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SYSTEMIC PATHOLOGY - 1 > 2 – Congenital Heart Defects > Flashcards

2 – Congenital Heart Defects Flashcards

1
Q

3 shunts in fetal circulation

A
  • Ductus venosus
  • Foramen ovale
  • Ductus arteriosus
  • *closed after birth
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2
Q

Severe cardiac malformations

A
  • Incompatible with INTRAuterine life=embryonic death or fetal abortion
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3
Q

Cardiac malformations compatible with INTRAuterine life

A
  • Result in postnatal heart failure or sudden death
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4
Q

Minor cardiac malformations well compensated by physiologic adaptive mechanisms

A
  • Cause no clinical signs
  • Defects are incidental finding at slaughter or post-mortem examination
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5
Q

Etiological diagnosis of congenital heart defects can be due to

A
  • Genetic
  • Maternal infections (parvovirus, BVD)
  • Nutritional deficiencies (vitamin A, zinc)
  • Drugs (ex. thalidomide)
  • Other teratogens (radiation, fetal hypoxia, maternal diabetes)
  • Multifactorial
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6
Q

Most common congenital heart defects: ‘groups’

A
  • Defects that cause volume overload
    o L to R shunts
    o Valvular regurgitation
  • Defects that cause pressure overload
  • Defects that cause early cyanosis (R to L shunts)
  • Miscellaneous
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7
Q

L to R shunts examples

A
  • Patent ductus arteriosus
  • Atrial septal defect
  • Ventricular septal defect
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8
Q

Valvular regurgitation

A
  • Valvular dysplasia
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9
Q

Defects that cause pressure overload

A
  • Aortic and pulmonic stenosis
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10
Q

Defects that cause early cyanosis (R to L shunts)

A
  • Tetralogy of Fallot
  • Transposition of great arteries
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11
Q

Miscellaneous congenital heart defects

A
  • Persistant right aortic arch
  • Ectopia cordis
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12
Q

Patent ductus arteriosus (PDA)

A
  • Communication between pulmonary artery and aorta=close after birth=ligament arteriosum
  • Particularly in DOG (make it after 3 weeks)
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13
Q

Hemodynamics of patent ductus arteriosus

A
  • L to R shunt between aorta and pulmonary artery
  • Increased pulmonary blood flow (hyperflux)
  • Pulmonary hypertension
  • Pressure overload in RV and volume overload in LV
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14
Q

Left to right shunts

A
  • Increased vascular resistance -> medial hypertrophy or irreversible obstructive intimal lesions
  • Shunt reverses (R to L)
  • Late cyanosis (Eisenmenger syndrome)
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15
Q

2 ways communication between L and R atrium may occur POSTnatally

A
  1. Persistence of the fetal foramen ovale
  2. True atrial defect in which there is a failed closure of atrial septum
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16
Q

Atrial septal defect (ASD)

A
  • Minor ones have little clinical significance
  • 20% of humans, probe can be passed through, but it is not functional=no shunt
17
Q

Hemodynamics of atrial septal defect

A
  • Large defect: excessive blood flow from L to R atrium -> volume overload of R ventricle -> R ventricle hypertrophy
  • Pulmonary congestion (O2 blood returns to the lungs)
18
Q

Ventricular septal defect

A
  • One of the most common defects in domestic animals
  • High (close to AV valve) or low (close to apex=rare)
19
Q

Hemodynamics of ventricular septal defect

A
  • L to R shunt
  • R ventricle pressure and volume overload
  • R ventricle hypertrophy
  • R heart failure (if uncompensated)
  • L ventricle hypertrophy
  • *blood shunt reverse to R to L and cause cyanosis (Eisenmenger complex)
20
Q

Valvular dysplasia

A
  • Often difficult to assess post-mortem (requires experienced practioner)
  • Tricuspid dysplasia
  • Mitral dysplasia
21
Q

Tricuspid dysplastic valves show one or more of the following features

A
  • Diffuse or focal thickening of leaflets
  • Missing or short chordae tendineae
  • Thick or short papillary muscles
  • Direct fusion of leaflets to papillary muscles or the ventricular wall
22
Q

Tricuspid dysplasia

A
  • Most common in cats (dogs, retrievers)
  • ECCENTRIC hypertrophy of R ventricle
  • Massive DISTENSION of R atrium
23
Q

Mitral dysplasia

A
  • Most common in cats
  • ECCENTRIC hypertrophy of L ventricle
  • DISTENSION of L atrium
24
Q

Mitral dysplastic valves show one or more of the following features

A
  • Short thick leaflets
  • Short thickened chordae tendineae
  • Upward malposition of atrophic or hypertrophic papillary muscles
25
Q

Pulmonic stenosis

A
  • Narrowing of pulmonic vavle
  • Valvular, subvalvular, supravulvular
  • Usually due to constricting band of fibrous or muscular tissue
  • Post-stenoic arterial dilation often found in artery, distal to stenosis
26
Q

Pulmonic stenosis hemodynamics

A
  • Pressure overload of RV
  • RV hypertrophy
  • If uncompensated=R heart failure
27
Q

Pulmonic stenosis necropsy findings

A
  • Heart has broad base
  • Hypertrophic RV
  • Narrow lumen of pulmonary artery (may show post-stenotic dilation)
28
Q

Aortic and subaortic stenosis

A
  • Dogs and pigs
  • Constricting band of fibrous or muscular tissue encircling LV outflow tract
29
Q

Hemodynamics in subaortic stenosis

A
  • Pressure overload of LV
  • LV hypertrophy (concentric)
  • Post-stenotic dilation of aorta
  • If uncompensated: L heart failure w/pulmonary edema
30
Q

Tetralogy of Fallot

A
  • 4 anomalies (3 congenital, 1 consequence)
    1. VSD
    2. Overriding aorta
    3. Pulmonic stenosis
    4. R ventricular hypertrophy
31
Q

Transposition of the great arteries

A
  • VENTRICULOARTERIAL DISCORDANCE
  • Aorta arises from R ventricle
  • Pulmonary artery arises from L ventricle
  • Not able to survive unless a shunt exists for adequate mixing of blood (R to L shunt and early cyanosis)
32
Q

Persistent right aortic arch

A
  • Dogs
  • Aorta incorrectly formed from right 4th arch rather then the left
  • Trachea and esophagus enclosed by aortic arch, pulmonary artery and ligamentum arteriosum
  • No hemodynamic abnormalities or signs of heart failure
33
Q

Esophageal constriction in persistent right aortic arch

A
  • Dysphagia
  • Regurgitation
  • Megaesophagus
34
Q

Ectopia cordis

A
  • Mostly found in stillbirths or aborted fetuses
  • Animals may survive for days, weeks or more

SYSTEMIC PATHOLOGY - 1 (11 decks)

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