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Pathology+101 Complete)

Pathology+101 Complete)

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Published by Goh Kah Yong
About everything you need that is not a bottle tute
About everything you need that is not a bottle tute

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Published by: Goh Kah Yong on Oct 04, 2010
Copyright:Attribution Non-commercial


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v1.0 For the last 2 weeks we have endured long days and sleepless nights to bring you these notes. Apologies to
future dermatologist and orthopaedic surgeons, we didn’t get to starting
musculo or skin, look out for them inthe second edition (may or may not be released next year, probably not).The main inspiration to keep us going to get these done was that Raj really needed them.
v2.0 So its 3wks in now and I’ve got an update, guess next year came quicker than expected. I know the
exam issoon but it might help. All the systems are there now and thanks to Tash we now have skin notes. Thanks toBen for his help with notes on demyelination.
The main inspiration to get this done was that Raj said he’d do dentistry if he didn’t get int
o orthopaedics.Tareq and Faran Publications, 2008
Heart failure occurs when the heart is unable to pump blood at a rate that meets the metabolicrequirements of the peripheral tissue.Compensatory Mechanisms: are triggered during reduced myocardial contractility or increasedhaemodynamic burden.
Activation of neurohormonal systems:noradrenaline, renin-angiotensin system, ANP.
Frank-starling mechanism: Cardiac failure causes
EDP resulting in increased stretch of cardiacmuscle
fibres contract more forcibly, hence
Myocardial structural changes (hypertrophy).This is an adaptation to chronic
workload and
since myocytes can’t proliferate, concentric or
eccentric hypertrophy occurs.
Adaptive mechanisms eventually aren’t sufficient with
sustained worsening of heart
pathologic changes (eg.myocyte apoptosis, cytoskeletal changes, altered ECMsynthesis) cause structural and functional disturbances.Classification: resulting failure can be classified by a variety of mechanisms:
Forward failure: diminished cardiac output, reduced tissue perfusion.vs Backward (congestive) failure: back pressure, venous congestion and oedema.
Systolic failure: inability to contract normally and expel blood.vs Diastolic failure: inability to fill ventricles.
High output failure: heart is pumping normally, however tissue demands have greatly increased.vs Low output failure: heart cannot keep pace with basic peripheral demands.
Acute heart failure: quick onset, usually systolic heart failure and hypotension but no oedema.vs Chronic heart failure: long term, often normal BP but with oedema.
Compensated heart failure: if compensatory mechanism produce sufficient COvs Decompensated heart failure: compensatory mechanisms, especially hypertrophy, increaseO
requirements, eventually leading to insufficient CO and increasing risk of ischaemic injury.
Pressure vs Volume Overload
Pressure overload state
(eg. hypertension, valvestenosis) causes increased SBP. Results in increaseddiameter of cardiac muscle (added myofibrils).
CONCENTRIC HYPERTROPHY: wall thickening withno change in chamber size.
Volume overload state
(eg. valve regurge, abnormalshunts) causes increased DBP. Results in increasedlength of muscle fibres (added sarcomeres).
ECCENTRIC HYPERTROPHY: chamber enlargementwith some wall thickening.
Left-Sided Heart Failure
More clinically significant, can be due to IHD, HHD, VHD,CMP (ie. main heart diseases). Can be further classifiedaccording to mechanisms above.Symptoms are primarily due to pulmonary congestion,oedema and ventricular dilation:
Dyspnoea, orthopnea
Cough (transudate in airway)
Tachycardia, cardiomegaly, 3
heart sound
Fine crepitant rales at lung bases (oedema in alveoli)
Mitral regurgitation (papillary muscle damage)
Atrial fibrillation (irregularly irregular heart beat)
 Right-Sided Heart Failure
Usually a consequence of left sided heart failure causingincreased pulmonary pressure. Isolated right heart failureis rare but can be due to:
Lung disease with chronic pulmonary hypertension
enlargement of right ventricle (cor pulmonale).
Congenital heart diseases with right to left shunts.Symptoms are mostly due to backward failure (congestion)causing engorgement of systemic and portal venoussystems:
Hepatic and splenic enlargement
Peripheral oedema, pleural effusion, ascites

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