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Year 1 Medicine Newcastle > Foundation 2 > Flashcards

Foundation 2 Flashcards

1
Q

What is the anatomical position

A

Head, gaze and toes directed forward
Arms adjacent to the sides with palms facing forward
Lower limbs close together with feet parallel

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2
Q

What is the medial plane

A

The vertical plane that passes directly through the body dividing it into left and right halves

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3
Q

What are sagittal planes

A

Vertical planes that pass through the body parallel to the medial plane

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4
Q

What are frontal planes

A

Planes that are vertical and split the body into anterior and posterior, right angle to the medial plane

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5
Q

What are transverse planes

A

Horizontal planes that pass through the body at right angles to the median and frontal planes

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6
Q

What does rostral mean

A

This is often used instead of anterior when describing the brain

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7
Q

What does medial mean

A

The location closer to the medial plane

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8
Q

What does lateral mean

A

This refers to something further away from the medial plane

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9
Q

What does superficial, intermediate and deep refer to

A

The position of body parts when they are underlying or overlying structures

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10
Q

What are bilateral structures

A

These are paired structures that have right and left members

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11
Q

What are contralateral structures

A

Structures found on opposite sides of the body

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12
Q

What is flexion

A

The bending or decreasing of the angle between the bones or parts of the body

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13
Q

What is extension

A

Increasing the angle between a bone or part of the body

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14
Q

What is dorsiflexion

A

Flexion at the ankle join

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15
Q

What is plantarflexion

A

This is extension of the ankle joint such as standing on your toes

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16
Q

What is abduction

A

Moving away from the medial plane such as spreading your fingers away from the middle digit

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17
Q

What is pronation of the forearm

A

Rotation of the arm so the palm faces posteriorly and the dorsum faces anteriorly

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18
Q

What is inversion of the sole of the foot

A

Moving it inwards towards the medial plane

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19
Q

What is elevation

A

The raising of parts superiorly such as shrugging

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20
Q

What is depression

A

The lowering of parts inferiorly

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21
Q

What is the thoracic plane

A

The plane at T4/5

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22
Q

Where is the subcostal plane

A

At T12 the 12th vertebrae just below the ribs

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23
Q

How many cervical levels are there

A

7

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24
Q

How many thoracic levels are there

A

12

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25
Q

How many lumbar levels are there

A

5

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26
Q

How many sacral levels are there

A

5

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27
Q

What is the sympathetic nervous system

A

This is involved in fight or flight

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28
Q

What is the parasympathetic nervous system

A

Rest and Digest

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29
Q

Where is the origin of the parasympathetic nervous system

A

Cranio-sacral origin with cranial from the brain stem

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30
Q

What is the make up of the sympathetic nervous system

A

It’s a thoraco-lumbar make up

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31
Q

What makes up the two-neurone model

A

The preganglionic and postganglionic neurone with a synapse between

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32
Q

How many neurones does the SNS have to go through after the spinal cord to a skeletal muscle

A

1

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33
Q

How many neurones does the ANS go through before reaching its effector

A

2

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34
Q

What ganglion is longer when comparing the sympathetic and parasympathetic nervous systems

A

The sympathetic contains short preganglionic neurones and long postganglionic whereas the parasympathetic is the other way round

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35
Q

What neurotransmitter is released by preganglionic neurones

A

Ach

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36
Q

What receptor does Ach bind to

A

N2

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37
Q

What is the most common neurotransmitter to the effector in the sympathetic nervous system

A

Norepinephrine

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38
Q

What is the most common neurotransmitter to the effector in the parasympathetic nervous system

A

Ach

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39
Q

What is the exception in which the sympathetic nervous system releases Ach

A

To the sweat glands

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40
Q

What is the anomaly with regards to the sympathetic nervous system when a postganglionic neurone is not involved

A

When going to the adrenal gland the preganglionic neurone directly releases Ach

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41
Q

What receptors bing epinephrine and norepinephrine

A

Adrenergic receptors

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42
Q

What two receptors make up cholinergic receptors

A

Muscarinic and nicotinic

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43
Q

What are metabotropic receptors

A

These are receptors that, upon activation, activate a G protein

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44
Q

What three receptor types are metabotropic

A

Alpha, beta (both adrenergic) and muscarinic

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45
Q

What are the three types of G-proteins with alpha subunits

A

G-protein-q
s
l

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46
Q

What does s and i refer to with regards to the g proteins

A

s is stimulatory of ATP and i is inhibitory of this

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47
Q

What is the role of the downstream enzyme linked with g-protein l and s

A

The conversion of ATP into cAMP

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48
Q

What is the downstream enzyme linked with g-protein q

A

Phospholipase C- it converts IP3 and DAG

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49
Q

What G protein do beta receptors release

A

G-protein s

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50
Q

What g protein do alpha 1 receptors release

A

G-protein q

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51
Q

What G protein do alpha 2 receptors release

A

G-protein l

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52
Q

What G-protein do recpetors M1, 3 and 5 release upon Ach binding and what does this produce

A

G-protein q to produce cAMP

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53
Q

What G-protein is released upon Ach binding with M2 or 4

A

G-protein l to inhibit cAMP production

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54
Q

What does binding of Ach to N1 and N2 receptors result in

A

Depolarisation and the opening of Na+ channels to initiate muscle contraction

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55
Q

What receptors have the highest affinity for binding norepinephrine?

A

Alpha adrenergic receptors

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56
Q

What receptor the highest affinity for epinephrine

A

Beta 2 receptors

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57
Q

What is the affinity for the neurotransmitters epinephrine and norepinephrine on beta 1 recpetors

A

Equal affinity for both

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58
Q

What is the epimysium

A

A sheet of fibrous elastic tissue surrounding a muscle

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59
Q

What is the myofibril

A

A repeated unit made up of thick and thin filaments

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60
Q

What is the plasma membrane in a muscle cell

A

Sarcolemma

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61
Q

What is the role of the m line

A

to anchor and align the thick and thin filaments

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62
Q

What is the I band

A

This contains only thin filament attached to the Z disc

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63
Q

Where are the thick filaments anchored to

A

The M line

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64
Q

What is the region of both thick and thin filaments

A

The A band

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65
Q

What is the region of only thick filaments

A

The H band

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66
Q

What are t-tubules

A

Extensions of the sarcolemma and connected to the sarcoplasmic reticulum

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67
Q

What connects the t-tubules with the sarcoplasmic reticulum

A

Terminal cristae

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68
Q

What three components make up the triad

A

Terminal cristae, sarcoplasmic reticulum and the t-tubules

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69
Q

What are the three different types of troponin and what do they bind

A

Troponin T- tropomyosin
Troponin C- Calcium
Troponin I- actin

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70
Q

What initiates the conformational change in troponin so that the actin filaments are exposed to the myosin heads

A

The binding of Ca2+ to troponin C

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71
Q

What does the myosin pull the actin filament towards during a power stroke

A

The M line

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72
Q

What occurs to the Z line, I band, H zone and A band during a power stroke

A

The Z line, I band and H zone all decrease whilst the A band remains unchanged

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73
Q

Where are the Ca2+ ions stored

A

The sarcoplasmic reticulum

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74
Q

What receptor does Ach bind in skeletal muscles following an influx of calcium ions in the presynaptic neurone

A

The N1 receptor

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75
Q

What does the activation of the N1 receptor in a skeletal muscle result in

A

The depolarisation of the membrane due to an influx of Na+ which results in the release of Ca2+ in the sarcoplasmic reticulum

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76
Q

What shape are smooth muscle cells

A

Spindle shaped with a central nucleus

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77
Q

What is the difference between single unit smooth muscle cells and multi unit

A

Single unit- when one depolarises they all do however in multi unit this doesn’t necessarily happen

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78
Q

What does calcium influx result in in smooth muscle cells

A

Ca2+ enters the cell and binds to calmodulin to form a calcium-calmodulin complex instead of binding to troponin C

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79
Q

How does the activation of cross bridges differ with smooth muscle in comparison to skeletal muscles

A

In smooth muscle the myosin heads are directly phosphorylated by the calcium-calmodulin complex

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80
Q

What three things are slower in smooth muscle cells in comparison to skeletal muscle

A

Slower Ca2+ influc
Slower cross bridge formation
Slower removal of Ca2+ so longer stages of depolarisation

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81
Q

What enzyme dephosphorylates the myosin heads in smooth muscle

A

Myosin light chain phosphotase

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82
Q

What hormone stimulates contraction of the uterus in pregnancy

A

Oxytocin

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83
Q

What hormone stimulates vasoconstriction and inhibits bronchioconstriction

A

Epinephrine

AGII only stimulates vasoconstriction

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84
Q

How does the Na+/K+ pump work

A

It actively pumps 3 Na+ out of every cell for every 2 K+ in

85
Q

Why does the membrane potential in neuromuscular cells settle at -70mV even if there is still a concentration gradient

A

This occurs as there is still an electrochemical gradient across the membrane due to the -70mV of charge difference
As a result Na+ doesn’t move across due to it’s attraction to the -ve inside of the cell

86
Q

Why does the movement of Na+ stop at +60mV despite Na+ still having a concentration gradient across the membrane

A

Because there is no longer an electrochemical gradient to power the movement of these ions so the movement across the membrane stops

87
Q

What is the positive peak of an action potential and why does it stop there

A

+40mV as here voltage gated Na+ channels close rapidly to stop Na+ from entering the axon
This also opens the voltage gated K+ channels which means K+ flows out of the axon to initiate repolarisation

88
Q

Why does hyperpolarisation occur

A

Because K+ channels close slowly so more K+ than desired is let out of the axon

89
Q

Why do myelinated neurones have a faster rate of action potentials

A

The action potential jumps between nodes of ranvier

90
Q

What is the structure of electrical synapses

A

These have proteins joining them called a connexon that allows neurons to flow through it and results in less delay of signal

91
Q

What is the structure of chemical synapses and how does it differ to electrical ones

A

These contain a synaptic cleft so the neurones aren’t connected and neurotransmitters have to carry the signal across these synapses
However these synapses can be modulated whereas electrical synapses cant

92
Q

What ions are at each synapse

A

The presynaptic neurones contain Ca2+ voltage gated channels whereas the postsynaptic neurone contains Na+ ligand gated channels

93
Q

What are the two classes of neurotransmitters

A

Excitatory and inhibitory

94
Q

What is the difference between excitatory and inhibitory neurotransmitters

A

Excitatory cause membrane depolarisation whereas inhibitory neurotransmitters do not cause depolarisation, instead they cause hyperpolarisation

95
Q

What are the major neurotransmitters and what is their function (8)

A 
Adrenaline (fight or flight)
Noradrenaline "
Dopamine (pleasure)
Serotonin (dictates mood and more means happier)
GABA (calming for sleep)
Ach (neuromuscular junctions)
Glutamate (excitatory in learning)
Endorphin (euphoria transmitter after exercise)
96
Q

What are ionotropic receptors coupled to

A

Ion channels

97
Q

What type of receptors are glutamate and GABA attached to

A

Both metabotropic and ionotropic

98
Q

What type of receptors does serotonin bind to

A

ionotropic receptors

99
Q

What type of receptors do dopamine and norepinephrine bind to

A

Metabotropic

100
Q

What are the five segemnts of the spinal cord

A

cervical, thoracic, lumbar sacral and coccygeal

101
Q

How many pairs of spinal nerves are there

A

31

102
Q

How many cranial nerves are there

A

12

103
Q

What type of neurone is the ventral root

A

A motor neurone

104
Q

What type of neurone is a dorsal root

A

Sensory

105
Q

Which side of the sign is anterior, ventral or dorsal

A

Ventral

106
Q

What kind of matter is in the spine and how is it arranged

A

Grey matter centrally surrounded by white matter

107
Q

What is the most abundant CNS neuroglia

A

Astrocytes

108
Q

What is the role of microglial cells

A

These are defensive cells in the CNS

109
Q

What cells line the cerebrospinal fluid filled cavities and what type of epithelium are they

A

Ependymal cells

simple cuboidal epithelial cells

110
Q

What is the role of oligodendrocytes in the CNS

A

They myelinate neurones by forming the myelin sheaths

111
Q

What cells myelinate neurones in the peripheral nervous system

A

Schwaan cells and satellite cells

112
Q

How do oligondendrocytes form myelin sheaths around Schwaan cells

A

They extend their plasma membrane to wrap around the neurone and they can do this on multiple different axons

113
Q

What is the difference between Schwaan cells and oligodendrocytes

A

Schwaan cells are much closer together and can only produce one myelin sheath

114
Q

What is the Therapeutic index of a drug

A

It is the toxic dose of a drug for 50% of the population, divided by the minimum effective dose for 50% of the population

115
Q

What does a high TI suggest

A

That the drug has a favourable safety and efficacy profile

116
Q

What can the lack of specificity of a drug result in

A

This can lead to unwanted side effects as it may be acting on a different area simultaneously as being effective on a target area

117
Q

What is tolerance

A

The reduction in drug response after repeated administration of that specific drug

118
Q

What is desensitisation

A

This is when a drug has stimulated it’s target and cannot stimulate it again rapidly after and thus doesn’t have an effect

119
Q

Why may a drugs effect be reduced (5)

A

The receptors may undergo a conformational change that makes them harder to activate
The receptors may be internalised by the cell upon repeated activation so fewer are on the surface
The neurotransmitters or mediators may be depleted by the drugs
Usage may result in metabolic degradation
Some drugs can cause physiological adaptations such as fluid in the body

120
Q

What can change the drugs effectiveness of a drug

A

The amount of water taken with it

The formulation and packaging of a drug

121
Q

What can alter in the GI tract effectiveness in absorbing drugs

A

Gut motility- excessive movement leads to decreased absorption
pH- poor absorption of strong acids and bases
Interactions with food
Particle size and formulation
Gut resistant coating

122
Q

What are hormones

A

Chemical messengers synthesised by specific tissues that are carried in the blood stream to non adjacent sites in order to elicit actions

123
Q

What hormones do white blood cells produce

A

Cytokines that act on tissues in the immune system

124
Q

What is endocrine signalling

A

When a cell signals to a distant cell via a hormone released into the circulatory system

125
Q

What is paracrine signalling

A

When a cell communicates to the cell next to it

126
Q

What is autocrine signalling

A

When a cell signals to itself

127
Q

What is synaptic or neurocrine signalling

A

When a neuron signals to a cell using neurotransmitter

128
Q

Where is the hypothalamus located

A

At the base of the forebrain

129
Q

What is located at the inferior part of the hypothalamus

A

The pituitary stalk that gives rise to the pituitary gland

130
Q

What are the two lobes of the pituitary gland

A

The anterior and posterior pituitary gland

131
Q

What is the role of the posterior and anterior pituitary gland

A

The posterior stores hormones produced by the pituitary gland whilst the anterior actually makes some

132
Q

Where are neurohormones produced by the hypothalamus secreted into

A

The capillary plexus in the posterior pituitary gland

133
Q

Where does the anterior pituitary gland secrete its hormones

A

Directly into the extracellular fluid

134
Q

How is the anterior pituitary gland hormone production controlled

A

It is instructed by the hypothalamus through hormone release

135
Q

What is the role of TRH

A

It stimulates the release of thyroid stimulating hormone and prolactin

136
Q

What is the role of GnRH

A

it stimulates FSH and LH production

137
Q

What is the role of CRH

A

It stimulates adrenocorticopic hormone (ACTH) and this is essential for adrenal gland functioning

138
Q

What is the role of GHRH (growth hormone regulating hormone)

A

It stimulates growth hormone release

139
Q

What is the role of PRF (prolactin release factor)

A

stimulates the release of prolactin

140
Q

What inhibits prolactin release

A

Dopamine

141
Q

What does growth hormone do

A

It stimulates growth and targets the liver

142
Q

What does thyroid stimulating hormone do

A

It targets the thyroid glands to release thyroid hormone that regulates the bodys metabolic rate

143
Q

What is the role of prolactin

A

It acts on the mammary glands and reproductive organs and stimulates milk production

144
Q

What does ACTH do

A

It targets the adrenal cortex to release cortisol

145
Q

What and how does excess growth hormone result in

A

Acromegaly which occurs when more growth hormone is produced despite the growth plates being closed
Gigantsim occurs when there is excess before the plates close

146
Q

What can growth hormone deficiency cause

A

Dwarfism

147
Q

What does a lack of ADH result in

A

Cranial diabetes insipidus that results in thirst and dilute urine production

148
Q

What is Kallmann syndrome

A

The lack of GnRH which reduces LH and FSH secretion

149
Q

What occurs when the brain feels physical or emotional stress

A

The brain releases corticotropin-releasing hormone that stimulates the pituitary gland to release ACTH
This stimulates the adrenal glands to release cortisol

150
Q

What does nervous stimulation of the adrenal glands result in

A

Release of adrenaline

151
Q

Where are the adrenal glands located

A

Above the kidneys

152
Q

What are the three layers in the cortex of an adrenal gland from superficial to deep and what do they secrete

A

Zona glomerulosa- mineralocorticoids
Zona fasciculata- secretes glucocorticoids involved in stress responses
Zona reticularis- secretes an androgen precursor DHEA and glucocorticoids

153
Q

What can excess cortisol lead to

A

Cushing’s syndrome

154
Q

What results in too little aldosterone and cortisol

A

Addison’s disease due to adrenal cortex insufficiency and this results in degradation of the adrenal glands

155
Q

What are examples of positive feedback

A

Oxytocin secretion during childbirth and oestrogen secretion in the menstrual cycle before ovulation

156
Q

What are steroid hormones synthesised from

A

cholesterol

157
Q

How can steroid hormones pass through the plasma membrane

A

They’re lipophilic so can diffuse through the plasma membrane

158
Q

How do steroid hormones travel in the bloodstream

A

They travel bound to plasma proteins as they’re hydrophobic

159
Q

Where are non-steroid hormones stored

A

secretory vesicles in cells

160
Q

What happens to the Cell surface receptor when a hormone binds to it

A

They undergo a conformational change on the intracellular domain

161
Q

How do steroid hormones interact with target cells

A

They bind to intracellular receptors and then cause a conformational change and enter the nucleus, binding to specific sections of DNA called hormone response elements to inhibit or stimulate it

162
Q

What is the first step of cell surface receptors upon activation

A

They phosphorylate proteins

163
Q

What does a G protein do upon activation

A

It gains GTP after losing GDP and breaks down this GTP into GDP

164
Q

How do tyrosine kinase receptors work

A

ATP is hydrolysed into ADP and the phosphate group phosphorylates tyrosine alongside tyrosine kinase
This triggers the release of relay proteins

165
Q

What effector protein converts ATP into cyclic AMP which acts as a secondary messenger

A

Adenylate cyclase

166
Q

What is PIP2 broken down into to form a secondary messenger

A

IP3

167
Q

What is the role of IP3

A

It binds to the ER to open ligand gated Ca2+ channels that activates multiple cellular responses

168
Q

What is a drug

A

A chemical, other than an essential nutrient, which when administered, produces a biological effect

169
Q

What is therapeutics in medicine

A

The area concerned with the treatment of disease

170
Q

What is pharmacokinetics

A

The measurement and formal interpretation of changes with time of drug concentrations in one or more different regions of the body

171
Q

What are the four phases of pharmacokinetics

A

Absorption
Distribution
Metabolism
Excretion

172
Q

What are the 5 different routes of drug administration

A

Oral or rectal, precutaneous (skin), intravenous, intramuscular and inhalation

173
Q

Why might some drugs be taken simultaneously with other drugs despite not having a target organ

A

They may increase the absorption of the other drug that has a specific function

174
Q

What molecules move through the membranes most effectively

A

small hydrophobic molecules

175
Q

How rapidly do small uncharged polar molecules move through the plasma membrane

A

Quite quickly although the polar nature provides a slight barrier

176
Q

How fast do large uncharged molecules diffuse through the membrane

A

Quite slowly due to their size

177
Q

How quickly to ions diffuse through the plasma membrane

A

They can’t

178
Q

What is the pKa of a drug

A

The value of the pH at which the drug exists in a 50% ionised state

179
Q

What is the volume of distribution

A

The volume of litres that the drug distributes in comparison to the entire body water volume over a given time

180
Q

What is Kel

A

This is the elimination rate constant of a drug

181
Q

What effects the rate of distribution of a drug

A

Membrane permeability and blood perfusion

182
Q

What effects the distribution of a drug

A

Lipid solubility

plasma protein binding and tissue bending

183
Q

How is there a constant elimination of drugs from cells

A

As the drug is eliminated from the plasma this sets up a concentration gradient for the drug to move out of cells and into the plasma

184
Q

If a drug is a high plasma bound protein drug will this have a slower or faster effect

A

Slower

185
Q

What effects can the liver and gut have on drug action

A

They may reduce drug action as they absorb the drug before it reaches its target

186
Q

What is bioavailability

A

The proportion of drug dose which appears in the systemic circulation following administration

187
Q

Why does IV have a bioavailability of 100

A

because it bypasses the gut and liver

188
Q

Why are oral drugs bioavailability almost always below 100%

A

Because they have to bypass the liver and GI tract

189
Q

What affects rectal bioavailability

A

The interference with the GI tract

However some drugs can be absorbed directly in the rectal area

190
Q

What is the main family of enzymes, commonly found in the liver and GI tract, that are frequently involved in drug metabolism

A

Cytochrome P450 enzymes

191
Q

What is phase 1 of drug metabolism

A

The chemical modification of a drug to produce a marked change in biological effect

192
Q

What is phase 2 of drug metabolism

A

Metabolic reactions that add groups to the drug in order to prepare it for secretion

193
Q

What is pharmacodynamics

A

What the drug does to the body and refers to the events after the drug interacts with it’s receptor

194
Q

What is a ligand gated ion channel with regards to drugs

A

When a drug binds this may open or close this channel

This may change the charge in a cell rapidly

195
Q

What are kinase linked receptors and what can they do

A

These are linked to phosphorylation pathways to affect things such as gene transcription or protein synthesis

196
Q

What is an agonist

A

This is a ligand that binds to a receptor to cause a biological cellular response

197
Q

What is the affinity of a drug

A

How easily the drug will bind with its receptor to form an agonist-receptor complex

198
Q

What is the EC50 concentration

A

The concentration of the drug that requires 50% effect and defines the affinity of the drug to its receptor

199
Q

What is the efficacy of an agonist

A

The ability of a drug to elicit a response upon binding to its receptor

200
Q

What is the efficacy of a full agonist

A

1

201
Q

What is an antagonist

A

This binds to a receptor but doesn’t activate it

202
Q

Do antagonists have affinity?

A

Yes

203
Q

What is the efficacy of antagonists

A

0 as it elicits no response upon binding to a receptor, it is merely competitive

204
Q

Do reversible antagonists bind to the same or different sites on a receptor as the agonist

A

The same

205
Q

How can you overcome reversible antagonists

A

Increasing the concentration of the agonist

206
Q

What is lowered in the presence of a competitive antagonist

A

The EC50

207
Q

Is the binding of a non-competitive antagonist reversible or irreversible

A

irreversible

208
Q

What changes in the presence of a non competitive antagonise, the efficacy or the EC50

A

The efficacy

Year 1 Medicine Newcastle (8 decks)

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