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It consists of two types of blocks: 1) Mobitz type I block, 2) Mobitz type II block. Mobitz type I It is also called as Wenckebach pattern. In this condition, each stimulus from the atria appears to have more difficult time to pass through the AV junction. Finally one stimulus is not conducted through the defective AV node. A characteristic ECG shows progressive lengthening of the PR interval until a beat is dropped. i.e. the P wave is not followed by a QRS complex. It is also important to note that the PR interval after the dropped beat is always shorter than that before the non conducted P wave. Also the R-R interval encompassing the non conducted P wave is less than twice the preceding R-R interval. This ECG is also shows a Wenckebach pattern and we can clearly see at first glance that the narrow QRS complexes appear to be clustered and separated by a pause. This is called as group beating. If ever you find such a pattern, look out for the progressively increasing P

In this condition, there is a delay in conduction between the atria and the ventricles. There is a prolongation of the PR interval to more than 200 ms. i.e > 5 small squares on a usual 25 mm/s ECG tracing. The normal duration for PR interval is 120 - 200 ms. A QRS complex follows each P wave and the PR interval is relatively constant from beat to beat. The pathology is usually due to a delay within the AV node if we have a normal QRS complex. But if the QRS complex is wide, the problem is more distal.

The 6 P's are: 1) Pain, 2) Pallor, 3) Pulselessness, 4) Paralysis, 5) Paraesthesia, 6) Perishingly cold.

As soon as a diagnosis of VTE / PE is strongly suspected, anticoagulant therapy should be started unless there are contraindications. Parenteral drugs like unfractionated heparin (standard heparin) and low molecular weight heparin (lovenox) are started and therapy shifted to a long term stable vitamin K antagonist like warfarin. Unfractionated heparin The anticoagulant action is by binding to and accelerating the activity of antithrombin III. This inactivates thrombin, factor IXa and Xa and thus prevents further clot formation. The classical regimen for the dosage is a loading dose of 5000 - 10000 units followed by a continuous infusion of 1000 - 1500 units/hour. Unfortunately we all do not have the same weight. So, a more appropriate dosage is a loading dose of 80 units/kg and a continuous infusion of 18 units/kg/hr. The aim is to achieve a target activated partial thromboplastin time (aPTT) aka partial thromboplastin time with kaolin (PTTK) of 2-3 times the normal laboratory val

Ingestion of alcohol makes you feel warm because it causes cutaneous vasodilation. Increased blood flow to the skin coupled with a low environmental temperature means that there is a more rapid loss of heat from the body. Furthermore, consumption of a large amount of ethanol leads to depression of the central temperature regulating mechanism. Thus drinking alcohol excessively in cold climates can lead to hypothermia and even death if appropriate measures are not taken.

1) First detected AF - It is the designation given when diagnosis has only recently been made. 2) Recurrent AF - When patient has experienced two or more episodes of AF. 3) Paroxysmal AF - Self terminating episodes that generally last less than 7 days (mostly <24 hr) 4) Persistent AF - Last more than 7 days and requires electrical or pharmacologic cardioversion. 5) Permanent AF - It has failed cardioversion and has been sustained for more than a year.

This is a continuation of the main article  Diabetes insipidus . It shows the effect of desmopressin in a case of central D.I. The changes seen are: 1) decrease in urine output, 2) increase in urine osmolarity, 3) decrease in plasma osmolarity and 4) slight increase in body weight. Desmopressin is 12 times more potent antidiuretic than ADH. It has a duration of action of around 8 hours and thus can be given in 3 divided doses per day. The intranasal route is preferred though the bioavailability is only 10-20%. Treatment is life long.

Definition: It is a syndrome characterized by the production of abnormally large volumes of dilute urine due to the decreased secretion or decreased action of AVP (arginine vasopressin). AVP is also commonly known as ADH i.e. Anti Diuretic Hormone. Cause: 1) Central D.I - aka pituitary D.I or neurohypophyseal D.I. 2) Nephrogenic D.I Central D.I occurs because of an inadequate release of ADH from the posterior pituitary. The usual causes are idiopathic, traumatic, iatrogenic (surgery,radiation), neoplastic, infective, granulomatous (TB,sarcoidosis) and congenital being a rarer cause. Nephrogenic D.I is due to the resistance to ADH at the level of the collecting duct cell. The most common cause of resistance is the use of drugs like lithium (bipolar disorders) and amphotericin. But it can rarely be due to a congenital cause. Pathogenesis: The antidiuretic effect of ADH is achieved by increasing the hydroosmotic permeability of cells that line the distal tubule and medullary

Group: macrolide Antimicrobial activity: Good against Gram positive and Gram negative organisms. Slightly less active than erythromycin against staphylococci and streptococci but more active against H.influenzae. It is also highly active against chlamydia, Mycobacterium avium complex and Toxoplasma gondii. Mechanism of action: It binds to the 50s ribosome subunit and hinders the translocation of the elongated peptide chain from the acceptor site to the peptidyl site. Thus the ribosome does not move along the mRNA to expose the next codon and peptide synthesis is prematurely terminated. Pharmacokinetic properties: Acid stability and more active in alkaline medium, rapid oral absorption but better given 1 hour before meals or 2 hours after meals, marked tissue distribution especially intracellular penetration (macrophages and fibroblasts), Half life : 2-4 days, therefore can be given as once a day dosing Clinical uses: 1) Legionnaire's pneumonia - 500 mg O.D for 2 wee

The use of I.V morphine in dyspnea from pulmonary edema due to left ventricular failure produces remarkable relief. The proposed mechanisms include:  1) reduced anxiety ( decreased perception of shortness of breath ),  2) reduced cardiac preload ( reduced venous tone ) and  3) decreased cardiac afterload (decreased peripheral resistance ).  However frusemide remains the treatment of choice.  Side effect is respiratory depression at a higher dosage which occurs because of inhibition of the brainstem respiratory mechanism.

 DIAGNOSIS  Hypoglycemia can be diagnosed by whipple's triad which consists of: 1) symptoms consistent with hypoglycemia, 2) a low plasma glucose concentration measured by an accurate method, 3) relief of the symptoms when the plasma glucose level is raised.  SYMPTOMS  Symptoms of hypoglycemia are: 1) Neuroglycopenic symptoms like behavioral changes, fatigue, seizures, altered consciousness, 2) Adrenergic symptoms like palpitations, tremors, anxiety, 3) Cholinergic symptoms like sweating, hunger and altered sensations The cut off value for hypoglycemia is 70 mg/dL which is equal to 3.9 mmol/L.  TREATMENT  Relief of symptoms can be done by: 1) an initial 20 g of carbohydrate containing fluid or food can be given if the patient can tolerate orally, 2) I.V glucose 25 g bolus at 2 mg/kg/min followed by 10 g/hr. 250 mL of 10% dextrose is better than 50 mL of 50 % dextrose as there is less thrombophlebitis. 3) Glucagon 1 mg subcutaneously or intramuscularly works as rap

It is caused by an organism known as Bacillus anthracis. The latter is a gram positive, spore-forming rod that is found in soil. The spores can remain viable for years. Anthrax came to public notice in September 2001 when it was used as a bioweapon delivered through the U.S Postal System causing infection in 22 persons of whom 5 died. In the past i.e. during World War II , anthrax was studied mainly for its potential use as a biological weapon but following the Biological and Toxin Weapons Convention Treaty in 1972, such research was no longer allowed. Still, some nations and extremist groups do work on this agent secretly. There are 3 major clinical forms of anthrax: 11)       Gastrointestinal anthrax – from ingestion of contaminated meat 22)       Cutaneous   anthrax – from introduction of spores through opening in skin 33)       Inhalational anthrax- inhalation of spores that deposit in the alveolar spaces. The inhalational form is the one usually used for biot

1)  Measurement of height, weight, waist, BMI 2) Measurement of blood pressure  3) Examination of feet for pulses, loss of sensation to touch/vibration, signs of  infection  4) Measurement of visual acuity  5) Urine tested for albumin, ketones and glucose  6) Record made of current physical activity/recreational exercise levels, smoking  history and alcohol consumption, addition of salt to prepared food  If the resources and laboratory facilities are available then the following may be desirable.  •  ECG as baseline  •  Fasting blood lipids-cholesterol and triglycerides, HDL, LDL  •  Serum urea and creatinine for those with proteinuria  •  Retinal examination by fundoscopy  •  Urine for microalbuminuria if dipstick –ve  •  Glycosylated haemoglobin (HbA1c) 

1) There is usually a tingling sensation in the throat in hemoptysis while in hematemesis the patient will usually complain from nausea and upset stomach. 2) The blood is usually frothy and bright red in hemoptysis while it is dark red in hematemesis, non-frothy and food particles may also be present at the same time. 3) Blood in hematemesis will give an acidic pH when tested with litmus paper whereas that in hemoptysis will be neutral to alkaline. 4) Stools will be almost always positive for occult blood in hematemesis while it is usually negative in case of hemoptysis. But it can also be positive at times if the patient has swallowed his sputum. Last reviewed on: 1 September 2015

Insulin binds to receptor on target sites. These sites have an intrinsic tyrosine kinase activity that lead to receptor autophosphorylation and recruitment of intracellular signalling molecules. The latter result in widespread metabolic and mitogenic effects of insulin as shown in the diagram above. Another effect is the activation of phosphatidylinositol 3 kinase that fastens the translocation of GLUT-4 containing vesicles to the cell surface. This is important to allow uptake of glucose by skeletal and fat cells. When insulin action ceases, the transporter-containing patches of membrane are endocytosed and the vesicles are ready for the next exposure to insulin. On the other hand, in the liver, this is not the mechanism of glucose uptake. Instead, it induces glucokinase, and this increases the phosphorylation of glucose, so that the intracellular free glucose concentration stays low, facilitating the entry of glucose into the cell by diffusion. Insulin-sensitive tissues l

The diagram shows a beta cell of the islet of pancreas and will explain how local factors regulate secretion of insulin from it. Glucose enters the cell via the GLUT-2 transporter. Inside the cell there is metabolism with the generation of ATP. This causes the ATP-sensitive K+ channel to close, as shown in A. Closure of this channel leads to cell membrane depolarization. This in turn allows calcium ions to enter the cell via another calcium channel, shown in B. Increased intracellular calcium activates calcium dependent phospholipid protein kinase. This leads to exocytosis of insulin granules.

Virchow's triad refers to the 3 primary influences for thrombus formation and it includes: 1) Endothelial injury 2) Stasis, turbulence or abnormal blood flow 3) Blood hypercoagulability. Endothelial injury Physical loss of endothelium leads to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, and local depletion of PGI 2 and plasminogen activators. Abnormal blood flow Turbulence can cause endothelial injury which is in itself a major influence for thrombosis. Apart from that abnormal blood flow can: 1) Disrupt laminar flow and bring platelets into contact with the endothelium 2) Prevent dilution of activated clotting factors by fresh-flowing blood 3) Retard the inflow of clotting factor inhibitors and permit the buildup of thrombi 4) Promote endothelial cell activation, resulting in local thrombosis, leukocyte adhesion, etc.  Hypercoagulability It can be primarily due to a genetic disorder and secondarily due to some acqui

The table above shows how chronic kidney diseases are classified. Risk factors include hypertension, diabetes mellitus, autoimmune disease, older age, African ancestry, a family history of renal disease, a previous episode of acute renal failure, and the presence of proteinuria, abnormal urinary sediment, or structural abnormalities of the urinary tract. Stage 0 Not commonly included in many classifications but in this stage there is no kidney damage evident but patients have one or more risk factors mentioned above. Stage 1 Kidney damage is there demonstrated by persistent proteinuria, abnormal urine sediment, abnormal blood and urine chemistry, abnormal imaging studies but GFR i.e kidney function will be normal. Stage 2 Kidney damage is there and slight decrease in kidney funtion. Stage 3-5 The older term chronic renal failure corresponds to these stages. It is characterized by a progressive, significant and irreversible kidney damage with a GFR < 60 for 3 month

We have 2 classic regimens that have been used on a large scale. 1) Multiple component insulin regimen Here, usually a basal insulin level is maintained by a long acting insulin like glargine insulin (lantus) injected at night. Then short acting insulin analogues are injected just after breakfast, lunch and supper. In total the patient has to do 4 injections per day. 2) Twice a day pre-mixed insulin This is more commonly used. It consists of twice daily injected mixture of an intermediate acting insulin like NPH insulin and a short acting insulin or regular insulin in a ratio of 70:30. 2/3rd of the total insulin requirement is given in the morning and the remaining 1/3rd at night. The total number of injections is 2 per day. For the patients' convenience, the second regimen seems better as he/she has to do only 2 injections but the first regimen i.e multiple component insulin regime is actually the better of the two. Studies have recently shown that a better HbA1c goal i

Bronchial asthma is considered to be well controlled if the patient experiences cough, shortness of breath and wheezing less than 3 times/week during the day, less than 3 times/month of night time awakenings and no asthma related interference with normal activity. Recently it has been found that only 1/3rd of asthma patients can be categorized as being into the well controlled group.