HLTH week 1 Flashcards
1
Q
common signs of inflammation
A
redness, swelling, pain, loss of function, heat, and pus
2
Q
cytokines
A
the proteins that controll the activity and growth of immune cells; released during an acute immune response
3
Q
2 stages of acute inflammation reactions
A
vascular and cellular
4
Q
what do disorders associated with inflammation end in?
A
-itis
5
Q
causes of inflammation
A
physical injury, chemicals, ischemia, allergic reactions, extreme temperatures, or forgein bodies
6
Q
bradykinin
A
released from injured cells and activates pain receptors
7
Q
what occurs during the vascular response?
A
vasodialtion and increased capillary permeability
8
Q
what occurs during the cellular response?
A
the movement of cells as a result a chemical stimulus
9
Q
chemotaxis
A
when chemicals released in respond to inflammation cause the movement of cells towards the site of injury
10
Q
what do chemical mediators release during inflammation?
A
histimine, serotonin, prostaglandins, and leukotrines into the interstial fluid and blood
11
Q
where is fever induced from?
A
the hypothalamus as this is the temperature regulator centre
12
Q
what attracts neutrophils to the injury site?
A
platlet aggregation and chemotatic factor released by mast cells
13
Q
examples of cytokines
A
interleukins and lymphokines
14
Q
what do interleukins and lymphokines do?
A
increase plasma proteins, RBC sedimentation rate, induce fever, and cause chemotaxis
15
Q
what besides histimine also causes the vascular response?
A
prostaglandins, bradykinin, and the complement system
16
Q
hyperemia
A
increased blood flow
17
Q
diapedesis
A
aka emigration; movement of cells from the capillaries to the interstital fluid
18
Q
basophils
A
release histimine
19
Q
eosionhils
A
increase during allergic reactions
20
Q
what act as phagocytes?
A
neutrophils and monocytea
21
Q
what is redness caused by?
A
increased blood flow
22
Q
what is swelling caused by?
A
the shift of proteins and WBC’s into the interstital fluid
23
Q
what is pain during inflammation caused by?
A
the pressure of fluid on the nerves
24
Q
what is loss of function during inflammation caused by?
A
cells lacking nutrients
25
what does serous fluid contain?
small amounts of proteins and WBCs
26
exudate
a collection of interstital fluid in the inflammed area
27
systemtic effects of inflammation
mild fever, headache, fatigure, and loss of apetite
28
pyrexia
a low grade or mild fever
29
what do fevers result from?
pyogens which are fever producing substances from WBCs or macrophages
30
what shows up on lab reports during inflammation?
increased WBC count, elevated serum-C reactive protein, higher erythrocyte sedimentation rate, and incresed plasma proteins like fibronigen and prothrombin
31
what are potential complications of inflammation?
local complications at the site of injury such as decreased joint mobility and infection
32
chronic inflammation
may develop following an acute episode or from chronic irritation such as smoking
33
characterisitcs of chronic inflammation
swelling and higher concentrations of lymphocytes, marcophages, and fibroblasts
34
common medications for inflammation
asprin, acetaminophen (tylenol), NSAID, and glucocorticoids
35
how does asprin act of inflammation
by decreasing prostaglandin synthesis at the site of inflammation, reducing pain and inflammatioin as a result
36
side effects of asprin
can cause ulcers and irritation in the stomach, as well as potential blood clotting
37
how does acetaminophen act on inflammation?
it helps with pain and fever but does not actually decrease inflammation
38
how does NSAID act on inflammation?
it helps to reduce the production of prostaglandins, but it especially effective in reducing muscle and skeletal inflammation
39
how do glucocorticods act on inflammation
decrease capillary permeability, block the immune response, and decreases the number of leukocytes
40
side effects of glucocorticods
can effect the natural feedback mechanisms occuring in the adrenal cortex
41
3 types of healing responses
resolution, regeneration, and replacement
42
resolution
the process that occurs when there is minimal tissue damage
43
regeneration
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
44
replacement
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
45
where are cells incapable of mitosis
the brain and the myocardium
46
healing by first intention
occurs when the wound is clean and free of foreign material and necrotic tissue; here the edges of the tissue are held close together
47
healing by second intention
occurs when there is a larger break in the tissue and more inflammation, hence the healing process is longer and scar tissue forms
48
when does the process of tissue repair begin?
when there is a blod clot forming
49
granulation tissue
starts developing about 3-4 days after injury and is a very vasculare, moist, and pink tissue
50
tissue engineering
a new method is which stem cells are used to replace damaged tissues
51
factors promoting healing
youth, good nutrition, adequate hemoglobin, effective ciruclation, and a clean, uneffected wound
52
factors inhibiting healing
advanced age, reduced mitosis, poor nutrition, dehydration, low hemoglobin (anemia), circulatory problems, diabetes or cancer, and prolonged use of glucocorticoids
53
what is a burn?
a thermal or nonthermal (electrical or chemical) injury to the body causing acute inflammation and tissue destruction
54
what occurs after a burn in the body?
an acute inflammatory response which causes the release of chemical mediators, a major fluid shift, edema, and decreased blood volume
55
what are burns classified based on?
the depth and the percentage of body surface area
56
first degree burns
damage the epidermis and the upper dermis; burns are red, painful, and usually don't leave a scar
57
second degree burns
aka partial thickness burn; the epidermis and part of the dermis are damaged; burns are red, blister, often scar, and can be easily infected
58
third degree burns
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
59
general effects of burns
shock, inflammation, damaged respiratory systems, infections, and damaged metabolism
60
shock effects of burns
decreased blood volume and pressure, increased hematocrit, and prolonged shock may lead to kindey failure and damage to other organs
61
hematocrit
% of RBCs in a volume of blood
62
respiratory problems of burns
inhaled hot air may damage brochi and trachea, as inhalation of carbon monoxide is dangerous as it bonds to hemoglobin, taking O2's place
63
how do burns cause infection
bacteria and fungi may invade open areas
64
metabolic needs after a burn
increased intake of protein and carbs
65
how are burns healed?
covering of the sound (nonstick dressings), new skin cultivation, surgery, and sometimes physio and occupational therapy
66
what suffix indicates a tumour?
-oma
67
benign tumours
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
68
malignant tumours
do not appear organised, grow faster than benign tumours, and infiltrate into surrounding organs and tissues
69
what may tumour cells secrete?
enzymes like collagenase which break down proteins or cells and growth factor which promotes angiogenesis
70
angiogenesis
the development of new capillaries in the tumour that promote further tumour development
71
warning signs of cancer
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
72
local effects of cancer
pain may be a sympton but usually not till later on, infection, ischemia, bleeding, obstruction of passagways, and tissue necrosis
73
systemic effects of cancer
weight loss through nutrient trapping of the tumours, fatigue, pneumoniam, and parneoplastic syndromes
74
parneoplastic syndromes
are associated with certain tumours when cells release substances that affect neurological function and blood clotting
75
diagnostic tests for cancer
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
tumour markers
substances, enzymes, antigens, and hormones produced by neoplastic cells; can be used to confirm a diagnosis
77
3 mechanisms for the spread of tumour cells
invasion, metastasis, or seeding
78
tumour invasion
a local spread in which the tumour grows into adjacent tissues
79
tumour metastasis
cells spread to distant sites by blood or lympathic channels; usually will first develop in the lymph nodes, liver, or lungs
80
tumour seeding
the spread of cancer cells in body fluids or among membranes; usually occurs in body cavities; common with ovarian cancer
81
what can chronic inflammation lead to?
rheumatoid arthritis, deep ulcers, or extensive scar tissue
82
carciongenesis
the process in which normal cells develop into cancer cells
83
what is staging?
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
3 factors of staging classification
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
what is carniongeneis a result of?
repeated exposure to a single risk factor (or a combination) that may lead to changes that activate or change gene expression
86
what are risk factors for ovarian carcinogenesis?
oncogenic viruses
87
the 4 stages of carcinogenesis
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
risk factors for carcinogenesis
genetic conditions, radiation, viruses, chemicals, biologic factors, age, diet, and hormones
89
preventative measures for carcinogenesis
avoid certain foods, avoid sun exposure, regular screenings, and a diet high in fibre, antioxidants, and vitamins A and E
90
host defences for carinogenesis
the immune reaction in which cytoloxic T lymphocytes, natural killer cells, and macrophages act as defence
91
two different immune responses
cell-mediated and humoural
92
treatments for cancer
chemotherpay, radiation therapy, surgery, and immunotherapy
93
why is leukaemia often treated with chemotherapy?
because the cells are circulating in the blood
94
how does immunotherapy work?
it stimulates the immune system to attack the cancer
95
two general types of treatment
curative or palliative (extends the life as long as possible)
96
adjuvant therapy
are additional preventative treatments that are used in cancers that spread quickly and are unseen
97
additional non-medical treatments for cancer?
physio, occupational therapy, and speech therapy which support the paitent psychologically
98
radiofrequency ablation
an alternative surgery and is less invasive by using CT's and ultrasound to guide a needle and electrolytes into the timour
99
what is radiofrequency abllation used for?
small tumours in the lungs and liver
100
how does radiation therapy work?
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
how does ionizing radiation work?
by using x-rays ro gamma rays, as well as high energy penetrating particles
102
adverse effects of radiotherapy
bone marrow depression, epithelial cell damage, fatigue and damage to the genitals
103
long term adverse effects of radiotherapy
inflammation, necrosis, and scar tissue
104
how does chemotherapy work?
involves the admistraiton of 2-4 drugs usually in 6 week intervals that fight against rapidly reproducing drugs
105
common chemotherapy drugs
antimiotics, antimetabolites, alklating agents, and antibiotics
106
how do chemotherapy drugs work?
they interfere with protien synthesis and DNA replication at different points in a tumours life
107
adriamycin
an antibiotic that binds DNA and inhibits synthesis of nucleic acids; acts on the S phase
108
bleomycin
an anitbiotic that inhibits DNA synthesis
109
vinblastine
an antibiotic that acts on the M cycle
110
decarbazine
an alkylating agent that acts on several differnt points in the cycle
111
adverse effects of chemotherapy
bone marrow depression, vomitting, hair loss, skin breakdown damaged skin and mucosa, and damaged gonads
112
why does hair loss and breakdown of the skin occur in chemotherapy?
because the epithelial layer is damaged
113
how does gene therapy work?
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
other drug treatments for cancer
prescription of hormones, glucorticods, angiogenesis inhibitors, and biologic response modifiers
115
side effects of cancer related to nutrition
change in taste, vomitting, anorexia, sore mouth, loss of teeth, and malabsorption due to inflammation of the GI tract
116
how to combat nutrition side effects of cancer?
ice mouth rinses, frequent small meals of palatable food, total parenteral nutrition, and antimetic drugs (these increase appetite)
117
total parenteral nutrition
injects a nutrtion mixture into veins
118
skin cancer recovery
ususally high recovery except for melanoma
119
what is skin cancer normally treated with?
surgery
120
most common skin cancer
basal cell carcinoma
121
ovarian cancer recovery
very poor, as symptons aren't obvious until later on and the tumour gets hidden in the periotneal cavity
122
signs of ovarian cancer
pressure on the bladder or intestine and irregular bladder and urinary patterns
123
what are risk factors for ovarian cancer?
hormonal and genetic factors
124
what is an elevated marker in ovarian cancer?
Ca1245
125
where does ovarian cancer often travel to?
the liver, pelvis, and uterus
126
treatment for ovarian cancer
surgery, radiation, and chemotherapy
127
when are brain stems vital
often (even beningn ones); very vital if in the cerebellum or brainstem as these inhibit respiratory functions
128
early signs of a brain tumour
seizures, headaches, drowsiness, vomitting, visual problems, or impaired motor function
129
treatment for brain cancer
surgery, radiation, and chemotherapy
130
allele
a specific version of a gene; ex. brown eyes are an allele
131
heterozygous genotypes
have two different alleles
132
homozygous genotypes
have the same alleles
133
recessive
opposite of dominant
134
phenotype
the observable expression of the genotype
135
genotype
the person's unique sequence of DNA as inherited by two people
136
function of RNA
provides communication links with DNA during actual protien synthesis and helps to maintain the control of cell activity
137
polygenic
more than one allele determines the genotype and thus the phenotype of the individual
138
what can gene mutations occur as a result of?
radion, chemicals, or drugs
139
congenital amomalies
refers to disorders present at birth; defects can be genetic or developmental
140
what can genetic disorders arise from?
a single gene trait or a chromosomal defect
141
what are single-gene disorders caused by?
a change in one gene within the reproductive cells; this is transferred to subsequent generations
142
what do chromosomal anomalies usually result from?
an error during meiosis, specifically when the DNA fragments are lost or displayed
143
developmental defects
can be spontaneous errors or may result from exposure to toxic factors in utero
144
teratogenic agents
those that cause damage during embryonic or fetal development
145
multifactorial disorders
involve genes or genetic influences, combined with environmental factors
146
cystic fibrosis
affects the exocrine glands in the lungs and the pancreas
147
sickle cell disease
ineffective hemoglobin
148
phenylketonuria
occurs when there is a missing metabolic enzyme
149
recessive disorder
both parents must pass on the defective gene to produce a homozygous child
150
recessive disorder for heterozygous children
no clinical signs appear
151
autosomal dominant disorders
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
examples of autosomal dominant disorders
huntington's disease, polycystic kidney disease, and neurofibromatosis
153
X-linked dominant disorders
occurs when an inherited dominant allele is carried on one of the X chromosomes
154
most common X linked dominant disorders
fragile X and this is the common cause of mental retardation, cognitive defects, and learning disorders
155
X-linked recessive disorders
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
examples of X-linked recessive disorders
hemophilia A and duchenne muscular dystrophy
157
tirsomy
when there are three chromosomes rather than 2 in the 21 position; results in down syndrome
158
translocation
a less common form of down syndrome when part of chromosome 21 is attracted to another chromosomes
159
monosomy X
occurs when only one sex chromosome (the X) is present; the individual therefore has only 45 chromosomes
160
common examples of multifactorial disordesr
cleft palate, congenital hip dislocation, congenital heart disease and type 2 diabetes
161
how is the risk for having a down syndrome child caused?
by damage to the oocytes which results from aging factors
162
characteristics of someone with down syndrome
small head, flat face, slanted eyes, open mouth, small hands, delayed development, cognitive impairment, and delayed or incomplete sexual development
163
cerebral palsy
a group of disorders that affect an individual's ability to move in certain ways through damage to motor brain areas
164
areas of the brain affected in cerebral palsy
cerebellum, motor cortex, and the basal ganglia
165
prenatal risk factors for cerebral palsy
genetic mutations and torch infections
166
perinatal risk factors for cerebral palsy
premature birth, O2 deprivation, and torch infections
167
postnatal risk factors for cerebral palsy
infections (bacterial meningitis)
168
developmental disorders risk factors
alcohol, cigarettes, radiation, pharmaceuticals, cocaine, and infections
169
what do developmental risk factors do?
damage the placental barrier and damage the rapidly dividing cells of the embryo and fetus
170
TORCH meaning
toxoplasmosis, other (hepatitis B, mumps, varicella, syphilis, and gonorrhea), robella, cytomegalovirus, and herpes
171
when are diagnostic test for genetic or chromosomal disorders recommended?
women over 35, those with genetic family history, and those will current children who have abnormalities
172
methods for genetic or chromosomal defect testing
ultrasonography, amniocentesis, and triple screen maternal blood tests
173
ultrasonography
can visualize structural anomalies
174
amniocentesis
involves an extraction of amniotic fluid from the uterus
175
benefits of prenatal screening
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
genetic engineering
the practices of manipulating genes in living organisms by changing DNA sequence by rearrangement, deletion, or substitution
177
goal of genetic engineering
to remove a defective gene and supply a normal one
178
gene therapy
involves the introduction of normal genes in living target cells by means of a harmless virus or bacteria
179
when is gene therapy effective?
for single gene disorders like cystic fibrosis, polycystic kidney disease, or huntington's disease
180
proteomic research
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
