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  • Elizabeth

    Galactorrhea. Lactation in men or women who are not breastfeeding. Usually due to a prolactin secreting pituitary adenoma. Diagnosis is by measure of prolactin levels and imaging. Treatments can include: dopaminergic agonists, and sometimes destruction or removal of the adenoma.

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Chest trauma: flail chest. Occurs when there is costal (rib) breakage, and one lung comes dislodged from the thoracic wall. The dislodged lung then causes paradoxical breathing, mediastinal shift, crepitus, JVD, tracheal shift, and can lead to skipped beats (no room for the heart to beat), shock, and death.

Here’s a good pic to help you distinguish eschar & slough. Remember, until enough slough and/or eschar is removed to expose the base of the wound, the true depth and stage cannot be determined.

Parenteral. Introducing medications, nutrition, or other substances into the body via a route that is not the GI tract.

Full-Thickness Burn: 4th-Degree. Caused by electrical current or prolonged contact with flame (such as an unconscious victim). Epidermins, dermis, epidermal appendages destroyed. Injury can also involve CT, muscle, and even bone. Wound is dry and looks charred. Mottled brown, white, red. No sensation, and limited or no movement of involved digits or extremities. This kind of burn requires skin grafting, amputation of involved extremities or digits is likely.

Full Thickness Burn: Third Degree. Caused by prolonged contact with flame, scalding liquids, or steam, hot objects, chemicals, or electrical current. Epidermis, dermis, and epidermal appendages are all destroyed. Wound is dry, leatherlike. Can be pale, mottled brown or red. Vessels are thrombosed and visible. The wound is insensitive to touch. Skin grafting is required.

Deep Partial Thickness 2nd-Degree Burn. Caused by intense radiant energy; scalding liquids, hot semisolids or solids, and flame. The epidermid is destroyed, underlying dermis is damaged, some epidermal appendages remain intact. Wound is pale and has decreased moistness. Absent or prolonged blanching. Intact sensation to deep pressure, but not to pin-prick. Prolonged healing of >21 days, which may require skin grafting to complete healing with functional outcome.

Superficial Partial Thickness 2nd-Degree burn. Caused by brief exposure to flash, flame, or hot liquids. The epidermis is destroyed, with minimal damage to superficial layers of dermis. Epidermal appendages remain intact. The wound is moist and weepy, with pink or red blisters. It blanches and is hypersensitive. Complete healing occurs in 21 days, with minimal to no scarring.

1st-Degree Burn. Caused by: sun, brief exposure to hot liquids. Injury is limited to the epithelium, and the skin remains intact. The wound is erythematous and hypersensitive, but without blister formation. Complete healing in 3-5 days without scarring.

Bronchiectasis. A condition of the bronchial tree that is caused by destruction of muscle and elastic tissue. The bronchi involved are dilated and inflamed, they easily collapse leading to airflow obstruction and an impaired ability to rid secretions. Because secretions stay stagnant, bronchiectasis is associated with an array of bacterial infections (staph, klebsilla, or B. pertussis). Cystic fibrosis is the leading cause. In children, inhalation of an object or substance can be responsible.

Secondary Polycthemia. Absolute erythrocytosis caused by increased stimulation of RBC production. Most often in response to tissue hypoxia in high altitudes or lung disease. Less often, it is caused by renal tumors that increase erythropoietin production. Phelbotomy is used to reduce CV workload, and oxygen administration can help. Prognosis depends on the underlying cause.

Polycthemia Vera, or Primary Polycthemia. An idiopathic chronic myeloproliferative disorder characterized by increase in RBC mass. Risk for thrombosis is increased, as are (though rarely) acute leukemia or myelofibrotic transformation. Aspirin is used to treat low-risk patients, and myelosuppressive therapy is used for those at higher-risk.

Allergic Transfusion Reaction. Often caused by antibodies to plasma proteins in the transfusion. Signs/symptoms: urticaria, flushing, wheezing, laryngeal edema, rarely it causes hypotension or anaphylaxis. Treatment: cease the transfusion, administer antihistamine, and if severe give epinephrine and/or steroids. To prevent this, pretransfusion antihistamine can be administered, and washed RBC components can be used.

Graft Versus Host Disease. Caused by viable T cells in transplant reacting against tissue antigens. Treatment: the goal is to suppress the immune response without damaging the new cells. Corticosteroids are the most effective treatment for GVHD, but antibodies to T cells and other meds are given to patients who do not respond to steroids. Complications can result in death; damage to liver, lungs, GI; severe infection; severe lung disease. Precautions: use gammma-radiated components to prevent

Delayed Transfusion Reaction. Hemolytic immune response. Caused by ABO incompatibility, but delayed 3-10 days post-transfusion. Signs/symptoms: fever, malaise, indirect hyperbilirubinemia, increased urine urobillinogen, falling hematocrit. Treatment: monitor hematocrit, renal function, coagulation profile. Usually, no acute treatment is required.

Acute Intravascular Hemolytic (immune) Transfusion Reaction. Caused usually by clerical errors. ABO or other erythrocyte antigen-antibodies are mislabeled. Signs/symptoms: hemoglobinemia and heoglobinuria, fever, chills, anxiety, shock, DIC, dyspnea, chest pain, flank pain, nausea/vomiting, headache, pain at needle site and along venous track. Treatment: STOP transfusion, hydrate, support BP and respiration, induce diuresis, treat shock and DIC.

Glasgow Coma Scale.

ACE Inhibitors (angiotensin inhibitors). Improves endothelial function; acts as antioxidant (LDL), and antiinflammatory.

Statins. For CHD: decreases LDL-C; increases HDL-C; improves endothelial function; antiinflammatory.

Aspirin. As a therapy for reducing coronary heart disease: inhibits thrombosis, and acts as an antiinflammatory.

Ventricular Septal Defect is the most common congenital cardiac malformation at birth, making up 42% of the total.

Tricuspid Atresia. Complete absence of a tricuspid valve. Accompanied often by right ventricular underdevelopment, and an atrial-septal defect (which allows blood flow from right to left). In some cases(but not all, as the picture would have you think), a ventricular-septal defect allows some blood into the right side and up into the pulmonary system. Other than that, a patent ductus arteriosus is required for any blood perfusion of the lungs. Cyanosis is present at birth, mortality is high.

Truncus Arteriosus. A cyanotic congenital malformation in which the aorta and pulmonary artery fail to separate. This leads to one large vessel that receives blood from both the right and left ventricles. A large ventricular septal defect below the single valvular structure leads to a mixture of blood from both sides being taken into systemic circulation. The amounts of blood entering systemic vs. pulmonary circulation depend on the degree of resistance in the two circulations.

MB band of Creatine Kinase (CK-MB). An "enzyme" marker for myocardial infarction, the MB band of CK-MB is indicative of injury in many muscles, but its release is a highly specific indicator for MI. It is only elevated for 48-72 hours afterwards, though, making it less useful than troponin I for diagnostic purposes.

Troponin. Considered a cardiac "enzyme." Troponin is an integral part of the myocardium (and every other muscle), and after a myocardial infarction has occurred troponin is released because of damage to the muscle. Troponins I and T (specific to myocardium) are choice markers for detecting MIs and considered to be diagnostic. However, their levels remain elevated and make detection of a reinfarction difficult.

Coarctation of the Aorta. Congenital acyanotic defect in which the aorta is constricted. Happens in males 3-4 times more often. Can occur anywhere on the aorta, but usually happens just before or after the ductus arteriosus. Preductal is more severe. This defect causes a high work load for the left side and may lead to heart failure in the early neo-natal period. Postductal coarcation is less severe and may be unrecognized into adulthood. Upper extremities have higher BP, low BP in lower body.