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Step1 > CV Pathology > Flashcards

CV Pathology Flashcards

1
Q

R –> L Shunts

A 
Blue babies (R-->L: eaRLy cyanosis)
5 T's:
  1. Truncus Arteriosus (1 vessel)
  2. Transposition (2 switched vessels)
  3. Tricuspid Atresia (3=Tri)
  4. Tetrology Of Fallot (4=tetra)
  5. TAPVR (5 letters)
Worsened by:
   i. ^ pulm resistance (crying, hypoventilation, acidosis)
   ii. Decreased SVR: hypotension, histamine, sepsis
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2
Q

Persistent Truncus Arteriosus

A

Truncus arteriosus fails to divide into pulm trunk & aorta
-lack of aorticopulmonary septum formation
Asc:
-VSD

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3
Q

Transposition of the Great vessels

A

=Failure of aorticopulmonary septum to spiral
Only viable if there’s shunt:
-VSD, PDA, Patent foramen ovale
Tx: surgery

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4
Q

Tricuspid Atresia

A

No tricuspid valve + hypoplastic RV

Only viable if: ASD & VSD

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5
Q

Tetrology of Fallot

A 
Characteristics: (PROVe)
  i. Pulmonary infundibular stenosis
  ii. RVH
  iii. Overriding aortaf
  iv. VSD
Tet spells:
   crying --> Pulm resistance --> ^shunt
Squatting: ^SVR --> decrease shunting
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6
Q

TAPVR (total anomalous pulmonary venous return)

A

Pulm veins drain into R heart

Asc: ASD or PDA to allow for R–>L shunting

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7
Q

Ebstein Anomaly

A

Displacement of Tricuspid valves into RV–>atrializing the ventricle
Can be caused by Lithium in utero

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8
Q

L to R shunts

A

L to R shunts: LateR cyanosis (due to Eisenmenger)

Frequency: VSD>ASD>PDA

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9
Q

Down Syndrome: asc cardiac defects

A
  • VSD
  • ASD
  • AV septal defects
  • tetrology of fallot

*have a lower baseline HR

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10
Q

Drugs that give SLE like symps

A
  • Quinidine

- Hydralazine

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11
Q

Congenital Cardiac Defect asc w/ Fetal Alcohol syndrome

A

VSD, ASD, PDA

Tetrology of Fallot

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12
Q

Congenital Cardiac Defect asc w/Congenital Rubella

A

PDA
Pulm artery stenosis
Septal defects

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13
Q

Congenital Cardiac Defect asc w/ Down Syndrome

A

VSD
ASD
AV septal defect (endocardial cushion defect)

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14
Q

Congenital Cardiac Defect asc w/ Diabetic mom

A

Transposition of great vessels

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15
Q

Congenital Cardiac Defect asc w/Marfan Syndrome

A

Mitral Valve Prolapse
Thoracic aortic aneuryms/dissection
Aortic Regurg

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16
Q

Congenital Cardiac Defect asc w/ fetal lithium exposure

A

Ebstein anomaly

17
Q

Congenital Cardiac Defect asc w/ Turner Syndrome

A

BAV

Coarctation of aorta

18
Q

Congenital Cardiac Defect asc w/ Williams Syndrome

A

Supravalvular aortic stenosis

19
Q

Congenital Cardiac Defect asc w/ 22q11

A

Truncus Arteriosus

Tetrology of Fallot

20
Q

Hyperlipidemia signs

A

Xanthomas:
-plaques/nodules of lipid filled histiocytes in skin
(esp eyelids)
Tendinous Xanthoma:
-lipid deposit in tendon (esp achilles)
Corneal Arcus:
-lipid deposit in cornea (ok in elderly)

21
Q

2 types of Arteriolosclerosis

A 
=Arteriosclerosis (Hardening, wall thickness, loss of elasticity) -small arteries & arterioles
1. Hyaline
   -thickening of BV walls
   -essential HTN, DM
2. Hyperplastic
  -thickening of BV walls + smooth m
  -severe HTN
  "onion skin layers"
22
Q

Atherosclerosis

A

-endothelial damage of muscular/elastic arteries
-due to cholesterol plaque build up in tunica intima
Abdominal aorta > coronary a>popliteal a>carotid a
-abd: no vasovorum after renal a’s –> ischemic damage
RF:
-smoking, ^LDL, HTN, diabetes
-age, sex (M/post menopause>F), FH
Pathogenesis:
1. Fatty streak:
Endothelial damage/dysfxn: LDL enter intima –>
macros phagocytose the oxidized LDL –> foam cells
2. Plat growth factor –>Smooth m migrate
–>proliferate, ECM deposition
3. Rupture –> thrombus formation
Complications:
-aneurysms
-ischemia, thrombus, emboli, infarcts
-peripheral vascular dz

23
Q

Arteriosclerosis

A

=hardening of BV + thickening + loss of elasticity

  1. Monckeberg (small-medium, medial calcific sclerosis)
  2. Arteriolosclerosis
  3. Atherosclerosis
24
Q

Most common location of Aortic rupture

A

Aortic Isthmus (beginning of desc aorta, after L subclavian artery)

25
Q

0-24 Hrs after MI

A 
2-4 hours: no changes
4-8 hrs: Early coagulative necrosis
  -release of cell contents into blood
  -wavy myofibers 
   (due to mix of intact contractile fibers & noncontractile)
4-24 hrs:
  -Dark mottling
       -Tetrazolium stain: pale
12-24 Hrs:
  -Contraction bands
       -reperfusion injury -->ROS-->^Ca-->hypercontraction
  -Neutrophils
Complications:
   -V arrhythmia
   -HF
   -Cardiogenic shock
26
Q

1-3 days Post Mi

A
  • Coagulative necrosis
  • yellow w/swelling
  • ^neutrophils, dilated BV (hyperemic)

Complications:

  • fibrinous pericarditis
  • Arrhythmias
27
Q

3-14 days post MI

A
  • max yellow w/hyperemic red borders
  • Clearance of necrotic myocardium
  • granulation @ margins
  • Macrophages

Complications;

  • myocardial rupture
    - ->tamponade, VSD, or mitral regurg
28
Q

2wks-months post MI

A
  • Completion of collagen deposition
  • Grey white scar (type I collagen)
  • mature fibrous tissue

Complications:

  • Dressler
  • HF
  • Arrhythmias
  • ventricular aneuryms (–> mural thrombus)
29
Q

What predisposes ppl to endocarditis

A
  • rheumatic heart dz
  • mitral valve prolapse
  • BAV
  • Prosthetic valves
  • Degenerative calcific valvular stenosis
  • congenital defects
30
Q

Tricuspid valve endocarditis:

Asc, causes

A 
Asc: IV drug use
Common causes:
   -Staph Aureus
   -psuedomonas Aeruginosa
   -Candida

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