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59 Cards in this Set
- Front
- Back
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Dual embryological origins of the pituitary gland
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The anterior pituitary is from
Rathke’s pouch, an invagination of the roof of the mouth The posterior pituitary is the neurohypophysis, (derived from the floor of the third ventricle) |
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Circumventricular organs
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Circumventricular organs
are breaks in the Blood- brain barrier that allow adjacent neurons to sample the contents of the blood |
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Inputs to hypothalamus
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Cortex
-Orbito frontal cortex Amygdala -via Bed nucleus of the stria terminalis -ventral amygdalofugal pathway Hippocampus -Via the fornix Septal area -Via the medial forebrain bundle Thalamus Retina -Via optic tract -Non reciprocal Brainstem nuclei & Spinal Cord -Nucleus of the Solitary tract via medial forebrain bundle -dorsal longitudinal fasciculus |
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Outputs of hypothalamus
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Follow reciprocity rule
Cortex -Amygdala --stria terminalis -Septal area (Forebrain) --medial forebrain bundle Brainstem and Spinal Cord: -Descending autonomic control to brainstem and spinal cord preganglionic neurons for autonomic outflow -Multi-synaptic --medial forebrain bundle, --dorsal longitudinal fasciculus --mammillotegmental tract -Thalamus - anterior thalamic nucleus --via mammillothalamic tract Pituitary Gland -Hypothalamo-Hypophyseal pathways (not reciprocal) |
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Hypothalamus and short term thermoregulation
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Two sets of temperature receptors allow comparison of external and internal temperatures
-Peripheral sensors - thermoreceptors in skin (anterolateral pathway) and viscera -Central sensors - thermoreceptors in hypothalamus -Peripheral input projects to warm and cold sensitive neurons Warm sensitive nuclei in preoptic and anterior hypothalamus -increase firing as body temp increases -project to PVN and lateral hypothalamus to activate a sympathetic response of vasodilation and sweating -lesions result in hyperthermia Cold sensitive neurons located in posterior hypothalams -activate a sympathetic response of vasoconstriction and shivering -lesions result in hypothermia |
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Hypothalamus and long term thermoregulation
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Temperature can control voluntary motor activities
-Get out o the sun -Build an igloo -Move from Cleveland to North Carolina Endocrine control of thermoregulation -upregulation of thyroxine production and release |
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Pyrogens and antipyresis
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Pyrogens are proteins that induce fever
-Temperatures outside physiological range -->100oF or 37.5o C -exogenous --microbial toxins like lipopolysaccheride -endogenous --Cytokines like IL-1, IL-6 &TNF-alpha Exogenous pyrogens act by increasing the levels of endogenous pyrogens -Activate PGE in OVLT & preoptic area to increase temperature set point |
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Antipyresis
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Vasopressin acts as an endogenous antipyretic agent in the anterior hypothalamus and ventral septal nuclei
-Only active at fever-level temperatures Aspirin and other NSAIDs inhibit cyclooxigenase to reduce the production of PGE |
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Classic view of hypothalamic regulation of food intake
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Stimulation of the lateral hypothalamus elicits feeding
-Lesions result in aphagia Stimulation of the ventromedical hypothalmus suppresses feeding -Lesions result in hyperphagia |
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Neurochemical circuitry of feeding
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The arcuate nucleus detects most humoral messengers
-Most effective VMH lesions included it Leptin-activated ARC neurons modulate eating-related activity in VMH to reduce feeding -ARC neurons express other feeding related peptides -co-express NPY & AgRP: Stimulate food intake -co-express POMC & CART: Inhibit food intake Orexin elicits feeding -Orexin-containing neurons are found in the LHA -Leptin inhibits orexin-containing neurons PVN = output to endocrine and brainstem feeding networks |
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Regulatory cues for feeding
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Short term:
Food stimuli -Food in mouth stimulates feeding -Food in stomach inhibits feeding Humoral satiation cues -CCK, CLP-1, -Grehlin -glucose Long-term responses: Hypothalamus regulates body weight around a set point -Endocrine involvement -Thyroid hormone Humoral signals about fat -Leptin -Insulin DBS near VMH reduced body weight and body fat in monkeys! |
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Hypothalamus and sexual and reproductive behavior overview
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Development and release of gametes regulated by pituitary gonadotropins
Preoptic region involved in male sexual behaviors such as arousal - erection, mounting and ejaculation Ventromedial nucleus important in female sexual behaviors (receptive behaviors e.g., lordosis in animal models) Sexually-dimorphic nuclei differ in males and females |
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Hypothalamic response to estrogen and female sexual behavior
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Circulating estrogen binds to receptors in neurons within the ventromedial nucleus of the hypothalamus.
Activated estrogen receptor alters neuronal gene expression to produce progesterone receptors Circulating progesterone stimulates the primed ventromedial neurons and VM activity results in proceptive sexual behaviors with ovulation to enhance fertilization |
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Hypothalamus medial preoptic area
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Medial Preoptic n is sexually dimorphic
-= 3rd interstitial nucleus of the anterior hypothalamus (INAH3) in humans -Releases gonadotropin releasing hormone -Plays a role in male copulation -1.7 times as large in heterosexual men as in women, who are equal to homosexual men -Some evidence that suprachiasmatic n is 2X as large in homosexual than heterosexual men -Male to female transsexuals have INAH3 nuclei that look female and female to male transsexuals have INAH# nuclei that look male |
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Hypothalamus and circadian rhythms
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Cylcical patterns of physiological and behavioral changes
-Sleep-wakefulness -Body temperature -Hormonal cycles Rhythm originates in suprachiasmatic nucleus -Direct retinal inputs -SC (suprachiasmatic) projects to PVN -PVN to intermiate lateral cell column -Projections to pineal gland via sympathetic outflow -Pineal secrete melatonin Lesion of the Suprachiasmatic Nucleus disrupts the sleep wake cycle (biological clock). |
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Hypothalamus projections to brainstem and spinal centers ANS
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Rostroventrolateral medulla controls sympathetic tone along with intermediolateral cells column
-PVN projects to RVLM and the intermediolateral cell column Dorsal motor n of the vagus and n ambiguous supply parasympathetic control -Dorsomedial and posterolateral nuclei supply activation -Anterior nuclei activate parasympathetics |
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Hypothalamus and endocrine control overview
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Hypothalamus converts complex CNS processing into direct and indirect endocrine responses via the pituitary gland
-Posterior hypothalamus – direct endocrine responses --Posterior pituitary -Anterior hypothalamus – indirect endocrine responses --Anterior pituitary Circulating hormones levels are regulated by feedback to the hypothalamus and pituitary gland |
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Hypothalamus response to both neural and humoral signals
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Neural input (stimulus) - neural output (response)
-e.g., behavioral control of body temperature Neural input - humoral output -e.g., milk ejection – Post. Pituitary release of oxytocin - lactation Humoral input - neural output -e.g., circulating leptin stops feeding behavior Humoral input - humoral output -e.g., control of ACTH secretion by cortisol feedback |
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ADH (vasopressin) and oxytocin
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ADH or vasopressin stimulates kidney tubules to reabsorb water and increase blood volume.
Oxytocin stimulates uterine contraction and milk let down. Neuroendocrine Control: Hypothalamic Release of Hormones in the Posterior Pituitary |
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Direct hypothalamic control of hormone secretion
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Magnocellular (i.e., large) neurons in paraventricular and supraoptic nuclei
Synthesize and release -vasopressin (ADH or antidiuretic hormone) -oxytocin Hormones released at axon terminals in posterior pituitary capillary bed for systemic circulation |
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Hypothalamus and fluid regulation
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Magnocellular neurons in the paraventricular and supraoptic nuclei secret ADH in response to measurements of low blood volume.
The hypothalamus is sensitive to changes in blood volume measured by: Tissue osmolarity is measured by osmoreceptors in the hypothalamus – at a high concentration threshold the kidney increases water resorption to increase the volume of water in plasma and dilute solutes. Fluid volume (i.e., pressure) is measured by baroreceptors in blood vessels – at a low pressure threshold the kidney increases water resorption to increase blood volume and increase blood pressure. Magnocellular neurons in the paraventricular and supraoptic nucleus produce arginine vasopressin (AVP) that is transported by axons to the posterior pituitary where it released by axons directly into blood |
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Hypothalamic control of urine production
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Hypothalamic control of urine production:
Low volume (high osmolarity) and low blood pressure signals from the carotid sinus and the aortic arch to the solitary nucleus provide the neural sensory limb to the hypothalamus for a neuroendocrine reflex. The sensory input increases firing of magnocellular neurons in the parvocellular and supraoptic neurons in the hypothalamus. This increased firing results in the increased synthesis and release of vasopressin (ADH) (the neuroendocrine motor limb of the reflex) by axons in the posterior hypothalamus. ADH increases water absorption in the kidney to restore blood volume, increase blood pressure and reduce tissue osmolarity |
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Diabetes insipidus and urine production
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Defect in vasopressin (or ADH) synthesis or ADH release
Often a result of hypothalamic damage – ADH deprivation (neurogenic DI) Can also arise from kidney insensitivity to circulating ADH (nephrogenic DI or vasopressin resistant DI) Characterized by polyuria and polydipsia -(large volume of pale urine, dehydration, extreme thirst) Treated with synthetic ADH analogs |
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Indirect hypothalamic control of endocrine function via anterior pituitary
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Mediated by parvocellular neurons in multiple nuclei
-Preoptic -Periventricular -Arcuate -Tuberal Neurons produce peptides that are released into hypophyseal portal system -Called releasing hormones (or factors) -first capillary bed in median eminence Carried to anterior pituitary portal veins Regulate the release of anterior pituitary hormones into the systemic circulation -Second capillary bed |
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Anterior pituitary and their releasing factors
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The hypothalamus indirectly regulates the secretion of 6 hormones synthesized and released by endocrine cells in the anterior pituitary gland. These are:
GH – growth hormone TSH – thyroid stimulating hormone ACTH – adrenocorticotropic hormone FSH – follicle stimulating hormone LH – luteinizing hormone prolactin |
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Hypothalamus and stress response
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Endocrine portion is the Hypothalamic-pituitary-adrenal axis
Corticotropin Releasing Hormone -Regulates the release of ACTH from the ant pituitary -Is a central neurotransmitter Norepinephrine is also a central & peripheral mediator of stress resonse Activation of the Sympathetic Nervous System leads to fight or flight response |
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Feedback control of cortisol levels
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The hypothalamic – pituitary – adrenal axis is important in mediating or translating complex cortical functions into a hormonal stress response.
The hypothalamic production of CRH (corticotropin releasing hormone) stimulates the synthesis and release of ACTH by endocrine cells in the anterior pituitary gland. ACTH stimulates the release of glucocorticoids and cortisol in the adrenal cortex which mediate a systemic stress response. High levels of cortisol provide negative hormonal feedback to reduce the synthesis and release of CRH in the hypothalamus and ACTH in the anterior pituitary. This is one example of the endocrine system regulating the hypothalamus via negative feedback. Prolonged negative feedback from high levels of endogenous adrenal corticosteroids or form treatment with high levels of exogenous glucocorticoid medications including cortisone, hydrocortisone, dexamehtasone or prednisone can permanently reduce or shut down the production of CRH and/or ACTH. Excess endogenous adrenal corticosteroids or exogenous glucocorticoid medications can produce Cushing’s Syndrome (a “spiderlike” body with round moon-shaped face, fat deposition on the trunk, as well as acne, poor wound healing, hypertension, diabetes, edema, immunosupression, amenenorrhea and psychiatric disorders). Cushing’s Disease is caused by an anterior pituitary tumor that over-secrets ACTH and is a principal cause of Cushing’s Syndrome. |
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Anorexia nervosa definition
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Significantly underweight (<85 % of normal body weight)
Intense fear of gaining weight Abnormal body image and or undue influence of body image on self-evaluation Amenorrhea Females predominate ~20:1 |
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Genetics and social factors in anorexia nervosa
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Genetics
-Sister 6% incidence -Monozygotic twins show greater concordance then dizygotic twins Social and cultural factors -Identified as early as 1689 -Increasing prevalence in the past 50 years -Primarily in affluent cultures and higher SES |
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Psychological theory of anorexia nervosa
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Failed early attachment
Chronic Feelings of Inadequacy Family Enmeshment Rigidity Control issues Low emotional expression Highly compliant, cautious |
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Physical findings in anorexia nervosa
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Lanugo hair
Bradycardia, hypotension, arrhythmias Anemia, leukopenia Electrolyte abnormalities (low K, Na, Cl) Alkalosis and elevated BUN/creatinine Delayed gastric emptying, constipation Low thyroxine, LH Elevated cortisol |
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Assessment in anorexia nervosa
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Current weight (<75 % normal consider hospitalization)
CBC, CMP, EKG Weight history (min, max, desired) R/O medical causes for anorexia (Chrohn’s disease, gastric outlet obstruction, brain tumor) |
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Course in anorexia nervosa
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20% mortality in 10-30 years
30-50% make full recovery 30-50% have re-hospitalization |
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Treatment of anorexia nervosa
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Education, health consequences
Family Therapy – esp. if early onset with < 3 years of symptoms Structured Behavioral Therapy Nutritional Counseling Individual therapy SSRI – especially with OCD type symptoms Mirtazapine (Remeron) – antiemetic, encourages appetite |
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Bulimia nervosa definition
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Binge eating – larger then normal amounts of food consumed
Sense of loss of control Purging – vomiting, use of emetics, laxatives, diuretics Fasting Over-exercising |
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Bulimia nervosa epidemiology
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1-4 % of young women
Females predominate 10:1 Co-morbidity with depressive disorders, anxiety disorders, substance abuse, and personality disorders Family history of obesity or depression |
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Bulimia nervosa physical signs
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Knuckle excoriations
Tooth enamel erosion Alkalosis Parotid gland hypertrophy Low K+, Na+, and Cl- |
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Treatment of bulimia nervosa
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Individual Therapy – CBT, Interpersonal, supportive/expressive
Antidepressants: Mainly SSRIs MAO-Is and Bupropion (Wellbutrin) contraindicated |
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Gerstmann syndrome
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Right-left confusion
Agraphia Acalculia Finger agnosia Indicates involvement of left angular gyrus (dominant parietal lobe) |
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Wernicke's encephalopathy, normal-pressure hydrocephalus, tabes dorsalis
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Ataxia of gait, oculomotor abnormalities, acute confusional state: Wernicke’s encephalopathy (due to thiamine deficiency)
Ataxia of gait, incontinence, dementia: normal-pressure hydrocephalus Ataxia of gait, lightning-like pains, incontinence, loss of proprioception and vibration in legs, positive Romberg sign, areflexia, Charcot joints, Argyll Robertson pupils: tabes dorsalis |
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Temporal patterns of illness
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Monophasic (single episode with recovery)
-This may not be known in the acute stage, but how the disease plays out over time can affect the ultimate diagnosis. Relapsing and remitting -Most common pattern in multiple sclerosis -Myasthenia gravis Chronic static (“static encephalopathies”) -Cerebral palsy due to birth asphyxia -Previous traumatic injury Chronic with gradual worsening -Neurodegenerative diseases -Growth of mass Chronic with stepwise worsening -Multiple infarcts |
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Motor unit definition and denervation
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Definition: a lower motor neuron and all the muscle fibers it innervates
Denervation of muscle results in: Atrophy Fasciculations: spontaneous twitching of all myofibers in an affected motor unit Fibrillations: spontaneous twitching of an individual myofiber -Cannot see these clinically except in tongue -Detected on electromyography |
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Disorders of tone
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Flaccidity: no resistance to passive stretch
Spasticity: -Increased tone + hyperreflexia -Resistance proportional to velocity of stretch -Antigravity muscles exhibit increased tone -Flexors of arms and extensors of legs -Clasp-knife phenomenon Rigidity (basal ganglia lesion): increased resistance in all directions of movement in all muscles Paratonia (gegenhalten): apparent active resistance to movement when limbs are passively moved (frontal lobe dysfunction) |
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Rating of strength
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0/5 = no contraction of muscle
1/5 = muscle flicker, but no movement 2/5 = movement, but not against gravity 3/5 = movement against gravity, but not against resistance by examiner 4/5 = movement against some resistance 5/5 = normal |
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Reflex scale
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0 = absent
1 = trace, seen only with re-enforcement 2 = normal 3 = brisk 4 = non-sustained clonus 5 = sustained clonus |
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Features of weakness due to muscle disorders
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Pattern of weakness:
-Proximal > distal muscle involvement is most common Tone: normal Atrophy: present late (< atrophy due to denervation) No fasciculations Reflexes: normal; decreased late No sensory loss |
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Features of weakness due to NMJ disorders
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Fluctuating weakness, especially increasing weakness with exertion is most characteristic sign
Pattern of weakness: -Proximal > distal -Ocular -Bulbar Normal tone and reflexes No atrophy or fasciculations No sensory loss |
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Features of weakness due to peripheral neuropathy or radiculopathy
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Pattern of involvement:
-In distribution of nerve root (radiculopathy) -In distribution of a single peripheral nerve (mononeuropathy) -In distribution of multiple peripheral nerves (mononeuropathy multiplex) -Distal symmetric polyneuropathy Sensory loss often present and in same pattern of distribution Tone: normal to decreased Reflexes: diminished to absent in involved areas Atrophy in denervated muscles Fasciculations: not usually visible, but are seen on electromyography |
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Features of weakness due to LMN dysfunction
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Pattern of weakness: motor units of involved LMNs
Changes due to denervation of muscle: -Atrophy -Fasciculations Tone: decreased to flaccid Reflexes: decreased to absent No sensory loss unless lesion also involves sensory tracts LMN signs with sensory loss -Mixed sensory and motor peripheral nerve(s) -Anterior and posterior spinal nerve roots LMN signs without sensory loss -Anterior spinal gray matter (e.g., polio, spinal muscular atrophy, tumors, syrinx, etc.) -Anterior spinal nerve roots -Pure motor peripheral nerve(s) -Motor axons |
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Features of weakness due to UMN dysfunction
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Hyperreflexia
Tone: -Spasticity is characteristic -In acute lesions, flaccidity may be present transiently. Atrophy from disuse (less severe that denervation atrophy) No fasciculations Does not cause sensory loss, but sensory findings may be present if lesion involves sensory tracts as well as UMNs. Pattern of weakness from a single lesion: -Group of muscles, never individual muscles; -Lesion above the level of facial nucleus weakness: UMN paresis of face and body on the same side and contralateral to the lesion. -Pontine lesion involving facial nucleus or nerve and corticospinal tract: LMN facial paresis ipsilateral to lesion and hemiparesis (of body) contralateral to weakness. -Between facial nucleus and decussation of pyramids: hemiparesis contralateral to lesion; no facial weakness. -Below decussation of pyramids: hemiparesis or monoparesis ipsilateral to lesion; quadriparesis or paraparesis (if both side of spinal cord involved); pattern depends on level of spinal cord injury |
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Localizing UMN lesions
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Is the problem in the cerebral cortex, subcortical white matter, brainstem, or spinal cord?
-Pattern of weakness: face, arm, and leg -Evidence of cortical dysfunction: --Higher cortical functions: aphasia, apraxia, agnosia, neglect --Cortical sensory loss --Homonymous visual field defect --Some horizontal gaze palsies |
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Horizontal conjugate gaze localization
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Lesion in frontal eye field: eyes deviate toward side of lesion
Lesion in MLF: internuclear ophthalmoplegia (INO); failure of adduction of ipsilateral eye; +/- nystagmus in contralateral abducting eye; bilateral INO almost always due to MS. Lesion in pons: eyes deviate away from side with lesion |
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Signs of brainstem lesion
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Cranial nerve dysfunction: tells level of lesion
Crossed weakness: ipsilateral cranial nerve palsy with contralateral hemiparesis Loss of pain and temperature on ipsilateral face and contralateral body (spinal tract of V + spinothalamic tract): lateral brainstem lesion Dissociated sensory loss: loss of sensory modalities of one sensory pathway but not the other (can also occur in spinal cord) -Involvement of medial lemniscus with sparing of spinothalamic tract: medial brainstem lesion -Involvement of spinothalamic tract with sparing of medial lemniscus: lateral brainstem lesion Some gaze palsies (see previous slide): medial brainstem lesion between oculomotor and abducens nuclei. |
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Transverse myelopathy
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Trauma
Extradural compression by herniated cervical disc, tumor, epidural abscess Inflammatory diseases (transverse myelitis) -May be seen with multiple sclerosis Complete spinal cord lesion |
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Brown Sequard syndrome
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Trauma
Compression by herniated cervical disc or extradural tumor Tumor in spinal cord Hematoma in spinal cord Rarely seen in pure form Hemicord lesion |
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Central cord syndrome
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Acute hyperextension injury, especially if accompanied by congenital stenosis of cervical spinal canal or cervical spondylosis
Tumor in spinal cord Hemorrhage in spinal cord Syringomyelia (syrinx) = cavity in spinal cord -Idiopathic -May be associated with obstruction of foramen magnum, e.g., Chiari I malformation = developmental defect resulting in downward displacement of cerebellar tonsil into cervical spinal canal. -May be associated with spinal cord tumor or result of trauma, inflammation, infarction, or cord compression Hydromyelia = dilation of central canal of spinal cord (developmental) Lesion in center of spinal cord |
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Posterior cord syndromes
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Posterior cord syndrome:
-Tabes dorsalis (a form of neurosyphilis) Posterior columns + corticospinal tracts -Subacute combined degeneration of spinal cord (demyelination due to Vitamin B12 deficiency) Posterior cord + corticospinal tracts + spinocerebellar tracts -Friedreich’s ataxia |
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Anterior cord syndrome
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Anterior spinal artery infarct
Compression by herniated cervical disc or tumor located anterior to cord |
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Conus medullaris and cauda equina syndromes
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Conus medullaris
Symmetrical saddle anesthesia Symmetrical weakness, if lesion involves segments rostral to S2 Early and complete loss of sphincter and sexual function -Distended, atonic bladder with overflow incontinence -Loss of rectal tone and fecal incontinence -Constipation Spontaneous pain usually absent Patellar reflexes usually spared Causes: trauma, spinal cord tumor, vascular malformation, infectious or inflammatory process Cauda equina Involvement of multiple nerve roots Radiating (radicular) pain common Asymmetrical sensory loss and weakness Sphincter dysfunction occurs late and is often incomplete Causes: nerve sheath tumor (schwannoma or neurofibroma), meningiomas, neoplastic meningitis, compression by herniated disc or epidural tumor, arachnoiditis, polyradiculitis |
