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BASIC Exam Study Guide > Science and Research > Flashcards

Science and Research Flashcards

1
Q

What structures are derived from mesoderm? (4)

A
  • Fibroblasts
  • Langerhans cells
  • Immune cells
  • Vessels
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2
Q

What embryological layer (ectoderm, mesoderm, endoderm) are adnexal structures derived from?

A

Ectoderm

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3
Q

What embryological layer (endoderm, mesoderm, ectoderm) are fibroblasts derived from?

A

Mesoderm

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4
Q

What embryological layer (endoderm, mesoderm, ectoderm) are Langerhans cells derived from?

A

Mesoderm

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5
Q

What embryological layer (endoderm, mesoderm, ectoderm) are inflammatory cells derived from?

A

Mesoderm

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6
Q

What embryological layer (endoderm, mesoderm, ectoderm) are Merkel cells derived from?

A

Ectoderm

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7
Q

What embryological layer (endoderm, mesoderm, ectoderm) are melanocytes derived from?

  • What specifically?
A

Ectoderm (specifically neural crest)

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8
Q

What skin structures are derived from ectoderm? (5)

A
  • Epidermis
  • Adnexal structures
  • Merkel cells
  • Melanocytes (neural crest)
  • Nerves (neuroectoderm)
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9
Q

What is meant by the term “power” in a study?

A

The probability of rejecting the null hypothesis when it is false.

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10
Q

How do you increase the power of a study? (3)

A
  • Increase the sample size
  • Increase the expected effect size
  • Increase precision of measurement
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11
Q

Assuming a normal distribution, what proportion of the population falls within:

  • 1 standard deviation (SD) of the mean?
  • 2 SDs of the mean?
  • 3 SDs of the mean?
A
  • 68%
  • 95%
  • 99.7%
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12
Q

What is meant by the term “standard error of the mean” in a study?

A

An estimate of how much variability exists between the sample mean and the true population mean

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13
Q

What is meant by the term “confidence interval” in a study?

A

Range of values in which a specified probability of the means of repeated samples would be expected to fall

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14
Q

How can 95% confidence intervals (CIs) be used to determine if there is a stastistically significant difference between the following:

  • For 2 group or variables;
  • For an odds ratio or relative risk?
A
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15
Q

Describe a cross-sectional study.

A
  • Collects data from a group of people to assess frequency of a disease at a snapshot in time
  • Measures disease prevalence
  • Can show risk factors associated with a disease, but cannot establish causality
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16
Q

Describe a case-control study.

  • What does it investigate or look for?
  • What can it be used to calculate?
A
  • Type of observational study; retrospective
  • Compares a group of people with a disease to a group of people without.
  • Looks for prior exposure or risk factor.
  • Asks “what happened?”
  • Can calculate odds ratios
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17
Q

How do you calculate odds ratio?

A

Calculated with a case-control study

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18
Q

Describe a cohort study.

  • What does it investigate or look for?
  • What can it be used to calculate?
A
  • Looks to see if an exposure increases the likelihood of disease
  • Compares a group with the exposure or risk factor to a group without it
  • Can be retrospective or prospective
  • Measures relative risk
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19
Q

How do you calculate relative risk?

A

Calculated with a cohort study

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20
Q

Describe a randomized control trial.

A
  • Type of interventional study
  • Gold-standard for clinical trials
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21
Q

Describe prevalence.

A

Prevalence = total number of cases at a given time divided by total population at risk

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22
Q

What is the difference between a case-control study and a cohort study?

A
  • In a case-control study, the outcome is already known
    • A diseased and non-diseased group are retrospectively compared with regard to an exposure
  • In a cohort study, the exposure is known
    • An exposed and non-exposed group are compared with regard to a past or future outcome
    • Can be retrospective or prospective
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23
Q

Describe incidence.

A

Incidence = number of new cases during a given time period divided by total population at risk

Note: people who already have the disease are NOT counted.

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24
Q

Define mosaicism.

A
25
Q

Define chromosomal translocation.

A
  • Caused by rearrangement of non-homologous chromosomes
    • Segments moves from one chromosome to another
  • Can either be balanced or unbalanced
26
Q

Define mitochondrial inheritance.

A

Note: heteroplasmy is the presence of both normal and mutated mtDNA, resulting in variable expression in mitochondrially inherited disease

27
Q

Define loss of heterozygosity.

A
28
Q

What is the difference betweeen aneuploidy and polyploidy?

A
  • Polyploidy: a numerical change in a whole set of chromosomes.
    • A cell has an entire extra set or is missing an entire set of chromosomes.
  • Aneuploidy: a numerical change in part of the chromosome set.
    • One or more extra or fewer chromosomes (like trisomy 21) in a cell.
29
Q

What is the difference between innate and adaptive immunity?

  • Which recognizes foreign and/or self-antigens?
A
  • Innate: Initial defense with no memory response
    • Present from birth
    • Recognize foreign antigens only
  • Adaptive: Lag phase before activation and differentiation of lymphocytes
    • “Memory” is created from reexposure to antigen
    • Can recognize both foreign and self-antigens
30
Q

What are the components of innate immunity and adaptive immunity?

A
31
Q

What are the three complement pathways?

A
  • Classical
  • Alternative
  • Lectin
32
Q

How do innate immunity and adaptive immunity recognize pathogens?

A

Innate immunity on left and adaptive immunity on right

33
Q

How is the classical complement pathway activated?

A

Activated by immune (antibody-antigen) complexes

  • C1 binds to the Fc portion of the antigen-bound antibodies and the cascade continues from there
34
Q

How is the alternative pathway activated?

A

Recognizes microbial cell surface structures without antibodies

  • Activated by the binding of spontaneously generated C3b to microbial surfaces
  • Microbial bound C3b binds factor B, which is converted to factor Bb, forming C3 convertase
35
Q

How is the lectin complement pathway activated?

A

Activated by mannose-binding lectin protein (without antibodies)

  • MBL binds to mannose residues on microbial surfaces
  • MBL binds MBL-associated serine proteases, which bind and cleave C4 and C2, forming C3 convertase.
36
Q

What is the main function of B-cells?

  • What can they differentiate into?
A
  • Antibody production
  • Differentiation into plasma cells and memory B-cells
37
Q

What role do CD4+ Th1 cells play in immunity?

  • What can they activate or promote?
  • What type of immunity do they maintain?
  • What hypersensitivity reaction are they involved in?
  • What do they downregulate?
A
  • Activate macrophages, promote complement deposition and opsonization
  • Maintain cell-mediated immunity and involved in delayed-type hypersensitivity reactions
  • Downregulate Th2 pathway
38
Q

What role do CD4+ Th2 cells play in immunity?

  • What can they activate or promote?
  • What do they downregulate?
  • What type of immunity do they maintain?
A
  • Activate eosinophils and promote IgE production by B-cells
    • Important in parasite defense
  • Downregulate macrophages
  • Important in humoral immunity
39
Q

What are the three phases of wound healing?

  • Chronic wounds are thought to be stuck in which phase?
A
  1. Inflammatory phase
  2. Proliferative phase
  3. Remodeling phase

Chronic wounds are thought to be stuck in the inflammatory phase.

40
Q

What role do CD4+ Th17 cells play in immunity?

  • What can they recruit?
A
  • Recruit neutrophils to destroy extracellular pathogens
41
Q

Describe the inflammatory phase of wound healing.

  • How long does it last?
  • What comes to the wound site first?
  • How is the clot cleared?
  • What cell type is absolutely required for wound healing?
A
  • Starts within 6-8 hours, lasts 3-4 days
  • Platelets come to site of wound first to form clot
    • Fibrin (first ECM component deposited) and fibronectin (helps provide a matrix for fibroblasts) are essential for clotting and coagulation
    • Clot is ultimately cleared by MMPs and plasminogen for proper scar formation
  • Influx of neutrophils in first 48 hours
  • Macrophages arrive next –> ABSOLUTELY REQUIRED FOR WOUND HEALING.
42
Q

What role do CD4+ Treg cells play in immunity?

A
43
Q

What role do CD8+ cells play in immunity?

A
44
Q

What cell lines are included under the broad term “lymphocyte”? (3)

A
  • T-cells
  • B-cells
  • NK-cells
45
Q

What cell lines are included under the broad term “monocyte”? (3 or 4)

A
  • Dendritic cells (including histiocytes)
  • Langerhans cells
  • Macrophages
46
Q

What cell lines are included under the broad term “granulocyte”? (3)

A
  • Neutrophils
  • Mast cells
  • Eosinophils
47
Q

What occurs during the proliferative phase of wound healing?

  • Around when does this start?
  • What do keratinocytes do during this time?
  • What do fibroblasts do?
  • What causes wound contraction?
A
  • Onset around day 5-7 of initial wound
  • Re-epithelialization
    • Keratinocytes from wound margins “leapfrog” over each other into defect
  • Granulation tissue (macrophages, fibroblasts, vessels): requires fibronectin
  • Deposition of collagen by fibroblasts
  • Wound contraction by myofibroblasts
  • Neovascularization/angiogenesis
48
Q

Describe the remodeling phase of wound healing.

  • When does this start?
  • What is formed?
  • What regresses?
  • What is remodeled?
A
  • Starts at 3-4 weeks and can take up to 1 year
  • Scar formation (via fibroblast production of collagen/fibronectin/hyaluronic acid)
  • Regression of granulation tissue (via apoptosis of cells)
  • Collagen remodeling
49
Q

What is the scar strength at:

1 week

3 weeks

3 months

1 year

A
  • 1 week = up to 5%
  • 3 weeks = 20%
  • 3 months = 50%
  • 1 year = 80%
50
Q

What wavelength is UV radiation, visible light, and infrared radiation in general?

A
  • UV: below 400 nm
  • Visible light: 400 - 760 nm
  • Infrared: beyond 760 nm
51
Q

How does UVB lead to the production of metabolically active vitamin D?

  • Think about where things are converted and what organs are involved
  • What form do we usually test for?
A
  • UVB converts _pro-_vitamin D3 to _pre-_vitamin D3
  • Pre-vitamin D3 is isomerized in the peripheral circulation to vitamin D3
  • Vitamin D3 is converted to 25-hydroxyvitamin D3 in the liver (which is what is measured to assess vitamin D3 stores)
  • 25-hydroxyvitamin D3 is converted to 1,25-hydroxyvitamin D3 in the kidneys
  • 1,25-hydroxyvitamin D3 is the metabolically active form
52
Q

What wavelengths are UVA and UVB made up of?

  • Which is constant during the day and which peaks?
A
  • UVB: 280-320 nm
  • UVA: 320-400 nm

Note: UVA is constant throughout the day while UVB peaks around noon.

53
Q

Which is more responsible for solar erythema: UVA or UVB?

A

UVB

54
Q

What are the two types of skin pigment changes that occur after UV exposure?

  • What happens first? What UV radiation causes this?
  • What happens in the longer term? What UV radiation causes this?
A
  • Immediate pigment darkening:
    • Within 10-20 minutes of UVA light exposure
    • Oxidation and redistribution of melanin already in the skin
    • NOT photoprotective
  • Delayed melanogenesis:
    • Peaks about 3 days after UVB light exposure
    • Increased melanin synthesis
    • Due to DNA damage and formation of cyclobutane pyrimidine dimers
55
Q

What occurs on a cellular level after a UVB-induced tan? (4)

A
  • Increased melanocytes
  • Increased melanin synthesis (melanogenesis)
  • Increased arborization of melanocytes
  • Increased transfer of melanosomes to keratinocytes
56
Q

Describe how chemical sunscreens work.

A
  • Organic aromatic compounds that absorb radiation and convert it into longer, lower-energy wavelengths
  • UVA blockers
    • Oxybenzone, avobenzone, ecamsule
  • UVB blockers
    • Octinoxate, PABA, cinnamates, octylocrylene, padimate O
57
Q

What is the definition of sun protection factor (SPF)?

  • How is it calculated?
A

SPF = MED of protected skin divided by MED of unprotected skin

Note: MED is the shortest exposure of UV radiation that produces erythema within 1-6 hours that disappears within 24 hours

58
Q

How do physical sunscreens work?

  • What are two examples?
A
  • Chemically inert compounds that reflect/scatter UV radiation
  • E.g., zinc oxide and titanium dioxide
  • More broad spectrum than chemical blocks and less irritating for sensitive skin

BASIC Exam Study Guide (11 decks)

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