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MHD I > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What does necrotic tissue look like under the microscope?

A
  • eosinophilia (cells stain bright pink)
  • pyknosis (nuclear shrinking + basophilia)
  • karyorrhesis (fragmentation of pyknotic nucleus)
  • karyolysis (loss of some DNA)
  • nuclei are lost
  • cell fragmentation
  • high neutrophil recruitment
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2
Q

Coagulation necrosis

A
  • associated w/ severe ischemia - best appreciated in solid organs - ghost-like remnants of intact cells w/o nuclei
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3
Q

Liquefactive necrosis

A
  • associated w/ bacterial infections and BRAIN ISCHEMIA - bacteria release enzymes which cause abscess (collections of pus)
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4
Q

Caseous necrosis

A

Associated w/ granuloma (dead cells in center of granulomatous cell reaction [multi-nucleated, giant “angry” macrophages])

Necrotic tissue is white/ friable, resembling cheese curds

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5
Q

Enzymatic fat necrosis

A
  • associated w/ focal death in pancreas/ adjacent fat cells (acute pancreatitis) - enzymes from damaged cells digest adipose cells - fatty acids combine w/ Ca2+ forming yellow/white insolable soaps
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6
Q

Gangrene

A
  • coagulative necrosis of the bowel, gall bladder or an extremity - wet = w/ infection (+liquefactive); dry = w/out infection
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7
Q

What type of cells dominate in acute inflammation? In chronic inflammation?

A
  • neutrophils - macrophages
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8
Q

Chemotaxis

A
  • unidirectional movement of leukocytes along a chemical gradient, towards an injury site - key for transmigration
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9
Q

Local clinical manifestations of inflammation

A

Rubor, Calor, Dolor and Tumor

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10
Q

Key interleukin of acute inflammation

A

IL-8; produced by innate immune cells; stimulates bone marrow to increase maturation, proliferation and release of PMNs.

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11
Q

Myeloperoxidase

A

Major enzyme in a granule that is used as a killing mechanism by leukocytes use at injury site.

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12
Q

Scale of severity for acute inflammation

A

SEROUS- least severe [aka transudate] –> pressure w/o endothelial opening (fluid leak only) FIBRONOUS- intermediate SUPPURATIVE/ABSCESS- most severe [aka exudate] –> hydrostatic pressure + endothelial opening (fluid + protein leakage) ULCERATIVE- special category

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13
Q

Left shift

A

When neutrophil populations shift to more immature precursors because the body is trying to quickly pump out neutrophils (as opposed to giving them time to mature). Indicates infection/inflammation.

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14
Q

NETS

A

PMN chromatin laden w/ granules, used to trap bacteria and fungi

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15
Q

Characteristics of chronic inflammation

A
  1. predominance of M1s, lymphocytes and plasma cells 2. collateral tissue damage 3. repair processes occurring in parallel w/ persistent inflammation
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16
Q

Chronic high levels of inflammatory cytokines cause…

A

(1) Increased rates of hepatic production of defense proteins (2) Increased hepcidin production (which thereby decreases Fe2+ in blood leading to anemia) (3) Increased growth factor for platelets and monocytes

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17
Q

Granulomatous Inflammation

A

Distinct form of chronic inflammation associated with persistent T-cell activation. Seen with TB, macrophage ingestion of foreign bodies and sarcoidosis/IBD.

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18
Q

Acute phase reactants

A

Biochemical changes which are the reflection of hepatic protein adjustments to inflammation (ex. decreased albumin as liver increases formation of defense proteins)

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19
Q

C-reactive protein

A

Liver produced factor closely linked to IL-6 levels which can be used to indirectly assess intensity of inflammation. Obesity can give a false positive.

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20
Q

Cell classifications

A

(1) LABILE- continuously divide [skin epithelium, gut, hematopoietic] (2) STABLE- divide when stimulated [ex. liver] (3) PERMANENT- non-dividing [cardiac, neural, skeletal]

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21
Q

Granulation tissue

A

IMMATURE PRE-SCAR Specialized tissue that fills defects in organs when non-regenerative cells or connective tissue framework is destroyed. Proliferative fibroblasts lay immature connective tissue elements.

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22
Q

Organization

A

MATURE SCAR The process of transforming granulation tissue into dense scar

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23
Q

Important cells of skin lac healing

A
  1. macrophages- remove debris
  2. fibroblasts- produce matrix
  3. myofibroblasts- contract wound
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24
Q

Hyperemia vs Congestion

A

HYPEREMIA: Active process of arteriolar dilatation and increased blood flow. Tissue appears redder. CONGESTION: Passive process of impaired outflow of venous blood from a tissue. Tissue appears “red-blue” color.

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25
Q

Hemostasis

A

A series of regulated processes that maintain blood in a liquid state and prevents uncontrolled bleeding.

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26
Q

Virchow’s Triad in Thrombosis

A
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27
Q

Types of Embolism

A
  1. Fragments of thrombi
  2. Amniotic fluid (enters placental membranes)
  3. Air (gas)
  4. Fat/marrow (soft tissue crush injury/ long bone injury)
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28
Q

What does protein C deficiency do?

A

Deficiency in protein C causes a hypercoagulative state because protein C is a zymogen whose active form works to counter different coagulative factors.

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29
Q

The 2 basic components of all neoplasias (benign and malignant)

A
  1. PARENCHYMA- the actual neoplastic cells
  2. ​STROMA- supporting cells (connective tissue, blood vessels, immune cells, etc.)
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30
Q

Teratoma

A

Rare tumors which contain cells from multiple germ layer origins

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31
Q

Mixed tumors

A

Cells which come from one germ layer but can diverge to multiple cell types (ex. salivary gland capable of epithelial and myoepitheial differentiation)

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32
Q

Key cell morphology of benign neoplasms

A

Cells can range from well differentiated to dysplastic. Never penetrate the basement membrane.

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33
Q

Dysplasia

A

Disorderly architecture of a neoplasm. Altered cell cytology. No penetration of the basement membrane. Often occurs in metaplastic epithelium. Reversible. Full thickness dysplasia → Carcinoma In-situ

34
Q

Cell morphology of malignant neoplasms

A
  1. Vary from differentiated to anaplastic
  2. Pleimorphic
  3. Abnormal nuclear morphology (high N/C ratio; hyperchromatic; prominent nuclei)
35
Q

Anaplasia

A

Cells that have changed so they don’t look like they did originally. Loss of differentiation.

36
Q

Pleimorphism

A

Variation in size and shape of cells or their nuclei

37
Q

Lymphatic spread is typical of what type malignant neoplasms?

A

Carcinomas

38
Q

Hematogenous spread is typical of what type of malignant neoplasm?

A

Sarcomas

39
Q

p53

A
  • Key cell regulator that puts a stop to cyclins (the workhorses driving the cell cycle) when there is an issue in the replication or DNA of a cell.
  • ​Most commonly mutated gene in cancers
40
Q

RAS

A
  • Most common proto-oncogene in human tumors
  • Normal active RAS stimulates downstream regulators of proliferation
  • Mutant RAS loses ability to be turned off so it is constantly sending signals to cyclins, pushing through the cell cycle.
41
Q

Li-Fraumemi Syndrome

A

Pts inherit one defective p53 so it only takes knocking out one more to cause cancer. 25x risk of cancer by age 5.

42
Q

What does Rb normally do?

A

It normally guards the transition from G1 to S via E2F

43
Q

Key anti-apoptotic genes

A

BCL-2; BCL-XL

44
Q

Key pro-apoptotic genes

A

BAX, BAK (Intrinsic); Fas death receptor (extrinsic)

45
Q

E-cadherins

A

Mediate adhesion of epithelial cells. Functional loss facilitates detachment of cells from primary tumor and use of collaganse to break through basement membrane, allowing for metastasis.

46
Q

Key inhibitors and inducers of angiogenesis

A

​INDUCER: ​VEGF

INHIBITOR: TSP-1

47
Q

Two main types of carcinogens and examples

A
  1. Direct acting require no metabolic conversion; carcinogenic by themselves (ex. alkylating agents)
  2. Indirect acting ​require metabolic conversion; partially genetics based (ex. cigarette smoke)
48
Q

Principles of radiation carcinogenesis

A
  • long latent period
  • radiation initiation is irreversible
  • continue exposure is additive
49
Q

HTLV-1

A

Virus which infects T-cells, causing polyclonal proliferation and neutralizing growth inhibitory signals. Can lead to T-cell leukemia/lymphoma.

50
Q

Methods used by neoplasms to avoid immune surveillence

A
  1. Failing to express HLA class I and escaping CTL attack
  2. Eliminating strongly immunogenic subloclones
  3. Suppressing host immune response (ex. expressing FasL, thereby inducing immune cell apoptosis)
  4. Producing a thicker coat of glycocalyx molecules, thereby blocking access to immune cells.
51
Q

Cancer cachexia

A

Loss of body fat, lean body mass, weakness, anorexia and anemia. Mediated by neoplasia produced cytokines.

52
Q

Paraneoplastic syndrome

A

Symptom complexes notreadily explained by local or distant spread of neoplasms. (ex. ACTH secretion by small cell lung carcinoma)

53
Q

Important tumor associated markers

A

AFP→ liver carcinomas, gonadal tissues

CEA → Colon, pancreas, lung, stomach, breast carcinomas

Both used for surveillance, not primary diagnosis

54
Q

Grading of Cancer

A

Based on cytologic differentiation of tumor. Estimates agressiveness based on degree of differentiation, pleomorphism, loss of normal architecture and mitotic index.

Well differentiated= low grade; poorly differentiated= high grade

Most clinically useful for prostate cancer and chondrosarcoma

55
Q

Staging of Cancer

A

The most clinical valuable way to assess cancer progression (except for with prostate cancer and chondrosarcomas).

Based on size (T1-4) , spread to LN’s (N0-3), and metastasis (M0 or 1).

TNM system stages 0-IV

56
Q

What is the relationship between hypoxia, sodium and cell damage?

Hypoxia and calcium?

A

Hypoxia means that there will be no O2​ to be used to accept electrons so you will lack ATP. ATP is needed to fuel the Na+/K+ pump. W/o this pump, Na+ will build up within the cell and water will follow, causing swelling and cell damage.

THe calcium pump is fueled by the same ATP mechanism causing calcium build-up and causing calcium to activate enzymes which it normally wouldn’t, causing cell damage.

57
Q

Key hallmark of reversible cell injury?

A

Cellular swelling (loss of microvilli, membrane blebbing, swollen RER, etc.)

58
Q

Key hallmark of irreversible cell injury?

A

Membrane damage

59
Q

The 3 components found in granulation tissue

A
  1. Capillaries (brings nutrients)
  2. Fibroblasts (secretes collagen– type III collagen is intially secreted and later is converted to type I when mature scar is formed)
  3. Myofibroblasts (contracts wound)
60
Q

What is the cofactor collagenase uses when removing type III collagen and replacing it with type I during scarring?

A

Zinc

61
Q

Dehissance

A

When a closed wound reopens

62
Q

What type of collagen characterizes a keloid?

A

Type III collagen

63
Q

Lactate and Cell Injury

A

A loss of ATP during hypoxic cell injury causes the cells to switch to anaerobic cell respiration (due to the lack of ATP needed for aerobic). Anaerobic cell respiration leads to a build-up of lactate and a state of metabollic acidosis as a result.

64
Q

Reperfusion and free radicals

A

The rush of blood to site of ischemia during reperfusion can lead to the production of oxygen derived free radicals. This, paradoxically, can lead to further cell injury.

65
Q

Acidophilic bodies are often a sign of what type of cell?

A

Apoptotic

66
Q

Inflammasome

A
  • Formed from DAMPS/PAMPS
  • Multi-protein complex defined by activation of caspase 1
  • ​​Cleavage of IL-1 to active form sets the inflammatory cytokines in action
67
Q

What is one of the key factors in making capillaries leaky during inflammation?

A

Damaged tissues release histamineS

68
Q

What are the 2 types of necrosis associated with the pancreas?

A

Liquefactive necrosis (when the pancreas breaks itself down with its own enzymes) and enzymatic fat necrosis (when pancreatic enzymes break down surrounding fat)

69
Q

Key mediator of apoptosis

A

Caspases (enzymes)

They activate proteases (break down cytoskeleton) and endonucleases (break down DNA)

70
Q

Cytochrome C and apoptosis

A

Cytochrome C activates caspases, thus turning on apoptosis. Normally Cytochrome C is trapped in mitochondria and held there by Bcl2 which is stabilizing the mitochondria.​ Bcl2 is knocked out when there is so stimulus which will result in apoptosis (DNA damage, hormone changes, etc.), allowing for caspases to leak out.

71
Q

Hemotoxylin

A

Basic dye which binds to acids (like DNA)

72
Q

Eosin

A

Acidic dye which binds bright pink to proteins (like those found in cytoplasm)

73
Q
A

Gram Stain

Stains bacteria

background yellow/ positive purple and pink

74
Q
A

Periodic acid-Schiff (PAS)

Stains fungi and glycogen

background light pink/ positive magenta

75
Q
A

Grocott methenamine silver stain (GMS)

stains fungi

background green/ postive black

76
Q
A

Acid Fast

Stains mycobacteria, actinomyces

background blue/ positive red

77
Q
A

IHC

Immunohistochemical stain

Antibodies combine with enzyme and produce a color when bound to certain antigens

Background negative blue/ positive brown and red

78
Q

Steps to neutrophil entering interstitial space

A
  1. Marginalization
  2. Rolling
  3. Adhesion
  4. Transmigration
79
Q

Key cytokines for ending inflammation

A

IL-10, TGF-B

80
Q

Sarcoma vs Carcinoma

A

S: Malagnancy of mesenchymal tissue (ex. bone, cartilage, fat etc.)

C: Epithelial tissue (breasts, lung, stomach, etc.)

MHD I (3 decks)

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