00:00 / 00:00
Bundle branch block
Pulseless electrical activity
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Rheumatic heart disease
Atrial septal defect
Coarctation of the aorta
Patent ductus arteriosus
Ventricular septal defect
Hypoplastic left heart syndrome
Tetralogy of Fallot
Total anomalous pulmonary venous return
Transposition of the great vessels
Pericarditis and pericardial effusion
Aortic valve disease
Mitral valve disease
Pulmonary valve disease
Tricuspid valve disease
Coronary steal syndrome
Polycystic kidney disease
Renal artery stenosis
Peripheral artery disease
Subclavian steal syndrome
Superior mesenteric artery syndrome
Human herpesvirus 8 (Kaposi sarcoma)
Chronic venous insufficiency
Deep vein thrombosis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
0 / 6 complete
Dysbetalipoproteinemia (Type III Familial Dyslipidemia)
Familial Hypercholesterolemia (Type IIa Familial Dyslipidemia)
Hyperchylomicronemia (Type I Familial Dyslipidemia)
Hypertriglyceridemia (Type IV Familial Dyslipidemia)
Jamie is a 24-year-old male presenting to the emergency department complaining of sudden onset chest pain and shortness of breath when playing soccer.
On further evaluation, his ECG showed ST-segment elevation and laboratory evaluation showed elevated troponin I levels.
After instituting treatment, Jamie and his family inquire about the odd early onset of his disease.
The physical examination of the skin showed numerous xanthomas.
A lipid panel is ordered and shows marked elevation of LDL.
Jamie had a myocardial infarction which was caused by an underlying lipid disorder.
Lipid disorders include both hyper and hypolipidemia.
Hyperlipidemia can manifest as a high level of cholesterol, a high level of triglycerides, or a combination of both.
Hypolipidemia is the opposite where there’s a low level of these lipids.
So let’s do a quick overview of the physiology of lipid metabolism.
After eating a fatty meal, cholesterol and fatty acids enter the intestinal cells.
The fatty acids are assembled into triglycerides, and then they, along with a small amount of cholesterol, are packaged together with lipoproteins to form chylomicrons.
Chylomicrons move into the lymphatic vessels and eventually end up getting emptied into the left and right subclavian veins where they enter into the blood.
Now an enzyme in capillaries called lipoprotein lipase breaks down the chylomicrons to free the triglycerides, and then it also breaks the triglycerides down into fatty acids.
These can be taken up by nearby tissues to generate energy, like in the muscle cells, or for storage, like in adipocytes.
The remains of the chylomicrons will contain lipoproteins and a small amount of triglyceride and cholesterol, so these chylomicron remnants head to the liver to deposit the leftover lipid molecules.
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