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GI Flashcards

1
Q

what constitutes the foregut

A

mouth to the common bile duct includes: pharynx, oesophagus, stomach and proximal half of the duodenum

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2
Q

what constitutes the midgut

A

common bile duct to 2/3 of the way across the transverse colon includes: distal half of the duodenum, jejunum, ileum, caecum, appendix, ascending colon and proximal 2/3 of transverse colon

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3
Q

what constitutes the hindgut

A

2/3 of the way along the transverse colon to the anal canal includes: distal 1/3 of the transverse colon, descending colon, sigmoid colon, rectum and the anal canal

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4
Q

what is the blood supply to the foregut?

A

celiac artery

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5
Q

what is the blood supply to the midgut?

A

superior mesenteric artery

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6
Q

what is the blood supply to the hindgut?

A

inferior mesenteric artery

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7
Q

what is embryonic folding

A

in the fourth week of development the trilaminar disc folds into a cylinder. it happens in the lateral plane and the medial plane. this results in two lateral body folds (horizontal folding) and cranial and caudal folds (medial folding)

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8
Q

endoderm gives rise to what in the primitive gut

A

i) epithelial lining of the digestive tract ii) hepatocytes of the liver iii) endocrine and exocrine of the pancreas

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9
Q

visceral mesoderm gives rise to what in the primitive gut?

A

i) muscle, connective tissue and peritoneal components of the wall of the gut ii) connective tissue of the glands

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10
Q

formation of the mouth

A

the cranial end of the gut tube ruptures at the end of the 4th week of development

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11
Q

what is the vitelline duct?

A

the midgut is connected to the yolk sac until the 5th week of development. as embryonic folding continues, the connection to the yolk sack narrows into a stalk called the vitelline duct

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12
Q

formation of the anus

A

the caudal end of the primitive gut tube remains closed by the cloacal membrane. this ruptures during the 7th week of development forming the anus

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13
Q

what are the pharyngeal arches?

A
  • There are 5, 1,2,3,4 and 6 (no five in humans)
  • formed by mesenchymal cells that are invaded by neural crest cells (forming clefts)
  • they’re covered externally by endoderm and internally by ectoderm (forming pouches)
  • each has
    • nerve supply
    • arterial supply
    • venous supply
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14
Q

when do the pharyngeal arches develop?

A

4th and 5th week

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15
Q

1st pharyngeal arch

A
  • innervation: mandibular nerve (V3)
  • Muscles:
    • muscles of mastication
    • tensor tympani
    • digastric
    • myolohyoid
  • Bones
    • maxilla
    • mandible
    • incus
    • malleus
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16
Q

2nd pharyngeal arch

A
  • innervation: facial nerve
  • muscles:
    • facial expression
    • stapedius
    • stylohyoid
  • bone:
    • stapes
    • styloid
    • lesser horn of hyoid cartilage
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17
Q

3rd pharyngeal arch

A
  • Innervation: glossopharyngeal (CN IX)
  • Muscles: stylopharyngeus of the pharynx
  • Bone: body and greater horn of the hyoid cartilage
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18
Q

4th pharyngeal arch

A
  • innervation: superior laryngeal of the vagus
  • Muscles: Cricothyroid
  • Bone:
    • thyroid cartilage
    • epiglottic cartilage
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19
Q

6th pharyngeal arch

A
  • Innervation: recurrent laryngeal nerve of vagus
  • Mucles:
    • All muscles of the larynx except for the cricothryoid
  • Bone:
    • Cricoid cartilage
    • Arytenoid cartelage
    • Corniculate and cuneiform cartilage
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20
Q

When and where do lung buds appear?

A
  • at the end of the 4th week
  • between the end of the pharynx and the beginning of the oesophagus
  • at the ventral wall of the foregut
  • they’re called respiratory diverticulum
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21
Q

development of the oesophagus

A
  • after the lung buds have formed, a septum grows to divide the respiratory tract from the dorsal foregut
  • at this point the ‘respiratory primordium’ is still part of the foregut
  • but the foregut is now spit into
    • ventral: respiratory primordium
    • dorsal: oesophagus
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22
Q

Mesenteries and their development

A
  • double layers of peritoneum that surround organs and connect them to the abdo wall
  • if something is in contact with the posterior abdominal wall and only covered on its anterior side by mesentary then it is ‘retroperitoneal’
    • e.g. kidneys
  • by the 5th week, most of the gut is suspended from the posterior abdominal wall by dorsal mesentary
  • dorsal mesentary extends form the lower part of the oesophagus to the cloacal region
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23
Q

initial development of the stomach

A
  • appears as a spiral shaped dilation in the foregut in the 4th week
  • is attached to the body walls by the dorsal and ventreal mesenteries
  • left and right vagus nerve flank it
  • dorsal wall grows faster than ventral wall
    • creates greater and lesser curves
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24
Q

stomach development: 7th week

A
  • stomach rotates 90° clockwise
  • this creates a space behind the stomach called the lesser sack
  • greater curve now faces left and lesser curve now faces right
  • the right vagus is now posterior and left vagus is anterior
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25
Q

stomach development: 8th week

A
  • stomach and duodenum rotate
  • pulls pylorus of stomach up and pulls duodenum into a C shape
  • dorsal mesentery (hanging from greater curvature of stomach) is now called greater omentum
  • the ventral mesentery is attached to the liver and is now called the lesser omentum
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26
Q

greater and lesser sac

A
  • lesser sac is the space behind the stomach
  • greater sac is the space in front of the stomach (basically the rest of the peritoneal cavity
  • they communicate through a small hole called the epiploic foramen which is a small hole behind the hilum of the liver
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27
Q

1st stage of swallowing

A
  • voluntary
  • tongue compresses food and pushes it towards oropharynx
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28
Q

2nd stage of swallowing

A
  • involuntary
  • nasopharynx blocked off by soft palate which tenses and elevates
  • hyoid bone elevates, shortening and widening the pharynx
  • swallowing centre inhibits respiration and closes the glottis
  • epiglotis tilts back covering the glottis - prevents aspiration
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29
Q

3rd stage of swallowing

A
  • involuntary
  • constrictor muscles contract sequentially
    • 3 overlapping muscles innervated by the vagus
  • hyoid bone returns
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30
Q

the oesophagus

A
  • skeletal muscle around the upper third of the oesophagus
  • smooth muscle around the lower two thirds of the oesophagus
  • the skeletal muscle ring around the oesophagus just below the pharynx is called the upper oesophageal sphincter
  • smooth msucle ring around the oesophagus just before it enters the stomach is called the lowe oesophageal sphincter
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31
Q

how long does one oesophageal peristaltic wave take to reach the stomach?

A

nine seconds

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32
Q

Gagging (wig)

A

reflex elevation of the pharynx, often followed by vomiting,

caused by irritation of the oropharynx

reflex arc between CN IX and X

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33
Q

saliva

A
  • lubricant for mastication
  • contains alpha amylase for starch digestion
  • also contains lipase to begin fat digestion
  • daily secretion 0.8 - 1.5L
  • pH maintained at about 7.4
  • serous, mucus or mixed secretion
    • serous: more liquid, more amylase for starch digestion
    • mucus: more viscous for lubricaton
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34
Q

salivary glands position and secretion

A
  • parotid = serous
  • submandibular = mixed
    • M for mandibular and M for mixed
  • sublingual = mixed but mainly mucous
  • submandibular and sublingual are continuously active
  • parotid only becomes the main source of saliva when it is stimulated
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35
Q

oral cavity defence

A
  • physical barrier of mucosa
  • saliva washes away food particles that bacteria could live off
  • palletine tonsils contain many immune cells
    *
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36
Q

what tissues are salivary glands made of

A
  • two distinct epithelial tissues
  1. acinar cells
    • acinus is the functional unit of the salivary glands
  2. ducts
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37
Q

serous acinus

A
  • dark staining nuclei
  • nucleus is in the basal third of the cell
  • small central duct
  • secretes water and alpha amylase
  • mainly found in the parotid gland
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38
Q

mucous acinus

A
  • pale staining and foamy
  • nucleus at the base
  • has a large central duct
  • secretes mucous (which contains water and glycoproteins)
  • found in the submandibular and sublingual glands
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39
Q

Parotid Gland

A
  • entirely made of acini with ducts interspersed
  • parotid duct crosses the masseter muscle
  • it then pierces the buccinator muscle where it enters the oral cavity near the upper molars
  • innervation:
    • sympathetic (limits secretion): auriculo temporal nerve (branch of V3)
    • Parasympathetic: glossopharyngeal
  • structures that pass through it:
    • external carotid
    • retromandibular vein
    • facial nerve
  • this is why the parotid capsule is very tough
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40
Q

submandibular glands

A
  • one larger superficial lobe
  • one smaller deep lobe in the floor of the mouth
  • duct begins in superficial lobe and empties into the oral cavity at the sublingual papillae
  • has both serous and mucous acini
  • innervation:
    • sympathetic: lingual nerve branch of facial nerve
    • parasympathetic: chorda tympani branch of facial nerve
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41
Q

sublingual glands

A
  • more anterior to submandibular
  • very small
  • mixed serous and mucous acini
  • innervation:
    • sympathetic: lingual nerve branch of facial nerve
    • parasympathetic: chorda tympani branch of facial nerve
    • same as sub-mandibular
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42
Q

Xerostomia

A
  • dry mouth
  • if salivary output falls to less than 50% normal
  • why it’s a problem:
    • low lubrication so oral function becomes difficult
    • low natural oral hygeine
    • poor pH control (saliva is slightly alkaline)
    • maybe opportunistic infections like thrush
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43
Q

salivary obstruction

A
  • saliva contains calcium & phosphate ions that can form salivary caliculi
  • most common in submandibular gland
    • it blocks the duct where it bends round the mylohyoid
    • or at the exit at the sublingual papillae
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44
Q

Functions of the stomach

A
  • store and mix food
  • digest food
  • regulate emptying into the duodenum
  • kill microbes
  • secreate proteases
  • secrete intrinsic factor (enables absorbtion of vit B12)
  • activate proteases
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45
Q

Stomach cell types and their roles

A
  • Mucous cells: produce mucous
  • Parietal cells: produce gastric acid and intrinsic factor
  • Chief cells: produce pepsinogen
  • Enterochromaffin-like cells (ECL): release histamine
  • G cells: release gastrin
  • D cells: release somatostatin
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46
Q

stomach epithelium

A
  • the epithelial layer invaginates into the mucosa to form many tubular glands
  • the upper portion of the body of the stomach is thin walled and it secretes
    • mucous
    • HCL (from parietal cells)
    • pepsinogen (from chief cells)
  • the antrum of the stomach is more thick walled with smooth muscle and is responsible for mixing the stomach contents.
  • the antrum secretes:
    • almost no acid
    • gastrin (from G cells)
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47
Q

Gastric acid secretion

A
  • pH: 2
  • ~2 L per day produced
  • energy dependent
  • in the cell H2O breaks down into OH- and H+
  • CO2 and H2O in the cell form carbonic acid (H2CO3) via carbonic anhydrase
  • H2CO3 spontaneously dissociates into HCO3- and H+
  • Some of the H+ reacts with OH- to regenrate broken down H2O
  • H+ also gets pumped into the stomach lumen by antiport H+/K+ ATPase pumps (active process) (1 K+ into cell for 1 H+ out)
  • elsewhere K+ can diffuse in and out of the stomach via channels
  • HCO3- is secreted into the capillary for the exchange of Cl- ions
  • in the stomach the H+ and the Cl- form HCL
  • can you draw the diagram?
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48
Q

what happens when the gastric acid secretion is regulated UP?

A
  • proton pumps (H+/K+ ATPase) present in the membranes of intracellular vesicles migrate to the plasma membrane
  • these vesicles fuse with the membrane
  • this increases the number of proton pumps in the membrane
  • this means more acid can be secreted
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49
Q

Cephalic Phase of stimulating gastric acid secretion

A
  • parasympathetic
  • initiated by the sight, smell, taste of food and chewing
  • acetyl choline is released
  • ACh acts on parietal cells
  • this triggers the release of:
    • Gastrin from the G cells in the pyloric antrum
    • Histamine from the ECL cells
  • these both increase the number of proton pumps on the PM
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50
Q

gastric phase of stimulating gastric acid secretion

A
  • initiated by gastric distention and the presence of peptides and amino acids from food
  • gastrin is released
  • gastrin triggers the release of histamine
  • both gastrin and histamine increase the numbers of proton pumps on the PM
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51
Q

Gastric phase of turning gastric acid secretion off

A
  • low luminal pH inhibits gastrin secretion and thereby inhibits histamine release
  • low luminal pH also stimulates somatostatin secretion
  • somatostatin inhibits parietal cell activity
    • NB protein in the stomach acts as a buffer causing increased pH production through decreased somatostatin release
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52
Q

Intestinal phase of turning off gastric acid secretion

A
  • happens in the duodenum
  • initiated by duodenal distention, low pH, the presence of amino acids & fatty acids
  • triggers the release of locally produced enterogastrones such as secretin and CKK
  • secretin inhibits gastrin release and promotes somatostatin release
  • CCK causes the gall bladder to release bile produced by liver
  • all enterogastrones trigger neural pathways that reduce ACh release
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53
Q

chemical factors that control gastric acid secretion

A
  • controlled by the brain stomach and the duodenum
  • 1 parasympathetic neurotransmitter: ACh (+)
  • 1 hormone: gastrin (+)
  • 2 paracrine factors: histamine (+) and somatostatin (-)
  • 2 key enterogastones: secretin (-) and CKK (-)
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54
Q

bacterial cause of peptic ulcers

A
  • an ulcer is a breach in the mucosal surface
  • commonly caused by helicobacter pylori infection
    • lives in the gastric mucus & secretes urease
    • urease splits urea into CO2 and ammonia
    • ammonia + H+ = ammonium
    • ammonia is toxic to the mucosa and causes less mucous to be produced
    • results in inflammatory response and less mucosal defence
    • treat with proton pump inhibitor and antibiotics
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55
Q

drug cause of peptic ulcers

A
  • NSAIDs inhibit both COX-1 and COX-2
  • the COX enzymes synthesize prostaglandin
  • prostaglandin stimulates mucous secretion
  • therefore prolonged use of NSAIDs can cause reduced mucosal defence
  • treat with prostaglandin analogues
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56
Q

how to synthetically reduce gastric acid secretion

A
  • proton pump inhibitors
    • block the H+/K+ ATPase pump
    • e.g. omeprazole and lansoprazole
  • H2 receptor agonists
    • block histamine receptors thereby reducing acid secretion
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57
Q

protective mechanisms of gastric mucosa

A
  • alkaline mucus on luminal surface
  • tight junctions
  • stem cells to replace damaged cells
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58
Q

Protease secretion

A
  • chief cells produce pepsinogen (zymogen)
    • so that it doesn’t digest the chief cells
  • secretion parallels HCL secretion
  • once secreted, the low pH of stomach causes pepsinogen is transformed into pepsin
    • most efficient when pH <2
  • the HCO3- released in the duodenum irreversibly inactivates pepsin
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59
Q

the stomach and protein digestion

A
  • the stomach is non-essential for protein digestion
    • it simply accelerates protein digestion
    • accounts for 20% protein digestion
    • breaks down collagen - meat shreds - greater SA
  • however because parietal cells produce intrinsic factor, if the stomach is removed then no B12 can be absorbed
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60
Q

what is the volume of an empty stomach?

A

50ml

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61
Q

how much volume can the stomach accomodate without massively increasing luminal pressure?

A

1.5L

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62
Q

how does the stomach accomodate more space?

A
  • receptive relaxation
  • smooth muscles in the body and fundus relax
  • afferent sensory information from the stomach is relayed to the brain by the vagus nerve
  • efferent signals to relax are also relayed by the vagus nerve
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63
Q

Peristalsis

A
  • begins in the body of the stomach
  • most powerful contraction are in the antrum which cause the best mixing
  • pyloric sphincter closes as peristaltic waves reach it
    • this means only a little chyme enters the duodenum
    • also means contents are forced back to antrum for more mixing
  • 3 waves every minute
    • pacemaker cells in the muscular propria (longitudinal smooth muscle layer)
    • PM cells undergo slow depolarisation-repolarisation cycles
    • gap junctions transmit depolarisations
  • no significant contraction in an empty stomach
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64
Q

How is the strength of a stomach contraction altered?

A
  • pacemaker cells are always active
  • but the action potential threshold can be altered by various factors
  • if the threshold is lowered there will be more action potentials and therefore stronger contractions
65
Q

Factors that increase the strength of stomach contraction?

A
  • Gastrin
  • gastric distention (mechanoreceptors)
66
Q

Factors that decrease strength of stomch contractions

A
  • Duodenal distention
  • increease in duodenal fat
  • increase in duodenal osmolarity
  • decrease in duodenal pH
  • increase in sympathetic ns stimulation
  • decrease in parasympathetic ns stimulation
67
Q

dumping syndrome

A
  • this is when the stomach empties too quickly
  • a hypertonic solution enters the duodenum
  • this draws water into the intestinal lumen
  • osmotic diarrhoea ensues
  • other symptoms:
    • vomiting
    • bloating
    • cramps
    • dizziness
    • fatigue
68
Q

Delayed gastric emptying

A
  • gastroparesis
  • can be caused by neuro issues like
    • MS
    • Parkinsons
  • can be caused by abdo surgery
  • can be caused by drugs like:
    • H2 receptor agonists
    • PPIs
  • more common in females
  • contents of stomach rots and smells
  • nausea
  • vomiting undigested food
  • early satiety
69
Q

GORD

A
  • gastro oesophageal reflux disease
  • caused by
    • pregnancy
    • obesity
    • smoking
70
Q

Water in the GI tract

A
  • 8L of water is secreted into the small intestine
  • but only 1.5L passes on to the large intestine
  • the jejunum absorbs the most water
  • stomach only absorbs a very small amount of water (smal SA)
  • only 200ml (<3%) is excreted in stool
71
Q

Water absorbtion in the small intestine

A
  • transport of solutes (mainly Na+) fromt he lumen into the epithelial cells of the ilium and the jejunum
    • could be symport with glucose and protein
  • this creates a gradient
  • water moves down this gradient out of the lumen
  • on the baso-lateral surface of the epithelial cells there are Na+/K+ ATPase transporters that reduce the intracellular Na+ so that Na+ can still move down it’s concentration gradient into these cells
72
Q

Water and solute reabsorbtion in the colon

A
  • contents are now iso-osmotic so Na+ has to be pumped out of the lumen - water follows
  • potassium reabsorbtion happens by passive diffusion depending on the potential difference beteween the lumen and the intestinal capillaries
    • diarrhoea can result in hypokalaemia
  • chloride reabsorbtion is in antiport with bicarbonate resulting in the intestinal contents becoming more alkaline
73
Q

functional states of digestion and energy use

A
  1. Absorbtive state
    • ingested nutrients are entering the blood from the GI tract
    • some of this ingested nutrients is used for energy
    • the remainder is added to stored
  2. Post absorbtive state
    1. GI tract is empty and the body’s own stores must be used
74
Q

what are the 3 main fatty acids we absorb?

A
  1. Palmitic (most abundant)
  2. Stearic
  3. Oleic
75
Q

what is a triglyceride

A

a glycerol molecule with three fatty acids attached

76
Q

action of lipase on fatty acids

A
  • synthesised in the pancreas
  • splits the bonds that link the fatty acids to the 1st and 3rd carbons of glycerol
  • this produces 2 fatty acids and a monoglyceride
  • SO under the action of lipase:
    • triglyceride –> monoglyceride and 2 fatty acids
77
Q

fat emulsification

A
  • insoluble so aggregate in droplets inthe upper portion of stomach
  • emulsification to 1mm droplets requires:
    1. mechanical disruption of large droplets by motility of stomach and GI tract
    2. emulsifying agent
      • amphipathic phospholipids from food
      • amphipathic bile salts (in bile) from the liver secreted by gall bladder
  • non-polar portions of emulsifying agents associate with non-polar lipids, coating them
  • the polar portions of the emulsifying agents are exposed to the water surface
    • exposed polar portions repel other lipid droplets, preventing their aggrregation into larger droplets
78
Q

how does lipase access the lipid in the lipid droplets

A
  • the lipids being coated by an emulsified makes them harder to access by lipase
  • the pancreas secretes colipase which binds to the lipid droplet surface as well as binding to lipase
  • this holds lipase onto the surface of the droplet
79
Q

further emulsification of lipids

A
  • bile salts then further emulsify the lipids into ‘micelles’ which are 4-7nm in diameter
  • the micelles contain
    • fat soluble vitamins A,D,E,K
    • cholesterol
    • fatty acids and monoglycerides
      • products of lipase action
80
Q

Fat absorbtion and processing in the enterocyte

A
  • micelles themselves are not absorbed
  • They transport the lipids to the membrane of the enterocytes where they can move into the enterocytes
    • because lipids are non-polar they can just diffuse accross
  • the lipids are resynthesised into triglycerides in the SER
  • this decreases the cytosolic concentration of free fatty acids and monoglycerides so theat they can still diffuse into the cell down a gradient
  • vesicles of triglycerides are formed and processed through the golgi where they are converted to chylomicrons
81
Q

Chylomicrons

A
  • chylomicrons are lipoprotein particles specialised for the transport of lipids in the circulation
  • they contain:
    • triglycerides
    • phospholipids
    • cholesterol
    • fat soluble vitamins A,D,E,K
  • chylomicrons can fuse with plasma membrane and enter interstitial fluid via exocytosis
  • they enter the lacteals (lymphatic vessels) in the intestinal villi
    • lacteals have large pores between endothelial cells
  • they cannot enter capillaries due to the basement membrane
  • from the lymph they’re eventually emptied into systemic veins
82
Q

what do chylomicrons contain

A
  1. triglycerides
  2. phospholipids
  3. fat soluble vitamins A,D,E,K
  4. cholesterol
83
Q

chylomicrons in the circulation

A
  • in adipose tissue capillaries, lipoprotien lipase breaks down the triglycerides into free fatty acids
  • these can diffuse into adipodicytes
  • in the adipodicytes they are once more converted into triglycerides
    • this requires alpha glycerol
    • this is a phosphorylated glycerol
    • glucose is essential to make this glycerol - dunno why
84
Q

3 mains sources of fatty acids for triglyceride synthesis

A
  1. broken down glucose can be built up into fatty acids
  2. glucose used in the liver to form VLDL triglycerides are transported in the blood and taken up by adipodicytes
  3. ingested triglycerides transported by chylomicrons
  • sources 2 and 3 require lipoprotein lipase to release fatty acids from the circulating triglycerides
85
Q

Water soluble vitamin absorbtion

A
  • with one exception (B12) water soluble vitamins are absorbed by diffision or facilitated diffusion in the jejunum
  • the exception is B12
    • very large and charged vitamin
    • needs to be bound to the protein intrinsic factor
    • intrinsic factor is produced by parietal cells in the stomach
    • intrinsic gactor binds B12 then binds specific receptors on enterocytes in the lower portion of the ilium
    • B12 is absorbed by endocytosis
  • B12 deficiency can be due to pernicious anaemia where you have deficient intrinsic factor
86
Q

where are proteins absorbed

A
  • mainly in the duodenum
87
Q

how many g of protein does a healthy adult need per day

A

50-60g

88
Q

how many amino acids do we need and how many are essential

A

20 overall

8 are essentia - we cannot produce them

89
Q

what is a zwitterion

A

carboxyllic acid group of a amino acid donates a protein to the amine group

in this way the amino acid has both positive and negative groups

90
Q

Protein Digestion

A
  1. stomach
    • pepsin cleaves some peptide linkages forming fragments
    • pepsins work best at pH 1.6-3.2 so stop working when they leave the stomach
  2. small intestine
    • further fragmented by pancreatic enzymes that can be divided into two groups:
      • endopeptidases: trypsin, elastase and chymotrypsin
      • exopeptidases: carboxyl dipeptidases and amino peptidases of the brush border
  3. intracellular
    • some di and tri-peptidases are absorbed and finally broken down by intracellular peptidases
91
Q

where are carbohydrates mainly absorbed

A

duodenum

92
Q

which of the sugar isomers is the one utilised in metabolism

A

D-isomers

93
Q

what is glycogen like?

A
  • it’s the principle dietary polysaccharide from animal sources
  • its a polymer of glucose
  • joined by alpha 1-4 glycosidic linkages
  • branches because of 1-6 glycosidic linkages
94
Q

what is starch like?

A
  • starch is a mixture of two glucose polymers
    • amylose - linear with alpha 1-4 glycosidic bonds
    • amylocpectin - branched with 1-4 but also 1-6 GBs
95
Q

what is cellulose like

A

it is not branched

only has 1-4 glycosidic linkages

96
Q

starch digestion in the mouth and stomach

A
  • the alpha amylase in the saliva hydrolises some of the alpha 1-4 glycosidic bonds
  • when starch reaches the stomach this stops because the optimal pH for this enzyme is ~7
  • the starch is now partially digested oligosaccharides and polysaccharides
  • in the small intestine is where most of the digestion of starch happens
97
Q

starch digestion and absorbtion in the small intestine

A
  • this is where the majority of the digestion and absorbtion of starch happens
  • when the starch reaches the small intestine it has been broken into oligosaccharides and small polysaccharides
  • pancreatic alpha amylase breaks down the 1-4 bonds even more
  • the enterocytes have brush border enzymes on their brush border. these include
    • maltase that will hydrolyse maltose
    • sucrase that will hydrolyse the remaining 1-4 glycosidic bonds and the 1-6 bonds (the branch points)
  • this will give us very many glucose molecules
  • Na+ glucose linked transporters on the apical surface of the enterocytes cotransport Na+ and glucose into the cell
  • once glucose is within the cell it can leave through the GLUT-2 transporter on the basal surface of the enterocyte
  • it can enter capillaries through capillary pores
98
Q

starch in the colon

A
  • ‘resistant starch’ is the name of the starch derived oligosaccharides that didn’t get totally digested and absorbed in the small intestine
  • the resistant starch undergoes fermentation in the colon (due to gut microbiota)
  • bacteria use RS to create short chain fatty acids which can then be used by the human body
99
Q

where is most carbohydrate absorbes

A

within the first 20% of the small intestine

i.e. the duodenum

100
Q

carbs after absorbtion

A
  • they enter the capillaries and then the hepatic portal vein
  • they travel to the liver where, no matter what type of saccharide they are, they are all converted to glucose
  • it may then be taken to the skeletal muscles where it will either be used or converted to glycogen and stored in the muscle for future use
  • during the absorbtive phase ther is a net uptake of glucose by the liver
  • the liver converts this glucose to glycogen for later use
101
Q

what is the major consumer of glucose

A

skeletal muscle - even at rest

102
Q

making triglycerides

A
  • a triglyceride is a glycerol molecule with three fatty acids attached
  • you need alpha-glycerol phosphate to attach the fatty acids to it
  • to make alpha glycerol phosphate you just reduce dihydroxyacetone phosphate, DHAP (which is made during glycolysis)
  • converting glucose into alpha glycerol phosphate via glycolysis (in order to make triglycerides) is done in the liver as well as adipodicytes

look at the attached image if you need reminding of how DHAP is produced in glycolysis

103
Q

How does excess sugar increase body fat

A
  • most of the triglycerides synthesised from excess glucose in the liver is packaged into lipoproteins
  • these are called VLDL because they contain more lipid than protein and protein more dense
  • VLDLs are made in the golgi and secreted
  • lipoprotein lipase, found, on the luminal surface of the capillary endothelial cells (particularly in adipose capillary beds) hydrolyses the triglycerides mainly to monoglycerides and free fatty acids
  • these can then diffuse into the adipodicytes easily
  • here the free fatty acids combine with alpha glycerol phosphate (from DHAP from glycolysis) to form new triglycerides
  • the monoglycerides also combine with fatty acids to form triglycerides
104
Q

what is BMI

A
  • body mass index
  • MBI = weight (kg) / height2 (m)
105
Q

BMI categories

A
  • <18.5 is underweight
  • 18.5 - 25 is normal
  • 25 - 30 is overweight
  • >30 obese
106
Q

tissue requirements of brain and liver

A
  • together they represent 4.6% of body weight
    • yet they consume 40% of energy requirement at rest
107
Q

What fuels can the brain use

A
  • glucose
  • ketone bodies
108
Q

what fuels can muscle use

A
  • glucose
  • ketone bodies
  • triacylglycerol (AKA triglycerides)
109
Q

what fuels can the liver use

A
  • fatty acids
  • amino acids
  • glucose
  • alcohol
  • even though ketone bodies are MADE in the liver, they cannot be used by the liver
    • this is because hepatocytes do not have the enzyme thiolase
110
Q

what fuels can be used by the kidney?

A
  • cortex
    • glucose and ketone bodies
  • medulla
    • glucose only
111
Q

what is BMR

A
  • basal metabolic rate
  • kcal expended/hr/m2
  • usually measured by O2 consumption in a person who is awake, restful and fasted for 12 hours
112
Q

vitamin A

A
  • fat soluble
  • stored in the liver
  • found in oily fish, dairy products and margarine
  • needed for:
    • vision
    • reproduction
    • embryogenesis
    • healthy skin
    • lymphocyte production
  • deficiency causes
    • night blindness
    • xeropthalmia (dry eye)
    • increased susceptibility to infection
113
Q

vitamin C

A
  • water soluble
  • important in synthesis of neurotransmitters, carnitine and collagen
  • can donate electrons to ROS - antioxidant
  • found in
    • green veg
    • citrus fruit
    • potatoes
  • deficiency causes
    • weakness
    • bleeding gums
    • 50-100 days without vitamin C = scurvy
114
Q

vitamin B

A
  • most important one is B12
  • water soluble
  • important for cell metabolism and energy production
  • absorbed in the terminal ileum
  • requries intrinsic factor to be absorbed
    • produced by parietal cells of the stomach
  • deficiency leads to pernicious anaemia
115
Q

Vitamin D

A
  • lipid soluble
  • vitamin D3 is formed by the action of UV light on a cholesterol derivative in the skin
  • vitamin D2 is derived from plants
  • both of these are collectively referred to as vitamin D
  • in the liver and kidneys hydroxyl groups are added which turn it into 1,25-dihydroxyvitamin D
    • this is the active hormonal form of vitamin D
  • its major function is to stimulate intestinal absorbtion of Ca 2+ and phosphate
116
Q

Vitamin D deficiency

A
  • the major consequence is decreased plasma Ca2+
  • this is detectd by Ca2+ receptors on the parathyroid gland
  • this causes the parathyroid gland to secrete PTH (parathyroid hormone)
  • this hormone has multiple actions:
    1. increases resorption of bone by osteoclasts which causes Ca2+ and phosphate ions to be released from bone but causes a decrease in bone mass - osteoperosis
    2. directly stimulates the production of 1,25 dihidroxyvitamin D which increases intestinal absorbtion of Ca2+
    3. increases Ca2+ reabsorbtion in the kidneys thereby reducing urinary Ca2+ excretion
    4. decreases the reabsorbtion of phosphate in the kidneys which increases its excretion in the urine. this compensates for the phosphate released from the bone
117
Q

Vitamin E

A
  • Fat soluble
  • antioxidant
118
Q

Vitamin K

A
  • Essential for the synthesis of clotting factors 10, 7 , 9 and 2
  • fat soluble
119
Q

coeliac disease

A
  • occurs in genetically predisposed individuals
  • partially degraded gluten triggers an autoimmune response against the villi and microvilli
  • this results in loss of the intestinal brush border
  • this results in decreased absorbtion of many vitamins
120
Q

cystic fibrosis

A
  • AR mutation for CFTR (an epithelial channel protein)
  • problems with salt and water movement across membranes
  • thickened secretions and a high incidence of lung infections
  • decreased digestion and absorbtion
121
Q

summarise the water reabsorbtion table

A
122
Q

what epithelia is the mouth?

A

stratified squamous non-keratinizing

123
Q

what’s this?

A

the lip

the arrow shows the abrupt transition from stratified squamous non-keratinising epithelium to keratinising

there is irregular connective tissue lying beneith the epithelium

124
Q

what kind of epithelium covers the tongue?

A

stratified, squamous

keratinised on the dorsal surface and non–keratinised on ventral

125
Q

what is this?

A

dorsal surface of the tongue

stratified squamous keratinising epithelium

underneith there are course bundles of skeletal muscle

Extrinsic: connect with the lower jaw

Intrinsic: connect only to the fibrous connective tissue under the mucosa

126
Q

what are the folds of the dorsum of the tongue called?

A

papillae

127
Q

what is this?

A

oesophagus cut longitudinally

there’s a thin lamina propria, beneith which there are the smooth muscle cells of the muscularis mucosa

128
Q

what is this?

A

These are tase buds which are positioned in the lateral walls of the tongue’s papillae

129
Q

what is this

A

parotid gland acini

this is a wholly serous gland

130
Q

what is this

A

sublingual gland

this is a wholly mucous secreting gland

ducts are pinker staining and the pale staining cells are the secretory cells

131
Q

what is this

A

submandibular gland

these are mixed serous and mucous

lie below the mandible either side of the tongue

theres often a bit of fat in the gland

because it’s mixed secretion they have both the dark staining serous acini of the parotid and the light staining mucous acini of the sublingual

132
Q

what interesting thing do the parotid gland and the sublingual gland both produce

A

epidermal growth factor

this promotes the growth of the epithelium of the GI tract

133
Q

what type of epithelium covers the epiglottis

A
  • Most of its surface is covered by a stratified squamous epithelium
  • The lower part of its posterior (lower) surface has a pseudostratified columnar ciliated epithelium (respiratory epithelium).
134
Q

what are the 4 layers of the GI tract

A
  1. innermost mucosa
  2. underlying sub-mucosa
  3. external coat of muscularis propria
  4. a serosa (mesentary)
135
Q

what epithelium is the oesophagus lined by

A

stratified squamous non-keratinized epithelium mostly

below the thoracic diaphragm the epithelium can be transformed into a simple columnar type (this is the type that lines the cardiac region of the stomach)

If there is abnormal growth here this is a pre-cancerous condition known as barrett’s oesophagus

136
Q

What does the oesophageal sub-mucosa contain

A
  • Many sero-mucous glands
  • At the distal end of the oesophagus it contains many large, thin-walled veins. These may become the site of oesophageal varicosities.
137
Q

what is the outermost layer of muscle of the oesophagus called? What kind of muscle is it?

A

Muscularis externa. At the proximal end it is skeletal and at the distal end it is smooth.

This muscle is what forms the upper and lower oesophageal sphincter

138
Q

what epithelium lines the stomach?

A

simple columnar punctuated by gastric pits into which the gastric glands drain

139
Q

What is this? label it and say where it is present.

A
  • FULL gastric glands are present in the walls of the body and fundus
  • Glands of the cardiua and the pylorus also have gastric glands but they are devoid of parietal and chief cells
    • so they’re just mucous neck cells lubricating
140
Q

what is this? What type of epithelia is it and what do the arrows point to?

A
  • simple columnar epithelium
  • this is the stomach
  • arrows point to gastric pits into which gastric glands open
141
Q

In gastric glands where do parietal cells mostly occur

A

in the upper bit closest to the pit

142
Q

what is this and what do the arrows point to?

A
  • gastric glands from the body of the stomach
  • arrows point to the parietal cells
  • the top of the picture is towards the lumen of the stomach
  • the parietal cells are towards the luminal side of the gland, near the gastric pits
143
Q

what is this and what are the arrows pointing to? what is the stain?

A
  • these are gastric glands
  • the arrows point to chief cells
  • the muscularis mucosa is at the bottom of the picture
  • most of the cells in this picture are chief cells
  • they are found in the lower part of the glands and they stain blue with H&E
  • they secrete pepsinogen and lipases
  • just like parietal cells they are only found in the glands of the body and the fundus of the stomach
144
Q

what is this and where is it?

A
  • gastric pits of the pylorus of the stomach
  • these pits produce gastrin and serotonin and somatostatin
  • these cells play an important role in regulating the delivery of chyme to the duodenum
  • here the glands are shorter and are coiled (so they look like individual holes) than those in the body
  • the ducts are deeper than those in the body
145
Q

what are the major absorptive cell in the small and large bowel?

A

enterocytes

146
Q

how long is the duodenum

A

12 inches

147
Q

what is this?

A
  • Duodenum
  • Leaf like villi
    • BUT this does not distinguish it fro the jejunum
  • The distinguisher is that the duodenum has brunner glands
    • White holes bottom right of pic
  • Brunner glands secrete alkaline mucous to neutralise chyme
  • The crypts are long
148
Q

What is this and what are some of the important cells?

A
  • This is a duodenal crypt
  • Paneth cells - bright pink staining
    • produce and secrete lysozyme to regulate bacterial flora of the gut
  • Dividing stem cells are at the bottom of the crypt a bit to the side and they are identified by very dark staining nuclei
149
Q

What is this and what distinguishes it

A
  • This is the jejunum
  • Does not have brunners glands like the duodenum does
  • Does not have payers patches like the ileum
  • Finger like villi
  • More goblet cells than duodenum (pale staining here cause no alician blue)
150
Q

What is this and what distinguishes it

A
  • This is the ileum
  • villi not as tall
  • more goblet cells towards disgal end
  • payers patches in the submucosa
  • muscularis externa towards the bottom of the picture
  • submucosa across the middle of the picture
151
Q

where do the taenea coli originate?

A
  • they originate at the base of the appendix and run the whole length of the large intestine
152
Q

what is it, what is the epithelium and what types of tissue are seen?

A
  • vermiform appendix
  • rudimentary crypts surrounded by lymphoid tissue
  • the epithelium is simple columnar
153
Q

what is the epithelia of the colon like

A
  • it has no villi
  • caecum, ascending, transverse, descending and sigmoid all have similar histology
  • instead of villi there are closely packed intestinal crypt
  • these mainly contain enterocytes and goblet cells
  • lymph nodules as part of GALT are present
154
Q

what is this

A
  • this is the colon
  • note the abundance of pale staining goblet cells
  • muscularis mucosa at the bottom
155
Q

what is the epithelia of the anal canal?

A
  • lined by mainly stratified squamous epithelia
  • it becomes keratinized at the distal end
  • submucosa contains fat and veins
  • these veins give rise to varicosities
156
Q

what is this?

A
  • This is the recto-anal junction
  • There’s an abrupt transition between simple columnar of the rectum (left) and the stratified squamous of the anal canal
157
Q
A
158
Q
A

EM: (14 decks)

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