Arterial disease

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Arterial disease

Cardiovascular system

Vascular disorders

Arterial disease

Angina pectoris

Stable angina

Unstable angina

Myocardial infarction

Prinzmetal angina

Coronary steal syndrome

Peripheral artery disease

Subclavian steal syndrome

Aneurysms

Aortic dissection

Vasculitis

Behcet's disease

Kawasaki disease

Hypertension

Hypertensive emergency

Renal artery stenosis

Coarctation of the aorta

Cushing syndrome

Conn syndrome

Pheochromocytoma

Polycystic kidney disease

Hypotension

Orthostatic hypotension

Abetalipoproteinemia

Familial hypercholesterolemia

Hypertriglyceridemia

Hyperlipidemia

Chronic venous insufficiency

Thrombophlebitis

Deep vein thrombosis

Lymphedema

Lymphangioma

Shock

Vascular tumors

Human herpesvirus 8 (Kaposi sarcoma)

Angiosarcomas

Congenital heart defects

Truncus arteriosus

Transposition of the great vessels

Total anomalous pulmonary venous return

Tetralogy of Fallot

Hypoplastic left heart syndrome

Patent ductus arteriosus

Ventricular septal defect

Coarctation of the aorta

Atrial septal defect

Cardiac arrhythmias

Atrial flutter

Atrial fibrillation

Premature atrial contraction

Atrioventricular nodal reentrant tachycardia (AVNRT)

Wolff-Parkinson-White syndrome

Ventricular tachycardia

Brugada syndrome

Premature ventricular contraction

Long QT syndrome and Torsade de pointes

Ventricular fibrillation

Atrioventricular block

Bundle branch block

Pulseless electrical activity

Valvular disorders

Tricuspid valve disease

Pulmonary valve disease

Mitral valve disease

Aortic valve disease

Cardiomyopathies

Dilated cardiomyopathy

Restrictive cardiomyopathy

Hypertrophic cardiomyopathy

Heart failure

Heart failure

Cor pulmonale

Cardiac infections

Endocarditis

Myocarditis

Rheumatic heart disease

Pericardial disorders

Pericarditis and pericardial effusion

Cardiac tamponade

Dressler syndrome

Cardiac tumors

Cardiac tumors

Cardiovascular system pathology review

Acyanotic congenital heart defects: Pathology review

Cyanotic congenital heart defects: Pathology review

Atherosclerosis and arteriosclerosis: Pathology review

Coronary artery disease: Pathology review

Peripheral artery disease: Pathology review

Valvular heart disease: Pathology review

Cardiomyopathies: Pathology review

Heart failure: Pathology review

Supraventricular arrhythmias: Pathology review

Ventricular arrhythmias: Pathology review

Heart blocks: Pathology review

Aortic dissections and aneurysms: Pathology review

Pericardial disease: Pathology review

Endocarditis: Pathology review

Hypertension: Pathology review

Shock: Pathology review

Vasculitis: Pathology review

Cardiac and vascular tumors: Pathology review

Dyslipidemias: Pathology review

Assessments

Arterial disease

Flashcards

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USMLE® Step 1 questions

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Flashcards

Arterial disease

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Questions

USMLE® Step 1 style questions USMLE

of complete

A 75-year-old man is brought to the emergency department due to sudden-onset confusion and headaches accompanied by nausea and vomiting. The patient has a history of poorly controlled hypertension and hyperlipidemia due to noncompliance with medications. The patient has smoked a pack of cigarettes daily for 40 years. The patient’s temperature is 37.0°C (98.6°F), pulse is 100/min, and blood pressure is 205/140 mmHg. On physical examination, the patient is dyspneic. Fundoscopic examination reveals bilateral papilledema. Laboratory results are obtained and shown below:  
 
Laboratory value  Result 
 Serum 
 Creatinine   1.9 mg/dL 
 Blood urea nitrogen  50 mg/dL 
 Urine  
 Erythrocytes  8/hpf 
 Leukocytes  2/hpf 
 Protein  3+ 
 Sediment   None 
Which of the following histologic findings would likely be seen if this patient’s renal artery was biopsied?  

External References

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Abdominal aorta p. 372

atherosclerosis in p. 308, 728

Aneurysms p. 533

atherosclerosis p. 308

Angina

atherosclerosis p. 308

Atherosclerosis p. 308

abdominal aortic aneurysms and p. 308

aortic aneurysms p. 728

diabetes mellitus and p. 352

familial dyslipidemias p. 92

homocystinuria as cause p. 83

sites of p. 728

stable angina with p. 310

transplant rejection p. 117

Carotid artery

atherosclerosis in p. 308, 728

Cholesterol

atherosclerosis p. 308

Claudication

atherosclerosis p. 308

Coronary arteries

atherosclerosis in p. 308

Coronary artery

atherosclerosis in p. 728

Diabetes mellitus p. 352-360

atherosclerosis and p. 308

Emboli

atherosclerosis p. 308

Fibrous plaque in atherosclerosis p. 308

Foam cells

in atherosclerosis p. 308

Hyperlipidemia p. 307

atherosclerosis and p. 308

Hypertension p. 306

atherosclerosis and p. 308

Infarcts

atherosclerosis p. 308

Inflammation

in atherosclerosis p. 308

Ischemia p. 208, 691

atherosclerosis p. 308

Popliteal artery p. 463

atherosclerosis in p. 308, 728

Smoking

atherosclerosis and p. 308

Smooth muscle (vascular)

atherosclerosis and p. 308

Thrombi

atherosclerosis p. 308

Transcript

Content Reviewers

Rishi Desai, MD, MPH

Contributors

Tanner Marshall, MS

Vincent Waldman, PhD

So these three words look the same: Arteriosclerosis, Atherosclerosis, and Arteriolosclerosis.

Arteriosclerosis is a general umbrella term describing diseases where the wall of the artery becomes thicker, harder, and less elastic than normal.

You can figure that out right from the name: “arterio” which is Greek for artery, and sclerosis which is Greek for “hardening”.

Now the word arteriolosclerosis is any sort of hardening of small arteries in arterioles.

This is also pretty easy to remember since the “olo” in the middle of the word indicates small arterioles.

And then finally, atherosclerosis is the hardening of any artery (even though it’s usually medium- to large-sized arteries) which is caused by the buildup of plaque.

These plaques are called atheromatous plaques and happen in the innermost wall of the blood vessel called the tunica intima or endothelium. Okay now that we’ve differentiated been all three of those words, let’s first take a look at atherosclerosis.

So the blood vessel endothelium is made up of a single layer of cells and does two jobs: First,it protects the rest of the blood vessel wall from the blood, like a coat of varnish on your wood furniture and then, secondly, it secretes proteins on its surface to prevent the blood from clotting, because blood just inherently likes to clot whenever it gets the chance.

Now, Your endothelium can become damaged in lots of different ways. Low density lipoproteins, chemicals from smoking cigarettes, and high blood pressure all wreak havoc on the endothelium because these irritants break down the endothelium.

The damaged endothelium allow low-density lipoproteins to enter the endothelial wall.

The white blood cells called monocyte follow the low-density lipoproteins and break them down through oxidation.

Okay, so you might think macrophages eating the embedded low-density lipoproteins is a good thing, but if there is a lot of low-density lipoprotein, then the macrophage will eat so much cholesterol that it can die. It basically eats itself to death.

Sources

  1. "The pathogenesis of atherosclerosis: a perspective for the 1990s" Nature (1993)
  2. "Atherosclerosis — An Inflammatory Disease" New England Journal of Medicine (1999)
  3. "Robbins Basic Pathology" Elsevier (2017)
  4. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  5. "What Are the Signs and Symptoms of Atherosclerosis? - NHLBI, NIH" NHLBI, NIH (22 June 2016)
  6. "Atherosclerosis" Harvard Health Publications Harvard Health Publications (2011)
Elsevier

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