Pathoma Flashcards
1
Q
Growth adaptations?
A
an increase, decrease or change in stress on an organ can result in growth adaptations.
2
Q
Hyperplasia and hypertrophy differences?
A
Hypertrophy is an increase in the size. Hyperplasia is an increase on the number of cells.
3
Q
Hypertrophy involves what type of mechanism?
A
gene activation, protein synthesis and production of organelles.
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.
5
Q
EXAMPLE OF HYPERTROPHY?
A
CARDIAC MYOCYTES UNDERGO HYPERTROPHY IN RESPONSE HTA SYSTEMIC.
6
Q
Pathologic hyperplasia can progress ?
A
dysplasia and eventually cancer. exception HPB.
7
Q
Atrophy. definition.
A
a decrease in stress leads to a decrease in organ size example: decreased hormonal stimulation in uterus.
8
Q
Which is the via that occurs atrophy?
A
via ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components.
9
Q
what happens in ubiquitin-proteosome degradation?
A
Intermediate filament of the cytoskeleton are tagged with ubiquitin and destroyed by proteasomas.
10
Q
what happens in autophagy?
A
cellular components involves generation of autophagic vacuoles, these fuse with lysosomes whose hydrolytic enzymes breakdown cellular components.
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
12
Q
example of metaplasia.
A
Barret esophagus ( cells are better able to hadle the new stress.
13
Q
Hyperplasia involves de production of?
A
of new cells from stem cells with them produce the new cell type.
14
Q
¿What changes occurs in Barret esophagus ?
A
nonkeratinizing squamous epithelium to nonciliated, mucin-producing columnar cells
15
Q
Metaplasia is reversible?
A
yes, removal od the driving stressor.
16
Q
The persistent of stress in metaplasia can progress a cancer?
A
yes, first dysplasia and eventually result in cancer.
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.
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.
19
Q
which is the Mesenchymal tissues chance in metaplasia?
A
connective tissue whithin muscle changes to bone during healing after trauma (myositis ossificans).
20
Q
Dysplasia. Definition?
A
Disordered in cellular growth.
21
Q
example the dysplasia?
A
NIE OR CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN).
22
Q
Aplasia definition?
A
is failure of cell production during embryogenesis. (unilateral renal agenesis).
23
Q
Hypoplasia definition?
A
is a decrease in cell production during embryogenesis resulting in a relative small organ.
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.
25
Causes of cellular injury?
Inflammation, nutritional deficiency or excess, hypoxia, trauma and genetic mutations.
26
Hypoxia definition?
Low oxygen delivery to tissue.
27
how occurs the hypoxia?
oxygen is the final electron acceptor in the electron transport chain of oxidative phosphorylation. Decreased oxygen impairs oxidative phosphorylation resulting in decreased ATP production.
28
Causes of Hypoxia?
Ischemia, hypoxemia and decreased on O2.
29
Ischemia. definition?
decreased blood flow through an organ.
30
Which is the mechanism of ischemia?
1. Decreased arterial perfusion (atherosclerosis) 2. Decreased venous drainage (budd chiari syndrome) 3. Shock.
31
Definition of Hypoxemia?
Is low partial pressure of oxygen in the blood.
32
Which is the mechanism of Hypoxemia?
High altitude, Hypoventilation and Diffusion defect. V/Q mismatch (blood bypasses oxygenated lung or oxygeneted air cannot reach blood.
33
Definition of Decreased O2?
Carrying capacity arises with HB loss or dysfuntion. Ex: Anemia, Carbon monoxide poisoning.
34
Carbon monoxide poisonig syntoms?
Classic cherry-red appearance of skin. headache, coma and death.
35
The early and the lattes sing of exposure of CO2 poisoning?
Headache. Lattest: coma and death.
36
Methemoglobinemia
Iron in heme is oxidized to Fe3+, which cannot bind oxygen-PaO2 Normal SaO2 Decreased
37
Classic finding in methemoglobinemia
cyanosis with chocolated colored blood.
38
treatment of methemoglobinemia
Methylene Blue. Helps reduce Fe2+ bac to Fe2+ state.
39
Low ATP disrupts key cellular functions including?
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.
40
The Hallmark of reversible injury is?
Cellular swelling.
41
How occurs the cellular swelling?
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.
42
The hallmark of irreversible injury is?
Membrane damage. (plasma membrane, mitochondrial and lysosome membrane.
43
How occurs the irreversible injury?
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.
44
Cell death loss his nucleus for three ways?
Pyknosis (nuclear condensation), karyorrhesis (fragmentation) and karyolysis (dissolution).
45
Mechanisms of cell death?
Necrosis and apoptosis
46
The hallmark of cell death is?
Loss of the nucleus whick occurs for 3 via.
47
Necrosis definition?
Death of large groups of cells fallowed by acute inflammation. Underlying pathologic process.
48
Necrosis is divided into?
1. Coagulative necrosis.
2. Liquefactive necrosis.
3. Gangrenous Necrosis.
4. Caseous necrosis.
5. Fat necrosis.
6. Fibrinoid necrosis.
49
Characteristics of Coagulative necrosis?
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)
50
Characteristics of Liquefactive necrosis?
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.
51
Characteristics of Gangrenous necrosis?
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).
52
Characteristics of Caseous necrosis?
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.
53
Characteristics of Fat necrosis?
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.
3. Metastatic calcification occurs when high serum calcium or phosphate levels lead to calcium deposition in normal tissues.
54
Saponification
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.
55
Characteristics of Fibrinoid necrosis?
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).
56
Apoptosis. definition.
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
57
Morphology of apoptosis
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)
58
Apoptosis is mediated by?
Caspases that active Proteases ( break down the cytoskeleton) and endonucleases (break down DNA).
59
Caspases are activated by?
1. Intrinsic mitochondrial pathway.
2. Extrinsic receptor-ligand pathway.
3. Cytotoxic cd8+ T-cell mediated pathway.
60
Intrinsic mitochondrial pathway
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.
61
Extrinsic receptor-ligand pathway.
FAS ligand bind death receptor (CD95) on the target cell. TNF bind TNF receptor on the target cell, activating caspases.
62
Cytotoxic cd8+ T-cell mediated pathway.
Perforins secreted by CD8+ T cell create pores in membrane of target cell. Granzyme from CD8+ T cell enters and active caspases.
63
Free radicals, definition?
Free radicals are chemical species with unpaired in their outer orbit.
64
When occurs of generation of free radicals?
Physiologic occurs during oxidative phosphorylation.
65
How occurs generation of free radicals?
Cytochrome C oxidase (complex iv) transfers electrons to oxygen.
O2-O2(superoxide)-H202-OH-H20.
66
How occurs pathologic generation of free radicals
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.
67
Free radicals causes cellular injury via?
1. Peroxidation of lipids and oxidation of DNA and proteins.
2. DNA damege is implicated in oncogenesis and aging.
68
Elimination of free radicals occurs by?
Antioxidants, enzymes and metals (metal carrier proteins like transferrin).
69
Elimination of free radicals by enzymas?
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.
70
Carbon tetrachloride CCl4
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.
71
Reperfusion injury.
Return of blood to ischemic tissue-O2-derived free radical. leads to a continued rise in cardiac enzymes after reperfusion of iam tissue.
72
Amyloidosis. definition.
Is a misfolded protein that deposits in the extracellular space thereby damaging tissues. Systemic or localized.
73
Microscopically look?
Congo Red staining and apple green birefringence under polarized litgh. B-pleated sheet configuration.
74
Systemic Amyloidosis divided in?
Primary and secundary.
75
Primary amyloidosis.
Is a systemic deposition of AL AMYLOID, which is derived from Immunoglobulin light chain. (associated with plasma cell dyscrasias).
76
Secundary amyloidosis.
Is a systemic deposition of AA amyloid wich is derived from serum amyloid-associated protein (SAA).
77
Clinical findings of systemic amyloidosis.
Nephrotic syndrome. Restrictive cardiomyopathy or arrhythmia. Tonge enlargement, malabsorption and hepatosplenomegaly.
78
Diagnosis of amyloidosis
tissue biopsy. (abdominal fat and rectum)
79
Localized Amyloidosis
Amyloid deposition usually localized to a single organ.
80
Senile cardiac amyloidosis
Non-mutated serum transthyretin deposits in the heart.
81
Familial Amyloidosis cardiomyopathy
mutated serum transthyretin deposits in the heart. restrictive patron.
82
Non insulin dependent DM
amylin (derived fron insulin)
83
Alzheimer disease
AB amyloid (precursor protein) in the brain plaques.
84
Dialysis amyloid associated
B2-microglobulin deposits in joints.
85
Carcinoma of the thyroid
calcitonin deposits within the tumor (tumor cells in an amyloid background)
86
Inflammation. definition
is allows inflammatory cells plasma proteins and fluid to exit blood vessels and enter the interstitial space.
87
Acute inflammation. Characterized.
Presence of edema and neutrophils i tissue in response to infection or tissue necrosis. Inmediate response with limited specifity.
88
Which are the mediators of acute inflammation?
1. Toll-like receptors.
2. Arachidonic acid metabolites.
3. Mast cells.
4. Complement.
5. Hageman factor (factor XII).
89
Toll-like Receptors (TLRs). Function
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).
90
PAMPs
CD14 ( a co-receptor for TLR4) on macrophages recognizes lipopoly-saccharide (a PAMPs) on the outer membran of gram negative bacteria.
91
AA metabolites.
Is a released from the phospholipid cell membrane by phospholipase A2 and then acted upon by cyclooxygenase or 5-lipoxygenase.
92
Cyclooxygenase produce?
Cyclooxygenase produce PG
2. PGI2 PGD2 AND PGE2 mediate vasodilatation and increase vascular permeability. PGE2 also mediates Pain and fever.
93
35-Lipoxygenase produce?
Leukotrienes. 1. LTB attracks and active neutrophils. 2. LTC4 LTD4 LTE4 mediate vasoconstriction, bronchospasm and increase vascular permeability.
94
Mast cells.
Widely distributed throughout connective tissue. 2. Activated by tissue trauma, complement proteins C3a an C5A or cross linked of cell surface IgE by antigen.
95
Inmediate responde in mast cells.
Released of preformed histamine granules, which mediate vasodilation of arteriales and increased vascular permeability.
96
Delayed response in mast cells.
Involves production of arachidonic acid metabolites particularly Leukotrienes.
97
Complement definition in acute inflammation?
Proinflammatory serums proteins that complement inflammation. Circulate as inactive precursors.
98
Classic pathway of complement?
C1 bind IgG or IgM that is bound to antigen.
99
Alternative pathway of complement?
Microbial products directly activate complement.
100
Mannose-Binding lectin (MBL) pathway of complement?
MBL binds to mannose on microorganism and activate complement.
101
Activation of complement occurs for 3 patways
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.
102
Activation of complement occurs for 3 patways
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.
103
Activation of complement occurs for 3 patways
Activation occurs for 3 via:
1. Clasical.
2. Alternative
3. MBL ( Mannosse- binding lectin)
104
Phases of the complement?
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.
105
Neoplasia. definition.
Is new tissue growth that is unregulated, irreversible and monoclonal. Or uncontrolled, monoclonal proliferation of cells.
106
Differences between cells monoclonal and polyclonal?
Monoclonal means that neoplastic cells are derived from a single mother cell and polyclonal are cells derivaded from multiples cells.
107
Dysplasia
Is the loss of uniformity in cell size and shape (pleomorphism), loss of tissue orientation and nuclear changes often reversible.
108
Clonality is determined by?
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.
109
Differences between Neoplasia and Hyperplasia?
Neoplasia is unregulated, irreversible and monoclonal and Hyperplasia is regulated
110
Clonality of lymphocytes B is determined by?
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.
111
Differences between Neoplastic benign and malignant?
Benign: Localized and do not metastasize.
Malignant tumors> invade localy and have the potential to metastasize.
112
In lymphoma, which type of changes occurs in the Ratio?
Ratio increases to 6:1 or is inverted (kappa to lambda 1:3) which is monoclonal.
113
Ratio can change in 3 via. Which?
Metastasize, infecction and lymphoma.
114
Tumor Nomenclature.
Epithelium: Benign Adenoma Malignant: Adenocarcinoma.
Mesenchyme: Benign: FAT= Lipoma. Malignant: Liposarcoma.
Melanocyte Nevus and Melanoma.
115
Tumor Nomenclature exceptions:
Lymphoma.
116
Epidemiology of cancer.
Is the Secund leading cause of the in adults and children.
117
Which is the incidence of cancer in adults?
1. Breast/Prostate.
2. Lung.
3. Colorectal.
118
Which is the incidence of death in children's?
1. Accidents.
2. Cancer
3. Congenital defects.
119
Which is the incidence of death in adults?
1. Cardiovascular disease.
2. Cancer.
3. Chronic Respiratory disease.
120
Which is the incidence of cancer mortality in adults?
1. Lung
2. Breast/Prostate.
3. Colorectal.
121
Which is the rol of screening?
Seek to catch dysplasia before becomes carcinoma or carcinoma before clinical symtoms arise.
122
Most common screening methods are?
1. PAP smear.
2. Mammography.
3. PSA.
4. Hem occult test and colonoscopy.
123
Definition of carcinogenesis?
Is the iniciated damage to DNA of stems cells. The damage overcomes DNA repair mechanisms.
124
Carcinogens definition.
Are agents that damage DNA, increasing the risk of cancer. DNA mutations eventually disrupt key regulatory systems.
125
Carcinogens agent?
1. Chemicals.
2. Oncogenic viruses.
3. Radiation.
126
What chemicals are carcinogenic agent?
Aflatoxins, alkylating agents, alcohol, arsenic, asbestos, cigarette smoke, nitrosamines, naphthylamine, vinyl chloride, nickel, chromium, beryllium or silica.
127
What kind oncogenic viruses are carcinogens?
EBV, HHV-8, HBV AND HCV, HTLV-1 and subtypes HPV (16,18, 31 and 33).
128
What types of radiation are related to cancer?
Ionizing (nuclear reactor accidents and radiotherapy) and Nonionizing ( UVB).
129
Aflatoxins are related to?
Aspergillus and Hepatocellular carcinoma.
130
Alkylating are related to?
Leukemia/lymphoma for de side effects of chemotherapy.
131
Alcohol are related to?
Multiples cancer like: squamous cell carcinoma of oropharynx (more Tabaco), upper esophagus and hepatocellular carcinoma (cirrhosis). Pancreatic carcinoma for pancreatitis.
132
Arsenic are related to?
Squamous cell carcinoma of skin, lung cancer ( cigarette smoke) and angiosarcoma of liver.
133
Asbestos are related to?
Lung carcinoma and mesothelioma.
134
Cigarette smoke are related to?
Carcinoma of orooharynx, esophagus, lung, kidney, bladder and pancreas.
135
Why cigarette smoke are the most common cause of carcinogens?
Because of polycyclic hydrocarbons are particularly carcinogenic.
136
How cigarettes produce cancer in the urothelial tissue?
The Kidney cleaning the residues that acumulate in the tissue to product the mutations and after cancer.
137
Nitrosamine are related to?
Stomach carcinoma.
Usually found in smoke food
Japonese love smoke food
Is the most frecuent cancer in japon
138
Where I can found nitrosamines and what type of cancer is related specific?
Is found in smoked food, for that is responsible of high rate of carcinoma in Japan. They have the type Intestinal mejorar aqui tambien.
139
Naphthymine are related to?
Urothelial carcinma of bladder, derived from smoke cigarettes.
140
Vinyl Chloride are related to?
Angiosarcoma of liver, which is a Occupational exposure.
141
Other metal related to occupational expusure and cancer are?
Nickel, chromium, beryllium or silica in Lung cancer.
142
EBV are related to?
Nasopharyngeal carcinoma, Burkitt lymphoma and CNS lymphoma in AIDS.
143
HHV-8 are related to?
Kaposi sarcoma.
144
Which is the symptoms of EBV?
In nasopharyngeal are chinase male or africam with a mass in the neck.
145
HHV-8 presentations?
1. Westerns Europe and male.
2. AIDS and the treatment is antiretroviral.
3. Patient that had transplant, so they need decreased the dosis.
146
HBV AND HCV are related to?
Hepatocellular carcinoma
147
What type of virus are HBV AND HCV?
HBC are ADN virus and HCV are ARN virus.
148
HTLV1 are related to?
Adult T-Cell leukemia/lymphoma.
149
HPV are related to?
Squamous cell carcinoma of cervix, vulva, anus and vagina. Adenocarcinoma of cervix.
150
Which type the radiation is releated to cancer?
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
In the Nonionizing radiation who results in cancer?
UVB result in formation of pyrimidine dimers in DNA whit normally excised by restriction endonuclease.
152
Dna mutations allowing?
1. Disrupt key regulatory systems.
2. Tumor promotion (growth).
3. Progression (spread).
153
DNA Disrupts systems include?
1. Proto-oncogenes.
2. Tumor suppressor genes.
3. Regulators of apoptosis.
154
Proto-oncogenes?
1. Are essential for cell growth and differentiation; mutations of proto-oncogenes form oncogenes that lead to unregulated cellular growth.
155
Oncogenes categories?
1. Growth factors.
2. Growth factor receptor mediate signals.
3. Signal transducer relay receptor activation to the nucleus.
4. Cell cycle regulators.
156
Mechanisms associated to activation of the nucleus?
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.
3. Activated Ras sen.ds growth signals to the nucleus.
4. Ras inactivates itself cleaving GTP>GDP; augmented by GTPase activating protein.
5. Mutated Ras inhibits the activit oh GTPase activating proteins, that prolongs the activate state Ras
157
Growth factors like oncogens?
Induce cellular growth. PDGFB in astrocytoma.
158
Grow factor receptor are mediate?
For signals from growth factor. ERBB2 in breast cancer.
159
Growth factor like Oncogenes and associated tumors.
PDGFB. Platelet-derived growth factor. Overexpression, autocrine loop. Astrocytoma.
160
Growth factor receptors like Oncogenes and associated tumors.
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
Signal transducers like Oncogenes and associated tumors.
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
Nuclear regulators like Oncogenes and associated tumors.
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
Cell cycle regulators like Oncogenes and associated tumors.
1. CCND1 (cyclin D1) > cyclin > Translocation (11:14) involving IgH > Mantle cell lymphoma.
2. CDK4 > Cyclin-dependent kinase > Amplification > Melanoma.
164
Regulation of cyclin and cyclin-dependent kinase in the cell.
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
Tumor suppressor genes. Definition.
Regulate cell growth and hence, decrease (suppress) the risk of tumor formation. Example: p53 y Rb.
166
Function of p53?
P53 regulates progression of the cell cycle from G1 to S phase.
167
In response to DNA damage how is the function of p53?
P53 slows cell cycle and upregulates DNA repair enzymes.
168
If DNA damage it not possible repair which is the function of p53?
P53 induces the apoptosis, by upregulates BAX which disrupts Bcl2 and Cytochrome C leads from de mitochondria activating apoptosis.
169
Knudson two-hit hypothesis are related to?
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
Rb also regulates progression from G1 to S phase for what mechanism?
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
Regulators of apoptosis. Functions?
In normal cells prevent apoptosis.
In mutated cell whose DNA cannot be repaird promote apoptosis. Ex: Bcl2.
172
Bcl2 stabilizes the mitochondrial membrane in normal cells by?
Blocking release of cytochrome C, this leave the mitochondria and activate the apoptosis.
173
If Bcl2 is overexpressed, what happens in the mitochondrial membrane?
Is further stabilized, prohibiting apoptosis and B cells that would normally undergo apoptosis during somatic hypermutation in the lymh node germinal center.
174
Other important features of tumor development are?
1. Telomerase.
2. Angiogenesis.
3. Avoiding immune surveillance.
4. Immunodeficiency.
175
Telomerase involt in tumor development by?
1. Cell immortality.
2. Cellular senescence (telomerase shorten with serial cells divisions).
3. Upregulated telomerase (preserved).
176
Angiogenesis in tumor development are reletad to?
1. Production of new blood vessels for tumor survival and growth.
2. FGF and VEGF are related like angiogenic factor.
177
Avoiding immune surveillance through what mechanism?
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
Tumor progression definition?
Is the accumulation of mutations eventually results in tumor invasion and spred.
179
Tumor invasion and spred occurs by?
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
Routes of metastasis are?
1. Lymphatic spread.
2. Hematogenous spread.
3. Seeding of body cavities.
181
Lymphatic spread route is?
1. To regional draining lymp nodes like in the case of breast cancer.
182
Hematogenous spread route is characteristic of?
Sarcomas and some carcinomas
183
Hematogenous spread is characteristic of sarcomas and some carcinomas except?
1. Renal cell carcinoma.
2. Hepatocellular carcinoma.
3. Follicular carcinoma of Thyroid.
3. Choriocarcinoma.
184
The ovarian carcinoma had a especific characteristic?
Seedinf of body cavities, which often involves the peritoneum. ex: omental caking.
185
Characteristics Clincal of Benign Tumor are?
1. Slow growing
2. Well circumscribed.
3. Distinct.
4. Mobile.
186
Characteristics Clinical of Malignant Tumor are?
1. Rapid growing.
2. poorly circumscribed.
3. Infiltrative.
4. fixed to surrounding tissues and local structures.
187
Histologic characteristics of benign are?
1. usually well differentiated.
2. Organized growth.
3. Uniform nuclei.
4. Minimal mitotic activity.
5. Lack of invasion.
6. No metastatic potential.
188
Histologic characteristics of Malignant are?
1. Poorly differentiated (anaplastic).
2. Disorganized growth.
3. Nuclear pleomorphism and hyperchromasia.
4. High mitotic activity with atypical mitosis.
5. Invasion.
189
Hallmark of malignancy is?
Metastatic potential.
190
Immunohistochemistry is?
Used to characterize tumors that are difficult to classify on histology.
191
Immunohistochemical most common are?
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
What are Serum tumor markers?
Proteins released by tumor into serum like PSA.
193
Which is the used of serum tumor markers?
Is useful for screening, monitoring response to treatment and monitoring recurrence.
194
If you have a patient with serum tumor marker elevated, which is the next step?
Tissue biopsy for diagnosis.
195
Grading of cancer are?
Microscopic assessment of diferentiation takes into account architectural and nuclear features.
196
Grading of cancer is divided in two types?
1. Well differentiated (low grade).
2. Poorly differentiated (high grade).
197
The gradinf of cancer is important for?
Determining prognosis; well differentiated cancer have better prognosis than poorly differentiated cancers.
198
Staging of cancer are?
Assessment of side and spread of a cancer. Key prognostic factor.
199
TNM staying system:
T - tumor size or depth.
N - spread to regional lymp nodes. 2nt.
M - Metastasis. The most important.
200
The final result of activation complement pathways is?
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
Components of production of MAC?
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
Hageman factor or Factor XII. Functions:
1. Inactive proinflamatory protein produce in liver.
2. Activated upon exposure to subendothelial or tissue collagen.
203
What activated factor xii?
1. Coagulation and fibrinolytic systems.
2. Complement
3. Kinin system - Kinin cleaves high molecular -weight kininogen (HMWK)
204
Kinin system - Kinin cleaves high molecular -weight kininogen (HMWK) Actives?
1. Bradykinin which mediates vadilatation and increased vascular permeability.
2. Pain.
205
Cardinal signal of inflammation?
A. Redness (rubor) and warmth.
B. Swelling tumor.
C. Pain.
D. Fever.
206
Redness and warmth occurs?
1. Due to vasodilatation, which increased blood flow.
2. Occurs via relaxation of arteriolar smooth muscle.
207
Key mediators on redness and warmth are?
1. Histamine.
2. Prostaglandins.
3. Bradykinin.
208
Swelling occurs via?
1. Due to leakge of fluid postcapillary venueles into the intersticial space (exudative).
2. Key mediators (histamine).
209
Key mediator in swelling are?
Are histamine which causes endothelial cell contraction and tissue damage resulting in endothelial cell disruption.
210
Pain occurs via?
1. Bradykinin ang PGE2 Sintetize sensory nerve endings.
211
Fever occurs via?
1. Pyrogenes (LPS) cause macrophages to release IL-1 and TNF which inceased cyclooxygenase activity in perivascular cells of hypothalamus.
212
What make PGE2 in fever?
Increased raise temperature set point.
213
Macrophages in the acute inflammation appears?
1. Appears predominate after neutrophils and peak 2-3 days after inflammation begins. Derived from monocytes in blood.
214
Macrophages arrived in tissue via?
1. Margination.
2. Rolling.
3. Adhesion.
4. Transmigration sequence.
215
Macrophages ingest organism via?
By phagocytosis (augmented by opsonins) and destroy phagocytosed material using enzymes in secondary granules.
216
Manage the next step of the inflammatory process produced by macrophages include?
1. Resolution and healing
2. Puss formation.
3. Abscess.
4. Chronic inflammation.
217
The resolution and healing produce in acute inflammation?
Anti inflammatory cytokines. (IL-10 and TGF-B) produces by macrophages.
218
The continued acute inflammation by macrophages are marked by?
Continued acute inflammation marked by persistent pus formation. IL-8 recruits additional neutrophils.
219
Abscess are manage by?
Acute inflammation surrounded by fibrosis, macrophages mediate fibrosis via fibrotic growth factor and cytokines.
220
Chronic inflammation are manage by?
Macrophages present antigen to activate CD4+ helper T cells which secrete cytokines that promete chronic inflammation.
221
Chronic inflammation is characterized by?
The present of lymphocytes and plasma cells in tissue. Delayed response but more specific ADAPTATIVE IMMUNITY that acute inflammation.
222
Chronic inflammation stiluli include:
1. Persist infection.
2. Infection with virus, mycobacteria, parasites and fungi.
3. Auto immune disease.
4. Foreign material
5. some cancers.
223
T Lymohocytes are?
Produced in bone marrow as progenitor T Cells.
224
T cells used for antigen surveillance?
TCR AND CD3.
225
TCR complex recognizes antigen and is presented?
On MHC molecules.
226
What type of T cells are recognized by MHC?
CD4+ T cells to MHC class II
CD8+ T cells to MHC class I.
227
Activation of T cell requires two signals?
1. Binding of antigen/MHC complex.
2. Additional 2 nd signal. ?
228
T Lymphocytes are develop in what part of body?
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
CD4+ helper T cell activation are for what via?
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
Which is the second signals?
B7 on APC bins CD28 ON CD4+ helper T cells providing 2nd activation signal.
231
Activated CD4+ helper T cell secrete cytokines that are divided into two?
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
Activated CD8+ cytotoxic T cell mediated by?
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
In Activated CD8+ cytotoxic T cells Killing occurs via?
1. Secretion of perforins and granzyme.
2. Expresion of FasL, activating apoptosis.
234
What made perforins and granzyme?
Perforins creates pores that allow granzyme to enter the target cell activating apoptosis.
235
What made the Expresion of FasL?
Binds Fas on target cells. activating apoptosis.
236
B lymphocytes o B cells.
Immature B cells are produced in the bone marrow and become in naïve B cells that express surface IgM and IgD.
237
B cell activation occurs via?
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
B cell antigen presentation occurs 2 via?
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
Granulomatous inflammation
Is a subtype of chronic inflammation.
Characterized by granuloma.
240
Granuloma. Definition
Is a collection of epithelial histiocytes that are macrophages with abundant pink cytoplasm usually surrounded by giand cells and a rim lymphocytes.
241
Granuloma division are?
1. Noncaseating granulomas
2. Caseating granulomas.
242
Noncaseating granulomas
Lack central necrosis. Common etiologies include reaction to foreign material sarcoidosis beryllium exposure Chron disease.
243
Caseating granulomas.
Exhibit central necrosis and characteristic of TB and fungal infections.
244
Steps involve in granuloma formation
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
Primary Immunodenficiency
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
Autoimmune Disorders. Basic principles
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
Generalities in autoimmune disorders.
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
Mechanisms that involves loss of self tolerance?
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
Polyendocrine syndrome is the result of which mutations?
AIRE.
250
Peripheral tolerance pathway?
1. Fas apoptosis pathway mutations result in autoimmune lymproliferative syndrome ALPS.
251
What type of regulatory t cells are releted to supress autoimmunity?
1. CD25 Polymorphims ( MS and type DM).
2. FOXP3 mutations leads to IPEX syndrome.
252
IPEX
I - Immune dysregulation.
P- Polyendocrinopathy.
E- Enteropathy
X- X-linked.
253
Etiology of Immune disorders?
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
LES characteristics.
Chronic systemic autoimmune disease. Flares and remissions. Middle aged-females. African American and hispanic. Antigen-antibody complexes damage multiples tissues.
255
Chronic inflammation. Definition.
Is the adaptive immune response or delayed response, characterized by the present of LYMPHOCYTES AND PLASMA CELLS in tissue. Is more specfic.
256
Causes of chronic inflammation
1. Persistent infecction.
2. Infection (virus, mycobacteria, parasites and fungi.
3. immune disease.
4. foreing material.
5. some cancers.
257
Severe Combined Immunodeficiency (SCID)
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
X-Linked Agammaglobulinemia.
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
Hyper IgM syndrome.
Elevated IgM, due to mutated CD40L on helper t cells or CD40 receptor on B cells. 2
260
What type Antigen-antibody complexes damage the tissue?
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
Type III HSR occurs?
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
IgA deficiency.
Low serum and mucosal IgA. Increased risk for mucosal infection. Most patients are asymptomatic.
263
Classic finding in SLE include?
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
Diagnosis of SLE`
1. Syntoms.
2. ANA
3. Anti ds DNA or Sm antibodies.
265
Antiphospholipid antibody is associated whith?
SLE
266
Antibodies releated to SLE and AP
1. Antibodies are made against proteins bound to phospholipid.
2. anticardiolipin Vdrl RPR are false +.
3. lupus anticoagulant falsely elevated PTT (paradojico) Hypercoagulation.
267
Antiphospholipid antibodies syndrome. Characteristic:
Hypercoagulable state due to antiphospholipid antibodies, lupus anticoagulant, that result in arterial and venous thrombosis. Required lifelong anticoagulation.
268
LUPUS drug induce.
Ant histone antibody by procainamide hydralazine and isoniazid, ANA positive. CNS and Renal are rare. removal of drug results in remission.
269
Sjogren Syndrome.
Autoimmune destruction of lagrimal and salivary glands, lymphocyte mediated damage type IV HRS.
270
Sjogren Syndrome. Clinical.
Dry eyes, mouth and recurrent caries in older woman. Keratoconjunctivitis sicca and xerostomia.
Lymphatic sialadenitis.
271
Rheumatoid arthritis and Sjogren Syndrome.
Are related, FR in often + even in absent of AR.
272
Sjogren Syndrome. Antibodies.
1. Anti SSA/Ro and Anti SSB/La.
2. ANA
273
Anti SSA/Ro and Anti SSB/La. are related to:
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
Systemic Sclerosis (scleroderma). definition.
Autoimmune disorder characterized by sclerosis of skin and viseral organs. In middle aged females.
Fibroblast activation leads to deposition of collagen.
275
Scleroderma occurs by
1. Autoimmune damage to mesenchyma.
2. Endothelial dysfunction leads to inflammation, vasoconstriction and secretion of growth factors.
3. Fibrosis.
276
Types of scleroderma:
1. Limited type skin or CREST.
2. Diffuse type-Skin
277
CREST.
Calcinosis anti/centromere antibodies.
Raynaud Phenomenon.
Esophageal dysmotility.
Sclerodactyly.
Telangiectasias.
278
Diffuse Type Skin involvement:
Vessels
GI tract
Lungs
Kindneys
Antibodies to DNA topoisomerase I anti scl-70
279
Digeorge Syndrome Definition and characteristics?
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
Severe Combined Immunodeficiency (SCID)
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
X-Linked Agammaglobulinemia.
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
Common variable immunodefiency CVID.
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
Hyper IgM syndrome.
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
IgA deficiency.
Low serum and mucosal IgA. Increased risk for mucosal infection. Most patients are asymptomatic.
285
Wiskott Aldrich syndrome
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
Complement deficiencies.
C5-C9 deficiencies- increased risk for Neisseria.
Hereditary Angioedema due to Cl inhibitor deficiency. LA NINA BONITA QUE RECIBIA PLASMA Y BERINERT.
287
Why APP need anticoagulation for long time?
Hypercoagulable state and lupus anticoagulant, that result in arterial and venous thrombosis.
288
Mixed connective tissue disease
Autoimmune mediated tissue damage with mixed features of SLE, systemic sclerosis and polymyositis.
ANA y RNP.
289
Wound healing
Is initiated when inflammation begins, occurs via a combination of regeneration and repair.
290
Regeneration.
Is the replacement of damaged tissue whith native tissue depend on regenerative capacity.
291
Regeneration are divided into 3 types.
1. Labile tissues.
2. Stable tissues.
3. Permanent tissues.
292
Regeneration of labile tissues is bases on?
Stem cells that continously cycle to regenerate the tissue. Example: stem cells in mucosal crypts, stem cell in basal layer, bone marrow.
293
Regeneration of Stable tissues is bases on?
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
Regeneration of Permanent tissues is bases on?
lack significant regenerative potential. example: myocardium skelertal neurons.
295
Repair.
Are the replacement of damaged tissue with fibrous scar. Occurs when regenerative stem cells are lost o present lack of regenerative capacity.
296
Hallmark of repair is?
Granulation tissue formation, that results in scar formation.
297
How is the formation of granuloma tissue in repair?
Fibroblast (deposit type III collagen).
capillaries (provide nutrients).
Myofibroblasts (contract wound)
298
Formation of scar is results by?
Type III collagen is pliable. Type I collagen has high tensile strength. Collagenase removes type III collagen and requires zinc as a cofactor.
299
Which is the mechanisms of tissue regeneration and repair?
1. Paracrine signaling via growth factor that target fibroblasts, this interaction with receptor that results in gene expresion and cellular growth.
300
Which are the mediator or key in tissue regeneration and repair?
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
Cutaneous healing occurs for 2 via?
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
Delayed wound healing occurs in:
1. Infection
2. Vitamin C and Zinc deficiency.
3. Cooper.
4. other causes. (dm, ischemia).
303
Where are 4 types of collagen found?
Type 1 bone.
Type 2 cartilage
Type 3 granulation tissue embrionic tissue.
Type 4 basemen membrane.
304
Explain formation and structure of collagen.
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
Why we need vitamin c in the process of wound healing?
Vitamin C is needed to hydroxylate proline and lysine procollagen residues.
306
Why we need Cooper as cofactor in the process of wound healing?
Crosslinking is done by lysyl oxidase which has copper as cofactor and hydroxy lysine to form stable collagen.
307
Why we need Zinc in the process of wound healing?
Is a cofactor for collagenase, with replaces the type 3 collagen of granulation tissue with type 1 collagen.
308
What is a Keloid?
1. Is excess production of scar tissue that is out of proportion.
309
Characteristic of Keloid?
1. Excess by type 3 collagen.
2. Genetic predisposition.
3. Classically affect earlobes, face an upper extremities.
310
Where are 4 types of collagen found?
Type 1 bone.
Type 2 cartilage
Type 3 granulation tissue embrionic tissue.
Type 4 basemen membrane.
311
Hypertrophic scar is?
Excess production of scar tissue that is localized to the wound.
312
TCR complex recognizes antigen presenti by?
CD4+ T cells in MHC class II
CD8+ T cells MHC class I
313
Hemostasis definitation
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
Hemostasis occurs in two stages:
Primary and secondary.
315
Hemostasis primary are?
Primary hemostasis forms a weak plug and in mediate by interaction between platelets and the vessel wall.
316
Secondary hemostasis are?
Stabilizes the platelet plug and is mediated by the coagulation cascade.
317
Primary hemostasis Steps?
1. Transient vasoconstriction.
2. Platelet adhesion
3. Platelet degranulation.
4. Platelet aggregation.
318
Transient vasoconstriction in the damage vessels?
1. Neural stimulation.
2. Endothelin release from endothelial cells.
319
Platelet adhesion occurs via?
1. vWF binds exposed subendothelial collagen (base membrane) binds to exposed subendothelial collagen.
2. Bind vWF using GPIb receptors.
320
vWF come from?
1. Weibel-Palade bodies of endothelial cells and
2. alpha granules of platelets.
321
Platelet degranulation occurs?
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
TXA2 promotes?
1. Platelet aggregation.
2. Is synthesized by platelet COX.
323
Platelet aggregation occurs?
1. Platelets aggregate at the site on injury via GPIIb/IIIa using fibrinogen results in formation of platelet plug.
324
Hematopoiesis occurs?
Maturation of stem cells CD34+
325
When WBC are low or high are call?
Leukopenia and leukocytosis
326
Neutropenia causes?
drug toxity like alkylating agents and severe infection
327
why alkalating agents produce neutropenia?
Damage to stem cells results in decreased wbc.
328
How severe infecctions cause neutropenia?
Increased movement of neutrophils into tissue in decreased circulating.
329
Lymphopenia causes?
Immunodeficiency.
High cortisol state.
Autoimmune destruction.
Radiation.
330
Lymphopeni causes for immunodeficiency are??
HIV and Digeorge Syndrome (they dont have thymus for abnormal en pounch 3 and 4)
331
How autoimmune destruction produce lymphopenia?
Ex: SLE. By destruccion for antibodys againts el cells.
332
Which are the cell is released in bacterial infection or tissue necrosis?
Nuetrophils with immature forms.
333
Wihich is the characterits of immature neutrophils?
decreased receptor Fe or CD16.
334
How high cortisol affect the leucocyte?
disrupted leukocyte adhesion, leading to release of marginated pool of neutrophils.
335
Neutrophilic leukocytosis
Are increased circulating neutrophils
336
Cuases of neutrophilic leukocytosis
1. Bacterial infection or tissue necrosis
2. High cortisol.
337
Monocytosis causes
Chronic inflamatory states and malignancy.
338
EOSINOPHILIA IS IMPORT BY?
Production of circulating eosinphilis in allergic reaction type I, parasitic and HY: Hodgkin Lymphoma like chemotatic by IL-5.
339
CD8+T in mononucleosis are response by?
1. LAD in the paracortex
2. Splenomegaly due to T cell hyperplasia in PALS (HY)
3. High WBC with atypical lymphocytes.
340
Complications in Mononucleosis
HY
1. Increased risk for splenic rupture.
2. rash if expose to AMPICILIN.
3. Recurrence
4. B cell lymphoma in ej HIV.
341
Bordetella pertussis what is the different between another bacteria's?
1. Produce Lymphocytosis leukocytosis
2. Lymphocytosis promoting factors.
3. from leaving the blood to enter the lymph node.
342
Que oncogen esta relacionado al Hairy cell leukemia?
BRAF
343
Cual es la relacion entre Mycosis fungoide and leukemia?
esta en photos
344
TTP is caused by?
Impaired function on the vWF-cleaving proteasa.
345
how looks Leukemoid reaction in bone marrow?
Can be normal or hypercellular and responds with increased bands and early mature neutrolphils precusor.
346
Leukocyte alkaline phosphatase are?
A serum blood test that can be normal or increased in LAP
347
Leukocyte alkaline phospatase is drecreased in?
Chronic myelogenos leukemia
348
What is the Dohle bodies?
Are ligth blue(basophilic) peripheral granules in neutrophils. They are seen in toxic systemic ilness and myelodysplasia
349
