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HR Block 6 > HR block 6 part 2 > Flashcards

HR block 6 part 2 Flashcards

1
Q

Lesion to Right PPRF–L/R gaze effect?

A

Left gaze is normalNeither eye can move to the right

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2
Q

Lesion to Left MLF–L/R gaze effect?

A

Left Gaze normalRight Gaze: Left eye unable to move medially; Right eye nystagmus

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3
Q

Left Abducens Lesion and Left MLF–gaze?

A

Left Gaze : Neither eye can moveRight Gaze: Left eye unable to move medially; Right eye nystagmus

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4
Q

Horizontal Gaze Zone

A

4th Ventricle–PPRF

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5
Q

Vertical Gaze Zone

A

Rostral Midbrain Reticular Formation

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6
Q

Horizontal and Vertical Gaze Control Zones connected by?

A

MLF

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7
Q

Ventral Part of Rostral Midbrain Reticular Formation is associated with _____ gaze

A

downward

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8
Q

Dorsal Part of Rostral Midbrain Reticular Formation is associated with _____ gaze

A

upward

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9
Q

Each Superior Colliculus receives input from _____ half of visual field

A

contralateral

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10
Q

______ divides superior colliculus into superficial and deep layers

A

stratum opticum ( retinal axons white matter )

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11
Q

Retinal axons terminate on neurons of _____ layer of superior colliculus

A

superficial

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12
Q

How is cell activity of superior colliculus affected when receiving multiple senses (touch, vision, auditory)? Which layer of S. Colliculus receives this information?

A

Cell activity increases due to additive effectDeep Layer

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13
Q

Which layer of superior colliculus contains premotor nuerons that compute saccades?

A

Deep

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14
Q

Which layer of superior colliculus contain cells that excite motor neurons?

A

Superficial

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15
Q

Relationship of tectospinal tract with MLF

A

tectospinal is ventral to MLF (and dorsal to Medial Lemniscus)

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16
Q

Lesion to superior colliculus will cause _________?

A

Loss (for the most part) of ability to make saccades in contralateral visual fieldSome saccades still form due to presence of fibers from frontal eye field bypassing superior colliculus

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17
Q

Tectospinal Tract Function?

A

Direct head movements to match eye movements

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18
Q

Why does S. Colliculus Lesion not eliminate all saccades

A

Frontal Eye Fieldhas some tracts run through S. Colliculus while others bypass S. Colliculus to serve as compensatory mechanism to produce saccades

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19
Q

______ and _______ arteries if stretched can compress Cranial Nerve 3

A

Posterior Cerebral ArterySuperior Cerebellar Artery

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20
Q

Anterior Cerebral Arteries supply _____ surface of cortex

A

median

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21
Q

Middle Cerebral Arteries supply _____ surface of cerebral cortex

A

Lateral

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22
Q

Posterior Cerebral Arteries supply ______ surface of cerebral hemisphere

A

caudoventral

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23
Q

Attractive cues stimulate G-actin to be incorporated into ______

A

F-actin

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24
Q

Repulsive Cues support G-actin towards _______

A

lamellipodium

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25
Q

actin and tubulin regulate assembly and disassembly of subunits; however changes in _____ also influence this process

A

intracellular Calcium

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26
Q

_____ are involved with axon growth and serve as both the ligand and receptor on growing axons

A

CAM

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27
Q

Function of Netrins? What molecule works in opposition?

A

Present at midline to facilitate axons that are crossing over to opposite hemisphereSlit- stops growth across midline to counteract Netrin

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28
Q

Purpose of Semaphorins

A

Stop Axonal Growth

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29
Q

Where are Ephrins mostly located? Function?

A

Hippocampus to aid in development related to plasticity

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30
Q

Name some Chemorepellant molecules. Function?

A

Slit; SemaphorinChange trajectory or avoid inappropriate target

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31
Q

Neurons depend on a minimum amount of ______ for survival and growth

A

trophic factor (NGF)

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32
Q

T/F NTFs (specific neurotrophic factor) has the same effect on all neuronal populations

A

False– NTFs have a range of effect determined by type of neuron

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33
Q

GDNF (glial derived growth factor) promotes _____ types of cells

A

Dopamine

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35
Q

Alterations in NTFs have been associated with which diseases? How does this occur?

A

Parkinson’s ; Alzheimer’s ; ALSIncrease in p75 receptors which promote cell death and a decrease in Trk receptors which promote cell survival. NTFs bind to both of these types of receptors; in old age there is an increase in p75 receptors

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36
Q

How is Baby talk is important for language development?

A

Axonal guidance to language centers during critical time frame

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37
Q

How is the effect different for a cat whose eye was sutured shut from two months to month 36 compared to one that was sutured shut from 12 months to 36 months and then re-opened?

A

First case will not have vision in that eye due to lack of light exposure during critical time periodSecond case will have some vision in the previously sutured eye; however, it will be diminished.This indicating that deprivations at later stages in life are not as detrimental as deprivation during childhood or critical time for development.

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38
Q

Hebb’s Postulate

A

Synapses in one (L) eye will increase if synapses are removed from opposite (R) eye

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39
Q

Sprouting with respect to Parkinson’s

A

cells that remain producing Dopamine will grow in an attempt to provide enough Dopamine to the system

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40
Q

Activity Dependent Plasticity

A

Ca Influx into cell induces transcription and translation of things such as growth factor to promote neuronal development and axonal development

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41
Q

Types of Repair in PNS

A

Regrowth of axons - recreation of myelin and regrowth via growth coneRestoration of damaged nerve cells - (glial scarring)Wholesale Genesis of new neurons to replace lost neurons

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42
Q

Types of peripheral nerve regeneration

A
  1. severed axon- axon segment distal to site of cut degenerates2. crush axon- damaged distal segments provide a guide for regenerating proximal axons3. completely severed axons- Schwann cells in distal stump of nerve stimulate and guide axon growth via NTFs
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43
Q

Describe pathway of apoptosis in CNS

A

Excses glutamate disregulates Bcl-2 (anti-apoptotic) ; therefore apoptosis is activated via caspase 3

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44
Q

Where in CNS can neurogenesis take place?

A

Olfactory ReceptorsTaste ReceptorsHippocampus

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45
Q

Describe neurogenesis process.

A
  1. Subventricular Zone generates new neurons (PROLIFERATION)2. Translocation to desired area3. Differentiation for desired axonal development
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46
Q

Future of Parkinson’s Treatment?

A

Fetal Tissue transferred to PD patient and does not reject fetal dopamine cells

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47
Q

Explain cytokine function in axonal regeneration

A

glial cells capable of releasing pro and anti inflammatory cytokines. If pro inflammatory are released this will lead to further damage and cell death.

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48
Q

Where is the hypothalmus located?

A

Floor of the 3rd ventricle ; most ventral diencephalon

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49
Q

Boundaries surrounding Hypothalmus

A

Laterally - optic nervesVentral - tuber cinerum(midline of tuber cinerum is median eminence)Posteriorly- coronal plane between mammilary body and posterior commissure

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50
Q

Location and function of median eminence?

A

midline of tuber cinerumneuroendocrine control of pituitary

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51
Q

Nuclei of anterior Hypothalmus

A

Preoptic Supraoptic Suprachiasmatic

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52
Q

Nuclei of posterior Hypothalmus

A

posterior, mammillary, tuberomammillary, dorsal

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53
Q

Nuclei of middle Hypothalmus

A

paraventriculardorsomediallateralperiventricularventromedialarcuate

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54
Q

Name functions of hypothalmus (8) and nuclei that contribute

A
  1. water/ electrolyte balance - supraoptic (ADH) and paraventricular (oxytocin)2. synthesis and secretion of hypothalmic releasing/inhibiting factors that control anterior pituitary3. temperature regulation - anterior and posterior hypothalmic nuclei4. activate sympathetic and adrenal medulla - ant/post hypothalmic areas5. thirst/regulation of drinking - lateral hypothalmus 6. hunger/satiety - lateral / ventromedial hypothalmus 7. regulation of gonadal / sexual fxn - anterior/ preoptic area and arcuate8. regulation of circadian rhythm - suprachiasmatic
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55
Q

What is anterior and posterior pituitary made from?

A

anterior - ectodermal tissueposterior- neural tissue

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56
Q

Pituitary gland lies in _______

A

sella turcica

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57
Q

Vascular supply of pituitary (ant/post)

A

anterior pituitary - no significant direct arterial blood supply – supplied by hypophyseal portal systemposterior pituitary- long/short portal vessels - superior and inferior hypophyseal A.

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58
Q

______ forms anastomoses between Superior and Inferior hypophyseal A.

A

trabecular A.

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59
Q

5 cell types of anterior pituitary and product

A
  1. somatotrophs - growth hormone2. mammotrophs/lactotrophs - prolactin3. thyrotrophs - TSH 4. corticotrophs - ACTH (and other products of POMC)5. gonadotrophs- LH / FSH
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60
Q

7 neurohormones from hypothalmus and target pituitary hormones

A
  1. thyrotropin RH - Thyrotropin / Prolactin2. GnRH - LH / FSH3. CRH - ACTH (B-LPH / B-endorphins)4. GH RH - growth hormones5. Somatostain [GH inhibiting hormone] - Inhibit release of GH / thyrotropin6. Dopamine [Prolactin inhibiting factor] - Inhibit prolactin release7. Prolactin releasing factor - Prolactin
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61
Q

Long loop vs short loop feedback in hypothalmus

A

long loop - from target gland hormone [more important]short loop - pituitary topic hormones inhibit secretion of hypothalmus

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62
Q

Precursor for ACTH? By products when producing ACTH?

A

POMC ;by products: B-LPH (equimolar to ACTH) ; N-terminal fragmentACTH can be broken down to form Melanocyte Stimulating hormone

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63
Q

Function of MSH?

A

increase skin darkness (pigmentation)

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64
Q

Receptor for ACTH in adrenal cortex

A

MC2R

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65
Q

Major regulator of ACTH / POMC

A

CRH (corticotropin releasing hormone)

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66
Q

Describe ACTH secretion pattern

A

released in response to stressreleased mostly in early AM hours

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67
Q

Structural similarities and differences between TSH, LH, FSH

A

all have same alpha subunit but beta chain is different for each

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68
Q

T3

A

triiodothyronine

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69
Q

T4

A

thyroxine

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70
Q

Growth Hormone function

A

post natal growth – bones and musclesalso functions in carbohydrate metabolism

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71
Q

______ , secreted by _____ and _____ , binds to _____ to provide (predominant) tonic inhibition of prolactin

A

dopamine, TIDA neurons, tuberohypophyseal dopaminergic neurons, D2 receptor

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72
Q

Prolactinoma can cause what?

A

galactorrhea gonadal dysfunction impotence in men

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73
Q

Hypothalmic tumors in kids can cause?

A

advanced pubertyaltered growth rate

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74
Q

Loss of all hormones of anterior pituitary is known as? can be treated by?

A

panhypopituitarismreplacement therapy

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75
Q

Aldosterone produced in?

A

Zona glomerulosa

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76
Q

Primary glucocorticoid

A

cortisol

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77
Q

Precursors for aldosterone are?

A

Doc ; corticosterone

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78
Q

sex steroid production occurs in?

A

zona reticularis

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79
Q

How is cholesterol taken into cell?

A

(Primary) via LDL receptors and endocytosisMay also be made de novo via acetyl CoA

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80
Q

Enzyme which converts cortisone (inactive) to cortisol

A

11-hydroxysteroid dehydrogenase I (HSD-1)

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81
Q

_____ is the inactive form of cortisol (examples include cortisone and prednisone)

A

11-keto

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82
Q

Major control of cortisol biosynthesis

A

ACTH

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83
Q

Process of how ACTH increases cortisol

A

ACTH binds MC2RStimulates LDL uptakecholesterol transferred by StAr (StAr synthesis is also promoted by ACTH)conversion of cholesterol to pregnenolone via desmolasecortisol synthesis

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84
Q

Atrophy of ______ and _____ can occur in the absence of ACTH

A

zona fasicularis and reticularis because ACTH promotes protein synthesis and growth of each

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85
Q

Cortisol is bound to ____ which is made in the _____

A

CBGLiver

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86
Q

DHEA is bound to

A

albumin

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87
Q

This controls the amount of steroids gaininga ccess to MR receptor

A

11B-HSD

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88
Q

Function of NF-kB

A

migrates to nucleus to upregulate cytokine genes

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89
Q

How does cortisol reduce inflammation

A

Cortisol binds to GR and is then able to interfere with NF-kB access to the gene to prevent cytokine productionGlucocorticoids also surpress phospholipase A2 and Cox-2

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90
Q

Cortisol effect on metabolism of carbohydrates

A

increase GluconeogensisHyperglycemiaIncrease Glucose 6 phosphatase

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91
Q

Cortisol effect on metabolism of protein

A

inhibit protein synthesisincrease blood urea nitrogenincrease nitrogen excretionpromotes muscle degradation in muscle to mobilize amino acids

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92
Q

Cortisol effect on metabolism of lipids

A

enhance lipolysisfree fatty acids typically migrate to trunk

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93
Q

Cortisol deficiency - effect on cardiovascular system

A

responsivenessto vasoconstricters is diminished thus producing hypotensive state

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94
Q

Cortisol effect on lymph response

A

decrease antibody productionlimite immune reactions so as to not damage the organism

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95
Q

cortisol effect on CNS

A

can pass blood brain barrierchanges in mood and behavior

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96
Q

Excess androgen production can lead to

A

appreciable masculinizaiton

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97
Q

fetal zone of adrenal cortex produces

A

DHEA and sulfated form

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98
Q

Hypofunction of adrenal cortex

A

loss of appetitefatigue; muscle weaknesshypoglycemia

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99
Q

Addisson’s Disease

A

adrenal gland is destroyedlack of negative feedback from cortisol ; therefore, ACTH and POMC are overproducedLeads to hyperpigmentation due to MSH

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100
Q

Cushing’s Disease

A

Hyperfunction of adrenal– excess cortisolbilateral adrenal hyperplasia (due to excess ACTH)HyperglycemiaMuscle WeaknessThin extremitiesFat redistribution to face and trunk

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101
Q

Congenital Adrenal Hyperplasia. Most commonly caused by?

A

cortisol not produced in adequate amounts to activate negative feedback loop; therefore, ACTH hypersecretion results causing adrenals to enlargeSalt wasting due to no aldosteroneMost commonly caused by deficiency in 21 hydroxylase

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102
Q

Congenital Adrenal Hyperplasia effect on males and females

A

Females: masculanizaiton of external genetaliaMales: precocious puberty

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103
Q

Goiter

A

Enlarged thyroid

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104
Q

Follicle of cells that secrete thyroid hormone contain ______

A

colloid

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105
Q

This gland is well vascularized and has one of the highest rates of blood flow per gram of tissue

A

thyroid gland

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106
Q

Colloid is surrounded by ____ type of epithelium

A

cuboidal

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107
Q

______ essential for synthesis of thyroid hormones

A

dietary iodine

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108
Q

Recommended iodine intake per day. If this is below the normal value what happens?

A

150 micrograms/day; if below 100 the gland will be unable to secrete normal levels of thyroid hormone leading to hypothyroidism along with goiter

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109
Q

What constitutes the iodine pump and what is it connected to

A

Na/I co transporter on basolateralcoupled with Na/K ATPase

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110
Q

Inhibitors of Na/I symporter

A

perchlorate (HClO4 -) and thiocyanate (SCN-)compete for sites on symporter

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111
Q

How does TSH affect the Na/I pump

A

increases synthesis of pump

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112
Q

Pendrin

A

apical transporter of iodine

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113
Q

Function of thyroid peroxidase

A

changes I to I+couples thyroglobulin to form MIT (iodinated in one location) or DIT (iodinated in two locations)

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114
Q

What is functional significance of thyroglobulin? Where is it made?

A

thyroglobulin is made in the thyroidIt contains tyrosine which is then incorporated with I+Forming MIT and DIT

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115
Q

Once TGB forms T3/4 how is T3/4 released?

A

TGB is endocytosed and then broken down via lysozymesT3/4 are then released through basolateral membrane into blood(Iodide is recycled)

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116
Q

Function of thiouracils

A

inhibit peroxidase enzyme to inhibit T3 and T4 production

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117
Q

TSH secretion is inhibited by ______

A

somatostatin– decreases pituitary response to TRH

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118
Q

Which steps of T3 and T4 synthesis is TSH involved with?

A

All of them (iodine symporter, coupling, endocytosis, proteolysis of thyroglobulin)

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119
Q

More potent thyroid hormone: T3 or T4?

A

T3many tissues can convert T4 to T3

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120
Q

Wolff Chaikoff effect

A

excess iodine inhibits synthesis of T3 and T4 via peroxidase enzyme

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121
Q

Is most of T3/4 bound or unbound? Which state(s) are the active form

A

BoundUnbound is active

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122
Q

Molecules which bind T3/4. which has the highest affinity

A

thyroxine binding globulin (TBG) – highest affinity (binds both)transthyretin (TTR) - binds T4 but low amounts of T3Albumin- binds both but with low affinity

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123
Q

Half life for T3?

A

~1 day

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124
Q

Half life for T4

A

~6/7 days

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125
Q

How does pregnancy affect amount of T3/4 in active state

A

estrogen increases binding globulins (including TBG) thus causing more to be bound and inactive

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126
Q

Enzymes involved in deiodination use

A

selenium

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127
Q

Which deiodinase are found in glial cells? Why?

A

Type IITo maintain high levels of T3 even if T4 concentrations drop

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128
Q

Is reverse T3 an active form? When do you see elevated levels of reverse T3

A

No does not bind to thyroid receptorstarvation (to decrease metabolic rate and fuel consumption)

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129
Q

How do T3 and T4 enter the cell?

A

Monocarboxylate transporter (MCT8)Organic Anion Transporting family (OATP)

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130
Q

what is function of T3 once it is converted from T4

A

alter transcription rate and production of mRNA

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131
Q

where is thyroid receptor in absence of ligand

A

in nucleus associated with chromatin

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132
Q

T3 effect on carbohydrate metabolism

A

increase uptake of glucose and glycolysisincreased carbohydrate metabolism

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133
Q

T3 effect on lipid metabolism

A

increase lipolysispromote mobilization of fatty acidsdecrease in plasma TAGs

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134
Q

how does hypothyroidism alter basal metabolic rate (BMR). why?

A

decreases it due to decrease in oxygen consumption

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135
Q

Thyroid hormone effect on heat? carbon dioxide?

A

increase both

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136
Q

Hypothyroidism associated with hypo or hyper thermia

A

hypothermia (generate less heat and lower tolerance to cold)

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137
Q

What happens if thyroid hormone is absent during development of fetus

A

Dimished growth ofcerebral cortexdecrease in proliferation of axonsdecreased myelinationlack of maturation for bone growth centers

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138
Q

Effect of elevated thyroid hormone in adults

A

emotional instabilityhyperexcitability

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139
Q

Effect of hypothyroidism in adults

A

slow speechdecreased memorydecreased conduction in peripheral nerves

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140
Q

Effect of thyroid hormone on catecholamines

A

increases number of receptors (NOT increase blood levels of catecholamines)

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141
Q

Hyperthyroidism on heart

A

increased contractility due to increase in alpha myosin heavy chain, calcium channels, calcium ATPase, B-adrenergic receptorsPositive inotropic and chronotropic effects

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142
Q

Common finding to explain hyperthyroidism

A

1) benign thyroid adenoma2) elevated levels of thyroid stimulating immunoglobulin which binds normal TSH receptors to over stimulate production of T4/T3

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143
Q

Grave’s Disease. Clinical findings? treatment?

A

TSI (produced by B-lymphocytes) binds to TSH receptor on thyroid gland causing enlarged/overactive thyroidEyes protrudeTreated with thioamides

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144
Q

Causes of hypothyroidism

A

Iodine deficiencyhypothalmic or pituitary dysfunctionchronic thyroid inflammationremoval of thyroid

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145
Q

myxedema. treated with?

A

synonym for hypothyroidismmucinous edema that gives skin puffy appearancetreatment: synthetic levothyroxine

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146
Q

(A nitpicky one) Name the positions of Iodine on T3, T4, and rev T3

A

T3: 3,5,3T4: 3,5,3,5Rev T3: 3,3,5

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147
Q

Where does thyroid hormone not increase oxygen consumption in humans

A

brain, gonads, spleen

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148
Q

How does somatostatin alter TSH secretion?

A

Somatostatin decreases pituitary response to TRH (RELEASING HORMONE!)

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149
Q

Why is such a large population of T3/T4 bound?

A

To insure hormone solubilitymaintain large circulating reservoir of T3/T4 that is unaffected by shifts in secretionminimize loss of hormones via kidney/liver

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150
Q

How does T3 impose its negative feedback?

A

reduces number of TRH receptorsinhibits gene responsible for TSH synthesisT4/T3 suppress mRNA levels for TRH

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151
Q

What is the name of the zone of adrenal cortex present in gestation that eventually proliferates at a young age?

A

Definitive Zone

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152
Q

How would you treat Cushing’s Disease

A

metyrapone - blocks 11 hydroxylase enzyme to lower cortisol levels

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153
Q

What is the most abundant hormone in the adenohypophysis?

A

growth hormone

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154
Q

What is the GH-like hormone secreted during pregnancy?

A

hCS

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155
Q

What hormone stimulates GH release?

A

growth hormone release hormone

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156
Q

What hormone inhibits growth hormone?

A

somatostatin

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157
Q

How does GHRH affect somatotrophs?

A

increase GH mRNA transcription,synthesis of GH protein, GH release

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158
Q

What tissue secretes somatostatin?

A

hypothalamus

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159
Q

How does somatostatin affect somatotrophs?

A

decrease GH secretion

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160
Q

What is another name for IGF1?

A

somatomedin

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161
Q

What tissue produces somatomedin?

A

liver

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162
Q

How does somatomedin affect somatotrophs?

A

GH transcription

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163
Q

In adults, when are the highest GH levels observed?

A

during sleep

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164
Q

How many GH surges are seen per day around puberty?

A

4-6

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165
Q

What conditions increase GH?

A

stressexerciselow glc

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166
Q

What is the assumed endogenous ligand for GH secretagogue receptor?

A

ghrelin

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167
Q

What carries GH in the blood stream?

A

GH binding protein

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168
Q

What downstream signaling mechanism does GH use?

A

JAK/STAT

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169
Q

What tissue has the most GH receptors?

A

liver

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170
Q

Which IGF isoform is the most important?

A

IGF1

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171
Q

What effects does IGF have?

A

increase:glc uptakemitosisbone cel differentiationcollagen productiongrowth of the epiphyseal cartilage plate

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172
Q

How does GH affect adipose tissue?

A

decrease glc uptakeincrease lipolysis

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173
Q

How does GH affect chondrocytes?

A

increase aa uptake and protein synthesis

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174
Q

How does GH affect metabolism?

A

increase plasma glc and FFAdecrease plasma aa

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175
Q

How does GH affect skeletal growth?

A

stimulate epiphyseal cartilageincreased chondrocyte metabolism

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176
Q

What happens to epiphyseal plates without GH?

A

narrowcartilage redued

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177
Q

How is hormone sensitive lipase affected by GH?

A

increase

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178
Q

How do insulin and GH cross-talk?

A

GH inhibits insulin in muscle and adipose

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179
Q

GH deficiency causes __.

A

dwarfism

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180
Q

GH excess causes __.

A

gigantism

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181
Q

What does octreotide do?

A

somatostain analog

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182
Q

perfusion of brain increases proportional to increase in _____________

A

arterial CO2

183
Q

Cerebral blood flow remains nearly constant between ____ and ___ mmHg. Beyond these limits blood flow becomes _____ dependent

A

60 and 160pressure dependent

184
Q

How does autoregulation in CNS blood flow work when BP is high or low?

A

Low BP- dilation of arterioles which decreases resistance to flow to promote flowHigh BP - constrict arterioles to increase resistanceThis promotes constant flow desired

185
Q

How does chronic Hypertension alter autoregulation of CNS blood flow. What negative effects can this have?

A

shifts autoregulation to the right (increasing autoregulation pressure boundaries)Neg Effect- brain is now at risk for damage during periods of low pressure as CBF will decrease

186
Q

Injuries such as ________ (multiple answers) can cause CBF to have a linear relationship with ______

A

head trauma, ischemia, subarachnoid hemorrhageCBF varies directly with Cerebral Perfusion Pressure

187
Q

Brain lacks ____ and ______ ; therefore, it requires continuous supply of _____

A

creatine phosphate / glycogenO2

188
Q

What is the normal extracellular [K+] and what happens when the value is below and above this normal

A

4 mMol is normalBelow 4- flow decreasesAbove 4- flow increases

189
Q

__________ causes the extracellular[K+] to be above ____ mMol which leads to this undesirable response (much higher than normal K value)

A

neuronal damage10arterioles contracting – shutting down flow to sacrifice local neurons to save surrounding neurons

190
Q

Lack of oxygen results in the release of ___________ which produce ______ and ______ blood flow

A

acid metabolitesvasodilationincreased

191
Q

Anterior Cerebral Artery supplies? Penetrating branches supply?

A

inferior frontal lobesmedial surface of frontal lobesmedial surface parietal lobesanterior corpus callosumPenetrating: Limbic structures, head of caudate, anterior limb of internal capsule

192
Q

middle cerebral artery supplies? penetrating branches?

A

frontal lobesparietal lobestemporaloccipitalinsularpenetrating: posterior internal capsule, putamen, outer globus pallidus, body of caudate

193
Q

Posterior cerebral artery supplies?

A

occipital lobeinferior temporal lobethalmusposterior limb of internal capsule

194
Q

penetrating anterior choroidal artery supplies?

A

anterior hippocampusposterior internal capsule

195
Q

What arteries supply the ventral side of the brain?

A

PCACerebellar arteries (superior, ant. inf. , post. inf. )Brainstem branchesAnterior Spinal Artery

196
Q

what is the most common brainstem stroke?

A

posterior inferior cerebllar artery stroke

197
Q

A stroke affecting this artery could lead to possible ________ (a disease) symptoms.

A

posterior inferior cerebllar arteryptosis and miosis

198
Q

posterior inferior cerebllar artery stroke is also known as what other syndromes?

A

Wallenberg SyndromeLateral Medullary Syndrome

199
Q

contralateral loss of pain and temp to the body andipsilateral loss of pain and temp to the face is seen in a stroke of _______

A

posterior inferior cerebellar artery (PICA)

200
Q

Other random symptoms of stroke to PICA

A

vertigodifficulty swallowingataxia

201
Q

Symptoms associated with stroke to AICA. also known as _______

A

vomitingvertigoipsilateral deafnessnystagmusipsilateral facial weaknesslateral pontine syndrome

202
Q

Interesting symptoms of stroke to superior cerebellar artery

A

ipsilateral ataxiaslurred speechipsilateral horner’s syndromecontralateral loss of pain/temppartial deafnessRARE

203
Q

What is contained in paramedian midline territory?

A

corticospinal tractmedial lemiscus

204
Q

what is contained in the paramedian short circumferential territory?

A

pontocerebellar fibersmedial leminiscusALS

205
Q

What is contained in the paramedian long circumferential territory

A

middle and superior cerebellar pedunclesvestibular and cochlear nerves/nucleiCN 5 (spinal and trigeminal nucleus)CN 7ALS

206
Q

How is spinal artery supplied with blood?

A

anterior spinal artery - anterior 2/3 of cordposterior spinal artery- posterior 1/3 of cord

207
Q

_____ strokes are when blood vessel in brain ruptures and blood seeps into brain. This is most commonly caused by ____ and ____

A

hemorrhagic strokehigh BPaneurysm (weakness of vessel wall causing it to balloon outward)

208
Q

What are some secondary mediators released from O2 deprived tissue? What does this cause?

A

glutamateCaprostaglandinsfree radicalsprolong and extend neuronal damage

209
Q

Major risk factors for stroke

A

High BPSmokingDiabetesCarotid artery disease ( narrow Cartoid artery can be blocked by clot)- peripheral artery disease- narrowed blood vesselAtrial FibrillationBlood disorder- sickle cell anemia or high RBC count

210
Q

Comparison of blacks vs whites for strokes

A

blacks 2x more likely to have stroke for first timeblacks have higher death rate

211
Q

What is an effective treatment for ischemia of brain. Who should this not be given to?

A

tissue plasminogen activatorsshould not be given to someone with hemorrhagic stroke b/c they will bleed out

212
Q

treatments for hemorrhagic stroke

A
  1. drain/remove blood2. endovascular coli embolization (insert coil to repairaneurysm3. Place clip around aneurysm
213
Q

Vessel Occluded : anterior spinal artery (posterior to last radicular artery)

A

bilateral paralysis caudal to blockagebilateral loss of Pain/Temp below blockage

214
Q

Vessel Occluded : branch from anterior spinal artery at C5

A

Ipsilateral UMN paralysis below C5Ipsilateral LMN paralysis at C5Contralateral loss of pain/temp below C5

215
Q

Vessel Occluded : lateral branch of vertebral artery

A

contralateral loss of pain/temp from neck downipsilateral loss of pain/temp from faceipsilateral unsteadiness on feet

216
Q

Vessel Occluded : Penetrating branch from anterior spinal artery

A

ipsilateral tongue deviationcontralateral loss of touch from neck downcontralateral paralysis (UMN) from neck down

217
Q

Vessel Occluded : Medial Penetrator from basilar artery

A

contralateral loss of touch from neck down and some facecontralateral paralysis (UMN) from neck down and vocal and tongue

218
Q

Vessel Occluded : Penetrator from AICA

A

contralateral loss P/T and ipsilateral faceipsilateral loss facial motoripsilateral eye- no lateral movement - abducens nucleusipsilateral vestibular response loss

219
Q

Vessel Occluded : long circumferential from basilar

A

CL loss P/TCL loss touch from body and faceIP LMN of jaw musclesdecrease CL auditory perception

220
Q

Vessel Occluded : Medial penetrating from Basilar

A

CL UMN from headIP CN3 PalsyIP ataxia

221
Q

Vessel Occluded : Penetrating branch of superior cerebellar

A

CL paralysis (UMN) from neck downCL loss of touch, P/T from face and bodyDecrease CL auditory perception

222
Q

Vessel Occluded : Blockage of penetrating branch of posterior cerebral artery

A

CL loss of touch, position, P/T from body face

223
Q

Anterior Limb of Internal capsule is supplied by

A

lenticulostriate branch of Anterior Cerebral Artery

224
Q

Genu/Rostral Internal Capsule blood supply

A

lenticulostriate from MCA and anterior choroidal

225
Q

Blood supply to caudal posterior limb

A

penetrating branches of PCA

226
Q

Vessel Occluded : Anterior Cerebral Artery (ACA)

A

CL UMN paralysis from waist downCL loss of somatic sensation from waist down

227
Q

Vessel Occluded : Posterior Cerebral Artery (PCA)

A

CL homonymous hemianopsia

228
Q

Vessel Occluded : Middle Cerebral Artery (MCA)

A

CL UMN paralysis from waist upCL loss of somatic sensation from waist up

229
Q

What is the last brain structure to mature?

A

uncinate

230
Q

ADHD is characterized by a __ in cortical maturation.

A

delay

231
Q

What is neuroplasticity?

A

gene expression changes that lead to learning and behavioral adaptation

232
Q

How do heteromodal cortices differ from primary?

A

They integrate signals from multiple sensory inputs

233
Q

What does the arcuate/association fiber connect?

A

cortical areas of same hemisphere

234
Q

What do corticofugal fibers connect?

A

subcortical structures

235
Q

Name the 2 main arcuate fibers for learning.

A

uncinate fasciculusarcuate fasciculus

236
Q

List the 4 parts of the corpus callossum.

A

rostrumgenutrunksplenium

237
Q

What tissue is made up of archicortex?

A

hippocampus

238
Q

What tissue makes up paleocortex?

A

temporal lobe

239
Q

What is the allocortex made up of?

A

hippocampusamygdalaprepyriform cortex

240
Q

How does the cortex connect to the pons?

A

radiationsinternal capsulecerebral peduncle

241
Q

List some components of the limbic lobe.

A

cingulate gyrushippocampusparahippocampal gyrusnucleus accumbensamygdaladentate

242
Q

The hippocampus is right on top of what cortex?

A

perirhinal

243
Q

What tracts go from the hippocampus to the thalamus?

A

fornix to mammillary body to mammillothalamic tract

244
Q

ADHD is characterized by a __ in cortical maturation.

A

delay

245
Q

How do heteromodal cortices differ from primary?

A

They integrate signals from multiple sensory inputs

246
Q

How does the cortex connect to the pons?

A

radiationsinternal capsulecerebral peduncle

247
Q

List some components of the limbic lobe.

A

cingulate gyrushippocampusparahippocampal gyrusnucleus accumbensamygdaladentate

248
Q

List the 4 parts of the corpus callossum.

A

rostrumgenutrunksplenium

249
Q

Name the 2 main arcuate fibers for learning.

A

uncinate fasciculusarcuate fasciculus

250
Q

The hippocampus is right on top of what cortex?

A

perirhinal

251
Q

What do corticofugal fibers connect?

A

subcortical structures

252
Q

What does the arcuate/association fiber connect?

A

cortical areas of same hemisphere

253
Q

What is neuroplasticity?

A

gene expression changes that lead to learning and behavioral adaptation

254
Q

What is the allocortex made up of?

A

hippocampusamygdalaprepyriform cortex

255
Q

What is the last brain structure to mature?

A

uncinate

256
Q

What tissue is made up of archicortex?

A

hippocampus

257
Q

What tissue makes up paleocortex?

A

temporal lobe

258
Q

What tracts go from the hippocampus to the thalamus?

A

fornix to mammillary body to mammillothalamic tract

259
Q

MDD patients have a __ activation of the limbic system.

A

high

260
Q

What frequency are EEG gamma waves?

A

25+ Hz

261
Q

What frequency are EEG beta waves?

A

13-25 Hz

262
Q

What frequency are EEG alpha waves?

A

13-Aug

263
Q

What frequency are EEG theta waves?

A

4-7 Hz

264
Q

What frequency are EEG delta waves?

A

<4 Hz

265
Q

What EEG wave occurs during deep sleep?

A

delta

266
Q

What EEG wave occurs during early sleep?

A

theta

267
Q

What EEG wave occurs during binding of information?

A

gamma

268
Q

What EEG wave occurs during the alert stage?

A

beta

269
Q

What frequency EEG wave is the awake but relaxed state?

A

8-13 Hz

270
Q

How does encephalitis affect EEG?

A

general slowing

271
Q

How do siezures present on an EEG?

A

hyperactivity of neurons

272
Q

What makes up the classic reticular activating system?

A

rostral ponsthalamic relay nucleiintralaminar thalamic nucleicortex

273
Q

What NTS are used by the reticular activating system?

A

AChNE

274
Q

What nuclei start the reticular activating system?

A

parabrachial nucleilocus ceruleuspedunculopontine nucleusdorsal and median raphe nuclei

275
Q

What fiber drives the secondary arousal pathway?

A

medial forebrain bundle

276
Q

What NTS are used in the secondary arousal pathway?

A

orexinAChhistamine

277
Q

How do thalamic neurons fire during a synchronized EEG?

A

oscillatoryhyperpolarization by inhibitory input from thalamic reticular cells, which leads to Ca influx

278
Q

How do thalamic neurons fire during a desynchronized EEG?

A

tonic modecholinergic brainstem afferents from the reticular activating system

279
Q

What would happen if you were napping and then your EEG became desynchronized?

A

You would be awake

280
Q

What neural structure secretes histamines?

A

tuberomammillary nucleus

281
Q

Non-REM is regulated by activation of GABA neurons in the __.

A

ventrolateral preoptic area (VLPO)

282
Q

How long is REM sleep in each sleep cycle?

A

5-15 min

283
Q

How long is a sleep cycle?

A

90-120 min

284
Q

How is muscle tone affected in REM sleep?

A

relaxed

285
Q

GABA inhibition of what neuron initiates sleep?

A

NE 5HT ACh neurons in the midbrain

286
Q

During REM sleep, what part of the sleep neurons turns back on?

A

AChNE/5HT axis stays off

287
Q

What does the NE/5HT axis of sleep control?

A

motor output

288
Q

What nucleus is the circadian pacemaker?

A

suprachiasmatic nucleus

289
Q

What happens in narcolepsy?

A

onset of sleep starts with REM sleep

290
Q

What happens in cataplexy?

A

loss of muscle tone by active inhibition of skeletal muscleduring consciousness

291
Q

What sort of stimuli does sleep help encode?

A

positive stimuli

292
Q

What is encoding?

A

newly learned info is attended to and processed

293
Q

What is consolidation?

A

hippocampus-dependent short memories being encoded into cortex-dependent long memories

294
Q

Hippocampal damage results in __.

A

anterograde amnesia

295
Q

What type of memory is the hippocampus important for?

A

spatialshort term

296
Q

What updates faster, visual or auditory memory?

A

visual

297
Q

Does short term memory require the hippocampus?

A

no

298
Q

What is the molecular basis of memory?

A

long term potentiation/depression

299
Q

What are examples of nonassociative learning?

A

habituationsensitization

300
Q

What is habituation?

A

repeated exposure to same stimulus decreases response

301
Q

What is sensitization?

A

repeated exposure to same stimulus increases response

302
Q

What neural structures are important in associative memory?

A

amygadala and hippocampus

303
Q

What brain region does the central amygdala go to?

A

brainstemhypothalamus

304
Q

What brain region does the basolateral amygdala go to?

A

orbital cortexanterior cingulatemedial thalamus

305
Q

What part of the amygdala controls emotional cognition?

A

basolateral

306
Q

What part of the amygdala controls autonomic response?

A

central

307
Q

Simple associative learning of emotional response involves __.

A

amygdala

308
Q

Simple associative learning of the skeletal muscle involves the __.

A

cerebellum

309
Q

What is the common example of procedural memory?

A

riding a bike

310
Q

What sort of memory underlies our ability to create stereotypes?

A

perceptual

311
Q

What is episodic memory?

A

remembering experiences

312
Q

What is semantic memory?

A

remembering specific facts

313
Q

What lobe do Alzheimer plaques concentrate on?

A

parietal

314
Q

How does frontal lobe damage affect memory?

A

more work to get info in and out of storage

315
Q

How does hippocampal damage affect memory?

A

impossible to get info into storagecan still get memory from cortex

316
Q

What does the basal ganglia motor loop do?

A

the putamen sequences somatic movements by the motor and premotor cortex

317
Q

What does the basal ganglia oculomotor loop do?

A

regulates saccades using the caudate and frontal eye fields

318
Q

What does the basal ganglia prefrontal loop do?

A

dorsolateral prefrontal cortex innervates the caudate to use memory

319
Q

What does the basal ganglia limbic loop do?

A

anterior cingulate and orbital frontal cortex innervate the ventral striatum to regulate emotional behaviors

320
Q

What causes syndrome of Cretinism

A

decreased thyroid hormone during fetal development which leads to poor mental development

321
Q

How is GH affected by presence of Thyroid Hormone?

A

Thyroid Hormone is required by pituitary somatotroph for GH synthesis and secretion. Also, maintains sensitivity to GH and IGF

322
Q

What is the purpose of carotid endarterectomy

A

Restore blood flow to the brain by removing atherosclerotic plaque

323
Q

Where does atherosclerotic plaque build up (what layer of vessel)

A

intimia (endothelial layer)

324
Q

What are some consequences of stable and unstable plaque

A

occlusionthrombosishemorrhageembolism

325
Q

layers of vessel. features?

A

intima- endothelial ; basement membranemedia- smooth muscle ; Extracellular matrixadventitia- loose connective tissue ; vaso vasorum

326
Q

Infection, Inflammation, trauma, or toxic exposure can cause this type of interaction between the layers of the vessel

A

smooth muscle cells invade intima (intimal thickening)

327
Q

Which specific vessels does atherosclerosis predominantly affect?

A

Coronary and Carotid vessels

328
Q

What is a stroke?

A

embolus from broken plaque reaches cerebral vessels thus causing ischemic hypoxia in the brain

329
Q

Describe events in pre-clinical phase of atheroma

A

normal artery – 1) fatty streak 2) fibrofatty plaque (can also skip fatty streak stage) 3)advanced vulnerable plaque —> clinical phase

330
Q

Describe clinical phase of atheroma

A

Continuation of advanced plaque from pre-clinical :1) mural thrombosis/ embolization/ leading to wall weakening–>aneurysm and rupture2) plaque ruptures or erodes/embolizaiton –> occlusion by thrombus3)progressive plaque growth –> critical stenosis

331
Q

Partial or complete blockage of internal carotid or vertebral arteries leads to what change in blood flow?

A

None. Patients come in with 80% blockage in both carotids without symptoms

332
Q

What percent of patients have an incomplete circle of willis

A

20-50%

333
Q

How are carotid occlusions detected?

A

cerebrovascular event may be first sign: 1) stroke ; 2) transient ischemic attack

334
Q

Whaaaaaat is a bruit?

A

rush sound heard with a stethoscope (blood moving past occlusion)

335
Q

What is used to assess degree of infarct in patients who have just had a stroke?

A

CT/MRI

336
Q

Carotid Endarterectomy is recommended for patients with what symptoms?

A

70%+ stenosisstroketransient ischemic attackSignificant carotid artery disease

337
Q

What are possible fatal events associated with carotid endarterectomy

A

cardiac eventspost op stroke : plaque emboli ; platelet clotting ; improper flushinghyperperfusion syndrome

338
Q

Describe vascular anatomy of Pre Carotid Endarterectomy patients

A

vertebral artery flow compenstates for lack of carotid flowcommunicating branches become strongerautoregulation functions to decrease resistance to maintain CBF

339
Q

Describe vasculature of post Carotid Endarterectomy patient

A

Higher BP and oxygen is sensed; therefore arterioles try to constrict to prevent excess CBF

340
Q

3 clinical features of hyperperfusion syndrome

A

ipsilateral headache - migrainefocal motor seizuresintracerebral edema and hemorrhage

341
Q

What is main impaired ability with respect to autoregulation after Carotid Endarterectomy

A

vessels are unable to constrict in presence of high blood pressure

342
Q

Characteristics, prior to operation, of patients who have hyperperfusion syndrome

A

had high grade carotid stenosis (>80%)recent infarctbilateral carotid occlusionpoorly regulated post operative systemic blood pressure

343
Q

How does cardiovascular reactivity % correlate to hyperperfusion syndrome

A

low % are likely to suffer from hyperperfusion syndrome

344
Q

How are free radicals produced in hyperperfusion?

A

when clamping is removed, influx of blood and oxygen results in free radical formation and thus produces evidence of lipid peroxidaiton (within minutes of declamping)

345
Q

How is baroreceptor affected during Carotid Endarterectomy

A

1) nerves to carotid body may be severed or damaged by cytokines (from inflammatory response)–> hypertension and tachycardia2) stimulation of carotid sinus during procedure –> leads to hypotension which cannot be handled by autoregulation as vessels cannot constrict

346
Q

Where does the hippocampus project to

A

limbic cortexmammallary bodyseptum(Kalivas diagram)

347
Q

What is the input to the nucleus accumbens

A

anterior cingulate (+)oribital cortex (-)

348
Q

What does the inucium griseum connect

A

hippocampus to anterior cingulate/orbital cortex

349
Q

What is the corticostriatal thalmic loop? Purpose?

A

limbic cortex (ant cingulate/orbital cortex) to accumbens to medial anterior thalmus back to limbic cortexmodifies behavior

350
Q

Phases of addiction.

A

social useregulated relapsecompulsive relapse

351
Q

Neurocircuitry associated with social use

A

mesocorticolimbicdopamine

352
Q

Neurocircuitry associated with regulated relapse

A

prefrontal cortexglutamate

353
Q

Neurocircuitry associated with compulsive relapse

A

striatal habit circuitry

354
Q

How does dopamine contribute to addiction?

A

the dopamine release caused by a drug is directly related to how addictive it is

355
Q

characteristics of drugs which cause addiction

A

1) more dopamine release2) rapid drug onset3) greater drug availability

356
Q

Primary pathology in addiction?

A

inability for prefrontal cortex to regulate behavior via nucleus acumbens due to imbalance of glutamate projection to accumbens

357
Q

What types of drugs may be useful in treating addiction

A

drugs that restore normal glutamate transmission

358
Q

Cocaine addiction reduced ______ activity

A

prefrontal metabolic (anterior cingluate and orbital cortex)

359
Q

When cocaine addicts watched a cocaine video where was the greatest stimulation seen?

A

amygdala and anterior cingulate

360
Q

Cocaine use leads to a loss of ______

A

plasticity – decreased LTP and LTD

361
Q

Replacement therapies are effective for what stage of addiction

A

regulated relapse as it provides similar effect

362
Q

This drug helps to restore LTP and LTD

A

N-acetylcysteine

363
Q

NAC reduced activity in ______ for cocaine users shown a cocaine video

A

anterior cingulate

364
Q

Why is addiction so common in adolescents?

A

Adolescents have 30% more dopamine enabling them to become more easily addicted

365
Q

Most drug addicts begin between what ages?

A

14 and 23

366
Q

How did NAC affect days to relapse in cocaine addicts

A

increased the number of days to relapse

367
Q

In experiment to determine NAC effect on marijuana users what was found?

A

NAC increased number of people who produced NEGATIVE urine samples for THC vs placebo

368
Q

Purpse of ventral stream of visual processing

A

visual cortex to anterior temporal lobefacial recognition

369
Q

Purpse of dorsal stream of visual processing

A

visual cortex to medial temporal and parietal cortexspatial orientation and spatial cognition

370
Q

If a patient could not recognize faces where would you look for a lesion

A

ventral temporal/occipital junctionmust be in right hemisphere but can also be bilateral

371
Q

prosopagnosia

A

inability to recognize faces

372
Q

what are some associated problems that arise in conjunction with prosopagnosia

A

achromatopsia- inability to recognize colormetamorphopsia- object has distorted shape

373
Q

Balint’s syndrome

A

bilateral lesions of parietal cortexsimultangagnosia- loss of awareness for overall object (big picture loss)optic ataxia- inability to reach out and grasp object (hand eye coordination)

374
Q

What is the function of the parietal cortex in dorsal stream visual processing

A

analysis of motion and spatial relations

375
Q

What is the function of the temporal cortex in dorsal stream visual processing

A

analysis of form and color

376
Q

A unilateral parietal lesion will cause what problems with respect to hand eye coordination

A

Normal function in the ipsilateral fieldContralateral hand makes errors when in contralateral visual field

377
Q

Explain relationship between R/L visual field stimulus and increased activity in R/L parietal cortex

A

stimulus presented in the L visual field will cause firing in right parietal cortexstimulus presented in R visual field will cause firing in both right and left parietal cortex

378
Q

Lesion in which parietal cortex (R or L) is more devastating? What is this known as?

A

Right because both L and R visual field excites right parietal cortexLEFT NEGLECT

379
Q

The Go circuit is ______ as it is involved in ____ and _____

A

anterior cingulatemotivationattention

380
Q

The Stop circuit is the ______ as it is involved in providing _____

A

Orbital Cortexinhibitory control over behavior

381
Q

Drug addicts show blunted activity in the ______ indicating compulsive behavior

A

orbital cortex(also Kalivas states diminished anterior cingulate in a different lecture)

382
Q

This portion of the cortex is activated during emotional pocesssing

A

Insula (and Amygdala)

383
Q

Lateral frontal cortex of temporal lobe provides memory about _____

A

objects

384
Q

Anterior Cingulate cortex provides memory about _____

A

people corresponding to emotional/motivational content

385
Q

In experiment where subject is given a series of nouns and required to provide a verb to fit. Where was brain activity most prominent for the naive subject

A

prefrontal cortex and temporal lobe

386
Q

In experiment where subject is given a series of nouns and required to provide a verb to fit. Where was brain activity most prominent for the novel subject (experienced but given new words)

A

prefrontal cortex and temporal lobe

387
Q

Broca’s area? Function?

A

posterior frontal lobe– production of language

388
Q

Lesion of Broca’s area

A

expressive aphasia- can understand but difficulty expressing

389
Q

Wernicke’s area? Function?

A

posterior temporal lobeunderstanding language

390
Q

Lesion to Wernicke’s area

A

receptive aphasia– can’t make sense but speaking is ok

391
Q

Arcuate fasiculus purpose?

A

connects Wernicke’s and Broca’s area

392
Q

Lesion to arcuate fasiculus

A

conduction aphasia – paraphrasic speech and inability to produce appropriate response

393
Q

Stroke to ____ of temporal lobe may cause loss of ability to read and spell

A

posterior

394
Q

How do brains of deaf people adapt?

A

more easily activated parietal and frontal area associated with visual attention

395
Q

Language functions are lateralized with ______ on the left and _____ on the right

A

speech on leftemotional context on right

396
Q

What is Aprosodia? It comes about with a lesion in ______.

A

loss of emotion in speechLesion to right Broca’s area

397
Q

Dyscalculia? Lesion/Damage to what?

A

poor numeric abilitylesion to parieto-temporal

398
Q

Damage to ______ causes prosopagnosia

A

Right ventral temporal lobe

399
Q

Capgras syndrome. Caused by Lesion to ?

A

delusion that familiar person is an impostorassociated with damage between amygdyla and right temporal lobe

400
Q

What causes persistent developmental stuttering

A

lack of asymmetry in planum temporale (should be L dominant (temporal lobe) )

401
Q

Naming color of ink in a word shows partnership between ______ and ____ (ex. green [ans: black]). What is this this is an example of

A

FrontalParietalExample of Spatial cognition and attention

402
Q

Deficits in working memory are often seen in patients suffering from _____ or ______

A

schizoparkinsons

403
Q

Working memory (as exemplified with monkey trying to remember which container food is in) is established by _____ providing input to ______ (both are parts of the brain)

A

parietalprefrontal cortex

404
Q

What is a severe and striking deficit in one cognitive function; memory?

A

amnesia

405
Q

What is an absence of recognition and use of verbal language?

A

aphasia

406
Q

What is impaired object recognition?

A

agnosia

407
Q

What is chronic and substantial decline in two or more areas of cognitive function?

A

dementia

408
Q

What are the two categories of memory?

A

declarative (what)non-declarative (implicit or procedural)

409
Q

What is the leading cause of dementia?

A

aphasia

410
Q

Which hemisphere is predominantly used in language?

A

left

411
Q

What is an aphasia where you speak short phrases that make sense but takes a lot of effort?

A

broca’s (non-fluent)

412
Q

What is an aphasia where you speak long meaningless sentences?

A

wernicke’s

413
Q

What is agnosia?

A

characterized by an inability to recognize and identify objects or persons

414
Q

Around what age does Alzheimer’s onset?

A

60

415
Q

Describe pathological qualities of Alzheimer’s.

A

beta-amyloid plaquestau tanglesloss of gray matter

416
Q

What causes Wernicke-Korsakoff syndrome?

A

thiamine deficiency

417
Q

What population has high risk for Wernicke-Karsakoff?

A

alcholics

418
Q

What characterizes Wernicke-Karsakoff?

A

nystagmusconfusionpupil responsecoma

419
Q

List some common causes of memory disorders.

A

strokeseizureconcussion

420
Q

How is mental retardation defined?

A

significant limitations in intellectual and adaptive function

421
Q

When does mental retardation occur?

A

before age 18

422
Q

What is the incidence of mental retardation?

A

1-3%

423
Q

How to diagnose mental retardation by IQ?

A

<70

424
Q

What sort of disease can resemble mental retardation?

A

metabolic disease

425
Q

What is the histologic commonality in mental retardation?

A

dendrite and synapse abnormality

426
Q

What causes down syndrome?

A

trisomy 21

427
Q

What is the most common inherited form of mental retardation?

A

X-linked mental retardation disorder (XLMR)

428
Q

What is the incidence of fragile X?

A

1:4000 in males1:6000 in females

429
Q

What is the molecular cause of fragile X?

A

CGG repeat in the 5’ UTR

430
Q

Rett syndrome is __ to males.

A

lethal

431
Q

What gene is mutated for Rett syndrome?

A

MeCP2

432
Q

When does autism typically present?

A

first 3 yrs of life

433
Q

What is the triad of autism impairements?

A

socializationcommunicationimagination

434
Q

What is the prevalence of autism?

A

2-6 cases per 1000

435
Q

In addition to autism, what are the four other pervasive developmental disorders?

A

asperger’schildhood disintegrative disorderrett’sPDD not otherwise specified

436
Q

How does autism affect language development?

A

delayed

437
Q

How does autism affect social development?

A

physical and emotional distance from others

438
Q

How does autism affect intellectual development?

A

poor verbal ability

439
Q

What are the 5 signs that a child might be autistic?

A

does not babble at 12 monthsdoes not gesture at 12 monthsdoes not say single words by 16 monthsdoes not say two word phrases on his or her own by 24 monthsloss of language or social skills

440
Q

What is the critical gene to activate male genital development?

A

srytestis-determining factor

441
Q

What is the difference between organizational and activational effects of steroid hormones?

A

organize - in uteroactivation - puberty

442
Q

What is wrong with female congenital adrenal hyperplasia patients?

A

masculanized females

443
Q

What causes androgen insensitivity syndrome?

A

hormone receptors are insensitive

444
Q

What are brain regions that are especially sex dimorphic?

A

hypothalamusamygdala

445
Q

How do spinal motor neurons differ in males and females?

A

perineal motor neuron numbers are different

446
Q

where does the tectospinal tract end?

A

cervical segment of spinal cord since it primarily innervates shoulders and neck to move to follow eye movements

447
Q

Hypothalamus function: what nuclei and hormone are responsible for water and electrolyte balance

A

Supraoptic (ADH)

448
Q

What hypothalamus nuclei regulates circadian rhythm

A

Suprachiasmatic

449
Q

What hypothalamus regulates of gonadal / sexual function

A

Anterior / preoptic, arcuate

450
Q

What hypothalamus nuclei regulates hunger/satiety - lateral / ventromedial hypothalamus

A

Lateral nuclei - stimulate = start eating

Ventromedial nuclei - stimulate = stop eating (satiety)

451
Q

What hypothalamus nuclei regulates thirst

A

Lateral hypothalamus

452
Q

What hypothalamus areas activate sympathetic and adrenal medulla

A

Anterior and posterior areas.

453
Q

What hypothalamus nuclei regulate temperature

A

Anterior and posterior nuclei

HR Block 6 (3 decks)

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