Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

general knowledge medicine > pathology intro > Flashcards

pathology intro Flashcards

You may prefer our related Brainscape-certified flashcards:
Get Smarter flashcards
1
Q

Acute vs. chronic inflammation

A

acute- short duration; exudation of fluid and plasma proteins predominantly neutrophil.
chronic - longer duration - vascular proliferation and scaring/fibrosis - predominantly macrophage and lymphocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

adaptive immunity cells

A

lymphocytes and their products:
Humoral immunity - B lymphocytes
cellular immunity - T lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adhesion pairs

A

Endothelial V-CAM 1 // VLA 4 (integrin) leukocytes

Endothilia I CAM 1 // CD11/CD18 (LFA-1, Mac-1) leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Apoptosis decision

A

a balance between the withdrawal of positive signal and the receipt of negative signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

apoptosis is needed for:

A
  • optimal development (tadpole metamorphosis)
  • removal of excess cells during embryogenesis (fingers and toe digitation)
  • maintain cells with high turnovers
  • eliminates autoreactive immune T cells in the thymus
  • eliminates damaged cell
  • central to hormone depended involution (endometrium, ovary, breast)
  • cell death in tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

atrophy

A

decrease in organ size WITHOUT the loss of cell number (loss of cell substance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

atrophy is the adaptive response to what? is it reversible?

A

stress; yes (regain in size when remove stress)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

autoreactive clones could result in what conditions?

A

hemolytic anemia, thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ca gradient is maintained by what?

A

the membrane associated, energy-dependent Ca, Mg, ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cytoplasmic changes in necrosis

A

denaturation of cytoplasmic proteins tends to be acidophilic, granular mass and have affinity for acid dyes (eosinophilia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

damage results in high conductance channels called?

A

MPT - mitochondrial permeability transition where cytochrome c and H+ leak out of mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

define cellular aging

A

progressive decline in the proliferative capacity and lifespan of cells and the effect of continuous exposure to exogenous influences that result in progressive accumulation of cellular and molecular damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

definition of apoptosis

A

the elimination of unwanted cells by an internally programmed series of events
modulated by dedicated gene products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diabetes is an acquired or inherited diseases with defects in leukocyte function

A

acquired: defects in adhesion, chemotaxis, multiple defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dysplasia

A

changes in size, shape, and organization of the cells

most commonly in hyperplastic squamous epithelium and preneoplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dystrophic

A

deposition of calcium and other minerals in DEAD tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

edema

A

excessive accumulation of fluid in tissue or part

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

elements of wound contraction

A

12-24 hrs: inflammation and reepithelization (neutrophil, platelets)
3-7 days: angiogenesis, fibroplasia, wound contraction-granulation tissue (neutrophil, macrophage, fibroblast, wound matrix, blood vessel
1-2 wks: tissue remodeling: keratinocyte close off blood clot, complete coverage of granulation tissue, myofibroblasts, wound matrix and blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

endothelial CD-34 pairs with

A

L-selectin of leukocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

endothelial E-selectin

A

Lectin (sialyl-lewis X) of leukocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

endothelial P selectin pairs with

A

Lectin (sialyl-lewis X) of leukocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

example of cellular aging

A

sequential shortening of telomeres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

examples of dystrophic

A

atheromas

old tuberculosis lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

examples of endogenous intracellular acuumulations

A

products of abnormal synthesis and metabolism including lipofuschin, hemosiderin, biliruben

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

examples of metaplasia

A

smoking: ciliated columnar to straified squamous
chronic gastric reflux: squamous to columnar
cancer transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Extrinsic (Death Receptor initiated) pathway of apoptosis

A
  1. Fas ligand binds onto Fas Receptor cause dimerization of death domain
  2. induction of FADD (Fas associated deadth domain
  3. Procaspase 8 gets activated into Active Caspase 8
  4. caspase 8 activate excutioner caspase 3 for apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

exudate

A

a fluid found in extravascular space derived from blood plasma that traverses the endothelial wall of inflamed small vessels (mostly venules) that is RICH IN PROTEINS AND WHITE BLOOD CELLS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Free radical is formed from what?

A

by product of metabolisms reactions P-450 oxidase in ER; NADPH oxidase in plasma membrane; Peroxisome oxidase in cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

goal of inflammation

A

to deliver leukocytes and antibodies to injury site

initial response –> mediators amplify –. vascular response and cellular response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Heterophagy vs. Autophagy

A

Heterophagy - when a foreign particle is taken into a cell (phagocytosis or endocytosis) and the primary lysosome form a phagocytic vacuole and the secondary lysosome dismantle particles and exocytose
Autophagy - when the cell’s own organelles is no longer useful, the primary lysosome fuse to form autophagic vacuole and residual body with lipofuscin pigment granule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

histamine is released when there are?

A 
IgE antibodies binding to receptor
peptides: anaphylatoxins 
cytokines IL -1 IL-8
toxins/drugs: mellintin, codein, morphine
physical trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do cells naturally neutralized the free radicals?

A

Cytosol: SOD, vitamin C, Glutathione peroxidase, ferritin, ceruloplasmin
All membranes: vitamins E and A, B-Carotene
Mitocondria: SOD, Glutathione peroxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how does cytochrome c induce apoptosis?

A

cytochrome c act on procaspase 9 and Apaf-1 dimerize to latch on procaspase 9 activating it into active caspase 9, which activate the executioner caspase 3 for apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how does HPV16 cause cervical cancer?

A

HPV16 produces E6 –> binds and inactivates p53 –> prevent apopotosis of bad cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does the cell nucleus look like when undergo apoptosis vs. necrosis

A

Apoptosis: pyknosis (condenses); karyorrhexis (fragmentation); non random DNA breakdown
Necrosis: swelling; karyolysis (dissolution); random

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does the EBV cause monnucleosis, NPC, lymphomas?

A

EBV produces Bcl-2 –> block and resist apoptosis because caspase activation cannot take place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hyperemia

A

greater than usual amount of blood in the microcirculation of a tissue or a part

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Hyperplasia

A

increase in number of cells usually resulting in increased volume of the organ or tissue (may or may not increase in size)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Hypertrophy

A

increase in the size of cells resulting in an increase in size of the organ
NO NEW CELLS, JUST LARGER CELLS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

If no new cells form in hypertrophy, what accounts for the enlargement?

A

the cells increase its metabolic activity and manufacture more proteins causing larger cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

inflammatory cells and their function in chronic vs. acute inflammation

A

neutrophil - phagocytosis - acute
eosinophil - modulates mast cells function - acute in allergy; chronic in infection
basophil - binds to IgE - acute (anaphylaxis)
platelets - thrombosi, growth factor - acute
monocyte (macrophages) - phagocytosis - chronic
lymphocyte - humoral immunity (B cells); cell mediated immunity (T cells) - chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

injury summary of mediators in wound healing processes

A

epithelialization - KGF, TGFa
angiogenesis - FGF, VEGF, angiogenin
fibroblast migration, proliferation - PDGF
ECM synthesis//granulation of tissue formation//wound contraction - TGF-B
bone development - BMPs (BMP-7, IGF-I)
Remodeling (fibroplasia) –> fibrous scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

innate immunity cells

A

plasma cells, phagocytic cells, NK cells, lung surfactant proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Intrinsic pathway (mitochondrial) pathway of apoptosis

A

death agonists cause changes in the inner mitochondrial permeability transition (MPT) and release of cytochrome c and other pro-apototic proteins into to the cytosol leading do the activation fo caspase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

leukocytes give rise to what cells?

A

granulocytes –> neutrophils; eosinophils; basophils (mast cells)
monocytes –> macrophages
lymphoctyes –> B-lymphocytes and T-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Major differences btw necrosis and apoptosis

A

Apoptosis: no inflammation (clean); single cell target, cell shrinkage; small areas affected
Necrosis: inflammation (messy); groups of cells affected; swelling; large tissue area affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

margination and rolling involves what pairs of proteins?

A

selectins from endothelial cells and silaylated oliogsaccharides from leukocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Mechanisms of apoptosis

A
  1. intrinsic (mitochondrial) pathway - withdrawal of growth factors, hormones
    extrinsic (death receptor-initiated) pathway- receptor ligand interactions (FAS, TNF receptor)
    cytotoxic T lymphocytes directly propagates teh process by activate granzyme B
  2. control and regulations by the Bcl-2 family
  3. executational caspases activate latent cytoplasmic endonucleases/proteases
  4. cytoplasmic bud to form apoptotic body and ligand for phagocytotic cell receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

mechanisms of cell injury

A
  1. ATP depletion (hypoxia)
  2. mitochondrial damage
  3. intracellular influx of Ca++/loss of Ca++ homeostasis
  4. accumulation of free radicals (oxidative stress)
  5. defects in membrane permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Melonomas inhibit what?

A

expression of Apaf1 which is needed for activation of procaspase 9 for intrinsic pathway of apoptosis

53
Q

Metaplasia

A

conversion of one differentiated cell type to another

54
Q

metaplasia is most commonly seen in what cell types?

A

most common in epithelium and less in mesenchymal cells

55
Q

Metastatic

A

calcium deposition in NORMAL tissue in HYPERCALCEMIC states

56
Q

mitochondrial injury is caused by what factors?

A

inc incytosolic Ca, oxidative stress, lipid peroxidation, and leakage of cytochrom c into the cytosol

57
Q

monocytes vs macrophages

A

monocytes within circulation and macrophages are moncytes that have found residents in the tissues

58
Q

Name 2 immune privileged sites

A

the EYES and the TESTICLES

59
Q

name some of the anti inflammatory mediators

A

IL-1 receptor antagonist

IL-4, IL-10, TGF-B, TIMPs, LXA4

60
Q

name some proinflammatory mediators

A

IL-1, IL-6, TNF-a, Interferon (IFN-y), PGE2, MMPs

61
Q

Name the chemokines in inflammation

A

IL-8, MCP-1, eotaxin

62
Q

Necrosis

A

Gross and histological cell death from irreversible exogenous injury
Always pathologic etiology
morphologic appearance due to denaturation of intracellular protein

63
Q

Nuclear changes in Necrotic cell death

A

Pyknosis - condensation of chromatin
Karyorrhexis - fragmentation of cell nucleus (non random in apoptosis, but random in necrosis)
Karyolysis - dissolution of cell nucleus//basophilia of chromatin fades
*normally normal nucle is basophilic (purple/blueish) and the cytoplasm is more pinkish, but in necrosis nuclei tends to be eosiphillic (pinkish)

64
Q

opsonins

A

specific: antibodies
nonspecific: C3bi, C5b, collectins, fibronectin

65
Q

patterns of necrosis: caseous

A

subset of coagulative specific to tuberculosis lesion in the lung
cheese like
unlike coagulative necrosis, tissue architecture is completely obliterated

66
Q

patterns of necrosis: coagulative

A

outlined of dead cell intact, firm tissue
increasing intracellular acidosis - dentatures structural proteins
ex. myocardial infarction, renal infarction (except in brain)

67
Q

patterns of necrosis: fat necrosis

A

enzymatic digestion of fat
trauma induced
ex. fat necrosis by pancreatic enzymes

68
Q

patterns of necrosis: gangrenous necrosis

A

secondary to ischemia
superimposed infection
not a distinctive pattern of necrosis
ex. distal limb in diabetes mellitus

69
Q

patterns of necrosis: liquifactive

A 
dead cell disintegrates
affected tissue liquifies (brain)
digestion greater than denaturation
progressive catalysis of cell surface
ex. cerebral infarction
70
Q

platelets

A

not cells; fragments of megakaryocytes

71
Q

Reactive oxygen species include

A

O2-; H2O2; OH-

72
Q

regeneration and the cell cycle

A

regeneration has to be activated for labile cells (skin)
regeneration is reduced in permanent cells (neurons, heart)
regeneration is enhanced in stable cells (hepatocytes)

74
Q

regulators of the cell cylce

A

cyclin A -cdk2 @ synthesis
cyclin B -cdk1 @ mitosis
cyclin D - cdk4/6; cyclin E -cdk2; RB-P-E2F –> RB-PPP +E2F; CKI:p21/p27/p15 @ G1 phase

75
Q

Some cancer cells can either produce decoys levels of this protein to competively bind to the receptors of cells mark for apoptosis

A

FasL - the decoys competitively binds to the dead domain receptors so that the real Fas ligands could not bind and could not initiate extrinsic pathway

76
Q

some cancer cells produce real fasL to target what cells?

A

the cytotoxic T cells so that these T cells will die of apoptosis and can not go after the cancer cells.

77
Q

The cells of the immunopriveged sites express high levels of what at all times?

A

FasL - so antigens reactive T cells expressing Fas enter these sites are killed

78
Q

the execution phase of apoptosis, what does the cytoplasm caspases digest?

A

cytoskeleton

79
Q

The removal of dead cells by phagocytosis is so efficient and without a trace of inflammation. T/F

A

True

80
Q

Transudate

A

fluid in extravascular space derived from blood plasma that traverses the endothelial wall of normal non-inflamed capillaries and venules, having a LOW CONCENTRATIONS OF PROTEINS AND FEW OR NO CELLS.

81
Q

Unlike hypertrophy, what has to involve for hyperplasia?

A

Mitosis - hyperplasia only takes place if the cell is capable of synthesizing DNA, and completion of mitosis (cell cycle and checkpoints)

82
Q

what accounts for the rapid decline in CD4+ cells?

A

A few of the CD4+ cells are infected by the HIV virus in which it takes over the genomic marchinary, it begins to elaborate the production of fas Ligand that will come to the other uninfected cells and mark them for apoptosis. The majority of the cells death is not due to infection of the virus, but by the apoptosis mechanisms from the increase production of FasL forcing the healthy cells to die.

83
Q

What are caspases?

A

proteases first discovered in Nematodes; the caspase families sites of action include cytoskeleton, nucleus, mitochondria, with intrinsic and extrinsic triggers

84
Q

what are some examples of hyperplasia?

A 
physiological:
-hormonal ex. breast/pregnancy
-compensatory ex. liver regeneration
pathological:
-hormonal ex. endometrial hyperplasia, benign prostatic hyperplasia
-wound healing
85
Q

what are the 2 ways ATP is produced?

A 
oxidative phosphorylation (major)
glycolytic pathway (minor)
86
Q

what are the cardinal signs of acute inflammation?

A 
redness (rubor)
swelling (tumor)
heat (calor)
pain (dolar)
loss of function
87
Q

what are the functions of inflammation

A

localizes and eliminates injury;
dilutes, neutralizes, sequesters harmful agents
removes damaged/necrotic cells and tissues
initiates/interwoven with repair events

88
Q

what are the negative signals for apoptosis?

A
  • increased level of oxidants within a cell
  • DNA damage by oxidants/agents (UV, Xrays, chemo)
  • accumulation of malfolded proteins
  • inc death activators (TNFa, lymphotoxin, FasL)
89
Q

what are the positive signals for growth?

A

GF for neurons

IL-2 essential for mitosis of lymphocytes

90
Q

what are vasoactive amines?

A

histamine and serotonin

92
Q

what can block the cyclooxygenase reaction but not the 5 lipooxygenase reaction that makes the arachinodonic acid metabolites?

A

aspirin, indomethacin, ibuprofen (NSAID) drugs

93
Q

what can block the phospholipase producing arachindonic acid?

A

steroids

94
Q

what cause fatty liver?

A

when protein manufacturing shuts down during hypoxia, the liver mobilized glycogen to the mitochondria for glycolyis
free fatty acids for enter liver and form triglycerides and oxidation to ketone bodies, phospholipids, cholesterol esters and lipoproteins that all lead to lipid accumulation

95
Q

what cell inuries caused by free radicals?

A

Attack the lipid membrane directly
DNA fragmentation
protein cross linking and fragmentation

96
Q

what changes in cellular injury are reversible?

A

cellular swelling

fatty change

97
Q

what complements are endogenous chemotactic factors?

A

C3a, C5a, C567

98
Q

What does atrophy cause?

A

REDUCED FUNCTIONAL DEMAND

mechanism is an imbalance between protein synthesis and degradation

99
Q

what effect does cytochrome c has?

A

it aids in apoptosis

100
Q

what effects does ATP depletion has?

A

dec. ATP pump - inc influx of Ca, H2O, and Na//inc efflux of K+ - swelling
inc anerobic glycolysis - dec. glycogen//dec. pH - clumbing of chromatin

101
Q

What effects incr in cytosolic Ca have?

A

with extracellular Ca moving in, and intracellular moving out of mito into cytosol caused increased in cytosolic Ca, which activates enzymes, ATPase (dec in ATP), Phospholipase and Protease (membrane damage), endonuclease (nucleus chromatin damage)

102
Q

what factor involves the interrelationship among clotting, kinin, fibrinolytic and complement systems?

A

factor 12 to 12a

103
Q

what give us the signs that a cells is aging?

A

when find a lot of lipofuscin in a cell

104
Q

What happen when ATP depletion from hypoxic and chemical injury?

A

protein synthesis decreased (detachment of ribosomes)
lipogenesis (fatty deposition)
deacylation and reacylation in phospholipid turnover

105
Q

what happens in AIDS?

A

Decline in CD4+ T cells

106
Q

what inflammatory mediators are in fever?

A

IL-1, IL-6, TNF-a

107
Q

what inhibit the extrinsic (death receptor initiated) pathway?

A

FLIP, produced by some viruses and normal cells, which binds to procaspase 8 but cannot cleave/activate procas 8 because FLIP lacks enzyme activity

108
Q

what is an important function of NO?

A

free radical; cytotoxic, bactericidal

109
Q

what is increased in hypersensitivity reaction?

A

IgE

110
Q

what is involved in anaphylatoxins reaction and what is not?

A

IgE is NOT involved, but C3a, C5a more than C4a are produced by basophil/mast cells.

111
Q

what is the first point of attack?

A

plasma membrane

112
Q

what is the function of the plasma membrane?

A
  1. maintain contant ionic environment: K inside (protein synsthesis), Ca outside (prevents membrane damage)
  2. regulates what is taken into the cell: receptor mediated, pinocytosis, phagocytosis
  3. envelop and compartmentalized metabolic reactions
113
Q

what is the goal of acute inflammation?

A

to deliver leukocytes, antibodies to injury site

114
Q

what is the mechanisms for hyperplasia?

A

physiological: increased in local production fo GFs, and GFRs; activation of intracellular signaling such as production of transcription factors

115
Q

what is the normal CD4+ count?

A

500 to 1000 cells/mm^3

If less than 200 cells = AIDS

116
Q

what is the process that takes place on apoptotic cells with macrophages?

A

opsonization - macrophages secrete substances that bind specifically to apoptotic cells but not to live cells, and opsonize these for phagocytosis

118
Q

what is the sequence of duration of injury?

A

Reversible cell injury show dec in cell function
Irreversibel cell injury show incr in cell death with structural changes:
-Ultrastructural changes - min to hours
-Light microscopic changes - hrs to days
-Gross morphologic changes - days

119
Q

what molecules is involved in transmigration?

A

immunoglobulin superfamily PECAM -1 (CD31) from both endothelial and leukocytes pair to activate surface receptors CD44 on leukocyte

120
Q

what regulatory enzyme inhibit apoptosis and how?

A

Bcl-2 can block the release of cytochrome c and block Apaf-1 from latching onto procaspase 9 preventing it from activating to active caspase 9

121
Q

what signs are indication of metabolic derangement in cells?

A

intracellular accumulations in abnormal amounts

  • excess of normal cell constituents
  • abnormal exogenous, endogenous
  • pigments
122
Q

what specific chemokines are chemotactic factors?

A

IL-8: PMN
eotaxin: eosinophil
MCP-1: monocytes

123
Q

what triggers the alternate pathway of the plasma proteases?

A

endotoxins, cobra venom, aggregated IgA

124
Q

What types of caspases relevant to our courses?

A

Caspase 8, 9, 3, 6

125
Q

whatcondition that has a germline mutation that is found in the apoptosis pathologic process of the immune system?

A

Autoimmune Lymphoproliferative Syndrome (APLS) - present with spleen enlargement because of the accumulation of non useful lymphocytes

126
Q

where did plasma cells come from?

A

Plasma cells come from differentiated B -lymphocytes, terminally differentiate and only produce antibodies

127
Q

where does histamine release from?

A

mast cells/basophils

128
Q

where does the intracellular Ca reside?

A

Ca sequestered in the mitochondria and ER

129
Q

which tissues in the oral cavity have unlimited capacity for regeneration and which tissues has limited capability?

A

unlimited: gingiva, PDL, alveolar bone
limited: cementum (periodontium)

general knowledge medicine (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions