Chapter 10 Morphology Flashcards

1
Q

Appearance of lungs in children who die early

A

necrotic cellular debris can be seen in terminal bronchioles and alveolar ducts

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2
Q

Necrotic tissue in lungs of infant in distress

A

become incorporated within eosinophilic hyaline membranes linign the respiratory bronchioles, alveolar ducts, and alveoli

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3
Q

Membranes of lungs of infant in distress

A
  1. Made up of fibrin mixed with cell debris derived from necrotic type II pneumocytes
  2. Neutrophilic inflammatory reaction
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4
Q

Lungs of infants who survive more than 48 hours (3)

A

Alvelolar epithelium proliferates
May detach into the airspace
Undergoes partial digestion or phagocytosis by macrophages

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5
Q

Lung appearance of children in RDS

A

normal size lungs, solid, airless, reddish purple, and sink in water

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6
Q

Where does necrotizing enterocolitis occur?

A

terminal ileum, cecum, and right colon

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7
Q

Appearance of involved segment in necrotizing enterocolitis

A

distended, friable, congested, or can be gangrenous

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8
Q

Microscopic necrotizing enterocolitis

A

mucosal or transmural coagulative necrosis
ulceration
bacterial colonization
submucosal gas bubbles

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9
Q

Reparative changes in necrotizing enterocoitis

A

formation of granulation tissue and fibrosis

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10
Q

Hydrops associated with fetal anemia (4)

A

Both fetus and placenta are pale
Liver and spleen are enlarged from cardiac failure and congestion
Bone marrow has hyperplasia of erythroid precursors
Extramedullary hematopoiesis in liver, spleen, and lymph nodes

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11
Q

Why is there increased hematopoietic activity in hydrops?

A

presence in peripheral circulation of large numbers of immature red cells including retinocytes, normoblasts, and erythroblasts
*erythroblastosis fetalis

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12
Q

What is the most serious threat in fetal hydrops?

A

CNA damage known as kernicterus

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13
Q

Brain appearance in kernicterus (2)

A

Enlarged and edematous

Has yellow color - particularly in basal ganglia

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14
Q

Bilirubin level in blood for kernicterus

A

greater than 20 mg/dL in infants

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15
Q

Mucus secretion defect in nonclassic CF (3)

A

Leads to defective mucociliary action
Obstruction of bronchi and bronchioles
Crippling fatal pulmonary infections

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16
Q

What is not morphologically affected in nonclassic CF?

A

sweat glands

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17
Q

Pancreatic abnormalities in CF for mild cases

A

accumulation of mucus in small ducts

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18
Q

Pancreatic abnormalities in CF for severe cases

A

ducts are completely plugged causing atrophy of exocrine glands and fibrosis

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19
Q

Results from loss of pancreatic exocrine secretion in CF

A

impairs fat absorption and avitaminosis A can cause squamous metaplasia in pancreatic ducts

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20
Q

Meconium ileus

A

thick viscid plugs of mucus found in the small intestine that cause small bowel obstruction

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21
Q

Liver involvement in CF

A

bile canaliculi are plugged by mucus materia

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22
Q

Findings of a CF liver

A

hepatic steatosis and focal biliary cirrhosis

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23
Q

Histologic changes in salivary glands in CF patients

A

progressive dilation of ducts, squamous metaplasia of epithelium and glandular atrophy, and fibrosis

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24
Q

Pulmonary changes in CF patients

A

*most serious complication
Secondary obstruction and infection of the air passages
Bronchioles are distended with thick mucus
Marked hyperplasia and hypertrophy of cells

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25
Q

What are the 3 most common organisms responsible for lung infection?

A

haemophilus influenzae
peudomonas aeruginosa
staphylococcus aureus

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26
Q

What causes chronic inflammation in CF patients?

A

alginate-producing P. aeruginosa

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27
Q

What Burkholderia Cepacia Complex is most common in CF?

A

B. cenocepacia

Associated with cepacia syndrome

28
Q

Adult males with CF

A

likely have azoospermia and infertility

congenital bilateral absence of vas deferens

29
Q

Postmortem findings in infants who died of SIDS

A

Multiple petechiae on tymus, pleura, epicardium

Lungs are congested

30
Q

Upper Respiratory findings of an infant who died of SIDS

A

larynx and trachea show evidence of recurrent infection

31
Q

CNS findings of infant who died of SIDS

A

astrogliosis of brainstem and cerebellum

32
Q

How many neuroblastomas arise in adrenal medulla?

A

40%

33
Q

Size range of neuroblastomas

A

minute nodules (in situ lesions) to large masses more than 1g in weight

34
Q

Regression of in situ neuroblastoma lesions

A

leave only focus of fibrosis or calcification in the adult

35
Q

Transection of neuroblastoma lesion

A

soft, gray-tan tissue

36
Q

Large neuroblastoma features (4)

A

necrosis, cystic softening, and hemorrhage, foci of punctate inta-tumoral calcification

37
Q

Class neuroblastoma histology (7)

A
small primitive-appearing cells
dark nuclei
scant cytoplasm
poorly defined cell borders growing in solid sheets
mitotic activity
nuclear breakdown (karyorrhexis)
pleomorphism
38
Q

Background of neuroblastoma

A

neuropil- eosinophilic fibrillary material

39
Q

Neuropil

A

neuritic processes of the primitve neuroblasts

40
Q

Homer-Wright pseudorosettes

A

rosettes found in neuroblastomas that are filled with neuophil

41
Q

Helpful features of neuorblastoma

A

positive immunohistochemical reactions for neuron-specific enolase
membrane-bound cytoplasmic catecholamine-containing secretory granules

42
Q

Membrane-bound cytoplasmic catecholamine-containing secretory granules of neuroblastoma

A

contain central dense cores surrounded by peripheral halo

43
Q

Ganglion cells

A

in neuroblastomas that are large and have abundant cytoplasm, large vesicular nuclei and prominent nucleolus

44
Q

Ganglioneuroblastoma

A

admixed with primitive neuroblasts

45
Q

Ganglioneuroma

A

lesions contain more large cells that resemble ganglion cells with few residual neuroblasts

46
Q

Maturation of ganglion cells

A

accompanied by appearance of Schwann cells

47
Q

Presence of Schwannian stroma

A

histologic prerequisite for the designation of ganglioneuroblastoma and ganglioneuroma

48
Q

Favorable outcome for neuroblastoma

A

documenting schwannian stroma is essential

49
Q

Metastases of neuroblastomas

A

local infiltration and lymph node spread, there is pronounced tendency to spread through the bloodstream to liver lungs bone marrow and bones

50
Q

Staging for neuroblastoma

A

used to rank neuroblastoma

51
Q

Stage 1 of neuroblastomas

A

localized tumor with complete gross excision with or without microscopic residual disease
ipsilateral nonadherent lymph nodes negative for tumor

52
Q

Stage 2A of neuroblastomas

A

localized tumor with incomplete gross resection; representative ipsilateral nonadherent lymph nodes negative for tumor microscopically

53
Q

Stage 2B of neuroblastomas

A

localized tumor with or without complete gross excision
ipsilateral nonadherent lymph nodes positive for tumor
enlarged contralateral lymph nodes negative for tumor microscopically

54
Q

Stage 3 of neuroblastomas

A

unresectable unilateral tumor infiltrating across the midline with or without regional lymph node involvement
or localized unilateral tumor with contralateral regional lymph node involvment

55
Q

Stage 4 of neuroblastomas

A

any primary tumor with dissemination to distant lymph nodes, bone, bone marrow, liver, skin, and/or other organs

56
Q

Stage 4S

A

S = special
localized primary tumor with dissemination limited to skin, live, and/or bone marrow
*limited t infants younger than 1 year

57
Q

Presentation of Wilms tumor

A

large, solitary, well-circumscribed mass

58
Q

Cut section of Wilms tumor

A

soft, homogenous, tan and gray

occasional foci of hemorrhage, cyst formation, and necrosis

59
Q

Microscopic Wilms tumor characteristics

A

recognizing attempts to recapitulate different stages of nephrogeneisis

60
Q

Classic triphasic combination of Wilms tumor

A

blastemal, stromal, epithelial cell types

61
Q

Distinctive features in blasternal component of Wilms tumor

A

sheets of small blue cells

62
Q

Epithelial differentiation in Wilms tumor

A

abortive tubules or glomeruli

63
Q

Stromal cells of Wilms tumor

A

fibrocytic or myxoid

64
Q

Anaplasia in Wilms tumor

A

presence of cells with large hyperchromatic, pleomorphic nuclei and abnormal mitoses

65
Q

Mutation associated with presence of anaplasia in Wilms tumor

A

TP53 mutation

resistance to chemotherapy

66
Q

Function of p53

A

pro-apoptotic signals in response to DNA damage

67
Q

Loss of p53 function in Wilms tumor

A

explain relative unresponsiveness of anaplastic cells to cytotoxic chemotherapy