CV Pathology

Question 1

R –> L Shunts

Answer 1

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

Question 2

Persistent Truncus Arteriosus

Answer 2

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

Question 3

Transposition of the Great vessels

Answer 3

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

Question 4

Tricuspid Atresia

Answer 4

No tricuspid valve + hypoplastic RV

Only viable if: ASD & VSD

Question 5

Tetrology of Fallot

Answer 5

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

Question 6

TAPVR (total anomalous pulmonary venous return)

Answer 6

Pulm veins drain into R heart

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

Question 7

Ebstein Anomaly

Answer 7

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

Question 8

L to R shunts

Answer 8

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

Frequency: VSD>ASD>PDA

Question 9

Down Syndrome: asc cardiac defects

Answer 9

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

*have a lower baseline HR

Question 10

Drugs that give SLE like symps

Answer 10

• Quinidine

- Hydralazine

Question 11

Congenital Cardiac Defect asc w/ Fetal Alcohol syndrome

Answer 11

VSD, ASD, PDA

Tetrology of Fallot

Question 12

Congenital Cardiac Defect asc w/Congenital Rubella

Answer 12

PDA
Pulm artery stenosis
Septal defects

Question 13

Congenital Cardiac Defect asc w/ Down Syndrome

Answer 13

VSD
ASD
AV septal defect (endocardial cushion defect)

Question 14

Congenital Cardiac Defect asc w/ Diabetic mom

Answer 14

Transposition of great vessels

Question 15

Congenital Cardiac Defect asc w/Marfan Syndrome

Answer 15

Mitral Valve Prolapse
Thoracic aortic aneuryms/dissection
Aortic Regurg

Question 16

Congenital Cardiac Defect asc w/ fetal lithium exposure

Answer 16

Ebstein anomaly

Question 17

Congenital Cardiac Defect asc w/ Turner Syndrome

Answer 17

BAV

Coarctation of aorta

Question 18

Congenital Cardiac Defect asc w/ Williams Syndrome

Answer 18

Supravalvular aortic stenosis

Question 19

Congenital Cardiac Defect asc w/ 22q11

Answer 19

Truncus Arteriosus

Tetrology of Fallot

Question 20

Hyperlipidemia signs

Answer 20

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)

Question 21

2 types of Arteriolosclerosis

Answer 21

=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"

Question 22

Atherosclerosis

Answer 22

-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

Question 23

Arteriosclerosis

Answer 23

=hardening of BV + thickening + loss of elasticity

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

Question 24

Most common location of Aortic rupture

Answer 24

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

Question 25

0-24 Hrs after MI

Answer 25

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

Question 26

1-3 days Post Mi

Answer 26

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

Complications:

• fibrinous pericarditis
• Arrhythmias

Question 27

3-14 days post MI

Answer 27

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

Complications;

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

Question 28

2wks-months post MI

Answer 28

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

Complications:

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

Question 29

What predisposes ppl to endocarditis

Answer 29

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

Question 30

Tricuspid valve endocarditis:

Asc, causes

Answer 30

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