Science and Research Flashcards
1
Q
What structures are derived from mesoderm? (4)
A
- Fibroblasts
- Langerhans cells
- Immune cells
- Vessels
2
Q
What embryological layer (ectoderm, mesoderm, endoderm) are adnexal structures derived from?
A
Ectoderm
3
Q
What embryological layer (endoderm, mesoderm, ectoderm) are fibroblasts derived from?
A
Mesoderm
4
Q
What embryological layer (endoderm, mesoderm, ectoderm) are Langerhans cells derived from?
A
Mesoderm
5
Q
What embryological layer (endoderm, mesoderm, ectoderm) are inflammatory cells derived from?
A
Mesoderm
6
Q
What embryological layer (endoderm, mesoderm, ectoderm) are Merkel cells derived from?
A
Ectoderm
7
Q
What embryological layer (endoderm, mesoderm, ectoderm) are melanocytes derived from?
- What specifically?
A
Ectoderm (specifically neural crest)
8
Q
What skin structures are derived from ectoderm? (5)
A
- Epidermis
- Adnexal structures
- Merkel cells
- Melanocytes (neural crest)
- Nerves (neuroectoderm)
9
Q
What is meant by the term “power” in a study?
A
The probability of rejecting the null hypothesis when it is false.
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
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%
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
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
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
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
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
17
Q
How do you calculate odds ratio?
A
Calculated with a case-control study
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
19
Q
How do you calculate relative risk?
A
Calculated with a cohort study
20
Q
Describe a randomized control trial.
A
- Type of interventional study
- Gold-standard for clinical trials
21
Q
Describe prevalence.
A
Prevalence = total number of cases at a given time divided by total population at risk
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
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.
24
Q
Define mosaicism.
A
25
Define **chromosomal translocation.**
* Caused by rearrangement of non-homologous chromosomes
* Segments moves from one chromosome to another
* Can either be balanced or unbalanced
26
Define **mitochondrial inheritance**.
Note: heteroplasmy is the presence of both normal and mutated mtDNA, resulting in variable expression in mitochondrially inherited disease
27
Define **loss of heterozygosity**.
28
What is the difference betweeen **aneuploidy** and **polyploidy?**
* **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
What is the difference between **innate** and **adaptive immunity**?
* Which recognizes foreign and/or self-antigens?
* **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
What are the components of innate immunity and adaptive immunity?
31
What are the three **complement pathways**?
* Classical
* Alternative
* Lectin
32
How do innate immunity and adaptive immunity recognize pathogens?
Innate immunity on left and adaptive immunity on right
33
How is the classical complement pathway activated?
**Activated by immune (antibody-antigen) complexes**
* C1 binds to the Fc portion of the antigen-bound antibodies and the cascade continues from there
34
How is the alternative pathway activated?
**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
How is the lectin complement pathway activated?
**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
What is the main function of **B-cells**?
* What can they differentiate into?
* Antibody production
* Differentiation into plasma cells and memory B-cells
37
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?
* Activate macrophages, promote complement deposition and opsonization
* **Maintain cell-mediated immunity** and involved in delayed-type hypersensitivity reactions
* Downregulate Th2 pathway
38
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?
* **Activate eosinophils** and promote IgE production by B-cells
* Important in parasite defense
* Downregulate macrophages
* **Important in humoral immunity**
39
What are the three phases of wound healing?
* Chronic wounds are thought to be stuck in which phase?
1. Inflammatory phase
2. Proliferative phase
3. Remodeling phase
Chronic wounds are thought to be stuck in the inflammatory phase.
40
What role do CD4+ **Th17 cells** play in immunity?
* What can they recruit?
* **Recruit neutrophils** to destroy extracellular pathogens
41
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?
* 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
What role do CD4+ Treg cells play in immunity?
43
What role do **CD8+** cells play in immunity?
44
What cell lines are included under the broad term "**lymphocyte**"? (3)
* T-cells
* B-cells
* NK-cells
45
What cell lines are included under the broad term "**monocyte**"? (3 or 4)
* Dendritic cells (including histiocytes)
* Langerhans cells
* Macrophages
46
What cell lines are included under the broad term "**granulocyte**"? (3)
* Neutrophils
* Mast cells
* Eosinophils
47
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?
* 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
Describe the **remodeling phase of wound healing**.
* When does this start?
* What is formed?
* What regresses?
* What is remodeled?
* 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
What is the **scar strength** at:
1 week
3 weeks
3 months
1 year
* 1 week = up to 5%
* 3 weeks = 20%
* 3 months = 50%
* 1 year = 80%
50
What wavelength is UV radiation, visible light, and infrared radiation in general?
* UV: below 400 nm
* Visible light: 400 - 760 nm
* Infrared: beyond 760 nm
51
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?
* **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
What wavelengths are **UVA** and **UVB** made up of?
* Which is constant during the day and which peaks?
* **UVB: 280-320 nm**
* **UVA: 320-400 nm**
Note: UVA is constant throughout the day while UVB peaks around noon.
53
Which is more responsible for solar erythema: UVA or UVB?
**UVB**
54
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?
* **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
What occurs on a cellular level after a UVB-induced tan? (4)
* Increased melanocytes
* Increased melanin synthesis (melanogenesis)
* Increased arborization of melanocytes
* Increased transfer of melanosomes to keratinocytes
56
Describe how **chemical** sunscreens work.
* **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
What is the definition of sun protection factor (SPF)?
* How is it calculated?
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
How do physical sunscreens work?
* What are two examples?
* 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
