L14 Flashcards

1
Q

When rosenthal et al. initially studied SAD, they recruited ___ patients from a local community with a history of ___ and who had experienced for at least __ consecutive years, depression that developed during the ___ or ____ and remitted during the following spring or summer.

A

29, MDD, 2, fall, winter

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2
Q

Symptoms of SAD included sadness, ___, and irritability, decreased __ ____, changes in appetite and a craving for _____, increased total ____ time, and daytime ____.

A

anxiety, physical activity, carbohydrates, sleep, drowsiness

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3
Q

Rosenthal discovered that the percentage of subjects experiencing depression in ____ was 100%, when the daily ____ and _____ for the town was the lowest of all months.

A

january, photoperiod, temperature

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4
Q

Subjects in rosenthal’s experiment got 2 weeks of ____ ____ 3 hours before dawn or 3 hours after dusk. They either received a ____ light (daytime sunlight mimic) or a dim ____ light (mimics sunrise / ____ light). There was a decrease in symptoms with the light mimicking ______ light, but not the dim yellow light.

A

light therapy, blue, yellow, sunset, daytime

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5
Q

type of recurrent major depression, wherein depression begins and ends during a specific season each year

A

seasonal affective disorder

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6
Q

mild symptoms of SAD can be considered the ___ ___, or ____ ____. Severe symptoms of SAD are often debilitating symptoms seen in non-seasonal ____.

A

winter blues, subsyndromal SAD, MDD

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7
Q

Hypotheses on SAD pathophysiology include ____ ___, ____ function, and ____

A

circadian rhythms, neurotransmitter, genetics

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8
Q

Circadian rhythmicity is maintained by the central pacemaker in the ____, the ____, which entrains internal circadian rhythms to external time cues (____). Circadian ____ occurs when there is asynchrony between the SCN rhythm and ____.

A

hypothalamus, SCN, zeitgeber, misalignment, behaviour

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9
Q

______ displays robust circadian rhythm and plays a critical role in synchronizing the sleep-wake cycle with the ____ cycle. It peaks a little after ____, and ___ in the morning.

A

melatonin, light-dark, midnight, decreases

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10
Q

Circadian rhythm phase of melatonin can be described by the ___ ___ ______ _____, or the temporal onset of melatonin rise. Light exposure in the evening results in a ____ ____ of melatonin rhythm. If the wake-up time remains constant, but light exposure is still given in the evening, the phase-delayed melatonin rhythms results in a smaller __ ____ with the sleep wake cycle (has shorter rise and fall). Light exposure in the ___ can correct a phase-delayed rhythm by causing a ______

A

dim light melatonin onset, phase delay, phase angle, morning, phase-advance

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11
Q

melatonin is a small, _____, ______ ____ derived hormone that is primarily synthesized and secreted on demand by ____ in the pineal gland. It is metabolized quickly, with a half life of ___ minutes, and production is tightly regulated by ________ _____ release.

A

non polar, amino acid, pinealocytes, 30, sympathetic norepinephrine

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12
Q

when there is light, the light reaches the ___ ____ ____, then travels to the ___ which inhibits the ____.

A

retinal hypothalamic tract, SCN, PVN

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13
Q

In the darkness, the RHT has ___ ____, leading to no activation in the SCN, and ___ of the PVN. This PVN activity travels to the _____ ___ ____, which release ____ onto alpha-1 or ____ receptors on the ______. This then leads to the activation of ___ and subsequently ____, which activates ____ directly or indirectly by _____. ____ returned to the cell by monoamine transporters is converted to ______. This product is then converted to ___ by a protein ____ by PKA. Then melatonin diffuses into the bloodstream

A

no activation, disinhibition, sympathetic nervous system, NE, beta-1, pinealocyte, DAG/IP3, PKC, PKA, cAMP, serotonin, N-acetylserotonin, melatonin, phosphorylated

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14
Q

Exposure to a ____ light induces a reduction in melatonin release, while this is not seen in a ___ shifted light.

A

white/blue, green

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15
Q

a ____ light perception is not necessary for photoregulation of melatonin release. This is shown in patients with ___ ____, who have a damaged _____ ______. In these people, light does ___ affect melatonin release, and they lack a typical ___ hour circadian rhythm. However, patients with ___ ___ ____, where the retinal-hypothalamic tract is preserved, light induced a ___ of melatonin release, even though the patient had no ____ awareness of the light

A

conscious, congenital glaucoma, retinal-hypothalamic tract, not, 24, congenital retinal dystrophy, suppression, conscious

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16
Q

Photosensitivity ___ with age. Older people wake up ___ in the morning and have ___ during the day

A

decrease, earlier, naps

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17
Q

Rodent models of SAD like symptoms exist. Nile grass rats are ___ and exposure to a short photoperiod cycle of _____ light and ____ dark for ___ weeks induces depressive like behaviours on ___ ___ test (anhedonia) and the ____ ___ ___ (helplessness) relative to controls.

A

diurnal, 5 hr, 19 hr, 6, sucrose preference, forced swim test

18
Q

Wistar rats that are exposed to constant darkness or constant ____ (disrupts it more) for ___ weeks disrupts daily rhythmic activity. Exposure to constant light but not constant darkness induced ____ and ___ like responses on the sucrose preference test and ________ on an ____ ___ ___ compared to controls. It also abolished circadian fluctuations of ____ and _____. instead of high CORT / melatonin at night and low CORT / melatonin in the day, there was ___ CORT in both night and day, and ___ melatonin in both. This was likely driven by ___ of the SCN cells

A

light, 8, depressive, anxiety, grooming, open field test, cortisol, melatonin, high, low, hypoactivity

19
Q

The hypothesis that SAD is induced by a shorter winter photoperiod

A

photoperiod hypothesis

20
Q

Support for the photoperiod hypothesis includes that SAD tends to be more prevalent in regions ___ from the equator in the ___ ____, such as the ____ and ____. Additionally, SAD patients show ___ melatonin duration in the winter than in the summer, which is not seen in ____ controls. Moreover, ______ ____ via an artificial light is effective in treating SAD. When a ___ light is paired with an _____ such as citalopram or ____, this is more effective in treating SAD

A

farther, northern latitude, UK, Alaska, longer, healthy, photoperiod extension, bright, antidepressant, sertraline

21
Q

Problems with the photoperiod hypothesis include that it doesn’t explain the phenomenon of ___ ___ SAD, which involves poor ____, ___, weight loss, ____, agitation, restlessness, anxiety, and episodes of ____ behaviour. Moreover, if SAD is induced by a shorter winter photoperiod, then light therapy should be equally effective whether you add on daylight in the ___ or in the ____. However, giving light therapy in the ___ seems to be more effective than therapy in the night.

A

summer pattern, appetite, irritability, insomnia, violent, morning, night, morning

22
Q

hypothesis proposed by lewy et al., that says that SAD results from internal circadian rhythms that are phase delayed relative to the external clock or other rhythms such as the sleep-wake cycle

A

phase-shift hypothesis

23
Q

support for the phase shift hypothesis comes from the fact that light therapy exerts its effects by correcting the ___ phase delay, ie. by brining the light-sensitive circadian clock to match that of the ____ cycle.

A

abnormal, sleep-wake

24
Q

problems with the phase-shift hypothesis include that while it is a stronger hypothesis than the photoperiod hypothesis, there is ___ evidence of phase shift in ____ patients. Moreover, other circadian rhythms should show ____, but they do not. ____ ____ rhythms, ____ rhythms, and ____ ____ hormone rhythms do not change post treatment

A

minimal, SAD, misalignment, body temperature, cortisol, thyroid stimulating

25
Q

predicts that the underlying pathophysiological basis of depression is a depletion in levels of NE, DA and 5-HT

A

monoamine hypothesis of depression

26
Q

support for the monoamine hypothesis are that acute depletion of ___ or ____ can induce ___ of depressive symptoms in SAD patients following light therapy.

A

tryptophan, catecholamines, relapse

27
Q

acute tryptophan depletion includes the ingestion of a mixture of large ___ ___ lacking tryptophan. These compete for __ ___, reducing the ____ of tryptophan.

A

amino acids, active transport, bioavailability

28
Q

In another study, the meteorological data on daily global ____ from ____ days prior to a PET scan was calculated. The PET scan used a radio-labelled _____ receptor ligand to examine serotonin receptor binding potential. The study found a ___ correlation between 5-HT1A binding potential in the amygdala and _____ ____ and the global radial accumulated within the past five days. In other words, there was higher regional _____ 5-HT1AR binding potential in high global radiation group compared with the low global radiation group in areas such as the amygdala, hippocampus and ___ __ ____

A

radiation, 1-90, 5-HT1A, positive, parahippocampal cortex, postsynaptic, posterior cingulate cortex

29
Q

In catecholamine depletion studies, ______ is given, as it is a ___ ___ enzyme inhibitor that inhibits the ____ step in catecholamine biosynthesis. Since AMPT has ___ effects, _____ is administered as an active control. The measures are ___ and ___ which are the metabolites of catecholamines

A

alpha-methyl-para-tyrosine, tyrosine hydroxylase, rate-limiting, sedative, diphenhydramine, HVA, MPHG

30
Q

In the 1800s, physicians reported increased incidence of ___ __ in thyroid disorders, and in 1873, Sir William Withey Gull described the relationship between ______ (undiagnosed hypothyroidism) and ____.

A

nervous affections, myxoedema, psychosis

31
Q

Several thyroid abnormalities have been associated with affective disorders, in particular, ___ and ____. But the majority of patients with affective disorders don’t have ____ evidence of thyroid dysfunction. Rather than thyroid abnormalities being a product of affective disorders, it’s more likely that thyroid dysfunction _____ to the ___ of them.

A

depression, anxiety, biochemical, contributes, development

32
Q

when the thyroid overproduces T4 that turns off the hypothalamus

A

hyperthyroidism

33
Q

Failure of the thyroid gland to produce T4, most common type, 94%

A

primary hypothyroidism

34
Q

when a pituitary disease causes reduced TSH (rare)

A

secondary hypothyroidism

35
Q

when a hypothalamic disease causes reduced TSH (very rare)

A

tertiary hypothyroidism

36
Q

It is difficult to parcel out symptoms due to a ___ ___ vs the induction of certain moods due to ____ symptoms. Thyroid disorders may be accompanied by various ____ symptoms ranging from mild depression and anxiety to _____.

A

mood disorder, physical, neuropsychiatric, psychosis

37
Q

Neuropsychiatric symptoms typical of hyperthyroidism include ____ (generalized dissatisfaction with life), ____, ____, and emotional ____ (mood swings), as well as impaired ____

A

dysphoria, anxiety, irritability, lability, concentration

38
Q

neuropsychiatric symptoms typical of hypothyroidism include ___, ___ dysfunction, ___ and ____ slowing

A

depression, cognitive, apathy, psychomotor

39
Q

some studies report anxiety and depressive disorders occurring in over ____% of patients with hypo/hyper thyroidism

A

60

40
Q

depression has been linked to abnormal ____ rhythm. An absence of TSH _____ ____ is shown, as well as a ____ TSH response to exogenous ____. This is because in hypothyroidism, the hypothalamus doesn’t regulate ___ __ to suppress TRH release, resulted in chronically elevated levels and a ____ of TRH receptors. TRH not only stimulates TSH, but also stimulate central ____ activity. Chronically elevated TRH levels in depression might therefore serve to both increase ____ production snd rescue ____ 5-HT activity

A

TSH, nocturnal surge, blunted,TRH, negative feedback, downregulation, 5-HT, thyroid, low

41
Q

thyroid hormones have been used together with ____ therapy since the late _____s to accelerate clinical response to antidepressants. ___ is effective in accelerating clinical response to ___ ___ in patients with treatment resistant / ____ __ depression. Effects showed that ____ might benefit more from this treatment

A

antidepressant, 1960s, T3, tricyclic antidepressants, non refractory, women