Fluid, Electrolyte Imbalance and Hemodynamic Disorders II Flashcards

1
Q

What is a thrombosis?

A

Thrombosis is the formation of a solid or semi-solid mass from blood components with the vascular system in life.

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2
Q

Both thombosis and hemostasis invole three components. They are:

A

i. Platelets
ii. Vascular wall
iii. Coagulation cascade

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3
Q

What are the 3 disposing factors (causes) for thrombus formation (Virchow’s triad)?

A
  1. Endothelial injury
  2. Stasis or turbulence of blood flow
  3. Blood hypercoagulability (changes in blood composition)
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4
Q

The size and shape of a thrombus depend on the ________ and _______.

A

The site of origin and the cause.

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5
Q

Arterial or cardiac thrombi begin at sites of ________ or _______, while venous thrombi characteristically occur at sites of _______.

A
  • Endothelial injury or turbulence
  • Stasis
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6
Q

Thrombi on the heart valves are called _________.

A

Vegetations

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7
Q

Deep vein thrombosis can be complicated by:

A

i. Advanced age, bed rest and immobilisation
ii. Trauma, surgery, burns
iii. Cardiac failure
iv. Peripartum, postpartum state
v. Thrombophilia
vi. Disseminated cancers

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8
Q

Atherosclerosis is a major initiator of thrombosis due to loss of endothelial integrity and abnormal flow.

True or False?

A

True.

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9
Q

How do you manage thrombosis?

A

i. Blood thinners e.g. Heparin, Warfarin.
ii. Clot busters (thrombolytics):- Streptokinase, Urokinase and tissue plasminogen activators (t-PA) such as Alteplase, Tenecteplase
iii. Endovascular surgical procedures
iv. Physical measures such as compression stockings, ambulation.

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10
Q

What is an embolus?

A

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

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11
Q

Mention 8 forms of emboli.

A
  1. Thromboemboli
  2. Fat emboli
  3. Bone marrow emboli
  4. Air emboli
  5. Foreign particle emboli
  6. Artherosclerotic emboli
  7. Tumour emboli
  8. Amniotic fluid emboli.
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12
Q

What is the clinical significance of thromboembolism?

A

It may cause infarction of downstream tissue.

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13
Q

How do you manage embolism?

A
  1. Hospitalisation
  2. Prompt diagnosis
  3. Blood thinners
  4. Thrombolytics
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14
Q

Pulmonary embolisms usually originate from the deep leg vein thrombi above the knee level.

True or False

A

True.
They often originate form the popliteal, femoral and iliac veins.

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15
Q

Depending on the size, a pulmonary embolus could settle within:

A

i. The main pulmonary trunk
ii. The bifurcation
iii. The main pulmonary arteries
iv. The medium pulmonary arteries
v. The smaller branching arteries and arterioles.

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16
Q

What is paradoxical or crossing embolism?

A

The crossing of a venous embolism into systemic circulation through an interartrial or interverntricular defect.

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17
Q

The clinical outcome of a pulmonary thromboembolism depends on:

A

i. the severity of the occlusion:- size of occluded artery and number of occluding emboli
ii. the cardiorespiratory status of the patent

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18
Q

Sudden death due to cardiovascular collapse or right ventricular failure occurs when 60% or more of pulmonary circulation is obstructed with emboli.

True or False?

A

True.

19
Q

Pulmonary hypertension with right ventricular failure may occur as a result of many emboli over a period of time.

True or False?

A

True.

20
Q

What is systemic thromoembolism?

A

This refers to emboli in arterial circulation.

21
Q

Mention 4sources of systemic thromboembolism.

A
  1. Intracardiac mural thrombosis
  2. Valvular vegetation
  3. Ulceration of atherosclerotic plaques
  4. Aortic aneurysms
22
Q

What are the major sites for arteriolar embolisation?

A

i. The lower extremities
ii. The brain
iii. The intestines, kidney, spleen.
The upper limbs ( least common site)

23
Q

The consequences of tissue embolism depend on what 3 factors?

A

i. Tissue vulnerability to ischemia
ii. Caliber of occluded vessel
iii. The efficiency of collateral blood supply

24
Q

Arterial embolisation causes infarction of the affected tissues.

True or False?

A

True.

25
Q

Fat and bone marrow embolisms occur in individuals with severe ________ injuries.

A

Severe skeletal injuries

26
Q

What is an infarction?

A

An infarction is a localised area of ischemic tissue necrosis resulting often from the sudden reduction or cessation of its arterial blood supply or occasionally its venous drainage.

27
Q

What are the causes of infarction?

A

i. Thrombotic or embolic events
ii. Coronary artery spasm
iii. Expansion of atheromatous plaque (atheroma) due to intraplaque haemorrhage
iv. Torsion of pedicle of mobile organ
v. External pressure on blood vessel e.g. from tumour.

28
Q

External pressure and torsion usually interfere with venous drainage.

True or False?

A

True.

Veins are more readily compressed than arteries.

29
Q

How are infarctions classified?

A

i. On the basis of their colour:- red (haemorrhagic) or white (pale, anaemic)
ii. On the basis of the presence or absence of microbial infection:- septic or bland

30
Q

How do you manage an infarction?

A

i. Thrombolytics e.g streptokinase, urokinase and t-PAs such as Alteplase and Tenecteplase.
ii. Tissue reperfusion
iii. Heparin
iv. Beta blockers
v. Magnesium
vi. Insulin

31
Q

What is shock?

A

Shock is a state of systemic hypoperfusion that is caused by either a reduced cardiac output or a reduced effective circulating blood volume.

31
Q

Mention 5 categories of shock.

A
  1. Cardiogenic shock
  2. Hypovolemic shock
  3. Septic shock
  4. Neurogenic shock
  5. Anaphylactic shock
32
Q

Briefly describe cardiogenic shock.

A

This is due myocardial pump failure occurring as a result of intrinsic myocardial damage, extrinsic pressure or obstruction of outflow.

E.g. myocardial infarction, ventricular rupture, arrhythmia and pulmonary embolism.

33
Q

Briefly describe hypovolemic shock.

A

This is due to inadequate circulating blood or plasma volume.

E.g. Haemorrhage, Fluid loss due to diarrhoea, emesis and severe burns.

34
Q

Briefly describe septic shock.

A

This is due to peripheral dilation, drop in blood pressure along with multiple organ failure in response to severe infections.

E.g. endotoxic shock, fungal sepsis, gram-positive septicemia.

35
Q

Briefly describe neurogenic shock.

A

This is due to a loss of vascular tone and peripheral pooling of blood.

E.g. anesthetic accidents, spinal cord injury.

36
Q

Briefly describe anaphylactic shock.

A

This is an Ig E mediated hypersensitivity reaction causing widespread vasodilation with pooling of blood, causing cellular anoxia.

e.g. Drug anaphylaxis.

37
Q

What are the stages of shock?

A
  1. Non-progressive (compensated) stage
  2. Progressive (decompensated stage)
  3. Irreversible stage
38
Q

Describe the non-progressive stage of shock.

A

Reflex compensatory mechanisms are activated to maintain cardiac output, blood pressure and perfusion of vital organs.
These mechanisms include:
i. arteriolar constriction to increase blood pressure
ii. Increased heart rate
iii. renal conservation of fluids through secretion of ADH and activation of RAAS.

39
Q

Describe the progressive stage of shock.

A

In this stage, there is widespread tissue hypoxia, causing intracellular shift to anaerobic glycolysis, with excessive lactic acid production, resulting in lactic acidosis, which further leads to arteriolar dilation and peripheral pooling.

With widespread tissue hypoxia, vital organs are affected and start to fail.

40
Q

Describe the irreversible stage of shock.

A

Without prompt intervention, the damage enters and irreversible stage where the resulting cellular and tissue injury are so severe that despite corrective measures, survival is no longer possible.

Widespread cell injury causes lysozyme leakage, further aggravating the shock state.
Myocardial contractile function worsens mostly due to nitric acid synthesis.
If intestinal flora leak into circulation due to ischemic bowel, endotoxic shock is superimposed. Renal shutdown occurs due to acute tubular necrosis.

41
Q

What are the pathological features of shock?

A

The brain: hypoxic encephalopathy

The heart: foci of haemorrhage and necrosis are seen in the sub-epicardial and sub-endocardial regions of the myocardium.

The lungs: shock lung or adult respiratory distress characterised by pulmonary edema and fibrin deposition on the alveolar walls.

The Kidneys: Acute tubular necrosis (ATN).

42
Q

How do you manage hypervolemic shock?

A

i. Rapid response at accident scene
ii. Application of pressure on site of external bleeding to prevent further blood loss
iii. Use of antisecretory agents e.g. somatostatin and octreotide for vasoconstriction.

43
Q

How do you manage anaphylactic shock?

A

i. Epinephrine injection.
ii. Hospitalisation
iii. Oxygen intubation or ventilator
iii. IV histamines and cortisone to reduce inflammation of air passages
iv. Bronchodilators e.g. albuterol