The individual muscle cell differs in so many respects to one another. The length of the muscle fibre, diameter of the muscle fibre, the contractile element contained and the load on the fibre affects the individual muscle force development. The normal length of a sarcomere is 2. 0 micrometer, and the muscle contract maximally at this length, any increase in this normal length will result in a decreased active force generation. Also skeletal muscle contract rapidly when no load is present but velocity of contraction reduces when load is present. B] Answer:
There are three main sources for reconstituting ATP in skeletal muscle cells. Firstly, the cells make use of phosphocreatine- which carries a high energy phosphate bond. Phosphocreatine is cleaved and the released energy causes bonding of new phosphate ion to ADP to reform ATP, it provide a short term energy source for contracting muscle. Secondly, substance that can be use to reconstitute ATP and phosphocreatine is glycogen which has been previously stored in the cells. They are rapidly degraded to form pyruvic acid to liberate energy that will be used to convert ADP to ATP.
This is majorly involved in the short term muscle contraction. Lastly oxidative metabolism which involves combination of oxygen with various food stuffs to liberate ATP. This is the mostly use during a long term muscle contraction. C] Answer: No, the fibres are made up of different length, size and diameter and they utilize these sources of energy according to these parameters. Some muscles react slowly over a long period of time while some react very fast and rapidly. D] Answer Smooth muscle contraction involves the contractile protein which is also employed by the skeletal muscle: Actin and Myosin.
Interaction between actin and myosin brings about contraction but smooth muscle does not possess troponin complex as in the skeletal muscle. The initiation of contraction is caused by an increase in intracellular calcium this increase can be caused by nerve stimulation, hormonal coordination and changes in the environment of the fibres. The contraction of the smooth muscle are prolonged this is why no tetanus can occur during contraction 2A] The electrocardiogram revealed a complete AV block in the heart.
This is seen in a situation where by the conduction of impulses from the atria to the ventricle is lost. It will cause the P wave to completely dissociate from the QRS wave (Guyton and Hall 2000). Also, the atria beat very rapidly whereas the ventricle beat very slowly. The ventricle has escaped the atria control, so it was beating at its own natural rate. This effect is commonly caused by ischemia of the AV bundles as a result of coronary insufficiency; it can also be cause by compression of the bundle of His by scar tissue that was caused by the insufficient arterial supply to the part of the heart.
B] Answer: Increase in the interstitial fluid potassium will result in the decrease in the repolarisation refractive period of the myocardial cell. Since during normal action potential, sodium moves in while potassium moves out, but when the potassium is already out it will readily allow new action potential to pass thereby reducing the refractive period. This will result in re-entrance circuit. Also, the elevated potassium ion surrounding the cardiac cells will increase irritability of the cardiac muscle which will result into fibrillation C] Answer:
TRUE: since the heart muscle is weak due to insufficient perfusion, the weak heart does not pump blood as expected into the arterial tree, this will elicit a sympathetic response that will now result in the increase slope of the depolarizing wave of the SA nodal cell 3] Answer: A] Nitroglycerin is a drug that is applied sublingually to relax the blood vessel allowing more blood to flow to the heart. Its effect reduces the workload of the heart and causes more perfusion to the heart muscles B] B-blockers act on the B receptor on the heart to block the effect of the sympathetic stimulation on the heart.
They act majorly on the B1 receptor to effect this. This is why a cardio selective B-blocker is recommended to reduce the side effect on B2 receptors. C] Ca channel blockers act mainly to block the entry of calcium into the cardiac cells. They also act by reducing the heart work through arteriolar vasodilatation and after-load reduction (Rang and Dale 2003). 4 Answers: Circulatory shock is define as a situation whereby there is a generalised inadequate flow of blood throughout the body resulting in the build up of toxic waste in the tissue which causes tissue damage.
It can be cause by many factors such as decrease in cardiac output as a result of decreased ability of the heart to pump blood or as a result of decreased venous return to the heart. In some situation where there is adequate cardiac output, shock can result from excessive metabolism of the body in which the cardiac output of the heart is insufficient. Circulatory shock can be divided into three main stages in which if untreated each stage lead to the other. a] non progressive stage: this stage can be reverse even without external interference.
b] Progressive stage: the shock progressively becomes worst if untreated. c] Irreversible stage: in this stage, no amount of therapy can be sufficient to bring the patient back to life. There are about four types of shock namely: hypovolemic shock, caused majorly by haemorrhage and fluid loss, neurogenic shock, resulting from the increased dilatation of the vessels, anaphylactic shock, caused by the release of histamine and other autacoids into the blood vessels and septic shock which is caused by bacteria infections.
Both shock are interrelated there is no much difference between the two shocks though one occur very rapidly while the other develop not as rapid as the first one. The student fainted because of the sudden vasoconstrictions which result in shortage of blood to the brain while the shock in the patient was as a result of excessive blood loss (haemorrhage).
REFERENCE:
Guyton AC and Hall JE (2000): Textbook of Medical Physiology, Membrane Physiology, Nerve and Muscle, 10TH Edition.Pages 71-76. Guyton AC and Hall JE (2000): Textbook of Medical Physiology, The Heart, 10TH Edition. Pages 134-138. Nitroglycerin-sublingual (2005) www. medicinenet . com/nitroglycerin-sublingual/article. htm. Date of retrieval 12th March 2008 from www. medicinenet . com/nitroglycerin-sublingual/article. htm. Rang HP, Dale MM, Ritter JM, Moore PK (2003): Pharmacology, The Heart. 5th Edition Pages 271-272.