Case 7 - Parkinson's disease Flashcards
1
Q
Define:
- mortality rate
- Morbidity rate
- Incidence rate
- Prevalence rate
A
- Number of deaths in 1 year compared with previous or subsequent years
- The incidence rate or prevalence rate
- Measure of morbidity based on the number of new episodes of illness in a population over time. e.g. affected persons per 1000 individuals at risk
- Measure of morbidity based on current levels of disease in population either at a time (Point prevalence) or stated period (Period prevalence)
2
Q
- What are the 3 methods of assessing Quality of Life?
- What are unidimensional measures?
- What are multidimensional measures?
- What are individual QoL measures?
A
- Unidimensional measures, multidimensional measures, and individual QoL measures
- Focus on 1 particular aspect of health e.g. pain
- Assess health in the broadest sense
- Ask the individual to rate their own health
3
Q
Define:
- Quality Adjusted life years (QALY)
- Disability adjusted life years (DALY)
A
- How long a successfully treated patient can expect to live. Each expected year = 1 point, Each year with degree of illness or disability – <1. Death = 0
- Seeks to minimise the buren of the disease
4
Q
- What is emotion?
- What part of the brain is most important for fear?
- What happens when a person has a bilateral amygdala lesion?
A
- Mental state that arises spontaneously rather than through conscious effor and is accompanied by physiological changes
- Amygdala
- Fear conditioning is abolished, impaired ability to recognise emotion, and fear.
5
Q
Identify the following:
- Cerebral cortex
- Corpus callosum
- Hypothalamus
- Amygdala
- Pituitary gland
- Thalamus
- Hippocampus
A
6
Q
- What are the 2 components of long term memory?
- What are the 2 components of Declarative memory?
- What are the 3 components of Implicit memory?
- What are the 2 components of short term memory?
- What is retrograde amnesia?
- What is anterograde amnesia?
A
- Declarative (Explicit) & Implicit memory
- Episodic (Events) & Sematic (Facts)
- Procedural (skills) & Priming & Conditioning
- Sensory & Working memory
- Cannot remember events prior to the brain damage
- Cannot later remember events that occur after the brain damage
7
Q
- What is long term potentiation?
- What happens to the receptors?
- Where does it happen?
A
- How we learn/memorise - Strenghtening of the synapses and causing long term increase in signal transmission b/w neurons.
- There is an increase in the number of receptors
- Happens in the Hippocampus
8
Q
- What cells in the brain produce the metabolites for neurons?
- What does the brain use for energy? (2)
- What is the danger of anaerobic respiration?
- Why is energy important in the brain?
A
- Astrocytes
- Glucose to produce ATP
- Produces lactic acid which is damaging to neurons
- To maintan the ionic gradients
9
Q
- What other metabolite does the brain use during starvation?
- What do neurons use for metabolism?
- What is the short term energy reserve astrocytes have?
A
- Ketone bodies
- Lactate and Pyruvate
- Glycogen
10
Q
- What are the 3 major classes of NT?
- What is a NT?
- What is a neuron that releases more than 1 NT called?
A
- Amines, Amino acids, & Peptides
- Molecule produced and stored in presynaptic neuron, released on stimulation and produces response in postsynaptic cell
- Co-transmitter
11
Q
- What NT do cholinergic neurons release?
- What enzyme is required to synthesise acetylcholine?
- Where is ACh synthesised?
- Where does the Acetyl come from?
- How is choline transported into the cell?
- What is exchanged in order for the ACh to enter the vesicle?
A
- Acetylcholine (ACh)
- Choline Acetyltransferase
- Cytosol of the neuron
- From Acetyl CoA
- Via choline transporter which is transported along with Na+
- H+ ion
12
Q
- What 2 receptors does ACh act on? What types of receptors are they?
- What enzyme is used to degrade ACh?
- What does ACh get broken down into?
- What happens if you inhibit the enzyme AChE?
A
- Muscarinic (G protein) receptors & Nicotonic receptors (Ionotropic)
- Acetylcholinesterase (AChE)
- Choline + Acetic acid
- ACh is not broken down and there is constant stimulation of the receptors e.g. in skeletal muscle and cardiac muscle
13
Q
1. What are the 3 catecholaminergic NTs?
- What are they all originally derived from?
- Fill in the following order of production:
- Tyrosine – ______ – ______ – _______
4. Where is noradrenaline produced?
A
- Dopamine (DA) & Noradrenaline & Adrenaline
- Tyrosine
- Tyrosine – Dopamine – Noradrenaline – Adrenaline
- Locus Ceruleus
14
Q
- Which enzyme catalyses NE from DA?
- Which enzyme converts NE to E?
- What does E also act as in the body? Where is it released?
- Which enzyme is used to degrade NE & E?
- What are the 2 reuptake transporters for NE?
A
- DBH
- PNMT
- Hormone, Adrenal glands
- MAO
- NET & NAT
15
Q
- What is seratonin also called? Where is it made?
- Which amino acid is it derived from?
- What is its role?
- Complete this: Tryptophan – ____ – ____
- Where do we get tryptophan from?
- How is 5-HT removed from the synaptic cleft? (2)
- What is used to degrade it?
- What type are its receptors except for 1?
- What type of receptor is the 5-HT3 receptor?
A
- 5-HT, Raphe Nuclei
- Tryptophan
- Regulation of mood, emotional behaviour, apetite, and sleep
- Tryptophan – 5-HTP – 5-HT
- Diet
- by the Serotonin Reuptake receptor & 5HTT
- MAO
- G-protein coupled
- Ligand gated cation channel
16
Q
- Which serotonin receptors are positive coupling?
- Why type of receptors are they?
- What does NA do to 5HT neurons?
- What do the a2 receptors do?
A
- All except for 5HT1 and 5HT5
- G protein except for 5HT3
- Activates a1 receptor, Increases firing of the 5HT cell
- Decrease firing, so switches off 5-HT release
17
Q
- What are the 3 amino acids used as NT?
- What are glutamate and glycine synthesised from?
- What are the 3 types of glutatame receptors?
- What is GABA synthesised from?
- Which enzyme converts it?
A
- Glutamate & Glycine & GABA
- Glucose
- AMPA, NMDA, Kainate receptors
- Glutamate
- Glutamic acid decarboxylase (GAD)
18
Q
- What molecules which is used for cellular metabolism is also used as a NT?
- What are cannabinoids?
- What is their mechanism of action?
A
- ATP
- Lipid molecules
- Reduce the opening of presynaptic Ca+ channels so reduce the ability of presynaptic terminal to release its NT
19
Q
- What are AMPA cahnnels permeable to?
- What does the opening of these channels lead to?
- What do NMDA receptors do?
- What molecule blocks the channel ordinarily?
- What opens the channel?
- What do GABA receptors do?
- Which sub-unit binds the NT?
A
- Na+ and K+ ions
- excess of cations into the cell, so there is a rapid depolarisation – Excitatory
- Excitation of the cell, they allow Na+ into the cell
- Mg+
- Glutamate
- Allows Cl- ions into the cell, so hyperpolarises it
- A sub-unit
20
Q
- What are the 3 sub-units of G proteins?
- In the resting state what is the a subunit bound to?
- When a ligand binds to the receptor what happens?
- What does the activated GTP bound G protein split into? (2)
- What does the G a sub-unit act as?
- At rest what is the combination of the sub-units?
- What do Gs and Gi mean?
A
- a, b, and gamma
- GDP
- The G protein releases its GDP and exchanges it for GTP from cytosol
- alpha sub-unit + GTP & G beta/Gamma sub-unit complex
- An enzyme that can break down GTP – GDP
- They are all joined together
- G stimulatory protein, and G inhibitory protein
21
Q
- What are the 2 types of effectors for G proteins?
- What happens when a G protein receptor is activated?
- What does Adenylyl cyclase do?
- What downstream enzyme is subsequently activated?
- What happens when an inhibitory G protein is activated?
A
- G protein gated ion channels & G protein activated enzymes (2nd messengers)
- G protein is activated, and this stimulates Adenylyl cyclase (membrane bound enzyme)
- Converts ATP to cAMP (Increase)
- PKA (Protein Kinase A)
- Suppresses the activity of adenylyl cyclase