disturbances of the endocrine system the adrenal gland
TRANSCRIPT
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DISTURBANCES OF THE ENDOCRINE SYSTEM
THE ADRENAL GLAND
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ADDISON’S DISEASE
• PRIMARY ADRENAL INSUFFICIENCY
• SECONDARY ADRENAL INSUFFICIENCY
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PRIMARY ADRENAL INSUFFICIENCY
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ADDISON’S DISEASE
• FAILURE OF ADRENAL CORTEX TO PRODUCE ADRENOCORITICAL HORMONES
• USUALLY CAUSED BY PRIMARY ATROPHY OF ADRENAL CORTEX
AUTOIMMUNITYTUBERCULOSISCANCER
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HORMAL DISTURBANCES
• MINERALOCORTICOID
• GLUCOCORTICOID
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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
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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
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AFFECT ON MUSCLES
• WEAKNESS IN MUSCLES EVEN WHEN EXCESS GLUCOSE AND OTHER NUTRIENTS ARE AVAILABLE
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THE UNTREATED INDIVIDUAL WILL DIE IN A FEW DAYS TO TWO WEEKS
DUE TO CONSUMING WEAKNESS AND CIRCULATORY
SHOCK
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SECONDARY ADRENAL INSUFFICIENCY
• SECONDARY ADRENAL INSUFFICIENCY DUE TO HYPOTHALAMIC OR PITUITARY DISEASE OR DESTRUCTION
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DIAGNOSIS
• MEDICAL HISTORY OF SYMPTOMS
• HYPERPIGMENTATION
• ELVATED BLOOD LEVEL OF POTASSIUM
• RATIO OF WHITE BLOOD CELLS
• ECG CHANGES
• CHEST X-RAY
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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
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TREATMENT OF ADDISON’S DISEASE
• MINERALOCORTICOIDS ADMINSTERED
• GLUCOCORTICOIDS ADMINISTERED
• MUST HAVE A HIGH SALT DIET
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ADDISONIAN CRISIS
• OCCURS DURING PHYSICAL OR MENTAL STRESS
UNABLE TO SECRETE EXTRA NEEDED
GLUCOCORTICOIDS
• BEFORE SURGERY MUST ADMINISTER MASSIVE AMOUNTS OF GLUCOCORTICOIDS
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DID HE OR DIDN’T HE
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HYPERADRENALISMS
• CUSHING’S DISEASE
• CONN’S SYNDROME
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CUSHING’S DISEASE
• EFFECTS OF EXCESS CORTISOL IN BODY– PITUITARY TUMOR– ADRENAL TUMOR– ADMINISTRATION OF PREDNISONE OR
OTHER GLUCOCORTICOIDS
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HORMONAL DISTURBANCES
• INCREASED CORTISOL
• SOMETIMES INCREASED ANDROGENS
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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
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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
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DIAGNOSIS OF CUSHING’S DISEASE
• MEDICAL HISTORY
• PHYSICAL EXAM
• LAB TEST
• X-RAYS
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DEFINITIVE DIAGNOSITC TEST
• 24-Hour Urinary Free Cortisol Level
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DIAGNOSTIC TESTS
• DEXAMETHASONE SUPPRESSION TEST
• CRH STIMULATION TEST
• DIRECT VISUALIZATION OF THE ENDOCRINE GLANDS (RADIOLOGIC IMAGING)
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TESTS THAT DIFFERENTIATE BETWEEN PITUITARY AND
ECTOPIC SOURCES OF ACTH• PETROSAL SINUS SAMPLING
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TEST THAT DISTINGUISHES BETWEEN CUSHING’S AND
PSEUDOCUSHING’S• THE DEXAMETHASONE-CRH TEST
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TREATMENT
• SURGERY
• RADIATION
• CHEMOTHEURAPY
• IMMUNOTHERAPY
• DRUGS THAT SUPPRESS CORTISOL PRODUCTION
• GRADUAL REMOVAL FROM PRESCRIBED GLUCOCORTICOIDS
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CONN’S SYNDROME
• HYPERALDOSTERONISM
• OVERPRODUCTION OF MINERALOCORTICOIDS
• TUMOR OF ADRENAL CORTEX
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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
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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
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TREATMENT
• SURGICAL REMOVAL
• HYPERTENSIVE MEDICATION
• MEDICATIONS THAT BLOCK ALDOSTERONE
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DISTURBANCES OF THE ENDOCRINE SYSTEM
THE THYROID
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HYPERTHYROIDSM
• TOXIC GOITER
• THRYOTOXICOSIS
• GRAVES DISEASE
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HYPERSECRETION OF THRYOID HORMONES
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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
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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.
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GRAVES DISEASE
• MOST COMMON CAUSE
• AUTOIMMUNE DISEASE
• ANTIBODIES MIMIC TSH
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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).
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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
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HYPERTHYROIDISM DUE TO A SINGLE NODULE
• BENIGN TUMORS
• SOMETIMES PRODUCE EXCESSIVE AMOUNTS OF THYROID HORMONES.
• TOXIC NODULAR GOITER
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HYPERTHYROIDISM DUE TO THYRODITIS
• CAUSES THE TYPICAL SYMPTOMS
• GENERALLY LAST ONLY A FEW WEEKS
• SUBACUTE THYROIDITIS– CAUSED BY A VIRUS
• POSTPARTUM THYROIDITIS.
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HYPERTHYROID IN PATIENTS WHO ABUSE THYROID MEDICATION
• ESPECIALLY FORMS
• ESPECIALLY T3 FORMS
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DIAGNOSIS OF HYPERTHYROIDISM
• BLOOD TESTS FOR– DECREASED TSH LEVELS
– INCREASED THYROID HORMONE LEVELS(T3, T4, T7)
• IODINE THYROID SCAN
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TREATMENT
• ADMINISTRATION OF DRUGS THAT DECREASE HORMONE PRODUCTION
• RADIATION TREATMENT
• SURGERY
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ADMINISTRATION OF DRUGS TO SUPRESS HORMONE
PRODUCTION• METHIMAZOLE
• PROPYLTHIOURACIL (PTU).
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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
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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
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HYPOTHYROIDISM
• LACK OF THYROID HORMONE
• EFFECTS ARE GENERALLY OPPOSITE OF HYPERTHYROIDISM
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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
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PHYSIOLOGICAL EFFECTS OF HYPOTHYROIDISM
• MYXEDEMA
• ATERIOSCLEROSIS
• CRETINISM
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MYXEDEMA
• EDEMA THROUGHOUT BODY
• IN PATIENT’S WITH ALMOST NO THYROID FUNCTION
• INCREASE IIN PROTEOGLYCANS CAUSES SWELLING
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ATERIOSCLEROSIS
• LACK OF THYROID INCREASES THE AMOUNT OF BLOOD LIPIDS– ESPECIALLY CHOLESTEROL
• OFTEN RESULTS IN PERIPHERAL VASCULAR DISEASE
• DEAFNESS
• EXTREME CORONARY SCLEROSIS
• DEMIS
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CAUSES OF HYPOTHYROIDISM
• HASHIMOTO’S THYROIDITIS– AUTOIMMUNE THYROIDITIS
• MEDICAL TREATMENTS– SURGERY
– RADIATION TREATMENT
• LACK OF TSH SECRETION
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CONSEQUENCES OF HYPOTHYROIDISM
• TSH MAY CAUSE THRYOID TO ENLARGE
• COMPENSATORY GOITER
• RARE CONSEQUENCES– SEVERE DEPRESSION– HEART FAILURE– COMA
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DIAGNOSIS OF HYPOTHYROIDISM
• DIAGNOSIS BASED ON AMOUNT OF THYROID HORMONE IN BLOOD
• MEASURE BLOOD LEVELS OF T4 AND TSH
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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.
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TREATMENT OF HYPOTHYROIDISM
• EASY TO TREAT WITH HORMONE REPLACEMENT– LEVOTHYROXINE
– SYNTHETIC T4
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PRETIBIAL MYXEDEMA
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MYXEDEMA
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DISTURBANCES OF THE ENDOCRINE SYSTEM
THE PARATHYROID GLAND
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HYPERPARATHYROIDISM
• OVER SECRETION OF PARATHYROID HORMONE
• OSTEOPENIA
• OSTEOPOROSIS
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CAUSE OF HYPERPARATHYROIDISM
• OVERSECRETION OF PARATHYROID HORMONE
• BENIGN TUMORS
• HYPERPLASIA
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BENIGN TUMOR
• ADENOMA– 87-93% OF ALL CASES
• HYPERPLASIA
• ,
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CANCERS OF THE PARATHYROID IS VERY
RARE• LESS THAN 1 %
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SYMPTOMS OF HYPERPARATHYROIDISM
• OSTEOPENIA
• OSTEOPOROSIS
• BONE FRACTURES
• KIDNEY STONES
• PEPTIC ULCERS
• PANCREATITIS
• NERVOUS SYSTEM COMPLICATIONS
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DIAGNOSIS
• INAPPROPRIATE LEVELS OF PTH WHEN EXCESS CALCIUM IS PRESENT
• CALCIUM LEVELS IN THE URINE
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TREATMENT
• DO NOTHING
• SURGERY
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HYPOPARATHYROIDISM
• RARE• DEFICIENT PARATHYROID HORMONE
SECRETION.• INABILITY TO MAKE AN ACTIVE FORM OF
PTH.• INABILITY OF THE KIDNEYS & BONES TO
RESPOND TO PTH.
• ...
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DEFICIENT PARATHYROID SECRETION
• SURGICAL.
• IDIOPATHIC..– CONGENITAL
– ACQUIRED
• HYPOMAGNESEMIA
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SURGICAL CAUSES
• REMOVAL OF PARATHYROID TO CURE HYPERPARATHYROIDISM
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IDIOPATHIC HYPOPARATHYROIDISM
• WITHOUT A DEFINE CAUSE
• CONGENITAL
• ACQUIRED
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CONGENITAL
• PRESENT AT BIRTH
• BORN WITHOUT PARATHYROID
• BABIES WHOSE MOTHERS HAVE OVERACTIVE PARATHYROID GLANDS
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ACQUIRED
• ANTIBODIES DESTROY THE PARATHYROID
• ANTIBODIES BIND TO PARATHYROID CELLS AND BLOCK STIMULATION
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HYPOMAGNESEMIA
• MAGNESIUM IS NECESSARY FOR PTH PRODUCTION
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SECRETION OF BIOLOGICALLY INACTIVE PTH
• RARE
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RESISTANCE TO PARATHYROID HORMONE
• (PSEUDO-HYPOPARATHYROIDISM
• RARE
• PTH IS PRODUCED
• TARGET CELLS DO NOT RESPOND
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TREATMENT
• ADMINISTRATION OF VITAMIN D
• ADMINISTRATION OF CALCIUM
• HYPOMAGNESEMIA IS TREATED WITH MAGNESIUM
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DISTURBANCES OF THE ENDOCRINE SYSTEM
THE PITUITARY
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ACROMEGALY
• EXCESS SECRETION OF GROWTH HORMONE AFTER EPIPHYSEAL PLATES HAVE CLOSED
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HYPOPITUITARISM