endocrine reviews undana

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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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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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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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



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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

Hyperpigmentation in Addisons Disease


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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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