Anatomy amp Physiology Tony Serino PhD Abdominal 1 Topic Objectives Be able to distinguish between lesser and greater peritoneal cavities Be able to locate viscera in abdominal quadrants and regions ID: 907822
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Slide1
Abdominal Region I
Clinical Anatomy & PhysiologyTony Serino, Ph.D.
Slide2Abdominal 1: Topic Objectives
Be able to distinguish between lesser and greater peritoneal cavities.Be able to locate viscera in abdominal quadrants and regions.Be able to identify all anatomical structures of bones and muscles of abdominal and pelvic areas.Be able to identify Camper’s and Scarpa’s fascia.Be able to list and identify all features of major abdominal organs and their functions.
Be able to differentiate between short and long term stress adaptations.
Be able to describe hyper and
hyposecretion
effects of adrenal cortex.
Be able to describe effects of absorptive and post-absorptive states on the body and how the body controls these states.
Be able to apply nutritional states to diabetes.
Slide3Peritoneal Cavity
Includes abdominopelvic cavity
Slide4Abdominal Regions
Midclavicular planes
Transtubercular plane
Subcostal plane
Slide5Abdominal Quadrants
Median Plane
Transumbilical Plane
Slide6Peritoneal Cavity
Lesser omenta bursa
Greater omenta bursa
(supracolic portion)
Greater omenta bursa
(infracolic portion)
Slide7Retroperitoneal Position
Slide8Bony structuresLast thoracic vertebra and ribs
Lumbar vertebraePelvisSacrum
Slide9Lumbar vertebra
Slide10Lumbar Vertebra
Slide11Pelvis
Slide12Innominate (coxal bone)
Slide13Sacrum
Slide14Camper’s and Scarpa’s Fascia
Aponeurosis of ext. oblique
Inguinal Ligament
Pubis
Scarpa’s (membranous) fascia
Camper’s (fatty) fascia
Slide15Potential space below Scarpa’s fascia
Scarpa’s fascia
Ruptured Urethra
Slide16Inferior Diaphragm
Slide17Abdominal Muscles
Slide18Abdominal Wall Layers
Slide19Rectus sheath
Slide20Abdominal Hernias
Slide21Superficial Inguinal Ring
Inguinal Ligament
Slide22Peritoneal Cavity Mesenteries
Slide23Mesenteries
Slide24Mesenteries
Slide25Greater and Lesser Sac
Omental Foramen
TC
St
Greater Sac
Lesser sac
Slide26Mesenteries
Slide27Digestion
The reduction through mechanical and chemical means (hydrolysis) of complex food substances into simple monomers and their absorption into the internal environment.
Slide28Functions of Digestive System
Motility(Propulsion)
Ingestion –food enters tract
Mastication -chewing
Deglutition -swallowing
Transportation through tract (peristalsis)
Mixing
Egestion (Defecation)
SecretionEndocrine and Exocrine secretionsDigestion mechanical and chemical breakdown of foodAbsorptionPassage of food particles from external to the internal environment
Slide29Major Organs of System
Slide30Accessory Organs
Teeth
Slide31GI Tract Development
Pylorus
Late Gastrulation
Post-gastrula
Slide32Basic Histology of Digestive Tract
(LOCI)
(Meissner’s)
(Auerbach’s)
Slide33Peristalsis
Slide34Segmentation
Slide35Control of Overall GI Tract Activity
Slide36Upper Abdominal XS
Slide37Stomach (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)
Slide38Stomach Anatomy
Mucosa: simple columnar folded into rugaeNo villiOpenings leading to gastric pits and glandsMuscularis:Has three layers
Slide39Rugae of Stomach
Temporary longitudinal foldings of the mucosa
Slide40Blood supply
Slide41Stomach Histology
Slide42Regulation of Gastric Juice
Slide43Gastric Emptying
Slide44Gastric Emptying
Slide45Spleen
Slide46Internal Spleen
Slide47Adrenal Location and Structure
Slide48Adrenal Layers
(Epinephrine (adrenalin))
(Mineralocorticoids,
(Aldosterone))
(Glucocorticoids
(cortisol))
(Androgens)
Slide49GAS (General Adaptation Syndrome)
Slide50Adrenal Malfunction
Hypersecretion Cushing’s syndrome –increase in glucocorticoidsUsually 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 aldosteroneSalt imbalance, water retention,
h
BP, muscle weakness
Adrenogenital syndrome –too much androgen
Premature sexual development in children or masculinization in women
Slide51Cushings
(buffalo hump)
Obesity of trunk
Slide52Adrenogenital syndrome
A 15 yo girl, note typical masculine
build, under developed breasts, and
excessive body hair
Slide53Adrenal Cortex Malfunction
Hyposecretion –Addison’s diseaseDue to decrease amounts of mineral and glucocorticoidsCan be due to over use of steroids or an autoimmune mechanism resulting in destruction of the glandDehydration, K+ loss, iBP, fatigue, pigmentation deepening (bronzing of skin) may be symptom of loss of negative feedback
Slide54Duodenum and Accessory Organs
Slide55Duodenal Papilla
Slide56Pancreas
Slide57Pancreas Histology
Slide58Pancreatic Acinus
Slide59Exocrine Secretions of Pancreas
Slide60Secretion of Pancreatic Juice
Slide61Energy 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 aliveEstimated by heat production, O
2
consumption, or CO
2
produced
Slide62Acquisition of Energy and Nutrients
GI tract mechanically and chemically digests food into their chemical “building blocks” for absorption into internal environmentProteins into amino acidsCHO into monosaccharidesFats into fatty acids and glycerolMost of the absorbed material is first processed by the liver
Slide63Review of Metabolic Pathways
Slide64Nutritional States of the BodyAbsorptive State
Body is assimilating nutrients and is able to use the energy of this food to surviveLasts about 4 hours (represents time for food to pass through small intestine)Post-absorptive State (Fasting State)Occurs after meal fully absorbed
Slide65Absorptive State
Slide66Absorptive State Summary
Energy source for body is absorbed glucoseGlucose 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
Slide67Post-Absorptive State
Slide68Post-Absorptive State Summary
Body energy provided by stored reservesGlycogenolysis in muscle and liver releasing glucose to blood (glycogen glucose)Protein catabolism (esp. in muscle) puts AA in bloodGluconeogenesis 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
Slide69Fuel Homeostasis Regulated by Pancreas
Both an exocrine and endocrine glandLocated in middle of upper right abdominal quadrantIslets of Langerhans secrete hormones
Slide70Islet of Langerhans
b-cells secrete insulin
a
-cells secrete glucagon
d
-cells secrete somatostatin
f
-cells secrete PP (pancreatic polypeptide)
Slide71Slide72Slide73Insulin Regulation
Stimulated to be secreted by:Increase blood glucoseIncrease blood AAIncrease GI hormone levels in bloodIncrease parasympathetic activityInhibited by:Decrease blood glucoseIncrease sympathetic activity
Somatostatin
Slide74Insulin Effects
Message: increase glucose utilizationIncrease uptake of glu in all cells except brain and liver (increase glucose transporter proteins)Increase FA and AA uptakeIncreases glycolysis, glycogenesis, lipogenesis, and protein synthesisNet: decrease glu, AA and FA in blood; increase fat , glycogen and protein production
Slide75Glucagon Regulation
Stimulated by:Decrease blood glucoseIncrease blood AAIncrease sympathetic stimulationEpinephrine secretionInhibited by:Increase blood glucoseIncrease parasympathetic stimulation
Somatostatin secretion
Slide76Glucagon Effects
Increases cytoplasmic cAMP which triggers kinase activity to activate enzymesIncreases lipolysis, glycogenolysis, gluconeogenesisNet: increases blood glucose, FA, glycerol and ketonesMost cells survive on FA and ketone metabolism (glucose sparing action)
Slide77Exercise EffectsEssentially a Fasting State but protein sparing
Skeletal muscle differs from normal response:Increases uptake and use of glucoseNo protein catabolism (after excerise; increase protein synthesis
Slide78Diabetes
Disease state characterized by polyuria, polydipsia, polyphagiaDiabetes Insipidus –triggered by decrease production of ADH in post. pituitaryDiabetes Mellitus –due to hyposecretion secretion of insulin or insulin hyporesponsivenessType I (Insulin dependent or Juvenile) results from loss of b-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
Slide79Slide80Organ Response to Insulin Deficiency
Slide81