Flashcards in Review of posters 25/04/2016 Deck (51):
Treatment of angina (stable)
GTN spray for when the chest pain comes on.
Beta blockers/Calcium channel blockers
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
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
Minimal alcohol intake
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.
LABA/LAMA (salmeterol or ipatropium bromide)
Acute exacerbation of COPD
Ipatropium bromide IV
Antibiotics (if infective)
What is streptococcal pneumonia also known as?
What colour sputum does pneumococcal pneumonia produce?
Rusty coloured sputum.
Describe the symptoms of streptococcal pneumonia.
Acute in onset
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
Deranged liver enzymes and elevated creatine kinase.
Past influenza involvement
Chest pain may develop
Common in pregnant women and infants.
Infants remain asymptomatic for three weeks.
Describe the stages of sarcoidosis
Stage 1: Bilateral hilar lymphandenopathy
Stage 2: BHL with pulmonary infiltrates
Stage 3: Pulmonary infiltrates without BHL
Stage 4: fibrosis
What is bilateral hilar lymphadenopathy?
Bilateral enlargement of the lymph nodes of the pulmonary hilar
Detected on chest X-ray.
Nearly always involves lung parenchyma
What are the differential diagnosis' of BHL
Lymphoma, TB, carcinoma of the bronchus
What are pulmonary infiltrates?
Substances denser than air e.g. blood, pus, protein. May show as 'nodular shadows'
What are the differentials of pulmonary infiltrates?
Pulmonary fibrosis, pneumocoinosis and alveolar cell carcinoma.
Treatment of sarcoidosis
Describe Churg Strauss syndrome?
Presents as a combination of what looks like asthma and rhinitis. Eosinophilic vasculitis and systemic vasculitis.
Patient may present with tender subcutaneous nodules on the skin. ANCA positive (anti-neutrophil cytoplasmic bodies).
Treatment of Churg Strauss syndrome
What is Wegners Granulomatosis?
Single/multiple nodular masses with pneumonic infiltrates
symptoms include :
Rhinorhea- nasal cavity becomes blocked with mucus
nasal mucosal ulceration
Treatment of Wegners Granulomatosis?
Cyclophosphamide or ritixamab
Pleural adhesions, thickening and effusions
Often unilateral effusion
Decreased chronic glucose content
gastro-oesophageal reflux disease- loss of tone of lower oesophageal sphincter.
Symptoms of GORD
Severe chest pain
Spasm of the oesophagus
Treatment of GORD
PPI e.g. omeprazole
Birds beak appearance on CT.
Lower oesophageal sphincter has gone into spasm.
Treatment of achalasia
Lower oesophageal rings
Two types- mucosal (shatzki or B rings)
Squamocolumnar mucosal junction- intermittent dysphagia.
Muscular (A rings)
Treatment- endoscopic dilatation.
Thin membranous tissue covered in squamous epithelium that may cause dysphagia. Generally present in the anterior oesophagus just below the cricoid cartilage.
Peptic and oesophageal stricture
Narrowing of the vessel due to fibrous scar tissue forming. Primary cause is acid reflux.
Treatment of peptic and oesophageal strictures
Pathology of NSAIDs and peptic ulcers.
Inhibit COX2 causing an increase in acid production.
Also decreasing angiogenesis (formation of new blood vessels).
Inhibit COX1- impairs platelets
Decreases mucus secretion
Also cytotoxic to epithelial cells- disrupts barrier.
Symptoms of peptic ulcers
Relieved or aggravated by eating
Treatment of peptic ulcers
Stop NSAIDs immediately
All patients tested for H-pylori. If positive- eradication therapy. If negative- anti-secretary therapy.
H pylori eradication therapy
PPI and amoxicillin (1g twice a day)
Clarithromycin (500mg bd)