Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

x1 - Cardiovascular > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Atherogenesis definition

A

The process of forming atheromas/ atheromatous plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Components of atheromatous plaques

A

Central lipid core (w/ rim of foamy macrophages),
Fibrous tissue cap,
Covered by arterial endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Main aetiological factor for atheroma

A

Hyperlipidaemia.

High levels of lipoproteins (especially LDL) irritate the arterial endothelium leading to injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signs of major hyperlipidaemia

A

Premature corneal archus - white ring around iris

Tendon xanthomata - mobile nodules in knuckles/ Achilles

Xanthelasmata - yellowish deposits of cholesterol under the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Role of atheroma in coronary heart disease

A

Atheroma in coronary artery:
Stenosis –> reduction of blood flow –> reversible tissue ischaemia + angina

Total occlusion –> irreversible ischaemia –> tissue necrosis + myocardial infarction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Role of atheroma in cerebrovascular disease

A

Atheroma in carotid/cerebral artery:

stenosis/ occlusion –> ischaemic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Role of atheroma in peripheral arterial disease

A

Atheroma causing stenosis in ileal/ femoral/popliteal etc…artery
–> intermittent claudication (cramping pain in legs during exercise due to inadequate blood flow)
= most prominent symptom of PAD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Process of arethomatous plaque formation

atherogenesis

A
  1. An irritant causes endothelial cell injury,
  2. LDL enters T. intima,
  3. Monocytes adhere to endothelium, migrate into T. intima, mature becoming macrophagesand phagocytose LDL,
  4. Macrophages die forming foam cells
  5. Activated platelets adhere to the injured endothelium and release growth factors,
  6. Growth factors cause intimal smooth muscle to proliferate and form a fibrous cap (enclosing the lipid core)
  7. smooth muscle cells lie down calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Results of endothelial cell injury to the endothelium

A

Increased permeability to LDL,
Enhanced expression of cell adhesion molecules
Increased thrombogenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fatty streak

A

Earliest significant lesion of arteriosclerosis, begins in young children.

A yellow linear elevation of the intimal lining, comprised of lipid laden macrophages (foam cells).

No clinical significance, may disappear but for patients at risk, may form atheromatous plaques.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Consequences of atheroma on the artery

A

Reduced arterial radius = increased resistance
Reduced arterial compliance

= increased MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathophysiology of stable ischaemic heart disease

A

Mismatch between supply of O2 and metabolites to myocardium and myocardial demand for them.

Usually due to a reduction in coronary blood flow to the myocardium - coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Reasons for reduction of coronary blood flow

causing coronary artery disease

A

Obstructive coronary atheroma

Coronary artery spasm,
Coronary inflammation/arteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Other causes of stable ischaemic heart disease

other than reduction of coronary blood flow

A

Reduced O2 transport (anaemia),

Pathologically increased myocardial demand.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Angina definition

A

Cardiac chest pain associated with myocardial ischaemia (but without myocardial necrosis)

brought on by excess myocardial oxygen demand
e.g. exertion, cold weather, emotional stress, following heavy meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Non-modifiable risk factors for coronary artery disease

A

Age,
Male,
Race (south Asian),
Family history/ genetic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Modifiable risk factors for coronary artery disease

A 
Smoking,
Diet and exercise,
Diabetes mellitus (glycaemic control),
Hypertenion (BP control),
Hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Stable Angina SOCRATES

A 
Site: Retrosternal
Character: pressure/ tightness
Radiation: Left neck/jaw/down arm
Aggravated by: exertion/ emotional stress
Relieved by: GTN/ physical rest.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Other symptoms of stable angina

apart from pain

A

Breathlessness on exertion,
Excessive fatigue on exertion,
Near syncope on exertion,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Signs of stable angina

A 
Centripedal obesity,
Xanthalasma and corneal arcus,
Hypertension,
Palpable abdominal aortic aneurysm,
Arterial bruits,
Absent/reduced peripheral pulses,
Diabetic/hypertensive retinopathy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Investigations of stable angina

A

ECG: Usually normal, can show LVH or evidence of previous MI
Bloods: FBC, lipid profile, fasting glucose, electrolytes, liver function, thyroid function, d-dimer.
CXR: differential diagnosis
Exercise tolerance test: Shows ST segment depression on exertion
Myocardial perfusion imaging: Tracer seen at rest, not at stress
Invasive coronary angiogram/ cardiac catheterisation: shows occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Exercise tolerance test

A

Can confirm diagnosis of angina with:

  • typical symptoms
  • ST segment depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Myocardial perfusion imaging

A

Radionuclide tracer injected, images obtained at stress and at rest.

Tracer seen at rest, but not stress = ischaemia
Tracer not seen at rest or stress = infarction

Localises ischaemia,
assesses size of area affected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

coronary angiography/ cardiac catheterisation

A

Radio-opaque contrast is injected into coronary arteries with a catheter and visualised on an x-ray.

shows sites, distribution and nature of atheromatous disease - enabling best treatment decision.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Drug treatment of stable angina

influencing disease progression

A

STATINS: Reduce LDL cholesterol deposition

ACE INHIBITORS: Stabilise endothelium and reduce plaque rupture

ASPIRIN: Protects endothelium and reduces platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Drug treatment of stable angina

Symptom relief

A

Druds that decrease myocardial demand (HR, contractility, afterload):
β-blockers,
CCBs,
nitrates(e.g. GTN),
K+ channel activators (prevent influx of Ca2+ to smooth muscle = coronary vasodilation), e.g. nicorandil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Percutaneous Transluminal Coronary Angioplasty (PTCA)/

Percutaneous Coronary Intervention (PCI)

A

A balloon catheter is inserted through femoral/ brachial artery into the coronary artery with stenosis.

The balloon is inflated to compress the blockage and widen the artery. A stent may also be used to keep the vessel open.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Coronary Artery Bypass Grafting (CABG)

A
  1. The left internal thoracic artery is diverted to the left coronary artery.
  2. A great saphenous vein is removed and used to join the aorta to the obstructed artery, immediately after the obstruction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Virchow’s Triad

A

3 Factors causing thrombosis:

Changes in blood vessel wall,
Changes in blood constituents,
Changes in the pattern of blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Relationship between atheroma and thrombosis

A

Arterial thrombosis is most commonly superimposed on atheroma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Changes in the blood vessel wall that could lead to thrombosis

A

ATHEROMA

atheroma = occlusion = turbulent flow/stasis = endothelial damage = thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Changes in blood constituents that could lead to thrombosis

A

HYPERVISCOSITY
-e.g. from dehydration

HYPERCOAGULABILITY

  • thrombophilia,
  • pregnancy,
  • drugs e.g. OCP,
  • Diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Changes in blood flow that could lead to thrombosis

A

STASIS

  • aeroplane,
  • post-op

TURBULENCE

  • atheroma,
  • aortic aneurysm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Process of thrombosis

A

Endothelial injury = collagen exposed

  • -> platelets adhere to collagen
  • -> thrombin converts fibrinogen to fibrin
  • -> fibrin mesh formed over platelet plug

= Further turbulence
–> damages endothelium + causes platelet deposition
= growth of thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Sources of systemic/arterial thromboemboli

A

Mural thrombus (formed in heart chamber),
Aortic aneurysm,
Atheromatous plaques,
Valvular vegetations,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Source of venous thromboemboli

A

Deep venous thrombi

most common type, often cause pulmonary thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Types of embolus

A 
Systemic/ arterial (thromboembolus),
Venous (thromboembolus),
Fat,
Gas,
Air,
Tumour,
Trophoblast (in pregnancy),
Septic material,
Amniotic fluid,
Bone marrow,
Foreign bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Ischaemia definition

A

Relative lack of blood supply to tissue/ organ leading to inadequate O2 supply to meet the needs of the tissue/organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Types of hypoxia

A

Hypoxic - low inspired O2/ low PaO2
Anaemic - abnormal blood
Stagnant - abnormal delivery
Cytotoxic - abnormal at tissue level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Hypoxia definition

A

Diminished availability of O2 to body tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Infarction definition

A

Ischaemic necrosis within a tissue/ organ in living body produced by occlusion of the arterial supply or venous drainage

*Cell death due to ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Effects of infarction

A

Tissue dysfunction,
Pain,
Physical damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Supply issues leading to ischaemic heart disease

A 
Coronary artery atheroma,
Cardiac failure (flow),
Low pulmonary function,
Pulmonary oedema,
Anaemia,
Previous MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Process of infarction

A

relative lack of O2 supply

  • -> anaerobic metabolism
  • -> ATP depletion
  • -> (loss of myocardial contractility)
  • -> cell death
  • -> liberation of enzymes
  • -> breakdown of tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Transmural infarction

A

Ischaemic necrosis affecting full thickness of the myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Subendocardial infarction

A

Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

probably non-STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Reparative process in myocardial infarction

A

Cell death

  • -> Cell membranes breakdown (=coagulative necrosis)
  • -> Proteins leak out
  • -> Neutrophils lyse dead muscle cells
  • -> Neutrophils die
  • -> Macrophages phagocytose debris
  • -> Granulomatous inflammation (angiogenesis + fibroblasts lay down collagen)
  • -> Fibrosis = scar tissue - non-contractile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Acute coronary syndrome (ACS)

A

Any sudden cardiac even due to myocardial ischaemia

e.g. Unstable angina, Non-STEMI, STEMI, Sudden Cardiac Death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Sudden Cardiac Death (SCD)

A

Death caused by sudden and unexpected cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Myocardial Infarction definition

major/minor

A

Cell death in the myocardium due to ischaemia

MAJOR MI = due to complete coronary artery occlusion

MINOR MI = due to a partial/ transient complete coronary artery occlusion

51
Q

Symptoms of Myocardial Infarction

main + associated

A

Chest pain/discomfort:

  • severe, not “agony”
  • may radiate to neck/arm

May be associated with:

  • nausea
  • sweating
  • dyspnoea
52
Q

Signs of Myocardial Infarction

on examination

A

May look very unwell/ fine,
Often no specific features to find,

CHECK:

  • HR
  • BP
  • Murmurs
  • Crackles
53
Q

ECG changes after an MI

A

Complete coronary occlusion –> ST elevation –> Q waves after 3 days

Partial coronary occlusion –> no ST elevation (+ T-wave inversion) –> No Q waves

54
Q

Location of MI caused by coronary occlusions in different coronary arteries

A

RCA = inferior/posterior

Anterior interventricular coronary artery = anterior

Circumflex = lateral/posterior

55
Q

Detecting Posterior MIs

A

Usually caused by a RCA occlusion, so may see inferior changes.

Opposite changes are seen in opposite leads

56
Q

Biomarker tests following MI

A

Myocyte death = membrane ruptures = proteins (cardiac biomarkers) leak out.

Most useful biomarkers = Cardiac troponin I & T

*There can be other causes of troponin rise!!

57
Q

Diagnosis of MI

A
  1. detection of cell death = elevated troponin
  2. AND one of…
    - symptoms of ischaemia
    - New ECG changes,
    - Evidence of coronary problem on angiogram,
    - other evidence for new cardiac damage
58
Q

Thrombolytic therapy mechanism

A

Serine proteases that convert plasminogen to plasmin (a natural fibrinolytic)

59
Q

Strengths of thrombolytic therapy

A

Works well if given early, especially with aspirin.

Used if PCI not possible within 2 hours

60
Q

Weaknesses of thrombolytic therapy

A

Increases risk of bleeding/haemorrhage:

  • don’t give if recent stroke or previous intracranial bleed,
  • Caution of recent surgery, on warfarin or severe hypertension.

May not work, especially if given late.

61
Q 
Aspirin therapy
(mechanism and benefit)
A

Aspirin inhibits platelet production of thromboxane,
(thromboxane stimulates platelet aggregation and vasoconstriction)

Daily aspirin reduces risk of MI and death in patients with ischaemic heart disease

62
Q

Common complications of MI

A 
Arrhythmia,
Cardiogenic shock,
Myocardial rupture,
Papillary muscle dysfunction,
Acute VSD
63
Q

Cardiogenic shock

A

Inadequate circulation of the blood due to ventricular failure

64
Q

Cardiac rehabilitation

A

Exercise programmes,
Information sessions,
Addresses risk factors

65
Q

Beta blockers in MI treatment

A

Reduce myocardial oxygen demand by lowering HR and myocardial contractility.

Reduces mortality following acute MI and reduces risk of secondary MI in survivors.

66
Q

Contraindications of beta blockers in MI treatment

A 
Asthma
Bradycardia
Heart block
Coronary vasospasm
Cocaine use
↑ risk cardiogenic shock ( Systolic BP<120, HR>110, age>70yrs)
67
Q

Goals of pharmacological treatment of myocardial infarction

A
  1. Increase Myocardial O2 Supply:
    - coronary vasodilation
  2. Decrease Myocardial O2 Demand:
    - decrease HR
    - decrease BP
    - decrease preload/ myocardial contractility
68
Q

Drugs for prevention of MI and Angina

A

Beta-blockers,
ACE inhibitors,
Aspirin,
Simvastatin (lipid-lowering therapy),

69
Q

Clopidogrel (mechanism)

A

Inhibits platelet aggregation

70
Q

Heparin (mechanism)

A

Inactivates thrombin (converts fibrinogin to fibrin)

71
Q

Risk factors for stroke

A

MODIFIABLE:

  • High BP
  • Atrial fibrilation

NON-MODIFIABLE:

  • Age
  • Race
  • Family history
72
Q

Stroke investigations

A 
Blood tests - FBC, Lipids,
ECG - For possible cause
CT - Better for haemorrhagic (shows blood)
MRI - Better for ischaemic
Carotid doppler - shows carotid stenosis
Echo - shows clots in heart
73
Q

Acute treatments for stroke

A

Thrombolysis,
Aspirin,
Hemicraniectomy,
Thrombectomy (clot retrieval)

74
Q

Hemicraniectomy

A

Part of the skull is temporarily removed to allow the brain to swell following a stroke without increasing intercranial pressure.

75
Q

Treatment for primary + secondary prevention of stroke

A 
Clopidogrel or Aspirin
\+
Statin
\+
BP drugs (even if normal BP)

*Carotid Endarterectomy (surgical removal of atheromatous plaque)

76
Q

Aortic aneurysm disease definition

A

Dilatation of all layers of the aorta, leading to an increase in diameter of >50%
(abdominal aorta >3cm)

77
Q

Symptoms of abdominal aortic aneurysm

nearing rupture

A

May be asymptomatic
Increasing back pain
tender abdominal aortic aneurysm

78
Q

Clinical presentation of abdominal aortic aneurysm rupture

A

Abdominal/back/flank pain
Painful pulsatile mass
Hypoperfusion
Haemodynamic instability (shock)

79
Q

Unusual presentations of AAA

A 
Distal embolisation
Aortocaval fistula
Aortoenteric fistula
Ureteric occlusion
Duodenal occlusion
80
Q

Carotid endarterectomy

A

Prophylactic surgical removal of an atheromatous plaque from a carotid artery

81
Q

Complications (weaknesses) of carotid endarterectomy

A 
Wound infection
Bleeding
Scar
Anaesthetic risks
Nerve damage
Perioperative stroke
82
Q

Strengths of carotid endarterectomy

+ when should it be done

A

Lower risk of stroke than from stenting

Should be offered for all symptomatic patients with >70% stenosis (but not if complete occlusion)

83
Q

Positives of iodinated contrast agents

A 
Differential x-ray attenuation
Inert
Stable in selected body compartments
Painless
Easy to use
Cheap
Localises in the vascular system

*All qualities of the ideal vascular contrast agent

84
Q

Problems with iodinated contrast

A

MAJOR REACTIONS:

  • renal dysfunction
  • disturbance of thyroid metabolism
  • disturbance of clotting
  • seizures
  • pulmonary oedema
  • Contrasts should only be administered by those who can recognise and treat potential reactions
85
Q

Carbon dioxide as a contrast agent

A

A negative contrast agent

Used in angiography

Useful in patients with poor renal function or sensitivity to iodinated contrast agents

86
Q

Compression ultrasound

A

A normal vein has low pressure and is compressible

A DVT vein is full of thrombus and is not

87
Q

Radionuclide imaging of vascular disturbances is used for…

A

Perfusion

Blood loss

88
Q

Advantages of CT

A

Gives information about other structures
Sensitive
IV injection only

89
Q

Limitations of CT

A

Radiation dose
High contrast dose
Expensive

90
Q

Main contraindication of contrast agents

A

Renal failure

May induce contrast nephropathy
Renal function should be checked before administering the contrast if the patient is likely to have renal impairment

91
Q

Doppler ultrasonography

A

Ultrasound scanning that uses the doppler effect to image the movement of blood

92
Q

B mode ultrasound scanning

A

Shows a still plane through the body

Also called “2D mode”

93
Q

M mode ultrasound scanning

A

Many pulses are emitted in quick succession creating an ultrasound “video”

94
Q

Housenfield Unit/ CT Number

A

An arbitrary unit of the X-ray attenuation of structures viewed on CT
e.g. water = 0, compact bone = >1000

95
Q

CT window width

A

The range of Housenfield units displayed. Tissues outside the range are shown as black or white

Maximum width = a wider range of densities represents one shade of grey. Contrast appears very low, used to view regions with wide ranges of density

Smaller width = a smaller range of densities is represented by a shade of grey. Subtler differences in density can be distinguished,

96
Q

CT window level

A

The Housenfield unit at the centre of the window width. Should be higher to view denser tissues

97
Q

Spiral (helical) CT

A

The scanner scans the body in a spiral path.

Images are more detailed and can be taken in a shorter time

98
Q

Causes of venous valvular failure

valvular/venous incompetence

A

Surgical or traumatic disruption of the valve

DVT: ↑ pressure

Pregnancy: Hormonal changes cause vein and valve weakness. Enlarges uterus causes mechanical obstruction = ↑ pressure

Large pelvic tumour: A mechanical obstruction = ↑ pressure

99
Q

Varicose veins investigations

A

DOPPLER ULTRASOUND:
Shows dynamic blood flow

TOURNIQUET TEST:

TAP TEST:
Tapping the saphenous vein at the knee will be felt at the saphenofemoral junction if the valves in between are incompetent

100
Q

Chronic venous insufficiency investigations

A

Ultrasound: shows flow/reflux

Ankle-brachial pressure index: excludes arterial disease where BP is lower in the leg

CT/MR Venography: Shows detailed venous anatomy

101
Q

Varicose veins treatment

A
  1. Endovenous/endothermal treatment:
    A heat/ laser catheter causes fibrosis and occlusion of the vein
  2. Ultrasound guided foam sclerotherapy:
    A chemical foam causes fibrosis and occlusion of the vein
  3. Open surgery:
    The vein is stripped out

If intervention unsuitable (DVT, pregnancy): Compression hosiery

102
Q

Lymphoedema

A

Pooling of lymph fluid in the tissue (usually lower limbs) due to improper lymphatic drainage.

Can be primary (genetic)
or secondary, due to:
 - malignancy
 - surgery
 - radiotherapy
 - infection

Treatment is elevation and drainage

103
Q

Stages of symptoms of arterial occlusive disease

A

Stage 1: Asymptomatic
Stage 2: Claudication on exertion
Stage 3: Pain at rest, mostly in feet
Stage 4: Necrosis/ gangrene of the limb

104
Q

Signs of arterial occlusive disease

A

Ulceration
Pallor
Hair loss

105
Q

Surgical interventions for arterial occlusive disease

A

Angioplasty
Surgical bypass
Amputation
Embolectomy

106
Q

Demand issues leading to ischaemic heart disease

A

High intrinsic demand
Exertion
Stress

107
Q

Clinical consequences of ischaemia

A

MI
TIA (Transient ischaemic attack)
Cerebral infarction
Peripheral vascular disease

108
Q

Beta blocker ADRs

A

Fatigue
Lethargy
Bradycardia
Bronchospasm

109
Q

Aspirin ADRs

A

GI bleed

110
Q

Nitrovasodilators ADRs

A

Headache

Hypotension (“GTN syncope”)

111
Q

Rate limiting CCBs ADRs

A

Ankle oedema
Flushing
Headache

112
Q

Vasodilating CCBs ADRs

A

Reflex tachycardia
Ankle oedema
Flushing
Headache

113
Q

ACEI ADRs

A

Cough
First dose hypotension
Renal impairment

114
Q

Purpose of coronary interventions in SIHD and angina

A

Symptomatic treatment

Prevention of MI

115
Q

Pathophysiology of valvular incompetence

A

Once one valve fails, venous pressure increases, the distal vein dilates causing further valvular incompetence

116
Q

Treatment of chronic venous insufficiency

A

Wound care
Elevation
Compression bandaging
Shockwave therapy (for ulcers)

117
Q

Symptoms of varicose veins

A 
Burning
Itching
Heaviness
Tightness
Swelling
Discolouration
Phlebitis (red lines)
Bleeding
Disfiguration
Eczema
Ulceration
118
Q

Signs of varicose veins

A

Twisting and bulging visible and palpable veins

Oedema

119
Q

Symptoms of chronic venous insufficiency

A 
Swelling
Heaviness
Pain
Itching
Varicose veins
Discolouration
120
Q

Signs of chronic venous insufficiency

A

Oedema
Telangiectasia (spider veins)
Eczema
Hyperpigmentation
Lipodermatosclerosis (hypodermis inflammation)
Ulceration (breach in skin btw/ knee and ankle)
Haemosiderin pigmentation

121
Q

Indications of ultrasound

A

Used for anatomical + functional vascular imaging
No radiation
Quick
Non-invasive

122
Q

Methods of administration of contrast agents

A

Parenteral e.g:

  • CT (coronary) angiogram
  • Ultrasound
  • Radionucleide imaging
  • CT

Catheterisation e.g:
- coronary angiography/ cardiac catheterisation

123
Q

Tourniquet test

A

Leg is raised above heart level so vein drains
A tourniquet is applied above upper thigh to compress superficial (not deep) veins
Patient stands

  • If superficial veins distal to tourniquet refill <20 seconds = deep valvular incompetence

Tourniquet is released after 20 seconds

*If sudden refilling of superficial veins now = superficial venous incompetence

x1 - Cardiovascular (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions