Flashcards
Week 8
Flashcards do conjunto (50)
- 1Describe asymmetric self-renewal of stem cells-2 cells produced
-1 is genetically identical and the other is slightly different
-Stem cells created are associated with tissues (reservoir created) - 2Describe symmetric self-renewal of stem cells-2 cells produced
-Both are genetically identical
-Transient stem cells are involved in embryonic development - 3Purpose of the stem cell niche-Provide growth factors and cytokines
-Gradient determines how the stem cell divides - 4Define adult stem cellArise in the foetus and serve to maintain organs throughout life
- 5Define embryonic stem (ES) cell-Derived from early embryo (represents a cell that normally doesn't exist)
-Have the potential to give rise to every cell type in the body - 6Sources of stem cells-Embryonic stem cells
-Tissue specific stem cells
-Mesenchymal stem cells
-Bone marrow stem cells
-Umbilical cord stem cells
-Induced pluripotent stem cells (iPSCs) - 7When and what is totipotency?-From fertilisation to 8 cell stage
-Cells are identical
-Can differentiate into all cell types - 8When and what is pluripotency?-Morula onwards
-Gene expression has changed
-Potency is more limited - 9What does the inner cell mass become?Epiblast (plutipotent)
Hypoblast - 10What are the 3 pluripotency factors associated with ES cells?-Nanog
-Oct4
-Sox2 - 11How does LIF and BMP affect the ES cell fate?LIF: inhibits differentiation
BMP: stimulates differentiation - 12The primitive streak indicated initiation of gastrulation. Describe what FGF8 does-Controls cell movement by downregulating E-cadherins (normally binds epiblast cells)
-Controls cell specification into the mesoderm - 13How can ES cells be used in future medicine?-Regenerative medicine
-Study of disease mechanisms in genetic disorders
-Drug therapeutic and toxicity screens - 14What are the challenges of the use of ES cells in regenerative medicine?-Production in sufficient numbers and in a pure form
-Delivery and proper incorporation
-Immune rejection - 15What 3 lineages do mesenchymal cells produce?-Oligodendrocytes
-Adipocytes
-Chrondrocytes - 16Why are ES cells rarely used in cardiovascular tissue engineering?They have the highest potency, so can easily differentiate into another tissue with the wrong signal
- 17What features must the ECM have? Where are the signals located?-Inert, high tensile strength and flexible
-Coats the matrix - 18What are iPS cells?-Fibroblasts infected by a combination of pluripotency inducing factors that form ES-like cells
-Show morphology/growth properties of ES cells and express ES cell marker genes
-Patient's DNA is matched
-iPS cells however can remember their origin - 19List some examples of totipotency and pluripotencyTotipotency: zygote
Pluripotency: ES cells, embryonal carcinomas, IPS cell
Unipotent: differentiated cell types - 20How does epigenetics pose a problem for iPS cell formation?-Epigenetics are a permanent structure
-DNA de-methylase removes them on egg/sperm in embryongenesis
-However this is not present in adult cells - 21Describe the cell cycle in ES cells-Do not have a normal cell cycle or checkpoints
-Divides rapidly
-Cells revert back to stem cell proliferation rates once they turn cancerous - 22Advantages of transdifferentiation over iPSC use-Cells reverse partway, not the entire way to ES cells
-Process is faster and more efficient
-Patient specific
-Avoids risk of triggering an immune response - 23Describe normal foetal growth between 4-20 weeks (1st phase)-Increase in foetal weight, protein content and DNA content
-Cellular hyperplasia - 24Describe normal foetal growth between 20-28 weeks (2nd phase)-Increase in protein and weight
-Less increase in foetal DNA content
-Hyperplasia and hypertrophy - 25Describe normal foetal growth between 28 weeks to term (3rd phase)-Continued increase in foetal protein and weight
-No increase in DNA
-Hypertrophy - 26Define intrauterine growth restriction (IUGR)Failure of a foetus to achieve his/her growth potential
- 27Define small for gestational age (SGA)Birth weight is <10th percentile for gestational age
- 28Define large for gestational age (LGA)Birth weight is >90th percentile
- 29Define low birth weight (LBW)Birth weight is less than a certain threshold (like 250g)
- 30Consequences of foetal growth restriction-Cause of perinatal mortality and morbidity
-Unexplained stillbirths
-More likely to die within 1 year, and suffer from neonatal problems
-Origin of adult disease - 31Long term consequences of foetal growth restrictionIncreased risk of:
-obesity
-type 2 diabetes
-stroke
-CHD - 32What are the intergenerational effects of SGA? Causes?Mothers who were SGA are more likely to have SGA babies and increased perinatal mortality
Epigenetics and fewer/poorer quality mitochondria - 33Define macrosomiaBirth weight >4500g
- 34Causes of LGA?-Higher gestational age
-Male sex
-Excessive maternal weight gain and obesity
-Multiparity
-Genetic disorders of overgrowth
-Maternal diabetes (pre-existing/gestational) - 35How do these risk factors cause LGA?-Increased maternal glucose concentrations crosses the placenta
-Foetus has increased insulin concentrations as a result
-Foetal [GF] rises - 36What are some maternal factors that cause abnormal growth?-Ethnicity (pre-disposed to diabetes)
-Drugs
-Nutrition (quality of diet)
-Maternal hypoxia - 37What are some foetal factors that cause abnormal growth?-Chromosomal disorders
-Growth factors: IGF, thyroxine
-Congenital infection: CMV, toxoplasmosis, rubella - 38What are some primary/secondary placental factors that cause abnormal growth?Primary: abnormality of placenta structure/function
Secondary: hypertension, CKD, vasculitis, pro-thrombotic disorders
-Increased maternal burden in multiple gestations - 39Describe malplacentation in IUGR-Poor trophoblast invasion of maternal spiral arteries
-Increased impedance to flow
-Change in Doopler indices (in the uterine artery) - 40Describe asymmetrical patterns in IUGR-Uteroplacental insufficiency
-Decreased glycogen stores
-Decreased abdominal circumference - 41Describe symmetrical patterns in IUGR-Early growth insult
-Disrupted regulation of growth processes
-Disruption at cell hyperplasia stage - 42What is IUGR a combination of?-Reduced growth velocity
-Placental insufficiency - 43What is assessed in foetal growth?-Symphsio-fundal height
-Ultrasound
-Measurement of foetal head, abdomen and femur bone
-Measurement of foetal HR (120-150 bpm) and uterine contractions
-Umbilical artery Doppler (second trimester)
-Liquor (foetal urine) volume - 44Define gestational diabetes mellitusAny degree of glucose intolerance with its onset (or first recognition) during pregnancy
- 45What are some pre-existing risk factors?-Pancreatic beta cell dysfunction
-Deficient insulin production
-Background chronic insulin resistance - 46Describe the screening process for gestational diabetes mellitus-16-18 weeks if past history
-24-26 weeks if have family history, PCOS, BMI>30, ethnicity, previous macrosomia, previous unexplained stillbirth, on steroids
-Urgent if have significant glycosuria, polyhyramnios or macrosomia - 47What are some maternal complications of gestational diabetes mellitus?-Pre-eclampsia
-Pre-term labour
-Instrumental delivery/caesarean section
-Diabetes in later life - 48What are some foetal complications of gestational diabetes mellitus?-Macrosomia
-Shoulder dystocia
-Polyhydramnios
-Perinatal mortality and morbidity
-Increased risk of adult diseases - 49How is gestational diabetes mellitus managed?-MDT
-Regular monitoring and strict control
-Diet changes
-Drugs eg. metformin
-Insulin - 50How is gestational diabetes mellitus managed obstetrically?-Regular growth scans
-Regular blood glucose monitoring
-Delivery around 38 weeks
-Offer a glucose tolerance test 6 weeks postnatal
Informações
- Descrição
- Stem cells Fetal growth Heart and lungs post partum (anatomy)
- Criado por
- Dolu Falowo
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