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Med 3 > EAR (pituitary/ Thyroid) > Flashcards

EAR (pituitary/ Thyroid) Flashcards

1
Q

Where is insulin secreted

A

Islets of langerhans in the pancreas

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2
Q

What is lipolysis

A

Breakdown of triglycerides into free fatty acids and glycerol
Inhibited by insulin
Stimulated by glucagon, cortisol, GH and catecholamines

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3
Q

What is synergistic activity of hormones

A

Produce much greater enhanced response than sum of either hormones alone

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4
Q

What is permissive action of hormones

A

Presence of one hormone allows a second hormone to act
Eg cortisol on catecholamine activity
And prolactin to allow oxytocin action

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5
Q

What is antagonistic actions of hormones

A

When effects of hormones oppose each other
Eg PTH increases blood Ca2+ ; calcitonin decreases blood Ca2+

And insulin / glucagon in blood glucose

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6
Q

When is highest growth rate in humans

A

During foetal development and just after birth (pre natal and post natal)

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7
Q

What factors affect growth

A

Genetic

Socioeconomic and nutritional

Chronic disease and stress (cortisol causes anti growth activity by blocking actions of GH)

Endocrine hormones (mainly GH, also thyroid, insulin, glucocorticoids and sex hormones)

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8
Q

Where is GH synthesised

A

Somatotrophs in the anterior pituitary

Most abundant hormone secreted here

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9
Q

Actions of growth hormone (direct)

A

Increases lipolysis in the adipose tissue

Increases AA uptake and protein synthesis in skeletal muscle

Increases gluconeogenesis in liver

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10
Q

Indirect effects of GH

A

Stimulates release of growth factors such as IGF-I (insulin like growth factor 1) and IGF-II (somatomedins) from liver and other cell types

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11
Q

Action of IGF-I on cells

A

Stimulates protein synthesis, increase cell size (hypertrophy) - increase in lean body mass

Stimulates cell division (hyperplasia) increase in size of individual organs

Promotes skeletal growth- linear growth (increased height)

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12
Q

What is the role of thyroid hormones in growth

A

Action of GH on growth requires the presence of thyroid hormones

  • permissive role on GH activity in promoting growth
  • key role in CNS development (mental retardation in infants)
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13
Q

Role of insulin in growth

A

Important growth promoter (anabolic)

Important intra uterine growth factor

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14
Q

Role of sex hormones in growth

A

Dramatic rise in growth during puberty
- linear growth, muscle building and stop bone elongation by promoting epiphyseal plate closure (no more cartilage formation and remodelling into bone tissue and no more lengthening of the shaft)

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15
Q

What tissues do the anterior pituitary hormones have effects on

A

Prolactin - breast
LH, FSH (gonadotropins) - testes, ovaries
TSH (thyrotropin) - thyroid
ACTH (corticotropin) - adrenal cortex

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16
Q

What is GH regulated by

A

Hypothalamic releasing hormones (growth hormone releasing hormone (positive influence) and somatostatin(small negative influence)

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17
Q

What is the dual effect of glucocorticoids and GH

A

Initial synergism on metabolism

If chronic high levels of glucocorticoids this could inhibit GH release (eg Cushing’s syndrome, long term use of high dose steroids)
Particularly important in children as can cause growth retardation

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18
Q

Explain pituitary dwarfism

A

GH deficiency
Can be treated with hormone replacements in the pasts from human cadaver pituitaries. Now as recombinant human growth hormone
Licensed in uk to teat GH deficiency

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19
Q

GHD in adults symptoms

A 
Psychological changes 
Malaise, tiredness, anxiety, depression 
Osteoporosis 
Poor muscle tone, decrease in lean body mass
Increase in adipose tissue 
Impaired hair growth
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20
Q

What is hypothyroidism

A

Insufficient thyroid hormones for GH activity

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21
Q

What is cushings syndrome

A

Excess cortisol
Inhibits GH release
Inhibits linear bone growth

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22
Q

What is congenital adrenal hyperplasia and sexual precocity

A

Increased androgens result in early / rapid bone maturation (closure of epiphyseal growth plates)

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23
Q

What is gigantism

A

Tumour or excess GH in childhood

Often look much older than age

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24
Q

What is acromegaly

A 
Excess GH in adults 
Coarsening of facial features 
Enlarged hands and feet 
Headaches, visual disturbances
Sleep apnoea, general tiredness 
Hypertension, cardiomegaly 
Glucose intolerance (diabetes) 
Irregular or loss of periods (female); impotence (males)
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25
Q

Treatment of gigantism and acromegaly

A 
Surgery or radiotherapy 
Somatostatin drugs (inhibit GH release)

Some tumours respond to dopamine receptors agonsits

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26
Q

What is hyperthyroidism

A

Excess THs promote GH activity

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27
Q

What is sexual precocity in accelerated growth

A

Initial accelerated bone growth (early growth spurt)

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28
Q

What is eunuchoidism

A

Hypogonadism

Low sex hormone levels result in extension of long bone growth (delayed bone maturation)

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29
Q

What does the hypothalamus control

A 
Emotional state 
Homeostasis 
Body temp 
Hunger / thirst 
Circadian rhythm 
Sleep / wake 
Reproductive functions
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30
Q

What does the hypothalamus act with

A

Limbic system
Endocrine system
Autonomic nervous system

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31
Q

Where is the hypothalamus

A

Frontal and inferior to thalamus (and smaller)

- part of the diencephalon

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32
Q

What is the hypothalamus connected to in the limbic system

A

Hippocampus via fornix
Brain stem via medial forebrain bundle (from olfactory bulb)
Thalamus via mammillothalmic tract

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33
Q

What does the hypothalamus do through the limbic system

A

Deals with emotion regulation

Gets regulatory input for the ANS

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34
Q

What is homeostasis

A 
Maintenance of a constant internal environment
BP 
HR
Water balance 
Food intake 
Metabolic rate  
Blood glucose level
Used feedback loops and regulatory centres in hypothalamus and brain stem
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35
Q

Describe thermoregulation.

A

Too hot:

  • anterior hypothalamus neurons
  • peripheral vasodilation
  • sweating
Too cold: 
- posterior hypothalamus neurons 
Peripheral vasoconstriction 
- piloerection 
- shivering 
- brown fat thermogenesis
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36
Q

What is brown fat thermogenesis

A

When brown fat burns it creates heat without shivering. The brown fat also burns calories.

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37
Q

What is rheostasis

A

Changes of the internal environment to counteract external changes

  • circadian rhythms
  • seasonal changes
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38
Q

What are circadian rhythms

A 
Sleep wake cycle 
Heart rate / BP 
Body temp 
Organ function 
Hormones: vasopressin and cortisol 
Mental ability: attention and reaction time
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39
Q

What are circadian rhythms driven by

A

Suprachiasmatic nucleus

Evidence for this comes from lesion studies

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40
Q

Why do we need circadian rhythms

A

To anticipate changes in the external environment so our bodies can adapt

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41
Q

What are branchial (pharyngeal) arches

A

In the 4-5 week old embryonic pharynx
Arches- mesodermal proliferation - grow centrally - meet in midline -
Only 4 visible, 5th degenerates, 6th indistinct
Each arch contains:

Structural components (cartilage / bone / connective tissue)

An artery

A nerve

A muscle

And between the arches almost touching ; pouches internally lined with endoderm, grooves or clefts externally lined with ectoderm

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42
Q

Describe the nerves of the branchial arches

A

Each arch has its own nerve which innervates the associated muscle. If muscle migrates it takes its nerve with it

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43
Q

Describe the arteries of the branchial arches

A

Paired dorsal aortae connect to paired ventral aortae by branchial arch arteries - thus they surround the primitive gut. Gives rise to various arteries

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44
Q

What are the different arches

A

1st- meckels cartilage: incus, malleus, maxillary process, anterior ligament of malleus and sphenomandibular ligament
2nd- reicherts cartilage: stapes, styloid process, stylohyoid ligament, lesser Cornu and upper body of hyoid
3rd- greater Cornu and most of body of hyoid
4th- thyroid cartilage and some other laryngeal cartilages
6th arch - cricoid cartilage

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45
Q

What do the different arches form

A

1s - middle ear cavity and eustachiuan tube
2nd - tonsillar crypts
3rd- ventral wing descends into thorax to form hassall’s corpuscles and epithelial reticulum of thymus
4th- ventral wing forms ultimobranchial body which gives rise to C cells in thyroid
Dorsal wing gives rise to superior parathyroid

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46
Q

How does the tongue form

A

1st arch - lateral lingual swellings - anterior 2/3rds - median swelling

2/3/4 arch - hypobranchial eminence (copula) posterior 1/3rd

6th arch - tracheo-bronchial groove (laryngeal opening)

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47
Q

Formation of thyroid

A

Pouch of epithelium grows down from foramen caecum (between 1st and 2nd arches) to thyroid cartilage thus forming
- thyroglossal duct

In adults may form:
Cysts
Ectopic thyroid tissue
Pyramidal lobe

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48
Q

Development of face

A

Face develops from 5 elevations

  • the fronto-nasal process
  • paired maxillary processes
  • paired mandibular processes
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49
Q

How does the face develop

A

Ectoderm all thickening gives rise to nasa placodes which then form nasal pits with medial and Lateral nasal elevations

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50
Q

How does the palate develop

A

Free communication between oral and nasal cavity
Palate makes these separate except in the oro and naso pharynx at posterior

Primary palate - intermaxillary segment
Palatine shelves - maxillary processes - vertical

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51
Q

How does cleft lip form

A

Failure to fuse anterior to incisive foramen

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52
Q

How does cleft palate form

A

Failure to fuse posterior to incisive foramen produces cleft palate

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53
Q

Tongue abnormalities

A

Cleft
Macroglossia
Microglossia
Any of these can cause speech defects

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54
Q

Nose abnormalities

A

Microstomia

Bifid

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55
Q

Facial abnormalities caused by fetal alcohol syndrome

A

Mid line facial abnormalities and effects on behaviour
Wide nose
Lack of philltrum
Heavy epicanthic folds and flattened nose

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56
Q

What is Graves’ disease

A 
Hyperthyroidism 
Fast HR 
Weight loss 
Wasting 
Heat sensitive 
Goitre
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57
Q

What happens in Graves’ disease

A

Antibodies that stimulate TSH receptors
To shut down production of TSH, suppressing further thyroid and hormone synthesis. Thyroid hormones shut down TSH production but have no effect on autoantibody production which continues to cause excessive thyroid hormone problems

58
Q

What happens in a preganant person with graves fisease

A

Patient with Graves’ disease makes anti TSHR antibodies
Transfer of antibodies across placenta into the foetus
Newborn infant also suffers from Graves’ disease
Plasmapheresis removes maternal anti- TSHR antibodies and cures the disease

59
Q

What is pre tibial myxoedema

A

Thickening and coarsening of skin seen in Graves’ disease

60
Q

What is Hashimoto’s thyroiditis

A 
Hypothyroidism
Low BMR 
Weight gain 
Pain, numbness 
Slow responses 
Goitre (swelling of thyroid gland that produces a lump at neck)
Cold sensitive
61
Q

Mechanism of B12 malabsorption in pernicious anaemia

A

Antibodies that block the binding of B12 to the plasma cell or antibodies that bind in the place of the B12

62
Q

Type 1 diabetes mellitus

A

The B cell specific T cells recognise peptides from insulin or glutamic acid decarboxylase
Islets of langerhans contain several cell types secreting different hormones. Each cell expresses different tissue specific proteins
Effector T cell recognises peptides from a B cell and kills the B cell
So insulin cannot be made

63
Q

What is myasthenia gravis

A

Autoantibodies that inhibit acetylcholine receptors
Acetylcholine receptors internalised and degraded so no Na+ influx and no muscle contraction

Tx: inject acetylcholinesterase which maintains the stimulation to the muscles for longer - makes person able to open eyes but is not a long term fix

64
Q

What is goodpastures disease (type II hypersensitivity)

A

Autoantibodies bind directly to glomerular basement membranes giving ‘smooth’ staining pattern
Can lead to kidney failure
Takes time to build up so not obvious when autoantibodies are first generated

65
Q

What is pemphigus vulgaris

A

Autoantibodies to epidermal cadherin

66
Q

What are the subdivisions of the larynx

A

Nasopharynx: end of nasal cavity

Oropharynx: area of the mouth

Laryngopharynx: opening of larynx into tube

Oesophagus: runs through pharynx

67
Q

What makes up the cranium

A

Neurocranium
Bony case of the brain
Viscerocranium
Made up of facial bones

68
Q

What makes up the neurocranium

A 
8 bones - 4 singular bones at midline 
1. Frontal 
2. Ethmoid 
3. Sphenoid 
4. Occipital 
4 bilateral pairs: 
- temporal 
- parietal
69
Q

What makes up the viscerocranium

A

14 bones - 2 singular bones at midline

  1. Mandible
  2. Vomer
    - 12 bilateral pairs
  3. Maxilla
    - inferior nasal concha (turbinate)
  4. Zygomatic
  5. Palatine
  6. Nasal
  7. Lacrimal
70
Q

What are sutures

A

Areas where the cranial bones have jointed together

  • fibrous or synarthoridal joints
  • cant move
71
Q

What is the zygomatic bone

A

Cheek bone
Easily palpated inferolateral to eye
Borders: maxilla, frontal bone, temporal none

72
Q

Layers of the scalp

A

Skin

  • thin layer except occipital region
  • dense connective tissue
  • thick layer, well supplied by aa/vv/nn
  • epicranial aponeurosis
  • rigid tendon outs sheet that covers top part of skull (calavaria)
  • loose connective tissue
  • spongy layer that can distend with fluid, allows movement over calvaria
  • pericranium
  • dense layer of connective tissue over bone
73
Q

Which layer of the scalp is most susceptible to infection

A

Loose connective tissue because emissary veins provide pathway to intracranial space

74
Q

What are the attachments of the scalp

A

Pericranium tightly adhered to calvaria

  • covers neurocranium from occipital to frontal bone
  • lateral: extends over temporal fascia to zygomatic arches
  • blood supply contained by pericranium
  • pericranium can be stripped from calvaria
75
Q

Osteology of the mandible

A

Lower jaw acts as receptacle for teeth
- articulates with temporal bone
Temporomandibular joint
- has horizontal body and 2 vertical rami

76
Q

Anatomical structure of the body of the mandible

A

2 borders:

  • superior: alveolar border (has sockets to hold lower teeth)
  • inferior: base (site of attachment for digastric mm medially)
  • mandibular symphysis (small ridge of bone at midline, encloses mental protuberance - chin)
  • mental foramen (passageway for inferior alveolar nn / aa)
77
Q

What is the anatomical structure of the rami of the mandible

A
  • 2 of them
  • each has: head, neck, coronoid process, mandibular foramen (internal surface)
  • head: posterior articulates w temporal bone forming TMJ
  • neck: attachment site of lateral pterygoid mm
  • Coronoid process: attachment site of temporalis mm
78
Q

What is the temporomandibular joint

A

Mandible + temporal bone
Anterior to tragus of ear (lateral)
- articulations b/w mandibular fossa, articular tubercle of temporal none, head of mandible
- articular bones separated by articular disk therefore never in contact
- splits joints into 2 synovial joint cavities (sup / inf)
- articular surfaces of bones covered by fibrocartilage

79
Q

Movements at the TMJ

A

Produced by mm of mastication and hyoid mm

  • protrusion (chin)
  • retrusion / retraction (chin)
  • elevation ( close mouth)
  • depression (open mouth)
  • lateral movements (grinding / chewing)
80
Q

What happens in TMJ dislocation

A

Blunt force to side of face / large bite / yawning
- head of mandible slips out of fossa and pulled anteriorly
Pt cant close mouth
Risk: damage to facial, auriculotemporal nn

81
Q

What are the muscles of mastication

A

Masseter
Temporalis
Medial pterygoid
Lateral pterygoid

82
Q

Action of the masseter

A

Elevates mandible, closes mouth

83
Q

Attachment of the masseter

A

Superficial - maxillary process of zygomatic bone
Deep- zygomatic arch of temporal bone
-> ramus of mandible

84
Q

Innervation of the muscles of mastication.

A

Mandibular nerve (branch of trigeminal nerve)

85
Q

Action of the temporalis

A

Elevates mandible, closes mouth

Retracts mandible, pulls jaw posteriorly

86
Q

Attachment of the temporalis

A

Temporal fossa -> coronoid process of mandible

87
Q

Action of the medial pterygoid

A

Elevates mandible, closes mouth

88
Q

Attachment of medial pterygoid

A

Superficial- maxillary tuberosity and pyramidal process of palatine bone
Deep - tuberosity of maxilla
-> ramus of mandible

89
Q

Action of lateral pterygoid

A

Bilateral: protracted mandible, pushes jaw forwards
Unilateral: side to side movement of jaw

90
Q

Attachment of lateral pterygoid

A

Superior - greater wing of sphenoid
Inferior - lateral pterygoid plate of sphenoid
- > neck of mandible

91
Q

Motor innervation of the tongue

A 
All mm (except palatoglossus) -> hypoglossal nn 
Palatoglossus mm -> vagus nn
92
Q

What is the facial artery

A

Origin: external carotid aa

- branches 4 cervical + 4 facial

93
Q

What is the facial vein

A

Origin: angular vv
Branches: cervical and facial

94
Q

What is the facial nerve

A

Important for facial expression
Origin: pons of brain stem
Mixed nn fibres
Motor, sensory and parasympathetic fields of innervation

95
Q

What is the parotid gland

A

Paired salivary gland
Superficial and deep lobes
Innervation: glossopharyngeal and auriculotemporal nn

96
Q

How do yo test the facial nerve

A 
Assess asymmetry at rest 
As pt to: 
- raise eyebrows 
- close eyes tightly 
- blow out cheeks 
- smile 
- add resistance
97
Q

What are the muscles of facial expression

A 
Orbital 
Nasal 
Oral 
Auricular 
Occipitofrontalis
98
Q

What is the trigeminal nerve

A

Sensory: innervate skin, mucous membranes and sinuses of face
Motor: only mandibular branch, innervates mm of mastication

99
Q

What is the anatomical course of the trigeminal nerve

A

Originates from 3 sensory nuclei and 1 motor nucleus
Midbrain -> medulla
Pons: sensory nuclei merge to form sensory root, motor nucleus continues to form motor root
- middle cranial fossa: sensory root expands to trigeminal ganglion, lateral to trigeminal cave
- motor root passes inferiorly to sensory and travels along floor of trigeminal cave (motor fibres only go to mandibular division)

100
Q

Divisions of trigeminal nerve

A 
Opthalmic division (V1) 
Maxillary division (V2) 
Mandibular division (V3)
101
Q

How do the divisions of the trigeminal nerve exit the cranium

A

Opthalmic: via superior orbital fissure
Maxillary via foramen rotundum
Mandibular via foramen ovale

102
Q

What is the buccal nerve

A

Sensory innervation to buccal membrane of mouth and 2nd / 3rd molar

103
Q

What is the lingual nerve

A

Acts as conduit for fibres belonging to chords tympani

Innervates anterior 2/3 of tongue and submandibular sublingual glands

104
Q

Sensory functions of the mandibular nerve

A

O facial skin in the lower third of the face, chin and lower liv
Oinferior row of teeth and gingiva
O anterior 2/3 of tongue

105
Q

Motor functions of mandibular never

A

Olnervates the muscles of mastication
Olnervates the mylohyoid and anterior belly of digastric
Olnervates the tensor tympani and tensor veil palatini

106
Q

What is the tensor tympani

A

Dampens sounds created by chewing by stabilising the malleus bone of the ear

107
Q

What is the tensor veil palatini

A

Elevates the soft palate to prevent regurgitation of food and liquid into the nasopharynx

108
Q

What is satiation

A

Feeling of fullness that terminates meal

109
Q

What is satiety

A

Feeling of depletion that inhibits further meals

110
Q

What is ghrelin

A

A hormone released from the GI tract that stimulates appetite
Secreted on anticipation of food
- acts centrally at ARC or brain stem to stimulate food intake through NPY and AgRP

111
Q

What is leptin

A

Peptide hormone secreted from adipose tissue
Decreased food intake leads to decreased leptin levels (reversed by refeeding or insulin)
- production of leptin correlates with amount of adipose tissue ie energy stores
- mutations causing absence of leptin leads to severe obesity

112
Q

What is PYY

A

Secreted from distal GIT dependent on nutrient intake (eg protein > fat or CHO)
Also stimulated by CCK, gastric acid and bile
Inhibits food intake possibly through vagal inputs
PYY levels stay elevated for 12 hours post meal
Decreases food intake in lean and obese - useful target for treatment of appetite in obese patients

113
Q

How is appetite linked to reward processes in the brain

A

Eg opiod receptors (endorphins)
Cannabinoid receptors
Dopamine - feeding is associated with dopamine release in the dorsal striatum

114
Q

What is bupropion

A

Dopamine reuptake inhibitor

Weight loss

115
Q

What is orlistat

A

Inhibits gastric and pancreatic lipase
Minimal absorption
Needs to be taken before each meal
About 30% inhibition of lipases at normal therapeutic doses (lose 200kcal per day)

Needs to be combined with a low fat diet - reinforces the need to restrict fat intake

Side effects:
Steatorrhea- fatty foul smelling faeces, may help reduce fat intake

Need to monitor fat soluble vitamin status - supplements?

116
Q

When would you prescribe orlistat

A

BMI >30 kg/m2 or BMI >28 kg/m2 if other risk factors eg type 2 diabetes, hypercholesterlaemia, hypertension

Should only be continued after 12 weeks if weight loss exceeds 5%
Treatment >12 months should only be done after discussion potential benefits and risks with patient

117
Q

What is Alli

A 
Reduced dose orlistat (OTC) 
Max 6 months 
Reduced dose 
Combined with reduced fat diet 
BMI >28 
Dietary approaches and physical activity should be tried before 
Review after 12 weeks
118
Q

What is saxenda

A

GLP1 agonist
Liraglutide is a glucagon like peptide 1 receptor agonist
Sc injection
Appetite suppression - increased secretion of POMC / CART anorexigenic neurons
GLP1 can also reduce high fat food intake by suppressing dopamine signalling - effect on reward pathways

119
Q

What is mysimba

A

Combination of naltrexone and bupropion
Effects on reward pathway
Similar efficacy as orlistat

Not recommended by NICE as cost effectiveness isn’t clear (orlistat is much cheaper)

120
Q

What is Sibutramine

A

Combined Noradrenaline and 5HT uptake inhibitor
Cf antidepressants
Appetite suppressant
No longer used - increase bp and hr

121
Q

Define obesity

A

Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health

122
Q

What comoribid conditions is obesity associated with

A 
Depression 
Stroke 
Coronary disease (dyslipideamia, hypertension, LVH, CHF) 
T2 diabetes, prediabetes 
Gynae abnormalities 
Infertility 
GI diseases 
Non alcoholic fatty liver disease 
Pulmonary disease 
Sleep apnoea
123
Q

What is a VLCD

A

Very low calorie diet

700-900 calories consumed each day for 10 weeks

124
Q

What does GLP 1 do

A

Activates areas of the brain involved in appetite regulation

The postprandial GLP-1 response is associated with activation of areas of the human implicated in regulation of appetite and food intake

Peak postprandial increases in plasma GLP-1 concentration are correlated with increases in regional cerebral blood flor in the left dorsolateral prefrontal cortex and the hypothalamus

125
Q

Types of intercellular messengers in the body

A

Endocrine
Autocrine and paracrine
Neuroendocrine
Neurotransmitter

126
Q

What is a paracrine molecule

A

Relating to or denoting a hormone that has effect only in the vincinity of the gland secreting it

127
Q

What is an autocrine molecule

A

A chemical signal that binds to and affects the cells that makes it

128
Q

What is a neuroendocrine molecule

A

A nerve cell that makes the hormone and secretes it into the blood where it travels to target cells

129
Q

What is preprohormone

A

‘Pre’: hydrophobic signal peptide - informs cells needs further processing and packaging because going to be exported out of cell
- large, inactive precursor

130
Q

How are hormones synthesised

A

No gene involved
Enzymatic conversation of cholesterol
- lipophilic: lipid soluble -> readily pass over phospholipid bilayer so cant be stored
- released by simple diffusion
- bound to plasma carrier proteins in blood because aqueous

131
Q

Difference in regulation of peptide vs steroid hormones

A

Peptide: regulation of release is control of exocytosis (presynthesised, stored hormone)
Steroid: regulation of release is regulation of synthesis

132
Q

What is the endocrine axis

A

Interactions between hypothalamus, pituitary and peripheral endocrine glands, showing feedback regulation

133
Q

General principles of treatment

A

Hormone deficiency: hormone replacement
Hormone excess: drugs to block production
Decreased target cell responsiveness: drugs to enhance cellular response to hormone
If tumour: radiotherapy / surgery

134
Q

What are chromophobes

A

Immature with only a few hormones
Recently released most of their hormones
Waiting in reserve so don’t have many hormones

135
Q

What are chromophils

A

Actively secreting cells

136
Q

What are pituitary tumours

A

Adenoma
Common, usually benign, don’t spread
Can cause bilateral hemianopia (loss of peripheral vision) because of proximity to optic chiasm

137
Q

What happens if there is damage to the pituitary stalk

A

Anterior pituitary hormones regulated by hypothalamic releasing factors which go down portal vessels
Hormone levels go down (other than prolactin which increases)
Posterior pituitary hormones: decrease ADP and oxytocin

138
Q

How does surgical removal of pituitary tumours work

A

1) craniotomy - through skull above eye

2) trans - sphenoidal - through nose (most common)

139
Q

What is the development of self concept

A

5-7 year olds can give description on range of dimensions but not relative to others

7-8 year olds can compare themselves to others - self esteem increases

140
Q

Presentation of depression in adolescence

A 
Reduced school / professional performance 
Social isolation 
Aggressive, violent behaviour 
Repeat consultations for ill defined complaints 
Family conflict 
Sleep disturbances 
Apathy 
Poor concentration 
Low self esteem

Med 3 (10 decks)

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