Hemodynamic Disorders Export

Front 1

Anasarca: defn

Back 1

severe generalized edema with swelling of subcutaneous tissue

Front 2

Transudate : defn

Back 2

Fluid without cells

Front 3

Transudate: drain?

Back 3

No. Will recur.

Front 4

Exudate: defn

Back 4

Fluid with inflammatory cells

Front 5

Alterations in hemodynamic forces cause ____________

while inflammation and increased vascular permeability cause ____________.

Back 5

transudate; exudate.

Front 6

2 causes of generalized increased hydrostatic pressure

Back 6

1) Heart failure: defect in pumping
2) renal failure: volume overload

Front 7

2 causes of localized increased hydrostatic pressure

Back 7

1) Venous stasis
2) ascites

Front 8

Precursor of congestive heart failure

Back 8

Left ventricular hypertrophy

Front 9

Longstanding hypertension can cause

Back 9

Left ventricular hypertrophy

Front 10

What happens in pulmonary edema?

Back 10

L ventricle failure causes leakage of fluid into alveolar spaces.

difficulty breathing, coughing up blood (classically seen as pink frothy sputum)

Front 11

Abdominal ascites are a result of what?

Back 11

Portal hypertension that causes increased resistance to venous return from heavily vascularized intestines.

Front 12

Hyperemia: defn

Back 12

Active process with increased blood flow into capillaries (ex. exercise

Front 13

Congestion

Back 13

Passive process resulting from impaired venous drainage

Front 14

What are "heart failure cells?"

Back 14

Macrophages that phagocytose RBCs (and thus contain hemosiderin) that find their way into the alveolar spaces due to breakdown of alveolar wall.

Front 15

What is hemosiderin?

Back 15

an iron-storage complex.
always found within cells (as opposed to circulating in blood). Hemosiderin is most commonly found in macrophages and is especially abundant in situations following hemorrhage suggesting that its formation may be related to phagocytosis of red blood cells and hemoglobin. Hemosiderin can accumulate in different organs in various diseases.

Front 16

What is cardiac tamponade?

Back 16

Pericardial hemorrhage,

fluid accum in pericardium

Front 17

A pathologic process denoting the formation of a clotted mass of blood within a non-interrupted vascular system

Back 17

Thrombosis.

Front 18

What 3 factors are hemostasis and thrombosis dependent on ?

Back 18

1) Vascular endothelium
2) Platelets
3) Coagulation system

Front 19

What antithrombotic properties do endothelial cells have?

Back 19

1) Antiplatelet effects : isolates blood from subendothelial collagen (repels negative charged platelets) + producing prostacyclin and nitric oxide

2) Anticoagulant properties: makes heparin and thrombomodulin

3) Fibrinolytic properties - helps make plasmin

Front 20

What prothrombotic properties do endothelial cells have?

Back 20

1) When broken, negatively charged platelets adhere to positively charged subendothelial collagen
2) Synthesis of von Willebrand’s factor (VWF)
3) Synthesis of tissue factor (TF)
(Activates extrinsic clotting pathway)

Front 21

What is the primary hemostasis?

Back 21

Activation of platelets when they adhere to subendothelial collagen, releasing chemicals stored within granules.

Front 22

What is the coagulation cascade?

Back 22

Activated by release of tissue factor from injured endothelial cells, ultimately forming a more stable plug with cross-linked fibrin

Front 23

What is the secondary hemostasis?

Back 23

Coagulation cascade

Front 24

What converts fibrinogen to fibrin?

Back 24

Thrombin

Front 25

What is lab assessment of hemostasis?

Back 25

1) Platelet count
2) Activated Partial Thromboplastic time (PTT): intrinsic path; monitors heparin
3) Prothrombin time (PT): extrinsic path; monitors coumadin
4) Specific coagulation assays for hemophilia, etc.

Front 26

Antithrombins inhibit ___________

Back 26

serine protease factors

Front 27

Proteins C and S inactivate factors __ and _____

Back 27

Va and VIIIa

Front 28

Plasminogen-plasmin system results in _________

Back 28

fibrinolysis

Front 29

Clot formation limited to appropriate sites by normal balance of ________________

Back 29

anticoagulation/coagulation/fibrinolysis

Front 30

Mass of blood constituents, (platelets, RBCs, WBCs, fibrin) formed w/in circulating bld stream

Back 30

thrombus

Front 31

What are predisposing/risk factors for thrombosis?

Back 31

Endothelial injury; Alterations to normal blood flow; Hypercoagulability states

Front 32

What chamber of heart do clots often form in?

Back 32

L atrium

Front 33

Arterial thrombi most often occur in what arteries?

Back 33

Coronary, cerebral, femoral

Front 34

What are Lines of Zahn?

Back 34

Lines that form antemortem from successive waves of clot formation

Front 35

Venous thrombi most often occur in what veins?

Back 35

90% in veins of the lower extremities

Front 36

What do arterial thrombi usually form from?

Back 36

Often attached to atherosclerotic lesion

Front 37

Detached mass carried by blood stream to site distal from its point of origin

Back 37

Embolus

Front 38

How to determine affected organ by embolus?

Back 38

Follow the blood flow (arterial vs. venous)

Front 39

Most arterial emboli arise from _____

Back 39

heart

Front 40

What increases risk of arterial emboli?

Back 40

Atrial fibrillation

Front 41

What problems do arterial emboli cause?

Back 41

Infarction to lower extremities and brain (especially)

Front 42

Most serious venous emboli

Back 42

pulmonary embolus frequent cause of death

Front 43

What is a saddle embolus?

Back 43

When embolus straddles bifurcation of the pulmonary artery. Can cause sudden death

Front 44

Broken bones can cause what kind of embolus?

Back 44

Fat embolus because vasculature to bone marrow is very connected to the circulation

Front 45

A cold pale distal extremity suggests (arterial, venous) embolus?

Back 45

Arterial. It suggests no blood is getting there (not venous)

Front 46

Area of ischemic necrosis within a tissue or an organ produced by occlusion of either its arterial supply or its venous drainage

Back 46

infarct

Front 47

Arterial occlusion in solid tissues results in _____________ infarct.

Back 47

pale (anemic)

Front 48

Venous occlusion, loose tissues, and extensive collateral blood supply are associated with _______ infarct.

Back 48

Red (hemorrhagic)

Front 49

widespread hypoxia of tissues caused by ineffective circulation of blood

Back 49

shock

Front 50

Clinical manifestations of shock

Back 50

Hypotension, Hypoperfusion, weak pulse, tachycardia, tachypnea, oliguria (low urine output)

Front 51

Stages of shock: nonprogressive phase. What happens?

Back 51

perfusion is preserved by neurohumoral mechanisms (rapidly acting mechanisms that restore blood pressure)

Front 52

Morphologic features of shock: kidney

Back 52

Acute tubular necrosis or diffuse cortical necrosis

Front 53

Morphologic features of shock: liver

Back 53

fatty change or central hemorrhagic necrosis

Front 54

Cause of septic shock

Back 54

Systemic release of endotoxins (gram negative bacterial cells walls, lipopolysaccharides) cause a cytokine cascade resulting in hypotension, decreased cardiac contractility, disseminated intravascular coagulation, and fibrinolysis.

Bleeding is due to consumption of coagulation factors and activation of fibrinolysis

Front 55

What is amniotic fluid embolism?

Back 55

obstetric emergency in which amniotic fluid, fetal cells, hair, or other debris enters the mother's blood stream via the placental bed of the uterus and triggers an allergic reaction. This reaction then results in cardiorespiratory (heart and lung) collapse and coagulopathy.

Front 56

What is disseminated intravascular coagulation?

Back 56

DIC= clotting where it is not supposed to happen.
pathological activation of coagulation. DIC leads to the formation of small blood clots inside the blood vessels throughout the body.
As the small clots consume coagulation proteins and platelets normal coagulation is disrupted and abnormal bleeding occurs from the skin, GI tract, resp tract, wounds

Front 57

What is acute tubular necrosis?

Back 57

Damage to tubule cells of kidney due to ischemia/hypoperfusion