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EMS - JL > 23,24,25 > Flashcards

23,24,25 Flashcards

1
Q

What is atherosclerosis

A

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

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2
Q

How does endothelial injury occur?

A

Generation of oxygen free radicals e.g. smoking.

Also haemodynamic injury, chemicals, immune complex, deposition and irradiation

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3
Q

How does an atherosclerotic plaque form

A

Hyperlipidaemia
Lipid accumulates in the intimal
Monocytes migrate to the the intimal (due to lipid and endothelial injury)
Monocytes ingest lipids and form foam cells - makes a fatty streak
Monocytes secrete cheekiness to attract neutrophils/macrophages/smooth muscle
Smooth muscle proliferates and makes connective tissue
Atherosclerotic plaque formed consisting of extracellular material, fat and leukocytes of smooth muscle cells

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4
Q

What is the structure of an athersclerotic plaque

A

Fibrous Cap
Necrotic core where macrophages due
Fibrosis at the shoulder

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5
Q

What is the difference between a macrophage and monocyte

A

It is monocyte in the blood and a macrophage when it enters the tissue

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6
Q

What are the 3 consequences of atherosclerosis

A

Occlusion
Haemorrhages - vessel wall weakened can lead to an aneurysm
Erosion - thrombosis forms if cap is eroded

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7
Q

What is emobolus

A

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

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8
Q

What is the most common type of embolus

A

A thrombosis

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9
Q

Features of a clot

A

Elastic
Enzymatic process
Takes shape of vessel
Stagnant blood

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10
Q

Features of a thrombosis

A

Forms during life
Platelet dependent
Firm

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11
Q

What is a thrombosis

A

Solidification of blood constituents formed in the vessel during life

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12
Q

Do platelets have a nucleus

A

No - they are just fragments of megakaryocytes

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13
Q

What do alpha granules in platelets secrete

A

Fibrinogen, fibrinonectin, PDGF

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14
Q

What do dense granules in platelets secrete

A

Chemotactic chemicals

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15
Q

What can cause arterial thrombosis

A

Plaque rupture - due to turbulent flow and intimal change
Hyperlipidaemia - change in blood constituents so more likely to clot
Platelets bind and fibrin is produced entrapping RBC’s as chemotactic chemicals are formed

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16
Q

What lines of Zahn

A

Show what atherosclerotic plaques look like

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17
Q

Describe blood flow around atherosclerotic plaques

A

Laminar flow on the way up

Turbulent flow on the way down - more likely to form clots here

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18
Q

Where are clots most likely to form with regards to an athersclerotic plaque

A

On the downside of the atherosclerotic plaque due to the turbulent flow

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19
Q

What is likely to cause venous thrombosis

A

Stagnation of blood e.g immobility
Change in constituents e.g. Factor V Leiden
Intimal changes e.g. valves

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20
Q

Effect of oestrogen on clotting

A

It is pro-thrombotic

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21
Q

What are thrombi in the heart known as

A

Mural thrombi

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22
Q

What increases the stickiness of the muscle wall

A

MI and myocarditis

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23
Q

Describe the sequelae of a thrombosis

A

Occlusion
Resolution
Incorporation of thrombus into the vessel wall
Recanalisation through the fibrotic thrombosis
Embolization of the thrombus detatches

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24
Q

Most common type of emboli

A

Pulmonary emboli

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25
Q

How to diagnose a pulmonary emboli

A

A CTPA

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26
Q

Congenital risk factors of thrombtic emboli

A

Protein S defeciency

Factor V Leiden

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27
Q

Acquired risk factors of thrombotic emboli

A

Paradoxical emboli e.g. hole in heart

Immobility, malignancy, smoking, oestrogen, obesity, pregnancy etc

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28
Q

What is saddle embolus

A

Sits where the pulmonary arteries bifurcate

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29
Q

Name the different types of emboli

A 
Systemic
Infective
Tumour
Air
Amniotic Fluid
Fat 
Foreign Body
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30
Q

Where do systemic emboli form

A

In the heart - following MI or AF

Or in arterial circulation

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31
Q

Types of systemic emboli

A

Atheroma - from eroded plaques

Platelet - often asymptomatic, arise from atherosclerotic plaques and responsible for causing TIA’s

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32
Q

What causes TIA’s

A

Platelet systemic emboli

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33
Q

What are infective emboli

A

Small emboli that break of from vegetations on infected heart valves

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34
Q

What can be the consequence of an infected emboli

A

Can form a microcytic aneurysm where it lodges

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35
Q

Who is infective endocarditis common in

A

young people with prosthetic heart valves and IV Drug Users

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36
Q

What happens in a tumour embolism

A

Small part of a tumour breaks off - often too small to be symptomatic but major route of tumour dissemination

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37
Q

Two types of gas embolism

A

Air

Nitrogen

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38
Q

How does an air embolism form

A

Due to obstetric or chest wall procedures

Only occurs if more than 100ml of air enters

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39
Q

How does a nitrogen embolism form

A

Occurs in divers/tunnel workers
Nitrogen dissolve in the blood under the pressure
When we surface the nitrogen bubble out of the blood
Nitrogen bubbles enter bones, joints lungs affecting all systems neurological/cardiac

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40
Q

How does an amniotic fluid embolism occur

A

High intrauterine pressure during labour forces some amniotic fluid into maternal veins (may contain foreignsbstance)

Emboli lodge in blood causing respiratory distress

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41
Q

What histological findings might you get in amniotic fluid embolism

A

May see shed skin cells in the lung

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42
Q

What usually causes a fat embolism

A

80% occur in patients with significant trauma
E.g. mainly bone fracture or severe burns (fat precipitates out at high temperature)
Fatal in 15%
Sudden onset respiratory distress

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43
Q

Why is it hard to detect fat emboli in a post mortem

A

as we don’t specifically stain for fat

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44
Q

What is a foreign body emboli

A

Emboli due to foreign material injected intravenously
E.g. IVDU’s
Leads to a granulomatous reaction!

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45
Q

What is hypoxia

A

state of reduced oxygen availability
general = anemia/altitude
can be tissue specific

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46
Q

what is ischaemia

A

pathological reduction on blood flow, can cause hypoxia

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47
Q

Problems with therapeutic reperfusion

A

Can get reperfusion injury

48
Q

What is reperfusion in jury

A

the generation of oxygen free radicals produced during hypoxia and released in repercussion
Activates inflammatory cascade causing widespread damage

49
Q

What is infarction

A

Ischaemic necrosis due to the occlusion of arterial supply

50
Q

Causes of infatction

A 
Thrombus/emoblus
Vasopasms
Atheroma spasm
Steal - at the branching of the vessels if one is narrowed blood goes down the path of least resistance
Venous occlusion
Extrinsic compression
Volvulus
Vasculitis
Hyperviscosity
51
Q

Morphology of infarction

A

Red (hemorrhagic) - occurs if there is dual blood supply/venous infarction e.g. pulmonary embolus

White (anaemia) occurs with single blood supply

52
Q

4 factors affecting the degree of ischaemic damage

A

Blood supply
Oxygen demands of tissue
Rate of occlusion
Blood oxygen content

53
Q

What areas have dual blood supply

A

liver, lungs, hands

54
Q

what areas have single blood supply

A

Kidney, testis, spleen
Watershed regions between anastamosis e.g. the splenic flexure
Portal vasculature e.g. part of exocrine pancreas

55
Q

How does rate of occlusion affect ischaemic damage

A

If slow can generate collateral circulation

E.g. coronary arteries have small anastomosis between main branches through which blood can be redirected

56
Q

Which tissue is most vulnerable to hypoxia

A

Brain - uses 20% of bodies oxygen
Neutrons die within 3 to 4 minutes
Cardiac myocytes can live for 20 to 30 minutes

57
Q

Why does congestive heart failure make ischaemic damage more likely

A

Poor cardiac output and pulmonary ventilation

Decreases the oxygen content in the blood

58
Q

What do we give to treat angina

A

GTN

59
Q

What is TIA

A

Stroke reduced within 24 hours

60
Q

When would we suspect ischaemic bowel disease

A

Pain after eating due to increased blood demand

61
Q

What are the 2 types of cerebrovascular disaese

A

Ischaemic stoke

Haemorrhagic stroke

62
Q

What is a hemorrhagic stroke

A

Intracerebral haemorrhage secondary due to hypertension
Get ruptured aneurysm e.g. berry aneurysm
common in patients with tissue disroders

63
Q

What type of incident is common in people with connective tissue disorders

A

Intracerebral haemorrhage

64
Q

What is gangrene

A

The infarction of entire portion of a limb or organ

65
Q

When do you get gas gangrene

A

Necrosis with superimposed infection of a gas producing organism e.g. clostridium perfringens

66
Q

What is shock

A

Significant reduction of systemic perfusion (HYPOTENSION) causing reduced oxygen delivery to the tissue

67
Q

Cellular effects of shock

A

Membrane ion pump dysfunciton
Cellular swelling
Leakage of intracellular proteins into extracellular space
Anaerobic respiration - makes lactic acid - inappropriate pH regulation

68
Q

Systemic effects of shock

A

Alteration in pH (Acidic)
Endothelial dysfunction - vascular leakage
Stimulation of inflammatory and anti-inflammatory cascades
End organ damage

69
Q

Cardiac output =

A

Stroke volume x heart rate

70
Q

What affects stroke volume

A

Skeletal pump
Respiratory pump
Blood volume

71
Q

Mean arterial prssure =

A

cardiac output x total peripheral resistance

72
Q

What affects total peripheral resistance

A

arterial radius

73
Q

Name the 3 main types of shock

A

Hypovolaemic
Cardiogenic
Distributive

74
Q

What happens in hypovolaemi stroke

A

Due to intravascular fluid loss

Decreased cardiac output - increased SVR (vasconstriction)

75
Q

Causes of hypovolaemic stroke

A

Haemorrhagic - e.g. trauma, GI leed, fractures etc

Non-haemorrhagic - DnV, burns, third spacing

76
Q

What is third spacing

A

Loss of fluid into body cavities - occurs commonly post op and in intestinal obstruction

Can cause hypovolaemic shock

77
Q

What is cardiogenic shock

A

Cardiac pump failure

Decreased cardiac output and increased systemic vascular resistacnce

78
Q

4 types of cardiogenic shock

A

Myopathy
Arrythmias
Mechanical
Extra-cardiac

79
Q

What is myopathy cardiogenic shock

A

Occurs after MI, RV Infarction =, cardiomyopathies etc

Stunned myocardium

80
Q

What is arrhythmia cardiogenic shock

A

Occurs with atrial and ventricular fibrillations, tachycardias and arrhythmias etc

81
Q

What is mechanical cardiogenic shock

A

Problems with valves, septal defects etc

82
Q

What is extra-cardiac cariogenic shock

A

Anything that impairs cardiac filling or ejection of blood from heart
E.g. massive PE, tension pneumothorax, restrictive pericarditis, cardiac tamponade

83
Q

What is distributive shock

A

Decreased SVR due to severe vasodilation. Increase cardiac output by increasing heart rate

84
Q

Types of distributibe shock

A

Septic
Anaphylactic
Neurogenic
Toxic shock

85
Q

What is septic distributive shock

A

Sever overwhelming systemic infections
Increase cytokine mediators causing vasodilation
Procoagulation - causes DIC

86
Q

What is anaphylactic distributive shock

A

Allergen causes IgE cross linking - mast cell degranulation - vasodilation
Contraction of bronchioles causing respiratory distress
Laryngeal oedema
Circulatory collapse - death

87
Q

When does laryngeal oedema occur

A

In anaphylactic shock

88
Q

What is neurogenic shock

A

Occurs in spinal injury/anaesthetic
Loss of sympathetic tone
vasodilation

89
Q

What is toxic shock syndrome

A

S. aureus and S. pyogenes produce exotoxins
Exotoxins do not require processing by APC
Non-specific binding of MHCII to T cells receptors
Upton 20% of all T cells activated - widespread release of cytokine - decreases of SVR

90
Q

What type of shock can tampons cause

A

Toxic shock syndrome (part of distributive shock)

91
Q

How can shock types combine

A

One type can lead to the next e.g.
Septic shock - primary causing inflammatory and anti-inflammatory cascades - increaes vascular permeability

Hypovolaemic opponent - decreased oral intake and insensible losses through VnD

Cardiogenic shock - sepsis-related myocardium dysfunction

92
Q

Mortality of septic shock

A

35-60% die within 1 hour

93
Q

Cardiogenic shock mortality

A

60-90%

94
Q

When do most inborn errors of metabolism present

A

In childrhood

95
Q

What are most inborn errors of metabolism defects in

A

Defects in enzymes

96
Q

What can occur if blockages occur in pathways in inborn errors of metabolism

A

Can get accumulation of one substance

This substance may then be converted into compounds not usually seen - potentially toxic

97
Q

Role of cofactors in inborn errors of metabolism

A

Need to determine it is an enzyme defect not a cofactor deficiency
Problems making co factors cause the same effects as a defecient enzyme
If we replace the cofactor we can maximise what residual enzyme activity might be remaining

98
Q

Mechanisms of disease in inborn errors of metabolism

A

Accumulation of toxins
Enzyme defeciency
Defecienct production of essential metabolite/structural component

99
Q

When does ammonia accumulate

A

Defects in the urea cycle

100
Q

What does the urea cycle aim to do

A

Remove ammonia produced from the breakdown of amino acids

101
Q

What are the symptoms of ammonia accumulation

A

Lethargy, vomiting, tachypnoea, convulsions, coma, death

102
Q

When does a childhood with defects in the urea cycle become recognised

A

Usually normal at birth as using the mothers metabolism

Usually presents over the next few days/weeks

103
Q

When do porphyrins accumulate

A

Problems in harm synthesis

can only have mild problems as severe problems are incompatble with life

104
Q

What are the 2 types of problems in porphyrias

A 
Acute attacks - only in times of stress
Photosensitivity porphyria (thought of as werewolfs)
105
Q

What happens in acute porphyria attacks

A 
Severe abdominal pain
Chest/back pain
Vomiting, constipation, diarrhoea
Red/brown urine
Insomnia/anxiety
Hypertension
Seizures/metnal changes
Breathing problems/muscle problem
106
Q

What happens in photosensitive porphyria attacks

A 
Sensitivity to sun/artifical light
Itching
Sudden painful erythema and oedema
Fragile skin
Increased hair growth
Red/brown urine
107
Q

When can enzyme defeciency present

A

Present due to defects in fatty acid oxidation e.g. could be hypotonic

Often well until the patient becomes ill

108
Q

Describe a type of deficient production of essential metabolties

A

Healthy female phenotype but the abnormal breast development and absent pubic hair - genetic male

Occurs due to defect in androgen receptor
Presentation of primary amenorrhoea, infertility and ambiguous genitalia
Usually needs surgical resection of residual gonads

109
Q

How to diagnose Inborn errors of metabolism

A

Pre-symptomatic screening

Investigating symptomatic individuals e.g. basic urine screens for amino acids etc.

110
Q

Problems of homocytinuria

A 
Mental retardation
Marfinoud habitus
Ectopia lentis
Osteoporosis
Thromboembolism
111
Q

What is the presence of hyperhomocystinanaemia

A

5%

112
Q

Complication of mild hyperhomocystinaemia

A

Higher risk of stroke, peripheral vascular disease and coronary artery disease

113
Q

What do classic organic acidaemias often defects in

A

Branched chain amino acid catabolism

114
Q

What are the 3 inborn errors commonly picked up

A

Leucine, isoleucine, valine

115
Q

What do we test for in the first trimester for Down’s syndrome

A

PAPA, hCG, nuchal translucency

116
Q

What do we test for in the second trimester for Downs Syndrome

A

Maternal serum AFP, hCG, inhibin and estriol

Also test free foetal DNA

EMS - JL (10 decks)

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