Flashcards in Topics B8-12. Cardio 3: Hypertensive Vascular and Heart Disease, Pericardial disease, Atherosclerosis2, Aneurysms and Dissections Deck (35):
At what point is blood pressure considered hypertensive? At what point is it "malignant?"
Of all hypertension, how many have idiopathic causes and how many are "secondary hypertension" where the cause is known?
HTN is BP > 140/90 mmHg. Malignant if systolic > 200 and diastolic > 120 mmHg
Idiopathic (we don't know a specific cause, combination of many factors) accounts for 90-95% of cases. This is called "essential hypertension"
Remainder is "secondary hypertension" - usually due to renal disease, renal artery narrowing, or adrenal disorders
What are two examples of rare genetic defects that can lead to hypertension?
1. Defects of aldosterone metabolism: increased aldosterone
2. Mutations of proteins that affect sodium resorption, causing increased resorption and/or increased sensitivity to aldosterone
4 Mechanisms of Essential Hypertension:
1. Reduced renal sodium excretion: very common. Increases fluid volume, elevating blood pressure, which causes excretion of more sodium - but this isn't balanced, it's at a higher steady state than would be healthy
2. Vasoconstriction / Structural Change in Vessel Walls
3. Genetic factors: some small angiotensin-related polymorphisms
4. Environmental Factors: stress, obesity, smoking, physical inactivity, caffeine, high-salt diet
3 Major Consequences of Hypertension / Causes of morbidity and mortality
1. Apoplexia: vessels usually need to be "preconditioned" with damage to have a stroke as a result of hypertension. Charcot-Bouchard Aneurysm or Hyalinic Arteriosclerosis associated with HTN
2. Cardiac Failure: overworked left ventricle, left ventricular hypertrophy, CIHD
3. Kidney Failure: Untreated hypertension can cause "renal fixation of the kidney" - where it permanently produces more renin. Best lab test for hypertension is proteinuria - tells if kidneys are functioning.
What are two morphological changes in small blood vessels that occur as a result of hypertension?
How do they relate to kidney failure that results from hypertension?
1. Hyaline arteriosclerosis: typical of "slowly progressive" hypertension. Homogenous, pink hyaline thickening of arteriolar walls, loss of structural detail, and luminal narrowing. Occurs many plaes but particularly important in the kidney, as "nephrosclerosis"
2. Hyperplastic arteriosclerosis: more in severe, "malignant" hypertension (sys > 200, dia > 120mmHg). Vessels have "onionskin" concentric laminated thickening of arteriolar walls, luminal narrowing. In kidney you see necrotizing arteriolitis with fibrinoid deposits and vessel wall necrosis
What is the Goldblatt kidney experiment?
Dr. Goldblatt put a ring around just one renal artery of a dog, and the loss of pressure caused the dog to respond to become hypertensive. When he removed the ring, the dog continued to be hypertensive - it underwent "renal fixation of the kidney."
The experiment went further and attempted to remove the kidney on the affected side. This did not fix the hypertension. On other dogs, he tried it again with the contralateral (unaffected) kidney. By removing the contralateral kidney, he could fix the hypertension that he had induced.
What are 3 "indirect effects" of hypertension?
(categorization is kind of weird, but that's how Matolcsy put it. Very similar to the other question about major causes or morbidity/mortality, but these are maybe more slowly progressing problems.. basically it's problems that haven't been mentioned yet)
2. Aortic Dissection
3. Subarachnoid Bleeding
There are many other ones
What is the normal heart weight? And in cardiac hypertrophy, how much would it weigh?
Normal left ventricular wall thickness? What about in LVH?
Normal right ventricular wall thickness?
Heart normally weighs about 300-350 grams. In hypertrophy it often weighs > 500g.
Normal left ventricle: 10-14 mm. Hypertrophy > 20 mm.
Normal right ventricle: 3-5 mm
What is the difference between concentric and eccentric left-sided hypertrophy of the heart?
Concentric: more common. Left ventricle hyptrophies so that the wall is thicker, but the chamber remains the same size (key difference). Occurs from hypertension [relation to this topic], aortic stenosis, aortic coartication (pressure overload)
Eccentric: hypertrophy but the chamber is dilated. Results in volume overload. Occurs from mitral and aortic insufficiency (volume overload)
Why might left-sided concentric hypertrophy be mistaken for eccentric hypertrophy in autopsy?
This would be the "left-sided concenctric hypertrophy with terminal dilation" - the heart was concentrically hypertrophized, but as it was failing it started to use the Frank-Starling forces and began to dilate.
So when you see this dilation, you have to check for other causes - if it was eccentric, then you would see mitral or aortic insufficiency. If it was concentric, you would see some form of stenosis or hypertension.
What is the clinical progression of hypertension-induced left-sided concentric hypertrophy?
Many patients asymptomatic
The poor ejection may cause regurgitation into the left atrium, causing it to dilate. This is a major risk for atrial fibrillation (and the major risk of A-fib is embolism to the brain)
Eventually heart grows to point where it can no longer compensate for the increased burden. This leads to degenerative changes in the myocardial fibers, including fragmentation and loss of myofibrillar contractile elements. Net result of changes are ventricular dilation and cardiac failure.
The other effects of hypertenion may cause atherosclerosis, stroke, or progressive renal failure. Atherosclerosis may contribute to ischemic heart disease, along with the hypertrophy.
What is cor pulmonale? (Robbins definition)
What would make it acute vs chronic?
Right ventricular hypertrophy and/or dilation (often with right heart failure) that are caused by pulmonary hypertension. The pulmonary hypertension is due to disorders of the lung or lung vasculature
Can be acute (rapid onset due to pulmonary embolism, shows only dilation) or chronic (long-standing disease of lung, shows hypertrophy, will also be dilated if the heart fails)
Some examples of specific causes of pulmonary hypertension that lead to cor pulmonale:
(5 are listed from Matolcsy lecture, shouldn't be that hard to think of some examples.. there are many others)
1. Emphysema (COPD): Alveoli dilate to become huge bullas, need higher force to push blood through lungs
2. Pneumoconiosis: Coal Miner's Lung, inhalation of harmful minerals
3. Pulmonary embolism: blocks flow, increases resistance
4. Vasculitis: pulmonary vessels inflamed, compressing them
5. Chest deformity: scoliosis can compress the lung
A person with significant cor pulmonale chronicum will probably have what effect in the liver too?
Also, what will they likely be a macroscopically visible change in their pulmonary vessels?
Nutmeg liver: backwards buildup in hepatic pressure causes congestion in hepatic venules and damage that makes it appear spotted, like cut nutmeg
Pulmonary atherosclerosis also visible due to the pro-atherosclerotic effect of hypertension
What are some examples of causes primary versus secondary pericarditis?
Which is more common?
Primary: Normally viral infections, but can be other microbe infections too.
Secondary: part of some other problem. May occur after MI, uremia is most common cause (urea in blood), SLE, rheumatic fever, metastatic malignancies
Primary pericarditis is very rare; normally pericarditis is not an isolated problem
What are the 2 possible clinical outcomes of pericarditis, if it does not resolve with no problem?
1. Immediate problem of effusion that leads to pericardial tamponade
2. Progresses to chronic fibrotic pericardium. If severe, may result in “constrictive pericarditis” where the heart cannot fully expand during diastole
Acute pericarditis can have different microscopic and macroscopic morphology based on the cause. How would it be described if it's:
-Viral or uremia cause:
-Malignant tumor cause:
(hopefully this is not important, but otherwise it's a very short and easy topic)
-Viral or uremia cause: "bread and butter pericarditis" - shaggy irregular appearance with fibrinous exudate
-Bacterial cause: fibropurulent exudate (and caseation if it's TB)
-Malignant tumor cause: shaggy fibrinous exudate + bloody effusion
What are 2 possible clinical symptoms and signs of pericarditis?
1. Atypical chest pain, not related to exertion and you can rule out STEMI
2. If constrictive or cardiac tamponade has formed, may cause jugular vein distension due to backflow from right side of heart not being able to fill up. Could also have faint heart sounds, weak pulses, etc.
How much serous fluid is normally in the pericardial cavity?
In the case of effusion, how much fluid can be tolerated?
Normally 30-50 mL of serous fluid.
A slow accumulation can allow for a large amount of fluid to be tolerated, up to 1L.
But a rapid effusion, such as after trauma or myocardial rupture, can be lethal with just 250 mL.
There are 3 types of fluid that can accumulate in the pericardium, what are they and what are some examples of how they might accumulate there?
1. Serous fluid: may result from hypoalbuminemia edema or congestive heart failure
2. Blood: blunt chest trauma, malignancy, ruptured MI, aortic dissection
3. Lymph: from blockage in mediastinal lymph nodes
Note: topic B11 is atherosclerosis, which is also topic A7. For that reason, just going to put a few more cards in here that could have been in that section too
What is the process by which hyperlipidemia makes intimal plaques?
(there's a lot of important stuff packed into the answer, not just bullet points)
With chronic hyperlipidemia, LDL accumulates in the intima, where they are oxidized by free radicals. Macrophages then use scavenger receptors to detect and phagocytose the LDL and making it into a foam cell.
The foam cell then secretes cytokines and chemokines which attract more monocytes and are toxic for endothelial cells. Combination of foam cells and platelet precipitation with PDGF release induces smooth muscle proliferation, collagen and other ECM deposition. Have significant extracellular lipids as plaque forms. Also, the cholesterol in them forms crystals which, along with necrotic cell debris, are strongly pro-thrombotic
What are the 3 categories of risk factors of the Framingham study?
1. Major Constitutional Factors: Age, Sex, Genetics
2. Major Modifiable Factors: hyperlipidemia, hypertension, smoking, diabetes mellitus
3. Additional risk factors: inflammation, obesity, low physical activity, stressful life, type A personality
What are 4 major clinical consequences of atherosclerosis?
1. Myocardial infarction
2. Cerebral infarction (stroke)
3. Aortic Aneurysm
4. Peripheral vascular disease: causes gangrene in extremities
What are 6 changes to an atherosclerotic plaque that make it "complicated" versus primary?
1. Aneurysm: plaque causes pressure atrophy on vessel wall
2. Thrombus formation: via Ulceration, Erosion, or Rupture
3. Bleeding: bleeding into plaque can cause hematoma and rupture. Bleeding can also occur from vaso vasorum
5. Stenosis: (related to calcification)
6. Cholesterol Embolism
What is an aneurysm?
What is a "true" vs "false" aneurysm?
What is an arterial dissection?
Aneurysm: congenital or acquired dilations of blood vessels or the heart
True: all 3 layers (intima, media, adventia) are affected
False: Just one or two layers, usually have a hematoma that communicates with the intravascular space. May have "pulsating hematoma"
Dissection: after a tear in the intima, a channel of blood forms in the tunica media.
What are 3 morphologies of true aneurysms?
1. Saccular: just pushes off to one side. Often have a contained thrombus.
2. Berry: small berry-shaped protrusion sticks out.. it's a type of saccular
3. Fusiform: both sides are equally pushed out
(definitely look up a picture if you haven't seen these)
What are the 3 examples of specific aneurysm diseases mentioned in lecture?
1. Abdominal Aortic Aneurysm (AAA): caused by atherosclerotis with arterial wall thinning. Typically between renal arteries and aortic bifurcation.
2. Syphilitic Aneurysm: thoracic aorta is distended and dilated. Granulomatosus reaction compresses vaso vasorum, causes ischemia of the wall, allows the aorta to have huge dilation.
3. Berry aneurysm: usually in cerebral arteries at their branches. Rupture causes subarachnoid bleeding. Need to clip it or artificially stimulate a thrombus in there that will close it off without harm.
What are 4 consequences or complications of Abdominal Aortic Aneurysm?
1. Rupture, fatal bleeding into peritoneal spaces (the most severe consequence). AAAs greater than 5cm are more likely to burst.
2. Strong association with mural thrombosis (which is also related to atherosclerosis)
3. Ischemia: mostly of the lower extremities
4. Diagnostic problems: hard to tell if it's a tumor or some other mass
What are 2 types of diseases that increase the risk for Berry Aneurysms?
1. Genetic predisposition: collagen weakness diseases like Marfans.
2. Hypertension: berry aneurysms normally appear in people with hypertension who are 40-50 years old. People with polycystic kidney disease tend to have severe hypertension and so can also form berry aneurysms.
Which 2 populations are most prone to aortic dissections?
1. Men between 40-60 years old with history of hypertension
2. Younger people with connective tissue disorders like Marfans. Collagen is needed in the aortic wall to maintain its integrity.
What are 4 possible consequences of aortic dissection?
1. False channel: a second, distal rupture in the intima forms and so blood can re-enter the circulation ("double-barrel aorta")
2. Compressing of branching arteries: often compresses mesenteric or renal arteries, causing ischemia and necrosis
3. Expands to the heart: disrupts the valves or fills the pericardial sac, causing tamponade
4. Rupture: major cause of death, massive bleeding into thorax or abdomen
What is the classic clinical symptom of aortic dissection?
Sudden onset of excruciating tearing or stabbing pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downwards as the dissection progresses. Also have respiratory distress.
May be confused with MI. Many are incorrectly diagnosed.
What are the two types of classification for aortic dissection based on their location?
(another one that you should see a picture of if you haven't before)
DeBakey: the O.G. of aortic dissections
I: Ascending and Descending aorta
II: Ascending aorta only
III: Descending aorta only
Stanford: trying to simplify it, but just makes us have to learn more crap
A: Ascending aorta, and may or may not involve descending aorta (DeBakey I or II). Very high mortality rate, up to 70%.
B: Descending aorta (DeBakey III). Significantly less dangerous than type A.