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Flashcards in Pathology Week 3 Deck (34):
1

Edema is...

characterized by an increase in intercellular fluid

2

What are the mechanisms of edema?

- 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

3

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

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

4

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

- low albumin: nephrosis, liver disease

5

Relating to edema what are the causes of: Lymphatic obstruction

- surgery, tumor, radiation, filaria

6

Relating to edema what are the causes of: Increased sodium

- renal disorders; secondary to CHF

7

Relating to edema what are the causes of: Inflammation

- Acute, chronic, angiogenesis

8

Describe subcutaneous edema:

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)

9

Describe pitting edema:

Pitting edema: finger shaped depression in subcutaneous tissue

10

Describe pulmonary edema:

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

11

Describe brain edema:

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

12

What is hyperemia?

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

13

What is congestion?

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

14

Explain edema's relationship to congestive heart failure

• 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

15

What is hemostasis?

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

16

What is thrombosis?

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

17

Describe Virchow's Triad

◦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

18

What are the steps in normal hemostasis?

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

19

Describe first step in hemostasis (vasoconstriction)

Transient vasoconstriction
- Caused by reflex neurogenic mechanisms
- Augmented by endothelin

20

Describe second step in hemostasis (primary hemostasis)

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

21

Describe third step in hemostasis (secondary hemostasis)

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)

22

Describe fourth step in hemostasis (thrombus and antithrombotic events)

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

23

What is the most common hypercoaguable mutation?

Factor V (Leiden) Mutation

24

What is an embolism?

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

25

What are the pathways of the coagulation cascade?

Extrinsic
Intrinsic
Common

26

Elevated PTT is indicative of problems in which pathway?

Intrinsic

27

Elevated PT is indicative of problems in which pathway?

Extrinsic

28

What are the possible fates of a thrombus?

Propagation
Embolization
Dissolution
Organization and recanalization

29

What is the etiology of shock?

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

30

What are the major types of shock?

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

31

What is the morphology of shock?

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

32

What are the stages of shock?

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

33

What is the clinical course for shock?

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

34

What is DIC?

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.

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