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BRS/POM MOCKS > BRS MOCK 11 - Neurotransmitters, adrenal, microcirculation > Flashcards

BRS MOCK 11 - Neurotransmitters, adrenal, microcirculation Flashcards

1
Q

Classes of neurotransmitters?

A

Amino acids, amines and neuropeptides.

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2
Q

Explain neurotransmitter release

A

Docking of vesicle containing neurotransmitter in synaptic zone. Ca2+ entry leading to membrane fusion and exocytosis

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3
Q

How does alpha latrotoxin act as a neurotoxin?

A

Activates calcium channels. Massive neurotransmitter release resulting in muscle cramping.

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4
Q

How does botulinum toxin act as a neurotoxin?

A

Inhibits vesicle exocytosis. Paralysis, no muscle contraction.

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5
Q

What is the main neurotransmitter and post synaptic neurotransmitter receptor in the CNS?

A

Glutamate and GABA receptor.

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6
Q

Examples of g protein coupled receptors?

A

Seretonin receptors, Dopamine receptors, noradrenaline receptors,
Muscarinic receptors (acetylcholine).

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7
Q

Main Inhibitory neurotransmitters in CNS?

A

GABA and glycine.

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8
Q

Main excitatory neurotransmitter in CNS?

A

Glutamate.

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9
Q

How can a receptor excite a neurone?

A

Lead to sodium influx.

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10
Q

How can a receptor inhibit a neurone?

A

Lead to hyperpolarisation. With GABA and glycine its a chloride influx.

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11
Q

What are the two types of glutamate receptors?

A

AMPA and NMDA.

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12
Q

NMDA vs AMPA in terms of influx of ions?

A

NMDA receptors activation results in the influx of calcium ions in addition to the sodium. AMPA is just sodium.

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13
Q

NMDA vs AMPA in terms of function?

A

NMDA is responsible for slow component of excitatory transmission while AMPA is responsible for majority of fast excitatory synapses.

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14
Q

What do glutamate receptors require to work?

A

Glycine bound to receptor.

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15
Q

What cell is involved in the reuptake of neurotransmitter?

A

Glial cell.

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16
Q

What are seizures associated with?

A

Excess glutamate.

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17
Q

Why is glutamine synthetase important?

A

Glutamate to glutamine conversion in glial cells. Reduces excess levels of glutamate in synapse and so no seizures.

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18
Q

Explain a synaptic transmission involving glutamate?

A

Glutamate reversibly binds postsynaptic receptors. Rapid uptake of glutamate by excitatory amino acid transporters on presynaptic terminal and glial cell. Glutamate enzymatically modified by glutamine synthetase to glutamine in glial cells

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19
Q

How is GABA synthesised?

A

GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD).

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20
Q

Explain a synaptic transmission involving GABA?

A

GABA reversibly binds post-synaptic receptors. Rapid uptake of GABA by GABA transporters on presynaptic terminal and glial cell. GABA enzymatically modified by GABA-transaminase to succinic semialdehyde in glial cells.

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21
Q

What does the zona glomerulosa produce?

A

Aldosterone.

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22
Q

What does the zona fasciculata produce?

A

Cortisol.

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23
Q

What does the zona reticularis produce?

A

Androgens.

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24
Q

Name 3 catecholamines

A

Adrenaline, noradrenaline and dopamine.

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25
Q

What converts cholesterol to pregnenolone?

A

Side chain cleavage.

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26
Q

What converts pregnenolone to progesterone?

A

3 beta hydroxy steroid dehydrogenase.

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27
Q

Series of enzymes that convert progesterone to aldosterone?

A

21,11,18 hydroxylase.

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28
Q

Series of enzymes that convert progesterone to cortisol?

A

17,21,11 hydroxylase.

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29
Q

How does aldosterone work?

A

Binds to intracellular receptor. Gene expression results in greater Na+ reabsorption from urine into blood by activating Na+ pumps in distal convoluted tube and cortical collecting duct in the kidney. Na+ is pumped into blood and K+, H+ are pumped out of blood into urine by active transport. Increased Na+ reabsorption results in increased water reabsorption and so increased blood volume.

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30
Q

How does the renin angiotensin system work?

A

Drop in blood pressure (drop is renal perfusion pressure). juxtaglomerular cells detect drop in renal perfusion pressure and macula densa can detect drop in Na+. Release of renin from kidney (juxtaglomerular cells). Renin converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by ACE (lots in the lung).

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31
Q

What does angiotensin II do?

A

Vasoconstrictor. Increases synthesis of aldosterone from zona glomerulosa of adrenal cortex. Also stimulates release of AVP from anterior pituitary.

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32
Q

Cortisol hormone effects in the body?

A

Increased peripheral protein catabolism, increased gluconeogenesis, increased lipolysis - increased blood glucose. Increased vascular permeability, increased urine output.

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33
Q

How does angiotensin II increase aldosterone synthesis?

A

Activates enzymes in the zona glomerulosa of adrenal cortex - side chain cleavage, 3 beta hydroxysteroid dehydrogenase, 21 hydroxylase, 11 hydroxylase and 18 hydroxylase.

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34
Q

How does ACTH result in release of cortisol from zona fasciculata?

A

Activation of enzymes - side chain cleavage, 3 beta hydroxysteroid dehydrogenase, 17,21,11 hydroxylase.

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35
Q

Markers for addison’s disease

A

High ACTH, low cortisol, high MSH, low aldosterone

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36
Q

Symptoms of addison’s disease?

A

Hyperpigmentation, low blood pressure, weakness and vitiligo.

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37
Q

What results in low blood pressure in addison’s disease?

A

Low aldosterone.

38
Q

What results in vitiligo in addison’s disease?

A

Autoimmune destruction of melanocytes.

39
Q

Explain why a patient with addison’s disease has a tan?

A

ACTH is a peptide hormone. It is produced from a prohormone called proopiomelanocortin. When proopiomelanocortin is cleaved it produces ACTH and another hormone called MSH. High production of ACTH results in high levels of MSH. Melanocyte stimulating hormone stimulates melanocytes to produce melanin resulting in patients having a tan.

40
Q

How would you treat an addison’s crisis? Explain your management.

A

Administer saline solution by iv to patient to treat hyponatremia caused by deficiency in aldosterone. Give dextrose to treat low blood glucose caused by deficiency in glucocorticoids. Give hydrocortisone if you know its addison’s disease to treat low cortisol.

41
Q

What is secondary hypoadrenocortism and what are the biomarkers?

A

When the pituitary gland doesn’t secrete enough ACTH. Results in reduced levels of cortisol and ACTH.

42
Q

What is cushing’s syndrome?

A

Excess cortisol or other glucocorticoid production.

43
Q

What is cushing’s disease?

A

Pituitary tumour resulting in too much ACTH release.

44
Q

What are the 4 causes of cushing’s syndrome?

A

Cushing’s disease - pituitary tumour causing too much ACTH release.
Adrenal tumour - too much cortisol release.
Taking oral steroids.
Ectopic ACTH - ACTH secreting tumour outside of pituitary gland (e.g lung cancer).

45
Q

Cushing syndrome symptoms

A

Depression, easy bruising, red stretch marks, poor wound healing, immunosuppression.

46
Q

What is the catecholamine pathway? Explain the biochemical changes that take place.

A

Phenylalanine to tyrosine. Tyrosine to dopa (hydroxylation). Dopa to dopamine (decarboxylation - removal of carboxyl group). Dopamine to noradrenaline (hydroxylation). Noradrenaline to adrenaline (methylation).

47
Q

How are catecholamines degraded and what are the degradation enzymes?

A

Monoamine oxidase(deamination) or catechol - O methyl transferase(methylation).

48
Q

Catecholamines effect in the body?

A

Tachycardia, sweating, increased blood glucose and vasoconstriction.

49
Q

What are adrenaline and noradrenaline bound to in blood?

A

Albumin.

50
Q

Arterioles main function?

A

Regulate blood flow by altering resistance by altering radius of blood vessel.

51
Q

How are arterioles adapted?

A

Extensive smooth muscle in their walls and display a partial state of contraction at rest allowing them to vasoconstrict and vasodilate.

52
Q

Arterioles detect an increase in O2 usage and vasodilate. What is this an example of?

A

Active hyperaemia.

53
Q

What can result in active hyperaemia?

A

Local metabolites sensed by arterioles. Increase in O2 usage.

54
Q

What can cause myogenic autoregulation?

A

Change in blood temperature and stretch due to an increase in blood pressure.

55
Q

What helps regulated systemic arterial blood pressure?

A

Cardiovascular control centre in medulla via sympathetic nervous system and endocrine hormones.

56
Q

What is the blood pressure equation?

A

Blood pressure = cardiac output x total peripheral resistance

57
Q

Using the blood pressure equation explain how the cardiovascular control centre can restore low blood pressure?

A

Increase total peripheral resistance by increasing vasoconstriction in certain areas such as the gut.

58
Q

Types of capillary structures?

A

Continuous, fenestrated and discontinuous.

59
Q

What moves lymph around the body?

A

Skeletal muscles and respiratory movement.

60
Q

What is inspiratory reserve volume?

A

Maximal volume of air that can be forcibly inspired after tidal inspiration.

61
Q

How to calculate inspiratory capacity?

A

Inspiratory reserve volume + Tidal volume.

62
Q

What is residual volume?

A

Volume of air the remains in lungs after forced expiration.

63
Q

How to calculate total lung capcity?

A

Residual volume + expiratory reserve volume + tidal volume + inspiratory reserve volume

64
Q

How to calculate vital capacity?

A

Total lung capacity - residual volume

65
Q

What is functional residual volume?

A

Total amount of air present in lungs after tidal expiration.

66
Q

How to calculate functional residual volume?

A

Expiratory reserve volume + residual volume

67
Q

How do you calculate alveolar ventilation?

A

[Tidal volume - dead space] x breathing frequency

68
Q

What is the function of the pleural fluid in the pleural cavity?

A

Reduces friction between the membranes when you breath.

69
Q

Why is normal breathing regarded as negative pressure breathing?

A

Pressure of alveolar reduced bellow pressure of atmosphere.

70
Q

What is positive pressure breathing?

A

Pressure of atmosphere increased above alveolar pressure.

71
Q

What is dalton’s law?

A

Pressure of gas mixture is equal to sum of partial pressure of gases in the mixture.

72
Q

What is henry’s law?

A

Solubility of gas is directly proportional to partial pressure of that gas in equilibrium with that liquid.

73
Q

Why does HbO2 saturation need to be interpreted with haemoglobin?

A

Someone who has lost lots of blood can still have a HbO2 of 100%.

74
Q

What are factors that increase Hb oxygen affinity?

A

A decrease in temperature, alkalosis, hypocapnia (low blood C02 levels) and low 2,3-DPG levels in blood.

75
Q

How does haemoglobin and haemoglobin oxygen saturation change in a normal person, anaemic patient and a patient with polycthaemia?

A

Haemoglobin oxygen saturation will be the same but haemoglobin would be different. Low Hb in anaemic and high Hb in polycthaemia patient.

76
Q

What does carbon monoxide do to blood O2 and HbO2 saturation?

A

Low blood O2 as its harder to release oxygen from carbon monoxide bound haemoglobin. Reduced HbO2 saturation as haemoglobin binds to carbon monoxide instead of oxygen.

77
Q

Why may the blood leaving the lungs not have 100% HbO2?

A

Due to bronchial circulation drainage of deoxygenated blood into pulmonary vein

78
Q

What are the 3 ways in which CO2 is transported in the blood?

A

CO2 in blood. CO2 that reacts with water to produce carbonic acid in the blood. Carbonic acid in haemoglobin.

79
Q

What happens to carbonic acid in haemoglobin?

A

H+ ions bind to haemoglobin chain. Bicarbonate leaves red blood cell in exchange of a chloride ion.

80
Q

Why isn’t total resistance to air flow and airway generation a linear relationship?

A

Increase in number of airways at a certain airway generation offsets decrease in radius of airways.

81
Q

Why does resistance to airflow decrease later in inspiration?

A

Greater lung volume and more dilated airways results in lower resistance.

82
Q

What is laminar blood flow?

A

Velocity of fluid is constant at any one point and flow in layers. Blood flows fastest closest to the centre of lumen; blood cells closest to the wall experience more friction.

83
Q

What is turbulent blood flow?

A

Blood flows in irregular manner and is prone to pooling.

84
Q

Why is there negative pressure in pleural cavity at rest?

A

Lungs trying to contract inwards and chest wall trying to contract outwards.

85
Q

What is compliance and how is it calculated?

A

Tendency to distort under pressure. Change in volume / change in pressure.

86
Q

What is elastance and how is it calculated?

A

Tendency to recoil to its original volume. Change in pressure / change in volume.

87
Q

What does an increase in arterial stiffness result in?

A

Increase in systolic blood pressure. Lower diastolic pressure as less diastolic flow.

88
Q

What can result in decreased arterial compliance?

A

Increase in stiffness of arteries as we age.

89
Q

How does an aneurysm happen?

A

Weak muscle fibres in artery wall. Inward force produced by artery wall doesn’t match the blood pressure and so blood vessel expands until it ruptures.

90
Q

Why is it important that veins are more compliant than arteries?

A

Veins store most of the body’s blood. A small increase in pressure expands the volume of veins a lot.

91
Q

When standing upright, why does the bottom of the lung have greater ventilation?

A

Smaller and more compliant alveoli at the bottom of the lungs and effects of gravity.

92
Q

When standing upright, why does the bottom of the lung have greater perfusion?

A

Due to gravity which results in higher flow rate.

BRS/POM MOCKS (23 decks)

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