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Phase 1 > IMMS > Flashcards

IMMS Flashcards

1
Q

How many chromosomes are there in a normal somatic cell?

A

46

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2
Q

Male genotype

A

XY

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3
Q

How many H bonds between A and T

A

2

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4
Q

How many H bonds between C and G?

A

3

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5
Q

How is a chromosome condensed?

A

Coils around nucleosides, coils again to suprcoil

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6
Q

What is an ideogram?

A

Diagrammatic form chromosome bands

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7
Q

What are the 4 centromere locations

A

Metacentric, sub-metacentric, Acrocentric, telocentric

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8
Q

What happens in G1

A

rapid growth, cell organelles produced, proteins in spindle formation made, normal metabolic function

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9
Q

how many genes are there in humans

A

22000

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10
Q

what happens in S phase of cell cycle

A

DNA replicated to 4n, centrosome replication, histone production

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11
Q

what happens in G2

A

growth, chromosomes condense, energy stores accumulate, mitochondria and centrioles double

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12
Q

what happens to cells in G0

A

dont undergo mitosis

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13
Q

whats the purpose of mitosis

A

turn 1 parent cell to 2 daughter cells

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14
Q

whats the lifespan of RBC

A

120 days

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15
Q

what happens in prometaphase

A

nuclear membrane breaks down, microtubules invade nuclear space, chromatids attach to microtubules

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16
Q

what is a microtubule

A

largest cytoskeleton fibres found in cell made of tubulin

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17
Q

what is a chromatid

A

2 identical chromsomes joined by centromere

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18
Q

what happens in metaphase

A

chromosomes line up along metaphase plate

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19
Q

what happens in anaphase

A

sister chromatids separate and are pulled to opposite poles of cell, microtubules condense

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20
Q

what happens in telophase

A

nuclear membrane reforms, chromosome unfolds to chromatin, cytokinesis begins

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21
Q

what happens in cytokinesis

A

cell splits and 2 daughter cells made

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22
Q

what is the general principle of chemotherapy

A

blocks different phases of cell cycle

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23
Q

how can you tell a cell is undergoing mitosis histologically

A

dark nucleus as chromatin condensed to chromosomes and nuclei are different sizes

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24
Q

how can you distinguish a malignancy histologically

A

too many mitotic figures i.e. lots of dark nuclei of different sizes

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25
Q

where does meiosis occur

A

gametes

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26
Q

when does crossing over occur

A

prophase 1

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27
Q

what happens in meisosis 1

A

Chromosome number halved

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28
Q

what happens in prophase 1

A

crossing over occurs at chiasma; between non-sister chromatids  diversity

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29
Q

what happens in metaphase 1

A

independent assortment

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30
Q

what is Mendel’s 2nd law of independent assortment

A

alleles of 1 gene sort into gametes independently of the alleles of another gene

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31
Q

what happens in meiosis 2

A

sister chromatids separate, haploid cells produced

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32
Q

sperm production basic pathway

A

Primordial germ cells -> lots of mitoses -> spermatogonia

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33
Q

what are spermatogonia

A

basic gametes

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34
Q

how are primary spermatocytes made

A

mitosis in embryonic stages

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35
Q

when do meiotic divisions in sperm production start

A

puberty

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36
Q

what happens in puberty in sperm production

A

cytoplasm divides evenly to form 4 equal gametes after meiosis II

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37
Q

how long does it take to make mature sperm

A

60-65 days

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38
Q

what is the basic pathway for egg production

A

primordial germ cell forms 30 mitoses forms oogonia

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39
Q

what is an oogonia

A

basic gamete

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40
Q

what happens to oogonia

A

enter prophase of meiosis I by 8th month of intrauterine life

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41
Q

what happens to oogonia in ovulation

A

cytoplasm divides unequally to form 1 egg and 3 polar bodies

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42
Q

what happens to polar bodies from egg production

A

apoptose

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43
Q

when is meiosis I completed in egg production

A

ovulation

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44
Q

when is meiosis II completed in egg production

A

if fertilisation occurs

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45
Q

what is non-disjuncture

A

Failure of chromosome pairs to separate in meiosis 1 or sister chromatids to separate properly in meiosis II

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46
Q

what is Down’s syndrome

A

regular trisomy 21

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47
Q

what is Turners syndrome

A

loss of 1 x chromosome

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48
Q

what is the general name for loss of 1 chromosome

A

monosomy

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49
Q

what is reciprocal translocation

A

swapped between 2 different chromosomes

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50
Q

what is Robertsonian translocation

A

2 chromosomes join

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51
Q

what is gonadal mosaicism

A

When precursors germline cells to ova/ spermatozoa are a mix of 2 or more genetically different cell lines

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52
Q

what increases risk of gonadal mosaicism

A

advancing paternal age

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53
Q

what genetic patterns are most commonly associated with gonadal mosaicism

A

autosomal dominant and X linked disorders

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54
Q

genotype

A

genetic constitution of an individual

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55
Q

Phenotype

A

appearance of individual which results from the interaction of environment and phenotype

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56
Q

multifactorial condition

A

disease that are due to combination of genetic and environmental factors

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57
Q

allele

A

one of several alternative forms of a gene at a specific locus

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58
Q

functional type allele

A

normal allele/ wild type

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59
Q

pathogenic allele

A

disease allele carrying pathogenic variant

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60
Q

polymorphism

A

frequent hereditary variation at a locus

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61
Q

polyploidy

A

the state in which an organism/ cell has more than 2 paired (homologous) sets of chromosomes

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62
Q

penetrance

A

proportion of individuals with a specific genotype showing the expected phenotype

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63
Q

complete penetrance

A

gene/ genes for trait are expressed in all the population

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64
Q

incomplete penetrance

A

genetic trait is only expressed in parts of population

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65
Q

expressivity

A

range of phenotypes expressed by a specific genotype

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66
Q

variable expression

A

variation in clinical features (type and severity) of genetic disorder between individuals with the same gene alteration

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67
Q

sex linked/ limited

A

condition inherited in autosomal dominant pattern that seems to affect 1 sex more than the other e.g. BRCA

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68
Q

somatic mosaicism

A

genetic fault present in only some tissues in the body

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69
Q

gonadal mosaicism

A

genetic fault present in gonadal tissue - not detected in genetic test

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70
Q

consanguinity

A

reproductive union beyween 2 relatives

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71
Q

Autozygosity

A

homozygous by descent i.e. inheritance of the same mutant allele through 2 branches of the same family

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72
Q

sex-limitation

A

expression of a characteristic limited to one of the sexes

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73
Q

karyotype

A

number and appearance of chromosomes in a cell

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74
Q

aneuploidy

A

presence of abnormal number of chromosomes in a cell

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75
Q

autosome

A

any chromosome other than sex chromosome

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76
Q

allelic hetrogeneity

A

where different mutations within the same gene result in the same clinical condition

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77
Q

locus hetrogeneity

A

variants in different genes give the same clinical condition

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78
Q

anticipation

A

whereby genetic disorders affect successive generations earlier or more severely - usually due to expansion of unstable triplet repeat series

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79
Q

predictive testing

A

testing for a condition in pre-symptomatic individual to predict their chance of developing the condition

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80
Q

imprinting

A

epigenetic phenomenon that causes genes to be expressed in parent-of-origin manner; non-mendelian - each gene has 2 alleles, requires equal contribution for most alleles but some only require contribution from specific parent e.g. Prader Willi = deletion of paternal gene

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81
Q

late-onset

A

condition not manifested at birth

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82
Q

congenital

A

disease manifested at birth

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83
Q

heritability

A

proportion of the aetiology that can be ascribed to genetic factors as opposed to environmental factors

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84
Q

prevalence

A

total number in population who have the disease

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85
Q

incidence

A

number of new cases per year in population who don’t have the disease

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86
Q

genetic counselling

A

process by which patients/ relatives at risk of a disorder that may be hereditary are advised of the consequences of the disorder, the probability of developing/ transmitting it and the wats it may be prevented or ameliorated

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87
Q

methods of genetic testing in pregnancy

A

chorionic villus sampling or amniocentesis

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88
Q

types of mendelian inheritance

A

autosomal dominant, autosomal recessive, x-linked

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89
Q

non-traditional inheritance

A

mitochondrial, imprinting, mosaicism

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90
Q

autosomal dominant definition and example

A

disease manifests in heterozygous state, Huntington’s

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91
Q

autosomal recessive definition and example

A

disease manifests in homozygous state e.g. CF, sickle cell

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92
Q

x linked definition and example

A

caused by pathogenic variants in genes on X chromosomes, Duchenne’s and haemophilia

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93
Q

what shape is male on family tree

A

square

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94
Q

what shape is female on family tree

A

circle

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95
Q

what does a diamond on a family tree mean

A

unspecified gender

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96
Q

what does a half shaded shape on a family tree mean

A

autosomal carrier

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97
Q

what does a circle with a dot in it mean on a family tree

A

x linked carrier

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98
Q

what does a double line between 2 people on a family tree mean

A

consanguineous marriage

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99
Q

what does a dotted line on a family tree mean

A

extramarital union

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100
Q

what do square brackets around someone mean on a family tree

A

adopted

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101
Q

what does a downwards line connecting to a black circle mean on a family tree

A

still birth or abortion

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102
Q

what does an arrow pointing to the bottom left of a shape mean on a family tree

A

person of reference

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103
Q

what do diagonal lines connecting 2 children with a single point of origin mean on a family tree

A

dizygotic (fraternal) twins

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104
Q

what do diagonal lines connecting 2 children with a single point of origin and with a line between the 2 children (making a triangle) mean on a family tree

A

monozygotic (identical) twins

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105
Q

autosomal recessive characteristics

A
  • Males and females equally affected
  • Affected individuals in single generation
  • Parents can be related i.e. consanguineous
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106
Q

risk to offspring with carrier parents autosomal recessive

A

1 in 4 risk

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107
Q

odds of healthy children being carriers for autosomal recessive disorder if parents are carriers

A

2 in 3

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108
Q

prevelance of CF

A

1 in 2500

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109
Q

odds of being a CF carrier

A

1 in 25

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110
Q

cause of CF

A

CFTR gene on 7q31.2

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111
Q

autosomal dominant inheritance main characteristic

A
  • Disease manifests in heterozygous state
  • Males and females equally affected
  • Affected individuals in multiple generations
  • Transmission by individuals of both sexes to both sexes
  • ONLY WAY TO HAVE MALE TO MALE INHERITANCE
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112
Q

examples of autosomal dominant inheritance

A

Huntington’s, Marfan’s, Polycystic kidney disease

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113
Q

3 reasons for unaffected parents having affected children with autosomal dominant condition

A
  1. Don’t have gene for it (mutation in child)
  2. Gonadal mosaicism
  3. Mother has reduced penetrance or variable expression
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114
Q

x linked inheritance characteristics

A
  • Usually only males affected
  • Transmitted through unaffected females
  • No male-to-male transmission
  • Affected male cannot have affected son, but all his daughters will be carriers
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115
Q

outcome for carrier female and unaffected male with x linked conditions

A

 ¼ having affected son

 ¼ having carrier daughter

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116
Q

outcomes for affected male and homozygous normal female with x linked condition inheritance

A

all daughters are carriers, sons not at risk

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117
Q

what is lyonization

A

inactivation of an x chromosome

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118
Q

when does deactivation of x chromosome occur in lyonization

A

early embryonic development

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119
Q

why does lyonization occur

A

prevent females having twice as many gene products from X chromosomes as male

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120
Q

what is a barrbody

A

inactive X chromosome since package in heterochromatin and so can’t be transcribed

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121
Q

what causes mitochondrial disease

A

mtDNA inherited from mother

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122
Q

what processes do mitochondrial diseases affect

A

energy heavy processes e.g. muscle, nervous, vision

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123
Q

what is homoplasmy

A

eukaryotic cells whose copies of mtDNA are all identical

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124
Q

what is heteroplasmy

A

multiple copies of mtDNA in each cell

o Level of Heteroplasmy can vary between cells in same tissue/ organ/ person/ individuals

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125
Q

trisomy 21 name

A

Downs

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126
Q

trisomy 18 name

A

Edwards

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127
Q

trisomy 13 name

A

Patau

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128
Q

47, XXY name

A

Kleinfelter

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129
Q

Downs cause

A

trisomy 21

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130
Q

Edwards syndrome

A

trisomy 18

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131
Q

Patau syndrome casuse

A

trisomy 13

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132
Q

Kleinfelters karyotype

A

47, XXY

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133
Q

when do constitutional abnormalities occur and what do they affect

A

gametogenesis, affect all cells of body so heritable

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134
Q

when do acquired abnormalities occur and what do they affet

A

during life, restricted to malignant tissue and non heritable

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135
Q

gain of function mutations

A

1 mutation

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136
Q

loss of function mutation

A

2 mutations; inheritance of 2 copies - to loose function both copies must be defective

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137
Q

Knudson’s 2 hit hypothesis

A
  • Gene mutations may be either inherited or acquired during a person’s life
  • Sporadic cancers = 2 acquired mutations
  • Hereditary cancers = 1 inherited mutation and 1 acquired mutation
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138
Q

3 causes of disease

A

genetic, multifactorial, environmental

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139
Q

F.I.S.H.

A
  • Fluorescence in situ hybridisation
  • Use DNA probes labelled with fluorophores – target specific regions of DNA
  • Are hybridised directly to the chromosome
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140
Q

Relative risk

A

risk of having disease compared to someone who doesn’t have the genotype

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141
Q

relative risk of 1

A

no increased risk

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142
Q

nucleotide definition

A

building block to make new DNA

o Free phosphate groups provide energy for reaction

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143
Q

DNA structure

A
  • Double helix; due to v.d.w. forces
  • DNA coils around histones (chromatin complex) and forms nucleosomes  supercoils  chromosomes
  • Double stranded, phosphodiester bonds
  • Anti-parallel strands with H bonds between complementary bp
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144
Q

functions of DNA

A

emplate and regulator for transcription/ protein synthesis

o Genetic material; structural basis of hereditary and genetic disease

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145
Q

describe the DNA code

A

degenerate but unambiguous, universal, non-overlapping without punctuation

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146
Q

describe RNA structure

A

single strand, uracil not thymine

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147
Q

describe mRNA function and structure

A

Accumulates following cell stimulation
Prints a long linear transcript; processing removes introns
o Has 5’CAP and 3’ PolyA tail

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148
Q

what does Poly-A tail on RNA do

A

stops RNA being broken down by stopping enzyme degradation

• Added to mRNA which facilitates nuclear export of RNA and translation

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149
Q

what does rRNA do

A

combines with proteins -> 80S ribosomes; abundant in cytoplasm

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150
Q

what does tRNA do

A

carries AA to ribosomes; checks incorporated in correct position

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151
Q

start codons

A

AUG

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152
Q

stop codons

A

UAG, UGA, UAA

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153
Q

what does topoisomerase do

A

relives supercoiling by breaking phosphodiester bonds and re joining them

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154
Q

what does helicase do

A

breaks H bonds

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155
Q

what do SSB proteins do

A

hold strands open and prevents reannealing so remain single stranded

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156
Q

where is new DNA made

A

behind the replication fork

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157
Q

describe the process of DNA replication

A

Topoisomerase, helicase, ssb proteins open DNA, primer binds, base sequence copied into complimentary daughter strand

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158
Q

what is primase

A

RNA polymerase that synthesis short RNA primers needed to start replication process

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159
Q

what does RNAs H do

A

removes the RNA primers that previously began DNA synthesis

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160
Q

what direction does DNA polymerase print

A

5 to 3

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161
Q

what direction does dna polymerase read

A

3 to 5

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162
Q

why does dna polymerase print 5 to 3

A

phosphate at 5 acts as energy source

163
Q

what is the substrate for dna polymerase

A

deoxyribonucleoside triphosphates

164
Q

what does DNA primase do

A

Joins adjacent nucleotides together via a phosphodiester bond in 5’ 3’ direction
o Enzyme remains on strand and at same time extends and proof reads
o Starts at primer

165
Q

what is a primer

A

short strand of DNA that is the start point for DNA synthesis

166
Q

what do ligase enzymes do

A

joins short DNA pieces (Okazaki fragments) to form 1 continuous strand

167
Q

what are Okazaki fragments

A

short DNA pieces

168
Q

where do TF bind

A

specific sequence on 5’ of 1st exon (promoter region)

169
Q

what are transcription factors

A

proteins which bind to promoter regions

170
Q

describe transcription

A
  • TF bind to promoter region
  • Transcription complexes form (around TATA box)
  • Topoisomerase relieves supercoiling
  • DNA helicase breaks H bonds  DNA separates
  • SSB’s coat single strand to prevent re-annealing
  • Free mRNA nucleotides line up next to complementary bases on template/ antisense strand
  • RNA polymerase 2 binds to DNA at specific sites adjacent to promoter sequence
  • Forms pre-mRNA; attaches free ribonucleotides bases together
171
Q

describe the journey of mRNA

A

moves through pores to cytoplasm to ribosome and attaches to 80s ribosome

172
Q

how are AAs attached to tRNA

A

covalent bonds at 3’ end

173
Q

what enzyme attaches AA to tRNA

A

aminoacyl-tRNA synthetase

174
Q

how does translation occur

A
  • tRNA molecule anticodon is complementary to specific codon on mRNA
  • Initiation; methionine (AUG) starts polypeptide chain
  • Elongated by successive addition of AA forming peptide bonds; condensation reaction
  • Terminates at sequence (UGA, UAG, UAA)
175
Q

what is nonsense mediated decay

A
  • Surveillance mechanism; eliminates mRNA transcripts that contain premature stop codons
176
Q

how are genes silenced

A

genes are in heterochromatin (H for hiding) so no transcription can occur

177
Q

what state do genes need to be to be transcribed

A

euchromatin

178
Q

mis sense variant

A

SNP changes AA in portein

179
Q

sickle cell gene change

A

SNP CAG to CTG

180
Q

non-sense variant

A

SNP creates premature stop codon

181
Q

what does SNP stand for

A

single nucleotide polymorphism

182
Q

types of deletion mutations

A

in frame and out of frame

183
Q

what is an in frame mutation and what does it do

A

deletes multiples of 3 and doesn’t alter gene sequence so may or may not affect protein

184
Q

what is an out of frame mutation and what does it do

A

non-multiple of 3; causes frameshift so more likely to cause damage

185
Q

what can happen in a splice site mutation

A

o Can cause disease as mutation at splice junction mean section isn’t spliced out
 Introns not accurately removed  non-functioning protein

186
Q

give an example of a disease caused by expansion of tri-nucleotide repeat

A

Huntingtons, CAG

187
Q

gene for Huntington’s

A

> 36 CAG repeats

188
Q

anticipation definition

A

tri nucleotide repeats get bigger when transmitted to next generation  earlier symptoms of greater severity

189
Q

aim of PCR

A

synthesise DNA fragments; basis for forensic testing

190
Q

respiration definition

A

oxidation of fuels to generate ATP

191
Q

fed state definition

A

period in which digestion and absorption of nutrients occurs

192
Q

metabolism definition

A

sequence of chemical reactions: a particular molecule is converted into some other molecule(s) in a defined fashion

193
Q

anabolic definition and use

A

synthesis of large molecules from smaller components

o Storage and biosynthesis

194
Q

catabolic definition and use

A

break larger molecules into smaller ones

o Usually with release of energy

195
Q

4 main pathways of dietary metabolism

A

biosynthesis, fuel storage, waste disposal, oxidative process

196
Q

anabolic metabolic processes example

A

biosynthesis and fuel storage

197
Q

catabolic metabolic process example

A

oxidative process

198
Q

example of a process that can be both anabolic and catabolic

A

waste disposal

199
Q

energy from carbohydrate

A

4kcal/ g

200
Q

energy storage of carbohydrate

A

glycogen;
200g in liver
150g in muscles

201
Q

energy from lipids

A

9kcal/ g

202
Q

energy storage of lipids

A

TG in adipose tissue; 15kg

203
Q

energy from proteins

A

4kcal/ g

204
Q

AA need

A

0.8g/kg/day

205
Q

energy storage of protein

A

6kg in muscles

206
Q

energy from alcohol

A

7kcal/ g

207
Q

BMR meaning

A

basal metabolic rate

208
Q

BMR definition

A
  • Measure if energy required to maintain non-exercise bodily functions
  • Energy needed to stay alive at rest
209
Q

BMR equation

A
  • 1kcal/kg body mass/ hour
210
Q

factors that cause decreased BMR

A

age, gender, dieting/ starvation, hypothyroidism, decreased muscle mass

211
Q

factors that increase BMR

A

weight, hyperthyroidism, low ambient temperature, fever/ infection/ chronic disease, caffeine/ stimulant, exercise

212
Q

DEE meaning

A

daily energy expenditure

213
Q

DEE definition

A
  • Energy to support BMR and physical activity and diet induced thermogenesis
214
Q

diet induced thermogenesis definition

A

energy required to process the food we eat

215
Q

how much glucose does the brain require per day

A

150g

216
Q

how much glucose is eft in the liver after an overnight fast

A

80g

217
Q

what mechanism does the body rely on during an overnight fast

A

glycogenolysis

218
Q

what happens in a fast lasting 2-4 days

A

o Insulin decreases, cortisol increases – lipolysis and proteolysis
Gluconeogenesis uses Lactate, amino acids (muscle, intestine, skin), glycerol (fat breakdown)

219
Q

what happens in a fast lasting more than 4 days

A

liver produces ketones from fatty acids

220
Q

malnutrition definition

A

state of nutrition with a deficiency, excess or imbalance of energy, protein or other nutrients causing measurable adverse effects

221
Q

what happens in re-feeding syndrome

A

insulin secretion decreases in food deprivation
insulin secretion increases when shifts back from fat to carbohydrate metabolism; phosphate and potassium needed to convert glucose to energy
re distribution of ions and electrolytes can be fatal

222
Q

how much sodium is allowed per day in prudent diet

A

2.4g = 6g

223
Q

what enzyme is used in the ATP/ ADP cycle

A

ATPase

224
Q

what happens when adenine attaches to ribose

A

forms adenosine

225
Q

how is amp formed

A

when 2nd phosphohydride bond in ATP (i.e. ADP) is hydrolysed

226
Q

nucleoside definition

A

sugar + base

227
Q

nucleotide definition

A

sugar + base + phosphate

228
Q

methods of ATP regeneration

A

glycolysis, krebs, oxidative phosphorylation, substrate level phosphorylation, electron transport cjain

229
Q

where is glucose oxidised

A

cytosol of cell

230
Q

equation for glycolysis

A

Glucose + 2ADP +2Pi +2NAD+  2 pyruvate + 2ATP + 2NADH + 2H+ + 2H20

231
Q

what regulates glycolysis rate

A

[ATP]/ [AMP] and insulin/ glucagon

232
Q

what does AMP stand for

A

adenosine monophosphate

233
Q

what is the rate limiting enzyme in glycolysis

A

phosphofructokinase-1 (PFK-1)

234
Q

what does phosphofructokinase-1 do

A

Converts fructose-6-phosphate  fructose-1, 6-biphosphate

235
Q

what are the functions of glycolysis

A 
o	Provides ATP
o	Generates precursor for biosynthesis
	Pyruvate transaminated to alanine
	Pyruvate substrate for FA synthesis
	Glycerol-3-P (G3P) = backbone of triglycerides
236
Q

what are the intermediates from glycolysis converted to

A

Ribose 5-P (nucleotides)

AA; serine, glycine, valine

237
Q

what happens to pyruvate in aerobic conditions

A

enters Krebs cycle

238
Q

what happens to pyruvate in anaerobic conditions

A

converted to lactate then back to pyruvate or precursor for gluconeogenesis

239
Q

what enzyme is used for conversion of glucose to lactatw

A

lactate dehydrogenase

240
Q

equation for conversion of glucose to lactate

A

Glucose + 2ADP + 2Pi  2 lactate + 2ATP + 2H20 + 2H+

241
Q

what happens if [H+] and [lactate] increase

A

pH decreases and ACIDOSIS occurs

242
Q

equation that PFK-1 catalyses

A

Fructose -6-phosphate + ATP  fructose-1, 6-biphosphate + ADP

243
Q

what does fructose-2, 6 bisphosphate do

A

allosterically activates PF1! and increases rate of glycolysis and thus fructose-1, 6 bisphosphate production

244
Q

what happens in fed state (regarding PFK1)

A

high insulin levels mean more fructose-2, 6-bisphosphate produced so increased PFKa activation so higher rate of glycolysis so glucose sequestered from blood more efficiently so prevents hyperglycaemia

245
Q

what happens in fasting state (regarding PFK1)

A

high glucagon levels so decreased fructose2, 6-bisphosphate production so less PFK1 production so glycolysis pathway less efficient so blood glucose concentration maintained

246
Q

what allosterically inhibits PFK1

A

citrate/ other ions

247
Q

what is AMP regarding PFK1

A

allosteric activator so increases PFK1 affinity for fructose-6-phosphate

248
Q

what does ATP do regarding PFK1

A

allosteric inhibitor so glycolysis inhibited

249
Q

what does acidosis do to glycolysis

A

inhibits it

250
Q

where does TCA cycle occur

A

mitochondrial matrix

251
Q

what is the rate limiting enzyme of the TCA cycle

A

isocitrate dehydrogenase

252
Q

what does ADP do to ICDH

A

allosteric activator

253
Q

what does NADH do to ICDH

A

allosteric inhibitor

254
Q

where does oxidative phosphorylation occur

A

inner membrane of mitochondria

255
Q

total ATP made from 1 glucose molecule

A

34-38

256
Q

how many ATP does NADH produce

A

2.5

257
Q

how many ATP does FADH2 produce

A

1.5

258
Q

what are essential fatty acids

A

FA that can’t be synthesised de novo; need to be consumed in diet

259
Q

what is acyl adenylate composed of

A

fatty acid and adenosine

260
Q

where are FA activated and then what happens

A

activated in cytoplasm before oxidised in mitochondrion

261
Q

what is the largest acyl-CoA carbon chain that can diffuse through mitochondrial membrane

A

12C

262
Q

what happens if acyl-coa is >14C

A

taken through mitochondrial membrane through carnitine shuttle

263
Q

is fatty acid b oxidation aerobic or anaerobic

A

aerobic

264
Q

is fatty acid b oxidation anabolic or catabolic

A

catabolic

265
Q

what enzyme oxidises acyl coa

A

acyl coa dehydrogenase

266
Q

what is produced in 1 round of FA B oxidation

A

1 NADH, 1 FADH2, 1 Acetyl CoA

267
Q

what happens if acetyl coa produced exceeds limit of TCA cycle

A

used in ketogenesis in the liver

268
Q

where is acetyl coa from FA B oxidation used

A

krebs cycle

269
Q

where are NADH/ FADH2 from FA B oxidation used

A

oxidative phosphorylation

270
Q

why can’t FA act as energy source for nervous system

A

can’t cross BBB

271
Q

what are ketones

A

molecules produced by liver from acetyl coa

272
Q

where are ketone bodies synthesised

A

mitochondrial matrix

273
Q

what are ketone bodies synthesised from

A

acetyl coa generated in b oxidation

274
Q

what enzyme converts acetyl coa to Acetoacetyl coa

A

thiolase enzyme

275
Q

who gets ketoacidosis

A

insulin dependent diabetics whose dose is inadequate/ have increased insulin requirements

276
Q

why do diabetics get ketoacidosis

A

o Insulin down-regulates ketone production

277
Q

what is the presentation of ketoacidosis

A

hyperventilation and vomiting

278
Q

what happens in ketoacidosis

A

excessive ketones lower the pH of blood

279
Q

aliphatic definition

A

carbon structures that don’t contain ring

280
Q

aromatic definition

A

carbon compounds that contain benzene ring/ similar

281
Q

what does ‘native conformation’ mean

A

every molecule of the same protein folds into the same stable 3D structure

282
Q

disaccharide definition

A

2 MS joined by glycosidic bond

283
Q

oligosaccharide definition and production

A

3-12 MS joined by glycosidic bond;

o Products of digestion of polysaccharides

284
Q

polysaccharides definition

A

multiple MS joined by glycosidic bond

285
Q

what do spingolipids form

A

cell membrane of brain and nervous system

286
Q

what shape are steroids and what are they derived from

A

cylindrical, cholesterol

287
Q

what are eicosanoids derived from and what are they metabolised to

A

derived from eicosanoid acid, metabolised to prostaglandins

288
Q

which is ‘good’ cholesterol

A

HDLP

289
Q

what is ‘bad’ cholesterol

A

LDLP

290
Q

why is LDLP bad

A

o Risk to CVD and atherosclerosis; can transport content into artery walls and attract macrophages

291
Q

what affects the charge of an amino acid

A

r group

292
Q

what affects the polarity of an aa

A

r group

293
Q

what charge does the carboxyl group on an aa have

A

negative

294
Q

what charge does the amino group on an aa have

A

positive

295
Q

what form are most natural aa found in

A

l form

296
Q

how are peptide bonds formed

A

condensation reaction

297
Q

what enzyme cleaves peptide bonds

A

proteolytic enzymes

298
Q

what determines folding in aa

A

charged interactions, flexibility, physical dimensions

299
Q

Supersecondary structure examples

A

 Helix-turn-helix
 β- barrel
 Leucine zipper
 Zinc zipper

300
Q

isoenzyme definition

A

have different structure/ sequence but catalyse the same reaction

301
Q

allosteric site definition

A

location other than the active site

302
Q

co-enzyme definition

A

complex nonprotein organic molecules that help maximise an enzymes active site

303
Q

what do activation-transfer coenzymes do

A

form a covalent bond and are regenerated at end of reaction

304
Q

what do oxidation-reduction coenzymes do

A

used in reactions where e- are transferred from 1 compound to another

305
Q

where is myoglobin found

A

muscles

306
Q

what does myoglobin do

A

erves as reserve supply of oxygen; also facilitates movement of O2 in muscles

307
Q

how are haemogolobin and myoglobin related

A

structurally related proteins with some common elements; same tertiary structure
o Core of both molecules = porphyrin ring; holds an iron atom

308
Q

VDW force definition

A

o Weak electrostatic attraction between atoms due to fluctuating electrical charges
o Only important when 2 macromolecular surfaces fit closely in shape

309
Q

what level of structure(s) are VDW forces found

A

all

310
Q

H-bond definition

A

strongest vdw forced, Interaction between polar groups

311
Q

what level of structure(s) are h bonds found

A

secondary

312
Q

how are hydrophobic forces formed

A

o As uncharged and non-polar side chains are repelled by water, hydrophobic side chains tend to form tightly packed cores in the interior of proteins, EXCLUSING WATER MOLECULES

313
Q

what level of structure(s) are hydrophobic forces found

A

3/4

314
Q

what level of structure(s) are ionic bonds found

A

3/4

315
Q

ionic bond formation

A

o Occur between fully or partially charged groups

316
Q

what happens to ionic bonds in aqueous systems

A

weakened by shielding by water molecules and other ions in solution

317
Q

what type of bond are disulphide bonds

A

covalent

318
Q

where are disulphide bonds found

A

between cysteine residues

319
Q

what level of structure(s) are disulphide bridges found

A

3/4

320
Q

homeostasis definition

A

maintenance of a constant internal environment

321
Q

autocrine definition

A

cell signals with itself via extracellular fluid

322
Q

paracrine definition

A

cell signals with adjacent cells via extracellular fluid

323
Q

how do paracrine signals get transmitted

A

o Signal diffuses across gap between cells
o Inactivated locally, so doesn’t enter bloodstream
o Immobilised by matrix structure of interstitial fluid
o Activated by enzymes in interstitial fluid
 e.g. ACh at neuromuscular junction

324
Q

endocrine definition

A

cell signals with cells elsewhere in body via the blood

325
Q

exocrine definition

A

secreted into ducts then organs

326
Q

endocrine v paracrine

A

o Endocrine; hormines travel in blood
o Paracrine; chemical messengers only travel in extracellular fluid
o Endocrine affects more things and travels further

327
Q

features of positive feedback

A

signal amplification; is exponential

328
Q

positive feedback examples

A

clotting cascade, oxytocin release in childbirth

329
Q

negative feedback general mechanism

A

o Products inhibit production

330
Q

pituitary thyroid axis mechanism

A

 TSH travels through blood from anterior pituitary  thyroid; produces thyroxine which travels in blood  target cell
 Thyroxine inhibits secretion of TSH by anterior pituitary

331
Q

primary hyperthyroidism

A

problem with endocrine gland e.g. thyroid

332
Q

secondary hyperthyroidism

A

problem with pituitary or hypothalamus e.g. 2ndary hypothyroidism; both TSH and thyroixine levels are low; pituitary not producing enough TSH

333
Q

hormone definition

A
  • Molecules that act as chemical messengers
334
Q

peptide hormone examples

A

insulin, growth hormones, TSH (made in pituitary)

335
Q

peptide hormone structure

A
  • Made of short chain amino acids
    o Size varies
    o Some have COH side chains  glycoproteins
336
Q

properties of peptide hormones

A

Hydrophilic – so can dissolve in water;
o Large, hydrophilic, charged; can’t diffuse across a membrane
 Bind to receptors on membrane
- Binds to extracellular receptors  chemical reaction  quick response from cell
o 2nd messenger released into cell = very fast;
o Signal transduction cascade

337
Q

what are amino acid hormones synthesised from

A

tyrosine

338
Q

examples of amino acid hormones

A

adrenaline and thyroid hormones

339
Q

steroid hormone examples

A

testosterone, oestrogen, cortisol

340
Q

steroid hormone response rate

A

slow

341
Q

what are steroid hormones made from

A

cholesterol

342
Q

properties of steroid hormones; solubility

A
  • Can’t dissolve in water but can dissolve in lipids

o Must bind to transport protein to move in blood

343
Q

what do steroid hormones target

A

intracellular receptors; made by cell and then diffuse out - not stored

344
Q

amount of water in average 70kg male

A

42L

345
Q

weight of ‘average man’ used

A

70kg

346
Q

intercellular fluid distribution

A

28L (40% of bodyweight, 66% of water)

347
Q

extracellular fluid distribution

A

14L (20% bw)

348
Q

2 components of extracellular fluid

A

intravascular and interstitial fluid

349
Q

intravascular fluid distribution

A

3L, 6% of water

350
Q

intravascular fluid example

A

plasma

351
Q

interstitial fluid distribution

A

11L, 26% of water

352
Q

what does interstitial fluid do

A

surrounds cells but doesn’t circulate

353
Q

permeability of water through ICF and ECF

A

freely permeable

354
Q

main contributor to ECF osmolality and volumes

A

sodium

355
Q

ECF osmotic contents

A

sodium, chloride and bicarbonate, glucose and urea, protein

356
Q

what does protein do in ECF

A

colloid osmotic pressure - stays in intravascular fluid and exerts fluid pulling water into intervascular space

357
Q

ICF cations

A

potassium

358
Q

cell cation/ anion distribution v intracellular space

A

 Cells have high intracellular potassium and low intracellular sodium; reverse of intracellular space

359
Q

examples of insensible water losses

A

sweat, breath, vomiting, faeces

360
Q

osmolality definition

A

concentration of a solution expressed as no. of solute per kg of fluid

361
Q

osmolality of pure water and of intra/ extracellular fluid

A

0 and equal

362
Q

osmolarity definition

A

concentration of solution expressed as no. of solute particles per L of fluid

363
Q

osmotic pressure definition

A

pressure that would have been applied to a pure solvent to prevent it from passing into a given solution by osmosis
o Often used to express the concentration of the solution

364
Q

oncotic pressure definition

A

orm of osmotic pressure exerted by proteins in blood vessel plasma that usually tends to pull water into the circulatory system
o Opposing force to hydrostatic pressure

365
Q

hydrostatic pressure definition

A

pressure difference between capillary blood (plasma) and interstitial fluid
o Water and solutes move from plasma into interstitial fluid

366
Q

what happens in increased ECF osmolality

A

o Osmoreceptors detect an increase in osmolality
o ADH released from posterior pituitary to increase water retention
 Increased permeability of DCT
 Small volume of highly concentrated urine produced
o Water moves from ICF  ECF
o Stimulation of thirst centres in hypothalamus to increase water uptake

367
Q

what happens in decreased ECF volume

A

RAAS system activation

368
Q

where is albumin produced

A

liver

369
Q

where is angiontensinogen produced

A

liver

370
Q

where is angiotensin 1 produced

A

from angiotensinogen

371
Q

where is angiotensin 2 produced

A

from angiotensin 1

372
Q

where is renij produced

A

kidney; juxtaglomerular cells

373
Q

where is aldosterone produced

A

adrenal cortex

374
Q

where is ADH formed

A

hypothalamus but released from posterior pituitary gland

375
Q

ADH other name

A

vasopressin

376
Q

what causes the release/ production of albumin

A

common plasma protein

377
Q

what causes the release/ production of angiotensinogen

A

always there

378
Q

what causes the release/ production of angiostensin 1

A

presence of renin

379
Q

what causes the release/ production of angiotensin 2

A

ACE

380
Q

what causes the release/ production of renin

A

low sodium concentration and low bp in macula densa cells

381
Q

where does albumin act

A

blood

382
Q

where does angiotensin 2 act

A

Adrenal gland cortex, posterior lobe of the pituitary gland, arterioles, hypothalamus

383
Q

where does renin act

A

released into blood

384
Q

where does aldosterone act

A

collecting ducts

385
Q

where does ADH act

A

collecting ducts

386
Q

what does albumin do

A

generate oncotic pressure

387
Q

what does angiotensinogen do

A

acts as substrate to turn into 1

388
Q

what does angiotensin 1 do

A

precursor for 2

389
Q

what does angiotensin 2 do

A

Increases aldosterone secretion. increased ADH secretion, constriction of arterioles activates the thirst centres, increases sympathetic activity, increased Na+ reabsorption

390
Q

what does renin do

A

breaks angiotensinogen to angiotensin 1

391
Q

what does aldosterone do

A

Stimulate sodium reabsorption by making more Na+/K+ pumps

392
Q

what does ADH do

A

Stimulates vesicles with aquaporins

393
Q

what happens in water excess

A

o Decreased ECF osmolality
 Movement of water  ICF
 No stimulation of thirst centre in hypothalamus
 Inhibition of ADH frpm [posterior pituitary so uincreased urine volume

394
Q

what are the consequences of water excess

A 
	Hyponatraemia
	Cerebral overhydration;
•	Headache
•	Confusion
•	Convulsions
	Volume overload
•	ECF volume expansion
o	Heart/ kindye failure and cirrhosis with ascites 
•	Renal sodium retention
•	Oedema
•	Serous effusion
395
Q

oedema definition

A

excess accumulation of fluid in interstitial space

396
Q

serous effusion definition

A

excess water in body cavity

397
Q

types of serous effusion/ oedema

A

inflammatory, venous, lymphatic, hypoalbuminemia

398
Q

inflammatory oedema

A

albumin leaves capillary and doesn’t re-enter

 Inflammation increases permeability so proteins leak into interstitial fluid

399
Q

venous oedema

A

very high hydrostatic pressure at venous end

 Water not reabsorbed

400
Q

lymphatic oedema

A

diseased lymph nodes leads to impaired water reabsorption to lymph nodes
 Low capacity; takes time to build up

401
Q

hypoalbuminic oedema

A

low albumin in plasma

 e.g. malnutrition, liver disease leads to low oncotic pressure

402
Q

normal capacity of pleural space

A

10mL of fluid

403
Q

transudate pleural effusion

A

= fluid pushed through capillary due to high pressure within the capillary

404
Q

exudate pleural effusion

A

fluid that leaks around cells of capillaries caused by inflammation and increasing permeability of pleural capillaries to proteins

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