogurt,
processed cheese.
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Structure:Adrenal medulla: centralportion. Irregularly shapedcells organized in groupsaround blood vessels.Connected with thesympathetic division of theautonomic nervous system.Modified post-ganglionic
neuronsAdrenal cortex: outerportion. Epithelial cells inlayers. Well supplied with
blood vessels.
Sits atop each kidney and is embedded in the
mass of adipose tissue that encloses the kidney
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ADRENAL GLAND
- Composed of two distinct units: steroidsecreting cortex &catecholamineproducingmedulla
- In the adult, the normal adrenal weighs 4 gm.
- The cortex consists of threefunctional zones:
1 - zona glomerulosa2 - zona fasciculata(75% of the cortex)
3 - zona reticularis
- The cortex secretes threetypes of steroid hormones:
1 - mineralocorticoids(aldosterone) - zona glomerulosa.2 - glucocorticoids(cortisol) - zona fasciculatamainly.
3 - sex steroids(testosterone) - zona reticularismainly.
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Table Adrenal gland: characteristics
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Alterations of Adrenal FunctionDisorders of the adrenal cortex
Hypersecretion of adrenal androgens and estrogens
Feminization
Virilization
Cushing disease
Excessive anterior pituitary secretion of ACTH
Cushing syndrome
Excessive level of cortisol, regardless of cause
Disorders of the adrenal medulla
Adrenal medulla hyperfunctionCaused by tumors derived from the chromaffin cells of the
adrenal medulla
Pheochromocytomas
Secrete catecholamines on a continuous or episodic basis
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ADRENAL GLAND Cushings
Assessments: Fatigue, muscle wasting
Frequent infections, slow wound healing
Suppressed immune response ( can mask S/S); kill lymphocytes
Truncal obesity, buffalo hump, moon-shaped face, scrawny arms andlegs (PICKLE WITH LEGS)
Fragile skin, purplish striae on abdomen, buttocks, breasts, bruises Masculinization in women, hirsutism (increased hair growth), acne
Hypertension
Osteoporosis
Labile emotions
Abnormal sleep patterns
Nitrogen, carbohydrate, and mineral metabolism Elevated blood glucose
Central Obesity in Cushings
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Central Obesity in Cushing s
Disease
Williams Textbook of Endocrinology. 8thEd. Foster, DW, Wilson, JD (Eds), WB Saunders, Philadelphia, 1996
B ff l H i St i i C hi
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Buffalo Hump in
Cushings Disease
Orth, D. UpToDate
Striae in Cushings
DiseaseProximal Muscle Wasting
C hi Di
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Cushing Disease
G S C S G S
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ADRENAL GLANDS CUSHINGS
Diagnostic tests:
Cortisol: high with no circadian variation
Urinary levels of steroid metabolites: high
RBC and granulocytes: high
X-rays, MRI, CAT scans
Dexamethasone suppression test: give 1 mg
at night, test at 8am; high level
ADRENAL GLAND CUSHINGS
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ADRENAL GLAND CUSHINGS
Interventions: Treat underlying cause; stop steroids
Remove tumors of pituitary or adrenalectomy
( uni or bi lateral) Drugs:
Mitotane to inhibit cortisol synthesis ( watch foradrenal crisis!!
Cyproheptadine: ACTH inhibitorAldactone: mineralocorticoid antagonist to relievehypertension and hypokalemia
ADRENAL GLAND CUSHINGS
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ADRENAL GLAND CUSHINGS
Complications: Fluid and e-lyte imbalances
Hypertension: Na+and water retention
CHF: excess volume in compromised heart Hypokalemia
Ventricular dysrhythmias: due to CHF and
hypokalemia
Increased risk for infections & fractures Skin breakdown
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PRIMARY HYPERALDOSTERONISM
= excessive secretion of aldosterone independent of renin-
angiotensin system.
Features: hypervolemia, hypokalemia, hypertension, low renin
Causes:
- MCC is aldosterone-secreting adenoma(Conns syndrome) in80% of cases
- Bilateral idiopathic hyperplasia (? due to an abnormal
secretagogue)
- Glucorticoid-suppressible hyperaldosteronism: hybrid cellsproduce both cortisol & aldosterone, aldosterone under
influence of ACTH, suppressible by administration of
dexamethasone
Prognosis: adenomas are curable by surgery.
CHRONIC ADRENOCORTICAL
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CHRONIC ADRENOCORTICAL
INSUFFICIENCY
Primary (adrenal) or secondary (hypothalamic/pituitary):
Primary (Addisons disease): MCC: autoimmune adrenalitis;tuberculosis, metastatic cancers (destruction of 90% ofthe cortex) decreased cortisol & aldosterone, with feed-
back elevation of ACTH (+ MSH)hyperpigmentation ofskin,K+, Na+, BP, weakness, anorexia, N&V,hypoglycemia
Secondary: to hypothalamic or pituitary lesions associated withdecreased ACTH bilateral adrenal cortical atrophy,sparing the zona glomerulosa(skin color is paleandaldosterone is normal, i.e. no sodium or potassiumabnormalities).
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Addi Di
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Addisons Disease
Clinical Presentation:
Looks chronically ill,
weight loss, lethargy,
weakness, low libido
Dehydration
Creases in elbows,
knees and lips
Nausea, vomiting,
chronic abdominal pain
Muscle cramps Hyper/hypo-
pigmentation
(unilateral, patchy)
Hyperpigmentation of lip
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ADRENAL GLANDS ADDISONS
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ADRENAL GLANDS ADDISONS
Interventions: Lifelong therapy with replacement
Drugs:Cortisone: twice daily, increase dose for stressful times
Florinef: aldosterone replacement
Salt food liberally Avoid fasting
Eat high carbs and proteins
Always wear medic alert identification
Carry emergency kit with 100mg hydrocortisone for injection
Prevent acute exacerbations
Avoid salt and fluid restriction with diuretics; may lead to crisis
ADRENAL GLANDS
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ADRENAL GLANDS
Complications: Adrenal crisis: due to insufficiency; can occur
gradually or abruptly (acute adrenal insufficiency)
Potentially lethal
Occurs in individuals who dont respond to therapy;
increased stress without increased meds; abrupt
corticosteroid withdrawal
ALWAYS WITHDRAW STEROIDS THERAPY
GRADUALLY
ADRENAL GLANDS ADRENAL
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CRISIS
Treatment:
Restore volume with D5 or NS
Be sure to assess fluid status frequently
Cortisol q 6 hr. (Solu-Cortef IV): if given withsaline, proves adequate to replace
Aldosterone
Do not give methyleprednisolone (Solu-Medrol: lack mineralocorticoid effects)
Reduce anxiety
Adrenal Medulla
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94
Adrenal Medulla(part of autonomic nervous system)
Releases:
epinephrine
norepinephrine
Stimulated by:
fear
angerstress
hemorrhage
hypoxiahypoglycemia
ADRENAL GLANDS
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PHEOCHROMOCYTOMA
Rare, benign tumor; arises in medullaResults in hypersecretion of epinephrine andnorepinephrine
Tumors appear more commonly on right side; middle-
aged womenCan occur with thyroidal cancer andhyperparathyroidism-Sipplessyndrome
Complications:
Severe hypotension
CVA
Heart problems
If left untreated, always leads to death
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Pheochromocytoma
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y
Signs & Symptoms
hypertension
tachycardia
excessive sweating
tremor
headache
Vertigo
blurred vision
flushing
tinnitus
dyspnea
anxiety
hyperglycemia
Diagnosis
PheochromocytomaSerum catecholamines epinephrine 400 pg/ml
norepinephrine 2000 pg/ml
Urine 24 hr. test forVanillylmandelic acid (VMA)
Clonidine test
MIBG scintigraphy (CT,
MRI, US used to localize thetumor)
EKG changes
Diagnostic tests mayprecipitate a crisis!!!
PHEOCHROMOCYTOMA
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PHEOCHROMOCYTOMA
Assessment: Exaggerated flight or fight reaction
High blood pressure (Hallmark sign) 200/150
End-organ damage; CVA, heart disease, kidney damage
Orthostatic hypotension
Attack occurs with sporadic release of catecholamines (Mayresult from exercise, lifting, emotional distress, exposure to cold,food, alcohol, sex, etc.
Pounding heart beat, deep breathing
Peripheral vasoconstriction
Hyperglycemia
anxiety
PHEOCHROMOCYTOMA
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PHEOCHROMOCYTOMA
Interventions: Alpha-blockage to control HTN (phenoxybenzamine) Surgical removal (adrenelectomi)
Prior to surgery, drugs to reduce the excessive adrenergic action(2 weeks)
Receive plasma volume expanders
During surgery, receive Regitine, alpha-adrenergic blocker toprevent hypertensive crisis
If unable to have surgery, may order drug, Demser, inhibits anenzyme promoting norepinephrine synthesis
Avoid drugs like opiates, histamines, OTC cold medications During attack, maintain bedrest, HOB elevated to at 300to
reduce orthostatic hypotension
Signs & Symptoms of
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g y p
Aldosterone Deficiency
Impaired Na+ conservation weight loss
hypovolemia
low renal perfusion
increased renin production
weakness
postural syncope
Azotemia
Impaired renal secretion of K+ & H+ hyperkalemia
cardiac asystole
mild acidosis
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Polycystic Ovarian Syndrome
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Polycystic Ovarian Syndrome
Common 8-22% of population
Commonest cause of Hirsuitism
Pathogenesis
Hyperandrogenism
Insulin resistance
Presentation: acne, obesity (50%),
hirsutism, insulin resistance (40%),
abnormal lipids, menstrual dysfunction
Treatment: weight loss, metformin
Clinical Features (PCOS)
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Clinical Features (PCOS)
Oligomenorrhoea
Anouvulation
Hirstuism
AcneObesity
Hypertension
Glucose intoleranceDyslipideamia
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Testes: producestestosterone
SUMMARY OF THE MAJOR COMPONENTS OF THEENDOCRINE SYSTEM
BRAIN
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TARGET TISSUES
PRL TSH CALCIUMGH ACTHLH/FSH
GONADS LIVERADRENAL
CORTEXPANCREASTHYROID
INSULIN
GLUCAGON
STEROIDS
IGF-1 T3 +T4 STEROIDS PTH
GLUCOSE
ANTERIOR LOBE
OF PITUITARY
POSTERIOR LOBE
OF PITUITARY
PARATHYROID
OXYTOCIN
MILK
BRAIN
BREAST
DIET
ADRENAL
CORTEX
VASOPRESSIN
FEEDBACK LOOPS
GHRHGnRH CRHTRH
What Questions Can You
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What Questions Can You
Answer For Me?
QUIZ
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What is diabetesmellitus??
What is diabetes
insipidus??
Whats the diseases that caused byHypersecretion of ADH ?
What the diagnosis if you find:
Retention of water,hyponatremiaAnd hypoosmolarity ?
For patients diagnosed with
pituitary tumors, what is the Which disease, caused by
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surgical treatment of
choice?
Hypersecretion of
GH in children and
adolescents ?
a deficit in antidiuretic
hormone, results in
massive
diuresis and is treated with
vasopressin?
Deficiency of growthhormone early in life will
leads ?
Whats the diseases that you will find : Skin tags
and acanthosis nigricans ?
What is the most
di
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common disease
form of hypothyroidism?
What causes
Cushings
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Cushings
syndrome?
What diagnosis is made when apatient has truncal obesity,
protein wasting, a moon face,
and osteoporosis?
Whats the diseases if
neoplasm composed ofchromaffin cells that secretes
catecholamines?
What causes Conn
Syndrome?
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Whats this ?
Virilization
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Virilization
This lady complains of fatigue, increasing
weight memory loss and constipation
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weight, memory loss and constipation
An elderly gentleman presents with confusion and
weight loss
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g
What is the abnormaility in this 32 year old woman
with amenorrhoea and bitemporal hemianopia?
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with amenorrhoea and bitemporal hemianopia?
This lady presented with weight loss and
palpitations
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palpitations
This woman has presented with hair loss,
amenorrhoea and fatigue
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amenorrhoea and fatigue
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Williams Textbook of Endocrinology. 8thEd. Foster, DW, Wilson, JD (Eds), WB Saunders, Philadelphia, 1996
Hyperpigmentation of lip
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Goiter
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Goiter
Bulge in the neck resulting from anenlarged thyroid gland.
Toxic Goiter Simple Goiter
Hirsutism
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Hirsutism
Excess hair growth, especially in women.
Virilism
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Virilism
Masculinization of a female.
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Hypogonadism
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Hypopituitarism:
InfertilityPallor
Low BMR
Intolerance to stress
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Congenital Hypothyroidism
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P ti t #P ti t # 22
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Patient #Patient # 22
50 year old male Chief complaints:
Fatigue sweating of hands and
feet Increasing shoe size Joint pains Headache
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The End