Medicine Hack

CEA is an oncofetal antigen, a glycoprotein that is usually produced only during fetal life and is not present in the healthy adult blood. It is associated with certain malignancies, particularly epithelial tumors. It is a very non-specific tumour marker. Normal values: Non-smokers: 0–3 ng/mL [μg/L] Smokers: 0-5 ng/mL [μg/L] Elevated levels in:   1) Adenocarcinoma of colon cancer (72%) (right side of colon>left side),  2) Pancreatic cancer (91%),  3) Lung cancer (76%),  4) Stomach cancer (61%),  5) Breast cancer,  6) Cancer of ovary,  7) Cholangiocarcinoma,  8) Gall bladder cancer. Other non-neoplastic conditions include:  1) Cigarette smokers,  2) Benign liver disease (acute 50% and chronic 90%),  3) Benign GI disease (peptic ulcer, pancreatitis, colitis,cholecystitis). Elevations >20 ng/mL are generally associated with malignancy and metastasis. Screening:   The test is not sensitive or specific enough to be useful in cancer screening

Right Axis Deviation I. Spurious: left-right arm electrode reversal (look for negative P wave and negative QRS complex in lead I) II. Normal variant III. Dextrocardia IV. Right ventricular overload A. Acute (e.g., pulmonary embolus or severe asthmatic attack) B. Chronic 1. Chronic obstructive pulmonary disease 2. Any cause of right ventricular hypertrophy (e.g., pulmonic stenosis or primary pulmonary hypertension) V. Lateral wall myocardial infarction

Low-Voltage QRS Complexes 1. Artifactual or spurious (especially unrecognized standardization of the ECG at half the usual gain, i.e., 5 mm/mV). Always check this first! 2. Adrenal insufficiency (Addison's disease) 3. Anasarca (generalized edema) 4. Cardiac infiltration or replacement (e.g., amyloid, tumor) 5. Cardiac transplantation, especially with acute or chronic rejection 6. Cardiomyopathies 7. Chronic obstructive pulmonary disease 8. Constrictive pericarditis 9. Hypothyroidism/myxedema (usually with sinus bradycardia) 10. Left

Liver Examination sequence: 1) Start the palpation in the right iliac fossa. If you start in the right lumbar or right hypochondrium you may miss a massively enlarged liver. 2) The radial border of the right hand is used to feel the liver. The hand must be placed flat on the abdomen. Make sure you do not poke the patient’s abdomen with your finger tips. 3) Now your right hand is kept stationary and the patient is asked to take a deep breath. During inspiration the diaphragm becomes flat and pushes the liver downwards. Try feeling the edge when the patient inspires. 4) As the patient breathes out, move your hand up the abdomen for 1-2cm. Step 3) is then repeated. 5) Repeat step 4) till you reach the costal margin or you detect the edge of the liver. 6) If you feel the edge, then you have to work out whether it is a true enlargement of the liver or the latter has been displaced downwards by a hyperinflated lung e.g. in a case of emphysema. To check this, you have to percu

Ventricular repolarisation produces the T wave. The normal T wave is asymmetrical, the first half having a more gradual slope than the second half. This is well shown below with an up-slope of a duration of nearly 3 squares and a down-slope in only around 1 and  1/2 squares.  T wave orientation usually corresponds with that of the QRS complex, and thus is inverted in lead aVR, and may be inverted in lead III.  But the T waves are discordant with the QRS complexes in Left Bundle Branch Block (LBBB) i.e. T is inverted while the QRS complex is positive or vice-versa. T wave is positive in lead II. Left-sided chest leads such as V4-V6 normally always show a positive T wave. In the T wave can be inverted in the right precordial leads in normal persons. T waves are commonly inverted in all precordial leads at birth but usually become upright as time passes. A persistent juvenile pattern with inverted T waves in the leads to the left of V1 occurs in 1-3% o

The criteria for separating transudates from exudates were published in 1972 by Light and coworkers. They were based on the measurements of serum and pleural fluid protein and LDH.  The criteria are as follows: If at least one of the following 3 criteria is present, the fluid is virtually always an exudate and if none is present then the fluid is virtually always a transudate: 1)      Pleural fluid : Serum protein ratio > 0.5 2)      Pleural fluid LDH > 2/3 of the upper limit of the serum reference range 3)      Pleural fluid : Serum LDH ratio > 0.6 An exception to using Light’s criteria is in the setting of CHF treated with diuretics. Normally, in CHF, the effusions are due to an increased capillary hydrostatic pressure and are therefore transudates. But the use of diuretics has been shown to increase the pleural fluid protein and LDH concentrations. Thus we will have a false positive result making the fluid appear as an exudate. It is believed to be

It is at times difficult to interpret a PA chest X-ray as the amount of information present is huge. A systematic approach should always be done.  One should have the understanding of what is normal. This must include an evaluation of the  1) soft tissues,  2) bones and joints,  3) pleura, lungs, major airways and pulmonary vascularity,  4) mediastinum and its contents,  5) heart and its chambers, as well as  6) the areas seen below the diaphragm and above the thorax. The heart borders are explained in this post.  On the right side of the heart the following structures can be identified: 1) Az - Azygous vein 2) A - Ascending aorta 3) S - Superior vena cava 4) RA - Right atrium On the left side of the heart, we can identify the following: 1) SC - Subclavian artery 2) AA - Aortic arch 3) PA - Pulmonary artery 4) LB - Lower border of pulmonary artery 5) LA - Left atrial appendage 6) LV - Left ventricle The x-ray on the right side i.e. B shows the actual positio

The search for and use of an antidote should never replace good supportive care. Specific systemic antidotes are available for many common poisonings as shown in the table above. Inadequate availability of antidotes at acute care hospitals can complicate the care of a poisoned patient.  An evidenced-based consensus of experts has recommended minimum stocking requirements for 16 antidotes for acute care hospitals. These recommendations may provide guidance to pharmacy and therapeutics committees in establishing a hospital’s antidote needs. Drugs used conventionally for non-poisoning situations may act as antidotes to reverse acute toxicity, such as glucagon for β-adrenergic blocker or calcium channel antagonist overdose and octreotide for sulfonylurea-induced hypoglycemia. As our understanding of drug toxicity increases, antidotes may have applications beyond contemporary indications, such as for acetylcysteine, which has shown promise for treating approximately 25 different

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 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