N351 Exam 3

Tuberculosis, Hypertension, Atherosclerosis, & Dyslipidemia, Diabetes, Heart Failure & Stable Angina

Pulmonary Tuberculosis Definition

Infectious disease of the lung parenchyma (specifically the alveoli) caused by Mycobacterium tuberculosis:

• Active TB → Host is actively showing signs and symptoms and is extremely contagious

• Latent TB → No sign of disease and host is not contagious, can become active if the host becomes immunocompromised

Etiology of Tuberculosis (TB)

• AIRBORNE TRANSMISSION → Bacteria are spread by to person to person when tiny airborne particles leave during speech, coughing, or sneezing

• How it enters a new host → Extended contact in poorly ventilated indoor spaces

Airborne Precautions for Tuberculosis

• N95 Respirator Mask

• Negative-pressure room or “anteroom”

Risk Factors of Tuberculosis (TB)

• Close contact with infected host

• Immunocompromised

• Crowded living environments

• Travel to regions with high TB rates

• Being a healthcare worker*

Pathophysiology of Tuberculosis (TB)

• Follows the same pathophysiology of infection

• Exudate from the inflammatory process and immune responses accumulates in the alveoli

• Macrophages surrounding the bacteria may become calcified and collagenous scar tissue

• Within this mass, the bacteria may become dormant (latent TB)

Clinical Manifestations of Tuberculosis (TB)

• NIGHT SWEATS

• Unintentional weight loss

• Low-grade fever

• Hemoptysis (coughing up blood)

• Cough

• Fatigue

Diagnostic Tests of Tuberculosis (TB)

• Surveillance Monitoring:

  • TB Skin Test

  • Interferon Gamma Release Assay (IGRA); also called QuantiFERON Gold

• Chest X-Ray

• Sputum Culture and Sensitivity

Drug Therapy for Tuberculosis Infection

6 MONTHS TOTAL:

• Initial Phase = First 2 Months

  • 4 Antibiotics = Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE)

• Continuation Phase = Last 4 Months

  • 2 Antibiotics = Rifampin and Isoniazid

• Requires Directly Observed Therapy (DOT)

Directly Observed Therapy (DOT)

When a healthcare worker physically watches a patient swallow every dose of their prescribed medication

Patient Education for Tuberculosis (TB) Infection

1. Adherence to Drug Therapy:

   1. Compliance is imperative

   2. The nurse may need to observe the patient taking each dose

2. Safety/Monitoring:

   1. Avoid alcohol because patients are at risk of hepatotoxicity

   2. Keep lab draw appointments for liver function testing

   3. Notify the provider if visual changes occur

3. Side Effects/Adverse Effects:

   1. Rifampin may turn urine, sweat, tears orange to red color

   2. Report signs of liver impairment → Yellow skin or eyes

Hyperlipidemia Definition

• Excess serum levels of: Low-density lipoproteins (LDLs), total cholesterol, and triglycerides

• Low serum levels of: High-density lipoproteins (HDLs)

Low-Density Lipoproteins (LDLs)

• Also known as “the bad cholesterol”

• Function: Carries cholesterol from your liver to the cells that need it. If you have high serum levels, it can deposit into the walls of your blood vessels, causing plaque buildup (atherosclerosis)

• Serum Levels: Normal is considered LESS THAN 100

High-Density Lipoproteins (HDLs)

• Also known as “the good cholesterol”

• Function: Acts as a scavenger in your bloodstream. It absorbs excess cholesterol from your blood vessels and carries it back to your liver, which flushes it out of your body

• Serum Levels: Normal is considered MORE THAN 60

  • Higher levels help protect against the buildup of artery-clogging plaque

Etiology & Risk Factors of Hyperlipidemia

• Familial hypercholesterolemia → Genetic factor, childhood manifestation

• Foods high in saturated and trans fats

• Sedentary lifestyle

• Obesity

• Smoking

• Excess alcohol

• Medications → Hydrochlorothiazide (HCTZ), steroids, some birth control

Pathophysiology of Hyperlipidemia

• Trigger = High LDL serum levels →

• Infiltration of vascular endothelium (vessel lining) →

• Inflammatory process begins →

• Vascular smooth muscle remodeling & dysfunction

Clinical Manifestations & Diagnostics of Hyperlipidemia

• NO SYMPTOMS → May be diagnosed when looking for cause of related diseases

• Serum Lipid Panel:

  • Total Cholesterol = <200

  • LDL = <100

  • HDL = >60

  • Triglycerides = <150

Hyperlipidemia Medications

Prescribed when lifestyle changes are ineffective and prevention of cardiovascular disease:

• Atorvastatin → STATINS = Gold Standard

• Bile Acid Sequestrants → Colesevelam & Cholestyramine

• Fibrates → Fenofibrate

• Niacin

Blood Pressure Equation

Blood Pressure = Cardiac Output + Systemic Vascular Resistance

Cardiac Output Equation

Cardiac Output = Heart Rate + Stroke Volume

Cardiac Output Definition

The total amount of blood your heart pumps per minute

Stroke Volume (SV) Definition

Volume of blood pumped out by one ventricle of the heart in a single heartbeat

Factors Determining Stroke Volume (SV)

• Preload → The volume of blood in the ventricle at the end of diastole

• Contractility (Inotropy) → Inherent strength or force of the heart muscle's contraction; Stronger contractions empty more blood from the ventricle, lowering ESV and increasing stroke volume

• Afterload → The resistance/pressure the ventricle must overcome to push blood into the aorta or pulmonary artery

Stroke Volume Equation

Stroke Volume (SV) = End-Diastolic Volume (EDV) - End-Systolic Volume (ESV)

Systemic Vascular Resistance (SVR) Definition

Amount of force or resistance that the blood vessels in the body's systemic circulation (excluding the lungs) oppose against the flow of blood

• Also called “Total Peripheral Resistance”

Factors Determining Systemic Vascular Resistance (SVR)

• Vessel Diameter:

  • Vasoconstriction = Increased resistance

  • Vasodilation = Decreased resistance

• Blood Vessel Length: Longer vessels = Increased resistance

• Blood Viscosity: Thicker blood (high cell count) = Increased resistance

Etiology of Hypertension (HTN)

• Primary Hypertension:

  • Effects 95% of patients

  • Gradually develops over years

  • No single or clear cause

• Secondary Hypertension:

  • Appears suddenly

  • Caused by underlying medication condition, substance, or medication

Risk Factors of Hypertension

• Modifiable Factors: Diabetes*, high sodium diet, sedentary lifestyle, obesity, excessive alcohol use, nicotine use (potent vasoconstrictor), hyperlipidemia, and chronic stress

• Non-Modifiable Factors: Age, race, gender, and family history

Pathophysiology of Hypertension

• Triggers: Increased SNS activity, increased RAAS, and increased Na⁺ →

• Vasoconstriction/Increased SVR and increased cardiac output →

• Increased pressure on vessel walls →

• Endothelial lining damage →

• Hardened or thickened vessels →

• End organ ischemia and/or dysfunction

*Body sets a new homeostatic pressure = upregulated BP is the new target of homeostasis

Clinical Manifestations of Primary Hypertension

ASYMPTOMATIC FOR YEARS:

• Headache, blurred vision, and dizziness if SBP >180

• Damage begins at SBP >130

Consequences of Uncontrolled Hypertension

END ORGAN DAMAGE:

• Heart → Heart failure

• Brain → Stroke or thrombotic events

• Peripheral vascular disease or artery disease (PVD & PAD)

• Kidney → Kidney failure

• Eyes → Vision changes

Diagnostics of Hypertension

• Blood Pressure Screenings → Technique matters; consider “white coat hypertension”

• Additional Diagnostics to Explore Cause & Organ Damage → Metabolic, cardiac, renal

Primary Hypertension Medications

Prescribed when prevention and/or lifestyle change are not successful; the goal is to limit end organ damage:

• Initial Therapy Guidelines:

  • ACEs (angiotensin-converting enzyme inhibitors) → LISINOPRIL

  • ARBs (angiotensin II receptor blockers) → LOSARTAN

  • Selective calcium channel blocker → AMLODIPINE

  • Thiazide diuretic → Hydrochlorothiazide

• How many drugs and what combination depends on risk and resistance

Nursing Implications of ALL Antihypertensive Medications

• Review and monitor for interactions

• Assess BP before and after administration

• Fall Risk → Implement fall precautions

• Notify provider of side effects (especially ACEs with dry cough)

• Hold and notify provider if SBP <100

Where do calcium channel blockers work in the body?

Vasculature

Hypertensive Crisis Parameters

• SYSTOLIC Blood Pressure >180 mmHg

• DIASTOLIC Blood Pressure >110 mmHg

*Rate of rise is more important than the absolute value!

Hypertensive Urgency

Hypertension that develops over hours to days and may not require hospitalization

Hypertensive Emergency

PERMANENT END ORGAN DAMAGE can result if prompt treatment is not obtained, requires hospitalization

Clinical Manifestations of a Hypertensive Crisis

• Hypertensive Encephalopathy → overall brain dysfunction or damage

  • Headache, nausea/vomiting, seizures, confusion, coma

• Renal Insufficiency

• Cardiac Decompensation → Myocardial infarction, heart failure, pulmonary edema, etc.

• Aortic Dissection → A tear develops in inner layer of aorta

Medication Management of a Hypertensive Crisis

Requires fast-acting medications with 100% bioavailability:

• Treated with IV antihypertensives

• Goal = Reduce SBP by <25% within 1 hour

• If stable, <160/100 over next 2-6 hours

*GRADUAL REDUCTION prevents end organ ischemia; it must be gradual to maintain perfusion to specific tissues

Arteriosclerosis Definition

Thickening and hardening of vessel walls; can occur with aging as vessels lose elasticity

Atherosclerosis Definition

Form of arteriosclerosis where fatty deposits, cholesterol, and other substances accumulate within arterial walls:

• Leads to atherosclerotic plaques

• Major contributor to cardiovascular disease

Risk Factors of Atherosclerosis

• Family history

• Increasing age

• Hypertension

• Hyperlipidemia

• Diabetes

• Nicotine use

• Diet

• Stress

• Sedentary lifestyle

Pathophysiology of Atherosclerosis

• Increased low-density lipoprotein (LDL) inflammation →

• Special macrophages eat LDL and make foam cells →

• Foam cells contribute to plaque formation in vessel lining →

• Decreased diameter of arteries (narrowing) →

• Tissue ischemia and thrombosis occur

Thrombosis Definition

Formation of a blood clot (called a thrombus) inside a blood vessel or heart chamber, which can slow or completely block normal blood flow

Complications of Atherosclerosis

• Chronic tissue ischemia from decreased blood flow

• Acute arterial thrombosis

• Myocardial infarction (MI)

• Ischemic stroke

• Peripheral arterial disease (PAD)

Connecting Hyperlipidemia, Hypertension & Atherosclerosis Pathways

1. Hyperlipidemia promotes lipid accumulation within blood vessels → LDL particles enter endothelium

2. Hypertension contributes to endothelial dysfunction and vascular injury

3. Chronic inflammation contributes to plaque progression → Macrophages and foam cells enlarge atherosclerotic plaque

4. Atherosclerosis compromises arterial blood flow → narrowed lumen

5. Plaque disruption/rupture and thrombosis (blood clot) can cause acute cardiovascular events

Order of Blood Flow Through the Heart

Blood enters the heart through the superior and inferior vena cava → Right atrium → Tricuspid valve → Right ventricle → Pulmonary valve → Pulmonary trunk → Lungs oxygenate blood → Pulmonary veins → Left atrium → Mitral valve → Left ventricle → Aortic valve → Aorta → Systemic circulation

Frank-Starling Mechanism/Starling’s Law

Stroke volume (SV) of the heart increases in response to an increase in the volume of blood filling the ventricles (the end-diastolic volume or preload)

• Like a rubber band, stretching it further releases more snap; up to a physiological limit

• If the muscle is overstretched past its optimal length, the contraction force drops

Preload Definition

Volume of blood in the ventricles at the end of diastole (end-diastolic pressure); immediately at the end of filling the ventricles with blood:

• Increased with hypervolemia, regurgitation of cardiac valves, and heart failure

Afterload Definition

Resistance the left ventricle must overcome to circulate blood:

• Increased in hypertension and vasoconstriction

• Causes increased cardiac workload when there is more resistance

Systems Regulating Cardiac Output (CO)

• Sympathetic Nervous System (SNS):

  • B-1 adrenergic receptor activation = Increased HR

  • Alpha-1 receptor activation = Vasoconstriction/smooth muscle contraction

• Antidiuretic Hormone (ADH)/Vasopressin:

  • Systemic vasoconstriction

  • Water retention

• RAAS:

  • Angiotensin II = Vasoconstriction, aldosterone release, ADH release

  • Increased systemic vascular resistance (SVR)

  • Aldosterone = Reduces Na⁺ & H₂O excretion

• Natriuretic Peptides:

  • BNP = Dilates vessels, excretes H₂O & Na⁺

Ejection Fraction Definition

Percent (%) of ventricular blood ejected with each heart beat:

• Normal Range = 55%-60%

• Reduced Range = 40% or less (often indicates heart failure)

Myocardial Oxygenation: Supply & Demand

Left ventricular coronary perfusion occurs predominantly when the heart is at rest (diastole):

• Influenced by heart rate, contractility, and ventricle wall stress

• When demand exceeds supply = Cardiac ischemia

Stable Angina Parameters

• Transient myocardial ischemia → Meaning it occurs with exertion

• Source of chest pain when there’s no infarction present

• PREDICTABLE and follows pattern of previous chest pain

Etiology of Stable Angina

• Coronary artery atherosclerosis

• Narrowed arteries have predictable exertional symptoms

Pathophysiology of Stable Angina

• Trigger = Coronary artery damage →

• Decreased lumen diameter (artery narrowing) →

• Increased physical exertion →

• Myocardial O₂ demand outpaces the supply →

• Ischemic heart muscle distal to the site of narrowing →

• PAIN and other symptoms

Clinical Manifestations of Stable Angina

• Chest Pain (maybe, not always)

• Shortness of breath

• Indigestions

• Nausea

• Anxiety

*Women and older adults frequently present differently.

Diagnostics of Stable Angina

• Rule out myocardial infarction (MI)

• Cardiac Stress Test (positive if symptoms occur)

  • Exercise (running)

  • Pharmacologic

• Coronary CT Angiography

  • Non-invasive CT scan of coronary arteries

• Invasive Coronary Angiography

  • Left heart catheterization

Medications for Stable Angina

Goal of Pharmacologic Therapy = Prevent ischemic events and improve quality of life

• Nitrate vasodilators → NITROGLYCERIN

• Beta blockers → METROPROLOL

• Calcium channel blockers → AMLODIPINE

Heart Failure (HF) Definition

Heart muscle is too weak or stiff to pump enough blood and oxygen to meet the body's needs; it cannot keep up with its normal workload:

• Can be chronic or acute → Majority are chronic

• Inefficiency of the heart

  • Inability to FILL → Thick and stiff cardiac muscles

  • Inability to PUMP → Thin and weak muscles

• Decreased cardiac output (CO) → HALLMARK SIGN

• Decreased perfusion → Biggest concern; precursor to other disease

Etiology of Heart Failure (HF)

• Coronary artery disease (CAD)

• Hypertension

• Heart valve disease → Valves become stenotic/incompetent

• Cardiomyopathy → Umbrella term for heart muscle disease

• Myocarditis → Heart infection = Inflammation and swelling

• Arrhythmias

• Congenital heart defects

Pathophysiology of Heart Failure (HF)

• Trigger = Myocardial Dysfunction (inability to pump or to fill) →

• Decreased cardiac output →

• Activation of RAAS and SNS →

  • VASOCONSTRICTION

  • RAAS = Na⁺ and H₂O retention

• Increased heart workload →

• VENTRICULAR REMODELING = Hypertrophy or over-stretching of ventricles

Heart Failure with Reduced Ejection Fraction (HFrEF) Definition

The left ventricle becomes weakened and cannot squeeze forcefully enough during a contraction:

• Left Ventricular Ejection Fraction = 40% OR LESS

• Systolic heart failure

Heart Failure with Preserved Ejection Fraction (HFpEF) Defintion

The left ventricle squeezes normally, but the heart muscle has become too thick and stiff to relax and fill properly with blood between heartbeats:

• Left Ventricular Ejection Fraction = 50% OR MORE

• Diastolic heart failure

Left-Sided Heart Failure Definition

Left ventricle cannot effectively pump blood into systemic circulation, leading to increased pressure in the left atrium and pulmonary circulation; Think LUNGS!

• Fluid backs up into the lungs → Increased pulmonary capillary pressure → Fluid moves into alveoli (pulmonary edema)

Right-Sided Heart Failure Definition

The right ventricle is too weak or stiff to pump deoxygenated blood effectively to the lungs; blood and fluid back up into the body's venous system and tissues, causing systemic congestion

• Think REST of body

• Right ventricular dysfunction → Increased pressure in systemic circulation → Fluid in peripheral tissues/organs

• Most commonly caused by left-sided heart failure

Clinical Manifestations of Left-Sided Heart Failure

• PULMONARY EDEMA (fluid in alveoli) = Impaired gas exchange, decreased O₂ levels, cough, crackles, wheezing, blood-tinged sputum

• Dyspnea (especially with exertion) and/or paroxysmal nocturnal dyspnea (wakes at night with shortness of breath)

• Orthopnea (uses multiple pillows)

• Tachypnea

• Restlessness and anxiety

• Fatigue

• Tachycardia

• Possible confusion or cyanosis in severe cases

Clinical Manifestations of Right-Sided Heart Failure

• Peripheral edema (dependent, pitting)

• Weight gain/fluid retention → 3lbs/day or 5lbs/week

• Jugular veinous distention (JVD)

• Ascites (abdominal distention)

• Hepatomegaly (liver enlargement, right upper quadrant fullness)

• Anorexia and GI discomfort (nausea and early satiety)

• Fatigue

• Increased peripheral venous pressure

• Enlarged liver and spleen in chronic cases

• May be secondary to left-sided heart failure or chronic pulmonary problems

Diagnostics of Heart Failure

• Echocardiogram = Ultrasound of the heart that gives ejection fraction and more

• Chest X-Ray = Heart size, ventricular remodeling?

• Liver Function Tests = Increased AST + ALT when congested

• 12 Lead ECG = Electrical issues can be seen

• Brain Natriuretic Peptide (BNP) = GOLD STANDARD

  • 300 = Mild heart failure

  • 600 = Moderate heart failure

  • 900 = Severe heart failure

• Baseline Electrolytes = Decreased Na⁺ with increased fluid, hemodilution

Medications for Heart Failure

Goal of Drug Therapy: To reduce mortality, prevent or minimize exacerbations, improve function and quality of life, and stop or reverse cardiac remodeling

• Angiotensin Pathway Inhibitors:

  • Angiotensin-Converting Enzyme (ACE) Inhibitor = LISINOPRIL

  • Angiotensin-II Receptor Blocker (ARB) = LOSARTAN

  • Angiotensin Receptor/Neprilysin Inhibitor = SACUBITRIL/VALSARTAN

• Beta Blockers = METOPROLOL

• Mineralocorticoid Receptor Antagonist/Diuretics = SPIRONOLACTONE & FUROSEMIDE

• Sodium-Glucose Cotransporter (SGLT2) Inhibitors = DAPAGLIFOZIN

• Cardiac Glycosides = DIGOXIN

*Number of medications and combination depends on the type of heart failure

Etiology of Type I Diabetes

• Autoimmune destruction of pancreatic beta cells

• Little to no endogenous insulin production

• Requires exogenous insulin administration

Etiology of Type II Diabetes

• Insulin RESISTANCE

• Progressive beta-cell dysfunction

• Relative insulin deficiency

Etiology of Gestational Diabetes

• Glucose intolerance first recognized during PREGNANCY

• Increased insulin resistance related to pregnancy hormones

Secondary Etiology of Diabetes Mellitus

• Pancreatic disease

• Endocrine disorders

• Medications → Especially high doses of steroids!

  • Risk of developing hyperglycemia

  • Immunosuppression

Pancreatic Beta Cell Function

Specialized endocrine cells in the pancreas that serve as the body's sole physiological source of insulin

Pathophysiology of Normal Glucose Regulation

• After a meal, blood glucose increases →

• Pancreatic beta cells release insulin →

• Glucose enters muscles and adipose cells →

• Liver stores glucose as glycogen →

• Blood glucose decreases →

• Final Result: Insulin lowers blood glucose

Pathophysiology of Type I Diabetes

• Trigger: Autoimmune destruction of pancreatic beta cells →

• Little or absolutely no insulin production →

• Glucose cannot effectively enter insulin-dependent cells →

• HYPERGLYCEMIA →

• Body begins breaking down fats for energy →

• Final Result: Ketone production = Risk forDiabetic Ketoacidosis (DKA)

Pathophysiology of Type II Diabetes

• Trigger: Insulin resistance (develops gradually) →

• Cells do not appropriately respond to insulin →

• Pancreas initially produces MORE insulin →

• Progressive beta-cell dysfunction →

• Insulin production becomes inadequate →

• Persistent hyperglycemia →

• Final Result: Involves BOTH insulin resistance and progressive loss of insulin secretion

Risk Factors of Type I Diabetes

• Family history/genetic susceptibility → Most common cause

• Autoimmune predisposition

• Environmental triggers (e.g. mass immune response to illness)

Risk Factors of Type II Diabetes

• Family history/genetic predisposition

• Overweight/obesity

• Physical inactivity

• Increasing age

• History of gestational diabetes → these patients are screened more frequently

• Prediabetes

Pathophysiology of Diabetic Ketoacidosis (SIMPLIFIED)

1. Lack of insulin: Without insulin, your cells cannot use glucose for fuel, leaving sugar to build up in your bloodstream (hyperglycemia)

2. Fat breakdown: To find energy, your body starts breaking down fat instead.

3. Ketone buildup: This fat-burning process produces acidic waste products called ketones

4. Blood acidity: When ketones build up too fast, they turn the blood dangerously acidic and cause severe dehydration

A1C Diagnostic

Blood test that measures average blood glucose level over the past 2-3 months:

• Normal Value = LESS THAN 5.7%

• Prediabetes = 5.7-6.4%

• Diabetes = GREATER THAN 6.5%

Prediabetes Definition

• Blood glucose levels are higher than normal, but not high enough to be diagnosed as type 2 diabetes.

• It is a serious warning sign that the body is developing insulin resistance.

Fast Acting Plasma Glucose Diagnostic

Blood test that measures the amount of blood glucose levels after fasting (excluding water) for at least 8 to 12 hours:

• Normal Values = LESS THAN 100 mg/dL

• Prediabetes = 100-125 mg/dL

• Diabetes = GREATER THAN 126 mg/dL

2-Hour Oral Glucose Tolerance Test

Measures how well your body processes glucose; commonly used to diagnose gestational diabetes:

1. Fasting Blood Draw: Fast for 8-12 hours prior to the test. A baseline blood sample is taken to measure fasting blood glucose level.

2. Glucose Drink: Drink a solution containing 75 grams of glucose dissolved in water, usually consumed within 5 minutes.

3. 2-Hour Blood Draw: Another blood sample is taken 2 hours after the drink to measure how effectively the body has cleared glucose from your bloodstream.

• Normal Values = LESS THAN 140 mg/dL

• Prediabetes = 140-199 mg/dL

• Diabetes = GREATER THAN 200mg/dL

Random Plasma Glucose Test

Measures blood glucose levels at any given time of the day without requiring fasting beforehand; often used when a person shows acute symptoms of hyperglycemia

• No normal or prediabetes values are applicable

• Diabetes = GREATER THAN 200mg/dL + Classic Symptoms

Clinical Manifestations of Hyperglycemia

THINK 3 P’s!

• Polyuria → Excessive urination

• Polydipsia → Excessive thirst

• Polyphagia → Excessive hunger

• Fatigue → Too much glucose in the blood, but cells cannot use it effectively for energy

• Blurred vision

“Hot and dry? Sugar is HIGH!”

Diabetes Type I Clinical Manifestations

• Unintentional weight loss

• Rapid onset

• Ketosis/DKA

Diabetes Type II Clinical Manifestations

• Gradual onset

• Recurrent infections

• Delayed wound healing

• May initially be asymptomatic

Clinical Manifestations of Hypoglycemia

THINK = “Cool and clammy? Needs some candy!”

• Shakiness

• Sweating

• Tachycardia

• Hunger

• Irritability/Confusion

• Severe: Seizure or loss of consciousness

Clinical Manifestations of Diabetic Ketoacidosis (DKA)

• Hyperglycemia

• Ketosis

• Metabolic acidosis

• Dehydration

• Kussmaul respirations → deep, rapid, and labored breathing pattern = automatic reflex when blood becomes too acidic

• Fruity breath

Clinical Manifestations of Hyperosmolar Hyperglycemia Non-Ketonic Syndrome (HHNS)

*Most SEVERE acute complication, more common in Type II Diabetes

• Severe hyperglycemia

• Profound dehydration

• Neurologic changes

• Minimal or absent ketosis

Nursing Implications of Hypoglycemia

HYPOGLYCEMIA = <70 mg/dL → 15-15 Rule

• Give 15g rapid-acting carbohydrate (e.g. juice, glucose tablets, etc.)

• Recheck glucose in 15 minutes

• Repeat if still <70 mg/dL

• Severe/Unable to Swallow → Glucagon or IV dextrose as appropriate

Long-Term Complications of Diabetes

• Microvascular: Retinopathy, nephropathy, neuropathy

• Macrovascular: Coronary artery disease (CAD), stroke, peripheral vascular disease (PAD)

• Additional Complications: Poor wound healing, infection, foot ulcers, amputation

• Chronic hyperglycemia damages blood vessels and nerves throughout the body

Diabetes Therapy

Goal of Therapy: To maintain glucose as close to target as safely possible while preventing acute and chronic complications

• Nutrition

• Physical Activity

• Medication

• Monitoring

Type I → Insulin required

Type II → Lifestyle + non-insulin medications ± insulin

Insulin Mechanism of Action

• Decreases blood glucose levels

• Increases glucose uptake into the muscle and adipose tissue

• Increases glucose storage as glycogen in the liver

• Decreases hepatic glucose production

• Key Action: Moves glucose out of the blood and into the cells

Rapid-Acting Insulin Onset, Peak, & Duration

• Onset: ~15 minutes

• Peak: ~1 hour

• Duration: ~2-4 hours

THINK: “15 minutes feels like an hour during 2-4 rapid responses.”

Regular (Short-Acting) Insulin Peak, Onset, & Duration

• Onset: 30-60 minutes

• Peak: 2-4 hours

• Duration: 5-8 hours

THINK: “Short-staffed nurses went from 30 patients two 8 patients.”

NPH (Intermediate-Acting) Onset, Peak, & Duration

• Onset: 1-2 hours

• Peak: 4-12 hours

• Duration: 12-18 hours

THINK: “Nurses play hero two 12 18-year-olds”

Long-Acting Insulin Onset, Peak, & Duration

• Onset: ~1-2 hours

• Peak: NO pronounced peak

• Duration: ~24 hours or longer

THINK: “Long shifts never peaked, but lasted 24 hours”