Vasculature Path...

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rpbardoul
Mind Map by rpbardoul, updated more than 1 year ago
rpbardoul
Created by rpbardoul about 9 years ago
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Resource summary

Vasculature Path...
  1. 1) This is composed of arteries, veins, capillaries and lymphatics. The composition of each is similar (differences in the relative thickness)
    1. 3 layers... 1) Intima which is continuous with the endo (fibrous CT and single endo layer), 2) Media- concentric bands of muscle, 3) Adventitia- stabilises
    2. In normal BV's it is the ENDOTHELIAL cells which prevent platelet adhesion. Secretes comps that prevent the CC and act as vasodialtors (hist)
      1. Vessel damage (endo) prevents this and initiates the CC!
        1. Haemostasis- four stages, advanced by the subendothelium exposure
      2. 3) Aneurysm and rupture
        1. any outpouching of the arterial wall after reduction in the wall strength (particularly the aventitia). They are rarely detected prior to causing death but may show CS's relating to surouding compression of organs/tissue
          1. Strongylus vulgaris in horses, idiopathic turkeys and cu deficiency in pigs
        2. 2) Arterial ruptures
          1. Usually follows trauma but ca occur idiopathically in horses/ dogs following exercise
          2. Arterial thrombosis
            1. Virchows triangle- A thrombus is an intravascular blood clot
              1. Animals commonly develop them due to an altered blood flow, yet endothelial damage is the main issue. Common: valvular damage, cardiomyopathies, CHF which slows the blood
                1. Most arise in the atria- travel to the coronary (myocardial infarct), iliacs (saddle) and renal arteries
                  1. These are due to an UNDERLYING issue which needs to be identified...
                    1. Recall the other causes of thrombo-embolism: Fibrocartilage, gas, septic endocarditis- adipose from limb fx, strongylus vulagris nfx
                2. Artherosclerosis...
                  1. The deposition of liquid within the intima of BV, common in ppl but only found in parrots/ hypothyroid dogs (usually without CS's)
                  2. Calcification
                    1. Variety of animals- Johnes in cattle- hose pipe aorta. In others: CKD or choleciferol toxicity
                    2. Fibrinoid Necrosis
                      1. This is an uncommon condition in all except pigs/ chickens due to Se deficiency.
                        1. Dogs and cats can develop this - gastric and oral BV's are effected due to uraemia (^creatine/urea) associated with renal faiure.
                      2. Infectious Arteritis
                        1. BACTERIAL
                          1. Erysipelas
                            1. This can effect all animals but particularly pigs and turkeys- thrombosis + infarction due to vascular damage. Pigs develop diamond shape lesions
                              1. Diamond skin lesions
                            2. PARASITIC
                              1. Strongylus Vulgaris- uncommon in NZ but ca cause a mesenteric arteritis- aneurysm/ infarction
                                1. Dirofilaria Imminitis
                                  1. This is rare in NZ but is found in North America and Australia, arteritis, CHF and pulmonary embolism
                                2. This is the result of endothelial damage and can be the result of various infectious diseases
                                  1. VIRAL
                                    1. FIP
                                      1. This is NOT a Peritonitis, NOR infectious... Its a vasculitis with only 50% having a peritoneal involvement
                                        1. In a small # of cats the ubiq FICV will mutate into FIP, escape the git and enter the bloodstream causing a generalised vasculitis. Protein rich fluid enters the body cavities (including peritoneum)
                                          1. The endothelial damage causes thrombosis, infarction. The organs effected depend on localised area- hepatic + renal most common. 25% have a CNS vasculitis sign only
                                            1. The PM signs depend on the severity of the BV damage- wet vs dry. Fibrin accumulates as multiple white foci (immune complex mediated)
                                              1. WET: FNA and cytology will show up N0 and "scaling" The transudtae that is aspirated is yellow, turbid, has a low cellular, high protein content and clots rapidly
                                                1. DRY: this is a common cause of death in NZ cats and should be suspected in any "unknown cause of fever". UBiq nature of dz makes interpretation difficult. Biopsy and histo are the only DD
                                        2. MCF
                                          1. There are two forms of this; OHV associated is the one that causes dz in NZ cattle. In a small % the lymphcyte suppressors are damaged, allowing Lymphocytes to cause damage
                                            1. Generalised vasculitis causes variable signs- Corneal oedema, GIT upset are the most common. Oral ulceration, crusting lesions, and at times ulceration of the C.band
                                              1. Histo: Lymphocytic inflam and BV degeneration
                                            2. Bad temper!
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