Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ANAT > LAter 1z > Flashcards

LAter 1z Flashcards

1
Q

What are the 4 connective tissues?

A
  • Connective tissue proper
  • Cartilage
  • Bone
  • Blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cartilage

  • What are the 3 types?
    • What are each made of?
    • What is an example of each
A

→ Hyaline

  • Smooth, translucent
  • Eg joint surfaces, ribs, trachea

→ Fibrocartilage

  • Many collagen fibres
  • Eg cartilaginous joints, menisci

→ Elastic

  • Elastin & collagen fibres
  • Eg ear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bone

  • What are the 2 types?
    • What are they made of?
    • Give an example
A

→ Compact

  • Osteons: resist tension
  • Eg diaphysis of long bones

→ Cancellous/spongy

  • Trabeculae: resist
  • Eg epiphysis of long bones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

LOOSE Connective tissue proper

  • What are the 3 types
    • Type?
    • Where?
    • What does it form
A

→ Areolar

  • Strong yet cushioning
  • Underlies epithelium, forms lamina propria

→ Reticular

  • Reticular fibres (supportive mesh)
  • Forms stroma to supports organs

→ Adipose

  • Adipocytes
  • White: stores energy
  • Brown: thermoregulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DENSE connective tissue proper

  • What are the two types?
    • What type of fibres?
    • Give example
A

→ Regular

- Parallel fibres (mainly type 1 collagen)
- Eg ligaments, tendons

→ Irregular

- Non-parallel fibres
- Eg in dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mature name for these precursors?

  • Fibroblast & Myofibroblasts
  • Chondroblasts
  • Osteoblasts
  • Lipoblasts
A
  • Fibrocytes
  • Chondrocytes
  • Osteocytes
  • Adipocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the Matrix components of:

  • Connective tissue proper?
  • Cartilage?
  • Osseous (bone)
  • Blood
A
  • Gel-like ground substance ; all three fiber types
  • Gel-like ground substance; collagen fibres, elastin fibres in some
  • Gel-like ground substance hardened with calcium salts; collagen fibres
  • Liquid plasma; no fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the general function of:

  • Connective tissue proper?
  • Cartilage?
  • Osseous (bone)
  • Blood
A
  • Acts as a binding tissue; resists mechanical stress, (tensions)
  • Resist compression, cushions & supports body structures
  • Rigidness that resist compression & tension; support
  • Fluid tissue; transports oxygen, carbon dioxide, nutrients, hormones, wastes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What makes up the Extracellular matrix?

A
  • Proteoglycans & glycosaminoglycans (GAGs)
  • Fibrillar proteins
    • Fibres provide strength or elasticity
  • Structural glycoproteins
    • Mediate interaction b/w cells & ECM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Proteoglycans & glycosaminoglycan

  • What do they form?
  • What type of properties?
  • What does the ECF bind to?
  • What do they interact with?
A
  • Form the ground substance - a gel like, amorphous material
  • Water-binding properties
  • ECF (water & salts) binds to molecules
    • Volume & compression resistance
  • Proteoglycans & glycosaminoglycan (GAGs) interact with:
    • Each other
    • With water & salts
    • Collagen
    • & other fibres & molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Glycosaminoglycan (GAGs)

  • What is this?
  • What is the most commone GAG?
  • What other GAGs attach to the proteoglycan core
A
  • Long unbranched polysaccharide chains
  • Hyaluronic acid (Hyaluronate) most common GAG
    • forms long linear molecules
  • Other GAGs (eg chondroitin sulphate, keratan sulphate) attach to proteoglycan core
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

GAGS

  • What does it stain?
  • What colour does collagen fibres stain?
A
  • GAG component of connective tissue stains blue with alcian blue
  • Collagen fibres are pink
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Fibrillar proteins

  • What are they
  • What do they form?
  • What are they involved in?
A

→ Collagen - gives tensile strength

→ Elastin - ellastic recoil

→ Fibrillin
- Forms microfibrils, found with elastin fibres, involved in adhesion mechanisms

→ Fibronectin
- Glycoprotein that forms fibrils, involved in adhesion mechanisms, binds collagen to cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Collagen

  • Is it abundant?
  • Where is it found?
  • What is it secreted by?
  • What does it stain?
A
  • Most abundant protein in human body
  • Found in most support tissues
  • Secreted by fibroblasts
  • Stains pink in H&E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Collagen structue

  • What is collagen a series of?
  • Fibres are banded under the electron microscope due to what?
A
  • Collagen is a series of twisted protein fibres

- Fibres are banded under the electron microscope due to the overlap between the microfibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Collagen

  • What does type I make up?
  • Type II?
  • Type III?
  • Type IV?
A
  • `90% of collagen in body. Makes up ligaments, tendons, bone, skin
  • Cartilage
  • Reticular tissue (forms reticular fibres)
  • Basement membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Elastin & Reticulin

Elastin

  • What is it produced by?
  • What is it abundant in?

Reticulin (reticular fibres)

  • What is it produced by?
  • What is it made of?
  • What does it form?
A

→ Elastin

  • Produced by fibroblasts
  • Abundant in blood vessels, skin, lungs, elastic cartilage

→ Reticulin (reticulare fibres)

  • Produced by fibroblasts
  • Made of type III collagen
  • Form mesh networks to supports soft tissue & organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Structural glycoproteins

  • What do they mediate?
  • What are 2 types?
A
  • Mediate interaction b/w cell cytoskeleton & extracellular matrix
  • Fibronectin & Laminin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Fibronectin & Laminin

→ Fibronectin

  • What does it connect
  • What does it allow
  • What does it bind?

→ Laminin

  • What does it bind cells to?
  • What does it bind integrins to?
A

→ Fibronectin

  • Connects cells to collagen in ECM
  • Allows movement of cells through ECM
  • Binds collagen to integrins on cell surface

→ Laminin

  • Binds cells to basement membrane
  • Binds integrins on cell surface to type IV collagen in basement membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cell-matrix adhesion mechanisms

  • What do focal contacts attach?
  • What do hemidesmosome attach?
A
  • Attach cells to substratum

- Attach cells to basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Focal adhesions

  • What do integrin molecules interact with?
  • What do migrating cells bind to?
A
  • Integrin molecules interact w/ other proteins on both sides of the lipid bilayer
  • Migrating cells bind to ECM via focal adhesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hemidesmosomes

  • What do stationary epithelial cells bind to? and how?
  • What components are present
A
  • Stationary epithelial cells bind to ECM via hemidesmosomes
  • Collagen
  • Intermediate filaments (cytokeratin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hemidesmosomes attach cells to basement membrane

  • What are the integrins linked to?
A
  • Intracellular intermediate filaments (cytokeratin) by a protein called plectin in the plaque
  • The basement membrane by anchoring filaments by a type of laminin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Tissue response to injury

  • What is inflammation?
  • Draw tissue damage cell diagram (L11 pg 4)
A
  • Inflammation is an almost universal response to tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute inflammation

What are the three main interrelated stages?

  • Type of dilation?
    • What is it mediated by?
  • What type of activation?
  • Another type of activation?
A

→ Vascular dilation (after initial brief phase of arteriole constriction)
- Mediated by histamine (tissue mast cells) & nitric oxide (endothelial clels)

→ Endothelial activation

→ Neutrophil activation & migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Acute inflammation

  • What is released from damaged tissue? What does it act on?
  • What do these casue?
    • What type of dilation?
    • Separation of?
    • Increased what?
  • Mediators & cytokines activate?
    • What is margination?
    • What is migration?
    • What is fibrinogen polymerized to?
A

→ Chemical mediators released from damaged tissue act on blood vessels

→ These cause:

  • Vasodilation
  • Separation of endothelial cells
  • Increased permeability-exudation of water, salt, proteins

→ Mediators & cytokines activate endothelium

  • Margination - neutrophils adhere to endothelium
  • Migration - neutrophils move into damaged tissue
  • Fibrinogen polymerized to fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

→ Outcomes of Acute Inflammation?

→ What are outcomes affected by?

  • Severity of?
  • Capacity of?
  • Type of?
A

→

  • Regeneration
  • Organisation & repair - healing by fibrosis
  • Chronic inflammation

→

  • Severity of tissue damage
  • Capacity of specialised cells to replicate & regrow (regenerate)
  • Type of agent which has caused the tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tissue responses to injury

For restoration of normal function w/out scarring:

  • What must be intact?
  • What must damaged cells be capable of?
A
  • Stroma (connective tissue framework of tissue) must be intact
  • And damaged cells must be capable of regeneration (eg epithelial cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Organisation & repair

  • What enters damaged area? What does it remove?
  • What is then laid down?
A
  • Macrophages emigrate into the area of damage & remove the debris
  • Granulation tissue is then laid down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Vascular granulation tissue

  • What is damaged area first replaced by?
  • Where to capillary buds grom? what do they from?
  • What do macrophages secrete?
  • What else is present?
A
  • Damaged area is first replaced by a complex of interconnecting capillaries, macrophages & support cells
  • Capillary buds grow into damaged area to form network
  • Macrophages secrete fibrinogenic & angiogenic factors
  • Fibroblasty/myofibroblast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Vascular granulation tissue

  • What does healing of inflammation involve?
  • What does this form?

→ Acute myocardial infraction healing
- Numerous what? What are they laid down on?

  • What does fibroblast deposit?
A
  • Healing inflammation involves ingrowth of capillaries & fibroblasts
  • This forms granulation tissue
  • Numerous capillaries & collagen laid down to form scar
  • Fibroblast increase in number & deposit collagen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Collagenous scar formation

  • Why do fibroblast align?
  • Collagen is?
  • Fibroblast become?
  • Vascularity is?
A
  • The fibroblast align so the collagen is deposited for maximum strength
  • Collagen is dense
  • Fibroblasts become inactive (fibrocytes)
  • Vascularity is reduce
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Scar formation

→ How is clotting caused?

  • What seeps into the injured area?
  • What is release from injury?

→What multiplies & what does it fill?
- What does granulation tissue restore?

→ What happens if the epithelium thickens?

A

→ Clotting occurs, caused by clotting proteins & plasma proteins, & a scab is formed

  • Inflammatory chemicals are released from injury
  • White blood cells seep into the injured are

→ Epithelial cells multiply and fill in over the granulation tissue
- Granulation tissue restores the vascular supply

→ Restored epithelium thickens; the are matures & contracts

34
Q

Fibrous scar formation

  • What type of scars form?
  • What may contraction result in?
A
  • Permanent scar forms

- Contraction may result in reduction of size of scar

35
Q

Connective tissue defects and deficiencies

  • > 200 disorders of what? Give example?
  • What are some a result of? (give example)
  • Some as result of?
  • Some are?
  • Others have no known what?
A
  • > 200 disorders of connective tissue
  • Some are result of infections (eg cellulitis)
  • Some as result of injuries (eg scars)
  • Some are genetic
  • Others have no known cause
36
Q

Diseases due to collagen defects

→ Usually arise from what?

→ What produced fragile bones?
- What is the name for ‘brittle bone disease’?

→ What produces abnormally stretchy skin & joint laxity?
- What is syndrome is ‘Rubber Man Syndrome’

A

→ Usually arise from mutations in genes for particular collagen types

→ Point mutation in collagen I gene produces fragile bones
- Osteogenesis imperfecta - brittle bone disease

→ Other mutations for collagen I produce abnormally strechy skin & joint laxity
- Ehlers-Danlos syndrome - ‘Rubber Man Syndrome’

37
Q

Osteogenesis imperfecta

  • Deficiency of what?
  • Less what?
  • Results in what?
A
  • Deficiency of Type I collagen
  • Less collagen/poorer quality
  • Results in weak/fragile bones
38
Q

Ehlers-Danlos Syndrome

→ Group of heritable what?

→ What can it affect?

→ Characterised by?

→ Increase risk of?

A

→ Group of heritable connective tissue disorder

→ Can affect skin, ligaments & internal organs

→ Characterised by:

  • Loose joints
  • Stretchy skin
  • Abnormal scar formation

→ Increased risk of

  • Dislocations
  • Scoliosis
  • Osteoarthritis
39
Q

Alport syndrome

  • Mutation in what gene?
  • Inherited what?
  • What is it characterised by?
  • What is disrupted?
  • What is excreted in urine?
A
  • Mutation in Type IV collagen gene
  • Inherited kidney disease
  • Characterised by glomerulonephritis, deafness & visual abnormalities
  • Glomerular basement membrane disrupted
  • Blood & protein (not normally filtered) are exreted in urine
40
Q

Marfan Syndrome

  • Mutation in what gene?
  • What is fibrillin iportant for?
  • What does this disorder cause?
A
  • Due to mutation of fibrillin gene on chromosome 15
  • Fibrillin important protein component of blood vessel walls, eyes, tendons & ligaments, and lung
  • Disorder causes skeletal defect & cardiovascular complications
41
Q

Marfan syndrome

  • What are some characteristics?
  • What is the cardiovascular abnormalities include?
A
  • Long limbs
  • Spiderlike fingers
  • Chest abnormalities
  • Curvature of spine
  • Facial features with highly arched palate, crowded teeth
  • Cardiovascular abnormalities incl. dilation of base of aorta
42
Q

What are the tree main types of muscle?

A
  • Cardiac muscle
  • Skeletal muscle
  • Smooth muscle
43
Q

Skeletal muscle structure

→ Description

- What shape & type cells?
- Striations?

→ Function
- What type of movement?

→ Location
- What muscles? Attached to what?

A
  • Long, cylindrical, multinucleated cells
  • Obvious striations
  • Voluntary movement
  • In skeletal muscles attached to bones or occasionally to skin
44
Q

Anatomy of skeletal muscle

→ Epimysium

- What type of tissue?
- What does it sheath

→ Endomysium
- What does it protect?

→ Perimysium
- What does it sheath?

→ Fascicles
- Bundles of?

A
  • Connective tissue sheathing the muscle
  • Protecting individual muscle fibres
  • Sheaths bundles of muscle fibres
  • Bundles of muscle fibres
45
Q

Muscle fibres

→ How many motor neurons per fibre?

→ Sarcolemma
- What?

→ Transverse (T)-tubule
- Invagination of what?

→ Sarcoplasmic reticulum

- Similar to what?
- Store & release what?
A
  • Motor neuron (1 per fibre)
  • Cell membrane of muscle fibre
  • Invagination of sarcolemma into cell
  • Similar to endoplasmic reticulum
  • Store & release Ca2+
46
Q

Myofilament structure

→ Actin
- What does it contain?

→ tropomyosin
- What does it cover and when?

→ Troponin

- What does it sit on? 
- What does it signal?

→ Myosin

  • Main protein of what?
  • Head binds & ‘walks’ along what?
A
  • Contain binding sites for thick filament
  • Protein strand that covers binding sites in relaxed state
  • Sits on tropomyosin & responds to signals for contraction
  • Main protein of thick filament, elongated with distinctive head
  • Head binds & walks along thin filament
47
Q

Sarcomere contraction

1) What are binding sites covered by?
2) Binding of Ca2+ to what, causes movement of tropomyosin? What does it expose?
3) What binds to actin (thin filament)
4) What changes shape? what does it pull? And where?
5) What binds to myosin? What for?
6) What does the myosin head bind to?

A

1) Binding sites of actin to myosin covered by tropomyosin
2) Binding of Ca2+ to troponin causes movement of tropomyosin, exposing binding sites
3) Myosin (thick filament) binds to actin (thin filament)
4) Myosin head changes shape & pulls thin filament to centre of sarcomere
5) ATP binds to myosin, and energy is utilized to detach myosin, reverting shape
6) Myosin head binds to another actin molecule further towards the Z-line

48
Q

Clinical Perspective
What causes Rigor Mortis?

1) Where does Ca2+ leak from? When? What does it expose?
2) What does myosin automatically bind to and pull?
3) What is not produced?
4) What does myosin remain as? What happens to the contracted muscle?

A

1) Ca2+ leaks from sarcoplasmic reticulum into muscle fibres following death, exposing actin binding sites
2) Myosin automatically binds & pulls thin filament (no ATP required)
3) New molecules of ATP needed for the unbinding of myosin & actin are not produced

4 Thus, myosin remains attached to actin, and the contracted muscles do not relax

49
Q

Nemaline myopathy

  • What does severity vary from?
  • What are some symptoms?
 Mutations in at least 10 different genes
→ NEB
   - How much % of cases?
   - What does nebulin govern?
→ ACTA1 
    - What % of cases?
    - What does it make up?
A
  • Severity varies from neonatal lethal to low end of normal strength spectrum
  • Muscle weakness, swallowing dysfunction, impaired speech

→ NEB (~50% of cases) Nebulin governs length of thin filament
→ ACTA1 (15-25% of cases) - Actin isoform making up thin filament

50
Q

Cardiac muscle structure

  • What type cells?
  • Function: As it contracts, What does it propel? What type of control?
  • Location: Where?
A

Description: Branching, striated, generally uninucleate cells that interdigitate at specialized junctions (intercalated discs)

Function: As it contracts, it propels blood into the circulation; involuntary control

Location: The walls of the heart

51
Q

Arrhythmogenic right ventricular cardiomyopathy

  • A disease of what?
  • What dies? & what is it replaced by?
  • What is irregular?
  • What does it lead to? Who?
  • What explains the prevalence?
A
  • A disease of desmosomes
  • Cardiac muscles die & are replaced by fatty infiltration
  • Irregular hear beat - arrhythmia
  • Leads to heart attacks in otherwise healthy individuals
  • Genes for desmosome proteins explains prevalence
52
Q

Arrhythmogenic right ventricular cardiomyopathy

  • A disease of what?
  • What dies? & what is it replaced by?
  • What is irregular?
  • What does it lead to? Who?
  • What explains the prevalence?
A
  • A disease of desmosomes
  • Cardiac muscles die & are replaced by fatty infiltration
  • Irregular hear beat - arrhythmia
  • Leads to heart attacks in otherwise healthy individuals
  • Genes for desmosome proteins explains prevalence
53
Q

Arrhythmogenic right ventricular cardiomyopathy

  • Fewer what?
  • What happens to the intracellular gap?
  • What happens to the cell?
  • What contributes to arrhythmogenicity?
A
  • Fewer desmosomes, those that are present fragmented, different lengths
  • Intracellular gap widening & disruption
  • Cell death
  • Widening of gap junction may contribute to arrhythmogenicity
54
Q

Smooth Muscle

  • Muscular component of what? Give examples
  • Under what type of control?
  • What type of contraction?
  • How does the whole muscle contract?
A
  • Muscular component of visceral tissue eg blood vessels, gastrointestinal tract, uterus, bladder
  • Under inherent autonomic & hormonal control
  • Ie involuntary
  • Continuous contractions of slow force
  • Often whole muscle contracting in a wave-like fashion
55
Q

Smooth muscle

Description
- What do the cells look like?

Function

  • What does it propel? & Where?
  • WHat type of control?

Location
- Where?

A
  • Spindle-shaped cells with central nuclei; no striations; cells arranged closely to form sheets
  • Propels substances or objects along internal passageways
  • involuntary control
  • Mostly in the walls of hollow organs
56
Q

Smooth muscle cell junctions

  • What are smooth muscle fibres connected to each other by?
  • What is the Nexus junction extended through?
  • What is spread from cell to cell through these junctions?
A
  • Smooth muscle fibres are connected to each other by specialised cell junction called nexus junctions or gap junctions
  • Nexus junctions extend through the external lamina
  • Signals for muscle contraction are spread from cell to cell through these junctions
57
Q

Hypertrophy

  • Whithout what? seeni in skeletal muscle?
  • What cant produce new muscle cells?
  • What expansion?
  • More what?
  • More what?
A
  • Hypertrophy w/out hyperplasia seen in skeletal muscle with extra work
  • Adult skeletal muscle cannot produce new muscle cells
  • Sarcomere expansion
  • More sarcoplasmic reticulum
  • More nuclei
58
Q

Hypertrophy - Physiological

  • What shows hypertrophy without hyperplasia? What cant the muscle cells do?
A
  • Adult skeletal muscle shows hypertrophy w/out hyperplasia as muscle cells cannot divide
59
Q

Skeletal muscle development

  • What are precursors of muscle cells?
  • What proliferate during development?
  • What do these fuse to form?
  • What can influence degree of proliferation?
  • What slows myoblast proliferation?
A
  • Myoblast are precursors of muscle cells
  • Myoblasts proliferate during development
  • They fuse to form muscle cells
  • Genes can influence degree of proliferation
  • Myostatin slows myoblast proliferation
60
Q

Hypertrophy + Hyperplasia due to gene mutation

  • Mice purposely made deficient in the myostatin gene also have remarkable what?
A
  • Mice purposely made deficient in the myostatin gene also have remarkable big muscles
61
Q

Cardia hypertrophy: physiological

  • Mice that swim have bigger what?
A

Mice that swim have bigger hearts

62
Q

Cardiac hypertrophy: pathological

  • mice with aortic restriction have bigger what?
A
  • Mice with aortic restriction also have bigger hearts
63
Q

Hypertrophy of smooth muscles

  • Obstruction of bladder leads to what?
  • What can have similar effects?
  • Mimicking bladder obstructions in animals shows what?
A
  • Obstruction of bladder lead to hypertrophy of smooth muscle, eg with prostate cancer
  • Obstruction of intestines can have similar effects
  • Mimicking bladder obstructions in animals shows smooth muscle hypertrophy
64
Q

Hyperplasia with hypertrophy

  • both occur together in response to what?
  • Give example
  • Cells in pregnant uterus are what? have larger what? Reflecting increased what? what is increased?
  • Following pregnancy what happens to the uterus? How? Termed?
A
  • Both occur together in response to increased functional requirements
  • Eg: pregnant myometrium
  • ells in pregnant uterus are enlarged and have larger nuclei reflecting their increased protein synthesis. Number of cells is also increased
  • Following pregnancy the uterus returns to normal size by physiological atrophy termed involution
65
Q

Muscle Atrophy
Examples

1) Disuse atrophy occurs from a lack of what? Is it reversible?
- Give example

2) neurogenic atrophy occurs when?
- Is it suddenly?
- Give example

A

1) Disuse atrophy occurs from a lack of physical exercise (reversible)
- Examples: bed-ridden people, astronauts

2) Severe type of muscle atrophy is neurogenic atrophy. It occurs when there is injury or disease to a nerve.
- Tends to occur more suddenly than disuse atrophy
- Example: poliomyelitis (polio)

66
Q

Muscle atrophy occurs in response to reduced endocrine stimuli

  • Reductions in what anabolic hormones can cause muscle atrophy?
  • What does Stat5b knockout mice show?
A
  • Testosterone
  • Growth hormone
  • IGF1
  • Stat5b knockout mice shows muscle atrophy
67
Q

What are the mechanisms underlying Atrophy & Involution?

A
  • Autophagy in cell atrophy

- Apoptosis - programmed cell death

68
Q

Neurons all have the same basic structure but they vary in size & shape

→ Multipolar neurone
- Where do dedrites project?

→ Bipolar neuron
- Where is the dendrite?

→ Pseudo-unipolar neurone

  • Axon & dendrite rise from?
A

Multipolar neurone
- Multiple dendrites project from cell body

Bipolar neurons
- Single dendrite opposite from axon

Pseudo-unipolar neurone
- Axan & dendrite rise from a common stem of the cell body

69
Q

Ultrasonic structure of a neuron

  • Large what?
  • Many what?
  • Lots of? Where?
  • Numerous?
A
  • Large nucleus
  • Many mitochondria
  • Lots of ER, particularly in large neurons
70
Q

Ultrasonic structure of a neuron

  • Large what?
  • Many what?
  • Lots of? Where?
  • Numerous?
A
  • Large nucleus
  • Many mitochondria
  • Lots of ER, particularly in large neurons
  • Numerous neurofilaments
71
Q

Central Nervous system

  • What is grey matter?
  • What is white matter?
A

Grey matter
- neuron cell bodies, dendrites & axons

White matter
- Axons; many myelinated

72
Q

Glial cells support the CNS

Oligodendrocytes
- CNS equivalent of what?

Astrocytes
- Provide what?

Ependymal cells

  • What type cells?
  • What does it line?

Microglia
- What type of specialised cells of the CNS?

A

Oligodendrocytes
- CNS equivalent of Schwann cell myelinate axons

Astrocytes
- Provide mechanical support (also from part of blood brain barrier)

Ependymal cells

  • Ciliated cuboidal epithelial cells
  • Line the cavities of the brain & spinal cord

Microglia
- Specialised immunological cells of the CNS

73
Q

Peripheral Nerves

  • What does a nerve consist of?
  • What are axons inside the fascicles surrounded by?
  • What are the fascicles enclosed in?
  • What are the fascicles bound together by?
A
  • A nerve consists of one or more bundles of nerve fibres called fascicles
  • Axons inside the fascicles are surrounded by collagenous support tissue called endoneurium
  • The fascicles are enclosed in dense collagenous tissue called perineurium
  • The fascicles are bound together by loose collagenous tissue called epineurium
74
Q

Myelinated nerves

  • What is invaginated into the Schwann cell cytoplasm?
  • What does the outer membrane of the scwann cell fuse to form?
  • What rotates around the axon? What does it wrap the axon in?
A
  • The axon is invaginated into the Schwann cell cytoplasm
  • The outer membran of the Schwann cell fuses to form a mesaxon
  • the mesaxon rotates around the axon - wrapping the axon in concentric layers = myelin sheath
75
Q

The resting membrane potential

  • What exists across the plasma membrane? What is negative? What is positive?
A

An electrical Potential exists across the plasma membrane of all cells. The fluid inside the cells has an excess of negative charges and the fluid outside the cell an excess of positive charges

76
Q

Multiple Sclerosis

  • What disease? what does it attack?
  • What does it slow down or block?
  • What does it cause?
  • Is there a cure for MS?
A
  • Autoimmune nervouse system disease where immune system attacks the myelin of the CNS
  • Slows down or blocks messages b/w the brain & the body

Causes:

  • Visual disturbances
  • Muscle weakness
  • Trouble with coordination & balance
  • Numbness, prickling (“pins & needles”
  • Thinking & memory problems
  • There is no cure for MS
77
Q

Multiple Sclerosis

  • What type of disease? what does it attack?
  • What does it slow down or block?
  • What does it cause?
  • Is there a cure for MS?
A
  • Autoimmune nervouse system disease where immune system attacks the myelin of the CNS
  • Slows down or blocks messages b/w the brain & the body

Causes:

  • Visual disturbances
  • Muscle weakness
  • Trouble with coordination & balance
  • Numbness, prickling (“pins & needles”
  • Thinking & memory problems
  • There is no cure for MS
78
Q

Guillain-Barre syndrome

  • What type of disease? What does it attack?
  • What is a symptom?
  • Progressing weakness of what?
  • Effects on autonomic nervous system lead to altered what?
  • What is GB associated with?
A
  • Autoimmune nervous system disease where immune system attacks the myelin of the PNS
  • Tingling in hands & feet
  • Progressing weakness of limbs & respiratory muscles
  • Effects on autonomic nervous system lead to altered heart rate & blood pressure
  • Usually associated with earlier infection
79
Q 
Synaptic transmission @ chemical synapses steps?
1
2
3
4
....
  • What do neurotransmitters include?
A

Neurotransmitters include

- Noradrenaline, glutamate, dopamine, acetyl-choline, serotonin

80
Q

Neurotransmitter disorders

  • Loss of enzyme GTP cyclohydrolase 1 leads to deficiency in what?
  • GTPCH deficiency features
A
  • Loss of enzyme GTP cyclohydrolase 1 leads to deficiereathingncy in several neurotransmitters

GTPCH deficiency

  • Early onset (4-5 months)
  • Intellectual disability
  • Convulsions
  • Irritability
  • Hypersalivation
  • Difficulty breathing
81
Q

Motor neurons & the neuromuscular junction

  • What is the neuromuscular junction the synapse between?
  • What is the neuromuscular junction also known as?
  • What can one motor neuron divide into?
  • What can one neuron innervate?
A
  • Neuromuscular junction is the synapse b/w motor neurons & muscle fibre
  • Neuromuscular junction also known as motor end plate
  • One motor neuron can divide into many branches each ending in a neuromuscular junction
  • One neuron may innervate thousands of muscle fibres

ANAT (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions