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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