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1
Q

What kind of stimuli leads to cellular aging? Calcification? Cell injury? Cell adaptation?

A

Cellular aging: Cumulative sub-lethal injury over long life span
Calcification: Metabolic alterations, genetic or acquired, chronic injury
Cell Injury: Reduced oxygen supply, chemical injury, microbial infection
Cell adaptations: Altered physiological stimuli or non-lethal injurious stimuli

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2
Q

Examples of the three groups of tissues?

A

Labile: hematopoietic cells, surface epithelia
Stable: endothelial, fibroblasts, smooth muscle cells, parenchyma of most solid organs
Permanent: neurons, cardiac muscle cells

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3
Q

Give example of physiologic and pathologic hypertrophy

A

Physiologic: skeletal muscle in weight lifting, uterus in pregnancy
Patholgoic: cardiac muscle in hypertension

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4
Q

When the liver grows back after resection, that is an example of _____ _____

A

physiologic hyperplasia

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5
Q

Hyperplasia occurs in ____ cells, while hypertrophy occurs in ____ cells

A

Hyperplasia: labile, stable
Hypertrophy: Cells with limited or no capacity to divide

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6
Q

What is an example of tissue hypertrophy and hyperplasia?

A

Enlargement of uterus during pregnancy

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7
Q

Atrophy leads to decreased cell function and death. True or false?

A

False; leads to decreased cell function but NOT death

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8
Q

Examples of physiologic and pathologic atrophy?

A

Physiologic: endometrium at menopause (loss of hormonal stimulation)
Pathologic: calorie or protein deficit (inadequate nutrition), trauma to peripheral nerve, etc

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9
Q

You can get hypertrophy and atrophy of muscle fibers in myopathy. True or false?

A

True

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10
Q

BPH hyperplasia is associated with a higher risk of prostate cancer. True or false?

A

False; but endometrial hyperplasia IS associated with higher risk of cancer

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11
Q

Pathologic hyperplasia is reversible/irreversible. Metaplasia is reversible/irreversible.

A

Both reversible

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12
Q

Metaplasia may be associated with risk of cancer. True or false?

A

True

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13
Q

What is metaplasia?

A

Adaptive process to chronic stress and/or persistent injury where one adult cell type is replaced by another adult cell type that is better able to handle the stress

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14
Q

Example of epithelial metaplasia? Mesenchymal metaplasia?

A

Epi: Squamous epi becomes gastric/intestinal type epi in distal esophagus in those with reflux

Mesenchymal: Bone formation in soft tissue (muscle, connective) at sites of injury

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15
Q

Describe metaplasia in the cervix

A

Endocervix: columnar becomes squamous and increases risk of HPV infection

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16
Q

Is aging a cause of cell injury? Why or why not?

A

Yes, decreased ability to repair damage

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17
Q

Necrosis in terms of cell size, nucleus, plasma membrane, cellular contents, adjacent inflammation, physiologic/pathologic role?

A 
Enlarged/swelling cell size
Pyknosis, karyorrhexis, karyolysis
Disrupted PM
Enzymatic digestion, may leak out 
Frequent adjacent inflammation
Pathologic
*Also increased eosinophilia
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18
Q

Apoptosis in terms of cell size, nucleus, plasma membrane, cellular contents, adjacent inflammation, physiologic/pathologic role?

A

Reduced/shrinkage cell size
Fragmentation into nucleosome-size fragments
Intact PM, altered structure
Intact cell contents, may be released in apoptotic bodies
No adjacent inflammation
Often physiologic, may be pathologic

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19
Q

What are the four cardinal signs of inflammation?

A 
Calor (heat) 
Rubor (redness)
Tumor (swelling)
Dolor (pain)
*Functio lasea (loss of function)
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20
Q

Prominent cell in acute vs chronic inflammation?

A

Acute: neutrophil
Chronic: monocyte/macrophages, lymphocytes

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21
Q

Extent of local and systemic signs of acute vs chronic inflammation?

A

Acute: Prominent
Chronic: less prominent, may be subtle

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22
Q

Tissue injury/fibrosis in acute vs chronic inflammation?

A

Acute: Mild, self-limited
Chronic: Often severe, progressive (bystander effect)

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23
Q

Causes of chronic inflammation?

A

Persistent infections thats difficult to eradicate (TB, syphilis, leprosy, some viruses/fungi/parasites)

Prolonged exposure to toxic agents (silicosis, atherosclerosis)

Autoimmune diseases

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24
Q

Stimuli of acute inflammation?

A 
Infections, microbial toxins
Physical trauma
Physical and chemical agents
Tissue necrosis
Foreign bodies
Immune/hypersensitivity reactions
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25
Initiation of inflammatory response: stimuli is recognized by receptors on:
Epithelial cells Dendritic cells Phagocytes
26
Compare TLR and inflammasome
TLR: - On PM, recognize bacteria/viruses/other pathogens - When activated, releases cytokines (TNF) Inflammasome: - Cytoplasmic, recognizes parts of DEAD cells (uric acid, ATP, etc) and SOME microbes - Triggers activation of caspase-1 --> activates IL-1 --> triggers leukocyte recruitment
27
Inflammation initiation, TNF and IL-1 release leads to what?
Major effect of TNF and IL-1 is endothelial activation --> leukocyte binding and recruitment --> production of more cytokines
28
Role of histamine?
Causes vasodilation and increases vascular permeability Released from mast cells in connective tissue near vessels May be released in response to cytokines (IL-1), trauma, complement, etc
29
Role of NO?
Causes vasodilation Released by endothelial cells in response to injury
30
Role of bradykinin?
Causes vasodilation, increased permeability and pain Endothelial injury site exposure --> activate kinin system --> bradykinin (plasma protein) release
31
Specific gravity of transudate vs exudate?
Transudate: low s.g. 1.020
32
What causes transudate vs exudate?
Transudate: imbalances in hydrostatic/osmotic pressures Exudate: alteration in normal vessel permeability
33
How long is chronic inflammation?
Weeks to months to years
34
Chronic inflammation = active inflammation, tissue injury and healing occur at the same time. True or false?
True
35
Monocyte role in inflammation?
Acute: Circulating monocytes become the tissue macrophages Chronic: same but persist
36
Why do macrophages persist in chronic inflammation?
Steady release of dead cells, microbes, etc Stimulation by cytokines (IFN-Y) from activated T cells ***Macrophages then secrete products that result in continued tissue injury
37
Other cells involved in chronic inflammation other than macrophages?
Lymphocytes (T&B cells migrate to site, respond to chemokines) Activated B plasma cells --> Ig production against persistent antigens Eosinophils --> parasitic infection and IgE mediated inflammation (allergies) Mast cells in connective tissues --> release histamine, arachidonic acid metabolites. Has receptor for IgE for environmental antigens, and central in allergic and anaphylatic reactions
38
Histology/morphology of chronic inflammation?
Mononuclear cell infiltrate (macro, lympho, plasma cells) Tissue destruction; ongoing attempted tissue replacement and repair - angiogenesis - fibrosis
39
What is granulomatous inflammation? What does it look like?
Distinctive pattern of chronic inflammation | Prominent activated macros with epithelioid appearance
40
Granulomatous inflammation develops in the response to?
Specific infections Inert foreign bodies Immune reaction against self or unknown antigens
41
Infectious and non-infectious causes of granulomatous inflammation?
``` Splinters TB Syphilis Leprosy Sutures Silica Cat scratch fever Crohn disease Some fungal infections ```
42
Granulomatous inflammation histology characteristics?
Aggregate of epithelioid histiocytes/macros Multinucleated giant cells (fusion of many macros, IFN-y induces giant cell formation) Collar of lymphocytes Surrounding fibrosis
43
How can you tell histologically if its TB?
Think granulomatous inflammation | PLUS central caseous necrosis
44
What do mast cells release in hypersensitivity?
Histamine Heparin Tryptase Chymase, Cathepsin G, Carboxypeptidase Cytokines (IL-3, 4, 5, 13, GM-CSF and TNF) Chemokines (MIP-1alpha, RANTES, Eotaxin) Lipid Mediators (Leukotrienes C4, D4, E4 and PAF)
45
When do you see elevated eosinophil count?
``` NAACP Neoplasia Asthma Allergy (atopic disease, drug allergy) Connective tissue disease Parasitic disease ```
46
Examples of Type I hypersensitivity?
Asthma Anaphylaxis Allergic Rhinitis Urticaria
47
What can substitute for mast cell in early phase type I hypersensitivity?
Basophils, but no tryptase or PGD2 release
48
How do steroids/corticosteroids affect eosinophils? How is it mediated?
- induce rapid apoptosis of eosinophils - inhibit production of IL-5 --> increased apoptosis and decreased release from marrow Steroid binds GR-alpha and inhibits AP-1 and NFkB
49
Main source of IL-5?
Th2
50
How does IL-5 affect eosinophils in vitro?
- Prolongs survival - Enhances LT production and cytotoxicity against parasites - Augments B2-integrin mediated adhesion and transendothelial migration
51
How does IL-5 affect eosinophils in vivo?
- Causes eosinophilia - Find high IL-5 in diseases with eosinophilia - Find high IL-5 in fluid from sites of experimental late stage allergic reactions
52
What are some select eosinophil products? and their roles?
Lysophospholipase - degrades lysophospholipids MBP - mast cell activation, helminthotoxic ECP - same as MBP + neurotoxin EDN - neurotoxin PAF - bronchoconstriction, activates "PEN" LTC4 - bronchoconstriction, edema, mucus hypersecretion
53
Allergic rhinitis is present in up to __% of the population. May also have associated ___
20% | Associated asthma
54
Symptoms of allergic rhinitis is due to _____
cross-linking of IgE in nasal mucosa and ocular conjunctiva
55
Asthma effects __% of the population. Symptoms are due to ______
5% | IgE mediated disease in lower airways
56
What are some anaphylaxis mediators?
Histamine Leukotrienes NO
57
Role of histamine as anaphylaxis mediator?
H1: Smooth muscle contraction, vascular permeability H2: vascular permeability Both: vasodilation, pruritis
58
Role of leukotriene as anaphylaxis mediator?
Smooth muscle contraction Vascular permeability Vasodilation
59
Role of NO as anaphylaxis mediator?
Smooth muscle relaxation Vascular permeability Vasodilation
60
What does irreversible cell injury/death mean?
- Inability to reverse mitochondrial dysfunction (no oxid phosph/ATP generation) - Disturbance of membrane function
61
What are the steps in leukocyte recruitment in acute inflammation?
``` Margination Rolling Adhesion Transmigration Chemotaxis ```
62
Describe how leukocytes roll and adhere to blood vessels
Adhesion molecules - Selectins and Integrins - Selectin (aid in rolling and LOOSE attachment): on endothelial, leukocytes, platelets - Integrin (results in STABLE attachment): on leukocytes
63
Are selectins always present on cell surfaces?
No, not until mediators activate (histamine, thrombin, etc)
64
Are integrins always expressed/activated on leukocytes?
No, they are activated by chemokines released by endothelial cells
65
Transmigration is driven by the chemokine:
CD31/PECAM1 on leukocytes & endo cells
66
What mediators are important in leukocyte recruitment/activation and chemotaxis?
IL-1 TNF Bacterial products
67
What mediators are important for tissue damage?
NO | ROS

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