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Alimentary System > Physiology > Flashcards

Physiology Flashcards

1
Q

CONTROL MECHANISMS INVOLVED IN SALIVARY SECRETION CONTROL

A

PARASYMP & SYMP BOTH STIMULATORY

PARASYMP = FACIAL (VII) & GLOSSOPHARYNGEAL (IX) NERVES = THIN WATERY SECRETION

SYMP = THICK VISCOUS SECRETIONS & SMALL VOL.

ALPHA-ADRENORECEPTORS = INCREASES MUCUS
BETA-ADRENORECEPTORS = INCREASES AMYLASE

ALSO ENETRIC REFLEXES = FOOD IN MOUTH IS DETECTED BY PRESSURE RECEPTORS/CHEMORECEPTORS OF ROOF OF MOUTH/TONGUE

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2
Q

EFFECTS OF PARASYMP. & SYMP. SYSTEM ON SECRETION & MOTILITY

A 
PARASYMP. = STIMULATORY
SYMP. = INHIBITORY (cept SALIVATION)
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3
Q

ARTERIAL SUPPLY & VENOUS DRAINAGE OF GIT

A

ARTERIAL SUPPLY:

COELIAC TRUNK (FOREGUT; DIVIDES INTO L GASTRIC ARTERY, SPLENIC ARTERY & HEPATIC ARTERY)

SUPERIOR MESENTERIC ARTERY (MIDGUT)

INFERIOR MESENTERIC ARTERY (HINDGUT)

VENOUS DRAINAGE:

SPLENIC VEIN & SUPERIOR MESENTERIC VEIN = HEPATIC PORTAL VEIN

ALSO INFERIOR MESENTERIC VEIN

ALSO SPLENIC VEIN (into IMA, for pancreas) & GASTRIC VEIN (into PORTAL VEIN, into stomach) & DUODENAL VEINS

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4
Q

PORTAL VENOUS SYTEM & ANASTOMOSIS WITH SYSTEM SUPPLY

A

PORTAL SYSTEM = STARTS & ENDS IN CAPILLARY BED, thru VEINS, w/o going thru HEART

PORTAL LIVER SYSTEM = RECEIVES BLOOD FROM GUT IN SERIES SO THAT LIVER CAN DETOXIFY/SCREEN BLOOD OF TOXINS

HEPATIC PORTAL VEIN GOES TO LIVER - HEPATIC VEIN TO IVC

PORTAL SYSTEM ALSO HAS ANASTOMOSES WITH SYSTEMIC SUPPLY = PORTOCAVAL ANASTOMOSES

IN ANAL CANAL
IN DISTAL OESOPHAGEAL
IN COLON
~UMBILICUS

IF PORTAL SYSTEM BLOCKED = AN CAUSES VARICES/ENLARGEMENTS

OESOPHAGEAL VARICES
CAPUT MEDUSAE
HAEMORRHOIDS/PILES

CAN TREAT USING PORTOCAVAL SHUNTS

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5
Q

GIT ANATOMY + GENERAL PHYSIOLOGICAL FUNCTIONS OF COMPONENTS

A

SAME STRUCTURE THROUGHOUT TUBE

4 LAYERS:

MUCOSA: EPITHELIUM, LAMINA PROPRIA (loose connective tissue, supports epithelium, muscularis mucosa = also support

EPITHELIUM: OESOPHAGUS & ANAL CANAL = STRATIFIED SQUAMOUS

IN BWTN = SIMPLE COLUMNAR
EPITHELIUM = SECRETES & CREATES MUCUS, HORMONES, ACID, DIGESTIVE ENZYMES + ABSORBS DIGESTIVE PRODUCTS

SUB-MUCOSA: provides services to other layers = blood vessels, lymph vessels, GLANDS IN OESOPHAGUS & DUODENUM; SUBMUCOSAL PLEXUS bwtn SUBMUCOSA & MUSCULARIS EXTERNA

MUSCULARIS EXTERNA: thick muscular layer, 2 layers: inner = circular, outer = longitudinal; constriction & shortens gut tube; MYENTERIC PLEXUS = bwtn muscular layers

SEROSA (inside peritoneum)/ADVENTITIA (outside peritoneum)

MOUTH = CHEWING, SPLITTING INTO SMALLER PARTICLES, AMYLASES IN SALIVA

OESOPHAGUS = MUSCULAR TUBE, TRANSPORTS FOOD

STOMACH = TEMPORARY FOOD STORAGE, STERILISES FOOD, PRODUCES INTRINSIC FACTOR, MIXES & GRINDS FOOD, CONTROLS DELIVERY TO S. INTESTINE

PANCREAS = PRODUCES DIGESTIVE ENZYMES FOR ALL MAJOR FOOD GROUPS

LIVER = BILES SALTS & DETOXIFIES BLOOD

GALL BLADDER = STORES & CONCENTRATES BILE

S. INTESTINE = FINAL STAGES OF CHEMICAL DIGESTION & FOOD IS ABSORBED

L. INTESTINE = H2O ABSORPTION, FAECAL AGGREGATION & BACTERIAL FORMATION

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6
Q

COMMON FEATURES OF ALIMENTARY CANAL WALL STRUCTURE

A

CONTINUOUS TUBE

SAME 4 LAYERS: MUCOSA, SUBMUCOSA, MUSCULARIS EXTERNA, SEROSA/ADVENTITIA

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7
Q

ORGANISATION OF ENTERIC NERVOUS SYSTEM

A

ENS = MYENTIC PLEXUS + SUBMUCOSAL PLEXUS

MYENTERIC PLEXUS = BWTN MUSCLE LAYERS OF MUSCULARIS EXTERNA

SUBMUCOSAL PLEXUS = BWTN SUBMUCOSA & MUSCULARIS EXTERNA

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8
Q

DIGESTIVE PROCESSS FOR CONVERSION OF COMPLEX CHOs TO MONOSACCHARIDES

A

MONOSACCHARIDES (GLUCOSE, GALACTOSE, FRUCTOSE)

DISACCHARIDES (LACTOSE - LACTASE = GLUCOSE + GALACTOSE; MALTOSE - MALTASE = 2 GLUCOSE; SUCROSE - SUCRASE = GLUCOSE + FRUCTOSE)

POLYSACCHARIDES ONLY BROKEN DOWN IF ALPHA-1,4 GLYCOSIDIC BONDS (STARCH = AMLYLOPECTIN & AMYLOSE) = BROKEN DOWN BY ALPHA-AMYLASES

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9
Q

MECHANISM OF MONOSACCHARIDE ABSORPTION BY INTESTINAL EPITHELIAL CELLS

A

GLUCOSE & GALACTOSE:

ABSORBED VIA NA-GLUCOSE SYMPORTER/SGLT1 (NEEDS NA & INDIRECTLY NEEDS ATP)

CONFORMATIONAL CHANGE DEPOSITS NA & GLUCOSE INSIDE INTESTINAL EPITHELIA

NA IMMEDIATELY PUMPED OUT BY NA-K PUMP (OSMOTIC EFFECT & DRAWS H2O PARACELLULARY/ACROSS TIGHT JUNCTIONS)

GLUCOSE TRANSPORTED INTO BLOOD VIA GLUT2 TRANSPORTERS (WHEN INTESTINAL CONC. > BLOOD CONC.)

FRUCTOSE = INTO CELLS VIA GLUT5 TRANSPORTERS & OUT OF CELLS VIA GLUT2 TRANSPORTERS (NO BLOOD CONC. SO IMMEDIATELY TRANSPORTED)

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10
Q

DIGESTIVE PROCESS FOR BREAKING DOWN PROTEINS INTO SMALLERS PEPTIDES/AMINO ACIDS

A

PROTEINS ~3-10 AMINO ACIDS = SMALLER PEPTIDES

PROTEINS BROKEN DOWN USING H2O HYDROLYSIS & PROTEASES/PEPTIDASES

ENDOPEPTIDASE = WORKS IN MIDDLE OF CHAIN
EXOPEPTIDASE = WORKS AT END OF CHAIN
CARBOXYPEPTIDASE = WORKS AT CARBOXY END
AMINOPEPTIDASE = WORKS AT AMINO END
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11
Q

MECHANISMS OF ABSORPTION FOR AMINO ACIDS & SMALL PEPTIDES

A

AMINO ACIDS:

AMINO ACID & NA TRANSPORTER = CONFORMATIONAL CHANGE = DEPOSITED INTO INTESTINAL CELLS

NA PUMPED OUT OF CELL VIA NA-K PUMP = DRAWS H2O

AMINO ACID TRANSPORTED INTO BLOOD

SMALLER PEPTIDES:

DEPENDANT ON BRUSH BORDER ACID MICROCLIMATE

PEPT1 = SMALLER PEPTIDE & H+ TRANSPORTED INTO CELL

SMALLER PEPTIDE TRANSPORTED OUT & H+ PUMPED BACK INTO CELL

H+ PUMPED BACK OUT WITH NA COMING INTO CELL (USING NHE3 = NA-H EXCHANGER)

NA PUMPED OUT OF CELL USING NA-K PUMP = DRAWS H2O

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12
Q

DIGESTIVE PROCESSES OF FATS TO TAG & MONOGLYCERIDES

A

MOST DIETARY FATS = TAG

TAG IS BROKEN DOWN BY H2O SOLUBLE LIPASE = 2FA & MONOGLYCERIDE

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13
Q

REQUIREMENT OF EMULSIFICATION OF INGESTED FATS

A

EMULSIFICATION REQ. AS FAT DROPLETS FAR TOO LARGE FOR H2O SOLUBLE LIPASE TO WORK QUICKLY AS CAN ONLY WORK ON OUTER SURFACE AREA

EMULSIFICATION NEEDS 2 THINGS:

MECHANICAL DISRUPTION (CHURNING MOTION OF MUSCULARIS EXTERNA = SPLITS LARGE DROPLETS INTO SMALLER DROPLETS)

EMULSIFYING AGENT (BILE SALTS + PHOPHOLIPIDS IN BILE = STOPS FAT DROPLETS FROM RE-AGGREGATING AS THEY ARE AMPHIPATHIC MOLECULES)

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14
Q

ROLE OF BILE SALTS IN PRODUCTION OF EMULSIFICATION DROPLETS + HOW ARE FATS TRANSPORTED INSIDE INTESTINAL CELLS & INTO BLOOD

A

BILE SALTS EMULSIFY SMALLER DROPLETS OF FAT

MICELLLES ARE FOR TRANSPORTING THE SMALL DROPLETS OF FAT TO INTESTINAL BRUSH BORDER (as unless fats come into contact with membrane it cannot diffuse across)

MICELLES = BILE SALTS + PHOSPHOLIPIDS + MONOGLYCERIDE + 2FA

FA BECOME PROTONATED IN ACID MICROCLIMATE OF BRUSH BORDER & SO MICELLE UNSTABLE & BREAKS DOWN & RELEASES MONOGLYCERIDE & FA

MICELLES REFORM ONCE AWAY ACID MICROCLIMATE

INSIDE CELL:

CYTOPLASM IS AQUEOUS SO MONOGLYCERIDE & 2FA GO TO SMOOTH ENDOPLASMIC RETICULUM

THERE GETS PACKAGED INTO TAG & FORMS VESICLES (FROM sER MEMBRANE)

VESICLES TRANSPORT TAG THRU GOLGI APPARTUS & RELEASED INTO ECF/BLOOD AT SEROSAL MEMBRANE BY FUSING AT BASOLATERAL MEMBRANE

OUTSIDE CELL:

RELEASED AS CHYLOMICRONS (PHOSPHOLIPIDS, CHOLESTEROL, FAT-SOLUBLE VITAMINS). WHICH ARE TOO BIG FOR CAPILLARY BM = PASSES THRU LACTEALS

In Tissue = broken down by lipoprotein lipase - absorbed by tissues/stored as TAG; transported by lipoprotein & serum albumin complex (free FA); VLDL, HDL, LDL

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15
Q

ABSORPTION OF FAT SOLUBLE & H2O SOLUBLE VITAMINS

A

VITAMINS ADEK = FAT SOLUBLE = FOLLOW SAME PATHWAY AS FATS

VITAMINS B GROUP, C & FOLIC ACID = FACILITATED TRANSPORT/PASSIVE DIFFUSION

VITAMIN B12 = LARGE & CHARGED = BINDS TO INTRINSIC FACTOR (of stomach) & FORMS COMPLEX = ABSORBED BY SPECIFIC TRANSPORT MECHANISM OF DISTAL ILEUM (intrinsic factor sent to be stored in liver)

IF B12 DEFICIENCY = PERNICIOUS ANAEMIA = RBCs DO NOT MATURE (takes ~3yrs to show up as liver has ~3yr supply of intrinsic factor)

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16
Q

ABSORPTION OF IMPORTANT DIETARY MINERALS

A

IRON:
INGESTED IRON ENTERS INTESTINAL CELLS VIA DMT1 (DIVALENT METAL TRANSPORTER) = H+ DEPENDANT

ONCE INSIDE CELL = BOUND TO FERRITIN = INTRACELLULAR STORE - INTESTINAL CELL EVENTUALLY SLOUGHS OFF AS ~5 DAY LIFE & TAKEN FERRITIN WITH IT

FERRITIN LVLS CHANGE ACCORDING TO BODY’S IRON STATUS

HYPERAEMIA = INCREASED FERRITIN EXPRESSION & MORE IRON STORED IN INTESTINAL ENTEROCYTES

ANAEMIA = DECREASED FERRITIN EXPRESSION & MORE IRON LEFT IN BLOOD

OTHER WISE, IRON TRANSPORTED SEROSAL MEMBRANE & BOUND TO TRANSFERRIN (eventually goes to liver & bound into Hb)

17
Q

STOMACH & OESOPHAGUS - ANATOMY + GENERAL PHYSIOLOGICAL FUNCTIONS

A

OESOPHAGUS = MUCOSA(stratified squamous), SUBMUCOSA (glands); MUSCULARIS EXTERNA (upper 1/3 = skeletal; lower 2/3 = sm); SEROSA/ADVENTITIA

SPHINCTERS

18
Q

DESCRIBE OESOPHAGUS

A

NORMAL 4 LAYERS

UPPER 1/3 = SKELETAL MUCLE, MUSCULARIS EXTERNA

LOWER 2/3 = SM, MUSCULARIS EXTERNA

GLANDS IN SUBMUCOSA
EPITHELIUM NOT KERATINISED

SPHINCTERS TO CONTROL GASTRIC REFLUX & PREVENT RESPIRATORY FAILURE

19
Q

REFLEX CONTROL MECHANISM INVOLVED IN SWALLOWING

A

MOUTH:

CHEWING + SALIVA (H2O, MUCINS, AMYLASES, LYSOZOMES, ELECTROLYTES)

VOLUNTARY (SOMATIC NN. OF SKELETAL MUSCLES OF JAW & MOUTH) & REFLEXIVE CONTROL (PRESSURE OF FOOD DETECTED BY MECHANORECEPTORS & INHIBITS JAW CONTRACTION = SWALLOWING)

ORAL PHASE: BOLUS PUSHED TO BACK OF MOUTH & TONGUE PUSHES UP & BACK

PHARNGEAL PHASE: BOLUS PRE

20
Q

REFLEX CONTROL MECHANISM INVOLVED IN SWALLOWING

A

MOUTH:

CHEWING + SALIVA (H2O, MUCINS, AMYLASES, LYSOZOMES, ELECTROLYTES)

VOLUNTARY (SOMATIC NN. OF SKELETAL MUSCLES OF JAW & MOUTH) & REFLEXIVE CONTROL (PRESSURE OF FOOD DETECTED BY MECHANORECEPTORS & INHIBITS JAW CONTRACTION = SWALLOWING)

ORAL PHASE: BOLUS PUSHED TO BACK OF MOUTH

PHARYNGEAL PHASE:

BOLUS PRESENCE = PHARYNGEAL MUSCLES CONTRACT (INVOLUNTARY) & SOFT PALATE REFLECTED UP & BACK (closes off nasopharynx)

WHEN FOOD REACHES OESOPHAGUS = UPPER OESOPHAGEAL SPHINCTER RELAXES & EPIGLOTTIS COVERS ENTRANCE TO LARYNX)

AFTER FOOD PASSES THEY RELAX

ALL CONTROLLED BY SWALLOWING CENTRE IN MEDULLA (close to respiratory centres & so swallowing & breathing do not occur at same time)

OESOPHAGEAL PHASE:

PASSES BOLUS TO STOMACH BY PERISTALTIC WAVE (wave of contraction & relaxation)

AS FOOD NEARS LOWER OESOPHAGEAL SPHINCTER = IT RELAXES & ALLOWS FOOD TO ENTER STOMACH

LOS RELAXATION ALSO CAUSES STOMACH RELAXATION (VIA VAGAL REFLEXES) = CAUSE THIN ELASTIC SM OF GASTRIC FUNDUS & BODY TO RELAX (vol. increase w/o change in pressure)

21
Q

STOMACH STRUCTURE & FUNCTIONS

A

CARDIA = TRANSFERS FOOD INTO BODY

FUNDUS = THIN ELASTIC SM LAYER, MAINLY AIR-FILLED, EXTRA-STORAGE FOR FOOD

BODY: STORAGE OF FOOD, MUCUS, PEPSINOGEN, HCl, INTRINSIC FACTOR

ANTRUM = MIXES/GRINDS FOOD TO FORM CHYME & ALSO PRODUCES GASTRIN

SIMPLE COLUMNAR EPITHELIUM, MUCOSAL GLANDS INVAGINATE DOWNWARDS & DISTAL END OF STOMACH HAS 3RD INNERMOST OBLIQUE LAYER OF MUSCLE OF MUSCULARIS EXTERNA

22
Q

ESSENTIAL ROLE OF INTRINSIC FACTOR IN VITAMIN B12 ABSORPTION

A

VITAMIN B12 = LARGE & CHARGED = CANNOT BE ABSORBED/TRANSPORTED THRU BODY W/O INTRINSIC FACTOR

IF VITAMIN B12 DEFICIENCY = PERNICIOUS ANAEMIA

23
Q

FUNCTIONS OF GASTRIC MUCUS

A

CYTOPROTECTIVE (from stomach:

PREVENTS AGAINST HCL CORROSION & PEPSIN DIGESTION

LUBRICATES & PROTECTS MUCOSA AGAINST MECHANICAL INJURY

24
Q

BASIC PHYSIOLOGY OF GASTRIC ACID SECRETION

A

BACKGROUND:

LOTS OF CO2 IN BLOOD = DIFFUSE INTO PARIETAL CELL, WHERE IT COMBINE WITH H2O (USING CARBONIC ANHYDRASE) = BECOMES CARBONIC ACID

CARBONIC ACID DISSOCIATES = H+ & BICARBONATE ION

BICARBONATE-CL EXCHANGER (BICARB INTO BLOOD & CL INTO CELL & THEN LUMEN)

PROTON PUMP = PUMPS H+ INTO LUMEN & K+ INTO CELL - REQUIRES LOTS OF ATP (LOTS OF MITOCHONDRIA NEAR FOR THAT)

ION TRANSPORT ALSO DRAWS H2O INTO LUMEN

H2O + CL + H = HCL ACID

POST-PRANDIAL ALKANISATION = AFTER MEAL = EXCESS BICARBONATE IN BLOOD

CAN BE STIMULATED:

GASTRIN & ACh = INCREASE INTRACELLULAR Ca & ACTIVATE PROTEIN KINASES = ACTIVATE PROTON PUMP

HISTAMINE (gut receptors diff. to other bodily receptors) = ATTACHED TO G STIMULATORY PROTEIN = ACTIVATES ADENYLYL CYCLASE & PROTEIN KINASE = ACTIVATES PROTON PUMP

CEPHALIC PHASE:

ANY FOOD STIMULI = STIMULATES VAGAL REFLEXES

VAGAL NN. RELEASES ACh = STIMULATES PARIETAL CELLS

ALSO INNERVATES G CELLS = RELEASES GASTRIN = STIMULATES PARIETAL CELLS

ACh/GASTRIN ACT ON ECL CELLS = RELEASE HISTAMINE = STIMULATE PARIETAL CELLS

GASTRIC PHASE:

STOMACH DISTENSION = VAGAL REFLEX = STIMULATES PARIETAL CELLS

SMALLER PEPTIDES PRESENT = STIMULATES G CELLS & GASTRIN RELEASE = STIMULATES PARIETAL CELLS

ACh/GASTRIN = STIMULAET ECL CELLS = RELEASE HISTAMINE & STIMULATES PARIETAL CELLS

CAN BE INHIBITED:

PROSTAGLANDINS ATTACHED TO G INHIBITORY PROTEIN - SWITCHES OF ADENYLYL CYCLASE

CEPHALIC:

STOP FOOD STIMULI = REDUCE VAGAL ACTIVITY

GASTRIC PHASE = INCREASED pH = REDUCE GASTRIN PRODUCTION (-ve feedback loop)

INTESTINAL:

ACID IN DUODENUM (expresses SECRETIN & ENTEROGASTRIC REFLEX = REDUCES GASTRIN RELEASE & EFFECTIVITY OF GASTRIN AT PARIETAL CELLS)

FAT IN DUODENUM (GIP RELEASED = GASTRIN REDUCED & HCL REDUCED)

ENTEROGASTRONES = HORMONES RELEASED BY DUODENAL MUCOSAL GLANDS WHEN HYPERTONIC SOLNS./FAT/ACID PRESENT IN DUODENUM (tells stomach to calm down)

WORKS BY:
INHIBITING GASTRIC SECRETIONS & PREVENTING MOTILITY/GASTRIC EMPTYING

25
Q

IMPORTANCE OF GASTRIC ACID & PEPSIN SECRETION

NEURAL & HORMONAL MECHANISMS OF CONTROL

A

GASTRIC ACID = STERILISES FOOD = PROTECTIVE

PEPSINOGEN (ZYMOGEM = INACTIVE PRECURSOR) = PEPSIN PRECURSOR = PROTEIN BREAKDOWN; inactivated by neutral pH

NEUROCRINE = ACh
ENDOCRINE = GASTRIN
PARACRINE = HISTAMINE

Alimentary System (5 decks)

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