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(Pharm) 01 > USMLE Pathology > Flashcards

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
Q

How are B cells activated independent of T cells?

A

BCR binds to antigen and becomes plasma cell expressing IgM, IgD

26
Q

How are B cells activated by T cells?

A

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
Q

What are the key cells in granulomas?

A

Epithelioid histiocytes (surrounded by giant cells and rim of lymphocytes)

28
Q

How are granulomas activated?

A

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
Q

What is the cause of DiGeorge syndrome?

A

Microdeletion 22q11

30
Q

High yield cause of SCID?

A

Adenosine deaminase deficiency (builds up in lymphocytes, kills it)

31
Q

Chronic candida, adrenal failure, hypoparathyroidism. Dx?

A

Autoimmune polyendocrine syndrome (AIRE deficiency)

32
Q

What receptors are expressed on Treg cells?

A

CD4, CD25 (IL2-R), FOXP3

33
Q

How do Tregs do their work?

A

Compete with B7 with CTLA4 and release IL-10/TGF-B to shut down MHC II, DC, macrophages, and B7

34
Q

How does peripheral tolerance work?

A

Induces anergy if TCR binds MHC II without B7/CD-28 (absent in non-inflammatory states), or self expresses Fas to apoptose

35
Q

Features of IPEX syndrome?

A

Immune dysfn, polyendocrinopathy, enteropathy, x-linked

36
Q

What causes hyper IgM syndrome?

A

CD40/CD40L mutation = only IgMs produced, susceptible to pyogenic infections

37
Q

What risks associated with common variable immunodeficiency?

A

Bacterial, giardia, enterovirus infxns + risk of AI disease/lymphoma

38
Q

What makes up granulation tissue?

A

Blood vessels, fibroblasts (for T3 collagen), and myofibroblasts

39
Q

T1 collagen?

A

Bone

40
Q

T2 collagen?

A

Cartilage

41
Q

T3 collagen?

A

Granulation tissue, embryonic tissue, blood vessels

42
Q

T4 collagen?

A

Basement membrance

43
Q

TGF-alpha

A

Epithelium and fibroblast GF

44
Q

TGF-beta

A

Fibroblast GF and anti inflammatory

45
Q

PDGF

A

Endothelium, smooth muscle, fibroblast GF

46
Q

FGF

A

Angiogenesis and skeletal development

47
Q

VEGF

A

Angiogenesis

48
Q

What kind of collagen is seen in keloid scars?

A

T3 collagen

49
Q

Aflatoxins

A

HCC, in Africa and stored grains

50
Q

Alkylating agents

A

Lymphoma, leukemia

51
Q

Alcohol

A

SqCC of oropharynx & upper esophagus, HCC, pancreatic cancer

52
Q

Arsenic

A

SqCC of skin, lung cancer, angiosarcoma of liver

53
Q

Nitrosamine

A

Intestinal type stomach cancer

54
Q

Vinyl chloride

A

Angiosarcoma of liver

55
Q

EBV cancer associations?

A

Nasopharyngeal cancer, Burkitt lymphoma, CNS in AIDS

56
Q

HHV 8

A

Kaposi’s sarcoma in E. European males, AIDS, transplant

57
Q

HTLV-1

A

ATLL

58
Q

Ionizing

A

AML, CML, Papillary thyroid carcinoma

59
Q

Ret

A

Associated with medullary carcinoma of thyroid in MEN2A/2B

60
Q

PDFG-B overexpression

A

Astrocytoma

61
Q

What is ABL responsible for?

A

9:22 translocation seen in CML and adult B-ALL

62
Q

What are you at risk of with germline mutation of Rb?

A

Bilateral retinoblastomas and osteosarcoma

(Pharm) 01 (23 decks)

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