Pathophysiology FINAL Exam REVIEW.

Pathophysiology FINAL Exam REVIEW. types of Skin Lesion-Chapter 8  Macule; small, flat, circumscribed lesion of a different color than the normal skin  Papule; small, firm, elevated lesion  Nodule; palpable, elevated lesion; varies in size  Pustule; elevated, erythematous lesion, usually containing purulent exudate  Vesicle; elevated, thin-walled lesion containing clear fluid (blisters)  Plaque; large, slightly elevated lesion with flat surface, often topped by scales  Crust; dry, rough surface or dried exudate or blood  Lichenification; thick, dry, rough surface (leatherlike)  Keloid; raised, irregular, and increasing mass of collagen resulting from excessive scar tissue formation  Fissure; small, deep, linear crack or tear in skin  Ulcer; cavity with loss of tissue from the epidermis and dermis, often weeping and bleeding  Erosion; shallow, moist cavity in epidermis  Comedone; mass of sebum, keratin, and debris blocking the opening of a hair follicle Type 1 Hypersensitivity-Chapter 7 Hay, fever; anaphylaxis; Mechanism of the type 1 hypersensitivity: IgE bound to mast cells; release of histamine and chemical mediators. Effects are; immediate inflammation and pruritus. The type 1 hypersensitivity begins when an individual is exposed to a specific allergen and for some reason develops IgE antibodies from B lymphocytes. These antibodies attach to mast cells in specific locations, creating sensitized mast cells. Mast cells: are connective tissue cells that are present in large numbers in the mucosa of the respiratory and digestive tracts. Type II hypersensitivity ABO blood incompatibility; the mechanism of the type II hypersensitivity are IgG or IgM reacts with antigen on cell-complement activated; the effects is cell lysis and phagocytosis Type III hypersensitivity Autoimmune disorders; systemic lupus erythematosus, glomerulonephritis; the mechanism are antigen-antibody complex deposits in tissue-complement activated; the effects are inflammation, vasculitis Type IV hypersensitivity Contact dermatitis: transplant rejection; Mechanism of the type IV hypersensitivity: Antigen bind to T lymphocyte; sensitized lymphocyte releases lymphokines. Effects are; delayed inflammation. This type of hypersensitivity is a delayed response by sensitized T lymphocytes to antigens, resulting in release of lymphokines or other chemical mediators that cause an inflammatory response and destruction of the antigen. Contact dermatitis, or an allergic skin rash, is caused by a type IV reaction to direct contact with a chemical. Such chemicals includes cosmetics, dyes, soaps, and metals. Other examples include skin reactions to plant toxins such as poison ivy. These skin reactions usually do not occur immediately after contact; these reaction usually takes more than 24 hours. Importantly: Type 1 hypersensitivity respond immediately while Type IV has a delayed response. Chapter 8 (all skin disorder) urticaria: this results from a type 1 hypersensitivity reaction, commonly caused by ingested substances such as shellfish or certain fruits or drugs. Signs and Symptoms of Urticaria  Eruption of hard, raised erythematous lesions on the skin, often scattered all over the body  Highly pruritic lesions  Hives can also develop in the pharyngeal mucosa this may cause an obstruction of the air ways, resulting in difficulty with breathing. Urticaria can be treated with over the counter antihistamines, in more serious cases where inflammation of the airways occurs, corticosteroids are prescribe, this drugs is used only in severe cases. For chronic cases of urticaria, a biologic drug, may be prescribed for pt. 12 and older. Psoriasis: is a common chronic inflammatory skin disorder that affects 1% to 3% of the population and is considered to be genetic in orgin.  Psoriasis usually occurs in the teen years and the course in marked by remissions and exacerbation.  Depending on severity and psoriatic arthritis is associated with psoriasis in some cases  psoriasis results from the abnormal activation of T cells and an associated increase in cytokines in affected tissues  epidermal shedding may occur in 1 day rather than the normal 2-week turnover period.  The lesion begins as a small red papule that enlarges.  A silvery plaque forms while the base remains erythematous because of inflammation and vasodilation  Lesions are commonly found on the face, scalp, elbow and knees and may be accompanied by an itching or burning sensation.  The fingernails may thickened, pitted or ridged. Signs and Symptoms of Psoriasis  Red patches of skin covered with silvery scales  Small scaling spots these are commonly seen in children  Dry, cracked skin that may bleed  Itching, burning, or soreness  Thickened, pitted, or ridged nails  Swollen and stiff joints Treatment for psoriasis Glucocorticoids, reduces cell proliferation Tar preparations In severe cases antimetabolite methotrexate Exposure to ultraviolet light is frequently part of the treatment regimen Pemphigus: is an autoimmune disorder There are 2 types of Pemphigus, the most common type is the Pemphigus Vulgaris, the other type is the Pemphigus foliaceus. With pemphigus the autoantibodies disrupt the cohesion between the epidermal cells, causing blister to form  Pemphigus Vulgaris; the epidermis separates above the basal layer  Blisters form initially in the oral mucosa or scalp and then spread over the face and trunk during the ensuing months  The vesicles become large and tend to rupture, leaving large denuded area of the skin covered with crusts Signs and symptoms of pemphigus vulgaris  Blisters in mouth  Blisters spreading to the skin  Blisters are painful but not pruritic  Breathing is difficult due to swollen mouth and throat Manifestation of pemphigus foliaceus are similar to vulgaris except there are usually no mouth blisters and the blisters are typically not painful. Treatment for pemphigus are systemic glucocorticoids such as prednisone and other immunosuppressants Furuncle: A furuncle (boil) is an infection, usually by S. aureus, which begins in a hair follicle (folliculitis) and spreads into the surrounding dermis. Furuncle is commonly located in the face, neck, and back. Signs and Symptoms of furuncle are as followed  Firm, red lesion  Painful nodule, which develops into large, painful mass called abscess  The abscess produces large amounts of purulent exudate (pus) composed of leukocytes, cellular debris from dead blood cells and bacteria, and a thin proteinrich fluid component  Squeezing boils can result in the spread of infection by autoinoculation to other areas of the skin, can cause cellulitis, or can force the bacteria in the abscess deeper in the dermis or the subcutaneous tissue  Compression of the furuncles in the nasal area may lead to thrombi or infection that spreads to the brain if the infected material reaches the cavernous sinus in the facial bones Carbuncles are a collection of furuncles that coalesce to form a large infected mass, which may drain through several sinuses are develop into a single large abscess. Treatment for furuncles/carbuncles  Warm compresses to promote drainage of the furuncles/carbuncles  Ibuprofen or acetaminophen can provide pain relief from inflammation  If no drainage is noted in a few days, a physician should be called to cut and drain the abscess, if necessary antibiotic may be prescribe Sodium Imbalance-chapter 2 Review of Sodium Sodium (Na+ ) is the primary cation (positively charged ion) in the extracellular fluid  It makes up 90% of the solute in extracellular fluid Diffusion of sodium occurs between the vascular and interstitial fluids  Sodium transport across the cell membrane is controlled by the sodiumpotassium pump or active transport, resulting in sodium levels that are high in extracellular fluids and low inside the body Sodium levels in the body are primarily controlled by the kidneys, through the action of aldosterone Hyponatremia Hyponatremia refers to a serum sodium concentration below 3.8 to 5 mmol per liter or 135 milliequivalent (mEq) per liter Causes of Hyponatremia Common causes of low serum sodium levels include:  Losses from excessive sweating, vomiting, and diarrhea  Use of certain diuretic drugs combined with low-salt diets  Hormonal imbalances such as insufficient aldosterone, adrenal insufficiency, and excess ADH secretion  Early chronic renal failure  Excessive water intake Effects of Hyponatremia  Low sodium levels impair nerve conduction and result in fluid imbalances in the compartments  Decreased osmotic pressure in the extracellular compartment may cause a fluid shift into cells, resulting in hypovolemia and decreased blood pressure  The brain cells may swell, causing confusion, headache, weakness, and seizures Hypernatremia is an excessive sodium level in the blood and extracellular fluids (more than 145 mEq per liter) Causes of Hypernatremia Excess sodium results from ingestion of large amounts of sodium without proportionate water intake or a loss of water from the body that is faster than the loss of sodium Specific causes include:  Insufficient ADH, which results in a large volume of dilute urine (diabetes insipidus)  Loss of the thirst mechanism  Watery diarrhea  Prolonged periods of rapid respiration Effects of Hypernatremia The major effect of hypernatremia is a fluid shift out of the cells owing to the increased osmotic pressure of interstitial or extracellular fluid This effect is manifested by the following:  Weakness, agitation  Firm subcutaneous tissues  Increased thirst, with dry, rough mucous membranes  Decreased urine output because ADH is secreted  If the cause of hypernatremia is fluid loss caused by lack of ADH, urine output is high Potassium Imbalance (chapter 2, pg. 24-25)  Potassium (K) is a major intracellular cation. Potassium is ingested in food and is excreted primarily in the urine under the influence of the hormone aldosterone.  The hormone insulin also promotes movement of potassium into cells  potassium levels are also influence by the acid-base balance in the body; acidosis tends to shift potassium ions out of the cells into the extracellular fluids, and alkalosis tends to move more potassium into the cells  Most important, abnormal potassium levels, both high in and low, have a significant and serious effect on the contraction on cardiac muscle causing changes in the electrocardiogram and ultimately cardiac arrest or standstill Hypokalemia In hypokalemia the serum level of potassium is less than 2 mmol per liter or 3.5 mEq per liter Causes of Hypokalemia low serum potassium levels may result from the following  Excessive losses from the body due to diarrhea  Diuresis associated with certain diuretic drugs  The presence of excessive aldosterone or glucocorticoids in the body  Decreased dietary intake, which may occur with alcoholism, eating disorders, or starvation  Treatment of diabetic ketoacidosis with insulin Effects of Hypokalemia  Cardiac arrhythmias, cardiac arrest  Anorexia, nausea, constipation  Fatigue, muscle twitch, weakness, leg cramps  Shallow respirations, paresthesias  Postural hypotension, polyuria, and nocturia  Serum pH elevated-7.45 (alkalosis) Hyperkalemia Causes  serum levels of potassium greater the 2.5 mmol per liter or 5 mEq per liter  Renal failure  Deficit of aldosterone  Use of “potassium-sparing” diuretic drugs, which prevent potassium from being excreted in adequate amounts  Leakage of intracellular potassium into the extracellular fluid in patients with extensive tissue damage such as traumatic crush injuries and burns  displacement of potassium from cells by prolonged to severe acidosis Effects of Hyperkalemia  Arrhythmias, cardiac arrest  Nausea, diarrhea  Muscle weakness, paralysis beginning in the legs  Paresthesias-fingers, toes, face, tongue  Oliguria  Serum pH decreased-7.35 (acidosis) Magnesium (chapter 2, pg. 28) Magnesium (Mg) is an intracellular ion that has a normal serum level of 0.7 to 1.1 mmol per liter. Serum levels are linked to both potassium and calcium levels. Magnesium imbalances are rare Hypomagnnesemia Results from malabsorption or malnutrition, often associated with chronic alcoholism Causes of Hypomagnesemia  Use of diuretic  Diabetic ketoacidosis  Hyperparathyroidism  Hyperaldosteronism Effects of Hypomagnesemia  Neuromuscular hyperirritability  Tremors or chorea(involuntary repetitive movements)  Insomnia  Personalty changes  Increased heart rate with arrhythmias Hypermagnesemia Cause of Hypremagnesemia  Usually occurs with renal failure Effects of Hypermagnesemia  Depressed neuromuscular function  Decreased reflexes  lethargy  Cardiac arrhythmias  Metabolic acidosis: results from a decrease in bicarbonate ions (base) because of metabolic or renal problems.  Metabolic alkalosis: results from the loss of hydrogen ions through the kidneys or the gastrointestinal tract.  Respiratory acidosis: result from an increase in carbon dioxide levels (acid) due to respiratory problems.  Respiratory alkalosis: result when increased respirations cause a decrease in carbon dioxide (less acid).  Compensated serum pH= 7.35 to 7.4 (Respiratory & Metabolic acidosis)  Decompensated serum pH <7.35 (Respiratory & Metabolic acidosis)  Compensated serum pH= 7.4 to 7.45 (Respiratory & Metabolic alkalosis)  Decompensated serum pH > 7.45 (Respiratory & Metabolic alkalosis).....