Questions and Answers on GIT Physiology by Dr Khaled A Abulfadle

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

How gastric reflux into oesophogus is prevented i.e. antireflux mechanisms ?

Gastric reflux into oesophogus is prevented by:
1. (LES)High pressure zone sphincter.
2. The intra abdominal small part of the esophagus is squeezed by the increased intra abdominal pressure.
3. The oesophagus enters the stomach in acute angle and act as a flap.
4. Gastrin hormone increases the tone in the lower oesophagus.

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

Mention the most common enzyme secreted by the stomach and mention the main function of this enzyme ?

The most common enzyme secreted by the stomach is pepsinogen.
It is activated by HCL into pepsin.
Function: protein digestion into proteases and polypeptides.

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What is the function of the M cells in the ileum ?

M cells (or microfold cells) are cells found in the follicle-associated epithelium of the Peyer's patch. They transport organisms and particles from the gut lumen to immune cells across the epithelial barrier, and thus are important in stimulating mucosal immunity.

Unlike their neighbouring cells, they have the unique ability to take up antigen from the lumen of the small intestine via endocytosis or phagocytosis, and then deliver it via transcytosis to dendritic cells (an antigen presenting cell) and lymphocytes (namely T cells) located in a unique pocket-like structure on their basolateral side

M cells differ from normal enterocytes in that they lack microvilli on their apical surface, but instead possess broader microfolds that give the cell its name. These cells are also far less abundant than enterocytes. M cells are readily accessible for antigens in the gut lumen to travel through to the Peyer's patch because they do not secrete mucus or digestive enzymes and the filamentous brush border glycocalyx (an extracellular polysaccharide layer found throughout the intestine attached to enterocytes) is much thinner or absent on M cells.

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

How local (myenteric) nerve plexus cause contraction or relaxation for LES?

It is a local axon reflex i.e.

Stimulus: food in esophagus
Receptor: stretch receptor in wall of LES
Afferent: dendrites of local mynteric nerve plexus
Center: cell body of local mynteric nerve plexus
Efferent: axon of local myenteric nerve plexus
Effector organ: LES
Response: relaxation of LES (through release of a certain chemical transmitter in response to certain types of food) or contraction of LES (through release of another chemical transmitter in response to other types of food).

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

QUESTION

What are the causes of vomiting in a case of acute appendicitis?

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ANSWER

Appendicitis is a painful inflammation, swelling and infection of the appendix.

Vomiting that occurs with acute appendicitis is caused by:

The severe abdominal (visceral) pain (reflex vomiting i.e. unconditioned). "The main cause".

The released inflammatory cytokines (stimulate CTZ and vomiting center i.e. central vomiting).

Acute appendicitis may irritate peritoneum which stimulates vomiting reflex

Acute appendicitis may be complicated by rupture appendix and peritonitis which stimulates vomiting reflex.

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

Question

How excessive vomiting causes hypokalemia?

Answer

Hypokalemia with excessive vomiting is due to:

a. K+ shift from ECF to ICF due metabolic alkalosis which causes H+ to leave the cells while K+ entered the cells to maintain electroneutrality.

b. Increased K+ loss from the body through:

i. Kidney (most important): the renin–angiotensin II–aldosterone system was activated by ECF volume contraction. A major action of aldosterone is to increase K+ secretion by the principal cells of the late distal tubule and collecting ducts, resulting in increased K+ loss in urine.

ii. Gastrointestinal tract: some K+ was lost in gastric juice in vomitus.

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

Q: Mention stimuli for VIP release
A:Esophageal and gastric distension, vagal stimulation, presence of fatty acids and ethanol in duodenum

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Q: List sites of peristaltic movement in GIT
A: Esophagus, Stomach, Small and Large intestines

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

Q: Compare between Obstipation and constipation

Answer

Obstipation is a condition of extreme and persistent constipation caused by an obstruction in the intestinal system i.e. Intractable constipation i.e. constipation that becomes refractory to cure or control
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Constipation is defined as the infrequent of difficult evacuation of feces but does not necessarily imply a permanent loss of function
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Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

Q: Differences between upper and lower esophageal sphincters
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Answer

Upper Esophageal Sphincter (UES) is an anatomic sphincter. The main functions of UES closure are to prevent esophageal air insufflation during negative intrathoracic pressure events, for example, inspiration, and to prevent esophagopharyngeal/laryngeal reflux during esophageal peristalsis. The UES is opened intermittently by relaxation of its sphincteric muscles, contraction of its distracting muscles, and bolus pulsion. The function of intermittent UES opening is to allow transphincteric flow of fluid or gas during orthograde events, for example, swallowing, or antegrade events, for example, emesis

Lower Esophageal Sphincter (LES) is a physiologic sphincter
It is an anti-reflux barrier prevents reflux of gastric contents into the esophagus, and its dysfunction leads to gastroesophageal reflux disease and or dysphagiA. It maintains tonic closure of the sphincter and relaxes upon swallowing. The LES is composed of smooth muscles, and it maintains tonic contraction owing to myogenic as well as neurogenic factors. It relaxes due to vagally mediated inhibition involving nitric oxide as a neurotransmitter

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

QUESTION

What are the so-called “good” and “bad” types of cholesterol?
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ANSWER

Lipoproteins are complexes made of lipids (triglycerides and cholesterol) and proteins. Lipoproteins present different densities according to the ratio of their protein to lipid quantities, since lipids are less dense than proteins. Low-density lipoproteins (LDL) are those with a low protein/lipid ratio; high-density lipoproteins (HDL) have a high protein/lipid ratio; another group is very low-density lipoproteins (VLDL) with a very low protein/lipid ratio.

LDL is known as “bad cholesterol” because it transports cholesterol from the liver to tissues and, as a result, contributes to the formation of atheroma plaques inside blood vessels, a condition called atherosclerosis (not to be confused with arteriosclerosis), which can lead to severe circulatory obstructions such as acute myocardial infarction, cerebrovascular accidents and thrombosis. HDL is known as “good cholesterol” because it transports cholesterol from tissues to the liver (to be eliminated with bile). A high amount of HDL in the blood reduces the risk of atherosclerosis. (VLDL transforms into LDL after losing triglycerides in the blood).

Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

Question: Mention factors that prevent autodigestion of the pancreas

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Answer

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Admin عدد المساهمات : 9680 تاريخ التسجيل : 06/08/2009

What are the Semi-essential amino acids?

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Semi-essential amino acids are those that can be synthesized by the body's metabolic pathways, but possibly not in sufficient quantity (especially in children or the ill), and therefore may have to be supplied at least in part by the diet. Examples in humans are histidine and arginine.

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