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FPP Flashcards

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
Q

Initiation of inflammatory response: stimuli is recognized by receptors on:

A

Epithelial cells
Dendritic cells
Phagocytes

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26
Q

Compare TLR and inflammasome

A

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
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27
Q

Inflammation initiation, TNF and IL-1 release leads to what?

A

Major effect of TNF and IL-1 is endothelial activation –> leukocyte binding and recruitment –> production of more cytokines

28
Q

Role of histamine?

A

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
Q

Role of NO?

A

Causes vasodilation

Released by endothelial cells in response to injury

30
Q

Role of bradykinin?

A

Causes vasodilation, increased permeability and pain

Endothelial injury site exposure –> activate kinin system –> bradykinin (plasma protein) release

31
Q

Specific gravity of transudate vs exudate?

A

Transudate: low s.g. 1.020

32
Q

What causes transudate vs exudate?

A

Transudate: imbalances in hydrostatic/osmotic pressures
Exudate: alteration in normal vessel permeability

33
Q

How long is chronic inflammation?

A

Weeks to months to years

34
Q

Chronic inflammation = active inflammation, tissue injury and healing occur at the same time. True or false?

A

True

35
Q

Monocyte role in inflammation?

A

Acute: Circulating monocytes become the tissue macrophages

Chronic: same but persist

36
Q

Why do macrophages persist in chronic inflammation?

A

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
Q

Other cells involved in chronic inflammation other than macrophages?

A

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
Q

Histology/morphology of chronic inflammation?

A

Mononuclear cell infiltrate (macro, lympho, plasma cells)

Tissue destruction; ongoing attempted tissue replacement and repair

  • angiogenesis
  • fibrosis
39
Q

What is granulomatous inflammation? What does it look like?

A

Distinctive pattern of chronic inflammation

Prominent activated macros with epithelioid appearance

40
Q

Granulomatous inflammation develops in the response to?

A

Specific infections
Inert foreign bodies
Immune reaction against self or unknown antigens

41
Q

Infectious and non-infectious causes of granulomatous inflammation?

A 
Splinters
TB
Syphilis
Leprosy
Sutures
Silica
Cat scratch fever
Crohn disease
Some fungal infections
42
Q

Granulomatous inflammation histology characteristics?

A

Aggregate of epithelioid histiocytes/macros

Multinucleated giant cells (fusion of many macros, IFN-y induces giant cell formation)

Collar of lymphocytes
Surrounding fibrosis

43
Q

How can you tell histologically if its TB?

A

Think granulomatous inflammation

PLUS central caseous necrosis

44
Q

What do mast cells release in hypersensitivity?

A

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
Q

When do you see elevated eosinophil count?

A 
NAACP
Neoplasia
Asthma
Allergy (atopic disease, drug allergy)
Connective tissue disease
Parasitic disease
46
Q

Examples of Type I hypersensitivity?

A

Asthma
Anaphylaxis
Allergic Rhinitis
Urticaria

47
Q

What can substitute for mast cell in early phase type I hypersensitivity?

A

Basophils, but no tryptase or PGD2 release

48
Q

How do steroids/corticosteroids affect eosinophils? How is it mediated?

A
  • 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
Q

Main source of IL-5?

A

Th2

50
Q

How does IL-5 affect eosinophils in vitro?

A
  • Prolongs survival
  • Enhances LT production and cytotoxicity against parasites
  • Augments B2-integrin mediated adhesion and transendothelial migration
51
Q

How does IL-5 affect eosinophils in vivo?

A
  • 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
Q

What are some select eosinophil products? and their roles?

A

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
Q

Allergic rhinitis is present in up to __% of the population. May also have associated ___

A

20%

Associated asthma

54
Q

Symptoms of allergic rhinitis is due to _____

A

cross-linking of IgE in nasal mucosa and ocular conjunctiva

55
Q

Asthma effects __% of the population. Symptoms are due to ______

A

5%

IgE mediated disease in lower airways

56
Q

What are some anaphylaxis mediators?

A

Histamine
Leukotrienes
NO

57
Q

Role of histamine as anaphylaxis mediator?

A

H1: Smooth muscle contraction, vascular permeability
H2: vascular permeability
Both: vasodilation, pruritis

58
Q

Role of leukotriene as anaphylaxis mediator?

A

Smooth muscle contraction
Vascular permeability
Vasodilation

59
Q

Role of NO as anaphylaxis mediator?

A

Smooth muscle relaxation
Vascular permeability
Vasodilation

60
Q

What does irreversible cell injury/death mean?

A
  • Inability to reverse mitochondrial dysfunction (no oxid phosph/ATP generation)
  • Disturbance of membrane function
61
Q

What are the steps in leukocyte recruitment in acute inflammation?

A 
Margination
Rolling
Adhesion
Transmigration
Chemotaxis
62
Q

Describe how leukocytes roll and adhere to blood vessels

A

Adhesion molecules - Selectins and Integrins

  • Selectin (aid in rolling and LOOSE attachment): on endothelial, leukocytes, platelets
  • Integrin (results in STABLE attachment): on leukocytes
63
Q

Are selectins always present on cell surfaces?

A

No, not until mediators activate (histamine, thrombin, etc)

64
Q

Are integrins always expressed/activated on leukocytes?

A

No, they are activated by chemokines released by endothelial cells

65
Q

Transmigration is driven by the chemokine:

A

CD31/PECAM1 on leukocytes & endo cells

66
Q

What mediators are important in leukocyte recruitment/activation and chemotaxis?

A

IL-1
TNF
Bacterial products

67
Q

What mediators are important for tissue damage?

A

NO

ROS

FPP (3 decks)

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