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

Sunday, October 28, 2012

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Ataxic gait

This type of gait can be seen in cases of cerebellar or sensory ataxia.

Cerebellar ataxia and gait:

The problem here lies with the coordinating mechanisms in the cerebellum and its connecting systems. The gait is a clumsy, staggering, unsteady, irregular, lurching, titubating and wide-based. The patient may sway to either side, back or forward. Leg movements are erratic, and step length varies unpredictably.
The patient is unable to follow a straight line on the floor (to walk tandem).

With a lesion of the cerebellar vermis, the patient will exhibit a lurching, staggering gait but without laterality, the ataxia will be as marked toward one side as the other.
Cerebellar ataxia is present with eyes both open and closed; it may increase slightly with eyes closed but not so markedly as in sensory ataxia.

A gait resembling cerebellar ataxia is seen in acute alcohol intoxication.

With a hemispheric lesion the patient will stagger and deviate toward the involved side. In disease localized to one cerebellar hemisphere or in unilateral vestibular disease, there is persistent swaying or deviation toward the abnormal side. As the patient attempts to walk a straight line or to walk tandem he deviates toward the side of the lesion.
A patient with acute vestibulopathy will drift toward the involved side walking forward, and continue to drift during the backward phase. The resulting path traces out a multipointed star pattern. Walking a few steps backward and forward with eyes closed may bring out “compass deviation” or a “star-shaped gait”.
When attempting to walk a fixed circle around a chair, clockwise then counterclockwise, the patient will tend to fall toward the chair if it is on the side of the lesion, or to spiral out away from the chair if on the opposite side.

Either unilateral cerebellar or vestibular disease may cause turning toward the side of the lesion on the Fukuda stepping test. For all the tests that bring out deviation in one direction, other findings must be used to differentiate between vestibulopathy and a cerebellar hemispheric lesion. Unilateral ataxia may be demonstrated by having the patient attempt to jump on one foot, with the eyes either open or closed. The patient with bilateral vestibular disease may seek to minimize head movement during walking, holding the head stiff and rigid; having the patient turn the head back and forth during walking may bring out ataxia.

Sensory ataxia and gait:

The patient in this condition is extremely dependent on visual input for coordination. When deprived of visual input, as with eyes closed or in the dark, the gait deteriorates markedly. The difference in walking ability with and without visual input is the key feature of sensory ataxia. If the condition is mild, locomotion may appear normal when the patient walks eyes open. More commonly it is wide based, and poorly coordinated.

The term “steppage gait” refers to a manner of walking in which the patient takes unusually high steps. Sensory ataxia is one of the causes of a steppage gait. The patient takes a high step, throws out her foot and slams it down on the floor in order to increase the proprioceptive feedback. The heel may land before the toe, creating an audible “double tap.” An additional sound effect may be the tapping of a cane, creating a “slam,slam, tap” cadence. The sound effects may be so characteristic that the trained observer can make the diagnosis by listening to the footfalls.

The patient with sensory ataxia watches her feet and keeps her eyes on the floor while walking. With eyes closed, the feet seem to shoot out, the staggering and unsteadiness are increased, and the patient may be unable to walk. There is less reeling and lurching in sensory ataxia than with a comparable degree of cerebellar ataxia. The difficulty is even worse walking backward, since the patient cannot see where she is going. The patient with bilateral foot drops, however, also has a steppage gait and a double tapping sound striking.

In all of these tests, sensory ataxia can be differentiated from predominantly cerebellar ataxia by accentuation of the difficulty with eyes closed; and unilateral cerebellar or vestibular disease from vermis involvement by laterality of unsteadiness.


Sunday, October 14, 2012

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Edema - Definition, pathophysiology, causes, clinical features


 DEFINITION 
Edema is an abnormal presence of excessive fluid in the interstitial space.

 PATHOPHYSIOLOGY 
The movement of water and low molecular weight solutes such as salts between the intravascular and interstitial spaces is controlled primarily by the opposing effect of vascular hydrostatic pressure and plasma colloid osmotic pressure. Normally the outflow of fluid from the arteriolar end of the microcirculation into the interstitium is nearly balanced by inflow at the venular end. A small residual amount of fluid may be left in the interstitium and is drained by the lymphatic vessels, ultimately returning to the bloodstream via the thoracic duct.


Either increased capillary pressure, diminished colloid osmotic pressure or inadequate lymphatic drainage can result in an abnormally increased interstitial fluid i.e. edema. An abnormal increase in interstitial fluid within tissues is called edema, while fluid collections in the different body cavities are variously designated hydrothorax (pleural cavity), hydropericardium (pericardial cavity) and hydroperitoneum (the last is more commonly called ascites). Anasarca is a severe and generalized edema with widespread subcutaneous tissue swelling.


The diagram above shows the actual change in pressure gradients at the capillary level. The numbers represent the pressure in the vessels in mmHg.
At the arteriolar end, the hydrostatic pressure (outward force) is 37 mmHg while the oncotic pressure and interstitial pressure (inward forces) are 25 and 1 mmHg respectively. Thus the net outward force is 37 – (25+1) = +11 mmHg. Since the net outward force is positive fluid moves from the capillary to the interstitial spaces.
At the venular end, the hydrostatic pressure is lower and has a value of 17 mmHg. The oncotic and interstitial pressure on the other hand remain the same i.e. a total of 26 mmHg (25+1). Thus the net outward force is 17 – (25+1) = -9 mmHg. Since the outward force is negative, it means fluid is not getting out of the capillary but instead it is moving into it.

The arrows in the diagram show the magnitude and direction of net fluid movement.

 CLASSIFICATION  
1) According to pathophysiological mechanism:
                a) Transudate (low protein content)
                b) Exudate (high protein content)
2) According to location:
                a) Localized
                b) Generalized
3) According to clinical finding:
                a) Pitting
                b) Non-pitting.

 LOCALIZED EDEMA 
It means that the edema is localized to a specific region of the body. It is commonly due to venous/lymphatic causes, allergy and inflammation.

1) Venous edema: It is due to high venous pressure or venous constriction. Intravascular venous obstruction e.g. Deep vein thrombosis (DVT) or an external compression like a mass (tumour) or plaster are the common causes but there can also be failure of venous pumps due to paralysis of muscles (Cerebro-vascular accident), immobilization of parts of the body (Post-op, fractures) and failure of venous valves (Varicose veins). It is more frequent to see localized edema in the lower limbs but the upper limbs may also be affected.

2) Lymphatic edema: It is due to a blockage in the lymphatic return. It commonly occurs in conditions like cancer/ post-radiation, infections like elephantiasis (Filaria nematodes), surgery or congenital absence or abnormality of lymphatic vessels. The edema is persistent and non-pitting type. In case of elephantiasis, the affected limb may be dramatically enlarged.

3) Allergy/Angioedema (Quincke edema): During a case of allergy there is release of histamine and other mediators that lead to vasodilation. The swelling can involve the face, lips, tongue and even glottis. Edema of the glottis is a medical emergency as it can lead to asphyxia if not treated quickly. This type of edema is usually itchy but transitory. It resolves with antihistaminics and steroids.

4) Inflammation: Here also there is vasodilation because of the inflammatory mediators. Edema is seen with superficial (cellulitis) or deep infections (abscess).

 GENERALIZED EDEMA 
In this case the edema involves more than 1 part of the body simultaneously. It is commonly due to cardiac, hepatic, renal or endocrine causes.

1) Cardiac edema: The initial pathology is because of increased venous pressure but as the condition becomes more severe, there is impairment of renal blood supply, activation of rennin-angiotensin-aldosterone system and finally hypoalbuminemia secondary to liver stasis. Left sided heart failure leads to pulmonary edema while right sided heart failure causes peripheral edema, ascites, hydrothorax and anasarca in severe and long standing cases. The edema is progressive. In ambulant individuals, it moves up with severity. The edema is usually of pitting type. In early stages of heart failure, there is improved renal circulation at night leading to nycturia. Thus the edema will be less in the morning and progressively increases towards the end of the day.

2) Hepatic edema: Liver pathology like cirrhosis leads to decreased synthesis of proteins. The hypoalbuminemia leads to decreased oncotic pressure. The scarred liver also causes a back pressure in the portal vein territory (portal vein hypertension) and increases the hydrostatic pressure there. These 2 factors combined lead to edema in the peritoneal cavity (ascites) and this in turn compresses the inferior vena cava and leads to edema in the lower limbs.

3) Renal edema: Kidney diseases like nephritic syndrome with decreased glomerular filtration rate and sodium/water retention or nephrotic syndrome where there is albumin loss in the urine lead to generalized edema. The edema frequently occurs in lax connective tissue like the face, periorbital area and genitalia. It is of pitting type. It occurs mostly during the morning and is associated with vasoconstriction. Thus it is called as ‘white’ edema.

4) Endocrine edema: Many endocrine problems can cause edema. In case of hyperaldosteronism (primary or secondary), there is retention of sodium and water. This leads to an increase in hydrostatic pressure. The edema is of pitting type. On the other hand, myxedema refers to a non-pitting type of edema seen in hypothyroidism. Finally, females experience edema as part of the pre menstrual syndrome due to hormonal changes.

 CAUSES OF EDEMA (ACCORDING TO PATHOPHYSIOLOGY) 
  1. Increased capillary pressure (increased hydrostatic pressure)
    1. Excessive kidney retention of salt and water
      1. Acute or chronic kidney failure
      2. Mineralocorticoid excess
    2. High venous pressure and venous constriction
      1. Impaired heart functioning (Congestive heart failure, constrictive pericarditis)
      2. Venous obstruction (Deep vein thrombosis, External compression like a mass or plaster)
      3. Failure of venous pumps
        • (a) Paralysis of muscles (Cerebro-vascular accident)
        • (b) Immobilization of parts of the body (Post-op, fractures)
        • (c) Failure of venous valves (Varicose veins)
    3. Decreased arteriolar resistance
      1. Excessive body heat
      2. Insufficiency of sympathetic nervous system
      3. Drugs (vasodilators, calcium channel blockers)
  2. Decreased plasma proteins
    1. Loss of proteins in urine (Nephrotic syndrome) or G.I.T (Protein-losing gastroenteropathy)
    2. Loss of protein from denuded skin areas
      1. Burns
      2. Wounds
    3. Failure to produce proteins
      1. Liver disease (Cirrhosis)
      2. Serious protein or caloric malnutrition
  3. Increased capillary permeability
    1. Immune reactions that cause release of histamine and other immune products (Allergy)
    2. Toxins
    3. Bacterial infections (Cellulitis)
    4. Vitamin deficiency, especially vitamin C
    5. Prolonged ischemia
    6. Burns
  4. Blockage of lymph return
    1. Cancer
    2. Infections (Filaria nematodes)
    3. Surgery
    4. Congenital absence or abnormality of lymphatic vessels
    5. Post-radiation.
 CLINICAL FEATURES 
In dependent edema, which is typically present in congestive heart failure and in conditions associated with a low plasma protein level, the swelling first appears at the ankles and over the dorsum of the foot and only gradually involves the legs, thighs and trunk. The best place to check for slight degrees of edema in an ambulant patient is behind the malleoli at the ankles. In bed-bound patients edema often appears first over the sacrum. To recognize pitting edema it is important to press firmly and for a sustained period of 20-30s over a bony prominence (tibia, lateral malleoli or sacrum) to provide effective compression. The 'pit' will be as easily felt as seen. If the finger pressure is not maintained for an adequate period of time then slight degrees of edema may be overlooked.

Edema can be recognized by the pallid and glossy appearance of the skin over the swollen part, by its doughy feel and by the fact that it pits on finger pressure.
The edema of lymphatic obstruction does not pit on pressure or there may be minimal pitting. The skin is usually thickened and tough.

 N.B 
1) Without redness and scaling, bilateral periorbital edema may indicate acute nephritis, nephrosis or trichinosis. If there is irritation, contact dermatitis is the probable diagnosis.
2) In local venous obstruction the edema is confined to the parts from which the return of blood is impeded. Local edema is sometimes seen over inflamed joints.
3) Edema of the whole upper part of the body may result from intrathoracic tumours.

Last reviewed on: 1 September 2015





Wednesday, October 3, 2012

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Type 2 Diabetes Mellitus - Exercise benefits and regime

The positive benefits of exercise in a diabetic patient include:
1) cardiovascular risk reduction,
2) reduced blood pressure,
3) maintenance of muscle mass,
4) reduction in body fat and weight loss,
5) lowering plasma glucose (during and following exercise) and
6) increasing insulin sensitivity.

Also since the diabetics lack the normal glucoregulatory mechanisms, they are more prone to be affected by either hypo or hyperglycemia if exercising. That is why it is better to have the blood glucose monitored before, during and after the exercises.
It is not advised to do exercises if the blood glucose level is below 5.6 mmol/L or more than 14 mmol/L with ketones present.

The exercise regime recommended is as follows:
1) At least 150 minutes of moderate to vigorous exercise per week distributed over at least 3 days. One example of such a moderately intense exercise is brisk walking.
2) Ideally resistance training should also be done for 3 non consecutive days per week. e.g. small weight lifting.

Use of pedometer applications in mobile phone devices is also favoured. Studies have found that doing 10,000 steps per day is a good indicator of proper physical activity and will be beneficial on the long run.

Another important finding in a recent study found that in diabetic patients who did little or no exercise at baseline, cut their risk of death by 2/3 if they substantially increase their physical activity level over a period of 5 years.

Monday, August 27, 2012

Statins and muscle weakness

Muscle weakness is a well known side effect of statin use. This symptom is very commonly ignored both by the patients and the doctors.
Recent studies suggest that the higher potency statins i.e the ones causing a bigger drop in cholesterol/mg of active product are also the ones more likely to cause muscle weakness as a side effect.
In order of potency the statins are as followed :
1) Rosuvastatin
2) Atorvastatin
3) Simvastatin
4) Pravastatin
5) Lovastatin

So, it is always better not just to look at the altered hepatic functions during follow up visits. Do ask about the adverse side effects also and use a less potent statin if required.

Sunday, August 26, 2012

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Colchicine - complete information


Introduction:
Colchicine is an alkaloid isolated from the autumn crocus, Colchicum autumnale. It is actually present in the corm of the plant, the underground swollen part of the stem.

Pharmacokinetics:
Colchicine is absorbed readily when taken in orally. It reaches peak plasma levels within 2 hours. 
It has a serum half-life of 9 hours. 
Colchicine is partially deacetylated in the liver and the unchanged drug and its metabolites are excreted in the bile and undergo intestinal reabsorption. Colchicine is found in high concentrations in leucocytes, kidneys, the liver and spleen. Most of the drug is excreted in the feces but 10 to 20% is excreted in the urine and this proportion rises in patients with liver disorders. For patients with creatinine clearance of < 50 mL/min, colchicine must be avoided or used at a lower dose. Colchicine is also distributed into breast milk.

Pharmacodynamics:
Colchicine relieves the pain and inflammation of gouty arthritis in 12-24 hours. It does not alter the metabolism or excretion of urates. It also does not have other analgesic effects.
It is an anti-inflammatory agent. 
The mechanism of action is that it binds to the intracellular protein tubulin, thereby preventing its polymerization into microtubules. This causes the inhibition of leukocyte migration and phagocytosis. It also inhibits the formation of leukotriene B4. Colchicine also blocks cell division by binding to mitotic spindles and arrests the cell division at metaphase. Several of colchicine's adverse effects are produced by its inhibition of tubulin polymerization and cell mitosis.

Indications:
NSAIDs have replaced colchicine in the treatment of acute gout because of the troublesome diarrhea associated with colchicine therapy and because of its low therapeutic index. Previously it was used to treat an acute attack. It relieved the pain in more than 95% of cases and also provided a diagnostic confirmation because it is more or less specific for relief of pain due to acute gout. Non-gouty arthritis are unaffected.
1) Colchicine is now used for the prophylaxis of recurrent episodes of gouty arthritis. Its effectiveness is up to 80%.
2) It is also effective in reducing frequency of attacks in acute Mediterranean fever. It also prevents amyloidosis and reverses proteinuria
3) It may have a mild beneficial effect in sarcoid arthritis and in hepatic cirrhosis.
Although it can be given intravenously, this route should be used cautiously because of increased bone marrow toxicity.

Adverse Effects:
Colchicine often causes diarrhea and may occasionally cause nausea, vomiting and abdominal pain. The GIT is most commonly affected because it is the route of intake and of major excretion. Rarely chronic use of colchicine may cause hair loss and bone marrow depression (aplastic anemia, neutropenia) as well as peripheral neuritis and myopathy.

Acute intoxication after overdoses is characterized by burning throat pain, bloody diarrhea, shock, hematuria and oliguria. Fatal ascending central nervous system depression has been reported. Treatment is supportive. The fatal dose is as low as 7 mg.

Dosage:
1) The prophylactic dose of colchicine is 0.5-0.6 mg 1-3 times daily.
2) If used to terminate an attack of gout, the traditional initial dose of colchicine is usually 0.6 or 1.2 mg, followed by 0.6 mg every 2 hours until pain is relieved or nausea and diarrhea appear. A lower dose regimen of 1.2 mg initially, followed by 0.6 mg oral is as effective as the high dose regimen.
Normally we should not exceed 6 mg per acute attack and the dose should not be repeated within 7 days.
3) For Mediterranean fever, 1-1.5 mg 3 times/day is the prophylactic dose.


N.B:
1) IV use of colchicine is not recommended.
2) Colchicine use is contraindicated in pregnancy.
3) 0.6 mg/day for a creatinine clearance of 35-50 mL/min, 0.6 mg every 2 to 3 days for creatinine clearances of 10-35 mL/min and avoidance in those with creatinine clearance of less than 10 mL/min or with combined hepatic and renal disease.
4) Use of colchicine with clarithromycin, erythromycin or tolbutamide may cause colchicine toxicity. Thiazide diuretics may increase serum uric acid and interfere with the activity of colchicine.
5) Colchicine may impair the absorption of vitamin B12.
6) Acute myopathy has been reported in patients with chronic renal impairment given colchicine with Simvastatin. This is so because both drugs are metabolized by the cytochrome P450 isoenzyme CYP3A4.
7) Tetraparesis developed in a patient who took colchicine with verapamil. This was considered to be due to a pharmacokinetic interaction which increased serum and CSF concentrations of colchicine. 

Friday, August 24, 2012

Unilateral edema in limbs - common causes

1) Lymphatic: Filariasis, Pressure by growths like tumours, Radiation, Chronic lymphangitis
2) Traumatic: Bruises, Sprains, Fractures
3) Infections: Cellulitis, Boils, Carbuncles
4) Metabolic: Gout
5) Venous: Varicose veins, Venous thrombosis
6) Hereditary: Milroy's disease

Saturday, August 18, 2012

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Pulmonary embolism due to metallic mercury


Above is a chest radiograph of a schizophrenic patient. He was delusional about being a doctor. He used to read a lot of medical books and mastered the art of taking blood pressure. During an episode of psychosis, he broke the blood pressure apparatus and injected the mercury into his vein. We can see in the X-ray that there is micro-embolism of the liquid mercury to the pulmonary arterioles, mostly to the dependent areas and the arrow indicates a small pool of the mercury in the right ventricle.

Popliteal artery cyst


This is a popliteal arteriogram of a 27 year old male who presented with pain in left calf when exercising. Signs of deep vein thrombosis were negative but there was minimal swelling at the left ankle. A palpable pulsatile mass could be felt on the popliteal fossa. On arteriography a filling defect was obtained as shown in the picture above. CT scan confirmed that the cyst was within the popliteal artery wall.

Sunday, August 5, 2012

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Insulin - Structure

Insulin is a protein hormone. It was the first protein to be shown to have a precisely defined amino acid sequence. This work was done by Federick Sanger in 1953. 
As shown above in two colours, the insulin molecule consists of 2 peptide chains. 
a) The blue coloured chain is the A chain. It has 21 amino acids and a sisulphide bond within itself. 
b) The yellow colour represents the B chain. It is larger with 30 amino acids. 
Both chains are connected by 2 disulphide bridges. 
Porcine and bovine insulins differ from human insulin at 1 and 3 positions of the amino acids respectively. 

Friday, July 20, 2012

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Diabetes Mellitus - Definition / Criteria for diagnosis

Definition:
It is a group of metabolic disorders that is characterized by hyperglycemia which is due to a relative or absolute deficiency in insulin. There is usually a defect in insulin secretion, a defect in insulin action or a combination of both. 


Criteria for diagnosis:
1) An Fasting Plasma Glucose ≥ 7.0 mmol/L (126 mg/dL), 
2) A Plasma Glucose  ≥ 11.1 mmol/L (200 mg/dL) 2 h after an oral glucose tolerance test,
3) An HbA1c    6.5% or
4) A Random Plasma Glucose concentration   11.1 mmol/L (200 mg/dL) accompanied by classic symptoms of DM (polyuria, polydipsia, polyphagia, weight loss). 


Note:
1) Fasting means no calorie intake for the past 8 hours.
2) For the glucose tolerance test, we must use 75 g of anhydrous glucose dissolved in water.
3) The diagnostic HbA1c test should be performed using a method certified by the National Glycohemoglobin Standardization Program (NGSP) and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference assay. The currently available assays are not accurate enough.
4) Random Plasma Glucose means without regard to time since last meal. 

Thursday, July 19, 2012

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Chronic Obstructive Pulmonary disease - Definition

COPD is a preventable and treatable systemic disease state characterized by a progressive airflow limitation that is not fully reversible and associated with an abnormal inflammatory response of the lungs to noxious particles and gas.

Note that the new definition according to GOLD/ATS and ERS does not talk anything about the disease being a mixture of chronic bronchitis and emphysema, though these conditions are very frequently encountered in COPD and also the fact of being 'not fully reversible' distinguishes this disease from the other chronic obstructive condition which is bronchial asthma.

Thursday, July 5, 2012

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Centriacinar / Centrilobular emphysema

In a classical lesion, dilated and destroyed respiratory bronchioles coalesce in series and in parallel to produce sharply demarcated emphysematous spaces. They are separated from the acinar periphery (the  lobular septa) by intact alveolar ducts and sacs of normal size, as shown by the diagram below. 


The lesions vary in quality and quantity even within the same lung. There is striking irregularity of involvement of lobules, and even within the same lobule. The lesions are usually more common and become more severe in the upper than in the lower zones of the lung. Most affected are the upper lobe, particularly the posterior and apical segments, and the superior segment of the lower lobe as depicted below. 


This type of emphysema is commonly seen in chronic cigarette smokers. For classification of emphysema, follow this link: Emphysema


Wednesday, June 27, 2012

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Aminotransferases (Transaminases)


Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are measured by the serum glutamic-oxaloacetic  transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) respectively. They are important markers of hepatocellular injury.

Normal values:  (varies from lab to lab but on average)
ALT : 7-41 U/L
AST: 12-38 U/L

AST can be found in various tissues like cardiac/skeletal muscles, kidney, brain and liver.
ALT is limited primarily to the liver and thus ALT is a more specific reflection of hepatocellular disease than AST.

The highest elevations of both enzymes are seen in viral, toxin-induced and ischemic hepatitis. On the other hand, alcoholic hepatitis usually gives a lower raise of around < 300 U/L. 

AST/ALT ratio is a useful indicator.
a) A ratio of > 2 is highly suggestive of alcohol-induced hepatic injury.
b) A ratio of > 1 and cirrhosis is often seen in patients of chronic hepatitis B infections.
c) A ratio of < 1 is commonly seen in acute/chronic viral hepatitis or in extra hepatic biliary obstruction.

Elevated AST or ALT are not definitive predictive indices of histologic findings. Instead serial measurements may reflect the extent of damage and give information about the progression of the disease.

A decrease in previously elevated enzymes does not always indicate recovery. In cases of fulminant hepatic failure, a decrease in the level of enzymes indicates that there is a low hepatic reserve after overwhelming hepatocyte necrosis. i.e. there is so much damage that the remaining normal hepatocytes are releasing only a small amount of the enzymes upon insult.
False low levels are seen in patients with uremia and chronic renal failure undergoing dialysis. False elevation is seen in patients treated with erythromycin.

Thursday, June 21, 2012

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Delirium - definition, common causes, physical examination


Definition:
Delirium is defined by the acute onset of fluctuating cognitive impairment and a disturbance of consciousness. Cognition includes memory, language, orientation, judgement, conducting interpersonal relationships, performing actions (praxis), and problem solving. Delirium is thus marked by short-term confusion and changes in cognition. There is also rapid improvement in most cases when the causative factor is identified and eliminated.

Abnormalities of mood, perception, and behavior are common psychiatric symptoms. Tremor, asterixis, nystagmus, incoordination, and urinary incontinence are common neurological symptoms.

Common causes of delirium:
1) Central nervous system disorder
Seizure (postictal, nonconvulsive status, status)
Migraine
Head trauma, brain tumor, subarachnoid hemorrhage, subdural, epidural hematoma, abscess, intracerebral hemorrhage, cerebellar hemorrhage, nonhemorrhagic stroke, transient ischemia
2) Metabolic disorder
Electrolyte abnormalities
Diabetes, hypoglycemia, hyperglycemia, or insulin resistance
3) Systemic illness
Infection (e.g., sepsis, malaria, erysipelas, viral, plague, Lyme disease, syphilis, or abscess)
Trauma
Change in fluid status (dehydration or volume overload)
Nutritional deficiency
Burns
Uncontrolled pain
Heat stroke
High altitude (usually >5,000 m)
4) Medications
Pain medications (e.g., postoperative meperidine or morphine)
Antibiotics, antivirals, and antifungals
Steroids
Anesthesia
Cardiac medications
Antihypertensives
Antineoplastic agents
Anticholinergic agents
Neuroleptic malignant syndrome
Serotonin syndrome
5) Over-the-counter preparations
Herbals, teas, and nutritional supplements
6) Botanicals
Jimsonweed, oleander, foxglove, hemlock, dieffenbachia, and Amanita phalloides
7) Cardiac
Cardiac failure, arrhythmia, myocardial infarction, cardiac assist device, cardiac surgery
8) Pulmonary
Chronic obstructive pulmonary disease, hypoxia, SIADH, acid base disturbance
9) Endocrine
Adrenal crisis or adrenal failure, thyroid abnormality, parathyroid abnormality
10) Hematological
Anemia, leukemia, blood dyscrasia, stem cell transplant
11) Renal
Renal failure, uremia, SIADH
12) Hepatic
Hepatitis, cirrhosis, hepatic failure
13) Neoplasm
Neoplasm (primary brain, metastases, paraneoplastic syndrome)
14) Drugs of abuse
Intoxication and withdrawal
15) Toxins
Intoxication and withdrawal
Heavy metals and aluminum




Physical examination of a delirious patient:




Parameter
Finding
Clinical Implication

1. Pulse
Bradycardia
Hypothyroidism
Stokes-Adams syndrome
Increased intracranial pressure

Tachycardia
Hyperthyroidism
Infection
Heart failure

2. Temperature
Fever
Sepsis
Thyroid storm
Vasculitis

3. Blood pressure
Hypotension
Shock
Hypothyroidism
Addison's disease

Hypertension
Encephalopathy
Intracranial mass

4. Respiration
Tachypnea
Diabetes
Pneumonia
Cardiac failure
Fever
Acidosis (metabolic)

Shallow
Alcohol or other substance intoxication

5. Carotid vessels
Bruits or decreased pulse
Transient cerebral ischemia

6. Scalp and face
Evidence of trauma

7. Neck
Evidence of nuchal rigidity
Meningitis
Subarachnoid hemorrhage

8. Eyes
Papilledema
Tumor
Hypertensive encephalopathy

Pupillary dilatation
Anxiety
Autonomic overactivity (e.g., delirium tremens)

9. Mouth
Tongue or cheek lacerations
Evidence of generalized tonic-clonic seizures

10. Thyroid
Enlarged
Hyperthyroidism

11. Heart
Arrhythmia
Inadequate cardiac output, possibility of emboli

Cardiomegaly
Heart failure
Hypertensive disease

12. Lungs
Congestion
Primary pulmonary failure
Pulmonary edema
Pneumonia

13. Breath
Alcohol

Ketones
Diabetes

14. Liver
Enlargement
Cirrhosis
Liver failure

15. Nervous system
a. Reflexes
Asymmetry with Babinski's signs
Mass lesion
Cerebrovascular disease
Preexisting dementia
Snout
Frontal mass
Bilateral posterior cerebral artery occlusion
b. Abducent nerve
(sixth cranial nerve)
Weakness in lateral gaze
Increased intracranial pressure
c. Limb strength
Asymmetrical
Mass lesion
Cerebrovascular disease
d. Autonomic
Hyperactivity
Anxiety
Delirium

Wednesday, June 20, 2012

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Left ventricular function - normal echocardiography values



Women
Men
Measure
Reference Range
Abnormal
Reference Range
Abnormal


Mildly
Moderately
Severely
Mildly
Moderately
Severely
Linear method

Endocardial fraction shortening, %
27-45
22-26
17-21
≤16
25-43
20-24
15-19
≤14

Midwall fractional shortening, %
15-23
13-14
11-21
≤10
14-22
12-13
10-11
≤10
2D method

Ejection fraction, %
55
45-54
30-44
<30
55
45-54
30-44
<30