past years snq answer by rcsi

8/10/2019 Past Years SNQ Answer by RCSI

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Past Years (2006 & 2007) Questions And Answers Compilation.

2006 Q1. A 70 year old womans blood pressureis found to be elevated on two

separate occasions (180/105). Describe the mechanisms of action and the possible

adverse effects of two drug classes that you would consider using to lower blood

pressure in this woman.

Antihypertensive Drugs: ABCD AVAC

ACE-Inhibitors

Beta-blockers

Calcium-channel blockersDiuretics

Angiotensin II antagonistsAlpha-blockers

VasodilatorsCentral sympathophlegics

ThiazideDiureticsEx.Hydrochlorthiazide

MOA:.Inhibition of NaCl reabsorption in early distal tubule of renal nephron, decrease waterreabsorption, decrease in blood volume.S.E.s Fatigue

HypokalaemiaImpotance

Glucose intoleranceDyslipidaemiaHyperuricaemia

Beta-blockers

ExamplesNon-selective; Propranolol,1 selective; Atenolol

With vasodilatation; Pindolol(1 selective antagonist and partial agonist at B2 adrenoceptors)Carvidalol (non-selective -blocker but also 1 blocker)

Nebivolol (releases NO)Mechanisms of action: decrease HR, and decrease COInhibition of rennin secretion- S.Es:Bronchospasm(non-selective)

Worsening of peripheral vascular disease (non-selective)Glucose intolerance

DyslipidaemiaNegative inotrophyImpotance

Fatigue CNS effects, nightmares

Q2. A 10 year old girl with asthma is still suffering recurrent moderately severe attacks of

asthma despite treatment with an inhaled beta-2 adrenoceptor agonist.Discuss the

mechanisms of action and side effects of two classes of drugs you would consider adding to

her treatment regimen, so as to reduce frequency and severity of attacks.


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Bronchodilators

B2 adrenoreceptor agonists

Muscarinic (M3) antagonists

Xanthines

Anti-inflammatory Drugs

Glucocorticoids

Cromones

Leukotriene synthesis inhibitors & receptor antagonists

1. MUSCARINIC ANTAGONISTS

Ipratropium Bromide - derivative of N-isopropylatropine

Tiotropium bromide - Newer long-acting :

Administration

Given by inhalation

not well absorbed -little systemic effects.

Mechanism of action

Inhibition of the action of acetyl choline at M1, M2,

and M3 muscarinic receptors. thus producing

bronchodilation and reducing mucous secretion.

Slower acting than B2 agonists.

2. XANTHINES

Caffeine

Theophylline

Oral.

Short T1/2.

Sustained release preparations available

Aminophylline

IV.


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MOA: Relax bronchial smooth muscle (bronchodilation)

by inhibiting phosphodiesterase resulting in increased

cAMP and cGMP.

Also anti-inflammatory actions (inhibit the late phase)

? inhibition of phosphodiesterase present in

inflammatory cells.

Selective PD4 inhibitors (Roflumilast, Cilomilast)

may be particularly beneficial in COAD)

Side Effects

Narrow therapeutic range (27-80mmol/l)

Side effects likely with concentrations >110mmol/l

gastrointestinal: nausea / anorexia

cardiovascular: arrhythmias can be fatal

CNS: nervousness, tremor, seizures

Pharmacokinetics

Metabolised in the liver

T1/2 increased by liver disease, heart failure and decreased by

smoking and heavy drinking

NB Drug interactions

Pharmacokinetic Drug Interactions occur with Theophylline because of extensive

Metabolism by Cytochrome P450 Enzymes

Cytochrome P450 1A2 is the main isoform responsible for the metabolism of theophylline

Erythromicin and Cimetidine are also metabolised by this isoform hence competitive

inhibition can occur when co-administered

Enzyme inducers such as; Phenytoin, Carbamazepine, Rifampicin, Barbiturates, Alcoholresult in reduced plasma concentrations and decreased effects of drugs (such as

theophylline) which are extensively metabolised by Cytochrome P450 enzymes

Note: Delayed onset (2-3 weeks) as enzyme induction requires synthesis of new protein.

Note: Pharmacokinetic drug interactions are most important for drugs, such as

theophilline, that have a low therapeutic index


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Q3. Describe the treatment of arrhythmias, giving special attention to the Vaughan

Williams classification and side effects of two classes of anti-arrhythmic drugs.

There are five main classes in the Vaughan Williams

classification of antiarrhythmic agents:

Class I agents interfere with thesodium(Na+) channel.

Class II agents are anti-sympathetic nervous systemagents. All agents in this class

arebeta blockers.

Class III agents affectpotassium(K+) efflux.

Class IV agents affect theAV node.

Class V agents work by other or unknown mechanisms.

Q4. The levels of plasma lipoproteins in humansubjects are used diagnostically to

evaluate cardiovascular risk. Name the two lipoproteins mainly responsible for

cholesterol transport and state FOUR of the properties by which these two may be

distinguished.

Low density lipoprotein(LDL)

Lower density, larger

Contain a larger proportion of cholesterol than HDL

Move cholesterol around to/from liver and peripheral tissues in the circulatory

system

As a result, cholesterol may be deposited in the walls of blood vessels and causecardiovascular diseases such as atherosclerosis

High density lipoprotein (HDL)

Higher density, smaller

Carry least amount of cholesterol

Carry cholesterol back to liver for elimination from body

Class IV

( Ca channel

blockers)

Verapmil

Diltaizem

Block the L-type of Ca channel.

Shorten phase 2 (plateau)

Reduce contractility of heart.

Act on AV node

Treat SVT

-Reduce cardia

contractility.

-Bradycardia

Class V

(Digitalis)

Digoxin Increases vagal activity via its central

action on the central nervous system.

Thus, decreasing the conduction of

electrical impulses through the AV node.

Positive inotropic effect

-Hypokalaemia

-Nausea &

vomiting.
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As a result, accelerate the removal of cholesterol from blood, reducing the likelihood

of cholesterol becoming deposited in arterial wallsprovide protection from

cardiovascular diseases

Q5. A family travel to Australia to visit their relations. On arrival in Sydney, the

mother experiences chest pain and is admitted to hospital. She is found to have apulmonary embolus. Describe how a pulmonary embolus interferes with respiratory

function.

Pulmonary embolus blockage of pulmonary artery by matters such as fat, tumour

or a clot from vein

Decrease perfusion / underperfusion

Larger ventilation/perfusion (V/Q) ratio

Increased physiological dead space, wasted ventilation

Increases PO2and decreases PCO2

Alveoli contract, pulmonary artery relax Symptoms: dyspnoea, tachypnoea, pleuritic pain, cough, haemoptysis

Q6. Describe the intrinsic ability of the heart to adapt to changes in venous return.

Illustrate your answer with a diagram.

Venous return: The rate of blood flow back to the heart is the venous return. It normally

limits cardiac output. VR at RA determines amount of blood flowing thru pulmonary circ

(L.Atrium) and hence through systemic circ (at L.Ventricle)

Cardiac output is affected by preload(:is the pressure stretching theventricleof theheart,

after passive filling andatrialcontraction / LVEDP: L.ventricle end diastolic pressure)

Preload affected by...VENOUS RETURN:

Left ventricle (LV) function curve, or Frank - Starling curve (1914):

Normal range of the LVEDP, 5-6 mmHg

Optimal initial preload, 15-20 mmHg (at optimal length of Sarcomere, 2.0

2.2 m)

When the LVEDP > 20 mmHg, LV work is maintained at almost the same level, does

not change with the increase of LVEDP

What affects LVEDP??

Period of the ventricle diastole (filling) heart rate

Speed of the venous return (difference between the venous pressure and

atrial pressure)
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Mechanism: VR increase, LV work inc, smooth muscle stretching inc, LVEDP

increase, more blood pumped out of heart, vice versa

Basically, heart gives away all that it receives.

Concept of heterometric regulation: regulation depending upon change in size (i.e. LVP)

Q7. In a group on a hiking tour to the historic site of Machu Picchu in the Peruvian

Andes, some develop acute mountain sickness but others acclimatise normally to the

high altitude. Describe the cardiovascular and respiratory changes that occur during

acclimatisation.

Physiological effects of altitude are due to decrease in barometric pressure

Air composition stays the same but PO2in the air fallsPAO2and PaO2fall

Lower amount of oxygen available to inhale (hypoxia), less oxygen reaches the

blood (hypoxemia)

Cardiovascular: pulmonary hypertension, increased HR and CO

Respiratory: ventilation increases by 65% to bring in more oxygen at rapid rate

PACO2and PaCO2decrease (hypocaptic)

Q8. On suddenly standing upright,you may feel dizzy and faint. Describe the reflex

physiological response which normally counteracts postural hypotension.

Drop in bpsensed by baroreceptorincrease firing rate to medullaactivate

sympatheticincrease hrincrease coincrease bp

Q9. Describe the changes in left ventricular pressure occurring during the cardiac

cycle.Illustrate your answer with a diagram giving absolute values of pressure.


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Q10. Prior to elective surgery for a hip replacement, a patient is found to have

haemoglobin of 8g/dl. Discuss the balance between oxygen availabilityand demand

in this situation.

Things need to know

o Source of oxygen

o

How body respond if

Demand increase

Demand decrease

o Effect to pO2 & pCO2

o Example for each situation

o Regulator

1.

Source of oxygen

o

From ventilation process

o Diffuse to blood

o Pump by heart

2. If demand increase

o Example exercise

o

Effect pO2 low, pCO2 high

o

How body respond

Ventilation increase (accessory muscle)

Blood flow increase to muscle (higher c. output, heart rate )

3.

If demand decrease

o

Example sleeping

o How body respond

Ventilation normal (not involve accessory muscle)

Blood flow not focus to muscle

4.

Regulator


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o

Detector chemoreceptor (central, peripheral)

o Central controller medulla, respiratory centre

o Effector respiratory muscleQ11. A young man is brought to the Accident and Emergency Department following a

stab wound to the 4thright intercostal space and has developed a pneumothorax. List

the layers of the chest wall that the knife has passed through. Where does theneurovascular bundle lie in the intercostal space and what does it contain? What are

the surface markings of the pleural cavities? Answers.

Layers of the chest wall that the knife has passed through:

- Skin

- Fat

- External intercostal muscle

-

Internal intercostal muscle

- Innermost intercostal muscle

- Endothoracic fascia

- Parietal pleura

-

Pleural cavity

-

Visceral pleura

Neurovascular bundle:

- Lies within the costal groove (upper part of the intercostal space)

- The contains, from top to the bottom, are intercostal vein, intercostal artery, and

intercostal nerve.

The surface marking of the pleural cavity:

- About 2 cm above the clavicle

- At 4thcostal cartilage, the left pleural line pass laterally, while the right line

continues down

-

The lines pass obliquely laterally across the 6thcostal cartilage- In the midclavicular line, the lines across the 8 thrib

-

In the midaxillary line, they cross the 10thrib

- In the midscapular line, they cross the 12thrib

Q12. During a routine physical examination, you auscultate your patients chest.

Describe or draw the surface markings of the heart and the heart valves. Indicate

where you would place a stethoscope to listen to each valve.

Heart border: upper left end: 2ndleft CC, upper right end: 3rdright CC, lower right end: 6th

CC, lower left end: 5thintercostal space, midclavicular line. Surface marking of the heart

valves: retrosternal.

Valve Surface marking Auscultation

Pulmonary 3rdCC, left sternal border 2ndcc, left sternal border

Aortic 3rdICS, right sternal border 2ndcc, right sternal border

Mitral 4thCC, left sternal border 5

thICS, midclavicular line

Tricuspid 4tdICS, right sternal border Left lower sternal border


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Openings:

T8 IVC, right phrenic nerve (at central tendon)

T10 oesophagus, R&L vagus nerve (and esophageal branches of left gastric

arteries&veins)

T12 aorta, azygos vein, thoracic duct

Q14. A 29 year old man develops shoulder pains following a tennis match. Explain

with reference to their attachments, how the muscles of the shoulder girdle control

rotation of the scapula when reaching out and opening a door.

1.

flexion of the shoulder when reaching out

a. anterior part of deltoid- attached from spine of scapula, acromium process,

lateral 1/3 clavicle to humerus

b.

pectoralis major (clavicular part)- attached from clavicle, sternum and costal

cartilages

c.

coracobrachialis

d.

biceps2.

extension of shoulder when opening a door

a.

latissimus dorsi (assist by teres major)attached from spinous process (T6-

T12), sacrum, iliac crest and ribs (10-12) to humerus (floor of the bicipital

groove)

b. posterior part of deltoid attached from spine of scapula, acromium

process, lateral 1/3 clavicle to humerus (deltoid tuberosity)

c.

teres major attached from inferior angle of scapula tointertubercular

sulcusof thehumerus(medial lip)

d.

triceps attached from:

i. long head: inferior glenoid tubercle of thescapula

ii.

lateral head: posteriorhumerus,above spiral grioove

iii.

medial head: posteriorhumerus,below the spiral grooveto olecranon process of ulna

3.

Abduction of Shoulder joint when reaching out

10 Supraspinatus Supraspinatus fossa of scapula Greater tubercle

Up to 90 Deltoid Spine of scapula, acromium

process, lateral 1/3 clavicle

Deltoid tuberosity

Rotation of

scapula,

allows

another 60abduction

Serratus anterior Upper 8 ribs Medial border of scapula

Trapezoid Occipital protuberance

Ligamentum nuchae

Spinous process of C1-T7

Origin of deltoid:

Spine of scapula, acromiumprocess, lateral 1/3 clavicle
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Q15. A 29 year old man accidentally puts his hand through a sheet of glass, causing a

laceration of his thenar eminence. Describe the movements of the thumb.Indicate the

muscles involved and their innervation.

Finger and Thumb MovementsFlexion

Thumbbends medially along the palmFingersbend anteriorlyExtension

Thumbpoints laterally

Fingers move posteriorly

Abduction/Adduction

Movement of thumb forward (anteriorly) is abduction and Movement of thumb forward

(anteriorly) is adduction

The thenar eminence (ball of the thumb)has a flexor pollicis brevis, an abductor pollicis brevis,and an opponens pollicis. Each of the muscles is supplied by T1 from median nerve.

Flexion bends medially along the palm FPL Median

FPB Median

Extension points laterally EPL Radial

EPB Radial

Abduction Movement of thumb forward (anteriorly) APL Median

APB Radial

Adduction Movement of thumb backward (posteriorly) AP Ulnar


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2006 (repeat)

Q1. A young women presents to the Accident & Emergency Department with

dysphagia (difficulty swallowing), after swallowing a large piece of biscuit. Describe

the structure, course and relations of the thoracic oesophagus. Describe the points at

which the oesophagus is narrowed.


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Q2. A young child is brought to the Accident and Emergency Department after

inhaling a peanut. Describe the trachea and bronchial tree within the thorax,

including their structure, position and relations. Into which segmental bronchus is an

inhaled foreign body most likely to lodge if a patient is standing upright? Or lying

down?

The right main bronchus is wider, shorter, and more

vertical than the left main bronchus.

The cartilage and mucous membrane of the primary

bronchi are similar to that in the trachea.

As the branching continues through the bronchial tree,

the amount of hyaline cartilage in the walls decreases

until it is absent in the smallest bronchioles. As the

cartilage decreases, the amount of smooth muscle

increases. The mucous membrane also undergoes a

transition from ciliated pseudostratified columnar

epithelium to simple cuboidal epithelium to simple

squamous epithelium.

Standing upright? Or lying down? (probably standing up,

because the trachea is straight vertically in this

positionprobably.)


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Q3. A patient presents to her GP with a mass in the lateral breast and fullness in her

axilla. Describe the structure of the female breast, including relations blood supply

and lymphatic drainage. What structures in the axilla might be damaged during

surgery?

What structures in the axillamight be damaged during

surgery?

It could be the brachial plexus,

axillary art and vein. The lymph

nodes can be removed surgically.


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Q4. A footballer dislocates his shoulder during a match, damaging the axillary nerve.

Describe this nerve, including its origin, course and distribution (motor and

cutaneous). What is its root value? How would you test for its function clinically?

Comes off the posterior cord of thebrachial plexus at the level of theaxilla (armpit) and

carries nerve fibers from C5 and C6. The axillary nerve travels through thequadrangular space with theposterior circumflex humeral artery and vein.

It supplies twomuscles,deltoid (a muscle of the shoulder), andteres minor (one of the

rotator cuff muscles).

Sensory information from theshoulder joint,as well as the skin covering the inferior

region of the deltoid muscle, regimental patch (Superior Lateral Cutaneous Nerve

branch).

It lies at first behind theaxillary artery,and in front of theSubscapularis,and passes

downward to the lower border of that muscle. It then winds backward, in company with

the posterior humeral circumflex artery, through a quadrilateral space bounded above

by the Teres Minor, below by theTeres major,medially by the long head of theTriceps

brachii,and laterally by thesurgical neck of the humerus, and divides into an anteriorand a posterior branch.

The anterior branch(upper branch) winds around thesurgical neck of the humerus,

beneath the Deltoideus, with the posterior humeral circumflex vessels, as far as the

anterior border of that muscle, supplying it, and giving off a few small cutaneous

branches, which pierce the muscle and ramify in the skin covering its lower part.

Theposterior branch(lower branch) supplies the Teres minor and the posterior part of

the Deltoideus; upon the branch to the Teres minor an oval enlargement

(pseudoganglion) usually exists. The posterior branch then pierces the deep fascia and

is continued as the lateral brachial cutaneous nerve, which sweeps around the posterior

border of the Deltoideus and supplies the skin over the lower two-thirds of the

posterior part of this muscle, as well as that covering the long head of the Tricepsbrachii.

The trunk of the axillary nerve gives off an articular filament which enters theshoulder-

joint below the Subscapularis.

The axillary nerve may be injured in anterior dislocations of the shoulder joint,

compression of the axilla with a crutch or fracture of the surgical neck of the humerus.

Clinical test includes

o Abduction of shoulder >10. Paralysis of the teres minor and deltoid muscles.

o Sensory of regimental patch

Q5. When putting up a shelf, you use a screwdriver to attach it to the wall. Define the

movements of pronation and supination of the upper limb. Name and briefly describethe joints involved in pronation and supination.Name two pronators and two

supinators.

Pronation : Rotation of forearm to bring the palm facing backward.

Supination : Rotation of forearm to bring the palm facing forward (supine position).

Joint involved : Proximal & distal radioulnar joints (Where the radius and ulnar articulate,

and both are synovial joints)

Pronators : Pronator Teres & Pronator Quadratus
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Supinators : Supinator (Synergist) & Biceps Brachii (Main)

Q6. In the human lung, the alveolar surface is composed of two main cell types.

Compare briefly the metabolic functions and capabilities oftype I and type II

pneumocytes.

Type I Pneumocyte Type II Pneumocyte

Flat, small cells (Squamous) Large cells (Cuboidal)Unable to repair or regenerate (Because itcannot replicate)

Able to repair and regenerate

Responsible for gas exchange in the alveolus(Because its oxygen consumption is nearly

zero)

Produce surfactant which helps to reducesurface tension of the alveolus

Q7. Draw and label a myocardial pacemaker potential. Relate each phase to the

corresponding change in ion conductance.

SA node is the cardiac pacemaker Resting potential : About -55mV (Since the fast Na+ channel only active at around -

60mV, therefore it is inactivated in SA node)

Na+ slowly gets into the fibre, thus depolarising it towards the threshold which is -40mV

Once it achieves the threshold, slow Ca2+/Na+ channel opens, leading to action potential

of SA node

After about 200msec, Ca2+/Na+ channel closes and K+ leak channel opens

K+ leaves the cell and leading to repolarisation of SA node to its resting potential (-

55mV)

Q8. Describe the cardiac actions of the neurotransmitters noradrenaline and acetylcholine.

Noradrenalin (NA) Comparison Acetylcholine (ACh)

Adrenergic (Beta 1 receptor) Receptor Cholinergic (M2 receptor)

Adenylate cyclise (IncreasecAMP production)

2messenger Adenylate cyclise (DecreasecAMP production)

Sympathetic Type of ANS Parasympathetic

Increase heart rate

Open Ca2+/Na+ channels

Ca2+/Na+ enters

Depolarise

Bring the base (-55mV)

Effect on SA node Reduce heart rate

Open K+ channels

K+ leaves cardiac cells

Hyperpolarise

Bring the base further away


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closer to threshold (-40mV),

thus making SA node fasterto be depolarized

from the threshold, thus

making SA node harder tobe depolarized

Increase contractility

Increase permeability ofcardiac cells to Ca2+

Increase Ca2+ influx

Effect on Atria Reduce contractility

Reduce the cAMPproduction

Q9. Compare and contrast the pressure differences in the systemic and pulmonary

circulations, accompanied by numerical values.

SYSTEMIC CIRCULATION: circulation of oxygenated blood from the left ventricle of the

heart to the various tissues and of venous blood back to the right atrium of the heart, is high

pressure circulation PRESSURES INVOLVED:

SYSTEMIC PRESSURES SYSTOLIC/DIASTOLIC NOTES

Systemic blood pressureaorta 120/80mmHg SBP mainly determinedby CO

DBP mainly determined

by Total Peripheral

Resistance

Pulse pressure (PP) 40mmHg SBP-DBP

Mean Arterial Pressure

(MAP)

93mmHg =DBP + 1/3PP

Pressure in capillary beds 17mmHg

Right Atrial Pressure

(RAP) and vena cava

0mmHg (range= 0-

4mmHg)

RAP~JVP~CVP

So people measure JVP

height to reflect venous

return/ hydration state

(i.e. as blood volume also

affects v.return) and

assess cardiac function

Raised JVP>2cm = right

side HF

PULMONARY CIRCULATION: Flow of blood from the right ventricle of the heart through the

blood vessels of the lungs and back to the left ventricle of the heart, is low pressure

circulation

PRESSURES INVOLVED:


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PULMONARY PRESSURES SYSTOLIC/DIASTOLIC NOTES

Pulmonary Artery 25/10mmHg

Pulse pressure 15mmHg SBP-DBP

Mean pulmonary artery P 15 mmHg DBP + 1/3 PP

Pulmonary capillaries ~7 mm Hg

Pulmonary venous P ~ 2 mm Hg (2-6)

Left atrial pressure ~2-6mmHg Falls to ~0 in cardiac cycle

Raised in Left Heart Failure

Pulmonary Capillary wedge

pressure (PWP)

~7 mmHg

A lil above LAP

-pressure measured in a

pulmonary artery after

occlusion of that artery.

-provides an indirectmeasure of the left atrial

pressure.

- measured by a catheter

wedged into the distal

pulmonary artery

-usually real LAP


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Blood O2 content is actually increased but none are being delivered to the tissuesQ12. Describe the effects of different levels of exerciseon heart rate, stroke volume

and cardiac output quoting approximate values.

Sympathetic cholinergic nerves are activated even before the exercise begins

Lets say initial HR=70bts/min, SV= 70mL/beat, so CO= 4.9L/min

When the exercise begins, sympathetic cholinergic nerves are activated by psychic

stimuli, central command, muscle ergoreceptor, joint receptor

These increases HR=200bts/min, SV=150mL/beat, so CO=30L/min

As exercise intensity raises eg by training, HR maintains at 200bts/min, CO and SVvaries at values that agrees with CO=HR X SV

In moderate exercise, HR increase by 200% (140 bts/min), SV increase by 120%(85mL/beat), CO increase by 240% (12L/min)

In severe exercise, HR increases by 300% (200bts/min), SV increases by 175%

(125mL/beat), CO increases by 500% (25L/ min)

In athletes, max CO=35L/min, max HR 200bts/min, SV=175mL/beat

Training does not affect:

- maximum heart rate

- diffusion capacity

- hemoglobin content

- resting CO

-

VO2 at rest

Training causes:

- reduced heart rate training bradychardia

- increased resting stroke volume

- increased SV, CO, VO2max, VE max

- increased O2debt, anaerobic threshold

-

increased oxidative and glycolytic capacity- increased capillary density

-

increased muscle fibre length type 12 transitionQ13. Explain why the combination of nitrates and beta blockers may be more

effective than either alone in treating a patient with angina.

Continuous exposure to high doses of nitrates can cause tolerance and marked

reduction in pharmacological effect, therefore need nitrate free period every

24hours

Nitrates causes extreme hypotension with phosphodiesterase-5 inhibitor such as

Sildenafil

Most beta blockers are cardioselective but not cardioselective at high doses

Both drugs treat angina using different mechanism nitrates work by increasingblood supply to myocardium by causing vasodilatation of large coronary arteries,

while betablockers work by decreasing myocardial O2 demand by decreasing heart

rate, blood pressure and contractility

Q14. Describe the difference between the two types of blockers of the rennin

angiotensin system with reference to:

a) Mechanism of action

b) Efficacy in treating blood pressure.


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c) Production of dry cough

Angiotensin Converting

Enzyme (ACE) inhibitorAngiotensin II antagonist

a Inhibits ACE, hence blocks the conversion

of Angiotensin I to Angiotensin II,therefore:

- reduces circulating AT II levels. This

causes a decrease in peripheral vascular

resistance, decreasing afterload.

- prevents release of aldosterone , hence

sodium and water retention, decreasing

preload

- decreases SNS activity (blocks release of

Noradrenaline)

- potentiate effect of diuretics in heart

failure

ACE is one of the kinases that break down

bradykinin, inactivating it. Therefore, ACE

inhibitor activates bradykinin. Bradykinin

causes vasodilation, decreasing afterload.

It blocks the angiotensin II receptors:

- AT1Areceptor (at the blood receptors)

causes vasodilation, decreasing afterload.

- AT1Breceptor (at the adrenal cortex and

pituitary gland) causes reduced secretion of

aldosterone and vasopressin, reducing

preload.

Combined effect of this causes reduction of

blood pressure

b Presumably ACE inhibitor has greater efficacy in treating high blood pressure since it acts

on the earlier part of the RAA system, hence inhibiting much more downstream effects of

the system. In addition, it also acts on bradykinin in which Angiotensin II antagonist does

not act on.

c Bradykinin is also thought to be the cause

of the dry cough in some patients on

angiotensin converting enzyme(ACE)

inhibitor drugs. This refractory cough is a

common cause for stoppingACE inhibitor

therapy (wiki)

Presumably, it does not cause dry cough

since it does not any effect on bradykinin.

Q15. Explain the advantages of inhaled therapy over systemic therapyin the

management of asthma and chronic obstructive airways disease. COPDFaster (in reaching the target site), hence

speed relief of symptoms.

Directly goes into the airway

Limits the numbers of area in the body

exposed to the medicine and. For example,

using inhaled B-blockers in asthma treatment

can avoid the B-receptors elsewhere e.g.: B-

Reduce the risk of systemic side effects
http://en.wikipedia.org/wiki/Angiotensin_converting_enzymehttp://en.wikipedia.org/wiki/Angiotensin_converting_enzymehttp://en.wikipedia.org/wiki/ACE_inhibitorhttp://en.wikipedia.org/wiki/ACE_inhibitorhttp://en.wikipedia.org/wiki/ACE_inhibitorhttp://en.wikipedia.org/wiki/ACE_inhibitorhttp://en.wikipedia.org/wiki/Angiotensin_converting_enzyme


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-but compressed by alveolar air pressure

(PALV = atmospheric = 0mmHg)

On Standing

The effect of gravity is it exerts hydrostatic pressure which influences

pulmonary blood flow within the alveolar capillaries

blood pressure is reduced above cardiac level (0.74mmHg per cm; lung

about 30cm high: so 22mmHg difference, base to apex)

Apex of lung is -14; base is +8 mmHg relative to cardiac level

This develops three possible zones in lung in relation to the blood flow in the

alveolar capillaries within lung at respective zones

Three Possible Zones in lungs

Zone 1 (at apex)

No flow

capillary systolic P less than alveolar.

but only under abnormal conditions, e.g. very low pulmonary

systolic pressure (e.g. due to blood loss) - no flow at apex.

Zone 2

intermittent flow

- capillary diastolic pressure less than alveolar

(at apex: 10-14= -4 mmHg)

Zone 3(at base)

continuous flow

- capillary diastolic pressure more than alveolar (most of lung).

Q.3: A 30 year old is investigated following a mini-stroke and found to have a

patent foramen ovale on echocardiogram. Describe the right atrium, including the

main internal features. Add a note on the development of the interatrial septum.

Answer: (CVR 22)

Two parts

Anterior

Rough surface contributed owing to the Pectinate Muscle

Includes atrial apendage

Posterior

Smooth


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The two parts are separated by Crista terminalis internally and sulcus terminalis

externally

Receives blood from SVC and IVC and coronary sinus

At the lower end of the crista terminalis, are two non functional valves of IVC and

coronary sinus which guard the orifices of these vessels

Valve of IVC is continuous with the limbus edge of fossa ovalis

Fossa ovalis= a cresentric ridge on atrial septum marking site of prenatal foramen

ovale (by which means blood pass from right to left atrium bypassing nonfunctional

lungs)

Outflow valve to right ventricle= tricuspid

Atrial septum

Thicker part of it is formed from embryological septum secundum and ends at the

limbus of fossa ovalis

while the thinner part in the floor of the fossa is formed by septum primum

two septa normally unite, crista terminalis marks the junction between the 2

embryological parts of RA.

Q.4: A patient is found to have a pulmonary embolus following a long-haul flight.

Describe anatomical and physiological dead space and explain how an embolus

affects the physiological dead space. Answer: (CVR 34&35)

Dead space:

dead space air is air that does not take part in exchange with the blood

of the 500 ml inspired with each breath, only 350 ml enters the alveoli for exchange

the rest (150 ml) occupies the dead space in the mouth, nose, pharynx, trachea etc

and does not exchange with the blood

anatomical dead space:

volume of the conducting airways,

decresed by a tracheostomy and increased by breathing through a tube

measured by Fowlers method

physiological dead space:

is this plus air in alveoli that does not exchange with blood

may increase in respiratory disease (e.g. obstructive/ interstitial lung disease).

measured by Bohrs method:

o VD is calculated by measuring the % CO2 in alveolar and expired air and

measuring the gradient

o all of the expired CO2 comes from the VA and none from the VD (which

contains atmospheric air which has no CO2)

o therefore VT X FE = VA x FA

o but VT = VA + VD so VA = VT - VD


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o

so VT X FE = (VT - VD) x FA

o so VD = VT X [(FA - FE)/ FA]

normally, the volumes are almost the same

and explain how an embolus affects the physiological dead space

During PE, embolised part of the lung ventilated but not perfused. So unperfused paart of

alveoli no longer able to expire CO2 to air.

i.e. increase in area of lung that gets air without air exchange occurring.

So physiological dead space increase in this case.

Extra: respiratory symptom of PE:Acute respiratory consequences of PE include increased

alveolar dead space, pneumoconstriction, hypoxemia, and hyperventilation. Later, 2 additional

consequences may occur: regional loss of surfactant and pulmonary infarction. Arterial

hypoxemia is a frequent but not universal finding in patients with acute embolism. The

mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts,reduced cardiac output, and intracardiac shunt via patent foramen ovale. Pulmonary

infarction is an uncommon consequence because of the bronchial arterial collateral

circulation

Q.5: A thirty-five year old man with a history of myocardial infarction and severe

familial hypercholesterolaemia is started on Atorvastatin and Gemfibrozil. Write

short notes on the potential benefits and risks of this therapy. (CVR20)

Atorvastatin is an HMG CoA reductase inhibitors

Statins are the most effective and best tolerated agents for treating dyslipidemia

HMG CoA reductase inhibitors are the most potent drugs at reducing LDLcholesterol (Strongly associated with atherosclerosis and CHD events)

Competitive inhibitors of HMG-CoA reductase, which catalyzes an early, rate-

limiting step in cholesterol biosynthesis. So, inhibit the early and rate limiting step

in cholesterol biosynthesis, which results in increased expression of the LDL

receptor.

Multiple trials have shown reduction in fatal and non fatal CHD events

Other effects of Statins

Endothelial function

Plaque stability

Inflammation

Lipoprotein oxidation

Platelet aggregation Generally well tolerated

Side effects: Hepatotoxicity and Myopathy

- Hepatitis

- Muscle aches

- Myositis

- Angio-oedema

- Sleep disturbance

Gemfibrozil is a fibrate


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Fibrates are most effective at lowering triglycerides

Mechanism of action unclear, involves interaction with the nuclear transcription

factor PPAR that regulates several genes involved in lipid metabolism

Increase activity of peripheral lipoprotein lipase

Reduce VLDL production, increase hepatic LDL uptake

Statin + gemfibrozil = increased mytotoxicity: Gemfibrozil, the drug most commonlyassociated with statin induced myopathy (GI disturbance and increased liver

enzyme)Other common side effects: nausea, skin rash, GIT disturbance, vommitting, diorrhea

Q.6: An individual has their blood pressure measured as 125/80 mmHg. Calculate

pulse pressure and estimate mean blood pressure and explain your reasoning. What

values would you estimate for left ventricular pressure in this individual

(systolic/diastolic).

blood pressure measured as 125/80 mmHg.

(Systolic BP determined by Cardiac output ,

Diastolic BP mainly by Total Peripheral Resistance)

Calculate pulse pressure :

(SBP DBP); 125 80 =45 mmHg

and estimate mean blood pressure :

diastolic + 1/3 pulse pressure = 80 + 15 = 95

What values would you estimate for left ventricular pressure in this individual

(systolic/diastolic). 125/0

Note in LVP (CVR 2):

Diastole

(i) falls to 0mmHg (diastolic recoil-enlarging the chamber - more than

counteracts filling from atrium

(ii) rises slowly as blood flows from atrium into ventricle (atrium has filled with

blood during ventricular systole)

(iii) ventricular pressure rises as atrium contracts and expels blood into

ventricle (a)

Systole Initially Isovolumetric Contraction of ventricle. Pressure rises rapidly - AV

valve closes (can't alter blood volume of ventricle until aortic valve opens) -

pressure rises until higher than aortic (~80mmHg) - aortic valve opens -

blood expelled.

Period of Ejection - until aortic valve closes.


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Isovolumetric Relaxation - as ventricle relaxes - pressure falls - aortic valve

closes (as blood in aortic pushes back) - pressure falls until AV valve opens -

fills with blood from atrium next cycleQ.7: You are called to examine a gentleman with a respiratory tract infection in the

middle lobe of his right lung. What are the surface markings of the right lung

including the fissures? Where would you place your stethoscope to auscultate the

right middle lobe?

Lung apex and its pleura extend 2cm above clavicle into the neck and the lower border

varies during breathing.

In forced expiration: (T8 median and T9 lateral)

In forced inspiration (T9 median and T12 lateral)

Right lung has 3 lobes, upper middle and lower that are demarcated by fissures:

Oblique: spine of vertebra T2/T3 to 6thcostal cartilage

Horizontal: level of 4thCC, sternal edge to the point where it meets the line of

oblique fissure.

Auscultate right middle lobe On anterior chest wall, place stethoscope at the right side and in the axilla

Q.8: A 75 year old ladys blood pressure is found to be elevated on two separate

occasions (180/105 mmHg). Describe the mechanism of action of a drug class that

you would use as your first choice to lower her blood pressure. If her blood pressure

improved but did not reduce to optimal levels of


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The preferred combinations in the general hypertensive population are represented as

thick lines.

The frames indicate classes of agents proven to be beneficial in controlled intervention

trials

Q.9: Flow-volume curves are very useful in the diagnosis of respiratory disease.

Draw and describe a normal flow-volume curve.

FVC:

Flow volume curve is a graphic plot that provides useful information about lung

functions and the relationship between lung volume and maximal rate of airflow.

This is achieved during inspiration and expiration using maximum effort against

relevant lung volumes.

A normal flow-volume curve

Peak

Expi

rator

y

Flow Rate is the highest flow rate achieved

during a maximal expiration and occurs at the beginning of expiration near

Total lung Capacity

The flow-volume curve during a normal inspiration and expiration (tidal loop), and

subsequently recorded during forced in- en expirations serve to demonstrate the

considerable ventilatory reserves available to a healthy subject. Compared to resting

ventilation inspiratory and expiratory flows can still be considerably increased.

During exercise the level of ventilation can be increased by greater inspiratory and

expiratory flows, as well as by increasing tidal volume and respiratory rate. In


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Q.12: A 30 year old male is stabbed in his axilla; he is brought to the Accident &

Emergency Department with profuse bleeding and a rapidly falling blood pressure.

Describe the course of the axillary artery,including its parts, branches and relations

to the brachial plexus.

Axillary artery

Is a continuation from subclavian artery

Starts at lateral border of 1strib until the lower border of teres major

is divided in to 3 parts by the pectoralis minor muscle

branch of 1stpart (medial to pectoralis minor)supreme/highest thoracic

branch of 2ndpart (behind pec minor)

thoracoacromial : supply upper chest and acromial region, breast

lateral thoracic : to breast and chest

branch of 3rdpart (between pec minor and lateral border of teres major)

subscapular : to scapular muscles, scapular anastomosis

anterior circumflex humeral

posterior circumflex humeral

Axillary artery passes between the lateral and medial cords of the plexus. The medial root of

median nerve crosses the axillary artery to unite with the lateral root to form the median nerve

which is lateral and anterior to the axillary artery.


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Q.13: Briefly describe the ventilatory responses to hypoxia and hypercapnia.

Hypoxia: PO2 less than normal

Hyeprcapnia: PCO2 greater than normal

These conditions will be detected by peripheral arterial receptors.

This stimulates the respiratory centre causing an increase in breathing hence increase PaO2

and decrease in PaCO2 (i.e. negative feedback control mechanism)

Central chemoreceptors are also triggered by increase in brain ECF PCO2 and H+ but not by

decrease in PO2.

This causes ventilator response to increase ventilation and remove more CO2.

Q.14: A man falls on his outstretched hand. Explain the likely consequences of this

injury. Describe the boundaries and contents of the anatomical snuff box.

Fall on outstretch hands:

Fractured clavicle

Colles fracture (of the distal radius)(presentation: dinner fork deformity)

Fractures scaphoidtenderness in anatomical snuffbox

Bennets fracture: fracture of first metacarpal (presentation: thumb is pronated

to bring it into opposition w/ non-displaced palmar fragment)

Dislocated lunatemedian nerve injurycannot abduct hands against resistance (abductthe thumb at right angles to the palm with fingertips in contact and forming a pyramid.)

Mid-shaft humeral fracture : radial nerve damage(presentation: cannot extend radial3.5 fingers , test: no sensation on skin over 1stdorsal interosseous muscle )

Anatomical snuffbox:

Boundaries: Ulnar: tendons of extensor pollicis longusRadial: tendons of Extensor pollicis brevis

deep/ floor on the radial side: tendons of abductor pollicis longus

Contents: radial artery

Q.15: Beta-blockers are an important group of drugs that are widely used in clinical

practice.

[a] Briefly explain their classification based on their action on beta receptors

providing one example of a drug on each;[b] List three clinical conditions in which the use of beta-blockers is indicated and

describe the mechanism of action of the drug in two of these three examples.

Non-selective; Propranolol, : binds on bot B1 and B2 receptors

1 selective;Atenolol :only bind to B1 receptor


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2007 ( repeat )

1. A 48 year old man complains of central chest pain. Describe or draw the arterial

blood supply of the heart, adding a note on its venous drainage. Add a brief note

on the embryology of the right atrium.

2. With the aid of a diagram, illustrate and explain the changes in left ventricularpressure during the cardiac cycle. Also, indicate when the AV and aortic valves are

open.

3. A 23-year-old woman is using salbutamol inhaler for frequent attacks of asthma.

a). How does salbutamol provide relief in such attacks?

b) Suggest three side effects that may occur with the long-termuse of

salbutamol.

c) If the patient is not well-controlled on salbutamol, name one drug that can be

co-administered.

4. Describe the boundaries and contents of the carpal tunnel. What is carpal tunnel

syndrome and what are the likely causes and consequences?


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5. Heterozygosity for the condition of familial hypercholesterolaemia (FH) has a

frequency of about 1/600 in the general population. What is the molecular defect

underlying this condition. State whether you think it would be responsive to statin

therapy, giving reasons for your answer.

-rare genetic disorder characterised by very high LDL cholesterol and early cardiovascular

disease running in families.

-mutation in either the LDL receptor or the ApoB100 protein

-defects in the cell surface receptor that normally removes LDL particles from the blood

plasma.

-In heterozygous FH, only one of the two DNA copies (alleles) is damaged, and there will be

at least 50% of the normal LDL receptor activity

-Heterozygous FH can be treated effectively with statins. These are drugs that inhibit the

body's ability to produce cholesterol by blocking the

enzyme hydroxymethylglutaryl CoA reductase (HMG-CoA-reductase) in cholesterolbiosynthesis.

- Maximum doses are often necessary.

-Statins work by forcing the liver to produce more LDL receptor to increase clearance of

LDL

-therefore statin can reduce the bodys cholesterol level.

6. A young tall and thin male presents with sudden onset of unilateral chest pain and

progressively increasing breathlessness. Chest X-ray confirmed the diagnosis of

pneumothorax.

a) Describe the various pressures acting on the wall of the alveoli.

b) What is tension pneumothorax and what are its cardiovascular consequences?

tension pneumothorax is a worsening condition of a simple pneumothorax associated with

the fromation of a one-way valve at the rupture site. during inspiration, pressure in the

thorax decrease, and air is sucked into the pleural space htrough a one-way valve. however,

during expiration, the pressure created to force air out of the pleural cavity is insignificant.

over time, air accumulates in the pleural cavity, and this creates an increasing amount of

pressure in the thorax. subsequently, the pressure will compress the mediastinum and the

heart, reducing the amount of diastolic filling of the ventricles. as a result, cardiac output

will decrease.


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7. A 45 year old lady is diagnosed with breast carcinoma. Describe the position,

blood supply and lymphatic drainage of the breast.What are the signs of breast

carcinoma?

-blood supply: internal thoracic artery

lateral thoracic artery(branches of axillary artery),

thoracoacromial artery,

and posterior intercostal arteries

-position:2nd rib to 6th rib, 2/3 lies on pect major and

1/3 on the serratus anterior, only lies in superficial

fascia

-lymphatic drainage: mainly to axillry lymph nodes,

some goes to parasternal nodes and along intercostal

artery vessels

sign of breast carsinoma: lump on the breast, dimpling sign, and swollen of the lymph nodes

at axillary region.

8. With the aid of a diagram, describe the changes in membrane potential occurring

in a myocardial SA node pacemaker cell during a normal cardiac cycle, and the ion

channels involved.

SA nodal action potentials are divided into three phases. Phase 4is the spontaneous

depolarization (pacemaker potential) that triggers the action potential once the membranepotential reaches threshold between -40 and -30 mV). Phase 0is the depolarization phase of the

action potential. This is followed by phase 3repolarization. Once the cell is completelyrepolarized at about -60 mV, the cycle is spontaneously repeated.


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The changes in membrane potential during the different phases are brought about by changes inthe movement of ions (principally Ca++and K+, and to a lesser extent Na+) across the membrane

throughion channelsthat open and close at different times during the action potential. When achannel is opened, there is increasedelectrical conductance(g) of specific ions through that ionchannel. Closure of ion channels causes ion conductance to decrease. As ions flow through openchannels, they generate electrical currents (i or I) that change the membrane potential.

9. Briefly describe how the elastic properties of the lung and chest wallcan

influence the effectiveness of ventilationand the efficiency with which ventilation is

performed.

10. A patient is suspected of having a right lung pulmonary embolism seven days

post- operatively. Describe or draw the structures in the hilum of the right lung,

including the arteries, veins and lymphatics. Which nerve travels anterior to the

hilum, and which nerve travels posterior to the hilum?

-Hilum is where the root of the lung enter and leave the lung. It consists of pulmonary

artery, bronchial vessels, pulmonary vein, bronchus, lymphatics and nerve.

-In the right hilum, bronchus is situated posteriorly. Bronchus is cartilages. Bronchus of the

right side gives it branch of superior lobe branches in the root, unlike on the left which

branches within the lung itself.

-Pulmonary artery is superiorly at the hilum. Its is longer than the left. It carries

deoxygenated blood from right ventricle to the lung.

-pulmonary vein is anterior and inferiorly. It carries oxygenated blood to the left atria.

- lymphatics system in the lung is drained into tracheobronchial nodes around the root of

lobar and main bronchi and along the trachea. It is then drained into mediastinal nodes atposterior mediastenum and to the thoracic duct.

- the nerve travel anteriorly to the hilum is the phrenic nerve.

-the nerve travel posteriorly to the hilum is the vagus nerve.

11. Two individuals plan to perform heavy exercise. Person A is a well-trained athlete

having a resting heart rate of 50 beat per minute. Person B does not perform

regular exercise and has a resting heart rate of 80 beat per minute.

A) Explain why it is advantageous for Person A to have a slower resting heart rate

than person B?

B) Discuss the cardiac adjustments that will occur as the two individuals perform

the planned heavy exercise.
http://www.cvphysiology.com/Arrhythmias/A019.htmhttp://www.cvphysiology.com/Arrhythmias/A019.htmhttp://www.cvphysiology.com/Arrhythmias/A019.htmhttp://www.cvphysiology.com/Arrhythmias/A007a.htmhttp://www.cvphysiology.com/Arrhythmias/A007a.htmhttp://www.cvphysiology.com/Arrhythmias/A007a.htmhttp://www.cvphysiology.com/Arrhythmias/A007a.htmhttp://www.cvphysiology.com/Arrhythmias/A019.htm


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A) - slower resting heart rate would meant less work for the heart to pump the same or

greater amount of blood for the tissue all over the body.

-Person A has larger cardiac output if compared with person B.

- The circulatory system is able to provide increase cardiac output for delivery of oxygen

and other nutrients to the muscles during exercises.

- Therefore it can give the strength for the muscles themselves in setting the limit for

continued muscle work.

B) The sympathetic effect and decrease in parasympathetic affect which results in

- increase heart rate and increase pumping to deliver blood.

-most of the arterioles of the peripheral circulation are highly contracted, exceptthe arterioles in the active muscles. Its aim is to supply more oxygen to the

active muscle.

-contraction of vein increases mean systemic filling pressure. It is then

promoting the increase in venous return in the blood to heart, therefore

increase cardiac ooutput.

All the effect eventually increase the arterial pressure from normal 100mmHg up to 130-

160 mmHg during exersice ,which means more force to pull the blood to the muscle tissue

during exercise.

Long term increase workload without excess load of the heart cause increases mass andcontractile strength for the heart. This result in cardiac muscle hypertrophy and therefore

increase cardiac output.

(guyton&hall chapter 21-total body circulatory readjustment during exercise)

12. A sixty year old male has had one episode of sudden cardiac death and a five year

history of heart failure secondary to ischaemic heart disease. Write short notes on

the optimal pharmacological approach to treating this patient.

1st,ischeamic heart disease means heart does not get enough 02..so we

need to give 02 to heart

by...increase preload BUT decrease the contraction of heart musle( as

blood will go to coronary circ. when heart relax)

so, i suggest we give beta blockers(hydralazine,to reduce

contraction)... also give nitrate like Isosorbide dinitrate,because hydralazine work best with

nitrates...then we give LOOP DIURETICS( e.g furosemide) which has an effect at preload

furosemide will acutely increased


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13. A footballer dislocates his shoulder during a football match. Describe the anatomy

of the shoulder joint, naming the structures which contribute to its stability. What

nerve may be damaged by a dislocated shoulder and what are the motor and sensory

tests for this nerve?

Shoulder joint (glenohumeral joint) -articulation btw scapula and humerus, sacrifices

stability for mobility

-unstable coz glenoid fossa is shallow

Structures contribute to stability:

- Rotator cuff muscles:

Teres minor (most posterior)

Infraspinatus

Supraspinatus

Subscapularis (most anterior)

1st 3 attach to greater tuberosity Humerus, Subscapularis on lesser tuberosity

- Glenohumeral ligaments

-Dislocated shoulder can damage Axillary nerve

-Tests:

- Motor: shoulder abd

14. A patient with chronic obstructive pulmonary disease (COPD) is given some

additional oxygen to breathe to try and improve the arterial blood PO2. Suddenly,the patient stops breathing. Explain why.

COPD would give rise to asphyxia where pO2 of O2 is low and the pCO2 is high.

This is a type 2 respiratory failure which is hypoventilation.During asphyxia, ventilation is

adjusted accordingly to adapt to hypercapnia but it does not counter hypoxia. During

asphyxia, ventilation is dependent on hypoxic reflex from the peripheral receptors. By

giving oxygen, it eliminates this reflex action which causes apnoea. Hypercapnia also

inhibits the nervous system and induces coma. Over dosage of oxygen given to a type 2

respiratory failure would even cause CO2 retention.

15. Describe how coronary blood flow varies with the cardiac cycle. Illustrate your

answer with a diagram.


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JC1 examinations (January 2008) Question 4

What are the physiological mechanisms for generating the resting membrane potentialin a

typical neurone?

A membrane potential is generated by separation of opposite charge across plasma membrane ofneuroneMain ions involved are K+, Na+ and large protein anions (A-)Establishment of concentration gradients for K+ and Na+ are by sodium-potassium ATPase


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JC1 HIS module short-notes paper January 2008

Question 1

Mary is a 52 year old lady recently diagnosed with breast cancer. Her left upper limb has

become noticeably swollen in the last month. How might this be related to her breast

cancer? Add a note on the structure of a lymph node.

The breast drains to the axillary (armpit/upper arm) lymph nodes thus cancer cells may spread

here from the breast & cause enlargement of the nodes, blocking lymphatic drainage from thearm.

Structure of lymph node:

A lymph node is surrounded by an outer capsule (collagen)septae (trabeculae) radiate into thegland from this capsule. Multiple lymphatics may enter a gland, a single efferent lymphatic willexit.

Within the gland, there is an outer cortex and an inner medulla.The cortex contains B cells, while the underlying paracortical areas contain T cells.

Following stimulation, clusters of B cells (follicles) may have a germinal centre.The medulla contains cords of tissue surrounding sinuses and is largely populated by plasma cells

(active B cells).

Question 2Briefly describe the structural changes that occur in hemoglobin on oxygen binding. How

do these changes affect hemoglobins affinity for oxygen, and how does this relate to

hemoglobins physiological role?

Haemoglobin is a tetrameric molecule with 4 polypeptide chains, 2 alpha ()chains and 2 beta ()chains. Each chain carries one haem moiety and can bind one molecule of oxygen. The overallstructure can be thought of as a dimer of dimers of the form ()

2, with strong non-covalent

bonds within the dimers, and weaker non-covalent bonds between them. It is primarily the bonds

between the dimers that are affected by oxygen binding. DeoxyHb has a taut structure withrelatively strong bonds between the dimers. When oxygen binds to deoxyHb a conformationalchange occurs that breaks some of the ionic bonds between the dimers, resulting in a structurallyrelaxed form of Hb. The conformational change occurs due to changes in the electronicconfiguration of the haem iron, which causes the iron to move more into the plane of the haem

ring structure, moving the proximal histidine and helix F to which it is attached.3 JC1 examinations (January 2008)


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The relaxed form of Hb has a higher affinity for oxygen that the taut, deoxy- form. This change inaffinity on oxygen binding means that oxygen binding to Hb is cooperative, and results in a

sigmoid oxygen binding curve. This has the effect of allowing almost twice as much oxygen to bedelivered to the peripheral tissues than would be the case if oxygen binding was not cooperative.The affinity of Hb for oxygen is also affected by other allosteric modulators, including CO2, pHand 2,3-BPG, all of which enhance Hbs physiological role by increasing the amount of O

2

released at the peripheral tissues, while not compromising the ability of Hb to bind O2

in the

lungs.

Question 4

Name 3 ways in which the intact endothelium of a blood vessel regulates thrombosis. For

one of these, describe how drugs are used to target this area.In general the intact endothelium prevents unwanted thrombus formation. It does this in a number

of ways:1. it synthesizes and secretes, in a tonic fashion , Nitric Oxide (NO); which inhibits platelet

activation by elevating intracellular cGMP levels

2. it synthesizes and secretes, in a tonic fashion , prostacyclin (PGI2); which inhibits platelet

activation by elevating intracellular cAMP levels.

3. Intact endothelial cells express heparan sulphate, a proteoglycan on their surface. Thisinhibits any unwanted, or inappropriate, activation of thrombin and Factor Xa,

thereby preventing the formation of fibrin. In other words an intact endothelial cellacts as an inhibitor of the coagulation cascade

4. Intact endothelial cells express tissue-Plasminogen-Activator (tPA) on their surface. Thisdegrades any unwanted, or inappropriate, fibrin clot that is formed. In other wordsintact endothelial cells acts as an promotors of the fibrinolytic cascade.

5. Intact endothelial cells express Thrombomodulin on their surface. Thrombomodulin bindsto thrombin and inhibits its procoagulant effect. The TT-complex also stimulates

fibrinolysis.6. intact endothelial cells produce and secrete Tissue factor pathway inhibitor (TFPI),

which inhibits the coagulation cascade. This prevents unwanted clot formation.

7. In addition, intact endothelial cells prevent exposure of subendothelail collagen orfigrinogen and thereby prevent platelet adhesion and thrombus formation.

8. it can also be considered that intact endothelia prevent release of Tissue factor.

Any one of these pathways could be elaborated on for the second half of the question. The twothat I most expect to see are :tPA- recombinant tPA is used therapeutically to degrade thrombi. It works by activating

plasminogen, which degrades fibrin polymers.Heparin, derived from beef lung or from porcine intestinal mucosa, is a therapeutic agent thatmimics the expression of heparan sulphate on the surface of intact endothelia. It is used to preventunwanted or inappropriate clotting in patients at risk of thrombosis or during thrombosis. Theseinclude patients who are immobilized following surgery and patients with recent myocardial

infarcts. It acts by binding with plasma antithrombinIIII, increasing its capacity to inhibitthrombin and the coagulation cascade.

Obviously drugs which target any of the other pathways identified above are also acceptable suchas NO-donors (inhibit platelet activation in addition to causing vessel dilation), Dipyridamole,inhibits platelet activation by elevating intrcellular cAMP.

Antithrombin drugs in general would also be acceptable as these inhibit the coagulation cascade.4 JC1 examinations (January 2008)


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JC1 NE module short-notes paper January 2008

Question 5

Describe cell membrane proteins and outlinehow they are involved in moving molecules

back and forth across the cell membrane. Discuss the requirements of energy in these

processes.

Answer: There are a variety of proteins that are found in the cell membrane. There are anchoring

proteins which attach cell membranes to each other or to internal or external structures.Recognition proteins also known as identifiers, identify the cell and prevent attack by immunesystem. Enzymes found in the cell membrane catalyse either intracellular or extracellularreactions. Specific ligands found in the extracellular matrix bind to receptor proteins on themembrane surface and in doing so send signals into the cell. Leak Channels permit continuousmovement of water and ions while gated channels close or open to regulate ion movement. It is

the carrier proteins that are primarily involved in the movement of molecules across themembrane and in doing so may require an energy source such as ATP. Transport of molecules

across a membrane requiring energy occurs against a concentration gradient. This form oftransport is known as active transport and there are 3 types: primary active transport, secondary

active transport and group translocation. An example of active transport is the Na+ K+ pump.This pump uses 1 molecule of ATP to transport 3 Na+ ions from the inside of the cell to the

outside with the subsequent transport of 2 K+ ions from the outside of the cell to the inside. Anexample of secondary active transport is the transport of glucose into the cell. Glucose can betransported into the cell only after Na+ has bound to the transport protein. In 3 cycles, 3 glucose

molecules and 3 Na+ are pumped into the cell. The Na+ is then pumped out via the Na+/K+pump with the expenditure of 1 ATP. In group translocation a sugar is phosphorylated as it istransported across the membrane. An example of this is the phospho-transferase system (PTS),

where the source of energy is phosphoenolpyruvate.

Question 6

Hyperphenylalaninaemia (PKU)is one of the more common inborn errors of metabolism in

Ireland. What is PKU and how may it be diagnosed

What is PKU?

_Autosomal recessive inborn error of phenylalanine metabolism

_~ 97% of case in Ireland due to mutation in gene which code for

the enzyme Phenylalanine Hydroxylase (PAH) and ~ 3% due to Mark >1

defective synthesis of the PAH enzyme cofactor, tetrahydrobiopterin

_Clinical Phenotype and management depends of residual PAH enzyme activity

_Phenylketonuria (PKU)

phe>600mol/L

o PAH deficiency

o DHPTR deficiency

_Hyperphenylalaninaemia Not required by pass students

phe >180 mol/L


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How may it be diagnosed? Newborn screen (Heel-prick / Guthrie) test and biochemical analysis of blood

phenylalanine levels

Question 8

Discuss the central role of the TCA cycle (Krebs cycle) in metabolism.

The TCA cycle is cyclical biochemical pathway which begins with the joining of oxaloacetateand acetylCoA to form citric acid, cycles through various intermediates and regeneratesoxaloacetate by the dehydrogenation of malate. The cycle serves two main purposes inmetabolism:[1] It provides most of the cells energy by extracting it from Acetyl CoA in the form of GTP and

NADH (which is fed into the electron transport chain and oxidative phosphorylation). The

oxidative extraction of energy using the krebs cycle and oxidative phosphorylation is far moreefficient than anaerobic glycolysis, yielding 38 molecules of ATP as opposed to 2 for glycolysis

alone. The acetylCoA entering the TCA may come from,for example, glycolysis, via pyruvatedehydrogenase or from the beta-oxidation of fatty acids. Allosteric control of TCA enzymes is

also an important factor in the overall control of energy metabolism[2] It provides intermediate molecules which are converted into a number of other important

molecules for the cell. For example alpha-ketoglutarate is converted via transamination to theamino acid glutamate, which further yields proline and glutamine; oxaloacetate is likewiseconverted to aspartate which further yields asparagine. In addition, the breakdown products of

many compounds enter energy metabolism via the TCA, notably the carbon skeletons of manyamino acids. This is a very important process in prolonged starvation where body protein isutilized to provide glucose via gluconeogenesis.

If students want to include the complete details of the TCA cycle reactions that is worthwhile, but

it should also show something of how the cycle is interconnected with other parts of metabolism.

A1 ANATOMY

1. Describe or draw a labelled diagram of the arterial blood supply of the hand.Add a note on points of clinical significance.

2. Describe the attachments, actions, and nerve supply of triceps surae(gastrocnemius/ soleus). Add a note on clinical conditions that commonly affect

these muscles.3. Describe the ulnar nerve and its branches.Explain the condition claw hand.

4. A Outline the structures contributing to the stability of the hip joint. Add a note onpoints of clinical significance.

ORB Outline the structures contributing to the stability of the ankle joint. Add a noteon points of clinical significance.

A2 PHYSIOLOGY5. In 3 sentences of less, describe the function of the following molecules:(i) Erythropoietin(ii) Haemoglobin(iii) Thrombopoietin

(iv) Thrombin(v) Albumins6. Describe the structural and functional differences between intra- and extrafusal


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Neuromuscular blocking drugs are usedas an adjunct to anesthesia. Discuss why such

drugs are used. Which drugs are best suited to this task and describe their mechanism of

action.

Q3. Neuromuscular Module (NM)

Hypertension is treated with drugs that relax arteriolar smooth muscle, a type ofvisceral smooth muscle. Describe the differences between visceral and multi unit smooth

muscle.

2008/2009Question 4

What are the physiological mechanisms for generating the resting membrane potential in a

typical neurone?

A membrane potential is generated by separation of opposite charge across plasma membrane ofneurone

Main ions involved are K+, Na+ and large protein anions (A-)Establishment of concentration gradients for K+ and Na+ are by sodium-potassium ATPase(which moves 3Na out for 2K in). Leaves potassium concentration high intracellularly, sodium

high extracellularly and contributes a small part of negative potential.There is selective permeability of plasma membrane to K+ ions, with the negative membrane

potential driven in large part by K+ ion movement out of cells at rest via leak channels, pluspresence of large protein anions (exclusively intracellular)Resting membrane potential (approx. -70mV)

Top answers/extra credit: giving specific concentrations of Na+/K+ ions, mentioning Nernst

equation gives equilibrium potential for an ion, how membrane potential might be measured

experimentally

Question 7A patient suffering from angina is given a calcium channel blocker to reduce heart muscle

contraction. Describe excitation-contraction coupling in heart muscle.The action potential propagates along the T system which penetrates the cell at the Z lines.The sarcoplasmic reticulum of heart muscle is less well developed than in skeletal muscle, having

diads instead of triads and with only one diad or triad per sarcomere.The action potential involves calcium entry into the cell through the dihydropyridine receptor

which causes calcium release from the SR through the ryanodine receptor i.e. calcium-inducedcalcium release.The calcium is bound by troponin which results in conformational changes in the troponin-

tropomyosin complex allowing cross-bridge formation between the myosin and actin.The myosin head is in a high energy state which allows for the power stroke and the pulling of

the actin filament towards the centre of the sarcomere during which phosphate and ADP arereleased.The myosin head then binds ATP which causes release of the head, ATP hydrolysis and thereturn of the head to the high energy state for further cycles.Relaxation occurs due to pumping of calcium back into the SR and by sodium/calcium exchange

at the sarcolemma.


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NM Question

There are three types of muscle, skeletal, cardiac, and smooth in the

human body. There are many diseases associated with each of these

muscle types.a. Describe and differentiate between excitation-contraction coupling

in smooth and skeletal muscle.(2 marks)

b. Describe the distinguishing features between multiunit and single-

unit smooth muscle.(2 marks)

Model Answer

a. The two things they have in common are that they contain actin and

myosin and that they use ATP as an energy source. The differences inthe excitation is that the skeletal muscle is excited by an impulse

traveling down a neuron which transmits an action potential into the T

tubules of the skeletal muscle which then opens voltage-sensitive

channels called dihydropyridine receptors that undergo a

conformational change allowing the ryanodine receptors to release

calcium from the sarcoplasmic reticulum. So it can be described as a

structural change in order to bring about the contraction in skeletal

muscle. Smooth muscle can be excited in a variety of ways including a

nerve impulse, temperature, stretch, chemicals such as hormones orthey can be self-excitatory an example would be Interstitial cells of Cajal.

Then the excitation and coupling also involves a rise in calcium but this

time the calcium comes from the extracellular fluid as well as the

sarcoplasmic reticulum. The calcium and an intracellular calcium binding

protein called calmodulin complex and activate the myosin light chain

kinaseand this goes onto phosphorylate the myosin light chain and this

leads to a chemical change allowing the phosphorylated myosin filament

to combine with the actin filament and the muscle contracts.

b. Multiunit smooth muscle is controlled by nerve input and is well

innervated. It has well developed neuromuscular junctions and hence is

stimulated through a full action potential which goes onto to ensure a

muscle contraction. Hence, there is no spontaneous activity and there is

an absence of gap junctions in this type of smooth muscle.


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Single-unit smooth muscle is self-excitable, so it does not require

nervous stimulation for contraction so there is sparse innervation of the

tissue. The self-excitable cells of the single-unit smooth muscle do not

maintain a constant resting potential. Instead their membrane potential

inherently fluctuates without any influences by factors external to thecell. Two major types of spontaneous depolarisation displayed by self-

excitable cells are pacemaker potential is pacemaker cells and slow

wave potential in interstitial cells of Cajal. Such independent contractile

activity initiated by the muscle itself is termed as myogenic activity in

contrast to the neurogenic activity of the skeletal and multiunit smooth

muscles. The contraction is potentiated by the presence of gap junctions

and is often described as a functional syncytium. This type of muscle is

able to contract as a single-unit.

past years snq answer by rcsi

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