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Clinical Neuroscience > Path- 5: Trauma > Flashcards

Path- 5: Trauma Flashcards

1
Q

Where does the blood accumulate in an epidural hematoma?

A

between the calvaria and the dura

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2
Q

What causes epidural hematomas?

A

blow to the side of the head

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3
Q

What vessel is ruptured in an epidural hematoma?

A

MMA

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4
Q

What is the pathogenesis to epidural hematomas?

A

Aympomatic for first 4-8hrs –> when volume gets to be 30-50mL they have Sx that resemble space occupying lesion –> ICP becomes more than cerebral venous pressure –> ischemia –> cortical impairment

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5
Q

What is the Cushing reflex?

A

protective response to increase CBF and oxygenation. HR decreases, ionotopy increases, BP increases

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6
Q

When volume increases to 60mL, what happens in the epidural hematoma?

A

brain is shifted laterally away from the side of hematoma, transtentorial herniation, III compression, dmg to reticular formation

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7
Q

What happens if epidurals are untreated with 4-48 hrs?

A

necrosis of the brainstem –> irreversible dmg –> death or coma

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8
Q

Why do you pass out when u get it in the head when boxing?

A

hit the reticular formation

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9
Q

Rupture of what vessels cause subdural hematomas?

A

bridging veins

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10
Q

Causes of subdural hematomas?

A

falls, assaults, accidents, kinky role-playing high-velocity activites because your gf’s mom is gone grocery shopping for 10 minutes.

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11
Q

What is the pathogenesis to subdural hematomas?

A

brain impacts skull –> shearing of veins in subdural space –> bleeding into subdural space –> stops bleeding at 25-50mL due to local tamponade effect

“When life gives you tampons… you make tamponade.”

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12
Q

What is the pathology if subdural hematomas are left untreated?

A

After several weeks, granulation tissue appears, which creates a membrane above hematoma by using fibroblasts

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13
Q

What are the 3 routes of evolution for static subdural hematomas?

A
  1. may be rabsorbed (good!)
  2. remain static with potential for calcification (eh…)
  3. hemorrhage may enlarge and re-bleeding within 6 mo. (no bueno)
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14
Q

What are the Sx of subdural hematomas?

A

headaches, CL weakness, szrs, cognitive dysfxn

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15
Q

What happens in subarachnoid hemorrhageS?

A

bleeding into the subarachnoid space

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16
Q

What causes subarachnoid hemorrhages?

A

rupture of pre-existing arterial aneurysm (mainly)

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17
Q

What is a super good procedure to treat aneurysms before they burst into subarachnoid hemorrhages?

A

coiling

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18
Q

What causes cerebral contusions?

A

usually AP displacement of the brain (kinda like subdurals), lesions at point of impact (coup injury), or lesion on opposite side of impact (counter coup)

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19
Q

What is the immediate life threat in penetrating wounds to the brain?

A

Hemorrhage

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20
Q

Describe the characteristics of high velocity penetrating wounds to the head

A

causes centrifugal blast (cylinder disruption), immediate death (explosive increase in ICP –> cerebellar tonsil herniation), boom

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21
Q

What is a big threat in a healed penetrating wound 6-12 mo after the trauma?

A

Seizures

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22
Q

What happens in hyperextension injuries?

A

forehead struck from front and driven posteriorly, tears ALL, cord damaged by posterior bony process

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23
Q

What happens in hyperflexion injuries?

A

head or shoulders hit from behind –> sharp angulation of the spinal cord

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24
Q

What happens in concussions?

A

Mild injury, transient and reversible of spinal cord fxn

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25
Q

What happens in contusions?

A

trauma randes from minor bruise –> hemorrhage

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26
Q

What are myelomalacias?

A

Spinal cord necrosis and edema caused by contusions

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27
Q

What are hematomyelia?

A

hematomas within the cord fromc ontusions

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28
Q

What are AVM’s?

A

arteriovenous malformations, unknown cause

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29
Q

What is the main clinical significance of AVMs?

A

szrs, intracranial/subarachnoid hemorrhages with stroke-like Sx

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30
Q

Where are AVM’s typically seen?

A

cerebral Cx

31
Q

True or false: AVM’s do not grow over time, they stay stagnant and keep out from growing into the white matter.

A

FALSE

32
Q

What are cavernous angiomas?

A

large, irregular, thin-walled vascular channels that contain many open spaces

33
Q

What are the Sx of cavernous angiomas?

A

typically asymptomatic but can cause intracranial bleeding, szrs, or focal neuro disturbances

34
Q

What are telangiectasias?

A

focal aggregates of small vessels

35
Q

Sx of telangectasias?

A

may cause szrs and rarely rupture

36
Q

What are venous angiomas?

A

focus of few enlarged veins, distributed randomly in the spinal cord and brain, usually asymptomatic and overlaps with cavernous angiomas

37
Q

Why do cerebral aneurysms burst?

A

Increase in vascular pressure and a weakened arterial wall

38
Q

What are berry aneurysms?

A

arterial defects during embryogenesis when arteries bifurcate

39
Q

Where are 90% of sacular aneurysms?

A

Branch pooints in the carotid system

40
Q

What happens if Berry aneurysms burst?

A

life-threatening SAH (subarachnoid hem.)

41
Q

Where are most Atherosclerotic aneurysms?

A

in major cerebral arteries (vertebral, basilar, internal carotid)

42
Q

What is the cause of Atherosclerotic aneurysms?

A

fibrous replacement of media, destruction of internal elastic membrane

43
Q

What is the major complication to Atherosclerotic aneurysms?

A

Thrombosis (typically to MCA). These rarely rupture

44
Q

What are fusiform aneurysms?

A

an outpouching of the wall on both sides of the artery and doenst have a stem.

45
Q

Hypertension causes bleeds into what brain structure?

A

Basal ganglia

46
Q

What are Charcot-Bouchard aneurysms?

A

theyre aneurysms of the brain vasculature which occur in SMALL blood vessels (berry happen in large). often in brainstem, assocaited with chronic HTN.

47
Q

Where are mycotic aneurysms?

A

They’re infections of the arterial wall –> septic emboli or cerebral abscesses/meningitis

48
Q

True or false: traumatic aneurysms are rarely cause dissecting aneurysms

A

true

49
Q

Where do > 65% of strokes from HTN occur?

A

Basal ganglia & thalamus

50
Q

When lipids and hyaline material are deposited in the arterial walls to cause strokes, what is that called?

A

lipohyalinosis

51
Q

What are the clinical features of progressive hemorrhages in strokes?

A

death within hrs –> days, transtentorial herniation and/or rupture into ventricle with massive hemorrhage –> distention of 4th –> compression of vital centers

52
Q

Premature infants (22-30 wks) have an increase of which type of hemorrhage soon after birth?

A

Intraventricular hemorrhage

53
Q

What are global ischemias?

A

patterns of injuries that are consistent with the anatomy of the cerebral vascualture.

54
Q

What are watershed infarcts?

A

ACA, MCA and PCA have overlapping territories –> not perfused well –> infarcts in these “watershed” areas

55
Q

What happens in laminar necrosis?

A

necrosis of the superficial layers of the cerebral Cx, typically focal, happens after temporary cardiuac arrest

56
Q

What are the 2 types of neurons that are selectively sensitive?

A
  1. purkinje cells of the cerebellum

2. pyramidal neurons of the Sommer sector I hippocampus

57
Q

Why are these 2 types of neurons called selectively sensitive?

A

cuz theyre very sensitive areas to ischemia induced hypoxia, and can easily develop localized necrosis

58
Q

Why can atherosclerosis cause regional ischemia and cerebral infarction?

A

Occlusion ir embolization can be hemorrhagic

59
Q

How do u treat atheroslerotic emboli so it doesnt cause hemorrhagic infarcts?

A

Anticoagulants (t-PA!)

60
Q

Infarcts initiated via thrombosis are show what on cross-section?

A

bland areas in the area of infarct

61
Q

Infarct cause the affected tissue to transform into what?

A

Friable (crumbly) tissue

62
Q

What causes the friable tissue from infarcts?

A

macrophages, cysts, liquefactive necrosis

63
Q

What happens whent he proximal and MCA get occuluded by atheroscleosis and thrombosis? What structure is effed?

A

internal capsule (CL hemiparesis)

64
Q

What are TIA’s?

A

focal cerebreal dysfxn that lsts less than 24 hrs, signifies a risk for infarcts

65
Q

What are strokes in evolution?

A

Progression of neurological Sx while pt is under observation, shows the PROPOGATION of a thrombus in the carotid or basilar a.

66
Q

What are complete strokes?

A

stable neurological defects resulting from cerebral infarcts

67
Q

What happens if large extracranial and intracranial arteries are occluded dur to atherosclerosis?

A

depends on where, but u can imagine the Sx when u knock out the ICA, MCA or ACA. yer effed.

68
Q

The deficits surrounding an occlusion to the circle of willis depend on what?

A

collateral circulation

69
Q

What typically damages parencymal arteries/arterioles?

A

HTN

70
Q

What happens in small lacunal infarcts?

A

occlusion of 1 of the penetrating arteries that provides blood to the deep brain structures gets damaged –> yer effed.

71
Q

What happens if there are multiple parencymal arterial occlusions?

A

multiple infarcts, dementia

72
Q

What causes occlusions in capillary beds?

A

small emboli like fat or air –> petechiae

73
Q

Venous sinus thrombosis is potentially lethal for which 4 conditions?

A
  1. systemic dehydration
  2. phlebitis
  3. obstruction by neoplasm
  4. sickle cell

Clinical Neuroscience (12 decks)

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