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1
Q

what is the Valleculae

what is the Piriform Fossa

what is the Sulcus Terminalis

A
  1. Vallecular: anterior superior portion of Epiglottis
    (when bolus reaches valleculae, epiglottis tipped inferiorly)
  2. Piriform Fossa: posterolateral to the Laryngeal opening (in the sides), guides food, fish bones get stuck here
  3. Sulcus Terminalis: V-shaped on tongue. Divides into Anterior Oral (presulcal) and Posterior Pharyngeal (postsulcal)
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2
Q
  1. which Pharyngeal Muscles Push Food Down
  2. which Pharyngeal Muscles Elevate the Pharynx during Swallowing
  3. Contraction of which Pharyngeal Muscles brings the Soft Palate back Inferiorly
  4. Oropharyngeal Cavity is Closed by Constriction of which pharyngeal muscle

*5. Relaxation of which muscle permits entry of Bolus into Oesophagus

A
  1. CIRCULAR PHARYNGEAL MUSCLES push food down
    - superior, middle, inferior Constrictors
  2. LONGITUDINAL PHARYNGEAL MUSCLES pull the pharynx up
    - STYLOPHARYNGEUS, SALPINGOPHARYNGEUS, PALATOPHARYNGEUS
  3. PALATOPHARYNGEUS contracts to bring SOFT PALATE back down
  4. UPPER/SUPERIOR PHARYNGEAL CONSTRICTORS constrict to CLOSE OROPHARYNGEAL CAVITY
  5. CRICOPHARYNGEUS relaxes so food into OESOPHAGUS
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3
Q

Where are the Constrictions of the Oesophagus and due to what

A

Cervical: C5-C6 due to CRICOID CARTILAGE (larynx)

Thoracic: due to AORTIC ARCH

Abdominal: T10

Oesophageal Hiatus (where crosses DIAPHRAGM)

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4
Q
  1. Pancreas is on the … Abdominal wall
  2. it is … to the Aorta and IVC
  3. and … to the Stomach
A

POSTERIOR ABDOMINAL WALL

ANTERIOR to AORTA & IVC

but POSTERIOR to STOMACH

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5
Q

What is A Mesentery

  1. what is THE Mesentery
  2. which structures have their Own Mesenteries and what are their names
A

DOUBLE layer of PERITONEUM where VISCERAL and PARIETAL single layers come together
- between organ and wall

  • Gap between offers a SAFE PASSAGEWAY for Blood, Nerves, Lymph
  1. THE Mesentery - biggest mesentery for the SMALL INTESTINE - JEJUNUM and ILEUM
  2. SI - THE MESENTERY
    TRANSVERSE COLON: TRANSVERSE MESOCOLON
    SIGMOID COLON: SIGMOID MESOCOLON
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6
Q

are Retroperitoneal or Intraperitoneal organs Mobile

A

RETROPERITONEA: IMMOBILE as covered anteriorly and fixed down to Posterior Abdominal Wall
ie Duodenum, Pancreas

INTRAPERITONEAL: MOBILE, free-flowing
ie Stomach, Jejunum, Ileum

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7
Q

Retroperitoneal Structures:

A
  • PANCREAS
  • DUODENUM
  • OESOPHAGUS
  • ASCENDING & DESCENDING COLONS
  • RECTUM
  • LIVER
  • KIDNEYS & SUPRENAL GLANDS & URETERS
  • AORTA & IVC
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8
Q
  1. Gut Tube derived from which Germ Layer.
  2. what comes from Foregut, Midgut and Hindgut
  3. at what week does Diverticula Bud develop from Duodenum to form the Accessory Organs and their Ducts
A

ENDODERM

FOREGUT:
- LOWER OESOPHAGUS
- STOMACH
- 1ST HALF DUODENUM (1st,2nd parts)
- LIVER
- PANCREAS
- GALLBLADDER

MIDGUT:
- 2ND HALF DUODENUM (3rd,4th parts)
- JEJUNUM
- ILEUM
- CAECUM & APPENDIX
- ASCENDING COLON
- FIRST 3/4TH TRANSVERSE COLON

HINDGUT:
- LAST 1/4TH TRANSVERSE COLON
- DESCENDING COLON
- SIGMOID COLON
- RECTUM

  1. WEEK 5
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9
Q

in Anorectal Canal,
1. what is the Pectinate Line?
2. what is the White Line?

A
  1. PECTINATE LINE DIVIDES UPPER and LOWER Portions of canal
  2. WHITE LINE is the transition between KERATINISED and NON-KERATINISED Epithelia
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10
Q

Sites of Portosystemic Anastomoses (connection between 2 vessels / communication between veins in hepatic and caval systems):

A
  • OESOPHAGUS
  • ANTERIOR ABDOMINAL WALL
  • RECTUM
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11
Q
  1. how much of Lymph comes from GI Tract
  2. from which Nodes?
  3. Drains into what?
  4. what does Lymph facilitate in the GI Tract
A
  1. 50% - 1-4 L a day
  2. COELIAC NODES & INFERIOR MESENTERIC NODES
  3. CYSTERNA CHYLI (above diaphragm becomes Thoracic Duct)
  4. LIPID TRANSPORT
    MUCOSAL IMMUNE FUNCTION (IgA) because vast absorption surface
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12
Q

levels of
Coeliac Trunk (CT):
SMA:
IMA:

A

Coeliac Trunk (CT): T12
SMA: L1
IMA: L3

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13
Q
  1. which Muscles of Mastication Open the jaw/mouth
  2. which Muscles of Mastication Close the mouth
A
  1. OPEN MOUTH:
    - LATERYAL PTERYGOID (sphenoid to mandible)
    - DIGASTRIC (jaw to hyoid)
    - INFRAHYOID (4 pairs) (hyoid to clavicle)
  2. CLOSE MOUTH:
    - TEMPORALIS (temporal fossa to mandible)
    - MASSETER (maxilla to mandible)
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14
Q

what is Ginglymoarthrodial joint

why does it have this name

A
  • TMJ

Articular Disc divides the TMJ into upper and lower compartments
Upper Compartment: SLIDING MOVEMENTS
= ARTHRODIAL

Lower Compartment: ROTATIONAL MOVEMENT
= GINGLYMUS

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15
Q

what is Ginglymoarthrodial joint

why does it have this name

A
  • TMJ

Articular Disc divides the TMJ into upper and lower compartments
Upper Compartment: SLIDING MOVEMENTS
= ARTHRODIAL

Lower Compartment: ROTATIONAL MOVEMENT
= GINGLYMUS

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16
Q
  1. what type of secretions come from each Salivary Gland?
    Parotid:
    Sublingual:
    Submandibular:
    Minor Glands:
  2. what do all salivary glands secrete?
  3. Superior Salivary Nuclei (PONS) acts on which Gland(s)? via which Nerve?
  4. Inferior Salivary Nuclei (MEDULLA) acts on which Gland(s)? via which Nerve?
  5. which gland wraps around Mandibular Ramus?
  6. which gland receives Blood from branches of the Facial and Lingual Arteries?
A
  1. Parotid: SEROUS (watery, with proteins & amylase)
    Sublingual: MUCOUS (mucus glycoproteins / mucins)
    Submandibular: MIXED
    Minor Glands: MUCOUS
  2. PROTEIN and FLUID
  3. SUPERIOR SALIVARY NUCLEI (Pons)
    -> SUBLINGUAL and SUBMANDIBULAR Glands
    via FACIAL NERVE (7)
  4. INFERIOR SALIVARY NUCLEI (medulla)
    -> PAROTID Gland
    via GLOSSOPHARYNGEAL NERVE (9)
  5. PAROTID is around MANDIBULAR RAMUS
  6. SUBMANDIBULAR receives BLOOD from FACIAL and LINGUAL ARTERIES
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17
Q
  1. what is needed for Saliva Protein secretion from Acinar cell
  2. what is needed for Saliva Protein - IgA - secretion from Acinar cell
  3. what is needed for Saliva Fluid secretion from Acinar cell
  4. what are the second messengers in Fluid Secretion from Acinar Cells
A
  1. SYMPATHETIC : NORADRENALINE
  2. PIgR RECEPTOR
  3. PARASYMPATHETIC: ACETYLCHOLINE (m3 muscarinic receptor)
  4. IP3 and INCREASED CA2+
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18
Q
  1. GI Tract Epithelium type
  2. Epithelium type in the Mouth
  3. where is the Submucosal (Meissner’s) Plexus in the GI Tract Layers?
  4. where is the Myenteric (Auerbach’s) Plexus in the GI Tract Layers?
A
  1. SIMPLE COLUMNAR Epithelium
  2. MOUTH = STRATIFIED SQUAMOUS Epithelium
  3. SUBMUCOSAL PLEXUS : between SUBMUCOSA and INNER CIRCULAR SMOOTH MUSCLE
  4. MYENTERIC PLEXUS: between OUTER LONGITUDINAL MUSCLE and INNER CIRCULAR MUSCLE (muscularis layer)
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19
Q
  1. what is the Crural Diaphragm
  2. what nerve and neurotransmitter stimulates its Contraction
  3. which Nerve goes to the Lower Oesophageal Sphincter (LOS)
  4. Which Neurotransmitters are used to Relax the LOS (open) for entry of food into the stomach
  5. which Neurotransmitter would Contract the LOS (close)
A
  1. Crural Diaphragm forms SLING AROUND LOWER OESOPHAGEAL SPHINCTER
  2. PHRENIC NERVE (C3-C5) innervate
    release ACETYLCHOLINE to CONTRACT and OPEN crural diaphgram
  3. LOS - VAGAL EFFERENT NERVE (VAGUS)
  4. RELAX/OPEN LOS : VIP (vasoactive intestinal polypeptide) and NO (Nitric oxide)
    released from VAGAL INHIBITORY FIBRES
  5. CONTRACT/CLOSE LOS: ACH
    from VAGAL EXCITATORY FIBRES
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20
Q
  1. what happens in the gut in the Interdigestive period (between meals)?
  2. what are the 4 phases?
  3. where does it happen most?
  4. what stimulates phase 3 in Antrum?
  5. what stimulates phase 3 in the Duodenum?
A
  1. MIGRATING MYOELECTRIC COMPLEX (MMC)
  2. 1-Quiescence
    2-Random contractions
    3- BURST OF CONTRACTIONS
    4- Rapid Decrease contractions
  3. Most (71%) in ANTRUM
    29% in Duodenum
  4. ANTRUM:
    MOTILIN, GHRELIN, VAGUS NERVE (parasympathetic)
  5. DUODENUM:
    SOMATOSTATIN, SEROTONIN, XENIN
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21
Q
  1. what is meant by Intestinal Movement: Segmentation and what does it facilitate?
  2. in Peristaltic Reflex for pushing the food down, what is released due to Distension of gut wall from Bolus, and what does it act on?
  3. for Contraction (back/orad end) what do Excitatory Motor Neurons release?
  4. for Relaxation (front/caudad end) what do Inhibitory Motor Neurons release?
A
  1. SEGMENTATION: ALTERNATE CONTRACTION and RELAXATION of ADJACENT Segments causing thorough MIXING of food contents.
    SLOWS CHYME PROGESSION.
    - facilitates ABSORPTION of products within SMALL INTESTINE
  2. PERISTALSIS
    Distension: SEROTONIN / 5-HT
    acts on INTRINSIC PRIMARY AFFERENT NEURONS (IPAN)
  3. CONTRACTION via ACH and TK (TACHYKININ)
  4. RELAXATION via VIP and NO
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22
Q
  1. Contraction of Colon and Rectum to push Faeces along is by which Nerve?
    which Neurotransmitter?
  2. Relaxation of the Internal Anal Sphincter by which factors?
A
  1. CONTRACTION:
    parasympathetic: VAGUS NERVE
    releasing ACETYLCHOLINE
  2. RELAX IAS: VIP and ATP
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23
Q

secretion from stomach cells
Surface Epithelia:
Chief (Zymogen) Cells:
Parietal Cells:
Enterochromaffin-like (ECL) cells:
G-cells:
D-cells:
I-cells:

A

Surface Epithelia: MUCUS, HCO3-
Chief (Zymogen) Cells: PEPSINOGEN
Parietal Cells: HCL, INTRINSIC FACTOR
Enterochromaffin-like (ECL) cells: HISTAMINE
G-cells: GASTRIN
D-cells: SOMATOSTATIN
I-cells: CCK

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24
Q

which stomach cells are in the
Fundus ?
Corpus?
Antrum?

  1. order of the cells in the Corpus
A

Fundus:
SURFACE EPITHELIA -> Mucus, HCO3-
& gastric lipase

Corpus:
SURFACE EPITHELIA -> Mucus, HCO3-
CHEIF (ZYMOGEN) CELLS -> Pepsinogen
PARIETAL CELLS -> HCL, Intrinsic factor
ECL -> Histamine

Antrum
SURFACE EPITHELIA -> Mucus, HCO3-
CHEIF (ZYMOGEN) CELLS -> Pepsinogen
G-CELLS -> Gastrin
D-CELLS -> Somatostatin

  1. SURFACE EPITHELIA
    -> MUCUS, HCO3- PROTECTIVE BARRIER

PROLIFERATING CELLS

PARIETAL CELLS -> HCL

ECL CELLS -> HISTAMINE (regulates release of Hcl and Pepsionogen

CHIEF (ZYMOGEN) CELLS -> PEPSINOGEN (migrate up and acid activates to pepsin)

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25
Q
  1. what activate Parietal cells to secrete Hcl?
  2. what activate D-Cells to secrete Somatostatin after eating in order to Inhibit Parietal cells / Acid, Pepsinogen and Histamine secretions
  3. what stimulate antral G-Cells to secrete Gastrin
A
  1. ACETYLCHOLINE, HISTAMINE (Gastrin activates histamine)
  2. antral: sense HIGH H+ / LOW PH
    NORADRENALINE (Sympathetic),
    CCK
    VIP
    CGRP (Calcitonin gene related peptide)
  3. PROTEINS/PEPTIDES/AMINO ACIDS
    & GRP (GASTRIN RELEASING PEPTIDE)
26
Q
  1. what is the Proton Pump in Parietal cells?
  2. what Inhibits the Proton Pump?
  3. What are H2 Receptor Agonists that prevent Histamine binding (Competitive Inhibitors) to Parietal Cells (to stimulate)
A
  1. H+/K+ ATP-ASE (Exchanger)
  2. proton pump inhibitor: OMEPRAZOLE
  3. TAGAMET
    ZANTAC
    PEPCID AC
27
Q
  1. what is Satiation?
    what is Satiety?
  2. what does Satiation determine?
    what does Satiety determine?
A
  1. SATIATION prompts us to STOP EATING
    SATIETY is the FULLNESS that persists AFTER EATING
  2. SATIATION determines HOW MUCH FOOD CONSUMED in one sitting

SATIETY determines LENGTH OF TIME UNTIL NEXT EATING OCCASION

28
Q
  1. what do Enteroendocrine cells (largest endocrine organ in body) secrete?
  2. How do EEC Cells secrete
  3. where is the Nodose Ganglion?
  4. what does Nodose Ganglion contain
A
  1. EEC Cells: Lipid Mediators & Gut Hormones
    CCK, GLP-1, PYY, SEROTONIN, GLP-2
  2. INCREASE INTRACELLULAR CA2+ causes secretory vesicle exocytosis
  3. NODOSE GANGLION: VAGAL AFFERENT NEURONS
  4. NG: RECEPTORS for GUT HORMONES
29
Q

sensation of Pain in the gut is derived from which nerves?
which nervous system?

A

SPLANCHNIC NERVES
- SYMPATHETIC Stimulation

(pelvic splanchnic are parasympathetic)

30
Q
  1. what does CCK stimulate? inhibit?
  2. what does GLP-1 stimulate? inhibit?
    from which cells?
  3. what does Ghrelin stimulate? inhibit?
  4. what are the vagal afferents insensitive to in Obesity
A
  1. CCK
    STIMULATE: PANCREATIC SECRETIONS & GALLBLADDER CONTRACTIONS

INHBIT: FOOD INTAKE & GASTRIC EMPTYING

  1. GLP-1
    STIMULATE: INSULIN Secretion

INHIBIT: FOOD INTAKE & GASTRIC EMPTYING

  1. GHRELIN
    STIMULATE: FOOD INTAKE & GASTRIC EMPTYING

INHBIT: ACTION of CCK ON VAGAL AFFERENT NEURONS

  1. Obesity: vagal afferents insensitive to CCK
31
Q
  1. CCK binds to Pancreas Acinar cells for release of what?
  2. what binds to Pancreas Ductal Cells for release of HCO3-?
  3. where is Trypsin activated?
  4. what is it activated/converted by?
  5. Pancreatic Enzyme Inhibitor - inhibits autoactivation of trypsinogen in acinar cell is called?
A
  1. CCK -> ACINAR:
    ZYMOGENS (precursor enzymes)
    including TRYPSINOGEN
  2. SECRETIN (from duodenum S cells) binds to DUCTAL cells of pancreas for HCO3- / H2O release (ALKALINE TIDE)
  3. TRYPSINOGEN converted into TRYPSIN in *DUODENUM
  4. activation by ENTEROKINASE
    (neutral pH environment)
  5. Inhibitor: SPINK1/PST1
32
Q

where are Liver Stellate Cells and what do they do?

A

PERISINUSOIDAL (edge of sinusoids)
- in SPACE OF DISSE

  • STORE FAT
  • STORE VITAMIN A (fat-soluble)
  • REGULATE the TURNOVER OF / SECRETE ECM
32
Q
  1. Bile Acids conjugated with what form Bile Salts
  2. which Receptors do Bile Acids use?
  3. Primary Bile Acids are synthesised by the Oxidation of what? using which mediator?
    examples?
  4. what enzyme is the Rate-Limiting step in Primary Bile Acid Synthesis by?
    what down-regulates, up-regulates and inhibits it?
  5. how are Secondary Bile Acids formed and where?
A
  1. with TAURINE or GLYCINE
    • FARSENOID X RECEPTOR
      (triglyceride & glucose metabolism, liver growth)
      - TGR5 / G-protein Couples Bile Acids Receptor
      (metabolism, endocrine, neurological functions)
  3. PRIMARY BILE ACIDS - OXIDATION of CHOLESTEROL
    - mediated by CYTOCHROME P450 (CP450)
    eg. CHOLIC ACID, CHENODEOXYCHOLIC ACID
  4. Rate-Limiting step in PRIMARY BILE ACID SYNTHESIS is the Addition of -OH GROUP on 7TH POSITION by CHOLESTEROL 7 ALPHA-HYDROXYLASE
    - down regulate: Cholic acid
    - up regulate: Cholesterol
    - Inhibit: FGF15/19 hormone
  5. SECONDARY BILE ACIDS: PARTIAL HYDROXYLATION of PRIMARY Bile Acids
    in the COLON

ie Cholic acid -> Deoxycholic acid
Chenodeoxycholic acid -> Lithocholic acid

32
Q
  1. what causes the Gallbladder to Contract?
  2. name of the Sphincter that allows Bile and Pancreatic secretions into the Duodenum major papilla (from hepatopancreatic ampulla of Vater)
  3. what Relaxes this Sphincter
A
    • CCK
      - SECRETIN -> Pancreas -> INCREASE HCO3- / H2O
      - STOMACH ACID in DUODENUM
  2. SPHINCTER OF ODDI
  3. CCK RELAXES
    and HCO3-/H20 (ALKALINE TIDE)
32
Q
  1. ENTEROHEPATIC CIRCULATION refers to how what is made into Bile?
  2. where are Red Blood Cells broken down
  3. 95% of Bile is reabsorbed into liver to be re-cycled from where?
    - via what?
  4. how are organs Protected from potentially Toxic effects of Circulating Bilirubin?
A
  1. HAEME broken down into Biliverdin -> Bilrubin
    (BILE)
  2. SPLEEN
  3. Reabsorbed from TERMINAL ILEUM
    - via HEPATIC PORTAL VEIN
  4. CIRCULATING BILIRUBIN is BOUND to ALBUMIN
    (unconjugated bilirubin detaches from albumin and is extracted by liver)
33
Q

what types of meals Delay Gastric Emptying

A
  • FAT rich
  • HYPERTONIC (high conc. solutes)
  • ACIDIC
  • HIGH VISCOSITY
34
Q

where are Fat-Soluble substances such as Alcohol and Aspirin absorbed?

A

STOMACH

35
Q
  1. Monosaccharides of
    Maltose:
    Sucrose:
    Lactose:
  2. from Small Intestine how is Glucose absorbed across the Enterocytes at the brush border and into the blood?
  3. from Small Intestine how is Galactose absorbed across the Enterocytes at the brush border and into the blood?
  4. from Small Intestine how is Fructose absorbed across the Enterocytes at the brush border and into the blood?
A
  1. Maltose: 2X GLUCOSE
    Sucrose: GLUCOSE & FRUCTOSE
    Lactose: GLUCOSE & GALACTOSE
  2. GLUCOSE across Brush Border with NA+
    (NA+-GLUCOSE SYMPORTER / SGLT-1)
    into blood via GLUT 2
  3. GALACTOSE same as Glucose.
    with NA+ ACROSS BRUSH BORDER (SYMPORTER)
    into blood via GLUT2
  4. FRUCTOSE ACROSS BRUSH BORDER via GLUT5
    into blood via GLUT2
36
Q

for efficient Absorption of Water what should NA+ Conc. be above in the small intenstine (jejunum)

A

NA > 90 MMOL/L

37
Q
  1. what is meant by Colonic Fermentation
  2. what does it generate?
  3. which is the main fuel?
  4. how does high Fruit and Legume diet cause healthy bowels?
  5. which diet is unhealthy for gut and why?
A

in the COLON, Undigestible CARBOYDRATES / Polysaccharides are BROKEN DOWN / FERMENTED by ANAEROBIC BACTERIA (FERMICUTES)

into *SHORT CHAIN FATTY ACIDS
(and Gases - H2 -> Methane)

  1. generates ENERGY (800kcal per day)
  2. MAIN FUEL: BUTYRATE (HIGH ENERGY SOURCE)

(others: Acetate, Propionate)
(further metabolised by liver)

  1. Fruit & Legume: MORE & BENEFICIAL SCFAs GENERATED
    MORE GRAM +, SACCHROLYTIC SPECIES
  2. MILK, FAT, PROTEINS generate LOW SCFA LEVELS, MORE GRAM -, PROTEOLYTIC BACTERIA,
    AMINO ACID METABOLISM
38
Q
  1. what does the Stomach do to Proteins
  2. which Enzymes in the Small Intestine break down the Shorter Polypeptides
  3. where are Proteins further broken down for absorption if not completely digested in small intestine
A

.1. HCL in STOMACH DENATURES and UNFOLDS 3D STRUCTURE to REVEAL POLYPEPTIDE CHAIN
- PEPSIN break down into SHORTER POLYPEPTIDES

  1. TRYPSIN, CHYMOTRYPSIN, PROTEASES further digest into Tri/Di peptides or Amino Acids
  2. Di/Tri Peptides into ENTEROCYTES of Villus by Brush Border PEPT1 transporter
  • INTRACELLULAR PEPTIDASES further digest into Amino Acids (-> Blood)
39
Q
  1. Lipid Digestion steps:
  2. which Fatty Acids use CHYLOMICRON and LYMPHATICS for absorption
  3. structure of MICELLE
  4. structure of Chylomicron
  5. what can you get when fat absorption isn’t correct
A
  1. large lipid droplet EMULSIFIED by BILE into small lipid droplets (Increases Surface Area)
  2. LIPASE digests TRIGLYCERIDES -> FATTY ACIDS and MONOGLYCEROL
  3. FATTY ACIDS and MONOGLYCEROL form MICELLE which TRANSPORTS them through AQ. environment to ENTEROCYTE
  4. in Enterocyte, combine to REFORM TRIGLYCERIDE
  5. in GOLGI, TRIGLYCERIDE + LIPOPROTEINS
    FORM CHYLOMICRONS
  6. Chylomicrons transport out of cell into LACTEAL (LYMPH CAPILLARY) which carries it away from intestines (to Liver)
  1. LONG CHAIN FATTY ACIDS and MONOGLYCERIDES (LARGE) are transported by CHYLOMICRON into LYMPHATIC CAPILLARY

SHORT & MEDIUM CHAIN and GLYCEROL (SMALL) are absorbed DIRECTLY INTO BLOOD CAPILLARY

  1. MICELLE :
    HYDROPHOBIC INNER CORE
    HYDROPHILIC OUTER SHELL
  2. CHYLOMICRON:
    TRIGLYCERIDES in MIDDLE
    PHOPHOLIPIDS on OUTSIDE
    embedded apolipoproteins and Cholesterol molecules
  3. STEATORRHOES
40
Q
  1. What brings Cholesterol into the Liver?
  2. what do Hepatocytes synthesise from the Cholesterol
A
  1. cholesterol from CHYLOMICRON REMNANT
    - mediated by APO E
  2. BILE SALTS
    (oxidation by cp450)
41
Q
  1. Prostaglandins are Cytoprotective in the GI Tract as they do what?
  2. what do Prostaglandins Inhibit
  3. Prostaglandins are synthesised from Arachidonic Acid via which host Enzyme
  4. what drug Inhibits Prostaglandin synthesis by blocking this enzyme
A
    • INCREASE MUCOSAL BLOOD FLOW
    • Enhance MUCUS & HCO3- PRODUCTION
    • enhance MOTILITY
    • enhance SECRETIONS
    • enhance CELL MIGRATION for EPITHELIAL RESTITUTION
  2. INHIBIT ACID SYNTHESIS from PARIETAL CELLS and INHIBIT HISTAMINE from ECL CELLS
  3. CYTOOXYGENASE ENZYMES (COX1)
  4. ASPIRIN BLOCKS
42
Q
  1. how much Vitamin D is bound to DBP (binding protein)
  2. how much Vitamin D is in Chylomicrons
  3. Vitamin A is for what?
  4. Vitamin E is for what?
  5. Vitamin K makes which blood clotting factors?
A
  1. 40% transported by DBP
  2. 60% transported in CHYLOMICRON
  3. A: VISION
  4. B: BIOLOGICAL ANTIOXIDANT
  5. VIT K makes factors 2, 7, 9, 10
43
Q
  1. what is Vitamin B12 for?

in B12 absorption:
2. what is it Bound to in the STOMACH?

  1. what is it Bound to in the DUODENUM?
  2. where does this come from?
  3. where is B12 Absorbed into Blood?
  4. what is B12 Bound to in the Blood and what is this complex known as
  5. from the blood B12 goes where?
A
  1. RBC FORMATION
  1. STOMACH: BINDS R-PROTEINS
  2. DUODENUM: cleaved from R-proteins and bound to INTRINSIC FACTOR
  3. IF comes from STOMACH PARIETAL CELLS
  4. ABSORBED in DISTAL 80CM of ILEUM
  5. in blood bound to TRANSCOBALAMIN (I,II or III)
    -> HOLOTRANSCOBALAMIN - ACTIVE B12

7 goes to LIVER and re-circulated

44
Q

what do Oral Rehydration therapies use

A
  • WATER
  • SODIUM CHLORIDE
  • GLUCOSE
  • Potassium (to replace what was lost)

Na+ reabsorbed by SGLT-1 and Na+/Proton exchanger
Chloride exchanged into cell with HCO3-
Glucose into cell via SGLT-1

45
Q

what are the Defensive measures against stomach Acid and Pepsin?

A
  • MUCUS-HCO3- BARRIER : slows H+ diffusion, mucus gel traps H2O and HCO3- to create barrier
  • TIGHT JUNCTIONS between cells : slow H+ diffusion
  • CELL SURFACE PHOSPHOLIPIDS - tougher barrier
  • CELL MIGRATION and REGENERATION
  • PROSTAGLANDINS:
    - INCREASE HCO3- PRODUCTION (buffer)
    - INCREASE MUCOSAL BLOOD FLOW: carry H+
    away if does permeate, helps Antioxidant
    function
  • BLOOD VESSELS DILATION by NO and CGRP (induces somatostatin releases)
46
Q

Stretch Reflex of the Duodenum causes what to also bind to Pancreatic Acinar Cells (as well as CCK)?
what triggers the CCK to be released and bind?

Stretch Reflex of the Duodenum causes what to also bind to Pancreatic Duct Cells (as well as Secretin)?
what triggers the Secretin to be released and bind?

A

ACINAR: ACH and CCK bind
- I cells sense Fats and Proteins and thus release CCK
- ACH released due to Stretch of Duodenum

DUCTAL CELLS: VIP and SECRETIN
- S cells sense high H+ and thus release Secretin
- VIP released due to stretch of Duodenum

47
Q

which are the Key Players in Epithelium Restitution / Repair?

A
  • GASTRIN - stimulates migration
    -> GROWTH FACTORS
  • PROSTAGLANDINS
  • REGENERATING PROTEIN (REG - from ECL Cells)
  • TREFOIL PEPTIDES
48
Q
  1. in Peyer’s Patches what do Microfold/ M CELLS do?
  2. what is Secreted in response?

3.what do Mast cells stimulate in response?

A

M CELLS TRANSPORT antigenic material / bacteria to the BASOLATERAL Side
- present to IMMUNOSURVEILLANCE CELLS :
MAST CELLS, MACROPHAGES, T-CELLS
T-cells: cytokines
activation B cells
(and mucus production for barrier)

  1. IgA is produced and SECRETED INTO LUMEN across M CELL
  2. MAST CELLS cause INNERVATION of GUT WALL to INCREASE MOTILITY therefore MOVE AWAY INFECTIOUS AGENTS
49
Q

how many Villus cells?
how Many Crypts?
how many Crypts per Villus?
How many cells are lost/shed per day from each villus?
How long do cells take to shed?

what are Paneth Cells?

A

3500 VILLUS
250 Crypts
6-10 crypts per villus
10 Minutes to shed

PANETH CELLS are at the Bottom of crypts - PROTECT STEM CELLS by secreting cytidines and defensins to attack any bacteria

50
Q

Where is the Vomiting Centre?

  1. what are the Efferent Fibres?
  2. in Vomiting Reflex, what are Contracted?
  3. what are Relaxed?
A
  • Medulla
  1. VAGUS NERVE & PHRENIC NERVE
    • PYLORIS, DUODENUM, ANTRUM contract to stop food going down
      - DIAPHRAGM FIXED CONTRACTION for INSPIRATION
      - INTERCOSTAL MUSCLES Contract for HIGH ABDOMINAL MUSCULAR PRESSURE (needed for reflex)
  3. Pharynx, LOS and UOS are relaxed (soft palate raised and epiglottis moves over trachea)
51
Q

1.Taste Receptors use which Nerves?

  1. which Taste Receptors detect Umami / L-Amino-Acids (Protein)?
  2. which Taste Receptors detect Sweet (sugars)?
  3. which Taste Receptors detect Bitter?
  4. which Taste Receptors detect Saltiness?
  5. which Taste Receptors detect Sour?
  6. Gustatory patway:
A
  1. FACIAL (7) & GLOSSOPHARYNGEAL (9)
  2. Umami / L-Amino-Acids: T1R1 & T1R3
  3. Sweet: T1R2 & T1R3
  4. Bitter: T2Rs (type 2 receptors)
  5. Saltiness: ENaC
  6. Sour: PKD2L1
  7. Gustatory pathway to NTS Solitary tract to the Thalamus and then to Cortex
52
Q
  1. which Gut cells are for Chemosensing/Nutrient sensing
  2. what tastes do I cells (CCK) taste receptors sense?
  3. what tastes do G cells (Gastrin) taste receptors sense?
  4. what tastes do D cells (Somatostatin) taste receptors sense
A

ENTEROENDOCRINE Cells (EECs)
- have Nutrient-sensing G-PROTEIN COUPLED RECEPTORS (GUSTDUCIN g-protein)

  1. I cells:
    PROTEIN (UMAMI), LONG CHAIN FATTY ACIDS, BITTER
  2. G-cells:
    Proteins / peptides
  3. D-Cells:
    SWEET, BITTER
53
Q
  1. when does development of faecal microbiota take place?
  2. what are the 1st bacteria to form?
  3. which bacteria forms on 3rd Day?
  4. which bacteria forms on 5th Day?
  5. what is meant by Dysbiosis?
  6. Intestinal Bacteria play a key role in the Production of what?
A
  1. FIRST 10 DAYS
  2. COLIFORM, LACTOBACILI, ENTEROCOCCI
  3. 3rd day: strains of BACTERIODES
  4. 5th day: BIFIDOBACTERIA
  5. IMBALANCE in MICROBIOME
  6. PRODUCTION OF VITAMINS ie VIT K, B VITAMINS
54
Q
  1. out of the 6 major phyla what are the main anaerobic bacteria?
  2. these make up what proportion?
  3. where in the GI Tract are most bacteria found?
  4. in Colonic mucus which Layer is Free from bacteria
  5. 2 mucus layers in Colon are arranged by what?
A
  1. FIRMICUTES & BACTEROIDETES
  2. > 90%
  3. ASCENDING & TRANSVERSE COLON
  4. INNER LAYER is FREE FROM BACTERIA
    (outer layer keeps bacteria away)
  5. MUC2 MUCIN (dominant mucin glycoprotein in intestines)
55
Q
  1. what is used for the Absorption of SCFAs from the Colon
  2. Butyrate (BT) can also be used as an Anti-Cancer agent how?
  3. SFCA Receptors have what other functions
  4. SCFAs that are passed into Portal Vein undergo what by the Liver
A
  1. MCT TRANSPORTER/RECEPTOR
    (monocarboxylate)
  2. BUTYRATE - INHIBITS HISTONE DEACETYLASE which Enhances TUMOUR SUPPRESSOR GENE EXPRESSION
  3. IMMUNOMODULATORY
    & Link Gut microbiota metabolic activity to ENERGY HOMEOSTASIS
56
Q
  1. what is used for the Absorption of SCFAs from the Colon
  2. Butyrate (BT) can also be used as an Anti-Cancer agent how?
  3. SFCA Receptors have what other functions
  4. SCFAs that are passed into Portal Vein undergo what by the Liver
  5. what 3 things can SCFAs undergo in Liver?
A
  1. MCT TRANSPORTER/RECEPTOR
    (monocarboxylate)
  2. BUTYRATE - INHIBITS HISTONE DEACETYLASE which Enhances TUMOUR SUPPRESSOR GENE EXPRESSION
  3. IMMUNOMODULATORY
    & Link Gut microbiota metabolic activity to ENERGY HOMEOSTASIS
  4. Liver: 1ST PASS METABOLISM
    • ACETATE and BUTYRATE can be CONVERTED INTO ACETYL CO-A and used to FORM LIPIDS & KETONE BODIES
  • may enter CITRIC ACID CYCLE for GLUCOSE PRODUCTION via GLUCONEOGENESIS
  • ACETATE may enter PERIPHERAL CIRCULATION and be found in peripheral blood
57
Q
  1. what is the name for Vitamin B1?
    what does it do?
  2. what is the name for Vitamin B2?
    what does it do?
  3. what is the name for Vitamin B3?
    what does it do?
  4. what is the name for Vitamin B6?
    what does it do?
  5. what is the name for Vitamin B12?
    what does it do?
  6. what does Folic Acid do?
A
  1. THIAMINE : CARBOHYDRATE METABOLISM
  2. RIBOFLAVIN: H TRANSFER
  3. NIACIN: H TRANSFER
  4. PYRIDOXINE: PROTEIN METABOLISM
  5. CYANOCOBALAMIN: RBC FORMATION
  6. FOLIC ACID: SINGLE-CARBON METABOLISM
58
Q

Functions of each mineral.

Copper:
Iron:
Chromium:
Manganese:
Iodine:
Zinc:
Selenium:

A

Copper: METALLOENZYMES
Iron: HAEMOGLOBIN SYNTHESIS
Chromium: CARBOHYDRATE METABOLISM
Manganese: ORGANIC MATRIX OF BONE
Iodine: THYROID HORMONES
Zinc: METALLOENZYMES
Selenium: T4 -> T3 CONVERSION

59
Q

where is Iron absorbed

A

Duodenum

Gastrointestinal (19 decks)

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