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Anatomy and Phyisology > HLTH week 1 > Flashcards

HLTH week 1 Flashcards

1
Q

common signs of inflammation

A

redness, swelling, pain, loss of function, heat, and pus

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2
Q

cytokines

A

the proteins that controll the activity and growth of immune cells; released during an acute immune response

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3
Q

2 stages of acute inflammation reactions

A

vascular and cellular

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4
Q

what do disorders associated with inflammation end in?

A

-itis

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5
Q

causes of inflammation

A

physical injury, chemicals, ischemia, allergic reactions, extreme temperatures, or forgein bodies

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6
Q

bradykinin

A

released from injured cells and activates pain receptors

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7
Q

what occurs during the vascular response?

A

vasodialtion and increased capillary permeability

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8
Q

what occurs during the cellular response?

A

the movement of cells as a result a chemical stimulus

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9
Q

chemotaxis

A

when chemicals released in respond to inflammation cause the movement of cells towards the site of injury

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10
Q

what do chemical mediators release during inflammation?

A

histimine, serotonin, prostaglandins, and leukotrines into the interstial fluid and blood

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11
Q

where is fever induced from?

A

the hypothalamus as this is the temperature regulator centre

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12
Q

what attracts neutrophils to the injury site?

A

platlet aggregation and chemotatic factor released by mast cells

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13
Q

examples of cytokines

A

interleukins and lymphokines

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14
Q

what do interleukins and lymphokines do?

A

increase plasma proteins, RBC sedimentation rate, induce fever, and cause chemotaxis

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15
Q

what besides histimine also causes the vascular response?

A

prostaglandins, bradykinin, and the complement system

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16
Q

hyperemia

A

increased blood flow

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17
Q

diapedesis

A

aka emigration; movement of cells from the capillaries to the interstital fluid

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18
Q

basophils

A

release histimine

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19
Q

eosionhils

A

increase during allergic reactions

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20
Q

what act as phagocytes?

A

neutrophils and monocytea

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21
Q

what is redness caused by?

A

increased blood flow

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22
Q

what is swelling caused by?

A

the shift of proteins and WBC’s into the interstital fluid

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23
Q

what is pain during inflammation caused by?

A

the pressure of fluid on the nerves

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24
Q

what is loss of function during inflammation caused by?

A

cells lacking nutrients

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25
Q

what does serous fluid contain?

A

small amounts of proteins and WBCs

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26
Q

exudate

A

a collection of interstital fluid in the inflammed area

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27
Q

systemtic effects of inflammation

A

mild fever, headache, fatigure, and loss of apetite

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28
Q

pyrexia

A

a low grade or mild fever

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29
Q

what do fevers result from?

A

pyogens which are fever producing substances from WBCs or macrophages

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30
Q

what shows up on lab reports during inflammation?

A

increased WBC count, elevated serum-C reactive protein, higher erythrocyte sedimentation rate, and incresed plasma proteins like fibronigen and prothrombin

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31
Q

what are potential complications of inflammation?

A

local complications at the site of injury such as decreased joint mobility and infection

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32
Q

chronic inflammation

A

may develop following an acute episode or from chronic irritation such as smoking

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33
Q

characterisitcs of chronic inflammation

A

swelling and higher concentrations of lymphocytes, marcophages, and fibroblasts

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34
Q

common medications for inflammation

A

asprin, acetaminophen (tylenol), NSAID, and glucocorticoids

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35
Q

how does asprin act of inflammation

A

by decreasing prostaglandin synthesis at the site of inflammation, reducing pain and inflammatioin as a result

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36
Q

side effects of asprin

A

can cause ulcers and irritation in the stomach, as well as potential blood clotting

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37
Q

how does acetaminophen act on inflammation?

A

it helps with pain and fever but does not actually decrease inflammation

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38
Q

how does NSAID act on inflammation?

A

it helps to reduce the production of prostaglandins, but it especially effective in reducing muscle and skeletal inflammation

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39
Q

how do glucocorticods act on inflammation

A

decrease capillary permeability, block the immune response, and decreases the number of leukocytes

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40
Q

side effects of glucocorticods

A

can effect the natural feedback mechanisms occuring in the adrenal cortex

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41
Q

3 types of healing responses

A

resolution, regeneration, and replacement

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42
Q

resolution

A

the process that occurs when there is minimal tissue damage

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43
Q

regeneration

A

occurs in damaged tissues when the cells are capable of mitosis; the damaged tissue is thus replacedf with idenitical tissue generated by the proliferation of nearby cells

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44
Q

replacement

A

occurs by CT by scar or fibrous tissue formation; this occurs when there is extensive tissue damage and the cells are incapable of mitosis; associated with chronic inflammation

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45
Q

where are cells incapable of mitosis

A

the brain and the myocardium

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46
Q

healing by first intention

A

occurs when the wound is clean and free of foreign material and necrotic tissue; here the edges of the tissue are held close together

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47
Q

healing by second intention

A

occurs when there is a larger break in the tissue and more inflammation, hence the healing process is longer and scar tissue forms

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48
Q

when does the process of tissue repair begin?

A

when there is a blod clot forming

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49
Q

granulation tissue

A

starts developing about 3-4 days after injury and is a very vasculare, moist, and pink tissue

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50
Q

tissue engineering

A

a new method is which stem cells are used to replace damaged tissues

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51
Q

factors promoting healing

A

youth, good nutrition, adequate hemoglobin, effective ciruclation, and a clean, uneffected wound

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52
Q

factors inhibiting healing

A

advanced age, reduced mitosis, poor nutrition, dehydration, low hemoglobin (anemia), circulatory problems, diabetes or cancer, and prolonged use of glucocorticoids

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53
Q

what is a burn?

A

a thermal or nonthermal (electrical or chemical) injury to the body causing acute inflammation and tissue destruction

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54
Q

what occurs after a burn in the body?

A

an acute inflammatory response which causes the release of chemical mediators, a major fluid shift, edema, and decreased blood volume

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55
Q

what are burns classified based on?

A

the depth and the percentage of body surface area

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56
Q

first degree burns

A

damage the epidermis and the upper dermis; burns are red, painful, and usually don’t leave a scar

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57
Q

second degree burns

A

aka partial thickness burn; the epidermis and part of the dermis are damaged; burns are red, blister, often scar, and can be easily infected

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58
Q

third degree burns

A

aka full thickness burn; the whole skin layers are damaged; the burn area may appear charred, the tissue shrinks, it scars, and skin grafts are often used for healing

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59
Q

general effects of burns

A

shock, inflammation, damaged respiratory systems, infections, and damaged metabolism

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60
Q

shock effects of burns

A

decreased blood volume and pressure, increased hematocrit, and prolonged shock may lead to kindey failure and damage to other organs

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61
Q

hematocrit

A

% of RBCs in a volume of blood

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62
Q

respiratory problems of burns

A

inhaled hot air may damage brochi and trachea, as inhalation of carbon monoxide is dangerous as it bonds to hemoglobin, taking O2’s place

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63
Q

how do burns cause infection

A

bacteria and fungi may invade open areas

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64
Q

metabolic needs after a burn

A

increased intake of protein and carbs

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65
Q

how are burns healed?

A

covering of the sound (nonstick dressings), new skin cultivation, surgery, and sometimes physio and occupational therapy

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66
Q

what suffix indicates a tumour?

A

-oma

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67
Q

benign tumours

A

consist of differentiated cells that reproduce at a ghiher than normal rate; does not expand into surronding tissues; not life threatening unless in the brain

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68
Q

malignant tumours

A

do not appear organised, grow faster than benign tumours, and infiltrate into surrounding organs and tissues

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69
Q

what may tumour cells secrete?

A

enzymes like collagenase which break down proteins or cells and growth factor which promotes angiogenesis

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70
Q

angiogenesis

A

the development of new capillaries in the tumour that promote further tumour development

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71
Q

warning signs of cancer

A

unusual bleeding, change in bowel or urinary habits, a change in a wart of mole, a sore that does not heal, unexplained weight loss, anemia, a persistent cough, or a solid lump

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72
Q

local effects of cancer

A

pain may be a sympton but usually not till later on, infection, ischemia, bleeding, obstruction of passagways, and tissue necrosis

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73
Q

systemic effects of cancer

A

weight loss through nutrient trapping of the tumours, fatigue, pneumoniam, and parneoplastic syndromes

74
Q

parneoplastic syndromes

A

are associated with certain tumours when cells release substances that affect neurological function and blood clotting

75
Q

diagnostic tests for cancer

A

self examination, blood tests that look at RBC and hemoglobin count (low in an indicator), tumour markers, X-rays, ultrasounds, CT’s, MRI’s, genomic tumour assesments, and cytologic tests

76
Q

tumour markers

A

substances, enzymes, antigens, and hormones produced by neoplastic cells; can be used to confirm a diagnosis

77
Q

3 mechanisms for the spread of tumour cells

A

invasion, metastasis, or seeding

78
Q

tumour invasion

A

a local spread in which the tumour grows into adjacent tissues

79
Q

tumour metastasis

A

cells spread to distant sites by blood or lympathic channels; usually will first develop in the lymph nodes, liver, or lungs

80
Q

tumour seeding

A

the spread of cancer cells in body fluids or among membranes; usually occurs in body cavities; common with ovarian cancer

81
Q

what can chronic inflammation lead to?

A

rheumatoid arthritis, deep ulcers, or extensive scar tissue

82
Q

carciongenesis

A

the process in which normal cells develop into cancer cells

83
Q

what is staging?

A

a classification process that is applied to a specific malignant tumour at the time of diagnosis; this provides a basis for treatment and prognosis

84
Q

3 factors of staging classification

A

the size of the primary tumour (T), the extent of involvement in the regional lymph nodes (N), and the spread which is invasion or metastatis (M)

85
Q

what is carniongeneis a result of?

A

repeated exposure to a single risk factor (or a combination) that may lead to changes that activate or change gene expression

86
Q

what are risk factors for ovarian carcinogenesis?

A

oncogenic viruses

87
Q

the 4 stages of carcinogenesis

A

intitating factors that cause the first irrevisble DNA changes; epxosure to promoters that cause further changes in DNA (incresed mitosis); continued exposure and changes in DNA that result in a malignant tumour; and changes in the regulation of growth result in cells that are capable of spreading

88
Q

risk factors for carcinogenesis

A

genetic conditions, radiation, viruses, chemicals, biologic factors, age, diet, and hormones

89
Q

preventative measures for carcinogenesis

A

avoid certain foods, avoid sun exposure, regular screenings, and a diet high in fibre, antioxidants, and vitamins A and E

90
Q

host defences for carinogenesis

A

the immune reaction in which cytoloxic T lymphocytes, natural killer cells, and macrophages act as defence

91
Q

two different immune responses

A

cell-mediated and humoural

92
Q

treatments for cancer

A

chemotherpay, radiation therapy, surgery, and immunotherapy

93
Q

why is leukaemia often treated with chemotherapy?

A

because the cells are circulating in the blood

94
Q

how does immunotherapy work?

A

it stimulates the immune system to attack the cancer

95
Q

two general types of treatment

A

curative or palliative (extends the life as long as possible)

96
Q

adjuvant therapy

A

are additional preventative treatments that are used in cancers that spread quickly and are unseen

97
Q

additional non-medical treatments for cancer?

A

physio, occupational therapy, and speech therapy which support the paitent psychologically

98
Q

radiofrequency ablation

A

an alternative surgery and is less invasive by using CT’s and ultrasound to guide a needle and electrolytes into the timour

99
Q

what is radiofrequency abllation used for?

A

small tumours in the lungs and liver

100
Q

how does radiation therapy work?

A

by causing mutations or alterations in the targeted DNA, as a result preventing mitosis or causing intermediate cell death; it also damages the blood supply to tumours

101
Q

how does ionizing radiation work?

A

by using x-rays ro gamma rays, as well as high energy penetrating particles

102
Q

adverse effects of radiotherapy

A

bone marrow depression, epithelial cell damage, fatigue and damage to the genitals

103
Q

long term adverse effects of radiotherapy

A

inflammation, necrosis, and scar tissue

104
Q

how does chemotherapy work?

A

involves the admistraiton of 2-4 drugs usually in 6 week intervals that fight against rapidly reproducing drugs

105
Q

common chemotherapy drugs

A

antimiotics, antimetabolites, alklating agents, and antibiotics

106
Q

how do chemotherapy drugs work?

A

they interfere with protien synthesis and DNA replication at different points in a tumours life

107
Q

adriamycin

A

an antibiotic that binds DNA and inhibits synthesis of nucleic acids; acts on the S phase

108
Q

bleomycin

A

an anitbiotic that inhibits DNA synthesis

109
Q

vinblastine

A

an antibiotic that acts on the M cycle

110
Q

decarbazine

A

an alkylating agent that acts on several differnt points in the cycle

111
Q

adverse effects of chemotherapy

A

bone marrow depression, vomitting, hair loss, skin breakdown damaged skin and mucosa, and damaged gonads

112
Q

why does hair loss and breakdown of the skin occur in chemotherapy?

A

because the epithelial layer is damaged

113
Q

how does gene therapy work?

A

it replaces mutated genes with a healthy copy of the gene, causes an inactivation of the gene and the introduction of a new gene

114
Q

other drug treatments for cancer

A

prescription of hormones, glucorticods, angiogenesis inhibitors, and biologic response modifiers

115
Q

side effects of cancer related to nutrition

A

change in taste, vomitting, anorexia, sore mouth, loss of teeth, and malabsorption due to inflammation of the GI tract

116
Q

how to combat nutrition side effects of cancer?

A

ice mouth rinses, frequent small meals of palatable food, total parenteral nutrition, and antimetic drugs (these increase appetite)

117
Q

total parenteral nutrition

A

injects a nutrtion mixture into veins

118
Q

skin cancer recovery

A

ususally high recovery except for melanoma

119
Q

what is skin cancer normally treated with?

A

surgery

120
Q

most common skin cancer

A

basal cell carcinoma

121
Q

ovarian cancer recovery

A

very poor, as symptons aren’t obvious until later on and the tumour gets hidden in the periotneal cavity

122
Q

signs of ovarian cancer

A

pressure on the bladder or intestine and irregular bladder and urinary patterns

123
Q

what are risk factors for ovarian cancer?

A

hormonal and genetic factors

124
Q

what is an elevated marker in ovarian cancer?

A

Ca1245

125
Q

where does ovarian cancer often travel to?

A

the liver, pelvis, and uterus

126
Q

treatment for ovarian cancer

A

surgery, radiation, and chemotherapy

127
Q

when are brain stems vital

A

often (even beningn ones); very vital if in the cerebellum or brainstem as these inhibit respiratory functions

128
Q

early signs of a brain tumour

A

seizures, headaches, drowsiness, vomitting, visual problems, or impaired motor function

129
Q

treatment for brain cancer

A

surgery, radiation, and chemotherapy

130
Q

allele

A

a specific version of a gene; ex. brown eyes are an allele

131
Q

heterozygous genotypes

A

have two different alleles

132
Q

homozygous genotypes

A

have the same alleles

133
Q

recessive

A

opposite of dominant

134
Q

phenotype

A

the observable expression of the genotype

135
Q

genotype

A

the person’s unique sequence of DNA as inherited by two people

136
Q

function of RNA

A

provides communication links with DNA during actual protien synthesis and helps to maintain the control of cell activity

137
Q

polygenic

A

more than one allele determines the genotype and thus the phenotype of the individual

138
Q

what can gene mutations occur as a result of?

A

radion, chemicals, or drugs

139
Q

congenital amomalies

A

refers to disorders present at birth; defects can be genetic or developmental

140
Q

what can genetic disorders arise from?

A

a single gene trait or a chromosomal defect

141
Q

what are single-gene disorders caused by?

A

a change in one gene within the reproductive cells; this is transferred to subsequent generations

142
Q

what do chromosomal anomalies usually result from?

A

an error during meiosis, specifically when the DNA fragments are lost or displayed

143
Q

developmental defects

A

can be spontaneous errors or may result from exposure to toxic factors in utero

144
Q

teratogenic agents

A

those that cause damage during embryonic or fetal development

145
Q

multifactorial disorders

A

involve genes or genetic influences, combined with environmental factors

146
Q

cystic fibrosis

A

affects the exocrine glands in the lungs and the pancreas

147
Q

sickle cell disease

A

ineffective hemoglobin

148
Q

phenylketonuria

A

occurs when there is a missing metabolic enzyme

149
Q

recessive disorder

A

both parents must pass on the defective gene to produce a homozygous child

150
Q

recessive disorder for heterozygous children

A

no clinical signs appear

151
Q

autosomal dominant disorders

A

the presence of the defect in only one of the alleles produces expression of the disease; 50% chance of passing the disease on to child

152
Q

examples of autosomal dominant disorders

A

huntington’s disease, polycystic kidney disease, and neurofibromatosis

153
Q

X-linked dominant disorders

A

occurs when an inherited dominant allele is carried on one of the X chromosomes

154
Q

most common X linked dominant disorders

A

fragile X and this is the common cause of mental retardation, cognitive defects, and learning disorders

155
Q

X-linked recessive disorders

A

the genes for this are recessive but are manifested in heterozygous males who lack the matching normal gene on the Y chromosome; females are carriers when they are heterozygous

156
Q

examples of X-linked recessive disorders

A

hemophilia A and duchenne muscular dystrophy

157
Q

tirsomy

A

when there are three chromosomes rather than 2 in the 21 position; results in down syndrome

158
Q

translocation

A

a less common form of down syndrome when part of chromosome 21 is attracted to another chromosomes

159
Q

monosomy X

A

occurs when only one sex chromosome (the X) is present; the individual therefore has only 45 chromosomes

160
Q

common examples of multifactorial disordesr

A

cleft palate, congenital hip dislocation, congenital heart disease and type 2 diabetes

161
Q

how is the risk for having a down syndrome child caused?

A

by damage to the oocytes which results from aging factors

162
Q

characteristics of someone with down syndrome

A

small head, flat face, slanted eyes, open mouth, small hands, delayed development, cognitive impairment, and delayed or incomplete sexual development

163
Q

cerebral palsy

A

a group of disorders that affect an individual’s ability to move in certain ways through damage to motor brain areas

164
Q

areas of the brain affected in cerebral palsy

A

cerebellum, motor cortex, and the basal ganglia

165
Q

prenatal risk factors for cerebral palsy

A

genetic mutations and torch infections

166
Q

perinatal risk factors for cerebral palsy

A

premature birth, O2 deprivation, and torch infections

167
Q

postnatal risk factors for cerebral palsy

A

infections (bacterial meningitis)

168
Q

developmental disorders risk factors

A

alcohol, cigarettes, radiation, pharmaceuticals, cocaine, and infections

169
Q

what do developmental risk factors do?

A

damage the placental barrier and damage the rapidly dividing cells of the embryo and fetus

170
Q

TORCH meaning

A

toxoplasmosis, other (hepatitis B, mumps, varicella, syphilis, and gonorrhea), robella, cytomegalovirus, and herpes

171
Q

when are diagnostic test for genetic or chromosomal disorders recommended?

A

women over 35, those with genetic family history, and those will current children who have abnormalities

172
Q

methods for genetic or chromosomal defect testing

A

ultrasonography, amniocentesis, and triple screen maternal blood tests

173
Q

ultrasonography

A

can visualize structural anomalies

174
Q

amniocentesis

A

involves an extraction of amniotic fluid from the uterus

175
Q

benefits of prenatal screening

A

can offer reassurance to families, gives time to provide a plan, gives time to decide on an abortion, and can help with certain disorders common in certain populations

176
Q

genetic engineering

A

the practices of manipulating genes in living organisms by changing DNA sequence by rearrangement, deletion, or substitution

177
Q

goal of genetic engineering

A

to remove a defective gene and supply a normal one

178
Q

gene therapy

A

involves the introduction of normal genes in living target cells by means of a harmless virus or bacteria

179
Q

when is gene therapy effective?

A

for single gene disorders like cystic fibrosis, polycystic kidney disease, or huntington’s disease

180
Q

proteomic research

A

this is research of proteins that are produced when the gene is activated; it strives to characterise all of the proteins that are significant in the metabolic pathway for the expression of a single allele

181
Q
A

Anatomy and Phyisology (71 decks)

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