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1. Essential Medical Science > Vascular Disease > Flashcards

Vascular Disease Flashcards

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1
Q

What is an Atheroma?

A

Intimal lesion that protrudes into a vessel wall. It consists of a raised lesion with a soft core of of lipid (mainly cholesterol and cholesterol esters) and is covered by a fibrous cap.

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2
Q

What are the two layers of an Atheroma?

A

fibrous cap and necrotic centre

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3
Q

What does the fibrous cap contain?

A

Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin

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4
Q

What does the necrotic centre contain?

A

Cell debris, cholesterol crystals, foam cells, calcium

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5
Q

What vessels are commonly affected by Atheroma? (6)

A

Bifurcations (sites of turbulent flow), Abdominal aorta, Coronary arteries, Popliteal arteries, Carotid vessels, Circle of Willis

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6
Q

What are Non-Modifiable risk factors for an Atheroma?

A

Increasing age, Male gender, Family history

Genetic abnormalities

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7
Q

What are Modifiable risk factors for an Atheroma?

A

Hyperlipidemia (LDL: HDL), Hypertension, Smoking

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8
Q

What are causes of an Atheroma?

A

Atherosclerosis starts with damage or injury to the inner layer of an artery. The damage may be caused by:
High blood pressure, High cholesterol, An irritant, such as nicotine, Certain diseases, such as diabetes

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9
Q

What is the pathophysiology of an Atheroma?

A

Atherosclerosis develops as a chronic inflammatory response of the arterial wall to endothelial injury.
Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the normal cellular constituent of the arterial wall.
The contemporary view of atherosclerosis is expressed by the response-to-injury hypothesis

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10
Q

What is the Response to Injury Hypothesis?

A

1) Chronic Endothelial injury
2) Endothelial dysfunction
3) SM emigration from media to intima and macrophage activation
4) Macrophages and SM cells engulf lipids
5) SM proliferation, collagen and ECM deposition, extracellular lipids

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11
Q

What causes Chronic Endothelial injury?

A

Hyperlipidemis, hypertension, smoking, homocysteine, haemodynamic factors, toxins, viruses and immune reactions

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12
Q

What is Endothelial dysfunction?

A

increased permeability, leukocyte and monocyte adhesion and emigration

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13
Q

What are fatty streaks?

A

The earliest lesion in atherosclerosis, Composed of lipid filled foamy macrophages, Begins as multiple minute flat yellow spots that eventually coalesce into streaks >= 1cm
These lesions are not significantly raised and do not cause flow disturbance
Not all fatty streak are destined to progress to atheromatous plaque
Nevertheless coronary fatty streaks begin to form in adolescence at the same anatomical sites that later tend to develop plaque

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14
Q

What is a Atherosclerotic plaque?

A

Consists of intimal thickening and lipid accumulation
Appears white yellow and superimposed thrombus on the plaque appears red
Plaque impinges on the vessel lumen

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15
Q

Stages in Atherosclerosis progression

A

Initial lesion, fatty streak, intermediate lesion, atheroma, fibroatheroma, complicated lesion

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16
Q

Histology of the Initial lesion? and its main growth mechanism

A

Normal histologically, macrophage infiltration, isolated foam cells. Growth mainly by lipid addition. From 1st decade

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17
Q

Histology of the fatty streak? and its main growth mechanism

A

Mainly intracellular lipid accumulation. Growth mainly by lipid addition

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18
Q

Histology of the intermediate lesion? and its main growth mechanism

A

intracellular lipid accumulation, small extracellular lipid. Growth mainly by lipid addition. From 3rd decade

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19
Q

Histology of the atheroma? and its main growth mechanism

A

intracellular lipid accumulation, core of extracellular lipid. Growth mainly by lipid addition.

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20
Q

Histology of the fibroatheroma and its main growth mechanism

A

Single/multiple lipid cores, fibrotic/calcific layers. Main growth mechanism: Increased SM and collagen. From 4th decade

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21
Q

Histology of the complicated lesion? and its main growth mechanism

A

Surface defect, haematoma- haemorrhage, Thrombosis. Main growth mechanism: thrombosis +/or hepatoma

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22
Q

What are the Sequelae of atherosclerosis?

A

Rupture, ulceration or erosion of the intimal surface exposes the blood to highly thrombogenic substances and induces thrombosis… Lumen occlusion…ischemia
/Haemorrhage into plaque/Atheroembolism/ Aneurysm formation

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23
Q

What is a Thrombus? What most commonly leads to venous/ Arterial thrombosis ?

A

A solid mass of blood constituents formed within the vascular system in vivo
Arterial thrombosis most commonly superimposed on atheroma
Venous thrombosis is most commonly due to stasis

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24
Q

What is Virchow’s Triad?

A

Endothelial Injury, hepercoagulability and abnormal blood flow

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25
Q

Arterial thrombosis Mechanism

A

Typically from rupture of atheromatous plaque

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26
Q

Arterial thrombosis main locations

A

Left heart chambers, arteries

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27
Q

Arterial thrombosis; main diseases?

A

Acute coronary syndrome

Ischaemic stroke claudication

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28
Q

Arterial thrombosis: composition

A

Mainly platelets

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29
Q

Arterial thrombosis: Treatment

A

Anti-platelet agents (clopidogrel)

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30
Q

Venous thrombosis Mechanism

A

Typically from combination of factors from Virchow triad

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31
Q

Venous thrombosis main locations

A

Venous sinusoids of muscle and valves of veins

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32
Q

Venous thrombosis; main diseases?

A

DVT/ Pulmonary embolism

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33
Q

Venous thrombosis: composition

A

Mainly fibrin

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34
Q

Venous thrombosis: treatment

A

Anticoagulants (heparin, warfarin)

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35
Q

Features of a clot vs thrombus:

A

Clot: Platelets not involved, Occurs outside vessel (test tube or hematoma) or inside (postmortem), Red, Gelatinous, Not attached to the vessel wall

Thrombus: Platelets involved (lines of Zahn), Occurs only inside vessel, Red (venous), pale (arterial), Firm, Attached to the vessel wall.

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36
Q

What are the Sequelae of thrombosis?

A

Occlusion of vessel / Dissolution/ Incorporation into vessel wall/ Recanalisation/ Embolisation!!!!!

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37
Q

What is an embolus?

A

A mass of material in the vascular system able to become lodged in the vessel and block its lumen
Most emboli are derived from thrombi
Most common – pulmonary embolus derived from DVT

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38
Q

Types of emboli?

A

Thrombus derived, Atheromatous plaque material, Vegetation on heart valves (infective carditis), Fragments of tumour (causing metastasis), Amniotic fluid, Gas, Fat

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39
Q

Pulmonary emboli consequences?

A

Effects dependent on size of embolus, Acute respiratory and cardiac problems, Sudden death

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40
Q

Systemic emboli causes/ consequences?

A

Generally originate from the heart or atheromatous plaque/ Sequelae of myocardial infarction/ Atrial fibrillation/ Infective endocarditis – heart valve vegetations
Can cause – CVA, TIA, gangrene, bowel necrosis

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41
Q

What can cause hypercoagulability?

A

Hereditary: Facter V leiden, Prothromin, Proton C and S deficiencies
Acquired: Cancer, Chemo, OCR?HRT, pregnancy, obesity, HIT

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42
Q

What can cause stasis?

A

immobility, polycythemia

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43
Q

What can cause endothelial dysfunction and damage?

A

dysfunction: smoking, hypertension
damage: Surgery, catheter (PICC lines) trauma

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44
Q

What is hypoxia?

A

A state of reduced oxygen availability in tissues which causes cell injury by reducing aerobic oxidative respiration

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45
Q

Is hypoxia reversible?

A

The effects can be reversible or can result in adaption (i.e. atrophy)

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46
Q

What type of cell death does tissue hypoxia cause?

A

necrosis

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47
Q

What are causes of hypoxia?

A

Inadequate blood oxygenation?
Cardio-respiratory failure
Low ambient oxygen (e.g. altitude)
Decreased blood oxygen-carrying capacity?
Anaemia
Carbon monoxide poisoning
Ischemia

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48
Q

What is ischaemia?

A

Localised tissue hypoxia resulting from a reduction in blood flow to an organ or tissues.

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49
Q

What is the most common cause of ischaemia?

A

Most commonly caused by obstruction to arterial supply by mechanisms such as Severe atherosclerosis, Thrombosis
Embolism
NB – Obstruction to venous outflow can also cause ischaemia

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50
Q

Which is better? Ischaemia or generalised hypoxia

A

hypoxia is better

Ischaemia injures tissues faster / more severely than non-ischaemic (generalised) hypoxia

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51
Q

What is non-ischaemic (generalised) hypoxia B?

A

–Impaired oxygen supply only

–Other metabolites still supplied e.g. glucose

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52
Q

What is the result of Ischaemia?

A

–↓ supply of metabolites including glucose
–Glycolytic anaerobic respiration fails due to lack of glucose
–Build up of metabolites impairs anaerobic respiration further

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53
Q

How harmful is ischaemic injury?

A

•If limited / short duration = cell injury is reversible
–RAPID RESTORATION OF BLOOD FLOW CAN BE THERAPEUTIC
–e.g. primary percutaneous coronary intervention for myocardial ischaemia / infarction

•But if prolonged / sustained = irreversible cell damage
–CELL DEATH by NECROSIS

54
Q

What is tissue necrosis called when caused by ischaemia?

A

infarction

55
Q

What is ischemia?

A

Localised tissue hypoxia due to decreased blood flow to an organ or tissue

56
Q

What is an infarction?

A

Tissue necrosis as a consequence of ischaemia (i.e. ischaemic necrosis)

57
Q

Is therapeutic reperfusion of ischaemia – a good thing?

A

•Yes - tissue reperfusion is generally good!
–But only if the ischaemia is reversible
–e.g. Rapid PCI for MI / thrombolysis for stroke
•If not reversible (sustained)……then damage permanent
–Reperfusion of infarcted tissues will have no effect

58
Q

Is reperfusion of non-infarcted but ischaemic tissues always good?

A

no

59
Q

What is Reperfusion of ischaemia in coronary occlusion?

A

Following coronary occlusion, contractile function is lost within 2 minutes and viability begins to diminish after approximately 20 minutes. If perfusion is not restored (A), then nearly all myocardium in the affected region suffers death. B, If flow is restored, then some necrosis is prevented, myocardium is salvaged, and at least some function can return. The earlier reperfusion occurs, the greater the degree of salvage. However, the process of reperfusion itself may induce some damage (reperfusion injury), and return of function of salvaged myocardium may be delayed for hours to days (postischemic ventricular dysfunction or stunning)

–Yes. Forms an element of injury in myocardial infarction / stroke
–Possibly up to 50% final infarct may be due to IRPI
But generally reperfusion is better than infarction

60
Q

What is an infarct?

A

An area of infarction in a tissue

61
Q

What are the main causes of infarctions?

A

–thrombosis / embolism

–rupture / thrombosis of atherosclerotic plaque

62
Q

What are rarer causes of infarctions?

A 
–Vasospasm
–Atheroma expansion
–Extrinsic compression (e.g. tumour)
–Twisting of vessel roots (e.g. volvulus)
–Rupture of vascular supply (e.g. AAA)
63
Q

Infarction- venous occlusion

A

Common clinical outcome
–venous obstruction & congestion but no infarction
–smaller branches (collaterals) open up and allow blood to bypass the obstruction

organs with a single venous outflow (testis / ovary) are vulnerable to venous infarction

64
Q

What are the two types of infarction ?

A

Red infarction (haemorrhagic)
Dual blood supply / venous infarction
White infarction (anaemic)
Single blood supply hence totally cut-off

65
Q

Why are most infarcts are wedge-shaped?

A

–Deeper into the tissue the vascular branches expand

–If obstruction occurs at an upstream point, the entire down-stream area will be infarcted

66
Q

What type of necrosis seen in infarction?

A

Coagulative necrosis

67
Q

What type of necrosis seen in infarction in the brain?

A

colliquative necrosis

68
Q

If a person dies suddenly (e.g. massive heart attack) what do you see in the tissues?

A

–nothing

–no time to develop haemorrhage / inflammatory response into the infarcted tissues

69
Q

What is low-flow infarction?

A

Infarction in areas of diminished blood flow in vulnerable anatomical regions

70
Q

What is “PORTAL” vasculature?

A

–Blood supplied via other parenchymal capillary beds

–Anterior pituitary (via hypothalamus), renal tubules (via glomeruli)

71
Q

What are “WATERSHED” regions?

A

–Point of anatomoses between 2 vascular supplies

–Splenic flexure colon (SMA,IMA), myocardium (ventricles & coronary art), regions in the brain

72
Q

What is shock?

A
  • A pathophysiological state of reduced systemic tissue perfusion resulting in decreased oxygen delivery to the tissues
  • Causes a critical imbalance between oxygen delivery and oxygen requirements of the tissues
  • Impaired tissue perfusion and prolonged oxygen deprivation leads to cellular hypoxia
  • Derangement of cellular biochemistry and eventually end organ dysfunction
73
Q

Is shock reversible?

A

Shock is initially reversible but rapidly becomes irreversible

74
Q

What are the sequential effects of shock?

A 
The result is sequential
–Cell death due to hypoxia
–End-organ damage
–Multi-organ failure
–Death
75
Q

What is the pathophysiology of shock?

A

Shock is essentially decreased systemic tissue perfusion (or mean arterial pressure MAP)
MAP = CO x SVR
–↓ Cardiac output / ↓ Systemic (peripheral) vascular resistance can result in shock
Remember! Systemic Vascular Resistance (SVR) and Total Perpheral Resistances (TPR) are the same thing!

76
Q

What is the classification of shock?

A 
–HYPOVOLAEMIC
–CARDIOGENIC
–DISTRIBUTIVE
•ANAPHYLACTIC
•SEPTIC
•TOXIC SHOCK SYNDROME
•NEUROGENIC
•Others.......
77
Q

What is Hypovolaemic shock?

A 
•Intra-vascular fluid loss (blood, plasma etc)
•↓ venous return to heart AKA “pre-load”
•↓ stroke volume à ↓ cardiac output
•How could you compensate for this?
•↑ SVR – (vasoconstrict)
–Cool, clammy, “shut down”
–Increase HR
78
Q

What are the causes of hypovolaemic shock?

A 
•Haemorrhage
–Trauma, gastrointestinal bleeding, ruptured haematoma,
–Haemorrhagic pancreatitis, fractures
–Ruptured aortic, abdominal, or left ventricular free wall aneurysm
–
•Non-haemorrhagic fluid loss
–Diarrhoea, vomiting, heat stroke, burns
, Third-space losses
79
Q

What’s “Third spacing“?

A

•Acute loss of fluid into internal body cavities
Third-space losses are common postoperatively and in intestinal obstruction, pancreatitis, or cirrhosis

can cause hypovolaemic shock

80
Q

Whats Cardiogenic shock?

A
  • Cardiac pump failure
  • ↓ CO
  • How could you compensate for this?
  • ↑ SVR
81
Q

What are causes of cardiogenic shock?

A

•4 categories
–Myopathic (heart muscle failure)
–Arrythmia-related (abnormal electrical activity)
–Mechanical
–Extra-cardiac (obstruction to blood outflow)

82
Q

What are causes of myopathic cardiogenic shock?

A

–Myocardial infarction (> 40% left ventricular myocardium)
–Cardiomyopathies
–“Stunned myocardium” following prolonged ischemia or cardiopulmonary bypass.

83
Q

What is Arrhythmia-related cardiogenic shock?

A

–When the heart muscle is okay but not beating correctly
–Atrial and ventricular arrhythmias
–Impaired ventricular contraction or filling = ↓ cardiac output

84
Q

What is Mechanical cardiogenic shock?

A

–Defects relating to blood flow through the heart
–Valvular defects (e.g. prolapse), ventricular septal defects
–Atrial myxomas, ruptured ventricular free wall aneurysm
–↓ cardiac output

85
Q

What is extra-cardiac cardiogenic shock?

A

–Anything outside the heart that impairs cardiac filling or ejection of blood from heart
–Massive pulmonary embolism, tension pneumothorax,
–Severe constrictive pericarditis, pericardial tamponade etc.

86
Q

What is Distributive shock?

A 
•↓ SVR due to severe vasodilation
•How could you compensate for this?
•↑ CO = Flushed / bounding heart
•Warm esp. with septic shock!!!
–Always check temperature 
Includes several familiar sub-types:
•septic shock
•anaphylactic shock
•neurogenic shock
•toxic shock syndrome
87
Q

What is Septic Shock?

A

•Severe, over-whelming systemic infections with Gram+ve, gram-ve bacteria or fungi
Immunocompromised, elderly, very young etc
•↑ Cytokines / mediators–vasodilation
•Pro-coagulation (DIC)–Ischaemia

88
Q

What is Anaphylactic shock?

A

Severe type I hypersensitivity reaction
–Sensitized individuals
•Hospital e.g. drugs (penicillin etc)
•Community e.g. peanuts, shellfish, or insect toxins
–Small doses of allergen = IgE cross-linking
–Massive mast cell degranulation =Vasodilation
–Contraction of bronchioles / respiratory distress
–Laryngeal oedema
–Circulatory collapse =shock / death

89
Q

What is Neurogenic shock?

A
  • Spinal injury / anesthetic accidents
  • Loss of sympathetic vascular tone
  • Vasodilation = shock
90
Q

What is Toxic shock syndrome?

A
  • NOT the same as septic shock
  • S. aureus / S. pyogenes produce exotoxins “superantigens”
  • Do not require processing by antigen-presenting cells
  • Non-specific binding of class II MHC to T cell receptors
  • Up to 20% of T cells can be activated at one time!!!!!
  • Widespread release of massive amounts of cytokines ↓SVR
91
Q

What is Combination of shock sub-types

A
  • Different types of shock can co-exist (mixed shock)
  • For example in patients with septic shock…..
–Primary distributive component
•Inflammatory and anti-inflammatory cascades ↑ vascular permeability / vasodilation
–Hypovolemic component
•Decreased oral intake
•Insensible losses
•Vomiting, diahorrhea
–Cardiogenic component
•Sepsis-related myocardial dysfunction
92
Q

What is the Mortality of spetic shock and Cardiogenic shock?

A
  • Septic shock - 35 – 60% die within one month of the onset

* Cardiogenic shock - 60 – 90% mortality

93
Q

What is GANGRENE?

A

Infarction of entire portion of limb (or organ)

94
Q

What is dry gangrene?

A

Ischaemic coagulative necrosis only

95
Q

What is wet gangrene?

A

Gangrene with superimposed infection

96
Q

What is gas gangrene?

A

Superimposed infection with gas producing organism e.g. clostridium perferinges

97
Q

What factors influence the degree of ischaemic damage?

A

•Effects of vascular occlusion is variable and depends on four factors

  1. nature of the blood supply
  2. the rate of occlusion
  3. the tissue vulnerability to hypoxia
  4. the blood oxygen content
98
Q

What are the effects of ischaemia: Nature of the blood supply?

A

An alternative blood supply will means less damage hence severe ischaemia required for infarction
•Alternative blood supply is THE MOST IMPORTANT FACTOR in determining if vascular occlusion will cause damage
•lungs - pulmonary and bronchial arteries
•liver - hepatic artery and portal vein
•hand - radial and ulnar artery
•Tissues with a dual vascular supply are generally resistant to infarction of a single vessel
•Kidneys, spleen, testis etc have end-arterial circulations (artery only blood supply) hence are vulnerable to infarction

99
Q

What are the effects of ischaemia: Rate of occlusion?

A

•Slow developing occlusions = less likely to infarct tissues
•allows time for development of alternative perfusion pathways (collateral supply)
•HEART
–Small anastomoses normally connect the major branches of the coronary artery system and have minimal flow
–If a coronary arterial branch is slowly occluded flow can be directed through these channels.
–Infarction can be avoided even if the main arterial branch is totally occluded.

100
Q

What are the effects of ischaemia: Tissue vulnerability to hypoxia (brain and heart)

A 
•BRAIN
–If a neurone is deprived of oxygen, how long does it take to undergo irreversible cell damage ?
–3 – 4 MINUTES
•HEART
–Slightly more resistant
–Cardiac myocyte death ???
•20 – 30 MINUTES
–Cardiac fibroblast death ??
•HOURS
•NOT AS METABOLICALLY ACTIVE AS HEART MUSCLE CELLS
101
Q

What are the effects of ischaemia: Blood oxygen content

A

•Reduced oxygen in the blood (anaemia etc) = more vulnerable to infarction!
•Congestive heart failure
–Poor cardiac output AND impaired pulmonary ventilation
–Infarct in a normally inconsequential narrowing of the vessels!
–DUE TO IMPAIRED OXYGENATION OF THE TISSUES

102
Q

What is thrombosis?

A

Local coagulation or the formation of a blood clot inside a blood vessel
Can be Arterial/ Cardiac/ Venous

103
Q

Where so the vast majority of venous thrombi occur

A

The vast majority of venous thrombi occur in the veins of the lower limbs (DVT) although they can occur in other sites

104
Q

How does a Thrombi grow?

A

•Thrombi grow by successive deposition of fibrin, red blood cells and some platelets

105
Q

What are risk factors for DVT development?

A

Hyper-coagulability, change in blood flow, endothelial injury

106
Q

What increases Hypercoagulability?

A 
–Dehydration
–Cancer
–Cancer treatment / chemotherapy
–Smoking
–Hormonal contraceptives / HRT
–Genetic*
–Pregnancy
–Inflammatory and autoimmune disorders

etc..

107
Q

What causes a change in blood flow?

A 
Stasis / turbulence
Stasis: lack of calf muscle pump action
Long distance travel
Elderly
Orthopaedic cast
Pregnancy
108
Q

What are clinical effects of DVT?

A
  • Tenderness
  • Swelling
  • Reddening
109
Q

What are potential outcomes of a thrombus? (4)

A
  1. Propagation
  2. Embolisation
  3. Dissolution
  4. Organisation & recanalisation
110
Q

What are the different types of emboli?

A 
•Thrombus (99%)
–Systemic – from arterial system 
–Pulmonary – from deep veins
•Atheroma / platelets
•Infective
•Tumour
•Gas – e.g. air or nitrogen
•Amniotic fluid
•Fat / bone marrow
•Foreign material
111
Q

What is a Pulmonary embolism?

A

•95% originate in the leg veins (rest usually pelvic)
•Effects dependent upon size
–Small emboli go un-noticed (60-80%) unless multiple = chronic pulmonary hypertension
–Larger emboli = acute respiratory & cardiovascular symptoms
–Massive emboli (>60% occlusion) or saddle emboli = sudden death

112
Q

What is wells score?

A

Two-level DVT Wells score
•Guides next stages in investigation/managemen
PE likely or not

113
Q

How may a PE present?

A 
–Right-sided chest pain, localised to upper zone
–Onset was sudden
–Sharp
–Associated with SOB
–Worse on inspiration
–Apyrexial
–BP – 124/80 mmHg
–Pulse – 112 bpm
–RR – 22
–SpO2 – 96% on room air
–Right upper zone crepitations
–Swollen left calf
114
Q

What are the Initial Investigations for a DVT?

A

•Blood tests
–Hb 114 Haemoglobin normal range (female)115-160 g/L
–WCC 6.0 White cell count normal range 4-11 x 109/L
–CRP <5 C-reactive protein normal level <10 mg/L
–D-dimer 2000 Negative predictor of VTE <275 ug/ml
USS/CT/Xray/ V/Q SPECT scan

115
Q

What is the Managment of a PE from a DVT?

A

•Acute
–ABC
–High flow oxygen
–Analgesia
•Other
–Thrombolysis for PE with haemodynamic compromise
–Catheter directed thrombolytic therapy for DVT
•Long term treatment
–Pharmacological: Subcutaneous low molecular weight heparin and convert to oral vitamin K antagonists and continue for 3 months
–Mechanical: Compression stockings, IVC filter

116
Q

What is Hereditary Thrombophilia?

A

Consider in patients with unprovoked DVT/PE and first degree relative with history of DVT/PE if planning to stop anticoagulation treatment
•Factor V Leiden
•Antithrombin deficiency
•Protein C deficiency
•Protein S deficiency
In patients with unprovoked DVT or PE planning to stop anticoagulation consider testing for antiphospholipid antibodies

117
Q

What is a Paradoxical embolism?

A

Thromboembolus originating in the deep calf veins passing through a patent foramen ovale and entering the systemic circulation. Can lead to ischaemic stroke

118
Q

What is Ischaemic Heart Disease

[CAD/CHD]?

A

Pathophysiological syndromes due to:
•inadequate blood supply to the myocardium
•resulting from:
–reduced coronary blood flow, almost always due to atheroma +/- thrombus [CAD/CHD]
–myocardial hypertrophy, usually due to systemic hypertension

119
Q

What is the significance of IHD?

A 
•Leading cause of death globally
•Trend: fewer IHD deaths in UK and USA
•IHD mortality has reduced thanks to:
–Prevention: risk modification
–Improved diagnosis and treatment
120
Q

What is the prevention of IHD?

A
  • No smoking
  • Lose/manage weight
  • Lower blood pressure
  • Encourage exercise
  • Calculate risk and ?prescribe
121
Q

What is IHD Pathogenesis?

A
  • acute &/or chronic ischaemia
  • loss of autoregulation of coronary blood flow with > 75% vessel occlusion (critical stenosis) - symptomatic
  • low diastolic flow; subendocardial hypoperfusion
  • myocyte dysfunction/death from ischaemia
  • recovery possible: rapid reperfusion (15-20min)
122
Q

What are Ischaemic heart disease syndromes?

A 
•angina pectoris
–typical/stable 
–crescendo/unstable
–variant/Prinzmetal
•acute coronary syndrome
–acute myocardial infarction (+/- ECG ST elevation)
–crescendo/unstable angina
•sudden cardiac death
•chronic ischaemic heart disease
123
Q

What happens in acute iscemia of the heart?

A
  • atheroma + acute thrombosis/haemorrhage
  • lipid rich plaques at most risk
  • regional transmural myocardial infarction
  • subendocardial MIs are different
124
Q

What is MI morphology?

A
  • <24h normal
  • 1-2dy: pale, oedema, myocyte necrosis, neutrophils
  • 3-4dy: yellow with haemorrhagic edge, myocyte necrosis, macrophages
  • 1-3wk: pale, thin, granulation tissue then fibrosis
  • 3-6wk: dense fibrous scar
125
Q

What is Subendocardial MI?

A

•The subendocardial myocardium is relatively poorly perfused under normal conditions
•Given:
–stable atheromatous occlusion of the coronary circulation
–an acute hypotensive episode
The subendocardial myocardium can infarct without any acute coronary occlusion

126
Q

What are Blood markers of cardiac myocyte damage?

A

•Troponins T & I [popular]–detectable 2 – 3h, peaks at 12h, detectable to 7 days
–raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
•Creatine kinase MB–detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
•Myoglobin –peak at 2h but also released from damaged skeletal muscle
•Lactate dehydrogenase isoenzyme 1
–peaks at 3days, detectable to 14days
•Aspartate transaminase–Also present in liver so less useful as a marker of myocardial damage

127
Q

What is the Prognosis of an MI?

A
  • 20% 1-2h mortality – sudden cardiac death
  • <25% sudden cardiac death have MI at PM
  • 10-15% early hospital mortality
  • 7-10% further 1y mortality
  • 3-4% mortality per year in subsequent years
128
Q

What are the Complications of MI (80-90%

A
  • arrhythmias, ventricular fibrillation & sudden death
  • left ventricular failure & shock
  • pericarditis
  • Cardiac mural thrombus & emboli
  • deep vein thrombosis & pulmonary embolus
  • myocardial rupture - tamponade, ventricular septal perforation, papillary muscle
  • ventricular aneurysm (true)
  • autoimmune pericarditis (Dressler’s syndrome) +/- pleurisy 2 weeks to months post-MI
  • Haemopericardium
129
Q

What is MI/ACS Treatment?

A

•M.O.N.A.: Morphine, Oxygen, Nitrates and Aspirin
•Reperfusion: PCI (percutaneous coronary intervention); better than thrombolysis
•Manage complications and secondary prevention
–ACE-I, anti-platelets, anti-coagulation
–Anti-arrhythmics, beta-blockers
–Statins

130
Q

What is Chronic ischaemic heart disease?

A
  • Decompensated myocardium or coronary artery atheroma produces relative myocardial ischaemia
  • possibly result of previous (occult) MIs
  • congestive heart failure–big heart, hypertrophied and dilated
  • risk of sudden cardiac death or MI
131
Q

What is Familial hypercholesterolaemia?

A

•Mutation in genes involved in cholesterol metabolism
•The commonest are
–Low density lipoprotein receptor gene (1 in 500)
–Apolipoprotein B (1 in 1000)
•Heterozygotes
–develop xanthomas – tendons, periocular, corneal arcus – and early progressive atherosclerosis
–Early primary treatment with statins (hydroxymethylglutaryl CoA reductase inhibitors) is effective
•Treatment of homozygotes is more complex and less effective

1. Essential Medical Science (8 decks)

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