JUSTIFICATIONS

1. PLATELET PLUG DOES NOT DISLODGE FROM THE DAMAGED                 ENDOTHELIAL SITE.

When vessel is injured, it disrupt the endothelium and expose the underlying connective tissue collagen fibers. Platelet adhere to collagen, largely via an intermediatry called von Willebrand factor (VWF), a protein secreted by endothelial cell and platelet. Binding of platelet to collagen triggers the platelet to release the content of their secretory vesicles. Some of agent changes cause new platelet to adhere to the old one, a positive feedback phenomena which rapidly create 'platelet plug'. The platelet plug can completely seal small break in blood vessel wall. Its effectiveness is further enhanced by another property of platelet contraction. Platelet contains a very high concentration of actin and myosin, which are stimulated to contract in aggregated platelets. This causes compression and strengthening of platelet plug makes it unable to dislodge from the damaged endothelial site.

2. DEFICIENCY OF VITAMIN K CAN LEAD TO CLOTTING DISORDER.

The fat soluble vitamin K is essential for the functioning of several protein involved in blood clotting. Vitamin K is a cofactor for synthesis of blood coagulation factor 2, 7,9 and 10 and inhibitors such as protein C and S and bone matrix protein. Vitamin K act as cofactor for an enzyme that enable specific protein to bind calcium ion. The ability to bind calcium ion is required for the activation of the seven vitamin-K dependent blood clotting  factors. The liver requires this vitamin to produce prothrombin and several other clotting factor. 

3. THE FLOW RATE IN THE CAROTID SINUS REGULATE THE MEAN            ARTERIAL PRESSURE.

Arterial pressure originates primarily with arterial receptors that respond to change in pressure. Two major vessel that supplying the head, the common carotid arteries divided into two smaller arteries. At these divisions, the wall of artery is thinner than usual and contain a large number of branching vine like nerve ending. this portion is called carotid sinus. Its nerve endings are highly sensitive to stretch or distortion. The degree of wall stretching is directly related to the pressure within the artery. Thus, the carotid sinuses serve as pressure receptor or baroreceptor. The primary integrating center for the baroreceptor reflexes is a diffuse network of highly interconnected neuron called the medullary cardiovascular center located in the medulla oblongata. The neuron in this center receives input from various baroreceptors. This input determines the action potential frequency from cardiovascular center along neural pathway that terminates upon the cell bodies and dendrites of the vegus neuron to heart and sympathetic neuron to heart, arterioles and veins. When the arterial baroreceptors increase their rate of discharge, the result in decrease in sympathetic outflow to the heart, arteries and veins and an increase in parasympathetic outflow to the heart. A decrease in baroreceptor firing rate result in opposite pattern. If arterial pressure decreases, the discharge rate of arterial baroreceptor also decreases. Fewer impulses travel up the afferent nerve to the medullary cardiovascular center and induces: (1) increased heart rate because of increased sympathetic activity to the heart and decreased parasympathetic activity. (2) increased ventricular contractility because of increased sympathetic activity to the ventricular myocardium. (3) arteriolar constriction (4) increased venous constriction. The net result is an increased cardiac output, increased total peripheral resistance and return of blood pressure toward normal. Conversely, an increase in arterial blood pressure for any reason causes increased firing of the arterial baroreceptor, which reflexly induce a compensatory decrease in cardiac output and total peripheral resistance.

4. IF THE SALIVARY GLANDS ARE UNABLE TO SECRETE AMYLASE,           STARCH DIGESTION IS NOT MUCH AFFECTED.

The digestion of starch begins in the mouth by the action of enzyme, salivary amylase secreted by salivary gland. Digestion briefly continues in the upper part of the stomach before gastric acid destroy the amylase. If salivary gland does not secrete amylase, starch get digested in the small intestine by pancreatic amylases. The exocrine portion of pancreas secrete bicarbonate ions and a number of digestive enzymes into duct that converge into pancreatic duct which joins common bile duct coming from the liver. The enzymes secreted by pancreas digest fat, polysaccharides, proteins, and nucleic acid. Starch digestion occur by non-proteolytic enzyme amylase into disaccharides. Theses are further broken down into monosaccharides which are transported across the intestinal epithelium into the blood. 

5. SA NODE FUNCTION AS A PACEMAKER FOR THE ENTIRE HEART.

The heart is a dual pump in which the left and right  side of the heart pump blood separately, but simultaneously into systemic and pulmonary vessels. Contraction of cardiac muscles, like that of skeletal muscle and smooth muscle, is triggered by depolarization of the plasma membrane  gap junction interconnected myocardial cell and allow action potential to spread from one cell to another. Thus, the initial excitation of one cardiac cell eventually result in the excitation of all cardiac cell. This initial depolarization normally arises in a small gap of conducting system cell called the sinoatrial (SA) node, located in right atrium near the entrance of the superior vena cava. The action potential then spread from SA node throughout the atria and then into and throughout the ventricles. The SA node is the normal pacemaker for the entire heart. Its depolarization normally generates the action potential the action potential that leads to the depolarization of all other cardiac muscle cells. The action potential initiated in the SA node spreads throughout the myocardium, passing from cell to cell by way of gap junctions. Depolarization first spreads through the muscle cell of the atria, with conduction rapid enough that the right and left atria contracts essentially at the same time. The link between atrial depolarization and ventricular depolarization is a portion of conducting system called atrioventricular (AV)node, at the base of the right atrium.