USMLE Pathology Flashcards

1
Q

PaO2 and SaO2 levels in CO poisoning?

A

PaO2 normal, SaO2 decreased

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2
Q

What cells can only undergo hypertrophy?

A

Skeletal muscle, heart, neurons

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3
Q

What cellular functions stop working with hypoxia?

A

Na/K pumps = swelling, Ca pumps = Enzyme activation, Aerobic to anaerobic glycolysis = lactic acidosis, lowers pH

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4
Q

Where is the electron transport chain located?

A

Inner mitochondrial membrane

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5
Q

What are the three stages of cell death?

A

Pyknosis (shrinks down), karyorrhexis (nucleus breaks down), karyolysis (broken down)

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6
Q

When do you get a red infarct?

A

When blood reenters an infarcted area (of loosely connected tissue)

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7
Q

Why is necrosis in the brain liquefactive?

A

Because microglial cell enzymes destroy everything

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8
Q

What situations do you see liquefactive necrosis in?

A

Brain ischemia, abscess, pancreatitis

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9
Q

How do you distinguish dystrophic calcification from metastatic calcification?

A

Dystrophic = normal Ca PO4 in serum, will be elevated in metastatic

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10
Q

What are the three apoptotic pathways?

A

1) Intrinsic mitochondrial pathway (Bcl2, cytC)
2) Extrinsic receptor-ligant pathway (FasL, TNF)
3) Cytotoxic T cell pathway (perforin, granzymes)

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11
Q

Delayed separation of umbilical cord?

A

Leukocyte adhesion deficiency

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12
Q

What factors mediate pain?

A

PGE2 and bradykinin

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13
Q

What factors mediate inflammation

A

Mast cells, arachidonic acid, TLRs, complement, Hageman’s factor

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14
Q

What are mast cells activated by?

A

Tissue trauma, C3a, C5a, and cross linking by IgE

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15
Q

What factors are responsible for neutrophil chemotaxis?

A

LTB4, C5a, IL-8, bacterial products

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16
Q

What is an important example of TLRs in action?

A

CD14 on macrophages binds LPS on G-ve bacteria to activate NfKB

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17
Q

Features of Chediak Higashi syndrome?

A
Dysfunctional primary hemostasis
Albinism
Peripheral neuropathy
Infections (pyogenic)
Neutropenia
Giant granules in leukocytes
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18
Q

Recurrent infections by catalase positive organisms?

A

Chronic granulomatous disease

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19
Q

How do macrophages continue acute inflamm?

A

IL-8

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20
Q

How do macrophages initiate resolution and healing?

A

IL-10, TGF-B

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21
Q

How are CD4 T cells activated?

A

TCR to MHC II with antigen and B7 to CD28 on T cell

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22
Q

How are CD8 T cells activated

A

TCR to MHC I with antigen and IL-2 from TH1 CD4+ helper cells

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23
Q

What cytokines are produced by CD4+ Th1 cells?

A

Helps CD8 T cells

IL-2 - promotes T cell proliferation, IFN-gamma: activates macrophages

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24
Q

What cytokines are produced by CD4+ Th2 cells?

A

Helps B cells
IL-4 - switch to IgG, IgE
IL-5 eosinophils and switch to IgA
IL-10 inhibits Th1 subtype

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25
How are B cells activated independent of T cells?
BCR binds to antigen and becomes plasma cell expressing IgM, IgD
26
How are B cells activated by T cells?
B cell presents antigen on MHC II to CD4+ Th2 cells, CD40 on B cell binds CD40L on T cell --> IL4/IL5 for class switching
27
What are the key cells in granulomas?
Epithelioid histiocytes (surrounded by giant cells and rim of lymphocytes)
28
How are granulomas activated?
Macrophage presents antigen on MHC II to T helper cell and secretes IL-12 to turn it into TH1 cell. TH1 cell secretes IFN-gamma to turn macrophages into EH cells
29
What is the cause of DiGeorge syndrome?
Microdeletion 22q11
30
High yield cause of SCID?
Adenosine deaminase deficiency (builds up in lymphocytes, kills it)
31
Chronic candida, adrenal failure, hypoparathyroidism. Dx?
Autoimmune polyendocrine syndrome (AIRE deficiency)
32
What receptors are expressed on Treg cells?
CD4, CD25 (IL2-R), FOXP3
33
How do Tregs do their work?
Compete with B7 with CTLA4 and release IL-10/TGF-B to shut down MHC II, DC, macrophages, and B7
34
How does peripheral tolerance work?
Induces anergy if TCR binds MHC II without B7/CD-28 (absent in non-inflammatory states), or self expresses Fas to apoptose
35
Features of IPEX syndrome?
Immune dysfn, polyendocrinopathy, enteropathy, x-linked
36
What causes hyper IgM syndrome?
CD40/CD40L mutation = only IgMs produced, susceptible to pyogenic infections
37
What risks associated with common variable immunodeficiency?
Bacterial, giardia, enterovirus infxns + risk of AI disease/lymphoma
38
What makes up granulation tissue?
Blood vessels, fibroblasts (for T3 collagen), and myofibroblasts
39
T1 collagen?
Bone
40
T2 collagen?
Cartilage
41
T3 collagen?
Granulation tissue, embryonic tissue, blood vessels
42
T4 collagen?
Basement membrance
43
TGF-alpha
Epithelium and fibroblast GF
44
TGF-beta
Fibroblast GF and anti inflammatory
45
PDGF
Endothelium, smooth muscle, fibroblast GF
46
FGF
Angiogenesis and skeletal development
47
VEGF
Angiogenesis
48
What kind of collagen is seen in keloid scars?
T3 collagen
49
Aflatoxins
HCC, in Africa and stored grains
50
Alkylating agents
Lymphoma, leukemia
51
Alcohol
SqCC of oropharynx & upper esophagus, HCC, pancreatic cancer
52
Arsenic
SqCC of skin, lung cancer, angiosarcoma of liver
53
Nitrosamine
Intestinal type stomach cancer
54
Vinyl chloride
Angiosarcoma of liver
55
EBV cancer associations?
Nasopharyngeal cancer, Burkitt lymphoma, CNS in AIDS
56
HHV 8
Kaposi's sarcoma in E. European males, AIDS, transplant
57
HTLV-1
ATLL
58
Ionizing
AML, CML, Papillary thyroid carcinoma
59
Ret
Associated with medullary carcinoma of thyroid in MEN2A/2B
60
PDFG-B overexpression
Astrocytoma
61
What is ABL responsible for?
9:22 translocation seen in CML and adult B-ALL
62
What are you at risk of with germline mutation of Rb?
Bilateral retinoblastomas and osteosarcoma