go back over this stuff Flashcards
Criteria to diagnose diabetic ketoacidosis
- hyperglycaemia
- low bicarb
- ketonuria
- low pH
Equation for A-a gradient
A-a gradient = 20- Pac0/0.8 - Pa02
Drugs to treat crohns disease
5-ASA - anti-inflammatories
Steroids - prednisone
Immunosupression - azathioprine
wheeze on expiration in asthma + a stridor on inspiration in extrathoracic obstruction.
Stridor is an extrathoracic obstruction, can be due to something like croup. What happens is that normally during inspiration negative pressure is generated in the airways which results in an increased tendency for the airway to collapse, given the extrathoracic pressure placed on the airway this causes airway obstruction during inspiratory phase, increased turbulence and therefore the sound of stridor heard. Expiration is passive and airway pressure is not negative therefore the tendency for the airway to collapse is reduced and no sound is heard on expiration
what are symptoms of cholangitis
- charcots triad
- fever
- jaundice
- RUQ pain
ERCP
Endoscopic retrograde cholangiopancreatography
-diagnostic and therapeutic
short term and long term response of systemic barorceptors
Systemic arterial baroreceptors are important in minimising variation in systemic arterial pressure, regulating beat-to-beat arterial pressure, and maintaining blood pressure in the short-term. The extent to which these baroreceptors regulate arterial pressure in the long-term remains controversial. Surgical denervation of arterial baroreceptors led to an increase in the variation of arterial pressure. However the average arterial pressure increased for a very short period before returning to control levels. This indicates that other mechanisms must be involved in maintaining this long-term set point.
Denervation of arterial and cardiac baroreceptors led to sustained hypertension with wide fluctuations in arterial pressure. Thus while systemic arterial baroreceptors do not set the long-term baseline, they do influence the long-term regulation of arterial pressure.
Inverted T waves
monomophic ventricular tachycardia
i) inverted T waves indicate that repolarisation is occurring in the opposite direction to normal, which can happen in ventricular hypertrophy, bundle branch block, ischaemia.
ii) The electrical activation of the ventricles is not occurring by the usual His-purkinge system, instead electrical activity is travelling from one myocyte to another. This is much slower - hence the wide QRS complexes. This can occur for example if there is a re-entry circuit within a ventricle.
clinical features of mitral stensois
Diastolic decrescendo murmur heard in the Left 5th intercostal space, mid-clavicular line. Chest X-ray = enlarged LA and pulmonary congestion
Transthoracic ultrasound = narrowed mitral valve orifice, reduced mobility of mitral valve leaflets.
Would expect reduced coronary reserve, and thus reduced exercise capacity (SOB with exertion). May see irregularity of heartbeat.
cholangitis
Cholangitis, characterised by charcot’s triad (RUQ pain, jaundice, fever). This is bacterial infection of the biliary tract as a result of obstruction. Obstruction leads to more conjugated bilirubin entering the urine instead of faeces → dark urine
How can you get arrhythmia during an acute MI?
- ATP reduces
- Redued Na/K pump
- increase in sodium inside the cell and potassium outside the cell
Slow conduction - increased extracellular K gives reduces the membrane potenital
-inactivates sodium channels and gives rise to slowed conduction
Reduce AP duration and non-uniform repolarisation - elevated ECF K - reduces AP duration in ischemic region - so get differences in repolarisation rates throuhgout the muscle tissue
After depolarisations
- reduce ATP - redceud Ca/ATPase - increase in calcium inside teh cell
- get more ca leave the cell via Na/Ca transporter
- this gets a large inward current of sodium causing an after depolarisation.
what is chest comfort caused by?
chemical, mechanical stimuli (eg K+, H+, adenosine) - sympathetic afferents / spinothalamic
- referral to somatic segments of chest & arms
Treatment for Long QT
- beta blockers
- Implatable cardioveter-defibrillator
- lifestyle modifications
what other factors can contribute to electrical instability of the heart?
Other factors that can contribute to electrical instability after MI are:
• the increased cardiac sympathetic activity that commonly occurs under these circumstances and
• possible effects of aberrant wall motion on stretch-activated channels.
• aberrant LV wall motion occurs because the mechanical function of the
ischaemic region is impaired.
• for instance, wall thinning and expansion can occur during systole in the infarct region in the presence of wall thickening over the rest of the LV.
why likely to get ectopic beats within the first 24 hours
Ectopic electrical activation (and reentrant arrhythmias) are most likely to occur in the first 24 hours after MI, because ischaemic myocytes in the region of the infarct and border zone are electrically active, though highly unstable.
• Over the 24 hours post-infarction, the affected cells either die or the ischaemia is resolved.
• NOTE: reperfusion of an infarcted region (as is now common clinically immediately after MI) increases acute electrical instability.
