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Basics of Path > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

APECED

A

Defect in AIRE gene - break in central tolerance - fungal infections, tan skin

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2
Q

ALPS

A

Mutation in Fas or FasL - failed peripheral tolerance - widespread lymphadenopathy, splenomegaly, autoimmune cytopenias

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3
Q

IPEX

A

FOXP3 mutation loss of Tregs - hypergammaglobulinemia very high IgE

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4
Q

What three factors contribute to autoimmune diseases?

A
  1. HLA - what gets presented 2. SNPs - AIRE, FOXP3, IL-2 (+T reg) 3. Environment - triggered (<60% twins, molecular mimicry, presented at same time as viral particles)
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5
Q

Type I Hypersensitivity

A

IgE mediated - requires Th2 development e.g. food allergies, asthma, allergic rhinitis

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6
Q

Type II Hypersensitivity

A

Antibody mediated

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7
Q

Type III Hypersensitivity

A

Antibody/antigen complexes

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8
Q

What is the mechanism of disease in Type III Hypersensitivity

A

Failure to clear immune complexes in circulation deposit on vasculature

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9
Q

Type IV Hypersensitivity

A

Delayed T cell mediated disease CD4 - see self and begin inflammation CD8 - see self and kill

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10
Q

What are some examples of Type IV Hypersensitivity?

A

T1D, MS, IBS, contact sensitivity, viral hepatitis, superantigen mediated shock syndrome

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11
Q

Neoplasia

A

New growth

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12
Q

Neoplasm

A

Abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue, and persists in the same excessive manner after cessation of the stimuli that evoked the change.

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13
Q

Benign tumors typically end in ____.

A

Oma

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14
Q

Malignant tumors end in __________ or ___________.

A

Carcinoma or sarcoma

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15
Q

Benign tumors are by definition __________ and do not ____________.

A
  1. Non-invasive/encapsulated
  2. Metastasize
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16
Q

Tumors arising from epithelial duct cells are refered to as _________ if benign and __________________ if malignant.

A
  1. Adenoma
  2. Adenocarcinoma
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17
Q

Tumors arising from mesoderm are referred to as a _________.

A

Sarcoma

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18
Q

What are 4 examples of hematolymphoid tumors?

A
  1. Lymphoma
  2. Leukemia
  3. Plasmacytoma
  4. Pseudolymphoma
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19
Q

Tumors of the melanocytes have what origin? What is the term for a benign and malignant tumor?

A
  1. Neural crest
  2. Nevus
  3. Melanoma
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20
Q

Define: Tumor grade or differentiation. Is this a visible on gross or microscopic analysis?

A

The degree to which tumor cells morphologically and functionally resemble normal tissue.

Microscopic

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21
Q

Anaplastic

A

A complete lack of differentiation - ugly

Large nucleoli, hyperchromatic nuclei, high N/C ratios, pleomorphism, loss of polarity, atypical bizarre mitoses

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22
Q

Tumor in situ

A

Preinvasive lesion - malignant cells do not penetrate beyond BM

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23
Q

Dysplasia

A

Disordered growth of epithelium

Loss of polarity maturation, architecture/org

Abnormally located mitoses

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24
Q

Is moderate dysplasia reversible?

A

Yes - may spontaneously resolve

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25
Q

Is severe dysplasia reversible?

A

No. It is CIS

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26
Q

Are all benign neoplasms encapsulated?

A

No

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27
Q

Next to the development of __________, _________________ is the most reliable feature that distinguishes malignant from benign tumors.

A
  1. Metastases
  2. Local invasiveness
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28
Q

What are the steps of local invasion?

A
  1. Loosening of intercellular junctions
  2. Attachment
  3. Degredation - Type IV collagen cleavage
  4. Migration
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29
Q

What are two examples of highly invasive cancers that don’t metastasize?

A
  1. Basal cell carcinomas
  2. Most primary tumors of the CNS
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30
Q

What are the 3 main ways that malignant neoplasms disseminate?

A
  1. Seeding within body cavities
  2. Lymphatic spread - carcinoma
  3. Hematogenous - sarcoma
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31
Q

What organs are most frequent secondary sites in hematogenous dissemination?

A

Lungs and liver

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32
Q

What are 5 barriers to immune elimination of neoplasms?

A
  1. Tumors evade recognition - downreg MHC and immune stimulating molecules
  2. Activate negative regulation pathways of effector T cells
  3. Secrete immune suppressive enzymes - TGF-beta and IL-10
  4. Expansion and recruitment of reg. cells - myeloid suppressors
  5. IDO overexpression
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33
Q

What are 3 main approaches to cancer immunotherapy?

A
  1. Antibodies
  2. Adoptive cellular immunity
  3. Vaccines
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34
Q

What are 4 examples of antibodies killing off tumor cells via non-cellular mechanisms?

A
  1. Bind complement
  2. Linked to radionucleotide/toxin
  3. Block survival signal
  4. Proapoptotic
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35
Q

TILs

A

Lymphocytes cultured from tumors, removed by surgery, are expanded in culture and given back to patients to provide large numbers of highly activated T cells

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36
Q

What problems are associated with using TILs?

A

Autoimmunity: vitiligo, uveitis, immune system targets non-mutated self-antigens overexpressed on cancercells

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37
Q

Chimeric antigen receptors (CARs)

A

Antibody w/ T cell signaling motifs - not MHC restricted

Activate when they bind tumor antigen

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38
Q

What are some limitations of CARs?

A
  1. Doesn’t work well for solid tumors
  2. Can create toxic shock like symptoms (control w/ IL-6)
  3. Tumor antigen may be lost
  4. Autoimmunity
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39
Q

Allogneic T cells (HSC transplantation) Graft vs. Tumor Effect

A

Donor T cells become activated to host alloantigens

Used in leukemias

Can cause GVHD

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40
Q

What are 2 reasons cancer vaccines aren’t very effective?

A
  1. Traditionally used to prevent disease
  2. Traditional targets are smaller
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41
Q

What are 5 main cancer gene targets?

A
  1. Protooncogenes/oncogenes
  2. Tumor suppressor genes
  3. Anti-apoptosis genes
  4. Apoptosis genes
  5. DNA repair genes
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42
Q

Who might benefit from a cancer vaccine?

A

People with premalignant lesions, or at high risk for a certain type of cancer

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43
Q

What are the 5 main classes of oncogenes?

A
  1. Growth factors
  2. Growth factor receptors
  3. Signal transducing proteins
  4. Transcription factors
  5. Cell cycle regulators
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44
Q

What is an example of a growth factor gene mutation?

A

SIS gene produces beta-PDGF

Overexpression leads to astrocytoma/osteosarcoma

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45
Q

What are two examples of GFRs that cause cancer?

A
  1. ERB B2 (Her2/Neu) - unresponsiveness to estrogen therapy
  2. C-kit - YK activity - Gleevec inhibits it
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46
Q

What are two examples of signal transducing proteins that cause cancer?

A
  1. Ras (pt mutated in 15-20%) - GTP-binding proteins w/ reduced GRPase activity
    • K-Ras in pancreas, colon CA
    • H-Ras in bladder, kidney CA
  2. C-ABL gene - transient YK, not receptor linked
    • t(9;22) Philadelphia Chromsome → bcr-abl fusion
    • **CML and ALL **
    • Constitutively active - Gleevec
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47
Q

What is an example of a TF that cause cancer?

A

Burkitt lymphoma t(8;14) co-expressed w/ Ig heavy chain on 14

  • C-MYC continuously expressed

**Neuroblastoma - **N-MYC continuously amplified

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48
Q

What is an exmpale of a cell cycle regualtor that causes cancer?

A

Cyclin D1 - t(11;14) cyclin D1-IgH fusion - mantle cell lymphoma

  • Activates CDK4
  • Involved in G1:S transition - hyperphos Rb
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49
Q

What is the 2 Hit Hypothesis?

A

Mutations in both alleles of tumor supressor genes are required for oncogenesis.

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50
Q

What are 3 examples of tumor supressor genes?

A
  1. RB
  2. APC
  3. p-53
51
Q

APC Gene

A

Involved in the destruction and down-regualtion of beta-catenin.

52
Q

What does beta-catenin accumulation lead to?

A

Complexes w/ TCF and stimulates transcription of GFs → 100s of adenomas

53
Q

Familial Adenomatous Polyposis (FAP)

A

APC gene mutation - 100-1000s of polyps on colon

54
Q

p53

A

Cell cycle arrest, initiation of apoptosis following DNA damage

55
Q

Li-Fraumeni Syndrome

A

Inheritance of mutated p53 allele

Develop multiple cancers at younger ages

25x risk developing CA by 50

56
Q

What 2 things are required for repair of tissue?

A
  1. Stroma (CT)
  2. Existing cells - to respond to GFs
57
Q

Stem cells self-renew and _____________ replicate.

A

Asymmetrically

58
Q

What are 4 examples of growth factors involved in tissue repair?

A
  1. VEGF - angiogenesis
  2. FGF - angiogenesis + fibroblast migration
  3. PDGF - induce fibroblast and sitm production of ECM
  4. TGF-beta - suppress endothelial prolif/mig stim. stim production of ECM proteins
59
Q

What are 3 sources involved in tissue repair?

A
  1. Leukocytes at site of injury
  2. Parenchymal cells
  3. Stroma
60
Q

ECM provides mechanical support and a scaffold for _________________.

A

Scarless healing

61
Q

What are the two main components of the ECM?

A
  1. Interstitial matrix - 3D amorphous gel - made by fibroblasts
  2. Basement membrane - highly organized IM around epi/endothelaia and sm. muscle cells - made by mesenchyme and epithelium
62
Q

What proteins make up the ECM and what is their function? (4)

A
  1. Collagen - tensile strength
  2. Elastin + fibrillin - recoil
  3. Proteoglycan and hyaluronon - compression and GF storage
  4. Fibronectin - major part of interstitial matrix
63
Q

Ehlers-Danlos Syndrome

A

Defect in collagen - 6 types

Poor tensile strength, wound healing, hyperextensible

Classic = Type V collagen

64
Q

Marfan Syndrome

A

Mutation effecting fibrillin

Degeneration of aorta, lens defects, abnormal vlaves, long arms and legs, hyeprextensible joints

65
Q

Keloid

A

Raised scar due to excessive collagen (Inc. TGF-beta and IL-1)

66
Q

What are the 4 steps to scar formation?

A
  1. Angiogenesis
  2. Fibroblast migration and proliferation
  3. Deposition of ECM
  4. Maturation of fibrous tissue
67
Q

Wound strength is at _____ after 1 week and plateaus by the 3rd month at ______.

A

10%

70-80%

68
Q

What are 7 factors that influence healing?

A
  1. Nutrition - vitamin c
  2. Metabolic Status - diabetes - impaired neutrophil fx and macrophage, impaired vessel formation and collagen
  3. Circulatory Status
  4. Hormones: Steroids block TGF-beta and dec. fibrosis
  5. Infection
  6. Mechanical Factors
  7. Foreign bodies
69
Q

Exuberant granulation

A

Protrudes above surrounding skin, prevents re-epithelialization

70
Q

Blood exposures to HIV are higher risk than sexual exposures because there is a _______________________________.

A

Higher average number of HIV particles per mL

71
Q

Why is there a greater chance of contracting HIV as a receptive partner of anal sex vs. vaginal sex?

A

Different tissues have different native immune populations. More immune cells/targets to invade in the GI tract than the vaginal canal

72
Q

What is the mechanism of HIV transmission?

A

Enter thru epithelial cells

Enter Langerhaans cells

Transport to regional lymph node

Infect CD4 T cells

73
Q

What are 4 natural defenses against HIV?

A
  1. Intact epithelium (vaginal stratified columnar vs. rectal single layer columnar)
  2. Mucous, pH, SLPI, lactoferrin, Trappin-2
  3. Adaptive mucosal immunity
  4. Presence of selective co-infection (Syphillis, HSV II, TB)
74
Q

Non-circumcised individuals have a _______ chance of acquiring HIV infection.

A

Higher

75
Q

What are symptoms of acute HIV?

A

Rash, diarrhea, fever, no cough, headache

76
Q

What is on the differential with acute HIV?

A
  1. Strep
  2. Mono (CMV, EBV)
  3. Influena
77
Q

Window period (HIV)

A

Routine HIV antibody tests are negative, but virus can be detected in blood

78
Q

What two tests must be ordered to cofirm a diagnosis of Acute HIV?

A

HIV antibody test - low/non-existant

HIV-1 RNA test - high

79
Q

Antibody/p24 antigen test

A

Cheaper than RNA test

Positive slightly later than RNA test (14 days post exposure)

80
Q

Over _______ viral particles are produced daily if untreated.

A

1 billion

81
Q

A strong ____ response is associated with _________________.

A

CTL

slow progression

82
Q

Why is HIV difficult to cure?

A

DNA is inserted into genome of T cells - resevoir exists in memory T cells

83
Q

Immune Reconstitution Inflammatory Syndrome

A

Deterioration in clinical status ~ 8 weeks after starting ART

In response to some other disease e.g. tB, MAC, p. jiroveci, histo, Hep B/C, Parvo,

84
Q

Due to CD4+ cells being impacted dramatically in the ____, patients with chronic HIV are more susceptible to ________.

A

Gut

Bacteremia - meausre plasma LPS levels

Higher immune activation is coorelated with inc. likelihood of AIDS related event

85
Q

Tumor killing follows ________________: A constant dose of drug kills a constant __________ of tumor cells

A

First-order kinetics

Fraction

86
Q

A 2-4 log-kill is need to ________ expected lifespan. To be considered curative a regiment must have 2-4 log-kill efficiency and be repeated for __________ of therapy

A

Double

4-12 cycles

87
Q

What are 3 mechanisms of anti-angiogenic therapy?

A
  1. Anti-VEGF
  2. Soulble VEGFR
  3. Peel off pericytes - toxic
88
Q

What are 4 mechanisms of resistance to anti-angiogenics?

A
  1. Vascular mimicry
  2. RTKs don’t syndergize well with chemotherapy
  3. Makes other pro-angiogenic factors
  4. Fibroblasts in tumor bed are not a genomically stable compartment
89
Q

What are 4 causes of edema?

A
  1. Increased hydrostatic pressure
  2. Decresaed plasma osmotic pressure
  3. Lymphatic obstruction
  4. Na/Water retention
90
Q

What diseases cause increased hydrostatic pressure?

A

Venous Obstruction - DVT, mass, inactivity, cirrhosis

Congestive Heart Fialure -hypoperfusion of kidney - 2˚ hyperaldosteronism

Arteriolar dilatation - heat,

91
Q

What are cuases of decreased plasma osmotic pressure?

A

Excessive loss of albumin and 2˚ hyperaldosteronism

Nephrotic Syndrome

IBS

Malnutrition

Cirrhosis

92
Q

What are cuases of lymphatic obstruction?

A

Inflammatory - parasitic infection

Neoplasms

Post-surgical scarring/removal of LN

93
Q

Na and Water Retnetion

A

· Cause inc. hydrostatic pressure and dec. colloid osmotic pressure

Excessive salt intake w/ renal insufficiency

94
Q

What are two common cuases of subcutaneous edema?

A

Congestive heart failure/renal failure

95
Q

What is a common cuase of pulmonary edema?

A

L ventricular failure

96
Q

What is the main difference between hyperemia and congestion?

A

Hyperemia is an active process - inflammation/exercising muslces

Congestion is a passive back up/impaired outflow of venous blood

97
Q

What factors are involved in primary hemostasis?

A

Platelet plug formation

Vasculature, blood flow, platelet count and fx, ECM proteins

98
Q

What are the steps of platelet plug formation?

A
  1. Trauma
  2. Vasoconstriction (endothelin release)
  3. vWF binds platelet
  4. Active platelets change shape and recruit more via ADP and TXA2
99
Q

What are the steps involved in secondary hemostasis

A
  1. Tissue factor released (begins extrinsic pathway)
  2. Phospholipid complex expression
  3. Thrombin activation
  4. Fibrin polymerization
100
Q

What are 4 ways we develop bleeding disorders?

A
  1. Vascular integrity - Ehlers-Danlos, Scurvy
  2. Defects in platelet count/fx - thrombocytopenia, Glanzmann throbasthenia
  3. vWF deficiency/dysfunction - vWF disease
  4. Clotting factor deficiencies/inhibition - Vita K def, liver disease, hemophilia (Factor 8 and 9 problems) Anticoagulation (Warfarin)
101
Q
A
102
Q

Hematoma

A

Accumulation of blood within tissue

103
Q

Petechial Hemorrhages

A

1-2mm in skin, mucuos memranes

Associated w/ thrombocytopenia, platelet dysfunction, loss of vascular wall support or local pressure

104
Q

Purpura

A

>3 mm

Assoicated with thrombocytopenia, platelet dysfunction, loss of vascular wall support or local pressure

Vasculitis and vascular fragility

105
Q

Ecchymoses

A

>1-2 cm

Bruises associated with traume

106
Q

Factors that inhibit thrombosis

A
  1. Tissue factor pathway inhbitor - shuts down extrinsic pathway
  2. Thrombomodulin - Protein C and Protein S shut down clotting cascade (Va and VIIIa)
  3. PGI2- inhibit platelets
  4. Antithrombin III (inactivates thrombin)
107
Q

Lab screen for anticoagulants?

A
  1. Protein C and S activity and antigen
  2. atIII activity and antigen
  3. Molecular abnormalities in Factor 5 or Porthrombin gnees
  4. Lupus anticoagulant and antiphospholipid antibodies
108
Q

What are factors that put someone at risk for hypercoag?

A
  1. Factor 5 Leiden
  2. Protein C, S, and atIII deficiency
  3. Malignancy
  4. Estrogens
  5. Antiphospholipid antibody syndrome
109
Q

Factor 5 Leiden

A

Most common inherited predisposition

Changes cleavage site for protein C

Increased clotting risk - 5-7% of Caucasians are heterozygous

110
Q

Antiphospholipid antibodies

A

Acquired autoantibodies that inhibit phospholipids

Important to clot formation

**Arterial and venous thrombosis **

Lupus anticoagulant - in vivo promotes clotting

In vitro prolongs clotting

111
Q

What three conditions help form thrombi?

A

Site of endothelial injury

Turbulent flow

Site of blood stasis

112
Q

What are causes of abnormal blood flow?

A

Ulcerated atherosclerotic plaques, aneurysms, acute MI

A fib, mitral valve stenosis

113
Q

What is a classic example of red infarct?

A

Lung infarct secondary to embolus (hemorrhagic)

Brain - colateral flow

Venous occlusions

114
Q

What is an example of white (anemic) infarct?

A

Kidney, spleen

Arterial end arterial circulation

115
Q

What is the differnece between a hematoma and hemorrhagic infarct?

A

Hemorrhagic infarct blood is intermixed with necrosis

Hematoma blood is collected and forms a solid mass

116
Q

DIC

A

Small vessel clotting - organ ischemia

Bleeding tendencies - consumptive coagulopathy (platelets and clotting factors)

117
Q

Shock

A

CV collapse

Systemic hypoperfusion

118
Q

Cardiogenic Shock

A
119
Q

Hypovolemic Shock

A

Hemorrhage, fluid loss – burns vomiting, diarrhea

120
Q

Septic Shock

A

Overwhelming microbial infection à Peripheral VD and pooling of blood, endothelial activation or injury, leukocyte induced damage, cytokine activation and DIC

121
Q
A
122
Q

Neurogenic Shock

A

Interruption of sympathetic vasomotor input – arteriolar and venous dilation – dec cardiac output

123
Q

What are the three stages of shock?

A
  1. Non-progressive phase - still perfusing organs
  2. Progressive phase - tissue hypoxia, lactic acidosis, lower pH
  3. Irreversible phase - multiorgan failure
124
Q

Hypovolemic and cardiogenic shock patients have skin that is ____________________.

A

Cool, clammy and cyanotic

Basics of Path (5 decks)

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