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142 Cards in this Set
- Front
- Back
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Cardio path
What are four requirements of tetralogy of fallot? |
Tetralogy:
1. overriding aorta 2. ventricular septal defect 3. pulmonary stenosis 4. right ventricular hypertrophy |
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What is the shape of the heart in tetralogy of fallot? |
Boot shaped
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What type of shunt is tetralogy? |
Right to left
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Do all tetralogy of fallot babies have cyanosis? |
The degree of cyanosis is dependant on pulmonary stenosis
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What two shunts are cardioprotective in tetrology? |
1. patent ductus (unoxy blood goes from aorta down into pulm a and comes into pulm vein) - so the blood that happens to get into aorta from right ventricle has a second chance to go into pulm a via ductus.
2. ASD: blood that ends up in left atrium has a second chance of getting into the pulm a. via the right ventricle (causes a Left to Right shunt) |
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If you have a patient with tetralogy of fallot but with higher than normal O2 in right atrium - what does this patient have? |
Concombinent atrial septal defect.
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What is transposition of great vessels? What is necessary for survival? |
When the aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle.
To survive: need patent ductus arteriosus, patent foramen ovale, other ASD, or VSD (L to R to step up O2 in RV) |
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What is the developmental cause of transposition of great vessels? |
Failure of the aorticopulmonary septum to spiral
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What is the most common congenital cardiac anomaly? |
VSD
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What do the heart sounds sound like in ASD's? |
ASD:
loud S1 wide, fixed split S2 Midsystolic pulmonary ejection murmur (L to R shunt causes volume overloading of right ventricle and increased flow across pulmonary valve) Diastolic murmur (may also be heard because of increased flow from right atrium into right ventricle) |
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What is septum secundum a defect in? |
Closure of the fossa ovalis
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Where is the sinus venous located? |
Near the upper part of the septum near the entrance of the superior vena cava in the fetal heart.
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What is Lutembacher syndrome? |
An atrial septal defect with mitral stenosis.
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Murmur in patent ductus arterosus? |
Machine-like murmur
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How does a patent ductus arterosus shunt change immediately after birth? |
In fetal life the shunt is from right to left but after baby is born, with first breath, lung resistance decreases and shunt becomes left to right --> RVH and possibly heart failure.
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What causes the sustained patency of a PDA? |
Patency is maintained by PGE synthesis and low oxygen tension. PGE then may me necessary to sustain life in conditions such as transposition of the great vessels
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What is used to close a PDA? |
Indomethacin
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What is given patients with transposition of great vessels and a ductus arterosis? Why? |
PGE - to maintain PDA
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Which is most common: ASD, VSD, PDA? Which is least? |
VSD > ASD > PDA
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In all L to R shunts (VSD, aSD, PDA) what can eventually happen? |
Because of increased load on pulmonary arteries, pulmonary resistance can occur from arteriolar thickening --> progressive pulmonary hypertension --> reverse shunt --> cyanotic (and get clubbing and polycythemia)
condition of reversal called: Eisenmenger's |
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Q: What are the distinguishing features of a PDA heart? |
enlarged left atrium
enlarged left ventricle continuous murmur cyanosis (if reversal) |
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Q: When is child cyanotic in only his lower body? |
Often with an infantile form of coarctation of aorta when associated with a PDA.
The stenotic segment is located proximal to the PDA. Since BP drops distal to PDA, blood shunts from pulmonary artery to aorta thru PDA (reverse of nL PDA) = cyanosis in lower part of body. |
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Male to female ratio of coarctation of aorta? |
Male: female
3:1 |
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In a coarctation of the aorta, what will the pressure be like in the aorta? |
Pressure will be low.
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What 12 things are associated with Adult coarctation of the aorta?!?!?! |
Coarctation of aorta:
1. increase blood flow to proximal vessels 2. decrease flow below contriction 3. systolic murmu produced from stretching of aortic valve (like in syphilis) 4. 50% of time: bicuspid aortic valve 5. Increased upper extremity BP 6. Decreased LE BP 7. leg claudication 8. decrease in renal blood flow (activates renin-angiotensin = increase BP!!!) 9. colateral circulation between intercostals 10. CXR: rib notching 11. increased blood to brain - risk of berry aneuryism 12. risk of aortic dissection |
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What congenital abnormality is assoc with coarctation of the aorta? |
Turner's = babies go right into heart failure.
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Q: Some coarctations of the aorta can fully compensate, explain what blood flow will look like: |
In a fully compensated coarctation blood flow is nL in both upper and lower body despite an increase in pressure in upper vs lower body. This is made possible by an increased vascular resistance induced in lower body vessels.
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Q: 5yo presents with HTN, increased BP in arm over leg, erosion of inferior ribs, tachypnea? |
Coarctation of aorta
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What are the clinical findings of a baby with congenital rubella syndrome? |
Congenital rubella syndrome:
Cardiovascular defects Microcephaly Mental retardation deafness cateracts growth retardation |
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How can we try and prevent congenital rubella syndrome? |
Determine mother's immune status by looking for antirubella antibodies of IgM class.
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Why is the circle of willis a common location for berry aneuryisms? |
At the junction between communicating brances and the main cerebral vessel we have no interal elastic lamina and no smooth m. layer. (its weak)
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What causes the HTN seen in coarctation of the aorta? |
Increased renin
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Q: How is collateral circulation formed in coarctation of aorta? |
Colateral circulation is formed from anterograde flow through the intercostal artery via the subclavian a. (aorta receives retrograde supply from intercostal)
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Cardiac defect associated with: 22q11 syndromes |
Truncus arterosis
Tetralogy of fallot |
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Cardiac defect associated with: Down syndrome |
Endocardial cushion defect (most common)
ASD VSD |
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Cardiac defect associated with: Congenital rubella |
Septal defects
PDA |
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Cardiac defect associated with: Turner's syndrome |
Coarctation of aorta
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Cardiac defect associated with: Marfan's syndrome |
Aortic insufficiency
Mitral valve prolapse |
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Cardiac defect associated with: Offspring of diabetic mother (Q) |
transposition of great vessels
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Cardiac defect associated with: Ehlor-danlos syndrome |
Mitral valve prolapse
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Goljan: Pt with Marfan's died SUDDENLY, cause? |
Mitral valve prolapse with conduction defects
(not dissecting aneuryism) |
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Five signs Downs baby has? |
1. Heart defect (ASD, VSD, endocardial cushion defect)
2. double bubble sign (gas in stomach and duodenum) 3. prominent epicanthal folds 4. simian crease 5. flat facial profile |
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What is the most important risk factor for coronary artery dz? |
Old age!!!
men > 45; women > 55 |
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Why do women have an increase risk of coronary artery dz when they turn 55? |
Because their estrogen levels go down --> decrease HDL!!
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What is 90% of hypertension caused by? |
Primary (essential) HTN that is caused from a long term increase in CO and TPR.
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What is malignant hypertension? |
Is it a form of renal disease associated with malignant or accelerated phase of hypertension. This dramatic pattern of hypertension may occasionally develop in normotensive patients but is more commonly found in patients with pre-existing hypertension or renal disease.
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In what disease is malignant hypertension a frequent cause of disease? |
Scleroderma
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Q: 43 yo female with BP of 200/140, retinal hemorrhages, and ECG left axis deviation will have a decreased what? |
Arteriolar density
Answr: malignant HTN causes left ventricular hypertrophy, hypertrophy of the arteries and arterioles, and arteriollar rarefaction (loss of arterioles) After prolonged HTN arterioles close off and are reabsorbed!! |
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Does HTN predispose you to atherosclerosis? |
Yes!
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Atheromata? |
Plaques in blood vessel walls
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Xanthoma? |
Plaques or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids
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Tendinous xanthoma? |
Lipid deposit in tendon, especially Achilles
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Corneal arcus? |
Lipid deposit in cornea, nonspecific (arcus senilus)
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What blood value matters most for risk of coronary artery disease? |
HDL!!!
It reverses cholesterol transflow --> HDL visits fatty streaks in vessels and sucks LDL out of it and gives it to liver to metabolize. |
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Q: what heart conduction defect is most commonly caused by coronary artery dz? |
Bundle branch blocks
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Q: Three main causes of coronary artery dz? (not blood component elevations) |
1. HTN
2. Diabetes 3. Smoking |
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What is Monckeberg arteriosclerosis? |
Mockeberg:
Calcific deposits in muscular arteries in people commonly over 50. Can be seen radiographically and are often palpable but do not encroach on vessel lumen Robbins, p.515 FA: benign, especially in radial or ulnar artery, called "pipesteam arteries" |
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VIP Two main causes of hyalinarterolsclerosis? |
Diabetes
HTN |
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VIP Describe the MOA of diabetes induces hyalinarterolsclerosis? |
Nonenzymatic glycosilization: hemo A1C is glycosilated by glucose (glucose causes both osmotic and glycosilation damage). This glycosilation causes the basement membrane of small vessels to be perimeable to proteins. The proteins in plasma will leak into basement membrane and go into vessel wall. This produces hyaline changes and narrows lumen.
Can also do this to glomerular basement membrane: microalbuminuria. |
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MUST KNOW What is the appearance of a kidney from a pt with long standing diabetic damage? |
Kidney is shunken with cobble stone surface (from hyalinartersclerosis --> causes fibrosis).
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What causes lacunar strokes? |
Hyalinartersclerosis
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What causes peripheral neuropathy in diabetes? |
The excess glucose damages schwann cells.
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What is the leading cause of acquired heart dz in children? |
Kawasaki syndrome: acute, self-limiting disease of infants/kids. Causes transmural inflammation and acute necrotizing vasculitis of small/medium sized vessels.
Fever, congested conjuntiva, changes in lips/oral mucosa, lymphadenitis. May develop into coronary aneurysms. |
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What is the MCC of: 1. abdominal aneuryism 2. aortic root aneuryism 3. berry aneuryism 4. dissecting aneuryism |
1. abdom: aterosclerosis
2. aortic root: syphilis 3. berry: congenital defects in vessels walls and are assoc with polycystic kidney dz 4. dissecting: cystic medial degeneration (Marfans) |
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Xanthoma |
plaques or nodules composed of lipid-laden histiocytes in the skin, esp eyelid. Can also be in tendons, esp achilles
Caused by hyperlipidemia |
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Corneal arcus? |
Lipid deposits in cornea, nonspecific sign of hyperlipidemia
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In risk factors for coronary artery dz: which value matter the most LDL or HDL? |
HDL: it visits fatty streaks in vessels and sucks LDL out of it and gives it to the liver to metabolize.
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At what ages do men and women begin to be at risk for coronary artery dz? |
Men >45
Women > 55 (menopause= decreased estrogen=decreased HDL down to men's level) |
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What is monckeberg arteriosclerosis? |
Calcification of the arteries, especially the radial or ulnar.
Can be see in radiographically and can be palpated but do not "encroach" on the vessel lumen. |
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Describe the process of arteriolosclerosis? |
Hyaline thickening of small arteries in essential hypertension (no specific medical cause can be found)>
In malignant hypertension arteriolosclerosis is seen as a hyperplastic "onion skinning" appearance in the small vessels. Both are most often assoc with HTN and DM and can cause ischemic injury |
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Atherosclerosis |
Fibrous plaques and atheromas from in intima of arteries. It is a disease of elastic arteries and large to medium sized muscular arteries (image 79)
Progresses to fatty streaks --> proliferative plaque --> complex atheroma. Most common in abdominal aorta. |
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Describe a reprofusion injury (that isn't caused by medical intervention): |
Reprofusion injury: occurs in loose tissue organs that have collateral supply (lungs, intestines, or liver) following reperfusion after infarction.
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What is the most posterior compartment of the heart? |
Left atrium
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What does the posterior descedning artery feed and where does it orginate? |
Posterior 1/2 of interventricular septum and lateral left ventricular wall.
It orginates from RIGHT CORONARY a. (in right dom people, 80%) or left circumflex a. (in a left dominant ciruclation - 20%) |
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What is the most common thrombosed a of the heart? What does it supply? |
Left anterior descending:
supplies entire anterior part of heart and ant 2/3 of intraventricular septum (pale infarct) and apex of left ventricle. |
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Where are most wall ruptures after MI? |
anterior wall (because LAD is most commonly infarcted)
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What is the second most common vessel infarcted and what does this uniquely supply? |
Right coronary a:
supplies the entire posterior of heart, posterior intraventricular septum, and entire right ventricle. Unique: feeds posterior medial papillary m of mitral valve and AV node (95% while SA node is 50/50 with L/R) |
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VIP A patient comes in with sinus bradycardia and mitral regurg, and atypical chest pain (like GERD): Dx? |
Right coronary a. infarction (infarcts papillary m and AV node)
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Why is subendocardial ischemia happen first? Compare EKG to complete myometrial infarction |
Because coronary a. penitrate from outside in so subendo tissue gets screwed since its the last stop --> pain and ST depression
Ischemia to the entire myometrium (transmural) --> ST elevation |
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What vein is used in CABG? Alternative? |
Great saphinous vein
Alt: internal mammary |
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If a pt dies of sudden cardiac death what do we absolutely know about that patients history? |
They had a history of ischemic dz as an underlying abnormality
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What to lab is used to dx a reinfarction? |
CK-MB (peaks 24hrs and disappears in 3d)
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What is the best serum marker for MI from 0-8hrs? |
Troponin (begins in 2-6hrs,
peaks in 15-24, ends 7d) Note: LDH doesn't start for 10hrs and CK-MB starts in 4-8hrs |
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What is an LDH flip? |
Normally LDH2>LDH1 but in heart infarction LDH1<LDH2
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Why does tissue plasminogen activator work? Compart arterial and venous clots |
It is able to easily break new arterial thrombosis since they are just made of platelets and fibrin (not even a lot of fibrin)
In venous clots: too much fibrin --> can't break |
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What is the best inticator of how pt will do post MI? |
pts ejection fraction
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Pt comes in 3wks post MI with his chest bulgind on systole: Dx? What is pt at risk for? |
Dx: post MI aneurysm (but it won't rupture because it is lined by scar tissue)
Complications: decreased CO, risk of arrhythmia, embolus from mural thrombus |
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Pt comes in 3-5d post MI with pain in his chest that is relieved with leaning forward. Dx? |
DxL fibrinous pericarditis secondary to MI
Friction rub: occurs within 1 week of a transmural infarct |
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Pt comes in 6wks post infarct with pain in his chest releved with leaning forward, fever, and muscle aches. Dx? Rx? |
Dresslers syndrome: autoimmune phenomenon causing fibrinous pericarditis due to antibody formed against pericardial tissue
Rx: nonsteroidals |
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Pt presents 3-4d postMI with chest pain and distended neck veins. You hear muffled heart sounds. Dx? |
Rupture of anterior wall (LAD)
Other presentation: pansystolic murmur that increases on expiration, have S3/S4 |
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VIP What is the MCD in ventricular aneuryism? |
Heart failure, not aneuryism
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Cardio
VIP VIP VIP What type of dysfunction occurs in dilated (congestive) cardiomyopathy? 7 causes |
SYSTOLIC dysfunction caused by:
alcholol abuse (thiamine def), Beriberi, Coxsackie B virus myocarditis (autoimmune destruction of insulin-beta cells), cocaine, Chagas (damages m.), doxorubicin, and peripartum cardiomyopathy. |
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VIP VIP VIP VIP VIP Findings of hypertrophic cardiomyopathy: |
aka idopathic hypertrophic subaortic stenosis
1. hypertrophy often asymptomatic 2. hypertrophy of all chamber walls esp. ventricular septum (asymmetric) 3. loud S4 4. systolic murmur 5. septum hypertrophy forms an obstruction (so obstruction in this is below the aortic valve) |
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Treatment for hypertrophic cardiomyopathy: explain |
Beta blockers or Ca channel blocker:
both increase preload to decrease obstruction by pulling leaflet away from septum (beta1=increases HR and force of contraction --> increase CO) Both beta blockers and Ca blockers -> decrease HR and increase CO. Remember CO = SV x HR |
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MCC of child needing heart transplant? |
restrictive cardiomyopathy
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4mo develops heart failure and dies three months later. Histo: heart is covered with thick white layer and microscopically can see bands of elastic tissue in the thick which layer. Dx? |
Endocardial fibroelastosis caused by intrauterine virus infection.
Most likely the mumps virus. Endocardium thickens secondarily to marked increase in fibrose and elastic tissue. |
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70yo man with dimished pulses and a history of angina and syncope with exercise has an ejection murmur radiating to carotid arteries. Dx? |
aortic stenosis
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58yo man with LHF has an S3 and S4 heart sound and a pansystolic murmur located at the apex that increases with expiration: Dx? |
mitral regurgitation
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29yo IV drug abuser has fever, a giant c-v wave, and a pansystolic murmur along the left sternal border that increases with inspiration: Dx |
tricuspid regurgitation
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Which Hep is assoc with pANCA antibodies? |
Hep B (polyarteritis nodosa)
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Midsystolic ejection click? What does it mean when click is closer to S1? closer to S2? |
Midsystolic click: occurs when valve prolapses into left atrium and is suddenly restrained by chordea tendiea
S1: there is less ventricular volume --> standing up, anxiety (tachycardia), Valsalva S2: closer when left vent volume is increased: lying down/squatting (get more blood return to heart) Counterintuitive: think that mitral valve tries to hold out until 75% of blood is out --> thats its goal. So the more blood that is coming out -> click is closer to S2 |
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MC pathogenesis of Mitral valve prolapse? |
mitral cusps under go myxomatous degeneration caused by increased glycosaminoglycans (dermatan sulfate) which causes voluminous leaflets
AD inheritance in some cases Assoc. with Marfan's and Ehlers Danlos syndrome. |
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What is the cause of sudden death in a pt with mitral valve prolapse? |
Ventricular tachycardia (seen in Marfan's)
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MCC of mitral regurgitation? |
Structural abnormality
ex. LHF = stretching of MV ring Dz: chronic rheumatic heart dz, infective endocarditis, rupture of pap muscle |
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What structural changes does the heart undergo from mitral valve regurgitation? |
LVH and dilatation (blood reflexes into LA during systole --> pansystolic murmur)
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MCC of aortic stenosis? |
Calcified congenital bicuspid valve
(reduction in the valve orifice area offers increased resistance to the ejection of blood during systole: decreased stroke volume/CO. Poststenotic dilatation of aorta owing to stream of blood hitting the wall under increased pressure. Pressure overload in the left ventricle leads to concentric LVH) |
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Clinical findings in a pt with aortic stenosis? |
Narrow pulse pressure (poststenoic dilitation)
concentric left vent hypertrophy |
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What is the MC valvular lesion assoc with angina? |
Aortic stenosis because a decreased CO leads to filling of coronary arteries during diastole
-and- hypertrophic heart receives less blood |
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MC cause of microangiopathic hemolytic anemia? |
Aortic stenosis form schistocytes
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MCC of aortic regurgitation? |
Long-standing essential HTN
(also MC left sided valve involved in IV drug users) |
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High pitched blowing early diastolic murmur heard immediately after S2 and increases in intensity with expiration? Dx? Causes (3) |
aortic regurgitation
Causes (all dilate aortic ring): syphilitic aortic aneurysm dissecting aortic aneurysm coarctation of the aorta infective endocard in IV drug users |
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Austin flint murmur? |
Regurgitant stream from AV valve regurge hits anterior leaflet of mitral valve causing it to vibrate and produce a diastolic murmur too --> significant aortic regurg --> surgery
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Tricuspid stenosis has what increased Jugular veinous pulse findign? |
increased a wave
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Pt with opening snap and accentuated S1, then a mid-diastolic rumbling murmur heard best in lateral dicub position? |
Mitral stenosis
-accentuated S1 due to closure of a non-pliable valve -opening snap occurs when the non-pliable valve gives way under increased L atrial pressure -middiastolic rumbling would increase with expiration (mid because that is when atria contracts -MOW) |
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What increased jugular venous pulse is seen in tricuspid regurg? |
giant c-v jugular venous pulse wave (blood regurgitates into the atrium during systole)
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In what two regurg's do you get both S3 and S4? |
tricuspid and mitral
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What causes the hemisiderin-containing macrophages to be present in left-sided heart failure? |
left sided heart failure causes increased pulmonary capillary pressure --> this causes tiny hemorrhages --> pulmonary alveolar macrophages phagocytose dead erythrocytes
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Compare pulmonary edema and pleural effusion and their relationship to sided heart failure: |
LHF: pulmonary edema
RHF: pleural effusion |
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Cause of orthopnea? |
Pt with CHF already will have pulmonary vascular congestion.
When lying down there is an increase in venous return which exacerbates pulmonary vascular congestion. |
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Virchow's triad? |
this is what can predispose to DVT
1. stasis 2. hypercoagulability 3. endothelial damage |
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Pt with colon CA and endocarditis: Dx? |
Strep Bovis infection
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Number 1 cause of acute endocarditis? #1 cause of endocarditis in IV drug users? |
Staph Aureus
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What congenital problem predisposes to infective endocarditis? |
Any septal defect can cause aortic regurgitation and predispose to infective endocarditis
(ex vegatitation on aortic valve: VSD assoc endocarditis) |
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HY What is Libman-Sacks endocarditis? Cause? |
Endocarditis occuring only in systemic Lupus erythematosus (note: in SLE pericarditis is more common than endo).
This is characterized by small vegatations on either sides of the valve |
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Mneumonic for Lupus symptoms: |
I'M DAMN SHARP
Immunoglobulins (anti-dsDNA, anti-Sm, antiphospholipid) Malar rash Discoid rash Antinuclear antibody Mucositis (oropharyngeal ulcers) Neurologic disorders Serositis (pleuritis, pericarditis) Hematologic disorders Arthritis Renal disorders Photosensitivity |
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Endocarditis produced from carcinoid syndrome: |
Carcinoid tumors secrete serotonin which can be detoxed in the lung so it mainly effects the right sided valves. (Note: carcinoid SYNDROME means you have to have had metastasis to the liver)
It produces thickened endocardial plaques on endocardium or valves. |
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Mneumonic for bacterial endocarditis: |
FROM JANE
Fever Roth's spots Osler's nodes (tender raised lesions on finger or pads and round white spots on retina) Murmur (MC mitral) Janeway lesions (small erythematous lesions on palms and soles) Anemia Nail-bed splinter hemorrhage Emboli |
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Four complications of bacterial endocarditis? |
1. chordea rupture
2. glomerulonephritis 3. suppurative pericarditis 4. emboli |
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VIP VIP What is the most common valvular lesion in acute rheumatic fever? |
NOT MITRAL STENOSIS (this takes 10+ yrs to form)
It is actually MITRAL REGURGITATION because all of the parts of the heart are inflammed --> can form vegatations on valves |
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Symptoms for acute rheumatic fever: |
FEVERSS:
Fever ESR Vegatations Erythema marginatum Red-hot jts (polyarthritis) SubQ nodules St.Vitus' dance (chorea) |
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What will the blood culture of a patient with rheumatic fever tell you? |
Nothing!
It is an immunologic disease |
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What is DDx for a child with polyarthritis? |
1. acute rheumatic fever
2. juvienile arthritis (rheumatoid) 3. Henlouch-Purpura 4. rubella |
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Why does Group A strep cause such problems in our body? |
It has an M protein that looks similar to proteins we have in our joints and organs.
Our body forms Ab against Group A strep M protein and those Ab's then attack our own body |
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Pt with diffuse ST elevations, upright T waves, pericardial rub. nL CK and nL CXR Dx? |
Pericarditis
(won't hear muffled heart sounds because heart is fibrosed --> pericardial knock) |
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Cardio Path
Coxsackie virus is the most common cause of what 4 types of problems? How do you dx? |
Coxsackie MCC: (ss+RNA, linear, no env)
mycarditis pericarditis viral meningitis Dx coxsackie myocarditis using lymphocytic infiltrate |
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Cardio Path
Clincial presentation of myocarditis? |
Biventricular heart failure in young persons who do not have valvular, rheumatic, or congenital heart disease
MCC: Coxsackie (ss+RNA, linear, no env, icosohedral) |
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Cardio Path
MC valvular lesion? |
Mitral prolapse
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Cardio Path
In carcinoid syndrome what causes the flushing? |
Not serotonin
It is actually caused by the secretion of kallikrein (the enzyme that catalyzes conversion of kininogen to lysyl-bradykinin) Serotonin does cause the diarrhea, pellegra-like symptoms, fibrotic lesions of the endocardium and valves. |
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Cardio Path
Pathogenesis of heart problem assoc with tertiary syphilis: |
Disruption of the vasa vasora of the aorta with consequent dilation of the aorta and valve ring.
May see calcification of aortic root Can result in aneuryism |
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Cardio Path
MC primary cardiac tumor in children? |
Rhabdomyoma and is assoc with TUBULAR SCLEROSIS (facial angiofibroma, seizures, mental retardation, hypopigmented "ash-leaf spots" on skin, cortical and retinal hamartomas --incomplete penetrance, variable presentation) (VIP)
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Cardio Path
Four signs of pericardial effusion: |
Pericardial effusion:
1. low BP with inspirtation (pulsus paradoxis) 2. muffled heart sounds 3. neck vein distention with inspiration 4. decreased pulse on inspiration |
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Cardio Path
Women wtih pericardial or pleural effusion has what until proven otherwise? |
LUPUS
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