CVD Flashcards
What’s CVD
What’s Stroke?
sudden onset of neurological symptoms due to either of the above. It’s the clinical label used when symptoms are acute
Note: > 24hr
But it’s
TIA if <24hr
whats the Classification CVD Based on Mechanism
Ischemic and Hemmorhagic
Among the classification which is more common.
List example of both
- Cause: Impaired blood supply → hypoxia → ischemia → infarction
- Can be:
- Global (e.g., cardiac arrest)
- Focal (e.g., MCA stroke)
- Mechanism:
- Embolism is more common than thrombosis in the brain
- Source: heart (e.g., atrial fibrillation), carotids, atherosclerotic plaque
- Cause: Vessel rupture → bleeding into brain tissue or subarachnoid space
- Common causes:
- Chronic hypertension → small vessel rupture (e.g., basal ganglia bleed)
- Aneurysms (especially berry aneurysms in Circle of Willis)
- Arteriovenous malformations (AVMs)
Clinical Implications (Only Where It Matters)
- Ischemic strokes → treat urgently with tPA (if within 4.5 hrs), or mechanical thrombectomy (up to 24 hrs in select cases)
- Hemorrhagic strokes → NO tPA; focus on BP control, neurosurgical evaluation, and managing ICP
- High oxygen demand: Brain is only 1–2% of body weight, but:
- Gets 15% of resting cardiac output
- Uses 20% of the body’s oxygen
- Why? Brain relies almost entirely on aerobic metabolism. No oxygen = no energy = neurons die.
whats the Mechanisms of Oxygen Deprivation with examples for each
-
Hypoxia (oxygen is low but blood may still be flowing)
- Low PO₂ (e.g., high altitude)
- Low O₂-carrying capacity (e.g., anemia, CO poisoning)
- Tissue can’t use O₂ (e.g., cyanide poisoning) -
Ischemia (blood flow is interrupted)
- Transient (e.g., TIA)
- Permanent (e.g., infarct from stroke)
- Can result from:
- Low perfusion pressure (e.g., shock)
- Vessel obstruction (e.g., thrombus, embolus)
— ### What are the factors that determines weather Tissue Dies or Not:
- Collateral circulation (Circle of Willis can save the day… sometimes)
- Duration of ischemia (short = reversible)
- Severity and speed of flow reduction
> The combination of these factors determines: > - The location of damage > - The size of infarct > - The type of neurological symptoms
What Is Global Cerebral Ischemia? and the possible causes
This happens when blood flow to the entire brain drops, not just one region. You typically see it in situations like:
- Cardiac arrest → no pump = no brain perfusion
- Severe hypotension → not enough pressure to push blood into brain vessels
- Shock (e.g., septic or hypovolemic)
Note: This isn’t a focal stroke; it’s a brain-wide event that causes diffuse injury, often called diffuse hypoxic-ischemic encephalopathy.
— ### Clinical Outcomes Depend on Severity - Mild cases: You might see a temporary confusional state, agitation, or delayed responsiveness. These patients often recover completely, with no lasting damage. - Moderate to severe cases: There can be permanent neuronal injury or brain death, depending on how long the brain went without oxygen. > Key point: Even brief episodes can cause selective vulnerability — some brain areas suffer even if others recover. —
What’s Watershed (Border Zone) Infarcts
In the cerebral hemispheres, the most vulnerable area is: and who does damage to this place look?
- In the cerebral hemispheres, the most vulnerable area is:
- The zone between the anterior cerebral artery (ACA) and middle cerebral artery (MCA)
- Damage here forms a sickle-shaped band of dead tissue just lateral to the midline (near the interhemispheric fissure)
> Clinical sign: Patients may have bilateral weakness affecting the proximal upper limbs (the so-called “man-in-a-barrel” syndrome), depending on which watershed zone is affected. —
What’s the hierarchy in how brain cells respond to ischemia.
- Neurons are the most sensitive — they die within minutes of oxygen deprivation.
- Glial cells (especially oligodendrocytes and astrocytes) are somewhat more resilient but still vulnerable.
Within neurons, some regions are especially fragile which are? :
- CA1 of hippocampus (Sommer’s sector) – first to go. It’s essential for short-term memory.
- Cerebellar Purkinje cells – responsible for fine motor coordination.
- Pyramidal neurons in the cortex, especially in layers 3 and 5 – critical for conscious thought and motor output. > Clinical tie-in: Damage to these areas often leads to memory loss, motor coordination deficits, or even persistent vegetative state. — Let me know if you want a quick summary diagram, or if you’re ready to move to focal ischemia or infarct evolution
Whats are the Gross Changes in Global Ischemia
When the entire brain suffers from low blood flow, you get generalized swelling.
- Brain appears edematous → it swells due to fluid accumulation.
- Gyri are widened and sulci are narrowed → classic sign of cerebral edema.
- On cut section, you lose the usual contrast between gray and white matter. This tells you there’s diffuse, severe injury—everything is becoming structurally disorganized.
Think of it as the brain “blurring” on both the surface and in cross-section.
12 to 24
24hr to 2weeks
After 2weeks
Early Stage (12–24 hours) — “Red Neurons”
- First sign of irreversible neuronal injury.
- Changes in neurons include:
- Microvacuolization (small holes in cytoplasm)
- Eosinophilia (cytoplasm turns bright pink/red → “red neurons”)
- Nuclear pyknosis and karyorrhexis (nucleus shrinks, fragments)
These neurons are toast — they’re undergoing apoptosis or necrosis and can’t be rescued.
- Astrocytes and oligodendrocytes also begin to show similar changes, but they lag slightly behind neurons.
Subacute Stage (24 hours – 2 weeks)
Now the brain starts reacting to the injury:
- Tissue necrosis becomes clear — affected areas break down.
- Neutrophils arrive early, but are quickly replaced by:
- Macrophages (microglia), which clean up the dead cells.
- Vascular proliferation starts — new capillaries form, trying to restore perfusion.
- Reactive gliosis kicks in — astrocytes proliferate to fill in the damage.
Clinically, patients in this stage may worsen neurologically or start to stabilize depending on the injury extent.
Repair Phase (After ~2 weeks)
The brain doesn’t scar like other tissues — it undergoes gliosis, not fibrosis.
- Necrotic tissue is cleared out by macrophages.
- Astrocytes lay down a glial scar — not true collagen, but a network that fills space.
- Normal architecture is lost — replaced by a mesh of glial cells.
- In the cerebral cortex, damage isn’t uniform:
- Some layers are destroyed while others are preserved.
- This pattern is called pseudolaminar necrosis — it looks layered, but it’s not organized, just patchy.
Clinical Takeaway
If a patient survives a severe hypotensive episode or cardiac arrest, imaging weeks later may show patchy cortical damage, gliotic scars, or volume loss — all reflecting this timeline. Their symptoms (like memory loss or motor issues) often reflect which areas suffered worst.
What Is Focal Cerebral Ischemia?
It’s a localized lack of blood flow to one part of the brain (focal = specific area). This happens when:
- A blood vessel gets blocked (like a clogged pipe), or
- There’s poor perfusion (not enough pressure to push blood through)
If this goes on long enough, it causes infarction (permanent tissue death).
What Determines the Outcome in focal ischemia?
The severity of damage depends on:
- How long the area goes without blood
- Whether there’s collateral circulation (backup blood supply through other vessels)
[Collateral circulation = alternate pathways that can reroute blood, like side streets during traffic] The main backup system is the Circle of Willis at the base of the brain. It connects major arteries and allows some compensation when one route is blocked. But areas deep in the brain — like the thalamus, basal ganglia, and deep white matter — get blood from small arteries that don’t have collateral supply. So they’re at higher risk of damage.
what are the Main Causes of Focal Ischemia
- Embolism (clot that travels)
- Most common cause.
- Clot usually forms in the heart and travels to the brain.
- From mural thrombi (clots on the heart wall) after heart attacks
- From valvular disease (damaged heart valves)
- From atrial fibrillation (irregular rhythm → stagnant blood → clots) > [Mural thrombus = clot stuck to the inner wall of the heart]
- These clots tend to lodge in the middle cerebral artery (MCA), which is a straight continuation of the internal carotid artery.
> [MCA = main artery supplying most of the lateral brain — speech, face, arm]
- Thrombosis (clot that forms right in the brain artery)
- Usually caused by atherosclerosis (plaque buildup in artery walls) - Common locations:
- Carotid bifurcation (where carotid artery splits in the neck)
- Origin of MCA
- Ends of the basilar artery (brainstem blood supply)
> [Thrombosis = blood clot forming at the site of damage, like a scab inside the pipe]
- Vasculitis (inflamed blood vessels) - Rare but important - Causes vessel walls to swell, narrow, and possibly occlude - Can be:
- Infectious (e.g., syphilis, TB, or in immunocompromised patients: CMV, aspergillosis)
- Autoimmune (e.g., lupus, primary CNS vasculitis) > [Vasculitis = immune system attacks blood vessels, narrowing or closing them]
Clinical Tie-In Knowing cause and territory helps you predict symptoms: - MCA infarcts → face/arm weakness, aphasia if dominant hemisphere - Small vessel strokes → pure motor or sensory deficits without cortical signs - Embolic strokes → often sudden, maximal at onset, may be multiple areas
🧠 Gross Morphology: What You’d See in the Brain Itself in focal ischemia
First 6 Hours
- Brain looks normal to the naked eye.
> [Even though cells are dying, you can’t see the damage yet]
By 48 Hours
- Tissue becomes:
- Pale
- Soft
- Swollen
- Corticomedullary junction (border between gray and white matter) becomes blurry
[Edema blurs normal brain structure]
2 to 10 Days
- Brain is gelatinous and fragile
- Edema starts to resolve, so now you can clearly see the dead area
10 Days to 3 Weeks
- Tissue liquefies (turns into mush)
- Forms a fluid-filled cavity as macrophages eat the debris
[Eventually, the body “cleans up” the dead tissue, leaving a hole where the infarct was]
🔬 Microscopic Morphology: What You’d See Under a Microscope
First 12–24 Hours
- Red neurons appear (dead neurons that stain red due to protein breakdown)
- Edema:
- Cytotoxic (cells swell due to water influx)
- Vasogenic (fluid leaks from blood vessels into brain)
- Neurons lose normal structure and color staining (aka “tinctorial characteristics”)
> [Cells swell, and normal brain structure starts falling apart]
24–48 Hours
- Neutrophils (first responders) flood in
- Microglia and monocytes start converting into phagocytes (cleanup crew)
2–3 Weeks
- Macrophages dominate and become full of:
- Myelin debris
- Sometimes blood products (if any minor bleeding happened)
- These macrophages can stick around for months to years
~1 Week Onward
- Reactive astrocytes kick in (brain’s support cells trying to wall off the damage)
- They:
- Enlarge
- Divide
- Grow “arms” to surround the lesion
[Think of astrocytes forming a fence to contain the damage]
Months Later
- Astrocytes shrink back
- What’s left:
- Glial scar (mesh of glial fibers)
- New blood vessels
- Some connective tissue
🔁 Summary Pattern
- Early (hours to 2 days): Cell death and swelling
- Middle (days to 2 weeks): Inflammation, phagocytosis begins
- Late (weeks to months): Repair and scarring by astrocytes
Hypertensive Cerebrovascular Disease: How High Blood Pressure Damages the Brain
what are the Main complications of Hypertensive Cerebrovascular Disease:
- Lacunar infarcts
- Slit hemorrhages
- Hypertensive encephalopathy
- Massive hypertensive intracerebral hemorrhage
[All these happen because chronically high pressure damages small vessels in the brain]
What’s Lacunar infarcts and it’s usually location of occurance
- What it is: Small, deep infarcts caused by occlusion of small arteries.
- Where: Common in:
- Lenticular nucleus
- Thalamus
- Internal capsule
- Deep white matter
- Caudate nucleus
- Pons
[These are all deep brain areas with tiny arteries]
What’s it’s size, morphological and microscopic appearance?
- Size: Less than 15 mm
- Appearance: Small, cavity-like (“lake”) spaces on imaging or gross inspection.
- Microscopy: Shows tissue loss with gliosis (scarring by glial cells)
[Think of it like small “potholes” in the brain from blocked deep vessels]
What’s Slit Hemorrhages it’s morphological and microscopic appearance
- What it is: Small hemorrhages (bleeds) from ruptured small vessels.
- Over time: Bleeds are reabsorbed, leaving behind slit-like cavities.
- Appearance: Brownish discoloration from blood breakdown products.
- Microscopy:
- Tissue destruction
- Macrophages filled with pigment
- Gliosis
[Imagine tiny vessel bursts → mini-bleeds → body cleans up → leaves a scar]
What’s Hypertensive Encephalopathyit’s symptoms , postmortem and microscopic features
- What it is: A brain emergency from sudden, extreme BP rise (malignant hypertension).
- Symptoms:
- Headache
- Vomiting
- Confusion
- Seizures
- Coma
[The brain can’t regulate blood flow fast enough — it swells and malfunctions]
- Postmortem findings:
- Swollen (edematous) brain
- May show herniation (brain gets pushed into abnormal spaces)
- Microscopy:
- Petechial hemorrhages (tiny bleeds)
- Fibrinoid necrosis of arterioles
[Fibrinoid necrosis = vessel wall damage with protein leakage and inflammation]
Big Picture
Hypertension causes:
- Clogging (lacunar infarcts)
- Bursting (slit hemorrhages)
- Swelling and dysfunction (encephalopathy)
- Massive bleeds (not discussed here yet, but coming up)
