Block 12 key things to learn Flashcards
What are the spinal levels of reflexes?
Biceps C5/ C6
Triceps C7
Patella L4
Achilles S1
What is the key difference between central and peripheral sensitisation?
Peripheral is linked with inflammatory mediators prostaglandins etc causing a reduced threshold for neuronal activation due to hyper excitability of peripheral nociceptors
Central is linked with increased glutamate and substance P leading to transcriptional changes and a reduced pain threshold
What are the fibular collateral ligaments of ankle and what happens when have inversion injury?
Anterior talofibular
Posterior talofibular
Calcaneofibular
So strong that more likely to break fibular than these
What are the medial collateral ligaments of ankle and what happens on eversion injury?
Anterior tibiotalar Posterior tibitalar Tibiocalcaneal Tibionavicular Get trimalleolar fracture due to injury to ligaments causing break of medial malleolus, tibia and lateral malleolus of fibular
Where does neural control of pupil come from?
Sympathetic (widen pupil) from superior cervical ganglion via oculomotor nerve
Parasympathetic from oculomotor nerve to ciliary ganglion to sclera muscle
How does the eye focus on close up and far away objects?
Distance- lens thin and suspensory ligament tense, ciliary muscles relaxed
Close- lend round, ciliary muscle tense, suspensory ligament relaxed
What visual loss would you get with an issue in different parts of visual system?
Optic nerve lesion- anopia of whichever eye
Optic chiasm- no crossing of visual fields- bitemporal hemianopia- can only see middle area not either side
Lateral geniculate nucleus- lose opposite side visual field, e.g. if in left nucleus then will get a right homonymous hemianopia
Optic tract- if just lose 1 fibre then you will only lose a quarter of your visual field- e.g. if on a fibre on the left you would get a right homonymous superquadrantopia
Occipital lobe- would lose the opposite sides visual field, same as if LGN lesion
What are the stages of anaesethscia?
1- induction:
immediately after administration until loss of consciousness. Big pupils react to light, irregular reps and heart rate, normal bp
2-Excitement:
After loss of consciousness
Excited and delirious activity, uncontrolled movements
Irregular resps and heart rate, big pupils react to light, high bp
3-surgical anaesthesia-
Pupils small and don’t react to light
Regular low resps and heart rate
Normal bp, skeletal muscle relaxation
4- overdose severe brainstem and medullary depression cardiovascular collapse big fixed pupils weak resps, weak thready pulse, low bp
What is wallenburg syndrome?
issue with artery supplying medulla- posterior cerebral artery, causes issues with cranial nerves 9-12
What happens if have oculomotor nerve lesion?
Eye points down and out, dilated pupil due to lack of parasympathetic innervation, partial ptosis
What is seen in horners syndrome
Issue with sympathetic innervation
Pupil constricted- mitosis
Droopy eyelid- ptosis
No sweating- anhidrosis
What does the ventricular system consist of and how does it work?
Otolith organs- utricle and saccule-
Utricle- detects left right head tilt- macula horizontal
Saccule- detects up down head tilt- macula vertical
Semicircular canals- detect rotation- ampulla with with hair cells in cupula inside is main unit of them and is pushed one way or other by endolymph
Where is hearing processed and how is sound localised?
Processed eventually by the medial geniculate nucleus
Superior olivary nucleus is where sound localisation is done:
Medial SON detects time difference in sound from each ear to localise. Done at low frequency sound
Lateral SON detect sound intensity difference between ears and done for high frequency sound
What is affected and what is the result of erbs palsy and klumfes paresis?
Erbs- damage to C5 root- arm hangs loosely at side- no bicep reflex
Klumpfe- T1 root damage- no sensation or use of small muscles of hand
How are osteoblasts and clasts regulated?
Calcitonin from thyroid encourages osteoblasts to lay down new bone.
PTH from parathyroid gland encourage osteoclast resorption.
Osteoblasts also regulate- produce RANKL to activate osteoclasts and produces OPG to block RANKL and stop osteoclast activation
What is the key triple therapy for rheumatoid arthritis?
Sulphasalazine, chloroquine and methotrexate
What is Alzheimers disease?
Most common form of dementia in all ages
Beta amyloid plaques, tau tangles and decreased acetylcholine
Mostly temporal lobe atrophy
1 in 6 chance over 80
2 x more common in women
Treat with Donepezil- acetylcholine esterase inhibitor and memantine- NMDA antagonist to block affect of excess glutamate and help memory
What is vascular dementia?
2nd most common dementia in over 65’s
Caused by issue with blood supply to brain- step wise progression
Affects more men than women
What is dementia with levy bodies?
Affects 15% of people with dementia
Mix of Alzheimers and Parkinson’s symptoms
Build of of Lewy bodies of alpha synucelin
Hard to treat- no specific treatment, give ACHe inhibitors for hallucinations
What are the 2 types of frontotemporal dementia?
Less common in over 65’s
Second most common in under 65’s
Often due to mutation in tau gene
Behavioural variant/ picks disease- more common change in personality and behaviour lose inhibitions change in appetite
Primary progressive aphasia-
language difficulties
reduced comprehension
speech problems
What is glaucoma and what is the treatment?
Issue with drainage of aqueous humour produced by ciliary body in anterior chamber of eye.
Usually drains via trabecular network into schlemms canal located at join of cornea and sclera.
Open angle glaucoma- trabecular network clogged over time, slow onset vision loss
Closed angle- iris bows and closes anterior chamber angle and blocks drainage- sudden onset vision loss and pain
Treatment:
beta blockers to reduce amount of aqueous humour
alpha agonists to reduce the amount
carbonic anhydrase inhibitors to reduce amount
Prostaglandin analogues to increase aqueous humour drainage
muscarinic agonists to increase trabecular outflow
How is vision processed?
From lateral geniculate nucleus it is sent to occipital lobe by magnocellular and parvocellular cells.
Magnocellular cells are the bottom 2 layers and are large cells that receive inputs from A parasol ganglion cells- greyscale
Parvoceullular cells are small cells in top 4 layers that get inputs from midget ganglion cells
Primary visual cortex sends things via 2 streams-
inferotemporal cortex- what pathway
posterior parietal cortex- where pathway
What are the areas of cerebellum and what happens in cerebellar dysfunction?
Vermis/ vestibulocerebellum- balance
Paravermis/ spinocerebellum- postural tone
Cerebellar hemispheres- fine coordination
V-vertigo A-ataxia N-nystagmus I-intention tremor S-lurred speech H-hypotonia D-dysmetria, dysdiadochokinesis
What is Menieres syndrome?
Increase in volume of endolymph disrupts function of labyrinth in ear, get temporary attacks of vertigo, deafness and nausea and vomiting
No cure but can treat nausea and vertigo
