Stroke

Front 1

3 types of stroke

Back 1

ABI Acute Brain Ischemia
ICH Intracerebral Hemorrhage
SAH Subarachnoid Hemorrage

Front 2

ID risk factors for each type of stroke

Back 2

ABH Atheroclerosis, cardioembolic, hypercoaguability, migraines, Sickle cell Dz
ICH HTN, bleeding Disorders, AVM's
SAH Congenital or Aquired aneurysms

Front 3

Identify Risk factors for ABI

Back 3

HTN, Incr risk by 50%
Smoking incr by 2-3 fold
Age>67, DM, Eliv Chol, Eliv C-Protein,
Male, Female post menapause, Family Hx, AFIB, Polycythemia Sickle Cell Dz, Birth control, HRT, Preg, thrombolitic DO,
Migraines esp w/ auras
TIA's 10% stroke w/in 90 days 1/2 w/in 48 hrs.
Surgery

Front 4

Name 4 major Classifications of the pathophysiology of ABI

Back 4

1. Atherothrombic Plaque infarcts
2. Cardioembolic Afib
3. Lacunar small vessel disease often due to hypercoagulable SCdz Deep brain Subtle
4. Hemodynamic Decr global cerebral perfusion

Front 5

In ABI describe the Neural response to ischemia. 6 steps

Back 5

1. Vessel occlusion
2. Cellular anaerobic metabolism
3, Granulocyte adhesion & O2 Radical
Inflam-TNFa, IL1, prostiglandins, O2
Radicals
Excitatory Amino Acids Glutamate, aspartate, Glycine
Lipid peroxidation, Loss of Na+ pump, Mitochondia inj, Release of protease, phosphlipase
4. Hyperexcitability & hyperpolerization, Ca+ accumulation
5. Cell injury
6. Apotosis, irrivers. cell injury

Front 6

ABI is
a) hemorrhagic
b) Ischemic

Back 6

b) Ischemic

Front 7

Patterns of ischemic neuronal injury, sparing and healing

Back 7

1) Dense infarction and necrosis forms at the center of ischemic brain tissue.
2) Spontaneous or therapeutic reperfusion results in the limitation of infarct size, but also contributes to oxygen radical production (reperfusion injury).
3) Selective neuronal necrosis - some neurons and glial cells survive, if reperfused 12 hours; sparing -rapid perfusion and neuroprotective therapy.

Front 8

Penumbra - tissue at the periphery of the ischemic zone
Describe

Back 8

1)CBF approximately 20 ml/100 gm/min.
neurons viable but no synaptic function. salvageable if perfusion is restored 90 minutes to several hours after initial event.
2) Ischemic -high extracellular potassium causing multiple repetitive depolarizations, ATP depletion and delayed cell death; new therapies are aimed at blocking peri infarct depolarizations.

Front 9

Acute Brain Ischemia is
a) Hemorrhagic or
b) Ischemia?

Back 9

b) ISCHEMIA

Front 10

Define autoregulation and its effect on Cerebral Blood Flow (CBF).

Back 10

"Autoregulation" regulates Cerebra vascular resistance (CVR)
to maintain CBF despite changes in MAP or ICP.
CBF= MAP-ICP/CVR

Front 11

To maintain CBF
What happens to CPP if MAP decreases or ICP increase??

Back 11

CPP will decrease and CVR will decrease.

Front 12

What are the acute or initial responses to ischemia causing neuronal damage?

Back 12

1.Inflammation,
2. excitotoxin release,
3. granulocyte adhesion,
4. oxygen radical production,
5. cytokine release cause not only acute neuronal damage

Front 13

Inflammation causes what delayed reaction leading to neuronal damage and death?

Back 13

delayed effects with T lymphocytes and macrophages infiltrating up to 2 weeks after the infarct.

Front 14

What occurs after Vessel occlusion?

Back 14

Anarobic metabolism & Lactate production, followed by Granulocyte adhesion & O2 Radical production

Front 15

Granulocyte adhesion & O2 Radical production lead to (3) responses

Back 15

1. release of inflammatory cytokines
2. Release of excitatory Amino Acids
3. Lipid Peroxidation

Front 16

inflammatory cytokines released are:

Back 16

TNF-a, IL1, prostaglandins. O2 Radicals

Front 17

Excitatory Amino Acids are:

Back 17

glutamate, Aspartate, glycine causing hyperexcitability & hyperpolarization, Ca+ accumulation

Front 18

Lipid Peroxidation results in:

Back 18

Loss of Na+ Pump, Mitocondrial Injury, Release of Protease and phospholipidosis

Front 19

Statins can reduce these Inflammatory markers after stroke and correlates with prognosis

Back 19

WBC, IL-1, IL-6 and C-reactive protein have been correlated with prognosis.

Front 20

Systemic responses to cerebral ischemia

Back 20

1)Arrhythmias (tachy or brady, arrhythmias, ST-T wave changes, increased creatinine phosphokinase MB [CPK-MB], brain natriuretic peptide [BNP], wall motion abnormalities) are believed to be due to a burst of catecholamines.
2)Neurogenic pulmonary edema (adult [acute] respiratory distress syndrome [ARDS])
3)Peptic ulcer disease (Cushing ulcer)
4)Endocrine abnormalities (syndrome of inappropriate antidiuretic hormone [SIADH])

Front 21

In response to ischemia, the cerebral autoregulatory mechanisms compensate for a reduction in CBF by (2)

Back 21

1. local vasodilatation,
2.opening the collaterals, and increasing the extraction of oxygen and glucose from the blood.

Front 22

Normal CBF is 50 -60 ml/100g/min. What happens when CBF decreases?

Back 22

If the CBF is reduced to below 20 ml/100g/min, an electrical silence ensues and synaptic activity is diminished to preserve energy stores. CBF of less than 10ml/100g/min results in irreversible neuronal injury

Front 23

Of the 3 types of stroke which one tends to be painless and the least level of decreased consciousnes?

Back 23

ABI tends to be painless with less change in level of consciousness than ICH or SAH.

Front 24

Which catagory of stroke tends to present with heasdaches and decreasing LOC?

Back 24

ICH and SAH are associated with severe headache and changes in level of consciousness (only 20-50% of patients with SAH have the classic “thunderclap headache”, and about half have prodromal headaches).

Front 25

3 findings that are most predictive of stroke:

Back 25

facial paralysis,
arm drift, and
abnormal speech.