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General Pathology > Haemodynamic Disorders > Flashcards

Haemodynamic Disorders Flashcards

1
Q

What are the 6 Haemodynamic Disorders

A
  1. Hyperaemia and Congestion (Passive Hyperaemia)
  2. Oedema
  3. Haemorrhages
  4. Shock
  5. Thrombosis and Embolism
  6. Infarction
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2
Q

What is the definition of Hyperaemia

A

Hyperaemia is the term used to mean that the vessels of the microcirculation contain more blood than normal.

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3
Q

What is the difference between Active Hyperaemia and Passive Hyperaemia (Congestion)

A

Active Hyperaemia: blood flow TO organ is INCREASED

Passive Hyperaemia: blood flow OUT of organ is DECREASED

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4
Q

What are the causes of Active Hyperaemia?

A
  1. Nervous Impulse (blushing)
  2. Functional Demand
    a. Muscles during exercise
    b. acute inflammation
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5
Q

What are the causes of Passive Hyperaemia (Congestion)?

A
  1. Local - Obstructed Vein

2. General - Congestive Heart Failure (both left and right)

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6
Q

How do congested organs look like?

A
  • Enlarged
  • Cynotic (bluish or purplish discoloration due to deficient oxygenation of the blood)
  • Firm and heavy
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7
Q

What is Oedema?

A

An excessive extravascular accumulation of fluid in interstitial tissues and body cavities (most severe/pronounced in areas that are gravity dependent like the lower limbs)
It can be localised or generalised.

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8
Q

What is Starling’s Law?

A

The amount of fluid that filters out of the arterial end of a capillary is about equivalent to the amount of fluid reabsorbed at the venous end (balance)

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9
Q

What factors affect Starling’s Law?

A

Hydrostatic Pressure of blood + interstitial fluid

Osmotic Pressure of blood + interstitial fluid

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10
Q

What is the Osmotic pressure of blood/plasma controlled by?

A

Albumin levels. Albumin tends to hold water hence as albumin levels increase, osmotic pressure increase.

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11
Q

What are the primary causes of oedema (due to changes in starling’s law)?

A
  1. Increased hydrostatic pressure of plasma
  2. Reduced osmotic (osmotic) pressure of plasma
  3. Increased endothelial permeability (inflammation)
  4. Lymphatic obstruction
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12
Q

What are the causes of Localised Oedema?

A
  1. Impaired venous drainage (venous occlusion due to thrombosis)
  2. Increased Vascular Permeability and Hyperaemia (Inflammation)
  3. Obstruction/Destruction of lymphatics (Filariasis - parasite, Cancer - clogs up lymph nodes)
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13
Q

What are the causes of General Oedema?

A
  1. Cardiac Cause
  2. Renal Cause
  3. Hepatic Cause
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14
Q

What is the pathogenesis of oedema in Heart Failure?

A

Mechanism 1:

  1. Increased central venous pressure due to a decrease in cardiac output (decreased HR or stroke volume in ventricular failure) resulting in blood backing up into the venous circulation
  2. Increase capillary hydrostatic pressure
  3. increase transudation
  4. Oedema

Mechanism 2:

  1. Decreased cardiac output
  2. Reduced renal blood flow
  3. Increase renin angiotensin
  4. Increase aldosterone secretion + Increase Anti-diuretic Hormone
  5. Renal salt and water retention
  6. Increased plasma volume
  7. Increased capillary hydrostatic pressure
  8. Increased transudation
  9. Oedema
Mechanism 3: 
1. Increased Transudation
2. Decreased plasma volume
3. Decreased Cardiac Output
Mechanism 2
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15
Q

What is transudation?

A

The movement of fluid from the vascular component to the tissue space

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16
Q

What is the pathogenesis of oedema in Nephrotic Syndrome?

A
  1. Protein loss in urine due to glomerular disease
  2. Hypoproteinaema (decreased oncotic pressure)
  3. Increased transudation
  4. Increase sodium retention via (RAA system)
  5. Increase anti-diuretic hormone
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17
Q

What is the pathogenesis of oedema in Chronic LIver Disease?

A
  1. Chronic liver disease causes defective albumin production
  2. Hypoproteinaema (decreased oncotic pressure)
  3. Increased transudation
  4. Increase sodium retention via (RAA system)
  5. Increase anti-diuretic hormone
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18
Q

What is an alternative cause to hypoproteinaemia that causes oedema

A

Malnutrition (lack of protein in diet)

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19
Q

What are the 2 types of oedema fluid?

A
  1. Exudate

2. Transudate

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20
Q

What is the cause of exudate oedema fluid?

A

Inflammation (Infection eg. pneumonia)

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21
Q

What is the cause of transudate oedema fluid?

A

Changes in oncotic/hydrostatic pressure (Starling’s Law) eg. Congestive Heart Failure

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22
Q

What is the difference between exudate and transudate oedema fluid?

A
  1. Protein content (Exudate - high; Transudate - low (<10g/L))
  2. Types of protein (Exudate - As in plasma fibrinogen (clot); Transudate - Albumin, no fibrinogen)
  3. Specific gravity (Exudate - high 1.018; Transudate - low 1.012)
  4. Cells (Exudate - Many inflammatory cells; Transudate - Few inflammatory cells)
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23
Q

What are the causes of Haemorrhage?

A
  1. Traumatic
  2. Spontaneous
    a. Abnormal Vessels
    b. Platelets - Thrombocytopenia, Qualitative Platelet Defect
    c. Coagulative Factor Deficiency
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24
Q

How are Haemorrhages classified by?

A

Size

< 2-3mm: Petechiae
1-2mm: Purpura
Larger: Ecchymoses

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25
Q

What is the cause of Petechiae?

A

Capillary fragility due to malnutrition (vit C deficiency) or decrease platelet count (eg. dengue)

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26
Q

How is coagulative factor deficiency shown on the skin?

A

Purpura or Ecchymoses

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27
Q

What happens if haemorrhage is not picked up on the skin and occurs in organs?

A

Death. :(

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28
Q

What are the effects of blood loss caused by haemorrhages?

A

Acute: Shock
Chronic: Iron-deficiency Anaemia

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29
Q

What are the bodies responses to blood loss caused by haemorrhages?

A

Initial:

  • Maintenance of BP and flow
  • Sympathetic response (Vasoconstriction)

Compensation for volume loss:

  • Fluid retention (RAA, ADH)
  • Redistribution of blood flow

Long term:
- Replacement of RBCs (dependent on functioning bone marrow)

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30
Q

What is shock?

A

Shock is a state of inadequate perfusion of cells and tissues leading to reversible hypoxic injury, and if severe of prolonged enough, to irreversible cell and organ injury and death

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31
Q

What are the different types of shock?

A
  1. Hypovolemic shock (>15-20% is severe) - haemorrhage, vomiting, diarrhoea, burns
  2. Cardiogenic shock - heart failure
  3. Distributive shock - generalised vasodilation, septic shock, anaphylactic shock, neurogenic shock
  4. Obstructive shock - pulmonary embolism, pericardial tamponade
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32
Q

What is septic shock caused by?

A

Infection by microbial antigens (usually gram -ve bacteria) eg. endotoxins (lipopolysaccharide)

33
Q

How do microbial antigens cause septic shock?

A
  1. Binds to endotoxin receptors of macrophages to produce cytokines which are initially protective but later cause vasodilation and decreased cardiac contractility
  2. Endothelial injury which promotes blood coagulation causing disseminated intravascular coagulation
34
Q

What are some clinical manifestations of early shock?

A 
Skin: pale and cold
Kidneys: low urine production
Gut: bowel stasis
Lung: Tachypnea (rapid breathing)
Liver: Fatty change
Brain: Reduced conscious level
Heart: Tachycardia (rapid HR)
35
Q

What are some clinical manifestations of late shock?

A 
Skin: Cyanosed (blue purple discolouration)
Kidneys: Necrosis of tubular epithelium
Gut: Necrosis of lining epithelium
Lung: Necrosis of alveolar epithelium
Liver: Necrosis of centrilobular cells
Brain: Necrosis of neurons, coma
Heart: Myocardial necrosis

Hence, this causes multi organ failure

36
Q

Why is time of the essence when treating shock?

A

Because it results in a vicious cycle of shock

Heart: myocardial damage –> heart failure
Gut: mucosal damage –> loss of fluid, liberation of bacteria
Liver: impaired lactate catabolism –> acidosis –> impairs cardiovascular function
Kidney: acute tubular necrosis –> renal failure –> acidosis –> impairs microcirculation
Lung: alveolar damage –> decreased oxygenation

37
Q

What are the treatment options for Shock?

A
  1. Basic Cardiac Life Support
  2. Advanced Cardiac Life Support
  3. Advanced Trauma Life Support

These must all be provided within the golden hour

38
Q

What is anaphylactic shock caused by?

A

Severe type I hypersensitivity allergic reaction mediated by IGE (histamine)
Treatment: Epinephrine pen

39
Q

What is a Thrombus

A

An intravascular mass formed during life from constituents of the blood

40
Q

What is Thrombosis?

A

The process in which a thrombus is formed

41
Q

What on endothelial cells helps to inhibit platelet aggregation?

A

PGI2

42
Q

What is found underneath endothelial cells?

A

Support tissue containing von Willebrand factor

43
Q

What is the function of platelets?

A
  1. Platelet-collagen fibril attachment (Adhesion) - mediated by von Willebrand’s factor
  2. Degranulation - releases dense granules (ADP, Ca2+, serotonin, histamine, adrenaline) and alpha granules (PF4, fibrinogen, PDGF, factor V, factor VIII, fibrinectin)
  3. Platelet-platelet interadherance (Aggregation) - mediated by ADP, thrombin, thromboxane A2
44
Q

What is a common antiplatelet agent?

A

Asprin - inhibits thromboxane synthesis

45
Q

What is the difference between an anticoagulative agent and an antiplatelet agent?

A

Anticoagulants such as heparin or warfarin slow down your body’s process of making clots. Antiplatelet drugs, such as aspirin, prevent blood cells called platelets from clumping together to form a clot.

46
Q

What is the intrinsic pathway of the Coagulation Cascade?

A

check notes :/ is too complicated to write here well

47
Q

What does thrombin activate in a positive feedback loop for the coagulation cascade?

A

8 to 8a

5 to 5a

48
Q

What are the counteracting mechanisms of the coagulation cascade?

A
  • Antithrombin III

- Fibrinolysis

49
Q

What is coagulative factor II

A

Prothrombin

50
Q

What catalyses the coagulative step of 10 to 10a?

A

8a, 9a, platelet factor 3, 7a

51
Q

What catalyses the coagulative step of prothrombin to thrombin?

A

5a, 10a, platelet factor 3

52
Q

What is the cause of thrombogenesis?

A

Virchow’s Triad

  1. Injury to endothelium
  2. Alteration in blood flow
  3. Alteration in blood coagulability
53
Q

What is deep vein thrombosis (in deep calf veins) caused by?

A

Stasis (build up of activated clotting factors)

54
Q

How does endothelial injury result in thrombosis?

A
  1. Loss of non-reactive interface
  2. Exposure of subendothelial collagen
  3. Local depletion of PGI-2 and plasminogen activator (anti clotting factors)
  4. Release of tissue thromboplastin (tissue factor)
55
Q

What are examples of diseases causing Alterations in Blood Flow?

A
  1. Atheromatous Disease - Turbulence (Eddy currents)

2. Aortic Aneurysm - Stasis

56
Q

What alterations in blood coagulability encourages thrombosis?

A
  1. Increase in the number and stickiness of platelets
  2. Increase in factor 5 (gene mutation)
  3. Increase in prothrombin (gene mutation)
  4. Antithrombin Deficiency
  5. Fibrinolysis defects
57
Q

What are some common clinical states that result in thrombosis?

A
  1. Atrial Fibrillation - thrombus in atria
  2. Prosthetic cardiac valves - thrombus on valves
  3. Post-operative or post-partum state
  4. Prolonged bed rest or immobilisation
  5. Disseminated cancer
  6. Oral contraceptives (oestrogen)
58
Q

What is the risk of thrombosis?

A

That it detaches and becomes an embolus and results in vascular occlusion of distant organs

59
Q

What is the most likely (and feared) destination of the thromboembolus from deep vein thrombosis?

A

Pulmonary artery

60
Q

What are the possible fates of a thrombus?

A
  1. Resolution/Lysis :D
  2. Propagation
  3. Organisation and Recanalisation
  4. Embolism
61
Q

What is an embolus?

A

An embolus is a detached intravascular solid/liquid or gaseous mass that is carried by the blood to a site distant from the point of origin (Embolism)

62
Q

What are the types of Emboli?

A

Solid:

  1. Detached thrombus
  2. Tissue Fragments
  3. Tumour clumps
  4. Foreign Bodies
  5. Atherosclerotic Plug (cholesterol)

Liquid:

  1. Fat
  2. Amniotic Fluid

Gas:

  1. Air
  2. Nitrogen
63
Q

What is the clinical significance of embolism in arteries?

A 
It causes vascular occlusion and hence ischemia and thus necrosis of target organs, leading to death.
Eg.
cerebral artery - brain necrosis
coronary artery - myocardial necrosis
renal artery - renal necrosis
64
Q

What is septic emboli?

A

An embolus caused by infection

65
Q

How does tumour disseminate?

A

Through embolism to spread to other organs and hence kills

66
Q

What are the effects of pulmonary embolism?

A
  1. Sudden Death
  2. Pulmonary Infarction
  3. Pulmonary Hypertension
67
Q

What is atrial fibrillation?

A

An irregular and often rapid heart rate that occurs when the 2 upper chambers of your heart experience chaotic electrical signals.
HR = 100-175 beats a min

68
Q

What is an example of an oral anticoagulant?

A

Warfarin

69
Q

What is fat embolism caused by?

A

Traumatic fracture of the bone marrow

70
Q

What are the effects of fat embolism?

A

Widespread vascular occlusion and damage

71
Q

What are hyperbaric chambers/ decompression chambers used for?

A

As treatment/therapy for air embolism

72
Q

What is air embolism caused by?

A

IV infusion

Deep sea diving injuries

73
Q

What are the effects of air embolism?

A

Lungs: Chokes - interferes with gaseous exchange
Muscle: Bends - very pain
Brain: Staggers - cerebral ischemia causing drowsiness and instability

74
Q

What is amniotic fluid embolism caused by?

A

When amniotic fluid (which is very dirty) gets into maternal uterine lining circulation. It is a rare obstetric complication occuring in 1 in 50.000 deliveries.

75
Q

What are the effects of amniotic fluid embolism?

A

It causes pulmonary embolism causing acute right heart failure. This results in the choking of the mum and has a very high mortality rate.
It also causes disseminated intravascular coagulation.

76
Q

What is Infarction?

A

Necrosis due to ischemia (usually occlusion of artery and sometimes occlusion of venous drainage)

77
Q

What is the difference between white and red infarcts?

A 
White infarcts:
Solid organs (eg. spleen, kidney)
Red infarcts (caused by superimposed haemorrhage over the infarction):
Spongy organs (eg. lungs)
78
Q

What is an example of infarction due to venous occlusion?

A

Testicular torsion
The spermatic artery and vein in the spermatic cord get twisted and blood cannot get out, hence the organ becomes very hemorrhagic (red infarct).

It can also occur to female overies.

79
Q

What are the effects of ischaemia?

A
  1. Remains viable/compensated :) - through anastomosis/blood flow from other vessels
  2. Infarction :(
  3. Healing by fibrosis eg. heart muscle - helps to maintain some integrity
  4. Ischaemic atrophy - organ becomes much smaller and hence has diminished function

General Pathology (10 decks)

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