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COM MOD 2 > Chapter 9 Morphology > Flashcards

Chapter 9 Morphology Flashcards

1
Q

Chronic poisoning by CO

A

carboxyhemoglobin is remarkably stable and rises to life-threatening levels in blood

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2
Q

Slow developing hypoxia in CO poisoning

A

evoke ischemic changes in CNS specifically the basal ganglia and lenticular nuclei

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3
Q

Diagnosis of CO poisoning

A

made by measuring carboxyhemoglobin levels in the blood

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4
Q

Cause of Acute poisoning by CO

A

accidental exposure or suicide attempt

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5
Q

Acute poisoning of CO in light-skinned individuals

A

marked by cherry-red color of the skin and mucous membranes

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6
Q

What causes the cherry-red color of skin and mucous membranes in CO poisoning?

A

high levels of carboxyhemoglobin

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7
Q

Brain appearance in acute CO poisoning (3)

A

slightly edematous, punctate hemorrhages, hypoxia-induced neuronal changes

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8
Q

Major anatomic targets of lead toxicity (5)

A

bone marrow, blood, nervous system, GI tract, kidneys

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9
Q

Blood and marrow changes in lead toxicity

A

inhibition of ferrochelatase by lead results in ring sideroblasts

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10
Q

Ring sideroblasts in lead toxicity

A

red cell precursors with iron-laden mitochondria that are detected by Prussian blue stain

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11
Q

Hemoglobin defect in peripheral blood in lead toxicity

A

Microcytic, hypochromic anemia and mild hemolysis

Punctate basophilic stippling of the red cells

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12
Q

Brain involvement in lead toxicity in children

A

brain damage from subtle to massive and lethal

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13
Q

Brain appearance in lead toxicity

A

edema, demyelination of cerebral and cerebellar white matter, necrosis and astrocytic proliferation

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14
Q

Adult impact by lead toxicity

A

peripheral demyelinating neuropathy

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15
Q

Peripheral demyelinating neuropathy appearance

A

involved motor nerves of most commonly used muscles

extensor muscles of wrist and fingers

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16
Q

GI tract and lead toxicity

A

lead “colic” characterized by extremely sensitive, poorly localized abdominal pain

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17
Q

Kidney and lead toxity

A

proximal tubular damage with intranuclear inclusions with protein aggretates
Can decrease uric acid excretion and cause gout

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18
Q

Gout associated with lead toxicity

A

saturnine gout

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19
Q

Appearance of full-thickness burns

A

white or charred, dry and painless

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20
Q

Appearance of partial-thickness burns

A

pink or marked with blisters and painful

21
Q

Histology of tissue in burns

A

coagulative necrosis adjacent to vital tissue that accumulated inflammatory cells and exudation

22
Q

Changes in chromosomes in cells surviving radiant energy damage

A

double stranded DNA breaks- deletions, translocations, fragmentations
nuclear swelling
abnormal nuclear morphologies

23
Q

Abnormal nuclear morphologies in cells surviving radiant energy damage

A

giant cells with pleomorphic nuclei

cell death- nuclear pynosis and lysis

24
Q

Cytoplasmic changes in cells surviving radiant energy damage (3)

A

cytoplasmic swelling
mitochondrial distortion
degeneration of endoplasmic reticulum

25
Q

Histologic constellation in cells involved in radiant energy damage (4)

A

cellular pleomorphism
giant cell formation
conformation changes in nuclei
abnormal mitotic figures

26
Q

Changes in irradiated tissues

A

vascular changes and interstitial fibrosis

27
Q

Immediate postirradiation period

A

vessels only dilated

28
Q

Over time during postirradiation period

A

degenerative changes- endothelial cell swelling and vacuolation
collagenous hyalinization
narrowing or obliteration of vascular lumens

29
Q

Main anatomic changes in PEM (3)

A

Growth failure
Peripheral edema in kwashiorkor
Loss of body fat and atrophy of muscles

30
Q

Liver in kwashiorkor

A

enlarged and fatty

31
Q

Small bowel in kwashiorkor

A

Decrease in mitotic index in the crypts of the glands

Loss of villi and microvilli

32
Q

Bone marrow in kwashiorkor and marasmus

A

hypoplastic from decreased number of red cell precursors

33
Q

Peripheral blood in kwashiorkor and marasmus

A

mild to moderate anemia

vitamin deficiency might contribute to this

34
Q

Brain in infants born to malnourished mothers (3)

A

show cerebral atrophy, reduced number of neurons, and impaired myelinization of white matter

35
Q

“Other” changes seen in PEM (3)

A

Thymic and lymphoid atrophy
Anatomic alterations from infections
Deficiencies of required nutritents

36
Q

2 vitamin D deficiencies

A

rickets and osteomalacia

37
Q

How do rickets and osteomalacia occur?

A

excess of unmineralized matrix

38
Q

Characteristics of Rickets (6)

A
  1. overgrowth of epiphyseal cartilage
  2. distorted irregular masses of cartilage
  3. deposition of osteoid matrix
  4. disruption of orderly replacement of cartilage
  5. abnormal overgrowth of capillaries and fibroblasts
  6. deformation of the skeleton
39
Q

What happens during the nonambulatory stage of infancy in rickets

A

Head and chest sustain greatest stresses

Softened occipital bones become flat

40
Q

Craniotabes

A

elastic recoil that snaps the bones back to original position in rickets

41
Q

What does excess osteoid in rickets cause?

A

frontal bossing and squared appearance to the head

42
Q

Chest abnormalities in rickets

A

rachitic rosary

pigeon breast deformity

43
Q

Rachitic rosary

A

overgrowth of cartilage or osteoid tissue at costochondral junction

44
Q

Pigeon breast deformity

A

weakened metaphyseal area of ribs pulls on respiratory muscles bending them inward

45
Q

Skeletal deformities in child with rickets

A

lumbar lordosis and bowing of the legs

46
Q

Osteomalacia

A

adults that lack vitamin D which deranges their normal bone remodeling

47
Q

Characteristic of osteomalacia

A

newly formed osteoid matrix laid down by osteoblasts is mineralized and excess of persistent osteoid

48
Q

Bones in osteomalacia

A

weak and vulnerable to gross fractures or microfractures

*more common in vertebral bodies and femoral necks

49
Q

Unmineralized bone in osteomalacia appearance

A

thickened layer of matrix arranged about the more basophilic, mineralized trabeculae

COM MOD 2 (9 decks)

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