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*MOD Exam 1 > Ch 2- Cell Responses and Adaptations (Dobson Lect) > Flashcards

Ch 2- Cell Responses and Adaptations (Dobson Lect) Flashcards

1
Q

Define:

Disease

A

“Any deviation from or interruption of the normal structure or function of a part, an organ, or system of the body as manifested by characteristic symptoms and sign ; the etiology, pathology, and prognosis may be known or unknown”

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2
Q

Define:

Disorder

A

“A derangment or abnormality of function; a morbid physical or mental state/condition”

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3
Q

Define:

Neoplasm

A

“Any new and abnormal growth; specifically a new growth of tissue in which the growth is uncontrolled and progressive”

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4
Q

Define:

Syndrome

A

“A set of symptoms that occur together; a symptom complex; the sum of signs of any morbid state”

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5
Q

What is an adaptation?

A

Adaptations are reversible functional and structural responses to changes in physiologic states and some pathologic stimuli

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6
Q

What are 4 examples of adaptation that were discussed in lecture?

A

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

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7
Q

Is cell injury reversible?

A

UP TO A CERTAIN POINT IT IS

If the stimulus persists or is severe enough, the cell will suffer from irreversible injury

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8
Q

Define:

Hypertrophy

A

Increase cell and organ size

*Hyper-trophy = you always want a BIG trophy*

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9
Q

Define:

Hyperplasia

A

Increased cell numbers

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10
Q

Define:

Atrophy

A

Decreased cell and organ size

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11
Q

Define:

Metaplasia

A

Change in phenotype of differentiated cells

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12
Q

What does the difference in heart size reveal?

What was the mechanism of this?

A

Hypertrophy

Increased production of cellular proteins

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13
Q

This comparitive image demonstrates what type of hyperplasia?

A

Physiologic hypertrophy of the uterus

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14
Q

A hallmark of cardiac metabolism before birth is?

A

The predominance of carbohydrate use for energy

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15
Q

After birth, cardiac metabolism switches energy source to the utilization of?

A

Oxidation of fatty acids

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16
Q

Why is it important to know the differences in fetal vs adult cardiac metabolism energy sources?

A

(*reminder: fetal uses carbohydrates, adult uses fatty acid oxidation)

It’s important because in several pathophysiologic conditions [ex: hypoxia, ischemia, hypertrophy, atrophy, diabetes, and hypothyroidism] the postnatal heart returns to “fetal” gene program

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17
Q

What is this image an example of?

A

(Left : Normal kidney)

(Right: (Physiologic compensatory hyperplasia)

***This is physiologic because it was due to loss of sister kidney. This kidney developed more renal cells to compensate.

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18
Q

What is one of the most concerning outcomes from repetitive hyperplasic events?

A

Transformation to malignancy

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19
Q

Where are the most common sites for developing cancerous malignancy?

A

Sites where hyperplasia are common!!!

Examples Include:

Breast

Endometrium

Prostate

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20
Q

What is this image revealing?

A

Hyperplasia can become cancerous if checkpoints go unregulated

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21
Q

What is this a picture of?

A

A patient with ALS that shows atrophy of the thenar eminence

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22
Q

What are the common reasons for atrophy? (6)

A
  • Decreased workload
  • Loss of innervation
  • Diminished blood supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure
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23
Q

What is the mechanism of atrophy?

A

Atrophy results from:

Decreased protein synthesis (due to reduced metabolic activity) and increased protein degradation in cells (proteosomes and/or autophagy)

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24
Q

What is the mechanism of metaplasia?

A

Result of a reprogramming of stem cells in normal tissues, or of undifferentiated mesenchymal cells present in connective tissue

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25
Q

The influences that predispose to metaplasia, if persistent, can intiate _______________

A

Malignant transformation

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26
Q

Which tissues do NOT have stem cells in them?

What does that mean in terms of metaplasia?

A

Heart & Brain

Cannot undergo metaplasia!!!

*Likely a test question* cough cough

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27
Q

What is this histologic slide revealing?

A

Bronchus Metaplasia!!!

Notice the difference in cell types that are directly adjacent to each other

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28
Q

What are the microscopic features of reversible cell injury?

A

Cell swelling

Fatty change

29
Q

Features of Necrosis and Apoptosis

Feature: Cell size

What happens with necrosis vs. apoptosis?

A

Necrosis: Enlarged (swelling)

Apoptosis: Reduced (shrinkage)

30
Q

Features of Necrosis and Apoptosis

Feature: Nucleus

What happens with necrosis vs. apoptosis?

A

Necrosis: Pyknosis –> Karyorrhexis –> Karyolysis

Apoptosis: Fragmentation into nucleosome-size fragments

31
Q

Features of Necrosis and Apoptosis

Feature: Plasma membrane

What happens with necrosis vs. apoptosis?

A

Necrosis: Disrupted

Apoptosis: Intact; altered structure

32
Q

Features of Necrosis and Apoptosis

Feature: Cellular contents

What happens with necrosis vs. apoptosis?

A

Necrosis: Enzymatic digestion; may leak out of cell

Apoptosis: Intact; may be released in apoptotic bodies

33
Q

Features of Necrosis and Apoptosis

Feature: Adjacent Inflammation

What happens with necrosis vs. apoptosis?

A

Necrosis: Frequent

Apoptosis: NONE!!!

34
Q

Features of Necrosis and Apoptosis

Feature: Physiologic or pathologic role

What happens with necrosis vs. apoptosis?

A

Necrosis: Invariably pathologic

Apoptosis: Often physiologic, means of eliminating unwanted cells, may be pathologic after some forms of cell injury, especially DNA damage

35
Q

Define:

Karyolysis

A

Nuclear fading

36
Q

Define:

Pyknosis

A

Nuclear shrinkage

37
Q

Define:

Karyorrhexis

A

Nuclear fragmentation

38
Q

Go read morphology box pages 42-44 of robbins

A

now

39
Q

What are these blue lines indicating?

A

Patterns of necrosis

Pie shaped/wedge shaped

(right: liquifactive necrosis of the brain)

40
Q

What type of necrosis is this?

A

Caseous necrosis

(Cheese like)

41
Q

Caseous necrosis is associated with what infection?

A

TB (mycobacterium tuberculosis)

42
Q

Caseous necrosis is described as?

A

Yellow-white and “cheese like”

43
Q

Caseous necrosis is described as:

“…the necrotic area appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border; this appearance is characteristic of a focus of inflammation known as a _____________”

A

Granuloma

44
Q

What are the principal biochemical mechanisms and sites of damage in cell injury?

A

Mitochondrial damage

Entry of Ca2+

Membrane damage

Protein misfolding, DNA damage

45
Q

Reduction in ATP levels is a fundamental cause of ______________

A

Necrotic cell death

46
Q

Increased production or decreased scavenging of ROS may lead to an excess of these free radicals, a condition called _________________

A

Oxidative stress

47
Q

Oxidative stress has been implicated in the following:

A
  • Cancer
  • Cell injury
  • Aging
  • Alzheimers disease
48
Q

ROS are produced in large amounts by ____________________

A

Activated leukocytes

49
Q

Why are ROS generated by neutrophils and macrophages?

A

Produced during inflammatory reactions aimed at destroying microbes and cleaning up dead cells and other unwanted substances

50
Q

Where are the most important sites of membrane damage during cell injury?

A

Mitochondrial membrane

Plasma membrane

Lysosomal membranes

51
Q

The release of _____________ into the bloodstream occurs by different sources, including primary tumor, tumor cells that circulate in peripheral blood, metastatic deposits present at distant sites, and normal cell types.

A

cfDNA (cell free DNA)

52
Q

What are the arrows pointing at?

A

Apoptotic bodies

53
Q

What are the two major mechanisms of apoptosis?

Which of the two is most common?

A

Mitochondrial (intrinsic) pathway ***more common***

Death receptor (extrinsic) pathway

54
Q

The process of apoptosis may be divided into two phases. What are they?

A

Initiation phase

Execution phase

55
Q

Caspases are associated with?

A

APOPTOSIS

56
Q

What are the major players in the mechanism of apoptosis?

A

BCL2 family

Cytochrome C

Caspases

Apoptosome

57
Q

What is the MAJOR anti-apoptotic protein?

A

BCL2

58
Q

What are the MAJOR pro-apoptotic proteins?

A

BAX and BAK

59
Q

Describe the death receptor (extrinsic) apoptotic pathway

A

This pathway is initiated by engagement of plasma membrane death receptors on a variety of cells with the ligand for Fas.

FasL is expressed on T cells that recognize self antigens and on some cytotoxic T lymphocytes.

60
Q

The death receptor (extrinsic) apoptotic pathway can be inhibited by a protein called?

A

FLIP

61
Q

What are specific examples of diseases caused by misfolding of protein?

A

Cystic Fibrosis

Familial hypercholesterolemia

Tay-Sachs disease

Alpha-1 antitrypsin deficiency

Creutzfeldt-Jacob disease

Alzheimer disease

62
Q

What is the purpose of autophagy?

A

Autophagy functions as a survival mechanism under various stress conditions, by maintaining the integrity of cells by recycling essential metabolites and clearing cellular debris.

63
Q

Dysregulation of autophagy can result in?

A

Cancer, IBS, neurodegenerative disorders

64
Q

What are the two examples of exogenous accumulations?

A

Anthracosis (carbon pigment)

Tattoo (pigment)

65
Q

What are the three examples of endogenous accumulations?

A

Lipofuscin

Melanin

Hemosiderin

66
Q

What are the two types of calcifications?

A
  1. Dystrophic
  2. Metastatic
67
Q

Where is dystrophic calcification found?

A

Areas of

Necrotic, damaged or aging tissue

68
Q

What causes metastatic calcification?

What are some disease states where you would find metastatic calcification? (4)

A

Hypercalcemia

  1. Hyperparathyroidism
  2. Resorption of bone due to bone tumors
  3. Vitamin D related disorders
  4. Renal failure
69
Q

What are the arrows pointing at?

A

Psammoma bodies

(a round collection of calcium)

–> Associated with benign and malignant lesions

*HE LOVED TALKING ABOUT THIS

*MOD Exam 1 (15 decks)

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