MEQ 2019

Question 1

Draw labelled diagram of relationship of parotid gland

Answer 1

The parotid duct runs through masseter , pierced into buccinator and enter through opposite second maxillary molar

Question 2

Clinical significance of parotid gland

Answer 2

Parotid Gland Tumours

The parotid gland is the most common site of a salivary gland tumour. These tumours are usually benign, such as an adenolymphoma. In contrast, tumours of the submandibular and sublingual glands are less common, but more likely to be malignant.

Treatment usually involves surgical excision of the tumour and parotid gland, known as a parotidectomy. During this procedure, it is critical to identify and preserve the facial nerve and its branches.

Damage to facial nerve or its branches will cause paralysis of the facial muscles. The affected muscles will lose tone, and the area will ‘sag’. The inferior eyelid can be particularly affected, falling away from the eyeball (known as ectropion).

Parotitis

Parotitis refers to inflammation of the parotid gland, usually as a result of an infection. The parotid gland is enclosed in a tough fibrous capsule. This limits swelling of the gland, producing pain.

The pain produced can be referred to the external ear. This is because the auriculotemporal nerve provides sensory innervation to the parotid gland and the external ear.

Question 3

Autonomic innervation, neurotransmotter, specific receptors thatlead to increase of heart beat

Answer 3

Sympathetic nervous system, epinephrine, norepinephrine, increase in high temperayure. Receptor, alpha adrenergic, beta adrenergic

Question 4

How oedema occurs

Answer 4

Occurs due to accummulation of excessive fluid in the interstitial space, leads to swelling of tissues.
Imbalance of Startling forces results in filtration more than reabsorption. Volume of interstitial fluid exceeds the ability of lymphatics to return it to circulation

Question 5

5 component of olfactory pathway

Answer 5

olfactory receptor cells.
olfactory nerves.
olfactory bulb.
olfactory tract.
olfactory striae.
olfactory cortex.
output targets of the olfactory cortex.

Question 6

Clinical significance of cribriform plate fracture

Answer 6

Fracture of the cribriform plate damaging the CN I results in Anosmia. If the nerve bundles on one side are torn, there will be complete loss of smell on that side.

Question 7

Anosmia

Answer 7

Loss, not only sense of smell but flavour of foods

Question 8

name condition (pain when eat cold food)

Answer 8

Dentine hypersensitivity

Question 9

Name 3 theories of dentine hypersensitivity

Answer 9

Hydrodynamic theory
Direct innervation theory
Odontoblast transducer theory

Question 10

Describe the hypersensitivity theory

Answer 10

Direct innervation = nerve ending penetrates dentinal tubules. Direct transudction occur at nerve ending of dentinal tubule

Odontoblast transducer = odontoblast is the sensory cell and receptor, couple to nerves in pulp

Hydrodynamic =pain producing stimuli increase dentinal fluid flow in tubules, kalau cold, fluid move inwards. Heat, fluid outwards

Question 11

Describe 2 jaw reflex

Answer 11

Jaw closing reflex
Tap chins, muscle spindle stretches, afferent fibre excited, activates jaw closing alpha motorneurons, muscle contract and close jaw

Jaw opening reflex
Stimulation of intraoral receptive fields, excites micosal receptor with afferent fibres, excitation of local circuit interneurons, activates jaw opening alpha motor neuron, muscle contracts

Question 12

provision of mineral is important during amelogenesis. explain the effect of excessive fluoride during this phase

Answer 12

Dental fluorosis
Excess of F- ions retain immature matrix proteins (amelogenin and ameloblastin) leading to accummulation of these proteins.
Results in incomplete crystal growth whereby there are wide gaps develop between enamel rods which cause porosity, less hydroxyapatite crystals formed leads to brittle enamel

Question 13

Function of carnitine in fatty oxidation & 1 deficiency.

Answer 13

Carnithine functions to transport acyl coA from cytosol to mitosol

Carnitine deficiency:
• Primary (due to gene mutation)
– low level in tissue of muscle, heart, kidney – Symptoms: muscle cramps
• Secondary (due to other metabolic disorders)
– Excessive lipid deposition in muscle and heart (cardiac and skeletal myopathy) and liver (hepatomegaly)
– Accumulation of acyl-carnitine excreted in urine (therefore depleting carnitine pool)