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Medicine year 2 semester 2 > Case 21- pharmacology and physiology > Flashcards

Case 21- pharmacology and physiology Flashcards

1
Q

Side effects of drugs- Nigrostriatal pathway

A
  • Extrapyramidal side effects
  • Extrapyramidal system- brainstem, cerebellum and basal ganglia. The fibres do not pass through the pyramids in the medulla. Controls both voluntary and involuntary movement
  • Hours to days- Dystonia, muscle tension particularly in the face and neck
  • Days to weeks- Akathisisia, restlessness
  • Weeks to months- Pseudoparkinsonism (Bradykinesia, Rigidity, Shuffling gait, Tremor)
  • Years- Tardive dyskinesia. Oral and facial movement, often untreatable. Thought to be due to super sensitivity after long term blockage
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2
Q

Side effects of drugs- Tuberoinfundibular pathway

A 
Blocking this pathway causes hyperprolactinaemia which results in:
• Sexual dysfunction- decreased libido
• Gynaecomastia
• Galactorrhoea
• Infertility
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3
Q

Side effects of the histamine

A

Blocking these receptors lead to sedation and weight gain due to lack of satiety and the development of sugar cravings. These effects could be a problem if the patient is taking the medication long term and needs to drive or attend work and it increases their chance of diabetes, MI or stroke

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4
Q

∝-1 adrenoreceptors

A

Blocking these receptors cause dizziness, postural hypotension and erection and ejaculation problems

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5
Q

Serotonin receptors (5HT2)

A

Blocking these receptors may increase anxiety and cause insomnia, It can also have a metabolic effect causing dyslipidaemia, weight gain and hyperglycaemia

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6
Q

Muscarinic aceetylcholine receptors (M1)

A

Blocking these receptors produce the typical anticholingeric side effects of dry mouth, urinary retention, constipation and blurred vision.

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7
Q

Other effects of antipsychotics

A
  • Prolonged QT interval- most common with haloperidol. It can cause arrhythmias -> cardiac arrest. Thought to be due to the effect of blocking a K+ channel involved in the repolarisation of ventricular cells
  • Neuroleptic Malignant syndrome- can be fatal. Muscle rigidity to rhabdomyolysis to renal failure. Hyperthermia, Sweating, Tachycardia and Labile blood pressure. Thought to be due to the reduction in the central dopaminergic activity
  • More common in individuals with predisposing factors i.e. older age, switching between antipsychotics or high doses of medication.
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8
Q

What type of drugs are antipsychotics

A

Antipsychotics tend to be dopamine antagonists. They have effects on other receptors causing side effects.

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9
Q

The typical or 1st generations

A
  • Grouped according to their structure and side effect profile. They have an affinity for D2 receptors but can also interact with histamine, cholinergic and ∝-adrenergic receptors.
  • These drugs allow the mesolimbic pathway to be blocked which reduces the positive symptoms associated with schizophrenia.
  • In the mesocortical pathway, inhibition may worsen the negative symptoms.
  • The typical antipsychotics also block the nigrostriatal and tuberoinfundibular dopamine pathways causing extrapyramidal movement disorders and hyperprolactinaemia.
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10
Q

The atypical or 2nd generation antipsychotic drugs

A
  • Act at D2 receptors, they cause a transient block of these receptors which can help to reduce extrapyramidal side effects.
  • They also block serotonin (5HT2a) receptors. Serotonin reduces the release of dopamine and blocking this inhibition increases dopamine in the mesocortical pathway
  • Both the transient blockade of D2 receptors and 5HT2a blockade may allow the treatment of the negative symptoms of schizophrenia.
  • Blocking serotonin receptors generates the main metabolic side effects of the second-generation drugs, dyslipidaemia, weight gain and hyperglycaemia.
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11
Q

First generation/ atypical antipsychotics

A

1) Phenothiazines
2) Thioxanthenes
3) Butyrophenones

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12
Q

Phenothiazines

A
  • Group 1 i.e. Chlorpromazine (pronounced sedative effects, moderate antimuscarinic and extrapyramidal side effects
  • Group 2: e.g. Pericyazine (moderate sedative effects, but fewer extrapyramidal side-effects than groups 1 or 3)
  • Group 3: e.g. Fluphenazine (fewer sedative and antimuscarinic effects, more pronounced extrapyramidal side effects than groups 1 and 2).
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13
Q

First generation antipsychotics- Thioxanthenes, Butyrophenes

A 
Thioxanthenes= Flupentixol and Zuclopenthixol- moderate sedative, antimuscarinic and extrapyramidal effects
Butyrophenones= Haloperidol and Benperidol, side effects are similar to group 3 phenothiazines
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14
Q

Group 1 Phenothiazine: Chlorpromazine

A
  • Lipophilic
  • It may be given as an oral, intramuscular (IM) or depot preparation
  • IM injection may be useful in acute episodes
  • High level of plasma protein binding
  • Liver metabolism= high first pass metabolism, the half life is erratic but around 1 day
  • Interactions= reduce the effectiveness of antiparkinsonian drugs. Potentiates the sedative effects of benzodiazepines and central antihistamines
  • Additional side effects- Blood dyscariasis, CV disease and diabetes, Predisposes to seizures/epilepsy, Depression, Myasthenia gravis, Photosensitation
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14
Q

Group 1 Phenothiazine: Chlorpromazine

A
  • Lipophilic
  • It may be given as an oral, intramuscular (IM) or depot preparation
  • IM injection may be useful in acute episodes
  • High level of plasma protein binding
  • Liver metabolism= high first pass metabolism, the half life is erratic but around 1 day
  • Interactions= reduce the effectiveness of antiparkinsonian drugs. Potentiates the sedative effects of benzodiazepines and central antihistamines
  • Additional side effects- Blood dyscariasis, CV disease and diabetes, Predisposes to seizures/epilepsy, Depression, Myasthenia gravis, Photosensitation
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15
Q

2nd generation/atypical antipsychotics MoA

A

Due to the low potency but high side effect profile of the typical antipsychotics the atypical antipsychotics were created.
These are still very non-specific drugs as they also have varied effects on dopamine, serotonin (HT), histamine (H), muscarinic, and ∝-1 receptors.
Some have a higher affinity for HT2A than dopamine receptors-this can help to increase the amount of dopamine release in the mesocortical area reducing the negative symptoms of schizophrenia.

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16
Q

Types of 2nd generation/atypical antipsychotics

A
  • Aripiprazole-D2 partial agonist, 5-HT1A, 5-HT2A
  • Risperidone-D2>D3=D4, 5-HT2, ∝-1, H1
  • Olanzapine- weak D2 (but limbic selective D2 affinity), muscarinic, 5-HT2, H1
  • Quetiapine-limbic selective D2 affinity, muscarinic, 5-HT2, ∝-2 , H1
  • Amisulpride-D2=D3 (limbic selective)
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17
Q

Clozapine side effects

A

Used for treatment resistant schizophrenia. Has a number of important side effects:
• Metabolic- weight gain which requires BMI, HbA1c, and lipid monitoring.
• Pericarditis/ myocarditis- requires ECG monitoring and cardiac function tests.
• Agranulocytosis- reduction in leukocytes, there is an increased risk of serious infections-requires regular blood tests for WCC.
• Can cause intestinal obstruction- make sure there is no PMH of this condition and that the patient seeks medical help if constipation develops.
• Risk of death due to toxicity-monitor the blood concentration if the patient changes any of their medication that may affect drug metabolism, stops smoking cigarettes, or has an acute concurrent illness.

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18
Q

Sequence of Schizophrenic drugs used

A

1st line-Atypical/Typical
2nd line-Atypical/Typical
3rd line-Clozapine-this is the most effective antipsychotic for treatment-resistant schizophrenia

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19
Q

How long should antipsychotics be taken

A

Start the patient on a low dose and titrate up. The patient should stay on the medication for 4-6 weeks at an optimum dose before concluding that there is no response to treatment.
You need to find the best response with the lowest amount of side effects.
Patients usually need to stay on medication for around 2 years after an initial presentation.

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20
Q

Sensory modalities

A
  • General senses= Somatic (Tactile, thermal, pain, proprioception). Visceral (conditions of internal organs).
  • Special senses= taste, smell, hearing, balance, vision
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21
Q

Sensory processing features shared between sensory modalities

A
  • Pre neutral stimulus enhancement
  • Sensory transduction- from light stimulus to action potentials, through photoreceptors
  • Adaption to stimulus intensity
  • Adaption to stimulus duration
  • Sensory acuity- different parts of the retina viea different parts of the visual world, more rods and cones in the fovea
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22
Q

Sensory processing

A
  • Pre-neural stimulus enhancement in the retina
  • Sensory transduction
  • Subcortical processing in the thalamus, before the primary sensory cortex (V1)
  • Cortical processing- where perception takes place. Cortical processing can affect sensory transduction where the brain expects to see certain patterns
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23
Q

What layer does light enter through the retina

A

Light enters the retina through the ganglion cell layer and has to pass all layers to reach the photoreceptors. The photoreceptors are at the back of the eye where they are connected to the blood vessels and connected to the pigmented epithelium which is very dark and feeds the cells. Also means the light doesnt scatter back into the eye

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24
Q

Retinal circuits- basic organisation

A
  • Vertical connections- Glutamate (photoreceptors, bipolar cells, ganglion cells). Continuous release from PRs and BCs]
  • Horizontal connections- GABA (horizontal and amacrine cells), Glycine (amacrine cells), Acetylcholine (amacrine), Dopamine (amacrine cells)
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25
Q

The retina

A
  • Outpost of the brain, part of the CNS complex, layered structure
  • Seven cell types organised in three nuclear layers and two synaptic layers
26
Q

Nuclear layers of the retina

A
  • Outer nuclear layer (ONL)- Photoreceptors: rods and cones
  • Inner nuclear layer (INL)- Horizontal cells, bipolar cells, amacrine cells
  • Ganglion cell layer (GCL)- Ganglion cells (output cells, axons from the optic nerve
27
Q

Synaptic layers of the retina

A
  • Outer plexiform layer (OPL)- synaptic contacts between photoreceptors, horizontal and bipolar cells
  • Inner plexiform layer (IPL)- synaptic connection between bipolar, amacrine and ganglion cells. IPL is divided into an On and Off layer
28
Q

Retinal haemorrhage

A
  • Flame-shaped haemorrhages: seen in the nerve fibre layer, fans out
  • Dot-blot haemorrhages: seen in both the inner nuclear or outer plexiform layers, look like dots
  • Hard exudates: extracellular protein and lipid deposits left after chronic edema, star-shaped due to location in Henle’s layer (part of the outer plexiform layer). White dots
  • Haemorrhage in all retinal layers- stormy look
29
Q

Retinal ischaemia

A
  • Cherry red spots: retinal edema, usually due to central retinal artery occlusion
  • Partial retinal ischemia
  • Cotton-wool spot: focal areas of ischemia in Ganglion Cell Layer and Nerve Fibre Layer
  • Central retinal artery occlusion
30
Q

Main features of the vertebrae retina

A

• The retina is inverted: photoreceptors are located behind other layers,
at the back of the eye, adjacent to the pigment epithelium.
• The fovea- only cones
• The optic disk.
• Macula- cones with some rods

31
Q

Why is the retina inverted

A
  • Evolutionary accident?
  • Receptors are “hungriest” of all retinal cells, and blood vessels are directly underneath, in choroid plexus.
  • Neurons are transparent, blood vessels are not.
  • Retinal pigment epithelium is black and therefore minimizes light scatter.
32
Q

The fovea

A

• In size, 2o visual angle (or 600mm in retinal distance).
• All inner layers pushed aside.
Foveola or foveal pit: no blood vessels, no ganglion cells, no INL cells, Contains only cones
All the bipolar, ganglion and support cells are pushed to the side creating the foveal pit gives the cones an unobstructed view of the outside world. The fovea’s ganglion cells are in the macula

33
Q

Normal optic disc

A 
• In size, 6o visual angle (1,800 mm).
In the nasal retina
• Located 15o nasal to fovea.
• Ganglion cell axons converge and leave eye together with blood vessels.
• Here, no receptors (cones, rods) 
• Corresponds to blind spot.
White disk in the centre
Cup to disc ratio of about 0.3
34
Q

Structure of rods and cones

A

• Rod membraneous disks- rhodopsin
• Cone membraneous disks- photopsin
Rods and cones are involved in phototransduction. In the centre are the cones which are smaller, near the outside are some rods which are a lot smaller. You have more rods then cones
The nucleus are in the central body, the photodetection areas are in the membranous disc in the outer segment

35
Q

Phototransduction

A
  • Enabled by a visual pigment in outer segment discs.
  • Consists of a protein - opsin (molecule sensitive to light) and a chromophore derived from vitamin A - retinal (manufactured from b-carotene in the food we eat) bound together. The chromophore is a particular colour which allows us to absorb that wavelength of light
  • Photoreceptor response- allows Na+ influx in the dark releasing Glutamate. Light closes the Na+ channels reducing the membrane potential (hyperpolarises). Ca+2 can also pass through these channels
36
Q

The process of Phototranduction

A

• Light absorbed by an opsin molecule in the membrane area of the disc triggers a signalling cascade.
• ‘11-cis retinal’ undergoes a conformational change to ‘all-trans’
• This change activates the G protein ‘transducin’
• The activated ‘transducing’ in turn activates ‘cGMP phosphodiesterase’
• ‘cGMP PDE’ now hydrolyzes ‘cGMP’ reducing its concentration
• The reduced concentration of ‘cGMP’ leads to closure of the sodium channels
• The closure of the sodium channels leads to a change in membrane potential
Phototransduction provides an enormous signal amplification system. Allows you to be sensitive to small changed in light. There is a change in membrane potential and a reduction in the amount of glutamate released from the bipolar cells

37
Q

Peripheral vision

A

• Rods, distributed throughout the retina but none in the fovea
• Responsible for our ability to see in dim light (scotopic vision)
• High sensitivity (can detect one photon)
• Monochromatic (colour-blind)
• Cannot discriminate fine image details (poor spatial acuity)
• Slow temporal responses to changes in illumination
Rods are good for seeing movement

38
Q

Central vision

A
  • Cones, concentrated around the fovea
  • Works only in daylight (photopic vision)
  • Low sensitivity (cannot detect very small luminance changes)
  • Chromatic (colour vision), tuned to specific light wavelengths.
  • Can discriminate fine image details (high spatial acuity)
  • Narrow angle of coverage
  • Fast responses to changes in illumination
39
Q

Why do we initially see almost nothing when we move from bright light to darkness

A
  • Shift operation from cones to rods
  • Initially we only see blackness because- cones slowly adapt to lower light levels but will stop functioning in a very dark environment. Rods are not functional because rhodoposin has bleached in the bright light
  • Rhodoposin starts regenerating in the dark and retinal sensitivity increases with time
  • Slow process- can take over 30 mins
40
Q

Optical refraction

A

Light is refracted onto the retina by the cornea and lens. Problems with this refractory process can result in a reduction in visual acuity as the light is not being focused correctly onto the retina. The cornea is fixed in shape and therefore its refractive power remains the same, this is where most refraction occurs. The shape of the lens can be changed meaning the refractive power here can be altered depending on the distance of the object that is being viewed.

41
Q

Myopia/near sighted

A

The refractive power is too great or the eyeball is too long. The image is focused in front of the retina

42
Q

Hyperopia/long sighted

A

The refractory power is too weak or the eyeball is too short. The image is focused behind the retina

43
Q

Presbyopia

A

An effect of aging. Impaired accommodation due to reduced elasticity of the lens or ciliary muscle dysfunction. This causes a problem when viewing objects close by.

44
Q

Where does the eye sit in the orbit

A

There is 23 degrees between the axis of the orbit and the axis of the eyeball

45
Q

Eye movements

A
  • Elevation- looking up
  • Intorsion- a medial rotation of the eye i.e. going from looking up to looking medially
  • Extorsion- a lateral rotation of the eye i.e. going from looking up to moving laterally
  • Abduction- looking laterally
  • Adduction- looking medially
  • Depression- looking down
46
Q

Lacrimation function

A
  • Contributes to the tear film: with the Lacrimal, Meibomian, mucous gland
  • Protection from pathogens
  • Removal of debris
  • Nutrient provisions to the cornea
  • Lubrication
  • Lacrimal gland is superolateral to the eye
47
Q

Lacrimal gland parts

A

Palpebral part, Orbital part. Supplied by the Levator palpebrae superioris muscle. The palpebral part is inferior to the muscle

48
Q

Conjunctiva

A
  • When the lids are closed a conjunctival sac is formed. The Palpebral conjunctiva covers the upper and lower surface of the eyelid and it extends back to form the Bulbar conjunctiva
  • The upper extension of the sac is the superior fornix
  • Fluid from the lacrimal gland is released into this region via the lacrimal ducts
49
Q

Lacrimation

A
  • The fluid released from the lacrimal gland moves across the surface of the eye to the lacrimal lake
  • Lacrimal puncta (upper and lower) on the medial surface of the eye which drain the secretions from the lacrimal lake. The fluid then drains into the Lacrimal canaliculi and then the Lacrimal sac. There is then drainage via the Nasolacrimal duct to the nose and drains via the inferior meatus into the lateral aspect of the nose
  • Lacrimal sac
  • Nasolacrimal duct
  • Lacrimal canaliculi (upper and lower)
50
Q

Control of lacrimation- via CNVII (facial) Parasympathetic

A
  • Preganglionic fibres- via the greater petrosal nerve and nerve of the pterygoid canal from the salivatory nucleus of the facial nerve (CNVII)
  • They then enter the Pterygopalatine ganglion
  • Postganglionic fibres- hitch hikes on divisions of the maxillary and ophthalmic branches of the trigeminal nerve (CNV) to the lacrimal gland
51
Q

Nerves involved in the control of lacrimation

A

Branches concerned are the Zygomatic and the Zygomaticotemporal branches of the facial nerve. The division of the Ophthalmic nerve is the Lacrimal nerve.

52
Q

Pathology of the Lacrimal gland

A
  • Sjorgen syndrome- autoimmune condition with lymphocyte infiltration of the lacrimal and parotid glands. Associated with rheumatoid arthritis. Symptoms are dry eyes and mouth
  • Dacryocystitis- inflammation of the lacrimal sac. Symptoms are pain, redness, swelling, excess tears (epiphora), discharge, fever. Can cause pre-septal and orbital cellulitis. Requires antibiotics or incision and drainage
53
Q

Where does fluid move from the Lacrimal gland

A

Lacrimal gland -> Lacrimal ducts -> Conjunctival sac -> Lacrimal lake -> Lacrimal puncta -> Lacrimal canaliculi -> Lacrimal sac -> Nasolacrimal duct -> Inferior nasal meatus -> Nasal cavity

54
Q

Where is aqueous humour produced from

A

The ciliary process

55
Q

Composition of Aqueous humour

A

Clear watery fluid, similar to plasma. Higher amount of ascorbate in it (ester of vitamin C) essential for supporting the health of the lens, lower protein then plasma, doesn’t contain any blood cells

56
Q

Function of aqueous humour

A

Nutrient supply to the avascular area (lens and cornea), wate removal, Intra-ocular pressure

57
Q

Flow of the aqueous humour

A
  • The ciliary circulation bring fluid and the metabolic components to this region
  • Ultrafiltration and active secretion into the posterior chamber
  • Flows into the front of the lens and through the pupil into the anterior chamber
  • Drains via the trabecular meshwork into the canal of Schlemm which is the angle of the eye between the cornea and the iris
  • The aqueous humour humour reaches the blood stream via the ciliary veins
  • The posterior chamber is in front of the lens and behind the Iris
58
Q

Pathology- Glaucoma

A
  • Primary glaucoma- open or closed angle
  • Open angle- flow is reduced through the trabecular meshwork, causes gradual decrease of peripheral vision
  • Closed angle- forward displacement of the iris onto the cornea issues with removal of the aqueous humour. Opthalmic emergency which rapidly leads to blindess
  • Both types- prevent aqueous humour from draining. Fluid backs up increasing intraocular pressure. Causes damage to the optic nerve
  • In Glaucoma you have an increased cup to disc ratio (enlarged cup) so some of the nerve fibres have died in the middle
  • Retinal ganglion axons pass along the nerve fibre layer to the disc then change course to go back past the nerve
59
Q

Branches of V1 in the eye

A

There are branches of the ophthalmic nerve (V1) entering the orbit via the superior orbital fissure.
These nerves remain at the superior aspect of the orbit

60
Q

The branches of the ophthalmic nerve include the

A
  • Nasociliary nerve -passes through the tendinous ring (the origin of the four rectus muscles) to travel medially. It terminates as the anterior ethmoidal and infratrochlear nerves
  • Frontal nerve -middle and largest branch, sits superficial to the levator palpebrae superioris which is superficial to superior rectus. It gives off the supratrochlear and supraorbital nerves.
  • Lacrimal nerve -lateral, heads towards the lacrimal gland
61
Q

Optic nerve

A

Enters the orbit via the optic canal, it is a large structure that is easily identifiable. It passes through the tendinous ring. Also passing through the optic canal is the ophthalmic artery which is a branch of the internal carotid

62
Q

The Oculomotor nerve- summary

A
  • The oculomotor nerve has superior and inferior branches
  • They both enter the orbit through the superior orbital fissure and pass through the tendinous ring.
  • The inferior branch innervates the medial rectus, inferior rectus and inferior oblique
  • The superior branch innervates the superior rectus and levator palpebrae superioris
63
Q

Muscles of the eye- summary

A
  • On the medial surface there is the superior oblique. It is easy to identify as it passes through the trochlea pulley system.
  • It is supplied by the trochlear nerve which you can see moving medially after passing through the superior orbital fissure to innervate this muscle.
  • On the lateral surface you can see the lateral rectus muscle. This is supplied by the abducent nerve which passes through the superior orbital fissure and tendinous ring.

Medicine year 2 semester 2 (47 decks)

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