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Anatomy (make or break marks) > Principles > Flashcards

Principles Flashcards

1
Q

In what direction does DNA replication occur?

A

5’ to 3’ (nay exceptions!)

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2
Q

What enzyme unwinds DNA into a leading strand and lagging strand?

A

Helicase.

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3
Q

Other than adding new nucleotides, what function does DNA polymerase have?

A

3’ to 5’ exonuclease activity - “proof reading” DNA for mistakes

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4
Q

What is the lagging strand called. How is it different to the leading strand?

A

Okazaki fragments. These do not have a free 3’ end, thus, new nucleotides cannot be added to it in the same way as in the leading strand.

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5
Q

How are new nucleotides added to Okazaki fragments?

A

RNA primer (short strand of nucleic acids, synthesised by primase) is used in order for DNA polymerase to add new nucleotides in a 5’ to 3’ direction.

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6
Q

What is the first step called in DNA to protein synthesis? What is the product of this step (before splicing)?

A

Transcription. producing a Primary RNA transcript.

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7
Q

What is required for transcription to begin? expand.

A

General transcription factors (proteins) are required to bind to the promoter region of DNA. This then recruits RNA polymerase II, which also binds to the promoter region.

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8
Q

What occurs when RNA polymerase II binds to the promoter region of DNA?

A

DNA chains separate and transcription begins, one nucleotide at a time.

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9
Q

What direction are nucleotides added in the “Elongation” process of transcription?

A

5’ to 3’

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10
Q

Describe the “termination” step in transcription.

A

the RNA forms a stem loop and a Poly A tail is added to the 3’ end. (poly A tail acts as a signal for the RNA to leave the nucleus and bind to ribosomes in the cytoplasm)

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11
Q

what does a primary RNA transcript contain? and what step must it undergo to become a proper mRNA?

A

contains exons (coding regions) and introns (non-coding regions). Must undergo splicing (with spliceosome) to remove introns

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12
Q

What step comes after transcription? How is it initiated?

A

Translation. initiated by Initiation factors binding to the mRNA.

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13
Q

What occurs after initiation factors have bound to mRNA?

A

Small ribosomal sub-unit moves along mRNA (5’ to 3’) until start codon (AUG) is found. This then brings in “initiator” tRNA which joins to the start codon. Large ribosomal subunit finally joins assembly line.

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14
Q

What is the last step in translation called? and what is involved?

A

Elongation - elongation factor (EF1α).

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15
Q

What is the function of EF1α?

A

Brings in the next tRNAs to the assembly line. (translation)

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16
Q

what is ribosomalRNA?

A

RNA that combine with proteins to form ribsomes (site of protein synthesis)

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17
Q

what does messengerRNA do?

A

carries information from DNA to cytoplasm.

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18
Q

what is the function of transferRNA?

A

brings in the amino acids to be incorporated into proteins (during translation)

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19
Q

What is a catabolic reaction?

A

exergonic - negative change in free energy (energy released, occur spontaneously)

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20
Q

What is an anabolic reaction?

A

endergonic - positive change in free energy (energy absorbed, cannot occur spontaneously)

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21
Q

During the oxidation (catabolism) of glucose, what is released and what picks them up?

A

High energy electrons. picked up by electron carriers: NAD+, FAD, NADP+ (each pick up 2 electrons)
Becoming: NADH + H+
FADH2
NADPH + H+

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22
Q

What are the electron carriers in the oxidation of glucose called?

A

oxidising agents (as they gain e-)

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23
Q

Which two electron carriers drive oxidative phosphorylation and which one is used for gluconeogenisis?

A

NAD+ , FAD drive oxidative phosphorylation.

NADP+ uses its captured electrons for gluconeogenisis (glucose synthesis)

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24
Q

What are 4 ways in which the body uses glucose?

A

1) storage (glycogen, conversion to lipids)
2) Oxidation via aerobic glycolysis (into pyruvate)
3) Fermentation by anaerobic glycolysis (pyruvate into lactate)
4) Oxidation via the pentose phosphate pathway (

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25
Q

in what form is glucose stored in the body?

A

Glycogen. Conversion to lipids.

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26
Q

Oxidation via aerobic glycolysis produces?

A

Pyruvate

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27
Q

Fermentation by anaerobic glycolysis involves? why is this important within the body?

A

Pyruvate + (NADH ) + (H+) —-lactate dehydrogenase—> Lactate + (NAD+) [allows for REGENERATION of NAD+, so that it can be used in oxidative phosphorylation]

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28
Q

What does oxidation of glucose via pentose-phosphate-pathway produce? what is this used for?

A

Ribose-5-phosphate (precursor for nucleotides and DNA repair)

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29
Q

What are the two ways in which glucose is transported within the body?

A

Na+/glucose symporters (secondary active transport. energy from Na+ concentration gradient)
GLUT (glucose transporters) - facilitated diffusion. no energy required.

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30
Q

Define glycolysis. Where does it occur?

A

the initial pathway for the conversion of glucose to pyruvate. occurs in the cytosol of cytoplasm

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31
Q

What kind of reaction is the conversion of glucose to pyruvate called?

A

Substrate level phosphorylation.

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32
Q

What is the net gain of ATP in glycolysis?

A

2 ATP

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33
Q

Where does the Krebs/ citric acid cycle occur?

A

in the mitochondrial matrix.

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34
Q

What is the Krebs cycle?

A

the generation of energy (GTP) via the oxidation of Acetly-CoA

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35
Q

What two things are required for the metabolism of pyruvate to Aceteyl-CoA?

A

NAD+ required to pick up electrons.

Pyruvate dehydrogenase complex.

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36
Q

In the Krebs cycle, 2 carbon atoms are uptaken and 2 carbon atoms released. what form do these take?

A

uptaken carbon = Acetly-CoA

released carbon = CO2

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37
Q

What does the last stage (stage 3) in the metabolism of glucose involve?

A

Oxidative phosphorylation.

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38
Q

what is involved in the “electron transport chain”?

A

electrons flow from NADH and FADH2 to reduce O2 into H2O in the cristae of the mitochondrial matrix. the energy produced from this flow of electrons is then used to pupm protons from the mitochondrial matrix into the intermembrane space.

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39
Q

What pumps the protons from the cristae of the mitochondrial matrix into the intermembrane space?

A

Complex I, III and IV. (complex II does not pump protons)

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40
Q

What is the electron transport potential? What is it used for?

A

The electron transport potential is the energy produced when the protons flow back across the innermembrane bak into the mitochondrial matrix, following their concentration gradient.

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41
Q

What is the energy from the electron transport potential used for?

A

for the oxidative phosphorylation of ADP + Pi into ATP!! (using ATP synthase)

42
Q

In neurotransmission, what kind of receptors are ligand-gated ion channels?

A

Nicotinic ACh receptors

43
Q

In neurotransmission, what kind of receptors are G-protein coupled receptors?

A

Muscarinic ACh receptors + adrenoceptors

44
Q

which receptor is found in both parasympathetic and sympathetic preganglions?

A

nicotinic ACh receptors

45
Q

What occurs in response to an action potential in the synaptic cleft of both pre and post-ganglions?

A

Voltage-gated calcium channels open, triggering calcium entry.

46
Q

What occurs when calcium enters a sympathetic and parasympathetic preganglion?

A

preformed ACh is released which then enters the postganglion (ACh for BOTH parasympathetic and sympathetic)

47
Q

What occurs when calcium enters a sympathetic and parasympathetic postganglion (in response to action potential, ACh, from preganglion)?

A

sympathetic: release of preformed NA from vesicles which then enter the effector cell.
parasympathetic: release of preformed ACh from vesicles which then enter effector cell.

48
Q

What is the neurotransmitters in parasympathetic and sympathetic pre-ganglions?

A

ACh for BOTH.

49
Q

What is the main neurotransmitter in sympathetic nerve transmission?

A

NA (adrenaline for B2 ADR)

50
Q

What is the main neurotransmitter in parasympathetic nerve transmission?

A

ACh

51
Q

How is nerve transmission terminated in the sympathetic postganglion?

A

NA is re-uptaken by U1 (postganglion) and U2 (effector cell)

52
Q

How is nerve transmission terminated in the parasympathetic postganglion?

A

acetylcholinesterase breaks down ACh into choline and acetate.

53
Q

Where do parasympathetic pregnglions originate from?

A

Cranium or sacrum

54
Q

Where do sympathetic nerve fibres originate from?

A

Thoracolumbar origin. (T1 - L2)

55
Q

What are the effects of M1, M2 and M3 muscarinic acetylcholine receptors?

A 
M1 = increase in HCL secretion.
M2 = decreases heart rate (negative chronotropic effect). also acts as autoreceptor, negative feedback inhibition.
M3 = increases salivary/gastric secretions. Bronchoconstriction. GI SMC constriction.
56
Q

What are the effects of B1, B2, α1, α2 adrenoceptors?

A 
B1 = increase FORCE (positive inotropic effect) of heart and rate
B2 = Bronchodilation, smooth muscle relaxation of muscle and liver. 
α1 = vasoconstriction 
α2 = autoreceptor. negative feedback inhibition.
57
Q

Where are the autoreceptors located?

A

presynaptic ganglions.

58
Q

What are the 3 equations for determining MAP?

A 
MAP = (2D + S)/3 
MAP = 0.3(S - D) + D
MAP = CO x TPR
59
Q

Where is the baroreceptor action initiated? How does it travel to the heart?

A

Medulla of brain. via the vagus nerve (vagal outflow)

60
Q

When is the baroreceptor initiated? what does it do?

A

When there is a change in MAP (a fall in MAP results in decreased firing of baroreceptors). Acts on M2 receptors on heart to increase heart rate (positive chronotropic effect), thus affecting TPR.

61
Q

Where are baroreceptors located?

A

Carotid sinus (bifurcation of external and internal carotid arteries) + the aortic arch.

62
Q

equation for CO?

A

CO = SV x HR

CO is the volume of blood pumped out of the heart every min

63
Q

What is meant by the vasomotor tone?

A

Vascular smooth muscles are partially constricted at rest due to tonic sympathetic discharge (causing a continued release of NA)

64
Q

what does an increase in vasomotor tone result in? why? what receptor is stimulated and by what?

A

increase in TPR. due to increased vasoconstriction. NA stimulates the α1 adrenoceptors.

65
Q

Where is the cold response initiated? describe.

A

posterior hypothalamus.
includes shivering, vasoconstriction, increase in muscle tone. (increase in basal metabolic rate due to increased muscle activity)

66
Q

Where is the warm response initiated? describe please.

A

anterior hypothalamus.
includes sweating, vasodilation, decease in muscle tone. (decrease in the basal metabolic rate due to decreased muscle activity)

67
Q

Which part of the ANS is responsible for control of body temperature?

A

Sympathetic.

68
Q

How is the basal metabolic rate modulated?

A

via the release of NA, adrenaline and thyroxine.

increasing/decreasing muscle activity

69
Q

What does prostaglandins, released by the hypothalamus do?

A

It resets the body temperature to a higher set point during the cold response.

70
Q

What temperatures constitute fever? hyperthermia? hypothermia?

A

fever = 38 - 40
hyperthermia > 40
hypothermia

71
Q

In a G-protein coupled receptor, what kind of protein is the G-protein and the receptor protein?

A 
G-protein = peripheral membrane protein
receptor = integral membrane protein
72
Q

What does the G-protein consist of? where is the guanine nucleotide binding site located?

A

consists of γ, β, α subunits. (γ/β subunits are a pair. α subunit contains guanine nucleotide binding site.)

73
Q

Describe how a G-protein coupled receptor works.

A

When there is no signal, all 3 subunits joined together, guanine nucleotide binding site contains GDP. When agonist activates recpetor (eg. ACh, NA), GTP replaces GDP and α subunit disassociates from the B/y. α subunit goes onto bind and modulate effector cell.

74
Q

How is the signal turned off in a G-protein coupled receptor?

A

α subunit acts as ATPase and hydrolysis GTP to GDP and Pi - signal turned off. α subunit recombines with other two subunits.

75
Q

What is the resting membrane potential?

A

-70mV

76
Q

Which cells are able to produce an action potential?

A

muscle and nerve cells. (excitable cells)

77
Q

What is the equilibrium potential of potassium?

A

-90mV

78
Q

What is the equilibrium potential of sodium?

A

+60mV

79
Q

What are the intra and extra-cellular levels of Na and K?

A

Na+: extra = 150, intra = 15

K+: extra = 5, intra = 150

80
Q

What occurs to the membrane potential in depolarisation and hyperpolarisation?

A

depolarisation: membrane potential becomes more positive (up)
hyperpolarisation: membrane potential becomes more negtive (back down)

81
Q

What is the membrane potential of the undershoot? what is it due to?

A

-80mV. Due to delayed closure of voltage-gated k+ channels (negative feedback control)

82
Q

What causes the upstroke in the action potential of nerve cell?

A

opening of voltage-gated Na+ channels (Na+ INFLUX, sodium in)

83
Q

What causes the downstroke in the action potential of nerve cell?

A

opening of voltage-gated K+ channels (K+ EFFLUX, potassium out).
also helped by inactivation of Na+ channels

84
Q

K+ channels are an example of…? Na+ channels are an example of..?

A 
K+ = negative feedback control (self-limiting)
Na+ = positive feedback control (self-reinforcing, domino effect)
85
Q

What are the 3 states of a voltage-gated Na+ channel?

A

closed: resting state, ready to conduct
open: currently conducting
inactivated: during sustained periods of depolarisation, Na channels enter a non-conducting, inactivated state. Repolarisation/hyperpolarisation required for it to return back to closed state.

86
Q

What are the 2 types of refractory periods? when do they occur? What do they mean?

A

Absolute refractory period - during upstroke/downstroke. No stimulus, however strong, can illicit a 2nd A.P.
Relative refractory period - during the undershoot, a stronger than usual stimulus may illicit a 2nd A.P.

87
Q

What causes the refractory periods?

A

Inactivated voltage-gated Na+ channels.

88
Q

What type of inhibition are non-competitive antagonists? what does this mean?

A

Allosteric inhibition - antagonist binds to a site other than the active site, changing the agonists conformation.

89
Q

What type of inhibition are competitive antagonists? what does this mean?

A

orthosteric inhibition - antagonist binds to the active site

90
Q

How is the Vmax and Km changed in 1) competitive antagonists 2) non-competive antagonists?

A

1) competitive: Vmax = no change (competitive folk always want the maximum) Km = change
2) non-competitive: Vmax = change, Km = no change

91
Q

What is meant by Vmax and Km

A 
Vmax = maximum velocity of a reaction
Km = the amount of substrate required to illicit half-maximum velocity of a reaction.
92
Q

What is Km related to? What does it mean if an enzyme has a low Km?

A

Affinity. enzyme with a low Km has a HIGH affinity for substrate.

93
Q

What changes are caused in the dose-response curve by competitive and non-competitive antagonists?

A 
competitive = parallel rightward shift, with no change in Vmax (shape/height of curve remains same) 
non-competitive = depresses the curve (max height on Y-axis not as high), but no change in position of X-axis.
94
Q

What does it mean if a drug exhibits first-order kinetics?

A

The rate of elimination of the drug is directly proportional to drug concentration.

95
Q

For drugs that exhibit first order-kinetics, how does the dose administered affect the plasma concentration of said drug? the half life? the rate of elimination?

A

plasma concentration directly proportional to dose administered. However, no change in half life or rate of elimination.

96
Q

What is the equation for rate of elimination (Kel)?

A

Kel = clearance (Cl) x plasma concentration (Cp)

97
Q

What is the rate of elimination in drugs with zero-order kinetics?

A

initial rate of elimination is constant .

98
Q

What is meant by the buffer capacity of a solution? and what is meant by pH?

A

how well a solution can resist changes in pH.

pH = the ratio between conjugate base and acid.

99
Q

What is meant by an enzyme?

A

A substance which can increase the RATE at which a reaction reaches equilibrium (however, there is no change in the position of equilibrium or change in free energy)

100
Q

How does an enzyme increase the rate of a reaction?

A

By reducing the activation energy by providing alternative reaction pathways and by stabilising the transition state.

101
Q

In a lineweaver-burke plot, what does the y and x-axis intersection give?

A 
Y-axis = Vmax
X-axis = Km

Anatomy (make or break marks) (9 decks)

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