P harmacology Stu dy Gu ide
Not es Summ ary Table
Mus l c e Relaxants Mus l c e Relaxant - Summary Table
Op o i id Drugs i id Drugs - Summary Table
Op o
a ea/ Vomiting
N us a ea/ Vomiting - Summary Table
N us
ANS Control O f Eye ANS Control O f Eye - Summary Table
a kinsonʼs Disease
P r a kinsonʼs Disease - Summary Table
P r
Alz heimer ʼs Disease Alzheimer ʼs Disease - Summary Table
Psy chiatric Medication Ant idepressants - Summary Table
Moo d Stabilisers Moo d Stabilisers - Summary Table
Dru gs/ Stimulants Dru gs/ Stimulants - Summary Table
How do drugs perform their action?
Action On Transmitter Synthesis
e
N urop harmacological agents can:
In rc ease transmitter synthesis
Decrease transmitter synthesis
a e synthesis of different transmitter that is more effective than the natural chemical
C us
Action On Storage And Release
Stor age: drugs can interfere with storage
e a i e
L ss tr nsm tt r stor ed →e
l eleased
ss r
Tar nsm tti er release: drugs can
Promot e release
In hibit release
Action On Receptor Binding
Dru gs can:
i d directly to receptors and activate them
Bn → g i
A on sts
i d to same site as agonist, prevent activation
Bn → e i i e antagonists
Comp t t v
i d to different site, cause conformational change preventing activation
Bn → c e i i e antagonists
Non- omp t t v
Action On Termination Of Transmitter
Blo ck reuptake → R upte ake inhibitors (e.g. SSRIs)
Inhibit enzymatic degradation
Bot h result in increased neurotransmitter action
Ext ernal Ampl ification v/s Int ernal Co chlear Impl ants
Ext ernal Amplification (Hearing Aids):
U ed f
s or m l i d to moderate hearing loss, conductive hearing loss
Ampl ifies sound to improve hearing, non-invasive and easily adjustable.
Int ernal Cochlear Implants:
U ed f
s or severe to profound sensorineural hearing loss, when hearing aids are ineffective
a e damaged parts of the ear and directly stim auditory nerve, requires surgical implantation
Byp ss s
,Chemical injected into ventricles/ subarachnoid space reachs nerve cells
a e
Intr v ntr icular injection (via an Ommaya reservoir) allows drugs to enter CSF in ventricles.
a hecal injection (into subarachnoid space, in lumbar region) allows direct CSF entry
Intr t
1. CSF C r i culation Pathway
: h
Flow C oro id plexus → Ve
ntr icles → barachnoid space
Su → SC & brain → Arachnoid granulations (reabsorption).
2. M echanisms of Drug Distribution
D iffusion into Brain Tissue
The e e d
p n ymal layer lining ventricles is more permeable than BBB, allowing drug diffusion.
:
Ex Intr t a hecal chemotherapy (methotrexate, cytarabine) for brain tumors.
CSF Flow Ass st- i ed Distribution
Dru gs injected into the lumbar subarachnoid space spread via bulk flow.
: i a anesthesia (bupivacaine, lidocaine).
Ex Sp n l
Entry v ia CSF-Brain Barriers: choroid plexus and pia mater regulate drug exchange with the brain parenchyma.
→ eh
M t otr x t e a e (a chemotherapy drug) is injected intrathecally to treat brain cancers and prev CNS leukemia.
Cl ni ical Applications of CSF Drug Administration
Intr athecal Drug Delivery – Direct injection into CSF (spinal canal or ventricles)
U ed f che
s or mot herapy, pain management (opioids), or antibiotics (meningitis treatment).
Ep idural vs. Intrathecal Injection
Ep idural: Drug stays outside the dura mater, slow diffusion (e.g., labor analgesia).
Intr athecal: Drug enters directly into CSF, acting faster (e.g., spinal anesthesia).
, Alz heimerʼs isease D
Therapies used:
1. M edications:
a. h i e e a e inhibitors
C ol n st r s
b. - e h - -aspartate (NMDA) antagonists
N m t yl D
c. Lecanemab and donanemab
2. St m e cell therapy
3. Ant i-Amyloid Therapies
4. Ant i-Tau Therapies
5. Ant i-Inflammatory Therapies
6. e
N uroprot ective Strategies
7. G n e e therapy
1a) Cholinesterase inhibitors:
a ients with AD have red cerebral content of choline acetyl transferase, which leads to a decrease in acetylcholine synthesis and impaired
P t
cortical cholinergic function. Cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) increase cholinergic transmission by
inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia.
1b) N-methyl-D-aspartate (NMDA) antagonists
Memantine is a NMDA receptor antagonist, the mechanism of action of which is distinct from those of the cholinergic agents; it is proposed to
be neuroprotective. Glutamate is the principal excitatory amino acid neurotransmitter in cortical and hippocampal neurons. One of the
receptors activated by glutamate is the NMDA receptor, which is involved in learning and memory. Excessive NMDA stimulation can be induced
by ischemia and lead to excitotoxicity, suggesting that agents that block pathologic stimulation of NMDA receptors may protect against further
damage in patients with vascular dementia. In addition, the physiologic function of the remaining neurons could be restored, resulting in
symptomatic improvement. Memantine appears to have modest benefits in patients with moderate to severe AD. There is little, if any, evidence
that pts with milder AD benefit from memantine.
1c) Lecanemab and Donanemab
1. L ecanemab and donanemab are FDA-approved immunotherapy drugs for the treatment of early Alzheimer ʼs. These drugs target the protein
beta-amyloid to help reduce amyloid plaques, one of the hallmark brain changes in Alzheimer ʼs. Clinical studies to determine the effectiveness
of lecanemab and donanemab were conducted in people with early-stage Alzheimer ʼs or mild cognitive impairment due to the disease. These
studies showed that the drugs slowed the rate of cognitive decline among some study participants over the course of 18 months and red the
levels of amyloid in the brain.
2) Stem cell therapy
SC t herapy is being explored as a potential treatment due to its regenerative and neuroprotective properties.
T e
yp s o f Stem Cells Used in AD Therapy
1. M s ne e chymal Stem Cells (MSCs)
D rve i ed from bone marrow, adipose tissue, or umbilical cord.
H v a e immunomodulatory and neuroprotective effects.
Red neuroinflammation by secreting anti-inflammatory cytokines.
Promot e neuronal survival and synaptic plasticity.
2. e a e
N ur l St m C lls e (NSCs)
D rve i ed from fetal brain tissue or induced pluripotent stem cells (iPSCs).
C n a differentiate into neurons and glial cells.
Improv e cognitive function in animal models by replacing lost neurons.
3. In duced Pluripotent Stem Cells (iPSCs)
e e a ed by reprogramming adult somatic cells.
G n r t
O ffer a patient-specific treatment approach, reducing the risk of immune rejection.
C n a be differentiated into neurons or glial cells to replace damaged brain cells.
4. e a
H m topo ietic Stem Cells (HSCs)
Foun d in bone marrow and blood.
Not es Summ ary Table
Mus l c e Relaxants Mus l c e Relaxant - Summary Table
Op o i id Drugs i id Drugs - Summary Table
Op o
a ea/ Vomiting
N us a ea/ Vomiting - Summary Table
N us
ANS Control O f Eye ANS Control O f Eye - Summary Table
a kinsonʼs Disease
P r a kinsonʼs Disease - Summary Table
P r
Alz heimer ʼs Disease Alzheimer ʼs Disease - Summary Table
Psy chiatric Medication Ant idepressants - Summary Table
Moo d Stabilisers Moo d Stabilisers - Summary Table
Dru gs/ Stimulants Dru gs/ Stimulants - Summary Table
How do drugs perform their action?
Action On Transmitter Synthesis
e
N urop harmacological agents can:
In rc ease transmitter synthesis
Decrease transmitter synthesis
a e synthesis of different transmitter that is more effective than the natural chemical
C us
Action On Storage And Release
Stor age: drugs can interfere with storage
e a i e
L ss tr nsm tt r stor ed →e
l eleased
ss r
Tar nsm tti er release: drugs can
Promot e release
In hibit release
Action On Receptor Binding
Dru gs can:
i d directly to receptors and activate them
Bn → g i
A on sts
i d to same site as agonist, prevent activation
Bn → e i i e antagonists
Comp t t v
i d to different site, cause conformational change preventing activation
Bn → c e i i e antagonists
Non- omp t t v
Action On Termination Of Transmitter
Blo ck reuptake → R upte ake inhibitors (e.g. SSRIs)
Inhibit enzymatic degradation
Bot h result in increased neurotransmitter action
Ext ernal Ampl ification v/s Int ernal Co chlear Impl ants
Ext ernal Amplification (Hearing Aids):
U ed f
s or m l i d to moderate hearing loss, conductive hearing loss
Ampl ifies sound to improve hearing, non-invasive and easily adjustable.
Int ernal Cochlear Implants:
U ed f
s or severe to profound sensorineural hearing loss, when hearing aids are ineffective
a e damaged parts of the ear and directly stim auditory nerve, requires surgical implantation
Byp ss s
,Chemical injected into ventricles/ subarachnoid space reachs nerve cells
a e
Intr v ntr icular injection (via an Ommaya reservoir) allows drugs to enter CSF in ventricles.
a hecal injection (into subarachnoid space, in lumbar region) allows direct CSF entry
Intr t
1. CSF C r i culation Pathway
: h
Flow C oro id plexus → Ve
ntr icles → barachnoid space
Su → SC & brain → Arachnoid granulations (reabsorption).
2. M echanisms of Drug Distribution
D iffusion into Brain Tissue
The e e d
p n ymal layer lining ventricles is more permeable than BBB, allowing drug diffusion.
:
Ex Intr t a hecal chemotherapy (methotrexate, cytarabine) for brain tumors.
CSF Flow Ass st- i ed Distribution
Dru gs injected into the lumbar subarachnoid space spread via bulk flow.
: i a anesthesia (bupivacaine, lidocaine).
Ex Sp n l
Entry v ia CSF-Brain Barriers: choroid plexus and pia mater regulate drug exchange with the brain parenchyma.
→ eh
M t otr x t e a e (a chemotherapy drug) is injected intrathecally to treat brain cancers and prev CNS leukemia.
Cl ni ical Applications of CSF Drug Administration
Intr athecal Drug Delivery – Direct injection into CSF (spinal canal or ventricles)
U ed f che
s or mot herapy, pain management (opioids), or antibiotics (meningitis treatment).
Ep idural vs. Intrathecal Injection
Ep idural: Drug stays outside the dura mater, slow diffusion (e.g., labor analgesia).
Intr athecal: Drug enters directly into CSF, acting faster (e.g., spinal anesthesia).
, Alz heimerʼs isease D
Therapies used:
1. M edications:
a. h i e e a e inhibitors
C ol n st r s
b. - e h - -aspartate (NMDA) antagonists
N m t yl D
c. Lecanemab and donanemab
2. St m e cell therapy
3. Ant i-Amyloid Therapies
4. Ant i-Tau Therapies
5. Ant i-Inflammatory Therapies
6. e
N uroprot ective Strategies
7. G n e e therapy
1a) Cholinesterase inhibitors:
a ients with AD have red cerebral content of choline acetyl transferase, which leads to a decrease in acetylcholine synthesis and impaired
P t
cortical cholinergic function. Cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) increase cholinergic transmission by
inhibiting cholinesterase at the synaptic cleft and provide modest symptomatic benefit in some patients with dementia.
1b) N-methyl-D-aspartate (NMDA) antagonists
Memantine is a NMDA receptor antagonist, the mechanism of action of which is distinct from those of the cholinergic agents; it is proposed to
be neuroprotective. Glutamate is the principal excitatory amino acid neurotransmitter in cortical and hippocampal neurons. One of the
receptors activated by glutamate is the NMDA receptor, which is involved in learning and memory. Excessive NMDA stimulation can be induced
by ischemia and lead to excitotoxicity, suggesting that agents that block pathologic stimulation of NMDA receptors may protect against further
damage in patients with vascular dementia. In addition, the physiologic function of the remaining neurons could be restored, resulting in
symptomatic improvement. Memantine appears to have modest benefits in patients with moderate to severe AD. There is little, if any, evidence
that pts with milder AD benefit from memantine.
1c) Lecanemab and Donanemab
1. L ecanemab and donanemab are FDA-approved immunotherapy drugs for the treatment of early Alzheimer ʼs. These drugs target the protein
beta-amyloid to help reduce amyloid plaques, one of the hallmark brain changes in Alzheimer ʼs. Clinical studies to determine the effectiveness
of lecanemab and donanemab were conducted in people with early-stage Alzheimer ʼs or mild cognitive impairment due to the disease. These
studies showed that the drugs slowed the rate of cognitive decline among some study participants over the course of 18 months and red the
levels of amyloid in the brain.
2) Stem cell therapy
SC t herapy is being explored as a potential treatment due to its regenerative and neuroprotective properties.
T e
yp s o f Stem Cells Used in AD Therapy
1. M s ne e chymal Stem Cells (MSCs)
D rve i ed from bone marrow, adipose tissue, or umbilical cord.
H v a e immunomodulatory and neuroprotective effects.
Red neuroinflammation by secreting anti-inflammatory cytokines.
Promot e neuronal survival and synaptic plasticity.
2. e a e
N ur l St m C lls e (NSCs)
D rve i ed from fetal brain tissue or induced pluripotent stem cells (iPSCs).
C n a differentiate into neurons and glial cells.
Improv e cognitive function in animal models by replacing lost neurons.
3. In duced Pluripotent Stem Cells (iPSCs)
e e a ed by reprogramming adult somatic cells.
G n r t
O ffer a patient-specific treatment approach, reducing the risk of immune rejection.
C n a be differentiated into neurons or glial cells to replace damaged brain cells.
4. e a
H m topo ietic Stem Cells (HSCs)
Foun d in bone marrow and blood.
