Pass MRCPUK

Obesity and Cardiovascular disease and Its management

2011-02-09T20:33:00.000-08:00

Obesity and Heart disease
Introduction:
Obesity is major public health problem in the united states. In the National Health and Nutritional Examination Survey(NHANES III) form 1988 to !991 it was 36% of the total population which was 25% in NHANES II from 1976 to 1980. The prevalence of obesity has continued to rise. Compared to NHANES data from 1988 to 1994, data from NHANES 1999 to 2000 demonstrates an increase in the prevalence of overweight and obese adults from 55.9 to 64.5 percent for overweight and from 22.9 to 30.5 percent for obese adults .
Similar results have been noted in the United Kingdom. The percentage of the population with a body mass index (BMI) above 30 kg/m2 increased between 1986 and 1993 from 6 to 13 percent in men and from 8 to 16 percent in women . These data and those from other countries are indicative of a major international epidemic .
There is a relationship between obesity and age. Approximately 20 percent of Americans between the age of 25 and 34 are obese; another 10 percent of the population becomes obese with each succeeding decade up to the age of 55
Obesity has long been associated with an increased risk for coronary heart disease (CHD). A recent meta-analysis observed a 29 percent increase in CHD for each five-unit increase in BMI . This association was slightly attenuated after adjustment for blood pressure and cholesterol level. The risk is compounded by the common coexistence of other risk factors associated with obesity such as hypertension, dyslipidemia, and abnormal glucose metabolism. How much of the risk is due to obesity alone has been uncertain. Furthermore, the mechanisms by which obesity, particularly abdominal obesity, cause or accelerate coronary atherogenesis are also uncertain.
Evidence does exist to suggest that obesity, particularly visceral adipose, among adolescents is associated with acceleration of atherosclerosis . More recently, long-term follow-up from Denmark demonstrated BMI during childhood was positively associated with increased risk of CHD during adulthood

DEFINITION OF OBESITY

The body mass index (BMI) is the most practical way to evaluate the degree of obesity. It is calculated from the height and weight as follows:
BMI = body weight (in kg) ÷ square of stature (height, in meters)
The BMI can be obtained from a nomogram or a table. BMI is correlated with body fat and is relatively unaffected by height.
Overweight is defined as a BMI between 25 and 30 kg/m2 and obesity as a BMI greater than 30 kg/m2. However, when estimating cardiovascular and other risks associated with obesity, both regional fat distribution and comorbid conditions must also be taken into account.
A BMI of 20 to 25 kg/m2 is associated with little or no increased risk unless visceral fat is high, or the subject has gained more than 10 kg since age 18.
• Subjects with a BMI of 25 to 30 kg/m2 may be described as having low risk, while those with a BMI of 30 to 35 kg/m2 are at moderate risk.
• Subjects with a BMI of 35 to 40 kg/m2 are at high risk, and those with a BMI above 40 kg/m2 are at very high risk from their obesity.

OBESITY AND CARDIOVASCULAR DISEASE

Despite uncertainties about the relationship between obesity and CHD, the American Heart Association has identified obesity as an independent risk factor. This action should heighten physician awareness about the importance of obesity and stimulate a more vigorous approach to prevention and treatment.

Coronary disease — The 27th Bethesda Conference classified obesity as a category II risk factor, that is, a risk factor for which intervention was likely to lower the incidence of CHD events, based upon the current pathophysiologic understanding and epidemiologic and clinical trial evidence . There is strong, consistent epidemiologic evidence for an association between obesity and CHD, but supporting data from clinical trials are lacking.

Many studies have demonstrated a linear, longitudinal relationship between obesity and CHD incidence in univariate analyses, but the relationship has been less certain in multivariate analyses that included serum lipids, diabetes, and hypertension. As an example, the Munster Heart Study (PROCAM) followed 16,288 men and 7325 women for up to seven years [17]. There was a graded positive relationship between BMI and other CHD risk factors including age, total serum cholesterol, low density lipoprotein (LDL) cholesterol, and systolic and diastolic blood pressure in addition to markers of inflammation and thrombosis. The increase of CHD death associated with BMI was completely accounted for and mediated by these risk factors.

In contrast, other studies have found that obesity is an independent cardiovascular risk factor .
• The Nurses' Health Study evaluated the relationship between BMI and total and cause specific mortality in 115,195 United States women [18]. In multivariate analyses of women who had never smoked, there was a significant trend for increasing risk of death with increasing BMI; compared to women with a BMI <19 kg/m2, the relative risk of death was: 1.2 for a BMI 19 to 24.9 kg/m2; 1.3 for a BMI 25 to 26.9 kg/m2; 1.6 for a BMI 27 to 28.9 kg/m2; 2.1 to 2.2 for a BMI >29 kg/m2. The risk of death was increased at BMI levels well below those considered to indicate obesity, with a striking increase in risk for truly obese women. Weight gain of 10 kg or more after the age of 18 was associated with increased mortality in middle adulthood.
There was also an association between BMI and cardiovascular mortality. Among women with a BMI of 32 or higher who had never smoked, the relative risk of death from cardiovascular disease was 4.1 compared with women who had a BMI below 19.0.
• Obesity was also found to be an independent risk factor for all-cause mortality in the Framingham Heart Study, which analyzed 30 year follow-up data on male participants . Using Metropolitan Relative Weight criteria, the minimum mortality was seen in the group of men with desirable weight (100 to 109 percent "normal"). Multivariate analyses showed a strong positive relationship between baseline weight and death occurring at any interval; the 30 year mortality rate for nonsmoking men who were overweight (weight more than 110 percent desirable weight) was up to 3.9 times higher than men of desirable weight.
• Another prospective study of over one million adults followed for 14 years found that obesity was strongly associated with an increased risk of all-cause mortality and cardiovascular death among nonsmokers and those without a history of CHD . All-cause mortality was lowest in adults with a BMI between 23.5 and 24.9 kg/m2 in men and 22 and 23.4 kg/m2 in women; mortality rates progressively increased at higher indices and were highest in the heaviest men and women who had a BMI ≥40 kg/m2 (relative risk 2.7 and 1.9, respectively). A high BMI was most predictive of death from cardiovascular disease, especially in men (relative risk 2.9); significantly increased risks of death from cardiovascular disease were found at all indices greater than 26.5 kg/m2 in men and 25 kg/m2 in women. The risk associated with BMI was greater for whites than blacks.
Thus, in several large, prospective, long-term studies using multivariate analyses, obesity was an independent risk factor for all-cause mortality and death from CHD in both women and men. However, other studies have observed reduced mortality risk with increasing BMI among patients with a prior history of heart disease . Data from over 9000 patients undergoing cardiac catheterization suggest obese patients tend to be younger, and more likely to have single-vessel disease. At one year, patients with normal BMI had higher rates of mortality compared to overweight and obese patients

Obesity and Other Complications:

There are a number of physiological and metabolic changes associated with obesity that may contribute to an increased risk of cardiovascular disease .
• Insulin resistance and hyperinsulinemia .
• Type 2 diabetes mellitus .
• Lipid abnormalities, including low HDL level, high triglyceride level, increased apolipoprotein B level .
• Systolic and diastolic hypertension .
• Left ventricular hypertrophy .
• Sympathetic nervous system dysfunction
• Endothelial dysfunction .
• Obstructive sleep apnea .

Metabolic syndrome — Visceral or abdominal obesity is associated with insulin resistance and an array of metabolic and hemodynamic disorders, including hyperinsulinemia, atherogenic blood lipid changes, hypertension, and type 2 diabetes. This constellation of findings has been called the metabolic syndrome (or insulin resistance syndrome or syndrome X). The prevalence of the metabolic syndrome is significantly higher in patients with than without a history of cardiovascular disease. In addition, the metabolic syndrome is associated with a significant increase in the subsequent risk of cardiovascular events.
Type 2 diabetes mellitus — Type 2 diabetes mellitus is strongly associated with obesity in all ethnic groups. More than 80 percent of cases of type 2 diabetes can be attributed to obesity, which may also account for many diabetes-related deaths. CHD is more common in diabetics than in the general population, affecting as many as 55 percent of patients.

Hyperlipidemia — Obesity is associated with several deleterious changes in lipid metabolism, including high serum concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL)-cholesterol, and triglycerides, and a reduction in serum HDL cholesterol of about 5 percent . The last effect may be most important since a low serum HDL cholesterol concentration carries a greater relative risk of CHD than hypertriglyceridemia.
Central fat distribution also plays an important role in the serum lipid abnormalities. Waist circumference alone accounts for as much or more of the variance in serum triglyceride and HDL cholesterol concentrations as either the WHR .

Hypertension — Blood pressure is often increased in obese subjects . In the Swedish Obesity Study, for example, hypertension was present at baseline in approximately one-half of subjects. In a report from the Nurses' Health Study, the BMI at age 18 years and at midlife was positively associated with the occurrence of hypertension . Weight gain was also associated with an increased risk; the relative risk of hypertension in those women who gained 5.0 to 9.9 kg and ≥25.0 kg was 1.7 and 5.2, respectively .

Left ventricular hypertrophy — Obesity is associated with volume overload resulting in a high end-diastolic volume and increased filling pressure. This, coupled with hypertension, can lead to left ventricular hypertrophy (LVH) . LVH is important clinically because it is associated with an enhanced incidence of heart failure, ventricular arrhythmias, death following MI, and sudden cardiac death .

Sympathetic nervous system — Obesity may be associated with abnormalities in sympathetic nervous system control. This can predispose obese individuals to prolonged QT intervals and arrhythmia .

Sleep apnea — Sleep apnea is associated with obesity.The syndrome is related to excess mortality, hypertension, left and right ventricular dysfunction, and arrhythmias.

Heart failure — There is an important association between obesity and heart failure. In an analysis from the Framingham Heart Study in which almost 6000 individuals without a history of heart failure (mean age 55 years) were followed for a mean of 14 years . heart failure developed in 496 (8.4 percent). The risk of heart failure was increased approximately two-fold in obese (body mass index [BMI] ≥30 kg/m2) compared with nonobese subjects. After adjusting for established risk factors (eg, hypertension, coronary disease, diabetes, left ventricular hypertrophy), the risk of heart failure increased 5 percent in men and 7 percent in women for each increment of 1 kg/m2 in BMI. Approximately 11 percent of cases of heart failure in men and 14 percent in women could be attributed to obesity alone. The risk was also increased in overweight (BMI 25 to 29.9 kg/m2) women but not men. However, among patients with a history of heart failure, increasing BMI appears protective. Several studies have observed lower rates of rehospitalization and death among heart failure overweight and obese heart failure patients .

ECG in morbid obesity — Morbid obesity can produce changes in cardiac morphology that can alter the surface ECG. This was revealed in a study that compared the ECG of 100 obese subjects and 100 controls; none of the subjects had clinical, ECG, radiographic, or echocardiographic evidence of coronary heart disease, systemic hypertension, valvular heart disease, heart failure, cardiomyopathy, or pericardial disease .Compared to controls, obese patients had the following alterations on the ECG:
• P, QRS, and T wave axes were more leftward
• Low QRS voltage, multiple ECG criteria for left ventricular hypertrophy and left atrial abnormality, and T wave flattening in the inferior and lateral leads were more common
•
Abdominal obesity — At any given level of BMI, the risk of the development of cardiovascular disease in both men and women is increased by more abdominal fat (increased waist to hip ratio, WHR) .
The relationship between abdominal obesity and cardiovascular mortality was evaluated in a cohort of 44,636 women in the Nurses' Health Study . The relative risk increased significantly from the lowest to the highest waist circumference quintiles (1.00, 1.04, 1.04, 1.28 and 1.99 respectively) after adjustment for body mass index and other confounders during 16 years of follow-up. This relationship persisted even among normal weight women (body mass index 18.5 to <25kg/m2).

BENEFITS OF WEIGHT LOSS — Weight loss can improve or prevent many of the obesity-related risk factors for cardiovascular disease . Benefits include:
• Decreased blood pressure in hypertensive patients .
• Decreased incidence of diabetes mellitus .
• Improved lipid profile
• Decreased insulin resistance.
• Reduced C-reactive protein concentration .
• Improved endothelial function .
Management of obesity:
Obesity can be managed by medical and surgical treatment. Medical treatment have some limitations and not applicable for those BMI is more than 40 and also those have visceral deposition of fat. At that case surgical procedure give good and excellent result
No randomized controlled clinical trial has demonstrated that voluntary weight loss alone has any effect upon long-term outcomes such as total mortality or cardiovascular disease . However, one prospective study of 28,388 overweight women ages 40 to 64 who had no preexisting illness found that intentional weight loss of more than 20 lb (9.1 kg) was associated with a 25 percent decrease in all-cause, cardiovascular, and cancer mortality . Among 15,069 women with comorbid conditions such as heart disease or diabetes mellitus, any amount of intentional weight loss was associated with a 10 percent reduction in cardiovascular disease and a 20 percent reduction in all-cause mortality, primarily due to a reduction in mortality from obesity-related malignancy.
Achieving and maintaining weight loss is made difficult by the reduction in energy expenditure that is induced by weight loss. In addition, recidivism (regaining of lost weight) is a common problem; of those subjects who lose weight during any treatment program, most do not maintain the weight loss.
Despite the limited data regarding the long-term benefits of weight loss and the difficulties with achieving and maintaining weight loss, physicians should urge patients with known cardiovascular disease or cardiovascular risk factors (eg, hypertension, dyslipidemia, type 2 diabetes mellitus) to lose weight. For persons free of disease, prevention of obesity beginning in early life is a sound recommendation. For individuals older than 75, excess body weight does not appear to be an important risk factor.
Drug therapy may be a helpful component of treatment for overweight subjects. However, among patients with CVD, certain drugs (such as sibutramine) may be contraindicated. Anti-obesity drugs have been used as an adjunct to diet and exercise for obese subjects with a BMI greater than 30 kg/m2. The role of drug therapy has been questioned, however, because of concerns about efficacy, the potential for abuse, and side effects. .
Surgery (gastric bypass or banding) is another option for patients at high risk of complications from obesity.
Like dietary weight loss, gastrointestinal obesity surgery can reduce cardiovascular risk factors, including blood pressure, diabetes incidence, and lipid profile . However, this does not appear to occur with liposuction suggesting that the negative energy balance associated with decreased nutritional intake may be necessary for achieving the metabolic benefits of weight loss.
PREOPERATIVE CONSIDERATIONS — As discussed above, the prevalence of coronary heart disease (CHD) or its risk factors is increased in obese patients.
Patients with established CHD are at increased risk for cardiovascular events at the time of non-cardiac surgery. The preoperative approach to obese patients scheduled to undergo non-cardiac surgery is discussed elsewhere.

RECOMMENDATIONS — The 2007 ACC/AHA focused update of the 2002 guidelines for the management of patients with chronic stable angina made the following recommendations for weight management :
• Regular assessment of BMI and waist circumference.
• Counseling on weight management at each patient visit, with a goal of a BMI between 18.5 and 24.9 kg/m2.
• The initial goal of weight loss should be approximately 10 percent from baseline.
• Recommend lifestyle changes and consider treatment strategies for metabolic syndrome in women if the waist circumference is ≥35 inches (89 cm) or ≥40 inches (102 cm) in men.

amazan

2010-12-30T07:27:00.001-08:00

Urinary Bladder

2010-11-10T07:07:00.000-08:00

large muscular bag, reservior of urine lies ant part of pelvic cavity.

Size shape and position:
varies in size , shape and position according to amount of urine contains
when empty lies in pelvis, reaches abdomen when filled with urine.

External features:
when empty:
tetra hedral. has apex, base, three surface, four boarder and one neck.

Ligaments of the bladder:

a. true ligaments:
lateral true ligaments of bladder.
lateral puboprostatic ligament
Medial puboprostatic ligament
median umblical ligaments

b.false ligaments
The median umblical fold
medial umblical fold
lateral false ligaments
Posteriaor false ligaments

Arterial supply:
Superior and inferior vesicular artery
additional supply from obturator and inferior gluteal artery.
acne treatments
Nerve supply:
parasympathetic s234
sympathetic T11-L2
Pudendal nerve s234

The urinary bladder

2010-11-04T08:42:00.000-07:00

Urinary Bladder:

Muscular reservior of urine which lies ant to

Ureters

2010-11-04T08:22:00.000-07:00

Thick wall muscular tube which convey urine to Urinary bladder from Kidneys.

Lies in posterior abdominal wall.
Measures about 25 cm, 12.5 cm lies in Abdomen and 12.5 cm lies in pelvis.

It has three constrictions.

Course:
Starts from renal pelvis , gradually narrows and lower end of kidneys it become
ureter proper. It runs downwards and slightly medially over psoas major muscle
enters pelvis infront of termination of common internal iliac artery.

In lesser pelvis it runs bownwards and slightly backwards and laterally following
ant margin of greater sciatic notch. Opposite the ischial spine it runs forward
meidally towards urinary bladder.

Normal constriction:
1. At pelvic ureteric junction
2.at the brim of lesser pelvis
3.At its passage through its bladder wall.

Relations:

Blood supply:
It is supplied by three set of arteries:
1.Upper part receives branches from renal artery
2.Middle part receives branchs from the abdominal aorta
3.The pelvic part receives branches from vesical, middle rectal or uterine arteries.

Nerve supply:
Sympathetic N T10-L1
ParaSYMPATHETIC S2-4

Anatomy(Kidneys and Ureters)

2010-11-02T09:42:00.000-07:00

KIDNEYS:

Pairs of Excretory organs situated on Both side of vertebral column
on the posterior abdominal wall, behind the peritonium.

Retroperitonial organs:
Kidneys
Supra renal glands
Inferior vena cava
Abdominal aorta
Pancreas
Sympathetic trunk
Ovarian or testicular veins

Main organ of excretion , remove metabolic waste products maintains
water and electrolyte balance.

Each kidney is bean shaped.
It has two pole upper and lower, two border medical and lateral and
two surface anterior and posterior.

Upper pole is broad and lies close contact with supra renal glands. Lower
pole is pointed.

The anterior surface is rough and posterior surface is smooth.

lateral border is convex and medial border is concave and shows depression
in the middle is called hilum. The following structure is seen from ant to post
Renal vein, Renal artery, renal pelvis (VAP)

Expanded upper pole of ureter is called renal pelvis.

Kidneys occupy epigasrium, hypochondrium,lumber,umblical

vertically extends from T12 (upper border) to L3(Middle of the body).
Right kidney is slightly lower than the left.Left kidney is little nearer to
median plane than the right.

Transpyloric plane pass through upper border of rt kidney and lower
border of left kidney.

Each kidneys is about 11,6,3 cm
Measuring about 150 gms in male and 135 gms in female.

long axis is directed downwards and laterally, transverse axis is directed
backwards and laterally.

Relation of Kidneys:

Capsules of Kidneys:

Fibrous capsules
Perirenal Fat
Renal Fasciae
Para renal Fat

Structure of Kidneys.
Outer Cortex. Cortex is further divided into a. cortical lobules or cortical arches
which overlays the base of pyramid and b. Renal columns which dips into between
two cortical lobules.

Inner Medulla. Renal medulla is consist of 9 conical mass of renal pyramids. Their apices
form the renal papillae which indents the renal calices.

Major calices: 2/3 in number
Minor calices: 7/13 in Number

Renal sinus: Space extends from kidneys to renal hilus.

Histologically kidneys consist of 1-3 milions of uriniferous tubules

Each tubules develops from two part 1. Secretory portion from Mesonephric blastoma from mesoderm and 2. Collecting part from ureteric bud.

Arterial supply:

Usually there is one renal artey on each side arising from abdominal aorta.
Acessory renal artey present in 30% case, usually arise from abdomianl aorta

Nerve supply:

sympathetic nerve T10-L1
No Parasympathetic supply

anomalies of Kidneys:

Congenital polycystic kidneys
Horse shoe shape kidneys
Pelvic kidneys
Aplasis/hypoplasia.

Bacterial Cell wall

2010-10-30T10:47:00.002-07:00

Composition:

1.Peptidoglycan(Provides tensile strengeth)
90% in gm(+) and 5-20% in gm(-)
2.Special Component
Gm(+).........Techeic acid,Polysaccharide
Gm(-)...........lipoprotein,Outer membrabne/lipopolysaccharide

Function:
1.Maintain Bacterial Shape
2.Protect internal envirnment
3. Helps in cell division

Peptidoglycan:
Composed of Glycan(sugar) and side chain peptide. Which are linked by
transpeptidase.

some extra matter:

Bacteria has three shape
1......................Cocci(sphere)
2.....................Bacilli(Rod)
3....................Spirochetes(spiral)

Cocci arranged in three pattern
1. ................pairs(diplococci)
2.................Chain(Streptococcus)
3.................Cluster(Staphylococcus)

Size of bacteria ranges from 1-----4 micrometer
Mycoplasma the smallest bacteria sizes .2micrometer.

All bacteria have cell wall of peptidoglycan except mycoplasma
which is surronding by membrabne.

Gm(-) bacteria has thin outer membrane where as gm(+)
do not have.

Outer membrane of gm(-) bacteria contains(LPS) the main cause of septic shock.

Endotoxin..composed of

Bacterial Cell wall

2010-10-30T10:47:00.001-07:00

Composition:

1.Peptidoglycan(Provides tensile strengeth)
90% in gm(+) and
2.Special Component

Bacterial Cell wall

2010-10-30T10:47:00.000-07:00

Composition:

1.Peptidoglycan(Provides tensile strengeth)
90% in gm(+)
2.Special Component

Microbiology

2010-10-30T10:38:00.001-07:00

Eukaryotes:

Fungi,protozoa,Algie, Slime mold, Helminths
Cell membrane......
nucleus complete
reprodruction
.........Mitosis
.........meiosis
Organelles are present
............lysosome, ER,Mitochondria
Chromosome
...................Many
ribosome
............80s
DNA
................present
Cell membrane contains
................Sterol

Prokaryotes:
1. Eubacteria(Medically important bacteria)
2. Archaebacteria

MRCP/FCPS/MD UK Coaching

2010-10-26T11:36:00.000-07:00

MRCP UK Coaching:

We do arrange MRCP coaching for MRCPUK part1 In every year. 3 time in a year. We take fees 300 pound for 3 months coaching. with regards. Dr Nizam.
email : nizammozumder@yahoo.com

Besides we do arrange MD/MS,FCPS part1 coaching. twice in a year . It takes 14000 BDT for 5 months coaching. Interested candidates are invited . With regards. Dr Nizam.
email: nizammozumder@yahoo.com or nizammozumder@gmail.com
Mobile: 01937206117

Infectious disease.... Toxoplasmosis

2010-10-26T10:35:00.000-07:00

Definitive Host:........................Cat
(where adult stage exist or sexual stage of protozoa occurs):
usually human is the definitive host most case except malarial parasite and hydatid tape warm)

Intermediate host: .....................Human,mouse
where asexual or larval stage occurs

routes of transmission:

1.Transplacental
2. Blood transfusion
3.Infected Meat(Bradyzoite)
4.Ocyst

Bradyzoite penetrates ..........>> enterocyte...........>>multiply
Tachyzoite.......>>> infect more enterocyte
(Usually it can not do so due to CMI, In AIDS it can do so)

Brain, retina, Muscle tissue, Liver and other nervous tissue it has special fascination.

Clinical feature:
a. Congenital toxoplasmosis(infant)
b.Acquired toxoplasmosis

a. Congenital toxoplasmosis

Consist of tetrod....RICH
R...........Retinochoroiditis
I............Intracerebral calcification
C............Convulsion
H............Hydrocephalus

Time of transmission
Ist trimester........50% brain
2nd trimester.......40%brain
3rd..........................11%brain

b.Acquired toxoplasmosis

Occurs only in immunosuppressed state(AIDS)
fever with rash with lymphadenopathy

Algorithm of Diagnosis:

IgG +ve /-ve

If igG negative no infection seen.

If IgG positive(Inf may be within 2/6 months) then go for IgM.

If IgM positive then

aplastic anaemia

2010-10-25T10:34:00.000-07:00

Aplastic anaemia

Anaemia due to bone marrow aplasia. Here all hematological cells are decreased. So pancytopenia occurs. you can know details in this link www.aplasticanaemia.co.uk

Type of apastic anaemia.

1.Primary Idiopathic Acquired aplastic anaemia
Most common in China. In Uk 3/6 case per mil.pancytopenia due to Bone marrow failure.
Cause: Mostly due to autoimmune disease, Viral infection, others; drugs.

a.Drugs: cytotoxic ,Idiosyncratic,Antibiotics:Chlorampenicol,Sulphonamide
penicillin, Gold,Indomethacin
Antithyroid
Anticonvulsant
b.Chemicals
DDT
OPC
benzene,toluine
c.Radiation
d.Viral hepatitis
e.Pregnancy
f.PNH

Investigation:
Bone Marrow: hypoplastic ,pancytopenia, Leucopenia, Normocytic normochromic anaemia

Management:

If pt before 20yrs. treat with allogenic bone marrow transplantation.if donor available.
If old age treat with antithymocyte globulin and cyclosporin, androgen.

Prognosis:
prognosis is poor 50% dies within 12 months.
Survival is better in ABMT.

2. Secondary aplasia.

Myelodysplastic syndrome

2010-10-25T10:28:00.000-07:00

Myelodysplastic syndrome

The word dysplasia is premalignant condition. Any dysplasia is premalignant.It is premalignant so malignancy of myeloid origin may occur. That is it may turn into leukaemia whether acute or chronic.

Here bone marrow dysplasia occur so cytopenia occurs. So we can call MDS as a group of disorder where .

the word.

Myelo means Blood cells.

Dysplasia means abnormal growth.

Here below the classification of MDS:

French American British (FAB) Classification System
Even though the newer WHO system updated the FAB system, the FAB system is still used by some doctors today.

The FAB system is based on four main factors:

* The percentage of blast cells in the bone marrow
* The percentage of peripheral blood blasts
* The percentage of red blood cell precursors with abnormal iron deposits called ring sideroblasts
* The percentage of monocytes in the blood

The FAB system divides MDS into 5 subtypes. These subtypes include:

1. Refractory anemia, also called RA
2. Refractory anemia with ring sideroblasts, also called RARS
3. Refractory anemia with excess blasts, also called RAEB
4. Refractory anemia with excess blasts in transition, also called RAEB-t
5. Chronic Myelomonocytic Leukemia, or CMML

Diagnosis:
BME: cytopenia with dysplastic feature.Hypercelluler marrow.
Blast cell must not more than 30 %. defect in chromosom 5/7

Management:
Treatment is unsatisfactory. Blood transfusion with antibiotics.
Agressive antileukaemic therapy is not effective.
Retenoic acid is not fulfilling the promise.
Low dose cytosin arabinose has little effect
ABMT has 30% success .

International Prognostic Scoring System (IPSS)
The IPSS gives each patient a score to help their doctor understand how quickly their MDS is progressing and what is likely to happen to their disease over time. The score is based on several factors that are linked to MDS. They are:

Percentage of blasts in the bone marrow
Changes in cell chromosomes, also called cytogenetics
Low blood cell counts or cytopenias

Each factor gets a score. Together, the scores tell which risk groups you fall into.

Your IPSS score helps your doctor to answer the following questions:

How severe is your case of MDS?
How likely is your case to become acute myeloid leukemia or AML if treated only with supportive care?
How long are you likely to live if you are treated only with supportive care?

Factor
Value
IPSS Score

Blasts in bone marrow

less than 5%
5% to 10%
11% - 20%
21% - 30%
0
0.5
1.5
2.0

Cell DNA changes (cytogenics)

Good
Intermediate
Poor
0
0.5
2.0

Low blood counts or cytopenias
0 or 1 cytopenia
2 or 3 cytopenias
0
0.5

Using the IPSS, a patient is given a score between 0 and 3.0. A patient can be put into one of four risk groups, two lower-risk and two higher-risk. Scores of less than 1.5 are considered lower-risk.

This score tells you what risk group you fall into. For example:

If your IPSS score is 0, you are in the low-risk group
If your IPSS score is 0.5 to 1, you are in the intermediate-1 risk group
If your IPSS score is 1.5 to 2, you are in the intermediate-2 risk group

If your IPSS score is more than 2.0, you are in the high-risk group

Learn about Treatments for MDS.

__________________________

Order an AA&MDSIF information packet containing detailed information about MDS and its treatment.

For more in-depth information on MDS and its treatment you can also visit our Online Learning Center and view webcasts by some of the leading medical experts on MDS.

Prognosis:

Lipoprotein

2010-10-25T10:26:00.001-07:00

Lipoprotein
VLDL:

Synthesized inLiver.
Mostly composed of TG.

Lipid 90-93%

Function:
Transport TG from liver to peripheral tissue.

Metabolism :
Extrahepatic tissue by lipoprotein lipase

Metabolic end product:
FFA
Glycerol
IDL/VLDL remnent

Fate:
Taken by liver
converted to LDL

LDL:

Composed of 79% lipid
Protein 21%

Contains cholesterol and cholesterol ester.

Derived from VLDL in the plasma

Chief pathogenic factor for atherosclerosis.

Functions:
Provides cholesterol to peripheral tissues.

Metabolism:
30% extrahepatic tissue
70% inside liver.

HDL:

Lipid 33%
Protein 67%

Synthesized inside the liver.

Function:
Transport Cholesterol from peripheral tissue to liver.

Usually biconcave shape. When it picks up cholesterol it become round.

Transfer cholesterol to VLDL,LDL in exchange of TAG/TG
carry CE(ester) to liver
Remove free cholesterol from extrahepatic tissue by LCAT(lecithin cholesterol actyl transferase)
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Lipoprotein
Protein part of lipoprotein is called apo protein.

Types of lipoprotein:
1. Chylomicron
2.VLDL(very low density lipoprotein)
3.LDL
4.HDL

Here one should be noted density will decrease if lipid amount increase.
So in VLDL, lipid is much more than in HDL

another matter;
Increase protein causes the increase elecrophoric mobility.

Basics of apoprotein:
maintenance the shape of liupoprotein.
B100. the apoprotein which synthesize by B gene 100%
B48... B gene synthesize 48% of the protein.

metabolism of Lipoprotein:

Chylomicron:
Site of synthesis: Small intestine.
Size 100 nano m
Low density
combines with C1,11,111 E in circulation.

lipid 98-99%
Protein 1%

Functions:
Transport dietary TG,Cholesterol,Cholesterol Ester from instestine to peripheral
tissue.

Metabolism:
Extrahepatic tissue by lipoprotein lipase.

Metabolic end product:
FFA
Glycerol
Chylomicron remnant(Removed by liver )
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Metabolism of TG/Triacyl glycerol
TG is consit of three molecule of fatty acid esterified into glycerol.

Storage:

Main storage: Adipose cell. Most of TG deposite as droplet.
Other store: Liver and muscle cell, Store small amount of TG.

Fate of TG:

1. Fate of Adipose tissue TG:
Store in cytosol as depot fat.
Ready to mobilize when body require fuel.
2. Liver: TG is packed with cholesterol, Cholesterol ester
Phospholopid ,protein forms various lipoprotein.

Biosynthesis:
Site : liver and adipose tissue.

Source : FFA.(free fatty acid)

Lipolysis of TG:

hydrolysis of TG is called lipolysis.

Enzyme required:
Lipase.
a. In adipose tissue: Hormone sensitive lipase.
b. In vessles. Lipoprotein lipase(chylomicron, VLDL)

hormone sensitive lipase
TG......................................................>>>DAG(diacylglycerol)+FFA

DAG....................................................>>>MAG+FFA

MAG..................................................>>>Glycerol+FFA

So the products of lipolysis are:
a. FFA
b.Glycerol

Fate of Glycerol:
a.In adipose tisssue..Can not utilize glycerol as there is no enzyme to metabolise
So glycerol is the excellent index of glycolysis in adipose tissue.
b.In liver. glycerol is converted to glycerol phosphate by glycerol kinase.
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Absorption of lipid
Primary product of lipid degradation are:
a. FFA
b.2-monoglycerol
c.Cholesterol.

Absorption:

Site of absorption:
Brush border of intestinal mucosal cell.

process of absorption:

Short and Medium chain fatty acid absorbs into directly into portal vein
Long chain fatty acid and 2-monoglycerol absorbs by brush border forming micelle.
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Tuesday, May 25, 2010Composition of Dietary lipid
TG
Sterol(Cholesterol)
Sterol Ester
Phospholipid

Fat.... Are all triester of tri hydric alcohol , glycerol and various fatty acid.
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Lipid and Lipid disorder.
Lipid classsification:

1. Simple lipid: (fatty acid with various alcohol)
a. Neutral fat
Fatty acid+Glycerol= TG
b. Wax
Fatty acid + High molecular wt alcohol

2.Compound Lipids:(Fatty acid +alcohol+others)

a. Phospholipids
Fatty acid+Glycerol+Phosphoric acid
b.Glycolipid
Lipid+CHO+Nitrogenous Base
c.Sulpholipid
Lipid+sulphergroup
d.lipoprotein
Lipid+Plasma protein

3. Derived lipid
Saturated and Unsaturated fatty acid
glycerol
sterol
vit A, Vit D

4.Miscelleneous Lipid.
Aliphatic hydrocarbon
carotinoid
Vit e, Vit K

Lipoprotein

2010-10-25T10:26:00.000-07:00

Lipoprotein

2010-10-25T10:20:00.000-07:00

Pancytopenia:

2010-07-31T09:25:00.000-07:00

Pancytopenia:
Aplastic anaemia
Administration of cytotoxic drugs
Radiotherapy
Overwhelming infection
Subleukaemic leukaemia
Bone marrow infiltration
Hyperspleenism
SLE
Megaloblastic anaemia

wbc

2010-07-31T09:21:00.001-07:00

Causes of Leucocytosis:A.Physiological
Erercise
Cold
Pregnancy
Diurnal variation(Slight raise in after noon)

B.Pathological
1. Infection
Bacterial
Viral poliomyelitis
All virus causes lymphopenia
2.Inflammation
RA
Gout
R fever
3.Malignancy
HD
CML
4.Haemorrhage
5.Tissue necrosis

Leucopenia:Viral: Influenza, Atypical pneumonia
Bacterial: Typhoid, Paratyphoid
Protozoal: malaria, kala zar
Autoimmune: SLE
Drugs:
Chlorampenical
Sulphonamide
Cotrimoxazole
Phenytoin
Maloprim
Chloropromazine
Chloropropamide
Hyperspleenism
Idiopathic
Congenital: Kostmann syndrome

Eosinophilia:1.Helminth
Filarial,Hydatid,Tape worm,Hookworm
2.Allergic
Asthma,Atopic,Eczema,Skin disease
3.Connective tissue
PAN
4.Malignancy
Lymphoma
CML
5.Pulmonary eosinophilia
Tropical> 2000 microfilaria
Loffelers 500-1500/mm
6.Familial
7.Drugs

Lymphocytosis:1.Bacterial: TB,Typhoid,para typh, Whoophing cough,syphilis
2.Viral: Hepatitis,Chicken pox,Measles,Rubella,Infectious mononucleosis
3.Protozoal: malaria ,Ka la zar
4.Malignancy: CLL, NHL
5.Post spleenectomy
6.Thyrotoxicosis

Lymphopenia:Inflammation: CTD
Lymphoma
Renal Failure
Drugs
Steroid
Cytotoxic
Congenital:SCID

Functions:
Basophil:
Secret5es heparin, Bradikinin
Contains dark blue granules
Prevents intravascular clotting
Acts as co factor for lipoprotein lipase , so it plays a rule in fat metabolism

Eosinophils:Phagocytsis Ab-ag complex
Bilobed red orange granules
Inactivation of hgistamine
Release fibrinolysin which dissolve fibrin clot

wbc

2010-07-31T09:21:00.000-07:00

Fe Metabolism:

2010-07-31T09:16:00.000-07:00

Source:Liver , Meat, Cereals
1.5-2.0 mg/day

Absorption: upper intestine(duodenum and jejunum)
Active transport
Ferrous form

Distribution of Iron:TBI; 4-5 gm
Hb 60-70%
Myoglobin 3-5%
Haeme enzyme
Plasma iron 0.1%
Ferritin and Haemosiderin 25%

Blood iron form:Hb
Transferrin

Hb contains 2/3 of total iron
Diet contains 15-20 mg/day
10% absorbs
Anaemic person absorbs 20-30 of dietary iron
An average menstrual loss 30 mg per period

Factors influencing iron absorption:

Factors increased absorption:Ferrous
Haem Iron
Fasting
Increased Acidity
Low iron store
Ascorbic acid
Alcohol
Increased erythropoiesis
Pancreatic secretion stimulate absorption

Factors decrease absorption:Ferric iron
Non haem
Full stomach
Decreased gastric acidity
Iron overload
Phosphate

MRCP part2 revision course

2010-07-21T22:21:00.001-07:00

MRCP (UK) Part II Written Exam Revision Course

The MRCP(UK) examination is crucial to the progress of physicians
through their training. With a pass rate of about 40% at each sitting
of the written papers, the exam is a challenge. With this in mind,
the College wishes to help candidates with their preparation and improve their prospects of passing the exam.

Therefore the Royal College of Physicians have created a revision
course for the part II written exam. Delivered over four or five-days,
the course allows focussed and intensive study. The course is facilitated
by doctors who are respected leaders in their specialties and have extensive experience in preparing candidates for the MRCP(UK).

The course was established in 2003 and feedback from delegates
has always been excellent:
“Excellent revision course – very relevant to forthcoming exam
and pitched at the appropriate level for part II written exam”

“This revision course has been extremely beneficial and has increased
my confidence in sitting the exam – thank you”

“An excellent course. The teaching levels were far superior
to other courses that I have attended”

Key features of the course• Comprehensive coverage of the Part II syllabus
• Course content that is updated to reflect current hot-topics of the exam
• Review of past question topics
• Attention paid to data interpretation, clinical pictures and analyses of functional tests
• Instruction on exam technique
• Course binder containing materials and key notes
• Stimulating learning environment utilising quality audiovisual aids
• Access to clinical revision materials held in the Jerwood Medical Education Resource Centre

Delegates who attend the course will also be given one week of free access to the Medical Masterclass website

Website users can access:
Mock MRCP (UK) exams
Over 2500 self-assessment questions of all types, including Best of five, N from many and picture tests, with detailed comments
The My History feature, which allows users to compare scores against their peers, provides average scores for each paper and every question and also ranks strongest and weakest specialty areas

For more information email the education dept at mrcpcourses@rcplondon.ac.uk
You can also downlaod an application form from: http://www.rcplondon.ac.uk/event/details.aspx?e=1268

MRCP part2 revision course

2010-07-21T22:21:00.000-07:00

tips for MRCP

2010-07-21T22:17:00.000-07:00

welcome fellow mrcp candidates i passed mrcp part one and 2 first time
with good score. and this is my advice to you
1- study from a small book not from big text book and the best
one in my opinion is oxford handbook of clinical medicine
because when i started prepairing for mrcp part one i
studied from different sources including this but when i
finished my exam i was surprised that i found all the answers
for the exam questions from this small book so i concentrated
on studing from this book in my study for part two and i got even higher score.

2- do at least one online mrcp course like onexamination or
pastest course because i found these courses much more valuable
than bof books and usually contains a lot of questions from
previous exams and many of these questions tend to be repeated
on the next exams and actually i personally know other candidates
who only studied online courses and still passed first time.

3 donot be tempted to study from books specially made for mrcp
as i find these books to have a lot of inaccurate information.
4-try to cover all branches and topics evenly in your study.
for example donot study hard in cardiology and leve some other
branch like nephrology not well coverd because in this way you
will miss so many easy questions in nephrology and still will
not get all cardiology questions right.

5- donot overlook small branches like ophthalmology, statistics,
and psychiatry because you will be able to collect a
lot of marks from this branches in only short period period of study.

6- mrcp is not that difficult so donot be put off by doctors who fail many times because these candidates simply donot prepare well for the exam.
study well and you will pass for sure.
thank you.

Haemolytic anaemia

2010-06-29T19:07:00.000-07:00

Classification:
a. Intracorpuscular
1. Hereditary
Hb defect .... thalassaemia, hb pathy
Membrane defect.......H spherocytosis, H elliptocytosis
Ezzyme defect.......... G6pD deficiency, EMP deficiency, Drug induced
2.Acquired
PNH
b.Extra corpuscular
1. Immune
Autoimmune..... warm antibody,cold antibody
Haemolytic disease of Newborn
Incompatible blood transfusion
2.Non Immune
Mechanical haemolytic..... cardiac, Microangiopathic
Drug and chemicals