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DISTURBANCES OF THE ENDOCRINE SYSTEM THE ADRENAL GLAND.

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Presentation on theme: "DISTURBANCES OF THE ENDOCRINE SYSTEM THE ADRENAL GLAND."— Presentation transcript:

1 DISTURBANCES OF THE ENDOCRINE SYSTEM THE ADRENAL GLAND

2 ADDISONS DISEASE PRIMARY ADRENAL INSUFFICIENCY SECONDARY ADRENAL INSUFFICIENCY

3 PRIMARY ADRENAL INSUFFICIENCY

4 ADDISONS DISEASE FAILURE OF ADRENAL CORTEX TO PRODUCE ADRENOCORITICAL HORMONES USUALLY CAUSED BY PRIMARY ATROPHY OF ADRENAL CORTEX AUTOIMMUNITY TUBERCULOSIS CANCER

5 HORMAL DISTURBANCES MINERALOCORTICOID GLUCOCORTICOID

6 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

7 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

8 AFFECT ON MUSCLES WEAKNESS IN MUSCLES EVEN WHEN EXCESS GLUCOSE AND OTHER NUTRIENTS ARE AVAILABLE

9 THE UNTREATED INDIVIDUAL WILL DIE IN A FEW DAYS TO TWO WEEKS DUE TO CONSUMING WEAKNESS AND CIRCULATORY SHOCK

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

11 DIAGNOSIS MEDICAL HISTORY OF SYMPTOMS HYPERPIGMENTATION ELVATED BLOOD LEVEL OF POTASSIUM RATIO OF WHITE BLOOD CELLS ECG CHANGES CHEST X-RAY

12 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

13 TREATMENT OF ADDISONS DISEASE MINERALOCORTICOIDS ADMINSTERED GLUCOCORTICOIDS ADMINISTERED MUST HAVE A HIGH SALT DIET

14 ADDISONIAN CRISIS OCCURS DURING PHYSICAL OR MENTAL STRESS UNABLE TO SECRETE EXTRA NEEDED GLUCOCORTICOIDS BEFORE SURGERY MUST ADMINISTER MASSIVE AMOUNTS OF GLUCOCORTICOIDS

15 DID HE OR DIDNT HE

16 HYPERADRENALISMS CUSHINGS DISEASE CONNS SYNDROME

17 CUSHINGS DISEASE EFFECTS OF EXCESS CORTISOL IN BODY –PITUITARY TUMOR –ADRENAL TUMOR –ADMINISTRATION OF PREDNISONE OR OTHER GLUCOCORTICOIDS

18 HORMONAL DISTURBANCES INCREASED CORTISOL SOMETIMES INCREASED ANDROGENS

19 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

20 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

21 DIAGNOSIS OF CUSHINGS DISEASE MEDICAL HISTORY PHYSICAL EXAM LAB TEST X-RAYS

22 DEFINITIVE DIAGNOSITC TEST 24-Hour Urinary Free Cortisol Level

23 DIAGNOSTIC TESTS DEXAMETHASONE SUPPRESSION TEST CRH STIMULATION TEST DIRECT VISUALIZATION OF THE ENDOCRINE GLANDS (RADIOLOGIC IMAGING)

24 TESTS THAT DIFFERENTIATE BETWEEN PITUITARY AND ECTOPIC SOURCES OF ACTH PETROSAL SINUS SAMPLING

25 TEST THAT DISTINGUISHES BETWEEN CUSHINGS AND PSEUDOCUSHINGS THE DEXAMETHASONE-CRH TEST

26 TREATMENT SURGERY RADIATION CHEMOTHEURAPY IMMUNOTHERAPY DRUGS THAT SUPPRESS CORTISOL PRODUCTION GRADUAL REMOVAL FROM PRESCRIBED GLUCOCORTICOIDS

27 CONNS SYNDROME HYPERALDOSTERONISM OVERPRODUCTION OF MINERALOCORTICOIDS TUMOR OF ADRENAL CORTEX

28 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

29 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

30 TREATMENT SURGICAL REMOVAL HYPERTENSIVE MEDICATION MEDICATIONS THAT BLOCK ALDOSTERONE

31 DISTURBANCES OF THE ENDOCRINE SYSTEM THE THYROID

32 HYPERTHYROIDSM TOXIC GOITER THRYOTOXICOSIS GRAVES DISEASE

33 HYPERSECRETION OF THRYOID HORMONES

34 SIGNS AND SYMPTOMS OF HYPERTHYROIDISM PALPITATIONS HEAT INTOLERANCE NERVOUSNESS INSOMNIA BREATHLESSNESS INCREASED BOWEL MOVEMENTS FATIGUE LIGHT OR ABSENT MENSTRUAL PERIODS FAST HEART RATE TREMBLING HANDS WEIGHT LOSS MUSCLE WEAKNESS WARM MOIST SKIN HAIR LOSS STARING GAZE

35 CAUSES OF HYPERTHYROIDISM GRAVES 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.

36 GRAVES DISEASE MOST COMMON CAUSE AUTOIMMUNE DISEASE ANTIBODIES MIMIC TSH

37 DISTINCT CHARACTERISTICS OF GRAVES 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).

38 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

39 HYPERTHYROIDISM DUE TO A SINGLE NODULE BENIGN TUMORS SOMETIMES PRODUCE EXCESSIVE AMOUNTS OF THYROID HORMONES. TOXIC NODULAR GOITER

40 HYPERTHYROIDISM DUE TO THYRODITIS CAUSES THE TYPICAL SYMPTOMS GENERALLY LAST ONLY A FEW WEEKS SUBACUTE THYROIDITIS –CAUSED BY A VIRUS POSTPARTUM THYROIDITIS..

41 HYPERTHYROID IN PATIENTS WHO ABUSE THYROID MEDICATION ESPECIALLY FORMS ESPECIALLY T 3 FORMS

42 DIAGNOSIS OF HYPERTHYROIDISM BLOOD TESTS FOR –DECREASED TSH LEVELS –INCREASED THYROID HORMONE LEVELS(T3, T4, T7) IODINE THYROID SCAN

43 TREATMENT ADMINISTRATION OF DRUGS THAT DECREASE HORMONE PRODUCTION RADIATION TREATMENT SURGERY

44 ADMINISTRATION OF DRUGS TO SUPRESS HORMONE PRODUCTION METHIMAZOLE PROPYLTHIOURACIL (PTU).

45 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

46 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

47 HYPOTHYROIDISM LACK OF THYROID HORMONE EFFECTS ARE GENERALLY OPPOSITE OF HYPERTHYROIDISM

48 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

49 PHYSIOLOGICAL EFFECTS OF HYPOTHYROIDISM MYXEDEMA ATERIOSCLEROSIS CRETINISM

50 MYXEDEMA EDEMA THROUGHOUT BODY IN PATIENTS WITH ALMOST NO THYROID FUNCTION INCREASE IIN PROTEOGLYCANS CAUSES SWELLING

51 ATERIOSCLEROSIS LACK OF THYROID INCREASES THE AMOUNT OF BLOOD LIPIDS –ESPECIALLY CHOLESTEROL OFTEN RESULTS IN PERIPHERAL VASCULAR DISEASE DEAFNESS EXTREME CORONARY SCLEROSIS DEMIS

52 CAUSES OF HYPOTHYROIDISM HASHIMOTOS THYROIDITIS –AUTOIMMUNE THYROIDITIS MEDICAL TREATMENTS –SURGERY –RADIATION TREATMENT LACK OF TSH SECRETION

53 CONSEQUENCES OF HYPOTHYROIDISM TSH MAY CAUSE THRYOID TO ENLARGE COMPENSATORY GOITER RARE CONSEQUENCES –SEVERE DEPRESSION –HEART FAILURE –COMA

54 DIAGNOSIS OF HYPOTHYROIDISM DIAGNOSIS BASED ON AMOUNT OF THYROID HORMONE IN BLOOD MEASURE BLOOD LEVELS OF T 4 AND TSH

55 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.

56 TREATMENT OF HYPOTHYROIDISM EASY TO TREAT WITH HORMONE REPLACEMENT –LEVOTHYROXINE –SYNTHETIC T 4

57 PRETIBIAL MYXEDEMA

58 MYXEDEMA

59 DISTURBANCES OF THE ENDOCRINE SYSTEM THE PARATHYROID GLAND

60 HYPERPARATHYROIDISM OVER SECRETION OF PARATHYROID HORMONE OSTEOPENIA OSTEOPOROSIS

61 CAUSE OF HYPERPARATHYROIDISM OVERSECRETION OF PARATHYROID HORMONE BENIGN TUMORS HYPERPLASIA

62 BENIGN TUMOR ADENOMA –87-93% OF ALL CASES HYPERPLASIA,

63 CANCERS OF THE PARATHYROID IS VERY RARE LESS THAN 1 %

64 SYMPTOMS OF HYPERPARATHYROIDISM OSTEOPENIA OSTEOPOROSIS BONE FRACTURES KIDNEY STONES PEPTIC ULCERS PANCREATITIS NERVOUS SYSTEM COMPLICATIONS

65 DIAGNOSIS INAPPROPRIATE LEVELS OF PTH WHEN EXCESS CALCIUM IS PRESENT CALCIUM LEVELS IN THE URINE

66 TREATMENT DO NOTHING SURGERY

67 HYPOPARATHYROIDISM RARE DEFICIENT PARATHYROID HORMONE SECRETION. INABILITY TO MAKE AN ACTIVE FORM OF PTH. INABILITY OF THE KIDNEYS & BONES TO RESPOND TO PTH....

68 DEFICIENT PARATHYROID SECRETION SURGICAL. IDIOPATHIC.. –CONGENITAL – ACQUIRED HYPOMAGNESEMIA

69 SURGICAL CAUSES REMOVAL OF PARATHYROID TO CURE HYPERPARATHYROIDISM

70 IDIOPATHIC HYPOPARATHYROIDISM WITHOUT A DEFINE CAUSE CONGENITAL ACQUIRED

71 CONGENITAL PRESENT AT BIRTH BORN WITHOUT PARATHYROID BABIES WHOSE MOTHERS HAVE OVERACTIVE PARATHYROID GLANDS

72 ACQUIRED ANTIBODIES DESTROY THE PARATHYROID ANTIBODIES BIND TO PARATHYROID CELLS AND BLOCK STIMULATION

73 HYPOMAGNESEMIA MAGNESIUM IS NECESSARY FOR PTH PRODUCTION

74 SECRETION OF BIOLOGICALLY INACTIVE PTH RARE

75 RESISTANCE TO PARATHYROID HORMONE (PSEUDO-HYPOPARATHYROIDISM RARE PTH IS PRODUCED TARGET CELLS DO NOT RESPOND

76 TREATMENT ADMINISTRATION OF VITAMIN D ADMINISTRATION OF CALCIUM HYPOMAGNESEMIA IS TREATED WITH MAGNESIUM

77 DISTURBANCES OF THE ENDOCRINE SYSTEM THE PITUITARY

78 ACROMEGALY EXCESS SECRETION OF GROWTH HORMONE AFTER EPIPHYSEAL PLATES HAVE CLOSED

79

80 HYPOPITUITARISM


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