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Pathology > Agenesis, Aplasia, Hypoplasia > Flashcards

Agenesis, Aplasia, Hypoplasia Flashcards

1
Q

What are the 2 major classes of disturbances of cell growth?

A
  • congenital

- acquired: after normal development

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2
Q

Growth

A

Increase in the parenchymal mass of a tissue, resulting from an increase in cell size or number, or both

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3
Q

Growth could be _____ or ______

A
  • developmental
  • response to abnormal stimulus: controlled (hypertrophy, hyperplasia, metaplasia), or uncontrolled (dysplasia, neoplasia)
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4
Q

________ is necessary to maintain the tissue and the animal

A

Continued cell proliferation

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5
Q

Quantitative

A
  • increased capacity (hypertrophy, hyperplasia)

- decreased capacity (atrophy)

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6
Q

Qualitative

A

Alteration of cell form to adapt (metaplasia)

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7
Q

_____, _____, and _____ are all lack of proper growth potential

A

Agenesis, aplasia, hypoplasia

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8
Q

-plasia

A

Change in the degree of cell proliferation

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9
Q

-ophy

A

Change in the degree of cell/tissue size

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10
Q

Effects of developmental defects on various organs

A
  • in vital organs: death in utero

- in dispensable tissues (spleen, kidney): relatively normal life

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11
Q

_____ and _____ are relatively common, especially in the reproductive tract

A

Agenesis and aplasia

- especially noted in males

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12
Q

What are the 3 stages of development?

A
  • chromosomes
  • gonad
  • tubular structures
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13
Q

Gonads develop from what 4 cell populations?

A
  • germ (yolk sac)
  • mesnechyme (supporting cells)
  • coelom epithelium (steroid cells)
  • mesonephros epithelium (epithelium)
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14
Q

Agenesis

A

Without beginning

- the complete failure of an organ to develop

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15
Q

Aplasia

A

Without formation

  • the organ had a beginning, but little else
  • rudimentary nub or cord of tissue
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16
Q

______ determines development of the gonad

A

Chromosomal sex

- absence of the Y chromosome causes ovaries to form

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17
Q

Y chromosomes

A

Mullerian inhibiting substance (from Sertoli cells) causes regression of the female tract and testosterone (from interstitial cells) stimulates Wolffian duct system

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18
Q

Suppressed testosterone leads to _____ of the male tract

A

Aplasia

- affects: epididymis, vas deferens, glands

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19
Q

Defects in the testosterone target tissue receptor

A

Testosterone causes virilization of Wolffian ducts, while dihydrotestosterone induces virilization changes in the urogenital sinus and external genitalia

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20
Q

Myriad abnormalities

A

Intricate timing of many events required

- failure of normal maturation, hypoplasia, aplasia of the genitalia

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21
Q

Segmental aplasia of paramesonephric duct

A

Any part affected, little known of etiology

  • absent segments of vagina, cervix, uterus
  • cattle: absence of uterine segments may allow CLs to persist (infertility)
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22
Q

3 categories of anomalies in external phenotype

A
  • abnormal/missing sex chromosome
  • female karyotype
  • male karyotype
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23
Q

Abnormal/missing sex chromosome

A
  • XXY: Klinefelter’s

- XX/XY: chimerism

24
Q

Female karyotype

A

XY disorders

  • testis development
  • androgen synthesis defects
25
Q

Male karyotype

A

XX disorders

  • ovary development
  • androgen excess
26
Q

XX and XY disorders are also divided into _____

A

SRY: sex determining region of Y chromosome

27
Q

Dysgensis

A

Defective development

28
Q

Chimerism

A

Where animals have 2 or more somatic cell types with different chromosome constitiutions

29
Q

Freemartins

A

Female twin of the male calf

  • vascular anastomoses allow the male calf’s gene products to alter the female’s phenotype
  • Sertoli cells, seminiferous cords in the ovaries
  • hypoplastic ovaries
  • hypoplastic/dysplastic tubular genitalia
30
Q

Phenotypic females with masculinization

A

XX, DSD, SRY -

  • hermaphrodites
  • polled goats
  • may interfere with fertility/parturition (are usually minor)
31
Q

XY, SRY+

A

Usually minor in nature (cystic remnants of ducts)

- more significant cases have a female phenotype

32
Q

Abnormal gonad development drives _______

A
  • phenotypic anomalies
  • abnormal androgen production
  • lack of androgen receptors
33
Q

Androgen receptors are lacking, testosterone is present, female genitalia

A
  • male pseudohermaphrodites
  • testicular feminization
  • XY sex reversal
34
Q

Persistent Mullerian duct syndrome

A

Occurs in mini schnauzers

  • XY males with normal sex organs (often cryptorchid) and a complete paramesonephric system (uterus)
  • lack anti-Mullerian hormone or its receptor
  • can still be fertile!
35
Q

Hypoplasia

A

Deficient formation

  • failure of an organ to obtain full size
  • found in young animals
  • difficult to differentiate from atrophy
  • may affect only part of an organ (especially tubular organs)
36
Q

Atresia

A

Lack of an orifice

37
Q

Hypoplasia/stenosis

A

Narrowing of lumen

38
Q

Fistula

A

Sinus tract leading from one hollow viscus to another

39
Q

Hypoplasia typically occurs ______ in development

A

Late

  • viruses, toxins that cause necrosis
  • genetic mutations in the embryo
40
Q

Congenital cerebellar hypoplasia

A

Neonatal ataxia due to viral infection during pregnancy

41
Q

What 3 diseases causes congenital cerebellar hypoplasia

A
  • feline panleukopenia virus
  • bluetongue virus in lambs
  • bovine viral diarrhea virus
42
Q

Pathogenesis of cerebellar hypoplasia

A

Germinal layer cells are specifically destroyed, and without their migration the internal granular layer doesn’t develop = cerebellar folia are small and fail to function

43
Q

Hereditary hypoplasia can occur in what 4 organs?

A
  • pituitary
  • thyroid
  • pancreas
  • kidney
  • all spontaneous!*
44
Q

Pancreatic hypoplasia in German Shepards

A

Malabsorption, weight loss, polyphagia, fatty feces

- succumb in early adulthood

45
Q

Renal hypoplasia

A

Well documented in many species

- unilateral or bilateral

46
Q

Auricular hypoplasia

A

Normal feature of some breeds

  • LaMancha goats (gopher and elf ears)
  • scottish fold cats: autosomal dominant trait, normal at birth, develop folding at 3 weeks –> may see osteodyschondroplasia
47
Q

Teratology

A

Study of congenital malformations

  • congenital
  • malformations: associated with aplasia/hypoplasia
  • abnormal genes, viruses, toxins in utero
  • deletion of critical primordial cells or substances that influence gene expression during development
48
Q

Small defects in tissues may lead to ______

A

Large lesions

- obstruction of fetal urinary tract leads to hydronephrosis

49
Q

Hydrocephalus

A

Most common congenital CNS abnormality

  • in utero virus infection, abnormalities in ependyma or ventricular system, infection with blockage of CSF outlfow or parenchymal loss
  • lesion: stenosis of mesencephalic aqueduct
50
Q

What 2 diseases result in hydrocephalus?

A
  • panleukopenia virus in cats

- parainfluenza in dogs

51
Q

Hydrocephalus pathogenesis

A

Obstruction –> ventricular pressure increases –> ventricles dilate –> ependyma atrophy –> CSF forced into brain –> edema –> degeneration and atrophy of brain –> expansion of ventricles

52
Q

Hydranencephaly

A

Cavitary anomaly of the cerebral hemispheres due to tissue necrosis in utero

53
Q

What disease results in hydranencephaly?

A

Bluetongue virus in lambs

  • due to vaccination of pregnant ewes
  • infection at 50-58 days = necrotizing encephalopathy
  • infection at 75-78 days = multifocal encephalitis leading to porencephaly
  • infection after 100 days = mild encephalitis and no malformations
54
Q

Cyclopia

A

Veratrum californicum

  • pregnant ewes ingesting plant at 10-15 gestation
  • 3 alkaloids: cyclopamine, jervine, cycloposine that inhibit sonic hedgehog pathway
  • eyes fail to divide
55
Q

Holoprosencephaly

A

Absence of midline structures leading to a proboscis with fused nasal cavities and a single eye
- single undivided cerebral lobe

Pathology (19 decks)

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