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Physiology Flashcards

1
Q

Fxn of frontal lobe?

A
  • reasoning, problem solving, parts of speech, movement, and emotion
    (prefrontal: is planning, consequences of action)
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2
Q

Fxn of parietal lobe?

A
  • perception of stimuli, orientation, recognition of stimuli and movement
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3
Q

Fxn of temporal lobe?

A
  • memory, perception/recognition of auditory stimuli and speech
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4
Q

Fxn of occipital lobe?

A
  • visual processing
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5
Q

Fxn of basal ganglia?

A
  • voluntary motor movemnt, coordination, cognition and emotion
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6
Q

Cerebrum fxn?

A
  • cerebral cortex: higher brain fxn: thought and action, controls all voluntary activity with help of cerebellum
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7
Q

Limbic system?

A
  • thalamus, hypothalamus, and amygdala(in temporal lobe, memory, emotion and fear), and hippocampus (learning, memory, converts short term memory into long memory)
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8
Q

Diencephalon 2 parts and fxns?

A
  • thalamus: deep in forebrain, processes almost all of sensory and motor info, relays info to and from overlying cortex, last relay site to all sensory input (except olfaction) before this info reaches cortex
  • hypothalamus: base of forebrain - controls homeostasis
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9
Q

Brainstem parts and fxn?

A
  • contrls vital life fxns: breathing, HR and BP
  • midbrain: controls eye movement, relays visual and auditory info
  • pons: regulates breathing, relay station b/t cerebral hemisphere and medulla (involved in motor control and sensory output)
  • medulla oblongata: extension of spinal cord, regulates vital body fxns (along with pons - HR, breathing, autonomic centers, swallowing, coughing)
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10
Q

Fxn of cerebellum?

A
  • maintains posture and balance, coord voluntary movement and control of head and eye movement
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11
Q

What are the brain motor descending pathways?

A
  • pyramidal (fine, isolated precise movements)

- extrapyramidal (gross synergistic movements)

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12
Q

Fxn of pyramidal system (direct pathway)?

A
  • directly reaches target in brainstem or spinal cord with only 1 synapse with cranial nerve (in brainstem) with the lower motor neuron in the spinal cord (anterior horn), direct connection allows for faster impulse transmission
    fxn: controls fine, precise body movements of head, neck and limbs (muscle groups that require concentration and conscious control)
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13
Q

What is the extrapyramidal system? Fxn?

A
  • indirect pathway (multisynaptic): don’t reach their targets by traveling through the pyramids and they make more than 1 synapse.
  • fxn: controls gross movement and autonomic movements involving larger muscles groups.
  • selective activation of movement and suppression of other movements ot prevent erratic movements
  • initiate movements, and coordiante movements
  • coord with ANS to help with posture and muscle tone, has more effect on midline structures instead of peripheral, controls facial expression (why parkinson pt has little facial expression)
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14
Q

What makes up the PNS? FXN?

A
  • CNs and spinal nerves

- fxn: communication lines b/t CNS and rest of body

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15
Q

What makes up the CNS? FXN?

A
  • brain and spinal cors

- integrative and control centers

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16
Q

Sensory (afferent) division of PNS?

A
  • somatic and visceral sensory nerve fibers

- conducts impulses from receptors to CNS

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17
Q

Motor (efferent) division of PNS? 2 sep divisions of this?

A
  • motor nerve fibers
  • conducts impulses from the CNS to effectors (muscles and glands)
  • ANS and SNS
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18
Q

ANS fxn?

A
  • visceral motor control (involuntary)
  • conducts impulses from CNS to cardiac muscles, smooth muscles and glands
  • has sympathetic division: mobilizes body systems during activity
  • has parasympathetic: conserves energy, promtes housekeeping fxns during rest
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19
Q

SNS fxn?

A
  • somatic motor (voluntary)

- conducts impulses from CNS to skeletal muscles

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20
Q

How does neural tube form?

A
  1. neural plate forms from surface ectoderm
  2. neural plate invaginates, forming neural groove, flanked by neural folds
  3. neural fold cells migrate to form neural crest, which will form much of PNS and many other structures
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21
Q

Prosencephalon (forebrain) will become?

A
  • telencephalon: cerebrum

- diencephalon (thalamus, hypothalamus)

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22
Q

Mensencephalon (midbrain) will become?

A
  • brain stem
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23
Q

Rhombencephalon (hindbrain) becomes?

A
  • Metencephalon: brain stem: pons, and cerebellum

- myelencephalon: brain stem: medulla oblongata

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24
Q

How does an AP work?

A
  • all or none event: threshold voltage is usually 15 mV positive to resting potential
  • initiated by depolarization, APs can be induced in nerve and muscle by extrinsic (percutaneous) sim
    • APs don’t summate, info coded by frequency not amplitude
  • have constant conduction velocity
  • APs only occur at nodes: increased velocity, and energy conservation
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25
Q

What fibers conduct faster? large or small diameter? Myelinated or unmyelinated?

A
  • fibers with large diameter conduct faster than small fibers
  • myelinated fibers conduct faster than unmyelinated fibers
26
Q

Role of ion channels in AP?

A
  • depolarization causes Na cahnnels to open (can cause activation and inactivation)
  • inactivated channels don’t pass any ions
  • K+ channels show activation but not inactivation
  • fall in current at end is deactivation
27
Q

Parts of brain involved in speech and language comprehension?

A
  • broca’s area

- wernicke’s area

28
Q

How does edema occur in CNS? Why is this such a problem?

A
  • increase in tissue mass that results from excess movement of body fluid from vascular compartment or its abnormal retention in tissue
  • problem in brain and spinal cord b/c: enclosed space, lack of lymphatics, and lack of anastomoses in venous drainage
29
Q

What is vasogenic edema?

A
  • occurs when blood-brain barrier is upset: inflammation due to infection, toxic agents that damage capillary endothelium, abnorm capillaries assoc with malignant neoplasm
  • leakage of protein fluid into interstitial - leads to swelling
  • plasma filtrate accum alters ionic balance and impairs fxn
30
Q

What is cytotoxic edema? Causes?

A
  • intracellular phenomenon
  • hypoxia: cardiac arrest, near drowning, strangulation, focal edema due to blockage of an end artery
  • toxic substances that: impair Na+/K+ pump, impair production of ATP
31
Q

Tx of CNS edema?

A
  • swelling often caused by both cytotoxic and vasogenic
  • tx is diff
  • if cytotoxicity the cause - can give IV bolus of hypertonic soln such as mannitol to draw water into vasculature and out of the brain
  • Can’t do this for vasogenic because fluid would be drawn into interstitial space and increase swelling
32
Q

Normal ICP? Causes of IICP?

A
  • norm: 5-15 mm Hg
  • IICP:
    tumor growth
    edema
    excess CSF
    hemorrhage
  • contents of cranium can cause IICP (tissue of CNS, CSF, blood)
33
Q

Clinical hallmarks of IICP?

A
  • headache
  • vomiting
  • papilledema: don’t do spinal tap (brain will herniate)
34
Q

Stage 1 of IICP?

A
  • since brain is encased in cranium, only way pressure can be relieved is by decreasing cranial contents, most readily displaced is CSF, and if ICP is still high, cerebral blood volume is altered:

stage 1: vasoconstriction and external compression of venous system. Compensating, so only few sxs

35
Q

Stage 2 of IICP?

A
  • if ICP continues to increase, may exceed brain’s ability to adjust

stage 2: IICP (gradually rising) causes a decrease of O2 of neural tissue

  • systemic vasoconstriciton occurs to increase BP to get blood to brain
  • clinical manifestations transient: episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes (hypoventilation)
36
Q

Stage 3 of IICP?

A
  • when ICP begins to = arterial pressure, there is a lack of compensation - beginning decompensation

stage 3: hypoxia and hypercapnia - lead to cytotoxic edema, decreasing levels of arousal, widening pulse pressure, may begin Cheynes-stokes respirations, bradycardia: due to increased pressure in carotid arteries, pupils are small and sluggish
* surgical or medical intervention is needed!!

37
Q

Stage 4 of IICP?

A
  • When all compensatory mech have been exhausted
  • stage 4:
    dramatic rise in ICP in a short time. Autoregulation is lost, and get vasodilation, further increasing intracranial volume. Decreased cerebral perfusion = severe hypoxia and acidosis
  • brain contents shift (herniate) from area of high pressure to areas of lower pressure - decreased blood flow
  • small hemorrhages develop, ipsilateral pupil dilation and fixation, progressing to bilateral fixed and dilate pupils
  • when mean systolic arterial pressure equals ICP - cerebral blood flow ceases
38
Q

What arteries make up 30% of CBF?

A
  • Basilar and vertebral arteries (verterbrals turn into basilar)
39
Q

Fxn of blood brain barrier?

A
  • prevent infections
  • protection from circulating AAs and otehr molecules that might act as neurotransmitters
  • protects against drugs and abx
  • has tight jxns and astrocyte foot processes that secure BBB
40
Q

Purpose of cervical and lumbar enlargements?

A
  • for innervation of upper and lower extremiteis
41
Q

Where would you perform a lumbar puncture at? Why?

A
  • b/t L4 and L5 b/c spinal cord has already ended (just nerve fibers), easy access of subarachnoid space
42
Q

Motor neurons route?

A
  • from ventral horn through ventral root and out of spinal nerve
  • (somatic and visceral motor neurons)
43
Q

sensory neruon route

A
  • Visceral and somatic sensory neurons coming in - into doral root ganglion (cell bodies) - and then into dorsal horn
44
Q

Classification of somatic sensations?

A

-mechanoreceptive: stimulated by mechanical displacement:
tactile
position or propioceptive
- thermoreceptive
- nociceptive: (touching hot stove - pull hand back)

45
Q

Spinocerebellar pathway?

A
  • remains on ipsilateral side up spinal cord and brainstem into cerebellum
46
Q

2 types of pain fibers?

A
  • neo-spinothalamic tract: fast- sharp pain, feel pain immediately, travel up through reticular formation along with paleo-spinothalamic tract and into ventrobasal compelx and posterior nuclear group
  • paleo-spinothalamic tract: slow - chronic pain, travel up through reticular formation into intralaminar nuclei of thalamus
47
Q

Process of reflex?

A

1 - afferent impulses from stretch receptor to spinal cord
2 - efferent impulses to alpha motor neurons cause contraction of stretched muscle that resists/reverses the stretch
3 - efferent impulses to antagonist muscles are dampened (reciprocal inhibition)

48
Q

Signs of UMNLs?

A
  1. paralysis or weakness of movements of the affected side but gross movements may be produced. No muscles atrophy seen initially but later on some disuse atrophy may occur
  2. Babinski sign in present: great toe dorsiflexes and other toes fan outward in response to sensory stimulation along lateral aspect of sole. Normal response = plantar flexion of all toes
  3. loss of performance of fine skilled voluntary movements esp at distal end of limbs (babinski)
  4. superficial abdominal reflexes and cremasteric reflex are absent
  5. spasticity or hypertonicity of muscles
  6. clasp-knife rxn: initial higher resistance to movement is followed by lesser resistance
  7. exaggerated DTRs and clonus may be present
49
Q

Signs of LMNLs?

A
  1. flaccid paralysis of muscles supplied
  2. atrophy of muscles supplied
  3. loss of reflexes of muscles supplied
  4. muscle fasciculations
  5. muslce fibrillation
  6. muscle contracture
  7. presence of muscle wasting
  8. rxn of degeneration to response to electrical stimulus
50
Q

Neurotransmitters in SNS?

A
  • initially acetylcholine is NT - at ganglion and adrenal medulla but NE and E are NTs that act on target (smooth muscle - gut, glands, cardiac muscle, blood vessel)
51
Q

Neurotransmitters of PNS?

A

Acetylcholine is NT at both ganglion and target organ (smooth muscle, glands, cardiac muscle, and blood vessels)

52
Q

Parasympathetic nerve orgins?

A
  • Cranial

- sacral

53
Q

sympathetic nerve origins?

A
  • sympathetic ganglion in Thoracic and lumbar
54
Q

Visceral reflex arc?

A
  • stimulus - travels up through sensory receptor through dorsal root ganglion into dorsal horn and integration center - and then ventral horn - to preganglionic axon which next travels to autonomic ganglion and then post ganglionic axon and to visceral effector - get a response
55
Q

What are neurotransmitters?

A
  • chemical substances that excite, inhibit or modify response of cerebral cells.
  • these include AAs, neuropeptides, and monoamines/
56
Q

GABA acts on what sites? FXN of GABA?

A
  • GABA (gamma-aminobutyric acid), AAs: glutamine, and glycine are NTs at most CNS synapses
  • GABA: mediates most synaptic inhibition in CNS
57
Q

3 processes a released transmitter can undergo?

A
  • 1: can be broken down into inactive substances by enzymes
  • 2: can be taken back up into presynaptic neuron (reuptake)
  • 3: it can diffuse into intercellular fluid until its concentration is too low to influence postsynaptic excitability
58
Q

Catecholamines?

A
  • NE, epi, dopamine
59
Q

NE and epi fxn?

A

Catecholamines can cause excitation or inhibition of smooth muscle contraction depending on set, dose and type of receptor present

  • NE: potent excitatory activity and low inhibitory activity
  • Epi: potent excitatory and inhibitory agent
  • produce excitatory effects on alpha receptors and inhibitory at beta receptors
60
Q

Cholinergic receptors?

A
  • receptors that respond to acetylcholine
  • 2 types:
    muscarinic: PNS and sweat glands
    nicotinic: skeletal muscle
  • acetylcholine is excitatory to most muscarinic and nicotinic receptors except those in heart and lower esophagus (inhibitory effect)

Neuro (19 decks)

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