Physiology, Gastrointestinal System

Front 1

Label.

Back 1

Front 2

Label.

Back 2

Front 3

Label.

Back 3

Front 4

Put labels on right places.

Back 4

Front 5

What does Musoca consist of? (3)

Back 5

Epithelium, Lamina propria, Muscalaris mucosae (thin specialised muscle).

Front 6

What does muscalaris externa consist of (2)?

Back 6

Circular muscle and Longitudinal muscle.

Front 7

Which part of the gastrointestinal system does not have villi in its structure?

Back 7

Stomach.

Front 8

What is the name of network of neurons that run in the structures of GT?

Back 8

Submucosal plexus (Meissner's plexus - in small and large intestine);
Myentric plexus (Auerbach's plexus - extends from mouth to anus).

Front 9

Name cells that are laying in large intestine epithelia of the GT (5).

Back 9

1. Absorptive cell
2. Goblet cell (mucous cell)
3.Microvacuolated columnar cell
4. Stem/progenitor cell
5. Enteric endocrine cell.

Front 10

Which membrane of cells is open to lumen of the intestine, apical or basolateral?

Back 10

Apical.

Front 11

Which membrane of cells has villi in it: apical or basolateral?

Back 11

Apical.

Front 12

Does water usually move across the intestinal epithelium using transcellular or paracellular pathway?

Back 12

Paracellular.

Front 13

If Cl- moves from interstitium to lumem of intestine, what fallows it?

Back 13

Na+ follow negative charge of Cl- and water follows because of osmotic imbalance.

Front 14

Name five major secretory tissues.

Back 14

Salivary glands,
Gastric glands,
Exocrine pancreas,
Liver-biliary system,
Intestin.

Front 15

Describe endocrine regulatory mechanism.

Back 15

Release of a transmitter (e.g. hormones: gastrin, CCK, secretin) into blood for delivery to distant target cell.

Front 16

Describe paracrine regulatory mechanism.

Back 16

Release of a transmitter (e.g.somatostatin) from a sensor cell to affect adjacent target cells without entering blood or activating neurons. Short distance affect of paracrines, they act locally, within the same tissue that secretes them.

Front 17

Describe neuronal regulatory mechanism.

Back 17

Electrical signalling via neurons. Via extrinsic and intrinsic regulation.

Front 18

What are neurocrines?

Back 18

Peptides that are synthesised in neurones of the GT and released following AP (e.g. ACh, GRP, norepineohrine, VIP, substance P).

Front 19

What is the site of secretion of the following hormones: Gastrin, CCK, Secretin, GIP?

Back 19

Gastrin - G cells of the stomach;
CCK - I cells of the duodenum and jejunum;
Secretin - S cells of the duodenum;
GIP - K cells in duodenum and jejunum.

Front 20

What are stimuli for secretion of the following hormones: Gastrin, CCK, Secretin, GIP?

Back 20

Gastrin - small peptides and amino acids, distention of the stomach, vagal stimulation (GRP);
CCK - Small peptides and amino acids, fatty acids;
Secretin - H+ in the duodenum, fatty acids in the duodenum;
GIP - fatty acids, amino acids, oral glucose.

Front 21

What are actions of Gastrin? (2)

Back 21

Increase H+ secretion, stimulating growth of gastric mucosa.

Front 22

What are actions of CCK? (5)

Back 22

Increase in pancreatic enzyme secretion;
Increase in pancreatic HCO3- secretion;
Stimulating contraction of gallbladder and relaxation of the spincter of Oddi;
Stimulating growth of exocrine pancreas and gallbladder;
Inhibition of gastric emptying.

Front 23

What are actions of Secretin? (4)

Back 23

Increase in pancreatic HCO3- secretion;
Increase in biliary HCO- secretion;
Decrease in gastric H+ secretion;
Inhibition of trophic effect of gastrin on gastric mucosa.

Front 24

What are actions of GIP? (2)

Back 24

Increase in insulin secretion from pancreatic beta cells;
Decrease in H+ secretion.

Front 25

Fill in the table using offered answers.

Back 25

Front 26

Which hormone inhibits gastric secretion and stimulates insulin release?

Back 26

GIP

Front 27

Which hormone stimulates growth of mucosa (of enterochromaffin-like cells)?

Back 27

Gastrin.

Front 28

Which hormone stimulates gallbladder contraction, pancreatic secretion?

Back 28

CCK.

Front 29

Which plexus lies between submucosa and the circular muscle?

Back 29

Submucosal plexus (Meissner's plexus).

Front 30

Which plexus lies between the circular muscle and the longitudinal muscle?

Back 30

Myenteric plexus.

Front 31

Innervation of GT is regulated by which two NS, which are part of ANS?

Back 31

Extrinsic NS (long reflexes) - sympathetic and parasympathetic innervation;
Intrinsic NS (short reflexes) - enteric NS.

Front 32

Put in names of transmitters.

Back 32

Front 33

Name two inhibitory transmitters of intrinsic NS.

Back 33

VIP and NO.

Front 34

Name two excitatory transmitters of intrinsic NS.

Back 34

ACh and substance P.

Front 35

Name three phases of gastrointestinal control.

Back 35

1. Cephalic phase -sight, smell, taste and chewing;
2. Gastric phase - distension, acidity, etc.;
3. Intestinal phase - distension, acidity, osmolarity, etc.

Front 36

Name three functions of motor activity of GI tract.

Back 36

Non-propulsive movements (Effectively mixes chyme and brings fresh chyme into contact with the mucosal surface);
Peristaltic movements (Propels chyme for a short distance);
Reservoir function.

Front 37

Name Two types of muscle contractions.

Back 37

Phasic and tonic.

Front 38

What are slow waves?

Back 38

Slow waves are not action potentials, but rather oscillating (колеблющийся) depolarization and repolarization of membrane potential of the smooth muscle cells.

Front 39

Fill in blanks about the electric activity in the smooth muscle in the GI tract:
The frequency of ___ ___ sets the frequency of ___ ___ and, therefore, sets the frequency of ____. ___ ___ cannot occur unless the ___ ___ brings the membrane potential to threshold.

Back 39

The frequency of slow waves sets the frequency of action potentials and, therefore, sets the frequency of contractions. Action potential cannot occur unless the slow wave brings the membrane potential to threshold.

Front 40

Where do slow waves originate?

Back 40

In interstitial cells of Cajal.

Front 41

What causes the depolarization of membrane potential of slow wave in GI tract cells?

Back 41

Cyclic opening of Ca++ channels.

Front 42

What causes the repolarization of membrane potential of slow wave in GI tract cells?

Back 42

Opening of Potassium channels.

Front 43

Name three components of gastric motility.

Back 43

1. Relaxation of the orad region of the stomach to receive the food bolus from the esophagus;
2. contractions that reduce the size of the bolus and mix it with gastric secretions to initiate digestion;
3. Gastric emptying that propels chyme into the small intestine.

Front 44

Name three anatomic divisions of the stomach.

Back 44

The fundus, the body and the antrum.

Front 45

Name two pats of the stomach, based on differences in motility.

Back 45

Orad and caudad.

Front 46

What are migrating motor complexes?

Back 46

During fasting, there are periodic contractions, that occur at 90-min intervals and function to clear the stomach of any residue remaining from the previous meal.

Front 47

What are spincters?

Back 47

Specialised circular muscles that separate two adjacent compartments of the GI tract. They effectively serve as one-way valves.

Front 48

Label.

Back 48

Front 49

What are the components of saliva?

Back 49

Mucin glycoproteins, lysozyme,
lipase, proline-rich proteins, alpha-amylase.

Front 50

Name three functions of saliva.

Back 50

1. Lubricate the food to make swallowing easier - mucin glycoproteins, water;
2. Clean and protect the cavity of the mouth - lysozyme, proline-rich proteins;
3. Reduce starch to oligosaccharide molecules - alpha-amylase.

Front 51

Name three major salivary glands.

Back 51

Parotid glands, submandibular glands and the sublingual glands.

Front 52

What does acinus of salivary gland soncist of?

Back 52

It is lined with acinar cells and in the middle of it there is intercalated duct.

Front 53

What do acinar cells produce?

Back 53

They produce initial saliva composed of water, ions (Na, K, Cl, HCO3), enzymes and mucus, which is isotonic to plasma.

Front 54

What do ductal cells of salivary glands do?

Back 54

They modify the initial saliva to produce the final saliva by altering the concentrations of various electrolytes. Secretion of K+ and HCO3- and reabsorbing Na+ and CL-. So saliva is hypotonic to plasma after going through ductal cells, it has less Na+ and CL-.

Front 55

Compare saliva and plasma osmolarity.

Back 55

Saliva is hypotonic to plasma, has lower osmolarity. It has higher K+ and HCO3- concentrations, but lower Na+ and Cl-.

Front 56

Acinar cells of salivary glands are often called leaky epithelia, and duct-lining epithelial cells are called tight epithelia. Why?

Back 56

Because acinar cells allows Na and water to move between them, but in duct cells secretion and reabsorption happens only through individual epithelial cells, nothing can move between the cells.

Front 57

Describe effect of flow rate on composition of saliva.

Back 57

The ionic composition of saliva changes with flow rate. Faster is flow rate, more closely is the composition of saliva to plasma or initial saliva. Low flow rates - low concentrations of Na and Cl, high flow rates - duct cells are not able to reabsorb these ions and their concentration remains high. Concentration of HCO3 and K do not change.

Front 58

Which hormones regulate saliva secretion in the mouth?

Back 58

There is no control by peptide hormones of excretion of saliva.

Front 59

Which NS increases salivary secretions - SNS or PNS?

Back 59

Both, but PNS has stronger effect and long-lasting.

Front 60

What is the effect of ACh in salivary glands?

Back 60

It decreases NaCl reabsorption.

Front 61

What is the effect of Noradrenaline in salivary glands?

Back 61

It stimulates HCO3- secretion.

Front 62

What is the effect of aldosterone in work of salivary glands?

Back 62

Aldosterone stimulates NaCl reabsorption and K+ secretion.

Front 63

How much of saliva is secreted every day?

Back 63

About 1 - 1.5 L per day.

Front 64

Name three phases of swallowing.

Back 64

1. Oral phase. Voluntarily.
2. Pharyngeal phase
3. Oesophageal phase (start of peristalsis).

Front 65

What is peristalsis?

Back 65

Sequential contraction of ring of muscle.

Front 66

What is receptive relaxation?

Back 66

Part of swallowing process - relaxation of the fundus of the stomach when food enters it.

Front 67

When does secondary peristalis occur?

Back 67

It occurs if after primary peristalis there is still food left in the oesophagus after lower oesophageal spincter is closed.

Front 68

Describe coordination of spincter activity during swallowing.

Back 68

When UES is open, LES is closed. And when LES opens, UES is closed.

Front 69

What coordinates vomiting reflex?

Back 69

Vomiting center in the medulla.

Front 70

Name 6 events of vomiting reflex in temporal sequence.

Back 70

1. Reverse peristalisthat begins in the small intestine
2. relaxation of the stomach and pyrolus
3. Forced inspiration to increase abdominal pressure
4. relaxation of the lower esophageal spincter
5. forceful expulsion of gastric contents
6. reflex relaxation of the upper oesophagus spincter and
vomiting.

Front 71

Fill in which substances and where are being secreted in the stomach.

Back 71

Front 72

What secretes gastric juice?

Back 72

Gastric mucosa.

Front 73

What are four major components of gastric juice?

Back 73

HCl, pepsinogen, mucus, intrinsic factor.

Front 74

Which substances of gastric juice initiate the process of protein digestion?

Back 74

HCl and pepsinogen.

Front 75

What is the major role of intrinsic factor?

Back 75

It is required for absorption of vitamin B12.

Front 76

What is the only essential component of gastric juice?

Back 76

Intrinsic factor.

Front 77

The body of stomach contains two types of glands. Which ones?

Back 77

Oxyntic and Pyloric.

Front 78

Which cells secrete HCl and intrinsic factor?

Back 78

Pariental cells.

Front 79

What do pariental cells secrete?

Back 79

HCl and intrinsic factor.

Front 80

Which cells in stomach secrete pepsinogen?

Back 80

Chief cells.

Front 81

Which stomach cells secrete Gastrin to circulation?

Back 81

G cells.

Front 82

Where to do G cells secrete gastrin?

Back 82

Into the circulation.

Front 83

To what level of pH does HCl acidifies gastric contents?

Back 83

pH between 1 and 2.

Front 84

What is the function of HCl in the stomach?

Back 84

It acidifies gastric contents. This is to convert inactive pepsinogen to its active form, pepsin, a protease that begins the process of protein digestion.

Front 85

Name 4 functions of HCl.

Back 85

1. Promotes the activation of pepsins; provides optimal environment for the action of pepsins;
2. Kills or inhibits microorganisms;
3. Stimulates secretions in the small intestine;
4. Helps iron and calcium absorption in the small intestine.

Front 86

What enzyme catalyzes in formation of H2CO3 from CO2 and water inside gastric pariental cells?

Back 86

Carbonic anhydrase.

Front 87

After dissociation of H2CO3 to H+ and HCO3- in the gastric pariental cells what happens with end products?

Back 87

H+ is secreted to lumen of the stomach and HCO3- is absorbed into the blood.

Front 88

In the pariental cells, how is H+ transported to the lumen of the stomach?

Back 88

Via H+-K+ATPase.

Front 89

In pariental cells of the stomach, how is Cl- transported to the lumen of the stomach?

Back 89

Diffusing through Cl- channels. Passive process.

Front 90

How do Cl- ions get to pariental cell of the stomach?

Back 90

The Cl- ions enter the cell across the basolateral membrane via the Cl-/HCO3- exchanger. No energy of ATP required.

Front 91

Which channels for ion transport do apical membrane of pariental cell in the stomach has?

Back 91

Cl- gated ion channel;
H+/K+ ATPase;
K+ gated ion channel.

Front 92

Which ion channels does basolateral membrane of pariental cells of a stomach have?

Back 92

Na+/K+ ATPase;
Cl-/HCO3- exchanger;
K+ gated ion channel.

Front 93

In pariental cells of the stomach how does HCO3- is absorbed from the cell to the blood?

Back 93

Through Cl-/HCO3- exchanger in basolateral membrane.

Front 94

What effect does HCO3- absorbed from pariental cells of a stomach has on blood?

Back 94

The effect is called 'alkaline tide', means high pH of the blood.

Front 95

What will happen with HCO3- absorbed by blood from pariental cells of the stomach?

Back 95

Eventually, it will be secreted back into the gastrointestinal tract in pancreatic secretions.

Front 96

In summary, what happens in apical and basolateral membrane of pariental cells in the stomach?

Back 96

Net secretion of HCl and net reabsorbtion of HCO3-.

Front 97

What is the function of intrinsic factor?

Back 97

It combines with vitamin B12 to resist digestion by pancreatic proteases (digestive enzymes secreted by the pancreas to break down proteins), it facilitates absorption of vitamin B12 in the ileum.

Front 98

What is the function of pepsins?

Back 98

They digest proteins.

Front 99

What environment is needed for pepsinogens to activate to pepsins?

Back 99

Very acidic (< or = 3 pH).

Front 100

Is the HCl needed for activity of pepsins (apart from activation of pepsinogen)?

Back 100

Yes.

Front 101

Why don’t HCl and pepsins damage the gastric mucosa?

Back 101

Because walls of a stomach are covered with gastric mucosal barrier.

Front 102

What are three protective components of gastric mucosal barrier?

Back 102

1. A compact epithelial cell lining, with very tight junctions that do not let the acid go through.
2. A special mucus covering, that holds HCO3 close to the epithelial cells.
3. Secretion of bicarbonate ions that in the lumen act to neutralize harsh acids. It combines with H+ and becomes H2CO3 and Water and CO2 later on.

Front 103

Which substances inhibit HCO3- secretion by epithelial cells of stomach?

Back 103

Aspirin, Adrenaline, noradrenaline.

Front 104

Name three phases of Gastrointestinal control.

Back 104

1.Cephalic phase (smell, sight, taste and chewing);
2. Gastric phase (distension, acidity);
3. Intestinal phase (distension, acidity, osmolarity).

Front 105

Describe control of gastric secretion in gastrointestinal Cephalic phase (1).

Back 105

The control is entirely dependent on vagal nerve. Stimulation via:
- direct effect on pariental cells
- indirect effect on ECL cell
- indirect effect on G cells.
Stimulation is also effected by inhibiting the secretion of somatostatin by D cells.

Front 106

Describe control of gastric secretion in gastric (2) phase of gastrointestinal control.

Back 106

Controlled by local and vagovagal reflexes and hormones.
The stimuli for secretion are distension of the stomach, presence of break-down products of protein, amino acids and small peptides.
- Distension causes direct vagal stimulation of periental cells and - indirect stimulation of the pariental cells via gastrin release from G cells.
- Distension of antum results in local reflexes and stimulates gastrin release.
- Alcohol and caffeine also stimulate gastric secretion.

Front 107

What effect do tonic contractions of the stomach have?

Back 107

It controls the emptying of food into the duodenum.

Front 108

What does tonic contraction of pyloric spincter control?

Back 108

The speed of stomach emptying.

Front 109

What is the driving force of gastric emptying?

Back 109

Pressure difference between the lumen of stomach and duodenum.

Front 110

Which of the following would have the fastest rate of emptying from the stomach: liver/glucose?

Back 110

Glucose --> liver.

Front 111

What is the amplitude of slow waves of smooth muscle?

Back 111

5 to 15 mV