Flashcards in Cardio Deck (81)
Complications from Artherosclerosis
TEA (and) PII
Peripheral Vascular Disease
Arteries effected by Atherosclerosis
AA > Coronary Arteries > Popliteal Artery > Carotid Artery
Causes of cardiogenic shock
Acute MI, HF, valvular dysfunction
(Increased EDV, increase Afterload, decreased CO)
Causes of obstructive shock
(Increased Preload (or decreased preload for tamponade or constrictive pericarditis) , increased afterload, decreased CO)
Causes of hypovolemic shock
hemorrhage, burn, GI bleed
(Decreased preload, increased afterload, decreased CO)
Causes of distributive shock
Sepsis, CNS injury, anaphylaxis
(decreased preload, decreased afterload, increased CO)
Early and late signs of shock
Tachycardia --> multiple organ failure
What is the vessel change in response to HT?
increase in media thickness with a relative decrease in lumen size
(arteriolosclerosis is a hypertensive change to arterioles)
What is the vessel change in atherosclerosis?
Intimal thickening (sub-endothelial matrix) due to inflammatory rxn to deposition of oxidized LDL
Atherosclerosis can be conceptualized as chronic inflammation
Pathogenesis/Pathway of HT
Initial increase in CO (not well understood) --> increase in BP --> Ateriole Wall stress --> Hypertrophy of media --> decreased lumen size --> increase PVR --> increased BP (CO returns to normal)
What is primary HT characterized by?
Structural changes in small arteries (SMASCH- small artery structural changes)
Angiotensin II role in primary HT
1.) Increases endothelial permeability (albumin leak, hyaline change)
2.) Increases VSMC calcification (monkeburg)
3.) Vasoconstriction (decrease NO, lumen narrowing)
4.) Smooth muscle expansion (medial hypertrophy, hyperplastic change)
5.) Matrix deposion, MMP action (reason for hyperplastic change, remodeling)
Role of Ang II in atherosclerosis
1.) Increases platelet aggregation (PA1 and PA2 receptors)
2.) increase expression of VCAM 1 and inflammatory cytokines (brings leukocytes in and bind)
3.) Decrease NADPH oxidase, increase ROS
2. CKD- grossly kidneys shrink and become granular
3. CVA: charcot /leticulostriate arteries of bg; dilation and rupture due to HT
4. Hypertensive retinopathy
What is the function of cholesterol in the body?
1. Membrane fluidity
2. Steroid hormones
3. Vit D
4. Bile salts
How does turbulent flow effect artherosclerotisis development?
Creates areas of high and flow shear stress, areas of low shear stress respond by trying to balance/increase shear stress by increasing subendothelial proteoglycans which bind LDL (body trying to equalize pressure to what it thinks are hypotension)
- Shear stress also increases inflammatory response by provoking transcription of inflammatory cytokines and decreasing NO synthase (vasoconstriction and inflammation)
- Get more LDL and more ROS = more oxidized LDL
Why do macrophages bind oxidized LDL?
Oxidized LDL mimics malaria infected erythrocytes, TB bacterium, and strep pneumo
Savenger receptors (CD36) on macrophages recognize these PAMPs and are activated
Macrophages release substances that induce a chronic inflammatory response
Phagocytose LDL --> foam cells --> decrease migration, increase lipid uptake, increase ROS genereation
How do LDL particles get oxidized?
-Extravascular reduced antioxidant exposure
- Aging (leaky ox phos enzymes)
- Inflammatory response
How do you get a necrotic core in atheroma formation?
Foam cells have ER stress which provokes apoptosis, enough of them undergoing apoptosis that efferocytosis (reabsorption of apoptotic cells), is diminished
Primary cause of hypertrophic cardiomyopathy
Missence ; AD mutation with uneven pentrance of beta myosin chain
Over 400 mutations but all associated with sarcomere proteins
Increase myofilament activation
What part of the heart is most hypertrophic in HCM
Bananna like config
What is arrythrogenic right ventricular cardiomyopathy?
AD disorder of cardiac muscle where the myocardium is replaced by fatty infiltrate and moderate fibrosis
Desmosomal junction mutations
Type of DCM
What is LV non compression cardiomyopathy
Congenital disorder that causes spongy ventricles
What populations is HCM associated with?
athletes under 35 (exertion = death)
Friedrisch ataxia patients
What are the three primary types of restrictive cardiomyopathy?
2. Endomyocardial fibrosis
3. Loeffler endomyocarditis
What type of amylodosis do you see in heart disease?
1. systemic (beta pleated sheets)- primary (AL) or secondary (AA)
2. senile cardiac amyloidosis (transthyretin- thyroxine and retinol transporter made in liver; found in older people and 4% of Af Am have gene mutations in transthryetin that predisposes)
Who gets endomyocardial fibrosis?
Children and young adults in Africa and other tropical areas
Dense diffuse fibrosis of endocardium and subendocardium that often effects M and T valves
Thought to be related to nutrational deficiency and helmith infection related inflammation
Most common cause of restrictive endocarditis globally
What is Loeffler endomyocarditis?
Large mural thrombi in all areas of the heart with peripheral and tissue infiltrates of eiosinophils (thought to release MBP which causes necrosis followed by layering of endocardium with thrombus)
Some people have PDGFR tyrosine kinase mutations and can reverse disease with tk inhibitors
What are the primary causes of myocarditis?
1. Viral (Cocksackie A and B- majority, CMV, HIV, influenza), often damage caused by immune response
2. Non viral- Chagas (trypanasoma cruzi) toxoplasma, trichinosis, lyme disease
3. Noninfectious: antibody mediated (SLE, drug rxns)
What are common causes of pericarditis?
Not often primary (Viral)
Secondary to MI, cardiac surgery, radiation, pneumonia, pleuritis, uremia, (less commonly RF, SLE, Mets)
What type of cancer is most common in the heart?
Lung cancer> lymphoma > breast> leukemia >melanoma>hepatocellular carcinoma > colon cancer
80-90% of primary heart tumors are _______?
What is the most common primary tumor of the heart?
Myxomas: LA mostly affected , singular arise around fossa ovalis
What are the most common primary tumors of the heart in infants and children?
Tuberous sclerosis mutations of TSC1 and TSC2 tumor suppressor genes
Most often regress spontaneously so are thought to be hamartomas
What are the most common causes of pericarditis?
most common is idiopathic (thought to be viral)
CIINA RUT (Cardiac - STEMI or Dressler; Infection, Idiopathic, Neoplasia- seeding of pericardial space causing reactive inflam changes, Autoimmune- SLE, RA, Radiation, Uremia, Trauma -contussion from compression )
What etiologies present with Pulsus Paradoxus?
Tamponade, Croup, Pericarditis, Asthma, Obstructive Sleep Apnea
Presenting features of pericarditis?
Pleuritic chest pain improved by leaning forward
Fever, chills, and dyspnea
Friction rub/cardiac rub --"leathery sound" "gratting sound"
EKG: STE and PR depression
Anti-inflam: naproxen, ibuprofen, steroids if refractory
CMV, HSV, HIV
(TB most common cause of pericarditis in 3rd world, esp constrictive)
Post MI fibrinous pericarditis
1-3 days post MI
Antibodies to DAMPS that attack the pericardium
What are risk factors for thoracic aneurysm?
HTN, bicuspid aortic valve (associated with Marfans and Ehlers Danlos = connective tissue disorders), 3 syphillis
CYSTIC MEDIAL DEGENERATION
What is CMD?
a disorder of large arteries, in particular the aorta, characterized by an accumulation of basophilic ground substance in the media with cyst-like lesions. CMN is known to occur in certain connective tissue diseases such as Marfan syndrome, Ehlers-Danlos syndrome, and annuloaortic ectasia, which usually result from degenerative changes in the aortic wall.
Congenital defects associated with alcohol exposure in utero?
ASD, VSD, PDA, Tetraology of Fallot
Congenital defects associated with rubella?
Septal defects, PDA, pulmonary stenosis
Congenital defects associated with Downs?
AV Septal defect, ASD, VSD
Congenital defects associated with diabetic mother?
Transposition of Great Arteries
Congenital defects associated with Marfans syndrome?
Mitral Valve Prolapse; thoracic aneurysm/disection, aortic regurg
Congenital defects associated with prenatal lithium exposure?
Ebstein abnormality (tricuspid valve displaced downward into the RV, 50% of people with ebstein anomaly have WPW
Congenital defects of Turner syndrome?
bicuspid aortic valve, aortic coarctation
Congenital defects associated with Williams syndrome?
Supravalvular aortic stenosis
Congenital defects associated with 22q11 syndromes?
truncus arteriosis, tetraology of fallot
What is the presentation of a patient with a myxoma?
Multiple syncope episodes due to ball valve obstruction of the LA M valve
Diastolic tumor plop sound
Risk factors for HTN
Increased age, obesity, diabetes, excess salt or alcohol intake, family history, physical inactivity
AD dominant disorder associated with multiple hamartomas (benign mixture of cells);
TSC1 gene mutation
"Child with seizures and skin finding"
Skin: hypopigmented ash leaf shaped macules on trunk and extremities or angiofibromas/adenoma sebatium "small papules on face"
Renal failure: high BP
Imaging, genetic testing, Everolimus: drug that inhibits tumor growth and proliferation
If bacterial endocarditis is culture negative, what are the most common etiologies?
HACEK (Hemophallus, Actinobacter, Cardiobacterium, Eikenella, Kingella)
First line HT in pregnancy
Hydralazine (often coadministered with a beta blocker to prevent reflex tachy)
- methyldopa, nifedipine, labetalol
Painful benign blue red tumor under nail
Due to modified SMCs of glomus body (thermoreg)
How do you differentiate bacillary angiomatosis from kaposi sarcoma?
BA has a neutrophilic infiltrate ; KS has a lymphocytic
Benign capillary hemangioma of the elderly
Often increases with age
Cavernous lymphangioma of the neck
Associated with Turners
Polypoid capillary hemangioma
Can rupture and bleed
Associated with pregnancy and trauma
Benign capillary hemangioma of infancy
Appears in the first few weeks of life and then regresses by 5-8 yrs old
Inhibit HMG-CoA reductase which converts HMG CoA to mevalonate (cholesterol precursor)
Up-regulates LDLR; decrease mortality in CAD patients
Decreases LDL, Increases HDL, decreases TAG
Side effects: myopathy, and hepatotoxicity
Bile resin that binds bile salts in the intestine and prevents reabsorption
Decreases LDL, slight elevation in HDL and TAGs
Side effects: GI upset and decreased absorption of certain drugs and DEAK vitamins
Prevents cholesterol from being absorbed into enterocytes (small intestine brush border)
Side effects: increased LFTs (rare), diarrhea
Increase LPL, activate PPAR-a to increase HDL synthesis
Decrease LDL, increase HDL, large decrease in TAGs
Side effects: myopathy and cholesterol gall stones
Inhibits lipolysis in adipose tissue, decreases VLDL synthesis
Decrease LDL, large increase in HDL, decrease in TAGs
Side effects: Face flushing (improved by NSAIDS); hypergylcemia, hyperuricemia
What are reversal agents for beta blockers?
Saline, atropine, and glucagon
Which beta blockers are contraindicated in angina and why?
Partial Beta antagonists that can increase myocardial O2 consumption
Congenital abnormality where you lack the tricuspid valve and have right ventricular hypoplasia
Need to also have ASD and VSD to be viable
Total anomalous pulmonary venous return
TAPVR, congenital defect where pulmonary veins drain into the RA
ASD and/or PDA allow for right to left shunting and oxygenation of the periphery
Continuous "machine like" murmur heard during diastole and systole
What are the signs of coarctation of the aorta?
Tends to be juxtaductal, Associated with bicuspid aortic valve and Turners
HT in upper extermities and weak/delayed pulses in lower extremities
Notched ribs on CXR over time as collaterals grow
What are the physical signs of Eisenmengers?
Clubbing of the fingers (hypoxia), let onset cyanosis, polycythemia
Pathophysiology of young athlete death with hypertrophic cardiomyopathy
large septum --> decreased ejection --> stiff ventricle, decreased diastolic filling --> during exercise increase HR --> increased HR means less time filling --> symptoms (dyspnea, chest pain, palpatations, syncope, S4, systolic ejection type murmur) worsen
Maneuvers that effect preload
Maneuvers that effect afterload
Heart defects that change w/ increased afterload
Increase: Aortic regurg; Mitral regurg; VSD; Mitral stenosis
Decrease: Aortic stenosis, HCM
Pathophys of the murmur in HCM
Outflow tract narrowed due to wide septum; slow blood flow creates a suction effect that pulls the anterior leaflet of the mitral valve towards the septum further narrowing it and causing mitral insufficiency
What does the valsalva maneuver do?
Decreases LV preload
What does squatting from a standing position do?
Pushed blood that was pooled in legs back to heart
(decreases HCM murmur because greater filling causes displacement of hypertrophic septum away from outflow tract)