Clinical Conditions (B) - 9 PDF

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This is a summary I put together to help me revise for the clinical exams....

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Clinical Conditions (B) - 9 Wrist fractures ● The two types of distal radius fractures Colles and Smith’s fracture. ● Colle’s fracture is a distal radius fracture which is displaced dorsally. It is otherwise known as dinner fork deformity. It is caused by falling on an outstretched hand. 3 features are: a) Transverse fracture b) Occurs 1cm proximal to the radio-ulnar joint c) Dorsal displacement. ● Smith’s fracture is a distal radius fracture which is displaced volarly. It is otherwise known as garden spade deformity. It is caused by falling backwards on an outstretched hand with the wrists flexed. ● Barton’s fracture is a distal radius fracture combined with radiocarpal dislocation. It is caused by falling onto an extended and pronated wrist. ● Monteggia’s fracture is a fracture of the proximal ulna and dislocation of the proximal radioulnar joint. This is caused by a FOOSH injury with forced pronation. Meanwhile, Galeazzi’s fracture is a fracture of the distal radius and dislocation of the distal radioulnar joint. The mnemonic for this is Manchester United (Monteggia ulna) and Galaxy Rangers (Galeazzi Radius). ● Bennet’s fracture is of the first metacarpal which extends into the first carpometacarpal joint. It is common in situations like fist fights. On X-ray you will see a triangular fragment at the ulnar base of the metacarpal. ● Fracture of the radial head causes tenderness over the head of the radius, impaired movements at the elbow and sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination). ● Scaphoid is the most common carpal to be fractured which forms the floor of the anatomical snuffbox and therefore presents with tenderness over the anatomical snuffbox. This is a surgical emergency because there is a risk of avascular necrosis because the dorsal branch of the radial artery runs in this area. ● The two main causes of a scaphoid fracture is a) FOOSH (falling on an outstretched hand) b) Contact sports. ● Other signs which may be present in a scaphoid fracture are a) Pain on ulnar deviation b) Wrist effusions.

Mallory-weiss tear ● This is when severe repeated bouts of vomiting leads to mucosal lacerations in the gastro-oesophageal junction resulting in haematemesis. ● It may also appear as old blood in the stool (malaena) but this is rare. ● The blood that appears is described to be bright red. ● It is common in alcoholics and bulimics. It may be a complication of hyperemesis gravidarum.

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Management: it usually resolves spontaneously in the next 24-48 hours but sometimes surgery/endoscopy is needed in which epinephrine injections are inserted to stop the bleeding. A common differential is Boerhaave’s syndrome but this usually also presents with chest pain and emphysema.

Peptic ulcer disease and gastritis ● The two types of peptic ulcers are duodenal ulcers and gastric ulcers with duodenal ulcers being the most common. They both result in the symptoms of nausea and epigastric pain. The difference between the two is that duodenal ulcers produce epigastric pain when hungry and is relieved by eating whereas gastric ulcer pain is worsened by eating. ● H. pylori is the most common cause which accounts for 95% of duodenal ulcers and 75% of gastric ulcers. Another cause includes drugs such as NSAIDs, corticosteroids, SSRIs and bisphosphonates (in NCS I met my B). Another cause (rare) is Zollinger-Elison syndrome where there is an excess of gastrin released from a gastrin producing tumour. Alcohol and smoking are thought to have some association too but this is not clear. ● The best way to diagnose H. Pylori induced ulcers are through urea breath test and then stool antigen sample. ● If H. Pylori is found to be the cause then the best management is eradication therapy which is either: a) PPI + clarithromycin + amoxicillin OR b) PPI + clarithromycin + metronidazole. If H. Pylori is not the cause then the best management is giving a proton pump inhibitor (PPI). ● Peptic ulcer disease may cause thrombocytopenia which can lead to pruritus. ● One complication of peptic ulcers is that they may become perforated which is managed through laparoscopy. Larger defects are managed through a partial gastrectomy. Investigation used is a chest X-ray (CXR) which shows free air in the abdomen. The main symptom is pain which initially is sudden onset but then later can become a more generalised sort of pain. ● Gastritis is inflammation of the stomach lining. Diffusive erosive gastritis is treated with proton pump inhibitors (PPI) and if not managed endoscopically and continue to bleed then may need to be treated with gastrectomy. It may be caused by the same causes as peptic ulcers e.g. H. Pylori / NSAIDs - the management is to remove the underlying cause e.g. eradication therapy / stop taking NSAIDs. ● Peptic ulceration, galactorrhoea, hypercalcaemia in a question is most likely to indicate multiple endocrine neoplasia type I (because this affects the pancreas, pituitary and parathyroid respectively - otherwise known as the 3 Ps).

Immune thrombocytopenic purpura (ITP)

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Immune thrombocytopenic purpura (ITP) is an immune mediated decrease in platelet count due to antibodies against glycoprotein IIb/IIIa or Ib/V/IX complex. There are two types - a) Acute - more common in children b) Chronic - more common in young/middle aged women. Evan’s syndrome refers to ITP in combination with autoimmune haemolytic anaemia (AIHA) - where cold agglutins (IgM) may lead to thrombocytopenia. Purpura describes bleeding into the skin from small blood vessels creating a non-blanching rash - this symptom usually arises as a result of low platelet count (but may also be seen with bleeding disorders such as von Willebrand’s disease). The acute type has a self limiting course of about 1 to 2 weeks whilst the chronic type has a relapsing-remitting course. One differential for (chronic) ITP is gestational thrombocytopenia which is a relatively common condition in pregnancy due to decreased production of platelets and increased destruction of platelets - the latter being due to the fact that in pregnancy the spleen is more at work, resulting in sequestration. Differentiating between chronic ITP and gestational thrombocytopaenia is hard work and often relies on history. GTP is considered more likely if platelet count falls continually as pregnancy progresses but this is an unreliable method for diagnosis. If her platelet count falls severely low, then she is treated with steroids and a diagnosis of GTP is assumed. GTP doesn’t affect the neonate but ITP can do if maternal antibodies cross the placenta. Depending on the severity of thrombocytopenia in the newborn, platelet transfusions may be considered. Drug induced thrombocytopaenia can come about due to firstly the 3As: a) Abciximab b) Antibiotics (penicillin/rifampicin/sulphonamides) c) Anticonvulsants i.e. carbamazepine/ valproate....and also d) Diuretics: furosemide e) Heparin f) NSAIDs g) Quinine. Platelet transfusions however should not be performed for anyone with: a) Heparin induced thrombocytopenia b) Thrombotic thrombocytopenia. ITP is often preceded by a viral illness.

Thrombotic thrombocytopenic purpura (TTP) ● There’s nothing on passmed specifically related to TTP (only ITP) therefore look this up closer to exam time. Myeloproliferative disorders ● Polycythaemia means an increase in haematocrit levels. There are 3 types which are listed below - followed by their causes: a) Relative - dehydration, hypertension/stress (otherwise known as Gaisbock syndrome) b) Primary - polycythaemia rubra vera c) Secondary - COPD, altitude, obstructive sleep apnoea, increased erythropoietin production. ● The latter two types are known as true polycythaemia and the way to differentiate this from relative polycythaemia is through measuring red cell mass - in true polycythaemia it is >35ml/kg in males and >32ml/kg in females.

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Polycythaemia rubra vera is a myeloproliferative disorder caused by excess proliferation of bone marrow stem cell leading to increased red cell mass, accompanied by increased neutrophils and platelets. It has the highest incidence in those in the 6th decade. JAK2 mutation is present in 95% of patients with PRV. The methods of diagnosing PRV are: a) Full blood count/film b) JAK2 mutation c) Serum ferritin levels d) Renal and liver function tests. The most useful test for diagnosing PRV is screening for a JAK2 mutation followed by red blood cell mass. If JAK2 mutation is negative, can also look at red cell mass, arterial oxygen saturations, serum erythropoetin levels, abdominal ultrasound, bone marrow aspirate or trephine, cytogenetic analysis, erythrocyte burst forming unit (BFU-E) culture. Features of polycythaemia rubra vera (main ones): a) Hyperviscosity b) Pruritus (esp after a hot bath) c) Splenomegaly. Other features include: hypertension (in 1/3rd of patients), haemorrhage, plethoric appearance, low ESR. First line management of polycythaemic rubra vera is venesection (removing excess blood cells) as well as: a) Aspirin (prevents anticoagulation) b) Hydroxyurea (slight increased risk of chronic leukamia) c) Phosphorus-32. The most significant complication is that thrombotic events can lead to mortailty and morbidities. 5-15% may develop acute leukaemia and 5-15% may also develop myelofibrosis. The pathophysiology behind chronic myeloid leukaemia is that there is a Philadelphia chromosome present in more than 95% of patients which causes a translocation between the long arm of chromosome 9 (ABL) and chromosome 22 (BCR) resulting in BCR-ABL gene which codes for a fusion protein that has higher tyrosine kinase activity than normal. Symptoms of CML are: a) Anaemia causing lethargy, weight loss, sweating b) Splenomegaly which may cause abdo discomfort (like polycythaemia) c) Decrease in leukocyte alkaline phosphatase (like polycythaemia) d) Increase in granulocytes at different stages of maturation +/- thrombocytosis e) May undergo blast transformation. First line management of CML is using imatinib which is a tyrosine kinase inhibitor. Another form of management is bone marrow transplant. Another form of management, like PVR, is using hydroxyurea. In addition there is interferon alpha. The pathophysiology behind myelofibrosis is that it is due to hyperplasia of megakaryocytes which results in increased release of platelet derived growth factor which stimulates fibrocytes which results in increased haematopoesis in the liver and spleen. This results in the symptom of splenomegaly (which can cause abdo discomfort) as is the case in chronic myeloid leukaemia, as well as hypermetabolic symptoms (weight loss, night sweats) as is also the case in chronic myeloid leukaemia. However the main symptom is anaemia which is found mostly in elderly patients. The main laboratory finding of myelofibrosis is tear shaped poikilocytes. There is also high urate and LDH levels which reflect the high cell turnover. 5-15% of patients with polycythaemia vera can go on to develop myelofibrosis (as well as acute myeloid leukaemia).

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Similarities between CML and myelofibrosis: splenomegaly, anaemia, hypermetabolic symptoms, Similarities between CML and PVR: hydroxyurea as treatment Similarities between PVR and essential thrombocytosis: hydroxyurea and aspirin as treatment, and JAK2 mutation being a predisposing factor. Similarities between CML and essential thrombocytosis: hydroxyurea and interferon alpha The main feature of the image below is tear drop shaped poikilocytes which are found in myelofibrosis:

One cause of pyoderma gangrenosum (a dermatological condition characterised by small red papules which later become deep red necrotic ulcers) is myeloproliferative disorders. Myeloproliferative disorders can result in increased uric acid production which can lead to the musculoskeletal condition called gout. Essential thrombocytosis is another myeloproliferative disorder - the pathophysiology behind which is megakaryocyte proliferation that can lead to increased platelet production. The features of essential thrombocytosis is: a) Platelet count > 600 x 10^9 b) Increased thrombosis (venous and arterial) and haemorrhage c) Burning sensation in the hands d) JAK2 mutation in 50%. Management of essential thrombocytosis includes: a) Hydroxyurea - in order to reduce platelet production b) Low dose aspirin - to reduce thrombotic risk c) Interferon alpha. Pruritis may be caused by polycythaemia and seen particularly after a hot bath. Patients may appear to have a ruddy complexion. They may also have a background of gout and peptic ulcer disease. One cause of secondary polycythaemia rubra vera is COPD and the pathophysiology behind this is impaired gas exchange in the lungs results in low oxygen saturations which stimulates EPO production and release in the kidneys which results in greater RBC production. Decreased leukocyte alkaline phosphatase is indicative of chronic myeloid leukaemia. One adverse effect of hydroxyurea (which treats polycythaemia rubra vera, chronic myeloid leukaemia and essential thrombocytosis) is myelosuppression/ agranulocytosis....