1. DISTURBANCES OF THE ENDOCRINE SYSTEM
THE ADRENAL GLAND

2. ADDISON’S DISEASE PRIMARY ADRENAL INSUFFICIENCY
SECONDARY ADRENAL INSUFFICIENCY

3. PRIMARY ADRENAL INSUFFICIENCY

4. ADDISON’S 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 ADDISON’S 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 DIDN’T HE

16. HYPERADRENALISMS
CUSHING’S DISEASE
CONN’S SYNDROME

17. CUSHING’S 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 CUSHING’S 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 CUSHING’S AND PSEUDOCUSHING’S
THE DEXAMETHASONE-CRH TEST

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

27. CONN’S 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
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.

36. GRAVES DISEASE MOST COMMON CAUSE AUTOIMMUNE DISEASE
ANTIBODIES MIMIC TSH

37. 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).

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 T3 FORMS
depending on the underlying cause.

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 PATIENT’S 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
HASHIMOTO’S 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 T4 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 T4

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
life.

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

80. HYPOPITUITARISM