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Hypertension
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Effective therapy for hypertension was first introduced in the 1940s, initially for hypertensive heart failure (Smirk and Alstad, 1951), then for malignant hypertension. Such therapy was withheld from Franklin Delano Roosevelt, whose accelerated hypertension was not treated and led to his fatal stroke in 1945 (Calhoun and Oparil, 1995; Messerli, 1995). Demonstration that lowering blood pressure could resolve fibrinoid necrosis confirmed Byrom’s research and Pickering’s views. Over the past 50 years, new, more effective and better tolerated antihypertensive drugs have been successively introduced by a pharmaceutical industry that has gained and contributed immensely. The pharmaceutical industry has played a major role in changing the natural history of hypertension—through providing drugs that can break the vicious cycle acting through renal damage—and has exerted considerable influence on the medical profession as well. Over this time also, the description of hypertension as “essential” disappeared from the medical nomenclature. The word “essential” implied that elevation of blood pressure was essential to maintain flow through organs. Sir George Pickering was the most influential in challenging this view (Pickering, 1968), but it was solidly based on work of Byrom (1969) and (Byrom and Dodson, 1948) and others who showed that the opposite was true—that the only way to treat “malignant” hyper-tension effectively was by reducing arterial pressure and thereby breaking the vicious cycle.
Tissue injury and repair
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The most frequently encountered is coagulative necrosis in which cell outlines are initially maintained but the protein constituents coagulate. To the naked eye, the area of necrosis appears pale yellow−white but initially of normal consistency. Histological examination shows loss of nuclear staining with increased eosinophilia of the cytoplasm, but retention of the cellular outlines. These are gradually lost and, eventually, the extracellular tissue architecture breaks down. At this stage, the tissue is soft and autolysed. Inflammatory cells infiltrate the necrotic tissue to phagocytose and digest the dead cellular debris. Colliquative or liquefactive necrosis is seen in the lipid-rich tissues of the central nervous system. The lack of extracellular architecture and the high lipid content lead to liquefaction of the necrotic nervous tissue. Caseous necrosis is seen in tuberculosis (TB). There is an amorphous white centre to the granulomas in TB because of the tissue digestion by activated macrophages. Fibrinoid necrosis is seen in the special circumstances of vascular damage. It is characterized by platelet activation, fibrin deposition, and usually cell death of the vascular smooth muscle. The terms ‘fat necrosis’ and ‘gangrenous necrosis’ (which refers to necrosis with putrefaction) are commonly used in clinical practice.
Immunopathology
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Intradermal injection of antigen into a previously immunized animal generates immune complexes at the injection site. These complexes consist of preformed antibody and the injected antigen. Complement activation leads to neutrophil infiltration of the injection site and tissue destruction. The reaction is detectable 1–3 hours post-injection and reaches a peak after 4–10 hours. The injection site becomes edematous, erythematous, and may ulcerate. This is called the Arthus reaction. Histologically, one observes fibrinoid necrosis. Antibody and complement are detectable with immunostaining. A “passive” Arthus reaction may be induced by simultaneous intradermal injection of antigen and antibody.
Neuropathology Evaluation of in Utero Correction of Myelomeningocele and Complications of Late-Onset GBS Infection
Published in Fetal and Pediatric Pathology, 2023
Sarah Edminster, Tai-Wei Wu, Alexander Van Speybroeck, Jason Chu, Denise A. Lapa, Ramen H. Chmait, Linda J. Szymanski
Histologic examination of the hematoxylin and eosin (H&E)-stained brain and spinal cord sections showed diffuse neutrophilic and scattered macrophagic inflammatory infiltrate involving the meninges around the circle of Willis, ventral brainstem, cerebellum, and the entire spinal cord. The vasculature was dilated with foci of extravasated erythrocytes and extensive intra- and extracellular bacteria, especially around blood vessels (Fig. 2c). Gram stain highlighted many ovoid to cocci Gram-positive bacteria arranged in pairs and chains (Fig. 2c, inset). Foci of fibrinoid necrosis were occasionally present within vessels. The inflammatory infiltrate also involved the Virchow–Robin spaces and areas of the midbrain. Frequent intraluminal thrombi were found in the leptomeningeal and parenchymal vessels.
Lung, Liver and Skin Changes in an Infant with Positive Methamphetamine
Published in Fetal and Pediatric Pathology, 2023
Kunasilan Subramaniam, Hilma bt. Hazmi, Yong Swee Guan, Khairul Anuar bin Zainun
The association between methamphetamine and pulmonary vessel damage is not well understood due to the paucity of available literature. There are reports of blood vessel fibrinoid necrosis associated with methamphetamine-induced strokes [10]. The pathophysiology of stroke related to methamphetamine is multifactorial with hypertension, tachycardia, and vascular disease often postulated as major mechanisms. Necrosis of blood vessel walls with destruction of the elastic and smooth muscle layer, without leukocytic infiltration of the blood vessel walls, has been observed in the cerebral vasculature of stroke patients who had previously been exposed to methamphetamine, a condition known as necrotizing angiitis or meth arteritis [11]. In our case, we observed fibrinoid necrosis in the pulmonary vasculature. High blood pressure, vasculitis, and infection are all known causes of fibrinoid necrosis. In our case, we ruled out infection and vasculitis by performing blood culture, viral studies and histopathological examination. There was no leucocytic infiltration seen around the necrosed vessels while the blood culture and viral studies were also negative. A plausible reason for the fibrinoid necrosis in the pulmonary arteries may be due to exposure to methamphetamine smoke.
The COVID rash that puts the ‘U’ in GROUCH!
Published in Baylor University Medical Center Proceedings, 2021
Landon Hope, Brianna Hope, Jeannie Nguyen, Richard Hope, Michelle Tarbox
A 44-year-old woman presented to the outpatient dermatology clinic with complaints of a new-onset rash on her lower back and inner thighs (Figure 1a). Biopsy of both locations showed a normal-appearing epidermis and a superficial and deep perivascular mixed inflammatory infiltrate in the dermis composed of eosinophils, neutrophils and neutrophil fragments, lymphocytes, and extravasated red blood cells. Focal fibrinoid necrosis of blood vessel walls was seen within the mid-dermis (Figure 1b, 1c). The patient’s clinical presentation and histologic findings from both biopsy specimens were consistent with early urticarial vasculitis. She was treated with a combination of oral steroids and high-dose antihistamines and had complete resolution of her lesions. Interestingly, 2 days after the biopsies, she tested positive for SARS-CoV-2—which adds urticarial vasculitis, as seen in our patient, to the soiree of potential cutaneous findings associated with COVID-19.