Q.1. a). What is saltatory conduction? Enlist its advantages? 1+1 marks b).

briefly mention the three determinants of resting membrane potential. 3 marks Ans: Q.1.a. SATTATORY CONDUCTION: 1 mark
Propagation of action potential along a myelinated nerve fiber from one node of Ranvier to other in jumping manner is called as saltatory conduction. Node to node conduction. Also called saltatory / jumping conduction. All ion channels are present at nodes of Ranvier. Myelin sheath is absent & only neurilemma is there at the node.

ADVANTAGES OF SALTATORY CONDUCTION: 1 mark

It increases velocity of conduction directly in proportion to the fiber diameter, Conservation of energy- less energy expenditure. No short circuiting

Q.1. b). briefly mention the three determinants of resting membrane potential. Any two= 2 marks 1. Contribution of the Potassium Diffusion Potential (-94 mVolts) 2. Net Contribution of Sodium Diffusion Through the Nerve Membrane (+8 mVolts) 3. Contribution of the Na+-K+ Pump (-4 mVolts) Nernst Equation: (0.5 MARK) EMF (mV) = +/- 61 log conc. inside / conc. Outside Nernst Potential for K is -94 mV Nernst Potential for Na is +61 mV (but net contribution is only 8 mV because Na is 100 TIMES less permeable thru leak channels than K)

Goldmanns equation: 0.5 mark

Q.2: a). Draw and label the neuromuscular junction. 2 marks

b). What is end plate potential? How is it produced? How is it affected in myasthenia gravis? (2004, 2008 UHS). 1+1+1 marks

END PLATE POTENTIAL: It is a local potential of motor end plate, i-e., the thickened muscle membrane that is supplied by a motor-neuron, thus forming a component of neuro-muscular junction. Production of EPP: When impulse is transmitted from motor nerve to the muscle, the impulse arriving in the end of the motor neuron increases the permeability of its endings to calcium ions. Calcium ions trigger exocytosis of acetylcholine containing vesicles acetylcholine diffuses to the muscle-type nicotinic acetylcholine receptors, which are concentrated at the tops of junctional folds of the membrane of motor end plate. Binding of acetylcholine to these receptors increased sodium & potassium conductance of the membrane influx of sodium depolarizing potential is produced called END PLATE POTENTIAL The current created by this local potential depolarizes the adjacent muscle membrane to its firing level. Purpose of EPP is to build the threshold potential (- 65 mV). If RMP is -90 mV, then threshold is -65 mV, we need 25 mV potential change. Purpose of EPP is to reach the threshold of action potential. So voltage of EPP is much more than required, because required is only 25 mV. It is called SAFETY FACTOR. In Myasthenia Gravis, Miniature End Plate Potentials (MEPP = 0.5 mV) are produced. A rare auto-immune disease. Voltage of EPP is very low (Miniature EPP) action potential is not followed. At rest normally, a few synaptic vesicles break to liberate Ach from synaptic vesicles small change in EPP (about 0.5 mV) called MEPP. Amplitude varies directly with [Ca++] and inversely with [Mg++]. Impulse fails to transmit through NMJ Severe muscle weakness & fatigue (Extra-ocular muscles ptosis, diplopia, difficulty in Swallowing, weakness of Respiratory and Facial muscles)

Q.3. a). What is latch phenomenon in a smooth muscle fiber? What is its importance and how is it regulated? 1,1,1 b). What is compound action potential? Draw and label it. 1+1

key: LATCH PHENOMENON 1 mark

Smooth muscle can maintain prolong contraction with expenditure of small amount of energy. This is called as Latch phenomenon or latch principle.

IMPORTANCE OF LATCH PHENOMENON: 1 mark

It can maintain prolong tonic contraction in smooth muscle for hours with little use of energy. Little continued excitatory signal is required from nerve fibers or from hormonal sources. Once smooth muscle has developed full contraction, the amount of continuing excitation usually can be reduced to far less than the initial level, yet the muscle maintains its full force of contraction. The energy consumed to maintain contraction may be as little as 1/300 the energy required for comparable sustained skeletal muscle contraction.

REGULATION OF LATCH PHENOMENON: 1 mark

When myosin kinase & myosin phosphatase enzymes are both strongly activated, the cycling frequency of myosin heads & velocity of contraction are great. As the activation of enzymes decreases, the cycling frequency decreases, but at the same time, the deactivation of these enzymes allows the myosin heads to remain attached to the actin filament at any given time remains large. (Slow ATPase activity of myosin head). Because of the number of heads attached to actin determines the static force of contraction, tension is maintained, or latched; yet little energy is used by the muscle, because ATP is not degraded to ADP except on rare occasion when a head detaches.
b). What is compound action potential? Draw and label it. 1+1

Key: Multi-peaked action potential recorded from a nerve trunk For example: Sciatic nerve has number of nerve fibers of different diameters & different velocity of conduction. When action potential from different nerve fibers are recorded multiple peaks. 3 main peaks: A, B, C. A is further divided into alpha, beta, gamma, delta. A & B types are myelinated & C type is unmyelinated. Compound action potential is basis of physiological classification of nerve fibers. A alpha fibers with maximum diameter have highest velocity of conduction, up to 120 m/sec.

Q.4. a). Compare and contrast visceral (unitary) and multiunit types of smooth muscle. 2.5 marks

Ans:
1. 2. 3. 4. 5. LOCATION TYPE OF JUNCTIONS ARRANGEMENT CONTROL ACTION POTENTIAL.

1. LOCATION: UNITARY: Wall of GIT, ureter, bile duct, uterus and large blood vessels. MULTIUNIT: Ciliary muscle of eye, Iris of eye and pilo-erector muscle. 2. TYPE OF JUNCTION: UNITARY: Diffuse junction. No contact with nerve fiber. Neurotransmitter is released near the fiber. MULTIUNIT: Contact junction.One of the autonomic nerves form junction with muscle fiber and releases neurotransmitter like nor-epinephrine. 3. ARRANGEMENT: UNITARY: Sheaths or bundles with gap junctions in between, so act as single unit. If one part is excited whole is excited. MULTIUNIT: Individual muscle fibers. Each fiber has insulating outer membrane with glycoprotein and collagen consistency. Independently each muscle fiber is excited. 4. CONTROL: UNITARY: Mainly non-nervous stimuli (hormonal stimuli like oxytocin and serotonin). Show spontaneous contraction. MULTIUNIT: Mainly through nervous stimuli. Does not show spontaneous contraction. 5. ACTION POTENTIAL: UNITARY: 3 types: Spike, Plateau and Slow wave. Rhythm due to increased or decreased pumping of sodium. MULTIUNIT: Not required as individual muscle fibers are too small to produce action potential. Only localized depolarization in response to excitation.
b). compare simple diffusion with facilitated diffusion. SIMPLE DIFFUSION Absent Absent Absent Absent O2, CO2 Transport through cell membrane 2.5 marks FACILITATED DIFFUSION Present Present Present Present Glucose transport through GLUT transpoters

PARAMETER stereospecificity competition saturation Vmax examples

Q5. a). A woman of 50 years presents with irregularly irregular pulse and pulse deficit. Her ECG shows small irregular waves replacing P waves and QRS complexes at unequal distance. i. ii. iii. which condition the woman is suffering from? (1) Give features of this condition. (1) Explain the mechanism of this condition. (2)

Ans. She is suffering from atrial fibrillation. 1 mark b. Features of atrial fibrillation: 1 mark The atrial rate is between 400-600/min. Ventricular response is completely irregular ranging from 80-180 /min. (irregularly irregular pulse) Occurs in rheumatic and other forms of valvular heart disease, dialted cardiomyopathy, atrial septal defect, hypertension, thyrotoxicosis and coronary heart disease The most serious consequence of atrial fibrillation is the risk for thrombus formation due to stasis in atria and consequent embolization. Cardiac filling is decreased

c. Mechanism of atrial fibrillation: 2 marks Ectopic focus 0.5 marks The basic mechanism underlying atrial fibrillation is the re-entry or the circus phenomena in which the impulse generated continues to travel around the muscle that has already been excited. The different conditions that can cause re-entry of an impulse are as follows: 1 mark The pathway of conduction is too long. For instance as occurs in dilated hearts. Decreased rate of conduction. It occurs frequently in blockage of the conducting pathway due to ischemia or long pathway which is again a feature of dilated hearts. Shortened refractory period Chain reaction of impuses 0.5 marks

b). Biefly describe the functions of Na/K ATPase pump. Any two 2*0.5= 1 marks Maintains the cell volume Electrogenic pump (contributes -4 m Volts in the generation of RMP) Creates the concentration gradient of Na and K across the cell membrane.

Q6. a). A 60 year old lady falls down while climbing stairs. On examination in a hospital emergency her blood pressure =60/40 mm Hg, pulse rate=30minute and irregular. ECG shows dissociation between p waves and QRS complexes. i. ii. iii. What type of heart block does the lady suffer from? (1) What can be the future management of this type of heart block? (1) What is Stokes Adams syndrome? (1)

. a. What type of heart block does the lady suffer from? (1) She is suffering from complete heart block. b. What can be the future management of this type of heart block? (1) ATROPINE, Permanent Pacemaker c. What is Stokes Adams syndrome? (1) In a person with complete AV block that is when impulses from the atria are not conducted to the ventricles, ventricles do not start beating until a delay of 5 to 30 seconds. This leaves the brain without blood supply for a while leading to fainting. The frequent fainting spells are known as Stokes Adams syndrome.

b). Differentiate between the action potential of SA node and the ventricle. make table for these points

2 marks

RMP in SA node is -55 m volts and it is -85 m volts in the ventricle Pre-potential is seen in SA node and not seen in the ventricle Depolarization is due to opening of Ca channels SA node, and due to opening of fast Na channels in the ventricle Phase 1 and 2 is absent SA node while is present in the ventricle Action potential is of longer duration ventricle SA node shows autorrhytmicity Plateau phase is present in the ventricle

Q7. Draw and label normal ECG. Show its waves, intervals and segments. Give the changes in the ECG in a patient of Acute MI. (3.5+1.5)

A normal ECG comprises of: Waves of ECG: P-wave, QRS complex, T-wave and U-wave Segments of ECG: PQ or PR segment and ST segment Intervals of ECG: PR interval, QT interval and RR interval

P wave: shows atrial depolarization QRS: ventricular depolarization T wave: ventricular repolarization

Two changes in ECG in a patient of MI: 0.5*3= 1.5 marks T wave inversion ST elevation Q waves

Q8. Enlist the pressure and volume changes which occur in left ventricle during it cardiac cycle. (3+2)

Changes in the volume/pressure of ventricles during the cardiac cycle: 1.Phase of Iso-volumic contraction of ventricle: At the start of ventricular systole L.V is full of blood 110-120 ml which is called the end diastolic volume . The volume does not change in this phase as all valves are closed. Pressure: from 2-3 mmHg rises to 80 mmHg

2.Phase of Ejection: The volume of blood ejected in systole is 70 ml and is called stroke volume. It is divided into following initial and late phases Maximal Ejection Phase (M.E.P) / Rapid Ejection Phase (R.E.P): 2/3 rd or 70% of blood volume is ejected Pressure: from 80 mmHg rises to 120 mmHg

Phase of Reduced Ejection Phase (R.E.P): Remaining 1/3 of stroke volume, 30% emptying occurs in last 2/3 of ejection phase. The volume of blood remaining in the ventricle at the end of systole is 40-50 ml and is referred to end systolic volume Pressure: from 120 mmHg falls back to 80 mmHg

3. Phase of Iso-Volumic Relaxation: No change in blood volume occurs. Pressure: from 80 mmHg falls back to 2-3 mmHg

4. Period of Filling: Phase of Rapid Inflow: 2/3 of ventricular filling Pressure: from 2-3 mmHg Phase of Diastasis or slow inflow: Only slight filling occurs Pressure: from 2-3 mmHg

Last rapid inflow phase or Atrial Systole: Remaining 1/3 filling (30%). Now filling of ventricles is complete & EDV of 115 ml is present in the ventricles. Pressure: from 2-3 mmHg rises to 5-6 mmHg.

Q.9: Write down the mechanisms of temperature regulation during hot and cold weather. During hot weather: 0.5*5= 2.5 marks Increase sweating Vasodilation in skin blood vessels No shivering Decrease chmical thermogenesis No piloerection

2.5+2.5 marks

During cold weather: 0.5*5= 2.5 marks shivering increase chemical thermogenesis piloerection no sweating Vasoconstriction in skin blood vessels

Q. 10: write short notes on: a) Acclimatization to heat. 2

1. 2. 3. Examples of people requiring acclimatization are soldiers on duty in the tropics and miners working in the 2-mile-deep gold mines of South Africa, where the temperature approaches body temperature and the humidity approaches 100 per cent. A person exposed to heat for several hours each day while performing a reasonably heavy workload will develop increased tolerance to hot and humid conditions in 1 to 3 weeks. Among the most important physiological changes that occur during this acclimatization process are an approximately twofold increase in the maximum rate of sweating, an increase in plasma volume, and diminished loss of salt in the sweat and urine to almost none; the last two effects result from increased secretion of aldosterone by the adrenal glands.

b) Mechanism of fever and the role of hypothalamus in temperature regulation. 2+1

When the set-point of the hypothalamic temperature-control center is suddenly changed from the normal level to higher than normal (as a result of tissue destruction, pyrogenic substances, or dehydration), the body temperature usually takes several hours to reach the new temperature setpoint. Because the blood temperature is now less than the setpoint of the hypothalamic temperature controller, the usual responses that cause elevation of body temperature occur. During this period, the person experiences chills and feels extremely cold, even though his or her body temperature may already be above normal. Also, the skin becomes cold because of vasoconstriction, and the person shivers. Chills can continue until the body temperature reaches the hypothalamic set-point of 103F. Then the person no longer experiences chills but instead feels neither cold nor hot. As long as the factor that is causing the higher set-point of the hypothalamic temperature controller is present, the body temperature is regulated more or less in the normal manner, but at the high temperature set-point level. Crisis, or Flush. If the factor that is causing the high temperature is removed, the set-point of the hypothalamic temperature controller will be reduced to a lower valueperhaps even back to the normal level, , but the hypothalamus is attempting to regulate the temperature to 98.6F. which causes intense sweating and the sudden development of hot skin because of vasodilation everywhere.This sudden change of events in a febrile state is known as the crisis or, more appropriately, the flush. In the days before the advent of antibiotics, the crisis was always anxiously awaited, because once this occurred, the doctor assumed that the patients temperature would soon begin falling.