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PHYL2064 > GIT > Flashcards

GIT Flashcards

1
Q

2 types of inflammatory bowel disease

A

Chron’s disease and ulcerative colitis

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2
Q

Structure and purpose of the mucosal layer

A

Mucosal layer present to ensure lubrication and fecal movement.

Under this layer are the epithelial cells which are arranged in the brick and motor arrangement (cells held together by proteins) to ensure cell adhesion. Some of these structures are impermeable to water.

This means that water can be absorbed through transcellular transport or paracellular transport.

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3
Q

Locations and segments in GIT effected by UC and CD

A

UC - Mucosa of the colon and rectum (not transmural)

CD - Any part from mouth to anus and involves transmural lesions

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4
Q

Pathophysiology of UC

A
  • Unknown factor changed the viscosity and chemical composition of mucosal layer allowing bacteria to enter
  • Changing the mucosal layer will expose dendrites. They will come in contact with bacterial becoming activated which leads to cascade resulting in destruction of mucosal cell, resident macrophages are also activated.
  • This leads to activation of pro inflammatory chemicals. Proinflammatory chemical will increase blood flow and recruit WBCs as well as further activating dendritic and macrophage cells.
  • T cell activation will causes further activation of other inflammatory mediators which will increase permeability for antigens.
  • This will further increase the already in place response
  • This is where the relapsing condition comes in as the body will run out of leucocytes and the diarrhoea will stop until more are required.
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5
Q

UC key features

A
  • No skip lesions and limited to mucosa (can sometimes go through wall)
  • Primary problem is the epithelia barrier is effected.
  • Sometimes will effected rectum
  • Hyperaemic walls of colon (increased BF - red)
  • Sever cases can cause ulcers which way lead to blood in stool
  • Necrosis → fibrosis that may obstruct colon
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6
Q

Clinical outcome for UC

A
  • Remissions and exacerbation due to leucocyte recruitment
  • Water diarrhoea (damage to epithelia lining will limit water reabsorption)
  • Mucosal destruction leads to constipation due to decreased lubrication
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7
Q

Risk factors for CD

A

Family history, tobacco use, Jewish as well as CARD15 and NOD2 gene mutation are all risk factors

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8
Q

Pathophysiology of CD

A
  • Begins in submucosa (UC begins in mucosal layer)
  • Neutrophil infiltration
  • Has skip lesions (happen anywhere)
  • Cobble stoning of the GIT
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9
Q

Clinical outcomes of CD

A
  • Irritable bowel, even small meals will cause pain due to holding large amounts of water
  • Can get blood and mucus with diarrhoea
  • Main issue is inability to absorb molecules
  • Diarrhoea occurs due to decrease absorption, increased bacteria, overuse of medications for pain and bile
  • Anal fissure and abscess can be very painful as they are close to cutaneous nerves
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10
Q

Does CD have systemic factors

A

Spread through the body, unlike UC

  • Eyes
  • Kidneys
  • Mouth
  • Liver
  • Joints
  • Circulation
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11
Q

Risk factors for UC

A

Risk factors include family history, Jewish and Caucasians
Nicotine may prevent

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12
Q

Purpose of saliva in mouth

A

alkaline environment to ensure enzyme activity

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13
Q

What does amylase do in the mouth

A

hydrolyses starch and glycogen to smaller poly-saccharides and maltose (carb digestion)

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14
Q

Pepsin, amylase and mucus in the stomach

A

Pepsin is present which hydrolyses proteins

Limited carb digestion as amylase is not longer active at low pH. Will recommence in duodenum once pH is increased.

Mucus present to neutralise the acid. If there is an imbalance between mucus and acid then stomach ulcers can form.

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15
Q

What are MMCs

A

migrating myoelectric contraction. Weak repetitive peristaltic waves that move a short distance.

Migrating myoelectric complexes start when there is an anticipation of food.

Starts in stomach and will go down, eventually reaching LI which will move fecal matter to make room.

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16
Q

Enzymes in the mouth

A
  • Amylase = poly → di and trisaccharides
  • Lipase = tri glycerides and fatty acids
  • Lysozyme = antibacterial
  • Lactoperoxidase = bactericidal (kill bacterial)
17
Q

3 types of salivary glands, amount contributed and what enzymes

A
  • Parotid - 25%, serous fluid and amylase
  • Submandibular - 70% mixed (s/m), lysozyme and lactoperoxide
  • Sublingual - 5%, mucus and lingual lipase
18
Q

BASIC control of salivary secretions via para and symp

A
  • Parasympathetic - AcH and NA activate the PIP2 pathway causing Ca2 and Cl channels to open resulting in watery saliva
  • Sympathetic - Beta adrenergic activation causes release of enzymes → mucus saliva
19
Q

Conditioned and simple reflex for salivary secretions

A

Conditioned and simple reflex will both result in increased salivary secretion.

Condition reflex relates to seeing, thinking or smelling food.

Simple reflex is concerned with the pressure receptors and chemoreceptors in the mouth.

20
Q

Taste pathways

A

Mediated through 3 cranial nerves (7, 9 and 10) as well as the medulla, thalamus and gustatory centre in the cerebral cortex.

21
Q

Parietal and Chief cells in the stomach

A

Remember PC - parietal and chief cells responsible for secretion of these. These are located on the edges of villi within the fundus and body.

Chief - Produce pepsinogen which is a precursor to Pepsin

Parietal - Secret gastric acid. HCI (denatures proteins) and IF (intrinsic factor, for vitamin B12)

22
Q

How is HCL produced by parietal cells

A
  • High quantities of bicarb circulating in blood to help keep pH neutral
  • Every bicarb that is pumped out, one Cl can move into the cell.
  • Cellular metabolism is taking place, water + Co2 will create carbonic acid which will further deteriorate into H ion and bicarb.
  • Cl will diffuse through the cell into the gastric lumen
  • The H ions can move out of the cell but the K channels must be manipulated through the K/K ATPase antiporters (K move out into lumen and then comes back in allowing H out) - energy dependent
  • Cl and H in gastric lumen can then be formed into HCI

Note that bicarb and H are present in the parietal cell from metabolism

23
Q

What is prostaglandin E2

A

Prostaglandin E2 (PGE2) can help control amount of acid being secreted, NSAIDS can limit PGE2.

24
Q

Activators and inhibitors of gastric secretion

A

Activators include - vagus CN, gastrin and histamine

Inhibitors - secretin and somatostatin

ACh at neuromsuclar junction to M3 receptors, Gastrin effecting CCKB and Histamine to H2-R receptors.

While acid is being secreted, also preparing for neutralisation of the acid via somatostatin at the liver and pancreases via bile. (somatostatin)

25
Q

Overview of what is absorbed where in SI

A

Duodenum - chyme mixes with bile and pancreatic jucies

Jejunum - absorption of AA, lipids, carbs, Fe and Ca2

Ileum - B12 and bile salts absorption

26
Q

Control of BILE secretion (as chyme enters SI)

A

Vagus nerve stimulate does effect but its weak and hormones have greater effect.

When food comes in contact with duodenum it stretches, this cause somatostatin and CCK secretion.

Somatostatin involved in gastric acid secretion decrease.

CCK causes gallbladder contraction and relaxation of sphincter (Oddi).

This is a positive feedback.

27
Q

Control of pancreatic secretion

A

Controlled by CCK and vagus (afferent and efferent)

Food coming in contact with duodenum activation of brain centers and use of vagus.

28
Q

Carbohydrate absorption

A
  • Disaccharides located in the brush border membrane of the SI cells reduce the carbs in absorbable monosaccharides.
  • Glucose absorbed by secondary active transport via symporters for Na, doesn’t directly use energy but relies on Na gradient established by NA/K pump (low inside the cell).
  • Fructose enters via facilitated diffusion (GLUT-5)
  • Passive carrier mediated (GLUT-2) allows both to move to basal border.
  • All exit the cell via passive facilitated diffusion into the interstiutiom
  • There is then an osmotic gradient causing them to diffuse into the blood vessel
29
Q

Protein absorption

A
  • Absorbed as either AAs or small peptides
  • AA absorbed by symporter that relies on concentration gradient for NA establish by NA/k pump. (symporters are selective for specific AAs)
  • Small peptides enter via tertiary active transport. Symporter with moving down its concentration gradient. This gradient is established by a symporter in the luminal membrane in which is driven by Na moving down its concentration gradient into the cell and H moving it. This occurs again due to the Na/K pump.

Peptides broken down into AAs within cell

30
Q

Lipid absorption

A
  • Triglycerides are emulsified by bile salts in smaller fat droplets. Lipase hydrolyses the TGs into monoglycerides and free fatty acids.
  • These are water insoluble so are carried to the luminal surface within water soluble micelles (formed by bile salts).
  • When micelle approaches the membrane the monoglycerides or fatty acid leave and passive diffuse through the lipid bilayer. Passive diffusion!
  • They are then resynthesised into triglycerides within the epithelia cells
  • TGs are coated in lipoprotein from the ER to form water soluble Chylomicrons
  • Exocytosis moves chylomicrons inter interstitial fluid.
  • Chylomicrons cannot cross membrane of capillaries so they enter lymphatic vessels instead
31
Q

Iron absorption

A
  • Only a portion of ingested iron is already in a digestible form, either heme or ferrous iron (Fe2+)
  • Iron absorbed via different energy dependent carriers for heme and Fe2+ (heme carrier protein and divalent metal transport 1)
  • Iron that is absorbed into epithelial cells and is immediately needed for RBC production is transferred into the blood by a membrane transport called ferroprotin.
  • In the blood the iron is carrier to the bone marrow via transferrin which is a carrier protein
  • Iron that is absorbed and not immediately needed is stored in epithelia cells as ferritin which if left unused is lost as the cell is sloughed.
32
Q

Sympathetic activation on salivary gland cell

A

Sympathetic - Adrenaline acting on beta adrenergic receptors

Adrenalin acts on beta adrenergic receptors. This activates phosphokinase a (PKA).

Creates small amount of mucus coming out making mucus saliva.

33
Q

Parasympathetic activation on salivary gland cell

A

Parasympathetic - NA acts on alpha adrenergic receptors and ACh acts on M3 (muscarinic type 3), the outcome is the same for both → acting on the IP3 and DAG pathway.

This pathway activate PKC (phosphokinase C)

PKC acts on NaCC receptors (sodium and potassium exchangers). It also mobilises calcium stores of the cell making Cl moving into lumen of acenes. Lots of chloride will need lots of Na to balance leading to watery saliva.

34
Q

How is salivary made in the salivary acinar cell

A

Cellular metabolism causes bicarb and H inside the cell.

When the cell is stimulated (olfactory feedback or tounge moving, physical and chemical changes)

Calcium will cause cl stores inside the cell to move into the lumen on the apical membrane. When this occurs calcium will open potassium channels on basolateral side, flushing out K. This will ensure membrane is depolarised.

Na/K exchanged, every 2K moved in will move 3Na out. Also happening is a Na and H exchange mechanism (Na in and H out). The Na moving in will move through the cell and go into lumen of acince, combing with cl to form an equilibrated molecule.

The net Na in the interstitium will move via paracellular transport will move into the lumen as well causing water to follow. Making watery environment into lumen. Also want the saliva to be alkain so bicarb is taken from the cell as well.

35
Q

Anatomical and motility in LI

A

Longitudinal muscle known as tenia coli which creates haustra.

No villi present

Deep pit glands secret mucus. Stimulated by parasympathetic nervous system

Motility is much slower in the large intestine due to haustration and mass movement.

Mass movement stimulated by the gastrocolic reflex when food enters the stomach.

36
Q

Main function of LI

A

Main functions are water and electrolyte reabsorption as well as storage of fecal matter

37
Q

Absorption in the LI

A

Na enters cells by multiple pathways (net movement)

Cl enters enters by exchanging bicarb (alkaline faeces)

Na/K pump actively pumps Na into the ECF

Na can then reenter the cell with Cl via co transport.

Cl enters the lumen via CFTR channel and Na is absorbed into the ECF via Na

Negative Cl in lumen attract Na by paracellular pathways which brings water with it

Water moving from ECF into LI lumen.

If CFTR cells is damaged then can’t hydrate the faeces.

38
Q

Pancreatic acinar cell

A

Na bicarb symporter and Na H exchanger (Na in H out) on the basolateral membrane

Na K pump on basolateral side ensure there is always Na outside the cell in the plasma, K is recycled.

CFTR (cystic fibrosis transmembrane regulator) will ensure there is constant flow of Cl into lumen, this will mean Na will follow and therefore water.

Salivary going past the ductal cells, water and sodium chloride can be pushed into the ductal cells. Want an alkaline saliva.

PHYL2064 (7 decks)

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