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Showing posts from March, 2012

Clinical case 1 - Dizziness in 78 year old man

A 78-year-old man is brought to hospital with an episode of dizziness. He was well until the last 6 months, since when he has had some falls, irregularly. On some occasions he lost consciousness and is unsure how long he has been unconscious. On a few occasions he has fallen, grazing his knees and on others he has felt dizzy and has had to sit down but has not lost consciousness. These episodes usually happened on exertion, but once or twice they have occurred while sitting down. He recovers over 10–15 min after each episode. Once, his wife was with him when he blacked out. Worried, she called an ambulance. He looked so pale and still that she thought that he had died. He was taken to hospital, by which time he had recovered completely and was discharged and told that he had a normal electrocardiogram (ECG) and chest X-ray. On examination He is pale with a blood pressure of 93/63 mm Hg.  The pulse rate is 35/min, regular.  There are no heart murmurs.  The jugular veno

Heparin induced thrombocytopenia

HEPARIN-INDUCED THROMBOCYTOPENIA Drug-induced thrombocytopenia due to heparin differs from that seen with other drugs in two major ways. (1) The thrombocytopenia is not usually severe, with nadir counts rarely <20,000/L. (2) Heparin-induced thrombocytopenia (HIT) is not associated with bleeding and, in fact, markedly increases the risk of thrombosis. Pathology: HIT results from antibody formation to a complex of the platelet-specific protein platelet factor 4 (PF4) and heparin. The antiheparin/PF4 antibody can activate platelets through the FcRIIa receptor and also activate monocytes and endothelial cells. Many patients exposed to heparin develop antibodies to heparin/PF4, but do not appear to have adverse consequences. 1) A fraction of those who develop antibodies will develop HIT, and a portion of those (up to 50%) will develop thrombosis (HITT). 2) HIT can occur after exposure to low-molecular-weight heparin (LMWH) as well as unfractionated heparin (UFH), alt

Sick sinus syndrome

Sick sinus syndrome is a term applied to a syndrome encompassing a number of sinus nodal abnormalities, including the following: (1) Persistent spontaneous sinus bradycardia not caused by drugs and inappropriate for the physiologic circumstance (2) Sinus arrest or exit block i.e. no P wave on ECG for > 2 s. (3) Combinations of SA and AV conduction disturbances and (4) Alternation of paroxysms of rapid regular or irregular atrial tachyarrhythmias and periods of slow atrial and ventricular rates (bradycardia-tachycardia syndrome). More than one of these conditions can be recorded in the same patient on different occasions, and their mechanisms often can be shown to be causally interrelated and combined with an abnormal state of AV conduction or automaticity. Incidence: 3 in every 10,000 persons are affected. Incidence increases with age, seen more after 65 years of age. Men and women are equally affected. Patients who have sinus node disease can be categorized

Hypertrophic scars

Pathology: In some cases, the scarring process remains in the remodelling phase for longer than usual. These hypertrophic scars are more cellular and more vascular than mature scars.  There is increased collagen production and collagen breakdown but the balance is such that excess collagen is produced.  Clinical features: The hypertrophic scars are red, raised, itchy and tender. They will eventually mature to become pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic scars from keloid scars.  Cause: Hypertrophic scars typically occur in wounds where healing was delayed, e.g. in cases where infection or dehiscence has occurred.  Incidence: They are more common in children and where skin tension is high such as the tip of the shoulder or any scar that runs across relaxed skin tension lines. Prevention and treatment: The risk of developing a hypertrophic scar can be minimised by ensuring quiet primary healing. Where hypertrophy

Differences between hypertrophic scar and keloid scar

Barrett's esophagus

Definition: Barrett’s esophagus is characterized by an intestinal metaplastic change in the lining mucosa of the esophagus in response to chronic gastro­esophageal reflux.  The condition is named after Norman Barrett, an Australian surgeon who drew attention to the columnar-lined esophagus in 1950. It is still not well understood why some people develop esophagitis and others develop Barrett’s esophagus often without significant esophagitis.  Pathology: In Barrett’s esophagus the junction between squamous esophageal mucosa and gastric mucosa moves proximally. The columnar epithelium is more acid resistant than the squamous epithelium. So this metaplasia appears to be a protective adaptation. The patient of chronic reflux esophagitis will find his symptoms decrease when he has developed Barrett's esophagus. Incidence: It is mainly seen in white man and the prevalence increases with age.  Several types of gastric-type mucosa may be found in the lower esophagus. When inte