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Concepts 3 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

QT Prolongation

Causes (5)
Risk
Treatment (4)

A

Causes
- electrolyte imbalance (hypokalemia, hypomagnesemia, hypocalcemia)
- bradycardia
- heart blocks
- PVC
- meds (antidysrhythmic (i.e. amiodarone), antibiotics, anesthetics, antidepressants, antiemetics, antipsychotics, opioids, sedatives)

Risk: torsades de pointes (v-tach)

Treatment: pacemaker, increase HR, stop meds, correct electrolytes

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2
Q

ST Segment

How many boxes is it deviated?
NSTEMI (3)
STEMI (3)

A
  • deviated 3 small boxes up or down

Non-ST elevation MI (NSTEMI)
- No ST elevation
- T waves may be tall and symmetric
- troponin is elevated

ST elevation MI (STEMI)
- ST elevation in 2 or more consecutive leads
- T wave inversion
- troponin elevated as well

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3
Q

Ventricular Dysrhythmias: Characteristics (3)

A
  • widened QRS complexes (> 0.12)
  • impulses from sinus and atrial nodes fail
  • lead to decreased perfusion and potential for cardiac arrest
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4
Q

Premature ventricular complexes (PVC)

What is it?
Causes (5)

A
  • Early ventricular contraction/irritability (misfiring in heart outside of SA node; unable to see P wave)

Causes
- electrolytes (hypokalemia, hypomagnesemia,
- drugs (smoking, caffeine, alcohol,,
- stress (infection or invasive procedure (cardiac cath, surgery))
- respiratory problems (hypoxemia, acidosis, COPD)
- heart problems (cardiomyopathy, ventricular aneurysms, CHF, MI, sympathomimetic drugs)

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5
Q

Premature ventricular complexes (PVC)

Multifocal vs. unifocal
Repetitive Waves (4)

A

Multifocal vs. Unifocal
- Multifocal looks different and occur in different areas (more serious)
- Unifocal look the same and occurring in same place of heart

Repetitive Waves
- 2 PVCs- Couplets (two consecutive PVC)
- Bigeminy (after every normal beat)
- Trigeminy (after every two normal beats)
- 3 or more PVC’s in a row = Nonsustained run of V-tach

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6
Q

PVCs: Nursing care (5)

A
  • if new or symptomatic, call HCP
  • If > 3 in a row, call MRT and give amiodarone or beta blockers
  • Check labs for hypokalemia or hypomagnesemia
  • check perfusion (HR, BP, palpitations, decreased peripheral pulses)
  • request 12-lead EKG
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7
Q

V-tach: Characteristics (4)

A
  • most common ventricular dysrhythmia
  • Repetitive ventricular firing greater than 140 beats/min
  • no P waves
  • Nonsustained V-tach = < 30 seconds (sustained can progress to v-fib)
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8
Q

V-Tach/v-fib: Causes (4)

A
  • Cardiac (MI, HF, Dig toxicity,valvular dysfunction, cardiomyopathy, hypotension, SVT)
  • Electrolytes (hypokalemia, hypomagnesemia)
  • Meds (steroids, antidysrhythmic drugs which prolong QT)
  • Drugs(cocaine)
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9
Q

V-tach: Care w/ carotid pulse (4)

A
  • slow pulse with amiodarone (alt: diltiazem, digoxin, lidocaine, procainamide)
  • use cardioversion (call HCP; can be elective or emergent)
  • give oxygen
  • Get informed consent and hold digoxin 48 hrs prior to elective cardioversion b-c increases risk of VF from shock
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10
Q

V-tach: Care w/o carotid pulse (4)

Note: same care for V-fib

A
  • Implement Code Blue/ ACLS Protocol
  • Defibrillate (priority after everyone clear and oxygen off)
  • CPR if no defibrillation and after defibrillation
  • Epinephrine q3 min if no HR and no pulse after IV established
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11
Q

V-fib: characteristics (4)

A
  • Total chaos in ventricle with no discernible waves or complexes
  • Ventricles quiver and no forward flow of blood which consumes oxygen
  • Non-perfusing rhythm (no BP, no HR, apnea; potential for seizures and acidosis)
  • fatal if not terminated in 3-5 min
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12
Q

Pulseless Electrical Activity (PEA)

Characteristics (3)
Care

A

Characteristics
- NSR w/o a pulse
- non-perfusing rhythm
- not a shockable rhythm

Care
- Code Blue/ACLS protocol (CPR, ambu, epi)

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13
Q

ACLS: 5 Hs

A
  • Hypovolemia (LR, NS, or blood fast)
  • Hypoglycemia
  • Hydrogen ion (acidotic) (bicarb)
  • hypo/hyperkalemia
  • hypoxia (ambu bag)
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14
Q

ACLS: 5 Ts

A
  • Trauma
  • Tension Pneumothorax (chest tube, decompression)
  • Cardiac Tamponade (pericardial effusion prevents heart contraction) (do pericardiocentesis (removal of fluid))
  • Toxins (give antidote (flumazenil, naloxone, acetylcysteine)
  • Thrombosis (PE, coronary emboli)
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15
Q

Asystole

Characteristics (3)
Care (2)

A

Characteristics
- straight line b-c no electrical activity
- no contraction = no perfusion
- not a shockable rhythm

Care
- Code Blue/ACLS protocol (CPR, ambu, epi)
- pacemaker (help heart maintain rhythm)- never first action

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16
Q

Sudden Cardiac Death

Care (5)

A
  • Call MRT and initiate ACLS
  • get 12-lead EKG
  • Assess for risk factors and cognitive defects (hypoxic brain injury)
  • May need therapeutic hypothermia to preserve brain function
  • allow family at bedside during ACLS
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17
Q

Myocardial Infarction

Process
Risk Factors (4)

A

Process: Decreased Blood Flow (perfusion) leads to irreversible myocardial necrosis (cell death) r/t atherosclerotic plaque rupture

Risk factors
- HTN
- Lifestyle (smoker, obese, stress, sedentary)
- hyperglycemia
- hyperlipidemia

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18
Q

Myocardial Infarction: Priority Meds (4)

A
  • Morphine: For pain, anxiety, fear, reduces preload and afterload
  • Oxygen: To maintain >90% O2 sat
  • Nitroglycerin sublingual (vasodilation and increase cardiac output)–Risk for hypotension (hold if systolic <90 OR PDE5 inhibitor (sildenafil) in hx for erectile dysfunction or pulmonary HTN)
  • Aspirin (ASA): Prevents clumping of platelets and reduces mortality
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19
Q

Myocardial Infarction: Areas from outer to inner

Area of ischemia (2)
Area of Injury (2)
Area of Infarction (3)

A

Ischemia
- transient and reversible due to O2 deprivation
- Seen on ECG as T-wave inversion and ST depression

Injury
- injured but potentially viable tissue if circulation adequate
- Seen on ECG as ST elevation

Infarction (irreversible)
- Area of dead muscle (necrosis) in the myocardium which becomes scar tissue
- Delayed treatment = increased damage/area of infarction
- Seen on ECG as pathologic Q waves (deeper and wider than normal)

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20
Q

MI: Clinical Manifestations (7)

A
  • Angina (abrupt and not relieved by NTG); may be crushing, tightness, radiating
  • systolic murmur or S3/S4 sounds (r/t papillary muscle rupture, HF, pulmonary edema)
  • Pulmonary (dyspnea, tachypnea, crackles, wheezes)
  • Skin (diaphoresis)
  • Decreased cardiac outout) (tachycardia, hypotension, slow cap refill
  • Neuro (syncope, denial)
  • Muscular (weakness)
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21
Q

Diagnostics for MI (3)

A
  • Cardiac monitoring (12 lead EKG within 10 min of arrival to determine where MI is in the heart)
  • daily chest x-ray
  • echocardiogram
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22
Q

Labs for MI (4)

A
  • troponin (q6-8h b-c not elevated immediately but elevated for 7-10 days)
  • Metabolic panel
  • CBC
  • B type natriuretic peptide (BNP) (Rule out heart failure)
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23
Q

MI: Other Drugs Purposes

  • Beta Blocker (2)
  • ACE Inhibitor and ARBs
  • Anticoagulant (2)
A

Beta Blocker
- Decrease mortality from ventricular dysrhythmias; lower BP, prevent reinfarction
- Hold if in cardiogenic shock, heart failure, heart block (PR >0.24) or active asthma

ACE Inhibitor and ARBs
- Prevent ventricular remodeling and HF

Anticoagulant (Heparin or Enoxaparin)
- enhance perfusion
- If thrombocytopenia, give direct antithrombotic (e.g., bivalirudin, argatroban)

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24
Q

MI: Other Drugs Purposes

Stool Softener
Inotropic (dobutamine, dopamine, milrinone)
Diuretic
Amiodarone (antidysrhythmias)

A

Stool softener
- prevent straining which can slow HR via vagal stimulation

Inotropic (dobutamine, dopamine, milrinone)
- Increase CO

Diuretic
- If elevated BNP, pulmonary edema, CHF exacerbation

Amiodarone (antidysrhythmias)
- If v-tach w/ pulse or a-fib w/ RVR

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25
Q

MI: Priority Non Pharmacological Care (4)

A
  • place two large bore IVs
  • Door-to-PCI within 120 minutes if need transfer to PCI-capable facility (90 min if PCI-capable hospital)
  • Balance myocardial oxygen supply and demand (use Bed rest w/ bathroom privileges and place upright for venous return, lower preload, decrease workload)
  • Prevent immobility complications (DVT, pneumonia) w/ early mobility and HOB 30 or more
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26
Q

Fibrinolytics (tPA (ateplase); Reteplase (rPA) or Tenecteplase (TNKase))

Eligibility (2)
Exclusion (4)

A

Eligibility
- Onset of STEMI within 12 hrs
- <30 min after STEMI diagnosis

Exclusion
- Uncontrolled hypertension (need antihypertensives first)
- Ischemic stroke within 3 months
- Recent surgery, facial or head trauma
- Unstable angina or NSTEMI

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27
Q

Fibrinolytics (tPA (ateplase); Reteplase (rPA) or Tenecteplase (TNKase))

Action
Care (5)

A

Action: lysis of acute thrombus to reopen obstructed coronary artery and restore blood flow; short half-life

Care
- Anticoagulants(heparin) for 48 hrs after
- Antiplatelets (clopidogrel) for 14 days to 1 year after
- Continue aspirin indefinitely
- Bleeding precautions (gently handling, avoid venipunctures, apply add’l pressure)
- STOP if IC bleeding or internal bleeding and give volume expanders and coagulation factors

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28
Q

MI complication: Pericarditis

What is it?
S/s (4)
Care (3)

A
  • inflammation of pericardial sac during or after MI or CABG leads to pericardium irritation

S/s
- Cardiac Friction Rub (grating, scraping, leathery scratching at sternal border)- most common initial
- Chest pain (exacerbated by deep breathing/coughing and supine)- most common
- Pericardial effusion
- ST elevation in all EKG leads

Care
- NSAIDS/Aspirin
- Rest
- Pericardiocentesis (removal of fluid)

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29
Q

PCI: Nursing Interventions r/t to risk of bleeding (4)

A
  • Watch for S/S of bleeding (hematoma, hypotension, tachycardia; Back pain (retroperitoneal bleeding))
  • Assess insertion site and apply direct pressure if bleeding
  • HOB should be less than 30 degrees
  • Bedrest: Instruct to keep limb straight/minimize movement for 4-6 hrs
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30
Q

PCI: Nursing Interventions r/t to risk for ineffective peripheral tissue perfusion (3)

A
  • Monitor neurovascular of affected extremity (distal pulses, cap refill, color, sensation, and temperature in involved extremity)
  • VS q15 for 1h, q30 for 1 hr, q1 for 4 hrs
  • Monitor for graft occlusion
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31
Q

PCI: Nursing Interventions r/t to risk of Angina (4)

A
  • Watch for increased chest pain r/t thrombosis or transient coronary vasospasm
  • Monitor EKG for ST elevation
  • Give IV NTG
  • Monitor labs for hypokalemia
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32
Q

PCI: Nursing Interventions r/t to risk of AKI (3)

A
  • Maintain hydration before and after (NS and/or sodium bicarb)
  • Check Crt, BUN, GFR prior
  • Avoid nephrotoxic drugs (NSAIDS, metformin)
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33
Q

MI: Signs of Reperfusion (4)

A
  • Chest pain stops due to return of blood flow
  • CK and troponin increase rapidly then decrease (a washout)
  • ST elevation returns to baseline (note Failure of fibrinolytic = inability to achieve 50% resolution of ST elevation within 60-90 minutes of med admin)
  • Reperfusion dysrhythmias (ex. PVCs, bradycardia, heart block, VT)- Usually self-limiting –> Care for PVCs: oxygen and correct f/e imbalance
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34
Q

Aortic Aneurysm

What is it?
Causes (5)

A

Localized dilation of arterial wall that results in alteration in vessel shape and blood flow

Causes
- systemic HTN
- Atherosclerotic changes in the thoracic and abdominal aorta
- Blunt trauma
- Pregnancy
- Smoking

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35
Q

Aortic Aneurysm: Diagnostics (4)

A
  • CT w/ dye - May use NTG to dilate coronary arteries or BB to reduce HR for better visualization
  • Aortic Angiogram (uses dye)
  • Ultrasound (Can assess collapse of inferior vena cava during respiratory cycle)
  • Transesophageal Echocardiography (TEE) - less barriers so easier to see heart than Transthoracic; NPO prior
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36
Q

Aortic Aneurysm: s/s (2)

A
  • may not have any
  • palpable, pulsatile mass in umbilical region to left of midline (avoid palpating)
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37
Q

Aortic Aneurysm: Care if <4 cm (5)

A
  • Outpatient management and education
  • Lifestyle (Weight loss, Smoking cessation)
  • BP control (most important)
  • Pain control
  • Prevention of complications i.e. Rupture
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38
Q

Aortic Aneurysm: Care if > 4cm (9)

A
  • Inpatient management- 1-hour assessments for 24-48 hrs in ICU
  • Evaluate the need for surgical repair (Prosthetic graft)
  • Abdominal (DO NOT PALPATE; listen to bruits)
  • BP checks w/ art line or in both arms ( HTN treated w/ vasodilator (sodium nitroprusside) or labetalol or clevidipine; Hypotension treated w/ vasopressors and volume replacement)
  • Heart (Monitor EKG for ischemia or dysrhythmias; Auscultate aortic murmur
  • Neurovascular checks (Bilateral peripheral pulses, Pain, pallor, paresthesia, paralysis, movement)
  • Pain assessments and management
  • Kidney function (Urine output)
  • Maintain calm environment (No heavy lifting, stress)
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39
Q

Aortic Dissection

What is it?
S/s (4)

A
  • Sudden onset of intense, severe, tearing pain localized in the chest, abdomen, or back when column of blood separates vascular layers

S/s
- Pain Radiates to back or lower extremities
- Pulsatile mass in umbilical region of the abdomen to the left of midline
- neuro (alt mental status or coma)
- CV (severe HTN, limb ischemia, new murmur)

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40
Q

Aortic Dissection

Diagnostics (5)

A
  • CT
  • Transthoracic Echocardiography (TTE)–On chest and noninvasive w/ transducer on skin
  • Transesophageal Echocardiography (TEE)– Down throat; lidocaine to reduce gag reflex, NPO prior
  • Chest X-R (only if mediastinum widened)
  • Aortogram (definitive invasive)
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41
Q

Aortic Dissection: Care (4)

A
  • Control of BP (IV antihypertensives or vasodilators)
  • control pain (opiates)
  • May need mechanical ventilation if profound hemodynamic instability
  • Emergency Surgery (Resection of the affected area w/ Graft placement and restoration of blood flow to major branches of the aorta)
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42
Q

Aortic Dissection: Complications

Cardiac tamponade - 3
Cardiogenic shock - 1

A

Cardiac tamponade
- Lethal r/t fluid accumulation in mediastinal space which impairs heart’s ability to pump
- S/s: elevated and equalized filling pressures (CVP, PADP, PAOP); Decreased CO (Decreased BP, Muffled heart sounds, Sudden cessation of chest tube drainage); JVD, pulsus paradoxes
- Care: emergency sternotomy or return to OR for clot retrieval

Cardiogenic shock
- Blood pressure support

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43
Q

Endocarditis: Risk Factors (7)

A
  • Foreign material in heart (Prosthetic heart valves, Implantable pacemakers , ICDs)
  • IV drug users (esp if right heart valves involved)
  • Strep throat infection (not completing full course of antibiotics)
  • Poor oral hygiene
  • Other heart problems (CHD, Valvular heart disease)
  • Body piercings
  • DM type 2
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44
Q

Endocarditis

What is it
Noninfectious vs infectious

A

inflammation on the endothelial surface of the heart, specifically thrombotic-fibrin vegetation on the cardiac valves.

  • Noninfectious: thrombotic lesion on cardiac valve or endothelium
  • Infectious: Due to bacterial/fungal organism in blood (bacteremia) or on cardiac valve lesion; most common: Streptococci, staphylococci, and enterococci
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45
Q

Endocarditis

General Signs and Symptoms (5)
Complications (2)

A
  • Cough and pleuritic chest pain
  • Fever w/ rigor, fatigue, malaise
  • Myalgias and joint pain
  • Heart murmurs
  • bleeding (Hematuria, Petechiae)

Complications
- Heart Failure (most frequent cause of death)
- Embolic (CVA, PE, septic on fingers and toes (osler nodes, splinter hemorrhages), liver, splenomegaly, kidney, peripheral)

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46
Q

Endocarditis: Labs/Diagnostics (4)

A

CBC- Elevated WBC
Blood cultures- may be negative
TEE- Visualize vegetations and abscesses
Chest x-Ray- Detect nodular infiltrates, cardiomegaly, enlarged pulmonary vessels

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47
Q

Endocarditis

Treatment (2)
Key patient education (3)

A

Treatment
- IV Antibiotics for 4-6 weeks (Broad Spectrum– risk for kidney dysfunction, vestibular dysfunction, diarrhea (c-diff) or colitis
- Surgery to replace valves, remove vegetation for persistent vegetation, valve dysfunction, perivalvular extension, antibiotic-resistant bacteria or fungus

Key Patient education
- Daily temp monitoring
- Prophylactic antibiotics for invasive procedures (dental) if artificial valve, ICDs, pacemakers
- Care for HF (activity, fluid and sodium restriction, diuretics, daily weights)

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48
Q

Hypertensive Emergency

Diagnosis Criteria (2)
Goal of treatment

A
  • Acute rapid or severe increase in blood pressure over 180/120
  • results in new or progressive end-organ damage (heart (acute MI), the brain (stroke), or the kidney (kidney failure))

Goal by discharge: 140/90 or 130/90 if HTN, CKD, DM, or CAD

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49
Q

Hypertension Emergency: S/s (5)

A
  • CNS- Headache; Blurred vision; Change in LOC -> Coma, stroke, seizures
  • Cardiac- Chest pain of ACS or aortic dissection
  • Abdominal or back pain r/t aortic aneurysm or dissection
  • AKI i.e. Sudden absence of urine output; high Crt or BUN
  • Catecholamine excess = vasoconstriction
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50
Q

Hypertension Emergency: Medical management (5)

A
  • Vasodilator (Sodium Nitroprusside; hydralazine if pregnant)
  • Beta Blockers (labetalol and esmolol)
  • ACE inhibitors (enalaprilat)
  • Calcium Channel Blockers (nicardipine)
  • Loop Diuretics
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51
Q

Sodium Nitroprusside

Indication (2)
Risks (4)
Care (3)

A

Indications: HTN emergencies, afterload reduction in severe HF

Risks
- cyanide toxicity (blurred vision, confusion, tinnitus) w/ long-term use
- Hypotension r/t peripheral vasodilation
- Headaches r/t cerebral vasodilation
- Reflex tachycardia

Care
- start IV drip via titration (no more than 10-15% drop in BP in first 24 hrs)
- nee art line and 2 IVs for monitoring
- Protect bag and lines from light (usually in brown bag)

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52
Q

Components of Hemodynamic Monitoring (4)

A
  • Invasive catheter (Art-line least invasive)
  • 250-300 mm Hg pressure tubing with 0.9% NS flush solution
  • Transducer to convert physiologic signal into electrical energy
  • Bedside monitor to display volume of electrical signal on digital scale
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53
Q

Care for Hemodynamic Monitoring (7)

A
  • separate pressure bags for separate lines
  • place transducer at phlebostatic axis (midaxillary 4th intercostal space) while HOB 0-60 degrees every shift
  • zero transducer once a shift (open to atmospheric pressure and close to patient and flush solution)
  • monitor for bleeding, infection (CLABSI), air embolus, thrombus, dislodgement
  • alarms should always be audible
  • do fast flush square wave test to ensure waveform not over or underdamped
  • daily x-ray for placement
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54
Q

Art-line

What is it?
Indications (4)

A

Continuous measurement of three BP parameters (Systole, Diastole, Mean arterial blood pressure (MAP))

Indications
- Shock
- Hyper or hypotension
- Post-op for major surgery
- Acute lung failure b-c need frequent ABGs

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55
Q

Art-line: Care (3)

A
  • perform Allen test to assess collateral circulation
  • assess wave form (Systole: highest point; Dicrotic notch: closure of aortic valve and start of blood flow into arterial vasculature; Diastolic: lowest point)
  • never put meds in ART
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56
Q

Mean Arterial Pressure

Range
Preferred values (2)
Equation

A

Range: 70-100 mm Hg

Preferred
- > 60 to perfuse coronary arteries
- > 65 to perfuse brain and kidneys

Equation: MAP= [(DBP(2) + SBP)/3)]

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57
Q

Central venous pressure (CVP)

What is it?
Indication
Placement (3)
Normal Range

A
  • Measures right ventricular end-diastolic pressure( filling pressures of the right side of the heart) and sits in superior vena cava

Indicated for alteration in fluid volume (high = overload; low = dehydration)

Catheter Placement
- Subclavian (SC- better if > 5 days)
- Internal jugular (IJ- has best blood flow and less risk for pneumothorax)
- Femoral (if others inaccessible b-c higher risk for infection)

Range: 2-5 mm Hg

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58
Q

Pulmonary Artery Catheter

Four Lumens

A
  • CVP (R atrial pressure and volume status b-c sits in superior vena cava)- Useful for blood samples, IV infusion, fluid injection for CO determination, CVP (Volume Status (EDV))
  • PAP (pulmonary artery pressure) (L volume status b-c sits in pulmonary artery on L side) - Useful fo blood samples to measure Oxygen supply and demand (ventricular function (PVR, SVR) and SvO2)
  • Pulmonary Artery Occlusion Pressure (PAOP/Wedge Pressure) –5-12 mm Hg general range (Gives HCP the CO, SVO2, Cardiac index, preload)
  • Thermistor (Measure thermodilution CO)
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59
Q

Pulmonary Artery Catheter

Indications (4)
Special Care (2)

A

Indications
- Open heart surgery
- Acute heart failure
- Acute pulmonary HTN
- Cardiogenic shock

Special Care
- must have ECG monitoring
- must have defibrillator and emergency resuscitation nearby

60
Q

Cardiac Output

What is it?
What does Starling Law say?
Equation
Normal range

A

Volume of blood ejected from the left ventricle in 1 minute

Starling Law: force of ventricular blood volume ejection is related to preload (Volume of blood in the ventricle at end-diastole) and Amount of stretch (force) placed on the ventricle

Equation: HR (# of beats per minute) X SV (amount of blood ejected by ventricle w/ each heartbeat) = CO

Normal range: 4-6 L/min

61
Q

Preload

What is it
Factors on left and right side (2)
When increased (2)
How to reduce (3)

A
  • pressures resulting from volume coming into ventricles (end diastolic pressure)

Factors on left and right side
- Left side (Pulmonary artery diastolic pressure and pulmonary artery occlusion pressure)
- Right (CVP aka right atrial pressure)

  • increased (hypervolemia, regurgitation of valves)

How to reduce
- diuretics
- vasodilators
- fluid restrictions

62
Q

Afterload

What is it
Factors on left and right side (2)
When increased (2)
Care (2)

A
  • resistance left ventricle must overcome to circulate blood/ overcome systolic ejection

Factors
- Left (SVR– high SVR = decreased CO)
- Right (PVR)

  • increased (HTN, vasoconstriction) = increased cardiac workload

Care
- to reduce, ACEI, ARBS, vasodilators (sodium nitroprusside, NTG)
- to increase, vasopressors and IV fluids (preferably w/ art-line)

63
Q

Contractility

What is it?
Relation to Afterload, Preload, Ventricle distention (3)
Drugs to improve contractility (3)

A

The heart’s ability to stretch and contract

Relation
- Afterload/SVR increases, contractility decreases
- Preload increases, contractility increases
- If ventricle overdistended, contractility decreases

Drugs:
- Cardiac glycoside (digoxin)
- Inotropic drugs (dobutamine, dopamine, milrinone
- Oxygen (Hypoxia = negative inotrope)

64
Q

Hyperglycemia w/ absence of insulin Symptoms (11)

A
  • Polyuria (r/t osmotic diuresis from excess glucose in urine; leads to hypokalemia)
  • Polydipsia
  • Polyphagia (R/t cellular starvation of glucose so need insulin vs food to push glucose into cells)
  • Ketonuria and ketonemia -> metabolic acidosis -> hyperkalemia
  • Kussmaul respirations (to blow off excess CO2 from anion gap) – compensatory respiratory alkalosis
  • Acetone exhaled (fruity odor)
  • Hemoconcentration and Hyperviscosity
  • Hypovolemia (low CVP, high HR, low BP) and hypoperfusion
  • Hypoxia -> lactic acid production
  • Pain (headache, abdominal
  • fatigue, weakness)
65
Q

Diabetic Ketoacidosis (DKA): Definition (5)

A
  • Glucose > 250 mg/dL
  • Low bicarbonate level (<18 mEq/L)
  • Acidosis (pH <7.30)
  • Moderate or severe ketonemia and ketonuria
  • Anion gap > 12
66
Q

DKA: Risk factors (6)

A
  • Illness/infection (most common = UTI)
  • Increased metabolic demand (Pregnancy, trauma, hospital or surgery, Growth spurts)
  • Psychosocial (stress, eating disorders, depression)
  • mismanagement of sick days (not taking insulin when sick)
  • Drugs (steroids, insulin shortage or malfunction in pump)
  • heavy sugary drinks
67
Q

DKA: Patho (4)

A
  • due to insulin deficiency preventing glucose from entering cells
  • Lipolysis (Triglycerides to glycerol and free fatty acids ) -> Ketogenesis (Free fatty acids -> Ketones (Ketonemia and ketonuria, and Acetone (fruity breath via lung excretion) ->
    Metabolic Acidosis (low bicarb; anion gap > 12
  • Glycogenolysis (glucagon leads to release of glucose from liver and skeletal muscle stores to increase glucose level in blood)
  • Gluconeogenesis (breakdown of fats) into glucose in absence of insulin) -> Hyperglycemia -> attempt to get rid of excess glucose leads to osmotic diuresis (Causes dehydration, hypotension, tachycardia, tissue hypoxia, shock)
68
Q

DKA: non-defining labs (6)

A
  • Leukocytosis
  • Urine: High specific gravity and osmolality
  • Glucosuria (Osmotic pull of glucose increases output)
  • BUN, Crt increase b-c risk for kidney impairment r/t decreased organ perfusion
  • K, Na, PO4 excreted in urine (may be low)
  • Serum osmolality (hyperosmolality)
69
Q

DKA: Hydration (3)

A
  • NS 1 Liter w/n first hour
  • Then NS 1/2 at 250-500ml/hr
  • When glucose < 200, change to D5W 1/2NS at 150-250ml/hr to prevent hypoglycemia and cerebral edema via replenishing cellular glucose
70
Q

DKA: Correct Electrolytes -5

A
  • replace sodium w/ fluids
  • If hypokalemic, give K immediately before insulin
  • If not hypokalemic, give 20-30 mEq of K+ within 2-3 hrs of treatments
  • If hyperkalemic, insulin and volume expansion will correct
  • Replace phosphate if < 1 mg/dL
71
Q

DKA: Replace insulin (4)

A
  • 0.1 unit/kg Regular Insulin IV Bolus (onset: 15 min)
    followed by 0.1 unit/kg/hr via continuous IV pump
  • Glucose should drop 50-70 points/hr
  • Switch to SubQ regular insulin 2 hours before discontinuing continuous pump
  • Patient must be stable w/ consistent glucose level, no ketosis, and able to eat prior to switch to subQ
72
Q

DKA/HHS: Monitoring response to therapy (5)

A
  • Hourly glucose checks until stable (once stable, q2-4h)
  • Use accuchecks unless CVP or art-line w/ blood conservation system
  • rate of blood glucose change = 50—70 (More important than actual level)
  • Monitor appearance, VS, I & O and Labs: BUN, Crt, K, ABGs
  • NPO until glucose is stable
73
Q

DKA: Markers for resolution (4)

A
  • Blood glucose below 200 mg/dL
  • Serum bicarbonate above 18 mEq
  • pH greater than 7.3
  • absence of ketones in urine and blood
74
Q

DKA/HHS: Complications from management and key care(6)

A

Fluid volume overload r/t HF or kidney disease
- Care: oxygen, reduce infusion, elevate HOB, assess fluid status

Hypokalemia or Hyperkalemia
- Care: ECG monitoring, potassium chloride

Hyponatremia
- Care: NGT intermittent suctioning if NV

Cerebral edema
- Care: hourly neuro assessment esp sudden headache, confusion, pupils

Infection
- Care: oral care, repositioning, sterile technique, check venipuncture sites q4h

Hypoglycemia
- Care: stop IV insulin, give D50 or subQ glucagon q15 until glucose > 70

75
Q

Hyperglycemic Hyperosmolar State (HHS): Definition (6)

A
  • Blood glucose > 600 mg/dL
  • Arterial pH > 7.3
  • Serum bicarb > 18 mEq/L
  • Serum osmolality > 320 mmol/kg (risk for coma if > 350)
  • Absent or mild ketonuria
  • Severe dehydration
76
Q

HHS: Risk Factors (5)

A
  • Geriatric b-c higher risk for dehydration b-c decreased thirst perception, urine concentration; and increased diuretic usage
  • Illness (UTI, pneumonia, pancreatitis, sepsis)
  • Perfusion morbidities (MI, stroke)
  • Stress of critical illness (trauma, surgery, stress hormones: cortisol, glucagon, epinephrine)
  • Drugs (glucocorticoids, diuretics, phenytoin, beta blockers, CCB)
77
Q

HHS: Patho (5)

A
  • Pancreas makes insufficient insulin for glucose needs (enough to prevent ketosis but not enough to prevent hyperglycemia
  • No ketogenesis so no fruity breath and Rapid and shallow respirations vs kussmaul
  • Gluconeogenesis (glucagon in liver creates glucose)
  • Hyperosmolar -> Osmotic diuresis -> Severe Dehydration (hypovolemia, oliguria) -> hyperglycemia (b-c conserves glucose and water) -> hyperosmolality (worsened)
  • Hemoconcentration (Increased blood viscosity r/t hyperglycemia -> Risk for clot, VTE, infraction)
78
Q

HHS: non-defining labs (3)

A
  • Elevated Hct
  • Low K, PO4 b-c lost in urine
  • Elevated BUN and Creatinine r/t lack of kidney perfusion
79
Q

HHS: Management (6)

A
  • NS 1 liter/hr for massive fluid replacement
  • Once hemodynamically stable (look at CVP or PAOP) or serum Na reaches 140mEq/L change to 1/2NS.
  • When plasma glucose reaches 300mg/dL, change to D5W 1/2NS 150-250 ml/hr
  • 0.15 unit/kg Regular Insulin IV Bolus followed by 0.1unit/kg/hr
  • subQ insulin once glucose stable and adequate food intake
  • Correct electrolytes (Potassium is added based on serum level (give if < 3.3))
80
Q

Older adults and glucose regulation (6)

A
  • reduced glucose metabolism r/t increased visceral fat and decreased lean muscle mass
  • reduced insulin production r/t decreased pancreatic islet function (unable to regulate and metabolize glucose concentrations)
  • Type 2 DM more common in older adults
  • DM in older adults = increased institutionalization and reduced functional status
  • DM presents as thirst, confusion, infection, poor wound healing in older adults
  • increased DM complications (ESKD, blindness, heart disease, CVA, neuropathy, depression, sexual dysfunction, periodontal disease)
81
Q

Older adults: Reason for increased hypoglycemia risk (3)

A
  • Decreased kidney function so reduced elimination of sulfonylurea and insulin
  • Reduced epinephrine and glucagon release r/t hypoglycemic unawareness
  • Impaired motor skills interfere w/ ability to correct glucose levels
82
Q

Older adults: Endocrine system (5)

A
  • cold intolerance (hard to distinguish from hypothyroidism) r/t decreased metabolism
  • dilute urine and dehydration risk r/t decreased ADH production
  • reduced thyroid hormone secretion (may not have s/s of hypothyroidism)
  • hypothyroidism is most common thyroid problem in older adults
  • start low and go slow w/ levothyroxine b-c risk of angina, dysrhythmias, HTN
83
Q

DI: Three types

A

Central Diabetes Insipidus AKA neurogenic DI
- Hypofunction of the posterior pituitary gland or hypothalamus leads to ADH (vasopressin) deficiency
- no ADH = kidneys not told to concentrate urine so lose excess H2O

Nephrogenic Diabetes Insipidus
- Inability of kidney tubules to respond to circulating ADH

Dipsogenic Diabetes Insipidus
- Compulsive water drinking (> 5 L/day)

84
Q

DI: Risk factors

  • Neurogenic/Central (6)
  • Nephrogenic (3)
A

Neurogenic
- Head trauma
- resection of pituitary tumor (malignancy)
- craniotomy (surgery)
- congenital disorders
- infection (encephalitis, meningitis)
- increased ICP

Nephrogenic
- pyelonephritis
- Polycystic kidney disease
- Drugs (lithium carbonate and demeclocycline)

85
Q

DI: labs (4)

A
  • High Serum Na+ > 145 mEq/L
  • High Serum Osmolality > 295 mOsm//L (Normal: 275-295)
  • Low Urine Osmolality < 300 mOsm/L
  • Low Urine specific gravity < 1.005
86
Q

DI: manifestations (3)

A
  • Dehydration (decreased skin turgor, dry mucous membrane, tachycardia, hypotension/hypovolemia, hemoconcentration, constipation, LOC change)
  • large dilute urine (polyuria and nocturia ; > 3L/24 hr) w/o hyperglycemia, diuretics, or fluid challenge
  • Polydipsia
87
Q

DI: Medical Management

General - 3
Central DI - 2
Nephrogenic DI - 1

A

General
- volume resuscitation (oral or IV hypotonic)
- may need lifelong care for chronic DI w/ daily weights (ED if > 2.2 lb overnight)
- monitor for fluid balance (overload or dehydration)- need urinary catheter

Central DI
- Vasopressin (antidiuretic and vasoconstrictor): risk for HTN, angina, vasospasm (MI, CVA) so not preferred
- Desmopressin (DDAVP- strong antidiuretic w/ little effect on BP - preferred

Nephrogenic DI
- Hydrochlorothiazide (HCTZ) - reduces amount of urine via resorption of sodium and water in proximal nephron

88
Q

Water deprivation Test

Purpose
Procedure
Results (2)

A

Purpose: measure ADH and determine type of DI

Procedure: give ADH (vasopressin)

Results
- If condition improves, there is central DI
- If condition does not improve, there is nephrogenic DI

89
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Definition (3)

A
  • More ADH than needed to maintain normal blood volume and serum osmolality
  • Excessive water reabsorbed at kidney tubule -> dilutional hyponatremia and overhydration
  • Increased kidney filtration of water inhibits Renin and aldosterone which prevents sodium resorption
90
Q

SIADH: Causes (5)

A
  • Pituitary gland problems
  • Malignancy (bronchogenic small cell carcinoma)
  • Skull fracture
  • Pulmonary infection or impairment
  • Meds that release or potentiate ADH (insulin, vasopressin)
91
Q

SIADH: Labs (5)

A
  • Hyponatremia (less than 125 mEq/L)
  • Decreased Serum Osmolality – < 275 mOsm/L
  • increased Urine osmolality – >100 mOsm/L
  • Elevated urine sodium
  • Elevated urine specific gravity (> 1.030)
92
Q

SIADH: Manifestations (9)

A
  • GI: loss of appetite, NV
  • Dilutional hyponatremia (Lethargy, NV, Headache, hostility, disorientation)
  • Severe Neurological Symptoms (Serum Sodium< 120 mEq/L)- > Decreased LOC, Seizures/ Coma, Apprehension
  • Hypothermia r/t CNS disturbance
  • Full and bounding pulse r/t increased fluid volume
  • Decreased DTR’s
  • Weight gain but no edema b-c water not salt is retained
  • Decreased urine output
  • increased thirst (polydipsia)
93
Q

SIADH: Nursing Management (6)

A
  • Meds (hypertonic NaCl, Vaptans, Diuretic(if normal Na))
  • Fluid restriction (usually 500 -1000 mL/day)
  • Oral care for comfort and to prevent dry mouth
  • If they need any free water, use saline vs tap water
  • Monitor for complications (I &O, daily weights, fluid status q2h; neuro status hourly if any changes in LOC)
  • Always seizure precautions and reduce stimulation if SIADH
94
Q

SIADH: Na replacement (3)

A
  • Hypertonic saline (3%NaCl) when Na level is too low to prevent extra volume
  • do not want rapid sodium increase (want gradual increase 8 mEq/L in 24 hr to prevent osmotic demyelination)
  • Monitor Na+ and K+ q4h during acute phase of sodium replacement
95
Q

Vaptans (Conivaptan (Vaprisol)- IV or Tolvaptan (Samsca) – PO)

Indication
Action
Risks (2)

A

Indication: euvolemic hyponatremia in SIADH

Action: excretes water and conserves sodium (aqua diuresis)

Risks
- For Conivaptan, hypotension (contraindicated in hypovolemia)
- For Tolvaptan, black box warning for rapid hypernatremia (risk for CNS demyelination) AND liver failure

96
Q

Thyroid Storm: Manifestations (7)

A
  • heat intolerance (fever, diaphoresis)
  • Cardiac (SVT, systolic HTN, a-fib, PVC, HF, hypovolemia, pulmonary edema)
  • GI (Jaundice, NVD, abd pain, increased appetite, weight loss; enlarged spleen
  • CNS (agitation, insomnia, delirium, lethargy, seizures, stupor, coma, emotional instability)
  • Muscle (weakness and wasting; increased DTR, tremors)
  • Pulmonary (tachypnea)
  • Epithelium (goiter (no palpate); exophthalmos; pretibial myxedema; vision changes; thin hair )
97
Q

Thyroid Storm: Labs (5)

A
  • high T3 and T4
  • Hyperglycemia
  • Decreased TSH
  • Hypercalcemia (confusion, short QT, bradycardia, increased DTR) - > 10.5
  • metabolic acidosis
98
Q

Antithyroid Drugs (Propylthiouracil (PTU) and Methimazole (Tapazole)

Action
Care (5)

A

Action: block synthesis and release of thyroid hormone

Care
– must be enteral route
- Avoid crowds and sick people b-c they reduce immune response (agranulocytosis i.e cough, fever, inflammation, rash)
- Report s/s hypothyroidism (cold intolerance, weight gain)
- If PTU, report hyperpigmentation (darkening of urine or yellow coloring of skin) b-c could be liver failure
- If methimazole, report pregnancy b-c teratogenic

99
Q

Thyroid Storm: Medical management (7)

A
  • isotonic and glucose solutions for fluid replacement to correct dehydration and prevent hyponatremia
  • Thyroidectomy (if swallowing or breathing difficult)
  • Antithyroid drugs (PTU and methimazole)
  • Radioactive iodine to remove goiter (give after antithyroid therapy; do not give if pregnant; radiation precautions)
  • Beta blockers (Propranolol (Inderal)) to control myocardial demand and slow HR and AV conduction rate (need ECG monitoring and CVP line)
  • reduce hyperthermia (acetaminophen, fan, cooling blanket)- NO ASPIRIN b-c increases free thyroid hormone via inhibition of binding
  • give steroids to prevent conversion of T4 to T3
100
Q

Thyroid Storm: Risk factors (6)

A
  • Autoimmune (Graves)
  • increased metabolic demand (Stress, Infection, Surgery or trauma, Pregnancy, DKA)
  • abruptly stopping antithyroid meds
  • Excess thyroid hormone intake (levothyroxine)
  • Iodine-induced hyperthyroidism r/t amiodarone
  • radioactive iodine therapy or excess iodine
101
Q

Myxedema Coma: Manifestations (8)

A
  • Cardiac (anemia, hypotension, bradycardia, peripheral vasoconstriction, cardiomegaly, narrow pulse pressure, prolonged QT/PR)- risk for shock and cardiac tamponade
  • Pulmonary (hypoventilation)
  • GI: constipation, anorexia, abdominal distention)
  • cold intolerance (< 36.1)
  • CNS (blank facial expression, apathy, slow speech, depression, delirium, stupor, coma)
  • Skin (thick tongue w/ husky voice, brittle/thin nails and hair, nonpitting edema (weight gain), poor wound healing
  • Muscle (decreased DTR, paresthesia of hands and feet r/t hyaluronic acid deposits)
  • Renal (decreased GFR, specific gravity, urine osmolality and output) b-c decreased blood flow
102
Q

Myxedema Coma: Labs (6)

A
  • Low T3 and T4
  • Hypoglycemia
  • Increased TSH
  • Hyponatremia (confusion, NV)
  • metabolic acidosis/respiratory acidosis
  • hypercholesterolemia (r/t incomplete metabolism)
103
Q

Myxedema Coma: Medical Management (8)

A
  • give IV levothyroxine then PO (risk for angina and dysrhythmias) - take on empty stomach
  • give IV NS, glucose, steroids as needed
  • mechanical ventilation for hypoventilation and respiratory acidosis
  • warm blankets for hypothermia
  • emollient and repositioning for skin (rough, edema, risk for breakdown)
  • continuous ECG monitoring b-c risk for dysrhythmias
  • communicate slowly and in written form b-c decreased comprehension
  • fiber and fluids for constipation
104
Q

Myxedema Coma: Risk Factors (8)

A
  • older adults
  • hashimoto (autoimmune)
  • Infection, trauma, stress
  • cold exposure
  • interruption of medication (levothyroxine)
  • Impaired perfusion (MI or stroke)
  • Thyroid damage r/t amiodarone, surgery
  • Meds (lithium, thiocynates, aminoglutethimide, sodium or potassium perchlorate or cobalt)
105
Q

Older Adults: GI system alterations (6)

A
  • decreased GI blood flow and motility
  • decreased Gastric emptying
  • increased risk of dehydration (decreased thirst sensation)-> constipation
  • More prone to GI bleeds b-c more prone to h. pylori
  • Decreased absorption -> nutrient deficiency and anemias
  • decreased swallowing = risk for aspiration and malnutrition
106
Q

GI bleed: General Management

Prevention of Shock (3)

NGT Placement (2)

A

Prevent hypovolemic or hemorrhagic shock
- large bore IV for IV crystalloids, blood products (plasma, platelet, PRBCs)
- if esophageal varices, avoid frequent swallowing or activities that could rupture varices like vomiting or straining
- give Supplemental oxygen to Increase oxygen delivery and tissue perfusion

Nasogastric Tube Placement (NGT)
- Purpose: Gastric lavage to confirm bleeding via irrigation w/ NS; aspiration prevention, decompression (low suction); feeding
- Care: Do Not place if esophageal varices ; Lie on left side; Secure to gown; irrigate q4h w/ NS

107
Q

Endoscopy

What is it?
4 types

A

What is it?
- direct visualization and evaluation of GI tract (for lesions, mucosal changes, obstructions, motility dysfunction, bleeding

Types
EGD
- esophagus to duodenum
- evaluate upper GI bleed, chronic gastritis

Colonoscopy: rectum to distal ileum
- screens for colon cancer, evaluate UC

Sigmoidoscopy: sigmoid colon
- screen for Crohn’s disease

Endoscopic retrograde cholangiopancreatography (ERCP)
- visualize the liver, gallbladder, bile ducts, and pancreas
- evaluate pancreatitis, cholecystitis

108
Q

Endoscopy: safety (6)

A
  • If contrast dye involved, ask about shellfish allergies and check kidney function (BUN, Crt, urine output)
  • If sedation or anything down throat, check gag reflex before oral feedings (risk for aspiration, vasovagal stimulation, oversedation)
  • Ensure HCP gets informed consent
  • need Two large IV catheters
  • NPO 6-12 hrs prior
  • Bowel prep if lower GI
109
Q

GI Bleed: Assessment findings (7)

A
  • bleeding labs and VS (low H/H; low BP, high HR, decreased peripheral pulses)
  • Change in LOC (r/t dehydration or anemia)
  • Coffee ground emesis r/t gastric acid converting hemoglobin to brown hematin
  • Bright red emesis r/t profuse bleeding with little contact with gastric secretions
  • Hematochezia (bright red stools) – rectum or sigmoid (lower GI bleed)
  • Melena (black, tarry, or dark red stools) due to digestion of blood in upper GI bleed
  • Gastric perforation (sudden severe abd pain w/ rebound tenderness and rigidity plus fever, leukocytosis, tachycardia)- emergency
110
Q

GI bleed: Diagnostics (5)

A

Endoscopy
- achieve control of GI bleeding via cauterization, vasopressin, or embolic material

Angiography (has contrast dye)
- evaluate status of GI circulation, cirrhosis, portal HTN, intestinal ischemia

Abdominal x-ray
- visualize bowel obstruction and perforation

GI bleeding scan
- evaluate presence and location of of active GI bleed not detected on EGD and assess need for arteriogram

MRI
- identify tumors, abscesses, hemorrhages, and vascular abnormalities

111
Q

Liver Failure/Cirrhosis: Diagnostics

Liver Biopsy (4)
Ultrasound
Hepatobiliary scan (3)
CT

A

Liver Biopsy
- For liver failure, cirrhosis, or hepatitis (or diagnosis GI bleed)
- Pre-op: NPO 6 hrs prior, blood drawn for coagulation
- Post-op: position on right side and bed rest 6-8 hrs
- Complications: damage to other organs, peritonitis (r/t gallbladder leakage of bile), hemothorax, infection

US
- more sensitive than x-ray for liver problems

Hepatobiliary scan (HIDA scan)
- visualize the gallbladder and liver and determine patency of the biliary system w/ dye
- Results: decreased bile flow = obstruction
- Care: NPO 2-4 hr prior; usually no sedation but be still

CT
- evaluate abdominal vascular space

112
Q

GI bleed: Medical Management

Misoprostol -2
Vasopressin - 3
Sandostatin - 3
Epinephrine -1

A

Misoprostol
- Prevention of GI bleed
- contraindicated if pregnant

Vasopressin (Pretessin)
- prevent esophageal varices rupture via decreasing portal HTN
- not preferred unless pt in shock
- Risk for systemic vasoconstriction (chest pain, HTN, HF, dysrhythmias, phlebitis, CVA), bradycardia, fluid retention

Sandostatin (Octreotide)
– preferred to prevent esophageal varices rupture unless pt in shock
- Decrease portal venous pressure when acute bleeding and cirrhosis
- Risk for hyper/hypoglycemia when initiating drip

Epinephrine
- Vasoconstrictor agent

113
Q

Crohn’s Disease: Complications (9)

A
  • acute gastritis (inflammation of gastric mucosa)
  • Perianal ulcerations/ fistulas (usually pyuria and fecaluria) – may need skin barrier if draining b-c intestinal fluid enzymes are caustic
  • hemorrhage/Perforation (lower GI bleed)
  • abscess formation
  • toxic megacolon (dilation leads to ileus then gangrene and peritonitis)
  • intestinal malabsorption (esp folic acid and vitamin B12)-> malnutrition -> weight loss
  • Anemia (r/t slow bleeding and poor nutrition)
  • nonmechanical bowel obstruction (r/t inflammation, edema - > fibrosis and scar tissue)
  • extraintestinal (polyarthritis, erythema, cholelithiasis, oral and skin lesions, iritis, osteoporosis)
114
Q

GI Bleed: main causes

Peptic Ulcer Disease (2)
Stress-related erosive syndrome (SRES) (4)

A

Peptic Ulcer disease
- Gastroduodenal mucosal breakdown results in damaged blood vessels from acid secretions
r/t H. pylori, NSAIDs, steroids
- Diagnostic: anti H.pylori antibodies (IgG or IgM OR C13 urea breath test) - discontinue antacids and PPI a week prior

Stress-related erosive syndrome (SRES)
- Acute erosive gastritis covers mucosal lesions; common in ICU
- Increased stress = increased gastric acid secretion
- decreased mucosal blood flow = ischemia and degeneration of mucosal lining
- Reason for prophylactic PPI or H2 antagonists

115
Q

GI Bleed: main causes

Esophagogastric Varices (2)
Medications (3)
Conditions (2)

A

Esophagogastric Varices rupture
- r/t portal HTN and liver dysfunction diverting blood from high pressure to low pressure
- Risk w/ increased abdominal pressure (vigorous physical exercise, heavy lifting); hard dry food, chest trauma

Exacerbated by medications (anticoagulants, steroids, NSAIDS)

Conditions (Hepatitis, necrotizing pancreatitis, Acute liver failure))

116
Q

GI Bleed: Antiulcer agents

Antacids - 3
H2 Antagonists - 2
PPI - 2
Sucralfate - 3

A

Antacids
- mag = diarrhea and avoid if CKD
- calcium or aluminum = constipation
- give 1-2 hrs within other drugs OR after meals

H2 antagonists (Famotidine-Pepcid)
- dose at bedtime
- risks: CNS toxicity (confusion,deliruim) and thrombocytopenia

Proton pump inhibitors (Pantoprazole-Protonix)
- Can give w/ antacids
- risk for VAP and C-diff

Sucralfate (mucosal barrier)
- dissolved in water to form slurry, not crushed
- hold feedings before and after
- No antacids within 30 minutes

117
Q

Crohn’s Disease: Clinical Manifestations (6)

A
  • RLQ Abdominal Pain and/or distention
  • Peritonitis (guarding, masses, rigidity, tenderness)
  • High pitched sound on auscultation r/t narrowed bowel loops
  • Diarrhea (5-6 nonbloody stools a day
  • Steatorrhea (mucusy fatty stools)
  • Fever r/t fistula, abscess, severe inflammation
118
Q

Crohn’s Disease: Basics (4)

A
  • Inflammatory disease causing thickening of walls of small intestine, colon, or both (esp. terminal ileum)
  • Recurrent with remissions and exacerbations.
  • Strictures and deep ulcerations (cobblestone appearance)
  • less severe than Ulcerative Colitis
119
Q

Crohn’s Disease: Labs (4)

A
  • Decreased Hgb/Hct (slow blood loss)
  • Elevated WBC/CRP/ESR (inflammation)
  • Hypokalemia, hypomagnesemia, hyponatremia, hypochloremia (diarrhea)
  • Hypoalbuminemia (malnutrition and lost protein in stool)
120
Q

Barium enema w/ air contrast

Purpose
Safety (3)

A
  • differentiate UC and Crohn’s Disease i.e. complications, mucosal patterns, depth of disease

Safety
- void after to remove contrast
- NPO prior to procedure
- expect light colored stools b-c barium is white

121
Q

Crohn’s Disease: Drug Therapy (6)

A
  • Aminosalicylates (ER Mesalamine)
  • Glucocorticoids (Methylprednisolone) - risk for infection
  • Antidiarrheal drugs (w/ caution b-c risk for toxic megacolon)
  • Immunosuppressive drugs/ Biologics - risk for infection
  • antibiotics if peritonitis
  • pain medication for pain
122
Q

Crohn’s Disease: Nutritional Support (6)

Risks of poor nutrition: inadequate fistula healing, loss of lean muscle mass, decreased immune response, increased morbidity and mortality

A
  • recore accurate I & O for calorie counts
  • proper hydration
  • TPN (if severe and malnutrition present)
  • high calorie, high protein, high vitamin, low fiber diet
  • if fistulas, need up to 3,000/day
  • Avoid caffeine, alcohol, milk, gluten
123
Q

Crohn’s Disease: Surgical management (3)

A
  • Laparoscopic Surgeries
  • Small bowel and ileocecal resections
  • Stricturoplasty: increases bowel diameter
124
Q

Acute Pancreatitis

Basics (3)
Main causes (3)

A

Basics
- inflammation of pancreas due to premature activation of enzymes
- Inflammation worsened due to leukocyte clustering around hemorrhagic and necrotic areas
- Proteolysis: split proteins of peptide bonds leading to thrombosis and gangrene

Main Causes
- Gallstone migration
- Alcoholism
- Other causes: ERCP, tumors, meds, hypocalcemia, trauma

125
Q

Acute Pancreatitis: Involved Enzymes (5)

A
  • Trypsin- causes autodigestion and fibrosis
  • Phospholipase – destroys phospholipids of cell membranes leading to pancreatic and adipose tissue necrosis
  • Lipase – fat necrosis -> pancreatic necrosis
  • Kallikrein and chymotrypsin – increased cap permeability and vasodilation (edema, hypovolemia)
  • Elastase – hemorrhage r/t dissolution of elastic fibers for BVs
126
Q

Acute Pancreatitis: Labs (10)

A
  • high amylase (Normal 25-125)
  • high lipase (Normal 20-240) - elevated longer
  • high trypsin and elastase
  • AST >250 units/L (liver involvement)
  • Increased LDH (> 350)
  • hyperbilirubinemia
  • Leukocytosis (>16,000/mm3) and thrombocytopenia
  • Hyperglycemia (>200 mg/dL; no diabetic history) r/t decreased insulin from destroyed islet cells
  • Hypocalcemia and hypomagnesemia
  • Also present ( increased BUN, ALP, ESR, CRP; Hypoalbuminemia; Hypertriglyceridemia)
127
Q

Acute Pancreatitis: Clinical Manifestations (10)

A
  • epigastric to periumbilical abdominal pain (boring i.e going through body)
  • Nausea and Vomiting
  • Shock s/s (tachycardia, hypotension, diaphoresis)
  • Hypoactive bowel sounds
  • Peritonitis (Abdominal tenderness, guarding, distention, tympany, rigidity)
  • Severe jaundice (swelling of pancreas head, blocking bile)
  • Palpable abdominal mass = pseudocyst or abscess
  • Dull to percussion = pancreatic ascites
  • Grey Turner sign (gray-blue discoloration of the flanks) r/t Pancreatic hemorrhage
  • Cullen sign (discoloration of the umbilical region) r/t Pancreatic hemorrhage
128
Q

Acute Pancreatitis: Diagnostics (3)

A
  • Abdominal CT with contrast (gold standard) –diagnosis pancreatitis, r/o pancreatic pseudocyst
  • Abdominal ultrasound –check for liver, gallbladder, biliary system; Gas, ascites, obesity may interfere w/ viewing
  • ERCP
129
Q

Acute Pancreatitis: Management

Pain (3)
Nutrition (5)
Fluids and electrolytes (2)

A

Pain
- w/ hydromorphone (morphine causes sphincter of Oddi spasm)
- relieved by knee-to-chest or fetal position
- ulcer prophylaxis (H2 antagonist and PPI)

Nutrition
- NPO to rest pancreas
- small frequent meals afterwards
- mod to high carb, low fat, high protein
- avoid caffeine (coffee, tea, cola) and alcohol
- NGT if vomiting, obstruction or distention

Fluids and electrolytes
- IV crystalloids (LR)
- correct hypocalcemia, hypomagnesemia, and hyponatremia as needed

130
Q

Acute Pancreatitis: Complications

Systemic (2)
Local

A

Systemic
- Hypovolemic or hemorrhagic shock r/t third spacing
- Acute necrotizing pancreatitis -> Multi-organ damage (ARDs, AKI, paralytic ileus, GI hemorrhage , DIC, Type 2 DM)

Local
- Pancreatic pseudocyst (pancreatic fluid enclosed in non epithelialized wall) w/ Risks: peritonitis (if rupture), erode BVs (hemorrhage), bacterial infection (abscess), invade surroundings (obstruction) – may drain on own

131
Q

Acute Liver Failure

Basics of ALF
Basics of Cirrhosis (3)

A

Basics of ALF
- severe and sudden liver cell dysfunction (necrosis of hepatocytes), coagulopathy, and hepatic encephalopathy

Basics of Cirrhosis
- Irreversible scarring of the liver
- Early stage: liver enlarged and firm from fat
- Progression: liver atrophy and harder -> decreased function due to scar tissue

132
Q

Acute Liver Failure: Clinical Manifestations (9)

A
  • yellow skin (jaundice) or sclera (icterus)
  • Changes in color of urine (dark) or stool (clay colored)
  • Pruritus (itching) or rash or dry skin
  • Ascites (r/t portal HTN and hypoalbuminemia)- risk for orthopnea or dyspnea; posture problems
  • Asterixis (downward flapping of hands when arm dorsiflexes wrist)
  • Pulmonary (hyperventilation)
  • CNS (Headache; Hepatic encephalopathy r/t breakdown of blood brain barrier) –Increased ICP and cerebral edema
  • Coagulation (Palmar erythema, Spider nevi, Bruises)
  • Peripheral edema
133
Q

Acute Liver Failure/Cirrhosis: Labs (8)

A

↑ ALT, AST, ALP (ALT more liver specific)
- Normal ALT: 10-40 m, 9-32 f
- Normal AST: 8-40 m, 6-34 f
- Normal ALP: 35-150

↑Bilirubin (Normal: < 1) - decreased fecal bilirubin

↑ LDH (Normal: 110-220)

↑ Ammonia (risk for hepatic encephalopathy

Decreased Albumin (b-c reduced synthesis)

Anemia, thrombocytopenia, and leukopenia

Prolonged PT and INR r/t decreased prothrombin production
- Normal PT: 10-13 s
- Normal INR: 0.9-1.3

↑ BUN

134
Q

Acute Liver Failure: Management (7)

A
  • Reduce Ammonia (lactulose or nonabsorbable antibiotics) - force out ammonia
  • stress ulcer prophylaxis (PPI, H2 antagonists)
  • Treat GI bleeding (Vitamin K, PRBCs, platelets, coagulation factor replacement, plasma or Beta blocker)
  • antibiotics to prevent infection
  • definitive treatment = liver transplant
  • paracentesis or diuretics for ascites (pre-op: coagulation labs, void, and give vitamin K if high INR)
  • avoid too many drugs b-c liver cannot metabolize (NSAIDS, acetaminophen, alcohol, smoking)
135
Q

Acute liver failure/Cirrhosis: risk factors (6)

A
  • Viral hepatitis (HCV)
  • Drug-induced or toxin liver damage (alcohol, acetaminophen)
  • Infections
  • Hypoperfusion (shock, thrombosis, ischemia,
  • Metabolic disorders (Reye syndrome, Wilson disease, galactosemia, frustose intolerance)
  • surgery
136
Q

Acute Liver Failure: Complications (9)

A
  • Impaired bilirubin conjugation (Result: jaundice)
  • Decreased clotting factor production (Result: bleeding)
  • Depressed glucose synthesis (Result: hypoglycemia)
  • Decreased lactate clearance (Result: metabolic acidosis -> respiratory alkalosis)
  • infection
  • altered carb, protein, glucose metabolism
  • Hepatic encephalopathy and Acute Neurologic changes (Care: Give mannitol, elevate HOB 30, treat fever HTN, minimize stimulation; may need restraints)
  • Respiratory failure (ascites -> increased abdominal pressure -> shallow breathing ->atelectasis) - care: intubation
  • Cardiac dysrhythmias due to acidosis, hypoxemia, cerebral edema
137
Q

Cirrhosis: Complications (6)

A
  • Portal hypertension (Risks: Splenomegaly, ascites, Bleeding esophageal varices (distended veins), hemorrhoids)
  • Coagulation defects (result: bleeding)
  • Biliary obstruction (Decreased bile production = decreased absorption of fat soluble vitamins i.e vitamin K and jaundice and itching)
  • Portal-systemic encephalopathy (PSE) with hepatic coma
    S/s: sleep disturbance, mood disturbance, mental status change, speech problems, asterixis (hand flap)
    Late s/s: altered LOC, impaired thinking, neuromuscular problems r/t nonrhythmic extension and flexion of wrists and fingers
  • Hepatorenal syndrome
    S/s: oliguria, elevated BUN, Crt, urine osmolarity
  • Spontaneous bacterial peritonitis r/t ascites or hypoproteinemia
    S/s: abd pain, fever, chills, tenderness; worsened encephalopathy, increased jaundice
    Drug of choice: antibiotics
138
Q

Abdominal Trauma

Types (2)
Risks (4)

A

Types
- Blunt trauma (MVA, Falls, Assault, Contact sports)
- Penetrating trauma (Gunshot wounds, stabbing, impalement)

Risks
- Hemorrhage
- Hollow viscus perforation (stomach, intestine) r/t GI bleeding and septic shock (intestinal contents can leak into peritoneum)
- Peritonitis
- Increased intra-abdominal pressure -> organ dysfunction (S/s: decreased CO, decreased tidal volume, increased pulmonary pressure, decreased UOP, hypoxia, taut tense abdomen) –Normal IAP: 5-7

139
Q

Abdominal Trauma: Clinical manifestations

Inspection (5)
Auscultation (2)
Percussion/Palpation (3)

A

Inspection
- Location of entry and exit sites
- Cullen’s sign (umbilicus)
- Grey Turner’s sign r/t RTB or pancreatic injury (flank)
- Hematoma in flank r/t kidney injury
- Distended abdomen r/t perforation or ruptured BV

Auscultation
- Diminished Bowel sounds/
- presence of Friction Rub

Percussion/Palpation
- Rebound tenderness r/t peritoneal inflammation
- Rigidity
- Ruptured Spleen has Ballance’s Sign (dullness) or Kehr’s sign (Left shoulder pain)

140
Q

Abdominal Trauma: Diagnostics (8)

A
  • NGT for decompression and evaluate drainage
  • Peritoneal lavage ( NS catheter in abdominal cavity flushed to assess for blood)
  • Chest radiograph: Fractured ribs
  • Arteriogram: May show vascular injuries
  • Liver and spleen scan
  • Pyelogram (kidney scan w/ contrast dye)
  • Abdominal or pelvic CT scan: retroperitoneal hematoma, liver or spleen injury, ruptured viscus (bowel) (PREFERRED)
  • FAST (Focused Assessment and Sonogram for Trauma): Quick assessment of abdomen in radiology
141
Q

Abdominal Trauma: Labs (6)

A
  • Decreased hgb and hct levels
  • Increased serum amylase level or lipase from ischemia of pancreas
  • Increased lactate = mesenteric hypoperfusion or sepsis
  • Increased WBC count b-c stress
  • Hematuria
  • Positive Stool Guaiac b-c GI bleed
142
Q

Abdominal Trauma: Management (5)

A
  • Optimize hemodynamic status w/ fluids
  • Transfusion protocol to minimize blood loss
  • Prevent infection (Pneumococcal, meningococcal vaccines if splenectomy)
  • Stabilize injuries (drains to prevent hematoma; Embolization to decrease spleen blood loss; surgical repair)
  • TPN until bowel healed
143
Q

GI bleed: Controlling bleeding (less invasive)

Tagged Red Blood Cell Scanning
EGD (4)

A

Tagged red blood cell scanning
- identify location of bleed and treat if able to view

EGD
- thermal therapy: heat to cauterize the bleeding vessel
- injection of sclerosing therapy (epi or alcohol, hypertonic saline) to induce localized vessel vasoconstriction and sclerosing to form thrombosis
- intraarterial embolization
- Endoscopic variceal ligation: band or clip around bleeding site to obstruct and control bleeding (Risk: mucosal ulcers)

144
Q

GI bleed: Trans-jugular Intrahepatic Portosystemic Shunting (TIPS) (most invasive management)

Indication
Procedure
Risks (3)

A

Indication: ascites or prevent esophageal varice rupture

Procedure: stent placed b/w systemic and portal venous system to redirect portal blood, decrease portal HTN, and decompress varices to control bleeding

Risks: hepatic encephalopathy, elevated pulmonary artery pressure, bleeding

145
Q

TPN: Indications (8)

A
  • cannot tolerate enteral nutrition (i.e GI bleed)
  • extensive burn injuries
  • poor wound healing
  • specific GI disease (UC, Crohns, GI fistula)
  • hepatic failure
  • pancreatitis
  • malignant diseases
  • malnourished
146
Q

TPN:Care (6)

A
  • need central line and filter b-c hyperosmolar
  • Keep it going! (Dextrose 10 % if bag not ready)
  • Scheduled Accuchecks q6h
  • IV site assessment (phlebitis)
  • Maintain aseptic technique
  • change bags/tubing per protocol (typically q24h)

Concepts 3 (4 decks)

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