1. What is a thrombus?

The passage defines a thrombus as a blood clot that forms within a blood vessel and
can obstruct blood flow. [ passage not specific on type of vessel]

2. Pathogenesis of thrombosis (Virchow's triad):

Virchow's triad refers to the three main factors that contribute to thrombosis:

• Endothelial injury: Damage to the inner lining of a blood vessel exposes

underlying tissues that can activate clotting factors and promote platelet
adhesion.
• Stasis or turbulent blood flow: Slow or irregular blood flow allows platelets
and clotting factors to come into contact with each other and form a clot,
particularly in areas of stasis.
• Hypercoagulability: An abnormally increased tendency of the blood to clot,
often caused by alterations in coagulation factors or inherited conditions.

The passage mentions that Virchow's triad is particularly important for arterial and
cardiac thrombosis, while hypercoagulability plays a more significant role in venous
thrombosis.

3. Difference between arterial and venous thrombi:

The passage doesn't directly compare arterial and venous thrombi, but it highlights
some key differences:

• Composition: Arterial thrombi are typically rich in platelets due to the high
flow rates in arteries. Venous thrombi may have more red blood cells due to
slower blood flow.
• Cause: Endothelial injury is a more frequent cause of arterial thrombosis,
while stasis is a major contributor to venous thrombosis.
• Location: Arterial thrombi can occur anywhere in the arterial system and
often obstruct critical vessels like coronary or cerebral arteries. Venous
thrombi most commonly form in the deep veins of the legs (deep vein
thrombosis) but can also occur in superficial veins.
• Consequences: Arterial thrombi can lead to serious consequences like
stroke or heart attack due to blockage of blood flow to vital organs. Venous
thrombi can cause pain, swelling, and the major concern is the risk of
pulmonary embolism if the clot dislodges and travels to the lungs.

4. Difference between ante-mortem and post-mortem clot:

• Antemortem thrombi:
o Often have visible lines of Zahn (pale platelet-fibrin deposits alternating
with darker red blood cell layers).
o Indicate the clot formed in flowing blood.
o Firm and focally attached to the vessel wall in venous thrombosis.
• Postmortem clots:
o Bland and non-laminated (no lines of Zahn).

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 o Gelatinous with a dark red dependent area (settled red blood cells) and
a yellow upper layer.
o Not typically attached to the vessel wall.

5. Morphology of thrombi:

General Features:

• Heterogeneous composition: Thrombi are a mix of various elements, with

the relative proportions influencing their characteristics.
• Fibrin network: A key component, fibrin forms a mesh that traps other
elements like platelets and blood cells.
• Lines of Zahn (arterial and venous thrombi): These are alternating layers
of pale platelet-fibrin and darker red blood cell rich regions, indicating
formation in flowing blood.
• Size and shape: Varies depending on location and cause.

Arterial Thrombi:

• Composition: Rich in platelets due to high flow rates in arteries.

• Structure: Often described as a "friable meshwork" containing:
o Platelets
o Fibrin
o Red blood cells
o Degenerating white blood cells
• Location: Frequently occlusive, blocking arteries like coronary, cerebral, and
femoral.
• Cause: Typically associated with ruptured atherosclerotic plaques but can
also form due to other vascular injuries.

Venous Thrombi (Phlebothrombosis):

• Composition: Tend to have more red blood cells and fewer platelets
compared to arterial thrombi due to slower venous flow.
• Structure: Often referred to as "red thrombi" or "stasis thrombi" due to the
high red blood cell content.
• Properties:
o Firm and focally attached to the vessel wall.
o May show lines of Zahn.
• Location: Most commonly occur in the lower extremities (90% of cases) but
can also develop in other veins

6. Mural thrombi:

• Location: Develops on the inner lining (endocardium) of the heart chambers

or within the large arteries (aorta) - mural refers to the "wall."
• Cause:

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 o Abnormal heart contractions (arrhythmias, dilated cardiomyopathy,
myocardial infarction).
o Endocardial injury (myocarditis, catheter trauma).
o Ulcerated atherosclerotic plaque or aneurysmal dilation of the aorta.
• Properties:
o Can be large and may impede blood flow.
o Prone to fragmentation and embolization (breaking off and traveling to
other organs).
• Example: A clot formed in the left ventricle of the heart due to a recent heart
attack.

7. Vegetation:

• Location: Develops on the surface of heart valves.

• Cause:
o Infective: Caused by bacteria or fungi adhering to previously damaged
valves (e.g., rheumatic heart disease).
o Sterile: Develop in people with hypercoagulable states (increased
clotting tendency) or on non-infected valves.
▪ Nonbacterial thrombotic endocarditis
▪ Libman-Sacks endocarditis (associated with lupus)
• Properties:
o Can be large and interfere with valve function.
o Infective vegetations may harbor bacteria and contribute to the spread
of infection throughout the body.
• Example: A vegetation on the aortic valve caused by bacterial endocarditis.

8. Phlebothrombosis (Venous thrombosis):

Phlebothrombosis is another term for venous thrombosis. The passage discusses

both superficial and deep vein thrombosis:

• Superficial venous thrombosis: Typically occurs in the saphenous veins of

the leg, often in association with varicose veins. Causes local swelling, pain,
and tenderness, but rarely embolize. However, they can increase the risk of
skin ulcers.
• Deep vein thrombosis (DVT): Occurs in the deep veins of the leg,
particularly above the knee. More serious than superficial clots because they
have a higher risk of embolizing to the lungs (pulmonary embolism). DVT can
be asymptomatic in up to 50% of cases.

9. Fate of a thrombus:

A thrombus can undergo several processes:

• Propagation: The clot can grow larger by accumulating additional platelets

and fibrin.

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 • Embolization: The clot can dislodge and travel through the bloodstream to
lodge in another vessel, potentially causing serious complications.
• Dissolution: Clot breakdown by the body's fibrinolytic system, which is more
effective for younger clots.
• Organization and recanalization: Over time, older thrombi can be infiltrated
by cells and eventually be replaced by connective tissue. In some cases,
channels may form within the clot, re-establishing some blood flow.

10. Saddle thrombus:

• Location: Lodges specifically at the aortic bifurcation (where the aorta splits
into the iliac arteries supplying the legs).
• Cause: Similar to other arterial thrombi, often caused by endothelial injury or
turbulence at the branching point.
• Properties:
o Due to its location, a saddle thrombus can obstruct blood flow to both
legs.
o Presents a high risk of limb ischemia (tissue death due to lack of blood
supply).
• Example: A blood clot formed at the aortic bifurcation due to a buildup of
plaque and turbulence in the blood flow.

Hyperemia and Congestion

1. Difference Between Hyperemia and Congestion:

• Hyperemia:
o Active process: Increased blood flow due to arteriolar dilation.
o Causes: Inflammation, exercise (increased skeletal muscle demand).
o Appearance: Red (erythema) due to oxygenated blood.
o Consequences: Generally minimal, but prolonged hyperemia can
damage tissues.
• Congestion:
o Passive process: Reduced venous outflow of blood.
o Causes: Cardiac failure, isolated venous obstruction.
o Appearance: Dusky reddish-blue (cyanosis) due to deoxygenated
blood.
o Consequences: Edema, ischemic injury, scarring, hemorrhage.

2. Chronic Venous Congestion (CVC):

• Definition: Long-standing impairment of venous blood flow from a tissue.
• Pathogenesis:
o Increased hydrostatic pressure in veins due to:
▪ Heart failure (systemic CVC)
▪ Localized venous obstruction (e.g., blood clot)
o Reduced venous return leads to capillary congestion and potentially:

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 ▪ Edema
▪ Ischemia (lack of oxygen)
▪ Cell death
▪ Scarring
▪ Hemorrhage (ruptured capillaries)
• Gross Features: Varies depending on the organ affected.
o Lungs (chronic pulmonary congestion): Brownish, firm due to
edema and fibrosis (scarring).
o Liver (chronic passive hepatic congestion - nutmeg liver): Red-
brown, slightly depressed areas alternating with tan, normal-looking
liver tissue.
• Microscopic Features:
o Congestion of capillaries and sinusoids.
o Hemorrhage (red blood cells leaking out).
o Hemosiderin deposits (breakdown products of red blood cells) in
macrophages (scavenger cells).
o Cell death and necrosis, particularly in areas furthest from oxygen
supply (e.g., centrilobular region in the liver).
o Fibrosis (scarring) in long-standing cases.

3. Acute Pulmonary Congestion:

• Causes: Sudden increase in hydrostatic pressure in the pulmonary veins.
o Common cause: Left-sided heart failure (heart can't pump blood
efficiently from the lungs).
o Other causes: Fluid overload, mitral stenosis (narrowing of heart
valve).
• Gross Morphology: Lungs appear heavy, wet, and may have frothy fluid due
to edema.
• Microscopic Features:
o Engorged (swollen) alveolar capillaries.
o Edema fluid in alveolar septa (tissue between air sacs).
o Focal intra-alveolar hemorrhage (bleeding into air sacs).

4. Congestive Splenomegaly:
• Enlargement of the spleen due to chronic venous congestion.
• Often occurs with portal hypertension (high blood pressure in the portal vein
that drains blood from the spleen).
• Can be caused by chronic liver disease, heart failure, or blood clots in the
splenic vein.

5. Hepatic Congestion (Acute and Chronic):

• Acute: Caused by sudden obstruction of hepatic veins or rapid blood flow
increase.
o Central vein and sinusoids (blood vessels) become distended.

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 o Centrilobular (central region) liver cells may undergo ischemic necrosis
due to lack of oxygen.
o Periportal (outer region) cells may show fatty changes.
• Chronic (passive hepatic congestion - nutmeg liver):
o Caused by long-standing impaired venous outflow, often due to right-
sided heart failure.
o Characterized by alternating red-brown, depressed centrilobular areas
and tan, normal-looking periportal areas.
o Microscopic features similar to chronic CVC in other organs.
• Nutmeg Liver: The characteristic appearance of chronic passive hepatic
congestion described above.
• Cardiac Cirrhosis: Severe consequence of chronic congestion leading to
extensive fibrosis (scarring) throughout the liver, disrupting its function.

Embolism
1. Embolus: A detached intravascular solid, liquid, or gaseous mass
that travels through the bloodstream from its origin to a distant site,
often causing tissue dysfunction or infarction (tissue death).
2. Types of Embolism According to Source:
o Thromboembolism (most common): Dislodged blood clots,
typically from deep vein thrombosis (DVT).
o Fat Embolism: Microscopic fat globules released from
fractured bones or soft tissue trauma.
o Air Embolism: Gas bubbles entering the bloodstream, often
during medical procedures or decompression sickness.
o Amniotic Fluid Embolism: Amniotic fluid and fetal material
entering the maternal circulation during childbirth.
o Cholesterol Embolism: Atherosclerosis debris breaking off
and traveling through the bloodstream.
o Tumor Embolism: Fragments of tumors detaching and
traveling in the bloodstream.
o Bone Marrow Embolism: Bone marrow elements entering the
bloodstream due to trauma.
o Foreign Body Embolism: Introduction of foreign objects into
the bloodstream.
3. Septic vs. Bland Emboli:
o Septic Embolism: An embolus containing infectious material
like bacteria or fungi, potentially causing infection at the lodged
site.
o Bland Embolism: An embolus not containing infectious
material, composed of blood clots, fat globules, air bubbles,
etc.
4. Systemic Thromboembolism:
o Source: Most commonly arise from intracardiac mural thrombi
(clots on the heart wall), often associated with left ventricular

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 wall infarcts or atrial fibrillation. Other sources include aortic
aneurysms, atherosclerotic plaques, and valvular vegetations.
o Consequences: Depend on the affected tissue and the
presence of collateral blood supply. Often leads to tissue
infarction (death) in organs like the brain (10%), intestines,
kidneys, spleen, and lower extremities (75%).
5. Paradoxical Embolism:
o A venous embolus (usually from DVT) that travels through a
heart defect (atrial or ventricular septal defect) into the arterial
circulation, bypassing the lungs and potentially lodging in the
brain or other organs.
6. Pulmonary Embolism (PE):
o Source: In over 95% of cases, originates from leg DVT.
Fragmented thrombi travel through the veins and right heart
before lodging in the pulmonary arteries.
o Predisposing Factors: Same as DVT risk factors - prolonged
immobilization, surgery, pregnancy, obesity, genetic
predisposition, etc.
o Clinical Presentations: Can be silent (small emboli) or cause
sudden death, acute right heart failure, or cardiovascular
collapse (large emboli). May also cause chest pain, shortness
of breath, coughing (with or without blood), and low oxygen
levels.
o Consequences and Complications:
▪ Obstruction of blood flow to lung tissue, leading to
hypoxia (lack of oxygen).
▪ Pulmonary hemorrhage (bleeding) in some cases, if
bronchial circulation is intact.
▪ Infarction (tissue death) in lung tissue with smaller
emboli.
▪ Pulmonary hypertension and right ventricular failure with
repeated emboli.
7. Fat Embolism:
o Microscopic fat globules, sometimes with bone marrow
elements, released into the bloodstream after fractures of long
bones or soft-tissue trauma (rare).
o Fat Embolism Syndrome (Symptomatic
form): Characterized by pulmonary insufficiency (difficulty
breathing), neurological symptoms (confusion, coma), anemia,
and low platelet count. Can be fatal in 5-15% of cases.
8. Amniotic Fluid Embolism:
o A rare but serious complication of childbirth, where amniotic
fluid and fetal material enter the maternal circulation.

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 oSymptoms: Sudden severe shortness of breath, bluish skin
(cyanosis), shock, neurological problems (headache, seizures,
coma), and disseminated intravascular coagulation (DIC -
widespread blood clotting).
o Mortality Rate: Up to 80%, with survivors often experiencing
permanent neurological deficits.
9. Air Embolism:
o Gas bubbles entering the bloodstream, often during medical
procedures (neurosurgery, central line insertion) or due to
negative pressure gradients.
o Can cause air bubbles to lodge in the brain (causing mental
impairment or coma) or lungs (leading to respiratory distress).
o Large volumes of air (>100 mL) can be fatal in the pulmonary
circulation.
10. Decompression Sickness (Caisson Disease):

Decompression Sickness (Caisson Disease) in

Detail:
Decompression sickness, also known as caisson disease, arises from rapid
decompression and formation of gas bubbles within the body tissues and
bloodstream. Here's a breakdown of the key points:

Cause:

• Occurs when individuals experience a sudden decrease in atmospheric

pressure. This is most common in scuba divers and underwater construction
workers who ascend too quickly after being exposed to high pressure
environments.
• During high pressure (e.g., deep dives), increased amounts of gas,
particularly nitrogen, dissolve in the blood and tissues.
• If ascent (decompression) happens too rapidly, the dissolved nitrogen comes
out of solution and forms gas bubbles.

Symptoms:

The location and size of the gas bubbles determine the specific symptoms, which
can range from mild to life-threatening:

• The Bends (Musculoskeletal): The most common manifestation. Pain

develops in muscles and joints, often described as a bending or aching
sensation, due to bubbles forming in these areas.
• Chokes (Respiratory): Bubbles lodge in the lungs, causing difficulty
breathing, cough (may be bloody), and chest pain.
• Neurological symptoms: Bubbles in the brain or spinal cord can lead to
dizziness, weakness, numbness, tingling, vision problems, confusion, or even
coma.

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 • Other: Skin mottling, fatigue, and dizziness can also occur.

Infarct:
Infarct: An area of tissue death (necrosis) caused by insufficient blood flow due to
either blockage of the arterial supply or obstruction of venous drainage.

Infarct Classification:
A. Based on Color:

• Red Infarct (Hemorrhagic):

o Occurs with venous occlusions, loose tissues (lungs), dual circulation
tissues (lungs, intestines), previously congested tissues, or re-
established flow to a previously occluded area.
o Blood can seep into the infarcted zone, causing a reddish appearance.
• White Infarct (Anemic):
o Occurs with arterial occlusions in solid organs with limited blood supply
(heart, spleen, kidneys).
o Tissue density prevents blood seepage from surrounding areas,
resulting in a pale appearance.

B. Based on Presence or Absence of Infection:

• Septic Infarct:
o Develops when infected material (e.g., from heart valve vegetations)
seeds the necrotic tissue.
o Involves a more prominent inflammatory response as the infarct
transforms into an abscess.
• Bland Infarct:
o No associated infection. The infarct undergoes a typical organization
process with scar formation.

Red vs. White Infarct:

Here's a table summarizing the key differences between red and white infarcts:

Feature Red Infarct White Infarct

Cause of Venous occlusion, loose Arterial occlusion in solid organs
Infarction tissues, dual circulation with end-arterial circulation

Color Reddish due to blood Pale due to limited blood seepage

seepage

Examples Lung, small intestine (with Heart, spleen, kidney

dual circulation)

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 Blood Supply to Some blood may flow from Limited blood flow to the infarcted
Infarct surrounding areas zone

Shock
1. Define shock: Shock is a life-threatening condition where inadequate blood
flow to tissues results in cellular hypoxia (oxygen deficiency). Initially, this
cellular injury is reversible, but prolonged shock can lead to irreversible tissue
damage and death.
2. Etiological classification of shock: There are three main types of shock
based on the cause:
o Cardiogenic shock: Results from low cardiac output due to heart
problems like myocardial infarction (heart attack), arrhythmias (irregular
heartbeat), or heart muscle weakness.
o Hypovolemic shock: Occurs due to low blood volume, often from
severe hemorrhage (bleeding) or fluid loss from burns.
o Septic shock: A complication of sepsis, a life-threatening condition
caused by a dysregulated response to infection. It involves widespread
inflammation, vascular abnormalities, and tissue hypoxia.
3. Hypovolemic shock:
o Pathogenesis: Reduced blood volume leads to decreased cardiac
output (blood pumped by the heart per minute). The body tries to
compensate through reflex mechanisms like increased heart rate,
vasoconstriction (narrowing of blood vessels), and release of hormones
to retain fluids.
o Causes: Severe bleeding, extensive burns, dehydration from severe
diarrhea or vomiting.
o Clinical presentation: Hypotension (low blood pressure), rapid and
weak pulse, rapid breathing, cool, pale or clammy skin, anxiety, and
weakness.
4. Cardiogenic shock:
o Causes: Myocardial infarction (heart attack), severe heart failure,
arrhythmias, valve problems.
5. Neurogenic shock:
o Causes: Spinal cord injury, severe pain, severe allergic reactions.
o Pathogenesis: Disruption of nerve signals controlling blood vessel
tone leads to widespread vasodilation and pooling of blood, decreasing
blood pressure and cardiac output.
6. Anaphylactic shock:
o Pathogenesis: A severe allergic reaction involving the release of
massive amounts of inflammatory chemicals. These chemicals cause
widespread vasodilation, bronchoconstriction (narrowing of airways),
and increased vascular permeability (fluid leakage from vessels),
leading to shock.
7. Septic shock (brief description with flowchart):
o Causes: Bacterial, fungal, or parasitic infections.

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 o Pathogenesis:
▪ Microbial components trigger an inflammatory response.
▪ Inflammatory mediators cause vasodilation, vascular leakage,
and microvascular dysfunction.
▪ Activation of coagulation cascade leads to disseminated
intravascular coagulation (DIC), formation of blood clots within
small vessels.
▪ Cellular hypoxia and metabolic derangements occur due to
impaired blood flow and oxygen delivery.
▪ Organ failure can develop in severe cases.

Flowchart (simplified):

Infection -> Inflammatory response -> Vasodilation, vascular leakage,

microvascular dysfunction -> DIC -> Cellular hypoxia, metabolic
derangements -> Organ failure (possible) -> Shock

. Stages of Shock

Shock is a progressive disorder that leads to death if the underlying problems are not
addressed. The exact mechanisms of shock-related death are still unclear, but the
process typically follows three general stages:

• Non-progressive stage (compensatory stage):

o In the initial stage, the body activates reflex mechanisms to maintain
blood pressure and vital organ perfusion despite the underlying cause
of shock.
o These mechanisms include:
▪ Increased heart rate (tachycardia) to pump more blood.
▪ Vasoconstriction (narrowing) of blood vessels in non-essential
areas like the skin to redirect blood flow to vital organs like the
brain and heart.
▪ Release of hormones like epinephrine (adrenaline) to stimulate
these effects.
▪ Activation of the renin-angiotensin-aldosterone system to
promote fluid retention by the kidneys.
o Due to these compensatory mechanisms, blood pressure and vital
organ perfusion might be maintained in this early stage.
• Progressive stage:
o If the underlying cause of shock persists, the body's compensatory
mechanisms become overwhelmed.
o Tissue hypoperfusion (reduced blood flow to tissues) starts to occur,
leading to cellular hypoxia (oxygen deficiency).
o This stage is characterized by:
▪ Widespread lactic acid production due to anaerobic metabolism
(energy production without oxygen) in oxygen-starved cells.
▪ Metabolic acidosis (increased blood acidity) due to lactic acid
accumulation.
▪ Further deterioration of blood pressure.

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 ▪ Potential for organ dysfunction as organs are not receiving
enough oxygenated blood.
• Irreversible stage:
o In the most severe stage, cellular and tissue injury becomes so severe
that even if the underlying cause is corrected, organ failure and death
can occur.
o This stage involves:
▪ Widespread cell death and damage in various organs.
▪ Release of harmful lysosomal enzymes from damaged cells,
further aggravating tissue injury.
▪ Potential for disseminated intravascular coagulation (DIC), a
condition where widespread blood clots form within small
vessels, further compromising blood flow.

9. Morphological Changes in Shock (Different Organs)

Shock can cause widespread cellular damage due to hypoxia (lack of oxygen) in
various organs. The severity of damage depends on the duration and severity of
shock. Here's a breakdown of potential changes in some organs:

• Brain: Brain cells are highly sensitive to oxygen deprivation. Shock can lead
to neuronal death, which can manifest as confusion, coma, and even death.
• Heart: Myocardial cells (heart muscle cells) can die due to hypoxia, leading to
weakened heart contractions and further compromising blood flow.
• Kidneys: Acute tubular necrosis (damage to kidney tubules) can occur,
leading to kidney failure and electrolyte imbalances.
• Adrenals: Adrenal glands may show signs of stress and depletion of
hormones.
• Gastrointestinal tract: The gut lining can become damaged, increasing the
risk of bacterial translocation (movement of bacteria from the gut into the
bloodstream) and sepsis.

10. Clinical Features of Shock

Clinical features of shock can vary depending on the type and severity of shock.
However, some common signs and symptoms include:

• Hypotension (low blood pressure): This is a hallmark sign of shock, but it

can sometimes be present late in the course.
• Rapid and weak pulse: The heart tries to compensate by pumping faster, but
the pulse may be weak due to decreased cardiac output.
• Rapid breathing (tachypnea): The body attempts to increase oxygen intake
to compensate for cellular hypoxia.
• Altered mental status: Confusion, lethargy, agitation, and coma can occur
due to decreased blood flow to the brain.
• Cool, pale, or clammy skin: Reduced blood flow to the skin leads to
coolness and pallor. In some cases, particularly septic shock, the skin may
initially be flushed due to vasodilation.
• Other signs: Depending on the type of shock, there might be additional
symptoms like nausea, vomiting, diarrhea, or severe pain.

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