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ACEM Primary VIVA > VIVA: Physiology - Nerve and muscle cell, and nervous system physiology > Flashcards

VIVA: Physiology - Nerve and muscle cell, and nervous system physiology Flashcards

1
Q

Draw a skeletal muscle action potential

A
  • need correct shape, axes, resting membrane potentials and durations (+/- 25%)
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2
Q

What is the sequence of events in the contraction of a skeletal muscle fibre, starting at the motor-end plate?

A

6/10 to pass:
1. Activation of voltage-gated Ca2+ channels in presynaptic membrane
2. Ca2+ influx into the cell
3. Exocytosis of preformed ACh into synaptic cleft
4. Diffusion of ACh across synaptic cleft
5. Binding of ACh to post-synaptic nicotinic receptor
6. Increased Na+ and K+ conductance in end-plate membrane of muscle
7. Generation of end-plate potential
8. Generation of action potential in muscle fibres
9. Inward spread of depolarisation along T tubules
10. Release of Ca2+ from terminal cisterns of sarcoplasmic reticulum, and diffusion to thick and thin filaments
11. Binding of Ca2+ to troponin C, uncovering myosin-binding sites on actin
12. Actin-myosin binding and sliding of thin on thick filaments, producing movement

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3
Q

What is the sequence of events in the relaxation of a skeletal muscle fibre?

A
  1. Ca2+ pumped back into sarcoplasmic reticulum*
  2. Release of Ca2+ from troponin C
  3. Cessation of interaction between actin and myosin*
  • needed to pass
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4
Q

Describe the synthesis of acetylcholine at the neuromuscular junction

A
  1. Acetylcholine is synthesised in the pre-synaptic terminal and stored in synaptic vesicles along with ATP and proteoglycan, until required for synaptic neuronal transmission
  2. Acetyl CoenzymeA + choline* is catalysed by the enzyme choline acetyltransferase to form acetylcholine
  • needed to pass
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5
Q

Once acetylcholine is released into the synaptic cleft, how is its effect terminated?

A

ACh removed from synaptic cleft by acetylcholinesterase -> broken down into acetate and choline
Choline reuptake into the presynaptic nerve terminal
Acetate to liver and metabolised

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6
Q

Draw a nerve action potential and indicate the sequence of events that occur

A

Dependent on changes in Na+ and K+ conductance:
1. When a depolarising stimulus occurs, the voltage-gated Na+ channels * become active and Na+ enters the cell
2. When the threshold potential* is reached, the voltage-gated Na+ channels overwhelm the K+ channels
3. Entry of Na+ causes opening of more voltage-gated Na+ channels and further depolarisation (positive feedback loop), resulting in the upstroke of action potential
4. The membrane potential moves close to the equilibrium potential for Na+ (+60mV)
5. The voltage-gated Na+ channels then enter an inactivated state for a few milliseconds before returning to the resting state
6. Reversal of membrane potential limiting further Na+ influx, and opening of voltage-gated K+ channels results in repolarisation* and end of action potential
7. Slow return of K+ channels results in hyperpolarisation
8. Returns to resting membrane potential

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7
Q

Describe the sequence of events that leads to release of acetylcholine at the neuromuscular junction

A
  1. Impulse arrives at the motor neuron ending which causes voltage-gated calcium channels* to open
  2. Influx of calcium triggers release of acetylcholine into the synaptic cleft
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8
Q

What happens to acetylcholine after release into the synaptic cleft?

A
  1. When vesicle releases ACh into the synaptic cleft, it is rapidly broken down into acetate and choline by the enzyme acetylcholinesterase
  2. Choline is actively transported back into the presynaptic terminal to be re-used
  3. ACh binds to nicotinic receptors on the motor end-plate leading to Na+ entry and a subsequent depolarising end-plate potential
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9
Q

Define resting membrane potential of a neuron

A

The potential difference* across the cell at rest, with inside negative relative to outside
Normal RMP of a neuron is -70mV

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10
Q

Explain how the resting membrane potential of a neuron is generated

A

The gradients are actively maintained by Na+ / K+ ATPase*
Na+ / K+ ATPase actively pumps Na+ out and K+ into the cell using ATPase for energy
Na+ then passively flows back into the cell via channels down its concentration gradient, and K+ passively flows out of cell via K+ channels down its concentration gradient
At rest, there are more open K+ channels than Na+ channels, so the passive permeability to K+ is greater (hence why RMP of neuron is close to equilibrium potential for K+)

  • needed to pass + concept of Na+ in and K+ out with passive flow in opposite direction
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11
Q

Why is a cell more excitable in hyperkalaemia?

A

RMP moves closer to threshold potential for eliciting an action potential (becomes less negative on inside of cell)

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12
Q

What factors affect cerebral blood flow?

A

3/5 to pass:
- MAP at brain level
- MVP at brain level
- ICP
- Viscosity of the blood
- Local constriction/dilatation of cerebral arterioles

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13
Q

What is the mechanism of the Cushing response?

A

Increased ICP results in decreased CBF
Ischaemia of vasomotor centre increases sympathetic nervous system output
BP increases, which stimulates baroreceptors to produce vagal response that decreases HR and RR

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14
Q

What is the Monro-Kellie doctrine?

A

The sum of the volume of blood (75ml), CSF (75ml) and brain (1400g) in the cranium must be relatively constant
An increase in one should cause a reciprocal decrease in either one or both of the remaining two
Negative effects on these therefore if addition intracranial volume (e.g. SDH/EDH) occurs

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15
Q

What is the pathogenesis of fever?

A

2 needed to pass + at least one of toxins and inflammatory pyrogens:
- Bacterial toxins (e.g. endotoxin) act on monocytes, macrophages, and Kupffer cells to produce cytokines that act as endogenous pyrogens
- Inflammatory endogenous pyrogens (IL-1, IL-6, IFN and TNF-a) can be independently produced to cause fever
- Cytokines can also be produced in the CNS and act directly on thermoregulation centres
- Acts on the circumventricular organs (e.g. OVLT) which activates the preoptic area of the hypothalamus causing release of prostaglandins -> resets the homeostatic set point resulting in a fever

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16
Q

What is the body’s response to hot and cold environments?

A

Mechanisms activated by cold* (posterior hypothalamus):
- Increasing heat production: shivering, hunger, voluntary activity, catecholamine release
- Decreasing heat loss: skin vasoconstriction, curling up, piloerection

Mechanisms activated by heat (anterior hypothalamus):
- Decreasing heat production: anorexia, apathy, inertia
- Increasing heat loss: cutaneous vasodilation, sweating, respiration

  • need 1 mechanism for each of heat production and loss in hot and cold environment
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17
Q

What are upper motor neurons?

A

Upper motor neurons usually refer to corticospinal neurons that innervate spinal motor neurons* (also includes brainstem neurons that control spinal motor neurons)

  • needed to pass
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18
Q

What clinical features are seen when upper motor neurons are injured?

A

Damage initially causes muscles to become weak and flaccid* but eventually leads to spasticity, hypertonia, hyperactive stretch reflexes* and abnormal plantar extensor reflex*

  • 2 needed to pass
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19
Q

What is the physiological basis of clonus?

A

Loss of descending cortical input to inhibitory neurons called Renshaw cells, and therefore loss of inhibition of antagonist* muscle groups, resulting in repetitive sequential contractions of ankle flexors and extensors

  • needed to pass
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20
Q

List the long term complications of spinal cord injury

A

2 to pass:
- Pressure ulcers
- Protein / muscle degradation
- Hypercalcaemia
- Renal stones (due to hypercalcaemia)
- Urinary tract infection

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21
Q

Describe the components of the stretch reflex

A

Monosynaptic reflex in which skeletal muscle is stretched with contraction of muscle as the response:
- Stretch receptor sensory neuron* makes an excitatory connection with the extensor motor neuron* of the same muscle, and an inhibitory interneuron projecting to the antagonistic muscle
- Sense organ is the muscle spindle, with impulses from the spindle transmitted to the spinal cord by fast sensory fibres passing directly to the motor neurons supplying the same muscle
- Neurotransmitter at the central synapse is glutamate
- Components include sensor (muscle spindle), afferent nerve, integrator (monosynapse on motor neuron), efferent nerve*, effector (intrafusal fibres)

*needed to pass

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22
Q

How is the stretch reflex different from the withdrawal reflex?

A

Withdrawal reflex is a polysynaptic reflex
Also has afferent and efferent limbs, but sensory organ is a nociceptor (responds to painful stimulus), and the central integrator consists of polysynaptic connections in the spinal cord* (i.e. one or more interneurons interposed between afferent and efferent neurons)
Efferent limbs are motor nerves to effector muscles on the ipsilateral and contralateral sides
Results in flexion and withdrawal of the ipsilateral limb*, and extension of the contralateral limb

  • needed to pass
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23
Q

What is a typical example of a stretch reflex?

A

Knee jerk response

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24
Q

How does the body lose heat?

A

3 to pass:
- Radiation and conduction, mediated by vasodilation (70%)
- Vaporisation of sweat (27%)
- Respiration (2%)
- Urination and defecation (1%)

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25
Q

What are the body’s adaptive responses to cold environments?

A

3 to pass:
- Muscular: shivering, increased voluntary activity, curling up
- Vascular: vasoconstriction
- Increased noradrenaline and adrenaline secretion
- Hunger
- Horripilation

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26
Q

How does the body produce heat?

A

Basal metabolic processes*
Food intake

  • needed to pass
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27
Q

What part of the brain controls the reflex responses activated by cold?

A

Posterior hypothalamus

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28
Q

Where is thirst regulated?

A

Hypothalamus in the diencephalon

29
Q

What factors increase thirst?

A
  1. Increased osmotic pressure in plasma*
    - Sensed by osmoreceptors in the anterior hypothalamus
  2. Decreased ECF volume*
    - E.g. in haemorrhage
    - Sensed by baroreceptors in heart and blood vessels to increase thirst
    - Increased in renin -> AT II -> acts on diencephalon neurons to increase thirst
  3. Psychological
    - E.g. acute psychosis
  4. Others:
    - Increased liquids during eating (prandial drinking)
    - Other poorly understood mechanisms such as increased osmolality as food is absorbed, and GI hormones acting on the hypothalamus
30
Q

In what situations may thirst sensation be blunted?

A

Hypothalamic disease
Direct damage to the diencephalon
Altered mental state*
Psychosis
Lesion of anterior communicating artery (supplies the hypothalamus)
Diet high in protein (products of protein metabolism cause water diuresis)

  • needed to pass + one other
31
Q

Describe the neural connections of the visual pathway

A

Retina* -> optic nerve* -> optic chiasm* -> optic tract* -> lateral geniculate body (hypothalamus) -> geniculocalcarine tract -> primary visual cortex (occipital lobe)*

At the optic chiasm, nasal fibres decussate to the contralateral side*

Other connections:
- Pupillary reflexes and eye movements: optic tract (via superior colliculus) to pretectal midbrain, then to Edinger-Westphal nuclei in the oculomotor nerve
- Refined eye movements (vergence, near-point response): frontal cortex
- Endocrine and circadian responses to day/night cycle: retinal ganglion cells to suprachiasmatic nucleus in the hypothalamus

  • needed to pass
32
Q

Why is the fovea important for visual acuity?

A

Fovea is the centre of the macula, a thinned out rod-free portion of the retina where cones are densely packed* and each synapses on a single bipolar cell which in turn synapses on a single ganglion cell, providing a direct pathway to the brain
It is the point where visual acuity is the greatest*

  • one of these + one other to pass
33
Q

What ocular factors influence visual acuity?

A
  1. Optical factors:
    - State of the image-forming mechanisms (e.g. cataracts, keratitis, astigmatism, myopia, hyperopia)
  2. Retinal factors:
    - E.g. state of cones (retinopathies, optic neuritis)
  3. Stimulus factors:
    - E.g. illumination, brightness of stimulus, contrast between stimulus and background, length of time exposed to stimulus
34
Q

Describe in brief the sequence of events involved in producing a stretch reflex

A
  1. Stimulus (stretch)
  2. Sensory organ (muscle spindle within muscle body)
  3. Afferent sensory nerve
  4. Synapse in spinal cord to efferent motor nerve supplying the same muscle (transmitter involved is glutamate)
35
Q

What is summation of contractions?

A

The electrical response of a muscle fibre to repeated stimulation:
- Contractile mechanism does not have a refractory period, so repeated stimulation before relaxation has occurred produces additional activation and a response added to the contraction already present
- With rapidly repeated stimulation, individual responses fuse into one continuous contraction (tetanus or tetanic contraction)
- Complete tetanus occurs when there is no relaxation between stimuli, and the tension developed reaches 4x that of an individual twitch contraction
- Incomplete tetanus occurs when there are periods of incomplete relaxation between summated stimuli

36
Q

How does tetanic contraction occur?

A
  • Contractile mechanism has no refractory period *
  • Repeated stimulation before relaxation has occurred results in summation of contractions *
  • Fast repeated stimulation causes a fused continuous tetanic contraction (may be complete or incomplete)
  • Series of maximal stimuli at a frequency just below tetanising causes increasing tension between each twitch, due to increased Ca2+ availability
  • needed to pass
37
Q

What are the major differences in types of skeletal muscle?

A

Type I *:
- Slow
- Oxidative
- Red
- Moderate Ca2+ pumping, diameter and glycolytic capacity
- Slow myosin ATPase rate
- High oxidative capacity

Type II *:
- Fast
- Glycolytic
- White
- High Ca2+ pumping, diameter and glycolytic capacity
- Fast myosin ATPase rate
- Low oxidative capacity

  • 3 differences needed to pass
38
Q

Describe the sequence of events in contraction and relaxation of visceral smooth muscle

A
  1. Binding of ACh to muscarinic receptors
  2. Increased influx of Ca2+ into the cell *
  3. Activation of calmodulin-dependent myosin light chain kinase *
  4. Phosphorylation of myosin
  5. Increased myosin ATPase activity and binding of myosin to actin
  6. Contraction
  7. Dephosphorylation of myosin light chain phosphatase
  8. Relaxation or sustained contraction due to latch bridge and other mechanisms
  • needed to pass
39
Q

What factors influence intestinal smooth muscle contraction?

A
  1. Stretch of visceral smooth muscle causes contraction in the absence of innervation *
  2. Cold increases activity
  3. ACh decreases smooth muscle potential and increases spike frequency so resulting in more active muscle
  4. Adrenaline and noradrenaline increase smooth muscle potential and decrease spike frequency causing decreased muscle activity
  5. Neural inputs
  • needed to pass
40
Q

Describe the differences between the two types of acetylcholine receptors

A

Divided on basis of pharmacological properties into muscarinic and nicotinic *:
1. Muscarinic:
- Actions mimicked by muscarine and blocked by atropine
- Found in smooth muscle, glands and brain
- G-protein coupled to adenylyl cyclase and/or phospholipase
- M1 brain, M2 heart, M3 and 4 smooth muscle, M4 pancreas

  1. Nicotinic:
    - Actions mimicked by nicotine
    - Found in neuromuscular junction, autonomic ganglia and the CNS
    - Ligand-gated sodium ion channels
    - 5 subunits, with Ach binding site on alpha subunit
  • needed to pass + 2 sites of distribution
41
Q

Outline the biosynthesis of adrenaline

A
  • Dietary tyrosine mostly (some formed from phenylalanine)
  • Tyrosine transported into catecholamine-secreting neurons by concentrating mechanism
  • Tyrosine converted to DOPA by tyrosine hydroxylase (rate-limiting step, subject to feedback inhibition by dopamine and NA)
  • DOPA converted to dopamine by DOPA decarboxylase in the cytoplasm
  • Dopamine enters granulated vesicles and is converted to NA by dopamine B-hydroxylase
  • NA converted to adrenaline by PNMT (phenylethalonamine methyltransferase)
42
Q

How is the action of noradrenaline terminated?

A
  1. Post-synaptic binding
  2. Pre-synaptic binding
  3. Reuptake:
    - Reuptake at presynaptic neuron, then metabolised by MAO to inactive deaminated derivates or recycled
  4. Catabolised in synaptic cleft:
    - By COMT (catecholamine methyltransferase) to normetanephrine
43
Q

Which catecholamines act as neurotransmitters?

A

Noradrenaline
Adrenaline
Dopamine

44
Q

Describe the sequence of events at a noradrenergic synapse, following stimulation of a sympathetic nerve

A
  • Noradrenaline, which has been stored in granulated vesicles *, is released into the synaptic cleft by exocytosis *
  • Noradrenaline acts on postsynaptic and to a lesser extent presynaptic and glial receptors
  • In addition to binding to receptors, noradrenaline is also removed from the synaptic cleft by reuptake and catabolism
  • Reuptake into presynaptic neuron occurs via neurotransmitter transporter (NTT), and then is broken down to inactive product by monoamine oxidase (MAO) located on mitochondria
  • Synaptic catabolism to inactive product occurs via catechol-O-methyltransferase (COMT) located on the postsynaptic membrane
45
Q

Where are ion channels distributed in myelinated neurons?

A

Voltage-gated Na+ channels concentrated in node of Ranvier * and initial segment

  • needed to pass
46
Q

What ionic fluxes occur during the action potential of a neuron?

A
  • At firing level, there is a rapid influx of Na+ towards it equilibrium potential (60mV)
  • Na+ channels rapidly close and enter an inactivated state, and Na+ inhibits further Na+ influx
  • Voltage-gated K+ channels open
  • Slow K+ efflux completes repolarisation
  • Decrease in extracellular Ca2+ decreases the Na+ and K+ conductance required for an action potential
47
Q

Discuss the factors that affect conduction along a nerve cell

A
  1. Myelinated vs demyelinated
  2. Saltatory vs non-saltatory
  3. Size
  4. Direction of conduction
48
Q

What are the different types of nerve fibres?

A
  • Diameter and speed of conduction
  • Function (e.g. large and fast responsible for proprioception, conscious touch, somatic motor; small and slow responsible for pain, temperature and autonomic NS)
  • Gasser classification (A - alpha, beta, gamma, delta; B; C)
  • Numerical (Ia, Ib, II, III, IV)
49
Q

What is the clinical relevance of the different types of nerve fibres to emergency medicine?

A

Pain fibres are smaller and better penetrated by local anaesthetic, leading to loss of pain before loss of touch or proprioception

50
Q

In the synapse, where can inhibition occur?

A
  1. Post-synaptic:
    - Direct during the course of an IPSP and not the consequence of a previous discharge
    - Indirect due to the effect of a previous postsynaptic neuron discharge
  2. Pre-synaptic:
    - Mediated by neurons that end on excitatory endings forming an axo-axonal connection
    - Ca2+, Cl- and GABA are the transmitters involved
51
Q

What mechanisms are involved in inhibition at the synapse?

A
  1. Increased Cl- conductance:
    - Reduces Ca2+ influx and amount of excitatory transmitter released
  2. Voltage-gated K+ channels:
    - K+ also decreases Ca2+ entry
  3. Direct inhibition of excitatory transmitter release, independent of Ca2+ influx
52
Q

Describe the biosynthesis and storage of norepinephrine at the synaptic junction

A
  • Dietary tyrosine mostly (some formed from phenylalanine)
  • Tyrosine transported into catecholamine-secreting neurons by concentrating mechanism
  • Tyrosine converted to DOPA by tyrosine hydroxylase (rate-limiting step, subject to feedback inhibition by dopamine and NA)
  • DOPA converted to dopamine by DOPA decarboxylase in the cytoplasm
  • Dopamine enters granulated vesicles and is converted to NA by dopamine B-hydroxylase
  • NA stored bound to ATP, with protein chromogranin A
53
Q

What conditions are required to create a resting membrane potential?

A
  • Lipid bilayer
  • Unequal distribution of ions
  • Membrane must be permeable to ions
  • Concentration gradient
54
Q

What are the functions of serotonin?

A
  1. Regulation of vomiting reflex
  2. Regulation of mood
  3. Control of respiration
  4. Platelet aggregation and smooth muscle contraction
  5. Facilitate GI secretion and peristalsis
  6. Regulation of circadian rhythms
55
Q

What are the steps in synthesis and catabolism of serotonin?

A
  1. Hydroxylation and decarboxylation of tryptophan to form serotonin
  2. Released serotonin from serotonergic neurons is recaptured by an active reuptake mechanism and inactivated by MAO to form 5HIAA
  3. 5HIAA is excreted as a urinary metabolite
56
Q

What are the two major mechanisms of deafness?

A
  1. Conductive deafness:
    - Due to impaired sound transmission in external or middle ear
    - Affects all frequencies
  2. Sensorineural deafness:
    - Due to loss of cochlear hair cells (most commonly) or problems with CN VIII or within central auditory pathways
    - Affects some frequencies
57
Q

Explain the causes of conductive and sensorineural deafness in physiological terms and give examples

A
  1. Conductive:
    - Blockage of external canals (e.g. by wax or foreign bodies)
    - E.g. otitis externa or media, perforated eardrum, osteosclerosis
  2. Sensorineural:
    - E.g. degeneration (presbycusis), damage to outer hair cells (such as from prolonged noise exposure)
    - Aminoglycoside antibiotics
    - CN VIII tumours or cerebellopontine angle
    - CVA in medulla
58
Q

How can one differentiate between conductive and sensorineural deafness using a tuning fork?

A

Weber/Rinne with 256 tuning fork

(Weber - centre of forehead; Rinne - mastoid)

59
Q

What is nystagmus?

A

Characteristic jerky movement of the eye seen at the start and end of period of rotation *

Different types:
- Horizontal (eyes move in horizontal plane) *
- Vertical (head tipped sidewise in rotation)
- Rotatory (head tipped forward)

Direction of eye movement is identified by the direction of the quick component

  • needed to pass + 1 other type of nystagmus
60
Q

Why does nystagmus occur?

A

Reflex that maintains visual fixation on stationary points while the body rotates, although not initiated by visual impulses:
- When rotation starts, the eyes move slowly in a direction opposite to the direction of rotation, maintaining visual fixation * (vestibulo-ocular reflex)
- When the limit of this movement is reached, the eyes quickly snap back to a new fixation point and then again move slowly in the other direction *

  • needed to pass
61
Q

How is nystagmus mediated?

A

Slow component is initiated by impulses from the labyrinths *
Quick component is triggered by a centre in the brainstem *

62
Q

Describe the neural connections of the visual pathways

A
  • Retina
  • Optic nerve *
  • Optic chiasm *
  • Optic tract *
  • Lateral geniculate body (thalamus)
  • Geniculocalcarine tract
  • Primary visual cortex (occipital lobe *, Brodmann 17)

Other connections:
- Pupillary reflexes, eye movements: lateral geniculate nucleus to pretectal midbrain and superior colliculus
- Refined eye movement (vergeance, near-point response): to frontal cortex
- Endocrine and circadian responses to day/night cycle: optic chiasm to thalamic suprachiasmatic nucleus

  • needed to pass
63
Q

Describe the visual field defects of nerve sectioning at optic chiasm and optic tract on the right

A
64
Q

Describe how pain is transmitted from the periphery to the brain

A
  1. Sense organ:
    - Naked nerve endings * peripherally
  2. Transmission via:
    - Large fast myelinated A-delta fibres *
    - Small slow unmyelinated C fibres *
  3. Spinal cord:
    - Cell bodies of both fibre groups in dorsal root ganglia
    - Terminate on neurons in dorsal horns of spinal cord (“gate”): A-delta fibres on neurons in laminas 1 and 4, C fibres on laminas 1 and 2
  4. From spinal cord to brain via ventrolateral system *:
    - Second order neurons via ventrolateral system (including lateral spinothalamic) to thalamus *
    - Then third order neurons on to cerebral cortex *
  • 3/6 to pass + dorsal horn
65
Q

How can acute pain by modulated?

A
  1. “Gate theory” *:
    - Stimulation of large touch/pressure afferents causes inhibition of pain pathways in dorsal horn of spinal cord
  2. Stress-induced analgesia
  3. Drugs (e.g. opioids)
  4. Higher centre interpretation
  • needed to pass + 1 other
66
Q

What sites do opioid peptides act on?

A
  1. Receptors in afferent nerve fibres
  2. Dorsal horn region of spinal cord
  3. Periaqueductal grey matter in brain
67
Q

What are the characteristics of the different types of pain fibres?

A
  1. A-delta:
    - Myelinated *
    - Large diameter (2-5microns)
    - Fast * conduction rates (12-30m/s)
    - Modulate “fast” pain
    - Neurotransmitter is glutamate
  2. C:
    - Unmyelinated *
    - Small diameter (0.4-1.2microns)
    - Slow * conduction rates (0.5-2m/s)
    - Modulate “slow” pain (dull, intense, diffuse)
    - Neurotransmitter is substance P
  • needed to pass
68
Q

Define the term “referred pain”. From which structure is pain referred to the shoulder? Give another example of referred pain

A

Irritation of a visceral organ causing pain in a distant somatic structure that developed from the same embryonic segment or dermatome as the structure from which the pain originates
Diaphragmatic irritation referred to C5 dermatome at shoulder
E.g. cardiac pain to arm, ureteric pain to testicle

ACEM Primary VIVA (45 decks)

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