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FoCM > EOB > Flashcards

EOB Flashcards

1
Q

Sensitivity

A

TP/(TP + FN)

Probability test detects disease when disease is present

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2
Q

Specificity

A

TN/(TN+FP)

Probability test indicates no disease when disease isnt present

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3
Q

Positive predictive value

A

TP/(TP+FP)

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4
Q

Negative predictive value

A

TN/(TN+FN)

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5
Q

Conceptus

A

Product of fertilization

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6
Q

Primordium

A

Organ or tissue in early stages

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7
Q

Embryonic Period

A

Weeks 3-8

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8
Q

Fetal period

A

Weeks 8-38

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9
Q

Trimesters

A

Month 1-3, 4-6, 7-9

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10
Q

Blastocyst parts (3)

A

Inner cell mass (Embryoblast)
Outer cell mass (trophoblast)
Blastocyst cavity

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11
Q

Blastocyst arrival in uterus (week)

A

Week 1

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12
Q

Implantation

A

Fusion of Trophoblast and endometrial epithelium

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13
Q

Cytotrophoblast

A

Unfused trophoblast cells

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14
Q

Syncytiotrophoblast

A

Divided trophoblast cells that are fused into endometrial epithelium

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15
Q

hCG

A

Human chorionic gonadotropin

Secreted by Syncytiotophoblast –> prevents menstruation

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16
Q

Gastrulation (in general)

A

Week 3
Bilaminar germ disk –> trilaminar germ disk

Endoderm
Mesoderm
Ectoderm

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17
Q

Formation of endoderm

A

Epiblast cells migrate through primitive streak to replace hypoblast –> form endoderm

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18
Q

Mesoderm formation

A

Epiblast cells migration through primitive streak lie between endoderm and epiblast –> mesoderm

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19
Q

Ectoderm formation

A

Non migrating epiblast cells –> ectoderm

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20
Q

Ectoderm develops into..

A

EpidermisCNS

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21
Q

Endoderm develops into..

A

Inner lining of digestive and respiratory tracts

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22
Q

Mesoderm develops into..

A

Muscles, bones, blood, connective tissues, fat

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23
Q

Sacrococcygeal teratoma

A

Occurs when primitive streak cells persist

Tumors have a lot of tissues in them, teeth/hair

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24
Q

Caudal regression

A

Due to failure of mesoderm formation

Cranial structures normal, inferior structures underdeveloped

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25
Q

Locations without mesoderm after gastrulation

A

Cloacal membrane
Buccopharyngeal membrane
Tightly bound ecto and endoderm
Will form oral and uro-genital-digestive openings

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26
Q

3 mesoderm tissues

A

Paraxial mesoderm
Intermediate mesoderm
Lateral plate mesoderm

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27
Q

Formation of intraembryonic coelom

A

Lateral plate mesoderm splits into somatic and splanchnic mesoderm

Space in between is intraembryonoic coelom

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28
Q

Somatic mesoderm development –>

A

Body wall, conscious sensation and movement

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29
Q

Splanchnic mesoderm development –>

A

Visceral, unconscious sensation and movement

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30
Q

Intraembryonic coelom development –>

A

Body cavities

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31
Q

Molar pregnancy

A

Organism only develops placenta, no embryo

Villi swell and must be removed

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32
Q

Neurulation

A 
Week 4 (end of week 3)
Notocord induces ectoderm to thicken = neuroectoderm

Neuroectoderm folds, creates neural groove

Neuroectoderm fuses –> neural tube formed (filled with amniotic fluid)

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33
Q

Surface ectoderm after neurulation becomes…

A

Epidermis

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34
Q

Direction of neural tube closure

A

First in middle, then cranially and caudally

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35
Q

Closing of neural tube (week)

A

Near week 4 end

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36
Q

Neural crest

A

Forms when ectoderm cells break off from neural tube and neuroectodermLateral to neural tube

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37
Q

Neural crest develops..

A 
Neural cells that are outside of CNS
Schwann cells
dorsal root ganglion
Cranial nerve ganglion
Postganglionic neurons
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38
Q

Paraxial mesoderm condensation results in

A

Somitomeres –> Somites

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39
Q

Somites develop into..

A

Bone (migrates aroung notochord), muscle, dermis

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40
Q

Somite divides into 2 parts

A

Sclerotome (bone)Dermomyotome (muscle and dermis)

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41
Q

B cell development (total)

A

Stem cell –> Pro B –> Pre B –> Immature B –> Mature B

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42
Q

Pro B cell development

A

D-J rearrangements in H chain

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43
Q

Pre B cell development and Ig expression

A

V-D-J rearrangement in H chainCytoplasmic mu and pre B cell receptors

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44
Q

Immature B cell development and Ig expression

A

VJ rearrangement = Single functional light chain IgM expressed on surfaceas receptor (can’t be activated by antigen)

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45
Q

Mature B cell

A

IgM and IgD expressionCell exits bone marrow

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46
Q

Bruton’s X linked Agammaglobulinemia

A

Defect in btk genebtk gene product = pro B cell –> further developmentDefect = lack of humoral immunity (no B cells)No tonsils of papable lymph nodes

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47
Q

2 T cell types

A

Alpha-beta

Gamma-Delta

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48
Q

T cell marker on all T cells

A

CD3

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49
Q

T cell markers on alpha beta

A

CD4 or CD8

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50
Q

Activation of T cell (3 steps)

A 
Adhesion
Signal 1 (Antigen recognition)
Signal 2 (co-stimulation, B7-CD28)
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51
Q

Cell adhesion

A

Adhesion molecules help connect Tcell and APC
LFA-1/CAM-1
Transient connection

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52
Q

Antigen recognition and adhesion

A

TCR recognizes MHC/peptide –> Increased affinity of LFA-1

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53
Q

Leukocyte adhesion deficiency

A

Affects beta2 integrin subunit of LFA-1

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54
Q

Antigen recognition

A

TCR binding induces CD3 signal cascade

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55
Q

Costimulatory Signal

A

CD28-B7 (Most studied)
B7 on APC activated by microbes or innate immune response
Connect with CD28 on Tcell

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56
Q

B-cell activation by T cell (general overview)

A

B cell binds antigen –> Peptide derived and presented by MHC –> T helper cell recognizes

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57
Q

Helper T cell action after connected to B cell

A

CD40Ligand and cytokines expressed (bind to resective receptors) –> B cell activation and proliferation

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58
Q

Hapten

A 
Small non immunogenic molecule
Needs carrier (eg BSA) Carrier-hapten complex is immunogenic and Ig will react to hapten alone

ONLY AFTER COMPLEX IMMUNIZATION

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59
Q

IL-2

A

Made by activated T-cellsBinds (autocrine) to t-cells (IL-2R) and induces clonal expansion and differentiation

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60
Q

3 CD4 subsets

A

Th1, Th2, Th17

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61
Q

Th1 cytokine

A

IFN-gamma

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62
Q

IFN-gamma

A

Activates macrophages–> increased MHC expression, cytokine secretion, reactive O-, NO, lysosomal enzymes

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63
Q

IL-12 and Th1

A

IL12 secreted by innate immunity –> promotes Th1 responses

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64
Q

Th2 cytokines

A

IL-4 –> IgE responseIL-5 –> Eosinophil activationIL-10 –> Suppress Th1IL-13 –> Like IL-4, hypersensitivity

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65
Q

IL-4

A

IgE response

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66
Q

IL-5

A

Eosinophil activation

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67
Q

IL-10

A

Suppresses Th1

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68
Q

Th17 cytokines

A

IL-17AIL17-FIL-22

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69
Q

IL-17

A

Inflammatory diseasesNeutrophil action

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70
Q

CD8 activation (overview)

A

AdhesionAg recognitionCo-stimulationIL-2 (made by CD4 or CTL)

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71
Q

CTL mechanism of action

A

Initiates apoptosis pathway of cellReleases granules (perforins/granzymes) = apoptotic pathway

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72
Q

NK cells

A

Natural killer, kill cells without MHC-1Inhibitory receptor binds to MHC-1/peptide –> no destruction

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73
Q

ADCC

A

Antibody dependent cellular cytotoxicityNK’s bind to cells coated in IgG –> Kill cell

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74
Q

3 groups of genes involved in birth defects

A

Growth factor receptorsTranscription FactorsExtracellular matrix proteins

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75
Q

Anencephaly

A

Incomplete development of cranial neural tube –> exposed brain, undifferentiated

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76
Q

Myeloschisis

A

Incomplete development of the caudal neural tubeLumbar spinal cord that is undifferentiated and exposed

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77
Q

Spina bifida occulta

A

AsymptomaticUnfused vertebral arch but not huge opening

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78
Q

Meningocele

A

Only meninges protrude through defective non fused vertebral arch

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79
Q

Meningomyelocele

A

Neural tube breaks from ectoderm, herniates through defect

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80
Q

Phenytoin

A

AnticonvulsantTeratogen –> Fetal hydantoin syndromeHeart malformations, facial clefts, limb defectsMetabolized by phase 1 enzyme of epoxide hydrolase

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81
Q

Mercaptopurine

A

Metabolized by thiopurine methyltransferase (TPMT)

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82
Q

Pili

A

Protein projections on surface of bacteria (made of pilin)Major role in adherence, attach to receptors on host cellAntigenic, anti-phagocytic, variable

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83
Q

Spores

A

Small metabolically quiescent forms of bacteria, produced as survival mechanismCan withstand extreme environments

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84
Q

Exotoxin

A

Proteins that bind to host cell (B domain) and damage/kill host (A domain)

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85
Q

Diptheria toxin

A

Stops protein synthesisA domain ADP-ribosylates elongation factor 2 –> no protein synthesis

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86
Q

Cholera toxin

A

A domain ADP-ribosylates GTP binding protein, constant cAMP –> diarrhea

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87
Q

Tetanus and Botulinum toxins

A

Cleave vesicle fusion proteinsBlock neurotransmitter release

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88
Q

Bacterial endotoxins

A
  1. Integral to bacteria structure2. Composed of lipopolysaccharide3. Gram negative ONLY
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89
Q

Steps for microorganism infection

A
  1. Entry2. Spread3. Multiplication4. Transmission5. Pathology
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90
Q

TNF-alpha

A

Endogenous pyrogen (fever)Made by macrophageIncreases vascular permeability –> complement and increased fluid drainage to lymph nodes

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91
Q

Type 1 Interferon response

A

Induce resistance to viral replication (RNA and Protein synthesis level)Increase NK cell receptor ligandsActivate NK cellsInterferons released when cell is killed by virus, induces response in neighboring cells

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92
Q

HIV and chemokine relationship

A

HIV binds to chemokine receptors (CXCR4, CCR5)

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93
Q

Th1 pattern of cytokines =

A

Enhanced phagocytosis

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94
Q

Th2 pattern of cytokines

A

M2 or alternative pattern, wound healing

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95
Q

M2 macrophage

A

Wound repair, fibrosis

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96
Q

Superantigen

A

Activates T cellsBinds to MHC class 2 outside of peptide binding groove and Vbeta of TCR

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97
Q

High endothelial venules

A

Path of naive T cell trafficking to specific peripheral lymphoid tissueHoming based on specific homing receptors interacting with HEV receptors

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98
Q

Difference between fungi and human cells

A

Plasma membraneCell wall

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99
Q

Fungi cell wall

A

90% polysaccharides10% proteinsMannansGlucansChitin

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100
Q

Mannan

A

Mannose polymersAttached to surface proteins

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101
Q

Glucans

A

Glucose polymersStrength

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102
Q

Chitin

A

N-acetylglucosamine polymerStrength

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103
Q

Moulds

A

Form hyphae-Tube like structuresHyphae fusion = mycelium (colony)

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104
Q

Yeast

A

UnicellularBudding reproduction

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105
Q

Aflatoxin

A

Food contaminant

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106
Q

Fungi virulence/pathogenesis(steps)

A

AdherenceInvasionTissue damageHost evasion

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107
Q

Fungi adherence

A

Fungal surface proteins/carbohydrates bind human cell receptors

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108
Q

Invasion

A

Hyphal pathogens

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109
Q

Tissue damage

A

Degradative enzymes

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110
Q

Host evasion

A

Avoid recognitionEscape phagocytic killing

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111
Q

Superficial fungi

A

Environmentally acquired

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112
Q

Opportunistic fungi

A

Emerge in diseased hosts only

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113
Q

Pneumocystis jirovecci

A

Acquired by inhalation, but held in check by immune systemPneumocystis pneumonia in diseased patients

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114
Q

Systemic fungi

A

Infects healthy host Environmental transmission

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115
Q

Histoplasmosis

A

Found in caves, bat is the host

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116
Q

Antifungal innate immunity

A

PAMP’s recognized by PRR’s

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117
Q

Common fungal PAMP and human PRR

A

PAMP: Beta GlucanPRR: Dectin-1

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118
Q

Azoles

A

Block ergosterol synthesisFluconazoleVoriconazolePosaconazole

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119
Q

Allylamines

A

Block ergosterol synthesisTerbinafine (Lamisil)

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120
Q

Polyenes

A

Bind ergosterol (form pore)Higher toxicityAmphotericin BNystatin (topical)

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121
Q

Echinocandins

A

Block glucan synthesisCaspofunginAnidulofunginMicafungin

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122
Q

Pyrimidine Analogs

A

Block DNA/RNA synthesisFlucytosineRapid resistance, works in combo therapy

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123
Q

Fertilization (sperm)

A

Burrow through corona radiata and zona pellucidaEnzymes released from acrosome

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124
Q

Fertilization (oocyte)

A

Release cortical granules (confirmation change to prevent polyspermy)Finish meiosis IIBegin metabolism

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125
Q

Schistosoma mansoni

A

Flatworm infestation

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126
Q

Tapeworm (alternate name)

A

Cestode

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127
Q

Fluke (alternate name)

A

Trematode

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128
Q

Entamoeba Histolytica

A

Amebic parasite found in dirty water/foodOr Butt stuff

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129
Q

Ciliated or flagellate protozoan parasites more common?

A

Flagellate

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130
Q

Trichomonas vaginalis

A

Sexually transmitted flagellate protozoan

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131
Q

T cell development stages

A

Double negative –> Double positive –> +/-+/- in medulla of thymus

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132
Q

Transition from +/+

A

Recognition of MHC Class II = CDR-4+Recognition of MHC class I = CD-8+No recognition/too strong recognition = apoptosis

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133
Q

Cytokine signal transduction

A

JAK/STAT pathway

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134
Q

IL-2 and T cell affinity

A

Only activated T cells express Alpha unit of IL-2R and will respond to IL-2

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135
Q

Th2 defends host against…

A

Helminthic parasites

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136
Q

Th1 defends hosts against…

A

Foreign intracellular microbes

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137
Q

Th17 defends host against…

A

Extracellular bacteria/fungi

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138
Q

Pyrogens

A

TNF-alphaIL-1IL-6

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139
Q

Path of virus after entry into body

A

Taken up by APC (dendritic cell) –> Travel to lymphoid tissue

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140
Q

M1 phagocytosis

A

Microbe binds to phagocyte receptor –> Phagocyte membrane envelopes microbe –> Fuse with lysosome –> microbe killedTh1 cytokines

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141
Q

Positive sense RNA viruses

A

Virion RNA = mRNAImmediate translation

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142
Q

Negative sense RNA viruses

A

RNA is complementary to mRNA Need RNA dependent RNA polymerase packaged with it to transcribe then translate

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143
Q

Double stranded RNA viruses

A

RNA polymerase needed to make mRNA

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144
Q

Problem of monocistronic RNAs in human?

A

Humans only operate with single mRNA’sViruses translate singe mRNA and cleave product to make multiple proteins

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145
Q

Forces driving viral diversity

A

MutationSelectionReassortmentGenetic drift/founder effect

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146
Q

Immune escape

A

Gradual accumulation of mutations (genetic drift)

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147
Q

Productive infection

A

Cell has appropriate receptors and machinery for viral replication, production, and release

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148
Q

Null

A

Cell does not have appropriate receptors

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149
Q

Abortive

A

No virion formation after entryInsufficient DNA/RNA production or non infectious virions produced

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150
Q

Restrictive

A

Cell is transiently permissive, only few viruses producedNo more production but virus genome still present

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151
Q

Gram+ bacteria

A

Thick peptidoglycanTeichoic acid

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152
Q

Gram- bacteria

A

Outer membrane with LPS

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153
Q

LPS

A

LipopolysaccharideLipid A portion responsible for endotoxin activity

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154
Q

FluconazoleVoriconazolePosaconazole

A

AzoleBlock ergosterol synthesis

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155
Q

Terbinafine (Lamisil)

A

AllylamineBlocks ergosterol synthesis

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156
Q

Amphotericin B

A

PolyeneBinds ergosterol, forms pore

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157
Q

Nystatin

A

PolyeneBinds ergosterol, forms pore

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158
Q

CaspofunginAnidulofunginMicafungin

A

EchinocandinsBlock glucan synthase

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159
Q

Flucytosine

A

Pyrimadine analogBlock DNA/RNA synthesis

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160
Q

Giardia lamblia

A

Most common intestinal protozoan in USDiarrheaWater borne cysts

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161
Q

Chagas disease

A

Parasite that causes heart disease

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162
Q

Ascariasis

A

Infestation of ascaris lumbridoidesNematodeFecal-oral transmission of eggs in contaminated food

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163
Q

Percent of babies born with birth defect

A

3%120,000/year in US

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164
Q

Most common birth defect

A

Congenital heart defect1% of all births40,000 new cases per year

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165
Q

Cleft lip prevalence/incidence

A

P: 1/1000I: 7000 a year

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166
Q

Down’s syndrome prevalence/incidence

A

P: 1/1000I: 6000 a year

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167
Q

3 major components of embryonic development

A

Pattern formationAxis specificationOrganogenesis

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168
Q

FGFR3 diseases

A

HypochondroplasiaThanatophoric dysplasiaAchondroplasia

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169
Q

FGFR2 disease

A

Apert syndromeDigit fusion, face hypoplasia

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170
Q

Hirschsprung disease

A

P: 1/5000Lack of nerve cells in enteric tractRET oncogene mutation

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171
Q

Hox genes

A

Anterior/posterior axis

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172
Q

Situs inversus caused by…

A

DyneinPolycystin-2

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173
Q

Type I hypersensitivity

A

Immediate - IgEAntigen exposure –> Th2 activation –> IL-4 and IgE –> IgE + mast cells –> Release of mediators (After repeat exposure)

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174
Q

Histamine

A

Immediately released

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175
Q

Late phase (activated mast cell)

A

Release of prostaglandins and leukotrienesAnd Cytokines (TNF-a, IL-4, IL-5)

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176
Q

Type II hypersensitivity

A

Tissue/organ specificAntibody/antigen complex –> Complement activation –> inflammation and tissue injury (neutrophils, ROS)

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177
Q

Drug induced hemolytic anemia

A

Drug (hapten) binds to RBC –> induces pathway for hapten Ab generation –> Ab bind to RBC –> lysis or phagocytosis or complement activated phagocytosisOccurs when hapten binds to own cell

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178
Q

Grave’s disease

A

HyperthyroidismAntibodies bind to TSH receptor –> constitutive release of thyroid hormonesCan pass from mother to to child

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179
Q

Rheumatic fever

A

Group A Streptococcal pyogenesStreptococcal cell wall stimulates Ab response –> antibodies cross react with heart tissue antigens

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180
Q

Type III hypersensitivity

A

Soluble immune complex - systemicComplex becomes larger –> complement mediated recruitment of activation of inflammatory cells

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181
Q

Serum sickness - Type III hypersensitivity

A

Patients given bolus of foreign antibody (against specific disease eg. tetanus) –> antibodies made against antigen –> antigen:antibody complexes form –> type III hypersensitivity

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182
Q

Arthus reaction

A

Inject antigen –> antigen:antibody complexes form –> complement activation –> inflammation (neutrophil recruitment)

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183
Q

Systemic Lupus Erythematosus

A

Systemic auto immune disease (Type III hypersensitivity)Making antibodies against nuclear antigens –> Ag-Ab complexes –> Complement levels decrease –> kidneys affected

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184
Q

Type IV Hypersensitivity (DTH)

A

Antigen introduced –> Processed by APC –> Th1 recognition –> macrophage activation CD4 or CD8

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185
Q

Contact hypersensitivity

A

DTH

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186
Q

Active immunization

A

Immunized individual acquires immunity to specific antigen

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187
Q

Passive immunization

A

Preformed antibodies providing temporary protection

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188
Q

T independent antigen

A

Repeating epitopes that cross link Ig receptors on B cellsActivates B cell without use of T cellNo memory, no H chain switching, no affinity maturation

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189
Q

Conjugate vaccine

A

Add T-I antigen to carrier protein –> internalized and presented by B cell –> t cell activation –> B cell activation –> Ab secreted

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190
Q

Conjugate vaccine examples

A

Hib, PCV14, Meningococcal

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191
Q

4 methods of resistance

A

Enzymatic degradationAltered target Decreased uptakeIncreased efflux

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192
Q

Concentrated dependent killing

A

Higher concentration = more rapid, complete cell kill. Decreased resistance

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193
Q

Time dependent killing

A

Saturation of killing occurs at low multiples of MIC

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194
Q

Cell wall inhibitors

A

Beta-lactamsGlycopeptides

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195
Q

Cell membrane inhibitors

A

DaptomycinPolymyxins

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196
Q

Nucleic acid inhibitors

A

Fluoroquinolones

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197
Q

Protein Synthesis inhibitors

A

50S ribosome30S ribosome

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198
Q

Metabolic inhibitors

A

SulfonamidesTrimethoprin

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199
Q

Difference between Penicillins and cephalosporins

A

Cephalosporins have 6 membered ring, penicillins have 5 Cephalosporins have 2 R groups

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200
Q

Penicillin binding protein

A

Enzymes that catalyze last step of cell wall synthesis

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201
Q

PBP and Beta lactam

A

B-Lactam is structurally analagous to D-Ala-D-Ala –> react with PBP and create intermediate so cell wall is not fully synthesized

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202
Q

Beta lactamase

A

Breaks bond in Beta lactam ringMolecule disabled

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203
Q

Beta lactamase inhibitor

A

Binds to beta lactamase so it can’t functionExtends life of beta-lactam drug

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204
Q

Natural penicillin

A

Narrow spectrumStreptococci, treponemaPenicillin G, VK

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205
Q

Anti-staphylococcal

A

Narrow spectrumStaph-MSSA onlyHas beta-lactamses

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206
Q

Amino penicillins

A

Broad spectrum - Gram+ (not MRSA), some gram(-)Augmentin

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207
Q

Ureido penicillin

A

Piperacillin+tazobactamVery broad spectrum (enhanced gram- incl. Pseudomonas)

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208
Q

1st generation Cephalosporin

A

Narrow (Gram +)Staphylococci, streptococciCefazolinCephalexin

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209
Q

2nd generation Cephalosporins

A

Broader than 1st gen, includes anaerobes

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210
Q

3rd generation cephalosporin

A

Broad, enhanced gram-PseudomonasCeftriaxone - does not cover pseudomonas

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211
Q

4th generation cephalosporins

A

Very broad spectrumEnhanced gram(-), includes PseudomonasCefepime

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212
Q

5th generation cephalosporins

A

CeftarolineBroad spectrum, MRSA coverageBinds to altered target site on MRSA

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213
Q

Monobactams

A

Inhibits gram negatives onlyPoor PBP binding of gram+Penicillin allergies

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214
Q

Carbapenems

A

Stable to most Beta-lactamasesVery broad, used rarely to avoid resistance

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215
Q

Beta lactam adverse effects: Common

A

GI: Nausea/loose stoolsTaking drug for a while/high doses

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216
Q

Beta lactam uncommon/rare adverse effects

A

Uncommon: Hypersensitivity - Non IgE mediated rashRare: Hypersensitivity - anaphylaxis

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217
Q

Vancomycin

A

Large, tricyclic glycopeptideCell wall inhibitor - binds to D-ala-D-ala so it cant bind to PBPStep before Beta lactam

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218
Q

Vancomycin spectrum and target

A

Only active vs gram (+)Drug of choice for MRSAClinical resistance is low

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219
Q

Vancomycin ADME

A

A: Not absorbed orallyD: Does not cross BBBM: NegligibleE: KidneyMonitor drug concentration, keep 10-20ug/mL

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220
Q

Vancomycin toxicity

A
  1. Nephrotoxicity2. Red-man syndrome- Flushing, erythema, angioedema-Not IgE3. Ototoxicity
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221
Q

Daptomycin

A

Cell membrane inhibitorGram(+) via Ca dependent interaction w/membraneMRSA - Alternative to Vancomycin

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222
Q

Polymyxins

A

Binds with negative LPS –> permeability changes, leakage, cell deathGram(-)Last resort for MDR-organisms

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223
Q

Polymyxins Adverse Effects

A

NephrotoxicityNeurotoxicityTopical combination products are safe

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224
Q

Most common Fluoroquinolones

A

Ciprofloxacin (Cipro)Levofloxacin (Levaquin)Moxifloxacin (Avelox)Gemifloxacin (Factive)

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225
Q

FluoroquinoloneMoA, Spectrum, Resistance, PK/PD

A

MoA: Inhibit DNA gyrase and topoisomerase- blocks DNA replication, inhibit nucleic acid synthesisBroad spectrum: Gram +/-, atypicals, TBOral absorption

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226
Q

Fluoroquinolone adverse effects

A

GI: Loose stoolsCNS: HA, lightheadedness, nervousnessSkin: PhotosensitivityBoxed warning: Tendonitis/rupture, peripheral neuropathy, dysclycemiaNot good for children or prego chicks (unless benefit > risk)

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227
Q

50S ribosomal unit protein synth inhibitor

A

MacrolidesOxazolidinonesLincosamidesChloramphenicol

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228
Q

30S ribosomal unit protein synth inhibitor

A

AminoglycosidesTetracyclines: Doxycycline

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229
Q

Aminoglycoside/Tetracycline MoA

A

Bind to 30S ribosomePrevent binding of incoming charged tRNA

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230
Q

50S subunit drug MoA

A

Bind to 50S subunit and block peptide bond formation

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231
Q

Macrolides

A

Azithromycin (Zithromax)Inhibit protein synthesisBacteriostatic, time dependent killing, anti-inflammatoryLow level resistance (efflux pump)High level resistance (target site modification)Broad spectrum: Gram+, Neisseria, TreponemaChoice for atypicals

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232
Q

Macrolides clinical use

A

STI: Chlamydia, GonorrheaRTI: Pharyngitis, otitis, CAP

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233
Q

Macrolide adverse effects

A

GI (higher than most classes)May increase QTc interval

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234
Q

Erythromycin Drug interactions

A

P450 inhibitor

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235
Q

Oxazolidinones (Linezolid)

A

Inhibits protein synthesis at early stageNarrow spectrum: Gram+Alt for MRSA

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236
Q

Linezolid Adverse effects

A

GISkin rashesSerotonin syndrome: SSRI’s use blocked because MAO inhibition by drug

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237
Q

Lincosamide: Clindamycin

A

50S inhibitorBroad spectrum: Gram(+), anaerobes, toxoplasmaAdverse effects: Diarrhea, C.difficile colitisOlder drug

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238
Q

Chloramphenicol

A

50S binding –> block peptide bond formationBroad spectrum: Gram(+), (-) anaerobes

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239
Q

Chloramphenicol adverse effects

A

Reversible bone marrow suppressionAplastic anemiaGray baby syndrome

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240
Q

Aminoglycosides

A

Irreversible binding to 30S –> enzyme modificationSpectrum: Gram (-), synergistic activity with gram(+) cell wall agentsHigh dose, extended intervalRequire serum level monitoring

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241
Q

Aminoglycoside toxicity

A

Nephrotoxicity (5-25%)-5-7 daysOtotoxicity (1-5%)Neuromuscular blockade

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242
Q

Tetracycline

A

Doxycycline, tigecycline (MDR)Bind to 30S, block initiation complexBroad spectrum: Gram(+/-)

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243
Q

Tetracycline adverse effects

A

GIPhotosensitivityBad in children

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244
Q

Tetracycline drug interaction

A

Cations impair absorptionMay decrease effect of oral contraceptives

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245
Q

Sulfonamide

A

Folate inhibitorsUsed in combinationBlock purine production and nucleic acid synthesisBroad spectrum: Gram(+/-)

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246
Q

Nitrofurantoin

A

Inhibits several enzyme systems: Acetyl CoA –> inhibit metabolismGram(-) - E.coliBladder infectionsGI, rash, pulmonary

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247
Q

Guanosine analogs

A

AcyclovirValacyclovirFamciclovirChain termination (inhibits DNA chain elongation)Genital herpesValacyclovir = acyclovir prodrugFamciclovir: HIgher doses, less frequent

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248
Q

CMV antivirals

A

Ganciclovir: similar to acyclovirValganciclovir (Ganciclovir prodrug)

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249
Q

CMV antivirals adverse effects/drug interactions

A

GI, insomnia/confusion, rashBone marrow toxicity, mutagenic/embryotoxicityInteract with myelosuppressive agents, seizure potential

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250
Q

Foscarnet MoA, spectrum/use

A

Inhibits DNA polymerase - pyrophosphate analogCMV, Acyclovir resistant HSV

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251
Q

Foscarnet Adverse effects/interactions

A

NephrotoxicityBone marrow toxicityElectrolyte imbalance

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252
Q

Cidofovir

A

Cytosine nucleotide analogInhibits DNA polymeraseCMV, acyclovir resistant HSV

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253
Q

Cidofovir adverse effects

A

NephrotoxicityBone marrow toxicityCarcinogenic, mutagenic

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254
Q

Adamantanes

A

Influenza antiviralInhibit viral uncoatingInfluenza A only

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255
Q

Adamantanes ADR

A

CNS: dizzy, nervous, insomniaGITeratogenic, embryotoxic

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256
Q

Sialic acid analogs

A

Inhibit viral neuraminidase: clumping of virionsInfluenza A/B

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257
Q

Sialic acid analog ADR

A

Zanamivir: CoughOseltamivir: GIPeramivir: Skin

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258
Q

Fiber types

A

CollagenReticularElastic

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259
Q

Collagen properties

A

Tensile strength

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260
Q

Reticular fiber properties

A

Tensile strength

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261
Q

Elastic fiber properties

A

Resiliency

262
Q

Proteoglycan properties

A

Rigidity, porosity

263
Q

Mast cells

A

Granules contain bioactive substances: Histamine, leukotrienes, proteolycansSlow release of granule regulates innate immune responses

264
Q

Histamine

A

Causes bronchoconstriction by inducing contraction of smooth muscleTriggers vasodilation, lowers BP

265
Q

Epinephrine

A

Binds to adernergic receptorsSmooth muscle relaxation in airways, smooth muscle contraction

266
Q

Exposure

A

Contact with a microbe

267
Q

Infection

A

Acquisition by a hostSynonymous with disease

268
Q

Commensalism

A

Microbe that co-exists with host

269
Q

Mutualism

A

Host and microbe benefit

270
Q

Colonization

A

Microbe found in non sterile site without causing disease

271
Q

Latency

A

Microbe harbored without causing damage

272
Q

Disease

A

Clinical evidence that microbe is causing damage to host tissues

273
Q

Pathogen

A

Microbe that causes disease or damage to host

274
Q

Sepsis

A

Systemic response to an infectious agent - bacterial, viral fungal

275
Q

Sepsis clinical responses

A

Change in temperatureTachycardiaTachypneaAlteration in white blood cell count

276
Q

Sepsis mediators

A

ComplementCoagulation cascadePro-inflammatory mediatorsAnti- inflammatory mediators

277
Q

Sepsis benefits? White cells, Tachycardia, Tachypnea, fever

A

White cells combat infectionTachycardia increase COTachypnea increases ventilationFever inhibits microbial growth

278
Q

Septic shock

A

Sepsis and evidence of insufficient organ perfusion and oxygen delivery

279
Q

Treating sepsis

A

Lactate measurementBlood culturesBroad spectrum antibioticsFluid resuscitation

280
Q

Sepsis epidemiology

A

~750,000 cases in N. America~40,000 children30-35% mortality in adults, 10% in children19,000,000 cases worldwide

281
Q

Acute inflammation causes

A

Foreign intruderTissue necrosisTraumaImmune reactions

282
Q

Vascular reactions

A

VasodilationIncreased permeabilityVascular stasis

283
Q

Cellular reactions

A

ExtravasationChemotaxisActivationPhagocytosis

284
Q

Vasodilation

A

Arteriolar dilation –> hyperemia –> Rubor, calorRedness/heat

285
Q

Increased permeability

A

Endothelial gapsNeutrophil entry is easierEdema

286
Q

Vascular stasis

A

Slowed blood flow, more time for leukocytes to contact endothelial cells

287
Q

Extravasation

A

Roll, bind, squeeze through epitheliumRoll: SelectinsAdhesion: IntegrinsTransmigration: PCAM-1

288
Q

Chemotaxis

A

Respond via receptors, locomotion based on chemical gradient

289
Q

Activation

A

Increase defensive functions - more enzymes

290
Q

Phagocytosis

A

OpsinizationEngulfmentKilling/degradation

291
Q

Chronic inflammation

A

Prolonged durationMacrophages, lymphocytes, plasma cell

292
Q

Chronic inflammation causes

A

Acute inflammationPersistent infectionsProlonged irritationAutoimmunity

293
Q

Lymphocyte-Macrophage interaction

A

Activate macrophage –> TNF-a/IL-1 activates lymphocyte –> Activated lymphocyte IFN-gamma –> Macrophage activated

294
Q

Granulomatous inflammation

A

Special form of chronic inflammationEpithelioid macrophagesMyobacterium TB, histoplasmosa capsulatum, non infectious materials resistant to degradation

295
Q

Leukocytosis

A

Increase in leukocytesAccelerated release from marrowImmediate release of storage pools (Vasculature, spleen)

296
Q

C-Reactive Protein

A

Liver response to inflammation’Binds to damaged tissue and microbes, activates complement/pro-inflammatory cytokines

297
Q

Hematopoietic cells

A

Erythroid precursorsMegakaryocytesLymphocytesPlasma cellsMonocytes/macrophages

298
Q

Stromal cells

A

Fibroblasts/reticulinAdiposeOsteoclasts/blastsEndothelial cells

299
Q

Hematopoietic stem cell

A

MultipotentSelf renewalDifferentiation

300
Q

Simple squamos cells

A

Wider than tallFried egg appearance Allows materials to pass through

301
Q

Simple squamos examples

A

Endothelium - lining of blood/lymph vessels, heart cavitiesMesothelium - lining of serous cavities: Pericardium, peritoneum

302
Q

Simple cuboidal

A

Width = depth = heightPrevalent in secretory/absorption

303
Q

Simple cuboidal examlpes

A

Thyroid folliclesSmaller ducts/glandsGerminal epithelium of ovaryKidney ducts

304
Q

Simple columnar

A

Taller than wide, oval nucleus @ baseProtection and secretion

305
Q

Plain tall columnar

A

Mucosa of stomachSI, LIGall bladderBigger ducts of glands

306
Q

Ciliated Columnar

A

Cells with ciliaUterus and oviducts

307
Q

Pseudostratified columnar

A

All cells touch BM but do not reach surface

308
Q

Pseudostratified columnar w/motile cilia

A

Respiratory system: Nasal, larync, trachea, oviducts

309
Q

Pseudostratified columnar w/motile cilia and goblet cells

A

Respiratory system

310
Q

Goblet cells

A

Mucous secreting cells

311
Q

Pseudostratified columnar w/non motile cilia

A

Epididymis

312
Q

Pseudostratified columnar non ciliated

A

Ductus deferens

313
Q

Stratified squamos example

A

Skin, lining of cavities opening to skin: Mouth, vestibule of nose, anusMore than 1 layer

314
Q

Keratinzed stratified squamos

A

Protective layer of keratin formedEpidermis

315
Q

Non keratinzed stratified squamos

A

Mucous membraneMoist cavities

316
Q

Stratified cuboidal: Description and example

A

Secretion2 layers, top layer is definitively cuboidalSweat glands, large ducts

317
Q

Stratified columnar

A

RareLarge ducts of exocrine glandsBasal layer is cuboidal, apical surface is columnar

318
Q

Transitional

A

Lines excretory passages of urinary tractTransition form between stratified squamos and columnarSurface cells binucleate

319
Q

Bladder fill and transitional epithelium

A

Full bladder: Surface cells stretched - squamosEmpty: Cuboidal surface domelike

320
Q

Apical surface specialization

A

MicrovilliaCiliaSterocilia

321
Q

Lateral surface specialization

A

Intercellular junctions

322
Q

Basal surface specializations

A

Basement membraneJunctional specializations

323
Q

Microvilli

A

Fingerlike extensions from apical surface (1-2um)Core of actin filamentsBrush borderAbsorptive epithelium

324
Q

Terminal web

A

Horizontal web of actin, anchor microvilli

325
Q

Glycocalyx

A

Extracellular coat bound to plasmalemma of enterocyte microvillia

326
Q

Cilia

A

Long (5-10um) cytoplasmic extensionsNo actin core9+2 doublet formation of tubulin - axonemeFacilitate flow of fluid over epithelium

327
Q

Intraflagellar transport

A

Cargo molecules loaded at base –> Use kinesin to move up –> dynein to move down

328
Q

Primary cilia dyskinesia: Males

A

SterilityMale flagellum of sperm affected, cilia in testis

329
Q

Primary cilia dyskinesia: females

A

Cilia in oviducts affectedFertile but increased ectopic pregnancy

330
Q

Hydrocephalus internus

A

PCDEpendymal cells in ventricles play role in CSF circulationFluid accumulation in brain

331
Q

Stereocilia

A

Long, immotile, branched microvilliaMale reproductive tractInner ear sensory hair cells

332
Q

Zona occludens

A

Extends around entire perimeter of cell, apical area

333
Q

Tight junctions

A

Fused ridges of tightly packed transmembrane proteinsRapidly formed and disassembled Block lateral movement of lipids and membrane proteins

334
Q

Zonula adherens

A

Basal to zona occludensAdjacent plams membranes separated by 15-20nm gap, filled with plaque containing e-E-cadherin between

335
Q

Macula adherens/desmosomes

A

points of adhesion, 25-35nm separationCadherin within space, tonofilaments anchor within cell

336
Q

Clostridium perfringens and j(x) complexes

A

Attacks zona occludens J(x)Food poisoningDehydration

337
Q

Heliobacter pylori and j(x) complexes

A

Binds to extracellular domain of zonula occludens in stomach –> decrease tyrosine kinase signalingGastric ulcers, carcinomas

338
Q

Viruses and j(x) complexes

A

Attachment and endocytosis of reovirus to JAM protein of zonula occludens

339
Q

Parasites and j(x) complexes

A

Dust mitesCleave zonula occludens proteins, loss of barrier in lungs results in exposure and immune response

340
Q

Gap junctions (Nexus)

A

2-3nm separationDirect electrical and chemical communication

341
Q

Connexon

A

Bridge between nexus’

342
Q

Connexin 26

A

Inner ear - deafness

343
Q

Connexin 32

A

PNSDegenerative disease, charcot-marie-tooth

344
Q

Connexin 50

A

Congenital cataracts - blindness

345
Q

Basement Membrane

A

Thin sheet of extracellular material at basal surfaceSeparation of epithelial cell and CT

346
Q

Basal lamina

A

Extracellular supportive structure - only EMLamina lucidaLamina densa

347
Q

Hemidesmosome

A

Anchors intermediate filaments of cytoskeleton to BMHalf desmosome

348
Q

Lamina propria

A

Below BMSupport to epithelium

349
Q

Exocrine glands

A

Ducts opening to surface

350
Q

Endocrine

A

Release products into blood or lymph

351
Q

Merocrine/eccrine

A

Release of products with cell membrane intact - Exocytosis

352
Q

Apocrine

A

Part of cell membrane released (mammary glands)

353
Q

Holocrine

A

Bulk release of whole cell or cytoplasm (Sebaceous glands)

354
Q

Epithelial metaplasia

A

Reversible conversion of one mature cell to another typeAll epithelial

355
Q

Cardiac muscle nuclei location

356
Q

Skeletal muscle nuclei location

357
Q

Cardiac muscle histological description

A

More redCentral nucleiLots of cytoplasmBranching

358
Q

Skeletal muscle histological description

A

Nuclei in peripheryWide cellsStriations

359
Q

Smooth muscle histological description

A

Many evenly scattered nuclei

360
Q

Calcium signaling for muscle contraction

A

Ca increase –> Ca2+/Calmodulin complex activates Myosin light chain kinase –> activates myosin light chains –> Myosin light chain phosphatase removes phosphate from LC

361
Q

Difference between smooth and skeletal muscle contraction

A

Smooth muscles twist and can lockUse less energy

362
Q

Multiunit smooth muscle synaptic transmission

A

Each cell receives synapse

363
Q

Unitary (visceral) smooth muscle synaptic transmission

A

Few synapses, transmitted via gap junctions

364
Q

3 blood vessel wall components

A

Tunica intima: InsideTunica media: MiddleTunica adventitia: Outisde

365
Q

Tunica intima composition

A

Endothelial cells and loose connective tissue

366
Q

Tunica media composition

A

Smooth muscle

367
Q

Tunica Adventitia composition

A

Dense irregular connective tissue

368
Q

Vessels ranked by thickness: Highest to lowest

A

Artery&raquo_space; Vein&raquo_space; Lymphatic vessel

369
Q

Difference between artery and vein TM

A

Smooth muscle in Artery

370
Q

Capillaries composition

A

Endothelial cells and basement membraneNo smooth musclePinocytotic cellsTight junctions

371
Q

Continuous capillaries

A

Least permeable, endothelial cells have tight junctions and no fenestrations

372
Q

Fenestrated capillaries

A

More permeable, endothelial cells have tight junctions with fenestrations

373
Q

Functions of basal laminae

A

Structural supportBarrier or selective filterInfluences cell polarity and differentiationPromotes and guides cell migration

374
Q

Fibronectin

A

Connects fibroblasts1 geneBinding sites for many components (collagen, fibrin, cells)

375
Q

RGD

A

Cell binding domain of fibronectin

376
Q

Integrins

A

Protein on cells that bind to fibronectinAlpha/beta chainsSome have RGD receptorsTransmembrane signaling

377
Q

Integrin activation

A

Leukocyte rolling on endothelial cells –> reaches point with activating factors (site of infection) –> signaling cascade –> integrin in active confirmation

378
Q

Leukocyte Adhesion Deficiency

A

Lack of integrin Beta2

379
Q

LAD I

A

Structural defects in integrin

380
Q

LAD II

A

Absence of selectin ligand

381
Q

LAD III

A

Defects in integrin activation

382
Q

Brown fat location

A

CervicalSupraclavicularParavertebral

383
Q

White fat function

A

Energy storageInsulationCushioning

384
Q

Brown fat function

A

Heat regulation

385
Q

Brown fat heat generation

A

Uncoupling of respirationRich vascularization spreads heat

386
Q

Cushioning locations

A

Palm of handButtocksOrbit of eyeKidney

387
Q

Hematochezia

A

Passage of blood through the anus

388
Q

Melena

A

Black feces resulting from upper GI bleed/upstream colon

389
Q

Peri-partum hemorrhage

A

Childbirth bleed

390
Q

Gross hematuria

A

Blood in urine

391
Q

Hemo-pericardium

A

Blood in lung/heart

392
Q

Ecchymosis

A

Hematoma associated with skin or mucous membraneBruise

393
Q

Hemostasis trio of components

A
  1. Vasculature and hemodynamics2. Platelets3. Coagulation cascade
394
Q

Vascular response of hemostasis

A
  1. Vasoconstriction2. Endothelium: When broken, collagen interacts with blood, release vWF –> Platelet adhesion trigger3. Formation of platelet plug
395
Q

Fibrinogen

A

Links one platelet to another

396
Q

Coagulation Cascade

A

Create fibrin glue to support platelet plug until endothelium/matrix remodeling

397
Q

Virchow’s triad

A

Increase risk for thrombosisInjuryBlood flow: Stasis/turbulenceCoagulation pathway: hypercoagulability

398
Q

Congenital Atresia

A

Valve does not form

399
Q

Mass effect

A

Pregnancy or tumor squeezing veins

400
Q

Ischemia

401
Q

Infarct

A

Ischemic necrosis (Death of downstream tissues due to vessel narrowing) caused by artery occlusion

402
Q

Embolus

A

Detached mass carried by bloodThromboemboli most common

403
Q

Cardiogenic shock

A

Heart Pump failure

404
Q

Hypovolemic shock

A

Massive blood loss, fluid loss from burns

405
Q

Enterococcus faecalis

A

Gram positive CocciNormal flora in gutHighly resistant, including vancomycin

406
Q

Gram Positive Cocci

A

Strep. pyogenes (group A)Strep. pneumoniaeStrep. viridans (normal flora)Staph. aureusStaph epidermidis (normal flora)Group B beta-hemolytic strep: Strep. agalactiaeEnterococcus faecalis

407
Q

Central tolerance

A

Deletion of self reactive clones of lymphocytes - negative selection

408
Q

Peripheral tolerance

A

Lymphocyte interacts with antigen –> no subsequent response

409
Q

Clonal anergy

A

T cell recognize self antigen but no Co-stimulatory signalFunctional unresponsiveness

410
Q

Regulatory T cells

A

FoxP3, CD25 - markers for regulatory T-cellsInhibit T cell activationInhibit T cell effector functions

411
Q

Activation induced cell death

A

Apoptosis induced by apoptotic proteinsDeath ligands

412
Q

Receptor editing (B-cell)

A

New light chain rearrangement replacing original VL chain in B cell

413
Q

Molecular mimicry

A

Normal foreign antigen response cross reacts with self antigen(Rheumatic fever)

414
Q

Celiac disease HLA typing

A

95% DQ2DQ8Used for diagnostic exclusion

415
Q

Multiple Sclerosis

A

Autoimmune response against myelin sheath –> demyelinationAnimal model: EAETransfer disease to healthy animal –> recipient gets disease

416
Q

Insulin dependent diabetes mellitus

A

Insulitis in islet cells

417
Q

Rheumatoid factor

A

Autoantibodies against Fc portion of IgG

418
Q

X-linked agammaglobulinemiaBruton’s

A

Defect in btk gene, disrupted B cell developmentPro –> pre blocked

419
Q

Selective IgA deficiency

A

Deficiency in IgAAnaphylactoid rxn to blood transfusion

420
Q

Hyper IgM immunodeficiency

A

Lack of CD40L (t cell help)Elevated IgM and low/no class switching to other Ig’sX-linked

421
Q

CVID - Common variable immunodeficiency

A

Immunoglobulin deficiencyB cell and Ig deficiencyWide varietyRecurrent infectionLymphoproliferative diseasesAutoimmune cytopenias

422
Q

DiGeorge syndrome

A

Thymic aplasia: Thymus doesn’t form –> low T cell countHypocalcemia, congenital heart defects

423
Q

Gamma chain deficiency

A

SCID: Common gamma chain that is subunit of cytokine receptors (IL-2, 4, 7, 9, 15)T cell and NK cell deficiencyB cell intact (but T cell count affects B cell activation)

424
Q

Adenosine deaminase deficiency

A

SCID: Severe absence of T cell functionAccumulation of toxic product that kills T cellsT, B, and NK deficiency

425
Q

Bare lymphocyte syndrome (II)

A

SCID: Lack of MHC class II expression (transcription factor defect)No CD4+ cells –> B cells affected

426
Q

Tcell receptor Excision Circles

A

Circular genome that is lost during T cell gene rearrangement - should have large amount as child while making T cellsScreen for TREC to diagnose immunodeficiencies

427
Q

PAMPS

A

Pathogen associated molecular patterns

428
Q

DAMPS

A

Danger associated molecular patterns

429
Q

PRR

A

Pattern recognition receptorsCell surface & Intracellular

430
Q

Familial Mediterranean Fever

A

Autosomal recessiveFever and localized inflammation (skin, serosal membranes, joints)- Neutrophil infiltrationDay-weeksTypically resolve, risk of amyloidosis

431
Q

FMF Genetics

A

MEFV: Encodes pyrin4 functional domains

432
Q

PYRIN domain

A

Domain shared by multiple proteins involved in inflammation and apoptosisMember of intracellular PRR family- Sense microbial products –> pro-IL-1beta to active form (NALP3)

433
Q

NALP3 associated autoinflammatory syndromes

A

Mutation in NACHT domain of NALP3 = 3 autoinflammatory syndromesAutosomal dominant

434
Q

Familial Cold (Urticaria) Autoinflammatory syndrome

A

Urticaria 30min after cold exposure: IL-1 developmentFever, chill, malaise, joint stiffness, sweating, thirst

435
Q

Muckle-Wells syndrome

A

Short episodesTemp change as triggerUrticaria-like rash: achingSensory neural Hearing lossHigher risk of amyloidosis (25% in N.America)

436
Q

Neonatal onset multisystem inflammatory disease

A

NOMIDEarly onset (infancy)Rash at birth- non pruritic urticaria- neutrophilic infiltrateCNS disease- non infectious meningitis- Low IQSensory anomalies-Deafness, optic nerve atrophyArthropathy-Arthritis during flares-Bone enlargement

437
Q

Anakinra

A

IL-1 blockerBinds to IL-1R blocking IL-1a and IL-1B

438
Q

Canakinumab

A

Neutralizes IL-1B

439
Q

Rilonacept

A

Neutralizes IL-1B and IL-1a

440
Q

Gout

A

Recurrent attacks of acute inflammatory arthritis (accumulation of uric acid)Uric acid crystals are DAMPS and result in IL-1 buildup

441
Q

Chronic Recurrent Multifocal Osteomyelitis

A

CRMORecurrent lytic bone lesions with swelling and painFevers, inflammation can spread to tissues

442
Q

CRMO treatment

A

NSAIDsSteroidsTNF-inhibiting agents

443
Q

TNF receptor associated periodic syndrome

A

TRAPS: Autosomal dominantLong duration of inflammation and feverMigratory erythematous rashMyalgiasConjunctivitis, periorbital swellingTNF binds –> initiate inflammatory response –> receptors don’t shed and inflammatory response continues

444
Q

TRAPS treatment

A

Etanercept: TNF receptor analog

445
Q

PFAPA

A

Common in childrenRegular occurring fevers, early age of onsetCyclicAphthous stomatitis, lymphadenitis, pharyngitisNormal growth and development

446
Q

Cyclic Neutropenia

A

Inherited form caused by ELA2 gene mutation21 day cycleANC

447
Q

Severe inflammatory diseases: Cyclic/non cyclicResolve/do not resolve by puberty

A

Non cyclicDo not resolve by puberty

448
Q

Omenn syndrome

A

2 weeks-3 monthsMany symptoms: Erythroderma, alopecia, diarrhea, lymphadenopathy, opportunistic infectionsNormal IgGHigh IgELow IgA, IgMMaternal T cells remain, expand and GVHDRAG disorderBMT therapy

449
Q

Allergic Rhinoconjunctivitis epidemiology

A

20million americans10% children, 10-30% adolescents/teens

450
Q

Quick relief medications for asthma

A

Bronchodilator: Albuterol, xopenex, maxair

451
Q

Long acting bronchodilators

A

Salmeterol, formoterol12hr bronchodilation but no anti inflammatory effect

452
Q

Anti inflammatory medications for asthma

A

Oral corticosteroids, inhaled corticosteroids, leukotriene blockersDecrease airway inflammation - long term use results in improved disease control

453
Q

Telodendria

A

Branching at end of axon

454
Q

Epineurium

A

Death connective tissue surrounding nerve

455
Q

Perineurium

A

Surrounds bundle of nerve fibers

456
Q

Endoneurium

A

Loose connective tissue, surrounds individual nerve fibers

457
Q

Function of multipolar neurons

458
Q

Function of bipolar neurons

A

Special sensory

459
Q

Function of unipolar neurons

A

Sensory system

460
Q

4 functions of glial cells

A
  1. Surround neurons and hold them in place2. Supply nutrients and oxygen3. Insulate one neuron from the other4. Destroy and remove dead neurons
461
Q

Oligodendrocyte

A

Form myelin sheath in CNS

462
Q

Astrocytes

A

Induce blood brain barrier phenotypeMaintain chemical environment for generation of nerve impulsesScaffolding Scar formation

463
Q

Microglia

A

Phagocytes of CNSMicroglial nodule when virus infects

464
Q

Ependymal cells

A

Cuboidal to columnar cells arranged in single layer that possess microvilli and ciliaLine the ventricles of the brain and central canal of the spinal cord.

465
Q

Sympathetic opthalmia

A

Ag sequestration in eye –> damage leads to released Ag –> Tgcells activated and attack antigen in both eyes

466
Q

IFN-gamma and autoimmune diseases

A

IFN-gamma induces MHC class II molecules to be presented —> MHC II may present sequestered AG which can induce a response

467
Q

Goodpasture’s syndrome

A

Type II hypersensitivityAbs bind to type IV collagen on basement membranes of kidney and lung

468
Q

Classic neurotransmitters

A

Contained in small vesicles, located in active zone

469
Q

Dense core vesicles

A

Contain neuropeptidesLocated further back from active zone

470
Q

Synapsins

A

Vesicle associated proteinsTether vesicle to cytoskeleton

471
Q

Docking complex

A

Voltage gated Ca channel and additional proteins

472
Q

Vesicle storage and release

A

Vesicles sequestered in storage compartment and releasable compartmentCa influx moves storage vesicles to release zone, with help of Rab3A

473
Q

Fusion pore

A

Similar to gap junction, opening associated with electrical signalMuch faster response

474
Q

Synaptic vesicle recycling

A

Vesicles release neurotransmitters –> Fused membrane coated in dynamin and clatharin –> taken to early endosome and recycled

475
Q

Ionotropic receptor

A

Ligand gated receptorDirect receptor channel coupling

476
Q

Metabotropic Receptor

A

G protein mediated receptor channel couplingSecond messenger mediated receptor/channel coupling

477
Q

End plate potential

A

EPP: evoked in muscle cell and triggers PSAP and muscle contractionSuper threshold for muscle contraction, safety factor150-200 quanta released

478
Q

MEPP

A

Miniature end plate potential Constantly happening, spontaneous release of AChMany MEPPS can result in AP

479
Q

Myasthenia gravis mechanisms

A
  1. Bind to ACh receptor and block binding and receptor activation2. Promote endocytosis of ACh –> AChR degradation3. Destroy Postsynaptic surface, less AChR’s
480
Q

Lambert-Eaton Myasthenic syndrome

A

Presynaptic diseaseReduction of Voltage gated calcium channels (Immune attack)Weakness improves with activityTreat with aminopyridines

481
Q

Clostridial neurotoxins

A

Botulinum toxin A: BotoxBotulinum toxin B: Myobloc- weaken nerve muscle 4-6monthsBind and cleave SNAP 25 (docking zone protein)

482
Q

Clostridium tetani

A

Passes retrograde along nerve fibersInhibits inhibitory neurons that control spinal motor neurons and brainstem excitabilityAttacks synaptobrevin

483
Q

Wired transmission

A

Direct connection between pre and post synaptic neurons

484
Q

Volume transmission

A

Release site of neurotransmitter is some distance from target cellSlower onset, longer effect

485
Q

CNS cessation of neurotransmitters

A

DiffusionRe-uptake into glial cells and synaptic terminal

486
Q

Retrograde neurotransmitter

A

Messenger that goes from post synaptic cell to presynaptic cell and induces further neurotransmitter release

487
Q

LTP requirement

A

Protein synthesis

488
Q

Pre-synaptic inhibition

A

Inhibitory neuron contacts the terminal of a second presynaptic neuronReleased NT by inhibitory neuron depresses calcium current –> reduces NT release by presynaptic cell

489
Q

Presynaptic facilitation

A

Facilitating neuron enhances release of NT by other presynaptic neuron

490
Q

Squamous metaplasia: Smokers

A

Ciliated columnar –> stratified squamous

491
Q

Desmoplasia

A

Way connective tissue respond to neoplasmsCollagenous stroma laid down by desmoplastic fibroblasts

492
Q

Nicotine

A

AChR agonist

493
Q

Physostigmine

A

AChE inhibitor

494
Q

D-tubocurarine

A

Competitive inhibitor of AChR

495
Q

Tetrodotoxin, Saxitoxin

A

Blocks Voltage gated Sodium channels

496
Q

Conotoxin

A

Blocks Voltage gated calcium channels

497
Q

Succinylcholine

A

AChR agonistInactivates end plate sodium channels, desensitization of AChR

498
Q

Organophosphate compounds

A

Irreversible inhibition of AChE

499
Q

4 mechanisms of Calcium level regulation in nerve terminal

A
  1. Binding to proteins (calmodulin)2. Na symport channel3. Active transport out4. Sequestration
500
Q

EPSP

A

Fast - ionotropic receptors that pass NA and KInward current = depolarization of postsynaptic membraneMagnitude proportional to amount of NT released

501
Q

IPSP

A

Fast - ionotropic GABA and Glycine receptorsIncrease Cl- conductance into cell (hypoerpolarization)Or increased K permeability = hyperpolarization

502
Q

ATP depletion

A

Reduced Oxygen - ischemic damageMitochondrial damageFailure of Na/K pumpDisruption of translational machinery Shift to anaerobic glycolysis –> decrease in pH

503
Q

Elevated cytosolic Ca2+

A

External: failure of Ca pumpInternal: release from mitochondria/EREnzyme activationDisruption of mitochondria membrane potential

504
Q

Oxidative stress

A

Reactive oxygen species: Superoxide, H2O2, hydroxyl radicalROS scavengers: Vit C and EEnzymes - superoxide dismutase, catalase, glutathione peroxidase

505
Q

Loss of membrane integrity

A

ATP depletionIncreased CaIncreased protease activity

506
Q

Protein misfolding

A

Unfolded protein response activatedUnresolved = apoptosis

507
Q

Genotoxic stress

A

p53 transcription factor activationCell cycle arrestApoptosis

508
Q

Necrosis

A

Damage exceeds repair capacityCells swell, leaky membranes, nuclear changesDue to energy failure

509
Q

Coagulative necrosis

A

Injury causes protein denaturing - infarct

510
Q

Liquefactive necrosis

A

Hydrolytic enzyme releaseFocal infections, brain infarcts

511
Q

Caseous necrosis

A

Focal infection and immune responseTB, histoGranuloma

512
Q

Fat necrosis

A

Focal destruction of fatAcute pancreatitis

513
Q

Gangrenous necrosis

A

Dry: ischemia, distal limbWet: Superimposed bacterial infectionGasL Deadly form, anaerobic bacterial infection

514
Q

Apoptosis

A

Intrinsic: Injury to mitochondria inducedExtrinsic: Growth factor trigger

515
Q

Necroptosis

A

Hybrid of necrosis and apoptosisTNFR ligation

516
Q

Pyroptosis

A

Self destructCapase-1Pro-inflammatory signals released

517
Q

Neonatal diabetes mutations

A

Kir6.2SUR1

518
Q

Kir6.2 mutation

A

Decrease ability of ATP to bind to K-ATP channelNo insulin release

519
Q

SUR1 mutation

A

Increase Mg2+ and ADP to bindStops ATP binding

520
Q

Myotonia Congenita

A

Defect in Cl- conductance, slow repolarization after AP –> chance for repeated AP’s and thus constitutive muscle contractions

521
Q

Bladder metaplasia

A

Transitional –> SquamousStones

522
Q

Esophagus metaplasia

A

Squamous –> ColumnarReflux

523
Q

Dysplasia

A

Pre-neoplastic changeCellular atypia: Aberrant mutation, enlarged nuclei, nuclear hyperchromasia

524
Q

General somatic afferent fibers

A

Bring conscious/unconscious sensory memory from body wall and limbs

525
Q

General visceral afferent fibers

A

Bring sensory information from visceral structures to CNS

526
Q

General somatic efferent fibers

A

Innervation of voluntary skeletal muscles

527
Q

General visceral efferent fibers

A

Innervation of cardiac muscles, smooth muscles, and glands

528
Q

Dorsal root ganglions

A

Afferent nerve fibers

529
Q

Dorsal horn

A

Entry of sensory information

530
Q

Ventral horn

A

Location of motor neurons

531
Q

Lateral Horn (Thoracolumbar)

A

T1-L2Location of preganglionic sympathetic neurons

532
Q

Craniosacral preganglionic nerves

A

Parasympathetic originsBrainstem and S2-S4

533
Q

Path of efferent sympathetic nerve transmission

A

Information from CNS –> Travel down to spinal cord –> Leave through lateral horn via ventral root –> Enter spinal nerve –> Enter sympathetic ganglion via white ramus –> Exit sympathetic ganglion via gray ramus –> Travel through spinal nerve to target

534
Q

White ramus

A

Myelinated connection between spinal nerve and sympathetic ganglionOnly T1-L2

535
Q

Gray ramus

A

Unmyelinated connection between sympathetic ganglion and spinal nerveAll levels

536
Q

Path of efferent sympathetic nerve transmission (to cervical/lumbar area)

A

Information from CNS –> Travel down to spinal cord –> Leave through lateral horn via ventral root –> Enter spinal nerve –> Enter sympathetic ganglion via white ramus –> TRAVEL UP OR DOWN SYMPATHETIC CHAIN –> Synapse –> Exit sympathetic ganglion via gray ramus –> Travel through spinal nerve to target

537
Q

Tyrosine –> Epinephrine synthesis pathway

A

Tyrosine –> DOPA –> Dopamine –> Norepinephrine –> Epinephrine

538
Q

Neurotransmitter synthesis enzymes (Tyrosine –> Epi)

A

Tyrosine HydroxylaseDOPA decarboxylase D-beta-hydroxylasePNMT

539
Q

Major mechanism for termination of NE action

A

Reuptake pumpUptake-1

540
Q

Monoamine oxidase

A

Oxidizes NE to be degraded

541
Q

Cocaine

A

Inhibits NE re-uptake into nerve terminalMore NE –> enhanced response

542
Q

Imipramine

A

Tricyclic antidepressantInhibits NE reuptake

543
Q

Tyramine

A

Indirectly acting sympathomimeticMimics NE activity by using NETaken up by uptake-1 pump –> oxidized by MAOIf MAO-inhibitor –> Not oxidized –> displaces NE from vesicles

544
Q

Resperpine

A

Root of Rauwolfia serpentinaInhibits vesicular uptake of NE –> depletes vesicle so less NT when released

545
Q

D-beta hydroxylase location

A

Within vesicle, released during exocytosis

546
Q

Readily Reversible AChE inhibitor

A

Binds to active site but no covalent bond formation

547
Q

Intermediate reversible AChE inhibitor

A

Covalent bond formation and then bond hydrolyzed - carbamates

548
Q

Irreversible AChE inhibitor

A

Non hydrolysable covalent bondOrganophosphate

549
Q

Regeneration

A

Proliferation of cells and tissue with host replacement tissueLiver regeneration after resection

550
Q

Repair

A

Combination regeneration and deposition of collagen (scar formation)Dermal wound healing

551
Q

Stimulatory control of cell proliferation and growth

A

Growth factors and cytokinesHormonesCell-cell interactionsCell matrix interaction

552
Q

Inhibitory control of cell proliferation and growth

A

Contact inhibitionGrowth factors

553
Q

Stages of liver regeneration

A

Priming: IL-6 produced by Kuppfer cells make hepatocytes competent to respond to growth factorsGrowth factors: HGF, TGF-a act on primed hepatocytesHepatocytes move from G0 to G1 phase of cell cycle

554
Q

Kuppfer cells

A

Resident liver macrophages

555
Q

Oval cells

A

Hepatic ductal cells which accumulate during toxin exposureReplace parenchymal cells and restore function

556
Q

Primary union of skin incision

A

Clean injurySpace clots –> neutrophil infiltrate –> epithelial cell migration/proliferation –> Macrophage –> Granulation tissue forms –> Collagen begins to bridge wound ~1 week

557
Q

Angiogenesis

A

Blood vessel formationNotch signaling pathway

558
Q

Secondary union of skin

A

Larger wound, more inflammation, more granulation tissue fills defect, longer healing timeWound contraction reduces size

559
Q

Labile cells

A

Continuously dividingEpidermis, bone marrow, GI mucosa

560
Q

Stable/Quiescent cells

A

Potential to divideHepatocytes, renal tubular epithelium, endothelium, connective tissue, smooth muscle

561
Q

Permanent cells

A

Unable to divideNeurons, cardiac myocytes, skeletal muscle

562
Q

Determinants of quality of healing

A

Regenerative capacity, stromal injury, contamination, proliferative activity of connective tissue

563
Q

Excessive repair

A

Hypertrophic scarsKeloids

564
Q

Characteristics of benign neoplasms

A

Pushing, smooth borderHistology looks like normal tissueDo no metastasize

565
Q

Malignant neoplasms

A

Hard tumorInfiltrating, invasive locallyLack of differentiation: anaplasiaMay extend into adjacent tissue or invade nerve sheaths (perineural invasion) and blood vessels (vascular invasion)

566
Q

Invasion of matrix across basement membrane

A

Tumor cells lose cohesion –> secrete proteolytic enzymes –> Attach to extracellular matrix via receptors for laminin/fibronectin –> locomote through matrix

567
Q

Alpha-1 receptor activation effects

A

Vasoconstriction

568
Q

Alpha-2 receptor activation effect

A

Inhibition of transmitter release (NE and ACh)

569
Q

Beta-1 receptor activation effects

A

Increased cardiac rate (SA node) and force (and output)

570
Q

Beta-2 receptor activation effects

A

Bronchodilation, vasodilation Only Epinephrine

571
Q

Beta-1 agonist activity

A

Increased cardiac output, HR

572
Q

Beta-1 antagonist activity

A

Prevent increase in cardiac output

573
Q

Beta-2 agonist activity

A

Dilate airways, decrease resistance

574
Q

Beta-2 antagonist activity

A

Constrict airways, increase resistance

575
Q

Alpha-1 agonist activity

A

Constrict blood vessels, increase BP

576
Q

Alpha-1 antagonist activity

A

Dilate vessels, decrease BP

577
Q

Pheochromocytoma

A

Tumor of adrenal gland, releases Epi and NEIncrease BP, HRHeadache, sweating, hypertensive crisis

578
Q

Route 1 for sympathetic transmission

A

Preganglionic axon enters sympathetic chain (white ramus) –> synapse –> exit via gray ramus –> postganglionic axon to target

579
Q

Route 2 for sympathetic transmission

A

Preganglionic axon enters sympathetic chain (white ramus) –> Travel up/down sympathetic chain –> synapse –> postganglionic axon to target

580
Q

Route 3 for sympathetic transmission (thoracic)

A

Preganglionic axon enters sympathetic chain (white ramus) –> synapse –> Travel to heart via splanchnic nerve

581
Q

Route 4 for sympathetic transmission (Abdominal)

A

Preganglionic axon enters sympathetic chain (white ramus) –> Splanchnic nerve to target organ –> synapse and postganglionic innervation

582
Q

Parasympathetic preganglionic synapse location

A

Intramural ganglia on wall of visceral structure

583
Q

Vagus nerve

A

Parasympathetic nerve which branches off to target organsInnervates GI tract up to splenic flexure

584
Q

Pelvic splanchnic nerves

A

Sacral portion of parasympathetic divisionPelvic viscera, GI tract distal to splenic flexure

585
Q

Heart muscle sympathetic vs parasympathetic

A

S: Increase rate/forceP: Decrease rate

586
Q

Bladder urethra sympathetic vs parasympathetic

A

S: Detrusor relaxation, constriction of sphincterP: Detrusor constriction, relaxation of sphincter

587
Q

Lungs sympathetic vs parasympathetic

A

S: BronchodilationP: Bronchoconstriction

588
Q

GI organs sympathetic vs parasympathetic

A

S: Decreased peristalsis/secretionP: Increased peristalsis/secretion

589
Q

Eye sympathetic vs parasympathetic

A

S: DilationP: Constriction

590
Q

Glands sympathetic vs parasympathetic

A

S: Less secretionP: Increased secretion

591
Q

Phenylephrine

A

Alpha adrenergic agonist

592
Q

Epinephrine

A

Alpha and Beta adrenergic agonist

593
Q

Scopolamine

A

Muscarinic receptor antagonist

594
Q

Pupil innervation

A

Cholinergic and AdrenergicACh = parasympathetic = constriction = miosis Circular muscle contractionNE = sympathetic = dilation Radial muscle contraction

595
Q

Ciliary muscle innervation

A

M: ContractionBeta2: RelaxationPrimarily Parasympathetic innervation

596
Q

Vascular smooth muscle innervation

A

Single innervation: SympatheticAlpha1: ContractionBeta2: RelaxationNO CHOLINERGIC

597
Q

Muscarinic receptors on endothelium

A

Can release NO which relaxes VSM

598
Q

Sinoatrial node innervation

A

Dual innervation: Primarily parasympatheticACh & NEBeta1: Increase HR, contractilityBeta2: Only EpiM: Decrease HR

599
Q

Atropine

A

Muscarinic receptor antagonist

600
Q

GI innervation

A

Dual innervation: primarily sympatheticM: Contract, peristalsisBeta2: Relax, no peristalsis

601
Q

Sphincter muscle innervation

A

Dual innervation: primarily sympatheticMuscarinic receptor mediated relaxation (via NO)Alpha1: Contraction, retention

602
Q

Isoproterenol and VSM

A

Activates B2 –> relaxation

603
Q

Sarin gas

A

AChE inhibitorIrreversible

604
Q

Wound contraction

A

Reduction of size of defectMyofibroblasts3-5 days after injury

605
Q

Wound strength

A

Early (week 1)- 5-10% original strength- Fibrin, re-epithelializationFirst month- Collagen content- 15%Month-years- Collagen linking/remodeling- Max 60% original strength

606
Q

Phases of wound strength

A

LagRapid increase Slow increasePlateau

607
Q

Keloids vs hypertrophic scars: Similarities

A

Excessive granulation tissueExcessive collagenInitial morphological similarity

608
Q

Keloids vs Hypertrophic scarsL Differences

A

Keloids do not regress, recur, extend beyond injury site

609
Q

Biological aging of cells: Increase and decrease

A

Increase: Organelle damageDecrease: Oxidative phosphorylation, protein synthesis, nutrient uptake, DNA repair

610
Q

Cardiovascular aging

A

Intimal thickeningVascular stiffnessHypertension, atherosclerosis

611
Q

Urinary aging

A

Bladder elasticity declines, glomerulosclerosisBladder control problems decline in kidney function

612
Q

Respiratory aging

A

Loss of elasticity, immunityInfection, reduced exercise tolerance

613
Q

Endocrine system

A

Hormone levels changeAge associated disease, diabetes, hypotension

614
Q

Liver aging

A

Decreased blood flow, loss of hepatocytesDrug metabolism declines, Adverse drug reactions

615
Q

GI aging

A

Gi hormone decrease, smooth muscle atrophyConstipation, Reflux, nutritional defecits

616
Q

Trauma and aging

A

Inflammation and re-epithelialization is delayed

617
Q

Cumulative damage and aging - Accumulation

A

Waste product accumulation: LipofuscinAdvanced glycation end products- non enzymatic addition of sugars to proteins- Affect multiple tissues-Skin collagen and lens

618
Q

Hutchinson Gilford Progeria syndrome

A

Hydrocephalic appearancePremature aging lookAge associated pathology - osteoporosis, insulin resistance, CVDLamin A gene-Splice disorder –> Deletes 50 amino acidsNew protein is progerinDisrupts nuclear envelope

619
Q

Werner’s Syndrome

A

Autosomal recessivePremature wrinkling and graying, age related pathologyCancerMutant gene: WRN-1 (helicase)

620
Q

Telomeres

A

Added by telomeraseLength shortens after division –> trigger p53

621
Q

Resveratrol

A

Extends lifespan in lower organisms

622
Q

Rapamycin

A

Increases lifespanEnhances progerin clearanceImmunosuppressive

623
Q

HPV protein E6

A

Mimics MDM2Ubiquination and degradation of p53 protein–> loss of tumor suppressor

624
Q

HPV protein E7

A

Eradicates function of RBRemove brake against proliferation

625
Q

EBV in immune suppressed patients

A

Activates BCL2Prevents apoptosis

626
Q

Chronic inflammation and cancer promotion

A

Release factors for cell proliferation by leukocytes or by protease digestion of ECM

627
Q

HER2/neu

A

Amplification in breast cancer

628
Q

N-myc

A

Amplification in neuroblastoma

629
Q

Acute leukemias defect

A

Translocation

630
Q

ZAP-70

A

Chronic lymphocytic leukemia

631
Q

Chronic phase CML

A

Elevated WBC, eosiniphilia and basophilia

632
Q

Accelerated phase CML

A

20% blasts

633
Q

Imatinib (Gleevec)

A

Inhibits bcr-abl tyrosine kinaseStops leukemia

634
Q

Familial breast cancer cause

A

BRCA-1, BRCA-2

635
Q

Familial polyposis cause

A

APC tumor supressor

636
Q

Hereditary nonpolyposis colon cancer cause

A

Double stranded DNA repair genes

637
Q

Xeroderma pigmentosum cause

A

Nucleotide excision repair genesUV light exposure –> Pyrimidine-pyrimidine dimers

638
Q

Order for cancerInitiator/promotor

A

Initiator first then promotor

639
Q

HTLV I

A

T-cell leukemia/lymphomaCommon in Japan and Caribbean

640
Q

SA node resting tone and effect of ganglionic blocker

A

ParasympatheticGanglionic blocker = tachycardia

641
Q

Myocardium ventricle resting tone and effect of ganglionic blocker

A

SympatheticGanglionic blocker = Reduced contractility

642
Q

Basic steps of wound healing

A

InflammationGranulation tissue formationRe-epithelizalizationWound contraction and ECM deposition

643
Q

Stimuli for GVA (pain)

A

pH (ischemia/hypoxia)distention (stretch)Spasms of strong activationChemical irritantsLowering of membrane potential for stimulation

644
Q

Granulation cell

A

ECMInflammatory cellsFibroblastsBlood vessels

645
Q

Wound healing cells

A

MyofibroblastsSmooth muscleParenchymalLeukocytesEndothelialFibroblasts

646
Q

Cytokines for wound healing

A

Platelet derived GFTGF betaBasic Fibrobalst GFEpidermal GFVascular endothelial GFIL-1,8

647
Q

Growth factor functions

A

ProliferationLocomotionDifferentiationAngiogenesisSurvival

648
Q

miRNA tumor suppressor

A

145Breast, colon

649
Q

Her2/neu treatment

A

Monoclonal antibody

650
Q

Perineoplastic syndrome

A

CushingsHypercalcemiaSIA-Dehydrogenase

651
Q

Rituximab

A

Drug that acts on CD20 of B cells

FoCM (6 decks)

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