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Disease and Defense > Unit II > Flashcards

Unit II Flashcards

1
Q

What is aplastic anemia?

A

Normocytic-normochromic anemia that results from a loss of blood cell precursors, causing hypoplasia of bone marrow, RBCs, WBCs, and platelets.

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2
Q

What are the four classic signs of inflammation?

A

calor (heat), rubor (redness), tumor (swelling), and dolor (pain)

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3
Q

What is the innate immune system?

A

nonspecific defense mechanism, immediately or very soon (minutes to hours) Includes physical barriers: skin, mediators in the blood, immune system cells

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4
Q

What is the adaptive immune system?

A

antigen-specific response. More complex than innate. Requires antigen processing. Involves creating cells specifically designed for that antigen. Also includes memory for faster future encounters

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5
Q

Signs of acute inflammation

A

rapid in onset and of short duration, lasting from a few minutes to as long as a few days, and is characterized by fluid and plasma protein exudation and a predominantly neutrophilic leukocyte accumulation.

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6
Q

What are the cellular infiltrates for acute inflammation?

A

neutrophils

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7
Q

Signs of Chronic inflammation

A

more insidious, is of longer duration (days to years), and is typified by influx of lymphocytes and macrophages with associated vascular proliferation and fibrosis (scarring).

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8
Q

What are the cellular infiltrates for chronic inflammation?

A

lymphocytes and macrophages

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9
Q

What are the agents that cause acute inflammation?

A

Infection, trauma, tissue necrosis, foreign material, and immune reactions

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10
Q

What is the roll of toll like receptors?

A

Pattern recognition receptors found on the surface and within the host cell that can detect foreign material. Once activated it triggers the production of transcription factors to create proteins that mediate inflammation, interfere with action of infectious agents (interferons) and promote lymphocyte activation.

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11
Q

What is an inflammasome?

A

receptors that stimulate inflammation via activation of caspase-1. Caspase-1 forms active Interleukin-1β (IL-1β), which then recruits leukocytes that come
in to clean up dead cells

**recognizes products of dead cells like ATP and free floating DNA

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12
Q

inflammasome induce the secretion of what molecule?

A

Interleukin-1β

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13
Q

What are exudates?

A

An exudate is formed in inflammation because vascular permeability increases as a result of the increase in interendothelial spaces.

**typical inflammation response

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14
Q

What are transudates?

A

A transudate is formed when fluid leaks out because of increased hydrostatic pressure or decreased osmotic pressure.

**noninflammatory conditions/ vascular wall still in tact

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15
Q

What are the two major changes during acute inflammation?

A

increased blood flow and increase vessel permeability

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16
Q

What mechanism contribute to increase vessel permeability?

A

Endothelial cell contraction leading to intercellular gaps in postcapillary venules

Injury of endothelial cells –> incomplete endothelial layer

Transcytosis

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17
Q

quick response endothelial contraction is stimulated by what molecules?

A

histamines

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18
Q

Longer-term contraction is prompted by what molecules?

A

Cytokines like IL-1 and TNF

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19
Q

What is fibrosis?

A

If the tissue cannot regenerate or if there has been significant tissue destruction then
instead connective tissue fills the void

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20
Q

What adhesion molecules grab onto sugars that are present on the surface of leukocytes to promote leukocyte rolling?

A

P and E selectins

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21
Q

What molecule stimulates P-selectins?

A

histamine

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22
Q

What molecule stimulates E-selectins?

A

IL-1

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23
Q

What is stasis?

A

caused when numerous dilated small vessels become packed with red blood cells and blood viscosity increases

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24
Q

What is a low concentrations of protein and few or no blood cells in the extravascular space indicative of?

A

transudates

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25
Q

explain the adhesion process for leukocytes

A

When the adherent leukocytes encounter the displayed chemokines, the cells are activated, and their integrins undergo conformational changes and cluster together, thus converting to a high-affinity form

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26
Q

explain the adhesion process of endothelial cells

A

cytokines, notably TNF and IL-1 (also secreted at sites of infection and injury), activate endothelial cells to increase their expression of ligands for integrins. These ligands include intercellular adhesion molecule-1 (ICAM-1),

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27
Q

Where does diapedesis take place?

A

mainly in the venules of the systemic vasculature

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28
Q

what are opsonins?

A

Host proteins that coat microbes and target them for phagocytosis

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29
Q

Name examples of opsonins

A

IgG, compliment system (C3b), collectins

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30
Q

What are neutrophil extracellular traps?

A

tracellular fibrillar networks that are produced by neutrophils to prevent the spread of microbes.

Essentially they release their own chromatin to trap these microbes in place.

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31
Q

What collateral tissue damage is associated with inflammation?

A
  1. Tissue surrounding infectious agents may become damaged.
  2. Cleaning up necrotic tissue by the inflammatory process may cause additional damage
  3. Inflammatory process is directed against host tissues (i.e. autoimmune diseases)
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32
Q

What are common causes for defective leukocyte function?

A
  1. aplastic anemia secondary to chemotherapy
  2. Diabetes
  3. Chédiak-Higashi syndrome which has mutations in the proteins responsible for trafficking of
    organelles; thus phagosomes and lysosomes cannot properly fuse.
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33
Q

What are the trademark cells for chronic inflammation?

A

monocytic cells - lymphocytes, macrophages, dendritic cells, plasma cells

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34
Q

What are the characteristics of chronic inflammation?

A
  • inflammation with mononuclear cells
  • tissue destruction
  • repair
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35
Q

Describe a smear with acute inflammation of the lung

A

neutrophils filled in the alveolar space and blood vessel congestion

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36
Q

what is pruritus?

A

severe itching the skin

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37
Q

What are macrophages in the liver called?

A

Kupffer cells

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38
Q

What induces classical macrophage activation?

A

microbial products such as endotoxin, by T cell–derived signals, importantly the cytokine IFN-γ

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39
Q

What do classically activate macrophages produce?

A

NO, and ROS, all of which enhance their ability to kill ingested organisms, and secrete cytokines that stimulate inflammation

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40
Q

What induces alternative macrophage activation?

A

cytokines other than IFN-γ, such as IL-4 and IL-13, produced by T lymphocytes and other cells, including mast cells and eosinophils

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41
Q

What do alternative activated macrophages produce?

A

growth factors that promote angiogenesis, activate fibroblasts and stimulate collagen synthesis.

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42
Q

What is the principal role for alternative activated macrophages?

A

tissue repair, fibrosis, anti-inflammatory effects

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43
Q

What do TH1 CD4+ T lymphocytes secrete?

A

IFN-ɣ which activates classical pathway macrophages

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44
Q

What do TH2 CD4+ T lymphocytes secrete?

A

IL-4, IL-5, IL-13 which activates alternative pathway macrophages; also activates eosinophils

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45
Q

What do TH17 CD4+ T lymphocytes secrete? I

A

L-17 which recruits neutrophils and monocytes

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46
Q

Which chemokine recruits eosinophils?

A

eotaxins

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47
Q

What type of antibody is found on mast cells?

A

IGE

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48
Q

What cells are central players in allergic reactions, including anaphylactic shock?

A

IgE armed mast cells

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49
Q

What is the characteristic of granulomatous inflammation?

A

aggregates of activated enlarged macrophages with scattered lymphocytes

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50
Q

What is the prototype of a granulomatous disease?

A

tuberculosis

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51
Q

What are diseases associated with Granulomatous inflammation?

A

Crohn’s disease and sarcoidosis

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52
Q

what are the cells of chronic inflammation?

A

Macrophages
Lymphocytes
Eosinophils
Mast cells

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53
Q

What are the cytokines associated with acute phase reaction aka systemic inflammation?

A

TNF, IL-1, and IL-6 are responsible for many of the systemic effects

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54
Q

what cells produces the cytokines associated with acute phase reaction?

A

leukocytes

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55
Q

What triggers a fever?

A

a response to substances called pyrogens that act by stimulating prostaglandin synthesis in the vascular and perivascular cells of the hypothalamus.

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56
Q

what is the role of IL-6 in acute phase reactions?

A

IL-6 stimulates the hepatic synthesis of a number of plasma proteins

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57
Q

What are the acute phase proteins?

A

C-reactive protein (CRP) and serum amyloid A (SAA) protein are known to adhere to cell walls and may act as opsonins

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58
Q

What is used to test for the presence of inflammation?

A

erythrocyte sedimentation rate (ESR)

Fibrinogen binds red blood cells causing them to form stacks that quickly form sediments

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59
Q

What cytokine cause an increased number of immature white blood cells (early release)?

A

TNF and IL-1

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60
Q

What infection is assocaited to neutrophilia?

A

Bacterial infection

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61
Q

What infection is associated with lymphocytosis?

A

viral infection

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62
Q

What infection is associated with eosinophilia?

A

asthma and parasitic infection

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63
Q

What infection is associated with leukopenia?

A

specific infection like typhoid fever

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64
Q

What triggers the production of leukocytes?

A

colony stimulating factor

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65
Q

What are the two vasoactive amines and where are they stored?

A

histamine and serotinin both stored in mast cells

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66
Q

What is the role of histamine?

A

arterial dilation and & endothelial contraction

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67
Q

What is the role of serotonin?

A

vasoconstriction to aid in clotting

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68
Q

Where is serotonin found?

A

in platelet granules that are released during platelet aggregations

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69
Q

What stimuli cause mast cells to release histamine?

A 
Physical features - trauma or heat 
Immune – Binding of IgE
Compliment (C3a, C5a)
Histamine releasing proteins (from leukocytes)
Neuropeptides
Cytokines (IL-1, IL-8)
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70
Q

name of the source of arachidonic acid metabolites

A

Leukocytes, mast cells, endothelium & platelets

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71
Q

how are AA metabolites inactivated?

A

by spontaneous decay and enzymes

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72
Q

What are the two major pathways of arachidonic acid metabolism?

A

cyclooxygenase and lipoxygenase pathway

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73
Q

The cyclooxygenase pathway leads to what products?

A

prostaglandins and thromboxanes

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74
Q

What is the role of prostaglandins?

A

causes vasodilation and inhibits platelet aggregation

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75
Q

What is the role of thromboxanes?

A

causes vasoconstriction and promotes platelet aggregation

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76
Q

The lipoxygenase pathway leads to what products?

A

leukotrienes and lipoxins

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77
Q

What is the role of leukotrienes?

A

causes bronchoconstriction and increased vascular permeability

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78
Q

What is the role of lipoxins?

A

inhibit neutrophil chemotaxis and adhesion to endothelium and thus serve as endogenous **antagonist of leukotrienes.

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79
Q

What medication would you use to block the cyclooxygenase pathway?

A

NSAIDs

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80
Q

What medication would you use to block the entire arachidonic acid metabolites?

A

glucocorticoid steroids

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81
Q

What enzyme does glucocorticoid sterioids inhibit?

A

phospholipase

**stops the release of all AA metabolites

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82
Q

What cell derived mediator contributes to pain and fever?

A

prostaglandins

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83
Q

What is platelet activating factor?

A

phospholipid-derived mediator with a broad spectrum of inflammatory effects.

Effects include: platelet aggregation, vasodilation, vascular permeability and bronchoconstriction along with stimulation of platelets and cells to form other mediators

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84
Q

What are important acute inflammatory cytokines?

A

TNF, IL-1, IL-6

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85
Q

What are the main functions of TNF and IL-1?

A

Cause endothelial activation (leukocyte binding and recruitment)
Also induce systemic effects of inflammation: Fever, acute phase protein synthesis, etc

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86
Q

What are the important chronic inflammatory cytokines?

A

IFN-γ and IL-12

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87
Q

What is the role of IFN-γ?

A

Stimulates classical macrophage activation

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88
Q

What is the role of IL-12?

A

Stimulate the growth and function of T cells

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89
Q

What induces the activation of IL-1?

A

inflammasome

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90
Q

What cells produce reactive oxygen species?

A

neutrophils and macrophages

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91
Q

What is the role of reactive oxygen species?

A

highly toxic oxidizers that not only damage microbes, but also host tissues

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92
Q

What is the function of nitric oxide in inflammation?

A

a free radical that can be used to kill microbes

A mediator of vasodilation, antagonizes platelet activation, & reduces leukocyte recruitment

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93
Q

How is Type II NOS stimulated?

A

induced in macrophages and endothelial cells

Induced by IL-1, TNF, IFN-γ and bacterial endotoxins

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94
Q

What pH conditions are ideal for intracellular lysosomal enzymes?

A

low pH

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95
Q

What pH conditions are ideal for extracellular lysosomal enzymes?

A

neutral pH

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96
Q

What is the role of alpha 1- antitripsin?

A

inhibits elastase **protease inhibitor

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97
Q

What is the role of alpha 2-macroglobulin

A

inhibits a large variety of proteinases (e.g. collagenase)

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98
Q

Give an example of a neuropeptide

A

Substance P, an 11 amino acid peptide
Secreted by nerves and inflammatory cells (macrophages, eosinophils, lymphocytes, dendritic cells)

**generates proinflammatory effects in immune and epithelial cells

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99
Q

What are neuropeptides active in?

A

vascular tone and permeability

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100
Q

What is the central complement factor?

A

C3

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101
Q

What are they three pathways for the formation of C3?

A

1) the classical pathway, triggered by fixation of the first complement component C1 to antigen-antibody complexes;
(2) the alternative pathway, triggered by bacterial polysaccharides (e.g., endotoxin)
(3) the lectin pathway, in which a plasma lectin binds to mannose residues on microbes and activates an early component of the classical pathway (but in the absence of antibodies).

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102
Q

What happens once C3 is cleaved?

A

It cleaves into C3a and B. C3b deposits on the cell or microbial surface where complement was activated and then binds to the C3 convertase complex to form C5 convertase; this complex cleaves C5 to generate C5a and C5b and initiate the final stages of assembly of C6 to C9.

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103
Q

What is the role of C3a and C5a?

A

increases vascular permeability and stimulates mast cells to release histamine

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104
Q

What complement molecule activates the lipogenous pathway for AA metabolism?

A

C5a

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105
Q

What complement molecules activate leukocytes increasing their endothelial adhesion?

A

C5a, C4a, C3a

**these are also chemotatic agents for neuts, eos, basophils and monocytes

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106
Q

What complement molecule acts as opsonin for enhanced phagocytosis?

A

C3b

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107
Q

What part of complement forms the MAC?

A

multiple C9 proteins

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108
Q

What protects host tissue from activated complement?

A

C1 inhibitor blocks activation of C1

**Decay-accelerating factor (DAF) and **factor H limit C3/C5 convertase formation

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109
Q

What is the role of clotting factor XII in inflammation?

A

important clotting factor that activates the kinin system –> ultimately leads to bradykinin which increases vascular permeability, vascular dilation and pain

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110
Q

What activates factor XII?

A

Intermediate product Kallikrein is chemotatic and activates Factor XII

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111
Q

what molecule down regulates macrophages?

A

IL-10

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112
Q

what molecule promotes fibrosis and is anti-inflammatory?

A

TGF-beta

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113
Q

What are the two main types of tissue repair?

A

Regeneration and scar formation

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114
Q

What cell is responsible for Growth Factor Secretion?

A

Macrophages

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115
Q

What cell is responsible for Neovascularization?

A

endothelial cells

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116
Q

What cell is responsible for Collagen deposition?

A

fibroblasts and myofibroblasts

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117
Q

What cell is responsible for Collagen remodeling / retraction?

A

fibroblasts

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118
Q

What cell is responsible for Re-epithelialization / Regeneration?

A

epithelial cells cells and hepatocytes

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119
Q

What are labile tissues?

A

Continuous turnover from stem cells and proliferation of mature cells (e.g. bone marrow, surface epithelia such as skin, oral cavity, GI, ducts, urothelium, etc.)

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120
Q

What are stabile tissues?

A

minimal replicative activity, although capable of proliferating in response to injury or loss of tissue mass (e.g. parenchyma of most solid organs such as liver, kidney, pancreas; also endothelial cells, fibroblasts, smooth muscle cells); with exception of liver, stable tissues have limited capacity to regenerate after injury

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121
Q

What are permanent tissues?

A

Terminally differentiated and nonproliferative. Most neurons and cardiac muscle cells. Limited stem cell replication and differentiation, but insufficient for regeneration. Thus, repair dominated by scar formation.

122
Q

What are two properties of stem cells?

A

Self-renewal

Asymmetric replication

123
Q

What is an embryonic stem cell?

A

most undifferentiated, present in inner cell mass of blastocyst can form all three germ cell layers: ectoderm, endoderm, mesoderm

124
Q

What is an adult stem cell?

A

less undifferentiated than ES cells and found among differentiated cells within an organ or tissue. More limited self-renewal capacity, and more restricted lineage potential. Important in tissue homeostasis.

125
Q

What is the basement membrane made up of?

A

**Type IV collagen
laminin
proteoglycans

126
Q

What is the interstitial matrix comprised of?

A

Fibrillar collagens
elastins
proteoglycans and hyaluronan

127
Q

What is the main function of the extracellular matrix?

A

Mechanical support
Control of cell proliferation
Scaffolding for tissue renewal
Establishment of tissue microenvironments

128
Q

What happens if the extracellular matrix (ECM) is damaged?

A

repair can be accomplished only by scar formation

129
Q

What is the most important cytokine for synthesis and deposition of connective tissue proteins?

A

transforming growth factor TGF-ß

130
Q

What enzyme is responsible for the degradation of collagens and other ECM components? aka remodeling of connective tissue

A

**metalloproteinases (MMPs)

131
Q

What is a hypertrophic scar?

A

accumulation of collagen outside boundaries of injury / regresses

132
Q

What is a keloid scar?

A

accumulation of excessive amounts of collagen outside boundary of injury that persists

133
Q

What is granulation tissue comprised of?

A

Comprised of fibroblasts, new capillaries (angiogenesis), loose extracellular matrix, and inflammatory cells (predominantly macrophages) (seen beneath scab of wound)

134
Q

steps to form normal scar?

A

angiogenesis -> granulation tissue -> maturation and reorganization of fibrous tissue
(remodeling) -> stable fibrous scar

135
Q

VEGF is used for what?

A

Vascular endothelial growth factor

angiogenesis!

136
Q

How much of the liver can be removed in liver donor transplantation?

137
Q

What are the three Gf involved in Deposition of Connective Tissue?

A

PDGF (platelet derived growth factor) , FGF-2 (fibroblast growth factor), and TFG-ß (transforming growth factor)

138
Q

what is a contracture scar?

A

Scar that crosses the joint line

139
Q

What is healing by first intention?

A

epithelial regeneration is the principal mechanism of repair

140
Q

What is healing by secondary intention?

A

combination of regeneration and scarring. You also get wound contracture due to myofirbroblast

141
Q

Which drug has no anti-inflammatory element?

A

acetaminophen

142
Q

Primary use of aspirin?

A

inhibition of platelet aggregation

143
Q

When should you prescribe celecoxib?

A

When your patient needs anti-inflammatory action but cant put up with GI upset

144
Q

action of endothelial cox II

A

makes anti sticky prostaglandins for platelets **antiaggretory

145
Q

action of endothelial cox I

A

pro sticky postaglandins for platelet. **proaggregation

146
Q

The cox I pathway in platelets makes..

A

makes thromboxane (TXA2)

147
Q

The cox II pathway in endothelial cells makes..

A

makes prostacyclin (PGI2)

148
Q

Why is the anti platelet effect of aspirin Cox 1 selective

A
  1. pharmacodynamics - the endothelial cells have nucleus where as platelets do not. When endothelial cells are inhibited they can make more enzymes to counteract. A platelet needs to be made from scratch once it has been inhibited
  2. Pharmacokinetics - acetylsalicyilic acid is presystemic in the hepatic portal vein and therefore interacts with platelets in the circulation more easily vs the tissue endothelial tissue cell COX II
149
Q

What effect does cox I have on GI tract?

A

It’s cytoprotective - decreasess acid / pepsin secretion and increases mucous / bicarbonate production

150
Q

What effect does cox I have on smooth muscle?

A

increases contraction (think increased platelet aggregation)

151
Q

What effect does cox I have on kidneys?

A

increases renal blood flow –> increased urine flow (diuresis)

152
Q

which cyclogenase pathway is induced?

153
Q

What effects does COX II have on uterine smooth muscle?

A

Contributes to labor contractions near parturition

154
Q

What effect does COX II have on ductus arteriosus?

A

Maintenance of patent ductus arteriosus via vasodilation

155
Q

What type of inhibition for tNSAIDS?

A

reversible inhibition COX I and COX II

156
Q

What type of inhibition for celecoxib?

A

reversible selective inhibition of COX-2

157
Q

What type of inhibition for acetaminophen?

A

reversible inhibition of Cox II in the **CNS no peripheral effect like anti inflammation

158
Q

What type of inhibition for aspirin?

A

irreversible inhibition of COX-1 and COX-2. Because its irreversible its selective for COX I

extra anti-platelet effect! Not so much against fever and pain

159
Q

What drug would you give for anti-platelet effect?

A

low dose aspirin

160
Q

What drug for analgesic effect?

A

moderate doses NSAID COX II selective and aspirin

161
Q

What drug dose for antipyretic effect?

A

moderate dose

162
Q

What drug dose of anti-inflammatory effect?

163
Q

What drug is a reversible inhibitor of COX I and II?

A

tNSAIDS: ibuprofen, naproxen

164
Q

Which drug in large doses is metabolized to product toxic to liver?

A

Acetaminophen (tylenol)

165
Q

COX II inhibitors reduce what symptoms?

A

pain, inflammation, fever, uterine contraction, ductus arteriosus dilation, renal dilation,

166
Q

COX I inhibitors (nSAIDS, aspirin) reduce what symptoms?

A

platelet agglutination, GI protection, renal blood flow

167
Q

Ketorolac

A

analgesic drug in IM/IV form

168
Q

Ibuprofen

A

antipyretic and as effective as aspirin and acetaminophen

169
Q

What drug should you give for anti-inflammatory response?

A

Efficacies similar - choice based on individual response or tolerance of side effects and half-lives or route

**Except acetaminophen which has no anti-inflammatory element

170
Q

Safest over-the-counter pain medication to recommend to patients with gastric ulcers?

A

Acetaminophen

171
Q

What side effect do tNSAIDS have on platelets?

A

increases bleeding! (COX I inhibitor)

172
Q

Safest agent for pain treatment in patients taking oral anticoagulants?

A

Acetaminophen (tylenol)

celecoxib inhibits the antithrombosis component in endothelial COX II

173
Q

Which NSAID if you are GI sensitive?

A

Ibprofen **inhibits COX II

174
Q

Which NSAID if you are at risk of cardiovascular failure?

A

Naproxen **inhibits COX I more than COX II

175
Q

NSAID alternatives for pain for elderly patients?

A

Acetaminophen, tramadol, and opioids

176
Q

what is omeprazole?

A

proton pump inhibitor

177
Q

Why does acetaminophen lack an anti-inflammatory effect?

A

Peroxide formation at sites of inflammation inhibits the activity of acetaminophen

178
Q

Safest agent to treat musculoskeletal pain in patients with kidney dysfunction?

A

Acetaminophen

179
Q

Relative to ibuprofen (Advil), agents that preferentially inhibit COX-2 over COX-1 will cause a higher incidence of

A

Clotting-related disorders

180
Q

Aspirin is often used in low doses to prevent platelet aggregation by inhibiting the synthesis of which substance?

A

Thromboxane A2

181
Q

A 16-year-old girl comes to the emergency department suffering from the effects of an aspirin overdose. Which of the following syndromes is this patent most likely to exhibit as a result of this drug overdose?

A

Hyperthermia, metabolic acidosis, and coma

182
Q

What is the major endogenous glucocorticoid?

183
Q

What is the major exogenous glucocorticoid?

A

prednisone

184
Q

What is the major endogenous mineralcorticoid?

A

aldosterone

185
Q

What is the benefit of administering a glucocorticoid?

A

anti inflammatory

186
Q

What is the effect of too much aldosterone?

A

retaining too much sodium and losing too much potassium

187
Q

What is adrenal crisis?

A

Insufficient adrenal response to environmental stressors occuring due to chronic use of exogenous glucocorticoids

188
Q

What are the glucocorticoid metabolic effects?

A

Carbohydrate: gluconeogenesis, blood glucose ( insulin) all increase

protein break down –> increased amino acids

fat break down –> free fatty acids

189
Q

Metabolic effects of iatrogenic cushing’s disease?

A

hyperglycemia, muscle wasting, centripetal obesity

insulin and cortisol compete. Cortisol wins in the periphery (fat breakdown) Insulin wins centrally (storage). Fat in the trunk! = centripetal obesity

190
Q

What are signs of hypertension, sodium fluid retention, hypokalemia, and metabolic alkalosis?

A

Increased aldosterone

191
Q

What is a key molecular component for functional cortisol?

A

You need a hydroxyl group at position 11

192
Q

What is the benefit of using dexamethosone?

A

glucocorticoid that does not increase mineralcorticoid activity

193
Q

What is the benefit of using fludrocortisone?

A

glucocoriticoid that increase mineralcorticoid activity

Useful if patient is **hyponatremic and dehydrated

194
Q

Which organ activates cortisol?

195
Q

Which organ inactivates cortisol?

196
Q

What is the primary clinical advantage of the alternate day glucocorticoid regimen?

A

Minimizes glucocorticoid block of ACTH release which can significantly reduce adrenal atrophy

**the anti-inflammatory result will withstand for 48 hours

197
Q

Which corticosteroids need to go through the liver to be activated?

A

cortisone and prednisone

198
Q

What is a key difference between prednisone and methylprednisolone?

A

Methylprednisolone you can administer topically!

199
Q

Which drug is the most potent anti-inflammatory agent, used in cerebral edema, chemotherapy-induced vomiting; no mineralocorticoid action, greatest suppression of ACTH secretion at pituitary?

A

Dexamethasone

200
Q

Which drug is a potent systemic agent - excellent topical activity; no mineralocorticoid action?

A

Triamcinolone

201
Q

What are disease modifying antirheumatic drugs (DMARDs) used for?

A

added as soon as the diagnosis of rheumatic disease is certain with the aim of suppressing disease progression

202
Q

When does thrombosis in the arterial system most commonly occur?

A

endothelial injury and turbulent blood flow, often associated with **atherosclerosis.

203
Q

Where does arterial thrombi most commonly occur?

A

in the coronary, cerebral and femoral arteries.

204
Q

What is an embolus?

A

A free floating, intravascular mass of a solid, liquid or gas

205
Q

Where do Emboli in the venous/right sided system commonly lodge?

A

In the lungs

206
Q

Where do Emboli in the arterial/left sided system commonly lodge?

A

any organ but most commonly the legs and brain

207
Q

What is Disseminated intravascular coagulation (DIC)?

A

a unique condition where thrombosis and hemorrhage can occur simultaneously.

208
Q

signs of acute onset of DIC

209
Q

signs of chronic onset of DIC

A

thrombosis

210
Q

What are infarcts?

A

Infarcts are areas of tissue death (necrosis) caused by

ischemia.

211
Q

What is petechia?

A

small hemorrhage 1-2 mm

212
Q

What is purpura

A

hemorrhage 3cm

213
Q

What is echymoses?

A

bruise 1-2cm hemorrhage

214
Q

Hematoma

A

large collection of blood in organ or tissue

215
Q

What is the virchow triad that leads to thrombosis?

A

endothelial injury, hyper coagulability, abnormal blood flow

216
Q

How do you tell if a thrombus is formed before death or post mortem?

A

lines of zohn indicate thrombus before death

217
Q

What is a white infarction?

A

an arterial blockage, a single blood supply, and a dense tissue that limits accumulation of blood in necrotic areas.

218
Q

What is a red infarction?

A

venous occlusion, a dual blood supply and loose tissue that permits movement of blood from adjacent areas into the necrotic area

219
Q

Shock due to?

A

inadequate blood flow to tissue

220
Q

Signs of shock?

A

coolness and pallor of their skin, tachycardia, and decreased urine output.

221
Q

Signs of septic shock?

A

Fever, DIC, ARDS
Widespread
Arterial vasodilation –> hypotension, warm, flushed skin
Vascular leakage –> hypotension, edema
Venous blood pooling –> reduced cardiac output, increased heart rate

222
Q

Define diapedesis

A

the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.

223
Q

Where are toll like receptors located?

A

On the plasma membrane or endosomes

224
Q

What is the step by step roll of a toll like receptor?

A

The TLR is activated and then triggers the production of transcription factors to produce mediators of inflammation and anti-microbial products

225
Q

What do inflammasomes recognize?

A

stuff from dead or damaged cells

226
Q

What is the role of a leukocyte once it has been activated?

A
  1. readily phagocytize materials
  2. are poised to kill/degrade engulfed material
  3. readily secrete material to kill/degrade
  4. Produce inflammatory mediators (amplifies inflammatory process)
227
Q

When do you expect to see a granulomatous infection?

A

In difficult to eradicate infections

228
Q

Where are eosinophils predominantly found

A

allergies and parasitic infections

229
Q

What blood measurement can you use to detect/monitor the presence of inflammation

A

serum amyloid A, c-reactive protein, and fibrinogen

230
Q

neutrophilia is classic for what type of infection

A

bacterial infection.

231
Q

What is meant by quiescent tissue/cells and give an example

A

normally little turnover but there is a capacity for proliferation.

example would be the liver

232
Q

What is hypertrophy?

A

increase in cell size

233
Q

What is hyperplasia?

A

increase in cell number

234
Q

What is metaplasia?

A

Change from one benign, differentiated cell type to another, usually in response to injury (eg: inflammation)

235
Q

Is neoplasia reversible or irreversible?

A

generally irreversible

236
Q

What type of neoplasm is typically circumscribed/encapsulated?

A

benign neoplasm

237
Q

adenoma originates from what type of tissue?

A

epithelial (benign)

238
Q

osteoma, chondroma, and fibroma originate from what tissue type?

A

mesenchymal

239
Q

sarcoma tissue origin?

A

mesenchymal

240
Q

carcinoma tissue origin?

A

epithelial (malignant)

241
Q

What type of cancer is the most common?

A

carcinomas (cancer of the epithelium)

242
Q

What is dysplasia and why is it significant?

A

means disordered cell growth and is a hallmark of early premalignant neoplasia

243
Q

Main difference between sarcoma and carcinoma?

A

sarcomas do not have a premalignant or in-situ phase

244
Q

What is invasion?

A

the infiltration of adjacent tissues by malignant cells.

245
Q

What is metastasis?

A

the transfer of malignant cells from the primary site to a non-connected (secondary) site.

**So metastases are tumors discontinuous with the primary tumor.

246
Q

What is meant by an in-situ epithelial cancer?

A

In situ epithelial cancers display the cytologic features of malignancy without invasion of the basement membrane.

247
Q

What are the methods of dissemination for cancer?

A
  1. direct seeding of body cavities or surfaces
  2. lymphatic spread
  3. hematogenous spread
248
Q

What are the steps in the metastatic cascade?

A
  1. invasion - invasion through the basement membrane and ECM
  2. intravasion- getting into the blood or lymph
  3. extravasion - getting out of the blood or lymph
  4. colonization
249
Q

epithelial cells are held together by what proteins?

A

e-cadherins

250
Q

How do tumor cells manipulate the system to dissociate one cell from another?

A

they down regulate the production of e-cadherins

251
Q

What is the second stage of invasion for cancer cells?

A

local degredation of teh basement membrane and interstitial connective tissue by secretion of proteolytic enzymes or inducing stromal cells to make them

**Matrix-Metallo Proteases (MMP)

252
Q

Describe what ameboid migration is

A

cancer cells squeeze through the spaces in the matrix instead of cutting through with proteases.

**quicker and why MMP inhibitors won’t work on their own.

253
Q

What is the 3rd stage of invasion in cancer cells?

A

changes in attachment of tumor cells to the extracellular matrix proteins to stimulate migration

254
Q

What are some of the transcription factors that repress transcription of the e-cadherin gene?

A

SNAIL, TWIST, ZEB1/2

255
Q

What does the repression of e-cadherin ultimately lead to?

A

epithelial to mesenchymal transition (EMT)

256
Q

What is CARCINOMA-ASSOCIATED “PARANEOPLASTIC SYNDROME” ?

A

consequence of the presence of cancer, but not due to the local presence of the cancer cells. Thought to be due to hormones or cytokines excreted by tumor cells and/or immune response triggered by the tumor.

**indirect.

257
Q

What is the most common route of metastasis for carcinomas?

A

Lymphatic spread

258
Q

What is the most common route of metastasis for sarcomas?

A

hematogenous spread

259
Q

What is the main cause of death due to cancer?

260
Q

What are some of the causes of mortality due to cancer?

A
  1. infection
  2. organ failure
  3. hemorrhage
  4. thromboembolism
  5. emaciation
261
Q

What are the 3 most common cancers among men?

A
  1. Prostate (26%)
  2. Lung (14%)
  3. colon/rectal (14%)
262
Q

What are the 3 most common cancers among women?

A
  1. Breast (29%)
  2. Lung (13%)
  3. colon/rectal (8%)
263
Q

What are the three leading types responsible for cancer mortality for men?

A
  1. Lung (28%)
  2. Prostate (9%)
  3. colon/rectal (8%)
264
Q

What are the three leading types responsible for cancer mortality for women?

A
  1. Lung (26%)
  2. Breast (15%)
  3. colon/rectal (9%)
265
Q

In order for a structure to be carcinogenic, what must happen?

A

must be activated by cytochrome p450

266
Q

What is emphysema?

A

a condition in which the air sacs of the lungs are damaged and enlarged, causing breathlessness.

267
Q

What are the four main groups of carcinogens?

A

polycyclic aromatic hydrocarbons
aromatic amines
nitrosamines and nitrosamides
aflatoxins

268
Q

what does the ames test do?

A

Identifies mutagenic products

269
Q

What is meant by “stage”

A

the extent of tumor spread at the time of diagnosis

270
Q

What does TNM classification stand for?

A

T: size of tumor
N: lymph node involvement
M: presences of metastasis

271
Q

What is meant by “grade”

A

refers to the state of differentiation of the tumor cells seen in histological sections.

272
Q

What is low grade

A

means cells are well differentiated and exhibit features of normal cells

273
Q

What is high grade?

A

The cells do not resemble normal epithelial cells

274
Q

What are the pathologic features of squamous cell carcinoma?

A

in major branches of the bronchial tree “centrally”
squamous cells (instead of ciliated columnar epithelial)
necrosis and hemorrahgic
well differentiated
positive for keratin **keratin pearls

275
Q

What are the pathologic features of adenocarcinoma?

A

centrally or in the periphery of the lung
forms primitive gland like structures
**stains positive for mucin

276
Q

What are the pathologic features of large cell carcinoma?

A

undifferentiated
high grade lung cancer
may not produce either keratin or mucin

277
Q

What are the pathologic features of small cell carcinoma?

A 
can happen anywhere in the lung
high grade cancer
cells are small and dark staining
cells form clusters
stains positive for neuroendocrine markers
278
Q

Which cancers are strongly linked to cigarette smoking?

A

squamous cell carcinoma

small cell carcinoma

279
Q

What are risk factors for pancreatic cancer?

A

age, smoking, chronic pancratitis from alcoholism, diabetes mellitus, family history

280
Q

What is the prognosis for pancreatic and lung cancer?

A

low/poor (pancreatic cancer even worse)

281
Q

What are the pathologic features of pancreatic cancer?

A

well differentiated adenocarcinoma
primitive gland like structures
mucin production

282
Q

What is desmoplasia and what cancer is it associated with?

A

a prominent connective tissue stroma

**the reason why pancreatic cancers feel rock hard

283
Q

What are risk factors for lung cancer?

A

smoking, age, occupational history (mining, exposure to metal vapors, etc), exposure to air pollutants, and family history.

284
Q

What are the three inherited conditions that increase risk of colorectal cancer?

A
  1. rare familial adenomatous polyposis (APC)
  2. Rare loss of mismatch DNA repair (HNPCC)
  3. mutY base excision DNA repair enzyme
285
Q

What are the pathologic features of colorectal cancer?

A

well differentiated adeocarcinoma

innermost, mucosal layer of bowel wall

286
Q

What is the Gleason system?

A

A grading system for prostate cancer. The Gleason grade of the predominant pattern and the Gleason grade of the subordinate pattern are added together.

Values of 8 to 10 indicate aggressive behavior → can kill Pt

287
Q

What type of lung cancer is not treating with surgery?

A

small cell carcinoma

288
Q

Which cancer is associated with EGFR mutations?

A

adenocarcinomas

289
Q

What cancer do these drugs treat? Gefitinib, erlotinib, afatinib, critzotinib

A

Adenocarcinoma

290
Q

Describe the nuclear changes that occur during the breakdown of DNA and chromatin

A

Pyknosis - nuclear shrinkage/ condenses
Karyorrhexis - nucelar fragments
Karyolysis - dissolution of nucleus

291
Q

What is coagulative necrosis?

A

tissue architecture preserved due to damage to structural proteins and enzymes
-appear as pale “ghost cells”

292
Q

When does coagulative necrosis typically occur?

A

myocardial infarcts

any organ after an infarct

293
Q

What is liquefactive necrosis?

A

Dead cell dissolves - lysosomal hydrolases digest cell compartments

294
Q

When does liquefactive necrosis typically occur?

A

bacterial / fungal infections

also CNS following hypoxic conditions

295
Q

What is Caseous necrosis?

A

a collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border

296
Q

When do you see caseous necrosis?

A

tuberculosis

297
Q

What is fat necrosis?

A

Necrotic adipose tissue - fats are hydrolyzed into free fatty acids → ppt with Ca2+ →chalky gray material

298
Q

When do you see fat necrosis?

A

acute pancreatitis or trauma

299
Q

What is fibrinoid necrosis?

A

immune reaction in which complexes of antiges and antibodies are deposited in the walls of arteries

300
Q

When do you see fibrinoid necrosis?

A

vasculitis

polyarteritis nodosa

Disease and Defense (4 decks)

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