Random points

Posted: March 12, 2014 in Uncategorized

primary lymphoid organs are thymus and bone marrow

VIII cranial nerve is affected in syphilis

mc glial tumor- astrocytoma


drugs causing acute tolerance-

Key Features of Biologic Agents Used as Bioweapons
1. High morbidity and mortality rates
2. Potential for person-to-person spread
3. Low infective dose and highly infectious by aerosol
4. Lack of rapid diagnostic capability
5. Lack of universally available effective vaccine
6. Potential to cause anxiety
7. Availability of pathogen and feasibility of production
8. Environmental stability
9. Database of prior research and development
10. Potential to be “weaponized
CDC Category A, B, and C Agents
Category A
 Anthrax (Bacillus anthracis)
 Botulism (Clostridium botulinum toxin)
 Plague (Yersinia pestis)
 Smallpox (Variola major)
 Tularemia (Francisella tularensis)
 Viral hemorrhagic fevers
 Arenaviruses: Lassa, New World (Machupo, Junin, Guanarito, and Sabia)
 Bunyaviridae: Crimean-Congo, Rift Valley
 Filoviridae: Ebola, Marburg
Category B
 Brucellosis (Brucella spp.)
 Epsilon toxin of Clostridium perfringens
 Food safety threats (e.g., Salmonella spp., Escherichia coli
 0157:H7, Shigella)
 Glanders (Burkholderia mallei)
 Melioidosis (B. pseudomallei)
 Psittacosis (Chlamydophila psittaci)
 Q fever (Coxiella burnetii)
 Ricin toxin from Ricinus communis (castor beans)
 Staphylococcal enterotoxin B
 Typhus fever (Rickettsia prowazekii)
 Viral encephalitis [alphaviruses (e.g., Venezuelan, eastern, and western equine encephalitis)]
 Water safety threats (e.g., Vibrio cholerae, Cryptosporidium parvum)
Category C
 Emerging infectious diseases threats such as Nipah, hantavirus, SARS coronavirus, and pandemic influenza

Aerobic gain of ATP from glycolysis – 7 atp

irreversible steps involve those catalyzed by pfk-1 ,hexokinase, pyruvate kinase

Major rate limiting step is by hexokinase and not by pfk-1 as previously believed

Enolase is inhibited by Fluoride
Iodo acetate inhibits G 3 P dehydrogenase

Reaction takes place in the cytoplasm

Hexokinase 2 and 4 regulated by insulin

Glucokinase has low affinity for glucose,high Km. It’s inhibited by fructose 6 P

Glut 4 in adipose and muscle

Rbc undergoes anaerobic glycolysis

Malate shuttle in liver, heart, kidney. ATP gained 32

Glycerophosphate shuttle in brain, white skeletal muscle. ATP gained 30 since it utilizes FAD

Planning and coordination of movements- cerebrocerebellum and basal ganglia

Nagler reaction seen in cl perfringens demonstrates the alpha toxin which is a lecithinase

Maroteaux-Lamy syndrome,
People with MPS VI are deficient in a lysosomal enzyme called N-acetylgalactosamine-4-sulphatase (or 4-sulphatase for short), which is essential in breaking down a mucopolysaccharide called dermatan sulphate. The amount of dermatan sulphate that is stored influences the extent of physical symptoms

Mutations in the ARSB gene cause MPS VI. The ARSB gene provides instructions for producing an enzyme called arylsulfatase B, which is involved in the breakdown of large sugar molecules called glycosaminoglycans (GAGs). GAGs were originally called mucopolysaccharides, which is where this condition gets its name. Mutations in the ARSB gene reduce or completely eliminate the function of arylsulfatase B. The lack of arylsulfatase B activity leads to the accumulation of GAGs within cells, specifically inside the lysosomes. Lysosomes are compartments in the cell that digest and recycle different types of molecules. Conditions such as MPS VI that cause molecules to build up inside the lysosomes are called lysosomal storage disorders. The accumulation of GAGs within lysosomes increases the size of the cells, which is why many tissues and organs are enlarged in this disorder. Researchers believe that the buildup of GAGs may also interfere with the functions of other proteins inside lysosomes, triggering inflammation and cell death.

A wide variety of acute-phase reactants have been evaluated in neonates with suspected bacterial sepsis. However, only C-reactive protein (CRP) and procalcitonin concentrations have been investigated in sufficiently large studies.72,73 CRP concentration increases within 6 to 8 hours of an infectious episode in neonates and peaks at 24 hours.74,75 The sensitivity of a CRP determination is low at birth, because it requires an inflammatory response (with release of interleukin-6) to increase CRP concentrations.76 The sensitivity improves dramatically if the first determination is made 6 to 12 hours after birth.

Procalcitonin concentrations increase within 2 hours of an infectious episode, peak at 12 hours, and normalize within 2 to 3 days in healthy adult volunteers.77 A physiologic increase in procalcitonin concentration occurs within the first 24 hours of birth, and an increase in serum concentrations can occur with noninfectious conditions (eg, respiratory distress syndrome).78 Procalcitonin concentration has a modestly better sensitivity than does CRP concentration but is less specific.

target HbA1c levels are ? 8% for patients 6-12 years old and < 7.5% for those 13-19 years.



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