Neuro Part 5

Front 1

MAC =

(2)

Back 1

1. concentration of an inhaled anth that prevents movements in 50% of pts

2. ED50 of anesthetics

Front 2

***relationship of MAC to potency:***

Back 2

INVERSELY proportional

- higher MAC = lower potency

Front 3

**more soluble in the blood = slower to:*

Back 3

get to the brain**

=> conversely, ***insoluble = faster-acting***

(blood/fat coefficient is important for getting from blood to brain)

Front 4

***LIPID solubility affects speed of onset, offset;***

Back 4

low lipid solubility = rapid onset, rapid offset


- High lipid solubility = gradual

Front 5

***lipid solubility is DIRECTLY proportional to:***

Back 5

potency

Front 6

the longer an anesthetic is in the body, the more likely:

Back 6

it will get deposited in body fat

=> slower offset

Front 7

**ALL inhaled anesthetics are:**

Back 7

respiratory depressants

Front 8

4 inhaled anesthetics:

Back 8

1. Insoflurane

2. Sevoflurane

3. Desflurane

4. NO

Front 9

3 features of N2O:

Back 9

1. ONLY non-volatile inhaled anesthetic

2. ONLY one with analgesic properties

3. extremely low potency => never used alone

Front 10

anesthesia is NOT:

Back 10

analgesia

Front 11

***Malignant Hyperthermia = ***

Back 11

rare, genetic hypermetabolic disorder in which Ca2+ is wrongly metabolised

Front 12

MH is triggered by:

(2)

Back 12

1. all VOLATILE inhaled anesthetics

2. succinylcholine

***REQUIRES genetic defect***

Front 13

symptoms of MH:

(6)

Back 13

1. muscular rigidity (particularly in the jaw)

2. tachycardia/other arrhythmias

3. tachypnea

4. acidosis

5. shock

6. hyperthermia (usually ≥ 40° C)

Front 14

***treatment of MH:***

(2)

Back 14

1. rapid cooling and aggressive supportive measures
(highest priority)

2. Dantrolene

Front 15

***mechanism of Dantrolene:***

Back 15

muscle relaxant -

abolishes excitation-contraction coupling in muscle cells, *AT the sarcoplasmic reticulum*

(used for both MH and NMS)

Front 16

pharmacokinetics =

Back 16

effects of the body on a drug

Front 17

4 IV anesthetics:

Back 17

1. Propofol

2. Etomidate

3. Thiopental

4. Ketamine

Front 18

IV anesthetics mechanism: ALL enhance ______________, except for ____________, which _________________________________________

Back 18

ALL enhance GABA

except for Ketamine, which inhibits excitation.

Front 19

***3 features of Ketamine:***

Back 19

1. hypnotic

2. ***ONLY one that doesn't make you stop breathing***

3. GREAT analgesic

Front 20

***2 main features of Propofol:***

Back 20

1. extremely RAPID onset AND offset

2. **NO risk of MH - use if suspected**

Front 21

***main feature of Etomidate:***

Back 21

***NO effect on CV***

=> use in ELDERLY

Front 22

***main feature of Thiopental:***

Back 22

= barbituate

- addictive

Front 23

***mechanism of local anesthetics:***

Back 23

block Na+ channels

- no influx = no depol

Front 24

**ALL local anesthetics are ________ ________**

Back 24

WEAK bases

- pKa's range from 7.4 to 9.0

Front 25

significance of local anesthetics being bases:

Back 25

***only NON-ionic forms can cross** to be effective

=>=> ***IV anesthetics do NOT work in acidic environments like abscesses***

Front 26

***pKa determines:***

Back 26

***onset of action***

- closer to 7.4 will have a greater % of nonionic form

=> FASTER onset

Front 27

**2 exceptions to pKa closer to 7.4 resulting in faster onset:**

Back 27

1. procaine

2. chlorocaine

- high pKa but VERY rapid onset

Front 28

2 classes of local anesthetics:

Back 28

esters and amides

- esters show allergic rxn to PABA

Front 29

3 ESTER local anesthetics:

Back 29

1. Procaine

2. Benzocaine

3. Tetracaine

Front 30

3 AMIDE local anesthetics:

Back 30

1. Lidocaine

2. Bupivocaine

3. Ropivacaine

Front 31

***2 adjuvants for local anesthetics:***

Back 31

1. Na Bicarb

2. EPI

Front 32

**why NaBicarb is used as an adjuvant:**

(2)

Back 32

1. alkalizes the anesthetic soln => inc. % of nonionic local anesthtic => inc. speed of onset

2. may also dec. pain of injection

Front 33

***why EPI is a great adjuvant:***

(2)

Back 33

1. allows you to tell that you've hit an artery instead of the tissue (via inc. HR, BP)

2. vasoconstriction => dec. systemic uptake of anesthetic => dec. risk of toxicity, inc. duration of anesthetic

Front 34

NMB's = muscle relaxants =

Back 34

**IV** drugs


- interrupt AP's at the NMJ

Front 35

how do NMB's work?

Back 35

***bind Nicotinic receptors***

at the NMJ, block ACH

=> no depol

Front 36

***3 main indications for NMB's:***

Back 36

1. intubation

2. surgery

3. mechanical ventilation

Front 37

**NMB's have NO intrinsic:**

(2)

Back 37

anesthetic OR sedative effects

- ONLY paralysis

Front 38

2 classes of NMB:

Back 38

1. depolarizing

2. non-depolarizing

Front 39

the only depolarizing NMB =

Back 39

succinylcholine

Front 40

mechanism of succinylcholine:

Back 40

acts at Nicotinic r's to produce an *initial depol*

=> results in inactivated channels that can't get activated until the drug is degraded

Front 41

***2 features of succinylcholine:***

Back 41

1. metabolized by *plasma pseudocholinesterases*

2. RAPID onset, SHORT duration => PERFECT for intubation

Front 42

***mechanism of non-depolarizing NMB's:***

Back 42

COMPETITIVE antagonists of ACH
for ACH r's

Front 43

goal of NMB use is to see:

Back 43

1-3 twitches

(4 twitches = not paralyzed enough, 0 = too much)

Front 44

action of NMB's is reversed by:

Back 44

adding ACH or cholinesterase inhibitors

Front 45

Halothane = inhaled anesthetic that causes:

(2)

Back 45

arrythmias, hepatitis

Front 46

Neostigmine =

Back 46

peripheral ACHE *inhibitor*

=> more ACH at NMJ's

- used to REVERSE NMB's
- always given with glycopyrrolate to avoid SE's

Front 47

***2 UNRELIABLE signs of NMB reversal:***

Back 47

1. TV

2. twitches

- DON'T accept these as signs of NMB reversal

Front 48

MG =

Back 48

AI loss of ACH r's

=> need to inc. ACH to be able to move normally

Front 49

MG is diagnosed with:

Back 49

Edrophonium

(short-acting ACHE inhibitor)

Front 50

arachnoid villi ~~

Back 50

one-way flow into venous sinuses/blood

Front 51

**indications for LP:**

(6)

Back 51

1. meningitis

2. subarachnoid hemorrhage

3. (rarely) MS

4. GB syndrome

5. carcinomatous meningitis (not inf)

6. therapeutic relief, dx of IC HTN

Front 52

contraindications of LP:

(3)

Back 52

1. infected skin over puncture wound

2. severe coagulopathy

3. risk of herniation

Front 53

***features of nl CSF:***

(5)

Back 53

1. clear like water

2. <20 opening Pressure

3. glucose should be >50

4. protein should be <50

5. NO cells
(maybe couple lymphocytes)

Front 54

CSF after subarachnoid hemorrhage:

(3)

Back 54

1. bloody OR xanthochromic

2. inc. RBC's

3. inc. protein

Front 55

CSF in bacterial (septic) meningitis:

(5)

Back 55

1. elevated opening P

2. dec. CSF glucose

3. inc. protein

4. inc. PMN's, pus

5. positive culture, +/- gram stain

Front 56

CSF in viral (aseptic) meningitis:

(1)

Back 56

1. inc. lymphocytes

otherwise nl

Front 57

CSF in fungal meningitis:

(2)

Back 57

1. inc. lymphocytes

2. dec. glucose

Front 58

CSF in MS:

Back 58

**oligoclonal bands**

Front 59

CSF in GB Syndrome:

(1)

Back 59

1. inc. prot

otherwise nl

Front 60

CSF in IC HTN:

(1)

Back 60

elevated opening Pressute

Front 61

CSF in carcinomatous meningitis
(meningitis caused by cancer cell infiltration of subarachnoid space)

(2)

Back 61

1. elevated prot.

2. + cytology

Front 62

CSF in TB meningitis:

(3)

Back 62

1. elevated opening pressure

2. dec. glucose

3. + AFB stain

Front 63

elevated opening Pressure will be seen with:

(3)

Back 63

bacterial, fungal, or TB meningitis

Front 64

empyema =

Back 64

purulent collection in body cavity, usually bacterial

Front 65

encephalitis =

Back 65

inf. of brain parenchyma, usually of viral etiology

(cerebritis = same, but of bact. or fungal etiology)

Front 66

gliosis =

Back 66

prolif/hypertrophy of glial cells, in response to CNS damage

Front 67

Kernig sign =

Back 67

knee pain with hip flexion

Front 68

Brudzinski sign:

Back 68

flexing the neck causes the knee/hip to flex

Front 69

neurosyphillis is caused by:

Back 69

Treponema pallidum

(spirochete bact.)

Front 70

neurosyphillis will result in __________________________________________, _______ ______________ if untreated

Back 70

1. syphilitic obliterative endarteritis
(multiple small infarcts)

2. tabe dorsalis
(loss of pos/vib due to SC involvement)

Front 71

+ Romberg sign indicates:

Back 71

severe DCML lesion

Front 72

3 features of Cryotococcus:

Back 72

1. m.c. cause of fungal meningitis

2. opportunistic inf. typically seen only in imm-comp

3. primary reservoir of spores = birds

Front 73

soap-bubble abscess ~~

Back 73

parenchymal Cryptococcal inf.

= microabscesses surrounded by fungal capsule

(granulomatous inflam if neoformans)

Front 74

poliomyelitis =

Back 74

inflammation of GRAY matter of SC

Front 75

histo fo HSV inf:

Back 75

Cowdry A bodies

*intranuclear* eosinophilic inclusions surrounded by a *halo*

Front 76

herpes encephalitis =

Back 76

fulminant infection of CNS by HSV1

- localizes to *Temporal* lobes

(HSV2 ~~ genital herpes)

Front 77

primary CNS lymphomas are typically caused by:

Back 77

EBV **in imm-comp**

Front 78

HIV encephalopathy =>

Back 78

mild dementia to bradykinesia to severe cognitive impairment

Front 79

features of Toxoplasmosis:

(3)

Back 79

1. CNS infection of Toxoplasma spp. (protozoan)

2. m.c. mass lesion in AIDS patients

3. ~~ONLY severely imm-comp

Front 80

features of neurocysticercosis:

(4)

Back 80

1. CNS infection by Taenia solium (the pig tapeworm)

2. parasitic cysts to grow in brain parenchyma

3. c.c. of epilepsy and intracranial mass lesions worldwide

4. treatment can lead to massive cerebral edema due to robust immune response

Front 81

Spongiform Encephalopathy =

Back 81

degenerative dz caused by prion prots, PrP(B)

(everyone has prion proteins in the brain, in alpha config.)

Front 82

PrP(B) is UNdegradable, =>

Back 82

will accumulate in neurons

=> damage to neurons, glial cells

=> ***intracellular vacuoles***

Front 83

3 general reasons why PrP(a) converts to PrP(B):

Back 83

1. sporadic

2. inherited

3. transmissible

Front 84

m.c. form of Spongiform Encephalopathy =

Back 84

CJD

Front 85

features of CJD:

(4)

Back 85

1. usually sporadic

2. presents as rapidly-progressing dementia, associated with ataxia and startle myoclonus

3. => vacuoles

4. ~~elderly

Front 86

2 other kinds of spongiform encephalopathy:

Back 86

1. variable CJD
(young, eating infected beef)

2. familial fatal insomnia

Front 87

iatrogenic =

Back 87

caused by medical treatment

Front 88

Rabies ~~

Back 88

destruction of BS

=> difficulty swallowing, Negro bodies