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ACEM Primary VIVA > VIVA: Pathology - Fluid and haemodynamics > Flashcards

VIVA: Pathology - Fluid and haemodynamics Flashcards

1
Q

List some common triggers of DIC

A
  1. Sepsis*:
    - Bacterial endotoxins
    - Ag-Ab complexes
  2. Major trauma/burns/surgery/snakebite*
  3. Certain cancers*:
    - AML (promyelocitic)
    - Adenocarcinoma of the lung, colon, stomach, pancreas
  4. Obstetric complications*:
    - FDIU
    - Amniotic fluid embolism
    - Pre-eclampsia

*3/4 needed to pass

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2
Q

How does endothelial injury initiate DIC?

A

3 to pass:
- Exposure of sub-endothelial matrix activates platelets and the coagulation cascade
- TNF causes tissue factor to be expressed from endothelial cells
- TNF upregulates the expression of adhesion molecules on endothelial cells to allow leucocytes to bind and damage endothelial cells
- Direct trauma to endothelial cells from Ag-Ab complexes, temperature extremes, or microorganisms

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3
Q

Draw the extrinsic pathway of the coagulation cascade

A
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4
Q

What would you expect to find on a full blood count and coagulation profile in DIC?

A
  • Decreased Hb (MAHA: microangiopathic haemolytic anaemia)
  • Increased WCC
  • Decreased Plt*
  • Decreased fibrinogen
  • Prolonged bleeding time
  • Increased PT/INR, APTT
  • Increased fibrin degradation products*

*needed to pass

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5
Q

What are the pathological consequences of DIC?

A

In DIC, major trauma releases tissue thromboplastins and both clotting pathways are activated

2 major consequences:
- Deposition of fibrin within microcirculation leading to ischaemic/microthrombosis* of vulnerable organs
- Consumptive coagulopathy* with decreased platelets and clotting factors leading to a bleeding diathesis*

*needed to pass

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6
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 its point of origin

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7
Q

Name the different types of emboli

A
  1. Thromboembolus*:
    - Venous: pulmonary
    - Arterial: systemic
  2. Fat embolus*
  3. Gas embolus*
  4. Amniotic fluid embolus*
  5. Air embolus*
  6. Septic embolus
  7. Tumour fragment embolus
  8. Foreign body embolus (e.g. catheter)

*3/5 to pass

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8
Q

What is systemic thromboembolism?

A

Systemic thromboembolism refers to emboli in the arterial circulation

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9
Q

Name the sources of systemic thromboembolism

A
  • Most (80%) arise from intracardiac mural thrombi*, 2/3 of which are associated with LV wall infarcts and 1/4 with LA dilation and fibrillation
  • Remainder originate from aortic aneurysms, thrombi on ulcerated atherosclerotic plaques or fragmentation of a valvular vegetation, with a small fraction due to paradoxical emboli
  • 10-15% of systemic emboli are of unknown origin

*needed to pass + 1 other

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10
Q

What are the differences in the lodgement of venous and arterial thrombi?

A
  • Venous thrombi tend to lodge primarily in one vascular bed (the lung)
  • Arterial thrombi can travel to a wide variety of sites; the point of arrest depends on the source and the relative amount of blood flow that downstream tissues receive
  • Major sites of arterial embolisation are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen and upper extremities involved to a lesser extent
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11
Q

Describe the process of infarction from arterial occlusion

A
  • Dominant histologic characteristic is ischaemic necrosis
  • White infarcts occur in solid organs with end-arterial circulation
  • Acute inflammation occurs within hours, and reparative response follows

Factors influencing infarct development:
- Nature of vascular supply (end-artery vs presence of collateral blood supply)
- Rate of occlusion
- Vulnerability to hypoxia
- Oxygen content of blood
- Calibre of occluded vessel

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12
Q

Describe the process of primary haemostasis

A

Primary haemostasis involves the formation of platelet plug:
- Endothelial damage exposes ECM (collagen, vWF)
- Platelet activation
- Platelet adherence via Gp1b to vWF
- Platelets change shape from flat to round
- Platelets secrete ADP, TXA2, Ca2+ and negatively charged phospholipids -> platelet aggregation (platelet GpIIB-IIIa receptors via fibrinogen)

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13
Q

How is the coagulation cascade activated following injury?

A
  • Vascular damage and exposure of tissue factor* converts factor VII to VIIa
  • This in turn causes a series of amplifying enzymatic reactions that leads to the deposition of a fibrin clot (secondary haemostasis)*
  • Factor X is converted to factor Xa, which in turn converts prothrombin (factor II) to thrombin, which then converts fibrinogen to fibrin (producing fibrin network)

*needed to pass + concept

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14
Q

What does prothrombin time measure?

A

Assesses the extrinsic and common coagulation pathways

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15
Q

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

A
  1. Arteriolar vasoconstriction*:
    - Reflex neurogenic
    - Enhanced by endothelin
  2. Primary haemostasis*:
    - ECM exposed
    - Platelet adherence/activation
    - Platelets aggregate and forms a plug
  3. Secondary haemostasis*:
    - Tissue factors exposed -> coagulation cascade triggers and platelet plug consolidated with generation of thrombin and fibrin
  4. Thrombus and antithrombotic effect*:
    - Fibrin polymerises to form permanent plug
    - tPA regulates

*3/4 steps with understanding of concept to pass

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16
Q

What laboratory tests are used to assess the function of the different pathways of the coagulation cascade?

A

Prothrombin time:
- Measures extrinsic and common pathways
- Factors VII, X, II, V, fibrinogen (including vitamin K dependent factors*)

Partial thromboplastin time:
- Measures intrinsic and common pathways
- Factors XII, XI, IX, VIII, X, V, II, fibrinogen

*identify test, pathways and which one tests vitamin K dependent factors

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17
Q

What is an infarct?

A

Area of ischaemic necrosis caused by arterial or venous occlusion

18
Q

What mechanisms lead to infarction?

A
  • Arterial thrombus*
  • Embolism*
  • Vasospasm
  • Haemorrhage into plaque
  • Extrinsic vascular compression (by tumour or oedema)
  • Torsion of vessel
  • Traumatic rupture
  • Entrapment in hernial sac
  • Venous thrombosis

*needed to pass + 2 others

19
Q

What factors determine the development of an infarct?

A

2/4 to pass:
- Nature of vascular supply (e.g. dual vs end-arterial)
- Rate of occlusion development (time for collaterals to develop)
- Tissue vulnerability to hypoxia
- Oxygen content of blood

20
Q

What is oedema?

A

Increased interstitial fluid

21
Q

What are some of the causes of oedema?

A
  1. Inflammatory* (acute/chronic):
    - Infection
    - Tissue necrosis
    - Foreign body
    - Immune
    - Traumatic
  2. Non-inflammatory*:
    - Increased hydrostatic pressure (e.g. cardiac failure, DVT)
    - Hypoproteinaemia (e.g. chronic liver disease, nephrotic syndrome)
    - Lymphatic obstruction
    - Sodium retention

*2 examples from each to pass

22
Q

What is the difference in the composition of the fluid between inflammatory and non-inflammatory oedema?

A
  1. Inflammatory:
    - Exudate
    - High protein concentration
  2. Non-inflammatory:
    - Transudate
    - Low protein concentration (essentially an ultrafiltrate of plasma)
23
Q

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

A

2/3 to pass:
1. Hydrostatic pressure
2. Colloid osmotic pressure
3. Normal capillary walls

Most protein remains intravascular, fluid leaks out of vessel at arteriolar end and is mostly returned at venular end (small amount also returns via lymphatics)

24
Q

What are the clinical features of heart failure?

A

3/5 to pass:
1. Cardiovascular:
- 3rd heart sound
- Murmurs
- Displaced apex beat
- JVP elevation
- AF
2. Respiratory:
- Dyspnoea
- Orthopnoea
- PND
- APO
- Pleural effusions
3. Renal:
- Fluid retention
- Pedal oedema
- AKI
4. Neurological:
- Confusion secondary to hypoxia
5. Hepatic:
- Congestion
- Ascites
- Cirrhosis (late)

25
Q

What is the pathogenesis of cardiogenic oedema?

A

Decreased CO -> decreased renal perfusion -> secondary aldosteronism -> increased blood volume -> increased venous pressure

26
Q

What are the mechanisms of oedema formation?

A
  1. Increased hydrostatic pressure*:
    - Increased local venous pressure: venous obstruction, compression, thrombosis
    - Increased local arteriolar pressure: dilation, heat, neurohumeral dysregulation
    - Systemic: CCF, constrictive pericarditis, ascites, impaired venous return (e.g. immobility, internal/external obstruction)
  2. Reduced plasma oncotic pressure*:
    - Protein loss: nephrotic syndrome
    - Reduced protein production/absorption: cirrhosis, malnutrition, gut loss
  3. Inflammation:
    - Acute or chronic inflammation
    - Angiogenesis
  4. Lymphatic obstruction:
    - Inflammatory
    - Neoplastic
    - Post-surgical
    - Post-irradiation
  5. Sodium retention with water:
    - Renal insufficiency
    - Activation of renin-angiotensin system
    - Renal hypoperfusion

*needed to pass + 1 other (with 5 specific examples total)

27
Q

Define shock

A

State of global circulatory failure that impairs tissue perfusion* and leads to cellular hypoxia*

*needed to pass

28
Q

Describe the principal mechanisms for three major types of shock and provide a clinical example for each

A
  1. Cardiogenic*:
    - Low CO due to myocardial pump failure
    - E.g. AMI, arrhythmia, myocarditis, cardiomyopathy
    - Also includes obstructive causes like cardiac tamponade and PE
  2. Hypovolaemic:
    - Low CO due to low blood or plasma volume
    - E.g. haemorrhage, massive fluid losses from GIT or skin/burns
  3. Distributive:
    - Shock associated with systemic inflammation / sepsis
    - Activation of cytokine cascades, peripheral vasodilation and pooling of blood, endothelial activation/injury, leucocyte-induced damage, DIC
    - E.g. overwhelming microbial infections, superantigens, burns, trauma, pancreatitis, neurogenic, anaphylaxis
  4. Obstructive:
    - E.g. tension pneumothorax, cardiac tamponade, PE

*cardiogenic + 2 others with correct example to pass

29
Q

What are the stages of shock?

A

2/3 to pass:
1. Initial non-progressive stage:
- Reflex compensatory mechanism maintaining vital end-organ perfusion
- Changes include vasoconstriction, tachycardia, renal fluid retention, shunting of blood away from the skin
2. Progressive stage:
- Tissue hypoperfusion continues, with worsening acidosis / metabolic derangement and widespread tissue hypoxia
- Intervention at this stage prevents vital organs developing irreversible damage
3. Irreversible stage:
- Tissue injury so severe survival is not possible even with correction of haemodynamic defects
- Vital organs fail and can result in death

30
Q

Describe the initial clinical presentation of shock

A

3 to pass:
- Narrowed pulse pressure
- Increased capillary refill time
- Tachycardia
- Hypotension
- Tachypnoea
- Cool clammy or cyanotic skin
- Oliguria
- Altered mental state

31
Q

What happens at the cellular and tissue level during the irreversible phase of shock?

A

3 to pass:
- Widespread cell injury
- Lysosomal enzyme release
- Nitric oxide -> decreased myocardial contractility
- Acute tubular necrosis -> acute renal failure
- Ischaemic gut -> bacteraemic shock
- Severe hypotension, loss of consciousness, anuria
- Pre-cardiac arrest -> death

32
Q

Which organisms commonly cause urosepsis?

A

Gram negative bacilli (80%):
- E. coli*
- Proteus
- Klebsiella
- Enterobacter

Gram positive:
- Enterococcus faecalis
- Staphylococci

*needed to pass + 2 others

33
Q

What is the pathogenesis of septic shock?

A

2 to pass:
1. Inflammatory and counter-inflammatory responses:
- Microbial products (pathogen-associated molecular patterns, PAMPs) triggers production of inflammatory mediators (TNF, IL-1, IFN-a), PAF, prostaglandins, cytokines, chemokines and complement cascade
2. Endothelial activation and injury:
- Causes widespread vascular leakage and tissue oedema
3. Induction of procoagulant:
- Decrease in production of anticoagulant factors
- Dampening of fibrinolysis
4. Metabolic abnormalities:
- Insulin resistance, hyperglycaemia
- Cellular hypoxia causes lactic acidosis
5. Organ dysfunction:
- Diminished myocardial contractility
- ARDS
- Multi-organ failure

34
Q

What factors affect the outcomes of septic shock?

A

2 to pass:
- Extent and virulence of infection
- Immune status of the host
- Presence of other co-morbidities
- Pattern and level of mediator production

35
Q

What are the mechanisms of Gram negative sepsis?

A

Combination of direct microbial injury* and activation of host inflammatory responses e.g. by endotoxins* (lipid A, O Ag):
1. Inflammatory mediator release TNF, ILs (1, 6, 8, 10), prostaglandins, NO, PAF, ROS, PAI-1 (plasminogen activator inhibitor 1)
2. Activation innate cells of immune system (neutrophils, macrophages, monocytes)
3. Humoral interaction to activate complement and coagulation pathways
4. Direct endothelial injury and activation
5. Metabolic abnormalities:
- Insulin resistance and hyperglycaemia
- Glucocorticoid excess/deficiency
6. Immune suppression:
Activation of counter-regulatory mechanisms with anti-inflammatory mediators
- Lymphocyte apoptosis
- Inhibition of neutrophils due to hyperglycaemia

*needed to pass + 2/6 components

36
Q

What are the potential outcomes of septic shock?

A

End-organ and systemic dysfunction, including (3/7 to pass):
- Cardiomyopathy
- Hypotension
- ARDS
- DIC
- Renal failure
- MSOF
- Death

37
Q

When DIC develops, what is the process?

A

Induction of procoagulant state by:
- Increased tissue factor production
- Decreased production of protein C
- Tissue factor pathway inhibitor thrombomodulin
- Decreased fibrinolysis by increasing plasminogen activator inhibitor

Combined with stasis (decreased washout of activated coagulation factors) results in activation of thrombin and fibrin-rich thrombi

38
Q

What pathological mechanisms may contribute to venous thrombus formation in a vessel?

A

Virchow’s triad:
- Endothelial injury (damage to vessel)*
- Alteration in blood flow* (stasis, turbulence)
- Hypercoaguability* of blood

*needed to pass

39
Q

What are some of the different risk factors for venous thrombosis?

A

Primary (genetic)*:
- Mutations (e.g. factor V leiden, prothrombin gene)
- Increased levels of factor VIII, IX, XI, fibrinogen
- ATS, protein C and S deficiencies
- Fibrinolysis defects, homozygous homocysteinuria
- Non O blood group

Secondary (acquired)*:
- Stasis (e.g. prolonged bed rest, immobilisation, long distance travel)
- Tissue injury (e.g. MI, surgery/burns/fractures)
- AF
- Cancer
- Prosthetic cardiac valves/devices
- Indwelling vascular devices (e.g. PICC, CVC)
- External vessel compression (e.g. pregnancy >20/40, May Thurner syndrome)
- Platelet abnormalities (e.g. DIC, HITS, thrombocytosis)
- Cardiomyopathy, nephrotic syndrome
- Hyperoestrogenic states (e.g. pregnancy, postpartum, OCP)
- Sickle cell anaemia
- Smoking
- Antiphospholipid syndrome
- Hyperviscosity states (e.g. polycythaemia rubra vera, leukaemia, hyperproteinaemia)
- Often multifactorial

*2 examples of each to pass

40
Q

What are possible outcomes of a venous thrombus in a vessel?

A

3/5 to pass:
- Propagation: accumulates more platelets and fibrin, eventually leading to vessel occlusion
- Embolisation: dislodges and travels to other sites
- Dissolution: removal by fibrinolytic activity
- Organisation: inflammation leading to fibrosis
- Recanalisation: vascular flow re-established or thrombus incorporated into a thickened vascular wall

41
Q

What is the coagulation cascade?

A

The coagulation cascade is essentially a series of conversions of inactive pro-enzymes to activated enzymes *, culminating in the formation of thrombin which then converts the soluble plasma protein fibrinogen into the insoluble fibrillar protein fibrin *

*needed to pass

ACEM Primary VIVA (45 decks)

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