Bms 6633 Cardio & Resp Test 1 Harder Stuff

Front 1

Non-SA node pacemaking

Back 1

Negative deflection of P wave in leads 1/2

Front 2

Left Ventricular hypertrophy

Back 2

chronic hypertension, aortic stenosis

causes increased voltage (more myocyte mass)

criteria: S wave V1 + largest R wave in V5 or V6 must be greater than 35mm

or R wave more than 11mm in aVL

Front 3

Right ventricular

Back 3

resultant from pulmonary hypertension or tricuspid stenosis

Axis shift (negative I, positive II, positive aVF)

Positive R wave in v1/2, reduced waves in V5/6

Front 4

Ischemic ECG changes

Back 4

Sloping or horizontal T wave depression (most specific)

Symmetric T wave inversion (less specific). Best seen in V2/3, deeper and more symmetric = worse.

HOWEVER if these changes are found with elevated cardio markers then non-ST elevation MI.

Front 5

Funky T wave normalities

Back 5

normally flat in V1 and aVL, negative in aVR

Front 6

Myocardial Infarction ECG changes

Back 6

ST segment elevation

Pathological Q waves

Front 7

Right coronary Artery

Left Anterior descending

Circumflex

Back 7

inferior and posterior wall of L ventricle, right ventricle

interventricular septum, anterior wall of L ventricle

Lateral wall of L ventricle

Front 8

V4R lead

Back 8

Used to see right ventricle, good to do if possible inferior MI because R coronary artery supplies R ventricle and inferior of L ventricle

Front 9

Lipoprotein Major factors

Back 9

Triglycerides = primarily VLDL (also chylomicrons)

Cholesterol = LDL

HDL = mostly protein, some cholesterol

Front 10

Basic lipoprotein physiology

Back 10

intestinal cells create chylomicrons to transport FA in blood, lipoprotein liipase cleaves them in adipose and muscle tissue capillaries allowing absorption of FA. Chylmicron remants taken up by liver.

Liver creates VLDL, also cleaved by lipoprotein lipase (skeletal and adipose) and converted to IDL, which are either taken up again by liver or cleaved again by lipoprotein lipase to LDL. LDL are either used by extrahepatic cells (such as gonadal cells) or taken up by liver

Chylomicrons and IDL aren't measured. Chylomicrons gone after 3-6 hours from digestion, IDL have very short half-life. Lipoprotein levels measured at fasting state.

Front 11

Fasting Plasma Lipid Profile

Back 11

Shows lipid concentrations

Total cholesterol, Triglycerides, HDL-C (cholesterol in HDL)

Front 12

LDL calculated

Back 12

Most triglycerides are in VLDL, but they have 1/5th their weight in cholesterol. So VLDL-C = TG/5

Total cholesterol = HDL-C + LDL-C + VLDL-C

LDL-C = TC - (HDL-C + (TG/5))

Only works if TG levels are less than 400, otherwise pathology causing chylomicron accumulation

Front 13

LDL-C ranges

Back 13

< 70 = optimal for high risk
< 100 = optimal
130-159 = borderline

LDL = driving force of atherosclerosis

Front 14

Triglyceride ranges

Back 14

<100 optimal
<150 normal

>= 500 very high

Very high means risk of acute pancreatitis, chylomicrons always in serum, large and when entering capillaries of pancreas can block, create ischemia leading to release of lipases to digest chylomicrons. FA released causing inflammatory cascade resulting in acute pancreatitis

Front 15

Clinical ASCVD (atherosclerotic cardiovascular disease)

Back 15

acute coronary syndromes, history of MI, stable or unstable angina, coronary revascularization, stroke, transient ischemic attack, peripheral arterial disease (from atherosclerosis)

Front 16

Statins MOA

Back 16

inhibit HMG CoA reductase, lowering mevalonate, reducing cholesterol synthesis.

Hepatocyte senses deficiency, SCAP is transported to golgi and cleaved, SREBP resulting from that cleavage. SREBP enters nucleus binding to promoter region to create more HMG-CoA reductase and more LDL receptors, REDUCING LDL IN THE BLOODSTREAM

Front 17

High intensity statins

Moderate - Low intensity statins

Which is only renal excretion?

Back 17

Atorvastatin, Rosuvastatin

Simvastatin, pravastatin, lovastatin, fluvastatin

pravastatin = only no hepatic excreted drug

Front 18

Statin effects

Back 18

Large reduction in LDL-C

moderate reduction in triglycerides

small increase in HDL-C

increased plaque stability, decreased osteoporosis

Front 19

Statin Adverse reactions

Back 19

hepatotoxicity, dose dependent

Rhabdo-myotoxicity. Myalgia, myopathy, rhabdomyolysis. Check for creatine phosphokinase levels to monitor myopathy, pain in calf muscles.

Rhabdomyolysis can cause myoglobinemia and myoglobinuria, acute renal failure

Front 20

Gemfibrozil and statins

Back 20

don't prescribe together, gemfibrozil prevents bile clearance of statins, additive myotoxicity

Front 21

MOA Niacin (nicotinic acid)

Back 21

Decreases APOA-1 clearance from serum (for HDL-C)

Binds to niacin receptors, decreasing hormone sensitive lipase, decreasing hydrolysis of triglycerides into bloodstream, liver then synthesizes less VLDL since it is broken down more slowly. Less VLDL also means less LDL.

Niacin = broad spectrum anti-lipidemia, moderate increase in HDL-C, moderate decreases in TG and LDL-C

Front 22

Niacin SE

Back 22

Niacin flush, red appearance. Prescribe with aspirin 30 minutes prior. COX inhibitor prevents prostaglandin, cyclin, and thromboxin formation preventing inflammation.

Hepatotoxicity, myotoxicity, hyperuricemia

Watch creatine phosphokinase levels if prescribed with statins. Contraindicated with gout (hyperuricemia) and liver disease.

Front 23

MOA Fibrates

Back 23

PPAR-a receptor agonist (receptor normally activated by triglycerides, increases expression of lipoprotein lipase). Accelerates clearance of chylomicrons, VLDL, IDL from circulation

Small increase in HDL-C, large decrease in TG, small decrease in LDL-C

Fenofibrate, gemfibrozil, clofibrate

Front 24

Fibrate SE

Back 24

Also myotoxic effect, monitor creatine phosphokinase

Don't combine Gemfibrozil with statins

Increase biliary cholesterol excretion, super saturates bile, increases risk of gall stones

Front 25

Bile acid sequestrants (bile acid binding resins) MOA

Back 25

form insoluble complexes with bile acids, preventing reabsorption. Tiny increase in HDL-C, large decrease in LDL-C

Cholestyramine, colestipol

Front 26

Bile acid sequestrant SE

Back 26

GI distress, constipation, bloating, flatulence

High dosages can prevent fat soluble vitamin absorption

Front 27

Cholesterol absorption inhibitors MoA

Back 27

NPC1L1 transporter of cholesterol on brush borders in enterocytes of small intestine. Drug blocks protein selectively, no absorption of biliary or dietary cholesterol.

ezetimibe

Can cause diarrhea

Front 28

Hyperlipidemia drug uses

Back 28

Statins: for LDL
Niacin: broad spectrum
Fibrates: for triglycerides
Bile acid sequestrants: for LDL
Ezetimibe: for LDL

Front 29

Mean arterial pressure MAP

Back 29

MAP = DP + 1/3 (SP-DP)
or

MAP = Cardiac output X systemic vascular resistance
CO = HR x Stroke volume
SV = inotropy x preload

MAP = HR (Inotropy x preload) x SVR

only tweak SVR (afterload), HR, or preload

Front 30

Upper limit of MAP autoregulation

Back 30

when surpassed, arterioles dilate, precapillary sphincter opens

Result = hyperperfusion, and edema

Front 31

Hypertensive crisis (malignant hypertension)

Back 31

220/140, papilledema must be present

generally want to decrease 10% in minutes

then another 10% over hours

Need to consider volume depletion, give with saline eventually

Front 32

Drug induced hypertensive crisis from cocaine

Back 32

cocaine: serotonin, norepinephrine, dopamine reuptake inhibitor (triple reuptake inhibitor), also sodium channel blocker (ester, one i)

Triple reuptake inhibitor causes an effect on Alpha1 receptors, resulting in vasoconstriction.

Good treatment = phentolamine

Avoid beta-blockers here, can push catecholamines into alpha receptors causing further vasoconstriction

Front 33

Other drug induced hypertensive crisis

Back 33

beta-blockers withdrawal (-olol)

alpha-2-agonists (clonidine) withdrawal

or alcohol withdrawal

Front 34

Iatrogenic causes of hypertensive crysis

Back 34

Chronic benzodiazepine (-zepam, -zolam) use treated with flumazenil IV or naloxone (dilute both highly IV)

Front 35

Pheochromocytoma

Back 35

neuroendocrine tumor in adrenal glands, secretes high levels of catecholamines (4/1 norepinephrine/epinephrine)

treat with phentolamine

Front 36

Drug of choice for hypertensive emergency

Back 36

Nitroprusside

immediate action, short half-life. Causes relaxation of smooth muscle. Can be titrated for specific blood pressure, dial a pressure. Used with an IV infusion pump and arterial line

Front 37

Nitroprusside MOA

Back 37

Breaks down in circulation, releasing NO, activating guanylate cyclase in vascular smooth muscle, increasing production of cGMP, stimulates calcium movement into ER. Prevents calcium from binding calmodulin. Relaxes vessels

Can cause cyanide toxicity

Front 38

Cyanide poisoning

Back 38

Higher risk with hepatic or renal impairment, mixed venous saturation, metabolic acidosis, syncope, abnormal breathing. Caused due to inactivation of cytochrome oxidase

HYDROXOCOBALAMIN = antidote, works intracellularly and extracellularly by binding cyanide and is excreted

Nitrites + sodium thiosulfate: nitrites oxidize some hemoglobin to methemoglobin, cyanide binds methemoglobin. Sodium thiosulfate converters cyanmethemoglobin to thiocyanate, sulfite, hemoglobin and is excreted in urine.

Methemoglobin can also be treated with methylene blue

Front 39

Nitroglycerin

Back 39

Can also be used. Slightly slower than nitroprusside. Nice because gives some coronary perfusion

Front 40

Fenoldopam

Back 40

DA1 (dopamine) receptor agonist

ROSA, vasodilation

Front 41

Magnesium sulfate

Back 41

cheap, vasodilator, reduces heart rate, few side effects

Front 42

Phentolamine

Back 42

reversible, nonselective alpha-adrenergic antagonist causing vasodilation.

Helps treat phaeochromocytoma controlling hypertensive emergency. Also good for cocaine hypertensive emergency.

Front 43

Phenoxybenzamine

Back 43

nonselective alpha-adrenergic antagonist, causing vasodilation

Front 44

Esmolol

Back 44

only beta blocker (-olol) used during hypertensive emergency because it is an ester, short half-life. Long acting beta-blockers can affect inotropy which you don't want.

Front 45

Enalapril

Back 45

ACE inhibitor (-pril), too slow acting for emergency

do not give with bilateral renal artery stenosis (angiotensin II constricts efferent arterioles preventing GFR from falling into renal failure)

Front 46

Heart rate effectors

Back 46

Beta-blocker (-olol) (b1 receptor) = only meaningful if hypertension due to increased heart rate

alpha2 agonist (-idine) = reduce heart rate

Both decrease renin secretion (good for control)

Front 47

Beta blockers

Back 47

-olol. Reduce heart rate, treat tachyarrhythmias and angina. Hyperthyroidism.

fat soluble (propranolol) treats anxiety and tremor.

don't use with obstructive pulmonary diseases (asthma, no bronchodilation from b2)

cause increase glucose and lipid levels, hallucinations (propranolol), sexual dysfunction

Front 48

Central alpha2 agonists

Back 48

decreases sympathetic activity, vasodilation

clonidine like drugs,

-idine

Front 49

Methyldopa

Back 49

converted to alpha-methylnorepinephrine, which is an a2 adrenergic receptor

SAFE for pregnancy, doesn't reduce GFR or RPF so also good for renal disease.

Causes Na+ retention, use with diuretic.

Improves insulin resistance (good for diabetics)

Front 50

Calcium channel blockers

Back 50

verapamil = decreases HR, increases digoxin, treats supraventricular tachycardia

diltiazem = decreases HR

nifedipine = arteriolar vasodilator, decreasing afterload. Also felodipine and nimodipine (longer t1/2)

there are others used for antiseizure

Front 51

ACE-I and ARB

Back 51

ACE-I = -pril, ACE inhibitors

ARB = -sartan = angiotensin II receptor blocker

decrease water retention, also increase glucose utilization

all cause dry cough, angioedema, hyperkalemia (often given with thiazides to help K+ secretion and volume)

Don't given either with bilateral renal artery stenosis. Angiotensin II responsible for vasoconstriction of efferent arteriole, without it you have a huge drop in GFR.

Front 52

Alpha1 blocker

Back 52

-osin, causing vascular relaxation,

alpha1a = uroselective for prostate (tamsulosin)

side effect = increased HR, give with beta blocker

Front 53

Beta blockers in conjunction with

Back 53

Calcium channel blockers (except verapamil, more cardioselective calcium channel blocker)

alpha 1 blockers (-osin)

Hydralazine

both decrease BP, causing an increase in HR

Front 54

Hydralazine

Back 54

direct smooth muscle relaxant. Causes increase in renin, and increased fluid retention. Combine with diuretic and beta-blocker.

not first line, high risk for drug induced lupus erythematosus (more likely in genetic slow acetylators) (reversible)

Front 55

Thiazide diuretics

Back 55

-thiazide

sulfonamide derivatives

secreted into tubule via PSOASS, inhibit Na/Cl cotransporter in early distal tubule

decrease glucose utilization (bad)

Front 56

Mild hypertension

Back 56

choice of diuretic, beta-blocker, ACE-I, ARB, alpha 1 blocker, alpha 2 agonist

Front 57

Moderate hypertension

Back 57

diuretic+

choice of: beta-blocker, ACE-I, ARB, alpha 1 blocker, alpha 2 agonist

Front 58

Severe hypertension

Back 58

diuretic, beta blocker +

choice of: ACE-I, ARB, alpha 1 blocker, alpha 2 agonist

Front 59

Diabetes with antihypertension

Back 59

-thiazide diuretics = decrease glucose utilization (bad)
beta blockers = increase insulin resistance (bad)
ace inhibitors = increase glucose utilization
a1 blockers = decrease insulin resistance
calcium blockers = neutral

Front 60

RAAS system and antihypertension

Back 60

all decrease renin secretion except

Ca channel blockers (mixed), alpha 1 blockers (mixed)

diuretics (increase)

Front 61

Drugs high risk for drug induced lupus erythematosus

Back 61

Hydralazine, procainamide, quinidine

Front 62

Normal Heart States

Back 62

250-350 grams (gender, age)

Endocardium, myocardium (<1.5cm max), epicardium

myocyte (spindle cells): cross striations (like skeletal) but also intercalated disks

Front 63

Hypertrophy

Dilation

Cardiomegaly

Back 63

increased myocyte size and myocardial thickness

increased myocyte length, and chamber size (stretch)

Overall increase size / weight of heart

Front 64

Valves

Back 64

composed of fibrous and loose connective tissue, avascular. Neovascularization if chronic inflamation

Front 65

Congestive heart failure CHF

Back 65

End point, usually from systolic dysfunction: ischemic heart disease (from atherosclerosis), 2ndary from hypertension

20-50% from diastolic dysfunction (secondary to systolic dysfunction, pulmonary disease, valvular disease)

Often starts as left sided problem, ends as a left and right side problem

Minority = high output failure, increased tissue demands (anemia)

Front 66

Systolic Dysfunction

Back 66

Failure of pump (common) = weak muscle (ischemic heart disease), or hypertension

Obstruction of flow (valve stenosis, coarctation (narrowing))

Regurgitant flow: valvular insufficiency

Disorder of conduction: arrhythmia, blockade

Front 67

Adaptive Neurohormonal Mechanisms to Systolic Dysfunction

Back 67

norepinephrine increases heart rate, contractility, and vascular resistance

RAAS system = increases blood volume (to increase end diastolic volume, and in turn SV), eventually hypertrophy

Atrial natriuretic peptide released in reaction to RAAS system, decreases blood volume when atria is stretched

Front 68

BNP test

Back 68

tests for amount of atrial natriuretic peptide in blood to determine heart failure

Front 69

Frank-Starling law

Back 69

increased end diastolic pressure, increases chamber size, requiring increased contractile force

Pressure overload results in increased fiber thickness
volume overload results in increased fiber length

Front 70

Adaptive mechanism status

Back 70

Adequate = maintains needed cardiac output

Inadequate = cannot supply enough oxygen

Hypertrophy eventually means that not enough blood can be supplied to heart because no new vascularization. Results in an MI.

Front 71

L sided heart failure

Back 71

L ventricle hypertrophied or dilated, L atrium dilated, atrial fibrillation, mural thrombus (from turbulence)

Lung = congested, edema, HF cell, pleural effusion

Clinically: dyspnea, orthopnea, paroxysmal nocturnal dyspnea

Front 72

Back 72

septa shouldn't have blood between them, alveoli should be clear. Macrophages escape to eat the red blood cells, become full of pigment hemosiderin and are heart failure cells.

Front 73

Right sided heart failure

Back 73

Liver: congested, centrilobular necrosis, cirrhosis
Spleen: fibrocongestive splenomegaly
Ascites (GI edema in peritoneal cavity), pleural and pericardial effusion, pedal edema, anasarca (generalized edema)

clinical: few respiratory symptoms unless biventricular, systemic & portal venous congestion, hepatosplenomegaly, edema

Front 74

Back 74

nutmeg liver vs normal liver

due to centrilobular necrosis from R heart failure

Front 75

Causes of congeital heart disease (1% births)

Back 75

Hypoplasia (lack of completion), aplasia (non-production), stenosis, failure of closure, transposition, duplication

VSD 42%, ASD 10%, Tetralogy 5%, Coarctation 5%, Transposition 4%

Most idiopathic, some environmental (rubella, teratogens), some genetic (22q11 = tetralogy)

Front 76

TBX5 mutation

NKXX mutation

22q11 deletion

Back 76

ASD and VSD, Holt Oram Syndrome

isolated ASD

Tetralogy of fallot, DiGeorge syndrome

Front 77

Left to Right shunts

Back 77

ASD, VSD, PDA

no cyanosis at first, if longstanding R sided pressure eventually exceeds left sided, reversing and causing cyanosis (Eisenmenger syndrome)

Front 78

Eisenmenger syndrome

Back 78

reversal of L to R shunt resulting in cyanosis

more often in VSD

Front 79

Atrial Septal Defect ASD

Back 79

Left to right shunt in interatrial septum

increased pulmonary blood volume

Ostium primum 90%, ostium secundum 5%, sonus venosus 5% (NKX2 mutation) (associated with pulmonary vein into right atria)

most commonly diagnosed in adults (ventricular septal defect more common at birth but often rectifies), well tolerated

Surgery prevents pulmonary hypertension, CHF, paradoxical embolization (emboli may skip through shunt during a sneeze, skipping pulmonic circulation and heading into systemic circulation)

Front 80

Ventricular septal defect VSD

Back 80

Left to right shunt in interventricular septum

increased pulmonary blood volume AND pressure

muscular (more likely to close) or membranous 90% types

Most close spontaneously, 30% are isolated

Cause pulmonary hypertension, shunt reverses sooner and more frequently than ASD (due to right ventricular hypertrophy)

Front 81

Back 81

Left = muscular VSD, lower in ventricles

Right = membranous VSD, higher in ventricles

Front 82

Patent ductus arteriosus PDA Left to right shunt

Back 82

Ductus arteriosus normally closes 1-2d after birth, remains open in PDA

90% isolated, 10% with VSD

Dilated pulmonary arteries, RV, RA (from pulmonary hypertension)

Gives harsh machine like murmur, may be asymptomatic

Can be life saving with aortic or pulmonic atresia, but can also allow for paradoxical emboli

Front 83

Right to left shunts

Back 83

Cyanosis at birth or soon after

Chronic = clubbing fingers, polycythemia (increased RBC count)

paradoxical emboli possible

Tetralogy of fallot and transposition of great vessels

Front 84

Tetralogy of fallot (R to L shunt)

Back 84

Most common cause of cyanotic congenital heart disease

Subpulmonic stenosis, VSD, overriding aorta (placed directly above VSD, gets blood from both ventricles), RV hypertrophy (boot shaped heart)

Severity dependent on RV outflow obstruction, gets worse with age as pulmonary trunk doesn't grow with heart

No pulmonary hypertension, polycythemia, hypertrophic osteoarthropathy (clubbing)

Front 85

Transposition of great arteries (R to L shunt)

Back 85

Two circles of blood flow, right heart to lungs, left heart systemic. Circles never cross

35% VSD, stable shunt, 65% PDA or patent foramen ovale, unstable shunt. If no shunt, incompatible with life. Must be corrected with surgery, PGE can help prevent ductus arteriosus from closing.

Front 86

Coarctation of aorta

Back 86

Twice as prevalent in men, associated with Turner syndrome (45,X)

Infant form: proximal to PDA
Adult: around ligamentum arteriosum

50% have bicuspid aortic valve (instead of three cusps)

Sometimes associated with berry aneurysm in circle of Willis, and other heart defects

preductal with PDA = cyanosis of lower half, weak femoral pulse
posductal without PDA = usually asymptomatic

Claudication / coldness of legs

Rib notching from collateral circulation (intercostal and internal mamary arteries)

Front 87

Ischemic heart disease (coronary artery disease)

Back 87

Due to atherosclerosis, #1 cause of death

>70% blockage = unstable angina

Clinical: angina pectoris, prinzmetal (angina from cyclic vasospasms of coronary arteries), unstable angina, MI, sudden cardiac death

Front 88

Myocardial infarction

Back 88

MI, AMI. 2/3 die, most over 65 years. Black = white, men > women. 90% from acute thrombosis

necrosis of myocardium form ischemia

Plaque disrupted, platelets aggregate / activate, platelet mediators released, vasospasm, extrinsic coagulation cascade, occlusion, possible lysis / embolus

Front 89

Ischemia

Back 89

reversible (if short), irreversible beyond 20 min resulting in coagulative necrosis. Endocardium survives. Can lead to sudden cardiac death from arrhythmia (Vfib)

Subendocardium = most fragile due to last to receive blood supply

Front 90

Myocardial distribution

Back 90

Most often in left anterior descending artery = 50%

Right coronary artery = 30%

Left circumflex = 20%

Front 91

MI microscopic changes

Back 91

Immediately: none (<4h)

Wavy fibers, contraction bands (pictured) (>12h)
coagulative necrosis (3-7 d)
Poly infiltration (3-7 d) (highest risk for rupture)
macrophages
granulation tissue (> 10 d)
dense fibrosis (>2months)

Front 92

Tetrazolium

Back 92

Used by an enzyme in LV, if cells are alive then reaction occurs

Front 93

Reperfusion injury

Back 93

If reperfusion occurs after ischemia, damage can be done from oxidative stress and inflammation. Can be seen as contraction bands.

Front 94

MI markers

Back 94

LDH = old and nonspecific

Myoglobin is good for immediate knowledge because peaks fast

CK-MB (heart specific) is ok, taken as a ratio of total CK to see if there's an injury

TROPONIN = most often used, specific

Front 95

MI prognosis

Back 95

50% = death, worse if women, older, DM, previous MI
Contractile dysfunction = (too damaged to supply blood)
Arrhythmias
Rupture (day 3-7) coagulative necrosis = weak
Ventricular aneurysm, mural thrombus (tough and don't rupture)
Pericarditis
Progressive heart failure (chronic ischemic heart disease)

Front 96

Back 96

Front 97

Chronic ischemic heart disease

Back 97

prior MI, cardiac decompensation
Severe coronary artery disease

results in left ventricle dilation / hypertrophy
micro: hypertrophy, subendocardial vacuolization, fibrosis

Clinical: CHF, angina, arrhythmia

Front 98

Sudden cardiac death SCD

Back 98

Cardiac death w/o symptoms, or within 24h of symptoms. 80-90% have coronary artery disease with 75% stenosis.

Die due to arrhythmia, defibrillators for those at risk

Young non-atherosclerotic causes: myocarditis, hypertorphy, cardiomyhopathy, conduction abnormality

Front 99

Systemic Hypertensive heart disease

Back 99

Left ventricular hypertrophy (without cardiac cause)

hypertension or pathologic evidence of HTN

Thick LV, box car nuclei, dilated L atrium, fibrosis

Clinical: asymptomatic or CHF, afib, IHD, stroke, SCD

Front 100

Pulmonary hypertensive heart disease

Back 100

RV hypertrophy

Acute: due to large pulmonary embolism (LV dilated, no hypertrophy)

Chronic: obstruction of pulmonary vessels, interstitial fibrosis, primary pulmonary hypertension, LV hypertrophy, atheromatous plaques in pulmonary arteries

Front 101

Valvular heart diseases

Back 101

Cardiac aortic stenosis, mitral regurgitation (degenerative changes)

Rheumatic valvular disease

Endocarditis

Carcinoid heart disease

Prosthetic valves

Front 102

Calcific aortic stenosis

Back 102

Most common cause of aortic stenosis, due to wear & tear (atherosclerosis contributes)

Seen in 70y/o (40y/o if bicuspid aortic valve)

Asymptomatic until: LV hypertrophy, ischemia, CHF, pulmonary edema, syncope

CHF leads to syncope and angina, 50% 2 year mortality. Large reason for valve replacement

Front 103

Back 103

calcific aortic stenosis, calcific aortic stenosis (bicuspid)

Enlarged nuclei, mitral valve calcifications (enlarge, eventually impinge into muscle and interfere with AV node conduction)

Front 104

Myxomatous mitral valve

Back 104

5% of adults, women 7x more than men

Degenerative change due to buildup of glycosaminoglycan in collagen

Can also be due to collagen synthesis disorder (such as marfan's) Or due to abnormal hemodynamics

Leaflets balloon out, chordae tendinae are thin, often rupture

usually asymptomatic, causes regurgitation. If rupture CHF

associated with endocarditis, SCD

Front 105

Rheumatic valvular disease

Back 105

common cause of mitral stenosis (99%), but rare in US

hypersensitivity type 2 (antibodies)

acute: aschoff bodies (fibrinoid necrosis), lymph cells, anitschkow cells in aschoff bodies (macrophages)

Chronic: fibrosis, neovascularization, thick chordae, fusion, stenosis (buttonhole). 75% mitral (25% mitral and aortic)

Adults often get arthritis rather than carditis (children)

Front 106

Rheumatic valvular disease diagnosis

Back 106

ASO titer (tests for antibodies to beta-hemolytic strep)

2 or more Jones criteria: Carditis, migratory polyarthritis, subcutaneous nodules (granulomas), erythema marginatum (red rings on skin), Sydenham chorea (involuntary movements)

Front 107

Back 107

Front 108

Back 108

Aschoff nodules

Front 109

Back 109

Seen in chronic rheumatic heart disease

aschoff nodules, thickened chordae tendinae

Fishmouth or buttonhole mitral valve

Fusion of aortic cusps

Front 110

Infective (bacterial) endocarditis

Back 110

Usually oral bacteria

acute = fast progression, virulent organism, normal valve, 50% mortality

Subacute: slow, low virulence organism, abnormal valve, usually recover with antibiotics. (fevers and malaise, blood cultures to diagnose)

Gross pathology: bulky, friable, destructive to aortic and mitral valve. Tricuspid involvement = IV drug abuse (staph aureus). Can cause emboli because friable.

Micro: fibrin, poyls, bacteria

Front 111

Organisms of bacterial endocarditis

Back 111

Normal valves / IV drug abuse = Staph aureus

Abnormal valves: streptococcus viridans

Others; HACEK (oral flora, slow growth)

Front 112

Nonbacterial thrombotic endocarditis (NBTE) or marantic endocarditis

Back 112

nondestructive, sterile, normal valves

hypercoagulable states (disseminated intravascular coagulation, or adenocarcinoma)

Create Lambl excrescences (nubs on valves which become thrombotic), create emboli, or bacterial environment

Front 113

Libman-Sacks endocarditis

Back 113

Systemic lupus erythematosus, prevented with steroids

Small vegetations, no site predilection

Front 114

Back 114

Front 115

Back 115

Staph aureus endocarditis, strep viridans endocarditis

Nonbacterial endocarditis, ???? mystery slide

Front 116

Carcinoid heart disease

Back 116

carcinoid tumors (neuroendocrine origin)

right heart = due to hepatic metastasis. results in tricuspid insufficiency, pulmonary stenosis

Left heart = due to pulmonary tumors (more often seen in right side of heart due to systemic metastasis)

Causes systemic syndrome (flushing, diarrhea) from mediators (serotonin, histamine)

Endocardial white plaques, fibroid plaques with smooth muscles changes and collagen

Front 117

Prosthetic cardiac valves

Back 117

Mechanical: anticoagulants necessary, may cause hemolysis from stress

Bioprosthetic: no anticoagulation necessary, matrix deteriorates, calcify, tear

Both subject to infection

Front 118

Cardiomyopathies classifications

Back 118

dilated: enlarged four chamber dilation, hypertrophy, flabby, mural thrombus (systole problem, can't contract)

Hypertrophic: hypertrophy (usually asymmetric), no dilation, diastole problem can't relax

Restrictive: normal heart size, but stiff firm myocardium, diastole problem can't relax

Front 119

Dilated cardiomyopathy

Back 119

most common, 30% genetic (autosomal dominant), 70% other

Often caused by alcohol abuse (acetaldehyde), uncommonly caused by pregnancy (often spontaneous recovery), myocarditis (coxsackie B)

Iron overload: interferes with enzymes using metal coenzymes (transfusions or hemochromatosis)

Front 120

Hypertrophic cardiomyopathy (IHSS)

Back 120

Caused by genetics, usually beta-myosin (heavy chain)

LV = banana shaped, 10% concentric, septum thicker

Endocardial plaque in LV outflow, thickened anterior mitral leaflet (from hitting ventricle)

Front 121

Hypertrophic cardiomyopathy clinical presentation

Back 121

Impaired filling / outflow obstruction
harsh systolic murmur
dyspnea
angina
arrhythmia, CHF, SCD

Surgery possible to reduce septal size

Front 122

Restrictive cardiomyopathy (infiltrate)

Back 122

Stiff non compliant wall, impaired filling

Cause: Deposition of: collagen, amyloid, iron, metabolic products, granulomas (sarcoidosis)

Front 123

Endomyocardial Fibrosis (restrictive cardiomyopathy)

Back 123

African children, most common worldwide

Dense fibrosis of endocardium and subendocardium in ventricles

Front 124

Loeffler endomyocarditis (restrictive cardiomyopathy)

Back 124

Endocardial fibrosis, mural thrombi

eosinophilia, degranulation, proteins cause endocardial damage, necrosis, then fibrosis

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Myocarditis

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Inflammation causes damage, often classified as a cardiomyopathy

often lymphocytic. Caused by Coxsackievirus A and B

May resolve or end in fibrosis (dilated cardiomyopathy cox B)

Less common causes: CMV, HIV, T cruzi (chagas), T gondii (toxoplasmosis), T spiralis (trichinosis), B burgdorferi (lyme)

Noninfectious: SLE, hypersensitivity (eosinophilic)

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Giant cell myocarditis

Chagas myocarditis

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poor prognosis for myocarditis

parasite seen inside myocytes (T cruzi)

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Types of myocarditis

Lymphocytic, Eosinophilic (hypersensitivity)

Giant cell, Chagas myocarditis

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Trichinella spiralis larva (myocarditis)

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Pericarditis

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Primary: infection, usually viral
if secondary: after MI, surgery, uremia, SLE, metastases

Fibrinous, fibrinopurulent, caseating

Acute: resolve without consequence
Chronic: delicate fibrous bands with dense scarring or CONSTRICTIVE pericarditis

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Pericarditis clinical features

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atypical chest pain from friction (rubbing)

Constrictive pericarditis = right sided venous distension, decreased cardiac output (like restrictive cardiomyopathy)

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Atrial myxoma

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usually singular, usually L atrial fossa ovalis

If polyp like, cause wrecking ball effect on mitral valve and require its replacement

can be friable, embolize, cause syncope due to ball valve effect

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Rhabdomyoma

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most common primary cardiac tumor in children, associated with tuberous sclerosis (genetic syndrome)

usually ventricular, gray-white mass, large myocytes and spider cells

Usually regress

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Papillary Fibroelastoma

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on valve, often aortic

Hair like projections, sometimes multiple

can embolize, mucopolysaccharide with elastic fibers

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Heart Metastases

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Most common tumor in heart

common ones: lung adenocarcinoma, breast cancer, leukemia / lymphoma, melanoma

Melanoma identified by brown pigment , lymphomas identified via markers

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Cardiac transplantation

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Usually for ischemic heart disease and dilated cardiomyopathy

graft coronary arteriosclerosis always occurs

Silent MI possibly due to denervated heart, no angina

Rejection occurs via T lymphocytes and necrosis via myocytes

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Giant cell arteritis, large vessels

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non-infectious vasculitis, larger vasculature, pulseless

Chronic granulomatous inflammation, affects vertebral and ophthalmic arteries

Idiopathic, but T cell mediated

Effects >50y/o, fever, fatigue, headache, ocular symptoms (blindness)

corticosteroids as therapy

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Takayasu arteritis, large vessels

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chronic granulomatous inflammation (same as giant cell)

fibrosis at aortic arch

<40y/o women, pulseless upper extremities

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Polyarteritis nodosa (PAN) medium vessels

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affects small / medium sized muscular visceral arteries, but NOT pulmonary. Attacked by immune cells

Affects only portion of circumference, usually branch points, early / late lesions are concurrent

30% have hepBAg present in blood

Affects young adults, renal arterial involvement can cause death

Steroids = treatment, may cure

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Kawasaki disease (mucocutaneous lymph node syndrome), medium vessels

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Infants and children (80% < 4 years)

delayed response of T cells after virus, causes inflammation of medium sized blood vessels

Skin / lymph node involvement

20% untreated develop coronary artery disease (leading cause of acquired heart disease for children)

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Wegener granulomatosis (small vessels)

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Triad: 1 = necrotizing granulomas of lungs. 2 = necrotizing granulomatous vasculitis of lungs. 3 = necrotizing crescent shaped glomerulonephritis (renal failure dangerous)

c-ANCA gene related (anti-neutrophil cytoplasmic antibodies) 95%

Men > women. 40y/o. Immunosuppressive and corticosteroid therapy

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Churg-Strauss Syndrome (small vessels)

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Variant of Wegener Granulomatosis

In addition, has asthma and eosinophilia

p-ANCA gene involvement

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Microscopic polyangiitis (leukocytoclastic), small vessels

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Affects Capillaries, arterioles, venules. Usually due to antibody response to drugs (penicillin), or bugs (strep)

Involves any organ, can palpate the purpura. Treated by removing agent

p-ANCA production in 70%

Small vessels, all lesions of the same age, glomerulonephritis and pulmonary capillaritis are common

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Thromboangiitis obliterans (Buerger disease) (small and medium sized)

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Inflammation & thrombosis of small / medium sized arteries of extremities. Secondary extension into veins & nerves. Leads to necrosis and ulceration

Occurs due to toxicity from tobacco or immune response to tobacco.

Affects middle aged heavy smokers. Cold sensitivity in hands and feet first, and foot pain (instep claudication)

Cessation of smoking make cure if early