Pathology: Cellular Injury Flashcards

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1
Q

What is hypertrophy?

A

increased size of the cells (increased structural proteins and organelles)

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2
Q

What is hyperplasia?

A

Controlled proliferation of stem cells. Increased number of cells, can lead to dysplasia and cancer

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3
Q

What is atrophy?

A

Decrease the size and number of cells- destruction of cytoskeleton via ubiquitin-proteasome pathway. Autophagy and apoptosis. Caused by not using, denervation, lack of blood supply, lack of hormone, poor nutrition

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4
Q

Metaplasia

A

Reprogramming the stem cells to adapt to an insult

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5
Q

Dysplasia

A

Disordered, precancerous stem cell growth. Pleomorphism, nuclear changes,

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6
Q

Apoptosis

A

ATP programmed cell death. Intrinsic and extrinsic pathways. Eosinophilic cytoplasm and basophilic nucleus. pyknosis

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7
Q

Intrinsic apoptosis pathway (mitochondrial pathway)

A

tissue remodeling following embryogenesis- decreased IL2BAK and BAX, cytochrome C released from mitochondrial membrane, then activates caspases. Bcl2 keeps mito membrane impermeable (tumorigenesis)

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8
Q

Extrinsic pathway (death receptor pathway)

A
  1. Ligand receptor (Fas and TNF)

2. Immune cell (cytotoxic T cell)

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9
Q

Necrosis

A

enzymatic damage b/c of injury (inflammatory)

  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat
  5. Fibrinoid
  6. Gangrenous
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10
Q

What are Granulomas?

A

macrophages with pink cytoplasm with surrounding multinucleated giant cells and lymphocytes. IFN-y and TNF-a

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11
Q

What are the two types of calcification?

A

Dystrophic: 2nd to necrosis/injury (normal calcium levels) LOCALIZED
Metastatic: because of high calcium, hyperPTH (abnormal Ca levels) WIDESPREAD

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12
Q

What is lipofuscin?

A

yellow-brown wear and tear pigment that you see in elderly autopsies, autophagocytosed organellar membranes

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13
Q

What are hemachromatosis, Wilson’s, acetaminophen OD, ROP and reperfusion injury all examples of?

A

Free radical injury- DNA damage, protein modification, lipid perioxidation. Can be from radiation, drug metabolism, heavy metals, inflam (NO), WBC oxidative burst. free radicals can be removed by catalase, antioxidants ACE, superoxide dismutase, glutathione peroxidase

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14
Q

Scar formation?

A

nonregenerated cells replaced by connective tissue, 70-80% tensile strength by 3 months

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15
Q

What are keloid vs hypertrophic scars?

A

keloid are type 1 and 2 collagen, disorganized, go beyond the wound, upper extrem and face. Hypertrophic is type 3 collagen, organized strands parallel, stays in confines of original wound.

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16
Q

What are the phases of wound healing?

A

(pg 217)

  1. Inflammatory (up to 3 days)
  2. Proliferative (3 days to weeks)
  3. Remodeling (1 week to 6 months)-fibroblasts, type 3 collagen is replaced by type 1 collagen
17
Q

What conditions give you delayed wound healing?

A

Vitamin C and copper deficiency, zinc def (breaks down type 3 collagen)

18
Q

What are lights criteria?

A

(pg 217) It’s exudative if it meets one of these criteria:

  1. pleural fluid protein/serum >0.5
  2. pleural fluid LDH/serum LDH >0.6
  3. pleural fluid LDH >2/3 upper limit normal for serum LDH
19
Q

What is transthyretin associated with?

A

familial amyloid cardiomyopathy and familial amyloid polyneuropathies

20
Q

carcinoma vs sarcoma

A

carcinoma= epithelial cells. Sarcoma= mesenchymal cells

21
Q

What is anaplasia?

A

complete lack of differentiation in cancer cell

22
Q

What is the grade vs stage of neoplasm and which matters more for prognosis?

A

Grade: differentiation and mitosis
Stage: degree of spread
Stage=survival (TNM)-tumour size, nodes, mets

23
Q

Whats the difference between an oncogene and a tumour suppressor gene?

A

oncogene is gain of function mutation, only need one allele vs tumour suppressor gene is loss of function mutation and you need two alleles

24
Q

What are psammoma bodies?

A

laminated , concentric spherules with dystrophic calcification. Seen in papillary cell carcinoma, serous papillary cystadenocarcinoma of ovary, meningioma, malignant mesothelioma