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Pathophysiology > Sections 1-4 > Flashcards

Sections 1-4 Flashcards

1
Q

The process where DNA is converted into RNA

A

Transcription

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2
Q

The process where RNA is converted into DNA

A

Translation

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3
Q

What is the end product of glycolysis

A

pyruvate

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4
Q

How many Na+ move out of the cell, and how many K move into the cell with the sodium/potassium pump?

A

3; 2

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5
Q

Glucose–>glycogen

A

glycogenesis

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6
Q

glycogen–>glucose

A

glycogenolysis

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7
Q

Proteins, fat–>glucose

A

gluconeogenesis

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8
Q

process by which a cell converts one kind of signal or stimulus (extracellular) into another [cellular responses]

A

signal transduction

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9
Q

T/F? Cardiomyocytes are terminal (cannot divide anymore)?

A

True

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10
Q

Mature cell type replaced by different mature cell type

A

Metaplasia

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11
Q

undifferentiated cells with variable nuclear and cell structure

A

anaplasia

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12
Q

Low oxygen to tissue

A

hypoxia

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13
Q

oxygen deprivation to tissue

A

ischemia

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14
Q

cell/tissue death from no oxygen

A

infarction

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15
Q

Piece of DNA at the end of a chromosome that is lost with each cell division

A

telomere

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16
Q

WBC granulocytes (3)

A

Neutrophils, basophils, eosinophils

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17
Q

WBC agranulocytes (2)

A

Monocytes, Lymphocytes

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18
Q

Neutrophils undergo

A

Phagocytosis

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19
Q

Basohpils undergo

A

histamine release

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20
Q

Eosinophils undergo

A

combat effect of histamine

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21
Q

Monocytes

A

can enter tissue to become macrophages

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22
Q

Lymphocytes

A

produce cytokines

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23
Q

Histamine

A

Vasodilation and increase capillary permeability

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24
Q

Bradykinin

A

vasodilation, pain, increase capillary permeability, and chemotaxis

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25
Q

Mediators of inflammation- released by damaged cells

A

leukotrienes, prostaglandins

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26
Q

Four cardinal signs of inflammation

A

redness (increased blood flow to area), warmth, swelling (increased fluid in interstitial space), pain (release of chemical mediators- bradykinin)

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27
Q

Systemic effects of inflammation

A

malaise, fatigue, headache, loss of appetite

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28
Q

Leukocytosis

A

Increase in WBCs, especially immature neutrophils

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29
Q

Where are glucocorticoids made?

A

adrenal cortex

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30
Q

Effects of glucocorticoids include

A

decrease capillary permeability, decrease # of mast cells and leukocytes, decrease immune response (immunosuppressant)

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31
Q

Adverse effects of glucocorticoids

A

decrease WBC’s (infection), increase tissue breakdown, delay healing, delay growth in children, retention of sodium and water (edema and high BP)

32
Q

Types of healing

A

Resolution
Regeneration
Replacement

33
Q

Resolution

A

minimal tissue damage

34
Q

Regeneration

A

damage tissue replaced with cells that are functional

35
Q

Replacement

A

functional tissue replaced by fibrous or scar tissue; loss of function

36
Q

Process in which lymphocytes are programmed to attack “non-self” cells to protect the body

A

Cell-mediated immunity

37
Q

Antigens

A

stimulate immune response (trigger production of matched antibodies; activate immune cells)

38
Q

MHC class I

A
  • present in all nucleated cells; endogenous

- tumor cells, virus infected cells, “self” antigen

39
Q

MHC class II

A

present on macrophages and some other immune cells; exogenous

40
Q

Immune cells develop and mature in

A

bone marrow (only matures in thymus)

41
Q

Macrophages

A
  • engulf foreign material
  • process foreign antigen (MHC class II)
  • display processed antigen on cell surface- presenting it to lymphocytes
  • secrete interleukins
42
Q

Lymphocytes

A

primary cells in immune response

43
Q

Types of Lymphocytes (3)

A

T cells, B cells, NK (natural killer)

44
Q

T lymphocytes

A

participate in cell-mediated immunity

45
Q

T lymphocytes subgroups

A
  • Cytotoxic (CD8+) -destroys cells
  • Helper T cells (CD4+)- secrete cytokines; activate and regulate all cells in the immune system
  • Suppressor T cells- suppress immune cells
  • Memory T cells- remember the antigen (fight off easier)
46
Q

B lymphocytes

A

humoral immunity; produces antibodies (immunoglobulins)

-become antibody producing plasma cells after exposure to antigen and with the help of helper T cells

47
Q

Most common antibody in blood

A

IgG

48
Q

Natural antibodies (ABO blood typing) and are prominent in early immune response

A

IgM

49
Q

Immunoglobulin in secretions (tears, saliva, mucus)

A

IgA

50
Q

Allergic response immunoglobulin (results in inflammation)

A

IgE

51
Q

Antibody attaches to B cells and needed for B cell maturation

A

IgD

52
Q

Type 1 hypersensitivity

A

allergic reactions; development of IgE’s

  • complications: anaphylaxis, decreased bp, edema, hypoxia
  • ex: asthma, eczema, rhinitis
53
Q

Type II hypersensitivity

A
  • antibody-mediated cytotoxic hypersensitivity
  • IgG’s react with antigen
  • ex: response to incompatible blood transfusion
54
Q

Type III hypersensitivity

A
  • immune complex mediated hypersensitivity
  • antigen combines with antibody and is deposited into tissue (attract neutrophils that degranulate and destroy tissue)
  • ex: RA, glomerulornephritis
55
Q

Type IV hypersensitivity

A
  • cell mediated or delayed
  • destruction of antigen, inflammatory response
  • ex: latex, contact dermititis
56
Q

How do bacteria divide?

A

binary fission

57
Q

Gram +

A

purple stain; color binds to thick peptidoglycan

  • NO outer membrane
  • penicillin only affects gram +
58
Q

Gram -

A

pink stain; thin layer of peptidoglycan

-outer membrane layer present

59
Q

exotoxins

A

produced by gram + bacteria usually; secreted by host cell and released into the body’s fluids

60
Q

endotoxins

A

present in cell wall of gram - bacteria and released when bacteria die

61
Q

reverse transcriptase

A

RNA to DNA

62
Q

pathogenicity

A

Ability of microbe to cause disease (non-pathogen can become pathogen)

63
Q

Virulence

A

degree of pathogenicity

64
Q

Septicemia

A

bacteria reproducing and circulating in bloodstream

65
Q

leukopenia

A

decrease in WBC (viral infection present)

66
Q

Increase in neutrophils is seen in acute or chronic infections?

A

acute

67
Q

Increase in lymphocytes and monocytes seen in acute or chronic infections?

A

chronic

68
Q

decrease rate of reproduction of bacteria

A

bacteriostatic

69
Q

adverse effects of radiation

A 
decreased leukocytes (infection)
decreased erthryocytes (anemia, fatigue)
decreased platelets (excessive bleeding)
70
Q

keratoses

A

harmless benign lesions usually associated with aging and skin damage
-seborrhic or acitinic

71
Q

ABCD of melanoma

A

increase in area
change in border
change in color
increase in diameter

72
Q

hydrostatic pressure

A

filtration: determined by pressure of fluid

moves from higher to lower pressure

73
Q

osmotic pressure

A

osmosis: determined by protein/electrolyte balance

- moves from lower to higher concentration of SOLUTES

74
Q

Amount of fluid filtered across a semi-permeable membrane is proportional to net filtration pressure

A

Starling’s Law

75
Q

Four Starling Law forces

A

1) hydrostatic pressure in capillary
2) hydrostatic pressure in interstitium
3) osmotic pressure in capillary
4) osmotic pressure in interstitium

Pathophysiology (9 decks)

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