NR283 Pathophysiology Worksheet 2 Q&A Rated A+.

NR283 Pathophysiology Worksheet 2 Q&A Rated A+.   Worksheet 2 NR283 Pathophysiology Worksheet 2 Q&A Rated A+. Questions: 1. Define epidermis, dermis, and subcutaneous tissue. • Epidermis: Consists of 5 layers that vary in thickness @ different areas of the body; no blood vessels or nerves are present; contains melanocytes (specialized pigment-producing cells);5 layers include: stratum basale (innermost layer located on the basement membrane and only layer where mitosis occurs), stratum spinosum, stratum granulosum, stratum lucidum (present primarily in thick skin), and the stratum corneum (outer most layer). • Dermis: A thick layer of connective tissue that includes elastic and collagen fibers and varies in thickness over the body; provide flexibility and strength in the skin; provides support for the nerves and blood vessels; contains many sensory receptors for pressure or texture, pain, heat, or cold • Subcutaneous Tissue (or Hypodermis): Consists of connective tissue, fat, cells, macrophages, fibroblasts, blood vessels, nerves, and is the base of many of the appendages 2. Define the following; a. Macule: Small, flat, circumscribed lesion of a different color than the normal skin. b. Papule: Small, firm, elevated lesion. c. Nodule: Palpable elevated lesion and varies in size. d. Pustule: Elevated, erythematous lesion, usually containing purulent exudate. e. Vesicle: Elevated, thin-walled lesion containing clear fluid (blister). f. Plaque: Large, slightly elevated lesion with a flat surface, often topped by scale. g. Crust: Dry, rough surface or dried exudate or blood. h. Lichenification: Thick, dry, rough surface (leather-like). i. Keloid: A raised, irregular, and increasing mass of collagen resulting from excessive scar tissue formation. j. Fissure: Small, deep, linear crack or tear in the skin. k. Ulcer: Cavity with the loss of tissue from the epidermis and dermis and often consists of weeping or bleeding. l. Erosion: Shallow, moist cavity in the epidermis. m. Comedone: A mass of sebum, keratin, and debris blocking the opening of a hair follicle. n. Urticaria: Known as hives; that results from a type I hypersensitivity reaction that is commonly caused by ingest substances like shellfish or certain fruits or drugs; the release of histamine causes the eruption of hard, raised erythematous lesions on the skin, often scattered all over the body. o. Furuncles: Known as a boil; infection usually caused by S. aureus that begins in a hair follicle and spreads into the surrounding dermis; commonly found on the face, neck, and back; initially the lesion is a firm, red, painful nodule that develops into a large, painful mass (an abscess) that eventually drains large amounts of purulent exudate (pus) which is composed of leukocytes, cellular debris from dead blood cells and bacteria, and a thin protein rich fluid component. 3. Discuss impetigo. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Impetigo: A common infection in infants and children, but can also occur in adults; primarily from S. aureus, but also can be from group A beta-hemolytic streptococci. • Pathophysiology: Lesions that commonly occur on the face; begin as small vesicles that rapidly enlarge and rupture to form yellowish-brown crusty masses; underneath the crust, the lesion is red and moist, and exudes a honey-colored liquid; additional vesicles develop around primary site; pruritus is common and leads to scratching and further spread of the infection. • Risk Factors: S. aureus can cause highly contagious infections in neonates and is a threat in neonatal nurseries; easily spread by direct contact via the hands, eating utensils, or towels; close or physical contact can result in rapid spread of the infection (i.e., wrestling teams). • Clinical Manifestations: • Treatments: Topical antibiotics in early stages, but systemic (oral and topical) administration of these drugs are necessary is the lesions are extensive. 4. Discuss psoriasis. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Psoriasis: A chronic inflammatory skin disorder that affects 1-3% of the population and is considered to be genetic in origin; onset occurs within teen years, followed by a course of remissions and exacerbations; cases vary in severity; often psoriatic arthritis develops, too. • Pathophysiology: Occurs when there is an abnormal activation of T cells, causing an associated increase in cytokines in the affected tissues that lead to excessive proliferation of keratinocytes, thus, causing the symptoms to arise. The increased proliferation leads to thickening of the dermis and epidermis, which will eventually result in epidermal shedding that occurs in 1 single day (compared to 2 weeks in normal individuals). • Risk Factors: If the plaque is removed, small bleeding points will result. • Clinical Manifestations: Lesion begins as a small red papule due to inflammation and vasodilation, that enlarges to form an outer layer silvery plague; commonly found on the face, scalp, elbows, and knees; accompanied by a itching or burning sensation; fingernails may be thickened, pitted, or ridged. • Treatments: Aided to reduce cell proliferation such as glucocorticoids, tar preparations, and in severe cases the antimetabolite methotrexate; exposure to UV light has been shown to drastically help, too. 5. Discuss herpes simplex. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Herpes Simplex: A viral infection with numerous types; HSV-1 is the common cause of cold sores or fever blisters; HSV-2 usually refers to occurrence in the genital region; Herpes zoster is the causative agent of shingles. • Pathophysiology: The virus remains in a latent stage in the sensory nerve ganglion of the trigeminal nerve, from which it can be reactivated to cause skin lesions. • Risk Factors: The virus may be present in saliva for weeks following healing of the lesion and since it is spread via direct contact with fluid from the lesion it can therefore, be easily and frequently spread to others or to the fingers (causing whitlow) if there’s a break in the skin or to the eyes (causing keratitis-an infection and ulceration of the cornea). • Clinical Manifestations: Initially a person is asymptomatic but due to an infection like the common cold, sun exposure, or stress the virus can become reactivated and will cause a burning or tingling sensation along the nerve and the at the site of the initial infection, which is then followed by painful vesicles that will eventually rupture to form a crust. Takes about 2 to 3 weeks for spontaneous healing to occur. • Treatments: During the acute stage, the viral shedding and spreading can be reduced by the topical application or oral medications of antiviral drugs such as acyclovir (Zovirax) or valcyclovir (Valtrex). 6. Discuss scabies. Include the pathophysiology, risk factors, and clinical manifestations. • Scabies: Is when the body is invaded by a mite called Sarcoptes scabiei. • Pathophysiology: The female mite burrows into epidermis to lay eggs over a period of several weeks as she moves into the stratum corneum; male dies after fertilizing the female; female dies after laying her eggs; larvae emerge from eggs and migrate to skins surface to borrow and search for nutrients; larvae mature into adults and the cycle is repeated; inflammation and pruritus results because of the damage to the skin from the burrowing and the presence of mite fecal material in the burrow. • Risk Factors: Spread via close contact. • Clinical Manifestations: The burrows appear on the skin as tiny, light brown lines, often with small vesicles and erythema; commonly found on areas between the fingers, the wrists, the inner surfaces of the elbows, and the waistline. • Treatments: Topical treatment with lindane is effective (Sklice). 7. Discuss pediculosis. Include the pathophysiology, risk factors, and clinical manifestations. • Pediculosis: Known as lice, which are small, brownish parasites that feed off of human blood.; Pediculus humanus corporis is body lice, Pediculus pubis is pubic lice, and Pediculus humanus capitis is head lice (referred to as cooties). • Pathophysiology: Female lice lay eggs on hair shafts, cementing the egg firmly to the hair close to the scalp. The egg (or nit) appears as a small, whitish shell attached to the hair. After hatching the louse bites the human host, sucking blood for its survival. • Risk Factors: • Clinical Manifestations: The site of each bite resembles a macule or papule that is highly pruritic owing to the mite salvia and excoriations result from scratching, which can also cause visible nits. • Treatments: Topical permethrin, malathion, or pyrethrin (although resistance to these drugs are known). Use of a fine-toothed comb and cleaning of all clothing, linen, and surrounding areas. 8. Discuss Tinea (tinea capitis, tinea corporis, and tinea pedis). Include the pathophysiology, risk factors, clinical manifestations and treatment. • Tinea: May cause several types of superficial skin infections (dermatophytoses or ringworm), depending on the area of the body that is affected. I. Tinea Capitis: Infection on scalp; school-aged children; from Microsporum canis via cats or dogs; from Trichophyton tonsurans via humans; circular bald patch because hair’s broken off above scalp; erythema or scaling; oral antifungal agents like griseofulvin. II. Tinea Corporis: the body, particularly the non-hairy parts; lesion’s round; erythematous right of vesicles or papules have clear center (ringworm) scattered over the body; pruritus or burning sensation present; topical antifungal’s like tolnaftate or ketoconazole. III. Tinea Pedis: known as athlete’s foot; involves the feet, particularly the toes; caused by Trichophyton mentagrophytes or Trichophyton rubrum; may be associated with swimming pools or gymnasium; skin between toes becomes inflamed and macerated, with painful and pruritic fissures; may have foul odor; secondary bacterial infections are common, which add to the inflammation and necrosis; topical tolnaftate is used. 9. Discuss necrotizing fasciitis. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Necrotizing Fasciitis: termed as the ‘flesh-eating’ disease because of its extremely rapid tissue invasion. • Pathophysiology: Tissue invasion results from reduced blood supply; tissue destruction results from secretion of protease enzymes; aerobic and anaerobic microbes present at site; the fulminant course of severe inflammation and tissue necrosis is primarily a result from a highly virulent strain of gram-positive, group A, beta-hemolytic Streptococcus (S. pyogenes), which also produces a toxin that causes toxic shock; superficial fascia in the subcutaneous tissue and fascia surround the skeletal muscle, as well as other soft tissues, become edematous and necrotic, with the occlusion of small blood vessels leading to gangrene. • Risk Factors: early diagnosis is difficult because signs/symptoms are similar to cellulitis, which can be extremely dangerous since this infection process is so rapid; could result in death; increase in cases during the ‘cold months’; often occurs when there was a history of a minor trauma or infection of the skin and subcutaneous tissue of an extremity. • Clinical Manifestations: systemic toxicity develops with fever, tachycardia, hypotension, mental confusion, disorientation, and possibly organ failure; infected areas appear inflamed and painful, and they rapidly increase in size, and there are dermal gangrene present. • Treatments: aggressive antimicrobial therapy, fluid replacement, excision of all infected tissue, high oxygen flow in hyperbaric chambers, and possibly even amputation to prevent further spread. 10. Discuss malignant melanoma. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Malignant Melanoma: serious skin cancer that develops from melanocytes and is increasing in incidence. • Pathophysiology: melanomas arise from melanocytes in the basal layer of the epidermis or from a nevus (mole); often extend down into the tissues and metastasize quickly to the regional lymph nodes, then, to other organs. • Risk Factors: depends on genetic factors, exposure to UV radiation, and hormonal influence; they grow very quickly, spreading to organs, which lead to poor prognosis. • Clinical Manifestations: Nevi that grow, change shape, color, size, texture, or bleed are warning signs (ABCD: Area of mole’s increased, Border’s irregular Color changes, Diameter of mole’s increased); malignant melanoma often appear as a multicolored lesion with an irregular border. • Treatments: surgical removal of infected area and an extensive amount of tissue around and below the lesion to ensure all of the malignant cells are gone; additional radiation and chemotherapy provides a 5-year survival rate in 99% of cases with localized tumors and some 7-10% of cases when the tumors already invaded or metastasized. 11. Define the following; a. Rales: A bubbly or crackling sound in the lungs caused by air mixing with in the airways; associated with serous secretions. b. Rhonchi: A deep and harsh sound resulting from air mixing with excessive secretions in the lungs; results from thicker mucus. c. Stridor: An abnormal high-pitched, crowing sound caused by obstruction in the trachea or larynx. d. Wheezing: A high-pitched whining sound typical of obstruction in the bronchioles and small bronchi. e. Dyspnea: Difficulty breathing; subjective feeling of discomfort that occurs when a person’s unable to inhale enough air; manifested as SOB, either with exertion or at rest. f. Orthopnea: Form of dyspnea; difficult or labored breathing; pulmonary congestion develops as more blood pools in the lungs, while the abdominal contents push upward against the lungs of a person laying down, and is usually relieved by an upright position. g. Paroxysmal nocturnal dyspnea: Sudden acute type of dyspnea; awakening in severe respiratory distress; usually associated with pulmonary edema because while asleep the body fluid is being redistributed; common in patients with left-sided congestive heart failure. h. Hemoptysis: Frothy sputum containing streaks of blood, usually bright red, and referred to as ‘spitting up blood’. i. Hypercapnia: An increased level of carbon dioxide (CO2) in the blood. j. Clubbing: a painless, firm, fibrotic enlargement at the end of the digit. k. Eupnea: Normal, regular, quiet breathing; 10 to 18 inspirations per minute; pattern is regular and effortless. l. Apnea: Lack of breathing; sleep apnea results when the pharyngeal tissues collapse during sleep leading to repeated and momentary cessation of breathing. m. Hypoxemia: Insufficient oxygen in the arterial blood (PaO2). n. Cyanosis: Bluish color of skin and mucosa that occurs when a large proportion of hemoglobin is unoxygenated. 12. Discuss acute sinusitis. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Sinusitis: a bacterial infection secondary to a cold or an allergy that obstructed the drainage of 1 or more of the paranasal sinuses in the nasal cavity. • Pathophysiology: commonly from pneumococci, streptococci or Haemophilus influenzae; as the exudate accumulates the pressure builds up in the sinus cavity to cause severe pain in the facial bone • Risk Factors: anyone with a primary infection, such as the cold. • Clinical Manifestations: severe facial bone pain, which could be confused with a headache (ethmoid sinus) or toothache (maxillary sinus); nasal congestion, fever, and sore throat. • Treatments: decongestants and analgesics are recommended until the sinuses are draining well; antibiotics required to eradicate the infection 13. Discuss lobar pneumonia. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Lobar Pneumonia: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 14. Discuss aspiration pneumonia. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Aspiration Pneumonia: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 15. Discuss cystic fibrosis. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Cystic Fibrosis: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 16. Discuss epiglottis. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Epiglottis: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 17. Discuss lung carcinoma. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Lung Carcinoma: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 18. Discuss asthma. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Asthma: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 19. Discuss chronic obstructive pulmonary disease (COPD). Include the pathophysiology, risk factors, clinical manifestations and treatment. • Chronic Obstructive Pulmonary Disease (COPD): • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 20. Discuss pulmonary edema. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Pulmonary Edema: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 21. Discuss bronchiectasis. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Bronchiectasis: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 22. Discuss pulmonary embolus. Include the pathophysiology, risk factors, clinical manifestations and treatment. • Pulmonary Embolus: • Pathophysiology: • Risk Factors: • Clinical Manifestations: • Treatments: 23. Discuss laryngotracheobronchitis (croup). Include the pathophysiology, risk factors, clinical manifestations and treatment. • Laryngotracheobronchitis (Croup): common viral infection, primarily in children between 1-2, but adults can get it, too. • Pathophysiology: caused from parainfluenza viruses and adenoviruses; infection starts as an upper respiratory condition; in children, the larynx and subglottic area becomes inflamed, leading to obstruction. • Risk Factors: more severe at night; children with allergic tendencies may result in smooth muscle spasms that exacerbate the obstruction and requires additional medical treatment. • Clinical Manifestations: begins with nasal congestion and cough; children experience swelling and exudate that leads to the characteristic ‘barking cough’ referred to as croup; hoarse voice and inspiratory stridor. • Treatments: cool, moisturized air from a humidifier, shower, or croup tent helps to relieve the obstruction 24. Discuss the different types of pneumothorax. Include the pathophysiology, risk factors, clinical manifestations and treatment for each. • Pneumothorax: refers to air in the pleural cavity; the presence of air at atmospheric pressure in the pleural cavity and the separation of the pleural membranes by air prevent expansion of the lung, leading to atelectasis I. Closed Pneumothorax: occurs when air can enter the pleural cavity via an opening directly from the internal airways; there’s no opening in the chest wall; can be simple or spontaneous pneumothorax, or secondary to another disease. II. Simple or Spontaneous Pneumothorax: occurs when a tear on the surface of the lung allows air to escape from inside the lung through a bronchus and the visceral pleural cavity; as lung tissue collapses, it seals off the leak; following collapse, the mediastinum can shift toward the affected lung, allowing the other lung to expand more; often occurs in young men with no prior lung disease, but rather from an idiopathic bleb or defect from the lung surface. III. Secondary Pneumothorax: associated with an underlying respiratory disease resulting from rupture of an emphysematous bleb on the surface of the lung or erosion by a tumor or tubercular cavitation through the visceral pleura; let’s inspired air pass into the pleural cavity. IV. Open Pneumothorax: refers to atmospheric air entering the pleural cavity through an opening in the chest call; can be a result from a trauma or surgery. V. Tension Pneumothorax: most serious form; may result from an opening through the chest wall and parietal pleura (open pneumothorax) or from a tear in the lung tissue and visceral pleura (closed pneumothorax) that causes atelectasis; damage creates a flap of tissue or one-way valve effect, whereby the opening enlarges on inspiration that promotes airflow into the pleural cavity and is sealed off during expiration that prevents removal of air from the pleural cavity; each inspiration leads makes it worse; pressure eventually pushes the mediastinal contents against the other lung, compressing it and the inferior vena cava; severe hypoxia and respiratory distress develops and can be life threatening. • Clinical Manifestations: atelectasis, dyspnea, cough, and chest pain; breath sounds reduced over atelectasis area; various signs related to chest movements, unequal expansion, and mediastinal shift vary depending on the type; hypoxia that leads to sympathetic responses like anxiety, tachycardia, and pallor; the interference with venous return leads to hypotension. • Emergency Treatment: i. Transport to a hospital as soon as possible/ ii. An open pneumothorax or sucking wound is covered with an occlusive dressing or covering to prevent the air moving in and out of the pleural cavity. The dressing should be checked to ensure that a tension pneumothorax hasn’t developed. iii. Penetrating objects shouldn’t be removed from chest wall until medical assistance is available. iv. If possible, tension pneumothorax should be converted to an open pneumothorax, by removing loose tissue or enlarging the opening. Match the types of skin disorders with their causative organisms. 25. Tinea (Fungal Infection). A. Bacterial infection 26. Impetigo (Bacterial Infection). B. Varicella virus 27. Chicken pox (Varicella Virus). C. Human Herpes Virus 8 28. Kaposi sarcoma (Human Herpes Virus 8). D. Fungal infection 29. Plantar Warts (Human Papillomavirus). E. Human Papillomavirus Match the pleural effusion fluid with its description. 30. Transudate (White Blood Cells). A. Pus 31. Exudate (Watery). B. White blood cells 32. Hemothorax (Blood). C. Watery 33. Empyema (Pus). D. Blood 34. Discuss the major types of leukemia. • The Leukemia’s: a group of neoplastic disorders involving the WBCs; survival rate of 45%; 1 or more leukocyte types are present as undifferentiated, immature, nonfunctional cells that multiply uncontrollably in the bone marrow; large quantities are released into the general circulation; as the number of cells increase, they can infiltrate the lymph nodes, spleen, liver, brain, and other organs; proliferation of bone marrow suppresses the production of normal cells and leads to anemia, thrombocytopenia, and a lack of normal functional leukocytes; rapid turnover rate of cells leads to hyperuricemia and a risk of kidney stones or kidney failure; as malignancy progressed, the increased number of cells cause congestion and enlargement of lymphoid tissue, lymphadenopathy, splenomegaly, and hepatomegaly; usual result is death because of the overwhelming infection or hemorrhage I. Acute Lymphocytic Leukemia (ALL): usually occurs in young children between 2-5 years; associated with chromosomal abnormalities, particularly translocations; evident in children with Down syndrome; characterized by a high proportion of very immature, nonfunctional cells (blast cells) in the bone marrow, and peripheral circulation; onset is usually abrupt. II. Acute Myelogenous (or myelocytic) Leukemia (AML): usually occurs in adults; malignant cells are the granulocytic stem cells III. Chronic Lymphocytic Leukemia: usually occurs in adults that are greater than 50 years old; malignant cells are the B-lymphocytes IV. Chronic Myelogenous Leukemia (CML): usually occurs in adults between 30-50 years old; malignant cells are the Granulocytic stem cells V. Acute Monocytic Leukemia: usually occurs in adults; the malignant cells are the monocytes VI. Hairy Cell Leukemia: usually occurs in males that are greater than 50 years old; the malignant cells are the B-lymphocytes 35. What would a Vitamin K deficiency do to a person’s ability to clot? • Vitamin K deficiencies may cause a decrease in prothrombin and fibrinogen levels and result in bleeding problems due to not having enough of one of the main clotting factors; Vitamin K is a fat-soluble vitamin produced by the intestinal bacteria that is required for the synthesis of most clotting factors 36. What is the major risk associated with leukocyte counts less than 1000/mm3? • It can predispose the patient to infection; it can greatly increase the risk of infection 37. Blood loss is associated with which anemia? • Iron-Deficiency Anemia 38. What are the two vitamin deficiencies responsible for the macrocytic-normochromic anemias? • Known as Pernicious Anemia-Vitamin B12 Deficiency (Megaloblastic Anemia); deficiencies of Folic Acid (Vitamin B9) or Cyanocobalamin (Vitamin B12). 39. Which lab value is commonly used to measure anemia? • The first test to diagnose anemia is a complete blood count (CBC); used to check hemoglobin and hematocrit levels; low levels of RBCs or hemoglobin indicates anemia. 40. List one non-modifiable risk factor for hypertension. • Age, gender, or genetics 41. List three modifiable risk factors for hypertension. • High sodium intake, excessive alcohol intake (small amounts of alcohol appear to decrease blood pressure), obesity, and prolonged or recurrent stress. 42. Differentiate angina from myocardial infarction with regard to its cause and the characteristics of pain associated with it. • Angina: *lack of oxygen causing chest pain; no permanent damage* known as chest pain; occurs when there’s a deficit of oxygen to the heart muscle. o Causes: when the blood or oxygen supply to the myocardium is impaired, when the heart is working harder than usual and needs more oxygen, or when a combination of these factors is present. o Characteristics of Pain: *pain in left arm, neck, radiate even to the back, too* classic or exertional angina, which is the normal chest pain from physical activity; variant angina, in which vasospasm occurs and rest; unstable angina, which is the most serious and refers to a prolonged pain at rest and of recent onset, perhaps the result of a break in an atheroma and can proceed to a myocardial infraction (heart attack). o Classic Angina (Exertional): caused from being active (mowing lawn, shovel snow, play sports); lasts until you sit down to rest. o Variant Angina: occurs while @ rest, too; lasts from a few seconds to a few minutes long; o Unstable Angina: biggest warning sign to MI; prolong (lasts a lot longer than a few minutes); can happen at rest or while active; recurrent; • Myocardial Infraction (MI): known as a heart attack; occurs when a coronary artery is totally obstructed, leading to prolonged ischemia and cell death, or infarction, of the heart wall. o Causes: most common cause is atherosclerosis, usually with thrombus attached. o Characteristics of Pain: sudden substernal chest pain that radiates to the left arm, shoulder, jaw, or neck; described as severe, steady, and crushing; no relief occurs with rest or vasodilators*the warning signs of a heart attack include: (1) the feeling of pressure, heaviness, or burning in the chest, especially with increased activity, (2) sudden SOB, sweating, weakness, and fatigue, (3) nausea and indigestion, and (4) anxiety and fear* o Body Releases Enzymes: troponin (2 types), which specially tell you there’s been specific tissue death in the heart; CMKB is an indicator, but not just the heart can release this. o If blood flow is reversed w/in 20-30 minutes, then it the damage CAN be reversed (i.e., it will not be irreversible). 43. If you had a client with persistent chest pain following rest and administration of nitroglycerin, what action would you take? • If after the first dosage of Nitroglycerin the patient is still experiencing chest pain, they may wait 3-5 minutes and take a second dose. They can repeat Nitro at a max of 3 times or 3 different dosages, but if chest pain does not go away, then that is a sign that an MI (heart attack) may be occurring. 44. Why would you recommend avoidance of prolonged stress for a patient with congenital heart disease? • B/C stress increases the demands of the heart, which can cause an increased heart rate and possibly result in congestive heart failure (CHF). 45. Explain how aortic stenosis may develop following rheumatic fever. • Rheumatic fever is an acute systemic inflammatory condition that appears to result from an abnormal immune reaction occurring a few weeks after an untreated infection, usually caused by strains of group A beta-hemolytic Streptococcus; antibodies are normal at first and then eventually react with connective tissue (collagen) in the skin, joints, brain, and heart, causing inflammation; 46. Explain why untreated essential hypertension is dangerous. • Essential hypertension increases diastolic BP, requiring the left ventricle to contract with more force to open the aortic valve and eject blood into the aorta; the left ventricle hypertrophies and eventually fails; BP can continue to increase due to vasoconstriction, leading to decreased blood flow; if untreated over a long period of the time there will be damages to the arterial walls, as they will become hard and thick (sclerotic), narrowing the lumen and thus, the wall will dilate or tear, forming an aneurysm, or encourage artheroma formation; damage will occur mostly in the kidneys, brain, and retina 47. Define and explain the term intermittent claudication. • Intermittent claudication is referred to as leg pain; is associated with exercise due to muscle ischemia; initially pain subsides with rest, but as obstruction advances, pain will be more severe at rest, particularly in the distal areas such as the feet and toes. 48. Describe three early signs of shock and the rationale for each. I. Hypovolemic: due to loss of blood or plasma; causes hemorrhage, burns, dehydration, peritonitis, and pancreatitis. II. Cardiogenic: due to decreased pumping capability of the heart; causes myocardial infarction of the left ventricle, cardiac arrhythmia, pulmonary embolus, and cardiac tamponade. III. Anaphylactic: due to systemic vasodilation and increased permeability owing to a severe allergic reaction; caused by insect stings, drugs, nuts, or shellfish. IV. Septic (Endotoxin): due to vasodilation owing to severe infection, often with gram-negative bacteria; causes virulent microorganisms (gram-negative bacteria) or multiple infections. 49. List four types of congenital heart defects and briefly describe each. I. Ventricular Septal Defect: most common; called a “hole in the heart”; it’s when there’s an opening in the interventricular septum, which may vary in size and location; 50. Atherosclerosis puts the individual at high risk for developing which cardiac disorder? • Angina, and MI or a heart attack 51. List one way to prevent DVT’s (Deep Vein Thrombosis). • If patient has prolonged bed rest then compression stockings are helpful; a filter can be surgically inserted in the inferior vena cava to remove blood clots; if due to thrombus then oxygen is administered and usually heparin or streptokinase (fibrinolytic agents); mechanical ventilation may be necessary; embolectomy may have to be performed 52. Aortic heart valve disorders, if left untreated, can lead to which cardiac condition? • An aneurysm due to hypertension can result from aortic heart valve disorders 53. A friction rub is associated with which cardiac condition? • A friction rub is painful and heard as a grating sound on the chest with a stethoscope and is most commonly associated with the cardiac condition Pericarditis, which is when there is inflammation or infection of the pericardium that causes effusion and impaired filling of the heart. 54. What is cor pulmonale? • Cor pulmonale is the term used to refer to right-sided CHF that’s due to pulmonary disease. 55. Which laboratory test is used to help diagnose a myocardial infarction? • An ECG is used to illustrate the conduction activity of the heart, as well as the effect of systemic abnormalities such as serum, electrolyte imbalance; nuclear imaging with radioactive substances such as thallium assess the size of an infarct in the heart, the extent of myocardial perfusion, and the function of the ventricles, and can identify dead or damaged areas of myocardial tissues in order to assess the extent of the myocardial damage after a MI has occurred. RIGHT-SIDED CONGESTIVE HEART FAILURE: • Peripherally edema in feet, ankles • Asities (sp?) edema in your abdomen • JVD, vein’s really distended and bulging • Headache LEFT-SIDED CONGESTIVE HEART FAILURE: • LEFT=LUNGS LEFT-SIDED CHF CAN LEAD TO RIGHT-SIDED CHF!!!!