Fluid and Haemodynamic ( 10% - includes physiology Circulating Body Fluids 5% )

Question 1

Regarding oedema

• Hypoproteinaemia is the commonest cause of systemic oedema
• Hepatic cirrhosis is the commonest cause of hypoproteinaemia
• Facial oedema is a prominent feature of anasarca
• Hereditary angioneurotic oedema involves skin only
• Infection does not cause pulmonary oedema

Answer 1

Facial oedema is a prominent feature of anasarca
Anascara = generalised and extreme oedema

Question 2

Oedema can be caused by

• Decreased hydrostatic pressure
• Sodium retention
• Hyperproteinaemia
• Polycythaemia
• Hypertension

Answer 2

• Increased hydrostatic pressure
• Sodium retention
• Hypoproteinaemia

Question 3

Oedema can be caused by

• Raised capillary hydrostatic pressure
• Reduced colloid osmotic pressure
• Vitamin C deficiency
• Elevated angiotensin II levels
• All of the above

Answer 3

All of the above, and more!

Question 4

peripheral oedema

• is caused by decreased hydrostatic pressure
• is caused by increased renin-angiotensin-aldosterone secretion
• is characterized by a fluid with specific gravity of 1.020
• is commonly caused by protein-losing gastroenteropathy
• is increased by salt restriction in the diet

Answer 4

• Increased hydrostatic pressure
• Increased RAAS secretion
• Exudate has a SG > 1.020, Transudate < 1.012. Peripheral oedema can be either
• Rarely/uncommonly caused by protein causing enteropathies
• Reduced by salt-restriction (if there is underlying kidney disease that is causing the oedema in the first place)

Question 5

With regards to oedema

• It is caused by increased interstitial osmotic pressure
• It results in gross cell swelling
• It is characterized by increased plasma volume
• Nephritic syndrome results in more severe oedema than cardiac dysfunction
• Outflow of fluid is from the venule

Answer 5

• It is caused by reduced interstitial osmotic pressure
• It results in gross insterstitial swelling
• It is characterized by increased (salt/water retention) OR reduced (hypoproteinemia) plasma volume, depending on the underlying cause
• Nephritic syndrome results in more severe oedema than cardiac dysfunction
  
  • ​?Due to low protein causing a generalised oedema
• Outflow of fluid is from the ?capillary

Question 6

non-inflammatory oedema

• has a high protein content
• has a SG greater than 1.012
• is caused by low levels of aldosterone
• is caused by elevated oncotic pressure
• is associated with elevated levels of ANP

Answer 6

• has a low protein content (is a transudate)
• has a SG less than 1.012
• is caused by raised levels of aldosterone
• is caused by reduced oncotic pressure
• is associated with elevated levels of ANP
  
  • ​?Due to distension of atria

Question 7

15. Tissue oedema is the result of

• a. Decreased intravascular hydrostatic pressure
• b. Increased plasma oncotic pressure
• c. Increased blood pressure
• d. Calcium retention
• e. Lymphatic obstruction

Answer 7

• a. increased intravascular hydrostatic pressure
• b. decreased plasma oncotic pressure
• e. Lymphatic obstruction

Question 8

17. Causes of pulmonary oedema include

• a. Increased hydrostatic pressure
• b. Hyperalbuminaemia
• c. Increased oncotic pressure
• d. Dehydration
• e. Low altitude

Answer 8

• a. Increased hydrostatic pressure
• b. Hypoalbuminaemia
• c. reduced oncotic pressure
• d. Fluid overload
• e. high altitude ( HAPE )

Question 9

38. Vascular hyperaemia

• a. Is caused by inflammatory mediators
• b. Results in cyanosis
• c. Results in oedema
• d. Results in brown induration

Answer 9

• a. Is caused by inflammatory mediators<= aka active hyperaemia
• b. Results in cyanosis
• c. Results in oedema
• d. Results in brown induration

Others are due to congestion.

Hyperaemia = active process due to increased delivery of oxygenated blood to tissue brought about by arteriolar dilation (eg exercising muscle, inflammation)

Congestion = passive process due to reduced outflow of deoxygenated blood from a tissue due to venous obstruciton (eg CHF, DVT) which causes cyanosis and oedema (transudate)

Question 10

Air embolism

• Cannot occur in bone
• Affects only skeletal muscle and joints
• Causes focal ischaemia
• Is unlikely to occur with 10cc of air.
• Is due to dissolved oxygen in divers.

Answer 10

Causes focal ischaemia

Amount needed varies with organ - small amount to effect heart or brain, 100ml to cause clinical symptoms in lung

Is due to dissolved nitrogen in divers

Affects muscles and joints, brain, heart, lungs

Question 11

with regard to embolism

• arterial emboli most often lodge in viscera.
• pulmonary emboli are rarely multiple
• amniotic fluid emboli are associated with the greatest percentage mortality
• most PEs produce clinical signs and symptoms of respiratory distress
• all emboli consist of either gas or solid intravascular mass

Answer 11

• arterial emboli most often lodge in lower limbs (75%) or brain (10%)
• pulmonary emboli are often multiple - if you have one, high chance of a second
• amniotic fluid emboli are associated with the greatest percentage mortality (80%; fat emboli 10%)
• 75% of PEs do not produce clinical signs and symptoms of respiratory distress
• all emboli consist of either gas or solid intravascular mass - also liquid eg amniotic fluid emboli

Question 12

With regard to amniotic fluid embolisation, which is false

• It can occur as a complication of labour
• There is lanugu hair in the pulmonary circulation
• Has a mortality of 70%
• DIC can occur
• It is characterized by severe dyspnoea, hypotensive shock and seizures

Answer 12

Has a mortality of 80%

Question 13

concerning systemic thromboembolism

• the majority are secondary to MI
• aortic aneurysms are the commonest site of origin
• most end in the lungs
• deep leg veins are the commonest site of origin
• most end in the brain

Answer 13

the majority are secondary to MI

80% from heart, of which 66% are from MI, 25% from AF, and rest from valves

10% from AA, VTE wtih PFO, or ulcerated atherosclerotic plaque

10% unknown

Most (75%) end in lower limbs or brain (10%)

Deep leg veins are the commonest site for DVT

Question 14

regarding air embolism, what amount is required to produce symptoms

• 10ml
• 20ml
• 100ml
• 1000ml
• 1ml

Answer 14

100ml

in the lungs

However much smaller volumes can cause problems in the coronary circulation (volume not specified in R&C however)

Question 15

Fat embolism syndrome is associated with

• Mortality of >20%
• A non-thrombocytopenic petechial rash

Answer 15

A non-thrombocytopenic petechial rash

Mortality 10%

Question 16

18. Pulmonary thromboembolism

• a. Is caused in greater than 95% by thrombi in the deep veins of the legs
• b. Causes symptoms in the majority of cases
• c. Results in infarction of the distal lung segments in 50% of cases
• d. Is not a cause of pulseless electrical activity.
• e. Normally arises in patients with no risk factors

Answer 16

• a. Is caused in greater than 95% by thrombi in the deep veins of the legs
• b. Causes symptoms in the minority of cases - 75% asymptomatic
• c. Results in infarction of the distal lung segments in 10% of cases
• d. Is a cause of pulseless electrical activity.
• e. Normally arises in patients with no risk factors - often have multiple risk factors, hence the utility of Wells and PERC scoring

Question 17

19. Pulmonary embolism

• a. Has a 90% chance of recurrence in the presence of an underlying factor
• b. Causes pulmonary infarction in 10% of cases
• c. Originates as a leg DVT in 50% of cases
• d. Is multiple in 10% of cases
• e. Contributes to 1% of acute in-hospital mortality

Answer 17

• a. Has a 30% chance of recurrence in the presence of an underlying factor
• b. Causes pulmonary infarction in 10% of cases
• c. Originates as a leg DVT in >95% of cases
• d. Is multiple in >50% of cases
  
  • Occur either sequentially or simultaneously as a shower of fragments from a larger single mass
• e. Contributes to 10% of acute in-hospital mortality

Question 18

21. Systemic emboli

• a. Arise from thrombi within the heart in 60-65% of cases
• b. Rarely cause infarction
• c. Usually lodge in the brain
• d. Smaller ones are never fatal
• e. Occasionally originate from venous thrombi

Answer 18

• a. Arise from thrombi within the heart in 80% of cases
• b. often cause infarction (depending on collaterals)
• c. Usually lodge in the: 75% lower extremities, 10% brain
• d. Smaller ones are never fatal - can depend where it ends up. In the heart small ones can kill
• e. Occasionally originate from venous thrombi
  
  • ​Via PFO etc

Question 19

23. pulmonary embolism (pg 706-707)

• a. leads to pulmonary infarction in 15% of cases
• b. must occlude 25% of the pulmonary circulation to cause acute right heart failure
• c. is generally symptomatic
• d. is the cause of death in 40-50% of hospitalized patients
• e. is most commonly due to hereditary hypercoagulable states

Answer 19

• a. leads to pulmonary infarction in 10% of cases
• b. must occlude 60% of the pulmonary circulation to cause acute right heart failure
• c. is generally asymptomatic – 60-80% clinically silent
• d. is the cause of death in 10% of hospitalized patients
• e. is most commonly due to hereditary hypercoagulable state

Question 20

37. Regarding air embolism

• a. It does not leave the heart because air is compressible
• b. 200ml of air is the lethal dose

Answer 20

100ml required for clinical effect in the lungs, less in heart and brain.

No obvious right answer here

Question 21

48. Regarding embolism

• a. Introduction to the circulation of >100ml of air is usually required to cause a clinical effect
• b. Fat embolism syndrome is characterized by a maculopapular rash
• c. Most pulmonary emboli produce clinical signs and symptoms
• d. Obstruction of medium sized pulmonary arteries usually causes pulmonary infarction
• e. Multiple pulmonary emboli over time may result in left heart failure. Right free

Answer 21

• a. Introduction to the circulation of >100ml of air is usually required to cause a clinical effect
• b. Fat embolism syndrome is characterized by a petechial rash
• c. Most pulmonary emboli (60-80%) do not produce clinical signs and symptoms
• d. Obstruction of medium sized pulmonary arteries usually causes pulmonary haemorrhage but not infarction due to collaterals
  
  • ​Smaller vessels may cause infarction
• e. Multiple pulmonary emboli over time may result in right heart failure.

Question 22

49. venous thromboses:

• a. are rarely occlusive
• b. never embolise to the cerebral circulation
• c. affect the lower extremities in 75% of cases
• d. tend to contain more erythrocytes and are therefore known as red thrombi
• e. can be easily distinguished from postmortem clots on autopsy

Answer 22

• a. are often occlusive (think DVT and oedema)
• b. Rarely embolise to the cerebral circulation
• c. affect the lower extremities in 75% of cases – this is arterial emboli
• d. tend to contain more erythrocytes and are therefore known as red thrombi
  
  • ​cf arterial thombi which are white
• e. can be easily distinguished from postmortem clots on autopsy
  
  • No as they are both caused by stasis

Question 23

52. In relation to embolic disease:

• a. Fat embolus typically occurs within 24 hours of injury
• b. Atrial septal defects may result in paradoxical embolism
• c. As little as 2ml of air may result in clinical air embolus
• d. DIC usually occurs as a primary disease
• e. Very few pulmonary emboli are clinically silent

Answer 23

• a. Fat embolus typically occurs 1-3 days following injury
• b. Atrial septal defects may result in paradoxical embolism
• c. As little as 100ml of air may result in clinical air embolus
• d. DIC usually occurs as a secondary disease
• e. Most pulmonary emboli are clinically silent (60-80%)

Question 24

53. Arterial thromboembolism is LEAST likely to produce an infarct in

• a. Brain
• b. Liver
• c. Kidney
• d. Heart
• e. Spleen

Answer 24

b) liver

Also has a dual blood supply so ?less likely to infarct

All others (except heart) are listed as sites in book: Lower limbs, brain, intestine, spleen, kidney, upper limbs

Heart produces 80% of arterial emboli but ?how often is effected

Question 25

31. Most pulmonary emboli

• a. Cause centrally located pulmonary haemorrhage
• b. Cause pulmonary infarction
• c. Cause acute right heart failure
• d. Are clinically silent
• e. Lead to pulmonary hypertension

Answer 25

• a. Cause centrally located pulmonary haemorrhage (75% lower lobes)
• b. Cause pulmonary infarction (10%)
• c. Cause acute right heart failure (need to affect 60% of pulmonary circulation)
• d. Are clinically silent – 60 – 80%
• e. Lead to pulmonary hypertension - only if multiple

Question 26

Infarction

• In tissues with a double circulation will be of the white type.
• thromboembolic events accounts for 60% of the cause of all types of infarct.
• usually has characteristic cytologic changes of liquefaction.
• of anaemic (white) type is initially darker than surrounding tissue
• of bland type is due to bacterial activity.

Answer 26

• In tissues with a double circulation will be of the red type.
  
  • eg lungs, gut
• thromboembolic events accounts for almost all of the cause of all types of infarct.
• usually has characteristic cytologic changes of coagulative necrosis, except in the brain where it is liquefaction.
• of anaemic (white) type is initially darker than surrounding tissue
  
  • ​Due to initial inflammation
• of septic type is due to bacterial activity. Bland is not due to infection.

Question 27

With regards to infarction

1. The characteristic cytologic change of all infarcts is ischaemic coagulative necrosis of affected cells.
2. Is caused only by the occlusion of arterial supply
3. Haemorrhagic (red) infarcts are typically seen in solid tissues.
4. In most cases the necrotic focus is replaced with scar tissue
5. Inflammatory exudates usually begins at the margins of an infarcted area within a few minutes.

Answer 27

1. The characteristic cytologic change of most infarcts is ischaemic coagulative necrosis of affected cells, but the CNS undergoes liquefactive necrosis
2. Is caused primarily by the occlusion of arterial supply, but also has can be caused by venous obstruction, such as torsion, compartment syndrome etc
3. Haemorrhagic (red) infarcts are typically seen in loose tissues, white (anaemic) infarcts are typically seen in solid tissues with a single blood supply
4. In most cases the necrotic focus is replaced with scar tissue
5. Inflammatory exudates usually begins at the margins of an infarcted area within a few days

Question 28

White infarcts

• May be transiently red
• Occur in the intestine.
• Result from venous occlusion.
• Are always septic.
• Occur predominately in the liver.

Answer 28

• May be transiently red
• Occur in the solid organs. Loose organs such as intestine or lung are Red
• Result from arterial occlusion. Red infarcts occur due to venous occlusion.
• Are sometimes septic - Nothing is always
• Occur predominately in the liver - Very rare to have liver infarct and would be red due to dual blood supply

Question 29

16. Infarcts

• a. Always result in ischaemic coagulative necrosis.
• b. Are classed as red when they occur in solid organs.
• c. Are always caused by occlusion of the tissue’s arterial blood supply
• d. Cause liquefactive necrosis only in the brain
• e. Are classed as white when occurring in the lung

Answer 29

• a. Mostly result in ischaemic coagulative necrosis (except CNS)
• b. Are classed as white when they occur in solid organs
• c. Are mostly caused by occlusion of the tissue’s arterial blood supply, but can also be due to venous obstruction
• d. Cause liquefactive necrosis only in the brain
• e. Are classed as red when occurring in the lung

Question 30

White infarcts occur in the

• Small intestines
• Kidney
• Lung
• Sigmoid colon
• Oesophagus

Answer 30

Kidney

White (anaemic) = solid organs

Red (haemorrhagic) = loose organs, or dual blood supply

Question 31

Regarding infarction

• tumour obstruction accounts for a significant amount of cases
• all vascular occlusions lead to infarction
• they can be classified as either haemorrhagic or septic
• white infarcts occur in the testis
• most infarcts are wedge shaped

Answer 31

• tumour obstruction accounts for a low and rare of cases
• some vascular occlusions lead to infarction - if there is dual blood supply or collaterals might not lead to damage, or if the rate of occlusion is very slow
• they can be classified as either haemorrhagic or anaemic, septic or bland
• red infarcts occur in the testis
• most infarcts are wedge shaped

Question 32

Regarding septic shock

• Endotoxin is the only cause
• Marked vasoconstriction occurs in the non-infected tissue.
• Cardiac output is as low as 75% in some places
• Endotoxin entering the circulation causes an effect very similar to anaphylaxis
• Blood viscosity is unchanged.

Answer 32

• Endotoxin is a cause, but gram negative and fungi can also cause
• Marked vasodilation occurs in the non-infected tissue.
• Endotoxin entering the circulation causes an effect very similar to anaphylaxis
• Blood viscosity is increased due to widespread inflammatory mediatort release and activation of endothelium

Question 33

Which best defines the pathophysiology of shock

• Widespread tissue hypoxia as a result of decreased blood volume
• Lactic acid production
• Low CO
• Decreased blood volume
• Cellular hypoxia resulting from impaired tissue perfusion

Answer 33

Cellular hypoxia resulting from impaired tissue perfusion

Question 34

With regard to shock

• There are 3 main types – cardiogenic, septic and anaphylactic.
• Gram positive bacteria and fungi cannot induce septic shock
• Higher dose LPS directly injures endothelial cells, triggering coagulation cascade
• Superantigens are a major cause of septic shock
• Most young, healthy patients survive septic shock.

Answer 34

• There are 3 main types – cardiogenic, septic and hypovolaemic.
• Gram positive bacteria and fungi can induce septic shock
• Higher dose LPS directly injures endothelial cells, triggering coagulation cascade
  
  • ​LPS are endotoxins from gram negative bacteria which cause septic shock (Lipopolysaccharides found in the cell membrane)
• Superantigens are a uncommon cause of septic shock
• Most young, healthy patients survive hypovolaemic shock (90% young and fit survive). Septic shock has a 20% mortality

Question 35

regarding the types of shock

• cardiogenic shock is most commonly due to tamponade
• septic shock is caused by gram negative bacteria endotoxin in 70% cases.
• anaphylactic shock is IgG mediated
• septic shock is caused by a low CO
• neurogenic shock can follow brachial plexus injury.

Answer 35

• cardiogenic shock is most commonly due to myocardial infarction
• septic shock is caused by gram negative bacteria endotoxin in 70% cases. Listed as correct answer and is stated in 7th ed of R&C.
  
  • Latest editions state that gram positive is most common cause (which agrees with other sources)
• anaphylactic shock is IgE mediated
  
  • Antigen-antibody complexes cause widespread histamine release
• Cardiogenic shock is caused by a low CO
  
  • Septic shock by widespread inflammation with secondary hypovolaemia, procoagulative state, and suppressed myocardial activtiy
• neurogenic shock can follow Spinal cord cord injury

Question 36

10. Septic shock is associated with

• a. Peripheral vasodilation and myocardial depression
• b. Interleukin 2 in a dominant role
• c. Endotoxin producing organisms in approximately 40% of cases
• d. A declining incidence due to better prevention strategies
• e. Peripheral vasoconstriction and myocardial depression

Answer 36

• a. Peripheral vasodilation and myocardial depression
• b. Interleukin 2 in a dominant role - wrong
  
  • TF, PAF, TNF, IL-1, IFN-γ, complement.
  • IL-2 is an autocrine GF for/by CD4 cells
• c. Endotoxin producing organisms in approximately 40% of cases
  
  • Most frequently caused by Gram positive bacteria. Endotoxins only produced by Gram negative bacteria
• d. A declining incidence due to better prevention strategies - wrong
  
  • Actually is increasing due to ICU, HIV and more

Question 37

12. Regarding stages in cardiogenic shock

• a. A variety of neurohumoral mechanisms help maintain cardiac output and blood pressure in the late non-progressive phase of shock
• b. The patient may become confused and the urine output declines in the progressive stage
• c. The skin may be warm and flushed because of vasodilation.
• d. Endotoxic shock may be superimposed in the progressive stage.
• e. Coronary and cerebral vessels are more sensitive to the compensatory sympathetic response in the early non-progressive phase of shock.

Answer 37

• a. A variety of neurohumoral mechanisms help maintain cardiac output and blood pressure in the early phase of shock
• b. The patient may become confused and the urine output declines in the progressive stage
• c. The skin may be cool due to peripheral shutdown
  
  • ​Septic shock can be warm and flushed.
• d. Endotoxic shock may be superimposed in the irreversible stage.
  
  • Due to ischamic damage to bowel wall allowing intestinal bacteria into the circulation
• e. Coronary and cerebral vessels are least sensitive to the compensatory sympathetic response in the early non-progressive phase of shock. - want to maintain blood flow to brain and heart so do not vasoconstrict until hypoxia is developing

Question 38

Acute compensatory mechanisms in shock include all except

• Baroreceptor reflex
• Reverse stress-relaxation of vascular smooth muscle
• The effects of increased aldosterone secretion
• Activation of renin-angiotensin system
• CNS ischaemic response

Answer 38

The effects of increased aldosterone secretion

(need to clarify why RAS but not this)

• Baroreceptor Reflex helps maintain blood pressure if it drops
• Reverse Stress-Relaxation is the contraction of arterial walls with a fall in blood volume (the opposite also occurs)
• RAS is activated
• CNS ischaemic response​ is an increase in systemic arterial pressure in response to CNS hypoxia

Question 39

Shock in burns patients is primarily due to

• Neurogenic factors
• Hypovolaemia
• Acute RBC haemolysis
• Myocardial depression factor
• All of the above

Answer 39

All of the above

Burns victim are hypovolaemic, and undergoe widespread inflammation which can cause myocardial depression

Need to clarify neurogenic factors and haemolysis

Question 40

Mediators of septic shock include all of the following except

• IL6.
• C5a
• PAF
• Catecholamines
• TNF antibodies

Answer 40

• IL6. (vasodilator)
• C5a. (chemotaxis)
• PAF. (vasodilator)
• Catecholamines (released as host response to shock for sympathetic stimulation)
• TNF antibodies

TNF listed as answer but R&C states this is released along with other interleukins. IL-6 not mentioned but is a pro-inflammatory cyto and chemoline.

??Catecholamines as they are part of the solution not problem

Question 41

Septic shock causes all except

• Myocardial depression
• Vasoconstriction
• DIC
• ARF
• ARDS

Answer 41

Vasoconstriction

Causes vasodilation due to inflammatory response -> interleukins and cytokines etc -> vasodilation and leaky capillaries -> protein-rich exudate -> stasis -> mo’ problems

Question 42

1. Regarding platelets (2006)

• (a) They are the main source of thrombin
• (b) they number 150-300 x103 per microlitre
• (c) They contain a nucleus
• (d) They are biconcave discs
• (e) They contain α and β granules

Answer 42

• (a)Thrombin is cleaved from a circulating precursor molecule thrombinogen by activated factor X and V, and is produced by the liver
• (b) they number 150-300 x103 per microlitre
• (c) They do not contain a nucleus
• (d) They are flat discs
• (e) They contain α and delta (dense) granules

Question 43

2. Non-inflammatory oedema

• (a) has a high protein content
• (b) is caused by low levels of aldosterone
• (c) has a SG >1.012
• (d) is associated with high ANP
• (e) is caused by raised plasma oncotic pressure

Answer 43

• (a) has a low protein content as it is a transudate (SG <1.012; protein <30g/L)
• (b) is caused by high levels of aldosterone , due to decreased perfusion of the kidneys in situations such as CHF (secondary aldosteronism).
• (c) has a SG less than 1.012
• (d) is associated with high ANP - eg CHF from cardiac hypertrophy
• (e) is caused by lowered plasma oncotic pressure or raised plasma hydrostatic pressure

Question 44

3. Vascular hyperaemia

• (a) is caused by inflammatory mediators
• (b) results in cyanosis
• (c) results in oedema
• (d) results in brown induration
• (e) causes haemosiderin laden macrophages

Answer 44

• (a) is caused by inflammatory mediators
• (b) Congestion results in cyanosis - due to acculumation of deoxygenated blood in tissues
• (c) Does not results in oedema - extra blood is within vascular bed
• (d) results in brown induration - congestion
• (e) causes haemosiderin laden macrophages - congestion

Question 45

4. Active hyperaemia is associated with (2006)

• (a) cyanosis
• (b) dilation of arteries and arterioles
• (c) release of a tourniquet on a peripheral limb
• (d) inflammatory mediators
• (e) the blood flow to all parts of the body except the brain

Answer 45

(b) dilation of arteries and arterioles

• (a) cyanosis (reactive)
• (c) release of a tourniquet on a peripheral limb (reactive)
• (d) inflammatory mediators (reactive)
• (e) the blood flow to all parts of the body including the brain, which has increased blood flow in times of increased mental activity

Question 46

6. Which of the following is involved in the initiation of the clotting cascade, complement and kinin systems? (2004)

• (a) Hageman factor (XII)
• (b) factor VII
• (c) antigen-antibody complex
• (d) Tissue factor
• (e) Platelet activating factor

Answer 46

• (a) Hageman factor (XII)
• (b) factor VII - initiates the intrinsic clotting pathway in the presence of TF
• (c) antigen-antibody complex - initiates the classical complement cascade
• (d) Tissue factor - extrinsic pathway co-factor (activates VII and along with VIIa, helps to activate X)
• (e) Platelet activating factor - actiates platelets?

Question 47

7. Activated Factor XII (factor XIIa, Hageman factor) (from old paper 2004)

• (a) activates clotting, the kinin cascade and fibrinolysis
• (b) activates the coagulation cascade via the extrinsic pathway
• (c) converts low molecular weight kininogen (LMWK) to high molecular weight kininogen
• (d) converts factor VIII to active factor VIII (factor VIIIa)
• (e) along with kallikrein, converts plasminogen to plasmin

Answer 47

• (a) activates clotting, the kinin cascade and fibrinolysis
• (b) activates the coagulation cascade via the intrinsic pathway
• (c) converts Prekallikrein to kallikrein, which in turn converts high molecular weight kininogen to bradykinin
• (d) converts factor XI to XIa (XII->XI->IX->X = intrinsic pathway)
• (e) XIIa converts prekallikrein to kallikrein. Kallikrein converts plasminogen to plasmin (and HMW kininogen to bradykinen)

Question 48

8. Post mortem features of clot include: (2004, 2006)

• (a) adherence to the vascular wall
• (b) absence of red cells in the supernatant
• (c) lines of Zahn
• (d) firmer texture and have more fibrin than venous clot
• (e) none of the above features

Answer 48

(a) adherence to the vascular wall is a feature of living clots
* *(b) absence of red cells in the supernatant**, and a chicken fat appearance (c) lines of Zahn: arterial thrombi
(d) firmer texture and have more fibrin =venous clot
(e) none of the above features

‘Clots that form after death are gelatinous and have a dark red dependent portion where red cells have settled by gravity and a yellow ‘chicken fat’ upper portion, and are usually not attached to the underlying vessel wall’

Question 49

9. Blood put in a glass tube

• (a) normally clots in 6 to 10 minutes
• (b) clots because of the extrinsic pathway
• (c) and then slowly tipped backwards and forwards gives a clinically useful clotting time
• (d) clots almost instantaneously
• (e) never clots

Answer 49

• (a) normally clots in 6 to 10 minutes, but varies with test method, so is not** **clinically useful
• (b) clots because of the intrinsic pathway
  
  • So called becuase it is the pathway that blood clots in vitro, whereas additional agents need to be added to activate the extrinsic pathway (ie was thought to be an intrinsic property of blood but is actually just the negatively charged glass ions acting as a phospholipid membrane)
  • No tissue trauma, therefore no Tissue Factor to acrtivate extrinsic pathway
• (c) and then slowly tipped backwards and forwards gives a clotting time, but time varies with test method, so is not clinically useful
• (e) Always clots unless anticoagulant is added

Question 50

10. The process of blood coagulation involves

• (a) prothrombin activator converting fibrinogen to fibrin
• (b) α-2 macroglobulin
• (c) the action of antithrombin III to promote clotting
• (d) the action of plasmin on fibrin
• (e) The removal of peptides from each fibrinogen molecule

Answer 50

• (a) Thrombin converting fibrinogen to fibrin
  
  • prothrombin activator converts prothrombin to thrombin
• (b) α-2 macroglobulin - is an immunboiglobulin
• (c) the action of antithrombin III prevents clotting, and is part of the anticoagulant properties of normal endothelium
  
  • ​Inactivates IXa, Xa, XIa, XIIa, and thrombin
• (d) the action of plasmin on fibrin
  
  • This is part of the fibrinolytic cascade
• (e) The removal of peptides from each fibrinogen molecule
  
  • ​Converts soluble polymers into insoluble monomers which are then polymerised

Question 51

11. White infarcts (2006)

• (a) may be transiently red
• (b) occur in the intestine
• (c) result from venous occlusion
• (d) are always septic
• (e) characteristically has lines of Zahn

Answer 51

• (a) may be transiently red - due to initial inflammation
• (b) occur in the intestine - red as loose tissue with dual blood supply
• (c) result from arterial occlusion (white=anaemic)
• (d) are rarely septic
• (e) characteristically has lines of Zahn - arterial thrombi have lines of Zahn

The colour of an infarct depends on whether or not there is bleeding. White (anaemic) infarcts are arterial occlusions in solid organs. They occur in the heart, spleen and kidney (end organs; do not occur in the liver as there is dual blood supply)

Question 52

12. White infarcts occur in

• (a) kidney
• (b) the small intestine
• (c) lung
• (d) sigmoid colon
• (e) oesophagus

Answer 52

(a) kidney, heart, spleen

Red infarcts occur with venous occlusions (ovarian torsion), loose tissue which allows blood to pool in the infarcted area (lung), and areas with dual circulation (lung, liver)

Question 53

13. Which of the following tissues/organs is most at risk of a venous infarct

• (a) appendix
• (b) stomach
• (c) ovary
• (d) brain
• (e) lung

Answer 53

?? Ovary - as example given for venous occlusion

Lung seems most common involved organ (more PEs than ovarian torsions) but text states that this is due to loose tissue allowing blood to pool rather than venous occlusion.

Red infarcts occur with venous occlusions (ovarian torsion), loose tissue which allows blood to pool in the infarcted area (lung), and areas with dual circulation (lung, liver)

Question 54

14. With regard to embolism

• (a) arterial emboli most often lodge in the viscera
• (b) pulmonary emboli are rarely multiple
• (c) amniotic fluid emboli are associated with the highest mortality
• (d) all emboli consist of either a gas or a solid intravascular mass
• (e) most pulmonary emboli produce signs of respiratory compromise or distress

Answer 54

• (a) arterial emboli most often lodge in the lower limbs (75%)
• (b) pulmonary emboli are often multiple
• (c) amniotic fluid emboli are associated with the highest mortality (80%)
• (d) all emboli consist of either a gas or a solid intravascular mass (or liquid eg amniotic fluid)
• (e) most pulmonary emboli do not produce signs of respiratory compromise or distress - 60-80% are clinically silent

Question 55

15. Fat embolism syndrome is associated with

• (a) symptoms within 24 hours after fracture of a long bone
• (b) severe skeletal injuries in 30% of such patients
• (c) thrombocytosis, and anaemia
• (d) mortality in up to 10% of patients
• (e) petechial rash, which is non-thrombocytopaenic

Answer 55

• (a) symptoms 1-3 days after fracture of a long bone
• (b) severe skeletal injuries in 1**0% of such patients
• (c) thrombocytopenia, and anaemia
  
  • Causes platelet and RBC aggregation due to endothelial insult
• (d) mortality in up to 10% of patients
• (e) petechial rash, which is thrombocytopaenic

Question 56

16. Regarding air embolism, what is the least amount required to produce symptoms

• (a) 10mL
• (b) 20mL
• (c) 100mL
• (d) 1000mL
• (e) 1mL

Answer 56

(c) 100mL

Question 57

17. Regarding air embolism

• (a) they do not leave the heart as the air is incompressible
• (b) 200mL is the lethal dose
• (c) Air may coalesce to form frothy obstructive masses
• (d) It generally does not cause focal ischaemia
• (e) It requires decompression as treatment

Answer 57

(c) Air may coalesce to form frothy obstructive masses

• a) they can leave the heart and cause areas of ischaemia in peripheral and central tissues including the lungs
• b) 100ml is required to produce symptoms (unsure of lethal dose - not in book)
• d) it can cause focal ischaemia
• e) It requires compression as a treatment

Question 58

18. Amniotic fluid embolism (subject in old MCQ paper)

• (a) is seen in 0.5% of all deliveries
• (b) is associated with a 20%to 40% mortality rate
• (c) causes profound haemorrhage, due to the haemophilic properties of amniotic fluid
• (d) is associated with disseminated intravascular coagulation in 20% of affected patients
• (e) is due to rupture of uterine arteries

Answer 58

They thought b), but seems very low, and all others apart from c) seem clearly wrong

• (a) is seen in 1:50,000 of deliveries, an important cause of maternal death (0.002%)
• (b) is associated with a 80% mortality rate
• (c) causes profound haemorrhage, (due to the haemophilic properties of amniotic fluid - not sure about this part)
  
  • Causes DIC which can cause haemorrhageic complications through consumption of coagluation factors and activation of fibrinolytic cascade
• (d) is associated with disseminated intravascular coagulation in 50% of affected patients
• (e) is due to rupture of uterine veins or a tear in the placental membranes

Question 59

19. What best describes the pathophysiology underlying shock

• (a) Widespread tissue hypoxia as a result of decreased effective blood volume
• (b) lactic acid production
• (c) low cardiac output
• (d) decreased blood volume
• (e) Cellular hypoxia resulting from impaired tissue perfusion

Answer 59

(e) Cellular hypoxia resulting from impaired tissue perfusion
* Regardless of the underlying pathology*

• (a) Widespread tissue hypoxia as a result of reduction in cardiac output, or decreased effective blood volume
• (b) lactic acid production ((is a result of hypoperfusion))
• (c) low cardiac output and/or decreased effective blood volume
• (d) decreased blood volume or low cardiac output

Question 60

20. Shock results in

• (a) decreases capillary hydrostatic pressure
• (b) decrease in lipopolysaccharide levels
• (c) Baroreceptor inhibition
• (d) paradoxical inhibition of the sensation of thirst by the actions of ADH
• (e) maximal sympathetic outflow after thirty minutes of profound hypotension

Answer 60

• (a) decreases capillary hydrostatic pressure
• (b) lipopolysaccharide is the bacterial endotoxin that can initiate shock
• (c) Baroreceptor activation
• (d) ADH stimulates thirst (and water/Na retention in the kidneys)
• (e) maximal sympathetic outflow after 30 seconds of profound hypotension

Question 61

21. In acute cardiogenic shock there is

• (a) a decrease in right atrial pressure
• (b) an increase in mean arterial pressure
• (c) a decrease in capillary hydrostatic pressure
• (d) oedema
• (e) a survival rate of 50%

Answer 61

• (a) an increase in right atrial pressure - (they thought decrease but I cannot find anything except studies showing an increase in RAP is associated with increased mortality in cardiogenic shock, and R&C referecning LV failure due to MI causing shock often causes acute pulmonary oedema due to congestion, should -> increased right sided pressures)
• (b) an decrease in mean arterial pressure
• (c) a decrease in capillary hydrostatic pressure
  
  • ​As per other questions, this occurs in shock, likely due to arterial vasocontriction
• (d) oedema - does not develop acutely
• (e) a survival rate of <15%

Question 62

22. Irreversible shock is characterised by

• (a) widespread peripheral vasoconstriction
• (b) increased intracellular adenosine
• (c) increased adenosine levels in the blood
• (d) distinct differences in renal function when compared with compensated shock
• (e) none of the above

Answer 62

• (a) widespread peripheral vasodilation (severe ischaemia affects the brain and vasomotor tone is lost)
• (b) increased extracellular adenosine as it leaches into blood with cellular injury
• (c) increased adenosine levels in the blood
  
  • after all the ATP has been degraded to ADP and then AMP, it is converted to uric acid
• (d) stages are indistinct and can pass imperceptibly from one to antoher

Question 63

23. Septic shock may cause all of the following except

• (a) myocardial depression
• (b) vasoconstriction
• (c) DIC
• (d) ARF
• (e) ARDS

Answer 63

(b) vasoconstriction

Causes vasodilation

Question 64

24. Disseminated intravascular coagulation is associated with

• (a) thrombocytosis
• (b) a bleeding diathesis presentation in a patient with malignancy
• (c) pregnancy in 50% of cases
• (d) a haemolytic anaemia due to splenic activation
• (e) bacterial exotoxins in the majority of patients with septic shock

Answer 64

• (a) thrombocytopenia and consumptive coagulopathy with consumption of platelets, which can result in a serious bleeding disorder
• (b) a bleeding diathesis presentation in a patient with obstetric complications or major trauma, whereas chronic DIC which occurs in cancer patients tends to present as complications of thrombosis
• (c) pregnancy in 50% of cases
  
  • ​Reversible with delivery
  • 33% have carinomatosis
  • Rest are mostly sepsis and major trauma
• (d) a microangiopathic haemolytic anaemia due to. Fibrin deposits narrow the microvasculature
• (e) bacterial endotoxins in the majority of patients with septic shock

Question 65

25. Bradykinin is (2006)

• (a) produced by the actions of kallikrein on a precursor molecule
• (b) is factor XII
• (c)
• (d)
• (e)

Answer 65

(a) produced by the actions of kallikrein on a precursor molecule

Kallikrein cleaves HMW kininogen to bradykinin (and also cleaves plasminogen to plasmin

XIIa cleaves prokallikrein to kallikrein