Review of posters 25/04/2016 Flashcards
Treatment of angina (stable)
GTN spray for when the chest pain comes on.
Beta blockers/Calcium channel blockers
Aspirin
Treatment of unstable angina
Medical emergency- treat as you would heart attack (MONAC)
Describe the shapes abdominal aortic aneurysms can form.
Saccular- like a yolk sac
Fusiform
Mycotic (after infection)
Define a true aneurysm
One that has all three parts of the vessel wall intact.
Define a false (psuedo) aneurysm
Breach in the vessel wall
Describe the pathophysiology of an AAA
Decreased collagen and elastin in vessel walls.
Smooth muscle cell loss
Causing aortic dilatation
Lifestyle advice for angina
Encourage weight loss-eating healthily
Smoking cessation
Minimal alcohol intake
Exercise regularly
Describe the mechanism of an atrio-ventricular re-entrant tachycardia.
Accessory pathway exists. Due to the AV node holding the signal for a while and the accessory pathway not doing this, the signal from the accessory pathway passes into the ventricles before the signal down the normal route. This causes an abnormal contraction of the ventricles. Also, the signal can pass back up into the atria via the accessory pathway because it has finished its refractory period.
WOLF PARKINSON WHITE SYNDROME
Describe the mechanism of atrioventricular nodal re-entrant tachycardia
When the signal reaches the AV node- it is split into a fast pathway and a slow pathway. The fast pathway however has a long refractory period where as the slow pathway has a short refractory period. Normally, the signal would be split, the fast pathway would transfer the signal down to the Purkinje fibres and enter the refractory period. The slow pathway would then meet the fast pathway in it’s refractory period and the signal would be terminated.
In AVNRT- a premature beat arrives when the slow track has recovered from its refractory period. This means it passes down this pathway however meets the fast pathway when it has just recovered from its refractory period. This means the signal can be transmitted back up into to atria and it bounces around.
Describe the process of atherosclerotic plaque RUPTURE.
Plaque rupture exposes sub-endothelial cells and von Willeband factors. The platelets notice this and start to respond as they would to injury. Initially they form a monolayer. However they become activated, and release factors such as thromboxane A2 and ADP which cause them to aggregate together with other platelets. Inflammation then occurs, blood clots form and the lumen of the vessel becomes occluded.
Describe the process of formation of an atherosclerotic plaque.
Toxins in the blood e.g. smoking, high levels of LDL cholesterol and high blood pressure can cause initial damage to the vascular endothelium.
When this occurs, LDL cholesterol migrates into the damaged endothelium and becomes oxidised. This is called a fatty streak and causes inflammation. The macrophages are then recruited into the site of injury where they digest some of the cholesterol, however they gorge on it (forming foam cells) and subsequently die (adding to the plaque). They release cytokines which attract other inflammatory cells which again aggregates the plaque. Smooth muscle cells start to notice this aggregation and migrate into the plaque to form a fibrous cap. They also release calcium which hardens the plaque.
Pathology of COPD
Toxins in cigarette smoke cause an inflammatory response by stimulating alveolar macrophages. Neutrophillic inflammation then occurs and proteases are released.
Pathology of emphysema
The proteases released from the neutrophillic inflammatory response digest the elastin in the alveolar cell walls. This causes impaired gas exchange and respiratory failure.
Pathology of chronic bronchitis
Goblet cells undergo hypertrophy and cause mucus hypersecretion. The mucocilliary escalator becomes paralysed. This means the mucus cannot be expelled. This along with smooth muscle spasm and hypertrophy leads to airway limitation.
Treatment of COPD.
SABA (salbutamol)
LABA/LAMA (salmeterol or ipatropium bromide)
Corticosteroids (Beclametasone)
Acute exacerbation of COPD
iSOAP Ipatropium bromide IV Salbutamol Oxygen (24-28%) Antibiotics (if infective) P- prednisolone
What is streptococcal pneumonia also known as?
Pneumococcal pneumonia
What colour sputum does pneumococcal pneumonia produce?
Rusty coloured sputum.
Describe the symptoms of streptococcal pneumonia.
Acute in onset
Chest pain
What makes you more susceptible to streptococcus pneumoniae?
Female, HIV, alcohol.
Symptoms of mycoplasma pneumoniae
Headache, confusion, muscle pain. Generally mild.
Can cause haemolytic anaemia, skin rashes and hepatitis.
Symptoms of legionella pneumoniae?
Diarrhoea and vomiting
After travel
Neurological symptoms
Deranged liver enzymes and elevated creatine kinase.
Staphylococcus aureus
Past influenza involvement
Skin rashes
Chylamydophila psittaci
Mucoid sputum
Chest pain may develop
PET BIRD
