Glucose Regulation & Diabetes Lecture Notes nur 176 wk1

Course Logistics & Housekeeping

  • Very fast-paced class; communicate early if you fall behind so help can be arranged.
  • Review the new student handbook (added ethical/code sections); pay special attention to the 5-minute rule for exams—late arrivals beyond 5 minutes may forfeit the exam.
  • Homework:
    • Due the first class of each week.
    • Worth few points but can decide borderline grades (e.g.
    • 79.9 \rightarrow 80.0
    • 77.99999 can round up with homework credit).
    • Instructor is flexible up to mid-term—email if upload issues.
  • Syllabus = master document:
    • Contains all due dates, topics, and exam schedule.
    • Keep a DIGITAL copy for future credit transfer; other colleges often accept courses if your syllabus matches their content.
  • Resources you already paid for: library databases, NCLEX question banks, peer tutoring (in-person & Zoom), instructor’s limited 1-on-1 tutoring.
  • Form or join study buddies/groups—nursing (and nursing school) is a "team sport." Collect notes, share due-date reminders.
  • Upcoming assessments:
    • HESI: Week 2, second class.
    • Major Exams: Weeks 3, 6, 9; cumulative Final in Week 11 (dates in syllabus & blueprint).
    • EAQs (Med-Surg & Pharm) posted on Evolve; some links currently broken—will fix.
    • Kahoot reviews and recorded sessions will be e-mailed before each exam.
  • HESI remediation: graded minimally; due 2 weeks after test. Use Evolve packets, upload forms + HESI report.

Why Glucose Regulation Matters

  • Diabetes prevalence: most patients in clinical settings will have diabetes + 4–5 comorbidities (often diabetes-related).
  • Understanding diabetes improves care for cardiovascular, renal, neuro, wound, and immune complications.

Key Terminology & “G-Words”

  • Endocrine gland: organ that secretes hormones into blood (e.g.
    pancreas).
  • Hormone: chemical messenger acting on specific target tissue with matching receptor sites.
  • Glucose: circulating blood sugar; immediate cellular fuel.
  • Glycogen: stored form of glucose ("many Lego bricks snapped together").
  • Glucagon: pancreatic hormone that raises blood glucose when “sugar is gone.”
  • Insulin: ONLY physiologic hormone that lowers blood glucose; drives glucose into cells & promotes glycogen synthesis.
  • Counter-regulatory hormones: act opposite of insulin (glucagon, cortisol, catecholamines, growth hormone).
  • Insulin resistance: hallmark of Type 2 diabetes—receptors fail to respond.
  • Gluconeogenesis: \text{Glucose} + \text{Neo (new)} + \text{Genesis (creation)} → liver creates new glucose from non-carbohydrate sources (fat/protein); prominent in DKA.
  • Negative feedback: physiologic loop maintaining homeostasis:
    1. Variable deviates from set-point.
    2. Receptor detects change.
    3. Integrator (hypothalamus/pancreas) triggers corrective hormone.
    4. Effector reverses change → variable returns to set-point → hormone stops.

Simplified Infinity-Loop Example

  1. Overnight fast → blood glucose drops ≈ 60 mg/dL.
    • Pancreas releases glucagon → liver breaks glycogen → glucose ↑ → homeostasis.
  2. Pancake breakfast → blood glucose spikes ≈ 200 mg/dL.
    • Pancreas releases insulin → cells uptake glucose & liver converts excess to glycogen → glucose ↓ to normal.

Populations at Increased Risk

  • Pregnancy: gestational diabetes; hormones + weight gain ↑ insulin resistance. History → lifelong Type 2 risk.
  • Infants of diabetic mothers (LGA babies):
    • In-utero hyperglycemia → fetal pancreas over-produces insulin.
    • At birth cord is cut → maternal glucose supply stops → newborn hypoglycemia.
  • Elderly: ↓ lean muscle, ↑ insulin resistance.
  • Ethnicity:
    • Type 1 risk: Northern European ancestry.
    • Type 2 risk: Native American, Alaska Native, African-American, Hispanic/Latino, Asian-American.
  • Genetics: strong family correlation for all forms.
  • Medications & Stress:
    • Systemic steroids (e.g., prednisone) & endogenous cortisol during stress/illness raise glucose → may need more insulin.

Hyperglycemia

  • Causes: insulin deficiency (Type 1), insulin resistance (Type 2), counter-regulatory hormone excess, missed meds, high-carb meal.
  • Mnemonic: “Hot & Dry, Sugar High.”
  • Signs/Symptoms:
    • Warm, flushed, dry skin.
    • 3 P’s: \text{Polyuria} + \text{Polydipsia} + \text{Polyphagia} (often described without medical terms on tests).
    • Fruity (ketone) breath, N/V, lethargy → possible DKA (metabolic acidosis; look for \text{Kussmaul’s} respirations).
  • Acronym FLUSHED:
    • Facial flush / fruity breath
    • Lethargy
    • Unusual thirst (polydipsia) & urine ↑ (polyuria)
    • Skin warm & dry
    • Hyperventilation (Kussmaul) if DKA
    • Emesis
    • Drowsiness / decreased appetite

Hypoglycemia

  • Kills faster than hyperglycemia—no fuel for the brain.
  • Causes: skipped meals, excess insulin, intense exercise, alcohol, malnutrition.
  • Mnemonic: “Cold & Clammy? Need some Candy.”
  • Early Acronym T.I.R.E.D.:
    • Tachycardia
    • Irritability
    • Restlessness
    • Excessive hunger
    • Diaphoresis / Depression
  • Late Neuro Acronym C.O.M.A.S.:
    • Confusion → decreased concentration → Coma
    • Orientation problems / ↓ LOC
    • Mental-status changes (psychotic behavior)
    • Apathy (profound lethargy)
    • Seizures or stroke-like presentation (always check glucose before stroke protocol!)

Diagnostic & Monitoring Labs

Fasting Plasma Glucose (FPG):

  • 8-hour fast.
  • 100 \leq \text{FPG} < 126\;\text{mg/dL} → pre-diabetes.
  • \text{FPG} \geq 126\;\text{mg/dL} on 2 occasions → diabetes (need repeat to avoid “RC-Cola & Moon-Pie” false positive).
    Random (Casual) Glucose: \geq 200\;\text{mg/dL} with symptoms → diabetes.
    Oral Glucose Tolerance Test (OGTT): most sensitive test of glucose metabolism; essential for gestational screening.
    Glycosylated Hemoglobin (HbA1c / A1C):
  • Averages ~3 months of glycemia (RBC lifespan).
  • \text{A1C} \geq 6.5\% → diagnostic for diabetes.
  • Therapeutic goal for diagnosed diabetics: < 7.0\% (some individualized exceptions).
    Type 1 Antibody Panel:
  • GAD-Ab (glutamic-acid decarboxylase antibodies) – autoimmune marker.
  • C-peptide: by-product of endogenous insulin production.
    • Low/absent C-peptide + positive GAD → Type 1.
      Lipid Profile: Hyperglycemia parallels ↑ triglycerides; diabetics often have ↓ HDL ("happy") & ↑ LDL ("lousy").
      Renal Function: \text{BUN}, \text{Creatinine}, and albumin/proteinuria—early sign of diabetic nephropathy.
      C-Reactive Protein (CRP): nonspecific inflammation marker; elevated CRP correlates with insulin resistance & cardiovascular risk.

Nursing Priorities & Patient Education

  • Diabetes self-management hinges on patient knowledge & adherence.
  • Type 1: must have exogenous insulin; diet & exercise fine-tune control.
  • Type 2: spectrum of treatment—lifestyle → oral agents → injectables → insulin.
  • Teach:
    • Glucose self-monitoring technique & action thresholds.
    • A1C targets and frequency.
    • Recognition & rapid treatment of hyper/hypoglycemia.
    • Effects of illness, infection, steroids, and stress (“sick-day rules”).
    • Nutrition: balanced carb intake; cultural adaptations; label reading.
    • Exercise: improves insulin sensitivity; caution for hypoglycemia.
    • Foot care, eye exams, renal follow-up.
  • Explore barriers to adherence: financial, cultural diet, knowledge deficit, family dynamics—interdisciplinary referrals (social work, dietitian, peer educator).

Concept Map Connections

  • Glucose Regulation intersects with:
    • Hormone Regulation (insulin, glucagon, cortisol).
    • Nutrition & Mobility (dietary carbs, muscular uptake of glucose).
    • Perfusion (macro/micro-vascular damage), Immunity, Sensory (neuropathy), Tissue Integrity (wound healing), Elimination (renal impact).

Sample Review Questions & Answers

  1. Only hormone that lowers post-prandial glucose?Insulin.
  2. Effect of infection/stress on insulin need? → Requirement increases due to cortisol surge.
  3. A1C level diagnostic for diabetes? → \boxed{> 6.5\%}.
  4. Do NOT give insulin if glucose is < 70 mg/dL—treat hypoglycemia first.

Whiteboard / Mag-Board Demo Highlights

  • Visual model: Blood stream, Pancreas (insulin = blue blocks; glucagon = orange), Liver (glycogen stack), Brain (glucose-only fuel).
  • Scenarios:
    • Hypo (40 mg/dL): glucagon released → liver splits glycogen → glucose ↑.
    • Hyper (600 mg/dL in DKA): exogenous Regular insulin drives glucose into cells & stores excess as glycogen; primary danger = metabolic acidosis → aggressive fluids + insulin.

Administrative Reminders

  • Bring workbook & clinical packet each class.
  • Know clinical site for current week.
  • Can’t access email/portal? → Contact Denise (IT/Student Services).
  • Instructor is “laid-back” but expects communication & initiative.

Quick Reference Thresholds (Keep handy)

  • Hypoglycemia: < 70 mg/dL (symptoms often at \approx 60, neuro signs < 50).
  • Euglycemia goal: 80–120 mg/dL (varies per facility).
  • Hyperglycemia concern: > 180 mg/dL; emergency > 250 mg/dL (DKA risk) or > 600 mg/dL (HHS risk).
  • Prediabetes FPG: 100–125 mg/dL.
  • Diabetes Dx (FPG): \ge 126 mg/dL (×2).
  • Random + symptoms: \ge 200 mg/dL.
  • HbA1c targets: diagnose \ge 6.5\%; treat to < 7.0\%.

Closing Tips

  • Master negative feedback loop and the roles of glucose, glycogen, insulin, glucagon—this underpins every diabetic emergency & drug mechanism.
  • Translate mnemonics into symptom clusters for exams (test writers love alternate wording).
  • Use provided videos (links emailed) to reinforce physiology.
  • Remember: “Cold & clammy → candy; Hot & dry → sugar high.”