i feel apple company releasing it's itunes 8.0.2 with out proper testing

i am having apple ipod classic 160GB , i had updated my tunes on 11th of December 2008 with the itunes 8.0.2, which has been released earlier i the month of November, but to my fascination my ipod is recognised neither by the by the itunes nor by the windows. windows beeps(sounds ) that the ipod is plugged in, but is not being shown it i the my computer nor in the itunes.

when i searched the web for remedy, many of the users s having the same problem, till date i have been of opinion that the apple company products shall stand 1st in the quality of the services provided but with the agony i faced for 2 days, now i feel apple company is not an exception to other companies in offering miseries to its customers

ok i feel it is very important of how to solve this
the problem is with itunes 8.o.2 only and not with the earlier one,
and even if u tend to uninstall the apple mobile device driver from add remove programs, then the ipod tends to be recognized by the windows, ( visible in My computer )
but to totally solve the problem, totally uninstall all the apple products, i mean apple itunes, quick time, and the mobile device driver and then install the previous versin 8.0.1
you can find that here

http://appldnld.apple.com.edgesuite.net/content.info.apple.com/iTunes8/061-5555.20081002.5Kij7/iTunes801Setup.exe

this shall solve your problem

Reye syndrome

1. characterized by acute noninflammatory encephalopathy and hepatic failure
2. the etiology of Reye syndrome is unknown , occurs after a viral illness, particularly an upper respiratory tract infection (URTI), influenza, varicella, or gastroenteritis, and it is associated with the use of aspirin during the illness.
3. more than 3-fold increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and/or ammonia levels
4. Inborn errors that may mimic Reye syndrome include fatty-acid oxidation defects, amino and organic acidopathies, urea-cycle defects, and disorders of carbohydrate metabolism
5. Reye syndrome is equally distributed between the sexes.
6. Reye syndrome rarely occurs in newborns or in children older than 18 years
7. Reye syndrome can occur after vaccination with live viral vaccines.
8. Clinical features : pernicious vomiting Lethargy Diarrhea and hyperventilation
9. No specific treatment exists. Continue careful monitoring.

snow : mnemonic

Snow

Southern blot: DNA analysis

Northern blot: RNA

Western blot :protein

Eponyms

Eponym	Explanation	Reference if any
Mollaret's meningits	Lymohocytic meningitis due to HSV	Micro arora, p.no 217
1st day disease	Measles{Rubeola}
2nd day disease	Scarlet fever
3rd	Rubella { german measles
4th	Fliator Dukes disease , variant of scarlet fever
5th	Erythema infectioosum
6th	Exanthema subitum
Cushing reflex	bradycardia, hypertension, and irregular respirations	p.no 2473 harrison 16 th ed
Cushing phenomenon, Cushing effect; Cushing response;	rise in BP when the intracranial pressure acutely increases, usually in excess of 50% of the systolic arterial pressure.

CSF analysis

Constituent	SI Units	Conventional Units
Glucose	2.22–3.89 mmol/L	40–70 mg/dL
Lactate	1–2 mmol/L	10–20 mg/dL
Total protein
Lumbar	0.15–0.5 g/L	15–50 mg/dL
Cisternal	0.15–0.25 g/L	15–25 mg/dL
Ventricular	0.06–0.15 g/L	6–15 mg/dL
Albumin	0.066–0.442 g/L	6.6–44.2 mg/dL
IgG	0.009–0.057 g/L	0.9–5.7 mg/dL
IgG indexb	0.29–0.59
Oligoclonal bands (OGB)	<2>
Ammonia	15–47 µmol/L	25–80 µg/dL
CSF pressure		50–180 mmH2O
CSF volume (adult)	~150 mL
Red blood cells	0	0
Leukocytes
Total	0–5 mononuclear cells per mm3
Differential
Lymphocytes	60–70%
Monocytes	30–50%
Neutrophils	None

Hepatitis viruses

1. human hepatitis viruses are RNA viruses, except for hepatitis B, which is a DNA virus
2. progressive chronic liver disease with cirrhosis and even hepatocellular carcinoma, common to the bloodborne types (HBV, HCV, and HDV)

Hepatitis A

1. ether-resistant RNA virus
2. Inactivation of viral activity can be achieved by boiling for 1 min, by contact with formaldehyde and chlorine, or by ultraviolet irradiation
3. one serotype.
4. Hepatitis A has an incubation period of approximately 4 weeks.
5. Its replication is limited to the liver, but the virus is present in the liver, bile, stools, and blood during the late incubation period and acute preicteric phase of illness
6. viral shedding in feces, viremia, and infectivity diminish rapidly once jaundice becomes apparent
7. Antibodies to HAV (anti-HAV) can be detected during acute illness when serum aminotransferase activity is elevated and fecal HAV shedding is still occurring
8. early antibody response is predominantly of the IgM class
9. During convalescence, however, anti-HAV of the IgG class becomes the predominant antibody
10. diagnosis of hepatitis A is made during acute illness by demonstrating anti-HAV of the IgM class.
11. After acute illness, anti-HAV of the IgG class remains detectable indefinitely, and patients with serum anti-HAV are immune to reinfection

Hepatitis B

1. a DNA virus
2. HBV is now recognized as one of a family of animal viruses, hepadnaviruses (hepatotropic DNA viruses), and is classified as hepadnavirus type 1
3. Instead of DNA replication directly from a DNA template, hepadnaviruses rely on reverse transcription
4. HBV is difficult to cultivate in vitro in the conventional sense from clinical material
5. Geographic distribution of genotypes and subtypes varies
6. Clinical course and outcome are independent of subtype,
7. hepatitis B surface antigen (HBsAg) hepatitis B core antigen (HBcAg), and its corresponding antibody is anti-HBc. A third HBV antigen is hepatitis B e antigen (HBeAg), a soluble, nonparticulate, nucleocapsid protein
8. HBeAg, which has a signal peptide that binds it to the smooth endoplasmic reticulum and leads to its secretion into the circulation
9. HBcAg is the protein product; it has no signal peptide, it is not secretedHBcAg particles remain in the hepatocyte, where they are readily detectable by immunohistochemical staining naked core particles do not circulate in the serum
10. HBeAg, provides a convenient, readily detectable, qualitative marker of HBV replication and relative infectivity.
11. HBsAg-positive with HBeAg is more highly infectious and associated with hepatitis B virions (and detectable HBV DNA, ) than HBeAg-negative or anti-HBe-positive serum. For example, HBsAg carrier mothers who are HBeAg-positive almost invariably (>90%) transmit hepatitis B infection to their offspring, whereas HBsAg carrier mothers with anti-HBe rarely (10 to 15%) infect their offspring
12. during the course of acute hepatitis B, HBeAg appears transiently; its disappearance may be a harbinger of clinical improvement and resolution of infection
13. Persistence of HBeAg in serum beyond the first 3 months of acute infection may be predictive of the development of chronic infection,
14. the presence of HBeAg during chronic hepatitis B is associated with ongoing viral replication, infectivity, and inflammatory liver injury.
15. DNA polymerase has both DNA-dependent DNA polymerase and RNA-dependent reverse transcriptase activities
16. hepatitis B x antigen (HBxAg), that is capable of transactivating the transcription of both viral and cellular genes
17. clinical association observed between the expression of HBxAg and antibodies to it in patients with severe chronic hepatitis and hepatocellular carcinoma

SEROLOGIC AND VIROLOGIC MARKERS

First virologic marker detectable in serum is HBsAg

1. Circulating HBsAg precedes elevations of serum aminotransferase activity and clinical symptoms
2. Remains detectable during the entire icteric or symptomatic phase of acute hepatitis B and beyond.
3. Typically HBsAg becomes undetectable 1 to 2 months after the onset of jaundice and rarely persists beyond 6 months.
4. After HBsAg disappears, antibody to HBsAg (anti-HBs) becomes detectable in serum and remains detectable indefinitely thereafter
5. variability exists in the time of appearance of anti-HBs after HBV infection, a gap of several weeks or longer may separate the disappearance of HBsAg and the appearance of anti-HBs : gap” or “window” period
6. persons with anti-HBs in serum are protected against reinfection with HBV suggest that anti-HBs is the protective antibody
7. HBsAg; its presence does not signal imminent clearance of hepatitis B.

HBcAg

1. sequestered within an HBsAg coat, and is not detectable in serum .
2. By contrast, anti-HBc is readily demonstrable in serum, beginning within the first 1

to 2 weeks after the appearance of HBsAg and

3. Anti Hbc preceeds anti-HBs Ab by weeks to months
4. anti-HBc may represent serologic evidence of current or recent HBV infection especially in window period
5. blood containing anti-HBc in the absence of HBsAg and anti-HBs has been implicated in the development of transfusion-associated
6. isolated anti-HBc does not necessarily indicate active virus replication; most instances of isolated anti-HBc represent hepatitis B infection in the remote past.
7. Anti-HBc of the IgM class (IgM anti-HBc) predominates during the first 6 months after acute infection, whereas IgG anti-HBc is the predominant class of anti-HBc beyond 6 months.
8. Generally, in persons who have recovered from hepatitis B, anti-HBs and anti-HBc persist indefinitely

HBeAg,

1. appears concurrently with or shortly after HBsAg.
2. Its appearance coincides temporally with high levels of virus replication and reflects the presence of circulating intact virions and detectable HBV DNA.
3. In self-limited HBV infections, HBeAg becomes undetectable shortly after peak elevations in aminotransferase activity, before the disappearance of HBsAg, and anti-HBe then becomes detectable
4. HBeAg is a qualitative marker and HBV DNA a quantitative marker of this replicative phase,

EXTRAHEPATIC SITES

1. Hepatitis B antigens and HBV DNA have been identified in extrahepatic sites, including lymph nodes, bone marrow, circulating lymphocytes, spleen, and pancreas
2. does not appear to be associated with tissue injury in any of these extrahepatic sites,
3. explains the recurrence of HBV infection after orthotopic liver transplantation

Explanation to medical instruments

Explanation to medical instruments

Pulmonary capillary wedge pressure

from bailey book

The pulmonary capillary wedge pressure (PCWP) is a better indicator of both circulating blood volume and left ventricular function. PCWP is obtained by a pulmonary artery flotation balloon catheter (Swan—Ganz). This can be used to differentiate between left and right ventricular failure, pulmonary embolus, septic shock and ruptured mitral valve, and can also be an accurate guide to therapy with fluids, inotropic agents and vasodilators. It may also be used to measure cardiac output by a thermodilution technique simply at the bedside.

Measurement of pulmonary capillary wedge pressure

This specialised procedure requires supervised training, practice, patience and experience in interpreting the values measured and waveforms indicated. Complications include arrhythmias, pulmonary infarction, pulmonary artery rup­ture, balloon rupture and catheter knotting, in addition to the complication from central venous cannulation. The catheter should not be left in situ for more than 72 hours; if further haemodynamic monitoring is required, a new catheter should be inserted.

Method. Strict aseptic central venous cannulation should be performed (e.g. via right internal jugular vein) and using the appropriate introducers, cannula and guidewire, the catheter, flushed and wiped with heparin saline, introduced into the right atrium. The balloon, inflated with 1.5 ml of air, should be advanced slowly via the right ventricle into the pulmonary artery, checked by x-ray and monitored by pressure tracing, which becomes characteristically flat when the balloon wedges in a small branch to give the capillary pressure (indicating left atrial pressure). When the balloon is deflated, the pulmonary artery pressure is obtained. The balloon must never be reinflated in the absence of a normal pulmonary artery waveform as this means that the tip alone is wedged and reinflation might therefore rupture the pulmonary artery. Withdrawal of 2—3 cm is mandatory until the waveform reappears and reinflation can be permitted.

The transducer should be placed at the midaxillary point (zero reference point); the normal PCWP is between 8 and 12 mmHg (10.5 and 15.5 cmH2O), and normal pulmonary artery pressure is 25 mmHg systolic and 10 mmHg diastolic.

Clinical monitoring

In summary, patient monitoring in shock should include:

• pulse;

• blood pressure (recording systolic and diastolic pressure, the pulse pressure, using an intra-arterial line if necessary);

• heart rate and rhythm (cardioscope);

• respiratory rate and depth;

• CVP;

• PCWP in severe shock when the diagnosis is in doubt;

• urine output;

• serial blood gases and serum electrolyte measurements.

Medical instruments

Instrument	parametre	Reference / explanation
Swan ganz catheter	Pulmonary capillary wedge pressure	Bailey 23 rd edition page 105 of 2809 next page shown
Two-dimensional echocardiography	four chamber sizes, regional and global systolic function, and chamber wall thickness valve motion, intracardiac masses, abnormal or absent cardiac structures, and pericardial fluid	Cmdt 2008 go there and search for this in cardiology section
PulsedDoppler ultrasound	semiquantitative or qualitative estimation of the severity of transvalvular gradients, RV systolic pressure, PA pressure, valvular regurgitation, and intracardiac shunts	CMDT 2008 go there and search for this in cardiology section
Color flow Doppler ultrasound	visual pattern of blood flow velocities superimposed over the anatomic two-dimensional echocardiographic image thus demonstration of turbulence from stenotic or regurgitant valves, and for the visualization of intracardiac defects	CMDT 2008 go there and search for this in cardiology section
Transesophageal echocardiography (TEE) with Doppler ultrasound	to derive information about posterior structures (especially the atria and AV valves), prosthetic heart valves, and intracardiac masses not seen on chest wall echocardiography (eg, vegetations in endocarditis or thrombi on pacemaker leads), and to monitor patients during surgery confirm the location of the pulmonary veins and define septal defects or the presence of a patent foramen ovale (PFO) superior to surface echocardiography in diagnosing LA appendage thrombi and regurgitant lesions associated with prosthetic valves quite sensitive in detecting aortic dissection and severe atherosclerosis of the ascending aorta,	CMDT 2008 go there and search for this in cardiology section
Stress echocardiography	used in valvular as well as ischemic heart disease.	CMDT 2008 go there and search for this in cardiology section
Cardiac MRI	useful for defining myocardial diseases such as sarcoidosis or amyloidosis. Flow measurements, valve orifice sizes, and shunt sizes can all be determined Contrast-enhanced images can provide accurate measurement of myocardial infarction size and location to screen for renal artery stenosis in patients with hypertension. However, patients with metal pacemakers or defibrillators are not candidates for MRI.	CMDT 2008 go there and search for this in cardiology section
Cardiac multislice CT (fast CT)	it is an excellent test to confirm normal coronaries used to screen patients for CAD. the effective dose equivalent is around 20 milliSieverts, about the same as a rest and exercise thallium study	CMDT 2008 go there and search for this in cardiology section

sympathetic & parasympathetic actions over Heart

Electrophsiology of heart

Ion channels in heart:

Ion	Channel type
Na+	Voltage
K+	Voltage & ligand

phase 0	initial rapid depolarization and the overshoot	due to opening of voltage-gated Na+ channels
phase 1	initial rapid repolarization	due to closure of Na+ channels & also opening of K+ channels
phase 2	plateau	due to a slower but prolonged opening of voltage-gated Ca2+ channels.
phase 3 to phase 4	Final repolarization to the resting membrane potential	due to closure of the Ca2+ channels and K+ efflux through various types of K+ channels.




Variations in the duration and shape of the cardiac action potential exist depending on its location in the heart:

• Different layers of the ventricle exhibit marked changes in the action potential

Phase	Blunted at	Prominent at
Phase 1	Endocardium	Epicardium
phase 2	Epi

• M cells found in the midmyocardium have the longest action potential duration and may contribute to the U wave seen on the surface electrocardiogram
• The J (Osborne) wave seen on the ECG in cases of hypothermia may be due to the increased prominence of phase 1 in the epicardial cells

Normal heart

SA node : at the lateral border of the superior vena cava and right atrial junction in the sulcus

Terminalis, measuring up to 2 cm long × 0.5 cm wide

: sinus node artery, branching from either the right coronary artery (55 to 60%) or the left

coronary artery (40 to 45%), runs through the middle of the sinus node

: Effect

:of adrenergic: -increases rate

:of cholinergic : decrease rate

: stretch receptors: ( coupled to Cl-channels ) : increase the atrial rate with increasing atrial pressure

AV node : arterial supply from the right coronary artery in 85 to 90% of cases

: Conduction is relatively slow through the AV node compared with atrial and ventricular tissue, in part because of the decreased density of gap junction proteins & intercalated discs leads to slower depolarization of neighboring cells -- PR interval depends on this slow AV node conduction

Bundle of His : Conduction through the His bundle is rapid,owing to the presence of rapidly acting sodium channels

: arterial supply of the bundle of His originates from the left anterior descending artery in 90% of cases

: right bundle branch trifurcates distally into a network that supplies the anterolateral papillary muscle, the low right septum, and the parietal band

Ventricular activation

from left to right septum

from apex to base

from endocardium to epicardium

Purinergic receptors are a third family of G protein-coupled receptors that are activated by adenosine

slowing of the pacemaker activity for SA and AV nodes and conduction delay through the AV node

Phases of action potential of cardiac muscle

phase 0	initial rapid depolarization and the overshoot	due to opening of voltage-gated Na+ channels
phase 1	initial rapid repolarization	due to closure of Na+ channels & also opening of K+ channels
phase 2	plateau	due to a slower but prolonged opening of voltage-gated Ca2+ channels.
phase 3 to phase 4	Final repolarization to the resting membrane potential	due to closure of the Ca2+ channels and K+ efflux through various types of K+ channels.

Long QT Syndrome :

Long QT Syndrome :

http://www.emedicine.com/med/topic1983.htm

1. Long QT syndrome (LQTS) is a congenital disorder characterized by a prolongation of the QT interval on ECG and a propensity to ventricular tachyarrhythmias, which may lead to syncope, cardiac arrest, or sudden death
2. The QT interval on the ECG, measured from the beginning of the QRS complex to the end of the T wave, represents the duration of activation and recovery of the ventricular myocardium. QT intervals corrected for heart rate (QTc) longer than 0.44 seconds are generally considered abnormal, though a normal QTc can be slightly prolonged in female individuals (up to 0.46 sec).
3. The Bazett equation is used to calculate the QTc, as follows: QTc = QT/root of the R-R interval
4. To measure QT interval accurately, the relationship of QT to the R-T interval should be reproducible. This issue is especially important when the heart rate is <50>120 bpm and when athletes or children have marked beat-to-beat variability of the R-R interval. In such cases, long recordings and several measurements are required
5. Prolonged recovery from electrical excitation increases the likelihood of dispersing refractoriness, when some part of myocardium might be refractory to subsequent depolarization.
6. QT prolongation can lead to polymorphic ventricular tachycardia, or torsade de pointes, which itself may lead to ventricular fibrillation and sudden cardiac death.
7. LQTS has been recognized as mainly
1. Romano-Ward syndrome (ie, familial occurrence with autosomal dominant inheritance, QT prolongation, and ventricular tachyarrhythmias) or
2. Jervell and Lang-Nielsen (JLN) syndrome (ie, familial occurrence with autosomal recessive inheritance, congenital deafness, QT prolongation, and ventricular arrhythmias).
8. LQTS is caused by mutations of the genes for cardiac potassium and sodium or calcium ion channels
9. LQTS usually present with cardiac events in childhood, adlescence, or early adulthood.
10. The risk of death from LQTS is higher in boys than in girls younger than 10 years, and the risk is similar in male and female patients thereafter.
11. Diagnostic Criteria for LQTS

Criterion	Points
ECG findings*
QTc, ms†	>480	3
	460-470	2
	450 in male patient	1
Torsades de pointes‡		2
T-wave alternans	1
Notched T wave in 3 leads		1
Low heart rate for age§		0.5
Clinical history
Syncope||	With stress	2
	Without stress	1
Congenital deafness		0.5
Family history¶
A. Family members with definite LQTS#		1
B. Unexplained sudden cardiac death <30>		0.5

*In the absence of medications or disorders known to affect these electrocardiographic features.

†QTc calculated by Bazett's formula

‡Mutually exclusive

§Resting heart rate below the second percentile for the age.

||Mutually exclusive

¶The same family member cannot be counted in A and B.

#Definite LQTS is defined by an LQTS score of more than 3 (>4).

Adapted from Circulation. 1993;88:782-84.

12. Definition of QTc Based on Age- and Sex-Specific Criteria

Group	Prolonged QTc, s	Borderline QTc, s	Reference Range, s
Children and adolescents (<15>	>0.46	0.44-0.46	<0.44
Men	>0.45	0.43-0.45	<0.43
Women	>0.46	0.45-0.46	<0.45

13. Beta-blockers are drugs of choice for patients with LQTS. The protective effect of beta-blockers is related to their adrenergic blockade that diminishes the risk of cardiac arrhythmias. They may also reduce the QT interval : Propranolol Nadolol Metoprolol Atenolol