31 Cardiovascular Diseases Flashcards
Describe the structure of blood vessels
Label the image
Blue = structural features
Red = Vessel type
What do the Aorta and muscular arteries have that other vessels do not?
Which vessel is involved in Blood pressure control? ?
What do the Aorta and muscular arteries have that other vessels do not? Internal Elastic Lamina
Which vessel is involved in Blood pressure control? Arterioles
Atherosclerosis
Atherosclerosis:
- Involves which vessels
- Estimated to cause approx how many deaths in the Western world
- Currently thought to represent a response to ?
Characterized by ? atherosclerotic plaques containing:
- ?
- Proliferating ? cells
- ?
- ? cells
Atherosclerosis:
- Involves medium-sized & large arteries
- Estimated to cause approx half of the deaths in the Western world
- Currently thought to represent a response to endothelial injury
Characterized by intimal atherosclerotic plaques containing:
- lipids
- proliferating smooth muscle cells
- Collagen
- Inflammatory cells
Consequences of Atherosclerosis
- Obstruction of ? -> ? injury
- Weakening of blood vessel wall -> ?
- Rupture or ulceration of the ? surface -> ? or ?
Clinical Manifestations:
- ? and ?
- ?
- ? (claudication, gangrene)
- ?
- Obstruction of lumen -> Ischemic injury
- Weakening of blood vessel wall -> aneurysm
- Rupture or ulceration of the plaque surface -> thrombosis or atheroembolism
Clinical Manifestations:
- Angina and myocardial infarction
- stroke
- peripheral vascular disease (claudication, gangrene)
- Aortic aneurysm
Ischemic Heart Disease
Ischemic Heart Disease:
- ? = imbalance between myocardial supply and demand for oxygenated blood
- In majority of cases, due to ? of ? arteries (?)
- Small number of cases due to ?, inflammation or ?
Clinical Manifestations
- ?
- ? (stable or unstable)
- Chronic ? w/ ?
- sudden ?
Ischemic Heart Disease:
- Myocardial ischemia = imbalance between myocardial supply and demand for oxygenated blood
- In majority of cases, due to obstructing atherosclerosis of coronary arteries (coronary artery disease)
- Small number of cases due to coronary artery spasm, inflammation or emboli
Clinical Manifestations
- myocardial infarction
- angina (stable or unstable)
- Chronic IHD w/ Heart Failure
- sudden Cardiac death
IHD = Ischemic heart disease
Myocardial infarction
- Decreased ? → cardiac ? dysfunction →→ ?
- Ischemic changes can be reversed if ? occurs early enough
- See ? of a zone of myocardium with ? infiltrate, followed by ? tissue, ? deposition and ? formation
- Over time, accumulated myocardial damage leads to ?
Myocardial infarction
- Decreased perfusion → cardiac myocyte dysfunction →→ myocyte necrosis
- Ischemic changes can be reversed if reperfusion occurs early enough
- See necrosis of a zone of myocardium with neutrophil infiltrate, followed by granulation tissue, collagen deposition and scar formation
- Over time, accumulated myocardial damage leads to congestive heart failure
Cardiac Hypertrophy
Cardiac Hypertrophy:
- Can be due to ? or ? overload (eg systemic ?, aortic ?)
- ??Morphology changes??
Problems:
- No corresponding increase in ?
- Hypertrophy also accompanied by ?
- Increased Cardiac Mass, contractlility etc all result in increased ?
Can compensate in short term but eventually leads to ? and ?
Cardiac Hypertrophy:
- Can be due to pressure or volume overload (eg systemic hypertension, aortic valve stenosis)
- **Cardiac myocytes INCREASE in SIZE)
Problems:
- No corresponding increase in capillary numbers
- Hypertrophy also accompanied by fibrosis
- Increased Cardiac Mass, contractlility etc all result in increased cardiac oxygen consumption
Can compensate in short term but eventually leads to Decompensation and symptomatic HF
Congestive HF
Congestive Heart Failure:
Characterized by some combination of:
- “forward failure” (decreased ? and ?) and
- backward failure (?)
Often described by which side of the heart is primarily affected which have different causes:
- Left: ? // systemic ? // ? or ? valve disease // primary ? disorders
- Right: ? heart failure // ? disease that causes ? htn
Congestive Heart Failure:
Characterized by some combination of:
- “forward failure” (decreased cardiac output and tissue perfusion) and
- backward failure (pooling of blood in venous circulation)
Often described by which side of the heart is primarily affected which have different causes:
- Left: Ischemic heart disease // systemic htn // mitral or aortic valve disease // primary myocardial disorders
- Right: Left heart failure // pulmonary disease that causes pulmonary htn
Congestive Heart FAILURE
Clinical Manifestations of Congestive HF:
- ? , cough
- ?
- ? Edema
- ? edema
- ? and ?
- ? enlargement -> atrial ?, ? formation
- ? dysfunction due to decreased perfusion
Decreased perfusion to ?
- Activation of ? -> increased volume -> exacerbate ?
- Impaired ?
Clinical Manifestations of Congestive HF:
- Dyspnea , cough
- Orthopnea
- Pulmonary Edema
- Peripheral edema
- Hepatomegaly and Splenomegaly
- Left atrial enlargement -> atrial fibrillation, Thrombus formation
- Cerebral dysfunction due to decreased perfusion
Decreased perfusion to Kidneys
- Activation of RAAS -> increased volume -> exacerbate edema
- Impaired excretion of wastes
Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing.
Dyspnea = SOB
Hepatomegaly = An enlarged liver is one that’s bigger than normal.
Splenomegaly = An enlarged spleen
Cardiac Troponin (cTn)
Cardiac Troponin (cTn)
Component of ? in cardiac myocyte
- Regulatory protein involved in ?
Complex of 3 subunits:
- Troponin found in ? and ? muscle
Troponin ? and ? have different isoforms depending on the mm origin
- ? seems to have slightly better specificity
Unlike other Cardiac Markers ? and ? almost absent from normal serum
Most ? marker of Myocardial injury we have
? levels rise a few hours following MI, peaks by 24 hours and then decreases over several days
Measured by ?
Cardiac Troponin (cTn)
Component of contractile apparatus in cardiac myocyte
- Regulatory protein involved in interaction of actin and tropomyosin
Complex of 3 subunits:
1. Troponin I (cTnI)
2. Troponin T (cTnT)
3. Troponin C (TnC)
- Troponin found in skeletal and cardiac muscle
Troponin T and I have different isoforms depending on the mm origin
- TnI seems to have slightly better specificity
Unlike other Cardiac Markers Troponin T and I almost absent from normal serum
Most specific marker of Myocardial injury we have
cTn levels rise a few hours following MI, peaks by 24 hours and then decreases over several days
Measured by immunoassays available as POC assay
How can you use cTn level to differentiate between Acute and Chronic injury?
Acute Injury = If see a rising and/or falling pattern of cTn values above 99th percentile URL
Chronic Injury = Persistently elevated cTn level
If have elevated cTn plus clinical evidence of ischemia (symptoms/ ECG changes) -> can diagnose acute myocardial infaction
If have elevated cTn plus clinical evidence of ischemia (symptoms/ ECG changes) -> can diagnose ?
If have elevated cTn plus clinical evidence of ischemia (symptoms/ ECG changes) -> can diagnose acute myocardial infaction
High sensitivity Troponin
- Newer assays have increased ? (can detect lower levels of circulating troponin than previous assays)
- Potentially allow for earlier detection of ?
- Increased ? that will need investigating
- Interest in prognostic value of ? in settings other than acute MI
- Significant interest in the value of ? assays to expedite evaluation of pts in ER
High sensitivity Troponin
- Newer assays have increased sensitivity (can detect lower levels of circulating troponin than previous assays)
- Potentially allow for earlier detection of Myocardial injury
- Increased positives that will need investigating
- Interest in prognostic value of cTn in settings other than acute MI
- Significant interest in the value of has-cTn assays to expedite evaluation of pts in ER
B-Type (Brain) Natriuretic Peptide
- peptides w/ natriuretic effects (increased urine flow) were found to be produced in human atria = ?
- Similar peptid found in rats = ?
- In humans, most ? is produced by Ventricles
- Detected by ? available as POC assay
- peptides w/ natriuretic effects (increased urine flow) were found to be produced in human atria = ANP
- Similar peptid found in rats = BNP
- In humans, most BNP is produced by Ventricles
- Detected by Immunoassay available as POC assay
Atrial natriuretic peptide
BNP
BNP:
- In humans, most BNP is produced by ?
- Secreted in response to ?
- Either ? can be measured in assays
- Detected by ? available as ? assay
Used for Ruling out ? when evaluating acute SOB in ER
Very ? but relatively ?
BNP:
- In humans, most BNP is produced by Ventricles
- Secreted in response to ventricular wall stretch
- Either fragment can be measured in assays
- Detected by Immunoassay available as POC assay
Used for Ruling out heart failure when evaluating acute SOB in ER
Very sensitive but relatively nonspecific (high negative predictive values)
