10 anatomy mcq
1? Where is the weakest point in the clavicle?
a. the middle point of clavicle
b. the lateral ends
c. point where middle 2/3rd meets lateral 1/3rd’
d. point where lateral 1/4th meets middle 3/4th
e. None
2. which of the following muscles are not attached to coracoid process?
a. Short head of biceps
b. longhead of biceps
c. corachobrachialis
d. pectoralis minor
e. none
3. which muscles origins from above the glenoid fossa?
a. short head of biceps
b. long head of biceps
c. corachobrachialis
d. long head of triceps
e. deltoid
4. which of the following muscles are not inserted on greater tubercle of humerus?
a. supraspinatus
b. infraspinatus
c. teres major
d. teres minor
5. which of he following muscle inserted in lesser tubercle?
a. Supraspinatus
b. infraspinatus
c. suscapularis
d. deltoid
e. corachobrachialis
6. which of the following muscles not inserted into intertubercular groove?
a. Lattissimus dorsi
b. pectoralis major
c. teres major
d. deltoid
7. Which of the following is NOT true regarding the clavicle?
(A) Its medial end is enlarged where it attaches to the sternum.
(B) Its lateral end is ?at where it articulates with the humerus.
(C) The medial two-thirds of the shaft are convex anteriorly.
(D) The clavicle transmits shock from the upper limb to the axial skeleton.
(E) The clavicle is a “long bone” that has no medullary cavity.
8 The trapezius attaches to which of the following regions of the clavicle?
(A) lateral one-third of the clavicle
(B) conoid tubercle
(C) subclavian groove
(D) trapezoid line
(E) quadrangular tubercle
9. Which of the following is true in respect to the scapula?
(A) The spine of the scapula continues laterally as the coracoid process.
(B) The lateral surface of the scapula forms the glenoid cavity.
(C) The acromion is superior to the glenoid cavity and projects anterolaterally.
(D) The scapula is fastened securely to the thoracic cage at the scapulothoracic joint.
(E) The acromioclavicular
Sunday, September 26, 2010
Pharmacology of Cardiovascular MCQs
Pharma -CVS MCQs
1. In PSVT the drug of choice is
a. Adenosine b. Propranolol c. Lignocaine d. Epinephrine
Ans. a
2. Propranolol is not used in
a. Hypertension b. Migraine c. Varient angina d. Thyrotoxicosis
Ans. c
3. Which of the following is not a cardioselective drug
a. Atenolol b. Metoprolol c. Labetalol d. Esmolol
Ans. c
4. Which of the following drug is contraindicated to treat hypertension with pregnancy ?
a. Enalapril b. Methyldopa c. Nifedipine d. Labetolol
Ans. a
5. All of the following are indications for use of ACE inhibitors , except
a. Hypertension b. Myocardial infarction
c. Left ventricular dysfunction d. Pheochromocytoma
Ans. d 6. Which of the following statements regarding ACE inhibitors is true
a. Has positive inotropic effect
b. No effect on preload
c. Decrease bradykinin level
d. Can result in increase plasma K level
Ans. d
7. The preferred drugs for hypertension in patients with heart failure ….
a. Verapamil b. Propranolol c. Diltiazem d. Captopril
ans. d
8. Which of the following statement regarding anti-arrhythmic drugs is false
a. Lignocaine ---- Na channel blocker
b. Verapamil ---- Ca channel blocker
c. Amiodarone ---- Na channel blocker
d. Propranolol ---- Beta receptor blocker
ans. c
9. The following persons have risk factors for developing hypertension EXCEPT:
a. A person with high total blood cholesterol
b. A person whose father developed hypertension at the age of 40 but the mother who is already age 50 and still normotensive
c. A person with a body mass index of 32
d. A person who drinks a large bottle of beer everyday
e. A person who works as an office worker and does not do any exercises
ans. d
10. A 50 year old female was given Digoxin for congestive heart failure. What is the cellular action of digoxin?
a. Inhibition of beta receptors
b. Inhibition of Na pump
c. Inhibition of ATP degradation
d. Inhibition of mitochondrial Ca ions release
ans. b
1. In PSVT the drug of choice is
a. Adenosine b. Propranolol c. Lignocaine d. Epinephrine
Ans. a
2. Propranolol is not used in
a. Hypertension b. Migraine c. Varient angina d. Thyrotoxicosis
Ans. c
3. Which of the following is not a cardioselective drug
a. Atenolol b. Metoprolol c. Labetalol d. Esmolol
Ans. c
4. Which of the following drug is contraindicated to treat hypertension with pregnancy ?
a. Enalapril b. Methyldopa c. Nifedipine d. Labetolol
Ans. a
5. All of the following are indications for use of ACE inhibitors , except
a. Hypertension b. Myocardial infarction
c. Left ventricular dysfunction d. Pheochromocytoma
Ans. d 6. Which of the following statements regarding ACE inhibitors is true
a. Has positive inotropic effect
b. No effect on preload
c. Decrease bradykinin level
d. Can result in increase plasma K level
Ans. d
7. The preferred drugs for hypertension in patients with heart failure ….
a. Verapamil b. Propranolol c. Diltiazem d. Captopril
ans. d
8. Which of the following statement regarding anti-arrhythmic drugs is false
a. Lignocaine ---- Na channel blocker
b. Verapamil ---- Ca channel blocker
c. Amiodarone ---- Na channel blocker
d. Propranolol ---- Beta receptor blocker
ans. c
9. The following persons have risk factors for developing hypertension EXCEPT:
a. A person with high total blood cholesterol
b. A person whose father developed hypertension at the age of 40 but the mother who is already age 50 and still normotensive
c. A person with a body mass index of 32
d. A person who drinks a large bottle of beer everyday
e. A person who works as an office worker and does not do any exercises
ans. d
10. A 50 year old female was given Digoxin for congestive heart failure. What is the cellular action of digoxin?
a. Inhibition of beta receptors
b. Inhibition of Na pump
c. Inhibition of ATP degradation
d. Inhibition of mitochondrial Ca ions release
ans. b
People who get less than 6 hours sleep per night had an increased risk of dying prematurely
People who get less than 6 hours sleep per night had an increased risk of dying prematurely in a recent study. Those who slept for less than that amount of time were 12% more likely to die early, though researchers also found a link between sleeping more than 9 hours and premature death.
The study aggregated decade-long studies from around the world involving more than 1.3 million people and found "unequivocal evidence of the direct link" between lack of sleep and premature death.
Just one sleepless night can hamper the body's ability to use insulin to process sugar in the bloodstream. Insulin sensitivity is not fixed in healthy people, but depends on the duration of sleep in the preceding night.
"Society pushes us to sleep less and less," one of the study investigators said, adding that about 20% of the population in the United States and Britain sleeps less than 5 hours.
Adults typically need between 7 and 9 hours sleep a night. If you sleep little, you can develop diabetes, obesity, hypertension and high cholesterol.
References:
Bad night's sleep can hamper body's insulin use. Reuters.
The study aggregated decade-long studies from around the world involving more than 1.3 million people and found "unequivocal evidence of the direct link" between lack of sleep and premature death.
Just one sleepless night can hamper the body's ability to use insulin to process sugar in the bloodstream. Insulin sensitivity is not fixed in healthy people, but depends on the duration of sleep in the preceding night.
"Society pushes us to sleep less and less," one of the study investigators said, adding that about 20% of the population in the United States and Britain sleeps less than 5 hours.
Adults typically need between 7 and 9 hours sleep a night. If you sleep little, you can develop diabetes, obesity, hypertension and high cholesterol.
References:
Bad night's sleep can hamper body's insulin use. Reuters.
Metformin on the incidence of vitamin B-12 deficiency
As many as 22% of people with type 2 diabetes could have vitamin B-12 deficiency.
This BMJ study evaluated the effects of metformin on the incidence of vitamin B-12 deficiency (lower than 150 pmol/l), low concentrations of vitamin B-12 (150-220 pmol/l), and folate and homocysteine concentrations in patients with type 2 diabetes receiving treatment with insulin.
Compared with placebo, metformin treatment was associated with a decrease in vitamin B-12 concentration of -19%.
The absolute risk of vitamin B-12 deficiency (lower than 150 pmol/l) at study end was 7.2 percentage points higher in the metformin group than in the placebo group with a number needed to harm of 13.8 per 4.3 years.
Long term treatment with metformin may increase the risk of vitamin B-12 deficiency, which results in raised homocysteine concentrations. Vitamin B-12 deficiency is preventable; therefore, regular measurement of vitamin B-12 concentrations during long term metformin treatment should be considered.
References:
BMJ 2010; 340:c2181
BMJ 2010; 340:c2198
This BMJ study evaluated the effects of metformin on the incidence of vitamin B-12 deficiency (lower than 150 pmol/l), low concentrations of vitamin B-12 (150-220 pmol/l), and folate and homocysteine concentrations in patients with type 2 diabetes receiving treatment with insulin.
Compared with placebo, metformin treatment was associated with a decrease in vitamin B-12 concentration of -19%.
The absolute risk of vitamin B-12 deficiency (lower than 150 pmol/l) at study end was 7.2 percentage points higher in the metformin group than in the placebo group with a number needed to harm of 13.8 per 4.3 years.
Long term treatment with metformin may increase the risk of vitamin B-12 deficiency, which results in raised homocysteine concentrations. Vitamin B-12 deficiency is preventable; therefore, regular measurement of vitamin B-12 concentrations during long term metformin treatment should be considered.
References:
BMJ 2010; 340:c2181
BMJ 2010; 340:c2198
Wednesday, July 21, 2010
Banting and best designed an experiment. What did they do and discover?
Fred Banting and Charles Best are credited with the discovery of insulin at the University of Toronto in 1921. Banting was the chief researcher, Best was his research assistant...chosen over another man by the toss of a coin.
The Nobel Prize for the discovery of insulin was shared by Banting and another man, a Scot by the name of John Macleod, head of the department where the research was carried out. It transpires that although history seems to give full credit to Banting and Best, the real glory should have gone to Macleod and another researcher, James Collip, who between them made all the most vital contributions to the project. In fact, without their contributions, Banting and Best could not progress any further than the previous work of Romanian Nicolai Paulescu who had already had far greater success in isolating active secretions from dog pancreases. It was Macleod's and Collip's suggestions which enabled the first successful trials on human diabetics.
Best was excluded from the Nobel Prize as his contribution was purely a functional pair of hands and not an intellectual one. Collip should've received far more credit than he actually did. Banting shared his prize fund with Best 50/50 and Macleod did the same with Collip.
Actual experiment:
Some dogs had their pancreases removed. Secretions were isolated from the pancreases of healthy dogs. These secretions were used to inject into the first set of dogs in an atempt to keep them alive. The Toronto University team were the first to complete successful trials with diabetic humans.
Source(s):
Fabulous Science, Fact and Fiction in the History of Scientific Discovery, by John Waller.
The Nobel Prize for the discovery of insulin was shared by Banting and another man, a Scot by the name of John Macleod, head of the department where the research was carried out. It transpires that although history seems to give full credit to Banting and Best, the real glory should have gone to Macleod and another researcher, James Collip, who between them made all the most vital contributions to the project. In fact, without their contributions, Banting and Best could not progress any further than the previous work of Romanian Nicolai Paulescu who had already had far greater success in isolating active secretions from dog pancreases. It was Macleod's and Collip's suggestions which enabled the first successful trials on human diabetics.
Best was excluded from the Nobel Prize as his contribution was purely a functional pair of hands and not an intellectual one. Collip should've received far more credit than he actually did. Banting shared his prize fund with Best 50/50 and Macleod did the same with Collip.
Actual experiment:
Some dogs had their pancreases removed. Secretions were isolated from the pancreases of healthy dogs. These secretions were used to inject into the first set of dogs in an atempt to keep them alive. The Toronto University team were the first to complete successful trials with diabetic humans.
Source(s):
Fabulous Science, Fact and Fiction in the History of Scientific Discovery, by John Waller.
Tales of the unexpected: Medicine's accidental discoveries
From Botox and viagra to penicillin, some of the greatest breakthrough cures have been discovered by happy serendipity. Roger Dobson reports
Viagra
The telephone call from a doctor in Merthyr Tydfil was one of the first clues. He had been running a small clinical trial on a new drug that had been designed for treating patients with angina. With other trials showing little efficacy for treating the disease, the future for the compound known as UK-92,480 was looking bleak.
When the doctor gave Pfizer the results, he mentioned that there had been some side effects among the healthy volunteers on the trial at Merthyr Tydfil, including indigestion and back pain. And, he added, some of the men had involuntary erections when they took the drug.
Scientists quickly discovered the scientific reason for the erections, and five years later and after much research, Pfizer applied for marketing approval for the drug – not for angina, this time, but for male impotence. Ten years on, Viagra has been used by more than 30 million men worldwide for impotence, and researchers are still finding new uses. The drug that nearly didn't make it is currently being used or investigated for treating more than a dozen diseases and health problems.
Vaccination
When Edward Jenner moved to practise medicine in rural Gloucestershire, he heard of a local saying that if a man wanted a woman who would not be scarred by the deadly smallpox disease, he should marry a milkmaid. This folk tale stemmed from the fact that milkmaids were vulnerable to cowpox, a chronic disease of cows that appeared as a rash on the milkmaids' hands.
As a result of this, in 1796 Jenner used cowpox to inoculate an eight-year-old boy called James, then exposed him, some weeks later, to smallpox. The cowpox was found to protect against smallpox.
Within six years, vaccination for the disease was an established practice, and it was Jenner's work that led to the eradication of smallpox in 1977, and the widespread use of vaccination.
Botulinum Toxin
In 1895, three members of a music club in Ellezelles, Belgium died and 34 fell ill, after eating a meal of raw salted ham. The culprit was eventually found to be Clostridium botulinum, which produces botulinum toxin, the most deadly poison of all. Work started in 1920, with researchers trying to isolate the toxin, but it wasn't until the 1950s that they discovered that the toxin could be used in tiny doses to treat "crossed eyes", spasms of the eyelids and excessive underarm sweating.
The cosmetically desirable effects of Botox were first discovered by Canadian surgeons Alastair and Jean Carruthers, a husband and wife team who noticed the softening of patients' frown lines following treatment for eye-muscle disorders.
"Its present cosmetic and non-cosmetic applications could certainly be considered a journey of serendipity,'' says Dr Arnold Klein of the University of California.
Later, Dr Richard Glogau, a dermatologist at the University of California, noticed a curious side effect when he injected Botox into the head and facial muscles of patients. The bacteria was being injected for cosmetic reasons, to temporarily get rid of wrinkles, but Glogau and his team noticed that patients who also had regular migraines were no longer getting them. Further research showed that botulinum toxin A injected into the muscles of the brow, eyes, forehead, side of the head and back of the head near the neck could induce immediate headache relief that may last for up to six months.
Penicillin
In 1928, after a period away from his laboratory at St Mary's Medical School in London, Alexander Fleming noticed that a mould had infected dishes where he had been growing experimental bacteria. Curiously, the area surrounding the mould growing in the dish was clear, suggesting that the bacteria could not survive near the mould. Fleming predicted that a compound produced by the mould must have an anti-bacterial action. He called the new chemical penicillin. Along with the other antibiotics, it revolutionised healthcare, and dramatically reduced mortality rates. He was awarded the Nobel Prize in 1945.
Librium and Valium
For months, the small box labelled Ro5-0690 had gathered dust. The product of work on synthetic dyes, it had been developed by Leo Sternbach, a pharmacist at Hoffmann-La Roche. During a routine clean-up, and Ro5-0690 was sent off to see if it had any pharmacological activity. The tests showed it to be highly effective. Ro5-0690 became the first anxiolytic benzodiazepine and was introduced in 1960 with the brand name Librium. Three years later, another anxiolytic benzodiazepine called diazepam (Valium) was introduced. Benzodiazepines revolutionised treatment for schizophrenia, depression and bipolar disorder. "They became one of the most lucrative drugs – thanks to luck," said Professor Ban.
Antidepressants
In 1956, Roland Kuhn, a Swiss psychiatrist, suggested to Geigy that its compound G 22,355 might have a therapeutic effect in schizophrenia. But tests showed it to be ineffective for the conditions. Just before he returned the drugs to the maker, Kuhn gave it to a patient with severe depression. Spurred by the apparent beneficial effect, Kuhn extended his trial. Not only did it have favourable effects, the patients relapsed when the drug was stopped. Within a year, G 22,355 had become the first tricyclic antidepressant, a family of drugs since used by millions.
Quinine
South American Indians discovered quinine and its anti-malarial powers by accident. The Peruvian natives found that if they drank from water close to cinchona trees, their fever would be eased. It is now known that the bark is a source of quinine, and Jesuit missionaries are recorded as having first used quinine from the tree to fight malaria in Peru in the 17th century. Quinine was brought to Europe in the same century, and the drug was eventually synthesised to become of a successful treatment for the condition, until it was superseded by other antimalarials.
Insulin
When two German doctors removed the pancreas from a dog, their plan was to study digestion processes. But they noticed that the dog's urine was attracting unusually large number of flies. Tests showed that they were attracted by high levels of sugar in the urine – a symptom of diabetes. The existence of diabetes in healthy animals led to an understanding of the pancreas's role in diabetes. It also led to the identification of insulin and treatment of the disease.
source:http://www.independent.co.uk/life-style/health-and-families/features/tales-of-the-unexpected-medicines-accidental-discoveries-826903.html
Viagra
The telephone call from a doctor in Merthyr Tydfil was one of the first clues. He had been running a small clinical trial on a new drug that had been designed for treating patients with angina. With other trials showing little efficacy for treating the disease, the future for the compound known as UK-92,480 was looking bleak.
When the doctor gave Pfizer the results, he mentioned that there had been some side effects among the healthy volunteers on the trial at Merthyr Tydfil, including indigestion and back pain. And, he added, some of the men had involuntary erections when they took the drug.
Scientists quickly discovered the scientific reason for the erections, and five years later and after much research, Pfizer applied for marketing approval for the drug – not for angina, this time, but for male impotence. Ten years on, Viagra has been used by more than 30 million men worldwide for impotence, and researchers are still finding new uses. The drug that nearly didn't make it is currently being used or investigated for treating more than a dozen diseases and health problems.
Vaccination
When Edward Jenner moved to practise medicine in rural Gloucestershire, he heard of a local saying that if a man wanted a woman who would not be scarred by the deadly smallpox disease, he should marry a milkmaid. This folk tale stemmed from the fact that milkmaids were vulnerable to cowpox, a chronic disease of cows that appeared as a rash on the milkmaids' hands.
As a result of this, in 1796 Jenner used cowpox to inoculate an eight-year-old boy called James, then exposed him, some weeks later, to smallpox. The cowpox was found to protect against smallpox.
Within six years, vaccination for the disease was an established practice, and it was Jenner's work that led to the eradication of smallpox in 1977, and the widespread use of vaccination.
Botulinum Toxin
In 1895, three members of a music club in Ellezelles, Belgium died and 34 fell ill, after eating a meal of raw salted ham. The culprit was eventually found to be Clostridium botulinum, which produces botulinum toxin, the most deadly poison of all. Work started in 1920, with researchers trying to isolate the toxin, but it wasn't until the 1950s that they discovered that the toxin could be used in tiny doses to treat "crossed eyes", spasms of the eyelids and excessive underarm sweating.
The cosmetically desirable effects of Botox were first discovered by Canadian surgeons Alastair and Jean Carruthers, a husband and wife team who noticed the softening of patients' frown lines following treatment for eye-muscle disorders.
"Its present cosmetic and non-cosmetic applications could certainly be considered a journey of serendipity,'' says Dr Arnold Klein of the University of California.
Later, Dr Richard Glogau, a dermatologist at the University of California, noticed a curious side effect when he injected Botox into the head and facial muscles of patients. The bacteria was being injected for cosmetic reasons, to temporarily get rid of wrinkles, but Glogau and his team noticed that patients who also had regular migraines were no longer getting them. Further research showed that botulinum toxin A injected into the muscles of the brow, eyes, forehead, side of the head and back of the head near the neck could induce immediate headache relief that may last for up to six months.
Penicillin
In 1928, after a period away from his laboratory at St Mary's Medical School in London, Alexander Fleming noticed that a mould had infected dishes where he had been growing experimental bacteria. Curiously, the area surrounding the mould growing in the dish was clear, suggesting that the bacteria could not survive near the mould. Fleming predicted that a compound produced by the mould must have an anti-bacterial action. He called the new chemical penicillin. Along with the other antibiotics, it revolutionised healthcare, and dramatically reduced mortality rates. He was awarded the Nobel Prize in 1945.
Librium and Valium
For months, the small box labelled Ro5-0690 had gathered dust. The product of work on synthetic dyes, it had been developed by Leo Sternbach, a pharmacist at Hoffmann-La Roche. During a routine clean-up, and Ro5-0690 was sent off to see if it had any pharmacological activity. The tests showed it to be highly effective. Ro5-0690 became the first anxiolytic benzodiazepine and was introduced in 1960 with the brand name Librium. Three years later, another anxiolytic benzodiazepine called diazepam (Valium) was introduced. Benzodiazepines revolutionised treatment for schizophrenia, depression and bipolar disorder. "They became one of the most lucrative drugs – thanks to luck," said Professor Ban.
Antidepressants
In 1956, Roland Kuhn, a Swiss psychiatrist, suggested to Geigy that its compound G 22,355 might have a therapeutic effect in schizophrenia. But tests showed it to be ineffective for the conditions. Just before he returned the drugs to the maker, Kuhn gave it to a patient with severe depression. Spurred by the apparent beneficial effect, Kuhn extended his trial. Not only did it have favourable effects, the patients relapsed when the drug was stopped. Within a year, G 22,355 had become the first tricyclic antidepressant, a family of drugs since used by millions.
Quinine
South American Indians discovered quinine and its anti-malarial powers by accident. The Peruvian natives found that if they drank from water close to cinchona trees, their fever would be eased. It is now known that the bark is a source of quinine, and Jesuit missionaries are recorded as having first used quinine from the tree to fight malaria in Peru in the 17th century. Quinine was brought to Europe in the same century, and the drug was eventually synthesised to become of a successful treatment for the condition, until it was superseded by other antimalarials.
Insulin
When two German doctors removed the pancreas from a dog, their plan was to study digestion processes. But they noticed that the dog's urine was attracting unusually large number of flies. Tests showed that they were attracted by high levels of sugar in the urine – a symptom of diabetes. The existence of diabetes in healthy animals led to an understanding of the pancreas's role in diabetes. It also led to the identification of insulin and treatment of the disease.
source:http://www.independent.co.uk/life-style/health-and-families/features/tales-of-the-unexpected-medicines-accidental-discoveries-826903.html
Friday, June 25, 2010
DEVELOPMENT OF CNS
Central nervous system (CNS).
Brain and spinal cord.
Both contain fluid-filled spaces which contain cerebrospinal fluid (CSF).
The central canal of the spinal cord is continuous with the ventricles of the brain.
White matter is composed of bundles of myelinated axons
Gray matter consists of unmyelinated axons, nuclei, and dendrites.
Peripheral nervous system.
Everything outside the CNS.
Spinal and cranial nerves
The cerebrum is derived from the embryonic telencephalon
The cerebrum is divided into left and right cerebrum hemispheres.
The corpus callosum is the major connection between the two hemispheres.
The left hemisphere is primarily responsible for the right side of the body.
The right hemisphere is primarily responsible for the left side of the body.
Cerebral cortex: outer covering of gray matter.
Neocortex: region unique to mammals.
The more convoluted the surface of the neocortex the more surface area the more neurons.
Basal nuclei: internal clusters of nuclei
Lateralization of Brain Function.
The left hemisphere.
Specializes in language, math, logic operations, and the processing of serial sequences of information, and visual and auditory details.
Specializes in detailed activities required for motor control.
The right hemisphere.
Specializes in pattern recognition, spatial relationships, nonverbal ideation, emotional processing, and the parallel processing of information.
The epithalamus, choroid plexus and the pineal gland thalamus, and hypothalamus are derived from the embryonic diencephalon.
Thalamus.
Relays all sensory information to the cerebrum.
Contains one nucleus for each type of sensory information.
Relays motor information from the cerebrum.
Receives input from the cerebrum.
Receives input from brain centers involved in the regulation of emotion and arousal. Hypothalamus.
Regulates autonomic activity.
Contains nuclei involved in thermoregulation, hunger, thirst, sexual and mating behavior, etc.
Regulates the pituitary gland.
• The Brainstem.
– The “lower brain.”
– Consists of the medulla oblongata, pons, and midbrain.
– Derived from the embryonic hindbrain and midbrain.
– Functions in homeostasis, coordination of movement, conduction of impulses to higher brain centers.
Midbrain. Develops from the mesencephalon
Contains nuclei involved in the integration of sensory information. visual reflexes & auditory reflexes. Relays information to and from higher brain centers
Cerebellum.Develops from part of the metencephalon.
Relays sensory information about joints, muscles, sight, and sound to the cerebrum.
Coordinates motor commands issued by the cerebrum
Pons. Develops from part of the metencephalon
Contains nuclei involved in the regulation of visceral activities such as breathing.
Relays information to and from higher brain centers
Medulla oblongata. Develops from the myelencephalon
Contains nuclei that control visceral (autonomic homeostatic) functions.
Relays information to and from higher brain centers
DEVELOPMENT OF URINARY SYSTEM
INDIANA UNIVERSITY
SCHOOL OF MEDICINE
The urogenital system develops from:
• the intermediate mesoderm (fig. 12-1B),
• the mesodermal epithelium (mesothelium) of the peritoneal cavity,
• and the endoderm of the urogenital sinus (fig. 12-20A).
The intermediate mesoderm used to lie lateral to the somites, then moved away from the somites during the lateral fold. It forms the urogenital ridge (fig. 12-1F) which is comprised of:
• a nephrogenic cord or ridge (fig. 12-2A)
• and a gonadal or genital ridge (fig. 12-29C).
3 successive sets of kidneys develop:
• The nonfunctional, rudimentary pronephroi develop early in week 4. But they degenerate, leaving behind the pronephric ducts which run to the cloaca (fig. 12-2). These ducts will remain for other kidneys.
• The mesonephroi develop later during week 4, serving as temporary excretory organs.
• The functional metanephroi or permanent kidneys develop early in week 5. They are functional by week 11-13 and excrete urine into the amniotic fluid. This excretion continues during fetal life and the fetus swallows this urine mixed in the amniotic fluid. It is then absorbed in the stomach and duodenum to the blood for transport to the placenta and disposal.
o If renal agenesis or urethral obstruction occurs, oligohydramnios results.
o If esophageal or duodenal atresia occurs, then polyhydramnios results.
The metanephros develops mesodermally from the metanephric diverticulum or ureteric bud which is a dorsal outgrowth from the mesonephric duct near the cloaca (fig. 12-6).
• Its stalk gives rise to the ureter (fig. 12-6C),
• its cranial end to the renal pelvis,
• its first 4 generations of tubules to the major calyces,
• its second 4 generations to the minor calyces (fig. 12-6D)
• and the remaining generations of tubules to the collecting tubules (fig. 12-6E).
The metanephric diverticulum or ureteric bud penetrates the metanephric mesoderm in the caudal part of the nephrogenic cord and stimulates the formation of the metanephric mass or cap (fig. 12-9).
The metanephric mesoderm gives rise to the nephrons (glomerulus, Bowman's capsule, proximal convoluted tubule, loop of Henle and distal convoluted tubule; fig. 12-7). The cortex of the kidney in the newborn contains mostly undifferentiated mesenchyme; the nephrons continue to develop several months after birth.
Ascension of the kidneys (fig. 12-10): The kidneys are first located in the pelvis ventral to the sacrum but gradually ascend to the abdomen. They reach the adult position by week 9 having touched the suprarenal glands (fig. 12-10). This is due to the disproportionate growth between the lumbar and sacral regions: the sacral region grows faster than the lumbar region.
The kidneys rotate 90 degrees from anterior to medial.
During their ascension, the blood supply changes continuously so that an adult may have 2 to 4 renal arteries (fig. 12-11).
The suprarenal glands ( fig. 12-27):
• The cortex forms from the mesoderm,
• the medulla from neural crest cells (receiving preganglionic sympathetic fibers from the celiac plexus).
The urinary bladder develops from the urogenital sinus and the surrounding splanchnic mesenchyme (fig. 12-20). The urogenital sinus is comprised of 3 regions:
• The cranial or vesical region which will form the bladder and which is attached to the allantois. After birth, the allantois degenerates and becomes the urachus forming the median umbilical ligament. The transitional epithelium of the bladder develops from endoderm of the urogenital sinus.
• The middle or pelvic region.
• and the caudal or phallic region.
The female urethra and almost all of the male urethra have the same origin.
The glans penis in the male develops from the ectodermal glandular plate (figs. 12-24, 12-25)
Developmental abnormalities of the kidney and excretory passages are common:
• Incomplete division of the metanephric diverticulum or ureteric bud results in double ureter (fig. 12-12B-D) and supernumerary kidney (fig. 12-12F).
• Failure of the kidney to "ascend" from its embryonic position in the pelvis results in an ectopic kidney that is abnormally rotated (fig. 12-12B).
• Various congenital cystic conditions of the kidneys may result from failure of nephrons derived from the metanephric mesoderm to connect with collecting tubules derived from the metanephric diverticulum.
Saturday, May 22, 2010
NOTES ON Osteoarthritis
Osteoarthritis
By: Sue Renfrow, RN, BSN
Osteoarthritis
* A form of Degenerative Joint Disease (DJD) * A common disabling joint disorder (problems with hips, knees, ankles) *Osteoarthritis is the most prevalent activity limitation among the elderly leading to disability *Affects 16- 20 million people in U.S.
Causes
*Idiopathic- Primary *No prior event or disease * Aging *Secondary *Resulting from previous joint or inflammatory disease *Congenital diseases ( Legg-Cave’-Perthes) *Gout *Obesity the more you weigh the harder it is on your joints
Clinical Manifestations
*Pain *Stiffness/ swelling *Functional Impairment/ asymetric *Heberden’s Nodes
Assessment/Diagnostic
*Physical assessment of musculoskeletal system *Location and pattern of pain *X-Rays- Show loss of joint cartilage, narrowing of joint space, osteophytes (bone Spurs) *Labs-ESR, RH-rule out RA (RH 40 or less)
Medical Management
*Decrease weight *Injury prevention *Ergonomic modifications
Conservative:
-heat/cold -avoid overuse -supports for joints -isometric, postural and aerobic exercise -Physical/Occupational therapy
Pharmacological
*Tylenol, Acetaminophen (drug of choice) worry about liver damage
*Salicylates, Aspirin - the “grandfather” *NSAIDS: Ibuprofen, Advil, Motrin & Nuprin (eventually will wind up on NSAIDs) *Cox-2 (Celebrex) worry about GI bleed *Opiates *Corticosteroids *Glucosamine/Chondroiton *Hyaluronic acid (Synivisc) *Topical- Capsain, methylsalicylate
Surgical Management
*Osteotomy-moderate to severe loss of function, may have this (realign joint) *Arthroplasty-surgical repair of the joint p. 1628
Treatment
*GOALS of treatment include: GOALS *decreasing joint pain and stiffness *improving joint mobility and stability *increasing ability to perform ADL’s *optimizing functional ability
Nursing Management:
*Chronic pain related to joint degeneration *Impaired physical mobility related to restricted joint mobility *Body image disturbance related to visible body changes *Self-care deficit related to immobility *Knowledge deficit *Ineffective individual/family coping or compromise
Preventative Measures:
*Joint Protection Joint *Correct body mechanics *Avoid grasping actions that strain finger joints *Spread weight of an object over several joints *Maintain good posture *Use strongest muscles and favor large joints
By: Sue Renfrow, RN, BSN
Osteoarthritis
* A form of Degenerative Joint Disease (DJD) * A common disabling joint disorder (problems with hips, knees, ankles) *Osteoarthritis is the most prevalent activity limitation among the elderly leading to disability *Affects 16- 20 million people in U.S.
Causes
*Idiopathic- Primary *No prior event or disease * Aging *Secondary *Resulting from previous joint or inflammatory disease *Congenital diseases ( Legg-Cave’-Perthes) *Gout *Obesity the more you weigh the harder it is on your joints
Clinical Manifestations
*Pain *Stiffness/ swelling *Functional Impairment/ asymetric *Heberden’s Nodes
Assessment/Diagnostic
*Physical assessment of musculoskeletal system *Location and pattern of pain *X-Rays- Show loss of joint cartilage, narrowing of joint space, osteophytes (bone Spurs) *Labs-ESR, RH-rule out RA (RH 40 or less)
Medical Management
*Decrease weight *Injury prevention *Ergonomic modifications
Conservative:
-heat/cold -avoid overuse -supports for joints -isometric, postural and aerobic exercise -Physical/Occupational therapy
Pharmacological
*Tylenol, Acetaminophen (drug of choice) worry about liver damage
*Salicylates, Aspirin - the “grandfather” *NSAIDS: Ibuprofen, Advil, Motrin & Nuprin (eventually will wind up on NSAIDs) *Cox-2 (Celebrex) worry about GI bleed *Opiates *Corticosteroids *Glucosamine/Chondroiton *Hyaluronic acid (Synivisc) *Topical- Capsain, methylsalicylate
Surgical Management
*Osteotomy-moderate to severe loss of function, may have this (realign joint) *Arthroplasty-surgical repair of the joint p. 1628
Treatment
*GOALS of treatment include: GOALS *decreasing joint pain and stiffness *improving joint mobility and stability *increasing ability to perform ADL’s *optimizing functional ability
Nursing Management:
*Chronic pain related to joint degeneration *Impaired physical mobility related to restricted joint mobility *Body image disturbance related to visible body changes *Self-care deficit related to immobility *Knowledge deficit *Ineffective individual/family coping or compromise
Preventative Measures:
*Joint Protection Joint *Correct body mechanics *Avoid grasping actions that strain finger joints *Spread weight of an object over several joints *Maintain good posture *Use strongest muscles and favor large joints
Thursday, May 20, 2010
LIVING WITH DISEASE
Great peoples and their disease.
.
Albert Einstein
Albert Einstein did not speak until the age of three. Even as an adult Einstein found that searching for words was laborious. He found schoolwork, especially math, difficult and was unable to express himself in writing. He was thought to be simple minded (retarded), until it was realized that he was able to achieve by visualizing rather than by the use of language. He work on relativity, which revolutionized modern physics, was created in his spare time.
Stephen Hawking
Stephen Hawking is a physicist/mathematician who has Lou Gehrigs Disease. He uses a wheelchair for mobility and a computer to speak.
Helen Keller
Helen Keller was suddenly shut off from the world at the age of 19 months by the loss of sight and hearing. Against overwhelming odds, she waged a slow and difficult but successful battle to re-enter the world. A near-savage deaf and blind mute child grew into a woman who wrote, spoke, and labored incessantly for the betterment of others and almost single-handedly destroyed age-old myths about people with disabilities.
John Milton
English Author/poet (1608-1674): He became blind at the age of 43. He went on to create his most famous epic, Paradise Lost.
Leonardo da Vinci
Leonardo da Vinci, an Italian painter, sculptor, writer, scientists, engineer, musician and architect. Renaissance genius. Strephosymbolis (unable to process symbols accurately).
George Washington
George Washington was unable to spell throughout his life and his grammar usage was very poor. His brother suggested that perhaps surveying in the backwoods might be an appropriate career for young George.
.
Albert Einstein
Albert Einstein did not speak until the age of three. Even as an adult Einstein found that searching for words was laborious. He found schoolwork, especially math, difficult and was unable to express himself in writing. He was thought to be simple minded (retarded), until it was realized that he was able to achieve by visualizing rather than by the use of language. He work on relativity, which revolutionized modern physics, was created in his spare time.
Stephen Hawking
Stephen Hawking is a physicist/mathematician who has Lou Gehrigs Disease. He uses a wheelchair for mobility and a computer to speak.
Helen Keller
Helen Keller was suddenly shut off from the world at the age of 19 months by the loss of sight and hearing. Against overwhelming odds, she waged a slow and difficult but successful battle to re-enter the world. A near-savage deaf and blind mute child grew into a woman who wrote, spoke, and labored incessantly for the betterment of others and almost single-handedly destroyed age-old myths about people with disabilities.
John Milton
English Author/poet (1608-1674): He became blind at the age of 43. He went on to create his most famous epic, Paradise Lost.
Leonardo da Vinci
Leonardo da Vinci, an Italian painter, sculptor, writer, scientists, engineer, musician and architect. Renaissance genius. Strephosymbolis (unable to process symbols accurately).
George Washington
George Washington was unable to spell throughout his life and his grammar usage was very poor. His brother suggested that perhaps surveying in the backwoods might be an appropriate career for young George.
Wednesday, May 19, 2010
NOTES ON SKULL TUTORIAL
NOTES ON SKULL TUTORIAL
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Notes on skull tutorial
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Notes on skull tutorial
Monday, May 17, 2010
Sunday, May 16, 2010
NOTICE
VERY SOON WE ARE GOING TO HAVE MAGAZINE/ARTICLE CORNER IN THIS BLOG IN WHICH WE ARE GOING TO POST CREATIVE WRITINGS ON ANY TOPICS RELATED AND NOT RELATED TO MEDICAL FIELDS...
THE ARTICLES WILL BE COLLECTED FROM MORE THAN 100 MEDICAL COLLEGES ALL OVER THE WORLD....
TO SUBMIT YOUR ARTICLE MAIL TO :
biveksingh@hotmail.com
PLEASE DO NOT COPY THE ARTICLES FROM OTHER SITE ,,,
THE ARTICLES WILL BE COLLECTED FROM MORE THAN 100 MEDICAL COLLEGES ALL OVER THE WORLD....
TO SUBMIT YOUR ARTICLE MAIL TO :
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PLEASE DO NOT COPY THE ARTICLES FROM OTHER SITE ,,,
Saturday, May 15, 2010
Musculoskeletal Pathology:Most know area
Musculoskeletal Pathology:Most know area
Hereditary Disorders
Osteogenesis imperfecta
· Many types
· Mutations of collagen type 1
· Multiple fractures
· Dentinogenesis imperfecta
Achondroplasia
· 20% autosomal dominant; 80% random mutations
· Most common form of inherited dwarfism
· Epiphyseal plates close prematurely
· Cor pulmonale
Osteopetrosis
· Autosomal dominant or recessive
· Osteoclast hypofunction causes very dense bone
· AR: severe, with anemia, nerve entrapment, hydrocephalus, infections, fractures
· AD: milder
Non-Neoplastic Disorders
Fracture
· Inflammatory phase (first week; clot and callus formation)
· Reparative phase (months; callus bridge)
· Remodeling phase (weeks-years; remodeling of callus)
Osteonecrosis
· Ischemic death of bone without infection
· Physical event: trauma, embolism, radiation
· Systemic disease: sickle cell, lupus, gout
· Toxic effect: corticosteroids, alcoholism
Myositis Ossificans
· Reactive bone formation within muscle
· Caused by trauma
· Looks like a neoplasm
· Lower limbs
Osteomyelitis
· Bone inflammation caused by infection
· Staph, Strep, E. coli, N. gonorrhea, H. influenzae, Salmonella
· Results from direct penetration or hematogenous spread
· Sequestrum (necrotic bone fragment) eventually covered by involucrum (new periosteal bone)
Osteoporosis
· Decreased bone mass per unit volume
· Normal ratio of mineral to matrix
· Primary occurs in elderly women (decreased estrogen, less exercise)
· Secondary occurs with corticosteroid use, alcoholism
Paget Disease
· Disorder of bone remodeling
· Three phases (hot, mixed, cold)
· Bones of skull: cotton wool appearance, hypercementosis of jaws
· Tests: alkaline phosphatase, urine hydroxyproline
Fibrous Dysplasia
· Monostotic
· Ground glass appearance on xray
· McCune Albright syndrome
· Jaffe syndrome
Osteoarthritis
· Most common joint disease
· Primary (cartilage defect), secondary (to trauma, crystal deposits, infection)
· Weight-bearing joints (knees, hips, spine) and hands
· Eburnated (very dense, ivory-like) bone, Haberden nodes
Rheumatoid Arthritis
· Chronic, systemic, autoimmune, inflammatory disease
· Symmetrical small-joint involvement
· Starts as synovial disease (hyperplastic synovium, pannus)
· Rice bodies, rheumatoid nodules
Gout
· Increased serum urate leads to urate crystals in joints, kidneys
· Primary or secondary (malignancy, alcoholism)
· Acute gout (podagra), tophaceous gout (tophi in ear, Achilles tendon)
· Histology: Granulomas with needle-shaped crystals
Muscle Disorders
Duchenne Muscular Dystrophy
· X-linked
· Deletion of dystrophin gene
· Degeneration of muscles
· Wheelchair-bound by age 10-15; death from respiratory insufficiency or arrhythmia
Myotonic Dystrophy
· Autosomal dominant
· Atrophy of type I fibers, hypertrophy of type II fibers
· Muscle weakness and sustained muscular contractions
· Gets worse from one generation to next
Hereditary Disorders
Osteogenesis imperfecta
· Many types
· Mutations of collagen type 1
· Multiple fractures
· Dentinogenesis imperfecta
Achondroplasia
· 20% autosomal dominant; 80% random mutations
· Most common form of inherited dwarfism
· Epiphyseal plates close prematurely
· Cor pulmonale
Osteopetrosis
· Autosomal dominant or recessive
· Osteoclast hypofunction causes very dense bone
· AR: severe, with anemia, nerve entrapment, hydrocephalus, infections, fractures
· AD: milder
Non-Neoplastic Disorders
Fracture
· Inflammatory phase (first week; clot and callus formation)
· Reparative phase (months; callus bridge)
· Remodeling phase (weeks-years; remodeling of callus)
Osteonecrosis
· Ischemic death of bone without infection
· Physical event: trauma, embolism, radiation
· Systemic disease: sickle cell, lupus, gout
· Toxic effect: corticosteroids, alcoholism
Myositis Ossificans
· Reactive bone formation within muscle
· Caused by trauma
· Looks like a neoplasm
· Lower limbs
Osteomyelitis
· Bone inflammation caused by infection
· Staph, Strep, E. coli, N. gonorrhea, H. influenzae, Salmonella
· Results from direct penetration or hematogenous spread
· Sequestrum (necrotic bone fragment) eventually covered by involucrum (new periosteal bone)
Osteoporosis
· Decreased bone mass per unit volume
· Normal ratio of mineral to matrix
· Primary occurs in elderly women (decreased estrogen, less exercise)
· Secondary occurs with corticosteroid use, alcoholism
Paget Disease
· Disorder of bone remodeling
· Three phases (hot, mixed, cold)
· Bones of skull: cotton wool appearance, hypercementosis of jaws
· Tests: alkaline phosphatase, urine hydroxyproline
Fibrous Dysplasia
· Monostotic
· Ground glass appearance on xray
· McCune Albright syndrome
· Jaffe syndrome
Osteoarthritis
· Most common joint disease
· Primary (cartilage defect), secondary (to trauma, crystal deposits, infection)
· Weight-bearing joints (knees, hips, spine) and hands
· Eburnated (very dense, ivory-like) bone, Haberden nodes
Rheumatoid Arthritis
· Chronic, systemic, autoimmune, inflammatory disease
· Symmetrical small-joint involvement
· Starts as synovial disease (hyperplastic synovium, pannus)
· Rice bodies, rheumatoid nodules
Gout
· Increased serum urate leads to urate crystals in joints, kidneys
· Primary or secondary (malignancy, alcoholism)
· Acute gout (podagra), tophaceous gout (tophi in ear, Achilles tendon)
· Histology: Granulomas with needle-shaped crystals
Muscle Disorders
Duchenne Muscular Dystrophy
· X-linked
· Deletion of dystrophin gene
· Degeneration of muscles
· Wheelchair-bound by age 10-15; death from respiratory insufficiency or arrhythmia
Myotonic Dystrophy
· Autosomal dominant
· Atrophy of type I fibers, hypertrophy of type II fibers
· Muscle weakness and sustained muscular contractions
· Gets worse from one generation to next
Asperger's Symptoms :A SYNDROME IN "MY NAME IS KHAN"
Asperger's Symptoms in Children
There are some simple, easy-to-use practical tips and techniques that can save you ALL that stress, worry, physical pain and embarrassment...
The Parenting Aspergers Resource Guide is an excellent resource that I would recommend to any parent who has a child with Aspergers Syndrome.
It is full of really practical and easy-to-use information to help parents with their Aspergers child and also the rest of the family.
Learn effective methods which can have a really positive effect on Asperger Symptoms and Asperger Syndrome Behavior:
Does your toddler have aspergers?
Asperger's Symptoms can be presented in a range of combinations. Both children and adults can exhibit any combination of aspergers behaviours in varying degrees of severity. This means that two children, both with the same diagnosis, can act very differently from one another and have varying skills.
The best way to understand Asperger syndrome is to think of it as a form of autism in smart kids.
The best way to understand Asperger syndrome is to think of it as a form of autism in smart kids.
10 Most Essential Asperger's Symptoms in Children
1. Not pick up on social cues and may lack inborn social skills, such as being able to read others' body language, start or maintain a conversation, and take turns talking.
2. Dislike any changes.
3. Lack empathy.
4. Be unable to recognize subtle differences in speech tone, pitch, and accent that alter the meaning of others' speech. Thus, your child may not understand a joke or may take a sarcastic comment literally. Likewise, his or her speech may be flat and difficult to understand because it lacks tone, pitch, and accent.
5. Have a formal style of speaking that is advanced for his or her age. For example, the child may use the word "beckon" instead of "call" or the word "return" instead of "come back."
6. Avoid eye contact or stare at others.
7. Have unusual facial expressions or postures.
8. Be preoccupied with only one or few interests, which he or she may be very knowledgeable about. Many children with Asperger's syndrome are overly interested in parts of a whole or in unusual activities, such as designing houses, drawing highly detailed scenes, or studying astronomy.
9. Talk a lot, usually about a favorite subject. One-sided conversations are common. Internal thoughts are often verbalized.
10. Have delayed motor development. Your child may be late in learning to use a fork or spoon, ride a bike, or catch a ball. He or she may have an awkward walk. Handwriting is often poor.
Source: WeBMD.com
2. Dislike any changes.
3. Lack empathy.
4. Be unable to recognize subtle differences in speech tone, pitch, and accent that alter the meaning of others' speech. Thus, your child may not understand a joke or may take a sarcastic comment literally. Likewise, his or her speech may be flat and difficult to understand because it lacks tone, pitch, and accent.
5. Have a formal style of speaking that is advanced for his or her age. For example, the child may use the word "beckon" instead of "call" or the word "return" instead of "come back."
6. Avoid eye contact or stare at others.
7. Have unusual facial expressions or postures.
8. Be preoccupied with only one or few interests, which he or she may be very knowledgeable about. Many children with Asperger's syndrome are overly interested in parts of a whole or in unusual activities, such as designing houses, drawing highly detailed scenes, or studying astronomy.
9. Talk a lot, usually about a favorite subject. One-sided conversations are common. Internal thoughts are often verbalized.
10. Have delayed motor development. Your child may be late in learning to use a fork or spoon, ride a bike, or catch a ball. He or she may have an awkward walk. Handwriting is often poor.
Source: WeBMD.com
How Asperger Syndrome Affects Daily Life
The syndrome manifests in many ways that can cause difficulties on a daily basis. Here are some examples of what to look for:
- Delayed motor milestones
- Difficulty in conversing
- Extreme shyness
- Mixing with inappropriate company
- Unusual and obsessional interests
- Quoting lists of facts
- Confusion
- Difficulty with multitasking
- Not understanding jokes or social interaction
- Being naive and trusting
- Delighting in fine details such as knobs on a stereo
- Lack of dress sense
- Difficulty in conversing
- Extreme shyness
- Mixing with inappropriate company
- Unusual and obsessional interests
- Quoting lists of facts
- Confusion
- Difficulty with multitasking
- Not understanding jokes or social interaction
- Being naive and trusting
- Delighting in fine details such as knobs on a stereo
- Lack of dress sense
Is There A Cure? NO!
There is currently no known 'cure' for Asperger Syndrome. This does not mean, however, that nothing can be done to help your asperger child.
One of the worst problems is that you can never really understand what is going on inside your child's head.
This makes it so difficult for you to understand their behaviour.
This can leave you feeling emotionally beat up and completely useless as a parent.
You have to cope with crisis on a daily, hourly or even minute by minute basis.
You experience problems when you are at home,...
One of the worst problems is that you can never really understand what is going on inside your child's head.
This makes it so difficult for you to understand their behaviour.
This can leave you feeling emotionally beat up and completely useless as a parent.
You have to cope with crisis on a daily, hourly or even minute by minute basis.
You experience problems when you are at home,...
Is There A Help? YES!
Although behaviors may change through the years, the problem will not go away. But there are strategies that can improve functioning and help families cope. Early diagnosis, behavior training programs, and careful educational management to help the children reach their maximum potential are well worth the effort.There are some simple, easy-to-use practical tips and techniques that can save you ALL that stress, worry, physical pain and embarrassment...
The Parenting Aspergers Resource Guide is an excellent resource that I would recommend to any parent who has a child with Aspergers Syndrome.
It is full of really practical and easy-to-use information to help parents with their Aspergers child and also the rest of the family.
Learn effective methods which can have a really positive effect on Asperger Symptoms and Asperger Syndrome Behavior:
Eating broccoli and cabbage can assist in lowering blood pressure
London, July 11: Eating broccoli and cabbage can assist in lowering blood pressure, suggests a latest study.
The probable reason behind this is the presence of glutamic acid in high volume in broccoli and cabbage.
For conducting the latest study, researchers scrutinized the quantity of five amino acids in the diets of 4,680 volunteers, ages between 40 to 59 years, from the U.S., UK, China and Japan.
It was discovered that with an increase in glutamic acid content in their food, their blood pressure dropped down.
Study author Dr Ian Brown, an epidemiologist at Imperial College, London, was quoted as saying, “Glutamic acid may partly explain the link between vegetable protein and lower blood pressure.”
He added, “However there is no ‘magic bullet’ for preventing high blood pressure, and vegetable protein and glutamic acid are individual elements of a broader healthy eating pattern.”
Glutamic acid and its sources
Glutamic acid is one of the most widely found amino acids and forms nearly one-fourth of vegetable protein and one-fifth of the animal protein.
It is found in all types of meats, dairy products, poultry, fish and the seaweed kombu. Rice, soy products, breads, cereals and similar whole grain foods are other excellent sources of glutamic acid.
Researchers recommend that people should not pop up glutamic acid pills, instead they should eat foods containing this acid.
DASH recommended for blood pressure
Experts say that the ‘Dietary Approaches to Stop Hypertension (DASH)’ diet, which reduces blood pressure and is developed by the U.S. National Institutes of Health, should be followed.
The DASH diet is rich in fruits, vegetables, whole grains, lean poultry, nuts and beans.
The new study has been published in Circulation: Journal of the American Heart Association.
The probable reason behind this is the presence of glutamic acid in high volume in broccoli and cabbage.
For conducting the latest study, researchers scrutinized the quantity of five amino acids in the diets of 4,680 volunteers, ages between 40 to 59 years, from the U.S., UK, China and Japan.
It was discovered that with an increase in glutamic acid content in their food, their blood pressure dropped down.
Study author Dr Ian Brown, an epidemiologist at Imperial College, London, was quoted as saying, “Glutamic acid may partly explain the link between vegetable protein and lower blood pressure.”
He added, “However there is no ‘magic bullet’ for preventing high blood pressure, and vegetable protein and glutamic acid are individual elements of a broader healthy eating pattern.”
Glutamic acid and its sources
Glutamic acid is one of the most widely found amino acids and forms nearly one-fourth of vegetable protein and one-fifth of the animal protein.
It is found in all types of meats, dairy products, poultry, fish and the seaweed kombu. Rice, soy products, breads, cereals and similar whole grain foods are other excellent sources of glutamic acid.
Researchers recommend that people should not pop up glutamic acid pills, instead they should eat foods containing this acid.
DASH recommended for blood pressure
Experts say that the ‘Dietary Approaches to Stop Hypertension (DASH)’ diet, which reduces blood pressure and is developed by the U.S. National Institutes of Health, should be followed.
The DASH diet is rich in fruits, vegetables, whole grains, lean poultry, nuts and beans.
The new study has been published in Circulation: Journal of the American Heart Association.
Friday, May 14, 2010
THE SPITTING COBRA
THE SPITTING COBRA
The species of snake called the spitting cobra is very unusual as it not only has a poisonous bite but it also spits venom into the eyes of its prey and aggressors. Contact of this venom with your eyes is very painful and can even blind you temporarily, therefore, if you get cobra venom in your eyes, irrigate them with water at once in order to prevent permanent tissue damage.
The King Cobra (Ophiophagus hannah) is also remarkable in this large family of snakes (elapidae) because it feeds almost entirely on other snakes with mice and small birds also falling prey to its poison.
The King Cobra is also a record-holder because of its size – it can reach almost twenty feet (585 cms) in length, which makes it the largest poisonous snake in the world. The most recent discovery of a new species of cobra was made in 2003 as part of an illegal shipment of exotic pets at London Zoo.
DNA studies revealed that this new species of snake is similar to the red spitting cobra but has different genes. It seems to originate from an area between Sudan and Egypt and it has been called the ‘Nubian Spitting Cobra’.
Though highly dangerous when it is threatened cobras will not attack if you leave them alone, although the spit is very accurate for about two meters. Compared to the strike of a rattlesnake, the cobra is fairly slow in its attack and furthermore, many bites prove to be blank, that is without venom.
Statistics of a study conducted on Malaysian cobra snake victims indicate that only 55% of the bites involved poison release and the same statistics indicate a mortality rate of only 10% for people bitten, since the poisons injected into the blood of the prey destroy the nerves (neurotoxins), which induces respiratory failure approximately half an hour after being bitten, so you have 30 minutes to seek help.
The colouration is variable from light green-grey to black, while juveniles are yellow and black banded. This snake can find a habitat all over south-eastern Asia.
Use Google as a calculator.
Use Google as a calculator.
Google has a built-in calculator — try entering a calculation like 110 * (654/8 + 3). Yes, your computer also has a calculator, but if you spend most of your day inside a browser, typing your calculation into the browser’s search box is quicker than firing up your calculator app.
Google has a built-in calculator — try entering a calculation like 110 * (654/8 + 3). Yes, your computer also has a calculator, but if you spend most of your day inside a browser, typing your calculation into the browser’s search box is quicker than firing up your calculator app.
Thursday, May 13, 2010
Liver, Pancreas, and Gallbladder Anatomy-Histology Correlate
Notes on Liver, Pancreas, and Gallbladder Anatomy-Histology Correlate
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Notes on Liver,Pancreas , and Gallbladder Anatomy-Histology Correlate
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Notes on Liver,Pancreas , and Gallbladder Anatomy-Histology Correlate
NOTES ON MUSCLE CONTRACTION
NOTES ON MUSCLE CONTRACTION
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NOTES ON MUSCLE PHYSIOLOGY
NOTES ON MUSCLE PHYSIOLOGY
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QUIZ ON GASTROINTESTINAL PHYSIOLOGY
Gastrointestinal System Quiz - II
1. Which of the following listed diagnostic tests to be performed at the last?
A. Gall bladde series
B. Barium enema
C. Barium swallow
D. Oral choleycystogram
Answer Key
2. What type of diet should be provided to the patient sheduled for oral choleycystogram on the evening before the test?
A. Low-protein
B. High-carbohydrate
C. Fat-free
D. Liquid
Answer Key
3. What type of diet is indicated for a patient with colostomy for the first 4 to 6 weeks foolowing the surgery?
A. High-protein
B. High-carbohydrate
C. Low-calorie
D. Low-residue
Answer Key
4. Which is the appropriate mode of suction pressure and control indicated for stomuch decompression?
A. Low and continous
B. High and intermittent
C. low and intermittent
D. High and continous
5. Gastric juice contains:
A. Pepsin, lipase and renin
B. Trypsin, lipase and rennin
C. Trypsin, lipase and lipase
D. Trypsin, pepsin and rennin
Answer Key
6. Succus entericus is the name given to:
A. Intestinal juice
B. Junction between ileum and large intestine
C.Swelling in the gut
D. Appendix
Answer Key
7. Glycogen is:
A. Synthesised in liver, source of energy, forming bile and lipase
B. Disacharide stored in liver, reacts with amonia to form protein
C. Synthesied in blood, stored in liver, and muscle to provide glucose.
D. Polysacharide synthesised and stored in liver
Answer Key
8. Which ones are absorbed in the alimentary tract without any breakdown?
A. Proteins
B. Polysacharides
C. fat soluble vitamins
D. Albumin of egg
Answer Key
9. pH suitable for ptylin action is:
A. 6.8
B. 7.8
C. 3.2
D. 9.3
Answer Key
10. Choose the correct pair
A. Rennin-Casein
B. Protein-Amylase
C. Carbohydrate-Lipase
D. Maltase-Lactose
Answer Key
10. What is common among amylase, rennin and lipase?
A. All proteins
B. Proteolytic enzymes
C. Produced in stomuch
D. Act at pH lower than 7.
Answer Key
11. Which is a spcific gastric hormone?
A. secretin
B. Srotonin
C. Amphetamine
D. Trypsin
Answer Key
12. secretion of cholecystokinin is for:
A. Controlling blood pressure
B. Inducing peristalsis
C. Bile functions
D. Release of insulin
Answer Key
13. Average human live weighs:
A. 6. 0 kg
B. 5.0 kg
C. 0.5 kg
D. 1.5 kg
Answer Key
14. Digesive juice contains catalytic agents called:
A. Vitamins
B. Hormones
C. Enzymes
D. Nitrates
Answer Key
15. Human digestive juice lacks:
A. Lactase
B. Cellulase
C. Amylase
D. Sucrase
Answer Key
16. Cobalamine is required for the formation of:
A. Platelets
B. Leucocytes
C. Lymph
D. Erythrocytes
Answer Key
17. Digestive hormones secretin and cholecystokinin are secreted by:
A. Oesophagus
B. Stomuch
C. Ileum
D. Duodenum
Answer Key
18. Number of milk teeth in an toddler is:
A. 12
B. 20.
C. 32
D. 46
Answer Key
19. Which is NOT correctly matched?
A. Vit B12 -- Pernicious anaemia
B. Vit B6 -- Loss of appetite
C. Vit B1 -- Beri-beri
D. Vit B2 -- Pellagra
Answer Key
20. Glisson's capule is associated with:
A. Liver
B. Pancreas
C. Lung
D. Kidney
Answer Key
Answer Key
1. C 2. C 3. D 4. C 5. A
6. A 7. D 8. C 9. A 10. B
11. A 12. C 13. C 14. C 15.B
16. D 17. D 18. B 19. D 20. A
1. Which of the following listed diagnostic tests to be performed at the last?
A. Gall bladde series
B. Barium enema
C. Barium swallow
D. Oral choleycystogram
Answer Key
2. What type of diet should be provided to the patient sheduled for oral choleycystogram on the evening before the test?
A. Low-protein
B. High-carbohydrate
C. Fat-free
D. Liquid
Answer Key
3. What type of diet is indicated for a patient with colostomy for the first 4 to 6 weeks foolowing the surgery?
A. High-protein
B. High-carbohydrate
C. Low-calorie
D. Low-residue
Answer Key
4. Which is the appropriate mode of suction pressure and control indicated for stomuch decompression?
A. Low and continous
B. High and intermittent
C. low and intermittent
D. High and continous
5. Gastric juice contains:
A. Pepsin, lipase and renin
B. Trypsin, lipase and rennin
C. Trypsin, lipase and lipase
D. Trypsin, pepsin and rennin
Answer Key
6. Succus entericus is the name given to:
A. Intestinal juice
B. Junction between ileum and large intestine
C.Swelling in the gut
D. Appendix
Answer Key
7. Glycogen is:
A. Synthesised in liver, source of energy, forming bile and lipase
B. Disacharide stored in liver, reacts with amonia to form protein
C. Synthesied in blood, stored in liver, and muscle to provide glucose.
D. Polysacharide synthesised and stored in liver
Answer Key
8. Which ones are absorbed in the alimentary tract without any breakdown?
A. Proteins
B. Polysacharides
C. fat soluble vitamins
D. Albumin of egg
Answer Key
9. pH suitable for ptylin action is:
A. 6.8
B. 7.8
C. 3.2
D. 9.3
Answer Key
10. Choose the correct pair
A. Rennin-Casein
B. Protein-Amylase
C. Carbohydrate-Lipase
D. Maltase-Lactose
Answer Key
10. What is common among amylase, rennin and lipase?
A. All proteins
B. Proteolytic enzymes
C. Produced in stomuch
D. Act at pH lower than 7.
Answer Key
11. Which is a spcific gastric hormone?
A. secretin
B. Srotonin
C. Amphetamine
D. Trypsin
Answer Key
12. secretion of cholecystokinin is for:
A. Controlling blood pressure
B. Inducing peristalsis
C. Bile functions
D. Release of insulin
Answer Key
13. Average human live weighs:
A. 6. 0 kg
B. 5.0 kg
C. 0.5 kg
D. 1.5 kg
Answer Key
14. Digesive juice contains catalytic agents called:
A. Vitamins
B. Hormones
C. Enzymes
D. Nitrates
Answer Key
15. Human digestive juice lacks:
A. Lactase
B. Cellulase
C. Amylase
D. Sucrase
Answer Key
16. Cobalamine is required for the formation of:
A. Platelets
B. Leucocytes
C. Lymph
D. Erythrocytes
Answer Key
17. Digestive hormones secretin and cholecystokinin are secreted by:
A. Oesophagus
B. Stomuch
C. Ileum
D. Duodenum
Answer Key
18. Number of milk teeth in an toddler is:
A. 12
B. 20.
C. 32
D. 46
Answer Key
19. Which is NOT correctly matched?
A. Vit B12 -- Pernicious anaemia
B. Vit B6 -- Loss of appetite
C. Vit B1 -- Beri-beri
D. Vit B2 -- Pellagra
Answer Key
20. Glisson's capule is associated with:
A. Liver
B. Pancreas
C. Lung
D. Kidney
Answer Key
Answer Key
1. C 2. C 3. D 4. C 5. A
6. A 7. D 8. C 9. A 10. B
11. A 12. C 13. C 14. C 15.B
16. D 17. D 18. B 19. D 20. A
NOTES ON SHOULDER JOINT
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Wednesday, May 12, 2010
NOTES ON KNEE JOINT
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vinay kumar (PATHOLOGIST)
Vinay Kumar, MBBS, MD, FRCPath
Alice Hogge & Arthur Baer Professor
Chairman, Department of Pathology
Executive Vice Dean, Division of Biological Sciences
Contact
* visit U of C Directory *
Department of Pathology
The University of Chicago
MC 3083, S329
5841 S. Maryland Avenue
Chicago, IL 60637
Phone: 773.702.0647
Fax: 773.702.9379
vkumar@bsd.uchicago.edu
Research Interests
Our laboratory is interested in the cellular and molecular biology of murine natural killer (NK) cells. These cells are believed to act as the first line of defense against tumors and viral infections. In addition they secrete a variety of cytokines including 1FN-g and GM-CSF that can influence the inflammatory response. Two aspects of NK cell biology are of particular interest to us: the development of NK cells from multipotent progenitor cells, and the identification of NK cell receptors and their ligands. Textbook Publications
Kumar V, Abbas AK, Fausto N, Aster JA. "Pathologic Basis of Disease." 8th edition, W.B. Saunders Co., 2009 in press (with translations into Spanish, Portuguese, Italian, German, Turkish and Arabic).
Kumar V, Mitchell RM, Abbas AK, Fausto N. "Basic Pathology." 8th edition, W.B. Saunders, 2007 (with translations into Spanish, Portuguese, Italian, Chinese, Japanese, Hungarian and Croatian).
Mitchell R, Kumar V, Abbas A, Fausto N. "Pocket Companion to Robbins and Cotran Pathologic Basis of Disease." 7th Edition, Elsevier Saunders, 2006.
Klatt E, Kumar V. "Robbins and Cotran Review of Pathology." 2nd Edition, Elsevier Saunders, 2005.
Kumar V, Fausto N, Abbas A. "Robbins and Cotran Pathologic Basis of Disease." 7th edition, Elsevier Saunders, 2004.
How to perform better in exams
How to perform better in exams
Tests and exams are an inevitable part of learning. They’re not there to trip you up, but to measure how well you have understood the subject. Even if you know the content well, there are ways to help yourself perform better on the day.
Before the exam
During the exam
After the exam
Some people thrive on exams, others aren’t so fortunate. A disciplined approach will make your task easier, and - hopefully - improve your results
Before the exam
Your success starts before you even sit down for the exam.
Look at previous tests, and analyse how well you did, and where there could be room for improvement
Always arrive early for an exam. Arriving late will just add to your stress levels
Arrive with a good attitude: be positive, smile, and be confident
If you suffer from exam anxiety, read our article on how to manage exam stress.
--------------------------------------------------------------------------------
During the exam
Read the directions carefully, and slowly. You don’t want to make a careless mistake
Read through the whole exam before answering, to give an overall picture of your task
Answer easy questions first; that way you won’t get stuck on a tricky question and run out of time
Look for the key words in the question: there are usually one or two that will give you a clue
Don’t leave when you’re finished; review all your answers and double-check you’ve answered all questions correctly
Double-check your spelling, punctuation and grammar.
--------------------------------------------------------------------------------
After the exam
Be positive: think about those tasks you know you did well on
Avoid a ‘post mortem’. Discussing with other students how well you and they did, or didn’t do, will only drag you down
After the exam, don’t go back to study or work right away: give yourself some time off to relax doing something you enjoy.
--------------------------------------------------------------------------------
Tests and exams are an inevitable part of learning. They’re not there to trip you up, but to measure how well you have understood the subject. Even if you know the content well, there are ways to help yourself perform better on the day.
Before the exam
During the exam
After the exam
Some people thrive on exams, others aren’t so fortunate. A disciplined approach will make your task easier, and - hopefully - improve your results
Before the exam
Your success starts before you even sit down for the exam.
Look at previous tests, and analyse how well you did, and where there could be room for improvement
Always arrive early for an exam. Arriving late will just add to your stress levels
Arrive with a good attitude: be positive, smile, and be confident
If you suffer from exam anxiety, read our article on how to manage exam stress.
--------------------------------------------------------------------------------
During the exam
Read the directions carefully, and slowly. You don’t want to make a careless mistake
Read through the whole exam before answering, to give an overall picture of your task
Answer easy questions first; that way you won’t get stuck on a tricky question and run out of time
Look for the key words in the question: there are usually one or two that will give you a clue
Don’t leave when you’re finished; review all your answers and double-check you’ve answered all questions correctly
Double-check your spelling, punctuation and grammar.
--------------------------------------------------------------------------------
After the exam
Be positive: think about those tasks you know you did well on
Avoid a ‘post mortem’. Discussing with other students how well you and they did, or didn’t do, will only drag you down
After the exam, don’t go back to study or work right away: give yourself some time off to relax doing something you enjoy.
--------------------------------------------------------------------------------
Tuesday, May 11, 2010
NOTES ON HYMENOLEPIS NANA (dwarf tapeworm) by BIVEK SINGH
HYMENOLEPIS NANA (dwarf tapeworm)
• smallest tapeworm infecting man
• only human tapeworm which can complete its entire life cycle in a single host
• does not require an obligatory intermediate host
• man can harbor both adult and larval stages of parasite
DISTRIBUTION
• worldwide among children
DISEASES
• hymenolepiasis
MORPHOLOGY
1. Adult Worm
- found in the ileum
- delicate strobila that measures 25 to 45 mm x 1 mm (lw)
- Scolex
o Subglobular
o 4 cup-shaped suckers
o retractable rostellum with a single row of 20 to 30 y-shaped hooklets
- Neck
o long and slender
- Proglottids
o Anterior = short
o Posterior = broader
o Measures 0.15 to 0.3 mm x 0.8 to 1.0 mm (lw)
o Mature proglottids : contain 3 ovoid testes and one ovary
o Gravid proglottids :
testes and ovary disappear
uterus hollows out and becomes filled with eggs
segments are separated from the strobila and disintegrate as they pass out of the intestines, releasing eggs in stool
- Segments
o 175 to 220 segments
o genital pores found along the side of segments
2. Eggs
- Shape : spherical or subspherical
- Measures 30 to 47 um in diameter
- Oncosphere
o thin outer membrane
o thick inner membrane with conspicuous bipolar thickenings
4 to 8 hair-like polar filaments arise
filaments are embedded in the inner membrane
H. nana cysticercoid
LIFE CYCLE
- Dual pathway
1. Direct
• host ingests eggs which hatch in the duodenum
• liberated embryos penetrate mucosal villi
• develop into infective cysticercoid larvae
• larvae break out of villi and attaches to intestinal mucosa 4 to 5 days later
• develop into adults
2. Indirect
• infection is usually via accidental ingestion of infected arthropod intermediate hosts like rice and flour beetles (Tenebrio sp.)
• cysticercoid larvae are released and will eventually develop into adult tapeworms in the intestines of the host
- takes 20 to 30 days from time of ingestion for eggs to appear in the feces
- eggs are viable immediately after discharge from bowel
- autoinfection can occur through the fecal-oral route or w/in the small bowel
- oncospheres from eggs are released and they invade the host villi to start new generation
PATHOGENESIS AND CLINICAL MANIFESTATION
• symptoms are produced because of patient’s immunological response to the presence of the parasite
• asymptomatic – light worm burden
• clinical manifestations:
o headache
o dizziness
o anorexia
o pruritus of nose and anus
o diarrhea
o abdominal pain
o pallor
• infected children
o restless
o irritable
o exhibit sleep disturbances
o convulsions (rare)
• Heavy infections
o Enteritis due to necrosis and desquamation of the intestinal epithelial cells
• Regulatory immunity
o (time) clears H. nana spontaneously.
DIAGNOSIS
• specific diagnosis = demonstration of characteristic eggs in stool
• light infections = need to concentrate stool specimens
• proglottids are not recovered because they undergo degeneration prior to passage with stools
TREATMENT
• *Praziquantel = 25mg/kg single dose
o causes vacuolization and disruption of tegument in the neck region
o dosage for hymenolepiasis is higher than for taeniasis because of relative resistant cysticercoids in the intestinal tissue
• examine stool after 2 weeks
o repeat treatment to cover for the worms emerging from remaining viable cysticercoids
EPIDEMIOLOGY
• found in warm countries
o Southern USA
o Latin America
o Mediterranean
o East Asia
o Philippines
• Transmission : poor sanitation, overcrowding, poor personal hygiene
• Direct contact plays an important role because eggs cannot survive long outside host
• Familial and institutional infection
• Found in mice and rats
PREVENTION AND CONTROL
• involves a single host and transmission is direct
• personal hygiene and environmental sanitation
• rodent control
• prevent food from infections by grain beetles
you can post comments ,likes ,suggestion and demand for other notes>
BIVEK SINGH
• smallest tapeworm infecting man
• only human tapeworm which can complete its entire life cycle in a single host
• does not require an obligatory intermediate host
• man can harbor both adult and larval stages of parasite
DISTRIBUTION
• worldwide among children
DISEASES
• hymenolepiasis
MORPHOLOGY
1. Adult Worm
- found in the ileum
- delicate strobila that measures 25 to 45 mm x 1 mm (lw)
- Scolex
o Subglobular
o 4 cup-shaped suckers
o retractable rostellum with a single row of 20 to 30 y-shaped hooklets
- Neck
o long and slender
- Proglottids
o Anterior = short
o Posterior = broader
o Measures 0.15 to 0.3 mm x 0.8 to 1.0 mm (lw)
o Mature proglottids : contain 3 ovoid testes and one ovary
o Gravid proglottids :
testes and ovary disappear
uterus hollows out and becomes filled with eggs
segments are separated from the strobila and disintegrate as they pass out of the intestines, releasing eggs in stool
- Segments
o 175 to 220 segments
o genital pores found along the side of segments
2. Eggs
- Shape : spherical or subspherical
- Measures 30 to 47 um in diameter
- Oncosphere
o thin outer membrane
o thick inner membrane with conspicuous bipolar thickenings
4 to 8 hair-like polar filaments arise
filaments are embedded in the inner membrane
H. nana cysticercoid
LIFE CYCLE
- Dual pathway
1. Direct
• host ingests eggs which hatch in the duodenum
• liberated embryos penetrate mucosal villi
• develop into infective cysticercoid larvae
• larvae break out of villi and attaches to intestinal mucosa 4 to 5 days later
• develop into adults
2. Indirect
• infection is usually via accidental ingestion of infected arthropod intermediate hosts like rice and flour beetles (Tenebrio sp.)
• cysticercoid larvae are released and will eventually develop into adult tapeworms in the intestines of the host
- takes 20 to 30 days from time of ingestion for eggs to appear in the feces
- eggs are viable immediately after discharge from bowel
- autoinfection can occur through the fecal-oral route or w/in the small bowel
- oncospheres from eggs are released and they invade the host villi to start new generation
PATHOGENESIS AND CLINICAL MANIFESTATION
• symptoms are produced because of patient’s immunological response to the presence of the parasite
• asymptomatic – light worm burden
• clinical manifestations:
o headache
o dizziness
o anorexia
o pruritus of nose and anus
o diarrhea
o abdominal pain
o pallor
• infected children
o restless
o irritable
o exhibit sleep disturbances
o convulsions (rare)
• Heavy infections
o Enteritis due to necrosis and desquamation of the intestinal epithelial cells
• Regulatory immunity
o (time) clears H. nana spontaneously.
DIAGNOSIS
• specific diagnosis = demonstration of characteristic eggs in stool
• light infections = need to concentrate stool specimens
• proglottids are not recovered because they undergo degeneration prior to passage with stools
TREATMENT
• *Praziquantel = 25mg/kg single dose
o causes vacuolization and disruption of tegument in the neck region
o dosage for hymenolepiasis is higher than for taeniasis because of relative resistant cysticercoids in the intestinal tissue
• examine stool after 2 weeks
o repeat treatment to cover for the worms emerging from remaining viable cysticercoids
EPIDEMIOLOGY
• found in warm countries
o Southern USA
o Latin America
o Mediterranean
o East Asia
o Philippines
• Transmission : poor sanitation, overcrowding, poor personal hygiene
• Direct contact plays an important role because eggs cannot survive long outside host
• Familial and institutional infection
• Found in mice and rats
PREVENTION AND CONTROL
• involves a single host and transmission is direct
• personal hygiene and environmental sanitation
• rodent control
• prevent food from infections by grain beetles
you can post comments ,likes ,suggestion and demand for other notes>
BIVEK SINGH
Gallstones
Bile contains cholesterol, bile pigments and phospholipids - if concentrations vary stones can form
Pigment stones - small, friable and irregular, caused by haemolysis
Cholesterol - large, often solitary. Associated with F, age and obesity
Occur in 8% over 40, 90% are asymptomatic.
Risks for becoming symptomatic - smoking, parity
Stones may cause;
Acute or chronic cholecystitis
Bilary colic
Pancreatitis
Obstructive jaundice
Acute cholecystitis
Follows stone or sludge impaction in the neck of the gallbladder
May cause continuous epigastric or RUQ pain (referred to right shoulder), vomiting, fever, local peritonism or a GB mass
The main difference from biliary colic is the inflammatory component - local peritonism, fever, raised WCC
If the stone moves to the CBD, obstructive jaundice and cholangitis may result
Murphy’s sign positive - place fingers over RUQ and get patient to breath in, then repeat on the LUQ
Tests - raised WCC, ultrasound - thick walled, shrunken GB, pericholestatic fluid, stones? CBD - dilated >6cm? AXR only shows up 10% of stones
Treatment
NBM, analgesics, IV fluids and antibiotics e.g. cefuroxime
Cholecystectomy
Chronic cholecystitis
Stones causing chronic inflammation and colic
Vague abdo pain, distension, nausea, flatulence and fat intolerance
US used to check for stones and CBD dilation
Treatment - cholecystectomy
Biliary colic
Occurs when gallstones become symptomatic with cystic duct obstruction or by passing into the CBD
Give RUQ pain, radiating to back plus jaundice
Give morphine plus an antiemetic
Elective cholecystectomy
Other presentations
Obstructive jaundice with CBD stones
Cholangitis - bile duct infection
Gallstone ileus - a stone perforates the GB entering the duodenum where it may obstruct the terminal ileum. Duodenal obstruction is rarer - Bouveret’s syndrome
Pancreatitis
Empyema
Complications of gallstones;
In the gallbladder;
Biliary colic
Acute and chronic cholecystitis
Empyema
Mucocoele
Carcinoma
In the bile duct
Obstructive jaundice
Pancreatitis
Cholangitis
In the gut;
Gallstone ileus
Pigment stones - small, friable and irregular, caused by haemolysis
Cholesterol - large, often solitary. Associated with F, age and obesity
Occur in 8% over 40, 90% are asymptomatic.
Risks for becoming symptomatic - smoking, parity
Stones may cause;
Acute or chronic cholecystitis
Bilary colic
Pancreatitis
Obstructive jaundice
Acute cholecystitis
Follows stone or sludge impaction in the neck of the gallbladder
May cause continuous epigastric or RUQ pain (referred to right shoulder), vomiting, fever, local peritonism or a GB mass
The main difference from biliary colic is the inflammatory component - local peritonism, fever, raised WCC
If the stone moves to the CBD, obstructive jaundice and cholangitis may result
Murphy’s sign positive - place fingers over RUQ and get patient to breath in, then repeat on the LUQ
Tests - raised WCC, ultrasound - thick walled, shrunken GB, pericholestatic fluid, stones? CBD - dilated >6cm? AXR only shows up 10% of stones
Treatment
NBM, analgesics, IV fluids and antibiotics e.g. cefuroxime
Cholecystectomy
Chronic cholecystitis
Stones causing chronic inflammation and colic
Vague abdo pain, distension, nausea, flatulence and fat intolerance
US used to check for stones and CBD dilation
Treatment - cholecystectomy
Biliary colic
Occurs when gallstones become symptomatic with cystic duct obstruction or by passing into the CBD
Give RUQ pain, radiating to back plus jaundice
Give morphine plus an antiemetic
Elective cholecystectomy
Other presentations
Obstructive jaundice with CBD stones
Cholangitis - bile duct infection
Gallstone ileus - a stone perforates the GB entering the duodenum where it may obstruct the terminal ileum. Duodenal obstruction is rarer - Bouveret’s syndrome
Pancreatitis
Empyema
Complications of gallstones;
In the gallbladder;
Biliary colic
Acute and chronic cholecystitis
Empyema
Mucocoele
Carcinoma
In the bile duct
Obstructive jaundice
Pancreatitis
Cholangitis
In the gut;
Gallstone ileus
High-risk profession: Suicide rate of U.S. doctors is one per day
More than a quarter of primary care doctors reported being "burnt out," in part due to worsening time pressures and a chaotic work pace, which were "strongly associated with low physician satisfaction."
300-400 doctors in the United States kill themselves every year, or roughly 1 per day. Male doctors have suicide rates 1.4 times that of the general population, while female doctors have twice the rate of depression and 2.3 times the suicide rate when compared with women who are not physicians.
References:
Help for Today's Tense, Frustrated Doctors. Medscape, 2009.
http://www.medscape.com/viewarticle/710904
Image source: Vincent van Gogh's 1890 painting At Eternity's Gate. Wikipedia, public domain.
Eating chocolate with high flavanol levels can protect the skin from UV light
Cocoa beans fresh from the tree are exceptionally rich in flavanols. Unfortunately, during conventional chocolate making, this high antioxidant capacity is greatly reduced due to manufacturing processes.
The researchers evaluated the photoprotective potential of chocolate consumption, comparing:
- specially produced chocolate with preserved high flavanol (HF) levels.
The minimal erythema dose (MED) was assessed at baseline and after 12 weeks.
In the high flavanol (HF) chocolate group the mean MED more than doubled after 12 weeks of chocolate consumption, while in the LF chocolate group, the MED remained without significant change.
The authors concluded that regular consumption of a chocolate rich in flavanols confers significant photoprotection and can thus be effective at protecting human skin from harmful UV effects. However, conventional chocolate has no such effect.
The researchers evaluated the photoprotective potential of chocolate consumption, comparing:
- conventional dark chocolate
- specially produced chocolate with preserved high flavanol (HF) levels.
A double-blind in vivo study in 30 healthy subjects was conducted, 15 subjects were randomly assigned to either a high flavanol (HF) or low flavanol (LF) chocolate group and consumed a 20 g portion of their allocated chocolate daily.
The minimal erythema dose (MED) was assessed at baseline and after 12 weeks.
In the high flavanol (HF) chocolate group the mean MED more than doubled after 12 weeks of chocolate consumption, while in the LF chocolate group, the MED remained without significant change.
The authors concluded that regular consumption of a chocolate rich in flavanols confers significant photoprotection and can thus be effective at protecting human skin from harmful UV effects. However, conventional chocolate has no such effect.
Can a Midday Nap Make You Smarter? Adults Who Nap for 90-minutes at 2 PM Learn and Perform Better at Tests
According to a new study, if you devote your lunch hour to a nap, you may perform and learn better in the afternoon.
Napping at midday, when the brain's ability to learn may have deteriorated, may clear the brain's memory "storage area" and make room for new information.
In the study, the nap group was given the chance for a 90-minute siesta at 2 p.m.; the no-nap group was asked to stay awake.
People in the group which didn't nap had a 10% reduction in their learning capacity. The people who had a nap improved their ability to learn by 10% (not much).
References:
Can a Mid-Day Nap Make You Smarter? WebMD.
Image source: Sleeping kitten. Wikipedia, Tilman Piesk, public domain.
B-BLOCKER BLOOD PRESSURE PILLS HAVE BEEN USED FOR STAGE FRIGHT BUT MAKE SOME DEPRESSED AND SLOW HEART RATE
Some people are so nervous that they are anxious about their anxiety. "A blood pressure pill could help people forget bad memories, according to a Dutch study published Sunday". I am not sure if this is exactly news because beta blockers in small doses have been profferred as a treatment for some kinds of anxiety for quite a long time. According to the interesting musician's web site below "Beta blockers have been called "the musicians underground drug." Often musicians form their opinions, and may risk their health, based on locker-room-type information". But like almost everything in medicine different people react differently to the same drug. Some people actually get more depressed on beta blockers.
Beta blockers are a class of heart cardiovascular and blood pressure pills that have the effect of slowing the heart beat. They work on the so called beta receptors. They can be dangerous in certain conditions such as when a person already has a slow heart rate and they can worsen diabetes and increase asthma problems.
"The generic beta-blocker propranolol weakened a person's fearful memories of spiders in the test group, making it a possible treatment for individuals with anxiety disorders and phobias.We could show that the fear response went away, which suggests the memory was weakened," said Merel Kindt, a psychologist at the University of Amsterdam, who led the study".
Beta blockers are a class of heart cardiovascular and blood pressure pills that have the effect of slowing the heart beat. They work on the so called beta receptors. They can be dangerous in certain conditions such as when a person already has a slow heart rate and they can worsen diabetes and increase asthma problems.
"The generic beta-blocker propranolol weakened a person's fearful memories of spiders in the test group, making it a possible treatment for individuals with anxiety disorders and phobias.We could show that the fear response went away, which suggests the memory was weakened," said Merel Kindt, a psychologist at the University of Amsterdam, who led the study".
What Does Monty Python Have to do with the Heart?
I went to a cardiologist yesterday and he told me to go watch the movie Ferris Bueller's Day Off or Monthy Python... Actually that didn't happen but it could have. Watching a funny movie could be good for your heart. "Laughing may be important to maintain a healthy endothelium, and reduce the risk of cardiovascular disease,” says principal investigator Michael Miller, M.D., director of preventive cardiology at the University of Maryland Medical Center". Using laughter-provoking movies to gauge the effect of emotions on cardiovascular health, researchers at the school suggest that laughter is linked to healthy function of blood vessels. The endothelium is the inner lining of the blood vessels. You may not know it but the blood vessels can dilate (become wider). One of the signs of good cardiovascular function is the flexibility of the blood vessels to dilate. Interestingly, drugs like Viagra improve the dilation qualities of blood vessels. That is how it was discovered when scientists were looking for new heart medicines. Too much dilation can cause low blood pressure and thus the warnings about these drugs in some people, but I digress.
Sunday, March 21, 2010
IRON METABOLISM
Presented By:
• Bivek Singh
• KISTMC
• Second year student
• Department of biochemistry
Describe Iron deficiency anemia
Describe the diagnostic test for iron
deficiency states.
Cause ,Diagnosis and Management of
Porphyria
Acute intermittent porphyria
Iron deficiency anemia
Commonest cause of anaemia worldwide
Cause of chronic ill health
CAUSE :-
• Increased physiologic demand eg. pregnancy, lactation, rapid growth
• Blood loss from GI tract, uterus, haemoglobinuria
• Malabsorption
• Diet
CLINICAL FEATURES :
IRON DEFICIENCY
Symptoms eg. fatigue, dizziness, headache
Signs
eg. pallor,
glossitis,
angular cheilosis,
koilonychia,
Plummer Vinson syndrome
LABORATORY DIAGNOSIS: IRON DEFICIENCY
• Microcytic hypochromic anaemia
• Often pencil cells and target cells on blood film
• Decreased serum ferritin
• Decreased serum iron, increased TIBC, decreased % transferrin saturation
• Absent bone marrow haemosiderin : (rarely required for diagnosis )
Things you need to know about Laboratory Testing for Iron Status
1. Serum ferritin most useful test
2. Low serum ferritin certain proof patient iron deficient
3. Normal serum ferritin does not always rule out iron deficiency
4. Certain conditions raise ferritin for reasons unrelated to iron status
Porphyria:
Heme is part of hemoglobin, myoglobin, catalases, peroxidases, and cytochromes
Heme is made in every human cell (85% in erythroid cells & much of the rest in the liver)
Classification of porphyrias
Porphyria is a disruption in the heme pathway
• Group of metabolic diseases resulting from a partial deficiency of an enzyme in the heme biosynthetic pathway
• Seven enzymes in the pathway
• Four of the porphyrias cause acute attacks
• Increased demand for heme can precipitate attacks secondary to overproduction of toxic heme precursors (porphyrins, ALA)
• The porphyrins have no useful function and act as highly reactive oxidants damaging tissues
Not a ‘vampire’s’ disease
Some symptoms of porphyrias have lead people to believe that these diseases
provide some basis for vampire legends:
• Extreme sensitivity to sunlight
• Anemia
This idea has been discarded both for scientific reasons:
• Porphyrias do not cause a craving for blood.
• Drinking blood would not help a victim of porphyria.
Acute Intermittent Porphyria
Most common porphyria
Deficiency of hepatic PBG deaminase
Autosomal dominant pattern
Affected individuals have a 50% reduction in erythrocyte PBG deaminase activity
Latent prior to puberty
Symptoms more common in females than males
Increased urinary ALA & PBG
Clinical Features
Gastrointestinal symptoms - Abdominal pain (most common presenting complaint), nausea/vomiting, constipation, and diarrhea.
Dehydration
Hyponatremia
Cardiovascular symptoms - tachycardia, hypertension, arrhythmias
Neurologic manifestations - motor neuropathy, sensory neuropathy, mental symptoms, seizures.
diagnosis
• PBG, uroprophryin, and 5-ALA
accumulate in the plasma and the urine
Cause diagnosis and treatment
of porphyrias
Porphyrias are metabolic diseases resulting from a partial deficiency of an enzyme in the heme biosynthetic pathway
Cause acute attacks secondary accumulation of heme precursors
Clinical features: abdominal pain, tachycardia, hypertension, hyponatremia, seizures, motor neuropathy etc.
Treat acute attacks with IV hemin
Prevent acute attacks with smoking cessation, avoidance of inciting agents
DIAGNOSIS
1. Erythrocyte fluorescence:Positive test suggests erythropoietic protoporphyria or congenital erythropoietic porphyria.
1. Plasma scan:highly specific for variegate porphyria.
1. Urine porphyrin and precursor analysis:may confirm a diagnosis of acute intermittent porphyria or porphyria cutanea tarda, and is the most appropriate way to assess the biochemical activity of variegate porphyria
1. DNA analysis:
1. Stool porphyrin analysis:usually for diagnosis of hereditary coproporphyria.
TREATMENT
Remove precipitating factors
Treat the pain
Expect and treat the complications
Specific therapy with hemin (haem arginate)
Prevent acute attacks with smoking cessation, avoidance of inciting agents
Presented By:
• Bivek Singh
• KISTMC
• Second year student
• Department of biochemistry
Describe Iron deficiency anemia
Describe the diagnostic test for iron
deficiency states.
Cause ,Diagnosis and Management of
Porphyria
Acute intermittent porphyria
Iron deficiency anemia
Commonest cause of anaemia worldwide
Cause of chronic ill health
CAUSE :-
• Increased physiologic demand eg. pregnancy, lactation, rapid growth
• Blood loss from GI tract, uterus, haemoglobinuria
• Malabsorption
• Diet
CLINICAL FEATURES :
IRON DEFICIENCY
Symptoms eg. fatigue, dizziness, headache
Signs
eg. pallor,
glossitis,
angular cheilosis,
koilonychia,
Plummer Vinson syndrome
LABORATORY DIAGNOSIS: IRON DEFICIENCY
• Microcytic hypochromic anaemia
• Often pencil cells and target cells on blood film
• Decreased serum ferritin
• Decreased serum iron, increased TIBC, decreased % transferrin saturation
• Absent bone marrow haemosiderin : (rarely required for diagnosis )
Things you need to know about Laboratory Testing for Iron Status
1. Serum ferritin most useful test
2. Low serum ferritin certain proof patient iron deficient
3. Normal serum ferritin does not always rule out iron deficiency
4. Certain conditions raise ferritin for reasons unrelated to iron status
Porphyria:
Heme is part of hemoglobin, myoglobin, catalases, peroxidases, and cytochromes
Heme is made in every human cell (85% in erythroid cells & much of the rest in the liver)
Classification of porphyrias
Porphyria is a disruption in the heme pathway
• Group of metabolic diseases resulting from a partial deficiency of an enzyme in the heme biosynthetic pathway
• Seven enzymes in the pathway
• Four of the porphyrias cause acute attacks
• Increased demand for heme can precipitate attacks secondary to overproduction of toxic heme precursors (porphyrins, ALA)
• The porphyrins have no useful function and act as highly reactive oxidants damaging tissues
Not a ‘vampire’s’ disease
Some symptoms of porphyrias have lead people to believe that these diseases
provide some basis for vampire legends:
• Extreme sensitivity to sunlight
• Anemia
This idea has been discarded both for scientific reasons:
• Porphyrias do not cause a craving for blood.
• Drinking blood would not help a victim of porphyria.
Acute Intermittent Porphyria
Most common porphyria
Deficiency of hepatic PBG deaminase
Autosomal dominant pattern
Affected individuals have a 50% reduction in erythrocyte PBG deaminase activity
Latent prior to puberty
Symptoms more common in females than males
Increased urinary ALA & PBG
Clinical Features
Gastrointestinal symptoms - Abdominal pain (most common presenting complaint), nausea/vomiting, constipation, and diarrhea.
Dehydration
Hyponatremia
Cardiovascular symptoms - tachycardia, hypertension, arrhythmias
Neurologic manifestations - motor neuropathy, sensory neuropathy, mental symptoms, seizures.
diagnosis
• PBG, uroprophryin, and 5-ALA
accumulate in the plasma and the urine
Cause diagnosis and treatment
of porphyrias
Porphyrias are metabolic diseases resulting from a partial deficiency of an enzyme in the heme biosynthetic pathway
Cause acute attacks secondary accumulation of heme precursors
Clinical features: abdominal pain, tachycardia, hypertension, hyponatremia, seizures, motor neuropathy etc.
Treat acute attacks with IV hemin
Prevent acute attacks with smoking cessation, avoidance of inciting agents
DIAGNOSIS
1. Erythrocyte fluorescence:Positive test suggests erythropoietic protoporphyria or congenital erythropoietic porphyria.
1. Plasma scan:highly specific for variegate porphyria.
1. Urine porphyrin and precursor analysis:may confirm a diagnosis of acute intermittent porphyria or porphyria cutanea tarda, and is the most appropriate way to assess the biochemical activity of variegate porphyria
1. DNA analysis:
1. Stool porphyrin analysis:usually for diagnosis of hereditary coproporphyria.
TREATMENT
Remove precipitating factors
Treat the pain
Expect and treat the complications
Specific therapy with hemin (haem arginate)
Prevent acute attacks with smoking cessation, avoidance of inciting agents
Friday, February 26, 2010
ANATOMY & PHYSIOLOGY
Skeletal System
I. Introduction
The skeletal system includes connective tissues such as bone, cartilage, tendons, and ligaments. These tissues are combined with the various types of muscle tissue to form the Musculo-Skeletal System.
1) Bone itself has five functions, including:
Movement
Support
Calcium Storage
Production of Red Blood Cells
Protection
2) Cartilage serves as the fetal template for bone formation, and covers the ends of bone, most especially at the joints, or points of articulation.
3) Tendons connect muscles to bone
4) Ligaments connect bone to bone
II. Bone Biology
1) Bone is composed of organic material (mostly collagen, a spongy protein), within an inorganic matrix called hydroxyapatite (mostly calcium and potassium).
2) Bone tissue consists of three specialized cell types, osteoblasts, osteocytes, and osteoclasts
a. Osteoblasts are bone-forming cells, which line the surface of a bone’s structure.
b. Osteocytes are bone cells and are found within the bone’s structure.
c. Osteoclasts are cells that resorb bone trough a degradation process.
3) Process of Bone Formation
At birth, most of the skeletal system is composed of cartilage, which over time is replaced by bone. By the early twenties, most bone growth is complete, although bone is remodeled throughout life.
Through the process of remodeling, osteoclasts circulate throughout the bone and look for old or damaged osteocytes to break down, which are then replaced by osteoblasts which lay down new bone tissue.
This breakdown and buildup occurs throughout the bone, but is most visible at the growth plates of the bone which form at the junction of the epiphysis (bone ends), and the diaphysis (bone shaft). This junction is called the epiphyseal plate, located towards the end of the bone shaft.
Finally, some growth occurs in the periosteum, which is a thin sheaf of tissue that covers the outside of the bone surface. The periosteum also serves as an intake of nutrition and gasses.
III. Bone Anatomy
1) There are approximately 206 bones in the human body
2) They can be classified into four main classes
a. Long bones: main components of limbs, include the femur, humerus, radius and ulna, tibia and fibula.
b. Short Bones: include metacarpals of hands and metatarsals of feet
c. Flat Bones: includes cranial bones, innominates and scapula, offer protection and large muscle attachments
d. Irregular Bones: includes vertebra, carpals (hand) and tarsals (feet), many of the cranial bones. These bones are generally complex in design and serve specialized
purposes
3) The skeleton can also be divided into two parts, the axial skeleton, and the appendicular skeleton.
a. The axial skeleton includes the skull or cranium, the vertebral column, and the ribs.
b. The appendicular skeleton includes the pelvic and pectoral girdles, as well as the upper and lower limb bones.
i. The pectoral girdle includes the scapula and clavicle, and forms the shoulder
ii. The pelvic girdle includes innominate or hip bones.
iii. The upper limbs include the humerus, radius, ulna, carpals, metacarpals, and hand phalanges.
iv. The lower limbs include the femur, tibia, fibula, patella, tarsals, metatarsals, and foot phalanges.