Nurs 351 Exam 1

Front 1

WHO definition of health

Back 1

Astate of complete physical, mental, and social well-being, and not merely theabsence of disease and infirmity

Front 2

Definition of disease

Back 2

Anydeviation from or interruption of the normal structure or function of a part,organ, or system of the body that is manifested by a characteristic set ofsymptoms or signs

Front 3

Organic disease vs. functional disease

Back 3

Organic=structural changes

Functional= no morphological abnormalities

Front 4

Ends of disease continuum

Back 4

One end=severe, life-threatening, disabling illness; other end=complete mental and physical well-being

Front 5

What are etiologic factors? What do they include? What is etiology?

Back 5

Causes of disease; include biologic agents, physical forces, chemical agents, and nutritional excesses or deficits; describes what sets the disease process in motion

Front 6

Disease risk factor categories

Back 6

Genetic, disease-associated (past illnesses that increase risk), treatment-associated, environmental, lifestyle/behavioral

Front 7

What is pathogenesis?

Back 7

-Sequence of cellular & tissueevents that take place from the time of initial contact with an agent until theultimate expression of disease -Describes how the disease processevolves

Front 8

Morphologic changes are concerned with what type of changes?

Back 8

Gross anatomic and microscopic changes

Front 9

What is histology? What is a lesion?

Back 9

Histology Dealswith the study of the cells & extracellular matrix of body tissues

A lesion representsa pathologic or traumatic discontinuity of a body organ or tissue

Front 10

What is a sign versus a symptom?

Back 10

Sign=objective manifestation of illness or disorder; can be seen, heard, measured, or felt by the clinician

Symptom= subjective evidence of an illness or disorder; changes in the body or its function that is perceived by the patient as indicating the presence of disease

Front 11

Define: syndrome

Back 11

A complication of signs and symptoms characteristic of a specific disease state

Front 12

Define: sequelae

Back 12

Lesions or impairments that follow or are caused by a disease

Front 13

Deductive vs. Inductive reasoning

Back 13

Deductive: from general to specific, concerned with rules for determining when an argument is valid, uses syllogism

Inductive: from specific to general, concerned with the soundness of inferences for which evidence is not conclusive, uses probability

Front 14

Validity vs. Reliability

Back 14

Validity: Accuracy; refers to the extent to which a measurement tool measures what it is intended to measure

Reliability: Consistency; refers to the extent to which an observation, if repeated, gives the same result

Front 15

How are references ranges used?

Back 15

Interpreted by comparison with lab specific values, defined by healthy volunteers and plotting the frequency distribution; generally conform to gaussian bell-shaped curve; reference ranges are reported as those values within 2 SD of the mean (range of values within 95% individuals)

Front 16

Acute v. chronic v. subacute disease

Back 16

Acute=usually self-limiting and relatively severe

Chronic disorder= implies long-term process, continuous symptoms/severity of disease over time, exacerbations

Subacute disease=intermediate between acute and chronic; not as severe as acute and not as prolonged as chronic

Front 17

Stages of disease

Back 17

Preclinical: disease is not clinically evident but is destined to progress clinical disease

Subclinical disease: not clinically apparent and not destined to become clinically apparent

Clinical disease: characterized by signs and symptoms

Carrier status: refers to an individuals who harbors an organism but is without clinical manifestation; person does not have disease but can still infect others

Front 18

What is metabolic disease? Neoplastic disease?

Back 18

Disturbances of cellular energy processes; characterized by abnormal cell growth (malignant or benign)

Front 19

What is homeostasis and how do the physiologic control systems operate?

Back 19

Purposeful maintenance of a stable internal environment maintained by coordinated physiologic processes that oppose change

The physiologic control systems that oppose change operate by negative feedback mechanisms

Front 20

The physiologic control systems that oppose change operate by negative feedback mechanisms that are composed of...

Back 20

A sensor that detects change, an integrator/comparator that sums and compares incoming data with a set point, an effector system that returns the sensed function to within the set point range

Front 21

What are control systems and what are they responsible for?

Back 21

A collection of interconnected components that function to keep a physical or chemical parameter of the body relatively constant: they regulate cellular function, control life processes, integrate functions of different organ systems

Front 22

What are negative feedback mechanisms?

Back 22

Maintains stability in system; when value decreases below set point, the feedback mechanism causes the function or value to increase, when the function or value is increased above the set point, the feedback mechanism causes it to decrease

Front 23

What are positive feedback mechanisms?

Back 23

Interjects instability in the system; produces a cycle inn which the initiating stimulus produces more of the same

Front 24

What is general adaptation syndrome?

Back 24

-General: Theeffect is a general systemic reaction

-Adaptation: Theresponse is in reaction to a stressor

-Syndrome: Thephysical manifestations are coordinated & dependent on each other

Front 25

What are the stages of General Adaptation Syndrome?

Back 25

Alarm

Resistance or Adaptation

Exhaustion

Front 26

What is the alarm stage of the general adaptation syndrome?

Back 26

CNS aroused and body defenses mobilized; E and NE released--increases heart rate, force of contraction, O2 intake, and mental activity

Front 27

What is the resistance or adaptation stage of the general adaptation syndrome?

Back 27

SNS response: Fight or Flight adrenaline rush; body responds to stressor and attempts to return to homeostasis and coping mechanisms are used

Front 28

What is the exhaustion phase of general adaptation syndrome?

Back 28

Continuous stress causes progressive breakdown of compensatory mechanisms; the body can no longer produce hormones and organ damage begins--marks the onset of disease

Front 29

What are Hans Selye's General Adaptation Syndrome (GAS) stages?

Back 29

Physical or psychological stressor-->alarm reaction-->resistance--> recovery or exhaustion

Front 30

Eustress v. distress

Back 30

Eustress: mild, brief, controllable periods of stress; perceived as positive stimuli to emotional and intellectual growth and development

Distress: severe, protracted, uncontrollable situations of psychological and physical stress, disruptive of health

Front 31

What are conditioning factors?

Back 31

Refers to influence of the adaptive capacity of the person: internal (genetic predisposition, age, sex) and external (exposure to environmental agents, life experiences, dietary factors, level of social support)

Relative risk for development of a stress-related pathologic process in part depends on these factors

Front 32

The stress response is mediated by:

Back 32

the combined efforts of the nervous and endocrine systems

Front 33

Purpose of the stress response

Back 33

To protect the person against acute threats to homeostasis and normally is time limited

Front 34

Stress and Body System Interaction Diagram

Back 34

Front 35

What are the neuroendocrine responses to stress?

Back 35

Hypothalamic-Pituitary Adrenal cortex (HPA) axis; Sympathetic Nervous System (SNS)

Front 36

The Hypothalamic-Pituitary-Adrenal cortex (HPA) is mediated by:

Back 36

glucocorticoids secreted by the adrenal cortex (cortisol)

Front 37

The Sympathetic Nervous System (SNS) is mediated by:

Back 37

catecholamines secreted in the adrenal medulla (E and NE)

Front 38

How does the HPA operate in times of stress? (Flow)

Back 38

With stressor, hypothalamus releases corticotrophin-releasing factor (CRH)-->goes to pituitary gland which releases adrenocorticatropoc hormone (ACTH)-->goes to adrenal cortex which releases corticosteroids (e.g. cortisol)--> give negative to hypothalamus and pituitary gland; also increases blood glucose, depressed the immune system, and is broken down to cholesterol

Front 39

What is cortisol? Why is it essential? What does it do? What is the permissive action of cortisol?

Back 39

Major form of glucocorticoid; is essential for life because of importnat direct effects on intermediary metabolism of carbs, proteins, and lipids

Stimulates protein breakdown to AAs, facilitates lipid breakdown in adipose tissue to fatty acids and glycerol, promotes hepatic gluconeogensis (synthesis of glucose) from AAs, glycerol and fatty acids (via oxaloacetate), making glucose available to brain by inhibiting utilization by other tissues

Permissive action is that a small amount is required for metabolisms, especially those promoted by catecholamines

Front 40

Actions of the parasympathetic nervous system division of the autonomic nervous system

Back 40

Constricts pupil, stimulates salivation, inhibits heart, contricts bronchi, stimulates digestive activity, stimulates gallbladder, contracts bladder, relaxes rectum

Front 41

Actions of the sympathetic nervous system division of the autonomic nervous system

Back 41

Dilates pupil, inhibits salvation, relaxes bronchi, accelerates heart, inhibits digestive activity, stimulates glucose release by liver, secretion of E and NE from kidney, relaxes bladder, contracts rectum

Front 42

The effects of the adrenal catecholamines E and NE in target organs are mediated by:

How is one type of hormone's actions effected by type of receptor?

Back 42

alpha and beta adrenergic receptors; tissues may have one or more receptor types

Actions of one hormone mediated by two classes of receptors often produce opposite effects; when exerted through the same type of receptor, NE and E exert similar effects

Front 43

Alpha receptor mediated actions of the adrenal catecholamines E and NE

Back 43

Increased gluconeogenesis, increased arterilar constriction, increased muscle contraction, increased growth hormone secretion, increased sweating, increased dilation of pupils, decreased insulin secretion

Front 44

Beta receptor mediated actions of the adrenal catecholamines E and NE

Back 44

Increased glycogenolysis, increased lipolysis and ketosis, increased arterior dilation, increased cardiac contractility, increased heart rate, muscle relaxation, increased insulin secretion, renin secretion, increased thyroid hormone secretion

Front 45

Major hormonal changes in stress response and their effects

Back 45

Increased E: prep for fight or flight; mobiliz of energy stores, increased blood glucose and fatty acids

Increased Cortisol: mobiliz of energy stores, increased blood glucose, AAs, and fatty aicds

Increased glucagon and decreased insulin: increase blood glucose and fatty acids

Increase in renin-angiotensin: conserve salt and water

Increase in aldosterone: increase plasma volume

Increase vasopressin: increase ateriolar basoconstriction, thus maintaining/elevating BP

Front 46

Flow or hormonal changes during the stress response

Back 46

Front 47

What are the detrimental affects of stress and its affiliated hormones?

Back 47

Affects growth hormone (decreased levels), thyroid hormone (increased), reproductive hormones (inhibited), interferes with immune function

Front 48

The integration of the stress response relies on communication along neuronal pathways of the:

Back 48

cerebral cortex, limbic system, thalamus, hypothalamus, pituitary gland, reticular activating system (RAS)

Front 49

Cerebral cortex stress actions:

Back 49

involved with vigiliance, cognition, and focused attention

Front 50

Limbic system stress actions:

Back 50

involved with emotional responses

Front 51

Thalamus stress actions:

Back 51

relay center: important in receiving, sorting, and distributing sensory input

Front 52

Hypothalamus stress actions

Back 52

Coordinates responses of the endocrine system and autonomic nervous system

Front 53

Pituitary gland stress actions

Back 53

Releases hormones that govern vital processes

Front 54

Reticular activating system stress actions

Back 54

Modulates mental alertness

Front 55

Diagram of interplay of stress pathways

Back 55

Front 56

What is stress? How does the stress response work?

Back 56

qAstate manifested by symptoms that arise from the coordinated activation of theneuroendocrine & immune systemsqThehormones & neurotransmitters (catecholamines& cortisol) that are released during the stress response function to nAlertthe individual to a threat or challenge to homeostasisnEnhancecardiovascular & metabolic activity of other systems in order to manage thestressornFocusthe energy of the body by suppressing the activity of other systems that arenot immediately needed

Front 57

What is physiologic stress?

Back 57

nChemical or physical disturbance inthe cells or tissue fluid produced by a change, either in the externalenvironment or within the body itself, that requires a response to counteractthe disturbance

Front 58

What are the components of physiologic stress?

Back 58

Exogenous or endogenous stressor initiating the disturbance; chemical or physical disturbance produced by the stressor, the body's counteracting (adaptational) response to the disturbance

Front 59

What is adaptation? What is it affected by?

Back 59

The ability to respond to challenges of physical or psychological homeostasis and to return to a balanced state

Appraisal of the event; coping strategies or coping mechanisms

Front 60

Factors affection adaptation

Back 60

Experience and previous learning, nutrition, genetic endowment and age, physiologic reserve, rapidity with which need for adaptation occurs, sleep-wake cycles, psychosocial factors

Front 61

What is PTSD? What are the causes? How is it characterized? What are the treatments?

Back 61

Shell shock/battle fatigue; caused by trauma; characterized by intrusion, avoidance, and hyperarousal; treatment includes debriefing, crisis intervention, medications for anxiety and depression

Front 62

Inflammatory response v. immune response

Back 62

Inflammatory=non-specific; fever and inflammation

Immune response=specific; antigen-antibody response

Front 63

Inflammatory response involves what types of cells

Back 63

phagocytic WBCs, antimicrobial substances, natural killer cells

Front 64

Functions of the immune response

Back 64

identifies self from non-self; recognizes and eliminates altered host cells, develops more slowly and involves specific cells to combat a particular pathogen

Front 65

What is the 1st line of defense in non-specific resistance to disease?

Back 65

Mechanical factors: skin, mucous membranes, mucus, hairs, cilia, lacrimal apparatus, saliva, urine, defection and vomiting

Chemical Factors: Acid pH of skin, unsaturated fatty acids, lysozyme, gastric juice, vaginal secretions

Front 66

What is the 2nd line of defense in non-specific resistance to disease?

Back 66

Internal defenses: antimicrobial proteins (interferons and complement system), natural killer cells, phagocytes, inflammation, fever

Front 67

Structures of the immune system

Back 67

Lymph nodes, thymus, spleen, spleen, tonsils, red bone marrow

Front 68

Role of lymph nodes in immune system

Back 68

Distrubuted along lymphatic vessels, filter lymph fluid and remove bacteria and toxins from circulation, proliferation of immune cells

Front 69

Role of thymus in immune system

Back 69

Located in mediastinum, produces T-lymphocytes

Front 70

Role of spleen in immune system

Back 70

Largest lymph organ, reservoir for blood, macrophages clear cellular debris and process hemoglobin

Front 71

Role of tonsils in immune system

Back 71

Produce lymphocytes, guard against airborne and injested pathogens

Front 72

Role of red bone marrow in immune system

Back 72

Houses stem cells that develop into lymphocytes

Front 73

Primary vs. secondary lymphatic organs

Back 73

Primary: provide environment for stem cells to divide and mature (red bone marrow, thymus)

Secondary: Sites where most immune responses occur (lymph nodes, spleen, lymphatic nodules)

Front 74

How does lymphatic flow operate?

Back 74

Upper right half of body drains to right lymphatic duct; rest of body drains to thoracic duct

Front 75

Factors of host response to disease

Back 75

Resistance: ability of the body to ward off disease

Susceptibility: vulnearability or lack of resistance to disease

Host factors

Front 76

What is the epidemiologic triangle?

Back 76

Agent; Environment; Host

Front 77

-emia =?

Back 77

it's in the blood

Front 78

Define sepsis, bacteremia, viremia, septicemia

Back 78

-Infection; contamination

-Presence of bacteria in the blood

-Presence of virus particles in the blood

-Systemic infection in which pathogens are present in the blood having spread from an infection in any part of the body

Front 79

Key aspects of viruses

Back 79

£Microscopic genetic parasites£Consist of a protein coat that surroundsa nucleic acid core which may contain RNA or DNA£Have no metabolic capability à most require a host cell to replicate(obligate intracellular parasites)£Some can reproduce outside of a livingcell£Capable of remaining dormant for longperiods of time & replicate / produce symptoms months or years afterinitial infection

Front 80

Key aspects of bacteria

Back 80

£Single-celled microorganisms£No true nucleus£Reproduce by cell division£Pathogenic bacteria contain cell-damagingproteinslEndotoxins – released when the bacterialcell wall decomposes; can cause fever and are not affected by antibioticslExotoxins – released during cell growth£Classified based onlShape: coccus (spherical), spirillium(helical), bacillus (elongated)lGrowth requirementslMotility (flagellated)lOxygen requirements (aerobic vsanaerobic)lGram stain: positively stains purple,negative do not retain stain

Front 81

What are mycoplasmas?

Back 81

Infection-causing microbes; 1/3 the size of bacteria, capable of reproducing independently, do NOT have a rigid cell wall, some cause pneumonia

Front 82

What is rickettsiae?

Back 82

Infection-causing microbes, depend upon host cell for nutrients, multiply by cell division, have a rigid cell wall, human infection caused by bite of an infected arthropod (ex. Typhus, Rocky Mountain spotted fever)

Front 83

Key Aspects of fungi

Back 83

lNon-photosynthetic microorganisms thatreproduce asexually (cell division)lRelatively large microorganismslContain a true nucleuslClassified as•Yeasts•Round, single-celled facultativeanaerobes (can live with or without oxygen)•Molds•Filament-like, multinucleated,aerobic microorganisms

Front 84

What are mycotic infections or mycoses?

Back 84

Infections caused by fungi that release mycotoxins

Front 85

What is the categorization of most fungal infections?

Back 85

£Most infections are mild (athlete’sfoot, candidiasis) unless they become systemic or the patient’simmune system is compromised àopportunistic infection

Front 86

What are parasites and what are the major kinds?

Back 86

Infection-causing microbes, depend on a host for food and protective environment

Protozoa, helminths, arthropods, ectoparasites

Front 87

What are protozoa?

Back 87

Infection-causing microbes; minute unicellular animals, transmission by arthropod vector or contaminated food/water (malaria, amebic dysentery)

Front 88

What are helminths?

Back 88

Worm-like parasites, transmitted by ingestion of fertilized eggs or larva penetration of the skin, most common in developing countries

Front 89

What are anthropods?

Back 89

Infection-causing parasites; have jointed exoskeleton and paired jointed legs, can serve as vectors for other diseases (ticks, mosquitoes, biting flies)

Front 90

What are ectoparasites?

Back 90

Infection-causing parasites; organism that lives on outside of the body, transmitted through contact with infected clothing, bedding, or grooming articles (mites, lice, chiggers)

Front 91

Important function of the intestinal flora

Back 91

help synthesize Vitamin K

Front 92

What are the links in chain of infection?

Back 92

Pathogen, reservoir (habitat of growth), portal of exit, transmission, portal of entry, new host

Front 93

Modes of transmission in chain of infection

Back 93

Direct: direct contact or droplet spread

Indirect: Airborne, vehicleborne, vectorborne

Front 94

Cellular elements of peripheral smear

Back 94

Granulocytes (Neutrophils, basophils. eosinophils), Agranulocytes (lymphocytes, monocytes). RBCs, Platelets

Front 95

Possible pathways for hematopoietic stem cell

Back 95

Front 96

What do WBCs do? What are the types?

Back 96

Protect body against harmful bacteria and infection; Granulocytes "ploys" or "segs" (neutrophils, basophils, eosinophils) and Agranulocytes (monocytes and lymphocytes)

Front 97

What is implied with neutrophils?

What are bands

Back 97

White Blood cell granulocyte involved with Phagocytosis "pyogenic" infections; Bands are immature neutrophilsW

Front 98

What does a "shift to the left" mean in a peripheral blood smear with bands?

Back 98

A shift to the left implies an increase in the number of bands, signaling the worsening of an infection because the full grown neutrophils are dying off

Front 99

What are basophils involved in?

Back 99

WBC Granulocyte involved in allergies and inflammatory responses

Front 100

What are eosinophils and what are they involved with?

Back 100

White Blood Cell Granulocyte; release heparin and histamine, involved in delayed allergic reaction, also has a role in parasitic infections

Front 101

What are monocytes and what are they involved with?

Back 101

Agranulocyte white blood cell; involved with phagocytosis-->severe infections

Front 102

What are lymphocytes, what are they involved with, and what are the types and functions?

Back 102

Agranulocyte white blood cell; viral infections; B cells: mature into plasma cells and release antibodies, T cells-->regulate cell mediated immunity

Front 103

Key features of macrophages

Back 103

£Lacksurface receptors for specific antigens£Havereceptors for Fc region and for complement£Ingestand process antigen & deposit it on its own surface in association with MHCII àpresentantigen-MHC complex to T-lymphocytes à activate T-lymphocytes£Secretecytokines: tumor necrosis factor (TNF) & interleukin-1 (IL-1) which producefever£Phagocyticeffector cells in both humoral & cell-mediated responses

Front 104

In a WBC differential what does each cell count indicate?

Back 104

Neutrophils: bacterial infections, inflammatory, stress, certain drugs

Eosinophils: allergic disorders and parasitic infestations

Basophils: inflammation and allergic reaction

Lymphocytes: viral infections

Monocytes: severe infections

Front 105

How is absolute value in a WBC differential count calculated?

Back 105

Absolute value= relative value (%) x Total WBC

Front 106

What are the terminologies for increased value in a WBC differential? What are the terminologies for decreased values in a WBC differential?

Back 106

Leukocytosis, neutrophilia, lymphocytosis, monocytosis, eosinophilia, basophilia

Leukopenia, neutropenia, lymphopenia, monocytopenia, eosinopenia, basopenia

Front 107

In what cases is an increased WBC count seen?

Back 107

Infection, inflammation, tissue, necrosis, or leukemic neoplasia; increases also observed in trauma, emotional/physical distress

Front 108

In what cases is a decreased WBC count seen?

Back 108

Chemotherapy, radiation therapy, marrow infiltrative diseases, overwhelming infections, dietary deficienicies, autoimmune diseases

Front 109

A persistent increased in serial WBC and differential counts indicates...

A drastic decrease indicates...

Back 109

worsening of an infection

bone marrow failure and risk of infection

Front 110

What are the critical values for WBC counts? WBC values tend to be...

Back 110

<2500 cells/mm3 or >30,000 cells/mm3

Tend to be age-related, normal newborns and infants have higher WBC values, elderly may not develop increased WBC even in the presence of severe bacterial infection

Front 111

How is absolute neutrophil count (ANC) calculated?

Back 111

ANC=WBC x (% neutrophils + % bands)

Front 112

What is erythrocyte sedimentation rate (ESR)?

What happens to ESR in acute infections?

Back 112

Rate that RBC's settle out of anticoagulated blood in 1 hour; is not diagnostic but provides information about disease processes that need to be investigated

In acute infections, the ESR usually does not elevate for 6-24 hours and peaks after several

Front 113

What is C-reactive protein (CRP)

Back 113

An abnormal protein synthesized by the liver and present in blood during any process that involves tissue necrosis, trauma, inflammation, or infection

NON-specific test

Front 114

How and when does C-reactive protein react?

Back 114

Appears rapidly in resposne to injurious stimulus, classic and most dramatic acute phase reactant, levels up to 1000x normal-->rapidly declines when inflammatory process regreesses-->provides good indicator of healing and response to Tx

Serum levels increase within 18-24 hours (rises earlier) and starts to decrease earleir as well

Front 115

What are markers of infection in urinalysis? What do these markers indicate?

Back 115

Appearance and color (cloudy urine may be caused by pus, RBCs, or bacteria; pseudomonoas may produce green urine)

Odor (foul odor may indicate UTI)

pH (bacteria increases, urea splitting bacteria causes alkaline)

Leukocyte esterase (screen test used to detect leukocytes in urine 90% accuracy)

Nitrites: screening test for identification of UTIs 50% accuracy

Front 116

What is nitrites evaluation in urinanalysis? What can give a false positive?

Back 116

Screening test for identification of UTIs; bacteria produce an enzyme called reductase which can reduce nitrates to nitrites (50% accuracy); false positive if contaminated with vaginal secretions

Front 117

Normally stool contains:

Bacteria that act as pathogens in stool:

Back 117

Many bacteria and fungi that are indigenous

Salmonella, Shigella, campylobacter, yersinia

Front 118

What might give a false negative culture in a stool culture?

When is stool culture taken? When can stool flora become pathogenic?

Back 118

Urine the sample may inhibit bacterial growth and give a false negative culture

Performed on patients with unrelenting diarrhea, fever, and abdominal bloating

Normal stool can become pathogenic if the host is immunocompromised

Front 119

"itis"=?

Back 119

inflammation

Front 120

What is the acute inflammatory response? What does it result in?

Back 120

Rapid and non-specific, protective response to cellular injury from any cause, can only occur vascularized tissue

Results in accumulation of fluid and cells at the inflammatory site

Front 121

Hallmarks of inflammation

Back 121

redness, swelling, heat, pain, loss of function

Front 122

The reaction of vascularized tissue to local injury is:

Back 122

active, aggressive, nonspecific

Front 123

Causes of inflammation

Back 123

infection by microorganisms; heat (burns) and cold (frostbite); radiation (UV, infrared or radioactive); trauma (abrasions, lacerations, bruising, crushing); chemicals (strong acids or bases, insect bites, allergens, toxins produced by microorganisms), ischemic damage

Front 124

What is hypoxia? What are some examples?

Back 124

Lack of sufficient oxygen

Ex. Decreased amount of oxygen in the air, loss of hemoglobin or hemoglobin funcction, decreased production of RBCs, diseases of the respiratory and cardiovascular systems, poisoning of the oxidative enzymes within the cells

Front 125

What is ischemia? What are some examples?

Back 125

Reduced blood supply (gradual progressive vs. sudden acute)

Ex. arteriosclerosis (gradual narrowing of arteries), thrombosis (complete blockage of an artery by a blood clot), embolus (a blood clot that has traveled

Front 126

What is anoxia? What is infarction?

Back 126

Total lack of oxygen; cell death

Front 127

What is the vascular response of the acute phase response?

Back 127

Immediate arteriolar vasoconstriction followed by vasodilation-->swelling (edema) and erythema (redness)-->hyperemia

Increased capillary permeability-->allows fluid to escape into tissue-->swelling (edema)

Pain and impaired function d/t tissue swelling and release of chemical mediators

Front 128

What is the cellular response of acute phase response?

Back 128

WBCs move toward damaged cells-->phagocytosis of dead cells & microorganisms

Platelets move toward damaged cells-->control any excess bleeding in the area

Mast cells-->release heparin to maintain blood flow to area

Involves granulocytes, mononuclear phago cytes, margination and emigration of leukocytes, chemotaxis, phagocytosis

Front 129

Action of neutrophils in acute phase response? what are the types?

Back 129

Primary phagocyte: arrives early, polymorphonuclear (PMNs or polys) or Segmented neutrophils (segs); bands (immature neutrophils)

Front 130

Action of eosinophils in acute phase response?

Back 130

Allergic reactions and parasitic infections; release chemical mediators-->inflammation

Front 131

Action of basophils in acute phase response

Back 131

Inflammation and allergic reactions; contain histamine-->mediator of inflammation

Front 132

What is leukocytosis?

Back 132

Increase in WBCs

Front 133

Key aspects of mononuclear phagocytes

Back 133

£LargestWBC (3-8% WBC)£3-4xlonger lifespan; longer in tissues£Matureinto macrophages£W/in48 hrs monocytes & macrophages arepredominant cell type£Canphagocytize larger material than neutrophils£Migrateto local lymph nodes & play role in specific immunity£Rolein chronic inflammation àwall off material that cannot be digested

Front 134

What is involved in margination and emigration of leukocytes?

Back 134

£Fluidleaves capillaries à­blood viscosity£Releaseof chemical mediators (histamine, leukotrienes, & kinins)and cytokines affect endothelial cells of capillaries à­expression of adhesion molecules àleukocytes marginate (pavementing)àemigration – diapedesis through capillary walls

Front 135

What is involved with chemotaxis?

Back 135

£Leukocyteswander through tissue guided by lSecreted cytokines (chemokines,IL-8) lBacterial & cellular debrislComplement fragments (C3a, C5a)£Migrationin response to chemical signal à increases probability of sufficientlylocalized cellular response

Front 136

What is phagocytosis? What steps are involved?

Back 136

Acute phase response; neutrophils and macrophages engulf and degrade bacteria and cellular debris

Involves 4 steps: chemotaxis, adherence plus opsonization, engulfment, and intracellular killing

Front 137

What is the chemotaxis step of phagocytosis?

Back 137

Chemical attraction of WBCs to area

Front 138

What is the adherence plus opsonization stage of phagocytosis?

Back 138

Coats the antigen with antibody (Fc) or complement (C3a)

Front 139

What is the engulfment stage of phagocytosis?

Back 139

Pseudopods surround and enclose particle in particle in phagocytic vesicle (phagosome)-->merges with lysosome-->antibacterial molecules and enzymes digest microbe

Front 140

What is the intraceullar killing stage of phagocytosis?

Back 140

Via enzymes, defensions, and toxic products

Front 141

Stages of phagocytosis

Back 141

Attachment, ingestion, fusion of the lysosome and phagosome, digestion, release of digested

Front 142

What are the changes in the body with the acute phase response?

Back 142

Changes in concentrations of plasma proteins, increase in erthyrocyte sedimentation rate, fever, increase in number of leukocytes, skeletal muscle catabolism, negative nitrogen balance

Front 143

How does histamine work?

Back 143

Main chemical mediator of inflammation; released by basophils, platelets, and mast cells

Responsible for BOTH parts of the vascular response to inflammation: vasodilation leads to increases blood flow and increases capillary permeability

Also stimulates bronchoconstriction (H1 receptors) and gastric acid secretion (H2 receptors)

Front 144

How do plasma proteases work?

Back 144

Inflammatory mediators; kinins, activated complement proteins, and clotting factors

Bradykinin increases capillary permeability and causes pain

They contribute to the vascular phase of inflammation through fibrinopeptides formed during final step of clotting process

Front 145

What are prostaglandins and what are their effects? Which are the most important ones for inflammation?

Back 145

Inflammatory mediator produced from arachodonic acid found in the cell membranes via cyclooxygenase metabolic pathway

Increase blood flow and increase capillary permeability, potentiate effects of histamine, cause fever in response to infection, stimulate pain receptors, blocked by NSAIDs

Front 146

How does leukotrienes operate? What kind is essential?

Back 146

Inflammatory mediators that increase vascular permeability, affects adhesion of WBC to capillary during injury or infection, act as chemo-attractants

SRSA=slow reacting substance of anaphylaxis-->key role in bronchoconstriction in asthma

Front 147

What is platelet activating factor? How does it operate?

Back 147

Inflammatory mediators, generated from a complex lipid in cell membranes, affects a variety of cell types, induces PLT aggregation, activates neutrophils, potent eosinophil chemo-attractant

Front 148

What are peptides? How do they function and what are their effects?

Back 148

Peptides produced by variety of immune and inflammatory cells: macrophages, monocytes, neutrophils, lymphocytes; also produced by non-inflammatory cells: fibroblasts and endothelial cells

Function as local hormones that affect host response to injury or infection

Multiple effects-->serve as communication links between immune and inflammatory

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How are cytokines named?

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Referred to by specific name according to their function or a numbered "interleukin"

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What kinds of cytokines induce inflammation?

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IL-1, IL-6, TNF, interferon-Y

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Chemical mediators of swelling, redness, and tissue warmth

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Histamine, prostaglandins, leukotrienes, bradykinin, platelet-activating factor

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Chemical mediators of tissue damage

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Lysosomal enzymes and products released from neutrophils, macrophages, and other inflammatory cells

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What is the chemical mediator of chemotaxis?

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Complement fragments

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What are the chemical mediators of pain?

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Prostaglandins, bradykinin

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Chemical mediators of fever

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IL-1 and IL-6

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Chemical mediators of leukocytosis

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TNF and IL-8

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What are inflammatory exudates? What are the types?

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Fluid, plasma protein, cell contents

Types: serous, fibrinous, membranous, purulent or suppurative, hemorrhagic

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What are the serous, fibrinous, and membranous types of inflammatory exudates?

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Serous: watery, low protein (plasma)

Fibrinous--fibrogen-->thick sticky meshwork like a clot

Membranous--develop on mucous membrane surface-->necrotic cells enmeshed in fibrino-purulent exudate

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What are the purulent or suppurative and the hemorrhagic types of inflammatory exudates

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Purrulent or suppurative: contains pus (WBCs--neutrophils and macrophages, proteins, tissue debris)

Hemorrhagic--leakage of RBCs

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What is acute inflammation?

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With intact immune system, usually self-limited and rapidly controlled by host defenses

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What is chronic inflammation? Types?

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Self-perpetuating and lasts for weeks or months, involves proliferation of fibroblasts instead of exudates-->increased risk of scarring; typically involves low-grade, persistent irritants (asbestos, talc, silica) or moderate to low virulence (tubercle bacillus, treponema pallidum, actinomyces) that are unable to penetrate deeply or spread rapidly; immune mechanisms thought to play a larger role

Types: non-specific, granulomatous

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What is an abscess?

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A localized area of inflammation containing a purulent exudate. Typically have a central necrotic core contianing purulent exudates surrounded by a layer of neutrophils. fibroblasts may eventually enter area and wall off area making it inaccessible to antibiotics-->often requires surgical incision and drainage

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What is ulceration?

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A site of inflammation where an epithelial surface has become necrotic and eroded, often associated with subendothelial inflammation; may also occur as a result of injury to epithelial surface or because of vascular compromise

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What happens with chronic lesions?

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The area surrounding the ulceration develops fibroblastic proliferation with scarring and accumulation of chronic inflammatory cells (macrophages and lymphocytes)

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How are granulomas formed?

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If acute inflammatory response is unsuccessful at ridding the body of invading foreign particle-->chronic inflammation--> granuloma formation

Formed when giant cells (fused macrophages) engulf large foreign particles

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What is a granuloma? What is it associated with.

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1-2 mm lesion--a mass of macrophages surrounded by lymphocytes (aka epitheloid cells); associated with foreign bodies such as splinters, sutures, silica, asbestos, and microorganisms that cause Tb and syphilis (agents that are poorly digested and not easily controlled)

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What is inside and outside of granulomas?

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Inside: debris decays and forms a liquid that may diffuse out leaving behind only the thick-walled casing

Outside: encased by a collagen network and may eventually calcify-->lesion becomes encapsulated and isolated

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What are the acute phase responses systemic manifestations?

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Changes in concentrations of plasma proteins, increased ESR, fever, leukocytosis and neutrophilia (in case of bacteria infections), eosinophilia (in case of parasitic infections and allergic reactions), neutropenia and lymphocytosis (in viral infections), leukopenia (in overwhelming infections in the presence of other debilitating diseases such as cancer); skeletal muscle catabolism and negative nitrogen balance; lethargy

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What is lymphadenopathy?

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Characterized by a localized or generalized enlargement of the lymph nodes or lymph vessels

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What is lymphadenitis?

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Inflammatory condition of the lymph nodes; nodes may be enlarged, hard, smooth, or irregular, may be red, feel hot, or tender to touch; location of the node is indicative of the site of origin of disease--affected nodes are proximally located along the lymphatic drainage pathway

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What are painful nodes associated with? What are non-painful lymph nodes associated with?

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Painful-->associated with inflammatory process

Non-painful lymph nodes-->more characteristic of neoplasms

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Weakened immune systems can lead to

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Opportunistic infections that occur as a result of altered or weakened host immune systems

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What might a hyperactive immune system result in?

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Autoimmune disorders which is an inflammatory response related to injury to one's own body tissues

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The body's thermostat is...

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hypothalamus

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What happens to body temperature after major surgery or MI?

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Low grade temperature for 1st 48-72 hours is normal

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What are pyrogens? Types?

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Fever producers; Exogenous (gram +/- bacteria, endotoxins, viruses, fungi, yeast, protozoans) or Endogenous (PMNs, macrophages, T4 cells, malignancies, Ag-Ab reactions and graft rejections)

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How to pyrogens lead to fever production?

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Endogenous pyrogens stimulate release of PgE from hypothalamus-->stimulates release of NE from adrenal medulla--> lowers Ca around hypothalamic cells--> increases firing rate

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What are the stages of fever?

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Prodromal: general malaise, fleeting aches and pains

Stage 1: cold or shaking chill stage: 10-40 min with rapid steady rise in T with increases cellular metabolism-->vasoconstriction and cessation of sweating

Stage 2: Flush: thermostat reset, cutaneous vasodilation-->skin warm and flushed-->dehydration

Stage 3: defervescence: initiation of sweating

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What are the patterns of fever?

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Intermittent: returns to normal at least every 24 hours

Remittent: varies a few degrees in either direction

Sustained or continuous: Increased T remains with minimal variation

Recurrent or relapsing: one or more episodes of fever each lasting several days with one or more days of normal T between episodes

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What is fever of unknown origin? Causes?

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Temperature greater than 101 present for >3 weeks

Causes: malignancies, infections, cirrhosis

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What is different about fever in children?

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2/3 of children <3 years qualify with fever (common); low vs. high risk based on probability of progression to bacteremia and menigitis

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How does S/S toxicity present in children?

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Lethargy, poor feeding, hypo ventilation & poor oxygenation, cyanosis

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How does fever different in the elderly?

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Normal body temperature and circadian pattern often altered in elderly; lower basal temperature; 20-30% with serious infection present with absent or blunted febrile response