Test 2

Front 1

delayed hypersensitivity reactions

Back 1

occurs several hours to several days

Front 2

IgE

Back 2

bind to Fc receptors on surface of mast cells

Front 3

IgE+antigen binds>

Back 3

degranulation of mast cells>histamine release

Front 4

anti histamines

Back 4

block release of mast cells and block histamine from binding to target site

Front 5

histamine effects tissue with large amounts of mast cells

Back 5

these area are skin GI and respiratory tract

Front 6

atopic individuals with a genetic predisposition

Back 6

1 parent with allergy=40%

Front 7

Tests for allergies

Back 7

food test, skin tests, lab

Front 8

desensitization

Back 8

small quantity desensitization

Front 9

Tissue specific (Type 2)

Back 9

cell is destroyed by antibodies and compliment

cell destruction through phagocytosis

soluable antigen enters the circulation and deposit on tissues

antibody-dependent cell mediated cytotoxicity

causes target cell malfunction

Front 10

Type 3 ( immune complex mediated)

Back 10

antigen antibody complexes formed in the circulation and deposited in vessel walls or extravascular tissues

causes releases of lysosomal enzymes (non specific) onto the tissue

not organ specific

Front 11

Type 3 immune coplex clearance

Back 11

hh

Front 12

serum sickness

Back 12

immunce complezes formed in blood and deposited in tissue

(fever, rash, pain and enlarged lymph nodes)

Front 13

Raynauds phenomenon

Back 13

complexes precipitates in cold tissues (fingers, toes, nose)

block circulation>pallor, numbness, cyanosis (o2 deprived)>can cause gangrene if circulation not restrored

Front 14

Arthus reaction

Back 14

localized type3 reaction, complexes deposited in local blood vessel walls

reaction begins after 1 hr peak by 6-12 hours

increase vascular permeability, neutrophils, edema, hemorrhage, clotting and tissue damage

ex; celiac disease gluten sensitive enterophath)

allergive alveolitis (inhalation of boldy hay

Front 15

Type 4 hypersensitvity does not involve

Back 15

antibodies

Front 16

ll

Back 16

ll

Front 17

Surface Coats

Back 17

inhibit phagocytosis (Carbohydrate/protein capsules)

have surface receptors to bind

Front 18

antigenic drigt

Back 18

mutations of surface antigen appearance

ex: influenza

allows emergence of new flue virus from year to year

Front 19

Antigeneic shifts

Back 19

recombination of H and N strains from different virus strains

ex worldwide pandemics

Front 20

gene switching

Back 20

multiple genes for antigen turned off/on

ex parasites (african trypanasome)

Front 21

Siderophores

Back 21

iron receptors on bacteria

bacteria must have iron to multiply

Front 22

Factors that contribute to bacterial virulence and infectivity

Back 22

-presence of polysaccharide capsules

-suppression of complement activation

-bacterial proliferation rates can surpass protective responses

-siderophores

Front 23

exotoxins

Back 23

enzymes released during growth causing specific responses

ex: cytotoxins, neurotoxins, ct

Front 24

Endotoxins

Back 24

gram- bacteria

lipopolysaccharides contained in cell walls that are released during lysis

cause hypotension or shock if bacteria is killed off too fast

Front 25

Bacteremia or septicemia

Back 25

presence of bacteria in blood due to defense failure

caused by gram -

toxins released in the blood cause the release of vasoactive peptides and cytokines

decreases bp and o2 delivery> cardiovascular shock

(most commonly caused by bowel ruptures)

Front 26

obligate intracellular parasites

Back 26

nucleic acids protected by layers of protein

very enviornmentally dependent

no metabolism

incapable of independent reproduction

permissive to the host cell

enter through endocytosis, fusion with membrane, or direct membrane crossing

self-limiting infection(spreads cell to cell)

Front 27

Viral Replication

Back 27

single or double stranded DNA or RNA

uncoating ect

Front 28

RNA viruses directly produce what in the cytoplasm?

Back 28

mRNA

Front 29

Phases of viral replication

Back 29

productive phase

latency phase

FINISH

Front 30

cellular effects of viruses

Back 30

inhibition of cell DNA, RNA, or protein synthesis

disruption of lysosomal membrains>cell death (herpes)

Promotion of apoptosis

fusion of infected, adjacent host cells

Front 31

cancer can be caused by

Back 31

transfromation of the host cells into cancerous cells from a virus ex: HPV

Front 32

viruses cause a promotion of secondary bacterial infections t/f

Back 32

true

Front 33

fungus

Back 33

large microorganisms with thick cell walls

ridgid and multilayered walls of polysaccharides

Front 34

can fungal infections resit penicillin

Back 34

yes, their pollysacchraide layer blocks the cell wall inhibiting antibiotics.

Front 35

are there vaccines for fungal infections?

Back 35

no

Front 36

pathogenicity of fungal infections

Back 36

can adapt to a wide range of temp variations, digest keratin, and survive low o2 areas.

suppress the immune defenses

Front 37

How do you diagnose a fungal infection

Back 37

KOH (potassium hydroxide)-enhances visualization

Front 38

mycoses

Back 38

diseases caused by fungi

Front 39

superficial mycoses

Back 39

fungi that invade skin hair or nails are dermatophytes

Front 40

dermatophytes

Back 40

fungi that invade skin hair or nails

Front 41

tineas

Back 41

diseases produced by dermatophytes

Front 42

deep fungal infections

Back 42

impact internal organs

associated with other diseases and opportunistic infections do to immunosuppression

invade through open wounds and inhalation

Front 43

endogenous pyrogens

Back 43

IL-1, TNF-apha

controlled by hypothalamus

fever

Front 44

exogenous pyrogens

Back 44

produces by infectious agents

controlled by hypothalamus

fever

Front 45

attenuated organisms

Back 45

weaked live virus

ex; MMR, Varicella(chix pox)

can cause life threatening illness in immunosuppressed

Front 46

recombinant viral protein countermeasures

Back 46

ex: hepatitis B

vaccine

Front 47

Vaccines

Back 47

induction of long-lasting protective immune responses that will not result in disease in a healthy recipient

boosters to develop sufficient # memory cells, t cells, and antibodies

Front 48

stress

Back 48

demand exceeds a person's coping abilities resulting in disturbances of cognition, emotion, and behavior that adversly affect well-being

Front 49

psychoneuroimmunology

Back 49

study of interaction between the conscious mind, spinal cord, and defense mechanisms of the body against infection and abnormal cell division

Front 50

general adaptation syndrome

Back 50

enlargment of adrenal gland

thymic and lymphoid atrophy

bleeding ulcers

Front 51

3 stages of GAS (general adaptation syndrome)

Back 51

-alarm (arousal of CNS/Fight or flight)

-Resistance or adaptation (mobilization contributes to fight or flight)

-exhaustion( continuous stress breaks down compensary mechanisms and causes the onset of disease)

Front 52

alarm

Back 52

stressor triggers the hypothalamic-pituitary-adrenal axis

Front 53

resistance stage

Back 53

begins with the actions of adrenal hormones (cortisol, epinephrine, and norepinephrine)

Front 54

exhaustion stage

Back 54

occurs only if stress continues

impairment of immune response

Front 55

reactive response

Back 55

heart rate increase and dry mount

physiologic response to physchological stressor

Front 56

anticipatory response

Back 56

physiologic response to anticipated disturbance in state

ie innate fear of predators

Front 57

conditional response

Back 57

situation dependent geers

Front 58

catecholamines

Back 58

leased from chromaffin cells of the adrenal medulla

(20%norepinephrin and 80% epinephrine)

Front 59

a-adrenergic receptors

Back 59

stimulated by epinephrine and norepinephrine

Front 60

b-adrenergic receptors

Back 60

stimulated by epinephrine

Front 61

norepinephrine

Back 61

cause vasoconstruiction, pupil dialation, sweating

Front 62

epinephrine

Back 62

heart rate increases

bronchidiolation

increase in blood glucose

Front 63

cortisol (hyrdrocortisone)

Back 63

activated by adrenocorticotropic hormone

stimulates gluconeogenesis (formation of glucose from fats and amino acids)> increase in blood glucose level

can be anti innflamatory agent

Front 64

glucocorticois and catecholamines

Back 64

decrease cellular immunity while increasing humoral immuninty

inhibits helper t1 cells

stimulates helper t2 cells

called th2 shift

increases acute inflamation

Front 65

b-endoriphins

Back 65

protiens in brain with pain relieving capabilities

Front 66

b- endorphins are released in response to a

Back 66

stressor

Front 67

b-endorphins modulate

Back 67

BP instability in cases of extreme hemorage

Front 68

somatotropin is a

Back 68

growth hormone

Front 69

somatotropin is produced by the

Back 69

anterior pituitary gland

Front 70

somatrotropin affects____while enhancing_____

Back 70

protien, lipid, and carbohydrate metabolism and enhances immune fuction

Front 71

chronic stress decreases the level of what growth hormone

Back 71

somatotropin

Front 72

prolactin is released from the

Back 72

anterior pituitary gland

Front 73

prolactin levels in the plasma increase as a result of what stimuli

Back 73

intense stress

Front 74

oxytocin is produced by what gland during what activities

Back 74

hypothalamus, childbirth and sec

Front 75

testosterone is produced by what cells

Back 75

leydig cells in the testies

Front 76

what does testosterone regulate

Back 76

secondary male sex characteristics and libido

Front 77

testosterone levels decrease due to

Back 77

stress

Front 78

stress is directly related to

Back 78

proinflammatory cytokines

Front 79

examples of disease caused by stress due to proinflammatory cytokines

Back 79

diabetes2, cardiovasucalar disease, COPD, and some cancers

Front 80

stress response decrease

Back 80

natural killer cells and t and b cell function

Front 81

tumor is also called

Back 81

neoplasm (new growth)

Front 82

not all tumors or neoplasms are cancer

Back 82

ie benign tumor

Front 83

benign

Back 83

slow growing, well defined capsule, non invasive, well differentiated, low mitotic index, does not metastize

Front 84

malignant

Back 84

grow rapidly, not encapsulated, invasive, poorly differentiated, high mitotic index, does metasitisis

Front 85

benign tumors are named according to the

Back 85

tissues from which they arise and include the suffix oma

Front 86

malignant tumors are named according to the

Back 86

the tissues from which they arise

Front 87

malignant epithelial tumor

Back 87

carcinoma

Front 88

adenocarcinoma

Back 88

ductual or glandular epithelium

Front 89

sarcomas

Back 89

malignant connective tissue tumors

Front 90

rhabomyosarcoma

Back 90

skeletal muscal malignant tumor

Front 91

lymphomas

Back 91

malignant tumors of the lymphatics

Front 92

hodgkins lymphoma

Back 92

specific lyphoma example

Front 93

malignant blood forming cell tumors

Back 93

lekemias

Front 94

chronic myelogenous leukemia

Back 94

specific malignant blood forming cell tumors

Front 95

carcinoma in situ (CIS)

Back 95

pre-incasive epithelial malignant tumros of glandular or epithelial orgin that have not broken through the basement membrane or invaded the surrounding stroma

Front 96

carcinoma in situ is classified by

Back 96

cellular disorganization, atypia, become mor invasive eventually

Front 97

autonomy

Back 97

cancer cells independence from normal cellular controls

Front 98

anaplasia

Back 98

loss of differentiation, increased nuclear size and pleomorphic (variable in size and shape)

Front 99

stem cells

Back 99

undifferentiated and replicating cells fond in intesinal, epidermal, or bone maroow

Front 100

can stem cells self-renew

Back 100

yes, cell divisions create new cells that will undergo differentiation

Front 101

are stem cells pluripotent

Back 101

yes they can differenciate into mulpe cell tyes

Front 102

tumor cell markers, biologic markers are substances that are produced by cancer cells that are found on the

Back 102

plasma cell membranes in the blood CSF or urine

Front 103

examples of tumor markers

Back 103

epinephrine-adtrenal medulla tumor pheochromocytoma (hormone)

prostate specific antigen(PSA)-antigen

multiple myeloma (antibodies)

enxymes

and genes

Front 104

tumor markers are used to

Back 104

screen high risk patients

diagnose specific types of tumors

Front 105

do non malignant cancers also alter tumor marker levels

Back 105

they can

Front 106

cancer is predominatly a disease of

Back 106

aging

Front 107

clonal proliferation or expanison

Back 107

result of mutation, cell acquires changes that allow it to have selective advantage over its nighbors

(ie increased growth or decrease apoptosis)

Front 108

colon cancer

Back 108

few mutation-small benign polyps

more mutatiosn-large benign/malignant polyps

many mutations-large carcinoma

accumulation of mutations-cancer

Front 109

types of mutated genes-ie secretionf of growth factors that stimulates its grown

Back 109

epidermal growth factor in breast cancer

mutation in ras-stimulates growth even when growth factors are missing

Front 110

inactivation of Rb tumor suppressor gene

Back 110

cell is unresponsibe to antigrowth signals ( ie contact with other cells, basement membrane,soluable factors)

Front 111

activation of protein kinases that drive the cell cycle renders the cell unresponsive to

Back 111

anti growth signals

Front 112

mutation in the p53 gene makesthe cell resistant to

Back 112

apoptosis

Front 113

angiogenesis

Back 113

growth of new vessels due to increase of size (needs more oxygen and nutrients

Front 114

advanced cancers can secrete angiogenic factors vascular endothelial growth factor

Back 114

vegf

Front 115

bevacizumab (avastin) inactivates ____ and is used in ____ treatment

Back 115

VGEF, colon cancer treatment

Front 116

oncogenes

Back 116

mutant genes that in thier normal state regulate protein sythesis and cellular growth

Front 117

tumor suppressor genes

Back 117

encode proteins that in their normal stat negativly regulate proliferation

aka antioncogenes

Front 118

point mutation

Back 118

changes in one or a few nucleotide base pair

ex ras gene mutation concerts it from a regulated pro-oncogen to and unregulated oncogene (accelrating cellular proliferation especially in pancreatic and colorectal cancers)

Front 119

chromosome translocation

Back 119

one piece of the chromosome is transfered to anotehr chromosome causing an inappropriate production of proliferation factor

Front 120

burkitt lymphoma

Back 120

aggressive b cell cancer caued by translocation from chromosome 8 to 14

Front 121

chronic myeloid leukemia

Back 121

uncontrolled growth of myeloid cells due to misregulated tyrosine kinase because of translocation of chromosome 9 to 22

Front 122

gleevec

Back 122

inhibits tyrosine kinase activity

Front 123

chromosome amplification

Back 123

duplication of a small piece of chromosome over and over (ie 10+ copies of the same gene)

results in an increased expression of an oncogene

n-myc oncogene in neuroblastomas

erbB2 in breast cancer

Front 124

N-myc oncogene in nerublastomas and erbB2 epidermal growth factors in breast cancer are examples of

Back 124

chromosome amplification

Front 125

mutation of a tumor-suppressor gene

Back 125

allows unregulated cellular growth

Front 126

retinoblastoma RB gene inhibits cell cycle growth, but when inactivated due to mutation it causes

Back 126

lung breast and bone cancers

Front 127

gene silencing

Back 127

whole regions of chromosomes are shut off

Front 128

DNA can be damaged during

Back 128

dna sythesis, mitosis, external mutagens ect

Front 129

caretaker genes

Back 129

encode for protiens that are involved in repairing damaged cells

Front 130

chromosome instability

Back 130

increased malignant cells

results in chromosome loss, loss of heterozygosity, and chromosome amplification

Front 131

tobacco

Back 131

leading preventable cause of death

Front 132

childhood cancer is the ___leading cause of death in chidren

Back 132

second

Front 133

9500 children under 15 are giadnosed with cancer

Back 133

annually

Front 134

most childhood cancer originates from where

Back 134

the mesodermal germ layer

Front 135

mesodermal layer gives rise to what tissues

Back 135

connective, bone, cartilage, muscle, blood, gonads, kidneys, and lymphatic system

Front 136

most comon childhood cancers are

Back 136

leukemias, sarcomas, and embryonic tumors

Front 137

embryonic tummors originate during

Back 137

uterine life

Front 138

embryonic tummors are typically diagnosed

Back 138

before the age of 5

Front 139

what is embryonic tumor

Back 139

tissue which is unable to mature or differentiate into fully developed cells

Front 140

leukemia

Back 140

most common malignancy in children

Front 141

1/3 childhood cancers

Back 141

leukemia

Front 142

children with downsyndrome are ____% more likely to develop leukemia

Back 142

10-20%

Front 143

sarcoma

Back 143

bone tumor

Front 144

types of bone tumors

Back 144

osteosarcoma and ewings sarcoma

Front 145

nueroblastoma

Back 145

malignant sympathetic nervous system

Front 146

wilms tumor

Back 146

malignancy of the kidneycommonin kids

Front 147

rhabomyosarcoma

Back 147

skeletal boe cancercommon in kids

Front 148

retinoblastoma

Back 148

retina cancer common in kids

Front 149

ecogenetics

Back 149

interaction of genetic and enviornmental factors

Front 150

genetic factors of childhood cancer

Back 150

chromosomal abnormalities ie aneuploidy, amps, deletions, translocation, and fragility

Front 151

franconis anemia

Back 151

oncogenes and tumor suppressor genes

acute myelogenous leukemia

high reoccurrence risk

Front 152

drugs and ionizing radiation

Back 152

diesthylstibestrol (avert early abortions

adenocarcinoma in vag of daughters

Front 153

children are ___ responsive to treatment

Back 153

more

Front 154

children have a reduces risk in developing

Back 154

2nd malignancy

Front 155

residual effects of treating childhood cancer

Back 155

soft tissue and bone atrophy, physical impairments, psychological sequelae, reo problems

Front 156

tobacco causes

Back 156

squamous cell carcinoma and small cell carcinoma of the luncs

is liknks to other typs as well

Front 157

ionizing radiation is a risk factor

Back 157

ie xrays and gamma rays

lekemia thyroid breast lung stomach colon and urinary and other myeloma cancers

Front 158

UV

Back 158

causes basal cell carcinoma. squamous cell carcinoma, and melanoma

Front 159

ultra violet a and ultraviolet b inuce what in the epidermis

Back 159

tnf which reduces immune surveillance of cancer

as well as promotes skin inflammation and the release of free radicals

Front 160

basal cell cancer of the head and neck are common in people of _____complections

Back 160

fair

Front 161

squamous cell cancer

Back 161

common for people who wor outdoors on head neck and upper extremities

Front 162

basal and squamous cell cancers are linked to _____uv exposure

Back 162

cummulative

Front 163

melanoma is related to

Back 163

episodes of intese intermittents uv expsure

Front 164

uv overdose leads to

Back 164

inflammation and cytokine production

Front 165

melanoma is common on the ____of men and ____s of women

Back 165

trunks of men and back of legs in women

Front 166

risks of meanoma are associated with

Back 166

family history, inability to tan, tendency to frecke, moles, and sunburn

Front 167

electromagnetic radiation

Back 167

no ionizing radiation (ie can break off electron

ex microwaves cell phones radar

Front 168

alcohol consumption is a risk factor for _____cancers

Back 168

oral phyarnx hypopharyncy larynx esophagus and liver cancers

Front 169

alcohol and ciggerette combo ______ a persons risk for cancer

Back 169

increases

Front 170

carinogenesis is related to

Back 170

cellular toxicity

oxidative stress from alchol metabolis

alcholoic liver injury

nutrition deficencies

decrease immune resposne

Front 171

hpv 16 causes

Back 171

50-60% of cervical cancer cases

Front 172

hpv 18 causes

Back 172

10-12% of cervical cancer cases

Front 173

hpv 31 and 45 cause

Back 173

4-5% each

Front 174

hpv2 and 11

Back 174

low cancer risk just g warts

Front 175

5yrs+ contraceptive use and 5+ prgnancies smoking and HIV

Back 175

increases cancer risk

Front 176

physical activity decreases

Back 176

cancer risk, insulin, obesity, free radicats

Front 177

physical activity

Back 177

increase gut motility

Front 178

occupational hazards > cancer

Back 178

meothelioma caused by asbestos

radon causes lung ca and small cell carcinomoma

Front 179

xenobiotics

Back 179

toxic mutagenic carinogenic chemicals found in food activated by phase 1 activation enzymes in liver

Front 180

cachexia

Back 180

most severe form of malnutrition associated with cancer

Front 181

acute phase protien response is linked to acceleration of weighloss and is produced in response to

Back 181

altered levels of cytokines, hormones and neuropeptides

Front 182

anemia is associated with cancer and is a

Back 182

decrease of hemoglobin in the blood

Front 183

20% of cancer patiens have concentration of hemoglobin below

Back 183

8g/dL of hemoglobin

Front 184

chemotherapy causes what time of anemia

Back 184

normocytic normochromic anemia

Front 185

methotrexate is what type of anemia

Back 185

abnormal folate metabolism

Front 186

how do you treat anemia

Back 186

erythropietin therapy

Front 187

thrombocytopenia

Back 187

decrease in platelets due to direct tumor invasion

Front 188

leukopenia

Back 188

decrease in white blood cells due to direct tumor invasion

Front 189

paraneoplastic syndrom

Back 189

symptoms that can be ecplaned by the spread of tumor

Front 190

chemotherapy

Back 190

nonselective cytoxic drugs that target metabolic pathways

Front 191

adjuvant chemotherapy

Back 191

chemotherapy following surgica rumor common in treatment of osteosarcomas