NR 283 Exam 1 study guide PDF

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NR283 Pathophysiology Study Guide for Exam 1

Chapter 1: Intro to Pathology 1 & 2. Describe the cellular adaptations made in each of the following processes and their causative factors: atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia Atrophy- a decrease in the size of cells, resulting in a reduced tissue mass. Common causes include reduced use of the tissue, insufficient nutrition, decreased neurologic or hormonal stimulation, and aging Hypertrophy- an increase in the size of individual cells, resulting in an enlarged tissue mass. This increase may be caused by additional work by the tissue, as demonstrated by an enlarged heart muscle resulting from increased demands Hyperplasia- an increased number of cells resulting in an enlarged tissue mass. Hyperplasia may be a compensatory mechanism to meet increased demands, or pathologic when there is a hormonal imbalance, or it may mean there is an increased risk of cancer Dysplasia- tissue in which the cells vary in size and shape, large nuclei are frequently present, and the rate of mitosis is increased. May result from chronic irritation infection, or may be a precancerous change. Detection of dysplasia is the basis of routine screening tests for atypical cells such as the Pap smear Metaplasia- when one mature cell type is replaced by a different mature cell type. May result from a deficit of vitamin A. Metaplasia is sometimes an adaptive mechanism that provides a more resistant tissue (i.e. when stratified squamous epithelium replaces ciliated columnar epithelium in the respiratory tracts of cigarette smokers. The new cells make a stronger barrier but they decrease defenses for the lungs because they lack cilia)

3. Identify the most common cause of cellular injury. The most common cause of cellular injury is ischemia (decreased supply of oxygenated blood to a tissue or organ, due to circulatory obstruction), which results in hypoxia (reduced oxygen in tissue) and reduced cellular metabolism Other causes of cell injury: ● ● ● ● ● ● ●

Physical agents - excessive health or cold or radiation exposure Mechanical damage such as pressure or tearing of tissue Chemical toxins Microorganisms such as bacteria, viruses, and parasites Abnormal metabolites accumulation in cells Nutritional deficits Imbalance of fluids or electrolytes

4. Describe cellular injury caused by infection and inflammation. Infectious diseases cause cell injury through microorganisms (i.e. bacteria & viruses). Some microorganisms induce pyroptosis (a type of cell death by lysis/dissolution of the cell), resulting in the rupture of the plasma membrane and release of destructive lysosomal enzymes into the tissue, which causes inflammation (swelling, redness, and pain) as well as damage to nearby cells and reduced function

5. Describe the major mechanism of tissue damage caused by chemical injury. Chemicals from both the environment (exogenous) and inside the body (endogenous) may damage cells, either by altering cell membrane permeability or producing free radicals, which continue to damage cell components

6. Discuss the manifestations of the four major types of necrosis, and give examples of the tissue types affected by each type of necrosis. Liquefaction necrosis- the process by which dead cells liquefy under the influence of certain cell enzymes. Occurs when brain tissue dies, or in some bacterial infections in which a cavity or ulcer develops in the infected area Coagulative necrosis- when the cell proteins are altered or denatured and the cells retain some form for a time after death. Occurs in a myocardial infarction when a lack of oxygen causes cell death Fat necrosis- when fatty tissue is broken down into fatty acids in the presence of infection or certain enzymes. These compounds may increase inflammation. Caseous necrosis- a form of coagulation necrosis in which a thick, yellowish, “cheesy” substance forms. When TB develops, the first stage is characterized by development of a Ghon complex a.k.a. granuloma (small solid mass of macrophages & lymphocytes covered by connective tissue). Caseous necrosis can be seen inside this mass. The Ghon complex heals like a scar, containing the infection. If the infection continues to develop, the area may undergo liquefaction necrosis, forming a cavity

7. Discuss apoptosis. Apoptosis- programmed cell death; a normal occurrence in the body. Cells self-destruct by digesting themselves enzymatically and then disintegrate into apoptotic bodies (vesicles), which are then phagocized without eliciting an inflammatory response. Apoptosis may increase when cell development is abnormal, cell numbers are excessive, or cells are injured or aged.

8. Discuss the types of tissue necrosis. 

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Coagulative o Cardiac o Kidney caused by ischemia Fat o Pancreas o Breast tissue Liquefactive o Abscess and hypoxic death o Commonly found in the brain Caseous o Spaces of cavitation (cystic spaces) o Found in TB patients and the bronchi o Lungs, kidney

Chapter 02: Fluids and Electrolytes, Acids and Bases 1. Discuss the two functional fluid compartments of the body. o Intracellular fluid compartment- fluid inside cells; makes up greater % of body weight than ECF o Extracellular fluid compartment- fluid outside the cells  Includes: – Intravascular fluid (blood/fluid in blood) – Interstitial fluid (intercellular fluid) – Cerebrospinal fluid – Transcelluar fluids (present in various secretions like pericardial (heart) cavity or synovial cavities) 2. Discuss the ways water moves between plasma and interstitial fluid. Water moves between the plasma (vascular component/blood vessels) and the interstitial compartment through a semipermeable capillary membranes based on hydrostatic pressure and osmotic pressure. At the arteriolar end of the capillary, the plasma hydrostatic pressure (blood pressure) is greater than the interstitial hydrostatic pressure and the plasma osmotic pressure of the blood so fluid moves/pushes out from the capillary into the interstitial compartment. At the venous end of the capillary, the plasma hydrostatic pressure is decreased and the osmotic pressure is increased (because of the greater concentration of plasma proteins and other solutes) so fluid is pulled back into the capillary from the interstitial compartment

3. Describe the causation, pathophysiologic process, and clinical manifestations of edema. Edema- an excessive amount of fluid in the interstitial compartment, which causes a swelling or enlargement of the tissues. Causes of Edema: 1. Increased capillary hydrostatic pressure (higher BP)- prevents return of fluid from the interstitial compartment to the venous end of the capillary, or forces excessive amounts of fluid out of the capillaries into the tissues (pulmonary edema). Specific causes of edema related to increased hydrostatic pressure include increased blood volume (hypervolemia) associated with kidney failure, pregnancy, CHF, or administration of excessive fluids. 2. Loss of plasma proteins (albumin)- results in decreased plasma osmotic pressure because there are less proteins/solutes in the plasma. Fewer plasma proteins in the capillary allows more fluid to leave the capillary and less fluid to return to the venous end of the capillary. Proteins are lost in urine through kidney disease; protein synthesis is impaired in patients with malnutrition/malabsorption diseases or with liver disease. Protein levels drop acutely in burn patients with large burn areas because the subsequent inflammation and loss of skin barrier allows proteins to easily leak out of the body Excessive Na+ levels in the ECF accompany the two causes just mentioned. When Na+ ions are retained, they promote accumulation of fluid in the interstitial compartment by increasing the ISF osmotic pressure and decreasing the return of fluid to the blood. Blood volume and BP are usually elevated. High Na+ levels are common in patients with heart failure, high BP, kidney disease, and increased aldosterone secretion. 3. Obstruction of the lymphatic circulation- causes localized edema because excessive fluid & protein are not returned to the general circulation. May occur if a tumor or infection damages lymph nodes or if lymph nodes are removed (cancer surgery) 4. Increased capillary permeability- causes localized edema; results from an inflammatory response or infection. Histamine and other chemical mediators released from cells following tissue injury cause increased capillary permeability and increased fluid movement into the interstitial area. Protein also leaks into the interstitial compartment, increasing the osmotic pressure in ISF and thus holding more fluid in the interstitial area. Increase in capillary permeability can result from some bacterial toxins or large burn wounds, leading to both hypovolemic and shock Signs & Symptoms of Edema: o Pale, gray, or red skin color o Weight gain o Slow, bounding pulse, high BP o Lethargy, possible seizures o Pulmonary congestion, cough, rales o Laboratory values: Decreased HCT, decreased serum Na+ o Urine: low specific gravity, high volume

4. Discuss the regulatory processes for sodium and water balance in the body, including the role of antidiuretic hormone, renin-angiotensin-aldosterone

Antidiuretic Hormone (ADH)- controls the amount of fluid leaving the body in the urine; helps retain Na+ and promotes reabsorption of water into the blood from the kidney tubules; prevents the production of dilute urine; released by the pituitary gland Aldosterone determines the reabsorption of Na+ ions and water from the kidney tubules; aldosterone conserves more fluid when there is a fluid deficit in the body. The kidneys detect low blood volume or Na+ levels, or blood K+ is high, and release renin (enzyme). Renin converts angiotensinogen (produced in the liver) to angiotensin I (hormone). Angiotensin-converting enzyme (ACE), found in the lungs, metabolizes angiotensin I into angiotensin II. Angiotensin II causes vasoconstriction and BP to increase. Angiotensin II stimulates the release of aldosterone in the adrenal glands, which causes the renal tubules to retain Na+ and water and excrete K+. Angiotensin II & aldosterone work to raise blood volume, blood pressure and Na+ levels in the blood. If the renin-angiotensin system becomes overactive, consistently high blood pressure results

5. Identify the basic causes and clinical manifestations of hypernatremia, hyponatremia, hyperkalemia and hypokalemia, hypocalcemia, hypercalcemia Causes of HYPERnatremia: o Excessive consumption of Na+ without proportionate water intake o Loss of water from the body that is faster than the loss of sodium o Insufficient ADH, which results in a large volume of dilute urine (diabetes insipidus) o Loss of the thirst mechanism o Watery diarrhea o Prolonged periods of rapid respiration Signs & Symptoms of HYPERnatremia: o Thirst; tongue and mucosa are dry and sticky o Weakness, lethargy, agitation o Edema o Elevated BP Causes of HYPOnatremia: o Losses from excessive sweating, vomiting, and diarrhea o Use of certain diuretic drugs combined with low-salt diets o Insufficient aldosterone, adrenal insufficiency, and excess ADH secretion (SIADH or syndrome of inappropriate antidiuretic hormone secretion) o Early chronic renal failure o Excessive water intake Signs & Symptoms of HYPOnatremia: o Anorexia, nausea, cramps o Fatigue, lethargy, muscle weakness o Headache, confusion, seizures o Decreased BP

Causes of HYPERkalemia: o Renal failure o Aldosterone deficit o “K+ sparing” diuretic drugs o Leakage of intracellular K+ into ECF in pts with extensive tissue damage/traumatic injuries o Displacement of K+ from cells by prolonged acidosis Signs & Symptoms of HYPERnatremia: o Arrhythmias, cardiac arrest o Nausea, diarrhea o Muscle weakness, paralysis beginning in leg o Paresthesias (fingers, toes, face, tongue) o Oliguria o pH < 7.35 (acidosis) Causes of HYPOkalemia: o Excessive losses from the body due to diarrhea o Diuresis associated with certain diuretic drugs o Excessive aldosterone or glucocorticoids in the body o Decreased dietary intake, which may occur with alcoholism, eating disorders, or starvation o Treatment of diabetic ketoacidosis with insulin Signs & Symptoms of HYPOkalemia: o Cardiac arrhythmias, cardiac arrest o Anorexia, nausea, constipation o Fatigue, muscle twitch, weakness, leg cramps o Shallow respirations, paresthesias o Postural hypotension, polyuria, and nocturia o pH > 7.45 (alkalosis) Causes of HYPERcalcemia: o Uncontrolled release of Ca2+ ions from the bones due to neoplasms; malignant bone tumors destroying bone, or tumors secreting PTH in excess of body needs o Hyperparathyroidism o Immobility, which may decrease stress on the bone, leading to demineralization o Increased intake of Ca2+ due to excess vitamin D or excess dietary Ca2+ o Milk-alkali syndrome associated w/ increased milk & antacid intake Signs & Symptoms of HYPERcalcemia: o Apathy, lethargy o Anorexia, nausea, constipation o Polyuria, thirst o Kidney stones o Arrhythmias, prolonged strong cardiac contractions, increased BP

Causes of HYPOcalcemia: o Hypoparathyroidism- decreased parathyroid hormone causes decreased intestinal Ca2+ absorption o Malabsorption syndrome- decreased intestinal absorption of vitamin D or Ca2+ o Deficient serum albumin o pH > 7.45 (alkalosis) Signs & Symptoms of HYPOcalcemia: o Tetany- involuntary skeletal muscle spasm, carpopedal spasm, laryngospasm o Tingling fingers o Mental confusion, irritability o Arrhythmias, weak heart contractions

6. Discuss the causes, clinical manifestations, complications of water deficit (hypovolemia). Hyponatremia results in decreased osmotic pressure in the extracellular compartment which may cause a fluid shift into cells, resulting in hypovolemia and decreased blood pressure Decreased volume of circulating blood in the body. Can be caused by severe diarrhea and vomiting, injury from deep cut or hard impact, illnesses like damage in organ like spleen, liver, kidneys, tear in heart or a large blood vessel. Problems with digestive track such as ulcers. S/S are dehydration, sunken, soft eyes, dry mucous membrane, concentrated urine, thirst, weight loss, fatigue, weakness, dizziness, possible stupor, increased body temperature, low blood pressure, thread pulse

7. Discuss the causes, clinical manifestations, complications, of water excess (hypervolemia). Increased hydrostatic pressure includes increased blood volume. It is associated with kidney `failure, pregnancy, congestive heart failure, or administration of excessive fluids. S/S are edema, weight gain, slow, bounding pulse, high blood pressure, lethargy, possible seizures, pulmonary congestion 8. Discuss the role of hydrogen ion concentration in cellular function and dysfunction. 9. Explain how the lungs and the kidneys regulate acid-base balance. 10. Differentiate between respiratory acidosis, respiratory alkalosis, metabolic alkalosis, and metabolic acidosis by causes and mechanisms of compensation.

Chapter 5: Inflammation * Physiology of inflammation; definition of inflammation; causes; and steps of inflammation Physiology - protective mechanism. Normal defense mechanism in the body and is intended to localize and remove an injurious agent.

Definition - is the body's nonspecific response to tissue injury, resulting in redness, swelling, warmth, pain, and sometimes a loss of function. Disorders ending -itis for inflammation. The root word is usually a body part or tissue - for example, pancreatitis, appendicitis, laryngitis Causes: associated with many different types of tissue injury, causes include direct physical damage such as cuts or sprains, caustic chemicals such as acids or alkali, ischemia or infarction, allergic reactions, extremes of heat or cold, foreign bodies such as splinters or glass and infection. Steps: an injury to capillaries and tissue cells will result in the following reaction 1. 2. 3. 4.

Bradykinin is released from the injured cells Bradykinin activates pain receptors Sensation of pain stimulates mast cells and basophils to release histamine Bradykinin and histamine cause capillary dilation a. This results in an increase of blood flow and increased capillary permeability 5. Break in skin allows bacteria to enter the tissue a. This results in the migration of neutrophils and monocytes to the site of injury 6. Neutrophils phagocytize bacteria 7. Macrophages leave the bloodstream and phagocytose microbes

* Pathophysiology of inflammation (acute vs. chronic); local effects and systemic effects of inflammation (including clinical manifestations); complications of acute and chronic inflammation Acute Inflammation: o Process of inflammation is the same, regardless of cause. o Timing varies with specific cause o Chemical mediators affect blood vessels and nerves in the damaged area: o Vasodilation o Hyperemia o Increase in capillary permeability o Chemotaxis to attract cells of the immune system o When tissue injury occurs, the damaged mast cells and platelets release chemical mediators including histamine, serotonin, prostaglandins, and leukotrienes into the interstitial fluid and blood. These chemicals affect blood vessels and nerves in the damaged area o The rapid release of chemical mediators results in local vasodilation (relaxation of smooth muscle causing an increase in the diameter of arterioles), which causes hyperemia, increased blood flow in the area. Capillary membrane permeability also increases, allowing plasma proteins to move into the interstitial space along with more fluid o The increased fluid dilutes any toxic material at the site, while the globulins serve as antibodies, and fibrinogen forms a fibrin mesh around the area in an attempt to localize the injurious agent. Any blood clotting will also provide a fibrin mesh to wall off the area. Vasodilation and increased capillary permeability make up the vascular response to injury o As excessive fluid and protein collects in the interstitial compartment, blood flow in the area decreases as swelling leads to increased pressure on the capillary bed, and fluid shifts out of the capillary are reduced. Severely reduced blood flow can decrease the nutrients available to the undamaged cells in the area and prevent the removal of wastes. This may cause additional damage to the tissue.

o Complications:  local complications depend on the site of inflammation (ex: inflammation in the lungs may impair he expansion of the lungs, decreasing the diffusion of oxygen)  Infection - may develop in an inflamed tissue because microorganisms can more easily penetrate when the skin or mucosa is damaged and the blood supply is impaired.  Skeletal muscle spasms - strong muscle contractions may be initiated by inflammation. o Local effects - redness (rubor or erythema), heat, swelling, and pain o Systemic effects - mild fever, malaise (feeling unwell), fatigue, headache, and anorexia (loss of appetite) Chronic Inflammation: o May develop after acute episode of inflammation when the cause is not eradicated o Pathophysiology - swelling and exudate but the presence of more lymphocytes, macrophages, and fibroblasts (connective tissue cells) than in acute inflammation o Complications  disorders such as rheumatoid arthritis are characterized by chronic inflammation with periodic exacerbations of acute inflammation  Deep ulcers may result from severe or prolonged inflammation because cell necrosis and lack of cell regeneration cause erosion of tissue  This in turn can lead to complications such as perforation (erosion through the wall) of viscera or the development of extensive scar tissue

* Types of healing o Resolution is the process that occurs when there is minimal tissue damage. The damaged cells recover, and the tissue returns to normal within a short period of time—for example, after a mild sunburn. o Regeneration is the healing process that occurs in damaged tissue in which the cells are capable of mitosis. Some types of cells (eg, epithelial cells) are constantly replicating, whereas other cells such as hepatocytes in the liver are ...