bio questionxxx

[hassam]

whats the link of long latency stage of TB and HIV with the difficulty in controlling these diseases?
sloths feed on leaves...they contain bacteria in their stomach that can digest cellulose...suggest advantage of this to sloth
why the programme to eradicate smallpox was successful

 

[aislam17]

Smallpox virus was stable. So therefore only one vaccine had to be administered. Smallpox patients were easy to identify. It did not infect animals. Virus did not linger in the body. Vaccine was freeze dried and could be kept at high temperatures. Vaccine was amde from harmless strain of similar virus. As leaves contain a high amount of cellulose, it needs to be broken down so therefore the bacteria in the stomach of the sloths do this job. And for your first question I think the link is that since HIV attacks T helper lymphocytes and their number are low therefore the AIDS pandemic allows the resurgence of TB virus which lingers in the body for a long time.

 

[hassam]

well..in first question...i thought like this...
latency stage means the period during which the virus or bacterium just stays in body and remains dormant i.e doesn't cause symptoms of disease and also does not cause production of antibodies in case of AIDS....SO symptomless carriers will be spreading the disease....and there ll be difficulty in testing people for HIV status since the test for HIV identifies whether the antibodies to virus have been produced or not...
but i dont know whether m ryt or wrong,.....
secondly i have to ask more questionsss
Q1. what are the problems with vaccines for TB....the vaccine has been there from 1921 but the disease is still there...why

 

[hassam]

 

[hassam]

well i can only think of dissolving point by forming hydrogen bods to polar or charged molecules......but this is for 4 marks....what other points i shud be writing

 

[hassam]

what is meant by DEGENERATE code...? any one explain me this

 

[hassam]

Describe how tar, deposited in the lungs from cigarette smoke, can lead to emphysema? (4)
i know that phagocytes come out of capillary to linnig of respiratory tract by releasing enzyme elastase...but what does it has to do with tar....do not they come because of bacteria that are breeding on respiratory lining....?

 

[hassam]

libra94...hamid ali....anyone help me out

 

[farrukh]

degenerate code means that many different triplet codons can code for the same amino acid.......
in the water question u can tell about the strenght of hydrogen bonds so the heat capacity of water is high and temperature changes are less..
u can also tell about surface tension and cohesion that help in transport of water in plants..

i dunno about that tar question...

 

[princesszahra]

u have to explain about the polarity, net dipole, formation of hydrogen bonds,
movement of water as a bulk transport ie water moves as a single body!

 

[Amna]

for how tar deposited in the lungs can lead to emphysema:
tar can inhibit the cleaning action of the respiratory pathway. it stimulates the goblet cells to make more mucous, cilia get paralyzed, goblet sells swell up, epithelial layer is replaced by fibrous scar tissue, smooth muscles become thicker, airways get blocked with mucous. this causes smoker's cough or chronic bronchitis. chronic bronchitis then leads to emphysema: there's inflammation, bronchi are prone to infection, so macrophages come to site. they secrete elastase to digest the elastin to reach the alveolar surface, normally this "digestion" is checked by elastase inhibitors, but smokers don't have much of the inhibitor, so elastin is lost, alveoli can't recoil as much, there's a build up of pressure, bronchioles collapse, air traps in alveoli, alveoli burst. which equals emphysema.

so basically you just have to make the connection between tar and chronic bronchitis, then link that to emphysema. that many details aren't really required. i know them because the more details i try to remember, the more chance i'll retain something of it on the exam day

 

[hassam]

WELL THANKS U reminded me of a powerful tool to answer questions....making links....well cn u tell me abt COMBINATION therapy for tuberculosis

 

[hassam]

why is their inflammation of bronchial lining

 

[hassam]

i am posting all reasoning questions i remember here....will help all of us on the nyt of 17...
describe the role of elastin in alveoli
why is it difficult to control hiv
why some people show poor response to TB vaccine
describe how tar in smoke can cause lung cancer
why transpiration is considered an inevitable consequence of gas exchange
describe ho plant in fig. is adapted for reducing water loss
what are adaptations of xylem/phloem
how water moves from root to leaves through xylem
how sucrose is loaded at source\
describe the role of tRNA In transcription
why is it important that an exact copy of dna is made during replication
graph...describe and explain how pH,Temp influences activity of enzyme
suggest how .....may inhibit following enzyme
explain why it is difficult to develop vaccine against malaria
explain distribution of malaria i.e why it is only restricted to tropics

 

[workinghard]

Describe how tar, deposited in the lungs from cigarette smoke, can lead to emphysema? (4)
i know that phagocytes come out of capillary to linnig of respiratory tract by releasing enzyme elastase...but what does it has to do with tar....do not they come because of bacteria that are breeding on respiratory lining....?

it is basically linked with chronic bronchitis and
well it goes like this...
The importance of cigarette smoking as a risk factor for developing emphysema cannot be overemphasized. Cigarette smoke contributes to this disease process in two ways. It destroys lung tissue, which results in the obstruction of air flow, and it causes inflammation and irritation of airways that can add to air flow obstruction.


Destruction of lung tissue occurs in several ways. First, cigarette smoke directly affects the cells in the airway responsible for clearing mucus and other secretions. Occasional smoking temporarily disrupts the sweeping action of tiny hairs called cilia that line the airways. Continued smoking leads to longer dysfunction of the cilia. Long-term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages. Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract. Furthermore, smoke causes mucous secretion to be increased at the same time that the ability to clear the secretions is decreased. The resulting mucous buildup can provide bacteria and other organisms with a rich source of food and lead to infection.


The immune cells in the lung, whose job it is to prevent and fight infection, are also affected by cigarette smoke. They cannot fight bacteria as effectively or clear the lungs of the many particles (such as tar) that cigarette smoke contains. In these ways cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the inflammation caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells.


Over time, enzymes released during this persistent inflammation lead to the loss of proteins responsible for keeping the lungs elastic. In addition, the tissue separating the air cells (alveoli) from one another also is destroyed. Over years of chronic exposure to cigarette smoke, the decreased elasticity and destruction of alveoli leads to the slow destruction of lung function.

hope it helps!!!!

 

[Amna]

inflammation of the bronchial lining occurs cuz tar's an irritant... so when it gets deposited on the lining, causes irritation/inflammation...

for the combination treatment for TB: combination therapy is when more than one drugs (= combination of drugs) are used to treat TB. the reason that more drugs are used at the same time is that the are a lot of mutant varieties of the TB-causing bacteria of which some are resistant to one drug... others are resistant to some other drug... meaning if "bacteria1" is resistant to "drug1" and "bacteria2" is resistant to "drug2", both drugs 1&2 are given to the patient... so "drug1" can take care of "bacteria2" and "drug2" can take care of "bacteria1"... so there are no bacteria left in the patient's body, so no re-infection due to drug resistant varieties... and no infecting other people after treatment...

that's an oversimplification though, cuz there are multiple drug resistant varieties of bacteria too... so u need like a lot of drugs. i think four are used these days in the "direct observation treatment shortcourse" implemented by WHO in which patient are kept under observation to make sure they take the drugs. isoniazid and rifampicin are two of them, but you don't need to remember the names i think...

 

[hassam]

yeah I remember that DOTS scheme and isoniazid......there is one more point which i read recently.....mycobacteria are slow growing and much less sensitive to drugs being used to kill it so a combination of drugs used over a long period of time reduces the risk of leaving out a reservoir of infection and destroys all the bacteria......thanks

 

[Amna]

hmm yeah makes sense and also because mycobacteria breed intracellularly or something so drugs aren't effective there... but i really didn't get that part...

 

[hassam]

why is it difficult to control aids......?

 

[Oronkira]

Describe how tar, deposited in the lungs from cigarette smoke, can lead to emphysema? (4)
i know that phagocytes come out of capillary to linnig of respiratory tract by releasing enzyme elastase...but what does it has to do with tar....do not they come because of bacteria that are breeding on respiratory lining....?

Tar deposits form on the lining of the ciliated epithelium in the airways. May also lead to inflammation of the lungs. Mucus is secreted in excess to capture this tar and cilia cannot beat and move it up the larynx to be swallowed. White blood cells(phagocytes) present in the airways attack the bacteria and dust but also secrete the enzyme elastase which destroys the elastic fibres of alveoli causing them to shrink and burst. Air spaces are left in the lungs, reducing surface area for gas exchange and leading to emphysema. Shortness of breath is one of the symptoms.

Something like that