EXAM QUESTIONS Flashcards
(58 cards)
“Describe the hormones involved in regulating fluid intake. Discuss whether drinking is a homeostatic process”
what would be in your introduction
1-2 sentences outline what fluid intake is and how it is typically regulated eg osmotic and hypovolemic thirst - refer to Fitzsimmons 1998
1-2 sentences about how fluid intake is a complex process and how it is regulated by the endocrine system
1-2 sentences link back to the question and what you will be addressing
“Describe the hormones involved in regulating fluid intake. Discuss whether drinking is a homeostatic process”
what would be in your first main paragraph
antidiuretic hormone ADH
points to include:
- refer to Nelson 2022
- ADH is released from hypothalamus after detection from the osmoreceptors.
- ADH enters pituitary gland where it travels to the kidneys
- increase permeability of renal tubes and narrow blood vessels
- this is done when fluid levels are low and the body stimulates thirst to encourage drinking behaviour and greater fluid intake
- talk about when fluid levels are high
“Describe the hormones involved in regulating fluid intake. Discuss whether drinking is a homeostatic process”
what would be in your second main paragraph
aldosterone
points to include:
- refer to Nelson 2022
- released by the adrenal glands before it properly enters the kidneys
- release is stimulated by ADH
- this is when solute and fluid levels are low
- conserves sodium chloride so its not lost in urine
“Describe the hormones involved in regulating fluid intake. Discuss whether drinking is a homeostatic process”
what would be in your third main paragraph
drinking is homeostatic
Answer the next bit of the question:
- define homeostasis
- evidence to believe it is homeostatic
- ADH, aldosterone, and angiotensin II are all released when fluid levels are low - dehydration
- Verbalis 2007 ADH is released in coordination with the thirst mechanism as restricting BV and RT it enhances thirst - drinking
- Stricker 1986 aldosterone and angiotensin II drove thirst and fluid intake
“Describe the hormones involved in regulating fluid intake. Discuss whether drinking is a homeostatic process”
what would you put in your fourth main argument
drinking isn’t homeostatic
points to include:
- drinking isn’t also performed due to physiological needs and may be influenced by the environment
- Wilk 1984 availability of fluids eg party influenced how much people drank, regardless of thirst
- Booth 1968 drinking is a conditioned response in certain conditions such as warm weather or socialising at a party
“Describe the hormones involved in regulating fluid intake. Discuss whether drinking is a homeostatic process”
what would you put in your conclusion
1-2 sentences about how there’s evidence to believe both
“From receptor to cortical level, describe how we feel touch and pain and discuss how a central factor of your choice alleviates pain”
what would be in your introduction
1-2 sentences on why touch and pain are important for our survivals
1-2 sentences about how they differ
1-2 sentences about how you will answer the question
“From receptor to cortical level, describe how we feel touch and pain and discuss how a central factor of your choice alleviates pain”
what would be in your first main paragraph
touch and pain
points to include:
- pain is detected by dermatomes
- anterolateral pathway - primary afferent nerves to spinal cord top thalamus to somatosensory cortex
- pain contralateral
- touch is detected by mechanoreceptors
- touch is medial lemnisucs pathway - mechanoreceptor to spinal cord to dorsal column to medulla to dorsal column nuclei to medial lemniscus to thalamus to somatosensory cortex
H: however not all pain is transmitted eg descending pain pathway which acts a way of suppressing pain
“From receptor to cortical level, describe how we feel touch and pain and discuss how a central factor of your choice alleviates pain”
what would be in your second main paragraph
central modulation yes
points to include:
- define
- how does it alleviate pain
- Wellington 2011 a way of suppressing the aching pain (C fibres) is mental power
- Larbig 1991 trauma ptsd due to endorphins released during the stressful moment blocking the pain
“From receptor to cortical level, describe how we feel touch and pain and discuss how a central factor of your choice alleviates pain”
what would be in your third main paragraph
central modulation no
points to include:
- effective for temporary pain but not chronic pain
- Mckracken 2003 found people with chronic pain still feel pain despite using cognitive coping strategies
- Engell 1977 distracting yourself away from the pain only activates your attentional abilities, when distraction is reduced you still feel the pain
- central modulation is a temporary factor for alleviating pain but not successful long term
“From receptor to cortical level, describe how we feel touch and pain and discuss how a central factor of your choice alleviates pain”
what would be in your conclusion
1-2 sentences about the effectiveness of central modulation
1-2 sentences about how future work should consider greater coping mechanisms for chronic pain
“Describe the pathophysiology of Parkinson’s disease. Discuss the current treatment options and their effectiveness.”
what would you put in your introduction?
1-2 sentences outlining what Parkinsons disorder is and how prevalent it is
1-2 sentences about why it is important to learn more about parkinsons due to the limited treatment options
1-2 sentences outlining what you will be discussing in this essay
“Describe the pathophysiology of Parkinson’s disease. Discuss the current treatment options and their effectiveness.”
what would you put in your first main paragraph
Lewy bodies and dopamine loss
P: Parkinsons disease is mostly characterised by the loss or absence of dopamine in the substantia nigra
E: the substantia nigra is located in the basal ganglia and is important for its role in reward (Samii, 2004). Due it it being centred around reward, the substantia nigra is known for producing the reward hormone, dopamine. However, people with Parkinsons have a gradual deterioration in dopamine producing neurons in the substantia nigra (Bear, 2020).
E: this absence means that people with parkinsons have uncoordinated, rigidity movement with slight tremors which is also heightened due to the lack of signalling to the wider parts of the basal ganglia which is involved in initiating and being being motivated to complete movement and the formation of Lewy bodies which interferes with normal brain functioning and signalling.
A: this lack of signalling and normal brain functioning explains why people with parkinsons disorder have uncoordinated and disrupted movement because of the lack of normal signalling in the motor coordinated areas of the brain, such as the substantial nigra.
L: therefore, the loss of dopamine producing neurons in the substantia nigra of people with parkinsons showcases how they have their innacurate and uncoordinated movements.
“Describe the pathophysiology of Parkinson’s disease. Discuss the current treatment options and their effectiveness.”
what would you put in your second main paragraph
levodopa
P: the most common type of treatment for people with parkinsons is the administration of levodopa
E: with the primary pathological issue of Parkinsons being the loss of dopamine producing neurons in the substantia nigra, psychologists looked for ways of administering more dopamine into the brain. However, dopamine was too large to cross the blood brain barrier which led to the development of levodopa. Levodopa is an administered drug which patients with Parkinsons take as it is small enough to cross the blood brain barrier and enter the brain (Cotzias, 1967). Once in the brain, it can be converted into dopamine, therefore increasing dopamine in the substantia nigra.
E: However, when arriving at the blood brain barrier, levodopa is broken down the dopa decarboxylase enzyme which means that less levodopa enters the brain, therefore minimising its true potential. To prevent this, doctors administer levodopa alongside dopa decarboxylase inhibitors such as carbidopa which prevent the breakdown so that more levodopa can enter the brain.
L: With more entering the brain, levodopa stands as the most effective treatment for parkinsons with symptoms like bradykinesia snd tremors improving (Salat, 2013).
H: However, whilst some have found levodopa administration to be effective at reducing symptoms, its long term effectiveness has been compromised. Many patients taking this drug have been found to take levodopa holidays where they go a period of time without taking the drug when they have discovered no improvement in symptoms. After this holiday, some of the drugs effectiveness should return. therefore, whilst is may be effective for a temporary reduction in symptoms, levodopa may not be effective for long term administration.
“Describe the pathophysiology of Parkinson’s disease. Discuss the current treatment options and their effectiveness.”
what would you put in your third main paragraph
fetal tissue neurotransplantation
P: Implanting fetal tissue into the brains of those with parkinsons have been found to effectively reduce the symptoms
E: Sladek 1987 conducted a study with monkeys who had Parkinsons disease. They implanted fetal tissue into the brains of the monkeys and found that after a short period of time, the fetal tissue formed connections with neighbouring tissue within the brain. These new found connections enabled and stimulated the release of dopamine which therefore effectively reduced the symptoms that were originally associated with the low dopamine, such as the tremors.
E: with greater dopamine within the brain, there was b=greater signalling within the basal ganglia and substantia striatum which therefore led to greater initiation of movement, helping to explain why some of the motor related deficiencies were reduced.
L: Therefore, fetal tissue neurotransplantation helps to showcase how the encouragement of the formation of new connections with the brain of those with parkinsons, otherwise known as neuroplasticity, helps to encourage the reduction in symptoms.
H: However, the majority of studies like Sladek 1987 of fetal tissue neurotransplantation were conducted on animals, such as monkeys. this means that there is little evidence of this kind of treatment being effective in humans, limiting its effectiveness as a treatment
“Describe the pathophysiology of Parkinson’s disease. Discuss the current treatment options and their effectiveness.”
what would be your fourth main paragraph
dopamine agonists
P: Another current treatment option for those with Parkinsons is dopamine agonists.
E: Dopamine agonists are a form of oral medication that once entered the brain, mimic the function of dopamine.
E: this is effective as it helps to restore the loss of dopamine in the substantia nigra, therefore encouraging healthy and normal functioning
L: This helps to show how dopamine agonists effectively restore the loss of dopamine in the brain, helping to reduce the symptoms.
H: However, despite their effectiveness, dopamine agonists have been found to be associated with many side effects for the patient such as vomiting and sleep disturbance. this can be quite distressing for the patient which may cause them to stop taking the drug, therefore limiting its true success due to a short administration time.
“Describe the mechanisms of neural reorganisation following brain injury. Discuss the role of constraint-induced therapy in promoting functional recovery.”
what would be in your introduction
1-2 sentences on what neural reorganisation is, how it occurs, and how it is important
1-2 sentences on how it is a complex form of neuroplasticity
1-2 sentences on what you will discuss in the essay
“Describe the mechanisms of neural reorganisation following brain injury. Discuss the role of constraint-induced therapy in promoting functional recovery.”
what would be in your first paragraph
neural reorganisation
points to include:
- body remapping itself
- Sanes (1990) whereby cut the whiskers off cats and found that the somatosensory cortex, the part what was responsible for movement of the whiskers, repurposed itself so that it moved to controlling and helping the movement of other facial structures
- strengthening of existing connections synaptic bridging
- building new connecting eg synaptic pruning
- Elbart 1992 - blind people had an expansion of the auditory cortex due to the parts of the brain that was originally made for the visual cortex relocated.
“Describe the mechanisms of neural reorganisation following brain injury. Discuss the role of constraint-induced therapy in promoting functional recovery.”
what would be in your second main paragraph
define constraint induced therapy - form of neuroplastic recovery which involves applying movement on the damaged limb
points to include:
- acts as cortical remapping - form of neural reorganisation (kwakkel, 2015)
- most effective when applied straight after injury
“Describe the mechanisms of neural reorganisation following brain injury. Discuss the role of constraint-induced therapy in promoting functional recovery.”
what would you put in your third paragraph
constraint induced therapy isn’t good at promoting functional recovery
point to include:
- most tasks encouraged from the patient in CIT are repetitive meaning they get really good at performing that certain task but this may not be effective for everyday tasks - may struggle with basic movement still
- patient demanding - requires intensive rehabilitation of around 6h a day which can be exhausting and also painful which can cause attrition rates
- only really effective for minimal impairments, not severe impairments as putting pressure on a severe damage can potentially worsen the area as it hasn’t had chance to heal
- focuses on using just one limb (the damaged one) but a lot of everyday tasks require both - if done for a long time it could cause impairment in the healthy limb due to the loss of functioning promoting neuroplasticity
“Describe the neuropathological changes found in both Parkinson’s and Alzheimer’s disease.
Discuss how understanding these changes informs the development of pharmacological treatments.”
what would you put in your introduction
1-2 sentences describing what parkinsons and Alzheimers are - link to dementia
1-2 sentences discussing why it is important to research into these diseases to help with the initiation of intervention
1-2 sentences about what the essay will include
Describe the neuropathological changes found in both Parkinson’s and Alzheimer’s disease.
Discuss how understanding these changes informs the development of pharmacological treatments.
what would you put in your describe paragraph
Parkinsons and Alzheimers
Parkinsons:
- formation of Lewy bodies - signal
- Klein 2007 - dopamine loss
- substantia nigra shrinks
- dopamine loss due to shrinkage
- basal ganglia signalling interference
Alzheimers:
- neurofibrillary tangles - tau protein
- amyloid plaques
- APOE-4 gene - Evans 1995, Small 2002
- AB42 (beta amyloid variant)
- toxic pathway
- Amyloid cascade theory Allsop 1991
Describe the neuropathological changes found in both Parkinson’s and Alzheimer’s disease.
Discuss how understanding these changes informs the development of pharmacological treatments.
what would you put in your discuss paragraphs
dopamine agonists:
- mimic dopamine
- effective
- side effects - sick, tired
Levodopa:
- Cotzias 1967 - fit through BBB
- Levodopa -> dopamine
- administered alongside dopa decarboxylase inhibitors eg carbidopa
Neurotransplantation:
- Sladek 1987 fetal tissue transplant
- connections to neighbouring tissue
Anti-amyloid immunotherapy:
- early stages
- lab made antibodies that bind to beta-amyloid and help slow down the build up to eventually clear it
Describe the neuropathological changes found in both Parkinson’s and Alzheimer’s disease.
Discuss how understanding these changes informs the development of pharmacological treatments.
what people could you include in this essay
- Evans 1995 - APOE-4 plaques
- Small 2002 - reduced activity in hippocampus and prefrontal cortex
- Klein 2007 - parkinsons dopamine loss
- Samali 2013 - parkinsons
- Sladek 1987 - fetal tissue transplant
- Cotzias 1967 - levodopa fits BBB
- Allsop 1991 - amyloid cascade theory
