Carotid Artery Stenosis, Baker’s Cyst, And Breast Fibrocystic Disease: Pathophysiology And Treatment

Carotid Artery Stenosis

 Carotid Artery Stenosis 

Carotid artery disease is progressive narrowing of carotid artery because of the atherosclerosis growth characterized by the thickening of the interior arterial wall (Diomedi et al., 2014). Carotid artery stenosis happens when atherosclerotic plaques that derive from fatty streaks that over time assemble into a lipid core clog blood vessels that deliver blood to the head and brain. This occlusion escalates the peril of stroke which is a medical emergency that happens when the supply of blood to the brain is disrupted. The classical kinds of lesions include the fibrous cap, fatty streaks along with complicated injuries based on the atherosclerosis progression. The fatty streaks become a fibroatheroma as fibrous structure gathers over the base and creats a fibrous cap.

The fibrous cap comprises smooth muscle cells, a dense connective structure which contains elastin, a basement membrane, collagen fibrils, few leukocytes, and proteoglycans. Furthermore, it is composed of a cellular region beneath that includes a mixture of T lymphocytes, macrophages, and smooth muscle cells. It also has a deeper necrotic core that consists of cholesterol crystal, calcium deposit, lipids, and cellular debris. Carotid plaques include of lipid core with infiltration of inflammatory cells which are wrapped with a fibrous cap (Diomedi et al., 2014). Few plaques become unstable leading to an enlarging lipid core, enlargement of the plaque, luminous thrombosis, fibrous cap rupture, intraplaque hemorrhage and ulceration via unknown mechanisms. However, the histomorphologic features have been related to the neurologic and atheroemboli symptoms.

Notably, the features have been observed frequently in explanted plaque specimens acquired from symptomatic patients. Consequently, the small lipid core which is located deeper within the plaque that has a thick fibrous cap has been observed in patients with asymptomatic carotid stenosis (Diomedi et al., 2014). The predominance of significant carotid artery stenosis is 9 percent in men and 7 percent in women. The current developments in magnetic resonance imaging and duplex ultrasound enable structure plaque characterization which is possible in defining high-risk lesions later. Atherosclerotic plaques grow entirely at branch Ostia and bifurcation of frequent carotid artery into internal together with external carotid artery (Xu et al., 2018). Along the inner carotid bulb wall, the flow of blood remains laminar and with high shears stress along with high velocity.

On the contrast, along with the outer wall, there are regions of a complex oscillating shear stress pattern, flow separation, turbulent flow and stasis that lead to atherosclerosis plaque expulsion. While rare neurologic events have been accredited to progressive stenosis and decreased the flow of blood from enlarging atherosclerotic plaques, most such incidents are secondary to atheroembolization and plaque rapture from the lesion. Exposure of the atherosclerotic debris together with the fibrous cap and disruption to the flow of lumen is responsible for the embolic complications (Diomedi et al., 2014). The primary risk factors incorporate of diabetes, cigarette smoking and lack of exercise. Also, dyslipidemia, C-reactive protein, hypertension, obesity, and advanced glycation end products along with its receptors which include RAGE and soluble RAGE play a contributory role.

Baker’s Cyst

Baker‘s Cyst

  Another name for Baker’s cyst is popliteal cyst which is a protrusion that unfolds behind the popliteal (Jiang and Ni, 2017). The cyst development result from an accretion of fluid in the semimembranosus tendon bursa  with communication between here and the joint yet with a one-way fluid flow  in the cyst’s direction limited by a valve. A baker’s cyst commensurate to a cyst situated amidst the medial head of the gastrocnemius muscle and the semimembranosus tendon and (Jiang and Ni, 2017). The pathology of baker’s cyst is elucidated via the existence of a link amidst the knee joint along with a bursa amidst the semitendinosus tendon and the gastrocnemius muscle permitting the fluid flow. It is filled with synovial fluid which is the lubricating fluid which is generally found inside the knee joint (Jiang and Ni, 2017).

This type of infection occurs in case there is an underlying problem with the knee like osteoarthritis (Inklebarger et al., 2017). Some of the symptoms may incorporate of tightness and swelling behind the knee and can rarely rupture and cause the same symptoms to a deep vein thrombosis (Frush and Noyes, 2015). Baker’s cyst can rupture and become complex by spreading fluid over the leg amid the muscles of the calf. This fluid could then tracks down the calf and result in a bruise around the ankle. Over time, baker’s cysts often get better and disappear by itself.

 Amidst adult victims who encounter magnetic resonance imaging of the popliteal, its predominance extends from 5-38 percent. Its commonness increases with the increase in age and is remarkably more persistent in individuals of 50 or more years. Although this infection may cause swelling and bring about discomfort, treating the possible underlying issue gives relief (Inklebarger et al., 2017) typically.

Multiple situations are related to baker’s cyst like arthritides, hemophilia, intraarticular lesions, infection, pigmented villonodular synovitis and systemic lupus erythematous (Grainger and O’Connor, 2015). In adults, the disease is related to intra-articular state whereas in children the development is obscure and elementary in 95 percent of the instances. Baker’s cysts do not need medication since 70 percent settles impulsively over the years or even months with traditional medicines. Radioactive synoviorthesis could be utilized to remedy erythrogenic arthritides and hemophilia, and extraction of the cyst can be endorsed when a baker’s cyst is insensitive to all other remedies (Grainger and O’Connor, 2015).
 Breast Fibrocystic Disease

Fibrocystic breast disease is a regular non-cancerous state which impacts mostly premenopausal females. It incorporates a broad variety of symptoms like sudden disappearance or appearance of noticeable benign masses in the breast, lumpy or free moving masses in the breast and breast inflammation (Talaei et al., 2017). The breast fibrocystic disease’s pathophysiology is driven by the progesterone insufficiency along with estrogen prevalence which leads to hyperproliferation of connective tissues. This is then preceded by facultative epithelial swelling, and this increases the risk of breast cancer to these victims from twofold to fourfold. Clinical correlation of fibrocystic breast disease is contemplated by the breast together with the axillary inflammation or pain in retaliation to the growth of fibrocystic lumps, fibrocystic plaques, macrocysts, and modularity.

Breast Fibrocystic Disease

This infection is majorly pronounced in women when they are in their 40s, and it proceeds with progressing premenopausal age but the adjustments in fibrocystic relapse during the period of postmenopausal. Prolactin, estrogen, and progesterone affect the breast tissues directly by causing the cells to grow and multiply (Talaei et al., 2017). There are other hormones that indirectly or directly impact the regulating or amplifying the growth of cells which include insulin, growth factors like TGF-beta, THS and growth hormone. Years of fluctuation finally produce small cysts and regions of dense or fibrotic tissue. Several small cysts along with the elevating breast pain level develop commonly during the 30s in females. However, larger cysts do generally not occur till after the age of 35, and it is presumably driven by aberrant development signals, lesions which may accumulate epigenetic, genetic and karyotypic changes like loss of heterozygosity along with modified expression of hormone receptors (Talaei et al., 2017).

Multiple variants of fibrocystic breast changes may be differentiated, and these may contain various causes and genetic predispositions. Other lesions seem to stem primarily from ductal epithelial origins, but adenosis includes density of lobular units and abnormal count. Iodine deficiency has been identified to be the preliminary contributor to fibrocystic breast infection through facilitating the sensitivity of breast structure to estrogen. To treat fibrocystic breast disease ovarian estrogen secretion is suppressed along a low estrogen oral contraceptive where the estrogen action on breast structure is resistant by the oral contraceptives progestin constituent which is 19-nortestosterone derivatives. Also, it can be treated by cyclic application of a progestogen that is progesterone, medroxyprogesterone acetate which regulates the estrogen mammary impacts (Talaei et al., 2017).

The medication modalities are equally superior and effective to danazol treatment that encompasses adverse impacts in most of the patients. For victims with abnormal or borderline lipid profiles, vitamin E along with adjuvant treatment of fibrocystic breast stenosis is of value that is, high plasma quantities of low-density lipoprotein and low plasma amounts of high-density lipoproteins. If there is a close follow up, thorough diagnostic assessment and proper treatment all patients can get successful treatment. In case of ultrasonic, mammographic or clinical evaluations are suspicious for carcinoma and patients with macrocysts needle aspiration biopsy should be conducted (Talaei et al., 2017). This infection is not a mild non-infection although a well-defined clinical system that needs medication to minimize the occurrence of breast surgical processes diminishes the peril of breast cancer together with bringing about relief.

References

Diomedi, M., Scacciatelli, D., Misaggi, G., Balestrini, S., Balucani, C., Sallustio, F., Di Legge, S., Stanzione, P. and Silvestrini, M., 2014. Increased common carotid artery wall thickness is associated with rapid progression of asymptomatic carotid stenosis. Journal of Neuroimaging, 24(5), pp.473-478.

Frush, T.J. and Noyes, F.R., 2015. Baker’s cyst: diagnostic and surgical considerations. Sports Health, 7(4), pp.359-365.

Grainger, A.J. and O’Connor, P., 2015. IMAGING OF JOINT DISEASE. Grainger and Allison’s Diagnostic Radiology: Musculoskeletal System, p.156.

Inklebarger, J., Galanis, N., Kumar, D., Krishaswa, K. and Leddy, J., 2017. Bakers Cyst Occurrence Following Arthroscopic Medial Meniscal Debridement in a Recreational Athlete: Some Potential Indications for Ultrasound-Guided Needle Aspiration.

Jiang, J., and Ni, L., 2017. Arthroscopic internal drainage and cystectomy of popliteal cyst in knee osteoarthritis. Journal of orthopedic surgery and research, 12(1), p.182.

Talaei, A., Moradi, A. and Rafidi, F., 2017. The evaluation of the effect of metformin on breast fibrocystic disease. Breast disease, 37(2), pp.49-53.

Xu, P., Liu, X., Zhang, H., Ghista, D., Zhang, D., Shi, C. and Huang, W., 2018. Assessment of boundary conditions for CFD simulation in a human carotid artery. Biomechanics and modeling in mechanobiology, pp.1-17.