Brainscape's Knowledge GenomeTM

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


See full index

PHAR 123 > CNS Pathology Introduction > Flashcards

CNS Pathology Introduction Flashcards

1
Q

The average brain has over how many neurons? How many synaptic connections?

A

> 100 billion
150 trillion synaptic connections

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

The bones of the ______ & _________ protect the CNS from mechanical injury.

A

Skull ; Vertebrae

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

The _________ & the ___ separate the CNS from the remainder of the body.

A

Meninges ; BBB (Blood Brain Barrier)

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

What are the three classical features of Neurons?

A

-Nondividing
-Permanent
-Postmitotic

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

CNS disease symptoms result from what?

A

Dysfunction of or loss of Neuronal function

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

What % of total cardiac output goes to the brain?

A

15%

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

What % of total bodily oxygen consumption is conducted by the brain?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What % of total bodily glucose consumption is conducted by the brain?

A

25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The brain extracts approximately ___% of Oxygen & ___% of Glucose from Arterial Blood in order to facilitate active Neuronal Cells.

A

50% O2 ; 10% Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why are Neurons particularly vulnerable to the effects of toxins?

A

-Fatty nature of Neurons (many organotoxins are fat soluble)
-High activity levels & specialization
-High concentration of Sulfur-Containing AAs (which bind toxic heavy metals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do Neurons respond following brain tissue injury?

A

-Axon &/or Cell Body swell
-Rapid Death results in Phagocytosis (via transformed Microglia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do Oligodendroglia respond following brain tissue injury?

A

-DO NOT REGENERATE (!!)… These cells are typically responsible for myelinating neuronal cells, but do not regenerate upon being damaged.

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

How do Microglia respond following brain tissue injury?

A

-Chemotactic Factors activate them & cause them to transform into Phagocytic Cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do Astrocytes respond following brain tissue injury?

A

-Hypertrophy / Hyperplasia (increase in size & number)… Rxn is called “Gliosis”.

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

How do Ependymal Cells respond following brain tissue injury?

A

-DO NOT REGENERATE (!!)… Typically line the ventricles of the brain, but do not regenerate upon being damaged (much like Oligodendroglia).

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

What differs in the presentation of acute brain injury (vs. damage to other bodily compartments)?

A

No Fibrotic Scarring (a hole is left instead)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Summarize the “Ischemic Cascade”.

A

1) Cerebral Blood Flow & Metabolic Demands are mismatched… Can bring about either Electrical Failures or induce Anaerobic Metabolism to kick in.

2) Electric Fail: Na+ Influx into Neurons (ie. Neuron Depolarization) stimulates Ca2+ Influx, leading to activated PLA2. PLA2 enzyme converts membrane phospholipids into Arachidonic Acid, which stimulates both the Cyclooxygenase & Lipooxygenase Pathways. COX Pathway activation leads to Potent Vasoconstriction & Platelet Aggregation, as well as Free Radical production. LPOX Pathway activation induces LT production, which promotes inflammatory response & brings about neuron damage.

3) Anaerobic Metabolism Activation: Induces Lactic Acidosis, as Ketone Bodies are being produced as alternative energy sources. The production of these Ketones causes neuronal damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does “Global Ischemia” mean?

A

Not enough O2 gets to brain tissues (ie. CHF / ASCVD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does “Cerebral Infarct” mean?

A

-Just means cell death in brain adam
:( the below part is what causes it
Blood Vessel bursts or leaks (Hemorrhagic)
-Blood Vessel blocked by a blood clot, plaque, embolism (Ischemic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is an “Intracerebral Hemorrhage”?

A

Brain bleed (ie. Weak / Malformed Vessel or Trauma)

21
Q

What is the number one risk factor for Strokes?

A

Elevated BP

22
Q

What are some other risk factors for Stroke?

A

-A Fib
-Diabetes
-Family History of Stroke
-High Cholesterol
-Increasing Age (> 55yrs especially)
-Heart Disease or Poor Blood Flow in Legs
-Fat
-Drink
-Diet
-Smoker
-Illegal Drug Use
-Oral Contraceptive Use

23
Q

What classes of medications increase one’s risk for suffering a Hemorrhagic Stroke?

A

-Antithrombotics
-Antiplatelets
-Sympathomimetics (ie. Ephedrine, Pseudoephedrine, Phenylpropanolamine)

24
Q

What ethnicities have a higher risk for suffering Hemorrhagic Stroke?

A

-African
-Hispanic
-Asian

25
Q

What factors increase death risk 30 days Post-Intracranial Hemorrhage (ICH)?

A

-Lg. Hematoma Volume
-Coma
-Old Age
-Oral Anticoagulant Use
-Increased INR
-Intraventricular / Infratentorial Hemorrhage

26
Q

Stroke symptoms… What are they?

A

-Headache (worsens when lying down, bent over, straining, coughing, changing positions)
-Unilateral face drooping / muscle weakness
-Slurred speech
-Loss of bladder / bowel function / coordination
-Dizzy (ie. Vertigo)
-Confusion / Memory Loss
-Sensory changes (ie. Hearing / Taste / Touch / Sight / Pain Sensation)

27
Q

Ischemic Strokes comprise __% of total Stroke cases; Hemorrhagic Strokes comprise __% of total Stroke cases.

A

80% (Ischemic) ; 20% (Hemorrhagic)

28
Q

Would a patient with higher or lower BP have a better prognosis post-Stroke?

A

Higher BP patient (as overall cerebral perfusion is enhanced with higher BP)

29
Q

Two patients suffer Ischemic Strokes… One in Mexico (at an outdoor resort), & one in Saskatchewan (outside & during a winter snowmobiling trip). Regarding the temperature differences, which patient has a better prognosis post-Stroke?

A

The one in SK (as cooler temps slow down brain metabolism & injury extent)

30
Q

One Stroke patient is hyperglycemic & another Stroke patient is hypoglycemic. Which one has a better prognosis post-Stroke?

A

The hyperglycemic one (as extent of glucose metabolism affects infarct size)

31
Q

What visible changes occur around the 5-6hr mark that enable us to distinguish an Infarcted Brain from a healthy one?

A

-Discoloration & fuzziness brought onto the usually clear border between Gray & White Matter.

32
Q

At the 72hr mark, what visual difference shows up between an Infarcted Brain & a healthy one?

A

-Well established Necrosis (that eventually liquifies & leads to holes).

33
Q

Neuronal Cells begin to die at a Cerebral Blood Flow value below what?

A

< 10mL / 100g / min

34
Q

Destructive processes that occur during a Stroke are somewhat reversible if reperfusion of infarcted brain tissues happens within how many hours?

A

2-4hrs

35
Q

Within how many hours post-Stroke are the following tPA agents effective:

Alteplase?
IV r-TPA?

A

Alteplase: 0 - 3hrs
IV r-TPA: 3 - 4.5hrs

36
Q

Who would be C/I to receive tPA treatments?

A

-Those with relative bleed risks (including HTN patients).

37
Q

If tPA is C/I, what other option can be considered? Within what window of time (how many hrs) must it be initiated in order to have effect?

A

Stent ; 6hr Window

38
Q

What parameters must be ensured prior to administering tPA?

A

-No intracranial hemorrhaging
-BP < 185 / 110 (but not too low, as low BP = Poor Perfusion)

39
Q

If BP is > 185 / 110, what must we administer prior to giving tPA?

A

One of the below options:

-Labetalol (10-20mg IV)
-Enalapril (1.25mg IV)
-Nitropaste (1-2in)

May repeat the above procedure once if necessary!

40
Q

Once BP is < 185 / 110, how much tPA should be administered?

A

0.9mg / kg (with a max dose of 90mg)

-10% should be Bolus over 1min… Remainder infused over 1hr.

41
Q

How long after tPA administration should we withhold Antiplatelet Therapies or Heparin?

A

24hrs

42
Q

Why is a single bolus dose of tPA favored over a 1hr infusion?

A

-Longer DOA due to less Plasminogen Activator Inhibitor inactivation.
-Thought to work better for large clots.

43
Q

How do we treat Hemorrhagic Stroke?

A

1) BP ctrl & supportive care (primary goal is reduce intracranial pressure)
2) Anti-Clotting agents in order to further reduce risk

44
Q

How do concussions & contusions differ in presentation?

A

Concussion: Widespread & microscopic bruising / bleeding
Contusion: Localized & macroscopic bruising / bleeding

45
Q

What is a laceration?

A

Tissue tearing

46
Q

What are some events that can bring upon Intracerebral Hemorrhages?

A

-Head Trauma Complications
-Intracerebral Vessel Rupture
-Gunshot Wound
-Nontraumatic Forms (ie. Stroke)
-Hematologic Disease (ie. Leukemia)

47
Q

What types of virally-induced diseases can cause Encephalitis?

A

-Rabies
-Polyomelitis
-Herpes Encephalitis
-MMR
-West Nile Disease

48
Q

How do mild & severe cases of Encephalitis differ in presentation?

A

Mild: Flu-like symptoms, headaches.

Severe: Severe headaches, high fever, drowsiness, vomiting, confusion, seizures, abnormal sensations or movements.

49
Q

Four types of Encephalitis?

A

PHAR 123 (18 decks)

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