Aneurysms

Aneurysms

Interna

Interna

Pericarditis and pericardial effusion
Pericardial disease: Clinical
Myocarditis
Endocarditis
Infective endocarditis: Clinical
Rheumatic heart disease
Mitral valve disease
Aortic valve disease
Aneurysms
Aortic aneurysms and dissections: Clinical
Aortic dissection
Coarctation of the aorta
Hypertension
Hypertension: Clinical
Pulmonary embolism
Cor pulmonale
Peripheral vascular disease: Clinical
Thrombophlebitis
Deep vein thrombosis
Arterial disease
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Clinical
Myocardial infarction
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Cardiomyopathies: Clinical
Cyanotic congenital heart defects: Pathology review
Acyanotic congenital heart defects: Pathology review
Congenital heart defects: Clinical
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Heart failure: Clinical
Syncope: Clinical
Shock
Shock: Clinical
Asthma: Clinical
Chronic obstructive pulmonary disease (COPD): Clinical
Acute respiratory distress syndrome: Clinical
Pneumonia
Pneumonia: Clinical
Lung cancer
Lung cancer: Clinical
Mycobacterium tuberculosis (Tuberculosis)
Tuberculosis: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Pleural effusion
Sarcoidosis
Diffuse parenchymal lung disease: Clinical
Nephritic and nephrotic syndromes: Clinical
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
Membranoproliferative glomerulonephritis
Focal segmental glomerulosclerosis (NORD)
IgA nephropathy (NORD)
Acute kidney injury: Clinical
Chronic kidney disease: Clinical
Kidney stones: Clinical
Esophageal disorders: Clinical
Esophageal cancer
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Gastric cancer
Peptic ulcers and stomach cancer: Clinical
Inflammatory bowel disease: Clinical
Colorectal cancer
Colorectal cancer: Clinical
Colorectal polyps and cancer: Pathology review
Viral hepatitis
Viral hepatitis: Clinical
Autoimmune hepatitis
Hepatitis A and Hepatitis E virus
Hepatitis C virus
Cirrhosis
Cirrhosis: Clinical
Jaundice
Jaundice: Clinical
Gastrointestinal bleeding: Clinical
Abdominal pain: Clinical
Irritable bowel syndrome
Benign liver tumors
Hepatocellular carcinoma
Gallbladder carcinoma
Gallbladder disorders: Clinical
Primary biliary cholangitis
Biliary colic
Acute cholecystitis
Cholestatic liver disease
Chronic cholecystitis
Ascending cholangitis
Acute pancreatitis
Chronic pancreatitis
Pancreatitis: Clinical
Pancreatic cancer
Malabsorption: Clinical
Short bowel syndrome (NORD)
Pituitary adenomas and pituitary hyperfunction: Clinical
Hypopituitarism: Clinical
Thyroid storm
Hyperthyroidism: Clinical
Hypothyroidism and thyroiditis: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Cushing syndrome: Clinical
Adrenal masses and tumors: Clinical
Adrenal insufficiency: Clinical
MEN syndromes: Clinical
Testicular and scrotal conditions: Pathology review
Anemia: Clinical
Macrocytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Microcytic anemia: Pathology review
Anemia of chronic disease
Leukemia: Clinical
Myeloproliferative neoplasms: Clinical
Bleeding disorders: Clinical
Thrombocytopenia: Clinical
Thrombophilia: Clinical
Disseminated intravascular coagulation
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Lymphoma: Clinical
Plasma cell disorders: Clinical
Blood products and transfusion: Clinical
Disorders of consciousness: Clinical
Hypercholesterolemia: Clinical
Hypertriglyceridemia
Diabetes insipidus
Diabetes insipidus and SIADH: Pathology review
Diabetes mellitus
Diabetes mellitus: Clinical
Peripheral artery disease
Fever of unknown origin: Clinical
Sepsis
Myelodysplastic syndromes
Rheumatoid arthritis
Rheumatoid arthritis: Clinical
Lower back pain: Clinical
Ankylosing spondylitis
Toxidromes: Clinical
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute intermittent porphyria
Lymphedema
Hodgkin lymphoma
Non-Hodgkin lymphoma
Glucocorticoids
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Aminoglycosides
Protein synthesis inhibitors: Tetracyclines
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Penicillins
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Electrolyte disturbances: Pathology review
Hydration
Hypernatremia: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Hyperphosphatemia
Metabolic and respiratory acidosis: Clinical
Metabolic and respiratory alkalosis: Clinical
Osteoporosis
Osteomalacia and rickets
Systemic lupus erythematosus (SLE): Clinical
Vasculitis: Clinical
Scleroderma
Sjogren syndrome: Clinical
Stroke: Clinical
Restrictive lung diseases
Incidence and prevalence
Advanced cardiac life support (ACLS): Clinical

Transcript

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Content Reviewers

The word “aneurysm” comes from the Greek word aneurysma, meaning “dilation.” This makes sense because aneurysms are defined as abnormal dilations in a blood vessel. A bulge in a blood vessel is officially labelled as an aneurysm when the diameter of the bulge is approximately one and a half times larger than the normal diameter of the blood vessel.

Aneurysms can happen to any blood vessel in your body, including the aorta, the femoral artery, the iliac artery, the popliteal artery, and the cerebral arteries. They can also happen in your veins too, but those are less common as blood pressure in veins is much, much lower than in the arteries.

There are two major categories of aneurysms: true aneurysms and pseudoaneurysms. In true aneurysms, all the layers of the blood vessel wall dilate together. True aneurysms that balloon out symmetrically on all sides of the blood vessel are called fusiform aneurysms, whereas asymmetrically shaped aneurysms balloon out on one side of the blood vessel. This asymmetrical shape usually happens because for some reason one side of the blood vessel wall experiences higher blood pressure than the rest of the vessel wall, or because the wall was weaker on one side to begin with. Asymmetrical true aneurysms can be called either “saccular” or “berry” aneurysms.

Pseudoaneurysms, on the other hand, are like false aneurysms because they are not actually aneurysms at all. They are caused by a small hole in your blood vessel which allows blood to leak out of the vessel and form a pool of blood that looks like a fusiform or berry aneurysm depending on where the hole is and its size. The blood pools because the surrounding tissues act as walls that contain the blood in one spot.

Arterial aneurysms occur most commonly in the aorta with about 60% of true aortic aneurysms happening in the abdominal section of the aorta, and the other 40% happening in the thoracic section. Of all the abdominal aortic aneurysms, you can find about 95% of them just below the point where the renal arteries branch off from the abdominal aorta but above the aortic bifurcation. This is because there is naturally less elastin[a] in the walls of this section of the aorta.

Aneurysms are caused by a weakness in the blood vessel wall, so anything (really anything!), that causes the wall to weaken can cause an aneurysm. When a blood vessel wall weakens, it struggles to contain the pressure of the blood pushing against the walls so the diameter of the blood vessel lumen increases. On top of this, pressure on the blood vessel walls increases as the diameter of the lumen also increases, thanks to LaPlace’s law. This makes the aneurysm diameter even bigger, creating a cycle of continuous bulging. You’ve likely experienced this when you blow up a balloon. The first breath into the balloon is tough, but the next several breaths are pretty easy. This positive feedback loop is why aneurysms usually get bigger over time.

So what underlying conditions might weaken the wall of blood vessels? Well one way is if all the layers of those blood vessel walls don’t receive oxygen. Typically, the cells of the vessel walls are able to get oxygen from blood as it flows by. However, in the first section of the aorta, where the walls are super thick and muscular in order to handle all that blood pressure coming from the heart, the cells need to have their own set of blood vessels that supply the tunica media and the tunica externa. We call these special blood vessels vasa vasorum.

In hypertension, the vasa vasorum can develop hyaline arteriolosclerosis, narrowing their lumen, and causing ischemia. This leads to atrophy of the smooth muscle of the tunica media, and overall all, weakening in the aortic wall.

The same thing can happen in blood vessels without vasa vasorum if we have a bunch of plaque building up on the tunica intima thanks to our friendly neighbourhood atherosclerosis. Oxygen just can’t penetrate all the vessel’s walls. You see this type of aneurysm often in the abdominal aorta, where blood pressure is high and the aorta walls are nourished by passing blood. If you think about this it’s no wonder, then, why both aneurysms and atherosclerosis share similar risk factors: usually people who are male, who are over the age of 60, who have hypertension, and who smoke.

If we look at tertiary syphilis, it affects the vasa vasorum as syphilis causes inflammation in the tunica intima of the vasa vasorum (which again are those blood vessels that deliver oxygen to the thick walls of larger blood vessels). This ultimately leads to a narrower lumen and restricts blood supply to the vessel walls of the thoracic aorta, causing atrophy. By the way, the name for this vasa vasorum inflammation is endarteritis obliterans. If you were to look at the vasa vasorum in tertiary syphilis, you’d see the inflammation causes fibrosis and scarring on the walls creating this cool to look at, but less cool to have, tree-bark like texture.

Other bacterial infections can also cause aneurysms, which we label as mycotic aneurysms. The bacteria from an infection somewhere else in the body can break off from the main infection and travel around in the blood. Usually these embolic bacteria will get stuck in the intracranial arteries, visceral arteries, or the arteries feeding the arms and legs. There, the bacteria enter and weaken the blood vessel walls leading to, you guessed it, an aneurysm. Some of the bacteria that commonly cause mycotic aneurysms are, and these can be tricky to pronounce so bare with me, Bacteroides fragilis, Pseudomonas aeruginosa, and anything in the Salmonella species. You’ll also see mycotic aneurysms are a complication of infective endocarditis. However, infection leading to aneurysm is not limited to just bacteria. Infection from the fungi Aspergillus, Candida, and Mucor are also a common cause of mycotic aneurysms.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Aneurysms in Vascular Access: State of the Art and Future Developments" The Journal of Vascular Access (2017)
  5. "Open and Endovascular Management of Aortic Aneurysms" Circulation Research (2019)
  6. "Abdominal aortic aneurysms" Current Opinion in Cardiology (1994)