Abdominal Region I Clinical - PowerPoint Presentation

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Abdominal Region I

Clinical Anatomy & PhysiologyTony Serino, Ph.D.

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Abdominal 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.

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Peritoneal Cavity

Includes abdominopelvic cavity

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Abdominal Regions

Midclavicular planes

Transtubercular plane

Subcostal plane

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Abdominal Quadrants

Median Plane

Transumbilical Plane

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Peritoneal Cavity

Lesser omenta bursa

Greater omenta bursa

(supracolic portion)

Greater omenta bursa

(infracolic portion)

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Retroperitoneal Position

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Bony structuresLast thoracic vertebra and ribs

Lumbar vertebraePelvisSacrum

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Lumbar vertebra

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Lumbar Vertebra

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Pelvis

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Innominate (coxal bone)

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Sacrum

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Camper’s and Scarpa’s Fascia

Aponeurosis of ext. oblique

Inguinal Ligament

Pubis

Scarpa’s (membranous) fascia

Camper’s (fatty) fascia

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Potential space below Scarpa’s fascia

Scarpa’s fascia

Ruptured Urethra

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Inferior Diaphragm

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Abdominal Muscles

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Abdominal Wall Layers

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Rectus sheath

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Abdominal Hernias

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Superficial Inguinal Ring

Inguinal Ligament

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Peritoneal Cavity Mesenteries

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Mesenteries

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Mesenteries

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Greater and Lesser Sac

Omental Foramen

TC

St

Greater Sac

Lesser sac

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Mesenteries

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Digestion

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

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Functions 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

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Major Organs of System

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Accessory Organs

Teeth

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GI Tract Development

Pylorus

Late Gastrulation

Post-gastrula

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Basic Histology of Digestive Tract

(LOCI)

(Meissner’s)

(Auerbach’s)

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Peristalsis

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Segmentation

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Control of Overall GI Tract Activity

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Upper Abdominal XS

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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)

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Stomach Anatomy

Mucosa: simple columnar folded into rugaeNo villiOpenings leading to gastric pits and glandsMuscularis:Has three layers

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Rugae of Stomach

Temporary longitudinal foldings of the mucosa

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Blood supply

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Stomach Histology

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Regulation of Gastric Juice

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Gastric Emptying

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Gastric Emptying

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Spleen

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Internal Spleen

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Adrenal Location and Structure

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Adrenal Layers

(Epinephrine (adrenalin))

(Mineralocorticoids,

(Aldosterone))

(Glucocorticoids

(cortisol))

(Androgens)

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GAS (General Adaptation Syndrome)

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Adrenal 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

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Cushings

(buffalo hump)

Obesity of trunk

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Adrenogenital syndrome

A 15 yo girl, note typical masculine

build, under developed breasts, and

excessive body hair

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Adrenal 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

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Duodenum and Accessory Organs

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Duodenal Papilla

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Pancreas

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Pancreas Histology

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Pancreatic Acinus

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Exocrine Secretions of Pancreas

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Secretion of Pancreatic Juice

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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 aliveEstimated by heat production, O

2

consumption, or CO

2

produced

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Acquisition 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

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Review of Metabolic Pathways

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Nutritional 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

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Absorptive State

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Absorptive 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

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Post-Absorptive State

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Post-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

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Fuel Homeostasis Regulated by Pancreas

Both an exocrine and endocrine glandLocated in middle of upper right abdominal quadrantIslets of Langerhans secrete hormones

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Islet of Langerhans

b-cells secrete insulin

a

-cells secrete glucagon

d

-cells secrete somatostatin

f

-cells secrete PP (pancreatic polypeptide)

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Insulin 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

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Insulin 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

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Glucagon Regulation

Stimulated by:Decrease blood glucoseIncrease blood AAIncrease sympathetic stimulationEpinephrine secretionInhibited by:Increase blood glucoseIncrease parasympathetic stimulation

Somatostatin secretion

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Glucagon 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)

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Exercise 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

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Diabetes

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

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Organ Response to Insulin Deficiency

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