Unit 3 - Formative 8 D2

Front 1

When does selection occur to violate Hardy-Weinberg equilibrium?

Back 1

When individuals with different genotypes have different abilities to reproduce

If in a dx w/ Aa genotype, suddenly aa can't reproduce, they can't contribute to gene pool in next generation and the frequency of allele a will decrease

Front 2

Founder Effect

Back 2

Observed when a few individuals leave one population to start a new population; results in the increase or decrease of alleles present in the original population (associated w/ population bottlenecks/disasters)

Front 3

How can you differentiate between heterozygote advantage or founder effect?

Back 3

If the increased prevalence of a disease results from a founder effect, most affected people should have the same ancestral mutation.
If the increased prevalence of a disease results from heterzygote advantage, a whole range of mutations might be common.

Front 4

Genetic Drift

Back 4

Fluctuations of gene frequency that can affect small populations (for example, only AA individuals participate in mating BY CHANCE)

Front 5

How does consanguineous mating affect gene frequencies?

Back 5

Close realtives share more genes than individuals picked randomly in a population and thus increase homozygosity at many loci

Front 6

What are the risks of consanguinity?

Back 6

Increases the risk that two carriers of the same recessive disease amte and have an ffected child; largest risk for rare diseases

Front 7

Assortive MAting

Back 7

Mating w/ similar individuals (positive assortive mating, increases range of variation) or with dissimilar indiivduals (negative assortive mating, decreases range of variation)

Two similar individuals will have similar genes and thus might bring out rare recessive phenotypes (disruptive selection) that would not occur otherwise (stabilized selection)

Front 8

Heterozygote Advantage

Back 8

Heterozygote genotype has a higher relative fitness to homozygote dominant or homozygote recessive genotypes

Front 9

Disease Prevalence Equation

Back 9

p^2 + 2pq + q^2 = 1

Front 10

Allele Prevalence Equation

Back 10

p + q = 1

Front 11

Heterozygote Prevalence Equation

Back 11

2pq = heterozygote prevalence

Front 12

The prevalence of an X linked recessive disease in males and females equations

Back 12

Males = q
Females = q^2

Front 13

Equation for P is dominant over q

Back 13

P^2 + 2Pq

Fraction w/ recessive phenotype = q^2

Front 14

Porphyrins

Back 14

Cyclic compounds that bind metal ions (Fe2+)

Front 15

Erythrocyte Metabolism: Glycolytic Pathway Function

Back 15

Provides ATP

Front 16

Erythrocyte Metabolism: Hexose-Monophosphate Shunt Function

Back 16

Provides NADPH and glutathione

Front 17

Erythrocyte Metabolism: Glycolytic Pathway FunctionRapoport-Leubering Pathway Function

Back 17

Forms 2,3 BPG

Front 18

Erythrocyte Metabolism: Glycolytic Pathway FunctionMethemoglobin Reductase Function

Back 18

Protects hemoglobin from oxidation

Front 19

What does the mean cell volume laboraty test tell you?

Back 19

Used to classify cells as normocytic, microcytic or macrocytic

Front 20

Ansiocytosis

Back 20

Variation in the size of the cells

Front 21

Poikilocytosis

Back 21

Variation in the shape of the red cells

Front 22

Hypochromic Cells

Back 22

Poorly hemoglobinized; associated with impaired/decreased hemoglobin cynthesis

Front 23

Anemia of Acute Blood Loss

Back 23

Blood loss -> water shifts from interstitial fluid compartment to intravascular compartment -> results in hemodilution causing a decrease in hematocrit = anemia

Front 24

Extravascular Hemolysis

Back 24

Premature destruction of RBC within splenic phagocytes; if persistent = splenomegaly secondary to phagocytic hyperplasia

Front 25

Haptoglobin

Back 25

Binds free hemoglobin, preventing its excretion in the urine

Front 26

Intravascular Hemolysis

Back 26

rupture/lysis of RBC within circulation due to mechanical injury, complement fixation, intracelullar parasites (malaria) or exogenous toxins (clostridial sepsis)