11. Clinical I - Coronary and Peripheral Circulation (atherosclerosis) Flashcards
ATHEROSCLEROTIC PLAQUES form in which WALL LAYER of LARGE and MEDIUM SIZED ARTERIES
TUNICA INTIMA
how are SYMPTOMS of ATHEROSCLEROTIC PLAQUES
usually ASYMPTOMIC,
BENIGN lesions
Life-Threatening ISCHAEMIC (tissue dies due to lack of blood supply) DAMAGE to vital organs may only occur when what forms
when an OCCLUSIVE (blocking) THROMBUS (clot) forms ON a SPONTANEOUSLY DISRUPTIVE PLAQUE (ATHEROTHROMBOSIS)
what are the possible SITES (arteries) of ATHEROSCLEROSIS
- CORONARY ARTERIES to HEART
(myocardial ischaemia, unstable angina, myocardial infarction) - PERIPHERAL ARTERIES ie to Legs
(limb claudication) - CEREBRAL ARTERIES to BRAIN
Stroke (embolic or thrombotic) - RENAL ARTERIES to KIDNEYS
(atheroembolic renal disease, renal artery stenosis)
what different events can happen as a result of ATHEROSCLEROSIS
- NARROWING of vessel by FIBROUS PLAQUE
- Plaque ULCERATION or RUPTURE
- Intraplaque HEMORRHAGE
- Peripheral EMBOLI (clot)
- WEAKENING of vessel WALL (can lead to ANEURYSM - balooning which may rupture)
FORMATION of ATHEROSCLEROSIS starts with the FORMATION of what in young children (earliest significant lesions)
FATTY STREAKS
what do FATTY STREAKS consist of
LIPID-CONTAINING FOAM CELLS in the arterial just BENEATH the ENDOTHELOUM
over time they can evolve into atherosclerotic plaques or remain stable or even regress
how are FOAM CELLS FORMED in the process of the formation of an ATHEROSCLEROSIS
- INJURY to the ENDOTHELIUM of vessel triggers MONOCYTE ADHESION, Loosening of endothelial cell junctions and MIGRATION of MONOCYTES
- monocytes DIFFERENTIATE into MACROPHAGES
- MORE PERMEABLE ENDOTHELIUM also permits LOW-DENSITY LIPOPROTEINS (LDL) to ENTER the INTIMA of the artery
- MACROPHAGES ENGULF the LDL by PHAGOCYTOSIS
- after macrophages become LADEN with LIPID they are referred to as FOAM CELLS
when ENDOTHELIUM of a VESSEL is INJURED what is drawn to the site
MONOCYTES
which differentiate into MACROPHAGES
INJURED, MORE PERMEABLE ENDOTHELIUM of a vessel permits the ENTRY of what into the INTIMA that causes formation of FOAM CELLS (FATTY STREAKS) & ATHEROSCLEROSIS
LOW-DENSITY LIPOPROTEINS (LDL)
LOW DENSITY LIPOPROTEINS are PHAGOCYTOSED by … to FORM FOAM CELLS
MACROPHAGES
in the production of FOAM CELLS and ATHEROSCLEROSIS, what are also present in the INTIMA that are SECRETING CYTOKINES
T LYMPHOCYTES
T LYMPHOCYTES in INTIMA SECRETE CYTOKINES which cause what migration
SMOOTH MUSCLE CELLS in the TUNICA MEDIA MIGRATE INTO the INTIMA
- begin to PROLIFERATE under the influence of GROWTH FACTORS
progressive ACCUMULATION of LIPID / FOAM CELLS and SMOOTH MUSCLE CELLS in the INTIMA of artery walls / GROWING LESION begins to RAISE the ENDOTHELIUM and ENCROACH (intrude) on the LUMEN of the artery.
this lesion is known as a…
ATHEROSCLEROTIC PLAQUE
ATHEROSCLEROTIC PLAQUES evolve in 2 possible ways (2 pathways)
- how are SLOWLY GROWING PLAQUES
expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells
- STABILISE
*NOT PRONE TO RUPTURE
- the FIBRIN-CAP (thick) on top of the lesion MATURES
ATHEROSCLEROTIC PLAQUES evolve in 2 possible ways (2 pathways)
- how are RAPID GROWING PLAQUES
grow more rapidly as a result of more rapid lipid deposition
- have THIN FIBRIN CAPS that are PRONE TO RUPTURE
once a RAPID GROWING PLAQUE (with thin fibrin cap) RUPTURES what can it TRIGGER
an ACUTE THROMBOSIS (CLOT)
- by activating PLATELETS and CLOTTING CASCADE
in CORONARY ARTERIES, ATHEROSCLEROTIC NARROWING that REDUCES the LUMEN of the artery MORE THAN 75% causes what…
ANGINA PECTORIS / STABLE ANGINA
- chest pain that results when PAIN-PRODUCING SUBSTANCES ACCUMULATE in the MYOCARDIUM
typically the pain comes during EXERTION / EXERCISE
and DISAPPEARS with REST as the substances are washed out by the blood
in ANGINA PECTORIS / STABLE ANGINA, PAIN-PRODUCING SUBSTANCES ACCUMULATE where
in the MYOCARDIUM
(washed out by blood during rest)
if a PLAQUE is UNSTABLE (RAPID GROWING, THIN FIBROUS CAP) and becomes DISRUPTED what are the three possible diseases
- UNSTABLE ANGINA or SUBENDOTHELIAL MYOCARDIAL INFARCTION (thin layer of tissue just under endothelium dies)
- MYOCARDIAL INFARCTION (complete death of cardiac muscle)
how are UNSTABLE ANGINA (pain even at rest or on minimal activity / exertion) and SUBENDOTHELIAL MYOCARDIAL INFARCTION CAUSED
- a MURAL THROMBUS FORMS on TOP of a RUPTURED PLAQUE (unstable, rapid forming plaque with thin cap has ruptured)
-> where thrombus (clot) is in CONTACT with the ENDOCARDIAL LINING of a large blood vessel / artery (attached to the wall)
but in NOT OCCLUSIVE
(not completely blocking artery lumen)
causing variable OBSTRUCTION to artery
how is ACUTE TRANSMURAL MYOCARDIAL INFARCTION caused (heart attack)
- THROMBUS FORMS on TOP of a RUPTURED PLAQUE and *OCCLUDES the LUMEN
(OCCLUSIVE THROMBUS)
leading to DEATH of full thickness of CARDIAC MUSCLE supplied by that artery (no blood supply)
STABLE ANGINA is knwon as … obstruction
FIXED CORONARY OBSTRUCTION
a PLAQUE DISRUPTION may HEAL to become ….
or may get MORE DISRUPTIVE to become…
heal : SEVERE FIXED CORONARY OBSTRUCTION (chronic ischemic heart disease)
worsen: MURAL THROMBUS (unstable angina or sunendothelial myocardial infarction or sudden death)
or OCCLUSIVE THROMBUS (acute transmural myocardial infarction or sudden death)
when does PERIPHERAL ARTERIAL DISEASE (PAD) occur
/ peripheral vascular disease
when ATHEROSCLEROSIS of the ARTERIES of the LOWER LEGS causes SYMPTOMS of ISCHAEMIA and/or INFARCTION to occur
what is the MOST COMMON PRESENTING SYMPTOM of PAD
INTERMITTENT CLAUDICATION (‘only happens sometimes’ severe constricting pain)
(pain in the legs that is relieved by REST)
in PAD if the CIRCULATION of a LIMB is SEVERELY COMPROMISED what can happen to the SKIN
can ULCERATE, producing LESIONS that are SLOW to HEAL
if infected, FRANK GANGRENE of the extremities may occur
PAD is when there is ATHEROSCLEROSIS of the ARTERIES where?
LOWER LEGS
PAD is the disease that results when ATHEROSCLEROSIS of the ARTERIES of the LOWER LEGS causes SYMPTOMS of…
ISCHAEMIA (blood flow restricted)
and/or
INFARCTION (tissue death)
how are ARTERIAL ULCERS
- PUNCHED OUT with DESTRUCTION of DEEP FASCIA
- TENDON, BONES and underlying JOINTS may be EXPISED
- covered with minimal granulation tissue
- presence of ischaemic changes:
PALLOR (pale),
DRY SKIN (death of sweat glands as no blood supply),
LOSS OF HAIR (hair follicles supply),
FISSURING of NAILS (nail beds supply)
when a MURAL THROMBUS (attached to endothelium) forms on top of a RUPTURED PLAQUE what diseases may present
UNSTABLE ANGINA
or
SUBENDOTHELIAL MYOCARDIAL INFARCTION
when an OCCLUSIVE THROMBUS (blocking) forms on top of a RUPTURED PLAQUE what diseases may present
ACUTE TRANSMURAL MYOCARDIAL INFARCTION
how is the ATHEROSCLEROTIC PLAQUE in STABLE ANGINA (ruptured?) (cap?)
STABLE PLAQUE, NOT PRONE TO RUPTURE
THICK FIBRIN CAP that MATURES on top
ATHEROSCLEROTIC PLAQUE in ARTERY WALL (INTIMA) is caused by a build up of what after injury
- LIPIDS IN FOAM CELLS
(macrophages engulf low density lipoproteins that come through damaged endothelium) - SMOOTH MUSCLE CELLS
(which have migrated from MEDIA into INTIMA under influence of T cell Cytokines and Proliferate under influence of growth factors)
