Mp Ch4

Front 1

What are the four non-inflammatory causes of inflammation?

Back 1

1. Increased hydrostatic pressure
2. Decreased osmotic pressure
3. Lymphatic obstruction
4. Preimary retention of Na

Front 2

What parasite causes the enlarged lymph node that is responsible for elephantitis

Back 2

Filaris

Front 3

What causes Peau d'orange?

Back 3

Obstruction of superficial lymph vessels in breast cancer

Front 4

What are three clinical correlations of edema?

Back 4

1. Impaired wound healing and infection clearance
2. Pulmoney edema decreases gas exchange and increases infection
3. Brain edema can cause herniation through the foramen magnum or even vascular compromise

Front 5

Describe hyperemia.

Back 5

It is an active process that results in the increase of blood flow to a certain tissue usually as a result of a dilated arteriole.

Front 6

Describe congestion.

Back 6

Congestion is a passive process that involves the accumulation of static blood due to venous obstruction or pressure.

Front 7

Describe the color of hyperemia and congestion.

Back 7

Hyperemia is usually red while congestion is cyanotic (blue-red).

Front 8

What is a wide variety of medical conditions that lead to the increased tendancy to hemorrhage?

Back 8

Hemorrhagic diathesis

Front 9

What are the causes for petechiae (4)?

Back 9

1. Increased intravascular pressure
2. Thrombocytopenia
3. Decrease in circulating clotting factors
4. Defective platelets

Front 10

What the causes for purpura(3)?

Back 10

1. Trauma
2. Amalyoidsis
3. Vascular inflammation

Front 11

Hemostasis and thrombosis are regulated by three components. What are they?

Back 11

1. Vascular wall
2. Platelets
3. Clotting factors (coagulation cascade)

Front 12

What endothelial compounds prevent the aggregation of platelets in normal situations?

Back 12

1. NO
2. PGI2
3. ADPase

Front 13

What are the different ways that coagulation is prevented by endothelium?

Back 13

1. HLMs interact with Antithrombin III to degrade IIa (thrombin)
2. Thrombomodulin activates Protein C and that results in the cleavage of Va and VIIIa.
3. Thrombomodulin can also turn thrombin into an anticoagulant
4. TFPI - tissue factor pathway inhibitor prevents the activation of the extrinsic pathway

Front 14

What anti-thrombolytic factor does endothelium secrete?

Back 14

Plasmin Activating Inhibtors

Front 15

Platelets contain two different types of granules. What are they and what do they contain?

Back 15

1. Alpha granules - fibrinogen, fibronectin, Factors V, VIII, platelet factor 4, PDGF, TGF-Beta
2. Dense bodies/Delta granuse - ADP, ATP, calcium, histamine, seratonin and epinephrine

Front 16

vW Factor acts as a bridge between what?

Back 16

Platelets receptors(glycoprotein-1b) and collagen

Front 17

What is a disorder of deficient vW Factor called? Glycoprotein-1b?

Back 17

1. vW disease
2. Bernard Soulier Disease

Front 18

What does ADP release augement besides aggregation of platelets?

Back 18

The release of ADP from other platelets

Front 19

Why are the phospholipid complexes on the platelets so important in clotting?

Back 19

They provide a stage for the platelet, factor and cofactor to aggregate on. Calcium also stabilizes this area.

Front 20

Besides ADP, what do platelets secrete to further their aggregation?

Back 20

TxA2

Front 21

What is it called when the platelets contract?

Back 21

Viscous metamorphisis

Front 22

What ADP activated substance encourages the crosslinking of platelets using fibrinogen?

Back 22

GpIIb-IIIa

Front 23

What disorder is a deficiency of GpIIb-IIIa?

Back 23

Glanzmann thrombasthenia

Front 24

Does thrombin stimulate neutrophil and monocyte adhesion?

Back 24

Yes

Front 25

The intrinsic clotting cascade is started with the activation of what?

Back 25

Hageman (Factor XII)

Front 26

The extrinsic clotting cascade is started with the actiavtion of what?

Back 26

Tissue Factor

Front 27

What are three natural anti-coagulants?

Back 27

1. Antithrombin III
2. Protein C and S - requires K
3. Tissue Factor Pathway Inhibitor - inactivates X and VII

Front 28

What three ways can plasmin be activated?

Back 28

1. Hageman Factor
2. Urokinase PA
3. Tissue PA

Front 29

What does free plasmin adhere to?

Back 29

Alpha-2 plasmin inhibitor

Front 30

What three influences make up Virchow's Triad?

Back 30

1. Endotheliam Injury (most dominant)
2. Alterationa in normal blood flow
3. Hypercoagability

Front 31

What is the main factor in venous thrombis formation?

Back 31

Stasis

Front 32

What are the four things that stasis or turbulent blood flow do to promotoe thrombis formation?

Back 32

1. Disrupt laminar flow and bring the platelets to the endothelial surface
2. Prevent dilution of circulating clotting factors
3. Prevent the influx of anti-coagulant factors
4. Activates the endothelial cells

Front 33

What is the aquired mutation of Factor V called and why is it hypercoagulative?

Back 33

1. Leiden Mutation
2. It makes Factor V resistant to cleavage by Protein C

Front 34

60% of people with DVT have what mutation?

Back 34

Leiden Mutation

Front 35

Elevated levels of what will lead you to be 3x more likely to get a DVT?

Back 35

Prothrombin

Front 36

Hyperhomocysteinemia causes what?

Back 36

Decreased activity of Antithrombin III and Thrombobodulin.

Front 37

When should you consider a hereditary hypercoagability disorder in a patient?

Back 37

If a patient is under 50 with no aquired causes of hypercoagability.

Front 38

What happens in Heparin-Induced Thrombocytopenia Syndrome?

Back 38

Unfractionated heparin causes an immune reaction where antibodies against heparin + Platelet Factor 4 complexes cause thrombocytopenia

Front 39

What happens in antiphospholipid antibody syndrome? What is seen in this disorder?

Back 39

1. Antibodies are produced against epitopes on plasma proteins that are only exposed when bound to phospholipids(carbolipin).

2. Repeat miscarriages, valve vegetations or thrombocytopenia

Front 40

What is the order in which you see predominating arterial thrombi? Are they usually occlusive?

Back 40

1. Coronary
2. Cerebral
3. Femoral
4. Yes

Front 41

What type of thrombis usually makes a long cast of the vessel it is in? Why?

Back 41

1. Venous thrombi
2. The blood is more static that arterial blood

Front 42

How can you tell the difference between post-mortem clots and red/stasis clots?

Back 42

1. Red/Stasis clots are usually attached to the wall of the vessel
2. Post-mortem clots are usually red all the way through the clot

Front 43

What type of endocarditis is caused by immune complexes dipositing on the valve?

Back 43

Verrucous Endocarditis (Libman-Sacks)

Front 44

What are the four fates of thrombi?

Back 44

1. Propagation
2. Dissolution
3. Embolization
4. Recanulization

Front 45

Dissolution of thrombi is only possible when?

Back 45

When the thrombus is very recent

Front 46

An organizaed thrombus can be reconstituted in what part of the vessel?

Back 46

Sub-endothelial area

Front 47

Bacterial thrombi result in what?

Back 47

Mycotic anuerysm

Front 48

Edema and swelling in superficial venous thrombi can cause what?

Back 48

Vericose ulcers

Front 49

Is there pain associated with DVT?

Back 49

Not very much

Front 50

What is a tumor associated disease that results in an increase in the release of procoagulant factors?

Back 50

Migratory Thrombophlebitis or Trousseau Syndrome

Front 51

What disease causes the dilation of the atrium due to mitral valve stenosis? What does this lead to?

Back 51

1. Rheumatic heart disease
2. Stasis of the blood in the atrium and thrombi formation

Front 52

What are the three main targets of arterial emboli? Why?

Back 52

1. Brain
2. Spleen
3. Kideny
4. High blood flow to these organs

Front 53

What is the worst type of PE?

Back 53

Saddle embolism

Front 54

What is it called when a PE crosses over into arterial circulation?

Back 54

Paradoxical embolism

Front 55

80% of systemic emboli are the result of what type of thrombis?

Back 55

Intracardiac Mural Thrombi

Front 56

What strange symptom is seen in 20-50% of patients with a fat embolis?

Back 56

Rash

Front 57

What is chronic decompression sickness called? What is the main sign of this disease?

Back 57

1. Cassion disease
2. Necrosis in the heads of long bones

Front 58

Amniotic fluid embolism is caused by tears in what vessel? What do the lungs show in this event?

Back 58

1. Uterine veins
2. Diffuse alveloar damage

Front 59

If the base of an infarct is seen near a serous cavity, what is usually seen?

Back 59

Fibrous exudate

Front 60

What is a difference in red a white infarcts over time?

Back 60

Red infarcts do not change while white infarcts get whitter with time.

Front 61

What four factors influence the development of an infarct?

Back 61

1. Nature of the blood supply
2. Rate of occlusion
3. Tissue's resistance to O2 deprivation
4. O2 content of the blood

Front 62

70% of septic shock is due to what?

Back 62

Gram (-) bacterail LPS

Front 63

Describe the interaction of LPS with the body

Back 63

1. LPS binds to LPS binding protein
2. That complex binds to CD14
3. This complex is bound to TLR4
4. This activates leukocytes

Front 64

What are the three phases of shock?

Back 64

1. Initial non-progressive stage
2. Progressive stage
3. Irreversible stage

Front 65

Why do the arterioles dilate in the progresive stage of shock?

Back 65

Decreasing pH causes a depression of the vasomotor reponse

Front 66

What pathological change is seen in the heart due to septic shock?

Back 66

Contraction band necrosis

Front 67

What pathological change is seen in the lungs as a result of septic shock?

Back 67

Diffuse alveloar damage - "shock lung"

Front 68

Is diffuse alveloar damage seen in hypovolemic show?

Back 68

No