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Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Thrombi may be formed anywhere in the circulation, either in the capillaries, arteries, veins, or chambers of the heart. They are usually attached to the endothelial surface of the vessel or to the lining of the heart. A mural thrombus adheres only to one side of the vessel and the blood continues to flow past the thrombus. However, if the entire lumen of the vessel is sealed by the clot, the ensuing occlusive thrombosis leads to a complete cut-off of the blood supply to the tissue. Thus depending on the importance of the thrombosed vessel, this event will lead to the death of the organ. This process is the infarction which occurs after extensive thrombosis or embolus blocking the circulation in an end artery. Sometimes diffuse clot formation of small vessels throughout a whole organ can have fatal consequences. This situation occurs frequently in patients with bacteremia, as they stimulate the process of an extensive blood coagulation. Consequently, in organs such as the kidney or the lung, the microcirculation becomes plugged with clots causing a sudden loss of supply vital constituents and subsequent immediate deterioration of function. If the diffuse, multiple thrombosis is severe and involves the greater part of an organ, the patient may die from shock.
More about balloon angioplasty: Keeping out of trouble
Published in Peter A. Schneider, Endovascular Skills: Guidewire and Catheter Skills for Endovascular Surgery, 2019
Spasm is not much of a clinical issue at the balloon angioplasty site. More commonly, it may be considered as a possibility in the outflow bed for an angioplasty site or in a neighboring segment of the artery being treated. If the operator is unable to visualize the end artery or outflow vessels, it may be due to poor technique, low flow, thrombosis, embolization, dissection, or spasm. Spasm should only be accepted as a diagnosis if the other possibilities have been ruled out. Be sure that an adequate bolus of contrast was delivered and that the concentration was appropriate. Check to see if there are reasons for a low-flow state. The usual setting where this comes up is in the course of an endovascular intervention when an area of the outflow can no longer be visualized or appears substantially different from the preintervention arteriogram.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
The outcome of ischaemia is determined by a variety of factors: The nature of the vascular supply (the most important factor). The presence of collaterals is protective against the effects of ischaemia. Conversely, blockage of an end-artery will almost always cause infarctionThe tissue involved. The brain and heart are more susceptible to the effects of hypoxiaThe speed of onset. Slowly developing occlusions are less likely to cause infarction since they provide time for the development of alternative perfusion pathwaysThe degree of obstruction and the calibre of the vessel occludedThe oxygen content of the blood supplying the ischaemic tissueThe presence of concomitant heart failureThe state of the microcirculation, as in diabetes mellitus
Nonthrombotic proliferative vasculopathy associated with antiphospholipid antibodies: A case report and literature review
Published in Modern Rheumatology, 2019
Jeong Seok Lee, Hyojin Kim, Eun Bong Lee, Yeong Wook Song, Jin Kyun Park
The majority of the reported cases had a poor outcome with death or permanent organ loss (amputation of the affected extremity in cases 1 and 2). This is contrasted by the relative good outcome in our patient. One possible explanation is that, his NTPV-aPL was confined to few pulmonary arteries. Since pulmonary circulation has a large functional reserve, occlusion of few arteries would not result in a life-threatening infarct. By contrast, involvement of end artery such as peripheral or intestinal arteries without collateral circulation would lead to critical ischemia with permanent organ loss or death. A delay in diagnosis could be a reason for the poor outcome of NTPV patients because this disease entity might be under-recognized. Since the pathophysiologic process is poorly understood, an effective treatment has not been defined to date. In classical APS, aPL bind to and activate endothelial cells, leading to the activation of a coagulation cascade with subsequent thrombus formation. Consequently, anticoagulation therapy has proven effective [1].
The Sub-Phenotypes of Sickle Cell Disease in Kuwait
Published in Hemoglobin, 2019
Adekunle D. Adekile, Sondus Al-Sherida, Rajaa Marouf, Nada Mustafa, Diana Thomas
The sickle cell disease clinical phenotype is, however, very heterogeneous, and the identified genetic modifiers include Hb F level, βS-globin gene haplotype and coexistent α-thalassemia (α-thal) trait [5]. It has been estimated that a patient with ≥20.0% Hb F will have a mild phenotype and less end-organ pathology [6]. Patients with the Arab/India haplotype carry the HBG2 –158 (C>T) XmnI allele, which is associated with a high Hb F expression, and are therefore protected against some of the complications of the disease [7]. Some other trans-acting quantitative trait loci influencing Hb F expression include the BCL11A on chromosome 2p16 and HBS1L-MYB intergenic polymorphisms (HMIP) on chromosome 6q23 [8–10]. Coexistent α-thal trait is associated with less anemia and protects the patients from leg ulcers, stroke, gallstones and splenic dysfunction, but may be associated with end-artery thrombotic phenomena leading to osteonecrosis and retinopathy [11–13].
Sensorineural hearing loss in children with sickle cell anemia and its association with endothelial dysfunction
Published in Hematology, 2018
Mara Renata Rissatto Lago, Luciene da Cruz Fernandes, Isa Menezes Lyra, Regina Terse Ramos, Rozana Teixeira, Cristina Salles, Ana Marice Teixeira Ladeia
In SCA, most investigators attribute SNHL to impaired blood flow in the cochlea or to the nerve pathways from the inner ear to the brain. The blood supply of the inner ear is provided by the labyrinthic artery, which is a functional end artery. Even occasional limited ischemia culminates in Corti’s Organ hypoxia and lesion of the OHC in the stria vascularis [3–5]. The base of the cochlea is typically involved because of its tonotopic organization; the hair cells of the basal turn of the cochlea are more sensitive to anoxia pathogena than the apex. This may explain why SNHL initially affects isolated frequency regions, and usually high frequencies. Changes in the other frequencies suggest diffuse damage to the cochlea, rather than damage limited to the basal turn [34].