Vascular diseases Flashcards

1
Q

Atherosclerosis

A

An inflammatory disease of large and medium-sized systemic arteries characterised by the formation of lipid-rich plaques in the vessel wall.

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2
Q

Atherosclerosis Epidemiology and modifiable RF

A

Almost universally present to some degree in all individuals with ageing.

Non modifiable RF: age, males, Family Hx

Modifiable RF: Smoking, alcohol, poor diet/high cholesterol, obesity/low exercise, stress.

Comorbidities that increase the risk:
Diabetes mellitus, hypertension, Inflammatory conditions e.g. RA, and hyperlipidaemia.

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3
Q

Atherosclerosis Pathology

A

Endothelial injury leads to an inflammatory and activation of the immune system - fibroproliferative reaction in the artery, culminating in lipid plaques as a response to injury.
May form stable or unstable plaques.
These plaques cause:
1) Artery wall to stiffen leading to hypertension.
2) Stenosis causing reduced blood flow E.g. PVD
3) Plaque ruptures giving of thrombus that can travel down the blood vessel, blocking it and causing ischaemia - main cause of Heart attack

  • Endothelium may be damaged by multiple factors: including smoking, hyperglycaemia, and oxidised LDL (Oxidized Low-Density Lipoprotein) - from bad cholesterol/fatty foods
  • Oxidised LDL is particularly potent at driving atherosclerosis through its proinflammatory and procoagulant effects. More likely to cause a thrombosis
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4
Q

Stable plaques

A

Few inflammatory cells and a thick fibrous cap narrow the lumen of the artery, but are less likely to cause acute complications.
Cause symptoms of reversible ischaemia in the supplied organ, e.g. angina pectoris, chronic lower limb ischaemia.

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5
Q

Unstable plaques

A

More inflammatory cells have a thin fibrous cap more liable to complications like erosion, cracking, or rupture.
Cause acute ischaemic events, e.g. acute coronary syndromes, stroke, acute lower limb ischaemia.

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6
Q

Peripheral Vascular Disease (PVD)

A

A narrowing or blockage of the arteries that supply blood to the extremities. PVD most commonly affects the arteries in the lower limbs but can also occur in the arms or other peripheral arteries.

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7
Q

PVD Epidemiology

A

Increasing age, especially after 65 (or after 50 if you have risk factors for atherosclerosis).
Smoking, diabetes, high blood pressure, high cholesterol levels, obesity, and a sedentary lifestyle.

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8
Q

PVD Pathology

A

Often caused by atherosclerosis, a condition characterised by the buildup of plaque (cholesterol, fat, and other substances) on the inner walls of the arteries. This buildup leads to a reduction in blood flow, resulting in inadequate oxygen and nutrient supply to the affected areas.

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9
Q

PVD S&S

A

Claudication: This is the most common symptom of PVD. It refers to pain, cramping, or fatigue in the muscles of the legs, particularly during physical activity or walking. The pain typically subsides with rest.

5Ps:
Pain
Paresthesia
Pulselessness
Palar
Pertin cold - cold to touch

  • Changes in skin colour, the affected area may appear pale, bluish, or discoloured.
  • Slow-healing wounds or ulcers
  • Slower growth of the toenails
  • Sores on the toes, feet or legs that won’t heal - trash toes
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10
Q

Leriche syndrome

A

PVD in the aortic or illiac vessels
Thigh = buttocks claudication
Male impotence
Pulslessness femoral pulse

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11
Q

PVD Investigations

A

Compare blood pressure in the arms and legs, Doppler ultrasound
MRA

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12
Q

PVD management

A

In severe cases, PVD can result in critical limb ischemia, a condition characterized by severe pain at rest, non-healing ulcers, and the risk of tissue damage or limb loss.
Lifestyle modifications
Surgical interventions to remove blockages or bypass the narrowed arteries.

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13
Q

Hypertension (S)

A

High blood pressure, characterised by persistently elevated blood pressure in the arteries

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14
Q

Hypertension Epidemiology

A

The risk of high blood pressure increases with age. Until about age 64, high blood pressure is more common in men. Women are more likely to develop high blood pressure after age 65.
Black people
Family history

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15
Q

Hypertension Patho

A

Blood pressure is product of cardiac output (Heart rate
x Stroke volume) and total peripheral vascular resistance.

Phsyiological process of BP: in the liver it creates angiotensin, when the kidney senses a low amount of water going through it it release renin which stimulates angiotensin to go through the lungs and ACE and converts it to ACE 2 which stimulates the medullary cortex to produce aldosterone in the adrenal glands that are on the kidneys and effectively increases the blood pressure.

Blood leaves the left ventricle through the aorta and influences specialised cells in the aortic arch (also within the carotid artery)
Increases and decreases in pressure are registered and sent to the medulla oblongata (cardiovascular centre)
If pressure is high the medulla stimulates vasodilation and a decrease in cardiac output
If the pressure is low the medulla stimulates vasoconstriction: an increase in cardiac output

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16
Q

In response to low cardiac output

A

1) In response to low cardiac output the sympathetic nervous system will cause Alpha and Beta-adrenoreceptor changes which stimulate an increase in cardiac output

2) In response to poorly oxygenated blood the nephrons of the juxtaglomerular apparatus will cause renin to be released which reacts with angiotensin 1reacts with angiotensin 2 reacts with blood vessels vasoconstrictionraises total peripheral resistance

3) Angiotensin 2 also reacts with the adrenal cortices which release aldosterone acts on nephrons to retain sodium and waterraises BP and increases blood volume

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17
Q

3 Types of hypertension

A

Primary
Secondary
Malignant

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18
Q

Primary

A

For most adults, there’s no identifiable cause of high blood pressure. It tends to develop gradually over many years. Atherosclerosis, increases the risk of high blood pressure.

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19
Q

Secondary

A

Caused by an underlying condition. It tends to appear suddenly and cause higher blood pressure than does primary hypertension. Conditions and medicines that can lead to secondary hypertension include:
Renal disease (80%): mechanism is generally sodium and water retention.
Adrenal gland tumors
Blood vessel problems present at birth, also called congenital heart defects
Kidney disease
Thyroid problems

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20
Q

Malignant

A

Results from extremely high blood pressure that only about 1% of those with high BP are affected, could happen from missing the medication dosage, or tumor of the adrenal gland, spinal cord injuries, illegal drugs such as cocaine
Usually have 180/120 and should be treated as a medical emergency and that’s when you should refer (when they have extremely high BP and have symptoms) could get blindness , chest pain
Arteries over time as you age stiffen more and more and so BP increases with age.

21
Q

Hypertension S&S

A

Most often asymptomatic - lots of S&S may indicate malignant hypertension.
Blurred vision
Nosebleeds
Shortness of breath
Chest P
Dizziness
Headaches - particularly in the morning
Tinnitus – ringing in ears
Nausea

Heart palpitations
Flushed skin
Pale skin

22
Q

Hypertension Investigations

A

BP reading
Normal- less than 120/80

Elevated blood pressure. The top number ranges from 120 to 139 mm Hg and the bottom number is below, not above, 89 mm Hg.

Stage 1 hypertension. 140-159/90-99
Stage 2 hypertension. 160+/100+
Hypertensive crisis- higher than 180/and/or higher than 120

23
Q

Hypertension management

A

A- ACE inhibitor
B- beta blocker
C- calcium channel blocker
D- diuretic
ARB- angiotensin receptor blockers- used in place of ACE inhibitor if Pt cant tolerate ACE (commonly due to dry cough)
Advise on lifestyle- healthy diet, stop smoking, reducing alcohol, caffeine and slt intake, regular exercise

24
Q

Abdominal Aortic Aneurysm (AAA) (S)

A

Abnormal enlargement or ballooning of the aorta, the largest artery in the abdomen.

25
Q

AAA Epidemiology

A

Inc age, most often in people age 65 and older.
Men - M:F 5:1
White
Family Hx
Smoking
Atherosclerosis
Hypertension
Connective tissue

26
Q

AAA Patho

A

Dilation of abdominal aorta, with diameter of more than 3cm
Part of aorta wall becomes weakened and large amounts of blood pass through puts pressure on weak spot, causing building outwards –> aneurysm
Causes turbulent and stagnant blood flow and thrombi that may embolise to different venous sites.

27
Q

AAA S&S

A

Mostly asymptomatic- may be discovered through screening or once ruptured
Symptoms may only present right before rupture.
Non-specific abdominal P - AAA level with L3
P may radiate to back.
Pulsatile and expansile mass in abdomen when palpated with both hands and heard as a bruit on auscultation.
Vascular claudication thats worse when exercising and partially walking uphill - relived by rest/raising legs.
May present with similar symptoms to PAD

28
Q

AAA Investigations

A

All men have screening ultrasound at 65 to detect asymptomatic AAA
Routine ultrasound considered for women over 70 with risks such as CV disease, COPD, family Hx, hypertension
Normal- less than 3cm
Medium- 4.5-5.4cm
Large- above 5.5cm (emergency)

29
Q

AAA Management

A

Treat reversible risks- smoking, healthy diet, optimise management of hypertension, diabetes
Yearly follow ups for 3-4.4cm
3 monthly for 4.5-5.4
Ruptured- mortality of 80%

30
Q

Cervical Arterial Dysfunction/Disection (CAD) (S)

A

Damage or tearing in the inner layers of the arteries in the neck, particularly the carotid or vertebral arteries. These arteries supply blood to the brain.
Carotid supplies the front, vertebral supplies the back and the spine.
Common heart disease involving atherosclerotic plaque formation in vessel lumen
Leads to impairment in blood flow and O2 delivery to myocardium

31
Q

CAD Epidemiology

A

Males
Family Hx
Obesity/seden
Smoking
High BP
Hypercholesterolemia (risk)

32
Q

CAD Patho

A

Injury/trauma to head or neck most common cause.
Causes tear in the itima, which can lead to the formation of a false lumen and hematoma or thrombosis causing atrial stenosis or occlusion. Less blood goes through the true lumen and to the brain.

Development of atherosclerotic plaques.

33
Q

CAD S&S

A

Symptoms may only present 30-70 days after injury and may present with retinal ischemia, TIA or Horner’s syndrome (partial ptosis, miosis)

Sudden/severe neck px and head px particularly behind one eye. Main presenting symptom.
Facial px
Dizziness
Blurred vision
Paresthesia
Horners syndrome may develop
- Affects involuntary functions of eyes/face
- Drooping eyelids
- Smaller pupil in one eye
Hypoglassal nerve palsy.

5Ds, 3Ns, 1A a later stage symptom.

34
Q

CAD Investigations

A

MRI
CT
Doppler Ultrasound

35
Q

CAD Management

A

Lifestyle changes- stop smoking, healthy diet, inc exercise
Mediation- Antiplatlet or anticoagulant medications
Big RF for strokes.

36
Q

Vertebral Artery Insuficiency (VBI) (S)

A

Reduced blood flow through the vertebral arteries, which are major arteries that supply blood to the brainstem, cerebellum, and other areas of the brain.

37
Q

VBI anatomy

A

Vertebral arteries are branches of subclavian arteries
Arise on each side of body, go up vertebral column into skull through foramen magnum
In skull, they join to form basilar artery at base of medulla oblongata
Basilar artery supplies arterial branches to brain stem, cerebella, and occipital lobes- control autonomic nervous system (breathing, HR), level of consciousness, coordination, balance and vision

38
Q

VBI Epidemiology

A

Older age
Men have higher risk before 75, women above 75
Family Hx
Smoking
Hypertension
Atherosclerosis
C1/C2 instability
Connective tissue disorders e.g. Marfan

39
Q

VBI Patho

A

Condition characterised by poor blood flow to back of brain
Blockage over time through atherosclerosis
Plaque made up of cholesterol, calcium, etc
Vertebrobasilar arteries supply oxygen and glucose to parts of brain responsible for consciousness, vision, coordination, balance
Restricted blood flow (ischemia) have serious consequences

40
Q

VBI S&S

A

Primary symptom is dizziness
5 Ds
3 Ns
1A
Diplopia, dizziness, drop attacks, dysarthria, dysphagia
Nausea, numbness, and nystagmus
Ataxia
May present with occipital region headaches.

41
Q

VBI Investigations

A

MRA and X-ray (using injected dye)- diagnose VBI
CT or MRI can be used to confirm a stroke has occurred

42
Q

VBI Management

A

Quit smoking
Attempt to lower cholesterol through diet, activity
Medication to control high blood pressure, lower cholesterol, block platelet function
Open surgical repair- restores blood supply to brain
Placement of catheter in artery of groin expands artery
Inc risk of TIAs, stokes
Lifestyle changes have good prog

43
Q

DVTs/PE (S)

A

Occurs when clot forms in one or more deep veins in body, usually legs

44
Q

DVTs/PE Epidemiology

A

Immobility
Recent surgery
Long haul travel
o Is suspected ask about above
Pregnancy
Hormone therapy with oestrogen- e.g., birth control

45
Q

DVTs/PE Patho

A

Associated with Virchows triad, this then causes sluggish blood flow, blood coagulability overcomes natural anticoagulant activity and causes a thrombosis to form in the deep leg veins .
Thrombus may enlarge as it propagates along the lumen of the vein.

Venous thromboembolism is a common and potentially fatal condition
Involves blood clots (thrombi) developing in circulation
Usually occurs secondary to stagnation of blood and hyper-coagulable states
When a thrombus develops in venous circulation, its called DVT
Once a thrombus has developed, it can travel (embolise) from deep veins, through right side of heart and into lungs, where it becomes lodged in pulmonary artieries
Blocks blood flow to areas of lungs and is called pulmonary embolism

46
Q

DVTs/PE S&S

A

Leg/calves swelling
Tenderness of calves
Leg P, cramping or soreness that often starts in calf
Change in skin colour on leg- red, purple
Feeling of warmth
Dilated superficial veins
Oedema

47
Q

DVTs/PE Investigations

A

Physical exam- check for swelling, tenderness or changes in skin colour
D-dimer blood test- D dimer is type of protein produced by blood clots, almost all with severe DVT have raised D dimer
Duplex ultrasound- non-invasive, creates pictures of how blood flows through veins
MRI- for DVT diagnosis in abdomen

48
Q

DVTs/PE Mangement

A

Anticoagulation- e.g., apixaban. Should be started immediately
Thrombolytics
IVCF to catch emboli before they reach the heart
Compression stockings
One third have recurrence within 10 years

49
Q

Pulmonary embolism

A

Common and potentially lethal due to its vague presenting symptoms. More frequently in pregnancy.
Usually arise from thrombi in the iliofemoral veins which is why its linked to DVT.
Small/medium: Breathlessness, pleuritic chest Px
Large: medical emergency.
Severe central chest pain, pale sweaty, tachypnoea, tachycardia, syncope. Central cyanosis, increased jugular venous pressure.