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Mind & Motion > Midterm 2: Buzzword Bingo > Flashcards

Midterm 2: Buzzword Bingo Flashcards

1
Q

Aphasia with decreased fluency, normal comprehension, decreased naming, decreased repetition

A

Broca’s aphasia

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2
Q

Clinical condition indicated by Brudzinski sign

A

Meningitis

Brudzinski sign is a test of nuchal rigidity. On passive flexion of neck, the patient will spontaneously and unconsciously flex legs and thighs.

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3
Q

Kernig sign

A

Flex patient’s hip to 90 degrees. In a positive Kernig sign, you won’t be able to extend that leg without the other leg flexing. This is also highly specific for meningitis (but not sensitive).

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4
Q

CNS inflammatory condition with abnormal brain function

A

Encephalitis - inflammation of the brain parenchyma.

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5
Q

Poorly demarcated focal infection of the brain

A

Cerebritis

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6
Q

Well-demarcated focal infection of the brain

A

Abscess

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7
Q

CNS inflammatory syndrome presenting with motor, sensory, autonomic dysfunction below the level of the lesion

A

Myelitis

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8
Q

Type of CNS inflammation indicated by a ring-enhancing lesion on head CT (referring to the clinical syndrome, not the specific pathology)

A

Abscess or cerebritis

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9
Q

Most common causes of bacterial meningitis in neonates

A

Gram negative rods, Group B strep

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10
Q

Most common causes of bacterial meningitis in kids

A

1) N meningitidis, 2) S pneumo

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11
Q

Most common causes of bacterial meningitis in adults

A

1) S. Pneumo, 2) N. Meningitidis

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12
Q

Most common causes of bacterial meningitis in older adults

A

N. Meningitidis, S. Pneumo, listeria

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13
Q

Appropriate empiric ABX for a neonate with suspected bacterial meningitis

A

Ampicillin + cefoxitime or aminoglycoside

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14
Q

Appropriate empiric ABX for a child or adult with suspected bacterial meningitis

A

Vancomycin + a third-generation cephalosporin

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15
Q

Appropriate empiric ABX for an older adult with suspected bacterial meningitis

A

Vancomycin + third-gen cephalosporin + ampicillin

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16
Q

What is the prognosis of a brain abscess?

A

10% mortality, 30% lasting deficits

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17
Q

Most common cause of fatal viral encephalitis

A

HSV viral encephalitis, involving temporal lobe. Presents like bacterial meningitis, but with seizures. Tx with IV acyclovir

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18
Q

Name the most likely etiology: Lumbar puncture shows very high PMNs, low glucose, high protein

A

Bacterial etiology

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19
Q

Name the most likely etiology for CNS infection based on lumbar puncture: high lymphocytes, normal glucose, high protein

A

Viral etiology

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20
Q

Name the most likely etiology for CNS infection based on lumbar puncture: normal to high mixed WBCs, normal glucose, high protein

A

Abscess

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21
Q

Red flags indicating a thunderclap headache

A

Sudden onset, very severe, hits its maximum intensity immediately

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22
Q

Presentation of a headache that doesn’t require imaging

A

Episodic with headache-free days, fulfills migraine criteria, onset <50 years

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23
Q

Serious causes of headache that can still have normal imaging

A

Temporal arteritis, pseudotumor, glaucoma, subarachnoid hemorrhage (if you delay the CT)

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24
Q

Motor unit

A

1 motor neuron and all the muscle fibers that it innervates

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25
Q

Neurotransmitter at the NMJ

A

Acetylcholine

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26
Q

Enzyme important for ACh synthesis

A

ChAT

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27
Q

This phenomenon is produced by the spontaneous release, without stimulation, of a single synaptic vesicle at the NMJ.

A

Miniature endplate potential (mEPP)

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28
Q

About how many quanta of ACh are released by an action potential?

A

200-300

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29
Q

Membrane potential of muscle

A

Around -85 mV

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30
Q

What is an EPP?

A

The sum of many mEPPs, formed when an action potential releases a large number of synaptic vesicles into the NMJ. It depolarizes the motor endplate by 30-50 mV.

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31
Q

Nicotinic ACh receptor channels are permeable to which ions?

A

Sodium and potassium, although the concentration gradient is such that the depolarization due to the EPP is driven by sodium.

32
Q

What contributes to the high safety factor in motor units, and what does that mean?

A

A high safety factor means that every AP in the motor neuron will produce an AP in the associated muscle fibers. This is due to the high number of vesicles released, high density of nAChR at the synapse, and lack of inhibitory motor neurons.

33
Q

How does ACh cause the EPP?

A

2 molecules of ACh bind to the nAChR, leading to a conformational change and opening of the channel pore to Na+ and K+ (although Na+ has a greater driving force, leading to a net excitatory event).

34
Q

How is the signal at the NMJ terminated?

A

ACh is broken down by acetylcholinesterase, which hydrolyzes it once it dissociates from the receptors. It can also diffuse out of the NMJ.

35
Q

Can the motor endplate generate an AP?

A

No - it has no voltage-gated sodium channels

36
Q

How is an AP generated in muscle?

A

Depolarization from the EPP spreads as a local current to adjacent muscle membrane, which can evoke an EP

37
Q

MOA of gallamine

A

Gallamine is a competitive ACh inhibitor. It competitively binds to the nAChR binding site for ACh, with higher affinity, blocking the development of EPPs. This causes paralysis.

38
Q

How is gallamine used clinically?

A

Paralytic drug for use in surgery

39
Q

MOA of succinylcholine

A

Depolarizing blocking agent: occupies nAChR for longer than ACh, causing an initial EPP/AP, but then doesn’t dissociate, leading to Na+ channel inactivation and desensitization of the nAChR

40
Q

How can you reverse the effects of succinylcholine?

A

Acetylcholinesterase

41
Q

How do anticholinesterases cause problems?

A

Anticholinesterases (sarin or nerve gas) block acetylcholinesterase, leading to long-term desensitization and Na+ channel inactivation

42
Q

How are anticholinesterases used medically?

A

To terminate action of competitive inhibitors like gallamine

43
Q

MOA of the AED vigabatrin

A

Irreversibly inhibits GABA transaminase

44
Q

MOA of tiagabine

A

Blocks GABA transport out of the synaptic cleft by inhibiting GAT-1

45
Q

MOA of valproate

A

Increases GABA concentration and decreases Na+ channels

46
Q

MOA of topiramate

A

blocks Na+ channels, increases GABA action, and inhibits kainate receptors

47
Q

MOA of gabapentin

A

Blocks high-voltage-activated calcium channels in pre synaptic terminal

48
Q

MOA of perampanel

A

Non-competitive AMPA receptor antagonist that decreases fast excitatory transmission

49
Q

MOA of phenobarbital

A

blocks AMPA receptors at the upper end of its therapeutic dose

50
Q

MOA of felbamate

A

Blocks NMDA receptors

51
Q

MOA of benzodiazepines

A

Make it easier for GABA-A chloride channels to open

52
Q

Guiding principles for choosing a second AED after the first one fails to control epilepsy

A

Pick one with a different MOA from the first drug

53
Q

MOA of carbamazepine, oxcarbazepine, phenytoin, lamotrigine

A

Prolong inactive state of sodium channels

54
Q

MOA of lacosamide

A

Changes the conformation of sodium channels to speed up inactivation

55
Q

Why choose oxcarbazepine over carbamazepine in terms of side effects?

A

Carbamazepine is metabolized to a stable epoxide by cytochrome p450, and that epoxide is responsible for most of the toxicity (plus tons of drug interactions). Oxcarbazepine doesn’t form an epoxide, and is more soluble.

56
Q

The older benzodiazepine clobazam can’t be paired with cannabidiol - why?

A

Increases a toxic metabolite

57
Q

Which glutamate receptor is implicated in seizure-like discharges?

A

AMPA receptors

58
Q

MOA of levatiracetam

A

Binds to a membrane glycoprotein in synaptic vesicles containing glutamate and prevents/slows release of glutamate

59
Q

What makes a good rational polypharmacy combination with lacosamide?

A

Traditional sodium blockers - the traditional ones prolong the inactive state, and lacosamide changes the speed of inactivation to make it occur sooner.

60
Q

Large muscle fatigue caused by antibodies against Ca++ channels at presynaptic terminals

A

Lambert-Eaton syndrome

61
Q

Fibrous tissue surrounding an entire muscle

A

Epimysium

62
Q

Fibrous tissue surrounding muscle fascicles

A

Perimysium

63
Q

Tissue surrounding individual muscle fibers

A

Endomysium

64
Q

Order the calcium concentrations of the following compartments: extracellular fluid, sarcoplasmic reticulum, myoplasm

A

Sarcoplasmic reticulum > extracellular fluid > myoplasm

65
Q

How many T-tubules are associated with each sarcomere (between its z lines)?

A

2

66
Q

Why can’t a single muscle twitch have maximal force?

A

Calcium removal is always more rapid than the process of troponin saturation, so twitch force is always partial because troponin never becomes fully saturated.

67
Q

Describe the layout of voltage-sensing molecules on the T tubule

A

Dihydropyridine receptors (L-type calcium channels, but function as voltage sensors) are clustered in tetras.

68
Q

Describe the receptors on the SR that allow for calcium release from the SR

A

Ryanodine receptors - calcium release channels. These are positioned pretty much right below dihydropyridine receptors, and then there’s an unpaired one next to it.

69
Q

Describe the mechanical hypothesis of EC coupling

A

Depolarization leads to a conformational change of the dihydropyridine receptor, which pulls open the ryanodine receptors, leading to calcium release

70
Q

Most common genetic myopathy characterized by a dystrophin mutation

A

Duchenne Muscular Dystrophy, more severe than the related form of Becker MD

71
Q

Patient can’t stand up from the ground without using hands - what is this called and what does it signify?

A

Gower’s maneuver - signifies hip girdle weakness

72
Q

Muscle biopsy showing fibers replaced by fatty tissue, with rounded fibers, excess connective tissue, internalized nuclei

A

Duchenne muscular dystrophy

73
Q

Histological features of congenital myopathies

A

Rods, cores, or central nuclei

74
Q

Muscle biopsy showing mononuclear inflammatory cells in a perivascular/perifascicular distribution with perifascicular atrophy

A

Dermatomyositis

75
Q

Muscle biopsy showing T cells invading non-necrotic muscle fibers and inflammatory response around individual muscle fibers

A

Polymyositis

76
Q

Muscle biopsy showing various sizes of muscle fibers, muscle fiber necrosis, not a ton of inflammatory cells

A

Immune-mediated necrotizing myopathy

77
Q

Muscle biopsy showing degeneration of fibers with vacuoles/inclusion bodies

A

Inclusion body myositis

Mind & Motion (7 decks)

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