Patho - Hemodynamic & Thromboembolic Disease

Front 1

What are the 4 mechanisms (causes) of edema?

Back 1

Increased capillary pressure/hydrostatic pressure
Diminished colloid osmotic pressure, loss of blood proteins (albumin)
Increase of intravascular fluid (renin-angio system)
Lymphatic obstruction

Front 2

How does malnutrition cause edema?

Back 2

Malnutrition --> decreased hepatic synthesis --> decreased albumin concentrations --> descreased osmotic pressure of plasma and loss of fluids from vasculature

Front 3

What is anascara?

Back 3

Generalized body edema

Related to nephrotic syndrome

Front 4

What is hydrothorax? Hydropericardium? Ascities?

Back 4

Pleural effusion - can cause collapsed lung due to pressure

Effusion of pericardial sac

Ascities: hydroperitoneium, abdominal effusion

Front 5

Exudate + pus =

Back 5

Purulent exudate

Front 6

Pulmonary edema is common with what chronic disease?

Back 6

Left ventricular heart failure
Renal failure
Pulmonary infection (bac favor endemic environments)

Front 7

What are the effects of edema in the brain?

Back 7

Can cause herniation of brain through foramen magnum, will cause brain stem to twist or compress

Front 8

Subcutaneous edema can indicate what disease?

Back 8

Cardiac or renal

Front 9

Compare hyperemia & congestion

Back 9

Hyperemia: active process of arteriolar dilation
--increased blood flow --> blood accumulation in tissues --> erythema of oxygenated blood

Congestion: passive process of reduced outflow via venous obstruction, cardiac failure
Can lead to cyanosis
Congestion + increased blood volume = edema

Front 10

How are hemosiderin-laden macrophages made in tissues?

Back 10

Congestion causes capillaries to rupture --> macrophages are recruited to clean up RBC excess --> iron is retained leading to pigment

Front 11

What is the mechanism of hemorrhage?

Back 11

Extravasion of blood into extravascular space

Front 12

Hemorrhagic shock is loss of ______% of blood

Back 12

>20%

Front 13

The range of hemorrhage sizes

Back 13

1-2mm, petchiae
>3mm, purpura
>1-2cm, subcutaneous hematoma

Front 14

Development of intravascular blood clots during pathologic hemostasis is

Back 14

Thrombosis

Front 15

Three factors that predispose thrombus formation include

Back 15

1) Endothelial injury - heart valve replacements, MI
2) Alteration in normal flow - turbulence, vegetative
3) Hypercoagulability - DVT, genetic mutations (coagulation cascade effects), MI, bedrest, atrial fib, cancer, DIC

Front 16

Thrombi on heart valves develop due to

Back 16

Blood-borne bacteria or fungi that adhere to valves to cause damage (vegetations)

Front 17

Mural thrombi are located

Back 17

In heart chambers or aortic lumen

Front 18

The three clinical locations of arterial thrombi are

Back 18

Coronary, cerebral, femoral

Front 19

Aortic emboli usually affect what anatomical sites?

Back 19

Brain
Kidney

Front 20

The propogation of thrombi is what process?

Back 20

Thrombi accumulates additional platelets and fibrin

Front 21

Dissolution of thrombi is what process?

Back 21

Thrombi go through rapid shrinkage and disappear via effects of fibrinolysis

Front 22

What is recanalization?

Back 22

Lumen that was once obstructed by a clot becomes reestablished by ingrowth of endothelial cells, smooth muscle and fibroblasts

Front 23

What is an embolism?

Back 23

Detached intravascular mass (liquid, solid, gas) carried to distant site from origin --> can lodge into vessels and cause partial to complete occlusion --> ischemia or infarction --> necrosis

Most common: blood in thromboembolism
Also: fat, nitrogen, cholesterol

Front 24

The most common source of venous emboli

Back 24

DVT

Front 25

The most common source of arterial emboli

Back 25

Coronary arteries --> MI

Front 26

The most serious thromboembolism form is

Back 26

PE

Can cause thrombi in R. side of heart that travels to pulmonary artery and causes occlusion --> pulmonary hypertension or R. side ventricular failure (can't pump blood through blocked vessels) also called cor pulmonale

How?
Infarct due to loss of blood --> necrosis --> inflammation --> scarring --> vasculature obstruction

Front 27

A PE that obstructs more than ____% of pulmonary circulation causes

Back 27

Right sided failure, cor pulmonale, sudden death via cardiovascular collapse

Front 28

What is Caisson's disease?

Back 28

Gas bubbles coalesce to form mass that obstructs vascular flow (decompression sickness)

Front 29

A fluid embolism cause from childbirth is

Back 29

Amniotic embolism from placental tear

Front 30

What is an infarct?

Back 30

Area of ischemic necrosis caused by occlusion of arterial supply OR venous draining

Front 31

What is hypoxia vs ischemia?

Back 31

Hypoxia: O2 loss only

Ischemia: O2 AND nutrients

Front 32

The most common location for coagulative necrosis is

Back 32

Heart/myocardium
Kidney

Front 33

Liquefactive necrosis occurs most frequently in

Back 33

Brain tissue/CNS

Front 34

Hemorrhagic necrosis/infarct most common where?

Back 34

Lung - dual-blood supply organ

Will become pale with progression of infarct

Front 35

What anatomical structures are most susceptible to infarct effects?

Back 35

Brain, heart

Front 36

What is shock?

Back 36

Systemic hypotension due to reduced cardiac output or reduction in blood volume --> impaired perfusion --> hypoxia

Front 37

The three categories of shock, and an example of their effects include

Back 37

Cardiogenic: low CO due to pump failure
Hypovolemic: low CO due to low blood volume (most common)
Septic: vasodilation and peripheral pooling from immune response or infection

Front 38

Clinical manifestations of shock include

Back 38

Hypotension, weak/rapid pulse, cool/clammy skin

Front 39

The stages of shock are

Back 39

1) nonprogressive: reflex mechanisms compensate to maintain perfusion

2) progressive: tissue hypoperfusion, worsening circulatory imbalance and acidosis

3) irreversible: cellular and tissue injury that cannot be repaired by reperfusion