Samenvatting
Summary Circulatie en Ademhaling II
- Instelling
- Maastricht University (UM)
Collection of all cases from block 2.1 Circulation and Breathing in English.
[Meer zien]Voorbeeld 6 van de 155 pagina's
Voorbeeld 6 van de 155 pagina's
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Door: drfahood • 8 jaar geleden
Voorbeeld van de inhoud
Samenvatting ‘Circulatie en Ademhaling II’Case 1……………………………………………………………………………………………………..2
Case 2…………………………………………………………………………………………………...20
Case 3…………………………………………………………………………………………………...32
Case 4…………………………………………………………………………………………………...48
Case 5………………………………………………………………………………………………...…50
Case 6…………………………………………………………………………………………………...64
Case 7……………………………………………………………………………………………….......89
Case 8…………………………………………………………………………………………………102
Case 9…………………………………………………………………………………………………119
Case 10……………………………………………………………………………………………….120
Case 11……………………………………………………………………………………….………134
Case 12………………………………………………………………………………………….……142
Case 13……………………………………………………………………………………….………149
1
,Case 1: Chest pain
Learning goals:
1. What are the causes of chest pain?
2. What is the chest pain? What is happening in relation to the plaque formation?
know the process of plaque formation
3. Mechanism of action for the drugs simvastatin, Acetylsalicylic acid and Isosorbide
dinitrate (why sublingual?)
4. How is cholesterol metabolism? How does simvastatin affect it?
5. What are the normal values of the lab results? What happens if they increase?
6. ITM: why is there a decline in cardiovascular mortality? What differences are
there in risk factors in different areas of the world? Why?
Learning goal 1: causes of chest pain
Chest pain = angina pectoris
- Ischemia causes the pain (ischemic heart disease)
- Adenosine released when ATP degrades
- Anaerobic not enough oxygen lactate
- A1 receptor
Referred pain left arm
Causes chest pain:
- Reduced blood supply
- Increased oxygen demand cause is hypertrophy
- Atherosclerosis occulusion of the coronary arteries,
Atheromas/atheromatous/atherosclerotic plague formation
- Occurs when 70% of the coronary arteries are closed
- Calcification of the arteries
- Reduced aortic compliance
- Injury to the endothelium causes activation of platelets and formation of fibrin
vasoconstriction of the vessel
Critical situations of IHD/CAD:
- Progressive atheroma formation
- Reduction in blood flow caused by occlusion due to plague formation
- Rupture of the plague foam cell formation, thrombi formation
Risk factors that increase the chance of forming plaques:
- Raised LDL cholesterol (ApoB100)
- Reduced HDL cholesterol (ApoA1 and ApoA2)
- Hypertension
- Diabetes mellitus
- Cigarette smoking
- Obesity
2
, - Physical inactivity
- Raised CRP
- Raised coagulation factors (Factor VII and fibrinogen)
- Raised homocysteine
- Raised lipoprotein A
Learning goal 2: What is chest pain? Process of plaque formation
Robbins, chapter 12, page 546
Angina pectoris is characterized by paroxysmal and usually recurrent attacks of
substernal or precordial chest discomfort (variously described as constricting,
squeezing, choking, or knifelike) caused by transient (15 seconds to 15 minutes)
myocardial ischemia that falls short of inducing myocyte necrosis.
The three overlapping patterns of angina pectoris
1. Stable or typical angina
2. Prinzmetal variant angina
3. Unstable or crescendo angina
Types are caused by varying combination of increased myocardial demand, decreased
myocardial perfusion, and coronary arterial pathology.
- Moreover, not all ischemic events are
perceived by patients (silent ischemia).
Stable angina, the most common form, is also called
typical angina pectoris. It is caused by an imbalance
in coronary perfusion (due to chronic stenosing
coronary atherosclerosis) relative to myocardial
demand, such as that produced by physical activity,
emotional excitement, or any other cause of
increased cardiac workload. Typical angina pectoris
is usually relieved by rest (which decreases demand)
or administering nitroglycerin, a strong vasodilator
(which increases perfusion).
3
,Robbins chapter 11: Blood vessels (8 th edition)
Atherosclerosis
Atherosclerosis is characterized by intimal lesions called atheroma’s (also called
atheromatous or atherosclerotic plaques) that protrude into vessel lumens.
An atheromatous plaque consists of a raised lesion with a soft, yellow, grumous core of
lipid (mainly cholesterol and cholesterol esters) covered by a white fibrous cap.
Consequences of plaques:
- Mechanically obstructing blood flow
- They can rupture, leading to vessel thrombosis
- Plaques can also weaken the underlying media and thereby lead to aneurysm
formation
Atherosclerosis causes roughly half of all deaths in the Western world. Because coronary
artery disease is an important manifestation of the disease, epidemiologic data related
to atherosclerosis mortality typically reflect deaths caused by heart disease.
Epidemiology
Risk factors have been identified through several prospective studies in well-defined
populations (Framingham Heart Study and Atherosclerosis Risk in Communities Study).
Risk factors have a multiplicative effect: two risk factors increase the approximately
fourfold.
Constitutional risk factors in IHD (ischemic heart disease)
- Age between ages 40 and 60 the incidence of myocardial infarction increases
fivefold. Death rates from IHD rise with each decade even into advanced age.
- Gender premenopausal woman are relatively protected against
atherosclerosis and its consequences compared to age-matched men. Thus,
myocardial infarction and other complications of atherosclerosis are uncommon
in premenopausal women in the absence of risk factors such as diabetes,
hyperlipidemia, or severe hypertension. After menopause, however, the
incidence of atherosclerosis-related diseases increases and at older ages actually
exceeds that of men.
4
, - Genetics family history is the most significant independent risk factor for
atherosclerosis. Many mendelian disorders associated with atherosclerosis, such
as familial hypercholesterolemia, have been characterized. Nevertheless, these
genetic diseases account for only a small percentage of cases.
Modifiable risk factors in IHD
- Hyperlipidemia major risk factor for atherosclerosis: even in the absence of
other factors, hypercholesterolemia is sufficient to stimulate lesion development.
High LDL levels increase the risk, high HDL levels reduce the risk. HDL mobilizes
cholesterol from tissue and transports it to the liver for excretion in the bile. - -
o Statins are a class of drugs that lower circulating cholesterol levels by
inhibiting hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase, the
rate-limiting enzyme in hepatic cholesterol biosynthesis.
- Hypertension hypertension increases the risk of IHD by around 60%
- Cigarette smoking prolonged smoking of one pack of cigarettes or more daily
doubles the death rate from IHD.
- Diabetes mellitus induces hypercholesterolemia and markedly increases the
risk of atherosclerosis. Other factors begin equal, the incidence of myocardial
infarction is twice as high in diabetics as in nondiabetics. There is also an
increased risk of strokes and a 100-fold increased risk of atherosclerosis-induced
gangrene of the lower extremities.
Addition risk factors: as many as 20% of all cardiovascular events occur in the absence
of hypertension, hyperlipidemia, smoking, or diabetes. Clearly, other factors contribute
to the risk.
- Inflammation inflammation is present during all stages of atherogenesis and
is intimately linked with atherosclerotic plaque formation and rupture.
Assessment of systemic inflammation has become important in overall risk
stratification (use of C-reactive protein, CRP, as a marker).
- Hyperhomocystinemia elevated levels of homocysteine causes a higher risk of
coronary artery disease, peripheral vascular disease, stroke, and venous
thrombosis. Elevated levels can be caused by low folate and vitamin B12 intake.
- Metabolic syndrome
- Lipoprotein (a) is an altered form of LDL that contains the apolipoprotein B-
100 portion of LDL linked to apolipoprotein A. Lipoprotein (a) levels are
associated with coronary and cerebrovascular disease risk, independent of total
cholesterol or LDL levels.
- Factors affecting hemostasis thrombin, through both its procoagulant and
pro-inflammatory effects, as well as platelet-derived factors both are increasingly
recognized as major contributors to local vascular pathology.
- Other factors include lack of exercise, competitive, stressful life style, obesity
Pathogenesis of atherosclerosis
Two dominant hypotheses on the mechanism of atherosclerosis: one emphasizes intimal
cellular proliferation, while the other focuses on the repetitive formation and
organization of thrombi.
5
, Response-to-injury hypothesis
- Atherosclerosis as a chronic inflammatory and healing response of the arterial
wall to endothelial injury. Lesion progression occurs through the interaction of
modified lipoproteins, monocyte-derived macrophages, and T-lymphocytes with
the normal cellular constituents of the arterial wall.
- According to this model, atherosclerosis is produced by the following pathogenic
events:
o Endothelial injury, which causes increased vascular permeability,
leukocyte adhesion, and thrombosis
o Accumulation of lipoproteins (mainly LDL) in the vessel wall
o Monocyte adhesion to the endothelium, followed by migration into the
intima and transformation into macrophages and foam cells.
o Platelet adhesion
o Factor release from activated platelets, macrophages, and vascular wall
cells, inducing smooth muscle cell recruitment, either from the media or
from circulating precursors.
o Smooth muscle cell proliferation and ECM production
o Lipid accumulation both extracellularly and within cells (macrophages
and smooth muscle cells)
Endothelial injury
The two most important causes of endothelial dysfunction are hemodynamic
disturbances and hypercholesterolemia.
Hemodynamic disturbances
- The importance of hemodynamic turbulence is illustrated by the observation that
plaques tend to occur at ostia of exiting vessels, where there are disturbed flow
patterns.
The mechanisms by which hyperlipidemia contribute to atherogenesis include the
following:
- Chronic hyperlipidemia can directly impair endothelial cell function by
increasing local oxygen free radical production, which can injure tissues and
accelerate NO decay, reducing its vasodilator activity
6
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