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:
- Variable deviates from set-point.
- Receptor detects change.
- Integrator (hypothalamus/pancreas) triggers corrective hormone.
- Effector reverses change → variable returns to set-point → hormone stops.
Simplified Infinity-Loop Example
- Overnight fast → blood glucose drops ≈ 60 mg/dL.
- Pancreas releases glucagon → liver breaks glycogen → glucose ↑ → homeostasis.
- 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
- Only hormone that lowers post-prandial glucose? → Insulin.
- Effect of infection/stress on insulin need? → Requirement increases due to cortisol surge.
- A1C level diagnostic for diabetes? → \boxed{> 6.5\%}.
- 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.”