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FoCM > Week 5 > Flashcards

Week 5 Flashcards

1
Q

General somatic afferent fibers

A

Bring conscious/unconscious sensory memory from body wall and limbs

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2
Q

General visceral afferent fibers

A

Bring sensory information from visceral structures to CNS

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3
Q

General somatic efferent fibers

A

Innervation of voluntary skeletal muscles

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4
Q

General visceral efferent fibers

A

Innervation of cardiac muscles, smooth muscles, and glands

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5
Q

Dorsal root ganglions

A

Afferent nerve fibers

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6
Q

Dorsal horn

A

Entry of sensory information

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7
Q

Ventral horn

A

Location of motor neurons

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8
Q

Lateral Horn (Thoracolumbar)

A

T1-L2Location of preganglionic sympathetic neurons

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9
Q

Craniosacral preganglionic nerves

A

Parasympathetic originsBrainstem and S2-S4

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10
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

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11
Q

White ramus

A

Myelinated connection between spinal nerve and sympathetic ganglionOnly T1-L2

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12
Q

Gray ramus

A

Unmyelinated connection between sympathetic ganglion and spinal nerveAll levels

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13
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

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14
Q

Tyrosine –> Epinephrine synthesis pathway

A

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

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15
Q

Neurotransmitter synthesis enzymes (Tyrosine –> Epi)

A

Tyrosine HydroxylaseDOPA decarboxylase D-beta-hydroxylasePNMT

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16
Q

Major mechanism for termination of NE action

A

Reuptake pumpUptake-1

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17
Q

Monoamine oxidase

A

Oxidizes NE to be degraded

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18
Q

Cocaine

A

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

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19
Q

Imipramine

A

Tricyclic antidepressantInhibits NE reuptake

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20
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

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21
Q

Resperpine

A

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

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22
Q

D-beta hydroxylase location

A

Within vesicle, released during exocytosis

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23
Q

Readily Reversible AChE inhibitor

A

Binds to active site but no covalent bond formation

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24
Q

Intermediate reversible AChE inhibitor

A

Covalent bond formation and then bond hydrolyzed - carbamates

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25
Q

Irreversible AChE inhibitor

A

Non hydrolysable covalent bondOrganophosphate

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26
Q

Regeneration

A

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

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27
Q

Repair

A

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

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28
Q

Stimulatory control of cell proliferation and growth

A

Growth factors and cytokinesHormonesCell-cell interactionsCell matrix interaction

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29
Q

Inhibitory control of cell proliferation and growth

A

Contact inhibitionGrowth factors

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30
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

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31
Q

Kuppfer cells

A

Resident liver macrophages

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32
Q

Oval cells

A

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

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33
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

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34
Q

Angiogenesis

A

Blood vessel formationNotch signaling pathway

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35
Q

Secondary union of skin

A

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

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36
Q

Labile cells

A

Continuously dividingEpidermis, bone marrow, GI mucosa

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37
Q

Stable/Quiescent cells

A

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

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38
Q

Permanent cells

A

Unable to divideNeurons, cardiac myocytes, skeletal muscle

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39
Q

Determinants of quality of healing

A

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

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40
Q

Excessive repair

A

Hypertrophic scarsKeloids

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41
Q

Characteristics of benign neoplasms

A

Pushing, smooth borderHistology looks like normal tissueDo no metastasize

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42
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)

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43
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

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44
Q

Alpha-1 receptor activation effects

A

Vasoconstriction

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45
Q

Alpha-2 receptor activation effect

A

Inhibition of transmitter release (NE and ACh)

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46
Q

Beta-1 receptor activation effects

A

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

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47
Q

Beta-2 receptor activation effects

A

Bronchodilation, vasodilation Only Epinephrine

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48
Q

Beta-1 agonist activity

A

Increased cardiac output, HR

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49
Q

Beta-1 antagonist activity

A

Prevent increase in cardiac output

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50
Q

Beta-2 agonist activity

A

Dilate airways, decrease resistance

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51
Q

Beta-2 antagonist activity

A

Constrict airways, increase resistance

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52
Q

Alpha-1 agonist activity

A

Constrict blood vessels, increase BP

53
Q

Alpha-1 antagonist activity

A

Dilate vessels, decrease BP

54
Q

Pheochromocytoma

A

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

55
Q

Route 1 for sympathetic transmission

A

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

56
Q

Route 2 for sympathetic transmission

A

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

57
Q

Route 3 for sympathetic transmission (thoracic)

A

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

58
Q

Route 4 for sympathetic transmission (Abdominal)

A

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

59
Q

Parasympathetic preganglionic synapse location

A

Intramural ganglia on wall of visceral structure

60
Q

Vagus nerve

A

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

61
Q

Pelvic splanchnic nerves

A

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

62
Q

Heart muscle sympathetic vs parasympathetic

A

S: Increase rate/forceP: Decrease rate

63
Q

Bladder urethra sympathetic vs parasympathetic

A

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

64
Q

Lungs sympathetic vs parasympathetic

A

S: BronchodilationP: Bronchoconstriction

65
Q

GI organs sympathetic vs parasympathetic

A

S: Decreased peristalsis/secretionP: Increased peristalsis/secretion

66
Q

Eye sympathetic vs parasympathetic

A

S: DilationP: Constriction

67
Q

Glands sympathetic vs parasympathetic

A

S: Less secretionP: Increased secretion

68
Q

Phenylephrine

A

Alpha adrenergic agonist

69
Q

Epinephrine

A

Alpha and Beta adrenergic agonist

70
Q

Scopolamine

A

Muscarinic receptor antagonist

71
Q

Pupil innervation

A

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

72
Q

Ciliary muscle innervation

A

M: ContractionBeta2: RelaxationPrimarily Parasympathetic innervation

73
Q

Vascular smooth muscle innervation

A

Single innervation: SympatheticAlpha1: ContractionBeta2: RelaxationNO CHOLINERGIC

74
Q

Muscarinic receptors on endothelium

A

Can release NO which relaxes VSM

75
Q

Sinoatrial node innervation

A

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

76
Q

Atropine

A

Muscarinic receptor antagonist

77
Q

GI innervation

A

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

78
Q

Sphincter muscle innervation

A

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

79
Q

Isoproterenol and VSM

A

Activates B2 –> relaxation

80
Q

Sarin gas

A

AChE inhibitorIrreversible

81
Q

Wound contraction

A

Reduction of size of defectMyofibroblasts3-5 days after injury

82
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

83
Q

Phases of wound strength

A

LagRapid increase Slow increasePlateau

84
Q

Keloids vs hypertrophic scars: Similarities

A

Excessive granulation tissueExcessive collagenInitial morphological similarity

85
Q

Keloids vs Hypertrophic scarsL Differences

A

Keloids do not regress, recur, extend beyond injury site

86
Q

Biological aging of cells: Increase and decrease

A

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

87
Q

Cardiovascular aging

A

Intimal thickeningVascular stiffnessHypertension, atherosclerosis

88
Q

Urinary aging

A

Bladder elasticity declines, glomerulosclerosisBladder control problems decline in kidney function

89
Q

Respiratory aging

A

Loss of elasticity, immunityInfection, reduced exercise tolerance

90
Q

Endocrine system

A

Hormone levels changeAge associated disease, diabetes, hypotension

91
Q

Liver aging

A

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

92
Q

GI aging

A

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

93
Q

Trauma and aging

A

Inflammation and re-epithelialization is delayed

94
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

95
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

96
Q

Werner’s Syndrome

A

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

97
Q

Telomeres

A

Added by telomeraseLength shortens after division –> trigger p53

98
Q

Resveratrol

A

Extends lifespan in lower organisms

99
Q

Rapamycin

A

Increases lifespanEnhances progerin clearanceImmunosuppressive

100
Q

HPV protein E6

A

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

101
Q

HPV protein E7

A

Eradicates function of RBRemove brake against proliferation

102
Q

EBV in immune suppressed patients

A

Activates BCL2Prevents apoptosis

103
Q

Chronic inflammation and cancer promotion

A

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

104
Q

HER2/neu

A

Amplification in breast cancer

105
Q

N-myc

A

Amplification in neuroblastoma

106
Q

Acute leukemias defect

A

Translocation

107
Q

ZAP-70

A

Chronic lymphocytic leukemia

108
Q

Chronic phase CML

A

Elevated WBC, eosiniphilia and basophilia

109
Q

Accelerated phase CML

A

20% blasts

110
Q

Imatinib (Gleevec)

A

Inhibits bcr-abl tyrosine kinaseStops leukemia

111
Q

Familial breast cancer cause

A

BRCA-1, BRCA-2

112
Q

Familial polyposis cause

A

APC tumor supressor

113
Q

Hereditary nonpolyposis colon cancer cause

A

Double stranded DNA repair genes

114
Q

Xeroderma pigmentosum cause

A

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

115
Q

Order for cancerInitiator/promotor

A

Initiator first then promotor

116
Q

HTLV I

A

T-cell leukemia/lymphomaCommon in Japan and Caribbean

117
Q

SA node resting tone and effect of ganglionic blocker

A

ParasympatheticGanglionic blocker = tachycardia

118
Q

Myocardium ventricle resting tone and effect of ganglionic blocker

A

SympatheticGanglionic blocker = Reduced contractility

119
Q

Basic steps of wound healing

A

InflammationGranulation tissue formationRe-epithelizalizationWound contraction and ECM deposition

120
Q

Stimuli for GVA (pain)

A

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

121
Q

Granulation cell

A

ECMInflammatory cellsFibroblastsBlood vessels

122
Q

Wound healing cells

A

MyofibroblastsSmooth muscleParenchymalLeukocytesEndothelialFibroblasts

123
Q

Cytokines for wound healing

A

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

124
Q

Growth factor functions

A

ProliferationLocomotionDifferentiationAngiogenesisSurvival

125
Q

miRNA tumor suppressor

A

145Breast, colon

126
Q

Her2/neu treatment

A

Monoclonal antibody

127
Q

Perineoplastic syndrome

A

CushingsHypercalcemiaSIA-Dehydrogenase

128
Q

Rituximab

A

Drug that acts on CD20 of B cells

FoCM (6 decks)

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