Cson S10 Patho Exam 2

Front 1

what is the first line of defense and give examples

Back 1

innate resistance
skin; vomiting; linings of gastrointestinal, genitourinary and respiratory tracts; coughing, sneezing, flushing, mucus and cilia

Front 2

second line of defense

Back 2

inflammation

Front 3

third line of defense

Back 3

adaptive (acquired) immunity

Front 4

what is the purpose of inflammation

Back 4

to neutralize and wall off the offensive agent and remove dead tissue and establish an environment suitable for healing

Front 5

when does inflammation occur

Back 5

almost immediately after injury

Front 6

what causes the inflammatory response

Back 6

infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation

Front 7

what are the key signs of inflammation

Back 7

redness, warmth, swelling, pain, loss of function

Front 8

is inflammation always present with infection?

Back 8

yes

Front 9

is infection always present with inflammation

Back 9

no

Front 10

local response of inflammation

Back 10

vascular and cellular stages

Front 11

systemic response of inflammation

Back 11

white blood cell response and acute-phase response

Front 12

etiology of inflammation

Back 12

heat, radiation, trauma, allergens, infection

Front 13

what determines the intensity of the inflammatory response

Back 13

extent and severity of injury; reactive capacity of injured person

Front 14

when might someone not show an inflammatory response

Back 14

if they are immunocompromised

Front 15

list four stages of inflammatory response

Back 15

vascular response, cellular response, formation of exudate, healing

Front 16

describe vascular response of inflammation

Back 16

arterioles undergo transient vasoconstriction; injured cells release histamine and other chemicals causing vasodilation (hyperemia); this results in hyperemia, increased blood flow to the area, raising of filtration pressure

Front 17

how does the vascular response appear to us?

Back 17

redness and edema in the tissue

Front 18

list the effects of vascular and chemical response in inflammation

Back 18

endothelial cell retraction, increased capillary permeability, movement of fluid from capillaries into tissues

Front 19

plasma protein fibrinogen is activated by products of injured cells to become what

Back 19

fibrin

Front 20

what is the function of fibrin

Back 20

strengthens a blood clot formed by platelets which traps bacteria to prevent spreading

Front 21

what is the purpose of the coagulation system at site of injury

Back 21

forms fibrinous meshwork at injured/inflamed site that prevents spread of infection, keeps microorganisms and foreign bodies at site of greatest inflammatory cell activity, forms clot that stops bleeding, provides a framework for repair and healing

Front 22

describe the first step in the cellular response of inflammation

Back 22

neutrophils and monocytes migrate through capillary wall to site of injury

Front 23

define chemotaxis and desccribe its purpose

Back 23

directional migration of wbcs along concentration gradient of chemotactic factors; mechanism for accumulation of neutrophils and monocytes at site of injury

Front 24

what do chemotactic factors do

Back 24

act as gps to direct wbc to injured tissue

Front 25

define margination

Back 25

lining up of wbc along sides of capillary wall

Front 26

define diapedesis

Back 26

migration out of capillary to site of injured tissue

Front 27

where do chemotactic factors originate from

Back 27

lipids in walls of cells release chemotactic factors as they break down

Front 28

neutrophils are also known as

Back 28

polymorphonucleated leukocytes (PMN)

Front 29

function of neutrophils in inflammatory response

Back 29

phagocytize bacteria, other foreign material and damaged cells

Front 30

life span of neutrophils

Back 30

24-48 hours

Front 31

first leukocytes to arrive at the site of injury

Back 31

neutrophils within 6-12 hours

Front 32

what does pus consist of

Back 32

dead neutrophils, digested bacteria, other cell debris

Front 33

what is the correct term for pus filled?

Back 33

purulent (not pussy)

Front 34

name for immature neutrophils

Back 34

bands, segmented neutrophils, segs

Front 35

what does it mean when segs are increased

Back 35

demand for neutrophils is so high that bone marrow releases immature neutrophils, or segmented neutrophils

Front 36

steps leading to phagocytosis

Back 36

pavementing = margination
diapedesis
chemotaxis

Front 37

steps of phagocytosis

Back 37

adherence, engulfment, phagosome formation, fusion with lysosomal granules/toxic oxygen production, destruction of the target

Front 38

what are monocytes

Back 38

second type of phagocytic cells to site of injury; biggest type of leukocytes

Front 39

when do moncytes arrive to site of inflammation

Back 39

3-7 days

Front 40

what do monocytes turn into

Back 40

macrophages

Front 41

functions of macrophages

Back 41

assist in phagocytosis of inflammatory debris; clean area so that healing can begin

Front 42

what is a multinucleated giant cell

Back 42

many macophages fused together; phagocytize particles too big for macrophage; become encapsulated by collagen leading to formation of granuloma

Front 43

function of lymphocytes

Back 43

cause the immune response; cell-mediated and humoral

Front 44

what are eosinophils and what do they do

Back 44

released in large quantities during allergic reaction
release chemicals that act to control effects of histamine and serotonin
involved in phagocytosis of allergen-antibody complex
slow down immune response to allow clean up and wound healing

Front 45

basophils

Back 45

carry histamine and heparin that are released during inflammation
limited phagocytic capabilities
similar to mast cell

Front 46

what is the most important activator of inflammation

Back 46

mast cell degranulation

Front 47

where are mast cells located

Back 47

throughout loose connective tissue surrounding blood vessels esp in lungs, gi tract and skin

Front 48

list the chemical mediators of the inflammatory response

Back 48

histamine, serotonin, kinins, complement components, prostaglandins, leukotrienes, cytokines

Front 49

describe the complement system

Back 49

major mediator of inflammatory response
when activated, components occur in sequential order involving two pathways
each activated complex can act on the next component

Front 50

what are the major functions of the complement system

Back 50

enhanced phagocytosis
increased vascular permeability
chemotaxis
cellular lysis

Front 51

functions of the kinin system

Back 51

activate and assist inflammatory cells
causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, leukocyte chemotaxis

Front 52

primary kinin is

Back 52

bradykinin

Front 53

function of prostaglandins

Back 53

potent vasodilators
inhibit platelet and neutrophil aggregation
pro inflammatory contributing to increased blood flow, edema and pain

Front 54

drugs that inhibit the prostaglandin synthesis

Back 54

NSAIDs, aspirin, corticosteroids

Front 55

what is exudate

Back 55

fluid and leukocytes that move from circulation to site of injury

Front 56

describe serous exudate

Back 56

watery; indicates early inflammation

Front 57

describe fibrinous exudate

Back 57

thick, clotted exudate; indicates more advanced inflammation

Front 58

describe purulent exudate

Back 58

pus, indicates bacterial infection

Front 59

describe hemorrhagic exudate

Back 59

contains blood, indicates bleeding

Front 60

clinical manifestations of local response to inflammation

Back 60

redness, heat, pain, swelling, loss of function
AKA cardinal signs

Front 61

clinical manifestations of systemic response to inflammation

Back 61

increased WBC count with shift to left
malaise
nausea
anorexia
increased pulse and respiratory rate
fever

Front 62

what does shift to left mean in reference to wbc

Back 62

increased #s of more immature leukocytes

Front 63

what are the causes of the systemic response to inflammation

Back 63

poorly understood but prob due to complement activation and release of cytokines

Front 64

beneficial aspects of fever

Back 64

increased killing of microorganisms, increased phagocytosis, increased proliferation of T lymphocytes

Front 65

what triggers fever

Back 65

release of cytokines --> they initiate metabolic changes in temp regulating center (epinephrine released from adrenal medulla increases metabolic rate)

Front 66

signs of fever

Back 66

chills and shivering; body is hot yet person seeks warmth until circulating temp reaches core body temp

Front 67

describe acute inflammation

Back 67

healing occurs in 2-3 wks usually leaving no residual damage
neutrophils are predominant cell at site

Front 68

describe subacute inflammation

Back 68

persists longer than acute
similar signs as acute
may be cause of vascular damage that leads to atherosclerosis
assoc with oral inflammation, pancreatic cancer and alzheimers

Front 69

describe chronic inflammation

Back 69

may last for years; injurious agent persists or repeats injury to site; predominant cell types are lymphocytes and macrophages; may result from changes in immune system (autoimmune); assoc with granuloma formation; lasts more than 2-3 weeks

Front 70

what are examples of chronic inflammation assoc with autoimmunity

Back 70

rheumatoid arthritis and tuberculosis

Front 71

final phase of inflammatory response

Back 71

healing

Front 72

describe regeneration

Back 72

replacement of lost cells and tissues with cells of same type

Front 73

do skeletal and cardiac muscle regenerate

Back 73

no; they are replaced with scar tissue

Front 74

describe repair

Back 74

healing as a result of lost cells being replaced with connective tissue; more complex than regeneration; most common type of healing; usually results in scar formation

Front 75

describe process of repair

Back 75

initial phase = 3-5 days
granulation phase = 5 days to 3 weeks
maturation phase and scar contraction = 7 days to several months or years

Front 76

what is the most common type of diabetes

Back 76

type 2

Front 77

where does diabetes rank in causes of death for the US

Back 77

5th

Front 78

where is insulin released from

Back 78

beta cells of pancreas

Front 79

where is glucagon released from

Back 79

alpha cells of pancreas

Front 80

what happens when blood sugar is too high

Back 80

insulin produced by the pancreas; liver stores glycogen

Front 81

what happens when blood sugar is too low

Back 81

glucagon produced by pancreas; liver releases glucose

Front 82

list and describe different types of diabetes

Back 82

type 1 - autoimmune, insulin absent, pediatric
type 2 - reduced insulin and insulin resistance; some cells produce but not enough
type 3 - from pancreatic trauma, drugs, other diseases
type 4 - gestational diabetes

Front 83

when does type 1 diabetes generally occur

Back 83

before age 30; peak onset between 11 and 13

Front 84

etiology of type 1 diabetes

Back 84

end result of auto immune process; beta cells destroyed by body's own T cells; related to genetic susceptibility, autoimmunity and environmental triggers

Front 85

symptoms of type 1 diabetes

Back 85

recent, sudden weight loss
polydipsia
polyuria
polyphagia

Front 86

why does weight loss occur with type 1 diabetes

Back 86

body is no longer able to absorb glucose and starts to break down protein and fat for energy

Front 87

types of test for diabetes

Back 87

IFG: impaired fasting glucose
IGT: impaired glucose tolerance

Front 88

which test is faster, less expensive and more easily tolerated for diabetes

Back 88

impaired fasting glucose

Front 89

if positive for pre diabetes, how long before diabetes generally develops

Back 89

usually within 10 years

Front 90

80 to 90% of people with type 2 diabetes are what?

Back 90

overweight

Front 91

symptoms assoc with type 2

Back 91

fatigue, blurred vision, unexplained weight loss

Front 92

what factors contribute to development of type 2 diabetes

Back 92

age, genetic basis, race (higher in blacks, asians, hispanics and natives), obesity, genetic mutations

Front 93

what are the metabolic abnormalitites assoc with type 2 diabetes

Back 93

insulin resistance
decreased ability to produce insulin
inappropriate glucose production
alteration in production of hormones (adipokines)

Front 94

where do adopokines come from?

Back 94

belly fat (cytokines of adipose tissue)

Front 95

what causes the pancreas to have decreased ability to produce insulin

Back 95

worn out beta cells; beta cells decrease in mass

Front 96

what are the two main adipokines

Back 96

adiponectin and leptin

Front 97

what is metabolic syndrome and what does it increase risk for

Back 97

cluster of abnormalities that increase risk for cardiovascular disease and diabetes; characterized by insulin resistance; abdominal obesity, high triglycerides, low HDL cholesterol, hyperglycemia, hypertension

Front 98

risk factors for metabolic syndrome

Back 98

central obesity, sedentary lifestyle, urbanization, certain ethnicities

Front 99

acute complications of diabetes

Back 99

hypoglycemia, diabetic ketoacidosis, hyperglycemic hyperosmolar syndrome (more common in older persons)

Front 100

common manifestations of hypoglycemia

Back 100

confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances

Front 101

what happens if hypoglycemia is not treated

Back 101

loss of consciousness, seizures, coma, death

Front 102

clinical manifestations of type 2 diabetes

Back 102

fatigue, recurrent infections, recurrent vaginal yeast or monilia infections, prolonged wound healing, visual changes (blurred vision)

Front 103

chronic hyperglycemia causes what

Back 103

micro and macrovascular disease and neuropathies; nonenzymatic glycosylation, shunting of glucose to polyol pathway, activation of protein kinase C

Front 104

describe nonenzymatic glycolysation

Back 104

reversible attachment of glucose to proteins, lipids w/o enzyme action; glucose can become permanently bound; leads to creation of AGEs which cause tissue injury

Front 105

how do AGEs cause injury

Back 105

procoagulant changes (clotting), production of free radicals, binding to macrophages inducing inflammation, thickening basement membranes which result in increased vascular permeability

Front 106

how does shunting of glucose to polyol pathway affect tissues

Back 106

polyol pathway is for tissues that do not require insulin for glucose transport; when glucose is shunted this increases osmotic pressure leading to tissue damage

Front 107

what tissues use polyol pathway

Back 107

RBCs, blood vessels, nerves, eye lens

Front 108

how does activation of protein kinase c injure tissues

Back 108

result in insulin resistance due to increased cytokines and increased permeability

Front 109

chronic complications of diabetes

Back 109

angiopathy, diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, infection

Front 110

describe angiopathy

Back 110

blood vessel damage; a major effect of diabetes; macrovascular and microvascular; symptoms usually appear 10-20 years after diagnosis

Front 111

which vascular changes are specific to diabetes

Back 111

microvascular

Front 112

areas most noticeably affected by microvascular angiopathy

Back 112

eyes, kidneys, skin

Front 113

what is the most common cause of new cases of blindness in people 20-74 years

Back 113

diabetic retinopathy (microvascular damage to retina as a result of chronic hyperglycemia)

Front 114

2 forms of diabetic retinopathy

Back 114

nonproliferative = most common, partial occlusion of small blood vessels in retina causing microaneurysms and retinal edema intraretinal hemorrhages
Proliferative = most sever form, retinal capillaries become occluded leading to retinal detachment

Front 115

leading cause of end stage renal disease

Back 115

diabetic nephropathy

Front 116

critical factors for prevention/delay of diabetic nephropathy

Back 116

tight glucose control
blood pressure management
yearly urine screening

Front 117

what is diabetic neuropathy

Back 117

nerve damage due to metabolic changes

Front 118

describe sensory neuropathy

Back 118

usually worse at night; can cause atrophy of small muscles of hands/feet; most common form is distal symmetric affecting hands and/or feet bilaterally; characterized by loss of sensation, abnormal sensation, pain and paresthesias (numbness)

Front 119

describe autonomic neuropathy

Back 119

complications include gastroparesis, sexual dysfunction, neurogenic bladder

Front 120

what is the most common cause of hospitalization with diabetes

Back 120

foot complications

Front 121

risk factors for complications of foot and lower extremity

Back 121

sensory neuropathy, peripheral artery disease
other contributors include smoking, clotting abnormalities, impaired immune function, autonomic neuropathy

Front 122

how is infection affected by diabetes

Back 122

diabetics are more susceptible; defect in mobilization of inflammatory cells; impairment of phagocytosis by neutrophils and monocytes; loss of sensation may delay detection; treatment must be prompt and vigorous

Front 123

when did modern antimicrobials first appear

Back 123

in the 1930s and 40s

Front 124

host

Back 124

any organism capable of supporting the nutritional and physical growth requirements of another

Front 125

infection

Back 125

presence and multiplication of a living organism on or within the host

Front 126

colonization

Back 126

bacteria present at site of entry; not necessarily in tissues

Front 127

microflora

Back 127

microorganisms normally living in or on your body; some are useful; many have no effect

Front 128

what are disease causing organisms called

Back 128

pathogens

Front 129

opportunistic pathogens

Back 129

those that normally would not cause disease but seize an opportunity provided by a person's decreased immune or inflammatory responses

Front 130

stages of infection

Back 130

colonization, invasion, multiplication, spread

Front 131

colonization

Back 131

presence of pathogen at portal of entry

Front 132

invasion

Back 132

may be aided by production of bacterial extracellular substances that break down primary or secondary defenses

Front 133

multiplication

Back 133

# of organisms increase

Front 134

spread

Back 134

movement to other tissues of the body

Front 135

stages of infectious disease

Back 135

incubation period
prodromal stage
acute stage
convalescent period

Front 136

incubation period

Back 136

pathogen begins active replication without producing recognizable symptoms in host

Front 137

prodromal stage

Back 137

inital appearance of symptoms in host

Front 138

acute stage

Back 138

host experiences maximum impact of infectioius process

Front 139

convalescent period

Back 139

containment of infection, progressive elimination of pathogen, repair of damaged tissue, resolution of associated symptoms

Front 140

insidious disease

Back 140

protracted prodromal phase

Front 141

fulminant illness

Back 141

abrupt onset of symptoms with little or no prodrome

Front 142

factors affecting infection

Back 142

mechanism of action, infectivity, pathogenicity, virulence, immongenicity, toxigenicity

Front 143

mechanism of action for infection

Back 143

direct damage of cells, interference with cellular metabolism, rendering a cell dysfunctional bc of accumulation of pathogenic substances and toxin production

Front 144

infectivity

Back 144

ability of pathogen to multiply in the individual

Front 145

pathogenicity

Back 145

ability of an agent to produce disease; depends on speed of reproduction, extent of tissue damage and production of toxins

Front 146

virulence

Back 146

potency of pathogen measured in terms of number of microorganisms or micrograms of toxin required to kill a host

Front 147

toxigenicity

Back 147

factor important in determining virulence such as production of soluble toxins or endotoxin

Front 148

kinds of infectious agents

Back 148

prions, viruses, bacteria, mycoplasmas, rickettsiae, chlamydiae, fungi, parasites

Front 149

prions

Back 149

small modified infectious proteins

Front 150

mechanism of action for prions

Back 150

cause normal proteins to change their shape and become new prions

Front 151

viruses

Back 151

protein coat surrounding nucleic acid core

Front 152

mechanism of action for viruses

Back 152

insert their genome into host cells' DNA and use that metabolic machinery to make new viruses

Front 153

cellular effects of viruses

Back 153

inhibition of host cell dna, rna or protein synthesis; disruption of lysosomal membranes, promotion of apoptosis, fusion of infected adjacent host cells; alteration of antigenic properties; transformation of host cells into cancerous cells; promotion of secondary bacterial infections

Front 154

bacteria

Back 154

cells without membrane bound organelles (prokaryotes)

Front 155

what feature of bacteria is important to antibiotic use

Back 155

cell wall that eukaryotes dont have

Front 156

exotoxins

Back 156

proteins released by bacteria that damage or kill host cells

Front 157

endotoxins

Back 157

parts of bacterial cell wall that cause host immune reactions

Front 158

what must bacteria have to multiply

Back 158

iron

Front 159

bacteremia or septicemia

Back 159

presence of bacteria in blood as a result of a failure of body's defense mechanisms; usually caused by gram negative bacteria; toxins released in blood cause widespread vasodilation resulting in seriously low blood pressure

Front 160

mycoplasmas, rickettsiae, chlamydiae

Back 160

smaller than bacteria; mycoplasmas lack cell walls; R and C have to live inside cell like virus

Front 161

fungi

Back 161

most fungal infections on body surface bc core temp is to high; deep fungal infections are life threatening and commonly opportunistic

Front 162

mechanism of action for fungal infections

Back 162

adapt to host environment; suppress immune defenses allowing fungi to grow

Front 163

diseases caused by fungi are called

Back 163

mycoses

Front 164

fungi that invade skin, hair or nails

Back 164

dermatophytes

Front 165

diseases produced by dermatophytes

Back 165

tineas

Front 166

types of parasites

Back 166

protozoa, helminths, arthropods

Front 167

examples of protozoan diseases

Back 167

malaria, amoebic dysentery, giardiasis

Front 168

examples of helminths

Back 168

roundworms, tapeworms, flukes

Front 169

examples of arthropods

Back 169

ticks, mosquitoes, mites, lice, fleas, itchmite, scabies, RMSF (rickettsiae)

Front 170

chain of infection

Back 170

causative organism, reservoir, portal of exit, mode of transmission, portal of entry, susceptible host

Front 171

antibiotic

Back 171

chemical produced by one microbe and has ability to harm other microbes

Front 172

antimicrobial drug

Back 172

any agent, natural or synthetic, that has the ability to kill or suppress microorganisms

Front 173

selective toxicity

Back 173

ability of a drug to injure a target cell or target organism without injuring other cells or organism that are in intimate contact with the target

Front 174

what makes antibiotics valuable

Back 174

selective toxicity

Front 175

how do we achieve selective toxicity

Back 175

disruption of bacterial cell wall; inhibition of an enzyme unique to bacteria; disruption of bacterial protein synthesis

Front 176

antibiotics kill bacteria by targeting what?

Back 176

cell wall synthesis; protein synthesis; nucleic acid synthesis; bacterial metabolism

Front 177

antiviral agents kill viruses by

Back 177

blocking viral rna or dna synthesis; blocking viral binding to cells; blocking production of the protein coats (capsids) of new viruses

Front 178

defense mechanisms of pathogens

Back 178

surface coats, viral-antigenic variation (mutation and recombination), parasites

Front 179

how bacteria acquire resistance to antimicrobials

Back 179

develop drug metabolizing enzymes; cease active uptake of the drug; drug receptors undergo changes decreasing the uptake; synthesize compounds that antagonize actions

Front 180

how do antibiotics promote resistance

Back 180

kill non resistant bacteria reducing the competition for resources which allows the resistant ones to flourish; promote overgrowth of normal flora that possess mechanism for resistance

Front 181

what can we do to help prevent antibiotic resistance

Back 181

culture and sensitivity tests; avoid casual use of antibiotics; use more narrow spectrum antibiotics

Front 182

MIC

Back 182

minimum inhibitory concentration; lowest concentration of abx that produces complete inhibition of bacterial growth (does NOT kill bacteria)

Front 183

MBC

Back 183

minimal bacterial concentration; lowest concentration to produce 99.9% decline in # of colonies indicating bacterial kill

Front 184

things we as nurses can do to delay emergence of drug resistance

Back 184

vaccinate, get the catheters out, target the pathogen, access the experts, practice antimicrobial control, use local data, treat infection not contamination, treat infection not colonization, know when to say no to vanco, stop treatment when infection is cured or unlikely, isolate the pathogen, break the chain of contagion

Front 185

things to consider when selecting antibiotics

Back 185

identify organism, drug sensitivity of organism, host factors, allergy, penetration to site of infection, patient variables

Front 186

misuses of antimicrobial drugs

Back 186

untreatable infection, fever of unknown origin, improper dosage, unidentified organism, omission of surgical drainage

Front 187

interfeurons

Back 187

protect against viruses and they also enhance the inflammation process