Cerebrovascular Pathology Flashcards
(162 cards)
1
Q
Hemorrhage between dura and skull
A
Epidural hematoma
2
Q
Epidural hematoma most often involves this artery
A
Middle meningeal artery
3
Q
Does Epidural hematoma require skull fracture?
A
Usually
4
Q
This type of hematoma appears lens-shape
A
Epidural hematoma
5
Q
Does Epidural hematoma involve arterial or venous pressure?
A
Arterial
6
Q
This hematoma forms biconcave (lentiform) hemorrhage
A
Epidural hematoma
7
Q
Does Epidural hematoma cross suture lines?
A
No
8
Q
Type of hematoma that occurs from trauma with loss of consciousness (concussion), lucid interval of couple hours or less, than rapid decompensation
A
Epidural hematoma
9
Q
Epidural hematoma usually occurs with skull fracture, and favors these two bones
A
Temporal and parietal
10
Q
Collection of hemorrhage between dura and meninges
A
Subdural hematoma
11
Q
Does Subdural hematoma involve arterial or venous pressure?
A
Venous
12
Q
This type of hematoma occurs in situations in which the brain moves relative to skull
A
Subdural hematoma
13
Q
Subdural hematoma is usually a rupture of this type of vessel
A
Bridging veins
14
Q
Type of hematoma that occurs from trauma and sheering of bridging veins
A
Subdural hematoma
15
Q
Type of hematoma that results in relatively low pressure venous bleeding
A
Subdural hematoma
16
Q
In a Subdural hematoma, does blood enter sulci?
A
No
17
Q
In a Subdural hematoma, does blood cross suture lines?
A
Yes - it can
18
Q
This type is a crescent shaped hematoma
A
Subdural hematoma
19
Q
Category of Subdural hematoma that is a rapid accumulation of blood due to high impact trauma
A
Acute Subdural hematoma
20
Q
With a Subdural hematoma, symptoms occur immediately within this many days
A
3
21
Q
Category of Subdural hematoma that may occur with mild or without any trauma
A
Chronic
22
Q
This type of hematoma may occur without trauma and typically in elderly patients
A
Chronic Subdural hematoma
23
Q
If symptoms develop in a chronic Subdural hematoma, they develop after this much time
A
3 weeks
24
Q
Shaken baby syndrome can involve this type of hematoma
A
Acute Subdural hematoma
25
Blunt force trauma or Acceleration-deceleration injury can cause this type of hematoma
Acute Subdural hematoma
26
Is there a lucid interval with Epidural hematoma?
Yes - of a couple hours or less
27
Is there a lucid interval with acute Subdural hematoma?
Possibly
28
A patient with a headache that may be unilateral and occurs when changing positions may have this type of hematoma
Acute Subdural hematoma
29
Are there focal signs with an acute Subdural hematoma?
+/-
30
Does acute Subdural hematoma affect intracranial pressure?
Increases
31
This type of hematoma requires high energy trauma
Acute Subdural hematoma
32
Increased ICP and herniation are possible with this type of hematoma
Acute Subdural hematoma
33
With this type of hematoma, blood is hyperdense on CT
Acute Subdural hematoma
34
Elderly, alcohol abuse, and anticoagulation are risk factors for this type of hematoma
Chronic Subdural hematoma
35
How might a chronic Subdural hematoma occur in pediatrics?
With trauma, including abuse
36
This type of hematoma involves stretched bridging veins, and the patient may not recall any trauma
Chronic Subdural hematoma
37
Are there focal signs with chronic Subdural hematoma?
May have focal signs
38
"Pseudodementia" may be seen with this type of hematoma
Chronic Subdural hematoma
39
With this type of hematoma, blood is hypodense on CT
Chronic Subdural hematoma
40
In an acute Subdural hematoma, is blood on CT hyperdense or hypodense?
Hyperdense (looks bright)
41
In a chronic Subdural hematoma, is blood on CT hyperdense or hypodense?
Hypodense (looks duller)
42
Is there a history of trauma with an Acute on chronic subdural hematoma?
Often with mild or no history of trauma
43
This type of hematoma may present weeks or months after trauma
Acute on chronic subdural hematoma
44
With this type of hematoma, the initial hematoma organizes (membrane), and granulation tissue veins are prone to rupture
Forms layers of repeat bleeding
Acute on chronic subdural hematoma
45
This type of hematoma shows layers and septation on CT
Acute on chronic subdural hematoma
46
This is an abrupt onset neurologic deficit, lasting >24 hours due to vascular cause
Stroke
47
How long does a stroke last?
>24 hours
48
This is also known as cerebrovascular accident/CVA
Stroke
49
Hypoglycemia may lead to an inability to use this, leading to hypoxic CVA
Oxygen
50
What CNS cells are the most vulnerable to ischemic injury?
Neurons
51
Transient ischemia may result in neuronal loss and preservation of these cells
Glial
52
This may result in neuronal loss and preservation of glial cells
Transient ischemia
53
What 3 brain regions are most vulnerable to ischemic injury?
Hippocampus (especially Sommer's sector (CA1))
Purkinje cells of cerebellum
Pyramidal neurons of cerebral cortex layers 3 and 5
54
This sector of the hippocampus is especially vulnerable to ischemic injury
Sommer's sector (CA1)
55
Purkinje cells in this part of the brain are vulnerable to ischemic injury
Cerebellum
56
Pyramidal neurons of these cerebral cortex layers are most vulnerable to ischemic injury
3 and 5
57
Watershed regions between vascular supplies occurs especially with this type of hypoperfusion
Global
58
This is a region of brain tissue that is at risk of dying but may be salvageable if blood flow is restored promptly
Penumbra
59
Is there recovery potential after ischemic/hypoxic CVA?
Yes - depends on blood flow
(ischemic penumbra exists at the 8-10 ml/100g/min range)
60
What is seen first morphologically in ischemic/hypoxic CVA?
Red neurons
(6-24 hours)
61
Is necrosis with neutrophils or macrophages seen first in an ischemic/hypoxic CVA?
Necrosis (usually liquefactive) with neutrophils (24-72 hours)
(macrophages appear after 3-4 days)
62
After how much time are red neurons seen in an ischemic/hypoxic CVA?
6-24 hours
63
After how much time is necrosis with neutrophils seen in an ischemic/hypoxic CVA?
24-72 hours
64
After how much time are macrophages seen in an ischemic/hypoxic CVA?
3-4 days
65
After how much time is gliosis seen in an ischemic/hypoxic CVA?
1-2 weeks
66
Morphology of this condition shows red neurons first, then necrosis with neutrophils, macrophages, edema, and gliosis
Ischemic/hypoxic CVA
67
What are three causes of shock?
Hypovolemia
Septic
Cardiogenic
68
This cause of ischemia results in a global decrease in mean arterial pressure or oxygenation
Entire brain is ischemic
Hypoperfusion
69
Watershed infarction is a pattern of this
Global ischemia
70
These regions of vascular supply are most vulnerable to hypoxia/low perfusion states
Terminal ends
71
What constitutes "watershed" zones of vascular supplies?
Overlap zones of vascular distributions
72
Overlap zones of vascular distributions (MCA, ACA, PCA) constitute this
Watershed zones
73
Infarcts at watershed zones are due to this
Low perfusion states (e.g. shock)
74
This is a preferential ischemia of cerebral layers 3 and 5, leading to a layer of necrosis between superficial and deep layers of viable tissue
Cortical laminar necrosis
75
Cortical laminar necrosis is a preferential ischemia of these cerebral layers
3 and 5
76
Cortical laminar necrosis can be seen in this cause of ischemia
Hypoperfusion
77
What are the three main causes of ischemia?
Hypoperfusion
Thrombosis
Embolism
78
Cause of vascular obstruction that tends to be pale/bland (non-hemorrhagic) infarct
Thrombosis
79
Cause of vascular obstruction that may be hemorrhagic with clot dissolution
Embolism
80
Vascular occlusion due to luminal blood clot
Thrombosis
81
Thrombosis of large vessels typically occurs at these types of vessels
Branching points; sites of atherosclerosis
(due to turbulence)
82
Thrombosis of this type of vessel is a common location for hypertensive vascular disease
Small vessels
83
Small vessels are common locations for this type of vascular disease
hypertensive
84
Lenticulostriate artery and pontine branches of basilar artery are common sites of this type of vascular disease
Hypertensive; small vessel thrombosis
85
Large vessel thrombosis is usually due to this type of vascular disease
Atherosclerotic
86
In large vessel thrombosis, plaque causes luminal narrowing, then ruptures to expose underlying lipid and collagen, causing this
Formation of fibrin clot (thrombus)
87
This is a condition characterized by the thickening and hardening of the walls of small arteries (arterioles)
Arteriolosclerosis
88
Does Arteriolosclerosis involve a thickening of small or large vessels?
Small
89
These two parts of the brain are common sites of small cystic lesions from hypertensive vascular disease
Basal ganglia and pons
90
Lacunar infarct occurs from this type of vascular disease
Hypertensive
91
This lesion is a hallmark of hypertensive cerebrovascular disease
Lacunar infarct
92
Small vessel stroke to this structure of the brain causes pure motor hemiparesis, especially face, arm, leg
Posterior limb of IC / pons
93
Small vessel stroke to this structure of the brain causes pure sensory stroke
Ventral thalamus
94
Small vessel stroke to this structure of the brain causes ataxic hemiparesis
Ventral pons / internal capsule
95
Small vessel stroke to this structure of the brain causes dysarthria and clumsy arm/hand
Ventral pons / IC genu
96
When this type of embolus reaches the lungs, it can cause hypoxia and dyspnea
Fat/marrow
97
How does a leg clot get to the brain?
Paradoxical embolus due to septal defect
98
This artery is the most common site in the brain where an emboli lodges
Middle cerebral artery
99
This type of embolus tends to send showers of emboli, leading to generalized CNS dysfunction
Fat and bone marrow
100
Symptomatic temporary ischemia with full recovery
Transient ischemic attack
101
How long does a Transient ischemic attack last?
<24 hours, usually less than an hour
102
This type of ischemia occurs without infarction of brain, cochlea, or retina
Transient ischemic attack
103
Transient ischemic attack is usually due to this
Embolism (from atherosclerotic plaque)
104
What results in restoration of function after a Transient ischemic attack?
Thrombolysis
105
After this, a patient has a subsequent high risk of embolic CVA
Transient ischemic attack
106
Patients with this often have carotid or vertebrobasilar symptoms
(Amaurosis fugax, weakness or sensory loss, aphasia, homonymous visual field defects)
Transient ischemic attack
107
What is the typical age of a patient with arteriosclerosis?
Middle age
108
What is the most common location in the brain for arteriosclerosis?
Basal ganglia
109
This occurs in hypertensive vasculopathy, and describes when muscle is replaced by hyalinized collagen and lipid, and elastic lamina is lost
Are fragile and prone to rupture and hemorrhage
Arteriolosclerosis (or lipohyalinosis)
110
These are tiny, saccular dilatations of arterioles in the brain
Charcot-Bouchard microaneurysms
111
Charcot-Bouchard microaneurysms are tiny, saccular dilatations of these vessels in the brain
Arterioles
(small, fragile vessels; seen in hypertensive vasculopathy)
112
This is the second most common cause of intraparenchymal hemorrhage
Cerebral amyloid angiopathy
113
Cerebral amyloid angiopathy is associated with this condition seen in elderly
Dementia
114
Cerebral amyloid angiopathy is often seen in patients of this age
Elderly
115
This is the most common location of Cerebral amyloid angiopathy
Cortical / lobar
(cerebrum and cerebellum)
116
Beta amyloid deposits in vessels walls near cortex, in this condition that can cause intraparenchymal hemorrhage
Cerebral amyloid angiopathy
117
In Cerebral amyloid angiopathy, this protein deposits in vessel walls near cortex
Beta amyloid
(same type as Alzheimer's)
118
Cerebral amyloid angiopathy is associated with this allele
ApoE
(alleles e2 and e4)
119
Cerebral amyloid angiopathy is associated with these 2 ApoE alleles
e2 and e4
120
Cerebral amyloid angiopathy is associated with mutations in this gene
APP (amyloid precursor protein)
121
This condition that can cause intraparenchymal hemorrhage is associated with ApoE alleles e2 and e4, and APP gene mutations
Cerebral amyloid angiopathy
122
Cerebral venous sinus thrombosis is usually secondary to this
Hypercoagulable state
123
Oral contraceptive use, dehydration, and Sickle Cell anemia are risk factors for this condition that is usually secondary to hypercoagulable state
Cerebral venous sinus thrombosis
124
This is a collection of abnormal blood vessels that may be parenchymal or on the surface, often with dysfunctional/weak wall structure and direct arterio-venous connection
Arteriovenous malformation
125
Malignancies, especially metastases, can cause this type of stroke
Intraparenchymal hemorrhage
126
This condition can cause intraparenchymal hemorrhage, and it involves recurrent small vessel subcortical infarcts, extensive white matter disease, and dementia
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukomalacia (CADASIL)
127
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukomalacia (CADASIL) can cause this type of stroke
Intraparenchymal hemorrhage
128
This condition that can cause intraparenchymal hemorrhage involves a deposition of PAS positive misfolded Notch 3 protein in vessel walls
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukomalacia (CADASIL)
129
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukomalacia (CADASIL) involves a deposition of this protein in vessel walls
PAS positive misfolded Notch 3 protein
130
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukomalacia (CADASIL) is an extensive white matter disease that can cause this condition
Dementia
131
Hemorrhage in the arachnoid space between pia and dura
Subarachnoid hemorrhage
132
Non-traumatic Subarachnoid hemorrhages are mostly due to this
Aneurysm rupture
133
Arterial dilation due to weakness of wall
Aneurysm
134
This is the most common morphological type of aneurysm
Saccular / Berry aneurysm
135
A pseudoaneurysm occurs due to this
Dissection
136
Hypertension, atherosclerosis, genetics, and fibromuscular dysplasia can cause this, which can lead to a non-traumatic subarachnoid hemorrhage
Aneurysm
137
This protein is defective in Marfans
Fibrillin
138
This protein is defective in Ehlers-Danlos syndrome
Collagen
139
This protein is defective in ADPKD
Polycystin
140
Valvular disease, bacterial endocarditis and paradoxical embolus can cause this type of aneurysm
Mycotic aneurysm
141
Arteriovenous malformation is mostly seen in this age group
Kids
142
This artery is the most common site of aneurysms in the brain
Anterior communicating artery
143
What type of arteries do aneurysms usually arise at?
Branch points
(anterior communicating, posterior communicating, MCA bifurcation, internal carotid terminus, basilar bifurcation)
144
Epidural hemorrhage stops at this
Suture lines
145
Subdural hemorrhage stops at this
Dural reflections
146
Does subarachnoid hemorrhage enter sulci?
Yes
147
This type of hemorrhage involves global bleeding around the whole surface of the brain
Subarachnoid hemorrhage
148
Blood in a lumbar puncture could indicate this type of hemorrhage
Subarachnoid hemorrhage
149
In the pathophysiology of a subarachnoid hemorrhage, aneurysm ruptures, often after this
Acute increase in BP
150
A Subarachnoid hemorrhage that irritates meninges will cause this
Meningitis signs
(neck stiffness, photophobia, Brudzinki sign, Kernig's sign)
151
A Subarachnoid hemorrhage that irritates the trigeminal nerve will cause this
Headache (very severe)
152
Subarachnoid hemorrhage that irritates the Circle of Willis will cause this
Vasoconstriction
153
How does Subarachnoid hemorrhage affect intracranial pressure?
Increases
(causing cerebral edema)
154
What is Brudzinski sign?
Meningeal sign - passive flexion of neck causes flexion of both legs and thighs
155
What is Kernig's sign?
Meningeal sign - patient cannot fully extend knee when supine with hip flexed 90 degrees
156
In a Subarachnoid hemorrhage, Circle of Willis vessels may constrict due to the irritation, causing this
Delayed cerebral ischemia
157
This is the 2nd most frequent cause of death from a Subarachnoid hemorrhage
Delayed cerebral ischemia
158
Delayed cerebral ischemia can occur this many days after Subarachnoid hemorrhage
3-20 days
(patient will seem like they recovered, then rapidly decompensate)
159
This is a late complication of Subarachnoid hemorrhage that occurs due to fibrosis of arachnoid granulations
Hydrocephalus
160
Is cerebral edema or Hydrocephalus a complication of Subarachnoid hemorrhage?
BOTH
(increased intracranial pressure leads to cerebral edema, possible fibrosis of arachnoid granulations leads to hydrocephalus)
161
This imaging is good for diagnosis of Subarachnoid hemorrhage
Non-contrast CT
162
Other than a non-contrast CT, what other test can be done to diagnose Subarachnoid hemorrhage?
Lumbar puncture
(will be bloody; Xanthochromia occurs later)
