Chapter 9 Morphology

Question 1

Chronic poisoning by CO

Answer 1

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

Question 2

Slow developing hypoxia in CO poisoning

Answer 2

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

Question 3

Diagnosis of CO poisoning

Answer 3

made by measuring carboxyhemoglobin levels in the blood

Question 4

Cause of Acute poisoning by CO

Answer 4

accidental exposure or suicide attempt

Question 5

Acute poisoning of CO in light-skinned individuals

Answer 5

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

Question 6

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

Answer 6

high levels of carboxyhemoglobin

Question 7

Brain appearance in acute CO poisoning (3)

Answer 7

slightly edematous, punctate hemorrhages, hypoxia-induced neuronal changes

Question 8

Major anatomic targets of lead toxicity (5)

Answer 8

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

Question 9

Blood and marrow changes in lead toxicity

Answer 9

inhibition of ferrochelatase by lead results in ring sideroblasts

Question 10

Ring sideroblasts in lead toxicity

Answer 10

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

Question 11

Hemoglobin defect in peripheral blood in lead toxicity

Answer 11

Microcytic, hypochromic anemia and mild hemolysis

Punctate basophilic stippling of the red cells

Question 12

Brain involvement in lead toxicity in children

Answer 12

brain damage from subtle to massive and lethal

Question 13

Brain appearance in lead toxicity

Answer 13

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

Question 14

Adult impact by lead toxicity

Answer 14

peripheral demyelinating neuropathy

Question 15

Peripheral demyelinating neuropathy appearance

Answer 15

involved motor nerves of most commonly used muscles

extensor muscles of wrist and fingers

Question 16

GI tract and lead toxicity

Answer 16

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

Question 17

Kidney and lead toxity

Answer 17

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

Question 18

Gout associated with lead toxicity

Answer 18

saturnine gout

Question 19

Appearance of full-thickness burns

Answer 19

white or charred, dry and painless

Question 20

Appearance of partial-thickness burns

Answer 20

pink or marked with blisters and painful

Question 21

Histology of tissue in burns

Answer 21

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

Question 22

Changes in chromosomes in cells surviving radiant energy damage

Answer 22

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

Question 23

Abnormal nuclear morphologies in cells surviving radiant energy damage

Answer 23

giant cells with pleomorphic nuclei

cell death- nuclear pynosis and lysis

Question 24

Cytoplasmic changes in cells surviving radiant energy damage (3)

Answer 24

cytoplasmic swelling
mitochondrial distortion
degeneration of endoplasmic reticulum

Question 25

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

Answer 25

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

Question 26

Changes in irradiated tissues

Answer 26

vascular changes and interstitial fibrosis

Question 27

Immediate postirradiation period

Answer 27

vessels only dilated

Question 28

Over time during postirradiation period

Answer 28

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

Question 29

Main anatomic changes in PEM (3)

Answer 29

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

Question 30

Liver in kwashiorkor

Answer 30

enlarged and fatty

Question 31

Small bowel in kwashiorkor

Answer 31

Decrease in mitotic index in the crypts of the glands | Loss of villi and microvilli

Question 32

Bone marrow in kwashiorkor and marasmus

Answer 32

hypoplastic from decreased number of red cell precursors

Question 33

Peripheral blood in kwashiorkor and marasmus

Answer 33

mild to moderate anemia | vitamin deficiency might contribute to this

Question 34

Brain in infants born to malnourished mothers (3)

Answer 34

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

Question 35

"Other" changes seen in PEM (3)

Answer 35

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

Question 36

2 vitamin D deficiencies

Answer 36

rickets and osteomalacia

Question 37

How do rickets and osteomalacia occur?

Answer 37

excess of unmineralized matrix

Question 38

Characteristics of Rickets (6)

Answer 38

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

Question 39

What happens during the nonambulatory stage of infancy in rickets

Answer 39

Head and chest sustain greatest stresses | Softened occipital bones become flat

Question 40

Craniotabes

Answer 40

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

Question 41

What does excess osteoid in rickets cause?

Answer 41

frontal bossing and squared appearance to the head

Question 42

Chest abnormalities in rickets

Answer 42

rachitic rosary | pigeon breast deformity

Question 43

Rachitic rosary

Answer 43

overgrowth of cartilage or osteoid tissue at costochondral junction

Question 44

Pigeon breast deformity

Answer 44

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

Question 45

Skeletal deformities in child with rickets

Answer 45

lumbar lordosis and bowing of the legs

Question 46

Osteomalacia

Answer 46

adults that lack vitamin D which deranges their normal bone remodeling

Question 47

Characteristic of osteomalacia

Answer 47

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

Question 48

Bones in osteomalacia

Answer 48

weak and vulnerable to gross fractures or microfractures | *more common in vertebral bodies and femoral necks

Question 49

Unmineralized bone in osteomalacia appearance

Answer 49

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