Peer Responses:
    Length: A minimum of 150 words per post, not including references
    Citations: At least one high-level scholarly reference in APA per post from within the last 5 years
    Citations need to be within 5 (Five)  years
    Context: Nursing in the USA

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T6 W8 D1 R2

            Pressure injuries and ulcers are very important to keep discussing because of their commonality, ease of being acquired amongst our vulnerable populations, and associated complications. Pressure ulcer damages from my experience can develop very quickly and complicate a patients condition severely. In Dlugasch and Story (2021) it is mentioned how pressure injuries can even result in as fast as one hour for some. They are also very expensive to treat and painful.

As for the pathophysiology of pressure injuries and ulcers, unrelieved and applied pressure against tissues, from ones own bones or devices, and reperfusion injury is involved. When pressure exceeds skin arteriolar pressure of 32 mmHg, hypoxia occurs (Dlugasch & Story, 2021). If this pressure isnt frequently relieved, for adequate perfusion to be restored, necrosis occurs. Often by this point, skin tissues die and slough off. The longer the pressure sustains, the more tissue becomes involved. Normally however, one frequently moves and constantly repositions themselves, even if it isnt noticed; therefore, avoiding pressure injuries without realizing it. Affected tissue, previously pale due to pressure cutting off circulation, might then be pink and have blanchable redness as reperfusion occurs; non-blanchable redness however might represent affected and dying tissue. Furthermore, pressure injuries also occur within the body over several tissue layers receiving increased pressure over a bony area. For example, when one sits, 300 mmHg of pressure is applied over the ischial tuberosities and onto surrounding tissues (Dlugasch & Story, 2021). Again, one might not realize it, but they often move and reposition their weight; constantly reperfusing tissues before they necrotize. One unable to reposition their weight and restore timely perfusion however, will develop necrosis in affected and deeper tissues. Additionally, the pathophysiology of pressure injuries also involves reperfusion injury (Dlugasch & Story, 2021). When reperfusion is restored, inflammation and reactive oxygen species further damage cellular membranes leading to further cellular death.

Lastly, the development of pressure injuries depend on various health factors, which is why some are more affected than others. Those developing pressure ulcers often have underlying diseases affecting circulation, have sensation impairments from neuropathies, cognitive or motor issues impairing mobility, and malnutrition making any wound healing more difficult than normally.

Reference
Dlugasch, L., & Story, L. (2021). Applied pathophysiology for the advanced practice nurse. Burlington, MA: Jones & Bartlett Learning.

Peer Responses:
    Length: A minimum of 150 words per post, not including references
    Citations: At least one high-level scholarly reference in APA per post from within the last 5 years
    Citations need to be within 5 (Five)  years
    Context: Nursing in the USA

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T6 W8 D1 R1

The pathophysiology of acne vulgaris is complex, with both internal and external triggers characterized by increased sebum production and abnormal desquamation of epithelial cells; this condition develops initially with the formation of microcomedo that obstructs the follicular canal, which is aggravated by the fusion of  corneocytes and hyperkeratosis of the follicular lining resulting in keratin and sebum formation in the follicle (Well, 2018). In addition, the process of acne vulgaris formation continues with the obstruction by the plug also called comedone that triggers the inflammatory process, the sebaceous gland duct and the cells continue to pack into the follicle, the plug expands behind a small follicular opening to the skin resulting in distension of the follicle and formation of a closed comedone, dilating the pores, and reopening the plug, and the final result is the formation of blackhead (Well, 2018). Acne vulgaris is caused by Propionibacterium that lives in the pilosebaceous follicle, originates from the normal flora of the skin and it causes inflammation  and irritation associated with acne vulgaris; hormonal changes such as menses, testosterones, sex hormones, androgen hormones, polycystic ovarian syndromes, medications like Litium, phenytoin, cosmetics products, tight clothing and under garments can all contribute to acne vulgariS as external factors (Well, 2018). Acne vulgaris pathophysiology mechanism follows four common steps including formation of excessive keratin in the hair follicles, overproduction of of sebum by the hair follicles, invasion of the bacteria called Propionibacterium that is part of the skin normal flora, and the inflammatory process; and acne vulgaris is generally noted on the face, neck, shoulders, trunk, arms, legs and buttocks, varying in severity (Dlugasch, Story, 2021). Overall, Acne Vulgaris affects over 65 millions people worldwide with physical, psychological, financial, esthetic impacts on the patients; usually diagnosed with history and physical examination and treated based on the severity using medications such as Azelaic acid, Salicylic acid, Benzoyl Peroxide; alternative therapies such as tea tree oil, brewers Yeast, micro dermal and laser therapies; diet and proper hygiene (Dlugasch, Story, 2021).
References:
Dlugasch, L; Story, L. (2021). Applied Pathophysiology for the Advanced Practice Nurse. P. 658-660.
Well, D. (2018). Lippincott William & Wilkins. Acne Vulgaris: A review of causes and Treatment of Options. p.1-8