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FMS 3 > Pathology: abnormalities of blood supply > Flashcards

Pathology: abnormalities of blood supply Flashcards

1
Q

Localized edema vs. systemic edema

A
  • Localized: local disturbance of fluid exchange of a tissue. Results from: inflammation, allergic rxn, venous obstruction, lymphatic obstruction
  • Localized edema can lead to non-pitting
  • Systemic edema: increased retention of total body Na/water. Results from CHF, renal disease (protein loss-> proteinuria), decreased protein synthesis in liver (cirrhosis), malnutrition
  • Systemic edema can lead to subcutaneous pitting
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2
Q

Transudate vs. exudate

A
  • Transudate: noninflammatory edema due to increased hydrostatic pressure, decreased oncotic pressure, or lymphatic obstruction (no change in vascular permeability)
  • Sp. Grav 1.015
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3
Q

Hyperemia and congestion

A
  • Hyperemia (redness) due to arteriolar vasodilation, leads to more blood flow (can be from inflammation, exercise)
  • Congestion (cyanosis) due to impaired venous outflow. May be local (obstructed veins) or general (CHF)
  • Blood looks blue due to deoxygenation. If chronic may lead to necrosis via hypoxia
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4
Q

Pulmonary edema

A
  • Acute: due to sudden left ventricular failure (left-sided HF, MI) causing increased hydrostatic pressure (transudate)
  • Transudate forms in interstitium within alveoli, eventually spills into airways
  • Capillaries my rupture (hemorrhage)
  • Chronic: persistent milder hydrostatic pressure increase. Alveoli respond by developing thick, fibrotic septae
  • Airspaces may contain macrophages w/ hemosiderin (heart failure cells)
  • If there is massive infiltration by leukocytes it is pneumonia (causes exudate)
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5
Q

Liver congestion

A
  • Acute: may be secondary to shock or hepatic vein thrombosis. Central vein and sinusoids are distended w/ blood
  • Centrolobular hepatocytes more vulnerable to hypoxic injury
  • Chronic: due to right sided (ventricular) HF, obstruction of venous outflow. Causes centrilobular congestion (nutmeg liver)
  • Centrilobular hepatocytes often atrophy and necrose, focal hemorrhages may be seen
  • Periportal hepatocytes not affected, mid-lobular may have fatty change
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6
Q

Centrilobular fibrosis

A
  • Due to chronic centrilobular congestion
  • Centrilobules will become hypoxic, resulting in infarct and coagulative necrosis, inflammation, scarring
  • Scar in middle of centrilobe (where vein used to be) surrounded by unhealthy hepatocytes
  • Cirrhosis: normal hepatocytes surrounded by fibrosis (from alcoholism or hepatitis (not A), but not from centrilobular congestion
  • Can distinguish btwn arterial obstruction and venous obstruction by presence of RBCs (color of tissue)
  • If the middle is hepatocytes, and the outside is scar then it is cirrhosis (usually alcoholism)
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7
Q

Hemostasis

A
  • Arrest in blood flow (usually due to thrombosis, embolism, atherosclerosis, vascular spasms at site of injury)
  • Depends on 3 components: injured vessel wall, platelets, coagulation cascade
  • Vessel walls (endothelial cells, ECs) are anticoagulant, when injured they become procoagulant
  • Exposure to subendothelial collagen leads to platelet binding and activation. Platelets adhere to form primary platelet plug. Coagulation cascade begins
  • Coagulation cascade: 7 steps but last 2 steps are most critical. Prothrombin is converted to thrombin, which cleaves fibrinogen into fibrin (insoluble) which creates mesh within platelet plug (definitive platelet plug)
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8
Q

Factors of hemostasis

A

-Hemostasis is a balance btwn 3 pathways: coagulation, fibrinolytic (contains coagulation), and anticoagulation (regulates actions btwn coagulation and fibrinolytic pathways)

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9
Q

Hemorrhage

A
  • Escape of RBCs across intact vessels or from vascular rupture (can lead to shock)
  • Can be secondary to congestion and increased hydrostatic pressure
  • Other causes: bleeding disorders (coagulopathy), abnormalities in coagulation, fragile vessels
  • Also trauma: atherosclerosis, aneurysms, inflammation, erosion by tumors
  • Extensive hemorrhage cal lead to jaundice
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10
Q

Hematoma

A
  • Type of hemorrhage, localized blood within tissue
  • Petechiae: smallest (pin point)
  • Purpura: slightly larger
  • Eccymoses: subcutaneous (bruises)
  • Large accumulations (hemothorax)
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11
Q

Thrombosis

A
  • Due to dysregulation or imbalance btwn pro and anti coagulation
  • Not the same as blood clot
  • Thrombosis is result of coagulation cascade and platelet activation within CVS of living person. Blood clots from coagulation cascade only and develops in extravascular space after blood is spilled over
  • Thrombosis is often attached to underlying ECs, displays orderly layering of platelets, RBCs, fibrin. Blood clots are not attached to underlying ECs, display random ordering of RBCs and fibrin
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12
Q

Causes of thrombosis

A
  • Virchow’s triad: EC injury, stasis/turbulence of blood, hypercoagulativity
  • EC injury exposes subendothelial collagen (ECM) and leads to platelets adherence/aggregation
  • EC injury can be due to loss of EC, denudation of EC (atherosclerosis), disturbances of local pro/anti coagulation
  • Changes in blood flow (from laminar flow): laminar flow is cells/platelets flow in center of vessel and plasma along periphery
  • Deviation form this increases chance that platelets contact underlying vessel wall and thrombus formation
  • Hypercoagulativity: alteration in hemostatic regulation that predisposes to thrombus formation (both genetic and acquired)
  • Other causes: prolonged immobilization, obesity, smoking, oral contraceptives, cancer, surgery, pregnancy, platelet hyperreacivity, missing natural anticoagulants
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13
Q

Arterial thrombosis

A
  • Usually due to atherosclerosis, turbulence
  • Turbulence increases as plaque enlarges
  • Turbulence also arises at bifurcations
  • Most common sites of arterial thrombosis: coronary, cerebral, femoral arteries
  • Thrombi have points of attachment to underlying vessel/surface
  • Arterial thrombi grow in retrograde direction (against blood flow) and appear more compact and white (fewer RBCs) b/c they are under higher pressures
  • Venous thrombi grow with blood flow, are less compact and often more red (more RBCs) b/c they are formed under lower pressure
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14
Q

Atherogenesis (pt. 1)

A
  • Chronic inflammatory, fibroproliferative process that is a response to damage to ECs
  • Causes include: hyperlipidemia (mostly LDL), hypertension (most significant), DM, smoking, genetics, age, obesity, gender, infections
  • LDL extravasate through leaky/injured EC to sub endothelial space
  • Upon injury, EC activation causes decreased NO secretion, leading to vasoconstriction, and up regulation of adhesion molecules for leukocytes
  • This converts anticoagulative surface into a procoagulative one
  • In sub endothelial space, LDL is oxidized by macrophages, ECs, platelets or SMCs. Oxidized LDL has pro-atherogenic properties
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15
Q

Atherogenesis (pt. 2)

A
  • Monocytes and T cells migrate across endothelial into intima where they internalize LDL and become foam cells (also SMCs and circulating stem cells)
  • Ox-LDL leads to T cell activation, causing release of cytokines and chemokines, perpetuating a chronic inflammatory response and plaque development
  • Endothelial dysfunction: reduced NO secretion leads to vasoconstriction. Can also include more adhesion molecules on surface, enhanced permeability, increase in cyto/chemokines
  • Fibrous cap: SMCs migrate from media to intima to proliferate and synthesize ECM proteins. Contributes to stability of fibrous cap
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16
Q

Cardiac (mural) thrombi

A

-Usually not occlusive, may develop due to MI (endocardial damage + inflammation) which results in loss of contractility b/c of fibrosis
-Leads to stasis of blood flow
-Left atrial dilation usually due to chronic mitral (bicuspid) valve stenosis (narrowing of valve) leads to stenosis
-Atrial fibrillation often occurs w/ atrial dilation. Uncoordinated beat does not allow atrium to fully empty into ventricle (more stasis)
Valvular disease: thrombi form on leaflets of valves (vegetations)
-Aortic thrombi are result of atherosclerosis + aneurysm (balloon-like dilation)
-Cardiac and aortic thrombi may contain stripes of red (RBCs, called lines of zahn) and white (flatelets, fibrin, leukocytes), which indicates the thrombus occurred during blood flow (not post-mortem)

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17
Q

Venous thrombosis

A
  • Frequently originate w/in valves as they produce eddies and stagnant blood
  • 2 types: superficial venous thrombosis (SVT) and deep vein thrombosis (DVT)
  • DVTs are prone to embolization but SVTs are not (only DVTs are affected by skeletal muscle contraction)
18
Q

SVT

A
  • Usually occur in saphenous veins of leg (accompanied by varicose- enlargement)
  • Can be result of infection, trauma, IV catheters
  • Clinical features: localized pain, warmth, hyperemia, edema, tenderness
  • Varicose veins form b/c superficial leg veins not dependent on milking action of leg muscles, so gravity is main cause of stasis
  • Not prone to embolize
19
Q

DVT

A
  • Occur in deep veins (femoral, popliteal, posterior tibial) in leg
  • Highest concern in post-surgicl patients (surgery/hypercoagulability + immobilization)
  • May present as distended superficial veins and tenderness, warmth, edema, cyanosis
  • Most common complaint is calf pain
  • Deep veins are constantly milked by movement of leg muscles, thus immobilization greatly increases chance of DTV (causes stasis)
  • Grow in direction of blood flow, and may not be firmly attached to ECs
  • Tails are often freely mobile and prone to breaking loose
  • Invariably occlusive and may traverse long distances in vessels
  • Formed under low pressure and contain more RBCs then arterial thrombi (red thrombi)
  • Hemorrhagic infarction can occur when drainage of blood supply is halted due to venous thrombi. Backup of blood can lead to hemorrhage, edema, infarction
20
Q

Outcome of thrombi

A
  • Formation may be triggered by any of virchows triad (EC injury most important)
  • They may propagate, resolve, organize, or embolize
  • Propagation: accumulation of more fibrin and gets bigger
  • Dissolution: removal of thrombus by fibrinolytic system
  • Organization/recanalization: conversation to vascularized mass of scar tissue w/ potential to reestablish blood flow (recanalization requires vessels lined w/ EC)
  • Embolization: detachment and transport to a distant site in CVS
21
Q

Thrombolysis

A
  • Activation of fibrinolytic system causes fibrin to be broken down by hydrolysis
  • Plasmin breaks down the fibrin, but must be activated from its pro-nz form plasminogen
  • Tissue plasminogen activator (tPa) and/or streptokinase/urokinase can activate plasminogen
22
Q

DIC: Disseminated intravascular coagulation

A
  • A burst of systemic coagulation w/ intravascular fibrin deposition
  • Arises form some complication of an event triggering generalized coagulation
  • Forms extensive micro thrombi and consumes a lot of the total supply of fibrin, platelets, and coagulation factors
  • Identify DIC via increase in prothrombin/partial thromboplastin time (thrombocytopenia), positive D-dimer test, anemia
  • Depletion in clotting factors plus activation of fibrinolytic system makes patient susceptible to hemorrhage
23
Q

Causes of DIC

A
  • 1) release of thromboplastic substances into circulation, and 2) widespread injury to endothelial cells
  • Thromboplastic substances: thromboplastin (tissue-released factor due to injury), endotoxin sepsis, amniotic fluid, premature placental detachment, malignant tumors (pancreas, lung), trauma/necrosis (burns, surgery, brain damage)
  • Mechanisms that cause EC injury: trauma, infection, Ag-Ab complexes, temp extremes (burn/frostbite)
24
Q

Clinical presentation of DIC

A
  • Patients present thrombosis and hemorrhage
  • Microthrombi in brain, kidney, heart, lungs mostly, produce microinfarctions
  • Cause pulmonary edea and respiratory failure, convulsions and coma, renal failure, circulatory collapse
  • May show skin and mucous membrane bleeding, other hemorrhage
  • Anemia due to shearing of RBCs as they bass through the fibrin threads of the micro thrombi
  • DIC is usually acute (can be low-grade chronic in some cancers)
  • Rx is usually heparin (anticoagulant) with procoagulants (platelets, clotting factors)
25
Q

Emboli

A
  • Detached mass (solid, liquid, gas) that is carried through CVS until it is lodged in a vessel
  • Almost all are from thrombi, other sources: fat, atherosclerosis, bone marrow, amniotic fluid, gas, tumors, parasites, foreign objects
  • Arterial emboli cannot end up in venous circulation
  • Venous emboli cannot end up in arterial circulation, unless there is a patent foramen
  • These are paradoxical emboli, which travel through a patent foemen ovale
  • Whether an embolus causes infarction depends on site of embolization and collateral circulation
26
Q

Systemic thromboemboli

A
  • Thromboemboli in arterial circulation, from 5 major sources (first 3 most common): 1) left ventricular wall (mural) thrombi (most common), 2) left atrial wall (mural) thrombi, 3) valvular vegetations, 4) ulcerated atherosclerotic plaque, 5) aortic aneurysm
  • Most common destination are lower extremities (75%) and brain (10%)
  • Usually lead to infarction
27
Q

Pulmonary embolism

A
  • 95% of the time from DVT
  • Lodge in bifurcation of pulmonary trunk if big enough
  • Most are small enough to remain asymptomatic and are lysed
  • Whether or not infarction occurs is based on size of disrupted blood
  • Lung has dual blood supplies (bronchial and pulmonary arteries), but bronchial arteries supply most of the lung oxygen
  • Thus pulmonary emboli generally cause hemorrhage but not infarction
  • But when a patient has left-sided CHF these emboli may cause infarct b/c the sluggish flow to bronchial arteries may not be enough to sustain tissue (congestion of lung)
28
Q

Fat embolism

A
  • Usually from bone fractures where fatty marrow is released into circulation
  • May also be from subcutaneous fat due to trauma
  • Often see diffuse petechial rash, respiratory distress, anemia, thrombocytopenia, neuro symptoms (these begin 1-3 delayed)
  • Can also have whole chunks of bone marrow being mobilized
29
Q

Atheroma embolism

A
  • Necrotic lipid debris form inside a plaque due to rupture
  • Can be accidentally released due to medical procedures
  • Usually embolize to small arteries (usually in kidney, spleen, brain, bowel) and produce infarcts
  • Identifiable by cholesterol clefts
30
Q

Amniotic fluid embolism

A
  • Amniotic membrane rupture, can cause DIC
  • Cells of fetal origin can be found in embolism, including epithelial cells, hair, mucous droplets, and meconium (feces)
31
Q

Gas embolism

A
  • Can be due to medical care, penetrating injury, negative pressure in veins of head/neck/chest during inspiration
  • At sufficient volume, molecules coalesce to behave as a solid
  • Caisson syndrome (decompression sickness): resurfacing too quickly brings dissolved N gas from tissues into circulation where it can form bubbles and cause EC damage, platelet activation, cerebral and cardiac ischemia, pulmonary hemorrhage
32
Q

Ischemia

A
  • Can be localized (arterial/venous obstruction) or generalized (HF, shock)
  • Local ischemia usually from arterial obstruction, based on: collateral circulation, integrity of collateral arteries, rate of obstruction development, tissue susceptibility, metabolic rate of tissue
  • 2 major organs w/ dual blood supply are lungs and liver
33
Q

Chronic ischemia

A
  • Chronic ischemia (usually from encroaching atherosclerosis, often in coronary artery disease) will cause affected region to decrease O2 tension by forming new collateral vessels
  • Chronic myocardial ischemia: increased O2 demands results in transient ischemia (angina)
  • Ischemia during sleep (or low cardiac activities) is sign of impending MI
  • Chronic muscle ischemia (atherosclerosis) leads to calf pain
  • Chronic ischemia leads to parenchymal atrophy (brain, kidney, heart)
  • Only heart capable of angiogenesis in response
34
Q

Ischemia from venous obstruction

A
  • If there is collateral circulation (generally more than arterial) it must be blocked, insufficient to prevent ischemia, or peripheral leading to spill-over to necrotic area
  • Will cause infarct (red) due to capillary rupture, ischemia
  • Seen in renal vein and superior sagittal sinus veins
35
Q

Infarction

A
  • Necrosis due to ischemia, vast majority due to arterial thrombosis or embolism
  • Venous infarcts in renal and superior sagittal sinus veins
  • Infarcts can be red (hemorrhagic, venous) or white (non-hemorrhagic, arterial) and wedged or triangle (based on vasculature)
  • White (anemic) infarcts usually due to arterial obstruction in the heart, kidney, brain, spleen (poor collateral circulation)
  • Wedge infarct occur in organs w/ hilum (lung, kidney, spleen)
  • Shape of infarct does not indicate presence or absence of collateral circulation
36
Q

Shock and hypovolemic shock

A
  • Systemic reduction in tissue perfusion. Impacts: delivery of O2 and nutrients, removal of waste, thermoregulation
  • 3 kinds: hypovolemic, cardiogenic, generalized vasodilation
  • Hypovolemic: large loss in blood volume (hemorrhage, fluid loss like vomiting or diarrhea, plasma loss from burns)
37
Q

Cardiogenic shock

A
  • Failure of heart to pump, usually due to MI but can also be from: arrhythmia, IV septal rupture, ventricular free wall rupture
  • Ventricular free wall rupture causes blood to flow in pericardial space (cardiac tamponade) and prevents ventricles from contracting properly
  • May also occur from massive pulmonary embolism (right can’t pump hard enough)
38
Q

Generalized vasodilation (w/ anaphylactic and neurogenic shock)

A
  • 3 types: anaphylactic, neurogenic, septic shock
  • Anaphylactic: allergy hypersensitivity rxn (histamine, bradykinin, LT released by mast and basophil cells) that causes vascular permeability and exudate
  • Neurogenic shock: from CNS injury or anesthesia, impairs neural control of vasomotor tone leading to increased vasodilation
  • Does not lead to loss of fluid outside vessels, just redirected to periphery (reduced effective circulating doses)
39
Q

Septic shock

A
  • Infectious agents in blood cause host reaction
  • Often due to endotoxin from GN (LPS) on cell wall binding to macrophages/PMNs and causing release of TNF and IL1
  • Result is systemic vasodilation, decreased myocardial contraction, and EC damage that can lead to DIC
40
Q

Stages of shock

A
  • Compensation (nonprogressive): sympathetic reflex causes tachycardia and peripheral vasoconstriction (for vital organs). Have rapid, shallow berating, cold, clammy and cyanotic/pale skin, low BP
  • Impaired tissue perfusion (progressive): prolonged vasoconstriction impairs tissue perfusion, resulting in hypoxia
  • LA acidosis causes vasodilation, peripheral blood pooling, decreased cardiac output. Necrosis begins (first in renal tubules), then lung hypoxia w/ edema, hemorrhage hyaline fibrin membrane (shock lung), then intestine and liver fatty change, DIC may initiate
  • Decompression (irreversible): complete loss of vasoconstriction, kidney failure due to acute tubular necrosis
  • BP and cardiac output drop to critical, cerebral hypoxia causes brain dysfunction
  • Bowel ischemia may result in bacterial seeding of bloodstream w/ superimposed endotoxic shock
41
Q

Acute tubular necrosis

A
  • Patchy or variable necrosis
  • Some tubules are dead, some aren’t (can still see some nuclei but in others you can’t)
  • Not due to infarct (unless it was transient),
  • Shock is most common cause of acute tubular necrosis (glomeruli receive enough O2 and don’t usually die)

FMS 3 (20 decks)

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