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Pathology > Cell Injury, Death, and Adaptations > Flashcards

Cell Injury, Death, and Adaptations Flashcards

1
Q

Molecular Cause of Hypereosinophilia

A

Degradation of cellular protein and cytoplasmic RNA

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2
Q

What is aplasia?

A

failure in cell production during fetal development or later by loss of precursor cells in proliferative tissue

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3
Q

Cell types unable to undergo hyperplasia

A

Cells that are incapable of mitotic division:

  1. Skeletal muscle
  2. Cardiac muscle
  3. Neurons
  4. Glomeruli
  5. Retinal epithelium
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4
Q

Cause (and tissue type) of thicking of uterus during normal cycle

A

Hyperplasia of the endometrial glands and stroma

(+) Estrogen

(-) Progesterone

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5
Q

Cause (and tissue type) of thicking of uterus during pregnancy

A

Hyperplasia of smooth muscle

(+) Estrogen

(-) Progesterone

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6
Q

Cause (and tissue type) of breast growth during puberty/pregnancy

A

hyperplasia of glandular epithelium

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7
Q

In cardiac m hypertrophy, what are the vasoactive compounds and growth factors that initiates gene activation?

A

Vasoactive compounds:

  1. Angiotensin II
  2. Endothelin

Growth factors:

  1. TGF-ß
  2. Insulin-like GF
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8
Q

What are the structural/molecular changes that accompany cardiac hypertrophy?

A
  1. change from a to fetal ß-myosin
    - decreases ATPase

slower, energy-efficient contraction

  1. Change to fetal ANF
    - increases Na excretion, with water, to decrease blood volume and pressure
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9
Q

What is Cachexia? What causes it? MOA?

A

Muscle wasting

Causes: Marasmus, chronic inflammation

Overproduction of TNF suppresses appetite and induces muscle atrophy

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10
Q

Mechanisms of protein degradation associated with atrophy

A
  1. Lysosomal enzymes
  2. Ubiquitin-proteasome pathway
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11
Q

What is shown in the picture? What does it signal?

A

Lipochrome pigment: autophagic granules signify atrophy

Also: lipofuscin pigments

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12
Q

What type of cellular process is shown? What is this condition called? What type of transformation? Cause?

A

Metaplasia

Barrett’s esophagus

In the esophagus: squamous to columnar (secreting) epithelium

Result of acid reflux disease

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13
Q

What type of cellular process is shown? What is this condition called? What type of transformation? Cause?

A

Metaplasia

Laryngeal metaplasia

Respiratory epithelium (columnar) to squamous

Smoking

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14
Q

What type of cellular process is shown? Characteristics?

A

Dysplasia of squamous epithelium of cervix

Hyperchromatic nuclei and mitotic spindles: Mitosis occurs at all tissue levels

Loss of cell polarity

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15
Q

Damage to cell following ischemia

A
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16
Q

Damage to mitochondria following increased Ca lvls, ROS damage, or lipid peroxidation

A
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17
Q

Cell damage following loss of Ca homeostasis

A
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18
Q

ROIs formed from radiation

A

Hydrolyzes water to hydroxyl and hydrogen free radicals

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19
Q

Metabolism of Superoxide

A

SOD and forms H2O2

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20
Q

Metabolism of H2O2

A
  1. Catalase: H20
  2. Glutathione peroxidase: Hydroxide + Hydroxy-radical
  3. Fenton reaction with iron or copper: Hydroxide + Hydroxy-radical
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21
Q

Significance of Malondialdehyde in blood or urine

A

oxidative damage (due to lipid peroxide radical formation)

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22
Q

Characteristics of necrotic cells

A
  1. cytoplasmic eosinophilia (degradation of cytoplasmic RNA and denaturation of proteins)
  2. Karyolysis, Pyknosis, and Karyorrhexis

**causes inflammation from leakage of cytoplasmic contents

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23
Q

Characteristics of Coagulative necrosis

A
  1. Results from hypoxic death (of all tissues except the brain)
  2. Denaturation of proteins (from low ATP -> anaerobic -> increased lactic acid) which results in preservation of outline of dead cells
  3. firm texture
  4. wedge-shape
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24
Q

Characteristics and causes of liquifactive necrosis

A

Causes:

  1. brain hypoxia (microglia)
  2. Abcess (neutrophils)
  3. Pancreatitis (proteases)
  4. Bacterial/fungal infection

Characteristics:

  1. viscous liquid mass (enzymatic digestion)
  2. focal accumulation of inflammatory cells
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25
Q

Dry gangrene

A

Coagulative necrosis from anoxic injury (frostbite)

26
Q

Wet gangrene

A

Liquefactive necrosis associated with secondary bacterial infection

27
Q

Causes and Characteristics of Caseous Necrosis

A

Causes:

  1. TB
  2. Fungal infection

Characteristics: (form of coagulative necrosis)

  1. cheesy appearance
  2. Granular center with inflammatory border
  3. Tissue architecture is obliterated
28
Q

Causes and Characteristics of Fat necrosis

A

Causes:

  1. Trauma to breast
  2. Acute pancreatitis

Characteristics:

  1. fat destruction
  2. fat saponification: FAs combine with Ca
29
Q

What is pictured? Cause?

A

Fibrinoid Necrosis

Deposition of immune complexes in the blood vessels causing vasculitis (fibrin leaks out)

30
Q

Type of necrosis?

A

Caseous necrosis

31
Q

Type of necrosis?

A

Coagulative

32
Q

Type of necrosis?

A

Coagulative

33
Q

Type of necrosis?

A

Coagulative

34
Q

Type of necrosis?

A

Fat necrosis

35
Q

Type of necrosis?

A

Fat necrosis with saponification

36
Q

Type of necrosis?

A

Liquifactive

37
Q

Type of necrosis?

A

Liquifactive

38
Q

What is shown? With what cellular process is it associated?

A

Myelin figures (swirls of phospholipids from membrane damage)

Associated with apoptosis

39
Q

Effect of mercuric chloride

A

binds sulfhydryl groups

increase membrane permeability

40
Q

Effect of cyanide

A

Inhibit oxidative phosphorylation (bind cytochrome C)

41
Q

Characteristics of apoptotic cells

A
  1. shrunken cell (results in eosinophilia)
  2. condensed chromatin (may form crescents)

3 Nucleus may break up into fragments

42
Q

Role of p53

A

cell cycle arrest if DNA damage is present

If irreparable, induces apoptosis.

43
Q

Extrinsic pathway apoptosis receptors

A

FAS ligand and TNF

44
Q

Causes of Intrinsic pathway apoptosis and MOA

A
  1. Withdrawal of GFs/Hormones
  2. Protein misfolding
  3. Cellular Injury

Mechanism: pro- vs anti-apoptotic molecule concentrations determine fate

45
Q

Proteins from Tc cells to induce apoptosis

A
  1. Perforin (punctures membrane to allow Granzyme in)
  2. Granzyme
46
Q

What is shown? With what disease is it associated?

A

Mallory bodies (or alcoholic hyaline) composed of IFs

Alcoholic liver disease

47
Q

Accumulation of Triglycerides

  1. Disease
  2. Causes
  3. Changes
A

Steatosis

Causes:

  1. Alcohol ((+) triglyceride synthesis)
  2. Protein malnutrition ((-) apolipoprotien)
  3. Malnutrition (increased FAs)

Changes:

  1. Liver enlargens and turns yellow
  2. liposomes in cells –> fatty cysts when cells lyse
48
Q

Atherosclerosis

  1. What is the accumulation?
  2. What are cell characteristics?
A
  1. Cholesterol
  2. Atheromas: foam cells and crystalized cholesterol clefts

Affects foam cells (macrophages) and smooth mm cells

49
Q

Xanthomas

  1. What is the accumulation?
  2. What are cell characteristics?
  3. Causes?
A
  1. Cholesterol
  2. Foamy macrophages (collect in connective tissue of skin, forming mass)
  3. Hyperlipidemia, neoplasms, xanthelasma (no underlying disorder
50
Q
  1. What is shown?
  2. What is the accumulation?
  3. What are cell characteristics?
A
  1. Cholesterolosis
  2. Cholesterol in the gall bladder
  3. Foamy macrophages
51
Q

Neimann-Pick type C

  1. Disease type?
  2. What is the accumulation?
A
  1. Lysosomal storage disease
  2. Cholesterol
52
Q

Alpha-anti-trypsin deficiency

  1. What is the accumulation?
  2. What is an associated disease?
A
  1. Protein (anti-trypsin) due to misfolding
  2. Emphysema
53
Q

Chloride Channel protein of lung deficiency

  1. What is the accumulation?
  2. With what disease is it associated?
A
  1. Protein (misfolded Cloride Channel)
  2. Cystic fibrosis
54
Q
  1. What type of accumulation is pictured?
  2. What diseases are associated with this type of accumulation?
A
  1. Glycogen
  2. Diabetes and Pompe’s disease (glycogen storage disease)
55
Q
  1. What type of accumulation is pictured?
  2. What is the disease? Characteristics?
A
  1. Carbon or coal dust
  2. Anthracosis: Transport via macrophage to regional lymph nodes, turning them black
56
Q
  1. What type of accumulation is pictured?
  2. What does it signal?
  3. Where does it come from?
A
  1. Lipofuscin
  2. Oxidative stress of cell
  3. End product of lipid peroxidation
57
Q

Hemosiderosis

  1. What is the accumulation?
  2. Causes?
A
  1. Hemosiderin
  2. Hb degradation or Fe overload
    - Hemorrage and lysis of RBCs (bruising)
    - Hemolytic anemia
    - Blood transfusion
    - Increased dietary iron or defective metabolism
58
Q

Jaundice

  1. What is the accumulation?
  2. What is the origin of the accumulation?
A
  1. Bilirubin
  2. derived from Hb but no iron
59
Q

Dystrophic vs Metastatic calcification

A

Dystrophic: occurs in dying tissue; calcium lvl normal

Metastatic: occurs in normal tissue; elevated calcium lvls

60
Q

Initiation of intracellular vs extracellular dystrophic calcification

A

Intracellular: Mitochondria (accumulates Ca)

Extracellular: phospholipids in membrane vesicles from dead cells

61
Q

Causes of Hypercalcemia

A
  1. Hyperparathyroidism (bone resorption)
  2. Bone destruction
  3. Increased Vit D (increases absorption of Ca from intestine and kidney)
  4. Renal failure (reuptake of PO4, secondary hyperparatyroidism)

Pathology (27 decks)

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