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Pearls Review Flashcards

1
Q

Metaplasias: Smokers transition

A

ciliated columnar epithelium -> squamous.

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2
Q

Metaplasias: GERD transition

A

squamous -> intestinal type
= Barrett Esophagus
(predisposes to carcinoma).

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3
Q

Metaplasia: HPV transition

A

columnar -> squamous

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4
Q

swelling, karyorrhexis, leakage, inflammation, ALWAYS pathological.

A

Necrosis:

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5
Q

shrinkage, fragmentation/condensation, either path or physiological.

A

Apoptosis:

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6
Q

Apoptotic Pathway: Instrinsic; Injury ->

A

Bcl-2 stops inhibiting -> mitochondria -> Cytochrome C -> caspases -> endonuclease activation and breakdown cytoskeleton.

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7
Q

Apoptotic Extrinsic

A

Fas + TNF receptor -> caspases -> etc.

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8
Q

Pathologic Calcification: Dystrophic;

A

damaged tissue, normal serum Ca (ex. Heart valves, atherosclerosis).

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9
Q

Pathologic Calcification:Metastatic;

A

normal tissue, hypercalcemia (ex. PTH, Vit D intoxication, Bone destruction, renal failure)

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10
Q

TRECs (T cell Receptor Excision Circles)

A

are circular pieces of DNA generated during T cell receptor editing. Absent in SCID (hence the screening test)

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11
Q

What is absent in SCID that you can test for

A

TRECs

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12
Q

obstructive lung disease due to inflammation/swelling and fibrosis of the lung. Some primary causes and also from recurrent infection

A

Bronchiectasis

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13
Q

IgE mediated, requires sensitization, not dose dependent.

A

Allergen

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14
Q

Not IgE mediated, dose dependent, will affect everyone at high dose.

A

Irritant

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15
Q

only made by Mast cells = best marker for Mast cell activation

A

Tryptase

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16
Q

Regulatory Tcells express_____ and suppress immune responses - disease is IPEX

A

Foxp3

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17
Q

Foxp3 messed up in this disease… thus no Tregs

A

IPEX

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18
Q

Acute inflammation dominant cell

A

neutrophils

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19
Q

Chronic inflammation dominant cells =

A

Monocytes & Lymphocytes

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20
Q

_______recognize PAMPs -> release TNF -> increase thrombogenicity.

A

TLRs

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21
Q

______ recognize dead cells (uric acid, ATP crystals) -> release IL-1 -> activates fibroblasts

A

Inflammasome

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22
Q

low protein/cells (SG <1.012) minimal flow.

A

Transudate -

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23
Q

high in protein/cells (SG > 1.020) high flow.

A

Exudate

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24
Q

Adhesion:_______ loose on endothelial, platelets, and leukocytes.
_______ tight, only on leukocytes.

A

Selectins

Integrins

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25
Q

Selectins present on

A

endothelial cells, platelets, leukocytes

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26
Q

Integrins present on

A

leukocytes

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27
Q

movement of leukocytes through vessel wall by CD31 (PECAM1)

A

Diapedesis:

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28
Q

How do leukocytes move through vessels wall?

A

CD31 or PECAM

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29
Q

Histamine present in:

A

mast cells, basophils platelets

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30
Q

Action of Histamine

A

vasodilation, increase permeability.

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31
Q

NO present in:

A

endothelium, macrophages

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32
Q

NO action:

A

vasodilation

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33
Q

Bradykinin present in:

A

(Liver - plasma)

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34
Q

Bradykinin action

A

Increase permeability, pain.

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35
Q

IL-1, TNF present in

A

(macrophages, endothelium, mast cells):

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36
Q

Action of IL-1 and TNF

A

chemotaxis, FEVER

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37
Q

Chronic granulomatous inflammation contains

A

Multinucleated giant cells (from monocyte fusions) caused by IFN-y

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38
Q

What causes giant cell fusion

A

IFN-y

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39
Q

Systemic Inflammatory Reponse Syndrome (SIRS):

A
  1. fever.
  2. elevated plasma levels of acute phase proteins.
    3 leukocytosis
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40
Q

Fever due to pyrogens (___,____,_____) -> production of PGE2 -> reset hypothalamus

A

(LPS, or IL-1, TNF)

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41
Q

; C reactive protein, fibrinogen, serium amyloid A.

A

Elevated acute phase proteins:

42
Q

What induces acute phase proteins

A

From liver (IL-6 induced)

43
Q

_______ causes RBC stacking = sedimentation = Erythrocyte sedimentation rate (ESR)

A

Fibrinogen

44
Q

(stimulate by TNF, IL-1) incerase in WBCS (to 15-20k) 4 types

A

Leukocytosis:

45
Q

What stimulates leukocytosis?

A

TNF and IL-1

46
Q

bacterial infection (causes left shift)

A

Neutrophilia:

47
Q

Lymphocytes signal a:

A

viral infection

48
Q

allergies, asthma, parasites will cause

A

Eosinphilia:

49
Q

typhoid, rickettsiae, some protozoa will cause

A

Leukopenia:

50
Q

defect in collagen. hyperflexible skin, joints, easily ruptured organs

A

Ehlers-Danlos Syndrome (EDS):

51
Q

specialized tissue seen in healing (present by 3-5 days)

A

Granulation Tissue:

52
Q

4 steps of scar formation:

A

1) angiogenesis.
2) fibroblast proliferation.
3) ECM deposition.
4) Remodeling of fibrous tissue

53
Q

Growth factors for fibroblasts:

Fibrogenic agent & inhibits lymphocytes.

54
Q

Growth factors for fibroblasts:

migration/proliferation of fibroblasts, SMCs, macrophages. FGF

55
Q 
Primary union (wound healing): 
Immediate -
A

fill w/ blood. W/ in 24 hrs-neutrophils, begin reepitheliazation.

56
Q 
Primary union (wound healing):  
Day 3-
A

neutrophils out macrophages in, granulation tissue present.

57
Q 
Primary union (wound healing): 
Day 5-
A

maximum granulation tissue, collagen fibers begin to bridge gap.

58
Q 
Primary union (wound healing): 
Weeks -
A

scar formation, decreased vessels.

59
Q

Secondary union:

A

More extensive damage (not a clean cut) - everything more intense. Substantial scar. More wound contracture by myofibroblasts

60
Q

reopening of wound.

A

Dehiscence

61
Q

too much collagen (African Americans).

62
Q

too tight around joint

A

Contracture -

63
Q

Wound strength:

A

10% at first week.

3 months - plateaus at 70-80%

64
Q

Why does having HSV2 or syphillis put you at higher risk of contracting HIV?

A

Having HSV-2 or syphillus puts you at higher risk for contracting HIV, as HIV prefers activated T cells (CCR5, etc)

65
Q

Acute HIV infection:

A

HIV virus can be detected, but Abs are not yet present.

66
Q

Symptoms at 1-4wks after exposure to HIV-

A

fever, lymphadenopathy, rash, joint pain, myalgia, anorexia, etc.

67
Q

We make Abs to HIV, but they don’t work, why?

A

Because HIV-1 Reverse Transcriptase make 1 in 10,000 errors. 10,000 is the size of its genome (1 error/each replication, and 1 billion replications/day = 1 billion mutations/day)

68
Q
  • a PARADOXICAL deterioration in status after immune system recover from HAART (typically w/ in 8 wks)
A

Immune Reconstituion Inflammatory Syndrome (IRIS)

69
Q

What happens to GALT in HIV patient?

A

lack of CD4 in the gut increases permeability to bacteria (LPS). ***This early insult is permanent! Continues even after HAART

70
Q

Direct recognition of alloantigen (acute rejection):

A

Recipient T cells reacts to Donor MHC.

71
Q

Indirect recogniton (chronic rejection):

A

Recipient T cell reacts to a peptide derived from the donor MHC.

72
Q

minutes, preformed Abs from blood transfusion, pregnancy, or prior transplantation (barrier to xeno).

A

Hyperacute rejection:

73
Q

Rejection that takes days to weeks, mostly by T cells (some Abs).

74
Q

Type of rejection that takes months to years, fibrosis of the graft (the major problem in kidney grafts now).

75
Q

Sources of Hematopoietic Stem Cells (for HSCT).

A

1) BM.
2) umbilical cord.
3) Mobilized Peripheral Blood (PBSC) induced by G-CSF and GM-CSF

76
Q

Host Disease (GVHD): 4 grades

A

(1-4, 4 being worst).

Based on amounts of rash, bilirubin, diarrhea (more = worse for all)

77
Q

: benign mass of disororganized but well differentiated tissue. ex) lung hamartoma contains cartilage, BVS, SMCS, alveoli, but all disorganized

78
Q

ecptopic tissue in a foreign location

A

Choriostoma:

79
Q

Grade/differentiation (different than staging):

A

how well differentiated it is.
Benign are well differentiated.
Malignant can vary.
Metestatic: well to poorly differentiated
(anaplastic = complete lack of differentiation)

80
Q

Metastasis pathway:

A

1) Hematogenous; veins over arteries (sacromas).
2) lymph (carcinomas).
3) body cavities.

81
Q

Carcinomas IG metastisize by

82
Q

Sarcomas IG metastisize by

A

hematogenous and VEINS more than arteries

83
Q

Clinical Stage is based on what three criteria

A

TNM
Tumor size,
Nodal involvement,
Metastasis

84
Q

differentiation and is based on HISTOLOGY. as opposed to stage.

85
Q

Non-hormonal or hormonal effect of tumor, UNRELATED to local spread or mets.
ex) a lung cancer which secretes ACTH causing Cushings.

A

Paraneoplastic syndromes**

86
Q

Tumor cells attempt to downregulate the immune response via

A

TGF-B, CTLA-4, PD1, IL-10, and recruiting Tregs

87
Q

have a modified receptor on them which directly binds an Ag on the tumor cell. No need for APC, MHC, or other peptides.

A

CAR (Chimeric Antigen Receptor) T cells (artificial)

88
Q

Possible problems with CAR

A

1) too much proliferation -> toxic shock.

2) autoimmunity

89
Q

Histology prep:

A

cassestes fixed in formalin, embedded in parafin. at 5 mm thick. stained with hematoxylin and eosin (H&E): H stains the nucleus blue. E stains the proteins orangeish

90
Q

What color does Hematoxylin stain the nucleus

91
Q

What color does eosin stain proteins?

A

pink/orange

92
Q

Whats the difference between direct acting and indirect acting carcinogens? How are they simular?

A

Direct acting carcinogens - electrophilic, direct.
Indirect - must be P450 activated.
Both target nucleic acids

93
Q

Polycyclic hydrocarbons result in lots of bad shit such as:

A

-> SCC of lungs, larynx, oral cavity; esophagus, pancreas, bladder CAs

94
Q

Alkylating agents cause

A

-> Hematolymphoid malignancies

95
Q

metabolizes polycyclic aromatic hydrocarbons. 10% caucasians have a highly induced form -> more carcinogen

96
Q

_______-> causes mutated DNA ->_______ -> causes replication of that mutated DNA

A

initiator

promoter

97
Q

EBV prefers______

98
Q

in an immunosuppressed patient it mulitplies in B cells. Then a t(8;14) can lead to Burkitt Lymphoma

99
Q

Killing of tumors follows

A

First Order Kinetics

Constant fraction. Not constant number. Log Kill (1=.9, 2=.99, 3=.99)

100
Q

To be curative you must have _____log kill for ____cycles.

A

2-4 (2-4 is necessary to double expected lifespan)

4-12

101
Q

VEGF, FGF, MMPs.

A

Angiogenic factors:

102
Q

PDGF, Angiopoetin, TGFB, Thrombospondin, Endostatin

A

Angiogenic Inhibitors

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