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
Q

Remission

A

When signs and symptoms subside; does not mean disease is gone

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26
Q

Exacerbation

A

Increase in the severity of signs and symptoms

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27
Q

Relapse

A

Disease returns after its apparent cessation

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28
Q

Complication

A

An abnormal state that develops in a person already suffering from a disease

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29
Q

Impacts that diseases have on a population

A

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

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30
Q

Classifications of disease

A
  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
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31
Q

Predisposing

A

Risk factors; NOT CAUSALITY

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32
Q

Predisposing factors of disease example

A

genetics, ages, gender, environment, lifestyle

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33
Q

Diagnosis

A

The use of scientific or clinical methods to determine nature and cause of disease

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34
Q

Factors utilized for diagnosis

A

Clinical history and the physical examination

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35
Q

Clinical history

A

A. Chief complaint
B. History of current illness
C. Past medical history (family health history & psychosocial sexual history)
D. Signs and symptoms

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36
Q

What are diagnostic tests utilized for?

A
  • diagnosing disease
  • monitoring treatment
  • screening
  • assessment of risk
  • prognosis
  • detection of complications
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37
Q

Accuracy

A

Are the results of the tests an indication of whats being measured?

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38
Q

Precision

A

Ability of test to provide the same result every time it is used.

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39
Q

Sensitivity

A

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
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40
Q

Specificity

A

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
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41
Q

Evaluation of diagnostic tests

A
accuracy
precision
sensitivity 
specificity 
risk/benefit/cost ratio
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42
Q

Screening tests for disease: Purpose

A
  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
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43
Q

To be a successful screening test:

A
  1. Suitable groups for screening
  2. Suitable screening tests
  3. Benefits of screening
  4. Screening for genetic disease
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44
Q

False positive

A

When person doesn’t have disease but test said they may have it

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45
Q

False negative

A

When person has disease but the test said they did not

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46
Q

Classification of diagnostic tests and procedures

A
  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
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47
Q

Clinical laboratory tests

A

Provides and interprets diagnostic testing related to patient care
- 60-70% of diagnosis relies on clinical tests

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48
Q

Qualitative

A

Describe quality, either positive or negative (either there or not there)

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49
Q

Quantitative

A

tests that have numerical results

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50
Q

Radiology =

A

imaging

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51
Q

types of radiology

A
  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
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52
Q

Types of radiologic procedures

A
  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
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53
Q

Diagnostic procedures

A
  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

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54
Q

Cytologic and histologic exams: techniques

A
  1. Biopsy (take tissue out)
  2. Fine Needle Aspiration (stick in needle and suck cells out)
  3. Collection of cells (ex. pap smear)
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55
Q

Palliative

A

Treatments designed to relieve and manage symptoms

ex. hospis

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56
Q

Organization of human body

A

Atoms, cells, tissues, organs, organ systems, organism

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57
Q

all cells ultimately come from

A

stem cells

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58
Q

Stem cells

A

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
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59
Q

Types of stem cells

A

Embryonic stem cell = pluripotent

Adult stem cell = progenitor cells

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60
Q

Progenitor cells

A

cells that can generate specialized cell; they are multipotent

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61
Q

All tissues originate from

A

all tissues originate from germ layers of inner cell mass of blastocyst

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62
Q

What are the 3 layers of the inner cell mass of the blastocyst

A
  1. Ectoderm (outside)
    - nervous tissue, skin
  2. Mesoderm (middle)
    - muscle
  3. Endoderm (inner)
    - inner tracts (GI tract)
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63
Q

Atrophy

A

shrinkage, decrease in cell size due to…
A. physiological (aging)
B. pathological (decreased blood supply, nutrition, lack or neural or hormone support)

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64
Q

Hypertrophy

A

Increase in cell size due to…
A. hormonal stimulation
B. increased functional demand

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65
Q

Hypertrophy results in…

A

increased protein synthesis within cell and decreased protein breakdown

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66
Q

Hyperplasia

A

Increase in cell number due to…
A. hormonal stimulation
B. increased functional demand
C, Chronic stress

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67
Q

Hyperplasia results in…

A

increased cell division if the cell can divide

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68
Q

Metaplasia

A

replacement of one cell type with another

  • most common in epithelium
  • reversible is the stress is removed
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69
Q

Dysplasia

A

change in cell resulting in abnormal cell size, shape, or organization

  • more severe than metaplasia
  • premaligant
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70
Q

Free radicals

A

atom or molecule with unpaired electron

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71
Q

Cell injury: morphological changes

A
  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
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72
Q

What is the exchange for the Na/K pump

A

3 Na out

2 K in

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73
Q

Cell death: Apoptosis

A

Programmed cell death or cell suicide

  • removes cells that are worn out
  • cell shrinks in on self
  • removes unwanted tissue
  • normal process/pathological
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74
Q

Apoptosis may be due to…

A
  • signaling factor attached to “death domains” of cell surface receptors
  • mitochondrial damage inside of cell
  • DNA damage
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75
Q

What is the main organelle that initiates Apoptosis

A

mitochondria

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76
Q

Cell death: Necrosis

A

Unregulated death - “sledgehammer”

- cells swell and rupture and they damage nearby cells and inflammation is a result

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77
Q

outcomes of cell injury

A

reversible, adaptation (may be permanent), death of cell

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78
Q

is aging programmed into cells?

A

we do not know

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79
Q

is aging the result of accumulated damage

A
  • older cells have more DNA damage
  • older cells have more free radicals
  • cells can lose their ability to repair their telomeres
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80
Q

Telomores

A

endcaps of chromosomes

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81
Q

Programmed Death-Telomeres

A

telomeres become too short; cell can no longer divide

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82
Q

Cellular aging indicators

A

Atrophy, decreased function and loss of cells

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83
Q

Tissue and systematic aging

A

progressive stiffness and rigidity (bone loss, less elastic CT)

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84
Q

Frailty

A

common clinical syndrome in older adults indicated functional decline, disability, disease and death

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85
Q

genotype

A

genetic info contain in DNA

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86
Q

phenotype

A

outward exp. of DNA (hair color, eye color)

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87
Q

Explain chromosomes

A

chromosomes exist in pairs, one derived from the male parent and one form the female parent; 46 total, 23 pairs

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88
Q

Types of chromosomes

A
  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
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89
Q

Gene

A

Fundamental unit of heredity

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90
Q

what is the functional product of gene

A

protein or RNA

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91
Q

how many genes in human genome

A

20,000; they can be dominant or recessive genes

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92
Q

Genes exist in ….

A

genes exist in pairs or alleles, one on each chromosome

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93
Q

Homozygous

A

both alleles are the same

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94
Q

Heterozygous

A

alleles are different

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95
Q

Genome

A

Sum total of all genes in a cell’s chromosomes

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96
Q

Human genome project

A

international collaboration of scientists that mapped nucleotide sequence of the entire human genome by determining the specific locations of individual genes

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97
Q

Genomics

A

study of gene structure to correlate gene structure with gene expression in individuals

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98
Q

Inheritance of genes of represented by ___.

A

Pedigree (it looks at genes inherited by offspring)

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99
Q

X-Chromosome Inactivation (Lyon Hypothesis)

A

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
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100
Q

Karotype

A

Studies the composition and abnormalities in chromosomes in terms of number and structure

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101
Q

To get a karotype…

A

cells must be stopped in metaphase

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102
Q

Chromosome smear

A

a layout of all 46 pairs of chromosomes

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103
Q

Genetic code

A

info carried by DNA

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104
Q

nucleotide

A
structural unit of DNA 
Bases: 
a. Purines (adenine, guanine)
b. pyrimidines (thymine, cytosine) 
*complementary base pairing*
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105
Q

DNA replication: semiconservative

A

One strand of DNA is kept, and makes a new strand with complementary base pairing

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106
Q

bases of DNA are held by _____.

A

H+ bonds

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107
Q

Translation of DNA to proteins: Protein synthesis steps

A
  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
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108
Q

if you see a “u” in complementary base paring, what does that tell you?

A

it tells you it is an RNA

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109
Q

MicroRNA (miRNA)

A

regulate gene expression; acts post-transcriptionally, a type of noncoding DNA

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110
Q

miRNA interacts with

A

miRNA interacts with mRNA and inhibits translation of mRNA

**implicated in many diseases

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111
Q

mitochondrial genes and inheritance

A

mitochondria contain own DNA (mtDNA), mitochondria inheritance is from the mother

  • hereditary diseases resulting from mitochondrial DNA mutations heterogeneous (ATP synthesis)
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112
Q

not all mature cells are able to divide such as

A

cardiac, skeletal muscle, nerve cells

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113
Q

Mitosis

A

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
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114
Q

Meiosis

A

Germ cells only

  • intermixing of genetic material between homologous chromosomes
  • DNA reduced by half
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115
Q

What are the 2 separate divisions of meiosis

A

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

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116
Q

Gametogenesis

A

process of forming gametes (egg and sperm)

- takes place in gonads (ovaries, testes)

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117
Q

Gametogenesis: types

A

Spermatogenesis: making of sperm
Oogenesis: making of eggs

*both have similarities and differences

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118
Q

Spermatogenesis

A

4 spermatozoa formed from each germ cell

- Spermatogenesis occurs continually once male begins puberty

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119
Q

Oogenesis

A

1 ovum formed from each precursor cell discarded as polar bodies

  • oocytes not produced continually (form in utero)
  • Oogenesis discontinues
  • 1 egg/month
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120
Q

Single nucleotide polymorphisms (SNPS)

A

Structural variations in single gene nucleotide of different individuals
- 10 mil. SNPS in human genome

basically, a change in one nucleotide

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121
Q

Single nucleotide polymorphisms (SNPS) affect gene functions resulting in individual differences in body functions such as:

A

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

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122
Q

Epigenetics

A

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
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123
Q

DNA = ___, Epigenetics = ____

A

hardware, software

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124
Q

Epigenetics mechanism: DNA methylation

A

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
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125
Q

Gene imprinting

A

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
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126
Q

How many genes are thought to be imprinted?

A

only 60-100 genes

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127
Q

Imprinting is a specific example of what?

A

methylation

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128
Q

X-Inactivation turns off entire chromosomes, while imprinting…

A

turns off specific genes

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129
Q

Gene therapy

A

delivery of therapeutic gene into a patients target cell; functional proteins are created returning cell to normal

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130
Q

Congenital

A

Abnormality present at birth, even though it may not be detected until some time after birth

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131
Q

Congenital malformation

A

intrinsic defect in development of baby; genetic, environment or both

*abnormal all the way through birth

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132
Q

Congenital deformation

A

abnormal external force, often occurs due to intrauterine pressures; common in twins because the womb is crowded

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133
Q

Congenital disruption

A

secondary destruction in tissue that was previously normal; starts normal, something goes wrong

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134
Q

hereditary or genetic disease

A

resulting from a chromosome abnormality or a defective gene

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135
Q

Hereditary and congenital malformations: causes

A
  • chromosomal abnormalities
  • abnormalities of individual gene
  • intrauterine injury to embryo of fetus
  • environmental factors
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136
Q

What percent of all newborn infants have congenital diseases?

A

2-3%

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137
Q

Causes of intrauterine injury

A
  1. Teratogens
  2. Radiation
  3. Maternal infections
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138
Q

Teratogens

A

harmful drugs and chemicals; drugs rated A, B, C, D, X by FDA

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139
Q

3rd - 8th week after conception…

A

embryo is most vulnerable to injury as organ systems are forming

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140
Q

what does TORCH stand for?

A
Toxoplasma = parasite
Other
Rubella = virus 
Cytomegalovirus 
Herpes Simplex Virus
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141
Q

fetal alcohol syndrome

A

1: 1000 births; mom consumes alcohol (how much determines the severity
- fetal growth restriction, CSN abnormalities, distinctive facial features

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142
Q

Genetic disorder

A

disease caused by abnormalities in DNA

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143
Q

Genetic disorder: monogenetic

A

single-gene disorders (small scale)

144
Q

Genetic disorder: chromosome disorders

A

large scale

145
Q

Genetic disorder: multi-factorial disorders

A

multiple genetic alterations and environment

146
Q

Genetic disorder: mitochondrial disorders

A

mitochondria has own DNA

147
Q

Genetic disorder: germline

A

passed to offspring

148
Q

Genetic disorder: somatic

A

cant be passed to offspring

149
Q

chromosome abnormalities

A
  • leading cause of genetic diseases, mental retardation, and pregnancy loss
150
Q

types of chromosome changes

A

aneuploidy (abnormal #), deletions (part of chromosome has been deleted eps. around tip), translocations (no loss of DNA but wrong place)

151
Q

Aneuploidy

A

Loss of gain of one or more chromosome; commonly results from non-disjunction during meiosis

*more common than changes in chromosome structure

152
Q

Monosomy

A

2n-1 condition (45 chromosomes)

- monosomy involving autosomes may have severe phenotypic effects in animals

153
Q

Non-disjunction

A

chromosomes don’t pull apart correctly, typically in meiosis

154
Q

Trisomy

A

2n+1 condition (47 chromosomes)
- somewhat less severe than monosomy when involves autosomes

ex. trisomy 21/18

155
Q

Down Syndrome

A

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
Q

Clinical features of Down Syndrome

A
  • intellectual impairment
  • slanted eyes
  • congenital heart disease
  • intestinal defects
  • abnormal creases in palms
157
Q

Down Syndrome causes

A

95% due to non-disjunction in meiosis 1

  • non-inherited
  • ovum is source of extra 21 in 95% of cases
158
Q

main risk for down syndrome?

A

maternal age –> older person, older eggs, more fragile, suspended in time

159
Q

Translocation down syndrome

A

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
Q

Sex chromosome abnormalities: Extra Y

A

no significant effect because it mainly carries genes concerned with male sexual differentiation

161
Q

Sex chromosome abnormalities: absent Y

A

body configuration is female

162
Q

Sex chromosome abnormalities: extra X in the female

A

little effect because one of the X chromosomes is inactivated

163
Q

Sex chromosome abnormalities: extra X in male

A

has adverse effect on male development

164
Q

turner syndrome

A

(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
Q

Klinefelter Syndrome

A

(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
Q

Triple X (47, XXX)

A

1: 1000 females

- benign characteristics because extra X chromosome is inactivated

167
Q

Jacobs syndrome

A

47, XYY

  • only through male disjunction
  • taller than avg.
  • delayed dev. speech and language skills
  • fertile
168
Q

Genetically transmitted diseases

A
  • Result from abnormalities of individual genes on the chromosomes
  • Chromosomes appear normal
169
Q

Genetically transmitted diseases causes

A
  • spontaneously (wrong base inserted)
  • environmental teratogen
  • inherited
170
Q

Genetically transmitted diseases: Transmission on autosomes

A

most hereditary diseases are transmitted on autosomes; can occur in…
- autosomal dominant/recessive inheritance

  • X linked inheritance (some are carried on sex chromosomes)
171
Q

autosomal dominant inheritance

A

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
Q

autosomal recessive inheritance

A
  • Need 2 copies of defective gene

- Parents of affected are usually heterozygous carriers

173
Q

Sex-linked inheritance

A
  1. X chromosome large
    - 2% of nuclear genome
    - X chromosome contains more genes than Y chromosome
  2. Y chromosome small
    - few dozen genes
174
Q

multifactorial inheritance

A
  • Combined effect of multiple genes interacting with environmental agents (diabetes, heart disease, hypertension)
  • congenital abnormalities (cleft lip/palate, clubfoot)
175
Q

Amniocentesis

A

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
Q

Amniocentesis risks

A

pregnancy loss 1 in 1,600

177
Q

Chronic Villi sampling (CVS)

A

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
Q

ultrasound examinations

A

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
Q

The inflammatory reaction

A

A non-specific response to any agent that causes cell injury

180
Q

The inflammatory reaction is part of what immune system

A

innate immune system

181
Q

The inflammatory reaction protects against

A

physical (heat or cold)
chemical (concentrated acid)
microbiologic (bacterium or virus)

182
Q

inflammation is a response to cell injury that

A
  • neutralizes harmful agents

- removes dead tissue

183
Q

inflammation is a combined response meaning…

A
  • local blood vessels
  • WBC
  • plasma proteins
  • surrounding tissue
  • systemic effects (fever)
184
Q

Cardinal signs of inflammation

A
  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
Q

Stages of acute inflammation

A
  1. Vascular stage
  2. movement of WBC into tissue
  3. Elimination of pathogen
  4. repair
186
Q

Explain vascular state of acute inflammation

A

Brief vasoconstriction, followed by vasodilation

- alterations in endothelial cells –> more permeable

187
Q

hypermia =

A

vasodilation

188
Q

Edema

A

accumulation of fluid in interstitial space

189
Q

Exudate

A

fluid mixture of protein, leukocytes, and tissue debris that results from inflammation

190
Q

Serous exudate

A

primarily fluid, little protein

191
Q

purulent exudate

A

largely inflammatory cells (pus)

192
Q

Fibrinous exudate

A

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
Q

hemorrhagic

A

Increased red blood cells due to capillary injury

194
Q

Cellular reaction follows vascular reactions

A

Leukocytes enter injured areas (neutrophils/macrophages)

STEPS:

  1. margination
  2. Emigration/diapedesis
  3. chemotaxis
  4. phagocytosis
195
Q

how do the phagocytes know where to go?

A

cytokines released by bacteria and macrophages which bring neutrophils to the site

196
Q

phagocytosis

A

Type of endocytosis - “cell eating”

  • neutrophils (die by apoptosis after)
  • macrophages (do not die after)
197
Q

role of lysosomal enzymes

A

digest bacteria

198
Q

chemical agents that intensify the inflammation process

A
  1. Cell-derived mediators
    a. mast cells
  2. mediators from blood plasma
    a. bradykinin
    b. complement
199
Q

Mast cells

A

(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
Q

Complement

A

activation by antigen-antibody reaction; series of proteins that interact in a regular sequence

201
Q

Arachidonic acid

A

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
Q

Mast cells make what

A

long chain fatty acids that come from Arachidonic acid

203
Q

The Kinin System

A

Functions to activate and assist inflammatory cells.

- causes vascular permeability and pain

204
Q

What is the primary kinin

A

bradykinin

205
Q

The complement system

A

activates or collaborates with other component of the inflammatory response (chemotaxis, phagocytosis, cell lysis)

206
Q

Chemotaxis, phagocytosis, cell lysis

A

chemotaxis - neutrophils coming to site
phagocytosis - cell eating
cell lysis - complement itself can result in lysis of bacteria

207
Q

Leukocytosis

A

increase WBC count (neutrophils)

208
Q

acute phase proteins

A

Proteins made by liver, help mediate inflammation to return body to homeostasis
ex. c-reactive protein (CRP) - help w phagocytosis

209
Q

infection

A

inflammatory process caused by disease-producing organisms

210
Q

“-itis”

A

suffix indicates an infection or inflammatory process such as appendicitis, hepatitis, colitis

211
Q

Cellulitis

A

acute spreading infection of skin and deeper tissues

212
Q

Abscess

A

formation of pus

213
Q

Septicemia

A

infection of pathogenic bacteria in blood

214
Q

pathogenic

A

Ability to cause disease

215
Q

virulence

A

degree of damage caused by a pathogen to the host

216
Q

host

A

affected ind. or animal

217
Q

factors influencing the outcome of disease

A

virulence of organism, numbers of invading organisms, host resistance

218
Q

Chronic infection/inflammation

A

state in which the pathogenic organism and the host are evenly matched; associated with repeated attempts of the body at healing

219
Q

Predominant cells in chronic infection/inflammation

A

lymphocytes (t&b cells), macrophages

220
Q

Inflammation ends with _____.

A

Repair

221
Q

explain the repair stage of the end of inflammation

A

Tissue can regenerate or repair; outcome depends on type of cells forming tissue (continuously dividing cells, non-dividing cells)

222
Q

Regenerate

A

nearly complete restoration

223
Q

repair

A

scar formation

224
Q

Wound healing: stages

A
  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
Q

Determinants of wound healing

A
  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
Q

Classifications of immune system

A
  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
Q

Leukocytes parts of innate immunity

A

macrophages, dendritic cells, polymorphonuclear granulocytes (PMNs)

228
Q

Leukocytes parts of adaptive immunity

A

lymphocytes - t and b cells

229
Q

CD

A

cluster of differentiation

  • CD4+ (helper T cells)
  • CD8+ (cytotoxic T cells)
230
Q

how can we distinguish leukocytes

A

we look at the CD

231
Q

Innate immunity

A

Always present

  • attacks non-self microbes
  • does not distinguish between different microbes (nonspecific)
232
Q

Components of innate immunity

A
  1. epithelial barriers (skin, tear, saliva, secretions)
  2. phagocytic cells (neutrophils, macrophages, dendritic cells)
  3. plasma proteins (complement)
  4. cell messenger molecules (cytokines)
233
Q

Cytokines

A

general term for chemical messengers involved in the immune process

234
Q

Polymorphonuclear cells include…

A

A. neutrophils (most numerous, phagocytosis)
B. basophils (allergic response)
C. eosinophils (parasitic infection)

235
Q

Monocytes

A

found in blood, immature macrophages

236
Q

Macrphages

A

found in tissue, mature monocytes

237
Q

Cells of the innate immune system

A
  1. Polymorphonuclear cells
    - neutrophils
    - basophils
    - eosinophils
  2. Monocytes/Macrphages
  3. Natural Killer Cells
238
Q

adaptive/acquired immunity

A
  • takes long time to respond, specificity, memory
239
Q

adaptive/acquired immunity components

A
  1. Humoral immunity (mediated by B cells)

2. Cell-mediated immunity (mediated by T cells)

240
Q

adaptive/acquired immunity : Mounting a response

A

Recognition –> specific receptor
Activation –> resting to active
Attack

241
Q

Humoral immunity

A

Mediated by B lymphocytes

–> B lymphocytes make antibodies such as plasma

242
Q

How do antibodies work?

A

neutralization, mobilize other components of immune system

243
Q

Cellular immune system

A

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
244
Q

Types of lymphocytes

A

helper T cells
Cytotoxic T cells
Suppressor T cells

245
Q

Cell mediated immunity

A

Antigen must first be “processed” and displayed on the cell membrane of the antigen presenting cell (APC) before activating T cells.

246
Q

Antigen presentation is done by…

A

APC

  • Macrophages
  • Dendritic cells
  • B cells
247
Q

Major Histocompatibility Complex (MHC) role

A

MCH present processed antigen to responding cells of the immune system; encoded by HLA genes

248
Q

MCH class restriction

A

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+)
249
Q

hypersensitivity

A

too much

250
Q

immunodeficiency

A

too little

251
Q

autoimmune disease

A

innapropriate

252
Q

malignancy

A

cancer

253
Q

Hypersensitivity reaction types

A
Type 1, 2 & 3 (mediated by B cell reactions)
Type 4 (mediated by T cell reactions)
254
Q

Type 1 hypersensitivity

A
  • Immediate hypersensitivity

- Preformed antibodies (person has already encountered antigen)

255
Q

Cells involved in Type 1 hypersensitivity

A

Mast cells and basophils

256
Q

Type 1 hypersensitivity: Mast cells

A
  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
257
Q

Allergic disease

A

Type 1 hypersensitivity to environmental substance (allergens); AKA atopy

258
Q

Most common allergen?

A

hay fever, urticaria (hives), atopic dermatitis (eczema), systemic anaphylaxis

259
Q

Anaphylaxis

A

TYPE 1 HYPERSENSITIVITY
- sensitizing antigen circulates throughout the body, triggers widespread mediator release from Ig-coated mast cells and basophils

260
Q

Systemic effects of anaphylaxis

A

Sever decrease in BP

  • Bronchoconstriction = severe respiratory distress
  • Prompt treatment required with epinephrine
261
Q

Hygiene hypothesis

A

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

262
Q

Cytotoxic hypersensitivity

A

TYPE 2 HYPERSENSITIVITY

  • antibody directly attached to antigen in target tissue (target host cell rather than foreign antigen
  • IgG antibody
263
Q

Type 2 hypersensitivity: 2 types

A
  1. Death of target cell
    a. killed by other components of immune system
  2. Antibodies block receptor function
    a. myasthenia (autoimmune disease)
264
Q

Immune complex hypersensitivity Type 3 hypersensitivity

A

TYPE 3 HYPERSENSITIVITY

  • antigen and antibody combine to form immune complex
  • deposition-induced inflammatory response (BV, kidneys, joints)
265
Q

What are some words you can remember to know the difference between each type of hypersensitivity?

A

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

266
Q

Delayed hypersensitivity

A

TYPE 4 HYPERSENSITIVITY

  • T lymphocytes are sensitized and activated on second contact with same antigen
  • Cytokines from T cells activate macrophages
267
Q

Type 4 hypersensitivity steps

A
  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
268
Q

Poison Ivy, metallic jewelry, celiac disease, TB test

A

Type 4 hypersensitivity - delayed

269
Q

Autoimmune disease

A

Self become foreign

  • systemic lupus erythematosus
  • rheumatoid arthritis
  • myasthenia gravis
  • type 1 diabetes
  • multiple sclerosis
270
Q

What hypersensitivity types are mechanisms of autoimmune diseases?

A

type 2, 3, and 4

271
Q

Autoimmune disease: Pathogenesis

A
  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
272
Q

Factors which predispose autoimmune disease

A
  1. gender (W 3x more likely)
  2. Genetic (certain HLA types)
  3. Infection (induction by microbes)
273
Q

Systemic Lupus Erythematosus (SLE) “Lupus”

A

Systemic autoimmune disease

  • circulating antibodies specific for constituents of nucleus (antinuclear antibodies)
  • TYPE 3 HYPERSENSITIVITY
274
Q

Systemic Lupus Erythematosus (SLE) “Lupus”: characteristics on body

A
  • butterfly rash
  • women (20-40)
  • fever
  • weakness
  • arthritis
  • kidney dysfunction
275
Q

Systemic Lupus Erythematosus (SLE) “Lupus”: clinical outcome

A
  • highly variable
  • episodic
  • eventual death due to organ failure (brain, kidney)
276
Q

Rheumatoid arthritis

A

Autoimmune disease

  • 1-3% of population
  • episodic
  • 20-40 years
  • rheumatoid factor –> antibodies against antibodies
277
Q

Multiple sclerosis

A

Autoimmune disease

  • autoimmune response against myelin sheaths
  • –> IgG autoantibodies against structural proteins of myelin
  • sclerotic plaques –> hard plaques that slow down conduction speed
278
Q

Why do you want to suppress immune system?

A

if you have autoimmune disease

279
Q

Main autosuppressive agents

A
  • radiation
  • immunosuppressive drugs that impede cell division or cell function
  • adrenal corticosteroid hormones
  • immunoglobin
280
Q

adrenal corticosteroid hormones

A
  • suppresses inflammatory reaction
  • impair phagocytosis
  • inhibit protein synthesis
281
Q

immunoglobin

A

interferes with normal immune response

282
Q

Neoplasm

A

uncontrolled growth of cells, benign or malignant

283
Q

Tumor

A

A non-specific term meaning lump or swelling

284
Q

Metastasis

A

discontinuous spread of a malignant neoplasm to distant sites

285
Q

Malignant

A

capable of metastasis

286
Q

Cancer

A

any malignant neoplasm or tumor

287
Q

Benign

A
  • slow growth rate
  • expansion of cells
  • tumor remains localized
  • well differentiated cells
288
Q

Malignant growth

A
  • rapid growth rate
  • infiltration (spreading)
  • metastasis by bloodstream or lymphatic channels
  • poorly differentiated cells
289
Q

“-oma”

A

Does not distinguish between benign or metastatic. However, more often used in conjunction with malignant neoplasms

290
Q

Carcinoma

A

malignancy of epithelial cells

291
Q

Sarcoma

A

malignancy of CT

292
Q

Melanoma

A

malignancy of melanocytes

293
Q

lymphoma

A

malignancy of lymphoid tissue

294
Q

lifetime risks:

a. developing cancer
b. dying from cancer

A

a. developing cancer
- men: 1 in 2
- women: 1 in 3

b. dying from cancer
men: 1 in 4
women: 1 in 5

295
Q

Explain how malignancies develop through pre-malignancies

A
  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
296
Q

Categories of mutant genes

A
  • oncogenes
  • tumor suppressor genes
  • DNA repair genes
  • genes regulating apoptosis
297
Q

Proto-oncogene

A

usually involved in cell growth/cell division

298
Q

oncogene

A

proto-oncogene thats been activated by mutation, gene amplification, translocation

299
Q

Tumor suppressor genes

A

Function to halt cell cycle

- P53 (protein 53)

300
Q

P53

A

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
301
Q

Development of cancer is a multistep process…explain

A

Cancer requires mutation of multiple genes; age relationship with cancer is consistent with this `

302
Q

Angiogenesis

A

new bv/capillary growth

303
Q

What cells are involved in the immune surveillance of cancer?

A

a. Natural Killer Cells (innate)

b. Cytotoxic T Cells ( CD8+, adaptive)

304
Q

Individuals at risk for cancer has inherited a set of genes that influence:

A

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

305
Q

What should you remember when looking for early warning signs of cancer?

A

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

306
Q

Tumor associated antigen tests

A

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*
307
Q

Tumor associated antigen tests: CEA (carnioembryonic antigen)

A

Present in amounts related to size of tumor.

- produced by most malignant tumors of the GI tract, pancreas, breast

308
Q

Tumor associated antigen tests: alpha fetoprotein

A

Normally produced by fetal tissues in the placenta but not adult cells; elevated in primary carcinoma of the liver

309
Q

Tumor associated antigen tests: Human chorionic gonadotropin

A

normally produced by placenta; elevated in testicular carcinoma

310
Q

Tumor associated antigen tests: acid-phosphatase

A

normally produced by prostate epithelial cells, may be elevated in prostate cancer

311
Q

Treatment depends on grading and scaling, what does grading and scaling mean?

A

Grading is a microscopic assessment; how abnormal do they look?

Scaling is behavioral assessment; size and extent of metastasis; help plan the treatment

312
Q

Gleason grading system

A

Scale of 1-5. 1 being the most differentiated, 5 being the least differentiated

313
Q

Tumor grading (stages)

A

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

314
Q

Cancer treatment: Surgery

A
  • to prevent cancer (polyps)
  • removal of abnormal tissue
  • biopsy for diagnosing and staging
  • lymph node sampling
  • debulking surgery (making smaller)
  • palliative surgery
315
Q

Hormone therapy

A
  • receptor activation or blockage

- interferes with cellular growth and signaling

316
Q

Ionizing radiation

A

Goal:

a. eradicate cancer without too much toxicity
b. avoid harm to normal structures
c. damage cancer cells DNA

317
Q

Chemotherapy

A

a. compounds targeting rapidly dividing cells
b. specific to cancer cells? –> hair, gut, hematopoietic
- hair loss, anemia, low weight/appetite, infection

318
Q

immunotherapy

A
  • stimulating own immune system to work harder or smarter to attack cancer cell
  • giving immune system components to attack cancer (tumor antibodies)
319
Q

Communicable disease

A

Disease transmitted from person to person

320
Q

Endemic

A

Communicable disease in which a small number of cases are continually present in the population

321
Q

Epidemic

A

Communicable disease concurrently affecting large numbers of people in a population

322
Q

Pandemic

A

Communicable disease concurrently affecting people worldwide

323
Q

STI

A

General term for any disease that can be spread by intimate/sexual contact

324
Q

Common signs/symptoms for STIs

A
  • Hematuria, urinary frequency, incontinence, purulent discharge, burning, itching on urination
  • pelvic/genital pain
  • any skin ulcerations, esp. in genital areas
  • fever, malaise
325
Q

Types of STIs

A
  1. Bacterial
    a. gonorrhea
  2. Viral
    a. genital warts
    b. human papillomavirus
  3. Protozoal
  4. Parasitic
  5. Fungal
326
Q

Syphilis

A
  • bacteria that infects body tissue
  • less common but more deadly because it can spread through blood
  • exists in 4 stages (primary, secondary, latent, tertiary)
327
Q

Stages of syphilis

A
  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
328
Q

Gummas

A

destructive skin, bone and soft tissue lesions

329
Q

Congenital syphilis

A

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

330
Q

Treatment for syphilis

A

Since it is a bacteria, you treat with antibiotic

331
Q

Gonorrhea

A

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)
332
Q

Gonorrhea symtosm

A
  • abdominal pain, fever, discharge (not bloody, purulent), asymptomatic (more likely in females)
333
Q

Gonorrhea: females

A

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
334
Q

Gonorrhea treatment

A

Since it is a bacteria, you treat with antibiotic

335
Q

Chlamydia

A

Intracellular bacterium

  • highly prevalent –> most common BACTERIAL STI
  • one of most potentially damaging STDs
336
Q

Chlamydia

A

Since it is a bacteria, you treat with antibiotic

337
Q

Chlamydia and Gonorrhea is where?

Syphilis is where?

A

Chlamydia and Gonorrhea is on the surface of cells. Syphilis is on the inside of cells.

i think

338
Q

Chlamydial infections: signs and symptoms

A
  • Silent STD
  • burning/itching in genitalia
  • mucopurulent vaginal discharge
  • discharge from penis
  • burning urination
  • swollen scrotum
339
Q

Chlamydia prognosis

A
  • good w early treatment
  • if untreated, such complications as pelvic inflammatory disease, infertility in females, epididymitis in males, sterility in both
340
Q

Genital herpes

A

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
341
Q

Genital herpes two stages

A
  • active w skin lesions
  • latent without symptoms
  • can be spread during both*
342
Q

Two types of genital herpes

A

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

343
Q

Human Papillomavirus (HPV)

A

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
344
Q

Human Papillomavirus (HPV) is a risk factor for?

A

cancer

  • 120 different types of HPV
  • –> divided into high-risk and low-risk types for caner
345
Q

HPV vs HSV

A

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

346
Q

AIDS

A

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)
347
Q

HIV transmission

A

HIV virus may enter body by any of several routes

  • sexual contact
  • blood/body fluids
  • mother to infant
348
Q

HIV transmission by blood and blood products: directly

A

Intimate sexual contact, linked to mucosal trauma from rectal intercourse

349
Q

HIV transmission by blood and blood products: transfusion

A

Contaminated blood or blood products, lessened by routine testing of all blood products

350
Q

HIV transmission by blood and blood products: sharing contaminated injection needles

A

mainly from illegal drugs

351
Q

HIV transmission by blood and blood products: transplacental or postpartum transmission

A

Via cervical or blood contact at delivery and in breast milk

352
Q

Group at risk for AIDS

A
  • homosexual or bisexual males
  • present or past IV drug users
  • patients with hemophila
  • recipients of transfusion of human blood
  • heterosexual contacts of the above
353
Q

HIV Targets…

A
  • helper T cells, macrophages

Entry depends on…

  • CD4+ receptor (helper T cells)
  • CCR5 (CXCR4) co-receptor
354
Q

Complications of AIDS

A
  • 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
355
Q

Treatment for HIV infections / AIDS

A

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
356
Q

Prevention of STIs

A
  1. Vaccines
    - HPV
  2. Safe sex
    - abstinence
    - condom (cannot prevent genital herpes or HPV)
  3. Limiting number of partners