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DESCRIBE THE ANS?
Autonomic nervous system. Maintains homeostasis.
Components are found in the PNS and the CNS . The peripheral autonomic nerves carry mainly EFFERENT fibers.
The motor component of the ANS is a TWO- NEURON system consisting of preganglionic (myelinated) and postganglionic neurons (unmeylinated).
Considered an INVOLUNTARY SYSTEM, and further broken down into the SNS and PNS.
DECRIBE THE FUNCTION OF THE SNS?
-Functions to mobilize energy stores in times of need (fight or flight)
-The SNS receives innervation from cell bodies located from T1 TO L2. Therefore is called "thoracolumbar division"
TRUE OR FALSE
THE PREGANGLIONIC FIBERS OF THE SNS FORM SYNAPES SHORTLY AFTER LEAVING THE CORD IN THE PARAVERTEBRAL GANGLIA,
TRUE
DESCRIBE THE FUNCTION OF THE PNS?
FUNCTIONS TO CONSERVE AND RESTORE ENERGY.
The nerve cells bodies are located in the cranial nerve nuclei, and in the sacral region of the spinal cord. Therefore constitute the "CRANIOSACRAL DIVISION"
The preganglionic fibers of the PNS, travel to ganglia close to the organs they innervate before forming synapses with the relatively short postganglionic neurons.
ACETYLCHOLINE?
Sympathetic preganglionic fibers and parasympathetic pre and postganglionic fibers release ACH.
Also released by somatic efferent neurons.
ENDOCRINE abnormalities can be caused by hypersecretion or hyposecretion of hormones, and also by which mechanisms?
ENDOCRINE abnormalities may also be caused by
a- A decrease in receptors
b- Receptor insensitivity to the hormone
c- Antibodies against specific receptors
d-Defects in second messenger generation or postreceptor defects.
DYSFUNCTION IN THE RELEASE OF HYPOTHALMIC HORMONES IS USUALLY A RESULT OF?
The interruption of the connection between the hypothalmus and the pituitary- namely the pituitary stalk.
CAUSES AND SYMPTOMS OF SIADH?
Disorder of posterior pituitary, characterized by abnormally high ADH secretion. HIGH ADH levels interfere with renal free water clearance, leading to hyponatremia, and hypoosmolality. Associated with certain cancers (ectopic secretion of ADH by tumor cells).
CAUSES AND SYMPTOMS OF DI?
Diabetes insipidus. May be neurogenic, caused by insufficient amounts of ADH.
Failure to concentrate urine, polydipsia, polyuria.
PITUITARY ADENOMA IS THE MOST COMMON CAUSE OF WHAT?
ACROMEGALY
GIVE EXAMPLES OF THE DIRECT EFFECT AND PERMISSIVE EFFECT OF HORMONES?
DIRECT- TSH stimulates secretion of thyroid hormone
PERMISSIVE-Cortisol enhances glucagon
DEFINE UP-REGULATION VS.
DOWN REGULATION?
UP REGULATION: IF synthesis of new receptors occurs faster than degradation of old receptors, the target cell will have more receptors and thus be more sensitive to hormones. Called up-reg. because the NUMBER of receptors goes up.
DOWN REGULATION- If the rate of the receptor degradation exceeds the rate of the receptor synthesis, the target cells number of receptors will decrease. Because the number of receptors and thus the sensitivity of the target cells goes down, this is called DOWN REGULATION.
EXAMPLES OF WATER SOLUBLE HORMONES?
CATECHOLAMINES
EXAMPLES OF LIPID SOLUBLE HORMONES?
STEROIDS, ANDROGENS, ESTROGENS, TESTOSTERONE, GLUCOCORTICOIDS, MINERALCORTICOIDS.
EXPLAIN THE HPA?
(HYPOTHALAMUS PITUITARY ACCESS)
Pituitary gland gets innervated from dorsal medial nuclei from CNS, info comes in from hypothalamus in, Pituitary will produce stimulation or inhibition of hormones.
WHERE IS THE PITUITARY IN RELATION TO THE HYPOTHALAMUS? (location)
Pituiary gland located in the sella turcica of the skull's sphenoid bones, and is connected to the hypothalamus by a stalklike infundibulum.
WHAT ARE THE HORMONES OF THE ANTERIOR PITUITARY?
FLAT PG
FSH
LH
ACTH
TSH
PROLACTIN
GROWTH HORMONE
WHICH CELLS ARE RESPONSIBLE FOR CALCITONIN SECRETION IN THE THYROID?
PARAFOLLICULAR
PARATHYROID LOCATION/ FUNCTION?
Located behind the upper and lower poles of the thyroid.
Regulate serum CALCIUM , antagonist to Calcitonin.
If dec. in Ca, will stimulate increased PTH secretion, will increase serum Ca levels.
Closely tied to magnesium levels and cAMP levels.
FUNCTION AND CHARACTERISITICS OF THE ADRENAL GLANDS?
80% OF ADRENAL GLAND'S TOTAL WEIGHT IS IN ADRENAL CORTEX.
-ZONA GLOMERULOSA MAKES ALDOSTERONE
-ZONA FASCICULATA MAKES CORTISOL
-ZONA RETICULARIS MAKES DHEA.
DESCRIBE INNERVATION OF ADRENAL MEDULLA?
Innervated by the SYMPATHETIC AND PARASYMPATHETIC NERVOUS SYSTEMS.
TRUE OR FALSE?
BOTH PSYCHOLOGICAL AND PHYSIOLOGICAL STRESSORS CAN STIMULATE THE PRODUCTION OF CORTISOL?
TRUE
DESCRIBE GRAVES DISEASE?
Most common form of hyperthyroidism, caused by an autoimmune mechanism that overrides normal mechanisms for control of TH secretion.
S/S include: diffuse thyroid enlargement, disorders of the skin, and enlargement of extraocular muscles. The cutaneous manifestation is pretibial myxedema.
WHICH CELLS SECRETE THE CATECHOLAMINES EPINEPHRINE AND NOREPINEPHRINE?
THE CHROMAFFIN CELLS IN THE ADRENAL MEDULLA.
"FIGHT OR FLIGHT"
PROMOTE HYPERGLYCEMIA (NUTRIENTS TO FIGHT)
PHENYLALANINE-TYROSINE-DOPA-DOPAMINE-NOREPINEPHRINE-EPINEPHRINE
WHAT ARE THE S/S OF SIADH AND THE PATHOPHYSIOLOGY?
HYPERSECRETION OF ADH.
FOR DIAGNOSIS: MUST HAVE
NORMAL ADRENAL AND THYROID FUNCTION.
THE PT WILL EXHIBIT HYPONATREMIA, HYPOOSMOLALITY.
DEFINE HASHIMOTO'S THYROIDITIS?
Hashimoto's is an AUTOIMMUNE disease in which the thyroid is attacked by T CELLS. Usually resulst in hypothryoidism, but can have bouts of hyperthyroidism.
On exam, hard goiter not painful to touch. Often misdiagnosed as depression or chronic fatigue syndrome. May have periorbital myxedema.
A TYPE 4 HYPERSENSITIVITY.
TREAT WITH LEVOTHYROXINE OR DESSICATED THYROID EXTRACT. TSH LEVELS SHOULD BE KEPT UNDER 3.0
ADDISON'S DISEASE?
CHRONIC ADRENAL INSUFFICIENCY. Rare Endocrine disorder where adrenal glands do not produce sufficient steroids (glucocorticoids/mineralcorticoids)
SYMPTOMS: Low BP, usually orthostatic hypotension, hyperpigmentation of skin, fatigue, muscle weakness, nausea, vomiting, diarrhea,
USUALLY TREATED WITH HYDROCORTISONE OR PREDNISONE,
IF IN CRISIS* IV INJECTIONS OF STEROIDS, AND SALINE SOLUTION WITH DEXTROSE.
CUSHING'S SYNDROME?
HIGH LEVELS OF CORTISOL IN THE BLOOD. Can be caused by tumors that secrete ACTH. Uusually an adenoma in the pituitary gland produces large amount of ACTH, which in turn elevates cortisol.
SYMPTOMS: RAPID WEIGHT GAIN, BUFFALO HUMP, MOON FACE, HYPERHIDROSIS, CENTRAL OBESITY. MAY HAVE POLYURIA AND POLYDIPSIA, PERSISTENT HTN AND POSSIBLY HYPOKALEMIA.
TREAT WITH:
TRUE OR FALSE? THE CHROMAFFIN CELLS OF THE ADRENAL MEDULLA RELEASE CATECHOLAMINES?
TRUE. Epinephrine and Norepinephrine.
TRUE OR FALSE?
The larger the diameter of the axon, the faster the conduction.
TRUE
Because more ions are able to come in, and depolarization occurs quicker.
Describe the action potential as it relates to neurons?
The action potential is passed down to the bottom of the axon, membrane potential change opens up Ca channels, Ca rushes in, vesicles are waiting to be released with neurotransmitters.
Describe the Limbic System?
Combination of overlapping regions. Numerous areas such as hippocampus. Modification/extensions of olfactory system. Involved in PRIMITIVE behavioral response: i.e. emotions, feeding behavior, sense of smell, biologic rhythms.
Limbic systems is everywhere.
Where is CSF made?
In the ventricles by Ependymal cells.
Which is the innermost part of the spinal cord that is closest to nervous system and adheres to spinal cord and brain?
PIA MATER.
What contributes to the grey color in GREY MATTER?
And conversely, the WHITE color in WHITE MATTER?
AND-
How is it distributed in brain vs spinal cord?
The grey matter consists of cell bodies and dendrites, which gives it the grey appearance.
Whereas, the white matter consist of myelin.
IN THE BRAIN, THE GREY IS OUTSIDE, AND THE WHITE INSIDE. IN THE SPINAL CORD, WHITE SURROUNDS THE GREY.
Frontal Lobe?
Prefrontal-Goal DIrected Behavior
Premotor-Basal Ganglia (initiate movement, restrict unwanted movement, if degeneration occurs, can lead to PARKINSONS.
PRIMARY MOTOR AREA, Broca Speech area as well.
Temporal Lobe?
Wernicke (speech)
Occipital Lobe?
Visual Cortex
MOTOR PATHWAYS?
CORTICOSPINAL=Goes thru pyramidal tract. MAIN MOTOR MVMT PATHWAY, info from cortex to spine. RESP. FOR VOLUNTARY AND FINE MVMTS.
RETICULOSPINAL- Takes info from reticular formation to spinal cord. Autonomic and gross mvmt.
RUBROSPINAL=red nuclei to spinal cord. Skeletal muscle, tone for posture.
TRUE OR FALSE?
UPPER MOTOR NEURONS CAN TRANSMIT INFO BUT CAN'T LEAVE THE CNS, SO IT SYNAPSES WITH LOWER MOTOR NEURON TO TAKE INFO TO MUSCLES?
TRUE!! :)
SENSORY PATHWAYS?
SPINOTHALAMIC- Pain and temp. Take info from spine up to thalamus. Cross over occurs right away as soon as enters spinal cord.
*Fine Touch and pressure. Kinethesis. DCML- Cross over at level of medulla.
What provides the major blood supply to the BRAIN?
The Internal Carotid and Vertebral Arteries.
Arterial circle- (circle of willis)
DESCRIBE the function and characteristic of the circle of willis?
The cerebral circle (circle of willis) is composed of:
Anterior cerebral artery (left and right)
Anterior communicating artery
Internal carotid artery (left and right)
Posterior cerebral artery (left and right)
Posterior communicating artery (left and right)
IF ONE PART BECOMES BLOCKED, THE BLOOD FLOW FROM THE OTHER VESSELS CAN PRESERVE CEREBRAL PERFUSION ENOUGH TO AVOID ISCHEMIA.
TRUE OR FALSE?
HYPERPARATHYROIDISM CAN CAUSE INCREASED OSTEOCLASTIC ACTIVITY?
TRUE
Posterior Pituitary gets innervation from where?
What hormones are produced there?
Gets innervation DIRECTLY from hypothalamus. Divided into the
pars nervosa, the infundibular stalk, the median eminence.
Hormones are: Oxytocin and vasopressin.
SIADH, hypersecretion of ADH from post. pituitary.
Anterior pituitary? Describe anatomy, function, hormones?
Located in sella turcica.
Composed of pars distalis, pars tuberalis, pars intermedia.
FLAT PG
FSH
LH
ACTH
TSH
PROLACTIN
GROWTH HORMONE
DESCRIBE THE HPA
(HYPOTHALAMUS-PITUITARY ACCESS)
HYPOTHALAMUS
PITUITARY GLAND
ANTERIOR PITUITARY
POSTERIOR PITUITARY
Pituitary gland gets innervated from medial nuclei from CNS, info comes in from hypothalamus, Piuitary gland will produce either stimulation of inhibition of hormones.
DESCRIBE THE ULTRA-SHORT, SHORT, AND LONG FEEDBACK LOOPS?
ULTRASHORT-target organ
SHORT-Goes back one step, from target organ to ant. pituitary or ant. pituitary to hypothalamus.
LONG- target organ feeds all the way back to hypothalamus.
TRUE OR FALSE
HORMONES OF THE POSTERIOR PITUITARY ARE MADE IN THE *HYPOTHALAMUS, AND HORMONES OF THE ANTERIOR PITUITARY ARE MADE IN THE *CELLS OF ANT. PITUITARY?
TRUE
WHAT ARE THE EFFECTS OF GROWTH HORMONE?
INCREASED CELL SIZE.
INCREASED MITOSIS.
DEVELOPMENT AND DIFFERENTIATION OF CELLS.
TRUE OR FALSE?
GLUCOCORTICOIDS STIMULATE PROTEIN CATABOLISM?
TRUE
TRUE OR FALSE?
THE MOST COMMON CAUSE OF HYPERPITUITARISM IS PITUITARY ADENOMA
TRUE
HYPERSECRETION OF GH CAUSES?
ACROMEGALY
DESCRIBE THE STEPS IN WALLERIAN DEGENERATION?
WHEN AN AXON IS CUT. WALLERIAN DEG. OCCURS DISTAL TO THE CUT.
1-A CHARACTERISTIC SWELLING
2-THE NEUROFILAMENTS HYPERTROPHY
3-MYELIN SHEATH SHRINKS AND DISINTEGRATES
4-AXON PORTION DEGENERATES AND DISAPPEARS.
DESCRIBE THE ROLE OF NEURO-GLIAL CELLS?
FOUND in the CNS, AND PNS,
and can provide structural support and nutrition for neurons, remove debris, increase the speed of nerve impulses, and play a significant role in memory.
WHICH PART OF THE SPINAL CORD IS INVOLVED IN PAIN TRANSMISSION?
SUSBSTANIA GELATINOSA
(located at the tip of the posterior horn)
DESCRIBE TEMPORAL SUMMATION?
Refers to the effects of successive, rapid impulses received from a SINGLE neuron on the same synapse.
WHAT IS THE FUNCTION OF THE THALAMUS?
MAJOR INTEGRATING CENTER FOR AFFERENT IMPULSES,
CEREBELLUM IS RESPONSIBLE FOR?
BALANCE AND POSTURE.
ALSO, CONSCIOUS AND UNCONSCIOUS MUSCLE SYNERGY.
FUNCTION OF PONS?
CONTROLS RESPIRATIONS AND IS THE LOCATION FOR CRANIAL NERVES V THROUGH VIII.
ALCOHOLICS ARE PRONE TO WHICH HEMATOMAS?
SUBDURAL HEMATOMAS.
ARTERIAL BLEED FROM BLD VESSELS THAT LINE THE SKULL.
TRUE OR FALSE?
EPINEPHRINE INDUCES GENERAL VASODILATION?
TRUE
TRUE OR FALSE?
PARASYMPATHETIC PRE AND POSTGANGLIONIC FIBERS RELEASE ACH?
TRUE
WHICH MEDICATIONS ARE USED TO TREAT THYROTOXIC CRISIS?
BETA BLOCKERS,
PTU
IODINE
WHAT IS THE CAUSE AND S/S OF MYXEDEMA COMA?
SEVERE HYPOTHYROIDISM
DIMINISHED LEVEL OF CONSCIOUSNESS, HYPOTHERMIA, HYPOVENTILATION, HYPOTENSION, HYPOGLYCEMIA, LACTIC ACIDOSIS.
TRUE OR FALSE
THYROID CARCINOMA IS THE MOST COMMON ENDOCRINE MALIGNANCY?
TRUE
allthough rare, it is the most common. Pt.'s have normal T3 AND T4 levels.
WHICH CRITERIA PROVIDE AN ACCURATE DISGNOSIS OF DIABETES?
An accurate diagnosis occurs with more than one fasting glucose greater than 126 mg/dl; plasma glucose value in the 2-hour sample of 200 mg/dl or greater; random glucose level greater than 200 mg/dl with symptoms of polydipsia, polyphagia, and polyuria; and impaired fasting glucose (IFG) as a fasting glucose greater than or equal to 110 mg/dl but less than 126 mg/dl.
WHICH TYPE OF DIABETES IS DEMONSTRATED BY PANCREATIC ATROPHY AND LOSS OF BETA CELLS?
TYPE 1 DIABETES.
DESCRIBE THE SOMOGYI EFFECT?
Unique combination of hypoglycemia followed by hyperglycemia.
TARGET CELLS FOR ALDOSTERONE LOCATED WHERE?
KIDNEYS
TRUE OR FALSE
PRIMARY EFFECT OF ADH IS WATER REABSORPTION?
TRUE
TRUE OR FALSE
PRIMARY PHYSIOLOGIC EFFECT OF INSULIN IS TO PROMOTE UPTAKE OF GLUCOSE INTO CELLS, TO BE STORED FOR METABOLISM.
TRUE
TRUE OR FALSE
HIGH LEVELS OF GLUCOCORTICOIDS SUCH AS CORTISOL CAN RESULT IN IMMUNOSUPPRESION?
TRUE
WHERE IS ACTH SYNTHESIZED AND RELEASED?
THE ANTERIOR PITUITARY
DECRIBE AUTONOMIC HYPERREFLEXIA?
A syndrome of a sudden and dangerous increase in blood pressure that may occur at any time after spinal shock resolves.
-Associated w massive CV response to stimulation of SNS.
-Usually affects indiv. w lesions at T6 or above.
-S/S: Paroxsymal hypertension, pounding headache, blurred vision, sweating above level of lesion,
nausea, piloerection.
-MOST COMMON CAUSE:
distended bladder or rectum.
BUT can be caused by stim. of skin or pain receptors.
TREAT WITH: Phenoxybenzamine
DESCRIBE BROWN-SEQUARD
SYNDROME?
(PARTIAL SPINAL CORD TRANSECTION)
-Associated with penetrating injuries, hyperextension and flexion, locked facets, and compression fractures.
S/S: Ipsilateral paralysis below level of injury, Ipsilateral loss of touch, pressure, vibration.
Contralateral loss of pain and temperature sensations below level of injury.
WATER SOLUBLE HORMONES?
EX: Insulin, Pituitary, Hypothamlic, and parathyroid hormones.
- Receptor/MOA= Plasma membrane receptors
-Circulate free unbound form
LIPID SOLUBLE HORMONES?
EX: Corticosteroids, sex hormones, T4, T3
Receptor/MOA= Easily diffuse across plasma membrane, Cytosol or nuclear receptors.
Circulate bound to a carrier or binding protein
TRUE OR FALSE
HYPERPARATHYROIDISM CAUSES INCREASED OSTEOCLASTIC ACTIVITY?
TRUE
INCREASED TSH, AND DECREASED T4?
PRIMARY HYPOTHYROIDISM
SECONDARY HYPERPARATHYROIDISM USUALLY CAUSED BY?
HYPOCALCEMIA DUE TO RENAL FAILURE (MOST COMMON)
CHARACTERISTICS OF MUSCLES?
Skeletal muscle attaches bone to bone.
Anatomical muscle moves from origin to insertion.
Muscle cells are the LARGEST CELLS.
MULTI-NUCLEATED.
One single cell can contain thousands of myofibrils.
Muscle is encased in the epimyseum.
DESCRIBE THE LOCATION AND ROLE OF THE T TUBULE?
Deep invagination of the sarcolemma (the plasma membrane of muscle cells)
Allows for DEPOLARIZATION of the membrane, to quickly penetrate the inside of the cell.
Major site for coupling of excitation and contraction.
SARCOPLASMIC RETICULUM?
STORES AND PUMPS CALCIUM IONS.
CALCIUM IS RELEASED INTO THE CYTOPLASM FROM THE S.R.
DIFFERENCE BETWEEN VOLTAGE DEPENDENT CHANNEL AND CALCIUM INDUCED CHANNEL?
Voltage dep= Open as a result of depolarization of sarcolemma.
Ca induced (Ryanedine) Channel=On sarcoplasmic reticulum, open in response to action from DHP receptors, allow Calcium in.
DESCRIBE THE STEPS OF MUSCLE CONTRACTION?
(BIND, FLICK, RELEASE, REPOSITION)
When calcium comes in to bind with troponin, it causes troponin to move tropomyosin, exposing the myosin site. Myosin then binds with actin, and muscle contracts.
BIND- Myosin head attaches to actin filament, when it binds it releases a phosphate
FLICK- the head flicks, moves actin past the width of one globular protein (one actin)
RELEASE-ATP binds to actin head, RELEASE
REPOSITION- ATP hydrolyzed, head repositions.
WILL CONTINUE AS LONG AS CALCIUM IS IN THE CYTOPLASM, TROPOMYSIN REMOVED, AND MYOSIN EXPOSED.
*Muscle is relaxed when there is no binding of actin and myosin*
*IF a muscle runs out of ATP, the step that stops is the release*
CREATINE PHOSPHATE?
CREATINE KINASE?
Stored energy in form of creatine phosphate. C.P. will give energy to ADP forming ATP. Smaller molecule and diffuses faster.
ATP in muscle cell good for a second or two, C.P. good for 7 or 8 seconds.
CREATINE KINASE- The enzyme that converts creatine to creatine phosphate.
CREATINE KINASE- IF in the bld, an indicator of muscle damage (appears quickly)
CK-MB (CARDIAC)
CK-MM (SKEL. MUSCLE)
CK-BB (BRAIN)
ROLE OF SATELLITE CELLS?
Respond to injury and provide additional nuclei for hypertrophied muscle.
Create daughter cells, fuse w muscle, new nucleus, now bigger and stronger to deal with whatever triggered myotrauma.
OSTEOBLASTS?
OSTEOCLASTS?
CHONDROBLASTS?
FIBROBLASTS?
OSTEOCYTES?
OSTEOBLASTS become osteocytes. (mesenchymal origin)
OSTEOCLASTS- resp. for bone breakdown (hematopoeitic origin)
CHONDROBLASTS- become chondrocytes, hyalin cartilage.
FIBROBLASTS- become fibrocytes, tendon and ligament.
OSTEOCYTES maintain serum calcium, long lived in matrix.
DUCHENNE'S MUSCULAR DYSTROPHY?
Most common musc. dz, mostly males, X linked recessive.
DEFECT W/DYSTROPHIN.
Tensions on sarcolemma, and is torn as muscle is used. Microtears in plasma membrane, whn muscle grows bk not stronger, end result, muscles DEGENERATE.
Initially elevated CK, later muscles so damaged don't leak CK.
test: muscle biopsy, serum CPK
TREAT: symptoms (pain)
encourage activity.
By age 12 most in wheelchair,
Usually die by age 25.
MYASTHENIA GRAVIS?
AUTO IMMUNE.
Auto-antibodies against Ach receptors. When Ach is dumped into the synaptic cleft, there are no receptors, so muscle contx. doesnt occur.
TREAT: ACH esterase inhibitor, slows the rate it is broken down
MYASTHENIC SYNDROME?
Auto antobodies against Calcium channel. Calcium channel is blocked, no calcium comes in, no release of Ach.
TRUE OR FALSE, MVA'S ARE THE MAJOR CAUSE OF TRAUMATIC CNS INJURY?
TRUE
DIFFERENT TYPES OF FOCAL BRAIN INJURY?
CONTUSION (BRUISING OF BRAIN)
LACERATION (TEARING OF BRAIN TISSUE)
EPIDURAL HEMATOMA (BLOOD ABOVE THE DURA MATER)
SUBDURAL HEMATOMA ( BLOOD BETWEEN DURA AND ARACHNOID MEMBRANE)
INTRACEREBRAL HEMATOMA (BLEEDING INTO THE BRAIN)
AND OPEN HEAD TRAUMA
Describe DAI?
Diffuse Axonal Injury.
Results from the effects of head rotation. Shearing stresses.
Basal skull fracture commonly associated with moderate DAI.
May exhibit decorticate or decerebrate posturing.
treat w hypothermia, mannitol, but not effective always.
CONCUSSIONS?
MILD-temporary axonal disturbances.
GRADE I= Confusion and disorientation accompanied by amnesia (momentary)
GRADE II=Momentary confusion and retrograde amnesia dev after 5-10 min
GRADE III= Confusion and retrograde amnesia present from impact.
GRADE IV= diffuse cerebral disconnection from the brainstem RAS, immediate LOC, which lasts up to 6 hours.
DISCUSS SPINAL CORD TRAUMA?
Usually males, mostly young adults. MVA'S, and falls. Older adults more at risk from falls.
FIRST STEP: IMMOBILIZATION
SECONDARY SPINAL CORD INJURY OCCURS WITHIN MINUTES. Microscopic hemmorrhages appear in grey matter and pia arachnoid. Edema in white matter. Within 4 hours, swollen axis cylinders develop. May progress to ischemia. Hemorrhages are maximal at level of injury and two cord segments above and below it.
In cervical region, can be life threatening bc of impairment of diaphragm function.
Circulation to white matter returns to normal in 24 hours, while grey matter circ. remains altered.
SPINAL SHOCK?
COMPLETE LOSS OF REFELX FUNCTION in all segments below the level of the lesion. Paralysis, flaccidity, absence of sensation, transient drop in BP.
Faulty control of sweating bc hypothalamus cant regulate body heat.
MAY LAST FOR 7-20 DAYS,
Signs of improvement: return of reflex activity, hyperreflexia,
spacticity, and reflex emptying of bladder.
NEUROGENIC SHOCK?=
Occurs with cervical or upper thoracic cord injury.
Loss of sympathetic outflow: Vasodilation,
Bradycardia, Hypotension, Hypothermia.
SUBDURAL HEMATOMA?
Blood gathers between dura and arachnoid.
MVA'S most common cause.
50% assoc. w skull fractures.
falls, alcoholics.
Tearing of bridging veins.
Burr holes or craniotomy.
BLUNT FORCE TRAUMA?
Basilar skull fractures occur because of blunt trauma and describe a break in the bones at the base of the skull. These are often associated with bleeding around the eyes (raccoon eyes) or behind the ears (Battle's sign). The fracture line may extend into the sinuses of the face and allow bacteria from the nose and mouth to come into contact with the brain, causing a potential infection.
Osteogenesis Imperfecta?
Genetic disorder of collagen.
Usually autosomal dominant.
Some have increased thyroxine levels.
RICKETS?
Growing bone fails to become mineralized (ossified).
Soft bones and skeletal deformities.
Insufficient vitamin D
S/S OF THYROTOXIC CRISIS AND TREATMENTS?
Can be triggered by extreme sickness or physical stress.
tachy, temp over 104F, arrhythmia, vomiting, diarrhea.
TREAT with PTU, beta blockers, steroids.
DESCRIBE DIFFERENCE BETWEEN BLOODFLOW TO ANT/PITUIARY VS POST. PITUITARY?
ANTERIOR PITUITARY IS MOST GREATLY AFFECTED BY LACK OF BLOODFLOW TO BRAIN!!
THE POST. PITUITARY GETS BLOOD FROM THE INTERNAL CAROTID.
HYPERPIGMENTATION ASSOCIATED WITH ADDISON'S IS DUE TO?
ELEVATED MSH
S/S OF PHEOCHROMOCYTOMA AND TREATMENTS?
SECRETE CATECHOLAMINES ON A CONTINUAL BASIS.
PERSISTENT TACHY, HTN, HEADACHE, SWEATING.
VERY VASCULAR, CAN RUPTURE.
SURGERY.
CAN TREAT BP W ALPHA ADRENERGIC OR BETA BLOCKERS.
PRIMARY ADRENAL INSUFFICENCY IS TERMED?
ADDISON'S DISEASE.
CHARACTERIZED BY ELEVATED ACTH LEVELS.
CHECK SERUM AND URINE LEVELS OF CORTISOL (DEPRESSED)
HYPONATERMIA COMMON.
*HYPERKALEMIA*
GLUCOCORTICOID AND MINERALCORTICOID REPLACEMENT THERAPY
OSTEOGENESIS IMPERFECTA?
COLLAGEN FIBRILS AND HYDROXYAPATITE CRYSTALS TO FORM BONE IS ALTERED.
*BLUE SCLERA*
DIFFERENCE BETWEEN SLOW OXIDATIVE MUSCLE AND FAST GLYCOLYTIC MUSCLE FIBERS? TYPE I AND TYPE IIA
*SLOW*
High fatigue resistance, work aerobically, many mitochondria,
glycogen content low, myoglobin content high (dark meat) many capillaries, recruited over and over again, smaller diameter and weaker.

*FAST* have ATP stored, anaerobic respiration, few mitochondria, capillarys low, glycogen content high, larger in diameter and stronger.