Chapter 10 Morphology Flashcards

(67 cards)

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
What are the 3 most common organisms responsible for lung infection?
haemophilus influenzae peudomonas aeruginosa staphylococcus aureus
26
What causes chronic inflammation in CF patients?
alginate-producing P. aeruginosa
27
What Burkholderia Cepacia Complex is most common in CF?
B. cenocepacia | Associated with cepacia syndrome
28
Adult males with CF
likely have azoospermia and infertility | congenital bilateral absence of vas deferens
29
Postmortem findings in infants who died of SIDS
Multiple petechiae on tymus, pleura, epicardium | Lungs are congested
30
Upper Respiratory findings of an infant who died of SIDS
larynx and trachea show evidence of recurrent infection
31
CNS findings of infant who died of SIDS
astrogliosis of brainstem and cerebellum
32
How many neuroblastomas arise in adrenal medulla?
40%
33
Size range of neuroblastomas
minute nodules (in situ lesions) to large masses more than 1g in weight
34
Regression of in situ neuroblastoma lesions
leave only focus of fibrosis or calcification in the adult
35
Transection of neuroblastoma lesion
soft, gray-tan tissue
36
Large neuroblastoma features (4)
necrosis, cystic softening, and hemorrhage, foci of punctate inta-tumoral calcification
37
Class neuroblastoma histology (7)
``` small primitive-appearing cells dark nuclei scant cytoplasm poorly defined cell borders growing in solid sheets mitotic activity nuclear breakdown (karyorrhexis) pleomorphism ```
38
Background of neuroblastoma
neuropil- eosinophilic fibrillary material
39
Neuropil
neuritic processes of the primitve neuroblasts
40
Homer-Wright pseudorosettes
rosettes found in neuroblastomas that are filled with neuophil
41
Helpful features of neuorblastoma
positive immunohistochemical reactions for neuron-specific enolase membrane-bound cytoplasmic catecholamine-containing secretory granules
42
Membrane-bound cytoplasmic catecholamine-containing secretory granules of neuroblastoma
contain central dense cores surrounded by peripheral halo
43
Ganglion cells
in neuroblastomas that are large and have abundant cytoplasm, large vesicular nuclei and prominent nucleolus
44
Ganglioneuroblastoma
admixed with primitive neuroblasts
45
Ganglioneuroma
lesions contain more large cells that resemble ganglion cells with few residual neuroblasts
46
Maturation of ganglion cells
accompanied by appearance of Schwann cells
47
Presence of Schwannian stroma
histologic prerequisite for the designation of ganglioneuroblastoma and ganglioneuroma
48
Favorable outcome for neuroblastoma
documenting schwannian stroma is essential
49
Metastases of neuroblastomas
local infiltration and lymph node spread, there is pronounced tendency to spread through the bloodstream to liver lungs bone marrow and bones
50
Staging for neuroblastoma
used to rank neuroblastoma
51
Stage 1 of neuroblastomas
localized tumor with complete gross excision with or without microscopic residual disease ipsilateral nonadherent lymph nodes negative for tumor
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Stage 2A of neuroblastomas
localized tumor with incomplete gross resection; representative ipsilateral nonadherent lymph nodes negative for tumor microscopically
53
Stage 2B of neuroblastomas
localized tumor with or without complete gross excision ipsilateral nonadherent lymph nodes positive for tumor enlarged contralateral lymph nodes negative for tumor microscopically
54
Stage 3 of neuroblastomas
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
Stage 4 of neuroblastomas
any primary tumor with dissemination to distant lymph nodes, bone, bone marrow, liver, skin, and/or other organs
56
Stage 4S
S = special localized primary tumor with dissemination limited to skin, live, and/or bone marrow *limited t infants younger than 1 year
57
Presentation of Wilms tumor
large, solitary, well-circumscribed mass
58
Cut section of Wilms tumor
soft, homogenous, tan and gray | occasional foci of hemorrhage, cyst formation, and necrosis
59
Microscopic Wilms tumor characteristics
recognizing attempts to recapitulate different stages of nephrogeneisis
60
Classic triphasic combination of Wilms tumor
blastemal, stromal, epithelial cell types
61
Distinctive features in blasternal component of Wilms tumor
sheets of small blue cells
62
Epithelial differentiation in Wilms tumor
abortive tubules or glomeruli
63
Stromal cells of Wilms tumor
fibrocytic or myxoid
64
Anaplasia in Wilms tumor
presence of cells with large hyperchromatic, pleomorphic nuclei and abnormal mitoses
65
Mutation associated with presence of anaplasia in Wilms tumor
TP53 mutation | resistance to chemotherapy
66
Function of p53
pro-apoptotic signals in response to DNA damage
67
Loss of p53 function in Wilms tumor
explain relative unresponsiveness of anaplastic cells to cytotoxic chemotherapy