NURS 384 Exam 2

Cardiovascular (hematology part 2 omitted) Hypertension (HTN)

● “silent killer” asymptomatic
Blood Flow ● Fatigue, dizziness, palpitations, angina,
(Deoxygenated) and dyspnea
1. SVC/IVC ● Primary (essential) hypertension -
2. Right Atrium elevated blood pressure without an
3. Tricuspid Valve identified cause
4. Right Ventricle ● Secondary hypertension - elevated blood
5. Pulmonary Semilunar Valve pressure with a specific cause can be
6. Pulmonary Artery Gas Exchange in the lungs identified and corrected
○ Common causes: Cirrhosis,
(Oxygenated) pregnancy, renal disease, sleep
7. Pulmonary Veins apnea, medications, Cushing
8. Left Atrium syndrome, thyroid disease
9. Mitral Valve ● Water and Sodium Retention
10.Left Ventricle ● Altered RAAS (incr conv of
11. Aortic Valve angiotensinogen to angiotensin 1)
12..Aorta ● Stress/ Incr SNS Activity
● Insulin Resistance & Hyperinsulinemia
Cardiac output - stroke volume or the amount of ● Endothelial Dysfunction
blood pumped out of the left ventricle per beat ○ Prolonged vasoconstriction
multiplied by the heart rate response or reduced vasodilator
CO = SV (mL per beat) * HR response
Systemic vascular resistance - the force
opposing the movement of blood within the blood Risk Factors for HTN
vessels (as arteries narrow, resistance to blood ● Age Alcohol Diabetes Ethnicity
flow increases) (Blacks) Excess sodium intake Family
history Gender (younger men, women
Increased SNS activity = vasoconstriction, incr after 65 years old)
heart rate, rel renin fr kidneys ● Incr serum lipids Obesity Sedentary
lifestyle Socioeconomic status Stress
Increased PNS activity = decr cardiac output and Tobacco use
HR (via vagus nerve)
HTN Crisis (epistaxis, headache, and dyspnea)
Orthostatic hypotension: pt moves from a supine ● Hypertensive urgency or emergency
to a standing position; decr 20 mmHg more in ● SBP > 180 mmHg and/or DBP > 120
SBP, decr of 10 mmHg more in DBP, and/or an mmHg
increase in the HR of 20 beats/min ● Encephalopathy, hemorrhage, HF, MI,
1. Patient rest supine position for 3 min and renal failure, dissect aortic aneurysm,
take baseline readings for BP and HR retinopathy
2. Have the patient sit and repeat the BP and ● Pt noncompliant with meds, cocaine or
pulse crack use, amphetamines, PCP, LSD use
3. Then have the patient stand and assess BP
and pulse again HTN Pt education
4. After the patient has been standing for 3 ● Risk Factor Modification
minutes, measure BP and pulse again ● Drug Therapy Adverse Effects
● Home Blood Pressure Monitoring
● Patient Adherence
HTN Lifestyle Modification Common Drugs for Hypertension *
● Weight loss (1kg = 1 BP mmHg) ● Central-Acting Adrenergic Agonists
● Nutrition Plant based and Mediterranean ○ decr sympathetic outflow from
diets fish CNS, produce vasodilation
● Sodium reduction 2300 mg/day ● Alpha Blockers
● Moderate alcohol use ○ Block alpha 1 Adrenergic effects,
○ Men - 2 drinks/day; Women - 1 produce vasodilation
drink/day ● Beta Blockers
● Physical activity (150 min mod exerc/ 75 ○ Block beta 1 adrenergic effects,
min vig exerc weekly) decrease renin secretion by
● Avoiding tobacco products kidneys
● Nicotine = vasoconstriction ● ACE Inhibitors
○ prev the conversion of
HTN Complications angiotensin 1 to angiotensin 2
● Hypertensive Heart Disease ● ARBs
○ Coronary Artery Disease ○ prev angiotensin 2 from binding
○ Left Ventricular Hypertrophy receptors in walls blood vessels
Heart Failure ● Calcium Channel Blockers
● Cerebrovascular Disease ○ prev the mvmnt Ca into cells
● Peripheral Vascular Disease (HTN speeds
up athero) Coronary Artery Disease
● Nephrosclerosis (renal ischemia) ● Leading cause of death worldwide
● Retinal Damage ● Atherosclerosis begins as soft deposits of
fat that harden w/ age in coronary arteries
Hypertension - Diagnostic Studies CAD Patho
● History and Physical ● Endothelial injury and inflammation
● Fasting blood glucose ● Tobacco use, hyperlipidemia, HTN,
● Routine urinalysis toxins, diabetes, inflammation, and
● Periodic BP monitoring infection
● 12-Lead ECG ● Develops in stages over many years
● Serum uric acid, calcium, and magnesium
● CBC Serum lipid profile BMP

Risk factors for CAD * Modifiable

Nonmodifiable ● High serum lipid levels - Normal: LDL <
● Age - Men over 45 & Women over 55 100 mg/dL ; HDL > 60 mg/dL ; Total <
● Gender - Women are more likely to die 150 mg/dL
from CVD ● High blood pressure - Normal B/P <
● Ethnicity - White and Black Males have 120/80 mmHg ; > 90/60 mmHg
higher incidence ● Tobacco use - Decreases estrogen levels
● Family history ● Physical inactivity
● Genetics - Mutation in LDLR gene, ● Obesity - Normal: BMI < 30
autosomal dominant ● Diabetes - Changes lipid metabolism
● Metabolic syndrome - rel to insulin
resistance
Pt education CAD Lipid lowering Drugs
● Smoking cessation ● HMG-CoA Reductase Inhibitors
● Decr saturated fats cholesterol and incr ○ Atorvastatin, Simvastatin
fiber ○ Block synth cholesterol and incr
● Avoid red meat, egg yolks, and whole LDL receptors in the liver
milk products high in saturated fats ○ Rhabdomyolysis/ muscle cramps
● Omega-3 fatty acids reduce triglyceride ● Fibric Acid Derivatives
levels but do not affect LDL levels ○ Fenofibrate, Gemfibrozil
○ decr hepatic synth and secretion
of VLDL
● Niacin
○ Inhibits synthesis/secretion of
VLDL and LDL
● Bile Acid Sequestrants
○ Cholestyramine, Colesevelam
Binds w/ bile acids in the intestine
and excretes in feces
■ Constipation

Diagnostic Chronic Angina

Chronic Stable Angina ● Exercise stress test with or without
● Clinical manifestation of myocardial imaging + ECG/Nuclear imaging
ischemia ● Cardiac catheterization
● Provoked by physical exertion, stress, or ● Percutaneous coronary intervention
emotional upset ○ Balloon angioplasty or stent mesh
● Pain is substernal and can radiate to the ● CABG surgery
jaw, neck, shoulders, and/or arms
● The pain subsides by resting, calming Nursing Actions for Complaints of Chest Pain
down, or using sublingual nitroglycerin 1. Position pt upright; apply supplemental
O2
Drug Therapy for Chronic Stable Angina 2. Assess vital signs
● Antiplatelet therapy (ASA,Clopidogrel) 3. Apply a continuous ECG monitor
● Nitrates - Always assess for Sildenafil use 4. Obtain a 12-lead ECG
prior to administering 5. Provide prompt pain relief, first with
● Store in cool dark place; take up to 3 sublingual or IV nitroglycerin followed by
tablets angina pain, start with 1 SL wait 5 an IV opioid analgesic (Morphine is
min, call 911, second one, then third if common)
still having anginal pain. 6. Obtain cardiac biomarkers
● NO more than 3 SL nitroglyc 7. Assess heart and lung sounds
tablets;headache common; NOT use if 8. Obtain a chest X-ray
taking ED medication will KILL
● ACE Inhibitors, ARBs Beta Blockers
Calcium Channel Blockers
● Lipid-Lowering Agents
Unstable Angina
● Chest pain that is new in onset, occurs at
rest, or occurs with increasing frequency,
duration, or less effort than the patient’s
chronic stable angina pattern
● The pain lasts for 10 minutes or longer
Must be treated immediately
ECG changes Angina
● ST depression (myocardial ischemia,
hypokalemia)
● ST elevation (myocardial infarction - a
total blockage)
● T wave inversion (myocardial ischemia)

Nursing Management MI
Myocardial Infarction ● Emergent Percutaneous Coronary
● Abrupt stoppage of blood flow through a Intervention
coronary artery with a thrombus caused ● Thrombolytic Therapy (if no cardiac cath
by platelet aggregation lab present at the facility)
● Irreversible necrosis in the heart ● Pain
● Troponin and CK-MB biomarkers ○ provide SL nitroglycerin,
● An emergency; PCI or thrombolytic morphine, supplemental O2
therapy are immediate treatments ● Monitoring
Symptoms: ○ Continuous ECG, Auscultate
● Pain Heavy pressure, burning, tight, heart and lungs
constricted, or crushing feeling ● Rest and Comfort
● Substernal or epigastric area that can ● Anxiety
radiate to the neck, lower jaw, and arms or ● Physical Activity
upper back ○ Gradually increase the patient’s
● SNS Stimul activity levels
○ Release of NE and EPI Complications
Diaphoresis, increased HR and ● Dysrhythmias
BP, vasoconstriction ● Heart Failure
● Cardiovascular Manifestations ● Cardiogenic Shock
○ Crackles, BP drops due to ● Papillary Muscle Dysfunction or Rupture
decreased CO, JVD, hepatic -> mitral valve regurg
engorgement, peripheral edema ● Left Ventricular Aneurysm
○ S3 or S4 ● Ventricular Septal Wall Rupture and Left
● N/V Fever STEMI or NSTEMI Ventricular Free Wall Rupture
● Pericarditis (inflamm of the pericardium)
● Dressler Syndrome (Pericarditis and
fever 1-8 weeks after MI)
 Right-Sided Heart Failure (Cor Pulmonale)
Heart Failure ● The most common cause of left- sided
● Inability of the heart to provide sufficient heart failure
blood to meet the oxygen needs of the Symptoms ** just look at pictures below
tissues and organs ● Elevated BNP, Tachycardia
● Decr cardiac output = decr tissue Drug Therapy
perfusion, impaired gas exchange, fluid ● Thiazide diuretics Loop diuretics
volume imbalance, and decreased Aldosterone antagonists Osmotic
functional ability diuretics
Left ventricular ejection fraction - percentage ● Digoxin - Positive Inotropic effect
blood volume in left ventricle at end diastole ● Nitrates - Vasodilators
pumped out of the left ventricle ● ACE Inhibitors and ARBs - Decrease
● Heart failure involves a defect in either afterload and systemic vascular resistance
ventricular systolic function/ LV ● Beta Blockers - Decrease afterload
contraction (reduced EJ) and/or a defect in
ventricular diastolic function/filling
(preserved EJ)
● HTN and CAD are the primary risk
factors for HF
● Cardiac output (CO) depends on preload,
afterload, myocardial contractility, and
HR
● CO = SV x HR
Left Sided Heart Failiure
● Inability of the LV to either: Empty
adequately during systole Fill adequately
during diastole Can be further classified
as HFrEF or HFpEF
● Normal ejection fraction is 55-65%
● HFrEF
○ The LV does not generate enough
pressure to eject blood forward
through the aorta
○ Over time, the LV dilates and
hypertrophies
● HFpEF
○ The inability of the ventricles to
relax and fill during diastole
○ HTN is the primary cause
○ LV is generally stiff and
noncompliant
 Aortic Aneurysm Complications
Aortic Aneurysm ● If rupture in retroperitoneal space =
● Permanent, localized, outpouching or ○ Bleeding may be controlled by
dilation of the vessel wall surrounding structures
● Common in white men ○ Back/blank bruising (Grey Turner
○ Rupture likely in people smoke sign)
tobacco ● If rupture into thoracic or abdom cavity
● Risk factors: age, male gender, ○ The patient can die from massive
hypertension, CAD, family history, hemorrhage
tobacco, high cholesterol, lower extremity ○ Hypovolemic shock is common
PAD, carotid artery disease, previous ○ Tachycardia, hypotension, pale
stroke, obesity clammy skin, decr urine output,
● True aneurysm - wall of the artery forms altered LOC, abdominal
aneurysm, with at least 1 vessel layer still tenderness
intact Aortic Aneurysm Diagnostic Studies
● False aneurysm - disruption of all ● Chest X-rays Abdominal X-rays
arterial wall layers with bleeding that is Ultrasound CT scan MRI echocardio
contained by surrounding anatomic Aortic Aneurysm Treatment
structures ● Early detection and prompt treatment
● For aneurysms 4.0-5.4 cm
Symptoms ○ Monitor aneurysm size ultrasound
● Thoracic (TAAs) or CT every 6- 12 months
○ asymptomatic ● For aneurysms > 5.5 cm
○ Deep, diffuse chest pain ○ Open aneurysm repair - large
● Abdominal (AAAs) abdominal incision; removes any
○ asymptomatic thrombus/plaque,
○ Back pain, epigastric discomfort, ○ Minimally invasive repair -
altered bowel elimination, sutureless aortic graft
intermittent claudication

Aortic Aneurysm Nursing management

● Graft patency (need adeq BP) Aortic Dissection (“dissecting aneurysm”)
● Cardiovascular status ● Type A = medical emergency
○ MI can occur in the periop period ● Type B = conservative management
○ Dysrhythmias bc electrolyte ● Caused by weakened elastic fibers in the
imbalances arterial wall
○ Infection ● Abrupt onset severe anterior chest or back
○ GI status (Postoperative ileus may pain Back, abdomen, or leg pain
develop due to anesthesia) Complications
○ Neurologic status ● Cardiac tamponade - blood leaks into
○ Peripheral perfusion status pericardial sac = hypotension, narrowed
○ Renal perfusion status pulse pressure, JVD, muffled heart
sounds, and pulsus paradoxus
Diagnostic studies= Similar aortic aneurysm
Treatment (pain relief, HR BP control, risk factor
modification)
 Drug Therapy for Venous Thromboembolism
Venous Thrombosis ● Low Molecular Weight Heparins
● Involves the formation of a thrombus ○ Enoxaparin, Dalteparin
(blood clot) with vein inflammation ○ No need to monitor apTT
Superficial vein thrombosis - a thrombus ○ Protamine sulfate is the antidote
in a superficial vein ● Factor Xa Inhibitors
● Deep vein thrombosis - a thrombus in a ○ Apixaban, Rivaroxaban,
deep vein Fondaparinux
● Venous thromboembolism - represents ○ Andexanet Alfa is the antidote
the spectrum from DVT to pulmonary ● Synthetic Thrombin Inhibitors
embolism (PE) ○ Dabigatran
● Virchow triad - three factors cause ○ Idarucizumab is the antidote
venous thrombosis ● Vitamin K Antagonist
● a. Venous stasis - when valves ○ Warfarin Monitor the INR
dysfunctional or the muscles of the ○ Avoid green, leafy vegetables
extremities are inactive ○ Vitamin K is the antidote
● b. Damage of the endothelium - caused by ● Heparin
surgery, IVs, trauma, burns, prior VTE ○ Monitor aPTT
● c. Hypercoagulability ○ Protamine sulfate is the antidote

Venous Thromboembolism
● Symptoms - Unilateral leg edema, pain,
tenderness with palpation, dilated
superficial veins, a sense of fullness in the
thigh or the calf, paresthesias, warm skin,
redness, or a systemic temperature of
100.4 F or greater
Diagnosis of an initial VTE
● D dimer testing and/or ultrasound
Prevention
● Teach patients to flex and extend their
feet, knees, and hips at least every 2-4
hours while awake
● Graduated compression stockings (TED
hose)
● Intermittent pneumatic compression
devices (SCDs)
● Medications - if at a high risk for VTE
development
Gastrointestinal Hypothalamus - regulates appetite
Neuropeptide Y - made in the hypothalamus is a
1.Mouth 2. Esophagus 3. Stomach 4. Small powerful appetite stimulant
intestine a. Duodenum b. Jejunum c. Ileum 5. Hormones and peptides made in the gut and
Large intestine a. Cecum b. Ascending colon c. adipocyte cells affect the hypothalamus
Transverse colon d. Descending colon e. Sigmoid Leptin - made in the adipocyte; acts on the
colon 6. Rectum 7. Anus hypothalamus to suppress appetite (full) and
increase fat metabolism
Obesity Ghrelin - gut hormone regulate appetite
● excessively high body fat adipose tissue inhibiting leptin; acts on hypothalamus and the
● Major risk factor for leading causes of brain’s pleasure centers to stimulate hunger
death including type 2 diabetes, heart ● Adipokines - made by adipocytes; plays role in
disease, and certain cancers glucose and lipid metabolism, insulin sensitivity,
● Altered body image, depression, low energy homeostasis, inflammation, immunity, and
self-esteem, and withdraw from social vascular function
interaction
● Energy imbalance = takes in more calories Health Risks Associated with Obesity
than one needs ● Cardiovascular Problems
● In obesity = incr number of adipocytes, or ○ Android obesity linked w/ an incr
fat cells, + incr in size risk of elevated LDL,
● Adipocyte hypertrophy triglycerides and decr HDL
● Primary obesity - Excess calorie intake ○ HTN (incr circ blood volume)
over energy expenditure ○ Stroke or CVD
● Secondary obesity - weight gain ● Diabetes (decr effect of insulin, pancr beta
(Endocrine, CNS disorders, medications cells overwork/worn)
such as steroids or antipsychotics) ● GERD
● Over 400 genes are linked to obesity ● Gallstones
● Fatty liver (NASH)
Classifications of Body Weight and Obesity ● Sleep apnea - incr neck circum; incr
● Body Mass Index (BMI) distribution of fat around the diaphragm
○ Obesity is a BMI > 30 ● Osteoarthritis
○ Morbid obesity >36 ● Hyperuricemia
○ Consider the BMI in relation to ● Cancer
the patient’s age, gender, and
body build Treatment for Obesity
● Waist circumference ● Reducing caloric intake compared to
○ Health risks incr if >40 inches in expenditure
men and 35 inches in women ● At least 150 minutes of moderate exercise
● Waist-to-Hip Ratio or 75 minutes of vigorous exercise per
○ Women should be 0.8 or less week
○ Men should be 1.0 or less ● Behavior Therapy
● Body shape ● Support Groups
○ Android obesity - fat mainly in ● Drug Therapy
the abdominal area (apple shaped)
○ Gynoid obesity - fat mainly in
the upper legs (pear shaped)
Drug Therapy for Obesity Bariatric Surgery
● Bupropion/Naltrexone (Contrave) ● Must have a BMI > 35
○ Nausea, vomiting, constipation, Restrictive Surgical Therapy
headache, dizziness, insomnia, ● Adjustable Gastric Banding (Lap-Band)
dry mouth ○ inflatable band placed around the
○ Can incr BP and HR and can fundus of the stomach
cause seizures ○ The stomach is divided into 2
○ Monitor for suicidal ideation portions and the upper part acts as
○ Naltrexone - opioid antagonist the “new” stomach
● Liraglutide (Saxenda) ○ Can be reversed
○ GLP-1 agonist ○ Causes delayed gastric emptying
○ Used to treat Type 2 DM ● Sleeve Gastrectomy (75% stomach is
○ Nausea, vomiting, diarrhea, removed)
fatigue, pancreatitis ○ Ghrelin is removed
○ Monitor for suicidal ideation ● Gastric Plication
● Orlistat ○ Folds the stomach wall inward
○ Need to supplement fat soluble and then places sutures to secure
vitamins (A, D, E, K) the folded stomach wall
○ Stool leakage, flatulence, ○ Can be reversed
diarrhea, abdominal bloating, ● Intragastric Balloon
liver injury, kidney stones
● Phentermine/Topiramate Malabsorptive Surgical Therapy
○ Dizziness, insomnia, dry mouth, ● Roux-en-Y Gastric Bypass
headache, increases BP and HR ○ Creating a small gastric pouch
● Semaglutide (Wegovy) and attaching it directly to the
○ GLP-1 agonist small intestine using a Y- shaped
○ Used to treat Type 2 DM limb of the small bowel
○ GI distress, hypoglycemia ○ Food bypasses 90% of the
stomach, the duodenum, and a
small segment of the jejunum
○ Complications include GI tract
leaks, gastric remnant distention,
ulcers, gallstones, and hernias
○ Bc sections of small intestine
bypassed = Poor iron absorption =
iron deficiency anemia
○ Chronic anemia due to cobalamin
(vit b12) deficiency
○ Dumping syndrome - gastric
contents empty too rapidly into
the small intestine, overwhelming
its ability to digest nutrients;
nausea, vomiting, weakness,
sweating, faintness, diarrhea
● Gastric Pacemaker
○ Blocks vagus nerve impulses, =
decr hunger and incr satiety
Gastroesophageal Reflux Disease (GERD) GERD - Diagnosis and Patient Teaching
● Reflux of acidic gastric contents into the ● Endoscopy (EGD) assess for return of gag
esophagus overwhelms the esophageal reflex
defenses ● Patient teaching
● Esophag inflamm or irritation caused by ○ Avoid triggers
reflux of stomach acid into the lower ○ Elevate the HOB to 30 degrees or
esophagus higher
● Primary factors causing GERD = ○ Should avoid lying supine for 2 to
incompetent lower esophageal sphincter 3 hours after a meal
● Obesity risk factor due to incr ○ Stop smoking
intraabdominal pressure ○ Avoid stress
● NSAIDs and potassium irritate esophageal ○ Avoid eating within 3 hours of
mucosa bedtime
○ Eat small, frequent meals
○ Avoid alcohol and caffeinated
beverages
○ Avoid chocolate, fatty foods,
peppermint

GERD - Manifestations GERD - Drug Therapy

● Hoarse voice ● Decr volume and acidity of reflux,
● Heartburn is the most common improving LES function, increasing
● GERD-related chest pain can mimic esophageal clearance, and protecting the
angina - burning, squeezing, or radiating esophageal mucosa
to the back, neck, jaw, or arms ● Proton pump inhibitors (PPIs)
● Dyspepsia - pain or discomfort centered ○ Omeprazole, Esomeprazole,
in the upper abdomen Pantoprazole
● Regurgitation - hot, bitter, or sour liquid ○ Short term use due to decrease in
coming into the throat or mouth bone density and risk for
● Respiratory problems such as wheezing, osteoporosis
coughing, or displeasure ● Histamine 2 (H2) Receptor Blockers
○ Cimetidine, Famotidine
GERD - Complications ● Antacids
● Effects of gastric acid on the esophageal ○ Aluminum hydroxide, Calcium
mucosa carbonate, Sodium bicarbonate,
● Esophagitis - inflammation esophagus = Maalox
scar tissue formation, stricture, and ○ Can cause constipation or
dysphagia electrolyte imbalances
● Barrett esophagus - flat epithelial cells in ● Sucralfate
the distal esophagus change into columnar ○ Form a protective layer and serve
epithelial cells; a precancerous lesion that as a barrier against acid
increases the patient’s risk for esophageal ● Metoclopramide
cancer ○ Increases gastric motility
● Cough, bronchospasm, laryngospasm, and ● Misoprostol
cricopharyngeal spasm ○ Protect stomach lining
● Dental erosion results from acid reflux in ○ Contraindicated in pregnancy
the mouth because it can cause uterine
contractions
Peptic Ulcer Disease PUD - Diagnosis and Management
● erosion of the GI mucosa hydrochloric ● Endoscopy (EGD) assess for return of gag
acid and pepsin reflex
● Classified as chronic or acute and by ● Serology, stool, and breath testing for the
location (gastric or duodenal) presence of H pylori
● Acute ulcer - causes superficial erosion ● Barium contrast study
and minimal inflammation; short duration ● CBC (reveal anemia)
and resolves quickly ● Surgery (Rare)
● Chronic ulcer - present continuously for ● Aspirin and NSAIDs stopped for 4-6
many months or intermittently throughout weeks
the person’s lifetime; or long duration ● Adequate rest
● Smoking cessation
● Restricting alcohol

PUD - Pathophysiology and Possible Causes PUD - Drug Therapy

● Back diffusion of HCl acid into the gastric ● Antibiotics for H pylori (Amoxicillin)
mucosa = cellular destruction and ● PPIs (reduce gastric acid secr and prom
inflammation ulcer healing)
● Histamine released from damaged mucosa ● H2 receptor blockers (prom ulcer healing)
= resulting in vasodilation, increased ● Antacids (Incr gastric acid pH neutral HCl
capillary permeability, and further acid)
secretion of acid and pepsin ● Misoprostol (prev gastric ulcers caused by
● (H pylori) infection NSAIDs)
● Medication-induced injury ● Sucralfate (mucosal protection for the
○ NSAIDs increase gastric acid esophagus, stomach, and duodenum)
secretion and reduce the integrity ○ Most effective at a low pH, give
of the mucosal barrier 60 minutes before or after an
● Lifestyle factors antacid
○ High alcohol intake and smoking
= stimulate acid secretion PUD - Complications
○ Psychological distress and stress ● GI Bleeding
can delay the healing of ulcers ● Perforation
once they develop ○ Spill gastric or duodenal contents
into peritoneal cavity
PUD - Manifestations ○ Sudden, severe upper abdominal
● Gastric ulcers pain that can radiate to the back
○ Discomfort high in the and shoulders
epigastrium ○ Abdomen appears rigid and
○ Symptoms occur 1-2 hours after board-like
meals ○ Bowel sounds absent
○ Food tends to worsen the pain ○ Bacterial peritonitis
○ ”Burning” or “Gaseous” ○ Patient will become septic
● Duodenal ulcers without immediate intervention
○ When gastric acid comes in ● Gastric outlet obstruction
contact with the ulcers ○ Pain is worse at the end of the day
○ With meals, food is present to as the stomach fills and dilates
help buffer the acid ○ Projectile Vomiting common
○ Symptoms occur generally 2-5 ○ NG tubes help to decompress the
hours after meals stomach
○ ”Burning” or “Cramplike”
Upper GI Bleeding Upper GI Bleed - Emergency Management
Hematemesis - Bloody vomitus appearing as ● Place IV lines (16 or 18 gauge needle for
fresh, bright red blood or “coffee-grounds” fluid and blood replacement)
appearance ● Intake and Output record
Melena - Black, tarry stools caused by digestion ● Measure urine output
of blood in upper GI tract (or taking iron) ● Apply ECG monitoring
Occult bleeding - small amounts of blood in ● Monitor vital signs closely
gastric secretions, vomitus, or stools not apparent ● Assess for signs and symptoms of
by appearance hypovolemic shock
● Stomach and Duodenal Origin ○ Decreased BP, increased HR, cool
○ Peptic ulcers due to H pylori and clammy skin, slow capillary refill,
NSAID use are the most common decreased urine output
cause ● Observe for fluid overload once products
○ Stress-related mucosal disease begin infusing
● Esophageal Origin ○ Auscultate lung sounds and
○ From esophagus; due to chronic observe respiratory effort, Assess
esophagitis or esophageal varices for edema
(occurs with cirrhosis) ● Assess stool and vomitus for blood
● Keep NG tube in proper position if one is
Upper GI Bleed - Diagnosis and Therapies placed
● Endoscopy (EGD) assess for return of gag ● Elevated the HOB to prevent aspiration
reflex
● Angiography
● CBC, CMP, PT, pTT
● Vomitus and stool testing for blood
● BUN (incr)
● Surgical therapy (bleed after rapid
transfusion of up to 2000 mL of whole
blood)
● Drug therapy (PPIs and antacids)
○ decr bleeding, decr HCl acid
secretion, and neutralize HCl acid
Acute Pancreatitis Acute Pancreatitis - Diagnosis (Turner’s and
● Acute inflammation of pancreas Cullens)
● Spill pancreatic enzymes = autodigestion ● Serum amylase and lipase high
and severe pain ● Liver enzymes, triglycerides, glucose,
● Most common cause is gallbladder bilirubin, calcium (hypocalcemia)
disease ● Abdominal ultrasound
● Second most common cause is alcohol use ● X-ray
● Other causes include pancreatic cancer ● CT scan
and hypertriglyceridemia ● Magnetic resonance
cholangiopancreatography (MRCP)
Acute Pancreatitis - Manifestations
● Abdominal pain Acute Pancreatitis - Complications
○ Distention of the pancreas, ● Can be life threatening
peritoneal irritation, and biliary ● Pseudocyst - accumulation of fluid,
tract obstruction pancreatic enzymes, tissue debris, and
○ Usually LUQ pain radiate to the inflammatory exudates surrounded by a
back due to the retroperitoneal wall next to the pancreas
location of the pancreas ● Pancreatic abscess - pseudocyst infected
○ Eating worsens the pain and extensive necrosis occurs in the
○ Severe, deep, piercing, and pancreas
continuous or steady ○ Can rupture or perforate into
● N/V Low-grade fever Leukocytosis adjacent organs
● Hypotension tachycardia Jaundice ● Pulmonary complications
● Bowel sounds decreased or absent ○ Atelactasis, pleural effusion,
● Paralytic ileus inflammation of the diaphragm
● Cullen sign
○ bluish periumbilical discoloration Acute Pancreatitis - Therapy
(occur due to seepage of ● Pain meds
bloodstained exudate from ● Monitor glucose for hyperglycemia
pancreas) ● Monitor for shock
● Grey Turner spots ● NPO status
○ A bluish flank discoloration ○ Suppress pancreatic enzymes and
(occur due to seepage of decrease pancreatic stimulation
bloodstained exudate from ● NG suction
pancreas) ○ Reduce vomiting and gastric
distention
○ Prevent gastric acid contents from
entering the duodenum
● Surgical therapy
○ Remove gallstones
● Monitor calcium levels (lipase + Ca2+)
○ Hypocalcemia can occur
● Drug Therapy
○ Antacids, Antispasmodics,
○ PPIs, Pancrelipase
Choleliathiasis (Gallbladder stones) Cholelithiasis - Manifestations
● lodge in the neck of the gallbladder or in ● Severity depends on whether stones
the cystic duct stationary or mobile and whether
● More common in women obstruction is present
● Risk factors = oral contraceptive use and ● When a stone is lodged in the ducts or
postmenopausal women when stones are moving through the
● Cholecystitis - inflammation of the ducts, spasms may result in response to
gallbladder wall the stone (biliary colic)
● Cholecystectomy - removal of the ● Tachycardia
gallbladder ● Diaphoresis, Fever, Chills
● Nausea and Vomiting
Cholelithiasis - Pathophysiology ● Jaundice
● Imbalance of cholesterol, bile salts, and ● RUQ pain or tenderness
calcium ○ Pain occurs 3-6 hours after a
● Mixed cholesterol stones are the most high-fat meal or when the patient
common lies down
● Factors ● Dark amber or brown urine
○ Supersaturation of bile with ○ If the common bile duct is
cholesterol obstructed = no bilirubin will
○ Decreased bile acids that dissolve reach the small intestine to be
cholesterol converted to urobilinogen
○ Excess mucus production
○ Gallbladder dismotility and stasis Cholelithiasis - Diagnosis
○ The liver excretes more ● Ultrasound
cholesterol than bile can dissolve ● Endoscopic retrograde
and the excess cholesterol may cholangiopancreatography (ERCP)
form into crystals and eventually ● Percutaneous transhepatic
stones cholangiography
● Stones may stay in the gallbladder or ● Hepatobiliary iminodiacetic scan (HIDA
migrate to the cystic duct or the common scan)
bile duct = pain as they pass through the ● Serum enzymes (AST, ALT)
duct ● WBC count
● Serum amylase (if pancreas is involved)
● Direct, indirect urinary, bilirubin levels
Cholelithiasis - Treatment
● Bile acids (dissolve stone)
● ERCP to remove stones
● Extracorporeal shock-wave lithotripsy
(ESWL)
● Laparoscopic cholecystectomy
● Transhepatic Biliary Catheter
● Drug therapy
○ Analgesics and Anticholinergics
Antispasmodics
○ Fat-soluble vitamins and Bile
salts (help digestion and vitamin
absorption)
 Type 2 Diabetes mellitus
For Diabetes mellitus ● Accounts for the majority of Diabetes
● A chronic multisystem disease cases
characterized by hyperglycemia from ● Characterized by a combination of
abnormal insulin production, impaired inadequate insulin secretion and insulin
insulin use, or both resistance
● Absent or insufficient insulin supply ○ The body either does not make
and/or ineffective use of the available enough insulin or does not use it
insulin effectively
Glucose and Insulin Metab ○ Prolonged high blood glucose
● Insulin = hormone made by the Beta cells levels require Beta cells to work
in the islets of Langerhans in the pancreas harder so that they can produce
● Pancreas continuously releases insulin enough insulin to lower blood
into the bloodstream in small amounts glucose levels
after ingesting food ● Risk factors include
● Insulin helps to transport glucose from the ○ Family history
bloodstream across the cell membrane ○ Overweight or obesity
into the cell ○ Being older
● Cells then break down glucose to make ● Common manifestations include
energy ○ Polyuria
● The liver stores excess glucose as ○ Polydipsia
glycogen ○ Polyphagia
● During fasting, fall in insulin levels ○ Recurrent infections
allows release stored glucose from the ○ Fatigue
liver, protein from the muscle, and fat ○ Recurrent vaginal yeast or
from adipose tissue candida infections
● Glycogenolysis then gluconeogenesis ○ Prolonged wound healing
○ Vision problems

Diagnostics:
Underlying medical conditions 1. A1C of 6.5% or higher
● DM occurs in some people because of 2. Fasting plasma glucose level of 126
another medical condition or treatment of mg/dL or higher
a medical condition that can cause 3. A 2-hour plasma glucose level of 200
abnormal glucose levels mg/dL or greater during an oral glucose
○ Cushing syndrome tolerance test (OGTT) using a glucose
○ Hyperthyroidism (red half life load of 75 g
insulin) 4. In a person with classic symptoms of
○ Pancreatitis hyperglycemia or hyperglycemic crisis, a
○ Cystic fibrosis random plasma glucose level of 200
○ Hemochromatosis mg/dL or greater
○ Parenteral nutrition (TPN)
○ Medications such as
corticosteroids, thiazides
(hypokalemia), phenytoin, and
atypical antipsychotics
● DM caused by medical conditions or
drugs usually resolves once the
underlying condition is treated or
removed
Type 1 Diabetes mellitus Gestational Diabetes
● Generally affects people under 40 years of ● Develops during pregnancy
age but can occur at any age ● Mother at a higher risk for cesarean
● An autoimmune disorder in which the delivery
body develops antibodies against insulin ● The baby is at a higher risk for perinatal
and/or the pancreatic Beta cells that make death, birth injury, or neonatal
insulin complications
● Patient not producing enough insulin to ● Risk factors include
survive ○ Obesity
● Strong genetic link ○ Advanced maternal age (>35
● Pancreas can no longer make enough years)
insulin to maintain normal glucose levels ○ Family history of DM
● The onset of symptoms is usually rapid ● Women are screened using an OGTT at 24
○ Ketoacidosis/DKA (a life to 28 weeks of gestation
threatening condition causing ● Most women‘s glucose levels return to
metabolic acidosis) normal within 6 weeks postpartum
■ Acid builds up in the ● Placental hormones can block insulin ->
blood to levels that can be hypoglycemia. Mom cant produce enough
life threatening insulin for the pregnancy*
■ Since the body cannot ● Fat baby = fetal macrosomia
produce insulin, fat is
then broken down for
energy
■ Ketones, which are acids,
build up in the blood and
collect in the urine
■ Fruity breath
■ Fast, deep breathing
(Kussmaul breathing)
○ Polydipsia (Excessive thirst)
○ Polyphagia (Excessive hunger)
body uses up all the fat and
protein for energy
○ Polyuria (Frequent urination)

Polyuria drives the polydipsia bc dehydration

Insulin Storage Insulin Pumps
● Insulin has special storage considerations ● Delivers a continuous subcutaneous
● Extreme temperatures alter insulin and insulin infusion through a small device
can make it less effective worn on the belt, in a pocket, or under
● Unopened insulin = stored in fridge clothing
● Opened insulin = room temperature for up ● Use rapid acting insulin
to 1 month ● The insulin is loaded into a cartridge and
● Avoid exposing insulin to sunlight is connected via plastic tubing to a
● Prefilled insulin syringes with 2 different catheter inserted into the subcutaneous
insulins are stable for up to 1 week when tissue
stored in the refrigerator ● All pumps are programmed to deliver a
continuous infusion 24 hours a day known
as the basal rate
Insulin Administration ● The basal rate can be adjusted based on
● Before injection, gently roll prefilled carbohydrate consumption, activity, or
syringes between the palms 10 to 20 times illness
to warm the insulin and resuspend the ● During mealtimes, the pumps can be
particles programmed to deliver a bolus dose of
● Rotate the injection site to prevent insulin
lipodystrophy ● The infusion set should be changed every
● 1 mL contains 100 units of insulin 2-3 days and placed in a new site to avoid
● It is preferred that an insulin syringe is infection
used to administer insulin ● Insulin pump users check their glucose
● 0.3 mL, 1.0 mL, or 0.5 mL syringes are levels at least 4 times per day or use a
also options continuous glucose monitoring (CGM)
● Do not recap used needles! system
● Insulin is typically injected at a 90 degree ● Type 1 Diabetics are more likely to have
angle and subcutaneously an insulin pump
● Some pumps offer the following features:
Steps to Administering Insulin ○ Alarms to alert you if your
1. Wash hands thoroughly glucose level is out of range if
2. Always inspect insulin vial before using it. your CGM communicates with
Check the expiration date your pump
3. Gently roll the insulin vial between the palms of ○ Connectivity to phone apps and
the hands to mix the insulin. Do not shake insulin other smart devices
to minimize the introduction of air bubbles ○ Options to manually increase or
4. Choose the right injection site decrease insulin
5. Ensure that the site is clean and dry ● The average cost is around $6,000 and
6. Push the needle straight into the skin (90-degree they last around 3-4 years
angle). If the patient is very thin, muscular, or you
are using an 8 or 12 mm needle, you may need to
pinch the skin and/or use a 45-degree angle
7. Push the plunger all the way down, leave the
needle in place for 5 seconds to ensure that all
insulin is injected, and then remove the needle
8. Destroy and dispose of single-use syringe safely

Problems with Insulin Inhaled Insulin

 ● Allergic reactions ● Afrezza is a rapid-acting inhaled insulin
○ Local reactions: itching, redness, ● It is given at the beginning of each meal
and burning around the injection or within 20 minutes after starting a meal
site ● Should not be used to treat DKA
○ A true insulin allergy is rare ● ● Contraindicated in patients who have
● Lipodystrophy asthma, COPD, chronic lung disease, or
○ Changes in subcutaneous fatty who smoke due to the risk of
tissue if the same site is used bronchospasm
frequently ● Side effects include hypoglycemia, cough,
● Somogyi effect: A high dose of insulin and throat pain or irritation
causes a decline in glucose levels during
the night which can stimulate Oral and Non-insulin injectable Agent
gluconeogenesis and ultimately causes
rebound hyperglycemia in the morning
○ Check glucose levels between 2-4
am for hypoglycemia
○ Treatment involves a bedtime
snack or reducing the dose of
insulin
● Dawn phenomenon: Hyperglycemia that
is present on awakening caused by GH
and cortisol that are excreted in increased
amounts in the early morning hours Glucagon Like Peptide-1 (GLP-1) Receptor
○ An increase in insulin or an Agonists
adjustment in administration time
is the most common treatment

Nutrition Therapy Blood Glucose Monitoring

● Carbohydrates ● A critical part of blood glucose
○ Fruits, vegetables, grains, management
legumes, and low-fat milk ○ ● Allows the patient to make decisions
○ Monitor by carb counting, about food intake, activity patterns, and
exchange lists, or appropriate drug dosages
proportions ● Produces accurate records of daily
○ Fiber intake at 14 g/1000 kcal/day glucose fluctuations and trends and alerts
● Protein and Fat ● People who perform BGM use portable
○ More than 2 servings of fish per blood glucose meters
week to provide polyunsaturated ● Disposable lancets are used to get a small
fatty acids ○ drop of capillary blood that is placed in a
○ Consume fats from plant products reagent strip
● Alcohol ● CGM uses a sensor inserted
○ Limit to a moderate amount (1 subcutaneously and display a new glucose
drink/day for women, 2 every 1-5 minutes and assesses interstitial
drinks/day for men) glucose which lags behind blood glucose
○ Consume alcohol with food to by 5-10 minutes
reduce the risk of hypoglycemic
episodes

Exercise Steps of Blood Glucose Monitoring

● Regular, consistent exercise is an essential 1. Wash and dry hands completely. It is not
part of DM management necessary to clean the site with alcohol, and it may
● ADA recommends people with DM interfere with the results (falsely lowers)
engage in at least 150 minutes/week of a 2. If it is hard to get an adequate drop of blood for
moderate-intensity aerobic activity and to monitoring, warm the hands in warm water or let
perform resistance training 2 to 3 times a the arms hang dependently for a few minutes
week unless contraindicated before making a finger puncture 3. Position the
● Exercise decreases insulin resistance and lancet on the side of the finger because there are
direct effect on lowering blood glucose fewer nerve endings
levels 4. Make a puncture just deep enough to get a
● People who use drugs that can cause sufficiently large drop of blood
hypoglycemia should exercise about 1
hour after a meal or have a 10-15 g carb
snack and check their glucose before
exercising
● Before exercise, if glucose is >250 mg/dL
in a Type 1 Diabetic and ketones are
present, delay vigorous activity until
ketones are gone to prevent a
hyperglycemic episode
Diabetic Ketoacidosis (DKA) Hyperosmolar Hyperglycemia Syndrome
● Profound deficiency of insulin (HHS)
● Hyperglycemia, ketosis, acidosis, and ● Life-threatening syndrome in patients
dehydration with DM able to make enough insulin to
● More likely occur in Type 1 DM prevent DKA but not enough insulin to
● Factors: illness, infection, inadequate prevent severe hyperglycemia
insulin dosage, undiagnosed Type 1 DM, ● Common causes: infections (UTIs,
lack of education/resources, neglect pneumonias, sepsis), an acute illness, and
Pathophysiology of DKA newly diagnosed type 2 DM
● Circulating supply of insulin insufficient, ● Impaired thirst sensation and/or a
glucose cannot be properly used for functional inability to replace fluids
energy ● Neurologic manifestations:
● The body compensates by breaking down ○ Somnolence, coma, seizures,
fat stores as a secondary source of fuel hemiparesis, and aphasia
● Ketones = acidic by-products of fat ● A glucose greater than 600 mg/dL
metabolism -> serious problems when ● Has a high mortality rate
excessive in the blood
● Ketosis alters pH balance = metabolic Hypoglycemic Episodes
acidosis develop ● Too much insulin proportion to available
Manifestations DKA glucose in the blood
● Dehydration (dry mucous membranes, ● Glucose level of less than 70 mg/dL
tachycardia, and orthostatic hypotension) ● Glucose level drops = autonomic nervous
● Lethargy and weakness system activated = releases epinephrine
● Soft and sunken eyes ○ Shakiness, palpitations,
● Kussmaul respirations (exhaling excessive nervousness, diaphoresis, anxiety,
CO2 to compensate for metabolic hunger, and pallor occur
acidosis) ● The brain needs glucose to function
● A blood glucose level of 250 mg/dL or efficiently (Difficulty speaking, visual
greater changes, stupor, confusion, and coma)
● Arterial blood pH of less than 7.3 and Hypoglycemia Emergency Management*
serum bicarbonate of less than 16 mEq/L ● Check glucose at the first sign of
DKA Emergency Management hypoglycemia (need an order)
1. Ensure patent airway ● Determine the cause of the hypoglycemia
2. Give O2 via nasal cannula/ non rebreather and correct condition
mask Conscious patient
3. Establish IV access w/ large-bore catheter ● Have pt eat or drink 15-20 g quick-acting
4. Begin fluid resuscitation with 0.9% NaCl carbs (4-6 oz of soda/OJ, 5-8 lifesavers, 1
solution 1 L/hour until blood pressure is tbsp syrup/honey, 4 tsp jelly)
stable and urine output is >30 mL/hour ● Wait 15 minutes and recheck the glucose
5. Begin continuous regular (short acting) ● If glucose is <70 mg/dL, have patient eat
insulin drip 0.1 units/kg/hour or drink another 15-20 g of carbs
○ It is important to prevent rapid ● Once the glucose level is stable = give
drops in serum glucose to avoid patient additional food of carbs plus
cerebral edema (give insulin protein or fat
slow) Unconscious patient
○ Insulin allows water, glucose, and ● 1 mg glucagon subcutaneous or IM or IV
potassium to enter into the cells administration of 20-50 mL of 50%
and can result in hypokalemia glucose
● Identify history of DM, time of last food, ● Turn the patient on the side to prevent
time and amount of last insulin injection aspiration
T3 and t4 low TSH high Thyroid Hormones
TSH low t3 and t3 high ● Thyroid stimulating hormone (TSH) ○
○ Produced by the anterior pituitary
Goiter = incr release thyroid hormones gland
○ Prompts the thyroid gland to
Throid Disorders make and release thyroid
hormones into the blood
Thyroid Anatomy and Physiology ● Triiodothyronine (T3)
● The butterfly-shaped organ located in the ○ A thyroid hormone with 3 iodines
neck ○ Active form
○ Wrapped around the trachea and ● Tetraiodothyronine/Thyroxine (T4)
is anterior to it ○ Thyroid hormone with 4 iodines
○ Just inferior to the larynx ○ Inactive form
○ The medial region, called the ○ 80% mainly secreted directly
isthmus, is flanked by left wing from the thyroid gland and is then
and ring wing lobes converted to T3 in a process
○ Each of the thyroid lobes are called deionization
embedded with parathyroid ● Thyrotropin releasing hormone (TRH)
glands on the posterior surfaces ○ Produced by the hypothalamus
○ Low levels of T3 and T4
stimulate the release
○ Triggers the secretion of TSH

Functions of Thyroid Hormones Goiter

● T3 and T4 influence the body’s basal ● An enlarged thyroid gland due to either an
metabolic rate (the amount of energy used overactive thyroid or an underactive
by the body at rest) thyroid
● T3 and T4 prompt cells to produce ATP ● Most common cause is a lack of dietary
○ An abnormal increase in level of iodine
heat is a byproduct of this process ● Goitrogens - foods or drugs that contain
○ hyperthyroidism have a heat thyroid- inhibiting substances can cause
intolerance (due to an increase in goiter
basal metabolism) ○ Broccoli, brussel sprouts,
● Thyroid hormones incr body’s sensitivity cabbage, cauliflower, mustard,
to catecholamines peanuts, strawberries,
○ High levels of thyroid hormones amiodarone, lithium
will increase SNS activity

Hyperthyroidism Graves Disease

● Hyperactivity of thyroid gland w/ sust incr ● Autoimmune disease; enlargement and
synth and rel thyroid hormones excess thyroid hormone secretion
● Most common form is Graves Disease ● The exact cause is unknown
● Other causes include: ● Risk factors: lack of iodine, smoking,
○ Toxic nodular goiter infection, genetic factors, and stress
○ Thyroiditis ● Develops auto antibodies to TSH
○ Excess iodine intake receptors which attach and stimulate the
○ Pituitary tumors release of T3 and T4 hormones from the
○ Thyroid cancer gland
● Diagnostic studies: ● Can lead to destruction of the thyroid
○ Low TSH; Elevated T4 levels tissue, causing hypothyroidism
Hyperthyroidism Manifests Hyperthyroidism - Drug Therapy
● Goiter ● Antithyroid drugs
● Exophthalmos ○ Propylthiouracil (PTU)
● Weight loss ■ Methimazole
● Acropachy (clubbing of the digits) ● Inhibit thyroid
● Increased appetite and thirst hormone
● Increased peristalsis synthesis
● Fatigue and weakness ● Block peripheral
● Vitiligo conversion of T4
● Tremors to T3
● Intolerance to heat ● Results seen betw
● Palmar erythema 4-8 weeks
● Dysrhythmias ● Iodine
○ Lugol solution [prepares for
Thyrotoxicosis/ Thyroid Storm thyroidectomy and antiseptic]
● Physiologic effects or clinical syndrome ○ Potassium iodine
of hypermetabolism resulting from excess ■ prep pt for thyroidectomy
circulating levels of T4, T3, or both by decr thyroid
● Caused by taking excessive thyroid vascularity
hormone, hyperthyroidism, or thyroiditis ■ Tx thyrotoxicosis by
● Signs and symptoms include: inhib release T3 and T4
○ Heat intolerance into circulation
○ Palpitations ■ Have patient mix the
○ Anxiety solution with water or
○ Fatigue juice and take after meals
○ Weight loss ■ Sip the solution through a
○ Muscle weakness straw to not stain the
○ Irregular menses teeth
Thyrotoxicosis - Nursing Considerations ■ Iodine toxicity: s/s
● Requires aggressive treatment - usually in include swelling of
the ICU buccal mucosa, excess
● Provide a calm, cool environment to salivation, N/V, skin
reduce the patient’s irritability and reactions
restlessness ● Beta blockers
● If exophthalmos is present, there is a risk ○ Block SNS and decrease
for corneal injury related to irritation and tachycardia, nervousness, tremors
dryness
○ Dark glasses reduce glare and
prevent irritation from smoke, air
currents, dust, and dirt
○ If the eyelids are unable to close,
tape them shut for sleep
● Monitoring for dysrhythmias [A fib
tachycardia] and decompensation,
ensuring adequate O2, and giving IV
fluids to replace electrolyte losses
secondary to GI loss or diaphoresis
○ [metaboic acidosis loss of bases]
Hyperthyroidism - Alternative Treatments Thyroidectomy - Nursing Considerations
● Radioactive Iodine Therapy (RAI) ● Monitor airway and respiratory status
○ The treatment of choice for most ○ Keep suction equipment, O2, and
nonpregnant adults tracheostomy tray available at the
○ Damages or destroys thyroid bedside
tissue and limits thyroid hormone ○ Keep the patient at a minimum of
secretion Semi Fowler’s
○ Delayed response and the effects ○ Assess the airway for s/s tracheal
may not be seen for up to 3 decompression, hemorrhage
months ■ Neck swelling, irregular
○ Home Precautions breathing, frequent
■ Use private toilet swallowing, choking,
facilities when possible sensations of fullness at
■ Flush 2 or 3 times after incision sites, blood on
each use the dressings
■ Launder separate towels, ● Monitor for postoperative complications
bed linens, and clothes ○ Hypothyroidism
■ Do not prepare food for ○ Damage to or inadvertently
others where it requires removing the parathyroid glands
prolonged bare hands (causes hypocalcemia)
● Thyroidectomy (surgery) ■ Have IV calcium
○ thyroid gland compressing on available at the bedside
their trachea, have thyroid cancer, ■ Monitor for Trousseau or
or do not respond to thyroid Chvostek signs
therapy ○ Laryngeal nerve damage and
○ Rapid reduction in thyroid levels vocal cord paralysis
● Nutrition Therapy ■ Laryngeal stridor - harsh,
○ A high-calorie diet of 4,000-5,000 vibratory sound due to
calories edema of the laryngeal
○ Avoid caffeine nerve
○ Avoid highly seasoned and high
fiber foods

Hypothyroidism Hashimoto’s Thyroiditis Disease

● Deficiency thyroid hormone = general ● An inflammation of the thyroid gland that
slowing of metabolic rate frequently causes goiter
● Increased TSH and decreased T4 levels ○ Compress structures in the neck
● Primary hypothyroidism (trachea, laryngeal nerves)
○ destruction of thyroid tissue or ● Caused by the autoimmune destruction of
defective hormone synthesis thyroid tissue by antibodies
● Secondary hypothyroidism ● Risk factors include female gender, a
○ Pituitary diseases with decr TSH family history, older age, white ethnicity
secretion or hypothalamic ● At first, T4 and T3 levels are increased
dysfunction with decr and then decrease with time
thyrotropin-releasing hormone ○ The antibodies destroy the thyroid
(TRH) secretion tissue and cause the release of
● Common causes include: hormones from the damaged
○ Iodine deficiency (most common) tissue
○ Atrophy of the thyroid gland
(Hashimoto or Graves disease)
 ○ Treatment of hyperthyroidism Hypothyroidism - Manifestations
○ Infancy (Cretinism) thyroid ● Cardiac hypertrophy [low SNS stim= low
hormone deficiencies during HR] ● Myxedema (Mask-like effect) ●
neonatal life Anemia ● Constipation ● Decreased
● Diagnostic studies include: appetite ● Weight gain ● Distended
○ Elevated TSH abdomen ● Enlarged, scaly tongue ●
○ Low T4 Celiac disease ● Fatigue/weakness ●
Forgetfulness ● Lethargy ● Cold
intolerance ● Goiter ● Thick, inelastic
cold skin thin brittle hair

Hypothyroidism - Drug Therapy Hypothyroidism - Nursing Considerations

● Replace the thyroid hormones ● Discuss the need for lifelong hormone
● Levothyroxine =T4, Liothyronine= T3 replacement therapy
○ The first dosages are low to ● Caution patient avoid switching thyroid
prevent increases in resting HR medications bc bioavailability of the
and BP hormones may differ
○ Instruct the patient to take the ● Comfortable, warm environment bc cold
medication first thing in the intolerance
morning on an empty stomach to ● Discuss ways to prevent constipation
prevent insomnia ○ Use of stool softeners
○ It can take up to 8 weeks before ○ Increase activity
the full effect of hormone therapy ○ Increase fiber and fluid intake
is seen ○ Pt avoid enemas bc cause vagal
○ Report HR greater than 100, chest stimulation and harmful if
pain, tremors, or insomnia cardiovascular manifestations

Renal and Urinary Classification UTI (ascending)

Function ● Upper or lower UTI
● Filter blood and create urine as waste ● Cystitis = inflammation bladder
byproduct ● Urethritis = inflammation of urethra
● Eliminate liquid waste called urea; keep ● Urosepsis = spread systematically, life
chemicals K+ Na+ and water in balance threat emergency
● Regulates blood pressure ● Pyelonephritis = inflamm renal
● Produce EPO = RBC prod in bone parenchyma and collect system
marrow
● Regulate acid base balance UTI Patho
● Urea prod when foods (meat poultry and ● Antibacterial properties urine (pH 6-7.5)
vegetables broken down) and antimicrobial proteins
● Nephrons = tiny filtering units ● Catheters = contribute to introd pathogens
● Each nephron has ball formed small blood
capillaries = glomerulus UTI Manifests
● Small tube = renal tubule ● Dysuria ● Hesitancy ● Urinary retention
● 30 mL/hr adequate urinary output or incomplete emptying ● Post Void
RAAS dribbling ● Incontinence ● Nocturia ●
● When BP falls, kidneys release renin Urgency ● Urinary frequency ●
● Renin -> angiotensinogen -> angiotensin I Suprapubic discomfort or pressure ●
-> angiotensin II via ACE -> Hematuria ● In older adults: impaired
vasoconstrictor cognition
UTI Urinary Tract Infection UTI Diagnostics
● E coli comon causing ● Dipstick urinalysis (presence of nitrites;
● Risk Factors (Congenital defects leading leukocyte esterase enzyme present in
to obstruction or urinary stasis, obesity, WBCs indicating pyuria)
shorter female urethra, colonization from ● Clean-catch urine sample
normal vaginal flora, catheters, foreign ○ Catheterization is an option if you
bodies, habitual delay urination (Nurse’s cannot obtain a clean-catch
bladder), sexual activity urinary retention specimen
poor personal hygiene constipation) ● Urine culture with sensitivity

UTI Drug Therapy Acute Pyelonephritis

● Trimethoprim/Sulfamethoxazole ● Inflammation of the renal parenchyma
(Bactrim) and collecting system, including the renal
○ Sulfonamides pelvis (mostly caused by infection)
○ Avoid in patients with sulfa ● Starts in the renal medulla and spreads to
allergies the adjacent cortex
○ Take this medication with a full ● Infection of the lower urinary tract via the
glass of water ascending urethral route
○ Do not mix with alcohol - ● May require hospitalization
Disulfiram reaction ○ IV antibiotics
● Nitrofurantoin (MacroBID) ○ Urosepsis = bacteriuria and
○ Nitrofuran bacteremia
○ Take with food ○ Pt dc when stable on PO
○ Do not mix with alcohol antibiotics
● Cephalexin (Keflex) ○ Pt w/ mild mod sympt tx out pt on
○ Cephalosporin antibiotics 5-14 days
○ Do not mix with alcohol ● Risk factors: (Pregnancy, Vesicoureteral
Disulfiram reaction reflux (backward mvmnt urine from lower
● Amoxicillin to upper urinary tract); Lower urinary
○ Penicillin tract obstruction (BPH, stones, stricture)
○ Increases risk for C diff Acute Pyelonephritis Manifestations
○ Take on an empty stomach with a ● Fever/chills ○ Nausea/vomiting ○ Malaise
full glass of water ○ Flank pain ○ Costovertebral angle
● Ciprofloxacin tenderness to percussion ○ Dysuria,
○ Fluoroquinolones urgency, frequency
○ Can cause an Achilles tendon Acute Pyelonephritis Diagnostic studies
rupture ● Ultrasound ○ CT scan ○ Urinalysis or
○ For complicated UTIs culture ○ Blood cultures
● Phenazopyridine (AZO)
○ Not recommended for longer than Nursing Care for UTIs
48 hours ● Maintain adequate fluid intake
○ Urine will be orange ● Avoid bladder irritants
○ Caffeine, alcohol, citrus juices,
Prevention CAUTIs chocolate, spicy foods,
● Avoid unnecessary catherization carbonated beverages
● Early removal indwelling catheters = most ● Apply heat to the suprapubic area or
effective means lower back
● Follow aseptic technique ● Taking the full course of antibiotics
● Educate patient on how to prevent UTIs
Urinary Tract Calculi (Renal Calculi) Types of Urinary Stones
● Nephrolithiasis (Renal calculi)
● Common in Whites and Asians
● More often in the summer months (hot
climate and dehydration)
Patho
● Crystal-forming substances are not diluted
by the kidney or the kidney’s ability to
keep crystals from sticking together is
reduced
● The higher the pH, the less soluble are
calcium and phosphate
● The lower the pH, the less soluble are uric Renal Calculi Manifests
acid and cystine ● Severe pain begins suddenly in flank area,
Risk Factors back, or lower abdomen
● Warm climates ● Renal colic - results from stretching,
● Excess tea or fruit juices that increase dilation, and spasm of the ureter in
urinary oxalate level response to the obstructing stone
● Large intake of proteins that increases uric ● ● Nausea and vomiting ● Manifestations
acid excretion can occur as a result of the obstruction of
● Large intake of salt, low calcium intake urine flow ○ Dysuria, fever, chills ●
● Low fluid intake that increases urine Diaphoresis ● Testicular or labial pain ●
concentration Costovertebral flank pain
● Family history
● Obesity or sedentary lifestyle Renal Calculi Diagnostics
● Metabolic abnorm incr urine pH, calcium, ● Noncontrast CT ● Ultrasound ● Complete
oxalate, or uric acid levels urinalysis ● Measuring urine pH Alkaline
● Genetics - Struvite stones ○ Acidic - Uric acid or
cystine stones ● Retrieval and analysis of
the stone ● Bloodwork ○ Serum calcium,
phosphorous, sodium, potassium,
bicarbonate, uric acid, BUN, creatinine
Renal Calculi Drug Therapy Endourologic Procedures
● Alpha Blockers ● If the stone is in the bladder, a cystoscopy
○ Tamsulosin, Terazosin is done to remove small stones
○ Help to relax the smooth muscle ● Transurethral or percutaneous suprapubic
of the ureter cystolitholapaxy
● NSAIDs ○ Ibuprofen, naproxen ○ ○ Ultrasonic or laser energy or an
Contraindicated in renal impairment ○ instrument called a lithotrite
Anti-inflammatory ○ Relieve colic pain ● (stone crusher) is used to break up
Opioids ○ Morphine, Hydromorphone, the stone
Fentanyl ○ Relieve colic pain ○ ○ Used for larger stones
Contraindicated in respiratory rate < 12, ○ The bladder is then irrigated and
low BP or HR the stone is washed out
● Cystoscopic lithotripsy
Renal Calculi Nursing Management ● Percutaneous nephrolithotomy
● Most stones are 4 mm or less in size and ○ A nephroscope is inserted into the
pass spontaneously kidney pelvis through a track in
● May take weeks for stones to pass the skin
● Educate pt on adequate hydration, sodium ○ The track is created in the
restrictions, diet changes, and medications patient’s back
● Prep pt for removal of stones if indicated ○ The kidney stones are
● Administer pain medications fragmented, removed, and the
● Obtain diagnostic tests pelvis is irrigated
○ A percutaneous nephrostomy tube
Renal Calculi Tx can be left in place to ensure the
● Endourology, lithotripsy, or open surgical ureter stays unobstructed
stone removal may be used if
○ Stone is too large for spontaneous Lithotripsy
passage (greater than 5 mm) ● A procedure to break up stones, allowing
○ Stones with bacteriuria or them to pass from the urinary tract
symptomatic infection are present ● Laser lithotripsy
○ Stones are causing impaired renal ● Extracorporeal shock wave lithotripsy
function (ESWL)
○ Stones are causing persistent pain, ● Ultrasonic lithotripsy
nausea, or paralytic ileus ● Electrohydraulic lithotripsy
○ Patient is unable to be treated
medically Renal Calculi Nutrition Therapy
○ Patient only has 1 kidney ● The patient should drink adequate fluids
to avoid dehydration (3 L/day)
○ When the patient has an active
stone present, do not force fluids
as this can increase renal colic
● A low-sodium diet is best
● Limit soda, coffee, and tea intake
Acute Kidney Injury (AKI) Acute Kidney Injury - Common Causes
● Encompass the entire scope of the ● Intrarenal AKI ○ direct damage to the
syndrome, ranging from a slight kidney tissue resulting in impaired
deterioration in kidney function to severe nephron function ○ Common causes ■
impairment Interstitial nephritis ● Allergies to
● Rapid loss of kidney function with or antibiotics, NSAIDs, or ACE inhibitors ●
without decreased urine output Infections ■ Nephrotoxic injury ●
● Progressive increases in blood urea Chemical exposure ● Contrast media ●
nitrogen (BUN), creatinine, and potassium Aminoglycosides, amphotericin B ●
● Result in azotemia (an accumulation of Hemolytic blood transfusion reaction ■
nitrogenous waste products such as urea Other ● Acute glomerulonephritis ●
nitrogen and creatinine) Malignant hypertension ● SLE ●
● Follows prolonged hypotension, Thrombotic disorders
hypovolemia, or exposure to a Intrarenal Patho
nephrotoxic agent ● Intrarenal ○ The damage from the
Intrarenal causes usually results from
Acute Kidney Injury Common Causes Causes prolonged ischemia, nephrotoxins,
● Prerenal AKI ○ Factors that reduce hemoglobin released from RBCs, or
systemic circulation causing decreased myoglobin released from necrotic muscle
renal blood flow ○ Common causes ■ cells ○ Acute tubular necrosis ■ Caused
Decreased Cardiac Output ● Cardiogenic by ischemia, nephrotoxins, or sepsis ■
shock ● HF or MI ● Dysrhythmias ■ Causes a disruption in the basement
Decreased Peripheral Vascular Resistance membrane and patchy destruction of the
● Anaphylaxis ● Neurologic injury ● tubular epithelium ■ Necrosis of the
Septic shock ■ Decreased Renovascular tubular epithelial cells slough off and plug
Blood Flow ● Embolism or renal vein the tubules
thrombosis ■ Hypovolemia ● Burns ● GI Acute Kidney Injury - Common Causes
losses ● Hemorrhage ● Dehydration ● Postrenal AKI ○ Involve mechanical
obstruction in the outflow of urine ○
Prerenal AKI Patho Common causes ■ BPH ■ Bladder cancer
● decrease blood flow = decreased ■ Calculi formation ■ Neuromuscular
glomerular perfusion and filtration of the disorders ■ Prostate cancer ■ Spinal cord
kidneys ○ decrease in blood volume, ■ disease ■ Strictures ■ Trauma
Increase in angiotensin ll, aldosterone,
norepinephrine, and antidiuretic hormone Postrenal AKI Patho
○ Prerenal problems can contribute to ● With the flow of urine obstructed, urine
intrarenal AKI refluxes into the renal pelvis, impairing
kidney function
● Bilateral ureteral obstruction leads to
hydronephrosis (kidney dilation), increase
in hydrostatic pressure, and tubular
blockage which results in a progressive
decline in kidney function
Acute Kidney Injury Oliguric Phase AKI Nursing Management
● Urinary Changes ● The first step is to determine if there is
○ Oliguria (less than 400 mL/day) adequate intravascular volume and cardiac
○ Anuria output to ensure adequate kidney
○ Some patients do not experience perfusion
oliguria ○ Possible loop or osmotic diuretics
● Fluid Volume if there is urinary output or
○ Anuria or oliguria lead to fluid diagnosis of AKI is not confirmed
retention ● Fluid restriction (600 mL plus previous 24
○ Neck veins may become hour fluid loss)
distended with a bounding pulse ● Manage hyperkalemia
○ Pulmonary edema, HF ● Dialysis
○ Edema and HTN ● Continuous renal replacement therapy
● Metabolic acidosis (RRT)
○ Impaired kidneys cannot excrete AKI Nutrition
hydrogen ions or the acid ● Adequate calories to prevent catabolism
products of metabolism despite restrictions that prevent electrolyte
○ HCO3 production decreases and fluid problems and azotemia
○ The patient may develop rapid, ● Fat intake is increased
deep respirations to compensate ● Adequate protein intake (0.8-1.0
● Sodium balance g/kg/day)
○ Damaged tubules cannot conserve ● Diet restrictions of sodium, potassium,
sodium phosphate
○ Urinary sodium excretion may
increase Manage Hyperkalemia
● Potassium Excess ● Can cause life threatening dysrhythmias
○ The serum potassium level ● Regular IV insulin
increases because the kidney’s ○ Shifts potassium into the cells
normal ability to excrete ● Sodium Bicarbonate
potassium is impaired ○ May be considered to correct
● Hematologic Problems acidosis and shift potassium into
○ Leukocytosis the cells
○ The most common cause of death ● Calcium Gluconate IV
in AKI is infection ○ Raises the threshold in which
● Waste Product Accumulation dysrhythmias occur
○ The kidneys are the main organs ● Sodium Polystyrene Sulfonate
for urea excretion (an end product (Kayexalate)
of protein metabolism) and ○ Produces osmotic diarrhea,
creatinine excretion (an end allowing for evacuation of
product of endogenous muscle potassium-rich stool
metabolism) ● Patiromer and Sodium Zirconium
● Neurologic Problems ○ Binds potassium in GI tract
○ Accumulation of nitrogenous ● Diet Restriction
waste products in the brain
○ Difficulty concentrating, seizures,
stupor, or coma
Acute Kidney Injury - Diuretic Phase Renal Replacement Therapy (RRT)
● Daily urine output around 1 to 3 L ● Encompass life-supporting treatments for
● High urine volume caused by osmotic renal failure
diuresis from the high urea concentration ● Common indications
in the glomerular filtrate and the inability ○ Volume overload
of the tubules to concentrate the urine ○ High serum potassium level
● Kidneys have recovered the ability to ○ Metabolic acidosis
excrete wastes but not to concentrate urine ○ BUN higher than 120 mg/dL
● Hypovolemia and hypotension can occur ○ Significant change in mental
due to massive fluid loss status
● Monitor electrolyte balances ○ Pericarditis, pericardial effusion,
Acute Kidney Injury - Recovery Phase or cardiac tamponade
● Begins when the GFR increases, allowing ● Peritoneal Dialysis
the BUN and creatinine levels to decrease ○ catheter inserted into abdominal
● Up to 12 months for kidney function to cavity and fill w/ cleansing
stabilize solution contains a type of sugar
● Some patients do not recover and progress that draws out waste and extra
to end-stage kidney disease fluid from the blood vessels into
the solution
AKI Diagnostic Studies ● Hemodialysis
● Urine output ○ Blood is run through a filter in a
● Serum creatinine (waste product in blood dialysis machine that acts as an
that comes from the muscles) artificial kidney to filter out waste
● Urinalysis products and cleans the blood
● Kidney ultrasound ○ Arteriovenous (AV) fistula
● CT scan or MRI needed
Questions I created based on what is important to know*********** please review these!
1. Matching. What are nonmodifiable and modifiable risk factors for CAD
a. Nonmodifiable: Age (Men over 45 and women over 55), Gender (Women), Ethnicity
(White/Black males), family hx, genetics (LDLR gene)
b. Modifiable: High serum lipid levels (LDL >100 mg; HDL <60 mg; total chol >150 mg);
High BP >120/80mmhg, Tobacco, inactivity, BMI >30, diabetes, metab syndrome
2. Whats the difference between primary (essential) HTN and secondary HTN?
a. Primary = unknown cause; secondary = underlying disease process
3. Assessing orthostatic hypotension: decr 20 mmHg or more SBP; decr 1- mmHg or more DBP;
tx drug is Midodrine
a. Step 1: Pt rest supine 3 minutes and take BP HR
b. Step 2: Pt sit, take BP HR
c. Step 3: Pt stand, take BP HR
d. Step 4: Pt stand 3 minutes, take BP HR
4. What are the drugs used for hypertension?
a. Central Acting Adrenergic Agonists (decr sympath outflow and incr vasodilation)
b. Alpha Blockers (block adrenergic effects and incr vasodilation)
c. Beta Blockers (block beta 1 adrenergic effects, decr renin secr)
d. ACE inhibitors (prev conv of angiotensin 1 to angiotensin 2)
e. ARBs (prev angiotensin 2 binding to recept)
f. Calcium channel blockers (prev mvmnt Ca into cells)
5. Chronic Stable Angina: by physical exertion stress, pain radiate to jaw neck shoulder,
subsides with rest, calming down, and SL nitroglycerin (DONT give to pt taking ED meds
Viagra)
6. Unstable Angina: occurs at rest, incr freq and duration, pain longer than 10 min, caused by
MI and emergency tx immediately
a. ST depression = myocardial ischemia or hypokalemia
b. ST elevation = MI
c. T wave inversion = myocardial ischemia
7. Steps for Chronic Stable Angina Nitrate use
i. Step 1: Stop activity
ii. Step 2: take one SL nitrate
iii. Step 3: Wait 5 min
iv. Step 4: Call 911
v. Step 5: 2nd dose nitrate
vi. Step 6: Wait 5 min
vii. Step 7: Take 3rd (max) dose nitrate
8. What are the biomarkers we look at for myocardial infarction (MI)
a. CKMB and Troponin
9. Select all that apply. Left and Right sided heart failure (elevated BNP)
a. Left sided: orthopnea, tachycardia, blood tinged sputum, crackles, wheezes, PND,
fatigue, cyanosis, confusion
b. Right sided (Cor pulmonale): Dependent edema, ascites, enlarged liver and spleen,
JVD, Fatigue
10. Venous Thromboembolism nursing interventions
a. Dont massage dont put on SCDs for active VTE, pillow not under knees, flex extend
feet knees every 2-4 hrs,
b. S/S: unilateral leg edema pain tenderness warmth fullness calf/thigh
11. Complication of MI = Dressler syndrome: pericarditis and fever 1-8 weeks after MI
12. CO= HR*SV (ml/beat)
13. HTN complications: Hypertensive Crisis (>180/ >120) and Left ventricular hypertrophy
heart failure
14. HTN lifestyle modification: Avoid tobacco (nicotine = vasoconstrict), Sodium reduction 2300
mg/day, weight loss (1kg = 1 BP mmHg), Mediterranean diet, Men 2 drinks Women 1 drink
day alcohol
15. Drugs for Hypertension:
a. Selective Beta Blockers (target heart specifically) = metoprolol atenolol esmolol
bisoprolol
b. Alpha Blockers: doxasozin, prazosin, terazosin
c. Central acting adrenergic agonists: Clonidine given PRN (sedative med)
d. ACEi (Captopril and Lisinopril) = Hyperkalemia, angioedema, dry hacking cough
e. ARBS (Losartan) = Hyperkalemia, angioedema, dry hacking cough
f. Calcium channel blocker (amlodipine, diltiazem, verapamil, nicardipine) “a very
nice day” interacts with grapefruit juice
16. Bile acid sequestrants (Cholestryramine, lipid lowering agent) = causes constipation
17. HMG-CoA Reductase inhibitors (Simvastatin/Atorvastatin) = causes leg muscle cramps and
rhabdomyolysis)
18. Aortic Dissection = can become cardiac tamponade
19. Aortic Aneurysm = common white men; if rupture retroperitoneal space = controlled
bleeding; if rupture thoracic abdom cavity = can die hypovolemic shock
20. Antidotes for VTE drugs: Heparin = Promatine Sulfate; Warfarin (vitam K antag) = vitamin
K, Factor Xa Inhib (Apixaban) = Andexanet Alfa; Synthetic Thrombin inhib (Dabigatran)
= Idarucizumab
21. What are the three factors of Virchow Triad regarding venous thrombosis
a. Hypercoagulation, Damage of endothelium, Venous stasis (HDV)
22. The nurse is assessing a patient with abdominal pain. How will the nurse document ecchymosis
around the area of umbilicus? a. Cullen‘s sign b. McBurney‘s sign c. Grey-Turner‘s sign
23. Acute Pancreatitis considerations and manifests: LUQ pain,
a. Cullen Sign: bluish periumbilical discoloration
b. Grey Turner: Bluish flank discoloration
c. Interventions: NPO status and NG suction
d. Common cause: gallbladder disease then alcohol use
e. can cause hypocalcemia
24. Labs for pancreatitis→ increased amylase and lipase
25. Complications of GERD: airway complications such as cough and bronchospasms Barret
esophagus→ flat epithelial cells turn into columnar epithelial cells, risk for esophageal
cancer
26. EGD procedure: assess for return of gag reflex; they are at risk for aspiration
27. Peptic ulcer disease PUD perforation: rigid boardlike abdomen and severe upper abdominal
pain radiate to back, can become septic
28. Gastric vs Duodenal ulcers
a. Gastric: epigastric discomfort, 1-2 hrs after meals, food worsen pain, “burning”,
“gaseous”
b. Duodenal: 2-5 hours after meals, “burning”, “Cramplike”, food/meals buffer acid,
gastric acid contact with ulcer
29. Cholelithiasis (Gallbladder stones) manifests and considerations: RUQ pain tenderness, dark
amber brown urine
a. Risk factors: oral contraceptive use and postemopausal women
30. Upper GI bleeding considerations:
a. Hematemesis: bright red blood coffee ground
b. Melena: black tarry stool, upper GI bleed or taking iron supplements
c. Occult Bleeding: small amout of blood in gastric sectretions vomitus or stool
31. Obesity body shapes: Android (apple) fat in abdomen, Gynoid (pear) fat in upper legs
32. Physical activity for HTN and obesity = (150 min mod exerc/ 75 min vig exerc weekly)
33. What is the difference between the hormones Ghrelin vs Leptin:
a. Ghrelin: inhibits leptin, stimulate hunger acts on hypothalamus;
b. Leptin: acts on hypothalamus and suppress appetite
34. People who use drugs that can cause hypoglycemia should exercise about 1hr after meal or
have 10-15g carb snack and check glucose before exercising
a. Before exercise, if glucose >250 mg in Type 1 DM and ketones present = delay
vigorous activity until ketones gone to prevent hyperglycemic epsiode
35. Gestational diabetes nursing considerations: placental hormones can block insulin causes
hypoglycemia; fat baby = macrosomia)
36. Inhaled insulin = Afrezza rapid acting; NOT used for DKA, contraindicated COPD asthma;
It is given at the beginning of each meal or within 20 minutes after starting a meal
37. Insulin pumps use what insulin type: Rapid acting (LAG Lispro Aspart Glulisine)
38. Somogyi Effect: high dose insulin = decline glucose at night = gluconeogenesis = rebound
hyperglycemia morning
a. Dawn phenomenon: hyperglycemia present awakening, GH and cortisol excreted incr
amts early morning; solution = incr insulin or adjust admin time
39. Alcohol causes hypoglycemia; give insulin for hyperkalemia
40. Diabetes Diagnostics and Interventions:
a. For diabetes: A1c > 6.5; fasting plasma glucose level of >126 mg;
41. For DKA (type 1 DM ): >250 mg blood glucose, Kussmaul respirations fruity breath
i. Give O2, establish large bore IV, give fluids NS, give regular (short acting
insulin), identify hx of DM, time of last food, time/amt of last insulin inject
42. For HHS (type 2 DM): blood glucose >600 mg; neurologic, not enough insulin prev severe
hyperglycemia
43. What are the nursing interventions for conscious and unconscious patient with hypoglycemia?
a. Conscious: Give pt 15-20g carbs (4-6 oz soda or OJ, 5-8 lifesavers, 1 tbsp honey or
syrup, 4 tsp jelly), reassess glucose lvl, then another 15-20g carbs
 b. Unconscious: 1 mg glucagon SQ or IM, 20-50mL of 50% glucose) and turn pt on side
prevent aspiration
44. Select all the possible goitrogens: Broccoli, brussel sprouts, cauliflower, mustard, peanuts,
strawberries, amiodarone, lithium
a. Goiter: overactive or underactive thyroid; lack of dietary iodine
45. Nursing considerations of pt taking levothyroxine: lifelong therapy, take first thing morning
empty stomach, may take up to 8 weeks full effect, report HR >100 bpm, chest pain tremor
insomnia
46. Thyroid hormones incr the body sensitivity to what? Catecholamines
47. During thyrotoxicosis (thyroid storm) what are some important nursing interventions?
a. If exopthalmos present, risk for cornea injury = dark glasses or if unable to close
tape them shut for sleep
48. Graves Disease: unknown cause, lack of iodine, autoimmune enlargement thyroid and excess
thyroid hormone secretion; exopthalmos, incr appetite thirst, weight loss, tremors, heat
intolerance (hyperthyroidism); incr uptake of iodine
49. Hypothyroidism: S/S constipation, dependent edema, dry coarse brittle hair, hoarseness,
forgetful, nausea vomit, thick brittle nails, cold intolerance, weight gain, dry skin, Celiac
Disease, myxedema (mask-like), low HR; 4000-5000 calorie diet, avoid caffeine an high fiber
a. Causes: iodine deficiency
50. Hyperthyroidism: S/S eyelid retract, hepatomegaly, hyperreflexia of DTR, incr appetite, heat
intolerance, weight loss, irritability, lack ability concentrate, velvety skin, Plummer’s nails, fine
soft hair;
a. Leads to irregular menses (incr prolactin prevents egg release)
b. Causes: excess iodine intake
51. Thyroidectomy considerations: [have trach tray, IV calcium available bedside, monitor
Trousseau (cuff) Chvostek (cheeks), numbness mouth, muscle weakness and cramping =
hypocalcemia]
a. Keep the patient at a minimum of Semi Fowler’s
b. Assess the airway for s/s tracheal decompression, hemorrhage
i. Neck swelling, irregular breathing, frequent swallowing, choking, sensations
of fullness at incision sites, blood on the dressings
52. What are T4 and T3 hormones called?
a. T3 = Triiodothyronine, T4= Thyroxine/Tetraiodothyronine
53. Acute pyelonephritis important nursing interventions: CVA costovertebral angle tenderness,
culture before full course IV Abx; inflammation of renal collecting system
54. What are important nursing considerations when giving insulin? Prevent rapid drops glucose to
avoid cerebral edema; Insulin can result in hypokalemia
55. Renal calculi risk factors: Warm climates, excess tea or fruit urinary oxalate levels, high
intake salt, low calcium intake, high intake proteins = incr uric acid, more common Whites
and Asians)
a. Renal colic: stretch dilation spasm of ureter response to stone
56. UTI most common agent: E. coli
a. Nurse’s Bladder: habitual delay of urination can cause UTI
57. UTI Drugs
a. Trimethoprim/ Sulfamethoxazole (Bactrim)
 i. Avoid in pt w/ sulfa allergy, take with full glass water, not mix alcohol
b. Nitrofurantoin (Macrobid)
i. Take with food, no mix alcohol
c. Cephalexin (Keflex)
i. Do not mix with alcohol
d. Amoxicillin
i. Incr risk for C diff, takes on empty stomach w/full glass water
e. Ciprofloxacin
i. Fluoroquinolones, Achilles tendon rupture
f. Phenazopyridine (AZO)
i. Not recommended longer than 48 hours, urine orange color
58. IVP Intravenous pyelogram nursing considerations: shellfish penicillin allergy
59. AKI nursing considerations: Fluid restriction (600 mL plus previous 25 hr fluid loss), loop or
thiazide diuretics, manage hyperkalemia, dialysis, RRT; diet restriction (sodium potassium
phosphate), adequate protein intake 0.8g to 1g /kg/day, High carb diet
60. Prerenal AKI: decr renal blood flow, decr blood volume
61. Intrarenal AKI: direct damage to kidney/nephron (prolong ischemia, sepsis, necrosis,
NSAIDS and ACE inhibs**)
62. Postrenal AKI: obstruction outflow of urine (BPH, renal calculi)
63. AKI Oliguric Phase: Oliguria (<400 mL/day), anuria, metab acidosis, hyperkalemia,
a. Hyperkalemia management = dysrhythmias, regular IV insulin, calcium gluconate,
sodium bicarbonate
64. AKI Diuretic Phase: daily urine output 1-3L, kidneys recovered ability excrete waste but not
concentrate urine, hypovolemia and hypotension occur;
65. AKI Recovery Phase: GFR incr allow BUN Cr decrease; some dont recover -> end stage
66. What is the most common cause of death in AKI? Infection
67. Stages of Kidney Disease
a. Stage 1 >90 ml/min
b. Stage 2 60-89 ml/min
c. Stage 3A 45-59 ml/min
d. Stage 3B 31-44 ml/min
e. Stage 4 15-29 ml/min
f. End Stage 5 <15 ml/min