Slides Picture of SMS 3033: Part 2
Tuesday, September 14, 2010
Can anyone help to explain these slides? All the slides are of histo-pathology. I am not sure of the name for each slides, but should I'm not mistaken, the arrangement are as follow:
1. Cervical Tumour
2. Endometrial Cancer
3. Endometrium Degeneration
4. Endometrium Interstitialoma
5. Ovary Cyst
Pathological changes of:
6. Placenta-Artery
7. Placenta-Vein
8. Umbilical Cord
Do inform me if the naming are wrong.









Slides Picture of SMS 3033: Part 1
Duchenne muscular dystrophy
Tuesday, July 20, 2010
Duchenne muscular dystrophy
Duchenne muscular dystrophy is an inherited disorder that involves rapidly worsening muscle weakness.
Causes
Duchenne muscular dystrophy is a rapidly-worsening form of muscular dystrophy. Other muscular dystrophies (including Becker's muscular dystrophy) get worse much more slowly.
Duchenne muscular dystrophy is caused by a defective gene for dystrophin (a protein in the muscles). However, it often occurs in people without a known family history of the condition.
Because of the way the disease is inherited, males are more likely to develop symptoms than are women. The sons of females who are carriers of the disease (women with a defective gene but no symptoms themselves) each have a 50% chance of having the disease. The daughters each have a 50% chance of being carriers.
Duchenne muscular dystrophy occurs in approximately 1 out of every 3,600 male infants. Because this is an inherited disorder, risks include a family history of Duchenne muscular dystrophy.
Symptoms
Symptoms usually appear before age 6 and may appear as early as infancy. They may include:
- Fatigue
- Mental retardation (possible, but does not worsen over time)
- Muscle weakness
- Begins in the legs and pelvis, but also occurs less severely in the arms, neck, and other areas of the body
- Difficulty with motor skills (running, hopping, jumping)
- Frequent falls
- Rapidly worsening weakness
- Progressive difficulty walking
- Ability to walk may be lost by age 12
By age 10, the person may need braces for walking. By age 12, most patients are confined to a wheelchair.
Exams and Tests
A complete nervous system (neurological), heart, lung, and muscle exam may show:
- Abnormal heart muscle (cardiomyopathy)
- Congestive heart failure or irregular heart rhythm (arrhythmias) -- rare
- Deformities of the chest and back (scoliosis)
- Enlarged calf muscles, which are eventually replaced by fat and connective tissue (pseudohypertrophy)
- Loss of muscle mass (wasting)
- Muscle contractures in the heels, legs
- Muscle deformities
- Respiratory disorders, including pneumonia and aspiration of food or fluid into the lungs (in late stages of the disease)
Tests may include:
- Electromyography (EMG)
- Genetic tests
- Muscle biopsy
- Serum CPK
Treatment
There is no known cure for Duchenne muscular dystrophy. Treatment aims to control symptoms to maximize quality of life. Gene therapy may become available in the future.
Activity is encouraged. Inactivity (such as bedrest) can worsen the muscle disease. Physical therapy may be helpful to maintain muscle strength and function. Orthopedic appliances (such as braces and wheelchairs) may improve mobility and the ability to care for yourself.
Outlook (Prognosis)
Duchenne muscular dystrophy leads to quickly worsening disability. Death usually occurs by age 25, typically from lung disorders.
Possible Complications
- Cardiomyopathy
- Congestive heart failure (rare)
- Deformities
- Heart arrhythmias (rare)
- Mental impairment (varies, usually minimal)
- Permanent, progressive disability
- Decreased mobility
- Decreased ability to care for self
- Pneumonia or other respiratory infections
- Respiratory failure
Alternative Names
Pseudohypertrophic muscular dystrophy; Muscular dystrophy - Duchenne type
Becker muscular dystrophy
Becker muscular dystrophy
Becker muscular dystrophy is an inherited disorder that involves slowly worsening muscle weakness muscle weakness of the legs and pelvis.
Causes
Becker muscular dystrophy is very similar to Duchenne muscular dystrophy, except that it gets worse at a much slower rate.
The disorder is passed down through families (inherited). Having a family history of the condition raises your risk.
Becker muscular dystrophy occurs in approximately 3 - 6 out of every 100,000 males. It is less common than Duchenne muscular dystrophy.
Symptoms
Females rarely develop symptoms. Males will develop symptoms if they inherit the defective gene. Symptoms usually appear in boys at about age 12, but may begin later.
Muscle weakness of the lower body, including the legs and pelvis area, slowly gets worse, causing:
- Difficulty walking that gets worse over time; by age 25-30 the person is usually unable to walk
- Frequent falls
- Difficulty with running, hopping, and jumping
- Loss of muscle mass
Muscle weakness in the arms, neck, and other areas is not as severe as in the lower body.
Other symptoms may include:
- Breathing problems
- Cognitive problems (these do not get worse over time)
- Fatigue
- Loss of balance and coordination
Exams and Tests
The health care provider will do a nervous system (neurological) and muscle examination. A careful medical history is also important, because the pattern of symptom development resembles that of Duchenne's muscular dystrophy. However, Becker muscular dystrophy gets worse much more slowly.
An exam may find:
- Abnormally developed bones, leading to deformities of the chest and back (scoliosis)
- Abnormality of heart muscle function (cardiomyopathy)
- Congestive heart failure or irregular heartbeat (arrhythmias) - rare
- Muscle deformities, including:
- Contractures of heels and legs
- Abnormal fat and connective tissue in calf muscles
- Muscle loss that begins in the legs and pelvis, then moves on to the muscles of the shoulders, neck, arms, and respiratory system
Tests that may be done include:
- CPK blood test
- Electromyography (EMG) nerve testing
- Muscle biopsy or genetic blood test
Treatment
There is no known cure for Becker muscular dystrophy. The goal of treatment is to control symptoms to maximize the person's quality of life. Some doctors prescribe steroids to help keep a patient walking for as long as possible.
Activity is encouraged. Inactivity (such as bed rest) can make the muscle disease worse. Physical therapy may be helpful to maintain muscle strength. Orthopedic appliances such as braces and wheelchairs may improve mobility and self-care.
Genetic counseling may be recommended. Daughters of a man with Becker muscular dystrophy may carry the defective gene and could pass it onto their sons.
Outlook (Prognosis)
Becker muscular dystrophy leads to slowly worsening disability, although the degree of disability varies. Some men may need a wheelchair, while others may only need to use walking aids such as canes or braces.
Possible Complications
- Heart-related complications such as cardiomyopathy
- Lung failure
- Pneumonia or other respiratory infections
- Increasing and permanent disability, that leads to:
Alternative Names
Benign pseudohypertrophic muscular dystrophy; Becker's dystrophy
NORMAL LABORATORY VALUES
Monday, July 19, 2010
NORMAL LABORATORY VALUES
| Laboratory Test | Normal Range in US Units | Normal Range in SI Units | To Convert US to SI Units |
| ALT (Alanine aminotransferase) | W 7-30 units/liter
| W 0.12-0.50 µkat/liter
| x 0.01667 |
| Albumin | 3.1 - 4.3 g/dl | 31 - 43 g/liter | x 10 |
| Alkaline Phosphatase | W 30-100 units/liter
| W 0.5-1.67 µkat/liter
| x 0.01667 |
| Amylase (serum) | 53-123 units/liter | 0.88-2.05 nkat/liter | x 0.01667 |
| AST (Aspartate aminotransferase) | W 9-25 units/liter
| W 0.15-0.42 µkat/liter
| x 0.01667 |
| Basophils | 0-3% of lymphocytes | 0.0-0.3 fraction of white blood cells | x 0.01 |
| Bilirubin - Direct | 0.0-0.4 mg/dl | 0-7 µmol/liter | x 17.1 |
| Bilirubin - Total | 0.0-1.0 mg/dl | 0-17 µmol/liter | x 17.1 |
| Blood pressure | Normal: 120/70 to 120/80 millimeters of mercury (mmHg). The top number is systolic pressure, when the heart is pumping. Bottom number is diastolic pressure then the heart is at rest. Blood pressure can be too low (hypotension) or too high (hypertension). | No conversion | |
| C peptide | 0.5-2.0 ng/ml | 0.17-0.66 nmol/liter | x 0.33 |
| Calcium, serum | 8.5 -10.5 mg/dl | 2.1-2.6 mmol/liter | x 0.25 |
| Calcium, urine | 0-300 mg/24h | 0.0-7.5 mmol/24h | x 0.025 |
| Cholesterol, total
| 239 mg/dL |
| x 0.02586 |
| Cholesterol, LDL
|
|
| x 0.02586 |
| Cholesterol, HDL
|
|
| x 0.02586 |
| Cortisol: serum | 0-25 µg/dl (depends on time of day) | 0-690 nmol/liter | x 27.59 |
| Cortisol: free (urine) | 20-70 µg/dl | 55-193 nmol/24h | x 2.759 |
| Creatine kinase | W 40-150 units/liter
| W 0.67-2.50 µkat/liter
| x 0.01667 |
| DHEA | W 130-980 ng/dl
| W 4.5-34.0 nmol/liter
| x 0.03467 |
| DHEA Sulfate | W Pre-menopause: 12-535 µg/dl
| W Pre-menopause: 120-5350 µg/liter
| x 10 |
| Eosinophils | 0-8% of white blood cells | 0.0-0.8 fraction of white blood cells | x 0.01 |
| Erythrocyte sedimentation rate (Sed Rate) | W<=30 mm/h
| W<=30 mm/h
| No conversion |
| Folate | 3.1-17.5 ng/ml | 7.0-39.7 nmol/liter | x 2.266 |
| Glucose, urine | <0.05> | <0.003> | x 0.05551 |
| Glucose, plasma | 70-110 mg/dl | 3.9-6.1 mmol/liter | x 0.05551 |
| GGT (Gamma glutamyl transferase) | W <=45U/L
| W <=45U/L
| No conversion |
| Hematocrit | W 36.0% - 46.0% of red blood cells
| W 0.36-0.46 fraction of red blood cells
| x 0.01 |
| Hemoglobin | W 12.0-16.0 g/dl
| W 7.4-9.9 mmol/liter
| x 0.6206 |
| LDH (Lactate dehydrogenase) (total) | <=270 U/L | <=4.5 µkat/liter | x 0.016667 |
| Lactic acid | 0.5-2.2 mmol/liter | 0.5-2.2 mmol/liter | No conversion |
| Leukocytes (WBC) | 4.5-11.0x103/mm3 | 4.5-11.0x109/liter | No conversion |
| Lymphocytes | 16%-46% of white blood cells | 0.16-0.46 fraction of white blood cells | x 0.01 |
| Mean corpuscular hemoglobin (MCH) | 25.0-35.0 pg/cell | 25.0-35.0 pg/cell | No conversion |
| Mean corpuscular hemoglobin concentration (MCHC) | 31.0-37.0 g/dl | 310-370 g/liter | x 10 |
| MCV (Mean corpuscular volume) | W 78-102 µm3
| W 78-102 fl
| No conversion |
| Monocytes | 4-11% of white blood cells | 0.04-0.11 fraction of white blood cells | x 0.01 |
| Neutrophils | 45%-75% of white blood cells | 0.45-0.75 fraction of white blood cells | x 0.01 |
| Phosphorus | 2.5 – 4.5 mg/dL | 0.81-1.45 mmol/L | x 0.323 |
| Platelets (Thrombocytes) | 130 – 400 x 10 3µL | 130 – 400 x 10 9L | No conversion |
| Potassium | 3.4-5.0 mmol/liter | 3.4-5.0 mmol/liter | No conversion |
| RBC (Red blood cell count) | W 3.9 – 5.2 x 106/µL3
| W 3.9 – 5.2 x 1012/L
| No conversion |
| Sodium | 135-145 mmol/liter | 135-145 mmol/liter | No conversion |
| Testosterone, total (morning sample) | W 6-86 ng/dl
| W 0.21-2.98 nmol/liter
| x 0.03467 |
| Testosterone, free
|
|
| x 34.67 |
| Triglicerides (fasting)
|
|
| x 0.01129 |
| Urea, plasma (BUN) | 8-25 mg/dl | 2.9-8.9 mmol/liter | x 0.357 |
| Urinalysis - pH
| 5.0-9.0
| 5.0-9.0
| No conversion |
| WBC (White blood cells, leukocytes) | 4.5-11.0x10 3 /mm 3 | 4.5-11.0x10 9 liter | No conversion |
UNITS:
gram : common measurement of weight. Used in this table: pg (picograms), g (grams), mg (milligrams), etc. per liter
katal (kat) : a unit of catalytic activity, used especially in the chemistry of enzymes. Used in this table: µkat (microkatals), nkat (nanokatals) per liter
micrometer (µm) : a unit of length. Mean Corpuscular Volume is expressed in cubic micrometers
mole : also “gram molecular weight,” a quantity based on the atomic weight of the substance. Many test results in the Système Internationale are expressed as the number of moles per liter. In US units, these measurements are usually in grams per liter. Used in this table: mmol (millimoles), µmol, (micromoles), nmol (nanomoles), pmol (picomoles) per liter
Some units of measurement include the following fractions and multipliers:
mega (M) : 10 6 or x1,000,000
kilo (k) : 10 3 or x1,000
deca or deka : 10 1 or x10
deci (d) : 10 -1 or ÷10
milli (m) : 10 -3 or ÷1,000
micro (µ) : 10 -6 or ÷1,000,000
nano (n) : 10 -9 or ÷1,000,000,000
pico (p) : 10 -12 or ÷1,000,000,000,000










