WELL FRIENDS I STARTING THIS NEW THREAD,I WILL BE POSTING CONFIRMED Q A EXPLANATION,FOR FEW Q OTHRS CAN ADD CONFIRMED QA,PLZ POST ONLY RELAVANT THINGS.SO THAT OTHRS CAN ACCESS IT WITH EASE.
kavish wrote:
Q.Malta fever is caused by?
a)
b)borrelia burgdorferi
c)brucella melitensis
d)pseudomonas
ans is c)brucella melitensis
Brucellosis, also called undulant fever, or Malta fever, in humans is a highly contagious zoonosis (infectious disease transmitted from animals to humans) caused by bacteria of the genus Brucella. Brucella spp. are small, gram-negative, non-motile, non-spore-forming rods. Brucella spp. are facultative intracellular parasites causing chronic disease, which usually persists for life. Brucellosis is a bacterial disease of both humans and animals recognized since the 19th century.
Brucellosis in humans is usually associated with the consumption of unpasteurized milk and soft cheeses made from the milk of infected animals, primarily goats, infected with Brucella melitensis and with occupational exposure of laboratory workers, veterinarians and slaughterhouse workers. Some vaccines used in livestock, most notably B. abortus strain 19 also cause disease in humans if accidentally injected. Brucellosis induces inconstant fevers, sweating, weakness, anaemia, headaches, depression and muscular and bodily pain.
Q.marker for granulocytic sarcoma?[/size][/color]
a)CD33
b)CD38
c)CD117
d)CD153
ans is c)CD117
ans is cd117 surely,they hv specifically asked about granulocytic sarcoma,
this q appear simple but are twisted.
for cd33 to hv been the ans AIIMS
cud hv simply asked marker for aml or for myeloid lineage.
i hv explained it fully in my book.
Q.In case of Post-ductal Coarctation distal anastomotic artery which is NOT involved?
A. Subscapular artery
B. Posterior intercostal artery
C. Vertebral arteries
D. Axillary arteries
Clinicall the cardinal sign of aortic coarctation is absent or diminished pulses in the femoral arteries of both lower limb.To compensate for the diminished volume of blood reaching the lower part of the body,an enormous collateral circulation develops with dilatation of the internal thoracic,subclavian,& post.intercoastal arteries.
THIS are the lines from Grey’s <a href="http://www.rxpgonline.com/forum97.html">Anatomy
</a>
In postductal coarctation of aorta,In the anterior thoracic wall,the thoraco-acromial,lateral thoracic & the subscapular arteries from the axillary,the suprascapular from the subclavian & the first & second post.intercoastal arteries from the coastocervical trunck anastamose with the third,& lower post.intercoastal arteries.
High Yield Point
Mnemonic For Branches of axillary artery
She Tastes Like Sweet Apple Pie
S: superior thoracic
T: thoracoacromial
L: lateral thoracic
S: subscapular
A: ant. circumflex humoral
P: post. circumflex humoral
Q.Irresistable sexual desire in a male is otherwise known as?
A.Nymphomania
B.Tribadism
C.Satyriasis
D.Sadism
Ans is C.Satyriasis
Hypersexuality is desire to engage in human sexual behavior at a level high enough to be considered clinically significant. Hypersexuality is characterized by a debilitating need for frequent genital stimulation which, once achieved, may fail to result in the expected long-term sexual—or emotional—satisfaction. This dissatisfaction is what is believed to encourage the heightened frequency of sexual stimulation, as well as additional physiological and neurological symptoms.
The concept of hypersexuality replaces the older concepts of nymphomania (or furor uterinus) and satyriasis. Nymphomania was believed to be a female psychological disorder characterized by an overactive libido and an obsession with sex. In males the disorder was called satyriasis (for etymology of the words, see nymph and satyr). "Nymphomania" and "satyriasis" are no longer listed as specific disorders in the DSM-IV, though they remain a part of ICD-10.
Option c)Tribadism or tribbing is a form of mutual masturbation, sometimes called frottage, in which a woman rubs her vulva against her partner's body for sexual stimulation.[1][2] The term is most often used in the context of lesbian sex, but is not exclusive to lesbians.
Q.siadh is caused by a/E?
a)vincristine
b)vinblastine
c)actinomycin d
d)cclophophamide
ans is c)actinomycin d SIADH
Definition: AVP excess associated with hyponatremia without edema or hypovolemia. The AVP excess is inappropriate in the face of hypoosmolality.
Ectopic secretion of AVP has been documented from neoplasms and pulmonary tissue. Intracranial lesions likely stimulate AVP release from the neurohypophysis, as do some drugs (e.g. chlorpropamide, vincristine, carbamazepine). Other medications (e.g. chlorpropamide, NSAIDS) potentiate the antidiuretic action of secreted AVP. Hypothalamic SIADH likely involves the baro (volume) receptor system, with a lesion of this system in the chest or CNS resulting in decreased tonic inhibition of magnocellular neuron AVP release.
CAUSES of SIADH BY PROBABLE MAJOR MECHANISM OF ACTION
Increased hypothalmic production of ADH
A. Neuropsychiatric disorders*
1. Infections: meningitis (tuberculous or bacterial), encephalitis, abscess, Herpes zoster
2. Vascular: thrombosis, subarachnoid or subdural hemorrhage, temporal arteritis, cavernous sinus thrombosis, cerebrovascular accident
3. Neoplasm: primary or metastatic
4. Skull fracture, head injury
5. Psychosis, delirium tremens
6. Other: Guillain-Barré syndrome, acute intermittent porphyria, autonomic neuropathy, hypothalamic sarcoidosis, postpituitary surgery, multiple sclerosis, epilepsy, hydrocephalus, lupus erythematosus, Shy-Drager syndrome, peripheral neuropathy, spinal cord lesions
B. Drugs
1. Intravenous cyclophosphamide* (increased sensitivity may also contribute)
2. Carbamazepine (though increased sensitivity is probably important). Hyponatremia is more common with oxcarbazepine.
3. Vincristine or vinblastine
4. Thiothixene
5. Thioridazine, other phenothiazines
6. Haloperidol
7. Amitriptyline, other tricyclic antidepressants or serotonin-reuptake inhibitors
8. Monoamine oxidase inhibitors
9. Bromocriptine
10. Lorcainide
11. Clofibrate
12. General anesthesia
13. Narcotics, opiate derivatives
14. Nicotine
C. Pulmonary disease
1. Pneumonia*: viral, bacterial, fungal
2. Tuberculosis
3. Lung abscess, empyema
4. Acute respiratory failure
5. Positive pressure ventilation (via inhibition of low-pressure cardiopulmonary baroreceptors)
6. Other: asthma, COPD, atelactasis, pneumothorax, cystic fibrosis
D. Postoperative patient*
E. Severe nausea
F. Pain
G. Infection with HIV
H. Idiopathic
Ectopic (nonhypothalamic) production of ADH
A. Carcinoma: Small cell carcinoma of lung* (2/3 of patients with small cell have impaired water excretion), bronchogenic, duodenum, pancreas, thymus, olfactory neuroblastoma, bladder, prostate, uterus
B. Lymphosarcoma, reticulum cell sarcoma, mesothelioma, Ewing sarcoma
C. Hodgkin's disease, leukemia
D. Pulmonary tuberculosis (?)
Potentiation of ADH effect
A. Chlorpropamide*
B. Carbamazepine
C. Psychosis
D. Intravenous cyclophosphamide
E. Tolbutamide
F. Prostaglandin-synthesis inhibitors (salicylates, NSAIDS)
Exogenous administration of ADH
A. Vasopressin, desmopressin
B. Oxytocin
Possible production of another antidiuretic compound (or increased sensitivity to very low levels of ADH)
A. Prolactinoma
B. Waldenstrom's macroglobulinemia
Retinitis pigmentosa, or RP, is a group of genetic eye conditions. In the progression of symptoms for RP, night blindness generally precedes tunnel vision by years or even decades. Many people with RP do not become legally blind until their 40s or 50s and retain some sight all their life. Others go completely blind from RP, in some cases as early as childhood. Progression of RP is different in each case.
RP is a group of inherited disorders in which abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina lead to progressive visual loss. Affected individuals first experience defective dark adaptation or nyctalopia (night blindness), followed by constriction of the peripheral visual field and, eventually, loss of central vision late in the course of the disease.
Signs
Mottling of the retinal pigment epithelium with [i]bone-spicule pigmentation is typically pathognomonic for retinitis pigmentosa. Other ocular features include waxy pallor of the optic nerve head, attenuated retinal vessels, cellophane maculopathy, cystic macular edema, and posterior subcapsular cataract
EXTRA INFORMATION About other options A.Usher syndrome
A leading cause of deaf-blindness, Usher syndrome (sometimes referred to as "Usher's syndrome") is a relatively rare genetic disorder that is associated with a mutation in any one of 10 genes. Other names for Usher syndrome include Hallgren syndrome, Usher-Hallgren syndrome, rp-dysacusis syndrome and dystrophia retinae dysacusis syndrome.[1] Usher syndrome is incurable at present; however, using gene therapy to replace the missing gene, researchers have succeeded in reversing one form of the disease in knockout mice.[2]
This syndrome is characterized by deafness and a gradual vision loss. The hearing loss is associated with a defective inner ear, whereas the vision loss is associated with retinitis pigmentosa (rp), a degeneration of the retinal cells. Usually, the rod cells of the retina are affected first, leading to early night blindness and the gradual loss of peripheral vision. In other cases, there is early degeneration of the cone cells in the macula, leading to a loss of central acuity. In some cases, the foveal vision is spared, leading to "doughnut vision"; central and peripheral vision are intact, but there is an annulus around the central region in which vision is impaired.
OPTION C.Kearns-Sayre syndrome
Kearns-Sayre syndrome (abbreviated KSS) or oculocraniosomatic syndrome is a disease caused by a 5,000 base deletion in the mitochondrial DNA. As such, it is a rare genetic disease in that it can be heteroplasmic, that is, more than one genome can be in a cell at any given time. Unlike most mitochondrial diseases, it is not maternally inherited. Rather, it occurs sporadically.
Kearnes-Sayre syndrome starts before the age of 20.
Presentation Its expression is systemic, but many of the most common expressions are in the eyes, with ophthalmoplegia and retinal degeneration, specifically retinitis pigmentosa, as common features.
Other characteristic features of KSS are dysphagia, proximal weakness, hearing loss, cerebellar ataxia and cardiac conduction defects.
White matter lesions are usually seen
OPTION D.Marfan syndrome
Marfan syndrome is an autosomal dominant genetic disorder of the connective tissue characterized by disproportionately long limbs, long thin fingers, a typically tall stature, and a predisposition to cardiovascular abnormalities, specifically those affecting the heart valves and aorta. The disorder may also affect numerous other structures and organs — including the lungs, eyes, dural sac surrounding the spinal cord, and hard palate.
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