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38 Cards in this Set

  • Front
  • Back
Largest Organ in the abdominal cavity
Liver
Location of liver
Intraperitoneal

Located in right hypochondriac region

Superior portion in contact with inferior portion of diaphragm. Gallbladder located in the inferior region of liver
Name the four lobes of liver
Quadrate, left, Cuadate, Right (largest)
Describe functional unit of liver
Functional unit called Liver Lobule

Liver lobule is constructed around a central vein that empties into hepatic veins --> inferior vena cava
Rate of blood flow to liver
Every minute 1.1 liter of blood flows from the portal vein into liver sinusoids. 350 mL come from arterial system.

Total of 1.45 L/min which is 29% of resting CO and 33% of total body blood flow.
How much blood can the liver store
Normal stores a blood volume of 450 ml or 10% of body's total blood volume
What cells clean the blood in sinusoids
Kupffer cells
Carbohydrate Metabolism in Liver
Stores Glycogen
Converts fructose & galactose to glucose
Gluconeogenesis
Form important chemical compounds for carb. metabolism
Sucrose
Glucose + Fructose
Lactose
Glucose + Galactose
Maltose
Glucose + Glucose
FAT METABOLISM
-OXIDATION OF FATTY ACIDS TO SUPPLY ENERGY
-FORMATION OF MOST LIPOPROTEINS
-SYNTHESIS OF CHOLESTEROL AND PHOSPHOLIPIDS (±80%OF THE CHOLESTEROL IS CONVERTED INTO BILE SALTS).
-CONVERSION OF CARBOHYDRATES AND PROTEINS INTO FAT
PROTEIN METABOLISM
-DEAMINATION OF AMINOACIDS
-FORMATION OF UREA (AMMONIA REMOVAL FROM THE BODY FLUIDS)
-FORMATION OF PLASMA PROTEINS.
-INTERCONVERSIONS AMONG THE DIFFERENT AMINOACIDS AND AMINOACIDS AND OTHER COMPOUNDS.
Vitamins stored in liver
Vitamin A, D, B12 and Iron
Other functions of liver
Remove ammonia by urea formation. If ammonia concentration too high --> hepatic coma and death

Form 90% of all plasma proteins

Form coagulation factors like FIBRINOGEN; PROTHROMBIN AND COAGULATION FACTORS V-VII-VIII-IX-X-XI-XII-XIII.

Excrete many drugs, metabolites and Ca2+ into bile/feces.
Name the four tunics/layer of the basic alimentary canal in GI tract.
--THE MUCOSA
--SUBMUCOSA
--MUSCULARIS
--SEROSA.

EACH LAYER CONTAINS A PREDOMINANT TISSUE TYPE THAT HAS A SPECIFIC ROLE TO PLAY IN THE FOOD BREAKDOWN PROCESS.
Describe Mucosa
MAJOR FUNCTIONS ARE:
--SECRETION
(OF MUCUS, DIGESTIVE ENZYMES, AND HORMONES)
--ABSORPTION
(OF THE END PRODUCTS OF DIGESTION INTO THE BLOOD)
--PROTECTION
(AGAINST INFECTIOUS DISEASE).

THE MUCOSA IN A PARTICULAR REGION OF THE GI TRACT MAY EXPRESS ONE OR ALL THREE OF THESE CAPABILITIES.
Describe Submucosa
AREOLAR CONNECTIVE TISSUE CONTAINING
BLOOD VESSELS, LYMPHATIC VESSELS, NERVE ENDINGS, AND EPITHELIAL GLANDS.
ITS LUXURIANT VASCULAR NETWORK SUPPLIES SURROUNDING TISSUES AND CARRIES AWAY
ABSORBED NUTRIENTS.
Submucosal Plexus
The nerve supply located in submucosa.

Its PART OF THE INTRINSIC NERVE SUPPLY OF THE GI TRACT WALL AND IS ACTUALLY PART OF THE AUTONOMIC NERVOUS SYSTEM.
Describe Muscularis
MIXES AND PROPELS FOOD STUFFS ALONG THE DIGESTIVE TRACT.
HAS AN INNER CIRCULAR LAYER AND AN OUTER LONGITUDINAL LAYER OF SMOOTH MUSCLE CELLS.
AT SEVERAL POINTS ALONG THE GI TRACT, THE CIRCULAR MUSCLE LAYER BECOMES THICKENED TO FORM SPHINCTERS THAT ACT AS VALVES TO PREVENT BACKFLOW AND CONTROL FOOD PASSAGE FROM ONE ORGAN TO THE NEXT
Myenteric Plexus
THE AUTONOMIC NERVE PLEXUS IN MUSCULARIS LAYER

PROVIDES THE MAJOR NERVE SUPPLY TO THE GI TRACT WALL AND CONTROLS GI MOTILITY.

IN GENERAL, ACTIVITY OF PARASYMPATHETIC FIBERS ENHANCES GI MOTILITY AND SECRETORY ACTIVITY, WHEREAS SYMPATHETIC FIBERS INHIBIT MOTILITY, THEREBY DEPRESSING DIGESTION.
Describe the Serosa
IT’S THE PROTECTIVE OUTERMOST LAYER OF MOST OF THE ALIMENTARY CANAL WALL AND
THE VISCERAL PERITONEUM.
Subserous Plexus
THIRD AUTONOMIC PLEXUS, IS ASSOCIATED WITH THE SEROSA.
Regulation of Gastric Secretion
Controlled by both neural and hormonal mechanisms.

Gastric Mucosa will pour out 2-3 L of gastric juices a day

Gastric secretions involved not only in chemical digestion but also in regulation of stomach contraction
STIMULATION OF SECRETION.
NERVOUS CONTROL IS PROVIDED BY THE LONG AND SHORT NERVE REFLEXES.

WHEN THE VAGUS NERVES ACTIVELY STIMULATE THE STOMACH, SECRETORY ACTIVITY OF VIRTUALLY ALL OF ITS GLANDS INCREASES DRAMATICALLY.

HORMONAL CONTROL OF GASTRIC SECRETION IS LARGELY THE PROVINCE OF GASTRIN, WHICH STIMULATES THE SECRETION OF BOTH ENZYMES AND HCL.
THREE DISTINCT PHASES OF GASTRIC SECRETORY ACTIVITY
1. THE CEPHALIC PHASE
2. THE GASTRIC PHASE
3. INTESTINAL PHASE
DESCRIBE CEPHALIC (REFLEX) PHASE
OCCURS BEFORE FOOD HAS ENTERED THE STOMACH AND IS TRIGGERED BY THE SIGHT, AROMA, TASTE, OR THOUGHT OF FOOD. DURING THIS PHASE, THE BRAIN GETS THE STOMACH READY FOR ITS UPCOMING DIGESTIVE CHORE.

INPUTS FROM ACTIVATED OLFACTORY RECEPTORS AND TASTE BUDS ARE RELAYED TO THE HYPOTHALAMUS, WHICH IN TURN STIMULATES THE VAGAL NUCLEI OF THE MEDULLA OBLONGATA, CAUSING MOTOR IMPULSES TO BE TRANSMITTED VIA VAGAL NERVE FIBERS TO THE STOMACH GLANDS.

THIS ACTIVITY IS CONDITIONED REFLEX AND OCCURS ONLY WHEN WE LIKE OR WANT THE FOOD. IF WE ARE DEPRESSED OR HAVE NO APPETITE, THIS PARTICULAR PART OF THE REFLEX IS DAMPENED.
ACTIVATION OF GASTRIC PHASE
WHEN FOOD REACHES THE STOMACH, NEURAL AND HORMONAL MECHANISMS INITIATE THE GASTRIC PHASE, WHICH ACCOUNTS FOR ABOUT TWO-THIRDS OF THE GASTRIC JUICE RELEASED.

STOMACH DISTENTION ACTIVATES STRETCH RECEPTORS AND INITIATES BOTH LOCAL (MYENTERIC) REFLEXES AND THE LONG VAGOVAGAL REFLEXES.

IN LONG VAGOVAGAL REFLEXES IMPULSES ARE TRANSMITTED TO THE MEDULLA ALONG VAGAL AFFERENTS AND THEN BACK TO THE STOMACH VIA VAGAL EFFERENTS.

BOTH TYPES OF NEURAL ACTIVITY LEAD TO ACETYLCHOLINE (ACH) RELEASE, WHICH STIMULATES THE OUTPUT OF MORE GASTRIC JUICE; HOWEVER, THE HORMONE GASTRIN IS PROBABLY MORE IMPORTANT THAN NEURAL INFLUENCES IN STIMULATING THE STOMACH GLANDS DURING THE GASTRIC PHASE.

CHEMICAL STIMULI PROVIDED BY FOODS, ESPECIALLY PARTIALLY DIGESTED PROTEINS AND CAFFEINE (PRESENT IN COLAS, COFFEE, AND TEA)DIRECTLY ACTIVATE GASTRIN-SECRETING CELLS. GASTRIN, IN TURN, STIMULATES THE GASTRIC GLANDS TO SPEW OUT EVEN MORE GASTRIC JUICE.
INHIBITION OF GASTRIN SECRETION (GASTRIC PHASE)
GASTRIN SECRETION IS INHIBITED BY HIGH ACIDITY, AND WHEN THE pH OF THE GASTRIC CONTENTS DROPS BELOW 2, ITS SECRETION IS DAMPED.
AS A GENERAL RULE, WHEN PROTEIN FOODS ARE IN THE STOMACH THE pH OF THE GASTRIC CONTENTS RISES BECAUSE PROTEINS ACT AS BUFFERS TO TIE UP H+. THE RISE IN pH REMOVES THE INHIBITION OF GASTRIN AND STIMULATES RELEASE OF HCL, WHICH IN TURN PROVIDES THE ACIDIC CONDITIONS NEEDED FOR PROTEIN DIGESTION.

IN ADDITION TO RESPONDING DIRECTLY TO CHEMICAL- STIMULI, THE GASTRIN-SECRETING CELLS ARE ACTIVATED BY THE NEURAL REFLEXES ALREADY DESCRIBED.
EMOTIONAL UPSETS; FEAR, ANXIETY, OR OTHER STATES THAT TRIGGER SYMPATHETIC NERVOUS SYSTEM ACTIVITY INHIBIT GASTRIC SECRETION, BECAUSE (DURING SUCH TIMES) THE SYMPATHETIC DIVISION OVERRIDES PARASYMPATHETIC CONTROLS OF DIGESTION.
GASTRIN-SECRETING CELLS
ENTEROENDOCRINE
INTESTINAL PHASE
IS SET INTO MOTION WHEN PARTIALLY DIGESTED FOOD BEGINS TO FILL THE INITIAL PART OF THE SMALL INTESTINE.

THIS FILLING STIMULATES INTESTINAL MUCOSAL CELLS TO RELEASE A HORMONE THAT ENCOURAGES THE GASTRIC GLANDS TO CONTINUE THEIR SECRETORY ACTIVITY.

ALTHOUGH THE PRECISE NATURE OF THIS HORMONE IS NOT KNOWN, ITS EFFECTS MIRROR THOSE OF GASTRIN, AND IT HAS BEEN NAMED INTESTINAL (ENTERIC) GASTRIN.
INHIBITION OF SECRETION (INTESTINAL PHASE)
ALTHOUGH THE PRESENCE OF FOOD IN THE SMALL INTESTINE STIMULATES GASTRIC GLAND ACTIVITY DURING THE INTESTINAL PHASE WHEN THE STOMACH IS ALMOST EMPTIED, IT INHIBITS GASTRIC SECRETION DURING THE GASTRIC PHASE WHEN THE STOMACH CONTAINS FOOD AND ITS SECRETORY ACTIVITY IS BEING REGULATED BY GASTRIC PHASE MECHANISMS.
DURING THE GASTRIC PHASE, FACTORS SUCH AS DISTENTION OF THE DUODENUM, LOW pH,
PRESENCE OF PARTIALLY DIGESTED PROTEINS, HYPERTONIC OR HYPOTONIC FLUIDS, AND IRRITANTS IN THE SMALL INTESTINE ALL TRIGGER THE ENTEROGASTRIC REFLEX.
THE ENTEROGASTRIC REFLEX
TRIO OF REFLEXES
--INHIBITS THE VAGAL NUCLEI IN THE MEDULLA
-- INHIBITS LOCAL REFLEXES
--ACTIVATES SYMPATHETIC FIBERS THAT CAUSE THE PYLORIC SPHINCTER TO TIGHTEN AND PREVENT FURTHER FOOD ENTRY INTO THE SMALL INTESTINE.
AS A RESULT, GASTRIC SECRETORY ACTIVITY DECLINES.

IN ADDITION, THE FACTORS JUST NAMED TRIGGER THE RELEASE OF SEVERAL INTESTINAL HORMONES, INCLUDING SECRETIN, CHOLECYSTOKININ(CCK), AND
GASTRIC INHIBITORY PEPTIDE (GIP).
ALL OF THESE HORMONES INHIBIT GASTRIC SECRETION DURING THE GASTRIC PHASE, WHEN THE STOMACH IS ACTIVELY SECRETING GASTRIN.
CONTRACTION OF STOMACH PERISTALTIC WAVES
THE RATE OF THESE CONTRACTIONS IS ALWAYS AROUND THREE CONTRACTIONS PER MINUTE.

SET BY THE SPONTANEOUS ACTIVITY OF PACEMAKER CELLS LOCATED WITHIN THE LONGITUDINAL SMOOTH MUSCLE LAYER
FACTORS THAT MODULATE AND INCREASE STRENGTH OF STOMACH CONTRACTION
SAME FACTORS THAT ENHANCE GASTRIC SECRETORY ACTIVITY.
DISTENTION OF THE STOMACH WALL ACTIVATES STRETCH RECEPTORS AND GASTRIN- SECRETING CELLS; THE ULTIMATE RESPONSE IN EACH CASE IS INCREASED GASTRIC MOTILITY.
ACTIVATION OF THE STRETCH RECEPTORS TRIGGERS BOTH LOCAL AND VAGOVAGAL REFLEXES, THAT, VIA ACETYLCHOLINE RELEASE, INTENSIFY THE STRENGTH OF PERISTALTIC CONTRACTIONS AND ELICIT GASTRIN RELEASE.
REGULATION OF GASTRIC EMPTYING
STOMACH USUALLY EMPTIES COMPLETELY WITHIN 4 HOURS AFTER A MEAL.

THE MORE LIQUEFIED ITS CONTAINED FOOD, THE FASTER THE STOMACH EMPTIES.

RATE OF GASTRIC EMPTYING DEPENDS AS MUCH, AND PERHAPS MORE, ON THE CONTENTS OF THE DUODENUM AS ON THE STATE OF FOOD DIGESTION IN THE STOMACH. THE STOMACH AND DUODENUM ACT IN TANDEM AND CAN BE THOUGHT OF AS A "COUPLED METER" THAT FUNCTIONS AT LESS THAN FULL CAPACITY.
ROLE OF SMALL INTESTINE IN REGULATING GASTRIC EMPTYING
AS CHYME ENTERS THE DUODENUM, RECEPTORS IN ITS WALL RESPOND TO CHEMICAL SIGNALS AND TO STRETCH, INITIATING THE ENTEROGASTRIC REFLEX AND THE HORMONE MECHANISMS

THESE MECHANISMS PREVENT FURTHER DUODENAL FILLING BY INHIBITING GASTRIC SECRETORY ACTIVITY AND BY REDUCING THE VIGOR OF PYLORIC CONTRACTIONS.

AS A RULE, A MEAL RICH IN CARBOHYDRATES MOVES THROUGH THE DUODENUM RAPIDLY, BUT FATS FORM AN OILY LAYER AT THE TOP OF THE CHYME AND ARE DIGESTED MORE SLOWLY BY INTESTINAL ENZYMES.

WHEN CHYME ENTERING THE DUODENUM IS HIGH IN FATS, FOOD MAY REMAIN IN THE STOMACH FOR AS LONG AS 6 HOURS OR MORE BEFORE GASTRIC EMPTYING IS COMPLETED.

ADDITIONALLY, THE PRESENCE OF FATS ELICITS THE RELEASE OF AN INTESTINAL HORMONE CALLED ENTEROGASTRONE, WHICH,
LIKE SECRETIN ELICITED BY LOW pH, ALSO INHIBITS GASTRIC MOTILITY.
MECHANISM OF VOMITING
INITIATED BY EXTREME STRETCHING OF THE STOMACH OR INTESTINE OR BY THE PRESENCE OF IRRITANTS SUCH AS BACTERIAL TOXINS, EXCESSIVE ALCOHOL, SPICY FOODS, AND CERTAIN DRUGS IN THOSE ORGANS.

SENSORY IMPULSES FROM THE IRRITATED SITES REACH THE EMETIC CENTER OF THE MEDULLA AND INITIATE A NUMBER OF MOTOR RESPONSES.

THE SKELETAL MUSCLES OF THE ABDOMINAL WALL AND DIAPHRAGM CONTRACT AND INCREASE THE INTRA-ABDOMINAL PRESSURE, THE SMOOTH MUSCLES OF THE GI TRACT CONTRACT FORCIBLY, THE GASTROESOPHAGEAL SPHINCTER RELAXES, AND THE SOFT PALATE RISES TO CLOSE OFF THE NASAL PASSAGES.

AS A RESULT, THE DUODENAL AND STOMACH CONTENTS ARE FORCED UPWARD THROUGH THE ESOPHAGUS AND PHARYNX AND OUT THE MOUTH.