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Year 2 > Christopher nolan- anxiety dementia > Flashcards

Christopher nolan- anxiety dementia Flashcards

1
Q

define Anxiety

A

Anxiety is an intense, excessive and persistent state of apprehension worry or fear about real or perceived threats or future uncertainties. It may be accompanied by physical symptoms such as restlessness, increased heart rate, muscle tension, sweating and difficulty in concentration.

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2
Q

Define pathological anxiety

A
  1. Fear is greatly out of proportion to risk/severity of the threat.
  2. The response continues even when the threat is gone or becomes generalized to other similar or dissimilar situations.
  3. Social or occupational functioning becomes impaired.
  4. The anxiety cannot be explained by an underlying medical condition e.g. metabolic, substance abuse, depression or psychosis.
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3
Q

Define generalized anxiety disorder

A

GAD is a persistent state of anxiety which is not specific to any particular circumstance with symptoms persisting for >6 months.

Atleast 3 of the following (“BE SKIMS”)

Blank mind/difficulty concentrating
Easily fatigued
Sleep disturbances (difficulty falling asleep or staying asleep)
Kept up or restless
Irritability
Muscle tension
Sympathetic overdrive

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4
Q

Describe the synthesis of serotonin

A

Tryptophan –> 5-hydroxytryptophan (tryptophan hydroxylase) –> 5-hydroxytryptamine (L-aromatic amino acid decarboxylase)

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5
Q

list 3 regions in the body where serotonin is found

List 4 functions of serotonin in the body

A

Found in:
(i) Chromaffin cells of GI tract
(ii) Platelets
(iii) CNS

Functions in
(i) Platelet aggregation
(ii) GI motility
(iii) Stimulation of peripheral nociceptors
(iv) Mood regulation

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6
Q

List 3 SSRIs

A

Sertraline
Fluoxetine
Citalopram
Paroxetine

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7
Q

list 2 SNRIs

A

Venlafaxine
Duloxetine

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8
Q

MOA of benzodiazepines in seizure control

A

Diazepam, Lorazepam, Midazolam

MOA
-Benzodiazepines enhance the activity of GABA to cause opening of neuronal chloride channels causing hyperpolarisation of the excitatory neuron—> reduces its excitability, preventing excessive depolarizations and seizure generation.
-It does so by binding to its site on the GABA-A receptor between the alpha-1 and gamma-2 subunit.
- Benzo’s only work in the presence of GABA

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9
Q

List 4 contraindications to benzos

A
  1. Hypersensitivity
  2. Closed angle glaucoma
  3. Respiratory depression
  4. Myasthenia gravis
  5. History of substance use disorder
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10
Q

Define tolerance and list 3 key underlying mechanisms for its development

A

Tolerance refers to a reduction in pharmacological/physiological effects of a drug after repeated use at a dose that was once sufficient to achieve the desired effect. It therefore means that the dose must be increased.

Mechanisms

  1. Receptor modulation: With chronic use of benzo’s, the GABA-A receptors can become down-regulated i.e. less receptors available for the drug to bind to or else they become less responsive to the drug. GABA-receptors with the alpha-2 subunit are especially effected in benzo use.
  2. Dose: The higher the dose, the more GABA receptors that benzos will be occupied which accelerates the development of tolerance.
  3. Duration of receptor occupancy
    Continuous use of benzos will likely cause greater receptor desensitization compared to intermittent or short term use (e.g. those using for sleeping aids will be less likely to develop tolerance than someone using long term at a much higher dose for seizure control)
  4. Metabolic tolerance: the liver produces extra enzymes resulting in increased metabolism and less drug in the blood.
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11
Q

Differentiate between tolerance and dependance

A

Tolerance occurs when a substance no longer produces the same physiological or pharmacological effect in the body at the same dose, following continued use. As a result, the person must take a higher dose to achieve the same effect. However, unlike in dependence, the body retains an intrinsic ability to maintain homeostasis without the substance.

Dependence occurs when, after prolonged use of a substance, the body adapts in such a way that it relies on the presence of the substance to maintain a degree of homeostasis. When the dose is reduced or the substance is stopped completely, the body experiences withdrawal symptoms due to dysregulation caused by the absence of the substance. For example, chronic alcohol use can lead to downregulation of GABA receptors and upregulation of NMDA receptors, as the body tries to counteract the inhibitory effects of alcohol on the central nervous system (CNS).

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12
Q

Describe the mechanism underlying dependance

A

Neuroplastic and neuroadaptive changes

Chronic exposure to benzodiazepines leads to neuroadaptive changes, including downregulation of GABA-A receptors and upregulation of NMDA receptors, as the brain attempts to compensate for the enhanced GABAergic inhibition caused by the drug. Upon withdrawal, there is continued underactivity of the GABAergic system due to reduced GABA-A receptor function, while the excitatory glutamatergic system remains hyperactive, primarily due to the upregulated NMDA receptors. This imbalance between inhibitory and excitatory transmission contributes to the withdrawal symptoms.

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13
Q

List 4 regions of the brain involved in language processing and describe the role of each region

A
  1. Angular gyrus
    -Located in the inferior parietal lobule
    -Receives information from the visual cortex
    -Helps in reading aloud by converting graphemes (written symbols) into phonemes (sounds) — a process known as phoneme retrieval.
    -Passes phoneme information to Wernicke’s area for comprehension and to Broca’s area for speech production.
    -Damage results in Alexia
  2. Wernicke’s area
    -Located in Superior temporal gyrus on dominant side (usually left)
    -Receives information relating to phenomes from bilateral primary auditory cortices and functions to comprehend the sounds heard, i.e. puts meaning to sounds.
    -Also receives information from the angular gyrus in relation to grapheme (understand written language).
    -Damage results in loss of comprehension of language/word salad
  3. Broca’s area
    -Located in inferior frontal gyrus
    -Allows for co-ordination and planning of speech output by communicating with the motor cortex to allow for appropriate muscle contraction to produce speech.
    -Also functions in the comprehension of syntax.
    -Damage results in telegraphic speech + Dysprosody (long gaps between words)
  4. Arcuate fasciculus
    - Channel of communication between wernickes and broca’s area.
    - Believed to function in comprehension of syntax
    - Damage results in loss of repetition of spoken words.
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14
Q

list 2 types of long term memory

A

(1) Explicit (declarative)
-> Episodic memory: Recall of personal experiences or events including geographic location, times, and other contextual info: Hippocampus, medial temporal lobe, pre-frontal cortex

-> Semantic memory: Recall of facts, general knowledge, concepts, familiar faces: Anterior temporal cortex, lateral prefrontal and neocortex.

Semantic memory would be remembering what a cat is, but episodic memory would be recalling a time when you were scratched by a particular cat.

(2) Implicit (non-declarative)
->Procedural memory: Does not require conscious recollection e.g. riding a bike, tying shoe laces: Basal ganglia, motor and associated cortex, cerebellum.

Key areas of brain for long term memory
Hippocampus: Encoding episodic and declarative memories.
Amygdala: Emotional modulation of memory.
Neocortex: Long-term storage of consolidated memories.
Lateral Prefrontal Cortex: Facilitates retrieval and organization of memories.

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15
Q

Outline the key areas of the brain involved in anterograde and retrograde amnesia

A

Anterograde
Inability to form new memories, old memories remain intact
(i) Hippocampus
(ii) Mamillary bodies
(iii) Fornix
(iv) Anterior thalamic nuclei
(v) Pre-frontal cortex

Retrograde
-Inability to remember old memories, new memories intact
(i) Medial temporal lobe (including the hippocampus)
(ii) Neocortex

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16
Q

list 4 acute effects of benzos

A

Acute

-Sedation due to GABAergic activity in limbic system, reticular activating system of brainstem and hypothalamus

-Anti-anxiety due to GABAergic activity mainly amygdala and
prefrontal cortex

-Anticonvulsant

-Muscle relaxant due to GABAergic activity in the spinal cord

-Anterograde amnesia due to GABAergic activity in hippocampus

17
Q

list 4 chronic effect of benzos

A

Chronic

(i) Emotional blunting
-chronic GABAergic activity in prefrontal cortex (involved in emotional processing)
-Reduced dopamine release in mesolimbic dopamine pathway also contributes to flattened affect

(ii) Rebound anxiety
- Cessation of benzo’s can lead to rebound anxiety, due to downregulated GABA receptors unable to counteract the now hyperactive excitatory neurons in areas like the amygdala

(iii) Depression
-Due to disruption of dopamine, noradrenalin and serotonin neurotransmission in the brain, particularly pre-frontal cortex

(iv) Cognitive deficits

(v) Loss of libido/sexual dysfunction
-Due to dampening of excitatory neuronal signals in areas like the hypothalamus and limbic system.

18
Q

Describe the key theories surrounding the aetiology of anxiety

A

(1) Reduced Functional Connectivity Between the Prefrontal Cortex and Limbic System:
-Prefrontal cortex is not sufficiently mediating emotional responses in the limbic system, particularly the amygdala –> leads to these regions becoming overactive/dysfunctional

(2) Single Nucleotide Polymorphism (SNP) Variations in the 5-HT Transporter
-Same as the monoamine hypothesis in depression –> reduces serotonin signaling in the brain leads to anxiety

(3) In anxiety disorders, the HPA axis can become dysregulated, often resulting in overactivation of the stress response. Chronic activation of the HPA axis and sustained elevated cortisol levels are thought to contribute to the development and maintenance of anxiety and related disorders.

19
Q

Differentiate between delirium and dementia

A

Delirium is a reversible, acute and transient state of confusion associated with altered and fluctuating levels of consciousness. It is often associated with organic causes such as polypharmacy, dehydration, infections. Its onset is rapid (hours to days) with symptoms including disorientation, hallucinations and altered levels of consciousness/attention. abnormal EEG

Dementia is an irreversible, chronic and progressive state of confusion associated with progressive decline in cognitive function independant of attention/level of consciousness. Its onset is slow and insidious (months to years) and is most commonly associated with neurodegeneration of the brain. normal EEG

20
Q

List 3 tests that may be done as a work up for delirium

A
  1. Bloods- FBC(anemia, infection, malignancy) U+Es, TFTs, LFTs (encephalopathy), Glucose, Cultures (sepsis), inflammatory markers (CRP, ESR), B12/folate
  2. Urine dipstick
  3. CT brain if concerns re intracranial hemorrhage
21
Q

what are the DSM-5 criteria to make a diagnosis of delirium

A
  1. Disturbance in attention and awareness
    –> Attention (focus, sustain, shift )
    –> Awareness (orientation to environment)
  2. Acute onset + fluctuating
  3. An additional disturbance in cognition
    –> memory, disorientation, language, perception, visuospatial
  4. Disturbances in cognition, attention and awareness are not explained by a pre-existing neurocognitive condition and don’t occur in the setting of coma/ reduced arousal.
  5. Direct physiological cause established through history, exam or labs
    –> intoxication, withdrawal, polypharmacy causing drug interaction
22
Q

DSM 5 criteria for dementia?

A
  1. Significant cognitive decline from baseline in one or more domains (memory, language, executive function, Complex attention, perceptual motor, social cognition)
  2. Interference with independence and daily functioning
  3. Progressive worsening
  4. Exclusion of delirium
  5. Exclusion of other medical conditions that could explain the symptoms.
23
Q

Describe the aetiology of early onset (familial) AD

A

Amyloid-beta protein

Early-onset Alzheimer’s disease (<60) is commonly associated with genetic mutations in the gene coding for amyloid precursor protein (APP) on chromosome 21, as well as mutations in PSEN1 and PSEN2, which regulate amyloid precursor protein cleavage. It is inherited in an autosomal dominant pattern.

Abnormal cleavage of APP by secretase results in accumulation of Beta-amyloid fibrillar peptides.

These peptides aggregate into beta-amyloid fibrils, contributing to the characteristic amyloid plaques seen in Alzheimer’s disease.

They can cause neuronal damage, impaired axonal transport, kinase activation (which can cause tau hyperphosphorylation) and eventually cell death.

Tau proteins

Hyperphosphorylation of Tau proteins, which normally stabilize microtubules, disrupts their ability to bind microtubules. This results in microtubule instability, impaired intracellular transport, and synaptic dysfunction, ultimately leading to the formation of neurofibrillary tangles (NFTs) and neuronal cell death.

End result

Neuritic plaques composed of a central amyloid core, and surrounded by microglia, reactive astrocytes and dystrophic neurites

Commonly seen in: Cerebral cortex, hippocampus, amygdala, neocortex

24
Q

Explain the aetiology of Late onset AD

A

o Late-onset Alzheimer’s disease (LOAD) is associated with genetic risk factors on chromosomes 12 and 19. Chromosome 12 encodes the protein alpha-2-macroglobulin (A2M), which is involved in the clearance of beta-amyloid. Certain genetic variants of A2M may impair this clearance, increasing the likelihood of beta-amyloid accumulation in the brain.

o On chromosome 19, the Apolipoprotein E (ApoE) gene encodes a cholesterol transporter that plays a critical role in lipid metabolism and beta-amyloid clearance. The ApoE4 allele is associated with an increased risk of Alzheimer’s disease because it is less effective in clearing beta-amyloid, leading to its accumulation as fibrillar plaques in the brain.

25
Q

define the following:

Aphasia

Alexia

Dysprosody

Dysarthria

Dysphonia

Agnosia

A

Aphasia: impaired production and/or comprehension of speech caused by loss of cerebral cortex +/- connecting white matter tracts between language centres. It can also affect reading and writing.

Dysprosody: Abnormal innotation, intensity or rhythm of word production e.g. long gaps between words

Dysarthria: Difficulty in execution of speech due to damage to motor component of speech production.

Dysphonia: Difficulty in production of speech sounds, commonly caused by inability to oscillate vocal cords

26
Q

Describe the synthesis and degradation of acetylcholine

A

**Synthesis*

-Choline is taken up into the pre-synaptic terminal via choline transporter
-In the cytosol, choline acetyltransferase combines choline with Acetyl CoA (from krebs) –> Acetylcholine + CoA
- Ach is then packaged into vesicles by vesicular acetylcholine transporter

Degradation
-Acetylcholinesterase or Butyrylcholinesterase (glial cells)–> choline and acetate

27
Q

Name the 3 acetylcholine breakdown inhibitors

A

(1) Donepezil –> Acetylcholinesterase inhibitor

(2) Rivastigmine –> Acetylcholinesterase + Butyrylcholinesterase

(3) Galantamine –> Acetylcholinesterase

28
Q

Why give Memantine

A

Amyloid plaques can cause excessive release of glutamate which leads to neuronal excitotoxicity through hyperexcitation of NMDA receptors –> calcium influx, toxic free radical production and cell death.

Memantine is a weak NMDA receptor antagonist that blocks the NMDA receptor’s ion channel during periods of excessive glutamate activation –> this prevents large amounts of calcium influx through the channel in response to excessive glutamate activation.

This prevents excitotoxicity.

Memantine’s voltage-dependent blockade allows it to selectively block calcium entry during periods of excessive or prolonged glutamate release, while its blockade can be reversed during phasic bursts of glutamate to allow for normal glutaminergic transmission

29
Q

List the domains assessed in the MMSE

A

ORAL-CR

Orientation - Time/Place

Registration - Immediate recall of 3 words

Attention + calculation - Count back from 100 in sevens or spell a word backwards

Language- name objects, repeat sentences, or follow verbal instructions.

Recall- Recall 3 words that were said earlier

30
Q

Interpret the MMSE scores

A

25-30: Normal

20-24: Mild

10-19: Moderate

<10: severe

31
Q

Differentiate between mild memory loss in normal ageing and dementia

A

Normal ageing

Unaffected: Procedural, immediate, semantic, speech and language.

Mildly affected: Memory retrieval, episodic, prospective and working memory, attention span, processing speed, learning speed.

None of these changes are severe enough to affect independance.

Dementia

In dementia, the earliest deficits typically involve immediate/short term memory

Episodic memory, particularly recent events may also be affected

As the condition progresses, it affects other types of memory, speech, and the ability to learn new information, ultimately disrupting daily functioning

32
Q

What are the two major pathological changes seen in alzheimer’s?

A
  1. Beta amyloid plaques
  2. Neurofibrillary tangles (tau)
  3. Narrow gyri
  4. Widened and deep sulci
33
Q

Give 4 causes of a low MMSE score other than dementia

A
  1. Metabolic abnormalities: Hypothyroidism, Hypoglycemia, Hypernatremia, hepatic encephalopathy
  2. Infection: UTIs causing delirium
  3. Drug use: Long term benzodiazepine or alcohol use disorder
  4. Previous traumatic brain injury
  5. Sleep disorders: Obstructive sleep apnoea
34
Q

Describe neurotransmission at the NMDA receptor

A
  1. Glutamate, released from presynaptic neurons
  2. NMDA activation requires 2 co-agonists to bind; glutamate and glycine.
  3. At resting membrane potential, the NMDA receptor channel is blocked by magnesium ions (Mg²⁺), preventing ion flow.
  4. Depolarization of the postsynaptic membrane, often mediated by AMPA receptor activation, expels Mg²⁺ from the NMDA receptor channel.
    Once Mg²⁺ is removed and glutamate and glycine are bound, the receptor channel opens, allowing ion flux.
  5. Calcium (Ca²⁺) and sodium (Na⁺) ions flow into the postsynaptic cell
  6. The calcium influx triggers signaling pathways involved in synaptic plasticity, such as long-term potentiation (LTP), which underlies learning and memory.

Overactivation of NMDA receptors can lead to excitotoxicity, while underactivation is implicated in disorders like schizophrenia.

35
Q

List 3 common bacteria causing UTIs

A
  1. E.coli
  2. Klebsiella pneumonia
  3. Enterococcus faecalis
36
Q

Nitrofurantoin and Co-trimoxazole can both be used to treat UTIs, describe the MOA of both

A

Nitrofurantoin
-This targets DNA integrity of the bacteria
-Within the cell it is reduced to a unstable metabolite by nitrofuran reductase which destroys the bacterial DNA.

Co-trimoxazole
-This is a combination of:
—>Sulfamethoxazole which inhibits dihydropteroate synthase
—> Trimethoprim which inhibits Inhibits dihydrofolate reductase.

This prevents the ability of bacteria to synthesise folate de novo thereby preventing the production of purines for incorporation into DNA.

37
Q

Name 4 differences between parkinsons disease + LBD

A

(1) Early symptoms
-LBD cognitive decline
-PD motor function decline

(2) Timing
-LBD cog + motor within 1 year
PD cog > 1 year of motor

(3) Visual hallucinations
- LBD common and frequent
- PD mostly in late stages

(4) Response to levo dopa
- LBD variable response, can worsen psychosis
- PD good response

Year 2 (19 decks)

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