Q51

What is an embolus?

  • A detached intravascular solid/liquid/gas mass that is carried by the blood stream from its site of origin to a distant site

Pass Criteria:

  • Bold to pass

Name the different types of embolus.

  • Thromboembolus
    1. Venous: pulmonary
    2. Arterial: systemic
  • Fat embolus: from bone marrow
  • Gas embolus: e.g. air/nitrogen
  • Amniotic fluid embolus
  • Tumour fragment embolus
  • Foreign body embolus e.g. catheter

Pass Criteria:

  • Bold + 2 to pass

What is systemic thromboembolism?

  • Definition: Emboli in arterial circulation

Pass Criteria:

  • Bold to pass

From where do systemic thromboemboli arise and where do they lodge?

  • Sources
    • 80% from intracardiac mural thrombi (2/3 left ventricular wall infarcts, 1/4 left atrial dilation/atrial fibrillation)
    • Other sources – aortic aneurysms, ulcerated atherosclerotic plaques, valvular vegetation, paradoxical emboli, unknown
  • Lodgement Sites
    • Lower limbs (75%)
    • Brain (10%)
    • Other – intestine, kidneys, spleen, upper limbs

Pass Criteria:

  • Bold + 2/4 sources and 2/4 sites to pass 

Describe the process of infarction from arterial occlusion.

PROMPT – What are the features that influence the development of an infarct?

  • Area of ischaemic necrosis: dominant histologic characteristic is ischaemic necrosis
  • White infarcts occur in solid organs with end-arterial circulation
  • Acute inflammation happens within hours; 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

Q52

What factors predispose to thrombus formation in a vessel?

  • Virchow’s triad
    1. Endothelial injury
    2. Alteration in blood flow (stasis or turbulence)
    3. Hypercoagulability of blood

Pass Criteria:

  • 3/3 bold to pass

How are hypercoagulable states categorised? What are some examples of each type?

  • Primary (Genetic)
    • Mutations – Factor V Leiden, Prothrombin
    • Increased levels – factors VIII, IX, XI, fibrinogen
    • Deficiencies – AT3, Protein C, S
    • Fibrinolysis defects, homozygous homocystinuria
  • Secondary (Acquired) – often multifactorial
    • Prolonged bed rest
    • Immobilisation
    • Myocardial Infarction
    • Atrial Fibrillation
    • Tissue injury (surgery, fracture, burn)
    • Cancer
    • Prosthetic valves
    • Disseminated Intravascular Coagulation
    • Heparin-Induced Thrombocytopaenia Syndrome
    • Anti-phospholipid Antibody Syndrome
    • Cardiomyopathy
    • Nephrotic syndrome
    • Hyperoestrogenic states (pregnancy, post partum)
    • Oral contraceptive pill
    • Sickle cell anaemia
    • Smoking

Pass Criteria:

  • 2 categories
  • Primary – 2 examples
  • Secondary – 3 examples

What are the possible outcomes for a vessel thrombus?

  • Propagation (e.g. resulting occlusion)
  • Embolisation
  • Dissolution
  • Organisation and recanalisation (e.g. to variable degree)

Pass Criteria:

  • 2/4 categories

Q53

What are the risk factors for development of abdominal aortic aneurysms?

  • Male
  • Smoking
  • Age >60
  • Family History
  • Connective tissue disease (e.g. Ehlers Danlos)
  • Vasculitis
  • Hypertension
  • Diabetes
  • Atherosclerosis

Pass Criteria:

  • 5 to pass

Describe the pathogenesis of AAA formation.

  • Atherosclerotic plaque in intima compresses media with degeneration and weakness of wall and cystic medial degradation
  • Local inflammation
  • Proteolytic enzymes with collagen degradation  role of matrix metalloproteinases (MMP)
  • Loss of vascular smooth muscle cells
  • Inappropriate synthesis of non-elastic ECM

Pass Criteria:

  • 2/3 bold to pass

What are the clinical consequences of an AAA?

  • Rupture: increase with diameter (higher if >5cm) and can be retroperitoneal OR intraperitoneal with rapid fatal haemorrhage
  • Obstruction: ischaemia from branch vessel obstruction e.g. mesenteric vertebral, renal
  • Embolism: plaque or thrombus
  • Impingement or compression of adjacent structures (e.g. ureter)
  • Painless mass

Pass Criteria:

  • Bold and 2 others

Q54

What are the consequences and complications of a myocardial infarction?

  • Contractile dysfunction/CCF
  • Arrhythmias
  • Myocardial rupture
  • Pericarditis
  • Right ventricular infarction & right heart failure
  • Infarct extension
  • Infarct expansion
  • Mural thrombus -> embolism
  • Ventricular aneurysm
  • Papillary muscle dysfunction
  • Progressive late heart failure
  • Remodelling
  • Death

Pass Criteria:

  • 6 to pass

What are the main cardiac rupture syndromes?

  • Free wall -> tamponade (most common of 3 occurs at 1-10 days)
  • Septum -> VSD and L->R shunt
  • Papillary muscle dysfunction -> severe Mitral Regurgitation

Pass Criteria:

  • 1 of 3 to pass

What changes occur in ventricular remodelling?

  • Hypertrophy and dilatation, increased oxygen demand -> ischaemia and depressed cardiac function, scar formation -> stiffening and hypertrophy

Pass Criteria:

  • 3 to pass

What systemic factors affect infarct healing?

  • Nutritional: protein, vitamin C
  • Metabolic: diabetes
  • Circulatory: arterial or venous
  • Hormonal: glucocorticoids

Pass Criteria:

  • 3 to pass

Q55

What is hypovolaemic shock?

  • Systemic hypoperfusion due to reduced effective circulating blood volume resulting in impaired tissue perfusion and cellular hypoxia

Pass Criteria:

  • Bold to pass

Describe the stages of hypovolaemic shock.

PROMPT – What compensatory mechanisms are involved?

  • A – Non-Progressive Phase
    • Reflex compensatory mechanisms activated to maintain vital organ perfusion
    • Variety of neurohumoral mechanisms activated to help maintain cardiac output and blood pressure – baroreceptors reflexes, release of catecholamines, activation of renin-angiotensin axis, ADH release and increased sympathetic output resulting in: tachycardia, peripheral vasoconstriction, and renal conservation of fluid with decreased urine output
    • Coronary and cerebral vessels less sensitive to sympathetic response and blood flow/O2 delivery spared
  • B – Progressive Phase
    • Tissue hypoperfusion and worsening circulatory and metabolic imbalance including acidosis
    • Widespread tissue hypoxia resulting in anaerobic glycolysis with excess lactic acidosis production blunts vasomotor response –> peripheral pooling, hypoxic injury, DIC, vital organs begin to fail
  • C – Irreversible phase
    • After body has incurred cellular and tissue injury so severe that even if haemodynamic defects are corrected, survival is not possible

Pass Criteria:

  • All 3 phases to pass
  • A – Bold to pass + 3 features
  • B – Bold to pass
  • C – Bold to pass

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

  • Widespread cell injury
  • Lysosomal enzyme release
  • Nitric oxide -> decreased myocardial contractility
  • Acute tubular necrosis -> acute renal failure
  • Ischaemic gut -> Bacteraemic shock
  • Severe hypotension, unconscious, anuric
  • Pre-cardiac arrest -> death

Pass Criteria:

  • 3 features to pass

Q56

Picture – ECG

Please describe and interpret this ECG.

  • Rate: Ventricular 75-100, Atrial approximately 300/min
  • Rhythm: Irregular. Variable block (3&4:1)
  • P waves: Atrial flutter waves (sawtooth)
  • Axis: Normal
  • QRS: Narrow complex, anterior Q waves.
  • T-waves: Difficult to comment
  • = Atrial flutter, variable block

Pass Criteria:

  • Bold to pass

Q57

Name the types of cardiomyopathy.

PROMPT – Based on function/pathology

  • Dilated cardiomyopathy (DCM)
  • Hypertrophic cardiomyopathy (HCM)
  • Restrictive cardiomyopathy

Pass Criteria:

  • Bold to pass

What are the causes of acquired cardiomyopathy?

  • Infections (viral, bacterial, fungal, protozoal)
  • Metabolic (hyperthyroidism, nutritional)
  • Infiltrative (sarcoid, carcinoma)
  • Immunological (autoimmune myocarditis
  • Drugs/toxins (alcohol, chemotherapy)
  • Ischaemic
  • Hypertensive
  • Valvular

Pass Criteria:

  • 3/5 bold and examples

How do dilated and hypertrophic cardiomyopathy differ?

PROMPT – Left ventricular structure and function

  • Dilated cardiomyopathycardiac dilatation, poor LV EF (<40%). Impaired contractility (systolic dysfunction)
  • Hypertrophic cardiomyopathy: myocardial hypertrophy, normal or high LV EF. Impaired compliance (diastolic dysfunction).

Pass Criteria:

  • Bold for each

Q58

Picture – ECG

Please describe and interpret the significant abnormalities in this ECG.

  • Sinus, rate ~100/min, normal axis
  • ST elevation (STEMI) Inferior leads
  • St depression and inverted T waves in I, aVL, V2, V3 (Reciprocal changes)

Pass Criteria:

  • Bold to pass

Q59

What sequence of changes occur in the vessel wall in aortic dissection?

  • Intimal tear into media of aorta, strips along laminar planes, formation of blood filled channel which may then rupture outwards.

Pass Criteria:

  • Bold to pass (conceptually)

What are the risk factors?

  • Men aged 40-60 with hypertension
  • Connective tissue disorders e.g. Marfan’s
  • Complication of arterial cannulation
  • Trauma

Pass Criteria:

  • Hypertension + one other

What are the types of aortic dissection?

PROMPT – Classification?

  • Stanford Type A – proximal ascending + (DeBakey I)/-(DeBakey II) distal, may rupture back through aortic valve.
  • Stanford Type B – beyond subclavian artery (DeBakey III)

Pass Criteria:

  • Concept (proximal and distal)

Q60

Hyperkalemia ECG

What are the abnormalities on the ECG?

  • Widespread peaked T waves
  • Mild Tachycardia
  • Some inverted T waves
  • ST elevation

Pass Criteria:

  • Bold to pass

What is the likely diagnosis?

  • Suggestive of hyperkalemia

Pass Criteria:

  • Bold to pass

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