DISTURBANCES OF THE ENDOCRINE SYSTEM THE ADRENAL GLAND.

DISTURBANCES OF THE ENDOCRINE SYSTEM

THE ADRENAL GLAND

ADDISON’S DISEASE

• PRIMARY ADRENAL INSUFFICIENCY

• SECONDARY ADRENAL INSUFFICIENCY

PRIMARY ADRENAL INSUFFICIENCY

ADDISON’S DISEASE

• FAILURE OF ADRENAL CORTEX TO PRODUCE ADRENOCORITICAL HORMONES

• USUALLY CAUSED BY PRIMARY ATROPHY OF ADRENAL CORTEX

AUTOIMMUNITYTUBERCULOSISCANCER

HORMAL DISTURBANCES

• MINERALOCORTICOID

• GLUCOCORTICOID

MINERALOCORTICOID DEFICIENCY

• GREATLY DECREASES SODIUM REABSORPTION

• INCREASES LOSS OF SODIUM, CHLORIDE AND WATER

• REDUCES EXTRACELLULAR FLUID VOLUMES

• HYPERKALEMIA DEVELOPS

• ACIDOSIS DEVELOPS

• PLASMA VOLUME DECREASES

• CIRCULATORY SHOCK MAY DEVELOP

GLUCOCORTICOID DEFICIENCY

• INABILITY TO MAINTAIN NORMAL GLUCOSE BETWEEN MEALS

• DUE TO INABILITY SYNTHESIZE GLUCOSE IN SUFFICIENT QUANTITIES

• DUE TO REDUCED ABILITY TO MOBILIZE FATS AND PROTEINS

• INCREASED SUSCEPTIBILITY TO STRESS

AFFECT ON MUSCLES

• WEAKNESS IN MUSCLES EVEN WHEN EXCESS GLUCOSE AND OTHER NUTRIENTS ARE AVAILABLE

THE UNTREATED INDIVIDUAL WILL DIE IN A FEW DAYS TO TWO WEEKS

DUE TO CONSUMING WEAKNESS AND CIRCULATORY

SHOCK

SECONDARY ADRENAL INSUFFICIENCY

• SECONDARY ADRENAL INSUFFICIENCY DUE TO HYPOTHALAMIC OR PITUITARY DISEASE OR DESTRUCTION

DIAGNOSIS

• MEDICAL HISTORY OF SYMPTOMS

• HYPERPIGMENTATION

• ELVATED BLOOD LEVEL OF POTASSIUM

• RATIO OF WHITE BLOOD CELLS

• ECG CHANGES

• CHEST X-RAY

DEFINITIVE DIAGOSIS

• TEST FOR LEVELS OF CORTISOL AND ALDOSTERONE– IN BLOOD AND URINE

• TEST FOR LEVELS OF ACTH– IN BLOOD

• ACTH IS ADMINISTERED AND CORTISOL AND ALDOSTERONE LEVELS ARE TESTED AGAIN

TREATMENT OF ADDISON’S DISEASE

• MINERALOCORTICOIDS ADMINSTERED

• GLUCOCORTICOIDS ADMINISTERED

• MUST HAVE A HIGH SALT DIET

ADDISONIAN CRISIS

• OCCURS DURING PHYSICAL OR MENTAL STRESS

UNABLE TO SECRETE EXTRA NEEDED

GLUCOCORTICOIDS

• BEFORE SURGERY MUST ADMINISTER MASSIVE AMOUNTS OF GLUCOCORTICOIDS

DID HE OR DIDN’T HE

HYPERADRENALISMS

• CUSHING’S DISEASE

• CONN’S SYNDROME

CUSHING’S DISEASE

• EFFECTS OF EXCESS CORTISOL IN BODY– PITUITARY TUMOR– ADRENAL TUMOR– ADMINISTRATION OF PREDNISONE OR

OTHER GLUCOCORTICOIDS

HORMONAL DISTURBANCES

• INCREASED CORTISOL

• SOMETIMES INCREASED ANDROGENS

GLUCOCORTICOID OVERSECRETION

• MOBILIZATION OF FAT FROM LOWER PART OF BODY– DEPOSITION IN UPPER PART OF BODY

• INCREASED BLOOD GLUCOSE– ADRENAL DIABETES

• UP TO 200mg/100ml

– MAINLY FROM GLUCONEOGENESIS

• INCREASED PROTEIN CATABOLISM

EFFECTS OF PROTEIN CATABOLISM

• MOST PROFOUND EFFECT– EXCEPT LIVER AND PLASMA PROTEINS

• LOSS OF IMMUNE PROTEINS LEAVES ONE SUSCEPTIBLE TO DISEASE– MANY DIE OF INFECTIONS

• DECREASE IN SUBCUTANEOUS TISSUE– STRIAE

• LOSS OF PROTEIN IN BONE CAUSES OSTEOPOROSIS

DIAGNOSIS OF CUSHING’S DISEASE

• MEDICAL HISTORY

• PHYSICAL EXAM

• LAB TEST

• X-RAYS

DEFINITIVE DIAGNOSITC TEST

• 24-Hour Urinary Free Cortisol Level

DIAGNOSTIC TESTS

• DEXAMETHASONE SUPPRESSION TEST

• CRH STIMULATION TEST

• DIRECT VISUALIZATION OF THE ENDOCRINE GLANDS (RADIOLOGIC IMAGING)

TESTS THAT DIFFERENTIATE BETWEEN PITUITARY AND

ECTOPIC SOURCES OF ACTH• PETROSAL SINUS SAMPLING

TEST THAT DISTINGUISHES BETWEEN CUSHING’S AND

PSEUDOCUSHING’S• THE DEXAMETHASONE-CRH TEST

TREATMENT

• SURGERY

• RADIATION

• CHEMOTHEURAPY

• IMMUNOTHERAPY

• DRUGS THAT SUPPRESS CORTISOL PRODUCTION

• GRADUAL REMOVAL FROM PRESCRIBED GLUCOCORTICOIDS

CONN’S SYNDROME

• HYPERALDOSTERONISM

• OVERPRODUCTION OF MINERALOCORTICOIDS

• TUMOR OF ADRENAL CORTEX

DIAGNOSIS

• ALDOSTERONE LEVELS IN BLOOD AND URINE

• SUPPRESSED PLASMA RENIN LEVELS

• OTHER ADRENAL HNORMONES

• PHYSIOLOGICAL CHANGES BETWEEN MORNING AND EVENING

• SODIUM CHALLENGE

• SODIUM RESTRICTION

• CT AND MRI

OVERSECRETION OF ALDOSTERONE

• HYPERKALEMIA– OCCASIONAL PERIODS OF MUSCULAR PARALYSIS

• SLIGHT INCREASE IN EXTRACELLULAR FLUID VOLUME

• SLIGHT INCREASE IN BLOOD VOLUME

• SLIGHT INCREASE IN PLASMA SODIUM CONCENTRATION – 2 TO 3%

• MODERATE TO SEVERE HYPERTENSION

TREATMENT

• SURGICAL REMOVAL

• HYPERTENSIVE MEDICATION

• MEDICATIONS THAT BLOCK ALDOSTERONE

DISTURBANCES OF THE ENDOCRINE SYSTEM

THE THYROID

HYPERTHYROIDSM

• TOXIC GOITER

• THRYOTOXICOSIS

• GRAVES DISEASE

HYPERSECRETION OF THRYOID HORMONES

SIGNS AND SYMPTOMS OF HYPERTHYROIDISM

• PALPITATIONS• HEAT INTOLERANCE • NERVOUSNESS• INSOMNIA• BREATHLESSNESS • INCREASED BOWEL

MOVEMENTS • FATIGUE

• LIGHT OR ABSENT MENSTRUAL PERIODSFAST HEART RATE

• TREMBLING HANDS• WEIGHT LOSS• MUSCLE WEAKNESS• WARM MOIST SKIN• HAIR LOSS• STARING GAZE

CAUSES OF HYPERTHYROIDISM

• GRAVE’S DISEASE• A SINGLE NODULE WITHIN THE

THYROID INSTEAD OF THE ENTIRE THYROID

• INFLAMMATION OF THE THYROID GLAND– THYROIDITIS,

• PATIENTS WHO TAKE EXCESSIVE DOSES OF THYROID HORMONE.

GRAVES DISEASE

• MOST COMMON CAUSE

• AUTOIMMUNE DISEASE

• ANTIBODIES MIMIC TSH

DISTINCT CHARACTERISTICS OF GRAVE’S DISEASE

• OVERACTIVITY OF THE THYROID GLAND (HYPERTHYROIDISM)

• INFLAMMATION OF THE TISSUES AROUND THE EYES CAUSING SWELLING

• THICKENING OF THE SKIN OVER THE LOWER LEGS (PRETIBIAL MYXEDEMA).

MORE CHARACTERISTICS

• AFFECTS WOMEN MUCH MORE OFTEN THAN MEN– ABOUT 8:1

• CALLED DIFFUSE TOXIC GOITER– ENTIRE GLAND IS ENLARGED

• COMMON IN THE 30'S AND 40'S

• TENDS TO RUN IN FAMILIES

HYPERTHYROIDISM DUE TO A SINGLE NODULE

• BENIGN TUMORS

• SOMETIMES PRODUCE EXCESSIVE AMOUNTS OF THYROID HORMONES.

• TOXIC NODULAR GOITER

HYPERTHYROIDISM DUE TO THYRODITIS

• CAUSES THE TYPICAL SYMPTOMS

• GENERALLY LAST ONLY A FEW WEEKS

• SUBACUTE THYROIDITIS– CAUSED BY A VIRUS

• POSTPARTUM THYROIDITIS.

HYPERTHYROID IN PATIENTS WHO ABUSE THYROID MEDICATION

• ESPECIALLY FORMS

• ESPECIALLY T3 FORMS

DIAGNOSIS OF HYPERTHYROIDISM

• BLOOD TESTS FOR– DECREASED TSH LEVELS

– INCREASED THYROID HORMONE LEVELS(T3, T4, T7)

• IODINE THYROID SCAN

TREATMENT

• ADMINISTRATION OF DRUGS THAT DECREASE HORMONE PRODUCTION

• RADIATION TREATMENT

• SURGERY

ADMINISTRATION OF DRUGS TO SUPRESS HORMONE

PRODUCTION• METHIMAZOLE

• PROPYLTHIOURACIL (PTU).

TREATMENT WITH RADIOACTIVE IODINE

• MOST WIDELY RECOMMENDED• BASED ON IODINE RELATIONSHIP TO

THYROID

• THYROID CELLS ARE KILLED

• TAKES ONE TO TWO

• HYPOTHYROIDISM IS ONLY COMMON SIDE EFFECT

SURGICAL REMOVAL OF THRYOID OR PORTIONS OF THYROID

• NOT USED AS OFTEN• HOT NODULES PRIME CANDIDATES

• GRAVES IS NOT

• DANGER OF DAMAGING LARYNGEAL NERVE

• HYPOTHYOIDISM TREATED WITH HORMONAL REPLACEMENT

HYPOTHYROIDISM

• LACK OF THYROID HORMONE

• EFFECTS ARE GENERALLY OPPOSITE OF HYPERTHYROIDISM

SIGNS AND SYMPTOMS OF HYPOTHYOIDISM

• FATIGUE• WEAKNESS

• WEIGHT GAIN OR DIFFICULTY LOSING WEIGHT

• COARSE, DRY HAIR

• DRY, ROUGH PALE SKIN

• HAIR LOSS

• INTOLERANCETO COLD

•

• MUSCLE CRAMPS

• MUSCLE ACHES

• CONSTIPATION

• DEPRESSION

• IRRITABILITY

• MEMORY LOSS

• ABNORMAL MENSTRUAL CYCLES

• DECREASED LIBIDO

• FROG LIKE VOICE

PHYSIOLOGICAL EFFECTS OF HYPOTHYROIDISM

• MYXEDEMA

• ATERIOSCLEROSIS

• CRETINISM

MYXEDEMA

• EDEMA THROUGHOUT BODY

• IN PATIENT’S WITH ALMOST NO THYROID FUNCTION

• INCREASE IIN PROTEOGLYCANS CAUSES SWELLING

ATERIOSCLEROSIS

• LACK OF THYROID INCREASES THE AMOUNT OF BLOOD LIPIDS– ESPECIALLY CHOLESTEROL

• OFTEN RESULTS IN PERIPHERAL VASCULAR DISEASE

• DEAFNESS

• EXTREME CORONARY SCLEROSIS

• DEMIS

CAUSES OF HYPOTHYROIDISM

• HASHIMOTO’S THYROIDITIS– AUTOIMMUNE THYROIDITIS

• MEDICAL TREATMENTS– SURGERY

– RADIATION TREATMENT

• LACK OF TSH SECRETION

CONSEQUENCES OF HYPOTHYROIDISM

• TSH MAY CAUSE THRYOID TO ENLARGE

• COMPENSATORY GOITER

• RARE CONSEQUENCES– SEVERE DEPRESSION– HEART FAILURE– COMA

DIAGNOSIS OF HYPOTHYROIDISM

• DIAGNOSIS BASED ON AMOUNT OF THYROID HORMONE IN BLOOD

• MEASURE BLOOD LEVELS OF T4 AND TSH

ADDITIONAL BLOOD TESTS• MEASUREMENT OF SERUM THYROID HORMONES: T4 BY RIA.

MEASUREMENT OF SERUM THYROID HORMONES: T3 BY RIA. THYROID BINDING GLOBULIN.

• MEASUREMENT OF PITUITARY PRODUCTION OF TSH.

• TRH TEST.

• IODINE UPTAKE SCAN.

• Thyroid Scan.

• Thyroid Ultrasound..

Thyroid Antibodies.

• Thyroid Needle Biopsy.

TREATMENT OF HYPOTHYROIDISM

• EASY TO TREAT WITH HORMONE REPLACEMENT– LEVOTHYROXINE

– SYNTHETIC T4

PRETIBIAL MYXEDEMA

MYXEDEMA

DISTURBANCES OF THE ENDOCRINE SYSTEM

THE PARATHYROID GLAND

HYPERPARATHYROIDISM

• OVER SECRETION OF PARATHYROID HORMONE

• OSTEOPENIA

• OSTEOPOROSIS

CAUSE OF HYPERPARATHYROIDISM

• OVERSECRETION OF PARATHYROID HORMONE

• BENIGN TUMORS

• HYPERPLASIA

BENIGN TUMOR

• ADENOMA– 87-93% OF ALL CASES

• HYPERPLASIA

• ,

CANCERS OF THE PARATHYROID IS VERY

RARE• LESS THAN 1 %

SYMPTOMS OF HYPERPARATHYROIDISM

• OSTEOPENIA

• OSTEOPOROSIS

• BONE FRACTURES

• KIDNEY STONES

• PEPTIC ULCERS

• PANCREATITIS

• NERVOUS SYSTEM COMPLICATIONS

DIAGNOSIS

• INAPPROPRIATE LEVELS OF PTH WHEN EXCESS CALCIUM IS PRESENT

• CALCIUM LEVELS IN THE URINE

TREATMENT

• DO NOTHING

• SURGERY

HYPOPARATHYROIDISM

• RARE• DEFICIENT PARATHYROID HORMONE

SECRETION.• INABILITY TO MAKE AN ACTIVE FORM OF

PTH.• INABILITY OF THE KIDNEYS & BONES TO

RESPOND TO PTH.

• ...

DEFICIENT PARATHYROID SECRETION

• SURGICAL.

• IDIOPATHIC..– CONGENITAL

– ACQUIRED

• HYPOMAGNESEMIA

SURGICAL CAUSES

• REMOVAL OF PARATHYROID TO CURE HYPERPARATHYROIDISM

IDIOPATHIC HYPOPARATHYROIDISM

• WITHOUT A DEFINE CAUSE

• CONGENITAL

• ACQUIRED

CONGENITAL

• PRESENT AT BIRTH

• BORN WITHOUT PARATHYROID

• BABIES WHOSE MOTHERS HAVE OVERACTIVE PARATHYROID GLANDS

ACQUIRED

• ANTIBODIES DESTROY THE PARATHYROID

• ANTIBODIES BIND TO PARATHYROID CELLS AND BLOCK STIMULATION

HYPOMAGNESEMIA

• MAGNESIUM IS NECESSARY FOR PTH PRODUCTION

SECRETION OF BIOLOGICALLY INACTIVE PTH

• RARE

RESISTANCE TO PARATHYROID HORMONE

• (PSEUDO-HYPOPARATHYROIDISM

• RARE

• PTH IS PRODUCED

• TARGET CELLS DO NOT RESPOND

TREATMENT

• ADMINISTRATION OF VITAMIN D

• ADMINISTRATION OF CALCIUM

• HYPOMAGNESEMIA IS TREATED WITH MAGNESIUM

DISTURBANCES OF THE ENDOCRINE SYSTEM

THE PITUITARY

ACROMEGALY

• EXCESS SECRETION OF GROWTH HORMONE AFTER EPIPHYSEAL PLATES HAVE CLOSED

HYPOPITUITARISM