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Fundamentals of Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

What are the three ways normal fluid homeostasis is maintained?

A
  • vascular wall integrity
  • intravascular hydrostatic pressure
  • osmolarity
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2
Q

What are the causes of edema?

A
  • Increased hydrostatic pressure
  • Reduced Osmotic pressure
  • Lymphatic obstruction
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3
Q

What are examples of why there could be increased capillary pressure?

A
  • venous obstruction: DVT, Mass, or Cirrohosis

- systemic: CHF, hypoperfusion to kidneys

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4
Q

Why could osmotic pressure be low causing edema?

A

Loss of albumin and decreased vascular volume, fluid remains in the interstitium.
Causes of low albumin:
- Damaged Nephrons (leaking through kidney)
- Protein loss through GI pathology
- Malnutrition
- Liver Disease, not making albumin

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5
Q

Causes of lymphatic source of local edema?

A
  • Inflammation
  • Neoplastic
  • Post surgical / Post radiation
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6
Q

How could excessive sodium intake contribute to edema?

A

Increases vascular volume, decreasing the colloid osmotic pressure preventing fluid from the interstitium from returning to circulation.

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7
Q

Where would edema be localized when the patient has left ventricular failure?

A

Pulmonary Edema

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8
Q

If a patient comes into the office with bilateral pedal edema and shortness of breath with a longstanding non-compliance with HTN management. What might be cause of his symptoms?

A

CHF, increased hydrostatic pressure

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9
Q

A patient has pretibial and ankle edema upon lab testing Creatinine is elevated.

A

Acute renal insufficiency, damaged nephrons leak protein int he urine and the liver cannot remake fast enough to keep up with leakage.
Edema from lowered osmotic pressure from the low Albumin levels

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10
Q

What is the difference between hyperemia and congestion, even though both are increased blood in tissues?

A

Hyperemia, active process of increased blood flow into a tissue due to inflammation
Congestion, passive process, decreased venous flow out of tissue.

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11
Q

What are long term consequences of congestion?

A

The blood can stay built up in the tissue and eventually not enough fresh blood can enter the tissue causing ischemia and necrosis in the congested areas.
Ex. CHF can cause congestion in the liver and can lead to necrosis of the hepatocytes.

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12
Q

What is primary hemostasis?

A

Primary hemostasis occurs when there is injury or trauma

  1. Platelet adhesion to vWF on the exposed endothelium
  2. Platelet changes shape and releases factors
  3. Factors recruit others and aggregation occurs
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13
Q

What are the steps in secondary hemostasis?

A

Clot formation

  1. Tissue factor is released from endothelial cells
  2. Phospholipid complex expression
  3. Thrombin Activation***
  4. Fibrin Polymerization
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14
Q

What lab screening can be performed to evaluate the primary hemostasis mechanism?

A

Primarily:

  • Platelet Count
  • Platelet Function
  • vWF function
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15
Q

What are common lab testing for secondary hemostasis?

A

Prothrombin Time - PT (extrinsic and common pathway)
Activated partial thromboplastin time - PTT (intrinsic and common pathway)
Fibrinogen Activity

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16
Q

How do long term anticoagulants reduce the body’s ability to clot?

A

Depletes Vitamin K reduction

Limiting function of Factors: 2, 7, 9, 10

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17
Q

What is a pathologic reason for depleted clotting factors?

A

Liver failure, limits production of clotting factors from the liver increasing chances to bleed significantly.

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18
Q

What is an example of pathologic vascular integrity compromise?

A

Scurvy, no Vitamin C, so defect in collagen and vessel walls

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19
Q

What is the difference between Hemorrhage and Hematoma?

A

Hemorrhage is when blood comes out of the vessel due to trauma or injury to the tissue.
Hematoma is where there is an injury and the blood is pooled into the tissue.

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20
Q

How can you tell the difference between hemorrhagic infarction vs. hematoma in the brain?

A

A hemorrhagic infarction will have mixed normal tissue and necrotic tissue and a hematoma will just have a collection of blood.

21
Q

What is a leading reason for Petechia and Purpura?

A

Low platelet counts
Loss of vascular wall support
Local pressure on vessels

22
Q

What surfaces do the Petechiae appear?

A

Throughout the skin, mucous surfaces, and serous surfaces

23
Q

What are the most common anticoagulants used by the body?

A
  • Anti-thrombin III
  • Protein C and Protein S
  • Tissue factor Pathway
  • PGI2
24
Q

What kind of factors promote thrombosis in the body?

A

Endothelial Injury

Abnormal Blood Flow

25
Q

What is the most common inherited hypercoagulability factor?

A

Factor 5 Leiden

26
Q

How does Factor 5 Leiden increase chances for a thrombosis?

A

Point mutation change of Factor V and Protein C cannot degrade Factor V and it continues to clot.
Increases chance for a thrombosis by between 5-50x%

27
Q

What are the most common external factors for hypercoagulable state?

A

Malignancy
Estrogens - birth control
Heparin-induced thrombocytopenia
Lupus Coagulation factor

28
Q

How can you acquire a hypercoagulable state?

A

Anti-Phospholipid Antibodies, which bind phospholipid complexes increasing chances of thrombosis of arterial and venous flow, high recurrent rates.

29
Q

How do you test for an acquired hypercoagulable state?

A
  • Lupus Anticoagulant

- Anti-cardiolipin antibodies

30
Q

What is odd about testing of Anti-phospholipid antibodies?

A
  • In Vivo they increase the risk of clotting

- In Vitro they inhibit clotting, increasing coagulation times

31
Q

What are the three main causes that can lead to a thrombosis?

A

Endothelial Injury
Abnormal Flow
Hypercoagulability

32
Q

What are common reasons for endothelial injury leading to thrombosis?

A
  • Trauma
  • HTN
  • Infection
  • Vasculitis
  • *Atherosclerotic Plaque
33
Q

Why does Turbulent blood flow increase chance of thrombosis?

A

The turbulance can cause the slowing down of the blood allowing the platelets more time to bind to the endothelial more easily contributing to development of a thrombosis.

34
Q

What can cause the turbulence in the blood vessels?

A
  • Atherosclerotic plaque
  • Aneurysm
  • MI
  • Afib
35
Q

What are the primary causes of a venous thrombi?

A
  • Prolonged statsis / immobilization

- Reduced activity of leg muscles

36
Q

What are the characteristics of a venous thrombosis?

A

50% of the time asymptomatic
DVT are most concerning, because they can break off and travel to the lungs or other parts of the body.
No inflammation involved

37
Q

What kind of embolus is associated with trauma and injury?

A

Fat Embolism

38
Q

What kind of embolus is associated with chest wall injuries and deep sea diving?

A

Air / Nitrogen Embolisms

39
Q

What is it called when a piece of thrombosis breaks off and travels to the lungs causing local ischemia?

A

Pulmonary Embolism, most commonly from DVT and can potentially cause sudden death.

40
Q

What are sources of thrombus embolisms?

A
  • Athrosclerosis
  • Heart Valves
  • Vessels
41
Q

What is the difference between Red and White infarction?

A

Red infarct involves hemorrhage from dual blood supply or blood leaking out of the vessels in the injured tissue.
White usually occurs in solid organs when there is only a single large vessel going into said organ.

42
Q

How is disseminated intravascular coagulation characterized?

A

Usually associated with serious injury, trauma, or sepsis. Begins with small vessel clotting resulting in organ ischemia, then clotting factors run out and they begin to bleed uncontrolled.

43
Q

What are the course of events that occur with “Shock”?

A

Cardiovascular collapse due to dysfunction of pumping of blood or severe blood volume loss.
Hypotension –> Impaired perfusion –> Hypoxia –> Tissue Death –> Person death

44
Q

What is the difference between Cardiogenic and Hypovolemic shock?

A

Cardiogenic is failure of myocardial pump due to infarction or obstruction to flow.
Hypovolemic is when there is severe fluid loss due to blood loss or fluids by means of GI

45
Q

How does Septic Shock occur?

A

Disseminated microbial activity in the blood with widespread immune response causing vasodilation of distal vessels blood pooling and clotting can occur and WBCs cause further damage with cytokinse and interlukins.

46
Q

How are Anaphylaxis and Neurogenic Shock different?

A

Neurogenic is where there is spinal cord or brain stem injury causing sympathetic output loss and vasodilation, hypotension.
Anaphalytic Shock is immune mediated

47
Q

What are the stages and symptoms of shock?

A

Initial: Tachycardia, peripherial vasoconstriction, kidney fluid retention with aldosterone.
Progressive: Tissue hypoxia / lactic acidosis, tissue hypoperfusion
Irreversible Phase: Cellular tissue damage preventing survival, excessive lactic acid production.

48
Q

What is the clinical manifestion of cardiogenic and hypovalemic shock?

A

Cold, Clammy, Cyanotic, Tachycardia, Tachpnea, Hypotension

49
Q

How does Septic Shock present?

A

Initially peripheral vasodilation, skin warm and flushed, typically gram POSTIVE bacteria

Fundamentals of Pathology (12 decks)

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