front 1 A CNS-resident cell phagocytoses pathogens after meningitis. Which
cell type is primarily responsible? | back 1 B. Microglia |
front 2 The main interface between brain parenchyma and the CSF compartment
is formed by: | back 2 C. Ependymal cells |
front 3 Structurally, neurotransmitters are divided into: | back 3 A. Small nitrogen molecules and neuropeptides |
front 4 Small nitrogen-containing neurotransmitters are generally synthesized
in the: | back 4 D. Presynaptic terminal |
front 5 Small nitrogen-containing neurotransmitters are synthesized mainly
from: | back 5 B. Amino acids and glycolysis intermediates |
front 6 Serotonin is synthesized from: | back 6 A. Tryptophan |
front 7 Glutamate (and its derivative GABA) is derived from the TCA
intermediate: | back 7 C. Alpha-ketoglutarate |
front 8 In the brain, glycine is synthesized from: | back 8 D. Serine |
front 9 After global cerebral ischemia, which process most directly amplifies
neuronal injury in many regions? | back 9 B. Glutamate excitotoxicity |
front 10 A neurodegenerative disorder is linked to oxidative damage. Which
pair is emphasized in pathogenesis? | back 10 C. Free radicals and nitric oxide |
front 11 During CNS development, which glial cell guides neuronal migration
and helps form a stabilizing matrix? | back 11 A. Astrocyte |
front 12 A cell population lines the ventricles and can be specialized to
secrete CSF. Which cells are these? | back 12 D. Ependymal cells |
front 13 Impaired ventricular ciliary beating would most directly
disrupt: | back 13 B. CSF circulation efficiency |
front 14 Glucose crosses brain capillary endothelium primarily via facilitated
diffusion through: | back 14 C. GLUT1 |
front 15 Neurons take up glucose from extracellular fluid primarily
via: | back 15 A. GLUT3 |
front 16 An infant has seizures and a low CSF glucose despite normal serum
glucose. This CSF finding is called: | back 16 D. Hypoglycorrhachia |
front 17 Large neutral amino acids enter CSF rapidly via: | back 17 B. A single amino-acid transporter |
front 18 High levels of one LNAA can reduce transport of others across the BBB
via: | back 18 A. Competitive inhibition |
front 19 Untreated PKU causes cognitive impairment; one proposed mechanism is
reduced BBB entry of other amino acids due to excess: | back 19 A. Phenylalanine |
front 20 In maple syrup urine disease, impaired CNS amino-acid balance is most
linked to excess blood: | back 20 B. Branched-chain amino acids |
front 21 A patient started on reserpine later reports severe anhedonia and
suicidal thoughts. The drug’s relevant primary action is: | back 21 D. Blocks catecholamine vesicular uptake |
front 22 Which adverse psychiatric outcome was historically observed in a
subset of patients taking reserpine? | back 22 A. Depression and suicidality |
front 23 The first and rate-limiting step in catecholamine synthesis from
tyrosine is catalyzed by: | back 23 C. Tyrosine hydroxylase |
front 24 Tyrosine hydroxylase requires which cofactor for activity? | back 24 B. Tetrahydrobiopterin |
front 25 The immediate product of tyrosine hydroxylase is: | back 25 A. L-DOPA |
front 26 The conversion of L-DOPA to dopamine requires which cofactor? | back 26 D. Pyridoxal phosphate |
front 27 Epinephrine synthesis depends on adequate vitamin support to generate
SAM, specifically: | back 27 B. Vitamin B12 and folate |
front 28 Conversion of tyrosine to L-DOPA and L-DOPA to dopamine occurs in
the: | back 28 C. Cytosol |
front 29 Reserpine was historically used clinically primarily as a(n): | back 29 D. Antihypertensive and antiepileptic |
front 30 Which set lists only major small nitrogen-containing
neurotransmitters from the provided material? | back 30 A. Glutamate, GABA, glycine, histamine |
front 31 A vesicular monoamine transporter shares homology with bacterial
drug-resistance transporters. Which example fits this family? | back 31 A. P-glycoprotein |
front 32 Vesicle transporters for monoamines typically span the membrane with
how many transmembrane domains? | back 32 C. 12 |
front 33 Catecholamines are concentrated inside storage vesicles by a
mechanism best described as: | back 33 B. Secondary active transport |
front 34 The catecholamine vesicular uptake process is ultimately driven by
a: | back 34 A. Proton pump gradient |
front 35 In storage vesicles, catecholamines most characteristically exist
complexed with: | back 35 B. ATP and chromogranins |
front 36 When chromogranins are released, they can be proteolytically
processed into: | back 36 C. Bioactive peptides |
front 37 A patient has episodic headaches, sweating, palpitations, and severe
hypertension (pheochromocytoma). Which circulating marker may be
elevated in this tumor type? | back 37 A. Chromogranins |
front 38 Two major enzyme systems mediating catecholamine inactivation
include: | back 38 B. COMT and MAO |
front 39 MAO is located primarily on the: | back 39 B. Outer mitochondrial membrane |
front 40 MAO catalysis oxidizes the amino-bearing carbon to an aldehyde and
releases: | back 40 C. Ammonium ion |
front 41 A drug selectively inhibiting MAO-A would most directly reduce
deamination of: | back 41 B. Norepinephrine and serotonin |
front 42 MAO-B has relatively broader activity against: | back 42 A. Phenylethylamines |
front 43 A child with hypopigmentation is suspected to have albinism due to
impaired tyrosine-to-melanin conversion. A potentially defective
enzyme is: | back 43 B. Copper-dependent tyrosine hydroxylase |
front 44 COMT inactivates catecholamines by transferring a methyl group
from: | back 44 C. SAM |
front 45 CSF homovanillylmandelic acid (HVA) is an indicator of: | back 45 A. Dopamine degradation |
front 46 Reduced CSF HVA would be most consistent with neuronal changes seen
in: | back 46 D. Parkinson disease |
front 47 A patient develops headaches, palpitations, nausea, vomiting, and
high blood pressure after ingesting large amounts of aged foods. The
culprit amine is: | back 47 C. Tyramine |
front 48 Tyramine is normally detoxified primarily by: | back 48 B. MAO-A |
front 49 A patient on an MAO inhibitor eats aged cheese and develops a
hypertensive crisis. The key immediate mechanism is: | back 49 A. Tyramine releases norepinephrine |
front 50 Free cytosolic catecholamines downregulate tyrosine hydroxylase by
competing for the enzyme’s: | back 50 C. Pterin cofactor binding |
front 51 Which acute event in a nerve terminal activates tyrosine
hydroxylase? | back 51 B. Depolarization |
front 52 With prolonged sympathetic firing, increased transcription of
tyrosine hydroxylase and dopamine β-hydroxylase occurs mainly in
neuronal: | back 52 D. Neuronal Perikarya |
front 53 The synthesis pathway of serotonin from tryptophan is most similar in
logic to norepinephrine synthesis from tyrosine because both begin
with: | back 53 B. Hydroxylation then decarboxylation |
front 54 In addition to catecholamines, serotonin is inactivated by: A. COMT | back 54 C. MAO |
front 55 The activity of several antipsychotic drugs is described here as
being based on inhibiting: | back 55 A. MAO |
front 56 Melatonin is synthesized from the amino acid precursor: | back 56 C. Tryptophan |
front 57 A patient develops thrombocytopenia and thrombosis after heparin
exposure due to antiheparin antibodies. This antibody-driven platelet
activation is associated with release of: | back 57 B. Serotonin |
front 58 Within the brain, histamine is produced by: | back 58 C. Mast cells and neuronal fibers |
front 59 Histaminergic neuronal cell bodies in humans are concentrated in
the: | back 59 C. Tuberomammillary nucleus |
front 60 The tuberomammillary nucleus lies within the: | back 60 A. Posterior basal hypothalamus |
front 61 Histamine synthesis from histidine is catalyzed by: | back 61 D. Histidine decarboxylase |
front 62 Histidine decarboxylase requires which cofactor? | back 62 B. Pyridoxal phosphate |
front 63 The catalytic mechanism of histidine decarboxylase most
resembles: | back 63 C. DOPA decarboxylase |
front 64 A serotonergic anorexigen decreases appetite via receptors
on: | back 64 A. POMC neurons |
front 65 The POMC neurons mediating Redux hypophagia are in the: | back 65 B. Arcuate nucleus |
front 66 A drug that raises synaptic serotonin most directly promotes: | back 66 D. Satiety signaling |
front 67 Chronically low serotonin is associated with: | back 67 A. Increased appetite |
front 68 Redux raised synaptic serotonin by SSRI action plus: | back 68 C. Increased serotonin secretion |
front 69 After neuronal release, histamine is thought to activate: | back 69 B. Pre and postsynaptic |
front 70 Relative to many transmitters, histamine shows little: | back 70 A. Presynaptic recycling |
front 71 Major CNS uptake/inactivation of histamine is attributed to: | back 71 D. Astrocytes |
front 72 A first-generation antihistamine most commonly causes: | back 72 C. Drowsiness |
front 73 “Nondrowsy” antihistamines minimize sedation mainly due to: | back 73 A. Poor BBB penetration |
front 74 Peripheral antihistamine effects primarily counter
histamine-driven: | back 74 B. Vasodilation permeability |
front 75 A proposed contributor to neurologic findings in B12 deficiency is
impaired: | back 75 D. Dopamine synthesis |
front 76 The key reaction supplying acetyl-CoA for acetylcholine synthesis
is: | back 76 C. Pyruvate dehydrogenase |
front 77 Pyruvate dehydrogenase is located in the: | back 77 A. Mitochondria |
front 78 Lecithin (phosphatidylcholine) supplementation has been used
for: | back 78 D. Tardive dyskinesia |
front 79 The highest physiologic demand for choline is in the: | back 79 B. Neonate |
front 80 Glutamate dehydrogenase forms glutamate by incorporating: | back 80 C. Ammonia |
front 81 An alternative major route to glutamate from α-ketoglutarate
uses: | back 81 A. Transamination |
front 82 The CNS recycling pathway conserving glutamate and GABA is
the: | back 82 D. GABA shunt |
front 83 A patient with epilepsy is given a drug that blocks GABA
reuptake: | back 83 C. Tiagabine |
front 84 Which amino acid cannot cross the BBB? | back 84 B. Aspartate |
front 85 Nitric oxide (NO) is synthesized from which amino acid
substrate? | back 85 B. Arginine |
front 86 A patient’s ABG shows PaO2 = 18 mm Hg during acute hypoxia. Most
likely clinical state? | back 86 D. Coma |
front 87 A shared metabolic consequence of all forms of hypoxia
is: | back 87 A. Decreased neurotransmitter synthesis |
front 88 Which enzyme represents a major anaplerotic reaction for the TCA
cycle? | back 88 C. Pyruvate carboxylase |
front 89 Valine and isoleucine degradation replenishes the TCA cycle by
producing: | back 89 A. Succinyl-CoA |
front 90 A peroxisome biogenesis disorder (e.g., Refsum) injures brain cells
largely due to failed metabolism of: | back 90 D. VLCFAs and branched-chain AAs |
front 91 Which lipid class is ~16% of myelin lipid and largely absent from
other membranes? | back 91 B. Cerebrosides |
front 92 Galactosylcerebroside is best described as having: | back 92 C. Single sugar on sphingosine OH |
front 93 Myelin lamellae are stabilized primarily by: | back 93 A. Protein–lipid and protein–protein |
front 94 Two proteins comprising ~60–80% of CNS myelin protein are: | back 94 D. Proteolipid protein and Myelin basic proteins |
front 95 What may help to stabilize the structure from within the membrane? A. Proteolipid protein | back 95 C. Myelin basic protein |
front 96 Pre-op management to mask catecholamine-excess signs in
pheochromocytoma most classically uses: | back 96 B. Phenoxybenzamine then propranolol |
front 97 Multiple sclerosis incidence is described as: | back 97 A. Near nil at Equator |
front 98 Modern MS treatment is now based mainly on blocking the: | back 98 C. Immune system blockade |
front 99 Inherited mutations in P0 (major PNS myelin protein) most directly
cause: | back 99 D. Charcot-Marie-Tooth disease |
front 100 The inheritance pattern classically described for Charcot-Marie-Tooth
is: | back 100 B. Autosomal dominant |
front 101 A PLP mutation in CNS myelin is associated with which
leukodystrophy? | back 101 C. Pelizaeus-Merzbacher disease |
front 102 The enzyme catalyzing NO formation from arginine is: | back 102 A. Nitric oxide synthase |
front 103 Which branched-chain amino acids contribute succinyl-CoA via
degradation? | back 103 B. Valine and isoleucine |
front 104 Mutations in the major CNS myelin protein can cause
Pelizaeus-Merzbacher and X-linked spastic paraplegia type 2. The
protein is: | back 104 D. Proteolipid protein |