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161 Cards in this Set
- Front
- Back
What is Down syndrome and what CHDs are related to it?
|
Trisomy 21
ASD |
|
What is Turner syndrome and what CHDs are related to it?
|
45, XO
left-sided obstruction |
|
What is Williams syndrome and what CHDs are related to it?
|
deletion of chromosome 7
supravalvular AS |
|
What is DiGeorge syndrome and what CHDs are related to it?
|
microdeletion in chromosome 22
outflow tract abnormalities |
|
What is Holt Oram syndrome and what CHDs are related to it?
|
Autosomal dominant disorder
ASD, VSD |
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What is Noonan syndrome and what CHDs are related to it?
|
Gene PTPN 11
PS |
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What 4 conditions are needed for pathogenesis of IE?
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1. Endocardial surface injury
2. Thrombus formation @ site of injury 3. Bacterial entry into circulation 4. Bacterial adherence to injured endocardial surface |
|
What are the 3 factors that determine the ability of an organism to cause IE?
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1. Access to bloodstream
2. Survival of organism in circulation 3. Adherence of organism to endocardium |
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What type of IE is found in previously normal valves?
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Acute IE
|
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What type of IE is found in previously abnormal valves?
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Subacute IE
|
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S. viridians typically causes what type of IE?
|
Subacute
|
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S. aureus typically causes what type of IE?
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Acute IE
|
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What lab abnormalities may be seen in IE?
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elevated WBCs w/leftward shift
Elevated ESR, CRP Can have elevated rheumatoid factor |
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What is the best way to visualize IE vegetations?
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TEE
|
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How is the entry of glucose into glycolysis regulated?
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PFK-1
PFK-1 is inhibited by ATP & activated by AMP. F2,6P2 is needed for PFK-1 fxn-->increased by insulin, glucose, & increased work |
|
What is the significance of PFK-2 in cardiac metabolism?
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PFK-2 is activated by NE & epinephrine-->increased glycolysis via increased F2,6P2 to affect PFK-1
|
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What is the main source of energy for the adult heart?
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Oxidative phosphorylation of FAs
|
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What prevents FAO in the liver?
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Malonyl CoA inhibits CPTI in liver which inhibits import of new FAs into mitochondria for FAO
|
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What is the difference between the creatine phosphate shuttle & the adenylate kinase shuttle?
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Adenylate kinase shuttle decreases local ADP by exchanging 2 ATP for 1 ADP each cycle.
|
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What is the change in substrate utilization in the heart in diabetes?
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Increased FAO
|
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What is the change in substrate utilization in the heart in fasting?
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Increased FAO
|
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What is the change in substrate utilization in the heart in hypoxia?
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Increased glycolysis/carb utilization
|
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What is the change in substrate utilization in the heart in heart failure?
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Increased glycolysis/carb utilization
|
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What is the change in substrate utilization in the heart in exercise?
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Increased glycolysis/carb utilization
|
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How does metformin work?
|
Insulin sensitizer which causes increased glycolysis to improve heart function.
|
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How does trimetazidine work?
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Anti-ischemic metabolic agent that works by inhibiting FAO
This causes increased glucose use in the heart HF treatment |
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How does GLP-1 work?
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Treats HF.
This is a insulin mimetic that can increase glucose metabolism |
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What is responsible for activation of LPL?
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ApoCII
|
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What are the 4 stages of cholesterol synthesis?
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1. Synthesis of mevalonate from acetyl CoA
2. conversion of mevalonic acid to activated isoprene (IPP & DPP) 3. condensation of 6 5-carbon isoprenes to 30C-squalene 4. conversion of 30C-squalene to 4-ring cholesterol (27C) |
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What enzyme converts cholesterol to cholesteryl ester?
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ACAT
|
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What is the rate-limiting step of bile acid synthesis?
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cholesterol 7-alpha hydroxylase
|
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What is the structure of FAS?
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7 enzymatic activities
Dimeric enzyme w/cysteinyl sulfhydryl group which touches the acyl carrier protein on the other half |
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What is activated in adipose tissue in fasted states?
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Low insulin/high glucagon increases cAMP concentration which activates protein kinase A (PKA)
PKA activates hormone-sensitive lipase by phosphorylation |
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What is the function of SR-B1?
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HDL receptor on liver cells
|
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What changes in lipids are seen in insulin resistance?
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Increased release of FAs from cells
Increased TGs, ApoB, VLDL Apo-A1 affects kidney once detached from HDL LDL gets too many TGs & becomes small dense LDL (depleted of TGs)-->BAD |
|
What can't the body make arachidonic acid?
|
Human desaturase cannot place double bond between C10 & omegaC-->canot make linolenic acid (an arachidonic acid precursor)
Must EAT omega3 & omega6 FAs |
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How does phospholipase A2 function in eicosanoid production?
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Phospholipase A2 & phospholipase C cleave bodns in phosphatidylinositol which produces prostacyclin
|
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Where is COX-1 found?
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GI
|
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Where is COX-2 found?
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Inflammation
Increases prostaglandins |
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What are the functions of aspirin?
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Irreversible COX-1 & COX-2 inhibition
Irreversible inhibition of platelet synthesis of TXA2 Blocks PGI2 synthesis in endothelial cells |
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What does ibuprogen & acetaminophen do?
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Reversible inhibition of COX1 & COX2
|
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What do vioxx & celebrex do?
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Inhibition of COX2
|
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What is adiponectin?
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Normal product of endothelium
Insulin-sensitizing Anti-atherogenic Anti-inflammatory |
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What is MCP-1?
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Monocyte chemoattractant protein expressed in response to modified lipoproteins
Causes diapedesis & inward migration of monocytes & macrophages |
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What produces the enzymes responsible for weakening of the fibrous cap?
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Collegenases from SMCs
|
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What is the significance of CD40L?
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Stimulated by platelets
Cuases adhesion molecules & MMPs |
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What side effect can P450s cause and what medication is it related to ?
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Myositis when using HMGCoA reductase inhibitors
|
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What is supplied by the LAD?
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IV septum
Apex Anterior & anterolateral LV |
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What is supplied by the left circumflex artery?
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Lateral LV wall
Posterior LV wall SA node (55%) |
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What is supplied by the RCA?
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RV
Inferior LV AV node SA node (45%) Inferior IV septum Posterior LV wall |
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What are the 3 major determinants of myocardial oxygen consumption?
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1. Myocardial wall stress: Stress=PR/h
2. HR (chronotropy) 3. Contractility (inotropy) |
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What is the primary determinant of CBF?
|
Myocardial O2 tension (pO2)
Increased adenosine=primary vasodilatory mediator (metabolic factor d/t break down of ADP and AMP) |
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What are the major coronary vasodilators?
|
NO
Prostacyclin EDHF |
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What are the major coronary vasoconstrictors?
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Endothelin-1
|
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What is related to coronary vascular reserve?
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Reactive hyperemia
Maximal CBF vs. % luminal stenosis |
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Obstructive arterial disease affects which vessels primarily?
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Large vessels
|
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What are some causes of small vessel obstruction?
|
Arteritis (collagen disease)
DM |
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What physical exam findings may be found in myocardial ischemia?
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S4
Apical impulse changes Systolic murmurs Bruits Xanthomas |
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What can sestamibi show?
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Perfusion defects during exercise stress test
|
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What are indications for coronary angiography?
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Pain refractory to treatment
Post-MI ischemia Markedly + treadmill test ACS Px undergoing valvular surgery Post-op eval. of graft & LV fxn |
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What are the major modifiable risk factors for CAD?
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Elevated lipids
Diabetes HTN Cigarette smoking Low HDL |
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What are the goals of angina treatment?
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Decreased MVO2
Increased CBF |
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Why might ACEi's be prescribed post-MI?
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Prevent LV remodeling-->decreased LVH
|
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What differentiates UA from NTSEMI?
|
cTnI & cTnT elevations or CK-MB
Same ECG readings |
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What is included in medical treatment of UA or NSTEMI?
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Statins
ASA Beta blockade Nitrates Clopidogrel Heparin IIb/IIIa platelet receptor agonists |
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What is included in calculating the TIMI risk score?
|
Age>65
History of CAD Use of ASA in last 7d At least 3 CAD risk factors ST segment changes 2 or more episodes of angina in last day Elevated cardiac enzymes |
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What does the development of Q wave represent?
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Death of myocardium
|
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What leads correspond to lateral heart?
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I, aVL
|
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What leads correspond to inferior heart?
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II, III, aVF
|
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What leads correspond to anteroseptal?
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V1, V2
|
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What leads correspond to anterolateral?
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V5, V6
|
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When does a Q wave develop?
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Hours after infarct
|
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What is classified by ECG as "old infarct"?
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Q waves w/ST segment elevation
|
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What is the treatment for ventricular tachycardia post-MI?
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Stable: beta blockers, IV lidocaine, IV amiodarone
Unstable: DC cardioversion, meds |
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What is treatment for ventricular fibrillation?
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Defib, ACLS, IV lidocaine, IV amiodarone
|
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When does LV aneurysm appear post-MI?
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weeks-months
|
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What does a persistent ST elevation in area of an MI indicate following an AMI?
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LV aneurysm
|
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When are vtach or PVCs considered BAD prognostic factors?
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Persistence after 72 hours
|
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What supplies the anterolateral papillary muscle?
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LAD and either RCA or LCX
|
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What supplies the posteromedial papillary muscle?
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RCA
|
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Which papillary muscle is more vulnerable to ischemia, infarction and/or rupture?
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Posteromedial PM
|
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What are risk factors for LV free wall rupture?
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Women
More likely in 1st MI Age>60 HTN Steroid use |
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When do most cardiac tissue ruptures occur?
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4-5 days post MI
|
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What is treatment for pericarditis?
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Indomethacin
High dose ASA Rarely, steroids |
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What is considered HTN?
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Diabetics>130/80
Nondiabetics>140/90 |
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A wide pulse pressure may indicate what?
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Systolic hypertension of the elderly
PP=SBP-DBP |
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What causes systolic HTN of the elderly?
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decreased compliance of aorta d/t calcification
|
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What 2 big signs may indicate systolic HTN of the elderly?
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1. Wide PP
2. Increased aortic PWV |
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What is the treatment for systolic HTN of the elderly?
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thiazide diuretics + vasodilators
|
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What indicates HTN d/t increased sympathetic outflow?
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Relative tachycardia (HR 86-90)
Young hypertensives |
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What is the treatment for increased sympathetic outflow causing HTN?
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Beta blcokers
Mixed alpha/beta blockers (carvedilol) |
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What might be indicated by increased PRA?
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PRA=plasma renin activity
Increased PRA w/o renal a. stenosis causing HTN |
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What is the treatment for HTN d/t increased PRA w/o renal a. stenosis?
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Lethal form of HTN
ACEis, ARBs, renin inhibitors |
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What is specific therapy for HTN in setting of CHF?
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Thiazide diuretics
ACEi/ARB Aldosterone antagonist Beta blocker |
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What is specific therapy for HTN in setting of post-MI?
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Thiazide diuretics
ACEi Aldosterone antagonist Beta blocker |
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What is specific therapy for HTN in setting of CAD?
|
Thiazide diuretics
ACEi Ca channel blocker Beta blocker |
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What is specific therapy for HTN in setting of DM?
|
Thiazide diuretics
ACEi/ARB Beta blocker |
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What is specific therapy for HTN in setting of a previous stroke?
|
Thiazide diuretics
ACEi |
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What is specific therapy for HTN in setting of renal dysfunction?
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Loop-type diuretic
ACEi/ARB |
|
What medication is most associated with LVH regression?
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ACEi
|
|
What are the criteria for metabolic syndrome?
|
Abdominal obesity (35-40inches)
TGs>150 HDL<40-50 BP>130/85 Fasting glucose>110 |
|
What is normal ABI?
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0.9-1.3
|
|
What does an ABI>1.3 indicate?
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Calcified vessels
|
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What is the gold standard for peripheral arterial disease diagnosis?
|
Invasive contrast arteriogram
|
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What are signs of anterior circulation obstruction?
|
Paralysis
Sensory deprivation |
|
What causes anterior circulation obstruction?
|
Carotid artery arterial disease
|
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What are signs of posterior circulation obstruction?
|
Dizziness
Syncope Nausea Diplopia |
|
What causes posterior circulation obstruction?
|
Vertebrobasilar arteries
|
|
What population commonly has subclavian artery artherosclerotic stenosis?
|
Smokers
|
|
What pattern of PAD is found in smokers?
|
proximal, large artery disease (aorta, iliac)
|
|
What pattern of PAD is found in diabetics?
|
distal, small vessel disease (below knee, tibial vessels)
|
|
What is cilostazol?
|
phosphodiesterase inhibitor w/vasodilatory effects used to treat claudication found in PAD
|
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What is pentoxyfylline?
|
increases RBC flexibility, used to treat claudication found in PAD
|
|
What pattern of claudication indicates aortoiliac disease?
|
Hip, buttock, thigh, calf claudication
|
|
What pattern of claudication indicates femoral artery disease?
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Thigh, calf claudication
|
|
What pattern of claudication indicates popliteal artery disease?
|
Calf, ankle, foot claudication
|
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What pattern of claudication indicates tibial artery disease?
|
Calf, ankle, foot claudication
|
|
Where are most atherosclerotic aneurysms?
|
Abdominal aorta
|
|
Where are most syphilitic aneurysms?
|
Thoracic aorta
|
|
What pathology is seen in atherosclerotic aneurysms?
|
medial atrophy
|
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Ischemic medial necrosis is seen in what type of aneurysm?
|
Syphilitic
|
|
Obliterative endarteritis is seen in what type of aneurysm?
|
Syphilitic
|
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Where is the intimal tear usually located which causes a dissecting aortic aneurysm?
|
Ascending aorta
Usually a split between the mid & outer 1/3 of the media |
|
What can cause a dissecting aortic aneurysm?
|
HTN or syphilis
|
|
What pathology is seen in a dissecting aortic aneurysm related to syphilis?
|
Medial degeneration
|
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What pathology is seen in a dissecting aortic aneurysm related to hypertension?
|
Normal media
|
|
What vasculitides affect large vessels?
|
Temporal arteritis
Takayasu arteritis |
|
What age group usually gets temporal arteritis?
|
Older than 50
F>M |
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What age group usually gets Takayasu arteritis?
|
Younger than 40
F>>M |
|
What symptoms accompany temporal arteritis?
|
Headache
Visual disturbances Fever Weight loss Swelling over temporal artery |
|
What symptoms accompany Takayasu arteritis?
|
Visual disturbances
Weak arm pulses d/t subclavian involvement Neurologic manifestations HTN |
|
What is the pathology of temporal arteritis?
|
Granulomatous inflammation
Intimal proliferation Segmental distribution Giant cells |
|
What is the pathology of Takayasu arteritis?
|
Intimal fibrosis
Granulomatous inflammation |
|
What arteries are involves in Takayasu arteritis?
|
Aortic arch & branches
|
|
What demographic does polyarteritis nodosa affect?
|
Young adults
|
|
What symptoms may be associated with polyarteritis nodosa?
|
HTN
Abdominal pain Renal failure GI hemorrhage Myalgias, neuritis, fever, weight loss, infarcts |
|
Hepatitis B is related to what condition?
|
Polyarteritis nodosa
|
|
What organs are affected by polyarteritis nodosa?
|
Kidney>liver>heart>GI
|
|
What pathology is seen in polyarteritis nodosa?
|
Fibrinoid necrosis w/PMN infiltration
Fibrosis-->intimal thickening Thrombosis & aneurysms may occur Segmental distribution |
|
What is the pathology of allergic granulomatosis?
|
Similar to polyarteritis nodosa.
Fibrinoid necrosis w/PMN infiltration Fibrosis-->intimal thickening Thrombosis & aneurysms may occur Segmental distribution Infiltration by eosinophils |
|
What organs are involved in allergic granulomatosis?
|
Lung, heart, spleen, peripheral nn., skin
|
|
What is the other name of Kawasaki disease?
|
Mucocutaneous lymph node syndrome
|
|
What causes Kawasaki disease?
|
?T cell response to infection
|
|
What demographic is affected by Kawasaki disease?
|
infants & children
|
|
What are symptoms of Kawasaki disease?
|
Oral mucosa erythema
skin rash lymphadenopathy of palms & soles Occurs in outbreaks |
|
What is important pathology of Kawasaki disease?
|
Coronary vasculitis may appear
|
|
What is the etiology of microscopic polyangiitis?
|
reaction to an antigen
|
|
What are clinical manifestations of microscopic polyangiitis?
|
skin rash
H-S purpura cryoglobulinemia malignancy |
|
What is the pathology of microscopic polyangiitis?
|
Fibrinoid necrosis
Karyorrhexis (breaking apart of nuclei) of PMNs |
|
What vasculitides involve small vessels?
|
Microscopic polyangiitis
Wegener granulomatosis Thromboangiitis obliterans |
|
What are clinical manifestations of Wegeners granulomatosis?
|
sinusitis, glomerulonephritis, renal failure, pneumonitis
|
|
What is the pathology of Wegeners granulomatosis?
|
Necrotizing granulomas
Vasculitis w/fibrinoid necrosis |
|
What demographic commonly gets thromboangiitis obliterans?
|
Young smoking males
|
|
What are symptoms of thromboangiitis obliterans?
|
Claudication of extremities
Gangrene Ischemic ulcers |
|
What is the pathology of thromboangiitis obliterans?
|
Vasculitis w/thrombosis
PMN collections in thrombi |
|
What disease are associated with pANCA?
|
allergic granulomatosis
Microscopic polyangiitis |
|
What diseases are associated with cANCA?
|
Wegener's granulomatosis
|
|
What are reversible early ultrastructural changes found in MIs?
|
glycogen depletion
cell swelling mitochondrial swelling disruption & clumping of nuclear chromatin |
|
What are irreversible early ultrastructural changes found in MIs?
|
disruption of sarcolemma
amorphous mitochondrial densities |
|
Is vacuolar degeneration reversible?
|
Can be reversible or irreversible
|
|
Is contraction band necrosis reversible?
|
NO.
Related to high [Ca] |