Download NU545 Patho Study Guide Unit 1 with Complete Solution and more Exams Pathophysiology in PDF only on Docsity!
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NU545 Patho Study Guide Unit 1 with
Complete Solution
1. What is metabolic absorption? (p.2): • 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)
2. What uses oxygen to remove hydrogen atoms in an oxidative reaction? (p.8): • 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
3. During cell injury what is released that is capable of cellular autodigestion? (p. 8): • Lysosomal enzymes (hydrolases), or
the digestive enzymes within the lysosome
• Autolysosomes, or autophagosomes
4. Where is the genetic info contained in the cell? (p. 2): Nucleus, specifically the nucleolus
5. Cell membranes contain which major chemical components? (p. 12): Lipids & Proteins in a complex lipid bilayer
6. What allows potassium to diffuse in and out of cells? (p. 31-32): • 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.
• Protein enzyme ATPase allows potassium to move in and out of the cell.
• Mediated transport = channel protein through which ions can dittuse (K+ leak channel).
7. How is a cell protected from injury? (p.12): • Plasma membrane - Acts as a barrier to toxic molecules, macromolecules, & foreign
organisms/cells.
• Exists in a state of change & modulation. Alternates receptor numbers & patterns.
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- Gating protects cells from release of Ca from injured cells by sealing ott or decreasing permeability at junctional complexes.
8. In cirrhosis, what does cholesterol have to do with the erythrocytes? (p.68): • Associated with chemical changes that result in
structural & metabolic abnormalities of the erythrocyte membrane leading to cell shape changes & hemolytic anemia.
- Increase in unesterified serum cholesterol owing to lecithin cholesterol acyl transferase (LCAT) deficiency in cirrhosis leads to expansion of the lipid bilayer & macrocytosis without megaloblastic changes in precursors. Substitutions of phosphatidyl choline (PC) moieties in the erythrocyte lipid bilayer lead to echinocytes (disaturated PC) or to stomatocytes (diunsaturated PC). In some patients, high density lipoprotein (HDL) abnormalities lead to erythrocyte surface changes causing rapid formation of echinocytes. (Ann Clin Lab Sci. 1990 May-Jun;20(3):169-74.Mechanisms of hemolysis in liver disease.Morse EE1. Department of Laboratory Medicine, University of Connecticut School of Medicine, Farmington 06032)
- Alters fluidity & function of cell membrane as well as intercellular transport
9. What is platelet-derived growth factor? (p.39): Stimulates production of connective tissue cells & neuroglial cells
10. What is cell communication? How does it occur? (p.20): • 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 attect the cell itself & cells that come in direct contact -via chemical signals that must enter the distant cells to attect the receptors inside of the distant cell (the most common means of communication).
- Primary modes of intercellular signaling are hormonal, neurohormonal, paracrine, contact-dependent, & neurotrans- mitters. There is also Autocrine signaling where the cell signals itself.
11. What is chemical signaling? (p.20): 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
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15. What are cytokines? (p.38-39)
Or cytokinesis? (p.37): • Cytokines are peptides that transmit signals within/between cells to stimulate tissue growth & development.
16. Do all cells continue to replicate or divide? (p. 39): • 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.
17. When normal columnar ciliated epithelial cells of the bronchial lining are replaced by stratified
squamous cells, the process is called? (p. 54): • Metaplasia: the reversible replacement of one mature cell by another, sometimes less ditterentiated cell type.
- However, lose protective ability, because new cells don't secrete mucus or have cilia.
- Bronchial metaplasia can be reversed if inducing stimulus is removed, such as cigarette smoking.
18. What is the relationship between ischemia and ATP? (p. 55-57): • When a hypoxic injury occurs to myocardium, which
causes an abrupt lack of contraction (caused by quick decline in mitochondrial phosphorylation), causing insuflcient ATP production.
- Lack of ATP leads to increase in anaerobic metabolism, which generates ATP from glycogen when there is insuflcient oxygen.
- When glycogen stores are depleted, even anaerobic metabolism ceases.
19. When does sodium enter the cell and cause swelling? (p. 57): • A reduction in ATP levels cause the plasma membrane's
Na-K pump & Na-Ca exchange to fail.
- Causes intracellular accumulation of Na & Ca & dittusion of K out of cell.
- Na & H2O enter cell freely, leading to cellular swelling.
20. What are free radicals in relation to cell damage? Progression of diseases? (p. 59-61): Membrane damage is initiated by
5 / 24 injury induced by free radicals, primarily by excess reactive oxygen species (ROS) called oxidated stress. Free radical is an electrically uncharged atom or group of atoms having an unpaired electron; thus causing the molecule to be unstable. To stabilize the molecule, it gives up an electron or steals one. This process is capable of injuries through chemical bond formation with proteins, lipids, & carbs. Free radicals aren't easily controlled & they initiate chain reactions. These reactive species are important in regard to cell injury by lipid peroxidation, alterations of proteins causing fragmentation of polypeptide chains, & alterations of DNA (breaking single strands). Diseases & disorders have been linked directly & indirectly to these reactive species.
21. Know all about lead poisoning. How does it cause damage within the cell? (p. 65-67): • 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 attected
- 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.
22. Know about the affects of fetal alcohol syndrome on infants. (p. 68-69): • Can lead to growth retardation, cognitive
impairment, facial anomalies, & ocular disturbances.
23. How does alcohol affect the nervous system? (p.67-68): • Acts as a depressant attecting the subcortical structures first (brainstem
reticular formation). Motor and intellectual activities then become distorted. At high levels, medullar centers become depressed, attecting respirations.
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30. After ovulation what happens to uterine endometrial cells? (p. 53, 780): • Hor- monal hyperplasia occurs chiefly in estrogen
dependent organs. After ovulation estrogen stimulates the endometrium to grow and thicken.
- After ovulation, then begins the secretory phase where glands in the endometrium secrete glycogen containing fluid, and if there is no ovum implantation, then we move to the ischemic phase where the endometrium sloughs ott monthly (P.780) During menstruation the functional layer of the endometrium falls apart and sloughs.
31. What happens to liver cells when a portion of the liver is removed? (p.52): - Compensatory hyperplasia is an
adaptive mechanism that allows some organs to regenerate in order to compensate for the loss. A protein, hepatocyte growth factor (HGF) is thought to be a mediator in vitro of liver regeneration; however other growth factors and cytokines are involved.
32. Understand necrosis in relation to pulmonary TB and gangrene. (p.90-91): • TB results in Caseous necrosis; a
combination of coagulative & liquefactive necrosis -coagulative = results from protein denaturation, where protein albumin changes from gelatinous, transparent to firm, opaque like cooked egg whites -liquefactive = digestive juices eat their own hydrolases, & tissue liquefies, gets walled ott from healthy tissue, & forms cysts
- Dead cells disintegrate but debris is not digested completely by hydrolases. Tissues appear soft & granular. A granulomatous inflammatory wall encloses areas of caseous necrosis.
- Gangrene is a term usually used to refer to death of tissue & results from severe hypoxic injury usually from arteriosclerosis. Hypoxia and bacterial invasion occurs.
- 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.
33. Infants are susceptible to significant total body water loss, why? (p. 104): 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
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34. Why are obese people at greater risk for dehydration? (p. 104 see table 3-3): • 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
35. With low plasma albumin you have edema, why? (p. 106-107): • Less plasma albumin
= decr plasma oncotic pressure = causes fluid to move into interstitial space.
36. Retention of sodium and water causes edema because of an increase in? (p. 106): Capillary hydrostatic pressure
through volume overload
37. What causes hypernatremia? (p. 111): • 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.
38. Can insulin be used to treat hyperkalemia? (p. 119): • 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.
39. What does hyperaldosteronism cause in relation to fluid and electrolyte balance? (p. 108-109,111):
Hypernatremia
40. 40. What causes the neuron symptoms in hypernatremia? (p. 111): • Alterations in membrane potential & shrinking of
brain cells.
41. Why does a pt have decreased urine output with SIADH?( Pg 112-114): • The amount of ADH is inappropriate r/t Na
levels.
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45. What causes hypermagnesemia? (pg. 121 table3-10): Usually caused by renal failure or mag-containing antacids
46. What influences calcium and phosphate balances? (pgs. 119-122): • Inversely proportional
- Regulated by: PTH, Vit D, & calcitonin. Acting together, they determine the amount of dietary Ca & Phos absorbed from intestine, the deposition/absorption in the bone, & the renal reabsorption/excretion in the kidneys.
47. What are Chvostek's and Trousseau's signs? (pg. 120): • 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
48. What causes hypocalcemia (serum Ca <8.5mg/dl)? (p.120): 1. Inadequate intestinal absorption - inadequate intake of dairy,
green leafy veggies; excessive dietary phosphorus binds Ca so neither are absorbed; malabsorption of fat.
2. Blood transfusions - citrate solution in storing whole blood binds with Ca
3. 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.
4. Vitamin D deficiency - can result from inadequate sunlight or malabsorption; causes decreased intestinal absorption.
5. Decreases in PTH - caused by removal of parathyroid gland.
6. Metabolic or respiratory alkalosis - changes in pH enhances protein binding of ionized Ca.
7. Hypoalbuminemia - decreases amount of bound Ca in plasma.
49. When someone vomits extensively, what causes the metabolic alkalosis? (p.128-129): • Depletion of ECF &
11 / 24 chloride (hypochloremic metabolic alkalosis), renal compensation becomes inettective 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.
50. What causes edema during inflammation? (p.107, 195): • Increases in capillary perme- ability = proteins escape from plasma &
produce edema through loss of capillary oncotic pressure & a gain in interstitial fluid proteins.
- Vasodilation
- Incr WBC accumulation
51. What is the purpose of inflammation?(p.191, 195-196): • 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
52. What causes the erythema and induration during inflammation? (p. 195): • 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.
53. After prolonged antibiotic therapy, what bacterium grows in the intestine? (p.194,1500): Clostridium
13 / 24 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 body with high concentrations of amino acids (glycine, proline, and lysine), collagen binds to form fibrils, which bond to form fibers. These provide strength when forming along lines of mechanical stress to create a final collagen matrix.
- Contraction = necessary for all wounds but more so for secondary intention. The granulation tissue contains myofibroblasts (specialized cells for contraction that contain both smooth muscle cells and fibroblasts). Contractions occurs as the extensions from the plasma membrane of myofibroblasts establish connections between neighboring cells, contract their fibers, and exert tension on the neighboring cells while anchoring themselves to the wound bed.
- Maturation Phase (starts several weeks after injury- 2 years) Involves cellular ditterentiation, scar formation and scar remodeling. Scar tissue is remodeled and capillaries disappear, leaving the avascular scar. At best repaired tissue only regains 80% of its original tensile strength.
58. How do vaccinations work to provide protection against certain microorgan- isms? (p.332-333): Active acquired
immunity = produced by an individual after either natural exposure to an antigen or after immunization
59. What can bacteria not multiply without? (p.301): 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)
60. How do bacteria become resistant to antibiotics? (p.310): • 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 attect the rate of intracellular accumulation of the antimicrobial by preventing entrance or increasing active efflux of the antibiotic.
61. How would you clean a wound that is healing by epithelialization? (Chapter 6, p.216-219): 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.
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62. What is a keloid? (p.219): • 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.
63. Why do some neonates have a transient depressed inflammatory response? (p.220): • Lack of phagocyte plasma
membrane fluidity impairs pseudopod formation & migration resulting in neutrophils (& perhaps monocytes) being incapable of eflcient chemoyaxis
- Neonates stressed by in utero infection or respiratory insuflciency - 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
64. Adults? (p. 220) impaired inflammation & wound healing in older adults: 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 ettects of hypoxia in the wound bed; Slow prolifer- ation of aging fibroblasts; Decreased number (alveolar macrophages) or activity (neutrophil chemotaxis, degranulation, & phagocytosis) of cellular components of innate resistance; Decreased inflammatory activity may be caused by decrease in expression & function of toll-like receptors
65. After the initial infection with herpes, why is the virus inaccessible to antibod- ies? (p. 319): • Symbiotic
relationship between cell & virus results in persistent unapparent infection (latency)
- Envelope - viral capsid completely surrounded by cellular plasma membrane highly similar to that of an uninfected cell
66. Which type of immunity is produced after natural exposure to an antigen? (p. 227): • Active acquired immunity- type of
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- 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 diflculties and slurred speech; More common in males
- Classifications by disease severity
o Grade I: Ocular disease
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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
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 transmis- sion, and incomplete/lack of muscle depolarization
- Clinical manifestation of MG:
o Typically insidious with first appearance during pregnancy, postpartum, or in conjunction with admin. of certain anesthetic agents
o Foremost complaint is fatigue and weakness with muscles of eyes, face, mouth, throat, and neck attected first
- Myasthenia crisis: Occurs when severe muscle weakness causes extreme quadriparesis or quadriplegia and possible respiratory arrest
- Cholinergic crisis may occur secondary to anticholinesterase drug toxicity and is treated by withholding the drug while providing ventilator support
- Evaluation and Treatment...
o Diagnosis made on basis of response to edrophonium chloride (tensilon), EMG, and detection of AChR and MuSK antibodies
o Treatment individualized with use of anticholinesterase drugs, steroids, immunosuppressants, azathioprine, and cyclosporines
o Plasmapheresis used during crisis, after thymectomy, and at the start of immunosuppressants
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- NK cells
- Neural cells of monocyte origin (macrophages and microglial cells)
78. What acts as a reservoir in which HIV can be relatively protected from antiviral drugs?(p.327): •
Cells in the CNS
79. Which cells are decreased with AIDS? (p.327): • CD4+Th cells; normal is 600- 1200
80. How long does it take for HIV antibodies to appear after infection thru blood products?(p.326): • Within 4-
7 weeks
81. After sexual transmission, a person can be infected but sero-negative for how long?(p.326): 6-
months
82. What is colonization?(p.300): Infectious organisms that exist in reservoirs, either in an environmental setting or colonization can occur in people:
microorganisms are deposited in a receptive environment,. Organisms that colonize are usually contained in specific areas where infections occur, i.e. respiratory, GU.
83. How are vaccines against viruses made? (p.332): Development of a vaccine includes: char- acterizing the desired protective
response, identifying the appropriate antigen to induce that response, determining the most ettective route of administration, optimizing the number and timing of vaccine doses, and deciding the most ettective and safe form to administer the vaccine. Most vaccines against viruses contain live viruses that are weakened to continue expressing the appropriate antigens but are unable to establish more than a limited and easily controlled infection.
84. What is the general adaptation syndrome?(p.339): A nonspecific response to noxious stim- uli. Includes 3 stages: alarm stage
(begins when stressor triggers the actions of hypothalamus/pituitary gland/adrenal gland)-CNS is aroused & the body's defenses are mobilized; stage of resistance or adaptation (begins with the actions of the adrenal hormones cortisol/norepi/epi); & stage of exhaustion (occurs if the stress continues & adaptation not successful)
85. How is the limbic system stimulated when there is an anticipatory response to stress? (pg 339, 341-
anticipatory learning of stressor, 343): • The limbic system indirectly elicits an endocrine stress response by stimulating neural pathways responsible
20 / 24 for receiving sensory info and central response by directly stimulating the locus ceruleus to release norepinephrine.
86. Which hormone causes anxiety and arousal during a stress response? Pg 339, 343: norepinephrine
87. During the response to stress what decreases lymphocytes, eosinophils, macrophages, and prostaglandin?
See page 348 (Ch. 11): Cortisol (glucocorticoid). Re- leased by the adrenal cortex which is activated by ACTH. Therapeutic levels of glucocorticoids inhibit the accumulation of leukocytes at site of inflammation, inhibit the release of kinins, plasminogen-activating factor, prostaglandins, and histamine from leukocytes, inhibit fibroblast proliferation and function at the site of an inflammatory response. Cortisol also promotes resolution and repair.
88. How does epinephrine affect the immune system during stress? See page 346 and 348 (Ch. 11): Epi causes
bronchodilation, increased force & rate of cardiac contraction, increases cardiac output and heart rate, increases circulating free fatty acids, attects pancreas by decreasing insulin released & increasing glucacon, attects liver by decreasing glycogen synthesis and increasing glycogenolysis, which all increase blood glucose. When injection of epinephrine in health individuals, a transient increase in the number of lymphocytes (T cells and NK cells) in peripheral blood. T cytotoxic and NK cells increase, but little change noted in B lymphocytes. Qualitatively, responsiveness to B and T lymphocytes is reduced. Similar response found at 5 to 6 minutes after exposure to stressor. This response only lasts about 2 hours. Has similar attect as glucocorticoids and can cause a decrease in Th1 activity and an increase in Th2 activity. Th1 and Th2 secrete cytokines. Th1 secretes cytokines that support innate immunity, while Th2 cytokines support adaptive immunity. A Th1 to Th2 shift promoting adaptive immunity by stimulating the growth and activation of mast cells, eosinophils, and the ditterentiation of B-cell immunoglobulins. These cytokines are often referred to as anti-inflammatory cytokines. A Th1 to Th2 shift can cause individuals to experience allergic responses, infections, and temporary worsening of autoimmune conditions (arthritis). Epinephrine can cause promotion of inflammatory response in the lungs by the release of cytokines that promote recruitment of leukocytes.
89. What catecholamines are secreted during stimulation of the adrenal medul- la? See page 345 (Ch. 11):
Epinephrine and norepinephrine
90. Is norepinephrine involved in the stress response? See page 345 (Ch. 11): • Yes, During stress, norepinephrine raises
blood pressure by constricting peripheral vessels, dilates the pupils of the eye, cause piloerection, and increases sweat gland action in armpits and palms. Very little adrenal norepinephrine reaches distal tissue, thus, the ettects caused by norepinephrine during the stress response are primarily elicited from the SNS.
