Q 1. Treated soda lime glass chemical
resistances is evaluated by following test?
A) Fused glass test B) Water attack test C) H2SO4 attack test D)Powdered glass test
A) Fused glass test B) Water attack test C) H2SO4 attack test D)Powdered glass test
Ans = B, Treated sodalime glass (Type-II)
used for Buffered Aqueous solution with pH below 7, Dry powders &
Oligogenic Substance.
Powdered glass test for = Brosilicate (Type-I),
Regular Sodalime Type-III), General purpose (Type-NP)
Q 2. Cab-O-sil used as
a) Lubricant b) Antiadherent c) Glidant d) Disintegrant
a) Lubricant b) Antiadherent c) Glidant d) Disintegrant
Ans = C, Cab-O-Sil fumed silica is a white,
free-flowing powder of extremely high purity. It is widely used as a glidant in
tablet and capsule formulations.
Q 3. Type I hypersensitivity mediated by
immunoglobulins is
A). IgE B). IgD C). IgM D). IgA
A). IgE B). IgD C). IgM D). IgA
Ans= A, In type-I reaction IgE antibody
involve, degranulation of mast cell, reaction occur with in 30 minutes, Ex.= anaphylactic
shock, hey fever, asthma.
Q 4. which of the following mediate secondary
response?
A) IgA B) IgD C) IgE D) IgG
A) IgA B) IgD C) IgE D) IgG
Ans = D, In type-II reaction IgM and IgG
antibody involve, reaction occur with in 5-12 hrs. Ex.= Rh incompatability
Q 5. Toxic features of atropine include the
following, except:
A). Tachycardia B). Blurred vision C). Urinary retention D). Hypothermia
A). Tachycardia B). Blurred vision C). Urinary retention D). Hypothermia
Ans = D , Atropine inhibits sweating and
stimulates the temperature-regulating center of the hypothalamus hence the body
temperature rises. Larger doses of atropine block the vagal effects on M2
muscarinic receptors on the SA nodal pace maker hence there is tachycardia. It
has a relaxant action on the ureter and the urinary bladder hence urinary
retention may occur in old males with prostatic hypertrophy. The lenss is fixed
for far vision hence near objects appear blurred.
Q 6. Cyclosporine :
A). Is excreted unchanged from the body.
B). Is derived from a bacterium.
C). Has a selective inhibitory effect on T-lymphocytes.
D). Is not absorbed orally.
A). Is excreted unchanged from the body.
B). Is derived from a bacterium.
C). Has a selective inhibitory effect on T-lymphocytes.
D). Is not absorbed orally.
Ans = C, Cyclosporine is obtained from a soil
fungus Tolypocladium inflatum gams. It has a selective inhibitory effect on
T-lymphocytes, suppressing the early cellular response to antigenic stimuli. It
can be administered both orally as well as intravenously. It gets metabolized
extensively in the liver and various drugs, which affect cytochrome P450,
affect its clearance.
Q 7. Choose the antimicrobial which acts by
interfering with DNA function in the bacteria:
A. Chloramphenicol
B. Ciprofloxacin
C. Streptomycin
D. Vancomycin
Ans. B. Chloramphenicol is a bacteriostatic broad-spectrum
antibiotic, alongside the tetracyclines . Chloramphenicol, also known as
chlornitromycin, is effective against a wide variety of Gram-positive and Gram-negative
bacteria, including most anaerobic organisms. Chloramphenicol is a bacteriostatic
drug that stops bacterial growth by inhibiting protein synthesis.
Chloramphenicol prevents protein chain elongation by inhibiting the peptidyl
transferase activity of the bacterial ribosome.
Ciprofloxacin is second-generation quinolones
are a family of synthetic broad-spectrum antibacterial drugs. Quinolones exert
their antibacterial effect by preventing bacterial DNA from unwinding and
duplicating.
Streptomycin is an antibiotic (antimycobacterial)
drug, the first of a class of drugs called aminoglycosides. It is derived from
the actinobacterium Streptomyces griseus. Streptomycin is a protein
synthesis inhibitor. It binds to the small 16S rRNA of the 30S subunit of the
bacterial ribosome, interfering with the binding of formyl-methionyl-tRNA to
the 30S subunit. This leads to codon misreading, eventual inhibition of protein
synthesis and ultimately death of microbial cells through mechanisms that are
still not understood. Speculation on this mechanism indicates that the binding
of the molecule to the 30S subunit interferes with 50S subunit association with
the mRNA strand. This results in an unstable ribosomal-mRNA complex, leading to
a frameshift mutation and defective protein synthesis; leading to cell death.
Vancomycin is of the glycopeptide antibiotic
class and is effective mostly against Gram-positive bacteria. Vancomycin acts
by inhibiting proper cell wall synthesis in Gram-positive bacteria. The large hydrophilic
molecule is able to form hydrogen bond interactions with the terminal
D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Under normal
circumstances, this is a five-point interaction.
Q 8. Absorption of oral iron preparation can
be facilitated by co-administering:
A. Antacids
B. Tetracyclines
C. Phosphates
D. Ascorbic Acid
Ans. D. A higher
bioavailability of the dietary iron can be achieved by increasing the content
of food components enhancing iron absorption (ascorbic acid, meat/fish) or by
decreasing the content of inhibitors (e.g., phytates, tannins). The key role of
ascorbic acid for the absorption of dietary nonheme iron is generally accepted.
The reasons for its action are twofold: (1) the prevention of the formation of
insoluble and unabsorbable iron compounds and (2) the reduction of ferric to
ferrous iron, which seems to be a requirement for the uptake of iron into the
mucosal cells.
It is often recommended to individuals who
have iron deficiency (anemia) that they take their iron supplements with orange
juice. This is because the vitamin C in the orange juice aids in iron
absorption. When vitamin C, also known as ascorbic acid, enters the stomach it
mixes with the iron supplement that contains non-heme iron. The ascorbic acid
is able to reduce iron from its non-heme form to a form called ferric iron. The
ferric iron then leaves the stomach and enters the small intestine. Iron
absorption in the small intestine is able to occur because the iron is in this
ferric form. Ferric iron has a low pH, which enables the mucous cells of the
small intestine lining to take up the iron. If it wasn't for the vitamin C
converting non-heme iron into ferric iron, the iron would pass through the body
and not be absorbed.
Q 9. Interferon is used in :
A. Hepatitis B
B. AIDS
C. Both A and B
D. None
Ans. C, Interferons (IFNs) are proteins made
and released by host cells in response to the presence of pathogens such as
viruses, bacteria, parasites or tumor cells. They allow for communication
between cells to trigger the protective defenses of the immune system that help
eradicate pathogens.
IFNs belong to the large class of
glycoproteins known as cytokines. Interferons are named after their ability to
"interfere" with viral replication by protecting cells from virus
infection. IFNs have other functions: they activate immune cells, such as
natural killer cells and macrophages; they increase host defenses by
up-regulating antigen presentation by virtue of increasing the expression of
major histocompatibility complex (MHC) antigens. Certain symptoms of
infections, such as fever, muscle pain and "flu-like symptoms", are
also caused by the production of IFNs and other cytokines.
More than twenty distinct IFN genes and
proteins have been identified in animals, including humans. They are typically
divided among three classes: Type I IFN, Type II IFN, and Type III IFN. IFNs
belonging to all IFN classes are important for fighting viral infections and
for the regulation of the immune system.
Q 10. Foscarnate inhibits viral:
A. DNA polymerase
B. Revese transcriptase
C. Both A and B
D. None
Ans. C, Foscarnet is the conjugate base of
the chemical compound with the formula HO2CPO3H2.
This phosphonic acid derivativeis an
antiviral medication used to treat herpes viruses, including drug-resistant
cytomegalovirus (CMV) and herpes simplex viruses types 1 and 2 (HSV-1 and
HSV-2). It is particularly used to treat CMV retinitis. Foscarnet can be used
to treat highly treatment-experienced patients with HIV as part of salvage
therapy.
Foscarnet is a structural mimic of the anion
pyrophosphate that selectively inhibits the
pyrophosphate binding site on viral DNA polymerases at
concentrations that do not affect human DNA polymerases.
MOA: inhibits viral DNA polymerase, RNA
polymerase and HIV reverse transcriptase directly without requiring activation
by phosphorylation -IV use only -large nephrotoxicity -very good against CMV,
herpes simplex and pts w/ acute flairs of HIV -second-line drug for CMV
retinitis, colitis, pneumonitis, esophagitis, as well as acyclovir resistant
VZV and HSV infections in immunocompromised pts
