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SMP Block 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

Where would edema be found in right and left sided heart failure?

A

Right - liver and lower extremities

Left - lungs

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2
Q

What is the function of endothelin?

A

Vasoconstriction after injury

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3
Q

What is the function of thrombin?

A

Fibrinogen to fibrin

Secondary hemostasis

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4
Q

What is the function of prostacyclin? Where is it produced?

A

Produced by endothelium

Vasodilation and inhibition of plt aggregation

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5
Q

What are the anti-thombotic factors produced by endothelium?

A

Prostacyclin
NO
ADPase

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6
Q

What is the function of NO in hemostasis? Where is it produced?

A

Endothelium

Inhibits plt aggregation

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7
Q

What is the function of ADPase? Where is it produced?

A

Expressed on endothelial cells

Degrades ADP, inhibits plt aggregation

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8
Q

What is the function of heparin-like molecules? Where is it produced?

A

Endothelium

Cofactors of antithombin III

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9
Q

What is the function of thrombomodulin? Where is it produced?

A

Endothelium

Activated by binding thombin - activates protein C, which works with protein S to cleave factors five and eight a

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10
Q

What is the function of tissue factor inhibitor? Where is it produced?

A

Endothelium

Inhibits activated tissue factor which stimulates secondary hemostasis

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11
Q

What are the anti-coagulant factors produced by endothelium?

A

Heparin-like molecules
Thrombomodulin
Tissue Factor Inhibitor

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12
Q

What is a prothombotic factor produced by endothelium?

A

Von Willibrand Factor

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13
Q

What is a procoagulant factor produced by endothelium? What does it do?

A

Tissue Factor

Initiates secondary hemostasis (extrinsic pathway)

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14
Q

What is an anti-fibrinolytic factor produced by endothelium? What does this do?

A

Plasminogen inhibitors

Inhibits the breakdown of clot - promotes clot

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15
Q

What is a fibrinolytic factor produced by endothelium? What does it do?

A

tPA - tissue plasminogen factor

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16
Q

What factor do the intrinsic and extrinsic pathways converge on?

A

X

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17
Q

Describe the intrinsic coag cascade

A

Negative surface - Factor 7 to 7a - Factor 11 to 11a - Factor 9 to 9a (factor 8a) - factor X - Xa - prothrombin to thrombin - fibrinogen to fibrin

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18
Q

Describe the extrinsic coag cascade

A

Tissue factor - Factor 7 to 7a - factor X - Xa - prothrombin to thrombin - fibrinogen to fibrin

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19
Q

Describe the clotting system in vivo

A

Tissue Factor - Factor 7 to 7a OR 11 to 11a - Factor 9 to 9a - factor X - Xa - prothrombin to thrombin - fibrinogen to fibrin

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20
Q

What are alpha granules and what do they contain?

A

Plt granules containing fibrinogen, fibronectin, factor 5 and vWF

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21
Q

What are dense bodies and what do they contain?

A

Plt granules containing ATP, ADP, calcium, histamine, serotinin, epi

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22
Q

How are M1 macrophages activated and what is their role?

A

Activated by IFN-gamma and microbial products
Enhances removal of organism – ROS, NO, lysosomal enzymes
Inflammation – IL-1, 12, and 23, chemokines

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23
Q

How are M2 macrophages activated and what is their role?

A

Cytokine activated (IL-4 and 13)
Tissue Repair - Growth factor, TGF-beta
Anti-inflammatory – IL-10, TGF-beta

24
Q

Where are plasma cells produced and what is their role?

A

Produced by B cells - antigen presenting

25
Q

What factors produce the physical symptoms of chronic inflammation and where do they come from?

A

IL-1, IL-6, TNF-alpha – macrophage derived

26
Q

What are 3 acute phase proteins of inflammation?

A

Fibrinogen, CRP, serum amyloid A protein

27
Q

Explain the cycle of lymphocyte and macrophage activation in chronic inflammation including specific cytokines and chemical mediators.

A

Macrophage is classically activated (microbes and IFN-gamma)
Activated macrophage secretes TNF and IL-1 to recruit leukocytes
Activated macrophage secretes cytokines IL-12, 6, 23 and presents antigens to T-lymphocyte

Activated T lymphocyte presents IL-17 and TNF to additionally recruits leukocytes
Activated T cell presents IFN-gamma to further activate macrophages continuing the cycle

28
Q

What are the primary pro and anti-inflammatory cytokines?

A

Pro-inflammatory: TNF and IL-1

Anti-inflammatory: IL-10, TGF-beta, lipoxins

29
Q

What is complement C5a?

A

Chemotaxis

30
Q

What is complement C3a?

A

Opsonin (antibody)

31
Q

What is complement Anaphylatoxin?

A

Release histamine – vasodilation and permeability

32
Q

Where is histamine released from?

A

Mast cells, basophils, platelets

33
Q

What role does histamine play in inflammation?

A

Vasodilation - arterioles

Vascular permeability of venules – immediate transient response

34
Q

What is the role of the kinin system?

A

Vasodilation – plasma proteins release bradykinin (vasoactive peptides)

Vascular permeability, vasodilation, pain

35
Q

Which chemical mediator is responsible for pain?

A

Kinin

36
Q

Differentiate between the two arachadonic acid pathways in inflammation

A

COX pathway – prostaglandins – pro-inflammatory
PGI2 – vasodilation, inhibits plt aggregation
Thromboxane A2 – vasoconstriction, promotes plt aggregation
PGd2/E2 – Vasodilation, vascular permeability

Anti-inflammatory pathway – Lipoxygenase – Leukotrienes
5-HETE – chemotaxis
C4, D4, E4 – bronchospasm and vascular permeability
Lipoxin A4 B4 – inhibition of inflammation

37
Q

Differentiate between parenchyma and stroma in neoplasia.

A

Parenchyma - basis for nomenclature - cell type

Stroma - environment - responsible for growth and spread

38
Q

What is an example of a common cancer point mutation?

A

RAS point mutation causing carcinoma - constitutively “on” activating transcription

39
Q

What are two examples of common cancer translocations?

A

ABL/BCR in CML - creates a new protein that overactivates ABL which is a cytoplasmic tyrosine kinase
8:14 promoter translocation in Burkitt’s Lymphoma which switches the myc and Ig promoters such that myc is produced in excessive quantities - too much normal protein

40
Q

What is an example of a common cancer gene amplification?

A

Her2 receptor overexpression in breast cancer due to gene duplication - causes sensitivity to growth factor

41
Q

What inhibits RAS/RAF?

A

NF1

42
Q

Describe a common regulation pathway for transcription

A

B-catenin promotes proliferation and transcription. It is inhibited by APC and E-cadherin - loss of APC or E-cadherin will lead to increased transcription

43
Q

What promotes progression through the cell cycle?

A

CDK-cyclin complexes

44
Q

What inhibits progression through the cell cycle?

A

p16 and Rb

45
Q

How does phosphorylation of RB affect transcription?

A

Phosphorylated - activates transcription

Dephosphorylated - blocks transcription

46
Q

What promotes apoptosis?

A

p53

47
Q

Describe the intrinsic apoptosis pathway

A

DNA damage activates p53 - P53 activates BAX and BAK in the mitochondria – activating cytochrome C and APAF-1 which activates caspase 9 to 3 to APOPTOSIS

48
Q

Describe the extrinsic apoptosis pathway

A

FasL binds Fas (CD 95) on membrane - Death-induced signaling complex – FADD and procaspase 8 – caspase 8- Caspase 3 – APOPTOSIS

49
Q

What inhibits caspase 9 and what is a consequence?

A

Inhibitor apoptosis protein (IAP) - blocks apoptosis

50
Q

What hormone is affected in Cushing’s Syndrome?

A

ACTH - retains sodium

51
Q

What hormone is affected in paraneoplastic hypercalcemia?

A

Parathyroid Hormone Related Protein - mobilizes Ca from bone

52
Q

What hormone is affected in SIADH?

A

ADH - leads to hyponatremia (low sodium)

53
Q

What Ig mediates eosinophil reactions?

A

IgE

54
Q

What protein is found in eosinophil granules?

A

Major Basic Protein

55
Q

What chemokine recruits basophils?

A

Eotaxin

SMP Block 2 (4 decks)

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