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 apoptoti.

1. 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).

2. 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

3. (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.

4. 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

5. (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.

6. 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

7. (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

8. 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,

9. 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).
References
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