Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Hailey - Neuro > Block 4 Shut the door > Flashcards

Block 4 Shut the door Flashcards

(105 cards)

Start Studying
1
Q

homeostasis example pathway

A

receptors: baroreceptors (peripheral) or temperature (central) > AFF > hypothalamus > EFF > hormones/ANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

homostasis fxn

A

integrates info for control of ENDOCRINE, ANS, and neural systems concerned with motivation (LIMBIC SYSTEM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

fornix

A

major projection from hypothalamus > mammillary bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pituitary structure

when head trauma…

A

lies at base of brain in sphenoid bone: sella turcica

infundibulum/stalk to pit can be severed = severs pit from thalamus&raquo_space;> increase in prolactin (because under inhibitory control)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

adenohypophysis

neurophypophysis

median eminence

A

anterior pituitary (more rostral)

posterior pituitary

infundibulum (intersection between hypothalamus and pit gland = impt relay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

posterior pituitary fxn

A

synthesis and secretion of VASOPRESSIN OR OXYTOCIN

synthesized in MAGNOCELLULUAR hypothalamic neurons in SUPRAOPTIC (SON) and PARAVENTRICULAR (PVN) nuclei (secrete directly into systemic circulation)
>
transported via axons to nerve terminals in posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Supraoptic nucleus (SON) and paraventricular nucleus (PVN) are where?

activated by

A

in medulla

limbic structures (motivation, emotions)
solitary nucleus (medulla) (requires AFF from baroreceptors and gi tract)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

nerve terminals in posterior pituitary >

A

vasopression and oxytocin axonal transported > terminal > vesicles > released by AP activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Vasopressin/ADH stimulus

A
  1. increased BLOOD OSMOLALITY: too much NaCl > hypothalamus > VP > kidney > INC WATER RESORPTION by kidney
  2. HYPOVOLEMIA: dec blood volume > receptors in heart > hypothalamus > VP > INC WATER RESORPTION
  3. HYPOTENSION: dec blood pressure > baroreceptor > hypothalamus > VP > VASOCONSTRICTION > inc BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Oxytocin stimulus

A

WOMEN

  1. SUCKLING/nursing > inc OT > “milk ejection reflex” via smooth muscle contraction in breast
  2. UTERINE SITMULATION > inc OT > uterine contraction > delivery of newborn
    * bonding idea, delivered intranasally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

anterior pituitary fxn

families

A

secretions of “families” of hormones into system circulation
1. somatomammotropins
GH
PROLACTIN

  1. glycoproteins
    TSH
    FSH
    LH
  2. opiomelanocortin peptides
    ACTH
    B-EP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

somatomammotropins

stimulus and effects

A

GH growth hormone

stimulus: EXERCISE, STRESS, SLEEP
effect: tissue growth, metabolism of fat, carbs, etc.

PROLACTIN

stimulus: SUCKING, STRESS
effect: development of mammary tissue, LACTATION (to be ejected by oxytocin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

glycoprotein

stimulus and effects

A

TSH thyroid-stimulating hormone

stimulus: COLD TEMPS
effects: increase TH > inc cell metabolism, inc metabolic rate, inc heat production *negative feedback

FSH follicle-stimulating hormone
gonadotropin regulated by hypothalamic peptide
effects: 
MEN inc SPERMATOGENESIS
WOMEN development of ovarian FOLLICLE

LH luteinizing hormone
gonadotropin regulated by hypothalamic peptide
effects:
MEN *required for SPERATOGENESIS (with FSH), stimulates TESTOSTERONE
WOMEN initiates OVULATION “trigger,” stimulates PROGESTERONE from spent follicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

opiomelanocortin peptides

stimulus and effects

A

opiate receptor binding, pigment action, adrenal cortex
common precursor: pro-imc: POMC

ACTH adrenocorticotropic hormone

stimulus: STRESS
effects: secretes CORTISOL/glucocorticoid from adrenal cortex

B-EP beta-endorphin

stimulus: STRESS (fight or flight)
effects: opiate-like ANALGESIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

POMC special because

A

when cleaved makes two biologically active peptides: ACTH and B-EP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

test used clinically to asses anterior pituitary function?

A

stress common stimulus, so induce insulin-induced hypoglycemia
inject small insulin: decrease blood glucose&raquo_space;> increase in ACTH, cortisol, prolactin, b-EP, GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hypothalamus controls anterior pituitary by _______ neurons,

which secrete _______ to median eminence

A

parvocellular neurons

hypothalamic releasing hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hypothalamic releasing hormone

function/pathway

A

synthesized in parvocellular neurons > transported via axons to median eminence > released from nerve terminals into hypophyseal portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

hypothalamic releasing hormones
excitatory
inhibitory

A

4 excitatory:
TRH thryotropin-releasing hormone = INC TSH
GnRH gonadotropin-releasing hormone = INC FSH and LH
CRH corticotropin-releasing hormone = INC ACTH and B-EP
GHRH growth hormone-releasing hormone = INC GH

2 inhibitory:
SOMATOSTATIN decrease GH secretion
DOPAMINE decrease PROLACTIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

only pituitary hormone controlled by excitatory and inhibitor HRHs

A

GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

diabetes insipidus

A

bitter urine
LOSS OF VASOPRESSIN SECRETION
etiology: head trauma (sever pit stalk), autoimm, idiopathic

POLYURIA excess urine
POLYDYPSIA excess drinking

Tx: desaminovasopression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

galactorrhea-amenorrhea

A

inappropriate lactation
cessation of menstruation
HYPERPROLACTINEMIA increased blood prolactin

etiology: tumor in pituitary = MICROADENOMA that release prolactin > dec LH and FSH > cessation of menstruatio > INFERTILITY

Tx: surgically remove microadenoma, block prolactin with DOPAMINE REC AGONIST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

signals from periphery that cause us to stop eating

A
  1. hormone CCK from gi tract thru vagus to brainstem
    (SHORT-TERM SIGNAL)
  2. LEPTIN from intestines from high fat content to hypothalamus
    (LONG-TERM SIGNAL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

short term signals of satiety (decreased food intake)

A

a. oropharyngeal: TASTE
b. GASTRIC DISTENSION/STRETCH and INTENSTINAL NUTRIENT
c. POST-ABSROPTIVE SATIETY: gi > liver through portal vein; SENSORS FOR GLUCOSE AND FREE FAs in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
satiety factors in CNS a. gastric distention b. CCK c. ghrelin
a. gastric distenion: MECHANORECEPTORS on VAGAL AFFERENTS > solitary nucleus (NTS) * add leptin, increased response to gastric stretch b. cholecystokinin CCK: hormone released from duodenum in response to meals -inc gallbladder contraction > inc bile release > inc fat digestion -inc pyloric constriction -inc gastric contractions CCK Rec > inc VAGAL AFF response > NTS c. ghrelin hormone: from stomach increased by fasting OREXIGENIC: INC APPETITE
26
Prader-Willi syndrome | Sx
``` fetal hypotonia mental retardation hypogonadotropic hypogonadism DEC FSH and LH ghrelin secretion HYPERGHRELINEMIA obesity hyperphagia EXCESSIVE EATING ```
27
long-term CNS signals of satiety
``` LEPTIN: adipocytes release leptin *morbid obesity: higher > normal amounts leptin site of action: 1. solitary nucleus in brainstem 2. hypothalamus ``` MULTIPLE HYPOTHALAMIC NUCLIE implicated in control of food intake: LHA, PVN, ARC
28
CNS nuclei of satiety: LHA lateral hypothalamic area PVN paraventricular nucleus ARC arcuate nucleus
activation of LHA > release of "anabolic" NT = OREXIN > increase in eating activation of PVN > release of "catabolic" NT = CRH (corticotropin releasing hormone) > decrease in eating ARC: integrates all this info two populations of neurons: i. NPY (neuropeptide Y) neurons project both to PVN and LHA to INC EATING ii. MELANOCORTIN neurons project both to PVN and LHA to DEC EATING
29
LHA lesion
APHAGIA cessation of eating 1. aphagia due to damage to MEDIAL FOREBRAIN BUNDLE = MESOLIMBIC SYSTEM dopeminergic system reduced MOTIVATION to eat reduced MOTOR FUNCTION to eat 2. aphagia due to loss of neurons that synthesis "orexigenic" peptide = OREXIN
30
actions of leptin on ARC
i. leptin acts in ARC to inhibit NPY: DEC FOOD INTAKE | ii. leptin acts in ARC to activate melanocortin neurons: DEC FOOD INTAKE
31
actions of ghelin on ARC
ghrelin acts in ARC to activate NPY neurons: INC FOOD INTAKE
32
what type of drug could be promising candidates for treating hyperphagia-induced obesity?
activate melanocrtin receptors
33
___% treated for mood disorders
over 50%
34
limbic system related structures
``` amygdala hippocampus septal nuclei nucleus accumbens medial prefrontal cortex and anterior cingulate cortex ventral segmental area anterior and dorsomedial nuclei of thalamus mamillary nuclei ```
35
limbic system pathways:
FORNIX: hippocampus > mammillary body and septal nuclei MAMMILLO-THALAMIC TRACT: mammillary body > anterior n of thalamus anterior n of thalamus > cingulate gyrus and prefrontal cortex STRIA TERMINAULIS: amygdala > septal nucleus MEDIAL FOREBRAIN BUNDLE: midbrain via hypothalamus > forebrain
36
all limbic areas receive rich innervation by _____ and _____ axons
monoaminergic and cholinergic axons a. NE from locus ceruleus (LC) in pons b. 5HT from raphe nuclei (Ra) midbrain, pons c. DA from mesolimbic system*** d. ACh from nucleus baseless and septal nucleus = general arousal, sleep wake cycles
37
ventral segmental area (VTA) projects to: | DA neurons
nucleus accumbens medial prefrontal cortex amygdala septal nuclei
38
mesolimbic system (DA)
i. self-stimulation studies: VTA > REWARDING ii. drug addiction COCAINE block DA repute: inc DA in synapse
39
lesion VTA, NAcc
decreased drug seeking behavior DA receptors permanently blocked ***has effects on our natural reward system (endorphins, natural opioids, nicotine, opioids)
40
natural rewards
SEX | FOOD
41
ACh neurons lost in AD in
nucleus basalis** | spetal nucleus
42
limbic system functions | AMYGDALA and lesion
amygdala fxns a. role in fear conditioning/type of learning Pavlovian classical conditioning lesions to amygdala: prevent fear conditioning
43
limbic system functions | PREFRONTAL CORTEX and syndrome
prefrontal cortex "The Case of Phineas Gage" rod through prefrontal while RR working Prefrontal Lobe Syndrome: GAAII a. impaired GOAL directed behavior, no job b. lack of emotion in decision-making APATHY c. poor social judgment ANTISOCIAL behavior d. poor emotional control INCREASED IMPULSIVITY etiology: dorsolateral PFC: working memory and executive function orbital frontal cortex: projections to amygdala
44
limbic system functions | HIPPOCAMPUS and injury
patient H.M. fell off bike > seizures *bilateral medial temporal lobectomy = removed hippocampus bilaterally >>> a. anterograde amnesia (no new memories) b. temporally graded retrograde amnesia (lost old memories, post surgery, can remember prior to surgery) c. explicity or declarative memory lost (semantic/facts and episodic/experiences) d. IMPLICIT MEMORY MOTOR SKILLS NOT LOST
45
limbic system dysfunction | Urbach-Wiethe disease
AMYGDALA dysfunction a. impaired recognition of emotion in facial expressions, INABILITY TO JUDGE "LIKE" EMOTIONS (fear vs anger, surprise vs. joy) b. MEMORY LOSS especially w/ EMOTIONAL CONTENT
46
limbic system dysfunction | PTSD
AMYGDALA dysfunction triad of symptoms: 1. re-experiencing phenomena/flashbacks 2. avoidance of situations that parallel initial trauma 3. hyperarousal: hypervigilance and increased anxiety etiology: increased amygdala activity in fMRI increased medial prefrontal cortex activity which usually inhbitis amygdala
47
Korsakoff's syndrome triad
1. DISORDER of immediate memory > no new memories 2. DISORIENTATION > to space and time 3. CONFABULATION > fabrication etiology: chronic alcoholism and thiamine B1 deficiency MAMMILLARY BODY DEGENERATION
48
Kluver-Bucy Syndrome
1. oral tendencies: all objects in mouth (Gary Busey has a big mouth) 2. changes in emotions ("k" is the most apathetic response) 3. hypersexuality ("luver") 4. visual agnosia: physchic blindness (Gary Busey has asymmetric eyes)
49
Alzheimer's Dementia AD
etiology: - loss of CHOLINERGIC input (in nucleus basalis) to HIPPOCAMPUS - presence of NFTs (intracellular, phosphorylated tau proteins) and beta-amyloid plaques (extracellular) Sx: 1. loss of memory 2. mood disorders: anx and dep 3. loss of motor fxn: slow 4. complete loss of cognitive fxn
50
___% over 85yo have AD
over 50% over 85yo have AD
51
according to engeland, treat AD with
donepezil (Aricept) | AChE
52
Schizophrenia | Sx and incidence
fragmentation of mood, thought, and movement Sx: positive: delusions and hallucinations negative: social withdrawal 1% US population diagnosed
53
Schizophrenia | neurochemical basis hypotheses
``` 1. "dopamine hypothesis" increase in DA rec activity > amphetamine psychosis Tx: antipsychotic: HALOPERIDOL block DA receptors (SE: parkinsonian) atypical anti-psychotic: CLOZAPINE block DA receptors block 5HT receptors block glutamate repute: increase glutamate in synapse ``` ``` 2. "glutamate hypothesis" PHENCYCLIDINE (PCP) "angel dust" blocks NMDA glutamate receptor Tx: increase glutamate receptor activity ```
54
Depression | Sx and incidence
Sx: lethargy, anhedonia, loss of sleep 15% US population 20% F, 13% M treated
55
Depression | neurochemical basis hypothesis
"monoamine hypothesis" decreased NE and/or decreased 5HT receptor activity Tx: increase NE and DA 1. MAOIs 2. TCAs: block repute of NE and/or 5HT 3. SSRIs: block repute of 5HT
56
Chronic Traumatic Encephalopathy (CTE)
progressive neurodegenerative disease cause by repeated head trauma TRIAD Sx: 1. cognition: ANTEROGRADE AMNESIA and LOSS EXECUTIVE FXN (prefrontal cortex and hippocampus) 2. mood: DEP and APATHY 3. behavior: DEC IMPULSE CONTROL and INC AGRESSIVENESS ~age 30-50 yo risk factors: HEAD TRAUMA etiology: generalized BRAIN ATROPHY including prefrontal cortex, temporal lobes (amygdala, hippocampus), and parietal lobes NFTs PRESENT
57
MCA stroke
weakness and snsory deficits to CONTRLATERAL side lateral side frontal, parental and temporal FACE and ARMS HOMONYMOUS HEMIANOPSIA "looking at their lesion" dominant hem: aphasia > problems speaking nondom hem: contralateral hemineglect
58
ACA stroke
weakness and sensory contralat SAME anterior and medial frontal and parietal and temporal LEGS PERSONALITY CHANGES
59
Lenticulostriate stroke
branch of MCA to DEEP STRUX OF BRAIN hallmark: LACK CORTICAL SIGNS pure motor: POSTERIOR LIMB OF IC (hemiparesis of legs, arms, face) pure sensory: LATERAL THALAMUS (numbness of legs, arms, face CONTRALAT)
60
Vertebral Artery stroke
supplies inferior cerebellum and lateral medulla VERTIGO, BLURRED VISION, VOMITING, NYSTAGMUS, ATAXIA WALLENBERG syndrome: numbness on one side of face and opposite side of body*****
61
Basilar artery stroke
supplies rostral brainstem and occipital lboes CN PALSIES, GAZE ISSUES, HEMIANOPSIA, MIOSIS may cause LOSS OF CONSCIOUSNESS
62
Posterior cerebral artery stroke (PICA)
supplies occipital lobes HOMONYMOUS HEMIANOPSIA (of contralateral) MACULAR SPARING ACROMATOPSIA difficulty naming colors nondom hem: neglect of affected vision field
63
intracerebral hemorrhage
HTN | decreased vascular elasticity
64
subarachnoid hemorrhage
rupture of intracranial aneurysms or trauma thunderclap sudden HA, "worst headache ever" N/V, nuchal rigidity, photophobia, change in consciousness
65
ischemia stroke
atherosclerosis via thrombosis of cerebral vessels OR embolism > inadequate oxygen delivery to brain > neuronal death as soon as 4 min sudden onset focal neurologic deficits, no HA
66
stroke imaging
non-contrast CT for intracranial bleeding, including SAH, intracerebral bleeding or hematoma MRI: ischemic stroke and focal cerebral ischemia
67
when is cerebral angiography indicated?
to evaluate patients with ischemic strokes in vertebrobasilar distribution and subarachnoid/intraparencymal hemorrhage
68
modifiable risk factors for stroke
``` HTN DM lipids sympathomimetic abuse smoking EtOH obesity Afib ```
69
non modifiable risk factors for stroke
age***most imp race ethnicity heredity Hispanic Americans, American Indians, Alaska Natives > white Americans African Americans 2X than white Americans**
70
tPA for stroke | MOA
enchances conversion of plasminogen to plamin by binding to fibrin > INITIATES FIBRINOLYSIS *helps restore potency to thromboses vessels considered for patients with ISCHEMIC stroke who can be treated WITHIN 3-4.5 HOURS OF SX ONSET
71
tPA contraindecations
``` HBP INTRACRANIAL HEMORRHAGE SAH rapidly resolving symptoms MI, stroke, head injury in past 3 mo GIB past 3 weeks active bleeding anticoagulation therapy ```
72
hypothermia is resisted by
heat conservation: VASOCONSTRICTION | heat production: SHIVERING
73
hypothalamus received input from ____ and ____ temperature receptors
skin (local) and spinal cord (central) | ***2 sensory receptors
74
local skin sensors cause release of ______ core SC temperature sensory send signals to CNS to activate _____
NO = VASODILATOR SYMPATHETIC NERVE OUTFLOW (adrengergic and cholinergic)
75
cold skin sensors release _____
NE = VASOCONSTRICTOR
76
fever involves a pyrogen which stimulates the hypothalamus to produce _____
PGE2 = causes shivering
77
hypothalamic temperature is special because
does not change in temperature (receives sensors from elsewhere)
78
sympathetic receptors related to blood pressure regulation
NE interacts with: Beta-1: stimulate HR, increase stroke volume Alpha-1: increase total peripheral resistance =increase BP
79
blood pressure regulation pathway
stretch receptors on carotid arteries and aortic arch > sense stretch/BP > as BP increases, firing rate incrases > glossopharyngeal IX and vagus X nere to medulla > solitary nucleus > rostral ventrolateral medulla suppressed baroreceptors inhibit: sympathetic PREganglionic neurons which usually increase BP
80
baroreceptors
attenuate (decrease) high BP
81
if blood pressure drops >
less activation of IX and X > less stimulation of NTs > LESS INHIBITION of rostral ventrolateral medulla > GREATER STIMULATION of PREganglionic sympathetics in thoracic cord > INC HR, SV, RESISTANCE using a1 and b1 receptors
82
orthostatic hypotension
LBP when stand up from sitting or laying down | young people, most common cause: dehydration, not enough fluids
83
inspiration requires
``` a PUMP (diaphragm and external intercostals) a PACEMAKER to initiate breathing (Pre-Boetzinger area of ventrolateral medulla) ```
84
stimulate _____ to innervate diaphragm
``` phrenic nerve (C3-5) ACh and nicotinic receptor ```
85
inputs to Pre-Boetzinger area
parafacial respiratory center SENSES CO2 (ACTUALLY H+) and DIRECTLY EXCITES ABDOMINALS
86
BTW, how do you get H+ from CO2?
CA carbonic anhydrase
87
Ondyne's curse
lack of CO2 sensors >>> HYPOVENTILATION | FATAL
88
sympathetics control _______ of _______ | parasympathetics affect ______ of _______
rate of breathing | dilation of bronchioles
89
urination is controlled by both
voluntary and involuntary mechanisms 1. external sphincter VOLUNTARY ACh and NICOTINIC 2. internal sphincter INVOLUNTARY ACh and MUSCARINIC PARAsympathetic
90
bladder full > sends AFF signals to
medial prefrontal cortex (usually suppresses voiding) | detected by STRETCH MECHANORECEPTORS
91
Pontine micturition center activates
the sacral cord to stimulate PREganglionic PARAsympathetic nerves > relaxation of external voluntary sphincter contraction of urinary bladder
92
urination involves dis-inhibitor of the micturition center when bladder is full, controlled by activation of which nerve
pudendal nerve > relax external sphincter
93
incontinence Tx
ANTIMUSCARINICS | M3 antagonists
94
HYPOkinetic disorders
DIRECT pathway INHIBITED INDIRECT pathway ACTIVE = decreased motor activity PARKINSON DISEASE = LOSS OF DOPAMINERGIC NEURONS
95
HYPERkineteic disorders
DIRECT pathway ACTIVE INDIRECT pathway INHIBITED = incrased motor activity HUNTINGTON DISEASE = expanded CAG repeats
96
parkinson disease Tx
RESTORE dopaminergic activity (not slow progression of disease) LEVODOPA (prodrug) plus CARBIDOPA (inh AAAD) = sinemet
97
adverse effects of L-DOPA
"peak dose" dyskinesia high plasma level, activating DIRECT too much diphasic sykinesia at onset and offset of loop effect "off" period dystonia when levels all off: no relief think morning/eve when dose is off "wearing off" phenomenon driven by progressive loss of DA neurons PRIMARY SIDE EFFECTS BECAUSE DA RECEPTORS IN ALL OF BODY
98
L-DOPA primary adverse effects
- confusion, anxiety, agitation, insomnia, nightmares, depression - psychotic reactions: schizophrenia-like delusions and hallucinations (because increased DA in limbic system) REVERSIBLE - orthostatic hypotension - nausea, vomiting, anorexia
99
COMT inhibitors
ENTACAPONE decrease peripheral metabolism of L-DOPA (like AAAD, but not into DA, will be excreted instead) smoother response longer on time
100
MAOI
SELEGINE MAO-a: metabolizes NE and 5HT MAO-b: priary metabolism of dopamine: USEFUL PD TX can be mono therapy in early stages smoothes out dosing
101
Dopaine receptor agonists
PRAMIPEXOLE D3 agonist ROPINIROLE D2 agonist direct action on D2 receptors in stiatum becoming more first line less SE
102
muscarinic antagonists
Ach is NT for a small amount of striatal interneurons TRIHEXYPHENIDYL
103
Amantadine
antiviral
104
PD Tx tissue transplantation?
human fetal adrenal medullary tissue into caudate nucleus
105
PD surgery
pallidotomy: allieviates akinesia

Hailey - Neuro (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions