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Winter 2016 > D&D Unit 1-2 > Flashcards

D&D Unit 1-2 Flashcards

1
Q

Human disease occurs mostly from injury to the _________

A

Epithelium

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2
Q

What is metaplasia?

A

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

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3
Q

5 types of necrosis

A

Coagulative Liquefactive Caseous Fat Fibrinoid

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4
Q

What is coagulative necrosis?

A

Tissue architecture is preserved for at least several days before they are digested

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5
Q

What is liquefactive necrosis?

A

Usually in infections where leukocyte enzyme digest tissue Also forms in hypoxic death of CNS cells

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6
Q

What is caseous necrosis?

A

Looks chalky white- like casein (milk) Central portion of an infection is necrotic (fragmented or lysed cells) and inflamed on borders

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7
Q

When does fat necrosis occur?

A

From release of pancreatic lipases Or from trauma to fat areas

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8
Q

4 reversible changes that occur in hypoxia

A

Decreased ATP

Decrease Na pump -> swelling

Increased glycolysis -> decreased pH

Decreased protein synthesis

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9
Q

3 irreversible changes that occur in hypoxia

A

Activation of lysosomal enzymes

DNA and protein degradation

Ca2+ influx

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10
Q

4 big picture cellular adaptations to stress

A

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

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11
Q

Metaplasia nomenclature

A

Metaplasia is named for whatever tissue replaces normal tissue

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12
Q

Why does fat accumulate in injured cells as lipid vacuoles in the cytoplasm?

A

Increased entry and synthesis of free fatty acids Decreased fatty acid oxidation

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13
Q

4 intracellular changes associated with reversible cell injury

A

Plasma membrane alterations (blebbing, blunting, distortion, loosening of intercellular attachments)

Mitochondrial changes (swelling and appearance of phospholipid-rich amorphous densities)

Dilation of ER with detachment of ribosomes and dissociation of polyribosomes

Nuclear alterations with chromatin clumping

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14
Q

Describe pyknosis

A

Nuclear shrinkage and increased basophilia (chromatin condenses) Step 1

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15
Q

Describe karyorrhexis

A

The pyknotic nucleus fragments Step 2

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16
Q

Describe karyolysis

A

The nucleus dissolves Step 3

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17
Q

What type of necrosis is gangrene?

A

A coagulative necrosis involving multiple tissue layers

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18
Q

What is fibrinoid necrosis?

A

An immune reaction in which complexes of antigens and antibodies are deposited in walls of arteries and combine with fibrin

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19
Q

How does ischemia cause mitochondrial damage and dysfunction?

A

Failure of oxidative phosphorylation causes:

ATP depletion

Formation of ROS

Formation of pores and loss of membrane potential

Release of proteins that activate apoptosis

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20
Q

Changes to intracelluar calcium in cellular damage

A

Release of calcium stores from inside

Increased influx accross plasma membrane

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21
Q

2 ways reactive oxygen species accumulate in cellular damage

A

Mitochondria

Phagocytes

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22
Q

3 important sites of cellular membrane damage

A

Mitochondria

Plasma membrane

Lysosome

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23
Q

The intrinsic apoptotic pathway is mediated by ________

A

Mitochondria

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24
Q

The extrinsic apoptotic pathway is mediated by ________

A

Death receptor

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25
Q

4 ways cells can accumulate shit

A

Inadequate removal

Accumulation of abnormal endogenous substance

Failure to degrade (storage diseases, usually genetic)

Deposition and accumulation of abnormal exogenous substance

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26
Q

What is steatosis?

A

Fat within cells

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27
Q

The inflammasome stimulates inflammation via activation of __________

A

Caspase-1

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28
Q

In the inflammasome, caspase-1 activates __________

A

IL-1 Beta

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29
Q

3 reasons why permeability occurs in inflammation

A

Endothelial cell contraction

Endothelial injury (they die or detach)

Transcytosis

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30
Q

Short-term vascular permeability is mediated by __________ and __________ while longer-term permeability is mediated by __________ and __________

A

Histamine
Bradykinin
(1 hr)

?

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31
Q

What is margination?

A

In initial phase of leukocyte recruitment, leukocytes accumulate on vascular endothelium so they move to the side of the laminar flow

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32
Q

Leukocytes stop rolling when __________ are engaged

A

Integrins

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33
Q

What is leukocyte transmigration

A

Pushing between endothelial cells

Usually occurs in venules

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34
Q

4 things macrophages produce via classical activation to fuck shit up

A

Reactive oxygen species

Nitrous oxide

Lysozymal enzymes

Proinflammatory cytokines

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35
Q

3 things that cause classical activation of macrophages

A

Endotoxin

IFN-gamma

Foreign material

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36
Q

What do alternatively activated macrophages do?

A

Produce growth factors for new vessel growth and fibroblast activation for tissue repair and fibrosis

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37
Q

What types of immune cells are hallmarkers of acute inflammation?

A

Neutrophils

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38
Q

3 places pro-inflammatory receptors can be on

A

Plasma membrane - extracellular triggers

Endosomes - ingested triggers

Cytosol - intracellular triggers

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39
Q

What does the inflammasome respond to?

A

Stuff from dead or damaged cells

(It is inside the cell)

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40
Q

Whta is the difference between exudate and transudate?

A

Exudate is a result of increased vascular permeability from inflammation

Transudate is a result of altered intravascular pressure from hemodynamic or osmotic changes

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41
Q

How is the phagocytotic target bound? (2 receptors)

A

Receptors for specific products of microbes or necrotic cells

Receptors for opsonins

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42
Q

How are ROS formed and what do they do? Like the process

A

ROS formed by oxidation of NDAPH which converts oxygen to a superoxide ion

Superoxide ion converts to H2O2

H2O2 converted to hypochlorous radical

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43
Q

How long to monocytes circulate for before they become macrophages in tissue?

A

About a day

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44
Q

3 roles of macrophages

A

Ingest stuff Initiate tissue repair Secrete inflammatory mediators like cytokines and eicosanoids that promote inflammation

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45
Q

Mast cells release __________ and __________ inflammatory mediators

A

Histamine Arachadonic acid

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46
Q

What is a granuloma?

A

Enlarged macrophages that form a nodule

Often surrounded by lymphocytes

Fibrosis often forms around longastnding granulomatous inflammation

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47
Q

3 chemical mediators responsible for many of the systemic effects of inflammation

A

TNF IL1 IL6

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48
Q

What about inflammation causes production of C-reactive protein and serum amyloid A? Where does this occur?

A

IL-6 induces hepatcytes to produce

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49
Q

What 2 chemicals cause the bone marrow to release more leukocytes in inflammation?

A

TNF

IL1

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50
Q

4 cell types that make arachidonic acid

A

Lekocytes

Mast cells

Endothelium

Platelets

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51
Q

What are lipoxins?

A

Are generated as leukocytes enter tissues Antagonize lekotrienes and are anti-inflammatory Inhibit neutrophil chemotaxis and endothelial adhesion

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52
Q

5 things platelet-activating factor does

A

Platelet aggregation

Vasodilation

Vascular permeability

Bronchoconstriction

Stimulation of platelets and other cells to make mediators

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53
Q

Production of platelet-activating factor

A

Phospholipase A2 cleaves lipids form cell membranes

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54
Q

What do chemokines do? (2)

A

Chemotaxis

Activate leukocytes

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55
Q

Production of NO

A

Made by nitric oxide synthase from L-arginine

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56
Q

What is the difference between type II and type III nitric oxide synthase

A

Type II is induced in macrophages and endothelial cells in inflammation

Type III is constitutively expressed in endothelial cells

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57
Q

What is substance P secreted by? What does it do?

A

Secreted by nerves and inflammatory cells

Binds the neurokinin-1 receptor

Generates proinflammatory effects in immune and epithelial cells

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58
Q

What does C3 convertase do in complement?

A

Cleaves C3 into C3a and C3b

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59
Q

What are 3 inhibitors of compliment?

A

C1 inhibitor blocks activation of C1

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

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60
Q

What does Factor XII/hageman factor do?

A

Activates the kinin system

Stimulates the clotting cascade

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61
Q

What does IL-10 do? What makes it?

A

Downregulates activated macrophages

Secreted by macrophages

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62
Q

What are the cells responsible for the following components of repair?

  1. Growth factor secretion
  2. Neovascularizaiton
  3. Collagen deposition
  4. Collagen remodeling/retraction
  5. Re-epithelization/regeneration
A
  1. Macrophage
  2. Endothelial cell
  3. FIbroblast
  4. Fibroblast
  5. Epithelial cells/hepatocytes
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63
Q

What is granulation tissue and what is it made of?

A

New tissue
Is pink and has a soft granular appearance
Made of fibroblasts, new capillaries, loose ECM, and inflammatory cells (mostly macrophages)

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64
Q

What is the difference between hydrostatic and oncotic pressure?

A

Hydrostatic pressure pushes fluid out into the interstitial space on the arterial end

Oncotic pressure pulls fluid back in to balance protein concentration on the venous end

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65
Q

How does the Virchow triad contribute to thrombosis?

A

Endothelial injury

Abnormal blood flow (stasis or turbulence)

Hypercoaguability

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66
Q

What are the 3 types of adrenal corticosteroids?

A

Glucocortigoids (cortisol)

Mineralocorticoids (aldosterone)

Adrenal androgens (DHEA, androstenedione)

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67
Q

ACTH is made by the _________

A

Pituitary

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68
Q

ACTH release is controlled by _________

A

corticotropin-releasing factor

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69
Q

Corticotropin-releasing factor is made by the _________

A

Hypothalamus

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70
Q

3 modes of regulation by the hypothalamic-pituitary-adrenal axis

A
  1. Diurnal rhythm of basal steroidogenesis
  2. Negative feedback by circulating corticosteroids
  3. Stress can override negative feedback and increase steroidogenesis
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71
Q

What are 3 drugs that decrease glucocorticoid production?

A

Metyrapone

Mitotane

Trilosane

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72
Q

What is the rate-limiting step in the glucocorticoid pathway? What is it stimulated by?

A

Conversion of cholesterol to pregnenolone

ACTH stimulates

The RAA system via angiotensin II also stimulates via the mineralocorticoid pathway

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73
Q

When are natural cortisol peaks in circadian rhythm?

A

Early morning

After meals

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74
Q

Is plasma-bound cortisol active?

A

No. Only free cortisol is active.

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75
Q

How is cortisol metabolised?

A

Reduced in liver

Conjugated in liver

Eliminated in uring

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76
Q

What are the effects of glucocorticoids on:

Carbohydrates

Protein

Lipids

Net effect

A

Carbs: Stimulates gluconeogenesis, increasing blood glucose.
Stimulation of glycogen synthase activity increases liver glycogen deposition

  • Proteins*: increased amino acid uptake into liver and kidney and decreased protein synthesis (except liver) leads to a transfer of amino acids from muscle and bone into liver
  • Lipids:* Inhibition of uptake of glucose by fat cells stimulates lipolysis. However, there is also insulin resistance leading to lipogenesis, especially in trunk -> central obesity

The net result is maintainin the glucose supply to the brain

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77
Q

What are permissive effects and what are 2 that happen wih glucocorticoids?

A

Permissie effects are responses that occur to an appreciable extent only in the presence of glucocorticoids, but don’t increase with increasing amounts of glucocorticoids

  1. Vasoconstrictuion and bronchodilation response to catecholamines
  2. Fat cell lipolysis response to catecholamines, ACTH, growth hormone
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78
Q

What happens when aldosterone binds to its receptor?

A

Cytosolic receptor migrates to the nucleus where it induces synthesis of membrane channels (Na/K ATPase, Na, K)

This increases reabsorption of Na+ from distal renal tubules that is coupled to increased secretion of H+ and K+

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79
Q

What are glucocorticoids used for pharmacologically?

A

To suppress inflammatory and immune responses

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80
Q

Glucocorticoid administration decreases synthesis of __________, __________, and __________ inflammatory and immune mediators

A

Cytokines

Leukotrienes

Prostaglandins

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81
Q

How do glucocorticoids reduce generation of leukotrienes and prostaglandins.

A

Decreases expression of COX-2 in inflammatory cells (decreased prostaglandins only)

Inhibits phospholipase A2 via lipocortin

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82
Q

How do glucocorticoids suppress the immune system? (3)

A

Suppress T cell activation

Supress cytokine production

Prevent eosinophils from releasing things

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83
Q

What effects do glucocorticoids have on lymphoid areas?

A

Decrease clonal expansion of T and B cells

Decrease cytokine production, but this has little effect on antibody formation at moderate doses

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84
Q

What effects do glucocorticoids have on the vasculature?

A

Reduce vasodilation

Decrease fluid exudation

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85
Q

What effects do glucocorticoids have on areas of acute inflammation?

A

Decrease number and activity of leukocytes by causing them to move to lymphoid tissues

Neutrophils move into circulation and out of peripheral tissues

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86
Q

What effects do neutrophils have on chronic inflammation?

A

Decreased activity of monocyte and lymphocytes

Decreased proliferation of blood vessels

Less fibrosis

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87
Q

What is a mineralocorticoid?

A

An agent that causes Na+ retention at the kidney

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88
Q

Are 11-hydroxy glucocorticoids physiologically active?

Are 11-keto glutocorticoids?

A

Yes

No. They are prodrugs that must be activated by 11beta-hydroxysteroid dehydrogenase (11B-HSD1)

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89
Q

What does the liver do to glycocorticoid drugs?

A

11beta-HSD1 converts cortisone to cortisol

Activating step

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90
Q

What does the kidney do to glucocorticoid drugs?

A

11Beta-HSD2 converts cortisol to cortisone

Inactivating step

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91
Q

What hormone actions does cortisol have as a drug?

How is it administered?

A

Glucocorgicoid and mineralcorticoid (1:1 ratio)

Oral and parenteral administration

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92
Q

What hormone actions does prednisone have?

A

Glucocorticoid and mineralcorticoid actions (13:1)

Activated to prednisolone in liver - must go through first pass metabolism

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93
Q

What hormone actions does dexamethosone (decadron) have?

A

No mineralocorticoid action, all glucocorticoid

94
Q

What hormone actions does methylprednisolone have?

A

Minimal mineralocorticoid action - mostly glucocorticoid

95
Q

What hormone actions does triamcinolone have?

A

No mineralocorticoid action - all glucocorticoid

96
Q

5 toxicities of systemic steroid drugs with high dose sustained therapy

A

In addition to acute effects,

Iatrogenic Cushing’s syndrome (hyperglycemia, muscle wasting, lipid deposition)

Hypothalamic-pituitary-adrenal axis suppression -> insufficient response to stress

Mood disturbance (initial euphoria, then letdown when reduced)

Impaired wound healing

Increased susceptibility to infection

97
Q

2 acute toxicities of systemic steroid drugs with short course therapy

A

Mineralocorticoid effects: Na+ and H2O retention -> edema -> increased BP, hypokalemia

Glucocorticoid effects: glucose intolerance, mood changes (up or down), insomnia, GI upset

98
Q

4 toxicities of systemic steroid drugs with large cumulative doses

A

Osteoporosis

Cataracts

Skin atrophy, loss of collagen support

Growth retardation in children

Peptic ulceration

99
Q

NSAIDS inhibit ___________ and ___________

A

Cyclooxegenase 1 and 2 (COX-1 and COX-2), which produce inflammatory prostaglandins and thromboxanes

100
Q

5 side effects of NSAIDS

A

GI: ulceration, bleeding, nausea

Bleeding problems

Renal: acute renal failure, interstitial nephritis

Uterine: interferes with contractions

Thrombosis: myocardial infarction, strokes

101
Q

What do traditionsl NSAIDS do chemically?

A

Reversible inhibition of COX-1 and COX-2

102
Q

What does acetophinophen do chemically?

A

Inhibits COX-2 onl in the CNS

103
Q

What does aspirin do chemically?

A

Irreversible inhibition of COX-1 and COX-2

104
Q

Contraindication for traditional NSAIDS

A

People at risk for peptic ulcer disease

  • old
  • history of PUD or prior NSAID gastropathy
    Concurrent glucocorticoid anti-inflammatory use
105
Q

What do traditional NSAIDS do the GI tract (side effect)

A

Interfere with gastric cytoprotection by inhibiting COX-1 PGE synthesis -> dyspepsia and gastric ulceration

106
Q

What do traditional NSAIDS do to platelets (side effects)?

A

Interfere with platelet aggregation by inhibiting COX-1 thromboxane A2 synthesis -> more bleeding

107
Q

What do traditional NSAIDS do to the kidneys?

A

Renal vasoconstriction by inhibition of COX-1 and COX-2 PGE synthesis and loss of vasodilator actions -> reversible renal insufficiency

Fluid retention

108
Q

What does celebrex/coloxib do chemically?

A

COX-2 selective inhibitor

109
Q

What side effects does Celebrex/coloxib have on the GI tract with different dosing levels?

A

Less GI toxicitiy at low doses

High doses yes

110
Q

Celebrex/coloxib effects on platelets

A

No increase in bleeding risk (no inhibition of COX-1 mediated TXA2 synthesis in platelets)

Increases risk of ischemic cardiovascular disease/heart failure

111
Q

What 4 patient populations do you avoid celebrex/coloxib use in?

A

Can cause acute renal railure in:

Chronic renal insufficiency
Severe heart disease
Volume depletion
Hepatic failure

112
Q

What are aspirin’s effects on:

Pain

Inflammation

Fever

Platelets

A

Reduces inflammatory pain, but not so much pain that is from direct stimulation of sensory nerves

Antiinflammatory

Reduces elevated (but not normal) body temperature

Inhibits platelet aggregation

113
Q

What is neoplasia?

A

Autonomous and progressive cell growth

114
Q

What does TXA2 (thromboxane 2) do?

A

Causes platelet aggregation

115
Q

What does COX-1 do to the GI tract, platelets, and kidneys?

A

GI: decreases acid/pepsin secretion, increases mucus/bicarb production

Platelets: pro-aggregatory

Kidneys: increases renal blood flow, promoting diuresis (a good thing)

116
Q

What does COX-2 do in endothelial cells, the uterus, ductus arteriosus, tissue damage, and the hypothalamus?

A

ECs: vasodilation, anti-aggregatory platelet effects

Uterus: labor contractions

Ductus arteriosus: maintains it open

Tissue damage: pain/inflammation through vasodilation, potentiation of bradykinin pain-producing activity

Hypothalamus: fever

117
Q

What is the chemical precursor of COX-1 and COX-2?

A

Arachadonic acid

118
Q

What does inhibiting CNS COX-2 do?

What does inhibiting peripheral COX-2 do?

A

Reduce pain

Reduce inflammation

119
Q

Where and what COX do you inhibit for analgesia?

What dosing level?

A

COX-2 at the site of tissue injury

Intermediate dosing

120
Q

Where and what COX do you inhibit for antipyritic effects? What dosing level?

A

COX-2 in hypothalamus

Intermediate dose

121
Q

Where and what COX do you inhibit for anti-inflammatory effects? What dosing?

A

COX-2 at sites of tissue njury

High doses, scheduling based on half-life

122
Q

Where and what COX do you inhibit for antithrombic uses? What dosing?

A

COX-1 in platelets

Low doses (daily)

123
Q

3 side effects of COX-1 inhibition

A

Gi ulceration, bleeding

Increased bleeding risk

Renal dysfunction

124
Q

3 side effects of COX-2 inhibition

A

Renal dysfunction

Delayed labor

Increased thrombotic events

125
Q

3 groups of patients at high risk for peptic ulcer disease

A

Being old

History of PUD or prior NSAID gastropathy

Concurrent glucocorticoid anti-inflammatory use

126
Q

What drug do you give people with NSAIDS to reduce GI side effects?

A

Proton pump inhibitors

Omeprazole

127
Q

How long is a platelet lifespan?

A

4-7 days

128
Q

Why should you be concerned about using traditional NSAIDS with cardiovascular disease?

A

They cause fluid retention,

May exacerbate heart failure

May raise blood pressure

May interfere wth cardioprotective effect of aspirin

129
Q

Which traditional NSAIDS have lowest and highest risk of GI problems?

A

Lowest- ibuprofen

Highest - naproxen

130
Q

Which traditional NSAIDS have lowest and highest risk of cardiovascular problems?

A

Lowest - naproxen

Highest - ibuprofen, celecoxib

131
Q

Greater COX-1 inhibition results in increased __________ system risk

Greater COX-2 inhibition results in increased __________ system risk

A

GI

CV

132
Q

When is aspirin COX-1 selective (as opposed to COX-2)

A

Low doses

133
Q

What are the 2 steps of aspirin metabolism?

A

Hydrolyzed by esterases

Conjugated with glycine or glucuronide

134
Q

What are hydrostatic and oncotic/osmotic pressures?

A

Hydrostatic pressure pushes blood out of arteries. Due to fluid pressure.

Osmotic pressure pulls blood into veins. Due to albumin.

135
Q

What is the difference between transudate and exudate?

A

Transudate is due to pressure differences

Exudate is due to increased vascular permeability (due to inflammation or endothelial damage)

136
Q

How do the protein, LDH, and glucose fluid/serum ratios differ etween transudate and exudate?

What about specific gravity and white blood cell count?

A

Exudate is has more protein, LDH

but less glucose

Specific gravity is increased in exudate

WBCs are increased in exudate

137
Q

What is hyperemia?

A

Physiologic/active increase in blood volume

Due to arteriolar dilation

Increase in oxygenated blood to tissue

138
Q

What is vascular congestion?

A

Pathologic/passive increase in blood volume

Impaired venous outflow

Increased deoxygenated blood

139
Q

How does conjestive heart failure work? (L heart failure)

A

Fluid buildup in lungs and pleural effusions

Low blood pressure (from cardiac insufficiency) -> kidney tries to retain fluid and sodium -> blood volume increases and blood dilutes -> peripheral edema

140
Q

What happens in liver congestion?

A

Portal backup -> splenic congestion, GI tract varices (dilated veins in the GI tract), pleural effusion, pericardial effusion, ascites

141
Q

What is a hematoma?

A

A hemmorhage within tissue

142
Q

What are the 3 sizes of small hemorrhages?

A

Petechiae (1-2 mm)

Purpura (>3 mm)

Ecchymoses (1-2 cm)

143
Q

What is disseminated intravascular coagulation?

A

Thrombosis and hemorrhage occur at the same time

Systemic activation of coagulation causes widespread fibrin depositon and consumption of platelets and clotting factors

144
Q

What is the difference between white and red (4 ways) infarcts?

A

White infarcts are in dense tissue where an artery is blocked off so there is no blood flow.

Red infacts are a venous blockage, when you restore blood flow after a tissue has died, loose tissue where blood can come form other places, or in organs that have dual blood flow like the lung

145
Q

What are 3 kinds of shocks?

A

Cardiogenic - due to inability to pump blood

Hypovolemic - low blood volume

Septic

146
Q

Glucocorticoids block the actions of ______________ and ______________

A

Prostaglandins

Leukotrienes

147
Q

Why can’t cortisone be given topically?

A

It is not active until first pass metabolism

148
Q

Glucocorticoid effects on carbs, protein, fat

A

Carbs: gluconeogenesis increases bloood glucose

Protein: decreased protein synthesis icreases synthesis of amino acids to glucose

Fat: lipolysis increases free fatty acids

149
Q

What does excess glucocorticoid do to carbs, protein, and fat?

A

Carbs: diabetes-like state

Protein: muscle wasting, skin-connective tissue atrophy

Fat: central lipogenesis (via insulin) leading to central obesity

We get iatrogenic cushing’s disease

150
Q

What do mineralocorticoids do?

A

Increase sodium absorption

-> increased blood volume and blood pressure

151
Q

What happens with excess mineralocorticoid(4)?

A

Sodium-fluid retention, hypertension, hypokalemia, metabolic alkalosis

152
Q

Glucocorticoid effects on vasculature, immune/inflammatory cells, immune/inflammatory mediators

A

Reduced vasodilation, decreased fluid exudation

Decrease in accumulation and activation of immune/inflammatory cells

Decrease in immune/inflammatory mediator synthesis

153
Q

How does glucocorticoid metabolism work with fetuses?

A

Placental 11beta-HSD2 is active, but fetal liver 11beta-HSD1 is not

so, we can treat the mother with glucocorticoids without effects on the fetus since the drug wil be inactivated by 11beta-HSD2 and not activated by 11beta-HSD1

To treat a fetus with GCs, we use agents that are poor substrates for 11beta-HSD2

154
Q

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

A

It minimizes the glucocorticoid block of ACTH relesae, which can significantly reduce adrenal atrophy

155
Q

What cell type characterizes granulomatous inflammation?

A

Epithelioid histiocytes

156
Q

4 steps of the metastatic cascade

A
  1. Dissociation of cells from one another
  2. Local degradation of the basement membrane and interstitial connective tissue
  3. Changes in attachment of tumor cells to ECM proteins. Lose adhesion, modify matrix
  4. Locomotion
157
Q

What protein holds epithelial cells together?

A

E-cadherin?

158
Q

Intracellularly, E-cadherins are connected to ___________ and ___________

A

Beta-catenin

Actin cytoskeleton

159
Q

2 types of tumor cell movement

A
  1. Secretion of proteolytic enzymes, or induction of stromal cells to produce them
  2. Ameboid migration - cell squeezes through spaces in matrix

Cancer cells often can switch between these

160
Q

What is tumor stage? Why is it important?

A

REfers to the extent of tumor spread at time of diagnosis.

For many types of carcinoma, stage is the best predictor of prognosis

161
Q

What are epithelial malignant neoplasms called?

Mesynchymal ones?

Hematopoietic ones (2 kinds)

A

Carcinoma

Sarcoma

Lymphoma
Leukemia

162
Q

3 characteristic histological features of dysplasia

A

Loss of cytologic uniformity

Loss of normal histologic maturation

Loss of architectural orientation

163
Q

What is histologic grade?

A

The degree of tumor histologic differentiation - like how much it resembles its normal tissue counterpart

Low grade - more differentiation/greater resemblance to normal

High grade - dedifferentiation/less resemblance to normal

164
Q

What are the 6 things that cause disease?

A

Trauma

Toxicity

Tumor

Infection

Inflammation

Idiopathic

165
Q

What is TNM tumor classification?

A

T - size of tumor (1-4)

N - lymph node involvement (number of lymph nodes)

M - metastasis (yes or no)

166
Q

Is small cell lung cancer treated surgically?

A

No. Only by chemotherapy.

167
Q

4 types of lung cancer

A

Squamous cell carcinoma

Adenocarcinoma (includes bronchioalveolar carcinoma)

Large cell carcinoma

Small cell (oat cell) carcinoma

168
Q

5 subtypes of lung adenocarcinoma

A

Acinar predominant

Papillary predominant

Micropapillary predominant

Solid predominant

Invasive mucinous

169
Q

What part of the pancreas does pancreatic carcinoma usually arise in?

A

Major ducts, not acini

170
Q

What is the most common mutation in pancreatic carcinoma?

A

K-ras

171
Q

What is the main cytologic feature of epithelial carcinoma in situ

A

Malignant without invasion of the basement membrane

This can be considered one step removed from invasive cancer

172
Q

What is the correlation between primary tumor size and risk of developing metastasis?

A

They are strongly positively correlated

173
Q

Epithelial cells are held together by _____________

On the intracellular side, this is connected to _____________ and _____________

A

E-cadherin

Beta-catenin

Actin cytoskeleton

174
Q

What are 2 ways matrix metallo-proteases regulate tumor invasion?

A
  1. Remodeling insoluble ocmponents o the basement membrane
  2. Releasing ECM-sequestered growth factors that cleave ECM components and promote cell growth
175
Q

What is paraneoplastic syndrome?

A

Hormones and cytokines excreted by tumor cells and/or immune response triggered by the tumor

->

Weird systemic effects

176
Q

What are 2 things carcinogenesis requires? (in terms of carcinogens)

A

Time (several years elapse after exposure to the carcinogen before cancer emerges)

Cell proliferation

177
Q

What cell type is at risk for becoming malignant?

A

The stem cell

Fully differentiated cells never become malinant

178
Q

What are cancer promoters?

A

Irritants that cause inflammation and cell proliferation

179
Q

What does kallikrein do?

A

Convertes high molecular weight kinin (HMWK) to bradykinin

180
Q

How do selectins work?

A

Selectins are on endothelial cells and interact with glycoprotein ligands on neutrophils. This is important during the rolling stage of neutrophil recruitment

181
Q

What are lipoxins derived from?

A

Arachadonic acid

182
Q

Is lipoxin pro or anti-inflammatory?

A

Anti-inflammatory

183
Q

Prostaglandins, leukotrienes, thromboxanes, and lipoxins are subfamilies of ____________

A

Eicosanoids

184
Q

Where do steroids act in the arachidonic acid metabolite pathway?

A

Steroids inhibit phopholipase. This prevents cell membrane phospholipids from becoming arachidonic acid, thus stopping production of many downstream meadiatiors of inflammation

185
Q

What are the adhesion molecules on endothelial cells that mediate the processes of margination and rolling in inflammation? What do they bind to on leukocytes?

A

E- and P- selectin on endothelial cells bind to sugars on the surface of leukocytes

186
Q

Where is bradykinin synthesized? Where is it activated?

A

Liver

Site of inflammation

187
Q

What is coughing up blood called?

A

Hemoptysis

188
Q

What secretes IL-12?

What does it do?

A

B cells secrete

Induces differentiation of T0 cells into Th1 cells
Activates NK cells

189
Q

What do catalase and glutathione peroxidase do?

A

Eliminate free radicals

190
Q

What are the 3 types of cancer chemotherapy?

A

Primary induction (drug treatment is the primary strategy)

Neoadjuvant (drug and then surgery/radiation)

Adjuvant (surgery/radiation and then drug)

191
Q

How does BH3 profiling work?

A

Mitochondria are exposed to titrated doses of BH3 and mitochondrial outer membrane permeabilization is measured.

Less BH3 is needed in cells that are closer to apoptosis.

Linked to clinical response to chemotherapy drugs

192
Q

BH3 is part of the ___________ protein

A

BCL, in the apoptosis pathway

193
Q

4 common mechanisms of chemoresistance

A

Drug inactivation

Alterations to drug target

Adaptive responses to the drug effect (often increased repair of cellular damage)

Dysfunctional apoptosis (cell doesn’t die when it should)

194
Q

How do alkylating agents work as chemotherapy agents?

A

Form covalent bonds and crosslink DNA

Prevents DNA replication

DNA damage activates apoptosis

195
Q

How do antimetabolites work as chemotherapy agents? What is the main example?

A

Intracellularly activated

Inhibits thymidylate synthase -> dTTP depletion -> inhibits DNA synthesis

INhibits DNA synthesis and activates apoptotic response because of DNA damage

5-Fluorouracil

196
Q

How do topoisomerase chemotherapeutic agents work?

A

Something about DS breaks

DNA damage -> apoptosis

197
Q

What category of chemotherapeutic agents causes cardiotoxicity? Why?

A

Anthracyclins

Reduced chelating ability -> radical damage (chelators and anti-oxidant enzymes are lower in cardiac tissue)

198
Q

How do Vinca alkaloids work as chemotherapeutic agents?

A

Anti-microtubule

Bind to tubulin and cause depolymerization

199
Q

How do taxanes work as chemotherapeutic agents?

A

Anti-microtubule

Stabilize against microtuble depolymerization -> blocks mitosis -> apoptosis

200
Q

What 3 substances cause vasodilation?

A

Prostaglandins

Nitric oxide

Histamine

201
Q

What 8 things cause increased vascular permeability?

A

Histamine

Serotonin

C3a

C5a

Bradyknin

Leukotrienes

Platelet-acivating factor

Substance P

202
Q

What 2 complement components cause chemotaxis of leukocyes?

A

C3a

C5a

203
Q

What 2 inflammatory substances cause pain?

A

Prostaglandins

Bradykinin

204
Q

What 3 inflammatory mediators cause fever?

A

IL-1

TNF

Prostaglandins

205
Q

Which cyclooxygenase inhibition is associated with each following symptom:

GI upset

Bleeding

Decreased renal function

Decrased uterine contraction

Increased clotting

A

1

1

1 & 2

2

2

206
Q

What is ulceration?

A

Where epithelium is missing

207
Q

What cell category lines the mesenteric surface?

A

Mesothelial cells

208
Q

What enzyme levels do we measure for pancreatitis?

A

Lipase is elevated in pancreatitis

209
Q

What hormone synthesize by the small bowel stimulates contraction of the gallbladder?

A

Cholecystokinin

210
Q

What is hematemesis?

4 possible sources

A

Vomiting blood

Oral lesion

Esophageal lesion

Stomach lesion

Blood from a lung lesion being swallowed

211
Q

What causes nutmeg liver?

A

Liver congestion

212
Q

What strucure do aenocarcinomas form?

A

Glands

213
Q

What cell type is small cell carcinoma (lung) derived from?

A

Neuroendocrine

214
Q

What is a uterine smooth muscle tumor called?

A

Leiomyoma (benign)

Leiomyosarcoma (malignant)

215
Q

What is a skeletal muscle tumor called?

A

Rhabdomyoma (benign)

Rhabdomyosacroma (malignant)

216
Q

What is an endothelial cell tumor called?

A

Hemangioma (benign)

Angiosarcoma (malignant)

217
Q

What are teh ABCDEs of moles?

A

Asymmetry

Border irregularity/bleeding

Color variation

Diameter

Evolution or elevation

218
Q

What is the difference between the light and dark zone of the germinal center?

A

Light zone is more mature cells

Dark zone is increased mitotic activity

219
Q

What is rituximab?

A

Anti CD20 antibody

220
Q

What are 2 ways cellular injury occurs in hypoxia?

A

ATP reduction

Production of free radicals following reperfusion

221
Q

What is an effusion?

A

Fluid accumulation in a body cavity

222
Q

What is dysplasia?

A

Disordered cell growth

223
Q

4 ways E-cadherin expression can be lost

A

Loss of heterozygosity

Inactivating mutation (rare)

Silencing of gene expression via hypermethylation of promoter

Transcriptional repressors like SNAIL, SLUG, TWIST< ZEB1/2

224
Q

The main 5 ways cancer kills you

A

Infection

Organ failure

Hemorrhage

Thromboembolism

Emaciation

225
Q

What 3 things are in the lymph node hilum?

A

Efferent lymph vessels

Afferent arteriole

Efferent venule

226
Q

Where are T cell precursors in the thymus? Where do they move?

A

Cortex and move inward as they mature

227
Q

What 2 things make up the integrin?

A

CD18

CD11

228
Q

Which cancer forms keratin pearls?

A

Squamous carcinoma of the lung

229
Q

What is stage IV cancer?

A

Metastasis

230
Q

What is stage III cancer?

A

Lymph node involvement

Winter 2016 (8 decks)

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