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ACEM Part 1 > Pathology - Fluid/Haemodynamics > Flashcards

Pathology - Fluid/Haemodynamics Flashcards

1
Q

What is edema and what are the causes and the difference in composition of fluid

A

-increased fluid in the interstitial spaces or body cavity

1) non-inflammatory (low protein transudates)
- increased hydrostatic pressure = chronic heart failure
- decreased plasma osmotic pressure = cirrhosis, nephrotic syndrome
- lymphatic obstruction = neoplastic
- sodium retention = excessive salt

2) inflammatory (high protein exudates)
- increased vascular permeability = acute/chronic inflammation, infection, tissue necrosis, foreign body, immune

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2
Q

What factors govern the movement of fluid between vascular and interstitial spaces

A

hydrostatic pressure
colloid osmotic pressure
normal capillary walls (most proteins remain intravascular)

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3
Q

What are the clinical features of heart failure

A
  • lung: dyspnea, orthopnea, APO, pleural effusions
  • cardiac: 3rd heart sound, displaced apex beat, AF, murmur, JVP elevation
  • renal: fluid retention, pedal edema, AKI
  • hepatic: congestion, ascites, cirrhosis
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4
Q

What is the pathogenesis of cardiogenic edema

A

decreased cardiac output and renal perfusion
secondary aldosteronism
increased blood volume/venous pressure

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5
Q

How does increased hydrostatic pressure cause edema

A

forces fluid out of vessels, mostly due to impaired venous return caused by:

heart = congestive heart failure 
veins = obstruction or compression (thrombosis, external pressure, inactivity) 
arteries = arteriolar dilation (heat)
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6
Q

What is the sequence of events that occurs to produce haemostasis after a vascular injury

A

1) arteriolar vasoconstriction: occurs immediately, reduced blood flow to area, augmented by endothelin
2) primary haemostasis: formation of platelet plug
3) secondary haemostasis: coagulation cascade leading to formation of a thrombus
4) activation of counter-regulatory mechanism: serves to restrict the haemostatic plug

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7
Q

Describe the process of primary haemostasis

A
  • the formation of a platelet plug
    1) endothelial injury exposes subendothelial vWF and collagen
    2) platelets bind to endothelial wall via vWF and collagen, which activates platelets to release some granules
    3) platelets change shape, which causes an increased affinity of glycoprotein to fibrinogen
    4) platelets secrete their granule content: alpha (fibrinogen, factor 5, PDGF), delta (ADP, ATP, Ca+2, TXA2)
    5) platelets aggregate by fibrinogen forming bridges between adjacent platelets (stimulated by TXA2 and ADP)
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8
Q

What are the 2 main roles of platelets

A

1) formation of primary haemostatic plug
2) provide surface to recruit and concentrate coagulation factors

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9
Q

How do platelets adhere at the site of vascular injury

A

vWF forms bridge between exposed collagen on endothelial wall and GP1b on platelet surface

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10
Q

What is the coagulation cascade (provide an overview, how is it activated post injury)

A
  • a series of steps leading to the deposition of fibrin and formation of a thrombus
  • involves sequential steps in which inactivated pro-enzymes are converted to activated enzymes to form thrombin
  • comprises of 2 pathways that converge on a final common pathway where activation of factor X occurs

1) extrinsic: activated by exposed tissue factor activating factor 7, measured by PT
2) intrinsic: activated by exposed collagen activating factor 12, measured by PTT

-common pathway involves the activation of thrombin and its subsequent conversion of fibrinogen to fibrin

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11
Q

In the normal coagulation cascade, what happens after factor X is activated

A
  • prothrombin is converted to thrombin (also requires calcium and activated factor 5a as cofactors)
  • thrombin catalyzes conversion of fibrinogen to fibrin (also requires calcium as cofactor)
  • fibrin conversion to a fibrin mesh is catalyzed by factor 13
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12
Q

What laboratory tests are used to assess different parts of the coagulation cascade

A
  • PT: extrinsic and common pathways: factors 2, 5, 7, 10, fibrinogen
  • PTT: intrinsic pathway: factors 2, 5, 8, 9, 10, 11, 12, fibrinogen
  • vitamin K dependent factors: 2, 7, 9, 10, protein c/s
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13
Q

Describe the normal process of fibrinolysis

A
  • circulating plasminogen is converted to plasmin by factor 12a or by tPA (produced by endothelial cells)
  • plasmin breaks down fibrin mesh into fibrinogen
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14
Q

What restricts the activity of the coagulation cascade (how is it limited to site of injury)

A

1) platelet inhibitory effects:
- intact endothelium blocks platelet access to subendothelial matrix
- PGI2 and NO inhibits platelet binding

2) anticoagulants:
- antithrombin III: endogenous anticoagulant that inactivates factors 2a, 9a, 10a, 11a, 12a
- thrombomodulin: produced by endothelium, binds thrombin, activates protein c/s, inactivates factor 5/8 and tPA
- tissue factor pathway inhibitor: forms a complex with Xa, which inhibits Xa, TF and 7a

3) fibrinolytics:
- plasmin: generated from plasminogen and cleaves fibrin mesh
- tPA: protease found in endothelial cells and converts plasminogen to plasmin, which degrades fibrin

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15
Q

What is DIC, what are the consequences?

A

-DIC is a complication of diffuse thrombi activation with consequences of:
widespread fibrin microthrombi in circulation leading to ischaemia of vulnerable organs
concurrent consumption of platelets and coagulation factors causing uncontrollable bleeding

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16
Q

Mechanism and lab findings of DIC

A

pathogenesis: pathological activation of the extrinsic and/or intrinsic pathway, TNF is an important mediator
1) release of tissue factor or thromboplastic substances into the circulation (extrinsic path)
2) widespread endothelial injury promotes platelet aggregation and exposes subendothelial collagen (intrinsic path)

lab: low Hb, high WCC, low platelets, low fibrinogen, high PT/INR, high ddimer

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17
Q

Common causes of DIC

A

causes:
- infection = gram negative sepsis, meningococcaemia, malaria
- obstetric complications = abruption, amniotic fluid embolism
- trauma = burns, extensive surgery
- malignancy = pancreatic cancer, prostate cancer

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18
Q

Describe the pathogenesis of thrombus

A

Virchow triad

1) endothelial injury: most important, cause exposure of subendothelium ECM
2) alterations in normal blood flow: stasis (thrombosis in veins), turbulence (thrombosis in arteries)
3) hypercoagulable state: any alteration in the coagulation pathway, may be primary or secondary

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19
Q

What are the potential fates of an intravascular thrombus

A

propagation
embolisation
dissolution
microbial seeding
organisation
recanalisation

20
Q

What are the risk factors for a hypercoagulable state

A
  • primary (genetic) = factor 5 leiden, deficiency in antithrombin III or protein c/s
  • secondary = OCP, pregnancy, stasis/immobilisation, malignancy, trauma
21
Q

What is an embolus

A

an embolus is any intravascular solid, liquid or gas mass carried by blood flow to a site distant from its origin

types: fat, air, amniotic, thrombi (venous or arterial), tumour fragment, foreign body

22
Q

What is a systemic thromboembolism and what are the sources and where do they lodge

A

refers to an emboli in the arterial circulation

sources: intra-cardiac mural thrombi (80%), aortic aneurysms, ulcerated atherosclerotic plaques, paradoxical
lodge: 75% to lower extremities, 10% to brain, rest to intestines, kidneys, spleen and upper extremities

23
Q

What are the features of fat embolism syndrome

A

associated with long bone fractures, <10% of fat embolism cases, 5-10% fatal

sudden pulmonary insufficiency 1-3 days post injury, associated with petechial rash and neurological symptoms

24
Q

From where do pulmonary thromboemboli originate and what are the clinical effects

A

origin: >95% from DVT
clinical: 60-80% clinically silent, cough, SOB, fever, chest pain, haemoptysis, tachycardia, CVS collapse, death

25
Q

What is an infarct and what are the mechanisms of infarction

A

an infarct is an area of ischaemic necrosis caused by occlusion of arterial supply or venous drainage in a tissue

mechanisms: arterial/venous thrombosis, embolism, vasospasm, haemorrhage into plaque, extrinsic compression

26
Q

What factors influence the development of an infarct

A

nature of vascular supply (dual or end arterial)
rate of occlusion
vulnerability to hypoxia
blood oxygen content

27
Q

Describe the process of infarction

A
  • dominant characteristic is ischaemic necrosis
  • tend to be wedge shaped with apex at site of occlusion and base at organ periphery
  • white infarct = occur in solid organs with end arterial supply (heart/spleen/kidney)
  • red infarct = occur in venous occlusion and tissue with dual circulation and re-perfusion sites
  • acute inflammation occurs within hours
28
Q

What are the metabolic and morphological changes in reversible and irreversible ischaemia

A

Reversible ischaemia

  • metabolic: depletion of ATP cause failure of Na+ pump and swelling, anaerobic metabolism causes lactic acidosis
  • morphologic: cell/organelle swell, membrane blebbing, nuclear chromatin clumping, ribosomes detach from ER

Irreversible ischaemia

  • metabolic: severe disturbance of membrane function and inability of mitochondria to make ATP
  • morphologic: nuclear destruction, lysosomal rupture, cell membrane disruption, severe mitchondrial vacuolization
29
Q

What is irreversible injury in cells after a period of ischaemia

A
  • irreparable structural and intracellular damage that results in necrosis or apoptosis
  • 2 consistent characteristics: severe disturbance of membrane function and inability of mitochondria to make ATP
  • changes in cell: nuclear destruction, lysosomal rupture, cellular membrane disruption, mitochondrial vacuolization
30
Q

What are the mechanisms of ischaemic cell injury

A
  • hypoxia leads to loss of oxidative phosphorylation and reduction in ATP
  • failure of Na+/K+ ATPase causes cell swelling
  • failure of Ca+2/Mg+2 ATPase causes increase in intracellular Ca+2 that degrades membrane phospholipids
  • accumulation of oxygen-derived free radicals causes damage to DNA and cell death
31
Q

What are the differences between ischaemic cell injury and hypoxic cell injury

A

Hypoxia = reduced oxygen carrying capacity, still allows delivery of substances and removal of waste

Ischaemia = reduced blood flow, injures tissues faster than hypoxia

32
Q

What is reperfusion injury and what are the mechanisms

A

when reperfused tissues sustain a loss of cells in addition to the cells already irreversibly damaged

mechanisms:
- reactive oxygen species = due to incomplete reduction of oxygen by damaged mitochondria
- inflammation = due to increased cytokine production from hypoxic cells recruiting inflammatory cells
- activation of complement = ischaemic tissue activates complem

33
Q

Define shock and what are the major categories

A

Tissue hypoperfusion due to either reduced cardiac output or reduced effective blood volume

Categories:
Cardiogenic = low cardiac output due to pump failure (AMI, arrhythmia)
Hypovolaemic = low cardiac output due to haemorrhage or volume loss (burns, bleeding)
Septic = vasodilatory state caused by infection (gram negative bacteraemia)
Neurogenic = loss of vascular tone and peripheral pooling (spinal injury)
Anaphylactic (distributive) = systemic vasodilation and increased vascular permeability (allergy)
Obstructive = low cardiac output due to obstructive cause (tension pneumothorax, tamponade

34
Q

What are the stages of shock

A

1) non-progressive: reflex neurohumoral compensatory mechanisms are activated and perfusion is maintained
- baroreceptor reflexes, catecholamines, RAAS, ADH release, peripheral vasoconstriction
2) progressive: tissue hypoperfusion and circulatory/metabolic abnormality causing lactic acidosis
- vasomotor response is blunted, leading to peripheral pooling, hypoxic injury, DIC, organs begin to fail
3) irreversible: even if perfusion is restored, survival is not possible
- widespread cellular injury, acute tubular necrosis leading to renal failure, ischaemic gut leading to septic shock

35
Q

What is the initial clinical presentation of shock

A

narrow pulse pressure
increased CRT
tachycardia
hypotension
tachypnea
clammy skin
oliguria
confusion

36
Q

Show the relationship between blood loss and cardiac output in haemorrhagic shock

A
  • turns down at around 20%
  • dead at 45%
37
Q

What are the physiological compensatory mechanisms of hypovolaemic shock

A
  • baroreceptor reflexes (seconds)
  • chemoreceptor reflexes (seconds)
  • circulating vasoconstrictors
  • renal reabsorption of sodium and water (minutes)
  • activation of thirst mechanisms
  • reabsorption of tissue fluids (minutes)
  • renal compensation via EPO (long term)
38
Q

What is the pathogenesis of septic shock (how do microbes initiate septic shock)

A
  • combination of direct microbial injury and activation of host inflammatory responses
  • bacterial toxin (endotoxin) binds to LPS binding protein in serum

1) interaction with the innate immune system: neutrophils, macrophages, monocytes
2) interaction with the humoral immune system: activate complement and coagulation pathways
3) inflammatory mediator release: TNF, IL-1, NO, PAF, reactive oxygen species, proteases, histamine, serotonin
4) endothelial activation and injury: causes elaboration of cytokines and vasoactive mediators
5) induction of a procoagulant state: may cause DIC
6) metabolic abnormalities: cytokines and stress-induced hormones causes insulin resistance and hyperglycaemia
7) organ dysfunction: hypotension, edema and thrombosis all reduce oxygen and nutrient delivery to tissues

39
Q

What is the effect of endothelial cell activation and injury during septic shock (what happens to the vessel)

A

thrombosis
increased vascular permeability
vasodilation

40
Q

How does endothelial activation in septic shock result in DIC

A

sepsis favours coagulation:
increased tissue factor production
decreased fibrinolysis
stasis

41
Q

When DIC develops, what is the process

A

-induction of a procoagulant state by:
increased tissue factor production
decreased production of protein c
tissue factor pathway inhibitor thrombomodulin
decreased fibrinolysis by increasing plasminogen activator inhibitor

42
Q

What is endotoxin

A
  • bacterial cell wall lipopolysaccharide (LPS) contained in the outer membrane of cell wall in gram negative bacteria
  • LPS is made up of lipid A and O antigen (lipid A has endotoxin activity)
  • effects of LPS: activates compliment, releases cytokines (TNF, IL-1, IL-6)
43
Q

How does endotoxin cause septic shock

A
  • activation of neutrophils, macrophages and monocytes causes mediator release and inflammatory response
  • causes: systemic vasodilation, widespread endothelial injury, decreased myocardial contractility, DIC
44
Q

How are specific organs effected in septic shock

A
  • heart: dysfunction, depression, dilation
  • vascular: hypotension, vasodilation
  • microcirculation: endothelial injury and activation
  • coagulation system: DIC
  • lungs: ARDS
  • liver/kidney: failure
45
Q

What determines the severity and are the possible outcomes of septic shock

A

severity:
extent and virulence of infection, immune status of host, co-morbid conditions

outcomes:
cardiomyopathy, hypotension, ARDS, DIC, renal failure, death

ACEM Part 1 (38 decks)

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