Neuro Part 3

Front 1

"extra-axial" =

Back 1

outside of brain parenchyma

Front 2

ischemic infarct = _______ on CT

Back 2

DARK on CT

Front 3

neoplasms can invade brain blood vessels and cause:

Back 3

bleeding in the brain

Front 4

pain is considered chronic if it lasts:

Back 4

>3 months

Front 5

nociceptive pain =

Back 5

somatic or visceral response due to tissue injury

somatic is stabbing or aching,

visceral is dull or crampy

Front 6

neuropathic path ~~

Back 6

abnormality of CNS or PNS response

- burning, tingling, electric shock

Front 7

3 types of analgesics:

Back 7

1. opioid

2. non-opioid

3. adjuvant/co-analgesic

Front 8

adjuvant/co-analgesics are used for some other primary effect (like depression) but ALSO provide analgesia; typically used for:

Back 8

cancer, chronic pain

Front 9

benzodiazapams are used for:

Back 9

muscle spasms

Front 10

ladder of analgesia disbursement:

(3)

Back 10

1. use non-opioids for mild pain

2. use WEAK opioid for mod. pain

3. use potent opioid for severe pain

(adjuvants may be given concurrently at each step)

Front 11

acute back pain usually improves in:

Back 11

1-4 weeks, with no intervention necessary

Front 12

chronic back pain before 40 y.o. is:

Back 12

RARE

Front 13

***radiation of pain down buttocks (sciatic pain) suggests:***

Back 13

compression of nerve root by HERNIATED DISC

Front 14

***pain that worsens with rest but improves with activity indicates:***

Back 14

ankylosing spondylitis,

esp when <40 y.o.

Front 15

***low back pain at night, unrelieved by rest or supine position, suggests:***

Back 15

malignancy

Front 16

***bilateral leg weakness or any other neurological problem below the waist suggests:***

Back 16

cauda equina issue

Front 17

+ straight leg test = pain <60 degrees; indicates:

Back 17

nerve root irritation

Front 18

get MRI immediately for suspected:

(2)

Back 18

cauda equina TUMOR or epidural MASS

- but NOT for herniated disc

Front 19

"muscle relaxants" don't really help:

Back 19

back pain

Front 20

_______ and ______ ______________ are INeffective for acute back pain

Back 20

rest and back exercises

are INeffective for acute back pain

Front 21

if neurological deficit is worsening, get ____________, ________________

Back 21

surgery IMMEDIATELY

Front 22

4 traits of chronic back pain:

Back 22

1. subjective complaint of pain with minimal objective findings

2. avoidance of work

3. use of passive instead of active PT

4. tolerance of progressively-higher opioid doses

Front 23

goal of tx with chronic back pain =

Back 23

improve activity lvls,

rather than decrease pain

Front 24

increased pain with increased activity does NOT indicate:

Back 24

worsening chronic back pain

- it will get worse before it gets better

Front 25

3 primary HA's:

Back 25

tension

migraine

cluster

Front 26

tx of tension HA:

(3)

Back 26

1. NSAID

2. sleep

3. stress reduciton

Front 27

**problem with taking analgesics all the time:**

Back 27

analgesic rebound HA

- like caffine - need the drug to NOT get HA's

Front 28

5 features of migraine:

Back 28

1. lasts few hours to days

2. severe throbbing

3. s/ts, n/v

4. trigemino-vascular system is affected

5. improved with sleep

Front 29

treatment of acute migraine:

(4)

Back 29

1. nonspecific
- NSAIDS
- anti-emetics

2. specific
- Triptans
- DHE

Front 30

prophylaxis of migraines:

(4)

Back 30

1. B-blockers

2. Ca2+ chan. blockers

3. tricyclic antidepressants

4. anticonvulsants

Front 31

mechanism of Triptans:

Back 31

as 5-HT r' agonist;

cause CONSTRICTION of cranial blood vessels

Front 32

3 SE's of Triptans:

Back 32

1. temporary but *significant* elevation of BP

2. myocardial ischemia (infarction or angina)

3. stroke

Front 33

Triptans should NEVER be mixed with ______________ or _______________________, due to potential for SER Syndrome

Back 33

MAOI's

or

dihydroergotamine (DHE)

Front 34

DHE mechanism:

Back 34

a-r' antagonist => constricts vessels

- same SE's as Triptans

Front 35

why DHE is rarely used:

Back 35

too many Cat. X drug interactions

Front 36

features of cluster HA's:

(6)

Back 36

1. occur in spring and fall, clusters span weeks to mths

2. last up to 2 hours

3. ALWAYS unilateral

4. ***autonomic symptoms - Horner's, runny nose, teary-eyed - on IPSI side as HA's

5. triggered by ***tiny amounts of alcohol***

6. NOT helped with rest

Front 37

tx of cluster HA's:

(3)

Back 37

1. Triptans

2. Prednisone

3. avoid EtOH

Front 38

**red flags for secondary HA's:**

(6)

Back 38

1. sudden onset

2. worsens

3. systemic illness

4. papilledema

5. triggered by cough, exertion, valsalva

6. worse in the morning

Front 39

3 examples of systemic illness:

Back 39

CA,

HIV,

renal failure

Front 40

some causes of secondary HA's:

(5)

Back 40

1. Dissection

2. Intracranial HTN

3. intracranial hypotension

4. temporal arteritis

5. analgesic rebound HA (from ANY pain med)

Front 41

dissection =

Back 41

lining of artery is torn

=> false lumen within vessel

(think chiropractor)

Front 42

m.c. vessels for dissection =

(2)

Back 42

1. carotid arteries

2. vertebral arteries

Front 43

**sympathetic fibers destined for the eye travel through:**

Back 43

the neck

Front 44

4 features of **intracranial HTN:**

Back 44

1. ~~ **young, obese females**

2. ONLY sign = papilledema

3. NORMAL imaging

4. inc. Pressure on LP

Front 45

2 results of papilledema:

Back 45

enlargement of blind spot,

blindness (eventually)

Front 46

treatment for intracranial HTN:

(2)

Back 46

1. acetazolamide

or

2. shunt

Front 47

intracranial hypotension =

Back 47

HA due to low Pressure from LP

=> resolved by lying down, hydration, caffeine

Front 48

5 features of temporal arteritis:

Back 48

1. HA

2. muscular pain in body, jaw

3. diplopia

4. ~~elderly

5. dx'd by biopsy of temporal artery

Front 49

if untreated, temporal arteritis will cause:

Back 49

blindness

Front 50

treatment for temporal arteritis =

Back 50

prednisone

Front 51

5 features of trigeminal neuralgia:

Back 51

1. ~~elderly

2. MOST SEVERE PAIN EVER

3. in V2/V3 fields

4. abrupt onset

5. UNILATERAL

Front 52

treatment of trigeminal neuralgia:

(2)

Back 52

1. anticonvulsants

2. surgery if 1. is refractory

Front 53

nonselective COX inhibitors:

(6)

Back 53

1. aspirin

2. ibuprofen

3. Naproxen

4. Diclofenac

5. Indomethacin

6. Ketorolac

Front 54

COX is the enzyme that catalyzes:

Back 54

the first step in TX/PG synthesis

- COX-2 is induced by inflammation

Front 55

***a COX-2-selective inhibitor: ***

Back 55

Celecoxib

Front 56

COX-1 => TXA2 => (functions)

(3)

Back 56

1. protection of gastric mucosa

2. creation of clots

3. constriction

Front 57

PG's are released at sites of inflammation, =>

(3 functions)

Back 57

1. sensitize nerves

2. promote inflammation

3. inc. fever

Front 58

***a COX-3-selective inhibitor:***

Back 58

Acetaminophen

Front 59

function of ALL NSAIDS:

(2)

Back 59

1. relieve fever by inhibiting PG synthesis in the hypothalamus

2. analgesics, by inhibiting PG synthesis in the tissue

Front 60

NSAID's use competitive inhibition, except for:

Back 60

ASPIRIN,

which IRREVERSIBLY binds COX

Front 61

NSAID SE's

(5)

Back 61

1. GI irritation

2. inc. risk of bleeding (ESP aspirin)

3. hepatic toxicity

4. teratogenicity

5. renal toxicity

Front 62

2 NSAID SE's that acetaminophen DOESN'T have, and one that it ESP has:

Back 62

1. teratogenicity, 2. renal toxicity

vs.

hepatotoxicity

Front 63

NSAID's + corticosteroids =>

Back 63

inc. risk of GI complications

Front 64

***aspirin should be avoided in:***

Back 64

CHILDREN,

due to risk of Reye syndrome

Front 65

4 symptoms of aspirin OD:

Back 65

1. fever

2. dehydration

3. hyperventilaiton

4. mixed resp. alkalosis-metabolic acidosis

Front 66

3 features of Acetaminophen:

Back 66

1. safe for children

2. ***lacks significant anti-platelet, anti-inflammatory activity***

3. anti-pyric, analgesic

Front 67

treatment for Aceta OD =

Back 67

acetylcysteine

Front 68

Indomethacin:

(3)

Back 68

1. most potent NSAID

2. tendency for adverse affects => reserved for *severe* inflammatory conditions

3. used for PDA too

Front 69

Celecoxiib => anti-inflammation WITHOUT:

Back 69

GI problems

(since it's COX-2 specific)

**but poses CV toxicity**

Front 70

what's the 1 partial opioid agonist?

Back 70

Buprenorphine

- high affinity, low efficacy

Front 71

what's the 1 mixed opioid agonist-antagonist?

Back 71

Nalbuphine

**limited use for analgesia, but t.o.c. for opioid-induced pruritis**

Front 72

what are the 2 opioid antagonists?

Back 72

1. Naloxone

2. Naltrexone

Front 73

SE's of opioid agonists:

(2)

Back 73

1. n/v

2. decreased respiration

3. many others

Front 74

classic withdrawal symptoms of opiates =

(6)

Back 74

1. anxiety

2. insomnia

3. sweating

4. fever

5. runny nose

6. GI issues

Front 75

ALL opioids =>

Back 75

tolerance/dependence

- NOT signs of addiction - ALL pts experience this

Front 76

interactions of opioids with MAOI's and tricyclics =>

Back 76

increased depressant effects

Front 77

interactions of opioids with alcohol, benzo's =>

Back 77

greater respiratory depression

Front 78

which opioid agonist is 100x stronger than Morphine?

Back 78

Fentanyl

Front 79

which is the opioid of choice for gall-bladder pain?

Back 79

Meperidine

Front 80

Codeine is used for:

Back 80

weak pain

Front 81

differences between Naloxone and Naltrexone:

Back 81

1. Naloxone acts in minutes, Naltrexone in hours

2. Naloxone is tx for **opioid OD**, Naltrexone for alcoholism

Front 82

Babinski sign is ______________ in adults

Back 82

ABNORMAL

- Big toe extends, other toes fan out

Front 83

risk factors for subDural hematoma:

(3 A's)

Back 83

age, anticoagulants, alcohol

Front 84

vegetative state = absence of responsiveness and awareness, but diencephalon and BS are spared to preserve reflexes and **sleep-wake cycles**

Back 84

=> eye movements without actual awareness

Front 85

coma ~~ NO:

Back 85

sleep-wake cycles

- continually off

Front 86

minimally conscious state ~~

Back 86

SOME awareness

Front 87

***weakness of face on SAME side as weakness of body signifies:***

Back 87

***lesions ABOVE BS***

(don't count the BS as a site of lesion when body is involved, unless cerebral peduncles are affected)

Front 88

midbrain lesion and CN's - think:

Back 88

CN 3 / pupillary reflex affected

Front 89

**in the SC, the CS tract is ______________, the ST is _________________, and the DCML is ______________

Back 89

CS is lateral;

ST is anterior;

DCML is Medial

Front 90

but in the BS, the CS and DCML are:

Back 90

Medial,

and the ST is Lateral

Front 91

***is the eye you're shining into doesn't constrict, the problem is with:***

Back 91

CN 2

- if the *opposite* eye doesn't constrict, it's a problem with CN 3 on the first side (check videos, diagram)

Front 92

gag reflex:

Back 92

9 = afferent,

10 = efferent

at MEDULLA

Front 93

baroreceptors in aorta and carotids, to lower BP:

Back 93

9 or 10 = afferent,

10 = efferent

Front 94

CN 11 palsy =>

(2)

Back 94

inability to shrug shoulders,

head turned AWAY from side of lesion (unopposed action of the other SCM)

Front 95

corneal reflex: afferent =

Back 95

CN 5;

efferent = CN 7

at PONS

Front 96

CN 12: muscle pushes tongue OUT on each side, so lesion on one side =>

Back 96

tongue pointing to that lesioned side

Front 97

ALL sensory afferents enter the SC's:

Back 97

dorsal horn