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Pathology Exam 2 > Chapter 4 > Flashcards

Chapter 4 Flashcards

1
Q

Edema

A

Abnormally increased interstitial fluid
Movement of water into tissues exceeds drainage
Can be caused by increased hydrostatic pressure or reduced plasma protein
Typically protein poor fluid
Seen in CHF, renal failure, hepatic failure, malnutrition
Clearing and separation of ECM, subtle cell swelling, commonly seen in subcutaneous tissues, lungs, brain

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2
Q

Anasarca

A

Severe and generalized edema
Widespread subcutaneous tissue swelling
Usually near death

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3
Q

Transudate

A

Typically protein-poor fluid

Edema caused by increased hydrostatic pressure and reduced plasma protein

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4
Q

Hydropericardium

A

fluid collection in the pericardial sac

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5
Q

Hydrothorax

A

fluid collection in the pleural spaces

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6
Q

Hydroperitoneum

A

Ascites

Fluid collection in abdomen

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7
Q

Inflammatory Edema

A

Protein-rich exudate

Result of increased vascular permeability in inflammatory response

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8
Q

Lymphedema

A 
Impaired lymphatic drainage
Chronic inflammation with fibrosis
Invasive malignant tumors
Physical disruption
Radiation damage
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9
Q

Parasitic Filariasis

A

Lymphatic obstruction caused by wucheria bancrofti, extensive inguinal lymphatic and lymph node fibrosis
Edema of external genitalia and lower limbs
Massive accumulation = elephantitis

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10
Q

Edema of upper extremity Axillary

A

Complicate surgical removal or irradiation
Breast/associated axillary lymph nodes
Breast cancer

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11
Q

Subcutaneous edema

A

Diffuse or more conspicuous in regions with high hydrostatic pressures
Distribution is influenced by gravity
Legs-standing, sacrum-sitting

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12
Q

Pitting edema

A

finger pressure displaces interstitial fluid leaving a depression

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13
Q

Periorbital edema

A

Characteristic finding in severe renal disease

Renal dysfunction produces edema in tissues with loose CT including eyelids

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14
Q

Soft tissue edema

A

Signals underlying cardiac or renal disease

Impairs wound healing or infection clearance

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15
Q

Pulmonary edema

A

Lungs are 2-3 times normal weight
Section yields frothy, blood tinged fluid
Common clinical problem
Left ventricular failure

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16
Q

Brain edema

A

Localized or generalized depending on injury
Severe edema can cause the brain to herniate towards the foramen magnum
Can injury medullary centers and cause death

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17
Q

Generalized Brain edema

A

Brain is grossly swollen, narrowed gyri, evidence of compression against skull

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18
Q

Hyperemia

A

Arteriole dilation at sites of inflammation or skeletal muscle during exercise
Increased blood flow, engorgement of vessels with oxygenated blood (erythema)

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19
Q

Congestion

A

Passive process
Reduced outflow of blood from a tissue
Systemic due to cardiac failure
Local due to isolated venous obstruction
Cyanosis, accumulation of deoxygenated hemoglobin (red cell stasis)

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20
Q

Longstanding chronic passive congestion

A

lack of blood flow causes chronic hypoxia
Ischemic tissue injury and scarring
Can cause capillary rupture
Small hemorrhagic foci
Catabolism of extravasated RBCs
Leave residual clusters of hemosiderin-laden macrophages

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21
Q

Acute Pulmonary congestion

A

engorged alveolar capillaries
Alveolar septal edema
Focal intra-alveolar hemorrhage

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22
Q

Chronic pulmonary congestion

A

Thickened septa
Fibrotic
Alveoli contain numerous hemosiderin-laden macrophages
Heart failure cells

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23
Q

Acute hepatic congestion

A

Central vein, sinusoids distended, centrilobular hepatocytes ischemic

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24
Q

Chronic passive hepatic congestion

A

Centrilobular regions are grossly red-brown
Areas are accentuated against uncongested parenchyma
Nutmeg liver

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25
Q

Hemorrhage

A

Extravasation of blood into extravascular space

26
Q

Hematoma

A

Hemorrhage contained within a tissue

27
Q

Petechiae

A

1-2 mm hemorrhages into skin, mucous membranes or serosal surfaces
Increased intravascular pressure
Low platelet count (thrombocytopenia)
Defective platelet function (uremia)

28
Q

Purpura

A

> 3 mm hemorrhages
Same disorders as petechiae
Secondary to trauma, vascular inflammation (vasculitis), increased vascular fragility (amyloidosis)

29
Q

Eccymoses

A

1-2 cm subcutaneous hematomas (bruises)
Possibly indicative of child abuse
RBCs in lesions are degraded and phagocytized by macrophages
Hemoglobin (red-blue) –>bilirubin (blue-green)–>hemosiderin (gold brown)

30
Q

Hemostasis

A

Tightly regulated process to maintain blood in a fluid state

Permit rapid formation of a hemostatic clot at the site of vascular injury

31
Q

Thrombosis

A

Pathologic counterpart of hemostasis

Blood clot formation

32
Q

3 Components of Hemostasis and Thrombosis

A
  1. Vascular wall
  2. Platelets
  3. Coagulation cascade
33
Q

T-PA

A

Protease that cleaves plasminogen to form plasmin

Plasmin cleaves fibrin to degrade thrombi

34
Q

Anti-Platelet Effects

A

Prevent platelet from engaging thrombogenic ECM
Nonactivated platelets do not adhere to endothelial cells
PGI2 and NO

35
Q

PGI2

A

Produced by endothelial cells impede platelet adhesion

36
Q

NO

A

Produced by endothelial cells and impede platelet adhesion

37
Q

Adenosine diphosphatase

A

Able to degrade ADP, inhibits platelet aggregation

38
Q

ADP function

A

Released from GPIb receptors that bind to vWF

39
Q

TxA2

A

Released from GpIb bound to vWF

Induces additional platelet aggregation through platelet GpIIb-IIIa receptor binding to fibrinogen

40
Q

Thrombomodulin

A

Binds to thrombin
Converts it from procoagulant into anticoagulant
Activates protein C, inhibits clotting by inactivating factors Va and VIIIa

41
Q

Tissue factor pathway inhibitor

A

inhibits tissue factor-factor VIIa and factor Xa

42
Q

Heparan like molecules

A

Indirect action
Cofactors that enhance the inactivation of thrombin and several other coagulation factors
Antithrombin III

43
Q

Antithrombin III

A

Inactivation of thrombin and other factors

44
Q

vWF

A

Adhesion of platelets through interaction with these factors

Product of normal endothelial cells and an essential cofactor for platelet binding to matrix elements

45
Q

Procoagulent effects

A

Response to cytokines (TNF or IL-1) or bacterial endotoxin
Tissue factor secreted from endothelial cells
Activate extrensic clotting cascade
Activated endothelial cells
Augment IXa and Xa

46
Q

PAIs

A

Endothelial cells secrete inhibitors of plasminogen activator
Limit fibrinolysis and favor thrombosis

47
Q

Glanzmann thrombasthenia

A

Defect in GpIIb-IIIa complex

Aggregation of platelets will not be able to occur

48
Q

Bernard-Soulier Syndrome

A

No GpIb receptor, no binding to vWFs

49
Q

von Willebrand disease

A

Deficiency in vWF

Unable to bind to subendothelial collagen and eventually glycoprotein Ib (GpIb platelet receptor)

50
Q

Platelets

A

Disc shaped
Anucleate cell fragments
Shed from megakaryocytes in bone marrow into bloodstream
Role in primary homeostatic plug formation

51
Q

2 Granule Types in Platelets

A

Alpha granules

Dense Granules

52
Q

Dense Granules

A

Found within platelets
Contain ADP and ATP
These recruit ionized Ca2+, histamine and 5HT and epinephrine

53
Q

3 Processes that Platelets undergo

A
  1. Adhesion and shape change
  2. Secretion
  3. Aggregation
54
Q

vWF-GpIb Associations

A

Necessary to overcome high shear forces of flowing blood

No vFW, no clotting occurs

55
Q

Dense Body Release

A

Ca2+ required for this to occur
Important process in coagulation cascade
ADP activates platelet aggregation

56
Q

ADP Release

A

Activates platelet aggregation
Causes additional ADP release
Amplifies aggregation process
Platelet activation

57
Q

Platelet activation

A

Negatively charged phospholipids appear on surface

Bind Ca2+ and serve as critical nucleation sites for assembly of complexes containing coagulation factors

58
Q

Aggregation Products released

A

Vasoconstrictor thromboxane A2

59
Q

Thromboxane A2

A

Important platelet-derived stimulus
Amplifies platelet aggregation
Formation of primary hemostatic plug

60
Q

What are the 2 mechanisms that stabilize the platelet plug?

A
  1. Thrombin binding to protease-activated receptor on platelet membrane, ADP and TXA2 causes platelet aggregation
  2. Thrombin converts fibrinogen to fibrin in vicinity of platelet plug, cements platelets in place
61
Q

Thrombin

A

Converts Fibrinogen –>Fibrin

62
Q

Plasmin

A
  1. Cleaves Fibrin

2. Blocks platelet aggregation, no clot

Pathology Exam 2 (6 decks)

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