Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Pathology Exam 4 > Primary CNS Diseases, Traumatic Brain Injury, CVD > Flashcards

Primary CNS Diseases, Traumatic Brain Injury, CVD Flashcards

1
Q

What 2 things are Neural Tube Defects associated with?

A
  • Increased alpha-fetoproteins (AFP) in amniotic fluid or maternal serum
  • Have been associated with maternal folic acid deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A majority of children and adolescents with spina bifida​ will test positive for what?

A

Hypersensitivity to latex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Cerebral Edema?

  • Resulting in…
  • Associated with…
  • Result of…
  • May occur following damage initiated by…
  • Tx:
A
  • Abnormal accumulation of fluid in the cerebral parenchyma
  • Resulting in cerebral swelling
  • Associated with raised ICP
  • Result of breakdown of BBB
  • May occur following damage intitiated by:
    • Ischemia (infarction)
    • Trauma (head injury)
    • Inflammation Encephalitis or Meningitis
    • Cerebral Tumors
    • Metabolic Disturbances (hyoantremia or hypoglycemia)
  • Tx: min formation of edema by use of osmotic agents or corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Hydrocephalus & What are the 3 possible mechanisms?

A
  • Increase in the volume of CSF within the brain resulting in the expansion of the cerebral ventricles
  • 3 Possible Mechanisms:
    1. Obstructive Hydrocephalus (obstruction to the flow of CSF)
    2. Impaired absorption of CSF at arachnoid villi (Rare)
    3. Overproduction of CSF by choroid plexus neoplasms (very rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Non-communicating Hydrocephalus?

A

Obstruction within the ventricular system leading to blockage of CSF flow from the ventricles to the subarachnoid space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Communicating Hydrocephalus​?

A

Extraventricular obstruction within subarachnoid space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Although, functional effects are seen earlier, When and Where is the morphologic evidence of injury in Brain Contusions seen?

A

Neuronal cell body, takes about 24 hours to appear

  • Nucelar pyknosis
  • Cytoplasmic eosinophilia
  • Cellular disintegration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Within a few hours of a brain contusion, blood extravasates through the involved tissue, across the width of the …, and into the … and …

A
  • Cerebral Cortex
  • White matter, and Subarachnoid spaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe a Concussion

A
  • Reversible altered consciousness from head injury in the absence of contusion.
  • Characteristic transient neurologic dysfunction includes:
    • Loss of Conciousness
    • Temporary Respiratory Arrest
    • Loss of Reflexes
  • Although neurologic recovery is complete, amnesia for the event persists.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is an Epidural Hematoma, describe it?

A
  • Traumatic Vascular Injury of the dural vessels (Middle Meningeal Artery)
    • Infants - traumatic displacement of the easily deformable skull may tear a vessel, even in the absence of a skull fracture
    • Children and Adults - almost always stem from skull fractures
  • Clinically - pts can be lucid for several hrs between the moment of trauma and the development of neurologic signs
  • May expand rapidly, and constitutes a Neurological Emergency necessitating promt drainage and repair to prevent death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a Subdural Hematoma, describe it?​

A
  • Rapid movement of the brain during trauma can tear the bridging veins that extend from the cerebral hemispheres through the subarachnoid and subdural space to the dural sinuses.**​
  • Infants - more susceptible because their bridging veins are thin-walled.
  • Elderly pts with brain atrophy - higher rate because their bridging veins are stretched out, and the brain has additional space to move.
  • Neurologic Symptoms:
    • nonlocalizing - headache, confusion, slowly progressive neurolgic deterioration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When do Subdural Hematomas typically become clinically evident?

A

Within the first 48 hrs after injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where are Subdural Hematomas most common?

A
  • Over the lateral aspects of the cerebral hemispheres
  • May be Bilateral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are Symptomatic Subdural Hematomas treated?

A

Surgical removal of the blood and associated reactive tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes Chronic Subdural Hematomas?

A

Subdural hematomas commonly rebleed during the healing process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do Acute Subdural Hematomas appear?

A

Appears as a collection of freshly clotted blood apposed to the contour of the brain surface, without extension into the depths of the sulci

17
Q

Describe the Morphology of Subdural Hematomas.

A
  • The underlying brain is flattened, and the subarachnoid space is often clear.
  • Typically, venous bleeding is self-limited with breakdown and organization of the hematoma takeing place over time:
    • 1 WEEK - subdural hematomas organize by lysis of the clot
    • 2 WEEKS - growth of granulation tissue from the dural surface into the hematoma
    • 1-3 MONTHS - fibrosis
    • Fibrosing lesions may eventually retract, leaving only a thin layer of CT = subdural membranes
18
Q

What is Cerebrovascular Disease (CVD)?

What is its Pathophysiology?

A
  • Characterized by injury to the brain as a consequence of altered BF
  • Stroke is the clinical designation
  • Pathophysiology Involes 1 of 2 Mechanisms:
    • Hypoxia, Ischemia, and Infarction resulting from impairment of blood supply and oxygenation of CNS tissue
      • Etiology: Embolism
    • Hemorrhage resulting from rupture of CNS vessels
      • Etiologies: Hypertension, and Vascular Anomalies (aneurysms and malformations)
19
Q

What are Cerebral Infarctions most commonly caused by?

A
  • Atherosclerotic Thrombi
    • ​​Usually due to Carotid Artery atherosclerotic disease (plaque rupture), most commonly at the Carotid bifurcation

OR

  • Emboli of Cardiac Origin secondary to:
    • Mitral Valve Pathology (valvular)
    • Acute anterior MI or Congestive Cardiomyopathies resulting in Cardiac Mural Hypokinesias or Akinesias with Thrombosis
    • Atrial Fibrillation (cardiac arrhytmias)
20
Q

What is the gross appearance of an ischemic cerebral infarct during the first 6 hours of irreverisble injury?

A

Little change in appearance

21
Q

What is the gross appearance of an ischemic cerebral infarct by 48 hours?

A
  • Tissue becomes pale, soft, and swollen
  • Corticomedullary Junction becomes Indistinct
22
Q

What is the gross appearance of an ischemic cerebral infarct from 2 to 10 days?

A
  • Brain becomes gelatinous and friable
  • Previously ill-defined boundary between normal and infarcted tissue becomes more distinct as edema resolves in the viable adjacent tissue
23
Q

What is the gross appearance of an ischemic cerebral infarct from 10 days to 3 weeks?

A
  • Liquefaction Necrosis, leaving a fluid filled cavity that continues to expand untill all of the dead tissue is removed.
24
Q

What is the RF most commonly associated with clinically significant deep brain Intracerebral Hemorrhages?

A

Hypertension (> 50% of cases)

25
Q

In Intracerebral Hemorrhage, Hypertension can causes Vessel Wall Abnormalities (making them weaker and more vulnerable to rupture). What are the 3 Abnormalities?

A
  • Accelerated Atherosclerosis in larger arteries
  • Hyaline Arteriolosclerosis in smaller arteries
  • Proliferative Changes and Frank Necrosis of arterioles (in severe cases)
26
Q

Where may Hypertensive Intracerebral Hemorrhage originate in most cases?

A
  • Putamen (50-60%)
  • Thalamus, pons, cerebellar hemispheres (rarely)
  • And other regions of the brain
27
Q

Describe how Intracerebral Hemorrhage occurs.

A

Rupture of an artery within brain tissue leads to extravasation of blood, which displaces brain tissue and causes Increased Intracranial Volume until the resulting tissue compression halts the bleeding.

28
Q

What is the most frequent cause of clinically significant Subarachnoid Hemorrhage?

A

Rupture of a Saccular Aneurysm in a Cerebral Artery

29
Q

What is the most common type of Intracranial Aneurysm?

A
  • Saccular “Berry” Aneurysm
    • Vessels within the circle of Willis are often affected
30
Q

What may a Subarachnoid Hemorrhage also result from (besides a rupture of a saccular aneurysm)? (5)

A
  • Extension of a traumatic Hematoma
  • Rupture of a Hypertensive Intracerebral Hemorrhage into the ventricular system
  • Vascular Malformation (arteriovenous, cavernous)
  • Hematologic disturbances
  • CNS Tumors

General Pathology Exam 4 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions