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CMOD-Path Block 1 > Adaptation, Injury, Death > Flashcards

Adaptation, Injury, Death Flashcards

1
Q

Differentiate anatomic and Clinical Pathology.

A

Anatomic - gross changes of cell or tissues

Clinical - biochemical alteration in body fluids (e.g. blood and urine)

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2
Q

Differentiate General and Systemic pathology.

A

General:
- focuses on the cellular and tissue alterations caused by pathologic stimuli in most tissues

Systemic:
- Examines reactions and abnormailities of different specialized organs

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3
Q

Differentiate Etiology and Pathogenesis.

A

Etiology - Origin of the disease and the underlying cause (Genetic, environmental, multifactorial)

Pathogesis - steps of the disease process

**Knowing both of these is essential to developing rational treatment

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4
Q

Diffentiate physiologic and pathologic adaptations.

A

Physiologic - normal adaption that are responses to hormones or endogenous chemical mediator

Pathologic - cell modifies its structure and function in order to escape injury

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5
Q

Differentiate mechanical and trophic triggers?

A

Mechanical triggers are things like stretch, where as trophic triggers are chemicals (soluble mediators)

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6
Q

What is infarction?

A

Cell Death

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7
Q

In the heart’s hypertrophic response to stress, what physical fluid or particle causes the enlargement?

A

Increase in Proteins

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8
Q

Differentiate Hypertrophy and Hyperplasia.

A

Hypertrophy - increase in cell size

Hyperplasia - increase in cell number

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9
Q

Does the uterus undergo hypertrophy or hyperplasia during pregnancy?

A

Hypertrophy

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10
Q

Differentiate physiologic and pathologic hyperplasia.

A

Physiologic:
- Hormonal or Compensatory

Pathologic:
- Excessive hormonal or growth factor stimulation (e.g. endometrial hyperplasia)

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11
Q

T or F: pathologic hyperplasia constitutes a fertile soil in which cancer can grow

A

True

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12
Q

What is atrophy?

  • necrosis, apoptosis, neither
  • Functionality
  • common causes
A

Loss of cell size due to loss of cell substance

Neither, cells simply shrink but are not dead

Common causes:

  • Decreased workload
  • loss of innervation
  • diminished blood supply
  • aging
  • loss of endocrine supply
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13
Q

What is the process of autophagy?

A

Starved cells eat their own components to survive

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14
Q

What two processes lead to cell atrophy?

A

Decreased Protein Synthesis
- because of decreased metabolic activity

Increased Protein degradation

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15
Q

Is metaplasia reversible?

- what typically causes it?

A

YES, this is very important

Usually caused by chronic irritation

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16
Q

Differentiate:

  • Hypertrophy
  • Hyperplasia
  • Dysplasia
  • Neoplasia
A

Hypertrophy - cells grow in size NOT number

Hyperplasia - cells increase in number

Dysplasia - disorganized growth (spotty hypertrophy)

Neoplasia - disorganized growth with an increase in the number of dividing cells

17
Q

What is the problem with monitoring gross structural changes in a tissue to monitor something like necrosis?

A

Gross changes seen on the microscope always lag behind actual cell death

By the time we see death its too late to start treating it

18
Q

What are two common reversible changes?

A
  • Swelling

- Fatty Change

19
Q

What are the two main determinants of whether damage to a cell will be reversible?

A
  1. Mitochondrial Dysfunction (lack of ox-phos and ATP etc.)

2. Disturbances in membrane function

20
Q

What are the 4 main factors causing cell death?

A
  1. Ischemia (lack of Blood Flow)
  2. Infections
  3. Toxins
  4. Immune Reaction
21
Q

Is necrosis or apoptosis more indicative of pathology?

A

Necrosis

22
Q

How do apoptotic and necrotic cells differ in:

  • Cell size
  • Nucleus
  • Plasma Membrane
A

Necrotic:

  • Size: Larger
  • Nucleus: Pyknosis, Karyorrhexis, Karyolysis
  • Plasma Membrane: Disrupted

Apoptotic:

  • Size: Reduced (shrinkage)
  • Nucleus: condensed
  • Plasma Membrane: intact with altered structure
23
Q

How do apoptotic and necrotic cells differ in:

  • Cellular Contents
  • Adjacent Inflammation
A

Necrotic:

  • Contents: enzymatic digestion that may leak out of cell
  • Inflammation: Frequent

Apoptotic:

  • Contents: in tact and may be released in apoptotic bodies
  • Inflammation: not present
24
Q

T or F: necrosis is invariably pathologic

A

True, apoptotic is most often physiologic

25
Q

Diffentiate

  • Karyolysis
  • Pynkosis
  • Karyorrhexis
A

Kayolysis - Faded Nucleus
Pyknosis - Nuclear Shrinkage (very purple)
Karyorrhexis - Nuclear fragmentation

26
Q

What is the end result of karyolysis, pynkosis, and karyorrhexis?

A

Nuclear dissolution and necrosis

27
Q

What is the characteristic pattern of infarcts in H and E stain in almost every organ?

A
  • Ghost outline (anoxic injury)
  • Darker band (Hemorrhagic zone)
  • Normal zone
28
Q

What is the difference between wet and dry gangrene?

A

Wet gangrene has a superimposed bacterial infection

**Note: both are usually found in the lower extremities

29
Q

What often causes liquifactive necrosis?

A
  • Focal bacterial or fungal infection
  • Inflammation and leukocytes “digest” tissue
  • HYPOXIA IN CNS
30
Q

What is caseous necrosis?

- characteristics

A

Cheese like necrosis

  • Tissue architecture is obliterated
  • Has an inflammatory border
  • Granuloma (from things like TB)
31
Q

What is Fibrinoid Necrosis?

  • what causes it?
  • H and E appearance?
A

Fibrin deposits

  • Typically immune reactions where antibody-antigen complexes desposit in arterial walls
  • Amphorous and Bright on H and E
32
Q

GO BACK AND LOOK AT THIS POWERPOINT TO REVIEW THE PICS

A

GO BACK AND LOOK AT THIS POWERPOINT TO REVIEW THE PICS

33
Q

What is Fat necrosis?

A
  • Focal areas of Fat destruction

**Pancreatitis causes pancreatic enzyme release and saponification results when the fats combine with calcium

**Also occurs in the breast in response to trauma (e.g. lump in the breast after having a car accident)

CMOD-Path Block 1 (10 decks)

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