Test 1 Flashcards

1
Q

Vitamins necessary for healing

A

Vitamin C (cofactor for hydroxylation reactions ie crosslinking of collagen)
Zinc (cofactor for metalloenzymes ie collagenases)
Copper (cofactor for lysyl oxidase ie cross-linking of lysine and hydroxylysine)

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2
Q

Keloid

A

Accumulation of exuberant amount of collagen –> raised scar beyond wound boundaries. More common in African-Americans.

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3
Q

Upregulation of P- and E- selectins and where P-selectin is released from.

A

P-selectin: histamine (Weibel-Palade body)

E-selectin: TNF-a and IL-1

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4
Q

Consequence of low NADPD in infection and why

A

Low NADPH means that H2O2 can’t be generated in lysosome bugs are not digested. H2O2 is converted to OH and OCl radicals, which are in turn converted to HOCl (bleach) by MPO (myeloperoxidase)

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5
Q

M1 v M2 macrophages

A

M1 - chronic inflammation. Assoc. with pro-inflammatory cytokines which lead to an increase in hepatic defense proteins (less albumin), increased hepcidin (anemia), and increased platelet and monocyte growth factors.

M2 - anti-inflammatory promoting tissue repair and fibrosis.

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6
Q

Granulomas have what kind of cells?

A

Necrotizing mass surrounded by giant cells, a cuff of CD4+ T cells, and proliferating fibroblasts. TMMI.

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7
Q

Acute phase reactants

A

Hepatic adjustments for inflammation.

High fibrinogen, ceruloplasmin, complement components, hepcidin, and growth factors.

Decreased albumin.

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8
Q

C-reactive protein

A

Levels closely linked to IL-6 levels, proxy for the level of inflammation in patients.

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9
Q

The basement membrane consists of…

A

Type IV collagen, laminin, proteoglycans

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10
Q

The interstitial matrix consists of…

A

Fibrillar collagen, elastin, proteoglycan, hyaluronan, and adhesive glycoproteins.

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11
Q

Angiogenesis requires what growth factors?

A

VEGF, FGF, PDGF, TGF-beta

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12
Q

Migration and proliferation of fibroblasts require what growth factors?

A

PDGF, FGF, TGF-beta

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13
Q

Trichrome stain for what cellular components?

A

Transformation of Collagen III (immature collagen) to Collagen I (mature collagen) in the healing process

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14
Q

Hyperemia

A

Arteriolar dilation leads to increased blood flow. Results from sympathetic discharge or chemical mediators. Ex - sites of inflammation, exercising skeletal muscle.

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15
Q

Virchow’s Triad

A

Endothelial injury (most important), abnormal blood flow, hypercoagulable state.

Three factors influencing the formation of a thrombus.

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16
Q

Which way do venous thrombosis propagate?

A

Towards the heart.

17
Q

White (Pale) vs Red infarction

A

White: arterial occlusions, solid organ with end arterial circulation (heart, spleen, liver, kidney)

Red: venous occlusion, tissue with dual circulation (lung, small intestine), and re-establishment of flow in white infarctions (re-perfusion).

18
Q

What are the three types of shock?

A

Cardiogenic - decreased cardiac output as a result of an MI, ventricular rupture, arrhythmia, or cardiac tamponade (fluid in the pericardium)

Hypovolemic - decreased C.O. secondary to decreased blood/plasma volume. Hemorrhage, fluid loss (vomiting, diarrhea, burns)

Septic - arteriolar vasodilation and venous pooling resulting from systemic immune response to infection (usu. gram positive bacteria)

19
Q

Parenchyma

A

The neoplastic cells.

20
Q

Stroma

A

The connective tissue, blood vessels, immune system cells that are supporting the growth of the neoplasm.

21
Q

Tumor names

A

Mesenchyme origin -
Benign = –oma Malignant = –sarcoma
Epithelium origin -
Benign = –oma Malignant = –carcinoma

22
Q

RAS protein

A

Oncogene - Active when bound to GTP, and upon hydrolysis to GDP turns off. When mutated, constitutively active and stimulating downstream promoters of proliferation. Dominant mutation.

23
Q

RB (“retinoblastoma”)

A

Tumor suppressor gene - When hyperphosphorylated, releases E2F to transcribe S-phase cyclins. Recessive mutation (need both genes to be hit in order to develop into cancer).

Retinoblastoma histology - you see “Flexner-Wintersteiner rosettes” and numerous mitotic figures.

24
Q

p53

A

Tumor suppressor gene. Normally involved in responding to DNA damage, puts the cell into quiescence (temporary), senescence (permanent), or signals for apoptosis.

Li-Fraumeni syndrome - inherit 1 defective p53 –>25x higher chance of cancer by age 5.

25
Q

Intrinsic/Mitochondrial apoptosis pathway

A

Bax/Bak punch a hole in the mitochondria, allowing cytochrome C to leak into the cytoplasm. This converts pro-caspase 9 to caspase 9 and leads to apoptosis.

Bax/Bak are inhibiting from dimerizing by Bcl-2/Bcl-XL (

26
Q

Extrinsic Apoptotic Pathway

A

Fas receptor bound by FasL, this leads to a conversion of pro-caspase 8 to caspase 8, starting to caspase cascade and leading to apoptosis.

27
Q

Thrombospondin-1 (TSP-1)

A

Inhibits angiogenesis

28
Q

Xeroderma pigmentosum

A

Defects in DNA repair resulting in an increased risk for skin cancer.

29
Q

Microbial oncogenesis

A

RNA viruses - HTLV-1

DNA viruses - HPV, Epstein-Barr virus, Hep B and C

Bacteria - helicobacter pylori

30
Q

Cachexia

A

Loss of body fat and lean body mass. Weakness, anorexia, anemia.

31
Q

HE Stain

A

Hematoxylin and eosin stain -

H is a basic stain that stains acids blue (nuclei)
E is an acidic stain that stains proteins pink (cytoplasm)

32
Q

PAS Stain

A

Periodic acid-Schiff - stains fungi and glycogen magenta and the rest light pink.

33
Q

GMS stain

A

Grocott methenamine silver - stains fungi black and everything else green

34
Q

Acid fast stain

A

Stains mycobacteria, actinomyces red, everything else blue

35
Q

Immunohistochemical stain

A

stains target brown/red, everything else blue.