Wednesday, January 30, 2013

OSA


The Epworth Sleepiness Scale (ESS) is used to provide a patient self-report of likelihood to fall asleep in a set of hypothetical situations, and has only a modest ability to predict OSA. Although an ESS score of 12 or greater is can be considered abnormal, patients with ESS scores lower than 12 with known risk factors for OSA should still raise clinical suspicion. However, the sensitivity of the ESS to detect clinically important OSA is insufficient to be used as a screening tool in the absence of other clinical data.


Maintenance of wakefulness test (MWT), in which the time it takes the patient to fall asleep or stay awake (respectively) is recorded via electroencephalographic readings over the course of a day.

The Berlin questionnaire addresses the presence and frequency of snoring, waketime sleepiness or fatigue, and history of obesity or hypertension, and has a sensitivity of 86% to detect sleep apnea (RDI>5) among patients who have persistent and frequent symptoms in any 2 of these domains.


The STOP-BANG questionnaire assesses the 8 most common factors associated with OSA: Snoring, Tiredness during daytime, Observed apneas, high blood Pressure, Body mass index (>35), Age (>50 years), Neck circumference (>40 cm), and Gender (male); research has shown that a BMI cutoff of 30 instead of 35 can be used in certain ethnic groups. STOP-BANG can be used preoperatively to assess patients who might be at higher-than-normal risk for surgical complications. A score of 5 to 8 has a high probability that a surgery candidate has moderate to severe OSA.


The NAMES assessment is a novel approach that combines neck circumference, airway classification, comorbidities, ESS score, and snoring, along with physical exam findings and patient history, to identify patients with moderate to severe OSA.


The goals of the PSG are (1) to quantify how much time is spent in the various sleep stages, and (2) to document any abnormalities or changes that occur during these stages.

Polysomnography results are reported using the AHI (Apnea-hypopnea index). An AHI score of less than 5 is normal. A patient can be diagnosed with OSA syndrome with an AHI of 5 to 14 along with daytime symptoms or an AHI of 15 or greater independent of other symptoms. Apnea-hypopnea index scores can also be used to assign severity: an AHI of 5 to 15 indicates mild OSA; 15 to 30 indicates moderate OSA, and scores greater than 30 indicate severe OSA.


The mainstay of therapy for OSA involves positive airway pressure (PAP). The most common form of PAP is continuous PAP (CPAP); other forms include variable or bilevel PAP (BiPAP or BPAP) and automatically-adjusting PAP (APAP).

CPAP uses continuous pressurized airflow to keep the patient's airway open during sleep using a compressor that has a snug-fitting mask covering the nose (or nose and mouth) to stabilize the upper airway and prevent collapse.
Typically, the initial amount of pressure is identified through the titration portion of the diagnostic PSG, while taking into consideration the patient's comfort. Titration should be to the lowest pressure required to decrease apneic and hypopneic episodes.

BiPAP may be used for patients who cannot tolerate CPAP or for patients with neuromuscular diseases who require assistance with nighttime ventilation. It employs 2 levels of pressure: a higher inspiratory PAP and lower expiratory PAP for easier exhaling. Automatically-adjusting PAP devices automatically titrate as necessary. Some of the newer models of CPAP also humidify the air, which diminishes dry mouth and may afford more comfort over the original models.


The optimal duration of CPAP use per night appears to be variable. A study involving nearly 150 patients with severe OSA reported that nightly CPAP use of longer durations -- but only up to a maximum of 7 hours -- leads to a greater percentage of patients achieving normal function.[52] Currently, patients are generally considered adherent if they use CPAP for at least 4 hours per night on at least 70% of all nights.
Patient complaints typically focus on dry mouth or throat, nasal irritation, discomfort with the pressure, and air leaks or problems with the masks.


CSA (Central sleep apnea) is characterized by episodes of disrupted breathing throughout the night; other symptoms include daytime sleepiness, restless sleep, and chronic fatigue, and may include morning headaches. Patients may report swallowing difficulties or changes in their voice; they may also report other symptoms based upon the causative pathophysiology of the disorder. Medical conditions that might lead to CSA include stroke or encephalitis affecting the brain stem, heart failure, some neurodegenerative disorders (Parkinson disease and multiple sclerosis), obesity, and the use of certain medications -- particularly narcotics. Patients with CSA may benefit from oxygen, nasal CPAP, or, in some cases, BiPAP. Treating the underlying comorbidity is imperative. Patients should avoid sedative medications, but may be prescribed medications to stimulate breathing. Adaptive servoventilation has been shown to be an effective treatment for CSA patients without heart failure.


Patients who live at higher altitudes and have moderate to severe OSA are significantly more difficult to treat with PAP. In addition, central apnea becomes significantly more common at increasing altitude in both diagnostic and treatment portions of PSG in patients with significant OSA. An alternative treatment approach for these patients is low-flow oxygen followed by titration with CPAP/BiPAP in patients who develop central “complex” apnea on PAP treatment. This approach can lead to overall good or optimal titration in 95% of titrated patients. One danger associated with central apnea that develops in OSA patients is an intolerance to PAP therapy.  This can result in a higher level of untreated OSA among these patients, which can, in turn, have negative effects on multiple disease processes, potentially leading to higher morbidity and mortality.



Wednesday, January 23, 2013


most common tumour of heart

A. adenoma
B. fibroma
C. myexoma
D. metastatic
E. leiomyoma


Ans: D


MC IN CHILDREN - RHABDOMYOSARCOMA

MC IN ADULTS - SECONDARIES

MC PRI TUMOR OF HEART IN ADULTS - MYXOMA

Kveim test,

The Kveim test, Nickerson-Kveim or Kveim-Siltzbach test is a skin test used to detect sarcoidosis, where part of a spleen from a patient with known sarcoidosis is injected into the skin of a patient suspected to have the disease. If granulomas are found (4–6 weeks later), the test is positive. If the patient has been on treatment (e.g. glucocorticoids), the test may be false negative.

Q: Potts puffy tumor is a complication of _____ sinusitis?
Potts puffy tumor is a complication of_____sinusitis
a)ethmoidal
b)frontal
c)maxillary
d)sphenoidal


Ans: B


Pott's puffy tumor, first described by Sir Percivall Pott in 1760, is characterized by an osteomyelitis of the frontal bone with frontal breakthrough, either direct or through haematogenic spread. This results in a swelling on the forehead, hence the name. The infection can also spread inwards, leading to an intracranial abscess.

Although it can affect all ages, it is mostly found among teenagers and adolescents.


Which of the anti tuberucular drug crosses the blood brain barrier.
a. INH
b.Rifmapaicn.
c. Ethambutol.
d. Streptomycin


Ans: A, B 

The literature relating to cerebrospinal fluid penetration of antituberculosis agents is reviewed. 
Amongst the essential antituberculosis agents isoniazid has the best CSF pharmacokinetics reaching peak concentrations (C(max)) only slightly less than in blood. 

Pyrazinamide also has good CSF penetration and in children receiving dosages of 40 mg/kg the CSF C(max) exceeds the proposed minimal inhibitory concentration of 20 μg/ml. 

Streptomycin other aminoglycosides and ethambutol have poor CSF penetration and cannot be agents of first choice for TBM treatment. 

Rifampicin at dosages used in adults seldom reaches CSF concentrations exceeding MIC, but does so more frequently in children when dosages of up to 20 mg/kg are used. 

The non-essential agents ethionamide, the fluoroquinolones, with the exception of ciprofloxacin, and cycloserine (terizadone) have relatively good CSF penetration and are recommended for TBM treatment.

Wednesday, January 9, 2013

Which Chromosome is involved in Lionisation


X-inactivation (also called lyonization) is a process by which one of the two copies of the X chromosome present in female mammals is inactivated. The inactive X chromosome is silenced by it being packaged in such a way that it has a transcriptionally inactive structure called heterochromatin.

As female mammals have two X chromosomes, X-inactivation causes them not to have twice as many X chromosome gene products as males, which only possess a single copy of the X chromosome .The choice of which X chromosome will be inactivated is random in placental mammals such as mice and humans, but once an X chromosome is inactivated it will remain inactive throughout the lifetime of the cell and its descendants in the organism. Unlike the random X-inactivation in placental mammals, inactivation in marsupials applies exclusively to the paternally derived X chromosome.

Normal females possess two X chromosomes, and in any given cell one chromosome will be active (designated as Xa) and one will be inactive (Xi). However, studies of individuals with extra copies of the X chromosome show that in cells with more than two X chromosomes there is still only one Xa, and all the remaining X chromosomes are inactivated. This indicates that the default state of the X chromosome in females is inactivation, but one X chromosome is always selected to remain active.

It is hypothesized that there is an autosomally-encoded 'blocking factor' which binds to the X chromosome and prevents its inactivation. The model postulates that there is a limiting blocking factor, so once the available blocking factor molecule binds to one X chromosome the remaining X chromosome(s) are not protected from inactivation. This model is supported by the existence of a single Xa in cells with many X chromosomes and by the existence of two active X chromosomes in cell lines with twice the normal number of autosomes.

Sequences at the X inactivation center (XIC), present on the X chromosome, control the silencing of the X chromosome. The hypothetical blocking factor is predicted to bind to sequences within the XIC.

Tuesday, January 8, 2013

Ozaena is characaterized by


a. Female patient.
b. Male patient.
c.Ansosmia
d Foetid smell from nose.


Ans: D
Ozaena: A chronic disease of the nose characterized by a foul-smelling nasal discharge and atrophy of nasal structures.
Atrophic rhinitis is of two types:
1. Primary and 
2. Secondary.

Primary Atrophic Rhinitis

Aetiology (Remember Mnemonic HERNIA)
The exact cause is not known. Various theories advanced regarding its causation are:

(a) Hereditary factors. Disease is known to involve more than one member in the same family.
(b) Endocrinal disturbance. Disease usually starts :Jt puberty, involves females more th an males, the
crusting and foetor associated with disease tends to cease after me nopause; these factors ha\'e r .Jl I::J the possibility of disease being an endocrina l dl ~ orde r.
(c) Racial factors. White and ye llow rae s are more susceptible than natives of equatorial Africd.
(d) Nutritional deficiency. Disease may be due to deficiency of vitamin A, D or iron or some other dietary factors. The fact that incidence of di:.ease is decreasing in western countries and is rarely seen in well-to-do families raises the possibility of some nutritional deficiency.
(e) Infective. Various organisms have been cul tureJ from cases of atrophic rhinitis such as Klebsiella ozaenae , (Perez bacillus), diphtheroids, P vulgaris, Esch. coli, Staphylococci and Streptococci but the ' are all considered to be secondary invade rs responsible for fou I smell rather than the primary ca usat ive organisms of the disease.
(f) Autoimmune process. The body reacts by a destructive process to the antigens released from the nasal mucosa. Viral infection or some other unspecified agents may trigger antigenicity of nasal mucosa.


Pathology
Ciliated columnar epithelium is lost and is replaced by strat ified squamous type. There is atrophy of seromucinous glands, ve nous blood sinusoid s and nerve elements.
Arteries in the mucosa, periosteum and bone show oblitt rati ve endarteritis. The bone of turbinates undergoes resorption causing widening of nasal chambers. Paranasal sinuses are small due to their arrested development.

Clinical Features
Disease is commonly seen in females and starts around puberty. There is foul smell from the nose making the patient a social outcast though patient himself is unaware of the smell due to marked anosmia (merciful anosmia) which accompanies these degenerative changes. 
Patient may complain of nasal obstruction in spite of unduly wide nasal chambers. This is due to large crusts filling the nose. Epistaxis may occur when the crusts are removed. 
Examination shows nasal cavity to be full of greenish or greyish black dry crusts covering the turbinates and septum. Attempts to remove them may cause bleeding. When the crusts have been removed, nasal cavities appear roomy with atrophy of turbinates so much so that the posterior wall of nasopharynx can be easily seen. 
Nasal turbinates may be reduced to mere ridges. Nasal mucosa appears pale. Septal perforation and dermatitis of nasal vestibule may be present. Nose may show a saddle deformity.
Atrophic changes may also be seen in the pharyngeal mucosa which may appear dry and gl8zed with crusts. Similar changes may occur in the larynx with cough and hoarseness of voice (atrophic laryngitis).
Hearing-impairment may be noticed because of obstruction to eustachian tube and middle ear effusion.
Paranasal sinuses are usually small and underdeveloped with thick walls. They appear opaque on X-ray.
Antral wash is difficult to perform due to thick walls of the sinuses.

Tache noir is seen after


1. 24 hrs after death
2.7-8 hrs after death
3.1hr after death
4.only in a drowned body after removing from water

Ans: 2


*Tache noir is one of the important postmortem changes seen in the eye after death.

*If the eyes remain open after death, the areas of the sclera exposed to the air dry out, which results in a first yellowish, then brownish-blackish band like discoloration zone called TACHE NOIRE.

*It is seen mostly after 7 to 8 hours after death.

TIME SINCE DEATH


Body temperature      Body stiffness               Time since death
warm                  not stiff                              dead not more than 3Hrs
warm                   stiff                              dead 3 to 8 hours
cold                            stiff                                      dead 8 to 36 hours
cold                           not stiff                              dead more than 36 hours

C1 C2 vertebra best seen in?



1)lateral view
2)oblique view
3)AP  view
4)odontoid view

Ans-4



Technique:
    - the patient is positioned as for the supine AP;
    - central beam directed perpendicular to the midpoint of the open mouth;
    - patient should softly say 'ah' to depress the tongue to the floor of mouth during exposure







- Done for:
    - to evaluate C1 (Jefferson), Dens, superior facets of C2;
    - for evaluating dens fractures, body of C2, & rotary C1-C2 dislocations;
    - mach lines - teeth, C1 arch;
    - open mouth view, along w/ lateral view, will reveal fractures of the dens ;
    - atlantoaxial articulation & integrity of dens and body of C2 are best seen on the odontoid view;
    - this is most technically most difficult film to obtain as it requires patient to open his mouth as wide as possible;
    - lateral masses of C1 should align over the lateral masses of C2;
    - lateral displacement of masses of C1 w/ respect to C2 may indicate Jefferson or burst fracture of the Atlas;
         - combined lateral mass displacement > 7 mm suggests that transverse ligament is torn;



    - children:
         - overlapping lateral masses can be a normal variant in children and therefore this view may not allos assessment of whether frx is
              stable or unstable;

Sweating is not seen in


1 heat stroke

2 heat cramps

3 heat fatigue

4 heat syncope



Ans: 1


Classic NEHS is characterized by hyperthermia, anhidrosis, and an altered sensorium, which develop suddenly after a period of prolonged elevations in ambient temperatures (ie, heat waves). Core body temperatures greater than 41°C are diagnostic, although heatstroke may occur with lower core body temperatures.

EHS is characterized by hyperthermia, diaphoresis, and an altered sensorium, which may manifest suddenly during extreme physical exertion in a hot environment.

Two forms of heatstroke exist.
Exertional heatstroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment.

Classic nonexertional heatstroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons.

Classic NEHS occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heatstroke are associated with a high morbidity and mortality, especially when therapy is delayed.

When heat gain overwhelms the body's mechanisms of heat loss, the body temperature rises, and a major heat illness ensues. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death.

Temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.

Factors that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness.

Wednesday, January 2, 2013

carrion's disease is also known as


1...trench fever

2...rocky mountain spotted fever

3...oroya fever

4...five day fever


Ans: 3


Oroya fever or Carrion's Disease is an infectious disease produced by Bartonella bacilliformis infection.

Carrion's disease is found only in Peru, Ecuador, and Colombia. It is endemic in some areas of Peru and is caused by infection with the bacterium Bartonella bacilliformis and transmitted by sandflies of genus Lutzomyia

The clinical symptoms of bartonellosis are pleomorphic and some patients from endemic areas may be asymptomatic.

The two classical clinical presentations are the acute phase and the chronic phase, corresponding to the two different host cell types invaded by the bacterium (red blood cells and endothelial cells).

Acute phase: (Carrion's disease) the most common findings are fever (usually sustained, but with temperature no greater than 102°F (39°C)), pallor, malaise, nonpainful hepatomegaly, jaundice, lymphadenopathy, splenomegaly. This phase is characterized by severe hemolytic anemia and transient immunosuppression. The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with Salmonella spp occurs. In a recent study the attack rate was 13.8% (123 cases) and the case-fatality rate was 0.7%.

Chronic phase: (Verruga Peruana or Peruvian Wart) it is characterized by an eruptive phase, in which the patients develop a cutaneus rash produced by a proliferation of endothelial cells and is known as "Peruvian warts" or "verruga peruana". Depending of the size and characteristics of the lesions, there are three types: miliary (1-4 mm), nodular or subdermic and mular (>5mm). Miliary lesions are the most common.
The most common findings are bleeding of verrugas, fever, malaise, arthralgias, anorexia, myalgias, pallor, lymphadeopathy, and hepato-splenomegaly.

Diagnosis during the acute phase can be made by obtaining a peripheral blood smear with Giemsa stain, Columbia-blood agar cultures, immunoblot, IFI, and PCR. Diagnosis during the chronic phase can be made using a Warthin-Starry stain of wart biopsy, PCR, and immunoblot.

The drug of choice during the acute phase is Quinolones (such as ciprofloxacin) or Chloramphenicol in adults and Chloramphenicol plus beta lactams in children.
For the chronic phase, Rifampin or macrolides are used to treat both adults and children.