Pathology Week 3

Question 1

Edema is…

Answer 1

characterized by an increase in intercellular fluid

Question 2

What are the mechanisms of edema?

Answer 2

• Increased hydrostatic pressure
• Decreased plasma osmotic pressure
• Lymphatic obstruction
• Increased sodium (increased hydrostatic pressure due to expansion of intravascular volume and reducing plasma osmotic pressure)
• Inflammation

Question 3

Relating to edema what are the causes of: Increased hydrostatic pressure

Answer 3

• Systemic: CHF
• Regional: Deep venous thrombosis
• venous obstruction, Iatrogenic fluid overload

Question 4

Relating to edema what are the causes of: Decreased plasma osmotic pressure

Answer 4

• low albumin: nephrosis, liver disease

Question 5

Relating to edema what are the causes of: Lymphatic obstruction

Answer 5

• surgery, tumor, radiation, filaria

Question 6

Relating to edema what are the causes of: Increased sodium

Answer 6

• renal disorders; secondary to CHF

Question 7

Relating to edema what are the causes of: Inflammation

Answer 7

• Acute, chronic, angiogenesis

Question 8

Describe subcutaneous edema:

Answer 8

Subcutaneous edema may be diffuse but tends to accumulate preferentially where body positioned greatest distance below heart (hydrostatic pressure highest there) and most pronounced in legs when standing and sitting when recumbent (termed dependent edema)

Question 9

Describe pitting edema:

Answer 9

Pitting edema: finger shaped depression in subcutaneous tissue

Question 10

Describe pulmonary edema:

Answer 10

lungs 2-3x normal weight, sectioning reveals frothy, sometimes blood tinged fluid consisting of air, edema fluid and extravasated red cells.

Question 11

Describe brain edema:

Answer 11

Localized or generalized depending on nature and extent of pathologic progress or injury
- Generalized edema, show narrowing of sulci while gyri are swollen and flattened against the skull

Question 12

What is hyperemia?

Answer 12

It is an active process (exercise, inflammation) that increases blood volume through arteriolar dilation.

Question 13

What is congestion?

Answer 13

Congestion is a passive process (local obstruction, CHF) that increases blood volume through capillary engorgement (decreased outflow) with possible associated cyanosis.

Question 14

Explain edema’s relationship to congestive heart failure

Answer 14

• Right heart failure, increased hydrostatic pressure in venous circuit
• Additionally, decreased renal perfusion causes kidneys to hold onto water
• Creates vicious circle because heart can’t handle more water

Question 15

What is hemostasis?

Answer 15

The balance between coagulation and anticoagulation, forming a hemostatic plug when needed in response to vascular injury.

Question 16

What is thrombosis?

Answer 16

The pathologic counterpart to hemostasis, causing formation of a blood clot within intact vessels.

Question 17

Describe Virchow’s Triad

Answer 17

◦Alteration in endothelium (endothelial injury)
◦Alteration in flow (abnormal blood flow = stasis or turbulence)
◦Alteration in coagulability (hypercoagulability) i.e. loss of platelet receptors or issues with factors in coagulation cascade

Question 18

What are the steps in normal hemostasis?

Answer 18

1. Vasoconstriction
2. Primary hemostasis
3. Secondary hemostasis
4. Thrombus and Antithrombotic events

Question 19

Describe first step in hemostasis (vasoconstriction)

Answer 19

Transient vasoconstriction

    - Caused by reflex neurogenic mechanisms
    - Augmented by endothelin

Question 20

Describe second step in hemostasis (primary hemostasis)

Answer 20

1. von Willibrand Factor (vWF) binds to exposed ECM
2. Platelets adhere to vWF through GP1b receptor
3. Platelets are activated by adhesion (shape change)
4. Platelets release granules (ADP, TXA2)
5. Platelets aggregate through GP2b/3a and fibrinogen
6. Primary hemostatic plug formed

Question 21

Describe third step in hemostasis (secondary hemostasis)

Answer 21

1. Tissue factor released
2. Activation of coagulation cascade
3. Activation of thrombin
4. Thrombin converts fibrinogen to fibrin
5. Thrombin cross-links fibrin forming hemostatic plug (thrombus)

Question 22

Describe fourth step in hemostasis (thrombus and antithrombotic events)

Answer 22

Counterregulatory mechanisms limit size of hemostatic plug
• Release of tissue plasminogen activator (t-PA) causes fibrinolysis
• Release of thrombomodulin blocks coagulation cascade

Question 23

What is the most common hypercoaguable mutation?

Answer 23

Factor V (Leiden) Mutation

Question 24

What is an embolism?

Answer 24

A detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.

Question 25

What are the pathways of the coagulation cascade?

Answer 25

Extrinsic
Intrinsic
Common

Question 26

Elevated PTT is indicative of problems in which pathway?

Answer 26

Intrinsic

Question 27

Elevated PT is indicative of problems in which pathway?

Answer 27

Extrinsic

Question 28

What are the possible fates of a thrombus?

Answer 28

Propagation
Embolization
Dissolution
Organization and recanalization

Question 29

What is the etiology of shock?

Answer 29

The hallmarks of shock include hypotension and hypoperfusion leading to cell death and eventually multi-organ failure

Question 30

What are the major types of shock?

Answer 30

Cardiogenic (MI, heart pump failure)
Hypovolemic (loss of blood or plasma)
Septic (host response to bacterial or fungal infection)
Allergic (IgE hypersensitivity)

Question 31

What is the morphology of shock?

Answer 31

◦BP low, <90 systolic by definition, with orthostatic changes possible initially
◦Weak, rapid, “thready” pulse
◦Skin clammy, mottled
◦Pt may be poorly responsive

Question 32

What are the stages of shock?

Answer 32

Nonprogressive stage - initial
Progressive stage - tissue hypoperfusion
Irreversible stage - cell injury too far gone

Question 33

What is the clinical course for shock?

Answer 33

◦Trendelenburg
◦Oxygen
◦Fluid balance
  ◾Foley catheter to monitor output
  ◾Central catheters used less often now
◦Monitor carefully
◦Diagnose and treat underlying problem

Question 34

What is DIC?

Answer 34

Disseminated Intravascular Coagulation (or consumption coagulopathy) is onset widespread thrombosis within microcirculation. It consumes platelets and coagulation proteins while activating fibrinolytic mechanisms.

Recognized by elevated D-Dimer levels.