Medical and surgical nursing notes for nle epinephrine thyroid what is anoxic encephalopathy

I. Cell s – A. Neu ron s properties and characteristics a. Exc ita bil ity – abi lit y of ne uro n to be af fec ted in exte rna l env iron men t. B. Condu ctivit y – abili ty of neur on to tran smit a wave of ex citat ion fr om on e cel l to a noth er c. Perma nent cells – once destro yed, cant regen erate (ex. Heart , retina , brain , osteoc ytes) regenerative capacity A. La bile – once d estroy ed ca nt rege nerate – epidermal cells, G IT cells, resp ( lung cells). GUT B. Stable – capable of regen eration BUT limited time only ex sa livary gland, pancreas cells cell of liver, kidney cells C. Perma nent cells – retina, b rain, heart, o steocytes can ’t regen erate. 3.) neuroglia – attached to ne urons.What is anoxic encephalopathy


supp orts neurons. Where brain tum ors are found. Types: 1 . A s t r o c y t e 2 . O l i g o d en d r i a astro cytom a – 90 – 95% bra in tum or from as trocy te. Mos t brain tu mors are f ound a t astroc yte. Astro cyte – main tain s integ rity o f bloo d brai n barrie r (BBB ). BBB – semi permea ble / s electi ve -toxic substance that destroys astrocyte destroy BBB. Toxins that can pass in BBB: 1. Am mo ni a- li ve r ci rr ho si s. 2. 2. C ar bo n M on ox id e – se iz ur e p ar kin so ns . 3. 3. Biliru bin- jaun dice, hepat itis, kernic terus /hype rbilirub enia .

– atrophy of brain tissue du e to a deficiency of acetylch oline. SSx: A – am ne si a – lo ss o f me mo ry A – apra xia – unab le t o det ermin e fun ction pu rpose of o bject A – agn osi a – un abl e to re cog niz e fam ili ar ob jec t A – a p h a s i a – – exp res siv e – bro cca ’s aph asi a – una ble to spe ak – rec ept ive – wer nic kes ap has ia – una ble to un der sta nd spo ken wo rds commo n to A lzhei mer – recept ive aph asia drug of ch oice – ARICE PT (tak en at bedti me) COGN EX.What is anoxic encephalopathy mgt: supp ortive palli ative. Microglia – stationary cells, en gulfs bacteria, en gulfs c ellular debris. II. Compositions of cord spinal cord 80 % – bra in ma ss 1 0 % – C S F 10 % – bl o od MONROE KELLY HYPOTH ESIS: the skull is a closed vault. Any increa se in one component will increase ICP. Normal ICP: 0-15mmhg brain mass 1 . C e r e b r u m – l a r g e s t – C o n n e c t s R L c e r e b r a l h e m i s p h e r e – corpus collu sum rt cerebral hemisphere, lt cerebral hemisphere function: 1 . S e n s o r y 2 . M o t o r 3 . In t e g ra t i ve lobes 1.) fro nta l a. Controls motor activity b. Controls personality development c. Where primitive reflexes are inhibited d. Site of development of sense of umor e.What is anoxic encephalopathy B rocca ’s a rea – speech cent er dam ag e – exp ress ive apha sia 2. ) te mp or al – a. Hearing b. Short term memory c. Wernic kes area – gen inte rpreta tive or know ing gno stic area dam age – rec epti ve apha sia 3.) pariet al lobe – appre ciati on disc rimat ion of s ensor y imp – pain, touc h, pressu re, heat cold 4. ) oc ci pi ta l – vi si on 5.) insul a/is land o f reil/ centra l lobe- contr ols vi scera l fx funct ion: – activ ities o f int ernal organ 6.) rhine nceph alon / limbe c – smell , libido, long- term memor y basal ganglia – areas of gray matte located deep within a cerebral hemisphe re

Change in VS = always late symptoms earliest sx: a.) change or decrease LOC – R e s t l e s s n e s s t o c o n f u s i o n W i d e p u l s e p r e s s u r e : I n c r e a s e d I C P – D i s o r i e n t a t i o n t o l e t h a r g y N a r r o w p p : C a r d i a c d i s o r d e r , s h o c k – stu por t o com a lat e sig n – cha nge in V /S 1.What is anoxic encephalopathy BP i ncr eas e (s yst oli c in crea se, dia sto le- sam e) 2. Wi den in g p ul se pr es su re normal adult BP 120/ 80 120 – 80 = 40 (norm al pulse press ure) increa se ICP = BP 1 40/80 = 1 40 – 80= 60 P P (wide ) 3. RR is de creas ed (ch eyne-S tokes = bet period of ap nea or hype rpnea with periods of ap nea) 4. T em p in cr ea se I n c r e a s e d I C P : I n c r e a s e B P S h o c k – d e c r e a s e B P – D e c r e a s e H R I n c r e a s e H R C U S H I N G S E F F E C T D e c r e a s e R R I n c r e a s e R R I n c r e a s e T e m p D e c r e a s e t e m p b.) headache projectile vomiting papil ledima (e dema of opt ic disk – outer su rface of reti na) decorticate (abnormal flexion) = damage to cortico spinal tract / decerebrate (abnormal extension) = damage to upper brain stem-pons/ c.) U ncal herni ation – unil atera l dila tion o f pu pil. (bila teral dilat ion of pupil – tentor ial h erni ation .) d.) possible seizure.What is anoxic encephalopathy nursing priority: 1.) maintain patent a/w adequate ventilation a. Prevention of hypoxia – (decrease tissue oxygen ation) h ypercarbia (increase in CO2 retention). Hyp oxi a – cer ebr al ede ma – inc rea se ICP hypoxi a – inad equat e tissue oxygen ation late sym ptoms o f hypo xia – B – bra dyc ard ia E – extrem e restles sness D – dy sp ne a C – cya nos is early symp toms – R – rest les sn ess A – agi tat ion T – tac hyc ard ia increase C O2 retention / hy percarbia – cerebral vasodilatation = in crease ICP