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Multiple sclerosis etiology

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175 Terms
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Multiple sclerosis etiology

- unknown cause

- unlikely related to a single cause

- genetics and environmental related to infectious, immunologic, and genetic factors

- precipitating factors can turn on MS in someone with a genetic disposition

- precipitating factors: infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poorer state of health

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Multiple sclerosis classification scheme


- clearly defined relapses with full recovery or minimal residual

- 80+% are diagnosed with this type of relapse


- accumulation of disease

- no distinct relapse or recovery

- 10% of MS


- start with relapse-remitting

- there is also progression

- 50% of patients diagnosed with relapse-remitting develop this within 10 years

Clinically isolated syndrome (CIS)

- episode that is indicative of MS

- clinical episode with symptoms similar to MS

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Multiple sclerosis diagnosis

- no definitive diagnostic test

- based on: history, clinical manifestations, and results of imaging studies

- diagnosis of exclusion

Imaging and tests that can assist in diagnosis


- CSF analysis

- evoked potentials: electrical events generated in by peripheral stimulation of a sensory organ to measure response time (somatosensory, visual, or brainstem auditory) (patients with MS have delayed visual response 50-90% of the time)

3 Criteria for Diagnosis

- lesions in 2 different locations

- damage/attack interval (usually a month apart)

- rule out

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Multiple sclerosis clinical manifestations


- weakness or paralysis

- double vision

- scanning speech

- muscle spasticity (interferes with speech and gait)


- Lhermitte's sign: electrical shock radiating down spine and neck

- numbness

- tingling

- blurred vision

- dizziness (vertigo)

- loss of balance

- patchy blindness

- reticular nerve root pain


- nystagmus

- involuntary eye movement

- ataxia

- dysarthria

- dysphagia

- difficulty swallowing


- increased energy needs

- heat

- decreased fluids

Bowel and Bladder

- constipation

- spastic bladder: possible dribbling or incontinence

- flaccid bladder

Sexual dysfunction

- erectile dysfunction

- decreased libido

- decreased vaginal lubrication

- pain during intercourse

Emotional changes


- 50% may experience short-term conversational or planning issues

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Multiple sclerosis pseudo relapse

- also known as pseudo-exacerbation or pseudo-flare

- common triggers: stress, fatigue, illness, and heat

- not causing new damage

- very distressing to patients

- treat underlying cause

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Impact of Pregnancy on a Patient with Multiple Sclerosis

- pregnancy can exacerbate symptoms and progression

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goals of disease modifying therapy

- decrease relapse rate

- slower accumulation of brain lesions on MRI

- will not heal scarring

- may not improve current functioning

- may have some effect on progression

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Adjunctive pharmacologic treatment for multiple sclerosis

- acute exacerbations: glucocorticoids (methylprednisolone, prednisone, etc.) (reduces edema at the site of demyelination) and plasma exchange (for a bad reaction to glucocorticoids)

- anticholinergics: treating bladder symptoms, increasing the amount of urine that can be held

- CNS stimulants for fatigue

- muscle relaxants for spasticity

- nerve conduction enhancer - improves walking speed (cautioned in CKD and seizure disorder)

- tricyclic antidepressants for chronic pain

- antispasmodics for spasticity (baclofen)

- anti seizure for chronic pain

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Functional limitation in patients with multiple sclerosis

- impaired physical mobility

- impaired urinary elimination

- interrupted family processes

- risk for falls

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Multiple sclerosis patient teaching

- good balance of exercise and rest

- nutrition

- treatment regimen (medication management and adherence)

- self-catheterization if necessary

- adequate intake of fiber to aid in regular bowel habits

- emotional adjustments

- lifestyle changes

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ALS etiology-classifications

- sporadic: without family history, random, 90-95% of cases

- familial: one occurrence in family, dominant inheritance

- onset: 40-70 years of age

- men vs. women - 2:1 men to women

- 5000 people in US diagnosed annually

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ALS clinical manifestions UMN vs. LMN

Typical manifestations: muscle weakness, dysarthria, dysphagia

Other manifestations: pain, sleep disorders, spasticity, drooling, emotional lability, depression, esophageal reflux, constipation

Upper Motor Neuron manifestations

- loss of dexterity or ability to coordinate movements

- weakness

- spasticity

- hyperreflexia

Lower Motor Neuron manifestations

- weakness

- paralysis

- hyporeflexia

- fasciculations

- flaccidity

- muscle cramps

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ALS diagnosis

- difficult to diagnose

- thorough neurological examination is key

- diagnosis of exclusion: electrodiagnostic tests, blood and urine studies, spinal tap, x-rays, MRI, pyelogram of cervical spine, and muscle and/or nerve biposy

- El Escorial criteria

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ALS drug therapy


- decreases body's level of glutamate

- slows progression of disease


- slows functional deterioration

- prevents oxidative stress

- came out 2 years ago

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ALS nursing interventions

Facilitating communication: over articulation, limit distractions, sit face to face, yes/no systems, eye blinking, smartphone, letter board, speech generating devices

Aspiration precautions: honey or nectar thick food, coughing and deep breathing exercises, secretion management with coughalator and chest physiotherapy, incentive spirometry, suctioning

Falls precautions: bed alarm, bed in lowest position, lifts, wheelchair safety, promote safe mobility

Skin management: turn q2hr, promote adequate nutritional intake, avoid boney prominences, reposition in wheelchair, incontinence management

Nutrition: appropriate consistency, small bites, eat slowly, positioning after eating, small frequent meals, high fiber, hydration, G tube, parenteral nutrition as the disease progresses

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ALS prognosis

- no cure

- death typically occurs from a respiratory tract infection

- 2-6 years after diagnosis

- focus on symptom management

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SLE etiology

- unknown

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SLE risk factors

- potentially due to genetics, hormones, or environmental factors

- possible environmental factors: sun or UV exposure, stress, viruses, chemicals, toxins, medications

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SLE pathophysiology

- the immune system produces auto reactive B cells and T cells, which make a type of protein called autoantibodies

- these autoantibodies in turn attack the bodies' cells, leading to inflammation

- these autoantibodies target various components of the cell nucleus and result in a Type III hypersensitivity response

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SLE clinical manifestations


- fever

- weight loss

- joint pain

- excessive fatigue


- malar/butterfly rash

- alopecia

- mouth ulcers

- photosensitivity


- arthritis

- swelling

- pain

- stiffness

- deformity

- subluxation

- swan neck of finger

- ulnar deviation


- pleurisy: inflammation of tissue that lines the lungs


- pericarditis

- myocarditis

- endocarditis

- fibrosis of sinoatrial and atrioventricular nodes (can lead to heart block)

- antiphospholipid syndrome: formation of abnormal blood clots

- Raynaud's phenomenon: narrowing of blood vessels


- mild proteinuria

- glomerulonephritis

Nervous System

- seizures

- headaches

- peripheral neuropathy

- cognitive problems: disordered thinking, disorientation, memory deficits

- depression

- anxiety


- anemia: low RBC

- leukopenia: low WBC

- thrombocytopenia: low platelets

- coagulation disorders: excess bleeding or clotting

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SLE diagnosis


- ANA test

- Anti-DSDNA test

- Anti-smith antibody

- antiphospholipid antibodies


- can be used to assess affected joints


- can be used to access cardiac abnormalities

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SLE pharmacologic treatment

- NSAIDS: reduce inflammation

- antimalarial agents: decrease autoantibody production

- corticosteroids: decrease inflammation (should be limited to the lowest dose)

- steriod-sparing medications: suppress immune system; control inflammation

- anticoagulants: increases blood clotting time

- monoclonal antibodies: target B-cells

- respiratory corticotropin injection: contains naturally occurring hormone ACTH, stimulates body to produce cortisol, helps reduce inflammation

- immunosuppressive medications: suppress the immune system

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SLE non-pharmacologic treatment


- no special diet

- consider: alcohol use, fat & salt intake, and calcium intake

- avoid alfalfa and garlic


- low impact: walking, swimming, yoga, pilates, cycling

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SLE complications

- infections

- end-stage renal disease

- stroke

- heart attack

- pregnancy complications

- skin scarring

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SLE nursing management

- pain management

- patient education

- maintain optimal role function

- positive self-image

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Primary prevention of abdominal trauma

- seatbelts: most effective way to reduce injury with MVC and reduces serious injury in crash by 50%

- helmets: most effective way to reduce injury in MCC; estimated to prevent 37% of fatal motorcycle injuries

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trauma primary survey

A - airway (with cervical spine protection)

B - breathing (and ventilation)

C - circulation (with hemorrhage control - stop the bleed)

D - disability (neurological status)

E - exposure and environmental control (completely undress patient but avoid hypothermia)

- vital signs, IV's, drugs, transfusions, foley, gastric tube, documentation

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trauma secondary survey

- History: AMPLE (allergies, medications, PMH, last meal, and events surrounding injury)

- physical examination: neurologic, head and skull, maxillofacial, neck, chest, abdomen, perineum/rectum, musculoskeletal, and tubes/fingers

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common injuries in blunt trauma

- liver laceration

- splenic laceration

- renal laceration

- bowel hematoma

- pelvic hematoma

- retroperitoneal hematoma

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pre-op nursing management of abdominal trauma

- prep for surgical intervention (pending diagnostic data)

- fluid resuscitation

- protection of ABC's

- management of pain

- frequent abdominal assessments (observe for abdominal distention and palpate for pain and firmness)

- prevention of lethal triad

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post-op nursing management of abdominal trauma


- protect and monitor airway and breathing

- ensure latency of airway

- monitor vital signs

- position patient to ensure optimal lung expansion

- monitor color and character of secretions (suction as needed)


- maintain hemodynamic stability

- monitor VS

- frequent assessment of peripheral vascular system

- monitor mental status

- provide fluid resuscitation

- crystalloid: lactated ringers or normal saline(20-30 mL/kg)

- colloids

- monitor I/O

- vasopressors: study at Penn showed that vasopressin along with crystalloid and colloid resuscitation had no mortality benefit but did show statistically significant benefit of less overall fluid resuscitation


- prevent trauma triad of death

- stop the bleed

- keep the patient warm: keep patient covered as much as possible, apply warm blankets, keep room temp. high

- administer fluids, both crystalloid and colloid

- ensure they are warm

- monitor and maximize oxygenation


- abdominal assessment: observe for increasing abdominal distention, auscultate for bowel sounds, and palpate to assess for pain or tenderness as well as firmness of abdominal wall

- trend bladder pressure: measures the intra-abdominal pressure and considered reliable only when patient is heavily sedated or chemically paralyzed

- nutrition: early involvement of nutrition team, advocate for 1.5-2.5g/kg/day of protein to start, monitor nutritional status with weekly labs (albumin, pre-albumin, C-reactive protein), monitor and replace electrolytes, weigh patient daily

- if contraindications to TEN exist, advocate for patient to start TPN within 48 hours of initial damage control procedure

Surgical Site

- incision assessment

- midline incision with full abdominal closure

- partial closure (such as a fascial closure where the skin remains open)

- open abdomen with ABThera, VAC, or other closure device

- indications for the open abdomen: damage control surgery, abdominal compartment syndrome, massive fluid replacement, requirement for second-look surgery (to assess bowel viability or to evaluate and treat continued intra-abdominal contamination)

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Neurologic exam

- glasgow coma scale

- pupils: CN II and III = midbrain

- not unilateral or bilateral dilated pupils (can be signed of increased ICP or herniation)

- extremity movement (equal?)

- in a comatose patient, checking protective reflexes such as blink (corneal reflex), gag, and cough are used to determine presence or absence of brain death

- observe for signs of trauma: lacerations, CSF rhinorrhea, peri-orbital hematoma, battles sign (bruising behind ear), raccoon eyes

- note PMH

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TBI classification and types of injury

Penetrating Injury

- a head injury in which the dura mater (outer layer of the meninges) is breached

- less common than closed head trauma but worse prognosis

- penetrating: foreign object penetrate and remains lodged

- tangential: foreign objects glances off skulls driving bone fragments into the brain

- perforating: through and through

- most common is GSW


- low velocity injury resulting in functional deficit without pathological injury

- most common symptoms is headache

- neuroimaging is typically normal

- recovery from symptoms within 7 days to 6 weeks

- balance and coordination may be affected

- concussion clinics and outpatient therapy are useful for symptom management (which can affect QOL)

Acceleration and Deceleration Injuries

- coup: site of impact with blunt object

- contrecoup: opposite the area of impact

Diffuse Axonal Injury

- long connecting fibers in the brain (axons) are sheared as the brain accelerates and decelerates

- causes injury to many places in the brain

- patients are often in a coma without obvious lesion on CT scan; punctate hemorrhages can be seen on MRI

- supportive care

- poor outcomes

Subdural Hematoma

- bleeding between dura and arachnoid membranes

- elderly are prone d/t fragile vessels and brain atrophy

- can occur with relatively low impact or be spontaneous

- typically venous (tearing of bridging veins)

- close near observation/serial near exams: gradually increasing headache and confusion can indicate expansion

- potential surgery for evacuation

- seizure prophylaxis (presenting symptom can be seizure)

- possible drain

Epidural Hematoma

- bleeding between skull and dura layer

- typically arterial

- close near observation/serial near exams: lucid initially to unconsciousness (can happen quickly)

- potential surgery

- seizure prophylaxis


- bleeding between the Pia mater and the arachnoid membrane

- trauma is most common cause of SAH

- seizure prophylaxis

- occurs in 35% of TBI, typically in combination with other hemorrhage

- rarely causes vasospasm

- medical management only

Intracerebral Hemorrhage

- intraparenchymal hemorrhage: blood in brain tissue

- intraventricular hemorrhage: blood in ventricles

- seizure prophylaxis

- surgery: possibly

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Potential complications of head injury

- cerebral edema and herniation

- seizures

- hydrocephalus

- alternations of neuroendocrine function of hypothalamus and pituitary system (diabetes isipidus and syndrome of inappropriate anti-diuretic hormone)

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Cushing's triad

- increased BP (sympathetic response to cerebral ischemia, worsening problem)

- decreased HR (HTN is detected and stimulates vagus nerve)

- decrease RR or irregular respiratory pattern (compression or respiratory center)

means acute herniation (near emergency)

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TBI nursing management


- serial neurologic exams (Q15min-Q4hours)

- monitoring/managing ICP; ICP

- manage pain/agitation

- EVD management

- repeat imaging - urgency

- seizures (clinical vs sub-clinical)

- HOB elevated (unless contraindicated)

- management of paroxysmal sympathetic hyperactivity


- BP goals: avoid HTN in bleed; avoid hypotension to optimize CPP

- monitor HR: high risk of arrhythmias d/t sympathetic surge

- treat shock (fluid/vasopressors)


- monitor status; GCS

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SCI: traumatic vs. non-traumatic


- flexion/extension/compression

- fractures

- hematomas


- tumors

- infection

- stenosis

- ischemic injury

- AVMs

- neuromuscular disease can present with weakness

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SCI major cause of death

- aspiration and shock

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ASIA scoring

A - complete; no motor or sensory function is preserved in the sacral segments S4-S5

B - incomplete; sensory but not motor function is preserved below the neurological level and includes sacral segments S4-5

C - incomplete; motor function is preserved below the neurological level and more than half of key muscles below the neurological level have a muscle grade less than 3

D - incomplete; motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more

E - norma; motor and sensory function are normal

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types of SCI injuries


- no residual function more than three levels below the injury affecting both sides equally


- any residual sensory or motor function below the injured level

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spine syndromes

Central Cord Syndrome

- most common type of incomplete injury

- injury to the center portion of the cervical cord - cervical motor fibers are located towards the center of the cord

- results in weakness in arms (loss of fine motor) more than legs

- surgical treatment remains controversial

- commonly found in hyperextension injury: older persons with cervical spondylosis/stenosis and younger persons with traumatic injury

- recovery is possible but variable

Brown-Sequard syndrome

- rare

- ipsilateral loss of motor and contralateral loss of sensation

- damage to half of the spinal cord; can be seen in patients with spinal cord tumor, trauma, infection and inflammatory disease, as well as disc herniation

Anterior Cord Syndrome

- complete motor paralysis and loss of temp. and pain perception distal to the lesion with preserved light touch, vibration, and proprioception

- caused by compression of the anterior spinal artery

- associated with burst fractures

Cauda Equina Syndrome

- nerve roots of the caudal equine are compressed (herniated disc, tumor, abscess)

- symptoms: weakness, difficulty urinating, loss of rectal tone, saddle anesthesia

- medical emergency

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Management of cardiogenic shock

- restore blood flow

- oxygen supply and demand

- thrombolytics

- angioplasty with senting

- coronary revascularization

- reduce workload of the heart with intra-aortic balloon pump (IABP) or ventricular assistive device (VAD)

- airway and oxygenation management

- drug therapy: positive inotropes (dopamine and dobutamine) ventodilation (nitroglycerin), and vasodilation (sodium nitroprusside), diuretics, and beta blockers

- supportive therapy

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common problems experiences by people who shift work

- characterized by insomnia, sleepiness, and fatigue

- sleep debt grows

- complications: mood, impact work performance, testosterone, higher accident risk, and substance use

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insomnia etiology

- behaviors

- lifestyle

- diet

- medical conditions

- medications

- stressful life events

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prevention of organ rejection

- both the donor and recipient are tested to identify HLA antigen variations, which minimizes rejection

- activation of lymphocytes are cellular rejection

- activation of antibodies are humoral rejection

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treatment of organ rejection

- calcineurin inhibitors

- corticosteroids

- antimetabolites

- antibody products

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diabetes insipidus clinical manifestations

- polydipsia

- polyuria

- excretion of large quantities of urine (2-20L/day, very low specific gravity, very low urine osmolality, serum osmolality is elevated)

- nocturia

- generalized weakness

- dehydration

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acute thyrotoxicosis management

- medical emergency

- propylthiouracil

- beta blockers

- IV fluids

- cardiac monitoring

- adequate oxygenation

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Cushing's syndrome etiology

- iatrogenic administration of exogenous corticosteroids

- ACTH-secreting pituitary adenoma: large cause of endogenous cases

- adrenal tumors: less common

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Hyperparathyroidism diagnosis

- serum PTH levels

- serum Ca

- serum P+

- bone density measurements

- urine

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Hyperparathyroidism management


- partial vs. complete (outpatient)

- auto transplantation of normal parathyroid tissue

Calcium supplementation for life if surgical interventions fail

Conservative approach if asymptomatic or mild symptoms

- labs

- annual x-rays or DEXA scans

- drug therapy

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Multiple sclerosis pathophysiology

Three Characterizing Pathologic Processes

- chronic inflammation

- demyelination

- gliosis in the CNS: scarring, nonspecific reaction-like changes

Primary Neuropathologic Condition

- autoimmune process orchestrated by activated T cells

- T cells migrate to the CNS, causing a blood-brain disruption


- insidious

- vague symptoms

- intermittent

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Golden hour vs. platinum 10

Golden hour

- the first hour after injury will largely determine a critically injured person's chances for survival

Platinum 10

- later coined to restrict the time of pre-hospital care of critically injured trauma patients to no more than 10 minutes of on-scene stabilization time prior to initiation of transport

- resulted in a scoop and run approach to encourage rapid transport to the local trauma center

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Etiology: blunt vs. penetrating




- pedestrian vs car

- assault with blunt force

- fall


- stab wound

- gunshot wound

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abdominal trauma complications

Abdominal compartment syndrome

- condition caused by abnormally increased pressure within the abdomen that is associated with organ dysfunction

- risk factors: trauma, surgery, infection

- intra-abdominal hypertension can impair the function of nearly every organ system

- clinical manifestations: abdominal distention worsening to tense, rigid abdomen; abdominal pain out or proportion to injury; tachypnea and/or dyspnea

- treatment: relief the pressure; emergency that needs to go to the OR immediately for exploratory laparotomy

Renal injury

- causes: pre-renal and intra-renal (secondary to prolonged hypotension; toxins such as antibiotics and IV contrast dye)

- monitor urine output

- inform provider if patient produces less than 0.5mL/kg/hr

- obtain labs as ordered

- monitor creatinine, BUN, and electrolytes


- prevent and treat

- monitor for sepsis (shivering, extreme pain or general discomfort, pale or discolored skin, sleepy/confused, "I feel like I might die" statements, shortness of breath

- antibiotics (prophylaxis and treatment)

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Trauma triad of death

- hypothermia

- coagulopathy

- acidosis

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Motor strength scaling

- musculoskeletal strength graded out of 5

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TBI signs

- use GCS

- decorticate (flexor) posturing: damage to cerebral hemispheres

- decerebrate (extensor) posturing: deeper brain structures, including midbrain, pons, brain stem

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TBI symptoms: mild vs. severe


- LOC for secs to min or none but state of being dazed/disoriented

- headache

- N/V

- fatigue

- speech problems

- dizziness

Moderate to Severe

- LOC for several mins to hours

- headache

- repeated N/V

- seizures

- dilation of one or both pupils

- clear fluids from nose or ears

- weakness

- agitation

- slurred speech

- come (GCS

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SCI etiology

- fractures

- dislocation

- masses such as tumors

- hematomas

- abscesses

- ischemic injuries (spinal stroke)

- penetrating injuries to the spine accounts for about half of spinal injuries in urban centers

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SCI mechanisms of injury

- must always be presumed until it is excluded (a missed injury can have devastating consequences)

- compression

- flexion

- extension

- rotation

- lateral bending/stress

- distraction

- penetration

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SCI acute complications

Spinal Shock

- transient depression or loss of reflex activity below the level of an acute spinal cord injury

Neurogenic shock

- form of distributive shock

- a sudden loss of autonomic tone due to spinal cord injury causes hypotension and bradycardia - unopposed parasympathetic innervation

- usually occurs in patients with injury T6 and above but can happen in any injury above L2

- management: airway support if needed, fluids and vasopressor support as needed, to maintain MAP

- atropine for bradycardia vs pacing (temporary or permanent?)

Autonomic dysreflexia

- uncontrolled sympathetic response secondary to a stressor in patients with a SCI T6 and above (unlikely to occur with injuries below T10)

- life threatening HTN and bradycardia when there is a noxious stimulus below the level of injury

- initial complaint is headache - any patient with headache and SCI above T6 should have their BP checked immediately

- common triggers are bladder dissension, fecal impaction/constipation, pressure injury

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SCI nursing management


- serial neurologic exams, especially motor strength and sensation

- maintain proper spinal precautions/alignment

- pain management (neuropathic pain)

- patient/family education and support

- encourage patient to be active participant in their care/recovery (give them back some control)


- close monitoring

- pulmonary toileting (cough assist, chest PT, quad cough)

- management of secretions


- BP monitoring

- HR/telemetry

- optimize perfusion - patients may require MAP goals of >80 or higher in initial injury period to optimize spine perfusion

- manage shock


- bowel regimen (may need standing suppository/rectal stimulation)

- strict bladder training


- frequent turns and skin assessments - offload pressure

- mobilize


- DVT prophylaxis

Discharge planning

- early PT/OT/Speech

- SCI rehabilitation/PM&R

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Medical management of spinal injury

- stabilization of spin

- distributive shock management: fluid resuscitation, atropine for bradycardia, vasopressors PRN

- no current support for steroids

- intensive support care

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causes of spinal tumors

- viruses

- defective genes

- exposure to certain chemicals and hazardous materials

- immune system disorders

- genetic diseases, such as tuberous sclerosis

- exposure to radiation

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SCI clinical manifestations

- trouble waking (abnormal gait)

- numbness/tingling

- bowel/bladder dysfunction

- general midback pain

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SCI diagnostic approach

- can take weeks

- often other causes ruled out first

- usually first diagnosed on MRI

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Management of spinal tumors

- surgical resection and stabilization of spine if possible

- radiation therapy

- chemo

- steroids to reduce swelling

- serial neuro assessments and spine exams

- pain management

- incentive spirometry

- prevent atelectasis

- peri-op abx

- wound and drain care/monitoring

- bowel regimen

- monitor for urinary retention

- mobilize

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leading causes of death in spinal cord injury after initial injury

- pneumonia

- PE

- sepsis

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Classifications of shock

- cardiogenic

- hypovolemic (absolute and relative)

- distributive (neurogenic, anaphylactic, and septic)

- obstructive

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Clinical manifestations of cardiogenic shock

- problem with the pump

- early: tachycardia, hypotension, narrowed pulse pressure

- respiratory: tachypnea, crackles, cyanosis, rhonchi

- cardiovascular: tachycardia, decrease in BP, decrease in cap refill, chest pain may or may not be present

- integumentary: pallor, cool, clammy

- renal: increase Na&H2O retention, decreased renal blood flow and urinary output

- neuro: anxiety, confusion, agitation

- GI: decreased BS, nausea, vomiting

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Clinical manifestations of hypovolemic shock

- dependent on age, extent of injury or insult, and overall state of health

- respiratory: tachypnea and bradypnea (late)

- cardiovascular: decreased preload, SV, and cap refill

- integumentary: pallor, cool, clammy

- renal: decreased u/o

- neuro: anxiety, confusion, agitation

- GI: absent bowel sounds

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Clinical manifestations of neurogenic shock

- main symptoms: hypotension, bradycardia, inability to regulate body temperature that leads to poikilothermia

-respiratory: related to injury level

- cardio: decreased BP, bradycardia, increase/decrease in temperature

- integumentary: pallor, cool, clammy

- renal: bladder dysfunction

- neuro: flaccid paralysis below level of lesion, loss of reflex activity

- GI: bowel dysfunction

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Clinical manifestations of anaphylactic shock

- main symptoms: dizziness, chest pain, incontinence, swelling of lips and tongue, wheezing, stridor, flushing, pruritus, uticaria, angioedema, and sense of impending doom

- respiratory: SOB, edema of larynx and epiglottis, wheezing, stridor, rhinitis

- cardio: CP, third spacing of fluid

- integumentary: flushing, pruritus, urticaria, angioedema

- renal: incontinence

- neuro: anxiety, feeling of impending doom, decreased LOC

- GI: cramping, ABD pain, diarrhea, vomiting, nausea

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Clinical manifestations of septic shock

- pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression

- respiratory: hyperventilation, crackles, respiratory alkalosis leading to acidosis, hypoxemia, ARDS (acute respiratory distress syndrome), and pulmonary hypertension

- cardio: increase/decrease in temp, myocardial dysfunction, ventricular dilation, decrease in EF

- integumentary: warm and flushed and then cool and mottled (late)

- renal: decreased urine output

- neuro: altered MS, confusion, agitation

- GI: GI bleed, paralytic ileus

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Clinical manifestations of obstructive shock

- main symptoms: decreased CO, increased afterload, and variable left ventricular filling pressure

- respiratory: tachypnea, SOB, bradypnea (late)

- cardio: decreased BP and preload

- integumentary: pallor, cool, clammy

- renal: decreased urine output

- neuro: anxiety, confusion, agitation

- GI: decreased or absent bowel sounds

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Management of hypovolemic shock

- treat the underlying cause

- large bore peripheral IVs or central venous catheter (CVC)

- fill the tank with crystalloids (LR, normal saline) and colloids (PRBCs, FFP, albumin, plasma volume expanders like hetastarch and dextran)

- invasive hemodynamic monitoring

- airway and oxygenation management

- no specific drug therapy

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Management of neurogenic shock

- based on the cause

- spine stability

- vasopressors (phenylephrine)

- atropine

- fluids must be used cautiously as there is a risk of fluid overload (change in resistance, not volume)

- body temperature

- airway and oxygenation management

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Management of anaphylactic shock

- prevention

- removal of offending cause

- airway and oxygenation management (endotracheal intubation or cricothyroidotomy)

- fluid resuscitation

- drug therapy: epinephrine, Benadryl, bronchodilators, corticosteroids

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Management of septic shock

- blood cultures identifying the organism

- labs

- abx

- aggressive fluid resuscitation

- vasopressors (norepinephrine)

- inotrope (dobutamine)

- prophylactic anticoagulants

- stress ulcer prophylaxis

- airway and oxygenation management

- invasive hemodynamic monitoring

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Management of obstructive shock

- treat the underlying cause: pericardiocentesis, needle decompression, chest tube insertion, embolectomy

- fluid resuscitation (temporary)

- airway and oxygenation management

- no specific drug therapy

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SIRS criteria

- temp over 100.9

- heart rate over 90 bpm

- respiratory rate of 22 bpm or PCO2 less than 32 mmHg

- WBC over 12 or WBC less than 4


- 2 SIRS + infection

Severe sepsis

- sepsis + 1 sepsis induced organ dysfunction

Septic shock

- severe sepsis + hypotension without response to fluid resuscitation

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Stages of shock

1. Initial

- cellular level

- usually not clinical apparent

- metabolism changes (lactic acid build-up)

2. Compensatory

- attempt to equilibrilate

- activation of neural, hormonal, and biochemical mechanisms

3. Progressive

- begins as compensatory mechanisms begin to fail

- changes in mental status

- CV system profoundly affected

- pulmonary system

- aggressive interventions (key to preventing MODS)

4. Irreversible/Refractory

- decreased perfusion, which leads to anaerobic metabolism

- decreased CO

- increasing capillary permeability

- increasing dilation

- profound hypotension and hypoxemia

- unlikely recovery

- sequelae: cerebral ischemia, worsening cardiac depression, and failure of one organ system

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How SVR, CO, and CVP relate to the presentation of cardiogenic shock

- increase in CVP, PAWP, and SVR

- decrease in CO

- related to systolic dysfunction (ineffective forward movement of blood) or diastolic dysfunction (ineffective filling)

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How SVR, CO, and CVP relate to the presentation of hypovolemic shock

- decrease in CVP, PAWP, and CO

- increase in SVR

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How SVR, CO, and CVP relate to the presentation of neurogenic shock

- decrease in blood pressure due to venous and arterial vasodilation

- decrease in CVP, PAWP, CO, and SVR

- due to loss of sympathetic tone and parasympathetic nervous system response

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How SVR, CO, and CVP relate to the presentation of anaphylactic shock

- decrease in CVP, PAWP, CPO, and SVR due to massive vasodilation of veins and arterioles

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How SVR, CO, and CVP relate to the presentation of septic shock

- selective vasoconstriction due to the activation of the CNS, the activation of endocrine system, and the release of pro inflammatory cytokines

- peripheral dilation due to the release of pro inflammatory cytokines

- decrease in CVP, PAWP, CO, and SVR

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How SVR, CO, and CVP relate to the presentation of obstructive shock

- decreased CVP, PAWP, and CO

- increased SVR

- caused by cardiac tamponade, tension pneumothorax, superior vena cava syndrome, abdominal compartment syndrome, and pulmonary embolism

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HIV transmission

- can occur from exposure to bodily fluids: blood, semen, pre-seminal fluid, rectal fluids, vaginal fluids, and breastmilk

- these fluids must come in contact with a mucous membrane (found inside rectum, vagina, penis, and mouth), damaged tissue, or the bloodstream

- not transmitted by air, water, saliva, sweat, tears, kissing, insects, pets, sharing toilets, food, drinks

- does not survive long outside the human body (such as on surfaces)

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Who should get tested for HIV?

- everyone aged 13 to 64 should get tested at least once

- sexually active gay and bisexual men may benefit from testing 3-6 months

- if you are pregnant or planning to get pregnant, get tested as early as possible

Should get tested once a year if:

- you're a man who has had sex with another man

- you've had sex with a partner with HIV

- you've had more than once partner since last test

- you have shared needles, syringes, or other equipment to inject drugs

- you've exchanged sex for drugs or money

- you have another STD, hepatitis, or TB

- you've had sex with anyone who has done any of the above or with someone with an unknown sexual history

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HIV diagnosis

Antibody Test

- only looks for antibodies to HIV in your blood or oral fluids

- sample from a blood draw can detect HIV sooner compared from samples taken through a finger prick or from oral fluid sample

- can tell if someone has HIV infection 23-90 days after exposure

- resulted within 20 minutes (finger prick or oral fluids) to a few days (sample from blood draw)

Antigen/Antibody Test

- looks for HIV antibodies and antigens

- can tell if someone has HIV infection 18-45 days after an exposure (sample taken from blood draw) or 18-90 days after an exposure (sample taken from finger prick)

- resulted in a few days (blood draw) or

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HIV prevention

- get tested

- use condoms

- increase financing

- end discrimination

- end mother to child transmission

- PEP and PrEP

- linkage to care

- needle exchange programs

- blood supply screening

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- post-exposure prophylaxis

- if started soon after exposure, PEP can reduce the risk of HIV infection by over 80%

- must be started within 72 hours of exposure and must complete the whole 28-day course

- pregnancy is not a contraindication

- follow-up HIV 4th generation Ab/Ag test at completion of treatment and then in 3 months

- if showing s/s of acute HIV infection, consider HIV viral load testing

- discuss prevention and risk reduction

- discuss appropriateness for PrEP


- pre-exposure prophylaxis

- when taken daily, PrEP reduces the risk of getting HIV through sexual transmission by 99%

- among those who inject drugs, PrEP reduces the risk of getting HIV by at least 74% when taken daily

- have had sex in the past 6 months and have a sexual partner with HIV, have not consistently used a condom, or have been diagnosed with an STI in the past 6 months

- PrEP is also recommended for people who inject drugs and have an injection partner with HIV or shared needles, syringes, or other equipment to inject drugs

- should be considered for those who have been prescribed PEP and report continued risk behaviors or have used multiple courses of PEP

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Stages of HIV

Acute HIV Infection (stage 0)

- typically begins within 28 days of infection with a median duration of 14 days

- flu-like illness: fever, sore throat, body aches, feeling fatigued

- initiating antiretroviral therapy is essential to accelerate resolution of symptomatic acute retroviral syndrome, minimize immunologic damage, diminish size of the latent HIV reservoir, and prevent transmission to others

Chronic HIV Infection (stage 1 and 2)

- defined when the CD4 is greater than 200 and the patient does not have any AIDS-defining condition

- staging can occur in either direction

- asymptomatic HIV infection or clinical latency

- HIV continues to multiply in the body

- if untreated, can remain in this stage for up to a decade

- those who take their antiretroviral therapy as prescribed and maintain an undetectable viral load have effectively no risk of transmitting HIV

AIDS (stage 3)

- acquired immunodeficiency syndrome

- applies to the most advanced stage of HIV infection as defined by CD4 less than 200 and/or presence of an opportunistic condition

- without treatment people with AIDS typically survive about 3 years

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Pharmacologic interventions for HIV

- nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs): targets the action of an HIV protein called reverse transcriptase by disrupting conversion of viral RNA into DNA halting its replication

- non-nucleoside reverse transcriptase inhibitors (NNRTIS): targets the action of reverse transcriptase by binding to it, blocking the reverse transcription process

- integrase strand transfer inhibitors: target the HIV protein stopping the virus from inserting itself into human DNA cells

- entry inhibitors: CCR5 inhibitors bind to the CCR5 receptor, preventing HIV viral entry into the cell; fusion inhibitors work by stopping the fusion of the HIV envelop protein with the CD4 cells

- protease inhibitors: targets the protease enzyme, which HIV uses to break up large polyproteins into smaller pieces required for assembly of new viral particles

- post-attachment inhibitor: binds to the CD4 receptor and prevents the HIV gp120 protein from changing its shape to engage with co-receptors after it engages with the CD4 receptors

- attachment inhibitor: binds to gp120 subunit and subsequently blocks the interaction of the virus with CD receptors preventing its attachment

- cabenuva: integrase inhibitor and NNRTI combined and administered once a month for 2 months followed by every 2-month administration (injectable)

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HIV complications

- can progress to AIDS without effective treatment

- when the immune system becomes severely suppressed, serious opportunistic conditions may arise

- pneumocystis pneumonia (PCP): leading cause of morbidity and mortality in patients with HIV, approximately 80% of people with AIDS will develop PCP, diagnosis requires detection of organism in respiratory secretions or in tissue

- toxoplasmosis: a protozoan parasite and can cause focal encephalitis; diagnosis is presumptive based on clinical manifestations, positive anti-toxoplasma ab and neuroradiographic finding

- kaposi sarcoma: vascular tumor caused by human hurpes virus-8, prevalence has decreased with antiretroviral use, requires biopsy to diagnose

- disseminated MAC disease: a group of nontuberculous mycobacteria

- oral candidiasis


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Management of HIV complications

- PCP: bactrim

- toxoplasmosis: the preferred treatment is pyrimethamine + sulfadiazine + leucovorin for at least 6 weeks followed by secondary prophylaxis of same regimen of lower dose. They will be on secondary prophylaxis until completion of initial therapy + no s/s of toxoplasma encephalitis + a CD4 of greater than 200 for at least 6 months

- kaposi sarcoma: antiretroviral, radiation, intralesional chemotherapy, topical therapy, surgical excision, cytotoxic chemotherapy, and other antiviral agents

- disseminated MAC disease: azithromycin

- oral candidiasis: anti-fungal pill (oral fluconazole)

- HPV: screening

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Leading cause of death in patients with HIV


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Implications of HIV stigma


- irrational or negative attitudes, behaviors, and judgments towards people living with or at risk of HIV

Impact of Stigma

- can discourage people learning their HIV status

- can discourage people from accessing treatment

- can discourage people from staying in care

- can discourage people from seeking HIV prevention tools and testing

- can discourage people from talking openly with their sex partners about safer sex options

Stopping Stigma

- talk openly about HIV and stigma

- choose supportive language

- speak out to correct myths and stereotypes

- educate yourself and others

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