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usmle > Pathology Basics > Flashcards

Pathology Basics Flashcards

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USMLE® Step 1 flashcards
1
Q

Cell injury; irreversible changes

A
  1. Plasma membrane damage (phospholipid membrane degradation);
    - leakage of cytosolic enzymes
    - Ca+ influx
  2. Lysosomal rupture/autolysis
  3. Nucleus:
    - shrinkage (pyknosis)
    - fragmentation (karyorrhexis
    - fading (karyolysis)
  4. Mitochondria permeability/vacuolization increases. (swelling alone is reversible)
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2
Q

What causes nuclear fragmentation (karyorrhexis)

A

Endonuclease mediated cleavage

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3
Q

What is a sensitive indicator of apoptosis

A

DNA laddering

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4
Q

Apoptosis pathways

A

Intrinsic (mitochondrial) pathway
Extrinsic (death receptor) pathway

-Both pathways activate caspases (cytosolic proteases)

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5
Q

Intrinsic pathway stimuli

A

Internal stimuli;

  • DNA Damage/stress
  • Cytokines (decreased IL-2 after an immunological reaction)
  • Injurious stimuli: Toxins, radiation, hypoxia
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6
Q

Extrinsic pathway stimuli

A

External stimuli; (2 pathways)

A. Extracellular Transmembrane ligands/receptor interaction;

  1. FASL binding to FAS (CD95)
  2. TNF-a binding to its receptor

B. T-cell release of perforin and granzyme B

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7
Q

Mitochondrial pathway is regulated by which family of proteins?

A

BCL-2.

Proapoptotic: BAX and BAK
Antiapoptotic: BCL-2 and BCL-xL

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8
Q

What is the function of BAX and BAK on the mitochondrial membrane?

A

Form pores in the membrane which allows the release of cytochrome C (leads to activation of caspases)

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9
Q

What is the function of BCL-2 on the mitochondrial membrane?

A

Keeps the membrane impermeable to keep cytochrome C from leaking out.

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10
Q

BCL-2 overexpression leads to decreased cascade activation which promotes tumor growth. Which malignancy is associated with this overexpression?

A

Follicular lymphoma t(14;18)

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11
Q

Extrrinsic pathway is regulated by which family of proteins?

A

TNF (tumor necrosis factor) family;

FAS (CD95)

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12
Q

What is the importance of FAS-FASL interaction in the thymic medulla?

A

FAS-FASL is important for the elimination of self-reacting T-cells. Normally, self reacting T-cells under go apoptosis. FAS mutation increases the number of self-reacting T cells in the circulation.

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13
Q

What autoimmune syndrome is associated with defective FAS-FASL interaction?

A

Autoimmune lymphoproliferative syndrome.

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14
Q

Leukocyte extravasation steps

A
  1. Margination/rolling
  2. Adhesion
  3. Transmigration
  4. migration
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15
Q

Margination/rolling: Molecules present on the blood vessel wall that serve as “speed bumps” so that rolling leukocytes can slow down to exit the blood vessel and to the site of injury.

A

Blood vessel:
E-selectin (in endothelial cells)
P-selectin (in platelets and endothelial cells)

Leukocyte:
L-selectin
Silly-Lewis

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16
Q

Adhesion molecules

A

Blood vessel:

  1. ICAM (CD54)
  2. VCAM (CD106)

Leukocyte:
1. CD11/18 integrins;
(LFA-1 and MAC-1)
2. VLA-4 integrin

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17
Q

Transmigration/Diapedesis; leukocyte squeezes through endothelial cells and exits blood vessel. Which molecules are involved in this step?

A

PECAM-1 (CD31)

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18
Q

Migration: leukocyte is guided to site of injury by ________________

A

Chemotactic signals

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19
Q

Although macrophage are the dominant mediators of chronic inflammation, they are also present in the late stages of acute inflammation (peak 2-3 days after onset) what is the role of macrophage in acute inflammation?

A

Influence the outcome of acute inflammation (4 outcomes; Resolution, healing by scarring, abscess formation or progression to chronic inflammation) by secreting cytokines.

20
Q

Outcomes of chronic inflammation?

A

Scarring, amyloidosis or neoplastic transformation

21
Q

Which mediators activate macrophage to create a pro inflammatory response?

A

INF-gamma (secreted by TH1), TNF

22
Q

Which mediators activate macrophage to induce an anti-inflammatory response?

A

IL-4 and IL-13 (Secreted by TH2)

23
Q

Oncogenes that encode Receptor Tyrosine Kinases. (With the associated neoplasm)

A

RET
HER2
ALK

24
Q

Oncogenes that encode Non-Receptor Tyrosine Kinase

A

JAK2

BCR-ABL

25
Q

Oncogenes that encode transcription factor

A

MYCL1
N-MYC
C-MYC

26
Q

Oncogene that encodes serine/threonine kinase

A

BRAF

27
Q

Oncogene that encodes GTPase

A

KRAS

28
Q

Oncogene that encodes cytokine receptor (Stem cell growth factor receptor)

A

C-KIT

29
Q

Tumor supressor gene that help repair damaged DNA

A

BRCA1/BRCA2

30
Q

Which tumor supressor genes prevent cells from dividing too fast (inhibit G1 to S phase progression)

A
  • Rb (Inhibits E2F; transcription factor)
  • TP53 (Activates P21 which is a cyclin dependent kinase inhibitor that slows down the cell cycle)
  • CDKN2A (P16)
31
Q

Which tumor supressor gene that inhibits hypoxia inducible factor 1a

A

VHL

32
Q

Which tumor supressor gene encodes a transcription factor that regulates urogenital development?

A

WT1

33
Q

Tumor suppressor gene that is a major antagonist of PI3K activity

A

PTEN (phosphatase and tensin homolog) negatively regulates the Pi3k/AKT pathway

34
Q

Tumor supressor gene that codes for Hamartin protein and Tuberin protein respectively

A

TSC1 and TSC 2

35
Q

Tumor supressor gene that codes Ras GTPase activating protein

A

NF1 (Neurofibromin)

36
Q

Negative regulator of B-catenin/WNT pathway

A

APC

37
Q

Carcinogens that cause hepatocellular carcinoma

A
  1. Aflatoxins (aspergillus)

2. Ethanol

38
Q

Carcinogens that cause angiosarcoma

A 
Vinyl chloride (pipes, plumbers)
Arsenic (Herbicides, metal smelting;iron)

Angiosarcoma: cancer that forms in the lining of blood vessels or lymph vessels. Common sites; skin, scalp, neck. Most common occupational association: Vineyard workers (arsenic) and plumbers (vinyl chloride)

39
Q

Carcinogens causing lung cancer

A
  1. Radon (airborne radioactive gas that accumulates in basements)
  2. Asbestos (Old roofing material, shipyard workers)
  3. Arsenic (Herbicides, metal smelting;iron)
40
Q

Cancer caused by radiation exposure from medical imaging equipment, Gamma rays, UV light

A

Papillary thyroid carcinoma (exposure to ionizing radiation)

41
Q

Most carcinomas spread through lymphatics with the exception of these four that spread via hematogenous route.

A

Follicular thyroid carcinoma, Choriocarcinoma, Renal Cell Carcinoma, Hepatocellular Carcinoma.

42
Q

Phases of wound healing

A
  1. inflammatory- up to 3 days after wound
  2. Proliferative - 3 days to weeks
  3. Remodeling- 1 week to more than 6 months.
43
Q

Cells and characteristics most likely seen in day 1 of wound healing

A

Cells: Platelets, neutrophils, macrophage

Characteristics:
1. Clot formation

  1. Migration of neutrophils to site of injury (step 4 of leukocyte extravasation)
  2. Macrophage clear debris 2 days later
44
Q

Cells and characteristics in proliferative (growth of new tissue) phase of wound healing

A

Cells: Fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophage

Characteristics:

  1. Clot lyses and is replaced by Granulation tissue
  2. Collagen type 3
  3. Epithelialization ( to form a barrier between wound and environment)
  4. angiogenesis
  5. wound contraction (mediated by myofibroblasts)
45
Q

Cells and characteristics seen in Remodeling/ maturation phase of wound healing.

A

Cells: Fibroblasts

Characteristics:

  1. Collagen 1 (replaces collagen 3 increasing tensile strength)
  2. Collagenases (require zinc to function) break down collagen 3
    - No zinc = no collagenases = collagen 3 doesn’t break down = delayed wound healing and decreased tensile strength.
46
Q

Part of kidney most susceptible to ischemia

A

Medulla

  1. Straight part of proximal tubule
  2. Thick ascending limb

usmle (15 decks)

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