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Foundations of Medicine > FOM Week 6 > Flashcards

FOM Week 6 Flashcards

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
Q

How is the D-V axis defined

A

BMP4 ventralizes the mesoderm

Chordin (activated by goosecoid), noggin, and follistatin dorsalizes the mesoderm and notochord

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26
Q

How do conjoined twins form

A

There is too little or too much goosecoid

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27
Q

Caudal Dysgenesis

A

Brachyrury gene is missing/mutated

Brachyrury is needed for cell migration/limb formation

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28
Q

How is the L-R axis defined

A

FGF8 is secreted by the node on the left side and establishes nodal
FGF8 on the right side is inhibited by SHH

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29
Q

Teratogenesis Associated with Gastrulation

A

During the 3rd week the embryo is very susceptible to teratogenic compounds
Alcohol can cause FAS at this stage

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30
Q

Sacrococcygeal Teratoma

A

When the primitive streak does not regress

Leads to a non malignant tumor on the fetus

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31
Q

Primary Villi
Secondary Villi
Tertiary Villi

A

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)

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32
Q

Screening Tests

A

A form of secondary prevention that is usually done on healthy people who are displaying no symptoms
Meant to reduce morbidity and mortality

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33
Q

Criteria for a Screening Test to be Good

A

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

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34
Q

Lead Time Bias

A

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

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35
Q

Length Time Bias

A

Individuals with longer pre clinical conditions/phases are more likely to be detected by screening
Leads to overdiagnosis

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36
Q

Sensitivity vs Specificity

A

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

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37
Q

How to Calculate Sensitivity and Specificity

A

Sens= TP/(TP+FN)

Spec= TN/(TN+FP)

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38
Q

PPV vs NPV

A

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)

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39
Q

Likelihood Ratio

A

Likelihood of test result when disease is present divided by likelihood of test result when disease is absent

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40
Q

Sequential Testing vs Simultaneous Testing

A

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

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41
Q

Cell Types in the Epidermis

A

Keratinocytes
Merkel Cells (come from neural crest)
Langerhan Cells
Melanocytes (come from neural crest)

42
Q

5 Layers of the Epidermis

A 
Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Statum Basale
43
Q

Psoriasis

A

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
Q

Bullous Pemphigoid
Pemphigus Vulgaris
Pemphigus Foliaceus

A

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
Q

Anagen
Catogen
Telogen

A

Anagen is hair growth
Catogen is intermediate/regression
Telogen is rest/shedding

46
Q

Regeneration vs Scar Fomation

A

Regeneration occurs with mild cuts that do not pass the epidermis
Scar formation occurs with more severe cuts that go into the dermis

47
Q

First Intention vs Second Intention Wound Healing

A

First only involves neutrophils, macrophages, and fibroblasts
Second involves those three but also myofibrilblasts to contract the ends of wound together

48
Q

Skin Grafting

A

Used to accelerate wound healing and minimize the amount of fluid lost
Can be self or non self

49
Q

Impact of Education on Health

A

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
Q

Which county in KS has the best education

Which county in KS has the worst

A

Johnson County has the best. It also has the best health outcomes and the highest income
Wyandotte County has the worst eudcation

51
Q

How does living in a rural area impact health

A

You have less access to quality care
You often have more risky occupations
Lots of rural areas have high poverty

52
Q

How does living in an urban area impact health

A

Often the neighborhoods are less safe
Pollution
Often there is a poorer quality of food

53
Q

Causes of Health Disparities

A 
Opportunity
Income
Education
Access
Location
54
Q

Derivatives of Ectoderm

A 
CNS
PNS
Epidermis/Hair/Nails
Mammary/Pituitary Glands
NC Cells
55
Q

High BMP4
Medium BMP4
Low BMP4

A

High produces epidermis
Medium produces NC cells
Low produces neural plate

56
Q

Neuralation

A

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
Q

What happens when the neural plate does not close

A 
Anencephaly when the cranial does not close
Spina bifida when the caudal end does not close
Folic acid (vitamin B9) can prevent this
58
Q

Derivatives of NC Cells

A 
Melanocytes
Perkel Cells
Facial cartilage and bone
Smooth muscle
PNS
59
Q

NC Cell Migration

A

The NC cells undergo EMT

They exit the head before the tube closes and they exit the caudal end after the tube closes

60
Q

Cause of Cranio-Facial Defects

A

Failure of the NC cells to migrate properly

61
Q

HOX Gene Organization

A

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
Q

Derivatives of Endoderm

A 
GI tract
Respiratory Tract
Urinary Tract
Liver
Pancreas
Bladder
63
Q

3 Stages of Adolescents

A

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
Q

Puberty in Girls

A

Takes about 4 years to complete
Is made up of 5 stages
Thelarche is the first step and begins with asymmetrical breast development

65
Q

Puberty in Boys

A

Takes about 3 years to complete
Is made up of 5 stages
98% of time the first step is testes enlarge

66
Q

Taking Adolescent History

A 
HEEADSSS
Home
Education
Eating
Activities
Drugs
Sex
Suicide
Safety
67
Q

Derivatives of the Paraxial Mesoderm

A

Somites

  • Vertabrae/ribs
  • Dermis
  • Skeletal Muscle
  • Limbs
68
Q

Derivatives of the Intermediate Mesoderm

A

Urogenital Structures

-Kidneys

69
Q

Derivatives of the Lateral Mesoderm

A

Heart/Blood Vessels

-Cardiac and smooth muscle

70
Q

Formation of Somites

A

Somatomeres form craniocaudally. These will then form somites in pairs
They are transient structures but help to form the segments of the body

71
Q

Formation of Kidneys

A

Occurs in the 4th week

Pronephric–> Mesonephric–> Metanephric

72
Q

Two Layers of Lateral Mesoderm

A

Somatic/Parietal- ventral body wall/limbs

Splanchnic/Visceral- wall of the gut and heart

73
Q

Vasculogenesis

A

De novo formation of new blood vessels

Stimulated by FGF2 and VEGF

74
Q

Angiogenesis

A

Branching/extension of existing blood vessels

Stimulated by VEGF

75
Q

Capillary Hemangiomas

A

Abnormal vascularization

Occurs in 10% of births and normally in facial area

76
Q

Areas of Hematopoesis

A

Starts out in the yolk sac–> mesonephros–> liver/spleen–> bone marrow

77
Q

Syndactyly

A

Fused digits due to failure of apoptosis

78
Q

Examples of Apoptosis

A

Formation of digits
Control of cell number
Deletion of structures
Deletion of abnormal cells

79
Q

Characteristics of Apoptosis

A 
Chromatin condenses
Membrane blebs
DNA cleavage
No energy required
Phosphatydalserine redistributes membrane to signal macrophages
80
Q

Extrinsic Pathway

A

An outside ligand binds to the death receptor
This recruits the initiator caspase8
Caspase8 will then activate other caspases and MOMP

81
Q

Active Site of Caspases

A

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
Q

IAPs

A

Inhibitors of apoptosis by binding to initiator and effector caspases

83
Q

What happens once caspases are activated

A 
Kinases become activated--> Ca influx
Cytoskeleton breaks down
PARP gets destruction--> no DNA repair
DNA gets fragmented
Nuclear lamin degrades
Flippases become degraded
84
Q

Intrinsic Pathway

A

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
Q

BAX

A

Forms a pore in the mitochondrial membrane that disrupts the ETC and releases cytochrome C (MOMP)

86
Q

Apoptosome

A

Cytochrome C forms a super complex with other proteins and this activates more caspases

87
Q

Health Policy

A

A formal statement that defines priorities and parameters for action

88
Q

Areas of Health Policy

A 
Public Health
Structural interventions
Health care delivery
Licensing of professionals
Accreditation of health care providers
89
Q

Sources of Health Policy

A

International/WHO
Government
Private Organizations

90
Q

Trends of Public Health in US

A

Worst in the SE and improves as you move NW

US spends the highest % of GDP on health spending

91
Q

How are free radicals generated

A 
Normal cellular redox rxns
Absorption of radiant energy (radiolysis of water)
Neutrophils
Fenton Rxn
NO productions
92
Q

Damages of ROS

A

Lipid peroxidation of membranes
DNA damage
Protein damage

93
Q

Reperfusion

A

Caused by ischemia

These cells are more likely to produce ROS

94
Q

Anti Apoptotic Proteins

A

BCL-2
BCL-XL
MCL1

95
Q

Pro Apoptotic Proteins

A

BAX
BAK
BH3

96
Q

Common Intracellular Accumulations

A 
Fat (clear)
Glycogen
Lysosomes
Iron (dark blue)
Lipofuscin (yellow-brown)
Melanin (brown-black)
Hyaline (red)
Carbon pigment (black)
97
Q

GPCRs

A

Signal Transduction Receptor
Has a 7 transmembrane domain
On the cytosolic side there is a heterotrimer protein that initiates the cascade

98
Q

Activation/Deactivation of GPCRs

A

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
Q

Ways to Inactivate the GPCR

A

Phosphorylate it and the G protein cannot bind
Hydrolyze the GTP
Block the ligand (ex is beta blockers)

100
Q

Cholera/Pertussis

A

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

Foundations of Medicine (5 decks)

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