>Would person with AIDS need to take immunosupressants for transplated organs?

Well, it's complicated.

First of all, AIDS is the acquired immunodeficiency syndrome. The HIV virus (human immunodeficiency virus) will, if untreated, eventually result in AIDS. People with AIDS are at very high risk for all sorts of infections, and if the HIV doesn't get treated, and if prophylactic antibiotics are not used, then they will ultimately die, often from infection, cancer, or both.

So if you have AIDS (as opposed to being HIV positive without immunodeficiency), you are at very high risk for serious problems, and you would not be a candidate for any kind of elective surgery, and certainly not a major surgery like an organ transplantation.

Until recently, even having HIV was generally a contraindication to getting an organ transplant. Because people with HIV have shorter lifespans, and because of the need for lifelong immunosuppressive medications, it was not thought that it was either a good use of limited resources, plus there is a risk that immunosuppressive medications could strongly interfere with HIV treatment.

Recently, some transplant centers have begun organ transplantation in HIV-positive patients. But we don't know whether this is going to result in longer lives for HIV-positive patients, as there could be worsening of HIV and the development of AIDS.

Now to specifically answer your question: no one really knows what to do in a situation like an HIV-positive patient with an organ transplant who develops AIDS. It's a no-win situation, and the person might well develop serious infections, organ rejection, or both.

First of all, people do not become resistant to antibiotics. Bacteria become resistant to antibiotics.

Basically, exposure to antibiotics can cause bacteria to evolve, as the bacteria that are not resistant are killed, and those that are survive. (Some bacteria have a way to share genes through a DNA structure called a plasmid, and antibiotic resistance can be passed along that way as well).

So the skin and the gastrointestinal tract are covered / filled with bacteria. If your bacterial microbiome has resistant bacteria in it, and you develop an infection from one of these bacteria, then the standard antibiotics might not work.

What does the doctor do?

Often, when treating a bacterial infection, the physician will obtain a test called a "culture and sensitivity". They take infected material (such as urine, pus, or sputum) and try to grow the bacteria that is causing the infection. After the lab grows it, then it can be identified through a series of tests (gram stain, for example). Once the bacteria is grown and identified, then they check sensitivities to antibiotics.

Sensitivity checking involves growing the bacteria again under new circumstances. Basically, a series of small paper discs impregnated with various antibiotics are placed on the Agar plate where they are growing the bacteria. By measuring the distance at which the bacteria can grown close to each disc, they can tell if the bacterium is likely to be sensitive or resistant to a particular antibiotic. Then the physician selects an appropriate antibiotic.

>my understanding that vasoconstriction means the same amount of blood flows through a smaller opening, thereby INCREASING blood pressure.

No. Let's look at a simple model of circulation:

There is a certain amount of pressure in the arterial system. Overall, the pressure is determined by the cardiac output, the amount of blood, and the vascular tone. If you change any of these variables, then you change the pressure in the system. If you constrict ALL of the blood vessels, then you could increase the overall pressure.

But in an injury, there is localized vasoconstriction in the arterioles proximal to the injury. Let's hold the other variables the same in this simplified model.

The cross section of the arteriole proximal to the injury is reduced. The pressure of the system as a whole is unchanged. Thus the VOLUME OF BLOOD passing through the constricted arteriole is smaller, and the pressure AFTER THE CONSTRICTION is reduced.

One of the things that is important to remember is that, while we talk about the arterial system as having a specific pressure, the "blood pressure", it does not have one pressure! In fact, for blood to flow (or any liquid to move in a system of pipes), there must be a pressure differential! The pressure of blood in the thoracic aorta is higher than the pressure of the blood in the peripheral arteries, or the blood does not move. The system is constantly adjusting the resistance of the arterioles to manage how much blood is sent here or there depending on need.

>both levocetirizne and fexofenadine are classified as second generation.

No.

Third generation antihistamines are metabolites or enantiomers of second generation antihistamines.

Levocetirizne is the L-enantiomer of cetirizine. Fexofenadine is a metabolite of terfenadine, another second generation antihistamine. They are third generation by definition.

>Which drugs are first gen and second gen antihistamines?

Commonly used 1st generation antihistamines include diphenhydramine, hydroxyzine and doxylamine.

Commonly used 2nd generation antihistamines include cetirizine and loratadine.

There are 3rd generation antihistamines as well, such as levocetirizne and fexofenadine. These may have even better efficacy and fewer side effects than the 2nd.

And is there a reason to take first gen at all if second gen exists now?

Because 1st generation antihistamines cross the blood-brain barrier, they have more effects. When we are treating allergic symptoms we call these effects "side effects" or "adverse effects". However, we might utilize these effects intentionally -- these drugs can reduce nausea, reduce anxiety, cause sedation, dry up secretions, reduce intestinal spasms, reduce the side effects of other medications. They are very useful in many clinical contexts.

>Are first generation better for anxiety?

1st generation are often prescribed of anxiety or insomnia because of the sedating effect. Second generation antihistamines are much less sedating, and would likely not be suitable for these uses.

>Not just that, the second generation antihistamines are generally first line for anything where an actual antihistamine would be required,

This is generally true. The exception would be in patients for whom oral medications are not optimal, such as those with nausea and vomiting or with severe allergic reactions -- some 1st generation antihistamines are available in parenteral formulations, whereas, to the best of my knowledge, 2nd generation antihistamines are only available in oral form.

>Are 1st gen safer ? wich do you reccommend ?

While I cannot recommend a specific medication for anyone (an interview, physical exam, and review of current and past medical issues is necessary before any such recommendations), in general, second-generation antihistamines such as cetirizine, fexofenadine, and loratadine are the first-line recommendations for symptoms of allergic rhinitis, as the side effects (such as sedation) are much less pronounced than the first-generation medications.

First generation antihistamines (i.e diphenhydramine) cross the blood-brain barrier, and thus can affect the brain directly. While we call them "antihistamines" because they affect histaminergic receptors (which are responsible for allergic reactions , among other things), they also have other effects, such as blocking cholinergic receptors. The overall effect on the brain is sedating.

Second generation antihistamines were designed not to enter the brain as easily, and thus the brain effects, such as sedation, seen commonly in first-generation antihistamines are much less pronounced.