Dr. RAJENDRAN S INSTITUTE OF MEDICAL EDUCATION

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1 Page 1 of 7 Dr. RAJENDRAN S INSTITUTE OF MEDICAL EDUCATION AIIMS NOVEMBER QUESTIONS AND ANSWERS PHYSIOLOGY This contains only 3 out of 7 questions. For complete questions with explanatory answers, click premium content at the top of the home page. 1) A man is shot in the back at the level of T8 vertebra. Immediately after the shot he loses all the sensation below level of lesion. Injured nerve is not able to regenerate due to all of the reasons below except: a. Lack of endoneural tubes b. Lack of growth factors c. Presence of glial scar d. Lack of myelin inhibiting substance Ans: D

2 Page 2 of 7 NERVE REGENERATION There are three types of nerve injuries: neurapraxia (focal demyelination), axonotmesis (interruption of axonal continuity but preservation of Schwann cell basal lamina), and neurotmesis (complete transection). After all types of injury, nerve regeneration involves three crucial steps: (a) survival of axonal cell bodies, (b) regeneration of axons that grow across the transected nerve to reach the distal stump, and (c) migration and connection of the regenerating nerve ends to the appropriate nerve ends or organ targets. Phagocytes remove the degenerating axons and myelin sheath from the distal stump (wallerian degeneration). Regenerating axonal sprouts extend from the proximal stump and probe the distal stump and the surrounding tissues. Schwann cells ensheathe and help in remyelinating the regenerating axons. Functional units are formed when the regenerating axons connect with the appropriate end targets. Several factors play a role in nerve healing, such as growth factors, cell adhesion molecules, and nonneuronal cells and receptors. Growth factors include nerve growth factor, brainderived neurotropic factor, basic and acidic fibroblastic growth factors, and neuroleukin. Celladhesion molecules involved in nerve healing include nerve-adhesion molecule, neuron-glia adhesion molecule, myelin adhesion glycoprotein, and N-cadherin. This complex interplay of growth factors and adhesion molecules helps in nerve regeneration. Some of the factors that have shown promise in nerve repair in the laboratory include triamcinolone, alpha melanocyte-stimulating hormone (alpha-msh) and its derivatives, leupeptin, and apolipoproteins. Nerve growth factor has yielded less encouraging results. Distant stump recovery is rare, and the damaged axons are unlikely to form new synapses. This is in part because CNS neurons do not have the growth-promoting chemicals needed for regeneration. In fact, CNS myelin is a potent inhibitor of axonal growth. In addition, following CNS injury several events astrocytic proliferation, activation of microglia, scar formation, inflammation, and invasion of immune cells provide an inappropriate environment for regeneration. Ganong's Review of Medical Physiology, 24e > Chapter 4. Excitable Tissue: Nerve > Neurotrophins > Other Factors Affecting Neuronal Growth Nerve Healing. CURRENT Diagnosis & Treatment in Orthopedics > Chapter 3. Musculoskeletal Trauma Surgery > The Healing Process

3 Page 3 of 7 2) False regarding increase in blood supply to muscle during exercise: a. Local metabolites b. Sympathetic stimulation c. Cholinergic stimulation d. Inhibition of beta receptor Ans: D The adjustments to exercise are mainly due to a large increase in sympathetic activity. During exercise, parasympathetic activity becomes attenuated, while sympathetic activity increases. The control of blood flow during exercise is extremely important to ensure that blood and oxygen are transported to the tissues that need them most. Transmission at the synaptic junctions between preganglionic and postganglionic neurons and between the postganglionic neurons and the autonomic effectors are chemically mediated. The principal transmitter agents involved are acetylcholine and norepinephrine. The autonomic neurons that are cholinergic (ie, release acetylcholine) are (1) all preganglionic neurons, (2) all parasympathetic postganglionic neurons, (3) sympathetic postganglionic neurons that innervate sweat glands, and (4) sympathetic postganglionic neurons that end on blood vessels in some skeletal muscles and produce vasodilation when stimulated (sympathetic vasodilator nerves). The remaining sympathetic postganglionic neurons are noradrenergic (ie, release norepinephrine). The adrenal medulla is essentially a sympathetic ganglion in which the postganglionic cells have lost their axons and secrete norepinephrine and epinephrine directly into the bloodstream. The chemical transmitter present at most sympathetic postganglionic endings is norepinephrine. Norepinephrine and its methyl derivative, epinephrine, are also secreted by the adrenal medulla. Epinephrine is not a mediator at postganglionic sympathetic endings. The sympathetic system releases norepinephrine directly through the sympathetic trunk to the sinus node and myocardium. In addition, the adrenal medulla releases both norepinephrine and epinephrine into the blood. During strenuous exercise, secretion of epinephrine is more than norepinephrine.

4 Page 4 of 7 Norepinephrine and epinephrine are approximately equipotent in stimulating beta 1 receptors present in heart. Norepinephrine and epinephrine both increase the force and rate of contraction of the heart. These responses are mediated by beta 1 receptors. Epinephrine and norepinephrine can increase the contractility of the heart by increasing the calcium concentration within the cardiac muscle fiber. This allows for greater myosin and actin interaction and an increase in force production. Norepinephrine is a potent alpha agonist and has relatively little action on beta 2 receptors; however, it is somewhat less potent than epinephrine on the alpha receptors of most organs. Norepinephrine produces vasoconstriction in most if not all organs via alpha1 receptors, but epinephrine dilates the blood vessels in skeletal muscle and the liver by stimulating beta 2 receptors. This usually overbalances the vasoconstriction produced by norepinephrine elsewhere, and the total peripheral resistance drops. Norepinephrine and epinephrine act to increase heart rate and increase myocardial contractility, as well as to redirect blood flow to working muscle by mediating peripheral vasoconstriction in relatively inactive tissues (eg, the kidneys and gut). Local metabolic conditions also control the shunting of blood to active muscles. The local response is primarily caused by the build-up of vasodilatory metabolites in exercising muscle. Vasodilatory metabolites help to maintain local increased flow to active skeletal muscles. A major change on the cardiovascular system during dynamic exercise is the great decrease in total peripheral resistance caused by metabolic vasodilator accumulation and decreased vascular resistance in the active skeletal muscle. Active muscles receive blood supply appropriate to their metabolic needs. At rest, approximately 20% of cardiac output is distributed to the skeletal muscle. However, during physical activity, the majority (85%) of the increased cardiac output is diverted to the working muscles. The tremendous increase in skeletal muscle blood flow is accomplished largely by increased cardiac output but also in part by diverting flow away from the kidneys and the splanchnic organs. Effect of Exercise. Cardiovascular Physiology > Chapter 10. Cardiovascular Responses to Physiological Stresses Chapter 100. Exercise in Health and Cardiovascular Disease. Hurst's The Heart Effects of Epinephrine & Norepinephrine. Ganong's Review of Medical Physiology, 24e > Chapter 20. The Adrenal Medulla & Adrenal Cortex > Adrenal Medulla: Structure & Function of Medullary Hormone

5 Page 5 of 7 3) Second messenger a. camp b. IP3 c. Guanylyl cyclase d. All Ans: D SECOND MESSENGER Nerve impulses and the binding of many hormones to cell surface receptors elicit changes within target cells by inducing the release or synthesis of specialized effectors called second messengers. Many hormones in the ECF bind to receptors on the surface of cells and trigger the release of intracellular mediators such as camp, IP 3, and DAG that initiate changes in cell function. Consequently, the primary, or "first," messenger is the hormone molecule or nerve impulse and the intracellular mediators are called "second messengers." Second messengers bring about many short-term changes in cell function. This mechanism provides amplification of the primary signal and distribution of the signal to appropriate targets within the cell. Second messengers include 3', 5'-cAMP, Ca2+, 3',5'-cGMP, nitric oxide, and the polyphosphoinositols. Many second messengers act by increasing the cytoplasmic Ca 2+ concentration. The increase is produced by releasing Ca 2+ from intracellular stores (primarily the endoplasmic reticulum) or by increasing the entry of Ca 2+ into cells, or by both mechanisms. IP 3 is the major second messenger that causes Ca 2+ release from the endoplasmic reticulum through the direct activation of a ligand-gated channel, the IP 3 receptor. In effect, the generation of one second messenger (IP 3 ) can lead to the release of another second messenger (Ca 2+ ).

6 Page 6 of 7 Ganong's Review of Medical Physiology, 24e > Chapter 2. Overview of Cellular Physiology in Medical Physiology > Intercellular Communication Harper's Illustrated Biochemistry, 29e > Chapter 9. Enzymes: Regulation of Activities GUANYLYL CYCLASE Cyclic guanosine monophosphate (cyclic GMP or cgmp) is important in vision in both rod and cone cells. In addition, there are cgmp-regulated ion channels, and cgmp activates cgmpdependent kinase, producing a number of physiologic effects. Guanylyl cyclases are a family of enzymes that catalyze the formation of cgmp. Two guanylyl cyclases are receptors for atrial natriuretic peptide and a third binds an Escherichia coli enterotoxin and the gastrointestinal polypeptide guanylin. The other form of guanylyl cyclase is soluble, contains heme, and is not bound to the membrane. There are several isoforms of the intracellular enzyme. They are activated by nitric oxide. Stimulation of receptors that raise intracellular cyclic GMP concentrations leads to the activation of the cyclic GMP-dependent protein kinase (PKG) that phosphorylates some of the same substrates as PKA. In this way, Guanylyl cyclases can also be considered as second messengers.

7 Page 7 of 7 Guanylyl Cyclase. Ganong's Review of Medical Physiology, 24e > Chapter 2. Overview of Cellular Physiology in Medical Physiology > Production of camp by Adenlyl Cyclase Second Messengers. Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e > Chapter 3. Pharmacodynamics: Molecular Mechanisms of Drug Action > Mechanisms of Drug Action For rest of the 4 questions in Physiology with explanatory answers, click premium content at the top of the homepage.

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