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EMS - MOD > week 6 > Flashcards

week 6 Flashcards

1
Q

what is atherosclerosis?

A

Degeneration of arterial walls characterised by fibrosis, lipid deposition and inflammation which limits blood circulation and predisposes to thrombosis

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2
Q

what are the nonmodifiable risk factors for atherosclerosis?

A

age, FH, gentics and MAle

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3
Q

what are the modifiable risk factors for atherosclerosis?

A

smoking, hyperlipideamia (LDL;HDL), diabetes, hypertension

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4
Q

what is the actions occur prior to atherosclerosis?

A

chronic injury and repair of the endothelium

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5
Q

What causes the first step of endothelial injury and therefore the initiation of atherosclerosis?

A

haemodynamic injury, chemicals, immune complex deposition, irradiation

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6
Q

what does injury to the endothelium cause?

A

the endothelium becomes leaky or permeable

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7
Q

How does damage to the endothelial lining caues the formation of foam cells in the fatXty streak stage?

A

Due to hyperlipideamia lipid will acumulate in the inner most part of the vessel –> intima
monocytes wil integrate to teh intima due to lipid and endothelium injury (VCAM1) and ingest the lipid to form foam cells
this is fatty streak

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8
Q

what does foam cells secrete and what is the action of that?

What do smooth muscle cells secrete and finally what is atherosclerotic plaque made up of?

A

They release chemokines that attract monocytes, macrophages, lymphocytes and smooth muscle cells

Smooth cells proliferate and secrete connective tissue

The mixture of fat, extracellular material, lymphocytes and smooth muscle cells form the ahterosclerotic plaque

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9
Q

what is in the necrotic center of atheromatous plaque?

A

foam cells, calcium, cholestrol crystals and cell debris

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10
Q

what is the fibrous cap made out of?

A

foam cells, lymphocytes, macrophage, smooth muscle cells, collagen, elastin, proteoglycans and neovascularization

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11
Q

what occurs to the smooth muscles during plaque formation?

A

ploriferation and secretion of connective tissues

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12
Q

what is the Sequelae of atherosclerosis?

A

Occlusion
Weakening of vessel walls –> aneurysm
Haemorrhage
Erosion –> thrombotic formation

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13
Q

what is an embolism?

A

A mass of material in the vascular system able to lodge in a vessel and block it

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14
Q

what is thrombosis?

How is it different to a clot pathogensis loand morphology?

A

the solidification/ solid mass of blood content formed in a vessel or heart during the life

Physiologically–> forms differently
Morphology–> looks different

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15
Q

what is a clot and what is its is the characterstics?

A

clot is stagnated blood that has amended clotting process either vivo ( the heart) or In vitro (test tube)

stagnant blood, enzymatic process, adopts shape of vessel and elsatic

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16
Q

what is the characterstics of thrombis?

A

firm, maintained throughout life, dependent on platelets

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17
Q

How are plateletes formed and where are they found? Do they have a nucleus?

A

they are fragment of megakaryocytes in the bone marrow that circulate around the blood stream

They do not have a nucleus

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18
Q

how are plateletes activated?

A

They attach to collagen which is exposed due to endothelium damage and become activated

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19
Q

what alpha granules do plateletes secrete?

A

fibrinogen, fibronectin, PDGF

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20
Q

what dense granules do plateletes secrete?

A

chemotactic chemicals

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21
Q

what are the sights where you get thrombusis?

A

heart, arteries, veins

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22
Q

Virchow triad says that to get platelett adhesion and subsequent thrombus formation requires changes in:

A

The intimal surface of the vessel
Change in pattern of blood flow
Blood constituents

All three is needed for thrombus formation

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23
Q

what three things cause the formation of arterial thrombus?

A

Plaque rupture- turbulent flow and intimal change
Hyperlipidaemia – change in blood constituents
Platelets bind and fibrin is produced entrapping RBC

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24
Q

Describe virchow triad for the cause of venous thrombosis

A

Intimal change especially around the valves

Chain in blood constituite:
Inflammatory mediators –> infection and malignancy
Factor v leiden –> common inherited disease
Oestrogen –> high levels of this

Change in blood flow:immobile

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25
Q

what drug increase your level of oestrogen and therefore increase risk factor for venous thrombosis?

A

the pill

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26
Q

what are thrombi in the heart usually called and what is the cause?

A

mural thrombi and occur over areas of endomyocardial injury –> MI and myocarditis

Can also occur due to arrythmias or cardiomyopathy

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27
Q

what is cardiomyopathy ?

A

chronic disease of the heart

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28
Q

what is the most common place where pulmonary embolism forms?

A

DVT in deep part of your legs

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29
Q

what is paradoxical embolus

A

type of arterial thrombosis where there is a blood clot of venous origion that goes through a lateral opening of the heart such as foramen ovale and then into the lungs

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30
Q

what are the acquired causes of pulmonary embolism?

A

immobility, malignancy, previous VTE, heart failure, oestrogens, obesity, pregnancy, renal disease, smokers

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31
Q

what are the genetic/hereditary cuases of pulmonary embolism?

A

thrombotic disorders –> Fv leiden and protein S defieiciency

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32
Q

what is the outcome of small pulmonary embolism?

A

asymptomatic at first —> multiple later will result in pulmonary hypertension

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33
Q

what would mediam pulmonary emboslism cause?

A

Cause acute respiratory and cardiac failure (V/Q mismatch, RV strain)

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34
Q

Where do systemic embolism occur

A

Within the heart after AF or MI

Within the arteries as a antheroma

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35
Q

what is platelet emboli?

A

Little emboli
Often asymptomatic
Arise from atherosclerotic plaque
Idea that this may what causes TIA

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36
Q

How are atheromas formed and where?

A

From eroded plaques

Often in lower limbs

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37
Q

how is infective embolism work?

A

Caused by vegetation of the infected heart valves

this will cause the bacteria present to cause infection and colonise which can lead to myocarditis aneurysm formation

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38
Q

which sub group of people is infective embolism commonly seen in?

A

intravenous drug uses and people wil prosthetic valves

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39
Q

what is the cause of tumor embolism?

A

Bits may break off as tumours penetrate vessels

Do not usually cause immediate physical problems

Major route of dissemination

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40
Q

How can air cause a gas embolism?

A

Have the vessels opened to air such as obstetric procedure and chest wall injury/surgery

Also need more than 100ml of air for it to have clinical effect

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41
Q

What is the consequence of too much nitrogen?

When do you get it and what is the consequence

A

Gas emboli

Decompression sickness (“the bends”)
Divers, tunnel workers
Nitrogen bubbles enter bones, joints and lungs
Little gas bulbels  
Bends --> terrible joint pains
Get neurological symptoms
Cardiac symptoms
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42
Q

how does amniotic fluid embolism happen?

What is the consequence

A

Increased uterine pressure during labour may force AF into maternal uterine veins and or the cervical veins

Lodge in lungs which can cause respiratory distress

Can see shed skin cells histologically –> contains debres and fetal cells that are not good for mother

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43
Q

When is fat emoblism seen?

What is the consequence

A

Microscopic fat emboli found in 90% patients with significant trauma and fractures bone
Mainly fractures but maybe seen in severe burns

Sudden onset of respiratory distress
Fatal in 10%

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44
Q

what is the cause of foreign body embolism?

A

Particles injected intravenously

Leads to a granulomatous reaction –> macrophage and lymphocyte reaction
Can affect lungs and heart

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45
Q

what are the two genetic factors that can lead to athersclorsis

A

familial hypercholesterolemia

inherited defected apoprotein A

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46
Q

what is the common site of athersclorsis?

A 
Bifurication ( site of turbulent flow)
Abdominal aorta -->AAA
Coronary arteries
Carotid vessel
Circle of willis 
Femoral and popliteal artery
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47
Q

what is hypoxia?

What process leads to hypoxia?

A

Any state of reduced tissue oxygen availability

Generalised - whole body e.g. altitude, anaemia
Regional - specific tissues affected

Ischaemia results in tissue hypoxia

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48
Q

what is ischaemia and what causes it?

A

Pathological reduction in blood flow to tissues

Usually as a result of obstruction to arterial flow
commonly as a result of thrombosis / embolism
Ischaemia results in tissue hypoxia

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49
Q

what factors need to occur for cell injury to be reversible?

A

short duration and limited injury to the cells

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50
Q

what factors need to occur for cell injury to be irreversible?

A

prolonged and sustained injury that leeds to necrosis of the tissue (infarction)

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51
Q

how is tissue reperfused after a myocardial infarction?

A

Percutaneous coronary intervention

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52
Q

how is tissue reperfused after a stroke?

A

Use of thromobolytic drugs that break down the clots

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53
Q

how can reperfusion of tissue be dangerous?

Reperfusion injury

A

Can produced oxygen free radicals from the inflammatory cells that can further damage the tissue and cause further problems such as inflammatory damage

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54
Q

when will reperfusion not having a effect?

A

if the tissue is infarcted

55
Q

what is infarction?

A

Ischaemic necrosis caused by occlusion of the arterial supply or venous drainage

56
Q

what is infarct?

A

An area of infarction in tissues

57
Q

what is the most common cause of infarction and where does it usually occur?

A

thrombosis and embolism most common cuase in the arteries

58
Q

what does spasm do to artery wall?

A

make them narrow

59
Q

Other than embolism and thrombus what are other caues of infarction?

A

Spasm
Antheroma expansion from the tunica intima
Steal
Compression
Vasculitis –> inflammation of the artery walls
Hyperviscosity
Volvus
Rupture of supply such as Abdominal aorta aneurysm

60
Q

what is the cause of compression on arteries?

A

the growth of a tumor underneath the blood vessel and therefore narrows the blood vessel

61
Q

what is the name of the condition where there is twisting of blood vessel causing infarction?

A

volvulus

62
Q

Infarction can be classified by morphology.

What are the 2 colours the groups are based on?

A

anemic –> white infarction

haemorrhagic –> red infarction

63
Q

what is red infacrtion?

A

Organ that has Dual blood supply / venous infarction

64
Q

what occurs in white infarction?

A

Single blood supply hence totally cut-off  in organs with one blood supply e.g. the heart

65
Q

what shape is most infarction and usually where is the point of obstruction?

A

Wedge shaped and the obstruction is usually at the upstream point.
Therefore all of the down stream is infarcted

66
Q

what is the usual histological characterstic of a infarct tissue?

A

Coagulative necrosis

67
Q

what is the histological characterstic of infarction in the brain?

A

Colliquative necrosis

68
Q

if some one dies of a heart attack (instant) why won’t there be any histological characterstic straight away?

A

this is because it takes at least a few hours for the tissue to show signs of damage –> not enough time for inflammatory response

69
Q

what factors infuence the degree of ischeamic damage?

A

Nature of the blood supply

Rate of occlusion

Tissue vulnerability to hypoxia

Blood oxygen content

70
Q

in terms of nature of blood supply what is key in the degree of ischaemic damage?

A

whether or not the organ has a dual blood supply or not. If they do then they have another route for blood supply and therefore damage is not as bad

71
Q

Give examples of organs with dual blood supply

A

Lungs (pulmonary and bronchial arteries)
Liver (hepatic artery and portal vein)
Hand (radial and ulnar artery)

72
Q

Give examples of organs with singal blood supply?

A

Kidneys, spleen, testis and heart and are prone to infarction

73
Q

What is the advantage of slow developing occlusion?

Give example in terms of coronary arteries?

A

Less likely for infarction to occur
Allows the development of alternative (collateral) perfusion pathway

In coronary arteries of the heart there are small anastomosis between the main branches.
This allows the flow of blood through these channels if there is a slow occlusion and can even divert and get around large occlusions.

74
Q

how quickly does irreversible cell damage occur to neurones in the brain?

A

within 3 to 4 minutes

75
Q

What is the weight of the brain and what does it require in terms of cardiac output and the percentage of oxygen consumption required?

A

1-2 of our body weight but requires 15% of cardiac output and 20% of body oxygen consumption

76
Q

how long does it take for irreversible cell damage of cardiac myocytes of the heart?

A

20 to 30 minutes

77
Q

what is a stable angina?

A

occurs after a certain distance and after taking a GTN spray it is relieved. Constant

78
Q

what is unstable angina?

A

patients develop chest pain after shorter and shorter distances or more frequently or when they are even sat a rest –> there atherosclerotic plaque is enlarging and therefore it is getting worse

79
Q

what is a TIA?

A

short lived –> blockage is overcome–> only last 24 hours –>blood flow restored

80
Q

what is difference beteen TIA and Stroke?

A

In stroke the blockage last for over 24 hours and therefore damage is perminant

81
Q

What occurs in 90% of cases in ischeamic heart disease?

A

Caused by Impaired coronary artery flow due to complications of athersclorotic diease

82
Q

what are the two types of stroke?

A

ischeamic caused by thrombosis secondary to atherscolorsis or embolism from mural thrombus (heart)
haemorrahagic –> bleeding

83
Q

what is the cause of haemorrahagic stroke?

A

Intracerebral haemorrhage cause by hypertension
Berry aneurysm (Ruptured aneurysm in the circle of Willis) –> subarachanoid
Tearing of small veins in the brain –> subdural
Trauma to middle meningeal artery –> Extradural haemorrahge

84
Q

how is haemorrahagic stroke treated?

A

controlling of blood pressure and coiling by blocking the aneurysm

85
Q

what is the cause of ischaemic bowel disease?

How is it presented?

A

Usually caused by thrombosis or embolism in the superior or inferior mesenteric arteries

Severe abdominal pain

86
Q

what is gangrene?

A

Infarction of entire portion of limb (or organ)

87
Q

what is gas gangrene?

A

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

88
Q

what is shock?

A

A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased oxygen delivery to the tissues.

89
Q

what balance in the body is affected by shock?

What affect does this have on oxygen levels of the cells and the biochemical arrangement?

A

Critical imbalance between oxygen delivery and oxygen consumption.

Impariment of tissue perfusion and ultimately prolonged oxygen deprivation leads to cellular hypoxia and dearanagement of biochemical properties firstly at cellular level and then systemic level

90
Q

what is the cellular effect of shock?

A

Membrane ion pump dysfunction
Intracellular swelling
Leakage of intracellular contents into the extracellular space
Inadequate regulation of intracellular pH
Anerobic respiration –> lactic acid

91
Q

what is the systematic effects of shock?

A

Alterations in the serum pH (acidaemia)
Endothelial dysfunction  vascular leakage
Stimulation of inflammatory and anti-inflammatory cascades
End-organ damage (ischaemia)

92
Q

what is the sequential result of shock?

A

Cell death
End-organ damage
Multi-organ failure
Death

93
Q

Is shock reversible or irreversible?

A

it is initially reversible but becomes quickly irreversible

94
Q

what are the three types of shock?

A

HYPOVOLAEMIC
CARDIOGENIC
DISTRIBUTIVE

95
Q

what is hypovolaemic shock?

A

Intra-vascular fluid loss (blood, plasma etc)

96
Q

what happens in hypovolaemic shock?

A

↓ venous return to heart AKA “pre-load”
↓ stroke volume –> ↓ cardiac output
Mean arterial pressure drops

97
Q

what is the bodies response to hypovolaemic shock?

A

Systemic vascular resistance (vasoconstriction). Causes increase in heart rate and increased meaning that blood does not go to the non vital organs and only blood going to vital organs.
Get cool and clammy hands.
Tachycardia and oliguria will occur –> Kidney reduced perfusion and capillary refill time will increase

98
Q

what are the haemorrahge causes of hypovolaemic shock?

A

Trauma, gastrointestinal bleeding (Internally) , ruptured haematoma
Ruptured aortic, abdominal, or left ventricular free wall aneurysm

99
Q

what are the non haemorrahge fluid loss?

A

diarrohea, vomiting, burns, heat stroke

100
Q

what is third spacing that also can cause hypovoleamic shock?

A

when you lose your blood volume into your body cavity

101
Q

what occurs in cardiogenic shock?

A

cardiac pump failure –> reduction in cardiac output

102
Q

what are the 4 categories of cardiogenic shock?

A

Myopathic (heart muscle failure)
Arrythmia-related (abnormal electrical activity)
Mechanical –> problem with the valves
Extra-cardiac (obstruction to blood outflow)

103
Q

Causes of myopathic cardiogenic shock

A

Myocardial infarction
Right ventricular infarction,
Dilated cardiomyopathies
Stunned myocardium” following prolonged ischemia or cardiopulmonary bypass.

104
Q

Causes of Arrythmia-related cardiogenic shock

A

Atrial and ventricular arrhythmias
Atrial fibrillation / flutter  ↓CO by impairment of co-ordinated atrial filling of the ventricles.
Ventricular tachycardia, bradyarrhythmias, and complete heart block ↓ CO, while ventricular fibrillation abolishes CO.

105
Q

causes of Mechanical cardiogenic shock?

A

Valvular defects (e.g. prolapse), ventricular septal defects
Atrial myxomas, ruptured ventricular free wall aneurysm. Valvular
Septum and the walls affected

106
Q

cause of extra cardiac cardiogenic scock?

A

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

107
Q

What occurs in distributive shock and how is it compensated?

A

reduction in systemic vascular resistance due to severe vasodilation
compensate by ↑ CO–> Flushed / bounding heart

108
Q

what are the different types of distributive shock?

A

SEPTIC SHOCK
ANAPHYLACTIC SHOCK
NEUROGENIC SHOCK
TOXIC SHOCK SYNDROME

109
Q

What is the cause of septic shock and in who’m does it occur in?

What is the outcome of septic shock

A

Severe or over-whelming infection caused by gram positive bacteria, gram negative bacteria or fungi

In Immunocompromised, elderly, very young

Outcome is increase in cytokines and mediators causing vasodilation

Can cause pro-coagulation (DIC) leading to ischaemia

110
Q

what is anaphlaytic shock?

A

Severe type I hypersensitivity reaction

111
Q

what are the two types sensitized individuals of anaphlaytic shock?

A

Hospital e.g. drugs (penicillin etc)
Community e.g. peanuts, shellfish, or insect toxins

Small dose of the allergen –> IgE cross linking

112
Q

what occurs in anaphylatic shock?

A

Massive mast cell degranulation –> Vasodilation –> widespread
Contraction of bronchioles / respiratory distress
Laryngeal oedema
Circulatory collapse –> shock / death

113
Q

what is neurogenic shock?

A

Spinal injury / anesthetic accidents

Loss of sympathetic vascular tone

114
Q

what is the cause of toxic shock syndrome?

A

S. aureus /S. pyogenes produce exotoxins –> “superantigens”

115
Q

How do S.aureus and S.pyogenes cause toxic shock syndrome?

A

The antigens produced do not need processing by APC

So they non-specific bind class 2 MHC to T cell receptors
Can have up to 20% of T cell activated
Get a huge amount of cytokine release and cause reduction in SVR

116
Q

what is the outcome of toxic shock syndrome?

Is it the same as septic shock

A

Widespread release of massive amounts of cytokines ↓SVR

Not the same as septic shock

117
Q

Different type of shock can co-exist, give an example of how distributive, hypovolaemic and cardiogenic components can all play a role in a patient with septic shock?

A

Primary distributive shock - inflammatory and anti-inflammatory cascades lead to increased vascular permeability/vasodilation

Hypovolaemic component - decreased oral intake, insensible losses, vomiting, diarrhoea

Cardiogenic component - sepsis-related myocardial dysfunctio

118
Q

what is the mortality of cardiogenic shock?

A

60 – 90% mortality

119
Q

what is the mortality of septic shock?

A

35 – 60% die within one month of the onset

120
Q

how does S.aureus cause toxic shock?

A

release anexotoxin called toxic shock syndrome toxin-1. This toxin alters the function of mononuclear phagocytes, thus impairing the clearance of other potentially toxic endotoxins.

121
Q

What part of the blood vessel does atherosclerosis form?

A

Tunica intima of the blood vessel

122
Q

What are common sites of athersoclerosis?

A

Bifurication of blood vessel –> turbulent flow
Circle of willis
Carotid arteries
Coronary artery –> occlusion will lead to MI but reduction in blood flow will lead to angina
Femoral and popliteal artery
Abdominal aorta

123
Q

What is the line of zahn?

A

It is a characteristic feature of thrombus especially when formed in the heart or aorta.
Can see microscopically alternative line of platelets mixed with fibrin which look light and then dark line of RBC.

124
Q

What can lead on from thrombosis?

A

Occlusion of vessel
Resolution or drugs to treat it
Recanalisation–> formation of new blood vessels
Incorporation of the thrombus into the vessel wall
Emoblism

125
Q

What is a emoblis and is it always dangerous?

A

It is a mass of material in the vascular system where it lodges into a vessel and blocks it

Might not be that important if it blocks vessel going to a tissue/organ with multiple blood supplies

Serious when it only has one blood supply

126
Q

What are the different states of embolism?

A

May be endo or exogenous

Solid, liquid or gas

127
Q

What is the pulmonary emboli common cause of?

A

Hospital morbiditiy and mortality

128
Q

What is vegetation and where does it commonly grow?

A

Commonly grows on valves and is abnormal growth that is made up of fibrin and platelets

129
Q

How does venous occlusion cause infarction and how common is it?

A

Occlusion causes vein to be blocked and a back log of blood

Not as common

130
Q

Why is oxygen blood content importent in terms of infarction?

A

If you have reduce blood concentration due to anemia more chance of having a infarct?

131
Q

How can a congestive cardiac failure (heart failure) caue infacrtion?

A

You have reduce cardiac output and poor pulmonary perfusion so therefore a small blood occlusion can lead to a infarction when normally it would not.

132
Q

What is the clinical manifestation of infarction in the intestines?

A

Ischeamic bowel

133
Q

What is the clinical manifestation of infarction in the extreimities?

A

Peripheral vascular disease

Gangrene

EMS - MOD (5 decks)

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