Archive for the ‘Repeated Topics In PG Entrance’ Category

PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML)

  • Cause: A progressive disease caused by JC virus

 

  • Affected cells: Oligodendrocytes

 

Pathology:

Since oligodendrocytes are concerned with myelination; PML is associated with multifocal areas of demyelination distributed throughout the brain but sparing spinal cord and optic nerve.

 

Cellular changes:

  • Oligodendrocytes: Densely staining enlarged nuclei containing viral inclusions
  • Astrocytes: Hyperchromatic, deformed, bizarre nuclei containing mitotic figures.

 

Associated conditions:

PML is predominantly seen in patients with immunosuppressive disorders: AIDS (80%), hematological malignancies, transplant recipients.

 

Symptoms:

  • Focal neurological signs: Aphasia, dysarthria, hemiparesis/ monoparesis, ataxia
  • Visual impairment (45%): Homonymous hemianopia
  • Mental impairment (38%): Behavioral change, confusion, dementia
  • Seizures (20%).

 

Diagnosis:

  • MRI is the investigation of choice for PML as it is superior than CT and shows classical asymmetric nonenhancing coalescing lesions in white matter located periventricularly.
  • PCR amplification of JCV-DNA in association with typical MRI lesion is diagnostic of PML.
  • Brain biopsy demonstrates multiple demyelinating lesion in white matter of cerebrum, cerebellum and brainstem.

 

Prognosis:

In most cases, death occurs within 3-6 months from the onset of neurological symptoms and even more rapidly in patients with AIDS.

 

Treatment:

  • Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity.
  • In the case of HIV-associated PML, immediately beginning ART will benefit most individuals.
  • Drugs that are being studies as potential treatment options (still not recommended): Cidofovir and Mefloquine.
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Papillary CA thyroid

 

In this post, we will discuss the physiology of appetite in a short as it is a frequent source of MCQs on PG examinations.

 

Physiology of appetite

 

  • The arcuate nucleus (ARC) is a key hypothalamic nucleus in the regulation of appetite and is involved in integrating peripheral satiety and adiposity signals via orexigenic and anorexigenic neuropeptide transmission to other hypothalamic and extrahypothalamic brain regions.

 

  • Proximity of ARC to the median eminence and the fact that it is not fully insulated from the circulation by the blood brain barrier makes it strategically positioned to integrate the great number of peripheral signals controlling food intake.

 

  • There are two major neuronal populations in the ARC implicated in the regulation of feeding:
  1. One population co-expresses Neuropeptide Y (NPY) and agouti-related protein (AgRP) and increases food intake. These are called orexigenic neurotransmitters.
  2. The second population of neurons co-expresses cocaine- and amphetamine-related transcript (CART) and proopiomelanocortin (POMC), the precursor to the melanocortin receptor agonist, α melanocyte-stimulating hormone (α-MSH) and inhibits food intake. These are called anorexigenic neurotransmitters.

–         Please follow the rest in the following pictures.

Figure 1:

General physiology of appetite: (at times of low and high body energy stores)

appetite

 

Figure 2: Hormones involved in appetite:

hormones involved in appetite regulation

Figure 3: Another picture showing preferential pathway towards anorexia just after a meal:

APPETITE2

Figure 4: The short form of Figure 3.

A simple diagram

Hope this post will help you understanding the physiology of appetite in a short time. Thank you.

Extended spectrum beta lactamase (ESBL):

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General description:

1. This is one important group of beta lactamase that is occasionally found in certain species of gram negative bacilli.

2. These enzymes are called Extended spectrum beta lactamases because they confer upon the bacteria the additional ability to hydrolyze the beta lactum rings of cefotaxime, ceftazidime or aztreonam.

History and present condition:

1. ESBLs were first described in the mid-1980s and during the 1990s were mostly found in Klebsiella species, mostly in hospitals and often in intensive care units treating the most vulnerable patients.

2. Until recently, the numbers of patients affected remained small and the problem showed little sign of growing.

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3. However, a new class of ESBL (called CTX-M enzymes) has emerged and these have been widely detected among E. coli. These ESBL-producing E. coli are able to resist penicillins and cephalosporins and are found most often in urinary tract infections – though not simple cystitis.

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4. Of the most concern is the emergence of KPC (Klebsiella pneumoniae carbapenemases), which confer resistance to 3rd and 4th generation cephalosporins and carbapenems.

5. Of concern, they have been found even in the community as well as in hospitals.

180213c_esbl_carriers_worldwide

Laboratory diagnosis of ESBL strains:

The presence of an ESBL is suggested if bacterial growth is observed despite a concentration of 1 microgram/ml of atleast one of the 3 extended spectrum cephalosporins (Ceftazidime/ Ceftriaxone/ Cefotaxime) or growth occurs despite a concentration of 4 microgram/ ml of Cefpodoxime.

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Treatment: 

1. Carbapenems (imipenem, meropenem etc.) are the most effective and reliable as they are highly resistant to the hydrolytic activity of the beta lactamases.

2. Amongst them, meropenem is the most active carbapenem active against ESBLs.

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I am writing this article because its a direct question frequently asked in PG examinations.

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What are the so called “osteoblastic meatstasis” and “osteolytic metastasis”?

  • Normal bone development and maintenance are sustained through a balanced communication between osteoclasts and osteoblasts.
  • Invasion of the bone compartment by cancer cells causes an imbalance in their activities and results in predominantly bone lysing or bone forming phenotypes depending on the origin of the cancer.
  • Tumor-induced bone lesions usually exhibit disturbances of both cell types.
  • Thus, osteolytic activity is activated in a predominantly osteoblastic lesion and vice versa.
  • The recent development of agents that target the osteolytic components of bone metastasis, including bisphosphonates and denosumab, showed promising results in osteolytic bone diseases such as multiple myeloma but were less effective in improving the osteoblastic bone disease found in prostate cancer.
  • Thus, while osteolytic components are present in both osteoblastic and osteolytic bone lesions, inhibition of the osteolytic component alone is not sufficient to alter the vicious cycle leading to tumors with an osteoblastic phenotype.

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Causes of Osteolytic and Osteoblastic metastases

*Causes of Osteolytic metastasis:
[Mnemonic: KT(LGB) : *LGB: Lateral Geniculate Body.]
– Kidney (expansile) and Thyroid : Expansile lytic osseous metastasis are characteristic of Renal cell carcinoma (kidney) and Thyroid cancers.
– Lung.
– Gastrointestinal tract (GIT).
– Breast (occasionally).
– Less commonly melanomacarcinoma of bronchus and pheochromocytoma may also present with expansile lytic lesions.

*Causes of Osteoblastic metastasis:

[Mnemonic: PSCO-BU: *PSCO: Posterior sub-capsular opacification]
 Prostate.
– Seminoma.
– Carcinoid. 
– Ovary.
– Breast (may be mixed).
– Uterus.

 

5aaa7037c105e944b629104406b6a3f9In this document, we have summarized one of the most important and confusing part of biochemistry, the “Acid and Base balance”. I called it important because if you are a regular PG question paper solver, then you know how much MCQs come only from this portion. And I called it confusing because although it is very easy to read, understand and remember; in exam times it suddenly appears difficult and very much confusing.

 

For these reasons I tried to summarize it in only 4 pages. I know that this much is not enough for concept building or first time reading but I think this will help PG aspirants a lot and will reduce the burden of fear of so-called “ABI” very much. So please go through at once. If any addition/ correction of any of my notes you think is necessary, then please don’t hesitate to contact me. Mail me at, “prithwiraj2009@yahoo.in”. See you soon.

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