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4630 Final > Exam 1 review sheet > Flashcards

Exam 1 review sheet Flashcards

1
Q

Insulin drip

A

atlanta multiplier methodstarting rate units/hour = (BG - 60) x .02

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2
Q

blood sugar 226

A

(226-60) x .02 = 3.32 …. 3 units/hour

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3
Q

correction bolus forumula

A

current BG - Ideal BG——————————–glucose correction factor

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4
Q

Ideal blood glucose

A

100

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5
Q

example:250-100————–30

A

= 5.0u

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6
Q

fasting glucose is 326ideal is 100correction factor of 30

A

326-100———–30 = 7.53 or 8 units

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7
Q

Notes

A

Will be given glucose correction factorIdeal is always 100Round up if the decimal is 5 or greater

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8
Q

hypoglycemia

A

glucose is 40how much d50 iv push should mrs. jones receive

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9
Q

D50 formula

A

= (100-bg) x 0.4 ml IV

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10
Q

(100-40) x 0.4 ml IV

A

24ml/IV

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11
Q

40 glucose is considered

A

a severe hypoglycemia

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12
Q

ABG Analysisph 7.35, pao2 60, paco2 50, hco3 30

A

compensated respiratory acidosis

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13
Q

ph 7.50, pao2 75, paco2 40, hco3 32

A

uncompensated metabolic alkalosis

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14
Q

ph 7.6, pa02 80, paco2 30, hco3 24

A

uncompensated respiratory alkalosis

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15
Q

ph 7.3 pa02 75, paco2 32, hco3 19

A

partially compensated metabolic acidosis

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16
Q

ph 7.45, pa02 75, paco2 28, hco3 20

A

fully compensated respiratory acidosis

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17
Q

Two challenge rule

A

f you call the provider and you don’t get a reasonable solution, restate what you think is approrpriate, restate why you think it’s appropriate, and if you still don’t get what you need, contact another provider

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18
Q

Compassion fatigue

A

Intrusive ThoughtsBlending of RolesLowered ToleranceDreadDepressionSelf-destructive ActionsHyper-vigilanceDecreased FunctioningLoss of Hope

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19
Q

Best level for hospital and NICU

A

Level 1 hospital: good. Teaching hospital with multiple care pathways and can handle multiple patients. NICU: level 3 is the best

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20
Q

Open vs. Closed unit

A

Open:-multiple staff is coming and going, physicians, ancilary staff, nurses, all managing a patient-most typically usedClosed:certain staff including an intensivist who managed your patient. Great, unless the intensivist missing something, or something special happens that’s not in the intensivists realm of specialty.

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21
Q

VAP bundle includes?

A

prevent ventilator associated pneumonia*head of bed elevated 30*oral care every 2 hours*turn Q2*sedation vacation every 24 hours*peptic ulcer prphylaxis within the first 24 hours of mechanical ventilation*DVT thrombosis w/i 24 hours on vent (DVT precautions)

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22
Q

Biggest problems for critical care patients

A

-they are vulnerable-communication issues-technology-complex, multiple-step process

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23
Q

Safe Medical Device Act

A

-Require that hospitals report serious or potentially serious device-related injuries to the U.S. Food and Drug Administration (FDA).-All implantable devices must be documented and tracked with the FDA

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24
Q

Weaning of morphine per london health center guidelines

A

Morphine: If dose is less than 4mg per hour , then decrease by half every six hours. If dose is more than 4mg an hour, decrease by 25% every 6 hours until less than 4

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25
Q

Most beneficial in reducing pain in patients

A

Touch and family

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26
Q

To provide adequate pain control, first rule out?

A

→ hypoxia→ hypoglycemia→ withdrawal→ sleep deprivation→ immobility→ fear

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27
Q

Three purposes of sedation

A

Amnesia: to forget what’s going onAgitation: Anxiety: go to sedation as last resort

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28
Q

Neonatal: Mother-Driven Interventions for pain

A

breastfeedingskin-to-skin carematernal voice, maternal heartbeat with NNSolfactory, aromatherapy recognition

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29
Q

Neonatal: Sensorial Interventions for pain

A

containment & swaddlingfacilitated tuckingvestibular stimulation (rocking)orotactal stimulation: non-nutritive sucking (NNS) sweet solutionsCombining interventions offers additional benefits

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30
Q

Delirium classifications

A

-Hyperactive (agitated): Most common. sudden change, hallucinated, hyperactive-Hypoactive (quiet) – often misdiagnosed as depression, become nonresponsive and sluggish-Mixed: Second most common, bipolar-ish

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31
Q

Treat Cause of Delirium Acronym

A

THINK-Toxic situations and medication: CHF, shock, dehydration, organ failure. Benzodiazepines, anticholinergics, and steroids-Hypoxemia-Infection/sepsis, inflammation, immobilization-Nonpharmacological interventions: sleep, reorientation/reassurance, familiar people/objects-K+ (potassium) or other electrolyte imbalance

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32
Q

Delirium

A

-Common in critically ill patients (esp. on ventilator)-Caused by neurotransmitter imbalance in brainPredisposing factors-Patient (age, substance use, sensory impairment)-Illness (infection, electrolyte imbalance, low HCT)-Iatrogenic (polypharmacy, sleep disruption, immobility)-causes hospitals not to get reimbursed

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33
Q

Sedation med used for long term, or low level sedation

A

Lorazepam (Ativan): benzodiazepine * intravenous onset: 15 to 30 minutes, duration ~8 hours * intermittent or continuous-can only be mixed with d5w-can cause renal tubular necrosis

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34
Q

When you want a sedation medication that acts rapidly and ends rapidly?

A

Propofol (Diprivan): short-acting general anesthetic agent * onset: 40 seconds, duration 3 to 5 minutes * sedation is necessary with rapid awakening * bolus, then continuous-usually on ventilated patients-containers it’s in can only be used for 12 hours-(lipid) generally used through central line or used large bore peripherally because it’s very irritating-if drip is stopped, expect them to wake up in 8

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35
Q

Ventilation vs. Respiration

A

Ventilation is the rate at which gases enter or leave the lungs whereas respiration is the transport of oxygen from the outside air to the cells within tissues, and the transport of carbon dioxide in the opposite direction

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36
Q

the volume of air breathed in or out of the lungs during normal respiration0.5

A

tidal volume

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37
Q

The Ventilation-Perfusion (V/Q) ratio (normal?)

A

The V/Q ratio is the ratio between the amount of air getting to the alveoli (the alveolar ventilation, V, in ml/min) and the amount of blood being sent to the lungs (the cardiac output or Q - also in ml/min).V/Q = (4 l/min)/(5 l/min)V/Q = 0.8

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38
Q

Shunt Unit

A

Inadequate ventilation to an alveolusExample: Pneumonia

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39
Q

Dead Space Unit

A

Alveolar cluster where perfusion failsExample: Pulmonary embolism

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40
Q

Normal ABG’s

A

PaO2: 80-100SaO2: 93-99pH: 7.35-7.45PaCO2: 35-45HCO3: 22-26

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41
Q

Type?Impaired Gas Exchange-Pneumonia-Pulmonary edema-ARDS-AtelectasisNursing Interventions?

A

Type I- HypoxemiNursing Interventions:-Cough and deep breathe-HOB elevated-administering of meds such as diuretics-Add some ventilator peep-incentive spirometry-Get up to allow lung expantion

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42
Q

Ineffective Breathing Pattern-COPD-Neurological Respiratory Failure-Muscular FailureType?Nursing Interventions?

A

Type II- HypercapneicNursing interventions:-Bipap-ventilate them and change inspiratory expiratory ratio to allow more time to breathe in (add paralytics)-mechanical ventilation-change position Q2-HOB elevated

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43
Q

Difference between CPAP and BIPAP

A

CPAP-Continuous Positive Airway Pressure-for patients who need continuous low pressure to keep lungs openBIPAP-Bilevel Positive Airway Pressure-can assist with low level pressure at inspiration and expiration to help lungs stay open

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44
Q

Volume Control

A

controlling the volume on the ventilator

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45
Q

pressure control

A

delivers volume until a certain pressure is acheived

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46
Q

synchronized intermitted mandatory ventilation

A

on the breaths that the ventilator is going to deliver, it will deliver the settings. Won’t assist on their own breaths

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47
Q

What is ECMO and how does it work?

A

-extracorporeal life support-De-saturated blood is drained via a venous cannula, CO2 is removed, O2 added through an “extracorporal” device (often misnamed an oxygenator), and the blood is then returned to systemic circulation via another vein (VV ECMO) or artery (VA ECMO)

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48
Q

Patho of ALI/ARDS phases

A

-Phase 1: (inflammation and exudation) Capillary membranes are compromised and alveoli begin to fill with protein rich fluid. Type I alveolar cells are destroyed. Hyaline membranes are formed.-Phase 2: (proliferation) Type II alveolar cells are damaged & surfactant production declines. Inspiratory pressures increase as compliance decreases resulting in a ventilation/perfusion mismatch.-Phase 3: (resolution) Fibrotic tissue develops resulting in increased pulmonary pressures and ventilation dead space.

49
Q

NON-PHARMACOLOGICAL interventions for ALI/ARDS

A

-Nutrition Support-Prone positioning: Guérin et al (2013) found early prone positioning decreased 30 & 90 day mortality-Mechanical Ventilation: Low VT and high PEEP,FiO2 below 60%, High Frequency Oscillation-Extracorporeal Life Support (ECLS): Lung bypass, ECMO

50
Q

Pharmacological interventions for ARDS/ALI

A

Anti-Inflammatories: Cases of hypoxia >7Days & started before Day 14VasodilatorsSurfactantB-AgonistsCytokine InhibitorsColloidsParalyticsOxygen

51
Q

-Leading cause of cancer deaths in the US-Main Types: SCLC, NSCLC (small cell: agressive & paliate care starts at the begginning, nonsmall cell is the other)

A

Lung Cancer

52
Q

Treatment options for lung cancer

A

-Proton therapy: A type of radiation that uses high energy beams.-Chemotherapy:The most commonly used drugs to treat small cell lung cancer are cisplatin or carboplatin with etoposide.-Brachytherapy: radiation beads or rods are inserted at the cancer site.

53
Q

-One of the most common congenital abnormalities-Incidence 1 in 2000 to 5000 births-One third of infants with this are stillborn, usually due to associated fatal anomalies like neural tube defects and cardiac defects-Defects are common on left side (80%) compared to right (20%)-expected risk in a 1st degree relative is 1 in 45combo with karyotype is associated with poor outcome-Bilateral is very rare

A

Congenital Diaphragmatic Hernias (CDH)

54
Q

two main CDH

A

-Bochdalek: most common-Morgani: much less common

55
Q

How to diagnose/treat CDH

A

-CXR showing displaced organs into the chest cavity-diagnosed with ultrasound usually in utero, can be diagnosed 1st day of life-EKG shows stress to heart-surgical treatment: Laparotomy, thoracotomy, laparoscopy and thoracoscopy. When diaphragmatic tissue is adequate, primary repair with nonabsorbable suture can be done. If the defect is too large, prosthetic material can be used for a tension-free repair-Meds: nitros oxide in lung and htn medicine

56
Q

RSD risk factors

A

-Develops in ~ 50% of infants born between 28-32 weeks gestation-Inversely related to prematurity-Males-Second born twins-C-section-Caucasian race

57
Q

RDS: Treatment

A

-Maintain FRC (CPAP vs. intubation)-Surfactant replacement (with temporary intubation)-Exogenous surfactants (if they don’t have any)-Survanta 4cc/kg-Infasurf 3cc/kg

58
Q

-Diffuse reticular granular or “ground glass”pattern-Air bronchograms (bronchi visible)-Underaeration

A

alveolar disease

59
Q

-(beta cells)-stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose

A

insulin

60
Q

-(alpha cells)-stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose

A

glucagon

61
Q

Functions of insulin

A

-Enables glucose to be transported into cells for energy for the body-Converts glucose to glycogen to be stored in muscles and the liver-Facilitates conversion of excess glucose to fat-Prevents the breakdown of body protein for energy

62
Q

-Usually under 30-Rapid onset-Normal or underweight-Little or no insulin-Ketosis common-Autoimmune plus environmental factors-Genetic Propensity possible-Treated with insulin, diet and exerciseType 1 or type 2?

A

Type 1

63
Q

-Usually over 40-Gradual onset-Most have insulin resistance-Ketosis rare-Part of metabolic insulin resistance syndrome-Strongly hereditary-Obesity in 80% of Cases-Diet & exercise, progressing to tablets, then insulinType 1 or type 2?

A

Type 2

64
Q

-Polydipsia – increased thirst-Polyuria – increased urine-Polyphagia – increased hunger-Fatigue-Blurred vision-Slow healing infections-Impotence in menType 1 or 2 clinical manifestations?

A

Type 2

65
Q

Major defect in individuals with type 2 diabetesReduced ability of beta-cells to secrete insulin in response to hyperglycemia

A

beta cell dysfunction

66
Q

-Most common form of diabetes (90%+ of all cases)-Risk factors: Obesity, Family history, Sedentary lifestyle, Ethnicity (African American, Hispanic, and Native Americans), Hypertension, Hyperlipidemia, –Over the age of 45 years-Combination of physiological factors contribute: —Impaired insulin production,-Insulin resistance-These individuals may have both-Hyperinsulinemia-Hyperglycemia

A

Type 2

67
Q

-Polyuria – increased urine-Polydipsia – increased thirst-Polyphagia – increased hunger-3 ‘Ps”-Weight loss-Fatigue-Nausea, vomiting-Ketoacidosis may be a presenting signclinical manifestations for?

A

Type 1

68
Q

-Not fully understood-Current thoughts-Viral exposure triggers immune response that also attack the beta cells in the Islets of Langerhans. -Genetic propensity also believed to be involved.-Some drug therapies destroy the beta cells-Pyrinuron (no longer used in the US)-Zanosar (used in the treatment of pancreatic cancer)

A

Type 1 diabetes

69
Q

AACE/ADA Recommended Target Glucose Levels in ICU Patients

A

ICU setting:-Starting threshold of no higher than 180 mg/dL-Once IV insulin is started, the glucose level should be maintained between 140 and 180 mg/dL-Lower glucose targets (110-140 mg/dL) may be appropriate in selected patients -Targets 180 mg/dL are not recommended 180: NOT RECOMMENDED

70
Q

AACE/ADA Target Glucose Levels in Non–ICU Patients

A

Non–ICU setting:-Premeal glucose targets <40

71
Q

Severe hypoglycemia is defined as a blood glucose level?

A

less than 40, less than 50 = decrease in cerebral glucose availability

72
Q

Events Triggering Hospital Hypoglycemia

A

-Transportation off ward, causing meal delay-Failure to measure blood glucose before insulin doses-New NPO status-Interruption of: IV dextrose therapy, Total parenteral nutrition, Enteral feedings, Continuous venovenous hemodialysis

73
Q

Features Increasing the Risk of Hypoglycemia in an Inpatient Setting

A

-Concurrent illness (cerebral vascular accident, congestive heart failure, shock, sepsis)-Concurrent medications (Beta-blockers, quinolones, epinephrine)-Advanced age-Renal failure-Liver disease-Ventilator use

74
Q

Continuous Variable Rate IV Insulin DripAtlanta Multiplier Method

A

-*(formula on test) Starting Rate Units / hour = (BG – 60) x 0.02, where BG is current Blood Glucose and 0.02 is the multiplier-Check glucose every hour and adjust drip-Adjust Multiplier to keep in desired glucose target range (90 to 120 in ICU; 100 to 140 on floor)

75
Q

Converting to SC insulin from IV protocol? What’s the exception?

A

-If More than 0.5 u/hr IV insulin required with normal BG, start long-acting insulin (glargine). ——-Exception: if no prior DM and normal A1C, may not need SC insulin-Must start SC insulin at least 1 to 2 hours before stopping IV insulin-Some centers start long-acting insulin on initiation of IV insulin or the night before stopping the drip

76
Q

Correction Bolus Formula

A

Current BG - Ideal BG/ Glucose Correction factorExample:Current BG: 250 mg/dlIdeal BG: 100 mg/dlGlucose Correction Factor: 30 mg/dlso 250-100/correction factor of 30= 5 units* ON TEST*Add that correction factor to current dose to calculate how much you’re giving

77
Q

-A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone.-Can occur in both Type I Diabetes and Type II Diabetes: In type II diabetics with insulin deficiency/dependence-The presenting symptom for ~ 25% of Type I Diabetics.

A

Diabetic Ketoacidosis (DKA)

78
Q

-An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia.-Occurs predominately in Type II DiabeticsA few reports of cases in type I diabetics.-The presenting symptom for 30-40% of Type II diabetics.

A

Hyperosmolar Hyperglycemic State (HHS)

79
Q

Severe DKA vs HHS. Which is which? ? ?Plasma glucose level: >250 >600Arterial pH: 7.30Sodium Bicarb: 15Urine Ketones: positive smallSerum Ketones: positive smallSerum Osmolality variable >320Anion Gap: >12 variableMental Status: Stupor/Coma

A

DKA HHSPlasma glucose level: >250 >600Arterial pH: 7.30Sodium Bicarb: 15Urine Ketones: positive smallSerum Ketones: positive smallSerum Osmolality variable >320Anion Gap: >12 variableMental Status: Stupor/Coma

80
Q

Treatment of DKA

A

HYDRATION!!!Normal Saline:500-1000 cc/hr for 4 hours, then 250 – 500 cc/hr for 4 hours, then 125-250 cc/hrOnce glucose is < 200, should change fluids to D5 ½ NS until insulin drip is stoppedInsulin-Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hrIdeally should decrease glucose 50-100 mg/dL per hourIn DKA: Change to subcutaneous regimen once anion gap has closed and patient is ready to eat.Need to give long-acting insulin dose several hours prior to stopping insulin drip.AccuchecksEvery 1 hour initially, then every 2 hours, and so on.Serial ElectrolytesPotassium repletionShould add potassium to IV fluids once potassium < 5

81
Q

Treatment of HHS

A

-Hydration!!!: Even more important than in DKA-Find underlying cause and treat!-Insulin drip: Should be started only once aggressive hydration has taken place. Switch to subcutaneous regimen once glucose < 200 and patient eating.-Serial Electrolytes: Potassium replacement.

82
Q

Five H’s of Pheochromocytoma

A

-hypertension, headache, hyperhidrosis (excessive sweating), hypermetabolism, and hyperglycemia.-Absence of hypertension excludes diagnosis.

83
Q

Primary- Decreased thyroid hormone production, most commonCauses:Hashimoto’s thyroiditisResult of thyroid surgeryRadioactive iodine treatment of hyperthyroidism Overtreatment of hyperthyroidismIodine deficiencySecondary- Originates from anterior pituitary gland not producing TSHMyxedema Coma- rare, serious complication

A

hypothyroidsm

84
Q

SUBJECTIVE:Weakness, fatigue, lethargyHeadachesSlowed memory, psychotic behaviorLoss of interest in sexual activityMenstrual disturbancesDepressionOBJECTIVE:NeurologicalCVPulmonaryMetabolicGIIntegumentaryPsychologicalReproductiveGoiter

A

Hypothyroid

85
Q

Clinical syndrome caused by excessive circulating thyroid hormonesAKA Thyrotoxicosis , Graves’ DiseaseGraves’ disease, the most frequent cause. Signs: goiter, exophthalmos, pretibial edemaThyroid scanUltrasonographyElectrocardiography

A

Hyperthyroidsm

86
Q

Graves’ Disease is most common causePossible autoimmune repsonseOccurs in 3rd or 4th decadeAffects women > menEmotional trauma, infection, increased stressOverdose of meds to tx hypothyroidismUse of certain weight loss products

A

Risk factors of hyperthyrodism

87
Q

Nervousness, mood swings, irritability, hyperactivity, decreased attention spanInsomnia, interrupted sleepIncreased appetite, weight lossPalpitations, widened pulse pressure, increased SBPHeat intolerance, increased perspirationDyspneaWeakness, exercise intoleranceVision changes, exophthalmos, staring gazeGoiterBruits over thyroid glandIrregular mensesS&S of?

A

Hyperthyroidism

88
Q

Exopthalamus treatment

A

Provide symptomatic treatment.Treatment of hyperthyroidism does not correct eye and vision problems of Graves’ disease.Elevate the head of bed at night.Instill artificial tears.Treat photophobia with dark glasses/patchesGive steroid therapy.Provide diuretics.

89
Q

postop treatment of thyroidectomy

A

HemorrhageRespiratory distress AIRWAY, SUCTION AND TRACH SET AT BEDSIDEHumidified O2Semi-fowlers with pillows on either side of neckHypocalcemia and tetanyLaryngeal nerve damage

90
Q

What are the Nurse-Patient Relationship Phases

A

Pre-interaction phaseIntroductory/orientation phaseworking phasetermination phase

91
Q

Pre-interaction Phase

A

initial task: self-exploration, self-analysischallenges of psychiatric setting may cause stress and fears,Analyze strengths, limitationsGather data about patientPlan for first interaction

92
Q

Introductory/orientation phase

A

Find out why patient sought helpExplore patient’s feelings, identify problemsEstablish trust, understanding, acceptance, open communicationEstablish goal consensus, collaborationFormulate contract, explaining roles, confidentiality, responsibilities, expectations of patient and nurse

93
Q

Working phase

A

Nurse and patient explore stressors Promote development of insight by linking perceptions, thoughts, feelings, actionsTranslate insight into action/behavior changeMaster anxieties, increase self-responsibility, develop constructive coping mechanismsStandoff, impasse, or plateau may develop if patient resists moving forward

94
Q

Termination phase

A

Learning maximized because of higher levels of trust, intimacyExchange feelings and memories to evaluate patient progress, goal attainmentEstablish reality of separation; explore feelings of rejection, loss, sadness, anger Make referrals if needed for continued care or treatment

95
Q

Therapeutic communication techniques

A

Listening is the foundationUse broad openings to encourage patient to communicate what is important to him/herRestate part of patient’s statementClarify vague ideas, thoughtsReflect on/validate patient’s behavior, feelings

96
Q

Authenticity

A

Comes with awareness of self. Helps with therapeutic alliance so the patient is more comfortable opening up to the provider.

97
Q

Nurse patient interactions

A

?????????

98
Q

Phases of schizophrenic disorder

A

Acute Relapsing: reduce stimulationStabilizing: Titration of medicationsStable: symptoms controlledRecovery: psychosocial goalsRefractory: cope with level of symptomsPersistent psychotic symptoms

99
Q

Schizophrenia Positive Symptoms

A

HallucinationsDelusionsIllusionsParanoiaSleep DisordersDisorganized SpeechLooseness of AssociationBizarre Behavior

100
Q

Schizophrenia Negative Symptoms

A

Poverty of SpeechAffective BluntingAnhedoniaSocial WithdrawalApathyAvolitionPoor GroomingAttentional ImpairmentAsocial behavior

101
Q

Alogia

A

lack of speech

102
Q

Anergia

A

lack of energy

103
Q

Anhedonia

A

lack of ability to experience pleasure

104
Q

Avolition

A

Cannot initiate or persist in goal-directed activities

105
Q

Laboratory tests for schizophrenia

A

complete blood count (CBC), other blood tests to rule out other conditions with similar symptoms, screening for alcohol and drugs, and imaging studies, such as an MRI or CT scan.Metabolic issues…lipid profile, HA1C, track weight.

106
Q

Medications for Schizophrenia

A

AtypicalTypical

107
Q

Atypical medications

A

treat both positive and negative symptoms. Risks:Metabolic syndrome…increased appetite, increased blood sugar, increased lipids.examples; Abilify, zypraxa, invenga, paloperidone, respridol, resperidone, clozaril

108
Q

Typical medications

A

As good as atypical for positive symptoms, but does not treat negative. Cheaper, but more side effects.examples; halidol, perfenazine, prolixine, trilifon

109
Q

Somatization Disorder

A

Physical complaintsCannot be explained medicallyUsual onset before age 30Extends to a period over yearsPain, GI, Sexual, Neuro symptomsSymptoms are not intentionally produced0.2-2% women, 0.2% men, prevalence

110
Q

Conversion Disorders

A

Voluntary motor/sensory functionsSymptom is initiated or exacerbated by stressorSymptoms not intentionally producedSymptoms cannot be explained medicallyImpaired social, occupational, or role functioning“La belle indifference”

111
Q

“La belle indifference”

A

Inappropriate lack of emotion

112
Q

Body Dysmorphic Disorder

A

Unrealistic focus regarding a deformed or defective featureExcessive grooming to disguiseClinically significant impairment of social, occupational or role functionNot better accounted for by another disorder

113
Q

Depersonalization disorder

A

persistent or recurrent feelings of depersonalization and/or derealization.

114
Q

Depersonalization

A

sense of personality is lost

115
Q

Derealization

A

external world is not real…a dream

116
Q

D50 coverage for hypoglycemia calculation

A

(100 (ideal BS) - actual BS) x 0.4

117
Q

emergency equipment for artificial airways

A

Ambu Bag, Obturator, Suction Equipment, Extra Tubes

118
Q

Cam ICU 4 sections

A
  1. Acute onset or fluctuating course: is pt. different from baseline, or had fluctuation in mental status last 24 hrs2. Inattention: letter attention test squeezing only on A’s3. Altered level of consciousness: present if RASS is anything other alert and calm (zero)4. Disorganized thinking: yes/no questions, commands
119
Q

How to tell if CAM ICU is positive for delirium?

A

Feature 1+ 2, and EITHER 3 OR 4 present = positive

4630 Final (11 decks)

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