Exam 1 Flashcards

1
Q

Disease

A

Any disturbance of structure or function of the body

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2
Q

Acute disease

A

quick, not as long (flu, broken leg)

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3
Q

Chronic disease

A

Progressive, has signs and symptoms, not as noticeable as an acute disease

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4
Q

Lesion

A

Characteristic structural changes in organs and tissues as a result of a disease

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5
Q

Structural (organic) disease

A

Associated with structural changes

  • gross examination
  • histologic examination
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6
Q

Functional Disease

A

No morphological abnormalities yet body functions are disturbed

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7
Q

How do you classify diseases?

A

they are either structural or functional

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8
Q

Are all diseases associated with structural or functional abnormality?

A

sometimes we do not know where it falls (depression)

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9
Q

Pathology

A

Study of structural and functional changes in body as a result of disease

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10
Q

Pathologist

A

Physician who specializes in diagnosing and classifying diseases by studying the morphology of cells and tissues

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11
Q

Clinician

A

Physician/health care professional that cares for patients

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12
Q

Pathogenesis

A

How a disease develops

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13
Q

Pathogen

A

Organism causing disease

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14
Q

Etiology

A

Cause of disease

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15
Q

Idiopathic

A

When you do not know the cause of a disease

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16
Q

Symptoms

A

Reported by patient, subjective

- pain

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17
Q

Signs

A

Measurable, objective

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18
Q

Asymptomatic

A

Without symptoms

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19
Q

Syndrome

A

Collection of clinical signs and symptoms

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20
Q

Health and disease is a _____.

A

continuum

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21
Q

Disease vs. Health

A

Presence or absence of a disease

- this does not refer to signs and symptoms

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22
Q

Normal vs. Abnormal

A

Determines whether disease is present by measurements and physical exam

Sometimes sick patients have normal test results

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23
Q

Prognosis

A

Predicted course and outcome of disease

  • chances of completed recovery
  • prediction of permanent loss of function
  • probability of survival
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24
Q

Terminal

A

Diseases that end in death

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25
Remission
When signs and symptoms subside; does not mean disease is gone
26
Exacerbation
Increase in the severity of signs and symptoms
27
Relapse
Disease returns after its apparent cessation
28
Complication
An abnormal state that develops in a person already suffering from a disease
29
Impacts that diseases have on a population
Prevalence - number of total cases at a given time Incidence - number of new cases at a given time Mortality - death Morbidity - how bad it makes you feel Epidemiology - the study of the occurrence, transmission, distribution, and control of disease
30
Classifications of disease
1. Vascular - heart disease 2. infectious (inflammatory) - flu, pneumonia, pink eye 3. Neoplastic - cancer 4. Degenerative (deficiency) - osteoarthritis 5. Idiopathic 6. Congenital - born with it 7. Allergic (autoimmune) - type 1 diabetes 8. Traumatic 9. Endocrine - type 1 diabetes 10. Metabolic - type 2 diabetes
31
Predisposing
Risk factors; NOT CAUSALITY
32
Predisposing factors of disease example
genetics, ages, gender, environment, lifestyle
33
Diagnosis
The use of scientific or clinical methods to determine nature and cause of disease
34
Factors utilized for diagnosis
Clinical history and the physical examination
35
Clinical history
A. Chief complaint B. History of current illness C. Past medical history (family health history & psychosocial sexual history) D. Signs and symptoms
36
What are diagnostic tests utilized for?
- diagnosing disease - monitoring treatment - screening - assessment of risk - prognosis - detection of complications
37
Accuracy
Are the results of the tests an indication of whats being measured?
38
Precision
Ability of test to provide the same result every time it is used.
39
Sensitivity
Ability of test to be positive in the presence of disease - 99% sensitivity = positive that 99 out of 100 people have disease - person has disease and test says they have disease
40
Specificity
Ability of a test to be negative in the absence of disease. - person does not have disease and test says they don't have disease
41
Evaluation of diagnostic tests
``` accuracy precision sensitivity specificity risk/benefit/cost ratio ```
42
Screening tests for disease: Purpose
1. Detection for disease - detect early asymptomatic diseases that can be treated to prevent or minimize late-stage organ damage 2. Screening for some genetic diseases - to screen for carriers of some genetic diseases transmitted from parent - allows affected persons to make decisions on future childbearing or management of current pregnancy
43
To be a successful screening test:
1. Suitable groups for screening 2. Suitable screening tests 3. Benefits of screening 4. Screening for genetic disease
44
False positive
When person doesn't have disease but test said they may have it
45
False negative
When person has disease but the test said they did not
46
Classification of diagnostic tests and procedures
1. Clinical laboratory tests - blood/urine 2. Imaging techniques - x-ray - computed tomography (CT) - magnetic resonance imaging (MRI) - ultrasound - positron emission tomography (PET) 3. Cytologic/Histologic examinations 4. Tests of electrical activity 5. Endoscopy/Laparoscopy
47
Clinical laboratory tests
Provides and interprets diagnostic testing related to patient care - 60-70% of diagnosis relies on clinical tests
48
Qualitative
Describe quality, either positive or negative (either there or not there)
49
Quantitative
tests that have numerical results
50
Radiology =
imaging
51
types of radiology
1. X-Ray - differing absorption properties of tissues ex. mammogram 2. Computed Tomography (CT) - 3D xray - good for imaging of internal organs - cons: high dose radiation
52
Types of radiologic procedures
1. Magnetic Resonance Imaging (MRI) - uses movement of hydrogen atoms to generate image - pros: does not use xrays, sensitive - con: stay till for long time, tight space, loud sound 2. Ultrasound - uses sound waves to view soft tissue structures; no radiation 3. Positron Emission Tomography (PET) - radioactive material is injected into patient and then the patient is scanned to determine where the material has settled
53
Diagnostic procedures
1. Endoscopy - non-surgical technique examining interior of body with flexible tube with light 2. Laparoscopy - surgical technique to examine structures within peritoneal cavity - small incision made in abdominal wall; often naval *both use flexible tube with light
54
Cytologic and histologic exams: techniques
1. Biopsy (take tissue out) 2. Fine Needle Aspiration (stick in needle and suck cells out) 3. Collection of cells (ex. pap smear)
55
Palliative
Treatments designed to relieve and manage symptoms | ex. hospis
56
Organization of human body
Atoms, cells, tissues, organs, organ systems, organism
57
all cells ultimately come from
stem cells
58
Stem cells
ability to become various types of cells 1. Totipotent = can become any cell in body as well as whole organism/cell of placenta 2. Pluripotent = any cell, but cannot become organism/cell of placenta 3. Multipotent = limited type of cell
59
Types of stem cells
Embryonic stem cell = pluripotent | Adult stem cell = progenitor cells
60
Progenitor cells
cells that can generate specialized cell; they are multipotent
61
All tissues originate from
all tissues originate from germ layers of inner cell mass of blastocyst
62
What are the 3 layers of the inner cell mass of the blastocyst
1. Ectoderm (outside) - nervous tissue, skin 2. Mesoderm (middle) - muscle 3. Endoderm (inner) - inner tracts (GI tract)
63
Atrophy
shrinkage, decrease in cell size due to... A. physiological (aging) B. pathological (decreased blood supply, nutrition, lack or neural or hormone support)
64
Hypertrophy
Increase in cell size due to... A. hormonal stimulation B. increased functional demand
65
Hypertrophy results in...
increased protein synthesis within cell and decreased protein breakdown
66
Hyperplasia
Increase in cell number due to... A. hormonal stimulation B. increased functional demand C, Chronic stress
67
Hyperplasia results in...
increased cell division if the cell can divide
68
Metaplasia
replacement of one cell type with another - most common in epithelium - reversible is the stress is removed
69
Dysplasia
change in cell resulting in abnormal cell size, shape, or organization - more severe than metaplasia - premaligant
70
Free radicals
atom or molecule with unpaired electron
71
Cell injury: morphological changes
1. Steatosis: fat 2. Cell Swelling: cause is a lot of ATP, failure of Na/K pump --> sodium remains in cells..water follows and makes it swell
72
What is the exchange for the Na/K pump
3 Na out | 2 K in
73
Cell death: Apoptosis
Programmed cell death or cell suicide - removes cells that are worn out - cell shrinks in on self - removes unwanted tissue - normal process/pathological
74
Apoptosis may be due to...
- signaling factor attached to "death domains" of cell surface receptors - mitochondrial damage inside of cell - DNA damage
75
What is the main organelle that initiates Apoptosis
mitochondria
76
Cell death: Necrosis
Unregulated death - "sledgehammer" | - cells swell and rupture and they damage nearby cells and inflammation is a result
77
outcomes of cell injury
reversible, adaptation (may be permanent), death of cell
78
is aging programmed into cells?
we do not know
79
is aging the result of accumulated damage
- older cells have more DNA damage - older cells have more free radicals - cells can lose their ability to repair their telomeres
80
Telomores
endcaps of chromosomes
81
Programmed Death-Telomeres
telomeres become too short; cell can no longer divide
82
Cellular aging indicators
Atrophy, decreased function and loss of cells
83
Tissue and systematic aging
progressive stiffness and rigidity (bone loss, less elastic CT)
84
Frailty
common clinical syndrome in older adults indicated functional decline, disability, disease and death
85
genotype
genetic info contain in DNA
86
phenotype
outward exp. of DNA (hair color, eye color)
87
Explain chromosomes
chromosomes exist in pairs, one derived from the male parent and one form the female parent; 46 total, 23 pairs
88
Types of chromosomes
1. Autosomes: 22 pairs in humans, similar in size, shape and appearance; homologous (1 mom, 1 dad) 2. Sex chromosomes - genetic male = XY - genetic female - XX
89
Gene
Fundamental unit of heredity
90
what is the functional product of gene
protein or RNA
91
how many genes in human genome
20,000; they can be dominant or recessive genes
92
Genes exist in ....
genes exist in pairs or alleles, one on each chromosome
93
Homozygous
both alleles are the same
94
Heterozygous
alleles are different
95
Genome
Sum total of all genes in a cell's chromosomes
96
Human genome project
international collaboration of scientists that mapped nucleotide sequence of the entire human genome by determining the specific locations of individual genes
97
Genomics
study of gene structure to correlate gene structure with gene expression in individuals
98
Inheritance of genes of represented by ___.
Pedigree (it looks at genes inherited by offspring)
99
X-Chromosome Inactivation (Lyon Hypothesis)
Females = XX Males = XY - potential dosage problem - Thus, one X chromosome is inactivated in all somatic cells, equalizing expression of X-linked genes * *random --> paternal or maternal - becomes barr body - inactivation occurs early in embryonic life
100
Karotype
Studies the composition and abnormalities in chromosomes in terms of number and structure
101
To get a karotype...
cells must be stopped in metaphase
102
Chromosome smear
a layout of all 46 pairs of chromosomes
103
Genetic code
info carried by DNA
104
nucleotide
``` structural unit of DNA Bases: a. Purines (adenine, guanine) b. pyrimidines (thymine, cytosine) *complementary base pairing* ```
105
DNA replication: semiconservative
One strand of DNA is kept, and makes a new strand with complementary base pairing
106
bases of DNA are held by _____.
H+ bonds
107
Translation of DNA to proteins: Protein synthesis steps
1. Transcription - in nucleus - unwinding of DNA, compl. base pairing to form mRNA - form mRNA (AU, GC) - exclusion of introns - mature mMRA leaves nucleus and goes to cytosol where it joins up with ribosome for translation 2. Translation - cytosol - formation of protein - need rRNA and tRNA
108
if you see a "u" in complementary base paring, what does that tell you?
it tells you it is an RNA
109
MicroRNA (miRNA)
regulate gene expression; acts post-transcriptionally, a type of noncoding DNA
110
miRNA interacts with
miRNA interacts with mRNA and inhibits translation of mRNA **implicated in many diseases
111
mitochondrial genes and inheritance
mitochondria contain own DNA (mtDNA), mitochondria inheritance is from the mother - hereditary diseases resulting from mitochondrial DNA mutations heterogeneous (ATP synthesis)
112
not all mature cells are able to divide such as
cardiac, skeletal muscle, nerve cells
113
Mitosis
Somatic cells only - somatic cells onlyq - each somatic cells contains 46 chromosomes (1-22 auto.) - no reduction in DNA - each of 2 new daughter cells receives identical DNA as in the parent cell
114
Meiosis
Germ cells only - intermixing of genetic material between homologous chromosomes - DNA reduced by half
115
What are the 2 separate divisions of meiosis
Meiosis 1: reduces number of chromosomes by half - daughter cells receive half of chromosomes by each parent cell - chromosomes are not exact duplicates of those in parent cell Meiosis 2: similar to mitosis, but each cell contains only 23 chromosomes
116
Gametogenesis
process of forming gametes (egg and sperm) | - takes place in gonads (ovaries, testes)
117
Gametogenesis: types
Spermatogenesis: making of sperm Oogenesis: making of eggs *both have similarities and differences
118
Spermatogenesis
4 spermatozoa formed from each germ cell | - Spermatogenesis occurs continually once male begins puberty
119
Oogenesis
1 ovum formed from each precursor cell discarded as polar bodies - oocytes not produced continually (form in utero) - Oogenesis discontinues - 1 egg/month
120
Single nucleotide polymorphisms (SNPS)
Structural variations in single gene nucleotide of different individuals - 10 mil. SNPS in human genome *basically, a change in one nucleotide*
121
Single nucleotide polymorphisms (SNPS) affect gene functions resulting in individual differences in body functions such as:
a. How rapidly cell inactivates drug or environmental toxin or repairs DNA damage b. variations in responses to food, antibiotics, or drugs c. ability to detoxify potential carcinogens or susceptibility to cancers
122
Epigenetics
refers to all heritable changes in gene expression and chromatin organization that are independent of the DNA sequence itself - normal regulation in human development and cellular differentiation - can switch genes on or off
123
DNA = ___, Epigenetics = ____
hardware, software
124
Epigenetics mechanism: DNA methylation
Adds methyl group to DNA on cytosine nucleotide located next to a guanine nucleotide (CpG cite) - methylation leads to gene silencing - when you methylate gene is decreases transcription
125
Gene imprinting
For some traits, expression of the phenotype depends on whether the allele is inherited from the mom or dad - gene is maternally imprinted, the copy of the imprinted gene from mother is always turned off - reversible - may be a problem if mutation on gene is not imprinted
126
How many genes are thought to be imprinted?
only 60-100 genes
127
Imprinting is a specific example of what?
methylation
128
X-Inactivation turns off entire chromosomes, while imprinting...
turns off specific genes
129
Gene therapy
delivery of therapeutic gene into a patients target cell; functional proteins are created returning cell to normal
130
Congenital
Abnormality present at birth, even though it may not be detected until some time after birth
131
Congenital malformation
intrinsic defect in development of baby; genetic, environment or both *abnormal all the way through birth
132
Congenital deformation
abnormal external force, often occurs due to intrauterine pressures; common in twins because the womb is crowded
133
Congenital disruption
secondary destruction in tissue that was previously normal; starts normal, something goes wrong
134
hereditary or genetic disease
resulting from a chromosome abnormality or a defective gene
135
Hereditary and congenital malformations: causes
- chromosomal abnormalities - abnormalities of individual gene - intrauterine injury to embryo of fetus - environmental factors
136
What percent of all newborn infants have congenital diseases?
2-3%
137
Causes of intrauterine injury
1. Teratogens 2. Radiation 3. Maternal infections
138
Teratogens
harmful drugs and chemicals; drugs rated A, B, C, D, X by FDA
139
3rd - 8th week after conception...
embryo is most vulnerable to injury as organ systems are forming
140
what does TORCH stand for?
``` Toxoplasma = parasite Other Rubella = virus Cytomegalovirus Herpes Simplex Virus ```
141
fetal alcohol syndrome
1: 1000 births; mom consumes alcohol (how much determines the severity - fetal growth restriction, CSN abnormalities, distinctive facial features
142
Genetic disorder
disease caused by abnormalities in DNA
143
Genetic disorder: monogenetic
single-gene disorders (small scale)
144
Genetic disorder: chromosome disorders
large scale
145
Genetic disorder: multi-factorial disorders
multiple genetic alterations and environment
146
Genetic disorder: mitochondrial disorders
mitochondria has own DNA
147
Genetic disorder: germline
passed to offspring
148
Genetic disorder: somatic
cant be passed to offspring
149
chromosome abnormalities
- leading cause of genetic diseases, mental retardation, and pregnancy loss
150
types of chromosome changes
aneuploidy (abnormal #), deletions (part of chromosome has been deleted eps. around tip), translocations (no loss of DNA but wrong place)
151
Aneuploidy
Loss of gain of one or more chromosome; commonly results from non-disjunction during meiosis *more common than changes in chromosome structure
152
Monosomy
2n-1 condition (45 chromosomes) | - monosomy involving autosomes may have severe phenotypic effects in animals
153
Non-disjunction
chromosomes don't pull apart correctly, typically in meiosis
154
Trisomy
2n+1 condition (47 chromosomes) - somewhat less severe than monosomy when involves autosomes ex. trisomy 21/18
155
Down Syndrome
Discovered in 1866 by John Langdon Down - now known to result from trisomy 21 (47, XY, +21) - most common chromosome abnormality - single most common cause of genetic intellectual impairment
156
Clinical features of Down Syndrome
- intellectual impairment - slanted eyes - congenital heart disease - intestinal defects - abnormal creases in palms
157
Down Syndrome causes
95% due to non-disjunction in meiosis 1 - non-inherited - ovum is source of extra 21 in 95% of cases
158
main risk for down syndrome?
maternal age --> older person, older eggs, more fragile, suspended in time
159
Translocation down syndrome
Familial down syndrome = about 5% of DS results from a translocation between chromosomes 21 and 14 - normal chromosomes in parent - translocation occurred during gametogenesis in one parent
160
Sex chromosome abnormalities: Extra Y
no significant effect because it mainly carries genes concerned with male sexual differentiation
161
Sex chromosome abnormalities: absent Y
body configuration is female
162
Sex chromosome abnormalities: extra X in the female
little effect because one of the X chromosomes is inactivated
163
Sex chromosome abnormalities: extra X in male
has adverse effect on male development
164
turner syndrome
(45, X) --> instead of XX she just has X - 1 in 2500 newborn girls, more common in miscarriages - short stature, failure to develop secondary sex characteristics, mal-developed ovaries, webbing
165
Klinefelter Syndrome
(47, XXY) - increased incidence with maternal age - 1:750 male births - delayed speech and lang. development - learning difficulties - tall - long arms and legs - hypogonadism - sterile - gynecomastia (breast dev.)
166
Triple X (47, XXX)
1: 1000 females | - benign characteristics because extra X chromosome is inactivated
167
Jacobs syndrome
47, XYY - only through male disjunction - taller than avg. - delayed dev. speech and language skills - fertile
168
Genetically transmitted diseases
- Result from abnormalities of individual genes on the chromosomes - Chromosomes appear normal
169
Genetically transmitted diseases causes
- spontaneously (wrong base inserted) - environmental teratogen - inherited
170
Genetically transmitted diseases: Transmission on autosomes
most hereditary diseases are transmitted on autosomes; can occur in... - autosomal dominant/recessive inheritance - X linked inheritance (some are carried on sex chromosomes)
171
autosomal dominant inheritance
Gene is expressed is only one copy of mutation is present - one allele is dominant - an affected person has 50% chance of passing it onto child - if neither parent has trait, none of the children have it
172
autosomal recessive inheritance
- Need 2 copies of defective gene | - Parents of affected are usually heterozygous carriers
173
Sex-linked inheritance
1. X chromosome large - 2% of nuclear genome - X chromosome contains more genes than Y chromosome 2. Y chromosome small - few dozen genes
174
multifactorial inheritance
- Combined effect of multiple genes interacting with environmental agents (diabetes, heart disease, hypertension) - congenital abnormalities (cleft lip/palate, clubfoot)
175
Amniocentesis
Fetal cells are collected. - detects about 1,000 of the more than 5,000 known chromosomal and biochemical problems - ultrasound is used to follow needle's movement
176
Amniocentesis risks
pregnancy loss 1 in 1,600
177
Chronic Villi sampling (CVS)
Fetal cells collected - performed during 10-12th week of pregnancy - earlier results than amniocentesis - less accurate than amniocentesis - greater risk of pregnancy loss (1%)
178
ultrasound examinations
Detection of major structural abnormalities - major structural abnormalities of nervous system - hydrocephalus - obstruction of urinary tract - failure of kidneys to dev - failure of limbs to form normally
179
The inflammatory reaction
A non-specific response to any agent that causes cell injury
180
The inflammatory reaction is part of what immune system
innate immune system
181
The inflammatory reaction protects against
physical (heat or cold) chemical (concentrated acid) microbiologic (bacterium or virus)
182
inflammation is a response to cell injury that
- neutralizes harmful agents | - removes dead tissue
183
inflammation is a combined response meaning...
- local blood vessels - WBC - plasma proteins - surrounding tissue - systemic effects (fever)
184
Cardinal signs of inflammation
1. Heat (dilated blood vessels) 2. Redness (dilated blood vessels) 3. Swelling (accumulation of fluid and exudate due to extravasation of plasma) 4. Tenderness and pain (irritation of nerve endings)
185
Stages of acute inflammation
1. Vascular stage 2. movement of WBC into tissue 3. Elimination of pathogen 4. repair
186
Explain vascular state of acute inflammation
Brief vasoconstriction, followed by vasodilation | - alterations in endothelial cells --> more permeable
187
hypermia =
vasodilation
188
Edema
accumulation of fluid in interstitial space
189
Exudate
fluid mixture of protein, leukocytes, and tissue debris that results from inflammation
190
Serous exudate
primarily fluid, little protein
191
purulent exudate
largely inflammatory cells (pus)
192
Fibrinous exudate
rich in fibrinogen; coagulates and forms fibrin; produces a sticky film on surface on inflamed tissue Can inform adhesions: bands of fibrous tissue that bind adjacent tissue together
193
hemorrhagic
Increased red blood cells due to capillary injury
194
Cellular reaction follows vascular reactions
Leukocytes enter injured areas (neutrophils/macrophages) STEPS: 1. margination 2. Emigration/diapedesis 3. chemotaxis 4. phagocytosis
195
how do the phagocytes know where to go?
cytokines released by bacteria and macrophages which bring neutrophils to the site
196
phagocytosis
Type of endocytosis - "cell eating" - neutrophils (die by apoptosis after) - macrophages (do not die after)
197
role of lysosomal enzymes
digest bacteria
198
chemical agents that intensify the inflammation process
1. Cell-derived mediators a. mast cells 2. mediators from blood plasma a. bradykinin b. complement
199
Mast cells
(WBC) specialized immune cells found in CT; filled with granules with vasoactive amines - histamine (a vasodilator) - prostaglandins (synthesized from arachidonic acid) - leukotrienes (synthesized from arachidonic acid) - serotonin
200
Complement
activation by antigen-antibody reaction; series of proteins that interact in a regular sequence
201
Arachidonic acid
a long chain fatty acid that acts as a hormone. it results in... 1. Prostaglandins (increase vascular permeability) 2. Leukotrienes (smooth muscle contractions, vascular permeability)
202
Mast cells make what
long chain fatty acids that come from Arachidonic acid
203
The Kinin System
Functions to activate and assist inflammatory cells. | - causes vascular permeability and pain
204
What is the primary kinin
bradykinin
205
The complement system
activates or collaborates with other component of the inflammatory response (chemotaxis, phagocytosis, cell lysis)
206
Chemotaxis, phagocytosis, cell lysis
chemotaxis - neutrophils coming to site phagocytosis - cell eating cell lysis - complement itself can result in lysis of bacteria
207
Leukocytosis
increase WBC count (neutrophils)
208
acute phase proteins
Proteins made by liver, help mediate inflammation to return body to homeostasis ex. c-reactive protein (CRP) - help w phagocytosis
209
infection
inflammatory process caused by disease-producing organisms
210
"-itis"
suffix indicates an infection or inflammatory process such as appendicitis, hepatitis, colitis
211
Cellulitis
acute spreading infection of skin and deeper tissues
212
Abscess
formation of pus
213
Septicemia
infection of pathogenic bacteria in blood
214
pathogenic
Ability to cause disease
215
virulence
degree of damage caused by a pathogen to the host
216
host
affected ind. or animal
217
factors influencing the outcome of disease
virulence of organism, numbers of invading organisms, host resistance
218
Chronic infection/inflammation
state in which the pathogenic organism and the host are evenly matched; associated with repeated attempts of the body at healing
219
Predominant cells in chronic infection/inflammation
lymphocytes (t&b cells), macrophages
220
Inflammation ends with _____.
Repair
221
explain the repair stage of the end of inflammation
Tissue can regenerate or repair; outcome depends on type of cells forming tissue (continuously dividing cells, non-dividing cells)
222
Regenerate
nearly complete restoration
223
repair
scar formation
224
Wound healing: stages
1. inflammation 2. Proliferation - granulation tissue stage - new capillaries - fibroblasts to area - epithelialization 3. Remodeling - maturation and reorganization - reorganization of collagen - may take years
225
Determinants of wound healing
1. Infection (will keep wound healing in stage 1) 2. Poor nutrition (protein bc collagen, vit. C. bc collagen synthesis) 3. age 4. steroid drugs 5. diabetes (lack of new capillary growth...delayed)
226
Classifications of immune system
1. Innate a. older b. faster c. nonspecific 2. Adaptive (aquired) immunity a. humoral / cell mediated (types) b. newer c. slower (7-10 days) d. specific f. memory
227
Leukocytes parts of innate immunity
macrophages, dendritic cells, polymorphonuclear granulocytes (PMNs)
228
Leukocytes parts of adaptive immunity
lymphocytes - t and b cells
229
CD
cluster of differentiation - CD4+ (helper T cells) - CD8+ (cytotoxic T cells)
230
how can we distinguish leukocytes
we look at the CD
231
Innate immunity
Always present - attacks non-self microbes - does not distinguish between different microbes (nonspecific)
232
Components of innate immunity
1. epithelial barriers (skin, tear, saliva, secretions) 2. phagocytic cells (neutrophils, macrophages, dendritic cells) 3. plasma proteins (complement) 4. cell messenger molecules (cytokines)
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Cytokines
general term for chemical messengers involved in the immune process
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Polymorphonuclear cells include...
A. neutrophils (most numerous, phagocytosis) B. basophils (allergic response) C. eosinophils (parasitic infection)
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Monocytes
found in blood, immature macrophages
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Macrphages
found in tissue, mature monocytes
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Cells of the innate immune system
1. Polymorphonuclear cells - neutrophils - basophils - eosinophils 2. Monocytes/Macrphages 3. Natural Killer Cells
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adaptive/acquired immunity
- takes long time to respond, specificity, memory
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adaptive/acquired immunity components
1. Humoral immunity (mediated by B cells) | 2. Cell-mediated immunity (mediated by T cells)
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adaptive/acquired immunity : Mounting a response
Recognition --> specific receptor Activation --> resting to active Attack
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Humoral immunity
Mediated by B lymphocytes | --> B lymphocytes make antibodies such as plasma
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How do antibodies work?
neutralization, mobilize other components of immune system
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Cellular immune system
Mediated by T lymphocytes - -> these are the main defense against viruses, fungi, parasites, and some bacteria - -> mechanism by which body rejects transplant organs - -> eliminates cancer cells
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Types of lymphocytes
helper T cells Cytotoxic T cells Suppressor T cells
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Cell mediated immunity
Antigen must first be "processed" and displayed on the cell membrane of the antigen presenting cell (APC) before activating T cells.
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Antigen presentation is done by...
APC - Macrophages - Dendritic cells - B cells
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Major Histocompatibility Complex (MHC) role
MCH present processed antigen to responding cells of the immune system; encoded by HLA genes
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MCH class restriction
MHC Class I: - present on all nucleated cells - restricted to cytotoxic T cells (CD8+) MHC Class II: - only on APC - restricted to Helper T cells (CD4+)
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hypersensitivity
too much
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immunodeficiency
too little
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autoimmune disease
innapropriate
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malignancy
cancer
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Hypersensitivity reaction types
``` Type 1, 2 & 3 (mediated by B cell reactions) Type 4 (mediated by T cell reactions) ```
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Type 1 hypersensitivity
- Immediate hypersensitivity | - Preformed antibodies (person has already encountered antigen)
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Cells involved in Type 1 hypersensitivity
Mast cells and basophils
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Type 1 hypersensitivity: Mast cells
1. Reside in tissue 2. Full of granules - degranulation - effect of granules when releases is vasodilation, increased capillary permeability, & accumulation of edema 3. May be local or systemic
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Allergic disease
Type 1 hypersensitivity to environmental substance (allergens); AKA atopy
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Most common allergen?
hay fever, urticaria (hives), atopic dermatitis (eczema), systemic anaphylaxis
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Anaphylaxis
TYPE 1 HYPERSENSITIVITY - sensitizing antigen circulates throughout the body, triggers widespread mediator release from Ig-coated mast cells and basophils
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Systemic effects of anaphylaxis
Sever decrease in BP - Bronchoconstriction = severe respiratory distress - Prompt treatment required with epinephrine
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Hygiene hypothesis
Prevalence of allergies increasing in the US - "westernized countries" have less exposure to different microbes because it is very sanitized living, which can lead to a weak immune system
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Cytotoxic hypersensitivity
TYPE 2 HYPERSENSITIVITY - antibody directly attached to antigen in target tissue (target host cell rather than foreign antigen - IgG antibody
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Type 2 hypersensitivity: 2 types
1. Death of target cell a. killed by other components of immune system 2. Antibodies block receptor function a. myasthenia (autoimmune disease)
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Immune complex hypersensitivity Type 3 hypersensitivity
TYPE 3 HYPERSENSITIVITY - antigen and antibody combine to form immune complex - deposition-induced inflammatory response (BV, kidneys, joints)
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What are some words you can remember to know the difference between each type of hypersensitivity?
Type 1: immediate hypersensitivity, atopy, anaphylaxis Type 2: Cytotoxic hypersensitivity, death of target cell, antibodies block receptor function Type 3: Immune complex hypersensitivity Type 4: Delayed hypersensitivity
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Delayed hypersensitivity
TYPE 4 HYPERSENSITIVITY - T lymphocytes are sensitized and activated on second contact with same antigen - Cytokines from T cells activate macrophages
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Type 4 hypersensitivity steps
1. Antigen uptake, presentation by APC 2. Presentation to Helper T cells 3. Memory T cells migrate to site 4. Second exposure = release mediators, attract other cells such as macrophages
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Poison Ivy, metallic jewelry, celiac disease, TB test
Type 4 hypersensitivity - delayed
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Autoimmune disease
Self become foreign - systemic lupus erythematosus - rheumatoid arthritis - myasthenia gravis - type 1 diabetes - multiple sclerosis
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What hypersensitivity types are mechanisms of autoimmune diseases?
type 2, 3, and 4
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Autoimmune disease: Pathogenesis
1. Alterations of patients own antigens, causing them to become antigenic, provoking an immune reaction 2. Formation of cross-reacting antibodies against foreign antigens that also attack patients own antigens 3. Defective regulation of the immune response by less regulator T lymphocytes
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Factors which predispose autoimmune disease
1. gender (W 3x more likely) 2. Genetic (certain HLA types) 3. Infection (induction by microbes)
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Systemic Lupus Erythematosus (SLE) "Lupus"
Systemic autoimmune disease - circulating antibodies specific for constituents of nucleus (antinuclear antibodies) - TYPE 3 HYPERSENSITIVITY
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Systemic Lupus Erythematosus (SLE) "Lupus": characteristics on body
- butterfly rash - women (20-40) - fever - weakness - arthritis - kidney dysfunction
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Systemic Lupus Erythematosus (SLE) "Lupus": clinical outcome
- highly variable - episodic - eventual death due to organ failure (brain, kidney)
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Rheumatoid arthritis
Autoimmune disease - 1-3% of population - episodic - 20-40 years - rheumatoid factor --> antibodies against antibodies
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Multiple sclerosis
Autoimmune disease - autoimmune response against myelin sheaths - --> IgG autoantibodies against structural proteins of myelin - sclerotic plaques --> hard plaques that slow down conduction speed
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Why do you want to suppress immune system?
if you have autoimmune disease
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Main autosuppressive agents
- radiation - immunosuppressive drugs that impede cell division or cell function - adrenal corticosteroid hormones - immunoglobin
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adrenal corticosteroid hormones
- suppresses inflammatory reaction - impair phagocytosis - inhibit protein synthesis
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immunoglobin
interferes with normal immune response
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Neoplasm
uncontrolled growth of cells, benign or malignant
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Tumor
A non-specific term meaning lump or swelling
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Metastasis
discontinuous spread of a malignant neoplasm to distant sites
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Malignant
capable of metastasis
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Cancer
any malignant neoplasm or tumor
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Benign
- slow growth rate - expansion of cells - tumor remains localized - well differentiated cells
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Malignant growth
- rapid growth rate - infiltration (spreading) - metastasis by bloodstream or lymphatic channels - poorly differentiated cells
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"-oma"
Does not distinguish between benign or metastatic. However, more often used in conjunction with malignant neoplasms
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Carcinoma
malignancy of epithelial cells
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Sarcoma
malignancy of CT
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Melanoma
malignancy of melanocytes
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lymphoma
malignancy of lymphoid tissue
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lifetime risks: a. developing cancer b. dying from cancer
a. developing cancer - men: 1 in 2 - women: 1 in 3 b. dying from cancer men: 1 in 4 women: 1 in 5
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Explain how malignancies develop through pre-malignancies
1. Dysplasia - premalignant state - tissue is atypical - usually epithelium - does not always progress to malignancy 2. Carcinoma in situ (CIS) - cancer in place - not invasive as basement membrane is intact 3. Progression to invasion
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Categories of mutant genes
- oncogenes - tumor suppressor genes - DNA repair genes - genes regulating apoptosis
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Proto-oncogene
usually involved in cell growth/cell division
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oncogene
proto-oncogene thats been activated by mutation, gene amplification, translocation
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Tumor suppressor genes
Function to halt cell cycle | - P53 (protein 53)
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P53
Tumor suppressor - guardian of the genome - mutated (inactivated) in more than 50% of all cancers - p53 regulates (activates of represses) transcription of more than 50 different genes - activated p53 levels rise rapidly is DNA is damaged or repair intermediates accumulate
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Development of cancer is a multistep process...explain
Cancer requires mutation of multiple genes; age relationship with cancer is consistent with this `
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Angiogenesis
new bv/capillary growth
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What cells are involved in the immune surveillance of cancer?
a. Natural Killer Cells (innate) | b. Cytotoxic T Cells ( CD8+, adaptive)
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Individuals at risk for cancer has inherited a set of genes that influence:
a. differences in circulating hormone levels b. variations in which cells metabolize cancer causing chemicals c. variations in ability to repair DNA d. variations in efficiency of immune system
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What should you remember when looking for early warning signs of cancer?
C - change in bladder/bowel habits or function A - A sore that does not heal U - unusual bleeding or discharge T - thickening or lump in breast or elsewhere I - indigestion or difficulty swallowing O - obvious change in wart or mole N - nagging cough or hoarseness
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Tumor associated antigen tests
Some cancers secrete substances that can be detected in the blood by lab tests * should never be used for strictly diagnosing* * should be used for monitoring treatment*
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Tumor associated antigen tests: CEA (carnioembryonic antigen)
Present in amounts related to size of tumor. | - produced by most malignant tumors of the GI tract, pancreas, breast
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Tumor associated antigen tests: alpha fetoprotein
Normally produced by fetal tissues in the placenta but not adult cells; elevated in primary carcinoma of the liver
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Tumor associated antigen tests: Human chorionic gonadotropin
normally produced by placenta; elevated in testicular carcinoma
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Tumor associated antigen tests: acid-phosphatase
normally produced by prostate epithelial cells, may be elevated in prostate cancer
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Treatment depends on grading and scaling, what does grading and scaling mean?
Grading is a microscopic assessment; how abnormal do they look? Scaling is behavioral assessment; size and extent of metastasis; help plan the treatment
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Gleason grading system
Scale of 1-5. 1 being the most differentiated, 5 being the least differentiated
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Tumor grading (stages)
Stage 0: CIS Stage 1: not spread into surrounding tissues, but larger than stage 0 Stage 2: May extend into nearby tissue Stage 3: Spread to nearby lymph-nodes but not other parts of body Stage 4: spread to distant tissues and organs
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Cancer treatment: Surgery
- to prevent cancer (polyps) - removal of abnormal tissue - biopsy for diagnosing and staging - lymph node sampling - debulking surgery (making smaller) - palliative surgery
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Hormone therapy
- receptor activation or blockage | - interferes with cellular growth and signaling
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Ionizing radiation
Goal: a. eradicate cancer without too much toxicity b. avoid harm to normal structures c. damage cancer cells DNA
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Chemotherapy
a. compounds targeting rapidly dividing cells b. specific to cancer cells? --> hair, gut, hematopoietic - hair loss, anemia, low weight/appetite, infection
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immunotherapy
- stimulating own immune system to work harder or smarter to attack cancer cell - giving immune system components to attack cancer (tumor antibodies)
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Communicable disease
Disease transmitted from person to person
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Endemic
Communicable disease in which a small number of cases are continually present in the population
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Epidemic
Communicable disease concurrently affecting large numbers of people in a population
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Pandemic
Communicable disease concurrently affecting people worldwide
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STI
General term for any disease that can be spread by intimate/sexual contact
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Common signs/symptoms for STIs
- Hematuria, urinary frequency, incontinence, purulent discharge, burning, itching on urination - pelvic/genital pain - any skin ulcerations, esp. in genital areas - fever, malaise
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Types of STIs
1. Bacterial a. gonorrhea 2. Viral a. genital warts b. human papillomavirus 3. Protozoal 4. Parasitic 5. Fungal
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Syphilis
- bacteria that infects body tissue - less common but more deadly because it can spread through blood - exists in 4 stages (primary, secondary, latent, tertiary)
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Stages of syphilis
1. Primary: Local manifestations a. Chancre b. painless but go unnoticed c. 4-6 weeks, resolves spontaneously d. highly contagious 2. Secondary: Systemic manifestations a. fever, malaise, sore throat, hoarseness, anorexia, joint pain, skin rash, lesions b. beings several months after chancre has healed c. highly contagious d. persists for several weeks, goes away spontaneously 3. Latent a. medical evidence of the infection, but asymptomatic b. unlikely contagious 4. Tertiary: Destructive systemic manifestations a. may emerge 5-20 years following latency b. most severe stage c. formation of gummas d. neurosyphilis
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Gummas
destructive skin, bone and soft tissue lesions
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Congenital syphilis
Transmission of disease from mother to child; may cause death of fetus *treatment early in pregnancy is important as bacteria are less likely to pass through placenta during first few weeks of pregnancy
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Treatment for syphilis
Since it is a bacteria, you treat with antibiotic
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Gonorrhea
Bacteria transmitted during sexual intercourse or other intimate sexual contact with infected partner. - 1:200 college ages females - transmission generally requires contact of epithelial surfaces (urethra, genital tract, pharynx)
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Gonorrhea symtosm
- abdominal pain, fever, discharge (not bloody, purulent), asymptomatic (more likely in females)
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Gonorrhea: females
infection may spread upward into fallopian tubes which can lead to tubal scarring and infertility - infected mother can infect child during vaginal delivery - can lead to infertility in both males and females
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Gonorrhea treatment
Since it is a bacteria, you treat with antibiotic
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Chlamydia
Intracellular bacterium - highly prevalent --> most common BACTERIAL STI - one of most potentially damaging STDs
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Chlamydia
Since it is a bacteria, you treat with antibiotic
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Chlamydia and Gonorrhea is where? | Syphilis is where?
Chlamydia and Gonorrhea is on the surface of cells. Syphilis is on the inside of cells. i think
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Chlamydial infections: signs and symptoms
- Silent STD - burning/itching in genitalia - mucopurulent vaginal discharge - discharge from penis - burning urination - swollen scrotum
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Chlamydia prognosis
- good w early treatment - if untreated, such complications as pelvic inflammatory disease, infertility in females, epididymitis in males, sterility in both
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Genital herpes
Herpes Simplex Complex (HSV) - multiple shallow ulcerations, pustules on genitals, mouth and anus - highly contagious VIRAL infection of genitalia - reoccurs spontaneously - life threatening form in infants during vaginal birth
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Genital herpes two stages
- active w skin lesions - latent without symptoms * can be spread during both*
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Two types of genital herpes
NOT restricted in distribution 1. Herpes Simplex Virus Type 1: HSV-1 - oral mucous membrane 2. Herpes Simplex Virus Type 2: HSV-2 - genitals - 80% of infections *skin can look normal, but still shed*
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Human Papillomavirus (HPV)
Genital Warts - soft, skin-colored, whitish pink to reddish brown benign growths - found on genitals (vag., cervix, anus) - very contagious - may not be visible to naked eye - most common STI - can be spread without seeing them - may go away without treatment
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Human Papillomavirus (HPV) is a risk factor for?
cancer - 120 different types of HPV - --> divided into high-risk and low-risk types for caner
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HPV vs HSV
Genital Warts vs Genital Herpes - Genital Herpes come and go away without treatment (no cure, antiviral meds to manage) - Genital Warts come but do not go away without treatment Genital Herpes = blistery sores causing pain, itching Genital Warts = small, painless, do not open or pus
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AIDS
Acquired Immune Deficiency - caused by HIV - end stage and most serious manifestation of HIV - low Helper T cell count (CD4+) - recurrent infections that are not observed in healthy people - certain kinds of neoplasms - cachexia (waisting away)
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HIV transmission
HIV virus may enter body by any of several routes - sexual contact - blood/body fluids - mother to infant
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HIV transmission by blood and blood products: directly
Intimate sexual contact, linked to mucosal trauma from rectal intercourse
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HIV transmission by blood and blood products: transfusion
Contaminated blood or blood products, lessened by routine testing of all blood products
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HIV transmission by blood and blood products: sharing contaminated injection needles
mainly from illegal drugs
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HIV transmission by blood and blood products: transplacental or postpartum transmission
Via cervical or blood contact at delivery and in breast milk
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Group at risk for AIDS
- homosexual or bisexual males - present or past IV drug users - patients with hemophila - recipients of transfusion of human blood - heterosexual contacts of the above
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HIV Targets...
- helper T cells, macrophages Entry depends on... - CD4+ receptor (helper T cells) - CCR5 (CXCR4) co-receptor
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Complications of AIDS
- Opportunistic infections from organisms not normally pathogenic or of limited pathogenicity - Malignant tumors in AIDs patients because helper T cells help B cells, innate immunity, and cytotoxic T cells...so when helper T cells are down so are cytotoxic T cells which leads to an increase in cancer because cytotoxic T cells fight cancer
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Treatment for HIV infections / AIDS
NO CURE Primary therapy is the use of various combinations of three different types of antiretroviral agents --> Drug cocktail Highly Active Antiretroviral Therapy (HAAT) - integrase inhibitor - reverse transcriptase inhibitor - protease inhibitor
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Prevention of STIs
1. Vaccines - HPV 2. Safe sex - abstinence - condom (cannot prevent genital herpes or HPV) 3. Limiting number of partners