formative summary revision Flashcards
what is Km increased by
competitive inhibition
what is Vmax decreased by
non-competitive inhibition
allosteric binding
sigmoidal curve
non-allosteric enzyme
hyperbolic curve
what are the 3 irreversible stages of glycolysis mediated by enzymes
- Hexokinase – substrate entry
- Phosphofructokinase – rate of flow
- Pyruvate kinase – product exit
what is metaplasia
mature cell transforms into another mature cell
dysplasia
disorder growth in abnormal cells in tissue
what are the hallmarks of cancer
- Resisting cell death
- Sustaining proliferative signalling
- Evading growth suppressors
- Activating invasion and metastasis
- Inducing angiogenesis
- Genome instability
when is steady state achieved
after 5 half lives
describe temp control/ negative feedback
- Central & peripheral thermoreceptors sense change in temp
- Send signals to hypothalamus
- Hypothalamus sends signals to effectors
- Effectors take action to oppose change
what is the test for gram positive
crystal violet dye
Pink
negative
purple
positive
endotoxin
negative
exotoxin
positive
what does an oncogene do
promote cell division
what does a tumour suppressor gene do
inhibit cell division
pyrimidine
cytosine, thymine, uracil
purine
guanine, adenosine
transcription
RNA polymerase
Topoisomerase
DNA rotation to help unwinding DNA
helicase
unzips DNA
DNA polymerase –
Adds nucleotides
Primase
Makes primer DNA
ligase
joins up Okazaki fragments
start codon =
AUG
what provides energy
GTP
what catalyses peptide bond formation between amino acids in P and A sites
Peptidyl transferas
autosomal dominant
in every generation
50% chance of passing onto offspring
autosomal recessive
2 genes needed and even so only a 25% chance of passing onto offspring
ectoderm
nervous tissue = controls
mesoderm
muscle tissue = moves
mesoderm
connective tissue = supports
endoderm
epithelial tissue = covers
IgM
first
IgA
secretory - breast milk
IgG
most abundant
IgE
allergy
high CO2 =
low affinity for O2
stroke volume
volume of blood each
ventricle ejects per heart beat
cardiac output
volume of blood pumped by each ventricle per minute
CO = SV x HR
MAP =
average arterial blood pressure during a single cardiac cycle. [70-105mm Hg]
Short term BP change:
When high blood pressure, firing rate to brain increases. Results in vessel dilation + HR falls.
Long term BP change: ACE
- RAAS – Renin stimulates Angiotensin 1 → Angiotensin 2 [produces aldosterone – vasoconstriction → increases SVR]
- NPs – counters RAAS
a. ANP – atrial distension
b. BNP – ventricles - ADH – regulates ECF – increases reabsorption of water, increasing MAP
Disaccharide =
Sucrose, Lactose
Polysaccharide =
Glycogen, Cellulose
∆G =
(energy products) – (energy reactants)
what is ∆G linked to
point of equilibrium
Primary protein =
Amino acids held together by peptide bonds
2nd protein =
Hydrogen bonds
3rd protein =
Amino acids interact [3D structure]
4th protein =
Disulphide bonds [multiple subunits]
Connective tissue –
Collagen triple helix
Phosphodiester bond
3’ OH group — 5’ triphosphate
mRNA “messenger”
Carries genetic information for protein synthesis – [Transcription]
trna: “transfer”
Carries amino acid to ribosome – [Translation]
how many types of eukaryotic cells are there
3 types
what are the 3 types of eukaryotic cells
Pol I, II (mRNA), III
how many types of prokaryotic cells are there
1 type
describe transcription
- RNA polymerase binding – finds promoters [initiation sites]
- DNA chain separation – Helicase
- Transcription initiation – 1st nucleotide added
- Elongation – Further nucleotides added to RNA chain
- Termination
what provides energy for translation
GTP
describe the process of translation
- Initiator tRNA located at A site – binds to start codon
- Elongation factor brings aminoacyl-tRNA to A site
- Peptidyl transferase catalyses bond formation between amino acids in P & A site 4. Termination when A site encounters stop codon
degenerate
amino acid with more than one codon
unambiguous
codon codes for one amino acid only
Apoenzyme =
enzyme, no cofactor
Halo-enzyme =
enzyme + cofactor
what happens to all enzymes in TCA
they are in matrix but succinate dehydrogenase at the inner mitochondrial membrane
mitosis
Diploid parent → 2 diploid daughter cells
meiosis
Diploid parent → 4 haploid daughter cells
Gene sequence variations due to:
Promoter sequence changes
Polymorphisms –
predispose to a disease
Mendelion –
single gene mutation = disease
Multifactorial –
multiple polymorphisms = risk of disease
aneuploidy:
whole missing/extra chromosome
Robertsonian translocation
two acro-centric chromosomes stuck end-end [trisomy]
Microarray CGH –
1st line chromosome test, detects abnormal chromosomes
FISH –
maps genetic material in a person’s cells (visualise specific genes)
PCR –
amplifies small piece of human genome [to find mutation]
Mosaicism –
having two genetically different types of cells in body
Penetrance –
likelihood of having a disease
Expression –
variation in disease severity
Autosomal dominant:
50% risk child affected
Autosomal recessive:
two faulty copies required, 25% risk, incest increases likelihood
x-linked:
recessive, only mum → child (50% risk), example – Haemophilia
Mitochondrial inheritance:
maternal only
Heteroplasmy –
daughter cells contain different proportions of mutant mitochondria
what genes are involves in cancer
Oncogenes [ras, PDGF, src]
- Tumour suppressor genes [p53]
- DNA repair genes
- Drug metabolism – genes that metabolise carcinogens
what is the breast cancer gene
BRCA1
Variolation –
Exposure to dried smallpox pustules from an infected patient
