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M2M - Niswander > Unit IV Week 1 > Flashcards

Unit IV Week 1 Flashcards

1
Q

Fusion in mitochondria
GTPase?
Mutations?

A

repairs damage
Mfn and OPA1
autosomal dominant optic atrophy, CMT 2A, ROS

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2
Q

Fission in mitochondira
GTPase?
Mutations?

A

required for mitophagy
Fis1 and Drp
ROS

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3
Q

TOM/GIP

A

translocase of outer membrane

passive, facilitated diffusion

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4
Q

TIM

A

translocase of inner membrane
gated channel with active transport
protein enters by N’, unwound
Hsp70 rewinds

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5
Q

1e- = ____ H+

____ H+ = 1 ATP

A

1e- = 5 H+

3 H+ = 1 ATP

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6
Q

ATP synthase F1

A

bound to F0

enzyme that makes ATP

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7
Q

ATP synthase F0

A

spans inner membrane, H+ channel

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8
Q

____ is final electron acceptor in ETC and makes _____

A

O2, H20

problems lead to ROS

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9
Q

Mitochondrial regulation of cell death

A

Bak/Bax make outer membrane permeable
Cytochrome C leaks into cytoplasm
Binds complex and forms apoptosome
Activates caspases

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10
Q

Ischemic injury leading to necrotic cell death

A

MPTP makes inner/outer membrane permeable
Cytochrome C release and disruption of H+ gradient
No ATP production (ATPsynth = ATPase)

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11
Q

Mitochondrial dysfunction consequences

A 
Can't produce ATP
Produces ROS (oxidize proteins, lipids, DNA)
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12
Q

Quality control

A

Mitochondrial proteases:
mAAA (mutation = hereditary spastic paraplegia)
iAAA
Lon
Fusion/fisson (redistribute or mitophagy)
Apoptosis

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13
Q

Arsenic toxin mechanism

A

inhibits oxidative phosphorylation and ATP production

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14
Q

Epithelial to mesenchymal transition

A

Epithelial loses polarity and cell adhesions

Migrates and becomes invasive

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15
Q

Functions of epithelial tissues

A 
protection
selective transport/absorption/secretion
biochemical modification and processing
sensory reception transduction
communication
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16
Q

Apical and basal polarity

A

Differences in:
transporters, ion channels, exo/endocytosis receptors, cell-cell, cell-lamina
Cytoplasm is also polarized

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17
Q

Cell junctions: tight junctions

A

highly selective
limit/control diffusion between cells
Core proteins: occludins, claudins

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18
Q

Cell junctions: adherence junctions

A

promote attachment, polarity, organization
decide stem cell behavior
Core protein: cadherins (actin to cyto)

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19
Q

Cell junctions: desmosomes

A

mechanical strength
resist shearing forces
Core protein: cadherins (intermediate filament to cyto)

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20
Q

Cell junctions: gap junctions

A

rapid communication between cells

joint cytoplasm

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21
Q

Apical modifications to epithelial cells

A

microvilli (actin bundles, increase surface area)
ex: stereocilia sensory cells (ear)

cilia
primary cilium (controls proliferation, fate, and function)
motile cilia
sensory cilia

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22
Q

Basolateral modifications to epithelial cells

A

infolds/outfolds to increase surface area
unorganized
seen in transport dependent cells

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23
Q

Components of basal lamina

A

collagen (type IV, network)
glycoproteins
laminins
entactin

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24
Q

Functions of basal lamina

A
  1. attach epithelia to underlying CT (via hemidesmosomes and focal adhesions, both using integrins)
  2. filtrations to/from epithelia
  3. establish/maintain polarity
  4. highways for cell migration through CT
  5. barrier to microbes/cancer
  6. control gene expression to affect proliferation
  7. scaffolding function - repair
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25
Q

2 ways cells can secrete

A

exocytosis

total cell disintegration

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26
Q

Exocrine glands

A

small consistent output (can be upregulated)
unidirectional secretion onto apical side
have secretory units: alveoli, acinar, tubular
have ducts: simple/compound

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27
Q

Endocrine glands

A

Hormonal control
no ducts, secrete to blood
surrounded by basal lamina and CT
secreted through basal lamina

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28
Q

Types of exocrine glands

A
  1. mucous (viscous, glycoprotein)
  2. serous (watery, salts)
  3. mixed
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29
Q

4 characteristics of stem cells

A
  1. competent for cell divsion
  2. self re-new (create mother)
  3. produce differentiated cells types specific to epithelia
  4. divide very slowly (lots of regulation)
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30
Q

Transit amplifying cells

A

daughter cells of stem cells that proliferate faster

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31
Q

Principles of stem cell pathways

A

Each path used by distinct cell lines/organs

Single path triggers different effects in different cell lines

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32
Q

Some examples of stem cell pathways/signal systems

A
  1. Wnt
  2. Shh
  3. TGF-ß
  4. Notch
  5. RTK (ex. EGFR, tx: Tarceva [erlotinib] anti=tumor
  6. FGF
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33
Q

Carcinoma

A

cancer with epithelial origin

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34
Q

Adenocarcinoma

A

cancer with glandular epithelial origin

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35
Q

Therapeutic targets for cancer

A

Signal systems that control development
Internal cell cycle control factors
Factors that control DNA repair
Factors that control apoptosis

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36
Q

Cystic fibrosis pattern of inheritance

mutation

A

Autosomal recessive

Chr 7 - CFTR gene, F508del

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37
Q

Cystic fibrosis pathophysiology

A

Problems in salt and water movement

Thick secretions

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38
Q

Cystic fibrosis clinical signs

A 
Sinus: chronic infections, nasal polyps
Lung: recurrent infections, bronchiectasis
Pancreas: exocrine pancreatic insufficiency (85%)
   greasy, bulky stool
   malabsorption, CF diabetes
meconium ileus
no vas deferens
clubbing
increased sweat chloride
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39
Q

Cystic fibrosis screening

A

newborn screen - asymptomatic or meconium ileus (15%)

older children - failure to thrive, abnormal stool

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40
Q

Cystic fibrosis treatment

A

nutrition
lung disease treatments (airway clearance, antibiotics, anti-inflammatory
CFTR modulators

41
Q

CFTR modulators

A 
Ivacaftor (Kalydeco): class III, potentiator
Lumacaftor/ivacaftor (Orkambi): class II, corrector and potentiator
42
Q

Components of cilia

A

Basal bodies
Axoneme
Transition zone
Ciliary membrane

43
Q

Intraflagellar transport

A

bidirectional
Anterograde: kinesin-2, IFT-B complex
Retrograde: dynein-2, IFT-A complex

44
Q

Ciliary formation/assembly

A

Basal body formation from older centriole (G1/S)

Ciliogenesis (subsequent G1/G0)

45
Q

Motile cilia

A

movement
dynein dependent sliding motion
9+2 (can be 9+0)

46
Q

Sensory cilia

A

9+0

lack dynein arms

47
Q

Pathways that function through cilia

A

SHh (glioma tumor)
Wnt
PDGF
FGF

48
Q

Advantage of cilia in signaling pathway

A 
cell antennae
concentrates signals
high receptor surface to volume ratio
positioned away from interfering cellular domains
mechanical detector of flow
49
Q

Cilia homeostasis function

A

Hh targets: limb, bone, nerve formation/homeo
Ciliary signaling: left/right asymmetry of body
9+0 motile leftward flow

50
Q

Examples of ciliopathies

A

Bardet-Biedl Syndrome (AR, vesice transport)

Polycystic Kidney Disease (AD and AR forms)

51
Q

Core cells of CT

A 
mesenchymal cells
fibroblasts
osteoprogenitor
chondrocytes
adipocyte
myofibroblast (smooth muscle)
52
Q

Immigrant cells of CT

A 
lymphocytes
macrophages
neutrophils/eosinophils
mast cells
osteoclasts
53
Q

Functions of macrophages

A

phagocytosis of cells and ECM
promote/control angiogenesis
send signals to other cells

54
Q

Types of collagen

A

Fibrillar (rope, head to tail, bone/tendon)
Fibril-associated (link collagen to collagen or other)
Network (thin sheets, basal lamina)

55
Q

Dense vs. loose CT

A

Dense: irregular or organized parallel (lig/ten)
high in ground substrate and low in cell density
Loose: thin irregular, (capillaries and nerves)
high in ground substrate and cell density

56
Q

Intracellular (first step) collagen synthesis

A
  1. polypeptides on ER
  2. translocated to ER lumen
  3. post-trans mods
  4. assembled to triple helix
57
Q

Extracellular (second step) collagen synthesis

A
  1. protease cleavage (N-telo peptide signal)
  2. formation of bundles/end to end polymers
  3. enzyme catalyzed crosslinks
58
Q

Ehlers-Danos syndrome

A

collagen disease

59
Q

Elastic fibers in ECM

A 
Elastin
Fibrillin (mutation = Marfans)
60
Q

Ground substrate in ECM

A

Proteoglycans
Other proteins (enzymes, GFs, proteases)
Inorganic solutes
Water

61
Q

ECM injury repair steps

A

Inflammation
New tissue formation
Tissue remodeling

62
Q

ECM injury - inflammation

A 
Fibroblasts/mast/macro increase H2O perm
Monocyte/lymphocyte migration
WBC to wound
Proliferation/differentiation monocytes to macro
Histamine
Cytokines (chemoattractant for WBC)
63
Q

ECM injury - new tissue formation

A

Fibroblasts divide/secrete ECM
Cytokines (regulate proliferation of fibroblasts) and GF’s
Macrophages: angiogenesis, repair, remodel

64
Q

ECM injury - tissue remodeling

A

CT extends
Cellularity is reduced
Scar formation (disorganized CT)

65
Q

Inflammatory disease in ECM

A 
Crohn's/UC
Rheumatoid arthritis
stomach ulcers
skin disorders
chronic inflammation = GI/colon cancer (promote angiogenesis)
66
Q

Function of cartilage

A

resilient/pliable support

directs formation of bone

67
Q

Types of cartilage growth

A 
appositional growth (from surface)
interstitial growth (within lacunae)
68
Q

3 types of cartilage

A

hyaline cartilage
elastic cartilage
fibrocartilage

69
Q

Hyaline cartilage

A

thin, irregular 3D
ground substrate has lots of proteoglycans
hyalurnoic acid (promotes hydration)
avascular (diffusion of metabolites)

70
Q

Elastic cartilage

A

interconnecting elastic sheets (lamellae)

ex: external ear, epiglottis, larynx

71
Q

Fibrocartilage

A

regularly arranged cartilage

extension of dense CT

72
Q

2 types of bone formation

A 
Intramembranous ossification (CT to bone, flat bones)
Endochrondral ossification
73
Q

Osteoblasts

A

secrete bone matrix (osteoid)

secrete matrix vesicles (Ca2+, PO43-)

74
Q

Osteocytes

A

Withdraw from cell cycle (G0)
Some matrix modifying
Long processes to surface for signals
Gap junctions b/t cells with processes

75
Q

Osteoclasts

A 
Hematopoiesis born (monocyte)
multinucleated
degrade bone/cartilage matrix
angiogenesis
CT migration
innervation
Ca2+ mobilization
76
Q

Fibrodysplasia ossificans progressive (FOP)

A

BMP-4 gene translocated to lymphocyte promoter in Bcell
BMP presence in ECM (with immune cells)
Acts on mesenchymal stem cells/fibroblasts

77
Q

Bone remodeling

A 
short range signals (shh, Notch, TGF-ß [BMPs])
long range signals (parathyroid hormone (up), calcitonin (down)
mechanical stress
neuronal stimulation (CNS stimulation)
78
Q

Smooth muscle contraction differences

A
  1. Ca2+ binds calmodulin
  2. Complex binds CaMkinase
  3. CaMkinase phosphylorates myosin light chain
    No troponin, still Ca2+
    Slower
    Ca2+ pumps/Na+-Ca2+ in sarcolemma
79
Q

Contractile and linker proteins in skeletal muscle

A

Dystrophin (actin to PM, not myofibril actin)
Titin (myosin to Z line, organizes thick filaments)
Nebulin (organizes thin filaments)
A-actinin (crosslinks actin at Z line)

80
Q

______ are wrapped into _______, wrapped by their own ______

A

myofilaments, myofibrils, SR

81
Q

T-tubule to SR biding triad

A

DHPR: in t-tubule membrane
Voltage gated Ca2+ channel
mutation: muscular dysgenesis
RyR: in SR membrane

82
Q

EC coupling differences in cardiac/smooth

A

Cardiac: Ca2+ entry causes depolarization
Smooth: no t-tubule/SR due to thin fibers

83
Q

Skeletal muscle fatigue

A

Decrease in both force and speed
Increased Pi, decreased pH
Affected steps:
1. AP propagation in t-tubule (K+ buildup, Na+ reduced)
2. Ca2+ release from SR (Pi buildup)
3. Ca2+ effect on troponin (H+ competition)
4. Force generation by myofilaments

84
Q

Satellite cells

A 
located on surface of fibers
differentiate into new fibers
Responsive to:
Growth factors, Nf-kB, NO, myostatin (TGF-ß)
Exercise (extra nuclei)
85
Q

Grading tension in skeletal muscle

A

increase frequency of AP
recruit additional motor units
length change (minimal, usually optimal)

86
Q

Grading tension in cardiac/smooth muscle

A

neurotransmitters/hormone regulation

cell length influences (since no bony attachments)

87
Q

Hypertrophic cardiomyopathy

A

AD, genetic heterogeneity, incomplete penetrance

88
Q

Hypertrophic cardiomyopathy clinical presentation

A 
cardiac murmur (if LV outflow obstruction)
pump fail (dyspnea, angina)
arrhythmia (syncope, sudden death)
89
Q

Hypertrophic cardiomyopathy molecular defects

A 
missense mutation in structural gene
cardiac hypertrophy (organ hypertrophy)
myocyte disarray (function compromised)
interstitial fibrosis (arrhythmia)
dysplastic intramyocardial arterioles (ischemia)
90
Q

Hypertrophic cardiomyopathy treatment

A

echo, EKG, MRI, family hx, genetic testing, chest xray

91
Q

Malignant hyperthermia

A

AD and environmental

92
Q

Malignant hyperthermia clinical presentation

A 
muscle rigidity (masseter spasm)
acidosis (increased CO2)
Rhabdomyolysis
Hyperthermia
Tachycardia, tachypnea, hyperkalemia
93
Q

Malignant hyperthermia molecular defects

A

RYR1 mutation (~70%)
Increased Ca2+ release
Increased O2 consumption and anerobic metabolism

94
Q

Malignant hyperthermia treatment

A 
Dantrolene (RyR1 antagonist)
Hypervent with O2
Bicarb
Cool patient
Treat arrhythmias (w/out Ca2+ blockers)
95
Q

DMD

A

X-linked, males only

96
Q

DMD clinical signs

A 
early onset (3-5 yrs)
abnormal gait (toe walking)
Gowers' sign
Calf pseudohypertrophy
High CK (1000s)
Cardiomyopathy
97
Q

DMD molecular defects

A

Dystrophin mutation

big deletions, framshift

98
Q

DMD treatment

A

corticosteroid (prolong ambulation, side effects)

M2M - Niswander (4 decks)

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