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Brain and Behavior T2 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What is hemiparesis?

A

weakness of the entire left or right side of the body.

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2
Q

What is hemiplegia?

A

Paralysis of one side of the body.`

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3
Q

Where does the brainstem begin

A

at FORAMEN MAGNUM

Mostly INFRATENTORIAL

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4
Q

What are the Crainial Nerves associated with,Midbrain,PonsMedulla?

A

Md-3&4, Pons 5-8, and Medulla 9-12

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5
Q

Cranial nerve func. ->sensory (Afferent)?

A

Pseudounipolar = GENERAL Sensory

Bipolar = SPECIAL Sensory

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6
Q

What are the nerve funct. of motor (efferent) fibers?

A

Multipolar:

  1. Skeletal Muscle
    - >Somites
    - >Branchial Arches
  2. Smooth Muscle
    - >PREganglionic
    - >Parasympathetics
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7
Q

What are the functions of the nuclei of Cranial Nerves?

A

Sensory =2nd Order

Motor= Alpha Motor or Pregang. Parasymp.

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8
Q

What are the ganglia in the the neurons of Cranial Nerves?

A

SENSORY-Pseudounipol. Bipolar

OR,Multipolar Parasymp. Gang

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9
Q

What is the order of the alar & basal plate org. @ medulla level?

A

Somatic Sensory,-> Visceral Sensory,->Visceral motor-pregang Para,-> Somatic motor- Alpha Motor

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10
Q

What sypmathetic muscle opens the eye?

A

Mueller’s Muscle

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11
Q

What Somatic muscle opens the eye?

A

Levator palpebrae

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12
Q

What is the trajectory of the upper motor neurons of the corticospinal tract?

A

It begins in the cerebral peduncle pierces the pons and goes inside the pons to go through the pyramid of the medulla

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13
Q

What are the somatic motor CNs in the head?Branchial?

A 
Somatic: EYE =  3, 4, 6
TONGUE =  12 
Branchial Arch Muscle:
Mastication = 5
Facial Expression =  7 
Pharynx & Larynx =  IX, X, XI (Nucleus Ambiguus)
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14
Q

What are the cranial nerves of the Medulla?

A

Hypoglossal (XII)
Accessory (XI, ambiguus)
Vagus (X)
Glossopharyngeal (IX)

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15
Q

Function of the Hypoglossal Nucleus?

A

TO Intrinsic and Extrinsic Muscles of the Tongue Somatic Motor (GSE)

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16
Q

What nerves innervate the Spinal Accessory Nucleus and what muscles does that affect?

A

Spinal Accessory Nucleus (Cervical 1-5,6)

TO Sternocleidomastoid & Trapezius muscles

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17
Q

What is the function of the dorsal motor nucleus of the vagus?

A

CN X; innervates the visceral motor to thorax and abdomen

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18
Q

What are the symptoms of a Lower Motor Neuron Lesion? Where can it be?

A

LOWER MOTOR NEURON = Atrophy, Fasciculations

Lesion could be in Medulla or Nerve

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19
Q

What are the symptoms of a Upper Motor Neuron Lesion? Where can it be?

A

UPPER MOTOR NEURON = Spasticity

Lesion in Cerebral Cortex or Corticobulbar Tract

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20
Q

What are the clinical signs and lesion location in the body of a alternating hemiplegia?

A

IPSILATERAL TONGUE LMN SIGNS; CONTRALATERAL BODY UMN SIGNS

CN XII lost

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21
Q

What are the ways YOU can GET AN UMN
LESION INVOLVING
TONGUE???

A
  • Corticobulbar Tract=Contralateral to hypoglossal nuc. (weak but no fasciculations)
  • If at the nucleus, ipsilateral
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22
Q

What it the path for the hypoglossal nerve from the cortex?

A

From cortex->into corticobulbar tract-> decusates to hypoglosal nucleus

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23
Q

What nerve would cause atrophy of trapezius?

A

Acessory Nerve (comes from medulla and cervical canal)

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24
Q

Vocal paralysis comes from what nerve? What nucleus caused it?

A

10, Nuc. Ambig.

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25
Q

What senses can be found at the Spinal Trigeminal Nuc.?

A

Somatic Sensory for skin of Outer Ear

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26
Q

What are the nuclei for the vestibulocochlear N. (VIII)

A

Somatic Sensory (SSA):

1) (Hearing) Organ of Corti Spiral Ganglion Cochlear Nuclei
2) (Balance) Cristae Amp. & Macula Vestibular Ganglion Vestibular Nuclei

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27
Q

What Are the nuclei of the Pons?

A

Vestibulocochlear (VIII)
Facial (VII)
Abducens (VI)
Trigeminal (V)

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28
Q

What are the nuclei and sensory responsibilities for the AFF for Facial N?

A

AFF:
1) Somatic Sensory:
GSA: FROM Skin of Outer Ear (gen. gang.) Spinal trigeminal Nuc.
2) Visceral Sensory:
SVA: FROM Taste Buds on Ant. 2/3 Tongue (chorda tympani - gen. gang. - nervus intermedius) Nuc. of Solitary Tract

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29
Q

What are the nuclei and sensory responsibilities for the EFF for Facial N?

A

EFF:
1) Visceral Motor:
GVE: Superior Salv. Nuc. = Parasympathetic TO
A) Pterygopalatine ganglion (via nervus intermedius then gr. Superficial petrosal n.) to Lacrimal Gland
B) Submandibular ganglion (via nervus intermedius then chorda tympani) to Submand. & Subling. Glands
2) Branchial Motor:
SVE: Facial Motor Nuc. = Branchial Motor TO Musc. Facial Expression, platysma, stapedius, stylohyoid, & post. belly digastric

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30
Q

Why would the a patient not be able to move his forhead?

A

Corticobulbar Tract synpses on 2 facial nerves so damage spares the forehead; LMN lesion to VII would cause paralysis to entire 1/2 of face (Bell’s Palsy)

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31
Q

What Nerve/Nucleus is responsible for Medial Strabismus?

A

Abducens!
LESIONS:
VI NERVE->NO Lateral Gaze Eye Same Side
VI NUCLEUS->NO Lateral Gaze Eye Same Side
NO Conjugate Contralateral Medial Gaze

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32
Q

Explain Internuclear Ophthalmoplegia

A

destruction of the medial longitudinal fasiculus inhibits Abducens->Oculomotor comm. Contralateral eye movement inhib.

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33
Q

What nerves does the Medial Longitudinal Fasciculus connect?

A

Connects the vestibular nucl. to 3,4,6

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34
Q

What are the functions of CN V AFF?

A

Somatic Sensory:
GSA:
FROM Skin of Face & ant. scalp, mouth & nasal Mucous Membrane, Dura (trigem. ganglion, V1,V2, V3)
Main Sensory Nuc. & Spinal Trigeminal Nuc.
FROM Stretch Receptors of Muscles of Mastication (JAW JERK)-> Mesencephalic Nucleus Motor Nucleus of V

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35
Q

What are the functions of CN V EFF?

A

Branchial Motor:
SVE: Motor Nucleus of V (Mandibular Nerve) TO Muscles of Mastication, tensor tympani, tensor veli palatini, mylohyoid, ant. belly digastric

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36
Q

What produces Aqueous humor and where does filter into?

A

Aqueous humor, continuously produced by the ciliary body, passes from the posterior chamber to the anterior chamber, then enters the Canal of Schlemm

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37
Q

Blockage of the aqueous flow can what disease?

A

Blockage of the aqueous flow can damage the optic nerve and cause glaucoma.

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38
Q

What is accommodation?

A

Changing the curvature of lens can help to bring an image to focus on the retina

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39
Q

Explain Presbyopia.

A

the lens looses its elasticity when it gets old and has trouble bringing a near image to focus

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40
Q

What are Cataracts?

A

problem of the lens, which occurs when the lens loses it opacity.

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41
Q

What is hyperopia? What lense fixes it?

A

The eyeball is too short, and light rays come to a focus behind the retina. Biconvex Lens

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42
Q

What is Myopia?

A

The eyeball is too long and light rays focus in front of the retina. Biconcave lens

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43
Q

What is Astigmatism?

A

curvature problems of the cornea or the lens

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44
Q

What are 4 major cell types in the internal nuclear layer?

A

Muller Supporting cell - is the major glia in the retina this extends the whole thickness of the retina.
Horizontal Cell - modulate signals sent out by photoreceptors
Bi-polar neuron - relay signals between cell layers.
Amacrine cell - modulate functions of ganglion cells.

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45
Q

What are the 3 layers in the retina?

A

External Nuclear, Internal Nuclear, and Ganglion Cells

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46
Q

What axon cells are collected into a bundle and to become the optic nerve?

A

Ganglion cells

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47
Q

What is the name of the area where sensory axons exit the eyeball? What is another name for it and where is it in the eye?

A

Papilla (optic disc) Blind Spot; medial to the macula densa

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48
Q

Why is the macula an area with high visual acuity? How is it related to the fovea?

A

Avascular so it has high visual acuity because light is not blocked by blood vessels and it has a high density of photoreceptors. The fovea has many cone photoreceptors!

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49
Q

What is the leading cause of blindness in the elderly population?

A

Macular Degeneration; looses central vision-external nuc. layer

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50
Q

What are the layers of meninges that wrap around the eyeball?

A

Choroid->Sclera->Retina

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51
Q

Possible cause(s) of high intracranial pressure

A

adsf

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52
Q

Why it can cause problems if you do lumbar puncture on a patient with papilledema?

A

adsf

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53
Q

What are the Biochemical events that happen in the photoreceptors?

A

light->rhodopsin conf. chg->transducin binds GTP->PDE activity incr->cGMP levels decreased->close Na+ ch.->hyperpolarization->Reduce Glu release

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54
Q

What causes retinitis pigmentosa?

A

mutations->severe degeneration of rod photoreceptors and patient has Impaired night vision
Impaired peripheral vision

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55
Q

Purposes of the visual info sent to LGN, Pretectal Nuc, and the suprachiasm?

A

LGN-Pattern, Pretectal Nuc.-Light reflex, Suprachiasmatic Nuc. of hypoth.->ciracadian rhythm

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56
Q

What areas of the brain cortex are responsible for visual info?

A

Areas 18-19 Visual Assoc., Sent here 1st->Area 17:Principal visual cortex, Areas 18-19 Visual associtation areas

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57
Q

What part of the brain initiates the pupillary reflex?

A

Information processing in the visual cortex

can initiate pupillary dilation reflex

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58
Q

What are the Nerves of the midbrain?

A

Trochlear (CN IV) & Oculomotor (CN VIII)

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59
Q

Where can CN 4 be found in the midbrain?

A

Somatic Motor (GSE, MYOTOME)

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60
Q

Where does CN4 decussate?

A

Superior Medullary Velum

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61
Q

Common place for LESIONS of TROCHLEAR?

A 
NUCLEUS (Rare):
	1) Contralateral SO
 	2) Possibly with Horner’s syn.
 NERVE:
	1) Before Decussation (Rare) = Contralat. SO
	2) At Decussation = Bilateral SO’s
	3) After Decussation = Ipsilateral SO
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62
Q

Signs of lesions in the trochlear?

A

1) Extorsion (Can’t Look Down & In)
2) Vertical Diplopia (Double Vision) when Reading or Walking Down Stairs
3) Head Tilt + Chin Down Contralat. to Affected SO

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63
Q

Oculomotor Nucleus myotome and function?

A

Somatic Motor (GSE, MYOTOME), Motor TO Levator Palpebrae Superioris & Extrinsic Eye Muscles

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64
Q

MM and Func. Visceral Motor (GVE)?

A

Nuc. of Edinger-Westphal->Parasymp. TO Ciliary Ganglion To Pupillary Constrictor & Ciliary Body

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65
Q

Common clinical causes of Oculomotor Palsy?

A 
Posterior Cerebral Artery Stroke
   JUST OCCULOMOTOR NERVE:
Posterior Communicating Aneurysm
Increased Intracranial Pressure
Diabetes (spares pupil)
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66
Q

Horner’s Syndrome vs. Lesion CN III

A 
Horner’s Syndrome
Sympathetics Lost: 
 Partial Ptosis (Muller’s m.), Miosis  (Pin Point Pupil), Anhydrosis
Lesion CN III
Somatic Motor Lost:
 Full Ptosis  (Levator m.)
 Down and Out	
Parasympathetics Lost:
 Mydriasis  (Dilated Pupil)
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67
Q

What are the parasymp. of the midbrain

A

3,7,9

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68
Q

Path of Optic nerve in Diencephalon? how are they myelinated?

A

Retinal Ganglion Cells TO Lateral Geniculate Body. Oligodendroglia

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69
Q

Why do both eyes blink w/ pupillary light reflex?

A

Optic Nerve Innervates both E-W and Pretectal Nucleus so both eyes are in conj.

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70
Q

What is th SVA fund. of the olfactory N

A

Bipolar Neurons Olfactory Epithelium to Olfactory Bulb

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71
Q

What is the SENSORY Component of “MOTOR” Cranial Nerves?

A

Proprioceptive Fibers (GSA) To Mesencephalic Nuc. of V (not in ganlia, scattered)

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72
Q

What supplies blood for the CN I & II?

A

Ant. Cerebral

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73
Q

What areas does PCA supply?

A

III Oculomotor Nucleus, Edinger-westphal, and Trochlear Nucleus

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74
Q

What Areas does AICA supply?

A

V Motor nuc. ,VI Abducens, VIII Facial Nucl., Sup Salvatory nuc, Facial n.

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75
Q

What Area does PICA supply?

A

VIII Cochlear nuclei Vestibular Nuclei, IX All components, X Nuc. amb.

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76
Q

What supplie blood to XI and XII?

A

ANT. SPINAL A. ->Accessory nuc. and Hypoglossal nuc.

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77
Q

Effects of Lesions of the Ventral Pons?

A

Raymond’s Syndrome LCST & CN VI=Contralateral Hemiparesis, Ipsilateral Medial Strabismus

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78
Q

Effects of lessions in the middle pons?

A

(Millard-Gubler Syndrome) LSCT & CN VII = Contralat., Hemiparesis, Ipsilat. Facial Paralysis

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79
Q

Effects of lessions in the Dorsal Pons?

A

LOCKED IN SYNDROME
Foville’s Syndrome
Nuc. VI (MLF) & VII and CN VII = Ipsilat. Medial Strabismus & Facial Paralysis,
Loss of Conjugate Movement of Contralat. Med. Rectus

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80
Q

What is Weber’s syndrome?

A

Lesion in LCST and CN II -> Contralat. Hemiparesis, Ipsilat. Ocular Paresis

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81
Q

What is Parinaud’s Syndrome?

A

Superior Colliculi-cant look up: Paralysis of Upward Gaze

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82
Q

What is the RF function? (PAPA D)

A

1) Pain Suppression System (Nuc. Raphe Magnus in Pons)
2) Autonomic Reflexes – Pattern Generators (Physiology)
RESPIRATORY CENTERS (Medulla, Pons)
CARDIOVASCULAR CENTERS (Medulla)
3) Descending Sympathetics (from Hypothalamus)
Lesion = ipsilat. HORNER’S SYNDROME
4) Arousal & Consciousness
-Ascending Reticular Activating System (ARAS)
5) Posture (Reticulospinal Tracts)

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83
Q

What are the 3 Longitudinal Zones?

A 
Median Zone:
 Raphe Nuclei (5-HT)
-Medial Zone: 
 Ascending & Descending Projections 
-POSTURE TRACTS: 
Medullary & Pontine Reticulospinal Tracts (Motor Sys. Lectures)
-Lateral Zone:
 CN Reflexes & Visceral Functions
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84
Q

Location and function of the NE Sys in the midbrain?

A

Located in the locus ceruleus,Solitary Nucleus, Lateral Area of Medullary Reticular Formation
has wide spread projections and is secreted for attention

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85
Q

Location and function of the DA Sys int the midbrain?

A

Initiation of Movement, Motivation, Cognition axons to striatum located in Substantia Nigra and axons to limbic system located in VTA where DA is made

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86
Q

Location and function of the 5-HT (serotonin) Sys in the midbrain?

A

Widespread Projections, Arousal, Pain Control. Located in Raphe Nuclei

87
Q

Location and function of the Ach Sys int the midbrain?

A
  • Muscarinic R’s in CNS, Sleep/Wake Cycle
  • -Reticular Formation (to Thalamus)
  • -Basal Forebrain (Nucleus Basalis of Meynert to Cortex, Amygdala, & Hippocampus)
  • -Striatum (Interneurons)
88
Q

Important meds of brainstem?

A

–Antipsychotics
Block DA receptors in VTA (Thorazine, Rx Schizophrenia)
–Antidepressants
NE (LC) & 5-HT (Raphe) receptor alterations?? (2o & 3o amines)
Increase levels of NE & DA (e.g., MAOI’s)
–Replacement Therapy
ACh (Nuc. Basalis) given to Alzheimer’s Disease Patients
DA (Substantia Nigra) given to Parkinson’s Patients

89
Q

AFF somatic and visceral sensory for CN IX?

A

1) Somatic Sensory:
GSA: FROM Skin of Outer Ear (sup. gang.)->Spinal Trigeminal Nuc.
2) Visceral Sensory:
GVA:
a) FROM Mucosa of Pharynx, & medial surf. Ear Drum, Carotid Body & Sinus (inf. gang.)->Solitary Nuc.
b) FROM Pharynx & post. Tongue (inf. gang.) Spinal Trigeminal Nuc.(pain)
SVA: FROM Taste Buds on Post. 1/3 Tongue (inf. gang.)->Solitary Nuc.

90
Q

EFF Branchial motor and visceral motor for CN IX?

A

1) Visceral Motor:
GVE: Inferior Salv. Nuc. = Parasymp. (via lesser petrosal n.) TO Otic Ganglion->Parotid Gld
2) Branchial Motor:
SVE: Nucleus Ambiguus = Branchial motor TO->Stylopharyngeus m

91
Q

What is nerves are responsible for Gag reflex? What about the Carotid Sinus Reflex?

A
  • AFF limb = Glossopharyngeal n. (IX, Solitary Nuc.)
  • EFF limb = Vagus n. (X, Nucleus Ambiguus)
  • Carotid Sinus Reflex involves AFF IX to EFF X Ambiguus or Dorsal Motor
92
Q

Which trigeminal system does Touch and proprioception travel through? Pain and Temperature?

A
  • Touch and prop.-Main sensory Nuc.

- Pain and Temp.-Spinal Tract Nucleus

93
Q

Where do the Trigeminothalsmics cross?

A
  • Spinothalamics crossed = Sp. Nuc. V (caudal = pain & temp) (rostral = gen. tactile, blink)
  • Medial Lemniscus - crossed = Main Sens. Nuc. (gen. tactile)*
  • Cerebellum->uncrossed = Mesenceph. Nuc.(joint position)
94
Q

What is the diff. btwn parasymp. and symp. axons?

A

symp.-short pre;long post

parasymp-long pre; short post

95
Q

What type receptors are at the somatic and cardiac/smoth musc?

A

Nicotinic Receptors Mediate Somatic Motor and the

Autonomic Ganglia Synapse

96
Q

What NT is released by Postsynaptic Parasympathetic Neurons
and Sympathetic Neurons Innervating Thermoregulatory Eccrine Sweat Glands? On what receptor?(cardiac and SM post para too)

A

Ach on Muscarinic (M1-5

97
Q

Diff. btwn Nicotinic Receptor versus Muscarinic Receptor Signalling?

A

Nicotinic-Ligand-Gated Ion Channel

Muscarinic-GPCR Receptors

98
Q

What NT do Sympathetic Ganglionic Neurons and Adrenal Medulla release?

A

Sympathetic Ganglionic Neurons Primarily Release Norepinephrine;
Adrenal Medulla Releases Epinephrine/Norepinephrine

99
Q

What type receptors are used for sympathetic neurons?

A

Adrenergic Receptors: Alpha: alp. 1, alp. 2 Beta: beta 1, Beta 2, (beta3)

100
Q

What are the different G protiens for alpha and beta receptors?

A
  • Alpha1 receptors-Gq->increase IP3, DAG
  • Beta receptors-Gs —> increase cAMP
  • Alpha2 recep-Gi-> decrease cAMP
101
Q

What muscle groups have Beta 1,2,3 receptors?

A

Beta1-Cardiac Muscle
Beta2-SM, liver, heart
Beta3-Fat cells

102
Q

What is the job of Presynaptic Alpha2 Adrenergic Autoreceptors?

A

Regulate Neurotransmitter

Release in the CNS and the PNS via neg. feedback

103
Q

What do dopaminergic receptors do?

A

Regulation of Renal and Splanchnic Vasculature Smooth Muscle; increase camp like Gs recep.

104
Q

Sympathetic response?

A

Blood from skin/visceral to skeletal, inc. sweat, inc. adrenalin

105
Q

What does parasymp not effect?

A

body wall and surarenal gland

106
Q

What is a lytic NT?

A

Blocks the action of endogenous neurotransmitter;Parasympatholytic
Sympatholytic

107
Q

Symp. and parasymp efects on Dilator pupillae mm

A

Symp.-contracts (mydriasis) alpha 1

-no para

108
Q

Symp. and parasymp efects on Sphincter pupillae mm

A

No symp

-Para-contracts (miosis) M recep.

109
Q

Symp. and parasymp efects on Ciliary mm?

A

No symp

-Para-contracts (miosis) M recep.

110
Q

Symp. and parasymp efects on heart SA node?

A

SA node

  • symp->accelerates, beta1 & 2
  • parasymp->decelerates on M recep
111
Q

Symp. and parasymp efects on Aqueous humor?

A
  • symp-inc. outflow and dec. secre.-alpa agonist and beta blocker
  • parasymp-dec. outflow on M recep.
112
Q

Symp. and parasymp efects on heart contractility?

A
  • Symp. incre. Beta1 & 2,

- Parasymp-decel on M recep.

113
Q

Symp. and parasymp efects on bld vess. of skin, splanic?

A

Symp-Constricts on alpha recep.

no para

114
Q

Symp. and parasymp efects on bld vess. of Renal (splanchnic)?

A

Relaxes on D1 recep.

no para

115
Q

Symp. and parasymp efects on bld vess. of Skeletal mus.

A

Relaxes on Beta 2 recep.

no para

116
Q

Symp. and parasymp efects on bronchilolar SM

A

Symp-relaxes Beta2

parasymp-Contracts on M recep.

117
Q

Symp. and parasymp efects on GI Smooth Wal mm

A

Symp-relaxes on Beta 2

Para-contracts on M recept

118
Q

Symp. and parasymp efects on GI Sphincters

A

Symp Contracts-Alpha 1

Parasymp-relaxes on m recep

119
Q

Symp. and parasymp efects on GI secretion

A

Sympathetic-Inhibits Alpha 2

Parasymp-Stimulates M recep.

120
Q

Symp. and parasymp efects on Genitournary SM mm Blad wall (detrussor)

A

-Symp. Relaxes on Beta 2 recep.

Parasymp-contracts M recep.

121
Q

Symp. and parasymp efects on Genitournary SM mm Sphincter (trigone)/prostate

A

Symp. Contracts-alpha 1

Parasymp relaxes on m recep

122
Q

Symp. and parasymp effects on Genitournary SM mm Uterus, pregnant?

A

Symp. Relaxes w/ Beta & contracts w/ Alpha

Parasymp. contracts w/ m recep

123
Q

Symp. and parasymp efects on Genitournary SM mm of penis, seminal vesicles?

A

Symp-Ejaculation on alpha recep.

Parasymp-erection on m recep

124
Q

Symp. and parasymp efects on metabolic renin, gluconeo, glycogenolys, and lipolysis

A

Symp. Stimulation on Beta 1, 2, and 3

No para

125
Q

Symp. and parasymp efects on Skin pilomotor, eccrine sweat, and apocrine sweat?

A

Symp. stim. on a alpha or M recep

126
Q

What neuronal tone is the sympathetic system responsible for?

A

Arterioles and Sweat glands

127
Q

What neuronal tone is the para-sympathetic system responsible for?

A

Iris, GI tract, Heart, Salavary glands, Urinary glands

128
Q

What fibers carry out baroreceptor sensory input?

A

CN IX and CN X afferent fibers to the vasomotor centers in the medulla.

129
Q

What is the Baroreceptor Reflex (also seen in Autonomic drugs)?

A

Monitors periph. bld. press. and activates barorecep. to alter CNS and provide quick homeostatic responses

130
Q

What is a sign of postural hypotension

A

Absent reflex in patients with autonomic failure (diabetic autonomic neuropathy)

131
Q

What are the Five Sites of Action for Pharmacological Manipulation of ANS?

A 
Synthesis
 Storage
 Release
 Termination
 Receptor
132
Q

Direct vs indirect effect of autonomic receptors?

A

Direct effect - Act directly on autonomic receptors

Indirect effect - Act indirectly through changes in endogenous transmitter levels in the terminal or synaptic cleft

133
Q

What are the Five Classes of Autonomic Drugs

A
  • Direct-acting cholinomimetics
  • Cholinoceptor blockers
  • Indirect-acting cholinesterase inhibitors
  • Sympathomimetics (direct/indirect)
  • Adrenoceptor blockers
134
Q

What are the Direct-Acting Cholinomimetics?

A

choline esters-acetylcholine, bethanecol

naturally occuring alkaloids-muscarine,nicotine,

135
Q

Use of Nicotinic agonists?

A

used to produce skeletal muscle paralysis (depolarization block) and smoking cessation

136
Q

Use of Muscarinic agonists?

A

clinically useful drugs are non-selective for the receptor subtypes (M1-5)

137
Q

Signs of Muscarinic toxicity? (Mushroom poisoning)

A

SLUDGE (Salivation, Lacrimation, Urination, Defecation, GI upset (diarrhea), Emesis

138
Q

How do muscarenic agonist activate the sympathetic system?

A

muscarinic receptors are located on endothelial cells (intima),
receptor activation->release of nitric oxide (NO).
NO diffuses to adjacent vascular smooth muscle (media)
activates guanylyl cyclase, increases cGMP
results in relaxation of vessels

139
Q

What are the sympath. effects of cholinomemetic musarenic agonist?

A

Vasodialation, tachycardia, and thermoregulatrory sweating

140
Q

What do Anti-nicotinic cholinoceptor blockers do?

A

Are ganglionic blockers that prevent nicotinic receptors from mediating the autonomic ganglia synapse

141
Q

What are 2 ex. of an anti-muscarinic cholinorecep. blocker?

A

Atropine-prototypical anti-muscarinic drug

Scopolamine- used as an anti-motion sickness drug

142
Q

What are 3 Anti muscarinic contraindications?

A

Glaucoma: elderly, especially acute angle-closure
Prostatic hyperplasia: Urinary retention
Children: danger of hyperthermia

143
Q

Signs of Atropine toxicity?

A
  • Dry as a bone: blocks thermoregulatory sweating, salivation, lacrimation
  • Red as a beet: Dilation of blood vessels “atropine flush” (unknown mechanism)
  • Mad as a hatter: CNS effects leading to delirium and hallucinations
144
Q

What are 3 cholinesterase inhibitor types?

A
  • carbamate esters (neostigmine)
  • phosphoric acid esters (organophosphates)
  • alcohol
145
Q

How do cholinesterase inhibitors work?

A

Indirect-Acting Cholinomimetics->compete with ACh for the enzyme
->hydrolysis by AChE
Augment the effects of physiologically released Ach (endogenous)

146
Q

Cholinesterase Inhibitor poisoning symptoms?

A

“DUMBBELSS”
-> diarrhea, urination, miosis, bronchoconstriction, bradycardia, excitation CNS/NMJ, lacrimation,
salivation, sweating

147
Q

Antidote for Cholinesterase Inhibitors?

148
Q

Contraindications for Cholinesterase Inhibitors?

A

Exacerbates COPD, asthma, peptic ulcers

149
Q

What receptors do epi act on? Norepi?

A

Epinephrine (protypical agonist) - acts at all alpha and beta receptors
Norepinephrine - acts at alpha and beta 1 receptors

150
Q

What receptors do phenylephrin and albuterol act on?

A

Phenylephrine-alpha agonists

Albutero-beta agonists

151
Q

What receptors does dopamine act on?

A

Dopamine > Beta> Alpha (DoPA = DoBA)

152
Q

Effects of Sympathomimetic Drugs: Indirect Acting?

A

Increase the concentration of “endogenous” catecholamines in the synaptic cleft

153
Q

2 modes of action for Sympathomimetic Drugs?

A
  • increase release of transmitter

- inhibit reuptake (thereby effectively increasing action

154
Q

Examples of Sympathomimetic Drugs?

A

Tyramine (in fermented cheeses)- induces release of stored catecholamines from terminal
Amphetamine (methamphetamine)- induces release of stored catecholamines from terminal
Cocaine - blocks reuptake at the NE or DA transporter
Tricyclic antidepressants- blocks reuptake at the NE transporter (NET)

155
Q

Examples of Adrenoreceptor blockers: alpha versus beta blockers

A

Prazosin-alpha 1 selective blocker)

Propranolol-(protypical) non-selective beta blocker

156
Q

Clinical uses of adrenoceptor blockers?

A

Glaucoma, Pheochromocytoma (adrenal tumour), cardioselective blockers (beta1), benign prostatic hyperplasia (alpha blkr)

157
Q

Where are the Barorecep. sensory afferent sensors and chemosensors?

A

aortic arch, carotid sinus, carotid body

158
Q

Where can centrl control of ANS output be found?

A

Presynaptic alpha 2 Receptors

159
Q

What is considered the ANS “head ganglia”?

A

Hypothalamus

160
Q

Causes and Incidence of Neurogenic Bladder Dysfunction?

161
Q

What do Muscle relaxants do different from anesthesia?

A

Cause paralysis NOT anesthesia. They DO NOT cause unconsciousness, amnesia or analgesia

162
Q

What subunits of Ach recp. bnd Ach?

A

Only two α subunits bind Ach molecules although there are

Five protein subunits; Two α; single β,δ and ε subunits

163
Q

What is the Muscle Relaxant Mechanism of Action?

A

They are water sol. and don’t cross lip. mem.

164
Q

What are the two types of muscle relaxants?

A

Depol. and non-depol.

165
Q

What is the Mechanism of Action for Succinylcholine?

A

Depolarizing N M Blockers bind to Ach receptor and generate action potential but stays at the recep and doesn’t move causing prolonged depolarization of muscle end plate

166
Q

Phase I block vs. Phase II block?

A

Prolonged end plate depolarization cause muscle relaxation due to time limited closure of lower gate sodium channel causes Phase I Block. More depol. causes conformational changes in Ach receptors causing Phase II Block

167
Q

Mech of Non-depolarizing N M Blockers like Rocuronium?

A

Bind to Ach receptors as Competitive antagonists but can NOT produce conformational changes for action potential

168
Q

How is Sch metabolized?

A

Once in blood, rapid metabolism into Succinyl-monocholine by blood enzyme Pseudocholinesterase

169
Q

Why is Sch is AVOIDED in pediatric patients?

A

high incidence of undiagnosed mypopathies and resulting severe hyperkalemia and associated complications

170
Q

Side effects & Clinical Considerations for Sch?

A

Severe hyperkalemia, Malignant hyperthermia,Increase in intracranial, intra-ocular and intra-gastric pressures

171
Q

Characteristics of Rocuronium?

A

Monoquarternary steroid; Non-depol. relaxant; elim. by liver can cause severe liver disease
Intubation 0.8 – 1.2 mg/kg; maintenance 0.15 mg/kg

172
Q

Charachteristics of action of Cistracurium?

A

Non-depo. Degraded in plasma by organ-independent Hofmann eliminationIntubating dose 0.2 mg/kg

173
Q

Charachteristics of action of Vecuronium?

A

Non-Depol. Intubating dose 0.12 mg/kg Biliary excretion (75%) and renal excretion (25%)
Women 30% more sensitive

174
Q

Charachteristics of action of Cholinesterase Inhibitors ?

A

Increase Acetylcholine (Ach) in Nicotinic AND Muscarinic Ach receptors and is used to reverse neuromuscular blockade by non-depolarizing muscle relaxants

175
Q

What are the effects of Excessive cholinesterase inhibitors?

A

potentiate non-depolarizing motor blockade Ach channel blockade

176
Q

How are muscarinic side effects avoided when using Cholinesterases Inhibitors?

A

by using specific Muscarinic Ach receptor blockers such as Atropine, Glycopyrrolate

177
Q

What MUST be present before reversal agent use is attempted?

A

Some evidence of spontaneous recovery from muscle relaxation

178
Q

Characteristics of Neostigmine?

A

Water soluble quaternary ammonium compound
Does not cross the blood brain barrier
Dose: 0.04 – 0.08 mg/kg; Maximum 5 mg.
Always given with Atropine 0.01 mg/kg or Glycopyrrolate 0.02 mg/kg iv to prevent the muscarinic side effects

179
Q

What is the Equilibration Time?

A

Amt of time it takes for the alveolar concentrations to equal inspired concentrations and maximum concentrations exist in the tissues (Fa=F1

180
Q

What is the FGF rate and how does it affect the F1?

A

F1=inspired gas conc. and is determined by Fresh Gas Flow (FGF) from the vaporizer, breathing circuit volume and circuit absorption

181
Q

With a drug existing in the lung, what are 3 determinants of rate of rise of lung concentrations?

A
  1. Inspired gas partial pressure
    1. Ventilation rate-minute alveolar ventilation-
    2. Functional residual capacity (FRC)
182
Q

What is the effect of FRC on inhaled drugs?

A

slows washin (i.e., flow of agent into the lung) ;induction time is increased (slowed);increases the volume of lung that must be filled to obtain an effect

183
Q

What are the three Primary Determinants of Tissue Uptake of a drug?

A
  1. Solubility of agent
  2. Pulmonary blood flow (i.e. cardiac output)
  3. Arterio(alveolar)-venous concentration gradient in lung
184
Q

Define solubility

A

relative content of a gas in 2 phases when (at equilibrium) the partial pressure of the gas in the 2 phases is equal

185
Q

Relationship of cardiac output and equilibration time?

A

Increases in CO decrease rate of alveolar concentration rise, and slow equilibration time

186
Q

What would using the same drug doses, with bigger volumes result in?

A

Decreasedblood concentrations, Reduced concentration gradients to drive drug into the brain, Slower (increased) equilibration time

187
Q

What is the relationship of tissue uptake and blood conc?

A

Increased tissue uptake decreases blood concentrations which increases blood uptake from lungs

188
Q

What are the usual targets of of inhailed drugs?

A
  1. Nicotinic acetylcholine (nACh) receptors
  2. 5-HT3 receptors
  3. Amino acid receptors (esp GABA)
189
Q

Mechanism of Action

for GABA?

A

Cl- conductance (freq and duration) increases, hyperpolarizes, and inhibits neuron

190
Q

Relationship btwn. GABA and Inhaled anesthetics

A

Inhaled anesthetics are GABA agonists

191
Q

What is the MAC?

A

Minimum alveolar concentratio-Primary measure of potency

equilibrium concentration required to prevent movement to skin incision at 1 ATM in 50% of patients

192
Q

Effects of distribution on drug anesthetics?

A

Results in termination of effects of most anesthetics

193
Q

What is the trend of drug distribution in the body?

A

Bld. 1st->1min-60% in brain,->4-256 min-80% in lean tiss and 40% in fat

194
Q

Thiopental charachtersitics?

A

Rapid unconsciousness
Good amnesia, poor analgesia
Poor muscle relaxation
Pleasant induction for the patient

195
Q

What is Thiopental’s Mechanism of Action?

A

Binds to Inhit neurons w/ GABAa receptor
Increases chloride ion flux into cell
Increases the duration channel opening

196
Q

What are Thiopental’s Effects on the brain?

A

Protects the brain BEST against hypoxic/ischemic injury Reduces cerebral metabolism, bld flw, and O2 use

197
Q

What are Thiopental’s cardiovascular effects?

A

Direct effects->hypotension and hrt contractility

Indirect effects->HR increased via barostatic reflex

198
Q

Pos. features of Benzodiazepines ?

A

Best amnestic agents,

Excellent anxiolytics, anti-convulsants, muscle relaxants

199
Q

Effect of Midazolam Physicochemical Properties?

A

In plasma, lipid solubility increases access to neuronal recept.

200
Q

Effects of Midazolam on the brain?

A

reduction in cerebral metabolism and blood flow

Raises seizure threshold. Antegrade, not retrograde amnesia

201
Q

Opioids Actions

A

Not reliable for amnesia used for postoperative pain control

202
Q

Opioid Effects?

A

Pruritis and forget to breathe

due to Chest wall rigidity

203
Q

Remifentanil

A

Shortest acting opioid

Termination of action is due to elimination, not redistribution

204
Q

Hydromorphone

A

Used as adjunct with inhaled agents for intraoperative and postoperative analgesia

205
Q

Meperidine

A

Only indicated for shivering

206
Q

Morphine

A

Used in all phases of anesthesia

207
Q

Alfentanil

A

Used intraoperatively as IV infusion

208
Q

What is Ketamine’s Mechanism of Action?

A

Non-competitive NMDA antagonist only iv agent discussed that works mainly by inhibition of stimulatory systems

209
Q

Ketamine: Organ System Effects

A

Sympathamimetic in increased heart rate, blood pressure, epinephrine and nor-epi levels
Causes bronchodilation via SM
Nystagmus and phonation!

210
Q

Etomidate Mechanism of Action

A

Imidazole derivative
Activates GABAA receptors
Not an analgesic

211
Q

Etomidate: Organ System Effects

A

Lowers cerebral blood flow, metabolic rate for O2 and thus intracranial pressure
Lower risk of apnea
good for short procedures

212
Q

What drug is best to use in patients with cardiovascular risk factors?

A

Etomidate-Best when hemodynamic stability is a must

Does NOT block sympathetic effects

213
Q

Propofol: Organ System Effects

A

Reduces cerebral blood flow and metabolism, burns going in, patient feels better next day, fast acting!

214
Q

Dexmedetomidine

A

Central a-2 stimulation results in sedation and analgesia

Brain and Behavior T2 (2 decks)

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