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343 Cards in this Set
- Front
- Back
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cause of brain problems
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Increased intracranial pressure
Traumatic brain injury Cerebral vessel changes (aneurysms, AVMs) Brain Tumors |
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what three things do you have in the cranium?
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spinal fluid
blood brain tissue |
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what controls vital signs for the body
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base of the brain
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Vintracranial=
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Vbrain+Vblood+VCSF
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Monro-Kellie Hypothesis
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To maintain normal intracranial pressure (ICP), a change in volume of brain, blood, or CSF must be accompanied by a change in either or both of the other components
If this does not occur, there is an increase in ICP |
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average intracranial volume
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1700 ml
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normal intracranial pressure
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5 - 13 mm Hg
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what happens if intracranial pressure gets too high
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your ventricles get enlaraged and you stop the perfusion of blood
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what is cerebral blood flow dependent on
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cerebral perfusion pressure (CPP)
(pressure you need to perfuse your brain) |
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cerebral perfusion pressure
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MAP ‑ ICP
{MAP = DBP+ 1/3 (SBP – DBP)} |
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Normal CPP =
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80 - 100 mm Hg
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A CPP below what is incompatible with life
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30
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what is the minimum CPP needed for life
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60-70
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when do you get ischemia with CPP
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less than 40-50
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If ICP = MAP what happens
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brain perfusion ceases and brain death results
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what does the brain need to survive
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o2 and glucose
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how does the body react when an increased in ICP
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1st - displacement of CSF into the spinal canal then external jugular veins
Next - reduction of blood volume in the brain Last - Herniation |
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displacement of brain tissue
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herniation
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what do the pupils look like when you are herniating
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big and none reactive
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what do you give people who are herniating
and what reaction do you look for |
Give manatol (a sugar) to these patients NOT Lasix bc it’s a osmotic diuretic
need large quantity of it --@ 100 grams of it so need a good IV for it so you don’t blow out the vein look at foley-they should start to diuresis when you give this meds |
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what cranial nerves are in the brainstem
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Cranial nerves III through XII
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BEST AND EARLIEST INDICATOR OF INCREASED ICP
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Change in LOC
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what are the parts of a glasscow coma scale
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eye opening
verbal responses motor response |
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types of abnormal posturing
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Decortication
Decerebrate |
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Decortication=
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abnormal FLEXION
Upper arms are close to the sides Elbows wrists & fingers are flexed Legs are extended with internal rotation Feet are planter flexed |
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when does Decortication occur
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Occurs with problems at the level of the corticospinal tracts of cerebral cortex
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Decerebrate
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EXTENSION
Neck extended with jaw clenched Arms are pronated, extended, and close to the sides Legs are extended straight out Feet are planter flexed Brain is so tight that even the slightest breeze will make they decerbrate After this you’ll be flat(no responsiveness) when they’ve done without oxygen |
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when does decerebrate occur
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Upper brain stem dysfunction (midbrain, pons or diencephalon)
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Cushing’s Triad-
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pt is herniating
Reflects rising ICP with direct pressure on the medullary center of brain Associated with IRREVERSIBLE brain stem damage |
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three parts of Cushings Triad
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Abnormal, irregular respiratory patterns
Decreased pulse/Bradycardia Hypertension with a wide pulse pressure |
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how is respiration associated with increased intracranial pressure
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Cheyne-Stokes
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Cheyne-Stokes
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Bilateral lesion in cerebral hemispheres, cerebellar sometimes, midbrain, upper pons
Rhythmic waxing and waning in depth followed by a period of apnea breathing starts and stops |
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what does cheyne strokes lead to
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Central neurogenic hyperventilation
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Central neurogenic hyperventilation
and where does it indicate damage |
Lesion in low midbrain or upper pons
Respirations are increased in depth, rapid (>24), and regular |
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what does Central neurogenic hyperventilation lead to
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Apneustic
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Apneustic
and what does it lead to |
Lesion in mid pons or low pons
Prolonged inspiration with a pause at the point where the respiration is at its peak, lasting for 2 – 3 seconds May alternate with an expiratory pause |
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what does Apneustic lead to
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Cluster breathing
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Cluster breathing
and where is the damage |
Low pons or upper medulla
Clusters of irregular breathing with periods of apnea that occur at irregular intervals |
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what does cluster breathing lead to
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Ataxic
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Ataxic
and where is damage what does it eventually lead to |
Respirations completely irregular with deep shallow random breaths & pauses
Eventually: Apnea |
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Pupillary reactions to light indicates functioning where
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upper brain stem function
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Anisocoria =
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unequal pupils
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Corneal reflex (blink) is associated with what nerves
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(CN V trigeminal & VII facial)
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Gag reflex is associated with what nerves
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(CN IX glossopharyngeal & X vagus)
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Swallow reflex is associated with what
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(CN IX glossopharyngeal & X vagus)
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CN III to CN XII indicate what is functioning
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brain stem functioning
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how do you test cranial nerve testing when a patient isn't awake
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oculocephalic (doll’s eyes) & oculovestibular (caloric)
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Oculocephalic reflex
normal and abnormal |
(Doll’s eyes)
Holding the patient’s eyes open briskly turn the head from side to side, pausing at each end point If brain stem intact = congugate eye movement opposite to the side the head is turned Positive Doll’s eyes If brain stem NOT intact = eyes remain stationary |
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Oculovestibular reflex (caloric)
normal and abnormal |
Cold caloric testing
Instill cold water into external auditory canal Observe direction of eye movements Normal = eyes deviate toward ear with irrigation flow Abnormal = slow movement toward instilled ear, dysconjugate eye movements, or absent eye movements |
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S & S of impending herniation
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LOC
Pupillary abnormalities Motor dysfunction (hemiplegia, decortication, decerebration) Impaired brainstem reflexes (corneal, gag, swallowing) Alteration in VS including respiratory irregularities |
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how do you monitor ICP and where can they be placed
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Fiberoptic monitor
Intraventricular catheter = most accurate Subarachnoid bolt |
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Intraventricular catheter
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“ventriculostomy”
Inserted into one of the lateral ventricles Diagnostic = to monitor ICP Therapeutic = permits drainage of CSF Has highest rate of infection |
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where can u place Fiberoptic monitor
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Can be placed
Into brain tissue (parenchyma) Subarachnoid space Epidural space Into a ventricle (draining only) ventriculostomy |
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Subarachnoid bolt
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Inserted through a burr hole in the skull into a small opening in the dura and into subarachnoid space
Allows pressure reading but not removal of fluid |
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treatment for elevated ICP
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Craniotomy:
Hydrocephalus: |
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Craniotomy:
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Remove or debulk masses/ lesions
Hematoma Abscess Tumor Remove or debulk infarcted and necrotic tissue after head trauma |
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Decompressive craniectomy
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Remove part of skull to allow brain expansion
Bone replaced at a later date |
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where do you put a temporary Ventriculostomy
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via Burr hole
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where do you put a Permanent: VP shunt
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from lateral ventricle to peritoneum
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where do you keep the brainage collection with a ventriclar drainage
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Collection bag usually level with auditory meatus
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how do you treat respiratory issues associated with ICP
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Collection bag usually level with auditory meatus, WHICH causes vasoconstriction & reduced CBF & ICP
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what medical treatment do you use with for elevated ICP -
and why do you use it |
Neuromuscular blockade
you use it bc when youre in coma your brain needs less o2 and less blood |
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Neuromuscular blockade
examples what do you monitor |
To induce paralysis
Pancuronium Vecuronium Pipecuronium Monitor by peripheral nerve stimulation check neuro exam eveyr2 hours |
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why do you control blood pressure when ICP
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high blood pressure increases ICP
which affects CPP |
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when do you treat hypertension when ICP
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Hypertension when SBP > 150 ‑160 in adult who was previously normotensive
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meds to decrease hypertension
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Labetalol (Normodyne; Trandate) = alpha & beta blocker
Sodium nitroprusside (nipride) infusion Calcium channel blockers |
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Drug treatment for elevated ICP
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Osmotic diuretics/hyperosmolar therapy
Promotes fluid removal from edematous brain tissue Bolus = Mannitol 1.0 g/kg IV over 20 minutes Mannitol 0.25 – 1.0 g/Kg continuous infusion Nsg: Monitor serum osmolality (Keep at 310 - 320 mosm/L), glucose, K+ Foley, I & O |
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what to avvoid with elevated ICP
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AVOID: prone
Trendelenberg Extreme neck flexion Hip flexion > 90 |
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Drug treatment for elevated ICP - Seizure prevention
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Phenytoin (Dilantin) 100 mg TID or QID; PO/IV/tube. Can be given quickly in push or drip
Fospheytoin Carbamezepine (Tegretol) Phenobarbital |
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Barbiturate coma
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When ICP does NOT respond to conventional therapy
Underlying therapeutic principle Decreased cerebral metabolism & decreased CBF = decreased ICP Pentobarbital (nembutal) Thiopental sodium (pentothal) |
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why shouldn't you use dextrose on a piggy back
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(increases cerebral edema and decreases serum osmolarity)
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If MAP/CVP/PCWP is low give what
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250 cc 5% albumin until CVP = 5-10/PCWP 10-15
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Acceleration-Deceleration coup-contrecoup
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When the accelerating skull, moving in a motor vehicle , suddenly decelerates when it hits an immobile object (steering wheel or windshield)
brain hits the skull in the direction of the movement and then rebounds and strikes the inner surface of the skull on the opposite side |
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Basilar skull fracture
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Occurs in bone over the base of the frontal & temporal lobes and blood pools around eye
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Linear fractures
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most common
Simple clean break in skull 70 ‑ 80% of skull fractures Occurs with low velocity injuries Subdural or epidural hematoma formation frequently underlie the fracture |
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Depressed skull fracture
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Inward depression of bone fragments
Usually due to a powerful blow to the skull Bone fragments may penetrate into the brain tissues Hair, dust, & debris may be found Dura may or may not be torn Can see CFS coming out of ear or nose-or down throat |
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dura matter
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Dura matter is the lning of the brain and spinal column where CFS flows underneath/ If torn you have open area from outside in and CFS can leak out
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Comminuted fracture
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Bone is crushed into small, fragments pieces
Usually seen with high impact injuries |
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Basilar skull fracture
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Base of skull
Linear, comminuted or depressed Anterior, middle or posterior fossa (frontal & temporal lobes) extension Results in CSF leakage from nose or ears Increased risk of meningitis Serious due to close proximity to vital brain stem structures! |
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surgical treatment of skull fracture
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Craniectomy (depressed, comminuted, or contaminated)
Cranioplasty Insertion of bone or artificial graft May be done immediately or postponed for 3 ‑ 6 months (if cerebral edema present) |
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Laceration =
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tearing of cortical surface blood vessels & may lead to secondary hemorrhage
More serious injury |
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types of Hemorrhage
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Epidural hematoma
Subdural hematoma Intracerebral |
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Epidural hematoma
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2% – 6% of head injuries
Bleeding between the skull & dura mater Usually caused by laceration of middle meningeal artery May also have temporal skull fracture usually seen in the young |
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Epidural hematoma signs & symptoms
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Momentary unconsciousness followed by a lucid period lasting for minutes to a few hours
Then Rapid deterioration in LOC (drowsiness to confusion to coma) pupils (ipsilateral dilation, sluggish, fixed), headache, hemiparesis, hemiplegia, seizures |
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treatment of Epidural hematoma
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emergency craniotomy needed
rupture of meningeal artery (skull fracture)> increased ICP > compression of brain > herniation rapid progression - immediate surgical drainage! lucid interval between trauma and progressive loss of consciousness |
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Subdural hematoma
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Bleeding between dura mater & arachnoid layer of the meninges
Usually venous in origin Occurs more slowly 29% of head injuries develop subdural hematomas |
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Categories of subdural hematoma
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3 categories based on interval between injury & appearance of symptoms
A) ACUTE = up to 48 hrs B) SUBACUTE = 2 days ‑ 2 weeks C) CHRONIC = 3 weeks to several months |
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signs of acute subdoral hematoma
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headache, drowsiness, agitation, slow cerebration, confusion
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signs of subacute hematoma
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same as acute but occurs slower
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signs of chronic subdoral hematoma
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Manifestations may not appear until weeks to months after injury
Confusion, slowed thinking, drowsiness |
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who do you usually see with subdural hematoma
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Elderly patients & chronic alcoholics prone to SDH
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treatment of subdoral hematoma
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Small ones = assessment & medical treatment
Large = craniotomy = Burr holes to evacuate clot & ligate bleeding vessels |
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Intracerebral hematoma
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Bleed into brain tissue (parenchyma)
14 ‑ 15% of head injuries Common sites: frontal or temporal lobes Acts like space-occupying lesions Common after hemorrhagic stroke, aneurysm rupture |
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Intracerebral hematoma signs & symptoms
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Unconsciousness
Headache Deteriorating consciousness progressing to deep coma Hemiplegia on contralateral side Dilated pupil on side of clot (ipsilateral) |
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Diffuse axonal injury classification
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Mild = loss of consciousness lasting 6 to 24 hours
May have associated short term disability Moderate = coma lasts < 24 hours Incomplete recovery on awakening Severe = injury to brain stem Abnormal posturing Coma |
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how do you detect a diffuse axonal injury and what is the prognosis
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94% die or remain in chronic vegetative state = long term care
MRI to detect |
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glasscow coma scale numbers
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Mild brain injury = GCS: 13 – 15
Moderate brain injury = GCS: 9 – 12 Severe brain injury = GCS: < 8 |
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when do you intibate with TBI
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GCS< 8
Fall in GCS of 3 Unequal pupils Inadequate respiratory effort or significant lung/chest injury Loss of gag apnea |
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most common cause of SAD
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aneurysms
Aneurysm usually forms in middle to older adulthood spontaneously will leak or rupture—you’ll see the worst headache of your life |
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who usually has SAD and how do they diagnose?
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Subarachnoid hemorrhage occurs more in the young females===hereditary
diagnosed by people having the intense headache and stiff neck(blood from aneurysm seeps out into subarachnoid space) they will do a spinal tap |
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Cerebral Aneurysm
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Localized arterial wall dilation that develops secondary to a weakness of the arterial wall
increased pressure can cause this to rupture |
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where do most anuerysms occur
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circle of willis
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risk factors for aneurysm
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Hypertension
Cocaine (mycotic) Head trauma Congenital |
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types of aneurysm
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Most (80% – 90%) are:
Berry: Shaped with a neck or stem Saccular: Any aneurysm that has a saccular outpouching Other types: Fusiform: Outpouching of a vessel wall without a stem Dissecting: Intimal layer pulls away from the medial layer and blood is forced between the two layers |
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S & S: Unruptured aneurysm
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Most are asymptomatic until the time of bleeding
Dilated pupil EOM’s deficits Ptosis Pain above & behind eye Localized headache Nuchal rigidity (neck pain on flexion) Possible photophobia |
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S & S: Ruptured aneurysm
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Meningeal irritation
stiff neck = nuchal rigidity Temperature low grade blurred vision Photophobia Change in LOC |
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what are you always at risk for with brain problems
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seizures
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goal of Intraparenchymal hemorrhage
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Fluid volume control
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drug therapy for intraparenchymal hemmorhage
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Nimodipine-
Dilantin-anti seizure Stool softeners Steroids-decreases swelling Analgesics for headache Acetaminophen or codeine Don’t give pain meds to neuro patient |
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3 Major Complications of hemorrhage
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Vasospasm
Most common = 30 - 70% Narrowing cerebral blood vessel- reduced blood flow distally = ischemia/infarction Hydrocephalus Blood circulating in CSF interferes with CSF reabsorption Rebleeding |
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Vasospasm prevention for hemorrhage
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Nimodipine (Nimotop)
Calcium channel blocker 60 mg Q 4 hour no later than 48 hours after hemorrhage 21 days monitor BP |
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Vasospasm treatment or prevention for hemmorrhage
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Hypervolemic
keep CVP 10 mm Hg Keep PCWP 14 - 18 Hg Albumin Q 6-8 hours IV fluids (0.9%NSS @ 150/hr) Hemodilution Keep Hematocrit at 32 - 35% Albumin IV fluids (0.9%NSS @ 150/hr) |
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drug treatment for vasospams in hemmorrhage
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Drugs
Dopamine (intropin) Phenylephrine (neosynephrine) = alpha agonist @ 0.5 ug/Kg/min |
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Communicating hydrocephalus including treatment
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Caused by blood in subarachnoid space
Prevents CSF reabsorption Contributes to increased ICP Treatment = shunt Ventriculoperitoneal |
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when do you start to worry about rebleeding with a hemorrahage
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2 weeks after initial bleed
Peaks 24 - 48 hours 7-10 days Rebleeding 24 to 48 hours cause of death |
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surgical treatment for berry and fusiform
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Berry (saccular ) = clip
Fusiform = wrap with special |
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Arteriovenous malformation (AVM)
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arteries & veins
Blood is directly shunted from the arteries (high resistance) to the veins (low resistance) rupture & hemorrhage A-V malformations=clumps of vessels |
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AVMs - Clinical Manifestations
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Hemorrhage
intraparenchymal Seizures Headache Progressive neuro deficits |
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AVMs - Diagnosis
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CT
MRI MRA (Magnetic Resonance Angiography) Blood vessels examined Angiography Definitive diagnostic procedure |
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AVM – treatment options
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Surgery
Embolization Curative, palliative, or adjunctive to surgery or radiosurgery Radiosurgery |
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signs of brain tumor
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Headache (not most common)
Seizures Neuro changes-FOCAL FINDINGS |
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Symptoms of frontal lobe tumors
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Personality & judgment disturbances
Inappropriate affect Motor dysfunction Aphasia ( Brocas area) expressive, motor Memory deficits |
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Occipital lobe signs and symptoms
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Visual disturbances
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temporal lobe signs and symptoms
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Olfactory, visual, or gustatory hallucinations
Complex partial seizures with automatic behavior Aphasia Receptive (Wernicke’s) Sensory Memory deficits |
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Symptoms of parietal lobe tumors
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Replicate pictures
Loss of right – left discrimination Paresthesias Sensory – perceptual defects Numbers, letters Neglect syndromes Visual filed cuts |
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Types of Brain Tumors in Adults
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Gliomas –originates from the tissue
Meningioma Neuroma Pituitary adenoma Developmental (congenital) Metastatic Genetic |
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Grading brain tumors
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Grades I to IV
Highly malignant grades III and IV astrocytoma type gliomas : primary brain tumors in adults |
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typews of Gliomas
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Astrocytomas (grades I and II) = 25-30% of gliomas
Less malignant Survival 5-6 years Anaplastic astrocytoma grade III Survival 15-28 months Glioblastoma multiforme [GBM] (also called astrocytoma grade IV) 20% brain tumors; 55%gliomas Highly malignant Survival = 12 months |
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Ependymoma
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Ventricles of the brain, fourth ventricle
slow or aggressive low = survival 5 - 10 years Very difficult to treat! |
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Developmental (congenital tumors)
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Dermoid, craniopharyngioma epidermoid,
Embryonic tissues Success of surgery depends on location & invasiveness Angiomas Vascular Difficult to resect(anything vascular is hard to resect) |
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medical treatments for tumors
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Control/decrease cerebral edema/ ICP
Corticosteroid Dexamethasone (Decadron) Prevent seizures Phenytoin (Dilantin) |
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levels of spinal cord preventions
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Primary
Education: accident prevention (helmets, etc) preventing falls Secondary Prompt intervention Tertiary Preventing complications |
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c4/cervical injury causes what
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quadriplegia
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C6 thoracic causes what
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quadraplegia
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T6, lumbar injury causes what
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paraplegia
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L1/sacral injury causes what
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paraplegia
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what causes problems with spinal cord injury
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Initial impact (primary injury = actual physical disruption of axons)
ongoing physiologic changes (secondary injury = ischemia, hypoxia, microhemorrhage, & edema) |
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how does spinal cord injury occur and what is it due to
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Occurs when something (e.g., bone, disk material, or foreign object) enters the spinal canal and disrupts the spinal cord or its blood supply
Injury due to cord compression: bone displacement interruption of blood supply to the spinal cord pulling on the spinal cord |
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mechanisms of spinal cord injury
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Hyperflexion (bending head forward too much)
Hyperextension (head bending backward) Axial loading and vertical compression-landing on feet Rotation Penetrating trauma-gun knife, etc |
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primary injuries of spinal cord trauma
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Concussion
temporary loss of function Contusion Bruising bleeding into the spinal cord, edema, and possible neuronal death Laceration tear in the spinal cord results in permanent injury Contusion, edema, and cord compression are seen with a laceration Transection severing of the spinal cord resulting in complete loss of function below the level of injury Hemorrhage is bleeding that occurs in and around the spinal cord, resulting in edema and cord compression Damage to the blood vessels that supply the spinal cord can result in ischemia & infarction |
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secondary injury of spinal cord injury
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secondary insults occur:-blood supply
cellular damage vascular damage, structural changes in the gray and white matter |
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how and where does nuerogenic shock occur
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Occurs (at or above T6)
Results from the loss of sympathetic nervous system influences from the T1 to L2 area of the spinal cord |
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what does nuerogenic shock cause
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BRADYCARDIA & DECREASED VASCULAR RESISTANCE (vasodilation)
Blood pools resulting in hypotension and ↓ Cardiac Output |
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Neurogenic shock contributes to
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hypoperfusion & secondary injury
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when can you determine extent of injury of spinal cord injuries
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after 72 hours
need spinal shock to be finished |
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complete spinal cord injury
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loss of sensory and motor function below the level of injury; complete interruption of motor & sensory pathways
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incomplete spinal cord injury
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mixed loss of motor & sensory function because some spinal tracts remains intact
Divided into syndromes |
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incomplete spinal cord injury syndromes
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Central cord syndrome
Anterior cord syndrome Brown-Sequard’s syndrome (lateral cord syndrome) |
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central cord syndrome
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Mechanism of injury
Hyperextension in cervical region Weakness UE > LE) Sensory deficits = same as motor distribution. Can’t move legs from waist down, they also can’t feel hot and cold from the same place from the waist down |
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Anterior cord syndrome
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caused by hyperflexion
Motor deficits Paralysis below injury level Sensory deficits posterior cord tracts are not injured Loss of temperature & pain sensation below injury level |
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Proprioception
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(sensations of touch, position, vibration and motion) remains intact ie “tell me if your toes is going up or down
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Brown-Sequard syndrome [Lateral cord syndrome]
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Mechanism of injury Penetrating trauma
Ipsilateral (same side as lesion) loss of motor & proproceptive (position & vibratory sense) functions Contralateral (opposite side from lesion) loss of pain & temperature sensation |
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Conus medullaris syndrome & Cauda equina syndrome
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damage to the very lowest portion of the spinal cord (conus) & the lumbar & sacral nerve roots (cauda equina = horse’s tail)
Spinal cord ends at L2 flaccid paralysis of the lower limbs & arreflexic (flaccid) bladder [causes urinary retention] & bowel dysfunction [loss of anal sphincter tone] |
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cervical cord associations
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C1-C2:
C3-4: Phrenic nucleus C4: Deltoids C4-5: Biceps C6: Wrist extensors C7: Triceps C8: Wrist extensors C8-T1: Hand muscles |
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relationship between level of injury and damage
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C1-C3: Absence of ability to breathe independently.
C4: Poor cough, diaphragmatic breathing, hypoventilation C5-T6: Decreased respiratory reserve T6 or T7-L4: Functional respiratory system with adequate reserve. |
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injury damage and problems in breathing of spinal cord injury
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bove C3: Immediate cessation of breathing
C3-C4: Have marked decrease in inspiratory volumes C5-T1: Can initiate breaths normally but experience hypoventilation because of loss of intercostal & accessory muscle strength (↓ VC & Inspiratory Force) Plus ↓ ability to cough |
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when medicine do you give in an SCI emergency
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methylprednisolone
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Specialty beds (roto rest)
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designed to maintain spinal immobilization & provide kinetic therapy available
Allow client to be moved in proper body alignment Allows more frequent movement Allows constant movement from side to side |
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Monitor pulmonary function
Ongoing assessment of: with SCI |
Maximal Inspiratory Pressure (MIP)
Vital Capacity If less than 10-15 ml/kg = respiratory insufficiency intubation & mechanical ventilation needed |
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Hypotension
inotropic support for sci |
Dopamine (Intropin)
Norepinephrine (Levophed) Goal: Avoid hypotension Maintain MAP of at least 85 to 90 mm Hg for the first 7 days after injury |
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Bradycardia treatment:
for sci |
Atropine
Temporary pacemaker |
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Administering Methylprednisolone (Solu-Medrol)
and what is it associated with |
SCI
Loading dose of 30 mg/kg IV over 15 minutes Followed 45 minutes later by an infusion of 5.4 mg/kg/hour |
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what do you need to monitor with Solu-Medrol
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Meticulous attention to side effects!
Prophylaxis against gastrointestinal ulcers Blood glucose monitoring & control |
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Subluxation =
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when one or more of the vertebrae move out of position and create pressure on, or irritate spinal nerves
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|
skeletal traction
|
For cervical injuries = skeletal traction is usually provided by:
Crutchfield, Vinke, or Gardner-Wells tongs |
|
|
Crutchfield tongs or halo vest…
what it is and what nursing care do you need |
early immobilization of cervical spine
Skeletal traction is applied Sterile pin care needed twice a day Clean with normal saline & ?antibiotic cream Be careful! Some antibiotic creams cause corrosion of the pins in the skull Skin assessment imperative! |
|
|
Rapid surgical intervention
|
is required if spinal cord compression is unrelieved by traction or if the fracture is unable to be reduced
|
|
|
Micturation reflex center
|
located in conus medullaris at S2-S4 (vertebral level (T12-L2)
Injury above this level affects UMN control of micturation Micturation center no longer connected to brain Reflex arc intact but voluntary control of urination lost |
|
|
Upper motor neurons
|
are any neurons that originate in motor region of the cerebral cortex and carry motor information down to the final common pathway, that is, any motor neurons that are not directly responsible for stimulating the target muscle
|
|
|
what carries the nerve impulses from upper to lower motor neurons.
|
neurotransmitter acetylcholine
|
|
|
what do you encourage with bladder training
|
Encourage fluids (2 to 4 L/day) to maintain high volume of dilute urine
|
|
|
Defecation center is where
|
at S2-S4
|
|
|
bowel management with SCI
meds |
Daily
Colace Glycerine or bisacodyl (ducolax) suppositories, and/or digital stimulation every other day or daily For patients with injuries at or above T6 Anesthetic jelly used to ↓ risk of autonomic hperreflexia ↑ fiber & fluid in diet |
|
|
medication for pain for SCI
|
Opiates
Muscle relaxants Baclofen (lioresal) Diazepam (valium) Methocarbamol (robaxin) Carisoprodol (soma) |
|
|
Orthostatic Hypotension
|
Blood pools in lower extremities due to loss of sympathetic vascular tone
Nursing strategies to ↓ orthostatic hypotension Application of graduated compression stockings Use of abdominal binder Maintain hydration Gradual progression to an upright position |
|
|
at what SCI level can you not control your temperature
|
Individuals with SCI at or above the T6
Hypothalamus cannot control temperature by vasoconstriction and increased metabolism Heat loss is compromised by the inability to sweat below the level of injury |
|
|
how do you decrease spasticity with SCI
|
b\Frequent range of motion exercises
Medications |
|
|
Medications for spasticity
|
Benzodiazepines
Valium® (Diazepam) Klonopin® or Rivotril® (Clonazepam) Tranxene® (Clorazepate) Lioresal® (Baclofen) Dantrium® (Dantrolene sodium) Neurotin® (Gabapetin) Zanaflex® (Tizanidine) Catapres-Tts® (Clonidine) |
|
|
where does Autonomic hyperreflexia
occur? |
Life-threatening with SCI at or above T6
Due to unopposed sympathetic response below the level of injury Exaggerated “fight or flight” response Occurs after the return of reflex activity, usually in the first year following injury |
|
|
Parasympathetic Response in Autonomic Dysreflexia
|
Parasympathetic Nervous system attempts to counteract ↑ BP by causing vasodilation
However—PNS impulses below level of injury are blocked—so the vessels below injury level remain constricted Parasympathetic responses in baroreceptors in cerebral vessels, carotid sinus, and aorta do respond and cause vasodilation above the injury |
|
|
what do you want to monitor with when a patient with a SCI complains of a “headache”
|
Important to measure BP
|
|
|
treatment for Autonomic hyperreflexia
|
Move the patient into a sitting position immediately or elevate HOB (provide orthostatic drop of BP)
Continual BP monitoring Q 2-5 minutes Identify & treat the underlying cause (e.g., bladder distention due to foley problem; impaction) Remove anything constricting client Assess for blocked catheter Assess for impacted stool |
|
|
Sexual reflex center @
|
S2-S4 (vertebral level T12-L2)
|
|
|
spinal cord tumor classification
|
Extramedullary tumors are located outside SC
Account for 80-90% of primary tumors Subdivided into: Extradural Intradural Intramedullary are located within the SC Extradural tumors Outside spinal dura Within the epidural space Usually malignant, metastatic lesions Can compress SC Type of tumor: chordomas & sarcomas |
|
|
treatment of extradural tumors
|
Tumors arise from bones of spine, in extradural space
Treatment = relief of cord pressure by surgical laminectomy, radiation, chemotherapy or combination approach Prognosis = poor |
|
|
Subdural tumors
|
Within spinal dura but outside SC
Also called intradural (extramedullary) Meningiomas Neurofibromas Schwannomas |
|
|
Intradural (extramedullary) tumors
|
Mostly benign
Treatment = complete surgical removal of tumor (if possible); partial removal followed by radiation Prognosis = very good if lack of damage to cord from compression |
|
|
Intramedullary
|
Within the spinal cord itself
Also called intradural (intramedullary) Astrocytomas Ependymonas Hemangioblastomas |
|
|
Intradural (intramedullary)
|
Least frequent
Treatment = Partial surgical removal, radiation therapy (resulting in only temporary improvement) Prognosis = very poor |
|
|
early symptoms of spinal cord tumor
|
Pain in the back with radicular pain simulating intercostal neuralgia, angina, or herpes zoster (shingles)
Radicular pain = pain experienced along the dermatome (or sensory distribution) of a nerve due to pressure on the nerve root Also know as sciatica |
|
|
where do you see symptoms of spinal cord tumors
|
same side as tumor
|
|
|
Amyotrophic Lateral Sclerosis
(ALS) ie LOU GEHRIG’S DISEASE |
Refers to the weakness & atrophy that occur from the degeneration of motor neurons
may be assoicaited with repeated blows to the head |
|
|
LMNs originate in the what and connect where
|
anterior horn of the SC
Axons of the LMNs connect the CNS with the voluntary muscles |
|
|
what is Essential for motor function & innervate the voluntary skeletal muscles
|
LMN
|
|
|
Lateral sclerosis
|
Refers to the scarring of the corticospinal tract in the lateral column of the SC
Refers to the UMN involvement |
|
|
what is damaged with ALS
|
Progressive, degeneration of both UMNs & LMNs from demyelination & scar tissue formation
|
|
|
stages of ALS
|
progressive degeneration of upper and lower motor neurons
progressive weakness muscle atrophy paralysis death due to respiratory failure |
|
|
classic pattern of ALS
|
LMN usually affected first
Muscles of upper body affected earlier than legs Begins with combination of: Weakness with tone Atrophy Fasciculations of limbs Fasciculations = Irregular twitching of muscle fibers or bundles |
|
|
what is not affected by ALS
|
Intellectual ability
Sensory function Vision Hearing Bowel Bladder |
|
|
diagnostic tests of ALS
|
none are definate
History Neurological exam Exclusion of other diseases EMG (electromyogram) demonstrates fibrillations Serum CPK |
|
|
treatment of ALS
|
No known cure
Management is supportive symptom management Goal is to keep patient as independent as long as possible & improve mobility & quality of life |
|
|
drugs for ALS
|
Riluzole (rilutek)
Inhibits release of glutamate in brain cells Dosage = 50 mg PO BID Taken on an empty stomach |
|
|
SIDE EFFECTS of riluzole
|
Side effect = abnormal liver function
Frequent check of alanine transaminase (ALT) & aspartate transaminase (AST) |
|
|
Baclofen (lioresal)
Zanaflex (tizanidine hydrochloride) Diazepam (valium) Dantrolene sodium (dantrium |
Spasticity drugs
|
|
|
Quinine sulfate (novoquinine, quinamm, quiphile)
Baclofen (lioresal) Klonopin (clonazepam) |
Cramps drugs
|
|
|
Trihexyphenidyl hydrochloride (catapres)
Amitriptyline hydrochloride (elavil) Scopolamine patch/cream Benadryl (diphenhydramine hydrochloride) Pamelor (nortriptyline hydrochloride) Robinul (glycopyrrolate) |
Increased salivation/drooling (sialorrhea)
drugs |
|
|
Colace (Docusate)
Dulcolax |
Constipation
|
|
|
Fluoxetine (prozac)
Paroxetine (paxil) Sertraline (zoloft) |
Depression
|
|
|
Non-narcotic & narcotic analgesics
|
Musculoskeletal pain
|
|
|
Amitriptyline hydrochloride (elavil)
Gabapentin (neurotin) Carbamazepine (tegretol) |
Neurogenic pain
|
|
|
Myasthenia Gravis (MG)
|
Chronic disease of neuromuscular junction
an autoimmune process destroys acetylcholine (Ach) receptors at postsynaptic muscle membrane |
|
|
pathology of MG`
|
Nerve impulse in peripheral nerve rely on release of acetylcholine (ACh) to transmit impulse across myoneural junction to muscle
|
|
|
what muscles are affected by MG
|
voluntary
|
|
|
signs of MG
|
Increasing weakness of voluntary muscles:
Chewing Swallowing Speaking Facial Ocular Weakness inc with repeated activity & improves with rest Improvement in strength with anticholinesterase drugs |
|
|
progressive signs of MG
|
Early = ptosis & diplopia
Ptosis may be unilateral or bilateral Becomes intensified when patient attempts to look upward Next Facial Flattening of nasolabial fold Masticator Speech Neck Head falls forward |
|
|
MYASTHENIA CRISIS
|
breathlessness & dyspnea
|
|
|
How is MG diagnosed?
|
History
Physical examination Have patient look upward for 2 to 3 minutes MG = droop of eyelids Person can barely keep the eyes open After rest, eyes can open Speech affected & voice often fades after a long conversation |
|
|
test for mG
|
Anticholinesterase Testing
Antibody Titer for AChR Repetitive Muscle Stimulation Single Fiber Electromyography Mediastinal MRI |
|
|
Tensilon (edrophonium chloride)
|
for MG diagnosis
An anticholinesterase drug = cholinesterase inhibitor Blocks enzyme acetylcholinesterase acetylcholine not broken down acetylcholine accumulates |
|
|
(Edrophonium chloride)
|
for MG
Ultra fast acting drug (30 seconds); duration 5 minutes 10 mg drawn into syringe Administer 2 mg IV if no symptoms then give 8 mg more Marked improvement in muscle strength in 30-60 seconds which lasts 5 to 10 minutes Also helps to distinguish myasthenic crisis/cholinergic crisis |
|
|
Antidote for Tensilon=
|
Atropine
Have handy during testing |
|
|
Repetitive Muscle Stimulation
|
Electrical shocks delivered to nerve at rate of 3 per second while surface electrodes over the muscle record electrical potentials
Positive test = the amplitude of the muscle’s response diminishes with progressive stimulation |
|
|
Single Fiber Electromyography
|
Detects delay or failure of neuromuscular transmission in pairs of muscle fibers supplied by branches of a single nerve fiber
99% sensitive in confirming MG |
|
|
treatmetn fro MG
|
Highly INDIVIDUALIZED management plan
Goal Achieve a quality of life that is as symptom free as possible |
|
|
drugs and surgery for treatment of MG
|
Anticholinesterase drug therapy
Immunosuppression Plasma exchange & IV immunoglobulin (IVIG) Thymectomy |
|
|
Anticholinesterase drugs
|
let Ach accumulate
First treatment step Pyridostigmine (Mestinon) |
|
|
when do you take anticholinesterase drugs
|
Important to have peak activity at meal time
Take before meals to enhance chewing & swallowing |
|
|
Pyridostigmine (Mestinon)
|
MUST BE GIVEN ON TIME
Daytime 30-120 mg PO Q 4 hours Night Time 180 mg timed release SE = muscarinic Diarrhea Abdominal cramps Antidote = ATROPINE |
|
|
two types of MG crisis
|
Cholinergic :
overmedicated Myasthenic : Undermedication |
|
|
cholinergic crisis
|
anticholinesterase drugs lets too much ACh accumulate
Profound, generalized weakness Excessive pulmonary secretions Impaired respiratory function |
|
|
Myasthenic crisis
|
Sudden relapse of myasthenic symptoms
Common precipitating event = infection (viral URI, bronchitis, pneumonia) Even with medication, patient develops: Difficulty with swallowing & breathing Respiratory paralysis Positive Tensilon test = inc muscle strength |
|
|
what is important to monitor in steroid use
|
Carefully monitor fluid & electrolyte levels
Monitor serum glucose Check potassium level ?dietary or supplemental K+ Observing for signs of GI bleeding such as gastric pain or blood in stool Antacids & proton pump inhibitors Documenting any changes in personality e.g., euphoria and insomnia Minimizing the patient’s exposure to people with communicable or infectious diseases |
|
|
Azathioprine (imuran)
Cyclosporine (neoral, sandimmune) Mycophenolate mofetil (CellCept) |
immunosupressants
|
|
|
Apheresis (pheresis)
|
Blood processing technique
Uses automated cell separator for selective removal of blood components Returns other components to patient |
|
|
Plasmapheresis =
|
Plasma exchange
Removing plasma Removes anti-ACh-R antibodies Used as short term intervention for sudden worsening of symptoms Goal = dec symptoms |
|
|
Intravenous immunoglobulin (IVIG)
|
Used as short term treatment for a serious relapse
Also called intravenous gamma globlulin IgG is one of five types of antibodies normally made by the body to fight infection 2 gms/kg infused IV over 2-5 hours |
|
|
Thymectomy
and teh two surgical approaches |
Removal of thymus gland
Induces remission of symptoms in 40% if done early in disease (first two years) 2 surgical approaches Suprasternal Transsternal |
|
|
Suprasternal
|
Less postoperative pain & morbidity
difficult to remove all of thymus due to dec access |
|
|
Transsternal
|
Complete thymus removal
sternum split so inc postoperative discomfort & inc convalescence |
|
|
Factors that predispose to exacerbation of MG
|
Infection
Stress Surgery Hard physical exercise Sedatives Strong cathartics |
|
|
Guillain-Barré Syndrome
|
Symptoms generalized and usually follow known viral illness
Not a disease, but a syndrome. Acute, rapidly progressing inflammatory polyneuropathy (polyneuritis) of unknown origin Characterized by varying degrees of motor weakness & paralysis |
|
|
what causes Guillain Barre syndrome
|
Immune-mediated response triggers destruction of myelin sheath surrounding peripheral nerves, nerve roots, root ganglia, & spinal cord
Myelin sheath destroyed by collections of lymphocytes & macrophages Demyelination occurs between the nodes of Ranvier Impairs or blocks transmission of impulses from node to node Nerve axons generally spared |
|
|
how does demyelination of GBS occur
|
Rapidly developing ascending weakness
Symmetrical involvement Distal parasthesias (numbness) and loss of deep tendon reflexes Absence of tendon reflexes important clue to diagnosis Loss of knee jerk reflex |
|
|
how does remyelination occur
|
proximally & proceeds distally
|
|
|
what viral infection do they think might cause GBS
|
Especially Campylobacter jejuni
C Jejuni gastroenteritis is thought to precede in 30% of cases C Jejuni found in poultry & eggs |
|
|
Ascending GBS
|
Most common form
Weakness & numbness begin in legs, then progresses upward 50% of patients experience respiratory insufficiency Sensory involvement usually present |
|
|
pure motor GBS
|
Similar to ascending form but without sensory involvement
Usually a milder form of GBS |
|
|
descending GBS
|
Begins with weakness in the muscles controlled by the cranial nerves & then progresses downward
Respiratory system quickly impaired Sensory involvement is present |
|
|
Miller-Fisher GBS
|
Rare
Is a triad of opthalmoplegia (paralysis of motor nerves of eye), areflexia, and pronounced ataxia Usually no sensory loss Rare respiratory involvement |
|
|
Stages of GBS
|
Stage 1 = Acute onset
Begins with first symptom Usually lasts 1-3 weeks 90% reach maximal degree of weakness in 3 weeks, most in first 2 weeks (14 days) Stage 2 = plateau period Lasts for several days to 2 weeks Stage 3 = recovery phase (remyelination & axonal regeneration process) Schwann cell produces myelin in peripheral nervous system & is spared in GB so remyelination can occur Takes months to years |
|
|
what is affected with GBS
|
Starts in LEascends to thorax, UE, face
Cranial nerves affected: V (trigeminal); VII (facial); IX (glossopharyngeal); X (vagus) |
|
|
S & S: Autonomic dysfunction
|
Orthostatic hypotension
Transient or persistent hypertension Paralytic ileus Bladder dysfunction Abnormal sweating |
|
|
symptoms of GBS
|
Pain & paresthesias present when sensory nerves are involved
Tingling or a pins-and-needles sensation Either numbness or a heightened sensitivity to touch may occur 25% experience pain “cramping” in the extremities |
|
|
GbS treatment
|
Respiratory support
Nursing care to minimize complications of immobility Plasmapheresis to remove antibodies Steroids ???? effective Drug = Intravenous IgG (IVIG) therapy |
|
|
when was the first case of AIDS
|
1981
|
|
|
what was the first drug available for AIDS and what was the problem with it?
|
Zidovudine
it was very expensive so many people didn't have access to it |
|
|
who is most affected by AIDS
|
gay Caucasian men
|
|
|
what is the most common route of transmission worldwide
of AIDS |
heterosexual contact
|
|
|
what are the routes of transmission of AIDS
|
Venereal-sexual
Parenteral-IV drug abuse |
|
|
what body fluids pass AIDS
|
Blood
Semen Vaginal fluid Breast milk |
|
|
What are the central lymph producing organs
|
bone marrow
|
|
|
What are the peripheral lymph producing organs
|
lymph producing cells, where are these found? Tonsils, gut, genital area, bronchial, skin, lymph nodes, and spleen
|
|
|
B Lymphocytes
Where do they originate and what is their function? |
the Bone Marrow and produce plasma cells including immunoglobins or antibodies.
|
|
|
T Lymphocytes
Where do they originate and what is their function? |
from the bone marrow to the Thymus gland where they mature and become differentiated
|
|
|
Killer (cytotoxic) T cells (T8)
|
Attach to foreign or abnormal cells (because they recognize the antigens on these cells)
Kill foreign or abnormal cells by making holes in the cell membrane and injecting enzymes into the cells. |
|
|
Helper T cells (T4)
|
Help B lymphocytes recognize and produce antibodies against foreign antigens
Help killer T cells kill foreign or abnormal cells. |
|
|
HIV is a what kind of virus
|
RNA
|
|
|
What is HIV called and why is it called it?
|
Called retrovirus because it replicates in a “backward” manner – goes from RNA to DNA
|
|
|
what happens when HIV virus is inside the cell?
|
Once inside the cell the single strand replicates itself and becomes double stranded DNA
|
|
|
how does HIV enter the cell
|
HIV attaches itself to a CD4 cell and enters
|
|
|
what happens once HIV is in the cell
|
It makes copies of itself inside the CD4 cell and then goes on to damage and destroy the cell.
The new HIV viruses burst out of the CD4 cell and goes off to find more cells to invade. |
|
|
what happens when CD4 is reduced
|
, the immune system has fewer cells to help it defend the body from other organisms. So, more likely to get sick.
When CD4 cells are attached they can’t work |
|
|
CD4 protein is also found on the surface of several other cells:
|
Monocytes
Macrophages Glial cells Gastrointestinal cells |
|
|
Immune dysfunction in HIV caused by
|
the dysregulation and destruction of CD4 T cells
|
|
|
The main target for HIV is
|
the T4 helper cell (T4 lymphocyte)
|
|
|
HIV possesses 3 enzymes that are essential for viral replication………….
|
reverse transcriptase
integrase protease |
|
|
reverse transcriptase
|
Viral RNA is converted into DNA by this
|
|
|
integrase
|
Viral DNA enters nucleus of the CD4 cell by using an enzyme called integrase, it splices itself into the genome
Becomes permanent part of cell’s genetic structure All daughter cells are infected Cells’ genetic code can direct cell to make HIV |
|
|
Protease
|
Production of HIV within cell results in long strands of HIV RNA that must be cut into appropriate lengths, cleaving of these genetic strands is accomplished with the assistance of the enzyme protease
New virus particles leave the cell, ready to infect other CD4+ cells |
|
|
HIV lifecycle
|
1) Attachment
GP120 & GP41 glycoproteins of HIV bind with host’s uninfected CD4 receptors = fusion of HIV & CD4 T cell membrane 2) Uncoating HIV viral core (2 single strands of viral RNA & 3 viral enzymes: reverse transcriptase; integrase; protease) are emptied into CD4 Tcell 3) DNA synthesis HIV changes genetic material from RNA to DNA through action of reverse transcriptase, resulting in double stranded DNA that carries instruction for viral replication 4) Integration New viral DNA enters the nucleus of the CD4 T cell and through action of integrase is blended with DNA of CD4 T cell RESULTS IN PERMANENT, LIFELONG INFECTION 5) Transcription When the CD4 T cell activated, double stranded DNA forms single-stranded messenger RNA (mRNA) which builds new viruses 6) Translation mRNA creates chains of new proteins and enzymes (polyproteins) that contain the components needed in construction of new viruses 7) Cleavage HIV enzyme protease cuts the polyprotein chain into individual proteins that make up the new virus 8) Budding New proteins & viral RNA migrate to membrane of infected CD4 T cell, exit from cell, and start process all over |
|
|
Two Types of HIV
|
: HIV-1 and HIV-2 HIV-1 is much more common worldwide
HIV-2 is found predominantly in West Africa, Angola, and Mozambique |
|
|
Viral load is
|
the amount of HIV in the blood
Measured by the HIV ribonucleic acid polymerase chain reaction blood test (HIV-RNA PCR) Viral load is very high shortly after primary HIV infection Falls steeply when the body develops antibodies; rises again after a number of years as the CD4 count drops |
|
|
High viral load
|
leads to higher transmission risk
is a sign of more severe disease as people develop AIDS |
|
|
Viral load is used to assess
|
the response to antiretroviral (ARV) treatment
|
|
|
normal adult level of CD4 T cells-helper cell
|
800 – 1200 per microliter (ul) of blood
|
|
|
CD4 T cells normal lifespan vs AIDS patients
|
Average life span is 100 days
HIV infected cells die in 2 days viral activity destroys about 1 billion CD4 cells every day |
|
|
CD4 T cell counts
|
200 to 499 CD4 T cell count: immune problems occur
< 200 severe immune problems |
|
|
what happens when HIV multiplies
|
it infects and kills CD4 T cells
|
|
|
Because of their key role in protecting against infection, the CD4 count reflects
|
the functional state of the immune system
|
|
|
how do you test for HIV
|
Tests for HIV detect either antibodies or antigens associated with HIV in whole blood, saliva, or urine
|
|
|
blood test results for HIV
|
A person whose blood test results show HIV infection is said to be “seropositive” or “HIV-positive”
A person whose blood test results do not show HIV infection is said to be “seronegative” or “HIV-negative” |
|
|
symptoms of HIV
|
Frequently accompanied by flu or mononucleosis like syndrome
Symptoms occur 1 – 3 weeks after initial infection Can last for 1 – 2 weeks Fever Lymphadenopathy Pharyngitis Headache Malaise Nausea Muscle & joint pain (myalgia) Diarrhea Photophobia Diffuse rash |
|
|
how long til HIV antibodies can be noticed
|
Delay of 6 weeks - 3 months after infection before detectable antibodies are produced
|
|
|
stages of HIV
|
Primary infection
HIV asymptomatic HIV symptomatic AIDS |
|
|
The US Centers for Disease Control and Prevention (CDC) categorizes HIV infection in adults on the basis of:
|
Associated clinical conditions (3 categories)
CD4+ T lymphocyte count (3 ranges) This results in a matrix of nine mutually exclusive categories (next slide) |
|
|
what does the CDC classification mean
|
Any HIV-infected individual with a CD4+ T cell count of <200/ml has AIDS (regardless of the presence of symptoms or opportunistic diseases), and
Any HIV-infected individual with an AIDS indicator (category C) condition has AIDS |
|
|
how does WHO categorize HIV
|
WHO identifies 4 clinical stages based on the performance level of the person and the associated illnesses
|
|
|
WHO classification of HIV
|
Clinical stage I
Asymptomatic Generalized lymphadenopathy Performance Scale 1: asymptomatic, normal activity Clinical Stage II Weight loss <10% of body weight Minor mucocutaneous manifestations (seborrhoeic dermatitis, prurigo, fungal nail infections, recurrent oral ulcerations, angular cheilitis) Herpes zoster within the last 5 years Recurrent upper respiratory tract infections (e.g., bacterial sinusitis) And/or Performance Scale 2: symptomatic, normal activity Clinical stage III Weight loss >10% of body weight Unexplained chronic diarrhea lasting for more than 1 month Unexplained prolonged fever (intermittent or constant) lasting for more than 1 month Oral candidiasis (thrush) Oral hairy leukoplakia Pulmonary tuberculosis Severe bacterial infections (e.g., pneumonia, pyomyositis) And/or Performance Scale 3: bedridden less than 50% of the day during the past month Clinical Stage IV HIV wasting syndrome Pneumocystis jiroveci pneumonia Toxoplasmosis of the brain Cryptosporidiosis with diarrhea lasting more than 1 month Cryptococcosis, extrapulmonary Cytomegalovirus (CMV) disease of an organ other than liver, spleen or lymph node (e.g., retinitis) Herpes simplex virus (HSV) infection, mucocutaneous (lasting for more than 1 month), or visceral Progressive multifocal leukoencephalopathy (PML) |
|
|
Confirmation of HIV infection can be done by:
|
isolation of the virus
detection of viral antigen detection of viral antibody |
|
|
what tests do you use to diagnose HIV
|
Enzyme-linked immunosorbent assay (ELISA) screening (now called EIA)
EIA has a high number of false positives so if + it is ALWAYS repeated If second test + then WESTERN BLOT TEST done (only 1% false +) |
|
|
Immediate HIV tests
|
OraQuick ®
uses saliva or whole blood results in about 20 minutes home testing? Uni-Gold™ Recombigen® HIV uses whole blood, serum or plasma results in about 10 minutes Implications informing HIV+, physical and psychological responses and follow-up |
|
|
AIDS criteria
|
CD4 T count < 200
development of one of following opportunistic infections (OI) Fungal= Candidiasis of bronchi, trachea, lungs; Pneumocystis carinii jiroveci pneumonia; histoplasmosis Viral = Cytomegalovirus (CMV), herpes simplex with chronic ulcer, or bronchitis or esophagitis, progressive multifocal leukoencephalopathy (PML), extrapulmonary cryptococcosis Protozoal = coccidioidomycosis, toxoplasmosis, cryptosporidiosis Bacterial = TB, Mycobacterium avium Development of one of the following opportunistic cancers Kaposi Sarcoma (most common) Invasive cervical cancer Burkitt’s lymphoma Wasting occurs (loss of 10% or more of ideal body mass) Dementia develops |
|
|
HIV monitoring
|
CD4 T cell count
Monitored q 3- 4 months rough measure of damage already done to the immune system by HIV virus used to determine risk of Opportunistic Infections (OI) Viral load HIV RNA levels reported as copies of RNA per milliliter (2 copies = 1 virion) |
|
|
detmining AIDS risk
|
< 10, 000 copies/ml = low AIDS risk
10, 000 - 100, 000 = risk doubles > 100, 000 copies/ml = high AIDS risk |
|
|
major signs of AIDS
|
Major signs
Weight loss >10% body weight Chronic diarrhea (lasting >1 month) Fever intermittent or constant (lasting >1 month) |
|
|
goals of treatment of AIDS
|
Clinical
Prolong survival - Delay development of HIV – related symptoms and opportunistic diseases Prevent disease progression Minimize drug toxicity Virological Maximal and durable decrease of viral load for as long as possible to below detectable levels (currently defined as <50 copies/ml) Immunological Preserve or raise CD4 T cell levels (CD4 cell count in normal range) Public health Reduce HIV transmission Preserve future treatment options |
|
|
benefits and risk of early AIDS treatment
|
Benefits of early therapy
Control of viral replication easier Prevention of immune system compromise Lower risk of resistance with complete viral suppression Possible decreased risk of HIV transmission Avoid irreversible immune system depletion Risks of early therapy Drug-related reduction in quality of life Greater cumulative drug-related adverse events Earlier development of drug resistance Limitation of future antiretroviral treatment options |
|
|
drugs and AIDS
|
Drug resistance increases if drugs not taken as ordered.
3 different drugs from at least 2 categories Take full dose prescribed Take on time Must know all meds d/t interactions with others Check viral load 2 weeks after change in meds Integrate drug schedule into pt’s daily schedule |
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goals of drug therapy for AIDS
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The goals of drug therapy are to:
Decrease the viral load Maintain or raise the CD4 count Delay the development of HIV-symptoms and opportunistic diseases |
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Highly Active Antiretroviral Therapy (HAART) Goals:for AIDS
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To decrease HIV RNA levels or VIRAL LOAD to < 5000 copies/ul (undetectable levels preferred)
Maintain or raise CD4 T cells counts to > 500 cells/ul (range of 800 – 1200 preferred) Delay the development of HIV related symptoms & diseases HAART is when three or four drugs are used in combination |
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Antiretroviral drugs
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Act by inhibiting the activity of the enzyme reverse transcriptase to synthesize DNA from viral RNA
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Nucleoside Analogue Reverse Transcriptase Inhibitors (NRTIs)
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for AIDS
Insert a piece of DNA into the developing HIV DNA chain, blocking further development of the chain and leaving the production of the new strand of HIV DNA incomplete |
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Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs) (Nucleoside analogs)
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for AIDS
Combine with reverse transcriptase enzyme to block the process needed to convert HIV RNA to HIV DNA |
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Protease Inhibitors
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Prevent the protease enzyme from cutting HIV proteins into the proper lengths needed to allow viable virions to assemble and but out from the cell membrane
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Entry inhibitors
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Prevent binding of HIV to cells, thus preventing entry of HIV into cells where replication would occur
for AIDS |
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Nucleotide reverse transcriptase inhibitors
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Inhibit the action of reverse transcriptase
FOr AIDS |
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Side Effects: NRTIs for AIDS
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Bone marrow suppression (AZT)
Pancreatitis Peripheral neuropathy |
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Nonnucleoside Reverse Trancriptase Inhibitors (NNRTIs)
and Side Effects |
Interfere directly with reverse transcriptase
Side effects: Rash Fetal anomalies* Dizziness Confusion |
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Efavirenz (Sustiva)*
Nevirapine (Viramune) Delavirdine (DLV)(Rescriptor) |
Nonnucleoside Reverse Trancriptase Inhibitors (NNRTIs) drugs
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Nelfinavir (Viracept)
Saquinavir soft gel cap (Fortovase) Ritonavir (Norvir) Indinavir sulfate (Crixivan) Amprenavir (Agenerase) |
protease inhibitors
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side effects of protease inhibitor
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Side effects
Hepatotoxicity Nausea, vomiting, diarrhea |
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CDC Recommended initial drug regimen
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Zidovudine (AZT) & Lamivudine (Epivir)or Combivir (which contains both)
AND Efavirenz (Sustiva) |
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recommendations for longer life in AIDS
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High protein, high calorie diet
Control stress = relaxation, support groups Exercise regularly Smoking cessation Food & water safety guidelines |
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baceterial infections and AIDS
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Mycobacterium Tuberculosis (TB)
Mycobacterium Avium Complex (MAC) |
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Prophylactic drug therapy if CD4 < 100
and side effects |
Clarithromycin (Biaxin) 500 mg PO BID then 500 mg per day
SE = Hepatotoxicity, nausea, abdominal pain, diarrhea Azithromycin (Zithromax) 1.2 g/ week PO SE = Hepatotoxicity, nausea, abdominal pain, diarrhea Rifabutin (Mycobutin) 300 mg/day po SE = Hepatotoxicity, neutropenia, turns urine/feces orange |
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Protozoal infections
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Pneumocystisis Jiroveci
formerly know as Pneumocystisis Carnii now thought to be fungal Toxoplasmosis Cryptosporidiosis |
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Most common severe Opportunistic Infection associated with HIV infection
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Pneumocystis Pneumonia (PCP
Loss of cellular immunity permits organism growth, exudate produced, profound V/Q mismatch Occurs in 90% of HIV infected persons in the U.S. Usual reason for ICU admission |
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treatment of Pneumocystis Pneumonia (PCP)
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Trimethoprin -sulfamethoxazole (Bactrim) IV/PO
Pentamidine isethionate IV second line if Bactrim doesn’t work |
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Fungal infections
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Histoplasmosis
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Conditions specific to HIV disease for IV Encephalopathy
and sings and symptoms |
HIV Encephalopathy
Formerly AIDs Dementia Complex (ADC) At risk: very young, older patients & those with anemia & weight loss Triad of S & S: Cognitive dysfunction decreased memory & judgment Motor problems weakness, ataxia, clumsiness Behavioral changes ranges from apathy to hyperexcitability |
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Conditions specific to HIV disease HIV Wasting Syndrome
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Profound involuntary weight loss of > 10% of total body baseline weight
PLUS Chronic diarrhea or chronic weakness & fever Weight loss in part due to catabolism of muscle mass Goal: Boost appetite & caloric intake |
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what do you do after being exposed to HIV needle stick etc
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Zidovudine (AZT) should be included in all regimens
Treatment within 1-2 hrs of exposure (animal studies > 24-36 hrs = ineffective) and continue for 4 weeks If source patient’s HIV status unknown, therapy initiated on case by case basis. HIV testing for 6 months after exposure: baseline, 6 weeks, 12 weeks, and 6 months |
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Genetics and HIV
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Zidovudine (AZT) should be included in all regimens
Treatment within 1-2 hrs of exposure (animal studies > 24-36 hrs = ineffective) and continue for 4 weeks If source patient’s HIV status unknown, therapy initiated on case by case basis. HIV testing for 6 months after exposure: baseline, 6 weeks, 12 weeks, and 6 months |
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true or false
Although HIV can be contracted in several ways, unsafe sex is the most frequent mode of transmission |
true
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Standard precautions apply to all body fluids except saliva.
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false
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true or false
An HIV patient with tuberculosis may manifest a negative response to a tuberculin skin test. |
true
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true or false
Recurrent vaginal candidiasis may be the first sign of HIV infection in women. |
true
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true or false
Although needle exchange programs reduce the incidence of HIV in IV drug users, they also increase the use of illegal drugs. |
false
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Mother-to-child transmission of HIV is most likely to occur during _________ .
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birth
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Loss of immune competence puts the patient with HIV at increased risk for _________ infections such as Pneumocystic jiroveci pneumonia .
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opportunistic
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_________ is a significant problem for the majority of AIDS patients due to enteric pathogens and the direct effects of HIV on intestinal cells.
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diarhea
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Results of antiretroviral therapy are evaluated using viral _________ tests.
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load
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Post-exposure prophylaxis for health care workers exposed to HIV involves taking antiretroviral drugs for _________ weeks
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four
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