In class
🩺 Type 1 Diabetes Mellitus (T1DM)
🧠 Pathophysiology:
Autoimmune destruction of pancreatic beta cells (which produce insulin).
NO insulin production → glucose can't enter cells → blood sugar rises (hyperglycemia).
Body burns fat for energy → produces ketones → risk for DKA (Diabetic Ketoacidosis).
📚 "3 P's" of Type 1 Diabetes Symptoms:
Polydipsia (excess thirst)
Polyuria (excess urination)
Polyphagia (excess hunger)
🛑 Often presents suddenly in children/young adults.
🩺 Type 2 Diabetes Mellitus (T2DM)
🧠 Pathophysiology:
Insulin resistance → cells ignore insulin signals.
Beta cells eventually wear out → reduced insulin secretion.
Blood sugar rises (hyperglycemia), but less chance of DKA (more likely HHS - Hyperosmolar Hyperglycemic State).
📚 "SLOW" for Type 2 Diabetes Symptoms:
Slow wound healing
Low energy
Overweight/obesity
Weird sensations (tingling/numbness)
🛑 Often develops slowly and seen in adults.
🩺 Thyroid Disorders
🧠 Pathophysiology:
The thyroid gland controls metabolism by releasing T3 (triiodothyronine) and T4 (thyroxine).
Hypothyroidism (underactive thyroid)
Low T3/T4, High TSH (pituitary trying to stimulate thyroid)
Slows down body functions.
📚 "Slow and Cold" Symptoms:
Weight gain
Cold intolerance
Fatigue
Constipation
Depression
Dry skin
Bradycardia (slow HR)
Puffy face, edema (myxedema if severe)
Mnemonic: "THYROID SLOW"
Tiredness
Hair loss
Yawning (fatigue)
Reflexes slow
Overweight
Intolerance to cold
Dry skin
Hyperthyroidism (overactive thyroid)
High T3/T4, Low TSH (pituitary tries to shut down thyroid)
Speeds up body functions.
📚 "Hot and Fast" Symptoms:
Weight loss
Heat intolerance
Anxiety, nervousness
Palpitations, tachycardia
Diarrhea
Sweating
Exophthalmos (bulging eyes in Graves’ disease)
Mnemonic: "THYROID HOT"
Tremors
High HR
Yelling (irritable)
Restlessness
Overheated
Intestinal issues (diarrhea)
Diaphoresis (sweating)
🌟 Quick Nursing Tip:
Always monitor TSH, T3, and T4 to assess thyroid function.
Type 1 DM = Insulin required for life.
Type 2 DM = May manage with diet, exercise, oral meds, or insulin if needed.
🩸 Acute Kidney Injury (AKI)
🧠 Pathophysiology:
Sudden decline in kidney function over hours to days.
Kidneys can’t filter waste, balance fluids, or maintain electrolytes.
Leads to azotemia (↑BUN and creatinine) and oliguria (low urine output).
3 Causes of AKI:
🩻 "P-I-P" Mnemonic
Pre-renal (↓blood flow to kidneys – eg: dehydration, hypotension)
Intra-renal (damage to kidney tissue – eg: nephrotoxins, glomerulonephritis)
Post-renal (obstruction – eg: kidney stones, BPH)
📚 Symptoms of AKI:
Decreased urine output (<400ml/day)
Fluid overload (edema, crackles)
Hyperkalemia (muscle cramps, ECG changes)
Fatigue, confusion (from toxins)
🩺 Chronic Kidney Disease (CKD)
🧠 Pathophysiology:
Gradual, irreversible loss of kidney function over months to years.
Kidneys can't remove wastes, regulate fluids, or control BP.
GFR (Glomerular Filtration Rate) slowly decreases.
🩻 "5 Stages" of CKD based on GFR:
Stage 1: Kidney damage with normal GFR (≥90)
Stage 2: Mild ↓ GFR (60–89)
Stage 3: Moderate ↓ GFR (30–59)
Stage 4: Severe ↓ GFR (15–29)
Stage 5: End-stage (GFR <15 → Dialysis needed)
📚 Symptoms of CKD:
🧠 "AEIOU" Mnemonic for signs dialysis needed:
Acid-base imbalance (metabolic acidosis)
Electrolyte imbalance (esp. high K⁺)
Intoxication (toxin build-up)
Overload of fluid (pulmonary edema)
Uremia (nausea, confusion, itchy skin)
Other symptoms:
Fatigue, anemia (↓erythropoietin)
Fluid retention (edema, hypertension)
Uremic frost (white crystals on skin in late stages)
🌟 Quick Nursing Tips:
Monitor I&O (intake/output)
Monitor electrolytes (especially K⁺ and Na⁺)
Control BP (ACE inhibitors common)
Educate on renal diet: low protein, low sodium, low potassium
Avoid nephrotoxic drugs (like NSAIDs)
🩺 Summary Table:
Condition | Onset | Reversible? | Key Feature |
|---|---|---|---|
AKI | Sudden (hours–days) | Often reversible | Oliguria, ↑ BUN/Creatinine |
CKD | Slow (months–years) | Irreversible | ↓ GFR, uremia, anemia |
🎯 Mnemonics to Remember
AKI Causes = "P-I-P" → Pre-renal, Intra-renal, Post-renal
Dialysis Indications = "AEIOU" → Acidosis, Electrolytes, Intoxication, Overload, Uremia
Metabolic Disorders Overview
Involves glucose control.
Differentiation between Type 1 and Type 2 Diabetes (etiology, pathogenesis, diagnostics, risk factors, consequences, complications).
Insulin's metabolic effects:
Increases glucose uptake.
Increases glycogen synthesis.
Increases triglyceride formation.
Enhances protein synthesis.
Reduces glucose and protein breakdown.
Insulin deficiency:
Decreased glucose uptake.
Increased blood sugar levels → diabetes.
Diabetes Mellitus (DM)
Metabolic disorder: elevated blood glucose levels.
Cause: lack of insulin, insulin deficiency, or tissues' insensitivity to insulin.
Clinical definitions: fasting blood glucose levels and oral glucose tolerance test results categorize into normal, pre-diabetes, and diabetes.
Leads to reduced glucose utilization → hyperglycemia, glycosuria, dehydration, increased fat mobilization, and protein depletion.
Type 1 Diabetes Mellitus
Peak onset: 11-13 years (rare after 30).
Autoimmune destruction of pancreatic β-cells.
Symptoms: polyuria, polydipsia, polyphagia, weight loss, fatigue.
Ketoacidosis from excessive fat breakdown.
Contributing factors: genetic susceptibility, environmental influences (viral infections), nutritional deficiencies.
Diabetic Ketoacidosis (DKA)
Insulin deficiency (primarily in type 1 diabetes).
Decreased glucose utilization and increased fat breakdown → heightened ketone production and metabolic acidosis.
Symptoms: fruity-smelling breath, deep Kussmaul respirations, nausea, vomiting, abdominal pain, electrolyte disturbances, severe dehydration.
Type 2 Diabetes Mellitus
Primarily from obesity, genetic factors, hypertension, and poor diet.
Leads to insulin resistance and relative insulin deficiency.
Obesity: increased adipokines and inflammatory cytokines → β-cell dysfunction.
Treatment: lifestyle changes (controlled diet and regular exercise) to enhance insulin sensitivity and manage glucose levels.
Long-term Complications of DM
Heart disease, peripheral vascular disease, neuropathy, retinopathy, and renal impairment.
Can lead to gangrene (amputations) and increase the risk of cerebrovascular accidents (CVAs).
Effective diabetes management is crucial to prevent these outcomes.
THYROID GLAND DYSFUNCTION
Role: regulates metabolism, heat production, and overall growth and development (thyroid hormones).
Hypothalamus releases thyrotropin-releasing hormone (TRH) → stimulates anterior pituitary to produce thyroid-stimulating hormone (TSH) → promotes synthesis of T3 and T4 hormones.
Understanding causes and symptoms of thyroid dysfunction (hyposecretion and hypersecretion) is essential.
Hypothyroidism
Cause: hyposecretion of thyroid hormones (iodine deficiency, autoimmune destruction, congenital defects).
Symptoms: myxedema, reduced basal metabolic rate (cold intolerance and weight gain), neurological depression (fatigue and confusion).
Increased TSH levels; goiter due to inadequate iodine intake.
Hyperthyroidism (Thyrotoxicosis)
Cause: issues within the thyroid or pituitary gland → overproduction of T3 and T4.
Graves’ Disease
Cause: thyroid-stimulating immunoglobulins (TRAb).
Symptoms: increased metabolic rate, heat intolerance, goiter, exophthalmos (connective tissue deposition), nervous system hyperexcitability (nervousness, irritability, fatigue).
Other symptoms: weight loss (despite increased appetite