hemodynamics

Question 1

edema/effusions

Answer 1

-Normal: hydrostatic pressure pushes water and salts out of capillaries into interstitial space; nearly balanced by tendency of plasma colloid osmotic pressure to pull water and salts back into vessels
-!!!!Elevated hydrostatic pressure or diminished colloid osmotic pressure disrupts balance, resulting in increased movement of fluid out of vessels!
-If net rate of fluid movement > rate of lymphatic drainage, fluid accumulates!
-Within tissues result is edema!
-If a serosal surface is involved, fluid may accumulate within the adjacent body cavity as an effusion!

Question 2

pathophysiologic categories of edema

Answer 2

-Increased hydrostatic pressure
-Impaired venous return (e.g., ascites (cirrhosis), congestive heart failure)
-Arteriolar dilation (e.g., heat)
-Reduced plasma osmotic pressure (hypoproteinemia): caused by decreased synthesis or increased loss of albumin from circulation
-Reduced albumin synthesis: severe liver diseases (cirrhosis), protein malnutrition
-Albumin loss: nephrotic syndrome - albumin leaks into urine through abnormally permeable glomerular capillaries
-Lymphatic obstruction: Trauma, fibrosis, invasive tumors, post-surgery, post-radiation and infectious agents - disrupt lymphatic vessels/impair clearance of interstitial fluid: resulting in lymphedema
-Sodium retention – Increased salt retention—with retention of associated water—causes both increased hydrostatic pressure (due to intravascular fluid volume expansion) and diminished vascular colloid osmotic pressure (due to dilution
-e.g., excessive salt intake with renal insufficiency, increased tubular reabsorption of sodium, renal hypoperfusion, increased renin-angiotensin-aldosterone secretion
-Inflammation

Question 3

congestive HF

Answer 3

-INCREASED VENOUS PRESSURE DUE TO HEART FAILURE
-Decreased renal perfusion results in activation of renin-angiotensin-aldosterone axis (sodium retention)
-Early: beneficial (retention of sodium and water and other adaptations, including increased vascular tone and elevated levels of antidiuretic hormone): improve cardiac output and restores normal renal perfusion
-As heart failure worsens and cardiac output diminishes, retained fluid increases hydrostatic pressure, leading to edema and effusions

Question 4

hepatic ascites

Answer 4

-PORTAL HTN
-HYPOALBUMINEMIA
-portal htn causes edema of organs and tissues within portal circulation- splenomegaly, hepatomegaly
-hypoalbuminemia may cause systemic edema

Question 5

renal edema

Answer 5

-SODIUM RETENTION
-PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)

Question 6

EDEMA

Answer 6

-Subcutaneous edema: distribution influenced by gravity (e.g., appears in legs when standing and sacrum when recumbent), aka, dependent edema
-Finger pressure over markedly edematous subcutaneous tissue displaces interstitial fluid and leaves a depression, aka pitting edema
-Edema resulting from renal dysfunction often appears initially in parts of the body containing loose connective tissue (e.g., eyelids); periorbital edema is characteristic finding in severe renal disease
-With pulmonary edema, lungs often 2 – 3 X their normal weight; sectioning yields frothy, blood-tinged fluid— mixture of air, edema, and extravasated red cells (heart failure)
-Cerebral edema: localized or generalized; swollen brain shows narrowed sulci and distended gyri, compressed by skull – herniation may occur
-ANASARCA - general swelling of the whole body, can occur when tissues of the body retain too much fluid

Question 7

brain herniation

Answer 7

1) Falx
2) Hippocampal cingulate gyrus
3) Cerebellar tonsillar
-dont need to know

Question 8

effusions

Answer 8

-Effusions may involve:
-pleural cavity (hydrothorax)
-pericardial cavity (hydropericardium)
-peritoneal cavity ( hydroperitoneum or ascites)
-Transudative effusions: typically protein-poor, translucent, and straw colored
-Exudative effusions: protein-rich and often cloudy due to the presence of white cells

Question 9

transudate vs exudate

Answer 9

-Transudate
-results from disturbance of Starling forces
-specific gravity < 1.012
-protein content < 3 g/dl, LDH LOW
-Exudate
-results from damage to the capillary wall
-specific gravity > 1.012
-protein content > 3 g/dl, LDH HIGH

Question 10

edema review

Answer 10

-Edema: result of movement of fluid from vasculature into interstitial spaces; the fluid may be protein-poor (transudate) or protein-rich (exudate)
-Edema may be caused by:
-Increased hydrostatic pressure (e.g., heart failure)
-Decreased colloid osmotic pressure caused by reduced plasma albumin, either due to decreased synthesis (e.g., liver disease, protein malnutrition) or to increased loss (e.g., nephrotic syndrome)
-Increased vascular permeability (e.g., inflammation)
-Lymphatic obstruction (e.g., infection or neoplasia)
-Sodium and water retention (e.g., renal failure)

Question 11

hyperemia vs congestion

Answer 11

-Hyperemia: active process - arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow; affected tissues turn red (erythema) because of increased delivery of oxygenated blood
-Congestion: passive process - reduced venous outflow of blood from a tissue; may be systemic (e.g., cardiac failure), or localized
-Congested tissues: abnormal blue-red color (cyanosis) from accumulation of deoxygenated hemoglobin in affected area
-As a result of increased hydrostatic pressures, congestion commonly leads to edema

Question 12

pulmonary edema

Answer 12

-pulmonary capillary pressure exceeds plasma colloid osmotic pressure
-Vessel borders become progressively hazier because of increasing extravasation of fluid into the interstitium.

Question 13

heart failure

Answer 13

-Heart failure cells are hemosiderin laden macrophages (broken down blood)
-in the lungs
-Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst.

Question 14

acute/chronic passive congestion: liver

Answer 14

-nutmeg liver
-aka “NUTMEG” liver - associated with necrosis in the CENTRAL part of the hepatic lobule.

Question 15

hemostasis

Answer 15

Physiologic blood clot at sites of vascular injury
-1. Arteriolar Vasoconstriction
-2. Primary Hemostasis (Platelet Plug) - adhesion, shape change, secretion of granules to induce aggregation, recruitment, aggregation
-3. Secondary Hemostasis (Coagulation Cascade)
-4. Clot Stabilization and Anti-Thrombotic Events
-Following a vascular injury:
-platelets adhere and aggregate to form primary hemostatic plug
-also promote key reactions in the coagulation cascade that lead to secondary hemostasis and formation of a fibrin clot

Question 16

thrombosis

Answer 16

Pathologic blood !clot within blood vessels or within! chambers of the heart

Question 17

hemorrhage

Answer 17

Excessive bleeding when hemostatic mechanisms are blunted, insufficient or defective
-EXTRAVASATION beyond vessel
-HEMATOMA (implies MASS effect)
-PETECHIAE (1-2 mm) (PLATELETS)
-PURPURA <1cm
-ECCHYMOSES >1cm (BRUISE)
-HEMO-: -thorax, -pericardium, -peritoneum, -arthrosis

Question 18

petechiae vs purpura vs ecchymossi

Answer 18

-Petechiae: 1-2 mm minute hemorrhage (1°) -> platelets
-Purpura: ≥3mm hemorrhage
-Ecchymosis or bruise: ≥1cm hemorrhage (2°)
-bigger- worry about coagulation factors
-dont memorize size

Question 19

hemostasis process: primary

Answer 19

-Involves platelets, clotting factors, and endothelium - at site of vascular injury; results in formation of a blood clot, to prevent/limit extent of bleeding
-Arteriolar vasoconstriction occurs immediately, greatly reduces blood flow to injured area - mediated by reflex neurogenic mechanisms; TRANSIENT
-Primary hemostasis: formation of the platelet plug
-!!Disruption of endothelium exposes subendothelial von Willebrand factor (vWF) and collagen, which promote platelet adherence and activation
-!!Activation of platelets results in dramatic shape change and release of secretory granules
-Within few minutes, secreted products recruit additional platelets that undergo aggregation to form a primary hemostatic plug !

Question 20

hemostasis: secondary

Answer 20

-Secondary hemostasis: deposition of fibrin; consolidates/stabilize initial platelet plug
-Vascular injury exposes tissue factor at site of injury
-What is tissue factor? membrane-bound procoagulant glycoprotein
-!!Tissue factor binds and activates factor VII resulting in coagulation cascade leading to thrombin generation
-Thrombin cleaves circulating fibrinogen into insoluble fibrin, creating a fibrin meshwork;
-Clot stabilization and resorption: Polymerized fibrin and platelet aggregates undergo contraction: form a solid, permanent plug that prevents further hemorrhage
-To limit clotting to injury site and eventual clot resorption: counterregulatory mechanisms(e.g., tissue plasminogen activator [t-PA]

Question 21

endothelium

Answer 21

-NORMALLY:
-ANTIPLETELET PROPERTIES
-ANTICOAGULANT PROPERTIES
-FIBRINOLYTIC PROPERTIES
-IN INJURY:
-PRO-COAGULANT PROPERTIES
-ACTIVATED by:
-Trauma
-INFECTIOUS AGENTS
-Hemodynamic forces
-Pro-inflammatory mediators

Question 22

platelets

Answer 22

-After traumatic vascular injury, platelets encounter parts of the subendothelial connective tissue, such as vWF and collagen
-On contact with these proteins, platelets undergo sequence of reactions that end in the formation of a platelet plug
-you can have enough platelets but have quality of platelet issues

Question 23

different disease (dont need to know)

Answer 23

-Gplb- no adhesion
-bernard soulier syndrome- no aggregation

Question 24

platelets: sequence: platelet adhesion (she barely went over this)

Answer 24

-Platelet adhesion: mediated by interactions between platelet surface receptor glycoprotein Ib (GpIb) and vWF in the subendothelial matrix;
-!!!!!!!Genetic deficiencies of vWF (von Willebrand disease) or GpIb (Bernard-Soulier syndrome) result in bleeding disorders (dont need to know this until we learn about this disease)
-Platelets rapidly change shape after adhesion - from smooth discs to spiky cells with increased surface area
-Secretion (release reaction) of granule contents occurs with changes in shape; (together referred to as platelet activation)

Question 25

platelets sequence: platelet activation (she barely went over this)

Answer 25

-Platelet activation - triggered by factors, including the coagulation factor thrombin and ADP
-Thrombin activates platelets
-ADP is a component of dense-body granules; platelet activation and ADP release causes more platelet activation, aka recruitment
-Activated platelets also produce the prostaglandin thromboxane A 2 (TxA 2 ), potent inducer of platelet aggregation
-Note: Aspirin, inhibits platelet aggregation and produces mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme required for TxA 2 synthesis

Question 26

platelet sequence: platelet aggregation (dont need to know)

Answer 26

-Platelet aggregation follows activation
-Conformational change in glycoprotein IIb/IIIa that occurs with platelet activation allows binding of fibrinogen (forms bridges between adjacent platelets, leading to their aggregation)
-!!!!!Inherited deficiency of GpIIb-IIIa results in a bleeding disorder called Glanzmann thrombasthenia
-!!!Activation of thrombin stabilizes platelet plug by causing further platelet activation and aggregation, and promoting irreversible platelet contraction
-Platelet contraction depends on the cytoskeleton: consolidates aggregated platelets
-Thrombin also converts fibrinogen into insoluble fibrin, cementing platelets in place and creating the definitive secondary hemostatic plug

Question 27

coagulation cascade (she didnt go over this)

Answer 27

-Series of amplifying enzymatic reactions that lead to deposition of an insoluble fibrin clot
-Each reaction step involves:
-an enzyme (an activated coagulation factor)
-a substrate (an inactive proenzyme form of a coagulation factor),
-a cofactor (a reaction accelerator)
-Assembled on a negatively charged phospholipid surface, provided by activated platelets
-Assembly of reaction complexes also depends on calcium, which binds to γ-carboxylated glutamic acid residues present in factors II, VII, IX, and X
-Note: the enzymatic reactions that produce γ-carboxylated glutamic acid use vitamin K as a cofactor and are antagonized by drugs such as coumadin, an anticoagulant.

Question 28

intrinsic vs extrinsic pathway

Answer 28

-Intrinsic pathway: activated by damage inside vasculature. Platelets, exposed/damaged endothelium,
subendothelial collagen, and other chemicals activate this arm of pathway
-Slower than extrinsic pathway, thought to generate a more robust coagulation response
-slower but more robust
-8 (hemophilia) ,9,11,12
-if PTT is prolonged -> problem is here
-Extrinsic pathway: activated by trauma that causes blood to leave vasculature. Tissue thromblastin factor is activated and sets off cascade
-Quicker than the intrinsic pathway
-most diseases have problems here
-high PT
-PT is prolonged -> factor 7 problem

Question 29

summary

Answer 29

-PT and PTT are prolonged in liver failure

Question 30

bleeding disorders: hemorrhagic diatheses: clinical lab tests

Answer 30

-Prothrombin time (PT): assesses extrinsic and common coagulation pathways
-Prolonged PT: deficiency/ dysfunction of factor V, factor VII, factor X, prothrombin, or fibrinogen
-Partial thromboplastin time (PTT): assesses intrinsic and common clotting pathways )
-Prolonged PTT: deficiency/dysfunction of factors V, VIII, IX, X, XI, or XII, prothrombin, or fibrinogen, or interfering antiphospholipid antibodies
-INR: International normalized ratio (INR) - calculation based on results of PT, used to monitor patients being treated with warfarin (anticoagulant)

Question 31

platelet counts/tests of platelet function

Answer 31

-Platelet counts: reference range: 150.000 - 350,000 platelets/µL
-Tests of platelet function:
-tests of platelet aggregation (measure ability of platelets to adhere to one another in response to agonists);
-quantitative and qualitative tests of von Willebrand factor
-Bleeding time – older test, not used much anymore
-Blood Smear: # platelet, size, and shape
-Bone Marrow Biopsy: Megakaryocytes

Question 32

disseminated intravascular coagulation

Answer 32

-Acute, subacute, or chronic thrombohemorrhagic disorder with excessive activation of coagulation and formation of thrombi in microvasculature
-Occurs as secondary complication of many disorders
-problems with platelets and factors
-platelets are busy making thrombi
-consumptive coagulopathy - platelets and factors are being consumed
-Consumption of platelets, fibrin, and coagulation factors and, secondarily, activation of fibrinolysis
-Signs and symptoms relate to tissue hypoxia and infarction caused by microthrombi; hemorrhage (because of depletion of factors and activation of fibrinolytic mechanisms; or both)
-Not a primary disease; acquired coagulopathy from different conditions!!!!!
-MC associated with obstetric complications, malignant neoplasms, sepsis, and major trauma
-Endotoxins from bacterial infections
-Massive trauma, extensive surgery, and severe burns: release of procoagulants (e.g., tissue factor)
-Obstetrics: procoagulants from placenta, dead retained fetus, or amniotic fluid may enter circulation
-Hypoxia, acidosis, and shock (often in very ill patients), also cause widespread endothelial injury
-Acute promyelocytic leukemia and adenocarcinomas of lung, pancreas, colon, and stomach most frequently associated with DIC

Question 33

consequences of DIC

Answer 33

-fibrin and platelets are deposited everywhere
-clots are forming everywhere
-Widespread deposition of fibrin within microcirculation: leads to ischemia of vulnerable organs and !!!microangiopathic hemolytic anemia!!!! (from fragmentation of rbcs as they squeeze through narrowed microvasculature)
-RBCs break up (become schistocytes) and burst when trying to get through all the clots -> anemia, thrombocytopenia
-Consumption of platelets and clotting factors and activation of plasminogen; leads to bleeding
-bleeding and clotting disease at the same time
-FIX THE UNDERLYING CAUSE
-Thrombi: in brain, heart, lungs, kidneys, adrenals, spleen, and liver (decreasing order of frequency) and other organs
-Many fibrin thrombi may be in alveolar capillaries, sometimes associated with pulmonary edema and fibrin exudation
-CNS: fibrin thrombi may cause microinfarcts

Question 34

common lab findings in DIC

Answer 34

-Low platelet count
-Prolonged PT / PTT
-Low fibrinogen (Can be elevated – Acute phase reactant)
-High levels of split products (Fibrinogen) and D-dimer (Fibrin)
-Decreased Factor V and Factor VIII
-Microangiopathic anemia – RBC damaged by fibrin thrombi (schistocytes aka helmet cells)

Question 35

thrombosis

Answer 35

-Pathogenesis
-Endothelial Injury
-Alterations in Flow
-Hypercoagulability
-Morphology
-Fate
-Clinical Correlations
-Venous
-Arterial (Mural)

Question 36

virchow triad in thrombosis

Answer 36

-Endothelial integrity most important factor
-Injury to endothelial cells changes local blood flow and affects coagulability.
-Abnormal blood flow (stasis or turbulence), can cause endothelial injury
-3 major risk factors for thrombosis: virchows
-1. Endothelial Injury
-Atherosclerosis / Hypercholesterolemia / Inflammation
-HTN / Vasculitis / Diabetes
-Toxins (Cigarette smoke) / Elevated Homocysteine
-2. Abnormal Blood Flow
-Stasis / Turbulence
-3. Hypercoagulable State
-Primary (genetic) or Secondary (acquired) disorders
-pregnancy, abnormal blood flow

Question 37

endothelial injury (barely went over)

Answer 37

-Severe endothelial injury exposes vWF and tissue factor: may trigger thrombosis
-endothelial injury causes abnormal clots
-Inflammation promotes thrombosis: shifts gene expression in endothelium to “prothrombotic.” (i.e., endothelial activation or dysfunction) – causes include:
-physical injury
-infectious agents
-abnormal blood flow
-inflammatory mediators
-metabolic abnormalities (e.g.,hypercholesterolemia or homocystinemia)
-toxins absorbed from cigarette smoke
-Procoagulant changes: endothelial cells activated by inflammatory cytokines downregulate expression of thrombomodulin, enhancing procoagulant and pro-inflammatory actions of thrombin
-Antifibrinolytic effects: activated endothelial cells secrete plasminogen activator inhibitors (PAIs) (limit fibrinolysis) – favors development of thrombi

Question 38

turbulence- abnormal blood flow

Answer 38

-Turbulence contributes to arterial and cardiac thrombosis by causing endothelial injury/ dysfunction and forming countercurrents (contribute to stasis)
-turbulence cause abnormal clots
-Turbulence and stasis:
-Promote endothelial activation, enhancing procoagulant activity and wbc adhesion
-Disrupt laminar flow: bring platelets into contact with endothelium
-Examples:
-Ulcerated atherosclerotic plaques expose subendothelial vWF and tissue factor, (also cause turbulence)
-Aneurysms result in local stasis
-Acute myocardial infarction - areas of noncontractile myocardium associated with stasis and flow abnormalities (promote formation of cardiac mural thrombi)

Question 39

hypercoagulability

Answer 39

-Hypercoagulability: abnormal tendency of blood to clot, usually caused by changes in coagulation factors; important in venous thrombosis - divided into primary (genetic) and secondary (acquired) disorders
-Primary include:
-Factor V Leiden (common)
-Prothrombin gene mutation (common)
-Elevated levels of homocysteine
-Rare inherited causes of primary hypercoagulability: deficiencies of anticoagulants (e.g., antithrombin III, protein C, or protein S) -
-Classically present with recurrent DVTs or DVT at young age (adolescence or early adulthood)

Question 40

hypercoagulability (acquired/secondary)

Answer 40

-Prolonged bed rest or immobilization
-Myocardial infarction
-Atrial fibrillation
-Tissue damage (surgery, fracture, burns)
-Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis)
-Prosthetic cardiac valves
-Disseminated intravascular coagulation
-Heparin-induced thrombocytopenia
-Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)
-Lower risk for thrombosis:
-Cardiomyopathy
-Nephrotic syndrome
-Hyperestrogenic states (pregnancy)
-Oral contraceptive use
-Sickle cell anemia
-Smoking, Obesity

Question 41

pathology of thrombosis

Answer 41

-Thrombi – gross and microscopic lines of Zahn, pale platelet and fibrin deposits alternating with darker red cell–rich layers; indicate thrombus formed in flowing blood (antemortem); versus bland, non-laminated, postmortem clots
-Thrombi in heart chambers or in aortic lumen aka mural thrombi; especially seen in abnormal myocardial contraction (arrhythmias, dilated cardiomyopathy, myocardial infarction)
-Arterial thrombi often occlusive; most common sites: coronary, cerebral, and femoral arteries (decreasing order of frequency)
-Venous thrombosis (phlebothrombosis) almost always occlusive; thrombus forms long luminal cast - forms in sluggish venous circulation, contains more enmeshed red cells (fewer platelets) aka red thrombi or stasis thrombi; firm, focally attached to vessel wall, contain lines of Zahn; veins of lower extremities most commonly involved (90% of cases)
-Postmortem clots - gelatinous with dark-red dependent portion (red cells settled by gravity) and yellow “chicken fat” upper portion

Question 42

pathology of thrombosis: lines of zahn

Answer 42

Pale -Platelet and Fibrin
Dark - RBC’s and Fibrin
clot is PRE-mortem
-Venous Thrombus – Stasis leads to “Red Thrombi” – More RBCs and less platelets

Question 43

post mortem clot: non laminated (no lines of zahn)

Answer 43

-Gelatinous with dark red dependent portion and yellow “chicken fat” upper portion
-Chicken fat/currant jelly consistency of POST-mortem blood clots

Question 44

fate of thrombus

Answer 44

-Propagation. thrombi accumulate additional platelets and fibrin
-Embolization: thrombi dislodge, travel to other sites in vasculature
-Dissolution: result of fibrinolysis, which can lead to rapid shrinkage and total disappearance of recent thrombi
-Organization and recanalization: older thrombi become organized by ingrowth of endothelial cells, smooth muscle cells, and fibroblasts; capillary channels eventually form - reestablish continuity of original lumen
-forms new vessels (holes) in the vessel for blood to flow there

Question 45

pathology of thrombosis

Answer 45

-Thrombi - vary in size and shape, depend on site and underlying cause, obstruct arteries or veins, or embolize
-Venous thrombi can cause painful congestion and edema distal to obstruction; also may embolize to lungs
-Arterial thrombi can also embolize, cause downstream infarctions; more likely to occlude critical vessels (e.g., coronary or cerebral artery)
-Arterial or cardiac thrombi usually begin at sites of turbulence or endothelial injury; venous thrombi usually occur at sites of stasis
-Thrombi - focally attached to underlying vascular surface; arterial thrombi (atherosclerotic plaques, MI) tend to grow retrograde, and venous thrombi (DVTs ) extend in direction of blood flow (both propagate toward heart)
-Aortic thrombi especially due to ulcerated atherosclerotic plaques and aneurysmal dilation

Question 46

venous thrombosis (phlebothrombosis)- she didnt go over this

Answer 46

-Most occur in superficial or deep veins of leg
-Superficial venous thrombi usually occur in saphenous veins in setting of varicosities; can cause local congestion, swelling, pain, and tenderness, rarely embolize
-Deep venous thrombus involving one of the large leg veins (e.g., popliteal, femoral, and iliac veins)— more often embolize to lungs
-DVTs may cause local pain and edema due to venous obstruction, but because of venous collateral channels, about 50% of DVTs asymptomatic; recognized only after embolization
-Lower extremity DVTs often associated with hypercoagulable states; common predisposing factors - bed rest and immobilization, congestive heart failure
-Trauma, surgery, and burns cause immobilization and also vascular insults (e.g., procoagulant release from injured tissues)
-Thrombotic diathesis of pregnancy: decreased venous return from leg veins and systemic hypercoagulability associated with hormonal changes of late pregnancy and postpartum period
-Tumor-associated inflammation and coagulation factors (tissue factor, factor VIII), as well as procoagulants (e.g., mucin) released from tumor cells: contribute to increased risk of thromboembolism in disseminated cancers (migratory thrombophlebitis or Trousseau syndrome)

Question 47

clinical features of venous thrombosis (stasis)

Answer 47

-Immobilization (Air Travel)
-Bed rest
-Congestive heart failure
-Pregnancy
-Trauma / Surgery
-Obesity
-Cancer

Question 48

arterial and cardiac thrombosis

Answer 48

-Atherosclerosis: major cause of arterial thromboses due to loss of endothelial integrity and abnormal blood flow
-Myocardial infarction can predispose to cardiac mural thrombi by causing dyskinetic myocardial contraction and endocardial injury
-Both cardiac and aortic mural thrombi prone to embolization to any tissue but especially brain, kidneys, and spleen

Question 49

embolism

Answer 49

-Embolus - Detached intravascular solid, liquid, or gaseous mass carried by blood from point of origin to distant site, often causing tissue dysfunction or infarction
-Vast majority are dislodged thrombi (thromboembolism)
-Other rare emboli - fat droplets, nitrogen bubbles (deep sea diving), atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or foreign bodies
-Emboli travel through blood, reach vessels too small to pass through, cause partial or complete vascular occlusion
-fat embolism- bone fracture -> bone marrow go into blood -> embolizes

Question 50

pulmonary embolism

Answer 50

-Originate from DVT (95%); most common form of thromboembolic disease; 100,000 deaths/year (US)
-Fragmented thrombi travel through progressively larger veins to right heart and “slam” into pulmonary vasculature; depending on embolus size can:
-occlude main pulmonary artery
-straddle pulmonary artery bifurcation (saddle embolus), or
-pass into smaller, branching arteries
-sudden death
-Most pulmonary emboli (60% to 80%) small and clinically silent

Question 51

major consequences of PE

Answer 51

-When emboli obstruct 60% or more of pulmonary circulation: sudden death, acute right heart failure (cor pulmonale), or cardiovascular collapse
-Embolic obstruction of medium-sized arteries with subsequent vascular rupture: can result in pulmonary hemorrhage – usually NOT pulmonary infarction (lung supplied by both pulmonary arteries and bronchial arteries; intact bronchial circulation can usually sufficiently perfuse affected area unless bronchial arterial flow compromised (e.g., left-sided cardiac failure), then infarction may occur)
-Embolic obstruction of small end-arteriolar pulmonary branches: often results in hemorrhage or infarction
-!Multiple emboli over time may cause pulmonary hypertension and right ventricular failure

Question 52

systemic (arterial) thromboembolism (didnt go over)

Answer 52

-Most systemic emboli (80%) from intracardiac mural thrombi
-2/3rds associated with left ventricular wall infarcts
-remainder originate from aortic aneurysms, atherosclerotic plaques, valvular vegetations, or venous thrombi (paradoxical emboli)
-10% to 15% unknown origin
-Arterial emboli can travel to many sites (v. venous thrombi, majority travels to lung); most go to lower extremities (75%) or brain (10%); other tissues (e.g., intestines, kidneys, spleen, and upper extremities) may be involved
-Usually result in tissue infarction

Question 53

infarction

Answer 53

-An area of necrosis secondary to decreased blood flow
-HEMORRHAGIC vs. ANEMIC
-RED (hemorrhagic) vs. WHITE (anemic)
-END ARTERIES vs. NO END ARTERIES
-ACUTE -> ORGANIZATION -> FIBROSIS

Question 54

shock

Answer 54

-State of systemic tissue hypoperfusion resulting from reduced cardiac output and/or reduced effective circulating blood volume
-Major types of shock:
-cardiogenic (e.g., myocardial infarction) - shock results from low cardiac output due to myocardial pump failure, ventricular arrhythmias, cardiac tamponade, outflow obstruction (pulmonary embolism)
-hypovolemic (e.g., blood loss)- shock results from low cardiac output due to low blood volume (massive hemorrhage or fluid loss from severe burns, severe vomiting or diarrhea)
-septic (e.g., infections)
-Less commonly, shock can occur in spinal cord injury ( neurogenic shock ), or an IgE-mediated hypersensitivity reaction (anaphylactic shock); In both, acute vasodilation leads to hypotension and tissue hypoperfusion
-Shock of any form can lead to inadequate tissue perfusion and hypoxic tissue injury; may be fatal

Question 55

shock: clinical stages: non-progressive stage

Answer 55

-Initial nonprogressive stage: reflex compensatory mechanisms activated; vital organ perfusion maintained; neurohumoral mechanisms help maintain cardiac output and blood pressure:
-baroreceptor reflexes, release of catecholamines and antidiuretic hormone, activation of renin-angiotensin-aldosterone axis, generalized sympathetic stimulation
-Net effect: tachycardia, peripheral vasoconstriction (pale), and renal fluid conservation
-Cutaneous vasoconstriction - characteristic “shocky” skin coolness and pallor (note - septic shock can initially cause cutaneous vasodilation; patient may present with warm, flushed skin)
-Coronary and cerebral vessels less sensitive to sympathetic signals, maintain relatively normal caliber, blood flow, and oxygen delivery; blood shunted away from skin to vital organs (e.g., heart and the brain)

Question 56

shock: clinical stages: progressive stage

Answer 56

-Progressive stage characterized by tissue hypoperfusion and worsening circulatory and metabolic derangement, including acidosis, blunting vasomotor response
-Arterioles dilate: blood pools in microcirculation
-Peripheral pooling worsens cardiac output
-With widespread tissue hypoxia, vital organs begin to fail

Question 57

shock: clinical stages: irreversible stage

Answer 57

Irreversible stage: cellular and tissue injury so severe that even if hemodynamic defects are corrected, survival is not possible
-necrosis
-sepsis- giving antibiotics will release bacterial toxins

Question 58

shock pathology

Answer 58

-MULTIPLE ORGAN FAILURE
-SUBENDOCARDIAL HEMORRHAGE
-ACUTE TUBULAR NECROSIS
-DAD (Diffuse Alveolar Damage, lung)
-GI MUCOSAL HEMORRHAGES
-LIVER NECROSIS
-DIC

Question 59

clinical progression of shock symptoms

Answer 59

-Hypotension ->
-Tachycardia ->
-Tachypnea ->
-Warm skin -> Cool skin -> Cyanosis
-Renal insufficiency->
-Obtunded mental status - depressed level of consciousness; cannot be fully aroused
-Death
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