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MCM > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Autosome

A

Chr1 - Chr22

Non sex Chromosome

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2
Q

Allosome

A

ChrX or ChrY
“Sex chromosome”
“gonosome”

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3
Q

Hemizygous

A

X-linked genes in males

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4
Q

Pleiotropy

A 
When one gene affects multiple phenotypes
Ex: The wolves turned dogs
- Behavior
- Floppy ears
- Curly tails
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5
Q

Incomplete dominant trait

A

The heterozygote expresses an INTERMEDIATE phenotype
Ex: Flower color
- red x white = pink

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6
Q

Codominant

A

The heterozygote expresses BOTH phenotypes

ex: ABO blood typing

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7
Q

Haploinsufficiency

A

A single gene copy does NOT have the ability to express the WT phenotype

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8
Q

Dosage compensation

A

One ChrX stochastically inactivated in each somatic cell
This is so each cell, in males or females, only have one copy of ChrX
- Random: 50/50 chance in any cell of either ChrX (dad’s or mom’s)
- Fixed: once inactivated, all descendent cells will follow suit
- Incomplete: some regions NOT inactivated

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9
Q

Barr body

A

Highly condensed Chr visible in nucleus during interphase

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10
Q

Expressivity

A

The severity of expression of the phenotype among individuals with the genotype
- Result of environmental factors (sex, exposure, …)

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11
Q

Penetrance

A

The probability that a gene will express a phenotype AT ALL

“Incomplete penetrance” = any penetrance under 100%

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12
Q

Early stage of embryogenesis

A
  • 0 to 2 weeks
  • starting with fertilization
  • not sensitive to teratogens b/c not connected to mom yet
  • right rate of lethality
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13
Q

Embryonic stage of embryogenesis

A
  • 3 to 8 weeks
  • period of greatest teratogen sensitivity
  • organogenesis (all organs formed here)
  • each organ system has its own period of peak sensitivity
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14
Q

Fetal stage of embryogenesis

A
  • 9 to 38 weeks
  • decreasing teratogen sensitivity
  • period of functional maturation
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15
Q

Teratogen

A

anything that causes birth defects

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16
Q

Congenital

A

Present at birth

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17
Q

Malformation

A
  • The tissue itself is flawed
  • Etiology: genetic, teratogenic —- morphogenic error
  • ex: spina bifida, myelomeningocele
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18
Q

Deformation

A
  • Due to extrinsic factor
  • Etiology: Extrinsic (fetal constraint), intrinsic (fetal akinesia) —> abnormla force
  • ex: club foot
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19
Q

Disruption

A
  • Normal development stops

- Etiology: vascular, compressive, tearing —> vasculor occlusion (any abnormal force)

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20
Q

Trisomy 21

A

Downs Syndrome

  • Extra copy of chr21
  • Growth/mental retardation
  • Craniofacial defects: brachycephaly, small nose, …
  • Cardiac defects: in 40%, septal defects of PDA
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21
Q

Trisomy 18

“18 year olds want to fight”

A

Edward Syndrome

  • Mental retardation
  • Clenched fists: flexion of fingers/hands
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22
Q

Trisomy 13

“13 in unlucky, people spit like puh-tooy for luck”

A

Patau Syndrome

  • Mental retardation
  • Deafness
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23
Q

Trisomy 8

“the 8 is long in the trunk”

A

Warkany Syndrome

  • Mental retardation
  • Long, slender trunk
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24
Q

47, XXY

A

Klinefelter Syndrome

  • Male
  • Presence of Barr bodies
  • Sterile, testicular atrophy
  • Gynechomastia
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25
Q

45, X

A

Turner’s Syndrome

  • In 80% of cases, due to paternal nondisjunction
  • Short stature, broad chest, short neck
  • Streak gonads (gonadal dysgenesis)
  • The only monosomy capable of life
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26
Q

47, XXX

A

Triple X Syndrome

  • Female
  • 2 Barr bodies
  • Amenorrheic
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27
Q

Cri du chat Syndrome

“quatre cinq sounds like ‘cat is 5’ “

A

Partial deletion of 5p (short arm)

- Characteristic cry like a cat because of malformed larynx

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28
Q

Deletion 4q syndrome

A

Partial deletion of 4q (long arm)

  • Cleft lip
  • Limb abnormalities
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29
Q

Angelman Syndrome

A

“Happy Puppet Syndrome”

  • Microdeletion on 15q (on the maternal chromosome)
  • Puppet-like gait
  • Aphasia (absent speech)
  • Prone to unprovoked periods of uncontrollable laughter
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30
Q

Prader-Willi Syndrome

A

Microdeletion on 15q (on paternal chr)

  • Obesity
  • Hypotonia
  • Hypogonadism
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31
Q

Miller-Dieker Syndrome

A

Microdeletion on 17p

  • Lissencephaly (smooth brain)
  • Microcephaly
  • Sever mental retardation
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32
Q

Maternal imprimting

A

Means that mom’s genes are silenced

Epigenetic

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33
Q

Primordial Germ Cells

A

Arise from epiblast (Week 2)

Give rise to all gametes

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34
Q

Monosomy

A

Diploid individual who has only 1 copy of a chr

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35
Q

Trisomy

A

Diploid individual who has 3 copies of a chr

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36
Q

Spermatogenesis Flow

A 
Starting at puberty
Anterior pituitary secretes LH/FSH
---> Leydig cells secrete testosterone
---> Stimulates primordial germ cells to differentiate
---> Spermatogonia Type A
---> Spermatogonia Type B
---> Primary spermatocytes
---> Meiosis 1
---> Secondary spermatocytes
---> Meiosis 2
---> Spermatids
---> Spermiogenesis
---> Mature spermatozoa
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37
Q

Sertoli cells

A

Supporter cells of primordial germ cells in males

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38
Q

Spermiogenesis changes

A
  • Condensed nucleus
  • Formation of acrosome (enzyme-filled)
  • Formation of tail for motility (flagellum)
  • Formation of middle piece (mitochondria)
  • Shedding of cytoplasm (polar body)
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39
Q

Oogenesis flow

A

All before birth
- Primordia germ cells —> Oogonia —> Mitosis —> Primary oocytes (rest at Prophase 1)

At puberty, one egg selected each month
- Finish Meiosis 1 —> Primary oocyte + polar body —> Meiosis 2 (rest at Metaphase 2 —> Ovulation

If fertilized
- Finish meiosis 2 —> Mature Ova + polar body

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40
Q

Follicle

A

Granulose Cells

  • The epithelial cells surrounding the oocyte as it goes through oogenesis
  • They make a capsule
  • Until puberty, they for a single squamous layer around primary oocyte
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41
Q

Folliculogenesis flow

+ Characteristics

A
  • Primordial follicle (single layer squamous cells)
  • Primary follicle (stratified cuboidal cells + zona pellucida)
  • Secondary follicle (bigger, + antrum)
  • Mature (Graafin) follicle (cumulus oophorus, secondary oocyte)
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42
Q

Zona pellucida

A
  • Layer between maturing oocyte and granulose cells

- Full of glycoprotein (secreted by both oocyte and follicle cells)

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43
Q

Antrum

A
  • Empty space found in the maturing follicle
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44
Q

Cumulus oophorus

A
  • The granulosa cells that exit the ovary along with the secondary oocyte during ovulation
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45
Q

Menstrual phase

A
  • If fertilization does not occur, endometrial lining sloughs off
    (requires progesterone)
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46
Q

Proliferative/Follicular phase

A
  • As follicle develops in ovary
  • Granulosa cells produce estrogen
  • Causes endometrial lining to thicken
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47
Q

Secretory/Progestational Phase

A
  • After ovulation

- Corput luteum produces progesterone to maintain endometrial lining

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48
Q

hCG

A

Human chorionic gonadotropic hormone

  • Secreted by an implated embry
  • Signals the corpus luteum to keep secreting progesterone
  • (Progesterone maintains a thick endometrial lining)
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49
Q

Lipoprotein

A
  • Transport lipids between intestines, liver, and other tissue
  • Globular particules
  • Core of triglycerides and cholesterol
  • Surrounded by coat of protein, phospholipid, and cholesterol
50
Q

5 Classes of lipoprotein

A
  1. VLDL
  2. IDL
  3. LDL
    (these 3 synth. in liver for lipid transport to other tissue)
  4. HDL
  5. Chylomicrons
51
Q

Order of lipoprotein density

?????

A

?????

Chylomicrons

52
Q

Apolipoprotein

A

Surround lipoproteins to hold them together

Ex: apoB-100

53
Q

Chylomicrons

A
  • Are de-lipidated in capillaries
  • Deliver dietary TG to tissue, deliver dietary cholesterol to liver
  • Their TG’s are hydrolyzed (lipoprotein lipase) and tissue takes up monoacylglycerol and FA
  • They are now cholesterol-rich chylomicrons that re-enter circulation —> liver
54
Q

Carbamoyl phosphate synthetase

A
  • Rate limiting step of Urea Cycle
  • 2 ATP + HCO3 + NH3 —> carbamoyl phosphate
  • In liver mitochondria
  • Enzyme is activated by N-acetylglutamate (made when there’s an excess of glutamate due to protein breakdown)
55
Q

Carniting palmitoyltransferase I

CPT I

A
  • Located in outer mitochondrial membrane, operates in intermembrane space
  • FA-CoA —> fatty acylcarnitine + CoA
56
Q

The 3 ketone bodies

A

D(-)3-hydroxybutyrate
Oxloacetate
Acetone

57
Q

All proucts released from full B-oxidation of Palmitate

A
  • Palmitate = C16
  • 8 rounds of B-ox (each round gives A-CoA + NADH + - FADH2)
  • Each A-Coa goes through Krebs (GTP + 3 NADH + FADH2)
  • In total, after Oxidative Phosphorylation —-> 106 AP
58
Q

Acyl CoA Synthetase

A

FA + CoA + ATP —-> FA-CoA + AMP + PPi

  • this is an activated FA
  • FA-CoA can now enter the outer mitochondrial matrix
59
Q

CPT-I

A

Carnitine palmitoyltransferase I

  • sits in outer mitochondrial matrix
  • FA-CoA + Carnitine —–> FA-carnitine + CoA
  • FA-carnitine can now enter the mitochondrial matrix using CAT (carnitine acylcarnitine transferase)
60
Q

CPT-II

A

Carnitine palmitoyltransferase II

  • sits in inner mitochondrial matrix
  • FA-carnitine + CoA —–> FA-CoA + Carnitine
  • Now, FA-CoA can do B-oxidation in the matrix
  • Now, Carnitine can go back to intermembrane space (here, carnitine in the shuttle for FA-CoA)
  • Shuttle = CAT (carnitine acylcarnitine transferase)
61
Q 
CPT-I deficiency
And treatment (3)
A
  • Only affects liver, liver can’t use FA’s
  • Hypoglycemia
  • Treated with
    1. Avoid fasting
    2. Lower LCFA in diet
    3. Carnitine supplement
62
Q 
CPT-II deficiency
And treatment (3)
A
  • Affects skeletal muscle (muscle weakness with exercise)
  • Hyperammonemia (brown urine)
  • Death
  • Treated with
    1. Avoid fasting
    2. Lower LCFA in diet
    3. Carnitine supplement
63
Q

Carnitine

A
  • Used to shuttle LCFA across inner mitochondrial membrane

- SCFA and MCFA (2C - 12C) can diffuse on their own

64
Q

HMG-CoA

A
  • A-CoA, instead of going into Krebs, will go to HMG-CoA (ketogenesis) during starvation because there is no oxaloacetate for it to enter Krebs
  • A-CoA —> HMG-CoA —> Ketone bodies (Acetone, Acetoac., 3-hydroxybutyrate)
65
Q

Brown urine

A

Hyperammonemia

66
Q

Ketone breath

A
  • Hyperketonemia
  • KB’s are water soluble so they entre blood streat and make it into lung where they are exhaled
  • Acetone has a slightly sweet smell
67
Q

Arginino succinate synthetase

A

Urea cycle enzyme

  • Allosteric inhibition my AMP
  • Citrulline + ATP —> Arginosuccinate
68
Q

Carbamoyl phosphate synthetase-1

A

Urea cycle enzyme

  • NH4+ + HCO3- + 2ATP —> Carbamoyl-P
  • Allosteric activation by N-acetylglutamate (made when there’s an excess of glutamate due to protein breakdown)
69
Q

Ornithine transcarbamoylase

A

Urea cycle enzyme

  • Allosteric activation by citrulline
  • Ornithine + carbamoyl-P —> Citrulline (in mit. matrix)
70
Q

Anticipation

A

Genetic disease gets worse with each generation

Usually due to expansion of trinucleotide repeats

71
Q

Epigenetic markers (3)

A

DNA Methylation - silencing (on C of CpG)
Histone Methylation - silencing
Histone Acetylation - expressing

72
Q

Gonadal Mosaicism

A

WT parent has unobservable mutation in sex cells, can pass on this mutation to offspring

73
Q

Anaphase lag

A
  • Another way to get aneuploidy (other than nondisjunction)

- One chr lags behind others during anaphase, left out of new nucleus

74
Q

Non-chromosomal mosaicism

A

Due to error in mitosis early in development, error passed to all offspring
Can results in 2+ populations of cells in an individual

75
Q

Chimera

A

Individual made of 2 genetically distinct cell populations arising from >1 zygote
Ex: Embryo fusion

76
Q

Isochromosome

A

One arm is lost and the other is duplicated

2 p arms or 2 q arms

77
Q

Robertsonian Translocation

A
  • Between two acrocentric Chr (very small p arm)

- Gives one large chr and one very small (usually degraded)

78
Q

Uniparental Disomy

A
  • Both in a pair of Chr come from single parent
79
Q

Linkage disequilibrium

A
  • SNP is in such physical proximity that it’s always inherited with disease loci
80
Q

RFLP

A

Restriction Fragment Length Polymorphism

  • When cut by restriction endonucleases, different alleles can have different lengths
  • Detectable with Southern Blot
  • Example of Indirect Genetic Diagnosis
81
Q

Hardy Weinberg Equilibrium

A

There is no change in allele or genotype freq. in a population over generations
Assumes
- Large pop
- Random mating
- No evolutionary forces (genetic drift, selection, …)

82
Q

STRP Analysis

A
  • Indirect genetic analysis

- Look for Short Tandem Repeat Polymorphisms of different lengths as markers for disease mutations

83
Q

Amniocentesis

A
  • Sample of amniotic fluid collected for genetic screening of embryo
84
Q

Chorionic villus sampling

A
  • Transabdominal/transcervical removal of chorionic villus sample
  • Villi are of fetal origin
  • Can do early in development, but higher risk to fetus (infection)
85
Q

Kartagener Syndrome

A

“Primary ciliary dyskinesia”

  • genetic
  • dynein arms are missing/dysfunctions
  • cilia/flagellum useless
  • affects ALL systems that use ciliary transport
  • high risk of ectopic pregnancy in females with syndrome
86
Q

Capacitation

A
  • Only capacitated sperm can penetrate zona pellucida

- Uterus secretions shed sperm of glycoprotein coat and seminal proteins

87
Q

Fimbrae

A
  • Finger-like projections on ampula of Fallopian tubes

- Work together with cilia on tube walls to beat and move egg down tube

88
Q

4 things to look for in pegidree analysis

A
  1. Any skipped generations? (skipped = recess, not = dom)
  2. M/F equally affected? (No = X-linked)
  3. M to M transmission? (Yes = NOT X-linked dom)
  4. All offspring of affected F affected? (Yes = mitochondrial)
89
Q

Heteroplasmy

A

Mitochondrial genomes may vary within a cell AND the proportion of each genome may be different cell to cell

90
Q

Allelic Heterogeneity

A

Different mutations at same locus cause same phenotype

91
Q

Locus Heterogeneity

A

A single disorder caused by mutations at different loci

92
Q

Preeclampsia

A

Pregnancy-related high BP
Can be due to synctiotrophoblast cells not differentiating and not invading mothers arteries during trophoblast formation (~Days 10-12)

93
Q

Synctiotrophoblasts

A

Part of the trophoblast

  • secrete hCG when implanted
  • secrete enzymes to break down endometrium ECM and invades endometrium
94
Q

Depo-Provera

A

Depot-medroxyprogesterone acetate

  • birth control
  • progesterone analogue
  • prevents ovulation
95
Q

RU-486

A

Mifepristone

  • Birth control
  • Acts as anti-progesterone to prevent/reverse implantation
96
Q

Placenta previa

A
  • When the placenta covers the utero-vaginal opening

- Due to ectopic pregnancy that plants near that bottom part of the uterus

97
Q

Hydatidiform Mole

A

Mole = “false pregnancy”

  • embryo fails to develop, trophoblast does develop
  • complete mole = results from fertilization of empty oocyte
  • partial mole = poorly developed embryo (usually triploid)
  • secrete high levels of hCG
98
Q

Persistent Trophoblastic Disease

A
  • If a mole is not completely removed, it can become invasive
  • ~5% of moles go on to form carcinomas
99
Q

Rhogam

A
  • To prevent hemolytic disease of the fetus (erythroblastosis fetalis)
  • Given ~Week 28
  • Rh- mom can attack Rh+ baby, especially if it’s her second Rh+ baby
  • Rhogam attacks Rh factors and mom is prevented from memory B-cell formation
100
Q

Chorion frondosum

A

The “rough” fetal placenta

  • the ticker part with villi
  • connects to the umbillical cord
  • the “smooth” side is the CHORION LAEVE
101
Q

Decidua basalis

A

The maternal part of the placenta

- “decidua” = it will shed with the placenta

102
Q

Placenta Accretia

A

When embryonic placenta eats through to the uterus

  • Accretia (75%) = eats through decidua basalis
  • Incretia (15%) = eats through some myometrium
  • Percretia (5%) = eats through entire myometrim/perimetrium
  • These can all require hysterectomy at birth because placental/uterine tissue won’t separate
103
Q

Fetal circulation

A

Umbilical artery

  • -> chorionic a
  • -> fetal capillary in villus
  • -> (exchange with maternal blood bath)
  • -> chorionic v
  • -> umbilical v
104
Q

Oligohydramnios

Causes and Complications

A 
Too little amniotic fluid
Causes
- Renal agenesis
- amnion rupture
- chr abnormalities
Complications
- Lung hypoplasia
- Limb malformation
- Low growth
105
Q

Polyhydramnios

Causes and Complications

A 
Too much amniotic fluid
Causes
- GI Obstruction
- Maternal diabetes
- Chr defecs
- High urine output by fetal kidneys
Complications
- High risk for placental abruption
106
Q

Competence

development

A

Actively aquiring the ability to espond to an inductive signal
must have two things:
1. signal receptor
2. the signaling pathway

107
Q 
Permissive interaction
(development)
A

All necessary genes are expressed but waiting for an environmental signal to proceed

108
Q

Mesenchyme

A
  • supporting cells
  • loosely packed connective tissue
  • mesodermal origin
109
Q

Juxtacrine

A
  • Non-diffusable signals

- Go to adjacent cells

110
Q

Sonic Hedgehog Pathway

A 
Ligand: Hedgehog (cholesterol-activated)
Receptor: Patched
Action:
- Activated Smoothened
- Inhibits proteins from P-ing and U-ing Ci
- Ci is now a TF
111
Q

Receptor Tyrosine Kinase Pathway

A 
Paracrine
Ligand: FGF's and other Growth Factors
Receptor: Receptor Tyrosin Kinase
Action:
- Induce dimers that are activate kinases
- Sequence of phosphorylating
- Ras-MEK-ERK pathway ---> TF's
112
Q

Smad pathway

A

Paracrine
Ligand: TGF-B family (ex: Nodal which does L-R axis)
Receptor: TGF-B Receptors( like Receptor Tyrosine Kinase)
Action: Receptors dimerize and P SMAD TF’s
(This pathway involved in mesoderm formation)

113
Q

JAK/STAT Pathway

A 
Paracrine
Ligand: Prolactin
Receptor: JAK (Tyrosine Kinase Receptor)
Action: P STAT TF's which dimerize
(fetal bone growth
114
Q

FGFR3

A

Fetal Growth Factor Receptor 3

  • Uses JAK/STAT Pathway
  • Signals chondrocytes to stop dividing and differentiate into cartilage
  • Gain-of-function mutation results in dwarfism
115
Q

Wnt Pathway

A 
Paracrine
Ligand: Wnt
Receptor: Frizzled
Action:
- ligand binding inhibits Disheveled
- APC complex now active (usually disheveled inhibits it)
- This frees up B-catenin (a TF)
(APC Complex is a tumor suppressor, implicated in colon cancer)
116
Q

Notch signaling

A

Juxtacrine
Ligand: Delta (transmembrane on inducing cell)
Receptor: Notch (transmembrane on responder cell)
Action:
- Cytoplasmic tail of Notch cleaved by proteases —> TF

117
Q

Integrins as receptors

A
  • Transmembrane proteins
  • Integrins bind ECM and IC actin
  • Allows cell movement via actin contraction
  • Involved in cell survival signaling
118
Q

Connexins as receptors

A
  • Found at gap junctions
  • Create a small opening between cells for small soluble molecules to pass
  • Can couple changes in ionic concentrations in two cells
119
Q

Animal/Vegetal poles

A
  • Dictated by polar body (polar body = animal pole)
120
Q

Dorsal/Ventral poles

A
  • Determined by location of Inner cell mass
  • Near blastocyst = ventral
  • Near edge = dorsal (contact with trophoblast)

MCM (3 decks)

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