Showing posts with label Internal medicine. Show all posts
Showing posts with label Internal medicine. Show all posts

Saturday, April 15, 2017

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Emphysematous pyelonephritis - Review

Emphysematous pyelonephritis is an acute necrotizing infection characterized by gas formation.
It is characterized by the presence of gas in and around the kidney.

E. coli (58%) and K. pneumoniae (21%) are the organisms most commonly isolated. Clostridium and Enterobacter spp may also be responsible, 7% each.

1) Diabetes mellitus (70-90%)- usually patients with poor glucose control. High levels of glucose in the urine serve as a substrate for these bacteria and large amounts of gas are generated through natural fermentation
2) Obstruction (25-40%)- it is another common predisposing factor for emphysematous pyelonephritis.

For non-diabetics, protein fermentation is a proposed source of gas formation.

7% of cases may be asymptomatic.
If symptomatic, patients may complain of pneumaturia, irritative lower tract voiding symptoms, flank pain or may present in a severe septic condition with an acute abdomen and high grade fever.

1) Plain radiograph of the abdomen can help us in 80-85 % of cases.
2) CT is considered the optimal imaging technique for confirming emphysematous infection and characterizing the extent of involvement.

According to radiological findings and CT scans, emphysematous pyelonephritis can be classified as follows:
Class 1— gas confined to the collecting system
Class 2— gas confined to the renal parenchyma alone
Class 3A— perinephric extension of gas or abscess
Class 3B— extension of gas beyond the Gerota fascia
Class 4— bilateral EPN or EPN in a solitary kidney
Emphysematous pyelonephritis

 Plain abdominal radiograph showing presence of air around the left kidney

Emphysematous pyelonephritis
 CT scan showing left emphysematous pyelonephritis with presence of gas and parenchymal destruction
Emphysematous pyelonephritis
CT scan of a diabetic patient with emphysematous pyelonephritis due to uncontrolled diabetes and renal stones.

1) Medical management includes antimicrobial therapy, bladder drainage and glycemic control.   effective.
2) Surgical intervention usually is required for only 10% of the cases. Emergency nephrectomy was traditionally considered necessary but currently, percutaneous drainage is the recommended initial approach.

 Later, elective nephrectomy may be required for some patients.

First published on: 15 April 2017

Monday, November 30, 2015


BMI versus waist to hip ratio

Obesity is a state of excess adipose tissue mass. It is often viewed as equivalent to an increased body weight. This is not true because muscular individuals may have increased body weight but are not obese.

Weight follows a continuous distribution pattern in human population. The point at which mortality and morbidity becomes statistically significant is the cut-off to call a patient obese.

Various methods have been used to measure obesity. These include:
1) Anthropometry (skin-fold thickness)
2) Densitometry (underwater weighing)
4) Electrical impedance.

Still the most common techniques used in clinical practice are:
1) BMI measurement
2) Waist-to-hip ratio measurement.

It is not an accurate measure of obesity but since it is simple to calculate, it is the most frequently measured parameter.

At similar BMI, women usually have more fat than men. When the BMI > 25 Kg/m2, morbidity starts to increase and if associated with risk factors then therapeutic interventions should be considered.

Intra-abdominal or abdominal subcutaneous tissue fat has more significant implications on morbidity than fat present in the buttocks and lower extremities. A WHR > 0.9 for women and > 1.0 for men is considered abnormal. (0.85 and 0.90 respectively according to WHO)

Insulin resitance, hypertension, dyslipidemia and diabetes mellitus are more strongly associated with intra-abdominal / abdominal subcutaneous tissue fat than to overall adiposity.

The probable explanation of this issue is that intra-abdominal adipocytes may be lipolytically more active than those from other depots. There is also release of free fatty acids into the portal circulation and this has adverse metabolic effects, especially on the liver.

A recent article published in the Annals of Internal Medicine concluded that
" normal-weight U.S. adults with central obesity have the worst long-term survival compared with participants with normal fat distribution, regardless of BMI category, even after adjustment for potential mediators. "

First published on: 30 November 2015

Tuesday, September 22, 2015

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Alcoholic liver disease

Chronic and excessive use of alcohol is one of the major causes of liver disease.

90% of daily heavy drinkers (>60 g alcohol/day) as well as binge drinkers have fatty liver but a smaller percentage (10-35%) of drinkers progress to alcoholic hepatitis which is a precursor for cirrhosis.

The long-term risk is 9 times higher in patients with alcoholic hepatitis compared to those with fatty liver alone.

Some population-based surveys have documented that men must drink 40 to 80 g of alcohol daily and women must drink 20 to 40 g daily for 10 to 12 years to achieve a significant risk of liver disease.

Liver pathology consists of 3 major lesions that are progressive and rarely exist in a pure form:
1) fatty liver (usually reverses quickly with abstinence),
2) alcoholic hepatitis and
3) cirrhosis.

histologic staging alcoholic liver disease

Prognosis of severe alcoholic liver disease (ALD) is bad. Mortality of patients with alcoholic hepatitis concurrent with cirrhosis id nearly 60% at 4 years.

Although alcohol is a direct hepatotoxin, it is unclear why only 10-20% of alcoholics will develop alcoholic hepatitis. It appears to involve a complex interaction of facilitating factors like drinking patterns, diet, obesity and gender.

Harmful use of alcohol results in 2.5 million deaths each yr. Most of the mortality is due to cirrhosis. The mortality is declining now because of decreased consumption of alcohol in the Western countries except in the U.K, Romania, Russia and Hungary.

a) Quantity and duration of alcohol intake - are the most important risk factors. Time taken to develop liver disease is directly related to the amount of alcohol consumed.
b) There is no clear role of the type of beverage and the pattern of drinking.
c) Genetic - some people are genetically predisposed  for alcoholism and subsequently to the ill effects of alcohol on the liver.
d) Gender - It is a strong determinant for ALD. Women are more susceptible to alcoholic liver injury. They develop advanced liver disease with substantially less alcohol intake. Gender-dependent differences may be due to the effects of estrogen, proportion of body fat and gastric metabolism of alcohol.
e) Chronic infection with Hepatitis C virus - It is an important comorbidity in the progression of ALD to cirrhosis in chronic and excessive drinkers. Even moderate alcohol intake of 20-50 g/day increases the risk of cirrhosis and hepatocellular cancer. Intake of more than 50 g/day decreases the efficacy of interferon-based antiviral therapy.

It is unclear but what is known is that alcohol can act as a direct hepatotxin and malnutrition does not play a major role.
- Alcohol is metabolised to acetyldehyde which in turn initiates an inflammatory cascade that results in a variety of metabolic responses.
- Steatosis from lipogenesis, fatty acid synthesis and depression of fatty acid oxidation occur secondary to effects on sterol regulatory transcription factor (SRTF) and peroxisome proliferator-activated receptor alpha (PPAR-alpha).
- Intestinal derived endotoxin initiates a pathogenic process through toll-like receptor-4 and TNF-alpha. This facilitates hepatocyte apoptosis and necrosis.
- Cell-injury endotoxin also activates innate and adaptive immunity pathways. There is release of pro-inflammatory cytokines (TNF-alpha) and proliferation of T/B cells.
- Production of toxic protein-aldehyde adducts, generation of reducing equivalents and oxidative stress also contribute to liver injury.

Finally hepatocyte injury and impaired regeneration are associated with stellate cell activation and collagen production which are key events in fibrogenesis. The resulting fibrosis causes architectural derangement of the liver and the associated pathophysiology.

Fatty liver is the initial and most common histologic response to hepatotoxic stimuli, including excess alcohol ingestion. Accumulation of fat within the perivenular hepatocytes coincides with the location of alcohol dehydrogenase. Continuing alcohol ingestion results in deposition of fat throughout the entire hepatic lobule.

Alcoholic fatty liver - traditionally regarded as benign but appearance of steatohepatitis and certain features like giant mitochondria, perivenular fibrosis and microvesicular fat are associated with progressive liver injury.

Hallmarks of alcoholic hepatitis include: (hepatocyte injury)
a) ballooning degeneration,
b) spotty necrosis,
c) polymorphonuclear infiltrate and
d) fibrosis in the perivenular and perisinusoidal space of Disse.

Mallory-Denk bodies are often present in florid cases but these are neither specific nor necessary to establish the diagnosis.

Usually the patients are asymptomatic.
Hepatomegaly is often the only clinical finding.
It is very important to assess the drinking history and estimate how much alcohol is consumed per day and for how long.
1 beer, 4-5 ounces of wine, 1.5 oz of 40% liquor and 1 ounce (approximately 30 mL) of 80% spirits all have around 12 g of alcohol.

Alcohol content of various beverages

- Patients with fatty liver may have:
1) right upper quadrant discomfort,
2) nausea and
3) rarely jaundice.

- Patients with alcoholic hepatitis may have:
1) fever
2) spider nevi
3) jaundice
4) abdominal pain.
We can also see portal hypertension, ascites and variceal bleeding even in the absence of cirrhosis.

These are most identified through routine screening tests.

Fatty liver - laboratory abnormalities are non-specific
Modest elevation of AST, ALT, GGTP are seen. Triglycerides and bilirubin may also be increased.

Alcoholic hepatitis
a) increased AST and ALT - by 2-7 fold but rarely greater than 400 IU.
b) AST/ALT ratio greater than 1.
c) hyperbilirubinemia
d) modest increase in alkaline phosphatase

If synthetic function is deranged then the condition is more serious. Hypoalbuminemia and coagulopathy are more common in advanced liver disease.

Ultrasonography is also a useful investigation as it can determine the size of the liver and detect any fatty infiltration. If it demonstrates portal vein flow reversal, ascites and intraabdominal venous collaterals then the condition has less potential for complete reversal.

Below is an ultrasonographic picture of hepatic steatosis. Fatty infiltration produces an increased reflectivity of hepatic parenchyma, known as ‘bright liver pattern’. This feature can be assessed by comparing liver parenchyma with the right kidney’s cortex, which normally presents an echogenicity equal to or slightly lower than that of the liver. Severe steatosis produces a strong attenuation in the deepest liver sections, resulting in poor explorability.

bright liver with posterior attenuation

Critically ill patients with alcoholic hepatatis have short term (30-day) mortality rates exceeding 50%.
A Discriminant Function (DF) above 32 and a Model for End-stage Liver Disease (MELD) greater than 21 is associated with poor prognosis.
Worse prognosis if there is associated:
a) ascites,
b) variceal hemorrhage,
c) deep encephalopathy and
d) hepatorenal syndrome.

mortality alcoholic liver disease

a) Complete abstinence from alcohol is the mainstay for treatment.
b) Patients with severe alcoholic hepatitis i.e. DF>32 and MELD>21 should be given Prednisone 40mg/day or Prednisolone 32mg/day for 4 weeks followed by tapering over 4 weeks.
c) Alternatively Pentoxifylline, a non-specific TNF inhibitor, can be used in a dosage of 400mg 3 times per day for 4 weeks.
d) Liver transplantation is an accepted indication for treatment in selected and motivated patients with end-stage cirrhosis.

Below is an algorithm showing how to manage alcoholic hepatitis:
algorithm alcoholic hepatitis

N.B Monoclonal antibodies that neutralize serum TNF-alpha should not be used as studies have reported an increase in the number of deaths secondary to infections and renal failure.

First published on: 23 September 2015

Tuesday, April 21, 2015



Homocysteine is a sulphur containing amino acid that is produced during the conversion of methionine to cysteine.

Hyperhomocysteinemia results when there is an abnormality in the homocysteine metabolism.
It is an independent risk factor for stroke, MI, peripheral arterial disease and venous thrombotic disease.

Even mild to moderate hyperhomocysteinemia is a significant risk factor for vascular disease.


The amino acid homocysteine is normally metabolized via the transsulfuration pathway by the enzyme cystathionine-β-synthase (CBS), which requires vitamin B6 as co-factor and via the
remethylation pathway by the enzymes methylenetetrahydrofolate reductase (MTHFR),
which is folate dependent and methionine synthase, which requires vitamin B12 as co-factor.

1 - Methylenetetrahydrofolate reductase
2 - Methionine synthase

Hyperhomocysteinemia can be either:
1) Inherited or
2) Acquired.

Inherited severe hyperhomocysteinemia (plasma level >100 µmol/L), as seen in classic homocystinuria, may result from homozygous MTHFR and CBS deficiencies and more rarely from inherited errors of cobalamin metabolism. Classic symptoms for homozygous patients include premature vascular disease and thrombosis, mental retardation, ectopic lens and skeletal abnormalities.

Inherited mild to moderate hyperhomocysteinemia (plasma level >15 to 100 µmol/L) may result from heterozygous MTHFR and CBS deficiencies, but most commonly results from the thermolabile variant of MTHFR (tlMTHFR) that is encoded by the C677T gene polymorphism. Heterozygous carriers of the tlMTHFR mutation have normal plasma homocysteine levels unless folate levels are

Acquired hyperhomocysteinemia may be caused by folate deficiency, vitamin B 6 or B 12 deficiency, renal insufficiency, hypothyroidism, type II diabetes mellitus, pernicious anemia, inflammatory bowel disease, advanced age, climacteric state, carcinoma (particularly involving breast, ovaries or pancreas) and acute lymphoblastic leukemia, as well as methotrexate, theophylline and phenytoin therapy.

VTE risk is most closely related to elevated fasting plasma homocysteine levels, regardless of etiology. Hyperhomocysteinemia (plasma level >18.5 µmol/L) has been associated with a two- to fourfold increased VTE risk.

The precise mechanisms underlying the thrombogenicity of homocysteine remain unclear. Several diverse mechanisms have been proposed, including endothelial cell desquamation, low-density lipoprotein (LDL) oxidation, promotion of monocyte adhesion to endothelium and factor V activation and promotion of thrombin generation.
Homocysteine also enhances platelet aggregation and adhesiveness as well as turnover, presumably as a result of endothelial cell injury.

Laboratory Diagnosis:
The initial step in the evaluation of the patient with suspected hyperhomocysteinemia involves measurement of fasting total plasma homocysteine (the sum of nonprotein-bound and proteinbound).
A normal value in the nonfasting setting does not normally require repeating.

Standardized methionine loading test
Testing 2 to 8 hours after an oral methionine load (100 mg/kg) increases the sensitivity of detecting occult vitamin B6 deficiency and obligate heterozygotes for CBS deficiency, but methionine loading is not routinely recommended.
Vitamin B12 and folate deficiency do not affect post-methionine loading homocysteine values.
After 4-6 hours the level of homocysteine is measured again.
A level 5 times that of the fasting one or an increase by 40 µmol/L is considered a positive test for hyperhomocysteinemia.
In patients found to have elevated levels of homocysteine, testing for vitamin B12 deficiency is advocated to avoid missing subclinical deficiency before
beginning oral folic acid therapy.

1) Folic acid supplementation is the mainstay therapy. The usual recommended dose is 0.4 to 1.0 mg daily. This causes a 25% decrease in the homocysteine level.
2) Because patients with subclinical vitamin B12 deficiency may be prone to developing
peripheral neuropathy if they receive folic acid supplementation alone, additional treatment with 0.5 mg/day of oral vitamin B12 has been advocated. An additional 7% reduction of homocysteine levels was noted with vitamin B12 supplementation.
Vitamin B12 administration results in normalization of homocysteine levels in B12-deficient individuals. In these patients, a monthly intramuscular injection of 200 to 1,000 µg of vitamin B12 is considered adequate replacement.
3) Vitamin B6 supplementation did not appear to have any effect on homocysteine levels.
4) Thrombotic events in hyperhomocysteinemic patients should be treated accordingly.

Monday, March 9, 2015

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kussmaul breathing pattern - description and causes

This type of breathing pattern was first described by Adolph Kussmaul, a german physician in 1874. He noticed that his patients with diabetic ketoacidosis had a pattern of breathing which he first labelled as having "air hunger".

In the Kussmaul type of breathing, the patient is breathing heavily i.e hyperventilating along with tachypnea.
So we will find that the amplitude of the breaths along with the rate will be increased.
There is usually no pauses between the breaths.

This is not specific for diabetic ketoacidosis. It can also appear in other types of severe metabolic acidoses e.g alcoholic ketoacidosis .

Saturday, April 26, 2014


Diaxozide - mechanism of action

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.

Diaxozide acts by opening the K+ channel. This leads to loss of K+ and causing membrane hyperpolarization. This prevents Ca2+ from entering, protein kinases are not activated and thus there is no exocytosis of insulin granules... 

Sunday, December 15, 2013


Prognostic scores in alcoholic hepatitis

1. Maddrey (modified) Discriminant Function score of greater or equal to 32 indicates a high risk (30-50%) risk of mortality at 30 days. The risk is even higher is there are signs of hepatic encephalopathy. Scores should be repeated at day 7.

2. MELD stands for Model for End stage Liver Disease. It is used to estimate 90 days mortality. Poor prognosis if score is greater than 18. Score should be repeated at day 7.

Sunday, October 6, 2013


Effect of weather on COPD

Exacerbations of COPD are more commonly seen during the winter season (nearly 1.6 times more frequently). The main cause of these exacerbations is infection with the respiratory virus, rhinovirus.
Frequent exacerbations have been shown to lead to a faster decline in the lung function, poorer quality of life and increased mortality.
A recent study showed that COPD exacerbations in colder periods of the year take longer to recover from and are more likely to involve cough or coryzal symptoms. The exacerbations in the cold seasons also have a greater impact on daily activity, with patients spending more time indoors and being more likely to be hospitalized with respiratory viral infection.

Sunday, June 2, 2013


Diabetes - 7 keys messages to the patients

1. Diabetes is self-managed.

Caring for diabetes is more than just taking a daily pill or doing your insulin injection. It may feel like a burden but the decisions you make about physical activity, what and when you will eat will affect both how you feel today and your future health and well-being.

2. Take diabetes seriously.

It is a multi-systemic disorder and indeed needs a lot of care. Since the symptoms and complications take time to appear you may think that it is a simple disease but it is not in reality!!!

3. Learn everything about the disease.

Since most of diabetes care is  about self-care, the more you know about it, the better you will be able to manage it. You can control your diabetes rather than letting your diabetes control you. If possible, try to get updated with latest developments in the field and read to drive away myths about the disease.

4. Your treatment will change over time.

Treatment of diabetes will eventually change over time. Changes in treatment do not mean that you have failed or that your diabetes is worse. It simply means that your body needs more help to keep your blood glucose level on target. Insulin therapy is part of the treatment and not a punishment.

5. Negative emotions are common.

It can be difficult to live with diabetes and researchers have shown that patients are about twice as likely to become depressed. Let your doctor know if your emotions are getting in the way of managing diabetes or enjoying your daily life. Do not hesitate to go for a psychological evaluation.

6. Step by step is the motto.

Diabetes often involves making changes in your food, exercise and other habits. It can quickly become too hard if you try to do it all at once. Start by choosing one thing that is important to you. Try to make small changes each day. It is likely that you will try different things along the way. Use what you learn about what does and does not work as a guide. Perfection is not the goal. It is what you do most of the time that counts.

7. Complications don't always happen.

You may have seen the toll of long-term complications on others. The good news is that these can be delayed or prevented by keeping your blood glucose and blood pressure levels in the target ranges. There are no guarantees, but you can greatly reduce your risk.

Living with diabetes is not easy. But with the help of your health care team and your family and friends, you can do it.

Thursday, May 2, 2013

Mediterranean diet and cognitive decline

A Mediterranean diet is one which comprises of fresh vegetables, fruits, beans, whole grains, nuts, olives, and olive oil along with some cheese, yogurt, fish, poultry, eggs, and wine.
A recent study has shown that this diet if adopted and followed leads to a slower decline in the cognitive function. The two main hypotheses are that it has a lot of anti-oxidants which prevent cell death in the brain and secondly it has a protective effect on the vasculature of the brain and thus prevents vascular dementia. Thus, the Mediterranean diet not only improve your looks and protects your cardiovascular system but also your brain cells benefit from it.

Wednesday, May 1, 2013


Highest prevalence of Diabetes Mellitus

Figures till November 2012 show that the top 5 countries with the highest prevalence of Diabetes Mellitus are from the pacific islands. They may be the smallest islands but the epidemic of diabetes is one of the worst there. More than a third of adults in some of these countries have diabetes and the combined toll of complications, deaths and loss of income make diabetes a real threat not just to the individuals experiencing the disease but also to the economies of the countries themselves.

Above is an image showing the locations of the pacific islands.


Top 10 countries with Diabetes Mellitus 2012

Data till November 2012 showed that together, these 10 countries make up 75% of the total prevalence of diabetes in the world.  Urbanisation and the accompanying changes in lifestyle are the main drivers of the epidemic in addition to changes in population structure where more people are living longer.

Friday, April 19, 2013


Anemia in diabetic patients - Erythropoietin treatment?

If you encounter a normochromic and normocytic anemia in a diabetic patient, do not forget that it may be a case of erythropoietin deficiency. This deficiency can occur early in diabetic nephropathy (well before stage 5 of chronic kidney disease).

In adults, about 85-90% of the erythropoietin comes from the kidneys and 10-15% from the liver. It is produced by interstitial cells in the peritubular capillary bed of the kidneys and by perivenous hepatocytes in the liver. In cases of decreased renal mass, the level of erythropoietin falls and does not increase much in response to hypoxia (anemia). This occurs even if the liver is normal as the latter cannot compensate for the kidney's loss of function.

Since the availability of recombinant human erythropoietin to patients in 1989, anemia and transfusion requirements have become relatively  rare in patients on hemodialysis.
After adequate treatment with erythropoietin, studies have demonstrated that there is an:
1) enhanced exercise capability, presumably partly because of improved cardiac function with reduction in ventricular hypertrophy,
2) improved quality of life with improved physical performance, work capacity and cognitive capacity,
3) improved sexual function,
4) reduced rates of hepatitis and iron overload because of fewer transfusions.

All of the erythropoietin preparations are now referred to collectively as erythropoiesis stimulating-agents (ESAs). So far, intravenous route has been the sole route of administration and is given during hemodialysis but investigations are going on about the possibility of subcutaneous administrations.

With subcutaneous administration, peak serum concentrations of about 4% to 10% of an equivalent IV dose are obtained at around 12 hours, and thereafter they decay slowly such that concentrations greater than baseline are still present at 4 days.
The bioavailability of subcutaneous epoetin is around 20% to 25%. Nevertheless, subcutaneous application
is more efficient than IV application, allowing an approximately 30% dose reduction to maintain the same hemoglobin concentration.
Presumably, the early peak concentrations of epoetin after IV injection are inefficient, but the more prolonged elevation of hormone concentrations after subcutaneous application allows a more sustained stimulation of red cells production. Thrice-weekly administration has remained the most popular dosage frequency for both IV and subcutaneous administration, although once-weekly, twice-weekly and
seven-times-weekly (once-daily) dosing have all been used.

The hemoglobin target should be in the range of 11-12 g/dL and should not be greater than 13 g/dL.

Above is a diagram showing the change in hemoglobin level (blue line) with respect to different dosage of erythropoietin from 1991 till 2009 in an attempt to keep the hemoglobin in the target range. Hemoglobin level should be tested at least once monthly. 

Thursday, March 7, 2013


Acanthosis nigricans - cause and significance

Acanthosis nigricans is a hyperpigmented velvety lesion usually found in the neck and the axillary region. It can also be seen elsewhere e.g. the belt line, creases over the dorsal surface of fingers. The palms and soles are typically not involved.

Pathologically, it is characterized by an increased number of melanocytes associated with hyperkeratotic epidermal papillomatosis.

It is strongly associated with insulin resistance but it is a non-specific condition and can also be found in obesity, polycystic ovarian syndrome, endocrine diseases like acromegaly and Cushing's syndrome, as well as some malignant tumours.

The severity of the acanthosis nigricans correlates with the degree of insulin resistance and the level of serum insulin.
The exact mechanism of its formation is still unclear but it is speculated that there are related IGF-1 receptors in the skin which are activated by ambient hyperinsulinemia.

If the insulting factor is removed, there may be a regression of the lesion.

Below are photos of a patient requiring more than 100 IU of insulin per day and despite dieting, the level of glycemia remained high.

It is an interesting case because it is an atypical location for acanthosis nigricans. The back of neck and axilla were free of any lesions.

Wednesday, March 6, 2013


Classification of Diabetes Mellitus

Diabetes is divided into 4 different classes:

1) Type 1 diabetes (results from beta-cell destruction, usually leading to absolute insulin deficiency)
2) Type 2 diabetes (results from a progressive insulin secretory defect on the background of insulin resistance)
3) Other specific types of diabetes due to other causes, e.g. genetic defects in beta-cell function, genetic defects in insulin action, diseases of the exocrine pancreas (such as cystic fibrosis, pancreatitis) and
drug- or chemical-induced (such as in the treatment of HIV/AIDS or after organ transplantation)
4) Gestational diabetes mellitus (GDM) (diabetes diagnosed for the first time during pregnancy that is not clearly overt diabetes).

Saturday, February 16, 2013


Respiratory failure - Definition, classification and difference between acute and chronic type

Respiratory failure may be classified as hypercapnic or hypoxemic.
Hypercapnic respiratory failure is defined as an arterial PCO2 (PaCO2 ) greater than 45mmHg.
Hypoxemic respiratory failure is defined as an arterial PO2 (PaO2 ) less than 55 mmHg when the fraction of oxygen in inspired air (FiO2) is 0.60 or greater.
In many cases, hypercapnic and hypoxemic respiratory failure coexist.

Distinctions between acute and chronic respiratory failure are summarized in the table below.

In general, acute hypercapnic respiratory failure is defined as a PaCO2 greater than 45 mmHg with accompanying acidemia (pH less than 7.30). The physiological effect of a sudden increase in PaCO2
depends on the prevailing level of serum bicarbonate anion. In patients with chronic hypercapnic respiratory failure e.g. COPD, a long-standing increase in PaCO2 results in renal compensation and an increased serum bicarbonate concentration. A superimposed acute increase in PaCO2 has a less dramatic effect than does a comparable increase in a patient with a normal bicarbonate level.

Distinction between acute and chronic hypoxemic respiratory failure may not be readily made on the basis of arterial blood gas values only. The presence of markers of chronic hypoxemia (e.g., polycythemia or cor pulmonale) provides clues to a long-standing disorder, whereas abrupt changes in mental status suggest an acute event.

Monday, February 11, 2013

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May-Thurner syndrome

As seen in the diagram above, the left common iliac vein is predisposed to be compressed by the right common iliac artery. This can lead to stasis and eventually causing thrombosis. Another effect is that the pulsatile nature of the artery over the vein leads to turbulence in the blood flow, thereby favouring thrombosis. 
Because of this anatomical predisposition, most Deep Vein Thrombosis (DVT) seen during pregnancy occur in the left iliac vein system. All the classic investigations done for cases of DVT should be performed here also.

Friday, November 23, 2012


Barrel shaped chest

Barrel shaped chest is commonly encountered in the clinical setting. It is seen in emphysema, hence also called as emphysematous chest. The anteroposterior diameter is increased (normally transverse:AP diameter is 7:5). The subcostal angle is wide (usually it is acute at around 70 degrees). The angle of Louis is unduly prominent with the sternum more arched. The spine is concave forwards and the ribs are less oblique.

The respiratory movements are diminished bilaterally, with the mediastinum remaining in the central position. On percussion, the lung is hyper-resonant. On auscultation, there is a diminished vesicular breathing with a prolonged expiration. Rhonchi may be present.

Wednesday, October 31, 2012

Body Mass Index - BMI

Body Mass Index is also known as the Quetelet Index, after the Belgian astronomer, statistician, sociologist and mathematician Lambert Adolphe Jacques Quetelet. It is a very easy and frequently used method to assess obesity, though it is not a direct measure of adiposity.

It is calculated by dividing the patient body mass (kg) by the square of his/her height (m).
BMI = kg/m2

Classification of weight status:

BMI (kg/m2)
Obesity Class Risk of Disease
Underweight < 18.5
Healthy weight 18.5–24.9
Overweight 25.0–29.9 Increased
Obesity 30.0–34.9 I High
Obesity 35.0–39.9 II Very high
Extreme Obesity > 40 III Extremely high

Obesity is defined as a BMI varying from 30-39.9 kg/m2. It is further classified into grades I, II and III. Extreme obesity with a BMI of greater than 40 is also called as morbid obesity. As seen on the right side of the table above, being overweight and the various classes of obesity is closely related to the risk of cardiovascular diseases.

The BMI is also used to categorize patient for appropriate therapies. The latter can range from lifestyle modifications for overweight, pharmacotherapy for obese and surgery for extremely obese patients.