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UWorld Questions

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SLOW ONSET OF ACTION

Before gas anesthetics can reach the brain, they must move through air -> lungs -> blood -> brain... Anesthesia occurs when enough has reached the brain.

AV conc gradient is difference b/w arterial and venous blood. If more soluble in peripheral tissues, then higher gradient. Means a lot of arteriolar delivered is taken up so low venous... As a result, saturation of blood requires further absorption of anesthetic in order to replace that which is absored in peripheral tissues... Since blood saturation is taking longer so brain saturation is slower onset.

In contrast, anesthetics w/ low peripheral solubility will have small AV gradients as there is less peripheral tissue uptake. Less anesthetic is required to replace the amount absorbed in peripheral tissue so blood saturation occurs quickly

Potency is determined by minimal alveolar concentration for 50% of patients to not realize they are being exposed to noxious stimuli. Potent anesthetics have low mAC. AV gradient influences rate of induction not anesthetic potency!!!

Inhaled air is determined by partial pressure of anesthetic... When air partial pressure equilibrates the blood, tissues are said to be saturated

Lungs (pulmonary ventilation rate) rate of rise of gas tension in alveoli is directly proportional to depth and rate of respiration

Blood... Solubility... higher means more anesthetic must be absorbed by blood to work effectively

Target organ.. solubility in peripheral tissues negatively affects brain saturation.
B cell precursors proliferate and mature in bone marrow... Then leave the BM and migrate to lymphoid organs and peripheral tissues where they are exposed to antigens..

On first exposure, new antigen, a clone of B cells becomes activated... Some differentiate into short lived plasma cell and release IgM through a T cell independent response

Most mature B cells though, migrate to lymphoid follicles located in lymph node cortex to undergo germinal centers. A portion of these activated B cells form long-lived memory cells that remain dormant in lymph node until next encounter with the same antigen, but majority transform into antibody-secreting plasma cells.

Isotype switching (IgM to others) occurs in germinal centers late in primary response... providing activated B cells the ability to produce antigen-specific antibodies of differing isotypes...

Heavy chain constant reigons are isotype specific and distinguish the 5 GAMED... While variable regions are antigen specific...

Light chains are antigen specific and do not determine the isotype...

Isotype switching first required CD40 on activated B cell to bind CD40L on (CD154) activatedT cell.. Afterwards the isotype switching and genetic rearrangement of heavy chain constant regions occurs... THis is mediated by cytokines... IgG response or IgA response at mucosa from here on out.

~~VDJ heavy and VJ light chains occurs via DNA rearrangement... After undergoing immunoglobulin rearrangement, each B cell makes antibodies of a single specificity. High variety... Recombo here occurs during B cell maturation w/in the bone marrow. Affinity maturation occurs in germinal centers w/ somatic hypermutation.
T lymphocytes are initially produced in the bone marrow, but migrate to mature during the first trimester of gestation in the thymus. In the thymus, TCR gene rearrangement, positive selection, negative selection, and expression of EC membrane markers/co-stimulatory molcls occurs.

Pro-T cells arrive at the thymus as "double negative" cells = indicating they lack CD4/CD8 and their differentiation in the subcapsular zone. Next, the process of TCR beta gene rearrangement occurs w/ simultaneous expression of both CD4 and CD8. Once in the thymic cortex, the alpha genes rearrange to produce a functional alpha=beta TCR.

Positive and negative selection occur w/ cells that fail either of the following two tests

1) Positive... T cells expressing TCR that is able to bind self MHC are allowed to survive. Those expressing a TCR that is not specific for MHC are eliminated. This occurs after TCR DNA rearrangement and prior to negative selection. It occurs in the thymic cortical epithelial cells (expressing self MHC). Positive selection is responsible for T cell recognizing self as normal

2) Negative... T cells w/ TCRs that bind w/ high affinity to self antigen or self MHC class 1/2 are elminiated. Occurs in the thymic medulla and involves interaction of developing T cells w/ thymic medullary epithelial and dendritic cells. This serves to eliminate T cells that may be autoreactive against self antigen. Prevents autoimmunity.

**Affinity maturation is enhancing the hypervariale reion antigen binding affinity after initial binding of an antigen to membrane-bound immunoglobulin on a naive B lymphocyte and subsequent migration of that B lymphocyte to a lymph node. W/in germinal center, B lymphocyte somatic hypermutates where DNA coding for immunoglobulin variable chain is mutated randomly at a high rate. THen sees how well it binds antigen. This selects for good binding. Does not occur in T cells.

**TCR DNA rearragnement is complex 10^15 possible antigen bindign sites out there. Join V,D,j,C regions of TCR and processes of junctional flexibility, N and P region NT addition, alternative joining of genes and mutlipe peptides. Matur eRCR