1. Abdominal Region I PA 481 Anatomy & Physiology Tony Serino, Ph.D. Biology Department Misericordia Univ.

2. Peritoneal Cavity Includes abdominopelvic cavity

3. Abdominal Regions Midclavicular planes Transtubercular plane Subcostal plane

4. Abdominal Quadrants Median Plane Transumbilical Plane

5. Peritoneal Cavity Lesser omenta bursa Greater omenta bursa (supracolic portion) Greater omenta bursa (infracolic portion)

6. Retroperitoneal Position

7. Bony structures Last thoracic vertebra and ribs Lumbar vertebrae Pelvis Sacrum

8. Lumbar vertebra

9. Lumbar Vertebra

10. Pelvis

11. Innominate (coxal bone)

12. Sacrum

13. Camper’s and Scarpa’s Fascia Aponeurosis of ext. oblique Inguinal Ligament Pubis Scarpa’s (membranous) fascia Camper’s (fatty) fascia

14. Potential space below Scarpa’s fascia Scarpa’s fascia Ruptured Urethra

15. Inferior Diaphragm

16. Abdominal Muscles

17. Abdominal Wall Layers

18. Rectus sheath

19. Superficial Inguinal Ring Inguinal Ligament

20. Peritoneal Cavity Mesenteries

21. Mesenteries

23. Greater and Lesser Sac Omental Foramen TC St Greater Sac Lesser sac

24. Mesenteries

25. Digestion The reduction through mechanical and chemical means (hydrolysis) of complex food substances into simple monomers and their absorption into the internal environment.

26. Functions of Digestive System Motility(Propulsion) –Ingestion –food enters tract –Mastication -chewing –Deglutition -swallowing –Transportation through tract (peristalsis) –Mixing –Egestion (Defecation) Secretion –Endocrine and Exocrine secretions Digestion –mechanical and chemical breakdown of food Absorption –Passage of food particles from external to the internal environment

27. Major Organs of System

28. Accessory Organs Teeth

29. GI Tract Development Pylorus Late Gastrulation Post-gastrula

30. Basic Histology of Digestive Tract (LOCI) (Meissner’s) (Auerbach’s)

31. Peristalsis

32. Segmentation

33. Control of Overall GI Tract Activity

34. Upper Abdominal XS

35. Stomach (cadaver) J-shaped muscular pouch Receives bolus and produces chyme Liquefies food by mixing it with HCl and vigorous churning Low pH stops amylase activity, but secretes pepsinogen (pepsin) that begins break down of proteins Absorbs little except imbibed water, electrolytes, and some drugs (ie. alcohol and aspirin)

36. Stomach Anatomy Mucosa: –simple columnar folded into rugae –No villi –Openings leading to gastric pits and glands Muscularis: –Has three layers

37. Rugae of Stomach Temporary longitudinal foldings of the mucosa

38. Blood supply

39. Stomach Histology

40. Gastric Gland

41. Regulation of Gastric Juice

42. Gastric Emptying

44. Spleen

45. Internal Spleen

46. Adrenal Location and Structure

47. Adrenal Layers (Epinephrine (adrenalin)) (Mineralocorticoids, (Aldosterone)) (Glucocorticoids (cortisol)) (Androgens)

48. GAS (General Adaptation Syndrome)

49. Adrenal Malfunction Hypersecretion Cushing’s syndrome –increase in glucocorticoids –Usually due to over secretion of ACTH by pituitary or from adrenal cortex tumors stimulating an increase in glucocorticoids. Characteristic obesity of trunk only and development of “buffalo hump” (a fat pad behind the shoulders). Will develop hypertension, atherosclerosis, muscular weakness and fatigue. Conn’s syndrome –excess amount of aldosterone –Salt imbalance, water retention,  BP, muscle weakness Adrenogenital syndrome –too much androgen –Premature sexual development in children or masculinization in women

50. Cushings (buffalo hump) Obesity of trunk

51. Adrenogenital syndrome A 15 yo girl, note typical masculine build, under developed breasts, and excessive body hair

52. Adrenal Cortex Malfunction Hyposecretion –Addison’s disease –Due to decrease amounts of mineral and glucocorticoids –Can be due to over use of steroids or an autoimmune mechanism resulting in destruction of the gland –Dehydration, K+ loss,  BP, fatigue, pigmentation deepening (bronzing of skin) may be symptom of loss of negative feedback

53. Duodenum and Accessory Organs

54. Duodenal Papilla

55. Pancreas

56. Pancreas Histology

57. Pancreatic Acinus

58. Exocrine Secretions of Pancreas

59. Secretion of Pancreatic Juice

60. Energy Metabolism Metabolic Rate (MR) –total rate of energy use in body (Kcal/min) -calorie = amount of heat needed to raise 1g of water one degree Celsius -1 Kcal (1000 calories) = 1 C (nutritional calorie) BMR –(basal MR) MR of conscious, relaxed person 12-14 hours after eating standardized for STP, diet and body size; represents the minimum energy required for individual to remain alive Estimated by heat production, O 2 consumption, or CO 2 produced

61. Acquisition of Energy and Nutrients GI tract mechanically and chemically digests food into their chemical “building blocks” for absorption into internal environment –Proteins into amino acids –CHO into monosaccharides –Fats into fatty acids and glycerol Most of the absorbed material is first processed by the liver

62. Review of Metabolic Pathways

63. Nutritional States of the Body Absorptive State –Body is assimilating nutrients and is able to use the energy of this food to survive –Lasts about 4 hours (represents time for food to pass through small intestine) Post-absorptive State (Fasting State) –Occurs after meal fully absorbed

64. Absorptive State

65. Absorptive State Summary Energy source for body is absorbed glucose Glucose utilization is favored (burn or store) Glycogenesis in skeletal muscles and liver: (Glucose  glycogen) Lipogenesis in adipose and liver: (FA  fat; also excess AA and glucose converted to FA in liver) Skeletal muscle and liver favor protein anabolism: (AA  protein) Dominated by insulin

66. Post- Absorptive State

67. Post-Absorptive State Summary Body energy provided by stored reserves Glycogenolysis in muscle and liver releasing glucose to blood (glycogen  glucose) Protein catabolism (esp. in muscle) puts AA in blood Gluconeogenesis in liver (creation of glucose from non- glycogen sources) –Lactate, pyruvate, glycerol, and AA Lipolysis (breakdown of fat  FA and glycerol) –FA used as energy source by most cells except brain –Liver can combine Co-A with FA to form ketones Dominated by glucagon

68. Fuel Homeostasis Regulated by Pancreas Both an exocrine and endocrine gland Located in middle of upper right abdominal quadrant Islets of Langerhans secrete hormones

69. Islet of Langerhans   -cells secrete insulin   -cells secrete glucagon   -cells secrete somatostatin  f -cells secrete PP (pancreatic polypeptide)

72. Insulin Regulation Stimulated to be secreted by: –Increase blood glucose –Increase blood AA –Increase GI hormone levels in blood –Increase parasympathetic activity Inhibited by: –Decrease blood glucose –Increase sympathetic activity –Somatostatin

73. Insulin Effects Message: increase glucose utilization Increase uptake of glu in all cells except brain and liver (increase glucose transporter proteins) Increase FA and AA uptake Increases glycolysis, glycogenesis, lipogenesis, and protein synthesis Net: decrease glu, AA and FA in blood; increase fat, glycogen and protein production

74. Glucagon Regulation Stimulated by: –Decrease blood glucose –Increase blood AA –Increase sympathetic stimulation –Epinephrine secretion Inhibited by: –Increase blood glucose –Increase parasympathetic stimulation –Somatostatin secretion

75. Glucagon Effects Increases cytoplasmic cAMP which triggers kinase activity to activate enzymes Increases lipolysis, glycogenolysis, gluconeogenesis Net: increases blood glucose, FA, glycerol and ketones Most cells survive on FA and ketone metabolism (glucose sparing action)

76. Exercise Effects Essentially a Fasting State but protein sparing Skeletal muscle differs from normal response: –Increases uptake and use of glucose –No protein catabolism (after excerise; increase protein synthesis

77. Diabetes Disease state characterized by polyuria, polydipsia, polyphagia Diabetes Insipidus –triggered by decrease production of ADH in post. pituitary Diabetes Mellitus –due to hyposecretion secretion of insulin or insulin hyporesponsiveness –Type I (Insulin dependent or Juvenile) results from loss of  - cells in pancreas (maybe autoimmune disease) (10% 0f diabetics) –Type II (insulin independent or Adult onset) results from loss of insulin membrane receptors in target tissues (Ab attachment to receptor or a chronic down regulation) (90% of diabetics) Chronic islets stimulation may result in hypertrophy and cell death; and thus insulin dependency

79. Organ Response to Insulin Deficiency