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Pathoma > Pathoma > Flashcards

Pathoma Flashcards

1
Q

Growth adaptations?

A

an increase, decrease or change in stress on an organ can result in growth adaptations.

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2
Q

Hyperplasia and hypertrophy differences?

A

Hypertrophy is an increase in the size. Hyperplasia is an increase on the number of cells.

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3
Q

Hypertrophy involves what type of mechanism?

A

gene activation, protein synthesis and production of organelles.

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4
Q

Hyperplasia and hypertrophy in permanent tissues?

A

cannot make new cells and undergo hypertrophy only example: cardia muscle, nerve. or response to systemic hta.

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5
Q

EXAMPLE OF HYPERTROPHY?

A

CARDIAC MYOCYTES UNDERGO HYPERTROPHY IN RESPONSE HTA SYSTEMIC.

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6
Q

Pathologic hyperplasia can progress ?

A

dysplasia and eventually cancer. exception HPB.

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7
Q

Atrophy. definition.

A

a decrease in stress leads to a decrease in organ size example: decreased hormonal stimulation in uterus.

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8
Q

Which is the via that occurs atrophy?

A

via ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components.

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9
Q

what happens in ubiquitin-proteosome degradation?

A

Intermediate filament of the cytoskeleton are tagged with ubiquitin and destroyed by proteasomas.

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10
Q

what happens in autophagy?

A

cellular components involves generation of autophagic vacuoles, these fuse with lysosomes whose hydrolytic enzymes breakdown cellular components.

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11
Q

Metaplasia definition

A

most commonly involves change of one type of surface epithelium to another or a change in stress on an organ leads to a change in cell type

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12
Q

example of metaplasia.

A

Barret esophagus ( cells are better able to hadle the new stress.

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13
Q

Hyperplasia involves de production of?

A

of new cells from stem cells with them produce the new cell type.

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14
Q

¿What changes occurs in Barret esophagus ?

A

nonkeratinizing squamous epithelium to nonciliated, mucin-producing columnar cells

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15
Q

Metaplasia is reversible?

A

yes, removal od the driving stressor.

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16
Q

The persistent of stress in metaplasia can progress a cancer?

A

yes, first dysplasia and eventually result in cancer.

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17
Q

which is the metaplasia exception in where not occurs dysplasia?

A

Apocrine metaplasia of breast, which carries no increases the risk of cancer.

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18
Q

Which is the roll of Vitamin A for differentiation of specialized surfaces (conjunctiva)?

A

the thin squamous lining of the conjunctiva undergoes into stratified keratinizing squamous epithelium is called keratomalacia.

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19
Q

which is the Mesenchymal tissues chance in metaplasia?

A

connective tissue whithin muscle changes to bone during healing after trauma (myositis ossificans).

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20
Q

Dysplasia. Definition?

A

Disordered in cellular growth.

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21
Q

example the dysplasia?

A

NIE OR CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN).

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22
Q

Aplasia definition?

A

is failure of cell production during embryogenesis. (unilateral renal agenesis).

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23
Q

Hypoplasia definition?

A

is a decrease in cell production during embryogenesis resulting in a relative small organ.

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24
Q

Cellular injury?

A

occurs when a stress exceeds the cell’s ability’s to adapt. And depend of the type of stress and the type of cell affected.

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25
Q

Causes of cellular injury?

A

Inflammation, nutritional deficiency or excess, hypoxia, trauma and genetic mutations.

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26
Q

Hypoxia definition?

A

Low oxygen delivery to tissue.

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27
Q

how occurs the hypoxia?

A

oxygen is the final electron acceptor in the electron transport chain of oxidative phosphorylation. Decreased oxygen impairs oxidative phosphorylation resulting in decreased ATP production.

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28
Q

Causes of Hypoxia?

A

Ischemia, hypoxemia and decreased on O2.

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29
Q

Ischemia. definition?

A

decreased blood flow through an organ.

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30
Q

Which is the mechanism of ischemia?

A
  1. Decreased arterial perfusion (atherosclerosis) 2. Decreased venous drainage (budd chiari syndrome) 3. Shock.
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31
Q

Definition of Hypoxemia?

A

Is low partial pressure of oxygen in the blood.

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32
Q

Which is the mechanism of Hypoxemia?

A

High altitude, Hypoventilation and Diffusion defect. V/Q mismatch (blood bypasses oxygenated lung or oxygeneted air cannot reach blood.

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33
Q

Definition of Decreased O2?

A

Carrying capacity arises with HB loss or dysfuntion. Ex: Anemia, Carbon monoxide poisoning.

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34
Q

Carbon monoxide poisonig syntoms?

A

Classic cherry-red appearance of skin. headache, coma and death.

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35
Q

The early and the lattes sing of exposure of CO2 poisoning?

A

Headache. Lattest: coma and death.

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36
Q

Methemoglobinemia

A

Iron in heme is oxidized to Fe3+, which cannot bind oxygen-PaO2 Normal SaO2 Decreased

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37
Q

Classic finding in methemoglobinemia

A

cyanosis with chocolated colored blood.

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38
Q

treatment of methemoglobinemia

A

Methylene Blue. Helps reduce Fe2+ bac to Fe2+ state.

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39
Q

Low ATP disrupts key cellular functions including?

A
  1. Na+-K+ pump, resulting in na and h20 buildup in the cell. 2. Ca+ pump resulting in Ca2+ buildup in the cytosol. 3. Aerobic glycolysis, switch to anaerobic glycolysis.
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40
Q

The Hallmark of reversible injury is?

A

Cellular swelling.

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41
Q

How occurs the cellular swelling?

A
  1. Cytosol swelling results in loss of microvilli and membrane bleebbing. 2. Swelling of the RER results in dissociation of ribosomes and decreased protein synthesis.
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42
Q

The hallmark of irreversible injury is?

A

Membrane damage. (plasma membrane, mitochondrial and lysosome membrane.

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43
Q

How occurs the irreversible injury?

A
  1. Plasma membrane: Cytosolic enzymes leaking into the serum and additional calcium entering into the cell 2. Mitochondrial: loss of the electron transport chain and cytochrome c leaking into cytosol (apoptosis). 3. Lysosome membrane: hydrolytic enzymes leaking into the cytosol are activated by the high intracellular calcium.
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44
Q

Cell death loss his nucleus for three ways?

A

Pyknosis (nuclear condensation), karyorrhesis (fragmentation) and karyolysis (dissolution).

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45
Q

Mechanisms of cell death?

A

Necrosis and apoptosis

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46
Q

The hallmark of cell death is?

A

Loss of the nucleus whick occurs for 3 via.

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47
Q

Necrosis definition?

A

Death of large groups of cells fallowed by acute inflammation. Underlying pathologic process.

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48
Q

Necrosis is divided into?

A
  1. Coagulative necrosis.
  2. Liquefactive necrosis.
  3. Gangrenous Necrosis.
  4. Caseous necrosis.
  5. Fat necrosis.
  6. Fibrinoid necrosis.
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49
Q

Characteristics of Coagulative necrosis?

A
  1. Necrotic tissue remains firm: cell shape and organ structure are preserved but the nucleus disappears.
  2. Area of infarcted tissue is often wedge-shape and pale (focus vascular occlusion renal example).
  3. Red infarction arises if blood re-enters a loosely organized tissue (testicular infarction)
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50
Q

Characteristics of Liquefactive necrosis?

A
  1. Necrotic tissue become liquefied; enzymatic lysis of cells and protein.
  2. Brain: Proteolytic enzymes from microglial cells.
  3. Abscess: Proteolytic enzymes fron neutrophils.
  4. Pancreatitis: Proteolytic enzymes from parenchyma.
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51
Q

Characteristics of Gangrenous necrosis?

A
  1. Coagulative necrosis that resembles mummified tissue.
  2. Ischemia of lower limb and GI tract.
  3. Superimposed infection od death tissues occurs the liquefactive necrosis ensues (wet gangrene).
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52
Q

Characteristics of Caseous necrosis?

A
  1. Soft and friable necrotic tissue with cottage cheese like.
  2. Combination of coagulative and liquefactive necrosis.
  3. Granulomatous inflammation due TB or fungal infection.
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53
Q

Characteristics of Fat necrosis?

A
  1. Necrotic adipose tissue with chalky-white appearance due to deposition of calcium.
  2. Fatty acids released by trauma (breast) or lipase (pancreatitis) join calcium.
  3. Saponification is a dystrophic calcification of dead tissues.
  4. Metastatic calcification occurs when high serum calcium or phosphate levels lead to calcium deposition in normal tissues.
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54
Q

Saponification

A

Is an example of dystrophic calcification in which calcium deposits on dead tissue. In dystrophic calcification the necrotic tissue Acts as nidus for calcification in the settings of normal serum calcium and phosphate.

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55
Q

Characteristics of Fibrinoid necrosis?

A

Necrotic damege to blood vessel wall. Leaking of proteins into vessel wall results in Bright pink staining of the wall microscopically. Malignant hypertension and vasculitis (preeclampsia, medical emergency).

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56
Q

Apoptosis. definition.

A

Energy ATP dependent genetically programmed cell death involving single cells or small groups of cells. ex> cd8+ t cell mediated killing of viral infected cells

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57
Q

Morphology of apoptosis

A

Dying cell shrinks, leading cytoplasm to become more eosinophilic. 2. Nucleus condenses and fragments in an organized manner. Apoptotic bodies fall from the cell are removed by macrophages (no followed by inflammation)

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58
Q

Apoptosis is mediated by?

A

Caspases that active Proteases ( break down the cytoskeleton) and endonucleases (break down DNA).

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59
Q

Caspases are activated by?

A
  1. Intrinsic mitochondrial pathway.
  2. Extrinsic receptor-ligand pathway.
  3. Cytotoxic cd8+ T-cell mediated pathway.
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60
Q

Intrinsic mitochondrial pathway

A

Cellular injury, DNA damage or decreased hormonal stimulation leads to inactivation of Bcl2. Lack of Bcl2 allows cytochrome C to leak from the inner matrix into the cytoplasm an activate caspases.

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61
Q

Extrinsic receptor-ligand pathway.

A

FAS ligand bind death receptor (CD95) on the target cell. TNF bind TNF receptor on the target cell, activating caspases.

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62
Q

Cytotoxic cd8+ T-cell mediated pathway.

A

Perforins secreted by CD8+ T cell create pores in membrane of target cell. Granzyme from CD8+ T cell enters and active caspases.

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63
Q

Free radicals, definition?

A

Free radicals are chemical species with unpaired in their outer orbit.

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64
Q

When occurs of generation of free radicals?

A

Physiologic occurs during oxidative phosphorylation.

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65
Q

How occurs generation of free radicals?

A

Cytochrome C oxidase (complex iv) transfers electrons to oxygen.
O2-O2(superoxide)-H202-OH-H20.

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66
Q

How occurs pathologic generation of free radicals

A
  1. Ionizing radiation (H2O TO OH)
  2. Inflammation-NADPH oxidase generate superoxide ions during oxygen dependent killing by neutrophils.
  3. Metals ( Fe2+ generantes Hydroxyl free radicals.
  4. Drugs and Chemicals: P450 System of liver metabolizes.
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67
Q

Free radicals causes cellular injury via?

A
  1. Peroxidation of lipids and oxidation of DNA and proteins.
  2. DNA damege is implicated in oncogenesis and aging.
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68
Q

Elimination of free radicals occurs by?

A

Antioxidants, enzymes and metals (metal carrier proteins like transferrin).

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69
Q

Elimination of free radicals by enzymas?

A
  1. Superoxide dismutase, in mitochondria 02.- H2O2.
  2. Glutathione peroxidase 2gsh+ free radical –GS-SG and H2O.
  3. Catalasa 9 (peroxisomes) H2O2-O2.- and h20.
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70
Q

Carbon tetrachloride CCl4

A
  1. Is an organic solvent used in the dry cleaning industry.
  2. Converted to CCl3 free radical by P450 system.
  3. Results in cell injury with swelling of RER. Ribosome detach, impairing protein synthesis.
  4. Decreased apolipoproteins lead to fatty change in the liver.
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71
Q

Reperfusion injury.

A

Return of blood to ischemic tissue-O2-derived free radical. leads to a continued rise in cardiac enzymes after reperfusion of iam tissue.

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72
Q

Amyloidosis. definition.

A

Is a misfolded protein that deposits in the extracellular space thereby damaging tissues. Systemic or localized.

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73
Q

Microscopically look?

A

Congo Red staining and apple green birefringence under polarized litgh. B-pleated sheet configuration.

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74
Q

Systemic Amyloidosis divided in?

A

Primary and secundary.

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75
Q

Primary amyloidosis.

A

Is a systemic deposition of AL AMYLOID, which is derived from Immunoglobulin light chain. (associated with plasma cell dyscrasias).

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76
Q

Secundary amyloidosis.

A

Is a systemic deposition of AA amyloid wich is derived from serum amyloid-associated protein (SAA).

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77
Q

Clinical findings of systemic amyloidosis.

A

Nephrotic syndrome. Restrictive cardiomyopathy or arrhythmia. Tonge enlargement, malabsorption and hepatosplenomegaly.

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78
Q

Diagnosis of amyloidosis

A

tissue biopsy. (abdominal fat and rectum)

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79
Q

Localized Amyloidosis

A

Amyloid deposition usually localized to a single organ.

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80
Q

Senile cardiac amyloidosis

A

Non-mutated serum transthyretin deposits in the heart.

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81
Q

Familial Amyloidosis cardiomyopathy

A

mutated serum transthyretin deposits in the heart. restrictive patron.

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82
Q

Non insulin dependent DM

A

amylin (derived fron insulin)

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83
Q

Alzheimer disease

A

AB amyloid (precursor protein) in the brain plaques.

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84
Q

Dialysis amyloid associated

A

B2-microglobulin deposits in joints.

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85
Q

Carcinoma of the thyroid

A

calcitonin deposits within the tumor (tumor cells in an amyloid background)

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86
Q

Inflammation. definition

A

is allows inflammatory cells plasma proteins and fluid to exit blood vessels and enter the interstitial space.

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87
Q

Acute inflammation. Characterized.

A

Presence of edema and neutrophils i tissue in response to infection or tissue necrosis. Inmediate response with limited specifity.

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88
Q

Which are the mediators of acute inflammation?

A
  1. Toll-like receptors.
  2. Arachidonic acid metabolites.
  3. Mast cells.
  4. Complement.
  5. Hageman factor (factor XII).
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89
Q

Toll-like Receptors (TLRs). Function

A
  1. Present on the cells of immune system (macrophages and dendritic cells)
  2. Activated by (PAMPs).
  3. TLRs activation results in upregulation of NF-kB a nuclear transcription factor that activated immune response genes.
    4.TLRs are also present on cells of adaptive immunity (lymphocytes).
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90
Q

PAMPs

A

CD14 ( a co-receptor for TLR4) on macrophages recognizes lipopoly-saccharide (a PAMPs) on the outer membran of gram negative bacteria.

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91
Q

AA metabolites.

A

Is a released from the phospholipid cell membrane by phospholipase A2 and then acted upon by cyclooxygenase or 5-lipoxygenase.

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92
Q

Cyclooxygenase produce?

A

Cyclooxygenase produce PG
2. PGI2 PGD2 AND PGE2 mediate vasodilatation and increase vascular permeability. PGE2 also mediates Pain and fever.

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93
Q

35-Lipoxygenase produce?

A

Leukotrienes. 1. LTB attracks and active neutrophils. 2. LTC4 LTD4 LTE4 mediate vasoconstriction, bronchospasm and increase vascular permeability.

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94
Q

Mast cells.

A

Widely distributed throughout connective tissue. 2. Activated by tissue trauma, complement proteins C3a an C5A or cross linked of cell surface IgE by antigen.

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95
Q

Inmediate responde in mast cells.

A

Released of preformed histamine granules, which mediate vasodilation of arteriales and increased vascular permeability.

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96
Q

Delayed response in mast cells.

A

Involves production of arachidonic acid metabolites particularly Leukotrienes.

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97
Q

Complement definition in acute inflammation?

A

Proinflammatory serums proteins that complement inflammation. Circulate as inactive precursors.

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98
Q

Classic pathway of complement?

A

C1 bind IgG or IgM that is bound to antigen.

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99
Q

Alternative pathway of complement?

A

Microbial products directly activate complement.

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100
Q

Mannose-Binding lectin (MBL) pathway of complement?

A

MBL binds to mannose on microorganism and activate complement.

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101
Q

Activation of complement occurs for 3 patways

A

Activation occurs for 3 via. Al pathways result in production of C3 convertase, in turns produces C5 convertase. C5b complexes with C6-C9 to form the Membrane attack complex.

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102
Q

Activation of complement occurs for 3 patways

A

Activation occurs for 3 via:
1. Clasical.
2. Alternative
3. MBL ( Mannosse- binding lectin) Al pathways result in production of C3 convertase, in turns produces C5 convertase. C5b complexes with C6-C9 to form the Membrane attack complex.

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103
Q

Activation of complement occurs for 3 patways

A

Activation occurs for 3 via:
1. Clasical.
2. Alternative
3. MBL ( Mannosse- binding lectin)

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104
Q

Phases of the complement?

A

C3a and C5a trigger mast cell degranulation, resulting in histamine-mediated vasodilatation and increase vascular permeability. C5a chemotactic for neutrophils. C3B opsonin for phagocytosis and MAC lyses microbes and creating a hole in the cell membrane.

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105
Q

Neoplasia. definition.

A

Is new tissue growth that is unregulated, irreversible and monoclonal. Or uncontrolled, monoclonal proliferation of cells.

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106
Q

Differences between cells monoclonal and polyclonal?

A

Monoclonal means that neoplastic cells are derived from a single mother cell and polyclonal are cells derivaded from multiples cells.

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107
Q

Dysplasia

A

Is the loss of uniformity in cell size and shape (pleomorphism), loss of tissue orientation and nuclear changes often reversible.

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108
Q

Clonality is determined by?

A

G6PD in multiples isoforms (G6PDa, G6PDb, G6PDC etc.). Can also be determined by androgen receptor isoforms, which are present on the X chromosome. Normal radio es 1:1 in cells of any tissue.

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109
Q

Differences between Neoplasia and Hyperplasia?

A

Neoplasia is unregulated, irreversible and monoclonal and Hyperplasia is regulated

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110
Q

Clonality of lymphocytes B is determined by?

A

Immunoglobulin (Ig) light chain phenotype. Each B cells expresses ligth chain that is Kappa or Lambda ratio 3:1. Is maintained polyclonal. if chain ratio higher than 6:1 is monoclonal.

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111
Q

Differences between Neoplastic benign and malignant?

A

Benign: Localized and do not metastasize.
Malignant tumors> invade localy and have the potential to metastasize.

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112
Q

In lymphoma, which type of changes occurs in the Ratio?

A

Ratio increases to 6:1 or is inverted (kappa to lambda 1:3) which is monoclonal.

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113
Q

Ratio can change in 3 via. Which?

A

Metastasize, infecction and lymphoma.

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114
Q

Tumor Nomenclature.

A

Epithelium: Benign Adenoma Malignant: Adenocarcinoma.
Mesenchyme: Benign: FAT= Lipoma. Malignant: Liposarcoma.
Melanocyte Nevus and Melanoma.

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115
Q

Tumor Nomenclature exceptions:

A

Lymphoma.

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116
Q

Epidemiology of cancer.

A

Is the Secund leading cause of the in adults and children.

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117
Q

Which is the incidence of cancer in adults?

A
  1. Breast/Prostate.
  2. Lung.
  3. Colorectal.
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118
Q

Which is the incidence of death in children’s?

A
  1. Accidents.
  2. Cancer
  3. Congenital defects.
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119
Q

Which is the incidence of death in adults?

A
  1. Cardiovascular disease.
  2. Cancer.
  3. Chronic Respiratory disease.
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120
Q

Which is the incidence of cancer mortality in adults?

A
  1. Lung
  2. Breast/Prostate.
  3. Colorectal.
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121
Q

Which is the rol of screening?

A

Seek to catch dysplasia before becomes carcinoma or carcinoma before clinical symtoms arise.

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122
Q

Most common screening methods are?

A
  1. PAP smear.
  2. Mammography.
  3. PSA.
  4. Hem occult test and colonoscopy.
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123
Q

Definition of carcinogenesis?

A

Is the iniciated damage to DNA of stems cells. The damage overcomes DNA repair mechanisms.

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124
Q

Carcinogens definition.

A

Are agents that damage DNA, increasing the risk of cancer. DNA mutations eventually disrupt key regulatory systems.

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125
Q

Carcinogens agent?

A
  1. Chemicals.
  2. Oncogenic viruses.
  3. Radiation.
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126
Q

What chemicals are carcinogenic agent?

A

Aflatoxins, alkylating agents, alcohol, arsenic, asbestos, cigarette smoke, nitrosamines, naphthylamine, vinyl chloride, nickel, chromium, beryllium or silica.

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127
Q

What kind oncogenic viruses are carcinogens?

A

EBV, HHV-8, HBV AND HCV, HTLV-1 and subtypes HPV (16,18, 31 and 33).

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128
Q

What types of radiation are related to cancer?

A

Ionizing (nuclear reactor accidents and radiotherapy) and Nonionizing ( UVB).

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129
Q

Aflatoxins are related to?

A

Aspergillus and Hepatocellular carcinoma.

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130
Q

Alkylating are related to?

A

Leukemia/lymphoma for de side effects of chemotherapy.

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131
Q

Alcohol are related to?

A

Multiples cancer like: squamous cell carcinoma of oropharynx (more Tabaco), upper esophagus and hepatocellular carcinoma (cirrhosis). Pancreatic carcinoma for pancreatitis.

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132
Q

Arsenic are related to?

A

Squamous cell carcinoma of skin, lung cancer ( cigarette smoke) and angiosarcoma of liver.

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133
Q

Asbestos are related to?

A

Lung carcinoma and mesothelioma.

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134
Q

Cigarette smoke are related to?

A

Carcinoma of orooharynx, esophagus, lung, kidney, bladder and pancreas.

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135
Q

Why cigarette smoke are the most common cause of carcinogens?

A

Because of polycyclic hydrocarbons are particularly carcinogenic.

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136
Q

How cigarettes produce cancer in the urothelial tissue?

A

The Kidney cleaning the residues that acumulate in the tissue to product the mutations and after cancer.

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137
Q

Nitrosamine are related to?

A

Stomach carcinoma.
Usually found in smoke food
Japonese love smoke food
Is the most frecuent cancer in japon

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138
Q

Where I can found nitrosamines and what type of cancer is related specific?

A

Is found in smoked food, for that is responsible of high rate of carcinoma in Japan. They have the type Intestinal mejorar aqui tambien.

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139
Q

Naphthymine are related to?

A

Urothelial carcinma of bladder, derived from smoke cigarettes.

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140
Q

Vinyl Chloride are related to?

A

Angiosarcoma of liver, which is a Occupational exposure.

141
Q

Other metal related to occupational expusure and cancer are?

A

Nickel, chromium, beryllium or silica in Lung cancer.

142
Q

EBV are related to?

A

Nasopharyngeal carcinoma, Burkitt lymphoma and CNS lymphoma in AIDS.

143
Q

HHV-8 are related to?

A

Kaposi sarcoma.

144
Q

Which is the symptoms of EBV?

A

In nasopharyngeal are chinase male or africam with a mass in the neck.

145
Q

HHV-8 presentations?

A
  1. Westerns Europe and male.
  2. AIDS and the treatment is antiretroviral.
  3. Patient that had transplant, so they need decreased the dosis.
146
Q

HBV AND HCV are related to?

A

Hepatocellular carcinoma

147
Q

What type of virus are HBV AND HCV?

A

HBC are ADN virus and HCV are ARN virus.

148
Q

HTLV1 are related to?

A

Adult T-Cell leukemia/lymphoma.

149
Q

HPV are related to?

A

Squamous cell carcinoma of cervix, vulva, anus and vagina. Adenocarcinoma of cervix.

150
Q

Which type the radiation is releated to cancer?

A
  1. Ionizing (nuclear reactor accidents and radiotherapy) AML, CML and Papillary carcinoma of thyroid.
  2. Nonionizing (UBV) Basal cell carcinoma, squamous cell carcinoma and melanoma of skin.
151
Q

In the Nonionizing radiation who results in cancer?

A

UVB result in formation of pyrimidine dimers in DNA whit normally excised by restriction endonuclease.

152
Q

Dna mutations allowing?

A
  1. Disrupt key regulatory systems.
  2. Tumor promotion (growth).
  3. Progression (spread).
153
Q

DNA Disrupts systems include?

A
  1. Proto-oncogenes.
  2. Tumor suppressor genes.
  3. Regulators of apoptosis.
154
Q

Proto-oncogenes?

A
  1. Are essential for cell growth and differentiation; mutations of proto-oncogenes form oncogenes that lead to unregulated cellular growth.
155
Q

Oncogenes categories?

A
  1. Growth factors.
  2. Growth factor receptor mediate signals.
  3. Signal transducer relay receptor activation to the nucleus.
  4. Cell cycle regulators.
156
Q

Mechanisms associated to activation of the nucleus?

A
  1. RAS is associated with Growth factor receptor in an inactive GDP-bound state.
    2.Receptor binding causes GPD to be replaced in an GTP, activating Ras.
  2. Activated Ras sen.ds growth signals to the nucleus.
  3. Ras inactivates itself cleaving GTP>GDP; augmented by GTPase activating protein.
  4. Mutated Ras inhibits the activit oh GTPase activating proteins, that prolongs the activate state Ras
157
Q

Growth factors like oncogens?

A

Induce cellular growth. PDGFB in astrocytoma.

158
Q

Grow factor receptor are mediate?

A

For signals from growth factor. ERBB2 in breast cancer.

159
Q

Growth factor like Oncogenes and associated tumors.

A

PDGFB. Platelet-derived growth factor. Overexpression, autocrine loop. Astrocytoma.

160
Q

Growth factor receptors like Oncogenes and associated tumors.

A
  1. ERBB2 (HER2/neu) > Epidermal growth factor receptor > amplification > subset of breast carcinoma.
  2. RET > Neural growth factor receptor > point mutation > MEN2A AND MEN 2B and sporadic medullary carcinoma of thyroid.
  3. KIT > stem cell growth factor > point mutation > GI stromal tumor.
161
Q

Signal transducers like Oncogenes and associated tumors.

A
  1. Ras gene family > GTP-binding protein > point mutation > Carcinomas, melanoma and lymphoma.
  2. ABL > tyrosine kinase > translocation 9: with BCR > CML and some types of ALL.
162
Q

Nuclear regulators like Oncogenes and associated tumors.

A
  1. c-MYC > Transcription factor > translocation (8:14) involving IgH > Burkitt lymphoma.
  2. N-MYC > Transcription factor > Amplification > Neuroblastoma.
  3. L-MYC > Transcription factor > Amplification > Lung carcinoma (small cell).
163
Q

Cell cycle regulators like Oncogenes and associated tumors.

A
  1. CCND1 (cyclin D1) > cyclin > Translocation (11:14) involving IgH > Mantle cell lymphoma.
  2. CDK4 > Cyclin-dependent kinase > Amplification > Melanoma.
164
Q

Regulation of cyclin and cyclin-dependent kinase in the cell.

A
  1. CDK’s form a complex which phosphorylates proteins that drive the cell through the cell cycle.
  2. CDK4 complex phosphorylates the retinoblastoma protein, promotes progression to G1 to S check point.
165
Q

Tumor suppressor genes. Definition.

A

Regulate cell growth and hence, decrease (suppress) the risk of tumor formation. Example: p53 y Rb.

166
Q

Function of p53?

A

P53 regulates progression of the cell cycle from G1 to S phase.

167
Q

In response to DNA damage how is the function of p53?

A

P53 slows cell cycle and upregulates DNA repair enzymes.

168
Q

If DNA damage it not possible repair which is the function of p53?

A

P53 induces the apoptosis, by upregulates BAX which disrupts Bcl2 and Cytochrome C leads from de mitochondria activating apoptosis.

169
Q

Knudson two-hit hypothesis are related to?

A

P53: Germline mutations results un Li-Fraumeni Syndrome characterized by the propensity to develop multiple types of carcinomas and sarcomas.
Rb: Germline mutations results Familial Retinoblastoma and osteosarcoma.

170
Q

Rb also regulates progression from G1 to S phase for what mechanism?

A

Rb holds the E2F transcription factor, E2F is released when Rb is phosphorylated by cyclinD/cyclin-dependent kinase 4 (CDK4) complex. Mutation of Rb results in free E2F allowing progression through the cell cycle and uncontrolled growth cells. Both copies of rb gene must be knocked out for tumor formation.

171
Q

Regulators of apoptosis. Functions?

A

In normal cells prevent apoptosis.
In mutated cell whose DNA cannot be repaird promote apoptosis. Ex: Bcl2.

172
Q

Bcl2 stabilizes the mitochondrial membrane in normal cells by?

A

Blocking release of cytochrome C, this leave the mitochondria and activate the apoptosis.

173
Q

If Bcl2 is overexpressed, what happens in the mitochondrial membrane?

A

Is further stabilized, prohibiting apoptosis and B cells that would normally undergo apoptosis during somatic hypermutation in the lymh node germinal center.

174
Q

Other important features of tumor development are?

A
  1. Telomerase.
  2. Angiogenesis.
  3. Avoiding immune surveillance.
  4. Immunodeficiency.
175
Q

Telomerase involt in tumor development by?

A
  1. Cell immortality.
  2. Cellular senescence (telomerase shorten with serial cells divisions).
  3. Upregulated telomerase (preserved).
176
Q

Angiogenesis in tumor development are reletad to?

A
  1. Production of new blood vessels for tumor survival and growth.
  2. FGF and VEGF are related like angiogenic factor.
177
Q

Avoiding immune surveillance through what mechanism?

A
  1. Mutations often results in abnormal proteins which are expressed on MHC class I.
  2. CD8+ T cells detect and destroyed.
  3. Tumor cells evade immune surveillance by downregulating expression of MHC class I.
178
Q

Tumor progression definition?

A

Is the accumulation of mutations eventually results in tumor invasion and spred.

179
Q

Tumor invasion and spred occurs by?

A
  1. Down regulation of E-cadherin leads to dissociation of attached cells.
  2. Cells attach to laminin and destroy BM (collagen type IV) via collagenase.
  3. Cells attach to fibronectin in the extracellular matrix spread locally.
  4. Entrance into vascular or lymphatic space.
180
Q

Routes of metastasis are?

A
  1. Lymphatic spread.
  2. Hematogenous spread.
  3. Seeding of body cavities.
181
Q

Lymphatic spread route is?

A
  1. To regional draining lymp nodes like in the case of breast cancer.
182
Q

Hematogenous spread route is characteristic of?

A

Sarcomas and some carcinomas

183
Q

Hematogenous spread is characteristic of sarcomas and some carcinomas except?

A
  1. Renal cell carcinoma.
  2. Hepatocellular carcinoma.
  3. Follicular carcinoma of Thyroid.
  4. Choriocarcinoma.
184
Q

The ovarian carcinoma had a especific characteristic?

A

Seedinf of body cavities, which often involves the peritoneum. ex: omental caking.

185
Q

Characteristics Clincal of Benign Tumor are?

A
  1. Slow growing
  2. Well circumscribed.
  3. Distinct.
  4. Mobile.
186
Q

Characteristics Clinical of Malignant Tumor are?

A
  1. Rapid growing.
  2. poorly circumscribed.
  3. Infiltrative.
  4. fixed to surrounding tissues and local structures.
187
Q

Histologic characteristics of benign are?

A
  1. usually well differentiated.
  2. Organized growth.
  3. Uniform nuclei.
  4. Minimal mitotic activity.
  5. Lack of invasion.
  6. No metastatic potential.
188
Q

Histologic characteristics of Malignant are?

A
  1. Poorly differentiated (anaplastic).
  2. Disorganized growth.
  3. Nuclear pleomorphism and hyperchromasia.
  4. High mitotic activity with atypical mitosis.
  5. Invasion.
189
Q

Hallmark of malignancy is?

A

Metastatic potential.

190
Q

Immunohistochemistry is?

A

Used to characterize tumors that are difficult to classify on histology.

191
Q

Immunohistochemical most common are?

A
  1. Keratin > epithelium.
  2. Vimentin > mesenchyma.
  3. Desmin > Muscle.
  4. GFAP > neuroglia.
  5. Neurofilament > neurons.
  6. PSA > Prostatic.
  7. Er > Breast
  8. Thyroglobulin > Thyroid follicular cells.
192
Q

What are Serum tumor markers?

A

Proteins released by tumor into serum like PSA.

193
Q

Which is the used of serum tumor markers?

A

Is useful for screening, monitoring response to treatment and monitoring recurrence.

194
Q

If you have a patient with serum tumor marker elevated, which is the next step?

A

Tissue biopsy for diagnosis.

195
Q

Grading of cancer are?

A

Microscopic assessment of diferentiation takes into account architectural and nuclear features.

196
Q

Grading of cancer is divided in two types?

A
  1. Well differentiated (low grade).
  2. Poorly differentiated (high grade).
197
Q

The gradinf of cancer is important for?

A

Determining prognosis; well differentiated cancer have better prognosis than poorly differentiated cancers.

198
Q

Staging of cancer are?

A

Assessment of side and spread of a cancer. Key prognostic factor.

199
Q

TNM staying system:

A

T - tumor size or depth.
N - spread to regional lymp nodes. 2nt.
M - Metastasis. The most important.

200
Q

The final result of activation complement pathways is?

A

All pathways result in production of C3 convertase, in turns produces C5 convertase. C5b complexes with C6-C9 to form the Membrane attack complex.

201
Q

Components of production of MAC?

A
  1. C3a and C5a (anaphylatoxins) -trigger mast cell degranulation, resulting in histamine-mediated vasodilatation and increase vascular permeability.
  2. C5a - chemotactic neutrophils.
  3. C3b- opsinin for phagocytosis.
  4. MAC (membrane attack complex).
202
Q

Hageman factor or Factor XII. Functions:

A
  1. Inactive proinflamatory protein produce in liver.
  2. Activated upon exposure to subendothelial or tissue collagen.
203
Q

What activated factor xii?

A
  1. Coagulation and fibrinolytic systems.
  2. Complement
  3. Kinin system - Kinin cleaves high molecular -weight kininogen (HMWK)
204
Q

Kinin system - Kinin cleaves high molecular -weight kininogen (HMWK) Actives?

A
  1. Bradykinin which mediates vadilatation and increased vascular permeability.
  2. Pain.
205
Q

Cardinal signal of inflammation?

A

A. Redness (rubor) and warmth.
B. Swelling tumor.
C. Pain.
D. Fever.

206
Q

Redness and warmth occurs?

A
  1. Due to vasodilatation, which increased blood flow.
  2. Occurs via relaxation of arteriolar smooth muscle.
207
Q

Key mediators on redness and warmth are?

A
  1. Histamine.
  2. Prostaglandins.
  3. Bradykinin.
208
Q

Swelling occurs via?

A
  1. Due to leakge of fluid postcapillary venueles into the intersticial space (exudative).
  2. Key mediators (histamine).
209
Q

Key mediator in swelling are?

A

Are histamine which causes endothelial cell contraction and tissue damage resulting in endothelial cell disruption.

210
Q

Pain occurs via?

A
  1. Bradykinin ang PGE2 Sintetize sensory nerve endings.
211
Q

Fever occurs via?

A
  1. Pyrogenes (LPS) cause macrophages to release IL-1 and TNF which inceased cyclooxygenase activity in perivascular cells of hypothalamus.
212
Q

What make PGE2 in fever?

A

Increased raise temperature set point.

213
Q

Macrophages in the acute inflammation appears?

A
  1. Appears predominate after neutrophils and peak 2-3 days after inflammation begins. Derived from monocytes in blood.
214
Q

Macrophages arrived in tissue via?

A
  1. Margination.
  2. Rolling.
  3. Adhesion.
  4. Transmigration sequence.
215
Q

Macrophages ingest organism via?

A

By phagocytosis (augmented by opsonins) and destroy phagocytosed material using enzymes in secondary granules.

216
Q

Manage the next step of the inflammatory process produced by macrophages include?

A
  1. Resolution and healing
  2. Puss formation.
  3. Abscess.
  4. Chronic inflammation.
217
Q

The resolution and healing produce in acute inflammation?

A

Anti inflammatory cytokines. (IL-10 and TGF-B) produces by macrophages.

218
Q

The continued acute inflammation by macrophages are marked by?

A

Continued acute inflammation marked by persistent pus formation. IL-8 recruits additional neutrophils.

219
Q

Abscess are manage by?

A

Acute inflammation surrounded by fibrosis, macrophages mediate fibrosis via fibrotic growth factor and cytokines.

220
Q

Chronic inflammation are manage by?

A

Macrophages present antigen to activate CD4+ helper T cells which secrete cytokines that promete chronic inflammation.

221
Q

Chronic inflammation is characterized by?

A

The present of lymphocytes and plasma cells in tissue. Delayed response but more specific ADAPTATIVE IMMUNITY that acute inflammation.

222
Q

Chronic inflammation stiluli include:

A
  1. Persist infection.
  2. Infection with virus, mycobacteria, parasites and fungi.
  3. Auto immune disease.
  4. Foreign material
  5. some cancers.
223
Q

T Lymohocytes are?

A

Produced in bone marrow as progenitor T Cells.

224
Q

T cells used for antigen surveillance?

A

TCR AND CD3.

225
Q

TCR complex recognizes antigen and is presented?

A

On MHC molecules.

226
Q

What type of T cells are recognized by MHC?

A

CD4+ T cells to MHC class II
CD8+ T cells to MHC class I.

227
Q

Activation of T cell requires two signals?

A
  1. Binding of antigen/MHC complex.
  2. Additional 2 nd signal. ?
228
Q

T Lymphocytes are develop in what part of body?

A

Further develop in the thymus where the T cells receptor (TCR) undergoes rearrangement and progenitor cells become CD4+ helper T or CD8+ cytotoxic T cells.

229
Q

CD4+ helper T cell activation are for what via?

A

Extracellular antigen is phagocytosed, processed and present on MHC class II, which is expressed by antigen presenting cells (APC). And de activation of second signals.

230
Q

Which is the second signals?

A

B7 on APC bins CD28 ON CD4+ helper T cells providing 2nd activation signal.

231
Q

Activated CD4+ helper T cell secrete cytokines that are divided into two?

A
  1. Th1 Subset secretes IFN-Gamma > B cells class > IgM to IgG.
  2. Th2 Subsets secrets IL-4 and IL 5> B cells > IgE and IgA.
232
Q

Activated CD8+ cytotoxic T cell mediated by?

A
  1. Intracellular antigen is processed and present on MHC class I, which is expressed by all nucleated cells and plaquets.
  2. IL-2 from CD4+ T h1 cell provides 2nd signal activation.
  3. Cytotoxic T cells are activating for killing.
233
Q

In Activated CD8+ cytotoxic T cells Killing occurs via?

A
  1. Secretion of perforins and granzyme.
  2. Expresion of FasL, activating apoptosis.
234
Q

What made perforins and granzyme?

A

Perforins creates pores that allow granzyme to enter the target cell activating apoptosis.

235
Q

What made the Expresion of FasL?

A

Binds Fas on target cells. activating apoptosis.

236
Q

B lymphocytes o B cells.

A

Immature B cells are produced in the bone marrow and become in naïve B cells that express surface IgM and IgD.

237
Q

B cell activation occurs via?

A
  1. Antigen binding to IgM or IgD results in maturation secreting plasma cells.
  2. B cells antigen presentation to CD4+ helper T cells via MHC class II.
238
Q

B cell antigen presentation occurs 2 via?

A

CD40 receptor on B cell bind CD40L on T cell, providing the 2nd activation signal.
Helper T the secrets IL-4 and IL-5 (B cell isotype switching hypermutation and maturation in plasma cells).

239
Q

Granulomatous inflammation

A

Is a subtype of chronic inflammation.
Characterized by granuloma.

240
Q

Granuloma. Definition

A

Is a collection of epithelial histiocytes that are macrophages with abundant pink cytoplasm usually surrounded by giand cells and a rim lymphocytes.

241
Q

Granuloma division are?

A
  1. Noncaseating granulomas
  2. Caseating granulomas.
242
Q

Noncaseating granulomas

A

Lack central necrosis. Common etiologies include reaction to foreign material sarcoidosis beryllium exposure Chron disease.

243
Q

Caseating granulomas.

A

Exhibit central necrosis and characteristic of TB and fungal infections.

244
Q

Steps involve in granuloma formation

A
  1. Macrophages process and present antigen via MHC class II to CD4+ helper T cells.
  2. Interaction macrophages to secrete IL-12 inducing CD4+ helper T cells to differentiate into Th1 subtype.
  3. Th1 cells secrete IFN gamma which convert macrophages to epithelial histiocytes and giand cells.
245
Q

Primary Immunodenficiency

A
  1. Digeorge Syndrome.
  2. Severe combined immunodeficiency (SCID).
  3. X linked agammaglobulinemia.
  4. Common variable immunodeficiency.
  5. IgA deficiency.
  6. Hyper IgM symdrome.
  7. Wiskott-Aldrich syndrome.
  8. Complement deficiencies.
246
Q

Autoimmune Disorders. Basic principles

A
  1. Characterized by immune-mediated damage of self tissues.
  2. Involves loss of self-tolerance.
  3. Central tolerance in bone marrow leads to receptor editing or B-cells apoptosis.
  4. Peropheral tolerance leads to anergy or apoptosis.
  5. Regulatory T cells suppress autoimmunity by blocking lymphoproliferative syndrome.
247
Q

Generalities in autoimmune disorders.

A
  1. More common in women on childbearing age. Because estrogen may reduce apoptosis of self- reactive B cells.
  2. Us prevalence 1-2%.
  3. Autoimmune disorders are clinically progressive with relapses and remissions and show overlapping features
248
Q

Mechanisms that involves loss of self tolerance?

A
  1. Self reactive lymphocytes are regularly generated.
  2. Central tolerance in thymus leads to T cell apoptosis generation of regulatory T cells. In bone marrow leads to receptor editing or B cells.
  3. Peripheral tolerance leads to anergy or apoptosis of T and B cells.
  4. Regulatory T cells supress autoimmunity by blocking T cell activation and producing anti-inflammatory cytokines.
249
Q

Polyendocrine syndrome is the result of which mutations?

A

AIRE.

250
Q

Peripheral tolerance pathway?

A
  1. Fas apoptosis pathway mutations result in autoimmune lymproliferative syndrome ALPS.
251
Q

What type of regulatory t cells are releted to supress autoimmunity?

A
  1. CD25 Polymorphims ( MS and type DM).
  2. FOXP3 mutations leads to IPEX syndrome.
252
Q

IPEX

A

I - Immune dysregulation.
P- Polyendocrinopathy.
E- Enteropathy
X- X-linked.

253
Q

Etiology of Immune disorders?

A

Is likely an environmental trigger in genetically susceptibles individuals. lead to bystander activation or molecular mimicry.
Association with certain HLA types (HLA-B27) and PTPN22 polymorphism.

254
Q

LES characteristics.

A

Chronic systemic autoimmune disease. Flares and remissions. Middle aged-females. African American and hispanic. Antigen-antibody complexes damage multiples tissues.

255
Q

Chronic inflammation. Definition.

A

Is the adaptive immune response or delayed response, characterized by the present of LYMPHOCYTES AND PLASMA CELLS in tissue. Is more specfic.

256
Q

Causes of chronic inflammation

A
  1. Persistent infecction.
  2. Infection (virus, mycobacteria, parasites and fungi.
  3. immune disease.
  4. foreing material.
  5. some cancers.
257
Q

Severe Combined Immunodeficiency (SCID)

A
  1. Cytokine receptor defects.
  2. Adenosine deaminase deficiency (ADA).
  3. MHC class II.
    Susceptibility to fungal bacterial and protozoal infections and LIVE VACCINES.
    Bubble baby.
258
Q

X-Linked Agammaglobulinemia.

A

Complete lack of immunoglobulin. Naive cells cannot mature in B cells.
Mutated Bruton tyrosune kinase, X linked.
Presents after 6 months recurral bacterial, enterovirus and gardia lambia. Don’t use Polio.

259
Q

Hyper IgM syndrome.

A

Elevated IgM, due to mutated CD40L on helper t cells or CD40 receptor on B cells. 2

260
Q

What type Antigen-antibody complexes damage the tissue?

A

Lupus is a systemic autoimmune disease in which autoantibodies can cause type II (cytotoxic -
antibody bind and kill cells) or type III hypersensitivity reaction (antigen-antibody complex form and deposit in tissue causing damage).

261
Q

Type III HSR occurs?

A
  1. Poorly cleared apoptotic debris produce antibodies to host nuclear antigens.
  2. Antigen-antibody complexes are taken by dendritic cells.
  3. DNA antigens activate TLRs.
  4. Antigen antibody complexes are deposit in multiples tissue.
  5. Deficiency of early complement proteins C1q C4 and C2.
262
Q

IgA deficiency.

A

Low serum and mucosal IgA. Increased risk for mucosal infection. Most patients are asymptomatic.

263
Q

Classic finding in SLE include?

A
  1. Fever, weigt loss, fatigue, lymphadenopathy and Raynaud.
  2. Malar butterfly rash. Discoid rash.
  3. Oral or nasopharyngeal ulcers.
  4. Artritis.
  5. Serositis.
  6. Psychosis.
  7. Renal damage.
  8. Alt hematologicas.
264
Q

Diagnosis of SLE`

A
  1. Syntoms.
  2. ANA
  3. Anti ds DNA or Sm antibodies.
265
Q

Antiphospholipid antibody is associated whith?

A

SLE

266
Q

Antibodies releated to SLE and AP

A
  1. Antibodies are made against proteins bound to phospholipid.
  2. anticardiolipin Vdrl RPR are false +.
  3. lupus anticoagulant falsely elevated PTT (paradojico) Hypercoagulation.
267
Q

Antiphospholipid antibodies syndrome. Characteristic:

A

Hypercoagulable state due to antiphospholipid antibodies, lupus anticoagulant, that result in arterial and venous thrombosis. Required lifelong anticoagulation.

268
Q

LUPUS drug induce.

A

Ant histone antibody by procainamide hydralazine and isoniazid, ANA positive. CNS and Renal are rare. removal of drug results in remission.

269
Q

Sjogren Syndrome.

A

Autoimmune destruction of lagrimal and salivary glands, lymphocyte mediated damage type IV HRS.

270
Q

Sjogren Syndrome. Clinical.

A

Dry eyes, mouth and recurrent caries in older woman. Keratoconjunctivitis sicca and xerostomia.
Lymphatic sialadenitis.

271
Q

Rheumatoid arthritis and Sjogren Syndrome.

A

Are related, FR in often + even in absent of AR.

272
Q

Sjogren Syndrome. Antibodies.

A
  1. Anti SSA/Ro and Anti SSB/La.
  2. ANA
273
Q

Anti SSA/Ro and Anti SSB/La. are related to:

A
  1. Extra glandular manifestations.
  2. Pregnant women with SSA with babis with neonatal lupus and congenital heart block.
  3. Increased risk for B cell lymphoma.
274
Q

Systemic Sclerosis (scleroderma). definition.

A

Autoimmune disorder characterized by sclerosis of skin and viseral organs. In middle aged females.
Fibroblast activation leads to deposition of collagen.

275
Q

Scleroderma occurs by

A
  1. Autoimmune damage to mesenchyma.
  2. Endothelial dysfunction leads to inflammation, vasoconstriction and secretion of growth factors.
  3. Fibrosis.
276
Q

Types of scleroderma:

A
  1. Limited type skin or CREST.
  2. Diffuse type-Skin
277
Q

CREST.

A

Calcinosis anti/centromere antibodies.
Raynaud Phenomenon.
Esophageal dysmotility.
Sclerodactyly.
Telangiectasias.

278
Q

Diffuse Type Skin involvement:

A

Vessels
GI tract
Lungs
Kindneys
Antibodies to DNA topoisomerase I anti scl-70

279
Q

Digeorge Syndrome Definition and characteristics?

A

Developmental failure of the Third and 4 pharyngeal pouches due to 22q11 microdeletion.
Most important T CELL DEFICIENCY.
C: T cell deficiency hypocalcemia and abnormalities in face heart.

280
Q

Severe Combined Immunodeficiency (SCID)

A
  1. Cytokine receptor defects.
  2. Adenosine deaminase deficiency (ADA).
  3. MHC class II.
    Susceptibility to fungal bacterial and protozoal infections and LIVE VACCINES.
    Bubble baby.
281
Q

X-Linked Agammaglobulinemia.

A

Complete lack of immunoglobulin. Naive cells cannot mature in B cells.
Mutated Bruton tyrosune kinase, X linked.
Presents after 6 months recurral bacterial, enterovirus and gardia lambia. Don’t use Polio.

282
Q

Common variable immunodefiency CVID.

A

Low immunoglobulin due to B cell or T cell defects (il). Risk for bacterial, enterovirus and giardia lamba in late childhood. Risk oh lymphoma and autoimmune disease.

283
Q

Hyper IgM syndrome.

A

Elevated IgM, due to mutated CD40L on helper t cells or CD40 receptor on B cells. 2do signal cannot be delivered so cytokines for immunoglobulin class switching are not produced.

284
Q

IgA deficiency.

A

Low serum and mucosal IgA. Increased risk for mucosal infection. Most patients are asymptomatic.

285
Q

Wiskott Aldrich syndrome

A

Trombocytopenia eczema and recurrent infections (defect in humoral and cellular immunity) Bleeding is a major cause of death. WASP gene C and X linked.

286
Q

Complement deficiencies.

A

C5-C9 deficiencies- increased risk for Neisseria.
Hereditary Angioedema due to Cl inhibitor deficiency. LA NINA BONITA QUE RECIBIA PLASMA Y BERINERT.

287
Q

Why APP need anticoagulation for long time?

A

Hypercoagulable state and lupus anticoagulant, that result in arterial and venous thrombosis.

288
Q

Mixed connective tissue disease

A

Autoimmune mediated tissue damage with mixed features of SLE, systemic sclerosis and polymyositis.
ANA y RNP.

289
Q

Wound healing

A

Is initiated when inflammation begins, occurs via a combination of regeneration and repair.

290
Q

Regeneration.

A

Is the replacement of damaged tissue whith native tissue depend on regenerative capacity.

291
Q

Regeneration are divided into 3 types.

A
  1. Labile tissues.
  2. Stable tissues.
  3. Permanent tissues.
292
Q

Regeneration of labile tissues is bases on?

A

Stem cells that continously cycle to regenerate the tissue. Example: stem cells in mucosal crypts, stem cell in basal layer, bone marrow.

293
Q

Regeneration of Stable tissues is bases on?

A

are compromised of cell that are quiescent (Go) but can reenter the cell cycle to regenerate tissue when is necessary. Example: Regeneration of liver after partial resection.

294
Q

Regeneration of Permanent tissues is bases on?

A

lack significant regenerative potential. example: myocardium skelertal neurons.

295
Q

Repair.

A

Are the replacement of damaged tissue with fibrous scar. Occurs when regenerative stem cells are lost o present lack of regenerative capacity.

296
Q

Hallmark of repair is?

A

Granulation tissue formation, that results in scar formation.

297
Q

How is the formation of granuloma tissue in repair?

A

Fibroblast (deposit type III collagen).
capillaries (provide nutrients).
Myofibroblasts (contract wound)

298
Q

Formation of scar is results by?

A

Type III collagen is pliable. Type I collagen has high tensile strength. Collagenase removes type III collagen and requires zinc as a cofactor.

299
Q

Which is the mechanisms of tissue regeneration and repair?

A
  1. Paracrine signaling via growth factor that target fibroblasts, this interaction with receptor that results in gene expresion and cellular growth.
300
Q

Which are the mediator or key in tissue regeneration and repair?

A
  1. TGF alpha epithelial and fibroblast growth factor.
  2. TGF beta fibroblast growth factor inhibits inflammation
  3. Platelet derived growth factor for endothelium smooth muscle, fibroblast.
  4. Fibroblast growth factor for angiogenesis
  5. Vascular endothelial growth factor.
301
Q

Cutaneous healing occurs for 2 via?

A
  1. Primary intention: leads minimal scar formation.
  2. Secondary intention edges are not approximated, granulation tissue fills the defect then contratc the wound forming scars.
302
Q

Delayed wound healing occurs in:

A
  1. Infection
  2. Vitamin C and Zinc deficiency.
  3. Cooper.
  4. other causes. (dm, ischemia).
303
Q

Where are 4 types of collagen found?

A

Type 1 bone.
Type 2 cartilage
Type 3 granulation tissue embrionic tissue.
Type 4 basemen membrane.

304
Q

Explain formation and structure of collagen.

A

Collagen is formed as multiple alpha strands inside cells. Multiple alpha strands intertwine to
make procollagen and come outside cell. Structure of alpha strand is Gly-X-Y, where X and Y are proline and lycine. multiple procollagen are crosslinked via hydroxyl group to make collagen.

305
Q

Why we need vitamin c in the process of wound healing?

A

Vitamin C is needed to hydroxylate proline and lysine procollagen residues.

306
Q

Why we need Cooper as cofactor in the process of wound healing?

A

Crosslinking is done by lysyl oxidase which has copper as cofactor and hydroxy lysine to form stable collagen.

307
Q

Why we need Zinc in the process of wound healing?

A

Is a cofactor for collagenase, with replaces the type 3 collagen of granulation tissue with type 1 collagen.

308
Q

What is a Keloid?

A
  1. Is excess production of scar tissue that is out of proportion.
309
Q

Characteristic of Keloid?

A
  1. Excess by type 3 collagen.
  2. Genetic predisposition.
  3. Classically affect earlobes, face an upper extremities.
310
Q

Where are 4 types of collagen found?

A

Type 1 bone.
Type 2 cartilage
Type 3 granulation tissue embrionic tissue.
Type 4 basemen membrane.

311
Q

Hypertrophic scar is?

A

Excess production of scar tissue that is localized to the wound.

312
Q

TCR complex recognizes antigen presenti by?

A

CD4+ T cells in MHC class II
CD8+ T cells MHC class I

313
Q

Hemostasis definitation

A

Are the integrity of the blood vessel to carry blood to tissues. Damage (endothelial cell and base membrane) to the wall is repaired by hemostasis, which involves formation of a thrombus or clot.

314
Q

Hemostasis occurs in two stages:

A

Primary and secondary.

315
Q

Hemostasis primary are?

A

Primary hemostasis forms a weak plug and in mediate by interaction between platelets and the vessel wall.

316
Q

Secondary hemostasis are?

A

Stabilizes the platelet plug and is mediated by the coagulation cascade.

317
Q

Primary hemostasis Steps?

A
  1. Transient vasoconstriction.
  2. Platelet adhesion
  3. Platelet degranulation.
  4. Platelet aggregation.
318
Q

Transient vasoconstriction in the damage vessels?

A
  1. Neural stimulation.
  2. Endothelin release from endothelial cells.
319
Q

Platelet adhesion occurs via?

A
  1. vWF binds exposed subendothelial collagen (base membrane) binds to exposed subendothelial collagen.
  2. Bind vWF using GPIb receptors.
320
Q

vWF come from?

A
  1. Weibel-Palade bodies of endothelial cells and
  2. alpha granules of platelets.
321
Q

Platelet degranulation occurs?

A
  1. Adhesion induces shape change in platelets.
  2. degranulation with release of multiple mediators: ADP, GPIIb/IIIa receptor on platelets and TXA2 to promotes platelet aggregation.
322
Q

TXA2 promotes?

A
  1. Platelet aggregation.
  2. Is synthesized by platelet COX.
323
Q

Platelet aggregation occurs?

A
  1. Platelets aggregate at the site on injury via GPIIb/IIIa using fibrinogen results in formation of platelet plug.
324
Q

Hematopoiesis occurs?

A

Maturation of stem cells CD34+

325
Q

When WBC are low or high are call?

A

Leukopenia and leukocytosis

326
Q

Neutropenia causes?

A

drug toxity like alkylating agents and severe infection

327
Q

why alkalating agents produce neutropenia?

A

Damage to stem cells results in decreased wbc.

328
Q

How severe infecctions cause neutropenia?

A

Increased movement of neutrophils into tissue in decreased circulating.

329
Q

Lymphopenia causes?

A

Immunodeficiency.
High cortisol state.
Autoimmune destruction.
Radiation.

330
Q

Lymphopeni causes for immunodeficiency are??

A

HIV and Digeorge Syndrome (they dont have thymus for abnormal en pounch 3 and 4)

331
Q

How autoimmune destruction produce lymphopenia?

A

Ex: SLE. By destruccion for antibodys againts el cells.

332
Q

Which are the cell is released in bacterial infection or tissue necrosis?

A

Nuetrophils with immature forms.

333
Q

Wihich is the characterits of immature neutrophils?

A

decreased receptor Fe or CD16.

334
Q

How high cortisol affect the leucocyte?

A

disrupted leukocyte adhesion, leading to release of marginated pool of neutrophils.

335
Q

Neutrophilic leukocytosis

A

Are increased circulating neutrophils

336
Q

Cuases of neutrophilic leukocytosis

A
  1. Bacterial infection or tissue necrosis
  2. High cortisol.
337
Q

Monocytosis causes

A

Chronic inflamatory states and malignancy.

338
Q

EOSINOPHILIA IS IMPORT BY?

A

Production of circulating eosinphilis in allergic reaction type I, parasitic and HY: Hodgkin Lymphoma like chemotatic by IL-5.

339
Q

CD8+T in mononucleosis are response by?

A
  1. LAD in the paracortex
  2. Splenomegaly due to T cell hyperplasia in PALS (HY)
  3. High WBC with atypical lymphocytes.
340
Q

Complications in Mononucleosis

A

HY
1. Increased risk for splenic rupture.
2. rash if expose to AMPICILIN.
3. Recurrence
4. B cell lymphoma in ej HIV.

341
Q

Bordetella pertussis what is the different between another bacteria’s?

A
  1. Produce Lymphocytosis leukocytosis
  2. Lymphocytosis promoting factors.
  3. from leaving the blood to enter the lymph node.
342
Q

Que oncogen esta relacionado al Hairy cell leukemia?

A

BRAF

343
Q

Cual es la relacion entre Mycosis fungoide and leukemia?

A

esta en photos

344
Q

TTP is caused by?

A

Impaired function on the vWF-cleaving proteasa.

345
Q

how looks Leukemoid reaction in bone marrow?

A

Can be normal or hypercellular and responds with increased bands and early mature neutrolphils precusor.

346
Q

Leukocyte alkaline phosphatase are?

A

A serum blood test that can be normal or increased in LAP

347
Q

Leukocyte alkaline phospatase is drecreased in?

A

Chronic myelogenos leukemia

348
Q

What is the Dohle bodies?

A

Are ligth blue(basophilic) peripheral granules in neutrophils. They are seen in toxic systemic ilness and myelodysplasia

349
Q
A

Pathoma (1 decks)

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