Abdominal Region I

PA 481 Anatomy & Physiology

Tony Serino, Ph.D.

Biology Department

Misericordia Univ.

Peritoneal Cavity

Includes abdominopelvic cavity

Abdominal Regions

Midclavicular planes

Transtubercular plane

Subcostal plane

Abdominal Quadrants

Median Plane

Transumbilical Plane

Peritoneal Cavity

Lesser omenta bursa

Greater omenta bursa (supracolic portion)

Greater omenta bursa(infracolic portion)

Retroperitoneal Position

Bony structures

• Last thoracic vertebra and ribs

• Lumbar vertebrae

• Pelvis

• Sacrum

Lumbar vertebra

Lumbar Vertebra

Pelvis

Innominate (coxal bone)

Sacrum

Camper’s and Scarpa’s Fascia

Aponeurosis of ext. oblique

Inguinal Ligament

Pubis

Scarpa’s (membranous) fascia

Camper’s (fatty) fascia

Potential space below Scarpa’s fascia

Scarpa’s fascia

Ruptured Urethra

Inferior Diaphragm

Abdominal Muscles

Abdominal Wall Layers

Rectus sheath

Superficial Inguinal Ring

Inguinal Ligament

Peritoneal Cavity Mesenteries

Mesenteries

Mesenteries

Greater and Lesser Sac

Omental Foramen

TC

StGreater Sac

Lesser sac

Mesenteries

Digestion

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

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

Major Organs of System

Accessory Organs

Teeth

GI Tract Development

Pylorus

Late Gastrulation Post-gastrula

Basic Histology of Digestive Tract

(LOCI)

(Meissner’s)(Auerbach’s)

Peristalsis

Segmentation

Control of Overall GI Tract Activity

Upper Abdominal XS

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)

Stomach Anatomy

• Mucosa: – simple columnar folded into

rugae

– No villi

– Openings leading to gastric pits and glands

• Muscularis:– Has three layers

Rugae of StomachTemporary longitudinal foldings of the mucosa

Blood supply

Stomach Histology

Gastric Gland

Regulation of Gastric Juice

Gastric Emptying

Gastric Emptying

Spleen

Internal Spleen

Adrenal Location and Structure

Adrenal Layers

(Epinephrine (adrenalin))

(Mineralocorticoids,(Aldosterone))

(Glucocorticoids (cortisol))

(Androgens)

GAS (General Adaptation Syndrome)

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

Cushings

(buffalo hump) Obesity of trunk

Adrenogenital syndrome

A 15 yo girl, note typical masculinebuild, under developed breasts, andexcessive body hair

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

Duodenum and Accessory Organs

Duodenal Papilla

Pancreas

Pancreas Histology

Pancreatic Acinus

Exocrine Secretions of Pancreas

Secretion of Pancreatic Juice

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, O2 consumption, or CO2 produced

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

Review of Metabolic Pathways

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

Absorptive State

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

Post-Absorptive

State

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

Fuel Homeostasis Regulated by Pancreas

• Both an exocrine and endocrine gland

• Located in middle of upper right abdominal quadrant

• Islets of Langerhans secrete hormones

Islet of Langerhans

-cells secrete insulin -cells secrete glucagon -cells secrete somatostatin f-cells secrete PP (pancreatic

polypeptide)

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

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

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

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)

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

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

Organ Response to Insulin Deficiency