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Physiology I > CNS S2 > Flashcards

CNS S2 Flashcards

1
Q

External ear anatomy

A

Pinna, ear canal, tympanic membrane

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2
Q

Inner ear anatomy/function of each

A

Cochlea (hearing), vestibular apparatus (equilibrium)

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3
Q

Frequency and hearing

A

Low-frequencies are low-pitched sounds, high-frequencies are high-pitched

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4
Q

What range of sounds do humans hear (Hz)

A

16-20,000 Hz (10 octaves)

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5
Q

Amplitude and hearing

A

Amplitude determines loudness; the larger the amplitude, the louder the sound

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6
Q

How do soundwaves produce sound

A

Canal > vibrates eardrum > vibrates malleus bones > incus moves stapes > oval window > cochlea > round window

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7
Q

Oval window anatomy

A

A membrane between the middle and inner ear (cochlea). Stapes pushes against the window

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8
Q

Ossicles

A

Smallest bones in the body and carry vibrations from the eardrum to the oval window

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9
Q

Organ of Corti

A

Inside the cochlear duct in the vestibular and tympanic duct. Has receptor cells for hearing

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10
Q

Organ of Corti receptor cells name

A

Hair cells (mechanoreceptors)

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11
Q

Hair cells

A

Epithelial cells with 50-100 stiff stereocilia which extend to the tectorial membrane

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12
Q

Hair cells mechanism

A

Cilia bend towards longest cilium, depolarizing neurons to release a neurotransmitter to activate primary sensory neurons. Axons from these form the auditory nerve

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13
Q

Basilar membrane

A

Narrow and stiff membrane near the round and oval windows. Helicotrema end (wider and flexible at one end)

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14
Q

Basilar membrane function

A

Responds to different frequencies. High-frequency waves displace membrane at oval window, low-frequency waves at other end

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15
Q

Auditory signal pathway

A

Auditory nerves > cochlear nuclei in medulla > midbrain > medial geniculate nucleus in thalamus > auditory cortex in temporal lobe

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16
Q

How is loudness coded

A

By firing frequency (louder sounds have faster firing)

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17
Q

Conductive hearing loss

A

Hearing can’t be transmitted through the external or middle ear

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18
Q

Sensorineural hearing loss

A

Damage to hair cells or elsewhere in the inner ear

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19
Q

Central hearing loss

A

Damage to the to the cortex or pathways from cochlea to cortex. Trouble with interpreting sounds, not detecting

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20
Q

Rinne test

A

Tuning fork held against mastoid bone and then beside ear to determine where it’s louder.

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21
Q

Rinne test results

A

If louder through bone, there is conductive loss since sound can be transmitted through the bone

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22
Q

Weber test

A

Tuning fork held against forehead and midline to see which ear is louder

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23
Q

Weber test results

A

Louder in good ear with sensorineural, louder in bad ear with conductive

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24
Q

Vestibular apparatus and equilibrium

A

Utricle and saccule contain hair cells that activate with head tilt. Semicircular canals contain fluid to detect head rotation

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25
Q

Equilibrium pathway

A

Vestibular hairs > primary sensory neurons in vesitbular nerve > cerebellum OR synapse in medulle OR thalamus > cortex

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26
Q

Somatic senses

A

Touch, temperature, proprioception (body position), nociception (pain/itch)

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27
Q

Free nerve ending receptors

A

Detect mechanical stimuli, temperature, chemicals

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28
Q

Merkel receptors

A

Mechanoreceptor nerve endings in contact with epithelial (Merkel) disks

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29
Q

Encapsulated receptors

A

Mesinner and Pacinian corpuscles. Sheathed in connective tissue

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30
Q

Merkel disks

A

At the bottom of the epidermis. Sensitive to deformation, signal contact. More tonic than phasic

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31
Q

Meissner Corpuscles

A

Top of dermis mainly in erogenous zones. Detect sideways shearing. Phasic

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32
Q

Pacinian Corpuscles

A

Deep in dermis. Sense tiny, quick, displacements. Phasic

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33
Q

Thermoreceptors

A

Free nerve endings with more cold than warm receptors. Phasic-tonic

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34
Q

Nociceptors

A

Free nerve endings that respond to noxious, harmful stimuli (ex, chemicals from damaged cells, heat)

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35
Q

Small fibre afferents

A

C and A-delta which come from free nerve endings. C fibres are unmyelinated (slow pain), A-delta’s are thicker/myelinated (fast pain)

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36
Q

Long fibre afferents

A

A-delta. Come from Merkel disks or encapsulated mechanoreceptors. Myelinated

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37
Q

Long fibre projection

A

upward upon reaching spinal cord, run ipsilaterally to the medulla tracts (dorsal columns) Synapse in medulla

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38
Q

Small fibre projection

A

Synapse directly/via interneurons and motor neurons or on dorsal-horn neurons who run in spinothalamic tracts

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39
Q

Large fibre main functions

A

Provide feedback to the brain, especially motor cortex to manipulate objects

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40
Q

Small fibre main functions

A

Evoke simple responses to specific stimuli. Don’t need immediate input from the brain

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41
Q

Thalamus to the cortex

A

spinal cord/head > ventroposterolateral nucleus of thalamus/ventroposteromedial nucleus > primary somtaosensory cotex

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42
Q

Nociceptors and TRP ion channels

A

Transient receptor potential (TRP channels) which are also found in thermoreceptors

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43
Q

TRPV1 channels

A

Vanilloid receptors which respond to damaging heat/chemicals including capsaicin in chili

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44
Q

TRPM8 channels

A

Respond to cold and menthol in mints

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45
Q

Nociceptive signals

A

Evoke responses from the CNS and reach the limbic and hypothalamus. Descending pathways in thalamus can block cells in spinal cord

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46
Q

Referred pain

A

Pain in internal organs that is felt on the body surface

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47
Q

Pain gated by A-beta activity

A

C fibres in dorsal horn contact secondary neurons which are inhibited by A-fibre activity

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48
Q

Acetylsalicylic acid

A

Asprin. Inhibits prostaglandins and inflammation, slowing transmission of pain

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49
Q

Opioids

A

Decrease neurotransmitter release from primary sensory neurons and postsynaptically inhibits secondary sensory neurons

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50
Q

Smell and taste similarities

A

Forms of chemoreception

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51
Q

Olfactory epithelium

A

Contains olfactory receptors at the top of the nasal cavity

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52
Q

Olfactory epithelium pigment

A

Richness of colour is correlated with olfactory sensitivity

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53
Q

Olfactory receptor cells

A

Contain a single dendrite that extends to the epithelium to form non motile cilia that catch odorant molecules

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54
Q

How many primary odors do we have

A

About 400 as we have about 400 kinds of receptor cells

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55
Q

Odorant molecule binding

A

Binds to a receptor, activating G proteins, increasing cAMP to open cation channels for depolarization

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56
Q

How many cells must react before smells are sensed

A

40 cells, or, 40 odorant molecules are required

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57
Q

Olfactory receptor cell properties

A

Pinocytotic, short-lived, send axons to the brain through holes in the cribriform plate, project to olfactory bulb

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58
Q

Olfactory bulb

A

An extension of the cerebrum and lies on the underside of the frontal lobes. Projects directly to olfactory cortex (frontal/temporal)

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59
Q

Limbic system

A

Linked to motivation and emotion. Made up of hippocampus, amygdala, cingulate gyrus. Bulb projects here

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60
Q

Vomeronasal organ (VNO)

A

Found in rodents to respond to sex pheromones. Disappears during fetal development in humans

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61
Q

Taste buds

A

Live 10 days, we have around 5000. Each contain 100 receptor cells (epithelial cells) and contact oral cavity through taste pore

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62
Q

5 kinds of taste receptor cells

A

Sweet/umami (sugar/glu), bitter (poison), salty/sour (Na+, H+ ions)

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63
Q

Type I taste receptors

A

Sense salt

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64
Q

Type II taste receptors

A

Sense sweet, bitter and umami (release ATP which act on type III)

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65
Q

Type III taste receptors

A

May sense sour (synapse with sensory neurons, activating them with serotonin)

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66
Q

Membrane proteins for taste receptor cells

A

Sweet, umami, bitter have G protein called gustducin for ATP release. Salt/sour is not G protein linked (uses ion channels)

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67
Q

Taste signal pathway

A

Receptor cells in taste buds excite cranial nerves VII, IX, X which synapse in the medulla and thalamus to the cortex

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68
Q

Simple reflexes

A

Sensory neurons synapse with motor neurons in the spinal cord (simplest form of motor control)

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69
Q

Reflexes

A

Innate and genetically determined. Efferent signals (sensory stimulus > motor response)

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70
Q

Monosynaptic pathway

A

Sesnory afferent neuron synapses directly to motor neurons in CNS to produce response

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71
Q

Polysynaptic pathway

A

Sensory neuron synapses with interneuron that synapses with motor neurons

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72
Q

Stretch reflex

A

Subconscious (ex, posture) that is triggered by passive muscle stretch from applied load/contraction, causing active contractive

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73
Q

Stretch reflex properties

A

Essential for posture, strongest in postural muscles, multisynaptic paths, suppressed during movement

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74
Q

Golgi tendon reflex

A

Contracted, relaxed. Afferents synapse on interneurons in the intermediate zone of spinal cord to inhibit motor neurons of the same muscle

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75
Q

Golgi tendon stimulus/response

A

triggered by active tension in muscle, causing relaxation through negative feedback

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76
Q

Flexion withdrawal reflex

A

Triggered by noxious inhurt of limb, causing flexion of proximal joints to the stimulus (slow, multisynaptic)

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77
Q

Reciprocal inhibition of reflexes

A

Activation of one motor nucleus is coupled to inhibition of antagonistic motor nuclei

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78
Q

Patellar tendon reflex

A

Patellar tendon tap causes quad stretch/contraction and hamstring contraction inhibition

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79
Q

Cross extension flex

A

Step on something sharp, causing flexion on leg where the pain is an extension on other (multisynaptic)

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80
Q

Extensor thrust reflex

A

Pressure on the sole of the foot causes activation of leg extensors (walking)

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81
Q

Babinski sign

A

Extensor thrust reflexes are influenced by the corticospinal tract.

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82
Q

Corticospinal tract damage

A

Reflex pattern is switched to flexion withdrawal

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83
Q

Vestibulo-spinal reflex

A

Downward deviation of head on one side activates otolith afferents for downhill limb extension on same size

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84
Q

Central pattern generators

A

Networks of interneurons in the spinal cord and brainstem that coordinate interaction of motor groups

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85
Q

Leg step cycle CPGs

A

2 CPGs for each leg; flexor burst generators, extensor burst generators

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86
Q

3 properties of the leg step cycle

A

1) Pacemaker neurons: diffuse excitation
2) Reciprocal inhibition: only one CPG on at a time
3) Phase-dependent reflexes

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87
Q

Flexor burst generator activation

A

Activates flexor motor neuron in the ventral horn causing flexion

88
Q

Which phase has a fixed duration

A

Flexion phase (swing phase when the leg is in the air)

89
Q

Extensor burst generator activation

A

Activates extensor motor neuron in ventral horn for leg extension

90
Q

What causes locomotion speed

A

Stance phase duration (extension phase)

91
Q

Phase-dependent reflexes in the stance phase

A

Reflexes that can be modulated based on phase.

1) Stretch reflex
2) Golgi tendon reflex
3) Extensor thrust reflex

92
Q

E3 (stance phase) ends when ___

A

1) leg is not bearing weight
2) hip is extended
3) opposite leg is in stance

93
Q

What causes arm motion during walking

A

CPGs in the cervical cord

94
Q

Arm swing mechanism

A

Flexion phase is synchronous with contra-lateral flexion in leg (diagonal)

95
Q

What links leg and arm CPGs

A

The propriospinal tracts (from one segment to another)

96
Q

What coordinates upper body motion and step cycles

A

Postural CPGs in the reticular formation of pons and medulla

97
Q

What maintains head angles when walking

A

Visual, vestibular and proprioceptive reflexes

98
Q

Complex/volitional movement

A

Motor output that is planned and refined by the motor cortex, basal ganglia and cerebellum. Learned

99
Q

Red nucleus

A

Found in the midbrain for sophisticated distal limb movements

100
Q

Rubrospinal cell pathway

A

Red nucleus > corticospinal/rubrospinal tract > midline > intermediate zone on other side

101
Q

Synergy

A

A group of muscles contracting together for a specific purpose

102
Q

Reticulospinal tract synergies

A

Widespread and cover over half the body for support postures

103
Q

Rubrospinal tract synergies

A

Highly localized in specific areas such as the face/distal limb

104
Q

Motor cortex location

A

Precentral gyrus of the central sulcus

105
Q

Somatotopic organization

A

Mapping of the body is upside down and isn’t proportionate

106
Q

Motor nuclei/motor columns

A

Motor nuclei are represented in columns at many loci and each muscle column is in a different neighbourhood

107
Q

Motor field

A

How one corticospinal axon synapses with a set of motor nuclei in more than 1 segment

108
Q

Somatosensory input

A

Only sensory input with direct access to the motor cortex after the thalamus (ex, proprioceptive)

109
Q

Premotor areas

A

Regions projecting to the motor cortex and determine the sequence of activation of synergies

110
Q

Premotor cortex vs motor cortex

A

Motor cortex: mainly somatosensory inputs

premotor cortex: receives all sensory input

111
Q

Broca’s area

A

Premotor zone for sequencing language elements for speech/writing. Involves input from Wernickes

112
Q

Sensorimotor cues

A

Sensory association areas recognize cues and send signal to frontal lobe (prefrontal and premotor cortex)

113
Q

When are premotor neurons active

A

During the preparatory phase of the movement, not during movement

114
Q

Supplementary motor area

A

Near the medial hemispheric wall. Controls bilateral coordination and processes internal volitional signals for movement

115
Q

Cingulate motor area

A

Below the SMA in the cingulate sulcus. Mediates emotional movements and autonomic functions

116
Q

Where are the hypothalamus and pituitary located

A

In the diencephalon

117
Q

Hypothalamus function

A

Controls feeding, plasma osmolarity, body temperature, sexual response (4Fs)

118
Q

Hypothalamic control

A

Always regulated through negative feedback

119
Q

Ventromedial and lateral hypothalamic lesions

A

Ventromedial lesions: mice overeat and become obese

Ventrolateral lesions: mice under eat

120
Q

Hypothalamic feeding control basic mechanism

A

Arcuate NPY cells drive feedings, arcuate POMC neurons inhibit feeding

121
Q

Arcuate NPY cells functions

A

Release neuropeptide Y, GABA, and agouti-related peptide (AgRP)

122
Q

Arc-NPY projection

A

Excite LH neurons, inhibit neurons in paraventricular hypothalamus (tells you you’re full)

123
Q

PVN

A

Acts on the sympathetic nervous system to inhibit feeding

124
Q

Lateral hypothalamus and feeding

A

Releases orexin which drives feeding and inhibits PVN

125
Q

Arc-POMC mechanisms

A

Cleave PMC to make alpha-MSH which is released at synapses to inhibit feeding

126
Q

Arc-POMC projections

A

Excited by sympathetic activity, inhibited by Arc-NPY. Project to hypothalamic nuclei

127
Q

a-MSH function

A

Released from POMC to excite PVN and VMH neurons which excite the sympathetic neurons

128
Q

DMH (dorsomedial hypothalamus) function

A

Inhibits the sympathetic system and is inhibited by Arc-POMC

129
Q

Leptin production

A

Released into the blood by fat cells. More fat, more circulating leptin

130
Q

Leptin function

A

Inhibits feeding centres Arc-NPY, LH, DMH and excited PVN, VMH and Arc-POMC

131
Q

What tells you to end a meal

A

Blood glucose; excites Arc-PMC and inhibits LH. Also sensors in the stomach/intestines

132
Q

Intestine sensors mechanism

A

Sense stretch/sugar/protein > release CCK, PYY and GLP-1 that inhibit feeding and excited the vagus nerve

133
Q

Ghrelin

A

Released from the stomach to encourage feeding by exciting Arc-NPY, LH and inhibited PVN

134
Q

Rimonabant

A

Blocks CB1 receptors leading to weight loss an other bad symptoms

135
Q

Leptin as a weight loss drug

A

Ineffective as most obesity is leptin resistant

136
Q

Liraglutide

A

A GLP-1 agonist weightloss drug

137
Q

Autonomic nervous system function

A

Deals with fight/flight and exercise, emotion, gravity, eating, etc

138
Q

Preganglionic neurons of ANS

A

located in CNS and project to ganglion between CNS and the target tissue (axons are autonomic ganglia)

139
Q

Postganglionic neurons of ANS

A

Project to target tissue and receive information from preganglionic neurons

140
Q

Preganglionic neurotransmitters

A

Sympathetic and parasympathetic neurons release ACh to nicotinic receptors

141
Q

Postganglionic neurotransmitters

A

Sympathetic secrete norepinephrine onto adrenergic receptors. Parasympathetic secrete ACh to muscarinic receptors

142
Q

Sympathetic nervous system

A

Preganglion in thoracolumbar spinal cord > postganglion in autonomic ganglion > short preganglion to sympathetic chain > long postganglion to effector organs

143
Q

Parasympathetic nervous system

A

Preganglion in brainstem > long preganglion to ganglia near effector organs > short postganglion from ganglion to effector organs

144
Q

Adrenal medulla

A

SNS neuroendocrine tissue. Preganglionic sympathetic neurons project to postganglion in medulla

145
Q

Chromaffin cells

A

Axonless cells in the adrenal medulla that secrete epinephrine into the blood

146
Q

Duel innervations

A

Any organ in the body is innervated by both the PSNS and SNS which have opposing effects on target organ

147
Q

Neuroeffector junction

A

The synpase between postganglionic autonomic neurons with its target cels

148
Q

Varicosities

A

Regions of axon swelling that contain vesicles filled with neurotransmitters

149
Q

Depression and neurotransmitters

A

Associated with a lack of serotonin and norepinephrine

150
Q

Pupillary light reflex location

A

organized in the pretectal area of the midbrain

151
Q

Pupillary light reflex function

A

Light carried by the ON afferent causes pupils to constrict

152
Q

Baroreflex pathway

A

Baroreceptors > nucleus solitary tract > VLM > sympathetic output

153
Q

Baroreflex

A

Regulates cardiovascular centre in the VLM. Includes noradrenergic vasoconstriction (tonic)

154
Q

VLM and BP

A

Caudal half inhibits rostral half, dropping BP and HR (opposite is also true)

155
Q

Periaqueductal Gray (PAG)

A

Found in the midbrain and is a premotor centre for autonomic behaviour. Organized in longitudinal columns according to behaviour

156
Q

Cholinergic modulatory system

A

Uses ACh. Involved in sleep-wake cycle, arousal, learning, sensory info

157
Q

Serotonergic modulatory system

A

Uses serotonin. Mood, emotional behaviour, aggression, depression

158
Q

Noradrenergic modulatory system

A

Norepinephrine. Attention, arousal, learning, memory, anxiety, pain, mood

159
Q

Dopaminergic modulatory system

A

Dopamine. Reward and addiction

160
Q

Histaminergic modulatory system

A

Histamine. Sleep-wake control, supports waking state, allergic reactions

161
Q

Period gene

A

Transcribed early in the night, mRNA abundant around 10pm, and PER is abundant 6 hours later

162
Q

TIM/PER general function

A

Form a dimer that represses transcription of tim and per. Highest at 4am and gradually falls

163
Q

TIM/PER mechanisms

A

Block CLK-CYC binding to DNA to repress per and tim transcription

164
Q

CLK-CYC

A

Binds DNA during the day to stimulate per and tim transcription.

165
Q

Doubletime gene

A

DBT binds PER, causing breakdown so that levels rise slower. Results in a lengthened cycle of 24 hours

166
Q

Mammalian cycle-regulation

A

PER forms a dimer with CRY instead ofTIM. clk, bmal1 and ck1e instead of clk, cyc, dbt

167
Q

Zeitgeber

A

Cues that keep cellular clocks in sync. Light, temp, feeding, social interaction, exercise

168
Q

Master clock

A

Suprachiasmatic nucleus in the hypothalamus above the optic chiasm. Light sensed by melanopsin is sent here

169
Q

Entrainment

A

The process of nudging the clock into synchrony with another rhythm

170
Q

Melatonin

A

Secreted by the pineal body at the back of the diencephalon at night. Acts on melatonin receptors in SCN to reset the clock

171
Q

SCN adjustment

A

Adjusts itself slowly to a new schedule of light by an hour a day

172
Q

Chronotypes

A

Different sleep times within diurnal and nocturnal animals. (ex, early birds/night owls)

173
Q

SCN in the day

A

Excited LH neurons to release orexin for arousal

174
Q

SCN at night

A

MCH is released from the LH to induce sleep

175
Q

Adenosine and sleep

A

Adenosine is created by ATP breakdown and increased during the day

176
Q

REM

A

30-40Hz brainwaves, vanished muscle tone, dreaming.

177
Q

When does REM occur

A

First stage after 90 minutes for 10 minutes. Gets longer throughout the night

178
Q

NREM

A

2-4Hz brain waves, dreamless, 3 stages

179
Q

What happens when you sleep after sleep deprevation

A

You first catch up on NREM but then will have more REM than usual the nights after

180
Q

3 types of muscle

A

Skeletal muscle, smooth muscle, cardiac muscle

181
Q

Skeletal muscle

A

activated by the somatic nervous system. Contractile filaments are in sarcomeres are striated. Well developed sarcoplasmic reticular

182
Q

Motor units

A

motor neurons + associated muscle fibres

183
Q

Neuro-muscular junction

A

Chemical signalling between motor neurons and skeletal muscle. The synapse between motor neurons and muscle fibres

184
Q

Muscle anatomy

A

Made up of fascicles

185
Q

Muscle fibres

A

Made up of myofibril which run the entire length of the muscle

186
Q

T-tubule system

A

Invagination of the sarcolemma into the muscle fibre. Transmits APs into the muscle

187
Q

Sarcoplasmic reticulum

A

intracellular calcium storage. Assists with reaction time

188
Q

Slow-twitch oxidative fibres

A

Slow contraction but with many mitochondria for oxidative metabolism. Non-fatiguing, low levels of force. Innervated by small diameter motor neurons

189
Q

Fast-twitch glycolytic fibres

A

Fast twitch time, large amounts of tension, rapid fatigue, few mitochondria. Innervated by large diameter motor neurons

190
Q

NMJ anatomy

A

Terminal bouton is the axon terminal and motor end plate is the specialized muscle membrane

191
Q

Motor neuron mechansism

A

Excited by the CNS for contraction and release ACh. Activation depends on summation of EPSPs and IPSPs

192
Q

Nicotinic receptor blocker

A

Prevents ACh binding, preventing APs

193
Q

Exocytosis blocker

A

Inhibits vesicle release, causing no ACh

194
Q

ACh-esterase inhibition

A

Prevents ACh breakdown, causing depolarization block from continuous depolarization so APs can’t be generated

195
Q

Skeletal muscle fibre

A

Thin filament is made up of actin, thick filament is myosin (creates muscular contraction)

196
Q

Sacromere structure

A

Actin and myosin overlap in units called sarcomeres. Contraction shortens these by sliding them

197
Q

Thin and thick filament structure

A

Thin filament actin has myosin binding site, thick filament myosin contains actin and ATP binding site

198
Q

Muscle relaxation anatomy

A

Myosin binding site on thin filament is covered by tropomyosin which is held by troponin. No crossbridges formed

199
Q

Muscle contraction anatomy

A

Calcium binds to troponin to move tropomyosin, allowing myosin and actin to bind. Crossbridges form

200
Q

Crossbridge cycle summary

A

How muscles generate force. Myosin head undergoes conformational changes, changing affinity for actin. Relies on ATP

201
Q

Contraction > relaxation

A

1) power stroke: myosin head moves thin filament to center of muscle
2) thick and thin filaments detach
3) myosin head returns to initial position

202
Q

ACh function (skeletal)

A

Allows Na+ entry > muscle AP > alteration in DHP > RyR release calcium from SR into cytoplasm

203
Q

Contraction Termination

A

Calcium most leave binding sites by Ca2+ ATPases in SR

204
Q

3 phases of muscle twitch + info for each

A

1) Latent: time require for Ca2+ to be released and bind troponin
2) contraction: Ca2+ high, crossbridge cycling occurs, tension rises
3) Relaxation: intracellular Ca2+ falls, tension falls

205
Q

Tetanus

A

Increased AP frequency causes successive twitches that fuse which each other into continuous contraction

206
Q

Single-unit smooth muscle

A

Most common, in GI tract, blood vessels. Spontaneous, active in the absence of external stimuli

207
Q

Multi-unit smooth muscles

A

Large airways, arteries. Innervated, each fibre is independent, contracts when there is stimuli

208
Q

Excitation-contraction coupling (smooth)

A

Ca2+ from ECF and SR, lacks specialized receptors, Ca2+ initiates cascade with phosphorylation of myosin

209
Q

Smooth muscle relaxation

A

Phosphatases remove phosphate from myosin. Ca2+ removed from cytoplasm by ATPase or Ca-Na counter transporter

210
Q

Cardiac muscles

A

Contractile filaments are striated, intermediate SR development, gap junctions, ANS modulation

211
Q

Cardiac muscle AP

A

Lasts 300ms (long), depolarization open Na+ and Ca2+ channels, Ca2+ prolongs AP from Na+. AP lasts as long as contraction and relaxation

212
Q

How is cardiac contraction force increased

A

Increasing muscle length by greater stretch (Sterling law)

213
Q

Systole

A

Contractile proteins from increased cytosolic calcium powers contraction

214
Q

Diastole

A

Calcium pump in SR removes Ca2+ from cytosol, allowing for relaxation

215
Q

Digitalis

A

A cardiac glycoside used to treat heart conditions by increasing Ca2+ levels, increasing contraction force

Physiology I (6 decks)

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