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194 Cards in this Set
- Front
- Back
What are the categories of congenital heart defects?
|
abnormalities of septation
abnormal valves or arteries abnormal connections between heart chambers and major blood vessels |
|
What shunts divert venous return in da fetalzzz circulation?
|
1. foramen ovale
2. ductus arteriosus |
|
Why does the foramen ovale close?
|
Low resistance placenta removed, peripheral vascular resistance increases
Breathing makes resistance in pulmonary circuit drop Fall in RIGHT atrial pressure, raise in LEFT atrial pressure (because increased aortic pressure makes foramen ovale close |
|
ASD/VSD/ AV septal defects are examples of what type of congenital heart disease?
|
abnormalities of septation
|
|
Truncus/hypoplastic left heart are examples of what kind of congenital heart disease?
|
abnormal valves or arteries
|
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Transposition is an example of what kind of congenital heart disease?
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abnormal connection
|
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What is the ostium secundum, and what is the foramen ovale?
|
The ostium secundum (or foramen secundum) is a foramen in the septum primum.
It should not be confused with the foramen ovale, which is a foramen in the septum secundum. |
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What is the foramen secundum?
|
Second hole in septum primum!
|
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Clinical features of fossa ovalis (ostium secundum) defects
|
normal pulmonary artery pressures until adult life, when modest increases develop
frequently exertional dyspnea and fatigue |
|
What's the function of prostaglandin E from mama?
|
Keeps ductus arteriosus open. When baby is born, lose prostaglandins
|
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What are ostium secundum/fossa ovalis defects?
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Atrial septal defect involving the foramen ovale, allows flow from right to left atrium
|
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What are ostium primum defects?
|
Atrial septal defects, involves midseptum
left to right shunting, increased pulmonary blood flow, chronic atrial fibrillation and heart block develop in later in life |
|
Where are most VSD's located?
|
membranous septum in the subaortic area
(perimembranous defects) |
|
What are muscular septal defects?
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VSD's below the membraneous septum
|
|
What are clinical features of VSD's?
|
size of defect determines defect. large defects= left to right shunting.
pulmonary artery pressure rises due to increased flow, so severe pulmonary hypertension Eisenmengr's complex exertional dyspnea and fatigue, respiratory infections, heart failure |
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A loud, holosystolic murmur best heart at the fourth interspace is assocaited with what defect?
|
VSD
|
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What determines the course of the disease of ASD's and VSD's?
|
size of defect and volume of left to right shunt
|
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What is a major clinical association with long-standing ASD's or VSD's?
Why? |
more pulmonary volume and pressure = pulmonary hypertension!
|
|
What is Eisenmenger's syndrome?
|
AV and VSD's make pulmonary pressure > systemic pressure, reversal of shunt from right to left-->cyanosis
|
|
What are clinical sxs of eisenmenger's syndrome?
|
exertional dyspnea, fatigue, respiratory
infections, congestive heart failure |
|
All 4 chambers are in communication → left-toright
shunt → pulmonary hypertension • Severe cardiac/congestive heart failure • Repeated respiratory infections, failure to thrive • Death: heart failure or pneumonia What defect? |
AV Septal Defect
|
|
Adult with exertional dyspnea, fatigue, respiratory
infections, congestive heart failure Dx? |
AVD or VSD
|
|
What is an atrioventricular septal defect?
|
one undivided common opening for the mitral and tricuspid orifices
basically a hole in the center of the heart through which all four chambers can communicate. |
|
Sx appear in infancy, severe cardiac failure, repeated resp infections, and failure to thrive, often die before age 15, median age death 2 yo
chief causes of death in infancy are heart failure and pneumonia. Dx? |
AV septal defects, all four chambers in communication
|
|
What is truncus arteriosus?
|
One great vessel leaves the base of the heart through a single semilunar valve. This single trunk supplies the coronary, pulmonary and systemic circulations.
|
|
Clinical features of truncus arterioles
|
if pulmonary arteries are hypoplastic, severe cyanosis
if pulmonary arteries are really sizable, volume overloading left heart chambers, congestive heart failure significant shunting from the aorta to the pulmonary arteries even during diastole depend on location and size of pulmonary arteries, since the magnitude of of blood flow into the lungs depends on pulmonary vascular resistance and whether truncal valve is competent or not. |
|
What left-to- right shunt lesion has significant shunting from aorta to pulmonary arteries even in diastole?
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Truncus arteriosus
|
|
What is hypoplastic left heart syndrome?
|
underdevelopment of left heart chambers, absence or stenosis of aortic and/or mitral orifices, and hypoplasia of aorta
Most severe= aortic valve atresia. aortic valve closed with fibrous membrane, fatal without surgery others: mitral valve atresia, mitral valve stenosis, hypoplasia of aortic arch |
|
Decreased systemic perfusion and shock often appear within hours
or days following birth, vascular collapse, decreased blood pressure, and heart failure inevitable. Dx? |
Hypoplastic left heart syndrome
|
|
Transposition of the Great Arteries- What is it?
|
pulmonary artery arises from the left ventricle
and the aorta (and coronary arteries) from the right ventricle The aorta is generally located in front of the pulmonary artery Normally incommunicable with life if not for patent ductus arteriosus, atrial septal defect, or ventricular septal defect |
|
Cyanosis! Cardiac failure!
Symptoms usually appear during the first weeks of life and include cyanosis (often marked), breathlessness at rest, cardiac failure, and respiratory failure. Death within 1st year. Dx? |
Transposition of the great arteries
|
|
Generic tem for thickening and inelasticity of arterial wall
|
arteriosclerosis
|
|
Form of arteriosclerosis, fibrofatty deposits produce arterial wall thickening; affects large and medium-sized arteries
|
atherosclerosis
|
|
Basic lesion of atherosclerosis, a raised intimal and subintimal local lesion containing a core of cholesterol and cholesterol esters covered by fibrous plaque
|
Atheroma
|
|
What layer of arteries does atherosclerosis begin?
|
Tunica intima (endothelial cells)
|
|
What is the principle locations you might find atheromas?
|
aorta, coronary arteries, and cerebral arteries
|
|
What is the first lesion of atherosclerosis?
|
The fatty streak
|
|
What are the three lesions of atherosclerosis?
|
1. fatty streak
2. raised lesion/atheromatous plaque 3. complicated plaquw |
|
What is a fatty streak? When is it seen? What kind of cells? What kind of lipid?
|
seen in children/teenagers
subendothelial collection of FOAM CELLS (fat-laden macrophages) lipid is cholesterol and cholesterol ester derived from LDL |
|
What's an atheroma?
structure type of lipids |
fibrous cap that overlies a lipid-rich necrotic core
inta-and extra-cellular lipids, cholesterol and cholesterol esters smooth muscle and extracellular matrix at edge of lipid core capillaries at edge of fibrous cap |
|
What type of lesion consists of a fibrous cap that overlies a necrotic core?
|
atheroma
|
|
Which type(s) of lesion(s) have smooth muscle at edge of lipid core? Why?
|
atheromas, complicated/advanced legions
smoo |
|
What type of lesion has a necrotic core + hemorrhage?
|
advanced/complicated
|
|
What are the hallmarks of advanced/complicated legions?
|
necrotic core + hemorrhage
calcium plaque rupture and thrombosis |
|
What are the components of atherosclerotic lesions?
|
Smooth muscle cells
macrophages lymphocytes connective tissue matrix (colalgen, elastin, proteoglycan) lipid (cholesterol esters, free cholesterol) |
|
When is the earliest onset of atheromas?
|
30s
|
|
Which lesion is marked by a fibrous cap overlying a localized deposit of lipids including cholesterol, and
cholesterol esters? |
atheromatous lesions
|
|
What are the preferential sites of atherosclerosis?
|
Intimal irregularities and sites of turbulent flow
|
|
What are compensatory measures for atherosclerotic obstruction of muscular arteries?
|
Increased arterial diameter
the formation of collateral vessel |
|
What causes localized vasoconstriction?
|
decreased nitric oxide and upped endothelin
|
|
Describe the difference between stable and unstable lesions
|
circumferential lesions are circumferential and lipid-poor
unstable lesions are eccentric and lipid-rich, ulcerated |
|
Where are the places where atherosclerotic lesions are most severe?
|
branch points!
carotid artery, subclavian artery, celiac artery, iliac artery, etc |
|
atherosclerosis risk factors
|
blood pressure
serum cholestrol smoking weight glucose intolerance age, sex |
|
How do we view the pathogenesis of atherosclerosis?
|
Atherosclerosis is a chronic immunoinflammatory,
fibroproliferative disease of large and medium-sized arteries. |
|
Describe the importance of CD40-CD40L interactions in atherosclerosis
|
activated platelets express CD40L (T cell surface) which triggers a cascade of inflammation (B cellzz)
activation of CD40-CD40L upregulates adhesion molecules, destabilizes lesions patients with unstable angina have mad CD40L |
|
What is the Marek virus?
|
plaques in chickens, causes paralysis and T cell lymphoma
|
|
describe role of c reactive protein in atherosclerois
|
acute phase reactant
inflammatory marker as good as cholesterol in predicting coronary events increased with hypertension, smoking inactivity and diabetes |
|
Describe early atherosclerosis
|
platelet aggregation
platelets release factors 3 and 4 (factor 3, procoagulant that activates prothrombin factor 4, procoagulant, chemotactic for monocytes) |
|
What mediates the expression of adhesion of monocytes to endothelium?
|
adhesion molecules on endothelial cells
upregulation of adhesion molecules are important in early atherogenesis! |
|
Upregulation of what molecules plays an important role in early atherogenesis?
|
Adhesion molecules!
|
|
What happens after adhesion molecules bind to endothelium in atherogenesis?
|
monocytes migrate into intima and become macrophage foam cells
|
|
Summarize the early events of atherogenesis
|
uptake of LDL by arterial wall
binding and migration of circulating monocytes into intima endothelial cell injury |
|
Late effects of endothelial injury!
|
smooth muscle cells proliferate!
fibroblasts make collagen damaged arterial wall permeable to lipids incomplete endothelial regeneration further sequesters liquid |
|
Summarize the events of atherosclerosis
|
LDL causes endothelial injury
Platelet adherence and aggregation release of PDGF smooth muscle cell proliferation, secretion of connective tissue matrix elements while cholesterol accumulates atheroma! |
|
Consequences of atherosclerosis
|
no effect
gradual occlusion leading to cerebral ischemia, myocardial ischemia, and renal ischemia sudden occlusion leading to thrombosis- myocardial infarction, cerebral infarction, embolism hemorrhage resulting from leakage or rupture of aortic aneurysm |
|
What is the QT interval?
|
ventricular contraction to ventricular repolarization
|
|
one "small box" on the graph is equiv to
|
.04 seconds
40 miliseconds |
|
normal ECG PR interval
|
one big box!
0.12- 0.20sec(onebigbox) |
|
Normal ECG measurements- QRS complex
|
.06-.1 second
(three small boxes is too long!) |
|
What are normal values for the QT interval?
|
normal values depend on heart rate!
for a given beat, QT determined by preceding RR interval As heart rate increases, the QT shortens As heart rate decreases, the QT lengthens! at resting heart rate, QT normally less than 1/2 RR interval |
|
What's the normal value for a PR interval?
|
.16 seconds
4 boxes! |
|
How do you find the end of the T wave in an ECG?
|
tangent to the steepest slope of the last limb of the T wave and the baseline
|
|
How would you measure the heart rate on an ECG strip if it is regular?
|
Measure R-R interval!
count big boxes (.2 sec) between intervals, divide into 300 |
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How would you measure the heart rate on an ECG if it is irregular?
|
Countthenumberofcomplexesin6sec(usingthe3sectimemarkersatthetopofthepage)andmultiplyby10
|
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18 : 2 ∆9, 12
|
18 carbons, 2 double bonds, located at 9 and 12
|
|
n-6 or OMEGA -6
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essential fatty acid, 6 carbons from methyl end is where double bond is located
|
|
n-7/OMEGA-7
n-6/ OMEGA-6 n-9/OMEGA-9 n-3/OMEGA-3 Which are the essential, which are the non-essential fatty acids? |
Essential fatty acids: Omega3, Omega6
Nonessential, Omega7, Omega9 |
|
Which FA are bent, and which are linear?
saturated, trans, cis |
saturated and trans FA= linear
cis FA= bent |
|
What is the function of albumin?
|
taxi cab! Carries free fatty acids only, and only a few per molecule.
Primary functions include building and transport of fatty acids, bilirubin, calcium and many other small molecules, maintenance of osmotic pressure in the blood |
|
Into what can a fatty acid be esterified?
|
phospholipid (PL)
triglyceride (TG) cholesterol ester (CE) |
|
Triglyceride structure
what are the different "flavors?" (aka different possibilities) |
3 fatty acids on a glycerol
can have saturated, monounsaturated, and polyunsaturated fatty acids! |
|
What are common dietary sources of triglycerides?
|
dairy products
oils and margarines meat and feeeeesh |
|
Where are triglycerides located in cells
Where are triglycerides located in plasma? |
cells= lipid droplets inside cells
plasma= triglycerides hang out in core inside liproproteins of plasma |
|
Structure of phospholipids
|
2 fatty acids on a glycerol phosphate backbone and a polar head group
|
|
Choline
Ethanolamine Inositol Serine are what? |
phospholipids!
|
|
Where are phospholipids located in cells? In plasma?
|
inner leaflet of membrane
in plasma, in shell of lipoproteins! |
|
What degrades phospholipids?
|
Phospholipases!
phospholipase cuts at the end of the fatty acids Phospholipase A2 is most important |
|
How can fatty acids be liberated from their phospholipids?
|
When the cell is activated by a ligand binding to a
cell surface receptor phospholipases, esp A2, cleave phospholipids and now they are free to chillax with their friends and also hurt you |
|
RELEASE OF ARACHIDONATE FROM PHOSPHOLIPIDS WITH AGONIST STIMULATION (pathway)
|
ligand binds receptor, Phospholipase A2 degrades, liberates fatty acid, fatty acid is oxygenated to become a biologic mediator, eicosanoids!
|
|
Dietary sources of cholesterol
|
dairy products
meatz certain fishezzz |
|
Where is cholesterol located in cells?
Where is cholesterol located in the plasma? |
in cells= inside membranes between lipid layerzzz
in plasma- cholesterol in shell of lipoproteins in plasma |
|
What are cholesterol esters?
|
cholesterols + fatty acids where hydroxyl group used to be, not soluble!
prominent component in plaque! |
|
Where are cholesterol esters located in cells?
In plasma? |
Cells= lipid droplets in cytoplasm
Plasma= in core of lipoproteins in plasma |
|
What's the basic concept off getting an eicosanoid from a polyunsaturated fatty acid?
|
Oxygenated Fatty Acids can have potent biological activity!
put hydroxyl groups 20 = eicosanoids 22= docosanoids 18= octadecanoids |
|
What's thromboxane?
|
An eicosanoid (arachidonate, cyclooxygenase) derivative that is involved in clumping platelets!
|
|
Why is aspirin therapy effective?
|
Aspirin reduces risk of occlusive thrombin formation by inhibiting cyclooxygenase, which makes thromboxane!
inhibits platelet formation |
|
Why is fish oil effective?
|
reduces triglyceride levels, may decrease cholesterol
|
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What are chylomicrons?
|
huge lipoproteins, carry most dietary fat (mostly triglyceride) when it first appears after a meal
|
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Where are VLDL's made?
|
liver
|
|
What's the inner composition of VLDLs?
|
about 5 triglycerides for every cholesterol ester!
|
|
What is the function of lipoprotein lipase?
|
clips fatty acids from triglycerides, releasing them from core, free fatty acids enter different cell types!
|
|
After lipoprotein lipase cleaves the fatty acids, what do muscle, adipose tissue, and liver do with them when they take them up>
|
muscle= energy
adipose tissue= triglyceride storage liver= triglyceride storage |
|
How are LDL particles made?
|
As a VLDL particle is degraded with removal of trglycerides from the core, and some proteins removed from shell, become LDL particles
|
|
What comprises the core of LDL particles? Where does it go?
|
core of product, LDL, is largely cholesterol ester, which is bad! it goes into cells and tissues
|
|
how do chylomicrons, VLDL, and LDL empty their contents?
|
chylomicrons and VLDL empty via puncture and leakage
LDL particles are ingested whole by cells, which have LDL receptors that bind Apolipoprotein B in the shell of the particle |
|
How do LDL particles get into cells?
|
LDL receptors!
|
|
When the apolipoprotein in LDL is modified, what happens?
|
it can no longer bind to LDL receptor, but it can bind to a scavenger receptor on macrophages!
|
|
How are foam cells created?
|
LDLparticlescanpenetratethrough
thebloodvesselwallandget trappedinit modificationofapolipoproteinB occurswithinthebloodvesselwall topermitentrapment ingestionofthemodifiedLDLby residentmacrophagesfollowsto createfoamcells |
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What particle attempts to clear the fat, primarily the cholesterol, from a plaque within a blood vessel? Where does it go?
|
HDL!
|
|
Equation to calculate LDL cholesterol
LDL = ? |
LDL= total cholesterol - HDL cholesterol - (triglycerides/5)
|
|
The direct measure LDL cholesterol test is more accurate and
precise than a calculated LDL - for which patients? |
Pts with elevated triglycerides
|
|
What are factors for metabolic syndrome?
|
hypertension, obesity (particularly truncal), high LDL, low HDL, dyslipidemia, insulin resistance
|
|
What is desirable and high level for total cholesterol? (mg/dL)
|
<200 mg/ DL desirable
240 mg/dL |
|
What are desirable and high levels for LDL?
|
<100 optimal
>160 high |
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What are desirable and low levels for HDL?
|
<40 bad
>50 good |
|
What are desirable and high levels for triglycerides?
|
<150 desirable
>200 high |
|
What are bruits?
|
heart sounds suggestive of turbulent flow
|
|
What is arcus?
|
white rim in periphery of iris, stigmata of dyslipidemia
|
|
What are xanthomas?
|
fat deposits under skin (joints), stigmata of dyslipidemia
|
|
What are xanthalasmas?
|
fatty depostis under eye- stigmata of dyslipidemia
|
|
How do you calculate fasting total cholesterol?
|
FTC= HDL+LDL+VLDL
|
|
How do you calculate non-HDL cholesterol?
|
Non-HDL cholesterol= total cholesterol - HDL
|
|
What are the overall treatment goals for the dyslipidemic patient?
|
1. Fix LDL first for CV risk reduction
2. Get triglycerides <500 mg/dl to prevent pancreatitis in severe hypertriglyceridemia |
|
What is the main risk of severe hypertriglyceridemia?
|
pancreatitis
|
|
What is Familial Combined Hyperlipidemia?
|
Most common genetic hyperlipidemia
High LDL, high VLDL, or both often associated with metabolic syndrome generally presents in adulthood |
|
What are HMG-CoA Reductase Inhibitors?
|
Most effective LDL lowering drug, inhibits rate limiting step in cholesterol synthesis
Lower hepatic intracellular concentration promotes increase LDL receptor expression – Increased hepatic LDL receptor expression leads to increased clearance of LDL lipoproteins and lower serum cholesterol level – Also reduce rate of VLDL synthesis Also have many ‘pleiotropic’ effects-increased nitric oxide synthesis, reduction of inflammatory macrophage cytokines, inhibition of smooth muscle proliferation – These effects likely contribute to clinical benefit, especially with stabilization of atherosclerotic plaque – However, LDL lowering is also essential for clinical risk reduction |
|
Adult with high LDL and VLDL, also metabolic syndrome, maybe low HDL, high triglycerides, might have what genetic disorder?
|
Familial Combined Hyperlipidemia
|
|
What are the effects of statins?
|
lower LDL by 25-50%
20-35% risk reduction of CHD events! |
|
What is a risk for taking statin medication?
|
myopathy
|
|
What is Familial Hypercholesterolemia?
|
Common heterozygous (1/500), rare homozygous
(1/106) disorder caused by mutations of the LDL Receptor Autosoma ldominant inheritance pattern for heterozygous state |
|
Patient with Cholesterol >300, LDL>180-250, tendon xanthomas, strong family history. Dx?
|
Familial Hypercholesterolemia!
heterozygous! |
|
Child with Chol>600, planar xanthomas,
CAD in childhood (<10 yrs of age), strong family hx. Dx? |
Familial Hypercholesterolemia!
homozygous! |
|
Colesevelam, Colestipol, and Cholestyramine are all examples of . . .
|
Gi- acting lipid agents!
|
|
What's the mechanism of action for intestinal acting agents?
|
makes bile get excreted, so you have to use more cholesterol to make the bile. WOW
|
|
Nicotinic Acid (Niacin). What does it do?
|
A B vitamin!
Reduces VLDL, raises HDL basically inhibits glycolysis, reduces LDL production |
|
What is the typical lesion of infective endocarditis?
|
vegetation!
|
|
Which valve does endocarditis strike most often?
|
Pulmonary!
second place is tricuspid third aortic fouth mitral |
|
What are the 4 cardinal manifestations of infectious endocarditis?
|
1.acute valvulitis
2. persistent bacteremia 3. immunologic mediated vascular phenomena 4. large vessel emboli |
|
Pathogenesis of Endocarditis
|
1. endothelial injury- regurgitant jets on left sided valves, IVDA/Nosocomial/PM on right sided valves
2. formation of clot- platelet/fibrin clump, aka "non-bacterial thrombotic endocarditis" 3. deposition of microorganisms |
|
What is non-bacterial thrombotic endocarditis?
|
Formation of clot- platelet "clump"
usually small, endothelial injury without the deposition of microorganisms! |
|
What is the main cause of native valve endocarditis?
|
valvular heart disease (esp mitral valve prolapse)
immunocompromsed |
|
What sort of valves tend to get infected in IV drug users? Why?
|
predisposition to infect right sided valves (tricuspid)
also, more highly virulent organisms |
|
What is the most important causative organism for infectious endocarditis?
|
80% is due to Staph or Strep!
*Gram positive Strep! Think gram positives |
|
What are the three main categories of clinical manifestations for infectious endocarditis?
|
1. local growth/destruction
2. constitutional symptoms 4. peripheral manifestations (like embolitic phenomena) |
|
Main constitutional Sx of infectious endocarditis
|
Fever
Malaise Anorexia Back Pain |
|
Fever, malaise, anorexia, back pain, frequently sick for weeks or months. heart problems?
|
Infectious endocarditis
|
|
What are Janeway lesions, and with what are they associated?
|
painless spots on palms and soles, associated with embolic complications of infectious endocarditis
|
|
What are osler's nodes, and with what are they associated?
|
Osler's Nodes are painful, red lesions on the hands and feet
associated with immunologic mediation of infectious endocarditis |
|
Are blood cultures and transesophageal echo sensitive for vegetation from infectious endocarditis?
|
Blood cultures are positive 85-90%
Transesophageal echo sensitive for vegetations 85-90% |
|
Therapy for endocarditis
|
IV antibiotics (high concentrations for protracted period (6 wks)
Surgery- for when failure to clear infection, recurrent emboli, etc |
|
Classify normal hypertension, prehypertension, stage 1 and stage 2 hypertension
|
normal <120/<80
Prehypertension 120-139/80-89 Stage I HT 140-159/90-99 Stage 2 HT >160/>100 |
|
Routine lab tests for dx-ing HT
|
ECG
urinalysis blood glucose hematocrit creatinine or GFR lipid profile w/LDL HDL, VLDL albumuin |
|
What is some organ damage associated with HT?
|
Changes in medium sized blood vessels, a/v nicking, arteries and veins cross
extracranial carotid disease peripheral vascular disease |
|
What are the major cardiovascular risk factors?
|
Hypertension
cigarette smoking obesity, especially truncal obesity physical activity dyslipidemia diabetes |
|
List some identifiable second causes of hypertension, explaining why they are pathologic
|
Sleep apnea- blood vessel wall damage, blood vessels less effective in regulating BP, also overactive sympathetic NS
Kidney problems- when glomeruli get swollen, high BP because they can't filter right (no waste and sodium out) aldosteronism- tumor in adrenal gland makes adrenal glands release too much aldosterone, which raises BP Renovascular disease- stenosis of arteries leading to kidneys, raises BP Cushing's syndrome/steroids Pheocrhomocytoma- rare tumor in adrenal gland, increases adrenaline and noradrenaline Thyroid/parathyroid disease- too much calcium! Boo! Or, too much or too little thyroid hormone! |
|
List main classes of medications used to treat hypertensions
|
• Angiotensin-converting enzyme inhibitors (ACEIs)
• Angiotensin receptor blockers (ARBs) • Beta Blockers (BBs) • Calcium Channel blockers (CCBs) • Thiazide-type diuretics |
|
List the main causes of resistant hypertension
|
Old age
Obesity |
|
Classify normal hypertension, prehypertension, stage 1 and stage 2 hypertension
|
normal <120/<80
Prehypertension 120-139/80-89 Stage I HT 140-159/90-99 Stage 2 HT >160/>100 |
|
Routine lab tests for dx-ing HT
|
ECG
urinalysis blood glucose hematocrit creatinine or GFR lipid profile w/LDL HDL, VLDL albumuin |
|
What is some organ damage associated with HT?
|
Changes in medium sized blood vessels, a/v nicking, arteries and veins cross
extracranial carotid disease peripheral vascular disease |
|
What are the major cardiovascular risk factors?
|
Hypertension
cigarette smoking obesity, especially truncal obesity physical activity dyslipidemia diabetes |
|
List some identifiable second causes of hypertension, explaining why they are pathologic
|
Sleep apnea- blood vessel wall damage, blood vessels less effective in regulating BP, also overactive sympathetic NS
Kidney problems- when glomeruli get swollen, high BP because they can't filter right (no waste and sodium out) aldosteronism- tumor in adrenal gland makes adrenal glands release too much aldosterone, which raises BP Renovascular disease- stenosis of arteries leading to kidneys, raises BP Cushing's syndrome/steroids Pheocrhomocytoma- rare tumor in adrenal gland, increases adrenaline and noradrenaline Thyroid/parathyroid disease- too much calcium! Boo! Or, too much or too little thyroid hormone! |
|
List main classes of medications used to treat hypertensions
|
• Angiotensin-converting enzyme inhibitors (ACEIs)
• Angiotensin receptor blockers (ARBs) • Beta Blockers (BBs) • Calcium Channel blockers (CCBs) • Thiazide-type diuretics |
|
List the main causes of resistant hypertension
|
Old age
Obesity |
|
What is the etiology of mitral stenosis?
|
rheumatic!
|
|
What is the etiology of mitral regurgitation?
|
mitral valve prolapse
Rheumatic! |
|
What is the etiology of aortic stenosis?
|
Congenital
Reumatic Senile Calcification |
|
What is the etiology of aortic regurgitation?
|
Rheumatic
Endocarditis |
|
What causes rheumatic fever?
|
2-3 weeks after pharyngeal infection by beta hemolytic group A strep
humoral and cell-mediated repsonses to cell membrane antigens with cross-reactivity to cardiac cells |
|
If gross pathology of the heart reveals fibrinous pericarditis, cardiomegaly, verrucuous vegetations,
and microscopic pathology reveals an Aschoff nodule, What's the dx? |
Rheumatic heart disease!
|
|
What is an aschoff nodule indicative of? (microscopic feature)
|
Most distinctive morphological feature microscopically of rheumatic heart disease
exutadive- acute inflammation, edema proliferative- aggregation of cells around an area of fibrinoid necrosive healed- scar |
|
Valve fibrosis, shortening, fusion and thickening of chordae, fusion of commissures, and McCallum's patches, valve stenosis and/or Regurgitation
likely diagnosis? |
rheumatic valve disease!
|
|
With which valve is rheumatic valve disease most often involved?
|
Mitral valve!
|
|
McCallum's patches in the heart are associated with what valvular disease?
|
rheumatic
|
|
When is mitral valve prolapse clinically significant?
|
Only in cases of regurgitation
|
|
Why do mitral valve prolapses have a sorta slimey appearance?
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"Myxomatous Degeneration"
aka, too many proteoglycans, GAGs, give mixoid appearance |
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What is myxomatous degeneration in mitral valve prolapse?
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It's not looking, so slimey, too many GAGs, not enough collagen
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What valvular disease is characterized by a systolic click and late systolic murmur?
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Mitral valve prolapse!
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What is the problem in aortic stenosis?
What does |
Pressure overload! Pventricles>>Paorta
concentric hypertrophy to compensate, replication of myocardial sarcomeres in parallel |
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What causes aortic insufficiency?
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leaflet abnormalities- congenital abnormalities, degenerative abnormalities, endocarditis
aortic root disease- Marfans, aortic disseaction, syphillis |
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What kind of hypertrophy takes place in chronic aortic regurgitation, and why?
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concentric and eccentric hypertrophy- chronic pressure AND volume state
replication of sarcomeres in parallel and in series LV gets thicker AND cavity size gets larger Volume overload is regurgitant volume during diastole, Stroke volume increased Pressure overlaod is that LV must generate more prssure to deal with more stroke volume |
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What sort of valvular heart disease results in the biggest hearts? Think cor bovinum
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Aortic regurgitation
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Shortness of breath, elevated left side filling pressures, angina decubitus (chest pain while lying down), and syncope are associated with what valvular disease?
Physical exam has an apical impulse that is displaced laterally a murmur that begins after A2, diastolic murmur! elevated systolic BP, widened pulse pressure |
chronic aortic regurgitation!
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a murmur that begins after A2, diastolic murmur!
elevated systolic BP, widened pulse Waterhammer pulse (collapsing pulse) de musset's sign (head bobbing) Quincke's sign (pulsation of blood in nail bed indicative of what valvular disease |
Chronic aortic regurgitation!
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Mitral regurgitation results in what changes in the left ventricle and why?
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volume overload! sarcomeres replicate in series, eccentric cardiac hypertrophy
every time the ventricle contracts, the blood has to go to the ventricle, a low pressure area! |
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What is the primary clinical finding of aortic regurgitation?
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shortness of breath!
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Physical exam of a patient reveals apical impulse is brisk, displaced laterally
blowing, high-pitched holosytolic murmur that's loudest at apex, radiates to axilla and infrascapular. If you reduce the preload (standing), murmur get smaller. If you increase the afterload, the murmur gets louder! shortness of breath, elevated pulmonary and venous pressures Dx? |
Mitral regurgitation!
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What is mitral stenosis?
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A roadblock between the left atrium and left ventricle!
can be from rheumatic, degenerative, or congenital |
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shortness of breath
fatigue, weakness, edema thromboembolism, endocarditis S1 is loud early and soft in advanced disease S2 has accentuated, with opening snap and diastolic rumble Dx? |
Mitral stenosis!
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Why is mitral stenosis a problem?
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In diastole, ventricle fills because mitral valve is open!
Pressure in atrium and ventricle will be equal in mitral valve stenosis, pressure in atrium develops to squirt into ventricle! |
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Shortness of breath, fatigue, and right sided heart failure are symptoms associated with which valvular disease?
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mitral stenosis!
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Patient with jugular venous distention, prominent systolic or "v" wave, RV lift, high-pitched, pansystolic murmur that increases with inspiration, pulsatile, enlarged liver, edema.
Dx? |
tricuspid regurgitation!
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What is the pathology and resulting symptoms of tricuspid stenosis?
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diastolic gradient between right atrium and right ventricle, results in systemic venous congestion
symptoms include fatigue, abdominal bloating, edema |
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Examination reveals decrescendo diastolic murmur at left sternal border
- increased with inspiration - PHT present: loud P2, right sided S3. Dx? |
pulmonary valve disease
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