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Final Flashcards

1
Q
  1. If chest pain is reproducible, is it indicative of an MI?
A
  1. Probably not
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2
Q
  1. How much urine output classifies as anuria?
  2. How much urine output classifies as oliguria?
  3. How much urine output classifies as Polyuria?
  4. T or F, polyuria occurs in the recovery phase? What might occur because of polyuria?
  5. What is the normal urine output in 1 day?
A
  1. <100ml in 24hr
  2. <400ml in 24hr
  3. > 2500ml in 24hr
  4. True. Polyuria can cause hypovolemia
  5. 800ml-2000ml
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3
Q
  1. What is the gold standard lab value for kidney function?
  2. What is creatinine a measure of, and how does it indicate kidney function?
  3. What is the normal serum creatinine level?
  4. What is normal BUN range?
  5. What is GFR? What is the normal level? At what level would we need dialysis?
A
  1. serum creatinine
  2. It’s a waste product of protein breakdown. When serum levels are high it means the kidneys aren’t doing their job of filtering it out of your blood, hence poor kidney function.
  3. 0.6-1.3mg for serum. For urine it’s 88-137mg/dL, with men having the higher range
  4. 5-20mg/dL
  5. Amount of blood filtered per minute. >60ml/min. If GFR is <30ml/min dialysis is needed
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4
Q
  1. Which electrolyte is excreted in urine, and what can happen in cases of polyuria?
  2. Acute kidney injury has a ………….. onset as opposed to chronic kidney disease.
  3. What is the most common cause of acute kidney injury? Chronic kidney disease?
  4. Diagnostic criteria of acute kidney injury is marked by an acute reduction in ………… ………….. or and elevation in ………… …………, Whereaschronic kidney disease is marked by GFR 3mos, or kidney damage >3mos.
  5. Is acute kidney damage reversible? Chronic disease?
  6. What is the most common cause of death in acute kidney disease? Chronic?
A
  1. K+, hypokalemia
  2. sudden
  3. acute tubular necrosis vs diabetic neuropathy
  4. urine output, or serum creatinine
  5. Potentially. Chronic disease is progressive and irreversible.
  6. infection. cardiovascular disease
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5
Q
  1. What are the 4 most common causes of pre-renal acute kidney injury?
  2. Name some causes of hypovolemia:
  3. What causes decreased cardiac output?
  4. What causes decreased peripheral vascular resistance?
  5. What causes decreased renal perfusion?
A
  1. Hypovolemia (most common cause of prerenal AKI in hospitalized patients), decreased cardiac output, decreased peripheral vascular resistance, decreased renovascular blood flow.
  2. dehydration, hemorrhage, diarrhea/vomiting, burns
  3. heart failure and MI
  4. anaphylaxis, and septic shock
  5. renal vein thrombosis
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6
Q
  1. What are the 4 intrarenal causes of acute kidney injury?
  2. What could cause a nephrotoxic injury?
  3. What could cause interstitial nephritis?
  4. why is hypertension considered intra-renal rather than pre-renal injury?
  5. What is acute tubular necrosis?
A
  1. nephrotoxic injury, interstitial nephritis, acute glomerulonephritis, malignant hypertension, thrombotic disorders (within the kidney itself)
  2. drugs, contrast media, or a crushing injury
  3. allergies (ie: to antibiotics) or bacterial infections
  4. the hypertension puts strain on the nephrons
  5. Most common cause intrarenal AKI in hospitalized patients. Ischemia , nephrotoxins, or sepsis cause disruption of basement membrane and necrosis of tubular epithelial cells.
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7
Q
      1. What are the 4 most common causes of post renal injury?
A
  1. Benign prostatic hypertrophy
  2. bladder cancer
  3. stones
  4. spinal cord disease
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8
Q
  1. What is RIFLE and what does it stand for?
  2. What constitutes Risk?
  3. What constitutes Injury?
  4. What constitutes Failure?
  5. What constitutes Loss?
  6. What constitutes End stage?
A
  1. Risk, Injury, Failure, Loss, and End-stage kidney disease. It is a classification for severity of kidney malfunction
  2. Risk stage is w/ increased creatinine x 1.5, GFR decrease of >25%
  3. Injury stage is w/ increased creatinine x 2, GFR decrease of >50%
  4. Failure stage is w/ increased creatinine x 3, GFR decrease of >75%
  5. Loss is when there has been a complete loss of renal function longer than 4 weeks.
  6. End stage is when theres no coming back.
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9
Q
  1. What are the parameters of the oliguric phase as far as when it starts, how long it lasts, and what might be seen in urinalysis?
  2. When urine output is decreased, what might we see elsewhere in body as far as physical manifestations?
  3. Would oliguria lead to acidosis or alkalosis? Why? What symptom might be seen?
  4. Describe what happens to Na+:
  5. What happens to potassium in oliguria?
  6. What happens with blood and neuro status?
A
  1. <400ml/day, occur within 1-7 days after injury, lasts 10-14 days, urinalysis shows casts, rbcs, and wbcs
  2. fluid retention, neck vein distention, bounding pulse, edema, hypertension, heart failure, pulmonary edema, pericardial and pleural effusions
  3. kidneys are major players in acid-base balance because they excrete H+. If not making urine, H+ stays in body. Kussmauls might be seen.
  4. Na+ gets diluted, leading to hyponatremia and cerebral edema. Look for neuro changes.
  5. Potassium excess! Hyperkalemia leads to ECG changes (peaked T wave)
  6. In blood we see leukocytosis, elevated BUN and creatinine, and neuro disorders like fatigue, seizures, stupor, coma.
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10
Q
  1. What happens in the diuretic phase of AKI?
  2. What happens to Na+, and K+
  3. Can patient become dehydrated in this phase?
  4. When does the recovery phase begin? When is the biggest improvement?
A
  1. Daily urine output is 1 to 3 L, but can even reach 5L or more!
  2. possible hypernatremia (from dehydration) and hypokalemia
  3. yes
  4. when GFR increases allowing BUN and creatinine to decrease. Biggest jump of improvement happens in 1st 1-2 weeks of this phase, but may take up to 12 months.
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11
Q
  1. Name 7 diagnostic techniques for AKI:
  2. What would be contraindicated in the diagnostic studies of AKI?
  3. Name the contrast medium that is less nephrotoxic than others:
A 
1. Thorough history
Serum creatinine
Urinalysis
Kidney ultrasonography
Renal scan
Computed tomography (CT) scan
Renal biopsy
  1. Contrast medium
  2. gadolinium
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12
Q
  1. What is a key goal in collaborative care of AKI patients?
  2. What drugs might be given?
  3. Would fluid intake be closely monitored during the oliguric stage?
A
  1. ensuring adequate intravscular volume and cardiac output
  2. Loop diuretics (furosemide) mannitol (strongest osmotic diuretic.
  3. yes, to avoid overload since it’s not being readily excreted.
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13
Q
      1. Name 5 drugs with a brief description that we use to treat AKI induced hyperkalemia:
A
  1. Dextrose:
    to counteract hypoglycemia related to insulin
  2. Insulin
    puts K+ back into the cell
  3. Sodium bicarbonate
    counteracts acidosis
  4. Calcium carbonate
    protects heart from dysrhythmias
  5. Sodium polystyrene sulfonate
    Kayexalate: binds with K+ in intestines and induces diarrhea to get K+ out of system quickly)
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14
Q
  1. In what 4 ways do we manage nutrition in AKI?
  2. When is renal replacement therapy (dialysis) indicated?
  3. Name 3 different types of dialysis:
A
  1. Maintain adequate caloric intake
    Restrict sodium
    Increase dietary fat
    Enteral nutrition
  2. Volume overload
    Elevated serum potassium level
    Metabolic acidosis
    BUN level higher than 120 mg/dL (43mmol/L)
    Significant change in mental status
    Pericarditis, pericardial effusion, or cardiac tamponade
  3. Peritoneal dialysis (PD)
    Intermittent hemodialysis (HD)
    Continuous renal replacement therapy (CRRT)
    (Cannulation of artery and vein)
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15
Q
  1. What is involved in the nursing assessment for AKI?
A 
1. Vitals
I&O
Examine urine
Assess general appearance
Observe dialysis access site
Daily weights
Mental status/ LOC
Oral mucosa
Lung sounds
JVD
Heart rhythm
Laboratory values
Diagnostic test results
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16
Q
  1. Name reasons why older adults are more susceptible to AKI:
A 
1. Polypharmacy
Hypotension
Diuretic therapy
Aminoglycoside therapy
Obstructive disorders
Surgery
Infection
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17
Q
  1. stroke risk ……… each decade after 55. Strokes are more common in women or men (but which dies more)? Which ethnicity has higher instances of death from stroke? Which ethnicities have higher risks than whites?
  2. What are the modifiable risk factors to strokes starting with the #1 cause (11)?
  3. If a person has TIAs what percentage doesn’t have another event? What percent progress to a stroke? What percent have subsequent TIA’s?
  4. What exactly is a TIA? How long do symptoms typically last?
A
  1. doubles. men (women die more). blacks. Hispanics, Native Americans, and Asian American.
  2. HTN, heart disease, diabetes, elevated cholesterol, smoking, obesity, sleep apnea, metabolic syndrome, lack of exercise, poor diet, drugs and alcohol
  3. 1/3, 1/3, 1/3
  4. A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of brain. Typically lasts < 1 hour.
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18
Q
  1. What is the ABCD score?
  2. What are the types of strokes, and which is most common?
  3. Thrombotic strokes are closely associated with ………………, ……………., and ………………. . Are these often preceeded by TIAs?
  4. Extent of a thrombotic stroke depends on what 3 factors?
  5. What is the onset of thrombotic strokes?
A
  1. a risk assessment tool designed to predict the risk of a stroke 2 days after a TIA
  2. Ischemic (comprised of embolic and thrombotic) and hemorrhagic (intercerebral or subarachnoid). ischemic/thrombotic are most common
  3. atherosclerosis, diabetes, and HTN. Yes.
  4. rapidity or onset, size of damaged area, ad presence of collateral circulation
  5. slow, gradual onset, often preceeded by TIAs
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19
Q
  1. What is the onset of an embolic stroke?

2. Do embolic strokes have warning signs? Do these often recur?

A
  1. sudden onset with severe manifestations

2. Not really. Yes.

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20
Q
  1. Which type of stroke has worst prognosis?
  2. Which is the main cause of hemorrhagic strokes?
  3. What is a symptom that shouldn’t be ignored that a hemorrhagic stroke is occurring?
  4. Name some other manifestations of intracerebral hemorrhage:
  5. where do most cerebral aneurysms occur? Incidence increases with …. . Is more common in ………. . Also dubbed the ………. ……….. .
A
  1. hemorrhagic
  2. HTN
  3. “worst headache of life”
4. Neurologic deficits
Headache
Nausea, vomiting
Decreased levels of consciousness
Hypertension
  1. circle of willis. age, women, “silent killer”
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21
Q
  1. What is FAST?
  2. When testing arm strength, what is one thing to look for?
  3. What important question do we ask of stroke patients?
  4. In regard to motor function post-stroke, there is an initial period of ………….. . This may last days or weeks. Then there is a period of ………….. .
A
  1. Face drooping, Arm weakness, Speech difficulty, Time to call 911
  2. pronator drift
  3. when did symptoms start (ask to know if thrombolytics can be used).
  4. flaccidity, spasticity
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22
Q
  1. What are the manifestations of a right-sided stroke?
  2. what are the manifestations of a left-sided stroke?
  3. What are the 3 types of aphasia? What word gets used interchangeably with aphasia?
  4. What is meant by fluent and nonfluent?
  5. what is dysarthria?
A
  1. paralysis of left side, impulsivity, impaired judgement, rowdy, short attention span, deny/minimize problems, spatial/perceptual problems.
  2. paralysis of right side, impaired language (aphasia), slow performance, cautious, depressed, anxious, impaired comprehension of reading and math
  3. receptive: loss of comprehansion
    expressive: loss of speech production
    global: total inability to communicate
    dysphagia
  4. fluent: Speech is present but has little meaningful communication
    nonfluent: Minimal speech activity with slow speech
  5. problems with muscular control of speech
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23
Q
  1. T or F, Patients who have a stroke may have a hard time controlling their emotions. Might their emotional responses be exaggerated or unpredictable? What types of problems will magnify emotional instability?
  2. T or F, both memory and judgement may be impaired by a stroke.
  3. Stroke on ………. side of brain is more likely to cause problems in spatial-perceptual orientation. They will have an incorrect perception of ………. and ……….. . Will they neglect the side of body that was affected in the stroke?
  4. What is homonymous hemianopsia?
  5. What is agnosia?
  6. What is apraxia?
A
  1. T, yes, Depression
    Changes in body image
    Loss of function
  2. T,
  3. right, self and illness, yes
  4. visual field defect involving either the two right or the two left halves of the visual fields of both eyes.
  5. can’t recognize people or objects
  6. trouble saying what he or she wants to say correctly and trouble performing tasks
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24
Q
  1. what happens to urinary and bowel function after a stroke?
  2. What is meant by wet and dry stroke? Why is it important to know which kind we are dealing with?
  3. Name 6 diagnostic techniques for strokes:
A
  1. luckily, most problems are temporary. If stroke affects only one hemisphere of brain, prognosis for bladder function is excellent
  2. wet = hemorrhagic, dry = ischemic. Important to know if thrombolytics are indicated.
  3. CT, MRI, cerebral angiography, digital subtraction angiography, transcranial doppler, lumbar puncture, LICOX
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25
Q
  1. What drugs are used to prevent strokes?
  2. What surgeries might be performed for patients suffering from TIAs from carotid disease?
  3. What do we do post op for these patients (6)
A
  1. aspirin 81, clopidogrel (Plavix), ticlopidine, ASA, dipyridamole, statins are effective after ischemic strokes.
  2. Carotid endarterectomy
    Transluminal angioplasty
    Stenting
  3. Neurovascular assessment
    BP management
    Assess for complications like Stent occlusion or
    Retroperitoneal hemorrhage
    Minimize risk of bleeding at insertion site
26
Q
  1. What drug might be given in a hemorrhagic stroke?
  2. What surgeries might be performed for hemorrhagic stroke?
  3. What info is critical?
A
  1. protamine sulfate (antidote for heparin) or vitamin K (antidote for coumadin), nimodipine (calcium channel blocker to treat vasospasm), vasoconstricting agents to increase cerebral blood flow, and seizure prophylactic drugs
  2. immediate evacuation of hematomas, drainage of CSF via ventriculostomy, and clipping or coiling of anuerysm.
  3. time of onset of symptoms
27
Q
  1. What are the acute care interventions for ischemic stroke patients?
  2. What is the window of time for TPA?
  3. TPA is for ….. whereas TNK is for ……… .
  4. Why do ischemic stroke symptoms get worse in the first 72 hours?
A
  1. manage abc’s, get baseline neuro assessment (remember that patients may get worse in first 24-48 hours), don’t lower BP too quickly (elevated BP is common after a stroke to maintain cerebral perfusion). Control fluid/elctrolyte balance, manage ICP by using interventions to improve venous drainage.
  2. 3-4.5 hours.
  3. brain, heart. Both are thrombolytics
  4. Because it takes that long to see the extento of progression of cerebral edema and infarction
28
Q
  1. After stroke patient has stabilized for 12 to 24 hours, interprofessional care shifts from ……….. ……. to ……………. ……… and reaching optimal function. Patient may be evaluated by a ……………. .
  2. what is a physiatrist?
  3. What is the 2nd most leading cause of an embolic stroke?
A
  1. preserving life, lessening disability, physiatrist.
  2. a rehabilitation physician treat a wide variety of medical conditions affecting the brain, spinal cord, nerves, bones, joints, ligaments, muscles, and tendons.
  3. a-fib
29
Q
  1. The primary nursing assessments of stroke victims are (3):
  2. If patient is stable what is the next thing to assess?
  3. What is included in the comprehensive neuro assessment?
A
  1. cardiac, respiratory, neuro status.
  2. patient description of current illness with attention to symptom onset and duration, current meds, hx or risk factors, family hx
  3. LOC, NIH stroke scale, cognition, and motor abilities, cranial nerve function, proprioception, cerebellar function, and deep tendon reflexes
30
Q
  1. post stroke, are patients susceptible to VTE? What is the best prevention of this?
  2. In regard to nutrition, what must be done on post stroke patients prior to eating and drinking?
  3. What is important to remember about infections?
A
  1. yes because of weakness or paralysis in lower extremities. Keep patient moving
  2. swallow eval and gag reflex present
  3. They can be a risk factor to developing clots because they put us in a hypercoagulatory state.
31
Q
  1. If muscles are still flaccid several weeks after stroke, prognosis for regaining function is ………
  2. Most patients begin to show signs of spasticity with exaggerated reflexes within ……….. after the stroke
  3. What is CIMT?
  4. When helping a patient out of bed, which side of the patient should you go to assist?
  5. Should we put IVs in the affected side?
  6. What is Bobath therapy?
A
  1. poor
  2. 48 hours
  3. an approach to regaining motor ability by targeting the affected side for use rather than compensating with the stronger side.
  4. The unaffected side
  5. Better to put in the unaffected side because of limited sensation on the bad side (maybe they wouldn’t feel the infiltrates).
  6. a method of assessment and therapy for neuro patients
32
Q
  1. what constitutes TBI?
  2. What is the most common cause of TBI?
  3. at what 3 points might a patient die after TBI?
A
  1. Any trauma to the
    Skull
    Scalp
    Brain
  2. auto collisions
  3. Immediately after the injury (from hemorrhage or shock. This is majority of cases)
    Within 2 hours after the injury
    3 weeks after the injury (death from multi system failure)
33
Q
  1. what is major complication of scalp laceration?
  2. linear fractures are associated with what?
  3. Why are basilar fractures so dangerous? what signs are associated with basilar fractures?
  4. What is rhinorrhea and otorrhea?
  5. What is halo sign?
  6. What does it mean if glucose is in the clear fluid collected?
A
  1. blood loss and infections. Nurse - apply pressure
  2. low velocity injuries
  3. Can cause leakage of CSF and high risk of infection. Raccoon eyes or Battle’s sign
  4. Leakage of CSF from the nose or ears
  5. a halo of clear CSF with blood in the middle when collected on a 4x4 pad.
  6. Positive for CSF because there’s glucose in CSF but not in normal mucous.
34
Q
  1. What are the classifications of head injuries, and the Glasgow numbers of severity?
  2. manifestations of diffuse injuries:
  3. Describe post concussion syndrome:
A 
1. Diffuse (generalized) 
Focal (localized)
Minor (Glascow Coma Scale 13-15)
Moderate (GCS 9-12)
Severe (GCS 3-8) - will likely die.

2. Concussion
Brief disruption in LOC
Retrograde amnesia
Headache
Short duration 
May result in postconcussion syndrome
  1. Occurs 2 weeks to 3 months post injury. Symptoms include: Persistent headache
    Lethargy
    Personality and behavior changes
    Shortened attention span, decreased short-term memory
    Changes in intellectual ability
35
Q
  1. focal injuries can be ……. to ……….. . They consist of which 4 types of injuries?
  2. What is a Diffuse Axonal Injury?
  3. What are the manifestations of DAI and what is the prognosis?
A
  1. can minor to severe and localized to an area of injury. Consists of lacerations, contusions, hematomas, and cranial nerve injuries.
  2. Widespread damage to axons occuring after a TBI. The damage changes the function of the axon resulting in swelling and disconnection. Takes 12-24 hours to develop.
3. Widespread axonal damage 
Decreased LOC
Increased ICP
Decortication, decerebration (worse of the 2)
Global cerebral edema
90% of peeps will be vegetables
36
Q
  1. Describe Lacerations and what they are associated with:
  2. How are they treated?
  3. How does intracerebral hemorrhage manifest?
A
  1. tearing brain tissue associated with depressed open fractures and penetrating injuries resulting in intracerebral hemorrhage. Surgical repair is impossible
  2. with antibiotics until meningitis is ruled out and preventing secondary injury related to ICP.
  3. as a lesion accompanied by unconsciousness, hemipalegia on contralateral side and dilated pupil omn ipsilateral side.
37
Q
  1. What is a contusion, what are they associated with, and what can they cause?
  2. What must the nurse watch for with contusions? What drugs must not be given and what population to look out for:
  3. What is coup, contrecoup?
A
  1. bruising of brain tissue associated with closed head injury and can cause hemorrhage, infarction, necrosis, and edema
  2. they can rebleed, seizures can occur (especially in first 7 days). No anticoagulants. Watch elderly who take blood thinners - worse contusions.
  3. brain moves inside of skull hitting front then back. Severe. Happens in car accidents.
38
Q
  1. Describe an epidural hematoma:

2. How do they present?

A
  1. Bleeding between the dura and the inner surface of the skull. Neurologic emergency
    Venous origin slow
    Arterial origin rapid
2. Initial period of unconsciousness
Brief lucid interval followed by decrease in LOC
Headache, nausea, vomiting
Focal findings
Requires rapid evacuation
39
Q
  1. Describe subdural hematoma, what its common source is:
  2. when do acute subdural hematoms develop? What are the symptoms?
  3. When do subacute develop?
  4. When do chronic develop and in who?
A
  1. Bleeding between the dura mater and the arachnoid. Most common source is the veins that drain the brain surface into the sagittal sinus. Can also be arterial. Can be chronic or acute or subacute.
  2. within 24-48 hours of injury. Decreased LOC, headache, ipsilateral pupil dilation (late sign)
  3. 2 - 14 days after injury - may appear to enlarge over time
  4. weeks or months after. Most common in older drinkers, often misdiagnosed
40
Q
  1. What is intracerebral hemorrhage?
  2. define ICP
  3. what is CPP? How much is necessary?
  4. How to calculate CPP? What is the magic number?
A
  1. bleeding within brain tissue particularly in frontal and temporal lobes
  2. amount of pressure in the brain and spinal fluid
  3. cerebral perfusion pressure. Amount of pressure required to get a sufficient blood to the brain.
  4. First get MAP (systolic + 2x diastolic).
    Divide answer by 3
    Answer Minus ICP
    Normal = 60 – 100 mg/hg (70 is magic #)
41
Q
  1. Describe Cushing’s Triad:
  2. What is the gold standard diagnostic for cerebral hemorrhage
  3. Name a few other diagnostic tools used in TBI:
  4. Can you get a 2 on GCS?
A
  1. Occurs when there is severe ICP.
    Cheyne Stoke)
    Bradycardia
    Systolic hypertension (widening pulse pressure)
  2. CT
3. MRI, PET
Evoked potential studies (measure brain activity)
Transcranial Doppler studies
Cervical spine x-ray
Glasgow Coma Scale (GCS)
  1. no. 3 is lowest
42
Q
  1. What factors can render faulty results on the GCS?
  2. What does widening pulse pressure possibly mean?
  3. What are the emergency nursing interventions for TBI?
A 
1. All of the following will cause decreased LOC and give a lower GCS score than the reality.
Glucose: 
Oxygenation:
ETOH
Drug
Psychological 
Age
  1. Cushing’s Triad - Severe ICP
  2. **Patent airway
    **    Stabilize cervical spine.
    Oxygen
    IV access
    Intubate if GCS <8.
    Control external bleeding.
    Remove patient’s clothing (get warm blankets)
    Ongoing monitoring
    Anticipate possible intubation.
    Assume neck injury.
    Administer fluids cautiously.
43
Q
  1. What subjective data do we collect?

2. What objective data must we obtain?

A 
1. Mechanism of Injury 
Alcohol/drug use; risk-taking behaviors
Headache
Mentation changes; impaired judgment
Aphasia, dysphasia
Fear, denial, anger, aggression, depression
* Anticoagulants 
2. Altered mental status
Lacerations, contusions, abrasions
Hematoma
Battle’s sign
Periorbital edema and ecchymosis
Otorrhea
Exposed brain
Rhinorrhea
Impaired gag reflex
Altered/irregular respirations
Cushing’s triad
Vomiting
Bowel and bladder incontinence
Uninhibited sexual expression
Altered LOC
Seizures
Pupil dysfunction
Cranial nerve deficit(s)
Motor deficit
Palmar drift
Paralysis
Spasticity
Posturing
Rigidity or flaccidity
Ataxia 
Abnormal CT scan or MRI 
Abnormal EEG
Positive toxicology screen or alcohol level
↑ or ↓Blood glucose level
↑ ICP
44
Q
  1. What is aniscoria?
  2. What med can quickly help to reduce ICP?
  3. What are the goals in treatment of head injury?
A
  1. difference in pupil size
  2. Mannitol (powerful diuretic)
3. Cerebral oxygenation & perfusion
Normothermic btw 36 and 37. No shivering
Control pain and discomfort
Free of infection
Adequate nutrition
Maximal cognitive, motor, and sensory function
45
Q
  1. What are the interventions for the patient leaking CSF?

2. If a patient is immobilized, what should we manage?

A 
1. Head of bed elevated
Loose collection pad 
No sneezing or blowing nose
***No NG tube 
No nasotracheal suctioning
  1. nausea, pain, infection, diuretics to decrease ICP, prep for surgery
46
Q
  1. Risk factors to osteoporosis:
  2. What meds might interfere w/bone density?
  3. Does hyperthyroidism cause osteoporosis?
  4. What is the gold standard of osteoporosis diagnosis? When should it be started for men and women?
A 
1. Advanced age (> 65) 
Female gender
Low body weight
Cigarette smoking
Nontraumatic fracture
Inactive lifestyle
Family hx of osteoporosis 
Diet low in calcium or vitamin D deficiency
Excessive use of alcohol (>2drinks a day) 
Postmenopausal, including premature or surgical menopause
White and Asian American descent 
Low testosterone in men
  1. corticosteroids, antiseizure meds (valproate and pheny), aluminum containing antacids, certain cancer drugs, barbituates, levothyroxine, heparin
  2. yes. stimulates too much turn over
  3. DEXA. Not routinely necessary for men. 65 for women
47
Q
  1. what are the parameters for osteoporosis, and osteopenia?
    What is ostemalacia?
  2. What are some other diagnostic studies for osteoporosis?
  3. What labs might be elevated that could reveal underlying causes for osteoporosis?
  4. T or F, magnesium is directly correlated to Ca+ levels?
  5. T or F calcium and phosphorus have an inverse relationship?
A
  1. Osteoporosis is a BMD >-2.5
    Osteopenia is a BMD > -1.0 but less than - 2.5. Osteomalacia is softening of bone.
2. History and physical exam
Hip, vertebra, or wrist fracture
Back pain
Loss of height 
Spinal deformities 
Kyphosis
Stooped posture 
Quantitative ultrasound
  1. ALT/AST (because alcoholism) TSH (because hyperthyroidism)
  2. T
  3. T
48
Q
  1. Parathyroid hormone causes:
  2. Calcitonin is secreted by the ………….. and its job is to move calcium from the ………… and into the …………… .
  3. Why does a smaller frame predispose one to getting osteoporosis?
  4. what bones do fractures most commonly occur on in osteoporotic patients?
  5. What is “The Silent Disease?”
A
  1. osteoclast activity
  2. thyroid, blood into bone
  3. because they have less bone mass to pull from before becoming osteoporotic.
  4. spine, hips, wrists
  5. Osteoporosis
49
Q
  1. What drugs are taken to prevent osteoporosis?
  2. What are the nursing interventions with bisphosphonates, and name a bisphosphonate?
  3. What is vertbroplasty?
  4. What is kyphoplasty?
  5. Aside from dairy, what foods are good for bones?
  6. When calcitonin is used, what is necessary to take to avoid secondary hyperparathyroidism?
A
  1. calcium supplementation, bisphosphonates, calcitonin, selective estrogen modulators
  2. take in morning, upright for 30 min (because causes reflux), full glass of water, watch for TMJ. Alendronate (Fosamax), Boniva
  3. bone cement injected into collapsed vertebra to stabilize. Wont correct deformity
  4. air bladder inserted into collapsed vertebra to stabilize it.
  5. greens, seafood
  6. calcium supplementation
50
Q
  1. Name a selective estrogen receptor modulator:

2. What is Teriparatide (Forteo)

A
  1. Raloxifene (Evista)
  2. Portion of parathyroid hormone
    First drug to stimulate new bone formation
51
Q
  1. What is the classic presentation of a hip fracture?
  2. What can be done for the extreme pain stemming from spasms associated with hip fracture?
  3. What is a big risk of hip surgery?
  4. what positions to avoid post- op for hips?
A
  1. shortening and external rotation of affected leg
  2. bucks traction
  3. DVT and infection
  4. no crossing mid line, no flexion beyond 90, keep legs abducted, ambulate by next day
52
Q
  1. What are the 5 P’s of neurovascular checks?
  2. can we turn patient onto the operative side?
  3. What signs indicate a dislocation post op?
A
  1. pain, paresthesia, paralysis, pulse, pallor
  2. not until approved by surgeon.
  3. Watch for sudden severer pain, a lump in the buttock, limb shortening and external rotation
53
Q
  1. How does rheumatoid arthritis differ from osteoarthritis?
A
  1. osteo only affects joints whereas rheumatoid affects joints in a symmetrical fashion especially fingers, wrists. Rheumatoid is systemic and can extend to heart, skin, eyes. Affects women more and happens at any age, 20-60.
54
Q
  1. What causes Hypernatremia?
  2. What are symptoms of Hypernatremia?
  3. How do we treat?
A
  1. Excess intake, DI, Cushings
  2. thirst, agitation, GI upset, muscle weakness, tetany, high (T, BP, ADH, aldosterone)
  3. hypotonic solutions (0.45% NaCl), Furosemide, Na+restriction, fluid replacement
55
Q
  1. What causes hyponatremia?
  2. What are the symptoms of hyponatremia?
  3. How do we treat hyponatremia?
A
  1. diuretics, kidney failure, diaphoresis, SIADH, hypoglycemia
  2. confusion (can happen in hyper, but worse in hypo), fatigua, N/V, headache, seizures
  3. hypertonic solutions (2-3% NaCl), increase Na+ intake, fluid restriction).
56
Q
  1. What causes hypercalcemia?
  2. What are the symptoms of hypercalcemia?
  3. How do we treat hypercalcemia?
A
  1. hyperparathyroidism, bone cancer, corticosteroids
  2. constipation, decreased reflexes, kidney stones, lethargy, weakness
  3. 0.9%NaCl, calcitonin, or dialysis.
    * Remember, Ca+ relaxes muscles. Too much causes mushiness - just like magnesium.

** remember the inverse relationship with phosphorus**

57
Q
  1. What causes hypocalcemia?
  2. What are the signs and symptoms of hypocalcemia?
  3. How do we treat hypocalcemia?
A
  1. diarrhea, insufficient Vitamin D, hypoparathyroidism.
  2. positive chvostek and trousseau, muscle spasms, tetany, hyperactive reflexes, numbness, tingling
  3. calcium supplementation
58
Q
  1. What causes Hyperkalemia?
  2. What are the signs and symptoms of hyperkalemia?
  3. How do we treat hyperkalemia?
A
  1. DKA, metabolic acidosis, kidney failure
  2. dysrhythmias, weakness, muscle spasms, N/V, tingling, leg pain/cramping
  3. Furosemide, kayexelate, insulin and dextrose, decrease K+ foods.
59
Q
  1. What causes hypokalemia?
  2. What are the signs and symptoms of hypokalemia?
  3. How do we treat hypokalemia?
A
  1. diuretics, GI losses, diaphoresis
  2. dysrhythmias, muscle weakness and spasms, low reflexes, fatigue, weak irregular pulse, prominent U wave, depresssed T wave
  3. K+ supplements in pill, IV, drink, or food
60
Q
  1. What causes hypermagnesemia?
  2. What are the signs and symptoms of hypermagnesemia?
  3. How do we treat hypermagnesemia?
A
  1. kidney disease, excess intake (from antacids)
  2. decreased reflexes, hypotension, lethargy, muscle weakness, cardiac arrest, respratory depression
  3. Furosemide, Ca+

** same as hypercalcemia

61
Q
  1. What causes hypomagnesemia?
  2. What are the signs of hypomagnesemia?
  3. How do we treat hypomagnesemia?
A
  1. GI loss, diuretics, alcohol abuse, malnutrition
  2. dysrhythmias (Torsade des Pointes), tremors, seizures
  3. magnesium supplementation
62
Q
  1. What is the range of pH?
  2. What is the range of paCO2?
  3. What is the range of HCO3?
A
  1. 7.35 - 7.45 (acidic to basic)
  2. 45-35 (acidic to basic)
  3. 22-26 (acidic to basic)

Med Surg 2 (3 decks)

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