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Pathology Exam 2 > Chapter 4 > Flashcards

Chapter 4 Flashcards

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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
Hemorrhage
Extravasation of blood into extravascular space
26
Hematoma
Hemorrhage contained within a tissue
27
Petechiae
1-2 mm hemorrhages into skin, mucous membranes or serosal surfaces Increased intravascular pressure Low platelet count (thrombocytopenia) Defective platelet function (uremia)
28
Purpura
>3 mm hemorrhages Same disorders as petechiae Secondary to trauma, vascular inflammation (vasculitis), increased vascular fragility (amyloidosis)
29
Eccymoses
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
Hemostasis
Tightly regulated process to maintain blood in a fluid state | Permit rapid formation of a hemostatic clot at the site of vascular injury
31
Thrombosis
Pathologic counterpart of hemostasis | Blood clot formation
32
3 Components of Hemostasis and Thrombosis
1. Vascular wall 2. Platelets 3. Coagulation cascade
33
T-PA
Protease that cleaves plasminogen to form plasmin | Plasmin cleaves fibrin to degrade thrombi
34
Anti-Platelet Effects
Prevent platelet from engaging thrombogenic ECM Nonactivated platelets do not adhere to endothelial cells PGI2 and NO
35
PGI2
Produced by endothelial cells impede platelet adhesion
36
NO
Produced by endothelial cells and impede platelet adhesion
37
Adenosine diphosphatase
Able to degrade ADP, inhibits platelet aggregation
38
ADP function
Released from GPIb receptors that bind to vWF
39
TxA2
Released from GpIb bound to vWF | Induces additional platelet aggregation through platelet GpIIb-IIIa receptor binding to fibrinogen
40
Thrombomodulin
Binds to thrombin Converts it from procoagulant into anticoagulant Activates protein C, inhibits clotting by inactivating factors Va and VIIIa
41
Tissue factor pathway inhibitor
inhibits tissue factor-factor VIIa and factor Xa
42
Heparan like molecules
Indirect action Cofactors that enhance the inactivation of thrombin and several other coagulation factors Antithrombin III
43
Antithrombin III
Inactivation of thrombin and other factors
44
vWF
Adhesion of platelets through interaction with these factors | Product of normal endothelial cells and an essential cofactor for platelet binding to matrix elements
45
Procoagulent effects
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
PAIs
Endothelial cells secrete inhibitors of plasminogen activator Limit fibrinolysis and favor thrombosis
47
Glanzmann thrombasthenia
Defect in GpIIb-IIIa complex | Aggregation of platelets will not be able to occur
48
Bernard-Soulier Syndrome
No GpIb receptor, no binding to vWFs
49
von Willebrand disease
Deficiency in vWF | Unable to bind to subendothelial collagen and eventually glycoprotein Ib (GpIb platelet receptor)
50
Platelets
Disc shaped Anucleate cell fragments Shed from megakaryocytes in bone marrow into bloodstream Role in primary homeostatic plug formation
51
2 Granule Types in Platelets
Alpha granules | Dense Granules
52
Dense Granules
Found within platelets Contain ADP and ATP These recruit ionized Ca2+, histamine and 5HT and epinephrine
53
3 Processes that Platelets undergo
1. Adhesion and shape change 2. Secretion 3. Aggregation
54
vWF-GpIb Associations
Necessary to overcome high shear forces of flowing blood | No vFW, no clotting occurs
55
Dense Body Release
Ca2+ required for this to occur Important process in coagulation cascade ADP activates platelet aggregation
56
ADP Release
Activates platelet aggregation Causes additional ADP release Amplifies aggregation process Platelet activation
57
Platelet activation
Negatively charged phospholipids appear on surface | Bind Ca2+ and serve as critical nucleation sites for assembly of complexes containing coagulation factors
58
Aggregation Products released
Vasoconstrictor thromboxane A2
59
Thromboxane A2
Important platelet-derived stimulus Amplifies platelet aggregation Formation of primary hemostatic plug
60
What are the 2 mechanisms that stabilize the platelet plug?
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
Thrombin
Converts Fibrinogen -->Fibrin
62
Plasmin
1. Cleaves Fibrin | 2. Blocks platelet aggregation, no clot

Pathology Exam 2 (6 decks)

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