Download NU545 PATHO STUDY GUIDE UNIT 1 WITH 100% CORRECT ANSWER and more Exams Nursing in PDF only on Docsity!
NU545 PATHO STUDY
GUIDE UNIT 1 WITH 100%
CORRECT ANSWER
Know the chemical mediators which induce pain during inflammatory response? See page 201, 207, 213 (Ch. 7) - CORRECT ANSWER- Pain is caused by prostaglandins and bradykinin. Prostaglandin is produced by mast cells which cause increased vascular permeability, neutrophil chemotaxis, and pain. Bradykinin is the primary kinin produced from the kinin system. Bradykinin causes dilation of blood vessels, and acts with prostaglandins to stimulate nerve endings and induce pain, causes smooth muscle cell contraction, increases vascular permeability, and may increase leukocyte chemostaxis. Know enzyme secreted in kidney when blood volume is decreased. See page 108 (Ch. 3) - CORRECT ANSWER- Renin is an enzyme secreted by the juxtaglomerular cells of the kidney when circulating blood pressure and renal blood flow or serum sodium concentrations are reduced. Renin stimulates the formation of angiotensin I (inactive peptide). Angiotensin-converting enzyme (ACE) in pulmonary vessels converts angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction to elevate BP and stimulates the secretion of aldosterone to promote NA and water reabsorption by the proximal tubules of the kidneys. Aldosterone also stimulates secretion (and excretion) of K by the distal tubule of the kidney which reduces K concentrations in the ECF. Know the difference between osmolarity and osmolality. See page 30 (Ch. 1) - CORRECT ANSWER- Osmolality controls the distribution of movement of water between body compartments and is the preferred measure of osmotic activity in clinical assessments of individuals. Osmolality is a measure of the number of milliosmoles per
kilogram (mOsm/kg) of water or the concentration of molecules per weight of water. Osmolarity is a measure of the number of milliosmoles per liter (mOsm/L) of solution, or the concentration of molecules per volume of solution. What is metabolic absorption? (p.2) - CORRECT ANSWER- • 1 of 8 cellular functions of eukaryote cell
- Chief function is to take in & use nutrients or other substances from surroundings
- Ex: kidney (fluid absorption and synthesize proteins) and Intestinal epithelial cells (fluid absorption/protein enzyme synthesis) What uses oxygen to remove hydrogen atoms in an oxidative reaction? (p.8) - CORRECT ANSWER- • Peroxisomes contain enzymes that use O2 to remove H+ in oxidative reactions that produces hydrogen peroxide which is then used by catalase to further oxidize other substances like: phenols, formic acid, formaldehyde, and alcohol During cell injury what is released that is capable of cellular autodigestion? (p. 8) - CORRECT ANSWER- • Lysosomal enzymes (hydrolases), or the digestive enzymes within the lysosome
- Autolysosomes, or autophagosomes Where is the genetic info contained in the cell? (p. 2) - CORRECT ANSWER- Nucleus, specifically the nucleolus Cell membranes contain which major chemical components? (p. 12)
- CORRECT ANSWER- Lipids & Proteins in a complex lipid bilayer What allows potassium to diffuse in and out of cells? (p. 31-32) - CORRECT ANSWER- • The Na+-K+-ATP pump. Uses direct energy of ATP; found in excitable tissues (muscles/nerves) & also in kidneys & salivary glands. Involves the movement of Na+ & K+ against a concentration gradient.
What is cell communication? How does it occur? (p.20) - CORRECT ANSWER- • Required for homeostasis, regulate cellular growth/division & development/organization into tissues, & coordinate cellular function.
- Occurs in 3 ways: -via protein channels & gap junctions that directly coordinate activities of adjacent cells (must be touching) -via plasma membrane-based signaling molecules (receptors) that affect the cell itself & cells that come in direct contact -via chemical signals that must enter the distant cells to affect the receptors inside of the distant cell (the most common means of communication).
- Primary modes of intercellular signaling are hormonal, neurohormonal, paracrine, contact-dependent, & neurotransmitters. There is also Autocrine signaling where the cell signals itself. What is chemical signaling? (p.20) - CORRECT ANSWER- Involves the secretion of chemicals, such as hormones, neurohormones, paracrine, autocrine, and neurotransmitters. Chemical signaling may occur through the bloodstream or in small discrete spaces How is glucose transported from the blood to the cell? (p. 33) - CORRECT ANSWER- Passive protein channels. Passive mediated transport or facilitated diffusion moves the glucose via a uniport mechanism into the cell. When all glucose-specific receptors are occupied, the transport system is saturated and operating at maximal capacity. Direction of movement is the same as passive simple diffusion-down the concentration gradient, from an area of high concentration to low concentration until equilibrium is achieved. Understand the transportation of potassium and sodium across plasma membranes. (p. 29-32) - CORRECT ANSWER- • The Na+ K+ antiport (opposite directions) system uses direct energy of ATP to move cations.
- ATPase is transporter protein.
- Concentration of ATPase in plasma membranes is directly related to Na+ K+ transport activity.
- Process:
- 3 Na+ ions bind to Na-binding sites on carrier's inner face.
- ATP molecule produced by cell's mitochondria binds to carrier.
- Carrier changes shape, releases 3 Na+ ions to outside of cell, & attracts 2 K+ ions to K-binding sites.
- Carrier returns to original shape, releasing 2 K+ ions & the leftover ATP molecule to inside of cell.
- Carrier can now repeat cycle. What is active transport? (p. 31-33) ch.1 - CORRECT ANSWER- • The movement of a substance across a membrane by a carrier protein. Requires metabolic energy (ATP) to move the molecules against the concentration gradient.
- Active transport also occurs by endocytosis (vesicle formation), where substances are engulfed by a segment of the plasma membrane, forming a vesicle that moves into the cell. What are cytokines? (p.38-39) Or cytokinesis? (p.37) - CORRECT ANSWER- • Cytokines are peptides that transmit signals within/between cells to stimulate tissue growth & development. Do all cells continue to replicate or divide? (p. 39) - CORRECT ANSWER- • No, all types of cells undergo mitosis during formation of the embryo, but adult cells including: nerve cells, lens cells, & muscle cells, lose the ability to replicate.
- When a need arises for new cells, as in the repair of injured cells, previously non-dividing cells must be rapidly triggered to reenter the cell cycle.
- Neurons are fixed at birth & are unable to be replaced. When normal columnar ciliated epithelial cells of the bronchial lining are replaced by stratified squamous cells, the process is called? (p.
fragmentation of polypeptide chains, & alterations of DNA (breaking single strands). Diseases & disorders have been linked directly & indirectly to these reactive species. Know all about lead poisoning. How does it cause damage within the cell? (p. 65-67) - CORRECT ANSWER- • A heavy metal, primary hazard to children.
- Can cause learning disabilities, hyperactivity, & ADD
- Found in paint, soil, dust, debris from houses, baby formula mixed with lead contaminated water, newsprint, water that flows through lead pipes, hair dyes, gasoline, & tin cans or pottery made with lead based glaze.
- Nervous system, hematopoietic system, & kidneys are primarily affected
- Interferes with Ca. Can increase intracellular Ca concentrations & become a substitute & some Ca-binding proteins are capable of binding with lead. PKC (protein kinase C) mediated lead induced rise in intracellular free Ca causing cellular disruption.
- Inhibits enzymes involved in hemoglobin synthesis (ie anemia)
- Other s/s: convulsions, delirium, & peripheral nerve involvement to the wrist, fingers, & feet, glycosuria, aminoaciduria, & hyperphosphaturia, n/v, loss of appetite, wt loss, & abd cramps. Know about the affects of fetal alcohol syndrome on infants. (p. 68-69)
- CORRECT ANSWER- • Can lead to growth retardation, cognitive impairment, facial anomalies, & ocular disturbances. How does alcohol affect the nervous system? (p.67-68) - CORRECT ANSWER- • Acts as a depressant affecting the subcortical structures first (brainstem reticular formation). Motor and intellectual activities then become distorted. At high levels, medullar centers become depressed, affecting respirations. Where do lipids accumulate? (p. 63, 75, 84-85) - CORRECT ANSWER- • During chemical injury lipids accumulate within the
cytoplasm, starting within cisternae of the endoplasmic reticulum (p.63).
- Lipids primarily accumulate in the cells of the spleen, liver, CNS (p.84).
- The most common site of intracellular lipid accumulation also known as fatty change is liver cells (p.85).
- Heart, liver, & muscle in hyperlipidemia (p.75). What is hemosiderosis? (p. 86) - CORRECT ANSWER- • Excess iron is stored as hemosiderin in the cells of many organs & tissues. Common w/multiple blood transfusions or prolonged parenteral administration of iron or excessive alcohol What causes free calcium in the cytosol? (p. 87 figure 2-24) - CORRECT ANSWER- • Calcium is usually stored in the mitochondria and endoplasmic reticulum and then pumped to extracellular space bound to calcium-binding proteins.
- Free calcium in the cytosol is caused by abnormal permeability of calcium-ion channels, direct damage to membranes, or depletion of ATP (i.e. hypoxic injury); therefore, causing uncontrolled enzyme activation causing further damage. What happens to sodium and water during cell injury? (p.84) - CORRECT ANSWER- In hypoxia ATP decreases, causing the Na/K pump & Na/Ca exchange to fail. Leading to increase of intracellular Na & Ca, & diffusion of K out of the cell; Na & water can then enter the cell freely causing swelling & dilation of the endoplasmic reticulum During cell injury caused by hypoxia, what happens to osmotic pressure? (p. 30, 56, and 98) - CORRECT ANSWER- • Osmotic pressure is the amount of hydrostatic pressure required to oppose the osmotic movement of water. (P.30)
- In hypoxia you have an increase in Na in the cell and an out flow of K+ (P.56). Resulting in a deficit of Na in the ECF which decreases the ECF osmotic pressure and water is attracted to the ICF space (P.98)
- Dry gangrene is d/t coagulative necrosis & the skin is dry & shrinks w/color changes (black).
- Wet gangrene occurs when neutrophils invade the site & cause liquifactive necrosis, usually in internal organs, causes site to be swollen, cold, & black. Foul odor is present produced by pus.
- Gas gangrene is caused by Clostridium that produces hydrolytic enzymes & toxins that destroy connective tissue, cellular membranes & causes gas bubbles to form in muscle cells. Can be fatal if enzymes lyse the membranes of the RBCs, resulting in shock. Infants are susceptible to significant total body water loss, why? (p.
- CORRECT ANSWER- In newborns, TBW is about 75%- 85%, w/a decr to about 67% during first year. Infants are susceptible to significant changes in TBW because of their high metabolic rate & accelerated turnover of body fluids caused by greater BSA Why are obese people at greater risk for dehydration? (p. 104 see table 3-3) - CORRECT ANSWER- • Fat is hydrophobic. Very little water is contained in adipose cells. Individuals with more body fat have proportionately less TBW &tend to be more susceptible to fluid imbalances that cause dehydration With low plasma albumin you have edema, why? (p. 106-107) - CORRECT ANSWER- • Less plasma albumin = decr plasma oncotic pressure = causes fluid to move into interstitial space. Retention of sodium and water causes edema because of an increase in? (p. 106) - CORRECT ANSWER- Capillary hydrostatic pressure through volume overload What causes hypernatremia? (p. 111) - CORRECT ANSWER- • NA > 147 mEq/L.
- Caused by incr Na or decr H2O
- DI, ADH deficiency, polyuria, profuse sweating, diarrhea, dehydration, gastric feedings w/deficient H2O, hypertonic saline,
hyperaldosteronism, Cushing's syndrome w/incr ACTH which causes incr aldosterone. Can insulin be used to treat hyperkalemia? (p. 119) - CORRECT ANSWER- • Management of hyperkalemia is r/t to treating causes & correcting K excess.
- Insulin facilitates cellular entry of K
- Calcium gluconate can restore normal neuromuscular irritability. What does hyperaldosteronism cause in relation to fluid and electrolyte balance? (p. 108-109,111) - CORRECT ANSWER- Hypernatremia
- What causes the neuron symptoms in hypernatremia? (p. 111) - CORRECT ANSWER- • Alterations in membrane potential & shrinking of brain cells. Why does a pt have decreased urine output with SIADH?( Pg 112-
- CORRECT ANSWER- • The amount of ADH is inappropriate r/t Na levels.
- Not caused by excess H2O intake but by incr renal absorption of H2O r/t inappropriate incr in ADH.
- Na & osmolality are reduced by dilution. The kidney continues to excrete sodium while urine sodium and urine osmolality are elevated. During acidosis how does the body compensate for increased hydrogen ion?( Pg 123-126) - CORRECT ANSWER- • Protein buffering = H+ binds with hemoglobin & CO2. Hemoglobin bound hydrogen becomes a weak acid. Venous blood (less saturated hemoglobin) = better buffer than arterial (saturated with O2).
- Renal buffering = distal tubule of the kidney secretes H+ into urine & reabsorbs HCO3. •Ammonia (NH3) is lipid soluble and can cross the cell membrane. Ammonia binds with H+ to form ammonia ion (NH4) which is eliminated in the urine. The renal buffering of H+ requires the use of CO2 & H2O to form HCO3.
What are Chvostek's and Trousseau's signs? (pg. 120) - CORRECT ANSWER- • Chvostek's: elicited by tapping on the facial nerve just below the temple; a positive sign is a twitch of the nose or lip.
- Trousseau's: contraction of the hand and fingers when the arterial blood flow in the arm is occluded for 5 min.
- Tests for hypocalcemia What causes hypocalcemia (serum Ca <8.5mg/dl)? (p.120) - CORRECT ANSWER- 1. Inadequate intestinal absorption - inadequate intake of dairy, green leafy veggies; excessive dietary phosphorus binds Ca so neither are absorbed; malabsorption of fat.
- Blood transfusions - citrate solution in storing whole blood binds with Ca
- Deposition of iCa into bone or soft tissue - pancreatitis releases lipases into soft tissues, which then binds Ca; neoplastic bone metastases inhibit bone resorption & increase Ca deposition into bone thereby decreasing serum Ca.
- Vitamin D deficiency - can result from inadequate sunlight or malabsorption; causes decreased intestinal absorption.
- Decreases in PTH - caused by removal of parathyroid gland.
- Metabolic or respiratory alkalosis - changes in pH enhances protein binding of ionized Ca.
- Hypoalbuminemia - decreases amount of bound Ca in plasma. When someone vomits extensively, what causes the metabolic alkalosis? (p.128-129) - CORRECT ANSWER- • Depletion of ECF & chloride (hypochloremic metabolic alkalosis), renal compensation becomes ineffective due to volume depletion & loss of electrolytes (Na, K, H, Cl).
- Kidneys increase Na & HCO3 reabsorption & excrete H+. HCO3 is reabsorbed to maintain anionic balance since the Cl in the ECF is decreased. H+ moves to the intracellular space when K is depleted & is excreted to maintain electrochemical balance. The urine is more acidic and the reabsorbed bicarbonate prevents correction of alkalosis.
What causes edema during inflammation? (p.107, 195) - CORRECT ANSWER- • Increases in capillary permeability = proteins escape from plasma & produce edema through loss of capillary oncotic pressure & a gain in interstitial fluid proteins.
- Vasodilation
- Incr WBC accumulation What is the purpose of inflammation?(p.191, 195-196) - CORRECT ANSWER- • Second line of defense; occurs in response to tissue injury or infection; protects against further injury, prevents infection of injured tissue, & promotes healing
- Incr local blood flow; incr RBC's & leukocytes, & biochemical mediators
- kill, contain, dilute bacteria
- promote clotting & prevent extensive inflammation What causes the erythema and induration during inflammation? (p.
- CORRECT ANSWER- • Vasodilation - incr blood flow & RBCs at site = warmth & redness.
- Increased vascular permeability & leakage of fluid out of the vessels
- biochemical mediators stimulate the endothelial cells lining the capillaries & venules to contract, creating spaces between cells which allows leukocytes & plasma to enter surrounding tissue.
- White blood cell adherence to inner walls of vessels and migration to site of injury. After prolonged antibiotic therapy, what bacterium grows in the intestine? (p.194,1500) - CORRECT ANSWER- Clostridium difficile When histamine is released from mast cells, what is the vascular effect? (p.199,206) - CORRECT ANSWER- • Constriction of large vessel walls & dilation of post capillary venules - results in increased blood flow into the microcirculation. (p.206)
- Increased capillary permeability and vasodilation(p.199)
tissue (epithelialization), macrophages secrete biochemical mediators and cytokines that promote healing. Fibroblasts, most important cell during this phase, they synthesize and secrete collagen and other connective tissue proteins which are deposited into debrided areas. Collagen most abundant protein in the bo How do vaccinations work to provide protection against certain microorganisms? (p.332-333) - CORRECT ANSWER- Active acquired immunity = produced by an individual after either natural exposure to an antigen or after immunization What can bacteria not multiply without? (p.301) - CORRECT ANSWER- Within the warm and nutrient filled environment of human tissue most microorganisms undergo rapid multiplication with production of many new infectious progeny. Some bacteria are intracellular pathogens and replicate in macrophages and other cells. Many extracellular bacteria form multi-cellular masses called biofilms, which provides an optimal environment for growth. (This was all I found in the book but online were answers like nutrients, oxygen, warmth, time, possibly moisture, and the correct pH) How do bacteria become resistant to antibiotics? (p.310) - CORRECT ANSWER- • Antibiotic resistance is usually a result of genetic mutations that can be transmitted directly to neighboring microorganisms by plasmid exchange. Microorganisms commonly develop the capacity to inactivate antibiotics.
- Other forms of resistance result from modification of the target molecule.
- A third mechanism of resistance is mediated by multidrug transporters in the microorganism's membrane. These transporters affect the rate of intracellular accumulation of the antimicrobial by preventing entrance or increasing active efflux of the antibiotic. How would you clean a wound that is healing by epithelialization? (Chapter 6, p.216-219) - CORRECT ANSWER- The ideal dressing is one that absorbs some drainage without being incorporated into the
clot or granulation tissue and keeps the wound moist. Normal saline should be used to cleanse or irrigate wound as other solutions might be desiccating to the wound. What is a keloid? (p.219) - CORRECT ANSWER- • A raised scar that extends beyond the original boundaries of the wound. Caused by excessive production of collagen causing surface over healing. It invades surrounding tissue, commonly recurs after surgical removal, familial tendency common, more common in blacks than whites, do not regress over time. Why do some neonates have a transient depressed inflammatory response? (p.220) - CORRECT ANSWER- • Lack of phagocyte plasma membrane fluidity impairs pseudopod formation & migration resulting in neutrophils (& perhaps monocytes) being incapable of efficient chemoyaxis
- Neonates stressed by in utero infection or respiratory insufficiency - neutrophils have diminished oxidative & bacterial responses
- Partially deficient in complement (esp. components of the alternative pathway)
- Relative deficiency of factor B
- Low levels of mannose-binding lectin
- May be deficient in some of the collectins & collectin-like proteins Adults? (p. 220) impaired inflammation & wound healing in older adults - CORRECT ANSWER- Can be linked to chronic illness (cardiovascular disease, diabetes mellitus); Medications (anti- inflammatory steroids interfere with healing process); Impaired sensation &/or mobility; Physiologic skin changes; Decreased subcutaneous fat (protective layer); Thicker collagen fibers; loss of elastin; Age-associated changes in epidermis (atrophy of underlying capillaries); Decreased perfusion - increased susceptibility to adverse effects of hypoxia in the wound bed; Slow proliferation of aging fibroblasts; Decreased number (alveolar macrophages) or activity (neutrophil chemotaxis, degranulation, & phagocytosis) of cellular components of innate resistance; Decreased inflammatory activity
Graves Disease (p.277, 726-728) - CORRECT ANSWER- • An autoimmune disease resulting in stimulation of the thyroid gland thus causing hyperthyroidism
- Generally consists of: Hyperthyroidism; Diffuse thyroid enlargement (goiter) due to increased iodide uptake and rate of metabolism; Ophthalmopathy (protrusion of the globe) double vision, irritation, pain, lacrimation, photophobia, & blurred vision; Dermopathy (shown as pretibial myexedema: subcutaneous swelling on anterior legs with indurated and erythema of skin)
- Genetic factors: major histocompatibility complex (MHC) genes associated with graves disease
- Pathology: Normal regularity mechanisms are overridden by abnormal immunologic mechanisms; T lymphocytes sensitized to antigens and B cells stimulated to produce IgG antibodies which bind to TSH receptors increasing release of TH; Autoantibodies known as thyroid-stimulating immunoglobulin's (TSI) or thyroid receptor antibodies (TRAb)
- Therapy: Anti-thyroid drugs (proiouracil and methimaxole), radioactive iodine, surgery Myasthenia Gravis: (p.277, 624-626) - CORRECT ANSWER- • Chronic autoimmune disease mediated by acetylcholine receptor (AChR) antibodies that act at the neuromuscular junction with unknown etiology (although some persons may have genetic susceptibility)
- Characterized by exertional fatigue, weakness that worsens with activity, improves with rest, and reoccurs with activity
- Increases risk for other diseases such as SLE, RA, polymyositis, and thyroitoxicosis
- Subtypes of MG: o AChR: Involves proximal musculature throughout body and has several courses including...
- Course with periodic remissions
- Slowly progressive course
- Rapidly progressive course
- Fulminating course
- AChR further subdivided by...
- Young persons, mostly female, with thymic hyperplasis
- Older adults, both sexes, with normal or involuted thymus glands
- Persons of both sexes with thymomas o Neonatal Myasthenia: Signs appear 1 to 3 days after birth and persist up to a few weeks; Myasthenia immunoglobulin transferred through the placenta o Ocular Myasthenia: Weakness of eye muscles and eyelids with swallowing difficulties and slurred speech; More common in males
- Classifications by disease severity o Grade I: Ocular disease o Grade IIa: Generalized mild weakness o Grade IIb: Moderate weakness o Grade III: Severe generalized weakness o Grade IV: Myasthenic crisis with respiratory failure
- Pathophysiology of MG... o Results from a defect in nerve impulse transmission at the junction o Main defect is formation of autoantibodies against ACh binding site receptors o Autoantibodies block AChR or cause loss of it o Eventual receptor site destruction occurs causing reduced number of receptors, diminished nerve impulse transmission, and incomplete/lack of muscle depolarization
- Clinical manifestation of MG: o Typically insidious with first appearance during pregnancy, postpartum, or in conjunction with a A patient reacts to a blood transfusion, what is this an example of? (p.
- CORRECT ANSWER- • An alloimmune reaction What is the positive reaction to a Tb skin test? (p. 270) - CORRECT ANSWER- A positive reaction is considered a type IV cell mediated hypersensitivity reaction
- Reaction follows injection of Tb antigen in a sensitized individual
- Considered a delayed hypersensitivity skin test d/t slow onset (24 to 72 hours)
