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OMS 1 > Molecular Medicine Exam Block 5 > Flashcards

Molecular Medicine Exam Block 5 Flashcards

1
Q

empiric therapy

A

dont know exact microbe

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2
Q

definitive therapy

A

culture returned and organism identified

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3
Q

determining which antibiotic to use utilizes

A

pharmokinetics

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4
Q

selective toxicity

A

must kill organism without damaging host

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5
Q

classification by

A

biochemical pathway and structure

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6
Q

prophylaxis

A

treat patients not yet infected

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7
Q

preemptive therapy

A

early targeted therapy in high risk patients who are asymptomatic but infected

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8
Q

suppressive therapy

A

initial disease controlled, therapy continued at lower dose

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9
Q

prokaryotic targets

A

inhibit cell wall synthesis
interfere with cell membrane function
disrupt ribosomal function reversibly (bacteriostatic) or irreversibly (bacteriocidal)
inhibit nucleic acid metabolism
block enzymes

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10
Q

minimum inhibitory concentration

A

lowest concentration that prevents visible growth after 18-24 hours

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11
Q

bactericidal concentration

A

concentration that kills organism

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12
Q

inoculum effect

A

efficacy decreases with increased bacterial density

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13
Q

inhibitory receptors (coinhibitors)

A

CTLA4 - recognize B7 1/2 on APC, role in suppressive function of regulatory T cells
PD1 - recognize PD-L 1/2
induced in activated T cells and terminate response

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14
Q

activation of CD8 cells

A

by class 1 MHC peptides
requires costimulator and helper T cells
requires cytosolic agent from 1 cell to be crossed with dendritic cell
differentiation into cytotoxic T lymphocytes and memory cells may require concomitant activation of CD4 helper T cells

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15
Q

CD4 helper T cells differentiate into 3 subsets of effector cells that produce distinct cytokines

A

TH1 produces IFN gamma
TH2 produces IL4/5/13
TH17 produces IL21

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16
Q

antibodies use what to to bind and block harmful effects of microbes and toxins

A

antigen binding Fab region

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17
Q

antibodies use what to activate diverse effector mechanisms that eliminate microbes and toxins

A

Fc regions

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18
Q

opsonization

A

antibodies coat microbes and promote ingestion by phagocytes
IgG1/3 Fc region binds to receptor (Fc gamme RI or CD64) expressed on neutrophils and macrophages

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19
Q

NK cells bind to antibody coated cells and destroy them

A

NK cells express Fc gamma receptor which is a NK cell activating receptor

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20
Q

mucosal immunity

A

IgA produced, transported across epithelia, bind and neutralize microbes in lumen of mucosal organs
B1 cell produces IgA in response to nonprotein antigens without T cell help

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21
Q

adaptation

A

cell changes to enable it to cope with excess stress

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22
Q

injury

A

if cell unable to adapt to stress
reversible - injurous agent removed and cell reverts to normal
irreversible - cell wont revert to normal and death innevitable

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23
Q

response to cell injury

A

death - apoptosis/necrosis, end or irreversible inury
atrophy, hypertrophy, hyperplasia, hypoplasia, aplasia, metaplasia, dysplasia

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24
Q

atrophy

A

decrease size of organ because decrease size of cells and number of cells
increase protein degradation and decrease protein synthesis
physiologic - embryologic structures, uterus after birth
pathalogic - decreased workload, lass of innervation or blood supply, no nutrition, aging

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25
Q

hypertrophy

A

increase cell size so increase organ size
increase protein production or organelles

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26
Q

hyperplasia

A

increase cell number so increase size of organ
hormonal - increase functional capacity of tissue under hormones
compensatory - increase tissue mass after damage or resection

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27
Q

hypoplasia

A

incomplete development of organ

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28
Q

aplasia

A

lack of development of organ

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29
Q

metaplasia

A

reversiible change in one adult cell type replaced by another (can lead to dysplasia)

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30
Q

dysplasia

A

abnormal increase in immature cells with decrease in number and location of mature cells
loss of uniformity of individual cells and organization
reversible or precedes development of cancer

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31
Q

hypoxia

A

decrease in oxygen delivery to tissue

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32
Q

morphological changes in reversible injury

A

cell swelling, fatty change, membrane blubbing/loss of microvilli, organelle swelling, detached ribosomes from ER, eosinophilia, nuclear chromatin clumping

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33
Q

injurous agents and calcium

A

calcium enters cytosol and denatures proteins

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34
Q

free radical induced cell injury

A

oxygen derived free radicals

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35
Q

ischemic/hypoxic injury

A

reversible - decrease or loss of ATP, increase anaerobic glycolysis, increase lactic acid, decrease pH, decrease enzymes
irreversible - ATP generation permanently lost, membrane function disturbed, loss of phospholipids, loss of intracellular amino acids

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36
Q

free radical injury

A

injurous agents increase production of free radicals, lipid peroxidation of membranes, oxidative modification of proteins, DNA damage

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37
Q

chemical injury

A

direct toxicity, conversion to toxic metabolites

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38
Q

necrosis

A

changes in individual cells, changes in tissues
morphological changes that follow cell death
lysosomal enzymes enter cytoplasm and digest cell

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39
Q

necrosis cytoplasmic changes

A
  1. eosinophilia - denatured proteins bind easin
  2. hyalinization - cytoplasm glossy and homogenous
  3. vacuolization - enzymatic digestion of organelles
  4. calcification - deposition of calcium
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40
Q

necrosis nuclear changes

A
  1. pyknosis - nucleus shrinks and becomes darker blue
  2. karyorrhexis - nucleus undergoes fragmentation
  3. karyolysis - nucleus stains pale blue
    2 days after necrotic cell death nucleus disappears
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41
Q

necrotic tissue

A

mass of dead cells in same physical area
pattern - liquefactive, coagulative, ganguenous, caseous, fat, fibrinoid

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42
Q

liquefactive necrosis

A

cell disappears due to digestion and destruction by hydrolytic enzymes from lysosomes or WBCs

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43
Q

coagulative necrosis

A

outlines of cells preserved , nucleus disappears, denaturation of proteins predominates, cells dont autolyze
hypoxic death outside of CNS

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44
Q

gangrenous necrosis

A

portion of limb or entire limb losses blood supply and dies
starts as coagulative and can become liquefactive

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45
Q

caseous necrosis

A

tissue appears soft and cheesy, necrotic focus of lysed cells and debris surrounded by border of granulomatous inflammation

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46
Q

fat necrosis

A

area of trauma or in peripancreatic fat in pancreatitis, damage and breakdown of fat cells release free fatty acids

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47
Q

fibrinoid necrosis

A

in vasculitis or severe hypertension
vessel walls damaged, fibrin deposited, immune complexes deposited

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48
Q

apoptosis

A

nuclear chromatin condenses and aggregates against nuclear membrane, apoptic bodies bud off, no inflammatory response
mitochondrial path
death receptor

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49
Q

pyroptosis

A

proinflammatory programmed cell death, swelling of cells, loss of plasma membrane integrity, release of inflammatory mediators

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50
Q

ferroptosis

A

iron induced programmed cell death, excess iron produces free radicals, decreased GPX-4 activity leads to lipid peroxidation
neurodegenerative diseases`

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51
Q

necroptosis

A

hybrid
mediated by tumor necrosis factor
triggered by genetically programmed signal transduction, doesnt result in capsase independent programmed cell death
kinases - receptor interacting protein 1 and 3, ligation TNFR1 recruits RIP1 and 3 into multiprotein complexes that contain caspase 8

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52
Q

lipid accumulation

A

fatty changes and steatosis refer to abnormal accumulations of triglycerides in parynchemal cells

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53
Q

protein accumulation

A

round eosinopilic droplets in cytoplasm

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54
Q

exogenous pigments

A

from outside body, most common carbon

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55
Q

endogenous pigments

A

melanin, lipofusion, hemosiderin, bilirubin, contusion

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56
Q

pathalogic calcification

A

dystophic - in damaged and dying tissues, localized
metastatic - calcium deposited in normal tissues, serum levels increased, widespread

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57
Q

specific gravity

A

ratio weight of solution compared to weight of equal colume of water

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58
Q

hydrostatic pressure

A

pressure fluid exerts on walls of its container, drives fluid out of circulatory system

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59
Q

plasma oncotic pressure

A

large proteins cant cross capillary walls, pulls fluid into circulatory system

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60
Q

inflammation

A

reaction of vascularized tissue to injury
2 parts - vascular and cellular`

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61
Q

types of leukocytes

A

neutrophils, lymphocytes, eosinophils, monocytes, basophils

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62
Q

acute inflammation

A

vascular changes - vasodilation, increased permeability, stasis because loss of blood

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63
Q

edema

A

excessive fluid in tissue and body cavity
transudate - filtrate of plasma from increased hydropstatic pressure or decreased oncotic pressure, no increase in permiability
exudate - increase permiability, cell and chemical mediators, high protein content

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64
Q

acute inflammatory leukocytes

A

expected - adhesion and transmigration, chemotaxis, recognition and activation, phagocytosis and killing, termination
undesired - release of products and tissue injury, defect function

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65
Q

acute neutrophil arrival and function

A

margination, rolling, activation, firm adhesion, transmigration, chemotaxis, phagocytosis

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66
Q

leukocyte activation

A

stimulation to produce response

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67
Q

phagocytosis

A

recognition and attachment, engulfment, killing and degradation

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68
Q

chemical mediators of inflammation

A

originate from plasma or cells
those from plasma circulate in precursor form and must be activated
cellular can be preformed and immediately available
most bind specific receptors on target cells
released mediators can bind other mediators
can act on one cell target or variety of types
short lives
most can have harmful effects

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69
Q

aarachedonic aci d metabolism

A

cyclooxygenase path produces prostoglandins which cause pain and fever
lipoxygenase path generates leukotrines and lipoxins

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70
Q

cytokines

A

proteins produced by cells that mediate and regulate immune and imflammatory reactions

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71
Q

chemokines

A

type of cytokine, small proteins that are primarily chemoattractants for leukocytes

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72
Q

plasma proteins

A

factor XII of clotting system activated by contact with injured tissue
kinin cascade produces bradykinin and kallikrein
clotting cascade produces thrombin
complement produces cleavage products
fibrinolytic paths produce plasmin

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73
Q

termination

A

mediators short lived, active mechanisms stop process

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74
Q

chronic inflammation

A

prolonged duration, inflammation by mononuclear cells, tissue destruction, healing by fibrosis, can result in granulomatous inflammation
cells - macrophages, B lymphocytes, plasma cells, eosinophils, mast cells cause granulomas and sometimes necrosis

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75
Q

outcomes of inflammation

A

resolution, abcess formation, healing

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76
Q

systemic effects of inflammation

A

fever, produce acute phase proteins, leukocytes, leukopenia, sepsis

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77
Q

hypersensitivity

A

failure of immune sysstem, reactions unwarranted and harmful to host, immune response responsible for inducction of disease, requires sensitization and antigen specific, classified by Gell and Coombs

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78
Q

type 1 hypersensitivity

A

immediate, IgE

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79
Q

type 2 hypersensitivity

A

cytotoxic, IgG and IgM

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80
Q

type 3 hypersensitivity

A

immune complexes, IgG and IgM

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81
Q

type 4 hypersensitivity

A

delayed, T cells (48 hours)

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82
Q

characteristics of hypersensitivity

A

first contact no symptoms, reexposure elicits reaction, reaction highly specific, reexposure increases or decreases severity of reaction

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83
Q

type 1 hypersensitivity

A

all hallmarks of normal immune response, secretion of IgE from plasma cells distinguishes it
IgE binds FcR on mast cells/basophils, coated cells sensitized, future allergen cross link sensitized cells and cause degranulation releasing pharmacologically active mediators, normal 0.1-0.4, severe allergic greater than 1

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84
Q

common allergens

A

small proteins, dried up particles, rehydrated on inhalation and presented by APCs to Th cells, development of Th2 response and increased IgE

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85
Q

primary reactions result of increased IgE and degranulation

A

prestored in granules with immediate short lived effects - histamine, heparin, TNF alpha, proteases, degradative enzymes, inflammatory mediators

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86
Q

histamine

A

binds histamine receptor (H1,2,3)
H1 on endothelial cells and blood vessels (increase permeability, constrict airway, increase mucous secretion)

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87
Q

secondary mediators

A

IL4, platelet activating factor, prostoglandins/leukotrienes, effects after primary and lasts longer

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88
Q

mast cell mediators

A

histatmine - smooth muscle contraction and increased vascular permiability
heparin - anticoagulant
eosinophil chemotactic factor A - chemotactic
prostoglandin D2, E2, F2alpha - increase smooth muscle contraction and vascular permeability
leukotriene C4, D4, E4 (lipooxygenase path) - increase smooth muscle contraction and vasular permiability
leukotriene B4 - chemotactic for neutrophils

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89
Q

system anaphylaxis

A

allergen enters blood and activates mast cells increasing vascular permeability and smooth muscle contraction

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90
Q

organ specific anaphylaxis

A

allergen effects target organ

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91
Q

systemic anaphylaxis

A

allergens - penicillin, insect stings, peanuts and brazil nuts
treatment - rapid administration of epinephrine

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92
Q

urticaria and hives

A

allergen activates mast cells on skin, most common cause insect bites
atopic dermatitis - increase IgE and allergies

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93
Q

type 2 hypersensitivity

A

antibodies binding cells or tissues
IgM
local complement activation, influx of leukocytes

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94
Q

type 3 hypersensitivity

A

immune complex mediated destruction of tissues
high levels of circulating immune complexes (IgG/M), systemic, deposit in tissues and activate complement, neutrophils try to remove causeing degranulation and tissue damage

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95
Q

type 4 hypersensitivity

A

Tcell mediated, takes 24-48 hours, Th1 response develops
can be activated by CD4 T cell cytotoxic production, direct killing of cells by cytotoxic CD8 T cells
celiac disease - Th CD4 T cell cytotokine secretion
poison ivy - CD4 and CD8 T cells because MHC class 1 and 2

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96
Q

tolerance

A

failure to amount an immune response to an antigen
when tolerance fails - autoimmune disease, hypersensitivity reactions, miscarriages

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97
Q

immunogens

A

antigens that induce an immune response

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98
Q

tolerogens

A

antigens that induce tolerance

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99
Q

central tolerance

A

T cells - in thymus, self reacting T cells eliminated by negative selection, strongly recognized antigen in thymus drives negative selection, some differentiate into Treg cells
defect in AIRE gene lead to autoimmune disease
Bcells - in bone marrow, self reactive B cells apoptosis or reedit receptor

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100
Q

peripheral tolerance

A

secondary lymphoid tissue, self reactive T and B cells apoptosis, anergy can render self reactice T/B cells unresponsive to future antigen presentation, Tregs circulate periphery and suppress immune responses
T cells - anergy, suppression, deletion

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101
Q

T cell suppression

A

CTLA4 binds B7 and removes it, PD1 blocks activation and TCR/MHC and B7/CD28
Tregs limit autoreactive cells, express CD25 (IL2 receptor), FoxP3 key transcription factor

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102
Q

T cell regulation by IL2 cytokines

A

stimulate T cell proliferation, inhibit immune response by maintaining functional regulatory T cells

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103
Q

Tregs

A

produce inhibitory cytokines (IL10, TGF beta)
express CTLA4 and consume IL2

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104
Q

T cell apoptosis

A

recognition of MHC/antigen T cell leaks proapoptic proteins (if costimulated and growth factors IL2 present this is countered by prosurvial proteins)
recognition of self antigen may increase death cell receptors and ligands (Fas receptor and FasL ligand)

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105
Q

B cell peripheral tolerance

A

anergy, suppression, deletion
without engagement CD4 T cells the B cells anergy or apoptosis
B cells have inhibitory receptors to inactivate and induce death by FcgammaRIIb, PD1

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106
Q

immune privilege

A

ability to tolerate antigens without eliciting inflammatory immune response

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107
Q

autoimmunity

A

failure of tolerance process
principle factors - genetics, environment triggers, trauma
microchimerism by mother/fetus, blood transfusion, organ transplant, twin to twin utero
environmental influences - infections break tolerance, molecular mimicry, alteration of self antigens, breakdown of antigen sequestration

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108
Q

rheumatic fever

A

complication of strep, production of cress reactive antibodies against protein M, difficult to generate response against it because of molecular mimicry

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109
Q

lupus

A

inflammatory immune disorder, fever/joint pain/rash

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110
Q

myasthenia gravis

A

autoantibodies agains Ach receptors on motor end plates of muscles
visual problems, muscle fatigue and weakness, weakness of neck and limbs

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111
Q

multiple sclerosis

A

autoreactive T cells from inflammatory lesions along myelin sheaths

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112
Q

extra cellular matrix

A

many componenets, form bulk of CT, basal lamina special form, hydration important for density and deformability of matrixf

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113
Q

function of ECM

A

provide structure and support, limits movement and migration, barrier to microorganisms and large molecules, damage leads to movement of things not normally mobile in matrix

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114
Q

collagen

A

in loose CT, bone, tendons, skin, vessels, cornea
triple helix structure
hydroxyproline for H bonds stability in helix, hyroxylysine for cross linking helices together

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115
Q

lack of vitamin C

A

less stability of collage and tissues

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116
Q

cross linking reactions for peptide fibril backbone

A

schiff base crosslinking of 2 allysine residues (generated by lysyl oxidase)
2 allysine residues (generated by lysyl oxidase) react by aldol condensation to lysinonorleucine

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117
Q

collagen 4

A

build mesh (important in basement membranes and basal lamina), globular domains at C termini make dimer, amino termini aggregate creating 7S domain

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118
Q

osteogenesis imperfecta

A

defect in collagen synthesis, blue sclera/brittle bone disease
sometimes collagen itself, maybe mutation at lysine
collagen mutations generally show type of dominant negative effect
processing of amino acid defects due to enzyme deficiencies more likely to be recessive

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119
Q

elastin

A

elastic fibers in smooth muscles, endothelium, near chondrocytes and fibroblasts
allow vessels to deform, lungs to expand
alternating hydrophobic and hydrophilic domains in protein

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120
Q

laminin

A

3 polypeptides in cross configuration
globular domains at N terminal then rigid coils, disulfide bond links cells, only alpha chain has C erminal that binds ECM, various combos of alpha beta gamma
most abundant in basal laminae ofter collagen, binds to ECM molecules and cell integrins, provide stability
defects lead to junctional epidermolysis bullosa

121
Q

proteoglycans

A

fibrous structural proteins embedded in gels (hyaluronic acid core with branching proteinscovered in glycosaminoglycans

122
Q

glycosaminoglycans

A

repeating disaccharides with 1 sugar N acetyl glucosamine or glycosamine, other acidic (glucuronic or iduronic acid)
sugars modified with sulfate added from PAPs

123
Q

proteoglycan linkage

A

GAGs added on serine/threonine residues, trimer of xylose and 2 galactose molecules link GAG to AA, GAG added to linker, repeat units added
addition of normal or modified sugar
modifications made to growing chain
sulfate added to existing chain sugars

124
Q

forming matrix

A

link proteins bing hyaluronic acid to proteoglycans with noncovalent bonds
negative charges bind positive ions or H bonds to H2O forming a hydrated gel

125
Q

proteoglycans bind fibronectin

A

fibronectin binds integrins in cell membranes and collagen fibrils, cells attach to matrix components

126
Q

cartilage

A

high number of negative charges attract cations (high osmotic pressure) water drawn in, tension balances swelling at equilibrium

127
Q

matrix lifecycle

A

components synthesized and degraded, near cells are less organized, intracellular matrix more organized, synovial fluid has smaller components

128
Q

matrix degradation

A

components taken up by endocytosis, endosomes from lysosomes, lysosomal hydroxylases break down ECM

129
Q

integrins

A

transmembrane proteins connect matrix and cytoskeleton, signals pass in either direction, composed of 18 and 10 beta subunits, some cells have inducible integrins

130
Q

matrix metalloproteinases (MMPs)

A

contain zinc, degrade all ECM proteins
important for migration and remodeling, can release growth factors
synthesized with propeptide containing cysteine blocking active site, removal necessary for activation
highly regulated, one method control of TIMP expression (tissue inhibitors of metalloproteinases)

131
Q

developmental genetics basics

A

many cell types due to differential gene expression

132
Q

types of genetic mediators

A

paracrine signaling, DNA transcription factors, ECM proteins

133
Q

paracrine signaling

A

secreted into intercellular space, diffuse to nearby cells
4 major families - fibroblast growth factor, hedgehog proteins, wingless family, transforming growth factor
need receptors, binding can change gene expression

134
Q

FGFR3 mutations

A

dwarfism
normally expressed in resting chondrocytes restraining chondrocyte proliferation and differentiation
most common dysplasia is achondroplasia activity inhibiting chondrocyte growth
milder form is hypochondroplasia

135
Q

transcription factors

A

find DNA and activate or repress gene expression, usually multiple targets
many families - homeobox, high mobility group HMG, T box family

136
Q

SOX family

A

prototype gene Sry - sex determining region fo Y
sox 9 regulates chondrogenesis, mutations cause comptomelic dysplasia
hirschprung neural crest defect - enteric neurons dont develop properly, sporadic and familial causes, sox 10 is one of several genes causing phenotype

137
Q

ECM mutations

A

type 1 collagen - osteogenesis imperfecta, bone formation disrupted
fibrillin 1 - marfan syndrome
elastin - supravulvar aortic stenosis
LAMC 2 - junctional epidermolysis bullosa

138
Q

pattern formation

A

established in developing organisms

139
Q

SHH

A

important in axis specification, induction of motor neurons, limb patterning
garlin syndrome - nevoid basal cell carcinoma syndrome - defect in tumor suppressor patched

140
Q

gastrulation

A

day 14-28 embryo becomes trilaminar, cell migration critical

141
Q

axis specification

A

patterning along AP axis bc HOX genes

142
Q

dorsal ventral axis

A

established before first cell division in fertilized embryo
noggin and chordin are dorsalizing signals
Bmp4 ventralizing signal
noggin and chordin bind Bmp4 preventing binding to receptor

143
Q

left right axis

A

defects random or reversed, most common zinc finger patterning of cerebellum (ZIC3 mutation)

144
Q

limb development

A

Fgf8 candidate for inductive signal, mediated by Fgf10 expression in mesoderm, Wnt2b and Wat8c maintain Fgf10 expression

145
Q

limb growth signals

A

proximal/distal stimulated by FGF2/4/8
zone of polarizing activity utilizes SHH to maintain apical epidermal ridge
ZPA signals positional info along proximal/distal axis

146
Q

limb defects

A

anterior - holt oram syndrome
posterior - ulnar mammary syndrome

147
Q

organs

A

beta cells require IPF1 to express insulin

148
Q

modes of aquisition for specific immunity

A

natural - passive is placental transfer, active is recovery from disease
artificial - passive is antiserum for rabies and tetanus, active is immunization

149
Q

passive immunizations

A

preformed antibodies transferred to recipient
no memory response
immediate protection

150
Q

active immunization

A

elicit protective immunity and immunologic memory

151
Q

attenuated vaccines

A

organisms cant cause disease but still grows in host, mimics natural infection

152
Q

inactivated vaccines

A

kill pathogen, critical to maintain structure of epitopes on surface antigens during inactivation, requires boosters, humoral response predominantly

153
Q

purified macromolecules

A

capsular polysaccharide, inactivated toxins, recombinant surface antigens

154
Q

polysaccharide vaccines

A

virulence factor of many organisms is polysaccharide, inability to activate Th

155
Q

conjugated polysaccharide vaccines

A

polysaccharide conjugated to protein antigen, changes immune system to T cell dependent, increase immunogenicity in infants, antibody booster response to multiple doses

156
Q

toxoid vaccines

A

exotoxins, entitoxoid antibodies bind toxin and neutralize effects, difficult to make in high quantities

157
Q

recombinant antigen vaccines

A

gene for immunologic protein isolated and cloned, induces humoral immunity

158
Q

mRNA vaccines

A

make proteins to trigger immune response

159
Q

live injected vaccines

A

coverage after first dose, second dose ensures seroconversion

160
Q

inactivated vaccines

A

not protected by first dose, may not be until second or third, antibody titer wanes over the years

161
Q

adverse reactions

A

local - common with inactive vaccines
systemic - common with whole cell/live attenuated vaccines
allergic - due to vaccine or vaccine component

162
Q

immunosuppressed

A

never get live attenuated vaccine

163
Q

cardinal features of inflammation

A

rubor, tumor, calor, dalor, functo laesa

164
Q

tissue damage

A

due to inflammatory or non inflammatory process

165
Q

healing

A

regeneration or scarring

166
Q

repair

A

synonym for healing or only means scarring

167
Q

regeneration

A

replacement of injured cells with healthy cells

168
Q

scarring

A

replacement of injured cells with fibrous connective tissue

169
Q

factors impairing tissue repair

A

persistent infection, diabetes, malnutrition, corticosteroids, mechanical factors, poor blood flow, foreign bodies

170
Q

cells of body divided into 3 groups

A

labile, stable, permanent

171
Q

labile cells

A

short G0, continually dividing

172
Q

stable cells

A

low level of replication, prolonged G0, reenter cell cycle under certain conditions

173
Q

permanent cells

A

left cell cycle, cannot undergo mitosis

174
Q

healing by regeneration IF

A

labile/stable cells, area must contain some surviving cells, CT intact
scarring in tissues unable to regenerate

175
Q

healing by scarring

A

inflammation, form new blood vessels, migration/proliferation fibroblasts, deposition/agragation of fibrous tissue

176
Q

growth factors

A

polypeptides, promote or inhibit cell proliferation

177
Q

events for repair by scarring

A

fibroblasts and vascular endothelial cells proliferate, formation of granulation tissue, remodeling

178
Q

granulation tissues

A

newly formed small vessels
edematous, synthesize collagen type 3, admixed inflammatory cells, myofibroblast proliferation

179
Q

remodeling

A

amount of collagen and ECM proteins increase, fibroblasts and vascularity decrease

180
Q

cutaneous wound healing

A

hemostasis, inflammation, proliferation, collagen accumulates and vascularity decreases, connective tissue formed

181
Q

stem cells

A

pluripotent, isolated from blastocysts, can be maintained undifferentiated or induced to differentiate

182
Q

adult stem cells

A

more restricted regeneration, generally lineage specific, located in niches

183
Q

beta lactam mechanism of antibacterial effect

A

bind beta lactam receptors, proteins have catalytic funtion which is inhibited by binding (bacteriostatic)
beta lactam activates autolysins of bacteria

184
Q

PBPs

A

transpeptiddases inhibited (catalyzes cross linking of murein) so synthesis of cell wall inhibited

185
Q

susceptibility to beta lactam depends on

A

constitution of outer layers of cell envelope antibiotic must cross and thickness of proteoglycan layer

186
Q

microbial resistance to beta lactam

A

acquired resistance - mainly extrachromosomal, mediated by plasmid
cross resistance among beta lactam sensitive penicillins
partial cross resistance among beta lactamase resistant penicillins and cephalosporins

187
Q

mechanisms of beta lactam resistanse

A

production of beta lactamase enzynes
develop PBPs wiht decreased affinity for antibiotic
decreased eprmeability of cell membrane
develop active efflux pump

188
Q

pharmokinetics of penecillin

A

absortption parental and oral
distribution - widespread
biotransformation variable
excretion - kidney
allergic reactions - highest with respiratory penicillins, lowest with oral, 1st and 2nd generations more cross reactivity so use a ceph, use alztreonam or macrolide

189
Q

cephalosporins

A

given after surgery
absorption - oral variable, parental very good
distribution - throughout body
biotransformation - variable
excretion - by kidney
adverse effects - hypersesitivity, thrombophlebitis, nephrotoxicity,

190
Q

monobactam

A

aerobic gram negative rods
IM/IV
allergic rections but major toxicity uncommon

191
Q

carbapenems

A

resistant to most betalactamases, parenteral, seizures and superinfections

192
Q

beta lactamase inhibitors

A

poor intrinsic antimicrobial activity
increase spectrum for beta lactam antibiotics against organisms producing beta lactamase

193
Q

non beta lactams

A

vancomycin
daptomycin’fosfomycin
colistin

194
Q

vancomycin

A

inhibits transglycosylate by binding D alamoyl D alanine of cell wall precursor

195
Q

daptomycin

A

depolarize cell membrane
pulmonary surfactant innactivates

196
Q

fasfomycin

A

inhibit bacterial cell wall synthesis, inhibits enolpyruvate transferase (bacteriacidal)

197
Q

colistins

A

cationic detergent

198
Q

neoplasia

A

new growth
abnormal, mass of tissue, growth exceeds and is uncoordinated with that of normal tissue, persists after cessation of inciting stimulus
genetic alterations passed down, clonal, excessive unregulated proliferation, altered differentiation of tumor cells, autonomous

199
Q

benign tumors

A

resemble normal tissues, function preserved, cannot metastasize

200
Q

malignant tumors

A

can metastasize, less differentiation and anaplastic, may be invasive

201
Q

benign leioyoma vs malignant leiomyosarcoma

A

benign leioyoma - small, well differentiated, slow growing, noninvasive, nonmetastatic
malignant leiomyosarcoma - large, poorly differentiated, rapidly growing, locally invasive, metastatic

202
Q

nomenclature

A

benign - end in oma
malignant - end in sarcoma or carcinoma
prefix based on origin

203
Q

acquired conditions predispose cancer

A

chronic inflammatory disorders, precursor lesions, immunodeficiency

204
Q

grading

A

varies with differentiation, relationship to growth rate, exact grade based on type of tumor

205
Q

staging denotes extent of diease

A

T - tumor size
N - nodal envolvement
M - metstases

206
Q

metastasis

A

genetic influence, stromal factors important
steps - loosening intracellular junctions, adherence to matrix proteins, degradation of matrix, locomotion, entry into circulation, travel to site, enter target organ, angiogenesis

207
Q

effects on host

A

local, hormonal production, cachexia

208
Q

treatment

A

depends on type, grade, stage
surgery, chemo, radiation, hormone therapy, immunotherapy

209
Q

fine needle aspiration

A

aspirating cells and attendant fluid with small bore needle
immunochemistry used to identify metastatic tumor

210
Q

tumor classification

A

carcinomas - epithelial tissue derived
sarcomas - CT derived
lymphomas - lymphatic tissue derived
gliomas - glial cells from nervous system
leukemias - hemotpoietic cells

211
Q

classes of cancer genes

A

oncogenes, tumor suppressors, DNA repair

212
Q

inherited cancer

A

defect in certain classes of genes, mutations can occur in germline, predisposed to cancer, all cells hace mutant gene, most loss of function mutation in tumor suppressor genes

213
Q

knudson two hit model

A

tumor requires mutations in both chromosomes so 2 mutations necessary

214
Q

identifying oncogenes

A

study of retroviruses, chromosomal rearrangement

215
Q

genomic instability

A

aneuploidy, translocations, DNA hypomethylation

216
Q

mapping cancer genes

A

array CGH, whole genome sequencing, STRs in linkage analysis, exome sequencing, GWAS

217
Q

loss of heterozygosity

A

missing markers, give probably gene locations

218
Q

refining

A

mutations in unrelated families examined, narrow the region with linkage studies, look for anomalies in region

219
Q

inherited TP53 mutation

A

rare Li-Fraumen syndrome
many tissues can show tumors, autosomal dominant, early age

220
Q

familial colon cancer

A

familial adencematous polyposis coli
hereditary nonpoluposis colon cancer
loss of both APC tumor suppressor genes
1. APC mutation
2. KRaas activation
3. TP53 mutations
4. other genes alteres

221
Q

HNPCC genes

A

1-5% colorectal cancers, autosomal dominant, causes other cancers
mutations in MSH 2 and 1

222
Q

breast cancer

A

BRCA 1 and 2
both repair double stranded DNA breaks

223
Q

melanoma

A

increased risk with affected relative
gain protooncogene CDK4
loss of function tumor suppressor gene CDKN2A

224
Q

many genes contribute to a trait

A

true for most quantitative traits
may show normal distribution (bell curve)

225
Q

threshold model

A

some diseases only present or absent, distribution not that of single genes
may be liability distribution - ends of curve effected (pyloric stenosis)

226
Q

recurrent risk

A

very complex, empirical risk derived

227
Q

specific indications

A

hard to distinguish from single gene with complicating factors
look for relative recurrent risk

228
Q

complex single gene traits

A

locus heterogeneity, background effects on major genes, many traits full into multiple categories

229
Q

twin pairs

A

concordant = both affected
discordant = 1 affected
heritability = 2(MZ-DZ)
adoption studies

230
Q

finding genes

A

some caused by genes, some caused by phenocopies
use population with affected and unaffected
perform genome scan
compare alleles at each locus with the trait
locate regions correlating with trait
screen region for candidate genes
alternate - affected sibling pair method, GWAS

231
Q

common multifactorial disorders

A

heart disease - coronary artery disease, athlerosclerosis
familial hypercholesterolemia - approximately doubles serum cholesterol, xanthomas, increases athlerosclerosis, autosomal dominant

232
Q

LDL receptor

A

binds LDL, LDL endocytosed, LDL delivered to lysosome where broken down
mutations -
1. no protein found
2. cannot leave ER, degraded
3. cannot bind LDL
4. do not migrate to coated pits
5. cannot dissociate from LDL, not recycled to cell surface
therapies - decrease intake of cholesterol or falts, bile acid binding resins, statins block cholesterol synthesis

233
Q

diabetes

A

type 1 - early onset, immune destruction of islet cells, no insulin, HLA DR314 mutation
type 2 - late onset (obesity), peripheral insulin resistance, TCF7L2, KCNJ11, PPAR gamma
MODY - intermediate onset, autosomal dominant, no obesity, glucokinase mutations or HNF 1 alpha/beta, HNF4 alpha, IPF 1 NEUROD2

234
Q

alzheimers

A

risk doubles if affected 1st degree relative
presenilin 1/2 and APP approximately 1/2 early onset cases
ApoE variations can increase risk

235
Q

clindamycin

A

not macrolide

236
Q

macrolides and tetracyclines good for

A

gram positive, nonvirulent gra negative, atypicals

237
Q

linezolid

A

potential serotonergic activity
2nd line for vancomycin

238
Q

2/3rd line drugs

A

linezolid, quinupristin/daflopristin, chloramphenizol, tigecycline

239
Q

MOA’s

A

50S ribosome - macrolides, clindamycin, linezolid, quinupristine/dalfopristin
30S ribosome - aminoglycosides, tetracyclines
all bacteriastatic except aminoglycides

240
Q

aminoglycosides

A

block initiation of translation and cause misreading of mRNA
streptomycin, gentamycin, tobramycin, neomycin, amikacin

241
Q

tetracyclines

A

block attachment of tRNA to ribosome
tetracycline, minocycline, doxycycline

242
Q

streptogramins

A

each interfere with distinct step of protein synthesis
quinupristin/dalfopristin

243
Q

macrolides

A

prevent continuation of protein synthesis
erythromycin, clarithromycin, azithromycin, telithromycin

244
Q

chloramphenicol

A

prevent peptide bonds from being formed

245
Q

lincosamides

A

prevent continuation of protein synthesis
clindamycin

246
Q

oxazolidinones

A

interfere with initiation of protein synthesis

247
Q

MOA aminoglycosides

A

penetration through cell envelope (passive diffusion via porin channels, active transport across inner membrane requires oxygen and alkaline), irreverisbly bind 30S and alter protein synthesis (interferes with initiation complex, block translation, misread mRNA)

248
Q

aminoglycosides

A

bactericidal, concentration dependent, post antibiotic effect
natural resistance - cell wall impermiable, anaerobic bacteria, lack receptor, plasmid production of transferase enzymes inactivated by adenylation/acetylation/phosphorylation
serious gram negative infections, synergistic with beta lactam (2nd line of defense)
IM/IV, kidney excretion
ototoxicity, nephrotoxicity, neuromuscular blockade

249
Q

spectromycin

A

like aminoglycosides but doesnt cause misreading of mRNA, bacteriastatic, IM only, for neisseria gonorrheam discontinued in US in 2001

250
Q

MOA macrolides, ketolides, lincosamides

A

antibacterial effect - bind 50S ribosome subunit, blockade of translocation, blockade of transpeptidation, bacteriostatic
resistance - plasmid encoded, increased activity of multidrug efflex pump

251
Q

macrolides

A

biliary excretion, some kidney
against gram positive and some nonvirulent gram negative
nausea, vomiting, diarrhea, acute cholestatic hepatitis, skin eruptions, fever
contraindications - QT prolongation

252
Q

clindamycin

A

50S ribosome, inhibits bacterial protein synthesis
diarrhea and colitis bc c difficile, nausea, vomiting
strep, staph, MRSA, good against anaerobes/bacteriodes

253
Q

tetracyclines/glycylcyclins

A

antibacterial effect - passive diffusion/active transport, bind 30S subunit and prevent tRNA binding
resistance - multidrug efflex pump

254
Q

tetracycline

A

absorption imparied by calcium cations, dairy products and antacids, excretion by kidney and bile, used against gram negative and positive and atypicals
effects - on microflora, bone/teeth growth inhibition or deformity, photosensitivity

255
Q

tigecycline

A

gram positive and negative
highly lipophilic, binds 30S and inhibits protein synthesis (bacteriostatic)
2/3rd line of defense

256
Q

chloramphenicol

A

reversibly bind 50S subunit inhibiting peptide formation (bacteriostatic)
used for bacterial meningitis and rickettsial disease
oral bioavailability, metabolized by liver
dose dependent toxicity, suppression of bone marrow, gray baby syndrome, aplastic anemia

257
Q

quinupristin/dalfopristin

A

50S blockade of translocation or conformation change (bactericidal)
hyper bilirubinemia, phlebitis
serious infections, not first line

258
Q

linezoid

A

bind 23S RNA of 50S subunit
myelosuppression
weak inhibition of MOA

259
Q

sulfonamides or trimethoprim alone

A

bacteriostatic

260
Q

sulfonamides and trimethoprim together

A

bactericidal

261
Q

sulfa drugs inhibit

A

dihydropteroate synthase

262
Q

trimethoprim inhibits

A

dihydrofolate reductase

263
Q

microbial resistance to sulfonamides

A

strep/steph/ecoli
increased production PABA, diminished sensitivity of dihydopteroate synthase, decrease permeability of cell wall to drug

264
Q

microbial resistance to trimethoprim

A

altered dihydrofolate reductase

265
Q

sulfonamides

A

acetylated in liver, excreted by kidney

266
Q

trimethoprim

A

100% oral absorption, distribute throughout body, biotransformation by liver about 35%, excreted by kidney

267
Q

adverse effects of sulfonamides

A

dose dependent toxicity, crystalluria, hemolytic/aplastic anemia, increased risk of kernicterus in newborns, allergic reactions, skin eruptions

268
Q

adverse effects trimethoprim

A

epigastric rash/nausea and vomiting, megoblastic anemia, rash/itching

269
Q

sulfonamide interactions

A

oral anticoagulants, sulfonylureas, phenyotoin, methotrexate, cyclosporine

270
Q

fluoroquinones

A

newer agents developed in 1990s
block topoisomerase 2 (DNA gyrase) and topisomerase 4
bacericidal, concentration dependent
microbial resistance - change in target enzyme, mutation decreases permiability of bacterium to drug
oral absorption impaired by cations, distributes throughout body, biotransformation by liver, excretion by kidney
gram positive and negative
adverse effects - cardiac arythmias, headache/dizziness/confusion/hallucinations
BBW - tendinitis, tendon rupture, photosensitivity

271
Q

metronidazole

A

form labile intermediates which inhibit DNA synthesis and damage DNA
anaerobic bacteria and protozoa
neurotoxicity, disulfiram like effects

272
Q

anaerobes

A

clindamycin used for those above the diaphram, metronidazole used for those below the diaphram

273
Q

fidaxomicin

A

inhibit RNA polymerase inhibiting protein synthesis (bactericidal), cofirst line for c diff, abdomineal pain/GI bleeding

274
Q

rifampin

A

antituberculosis

275
Q

nitrofurantoin

A

uncomplicated UTI

276
Q

cell growth and differentiation

A

growth factors and receptors, signal transduction pathways, transcription factors

277
Q

stages of cancer

A

start as single mutated cells, proliferate in situ, accumulates more mutations, inclusion of nearby tissue/blood vessels/lymphatics, small clusters and single cells migrate and metastasis

278
Q

cause of cancer

A

genetic aspects and environmental aspects

279
Q

chemical initiation

A

damage to DNA can change genes, mutations can be inherited at mitosis

280
Q

classes of cancer genes

A

oncogenes - enhance cell proliferation
tumor suppressor genes - normally control cell cycle and proliferation
DNA repari genes - help maintain integritiy of genome

281
Q

protoconcogenes

A

normally regulate cell cycle, modified or expressed inappropriately, stimulate cell division at inappropriate times
points - growth factor may be overexpressed or another molecule may bind receptor, receptor may signal without ligand, proteins may act without signal, G proteins may be active without GTP or lose GTPase, kinases active by themselves, TF active/overexpressed

282
Q

Ras path

A

monomeric G protein, activates Raf when GTP bound, Raf is MAP3K and activates MEP which activates MAP kinase which activates transcription factors

283
Q

cyclins in cell cycle

A

stimulate change from 1 stage to another, only made at certain stages, stimulate cyclin dependent kinases that are always present

284
Q

cyclin dependent kinases

A

only active when proper cyclin bound and have proper phosphorylation, inactivated by cyclin dependent kinase inhibitor proteins

285
Q

cell cycle checkpoint

A

Ras/Raf induce cyclin D which binds Cdk4/6, phosphorylates Rb and release E2F which enters nucleus and induces expression of genes for cell cycle progression

286
Q

RP53 gene

A

codes p53 protein, 50 tumor typers have mutations, loss of 17p in colon tumor cells, small deletions loclize to TP53 region, most mutations missense in DNA binding domain

287
Q

p53 function

A

CKI, inhibit cell cycle, DNA damage sensing, direct damaged cells undergo apoptosis, interacts with PTEN and BAX, specific carcinogens cause characteristic mutations in gene

288
Q

DNA damage and p53

A

p53 increases in response to mutagens, acts as TF for genes that repair damaged DNA, successful repair down regulates p53, stimulates Bax and IGF BP3 which blocks signaling

289
Q

tumor suppressors and Ras

A

Ras in hormon and growth factor signaling paths, GTPase activating proteins interefere with this, NF1 has loss of Ras

290
Q

combinations

A

tumor suppressors and oncogenes work together normally, patched is tumor suppressor and smoothened is protooncogene
tumor when patched looses function and smoothened gains function

291
Q

cadherins

A

mediate calcium dependent cell to cell adhesion, anchored by cadherins to actin incytoskeleton, loss of E cadherin can allow metastasis of tumor cells

292
Q

catenins dual function

A

affect gene transcription, beta catenin can enter nucleus as TF, degraded by complex including APC

293
Q

telomerase

A

maintain length and prevent senescence

294
Q

apoptosis

A

removes damaged cells

295
Q

caspases

A

cysteine proteases, cleave near aspartates, activates from zymogens by proteolysis, some are initiators which activate protecaspases (execution caspases)

296
Q

Bcl-2

A

apoptic and atiapoptic signals in cells, have Bcl-2 homology domains
3 types - anitapoptic, channel forming, proapoptic

297
Q

death receptor path

A

subset of TNF 1 receptors, trimer binds ligand, 2 procaspase molecules bind (initiators 8/10), autocatalytically cleave each other and become active, cleave procaspases 3,6,7 to activate execution ccaspases

298
Q

mitochondrial integrity path

A

induced by growth factor withdrawal/cell injury, cytochrome c released, bind Apaf 1 which binds/activates procaspase 9 forms apoptosome which cleaves procaspase 3/6/7 activating execution caspases

299
Q

cancer cells

A

resistant to apoptosis

OMS 1 (8 decks)

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