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Pathoma > Chapter 1 > Flashcards

Chapter 1 Flashcards

Note; ALL CAPS = either means high yield, or just making it easier to tell the difference between to words (like ABduction vs ADduction)

1
Q

Which permanent tissues only undergo hypertrophy and not hyperplasia?

A

-Cardiac muscle, skeletal muscle, and nerve

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2
Q

How does hyperplasia lead to cancer? Is there an exception to this rule?

A
  • When hyperplasia occurs secondary to a pathologic process
  • Pathologic hyperplasia (ex. Endometrial hyperplasia) can progress to dysplasia and eventually cancer.
  • EXCEPTION: BPH - NO increase risk for prostate cancer
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3
Q

Name of process that results in a decrease in cell #

A

apoptosis

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4
Q

Name of processes that results in decrease cell size

A

Ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components

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5
Q

What is Metaplasia?

A

A change in stress on an organ leads to a change in cell type.

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6
Q

Barret esophagus is a classic example of what type of growth adaptation?

A

Metaplasia

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7
Q

What type of tissue changes occur most commonly in metaplasia?

A

Change of one type of surface epithelium (squamous, columnar, urothelial) to another

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8
Q

What type of metaplasia do we see with Barret esophagus?

A

Non-keratinizing squamous epthelium –> nonciliated, mucin-producing columnar cells

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9
Q

Metaplasia is (reversible or irrreversible)?

A

reversible - in theory, with removal of the driving stressor

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10
Q

Can metaplasia progress to cancer?

A

Yes - under persistent stress:
-metaplasia –> dysplasia –> cancer
ex) Barret’s –> adenocarcinoma of the esophagus
EXCEPTION:apocrine metaplasia of breast - no increased risk for cancer

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11
Q

What vitamin deficiency can result in metaplasia?

A

Vitamin A.

-is necessary for differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye

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12
Q

How will a Vitamin A deficiency manifest?

A

Night blindness
Thin squamous lining of the conjunctiva undergoes metaplasia into stratified keratinizing squamous epithelium. Change = KERATOMALACIA

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13
Q

MYOSITIS OSSIFICANS is an example of what?

A
  • Mesenchymal (connective) tissue undergoing metaplasia

- muscle tissue changes to bone during healing after trauma (inflammation)

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14
Q

Define Dysplasia in 3 words

A

Disordered cellular growth

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15
Q

Cervical intraepithelial neoplasia (CIN) is an example of what growth adaptation?

A

Dysplasia

  • refers to a proliferation of precancerous cells (as most dysplasias do).
  • Represents dysplasia and is a precursor to cervial cancer
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16
Q

How does dysplasia arise?

A

-often from longstanding pathologic hyperplasia (endometrial hyperplasia) or metaplasia (Barrett)

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17
Q

IS DYSPLASIA REVERSIBLE?

A

Yes, in theory, with alleviation of inciting stress

-if the stress persists and it progresses to carcinoma –> that is irreversible

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18
Q

Define Aplasia:

A

Failure of cell production during embryogenesis

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19
Q

Define Hypoplasia

A

Decrease in cell production during embryogenesis resulting in a relatively small organ (ex streak ovary in turner syndrome)

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20
Q

What type of cells are highly susceptible to ischemic injury?

A

NEURONS (occurs after 3-5 minutes)

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21
Q

What does slowly developing ischemia result in?

A

Results in atrophy

In contrast to acute ischemia - which results in cellular injury

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22
Q

Define Hypoxia

A

Low oxygen delivery to tissue

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23
Q

What are the 3 causes of hypoxia?

A
  1. Ischemia (decreased blood flow through an organ)
  2. Hypoxemia (low partial pressure of oxygen in the blood)
  3. Decreased O2 - carrying capacity
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24
Q

What are 3 causes of ischemia?

A
  1. Decreased arterial perfusion (atherosclerosis)
  2. Decreased venous drainage (Budd-Chiari syndrome - from Polycythemia vera or Lupus causing a thrombosis in hepatic vein)
  3. Shock:
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25
Q

What lab values constitute Hypoxemia?

A

PaO2 < 60 mmHg;

SaO2 <90%

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26
Q

4 Causes of hypoxemia:

A
  1. High altitude
  2. Hypoventilation [Increased PACO2 –> Decreased PAO2)
  3. Diffusion Defect (Interstitial pulmonary fibrosis)
  4. V/Q mismatch (right-to-left shunt; atelectasis)
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27
Q

How does a decreased O2 carrying capacity of the blood occur?

A

Arises with hemoglobin (Hb) loss or dysfunction.

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28
Q

What are 3 examples of decreased O2-carrying capacity?

A
  1. Anemia [PaO2 normal; SaO2 normal]
  2. CO poisoning [PaO2 normal; SaO2 decreased]
  3. Methemoglobinemia [PaO2 normal; SaO2 decreased]
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29
Q

**What is the classic physical finding in CO poisoning?

A

Cherry-red appearance of skin

-Headache =early sign; then lead to coma and death

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30
Q

Explain Methemoglobinemia

A

Iron in heme is oxidized to Fe3+, which cannot bind O2

-Seen with oxidant stress (sulfa and nitrate drugs) or in newborns [‘cause babies suck at reducing Fe3+ to Fe2+]

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31
Q

What is a classic finding in methemoglobinemia?

A

Cyanosis with chocolate-colored blood

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32
Q

What is the treatment for Methemoglobinemia?

A

Intravenous methylene blue

- helps reduce Fe3+ back to Fe2+ state

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33
Q

What is the hallmark of reversible injury?

A

Cellular swelling

34
Q

What is the hallmark of irreversible injury?

A

Membrane damage:

35
Q

Where does the electron transport chain occur?

A

INNER MITOCHONDRIAL MEMBRANE

36
Q

What is cytochrome C?

A

an enzyme found in the mitochondria used in oxidative phosphorylation. When this leaks into the cytosol (when mitorchondrial membrane is damaged), will activate apoptosis

37
Q

What is the morphologic hallmark of cell death?

A

loss of the nucleus:

-Nuclear condensation (pyknosis) –> Fragmentation (Karyorrhexis) –> Dissolution (Karyolysis)

38
Q

In general, describe Necrosis (i.e. - how it will be differentiated from the other form of cell death)

A
  • Death of LARGE group of cells followed by ACUTE inflammation
  • Due to some underlying pathologic process; never physiologic
39
Q

What are the 6 gross patterns of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. Caseous
  5. Fat
  6. Fibrinoid necrosis
40
Q

Which pattern of necrosis is characteristic of ischemic infarction of any organ (except the brain)?

A

Coagulative

41
Q

What is a red infarction?

A

Coagulative necrosis: arises if blood re-enters a lossely organized tissue (pulmonary or testicular infarction)

42
Q

How would coagulative necrosis appear? (i.e firm, squishy, circular….?)

A

Tissue remains firm (cell shape preserved)

  • Wedge-shaped (pointing to focus of vascular occlusion)
  • Pale
43
Q

What type of necrosis is characteristic of brain infarction?

A

Liquefactive

Proteolytic enzymes from microglial cells liqeufy the brian

44
Q

What type of necrosis is characteristic of Abscess and Panceatitis?

A

Liquefactive

  • Abscess: Proteolytic enzymes from neutrophils
  • Pancreatitis: Proteolytic enzymes from pancreas liquefy parenchyma
45
Q

What type of necrosis is characteristic of ischemia of lower limb and GI tract?

A

Gangrenous necrosis

46
Q

What is wet gangrene?

A

When there is gangrenous necrosis with superimposed infection of dead tissues ( and liquefactive necrosis ensues)

47
Q

How would you describe a gangrenous necrosis?

A

Coagulative necrosis that resembles mummified tissue

48
Q

How would you describe a Caseous necrosis?

A

Soft and friable necrotic tissue with “cottage cheese-like” appearance
-A combination of coagulative and liquefactive

49
Q

What type of necrosis is characteristic of granulomatous inflammation due to tuberculous or fungal infections?

A

Caseous necrosis

50
Q

What is saponification?

A

Fatty acids released by trauma or lipase join with calcium

-Is an example of dystrophic calcification

51
Q

What is dystrophic calcification?

A

Calcium deposits on dead tissues.

  • necrotic tissue acts as a nidus for calcification
  • occurs in setting of NORMAL serum calcium and phosphate
52
Q

What is metastatic calcification?

A

HIGH serum Ca or P levels lead to Ca deposition in normal tissue (hyperparathyroidism leading to nephrocalcinosis)

53
Q

What type of necrosis is characteristic of trauma to fat and pancreatitis-mediated damage of peripancreatic fat?

A

Fat necrosis

-Will have a chalky-white appearance due to deposition of Ca

54
Q

What type of necrosis is characteristic of malignant hypertension and vasculitis?

A

Fibrinoid necrosis

55
Q

Define fibrinoid necrosis

A

Necrotic damage to blood vessel wall

-Leaking of proteins (fibrin) into vessel wall resulting in bright pink staining of the wall microscopically

56
Q

Define apoptosis:

A

ATP-dependent, genetically programmed cell death involving single cells or small groups of cells

57
Q

Give 3 examples of apoptosis

A
  1. Endometrial shedding during menstrual cycle
  2. Removal of cells during embryogenesis (digits)
  3. CD8 T cell-mediated killing of virally infected cells
58
Q

After apoptotic bodies are removed by macrophages, what type of inflammation occurs?

A

NONE - apoptosis is not followed by inflammation (BUT necrosis does have inflammation!)

59
Q

What mediates apoptosis?

A

Caspases: activate proteases and endonucleases

  • Proteases break down cytoskeleton
  • Endonucleases break down DNA
60
Q

How are caspases activated by the intrinsic mitochondrial pathway?

A
  • Inactivation of Bcl2 via cellular injury/DNA damage/loss of hormonal stimulation allows CYTOCHROME C to leak from the inner mitochondrial matrix into the cytoplasm and activate caspases
61
Q

How are caspases activated by the extrinsic receptor-ligand pathway?

A

FAS ligand binds FAS death receptors (CD95) on the target cell –> activating caspases (negative selection of thymocytes in thymus)
-TNF binds TNF receptors on target cell, also activating caspases

62
Q

How are caspaces activated by the Cytotoxic CD8 T cell-mediated pathway?

A
  • Perforins secreted by CD8 T cells create pores in membrane of target cells
  • Granzyme (really) from CD8 T cell enters pores and activates caspases
63
Q

How are free radicals generated physiologically?

A

Oxidative phosphorylation

  • Cytochrome c oxidase (complex IV) transfers electrons to oxygen
  • Partial reduction of O2 yeilds Superoxide (O2 -), hydrogen peroxide (H2O2), and Hydroxyl radicals (OH-)
64
Q

Which oxygen free radical is the devil of free radicals?

A

Hydroxyl radicals are the most dangerous

65
Q

What are 4 ways free radicals are generated pathologically?

A
  1. Ionizing radiation: Water –> Hydroxyl free radical
  2. Inflammation: NADPH oxidase generates superoxide ions during oxygen-dependent killing by neutrophils
  3. Metals: Fenton reaction (Fe2+ generates hydroxyl)
  4. Drugs and chemicals: during metabolism via P450
66
Q

How do free radicals cause cellular injury?

A

Via peroxidation of lipids and oxidation of DNA and proteins

DNA damage is implicated in aging and oncogenesis

67
Q

What are 3 enzymes that eliminate free radicals?

A

Superoxide dismutase (in mitochondira): Superoxide –> H2O2

  1. Glutathione peroxidase (in mitochondria): Hydroxyl –> water
  2. Catalase (in peroxisomes): H2O2 –> H2O
68
Q

What is Carbon Tetrachloride (CCl4), and why is it bad?

A
  • organic solvent used in dry cleaning
  • Converted to CCl3 by P450
  • Results in cell injury with swelling of rER –> ribosomes detach, impairing protein synthesis
  • Decreased apolipoproteins leads to FATTY CHANGE IN THE LIVER
69
Q

What are 2 shared features of proteins that can be deposited as amyloid?

A
  1. Beta-pleated sheet configuration

2. Congo red staining and apple-green birefringence when viewed microscopically under polarized light

70
Q

Define Primary amyloidosis

A

Systemic deposition of AL amyloid, which is derived from Ig light chain
-Associated with plasma cell dyscrasia (multiple myeloma)

71
Q

Define Secondary amyloidosis

A

Systemic deposition of AA amyloid, which is derived from serum amyloid-associated protein (SAA)

72
Q

What is serum amyloid-associated protein (SAA)?

A

an acute phase reactant that is increased in chronic inflammatory states, malignancy, and familial mediterranean fever (FMF - rare)

73
Q

What are the clinical findings of systemic amyloidosis?

A
  1. NEPHROTIC SYNDROME: KIDNEY IS THE MOST COMMON ORGAN INVOLVED
  2. Restrictive cardiomyopathy or arrhythmia
  3. Tongue enlargement, malabsorption, hepatosplenomegaly
74
Q

How do you diagnosis Systemic Amyloidosis:

A

Tissue biopsy
Abdominal fat pad and rectum are easily accessible biopsy targets. If you think convincing a patient sticking a needle up their butt will be easy anyway…

75
Q

What is the treatment for systemic amyloidosis?

A

Damage organs must be transplanted. Amyloid cannot be removed

76
Q

What is senile cardiac amyloidosis?

A

Localized amyloidosis

  • NON-MUTATED serum transthyretin deposits in the heart
  • usually asymptomatic. Common (25% of pts >80 years old)
77
Q

What is Familial amyloid cardiomyopathy?

A
  • Localized amyloidosis

- MUTATED serum transthyretin deposits in the heart leading to restrictive cardiomyopathy

78
Q

When would you see Amylin depsoited in the islet of the pancreas?

A

Type II diabetes mellitus.

Amylin is derived from insulin

79
Q

What amyloid is present in Alzheimer disease?

A
  • Abeta amyloid (derived from Beta-amyloid precursor protein) deposits in the brain forming amyloid plagues.
  • Gene for beta-APP is present on Chromosome 21 - which is where the association with Down syndrome comes from
80
Q

What do you see in Dialysis-assoicated amyloidosis

A

B2-microglobulin deposits in joints

81
Q

How is Medullary carcinoma of the thyroid associated with amyloidosis

A

Calcitonin (Produced by tumor cells) deposits within the tumor
-“TUMOR CELLS IN AN AMYLOID BACKGROUND”

Pathoma (15 decks)

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