Pathophysiology

Rapid atrial tachycardia outside normal locations. Can be caused by a reentry of a rythm in the right atrium

Sawtoot pattern instead o P-Wave. QRS may be normal or abnormal

Uncoordinated contraction of atria. Occurs when cells in atrium can not repolarize in time before next stimulus. QRS appears irregularly due to blocked random conduction through AV-node

extra heartbeat in the ventricles that disturbes the normal rythm.

An obvious QRS wave might be missing or much smaller, but an additional (wrong timed) QRS can maybe be seen

Ventricular rate ov 70-250 beats/min. Wide, tall and bizzare looking QRS. Can be uniform and randomly.
Dangerous because it eliminates atrial filling and thus reduce CO significantly

Severe derangements of cardiac rhythm. ECG looks sine-wave-like with fast oscillation rates (150-300).

Dangerous because ventricular filling is disturebed and CO decreases significantly

The hosts immune system must recognize the graft as "self" and not as "non-self". This depends on the MHC (major histocompability complex) molecules or HLA (Human leukocyte Antigens) expressed on the surface of cells (T- and B Lymphocytes destroy unfamiliar ones).

Autograft: Donor is also the Recipient (same person)
(Synergenic: Donor and recipient are idendtical twins)
Allograft: Donor and recipient are unrelated but same species
Xenograft: Donor and recipient are different species

Complex but coordinated cell mediated and antibody mediated immune response.
 

Cellular rejection: T-cell mediated, initiated by presentation of antigens to host T lympocytes and macrophages. Most antigens are presented by MCH (Major histocompatibility complex) molecules and T-cells transform into CTL (Cytotoxic t Lymphocytes) that kill graft tissue. CD4+ or T helper cells recognize MHC II and secrete cytokines that incluence almost all immune cells.

Antibody rejection: B-lymphycyte proliferation and differentiation into plasma cells that produce donor specific antibodies. Acute (within days) or hyperacute (immediately after vascular reperfusion)

Chronic rejection: Immune medaiated inflammatory injury to a graft that occurs over a prolonged time

Antibody: Y-shapaed protein used by immune system to inddentify and neutralize foreign objects. The antibody recognizes a uniqe molecule of the pathogen.

Antigen: Unique molecule of the pathogen

Abnormality in one or more parts of the immune system that result in increased susceptibility to diseases (which could normally be eliminated). Can be primary or secondary (aquired later in life)

Primary: Congenital or genetically inherited. Mostly by genetic mutations that affect signaling pathways (e.g. cytokines) that dictate immune cell development/function

Secondary: Use of certain drugs or another disorder such as cancer, or Human immunodeficiency virus (HIV)

Primary humoral: Most common, affects B-cell differentiation and antibody production

Primary cell mediated: T-cell mediated are most severe. Results from defective T-cell receptors and defective T-cell activation

Humoral: Affects B-cell differentiation and antibody production. Immature B-cells express antibodies, which undergo a switch after stimulation and loose surface antibodies and express other antibodies. Can interrupt the production of all or none antibodies

Cell mediated: Defective T-cell Receptors, cytokines production and defects in t-cell activation. Reduces numer of lymphocytes including T,B,NK-cells and depressed T-cell response to antigen stimulation

Can also occure combined

Depend on degree of immune system dysfunction.
Generally more prone to diseases and infections. Humoral leads to less resistance against influenza and gram-negativ organisms. Cell mediated to impaired response to viruses

1. Immediate Hypersensitivity Disorder
2. Antibody mediated disorders
3. Immune complex mediated disorders
4. Cell mediated hypersensitivity disorder

Immediate Hypersensitivity Disorder:
IgE (immunoglobulin E, Antibody) mediated, classic allergic response (antigen are referred to as allergens). Provoked by re-exposure to specific antigen/allergen.
Key role of type 2 helper T-cels (T2H) and mast cells (basophils). 1. mast cell degranulation -> vasodilation, smooth muscle contraction 2. inflammatory response (cytokine release), leukocytes migrate to site of allergene -> intense infiltration wiht inflammatroy cells -> tissue destruction

Local allergic reactions, sneezing, itchin, watery nose. If severe can lead to anaphylaxis (flood of chemicals leads to shock) which is life threatening.

Antibody mediated disorder:
Hypersensitivity reaction mediated by IgG (Immunoglobulin G, Antibody) or IgM, directed against target antigens on specific host cell surfaces of tissues (part of cell or incorporated after exposure to infectious agent).
Clinical manifestations depend on tissue that expresses target antigen. 

Immune complex mediated disorders:
Caused by formation of antigen antibody immune complexes (IgG, IgM) in blood. Deposition of those in tissue  activates complement system and iniciate massive inflammatory response. 
Comaring to type 2. here the complexes forme in the plasma and only then go to tissue.
Clinical manifestation depend on location but always inflammation that leads to tissue injury

Cell mediated hypersensitivity disorder:
Cell mediated and delayed (rather than anti-body as the other ones), hypersensitive T-cell mediated. Divided in 4 subtypes:

4a. CD4+ T1 helper cells activate monocytes and macrophages, those stimulate antibodies and proinflammatory response
4b. T2H helper cells activation and eosinophilic infiltration of tissue. T2H cells secrete cytokines that activate mast cells and stimulate production of antibodies
4c. involves recruitment and activation of neutrophils by T-cells
4d. cytotoxic response mediated by lymphocytes (CD4+ and CD8+)

Group of disorders that occur when bodys immune system fails do differ self from non-self (immunologic response to host tissue).
Can affect any cell type or organ, but some disorders are tissue specific

The capacity of the immune system to differentiate self from non-selfe.  Consists of two coordinated processes:
Central tolerance: eliminate autoreactive lymphocytes during maturation
Peripheral tolerance: Suppression of autoreactive lymphocytes that have escaped destruction in thymus

(Autoreactive = acts against itself)

Can be triggered by environmental or genetic factos. May also be triggered by infections

Depends on affected organ/s.
Tissue damage, alteret growth and function.

Diabetes Mellitus type 1, Graves disease (overproduction of thyroid hormones), Addisons disease (not enough of certain hormones) and multiple sclerosis (immune system attack myelin of nerves)

Inflammation is a reactoin of vascularized tissue to injury. Characterized by inflammatory mediatiors. Usually localizes and eliminates microbes, foreing particles, abnormal cells.

commonly named by adding suffix -itit to affected organ/system

Redness, swelling, heat, pain and loss of functions

Other signs such as fever may apper as chemical mediators (cytokines) are produced

Multiply factors, such as duratoin of insult, typre of foreign agent, degree of injury, microenvironment

Acure inflammation: short time, characterized by outflux of fluid and plasma components and leukocytes in extravascular tissues

Chronic inflammation: longer duration and associated with presence of lymphocytes, macrophages. Proliferation of blood vessels. Fibrosis and tissue necrosis (death of tissue)

Vascular phase: increased blood flow

Cellular stage: migration of leukocytes

Many different ones!

Endothelial cells (line blodvessels), connective tissue cells (mast cells, fibroblasts, macrophages, lymphocytes) and components of ECM (collagen, elastin)

Inflammatroy cells include: Edothelial cells, basophils, neutrophils, eosinophils, platelets, mast cells, macrophages, monocytes, fibroblasts, elastin, collagen, proteoglcan filaments

Changes in small blood bessels at site of injury. Begins with vasoconstriction followed by vasodilation -> increased blood flow (heat, redness) and vascular permeability (proteinrich fluid pours out and produces swelling, pain)

Leukocytes migration to site of injury to perform phagocytosis. Endohelial damage starts recruitment of leukocytes, the slowed down blood flow at injury helps with migration into tissue and along chemotaxins to the site of injury.
Start of phagocytosis and cell killing once leukocytes are at site of injury