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Final FA review > 3/26 Neuro > Flashcards

3/26 Neuro Flashcards

1
Q

fovea: nasal or temporal?

optic disc: nasal or tempora?

A

fovea: temporal

optic disc: nasal

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2
Q

anopia/anopsia

-define:

A

defect in field of vision
-so when its describing it, like bilateral temporal hemianopsia, it means the temporal visual field is fucked up on both sides.

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3
Q

optic radiations

-the path from what to what?

A

LGN => V1 via optic radiations.

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4
Q

optic radiations

-what are the two paths?

A

1) Meyers loop

2) Dorsal optic radiation

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5
Q

Brain lesion where can damage meyers loop?

-stroke in which art dmgs meyers loop?

A
  • temporal lobe

- MCA

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6
Q

Meyers loop

  • inf or sup retina?
  • inf or sup visual field?
  • mnemonic?
A
  • inferior retina (on that side) which obviously = superior VF.
  • (Max) Myers: lower in brain (inf. 1/2 of neurons) but superior in appearance (sup. 1/2 of VF).
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7
Q

What visual process loops around inferior horn of lateral ventricle?

A

Meyers loop

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8
Q

What visual path runs thru the internal capsule?

A

Dorsal optic radiation

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9
Q

Lesion where damages the Dorsal optic radiation?

-stroke in which art dmgs dorsal optic radiation?

A
  • Parietal lobe

- MCA.

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10
Q

Dorsal optic radiation

  • inf or sup retina?
  • where in brain is it located?
  • mnemonic
A
  • sup. retina
  • parietal lobe
  • “parietal lobe is higher up than temporal lobe, DOR is superior 1/2 of retina.”
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11
Q

4 destinations of optic tract fibers?

A

1) LGN
2) pretectal nucleus
3) superior colliculus
4) suprachiasmatic nucleus (of hypoT)

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12
Q

Sturge-Weber syndrome

  • somatic or inherited?
  • developmental anomaly of what tissue derivatives?
  • ectoderm? mesoderm? endoderm?
A
  • somatic
  • neural crest cells.
  • ectoderm & mesoderm.
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13
Q

Sturge-Weber syndrome

  • what type of mutation?
  • which gene?
A
  • activating mutation

- GNAQ gene

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14
Q

Sturge-Weber syndrome

-in basic terms, whats the problem here?

A
  • problem w/blood vessels.

- you get port-wine stain on face & neurological problems from excessive blood vessel growth on brain (angiomas).

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15
Q

Sturge-Weber syndrome

  • Sxs:
  • mnemonic:
A

STURGE:

  • Sporadic, port-wine Stain
  • Tram track Ca2+ (opposing gyri)
  • Unilateral
  • Retardation
  • Glaucoma, GNAQ gene
  • Epilepsy.
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16
Q

Tuberous sclerosis

  • Sxs:
  • mnemonic?
A

HAMARTOMAS

  • Hamartomas in CNS and skin
  • Angiofibromas
  • Mitral regurgitation
  • Ash-leaf spots
  • cardiac Rhabdomyoma
  • Tuberous sclerosis
  • autosomal dOminant
  • Mental retardation
  • renal Angiomyolipoma
  • Seizures, Shagreen patches
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17
Q

Tuberous sclerosis

-inheritance pattern

A

auto dom.

-must have variable expressivity.

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18
Q

Neurofibromatosis type I (von Recklinghausen disease)

  • mutation in what gene?
  • whats the gene product?
  • which chrom?
  • inheritance pattern?
A

-NF1 tumor suppressor gene
-neurofibromin, a negative regulator of Ras
-chrom 17
-

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19
Q

Neurofibromatosis type I

-Sxs:

A

Its a PNS tumor syndrome

  • Café-au-lait spots
  • Lisch nodules (pigmented iris hamartomas)
  • neurofibromas in skin
  • optic gliomas
  • pheochromocytomas.
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20
Q

von Hippel-Lindau disease

  • inhertiance pattern?
  • which gene?
  • which chrom?
A
  • auto dom
  • VHL tumor suppressor gene
  • chrom 3
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21
Q

von Hippel-Lindau disease

-gene products that are over-expressed?

A

-constitutive expression of HIF (transcription factor) and

activation of angiogenic growth factors.

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22
Q

von Hippel-Lindau disease

A
  • Cavernous hemangiomas in skin, mucosa, organs
  • bilateral renal cell carcinomas
  • hemangioblastoma in retina, brain stem, cerebellum
  • pheochromocytomas.
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23
Q

do meningiomas stain for GFAP?

A

no

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24
Q

butterfly glioma =?

A

glioblastoma multiforme

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25
Q

“Pseudopalisading” pleomorphic tumor cells—border central areas of necrosis and hemorrhage.
-which tumor?

A

glioblastoma multiforme

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26
Q

meningioma

  • typically found where?
  • tumor of what cell?
A
  • near the surface of brain & parasagittal.

- arachnoid cell.

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27
Q

Spindle cells concentrically arranged in a whorled pattern; psammoma bodies.
-which tumor?

A

meningioma

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28
Q

new-onset seizures in adult female

-imaging shows mass attached to the dura

A

meningioma

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29
Q

Hemangioblastoma

  • child or adult?
  • cerebral or cerebellar?
A
  • adult

- cerebellar

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30
Q

Cerebellar hemangioblastoma w/retinal angiomas

-what disease?

A

VHL

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31
Q

Hemangioblastoma

-which paraneoplastic hormone?

A

EPO

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32
Q

Oligodendroglioma

-most commonly found where?

A

frontal lobes

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33
Q

Pilocytic astrocytoma

  • benign or malignant?
  • marker?
A
  • benign.

- GFAP

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34
Q

Rosenthal fibers

  • what do they look like?
  • what disease are they found in?
A
  • eosinophilic, corkscrew fibers.

- pilocytic astrocytoma

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35
Q

Pilocytic astrocytoma

-gross appearance?

A
  • cystic + solid

- Mural node = small mass of tissue that adheres to the wall of the cyst.

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36
Q

Ependymoma

-most often found in which ventricle?

A

4th ventricle

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37
Q

Perivascular rosettes & rod-shaped blepharoplasts

-which disease?

A

ependymoma

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38
Q

Subfalcine herniation

  • what is it?
  • what can be compressed?
A
  • Cingulate gyrus herniation under falx cerebri.

- ACA can be compressed

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39
Q

Uncal herniation

  • what is it?
  • what CN be compressed?
A
  • Uncus = medial temporal lobe, herniates thru tentorium cerebelli.
  • Compressed CN 3 => CN3 palsy + blown pupil.
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40
Q

Uncal herniation

-what visual defect?

A

-Compressed ipsilateral PCA => contralateral homonymous hemianopia.

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41
Q

Uncal herniation

-what type of paralysis?

A

-compressed contralateral crus cerebri => ipsilateral paralysis, “false localization” sign.

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42
Q

First sign of uncal hernation?

A

fixed & dilated pupil

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43
Q

Cerebellar tonsillar herniation

  • herniates into where?
  • Sxs:
  • causes of death:
A
  • foramen magnum

- Coma and death result when these herniations compress the brain stem (and inhibit respiration).

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44
Q

Brimonidine

  • what is it?
  • whats it used for?
A

alpha2-agonist

-glaucoma: dec. humor prod

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45
Q

Epinephrine

  • how does it treat glaucoma?
  • which glaucoma does it treat?
A
  • dec. aqueous humor synthesis via vasoconstriction.

- do NOT use on closed-angle bc it causes mydriasis!

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46
Q

Emergency closed-angle glaucoma

-Tx:

A

pilocarpine

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47
Q

loperamide

  • what is it?
  • common use?
A
  • opiate

- Its an anti-diarrheal.

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48
Q

diphenoxylate

  • what is it?
  • common use?
A
  • opiate

- Its an anti-diarrheal.

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49
Q

Opiates

-what does pt never develop tolerance to?

A

miosis & constipation.

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50
Q

naloxone

-route of admin?

A

IV

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51
Q

Which opiate do you use in biliary & colic pain?

A

meperidine

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52
Q

meperidine

  • how is it metabolized?
  • what is its metabolite?
A
  • P450 metabolism.

- Its metabolite (normeperidine) = SSRI

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53
Q

Why should you be careful prescribing an opiate to a pt w/hypotension?

A

-all mu opioids cause histamine release => vasodilation & itching.

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54
Q

Mu receptors

-what type of receptor?

A
  • Gi coupled
  • open K channels = hyperpolarization.
  • close Ca channels & prevent release of NTs.
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55
Q

Opiates

-inhibit release of what chemicals?

A

Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

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56
Q

Pentazocine =

A
  • partial agonist @ Mu receptor.

- can cause withdrawals to opiate addict.

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57
Q

Meperidine overdose

-can you give naloxone?

A

No

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58
Q

How do opiates treat acute pulmonary edema?

A

-Improves pulmonary hemodynamics, helps normalize ventilation, helps allay anxiety.

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59
Q

How do opiates depress your central respiratory center?

-if your respiratory center is depressed, what keeps your ventilation going?

A
  • Your pCO2 centers in your medulla (central respiratory center) have mu receptors, so morphine will shut them down.
  • You also have peripheral O2 receptors (carotid body/aortic body) called your “hypoxic drive”. This is what will remain when a pt is under the influence of an opiate b/c central respiratory center is shut down.
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60
Q

Can you give O2 to a pt under opiates?

A
  • Do NOT give O2 to pt under opiates unless pt is mechanically ventilated.
  • Lots of oxygen will turn off the pO2 centers (carotid/aortic bodies) so there wont be any signals to breathe.
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61
Q

Butorphanol

  • what is it?
  • how do you treat OD?
A
  • Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia.
  • Overdose not easily reversed with naloxone.
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62
Q

Tramadol

  • mech?
  • mnemonic?
A
  • Weak opioid agonist; also inhibits serotonin and NE reuptake
  • works on multiple neurotransmitters—“tram it all” in with tramadol.
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63
Q

Tramadol

-tox:

A
  • Similar to opioids
  • Decreases seizure threshold
  • Serotonin syndrome
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64
Q

MI presenting w/brady & hypotension?

  • wheres the infarct?
  • which artery?
  • which leads?
A
  • SA node.
  • RCA
  • 2, 3, aVF
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65
Q

pseudogout

  • deposition of what type of crystals?
  • shape?
  • are they +/- birefringent?
A
  • calcium pyrophosphate
  • rhomboid
  • weakly positively birefringent.
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66
Q

gout

  • what are crystals made of?
  • are crystals +/- birefringent?
A
  • monosodium urate

- neg. birefringent.

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67
Q

Gout

-what color are crystals in parallel light?

A

yellow

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68
Q

Pseudgout

-what color are crystals in parallel light?

A

blue

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69
Q

Destructino of oligodendrocytes seen in which diseases?

A

MS & PML

*which is funny bc natalizumab is used to treat MS but can cause PML.

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70
Q

pleomorphic

-define:

A

differing in size & shape.

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71
Q

cutaneous facial angiomas & leptomeningeal angiomas

A

Sturge Weber syndrome

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72
Q

femoral neck fx

-which artery is at risk?

A

medial circumflex art.

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73
Q

inc or dec levels of hepcidin in hemochromatosis?

-how about ferroportin expression?

A

decreased levels of hepcidin which will upregulate (basolateral) ferroportin which allows enterocytes to release more iron into circulation.

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74
Q

Hemochromatosis

-which pancreatic functions are destroyed and which are retained?

A
  • endocrine destroyed
  • bc iron overload in blood, and endocrine part is much more highly vascularized.
  • exocrine retained (so no malabsorption).
75
Q

How do OCPs reduce risk of ovarian cancer?

A
  • when you ovulate/rupture a follicle, you have to then repair surface of ovary. This repairative process can lead to ovarian surface cancers.
  • OCPs reduce number of times a woman ovulates, so it reduces these risks.
76
Q

If cell wants to go from G1 to S, does Rb need to be phosphorylated or not-phosphorylated?

A

-phosphorylated means the cell cycle can continue.

77
Q

primary cell in gout thats causing problems?

A

neutrophils phagocytose the crystals and release inflammatory cytokines.

78
Q

Ethosuximide

  • mech?
  • use?
A
  • Blocks thalamic T-type Ca2+ channels.

- absence seizures.

79
Q

first line for acute status epilepticus.

A

Lorazepam

80
Q

phenytoin & megaloblastic anemia

-how?

A

phenytoin blocks intestinal conjugase needed to absorb folate.

81
Q

How does phenytoin dec. vit D levels?

A

by inc. P450.

-P450 system metabolizes vitamin D.

82
Q

Which drugs follow 0 order kinetics?

-mnemonic?

A

PEA (looks like 0)

-phenytoin, ethanol, aspirin.

83
Q

Phenytoin

-side effects?

A
  • gingival hyperplasia
  • hirsutism
  • P450 induction
  • megaloblastic anemia
  • teratogen
84
Q

Do 0-order drugs have wide or narrow therapeutic window?

A

narrow therapeutic window

85
Q

Unique use of carbamazepine

A

neurogenic pain

-ie. trigeminal neuralgia

86
Q

Carbamazepine

-side effects?

A
  • agranulocytosis
  • SIADH
  • aplastic anemia
  • P450 inducer
87
Q

Valproic acid

-mech:

A
  • Na channel inactivation
  • inhibit GABA transaminase
  • T-type Ca channel blocker
88
Q

Besides ethosuximide, which drugs can be used for absence seizures?

A

Valproic acid, Lamotrigine.

89
Q

Valproic acid

-side effects

A
  • hepatotoxicity
  • P450 inhibitor
  • neural tube defects
  • pancreatitis
  • teratogen
90
Q

Valproic acid

-besides seizures, what can it be used for?

A

bipolar disorder

91
Q

Gabapentin

-what is it?

A

Ca channel inhbitor + GABA analog

-anti-epileptic

92
Q

Topiramate

-what is it?

A
  • blocks Na channels, inc GABA action

- anti-epileptic

93
Q

Lamotrigine

  • what is it?
  • tox:
A
  • blocks Na channels
  • anti-epileptic
  • steven johnsons
94
Q

Levetiracetam

-what is it?

A

-anti-epileptic

95
Q

Tiagabine

-what is it?

A
  • GABA reuptake inhibitor

- anti-epileptic

96
Q

Vigabatrin

-what is it?

A
  • irreversible GABA transaminase inhibitor

- anti-epileptic

97
Q

Which one can you OD harder on, benzos or barbs?

A

barbs.

-benzos reach a plateau.

98
Q

Barbs & benzos

  • analgesia?
  • sedation?
A

pure sedation, no analgesia.

99
Q

Barbiturates

-C/I: if pt has what disease?

A

porphyrias

100
Q

which barb is used to induce anesthesia?

A

thiopental

101
Q

P450 induction

-what happens on lineweaver plot?

A

inc. Vmax.

102
Q

Benzos

-effect on sleep?

A

-dec. REM sleep.

103
Q

Short acting benzos:

-mnemonic?

A

triazolam, oxazepam, midazolam, alprazolam.

-TOM & AL bundy has a short fuse.

104
Q

Barbs/Benzos/ethanol

-bind GABAa or GABAb?

A

GABAa

105
Q

Night terrors, sleepwalking

-Tx:

A

benzos

106
Q

Benzo OD

-Tx:

A

flumazenil

107
Q

Which sedative has anterograde amnesia?

A

benzos

108
Q

Zolpidem

-what is it?

A
  • BZ1 subtype of the GABA receptor.

- Insomnia.

109
Q

Zaleplon

-what is it?

A
  • BZ1 subtype of the GABA receptor.

- Insomnia.

110
Q

esZopiclone

-what is it?

A
  • BZ1 subtype of the GABA receptor.

- Insomnia.

111
Q

Blood/gas ratio

-if you want fast on/off, do you want high or low blood/gas ratio?

A

low blood/gas ratio = fast on/off.

112
Q

Anesthetic: solubility in blood

-if you want fast on/off, do you want high or low solubility in blood?

A

low solubility in blood = fast on/off

-will = low blood/gas ratio

113
Q

Steepness of arterial tension curve for anesthetic

-if you want a steep curve, do you have high or low solubility in blood?

A
  • less soluble = steeper curve

- Partial pressure in the blood rises more quickly w/less soluble anesthetics, producing a steeper curve.

114
Q

Nitrous oxide

-how is it cleared/eliminated?

A

-not metabolized, just exhaled.

115
Q

Inhaled anesthetics

-mechanism of action:

A

mechanism unknown.

116
Q

Inhaled anesthetics

  • effect on cerebral blood flow?
  • effect on cerebral metabolic demand?
A
  • inc. cerebral blood flow (inc. ICP).

- dec. cerebral metabolic demand (working less so needs less energy, obviously).

117
Q

N2O

  • name?
  • is there resp. depression?
A
  • nitrous oxide

- no respiratory depression.

118
Q

Do inhaled anesthetics cause analgesia?

A

yes

-they do everything you want in a general anesthetic.

119
Q

A good inducer:

  • solubility in blood:
  • A-V conc. diff:
  • blood/gas ratio:
A
  • low solubility in blood
  • low A-V conc. diff
  • low blood/gas ratio.
120
Q

Which inhaled anesthetic can cause:

-hepatotoxicity

A

halothane

121
Q

Which inhaled anesthetic can cause:

-nephrotoxicity

A

methoxyflurane

122
Q

Which inhaled anesthetic can cause:

-seizures

A

enflurane

123
Q

Which inhaled anesthetic can cause:

-expansion of trapped gas in a body cavity

A

nitrous oxide

124
Q

Which inhaled anesthetic can NOT cause malignant hyperthermia?

A

nitrous oxide

125
Q

Malignant hyperthermia

  • most common causes:
  • Tx:
A
  • halothane, succinylcholine.

- Tx: dantrolene.

126
Q

Which inhaled anesthetic should pregnant women not use?

A

N2O can cause spontaneous abortion.

127
Q

Halothane hepatitis

  • how long after does it happen?
  • where is the necrosis?
A
  • 2 days to 4 weeks after surgery

- centilobular necrosis

128
Q

Malignant hyperthermia

-where is the problem?

A

ryanodine receptor

129
Q

Dantrolene

-mech:

A

Blocks Ca release from SR.

130
Q

IV anesthetics

-whats the pro?

A

Do not cause N/V.

131
Q

Anesthetics

-What does lipid solubility correlate with?

A

High lipid solubility = high potency = lower the MAC.

132
Q

IV barbs

-effect on cerebral blood flow?

A

dec. cerebral blood flow

- opposite inhaled anesthetics which inc. cerebral blood flow.

133
Q

What does potency tell you about the anesthetic?

A

Just tells you how much you have to use to get the job done, thats pretty much it.

134
Q

What risk is associated w/IV barbiturates?

A

laryngospasm

135
Q

ketamine

  • mech:
  • is it analgesic?
  • what type of anesthesia do they cause?
A
  • Block NMDA receptors
  • good analgesic.
  • dissociative anesthesia.
136
Q

ketamine

  • side effect?
  • C/I in what pts?
A
  • nightmares

- C/I in PTSD pts.

137
Q

ketamine

  • effect on CV system?
  • effect on cerebral blood flow?
A
  • CV stimulant.

- inc. cerebral blood flow.

138
Q

Which anesthetics inc. cerebral blood flow?

A

inhaled anesthetics, ketamine.

139
Q

Which anesthetics dec. cerebral blood flow?

A

barbiturates.

140
Q

Binding of what is required for NMDA receptor activation?

A

glutamate & glycine.

141
Q

Propofol

  • mech:
  • effect:
  • s/e:
A
  • potentiates GABAa
  • sedative, no analgesia = INDUCTION AGENT.
  • hypotension, its a vasodilator.
142
Q

Most ORs use what as the induction agent?

-why this one?

A

propofol

-less post-op N/V than thiopental.

143
Q

Propofol

-same mech as what other drugs?

A

benzos

144
Q

Local anesthetics

-esters vs amides: how do you remember, whats the mnemonic?

A

-amIdes have 2 I’s in name!

145
Q

tetracaine

-what is it?

A

ester local anesthetic

146
Q

procaine

-what is it?

A

ester local anesthetic

147
Q

local anesthetics

  • mech?
  • which channels do they preferentially bind?
A
  • Block Na+ channels (from inside the nerve).

- Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.

148
Q

local anesthetics

  • what needs to happen before they can work?
  • explain the different forms:
A

Need to get into the nerve.

  • They’re weak bases so need an alkaline environment so they remain neutrally charged so they can get in.
  • Then, once inside, the acidic pH of the cell ionizes them so they can function.
149
Q

local anesthetics

-amides: where are they metabolized?

A

Liver

150
Q

local anesthetics: which nerve fibers are blocked first

  • small or large?
  • myelinated or non-myelinated?
A
  • small

- myelinated

151
Q

local anesthetics: which nerve fibers are blocked first

-small unmyelinated or large myelinated?

A

small unmyelinated

-size predominates over myelination.

152
Q 
local anesthetics: order of loss, put these in order:
touch
pain
pressure
temperature
A

(1) pain
(2) temperature
(3) touch
(4) pressure

*-PTTP: pressure is last.

153
Q

Which local anesthetic can cause:

-severe cardiovascular toxicity

A

bupivacaine

154
Q

Which local anesthetic can cause:

-arrhythmias

A

cocaine

155
Q

Neuromuscular blocking drugs

-what kind of paralysis do they cause?

A

flaccid paralysis

-you wouldn’t ever want to cause a spastic paralysis - thats what happens in malignant hyperthermia!

156
Q

succinylcholine

-phase 1: how do you reverse it?

A

-pseudocholinesterase metabolizes the succinylcholine.

157
Q

succinylcholine

-phase 2: how do you reverse it?

A

AChE inhibitors

158
Q

succinylcholine

-tox:

A

hypercalcemia, hyperkalemia, and malignant hyperthermia.

159
Q

Non-depolarizing NMJ blockers

  • suffix?
  • mech?
A
  • curium
  • curonium
  • competetive inhibitors of ACh at Nm.

*Tubocurarine as well.

160
Q

Tubocurarine

-what is it?

A

Non-depolarizing NMJ blockers

161
Q

Malignant hyperthermia

-what do 50% of these pts have?

A

-auto dom. mutation in ryanodine receptor, causing LOTS of Calcium release from SR.

162
Q

carbidopa

-mech:

A

noncompetetive inhibitor of dopa decarboxylase.

163
Q

Amantadine

  • use in parkinsons?
  • tox?
A
  • inc. dopamine release

- tox = ataxia

164
Q

Selegiline

  • mech:
  • use:
A
  • selective MAO type B inhibitor
  • parkinsons

*MAO-B metabolizes dopamine.

165
Q

entacapone, tolcapone

  • mech:
  • use:
A
  • COMT inhibitors => prevent l-dopa degradation Ž=> inc. dopamine availability.
  • parkinsons
166
Q

entacapone vs tolcapone

-whats the diff?

A
  • entacapone only works in the periphery.

- tolcapone work in both periphery & central.

167
Q

MAO-A

-what does it metabolize?

A

NE & serotonin

168
Q

Which anti-muscarinic used most commonly in parkinsons?

A

benztropine

-“Park my Benz”

169
Q

What do anti-muscarinics do in parkinsons? Which Sxs do they manage?

A

-Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia.

170
Q

Which vitamin inc. peripheral degradation of levodopa?

A

B6

171
Q

Levodopa/carbidopa

-tox:

A
  • Arrhythmias from inc. peripheral formation of catecholamines.
  • Long-term use can lead to dyskinesia (on-off phenomenon).
172
Q

Selegiline

  • what are its metabolites?
  • what can they cause?
A
  • amphetamines

- insomnia, agitation.

173
Q

Memantine

  • mech:
  • use:
  • tox:
A
  • NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).
  • Huntingtons
  • Dizziness, confusion, hallucinations.
174
Q

Donepezil, galantamine

  • mech:
  • use:
A

AChE inhibitors
-Alzheimers

*also rivastigmine.

175
Q

Sumatriptan

-tox:

A

coronary vasospasm

176
Q

Sumatriptan

  • mech:
  • use:
A
  • 5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction.
  • acute migraine, cluster headache.
177
Q

myoclonic seizures

-1st line med:

A

valproic acid.

178
Q

clonic

-define

A

movement

179
Q

postictal

-define:

A

following a seizure

180
Q

Which ABx can cause serotonin syndrome if taken w/SSRI?

A

linezolid

-its a weak MAO inhibitor.

181
Q

migraine

-abortive therapy:

A

sumatriptan

182
Q

which nerve is responsible for migraine headaches & releasing vasoactive peptides to meninges?

A

trigeminal n.

-activated by meningeal irritation.

183
Q

Which NT is released in all ganglia?

A

ACh

Final FA review (52 decks)

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