Atherosclerosis Flashcards
(21 cards)
Definition
Disease of large or medium muscular arteries characterised by vascular inflammation endothelial dysfunction building upof lipids formation of plaques and leads to narrowing and hardening of vessels causes ischemia
Multifactorial disease
Causes or provoking or risk factors
Increase in low- density lipoprotein LDL
Male
Age for-men > 55 years and women >65
Smoking
Diabetes
Obesity
Sedentary lifestyle
Family history of CVD
Hypertension
Endothelial injury
Types of atherosclerosis
Coronary artery A.
Non-coronary artery A.
Extra cranial cerebrovasculardisease
Mesenteric artery A.
Cerebral vessels A.
Lower extremity occlusive disease
Mechanism of action
Presence of endothelial dysfunction
High level of glucose
Neuropathy - damage or dysfunction of nerves
High or increase level of cholesterol
Systemic infarction _ condition where multiple organs or tissues in the body are affected by restricted blood flow due to blockage in blood vessels
Pathogenesis
Endothelial dysfunction due to obesity DM hypercholesterolemia smoking genetic predisposition
Accumulation of calcium fat LDL macrophages cholesterol in intima
Macrophages take up LDL to become foam cells transform phagocytes to foam cells
Translocation of smooth muscle cells from intima to media layer production of collagen accumulation of calcium
Formation of plaque capsule
Plaques formed by atherosclerosis can be stable or unstable
Characteristics of stable plaques
Thick capsule with smooth muscle
Calcium with thick capsule has lower risk of rupture
Lipid core is small
Characteristics of unstable plaque
Thin capsule with high risk of sudden cardiac events like MI unstable angina
Big lipid core
Clinical picture of stable plaque
In coronary arteries
it’s manifested by chronic forms of ischemic heart diseases examples stable angina, acute MI, chronic coronary syndrome
Ischemic cardiomyopathy
In brain-carotid artery
Chronic hypoxia
Cognitive disorder decrease memory
In mesentrial arteries
Sign of chronic intestinal is chemical syndrome ofmaldigestion malabsorption and intestinal dyspepsia
Femoral arteries(leg)
Intermittent claudication
Renal arteries
Chronic renal failure
Clinical picture of unstable plaque
Coronary A
Acute MI and unstable angina
Brain - carotid A.
Stroke and transient ischemic attack
Mesentrial A.
Gangrene of intestine
Femoral A.
Gangrene/necrosis
Renal A.
Kidney infarction
Symptoms of atherosclerosis
Heart
Chest pain of angina
Shortness of breath
Sweating
Nausea
Dizziness
Light headedness Palpitations
Legs crampy
leg pain
Brain - dizziness confusion weakness paralysis on the size of the body
Severe numbness
Abdomen - dull or cramping pain 15 to 30 minutes after meal
Severe abdominal pain,vomiting,bloody stool and abdominal swelling
Xantelasms
•general signs
cardiovascular signs
Weight/Height ratio (BMI)
- Xantomas, xantelasmas, arcus senilis
- Gout tophi
- abdominal pain (primary hyperlipidemia)
- Hepatosplenomegalia (primary hyperlipidemia)
cardiovascular
- signs of AH
- murmurs on aorta
- Pathological sounds on vessel
Treatment targets and goals for cardiovascular
disease prevention
Smoking No exposure to tobacco in any form.
• Diet Healthy diet low in saturated fat with a focus on wholegrain
products, vegetables, fruits, and fish.
• Physical activity 3.5–7 h moderately vigorous physical activity per
week or 30–60 min most days.
• Body weight BMI 20–25 kg/m2
, and waist circumference <94 cm
(men) and <80 cm (women
Blood pressure <140/90 mmHg.
• LDL
Very-high risk in primary or secondary prevention: a therapeutic
regimen that achieves ≥50% LDL reduction from baseline and an
LDL goal of <1.4 mmol/L (<55 mg/dL).
High risk: A therapeutic regimen that achieves ≥50% LDL-C
reduction from baseline and an LDL goal of <1.8 mmol/L (<70
mg/dL).
Moderate risk: a goal of <2.6 mmol/L (<100 mg/dL).
Non-HDL
secondary goals are <2.2, 2.6, and 3.4 mmol/L (<85, 100, and 130
mg/dL) for very-high-
, high-
, and moderate-risk people, respectively.
ApolipoproteinB secondary goals are <65, 80, and 100 mg/dL for very-
high-
, high-
, and moderate-risk people, respectively.
Triglycerides - goal is <1.7 mmol/L (<150 mg/dL), this level indicates
lower risk and higher levels indicate a need to look for other risk
factors.
Diabetes HbA1c (glycated haemoglobin): <7% (<53 mmol/mol
Low risk: A goal of <3.0 mmol/L (<116 mg/dL
Drugs for treatment of
hypercholesterolaemia
Statins
Statins reduce the synthesis of cholesterol in the liver by competitively
inhibiting HMG-CoA reductase (3-hydroxy-3-methyl-glutaryl-
coenzyme A reductase) activity.
The reduction in intracellular cholesterol concentration induces an
increased expression of LDL-receptors on the surface of the
hepatocytes, which results in increased uptake of LDL from the blood
and a decreased plasma concentration of LDL and other apoB-
containing lipoproteins, including TG-rich particles.
atorvastatin, fluvastatin, lovastatin, pitavastatin,
pravastatin, rosuvastatin, simvastati
Bile acid sequestrants
Bile acids are synthesized in the liver from cholesterol and
are released into the intestinal lumen,
but most of the bile acid is returned to the liver from the terminal
ileum via active absorption.
The two older bile acid sequestrants, cholestyramine and colestipol,
are both bile acid-binding exchange resins.
By binding the bile acids, the drugs prevent the reabsorption of both
the drug and cholesterol into the blood, and thereby remove a large
portion of the bile acids from the enterohepatic circulation.
The liver, depleted of bile, synthesizes more from hepatic cholesterol,
therefore increasing the hepatic demand for cholesterol and
increasing LDL-receptor expression, which results in a decrease of
circulating L
Coronary artery
disease
CAD is a dynamic process of atherosclerotic plaque accumulation
and functional alterations of coronary circulation that can be
modified by lifestyle, pharmacological therapies, and
revascularization, which result in disease stabilization or regression.
• The clinical presentations of CAD can be categorized as either
acute coronary syndrome (ACS) or chronic coronary syndrome
(CC
Coronary artery
disease
Chronic coronary syndrome (CCS)
(i) patients with suspected CAD and ‘stable’ anginal symptoms, and/or
dyspnoea;
(ii) patients with new onset of heart failure (HF) or left ventricular (LV)
dysfunction and suspected CAD;
(iii) Asymptomatic and symptomatic patients with stabilized
symptoms <1 year after an ACS, or patients with recent
revascularization;
(iv) asymptomatic and symptomatic patients >1 year after initial
diagnosis or revascularization;
(v) patients with angina and suspected vasospastic or microvascular
disease;
(vi) asymptomatic subjects in whom CAD is detected at
screeni
Coronary artery disease
Stable coronary artery disease (SCAD)
generally
characterized by episodes of reversible myocardial
demand/supply mismatch, related to ischaemia or
hypoxia, which are usually inducible by exercise,
emotion or other stress and reproducible - but,
which may also be occurring spontaneously.
Such episodes of ischaemia/hypoxia are commonly
associated with transient chest discomfort (angina
pectoris
SCAD various clinical presentations
plaque-related obstruction of epicardial
arteries;
(ii) focal or diffuse spasm of normal or
plaque-diseased arteries;
(iii) microvascular dysfunction
(iv) left ventricular dysfunction caused by
prior acute myocardial necrosis and/or
hibernation (ischaemic
cardiomyopathy
risk factors for the
development of CAD
hypertension,
• hypercholesterolaemia,
• Diabetes,
• sedentary lifestyle,
• Obesity,
• Smoking,
• family history of CVD
initial diagnostic
management of patients with angina and suspected
obstructive CAD
he first step is to assess the symptoms and signs, to identify
patients with possible unstable angina or other forms of ACS
(step 1).
2. In patients without unstable angina or other ACS, the next step
is to evaluate the patient’s general condition and quality of life
(step 2). Comorbidities that could potentially influence
therapeutic decisions are assessed and other potential causes of
the symptoms are considered
Step 3 includes basic testing and assessment of LV function.
4. Thereafter, the clinical likelihood of obstructive CAD is estimated
(step 4) and, on this basis,
5. diagnostic testing is offered to selected patients to establish the
diagnosis of CAD (step 5).
6. Once a diagnosis of obstructive CAD has been confirmed, the
patient’s event risk will be determined (step 6) as it has a major
impact on the subsequent therapeutic decisions
Angina pectoris chest pain The duration of the discomfort is brief—no more than 10
min
The discomfort caused
by myocardial
ischaemia is usually
located in the chest,
near the sternum, but
may be felt anywhere
from the epigastrium
to the lower jaw or
teeth, between the
shoulder blades or in
either arm to the wrist
The discomfort is
often described as
pressure, tightness
or heaviness;
sometimes
strangling,
constricting or
burning. It may be
useful to directly
ask the patient for
the presence of
‘discomfort’ as
many do not feel
‘pain’ or ‘pressure’
in their ches
Traditional clinical classification
o f c h e s t p a i n
Typical a n g i n a (definite)
Meets all three of t h e following characteristics:
• substernal chest discomfort of characteristic quality and
d u r a t i o n ;
• provoked by exertion or emotional stress;
• relieved by rest and/or nitrates within minutes.
Atypical angina (probable) Non-anginal chest pain
M e e t s two o f t h e s e characteristics.
Atypical angina (probable) Non-anginal chest pain
Lacks or m e e t s only o n e or n o n e of t h e characteristics.w
