Circulation 2 (Second half of lecture. See Julia's for 1st half) Flashcards Preview

Pathology Quiz 1 > Circulation 2 (Second half of lecture. See Julia's for 1st half) > Flashcards

Flashcards in Circulation 2 (Second half of lecture. See Julia's for 1st half) Deck (30)
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1

What is Heparin-induced thrombocytopenia (HIT)?

• unfractionated heparin induces the formation of anti heparin-Platelet Factor 4 antibodies ->> activation and aggregation of platelets and endothelial damage >> procoagulant state
- newer heparin preparations induce less antibodies; they induce platelet aggregation if the antibodies are formed already

2

What is Anti phospholipid antibody syndrome (lupus anticoagulant syndrome)?

• protean clinical manifestations
• misnomer - the effects are mediated by the binding of antibodies to plasma proteins
(i.e. prothrombin) causing endothelial damage, platelet and complement activation >> hypercoagulable state

3

What thrombus occurs in microcirculation?

Disseminated Intravascular Coagulation (DIC)

4

What is Disseminated Intravascular Coagulation (DIC) ?

• widespread fibrin thrombi in the microcirculation causing diffuse circulatory insufficiency
• thrombi are apparent only by microscopic inspection

• The massive formation of thrombi consumes platelets and coagulation proteins at the same time activating the fibrinolytic mechanisms

5

What are the clinical manifestations of DIC?

• clinical manifestation: can evolve into a serious bleeding disorder

6

What are the steps of Disseminated Intravascular Coagulation (DIC)?

Widespread microscopic
fibrin thrombi >> Consumption of
Coagulation Factors >> Activation of Fibrinolysis >> Bleeding

7

What are fat embolism?
What are the origins of fat embolism?

Microscopic, multiple fat globules enter the circulation and obliterate an artery

• fractures of long bones with fatty bone marrow
• trauma of fat tissue
• burns

8

What are the symptoms of Fat Embolism Syndrome in severe cases?

• pulmonary insufficiency: tachypnea, dyspnea, tachycardia (ARDS)
• neurologic symptoms: irritability, restlessness, delirium, coma
• anemia and thrombocytopenia, widespread petechiae due to local RBC and platelet aggre
gation

9

What are the consequences of fat embolism?

• mechanical obstruction
• local biochemical injury of endothelium
• release of free fatty acids from fat globules
• platelet aggregation and granulocyte activation

10

What are air embolisms?

Gas bubbles within the circulation cause physical obstruction by themselves
or coalesce forming “frothy masses” that can occlude large arteries or atria.

11

When do air embolisms occur?

• obstetric procedures,
• large chest trauma,
• decompression sickness

12

What is Acute decompression sickness?

• due to sudden transition from high to low pressure environment (scuba divers, unpressurized aircraft)
• The breathed gas bubbles out of solution in the blood to form gas emboli

13

What are the symptoms os acute decompression sickness?
What is the treatment?

• the bends - pain due to rapid formation of air bubbles in the muscles and supporting tissue of the joints
• focal ischemia in brain and heart
• the chokes - lung edema, hemorrhages, focal atelectasis or emphysema
• Treatment : high pressure with slow decompression

14

What is Chronic Decompression Sickness aka Caisson Disease?

• persistence of gas emboli in the skeletal system results in focal necrosis (femur, humerus, tibia)

15

What is Amniotic Fluid Embolism?
When does it occur?

Infusion of amniotic fluid or fetal
masses in the maternal circulation
via a tear in the placenta or
rupture of uterine veins.

During labor or immediately postpartum

Very Rare (1:50,000)
Very Fatal: 30% mortality

16

How is Amniotic Fluid Embolism diagnosed in histopathology?

presence in pulmonary circulation of fetal squamous skin cells, lanugo hair, vernix caseosa fat and mucin from fetal intestine.

17

What is Shock?

decreased systemic perfusion of tissues

18

What are the causes of shock?
(name two categorical, we'll do specifics next)

• decreased effective circulating blood volume
• decreased cardiac output

19

What are the consequences of shock?

hypotension >> impaired tissue perfusion >> cellular hypoxia

20

What are the causes of decreased cardiac output in shock?

• myocardial pump failure

21

What are the causes of decreased effective circulating blood volume in shock?

• decreased blood volume
• hemorrhage
• increased vascular permeability (inflammation)
• increased system volume (vasodilation)

22

What are the three phases of shock?

1) nonprogressive or compensated
2) progressive but still reversible
3) irreversible

23

Name the characteristics of... in shock...
1) nonprogressive or compensated
2) progressive but still reversible
3) irreversible

1. nonprogressive or compensated: compensatory mechanisms maintain cardiac output and blood pressure enabling the perfusion of vital organs such as heart and
brain

2. progressive but still reversible:
generalized tissue hypoperfusion and worsening of circulatory and metabolic imbalances

3. irreversible
severe tissue and cellular injury that results in multiple organ failure and death even in the conditions of correction of hemodynamic defects

24

What are the cellular and tissue changes in shock?

hypoxic injury (Hypoxia means less oxygen being brought to the tissues)

25

In shock...
What is oxygen supply determined by?

• Cardiac output (decreased in cardiogenic shock)
• Amount of circulating hemoglobin (decreased in hypovolemic shock)
• Arterial O2 saturation (decreased in cardiogenic and hypovolemic shock)

26

How is shock pathology similar to DIC?

- widespread thrombi
- multiple foci of ischemic necrosis
- hemorrhage

27

Summary: What is...
Thrombosis?
Embolism?
Shock?

Thrombosis - inappropriate intravascular clotting in a living person
• clot formation on uninjured endothelium
• thrombotic occlusion of vasculature after minor injury

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

Shock - decreased systemic perfusion of tissues caused by decreased effective circulating blood volume or decreased cardiac output.

28

Extra:
What is Cardiogenic Shock?

1) low cardiac output
normal volume,
low blood pressure,
increased central venous pressure,
increased cardiac filling pressure

2) variable pulse rate
peripheral vasoconstriction
diminished perfusion of all organs
except heart and brain
decreased arterial pO2
increased arterio-venous O2 difference
increased arterial blood lactate
normal viscosity

3) decreased urine flow (oliguria)

29

Extra:
What is hypovolemic shock?

1) low circulating volume
low blood pressure
decreased central venous pressure
low cardiac filling pressure

2) increased pulse rate
peripheral vasoconstriction
diminished perfusion of all organs
except heart and brain
decreased arterial pO2
increased arterio-venous O2 difference
increased arterial blood lactate
increased viscosity

3) decreased urine flow (oliguria)

30

Extra:
What is septic shock?

Is mostly due to gram-negative bacteria (also called endotoxic shock)
Endotoxins - bacterial wall lipolysaccharides (LPS)

• Also called hyperdynamic shock
1) Normal circulating volume, low blood pressure, increased pulse rate, cardiac output, ventilation and central venous pressure
2) Alkalosis (with hyperventilation), warm dry extremities, low peripheral resistance (due to vasodilation)
3) decreased urine flow (oliguria)

Main pathophysiologic mechanism - peripheral vasodilation and pooling of the blood