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Molecules to Medicine > Unit 4 > Flashcards

Unit 4 Flashcards

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Organic Chemistry 101 flashcards
1
Q

Mitochondrial membrane permeability

A

Outer membrane: super permeable

Inner membrane: not very permeable

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2
Q

Infoldings in mitochondrial inner membrane

A

cristae

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3
Q

TOM

A

Translocase of outer membrane

passive transport

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4
Q

TIm

A

Translocase of inner membrane
ATP-dependent
Targeting sequence binds to TIM and opens the pore, only that protein will fit, and it’ll be fed through as a polypeptide strand.

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5
Q

Mitochondrial Fusion cellular GTPases

A

OPA1 and Mfn

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6
Q

Mitochondrial Fission cellular GTPases

A

Fis1 and Drp

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7
Q

F0 ATP synthase subunit

A

protein complex that spans the inner mitochondria membrane and contains a proton channel

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8
Q

F1 ATP synthase complex

A

bound to F0, enzyme that actually makes ATP from ADP and phosphate

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9
Q

Number of proton transfers needed to make 1 ATP

A

3

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10
Q

How is ATP transported out of the mitochondria?

A

ATP/ADP transporter

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11
Q

Role of mitochondria in cell death (apoptosis)

A

cell damage induces Bak/Bax-permeabilization of the outer mitochondrial membrane, which leads to cytochrome c release, which assembles an apoptosome

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12
Q

Role of mitochondria in necrosis

A

ischemic injury leads to MPTP-dependent permeabilization of the inner and outer mitochondrial membrane resulting in cytochrome release and elimination of the proton gradient, which prevents ATP synthesis and actually causes ATP synthase to reverse directions and use things up more quickly!

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13
Q

Mitochondria and quality control

A

1) mitochondrial proteases degrade misfolded proteins (mAAA, iAAA, Lon)
2) mitochondria can be fixed by fusing with healthy mitochonria
3) mitochondria can be eliminated by mitophagy

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14
Q

Why is mitochondrial QC important?

A

Mitochondrial damage and resulting increase in RUS is related to increased senescence and increased sensitivity to neuronal degeneration

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15
Q

Mitochondrial associated disease

A

mutation in OPA1 causes dominant optic atrophy
mutation in Mfn2 gene causes Charcot-Marie-Tooth neuropathy
mAAA protease mutation –> hereditary spastic paraplegia

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16
Q

Asenic mxn

A

inhibits oxidative phosporylation and ATP production

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17
Q

3 functions of mitochondria

A

1) ATP generation
2) Apoptosis
3) regulation of intracellular Ca2+

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18
Q

Outer membrane mitochondrial import

A

GIp= general import pore

Tom 70 and Tom 20 are import proteins

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19
Q

mtHSP70

A

recognizes the sequence for inner mitochondrial membrane import, binds it and TIM, hydrolyzes ATP, and pulls the protein through the membrane

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20
Q

ATP synthase structure

A

F1: 3 α and 3 β subunits, spins around and goes through 3 conformations

1) binds ADP
2) squishes phosphate and ADP together
3) ATP gets released

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21
Q

Cytochrome C and apoptosis

A

if cytochrome C is OXIDATED, it’ll form an apoptosome. It’s reversible if it’s small enough by reduction

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22
Q

Blood supply of epithelial cells

A

Epithelial cells are avascular. Nutrients and oxygen diffuse through basal lamina and connective tissue to reach epithelial cells

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23
Q

Epithelial funtions (7)

A

1) Barrier
2) Selection absorption and transport
3) Selective secretion
4) Movement of particles and movement through passageways
5) Biochemical modification of molecules
6) Communication to/from other tissues and organs
7) reception of sensory stimuli

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24
Q

endothelium

A

a tissue that faces blood and lymph

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25
Q

mesothelium

A

sheets of cells that line enclosed internal spaces of the body cavities

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26
Q

Organs that are composed mostly of epithelial cells in which epithelia are primary functional units

A

Liver, kidney, pancreas

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27
Q

Developmental origins of epihthelia

A

Developed from all 3 primary germ layers
There’s a lot of fluctuation in where the epithelia goes through early development.
-Many cells undergo epithelial to mesenchymal transition

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28
Q

Exceptions to generalized epithelia/CT/muscle/nerve relationships

A
  • Some specialized neurons make contact with specific epithelial cells (ie taste buds)
  • dendritic cells can infiltrate epithelia and migrate in and out of CT and can enter blood or lymph
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29
Q

lamina propria

A

the CT directly under the epithelium; typically contain lots of immune cells and small blood cells

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30
Q

submucosa

A

Layer of CT deep to the lamina propria. Typically contains larger muscles/vessels/nerves

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31
Q

Simple epithelia

A

all cells arranged in a single layer or sheet.

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32
Q

Stratified epithelia

A

more than one layer of cells in which cells of the outer layers do not directly contact the basal lamina.

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33
Q

pseudostratified

A

a special case where some cells do not reach the free surface
(giving a stratified appearance), but all directly rest on the basal lamina

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34
Q

Cell shapes relative to apical/basal axis

A

squamous=flat
cuboidal=cube-like
columnar=taller than wide

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35
Q

Naming stratified epithelia

A

Name them according to outer layer

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36
Q

Transitional epithelia (in bladder)

A

stratified,
but when stretched change their shape from cuboidal to squamous, and appear to decrease the
layering: this is indicative of a tightly adherent epithelium that is very resilient and stretchable.

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37
Q

Tight junctions

A

Key core proteins are claudins and occludins

In some epithelia the “tightness” of the barrier is regulated

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38
Q

Adherence junctions

A

Promote attachment, but also polarization, morphological organization and stem-cell behavior
cadherins link to actin filaments
and interact with other cells’ cadherins and intracellular proteins

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39
Q

Desmosomes

A

Promote mechanical strength

Contain a different type of cadherins that link to intermediate filaments and adapter proteins

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40
Q

location of tight junction complexes

A

Typically toward the apical side of cells

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41
Q

Are the basal and lateral membranes the same in protein composition, etc.

A

Not necessarily. Sometimes they’re different

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42
Q

Transcytosis

A

Transfer of vesicles from one side of the epithelium to the other

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43
Q

Microvilli

A

Protrusions that contain actin bundles connected to internal cytoskeleton
-Primary function= increase surface area

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44
Q

Stereocilia

A

a special type of microvilli found in the epididymis and sensory cells in ear.

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45
Q

Primary cilium

A

1 non-motile, microtubule based extension found on many cell types
-promote/organize signal transduction systems that control cell division, fate, and fxn

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46
Q

motile cilia

A

micotubule extensions that move like a boat oar to move mucus and other materials along.

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47
Q

Sensory cilia

A

not motile, have sensory fxn. ie. hair cells in ear

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48
Q

Location of villi and cilia

A

typically apical membrane. Sometimes there will be pockets for surface area in the basolateral membrane as well

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49
Q

Basal lamina

A

Formed by a special type of network-forming collagen (Type IV) interwoven with glycoproteins, laminins, and entactin

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50
Q

Basal laminae functions

A
  • Attachment
  • selective filtration to/from epithelia
  • necessary for establishment of cell polarity
  • “highways” for cells migrating through CT
  • barrier to movement of microbes and cancer cells to other tissues
  • control gene expression to effect proliferation or development
  • Control development of epithelial cells by providin g a”tissue scaffolding” function (essential for repair following disease/injury)
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51
Q

Attachments of epithelial cells to basal laminae

A

hemidesmosomes (integrin attaches to IF’s) and focal adhesions (integrins attach to actin) on basal surface
**all of these are made primarily from integrins*
=Focal adhesions regulate polarity and function through signaling, and are probably important in healing/cell turnover

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52
Q

Three qualities of all epithelial stem cells

A

(i) are competent for cell division, (ii) self renew:
regeneration of a “mother” stem cell with each division, and (iii) produce differentiated cell types
specific to each epithelia.

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53
Q

Transit amplifying cells

A
  • Daughter cells from stem cells that also proliferate, often at a faster rate
  • They themselves produce differentiated cells
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54
Q

Cell lineage

A

A specific stem cell type, its intermediate progeny, and their differentiated progeny

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55
Q

Epithelial stem cell signaling source

A

secreted by cells within the same epithelium or in nearby CT

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56
Q

Core groups of signaling pathways that control tissue development

A

Wnt, Sonic Hedgehog, TGFβ, Notch, FGF, receptor tyrosine kinase family

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57
Q

Tarceva (erlotinib)

A

a lung and pancreatic cancer treatment

inactivates EGF receptor

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58
Q

2 mechanisms of glandular secretion

A

1) Exocytosis

2) Total cellular disintegration (these glands are called holocrine glands)

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59
Q

Exocrine glands

A

secrete on the apical side of epithelium, generally multicellular (but some are unicellular ie Goblet cells)

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60
Q

Exocrine secretory units

A

bowl/flask shaped: alveoli/acini->alveolar/acinar gland

tubes: tubular gland

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61
Q

Ducts

A

Tubular structure that emanates from the secretory unit, pathway for secretion to reach its destination
1 duct–> simple gland
>1 duct–> compound gland

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62
Q

3 types of exocrine glands

A

1) mucous–> viscous glycoprotein produced
2) serous–> watery/ salty fluid is produced
3) mixed–> both types of secretions released

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63
Q

Endocrine glands

A

-No ducts, secrete directly into blood stream

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64
Q

Organization of endocrine gland

A

generally a clump of cell embedded with surrounding CT containing extensive capillary networks (each clump surrounded by a basal lamina)

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65
Q

Direction of endocrine secretions

A

Typically basolateral (hormone must cross basal lamina)

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66
Q

Regulation of exocrine/endocrine glands

A

Regulated by autonomic input, blood hormones, or both

Endocrine secretions are tightly regulated, exocrine less so

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67
Q

carcinoma

A

cancer of epithelial origin

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68
Q

adenocarcinomas

A

cancers developed from glandular epithelium

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69
Q

Typical progression of tumors

A

Tumors most commonly develop within an epithelial sheet but then can metastasize

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70
Q

Treatment targets for carcinomas

A

1) development signaling systems (wnt, EGF, notch)
2) internal cell cycle control factors
3) factors that control DNA repair and apoptosis

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71
Q

Epithelia and wound healing

A
  • If basal epithelial stem cells and lamina are intact–> intrinsic mxns work!
  • If damaged extensively, skin grafts may be required.
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72
Q

Cilia Base anchor

A

Basal bodies/centrioles

  • microtubule rich cylindrical structures formed from nine triplet microtubules
  • Polarized structure: proximal end forms first, distal-end nucleates the cilium
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73
Q

Axoneme

A
  • structural skeleton of the cilium
  • 9 fold symmetry
  • Each individual microtubule subunit contains A-B tubules
  • Plus ends at ciliary tip
  • provide tracks for movement within cilia
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74
Q

Linkage domain/Transition zone of cilia

A

“gatekeeper” of the cilia

  • attaches basal body to axoneme and ciliary membrane
  • Limits diffusion of both membrane and soluble proteins into cilia
  • *many disease mutations occur in this domain**
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75
Q

Ciliary membrane

A

compositionally distinct from plasma membrane because of transition zone

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76
Q

Intraflagellar transport

A

Anterograde: Kinesin 2 and IFT-B
Retrograde: dynein 2 and IFT-A
Lipid rafts are transported back and forth

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77
Q

Which centrosome becomes the basal body?

A

The older/mother centrosome

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78
Q

When in the cell cycle are cilia formed? replicated?

A

Formed- Early G1/G0

Replicated-S (along with DNA)

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79
Q

Steps of ciliogenesis

A

1) Mother centriole recruits vesicle from the golgi (“ciliary vesicle”)
2) Doublet appendages form and elongate
3) The structure hits the plasma membrane and fuses, axoneme is formed.

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80
Q

Motile cilia structure

A

Typically have a 9+2 axonemal microtubule arrangement (but a few exceptions are 9+0)

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81
Q

Distinguishing factor between motile and sensory cilia

A

Motile cilia have axonemal dynein arms

Primary/Sensory are 9+0 without axonemal dynein arms

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82
Q

3 types of stimuli detected by receptors in cilia

A

1) Physical stimuli (mechanical, temp, osmolarity)
2) Light
3) Chemical stimuli

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83
Q

Reasons why cilia is an optimal signaling molecule

A
  • Concentration of signal
  • localized/polarized signal
  • fluid mechanics (able to detect signals further from surface)
  • can detect mechanical flow
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84
Q

Hedgehog signaling pathway

A
  • Well established to act through cilia

- Target is the Glioma tumor transcriptional activator

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85
Q

Hedgehog downstream targets

A

Limb formation
bone formation
neurogenesis

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86
Q

Ciliary node

A
  • an invagination of ciliary cells that forms during gastrulation
  • cells beat in a rotary fashion producing a net leftward flow of signaling molecules
  • Determines laterality of body
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87
Q

Bardet Biedl Syndrome

A

Autosomal recessive
-19+ genes id’d
-BBS proteins affect vesicle transport in the clilum
Symptoms: photoreceptor degeneration, anosmia, developmental delay, neural tube defects, obesity, hypogonadism, kidney defects, diabetes, situs inversus

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88
Q

Polycystic kidney disease

A

Autosomal dominant (polycystin 1 or 2 mutation) or recessive (fibrocystin mutation)

  • genes encode Ca++ that sense mechanical flow of urine in kidney lumen
  • renal, pancreatic, and hepatic cysts and intracranial aneurysms
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89
Q

CF genetics

A

Autosomal recessive
All mutations occur in CFTR gene (there are many)
ΔF508 is the most common mutation

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90
Q

CFTR function

A

Chloride ion channel
controls the movement of salt and water in/out of cells
Loss of this movement alters host defense in the lung

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91
Q

CF Class 1

A

No CFTR synthesis occurs

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92
Q

CF Class 2

A

Block in processing- CFTR synthesis starts but processing isn’t completed/ membrane insertion does not occur

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93
Q

CF class 3

A

Block in gating

Channel is made and put in the membrane, but Chloride can’t actually get through at all

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94
Q

CF class 4

A

Altered conductance

CFTR is made and inserted, but it doesn’t conduct chloride as well

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95
Q

CF class 5

A

Reduced synthesis

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96
Q

Newborn screen in in colorado

A

IRT/IRT/DNA

IRT= immunoreactive trypsinogen, a pancreatic enzyme

97
Q

CF diagnosis

A 
Diagnosed through: 
-	Positive NBS OR
-	≥1 clinical feature of CF OR
-	Family hx of CF
PLUS
-	Sweat Cl ≥ 60 mmol/L AND/OR
-	2 CF mutations
98
Q

GI treatments for CF

A
  • Salt supplement

- Pancreatic enzyme supplement

99
Q

Lung treatments for CF

A

Daily airway clearance (percussive therapy, inhaled pulmozyme, inhaled saline/bronchodilators)
Antibiotic therapy for common CF related bacteria

100
Q

Anti-inflammaory treatments

A

Ibuprofen

Chronic azithromycin

101
Q

Ivacaftor

A

CFTR “potentiator” FDA approved for people 2 and over with Class III CF
G551D protein mutation

102
Q

Orkambi (Lumacaftor/Ivacaftor)

A

Combination CFTR “corrector” and “potentiator” for Class II CF ( 2 copies of the F508del mutation)

103
Q

Mesenchymal cells

A

stem cell precursors to all CT family cells

Most active during embryogenesis, a few will persist to adulthood

104
Q

Fibroblasts

A

pre-eminent cells of most connective tissues in body

105
Q

ECM functions (6)

A

a. control of epithelial cell polarization and shape
b. guidance and regulation of cell migration through matrix
c. control of cell proliferation, differentiation, metabolism
d. defense against infectious agents
e. control of tissue formation, organization, modification
f. Control of inflammation and repair due to injury

106
Q

Myofibroblasts

A

derivatives of fibroblasts capable of smooth-muscle like function (Often found in CT sites that require contractile function)
often generated at the sight of wounds, contributes to shrinkage of scar tissue

107
Q

Fibroblast derivatives

A

Adipocytes

108
Q

Adipocytes

A

store fat as energy for other cell types
“white fat’-adults
“brown fat”= a distinct type that converts fatty acids to heat in kids

109
Q

Osteoblasts

A

Make bone

110
Q

Osteocytes

A

Are left behind and actually hang out in bone

111
Q

Chondrocytes

A

make cartilage

112
Q

Smooth muscle cells

A

Exist in CT

A few of them (esp ones in blood vessel walls) make ECM components

113
Q

Cells that secrete ECM components

A

msenchymal cells, fibroblasts, myofibroblasts, adiiposytes, osteoblasts/cytes, chondrocytes, some smooth muscles

114
Q

Lymphocytes

A

central to acquired immunity

115
Q

Macrophatges

A

large” engulfing cells that phagocytose, signal for angiogenesis, remodel damaged tissue and normal tissue as part of development

116
Q

neutrophils and eosinohpils

A

white blood cells important for defense against microorganisms

117
Q

Mast Cells

A

Secretory cells that release various substances, including vasodilators that promote swelling in CT’s (important in edema and allergies)

118
Q

Osteoclasts

A

phagocytotic cells derived from blood monocytes, function in bone resorption

119
Q

Immigrant Blood derived cells in CT

A

Lymphocytes, macrophages, eosinophils and neutrophils, mast cells, osteoclasts

120
Q

Fibrillar collagen

A

assembled into large bundles (aligned head to tail for length, stacked for thickness.)
Great tensile strength, most abundant in body, Type 1 collagen

121
Q

3 types of collagen

A

Fibrillar, fibril-associated, and network-forming

122
Q

Fibril associated collagen

A

Decorate the surface of collagen fibrils and link them to each other/other tissue components

123
Q

Network-forming collagen

A

Very thin fibers that assemble into interlaced networks that formed porous sheets (basal laminae!)
Some also function as filtration barrier (kidney)
Type IV collagen is big

124
Q

Loose connective tissues

A

thin colagen fibrils in sparse networks - cell densities and ground substance components, capillaries, and nerves are relatively concentrated

125
Q

Dense connective tissue

A

Thick collagen fibrils more abundant than ground substance, low number ofcells

126
Q

Collagen organization in ligaments and tendons

A

parallel-organized sheets

127
Q

Collagen synthesis

A
  • Made by CT cells
  • Polypeptides synthesized on ER, post-translationally modified and assembled into a triple helix
  • N and C termini are cleaved and the collagen fibrils are polymerized, with enzymes forming cross links
128
Q

CT response to wounds

A

stimulation of fibroblast regulation and stimulation of ECM production

129
Q

N-Telo peptides

A

Bits cleaved off collagen monomers when they are first secreted. Used as a marker of CT/bone disease in urine

130
Q

Elastic fibers

A

Elastin-filamentous protein that exists in a random coil conformation that can stretch and recoil. These networks are interwoven with fibrillin that appears to organize the elastic elements

131
Q

Hyaluronic acid

A

A GAG that isn’t covalently attached to a protein

132
Q

3 properties of GAG’s relavent to function

A

1) highly negatively charged
2) Rigid extended structure causes them to readily form gels-they promote hydration of ground substance and allow diffusion of small metabolites while inhibiting movement of large structures and allows it to resist compression
3) Some can bind and inactivate other proteins (growth factors and ECM-modifying enzymes)

133
Q

4 ECM components

A

1)Proteoglycans (with GAG’s attached)
2)other secreted proteins/glycoproteins
inorganic and small organic 3)solutes
4)water

134
Q

Inflammation and clotting- role of CT

A

1) Blood clots temporarily seal wound

2) CT fibroblasts and Mast cells, etc. release signaling compounds to increase inflammation

135
Q

Inflammation processes

A

(i) Increase water permeability of capillary–> swelling
(ii) increase cellular permeability of endothelia to allow monocytes, lymphocytes, and other blood cells to enter C.T.
(iii) attract white cells to wound (chemotaxis)
(iv) stimulate proliferation of fibroblasts and differentiation of monocytes into macrophages

136
Q

Histamine’s effect

A

promote endothelial permeabilization

137
Q

cytokines

A

promote inflammatory processes and go back to hematopoeitic tissue to stimulate more WBC production

138
Q

Angiogenesis triggers after injury

A

macrophages secrete cytokines that promotes angiogenesis

139
Q

Cartilage

A

Avascular and unable to repair in adults

140
Q

Origin of chondrocytes

A

Mesenchymal stem cells

141
Q

perichondrium

A

external layer of CT surrounding cartilage

142
Q

Lacuna

A

Chondrocytes secrete ECM around themselves, forming lacuna

143
Q

Hyaline Cartilage

A

thin, irregular collagen fibrils. Ground substance rich in proteoglycans and hyaluronic acid
(At joints and temporary during bone growth)

144
Q

Elastic cartilage

A

Also contains thin collagen fibrils and proteoglycans, but distinguished by abundant elastic fibers and lamellae of elastic material
Does not calcify

145
Q

Fibrocartilage

A

Large bundles of regularly arranged collagen that’s similar to dense connective tissue (continuation of this tissue where tendons attach to bone and in intervertebral discs)
Resists compression and sheer forces

146
Q

spongy bone

A 
contains trabeculae (anastomosing spicules) 
Bone marrow is between trabeculae
147
Q

Bone marrow

A

hematopoeitic tissue or atipose cells surrounded by loose connective tissue containing blood vessels

148
Q

Outer surface covering bone

A

periosteum

149
Q

endosteum

A

inner surface where trabeculae contact CT

150
Q

Osteoprogenitor cells

A
  • generate osteoblasts and osteocytes

- present on periosteal and endosteal surfaces and in soft connective tissue

151
Q

osteoblasts

A

periosteal and endosteal surfaces where growth or remodeling occurs
secretes osteoid
Pinch off matrix vesicles that contain enzymes to initiate calcification

152
Q

osteocytes

A

derived from osteoblasts
become surrounded by bone matrix and a lacuna
no cell division
extend long processes through canaliculi in the calcified matrix and form gap junctions with other osteocyte processes

153
Q

Osteoclasts

A 
derived from monocytes
resemble macrophages
degrade cartilage/bone for 3 purposes:
1)allow inward growth of blood vessels
2)remodeling
3)Ca++ store release
154
Q

Bone matrix

A
  • calcified and packed with parallel collagen
  • contains glycoproteins
  • contains lots of hydroxyapatite crystallized onto collagen and in the ground substance
155
Q

Bone vascularization and innervation

A

-Travel through channels

Long axis channels in long bones are called Haversian canals. Bone lamellae surround them in concentric rings

156
Q

Osteon

A

Haversian canal + lamellae (concentric rings of compact bone)

157
Q

Volkmann’s canal

A

canals that link Haversian canals to each other and to the periosteum at the bone surface

158
Q

Intramembranous ossification

no pre-made cartilage

A

1) A group of mesenchymal cells come together in a sheet of connective tissue (condensation)
2) These mesenchymal cells differentiate into osteoprogenitors and then osteoblasts
3) This process forms “bone islands” that develop in a trabecular network

159
Q

Flat bone formation

A

intramembranous ossification

160
Q

Cartilage formation

A

Mesenchymal cells divide and differentiate to form chondrocytes. Chondrocytes then secrete hyaline cartilage matrix and individual chondrocytes become encased in lacunae

161
Q

Appositional growth

A

Growth at the surface

162
Q

Interstitial growth

A

growth from within
Early in development chondrocytes in the matrix continue to proliferate. Groups of chondrocytes that are clones derived from mitoses are “isogenous groups”

163
Q

Epiphyseal plate

A

Remaining region of proliferative cartilage after birth

aka growth plate

164
Q

Growth of long bones

A

1) Chondrocytes replicate in their lacunae in the direction of the long axis of the bone and deposit hyaline matrix
2_ Osteoblasts, osteoclasts, and capillaries encroach on the cartilage from the diaphyseal side causing a continued wave of bone formation

165
Q

Articular cartilage

A

The only sheath of non-proliferative cartilage left at the end of the epiphysis after bone growth

166
Q

Growth of bone diameter

A

occurs on periosteum, requires continued proliferation of osteoprogenitors in the periosteum and their differentiation into osteoblasts

167
Q

Bone resorption in adults

A

primarily on the endosteal surface

168
Q

Osteoporosis

A

decrease in bone mass due to defects in resorption/formation coupling

169
Q

Osteopetrosis

A

defective bone resorption and increased bone mass

170
Q

Osteomalacia rickets

A

abnormal increases in uncalcified osteoid (interferes with mineralization

171
Q

Matrix vesicles

A

Pinch off of osteoblasts and serete calcium, alkaline phosphatase, and phosphate bound to other molecules. Alkaline phosphatases are activated to form free phosphate, which precipitates with calcium to form hydroxyapatite, causes vesicle rupture, and then acts as a nucleation site

172
Q

Short range signals that regulate bone

A

Bone morphogenetic proteins (BMP’s)are secreted by the cell, then bind receptors and alter gene expression to control bone development and maybe other pathways
Other important pathways: FGF, Notch, Wnt

173
Q

Other sources of Bone regulation

A

1) Long-range signals (steroid hormones and Ca hormones)
2) Mechanical stress
3) Neuronal stimulation

174
Q

Parathyroid hormone and Calcium

A

Stimulates calcium liberation from bone

175
Q

Calcitonin

A

Stiumlates calcium uptake into bone by controlling osteoblasts and osteoclasts

176
Q

Vitamin D

A

important for calcium uptake from intestine

177
Q

Tunica intima

A

layer of endothelial cells and a layer of elastic and loose collagenous tissues

178
Q

Tunica media

A

Multiple layers of elastic laminae, smooth muscle cells, or collagen

179
Q

Tunica adventitia

A

Comprised of collagenous tissue

180
Q

vasa vasorum

A

blood vessels in the tunica adventitia of larger vessels

181
Q

Pericytes

A

Half moon like cells that surround capillaries and may develop smooth muscle cells during vessel growth and wound healing

182
Q

capillaries

A

1-2 endothelial cells surround lumen and pericytes

All surrounded by collagenous fibrils which anchor capillary to nearby CT

183
Q

Continuous capillaries

A

Endothelial cells form uninterrupted lining, transfer across lining is through pinocytotic vesicles

184
Q

Fenestrated capillaries

A

Pores or fenestrations occur in endothelial cells that permit bulk flow

185
Q

Post-capillary venules

A

Similar to capillaries but larger
also have pericytes
slow flow, common site of leukocyte diapedesis
endothelium is responsve to vasoregulatory substances like serotonin and histamine

186
Q

Arteriovenous shunt

and metarterioles

A

Connects larger arteries and venules

Constriction/dilation can control whether blood flows through a capillary bed

187
Q

End Artery

A

artery that supplies a section of tissue that has no alternate supply

188
Q

Portal system

A

begins in a capillary bed and ends in a capillary bed

189
Q

Pampiniform plexus

A

Countercurrent arrangement between artery and venous network

190
Q

EGFR in lung cancer

A

dysregulation can be due to ligand overexpression, receptor overexpression, or mutation in receptor

191
Q

EGFR treatments for lung cancer

A

TKI’s

Antibiodies

192
Q

ALK gene rearrangement

A

3% of lung cancer

can be targeted chemotherapeutically

193
Q

Immunotherapy for Lung cancer

A

PDL1 and PD1 upregulate apoptosis when they bind. In cancer, they don’t bind properly, but immunotherapy could fix this

194
Q

Centrally located nucleus in skeletal muscle

A

Healing cell

195
Q

Sarcomere boundaries

A

Z line to Z line

196
Q

myofibrils

A

bundles of contractile muscle fibers

197
Q

Troponin and tropomysin

A

Ca++ binds troponin and undergoes conformational change with tropomysin exposing a myosin binding site

198
Q

Myosin head dynamics

A

Myosin is already a loaded spring when it binds actin. It does a powerstroke automatically.
ATP then reloads the spring before it binds again

199
Q

Smooth muscle contractsion

A
  • No troponin or tropomysin
  • Calcium binds calmodulin, then ca-calmodulin binds CaM kinase, which phosphorylates myosin light chains allowing myosin to bind actin
200
Q

Smooth muscle contraction vs. skeletal muscle contraction

A
  • Ca++ signaling for smooth muscle is slower
  • Calcium is removed by Ca pumps and Na-Ca exchangers in sarcolemma
  • smooth muscle can remain in a bound state without consuming ATP
201
Q

Mutation in Duchenne Muscular dystrophy

A

Dystrophin- a protein that links actin/myosin with ECM

202
Q

titin

A

an enormous protein hat links myosin thick filaments to the Z-line

203
Q

Nebulin

A

large protein associated with actin thin filaments thought to be important for keeping thin filaments organized

204
Q

alpha actinin

A

the molecule that crosslinks actin filaments at the z-line

205
Q

FHC mutations

A

Usually in cardiac myosin head

206
Q

diffusion equation

A

= 6Dt,
D=diffusion coefficient
t=time
r=mean distance from starting point

207
Q

Parvalbumin

A

Calcium binding protein that can bind and release calcium and diffuse faster than calcium in muscle cells

208
Q

Myoglogin

A

An oxygen binding protein that is found in oxidative muscle in large quantities

209
Q

Creatine/phosphocreatine

A

Molecules that replenish ATP during times of high metabolic demand

210
Q

Transverse tubule system

A

Membrane structure that is basically a series of membrane invaginations throughout the muscle cell that allows AP propatagion

211
Q

Sarcoplasmic reticulum

A

Each myofibril has a “stocking” of SR that stores Calcium for release

212
Q

EC coupling

A

Action potential travels toward tendons and also inward into the t-system. The
membrane depolarization in the t-system is translated into Ca+2 release from the SR

213
Q

T-tubule/SR coupling

A

DHPR in the T-tubule is a complex of several subunits, one is a vg Ca++ channel
RyR is in the SR membrane
A conformational change in DHPR causes RyR receptor to open and flood the cell with calcium

214
Q

Malignant hyperthermia

A

abnormal SR calcium release channel causes catastrophic rise in temperature when given certain volatile anesthetics

215
Q

Treatment of malignant hyperthermia

A

dantrolene injection –> blocks Ca++ release from SR

216
Q

DHP receptor mutation

A

causes muscular dysgenesis –> embryonic lethal
Gene therapy might be possible
Cardiac DHP is coded by a different gene

217
Q

Difference between cardiac and skeletal muscle EC coupling

A

Ca2+ entry is required to trigger ca++ release by the SR receptor because it has a Ca++ binding site

218
Q

Gap junctions in muscle

A

Couple both smooth and cardiac muscle cells, but not skeletal muscle skells

219
Q

3 ways to grade tension in skeletal muscle

A

(1) Increase the frequency of action
potentials. This will increase tension until a maximal (tetanic) contraction is achieved. (2)
Recruit additional motor units. This increases tension until all motor neurons innervating the
muscle are stimulated. (3) Changing the length of the muscle is a minor factor for skeletal
muscle because it normally operates near the optimal length.

220
Q

Grading tension in cardiac and smooth muscle

A

both respond to NT’s and hormone-like molecules

221
Q

satellite cells

A

stem cells that are source for new myoblasts to repair injured muscle

222
Q

Signalling molecules for satellite cells

A

Fibroblast growth factor, insulin growth factor, hepatocyte growth factor, NFkappaB, NO, myostatin (promotes muscle cell degradation), LIF ( promotes satellite cell proliferation

223
Q

fibroblasts and satellite cells

A

Fibroblasts interact with satellite cells to influence which cell types will be produced

224
Q

Repair of cardiac muscle

A

doesn’t really happen. There aren’t satellite cells and mostly fibroblasts just make scar tissue

225
Q

Smooth muscle repair

A

Smooth muscle cells can dedifferentiate, enter mitosis, and regenerate smooth muscle cells (this might be related to how good they are at proliferating)

226
Q

Metabolic muscle fatigue

A

primarily an increase in inorganic
phosphate and a decrease in pH (from 7 to 6.5) that lead to decreased ca++ release. ATP levels change very little, but phosphocreatine levels are depleted

227
Q

Duchenne Muscular dystrophy common clinical features

A

cardiomyopathy!!
High creatine kinase
toe walking
Gower’s sign

228
Q

Treatment of DMD

A

Corticosteroids

229
Q

Myostatin

A

Muscle growth inhibitor
Potential treatment for DMD=inhibit myostatin!
May be involved in muscle wasting in AIDS patients

230
Q

Clinical signs of malignant hyperthemria

A

Masseter spasms
Increased CO2 production
Rhabdomyolysis (muscle breakdown)

231
Q

Tests for Malignant Hyperthermia

A

Halothane/caffeine test

232
Q

anesthesia’s that are deadly in malignant hyperthermia

A

Halothane and succinylcholine

233
Q

Hypertrophic Cardiomyopathy

A

***myocyte disarray
fibrosis–>arrhythmia
dysplastic intramyochardial arterioles–> ischemia

234
Q

Endomysium

A

Surrounds myocytes

235
Q

perimysium

A

surrounds muscle fascicules

236
Q

epimysium

A

surrounds entire muscles

237
Q

Clinical presentations of Hypertrophic cardiomyopathy

A

1) murmur if LV outflow is obstructed
2) Pump failure (dyspnea, angina)
3) arrhythmia (syncope/sudden death)
4) Sports/family screening

238
Q

Potential Hypertrophic cardiomyopathy cure

A

Rnai

239
Q

Genetic cause of malignant hyperthermia

A

mutation in RyR, they stay chronically open when people are given triggering antibiotics

Molecules to Medicine (5 decks)

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