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Posted: December 27th, 2022
Psoriasis is a chronic skin condition that causes cells to build up rapidly on the surface of the skin. The extra skin cells form scales and red patches that are sometimes itchy and painful. Psoriasis is a non-contagious condition that can affect any part of the body, but it is most commonly found on the scalp, knees, elbows, and lower back.
There are several types of psoriasis, including plaque psoriasis (the most common type), guttate psoriasis, inverse psoriasis, pustular psoriasis, and erythrodermic psoriasis. The severity of psoriasis can range from mild, with a few scattered patches, to severe, with widespread, thick patches covering large areas of the body.
The exact cause of psoriasis is unknown, but it is thought to be related to an immune system problem. There is no cure for psoriasis, but it can be managed with medications, lifestyle changes, and self-care measures. Treatments for psoriasis may include topical creams, light therapy, and oral or injectable medications.
Psoriasis is a chronic inflammatory, proliferative, relapsing skin, scalp, and nail illness (McCance and Huether, 2014).
Pathophysiology: Psoriasis is a complex inflammatory illness characterized by reactive aberrant epidermal differentiation and hyperproliferation; current research indicates that the causes are immune-mediated and include T-cells in the dermis (Lui, 2022). Langerhans antigen-presenting cells in the skin interact with T-cells as they migrate from the skin to the regional lymph nodes. T-cells are then activated, and cytokines are released, resulting in co-stimulatory signals from T-cell CD2 and LFA-1 receptors that interact with lymphocyte function-associated antigen (LFA)-3 and intercellular adhesion molecule-1 adhesion molecules (Lui, 2022). T cell reactivation and cytokine local effects in the dermis and epidermis cause inflammation, cell-mediated immune responses, and epidermal hyperproliferation (Lui, 2022).
Patients will have raised and palpable plaques that are irregular or oval in shape, one to a few centimeters in size, defined and demarcated boundaries, rich red color or blue violaceous tint specifically on legs, dry, thin, silvery-white or micaceous scale, uniform, symmetrically throughout the body on the scalp, trunk, and limbs, more commonly on the extensor surfaces (Lui, 2022).
Diagnosis is typically based only on clinical findings. In the case of unusual symptoms, a skin biopsy can be performed (Lui, 2022).
Treatment: Patients are given a cocktail of medications, including a topical corticosteroid and phototherapy (Lui, 2022). If the first approach fails, biological therapy that targets the unique etiology of psoriasis may be undertaken as a second line of treatment (Lui, 2022).
Lichen planus is an unknown cell-mediated immunological reaction (Chuang, 2021). It is frequently found with other diseases characterized by a weakened immune system, such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis (Chuang, 2021). It has also been linked to hepatitis C virus infection.
Pathophysiology: There is no recognized or understood pathophysiology (Chuang, 2021). This disease’s onset has been connected to stressful circumstances.
Clinical Manifestations: A thorough patient history is essential in the diagnosis of lichen planus. Lesions will form on the flexural surfaces of the limbs first, with generalized maximum spreading from 2-16 weeks, and can be found on mucous membranes, genitalia, nails, and the scalp (Chuang, 2021). The patient may also have pruritus and asymptomatic oral lesions, as well as burning or pain (Chuang, 2021).
A direct immunofluorescence study is used to diagnose this condition, which will reveal globular deposits of immunoglobulin M (IgM) and complement mixed with apoptotic keratinocytes (Chuang, 2021). There is no need for any additional imaging. Furthermore, due to the high occurrence of hepatitis, any patient with an unusual presentation should be checked for it (Chuang, 2021).
Treatment: The disease is self-limiting and resolves about 12-18 months with fluorinated topical steroids (Chuang, 2021). Immunosuppressants such as cyclosporine may be prescribed in severe situations.
The most frequent benign tumor in older people is seborrheic keratosis.
Pathophysiology: The exact pathophysiology is uncertain, however it is thought to be benign proliferation of cutaneous basal cells, resulting in smooth or warty raised lesions (McCance and Huether, 2014).
Patients typically show with many lesions on the chest, back, and face that range in hue from tan to waxy yellow, flesh-colored, or dark brown-black (McCance and Huether, 2014). Lesions range in size from a few millimeters to centimeters and have an oval greasy hyperkeratotic stuck-on scaly appearance (McCance and Huether, 2014).
A shave biopsy is collected and examined in the lab to rule out any disease conditions (Balin, 2021). There is no need for additional testing or imaging.
“Both cryotherapy with liquid nitrogen and electrocautery are effective treatments, and lesions normally slough 2 to 3 weeks following treatment,” says the doctor (McCance and Huether, 2014).
Actinic keratosis is a premalignant lesion caused by chronic UV radiation exposure that consists of abnormal epidermal proliferations (McCance and Huether, 2014).
Pathophysiology: It happens as a result of extended sun exposure to UV light, which causes mutations in certain genes such as TP53 and deletion of the gene coding for the p16 tumor suppressor protein (Spencer, 2021). These lesions could develop into aggressive squamous cell cancer.
Clinical Signs and Symptoms: Individuals with fair skin who do not use sunscreen are more likely to be affected. The patient has rough or scaly lesions with poorly defined pink to reddish or dark reddish raised papules (McCance and Huether, 2014). The papules can be present on the cheeks, ears, bald head, forearms, and hands’ backs (Spencer, 2021). Telangiectasias, or tiny, enlarged blood vessels on the skin, are also possible.
To assess the lesions, patients will have a dermoscopy and a biopsy (McCance and Huether, 2014). Patients will also need to be checked on a frequent basis for progression to progressive squamous cell carcinoma.
Patients are advised to apply sunscreen and protective gear to protect their skin from the sun. Topical therapies such as 5-FU and imiquimod are available (McCance and Huether, 2014). Ablative treatment is another possibility.
A. K. Balin, MD, PhD. (2021, November 8). Background, Pathophysiology, and Etiology of Seborrheic Keratosis. https://emedicine.medscape.com/article/1059477-overview
T. Chuang, M.D. (2021, May 18). Lichen Planus: Practice Requirements, Background, and Pathophysiology. https://emedicine.medscape.com/article/1123213-overview
H. Lui, M.D. (November 29, 2022). Plaque Psoriasis: Practice Essentials, Background, and Pathophysiology. https://emedicine.medscape.com/article/1108072-overview
McCance, K.L., and S.E. Huether (Eds.). (2014). Pathophysiology is the biological underpinning of disease in both adults and children. (7th. ed.). Mosby Elsevier. https://online.vitalsource.com/books/9780323088541
J. M. Spencer, M.D. (2021, July 12). Actinic Keratosis: Practice Requirements, Background, and Pathophysiology. https://emedicine.medscape.com/article/1099775-overview
Sepsis is defined by Koya and Paul (2022) as a potentially fatal organ failure caused by a dysregulated host response to infection. Septic shock is a subtype of sepsis characterized by severe circulatory, cellular, and metabolic abnormalities that result in tissue hypoperfusion expressed as hypotension requiring vasopressor therapy and increased lactate levels. Gram-positive bacteria, streptococcal pneumonia, and Enterococcus are the most prevalent pathogens associated with septic shock (Koya & Paul, 2022). According to McCance and Huether (2014), the condition begins with systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, and septic shock. In the intensive care context, sepsis is connected with the six most prevalent infection sites (pneumonia, bloodstream, intravascular catheter, intra-abdominal, urosepsis, and surgical wound infection). Septic shock begins with bacteria and fungus entering the bloodstream and causing bacteremia, either directly from the site of infection or indirectly through harmful chemicals produced directly into the bloodstream by the bacteria. Endotoxins produced by gram-negative microbes, lipoteichoic acids and peptidoglycan produced by gram-positive microorganisms, and superantigens are examples of harmful chemicals. The triggering chemicals initiate a proinflammatory response in the host. Proinflammatory cytokines stimulate tissue factors, which initiate coagulation. As a result, the host is likely to experience a mixed antagonistic response syndrome as proinflammatory and anti-inflammatory mediators respond, intensify, and contribute to MODS (McCance & Huether, 2014).
Clinical signs include persistently low arterial pressure, decreased SVR due to vasodilation, and a change in oxygen extraction by all cells. Septic shock and protracted shock, which cause tissue hypoxia with lactic acidosis, activate ATP-sensitive and calcium-regulated potassium channels in vascular smooth muscle, leading to ADH depletion. Tachycardia causes cardiac output to remain normal or increase, despite decreased myocardial contractility. Temperature instability exists, with temperatures ranging from hyperthermia to hypothermia. Other organ system effects may include unstable renal function, gastrointestinal mucosa changes that result in the release of bacteria from the stomach, jaundice, coagulation irregularities, mental status worsening, and tachypnea, which frequently escalates to ARDS (McCance & Huether, 2014).
Treatment consists of an IV fluid bolus of normal saline. Vasoactive drugs are used in pharmacologic hemodynamic support and adjunctive therapy to maintain tissue perfusion. The first vasopressor of choice is norepinephrine. Others include dopamine, epinephrine, phenylephrine, and vasopressin. Corticosteroids are used to compensate for the natural loss of cortisol, but only when blood pressure remains resistant to volume. Blood products are used to maintain hemoglobin levels between 7 and 9 g/dl. A lot of the therapies are done to keep anything else from happening. Patients, for example, are on PPi to avoid ulcers and DVT prophylactic therapies. Antibiotics will be administered based on the bacteria found (McCance & Huether, 2014).
Shock from Anaphylactic Reaction
Anaphylactic shock is a clinical illness characterized by a severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiac arrest and respiratory difficulties due to bronchospasm. The initial hypersensitivity reactions might occur seconds to minutes after the triggering antigen is presented. Drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex are all common allergies (Koya & Paul, 2022). Anaphylactic shock is frequently severe and involves early symptoms such as an itchy rash, throat swelling, and low blood pressure caused by extensive vasodilation and systemic inflammation, which can lead to death in minutes if emergency treatment is not received. Foods, insect and snake venoms, pollens, pharmaceuticals, and latex are examples of allergens known to produce hypersensitive reactions (McCance & Huether, 2014).
Anxiety, difficulty breathing, stomach cramps, edema, hives (urticaria), burning or itching of the skin, fever, and hemolysis are some of the clinical symptoms. Other symptoms include a drop in SVR and oliguria (McCance & Huether, 2014).
Treatment – Begin by removing whatever is causing the reaction. The drug epinephrine is used to generate vasoconstriction and reverse airway constriction. Volume expanders, such as IV fluids, are used to treat hypovolemia, while antihistamines and corticosteroids are used to reduce the inflammatory response (McCance & Huether, 2014).
Shock of Neurogenic Origin
Neurogenic shock can arise as a result of spinal cord or brain injuries. The fundamental process is autonomic system disturbance, which results in lower vascular resistance and changes in vagal tone (Koya & Paul, 2022). This is also known as vasogenic shock, which is characterized by extensive vasodilation caused by an imbalance in parasympathetic and sympathetic activation of the vascular smooth muscle. “Relative hypovolemia” is caused by neurogenic shock (McCance & Huether, 2014).
Causes- Normally, sympathetic activation keeps muscle tone stable. Vasodilation occurs when sympathetic activation is halted or blocked. Trauma to the spinal cord or medulla, conditions that disrupt the flow of oxygen to the medulla, or conditions that deplete the medulla of glucose all result in a neurogenic shock by disrupting sympathetic activity. Other causes of neurogenic shock include antidepressants, anesthetic medications, and extreme emotional stress and pain (McCance & Huether, 2014).
Clinical symptoms include low SVR, increased parasympathetic activity, and bradycardia. If blood pressure drops to the point where brain metabolism is insufficient to support awareness, the neurogenic shock induces fainting (McCance & Huether, 2014).
Hypovolemic shock is distinguished by a reduction in intravascular volume and an increase in systemic venous assistance (a compensatory mechanism to maintain perfusion in the early stages of shock). Cardiovascular output declines in the later stages of shock due to gradual volume depletion, resulting in hypotension. Hypovolemic shock is classified into two types: hemorrhagic and non-hemorrhagic (Koya & Paul, 2022).
Causes include gastrointestinal bleeding, trauma, vascular etiologies, and anticoagulant-related spontaneous bleeding. Non-hemorrhagic hypovolemic shock is associated with GI, renal, cutaneous, or insensible losses, and third-space loss (McCance & Huether, 2014).
Clinical Significance- Catecholamine release causes an increase in heart rate and SVR. High SVR, poor skin turgor, increased thirst, oliguria, low systemic and pulmonary preloads, and rapid heart rates are all symptoms. This increases cardiac output as well as tissue perfusion pressures. To enhance blood pressure and perfusion to the body’s essential organs, hypovolemic shock causes compensatory vasoconstriction and increased SVR and afterload. These coping techniques are constrained. If fluid loss is not replenished, tissue perfusion will suffer. Nutrient transport to cells is hampered, and cellular metabolism is hampered (McCance & Huether, 2014).
Treatment-Prompt bleeding control is the preferred treatment. Fluid replenishment is also necessary (McCance & Huether, 2014).
Shock of Cardiogenic Origin
Cardiac problems result in reduced cardiac output and systemic hypoperfusion. Cardiomyopathies, arrhythmias, mechanical (aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm) are examples of these conditions (Koya & Paul, 2022). Cardiogenic shock is caused by the heart’s inability to pump enough blood to tissues and organs for any reason, the most common being the short-term repercussions of an acute myocardial infarction or a severe bout of myocardial ischemia. In the presence of appropriate intravascular volume and left ventricular filling pressure, cardiogenic shock is characterized as persistent hypotension and tissue hypoperfusion induced by cardiac failure. As cardiac output falls, compensatory adaptive reactions kick in (McCance & Huether, 2014).
Clinical signs resulting from insufficient perfusion of the heart and end organs Chest discomfort, dyspnea, faintness, impending doom, tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output are common complaints. Cyanosis, irregular pulses, poor urine production, and sometimes peripheral edema are other symptoms (McCance & Huether, 2014).
H. H. Koya and M. Paul (2022). StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK531492/ McCance, K.L., and S.E. Huether (Eds). (2014). Pathophysiology is the biological underpinning of disease in both adults and children. (7th. ed.). Mosby Elsevier, https://online.vitalsource.com/books/9780323088541.
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