CONTENT EX 1 Flashcards

1
Q

Type 1
Type 2
Type 2b

A
  1. Slow-oxidative (type I) fibers (red, slow twitch)
  2. Fast-oxidative (type IIa) fibers (red, fast twitch)
  3. Fast-glycolytic (type IIb, also known as type IIx) fibers (white, fast twitch)
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2
Q

Dermatome of hand

A

C6 thumb
C7 Index Finger
median nerve also does appropriate finger tips

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3
Q

Type Ia fiber
Type Ib fiber
Type II fiber
gamma motor neurons

A

Type 1a primary, respond to the RATE of change in muscle LENGTH, as well to change in VELOCITY, rapidly adapting. ACTIVATE WHEN THE MusCLE IS PASSIVELY stretched
Type 1b in Golgi tendon organ, when the muscle is ACTIVEly strecthed
Type II provide position sense of a still muscle, fire when the muscle is static
gamma motor neurons Adjust the sensitivity of the spindle

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4
Q

titin
Desmin
nebulin
Dystrophin

A

Titin acts like a spring limits how far the sarcomere can be stretched

Z disks of one myofibril are bound to the Z disks of its neighbors via intermediate filament Desmin. Also links Z disks to attachment sites on the plasma membrane, Costameres. Costameres contain several cytoskeletal proteins, including vinculin, talin, spectrin, and ankyrin. Desmin mutations→ disorganization of myofibrils→generalized muscle failure.

nebulin Actin

Dystrophin (a member of the alpha-actinin protein superfamily) is a key component of dystroglycan-sarcoglycan transmembrane complex that links the CORTICAL CYTOSKELETON to the BASAL LAMINA and, therefore, to the extracellular matrix outside Looks like ACTIN filaments to sarclemma
{In patients with Duchenne’s muscular dystrophy, dystrophin is defective or absent that leads to a
disruption of the sarcolemma, which allows an unregulated Ca2+ entry, causing myofiber necrosis.}
Cytoskeletal actin to the dystroglycan complex

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5
Q

Diflusinal

A

DIFLUNISAL [Dolobid] A difluorophenyl derivative of salicyclic acid
Distinctive features of diflunisal
1) Longer half-life that allows twice daily dosing
2) Lower incidence of gastrointestinal irritation than aspirin (recall that GI effects result
from systemic action)
3) Not useful in the treatment of fever as diflunisal does not cross blood brain barrier
4) Effect on platelet aggregation is not significant in therapeutic doses

SALICYLATE

  • ASPIRIN
  • diflusinal
  • salicylates
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6
Q

DHP receptors

A

T tubules

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7
Q

Hepcidin

A

States of high hepcidin levels (including inflammatory states), serum iron levels can drop because iron is trapped inside macrophages. This may lead to anemia.

Hepcidin inhibits iron transport by binding to the iron export channel ferroportin, Inhibiting ferroportin prevents iron from being exported and the iron is sequestered in the cells

IL- 6 AFFECT

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8
Q

Protein C

A

Protein C also known as autoprothrombin IIA and blood coagulation factor XIV. Proteolytically inactivates protein 5a and Factor 8a. ANTICOAGULANT.
VITAMIN K dependent!!!

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9
Q

Ankyrin

A

Ankyrins are a family of adaptor proteins that mediate the attachment of integral membrane proteins to the Spectrin-Actin based membrane cytoskeleton. Ankyrins have binding sites for the beta subunit of Spectrin and at least 12 families of integral membrane proteins. This linkage is required to maintain the integrity of the plasma membranes and to anchor specific ion channels, ion exchangers and ion transporters in the plasma membrane.

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10
Q

MHC1 innnate immunity

A

proteosome of the MHC 1
Into ER through the TAP transport
CALENEXIN bound to MHC 1, Beta 2 Microglobulin binds to MHC1
-Calreticulin ERPs and Tapasin bind to the MHC 1 molecule, this allow the Beta macroglobulin peptide to be added Antigen presentation
MHC 1 molecule then leaves the ER in an endosome.

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11
Q

MHC 2 lysosome mediated

A
Lysosome binds in to the endosome 
MHC class 2 (alpha, beta) is within the endosome it is bound by LI so nothing can bind to it, LI blocks the site of binding 
Acidic environment of endosome breaks down LI (invariant chain peptide) to CLIP (class 2-associated invariant chain peptide) 
HLA-DM binds to MHC 2 releasing CLIP 
•MHC 2 endosome binds to endosome containing the pathogen and lysosome
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12
Q

“never liked more acid base”

A
neutrophils   			over half 
•	Lymphocytes			over 25% 
•	Monocytes 			around 5% 
•	Acidophils				1-3%
•	Basophils 			          1%
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13
Q

T helper cell 1

T helper cell 2

A

Th1 - macrophage, interferon gamma and TGF beta

Th2 - B cell, IL4, IL5

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14
Q

Thrombin positive feedback
Antithrombin 3?
ABO

A
  • affects factors 11,5,8…. thrombin is factor 2!
  • An endogenous inhibitor of factor 10a, and thrombin
  • B antigen galactose
  • A antigen galactosamine
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15
Q

Troponin

A

Troponin is a complex of three globular proteins:
-Troponin T (“T” for tropomyosin) attaches the troponin complex to tropomyosin.
-Troponin I (“I” for inhibition) inhibits the interaction of actin and myosin.
-Troponin C (“C” for Ca2+) is the Ca2+-binding protein that, when bound to Ca2+,
permits the interaction of actin and myosin.

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16
Q

3 phases in the healing process of an injured muscle

A
  1. Destruction
    - A haematoma, necrosis of muscle tissue,
    - degeneration, and an inflammatory -cell response
  2. Repair Phase
    - a haematoma, necrosis of muscle tissue, degeneration, and an inflammatory-cell response.
  3. Remodeling Phase
    - The regenerated muscle matures and contracts with reorganization of the scar tissue. There is often incomplete restoration of the functional capacity of the injured muscle.
17
Q

Muscle Healing

A

Activated SATELLITE CELLS (become MYOBLASTS, between the Basal Lamina and plasma membrane of each individual Myofiber, fibroblasts invade the at the same time, fibroblasts invade the gap and begin to produce extracellular matrix to restore the framework of the connective tissue. The physiological role of this scaffold is to transmit load across the defect so that the injured limb can be used before the repair process is complete. 2 In extensive muscle injury, the proliferation of fibroblasts can quickly lead to an excessive formation of dense scar tissue, which impedes regeneration of the muscle and results in an incomplete recovery. This has already been shown in several injuries including strains, contusions and muscle lacerations.

18
Q

What muscles are involved in flexion of the trunk?

A

AMERICAN COUNCIL ON EXERCISE
Primary lifting: Gluteus Maximus, Quadriceps, hamstrings
Secondary muscles: Synergists and stabilizers
Secondary muscles: Erector spinae, Transverse abdominus, gluteus medius/ minimus (abductors), adductors, soleus, gastrocnemius

19
Q

Satellite cells

A

Between the plasma membrane of the muscle fiber and its external lamina. Early myoblasts and late myoblasts. More specifically, upon activation, satellite cells can re-enter the cell cycle to proliferate and differentiate into myoblasts. Myosatellite cells are located between the basal lamina and sarcolemma of muscle fibers, and can lie in grooves either parallel or transversely to the longitudinal axis of the fiber. Their distribution across the fiber can vary significantly
In undamaged muscle, the majority of satellite cells are quiescent; they neither differentiate nor undergo cell division. In response to mechanical strain, satellite cells become activated. Activated satellite cells initially proliferate as skeletal myoblasts before undergoing myogenic differentiation.

**Muscular dystrophies are characterized by progressive degeneration of skeletal muscle fibers, which places a constant demand on the satellite cells to replace the degenerated fibers. Ultimately, the satellite cell pool is exhausted. satellite regeneration is outplaced by degradation

Between plasma membrane and basal lamina

20
Q

CSF flow brain to heart

A
  • Choroid plexus—(apertures in the 4th ventricle)→ subarachnoid space —(arachnoid villi)–→ Dural sinus-→ jugular vein–→ internal carotid -→ anterior choroidal artery-→ choroid plexus
  • 500 ml per day of CSF produces
21
Q

What muscles are involved in flexion of the trunk?

A

american council on exercise
Primary lifting: Gluteus Maximus, Quadriceps, hamstrings
Secondary muscles: Synergists and stabilizers
Secondary muscles: Erector spinae, Transverse abdominus, gluteus medius/ minimus (abductors), adductors, soleus, gastrocnemius

22
Q

what makes articular cartilage and fibrocartilage more vulnerable to degenerative processes than non-articular hyaline or elastic cartilage?

A

The absence of a perichondrium in articular and fibrocartilage

23
Q

smooth vessels
tunica intima
Tunica media
tunica adventitia

A
  • Muscular venules are distinguished from postcapillary venules by the presence of a tunica media.
    o Pericytes are not found in muscular venules
    Tunica Intima, endothelium with basal lamina
    Tunica Media Longitudinally arranged smooth muscle cells
    Tunica adventitia elastic fibers
24
Q

T helper cells

A

Th1 helper cells MACROPHAGE are the host immunity effectors against intracellular bacteria and protozoa. They are triggered by IL-12, IL-2 and their effector cytokine is IFN-γ. The main effector cells of Th1 immunity are macrophages as well as CD8 T cells, IgG B cells, and IFN-γ CD4 T cells.
Th2 helper cell are B CELLS the host immunity effectors against multicellular helminths. They are triggered by IL-4 and their effector cytokines are IL-4, IL-5, and IL-13. The main effector cells are eosinophils, basophils, and mast cells as well as IgE B cells, and IL-4/IL-5 CD4 T cells.

25
Q

Inteferon gamma

A

IFNγ, or type II interferon, is a cytokine that is critical for innate and adaptive immunity against viral and intracellular bacterial infections and for tumor control. IFNγ is an important activator of macrophages. Aberrant IFNγ expression is associated with a number of autoinflammatory and autoimmune diseases.

26
Q

propionic

acetic acid

A

propionic

  • indomethacin
  • ketorolac
  • diclofenac

acetic acid

  • ibuprofen
  • naproxen

enolic acid
-meloxicam