Pathology Exam 1

Front 1

Anthracosis

Back 1

Anthracosis: Accumulation of carbon in the lungs from inhaled smoke or coal dust

Front 2

Pneumoconiosis

Back 2

Pneumoconiosis: A disease of the lungs, such as asbestosis or silicosis, Anthracosis) caused by long-term inhalation of particulate matter, especially mineral or metallic dust.

Front 3

Carotenoid pigments

Back 3

Fat soluble pigments of plant origin, includes precursors of Vit-A (B-carotene)

Front 4

cyanosis

Back 4

Non Oxygenated Hb: giving bluish appearance to skin & tissues, term cyanosis

Front 5

hemosiderosis

Back 5

hemosiderin accumulation is called: hemosiderosis

Front 6

Thrombosis

Back 6

Formation of a blood clot inside of a blood vessel

Front 7

Virchow's triad leading to thrombus formation

Back 7

endothelial injury
Abnormal Blood flow
Hypercoagulability

Front 8

Endothelial Cell Injury Pathogenesis

Back 8

EC injury leads to exposure of TF or subendothelial collagen or fibronectin which is the stimuli for platet aggregation and coagulation

Front 9

Some etiologies for endothelium injury

Back 9

CAV-1, Equine Morbillivirus ( hendra), EHV-1, Equine arteritis virus ( EAV), Pestviruses ( Hog cholera, BVD, Border dz., flaviviruses: WNV), Elephant endotheliotropic Herpesvirus

Bacteria: Salmonella typhimurium, manheimia haemolytic, erysipelothrix rhusiopathiae, hemophilus somnus

Front 10

Altered Blood flow

Back 10

Stasis: reduced blood flow is more important in veins: Venous thrombosis ( Common in horses with occlusion of intestinal veins)

Turbulent flow: happens at narrowing of the vessel lumenor venous or lymphatic valves (disrupts laminar blood flow, physically can damage EC, and mixing of the blood can lead to a greater opportunity for coagulation factors)

Front 11

Causes of Altered blood Flow

Back 11

Cardiac diseases, Hypovolemia, Aneurysm

Front 12

Hypercoagulabiliy ( thrombophilia)

Back 12

it is the lesser than frequent contributor to thrombotic states, it is associated with alteration of coagulation pathways

Front 13

Causes of Hypercoagulability

Back 13

-Inflammation, tissue necrosis ( increase in factor I)

-Trauma, acute illness, surgery, increased metabolism ( increase in Factors I, VIII)

- Nephrotic syndrome ( Deficient ATIII, which is lost through damaged glomeruli)

- heartworm disease, nephrotic syndrome, neoplasia ( increase in platelet activation)

Front 14

Thrombus

Back 14

can develop anywhere in the cardiovascular system ( Cardiac chambers, valves, arteries, veins ,capillaries. Focally attached to the underlying vascular surface

***Propagation portion of a thrombus is often poorly attached and so it is prone to fragmentation --> emboli

Front 15

Recanalization

Back 15

regrowth of endothelium over the surface of the scar produce narrowing of the vessel lumen.

Front 16

Embolus

Back 16

detached intravascular solid, liquid, gaseous masses that are carried by the blood to a site distant from its point of origin

Front 17

Venous Thromboemboli

Back 17

Typically end up in the pulmonary circulation ...pulmonary infarcts or right side heart failure

Front 18

Arteral Thromboemboli

Back 18

end up mostly within a smaller artery downstream from the site of the thrombuis, near a bifucation; infarction

Front 19

Cardiac Thromemboli

Back 19

end up mostly at the birfurcation of the external iliac arteries therefore producign a saddle thrombus

Front 20

infarcts

Back 20

seen in areas of ischemic necrosis
caused by occlusion of either arterial supply or the venous drainage

The dominant histologic characteristic of infarcts is coagulative necrosis

Front 21

Red Infarcts

Back 21

occur with venous occlusion in losse tissue, tissue with dual circulation ( lung, small intestine). Also seen when flow is reestablised to a site of previous arterial occusion and necrosis

Front 22

White infarcts

Back 22

occur with arterial occlusionin solid organs with end arterial circulation ( heart, spleen, kidney)

Front 23

What do factors I, V, and VIII all have in common?

Back 23

The all rely on thrombin to be activated

Front 24

Disseminated Intrvascular coagulation (DIC)

Back 24

manifestation of abnormal coagulation ( not a primary disease)

cause: any condition associated with widespread activation of thrombin

Front 25

Septicmia

Back 25

Systemic infection of the blood with virulent bacteria that release their toxins

Front 26

Endotoxemia

Back 26

endotoxins (derived from gram negative bactera) Circulating in the blood

Front 27

Bacteremia

Back 27

presence of ive bacteria in the blood. Bacteremia precedes septicemia

Front 28

Shock

Back 28

it is the final common pathway for several potentially lethal clinical events including severe hemorrhage, extensive trauma or burns, diarrhea, microbial sepsis

Front 29

Three Types of Shock

Back 29

Cardiogenic shock
Hypovolemic shock
septic shock

Front 30

Cardiogenic shock

Back 30

failure of the heart to adequately pump blood

Front 31

Hypovolemic shock

Back 31

Decrease in circulating blood volume due to loss

caused by hemorrhage, fluid loss secondary to vomiting, diarrhea, burns. Leads to hypoperfusionS

Front 32

Septic Shock

Back 32

Peripheral vasodilation and pooling of blood, endothelial cell activation/ injury, WBC induced damage, DIC, activation of cytokine cascade

causes: systemic immune reaction ( release of excessive vascular and inflammatory mediators) to bacterial or fungal infection, most commonly initiated by endotoxins ( LPS complex), less common: peptidoglycans, lipotheichic acids or G+.

Front 33

What are the Effects of LPS on endothelium

Back 33

Inhibit production of anticoagulants ( TFPI, Thrombomodulin)

Front 34

What are the Effects of LPS on Monocytes and Macrophages

Back 34

Direct and indirect release of TNF, IL-2, IL-6, Chemokines

Front 35

LPS directly activates Factor XII

Back 35

initiates intrinsic coagulation pathway; and related XIIa activated pathways ( Kinin, fibrinolysis, complement)

Front 36

LPS directly activates the complement pathway

Back 36

generation on anaphylations ( C3a, C5a)

Front 37

Detrimental effects of LPS

Back 37

IL-1, TNFa and other cytokines; the secondary effects of these cytokines become more prominent

WHen? if the response is very pronounced like in heavy bacterial infections or when prolonged intestinal ischemia results in breakdown of the muscosal integrety and leakage of bacteria and toxins into the blood

Front 38

Effects of inflammatory mediators: IL-1

Back 38

activates lymphacytes, increase EC expression of adhesion molecules (E-selectin, ICAM-1, 2, VCAM-1) that mediate WBC extravasation and secrete chemokines (CXCL8) that lead to the activation of WBCs
- Stimulate the production of nuetrophils and platelets by the BM

- Acute-phase reaction:
stimulates hepatocytes to synthesize increase levels of acute phase proteins in response to inflammation

-In nervous system: acts on the brain to cause fever, lethargy, malaise, lack of appetite

Front 39

Effects of inflammatory mediator: TNF

Back 39

activated vascular endothelium to express adhesion molecules and synthesis of chemokines

- Activates nuetrophile, macrophages, enhancing their microbialcidal activities

-stimulates synthesis of acute phase proteins

-In very large amounts it is the principal mediator in septic shock which leads to inhibition of muscle tone and cardiac contractility decrease blood pressure and shock

Front 40

Stages of Shock

Back 40

- Non progessive: during which reflex compensatory mechanism are activated and perfusion of vital organs is maintained

-Progressive stage: characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances

- Irreversible Stage: sets in after the body has incurred cellular and tissue injury that is so severe that even if the hemodynamic defects are corrected, no way to survive

Front 41

Neurogenic shock

Back 41

Peripheral vasodilation

Mechanism: autonomic discharges lead to loss of vascular tone, peripheral pooling of blood as it occurs due to trauma, stress to the nervous system

Front 42

Effects of inflammatory mediators: IL-1

Back 42

activates lymphacytes, increase EC expression of adhesion molecules (E-selectin, ICAM-1, 2, VCAM-1) that mediate WBC extravasation and secrete chemokines (CXCL8) that lead to the activation of WBCs
- Stimulate the production of nuetrophils and platelets by the BM

- Acute-phase reaction:
stimulates hepatocytes to synthesize increase levels of acute phase proteins in response to inflammation

-In nervous system: acts on the brain to cause fever, lethargy, malaise, lack of appetite

Front 43

Anaphylactic shock

Back 43

Systemic vasodilation and increase vascular permeability leads to hypptension and tissue hypoperfusion

Mechanism: interaction of Ag ( allergen, drug, vaccine) with Ig-E bound to mast cells which leads to widespread MC degranulation and realease of histamine and vasoactive mediators ( Type 1 hypersensitivity)

Front 44

Effects of inflammatory mediator: TNF

Back 44

activated vascular endothelium to express adhesion molecules and synthesis of chemokines

- Activates nuetrophile, macrophages, enhancing their microbialcidal activities

-stimulates synthesis of acute phase proteins

-In very large amounts it is the principal mediator in septic shock which leads to inhibition of muscle tone and cardiac contractility decrease blood pressure and shock

Front 45

Stages of Shock

Back 45

- Non progessive: during which reflex compensatory mechanism are activated and perfusion of vital organs is maintained

-Progressive stage: characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances

- Irreversible Stage: sets in after the body has incurred cellular and tissue injury that is so severe that even if the hemodynamic defects are corrected, no way to survive

Front 46

Neurogenic shock

Back 46

Peripheral vasodilation

Mechanism: autonomic discharges lead to loss of vascular tone, peripheral pooling of blood as it occurs due to trauma, stress to the nervous system

Front 47

Anaphylactic shock

Back 47

Systemic vasodilation and increase vascular permeability leads to hypptension and tissue hypoperfusion

Mechanism: interaction of Ag ( allergen, drug, vaccine) with Ig-E bound to mast cells which leads to widespread MC degranulation and realease of histamine and vasoactive mediators ( Type 1 hypersensitivity)