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Modules > Cardio > Flashcards

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
Q

What are the three primary types of restrictive cardiomyopathy?

A
  1. Amylodosis
  2. Endomyocardial fibrosis
  3. Loeffler endomyocarditis
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26
Q

What type of amylodosis do you see in heart disease?

A
  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)
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27
Q

Who gets endomyocardial fibrosis?

A

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

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28
Q

What is Loeffler endomyocarditis?

A

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

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29
Q

What are the primary causes of myocarditis?

A
  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)
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30
Q

What are common causes of pericarditis?

A

Not often primary (Viral)

Secondary to MI, cardiac surgery, radiation, pneumonia, pleuritis, uremia, (less commonly RF, SLE, Mets)

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31
Q

What type of cancer is most common in the heart?

A

Mets

Lung cancer> lymphoma > breast> leukemia >melanoma>hepatocellular carcinoma > colon cancer

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32
Q

80-90% of primary heart tumors are _______?

A

benign

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33
Q

What is the most common primary tumor of the heart?

A

Myxomas: LA mostly affected , singular arise around fossa ovalis

34
Q

What are the most common primary tumors of the heart in infants and children?

A

Rhabdomyomas
Tuberous sclerosis mutations of TSC1 and TSC2 tumor suppressor genes
Most often regress spontaneously so are thought to be hamartomas

35
Q

What are the most common causes of pericarditis?

A 
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
Q

What etiologies present with Pulsus Paradoxus?

A

Tamponade, Croup, Pericarditis, Asthma, Obstructive Sleep Apnea

37
Q

Presenting features of pericarditis?

A

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
Q

Pericarditis viruses

A

CMV, HSV, HIV

TB most common cause of pericarditis in 3rd world, esp constrictive

39
Q

Post MI fibrinous pericarditis

A

1-3 days post MI

Antibodies to DAMPS that attack the pericardium

40
Q

What are risk factors for thoracic aneurysm?

A

HTN, bicuspid aortic valve (associated with Marfans and Ehlers Danlos = connective tissue disorders), 3 syphillis
CYSTIC MEDIAL DEGENERATION

41
Q

What is CMD?

A

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
Q

Congenital defects associated with alcohol exposure in utero?

A

ASD, VSD, PDA, Tetraology of Fallot

43
Q

Congenital defects associated with rubella?

A

Septal defects, PDA, pulmonary stenosis

44
Q

Congenital defects associated with Downs?

A

AV Septal defect, ASD, VSD

45
Q

Congenital defects associated with diabetic mother?

A

Transposition of Great Arteries

46
Q

Congenital defects associated with Marfans syndrome?

A

Mitral Valve Prolapse; thoracic aneurysm/disection, aortic regurg

47
Q

Congenital defects associated with prenatal lithium exposure?

A

Ebstein abnormality (tricuspid valve displaced downward into the RV, 50% of people with ebstein anomaly have WPW

48
Q

Congenital defects of Turner syndrome?

A

bicuspid aortic valve, aortic coarctation

49
Q

Congenital defects associated with Williams syndrome?

A

Supravalvular aortic stenosis

50
Q

Congenital defects associated with 22q11 syndromes?

A

truncus arteriosis, tetraology of fallot

51
Q

What is the presentation of a patient with a myxoma?

A

Multiple syncope episodes due to ball valve obstruction of the LA M valve
Diastolic tumor plop sound

52
Q

Risk factors for HTN

A

Increased age, obesity, diabetes, excess salt or alcohol intake, family history, physical inactivity

53
Q

Tuberous sclerosis

A

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
Q

If bacterial endocarditis is culture negative, what are the most common etiologies?

A

Coxiella burnetti
Bartonella
HACEK (Hemophallus, Actinobacter, Cardiobacterium, Eikenella, Kingella)

55
Q

First line HT in pregnancy

A

Hydralazine (often coadministered with a beta blocker to prevent reflex tachy)
- methyldopa, nifedipine, labetalol

56
Q

Glomus tumor

A

Painful benign blue red tumor under nail

Due to modified SMCs of glomus body (thermoreg)

57
Q

How do you differentiate bacillary angiomatosis from kaposi sarcoma?

A

BA has a neutrophilic infiltrate ; KS has a lymphocytic

58
Q

Cherry hemangioma

A

Benign capillary hemangioma of the elderly
Doesn’t regress
Often increases with age

59
Q

Cystic hygroma

A

Cavernous lymphangioma of the neck

Associated with Turners

60
Q

Pyogenic granuloma

A

Polypoid capillary hemangioma
Can rupture and bleed
Associated with pregnancy and trauma

61
Q

Strawberry hemangioma

A

Benign capillary hemangioma of infancy

Appears in the first few weeks of life and then regresses by 5-8 yrs old

62
Q

Lovastatin

A

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
Q

Cholestyramine

A

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
Q

Ezetimibe

A

Prevents cholesterol from being absorbed into enterocytes (small intestine brush border)
Decreases LDL
Side effects: increased LFTs (rare), diarrhea

65
Q

Gemfibrozil

A

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
Q

Niacin

A

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
Q

What are reversal agents for beta blockers?

A

Saline, atropine, and glucagon

68
Q

Which beta blockers are contraindicated in angina and why?

A

Acebutolol, pindolol

Partial Beta antagonists that can increase myocardial O2 consumption

69
Q

Tricuspid atresia

A

Congenital abnormality where you lack the tricuspid valve and have right ventricular hypoplasia
Need to also have ASD and VSD to be viable

70
Q

Total anomalous pulmonary venous return

A

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
Q

PDA murmur

A

Continuous “machine like” murmur heard during diastole and systole

72
Q

What are the signs of coarctation of the aorta?

A

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
Q

What are the physical signs of Eisenmengers?

A

Clubbing of the fingers (hypoxia), let onset cyanosis, polycythemia

74
Q

Pathophysiology of young athlete death with hypertrophic cardiomyopathy

A

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
Q

Maneuvers that effect preload

A

Decreased: valsalva
Increase: squatting

76
Q

Maneuvers that effect afterload

A

Increase: handgrip
Decrease: vasodilators

77
Q

Heart defects that change w/ increased afterload

A

Increase: Aortic regurg; Mitral regurg; VSD; Mitral stenosis
Decrease: Aortic stenosis, HCM

78
Q

Pathophys of the murmur in HCM

A

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
Q

What does the valsalva maneuver do?

A

Decreases LV preload

80
Q

What does squatting from a standing position do?

A

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
Q

What do handgrip exercises do?

A

Increase afterload
Make regurgitant murmurs worse
No effect on aortic stenosis murmurs
Helps differentiate between MR and AS

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