Diabetes Mellitus: Pathophysiology

Pathophysiology of Type 1 Diabetes Mellitus

• Type 1 diabetes is an autoimmune condition.
• The immune system attacks pancreatic beta cells, which are essential for insulin production.
• Destruction of β-cells within the islets of Langerhans leads to a complete insulin deficiency.
• Without insulin, glucose cannot enter cells, causing it to remain in the bloodstream, resulting in hyperglycemia.
• Key symptoms include polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (excessive hunger).
• Onset typically occurs during childhood or adolescence.

Pathophysiology of Type 2 Diabetes Mellitus

• Type 2 diabetes involves insulin resistance, where body cells fail to respond effectively to insulin, and eventual β-cell dysfunction.
• Insulin production continues, but it is not effective in facilitating glucose entry into cells, leading to elevated blood glucose levels.
• The pancreas initially attempts to compensate by producing more insulin, but this can lead to β-cell fatigue and decreased insulin production over time.
• Risk factors include obesity, poor diet, sedentary lifestyle, and family history.

DKA – Diabetic Ketoacidosis

• DKA is a dangerous complication of type 1 diabetes that arises from severe insulin deficiency.
• Cells cannot use glucose without insulin, leading the body to break down fat for energy.
• Fat metabolism generates ketones, which are acidic, leading to metabolic acidosis as they accumulate.
• High blood glucose levels result in osmotic diuresis causing dehydration and electrolyte imbalances.
• Symptoms include fruity-smelling breath and Kussmaul breathing (deep, labored).
• Further symptoms include confusion, lethargy, nausea, vomiting, polyuria, and polydipsia.
• Indicative lab values are blood glucose above 14 mmol/L, low pH, and ketones present in blood/urine.

HHS – Hyperosmolar Hyperglycemic State

• HHS predominantly affects those with type 2 diabetes, characterized by severe hyperglycemia and dehydration without ketone production.
• The presence of some insulin prevents ketosis, but not hyperglycemia.
• Extreme hyperglycemia leads to osmotic diuresis and significant dehydration.
• Elevated serum osmolarity results in neurological symptoms such as confusion and coma.
• Symptoms include glucose levels exceeding 30 mmol/L, very dry mouth, and polyuria.
• Further symptoms include lethargy, confusion, seizures, hypotension, and tachycardia.
• There are no significant ketones or acidosis present.

Nursing Management for DKA and HHS (A–E)

• Airway: Ensure the airway is clear; administer oxygen if the patient is hypoxic.
• Breathing: Provide oxygen via a non-rebreather mask at 15L, and monitor the respiratory rate.
• Circulation: Establish IV access, administer 0.9% saline, and monitor heart rate, blood pressure, and ECG changes related to potassium levels.
• Disability: Monitor Glasgow Coma Scale (GCS) scores, check blood glucose levels hourly, and assess mental status.
• Exposure: Perform a full-body check for potential infection triggers; check temperature and skin turgor.

Chronic Complications of Type 2 Diabetes

• Neuropathy: Nerve damage results in numbness and tingling in the extremities.
• Nephropathy: Kidney damage leads to proteinuria and chronic kidney disease.
• Retinopathy: Damage to blood vessels in the eyes can cause vision loss.
• Peripheral vascular disease: Poor circulation results in delayed wound healing, ulcers, and potential gangrene.
• There is an increased susceptibility to infections.

Relationship Between Insulin and Potassium

• Insulin facilitates the movement of potassium into cells
• As insulin is administered, serum potassium levels decrease.
• Monitoring potassium levels during DKA treatment is critical to prevent hypokalemia, which can lead to arrhythmias.

Pathophysiology of Acute Renal Failure (Acute Kidney Injury – AKI)

• AKI is a sudden decline in kidney function occurring over hours or days.
• This decline leads to the accumulation of waste products, fluid, and electrolyte imbalances.
• Types of AKI:
  • Pre-renal: Reduced blood flow to the kidneys caused by hypovolemia, hypotension, or heart failure.
  • Intra-renal: Direct kidney damage from nephrotoxic drugs or glomerulonephritis.
  • Post-renal: Obstruction due to kidney stones or an enlarged prostate.
• Reduced perfusion or injury leads to decreased glomerular filtration rate (GFR) and decreased urine output (oliguria or anuria).
• Accumulation of urea and creatinine results in increased serum creatinine and BUN levels.
• This condition can cause fluid overload, electrolyte imbalances (hyperkalemia, metabolic acidosis), and hypertension.
• The condition can potentially recover fully or progress to chronic kidney disease if not resolved.
• Symptoms include decreased urine output, edema, confusion, fatigue, nausea, vomiting, and elevated creatinine and potassium levels.

Pathophysiology of Chronic Kidney Disease (CKD) & Related Signs/Symptoms

• CKD involves progressive, irreversible kidney damage that happens over months to years.
• Ongoing damage from conditions like diabetes or hypertension leads to nephron loss.
• Remaining nephrons undergo hypertrophy and eventually fail, reducing GFR.
• In turn, this leads to the accumulation of urea, creatinine, fluid, and electrolyte imbalances.
• Key Complications:
  • Anemia: Decrease in erythropoietin leads to reduces red blood cell production.
  • Hyperphosphatemia and Hypocalcemia: Results in bone disease (renal osteodystrophy).
  • Metabolic acidosis.
  • Fluid retention: Leads to edema, hypertension, and pulmonary edema.
  • Uremia: Results in confusion, nausea, and itchy skin.

Pathophysiology of Metabolic Acidosis in Kidney Injury

• The kidneys cannot effectively excrete hydrogen ions (H⁺) or reabsorb bicarbonate (HCO₃⁻).
• The impairment results in increased retention of H⁺ ions and decreased production/reabsorption of bicarbonate.
• These issues lead to a decrease in blood pH.

Pathophysiology of Hypernatremia

• Hypernatremia indicates high serum sodium levels ( 145 mmol/L), typically due to fluid loss (e.g., diarrhea, vomiting, dehydration).
• High sodium levels draw water out of brain cells via osmosis.
• This process leads to cellular dehydration and shrinkage of brain cells.
• Neurological symptoms include lethargy, irritability, confusion, and, in severe cases, seizures.
• Treatment involves IV administration of Dextrose 5% or 0.45% NaCl (hypotonic fluid).
• Sodium levels must be corrected gradually to prevent cerebral edema.

ABG Interpretation & Acid-Base Imbalances

• Respiratory Acidosis:
  • Cause is hypoventilation (e.g., COPD, sedation, respiratory depression).
  • ABG results show decreased pH, increased CO₂, normal or increased HCO₃⁻ (compensation).
  • Symptoms are confusion, drowsiness, and shallow breathing.
  • Kidneys retain bicarbonate to compensate.
• Respiratory Alkalosis:
  • Cause is hyperventilation (e.g., anxiety, pain, early asthma attack).
  • ABG findings are increased pH, decreased CO₂, normal or decreased HCO₃⁻.
  • Symptoms are dizziness, light-headedness, and tingling.
  • Kidneys excrete bicarbonate to compensate.
• Metabolic Acidosis:
  • Cause is DKA, kidney failure, or diarrhea (loss of HCO₃⁻).
  • ABG shows decreased pH, decreased HCO₃⁻, and normal or decreased CO₂.
  • Symptoms include Kussmaul breathing, nausea, and confusion.
  • Lungs increase respiratory rate to eliminate CO₂ as compensation.
• Metabolic Alkalosis:
  • Cause is vomiting, diuretics (loss of H⁺), or excess antacids.
  • ABG findings are increased pH, increased HCO₃⁻, and normal or increased CO₂.
  • Symptoms include weakness, cramps, and slow breathing.
  • Lungs slow down breathing to retain CO₂ as compensation.

Two Organs for Acid-Base Regulation

• Lungs: Regulate CO₂ via ventilation in the short term.
• Kidneys: Regulate HCO₃⁻ and excrete H⁺ in the long term.

Pathophysiology of Alcoholic Liver Cirrhosis

• Chronic alcohol intake results in inflammation and fibrosis of the liver.
• Repeated injuries lead to scar tissue replacing functional tissue.
• Disrupts essential liver functions such as detoxification, protein synthesis, and clotting.

Complications of Chronic Liver Failure

• Ascites:
  • Portal hypertension and low albumin levels cause fluid to leak into the peritoneal cavity.
  • Signs include abdominal swelling and shortness of breath.
• Esophageal Varices:
  • Increased portal pressure results in dilated veins in the esophagus.
  • There is a risk of rupture and bleeding.
  • Signs include vomiting blood (hematemesis) and melena (black, tarry stools).
• Jaundice:
  • The liver's inability to metabolize bilirubin causes a buildup in the blood.
  • This results in yellowing of the skin and eyes.

Hepatic Encephalopathy

• The failing liver cannot convert ammonia to urea, leading to a buildup of ammonia.
• Ammonia crosses the blood-brain barrier, causing CNS toxicity.
• Signs include altered level of consciousness, confusion, tremors (asterixis), and coma.

Nursing Priorities for Liver Cirrhosis

• Monitor fluid balance through daily weights and assessment of ascites.
• Implement a low-sodium diet.
• Monitor for bleeding risks due to low platelet levels.
• Administer lactulose to reduce ammonia levels.
• Monitor neurological status for signs of encephalopathy.
• Prevent infection through vigilant care.
• Promote nutrition by providing small, frequent meals.
• Educate the patient on the importance of alcohol abstinence.

Why Do a CT Scan Before Thrombolytics?

• A CT scan distinguishes between ischemic and hemorrhagic stroke.
• Thrombolytics, such as tPA, can cause fatal bleeding in hemorrhagic stroke, so it must be ruled out first.

Diffuse vs Focal Brain Injury

• Diffuse brain injury: Widespread axonal injury (e.g., shaking, TBI) that results in a decreased level of consciousness.
• Focal brain injury: Localized injury (e.g., contusion, hematoma) which causes specific deficits such as limb weakness.

Coup-Contrecoup Injury

• The initial brain injury occurs at the site of impact, known as the coup.
• The secondary injury occurs on the opposite side as the brain bounces inside the skull, termed the contrecoup.
• This type of injury is common in car accidents or falls.

Pathophysiology of Stroke (CVA)

• Stroke involves the disruption of cerebral blood flow, leading to brain ischemia.
• The event can be ischemic (blockage) or hemorrhagic (ruptured vessel).
• Lack of oxygen and glucose causes brain tissue death.
• Signs include facial droop, weakness, slurred speech, and visual disturbances.

Types of Seizures

• Generalized Tonic-Clonic: Involves full body convulsions and loss of consciousness.
• Focal (partial): Affects one area of the brain/body, and may or may not alter consciousness.
• Absence: Characterized by brief staring spells without convulsions, common in children.

Post-Ictal A–E Seizure Nursing Care

• A: Airway – Place the patient in the recovery position and suction as needed.
• B: Breathing – Administer oxygen if needed and monitor the respiratory rate.
• C: Circulation – Check vital signs, ECG, and blood glucose levels.
• D: Disability – Assess the Glasgow Coma Scale (GCS) and perform neurological checks.
• E: Exposure – Look for any injuries or signs of infection, and take the patient's temperature.

Stroke Nursing Interventions

• Administer thrombolytics if the stroke is ischemic and within the appropriate time window.
• Provide anticoagulants and antiplatelets such as aspirin.
• Monitor neurological status and vital signs closely.
• Perform a swallowing assessment to prevent aspiration.
• Reposition the patient regularly to prevent pressure sores.
• Promote early mobilization if the patient is stable.
• Provide referrals for speech and physical therapy.
• Manage blood glucose levels.
• Offer education and emotional support to the patient and family.

Herpes Varicella vs. Zoster + Precautions

• Varicella (chickenpox): Primary infection characterized by vesicles and an itchy rash.
• Herpes Zoster (shingles): Reactivation of the varicella virus, following a dermatome pattern.
• Both are spread through airborne and contact routes.
• Precautions include placing the patient in a negative pressure room, using an N95 mask, gloves, and gown.

Scabies Pathophysiology & Care

• Scabies is caused by the Sarcoptes scabiei mite.
• The female mite burrows under the skin to lay eggs, causing intense itching, especially at night.
• Common areas affected include the arms, groin, and fingers.
• It is highly contagious.
• Nursing management:
  • Use PPE (gloves, gown).
  • Wash linens and clothes in hot water.
  • Apply Permethrin cream and repeat in 7–14 days.
  • Treat all close contacts.
  • Watch for secondary infections such as cellulitis.

Burn Injury Pathophysiology

• Burn damage to skin layers triggers an inflammatory response.
• Increased capillary permeability causes fluid shifts from the intravascular to the interstitial space.
• This leads to fluid loss, hypovolemia, and electrolyte imbalances.
• There is an increased risk of infection and compartment syndrome, especially with circumferential burns.
• Protein loss, including albumin, decreases oncotic pressure, causing edema.