05a: Muscle relaxants

Question 1

Cisatracurium is in (X) class of drugs and works by which MOA?

Answer 1

X = non-depolarizing (competitive) neuromuscular blocker

Competitive inhibition of ACh binding to nicotinic receptor

Question 2

Cisatracurium has (slow/quick) onset of action and (can/cannot) cross BBB.

Answer 2

Quick (2-8 min)

Cannot (quat amine)

Question 3

Cisatracurium effect can be antagonized by

Answer 3

ACEi (due to increased ACh overcoming competitive inhibition)

Question 4

Succinycholine is in (X) class of drugs and works by which MOA?

Answer 4

X = depolarizing (non-competitive) neuromuscular blocker

Binds to nicotinic ACh receptor and evokes receptor desensitization and channel inactivation

Question 5

Succinycholine stages of block

Answer 5

1. Fasciculation
2. Phase I block (depolarizing)
3. Phase II block (desensitizing)

Question 6

T/F: Muscle is depolarized in all stages of block by succinylcholine.

Answer 6

False - repolarizes in Phase II (but ACh receptors still not responsive)

Question 7

(Succinylcholine/Cisatracurium) degraded by plasma esterases.

Answer 7

Both

Question 8

Succinylcholine has (slow/quick) onset of action.

Answer 8

Quick (1 min!)

Question 9

Malignant hyperthermia is a dangerous side effect of (X) neuromuscular blocking agent. What’s the antidote?

Answer 9

X = succinylcholine

Dantrolene (Ryanodine-R antagonist)

Question 10

Malignant hyperthermia in patients with hereditary deficiency in (X). What’s the mechanism of this Sx?

Answer 10

X = plasma cholinesterase

High succinylcholine causes excess Ca2+ release in muscle, causing ATP use to increase as muscle attempts to reabsorb Ca2+ (this generates heat)

Question 11

Brain abscess (bacterial): what are the layers (from inside to out)?

Answer 11

1. Purulent/pus-filled center (degenerating PMNs and bac)
2. Neovascularization around central necrotic zone
3. Dense fibrous capsule
4. Reactive astrocytosis around capsule

Question 12

T/F: Zika can be spread via sex.

Answer 12

True - also mosquitos, vertically, and blood transfusion

Question 13

Which autoimmune disease is strongly associated with Zika?

Answer 13

Guillain-Barré (but only small portion of people with Zika get it)

Question 14

Which category of CNS infections associated with formation of microglial nodules and neuronophagia?

Answer 14

Viral Meningoencephalitis

Question 15

Which category of CNS infections likely associated with perivascular lymphocytes?

Answer 15

Viral Meningoencephalitis

Question 16

A characteristic feature of HSV meningoencephalitis is involvement of (X) parts of brain

Answer 16

X = inferior and medial temporal lobes; lower frontal lobes

Question 17

Which CNS infection associated with Cowdry type A eosinophilic intra-(cytoplasmic/nuclear) inclusions?

Answer 17

Intranuclear;

HSV-1 meningoencephalitis

Question 18

Which CNS infection associated with Negri bodies, intra-(cytoplasmic/nuclear) inclusions?

Answer 18

Intracytoplasmic;

Rabies

Question 19

Which CNS infection (in immunocompromised) associated with patchy demyelination/gliosis, microglial nodules, and multinucleated Giant cells.

Answer 19

HIV-1 meningoencephalitis

Question 20

T/F: Fungal Meningoencephalitis almost always originates from CNS tissue.

Answer 20

False - almost always spread from primary focus elsewhere in body

Question 21

(X) meningoencephalitis: Multiple intraparenchymal microabscesses stained purple in whole mount section.

Answer 21

X = candida

Question 22

(X) meningoencephalitis: hemorrhagic infarct, secondary to (Y).

Answer 22

X = aspergillus or mucor
Y = angioinvasion (invades artery)

Question 23

Aside from causing brain infarcts, (X) fungal species may cause multiple (Y)

Answer 23

X = aspergillus or mucor
Y = hemorrhagic abscesses

Question 24

(X) meningoencephalitis: cribiform appearance (“bubbles”) from infectious agent’s proliferation in perivascular space

Answer 24

X = cryptococcal

Question 25

T/F: Crytpo is most common opportunistic fungal CNS | infections in AIDS

Answer 25

True

Question 26

Your pt with AIDs has fungal meningoencephalitis. The capsule of (X) fungus may be easily seen with (Y) stain

Answer 26

``` X = Cryptococcus Y = mucicarmine ```

Question 27

T/F: Prions have no nucleic acid component

Answer 27

True - composed solely of protein

Question 28

T/F: PrP(SC) and PrP(C) are encoded by the same gene and are therefore identical in sequence.

Answer 28

True - differ due to post-translational modifications

Question 29

PrP(C) is protease (sensitive/resistant) and found where in/on cells?

Answer 29

Sensitive (normal protein); | On cell surface

Question 30

PrP(SC) is protease (sensitive/resistant) and found where in/on cells?

Answer 30

Resistant; | In intracellular vesicles and is secreted

Question 31

Incubation period for Prion diseases can be as long as (X).

Answer 31

X = 30 y

Question 32

T/F: There is no immune response in prion diseases.

Answer 32

True

Question 33

List procedures that can inactivate prions

Answer 33

1. Autoclave (for hours) 2. NaOH 3. Hypochlorite

Question 34

Killed (inactivated) Rabies virus vaccine prepared by chemical inactivation of rabies-infected (X) cells.

Answer 34

X = human diploid HDCV (human diploid cell vaccine)

Question 35

T/F: Previously vaccinated patient was bitten by animal with rabies. There's no need to give the rabies Ig (only the vaccine).

Answer 35

True

Question 36

Prion diseases: post-morten brain shows (X) in (cortex/cerebellum) (with/without) inflammation.

Answer 36

X = large vacuoles Both Without

Question 37

Prion disease clinical Sx:

Answer 37

loss of muscle control & coordination, | tremors, progressive dementia

Question 38

Prion appearance on EM:

Answer 38

filamentous rods

Question 39

PrP(SC) has more (alpha helices/beta sheets) than PrP(C).

Answer 39

Beta sheets

Question 40

T/F: Prion disease can be inherited.

Answer 40

True

Question 41

(X) Prion disease generally found in patients over 50 with clinical Sx initially similar to psych disorders. Progress to dementia and which other Sx?

Answer 41

X = Creuztfeldt-Jakob (CJD) Change in gait, involuntary movement, seizure

Question 42

Unlike CJD, nvCJD seen in (X) patients and transmitted by (Y).

Answer 42

``` X = younger Y = eating infected beef (similar to BSE, bovine spongiform encephalopathy) ```

Question 43

How do you assess CN II in comatose patient?

Answer 43

Pupillary reflex (CN II, III)

Question 44

Disrupted pupillary reflex can be either due to brainstem lesion, (X) herniation, and/or lateral shift of (Y).

Answer 44

``` X = uncal Y = supratentorial compartment (with stretching of CN III against clivus) ```

Question 45

Disrupted pupillary reflex can be either due to brainstem lesion, (X) herniation, and/or lateral shift of (Y).

Answer 45

``` X = uncal Y = supratentorial compartment (with stretching of CN III against clivus) ```

Question 46

Pupils in mid-position and fixed. Where do you suspect lesion to be?

Answer 46

Midbrain

Question 47

Pupils are small and reactive. Where do you suspect lesion to be?

Answer 47

Diencephalon

Question 48

How do you assess CN V in comatose patient?

Answer 48

Corneal reflex (V, VII)

Question 49

How do you assess CN V in comatose patient?

Answer 49

Corneal reflex (V, VII)

Question 50

(X) causes of comas represent 65% of etiologies, so they need to be ruled out, even while pursuing others.

Answer 50

X = Toxic/metabolic