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Med surg 3 exam 3
exam 3
| Question | Answer |
|---|---|
| protects spinal cord & supports body frame | spinal column |
| transmits neural impulses from the brain to the rest of the body, coordinates reflexes | spinal cord |
| type of injury examples: motor vehicle crashes, falls, violence, recreational sports | traumatic injury |
| type of injury examples: anklyosing spondylitis, RA, tumors | nontraumatic injury |
| spinal cord injury classification: paraplegia, tetrapeligia | complete spinal cord injury |
| spinal cord injury classification: spastic paralysis, flaccid paralysis | incomplete spinal cord injury |
| spinal cord injury classification: cervical, thoracic or lumbar | level spinal cord injury |
| spinal cord injury classification: neurologic damage that occurs at moment of impact | primary spinal cord injury |
| spinal cord injury classification: occurs within minutes of injury and can last for days to weeks, similar to TB!! | secondary spinal cord injury |
| what does radiography look at? | the stability of vertebral column |
| what is a CT scan used for? | better visualization |
| what identifies injuries to cord, ligaments, disks, can detect tumors, inflammation, infection, and vascular disruptions? | MRI (takes more time than CT) |
| what is done to visualize damage to vertebral artery (looking at bloodflow?) | angiography |
| what establishes functional prognosis after spinal cord edema resolves? | somatosensory evoked potentials |
| to assess motor strength, start where and move to what? | start at head and move to toes |
| eliminate gravity, assess movement against gravity, ROM against resistance: | motor assessment |
| examining where exact point where sensation is normal | sensory assessment |
| move from where to where to assess sensory? | move from lower to upper |
| assess presence of deep tendon reflexes | reflex activity |
| temporary state: usually occurs within 1st hour; resolves in a couple days | spinal shock |
| bradycardia is what sets this apart from the other types of shock | neurogenic shock |
| decompression & fusion (usually reserved for cervical injuries & injuries that can't be aligned with manual stabilization | surgical stabilization |
| to reduce fracture, screws implanted in skull, traction with weights added (invasive) | skull tongs (more temporary than halo device) |
| external fixation to keep spine aligned, prevents flexion, extension, and rotation of head & neck, 4 pins inserted in skull (invasive) | halo device (more long term) |
| type of stabilization: skull tongs, halo device, braces | manual stabilization |
| type of stabilization: methylprednisolone to prevent secondary injury, controversial (must be weaned off of steroids, doesn't always have positive outcomes) | steroid therapy |
| spinal cord injuries are more prone to what? | infections! (life threatening) |
| CNS dysfunction: life threatening, exaggerated sympathetic response (think about fight or flight response) | autonomic dysreflexia |
| occurs after spinal shock has resolved, lesions above T6 (higher up); sympathetic nervous system responses are exaggerated; life threatening to patient | autonomic dysreflexia |
| S/Sx: hypertension, sweating, goose bumps, HA, blurred vision, anxiety; parasympathetic system tries to response & can only function above injury resulting in flushing of skin, pupil constriction, stuffy nose, bradycardia | autonomic dysreflexia |
| what do you want to do if a patient has autonomic dysreflexia? | lower BP & determine cause- commonly bladder distention, bowel impaction, temp. change, UTI, pain, some kind of infection |
| class of stroke: blood supply to a part of the brain is suddenly interrupted, usually caused by thrombus or embolus- most commonly d/t atherosclerosis | ischemic stroke |
| class of stroke: blood clot that obstructs arterial blood flow (stays in one spot) usually happens when patient is at rest | thrombotic stroke |
| class of stroke: blood clot that travels from its original site & becomes lodged in an artery that feeds the brain (think of PE-travels)- usually occurs when a patient is up & moving | embolic stroke |
| what valve disorder commonly causes embolic strokes? | afib |
| class of stroke: brief episodes of focal neurologic deficits that usually resolve in a few minutes or hours, do not cause permanent damage, may precede a stroke, WARNING OF AN IMPEDING STROKE! | transient ischemic attack (TIA) |
| class of stroke: bleeding into brain tissue or cranial vault (actually bleeding) | hemorrhagic stroke |
| type of hemorrhage: cerebral blood vessel ruptures & blood accumulates in brain tissue | intracerebral hemorrhage |
| type of hemorrhage: due to trauma or rupture of an aneurysm, EMERGENCY! | subarachnoid hemorrhage |
| most common site of stroke is at the bifurcation of what? | the common carotid artery |
| what happens when clot, plaque, or platelet plug breaks off and blocks an artery? | stroke occurs |
| stroke impairs oxygen delivery resulting in impaired cellular function leading to what? | cell death |
| within a stroke there are cells that are dead & have no function & around those cells are minimally perfused cells that are still viable | penumbra |
| what is the goal of penumbra? | prevent secondary injury-optimize perfusion |
| after a stroke, reperfusion needs to occur in under what? | an hour "golden hour", however, we do allow more time due to the ability to still save of the cells |
| what is the goal after a stroke occurs? | restore cerebral blood flow & limit the size of infarcted zone |
| TPA (thrombolytic) therapy for reperfusion should occur up to how many hours from onset of symptoms? | 4.5 hours |
| modifiable risk factors for stroke: | BP, cardiac disease, diabetes (type II), dyslipidemia, smoking |
| nonmodifiable risk factors for stroke: | age, gender, race/ethnicity, genetic factors |
| who is more at risk for having strokes? | older adults, males |
| common manifestations of stroke: | numbness & weakness of face & arm, difficulties with balance or speech, loss of vision in one eye |
| thrombotic stroke speed of onset & rate of progression | slow progression (blood supply becomes smaller & smaller) |
| embolic stroke speed of onset & rate of progression | appears suddenly causing immediate neurologic deficits |
| hemorrhagic stroke speed of onset & rate of progression | appears suddenly & varies depending on location |
| what should be focused on when doing an assessment of stroke? | gag reflex (NPO until pass swallow evaluation) |
| what should be differentiated with a stroke in older adults? | dementia |
| what is critical when it comes to having a stroke? | TIME |
| what should be quickly determined when a patient is having/had a stroke? | hemorrhagic or ischemic- guides treatment, only have so much time |
| what is the golden standard test for stroke? | CT scan |
| what is used to see small clots in the heart? | TEE (if patient is to be cardioverted, they should have a TEE first) |
| what clotting times are important with stroke? | PT/INR, PTT |
| what mimics a stroke and should be ruled out when diagnosing? | hypoglycemia & electrolyte imbalances |
| what is the National Institutes of Health Stroke Scale (NIHSS)? | extensive assessment to assess all patients the same way |
| in an ischemic stroke, what medication should be given if patient is not receiving TPA? | aspirin- stops platelets from sticking together |
| thrombolytic therapy (TPA) must be given within how many hours? | 3-4.5 hours |
| thrombolytic therapy (TPA) can cause what major problem? | hemorrhage!! |
| TPA: what to give & when? | bolus within 3-4.5 hours followed by continuous infusion over an hour |
| what should be preformed frequently when administering TPA? | neurological assessments & BP checks |
| discontinue TPA infusion if what occurs? | N/V, severe headache, or hypertension develops |
| what serum glucose is good involved w/ strokes? | less than 180 is good |
| permissive hypertension is used to get blood supply/oxygen to those damaged sites in what kind of stroke? | ischemic stroke only |
| what is the highest BP acceptable for ischemic strokes, only allowed 1st 24 hours for a patient not receiving TPA? | 220/120 |
| what dysrhythmia is focused on that could cause a stroke? | afib (clots in heart could cause stroke) |
| contraindications to TPA? | hemophilia (bleeding clotting disorders), recent/major surgery, recent hemorrhagic stroke (within the last 3 months) |
| if a patient can not have TPA, what should be administered to them instead? | aspirin |
| if patient is receiving thrombolytic therapy (TPA), don't let BP higher than what? | 185/110 (to avoid massive hemorrhage) |
| invasive procedures for patient with angiosclerosis? | angioplasty & stenting (balloon to dilate vessels)-carries risk for hemorrhage |
| invasive procedure performed for hemorrhage or cerebellar infarction that compresses brainstem & increases ICP (for hemorrhagic stroke)? | craniotomy |
| for hemorrhagic stroke, procedure performed within 72 hours of the bleed, opening the cranium & putting a metal clip around the aneurysm to prevent rebleeding | aneurysm clipping |
| what is recommended when patient has had an aneurysm clipping? | triple H therapy (hypertension, hypovolemia, hemadilution) - maintain perfusion to brain |
| invasive procedure for ischemic disease, used to prevent recurring infarcts & TIAs | carotid endarterectomy |
| Priority to prevent when managing a stroke patient | prevent hypercapnia (causes vasodilation) |
| brain insult resulting from a mechanical disruption of brain tissue from an external impact or injury to the head | traumatic brain injury (TBI) |
| traumatic brain injury can be linked to what? | PTSD |
| mechanism of TBI: blunt moving object strikes the head | acceleration |
| mechanism of TBI: when an individual's head hits an immovable object | deceleration |
| what is the most severe type of traumatic brain injury? | when acceleration & deceleration occur together |
| mechanism of TBI: force impacting the head transfers energy to the brain in a nonlinear fashion, head rotates on its axis resulting in a shearing force throughout the brain & its axons (think of baking- head rotates) | rotational |
| mechanism of TBI: foreign object invades the brain (bullet, stabbing, other objects) | penetrating |
| skull fracture: not life threatening | linear |
| skull fracture: something has pushed skull inward | depressed |
| skull fracture: a part of skull missing (think of infection) | open |
| skull fracture: think of base of skull (back of head), can cause patient to immediately die-more distinct- leaking clear CSF! | basilar |
| the direct mechanism injury caused by the force or impact; causes immediate damage to neurons; often irreversible damage | primary traumatic brain injury |
| in response to the primary injury & results from local tissue & system response such as ischemia, more neuronal death, INFLAMMATION; can worsen patient outcomes | secondary traumatic brain injury |
| hypoxemia or hypercapnia results in what? | vasodilation |
| focal brain injury: accumulation of blood | cerebral hematoma |
| focal brain injury: accumulation of blood between the dura & arachnoid layers | subdural hematoma |
| do subdural hematomas have a fast or slow onset? | slow onset (usually venous injury) |
| when do manifestations develop in a subdural hematoma? | under 48 hours (acute), drowsy to comatose |
| when do subacute subdural hematomas occur? | 48 hours to 2 weeks, HA, drowsiness, confusion |
| when do chronic subdural hematomas occur? | manifestations develop more than 2 weeks after injury; vague manifestations can include HA, lethargy, absent-mindedness |
| focal brain injury: accumulation of blood between dura & skull, classic presentation includes LOC followed by being alert & oriented & then LOC again | epidural hematoma |
| focal brain injury: accumulation of blood in the parenchyma (brain tissue), manifestations vary according to location (common: HA, decreased LOC, dilation of one pupil, hemiplegia, symptoms similar to stroke/one sided) | intraparenchymal hematoma |
| focal brain injury: bruising of soft tissue; begins locally & may become diffuse over time (can spread throughout brain-unpredictable!) | contusion |
| diffuse brain injury: blunt trauma to head, cerebral damage at microscopic level, not detectable through radiographic or other testing, clinical presentation can include unconsciousness followed by amnesia; postconcussive symptoms can continue for months | concussion |
| what test is usually done in a concussion? | CT scan |
| diffuse brain injury: shearing forces disrupt structure of neurons & blood vessels; does not require bleeding (makes it difficult to detect); causes multiple, small diffuse hemorrhages | diffuse axonal injury |
| diffuse brain injury: accumulation of blood between meningeal arachnoid & the brain | subarachnoid hemorrhage |
| subarachnoid hemorrhages are commonly caused by what? | aneurysm (thunder clap headache!!!) |
| management of diffuse brain injuries: | lower ICP, increase CPP, stabilize vitals, prevent complications |
| assessment to see severity of brain injury | glasgow coma scale- initiate after initial resuscitation & before sedation or anything that can alter LOC |
| mild injury GCS: | 13-15-confused patient |
| moderate injury GCS: | 9-12- risk for increased ICP & cerebral edema |
| severe injury GCS: | 8 or less- critically ill, usually requires vent & ICP monitoring |
| what is an important rule when assessing a brain injury? | always assume patient has spinal cord injury until you can rule it out |
| golden standard when diagnosing brain injury | CT scan- fast, doesnt always need dye (MRI may be needed to get better image) |
| management of brain injury? | focus on maintaining CPP & controlling ICP |
| treat hypoxia & hypotension to minimize what kind of brain injury? | secondary injury |
| hyperthermia (r/t brain injury) requires more of what? | more oxygen |
| ideal MAP r/t brain injury? | greater than 90 to maintain CPP sufficiency (good for perfusion to brain) |
| questionable use for TBI, used for some cardiac arrest patients (protects brain tissue/functioning) | therapeutic hypothermia (TH) |
| to promote venous return in TBI patients, HOB should be what? | elevate HOB 30 degrees (unless cervical spine injury) |
| what may be used to produce vasoconstriction of cerebral vessels r/t TBI? | therapeutic hyperventilation |
| Normal ICP: | 0-15 (>20 for more than 5 min. need to intervene!!) |
| traumatic injuries are at risk for what? | ARDS |
| CSF drainage requires what? | IVC (requires an order) |
| what should be administered for hyperosmolar therapy? | mannitol (osmotic) |
| what is the most aggressive form of ICP? | level 3 |
| paralytics for patient to rest? | neuromuscular blockade |
| what are used to reduce ICP? | barbituates |
| typically occurs 5-10 days after TBI; produce large amounts of dilute urine with increase sodium & osmolality (r/t not secreting enough hormones); give vasopressin or desmopression | Diabetes Insipidus (complication of TBI) |
| complication of TBI: small amounts of concentrated urine w/ a decrease in sodium (dilute fluid); should restrict fluids | Syndrome of inappropriate antidiuretic hormone (SIADH) |
| complication of TBI: similar to SIADH, low sodium & urine osmolarity; state of hypovolemia; give IV saline or oral salt tablets | Cerebral salt wasting |
| complication of TBI: early-onset* (occurs within 7 days); late onset* (more than 7 days after injury) | seizires |
| complication of TBI: catastrophic*, drastic deterioration in neuro status & VS, unequal pupils followed by bilateral fixed, fully dilated | brain herniation |
| most severe complication of TBI (irreversible) | brain death |
| any alteration in brain functioning (can be long term or not) is known as what? | encephalopathy |
| acute confusional disorder characterized by attention deficits, fluctuating mental status, disordered thinking, altered LOC | delirium |
| type of delirium: ICU psychosis, agitation & restlessness | hyperactive |
| type of delirium: lethargy, withdrawal, flat affect, decreased responsiveness (gets missed a lot- gets labeled w/ encephalopathy often) | hypoactive |
| increased permeability can cause inflammatory mediators to cross the blood brain barrier causing edema, SIRS response (important to identify) | septic encephalopathy |
| delirium meds | antipsychotics (haloperidol, risperidone, seroquel) |
| persistent state of unresponsiveness from which a person cannot be aroused for more than 6 hours | coma |
| patient maintains arousal but not awareness (responses are spontaneous-patient looks alert but really isn't) | persistent vegetative state |
| irreversible loss of all brain & brainstem function (can maintain for period of time, but once brain stem stops functioning, they will deteriorate) | brain death |
| can result from drug intoxication, withdrawal, infections, brain trauma, ischemic injury, lesions, or metabolic issues | seizures |
| 1st line seizure meds? | benzodiazepines (lorazepam, diazepam) |
| continuous seizures for more than 5 minutes or recur without recovery of consciousness, mortality is highest with this type of seizure d/t respiratory risk & long term neurologic damage | status epilepticus |
| What is at risk with a valve less brain system? | pooling, limit blood flow out of brain |
| ICP: 80%, mainly water, disruption of blood-brain barrier results in cerebral edema | brain volume |
| ICP: 10%, maintained at a constant level through cerebral blood flow | cerebral blood volume |
| ICP is measured in the CSF & ranges from what? | 0-15 mm Hg = normal ICP |
| what is the easiest to influence with ICP? | cerebrospinal fluid |
| hypercapnia is what? | high CO2 |
| pressure gradient associated with cerebral blood flow that is necessary to supply blood in adequate amounts to the brain tissue (how much blood flow needed to go to brain) | Cerebral perfusion pressure (CPP) |
| what is CPP? | difference between MAP & ICP |
| normal CPP range? | 70-100 mm Hg |
| individual's ability to respond to environmental stimuli | arousal |
| patient's orientation | content |
| scores range from 15-3, score less than 7 is a coma state | Glasgow Coma Scale |
| inability to understand written or spoken words (can't receive it) | receptive aphasia |
| inability to write or use language appropriately | expressive aphasia |
| inability to use or understand language (both receptive & expressive) | global aphasia |
| abnormal flexion, indicates cerebral dysfunction (think of core- postures inward) | decorticate |
| abnormal extension, indicates brainstem dysfunction, more ominous (postures outward-worst of the 2) | decebrate |
| both pupils dilated & fixed signifies what? | emergency!!! think ischemia (no blood flow somewhere in brain) |
| pinpoint pupils signify what? | opiate drug overdose |
| blood pressure (systolic high/diastolic low) = what? | impending brain herniation |
| intracranial pressure monitoring is only recommending with GCS of what? | 8 or less who have abnormal findings on CT |
| what is the gold standard for cerebral perfusion? | intraventricular monitoring (can drain CSF) |
| most invasive procedure for cerebral perfusion | intraventricular catheter (can drain fluid) |
| what is a common contributor to acute kidney injuries? | sepsis |
| rapid onset & can be reversible, decrease in renal function often first noted by decrease in urine production (oliguria); high BUN/Creatinine | acute kidney injury |
| acute kidney injury is also known as what? | acute renal failure |
| kidney dysfunction resulting from decrease in blood volume; decreased CO, arterial occlusion, drug induced | prerenal AKI |
| problems that target actual renal tissue; drug induced, hepatorenal syndrome, rhabdomylosis (tea colored/dark urine, confused) | Intrisic AKI |
| obstruction of outflow of urine | Postrenal AKI |
| most at risk for AKI? | diabetics, hypertension patients, older patients (aging kidneys) |
| how do you prevent kidney injury? | treat hypertension early, early detection of family history |
| replaces certain functioning of kidneys; can correct fluid, electrolyte, & acid/base imbalances; removes waste | Renal Replacement Therapy (RRT) |
| Types of Renal Replacement Therapy (RRT)? | Intermittent hemodialysis, continuous renal replacement therapy, Peritoneal dialysis |
| gradual loss of renal function, impacts all other organs; can lead to full blown renal failure; progressive, irreversible; staged 1-5 | Chronic Kidney Disease (CKD) |
| must have evidence of kidney damage lasting 3 months along w/ decrease in glomerular filtration rate or structural/functional abnormalities | Chronic Kidney Disease (CKD) |
| manifestations: HF, hyperlipidemia, heart disease, pericarditis, chronic anemia, anorexia, sleep disorders, memory loss, impaired judgment, muscle cramps/twitching, encephalopathy, more susceptible to infections | Chronic Kidney Disease (CKD) |
| Treatment: dialysis, erythropoietin, iron supplements, vitamin D/ Calcium, diuretics, ACE inhibitors, beta blockers | Chronic Kidney Disease (CKD) |
| damage to glomerular membrane; causes increased permeability to plasma proteins (proteinuria); hypoalbuminemia & edema result; can be related to glomerulonephritis, diabetes, amyloidosis, multiple myeloma; treatment includes ACE inhibitors & diuretics | Nephrotic Syndrome |
| most often asymptomatic, late stages include blood in urine, flank pain, weight loss, fever; risk factors: smoking HTN; diagnostics: IVP, US, cystoscopy, biopsy, CT; treatment: nephrectomy, tumor removal, biological therapies, radiation; can easily spread | Renal Cancer |
| facilitates movement of food & fluid | esophagus |
| food storage, digestion, propulsion | stomach |
| absorption of nutrients & water, hormone secretion to regulate digestion | small intestine |
| completion of water & nutrient absorption, formation & expulsion of feces | large intestine |
| arterial blood comes from what? | abdominal aorta |
| fat metabolism, excretion of bile, maintains normal blood glucose, protein metabolism, vitamin absorption, iron storage, engulf & destroy bacteria, formation of clotting factors, metabolizes fat soluble drugs | Liver |
| secretes insulin & glucagon, releases enzyme fluids to aid in digestion of fats, starches, proteins, part of hepatic portal system | Pancreas |
| causes: peptic ulcers, erosive gastritis, tears, varices | upper GI bleed |
| causes: diverticulosis, AV malformation | lower GI bleed |
| blood that is present but not visible | occult blood |
| vomiting of blood | hematemesis |
| black, tarry, foul-smelling stools | melena |
| bright red or maroon stool | hematochezia |
| most common causes of upper GI bleeds? | peptic ulcer disease (PUD)!!! H. Hylori infection, NSAIDs, family history, smoking |
| manifestations: severe pain, if bleeding present-occult, hematemesis, melena, hematochezia | Upper GI bleeding |
| diagnosis & treatment: endoscopy, H. pylori testing, antibiotic therapy, proton pump inhibitors, H2 receptor blockers, sucralfate, antacids | upper GI bleeding |
| less common & usually less severe than upper GI bleeding | lower GI bleeding |
| lower GI bleed: self-limiting in most cases | diverticular bleeding |
| bloody diarrhea, typically light to moderate | inflammatory bowel disease |
| colorectal cancer, usually slow & chronic | neoplasms/polys |
| typically slow & chronic, may require arterial embolization | AV malformation |
| occlusion of artery, small vessel disease, venous obstruction, low-flow states, intestinal obstruction, typically tied to anticoagulant use | ischemic bowel disease |
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