1. D. C. MIKULECKY PROFESSOR OF PHYSIOLOGY AND FACULTY MENTORING PROGRAM

2.  NERVOUS SYSTEM  “WIRED”  CHEMICAL SIGNAL AT TARGET CELL  RAPID  BRIEF DURATION  CLOSE ANATOMICAL PROXIMITY  ENDOCRINE SYSTEM  “WIRELESS”  CHEMICAL SIGNAL AT TARGET CELL  SLOW  LONG DURATION  SPECIFIC RECEPTORS

3.  PEPTIDES  AMINES  STEROIDS

4.  HYDROPHILIC  DISSOLVED IN PLASMA  RECEPTOR ON CELL SURFACE  cAMP OR CALCIUM AS SECOND MESSENGERS  ACTIVATE SPECIFIC GENES TO INITIATE PROTEIN SYNTHESIS

5.  HYPOTHALAMIC  PITUITARY  PANREATIC  PARATHYROID  GI  KIDNEY  LIVER  HEART

6.  THYROID HORMONE  CATECHOLAMINES  ALL DERIVED FROM AMINO ACID TYROSINE  UNIQUE SYNTHETIC AND SECRETORY PATHWAYS

7.  LIPOPHILIC  RECEPTOR IN CYTOPLASM  ACTIVATE SPECIFIC GENES TO INITIATE PROTEIN SYNTHESIS  ADRENAL CORTICAL  GONADAL  PLACENTAL

8.  DEPENDS ON RATE OF SECRETION  NEGATIVE FEEDBACK  NEUROENDOCRINE REFLEXES  DIURNAL RHYTHMS

9.  HORMONE EXCESS  HORMONE DEFICIENCY  DECREASED RESPOSIVENESS OF RECEPTORS

10. HYPOTHALAMUS NEUROSECRETORY NEURONS ANTERIOR PITUITARY POSTERIOR PITUITARY SYSTEMIC ARTERY SYSTEMIC VEIN VASOPRESSIN OXYTOCIN

11. HYPOTHALAMUS NEUROSECRETORY NEURONS ANTERIOR PITUITARY: TSH ACTH PROLACTIN GROWTH HORMONE LH FSH POSTERIOR PITUITARY

12.  VESSELS PASS THROUGH STALK OF PITUITARY FROM HYPOTHALAMUS TO ANTERIOR PITUITARY  CARRY HYPOTHALAMIC REGULATORY HORMONES

13.  TROPIC HORMONES  CONTROL THE SECRETION OF OTHER HORMONES BY ACTING ON ENDOCRINE TISSUE

14.  CONTROL THE SECRETION OF ANTERIOR PITUITARY TROPIC HORMONES  TRH:THYROTROPIN-RELEASING HORMONE  PRH:PROLACTIN RELEASING HORMONE  PIH:PROLACTIN INHIBITING HORMONE  GHRH:GROWTH HORMONE RELEASING HORMONE  GHIH: GROWTH HORMONE INHIBITING HORMONE  CRH:CORTICOTROPHIN RELEASING HORMONE

15. INPUT HORMONE 1 (RELEASING/INHIBITING) HORMONE 2 (TROPIC) HORMONE 3 TARGET CELLS SYSTEMIC CIRCULATION H/H PORTAL SYSTEM HYPOTHALAMUS ANTERIOR PITUITARY ENDOCRINE GLAND

16. INPUT HORMONE 1 (RELEASING/INHIBITING) HORMONE 2 (TROPIC) HORMONE 3 TARGET CELLS SYSTEMIC CIRCULATION H/H PORTAL SYSTEM HYPOTHALAMUS ANTERIOR PITUITARY ENDOCRINE GLAND

17.  THYROID GLAND  THYROID HORMONES (T 3 & T 4 )

18.  ADRENAL CORTEX  CORTISOL

19.  MAMMARY GLANDS  BREAST GROWTH AND MILK SECRETION

20.  LIVER  SOMATOMEDINS  BONE  SOFT TISSUE  GROWTH  MANY TISSUES  INTERMEDIARY METABOLISM  INCREASE OR DECREASE

21.  LH:LETEINIZING HORMONE  SEX HORMONE SECRETION  F: ESTROGEN AND PROGESTERONE  M: TESTOSTERONE  FSH:FOLLICLE STIMULATING HORMONE  GAMETE PRODUCTION  OVA  SPERM

22.  GENETIC  DIET  DISEASE  HORMONES

23.  LIVER  SOMATOMEDINS  BONE  SOFT TISSUE  GROWTH  MANY TISSUES  INTERMEDIARY METABOLISM  INCREASE OR DECREASE

24.  MOBILIZES TRIGLYCERIDE FAT STORED IN ADIPOSE TISSUE  CONSERVES GLUCOSE FOR BRAIN

25.  SOFT TISSUES: STIMULATES CELL DIVISION, INCREASES SIZE OF CELLS  STIMULATES ALMOST ALL ASPECTS OF PROTEIN SYNTHESIS  INHIBITS PROTEIN DEGRADATION  PROMOTES UPTAKE OF AMINO ACIDS

26.  BONE: PROMOTES GROWTH OF LONG BONES  THICKNESS  LENGTH  AT END OF ADOLESCENCE, SEX HORMONES STOP THIS ACTION

27.  PEPTIDE MEDIATORS  PRODUCED IN LIVER AND OTHER TISSUES  ALSO PARACRINE EFFECTS

28.  ANTAGONIST IN CONTROL OF GROWTH HORMONE SECRETION  NEGATIVE FEEDBACK  DIURNAL RHYTHM: GH SECRETED AT NIGHT  EXERCISE, STRESS, HYPOGLYCEMIA

29.  DEFICIENCY: DWARFISM, REDUCED MUSCLE STRENGTH, DECREASED BONE DENSITY  EXCESS:GIGANTISM, ACROMEGLY

30.  OVER TRACHEA  THYROGLOBULIN  TETRAIODOTHYRONINE  TRIIODOTHYRONINE  IODINE REQUIRED FROM DIETARY INTAKE

31.  METABOLIC RATE: INCREASED BMR  CALOROGENIC: INCREASED HEAT PRODUCTION  SYMPATHOMIMETIC: FLIGHT OR FIGHT  CARDIOVASCULAR:INCREASES RESPONSIVENESS OF HEART  GROWTH: ESSENTIAL FOR NORMAL GROWTH  NERVOUS SYSTEM:DEVELOPMENT AND ADULT ACTIVITY

32. HYPOTHALAMUS TRH ANTERIOR PITUITARY TSH THYROID GLAND TARGET ORGANS THYROID HORMONE STRESS COLD IN CHILDREN - +

33.  HYPO  REDUCED BMR  POOR TOLERANCE OF COLD  GAIN OF WEIGHT  FATIGUE  SLOW, WEAK PULSE  SLOW REFLEXES AND MENTATION  MYXEDEMA  GOITER  CRETINISM  HYPER  GRAVE’S DISEASE:TSI  EXOPHTALMOS  GOITER

34.  CORTEX: STEROID HORMONES SECRETED  MEDULLA: CATECHOLAMINES

35.  MINERALOCORTICOIDS  GLUCOCORTICOIDS  SEX HOMONES

36.  ALDOSTERONE  ELECTROLYTE BALANCE  BLOOD PRESSURE  RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

37.  CORTISOL  GLOCONEOGENESIS  PERMISSIVE ACTIONS  STRESS ADAPTATION  ANTI-INFLAMITORY AND IMMUNOSUPPRESSANT

38. HYPOTHALAMUS CRH ANTERIOR PITUITARY ACTH ADRENAL CORTEX TARGET ORGANS CORTISOL STRESS DIURNAL RHYTHM + + - - INCREASED BLOOD GLUCOSE BLOOD AA BLOOD FATTY ACIDS

39.  ANDROGENS (TESTOSTERONE)  ESTROGENS  LESS THAN GONADS

40.  MINERALCORTICOIDS: SODIUM RETENTION, POTASSIUM DEPLETION  CORTISOL:EXCESS GLUCONEOGENESIS- EXCESS GLUCOSE DEPOSITED AS FAT  ANDROGEN:MASCULINIZATION, PSEUDOHERMAPHODITISM, PRECOCIOUS PSEUDOPUBERTY, NO EFFECT IN ADULT MALES

41.  CORTEX: ADDISON’S DISEASE  POOR RESPONSE TO STRESS  LACK OF PERMISSIVE ACTION  POTASSIUM RETENTION  HYPOTENSION

42.  A MODIFIED SYMPATHETIC POST GANGLIONIC NEURON  EPINEPHRINE

43.  MIMICS SYMPATHETIC NS  MOBILIZES STORED FAT AND CARBOHYDRATE  HEART AND BLOOD VESSELS

44.  FLIGHT OR FIGHT  EPINEPHRINE  CRH-ACTH-CORTISOL  RENIN-ANGIOTENSIN-ALDOSTERONE  VASOPRESSIN  COORDINATED BY HYPOTHALAMUS  CAN BE INDUCED PSYCHOSOCIALLY

45.  GLYCOGENESIS  GLYCOGENOLYSIS  GLUCONEOGENESIS  PROTEIN SYNTHESIS  PROTEIN DEGRADATION  FAT SYNTHESIS  FAT BREAKDOWN

46.  BUILD UP VS BREAKDOWN OF LARGE MOLECULES  ANABOLISM REQUIRES ENERGY (ATP)  CATABOLISM:ENERGY PRODUCTION

47.  INSULIN  GLUCAGON

48.  BETA CELLS IN ISLETS OF LANGERHANS: INSULIN  FACILITIES GLUCOSE ENTRY INTO CELLS  STIMULATES GLYCOGENESIS  INHIBITS GLYCOGENOLYSIS  INHIBITS GLUCONEOGENESIS

49.  INCREASES TRANSPORT INTO ADIPOSE CELLS  PROMTES TRIGLYCERIDE SYNTHESIS  INHIBITS LIPOLYSIS

50.  PROMOTES UPTAKE OF AA BY MUSCLE AND OTHER TISSUE  PROMOTES PROTEIN SYNTHESIS  INHIBITS PROTEIN DEGRADATION

51.  NEGATIVE FEEDBACK: BLOOD SUGAR  BLOOD AA  GI HORMONES  PARASYMPATHETIC ACTIVITY

52.  TYPE I: AUTOIMMUNE DESTRUCTION OF BETA CELLS, LACK OF INSULIN SECRETION  TYPE II: REDUCED SENSITIVITY OF INSULIN RECEPTORS

53.  EXTRACELLULAR GLUCOSE EXCESS  GLUCOSE IN URINE  EXCESS FLUID LOSS  CIRCULATORY FAILURE  RENAL FAILURE  NERVOUS SYSTEM MALFUNCTION DUE TO DEHYDRATION  EXCESSIVE FOOD INTAKE  PROGRESSIVE WEIGHT LOSS  MOBILIZTION OF FAT  KETOSIS  ACIDOSIS  COMA AND DEATH

54.  PANCREATIC ALPHA CELLS  GENERALLY OPPOSES ACTIONS OF INSULIN  DECREASE GLYCOGEN SYNTHESIS  PROMOTE GLYCOGENOLYSIS  STIMULATE GLUCONEOGENESIS  PROMOTES FAT BREAKDOWN  ONLY IN LIVER: PROTEIN CATABOLISM

55.  ALL INCREASE BLOOD GLUCOSE AND FATTY ACIDS  CORTISOL INCREASES BLOOD AA AND DECREASES MUSCLE PROTEIN  GH DECREASES BLOOD AA AND INCREASES MUSCLE PROTEIN

56.  PARATHYROID HORMONE  CALCITONIN  VITAMIN D

57.  RAISES FREE PLASMA CALCIUM  FROM BONE  CONSERVATION IN KIDNEYS  INCREASES INTESTINAL ABSORPTION (VIA VITAMIN D ACTIVATION)  REGULATED BY FREE CALCIUM IN PLASMA (NEGATIVE FEEDBACK)

58.  C CELLS OF THYROID GLAND  DECREASE IN CA MOBILIZATION FROM BONE  NOT AS IMPORTANT AS PTH AND VITAMIN D

59.  ACTUALLY A HORMONE  RELEASED FROM SKIN BY SUNLIGHT  TWO STEP ACTIVATION: LIVER AND KIDNEYS  INCREASES CALCIUM ABSORPTION IN INTESTINE

60.  LOW CALCIUM AND HIGH PHOSPHATE  MUSCLE SPASMS  MENTAL CHANGES

61.  IMPARED ABSORPTION OF CALCIUM  PTH MAINTAINS PLASMA LEVEL AT EXPENSE OF BONES  RICKETS IN CHILDREN  OSTEOMALACIA IN ADULTS