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cardiology > atherosclerosis > Flashcards

atherosclerosis Flashcards

1
Q

define hypertension

A

high blood pressure

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2
Q

aetiology of hypertension

A

genes
environment

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3
Q

characteristic of hypertension

A

140/90 BP

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4
Q

describe stage 1 treatment of hypertension

A

offer antihypertensive drug treatment to patients younger than 80

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5
Q

describe stage 2 treatment of hypertension

A

antihypertensive drug treatment

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6
Q

step 1 of treatment of hypertension for aged over 55

A

or black people of african/caribbean descent = calcium channel blocker or thiazide

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7
Q

step 1 of treatment of hypertension for aged under 55

A

ACE inhibitor or ARB

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8
Q

step 2 of treatment of hypertension

A

add thiazide type diuretic to step 1

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9
Q

step 3 of treatment of hypertension

A

add CCB, ACEi and diuretic together

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10
Q

step 4 of treatment of hypertension

A

resistant hypertension:
- unable to achieve target BP

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11
Q

strengths of antihypertensive therapy

A

help many people lower their high blood pressure and keep their hearts from becoming overworked.

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12
Q

weakness of antihypertensive therapy

A
  • renal artery stenosis
  • impaired renal function
  • hyperkalaemia
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13
Q

treatment of hypertension during pregnancy

A

V hydralazine, labetalol and oral nifedipine

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14
Q

what is atherogenesis

A

formation of focal elevated lesions in intima of large and medium sized arteries

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15
Q

describe atherogenesis

A

Atheromas formalong the inside lining of your arteries and interrupt blood flow through your body

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16
Q

development of atheromatous plaques

A
  • injury to endothelial lining of artery
  • chronic inflammatory and healing response of vascular wall to agent causing injury
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17
Q

what characterises early atheromatous plaque

A

smooth yellow patches in intima

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18
Q

what characterises complicated atheroma

A

atheromatous plaque and haemorrhage into plaque

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19
Q

what characterises a fully developed atheromatous plaque

A

form at arterial branching points

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20
Q

risk factor of atheroma

A

hypercholesterolaemia
- lipids are involved in plaque formation and growth

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21
Q

what are the signs of hyperlipidaemia

A
  • familial/primary vs acquired/secondary
  • LDL, HDL, total cholesterol, triglycerides
  • corneal arcus
  • tendon xanothmata
  • xanthelasmata
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22
Q

what is corneal arcus

A

white, blue or gray crescent shape (arc) made of lipid (fatty) deposits that curves around the outer edges of the cornea of the eye

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23
Q

what is tendon xanthomata

A

slowly enlarging subcutaneous nodules usually found attached to the Achilles tendon or tendons over the knuckles

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24
Q

what is xanthelasmata

A

a sharply demarcated yellowish deposit of cholesterol underneath the skin

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25
Q

describe ruptured atheromatous abdominal aortic aneurysm

A

media beneath atheromatous plaques gradually weakened - sudden rupture can cause massive haemorrhage

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26
Q

describe embolisation of distal arterial bed

A

detachment of small thrombus fragments from thrombosed atheromatous arteries

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27
Q

describe acute atherothrombotic occulsion

A

rupture of plaque can cause irreversible ischaemia and necrosis of tissues

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28
Q

what is thrombosis

A

the formation of a solid mass from the constituents of blood within the vascular system

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29
Q

pathogenesis of thrombosis

A
  • atheromatous coronary artery
  • turbulent blood flow
  • loss of intimal cells
  • collagen exposed
  • platelets adhere
  • RBC’s become trapped
  • lines of Zahn
  • propagation
  • consequences
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30
Q

what are the factors causing thrombosis

A
  • endothelial injury
  • stasis or turbulent blood flow
  • hypercoagulability of the blood
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31
Q

what is embolism

A

detached intravascular mass

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32
Q

factors causing embolism due to thrombus

A

mural thrombosis often associated with MI or left atrial dilation + AF)

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33
Q

factors causing embolism due to fat

A

after major fractures

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34
Q

factors causing embolism due to gas

A

decompression sickness - Na2 forms as bubbles which lodge in capillaries

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35
Q

factors causing embolism due to air embolus

A

head and neck wounds, surgery, CV lines

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36
Q

factors causing embolism due to trophoblast

A

pregnant women - lungs

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37
Q

define ischaemia

A

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

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38
Q

describe hypoxic hypoxia

A

O2 level = low
inspired O2 = normal
PaO2 = low

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39
Q

describe anaemic hypoxia

A

inspired O2 = normal
blood = abnormal

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40
Q

describe stagnant hypoxia

A

inspired O2 = normal
O2 delivery = abnormal

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41
Q

describe cytotoxic hypoxia

A

inspired O2 = normal
tissue level = abnormal

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42
Q

describe cytotoxic hypoxia

A

inspired O2 = normal
tissue level = abnormal

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43
Q

what is infarction

A

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

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44
Q

relationship between atheroma and ischaemia

A

Most ischemic strokes are caused by atherosclerosis

45
Q

describe biochemical consequences of ischaemia

A

reduced O2 leads to anaerobic metabolism which leads to cell death

46
Q

describe the process of infarction

A

anaerobic metabolism leads to cell death leads to liberation of enzymes leads to breakdown of tissue

47
Q

describe transmural infarction

A

ischaemic necrosis affects full thickness of the myocardium

48
Q

describe subendocardial infarction

A

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

49
Q

what is stable angina

A

a discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis

50
Q

what causes stable angina

A

reduction in coronary artery blood flow to the myocardium

51
Q

non-modifiable risks of stable angina

A

Age, gender, creed, family history & genetic factors.

52
Q

modifiable risks of stable angina

A

Smoking, Lifestyle- exercise & diet, Diabetes mellitus, Hypertension & Hyperlipidaemia

53
Q

clinical presentation of stable angina

A
  • Tar stains on fingers.
  • Obesity (centripedal).
  • Xanthalasma and corneal arcus (hypercholesterolaemia).
  • Hypertension.
  • Abdominal aortic aneurysm arterial bruits, absent or reduced peripheral pulses.
  • Diabetic retinopathy, hypertensive retinopathy on fundoscopy
54
Q

what investigation should higher risk patients with suspected stable angina undergo

A

coronary angiography

55
Q

what medicines are used for relief of stable angina symptoms

A

B blockers
Ca channel blockers
Lk channel blockers
all to achieve resting heart rate of under 60 BPM

56
Q

medicines used to manage stable angina

A

statins, ace inhibitors and aspirin

57
Q

what causes myocardial infarction

A

thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque

58
Q

symptoms of myocardial infarction

A
  • chest pain, which travels from left arm to neck,
  • shortness of breath,
  • sweating,
  • nausea,
  • vomiting,
    abnormal heart beating
59
Q

describe rate limiting drugs

A

for symptom relief
beta-adrenoreceptor antagonist

60
Q

describe vasodilator drugs

A

for symptom relief
examples: nitrates, calcium channel blockers

61
Q

describe sodium channel activator drugs

A

ranolazine

62
Q

function of beta blockers

A

block the sympathetic system

63
Q

example of beta blocker

A

bisoprolol

64
Q

adverse effects of beta blockers

A

asthma, acute heart failure and bradycardia

65
Q

benefits of beta blockers

A

reduces myocardial workload, reduces rate of ischaemic events and mortality

66
Q

function of calcium channel blockers

A

Prevent calcium influx into myocytes and smooth muscle arteries/arterioles by blocking L-type Ca channel

67
Q

examples of calcium channel blockers

A

amlodipine (DHP) verapamil (N-DHP)

68
Q

function of vasodilators

A

Nitric Oxide mediated smooth muscle relaxation

69
Q

examples of vasodilators

A

nitrates

70
Q

describe the mechanism of action of thrombolytic therapy

A
  • converting plasminogen to plasmin, an enzyme that breaks down fibrin, a protein that forms the backbone of blood clots.
  • By breaking down fibrin, thrombolytics can dissolve blood clots and restore blood flow to the affected area
71
Q

common complications of myocardial infarction

A
  • ventricular septal defect (VSD),
  • papillary muscle rupture or dysfunction,
  • cardiac free wall rupture,
  • ventricular aneurysm,
  • dynamic left ventricular (LV)
  • outflow tract (OT) obstruction
  • right ventricular (RV) failure
72
Q

what is the role of beta-blockers in angina

A

reducing myocardial oxygen demand by decreasing heart rate and myocardial contractility

73
Q

what is the role of statins

A

preventing myocardial infarction = lowering cholesterol levels

74
Q

what are the potential adverse drug reactions following treatment of ischaemic heart disease

A

bradycardia, dizziness, hypotension, hyperkalemia, cough, and renal impairment

75
Q

what is stroke

A

neurological deficit of sudden onset due to a blocked (ischemic) or ruptured (hemorrhagic) blood vessel in the brain

76
Q

causes of stroke

A

blockage with thrombus or clot, disease of vessel wall, disturbance of normal properties of blood, rupture

77
Q

risk factors for stroke

A
  • Age
  • Hypertension
  • Cardiac Disease (esp atrial fibrillation)
  • Diabetes
  • Smoking
  • Family history
  • Cholesterol
  • Bleeding disorders
78
Q

treatments for stroke

A

thrombolysis via atleplase
tissue plasminogen activator - within 3 hours of treatment

79
Q

treatments for stroke

A

thrombolysis via atleplase
tissue plasminogen activator - within 3 hours of treatment

80
Q

what is primary stroke prevention

A

Primary stroke prevention refers to the treatment of individuals with no history of stroke.

81
Q

what is secondary prevention of stroke

A
  • Secondary stroke prevention refers to the treatment of individuals who have already had a stroke or transient ischemic attack
  • Measures may include the use of platelet antiaggregants, antihypertensives, statins, and lifestyle interventions
82
Q

layers of thoracic aorta

A

tunica intima
tunica media
tunica adventitia

83
Q

what is tunica intima

A

inner layer - endothelial

84
Q

what is tunica media

A

middle layer - smooth muscle

85
Q

what is tunica adventitia

A

outer layer - thin connective tissue

86
Q

what is an aneurysm

A

localised enlargement of an artery caused by a weakening of the vessel wall

87
Q

describe a true aneurysm

A

weakness and dilation of wall involving all 3 layers

88
Q

describe a false aneurysm

A

rupture of wall of aorta contained by adventitia or soft tissue

89
Q

clinical presentation of acute thoracic aneurysm

A

can be asymptomatic
- Shortness of breath (associated aortic regurgitation)
- Dysphagia and hoarseness
- Back pain
- Symptoms of dissection - sharp chest pain radiating to back (between shoulder blades), hypotension
- Pulsatile mass

90
Q

what is aortic disection

A

tear in inner wall of aorta

91
Q

presenting symptoms of acute aortic disection

A
  • Chest pain – severe, sharp, radiating to back (inter-scapular)
  • Collapse (tamponade, acute AR, external rupture)
  • Stroke (involvement of carotid arteries)
92
Q

examined symptoms of acute aortic dissection

A
  • Reduced or absent peripheral pulses
  • Hypertension or hypotension
  • BP mismatch between sides
  • Soft early diastolic murmur (aortic regurgitation)
  • Pulmonary oedema
  • Signs of CVA
93
Q

what is coarctation

A

aortic narrowing close to where ductus arteriosus inserts

94
Q

signs of coarctation

A
  • Cold legs
  • Poor leg pulses
95
Q

what is marfans syndrome

A

an inherited disorder that affects connective tissue (fibrillin 1 gene)

96
Q

what are possible aortic manifestations

A
  • aortic/mitral valve prolapse - regurgitation
  • aneurysm and dissection
  • vascular - aneurysm, disection
97
Q

clinical presentation of arterial occlusive disease

A

“six Ps”:
-pallor
- pain
- paresthesia
- paralysis
- pulselessness
- poikilothermia

98
Q

clinical presentation of aneurysmal disease

A

abdominal or back pain with a pulsatile abdominal mass

99
Q

what is carotid endarterectomy

A

surgical procedure to remove a build-up of fatty deposits (plaque), which cause narrowing of a carotid artery

100
Q

benefits of carotid endarterectomy

A
  • Reduces Risk of Additional Stroke
  • Reduces Risk of First Time Stroke
  • Safe Procedure
  • The Procedure Has Durable Outcomes
101
Q

complications of carotid endarterectomy

A
  • surgical complications
  • restenosis = plaque returning
  • limited benefits for mild to moderate blockage
102
Q

function of the venous system in the lower limbs

A

A system of muscular venous pumps and bicuspid valvesensure flow from superficial to deep and from caudal to cephalad within the lower extremity

103
Q

what are the complications with venous incompetence

A
  • Recruitment of veins
  • DVT.
  • Pulmonary embolism (PE)
  • Venous ulceration.
  • Secondary lymphedema.
104
Q

symptoms of chronic venous insufficiency

A
  • Swelling in your legs or ankles.
  • Tight feeling in your calves or itchy, painful legs.
  • Pain when walking that stops when you rest.
  • Brown-colored skin, often near the ankles.
  • Varicose veins.
  • Leg ulcers that are sometimes hard to treat
105
Q

clinical presentation of CLI

A
  • Stage I: Asymptomatic, incomplete blood vessel obstruction
  • Stage II: Mild claudication pain in limb
  • Stage IIA: Claudication when walking a distance of greater than 200 meters
  • Stage IIB: Claudication when walking a distance of less than 200 meters
  • Stage III: Rest pain, mostly in the feet
  • Stage IV: Necrosis and/or gangrene of the limb
106
Q

clinical presentation of compartment syndrome

A
  • Inflammation,
  • oedema,
  • venous obstruction
  • tense, tender calf
107
Q

what is balloon angioplasty

A

procedure in which your vascular surgeon inserts a balloon catheter into a narrowed portion of an artery to treat arterial occlusive disease

108
Q

what is bypass grafting

A

surgical procedure to redirect blood flow around an area of blockage to treat arterial occlusive disease

cardiology (3 decks)

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