WEEK 7 Flashcards
Beta blocker receptors
BETA 1 RECEPTORS
- Receptive in the heart - SA, AV nodes and myocardial cells
- Kidneys - reduce secretion of Renin
- BisoprOLOL
- AtenOLOL
- PropanOLOL
BETA 2 RECEPTORS
- Smooth muscle - eg airways
- Skeletal muscle - reduces tremor
- Propanolol
Describe common symptoms of acute limb ischaemia (the 6 P’s)
(ALSO PRESENT IN CLTI)
- Pain
- Pallor
- Pulseless
- Perishingly cold
(LATE SIGNS)
- Paraesthesia (Pins and needles)
- Paralysis
Outline the surgical management of symptomatic carotid stenosis
CAROTID ENDARTERECTOMY (CEA)
Understand the difference in pathophysiology and risk factors between acute limb ischaemia and critical limb threatening ischaemia
ACUTE LIMB ISCHAEMIA
PATHOPHYSIOLOGY
- Sudden blockage to blood flow in a normal artery
- Ischaemia
- Cell death (necrosis)
RISK FACTORS
- Atrial Fibrillation
- thrombophilias
- Obesity
- Cancer
- If thrombotic, risks as for atherosclerosis
CRITICAL LIMB THREATENING ISCHAEMIA
PATHOPHYSIOLOGY
- Progressive atherosclerosis causes severe narrowing or complete occlusion in arteries
- Without gravity, supply cannot match demand even at rest
- Anaerobic metabolites released = pain
- Patients keep leg(s) hanging down
- causes oedema
- skin breakdown/ulceration which doesnt heal
RISK FACTORS
- Smoking
- Hypertension
- Diabetes
- Hypercholesterolaemia
Outline options for management of critical limb threatening ischaemia and investigations
MANAGMENT
OPERATIVE
- Conservative / Palliative
- Endovascular intervention
- Open surgery
- HYBRID PROCEDURE
= endovascular intervention and open surgery
DRUGS
- Antiplatelet, statin
- Analgesia
- DVT prophylaxis
- +/- Antibiotics
INVESTIGATIONS
- TEST FROM PATIENT
- Full blood count (FBC)
- Urea and electrolytes (U&Es)
- Coagulation
- G&S (incase blood transfusion required
- ECG
- CT ANGIOGRAM
Know the components of atheromatous plaques
- Early atherommatous plaque
- Lipid-laden macrophages
- Young adult onwards
- Fully developed atheromatous plaque
- Central lipid core with fibrous tissue cap, covered by arterial endothelium
- Collagens in cap provide strength
- Inflammatory cells (macrophages, T-lymphocytes, mast cells) reside in fibrous cap
- Central core lipid rich in cellular lipids/debris derived from macrophages
- Form at arterial branching points/bifurcations (tubulent flow)
- Central lipid core with fibrous tissue cap, covered by arterial endothelium
Describe the process of atherogenesis and understand how atheromatous plaques form
PATHOGENESIS OF ATHEROSCLEROSIS
- Endothelial injury and dysfunction
- Accumulation of lipoproteins (LDL) in vessel wall
- Monocyte adhesion to endothelium → migration into intima and transformation to foamy macrophages
- Platelet adhesion
- Factor release from activated platelets, macrophages → smooth muscle cell recruitment
- Smooth muscle cell proliferation, extracellular matrix production and T-cell recruitment
- Lipid accumulation (extracellular and in foamy macrophages)
DEVELOPMENT OF ADVANCED PLAQUE FORMATION
- Large numbers macrophages, T-lymphocytes
- Lipid-laden macrophages die through apoptosis → lipid into lipid core
- Response to injury = chronic inflammatory process: 1. inflammatory reaction 2. process of tissue repair
- Growth factors (PDGF) → proliferation intimal smooth muscle cells, subsequent synthesis collagen, elastin, mucopolysaccharide
- Fibrous cap encloses lipid rich core
- Growth factors secreted by platelets, injured endothelium, macrophages and smooth muscle cells
STEP 1 - Injury to endothelial lining of artery
STEP 2 - Chronic inflmmatory and healing response of vascular wall to agent causing injury
Chronic/episodic exposure of arterial wall to these processes causes formation of atheromatous plaque
Describe the consequences of ischaemia.
- TIA
- Cerebral infarction
- Abdominal aortic aneurysm
- Peripheral vascular disease
- Coronary artery disease –> MI –> cardiac failure
Know the reparative process involved in myocardial infarction. (6)
- Cell death
- Acute inflammation
- Macrophage phagocytosis of dead cells
- Granulation tissue
- Collagen deposition (fibrosis)
- Scar formation
Understand the difference between subendocardial and transmural infarction of the myocardium and the clinical significance of the two type of infarct.
Histological features are the same!!!!!
TRANSMURAL INFARCTION:
Ischaemic necrosis affects full thickness of the myocardium
SUBENDOCARDIAL INFARCTION:
Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
Know the aetiology of hypertension.
- major genes (single genes abnormalities )
- poly genes (multiple genes involved).
- There are >30 genes recognized
- Increased reactivity of resistance vessels and resultant increase in peripheral resistance
- Hereditary defect of the smooth muscle lining of arterioles
- A sodium homeostatic effect
- In hypertensive individuals, the kidneys are unable to excrete appropriate amounts of sodium for any given BP (Pressure naturesis). As a result sodium and fluid are retained and the BP increases
List the factors causing embolism.
- Cardiac failure
- Sever trauma/burns
- Post-op/post-partum
- Oral contraceptive
- Increased age
- Bed rest/immobilisation
- Obesity
- PMH of DVT
Know the clinical presentation of stable angina.
- Chest pain on left side
- Radiating pain down left shoulder and arm
- Tar staining on fingers
- Obesity
- Hypertension
- Abdominal aortic aneurysm
- Absent or reduced peripheral pulse
Describe the pathophysiology of stable angina.
Mismatch between supply of O2 and metabolites to myocardium and the myocardial demand for them.
By far most commonly due to: a reduction in coronary artery blood flow to the myocardium, caused by:
- Obstructive coronary atheroma (Very common)
- Spasm of a portion of coronary artery (Uncommon)
- Abnormal coronary flow (Uncommon).
Uncommonly due to reduced O2 transport:
Anaemia of any cause.
Uncommonly due to pathologically increased myocardial O2 demand:
- Left ventricular hypertrophy caused by years of persistent hypertension, significant aortic stenosis or hypertrophic cardiomyopathy.
- Thyrotoxicosis.
Most common cause of angina is coronary atheroma.
When there is increased myocardial oxygen demand the increase of coronary blood flow is obstructed and this leads to myocardial ischaemia and then angina symptoms.
Myocardial oxygen demand increases in situations where HR and BP rise for example: exercise, anxiety/emotional stress and after a large meal.
Discuss relevant investigations of stable angina.
- BLOODS
Full blood count, lipid profile and fasting glucose; Electrolytes, liver & thyroid tests would be routine. - CXR
- ELECTROCARDIOGRAM
- Normal in over 50% of cases.
- May be evidence of prior myocardial infarction i.e. pathological Q-waves.
- May be evidence of left ventricular hypertrophy i.e. high voltages, lateral ST-segment depression or “strain pattern”. - EXERCISE TOLERANCE TEST/ETT
- Often can confirm diagnosis of angina. - MYOCARDIAL PERFUSION IMAGING
- Superior to ETT in detection of CAD, localisation of ischaemia and assessing size of area affected.
- Expensive, involves radioactivity; depending on availability used where ETT not possible/equivocal.
- Either exercise or pharmacological stress: adenosine, dipyridamole or dobutamine. - CT (coronary angiography)
- INVASIVE ANGIOGRAPHY IF:
- Early or strongly positive ETT (suggests multi-vessel ds).
- Angina refractory to medical therapy.
- Diagnosis not clear after non-invasive tests.
- Young cardiac patients due to work/life effects.
- Occupation or lifestyle with risk e.g. drivers etc.
