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Pathology > Cellular Responses to Stress and Inflammation and Repair > Flashcards

Cellular Responses to Stress and Inflammation and Repair Flashcards

1
Q

Increase in SIZE of the cells — increased size of organ

Cellular adaptation of NON DIVIDING CELLS - myocardial fibers

A

HYPERTROPHY

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2
Q

Increase in NUMBER of cells

A

HYPERPLASIA

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3
Q

REDUCTION in cell SIZE and NUMBER — decreased size of organ

A

ATROPHY

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4
Q

A REVERSIBLE change wherein one differentiated cell type is REPLACED by ANOTHER cell type

A

METAPLASIA

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5
Q

55/M
long standing HPN, expired from MI
autopsy showed INCREASED thickness of the L ventricular wall w/ large areas of fibrotic scars

diagnosis and cellular adaptation

A

Myocardial Infarction
Left Ventricular Hypertrophy
Pathologic HYPERTROPHY

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6
Q

47 G0 w/ granulosa cell tumor presented w/ menorrhagia
UTZ showed endometrium
Px underwent diagnostic curettage
Biopsy showed BACK TO BACK ENDOMETRIAL GLANDS w/ NUCLEAR ATYPIA

diagnosis and cellular adaptation

A

Complex Atypical Hyperplasia

Pathologic Hyperplasia

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7
Q

35/M w/ hx of poliomyelitis presented w/ disproportionately thinner R lower extremity
Muscle biopsy showed DECREASE in size of skeletal myocytes

cellular adaptation

A

Denervation Atrophy

Pathologic Atrophy

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8
Q

The FIRST MANIFESTATION of almost all forms of injury to the cells
Change is d.t. INFUX of IONS (and water) d.t. FAILURE of ENERGY DEPENDENT ION PUMPS (NaKATPase)

A

CELLULAR SWELLING

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9
Q

Appearance of LIPID VACUOLES in the CYTOPLASM

Often seen in cells participating in fat metabolism (LIVER, HEART)

A

Steatosis

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10
Q

Type of cell death that results from PATHOLOGIC cell injury

A

Necrosis

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11
Q

Type of cell death that is energy dependent tightly regulated and associated w/ normal cellular functions often physiologic
PROGRAMMED CELL DEATH

A

Apoptosis

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12
Q

Component cells are dead but the basic structure is PRESERVED (acidophilic tombstone)
ISCHEMIC INJURY to MOST SOLID ORGANS (heart, spleen, kidney) EXCEPT BRAIN

A

Coagulative Necrosis

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13
Q

Digestion of dead cells — transformation of the tissue into a VISCOUS LIQUID MASS
Often seen in INFECTION (PUS) and hypoxic death of cells w/n CNS

A

Liquefactive necrosis

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14
Q

The term reserved for ISCHEMIC COAGULATIVE NECROSIS of the LIMBS (dry)
May have superimposed bacterial infection w/ liquefactive necrosis (wet)

A

Gangrene necrosis

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15
Q

CHEESE LIKE gross appearance of necrotic areas
Often seen in TUBERCULOUS INFECTIOUS
Tissue architecture is NOT PRESERVED

A

Caseous necrosis

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16
Q

Focal areas of fat destruction seen in ACUTE PANCREATITIS
Foci of necrosis contain SHADOWY OUTLINES OF NECROTIC FAT CELLS with basophil calcium deposits (SAPONIFICATION) surrounded by INFLAMMATORY REACTION

A

Enzymatic Fat Necrosis

17
Q

Seen in IMMUNE REACTIONS involving BLOOD VESSELS; deposits of immune complexes together w/ FIBRIN that have leaked out vessels — BRIGHT PINK and AMORPHOUS APPEARANCE

A

Fibrinoid necrosis

18
Q

Inactivation of anti-apoptotic BCL2 protein that leads to activation of BAX/BAK channel allowing cytochrome c to leak out of the mitochondria activating apoptosis

A

Intrinsic (Mitochondrial) Pathway

19
Q

Activation of DEATH RECEPTORS by appropriate ligands that leads activation of apoptosis

A

Extrinsic (Death Receptor) Pathway

20
Q

Calcium deposition occurring in DEAD TISSUES in the ABSENCE of CALCIUM METABOLIC DERANGEMENTS

i.e. Psammoma bodies (cancers w/ papillary architecture and meningioma)

A

Dystrophic Calcifications

21
Q

Calcium deposition in NORMAL TISSUES occurring in the setting of HYPERCALCEMIA

i.e. Calcinosis

A

Metastatic Calcifications

22
Q

ACUTE INFLAMMATION

A

fast; minutes or hrs
NEUTROPHILS
mild and self limited
prominent local and systemic signs

23
Q

CHRONIC INFLAMMATION

A

slow, days
MONOCYTES/MACROPHAGES and LYMPHOCYTES
severe and progressive
less local and systemic signs

24
Q

Components of Acute Inflammation

A
  1. DILATION of small vessels
  2. INCREASED microvascular PERMEABILITY
  3. EMIGRATION of leukocytes and their ACTIVATION
25
Q

Initial vascular response to injury

A

VASOCONSTRICTION

26
Q

Most notable mediator in acute inflammation that produces VASODILATION; stored in MAST CELLS, BASOPHILS and PLATELETS

27
Q

MC mechanism of INCREASED MICROVASCULAR PERMEABILITY in acute inflammation

A

Endothelial Cell Contraction

28
Q

Morphologic hallmarks of Acute Inflammation

A
  1. VASODILATION

2. Accumulation of leukocytes and fluid in the extravascular tissue

29
Q

Outcomes of Acute Inflammation

A
  1. Resolution
  2. Pus formation (ABSCESS)
  3. Healing by FIBROSIS
  4. Progression to CHRONIC

Pathology (24 decks)

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