FOM Week 6 Flashcards

(100 cards)

1
Q

PML

A

A growth suppressor protein that induces cell death

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2
Q

RARalpha

A

Induces promyelocyte differentiation into specific WBCs

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3
Q

What happens in APL

A

There is a chromosomal translocation and the PML and RARalpha proteins become fused together through non homologous end joining
The fused protein now inhibits apoptosis and differentiation

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4
Q

How does retinoic acid/arsenic help to treat APL

A

It removes the PML-RARalpha protein from the DNA

Apoptosis and differentiation can now occurs

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5
Q

How do steroids affect the estrogen receptor

A

Steroids will diffuse into the cell and bind to the ER
This will then cause two ERs to dimerize and bind to a specific DNA sequence
This then recruits HATs for transcription

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6
Q

Bilaminar Embryo

A

Early on when the ICM divides into the epiblast and the hypoblast

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7
Q

Trilaminar Embryo

A

When the epiblast undergoes gastrulation to divide into the ectoderm, the mesoderm, and the endoderm

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8
Q

3 Stages of Pregnancy

A
Period of Ovum (fertilization-->blastocyst)
Embryonic Period (implantation-->organogenesis)
Fetal Period (week 9-->birth)
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9
Q

What happens when you scramble two different types of sponge cells

A

They will reaggregate into their groups

Like cells recognize like cells

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10
Q

Expression of CAMs

A

High during aggregation
Low during migration
Important for NC migration/aggregation

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11
Q

Expression of Fibronectin

A

Low during aggregation
High during migration
Important for NC migration/aggregation

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12
Q

Totipotent/Pluripotent/Multipotent Stem Cells

A

Totipotent stem cells can become any cell in the body. They end after the 4 cell stage
Pluripotent stem cells can become any cell in a certain germ layer
Multipotent stem cells can become any cell of a certain lineage belonging to a germ layer

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13
Q

Differentiation

A

The process of restriction and determination resulting in a particular cell type with a specific function

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14
Q

Evagination vs Invagination

A

Evagination forms an outpocket of cells (eyes)

Invagination forms an ingrowth of cells (glands)

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15
Q

What two rxns must sperm undergo

A

Capacitation- removal of head proteins to expose receptors for binding to the oocyte
Acrosomal Rxn- digestive enzymes migrate through the zona pallucida

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16
Q

What two rxns follow fertilization

A

Cortical Rxn- cortical granules release lysosomal enzymes to prevent any sperm from passing
Zona Rxn- zona pallucida properties are altered to prevent sperm binding

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17
Q

Cleavage

A

Takes 3 days
The cell rapidly divides from 1 to 16 without increasing in size
Compaction keeps the cells close together

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18
Q

Morula

A

16 cell stage
The inner cells become the ICM
The outer cells become the trophblast (placenta)

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19
Q

Blastocyst

A

When the morula creates the ICM and the cavity

This is the structure that will undergo implantation once the zona pallucida hatches

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20
Q

After implantation, what happens to the ICM

A

It divides into the epiblast (columnar) and the hypoblast (cuboidal)

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21
Q

Ectopic Pregnancies

A

When the zygote implants somewhere other than the uterine wall
Usually leads to a miscarriage
Usually occurs in the ampulla of uterine tube or abdominal

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22
Q

Gastrulation

A

Occurs around week 3-4
Begins at the primitive streak and is organized by the primitive node/FGF
The process by which the germ layers are formed

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23
Q

Notochord

A

Forms from the endoderm in cranial to caudal direction around same time as gastrulation.
It is important for inducing the neural plate and ectoderm

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24
Q

How is the A-P axis defined

A

AVE expresses genes that define the anterior region

The primitive streak defines the posterior end

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25
How is the D-V axis defined
BMP4 ventralizes the mesoderm | Chordin (activated by goosecoid), noggin, and follistatin dorsalizes the mesoderm and notochord
26
How do conjoined twins form
There is too little or too much goosecoid
27
Caudal Dysgenesis
Brachyrury gene is missing/mutated | Brachyrury is needed for cell migration/limb formation
28
How is the L-R axis defined
FGF8 is secreted by the node on the left side and establishes nodal FGF8 on the right side is inhibited by SHH
29
Teratogenesis Associated with Gastrulation
During the 3rd week the embryo is very susceptible to teratogenic compounds Alcohol can cause FAS at this stage
30
Sacrococcygeal Teratoma
When the primitive streak does not regress | Leads to a non malignant tumor on the fetus
31
Primary Villi Secondary Villi Tertiary Villi
1 is two trophoblast layers 2 is two trophoblast layers with a mesoderm core 3 is when capillaries become present in the core (3rd week)
32
Screening Tests
A form of secondary prevention that is usually done on healthy people who are displaying no symptoms Meant to reduce morbidity and mortality
33
Criteria for a Screening Test to be Good
Disease has to have a high enough prevalence Disease has to be treatable Disease has to be accurately identifiable Patient has to be okay with the form of screening
34
Lead Time Bias
The time from when the disease becomes detectable to when it can be diagnosed by symptoms Lead time bias is extra time added onto the screened group In reality screening has no effect on the course of a disease
35
Length Time Bias
Individuals with longer pre clinical conditions/phases are more likely to be detected by screening Leads to overdiagnosis
36
Sensitivity vs Specificity
Sensitivity is the ability of a test to accurately identify those with the disease Tests with high sensitivity often give false positives Specificity is the ability of a test to accurately identify those without the disease Test with high specificity often give false negatives
37
How to Calculate Sensitivity and Specificity
Sens= TP/(TP+FN) Spec= TN/(TN+FP)
38
PPV vs NPV
PPV is the probability that disease is present given a positive result PPV= TP/(TP+FP) NPV is the probability that disease is not present given a negative result NPV= TN/(TN+FN)
39
Likelihood Ratio
Likelihood of test result when disease is present divided by likelihood of test result when disease is absent
40
Sequential Testing vs Simultaneous Testing
Sequential involves a cheap first test that has a high specificity. If you test negative you stop. If you test positive you move on to the next Simultaneous testing is used for large groups If you test positive to one, you are positive If you test negative to both, you are negative
41
Cell Types in the Epidermis
Keratinocytes Merkel Cells (come from neural crest) Langerhan Cells Melanocytes (come from neural crest)
42
5 Layers of the Epidermis
``` Stratum Corneum Stratum Lucidum Stratum Granulosum Stratum Spinosum Statum Basale ```
43
Psoriasis
Normal turnover of the epidermis is 1-2 months In psoriasis it is 3-4 days This is due to localized inflammation and increased cytokines
44
Bullous Pemphigoid Pemphigus Vulgaris Pemphigus Foliaceus
BP is Abs that attack the hemidesmsomes Pemphigus vulgaris is Abs that attack desmoglein 3 which is high in the basal layer Pemphigus foliaceus is Abs that attack desmoglein 1 which is high in the corneum layer
45
Anagen Catogen Telogen
Anagen is hair growth Catogen is intermediate/regression Telogen is rest/shedding
46
Regeneration vs Scar Fomation
Regeneration occurs with mild cuts that do not pass the epidermis Scar formation occurs with more severe cuts that go into the dermis
47
First Intention vs Second Intention Wound Healing
First only involves neutrophils, macrophages, and fibroblasts Second involves those three but also myofibrilblasts to contract the ends of wound together
48
Skin Grafting
Used to accelerate wound healing and minimize the amount of fluid lost Can be self or non self
49
Impact of Education on Health
The higher your education level, the more likely you are going to have better health People who dont graduate high school have a 3 times higher mortality rate than those who do
50
Which county in KS has the best education | Which county in KS has the worst
Johnson County has the best. It also has the best health outcomes and the highest income Wyandotte County has the worst eudcation
51
How does living in a rural area impact health
You have less access to quality care You often have more risky occupations Lots of rural areas have high poverty
52
How does living in an urban area impact health
Often the neighborhoods are less safe Pollution Often there is a poorer quality of food
53
Causes of Health Disparities
``` Opportunity Income Education Access Location ```
54
Derivatives of Ectoderm
``` CNS PNS Epidermis/Hair/Nails Mammary/Pituitary Glands NC Cells ```
55
High BMP4 Medium BMP4 Low BMP4
High produces epidermis Medium produces NC cells Low produces neural plate
56
Neuralation
Occurs during the 4th week Part of the ectoderm becomes induced by the notochord to form the neural plate Forms craniocaudally and it is when the neural plate folds
57
What happens when the neural plate does not close
``` Anencephaly when the cranial does not close Spina bifida when the caudal end does not close Folic acid (vitamin B9) can prevent this ```
58
Derivatives of NC Cells
``` Melanocytes Perkel Cells Facial cartilage and bone Smooth muscle PNS ```
59
NC Cell Migration
The NC cells undergo EMT | They exit the head before the tube closes and they exit the caudal end after the tube closes
60
Cause of Cranio-Facial Defects
Failure of the NC cells to migrate properly
61
HOX Gene Organization
3' end has lower number 5' end has higher number Lower number genes are expressed in head region Higher number genes are expressed in tail region
62
Derivatives of Endoderm
``` GI tract Respiratory Tract Urinary Tract Liver Pancreas Bladder ```
63
3 Stages of Adolescents
Early- puberty begins, they are concerned about body, they separate from family, concrete thinking Middle- puberty is usually complete, some abstract thinking Late- physical maturation complete, body image secure, develop life goals
64
Puberty in Girls
Takes about 4 years to complete Is made up of 5 stages Thelarche is the first step and begins with asymmetrical breast development
65
Puberty in Boys
Takes about 3 years to complete Is made up of 5 stages 98% of time the first step is testes enlarge
66
Taking Adolescent History
``` HEEADSSS Home Education Eating Activities Drugs Sex Suicide Safety ```
67
Derivatives of the Paraxial Mesoderm
Somites - Vertabrae/ribs - Dermis - Skeletal Muscle - Limbs
68
Derivatives of the Intermediate Mesoderm
Urogenital Structures | -Kidneys
69
Derivatives of the Lateral Mesoderm
Heart/Blood Vessels | -Cardiac and smooth muscle
70
Formation of Somites
Somatomeres form craniocaudally. These will then form somites in pairs They are transient structures but help to form the segments of the body
71
Formation of Kidneys
Occurs in the 4th week | Pronephric--> Mesonephric--> Metanephric
72
Two Layers of Lateral Mesoderm
Somatic/Parietal- ventral body wall/limbs | Splanchnic/Visceral- wall of the gut and heart
73
Vasculogenesis
De novo formation of new blood vessels | Stimulated by FGF2 and VEGF
74
Angiogenesis
Branching/extension of existing blood vessels | Stimulated by VEGF
75
Capillary Hemangiomas
Abnormal vascularization | Occurs in 10% of births and normally in facial area
76
Areas of Hematopoesis
Starts out in the yolk sac--> mesonephros--> liver/spleen--> bone marrow
77
Syndactyly
Fused digits due to failure of apoptosis
78
Examples of Apoptosis
Formation of digits Control of cell number Deletion of structures Deletion of abnormal cells
79
Characteristics of Apoptosis
``` Chromatin condenses Membrane blebs DNA cleavage No energy required Phosphatydalserine redistributes membrane to signal macrophages ```
80
Extrinsic Pathway
An outside ligand binds to the death receptor This recruits the initiator caspase8 Caspase8 will then activate other caspases and MOMP
81
Active Site of Caspases
To become active they have a sequence that needs to get cleaved The active site is a cysteine protease that cleaves at Asp residues
82
IAPs
Inhibitors of apoptosis by binding to initiator and effector caspases
83
What happens once caspases are activated
``` Kinases become activated--> Ca influx Cytoskeleton breaks down PARP gets destruction--> no DNA repair DNA gets fragmented Nuclear lamin degrades Flippases become degraded ```
84
Intrinsic Pathway
Activated by cellular stress (DNA damage, heat, hypoxia, etc) This activates P53 and BH3 proteins that inactivate the anti apoptotic BCL2 genes and activate the pro apoptotic BCL2 genes
85
BAX
Forms a pore in the mitochondrial membrane that disrupts the ETC and releases cytochrome C (MOMP)
86
Apoptosome
Cytochrome C forms a super complex with other proteins and this activates more caspases
87
Health Policy
A formal statement that defines priorities and parameters for action
88
Areas of Health Policy
``` Public Health Structural interventions Health care delivery Licensing of professionals Accreditation of health care providers ```
89
Sources of Health Policy
International/WHO Government Private Organizations
90
Trends of Public Health in US
Worst in the SE and improves as you move NW | US spends the highest % of GDP on health spending
91
How are free radicals generated
``` Normal cellular redox rxns Absorption of radiant energy (radiolysis of water) Neutrophils Fenton Rxn NO productions ```
92
Damages of ROS
Lipid peroxidation of membranes DNA damage Protein damage
93
Reperfusion
Caused by ischemia | These cells are more likely to produce ROS
94
Anti Apoptotic Proteins
BCL-2 BCL-XL MCL1
95
Pro Apoptotic Proteins
BAX BAK BH3
96
Common Intracellular Accumulations
``` Fat (clear) Glycogen Lysosomes Iron (dark blue) Lipofuscin (yellow-brown) Melanin (brown-black) Hyaline (red) Carbon pigment (black) ```
97
GPCRs
Signal Transduction Receptor Has a 7 transmembrane domain On the cytosolic side there is a heterotrimer protein that initiates the cascade
98
Activation/Deactivation of GPCRs
Once the ligand binds it will induce a conformational change that will swap GDP for GTP. This causes the alpha subunit to dissociate from the beta/gamma unit. These two unit will then lead to downward actions It is turned off by a GTPase that hydrolyzes the GTP and the units will then rejoin. This process is sped up by RGS
99
Ways to Inactivate the GPCR
Phosphorylate it and the G protein cannot bind Hydrolyze the GTP Block the ligand (ex is beta blockers)
100
Cholera/Pertussis
Cholera prevents the GTP from being hydrolized so the signal is not turned off Pertussis binds the the alpha subunit of the Gi protein and prevents it from binding to the GPCR