Nevada State College: School of Nursing
NURS 380
Exam 2 Study Help Sheet
CAD/ACS/MI (approx. 10 questions) 34, 32
 Risk factors: Modifiable and non-modifiable (know difference)
o Nonmodifiable
 Whites: white men have the highest incidence of CAD
 African American: early age onset of CAD, deaths from CAD and stroke are higher, women have a higher
incidence and death rate
 Native American: die from heart disease earlier than expected, mortality rates for those >65 are twice as high
 Hispanics: slightly lower rates of CAD, lower death rates from CAD
o Modifiable focus teaching plan on this
 Elevated serum lipidsLDL
 HTN
 Tobacco use
 Physical inactivity
 Obesity
 Diethighest percentage of calories should come from monosaturated fats
(nuts, olive oil, canola oil. Na, cholesterol
 Contributing modifiable risks: DM, metabolic syndrome, psychologic states, homocysteine, substance abuse
 Clinical manifestations/assessment
o Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO). Crackles. Jugular venous distention. Abnormal heart
soundsS3 or S4 heard with bell of the stethoscope with the patient in the left
lateral position. New murmur. Nausea and vomiting. Fever
o how to differentiate cardiac pain from musculoskeletal/pulmonary?
 Changes in pain that occur with raising arms or deep breathing are more typical with musculoskeletal pain or
pericarditis
o Time differentiation for MI vs. angina or pain from other etiologies
 >30min, last 3-6hours
Unstable vs stable angina—from class
 Stable angina usually relieved by rest or with nitroglycerine
 Pain occurring at rest or with increased frequency is typical of unstable angina
Provoking factors
Quality
Radiate
Severity
Time
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MI- diaphoresis, NV
anything/ nothing
GI
changes with food
Resp
resp, cough
pressure, crushing,
tightness, numbness
arm, cold, stiff
Numbness arm
10/10
*>30min, Lasts 3-6hr
burning pain,
cholecystitis
sharp
Musculo
movement,
palpation
Dull, achy
right to left shoulder
Depends on what it is
Psych
Fight
All over the
place
everywhere
situational
How does improving oxygenation change angina pain?
o Decreases workload on heart. Can cause coronary spasms (narrowing) if they have sufficient O 2 sat
*Nursing management/interventions/priorities
o Assess ABCs
o Aspirin administration
o Administer O2 (only if O2 is low) – new studies show O2 causes vasoconstriction
o May repeat 12-lead ECG, monitor & baseline blood work
o Prompt pain relief first with a nitrate followed by an opioid analgesic if needed
o Auscultation of heart and lung sounds
o Comfortable positioning of the patient
o Anxiety
o Emotional and behavioral reaction
 Maximize patient’s social support systems
 Consider open visitation
o Rest and comfort
 Balance rest and activity
 Begin cardiac rehabilitation
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Collaborative interventions – PTCA – what happens with Glucophage and contrast dye?
o IV contrast media that contain iodine poses a risk of acute kidney injury, which could exacerbate metformin induced lactic
acidosis
 To reduce risk of kidney injury, discontinue metformin a day or two before the procedure
 May be resumed 48 hrs after the procedure, once serum creatinine has been checked and is normal
ST elevation – why is this important?
o Left bundle branch block
o Immediate therapy with percutaneous coronary intervention (PCI) or thrombolytic medication is indicated to minimize
myocardial damage.
Prinzmetal’s angina – What is this? Meds and treatments?.
o Variant angina is a rare form of angina that often occurs at rest and not with increased physical demand.
o Sometimes seen in patients with a history of migraine headaches, Raynaud’s phenomenon, and heavy smoking
o Usually due to spasm of a major coronary arteryresults from increased intracellular calcium
o When spasm occurs, the patient experiences angina and transient ST segment elevation
o May occur during REM sleep when myocardial O2 consumption increases or when exposed to cold temperature
o Calcium channel blockers and/or nitrates are used to control the pain, as well as stopping any offending substances
Why is putting a patient on a monitor so important if they have acute coronary syndrome?
o The priority for the patient is to determine whether an acute myocardial infarction (AMI) is occurring so that reperfusion
therapy can begin as quickly as possible.
o ECG changes occur very rapidly after coronary artery occlusionan ECG should be obtained as soon as
possible!
What is a lethal arrhythmia?
o Vfib and vtach
o Amiodarone is the drug of choiceconduction
High cholesterol - dietary and exercise recommendations
o Exercise as toleratedlow saturated fats
o Cholesterol-lowering drugsstatins are drug of choice
 Assess liver enzymes (ALT and AST)
 Assess for rhabdomyolysis – ***muscle pain
Cardiazem – how does this medicine work? Diltiazem – various actions of this medication, adverse effects
o Calcium channel blocker. It has a chronotropic effectdecreases contractions=  O2 demand. Reduction in Afib flutter
o Coronary vasodilation resulting in  frequency and severity of angina attacks
o Systemic vasodilation resulting in  BP
Meds
 Nitroglycerinvasodilation, do not take with Viagra b/c severe hypotension can occur
o Goal is to relieve chest pain by improving the balance between myocardial oxygen supply and demand
o Can be taken to prevent chest pain or others symptoms from developing (e.g., before intercourse)
o Causes headachevasodilate
o Keep in dark place
o The emergency medical services (EMS) system should be activated when chest pain or other symptoms are not completely
relieved after 3 sublingual nitroglycerin tablets taken 5 minutes apart.
 Aspirin
o Action: produce analgesia and reduce inflammation and fever by inhibiting the production of prostaglandins
o Classification: antipyretic, nonopioid analgesic
o Indication: Fever and prophylaxis of transient ischemic attacks
o Nursing intervention: Monitor temperature, hepatic function, H&H and RBC count
o Main side effects: Tinnitus, GI bleeding and nausea
 Morphine – vasodilatesdecreases workload of the heart
 Heparin – what is the action? Nursing interventions and labs for therapeutic level
o Helps prevent conversion of fibrinogen to fibrin and decreasing coronary artery thrombosis does not dissolve
clots that are already formed!
o aPTT: 30-40 sec
o Therapeutic values for heparin: aPTT: 45-100 sec
 TNK – what is the safe window to administer this drug and why, adverse effects? Contraindications?
o ThrombolyticClot buster used for heart muscle
o Contraindications: Intracranial hemorrhage, AVM, neoplasm, < 3 mo CVA, trauma, spinal surgery, uncontrolled HTN,
aortic dissection, bleeding, recent surgery, pregnant
o ***Cautious use: PUD, anticoags, pregnancy, dementia, stroke > 3 monthsdamaged tissue can easily
bleed, recent bleeding, CPR, >65yrs
o Monitor bleeding times – PT, aPTT, INR, fibrinogen, and CBC
o Adverse effects: Bleeding. thrombocytopenia, anemia, or hemorrhage
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o Administer slowly
o Start IVs prior to administration
o Safety precautions for bleeding, bruising, etc
o Thrombolytic therapy should be started within 6hrs of onset of MIask when chest pain began
o Stop infusion if there is a change in LOCmay be experiencing intracranial bleeding
 Calcium channel blockers …they are Very Nice Drugs
Ca+=Depolarization(contraction)
Ca+slow conduction through SA and AV node and refractory period (they really are
nice!). They reduce spasm!
Contractility +Conductivity of the heart=  Demand for O2
o Verapamil, Nifedipine, Diltiazem (Cardiazem)
 HR, BP(vasodilates), Blood vol, contraction
 No grapefruit, check HR before giving
 Use for angina, arrhythmias, hypertension
 Use if pt can’t tolerate beta blockers
 Negative inotropicCa=Contraction
 Can cause CHFlisten to lungs and check for edema
 Beta blockers  contractility= oxygen demand. Decrease sympathetic stimulation of the
heart palpitations
o Metoprolol
 Side effects are hypotension and bradycardiabeta blockers inhibit SNS
o Propranolol
 HR, Blood vol (preload), BP (afterload), contraction
 Hold HR <60
 Negative inotropic
 check for rebound tachycardia (happens when suddenly discontinued)
 enhance oral hypoglycemic meds and also decrease the heart rate, thus masking symptoms of hypoglycemia
HR increases with hypoglycemia, so stopping that will mask this effect and
pt will not know that they have hypoglycemia
o Labetalol
 decreases sympathetic nervous system activity by blocking both á- and β-adrenergic receptors, leading to
vasodilation and a decrease in heart rate, which can cause severe orthostatic hypotension.  request
assistance when getting out of bed
 How are metoprolol and propranolol different and similar? Any problems taking concurrently with lung
conditions?
 Nonselective β-blockers block β1- and β2-adrenergic receptors and can cause bronchospasm,
especially in patients with a history of asthma. do not give propranolol if they
have asthma, they may also develop wheezing (take O2 sat, apply O2
and notify physician)
Labs
 LDL lethal
o <70
 HDL healthy
o 60 or higher
 Triglycerides
o Normal: below 150
Borderline high: 150—199, High: 200—499
o Very high: above 500
 Total Cholesterol
o Ideal: below 200
o Borderline: 200—240, High: above 240
 Troponin I and T (high or low) Troponin levels increase about 4 to 6 hours after the onset of
myocardial infarction (MI) and are highly specific indicators for MI.
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Troponin I
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Normal = < .2 ng/L
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Onset 3-5 hours
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No longer evident after 7 days
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Troponin T
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Normal = < .03 ng/L
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Onset 3 hours
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No longer evident after 14 days
 CPK (high or low)
3
o
o
Released into blood from necrotic heart muscle
CK-MB rises in 6hrs and peaks 18hrs
Pulmonary Embolism (approx. 3 questions) 38
 Signs, symptoms and etiology
o PE is the blockage of one or more pulmonary arteries by a thrombus, fat, or air embolus, or tumor tissue
o Most arise from DVT. Venous thromboembolism (VTE) = DVTPE If pt has VTE and has an onset of
shortness of breath, this suggests PEimmediate action: O2 administration and
notify physician
 Other sites include femoral or iliac veins, right side of the heart (atrial fibrillation), and pelvic veins (esp. after
surgery or childbirth). Upper extremity DVT occasionally occurs in the presence of central venous catheters or
arterial linesmay resolve with removal of the catheter
o Less common causes include fat emboli (fractured long bones), air emboli (improper IV therapy), bacterial vegetation on
heart valves, amniotic fluid, and tumors
 Risk factors
o Immobility or reduced mobility
o Surgery within the last 3 months (esp. pelvic and lower extremity surgery)
o History of DVT
o Malignancy
o Obesity
o Oral contraceptives
o Hormone therapy
o Cigarette smoking
o Prolonged air travel
o Heart failure
o Pregnancy
o Clotting disorders
 Nursing management/interventions
o Bed rest in a semi-Fowler’s positionfacilitates breathing
o O2 therapy as ordered
o Assess cardiopulmonary status monitor V/S, cardiac rhythm, pulse oximetry, ABGs, lung
sounds
o Maintain IV linemedications and fluid therapy
o Monitor lab results therapeutic ranges of INR (warfarin) and aPTT (IV heparin)
o Monitor complications of anticoagulant and fibrinolytic therapy bleeding, bruising, hematoma
o Pt teaching regarding long-term anticoagulant therapy continues at least 3 months to indefinitely
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INR levels drawn at intervals and warfarin dosage is adjusted
 Collaborative interventions and priorities
o Prevention of PE begins with prevention of DVT compression device, early ambulation,
anticoagulants
o Treatment objectives: prevent further growth or extension of thrombi in the lower extremities, prevent embolization from
the upper or lower extremities to the pulmonary vascular system, and provide cardiopulmonary support
o Supportive therapy:
 O2 given via mask or cannula, or endotracheal intubation.
 Respiratory measuresturn, cough, deep breathe, IS.
 Manifestations of shock IV fluids administered followed by vasopressor to support
perfusion
 Heart failure diuretics
 Pain from pleural irritation or reduced coronary blood flow opioids
o Drug Therapy
 SQ low-molecular-weight-heparin (LMWH)enoxaparin (Lovenox) once daily safer and more
effective than unfractionated heparin
 Warfarin for at least 3 months and then reevaluated
 VTE can be treated with Lovenox and warfarin Lovenox will work right away, but
Coumadin takes several days to have an effect on preventing clots.
 Direct thrombin inhibitors are not common, but used in Tx of PE
 Fibrinolytic agents (tissue plasminogen activator, tPA or alteplase, Activase) dissolve PE
o Surgical Therapy
 For hemodynamically unstable pts with massive PE in whom thrombotic therapy is contraindicated
 Embolectomy, removal of emboli to help decrease right ventricular afterload, can be achieved via a vascular
catheter or surgical approach
 To prevent further emboli, an inferior vena cava (IVC) filter may be the Tx of choice in pts who remain high risk
for whom anticoagulation is contraindicated
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Gold standard test for dx (CT with contrast)
o D-dimer measures amount of cross linked fibrin fibersresult of clot degradation
 Neither specific nor sensitive
 Pts suspected of PE and an  D-dimer, but normal venous ultrasound need a spiral CT or lung scan
o A spiral (helical) CT scan (AKA CT angiography or CTA) is most frequently used to diagnose PE
o If pt cannot have contrast media, a ventilation perfusion (V/Q) scan is done. It has two components and most accurate
when both are performed: Perfusion scanning and Ventilation scanning
o Pulmonary angiography is most sensitive and specific test for PE.
 It is expensive and invasive
 The accessibility and accuracy of spiral CT have greatly diminished the need for pulmonary angiography
Labs
D-Dimer(high or low)
o Measures amount of cross linked fibrin fibersresult of clot degradation
o Neither specific nor sensitive
o Pts suspected of PE and an  D-dimer, but normal venous ultrasound need a spiral CT or lung scan
DVT (approx. 1 question)
 Risk factors
o Venous stasis
 Occurs more frequently in people who are obese or pregnant, CHD or AFib, have been traveling on long trips
without regular exercise, have a prolonged surgical procedure, or are immobile for long periods (spinal cord
injury, fractured hip, limb paralysis)
o Endothelial damage
 Direct: surgery, intravascular catheterization, trauma, burns, prior VTE
 Indirect: chemotherapy, diabetes, sepsis
 Damaged endothelium stimulates plt activation and starts the coagulation cascade
o Hypercoagubility of blood
 Occurs in many disorders: severe anemias, polycythemia, malignancies, nephrotic syndrome,
hyperhomocysteinemia, protein C, protein S, and antithrombin deficiency
 sepsisendotoxins are released
 certain drugscorticosteroids, estrogens
 women of childbearing age who take estrogen-based oral contraceptives or postmenopausal women on oral
hormone therapy are at increased risk for VTE
 Smoking  plasma fibrinogen and homocysteine levels and activating
intrinsic coagulation pathway
 Prevention
o Ambulation, compression
 Clinical manifestations/assessment
○ May or may not have unilateral leg edema if IVC involved then both legs will have edema
○ Pain
○ Tenderness with palpation
○ Dilated superficial veins
○ Sense of fullness in the thigh or calf
○ Paresthesia
○ Warm skin
○ Erythema/spider veins
○ Systemic temperature greater than 100.4
○ cyanotic/increase pigmentation
 Nursing management/interventions
o Prevention and prophylaxis is priority
o ***Heparin monitor aPTT (1.5- 2 times normal), watch for bleeding
o Coumadin monitor PT/INR (INR 2-3), watch for bleeding and food/drug interactions
 Collaborative interventions
○ Lab – PTT, INR, bleeding time, hgb, hct, platelet count, d-dimer
○ Venous compression ultrasound, duplex ultrasound
○ Computed tomography venography, magnetic resonance venography
Meds
 Rivaroxaban
o anticoagulant
o Prevents DVT that may lead to PE following a knee or hip replacement
GERD (approx. 3 questions) 42
5
A chronic syndrome of mucosal damage caused by reflux of stomach acid into the lower esophagus
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Risk factors: One of the primary etiologic factors in GERD is an incompetent LES
o Increased Pressure
 bethanechol (Urecholine) Beth wants to pee, so make her pee
 methoclopramine (Reglan) motility of upper gI and rate of gastric emptying
o Decreased pressure
 Alcohol
 Chocolate (theobromine)
 Fatty foodspeanut butter
 Nicotine
 Peppermint, spearmint
 Tea, coffee (caffeine)
 Drugs: Anticholinergics, -Adrenergic blockers, Calcium channel blockers, Diazepam (Valium), Morphine
sulfate, Nitrates, Progesterone, Theophylline
Clinical manifestations/assessment
o The persistence of mild symptoms (more than twice a week) or moderate to severe once a week is considered GERD
o Heartburn (pyrosis) is the most common manifestation
 Burning, tight sensation felt intermittently beneath the lower sternum and spreading upward to the throat
 May occur after ingesting food/drugs that LES pressure directly or irritate the esophageal mucosa
o Dyspepsiapain or discomfort midline in the upper abdomen
o Regurgitationhot, bitter or sour liquid coming into the throat or mouth
o Respiratory wheezing, coughing, dyspnea
o Otolaryngologic hoarseness, sore throat, global sensation (sense of lump in throat),
hypersalivation, choking
o Chest pain burning, squeezing, or radiating to the back, neck, jaw, or arms.
Relieved with antacids
Nursing management/interventions
o Elevate HOB approximately 30 degrees
o Not be supine for 2-3 hours after meal
o Avoid food/activities that cause refluxlate night eating
o Post-op prevent resp complications by maintaining fluid and electrolyte balance,
and preventing infection
o Laparoscopic fundoplication often outpatient
pharmacological and nonpharm interventions – teaching
o Proton pump inhibitors Omeprezole (Prilosec) stomach acid production
 Take before the first meal of the day
 Side effects: headache, abdominal pain, N/V/D, flatulence
 Frequently used for a short period as the first step in diagnosis of GERD
o H2- receptor blockers Famotidine (Pepcid) secretion of stomach acid
 Inhibits the development of stress ulcers
 Take as prescribed and do not stop without checking with HCP
 Side effects: headache, abdominal pain, constipation, diarrhea
o Prokinetic drug therapy
 Side effects: CNS side effects ranging from anxiety to hallucinations. Tremor and dyskinesias similar to
Parkinson’s disease
o Cholinergic drugs
 Side effects: lightheadedness, syncope, flushing, diarrhea, stomach cramps, dizziness
o Antacids neutralize stomach acid and work rapidlyperiodically aspirate and test
gastric pH
 Aluminum hydroxide: constipation, phosphorus depletion with chronic use
 Calcium carbonate: Constipation or diarrhea, hypercalcemia, milk-alkali syndrome, renal calculi
 Magnesium preparations: Diarrhea, hypermagnesemia
 Sodium preparations: milk-alkali syndrome if used with large amounts of calcium. Use with caution in pts with
sodium restrictions
Collaborative interventions
o Diagnostic assessment
 History and physical
 Upper GI endoscopy with biopsy and cytologic analysis
 Esophagram (barium swallow)
 Motility (manometry) studies
 pH monitoring ( laboratory or 24hr ambulatory)
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 Radionuclide studies
Management conservative
 Elevate HOB on 4-6in blocks
 Avoid reflux-inducing foods fatty foods, chocolate, peppermint
 Avoid alcohol
 Reduce or avoid acidic pH beverages colas, red wine, orange juice
Surgical therapy: reserved for pts with complications including esophagitis, med intolerance, stricture, Barrett’s
esophagus, and persistent severe symptoms. Most procedures are done laparoscopically. Fundus of the stomach is wrapped
around the lower portion of the esophagus to reinforce and repair the defective barrier
 Nissen fundoplicationimmediately address absence of breath sounds post-op,
breath sounds on one side indicates pneumothorax
 Toupet fundoplication
Endoscopic therapy
 Intraluminal valvuloplasty
 Radiofrequency therapy
Peptic Ulcer Disease (PUD) (approx. 2 questions) 42
Condition characterized by erosion of the GI mucosa from the digestive action of HCI acid and
pepsin
 Risk factors
 Clinical manifestations/assessment (difference between gastric and duodenal)
o Gastric
 Burning or gaseous pressure in epigastrium
 Pain 1-2 hrs after meals
 If penetrating ulcer, aggravation of discomfort with food
o Duodenal
 Burning, cramping, pressure-like pain across midepigastrium and upper abdomen. Back pain with posterior
ulcers
 Pain 2-5 hrs after meals and midmorning, midafternoon, middle of night. Periodic and episodic
 Pain relief with antacids and food
 Nursing management/interventions
o Treatments for H.pylori
 Antibiotics and a PPI
 Amoxicillin, clarithromycin (Biaxin), and omeprazole
o Treatment of peptic ulcer: antacids and sucralfate (Carafate)
 Take antacids after meals and sucralfate 30 minutes before mealsSucralfate is most effective
when the pH is low and should not be given with or soon after antacids.
Antacids are most effective when taken after eating. Administration of
sucralfate 30 minutes before eating and antacids just after eating will
ensure that both drugs can be most effective.
 Complications
o The three major complications of chronic PUD are hemorrhage, perforation, and gastric outlet obstruction
o Hemorrhage
 Most common complication
 Duodenal ulcers account for a greater percentage of upper GI bleeding episodes than gastric ulcers
o Perforation
 Ulcer penetrates the serosal surface with spillage of gastric or duodenal contents into the peritoneal cavity
 Most lethal complication of PUD
 Duodenal ulcers are more common and perforate more, but mortality associated with perforation of gastric ulcers
is higher
 Larger perforations require immediate surgical closure
 Small perforations may spontaneously seal and symptoms cease
 Can lead to fibrinous fusion of the duodenum or gastric curvature to adjacent tissueliver and
structures that can obstruct flow of intestinal contents and passage of stool
 Manifestations are sudden and dramatic in onset
 Initial phase0-2hrs the pt has sudden, severe abdominal pain that quickly spreads throughout
abdomen. Pain radiates to the back and shoulders. Food or antacids do not relieve pain. Abdomen
appears rigid and boardlike as abdominal muscles attempt to prevent further injury. Respirations
become shallow and rapid, tachycardia, weak pulse, absent bowel sounds, N/V may occur
 Development of sudden, severe upper abdominal pain, diaphoresis, and
a firm abdomen=symptoms of acute perforationassess vital signs for
hypovolemic shock
 Bacterial peritonitis may occur within 6-12hrs
7
o
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Gastric outlet obstruction
 Obstruction in the distal stomach and duodenum is the result of edema, inflammation, or pylorospasm and
fibrous scar tissue formation
 Pt reports discomfort or pain that is worse toward the end of the day as the stomach fills and dilates
 Belching self-induced vomiting may provide some relief. Vomiting is common and often projectile
 Constipation occurs because of dehydration and decreased diet intake secondary to anorexia
 Over time dilation of stomach and visible swelling in upper abdomen may occur
Stress ulcers – risk and prevention
Stress-related mucosal disease (SRMD) also called physiologic stress ulcers, is a
continuum of conditions ranging from stress-related injury( superficial) to stress
ulcers (deep)
o Commonly seen in critically ill pts who have had severe burns, trauma, or major surgery
o Pts with coagulopathy and those who experience respiratory failure resulting in mechanical ventilation for more than 48
hrs are at highest risk for SRMD
o Prophylaxis- Cytoprotective (Sucralfate), H2Blockers, PPIs, Enteral feedings
o Famotidine (Pepcid) Inhibits the development of stress ulcers
GI Bleed (approx. 3 questions) 42
 Clinical manifestations/Priority assessment (i.e., for fluid balance what two things do you check first?)
o Obvious bleeding
 Hematemesis: Bloody vomitus appearing as fresh, bright red blood or coffee-ground appearancedark,
grainy digested blood
 Melena: Black, tarry stools ( often foul smelling) caused by digestion of blood in the GI tract Black appearance is
from the presence of iron
o Occult bleeding
 Small amounts of blood in gastric secretions, vomitus, or stools not apparent by appearance. Detectable by
guaiac test
o Priority assessment
 A complete history and physical of events leading to the bleeding episode is deferred until emergency care has
been started
 Focus physical examination on identifying signs and symptoms of shocktachycardia, hypotension,
weak pulse, cool extremities prolonged capillary refill, and apprehension.
BP and pulse are best indicators
 Nursing management/interventions
o Perform an immediate nursing assessment while you are getting the pt ready for initial Tx
o Include LOC, vital signs, skin color and capillary refill
o Abdomen distension, guarding and peristalsis
o Immediate determination of VS indicates whether the pt is in shock from blood loss and provides baseline BP and pulse
for monitoring the progress of Tx
 Monitor VS q 15-30min
 Collaborative management
o Emergency Management
 The amount of fluids infused are based on physical and laboratory findings
 Generally, an isotonic crystalloid solutionLactated Ringers is started
 Whole blood, packed RBCs, and fresh frozen plasma may be used for volume replacement in massive
hemorrhage
 When upper GI bleeding is less profuse, infusion of isotonic saline solution followed by packed RBCs restores
Hct more quickly and does not create complications r/t fluid volume overload
o Endoscopic Therapy primary tool for visualization and diagnosis of upper GI bleeding.
 First-line management of upper GI bleeding
 Performed within the first 24hrs and is important for diagnosis, determining the need for surgical intervention,
and providing treatment
 Goal is to coagulate or thrombose the bleeding vessel. Several techniques are used including:
 Thermal (heat) probecoagulates tissue by directly applying heat element
to the bleeding site
 Multipolar and bipolar electrocoagulation probe
 Argon plasma coagulation (APC) noncontact coagulation that delivers
monopolar current to tissue
 Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser
 Mechanical therapy with endoscopic clips and bandsdirectly compress the bleeding
vessel
o Surgical therapy
8
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o
Indicated when bleeding continues regardless of the therapy provided and when the site of bleeding has been
identified
 May be necessary when pt continues to bleed after rapid transfusion of up to 2000mL of whole blood or remains
in shock after 24hrs
Drug therapy
 During acute phase, drugs are used to  bleeding,  HCI acid secretion, and neutralize HCI acid that is present
 Empiric PPI therapy with high-dose IV bolus and subsequent infusion to acid secretion is often started before
endoscopy acidic environment can alter platelet function and interfere with
clot stabilization
 Injection therapy with epinephrine during endoscopy is effective for acute hemostasis Epi produces
tissue edema and ultimately, pressure on the source of bleeding
 Octreotide (Sandostatin) or vasopressin may be given when upper GI bleeding is from esophageal or gastric
varices
 If NSAID induced GI bleeding, use misoprostol (Cytotec) to protect the GI mucosa this
prostaglandin analog reduces acid secretion and the incidence of upper GI
bleeding associated with NSAID use.
Labs
H and H – know normal values
o Hct: Male: 42-52% Female:37-48%
o Hgb: Male: 14-18 Female: 12-16
o Lowbleeding or dehydration
o Gi bleed, any condition causing vomiting (SBO, Cholelithiasis/cholecystitis, pancreatitis)
Small Bowel Obstruction (approx. 2-4 questions) 43
 Risk factors
o Crohn’s disease, abdominal surgery, hernia, appendicitis, intussusception, foreign body ingestion
 Clinical manifestations – onset fast or slow?
o Fast onset, persistent vomiting, and abdominal pain
 Nursing management/interventions
o NPO, NG tuberest GI
o Antiemetics, pain meds, potassium supplements
 Collaborative management
o Imaging to determine location of obstruction
o Possible surgical removal if it does not resolve on its own
 After a small bowel resection, ambulation will improve peristalsis and help the patient eliminate flatus and
reduce gas painEncourage the patient to ambulate.
 What electrolyte and acid base imbalances are likely?
o Potassium hypokalemia
o VomitingMetabolic alkalosis
Gallbladder Disease (approx. 3-5 questions) 44
 Risk factors
o Forty
o Female
o Fat
o Genetics
o Older than 60
o DM I (high triglycerides)
o High protein, low calorie diets
o Weight loss (increases cholesterol)
 Clinical manifestations/assessment
o Pain RUQ or epigastric area
o Radiates to right shoulder
o Pain with deep inspiration
o Murphy’s sign (pain with palp RUQ under ribs)
o Intense pain
o Rebound tenderness
o Fever
o Dyspepsia, belching, flatulence
o Itching*** calamine bath, oatmeal in bath tub can help
o Clay colored stools***bile flow problem
o Tea colored urine*** bile flow problem
 Nursing management/interventions
9
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Analgesics
*** Demerol may cause spasms in sphincter of oddi causing pain, give morphine instead
 *Recent studies show there is no substantial difference between choice opioids used for cholecystitis
 NEVER give with gallbladder disease
o Dicylomine (bentyl)anticholinergic decreases spasms, Bile acid to aid in digestion
o Benadryl or calamine for itching, cool oatmeal baths
o IV fluids
o Keep NPO
o Continually assess for signs of sepsis, think… “what could kill this patient”

o May undergo lithotripsy
 Ultrasonic procedure to break up stones
 T tube may be placed in common bile duct –
 Monitor drainage – keep insertion site clean and dry, bile can be irritating to skin
 Inspect for infection
 Maintain flow by gravity
 Clamp tube 1-2 hours before and after food to assess tolerance of food post cholecystectomy
 Assess for stool color  make sure bile is traveling.. bile makes stool
brown. Clay color if no bile
o Tan or grey stools indicate biliary obstruction!
 Assess for bile peritonitis (pain, fever, jaundice)
 Patient dc home in 24 hours if laparoscopic
 Collaborative management
o After a laparoscopic cholecystectomy- removal of gallbladder, the patient will have Band-Aids in place over
the incisions. Patients are discharged the same (or next) day and have few restrictions on activities of daily living.
they can remove their own bandages and take a shower the next day
Labs
Bilirubin (high or low)
o Normal <1.0 mg/dL
o Cholelithiasis/cholecystitis
o RBC breakdown results in bilirubinliver converts bilirubin and makes it water-solubleexcreted via bile salts into
intestineexcreted in feces
o Gallbladder conditionsno breakdown of bilirubin pale stools, dark urine
Pancreatitis (approx. 4 questions) 44
 Clinical manifestations/assessment/complications
Use of alcohol is most common risk factor for pancreatitisAsk specifically about
alcohol consumption!
o Manifestations:
 Abdominal pain is the predominant manifestation
 Due to distension of the pancreas, peritoneal irritation, and obstruction of the biliary tract
 Usually located LUQ, but may be mid-epigastric
 Radiates to back and left shoulderretroperitoneal location of pancreas
 Sudden onset described as severe, deep, piercing, and continuous or steady
 Aggravated by eating and frequently has an onset when pt is recumbent
 May be accompanied by flushing, cyanosis and dyspnea
 N/Va lot of vomiting!, low-grade fever, leukocytosis, hypotension, tachycardia, jaundice, crackles
 Abdominal tenderness with muscle guarding is common
 Bowel sounds decreased or absent
 Paralytic ileus may occurmarked abdominal distention
 Cyanosis or greenish to yellow-brown discoloration of the abdominal wall
 Shock may occurhemorrhage into the pancreas, toxemia, from activated pancreatic enzymes, or hypovolemia
as a result of fluid shift into the retroperitoneal space
o Serious assessment findings:
 Seepage of blood stained exudates into tissues
 Ecchymosis on the flanks (Turner’s sign)***
 Bluish discoloration of the periumbilical area (Cullen’s sign)***
 Tetany caused by hypocalcemia (this is caused by fat necrosis from enzymes)
 Trusseau’s sign***blood pressure cuff, wrist goes incheck calcium level
if this happens!
 Chvostek’s sign*** stroke face, cheek twitches
 Twitching of fingers, spasms
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Report muscle twitching and finger numbness to providerhypocalcemiacan lead to
tetany unless calcium gluconate is administered!
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Complications:
 highest priority is maintaining normal respiratory function! Respiratory failure can occur as
a complication of acute pancreatitis, and maintenance of adequate
respiratory function is the priority goal.
 Pseudocyst
 pancreatic pseudocyst is a cavity continuous with or surrounding the outside of the pancreas
 Can rupture and hemorrhage
 Abscess
 A palpable abdominal mass may indicate the presence of a pancreatic abscess requires rapid surgical
drainage to prevent sepsis!
Nursing management/interventions
o NPO! And NG suctionNG suction and NPO status will decrease the release of pancreatic
enzymes into the pancreas and decrease painabdominal pain decreased suggest
these therapies are workin!
o Antiemetic
o Pain management (may require large amounts of opioids)
o TPN
o Limit stress, no smoking or etoh
o IV fluids (up to 6 L can be third-spaced)
o Monitor vital signs, electrolytes
o Teach to splint chest to prevent atelectasis
Collaborative management
o Chronic pancreatitis- take the prescribed pancrelipase (Viokase) with each mealPancreatic enzymes are used
to help with digestion of nutrients and should be taken with every meal.
Which lab value tracks improvement in symptoms best?
o Lipase Amylase
o Lipase rises slower than amylase but lasts 2 weeks (best marker***)
Labs
Lipase (high or low)
o Digestive enzyme
o Cholecystitis (if pancreas is involved)
o Pancreatitis
o Better than amylase
Obesity (approx. 5 questions) 41
 Clinical manifestations/assessment/complications
Assessment:
o Subjective: the first step is to determine whether any physical conditions are present that may be causing or contributing to
obesity
 HTN, cardiovascular problems, stroke, cancer, chronic joint pain, respiratory problems, diabetes, cholelithiasis,
metabolic syndrome.
 Functional health patterns: Health perception-health management, Nutritional-metabolic, EliminationConstipation, Activity-exercise, Sleep-rest, Cognitive-perceptual, Role-relationship, sexuality-reproductive
o Objective:
 Body mass index 30 kg/m2; waist circumference: women >35in(89cm),man >40in(102cm)
 Increased work of breathing; wheezing; rapid, shallow breathing
 HTN, tachycardia, dysrhythmias,
 Decreased joint mobility and flexibility; knee, hip, and low back pain
 Gynecomastia and hypogonadism in men
 glucose, cholesterol, triglycerides; chest x-ray enlarged heart; electrocardiogramdysrhythmia;
abnormal liver function tests
Complications:
o Psychosocial: depression, low self-esteem, suicide, discrimination, social isolation
o Endocrine/Metabolic: Type 2 DM, metabolic syndromeBP, glucose test >100mg/dL, waist size,
polycystic ovary syndrome
o Respiratory: Obesity hypoventilation syndrome, sleep apnea, asthma, pulmonary hypertension, exercise intolerance
o Reproductive: Women- menstrual irregularities, infertility, gestational diabetes. Men-hypogonadism, gynecomastia, sexual
dysfunction
o Musculoskeletal: osteoarthritis, impaired mobility and flexibility, gout, lumbar disk disease, chronic low back pain
o Cardiovascular: hyperlipidemia, sudden cardiac death, right-sided heart failure, left ventricular hypertrophy, CAD, DVT,
AFib, HTN, cardiomyopathy, venous stasis, varicose veins
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o GI: nonalcoholic steatohepatitis (NASH), gallstones, GERD
o GU: kidney cancer, chronic kidney disease, stress incontinence
o Cancer: esophagus, pancreas, thyroid, colorectal, and gallbladder cancer, women- endometrial, breast, and ovarian
Nursing management/interventions
o Overall goals
 1. Modify eating patterns
 2. Participate in a regular physical activity program
 3. Achieve and maintain weight loss to a specified level
 4. Minimize or prevent health problems r/t obesity
o Interventions
 Nutritional therapyrecommend a diet that includes adequate amounts of fruits and vegetables, enough bulk to
prevent constipation, meets daily vit A and vit C requirements. Lean meat, fish, and eggs provide sufficient
protein and the B-complex vitamin. Restrictive diets are difficult to maintain on a long-term basis. Recommend a
dietary approach in which calorie restriction includes all food groups. Set a realistic goallose 1-2lbs/wk
 Exercise Daily, preferably 30min-1hr. Explore possible ways to include exercise in daily routinespark
farther, take the stairs. Encourage goal of 10,000 steps/day. Muscle involvementcardiovascular conditioning
 Behavior Modification assumption is
 1. Obesity is a learned disorder caused by overeating ask about situations that tend
to appetite
 2. The difference between an obese person and a normal person is the cues that regulate eating
behavior. Teach to restrict eating to designated meals and increase their physical activity.
 Behavioral techniques: 1. Self-monitoring 2. Stimulus control 3. Rewards
Collaborative management
o Management of co-morbidities
o Lifestyle interventions
 Participation in weight loss program
 Support groups
 Behavior modificationideally with a trained interventionalist
o Nutritional therapy
o Exercise
o Behavior modification
o Support groups
o Drug therapy
o Surgical therapy
 vertical banded gastroplasty-support the incision during coughing and turning in bed
to prevent dehiscence
 gastric bypass- drink fluids between meals and not with meals to prevent dumping
syndrome and diarrhea
Colon Cancer (approx. 1 question)
 One question from group presentation
o Colonoscopy at age 50 for average risk
o Manifestations: blood in stool
Diabetes Mellitus (approx. 12 questions) 49
 Differentiate Type I & Type II
o How do lifestyle changes impact both Type I and II?
 Changes in diet and exercise may control blood glucose level in Type II
 Assessment findings (i.e., 3 Ps and weight loss – how will the patient appear, breathing, skin turgor?)
o Type 1: onset is rapid and initial manifestations are usually acute.
 Classic symptoms: polyuria, polydipsia, polyphagia
 Weight lossbreakdown of fat and protein because body needs energy that it
isn’t getting from glucose
 Weakness and fatigue cells lack energy
 Ketoacidosis most common complication
o Type 2: often non-specific, but can also experience the 3 Ps
 Fatigue
 Recurrent infection
 Recurrent vaginal yeast or candida infections
 Prolonged wound healing
 Visual changes
 Lab & diagnostic tests (including prediabetes )
o Diagnosis of diabetes mellitus is made using one of the four methods:
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
A1C of 6.5% or higherGlycosylated hemoglobin shows overall control of glucose
over 90-120 days
 Fasting plasma glucose (FPG) level greater than or equal to 126mg/dL (7.0mmol/L). Fasting is described as no
caloric intake for at least 8hrs
 Avoid smoking before testaffects results
 Several blood samples are obtained 30, 60, and 120 minutes
 Requires fasting for accuracy
 Two-hour plasma glucose level greater than or equal to 200mg/dL (11.1 mmol/L) during an OGTT, using a
glucose load of 75goral contraceptives may falsely elevate OGTT values
 In a patient with classic symptoms of hyperglycemia (3Ps and unexplained weight loss) or hyperglycemia crisis,
a random plasma glucose greater than or equal to 200 mg/dL
o Prediabetes: defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. Blood glucose levels
are elevated but not high enough to meet the diagnostic criteria for diabetes
 OGTT values are 140-199 mg/dL (7.8 to 11.0 mmol/L)
 IFG values are 100-125 mg/dL (5.56-6.9 mmol/L)
Collaborative care/management & nursing interventions/management –
o Nutrition, medications (insulins and metformin)
 Metformin is the most widely used oral diabetic agent and most effective first-line Tx for Type 2 DM
 Primary action is to glucose production in the liver
  insulin sensitivity  improves glucose transport into the cells
 May cause moderate weight loss use for overweight Type 2 and prediabetics
 Proper GFR is important to continue this medication
o Metformin – Can this be taken with iodine based contrast prior to tests like angiograms or CT of chest with contrast?
Why? What would happen? Lactic acidosis
 To avoid lactic acidosis, metformin should be discontinued a day or 2 before the angiogram
 Should not be used for 48hrs after IV contrast media are administered
o Know insulin – types and when to administer in terms of meals and when to assess for hypoglycemia
Rapid acting used for mealtime coverage
Onset: 10-30min
Peak: 30min-3hr
lispro (Humalog)
Duration: 3-5hr
aspart (NovoLog)
glulisine (Apidra)
Short acting
Onset: 30min-1hr
Regular ( Humulin R, Novolin R)
Peak: 2-5hr
Duration: 5-8hr
Intermediate acting
NPH (Humulin N, Novolin N)
Onset: 1.5-4hr
Peak: 4-12hr
Duration: 12-18hr
Long acting DO NOT MIX, given once
daily
glargine (Lantus)
detemir (Levemir)
degludec (Tresiba)
Inhaled
Afrezza
Onset: 0.8-4hr
Peak: none
Duration: 16-24hr
Onset: 12-15min
Peak: 60min
Duration: 2.5-3hr
Insulins
 how to give, what site is best, and why?
o Cleans skin with soap and water or alcohol
o Leave the syringe in place for about 5sec after injection to be sure that all insulin is injected
o The upper abdominal area is one of the preferred areas for insulin injection
o Do not administer into a site that will be exercisedexercise will rate of absorption
o No need to rotate sitesthere is more consistent insulin absorption when the same
site is used consistently
o Preparing NPH and regular using same syringe: clear before cloudy
1. Rotate NPH vial
2. Inject correct units of air into NPH vial
3. Inject correct units of air into regular insulin vial
4. Withdraw regular insulin
5. Withdraw NPH
13
o
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Exercise and insulin resistance
 Exercise decreases insulin resistance and can have a direct impact on lowering glucose. Weight loss further
decreases insulin resistance. Regular exercise may help triglycerides, LDL, HDL, BP, improves
circulation
 Patients who use insulin, sulfonylureas, or meglitinides are at increased risk for hypoglycemia when they
increase physical activity, especially if they exercise at the time of peak or eat too little to maintain adequate
glucoseneed medical clearance to begin new exercise program. Start slowly with gradual progress
 Glucose lowering effects of exercise can last up to 48hr after activity
 Exercise about 1hr after a meal or have a 10-15g carbohydrate snack and check glucose before exercise
 Can eat small carb snacks q 30min during exercise to prevent hypoglycemia
 Always carry a fast-acting source of carbs when exercisingglucose tablets, hard
candies
 Strenuous activity can be perceived by the body as stress, causing a release of counterregulatory hormones and a
temporary elevation of blood glucose
 In a Type 1 diabetic with hyperglycemia and ketones, exercise can worsen these conditions
 Delay activity if glucose is over 250mg/dL and ketones are present in the urine
 They can exercise if hyperglycemia is present without ketosis
o Symptoms and treatment of hypoglycemia (15 – 15 – 15)
 <70mg/dL
 Shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, pallorcaused by release of
epinephrine
 Difficulty speaking, visual disturbances, stupor, confusion, and comainsufficient glucose for
brain to function properly
 Manifestations mimic alcohol intoxication. Can progress to loss of consciousness, seizures, coma, and death
 “Rule of 15” to treat hypoglycemia
 A blood glucose <70mg/dL ingest 15g of a simple carb (4-6oz regular soda or juice, 5-8 LifeSavers,
1 Tbsp syrup or honey, 4tsp jelly)
 Wait 15 min. Then check glucose again
 If blood glucose <70mg/dL, repeat treatment of 15g of carb and recheck in 15min
 Once the glucose level is stable and the next meal is more than 1hr away, give patient additional food of
carb plus protein or fat (crackers with peanut butter or cheese) after symptoms subside. Give additional
food if patient is engaged in physical activity regardless of time until next meal.
 Immediately notify HCP or emergency service (if patient outside the hospital) if symptoms do not
subside after two or three administrations of quick-acting carb.
Acute complications
o Hyperglycemic hyperosmolar nonketotic coma (HHNC)
Hyperosmolar hyperglycemic syndrome (HHS) life threatening syndrome that can occur
in the patient with diabetes who is able to produce enough insulin to prevent DKA,
but not enough to prevent severe hyperglycemia, osmotic diuresis, and
extracellular fluid depletion. HHS produces fewer symptoms in the earlier stages
and blood levels can climb high before the problem is recognizedsevere
neurological manifestations: somnolence, coma, seizures, hemiparesis, and aphasia.
 Priority treatment
 Manifestations resemble stroke, so immediate determination of the glucose level is critical for correct
diagnosis and Tx.
 Laboratory blood glucose >600 mg/dL and a marked increase in serum osmolality. Ketones absent or
minimal in blood and urine
 Management:
o Immediate IV administration of regular insulin and either 0.9% or 0.45% NaCl
o Usually requires large volumes of fluid replacement administered slowly and
carefullythey are super dehydrated!
o When glucose levels fall to approximately 250mg/dL, IV fluids containing dextrose are
administered to prevent hypoglycemia
o Electrolytes are monitored and replaced as needed Hypokalemia is not as
significant in HHS as it is in DKA, although fluid losses may
result in milder potassium deficits that require replacement
o Assess vs, I&O, tissue turgor, laboratory values, and cardiac monitoring to check the efficacy
of fluid and electrolyte replacement.
o Monitor serum osmolality and frequently assess cardiac, renal, and mental status
Long term complications
o Teaching foot care – type of shoes, examination of feet, nails, etc.
 Neuropathyno feeling, Poor circulation to combat infection, Bacteria loves sugar
 Use lotion on dry areas of feet, but avoid between the toesprone to bacterial growth
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Dry feet thoroughly after washing to prevent bacterial growth between toes
Wear closed-toe shoes to prevent injury to feetchoose flat-soled leather shoes
Examine skin and feet daily
Trim toenails straight across and smooth edges with an emery board
Use a bath thermometer to ensure a water temperature below 43.3 C (110 F)
Do not use on topical over-the-counter medicationcan impair skin integrity and lead to
further injury
Somogyi and Dawn Phenomenon
o Somogyi effect: a high dose of insulin produces a decline in blood glucose levels during the nightcounterregulatory
hormones-glucagon, epi, GH, cortisol releasedlipolysis, gluconeogenesis, and glycogenolysishyperglycemia in the
morningdangerous because the patient or the HCP may increase the insulin dose
 If experiencing morning hyperglycemia, check blood glucose between 0200-0400 for hypoglycemia to determine
cause to be Somogyi effect.
 May report headaches on awakening and recall having night sweats or nightmares.
 A bedtime snack, reduction in insulin dose, or both can prevent Somogyi effect
o Dawn phenomenon: Also characterized by hyperglycemia present in the morning. Two counterregulatory hormones-GH
and cortisol, which are expected in increased amounts in the early morning hours, may be the cause of this phenomenon.
Affects most diabetics, but most severe when GH is at its peak in adolescence and young adulthood
 Tx is an increase in insulin or an adjustment in administration time.
 If 0200-0400 ifs high, the insulin dose should be increased.
Labs
Tests important for individuals with DM to have annually
 BP, creatinine, eye exams, microalbuminuria and why?
o BP, serum creatinine, urine testing for microalbuminuria, and monofilament testing of the foot are all
recommended at least annually to screen for possible macrovascular and microvascular complications of
diabetes
o the goal BP is usually 130/80
o because many patients have some diabetic retinopathy when they are first diagnosed with type 2 diabetes, a
dilated eye exam is recommended at the time of diagnosis and annually thereafter.
o Patients with type 1 diabetes should have dilated eye exams starting 5 years after they are diagnosed and
then annually.
Thyroid Disorders (approx. 7 questions) 48
 Hyperthyroidism- Clinical manifestations/Assessment
o Manifestations:
 Cardiovascular: systolic hypertension, rate and force of contractions, bounding and rapid pulse, CO, cardiac
hypertrophy, systolic murmurs, dysrhythmias, palpitations, angina
 Respiratory: dyspnea on mild exertion, RR
 GI: appetite, thirst, weight loss, peristalsis, diarrhea, frequent defecation, bowel sounds, splenomegaly
 Integumentary: warm, smooth, moist skin, onycholysis (thin, brittle nails detached from nail bed), hair loss
(may be patchy), clubbing of fingers (thyroid acropachy), palmer erythema, fine, silky hair, premature graying
(in men), diaphoresis, vitiligo, pretibial myxedema (infiltrative dermopathy)
 Musculoskeletal: fatigue, weakness, proximal muscle wasting, dependent edema, osteoporosis
 Nervous: difficulty focusing eyes, nervousness, fine tremor of fingers and tongue, insomnia, lability of mood,
delirium, restlessness, personality changes of irritability, agitation, exhaustion, hyperactive deep-tendon reflexes,
depression, fatigue, lack of ability to concentrate, stupor, coma
 Reproductive: menstrual irregularities, amenorrhea, decreased libido, impotence in men, gynecomastia in men,
decreased fertility
 Other: heat intolerance, elevated basal temperature, lid lag, stare, eyelid retraction, exophthalmos, goiterwill
feel a lump in throat when swallowing, DO NOT palpate! Can release thyroid
hormones, rapid speech
 Hyperthyroidism – Collaborative management/ Nursing management & surgery – pre and post op
o Special considerations with iodine therapy
 Radioactive iodine (RAI) damages or destroys thyroid tissue, thus limiting thyroid hormone secretion.
 RAI has a delayed response usually treated with antithyroid drugs and propranolol before and for up to 3
months after starting RAI until effects of radiation become apparent
 Radiation thyroiditis and parotiditis are possible and may cause dryness and irritation of the mouth and throat
relief with frequent sips of water, ice chips, or a salt and soda gargle 3 or 4 times per day
 Limit radiation exposure to others
 Use private toilet facilities and flush two or three times after each use
 Separate laundering towels, bed linens, and clothes daily at home
 Do not prepare food for others that requires handling with bare ands
 Avoid being close to pregnant women and children for 7 days after therapy
15
o
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What electrolyte imbalance will you assess for?
 Postoperative complications include hypothyroidism, damage to or inadvertent removal of parathyroid glands
hypoparathyroidism hypocalcemia, hemorrhage, injury to the recurrent laryngeal nerve,
thyrotoxicosis, and infection
 Important nursing interventions after thyroidectomy:
 Assess q 2hrs for 24hrs for signs of hemorrhage of tracheal compression irregular
breathing, neck swelling, frequent swallowing, choking, blood on
dressings, sensations of fullness at the incision sight
 Semi-fowler’s and support head with pillows. Avoid flexion of the neck and any tension on suture lines
 Monitor VS and calcium levels. Assess for signs of tetany secondary to hypoparathyroidism
tingling in toes, fingers, around the mouth; muscular twitching;
apprehension, and any difficulty speaking and hoarsenessnormal for 3-4 days after
surgery because of edema. Monitor Trousseau’s sign and Chvostek’s sign
 Control post-op pain with medication
Hypothyroidism – Diagnostic studies (i.e., increased TSH, decreased T3, T4)
o The most reliable laboratory tests for thyroid function are TSH and free T4. These values, correlated with symptoms
obtained from the history and physical examination, confirm the diagnosis of hypothyroidism.
o Serum TSH levels help determine the cause
 TSH the defect is in the thyroid (primary)
 TSHpituitary or hypothalamus (TRH function of hypothalamus) (secondary)
o Total serum T3 and T4
o Thyroid peroxidase (TIPO) antibodies suggests autoimmune in origin
o cholesterol, triglycerides, anemia, creatine kinase(CK), Basal metabolic rate (BMR), LDL
Hypothyroidism – Nursing management (what medications may increase myxedema?)
o Thyroid-inhibiting drugs:
 Propylthiouracil (PTU)
 Methimazole (Tapazole)
 Iodine in large doses
o Other Drugs:
 Sulfonamides
 Salicylates
 p-Aminosalicylic acid
 lithium
 amiodarone
Priority assessments – what can kill the patient?
o The mental sluggishness, drowsiness, and lethargy of hypothyroidism may progress gradually or suddenly to a notable
impairment of consciousness or coma myxedema coma
 Can be precipitated by infection, drugs (opioids, tranquilizers, and barbiturates), exposure to cold, and trauma
 Characterized by subnormal temperature, hypotension, and hypoventilation
 Cardiovascular collapse can result from hypoventilation, hyponatremia, hypoglycemia, and lactic acidosis
 Tx: Vital functions must be supported and IV thyroid hormone replacement administered
Surgical complications and nursing assessments and interventions
o Health promotion
 Risk factors: female, white, advanced age or DM type 1, Down syndrome, family history of thyroid disease,
goiter, and external beam radiation in the head and neck area
o Acute Caremyxedema coma
 Most people with hypothyroidism are treated on an outpatient basis unless myxedema coma developsoften
ICU, mechanical respiratory support and cardiac monitoring are frequently necessary
 Give thyroid hormone therapy and meds IVgastric motility may prevent absorption of
oral meds
 Monitor core temperature for hypothermiaoften occurs in myxedema and coma
 Gentle soap and moisturize frequently, position changes, low-pressure mattress prevent skin
breakdown
 Monitor progress VS, weight, I&O, and edema
 Cardiac assessment is importantresponse to hormone therapy determines the
medication regimen
 Note energy levels and mental alertnessshould improve 2-14days and progress to normal
levels
 Neurologic status and TSH levels determine continuing Tx
o
Ambulatory Carepatient education
 Need for life long therapy*T4- Levothyroid, T3- Liothyrone , monitor HR and BP, take in
the morning before food, need for regular follow-up care
 Do not switch brands of the hormone unless prescribed, since bioavailability of thyroid may differ
16
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Cold intoleranceneed comfortable, warm environment
Prevent skin breakdownuse soap sparingly and apply lotion to skin
Avoid sedatives and suggest lowest dose if must be used, caregiver should closely monitor mental status, LOC,
and respirations
 Minimize constipationgradual  in activity and exercise, fiber, stool
softeners, regular bowel elimination time
Labs- Thyroid function studies
 Thyroid stimulating hormone (TSH)
o 0.2-5.4 mU/L
 Thyroxine (T4)
o 5.4-11.5 mcg/dL
 Free Thyroxine (Total T4 F4)
o 0.7-2.0 ng/dL
 Triiodothyronine (Total T3)
o 75-200 ng/dL
Meds
 Levothyroxine – adverse effects, how and when should patient take this med
 PTU – onset of action for patient to feel and see an improvement
o Antithyroid used for hyperthyroidism
o Onset is 10-21 days
Hypertension (approx. 5 questions) 33
BP is primarily a function of cardiac output (CO) and systemic vascular resistance (SVR). CO
is the total blood flow through the systemic or pulmonary circulation per minute. Stroke
volume is the amount of blood pumped out the left ventricle in one beat. CO= SV x HR. SVR is
the force opposing the movement of blood within the vessels. Radius determines SVR narrow =
BP and dilate=BP
HTN affects eyes, heart, brain, and kidney!
 Risk factors – teaching – at least one question from student presentation
Primary Hypertension (essential or idiopathic): has no identified cause and accounts for 9095% of cases. Risk factors:
o Vasoconstricting or vasodilating agents
o Increased SNS activity
o Overproduction of sodium retaining hormonesAldosterone
o Excessive sodium intake
o Elevated serum lipids
o Obesity
o Diabetes
o Tobacco use
o Family history
o Sedentary lifestyle
o Stress
o Ethnicity 2 times greater in African Americans than in white
o Gender  men in young adult hood and women after 64yrs of age
o Socioeconomic status lower socioeconomic groups and the less educated
Secondary Hypertension: has a specific cause. Suspected if people suddenly develop BP,
especially if severe. Causes include:
o Cirrhosis
o Coarctation or congenital narrowing of the aorta
o Drug related estrogen replacement, oral contraceptives, NSAIDS, sympathetic
stimulants
o Endocrine disorders
o Neurologic disorders
o Pregnancy induced hypertension
o Renal disease
o Sleep apnea
 Clinical manifestations/assessment
Hypertension is often called the “silent killer” because it is freely asymptomatic until
it becomes severe and target organ disease occurs. Severe hypertension may experience
symptoms secondary to the effects on BVs in the various organs and tissues or the
increased workload of the heart. These secondary symptoms include:
o Fatigue, dizziness, palpitations, angina, dyspnea
o Hypertensive crisis severe headaches, dyspnea, anxiety, nosebleeds
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o
Cardio: SBP consistently >140 or DBP >90 for patients <60yr or >150 or DBP >90 for patients >60yr. Orthostatic
changes in BP and HR. Bilateral BP significantly different. Abnormal heart sounds. Laterally displaced apical pulse.
Diminished or absent peripheral pulses. Carotid, renal, or femoral bruits. Peripheral edema.
o GI: Obesity (BMI 30 kg/m2). Abnormal waist-hip ratio.
o Neuro: mental status changes.
o Diagnostic: abnormal serum electrolytes (especially potassium). BUN, creatinine, glucose, cholesterol,
triglyceride. Proteinuria, albuminuria, microscopic hematuria. Evidence of ischemic heart disease and left ventricular
hypertrophy on EKG. Evidence of structural heart disease and left ventricular hypertrophy on echocardiogram. Evidence
of arteriovenous nicking, retinal hemorrhages, and papilledema on funduscopic examination
 Nursing management/interventions – how to maintain safety after administering
o Changes in diets (DASH Eating Plan) that reduce the amount of fat, red meat, and salt intake but seeks increases in fresh
vegetables and fruits with more whole grains are often hard to achieve in people who have limited income or rely on
government help for food ( food stamps and WIC).
 DASH Eating Plan: diet that emphasizes “fruits, vegetables, fat free or low fat milk and milk products, whole
grains, fish, poultry, beans, seeds, and nuts.” ( Lewis, Dirksen, Heitkemper, Bucher; p 715, 2014)
o Physical activity as either moderate activity 30 minutes a day for 5+ days a week or 20 minutes 3+ days a week of
strenuous activity ( Lewis et al., 2014).
o Weight reduction, especially in abdominal area, to be monitored by checking weight and BMI; which should be reduced to
decrease risk for hypertension.
o Reduction of drug and alcohol use, including the overuse of NSAIDs, to limit secondary hypertension from liver or kidney
damage as well from damage to the arteries from smoking
o Encourage compliance with medication regimen to avoid rebound hypertension and ensure that the hypertension is being
treated constantly.
o Continuation of medical care to re-screen for effectiveness of medication or other suggested methods to reduce
hypertension.
 Collaborative interventions
o RN- develop and conduct HTN screening programs, assess risk factors and develop risk modification plans, teach about
lifestyle management and drug use, evaluate the effectiveness of lifestyle management and drugs, teach about BP
monitoring, make appropriate referrals to other HCPsdieticians or stress management programs,
monitor for complications of HTN, assess the pt with hypertensive crisis for evidence of target organ
diseaseencephalopathy, renal insufficiency, cardiac decompensation, manage the pt with
HTN urgency or emergencyadminister drugs and evaluate for resolution of the crisis
o LPN- administer HTN drugs to stable pts, monitor for adverse effects of HTN drugs, reinforce teaching about drugs and
lifestyle management
o UAP- obtain accurate BP readings, report high or low readings immediately to the RN, check for postural changes in BP
as directed
o Dietician- obtain diet history, teach components of the DASH diet, provide instructions for dietary changes as needed
o Physical therapist- assess pts current level of fitness, develop an exercise plan with the pt
 Assessing blood pressure measurements
o Patient should not have smoked, exercised, or ingested caffeine within 30min
o Legs uncrossed, feet on floor, back supported, arm supported at heart level
o Palpate radial pulse, inflate until pulse disappears, and inflate 20-30mm Hg above this level
o Deflate at a rate of 2-3 mm Hg/sec
o SBPwhen the first of two or more Korotkoff sounds are heard
o DPB when sounds disappears
 How to assess for end organ damage including labs
Hypertensive crisis is a term used to indicate either a hypertensive urgency or emergency.
Systolic >180 or diastolic >110. Hypertensive urgency develops over hours or days and does not
have clinical evidence or target organ disease. Hypertensive emergencies have target organ
disease and most often require hospitalization for prompt, controlled reduction of BP. Can
lead to encephalopathy, intracranial or subarachnoid hemorrhage, heart failure, MI, renal
failure, dissecting aortic aneurism, and retinopathy HTN affects eyes, heart, brain, and
kidney! The rate of increase BP is more important than the value in determining the need for
emergency treatment
o Sudden withdrawal of antihypertensive meds can cause rebound hypertension and hypertensive crisis ask if they
stopped taking their HTN meds
o Assessment is extremely important, monitor for signs of: neurologic deficits, retinal damage, heart failure, pulmonary
edema, and renal failure
o Often manifested as hypertensive encephalopathy, a syndrome in which sudden rise in BP cerebral capillary
permeabilitycerebral edema  severe headache, N/V, seizures, confusion, coma
o Retinal examinationexudates (mass of cells and fluid seeped out of BVs or an organ),
hemorrhages, papilledema (swelling of optic disc)
o Renal insufficiency ranging from minor injury to complete renal failure
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o
Rapid cardiac decompensation ranging from unstable angina to MI and pulmonary edema is also possible. Pts can have
chest pain and dyspnea. Aortic dissection can develop and will cause sudden, excruciating chest and back pain and
possible reduced or absent pulses in the extremities
o IV drugs given for HTN emergencies include: vasodilators (sodium nitroprusside),
adrenergic inhibitors, and the calcium channel blocker clevidipine. Sodium
nitroprusside is the most effective for this treatment
 MAP how to calculate
When treating hypertensive emergencies, the mean arterial pressure (MAP) is often used
instead of BP readings to guide and evaluate drug therapy. The initial goal is to
decrease MAP by no more than 20-25%, or 110-115 mm Hg. Lowering the BP too quickly or
too much may decrease cerebralstroke, coronaryMI, or renal perfusionrenal failure.
o MAP= (SBP + 2DBP)  3
 Ace inhibitors (“prils” – labs to access
o K+
Antihypertensives
Antihypertensive drugs affect RAAS
First dose hypotension is a phenomenon that occurs with many HTN meds
 Calcium channel blockers
 ACE Inhibitors
They inhibit ACE in the lungsBP, HR
Prevent changes in heart muscle ventricular remodeling
The angiotensin-converting enzyme (ACE) inhibitors frequently cause orthostatic
hypotension, and patients should be taught to change position slowly to allow the
vascular system time to compensate for the position change.
o Lisinopril
o Enalapril (most pril suffixes)
Unique side effects: BP, K+, cough (ACE in lungs), not effective on black population, angioedemaif any
swelling of the face or oral mucosa occurs, the health care provider should be
immediately notified because this could be life threatening.
Angiotensin receptor blockers
o Losartan (most artan suffixes)
o

Diuretics
 Furosemide
o Classification: Loop diuretic
o Indication: HF, acute pulmonary edema, hypertension, edema of HF, renal disease, and liver disease
o Nursing intervention: monitor potassium levels (check for hypokalemia, if give furosemide too fast can cause
tinnitus and/or hypotension. May take with food or milk to decrease stomach upset. Take when they wake up (or else
they will be peeing all night). Check BP before and throughout…can BP
o Main side effects: Related to imbalance in electrolytes and fluid, Hypokalemia, Alkalosis, Hypocalcemia, hypotension
 Spironolactone
o Classification: Potassium sparing diuretic
o Indication: adjuncts with thiazide or loop diuretics… they are not as powerful
o Nursing intervention: watch for hyperkalemia
o Main side effects: Hyperkalemia, dizzy, headache, hypotension
 Potassium sparing vs. potassium wasting
o Diet- Potassium wasting give foods high in potassium e.g., green leafy vegetables, whatever ends in os (potatoes,
avocado), melons, bananas, OJ
o Nursing interventions: monitor K+, BP, caution with digoxin
Labs and Medications
MEDICATIONS
Atrovastatin (Lipitor) what time of day to take it and why? Adverse effects to teach patient?
o Muscle aches and painRhabdomyolysis
Prednisone/solumedrol – what does this do to blood pressure?
o BP
o glucose
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