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Cardio Flashcards

1
Q

Complications from Artherosclerosis

A 
TEA (and) PII
Thrombosis
Embolism 
Aneurysm
Peripheral Vascular Disease
Ischemia
Infarction
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2
Q

Arteries effected by Atherosclerosis

A

AA > Coronary Arteries > Popliteal Artery > Carotid Artery

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3
Q

Causes of cardiogenic shock

A

Acute MI, HF, valvular dysfunction

Increased EDV, increase Afterload, decreased CO

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4
Q

Causes of obstructive shock

A

PE, tamponade
(Increased Preload (or decreased preload for tamponade or constrictive pericarditis) , increased afterload, decreased CO)

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5
Q

Causes of hypovolemic shock

A

hemorrhage, burn, GI bleed

Decreased preload, increased afterload, decreased CO

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6
Q

Causes of distributive shock

A

Sepsis, CNS injury, anaphylaxis

decreased preload, decreased afterload, increased CO

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7
Q

Early and late signs of shock

A

Tachycardia –> multiple organ failure

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8
Q

What is the vessel change in response to HT?

A

increase in media thickness with a relative decrease in lumen size
(arteriolosclerosis is a hypertensive change to arterioles)

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9
Q

What is the vessel change in atherosclerosis?

A 
Intimal thickening (sub-endothelial matrix) due to inflammatory rxn to deposition of oxidized LDL
Atherosclerosis can be conceptualized as chronic inflammation
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10
Q

Pathogenesis/Pathway of HT

A

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)

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11
Q

What is primary HT characterized by?

A

Structural changes in small arteries (SMASCH- small artery structural changes)

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12
Q

Angiotensin II role in primary HT

A
  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)
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13
Q

Role of Ang II in atherosclerosis

A
  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
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14
Q

Hypertensive Injury

A
  1. LVH
  2. CKD- grossly kidneys shrink and become granular
  3. CVA: charcot /leticulostriate arteries of bg; dilation and rupture due to HT
  4. Hypertensive retinopathy
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15
Q

What is the function of cholesterol in the body?

A
  1. Membrane fluidity
  2. Steroid hormones
  3. Vit D
  4. Bile salts
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16
Q

How does turbulent flow effect artherosclerotisis development?

A

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
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17
Q

Why do macrophages bind oxidized LDL?

A

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

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18
Q

How do LDL particles get oxidized?

A
  • Extravascular reduced antioxidant exposure
  • Smoking
  • Diabetes
  • Aging (leaky ox phos enzymes)
  • Inflammatory response
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19
Q

How do you get a necrotic core in atheroma formation?

A

Foam cells have ER stress which provokes apoptosis, enough of them undergoing apoptosis that efferocytosis (reabsorption of apoptotic cells), is diminished

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20
Q

Primary cause of hypertrophic cardiomyopathy

A

Missence ; AD mutation with uneven pentrance of beta myosin chain
Over 400 mutations but all associated with sarcomere proteins
Increase myofilament activation

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21
Q

What part of the heart is most hypertrophic in HCM

A

ventricular septum

Bananna like config

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22
Q

What is arrythrogenic right ventricular cardiomyopathy?

A

AD disorder of cardiac muscle where the myocardium is replaced by fatty infiltrate and moderate fibrosis
Desmosomal junction mutations
Type of DCM

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23
Q

What is LV non compression cardiomyopathy

A

Congenital disorder that causes spongy ventricles

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24
Q

What populations is HCM associated with?

A

athletes under 35 (exertion = death)

Friedrisch ataxia patients

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25
What are the three primary types of restrictive cardiomyopathy?
1. Amylodosis 2. Endomyocardial fibrosis 3. Loeffler endomyocarditis
26
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)
27
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
28
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
29
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)
30
What are common causes of pericarditis?
Not often primary (Viral) | Secondary to MI, cardiac surgery, radiation, pneumonia, pleuritis, uremia, (less commonly RF, SLE, Mets)
31
What type of cancer is most common in the heart?
Mets | Lung cancer> lymphoma > breast> leukemia >melanoma>hepatocellular carcinoma > colon cancer
32
80-90% of primary heart tumors are _______?
benign
33
What is the most common primary tumor of the heart?
Myxomas: LA mostly affected , singular arise around fossa ovalis
34
What are the most common primary tumors of the heart in infants and children?
Rhabdomyomas Tuberous sclerosis mutations of TSC1 and TSC2 tumor suppressor genes Most often regress spontaneously so are thought to be hamartomas
35
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 ) ```
36
What etiologies present with Pulsus Paradoxus?
Tamponade, Croup, Pericarditis, Asthma, Obstructive Sleep Apnea
37
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 CXR: Cardiomegaly Echo: Effusion Anti-inflam: naproxen, ibuprofen, steroids if refractory
38
Pericarditis viruses
CMV, HSV, HIV | TB most common cause of pericarditis in 3rd world, esp constrictive
39
Post MI fibrinous pericarditis
1-3 days post MI | Antibodies to DAMPS that attack the pericardium
40
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
41
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.
42
Congenital defects associated with alcohol exposure in utero?
ASD, VSD, PDA, Tetraology of Fallot
43
Congenital defects associated with rubella?
Septal defects, PDA, pulmonary stenosis
44
Congenital defects associated with Downs?
AV Septal defect, ASD, VSD
45
Congenital defects associated with diabetic mother?
Transposition of Great Arteries
46
Congenital defects associated with Marfans syndrome?
Mitral Valve Prolapse; thoracic aneurysm/disection, aortic regurg
47
Congenital defects associated with prenatal lithium exposure?
Ebstein abnormality (tricuspid valve displaced downward into the RV, 50% of people with ebstein anomaly have WPW
48
Congenital defects of Turner syndrome?
bicuspid aortic valve, aortic coarctation
49
Congenital defects associated with Williams syndrome?
Supravalvular aortic stenosis
50
Congenital defects associated with 22q11 syndromes?
truncus arteriosis, tetraology of fallot
51
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
52
Risk factors for HTN
Increased age, obesity, diabetes, excess salt or alcohol intake, family history, physical inactivity
53
Tuberous sclerosis
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 Heart: rhabdomyoma Brain: seizures! Imaging, genetic testing, Everolimus: drug that inhibits tumor growth and proliferation
54
If bacterial endocarditis is culture negative, what are the most common etiologies?
Coxiella burnetti Bartonella HACEK (Hemophallus, Actinobacter, Cardiobacterium, Eikenella, Kingella)
55
First line HT in pregnancy
Hydralazine (often coadministered with a beta blocker to prevent reflex tachy) - methyldopa, nifedipine, labetalol
56
Glomus tumor
Painful benign blue red tumor under nail | Due to modified SMCs of glomus body (thermoreg)
57
How do you differentiate bacillary angiomatosis from kaposi sarcoma?
BA has a neutrophilic infiltrate ; KS has a lymphocytic
58
Cherry hemangioma
Benign capillary hemangioma of the elderly Doesn't regress Often increases with age
59
Cystic hygroma
Cavernous lymphangioma of the neck | Associated with Turners
60
Pyogenic granuloma
Polypoid capillary hemangioma Can rupture and bleed Associated with pregnancy and trauma
61
Strawberry hemangioma
Benign capillary hemangioma of infancy | Appears in the first few weeks of life and then regresses by 5-8 yrs old
62
Lovastatin
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
63
Cholestyramine
Colestepol, Cholesevelam 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
64
Ezetimibe
Prevents cholesterol from being absorbed into enterocytes (small intestine brush border) Decreases LDL Side effects: increased LFTs (rare), diarrhea
65
Gemfibrozil
Fibrates Increase LPL, activate PPAR-a to increase HDL synthesis Decrease LDL, increase HDL, large decrease in TAGs Side effects: myopathy and cholesterol gall stones
66
Niacin
Vitamin B3 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
67
What are reversal agents for beta blockers?
Saline, atropine, and glucagon
68
Which beta blockers are contraindicated in angina and why?
Acebutolol, pindolol | Partial Beta antagonists that can increase myocardial O2 consumption
69
Tricuspid atresia
Congenital abnormality where you lack the tricuspid valve and have right ventricular hypoplasia Need to also have ASD and VSD to be viable
70
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
71
PDA murmur
Continuous "machine like" murmur heard during diastole and systole
72
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
73
What are the physical signs of Eisenmengers?
Clubbing of the fingers (hypoxia), let onset cyanosis, polycythemia
74
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
75
Maneuvers that effect preload
Decreased: valsalva Increase: squatting
76
Maneuvers that effect afterload
Increase: handgrip Decrease: vasodilators
77
Heart defects that change w/ increased afterload
Increase: Aortic regurg; Mitral regurg; VSD; Mitral stenosis Decrease: Aortic stenosis, HCM
78
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
79
What does the valsalva maneuver do?
Decreases LV preload
80
What does squatting from a standing position do?
Pushed blood that was pooled in legs back to heart Increases preload (decreases HCM murmur because greater filling causes displacement of hypertrophic septum away from outflow tract)
81
What do handgrip exercises do?
Increase afterload Make regurgitant murmurs worse No effect on aortic stenosis murmurs Helps differentiate between MR and AS

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