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Block 2 > General > Flashcards

General Flashcards

0
Q

What 3 features of a ligand will allow it to cross membranes to bind to intracellular receptors?

A

Small
Uncharged
Lipophilic

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1
Q

What are the 5 functions of the blood, lungs and heart?

A

Transport of nutrients
Oxygen delivery
Transport of hormones and other mediators
Removal of CO2 and waste products
Production, transport and delivery of protective mechanisms

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2
Q

What can intracellular receptors be?

A

Transcription factors

Enzymes

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3
Q

Name 4 steroid hormones that use intracellular receptors

A

Progesterone
Testosterone
Estradiol
Cortisol

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4
Q

Name 2 small lipophilic molecules that use intracellular receptors

A

Thyroxine

Retinoic acid

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5
Q

Which mechanism of cell signalling is common in development and differentiation?

A

Intracellular receptors

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6
Q

What are steroid hormones derived from?

A

Cholesterol

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7
Q

What do progesterone and estradiol do and where are they made?

A

Control development of female sex characteristics

Produced by ovary and placenta

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8
Q

What does testosterone do and where is it made?

A

Controls development of male sex characteristics

Produced in testes

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9
Q

What does cortisol do and where is it made?

A

Controls metabolic rate of many cells

Produced in adrenal cortex

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10
Q

What is the receptor for cortisol?

A

Glucocorticoid receptor (intracellular)

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11
Q

Where does the conversion of cholesterol to pregnenalone occur?

A

Mitochondria - cytochrome p450 enzymes

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12
Q

Which steroid hormones are formed from conversion of pregnenalone?

A 
Progesterone 
Testosterone 
Aldosterone 
Cortisol 
Estradiol
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13
Q

What is the alternative name for thyroxine?

A

Tetraiodothyronine

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14
Q

Where is the thyroid hormone receptor located?

A

Cell nucleus

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15
Q

What does thyroxine do and where is it made?

A

Broad effects on gene expression

Produced in thryoid gland by proteolysis of thyroglobulin

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16
Q

What is retinoic acid made from?

A

Vitamin A - retinol

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17
Q

Give an example of an intracellular receptor which is an enzyme

A

Intracellular soluble guanate cyclase - Nitric oxide is its ligand

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18
Q

Describe how NO leads to blood vessel dilation or peristalsis of gut

A

NO diffuses across membrane and binds to guanylate cyclase
This converts GTP to cGMP
This activates protein kinase G in smooth muscle
PKG phosphorylates myosin light chain
This causes muscle relaxation
This controls blood vessel dilation and peristaltic movement

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19
Q

Why are the effects of NO transient?

A

Quickly oxidised to nitrite and nitrate

cGMP is soon converted to GMP by phosphodiesterases so target proteins are no longer active

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20
Q

What is sildenafil citrate? And how does it work

A

Viagra
cGMP phosphodiesterase inhibitor particularly type 5 (principle type in corpus cavernosum)
Reduces degradation of cGMP and so prolongs the vasodilatory effects of NO

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21
Q

Give 3 examples of ligand gated ion channels

A

Nicotinic acetylcholine receptor in sympathetic nervous system
Glutamate receptors
5HT3 serotonin receptors

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22
Q

Give 2 examples of inhibitory transmitters which lead to opening of a Cl- channels

A

GABA

Glycine

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23
Q

Give 3 examples of second messengers which act as intracellular ligands

A

cAMP - olfaction
cGMP - photo transduction
Ca2+ - Ca induced Ca release

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24
Q

Give 3 examples of types of mechanoreceptors

A

Sound
Touch
Stretch

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25
Q

Name the 3 types of ion channel

A

Voltage gated
Ligand gated
Mechanically gated

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26
Q

How does cocaine function as a local anaesthetic?

A

Prevents action potential firing by blocking sodium channels

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27
Q

What do natriuretic peptides do?

A

Released by different organs in response to high blood pressure
Modulate CV and renal physiology to lower pressure

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28
Q

What is the main route of communication between heart and kidneys?

A

Atrial natriuretic peptide

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29
Q

What is the receptor for ANP?

A

Receptor guanylate cyclase

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30
Q

How does ANP release lead to increased salt excretion by the kidneys?

A

Guanylate cyclase converts GTP to cGMP
cGMP activates protein kinase G
Increased salt excretion and urine production due to phosphorylation of Na+ channels which reduces Na+ reabsorbtion.

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31
Q

How do receptor protein kinases work?

A

Binding of ligand causes receptor subunits to dimerise
Dimerisation activates the kinase, phosphorylating target proteins
2 types:
Receptor serine/threonine kinases
Receptor tyrosine kinases

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32
Q

Give an example of a receptor serine/threonine kinase ligand

A

Transforming growth factor B like ligands (TGF-B1). Inhibitory growth factor. Defects in signalling can lead to unrestricted growth (cancer)

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33
Q

What are SMADs?

A

Target proteins of TGF-B1 - intracellular transducers which activate downstream transcription factors. Receptor serine/threonine kinase dimers phosphorylate SMADs

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34
Q

Give 2 examples of receptor tyrosine kinase ligands

A

Growth factors - EGF and FGF

Insulin

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35
Q

What can receptor tyrosine kinases phosphorylate?

A

Transcription factors
Ion channels
Enzymes - PK, PLC, PI3K
Themselves - Ras activated by binding to phosphorylated receptor

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36
Q

Describe the signalling cascade for growth factors

A

Binding of growth factor induces receptor dimerisation
Dimerisation triggers phosphorylation of receptors
Adaptor and Ras-GDP bind to phosphorylated receptors
Nucleotide exchange generates activated Ras-GTP

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37
Q

Why is Ras signalling important?

A

20% human cancers due to mutations in Ras

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38
Q

Give an example of a receptor pathway which use soluble tyrosine kinases

A

Ligand - EPO
Receptor - EPO receptor
Activate janus kinases (JAK) - tyrosine kinase
Frequently use STAT pathway
Increases gene transcription therefore creating of more red blood cells

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39
Q

What are interleukines?

A

Type 1 cytokines

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40
Q

What are interferons?

A

Type II cytokines

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41
Q

How do cytokines exert their effects?

A

Autocrine and paracrine

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42
Q

What is bound to a G protein when it is in its active state?

A

GTP

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43
Q

Which G protein subunits change activity of target proteins?

A

G-aGTP and G-ByGTP

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44
Q

What target proteins can GPCRs act on?

A 
Transcription factors 
Ion channels 
Protein kinases and phosphatases
Phospholipase C 
Phosphoinositide 3-kinase 
Cyclases and phosphodiesterases
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45
Q

Give examples of ligands/receptors which act via G-aS to activate adenylate cyclase

A 
Glucagon 
ACTH
D1 and D5 dopamine receptors 
5HT 4,5,6 and 7 receptors 
Adrenergic B receptors
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46
Q

Give examples of ligands/receptors which act via G-ai to inhibit adenylate cyclase

A 
PGE1
Adenosine 
D2, D3 and D4 dopamine receptors 
M4 muscarinic receptors 
5HT1 receptors 
Adrenergic a2 receptors
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47
Q

Give an example of a ligand which acts via G-aT which activates cGMP phosphodiesterase

A

Photons (rhodopsin)

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48
Q

Give examples of ligands/receptors which act via G-aQ which activates phospholipase C

A

Vasopressin
M1, M3 and M5 muscarinic ACh receptors
5HT2 receptor
Adrenergic a1 receptors

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49
Q

Give an example of a ligand which acts via G-a13 which activates ion channels

A

Thrombin

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50
Q

How does stimulation and inhibition of adenylate cyclase affect signalling in cardiac myocytes?

A

Contraction is regulated by stimulatory and inhibitory signals
B-adrenergic receptors stimulate adenylate cyclase
a-adrenergic receptors inhibit adenylate cyclase
Adenylate cyclase converts ATP to cAMP

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51
Q

What is an acid?

A

Chemical that can donate H+

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52
Q

What is a base?

A

Chemical that can accept H+

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53
Q

What is a buffer?

A

Chemical that reversibly binds H+

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54
Q

How is pH calculated?

A

pH= -log10 [H+]

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55
Q

Increasing pH by 1 corresponds to what increase in H+ concentration?

A

10 fold increase

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56
Q

What is the normal range of pH?

A

7.36-7.44

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57
Q

What is pKa?

A

Ratio of concentrations of dissociated and undissociated weak acid

Measure of buffering

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58
Q

What is the pKa of the CO2/HCO3- system?

A

6.1

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59
Q

Which is more soluble in water, CO2 or O2?

A

CO2

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60
Q

What is formed when CO2 reacts with water?

A

Carbonic acid

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61
Q

What is the most important controller of pH in the blood?

A

CO2

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62
Q

In what form is CO2 mainly transported?

A

As bicarbonate

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63
Q

In what 3 ways can CO2 be transported in the blood?

A

Dissolved CO2
Bicarbonate
Carbamino compounds

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64
Q

Why are there negligible levels of carbonic acid present in the blood?

A

It is not stable so dissociates rapidly

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65
Q

What is the Henderson Hasselbach equation?

A

pH= pKa + log10 ( [base]/[acid] )

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66
Q

What is respiratory buffering?

A

Body produces acid, H+ reacts with HCO3 to form CO2 which is breathed out
Rapid

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67
Q

What is renal buffering?

A

If pCO2 levels are too high, kidneys excrete less HCO3, plasma levels are higher so buffering of acid occurs
Slow

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68
Q

Why can’t Hb be free in the blood and so requires blood cells to store it?

A

Would be filtered at the glomerulus out of the blood

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69
Q

By what 3 mechanisms can CO2 enter the red blood cell?

A

Diffusion through plasma membrane
Via aquaporin 1 receptor
Via rhesus complex

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70
Q

Why does the dissolving of CO2 in the blood occur very slowly?

A

No carbonic anhydrase present there, only in the red blood cell

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71
Q

What triggers the release of O2 from Hb-O2?

A

H+

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72
Q

What is the Bohr effect?

A

In acid conditions, oxygen dissociation curve shifts right for a given pO2 so Hb binds less O2

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73
Q

What is the Haldane effect?

A

Increasing oxygen binding reduces the affinity for CO2 and H+ ions by modifying quaternary structure

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74
Q

Give an example of a metabolic acidosis?

A

Diabetic ketoacidosis

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75
Q

What can cause a respiratory alkalosis?

A

Hyperventilation

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76
Q

What is Hb called when bound to CO2?

A

Carbaminohaemoglobin

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77
Q

How does Hb buffer H+?

A

H+ binds to imidazole group of histidine residue
6x more important than albumin as acid buffer
Deoxyhemoglobin buffers more than oxyhemoglobin

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78
Q

What is the difference between a weak and strong acid?

A

Strong acids dissociate completely in solution whereas weak acids will only partially dissociate

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79
Q

What is special about weak acids in relation to their buffering ability?

A

Weak acids form an equilibrium with its conjugate base forming a buffer pair that can respond to changes in H+

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80
Q

What is the average pH of the urine?

A

6

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81
Q

What is the average pH of saliva?

A

6.8

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82
Q

What is the normal concentration of H+ in the blood?

A

36-44 nanomoles / litre

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83
Q

A balance of what factors is required to maintain homeostasis of ion concentrations?

A

Intake
Production
Excretion

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84
Q

What effect does H+ have on protein function and why?

A

Small and charged
Alters protein activity, especially enzymes, by disrupting H+ bonding and denaturing them
Can affect the binding of other ions eg low [H+] increases Ca binding to albumin

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85
Q

What is a volatile acid?

A

Can leave solution and enter atmosphere
Generated in body from CO2 and H2CO3 due to aerobic respiration
Excreted by lungs

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86
Q

What is a non volatile acid?

A

Fixed or non respiratory
Sulphuric acid, lactic acid, keto acids
Excreted by the kidneys combined with bicarbonate

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87
Q

What 3 main mechanisms are in place to minimise changes in pH?

A

Buffers - unable to change overall body pH
Lungs - adjust excretion of CO2
Kidneys - adjust H+ excretion into urine and alter production of bicarbonate buffer

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88
Q

What is a buffer?

A

Any substance that can reversibly bind H+

89
Q

What are the 3 main buffer systems in the body?

A

Bicarbonate - extracellular
Phosphate - intracellular and urine
Protein - intracellular

90
Q

What 3 proteins can act as buffers?

A

Haemoglobin
Amino acids
Plasma proteins

91
Q

What does carbonic anhydrase do?

A

Catalyses inter conversion of CO2 and H2O to bicarbonate and H+
Type II free in cytosol
Type IV luminal side of proximal convoluted tubules

92
Q

What does the bicarbonate buffer system connect?

A

Lungs control of CO2 with kidneys control of bicarbonate

Shows they can compensate for one another

93
Q

What is the Henderson Hasselbach equation?

A

pH = pK + log10 ( [HCO3]/[CO2] )

94
Q

What is the normal ratio of HCO3 to CO2?

A

20:1

95
Q

How much H+ a day must the kidneys excrete in order to maintain acid base balance from non volatile acids?

A

70-100 mmol /day

96
Q

By what 2 main processes do the kidneys maintain pH?

A

Reabsorption of filtered HCO3

Excretion of H+

97
Q

Where is the majority of bicarbonate reabsorbed?

A

Proximal convoluted tubule

98
Q

Describe the process of reabsorption of bicarbonate in the proximal convoluted tubule

A

Na/H exchanger releases H+ into lumen
This combines with HCO3 to form H2CO3
Carbonic anhydrase on tubular cells catalyses conversion of this to H2O and CO2
These diffuse into the cell
Carbonic anhydrase catalyses conversion back to H+ and HCO3
HCO3 is symported with Na into renal interstitial fluid

99
Q

What happens differently to the PCT in bicarbonate reabsorption in the distal tube and collecting duct?

A

H+ ATPase present to secrete H+ rather than Na / H antiporter

100
Q

What are the 2 main urinary buffers?

A

Phosphate and ammonia

101
Q

Why does the process of excreting H+ generate new HCO3-?

A

Some HCO3 is consumed when buffering the non volatile acids

102
Q

What does the urinary phosphate buffer depend on?

A

Amount of phosphate taken in in the diet

103
Q

What 2 forms of filtered phosphate create a buffer pair in the tubular fluid? And which is in excess?

A

Mono protic HPO4 2- relative excess so can pick up H+

Diprotic H2PO4 -

104
Q

Which urinary buffer is better able to respond to the body’s needs?

A

Urinary ammonia buffer

105
Q

Which kidney cells produce glutaminase and what does it do?

A

Proximal convoluted tubule

Catalyse conversion of glutamine to ammonia

106
Q

What 2 substances form the buffer pair in the ammonia buffer?

A

Ammonia (NH3) and ammonium (NH4+)

107
Q

What does a decrease in pH stimulate the urinary ammonia buffer to do?

A

Metabolise more glutamine to ammonia which can pick up more H+

108
Q

Why are renal responses to pH more slow than respiratory?

A

Because they require protein synthesis eg glutaminase production to power the urinary ammonia buffer

109
Q

What 3 things can stimulate H+ secretion?

A

Increase in pCO2
Decrease in pH
Increased aldosterone levels

110
Q

What is compensation in terms of acid base balance?

A

Body’s attempt to minimise changes in pH, to restore back towards normal

111
Q

What would happen to [HCO3] and [CO2] levels in a compensated disorder?

A

Both levels would lie outside normal range, both in the same direction

112
Q

What can cause a respiratory acidosis?

A

Disorder affecting lungs, chest wall, nerves, muscles or CNS that leads to hypo ventilation

113
Q

What can cause a respiratory alkalosis?

A

Hyperventilation

High altitude

114
Q

What can cause a metabolic acidosis?

A

Addition of acid - exogenous methanol or endogenous lactic or keto acid
Failure of H+ excretion
Loss of HCO3 eg in severe diarrhoea

115
Q

What can cause a metabolic alkalosis?

A

Addition of alkali
Excess loss of H+ eg prolonged vomiting
Excess aldosterone eg due to dehydration

116
Q

How do you treat acid base disorders?

A

Treat the underlying cause
Sodium bicarbonate to neutralise acid
Ammonium chloride to neutralise alkali

117
Q

What is blood pressure a product of?

A

Systemic vascular resistance

Cardiac output

118
Q

What is the 5th korotkoff sound?

A

Absence of sound - diastolic pressure

119
Q

What is a normal pressure in the pulmonary artery?

A

25/10

120
Q

Describe the pressure volume loop in the left ventricle

A

Isovolumetric relaxation, pressure decreases, both valves closed
Atrial pressure exceeds ventricular and the mitral valve opens
Passive ventricular filling occurs so pressure and volume increase, atrial contraction completes filling
Pressure in ventricle exceeds atria so mitral valve closes
Ventricle contracts but both valves close so isovolumetric contraction, pressure increases until it exceeds aortic pressure
Aortic valve opens and blood flows out of ventricle. Volume decreases but pressure increases as ventricle continues to contract
Pressure starts to decrease and drops below that of aorta so aortic valve closes. Isovolumetric relaxation occurs and process starts again

121
Q

Why does pressure curve look different for aorta to femoral artery?

A

Aorta is elastic artery, has capacitance to expand. This smooths out the pressure differences between systolic and diastolic so that there is continual blood flow rather than a bolus which leaves the heart
Femoral artery is muscular and so pressure is more distinct

122
Q

What factors affect vessel calibre?

A

Local factors - endothelins, NO, CO2, K, lactate

Hormonal factors - adrenaline, noradrenaline, dopamine, angiotensin II

123
Q

What are the main roles of veins and lymphatics?

A

Capacitance and return of volume to CV system

124
Q

Describe lymphatic drainage

A

Contain valves to prevent backflow

Lymphatic drainage both passive and peristaltic, aided by skeletal muscle contraction

125
Q

What neural control exists of blood pressure?

A

Blood vessel innervation - vasomotor control

Cardiac innervation

126
Q

How are blood vessels innervated?

A

Noradrenergic nerve endings on all vessels
Vasoconstrictors - constant tone
Cholinergic fibres travel with sympathetic nerves
Vasodilators - no constant tone

127
Q

Describe cardiac innervation

A

Sympathetic stimulation to heart causes positive ionotropism and chronotropism
Constant opposition with vagal tone

128
Q

Where is the vasomotor area?

A

Medulla oblongata

129
Q

How does the vasomotor centre modulate sympathetic outflow?

A

Operates via RVLM (Rostro ventrolateral medulla) then IML (intermedio lateral cell column) of spinal cord
Balanced by vagal outflow also from medulla

130
Q

What hormonal control of blood pressure exists?

A

Renin-Angiotensin system
Anti-Diuretic Hormone
Atrial Natriuretic Peptide
Local mediators

131
Q

What factors can result in the release of renin?

A

Decreased renal arterial pressure
Decreased Na in renal tubular fluid
Increased renal sympathetic nerve activity

132
Q

What are the actions of angiotensin II?

A

Potent vasoconstrictor
Increases sympathetic tone centrally as well as local effects
Constricts renal afferent and efferent arterioles reducing
renal blood flow
Increases thirst and water intake
Stimulates ADH secretion
Directly inhibits secretion of Renin - -ve feedback loop

133
Q

What are the actions of aldosterone?

A

Controls reabsorption of sodium in renal cortical collecting duct
Induces production of proteins in collecting duct including membrane channels for Na and K
Increases Na reabsorption from gut, sweat and salivary glands

134
Q

What are the actions of anti diuretic hormone?

A

Synthesised in hypothalamus then secreted from posterior pituitary
Increases the water permeability of the collecting duct luminal membrane
Allows medullary interstitium to reabsorb water
Inserts protein channels for water into luminal membrane
Acts as vasoconstrictor at higher levels
Can reduce renal blood flow and GFR

135
Q

What are the actions of atrial natriuretic peptide?

A

Stretch receptors in cardiac atrial cells, stimulation causes release of ANP
Causes increased renal excretion of sodium and water
Also increases GFR by dilating afferent and constricting efferent renal arterioles - increasing filtration pressure
Inhibits renin secretion and aldosterone release

136
Q

What is the response protocol for a major trauma/haemorrhage?

A 
TRAUMATIC
T - tranexamic acid 
R - resuscitation 
A - avoid hypothermia
U - unstable? Damage control surgery
M - metabolic, avoid acidosis
A - avoid vasoconstrictors
T - test clotting
I - imaging
C - calcium
137
Q

What cardiovascular changes occur in sepsis?

A 
Hyperdynamic - Tachycardic, elevated CO, leaky vessels
Relative hypovolaemia 
Local factor vasodilatation 
Increased tissue oxygen demand 
Decreased cardiovascular supply
138
Q

What can be used as anti hypertensive agents?

A 
ABCD
A - ACE inhibitors/ AAs (angiotensin II receptor antagonists)
B - b blockers
C - calcium channel blockers
D - diuretics
139
Q

How can diuretics be used as anti hypertensive agents?

A

Decrease blood volume
Thiazide diuretics - bendroflumethiazide
Carboxylic acid derivatives - furosemide
Potassium sparing - spironolactone
Carbonic anhydrase inhibitors - acetazolomide
Osmotic - Mannitol

140
Q

How can ACE inhibitors be used as anti hypertensives?

A

Initial drop in BP by lowering peripheral vascular resistance - arterial tone rather than venous
HR unchanged, postural hypotension rare
Renal blood flow increased causing increased sodium and water
loss
Caution in renal artery stenosis as may cause worsening of renal
function and hyperkalaemia
Captopril, Enalapril, Lisinopril
Cough associated with bradykinin most common side effect

141
Q

What is nifedipine?

A

Calcium channel blocker

Vasodilatation and some negative ionotropism

142
Q

Name the 4 hormones which exert an effect on the circulation?

A

Agiotensin II
Aldosterone
Anti diuretic hormone
Adrenaline

143
Q

At what 3 sites does angiotensin II exert its effects?

A

Adrenal cortex - causes secretion of aldosterone
Hypothalamus - increases thirst, causes secretion of ADH
Arteries - vasoconstriction

144
Q

Define shock

A

Inadequate tissue perfusion

145
Q

What happens when blood pressure and/or flow decrease below the autoregulatory range?

A

Shock

146
Q

What are the 5 kinds of shock?

A 
Anaphylaxis 
Cardiogenic 
Hypovolaemic
Neurogenic 
Septic
147
Q

Which 3 types of shock present in a similar way?

A

Anaphylaxis
Neurogenic
Septic

148
Q

What physiological processes occur to maintain flow?

A 
Vasomotor tone 
Metabolites 
Supply pressure 
Transmural pressure 
Myogenic contraction 
Local vasoactive agents 
Systemic hormonal effects
149
Q

What is MAP?

A

MAP = CO x SVR (systemic vascular resistance)

150
Q

What is Starlings law?

A

The force of contraction of the cardiac muscle is proportional to its initial length
The heart pumps out the blood that is returned to it

151
Q

What are the accepted definitions of hypotension?

A

Reduced systolic BP below 90
Pressure 20mmHg below patients normal
Children, athletes, pregnant young women may have low BP normally

152
Q

What are the 3 mechanisms that can cause shock?

A

Inadequate circulating volume
Failure of the pump
Damage to control of resistance

153
Q

What can be problems of capacitance?

A

Hypovolaemia
Vasodilatation
Heart Failure

154
Q

What is the prime problem in hypovolaemia?

A

Inadequate volume so fall in cardiac output

155
Q

What compensation occurs in hypovolaemia?

A

Increased resistance

Tachycardia but cardiac output falls as stroke volume affected

156
Q

What will be seen clinically in someone with hypovolaemia?

A 
Cold, clammy peripheries
Tachycardia 
Prolonged cap refill time 
Empty Veins 
Weak thready fast pulse
157
Q

What can cause hypovolaemia?

A

Haemorrhage, dehydration, D+V, polyuria in diabetes, burns

158
Q

What is a clinical consequence of hypovolaemia?

A

Hypotension

159
Q

What is the prime problem with pump failure?

A

Fall in cardiac output

160
Q

What compensation occurs with pump failure?

A

Increased resistance
Tachycardia
Increased capacitance

161
Q

What can cause pump failure?

A

Ischemic heart disease, valvular disease, arrhythmia, PE, pneumothorax, cardiac tamponade

162
Q

What will you see clinically in a patient with pump failure?

A

Cold, clammy peripheries
May have tachycardia
Prolonged cap refill time
May have raised JVP

163
Q

What will you see clinically in a patient with excessive dilatation?

A

Warm, dry peripheries
Tachycardia
Short cap refill time
BOUNDING pulse

164
Q

What may happen to CO in early sepsis?

A

Massive increase due to activation of sympathetics to increase HR and contractility and increased capacitance of vessels

165
Q

What are signs of shock?

A

Poor tissue perfusion - oliguria, altered consciousness

166
Q

What signs of correction of acidosis might be seen in shock?

A

Lactate increase levels so metabolic acidosis

Increased respiratory rate to compensate

167
Q

What is the initial management of someone with shock?

A

Airway - give high flow oxygen
Breathing - Inspect, palpate, percuss, auscultate to assess
Circulation - with fluid resuscitation, Peripheral perfusion – cool & clammy v warm & dry, Pulse – volume/rate, IV access (blood for investigation, which tests?), Fluid challenge is nearly always the first ‘C’ treatment, Crystalloids v Colloids?, Indications for blood transfusion?
Hypotension is NOT required for shock to exist
Disability - Conscious level – AVPU v GCS, Pupils
Exposure - environment, other examination, causes – e.g. revealed bleeding, concealed bleeding, peripheral oedema

168
Q

What effects do a1 receptor agonists have?

A

Vasoconstriction

169
Q

What effects do B1 agonists have?

A

Tachycardia
Increased force of contraction
Vasodilation
Renin secretion

170
Q

What receptors does adrenaline act on and what are its effects?

A

a and B

Increased HR and ionotropism, vasoconstriction

171
Q

What receptors does noradrenaline act on and what are its effects?

A

a receptors

Vasoconstriction

172
Q

Which receptors does isoprenaline act on and what are its effects?

A

B receptors

Increase HR, ionotropism, vasodilation

173
Q

Which receptors does dobutamine act on and what are its effects?

A

B1

Increase HR, ionotropism, vasodilation

174
Q

What is DNA?

A

Polymer of nucleotides

Base, sugar and phosphate

175
Q

What are differences between RNA and DNA?

A

Ribonucleic acid in RNA, deoxyribonucelic acid in DNA

T in DNA, U in RNA

176
Q

Which direction does DNA replication proceed in?

A

5’ to 3’

177
Q

What bond forms between nucleotides?

A

Phosphodiester bonds

178
Q

What are purines?

A

Adenine and guanine

Double ring structure

179
Q

What are pyrimidines?

A

Cytosine and thymine

Single ring structure

180
Q

Why are TATA boxes present at start of genes?

A

TATA box at start of gene, less strong bonds as only double bond not triple so easier to separate to initiate replication/translation

181
Q

How many nucleotide pairs in a DNA helix turn?

A

10.4

182
Q

What are the two new strands of DNA formed during replication called?

A

Leading strand

Lagging strand - formed from Okazaki fragments

183
Q

How is DNA compacted into chromosomes?

A

Beads on a string form chromatin
Chromatin packed into nucleosomes
Condensed into chromosomes

184
Q

Which direction is the non coding strand transcribed into mRNA?

A

3’ to 5’

185
Q

How is transcription initiated?

A

Transcription factors first recognizes the promoter sequence (allows different cells to turn on and off different genes)
RNA polymerase can then be recruited (forms a transcription initiation complex)

186
Q

What is RNA splicing?

A

Exons code for proteins, introns junk. Removes introns. Can occur in different ways to produce different isoforms in different cell types

187
Q

What is a start codon?

A

AUG - methionine

188
Q

What are tRNA?

A

Adapter molecules made from RNA that are linked to an amino acid. They have an anti-codon

189
Q

What is rRNA?

A

Major component of ribosome which catalyses peptidyl transfer reaction

190
Q

Which subunit of ribosome binds to mRNA first?

A

Small subunit

191
Q

What is a zwitterion?

A

Molecule that contains a positive and a negative charge

Amino acids are zwitterions

192
Q

What type of reaction forms a peptide bond?

A

Dehydration reaction

193
Q

Which amino acids in proteins tend to be sites for phosphorylation?

A

Serine
Threonine
Tyrosine
All uncharged polar

194
Q

What are the 4 types of amino acid side chain?

A

Acidic, basic, uncharged polar, non polar

195
Q

Which is the simplest amino acid?

A

Glycine - H as its R side chain

196
Q

Why can’t peptide bonds between amino acids partake in H bonding?

A

Electron delocalisation

197
Q

Which bond in an amino acid chain allows rotation?

A

C-C bond

198
Q

Which diseases can be caused by a single amino acid change?

A

Sickle cell anaemia due to Hb mutation

Cardiomyopathy due to tropomyosin mutation

199
Q

What are the 5 factors that can influence the conformation of peptide chains folding into proteins?

A

Planarity of peptide bonds. Conformations are defined by dihedral angles Φ & Ψ
Hydrogen bonding of amide carbonyl groups to N-H donors
Steric crowding of neighboring groups
Repulsion and attraction of charged groups
Hydrophilic and hydrophobic character of groups

200
Q

Between which amino acid groups can disulphide bridges form?

A

Cysteine

201
Q

What forces exist in proteins which hold them together in their conformation?

A

Hydrogen
Electrostatic
Van der waals

202
Q

Which amino acids in an alpha helix form hydrogen bonds?

A

Every 4th amino acid

203
Q

Which molecule may involve a coiled coil structure forming?

A

Tropomyosin

204
Q

What are the 5 R steps in inflammation?

A 
Recognition of the injurious agent
Recruitment of leukocytes 
Removal of the agent 
Regulation of the response 
Repair or resolution
205
Q

There are acquired and genetic defects in leukocyte function. The genetic ones can be mainly categorized how?

A

Defects in leukocyte adhesion
Defects in microbicidal (killing) activity
Defects in phagolysosome function or formation

206
Q

What are the morphological patterns of acute inflammation?

A

Serous
Ulcerative
Suppurative
Fibrinous

207
Q

What 3 systems does factor XII activate?

A

Kinin system
Fibrinolytic system - plasmin - complement
Coagulation system - fibrin

208
Q

What are major groups of cell-derived mediators?

A

Vasoactive amines, arachidonic acid metabolites, platelet-activating factor, cytokines, reactive oxygen species, nitric oxide, lysosomal enzymes and neuropeptides

209
Q

What is the major vasoactive amine involved in acute inflammation?

A

Histamine

210
Q

Aspirin inhibits all 3 branches of cyclo oxygenase pathway including prostacyclin and thromboxane A2 which have opposing effects, why does it have its specific effects?

A

Endothelial cells produce prostacyclin which is temporarily blocked by aspirin, however these cells have machinery to create more
Platelets do not have the cellular machinery and so thromboxane production is permanently affected and hence its affects are reduced platelet aggregation and vasodilation

211
Q

What are the three ways of activating the complement system?

A

The alternative pathway (microbe), the classical pathway (antibody mediated) and the lectin pathway (lectin expressed on surface)

212
Q

What does C3b of the complement system do?

A

It opsonises particles to target them for destruction

Leads to cleavage of the remaining C4-9, which ultimately produces the membrane attack complex- C5b-C9

213
Q

The major product of the kinin system is Bradykinin. What is the effect of Bradykinin?

A

Vasoactive amine that functions similarly to Histamine

214
Q

What do macrophages do when they are activated?

A

They secrete proteases and ROS, cytokines (IL-1 and TNF) and arachidonic acid metabolites to contribute to the ongoing inflammation and tissue injury. They also secrete growth factors to start the repair process

215
Q

What are granulomas?

A

They are aggregates of activated or epithelioid macrophages

216
Q

What causes granulomatous inflammation?

A

Granulomatous inflammation is caused by persistent T cell responses to certain microbes i.e. TB (as we know T cells cause macrophage activation and Macrophages cause T Cell activation so this forms a cycle) and inert foreign bodies. Some granulomatous disease e.g. sarcoidosis or Crohns disease

217
Q

How is fever induced in inflammation?

A

Bacterial products and Il-1 and TNF cause AA metabolism, leading to increased prostaglandins, in the vascular a peri-vascular cells of the hypothalamus, which resets the core body temperature by 1-
4oC

218
Q

A patient is diagnoses with acute appendicitis, which is removed laproscopically. What would you expect to be covering the inflamed appendix?

A

Purulent exudate, pus

219
Q

Why do inflamed appendices appear plumper than normal?

A

Accumulation of oedema fluid and inflammatory exudate

220
Q

Why would appendicitis cause a risk of peritonitis?

A

Transmural necrosis accompanying the inflammation could lead to perforation

221
Q

What is the link between gallstones and hepatic abscess?

A

Ascending cholangitis- ascending infection

Block 2 (9 decks)

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