NR667 - CEA Week 1-6 Comprehensive Review before Chicago 2026 NR667- CEA FNP NR 667 CEA prep with 100% accurate solutions + rationales -Chamberlain

Hypertension

Hypertension is defined as BP ≥140/90 mmHg (per JNC8).

Non-Black population treatment

Start with thiazide diuretic, ACE inhibitor, ARB, or CCB.

Black population treatment

Start with thiazide diuretic or CCB.

DM or CKD treatment

Include ACE inhibitor or ARB for kidney protection.

Age ≥60 years treatment

Treat if BP ≥150/90 mmHg.

Age <60 years treatment

Treat if BP ≥140/90 mmHg.

Contractility

Force of cardiac muscle contraction.

Preload

Volume in ventricles at end-diastole (central venous volume).

Afterload

Resistance heart must pump against (arterial pressure).

Aortic Stenosis (AS)

Calcification narrows aortic valve → outflow obstruction.

Aortic Regurgitation (AR)

Incompetent aortic valve due to root dilation or endocarditis.

Mitral Stenosis (MS)

Often post-rheumatic fever, calcification of mitral valve.

Mitral Regurgitation (MR)

Commonly due to MI, CHF-induced LV dilation, papillary rupture, or endocarditis.

Direct Oral Anticoagulants (DOACs)

Do NOT require INR monitoring.

Factor Xa inhibitors

Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa).

Direct thrombin inhibitor

Dabigatran (Pradaxa).

Warfarin (Coumadin)

Onset: Delayed — requires bridging with LMWH or heparin.

Bridging with Warfarin

Bridging is required until INR reaches ≥2.0 for at least 24 hours.

Dopamine

Dose-dependent: low = renal perfusion, high = pressor.

Dobutamine

Inotrope (↑ contractility).

Norepinephrine (Levophed)

Vasoconstrictor + mild inotrope.

Epinephrine

Mixed alpha & beta agonist.

Nitroglycerin

Venodilator; ↓ Preload; avoid if hypotensive.

Nitroprusside

Potent arterial/venous vasodilator; risk of cyanide toxicity with prolonged use.

Statins

HMG-CoA reductase inhibitors used as first-line therapy for lipid management.

High-intensity statins

Atorvastatin 40-80 mg daily and Rosuvastatin 20-40 mg daily.

Indications for high-intensity statins

Clinical ASCVD (e.g., MI, stroke), LDL ≥190 mg/dL, Diabetes age 40-75 with ≥7.5% 10-year ASCVD risk.

Ezetimibe

A secondary therapy for mild LDL-lowering, often required before insurance approval of PCSK9 inhibitors.

PCSK9 inhibitors

Injectable monoclonal antibodies reserved for very high-risk patients or statin-intolerant.

ASCVD

Atherosclerotic Cardiovascular Disease, includes MI, stroke, angina, revascularization, and peripheral artery disease.

10-year risk categories

Low risk: <5%, Moderate risk: 5%-7.4%, High risk: ≥7.5%, Very high risk: ≥20% or known ASCVD.

Aortic Stenosis (AS)

Caused by calcification of the valve leading to outflow obstruction, with a classic triad of angina, syncope, dyspnea.

Aortic Regurgitation (AR)

Occurs when the valve fails to close, leading to wide pulse pressure and bounding pulses.

Mitral Stenosis (MS)

Often caused by post-rheumatic fever, symptoms include dyspnea, orthopnea, and atrial fibrillation.

Mitral Regurgitation (MR)

Caused by papillary muscle rupture, dilated LV, or endocarditis, characterized by a holosystolic murmur.

HFrEF

Heart failure with reduced ejection fraction, defined as EF <40% and associated with systolic dysfunction.

HFpEF

Heart failure with preserved ejection fraction, defined as EF ≥50% and associated with diastolic dysfunction.

First-line medications for HFrEF

Include beta-blockers (Carvedilol, metoprolol succinate, bisoprolol), ACE inhibitors or ARBs, loop diuretics, and spironolactone.

Shock categories

Include hypovolemic, cardiogenic, distributive, and obstructive types.

Hypovolemic shock

Caused by hemorrhage or dehydration, treated with fluids and blood products.

Cardiogenic shock

Caused by MI or CHF, treated with inotropes (dobutamine) and vasopressors.

Distributive shock

Caused by sepsis or anaphylaxis, treated with vasopressors (norepinephrine) and fluids.

Obstructive shock

Caused by PE, tamponade, or tension pneumothorax, treated by relieving the obstruction.

Norepinephrine (Levophed)

First-line treatment in septic shock.

Dobutamine

Used for low-output states in cardiogenic shock to improve contractility.

Fluid optimization

Must occur before giving vasopressors; check CVP or physical signs.

Vasodilator agents

Used for HTN emergencies or cardiac ischemia; avoid if volume depleted.

NOACs

Do not require INR monitoring (e.g., apixaban, rivaroxaban).

Warfarin

Requires bridging and INR goal 2.0-3.0 in most cases.

Type 1 Diabetes

Pathology: Autoimmune destruction of β-cells in the pancreas; no insulin production; classic triad: Polyuria, polydipsia, weight loss; presents with: Hyperglycemia and ketonuria.

Type 2 Diabetes

Pathology: Peripheral insulin resistance + decreased secretion over time; most are asymptomatic — diagnosed via labs; associated with: Obesity, metabolic syndrome.

Metabolic Syndrome

Must meet 3 of the 5 criteria: Waist circumference: 40 in (men), 35 in (women); Blood pressure: >130/80 mmHg; Triglycerides: >150 mg/dL; HDL: <40 mg/dL (men), <50 mg/dL (women); Fasting glucose: >100 mg/dL; increases risk for Type 2 diabetes and cardiovascular disease.

DKA (Diabetic Ketoacidosis)

Cause: Insulin deficiency (common in Type 1); key signs: Fruity breath, polyuria, polydipsia, N/V, abdominal pain, Kussmaul breathing; treatment: IV fluids first, then IV insulin; potassium correction; identify and treat underlying cause.

HHS (Hyperosmolar Hyperglycemic State)

Seen in Type 2 DM, elderly, not insulin dependent; very high glucose (600-1200 mg/dL); hyperosmolality, profound dehydration; little/no ketones or acidosis; often presents with neurologic symptoms; treatment: IV fluids, insulin, electrolytes.

Preventative Care for Diabetes Patients

Annual dilated eye exam, annual foot exam (podiatry), dental exam; vaccines: Pneumococcal, Influenza, Tdap, Hepatitis B, Zoster; BP goal: <130/80 mmHg; exercise: ≥150 minutes/week.

Biguanides

e.g. Metformin; ↓ Gluconeogenesis, ↓ GI glucose absorption; improves insulin sensitivity; first-line for T2DM; SE: GI upset (nausea, diarrhea).

Sulfonylureas

e.g. glipizide, glyburide, glimepiride; stimulate β-cell insulin secretion; can be used with metformin; SE: Hypoglycemia, weight gain, rash.

Thiazolidinediones (TZDs)

e.g. pioglitazone, rosiglitazone; ↑ Insulin sensitivity in muscle, liver, fat; ↓ Glucagon production; SE: Fluid retention, weight gain, fracture risk.

Meglitinides

e.g. repaglinide, nateglinide; stimulate insulin secretion (rapid-acting); very short half-life; SE: Hypoglycemia, weight gain.

Bile Acid Sequestrants

e.g. colesevelam; modestly lowers LDL and A1C; take with meals; SE: Bloating, constipation, GI upset.

Alpha-Glucosidase Inhibitors

e.g. acarbose, miglitol; delay carbohydrate absorption; SE: Gas, diarrhea, no hypoglycemia.

GLP-1 Receptor Agonists

e.g. liraglutide, exenatide; ↑ Insulin, ↓ glucagon, delayed gastric emptying; A1C ↓ 1-1.5%, weight loss; avoid in thyroid cancer history; SE: N/V, diarrhea, decreased appetite.

SGLT2 Inhibitors

e.g. canagliflozin, empagliflozin; ↑ Glucose excretion via kidneys; ↓ A1C + CV benefit; avoid in patients with frequent UTIs; SE: Genital infections, weight loss, polyuria.

DPP-4 Inhibitors

e.g. sitagliptin, linagliptin; enhance GLP-1, increase insulin release; not for initial monotherapy; SE: Severe joint pain (FDA warning).

Amylin Analog

e.g. pramlintide; SQ injection (with insulin); ↓ Glucagon, slows gastric emptying; SE: N/V, weight loss; use with insulin ↑ hypoglycemia risk.

Insulin Types: Onset, Peak, Duration

Rapid-acting (Lispro, Aspart, Glulisine): 15-30 min onset, 1-3 hrs peak, 4-6 hrs duration; Short-acting (Regular insulin): 30 min onset, 1.5-3.5 hrs peak, 8 hrs duration; Intermediate-acting (NPH): 4-6 hrs onset, 4-6 hrs peak, 12 hrs duration; Long-acting (Glargine, Detemir): U-100: 12 hrs onset, no peak, 20-24 hrs duration; U-300 (Glargine): 19 hrs onset, no peak, 20-24+ hrs duration.

Hypoparathyroidism

Definition: Low calcium due to deficient or absent parathyroid hormone (PTH); causes: most commonly surgical removal (e.g., post-thyroidectomy), autoimmune damage, genetic syndromes, radiation therapy to the neck.

Signs and Symptoms of Hypoparathyroidism

Neuromuscular irritability: Tetany, muscle cramps, paresthesias (especially in fingers/toes), carpopedal spasm, facial twitching (Chvostek & Trousseau signs), seizures, arrhythmias, bone pain, possible fractures, hypocalcemia → QT interval prolongation on ECG.

Diagnostic Workup for Hypoparathyroidism

Low serum calcium, elevated phosphate, low or inappropriately normal PTH; consider checking: Vitamin D levels, magnesium (needed for PTH secretion).

Treatment for Hypoparathyroidism

Calcium supplementation, vitamin D (calcitriol), magnesium correction if low, recombinant PTH in severe/refractory cases; always monitor serum calcium, phosphate, and PTH levels in patients post-thyroidectomy or with neuromuscular symptoms.

Eosinophilic Esophagitis (EoE)

Allergic/immune-mediated inflammation of the esophagus

Common demographics for EoE

Common in young men with atopic history (asthma, eczema, allergies)

Symptoms of EoE

Dysphagia, especially with solid foods; food impaction; chest pain not responsive to antacids; GERD-like symptoms or refractory heartburn; upper abdominal pain

Diagnosis of EoE

EGD with biopsy (shows eosinophils >15/HPF) and exclude other causes of esophageal eosinophilia

Gastroesophageal Reflux Disease (GERD)

Reflux of stomach acid into esophagus

Complications of GERD

May progress to erosive esophagitis or Barrett's esophagus

Lifestyle Modifications for GERD

Weight loss (obesity = risk factor), smoking cessation, avoid trigger foods (e.g., chocolate, caffeine), elevate head of bed

Pharmacologic Therapy for GERD

Start with PPI daily x 8 weeks, step down to H2 blockers once controlled, discontinue acid suppression if asymptomatic

Chronic therapy for GERD

For severe erosive disease and Barrett's esophagus

Hiatal Hernia Definition

Herniation of abdominal contents through esophageal hiatus

Types of Hiatal Hernia

Type I (sliding): 95%, manage like GERD; Types II-IV (paraesophageal): 5%, may require surgical correction if symptomatic

Diagnosis of Hiatal Hernia

EGD or Barium swallow

Barrett's Esophagus Cause

Metaplasia from chronic GERD

Cell change in Barrett's Esophagus

Stratified squamous → columnar epithelium

Risk of Barrett's Esophagus

Adenocarcinoma of the esophagus

Risk Factors for Barrett's Esophagus

Chronic GERD, central obesity, smoking, family history

Management of Barrett's Esophagus

Screen high-risk patients; if positive dysplasia, refer to GI for surveillance and ablation

Hepatitis B Diagnosis - HBsAg

Active infection (acute or chronic)

Hepatitis B Diagnosis - Anti-HBs

Immunity from vaccine or resolved infection

Hepatitis B Diagnosis - Anti-HBc

Indicates past or current infection

Hepatitis B Diagnosis - IgM Anti-HBc

Acute infection

Hepatitis B Diagnosis - HBeAg

Active viral replication (↑ infectivity)

Hepatitis B Diagnosis - Anti-HBe

Seroconversion (↓ infectivity)

Key for Acute Hepatitis B

Positive HBsAg and positive IgM anti-HBc; may have positive HBeAg if high replication

General GI Patient Evaluation

Always ask about food history, character of symptoms, recent exposures or travel, medical history

Common GI Symptoms

Abdominal pain (localized vs. diffuse), change in bowel habits (diarrhea, constipation), fatigue, weight loss, nausea/vomiting, GI bleeding (occult or visible)

Board Tip for Elderly Patients

In elderly patients with vague GI complaints and fatigue or weight loss, always think about colon cancer or pancreatic cancer

Microcytic Anemias

MCV < 80

Thalassemia

Hereditary anemia, especially in Mediterranean descent

Thalassemia Labs

↓ MCV and ↓ MCH, RDW normal (unlike IDA), Normal or high ferritin/TIBC, Confirmed via hemoglobin electrophoresis