Friday, 17 May 2013

Pharmacology: Receptor types


Receptor types:

1.       Ligand gated ion channels:
These are membrane proteins similar to other ion channels and incorporate a ligand binding site. Usually these are receptors on which fast neurotransmitters act. Generally cause an increase in Na+ and K+ permeability. Direct coupling between receptor and ion channel and no intermediate steps are needed in the transduction process.

E.g. Nicotinic acetylcholine receptor: 4 subunits: α, β, γ, δ (each 40 – 58 kDa). Two acetylcholine binding sites, each at the interface between one of the two α subunits and its neighbour. Each subunit spans the membrane 4 times.

Other examples:
GABAA receptor, 5-HT3 receptor

Ion channels:
·         4-5 subunits
·         Ligand gated
·         Conduct Na+, K+, Cl-, Ca2+
·         Alter cell membrane potential or intracellular ionic composition
·         Fast communication (µs-ms)
o   Examples:
o   Nicotinic Acetylcholine receptor (nAChR)
o   GABAA receptor
o   Glycine receptor
o   Glutamate receptor
o   5-HT3 receptor
o   P2x purine receptor


2.      G-protein coupled receptors:
GCPRs are the most targeted receptor type for therapeutic drugs. Many neurotransmitters can interact with both GCPRs and ligand-gated channels leading to a wide variety of effects.

GCPRs consist of a single polypeptide chain of up to 1100 residues. They have a characteristic seven transmembrane α helix structure, with an extracellular N-terminal and an intracellular C terminal domain.

The G-protein consists of three subunits, α, β, γ, the α subunit having GTPase activity. When this binds the agonist-occupied receptor, the α subunit dissociates and activates the effector (usually adenylyl cyclase, phospholipase C or ion channel). Activation is terminated when the bound GTP molecule is hydrolysed, which allows the α subunit to recombine.

E.g.
mAChRs, adrenoceptors, dopamine receptors, 5-Ht receptors, opiate receptors, purine receptors.

G-protein-coupled receptors
·         Receptors linked to effectors (adenylate cyclase/ phospholipase C/ ion channels) that change intracellular levels of second messenger via GTP-binding proteins
·         Spans membrane 7 times
·         Third intracellular loop couples to G-protein and determines G-protein selectivity
·         Nitrogen side extracellular, Carbon side intracellular
o   Examples:
o   Muscarinic acetylcholine receptor (mAChR)
o   Adrenoceptors
o   5-HT (serotonin) receptors (except 5-HT3)
o   Histamine H2 receptor
o   Eicosanoid receptor,
o   Many peptide receptors
o   Purine receptor
o   Chemorectors
o   Thrombin and other protease receptors
o   GABAB receptor
o   Dopamine receptors
o   Opioid receptors
§  Thrombin receptor activated by protease cleavage of N-terminus domain,à tethered agonist
·         Subtypes:
o   Activate (Gs, Gq)
o   Inhibit (Gi, G0)
·         Seconds to minutes
·         Signal amplification
·         Second messengers activate protein kinases:
o   PKA
o   PKG
o   PKC
o   DAG-dependent PKC


3.      Kinase linked receptors:
Most are large proteins with a single membrane spanning helical region with a large extracellular binding domain and a variable intracellular domain. They play a major role in controlling cell division, growth, differentiation, inflammation, tissue repair, apoptosis and immune response.

Main types:
·         Receptor tyrosine kinases:
·         Serine/ threonine kinases:
·         Cytokine receptors
·         Guanylyl cyclase – linked receptors

Signal transduction generally involves dimerization of receptors, followed by autophosphorylation of tyrosine residues. These act as acceptors for SH2 domains of intracellular proteins.

The two important pathways are:
-         The Ras/ Raf/ mitogen activated protein (MAP) kinase pathway, which is important in cell division, growth and differentiation
-         The Jak/ Stat pathway activated by many cytokines, which controls the synthesis and release of many inflammatory mediators

Receptors with direct kinase activity (Kinase-linked receptors):
·         For hormones regulating proliferation and differentiation (growth factors)
·         Monomers (single polypeptide chain)
o   Ligand binding site
o   Single α-helix crossing membrane
o   Intracellular domain with catalytic activity:
§  Tyrosine kinase
·         Regulate growth, differentiation, development
·         E.g. insulin, EGF, PDGF
§  Serine/threonine kinase
·         E.g. TGF β receptor
§  Guanylate cyclase



4.      Nuclear receptors
Located in the cytoplasm. The liganded receptor complexes initiate changes in gene transcription by binding to hormone response elements in gene promoters and recruiting coactivator or corepressor factors

Intracellular receptors
·         Minutes to hours
·         *Lag in response à slow onset anti-inflammatory effect of glucocorticoids can persist long after agonist concentration is reduced to zero
·         Mediate response to:
o   Steroids
o   Vitamin D
o   Thyroid hormone
o   Inducers of drug metabolism (via Ah receptor)
§  Barbituates,
§  TCDD
·         Eg.
o   Glucocorticoid receptor
(The glucocorticoid receptor is expressed in almost every cell in the body and regulates genes controlling the development, metabolism and immune response. When the glucocorticoid receptor binds the glucocorticoids, its primary mechanism of action is the regulation of gene transcription. The unbound receptor resides in the cytosol. The receptor-glucocorticoid complex up-regulates the expression of anti-inflammatory proteins in the nucleus or represses the expression of pro-inflammatory proteins in the cytosol)

Wednesday, 15 May 2013

Four Habits Model of Communication


The Four Habits Model of Communication is a useful guide for each consultation a doctor has with a patient. The aim of the model is to incorporate certain practices into a doctor’s normal consultation to create a positive relationship with the patient and increase diagnostic accuracy. It improves medical communication skills and will ultimately save lives.

The Four Habits are:
·         Invest in the Beginning
·         Elicit the patient’s perspective
·         Demonstrate Empathy
·         Invest in the End

Invest in the Beginning means establishing a welcoming atmosphere for the patient and creating a good rapport. This allows faster access to the real reason for the visit and minimises the “oh by the way …” statements at the end of the visit. This will increase diagnostic accuracy and decrease the potential for conflict later on.

The second habit, elicit the patient’s perspective, involves asking for the patients ideas and elicit any specific requests. History taking is the initial and most important step in any diagnosis and it is what steers the doctor in a certain direction. Therefore it is vital that it is done correctly as it will result in a better understanding of the patient’s illness, how it is affecting them and what they have already tried to resolve the problem (e.g. alternative medicine). By talking to the patient and allowing them to plan and negotiate the course of the consultation the patient is more likely to remember instructions and advice and be more compliant.

The third habit, demonstrate empathy, allows the doctor to e caring and compassionate towards the patient. Investing in the relationship in this way and getting to the heart of the problem by showing empathy is a rewarding strategy. It is important for the relationship and its potential for healing.

“The secret of the care of the patient is in caring for the patient” – Francis Peabody

The fourth habit, invest in the end, involves delivering diagnostic information, providing education, involving the patient in making decisions and completing the visit. In my opinion it is the most important part in preventing avoidable medical error. If the patient understands the treatment and why they need it, then they are less likely to make a mistake and cause themselves unnecessary harm. Ensuring the patient will be able to do as instructed once they leave the consultation is of utmost importance in avoiding medical error. It is the doctor’s responsibility to provide adequate information and education that the patient can understand. If written instruction is required it should be clear, legible and written at a low literacy standard.

Sunday, 12 May 2013

Neuroanatomy - Autonomic Nervous System


ANS
ANS innervates everything except skeletal muscle
Sympathetic nervous system only needed to respond to stress
Parasympathetic nervous system maintains normal physiological function

Autonomic nerves:
  • ganglia are outside cerebrospinal axis,
  • produce extensive nerve plexuses,
  • ACh and Noradrenaline,
  • post-ganglionic fibres are non-myelinated,
  • on interruption -> incomplete paralysis (because organs have inherent activity and autonomic nerves only modify their activity)

Somatic nerves:
  • ganglia are inside cerebrospinal axis (no peripheral ganglia),
  • do not produce extensive nerve plexuses,
  • ACh,
  • post-ganglionic fibres are myelinated,
  • on interruption -> complete paralysis

Hypothalamus and Subthalamic nucleus are the main centres of autonomic regulation

Generally both sympathetic and parasympathetic innervate together having opposite effects. exceptions include:

Sympathetic only:
  • blood vessels,
  • spleen,
  • sweat glands,
  • hair follicles

Parasympathetic only:
  • gastric glands,
  • ciliary muscles,
  • pancreatic glands

Sympathetic:
  • thoracolumbar output,
  • wide distribution,
  • ganglia are away from organs,
  • long postganglionic fibres,
  • Noradrenaline and ACh,
  • necessary in stress [1st neuron is short (ACh),
  • 2nd is long (Noradrenaline),
  • synapsing occurs in chain ganglia or collateral ganglia,
  • excitatory to many organs,
  • inhibitory to others (digestive),
  • effects widespread and persistent].
  • can cause glycogenolysis, glycolysis, vasoconstriction at site of bleed, release of RBCs from spleen, bronchodilation, vasodilation in blood vessels of skeletal muscle and vasoconstriction in blood vessels of skin.

Parasympathetic:
  • craniosacral output,
  • limited distribution to head,
  • neck and trunk,
  • ganglia are near organs,
  • short postganglionic fibres,
  • ACh. [1st neurons are long, emerge from brain stem or sacral spinal cord, run with spinal or pelvic nerves, ACh. 2nd neurons are short, ACh, excitatory/ inhibitory].
  • decreases HR and Respiration,
  • moves cilia,
  • stimulates GI and causes defecation, urination, stimulates digestion, miosis (protection from excess light??)

In the entire PNS adrenaline is released only in adrenal medulla as NT.
Dopamine is also released on renal vasculature
*ganglia - nicotinic receptor

Enteric Nervous System:
Auerbach’s plexus: ACh, CGRP, NPY
Meissner’s plexus: substance P, 5-HT, ACh, Noradrenaline

Disorders of ANS:
  • erectile dysfunction,
  • orthostatic hypotension,
  • gastroparesis,
  • urinary incontinence,
  • decreased or absent sweating

Saturday, 11 May 2013

Neuroanatomy - Limbic System


Limbic System

Cortical parts: Cingulate gyrus, Parahippocampal gyrus.
Subcortical parts: Hippocampal formation (hippocampus, parahippocampal gyrus (subiculum), dentate gyrus), Septal nuclei, Amygdala


Papez circuit



Amygdala: in temporal lobe, deep to uncus on parahippocampal gyrus.
2 masses of nuclei: corticomedial-central, basolateral

afferents to amygdala: olfactory bulb, dorsomedial nucleus of thalamus, hypothalamus, septal nuclei, brainstem autonomic nuclei, prefrontal, temporal, occipital and insular cortices, olfactory cortex

The 2 amygdala communicate with each other via stria terminalis and anterior commissure

Bilateral destruction of amygdala = inability to recognise fear

Septal nuclei

Magnocellular system: Vasopressin and oxytocin
Parvocellular system: releasing or release-inhibiting hormone

Friday, 10 May 2013

Neuroanatomy - Cerebellum


Cerebellum

  • anterior lobe,
  • posterior lobe,
  • floccular-nodular lobe vermis,
  • superior,
  • middle,
  • and inferior cerebellar peduncle

  • Fastigial nucleus,
  • globose nucleus,
  • emboliform nucleus,
  • dentate nucleus

Cerebellar afferents:
  • mossy fibres (spinocerebellar, pontocerebellar, vestibulocerebellar),
  • climbing fibres (inferior olivary nucleus)
cerebral cortex via pontine nuclei (Ponto-cerebellar tracts) - middle cerebellar peduncle
from anterior spino-cerebellar tract - superior cerebellar peduncle
from posterior spino-cerebellar tract - inferior cerebellar peduncle
from vestibular nuclei - vestibulo-cerebellar tracts
from inferior olivary nucleus - olivo-cerebellar tracts

arbor vitae = white matter
layers: molecular layer, purkinje cell layer, internal granular layer

Purkinje cell receives synapses from 1000s of granule cells. Parallel fibre synapses on 400 purkinje cells. Purkinje cell receives 1000s of synapses from one climbing fibre. Purkinje cells project to deep cerebellar nuclei (inhibitory)

Cerebellar Efferents: all efferents from deep cerebellar nuclei
Fastigial nucleus à vestibular nuclei and reticular formation à spinal cord
Globose and emboliform nuclei à red nucleus à spinal cord
Dentate nucleus à (red nucleus) à ventrolateral nucleus of thalamus à motor cortex

^all leave in superior cerebellar peduncle except from fastigial

Neurons in the intermediate and lateral parts of the cerebellar hemisphere project to the contralateral red nucleus and motor cortex (influence ipsilateral muscles)
Neurons in the vermis and flocculonodular lobes project to the vestibular and reticular nuclei controlling proximal muscle and limb extensors

Cerebellar Damage:
to lateral hemisphere - ataxia (lack of voluntary coordination), intermittent jerky gait (reduced muscle tone, reflexes, intention tremor)
to vermis - lack of limb coordination, staggering ataxic gait, nystagmus
to floccular-nodular lobe - loss of balance

Thursday, 9 May 2013

Neuroanatomy - Motor pathways


Motor - primary motor cortex, cortico-spinal tract

Cortico-spinal tract = primary motor cortex (UMN) à Ventral horn of spinal cord (LMN) à skeletal muscle of body

precentral gyrus = primary motor cortex

rostral to precentral gyrus = secondary motor regions

upper motor neuron = corticospinal neuron

lower motor neuron cell body is located in anterior horn grey matter of spinal cord

one upper motor neurone can influence many lower motor neurons which can innervate less than 10 muscles or several hundred.

Motor unit = spinal cord lower motor neuron, its axon and the muscle fibre it innervates.

Somatotopic map is contralateral, inverted and disproportionate.

Motor - cranial nerve motor nuclei, cortico-nuclear tract

Cortico-nuclear tract = primary motor cortex (UMN) à Cranial nerve motor nuclei (LMN) à skeletal muscle of head

Trigeminal (V) motor nucleus - rostral pons - muscles of mastication

Facial (VII) nucleus - caudal pons - muscles of facial expression

Nucleus Ambiguus (IX, X) - rostral medulla oblongata - muscles of larynx, pharynx and oesophagus

Hypoglossal nucleus (XII) - antero-medial rostral medulla oblongata - intrinsic and some extrinsic tongue muscles

Accessory nucleus (XI) - caudal medulla - two muscles in the neck, sternocleidomastoid and trapezius

also: Oculomotor nucleus (III) - midbrain - inferior oblique, medial, superior and inferior recti eye muscles

Trochlear (IV) nucleus - midbrain - superior oblique eye muscle

Abducens (VI) nucleus - pons - lateral rectus eye muscle

Upper Motor Neuron Lesion:
  • stroke, cortical damage, multiple sclerosis, amyotrophic lateral sclerosis (ALS) –
  • weakness (paresis) / paralysis (plegia) of specific movements,
  • no muscle wasting,
  • spasticity (increased resistance to passive stretch),
  • hyper-reflexia (hyperactivity of deep tendon reflexes),
  • Babinski reflex (extensor plantar reflex),
  • Spastic paralysis

Lower motor neuron lesion:
  • poliomyelitis, ALS, slipped discs, toxins –
  • weakness, paralysis of individual muscles,
  • muscle wasting,
  • Fasciculation (visible spontaneous contraction of motor units),
  • hyporeflexia/ areflexia (decrease/ loss of deep tendon reflexes),
  • flaccid paralysis

Motor 3 extrapyramidal pathways and basal ganglia

Extrapyramidal pathways=
  • rubrospinal tract,
  • tectospinal tract,
  • reticulospinal tract,
  • vestibulospinal tract

Basal ganglia connections:
  • cortico-striatal (cortex to caudate nucleus + putamen),
  • striato-pallidal,
  • pallidal-pallidal,
  • pallidal-thalamo,
  • thalamo-cortical

The corpus striatum includes the caudate nucleus, putamen and globus pallidus. These structures are concerned with control of posture and movement.
The Lentiform nucleus = putamen + globus pallidus
Functionally the caudate nucleus and putamen form a single entity = striatum
The caudate nucleus lies in the wall of the lateral ventricle.
The most ventral part of the striatum is the nucleus accumbens

The striatum is the input region. It receives afferents from the cerebral cortex, intralaminar thalamic nuclei and the substantia nigra pars compacta.
Efferent fibres are directed at the globus pallidus and the substantia nigra pars reticulata