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Boards Path > Cardio Path > Flashcards

Cardio Path Flashcards

1
Q

Blubus Cordis

A

-Superior portion of the primitive heart tube, desdends and moves anterolaterally, forms a major part of RV

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2
Q

Primative Ventricle

A

-Forms the majority of left ventrile and moves laterally in the chest

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3
Q

Primative Atria

A

-Is located on the inferior aspect of the heart tube and moves posterior and superioly (looping around) to form atria

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4
Q

Sinus Venosus

A
  • Bilateral structures at the base of the primitive heart tube the get pulled along with atrium
  • Form portion of atria and coronary sinus.
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5
Q

Truncus Arteriosus

A
  • Forms from the superior aspect of the primative heart tube and comes off bulbus chorus/primative Vent
  • Neural Crest and endochardial cushion tissue are crucial to proper spinning and septation
  • Transposition of GV: DM
  • Tetrology of Fallot: DiGeorge
  • Persistant Truncus: Di George
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6
Q

Interventricular Septation

A
  • Muscular portion comes from the bottom
  • Membranous portion forms from joining with the AP septation and neural crest
  • Endochardial Cushion Tissue grows to form the atrial/ventricular sepations
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7
Q

Endochardial Cushion Tissue

A
  • Forms the atrial/ventricular sepations

- Problems commonly with trisomy 21

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8
Q

Membranous Septal Defects

A
  • Much more common than muscular
  • Result in left to right shunt along pressure gradient. Leads to hypertrophy of Right Ventricle and eventual reversal of shunt
  • Eisenmeingers Syndrome
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9
Q

Atrial Septation

A
  • Begins with the formation of a membranous septum primum that grows from the superior aspect to join with the endochardial cushion tissue at the AV border
  • Foramen secundum forms when there are partial disintigration of the septum primum.
  • Development of rigid Septum secundum on the right ventricle side of septum primum, grows from superior and inferior
  • Septum primum is now flappy and acts like a one way valve allowing for flow during fetal development. Foramen Ovale
  • At birht, increased LA pressure closes spetums and they fuse. Failure is patent foramen Ovale
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10
Q

Down Syndrome

A
  • Associated with defects in endocardial cushion tissue
  • Membranous VSD
  • ASD with osteum primum
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11
Q

1st aortic Arch

A

-Maxillary artery gives rise to middle meningeal that exits through foramen spinosum and can lead to epidural hematomas

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12
Q

2nd aortic arch

A

-Stapedial artery

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13
Q

3rd aortic arch

A
  • Common carotid and internal carotid

- Pouch 3 is 9th CN, which innervates carotid baroreflex

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14
Q

4th aortic arch

A
  • Arch of aorta

- Pouch 4 is CN 10 which innervates the baroreflex

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15
Q

Aortic arch 6

A

-Pulmonary artery and ductus arteriosus

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16
Q

Eryhtropoesis in fetal life

A
  • 3-10 weeks is in yolk sac
  • 6 weeks to birth is in liver
  • Some is made in spleen around the time of birth
  • Bone marrow, especially sternum, skull, etc take over
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17
Q

Fetal hemoglobin

A

-Has decreased affinity for 2,3 BPG which leads to stronger bonding with oxygen, allowing it to be picked up at umbilical vein

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18
Q

Fetal Circulation

A
  • Umbilical Vein to ductus venosus to IVC to RA through foramen ovale to aorta to umbilical arteries
  • Blood can also be sent from RA to RV through pulmonary artery and then through ductus arteriosus
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19
Q

Ductus Venosus

A
  • Umbilical vein to IVC
  • Bypasses portal circulation
  • Become ligamentum teres heptis
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20
Q

Ductus arteriosus

A
  • Pulmonary artery to arch of aorta

- Becomes ligamentum arteriosum

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21
Q

Ligamentum Arteriosum

A
  • Anchors aorta to pulmonary veins and can be a site of traumatic rupture
  • The recurrent laryngeal nerve (Phonation arch 6) goes around the ligamentum arteriosum
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22
Q

Foramen ovale

A
  • Septum primum acts as floppy protion and secundum as strong portion of one way valve.
  • Permits flow from RA to LA bypassing pulmonary and RV
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23
Q

Changes at Birth

A

Inflation of lungs leads to decreased pulmonary pressure and increased LAP this closes foramen ovale.

  • Increased Oxygen leads to decrese in prostaglandins and a closure of the ductus arteriosus
  • If want to keep open give PGE1/2
  • If want to close foramen ovale give indomethacin
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24
Q

Umbilical Arteries remnant

A

-Medial umbilical ligaments

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25
Q

Median umbilical ligament

A
  • Urachus, derivative of allantois

- Normally functions to connect the yolk sac and the bladder

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26
Q

Urachal cyst

A

Extraperitoneal mass that may cause pain and inflammation

-May lead to bladder adenomcarcinoma

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27
Q

Coronary Arteries

A

-Fill during diastole, occlusion causing ischemia and coagulative necrosis

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28
Q

RCA

A
  • Supplies Right atrium and ventricle
  • Supplies SA and AV in nearly all individuals
  • 85% are right dominant, meaning RCA gives rise to posterior descending branch that supplies the posterior 1/3 of the interventricular septum
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29
Q

LCA

A
  • Supplies posterior half of left ventricle and atrium.
  • Can rarely supply AV node
  • Left dominant circulation means gives rise to posterior descending and posterior 1/3 of interventricular septum.
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30
Q

LAD

A
  • Supplies anterior surface of left heart and is most commonly occluded artery
  • Supplies anterior 2/3 of interventricular septum
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31
Q

Coronary Sinus

A
  • Drains all blood from heart except for anterior veins which drain directly into the heart
  • Embryologic origin is sinus venosus (also SVC)
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32
Q

Anterior heart (facing sternum)

A

-RV and RA

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33
Q

Base of heart, posterior

A
  • Left atrium
  • In close opposition to esophagus and recurrent laryngeal nerve.
  • Atrial enlargment from CHF/DCM leads to dysphagia and hoarsness
  • TEE can be used to visualize LA and other vascular structures
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34
Q

Diaphragmatic surface of heart

A

-Both ventricle, mainly left ventricle

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35
Q

Stroke Volume

A

-Effected by contractility, preload, and afterload

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36
Q

Contractility Increase

A
  • Increased Intracellular Ca
  • Caetacholamines (increase intracellular Ca)
  • Digoxin (inhibit Na/K pump leading to increased Na intracellularly and decreased Na leaving through Na/Ca channel)
  • Increased Preload (sarcomere stretch) Starling Law
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37
Q

Contractiliy Decrease

A
  • Decreased intracellular Ca
  • Beta 1 blockers
  • Acidosis
  • Hypokia
  • Ca Channel blockers (non DHP)
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38
Q

P=QR

A 
Pressure = Flow* resistance
Flow = delta P / Resistane
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39
Q

Preload

A
  • increased preload will increase cardiac output
  • Caetacholamines, increased filling time, increase blood volume (increase venous return)
  • Decrease preload will decrease oxygen requirements
  • Nitroglycerin used in angina
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40
Q

Afterload

A
  • Pressure needed to pump against

- Vasodilators will decrease this and decrease oxygen demands

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41
Q

Resistance

A
  • Mainly inverse function of radius to the 4th power

- Can also be effected by viscosity (Multiple Myeloma hyperprotein, Polycythemia, Spherocytosis

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42
Q

Heart Failure/DCM

A

Increasd preload with decreased ejection fraction

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43
Q

S1

A

Caused by mitral and tricuspid closure

  • End diastole
  • Occurs after the isovolumetric filling phase of ventricles
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44
Q

S2

A
  • Aortic and pulmonic closing
  • End systole
  • Occurs after ejection phase
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45
Q

S3

A
  • Early Diastolic Murmur
  • Caused by elevated filling volumes
  • Increased atrial pressure necessary to fill increased volume
  • CHF, DCM, Mitral Regurg
  • Normal in pregnant and kids
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46
Q

S4

A
  • Late diastolic murmur
  • From increased pressure/stiff ventricular walls that oppose atrial kick and cause murmur
  • LVH most commonly
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47
Q

JVP Wave form

A
  • initial a wave from atrial contraction followed by brief descent to c wave
  • C wave is ventricular contraction against closed tricuspid
  • X descent is relaxation of atria
  • V wave is filling of atria passively
  • Y descent is opening of tricuspid valve and RV filling/RA emptying
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48
Q

Elevated JVP

A

-Pericardial effusion, pHTN, CHF

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49
Q

Absent Pulsation elevated JVP

A

-Superior vena cava syndrome

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50
Q

Large A wave

A
  • Elevated RA pressures

- RV failure/thickening, tricuspid steonosis

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51
Q

Absent A wave

A

-Atrial fibrillation

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52
Q

Paradoxical JVP, Kussmauls

A
  • During inspiration there is an increase in JVP (normally would expect less because of reduced intrathoracic pressures)
  • Seen with Pericardial effusion, cardiac tamponade
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53
Q

Normal Splitting of S2

A
  • Normally during inspiration there is an increase in venous return to the RV because of decreased intrathoracic pressures. This leads to a longer time for volume to be expelled and a delay in the pulmonic portion of S2
  • Normal!
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54
Q

Wide splitting

A
  • Splitting still increases during inspiration, but the splitting is wider than would be expected because of exageratedly long RV emptying
  • Pulmonic stenosis, RBBB
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55
Q

Fixed Splitting

A
  • There is no relative change in ventricular pressures with the intrathoracic changes of breating.
  • ASD and VSD allow for blood to flow between chambers regargless of pressure.
  • ASD, VSD
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56
Q

Paradoxical Splitting

A
  • There is a longer time for LV emptying meaning the aortic portion of S2 will come before the pulmonic on normal breathing and the two will converge on inspiration (longer pulmonic component)
  • Aortic Stenosis, LBBB
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57
Q

Inspiration Effects on on heart sounds

A

Increase Right heart sounds

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58
Q

Expiration

A

Increase Left Heart Sounds

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59
Q

Handgrip

A

-Increases systemic resistance and increases regurgitations and decreases stenosis/S4

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60
Q

Valsalva

A
  • Increase in intrathoracic pressure

- Decreases all murmurs except increases MVP, LVH

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61
Q

Mitral Regurgitation

A
  • Holosystolic blowing murmur begining at apex and radiating to axilla
  • Increased with elevated systemic resistance, decreased with valsalva (increased intra thoracic)
  • Endocarditis, Rheumatic Fever, MVP, DCM
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62
Q

Tricuspid regurg

A

-Holosystolic heard best at tricuspid area a radiating to the right sternal border

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63
Q

Aortic Stenosis

A
  • Crescendo decrescendo systolic murmur that may have a click, heard best at apex and radiating to the carotids
  • Patient will have weak and delayed pulses and may have syncope, angina, DOE
  • Dystophic senile clacification, time course is increased with bicuspid aortic valve (turners)
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64
Q

VSD

A
  • Harsh holosystolic murmur heard best at left sternal border
  • Most commonly a membranous defect and is associated with endochardial cushion defects and Down’s Syndrome
  • Worsened with handgrip and increased systemic resistance
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65
Q

MVP

A
  • Most common murmur, often hear a mid systolic click with late systolic crescendo murmur. Heard at apex.
  • Click is from tightening of chorda
  • Marfans, myxametous degeneration, ehlers danlos, ruptured papillary
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66
Q

Aoritc Regurg

A
  • High pitched, mid and late diastolic blowing murmur.
  • Widened pulse pressure and may have headbobbing
  • Syphilis, dilated aortic root (Marfans) endocarditis, rheumatic fever
  • Worsened with handgrip and increased systemic resistance
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67
Q

Mitral Stenosis

A
  • Diastolic blowing murmur with opening snap
  • Rheumatic Fever
  • May lead to LA dilation and compression of esophagus and laryngeal nerve leading to impaired phonation and dysphagia
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68
Q

Patent Ductus

A
  • Contunous machine like murmur heard best at infraclavicular level
  • Prematurity or congential rubella
  • Close with indomethacin and keep open with PGE
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69
Q

Ventricular Action Potential

A
  • Phase 0: Na inward current upstroke
  • Phase 1: Na inactiavtion and begining of K opening
  • Phase 2: L-Type Ca opening and plateau phase
  • Phase 3: L-Type Ca close and K open causing repolarization
  • Phase 4: High K conductance and resting potential
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70
Q

Nodal Action Potential

A
  • Phase 0: T-Type and L-Type Ca channels opening leading to deoplarization
  • Phase 1 and 2 absent Na V-gated channels and no Plateau
  • Phase 3: T-Type and L-Type Ca channels closing and K opening allowing influx
  • Phase 4: HCN channels allow Na inward current to reach T-Type and L-Type Threshold
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71
Q

HCN Channels

A
  • Located most explicitely on nodal cells
  • Hyperpolarization and cyclic nucleotide gated channels
  • Cause a ramp potential
  • Increased by cAMP in response to B1 Gs activation
  • Slope will be decreasd by adenosine and Ach which bind M2 Gi receptor leading to decreased cAMP
  • Adensoine binds A1 receptor leading to decreased cAMP and increased K efflux
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72
Q

Ca Channels

A
  • T Type are enriched on nodal cells and almost gone in ventricular cells. Mediate lower potential (early opening) rapid increase, but close rapidly
  • L-Type stay open longer and are responsible for plateau phase
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73
Q

Muscle Contraction

A
  • Driven by Ca induced Ca release from sarcoplasmic reticulum
  • Influx through DHP (L-Type) ca channels opens ryr on SR
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74
Q

Na/Ca exchanger

A
  • Increases Ca efflux and Na influx driven gradient

- Decreased in digitalis leading to increased inotropy

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75
Q

Ionotropy

A
  • Strength of contraction, mediated by Ca levels

- Increased with SANS

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76
Q

Chronotropy

A
  • Heart rate, mainly Ca and Na dependent

- Negative by verapamil (L-type) positive SANS

77
Q

Dromotropy

A
  • Conduction through AV node

- Slowed with slower Ca current (digitalis, Verapamil, beta blockers)

78
Q

Mechanical Contraction

A
  • Occurs following Ca induced Ca release (L-type to RyR)
  • Occurs during the QT interval (Q is depolarization, T is repolarization) occurs from plateau phase 2 to phase 3 repolarization.
79
Q

U wave

A
  • Thought to represent papillary or perkinje repolarization

- Seen in hypokalemia and bradychardia

80
Q

Torsades De Points

A
  • Due to impaired K conductance usually, can be Na.
  • Can be a progression of long QT
  • Tx: magnessium sulfate
81
Q

Congenital Long QT

A
  • Commonly caused by K channel problem

- Can be accompanied by sensioneural hearing loss

82
Q

Drugs Long QT

A
  • Clarithromycin, Levofloxacin
  • Haloperidol
  • In combination with inhibitors of CYP 450 can cause effects
83
Q

Atrial Fibrillation

A
  • Ectopic atrial pacemaking cells make irregular rythm with complete lack of P waves.
  • Pulse will be irregularly irregular because of rate at which AV node allows current to pass.
  • May present with palpitations, dyspnea, syncope
  • Need to treat with anticoagulants to prevent clot formation, common cause of stroke
  • A fib may be caused by anything that causes atrial stretch: Mitral stenosis, DCM, Sleep apnea. Alcohol may as well
  • May be conducted faster and lead to v Tach if there is WPW connection
84
Q

Atrial Flutter

A
  • Saw tooth EKG that may regress into A Fib
  • SVT that should be treated
  • May go through AV node if WPW present
  • Syncope, Palpitations, Dyspnea
85
Q

V Fib

A

-Fatal, needs to be shocked

86
Q

Wolf-Parkinson-White

A
  • Anamoulous connection through fibrous layer separating atria and ventricles.
  • Will conduct SVT at faster rythm and may cause V Tach
  • Delta wave will be present on EKG
87
Q

1st degree A/V block

A
  • Lengthening of PR interval to more than .2 seconds

- Generally assymptomatic but may progres

88
Q

Second Degree type 1

A
  • Continually lenghtening PR until finally a QRS is dropped

- May progress, but is usually assymptomatic

89
Q

Second Degree Type 2

A
  • There are regular P intervals that are not followed by QRS

- May need to be paced and may progress to third degree

90
Q

Third Degree Heart Block

A
  • Complete disconnection between atria and ventricles
  • Can be caused by Lyme Disease, Lupus
  • Inferior wall MI can damage AV node
91
Q

Atrial Naturetic Peptide

A
  • Peptide hormone released by atrial myocytes in response to stretch. Indicates hypervolemic state.
  • Directly opposes aldosterone and even inhibits release
  • Works through a cGMP mediated second messenger system to: Increase Diuresis (Constrict efferent and dilate afferent), Inhibit ENaC in Collecting Duct and NCC in DCT, Direct vasodilation, prevents unfavorable ang 2 mediated cardiac remodelling
92
Q

Aortic Arch

A
  • Chemo and Baroreceptors transmit signals via CN 10 to nucleus solitarius
  • Aortic arch only responds to elevated BP through vagal induced bradychardia
93
Q

Carotid Body

A
  • Chemo and Baroreceptors transmit signals via CN 9 to nucleus solitarius
  • Carotid body responds to both increase and decrease BP
94
Q

Baroreceptors

A
  • Firing rate is proportional to stretch. Increased stretch means increased firing rate and hypertension induced vagal stimulation. M2 is Gi
  • Decreased stretch from hypotension is sensed as decreased firing rate and SANS stimulation
95
Q

Cushing Reflex

A
  • Increased ICP means cerebral ischemia and increased SANS tone to increase perfusion. Leads to systemic hypertension
  • Hyperstension leads to baroreceptor stretch and vagally mediated bradychardia
96
Q

Peripheral Chemoreceptors

A
  • Located in carotid body and aortic arch. Sense O2, CO2, and pH
  • Under normal circumstances play a minimal role in respiratory drive
  • If patient has COPD or sleep apnea, or Narcotic overdose then these take over and oxygen may cause apnea (Mainly with narcotics)
97
Q

Central Chemoreceptors

A
  • Chemoreceptor trigger zone in medulla at wall of 4th ventricle next to area postrema senses pH of CSF which is proportional to CO2 concentration.
  • CTZ also plays a role in vommiting
98
Q

Carotid Massage

A

-Increases pressure in carotid artery and increases firing rate leading to vagal stimulation from nucleus solitarius and M2 mediated Gi decrease in HR

99
Q

Pulmonary Capillary Wedge Pressure

A
  • Can be used to measure LAP

- Increased in aortic stenosis

100
Q

Autoregulation Heart

A

-Co2, O2, NO

101
Q

Autoregulation Skin

A

SANS

102
Q

Autoregulation Muscle

A

Lactate, K, NO

103
Q

Autoregulation Lungs

A

-Hypoxic induced vasoconstriction

104
Q

Congenital Heart Defects

A
  • Occur during embryogenesis weeks 3-8
  • Can cause early cyanosis (R to L)
  • Late Cyanosis (Eisenmiengers with L to R)
105
Q

Tetrology of Fallot

A
  • Pulmonary Stenosis determines extent of shunt and disease. RVH, VSD, Overriding Aorta
  • Associated with DiGeorge and is most common cause of early cyanosis, clubbing, polycythemia, etc
  • Boot shaped large heart from RVH
  • Patients will squat when they get “Tet” or hypoxic spells to increase systemic resistance and shunt more blood through stenosed pulmonary artery, increasing oxygen saturations
106
Q

Transposition of the great vessels

A
  • Right heart circulation returns to right heart, Left to Left
  • most commonly seen in DM mothers
  • Must have ASD or more likely PDA or else child will die. Tx with PGE1
  • Absence of aorticopulomary spiraling during development (NC involved)
107
Q

Presistent Truncus Arteriosis

A
  • Failure of septation of truncus leads to conjoined outflow tract.
  • Early cyanosis with splitting of blood between circulations.
  • Failure of Neural Crest cells to properly migrate, seen in DiGeorge Syndrome.
  • VSD is almost always present with associated cardiomegally and pulmonary hypertension
108
Q

Tricuspid Atresia

A
  • Lack of development of tricuspid valve and hypoplasia of RV
  • Requires ASD to get blood from RA to LA and VSD to get blood from LV to pulmonary circulation
  • Early Cyanosis and LVH
109
Q

TAPVR

A
  • Pulmonary veins drain into the SVC (Common Cardinal Vein) and coronary sinus
  • Cyanosis, must maintain PDA or else die, give PGE1. Also often require ASD.
110
Q

VSD

A
  • Most common congenital anomaly
  • Almost always occurs in the membranous portion and commonly is small and not clinically detectable. Often regresses.
  • Highly associated with FAS
  • Initially a L to R shunt that may cause pulmonary hypertension and right ventricular hypertrophy, reversing shunt. Eisenmiengers syndrome.
  • Holosystolic harsh murmur at left sternal border
111
Q

Osteum Secundum Defect

A
  • Most common ASD, too large of osteum secundum or failed closure
  • Also highly associated with FAS
  • Fixed splitting of S2
  • May progress to eisenmiengers depending on severity
  • May present with MVP
112
Q

Osteum Primum Defect

A
  • Problem with endochardial cushion tissue that forms AV septation.
  • Seen almost exclusively in downs syndrome
  • Fixed split S2 that may progress to Eisenmiengers
113
Q

Patent Foramen Ovale

A
  • Very common, incomplete fusion of septum secundum and primum after birth
  • Can lead to paradoxical embolism where DVT can cause a stroke
114
Q

Eisenmiengers Syndrome

A
  • L to R shunt reversal that leads to late cyanosis

- Polycythemia, clubbing, heart failure, arrythmia

115
Q

Ebstiens Anomaly

A
  • Displacement of tricuspid valve towards the apex of the heart
  • Hypoplastic RV with enlarged RA
  • Seen in mother taking Lithium for bipolar
  • May also show conduction defects
116
Q

PDA

A
  • Ductus arteriosus normally bypasses lungs during fetal life
  • With increased oxygen sat of blood, loss of PGE leads to closure
  • If persistent may cause lower extremetiy cyanosis, pulmonary hypertension, RVH,
  • Continuous Machine like murmur at infraclavicular line, widened pulse pressures
  • Congenital Rubella is common cause, also preterm birth and downs syndrome
117
Q

Congenital Rubella

A
  • PDA, Deafness, and cataracts

- Mother will have flu like symptoms, aches, and rash

118
Q

Infantile Coarctation

A
  • Preductal coarctation means that a large portion of systemic blood volume will be coming from pulmonary deoxygenated blood.
  • Leads to differential cyanosis of lower extremeties
119
Q

Adult Coarctation

A
  • Post ductal coarctation
  • Upper extremity hypertension means there will be minimal mixing but there will be lower extremity hypotension/weakened pulses
  • Will cause internal thoracic arteries to increase and provide collateral circulation leading to characteristic rib notching on X-Ray
120
Q

22q11 DiGeorge

A

Neural Crest impaired migration

  • CATCH 22
  • Tetrology of fallot, persistant truncus
121
Q

Downs

A
  • Endochardial cushion defect which normally makes AV septum
  • ASD osteum primum
  • VSD
122
Q

Rubella

A
  • Mother gets rash, cold like symptoms
  • Baby gets PDA, Cataracts, Deafness
  • Can also have septal defects
123
Q

Turner Syndrome

A

-Bicuspid aortic valve and infantile coarcration (Cyanosis because of preductal coarctation)

124
Q

Marfans/ED

A
  • Medial Cystic Necrosis””

- Ascending Aortic anyeruism that leads to aortic root dilation and aortic insufficency

125
Q

Diabetes in Mother

A

Transposition of Great Vessels

126
Q

HTN

A

Classified as greater than 140/90

  • Predisposes to atherosclerosis, arteriolosclerosis, anyeurism
  • Most primary and multifactorial
127
Q

Fibromuscular Dysplasia

A

-Seen in a female most comonly in renal artery and causes seondary HTN

128
Q

Malignant HTN

A

greater than 200/120

  • Often caused by runaway loop with kidney
  • Fibrinoid necrosis and hyperplastic arterioloscerosis
  • Risk of subarachnoid hemorrhage and neurologic sequella
  • Kidney often has a shrunken flea bitten appearance
129
Q

Fibrinoid Necrosis

A

-Malignant Hypertension, Vasculitis, and Pre-eclampsia

130
Q

Hyperlipidemia Signs

A

-Atheromas, Corneal Arcus (Seen commonly in elderly)

131
Q

Mockenbergs medial calcification

A
  • Calcific deposits in the media, most commonly in the radius and the ulnar arteries
  • Usually clinically silent, but can reduce arterial compliance
132
Q

Hyaline arteriolosclerosis

A
  • Deposition of proteinacous material in the ECM of arterioles
  • Most commonly secondary to diabetic NEG and HTN
133
Q

Nephroclerosis

A

-Hyaline arteriolosclerosis of renal arterioles leads to positive feedback loop of occlusion, decreased GFR and increased renin/HTN

134
Q

Atherosclerosis

A
  • Intimal Thickening!!!
  • Complex long term process, begins with endothelial injury (bifurcations, HTN, etc) allows for entry of LDL that is subsequently oxidized and consumed by macrophages through scavenger receptors
135
Q

Fatty Streaks

A
  • Oxidized lipid inside functional macrophages. Macrophages then die and spill contents leading to further inflammation
  • Endotheilial cells release cytokines (PDGF, FGF) that cause smooth muscle migration from medial layer to lay over top of the necrotic lipid core
136
Q

Atheroma

A
  • Has lipid core and fibromuscular cap. Smooth muscle cells are most imporatant regulators of smooth muscle cap. Platelets can release cytokine to call in smooth muscle cells. Reorganization fo fibromusclar cap with colalgenous changes and calcification lead to mature atheroma
  • Mature atheroma can rupture at neck exposing lipid core, collage, and tissue thromboplastin leading to activation of coagulation cascade
137
Q

Consequences of atherosclerosis

A
  • Anyeurism: Increased diffusion barrier and altered wall stresses lead to anyeurism formation, especially AAA
  • Stenosis: Plaque occlusion of 70% of lumen leads to iscehmic damage to cells downstream (Stable angina)
  • Infarction: Rupture leads to occlusion and ischemic cell death
138
Q

Atheroma locations

A
  • Often form at bifurcations, turbulent flow leads to increased risk of endothelial damage
  • AAA most common then coronary, then popliteal, then carotid
139
Q

Aortic Anyeurism (non AAA)

A
  • Located in the proximal aorta
  • Related to CT disease (Marfans, ehlers danlos, cystic medial necrosis), syphilis causing and endarteritis, HTN
  • Most commonly located in ascending aorta
  • Major risk is dissection and rupture
  • Also cause aortic regurgitation
140
Q

AAA

A
  • Lack of vasovasorum combined with atherosclerotic induced diffusion barrier leads to increased weakness of intima and formation of AAA
  • Rupture can lead to hypotension, pulsating mass, and flank pain
141
Q

Aortic Dissection

A
  • Blood breaks through intimal layer and dissects along the medial layer
  • Most common in thoracic aorta and associated with marfans, HTN, syphilis, Bicuspid Aortic valve
  • Goes forward and can lead to rupture, blood loss
  • Goes backward can bleed into pericardial sac and lead to tamponade
142
Q

Stable Angina

A
  • Pain that is releived by rest, caused by stenosis
  • ST depression on EKG
  • Tx: Rest and nitrates
143
Q

Prinzmetals angina

A
  • Pain unrelated to exercise caused by vasospasm
  • ST elevation because of transmural ischemia
  • Rest
144
Q

Unstable angina

A
  • Pain at rest that is caused by plaque rupture and incomplete occlusion, carries risk of MI
  • Tx: rest and nitrates, and ER eval
  • ST depression because of subendochardial ischemia
145
Q

Coronary Steal

A

-Vasodilation causes a non-stenosed portion of the heart to steal perfusion pressure from a stenosed portion of heart

146
Q

Sudden Cardiac Death

A
  • Death within one hour of onset of cardiac ischemia almost always caused by arryhtmias.
  • Vast majority caused by MI
147
Q

Chronic Ischemia

A

-Longstanding ischemic damage leads to CHF

148
Q

Hibernating Myocardium

A
  • Oxygen deprivation leads to ATP depletion and loss of contraction in 60 seconds.
  • Cells are still viable beyond that phase and minimal oxygen may keep alive but not functioning.
  • Reprofusion leads to reactivation of myocardium
149
Q

LAD MI

A
  • Most Common, appears in leads V1-V4

- Supplies the anterior wall of left ventricle and anterior 2/3 of interventricular septum

150
Q

RCA MI

A
  • Second most common, leads I, II, AvF
  • Supplies AV and SA nodes, also right ventricle, and in most indivudials (R dominant 85%) posterior 1/3 of interventricular septum
151
Q

LCX MI

A
  • Third most common, leads v5-v6 and AvL
  • Supplies the posterior left ventricular wall and the lateral free wall. In left dominant circulation (5-10%) supplies posterior 1/3 of interventricular septum
152
Q

MI Changes 0-4 hours

A
  • No gross or histologic changes. May appear reddened grossly.
  • Arryhtmia, cardiogenic shock are most important risk factors
153
Q

MI 4-24 hours

A
  • Coagulative necrosis occurs and contraction bands with the return of Ca
  • No cellular infiltrate
  • Biggest risk is Arrythmia
  • Enzymes become visible 2-4 hours post, before best diagnosis is clinical and EKG
154
Q

MI 1-3 Days

A
  • Neutrophilic infilration.

- If infarction is transmural there is risk of fibrinous pericarditis with friction rub.

155
Q

MI 3-7 Days

A
  • Macrophage infiltration
  • Risk is rupture of ventricular free wall (LCX) causing tamponade. Rupture of interventricular septum (RCA, LCA) leading to VSD
  • Can also be anyeurism and mural thrombus.
  • Papillary rupture leading to mitral regurg
156
Q

MI 1-3 weeks

A
  • Granulation tissue (type 3 collagen)

- Risk in anyeurism

157
Q

MI 3 weeks +

A
  • Granulation tissue replaced by scar (type 1 collagen)

- Dresslers syndrome - autoimmnue pericarditis due to exposure to pericardial antigens

158
Q

Dilated Cardiomyopathy Pathophys

A
  • Eccentric hypertrophy, sarcomeres added in series leads to dilated heart and systolic dysfunction
  • Most are idiopathic, can be familial and multifactorial
  • Will have S3 (Excess volume), enlarged heart massively on imaging
  • TX: ACEI, Digoxin, Diuretics, Transplant
159
Q

Dilated Cardiomyopathy Causes

A
  • Alcohol
  • Wet Beri Beri (Thiamine). Wet is Cardiovascular, dry is skin, muscle, neuro
  • Chagas
  • Doxyrubicin/Danorubicin/Adriomycin
  • Coxackie B
  • Tachychardia prolonged (cocaine, thyrotoxicosis)
  • Peripartum (Elevated volume of pregnancy not appropriately compensated)
  • Hemochromatosis (can also be restrictive)
160
Q

Hypertrophic Cardiomyopathy

A
  • Diastolic dysfunction caused by disorganized growth of cardiac myocytes. Assymetric concentric hypertrophy
  • Inherited in an AD pattern, most commonly related to myosin heavy chain
  • Biopsy will show disorganized cardiomyocytes
  • Also seen in Friedrichs ataxia and is cause of death in these patients
  • S/S: Normal size heart on imaging, S4 because of increased resistance to fill, dynamic outflow obstruction caused by mitral leaflet and enlarged septum leading to frequent fainting and a systolic murmur.
  • Most common cause of death is arryhtmia
  • Tx: Beta blockers and Ca Channel Blockers
161
Q

Restrictive or Obliterative Cardiomyopathy

A
  • Deposition of material or fibrosis of endochardium leading to impaired filling and diastolic failure
  • Decrease preload, increase RAP
  • Caused: Sarcoidosis, Amyloidosis, Loefflers (Eosiniophils in lungs release MBP and damage endocardium), Endocardial fibroelastosis (Seen in kids, also hydrocephalus and cataracts), Post radiation fibrosis, hemochromatosis.
162
Q

CHF

A
  • Defective heart function leads to backup of blood and systemic hypoperfusion.
  • Most commonly from DCM, longstanding HTN, etc
  • Dyspnea, fatigue, rales, edema
  • Tx: ACEI, Beta blockers if not decompensating, spironolactone, Thiazides and furosemide for symptomatic relief (Pulmonary edema)
163
Q

Left Heart Failure

A

Most commonly occurs first

  • Pulmonary edema, crackles, PND, orthopnea
  • Hemosiderin laden macrophages in lungs
164
Q

Right Heart

A
  • Generally caused by left heart failure but also cor pulmonale
  • Cor pulmonale: Hypoxic vasoconstriction, lung parenchyma tissue damage
  • Hepatomegally with nutmeg liver possibly causing cardiac cirrhosis
  • Edema, JVD
165
Q

Acute Bacterial Endocarditis

A
  • Caused by Staph Aureus most commonly
  • Commonly effects the tricuspid valve
  • Suppurative vegetations with new strong murmur, may cause chorda rupture and regurgitation
  • May throw septic emboli
  • Drug users can also get: Pseudomonas, candida endocarditis.
166
Q

Subacute Bacterial Endocarditis

A
  • Takes time to progress and presents with a new murmur. Most commonly mitral valve
  • Damaged valves (RF) create nidus and increase risk
  • Fever, Roth’s spots (retinal hemorrhages), Nodes, Elevated ESR. May have ACD from longterm infection
  • Strep viridans: commonly from bacteriemia following dental procedure.
  • Staph epidermididis: Prosthetic valves (biofilm)
  • Step Bovis: Colorectal carcinoma
167
Q

Nonbacterial Endocarditis

A
  • Liebmann Sacs: Sterile vegetations on both sides of mitral valve
  • Hypercoagulability: Mucinous adenocarcinoma commonly
168
Q

Rheumatic Fever

A
  • Post GAS infection leads to type 2 mediated molecular mimicry of cardiac CT and muscle. Based on M protein
  • Elevated ASO titer is necessary
  • JONES: Joints, Pancarditis, Nodes, Erythema Marginatum, Syndenham corea
  • Prevented with antibiotics
  • Can damage Mitral valve and lead to early mitral regurg and later to mitral stenosis: Fibrosis of chorda
169
Q

Rheumatic myocarditis

A
  • Type 2 to CT of heart. T cell and macrophage infiltration generally
  • Aschoff bodie is casseating granuloma in heart tissu
  • Anitschkow cells are macrophages with catipillar nuclei
170
Q

Acute pericarditis

A
  • Inflammation of the pericardial sac.
  • Presents with Pain that is worse with breathing a lying on back and better with leaning forward
  • EKG will show diffuse elevations in ST segments and PR depression
  • Heart sounds will be distant
171
Q

Fibrinous Pericarditis

A
  • Post transmural MI neutrophil exudate
  • Uremia, Radiation, Dressler’s
  • A friction rub can be heard
172
Q

Serrous pericarditis

A
  • Complication of viral infection (Most Common) and Chronic inflammation (RA/Lupus)
  • If chronic can get restrictive pericarditis with Kussmaul sign and pericardial knock
173
Q

Suppurative Pericarditis

A

-Acute bacterial infection, rare anymore

174
Q

Cardiac Tamponade

A
  • Fluid in pericardial sac that inhibits filling leading to hypotension
  • EKG will show diffuse blunting because of interference with electrical signal
  • Pulsus paridoxus, JVD, Distant heart sounds and tachycardia
175
Q

Pulsus Paridoxus

A
  • Decrease in systolic blood pressure by greater than 10mmHG during inspiration.
  • Caused by compression of LV from increased intrathoracic pressure
  • Tamponade, pericarditis, COPD, Asthma, OSA, Croup
176
Q

Syphilitic Heart Disease

A
  • 3 Syphilis causes an endarteritis that compromises bloodflow to aortic vaso vasorum
  • Leads to medial weakening and dilation (Anyeurism)
  • Ascending aortic rupture, or more commonly aortic regurgitation
177
Q

Caridac Myxoma

A
  • Most common primary cardiac tumor in adults.
  • Tumor of connective tissue and is a myxoid stroma,
  • Almost always presents in atrium and may cause a ball valve with the ventricle
  • Frequent syncopal episodes.
178
Q

Rhabdomyoma

A
  • Most common primary cardiac tumor in kids.
  • Associated with Tuberous Sclerosis (TSG mutation)
  • Nonmalignant
  • Most common associations with TS cause brain hamartomas
179
Q

Kussmauls Sign

A
  • Increase in JVP with inspiration. Normally there should be a decrease.
  • Caused by obstruction of RV filling
  • Tamponade, Cardiac Tumor, restrictive cardiomyopathies, also constrictive pericarditis (pericardial knock)
180
Q

Raynauds phenomenon

A
  • Vasopspasm of the peripheral vessels in response to cold and stress.
  • Painful blue discoloration
  • Can be idiopathic in young women
  • Also sign of systemic autoimmune disease: SLE, Scleroderma, Mixed connective tissue, CREST
181
Q

Giant Cell Arteritis

A
  • Granulomatous segmental inflammation of branches of carotid artery
  • May cause Headache, jaw pain, blindness
  • May also present with systemic symptoms and polymyalgia rheumatica (Pain and stiffness in large joints of neck, hips, and shoulders)
  • Massively elevated ESR
  • Emergent treatement with steroids
182
Q

Takyosu arteritis

A
  • Granulomatous thickening of branches of the aortic arch
  • Most commonly seen in younger asian females
  • Pulseless disease because of weakness of pulses in upper extremeties
  • Often accompanied by systemic signs
  • Tx: Steroids and cyclophosphamide
183
Q

Polyarteitis Nodosa

A
  • Young Adults, Involves smaller arteries of end organs.
  • Immune complex mediated
  • FIbrinoid necrosis in certain sections with healing and fibrosis leading to scar. Get anyeurism and scars leading to pearls on a sting appearance
  • Commonly effects renal aretry leading to HTN
  • Also effects GI arteries leading to melena and abdominal discomfort
  • Also commonly palpable purpura on the skin
184
Q

Kawasaki Disease

A
  • Medium vessel inflammation most comonly occuding in the coronary vasculature.
  • MI in young kids. Most commonly seen in young asians.
  • Presents similiarly to viral illness with conjunctivits, strawberry tongue. Also will have palms and soles rash.
  • Tx: ASA to prevent clots and MI and IVIG.
  • Usually self resolves.
185
Q

Beurger Disease

A
  • Thrombosing vasculitis of the distal digets leading to gangrenous necrosis and autoamputation.
  • Seen only in smokers. Commonly males less than 40.
  • Tx is smoking cessation
186
Q

Wegners

A
  • Small vessel granulmoatous inflammation with necrosis
  • Involves nasal mucosa, hemoptysis (lung) and Pauci immune RPGN with nephrititc syndrome
  • C-ANCA positive
  • Tx: steroids and cyclophosphamide
187
Q

Microscopic Polyangitis

A
  • Necrotizing, non-granulomatous vasculitis of small vessels with neutrophilic infiltrate
  • Can be a cause of pauci immune RPGN, palpable purpura are often commonly felt
  • P-ANCA
188
Q

Churgg-Straus

A
  • Necrotizing granulomatous vasculitis of small vessels with eosinophilic infiltrate.
  • Presence of elevated IgE, Eosinophils, asthma
  • P-ANCA positive.
  • Can be a cause of RPGN
189
Q

HSP

A
  • IgA immune complex deposition in small arteries
  • Presents most commonly in kids following URI with palpable purpura on the extensor surfaces and with GI pain.
  • Arthritis is also a common complaint.
  • May also cause IgA nephritic syndrome in kidney.

Boards Path (20 decks)

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