Block 4 Shut the door Flashcards

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
Q

satiety factors in CNS

a. gastric distention
b. CCK
c. ghrelin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Prader-Willi syndrome

Sx

A
fetal hypotonia
mental retardation
hypogonadotropic hypogonadism DEC FSH and LH
ghrelin secretion HYPERGHRELINEMIA
obesity
hyperphagia EXCESSIVE EATING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

long-term CNS signals of satiety

A
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

CNS nuclei of satiety:
LHA lateral hypothalamic area
PVN paraventricular nucleus
ARC arcuate nucleus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

LHA lesion

A

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

  1. aphagia due to loss of neurons that synthesis “orexigenic” peptide = OREXIN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

actions of leptin on ARC

A

i. leptin acts in ARC to inhibit NPY: DEC FOOD INTAKE

ii. leptin acts in ARC to activate melanocortin neurons: DEC FOOD INTAKE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

actions of ghelin on ARC

A

ghrelin acts in ARC to activate NPY neurons: INC FOOD INTAKE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what type of drug could be promising candidates for treating hyperphagia-induced obesity?

A

activate melanocrtin receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

___% treated for mood disorders

A

over 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

limbic system related structures

A
amygdala
hippocampus
septal nuclei
nucleus accumbens
medial prefrontal cortex and anterior cingulate cortex
ventral segmental area
anterior and dorsomedial nuclei of thalamus
mamillary nuclei
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

limbic system pathways:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

all limbic areas receive rich innervation by _____ and _____ axons

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

ventral segmental area (VTA) projects to:

DA neurons

A

nucleus accumbens
medial prefrontal cortex
amygdala
septal nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

mesolimbic system (DA)

A

i. self-stimulation studies: VTA > REWARDING
ii. drug addiction
COCAINE block DA repute: inc DA in synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

lesion VTA, NAcc

A

decreased drug seeking behavior
DA receptors permanently blocked
***has effects on our natural reward system (endorphins, natural opioids, nicotine, opioids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

natural rewards

A

SEX

FOOD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

ACh neurons lost in AD in

A

nucleus basalis**

spetal nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

limbic system functions

AMYGDALA and lesion

A

amygdala fxns
a. role in fear conditioning/type of learning
Pavlovian classical conditioning

lesions to amygdala: prevent fear conditioning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

limbic system functions

PREFRONTAL CORTEX and syndrome

A

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
Q

limbic system functions

HIPPOCAMPUS and injury

A

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
Q

limbic system dysfunction

Urbach-Wiethe disease

A

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
Q

limbic system dysfunction

PTSD

A

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
Q

Korsakoff’s syndrome triad

A
  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
Q

Kluver-Bucy Syndrome

A
  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
Q

Alzheimer’s Dementia AD

A

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
Q

___% over 85yo have AD

A

over 50% over 85yo have AD

51
Q

according to engeland, treat AD with

A

donepezil (Aricept)

AChE

52
Q

Schizophrenia

Sx and incidence

A

fragmentation of mood, thought, and movement
Sx:
positive: delusions and hallucinations
negative: social withdrawal

1% US population diagnosed

53
Q

Schizophrenia

neurochemical basis hypotheses

A
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
Q

Depression

Sx and incidence

A

Sx:
lethargy, anhedonia, loss of sleep

15% US population
20% F, 13% M treated

55
Q

Depression

neurochemical basis hypothesis

A

“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
Q

Chronic Traumatic Encephalopathy (CTE)

A

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
Q

MCA stroke

A

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
Q

ACA stroke

A

weakness and sensory contralat SAME
anterior and medial frontal and parietal and temporal
LEGS
PERSONALITY CHANGES

59
Q

Lenticulostriate stroke

A

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
Q

Vertebral Artery stroke

A

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
Q

Basilar artery stroke

A

supplies rostral brainstem and occipital lboes
CN PALSIES, GAZE ISSUES, HEMIANOPSIA, MIOSIS
may cause LOSS OF CONSCIOUSNESS

62
Q

Posterior cerebral artery stroke (PICA)

A

supplies occipital lobes
HOMONYMOUS HEMIANOPSIA (of contralateral)
MACULAR SPARING
ACROMATOPSIA difficulty naming colors
nondom hem: neglect of affected vision field

63
Q

intracerebral hemorrhage

A

HTN

decreased vascular elasticity

64
Q

subarachnoid hemorrhage

A

rupture of intracranial aneurysms or trauma
thunderclap sudden HA, “worst headache ever”
N/V, nuchal rigidity, photophobia, change in consciousness

65
Q

ischemia stroke

A

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
Q

stroke imaging

A

non-contrast CT
for intracranial bleeding, including SAH, intracerebral bleeding or hematoma

MRI: ischemic stroke and focal cerebral ischemia

67
Q

when is cerebral angiography indicated?

A

to evaluate patients with ischemic strokes in vertebrobasilar distribution and subarachnoid/intraparencymal hemorrhage

68
Q

modifiable risk factors for stroke

A
HTN
DM
lipids
sympathomimetic abuse
smoking
EtOH
obesity
Afib
69
Q

non modifiable risk factors for stroke

A

age*most imp
race
ethnicity
heredity
Hispanic Americans, American Indians, Alaska Natives > white Americans
African Americans 2X than white Americans

70
Q

tPA for stroke

MOA

A

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
Q

tPA contraindecations

A
HBP
INTRACRANIAL HEMORRHAGE
SAH
rapidly resolving symptoms
MI, stroke, head injury in past 3 mo
GIB past 3 weeks
active bleeding
anticoagulation therapy
72
Q

hypothermia is resisted by

A

heat conservation: VASOCONSTRICTION

heat production: SHIVERING

73
Q

hypothalamus received input from ____ and ____ temperature receptors

A

skin (local) and spinal cord (central)

***2 sensory receptors

74
Q

local skin sensors cause release of ______

core SC temperature sensory send signals to CNS to activate _____

A

NO = VASODILATOR

SYMPATHETIC NERVE OUTFLOW (adrengergic and cholinergic)

75
Q

cold skin sensors release _____

A

NE = VASOCONSTRICTOR

76
Q

fever involves a pyrogen which stimulates the hypothalamus to produce _____

A

PGE2 = causes shivering

77
Q

hypothalamic temperature is special because

A

does not change in temperature (receives sensors from elsewhere)

78
Q

sympathetic receptors related to blood pressure regulation

A

NE interacts with:
Beta-1: stimulate HR, increase stroke volume
Alpha-1: increase total peripheral resistance

=increase BP

79
Q

blood pressure regulation pathway

A

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
Q

baroreceptors

A

attenuate (decrease) high BP

81
Q

if blood pressure drops >

A

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
Q

orthostatic hypotension

A

LBP when stand up from sitting or laying down

young people, most common cause: dehydration, not enough fluids

83
Q

inspiration requires

A
a PUMP (diaphragm and external intercostals)
a PACEMAKER to initiate breathing (Pre-Boetzinger area of ventrolateral medulla)
84
Q

stimulate _____ to innervate diaphragm

A
phrenic nerve (C3-5)
ACh and nicotinic receptor
85
Q

inputs to Pre-Boetzinger area

A

parafacial respiratory center SENSES CO2 (ACTUALLY H+) and DIRECTLY EXCITES ABDOMINALS

86
Q

BTW, how do you get H+ from CO2?

A

CA carbonic anhydrase

87
Q

Ondyne’s curse

A

lack of CO2 sensors&raquo_space;> HYPOVENTILATION

FATAL

88
Q

sympathetics control _______ of _______

parasympathetics affect ______ of _______

A

rate of breathing

dilation of bronchioles

89
Q

urination is controlled by both

A

voluntary and involuntary mechanisms
1. external sphincter VOLUNTARY
ACh and NICOTINIC

  1. internal sphincter INVOLUNTARY
    ACh and MUSCARINIC
    PARAsympathetic
90
Q

bladder full > sends AFF signals to

A

medial prefrontal cortex (usually suppresses voiding)

detected by STRETCH MECHANORECEPTORS

91
Q

Pontine micturition center activates

A

the sacral cord to stimulate PREganglionic PARAsympathetic nerves >
relaxation of external voluntary sphincter
contraction of urinary bladder

92
Q

urination involves dis-inhibitor of the micturition center when bladder is full, controlled by activation of which nerve

A

pudendal nerve > relax external sphincter

93
Q

incontinence Tx

A

ANTIMUSCARINICS

M3 antagonists

94
Q

HYPOkinetic disorders

A

DIRECT pathway INHIBITED
INDIRECT pathway ACTIVE
= decreased motor activity

PARKINSON DISEASE = LOSS OF DOPAMINERGIC NEURONS

95
Q

HYPERkineteic disorders

A

DIRECT pathway ACTIVE
INDIRECT pathway INHIBITED
= incrased motor activity

HUNTINGTON DISEASE = expanded CAG repeats

96
Q

parkinson disease Tx

A

RESTORE dopaminergic activity (not slow progression of disease)

LEVODOPA (prodrug) plus CARBIDOPA (inh AAAD) = sinemet

97
Q

adverse effects of L-DOPA

A

“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
Q

L-DOPA primary adverse effects

A
  • 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
Q

COMT inhibitors

A

ENTACAPONE

decrease peripheral metabolism of L-DOPA
(like AAAD, but not into DA, will be excreted instead)

smoother response
longer on time

100
Q

MAOI

A

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
Q

Dopaine receptor agonists

A

PRAMIPEXOLE D3 agonist

ROPINIROLE D2 agonist

direct action on D2 receptors in stiatum
becoming more first line
less SE

102
Q

muscarinic antagonists

A

Ach is NT for a small amount of striatal interneurons

TRIHEXYPHENIDYL

103
Q

Amantadine

A

antiviral

104
Q

PD Tx tissue transplantation?

A

human fetal adrenal medullary tissue into caudate nucleus

105
Q

PD surgery

A

pallidotomy: allieviates akinesia