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Patho > Remediation Exam > Flashcards

Remediation Exam Flashcards

1
Q

What is the process of necrosis?

A

Necrosis is when cellular membranes fall apart and cellular enzymes leak out and ultimately digest the cell →causing inflammation

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2
Q

What is the process of apoptosis?

A

Apoptosis is programmed cell death when cells degrade their own DNA and nuclear/cytoplasmic proteins by the activation of caspases → apoptotic cells break up into fragments and apoptotic bodies (which are targets for phagocytes)

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3
Q

What are caspases?

A

Caspases are enzymes that control nuclear fragmentation & formation of apoptotic bodies

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4
Q

Explain size in apoptosis vs. necrosis.

A

Necrosis causes cellular swelling → cellular lysis

Apoptosis causes cellular shrinkage → apoptotic bodies form

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5
Q

How many cells are affected in apoptosis vs. necrosis?

A

Apoptosis → One one cell is affected

Necrosis → Many cells are affected bc trauma

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6
Q

What causes apoptosis?

A

External & Internal Agents

like DNA Damage or IC Stress

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7
Q

What causes necrosis?

A

External Agents

like ischemia, exposure to toxins, infections, or trauma

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8
Q

Explain uptake of cells (Necrosis vs. Apoptosis)

A

Apoptosis → Cell contents are digested by neighboring cells

Necrosis → Cell contents are digested by macrophages

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9
Q

Which is pro-inflammatory: necrosis or apoptosis?

A

Necrosis

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10
Q

What happens to organelles in necrosis vs. apoptosis?

A

Apoptosis → Leaky mitochondria release pro-apoptotic proteins

Necrosis → Organelle swelling causes mitochondrial membrane damage resulting in lysosomal leakage

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11
Q

DNA Degradation (Necrosis vs. Apoptosis)

A

Apoptosis → Chromatin condensation and non-random DNA degradation

Necrosis → Random DNA degradation

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12
Q

What are the pathologic patterns of apoptosis?

A
  • DNA Damage
  • Accumulation of misfolded proteins
  • Infections
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13
Q

What are the physiologic patterns of apoptosis?

A
  • Occurs during embryogenesis
  • Turnover of Proliferative Tissues
  • Involution (shrinkage) of hormone-dependent tissues
  • Decline of leukocyte #’s at the end of immune/inflammatory response
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14
Q

What is calcification?

A

The abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other minerals

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15
Q

What is dystrophic calcification?

A

Occurs when calcium metabolism is normal but calcium deposits in injured or dead tissue, such as areas of necrosis

(when this occurs in the aortic valves it causes aortic stenosis in elderly persons)

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16
Q

Where does metastatic calcification occur?

A

Occurs in normal tissues with hypercalcemia

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17
Q

Dystrophic vs. Metastatic Calcification

A

Metastatic Calcification → occurs with abnormal calcium metabolism but no cell death

Dystrophic Calcification → occurs when calcium metabolism is normal but cell death happens

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18
Q

4 Principal Causes of Metastatic Calcification

A
  • Elevated parathyroid hormone
  • Bone Destruction (due to the effects of accelerated turnover or malignancies)
  • Vitamin D Related Disorders
  • Renal Failure, Phosphate Retention → secondary hyperparathyroidism
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19
Q

What is hypertrophy?

A

An increase in the size of cells leads to the increase in the size of the affected organ but no new cells

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20
Q

Where does hypertrophy occur?

A

Occurs in cells that cannot form new cells or divide

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21
Q

Why does hypertrophy occur?

A

Hypertrophy is due to the synthesis and assembly of additional intracellular structural components

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22
Q

Compare examples of the physiological and pathological patterns of hypertrophy.

A

Physiological → Body Building or Pregnancy

Pathological → Hypertension or Increased Cardiac Hypertension

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23
Q

What is hyperplasia?

A

An increase in the number of cells in an organ or tissue in response to a stimulus

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24
Q

Where does hyperplasia occur?

A

Hyperplasia can only occur in tissue where cells are capable of dividing

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25
Q

Why does hyperplasia occur?

A

Hyperplasia is the result of growth factor-driven proliferation of mature cells or by an increased output of new cells from tissue stem cells

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26
Q

Compare examples of the physiological and pathological patterns of hyperplasia.

A

Physiological → Liver Tissue, Bone Marrow Tissue or Breast Tissue

Pathological → Thyroid (Goiter) Tissue or Benign Prostate Hyperplasia

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27
Q

What is atrophy?

A

A reduction in the size of an organ or tissue due to a decrease in cell size and number

(OPPOSITE OF HYPERTROPHY)

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28
Q

Compare examples of the physiological and pathological patterns of atrophy.

A

Physiological → Thymus Gland Shrinkage

Pathological → Decrease workload, loss of innovation, diminished blood supply, inadequate nutrition, loss of endocrine simulation

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29
Q

Which is reversible: atrophy or dystrophy?

A
  • Atrophy is reversible

- Dystrophy is irreversible cell death

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30
Q

What is the mechanism of atrophy?

A

DECREASED metabolic activity → DECREASED protein synthesis and INCREASED protein degradation → leads to atrophy

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31
Q

What is metaplasia?

A

A reversible change in which one adult cell type is replaced by another cell type

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32
Q

What type of response is metaplasia?

A

Metaplasia often represents an adaptive response in which one cell type that is sensitive to a particular stress is replaced by another cell type that is better able to withstand the adverse environment

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33
Q

What happens when you have persistent metaplasia?

A

The influences that induced metaplastic change in an epithelium, if persistent, may predispose to malignant transformation

34
Q

Compare examples of the physiological and pathological patterns of metaplasia.

A

Physiological → Body’s normal response to inflammation, monocytes that migrate to inflamed tissue transform into macrophages

Pathological → Chronic Irritation of Respiratory Epithelium (squamous epithelium) or Gastric Acid Reflux (columnar epithelium)

35
Q

What are the two types of lysosomal degradation?

A

Heterophagy and Autophagy

36
Q

What is heterophagy?

A

Occurs when endosomes and phagosomes fuse with lysosomes to facilitate the degradation of their internalized contents

37
Q

What is autophagy?

A

“Self-Eating” Mechanism

Occurs when senescent organized or denatured proteins are encircled with a double membrane which fuses with the lysosome and is degraded

38
Q

What is the mechanism of lysosomal degradation?

A

Lysosomes chop down things it comes into contact with and acid hydrolases cause the degradation

39
Q

What are lysosomes?

A

Lysosomes are vesicles containing digestive enzymes that are produced by the golgi apparatus. Lysosomes are used to defend against bacteria by cleaning up cellular debris & recycle worn out organelles.

40
Q

What is a proteasome?

A

Enzymes involved in breaking down proteins that are tagged with ubiquitin molecules. The proteins are degraded because they are misfolded or not needed by our body.

41
Q

How does a proteasome break down the protein?

A

Proteasomes break down the proteins (polypeptides) in to 6-12 amino acid chunks, which have to be further broken down into individual amino acids by other cellular
proteases.

42
Q

What are reactive oxygen species?

A

ROS are free radicals that have a single unpaired electron.

Oxidative stress is induced by ROS

43
Q

Describe normal production of ROS.

A

Produced normally at very low levels in all cells during the reduction oxidation (redox) reactions

44
Q

Where are ROS produced?

A

ROS are produced in phagocytic leukocytes, mainly neutrophils and macrophages.

45
Q

What increases ROS?

A

Hypoxia and toxic injury increase ROS → resulting in cell cycle arrest or apoptosis

46
Q

What is an ischemia-reperfusion injury?

A

Injury due to the restoration of blood flow to ischemic but viable tissue

47
Q

How does ROS affect an ischemia-reperfusion injury?

A

There is increased generation of ROS in the reperfused organ → complement activation & increased inflammatory infiltrate

48
Q

What are examples of an ischemia-reperfusion injury?

A

MI, ARF, Stroke

49
Q

How is accumulation of ROS determined?

A

Rates of production and removal

50
Q

What is the definition of granulomatous inflammation?

A

Characterized by local accumulations of activated macrophages (granuloma), surrounded by lymphocytes and surrounded with central necrosis.

51
Q

What type of inflammation is granulomatous inflammation: chronic or acute?

A

Chronic Inflammation

52
Q

What are the two types of granulomas?

A

Foreign Body Granulomas and Immune Granulomas

53
Q

What is a Foreign Body Granuloma?

A

A granuloma that is induced by particles that can be phagocytized

54
Q

What is an Immune Granuloma?

A

A granuloma formed by T-Cell-Mediated responses to persistent microbes or self-antigen

55
Q

What are the 3 steps in repair by scar formation?

A
  1. Inflammation
  2. Cell Proliferation
  3. Remodeling of Connective Tissue
56
Q

Compare the length from injury of the three steps of inflammation.

A

Inflammation– 6 to 48 hours
Cell Proliferation– up to 10 days
Remodeling of Connective Tissue– 2 to 3 wks after injury

57
Q

Explain the first step of scar formation.

A

-Inflammation

→ Typical acute and chronic inflammatory responses
→ Macrophages are a major player

58
Q

Explain the second step of scar formation.

A

-Cell Proliferation

→ Granulation tissue forms when epithelial cells respond to growth factors and migrate over to injury site
→ Angiogenesis: new blood vessel production (sprouting occurs)
→ Proliferating fibroblasts produce collagen fibers

59
Q

Explain the third step of scar formation.

A

-Remodeling of Connective Tissue

→ The replacement of granulation tissue with a fibrous scar
→ TGF-beta is involved in synthesis & deposition of connective tissue proteins which then forms the scar

60
Q

What are the 4 systemic factors that influence tissue repair with examples?

A

→Nutritional Status (ex: decreased vitamin c intake)

→Metabolic Status (ex: diabetes patient don’t heal well)

→Circulatory Status (ex: need blood to repair stress)

→Hormones (ex: steroids can slow healing process and make you more susceptible to fungal infections)

61
Q

What are the 4 local factors that influence tissue repair?

A

→Infections
→Size (location & type of wound)
→Mechanical Forces
→Foreign Bodies

62
Q

What is the definition of an aneurysm?

A

An aneurysm is an abnormal vascular dilation (bulging of blood vessels)

63
Q

What are the 3 types of aneurysms?

A

→True Aneurysm
→False Aneurysm
→Dissection

64
Q

What is a true aneurysm?

A

Occurs when all 3 vessel wall layers dilate, although layers can be individually weakened

65
Q

What is another name for false aneurysm?

A

Pseudoaneurysm

66
Q

What is a false aneurysm?

A

An extravascular hematoma that freely communicates with the intravascular space

Occurs when part of vessel wall has been lost and starts to form a collection of blood and connective tissue outside of aortic wall

67
Q

What is a dissection?

A

Occur when blood enters the arterial wall itself with no communication to intracellular space

68
Q

What is the pathogenesis of aneurysms?

A
  • Inflammation → weakening of blood vessels
  • Inadequate production or degradation of extracellular matrix
  • Apoptosis of smooth muscle cells due to ischemia
69
Q

What is the major etiology of Abdominal Aortic Aneurysms (AAA)?

A

Atherosclerosis

70
Q

What is the pathogenesis of Abdominal Aortic Aneurysms (AAA)?

A
  • Inflammatory infiltrates in atherosclerotic lesions that produce proteolytic enzymes → ECM degradation
  • ECM can’t protect itself → leading to weakened vessels
71
Q

Where do Abdominal Aortic Aneurysms (AAA) occur?

A

Below the chest

72
Q

What are the clinical features of Abdominal Aortic Aneurysms (AAA)?

A
  • Rupturing into the peritoneal cavity with massive hemorrhage (the risk of rupture increases as the size of the AAA increases)
  • Occlusion of a branch vessel
  • Compression of adjacent structures
  • Artheroembolism occurs which releases cholesterol crystals from a ruptured plaque which leads to more clotting in the distal arteries
73
Q

What is the major etiology of Thoracic Aortic Aneurysms?

A

Hypertension

74
Q

What are the clinical features of Thoracic Aortic Aneurysms?

A
  • Respiratory or Feeding Difficulties
  • Persistent cough
  • Pain
  • Cardiac Abnormalities
  • Aortic Dissection / Aortic Rupture
75
Q

Where do Thoracic Aortic Aneurysms occur?

A

Within the chest → clinical features encapsulate respiratory consequences

76
Q

What is the definition of an aortic dissection?

A

Blood dissects the media vessel layer and enters the aortic wall, forming a blood-filled channel

77
Q

What is the major clinical consequence of an aortic dissection?

A
  • Often leads to rupture → causing sudden death through massive hemorrhage
  • Death is usually the result of rupture into the pericardium, thorax, or abdominal cavities
78
Q

What are the main clinical targets of an aortic dissection?

A
  • Sudden onset of excruciating chest pain

- The pain can be confused with that of a heart attack

79
Q

What is the pathogenesis of aortic dissection?

A

-Once the tear is initiated, blood flow under systemic pressure advances the dissection area

→In hypertensive patients, aorta shows medical degeneration that is associated with loss of medical smooth muscle cells and disorganized extracellular matrix

80
Q

What are the main risk factors of aortic dissection?

A

→Hypertension
→Atherosclerosis
→Connective tissue defects that affect the aorta

Patho (2 decks)

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