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Semester 5 November > Histology > Flashcards

Histology Flashcards

0
Q

4 components of crista ampullaris

A

Crista
Hair cells
Capula
Ampulla

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1
Q

Function of crista ampullaris

A

Detect rotation of head

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2
Q

Location of crista ampullaris

A

Semicircular canals

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3
Q

Adaption of basal laminate for tonotopic mapping

A

Base - thicker and closer for high frequency

Apex - thinner and further for low frequency

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4
Q

Function of macula

A

Detection of linear movement and gravity

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5
Q

Components of macula

A 
Otoliths
Otolithic membrane 
Hair cells
Supporting cells
Nerve endings
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6
Q

Types of nerve endings

A 
Hair follicle ending
Ruffini ending
Krause corpuscle
Pacinian corpuscle
Meissners corpuscle
Free nerve endings
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7
Q

Fx ruffini ending

A

Pressure on skin

Dermis of hairy and glabrous skin

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8
Q

Fx pacinian corpuscle

A

Responds to vibration

Deep dermis

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9
Q

Fx meissners corpuscle

A

Responds to vibration

Found in glabrous skin

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10
Q

Fx free nerve endings

A

Pain, temp

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11
Q

Two parts of tympanic membrane

A

Pars tensa

Pars flaccida

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12
Q

Define process of Wallerian degeneration

A 
Chromatolysis
Swelling of cell body
Degeneration of disconnected axon
Degeneration of myelin sheath
Macs and Schwann mop up
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13
Q

Outline role of Schwann cells in regeneration in PNS

A 
Remove debris
Provide growth promoting substrate
Guide regenerating axon
Promote neuron survival = neurotrophic factors
Re-myelinate
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14
Q

Briefly explain how B amyloid fragment implicated in Alzheimer’s

A

Direct toxicity to neurons causes:
Neuronal damage
Disruptions of synaptic contacts

Promotes glial reactivity and inflammatory respose which damages and kills neurons.

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15
Q

Three true barriers on BBB

A

Cerebral capillaries
Choroid plexus
Arachnoid mater

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16
Q

Why blind spot not perceived in field of vision

A

Visual centers extrapolate info from adjacent areas of visual field and ‘fill’ the space.

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17
Q

Two main functions of neuronal cytoskeleton

A

Cellular structure

Axonal transport

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18
Q

How do cells in CNS contribute to regeneration failure

A

Astrocytes - become reactive, form glial scar and express axon-growth inhibiting proteoglycans.
Oligodendrocytes - up regulate release of axon-growth inhibiting proteins.
Microglia - remove debris but can release cytotoxic agents.

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19
Q

Principle function of each support cell type in CNS

A

Astro - metabolic/structural support, BBB, regulate ECM
Oligodendrcytes - myelination, membrane protein channels
Microglia - immune defense
Ependyma - movement of CSF (?neurogenesis)

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20
Q

Types of sensory axons and nature of stimuli

A

Aa - proprioception
Abeta - mechanoception
Adelta - pain, temp
C - pain, temp, itch

21
Q

Fast axonal transport uses what protein

A

Kinesin

22
Q

Fx of pericyte in CNS

A

Structural stability
Phagocytosis
Vasodynamic capacity

23
Q

Transport mechanisms across cerebral caps

A 
Carries systems (highly specific) eg D glucose, amino acids
Receptor mediated endocytosis eg insulin
Diffusion
24
Q

Structural differences between BMEC and normal endothelial cells

A

Absence of fenestrations

More extensive tight junctions

25
Q

Functional differences between BMEC and normal endothelial cells

A
  • impermeable to most substances
  • space pinocytotic vesicular transport
  • increased expression of transport and carrier proteins
  • no gap junctions
  • limited para cellular and trans cellular transport
26
Q

What is the role of astrocyte foot process in the BBB?

A
  • provide biochemical support
  • influence organisation of vessel wall
  • involved in postnatal maturation of BBB
  • co-regulate function be secretion of soluble cytokines
27
Q

Regions not enclosed by BBB

A
  • area postrema
  • median eminence
  • neurohypophysis
  • pineal gland
  • subfornical organ
  • lamina terminalis
28
Q

Type of molecules that can cross the BBB

A 
Hydrophobic (CO2, O2, N2)
Small polar (water, urea)
29
Q

Type of molecules that can’t cross the BBB

A

Large polar molecules (glucose, sucrose)

Ions

30
Q

Things that are carried across the BBB

A
  • D glucose
  • large neutral amino acids (NT precursors)
  • glycine
31
Q

How can pathogens be transferred across the BBB?

A
  • physical damage to BBB
  • ligand receptor interactions followed by host cell actin cytoskeleton rearrangements
  • trans cellular transport
32
Q

Types of neuronal death after injury

A
  • necrotic cell death (first wave)

- apoptotic (second wave)

33
Q

Requirements for functional axon regeneration

A
  • injured nerve must be able to survive after lesion and re-express genes required for outgrowth
  • surrounding tissue must be conducive to axon re growth
  • re-growing axons must be able to find their proper targets and establish contact
34
Q

Growth cone

A

Tip of a growing axon

35
Q

Sequence of events after a nerve injury

A

Wallerian degen
Schwann cells form a substrate for axon growth
Functional connection is restored

36
Q

How can regeneration go wrong?

A
  • gap in nerve too wide to bridge
  • axons grow down wrong endoneurial tubes
  • loss of target contact may cause death of motoneurones
37
Q

How do Schwann cells support axon regeneration?

A
  • phagocytose and recycle cellular debris
  • provide a growth-promoting substrate for axons
  • support neurones survival and axon re-growth through production of neurotrophic factors
38
Q

Why do axons not regenerate in the CNS?

A

Micro environment

  • oligos express proteins that actively inhibit atonal growth (contact inhibition)
  • Astros form a scar-like tissue at site of injury (mechanical barrier)
  • micro glia may kill injured CNS neurones
39
Q

Other factors contributing to failure of CNS axon regeneration

A
  • poor survival of injured neurons
  • failure to up-reg genes necessary for axon growth
  • lack of neurotrophic factors
  • lack of axon growth promoting substances
  • no re-expression of guidance cues
40
Q

Role of thalamic processing in the visual pathway

A
  • relay info on movement
  • segregate the retinal axons in preparation for depth perception
  • emphasize visual inputs from regions of high cone density
  • sharpen the contrast info received by the retina
41
Q

Sound pathway

A 
Oval window
Scala vestibuli
Basilar membrane 
Organ of corti 
Helicotrema 
Scala tympani 
Round window
42
Q

How does the amyloid beta protein fragment contribute to nerve degen in Alzheimer’s?

A
  • direct toxicity to neurons causes neuronal damage and disruption of synaptic contacts
  • promotes glial reactivity and inflammatory response which further damages and kills neurons
43
Q

Why is blind spot not perceived in vision

A

Visual centres use binocular vision to fill the space of the receptor free area

44
Q

Structural specialisations of cerebral capillaries

A
  • endothelium with tight junctions
  • lack of fenestrations
  • few pinocytotic vesicles
  • thick basement membrane

Blocks non-selective exchange of substances

45
Q

3 receptive structures in the inner ear

A
  • organ of corti (detection of sound waves)
  • macula (static equilibrium)
  • cristae ampullaris (dynamic equilibrium)
46
Q

Role of Schwann cell in regeneration of nerves

A
  • remove debris
  • provide growth promoting substances
  • guidance for regenerating axon
  • promote neuron survival by secreting neurotrophic factors
  • re myelinated
47
Q

3 BBBs

A
  • cerebral capillaries
  • choroid plexus
  • arachnoid mater
48
Q

Histological features of Graafian follicle just prior to ovulation

A
  • large astral follicle lined by multiple rows of cuboidal shaped granulosa cells
  • surrounded by theca interna containing typical steroid secreting cells
  • outer fibrous theca externa
  • oocyte surrounded by single row of cells (corona radiate)
  • attached to wall of follicle by cumulus oophorus
49
Q

Functional relationship leading to oestradiol production by Graafian follicle

A
  • theca interna cells take up chol to produce androstenedione
  • secreted and taken up by granulosa cells
  • aromatase cleaves androstenedione to form oestradiol
50
Q

Main functions of the neuronal cytoskeleton

A
  • mainataining cellular structure

- axonal transport

Semester 5 November (14 decks)

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