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BRS/POM MOCKS > POM MOCK 6 - enzyme kinetics, hypersensitivity, complex disease, chromosomal abnormalities, modes of inheritance > Flashcards

POM MOCK 6 - enzyme kinetics, hypersensitivity, complex disease, chromosomal abnormalities, modes of inheritance Flashcards

1
Q

What is Km used for?

A

The Km value is useful as a means of comparing the strength of Enzyme-Substrate complexes.

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2
Q

What does a low Km indicate?

A

Tight binding of a substrate to an enzyme.

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3
Q

What does a high Km indicate?

A

Weak binding of a substrate to an enzyme.

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4
Q

In a Lineweaver-Burk plot what does the gradient of the curve represent?

A

Km / Vmax

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5
Q

In a Lineweaver-Burk plot what does the y intercept represent?

A

1/Vmax

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6
Q

In a Lineweaver-Burk plot what does the x intercept represent?

A

-1/Km

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7
Q

How do competitive enzyme inhibitors work?

A

Occupies all or part of the active site of an enzyme.

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8
Q

Competitive enzyme inhibitor effects on Km and Vmax?

A

Inhibits KM but have no effect on Vmax. Simply adding enough substrate will outcompete the antagonist.

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9
Q

How do non competitive enzyme inhibitors work?

A

Bind outside of the enzyme active site and induce conformational changes in such that enzyme function is inhibited.

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10
Q

Non competitive inhibitor effects on Km and Vmax?

A

Non-competitive inhibitors have no effect on KM but act to lower Vmax.

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11
Q

How is turnover number (kcat) calculated?

A

Vmax / concentration of enzyme.

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12
Q

What does the turnover number (kcat) mean?

A

Number of molecules that an enzyme can process in a given unit of time.

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13
Q

What immunoglobulin activates classical complement pathway?

A

IgM and IgG3.

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14
Q

What class of antibody can cross muscosal epithelium?

A

IgA and sometimes IgM.

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15
Q

What class of antibody binds to Fc receptors on phagocytes?

A

IgG

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16
Q

What class of antibody is present on membrane of mature B cells?

A

IgM.

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17
Q

Which T helper cells activate B cell in type 1 hypersensitivity?

A

Th2 and T follicular helper cells.

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18
Q

What cytokines cause B cells to produce IgE (class switch) in type 1 hypersensitivity?

A

IL-4 and IL-13.

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19
Q

What cells are seen in early phase of type 1 hypersensitivity?

A

Mast cells.

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20
Q

What is seen later (within few hours) on in type 1 hypersensitivitiy?

A

Recruitment of neutrophils.

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21
Q

What do we seen in late response (3-5 days) to type 1 hypersensitivity?

A

High frequencies of eosinophils.

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22
Q

What two antibodies are involved in type II hypersensitivity?

A

IgG or IgM.

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23
Q

How can antibodies cause type 2 hypersensitivity?

A

Activation of complement system (C3a, C4a and C5a) recruit neutrophils which can destroy cells by degranulation. Formation of MAC complex (C5b, C6-C9) which can creates a channel in cell membrane leading to lysis. Opsonisation and phagocytosis. Antibody dependent cell mediated cytotoxicity where NK cells bind to fc region and release toxic granules. Antibody mediated cellular dysfunction where antibody binds to receptor blocking it or activating it.

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24
Q

What is type 3 hypersensitivity?

A

Immune complex driven disease. Immune complexes cannot be efficiently cleared, immune complexes end up being deposited in the blood vessel walls and tissues, promoting inflammation and tissue damage.

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25
Q

How can type 3 hypersensitivity lead to tissue damage?

A

Activation of complement system (C3a,C4a,C5a) increase vascular permeability which can lead to oedema. Neutrophils can’t phagocytose complexes and so degranulate which can lead to vasculitis.

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26
Q

What class of disease involve type 3 hypersensitivity?

A

Auto immune disease.

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27
Q

What is type IV hypersensitivity?

A

Delayed type hypersensitivity involving T cells.

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28
Q

What is the first exposure to antigens in hypersensitivity called?

A

Sensitisation.

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29
Q

Difference between type II hypersensitivity and type III?

A

Type II involves antibodies binding to antigens on cell surfaces while type III involves antibodies binding to soluble molecules to form complexes. Type 2 inflammation occurs where antigen is present in the body while type 3 is where the antigen-antibody complexes are deposited. Type 2 small amount of complement is produced while type 3 lots of complement proteins are released. Levels of complement protein can be tracked to see progression of type 3 hypersensitivity.

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30
Q

Why is type IV delayed?

A

Memory T cell response is slightly slow. 48 -72 hours.

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31
Q

What causes contraction of pulmonary smooth muscle?

A

Leukotrienes and prostaglandins.

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32
Q

What are the rate limiting molecules in all hypersensitivity reaction?

A

Antigens.

33
Q

What are the characteristics of the infiltrate in a delayed hypersensitivity reaction?

A

An infiltrate composed of helper T cells and macrophages.

34
Q

What is a hapten? Give an example

A

A small molecule which on its own is not antigenic, but when associated with a large carrier such as a protein can form an antigen. Penicillin binding to surface antigen on red blood cells causing haemolysis.

35
Q

When is a coombs test done?

A

Autoimmune hemolytic anemia. Drug-induced immune hemolytic anemia.

36
Q

Describe and explain the coombs test?

A

Blood sample from patient is taken. Red cells from patient are washed to remove any unbound antibodies. Coombs reagent (anti human globulin) is added. If antibody is present on the surface of the red blood cells this results in agglutination.

37
Q

Limitations of genome wide association studies?

A

Can’t identify causal variants. Threshold for amount of genome you can check. Environmental influence (epigenetic).

38
Q

Benefits of genome wide association studies?

A

Identify at risk individuals.

39
Q

How can heritability be studied?

A

Comparing trait between two monozygotic twins. Comparing trait between two dizygotic twins. If trait is presented similar between identical twins and not similar between non identical then it is a heritable trait.

40
Q

What is a mendelian trait?

A

Trait controlled by single gene.

41
Q

What is a complex Trait?

A

Controlled by multiple genes + the effect of environment.

42
Q

What staining leaves a recognizable pattern of bands in chromosomes?

A

Giemsa staining.

43
Q

What is the p arm?

A

Short arm of chromosome.

44
Q

What is the q arm?

A

Long arm of chromosome.

45
Q

What do the dark areas (heterochromatin) on a karyotype mean?

A

Highly condensed, gene-poor, and transcriptionally silent,

46
Q

What do the light areas (euchromatin) on a karyotype mean?

A

Less condensed, gene-rich, and more easily transcribed

47
Q

What is aneuploidy?

A

Abnormal number of chromosomes (not a multiple of 23).

48
Q

What is non disjunction?

A

Uneven number of chromosomes in meiosis daughter cells. Results in +1 or -1 leading to trisomy and monosomy.

49
Q

Most common form of aneuploidy?

A

Sex chromosome aneuploidy.

50
Q

Why is sex chromosome aneuploidy better tolerated?

A

X chromosome inactivation of extra x chromosomes and low gene content of Y chromosome.

51
Q

Why if extra x chromosomes are inactivated does sex chromosome aneuploidy still have an effect?

A

Both X and Y chromosome have a pseudo autosomal region.

52
Q

How would you write the karyotype of an individual with trisomy 21?

A

47 +21 or 47,XX +21

53
Q

Why is maternal meiosis the main cause of trisomy 21?

A

As woman age the chromatids in the gametes they were born with become less organised. In males, sperm cell are continually generated.

54
Q

What is mosaicism?

A

Presence of two or more population of cells with different genotype.

55
Q

How can sex chromosome aneuploidy be an example of mosaicisim?

A

X chromosome becomes inactivated during early development.

56
Q

When does crossing over of chromatids occur?

A

Prophase I.

57
Q

What can unequal crossover of chromosomes lead to?

A

Duplication and deletion of genes.

58
Q

If there is an unequal crossover of chromosomes but it is balanced what can result?

A

Carrier not affected but offspring can be affected. Offspring can be normal, balanced carrier or unbalanced (affected).

59
Q

What does philadelphia chromosome lead to?

A

CML (Chronic myeloid leukemia).

60
Q

What is philadelphia chromosome?

A

Chromosome 9 and 22 break and exchange portions. Can occur as somatic mutation.

61
Q

What is a metacentric chromosome?

A

Short arm and long arm are the same length.

62
Q

What is a submetacentric chromosome?

A

Short arm is shorter than long arm.

63
Q

What is an acrocentric chromosome?

A

Short arm encodes no genes.

64
Q

What is a Robertsonian translocation?

A

Two acrocentric chromosomes form one chromosome.

65
Q

When does a Robertsonian translocation cause problems?

A

Can cause problems in offspring. Offspring can either be normal, balanced (carrier), unbalanced (affected).

66
Q

Type of pattern in autosomal dominant?

A

Vertical pattern.

67
Q

What are the ways that cause a certain disorder to be dominant?

A

Gain of function, dominant negative effect and insufficient.

68
Q

What is a gain of function mutation?

A

Gene now makes a protein with a new function.

69
Q

What is a dominant negative mutation?

A

The mutant form interferes with the activity of proteins it binds to.

70
Q

What is an insufficient mutation?

A

Mutant in one gene results in half the amount of protein which is not enough for normal function.

71
Q

What is the most common kind of mutation in autosomal dominant conditions?

A

Gain of function.

72
Q

What is the most common kind of mutation in autosomal recessive conditions?

A

Loss of function.

73
Q

Type of pattern in autosomal recessive?

A

Horizontal pattern.

74
Q

A man has an x linked recessive disorder, what will the genotype of the daughter be?

A

Carrier.

75
Q

What are the characteristics of y linked disorders?

A

Affects only males. All sons of affected father. Vertical degree of pattern.

76
Q

How are Mitochondrial disorder inherited?

A

All mitochondrial DNA is inherited from the mother. Children of affected father are never affected but from mother they may be affected. Vertical degree pattern.

77
Q

Mitochondrial disorders nature?

A

Multiple copies of genome; some normal, some mutant. If mutant genome is above a certain threshold then it is expressed.

78
Q

Mitochondrial disease variability?

A

Number of mutant mitochondria in cell. Develop with age due to accumulation of mutant mitochondria.

BRS/POM MOCKS (23 decks)

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