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Phase 2- HNN > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Describe the palatine tonsils:

A
  • Grape-like structures
  • Visible on inspection of the mouth
  • Lies between the palatoglossal and palatopharyngeal folds
  • Well developed in children -> immune
  • Adulthood -> tend to involute
  • Rich arterial supply from the facial artery
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2
Q

Describe the pharyngeal tonsils:

A
  • Also known as the adenoid tonsil
  • Located in the upper posterior part of the nasopharynx
  • Large collection of lymphocytes
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3
Q

Describe the tubal tonsil:

A
  • Around the tubal elevation

- Large mass of lymphoid tissue

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4
Q

Describe the lingual tonsil:

A
  • Posterior third of the tongue

- Beneath the mucosa contains a large amount of lymphoid tissue

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5
Q

What do the tonsils form?

A

Waldeyer’s ring: an interrupted ring around the start of the respiratory tract

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6
Q

What is the function of tonsils?

A
  • Hold a lot of micro-organisms that are around the throat area -> mount an immune response against them
  • Protect respiratory tract from infection
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7
Q

What does the external ear consist of?

A

Auricle, external auditory canal and eardrum

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8
Q

What is the auricle?

A
  • Flap of elastic cartilage covered by skin
  • Rim of the auricle is the helix and inferior portion is the lobule
  • Ligaments and muscles attach the auricle to the head
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9
Q

What is the external auditory canal?

A

Curved tube that lies in the temporal bone and leads to the eardrum

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10
Q

Describe the tympanic membrane:

A
  • Tympanic membrane is a thin, semitransparent partition between the external auditory canal and middle ear
  • Tympanic membrane is covered in epidermis and lined by simple cuboidal epithelium
  • Between the epithelial layers is CT composed of collagen, elastic fibres and fibroblasts
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11
Q

Where and what are ceruminous glands?

A
  • Near the exterior opening, the external auditory canal contains a few hairs and specialised sweat glands called ceruminous glands
  • Ceruminous glands -> secrete cerumen that helps prevent dust and foreign objects from entering the ear
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12
Q

Describe the middle ear:

A
  • Small, air-filled cavity in the petrous portion of the temporal bone
  • Separated from the external ear by tympanic membrane
  • Separated from internal ear by a thin bond partition that contains two small membrane-covered opening -> oval and round window
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13
Q

What extends across the middle ear?

A

Three auditory ossicles, which are attached by ligaments and are connected by synovial joints

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14
Q

Where does the malleus attach and articulate?

A
  • Handle of the malleus attaches to the internal surface of the tympanic membrane
  • Head of the malleus articulates with the body of the incus
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15
Q

Where does the incus attach and articulate?

A

Incus articulates with he head of the stapes

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16
Q

Where does the stapes attach and articulate?

A

Base of the stapes finds into the oval window

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17
Q

Where is the round window and what is it enclosed by?

A

Directly below the oval window, and enclosed by the secondary tympanic membrane

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18
Q

Describe tensor tympani:

A
  • Innervated by mandibular branch of CN V

- Limits movement and increases tension on the eardrum to prevent damage to the inner ear from loud noises

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19
Q

Describe stapedius:

A
  • Supplied by the facial nerve
  • Smallest skeletal muscle
  • Dampens large vibrations of stapes due to loud noises -> protects the oval window
  • Decreases the sensitivity of hearing
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20
Q

What does the anterior wall of the middle ear contain?

A

An opening that leads into the auditory tube- composed of both bone and elastic cartilage and connects the ear with the nasopharynx

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21
Q

Is the auditory tube open or closed?

A

Normally closed at the pharyngeal end but opens during swallowing and yawning allowing air to enter and leave the middle ear

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22
Q

What does the inner ear consist of?

A
  • A complicated series of canals
  • Two main divisions;
    • Outer bony labyrinth
    • Inner membranous labyrinth
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23
Q

What is the bony labyrinth?

A

A series of cavities in the petrous portion of the temporal bone divided into three areas

  • semicircular canals
  • vestibule
  • cochlea
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24
Q

What lines the bony labyrinth?

A

Periosteum, and it contains perilymph which surrounds the membranous labyrinth

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25
Q

What is the membranous labyrinth?

A
  • A series of epithelial sacs and tubes within the bony labyrinth that have the same general form as the bony labyrinth and contain receptors for hearing and equilibrium
  • Epithelial membranous labyrinth contains endolymph
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26
Q

Describe the vestibule:

A
  • Oval central portion of the bony labyrinth
  • Membranous labyrinth in the vestibule consists of two sacs called the utricle and the saccule which are connected by a small duct
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27
Q

Where are the semicircular canals?

A

Projecting superiorly and posteriorly from the vestibule are three bony semicircular canals, each of which lies at right angles to the other two

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28
Q

How are the semicircular canals named?

A
  • Based on their positions, they are named the anterior, posterior and lateral semicircular canals
  • Anterior and posterior are vertically orientated and lateral is horizontally orientated
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29
Q

What lies at one end of each canal?

A

A swollen enlargement called the ampulla

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30
Q

What are the semicircular ducts, and what do they connect with?

A

Portions of the membranous labyrinth that lie inside the semicircular canals, connect with the utricle

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31
Q

What does the vestibular branch of the vestibulocochlear nerve consist of?

A

Ampullary, utricular and saccular nerves

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32
Q

What is the cochlea?

A
  • Anterior to the vestibule is the cochlea, a bony spiral canal that makes almost three turns around a central bony core called the modiolus
  • Divided into three channels
    • cochlear duct
    • scala vestibuli
    • scala tympani
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33
Q

What is the cochlear duct?

A

A continuation of the membranous labyrinth into the cochlea which is filled with endolymph

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34
Q

What is the scala vestibuli?

A

Channel above the cochlear duct, which ends at the oval window

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35
Q

What is the scala tympani?

A

Channel below the cochlear duct, which ends at the round window

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36
Q

Describe the scala vestibuli and tympani:

A
  • Both are part of the bony labyrinth and are therefore filled with perilymph
  • Completely separated by the cochlear duct except for an opening at the apex of the cochlea -> helictrema
  • Cochlea adjoins the wall of the vestibule into which the scala vestibuli opens
  • Vestibular membrane separates the cochlear duct from the scala vestibuli
  • Basilar membrane separates the cochlear duct from the scala tympani
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37
Q

What rests on the basilar membrane ?

A

Spiral organ of Corti, a coiled sheet of about 16,000 hair cells which are the receptors for hearing

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38
Q

What are the two groups of hair cells?

A
  • Inner hair cells: arranged in a single row

- Outer hair cells: arranged in three rows

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39
Q

What is at the apical tip of each hair cell, and what is its physiological significance?

A
  • 40-80 stereocilia that extend into the endolymph of the cochlear duct
  • Stereocilia are long hairlike microvilli arranged in several rows of graded height
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40
Q

How do hair cells connect to the CNS?

A
  • At their basal ends, inner and outer hair cells synapse both with first order sensory neurons and with motor neurons from the cochlear branch of CN 8
  • Cell bodies of their sensory neurons are located in the spiral ganglion
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41
Q

What is otitis media?

A

Inflammation of the middle ear

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42
Q

How can OM present?

A
  • As acute otitis media (AOM) or otitis media with effusion (OME)
  • AOM: refers to an acute middle ear infection which has abrupt onset of signs and symptoms related to middle ear inflammation and effusion
  • OME: refers to the presence of fluid in the middle ear without signs and symptoms of AOM and may occur spontaneously due to poor auditory tube function or as an inflammatory response following AOM
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43
Q

What are the risk factors for OM?

A
  • Pre-school age (infants between 3 months and 3 years)
  • Premature birth
  • Male gender
  • Ethnicity: Native American, Inuit
  • Family history of recurrent OM
  • Siblings in household
  • Genetic syndromes
  • Low socioeconomic status
  • Orofacial abnormalities: cleft lip and palate
  • Dysfunction of the auditory tube that allows reflux of fluid and bacteria into the middle ear space from the nasopharynx
  • Shorter, wider and more horizontal auditory tube in children
  • Lying in supine position
  • Bottle-fed infants
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44
Q

Briefly describe the aetiology of OM:

A
  • Most cases follow an uncomplicated upper respiratory tract infection that has been present for several days
  • Evidence of respiratory viruses is also found in middle ear exudates
  • Aetiology of AOM and OME are interrelated
  • Acute infection is usually followed by residual inflammation and effusion that in turn predisposes to recurrent infection
  • Middle ear effusion is an expression of underlying mucosal inflammation
  • Persistent middle ear effusion results in decreased motility of the tympanic membrane and serves as a barrier to sound conduction
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45
Q

Briefly describe the pathophysiology of OM:

A
  • Tubal tonsil hypertrophy in response to infection: block the opening of the auditory tube
  • New air cannot gain access to the middle ear
  • Middle ear is lined by respiratory epithelium and also contains mucus-secreting goblet cells
  • Mucus builds up in the middle ear
46
Q

How is hearing loss classified?

A
  • Conductive hearing loss
    • occurs usually in the external and middle ear
    • interference of the ability of the sound to be transmitted to the inner ear
    • many causes can be treated successfully with surgery
  • Sensorineural hearing loss
    • occurs in the inner ear (sensory) or auditory nerve/auditory pathway (neural)
    • many sensorineural hearing losses are permanent because the human inner ear and hair cells have only limited ability to repair themselves
47
Q

Describe Rinne’s test:

A
  • Tuning fork is placed on the mastoid bone (bone conduction) and then placed next to the external ear (air conduction)
  • Usually air conduction is heard louder than bone conduction -> positive Rinne’s test
  • If bone conduction is louder than -> negative Rinne’s test and indicates conductive hearing loss in that ear
48
Q

Describe Weber’s test:

A
  • Tuning fork is placed on the forehead
  • Patient is asked in which ear the sound is louder
  • If the patient hears the sound equally in each ear or cannot localise then normal and termed a mid-line Weber’s
  • Weber’s lateralises towards a conductive hearing loss and away from a sensorineural hearing loss
49
Q

What are grommets?

A
  • The most common effective treatment for OM
  • Performed under general anaesthetic, takes 15 mins
  • A small ventilation tube, a grommet, is inserted into the child’s ear through a small incision in their eardrum
  • Helps to drain away fluid in the middle ear and helps maintain the air pressure in the middle ear cavity
  • Helps to keep the eardrum open for several months
50
Q

How do grommets fall out?

A
  • As the eardrum starts to heal, the grommet will slowly be pushed out of the eardrum and in most cases eventually falls out
  • Processes happens naturally and should not be painful
  • Majority of grommets fall out between 6 to 15 months after they have been inserted
51
Q

What are the four major ways in which hearing loss affected children?

A
  • Causes delay in the development of receptive and expressive communication skills (speech and language)
  • Language deficit causes learning problems that result in reduced academic achievement
  • Communication difficulties often lead to social isolation and poor self-concept
  • May have an impact on vocational choices
52
Q

How does hearing loss affect development of vocabulary?

A
  • Vocabulary develops more slowly in children who have hearing loss
  • Learn concrete words like cat, jump, five and red more easily than abstract words like before, after, equal to and jealous
  • Also have difficulty with function words like the, an, are and a
  • Gap between vocabulary of children with normal hearing and those with hearing loss widens with age
  • Children with hearing loss do not catch up without intervention
  • Have difficulty understanding words with multiple meanings
53
Q

How does hearing loss affect development of sentence structure?

A
  • Comprehend and produce shorter and simpler sentences than children with normal hearing
  • Difficulty understanding and writing complex sentences
  • Often cannot hear word endings such as -s or -e, leads to misunderstanding
54
Q

How does hearing loss affect development of speaking?

A
  • Often cannot hear quiet speech sounds such as s, sh, f, t and k, and do not include them in their own speech
  • May not hear their own voices when speaking
55
Q

How does hearing loss affect academic achievement?

A
  • Difficulties in all aspects of academic achievement, especially reading and mathematical concepts
  • On average achieve one to four grade levels lower than their peers with normal hearing
  • Gap in academic achievement between children with normal hearing and those with hearing loss usually widens as they progress through school
56
Q

What does newborn hearing screening involve?

A
  • Placing a soft-tipped probe into the baby’s ears, playing sounds and trying to detect a response (echo) from the baby’s cochlea
  • Well babies who do not have a clear response are referred for an automated auditory brainstem response (AABR) screening test
  • AABR involves playing sounds to the baby and trying to detect responses from their brainstem via electrodes placed on the baby’s head and neck
  • Measures not only the integer it of the inner ear, but also the auditory pathway, and can therefore detect the rare condition of auditory neuropathy in children who are deaf but have normal ono-acoustic emissions (because the cochlea is normal)
57
Q

What is declarative memory?

A

Factual memory, life events, available to consciousness, easily formed and forgotten

58
Q

What is non-declarative memory?

A

Procedural memory, motor skills, not available to consciousness, less easily formed and forgotten

59
Q

What is ballistic movement?

A
  • Movement based largely on a set of pre-programmed instructions
  • Rapid but at expense of accuracy: little opportunity for compensation for unexpected changes
60
Q

What is pursuit or visual feedback movements?

A
  • Motor command continually updated according to sensory feedback (e.g. visual)
  • Highly accurate: can be modified while in progress
  • Slow
  • In practice most movements involve a mixture of both feedback and ballistic strategies
61
Q

Where is the primary motor cortex?

A

Area of the brain responsible for movement, found in dorsal portion of the frontal lobe

62
Q

What is the clinical relevance of decussation of pathways?

A
  • Pathways providing connections between primary sensory motor area and the periphery are crossed
  • Functions lost following stroke depend on the extend of the haemorrhage
  • Paralysis and loss of sensation will be contralateral to the side of the haemorrhage
63
Q

How is sensory information involved in movement?

A
  • Sensory information is crucial for co-ordinated movement
  • Proprioception: feedback from peripheral sensory receptors on the positions and movements of limbs
  • Vision: eyes, visual system and visual cortex
  • Vestibular: feedback from organs of balance- cortical
64
Q

How is the basal ganglia involved in movement?

A
  • Input mainly from prefrontal cortex: intended movement
  • Output to premotor area via thalamus
  • Functions
    • initiation of movement: putting motor plan into action
    • planning of complex voluntary movement
65
Q

How is the cerebellum involved in movement?

A
  • Input mainly from sensory cortex
  • Output to primary motor cortex via thalamus
  • Functions
    • coordination and smooth execution of movements
    • motor learning
    • error detection
  • Damage to cerebellum produces cerebellar ataxia: poor coordination
66
Q

How do descending pathways control motor function?

A
  • Lateral pathways: corticospinal and rubrospinal
    • pyramidal neurons in M1 project to the spinal cord (corticospinal tract) and red nucleus (rubrospinal)
    • main function: control of voluntary movement
  • Ventromedial pathways
    • control of axial muscles: control of posture
  • Descending systems synapse on motor neurons or on interneurons in the spinal cord
67
Q

How is dopamine synthesised?

A
  • Tyrosine enters the neuron via active transport
  • In the cytoplasm of the dopaminergic neuron, tyrosine is converted to DOPA via tyrosine hydroxylase
  • DOPA is converted to dopamine via DOPA-decarboxylase
  • Dopamine is then actively transported into storage vesicles by the vesicular transport mechanism
68
Q

What channel is involved in dopamine transport back into the neuronal terminal from the synaptic cleft?

A

Reuptake-1

69
Q

What is the fate of dopamine after re-uptake?

A
  • About 50% is transported into vesicles for storage and release
  • Remaining dopamine that enters the neuronal terminal is destroyed by monoamine oxidase (a mitochondrial enzyme)
70
Q

What is the fate of dopamine in the synapse when it is not transported back into the neuronal terminal?

A
  • Some of the dopamine that is released into the synaptic cleft (about 10%) is actively transported into the effector cell (via reuptake-2)
  • Dopamine entering the effector cells is inactivated primarily by an enzyme: catchol-O-methyltransferase (COMT)
  • Remaining dopamine in the synaptic cleft diffuses into the circulation and is destroyed in the liver by COMT and MAO
71
Q

What are the end products of dopamine metabolism?

A

Organic acids and alcohol which are excreted in the urine

72
Q

What are the 4 main dopamine pathways in the CNS?

A

Nigrostriatal pathway, mesolimbic pathway, mesocortical pathway and tuberohypophyseal system

73
Q

Describe the nigrostriatal pathway:

A
  • Accounts for about 75% of dopamine in the brain
  • Cell bodies largely in the substantia nigra
  • Axons terminate in the corpus striatum
  • Fibres run in the medial forebrain bundle along with other monoamine containing fibres
74
Q

Describe the mesolimbic pathway:

A
  • Cell bodies occur in the midbrain ventral tegmental area (VTA) adjacent to the substantia nigra
  • Project via the medial forebrain bundle to parts of the limbic system, especially the nucleus accumbens and the amygdaloid nucleus
75
Q

Describe the mesocortical pathway:

A
  • Cell bodies lie in the VTA

- Project via the medial forebrain bundle to the frontal cortex

76
Q

Describe the tuberohypophyseal system:

A
  • Group of neurons running from the ventral hypothalamus to the median eminence and pituitary glands
  • Regulate secretions
77
Q

What are the two families of dopamine receptors and what receptors are in each?

A

D1 family: D1 and D5

D2 family: D2, D3 and D4

78
Q

Where are D1 receptors most abundant?

A

In areas receiving a dopaminergic innervation (namely the striatum, limbic system thalamus and hypothalamus)

79
Q

Where are D2 receptors most abundant?

A

Same as D1, also the pituitary

80
Q

Where are D3 receptors found?

A

In the limbic system but not the striatum

81
Q

Where are D4 receptors found?

A

D4 is more weakly expressed, mainly in the cortex and limbic systems

82
Q

What effects do dopamine (D1) receptors mediate in the periphery?

A

Renal vasodilation and increased myocardial contractility

83
Q

What are the functions of dopamine?

A

Motor control in the nigrostriatal system, behavioural effects in the mesolimbic and mesocortical systems and endocrine controls in the tuberhypophyseal system

84
Q

Which neurons use the noradrenerigic system?

A

Neurons of the locus coeruleus in the pons, and there is one on each side

85
Q

What structures does the noradrenergic system innervate?

A

Axons leave the locus coeruleus in several tracts, but fan out to innervate almost every part of the brain:

  • All of the cerebral cortex
  • Thalamus
  • Hypothalamus
  • Olfactory bulb
  • Cerebellum
  • Midbrain
  • Spinal cord
86
Q

What is the noradrenergic system involved in?

A

Regulation of attention, arousal and sleep-wake cycles, as well as learning and memory anxiety and pain, mood and brain metabolism

87
Q

Where are serotonergic neurons found?

A

Mostly clustered within the nine nine raphe nuclei, and lie either side of the midline of the brainstem

88
Q

Describe the raphe nuclei:

A
  • Each nucleus projects to different regions of the brain
  • Those more caudal, in the medulla, innervate the spinal cord, where they modulate pain-related sensory signals
  • Those more rostral in the pons and midbrain innervate most of the brain in much the same diffuse way as the locus coeruleus neurons
  • Fire most rapidly during wakefulness, and are most quiet during sleep
89
Q

What is the reticular activating system?

A
  • Locus coeruleus and the raphe nuclei are part of the RAS, which implicates the reticular core of the brainstem in processes that arouse and awaken the forebrain
  • Intimately involved in the control of the sleep-wake cycles, as well as the different stages of sleep
  • Also been implicated in the control of mood and certain types of emotional behaviour
90
Q

What is Parkinson’s disease?

A

Progressive degenerative disorder of the basal ganglia that results in variable combinations of tremor, rigidity and bradykinesia

91
Q

What is parkinsonism?

A

Clinical syndrome arising from degenerative changes in the basal ganglia function is often referred to as Parikinsonism

92
Q

What characterises parkinson’s disease?

A

Dopamine depletion, resulting from degeneration of the dopamine nigrostriatal system

93
Q

How else can Parkinsonism develop?

A
  • Postencephalitic syndrome
  • Side effect of therapy with antipsychotic drugs that block dopamine receptors
  • Toxic reaction to a chemical agent
  • Outcome of severe CO poisoning
94
Q

What is the primary brain abnormality found in PD?

A

Degeneration of the nigrostriatal pathway -> subsequent reduction in stratal concentrations of dopamine

95
Q

What pathological processes have been identified in PD?

A
  • Oxidative stress
  • Apoptosis
  • Mitochondrial disorders
96
Q

What are the theories of PD pathophysiology?

A
  • Auto-oxidation of catecholamines such as dopamine may injure neurons in the substantia nigra
  • Increasing evidence that the development of PD may be related to oxidative metabolites of this process and the inability of neurons to render these products harmless
97
Q

What genetic mutations are associated with PD?

A
  • First genetic mutation associated with PD was the gene encoding a-synuclein, a member of a small family of proteins that are expressed preferentially in the substantia nigra
  • Mutations in a-syn cause a very rare, autosomal dominant form of the disease
  • a-syn is a major component of the Lewy bodies that are found in the brain tissue in people with PD
  • Mutations in the protein parkin is associated with an autosomal recessive, early-onset form of PD
98
Q

What are the clinical manifestations of PD?

A

Tremor, rigidity and bradykinesia

99
Q

Describe tremor in PD:

A
  • Most visible manifestation of the disorder
  • Affects the distal segments of the limbs, mainly the hands and feet, head, neck, face, lips and tongue
  • Characterised by rhythmic, alternating flexion and contraction movements
  • Usually unilateral, occurs when the limb is supported and at rest, and eventually disappears with movement and sleep
  • Tremor eventually becomes bilateral
100
Q

Describe rigidity in PD:

A
  • Resistance to movement of both flexors and extensors full range of movement
  • Most evident during passive joint movements and involves jerky, cogwheel-type or rachetlike movements that require considerable energy to perform
  • Flexion contractions may develop as a result of the rigidity
  • Usually begins unilaterally but eventually progresses bilaterally
101
Q

Describe bradykinesia in PD:

A
  • Slowness in initiating and performing movements and difficulty with sudden, unexpected stopping of voluntary movements
  • Unconscious associative movements occur in a series of disconnected steps rather than in a smooth, coordinated manner
  • Most disabling symptom of pD
  • Difficulty initiating walking and difficulty turning
  • While walking, they may freeze in place and feel as if their feet are glued to the floor, especially when moving through a doorway or preparing to turn
  • When they walk, they lean forward to maintain their centre of gravity
  • Take small, shuffling steps without swinging their arms and have difficulty changing their stride
102
Q

What are manifestations of advanced PD?

A
  • Falls
  • Fluctuations in motor function
  • Neuropsychiatric disorder
  • Sleep disorders
103
Q

What are other symptoms of PD?

A
  • Loss of postural reflexes predisposes to falling, often backwards
  • Emotional and voluntary facial movements become limited and slow as the disease progresses
  • Facial expression becomes stiff and mask-like
  • Loss of blinking reflex and failure to express emotion
  • Tongue, palate and throat muscles become rigid: patient may drool because of difficulty in moving the salvia to the back of the mouth and swallowing it
  • Speech become slow and monotonous, without modulation and poorly articulated
104
Q

What ANS symptoms accompany PD?

A
  • Because the basal ganglia also influence the ANS, people with PD often have excessive sweating, sebaceous gland secretion and salivation
  • Autonomic symptoms such as lacrimation, dysphagia, orthostatic hypotension, thermal regulation, constipation, impotence and urinary incontinence may present, especially late in the disease
105
Q

What is levodopa?

A

Metabolic precursor of dopamine

106
Q

How does levodopa work?

A

Restores dopaminergic neurotransmission in the corpus striatum by enhancing the synthesis of dopamine in the surviving neurons of the substantia nigra

107
Q

How does treatment with levodopa slow PD?

A
  • In patients with early disease, the number of residual dopaminergic neurons in the substantia nigra (typically about 20% is normal) is adequate for conversion of levodopa to dopamine
  • With time, number of neurons decreases and fewer cells are able to take up levodopa and convert it to dopamine
  • Consequently, motor fluctuation develops
108
Q

Describe relief by levodopa:

A
  • Relief provided by levodopa is only symptomatic and lasts only as long as the drug remains in the body
  • Effects of levodopa on the CNS can be greatly enhanced by co-administration of carbidopa
109
Q

What is carbidopa?

A

A dopa decarboxylase inhibitor that does not cross the blood brain barrier

110
Q

What is the MoA of L-dopa?

A
  • Because parkinsonism results from insufficient dopamine, attempts have been made to replenish the dopamine deficiency
  • Dopamine itself does not cross the BBB, but levodopa can
  • Levodopa is converted to dopamine in the brain
  • Large amounts are required because most of the drug is decarboxylated to dopamine in the periphery
111
Q

What is the MoA of C-dopa?

A
  • Dopa decarboxylase inhibiter
  • Diminishes metabolism of L-dopa in the periphery
  • Increases availability of levodopa for the CNS
  • Addition of C-dopa lowers the dose of L-dopa needed by about 5-fold
  • Decreases the severity of the SEs arising from peripherally formed dopamine

Phase 2- HNN (6 decks)

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