Urinalysis
Testing of urine is a basic test for the presence and severity of kidney diseases. 24-hour-collection is a general investigation for kidney diseases. The collected urine is then analysed through dipstick, or microscopy.
What to look for?
- Clear / cloudy?
- Colour change
>>>large amount of RBC stains urine pink or red i.e. haematuria
- Urine pH
>>>normal pH between 4.6 – 8
- Urine volume in 24 hours
- Presence of haemoglobin / glucose / protein / leucocyte esterase / nitrites / ketones / creatinine
>>>the above substances is sometimes present in small quantities in the normal population
>>>protein : creatinine ratio is almost as accurate as 24hr urine collection in diagnosing nephrotic syndrome
- Casts / lipids / organisms can be identified through urine microscopy
Any positive findings should be further investigated as they can be transient, of no prognostic importance, or indicative of other diseases. Other evidences of renal disease e.g. abnormal renal function, or clues from patient’s history, examination etc. should be taken into account for the diagnosis.
Blood test
- Blood urea nitrogen (BUN) & serum potassium increase in kidney diseases
- Serum creatinine increases due to decrease excretion via urine in kidney diseases
Glomerular Filtration Rate
The functional unit of kidneys, nephrons, is responsible for the controlling the amount of substances that stay in plasma or excreted via urine. To assess the renal excretory capacity, the ideal substance should be freely filtrated across the glomerulus, neither reabsorbed nor excreted into renal tubules, in a steady state concentration in plasma, and easily and reliably measured – which, does not exist.
Creatinine is universally used for the test, despite its varying concentration with diet, gender, muscle mass etc. With an impaired renal function there is correspondingly more tubular creatinine secretion, while a fall in GFR.
Renal imaging
Ultrasound is by far the most commonly used technique for screening and investigation. The imaging provides information of:
- Renal size, which is usually in proportion to body weight, between 9 - 12cm
- Shape, symmetry of kidneys
- Renal cysts, tumour, stone, obstruction
Small kidneys are noted in person with chronic renal disease.
Contrast study of kidneys is less common as person with pre-existing renal impairment, advanced age, diabetes etc. have an increased risk of contrast-induced nephropathy.
Renal biopsy
This is a highly specialized investigation to diagnose renal disease, especially when person presents with unexplained reduction in renal function. The test however, should only be performed after careful consideration of the risk to benefit ratio.
Showing posts with label dilys. Show all posts
Showing posts with label dilys. Show all posts
Wednesday, May 20, 2009
Thursday, April 30, 2009
Investigation
Serum creatinine & urea
Production of creatinine principally comes from metabolism of skeletal muscles. Since the level varies a little throughout the day, 24-hour urine collection is needed to reduce errors. The variations are due to changes in hydration or posture, tubular creatinine secretion etc. It is freely filtered by glomerulus, not metabolised, little or none is reabsorbed while small amount is secreted. These properties mean the amount of creatinine filtered almost equals to that excreted. Also, it is important to note that creatinine level is related to age, sex and muscle mass. Normal range is between 0.8-1.5mg/dL (70-135μmol/L).
Urine creatinine level is also taken to calculate glomerulus filtration rate (GFR):
U x V/P where U = urine concentration of creatinine; V = urine flow (mL/min); P = plasma concentration of creatinine. Normal rages are 90-140 and 80-125 mL/min for men and women respectively.
Renal failure results in reduced excretion of nitrogenous waste, e.g. urea, in which the serum concentration would be raised. Normal range lies between 2.5 - 7.5 mmol/L.
In renal diseases, a reduced renal blood flow, damage to or loss of glomeruli, or obstructed ultrafiltration along the tubules reduce GFR. Creatinine and urea are retained and give a raised serum level. However, both serum urea and creatinine do not rise above the normal range until there is a reduction of 50-60% in GFR.
Serum potassium
One of the functions of kidney is the body regulation of electrolytes e.g potassium. When kidney function is impaired, there is a reduced reabsorption of potassium, thus increases serum potassium concentration. Hyperkalaemia particularly increases the risk of cardiac dysrhythmia. Normal level is about 190mg/L.
Renal ultrasound
This can be used to differentiate between chronic and acute renal failure, in which the former usually results in a smaller kidney. Likewise, the images confirm the presence of any bladder outflow obstruction, urethral or ureteric stricture or obstruction etc. – suggesting post-renal cause of renal failure.
Production of creatinine principally comes from metabolism of skeletal muscles. Since the level varies a little throughout the day, 24-hour urine collection is needed to reduce errors. The variations are due to changes in hydration or posture, tubular creatinine secretion etc. It is freely filtered by glomerulus, not metabolised, little or none is reabsorbed while small amount is secreted. These properties mean the amount of creatinine filtered almost equals to that excreted. Also, it is important to note that creatinine level is related to age, sex and muscle mass. Normal range is between 0.8-1.5mg/dL (70-135μmol/L).
Urine creatinine level is also taken to calculate glomerulus filtration rate (GFR):
U x V/P where U = urine concentration of creatinine; V = urine flow (mL/min); P = plasma concentration of creatinine. Normal rages are 90-140 and 80-125 mL/min for men and women respectively.
Renal failure results in reduced excretion of nitrogenous waste, e.g. urea, in which the serum concentration would be raised. Normal range lies between 2.5 - 7.5 mmol/L.
In renal diseases, a reduced renal blood flow, damage to or loss of glomeruli, or obstructed ultrafiltration along the tubules reduce GFR. Creatinine and urea are retained and give a raised serum level. However, both serum urea and creatinine do not rise above the normal range until there is a reduction of 50-60% in GFR.
Serum potassium
One of the functions of kidney is the body regulation of electrolytes e.g potassium. When kidney function is impaired, there is a reduced reabsorption of potassium, thus increases serum potassium concentration. Hyperkalaemia particularly increases the risk of cardiac dysrhythmia. Normal level is about 190mg/L.
Renal ultrasound
This can be used to differentiate between chronic and acute renal failure, in which the former usually results in a smaller kidney. Likewise, the images confirm the presence of any bladder outflow obstruction, urethral or ureteric stricture or obstruction etc. – suggesting post-renal cause of renal failure.
Thursday, April 23, 2009
Pathophysiology of Cystic Fibrosis
Cystic fibrosis is an autosomal recessive disorder in which mutation occurs on the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The gene encodes a protein, CFTR that regulates multiple ion channels, the chloride channel – CFTR, sodium channel – EnaC etc. that involve in mucus secretion and other cellular processes.
Dehydration of mucus layer in cystic fibrosis
In epithelial cells, epithelial sodium channel (ENaC) is normally inhibited by CFTR. However in cystic fibrosis, ENaC activity is markedly increased while chloride secretion into the lumen is reduced. This leads to an increased reabsorption of sodium into the cells. The ion changes increase passive water reabsorption. Thus in cystic fibrosis, the mucus layer coating respiratory and intestinal epithelial cells becomes dehydrated, thick and sticky. In the lungs, the dehydration leads to defective action and the accumulation of hyperconcentrated secretions. This may obstruct the air passages and predispose to recurrent pulmonary infections.
CFTR in transport of bicarbonate ions
In pancreas, a mutated CFTR can have completely or partially preserved chloride transport, but markedly abnormal bicarbonate transport. The absence of bicarbonate ions decreases luminal pH, which leads to a variety of adverse effects.
Increased salt content in sweat
The function of CFTR in the sweat gland ducts is to reabsorb luminal chloride ions and ENaC to reabsorb sodium. Thus, in the sweat ducts, mutated CFTR gene results in a decreased reabsorption of sodium chloride.
Dehydration of mucus layer in cystic fibrosis
In epithelial cells, epithelial sodium channel (ENaC) is normally inhibited by CFTR. However in cystic fibrosis, ENaC activity is markedly increased while chloride secretion into the lumen is reduced. This leads to an increased reabsorption of sodium into the cells. The ion changes increase passive water reabsorption. Thus in cystic fibrosis, the mucus layer coating respiratory and intestinal epithelial cells becomes dehydrated, thick and sticky. In the lungs, the dehydration leads to defective action and the accumulation of hyperconcentrated secretions. This may obstruct the air passages and predispose to recurrent pulmonary infections.
CFTR in transport of bicarbonate ions
In pancreas, a mutated CFTR can have completely or partially preserved chloride transport, but markedly abnormal bicarbonate transport. The absence of bicarbonate ions decreases luminal pH, which leads to a variety of adverse effects.
Increased salt content in sweat
The function of CFTR in the sweat gland ducts is to reabsorb luminal chloride ions and ENaC to reabsorb sodium. Thus, in the sweat ducts, mutated CFTR gene results in a decreased reabsorption of sodium chloride.
Tuesday, April 14, 2009
Bronchiectasis
The term ‘bronchiectasis’ (bron-kee-ek’-tas-is) describes the condition where airways are abnormally and permanently dilated. Causes can be of congenital or acquired origin.
An infection or any condition that injuries the airways may slowly impaired airways’ ability to clear out mucus i.e. bronchiectasis itself is not an infection, but a condition developed secondary to an infection or injury to the airways. As mucus builds up, the environment favours ongoing infections, e.g. pneumonia, tuberculosis, fungal infections etc. Each infection or injury causes more damage to the airways.
The recurrent inflammation of the bronchial walls causes the airways to become stretched out, flabby and scarred. The thickening and damage to the bronchial walls are irreversible and incurable.
Congenital causes of bronchiectasis:
- Pulmonary sequestration
- Deficiency of bronchial elements
Acquired causes of bronchiectasis:
- Pneumonia
- Tuberculosis
- Lungs tumors
- Foreign bodies
Person with bronchiectasis develops symptoms gradually. This includes:
- Coughing up yellow sputum
- Dypsnoea due to airflow limitation
In severe cases, patient may suffer from:
- Cough up blood (haemoptysis)
- Bad breath (halitosis)
- Episodes of pneumonia
- Weight loss
- Fatigue
On examination, patients presents with signs including:
- Wheeze
- Crackles
- Clubbing
Possible investigations are:
- Chest x-ray and CT to locate bronchial dilation or wall thickening
- Sputum culture to determine presence of bacteria
- Lung function test to find out severity of damage to lungs
Treatment
- Antibiotics to treat recurrent respiratory infections
- Corticosteroids help reduce inflammation of lungs
An infection or any condition that injuries the airways may slowly impaired airways’ ability to clear out mucus i.e. bronchiectasis itself is not an infection, but a condition developed secondary to an infection or injury to the airways. As mucus builds up, the environment favours ongoing infections, e.g. pneumonia, tuberculosis, fungal infections etc. Each infection or injury causes more damage to the airways.
The recurrent inflammation of the bronchial walls causes the airways to become stretched out, flabby and scarred. The thickening and damage to the bronchial walls are irreversible and incurable.
Congenital causes of bronchiectasis:
- Pulmonary sequestration
- Deficiency of bronchial elements
Acquired causes of bronchiectasis:
- Pneumonia
- Tuberculosis
- Lungs tumors
- Foreign bodies
Person with bronchiectasis develops symptoms gradually. This includes:
- Coughing up yellow sputum
- Dypsnoea due to airflow limitation
In severe cases, patient may suffer from:
- Cough up blood (haemoptysis)
- Bad breath (halitosis)
- Episodes of pneumonia
- Weight loss
- Fatigue
On examination, patients presents with signs including:
- Wheeze
- Crackles
- Clubbing
Possible investigations are:
- Chest x-ray and CT to locate bronchial dilation or wall thickening
- Sputum culture to determine presence of bacteria
- Lung function test to find out severity of damage to lungs
Treatment
- Antibiotics to treat recurrent respiratory infections
- Corticosteroids help reduce inflammation of lungs
Thursday, April 2, 2009
Pathophysiology of asthma
'Intrinsic' asthma is triggered by e.g. exercise, cigarette etc.
'Extrinsic' asthma is the allergic type of asthma which involves IgE antibodies and mast cell degranulation.
The pathogenesis of asthma involves both genetic and environmental factors, and is triggered by exposure of allergens. When come into contact with antigens (allergens), dendritic cells react and present the antigens to lymphocytes. Helper T cells are then activated, releasing cytokines (IL-2, IL-4), which results in the activation of B cells to secret IgE antibodies. In extrinsic asthma, patients have a tendency to form abnormally large amounts of IgE antibodies. Migration and activation of mast cells and eosinophils are also stimulated by lymphocytes activation and cytokines generation.
The IgE antibodies attach to mast cells present in the lung interstitium. As the antigens react with the mast cell attached-antibodies, the mast cell is activated and sends signal for 1) degranulation; 2) phospholipase activation; 3) cytokine gene activation.
1) Substances released in mast cell degranulation are primary mediators of the allergic response. One of which is histamine.
2) Phospholipase activation leads to the release of leukotrienes and prostaglandin.
3) Cytokine IL-5, secreted upon cytokine gene activation, is responsible in activation of eosinophils.
Mast cell activation or, the mediators released, thus results in spasms of smooth bronchial muscles, increased mucus secretions into bronchiolar lumens, and localized oedema in the walls of the small bronchioles. The increased airway resistance creates obstruction in respiration.
The obstruction is, however, more severe during expiration. Despite the occlusion in asthmatic lungs, during inspiration, the positive pressure of the lungs in compare to the atmospheric pressure keeps the airway open. Thus the effect of obstruction is less. In expiration, the partially obstructed airway is further compressed by the greater atmospheric pressure. This gives a more reduced bronchiolar diameter and patients experience great difficulty expiring.
The activated eosinophils release mediators such as eosinophil cationic proteins that are toxic to epithelial cells. Epithelial cell loss in the chronic phase of asthma makes it more vulnerable to irritant stimuli -- resulting in bronchial hypersensitivity.
The theory behind airway remodeling is unknown. Nevertheless, various growth factors cause hypertrophy and hyperplasia of the smooth muscles in the chronic phase. Increased deposition of collagens due to fibroblasts activation creates an environment for ongoing inflammation, and eventually structural and functional alterations.
Reference: Kumar & Clark, Rang & Dale, Guyton
'Extrinsic' asthma is the allergic type of asthma which involves IgE antibodies and mast cell degranulation.
The pathogenesis of asthma involves both genetic and environmental factors, and is triggered by exposure of allergens. When come into contact with antigens (allergens), dendritic cells react and present the antigens to lymphocytes. Helper T cells are then activated, releasing cytokines (IL-2, IL-4), which results in the activation of B cells to secret IgE antibodies. In extrinsic asthma, patients have a tendency to form abnormally large amounts of IgE antibodies. Migration and activation of mast cells and eosinophils are also stimulated by lymphocytes activation and cytokines generation.
The IgE antibodies attach to mast cells present in the lung interstitium. As the antigens react with the mast cell attached-antibodies, the mast cell is activated and sends signal for 1) degranulation; 2) phospholipase activation; 3) cytokine gene activation.
1) Substances released in mast cell degranulation are primary mediators of the allergic response. One of which is histamine.
2) Phospholipase activation leads to the release of leukotrienes and prostaglandin.
3) Cytokine IL-5, secreted upon cytokine gene activation, is responsible in activation of eosinophils.
Mast cell activation or, the mediators released, thus results in spasms of smooth bronchial muscles, increased mucus secretions into bronchiolar lumens, and localized oedema in the walls of the small bronchioles. The increased airway resistance creates obstruction in respiration.
The obstruction is, however, more severe during expiration. Despite the occlusion in asthmatic lungs, during inspiration, the positive pressure of the lungs in compare to the atmospheric pressure keeps the airway open. Thus the effect of obstruction is less. In expiration, the partially obstructed airway is further compressed by the greater atmospheric pressure. This gives a more reduced bronchiolar diameter and patients experience great difficulty expiring.
The activated eosinophils release mediators such as eosinophil cationic proteins that are toxic to epithelial cells. Epithelial cell loss in the chronic phase of asthma makes it more vulnerable to irritant stimuli -- resulting in bronchial hypersensitivity.
The theory behind airway remodeling is unknown. Nevertheless, various growth factors cause hypertrophy and hyperplasia of the smooth muscles in the chronic phase. Increased deposition of collagens due to fibroblasts activation creates an environment for ongoing inflammation, and eventually structural and functional alterations.
Reference: Kumar & Clark, Rang & Dale, Guyton
Wednesday, March 25, 2009
Shock
When SHOCK occurs, generally there is an inadequate delivery of nutrients to critical tissues and organs, and also an inadequate removal of cellular waste products from the tissues. The cause of this inadequacy can be of cardio- / hypovolemic- / neurogenic- / anaphylactic-/ septic origin, however ultimately, lead to the deterioration of different body parts.
In the case of cell hypoxia, the non-progressive phase of shock then kicks in, in which our body’s negative feedback mechanisms attempt to return normal cardiac output and arterial pressure i.e. to recover from shock, by, namely, baroreceptors, renin-angiotensin system etc. However, when failing to recover from shock, shock proceeds to the progressive phase. The cause of shock and its resulting effects on, say, low systemic filling pressure, or reduced venous return etc., become a vicious circle that eventually leads to an irreversible deterioration of circulation and, to death.
Cadiogenic shock
i.e. body suffers from lack of nutrition and deteriorates due to inadequate cardiac pumping, in which, 1) often occurs after acute heart attacks or prolonged periods of slow progressive cardiac deterioration; 2) caused by a decreased venous return
- problem can be compounded by a low arterial pressure e.g. in circulatory shock, which reduces the coronary blood supply even more
- the condition thus becomes a vicious circle i.e. shock causes more shock
∴elevate arterial pressure!!! By infusion of whole blood / plasma, or blood-pressure raising drug
Hypovolemic shock
i.e. diminished blood volume caused by, most commonly, haemorrhage, which then decreases the filling pressure of the circulation and, as a consequence, decreases venous return; as the result, cardiac output falls, and shock comes after.
Neurogenic shock
When there is massive dilation of veins, mean systemic filling pressure decreases; thus, filling the circulatory system adequately had become incapable even with a normal amount of blood. Venous pooling of blood reduces cardiac output, therefore limits the gaseous and nutrition exchange around the body.
Anaphylactic shock
In anaphylaxis, basophils and mast cells release histamine, which causes dilation of veins and arterioles, as well as an increased permeability in capillaries. The effect of these is a great reduction in venous return, and shock.
Septic shock
A septic shock occurs when a blood-borne bacterial infection widely spread around the body, causing extensive damage. Signs of circulatory collapse often include marked vasodilation in patients with septic shock, while high fever from the infection is a possible cause. As the infection becomes more severe, the circulatory system deteriorates at the same time, and shock becomes more progressive.
Reference: Guyton
In the case of cell hypoxia, the non-progressive phase of shock then kicks in, in which our body’s negative feedback mechanisms attempt to return normal cardiac output and arterial pressure i.e. to recover from shock, by, namely, baroreceptors, renin-angiotensin system etc. However, when failing to recover from shock, shock proceeds to the progressive phase. The cause of shock and its resulting effects on, say, low systemic filling pressure, or reduced venous return etc., become a vicious circle that eventually leads to an irreversible deterioration of circulation and, to death.
Cadiogenic shock
i.e. body suffers from lack of nutrition and deteriorates due to inadequate cardiac pumping, in which, 1) often occurs after acute heart attacks or prolonged periods of slow progressive cardiac deterioration; 2) caused by a decreased venous return
- problem can be compounded by a low arterial pressure e.g. in circulatory shock, which reduces the coronary blood supply even more
- the condition thus becomes a vicious circle i.e. shock causes more shock
∴elevate arterial pressure!!! By infusion of whole blood / plasma, or blood-pressure raising drug
Hypovolemic shock
i.e. diminished blood volume caused by, most commonly, haemorrhage, which then decreases the filling pressure of the circulation and, as a consequence, decreases venous return; as the result, cardiac output falls, and shock comes after.
Neurogenic shock
When there is massive dilation of veins, mean systemic filling pressure decreases; thus, filling the circulatory system adequately had become incapable even with a normal amount of blood. Venous pooling of blood reduces cardiac output, therefore limits the gaseous and nutrition exchange around the body.
Anaphylactic shock
In anaphylaxis, basophils and mast cells release histamine, which causes dilation of veins and arterioles, as well as an increased permeability in capillaries. The effect of these is a great reduction in venous return, and shock.
Septic shock
A septic shock occurs when a blood-borne bacterial infection widely spread around the body, causing extensive damage. Signs of circulatory collapse often include marked vasodilation in patients with septic shock, while high fever from the infection is a possible cause. As the infection becomes more severe, the circulatory system deteriorates at the same time, and shock becomes more progressive.
Reference: Guyton
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