Week 8 answers

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please respond to each discussion post with apa references  Thank you!

Discussion 1

Psoriasis is chronic inflammatory, proliferative, relapsing disorder that involves the skin, scalp and nails (McCance and Huether, 2014).

Pathophysiology: Psoriasis is a complex inflammatory disorder, that involved reactive abnormal epidermal differentiation and hyperproliferation, the current research reflects that the mechanisms are immune based and involves the T-cells in the dermis (Lui, 2022).  Langerhans antigen presenting cells in the skin, travel from the skin to the regional lymph nodes interacting with T-cells.  The T-cells are then activated and cytokines are released resulting in co-stimulatory signals from the T-cell CD2 and LFA-1 receptors that interact with adhesion molecules of lymphocyte function-associated antigen (LFA)-3 and intercellular adhesion molecule-1 (Lui, 2022).  The reactivation of T cells and local effects of cytokines in the dermis and epidermis lead to inflammation, cell-mediated immune responses, and epidermal hyperproliferation (Lui, 2022). 

Clinical Manifestations: Patients will present with raised and palpable plaques that are irregular or oval shaped, 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). 

Evaluation: Diagnosis is made generally on the clinical manifestations alone.  If needed, a skin biopsy can be completed is atypical presentations (Lui, 2022). 

Treatment: Patients are prescribed a combination of treatments including a topical agent such as a corticosteroid and phototherapy (Lui, 2022).  As a second line of treatment if the first option is unsuccessful, biological therapy may be initiated that target the specific pathogenesis of psoriasis (Lui, 2022). 

Lichen planus is a cell-mediated immune response of unknown origin (Chuang, 2021). It is commonly present in other disease with altered immunity, such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis (Chuang, 2021). It has been also been associated with hepatitis C virus infection.

Pathophysiology: The pathophysiology is not known or understood (Chuang, 2021).  Onset of this disease has been linked to stressful events. 

Clinical Manifestations: Obtaining an extensive patient history is very important in the diagnosis of lichen planus.  Lesions will initially develop on the flexural surfaces of limbs with generalized maximum spreading at 2-16 weeks that can be found on mucous membranes, genitalia, nails, and scalp (Chuang, 2021).  The patient may also experience pruritus and oral lesions that may be asymptomatic, burning or pain (Chuang, 2021). 

Evaluation: To diagnose this disorder a direct immunofluorescence study is completed which will show globular deposits of immunoglobulin M (IgM) and complement mixed with apoptotic keratinocytes (Chuang, 2021).  No further imaging is required. Additionally, a patient with any atypical presentation should be tested for hepatitis due to the high incidence (Chuang, 2021). 

Treatment: Disease is self-limiting, self-resolving within 12-18 months and can be treated with fluorinated topical steroids (Chuang, 2021).  In severe cases, immunosuppressants such as cyclosporine may be prescribed.

Seborrheic keratosis is the most common benign tumor in older individuals.

Pathophysiology: The specific pathogenesis is unknown, but is benign proliferation of the cutaneous basal cells that results in smooth or warty elevated lesions (McCance and Huether, 2014).

Clinical Manifestations: Patients will usually present as multiple lesions on the chest, back and face that will appear from a tan to a waxy yellow, flesh colored or dark brown-black (McCance and Huether, 2014).  The lesions will vary in size from a few millimeters to centimeters with an oval greasy hyperkeratotic stuck-on scaly appearance (McCance and Huether, 2014).

Evaluation: To rule out other pathological processes, a shave biopsy is obtained and evaluated in the lab (Balin, 2021). No other testing or imaging is necessary.

Treatment: “Both cryotherapy with liquid nitrogen and electrocautery are effective treatments, and the lesions usually slough 2 to 3 weeks after treatment” (McCance and Huether, 2014).

Actinic keratosis is a premalignant lesion made of aberrant proliferations of epidermal caused by prolonged exposure to UV radiation (McCance and Huether, 2014).

Pathophysiology: It occurs following prolonged sun exposure to UV light that results in mutations in specific genes including TP53 and deletion of the gene coding for p16 tumor suppressor protein (Spencer, 2021).  These lesions have the potential to progress to invasive squamous cell carcinoma. 

Clinical Manifestations: Most commonly diagnosed in individuals with light skin that do not wear sun protection.  The patient presents lesions with rough or scaly, poorly defined pink to reddish or brown reddish elevated papules (McCance and Huether, 2014). The papules are found on the face, ears, bald scalp, forearms, and backs of the hands (Spencer, 2021).  They may also have telangiectasias which are small, widened blood vessels on the skin. 

Evaluation: Patients will have a dermoscopy and biopsy done to evaluate the lesions (McCance and Huether, 2014).  Patients will also need regular examinations to check for progression to progressive squamous cell carcinoma.

Treatment: Patients are recommended to wear sunscreen and wear protective clothing to protect their skin from the sun.  Topical therapy options including 5-FU and imiquimod (McCance and Huether, 2014).  Another option is ablative therapy. 


Balin, A. K., MD PhD. (2021, November 8). Seborrheic Keratosis: Background, Pathophysiology, Etiology. https://emedicine.medscape.com/article/1059477-overview

Chuang, T., MD. (2021, May 18). Lichen Planus: Practice Essentials, Background, Pathophysiology. https://emedicine.medscape.com/article/1123213-overview

Lui, H., MD. (2022, November 29). Plaque Psoriasis: Practice Essentials, Background, Pathophysiology. https://emedicine.medscape.com/article/1108072-overview

McCance, K.L. & Huether, S.E. (Eds.). (2014). Pathophysiology: The biologic basis for disease in adults and children. (7th. ed.). Elsevier Mosby. https://online.vitalsource.com/books/9780323088541

Spencer, J. M., MD. (2021, July 12). Actinic Keratosis: Practice Essentials, Background, Pathophysiology. https://emedicine.medscape.com/article/1099775-overview

Discussion 2

Septic Shock

          Koya and Paul (2022) describe sepsis as a life-threatening organ dysfunction resulting from dysregulated host response to infection. Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels. The most common pathogens associated with septic shock are gram-positive bacteria, streptococcal pneumonia, and Enterococcus (Koya & Paul, 2022). McCance and Huether (2014) further point out that the syndrome begins with systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, and septic shock. The six most common infection sites (pneumonia, bloodstream, intravascular catheter, intra-abdominal, urosepsis, and surgical wound infection) are associated with sepsis in the intensive care setting. The septic shock starts with bacteria and fungi entering the bloodstream to produce bacteremia either directly from the site of infection or indirectly from toxic substances released by the bacteria directly into the bloodstream. These toxic substances include endotoxins released by gram-negative microorganisms, lipoteichoic acids and peptidoglycan released by gram-positive microorganisms, and superantigens. The triggering molecules cause the host to initiate a proinflammatory response. The proinflammatory cytokines enhance tissue factors, which start coagulation. Presumably, the result is a mixed antagonistic response syndrome as proinflammatory, and anti-inflammatory mediators respond, intensify, and lead the host into MODS (McCance & Huether, 2014).

          Clinical manifestations- persistent low arterial pressure, low SVR from vasodilation, and an alteration in oxygen extraction by all cells. Septic shock and states of prolonged shock causing tissue hypoxia with lactic acidosis increase, activate ATP-sensitive and calcium-regulated potassium channels in vascular smooth muscle and lead to depletion of ADH. Tachycardia causes cardiac output to remain normal or elevate, although myocardial contractility is reduced. Temperature instability is present, ranging from hyperthermia to hypothermia. Effects on other organ systems may result in unstable renal function, gastrointestinal mucosa changes that result in the release of bacteria from the gut, jaundice, clotting abnormalities, deterioration of mental status, and tachypnea that often progresses to ARDS (McCance & Huether, 2014).

          Treatment- Fluid bolus of normal saline IV. Pharmacologic hemodynamic support and adjunctive therapy to maintain tissue perfusion include vasoactive agents. Norepinephrine is the initial vasopressor of choice. However, there are others like Dopamine, epinephrine, phenylephrine, and vasopressin. Corticosteroids are given to help replace the intrinsic loss of cortisol, but only when blood pressure remains unresponsive to volume. Blood products are given to keep hemoglobin levels between 7 and 9 g/dl. A lot of the treatments done are to prevent anything else from occurring. For example, patients are on PPi to avoid ulcers and DVT prophylactic treatments. Antibiotics will be given depending on the identified bacteria (McCance & Huether, 2014).

Anaphylactic Shock

          Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur seconds to minutes after the presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex (Koya & Paul, 2022). Anaphylactic shock is often severe and has immediate symptoms, including an itchy rash, throat swelling, and low blood pressure, related to the massive vasodilation and systemic inflammation that may progress to death in minutes if emergency treatment is not rendered. Some allergens known to cause hypersensitivity reactions are foods, insect and snake venoms, pollens, medications, and latex (McCance & Huether, 2014).

          Clinical manifestations- include anxiety, difficulty in breathing, gastrointestinal cramps, edema, hives (urticaria), burning or itching of the skin, fever, and hemolysis. Other signs include decreased SVR and oliguria (McCance & Huether, 2014).

          Treatment – Start with removing what is causing the reaction. Epinephrine is administered to cause vasoconstriction and reverse airway constriction. Volume expanders like IV fluids to help with hypovolemia, and antihistamines and corticosteroids are given to stop the inflammatory reaction (McCance & Huether, 2014).

Neurogenic Shock

         Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain. The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone (Koya & Paul, 2022). This is also known as vasogenic shock, a massive vasodilation resulting from an imbalance between parasympathetic and sympathetic stimulation of the vascular smooth muscle. Neurogenic shock creates “relative hypovolemia” (McCance & Huether, 2014).

        Causes- Normally, sympathetic stimulation maintains muscle tone. If sympathetic stimulation is interrupted or inhibited, vasodilation occurs. Therefore, trauma to the spinal cord or medulla, conditions that interrupt the supply of oxygen to the medulla, or conditions that deprive the medulla of glucose cause a neurogenic shock by interrupting sympathetic activity. Depressive drugs, anesthetic agents, and severe emotional stress and pain are other causes of neurogenic shock (McCance & Huether, 2014).

         Clinical manifestations- Very low SVR, excessive parasympathetic activity, bradycardia. The neurogenic shock causes fainting if blood pressure decreases to the point that cerebral metabolism is insufficient to support consciousness (McCance & Huether, 2014).

Hypovolemic Shock

        Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (a compensatory mechanism to maintain perfusion in the early stages of shock). In the later stages of shock, due to progressive volume depletion, cardiac output decreases and manifests as hypotension. Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic (Koya & Paul, 2022).

        Causes- Gastrointestinal bleed, trauma, vascular etiologies, spontaneous bleeding related to the use of anticoagulant. Non-hemorrhagic hypovolemic shock is related to GI losses, renal losses, skin or insensible losses, and third-space loss (McCance & Huether, 2014).

         Clinical Manifestation- Heart rate and SVR increase due to catecholamine release. So high SVR, poor skin turgor, increased thirst, oliguria, low systemic and pulmonary preloads, and rapid heart rates. This boosts cardiac output and tissue perfusion pressures. Hypovolemic shock results in compensatory vasoconstriction and increased SVR and afterload to improve blood pressure and perfusion to the body’s core organs. These compensatory mechanisms are restricted. If fluid loss is not replaced, this will decrease tissue perfusion. Nutrient delivery to the cells is impaired, and cellular metabolism fails (McCance & Huether, 2014).

         Treatment-Prompt control of hemorrhage is the treatment of choice. Fluid replacement is also essential (McCance & Huether, 2014).

Cardiogenic Shock

         Cardiac issues cause decreased cardiac output and systemic hypoperfusion. Those are cardiomyopathies, arrhythmias, mechanical (aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm) (Koya & Paul, 2022). Cardiogenic shock results from the inability of the heart to pump adequate blood to tissues and end organs from any cause, the most common being the short-term consequences of acute myocardial infarction or a severe episode of myocardial ischemia. Cardiogenic shock is defined as persistent hypotension and tissue hypoperfusion caused by cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure. As cardiac output decreases, compensatory adaptive responses are activated (McCance & Huether, 2014).

        Clinical manifestations- caused by inadequate perfusion to the heart and end organs Patients’ complaints are chest pain, dyspnea, faintness, impending doom, tachycardia, tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac output. Signs are also cyanosis, irregular pulses, low urine output, and occasional peripheral edema (McCance & Huether, 2014).



Koya, H. H., Paul, M. (2022). Shock. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK531492/

McCance, K.L. & Huether, S.E. (Eds.). (2014). Pathophysiology: The biologic basis for disease in adults and children. (7th. ed.). Elsevier Mosby. https://online.vitalsource.com/books/9780323088541


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