Apprenticeship Learning Log
Date of Learning: 15/10/25
Time: 9:30 – 16:30
Title of learning activity: Understanding Learning Disabilities and Long-Term Conditions – Core considerations for TNA.
Renal Patients and decision-making AKI
Diary of Learning activity
(itemise learning activity and reflect on the main points of learning from each. You should identify for each entry the relevant KSB)
Reflection on Learning Activity (include model of reflection e.g. Driscoll or Gibbs):
Today’s session facilitated discussion on:
Learning disability (LD) is a significant, lifelong condition that affects a person’s ability to learn new information, understand complex ideas, and cope independently.
Key Characteristics
- Reduced intellectual ability (IQ <70)
- Difficulty with everyday activities (e.g., communication, social skills, self-care)
- Onset before adulthood
Key long-term conditions within the LD population
- Diabetes: Poor diet, limited physical activity, and challenges with self-management
- Epilepsy: Often co-occurs with neurological disorders like cerebral palsy or Down syndrome
- Respiratory Diseases: Higher risk due to aspiration, poor posture, and reduced mobility
- Cardiovascular Diseases: Linked to obesity, sedentary lifestyle, and lack of routine health checks
- Mental health disorders: Anxiety, depression, and behavioural challenges are frequently under-recognized
Core Considerations for TNA
| 1. Holistic assessment |
| Consider physical, emotional, social, and spiritual aspects of living with a chronic condition. | |
| 2. Self-management | |
| Support independence — encourage medication adherence, healthy lifestyles, and self-monitoring. | |
| 3. Continuity of care | |
| LTCs require coordinated care across primary, secondary, and community settings. |
| 4. Monitoring and escalation |
| Recognise early signs of deterioration and escalate promptly following clinical governance pathways. | |
| 5. Empowerment and education | |
| Provide health education and involve patients in goal setting and care planning. | |
| 6. Psychological impact | |
| Be mindful of anxiety, depression, and the emotional toll of long-term illness. |
During afternoon session, we discussed: Renal Patients and decision-making AKI (Acute Kidney Injuries)
Anatomy and Physiology of the Kidneys
The kidneys are two bean-shaped organs located on either side of the spine between the twelfth thoracic and third lumbar vertebrae. Each kidney is around 10–12 cm in length and protected by the ribs, adipose tissue, and a fibrous capsule, with the right kidney positioned slightly lower due to the liver.
Each kidney consists of the renal cortex, medulla, and pelvis. The cortex contains nephrons, the functional units responsible for blood filtration and urine formation. Urine passes from the renal pyramids in the medulla to the pelvis and then to the ureter.
Physiologically, the kidneys filter waste products, maintain fluid and electrolyte balance, and regulate blood pressure via the renin–angiotensin–aldosterone system. They also control acid–base balance, stimulate erythropoietin production for red blood cell formation, and activate vitamin D to support calcium regulation and bone health.
Acute Kidney Injury (AKI) is a sudden decline in kidney function that occurs over hours to days, leading to an accumulation of waste products, fluid imbalance, and electrolyte disturbances. It is identified by a rapid rise in serum creatinine, a reduction in urine output, or both.
Classification (KDIGO Staging, 2012):
| Stage | Serum Creatinine Criteria | Urine Output Criteria |
| Stage 1 | Increase in serum creatinine ≥ 26 µmol/L within 48 hours, or 1.5–1.9 times baseline | < 0.5 mL/kg/hr for 6–12 hours |
| Stage 2 | Serum creatinine 2.0–2.9 times baseline | < 0.5 mL/kg/hr for ≥ 12 hours |
| Stage 3 | Serum creatinine ≥ 3 times baseline, or ≥ 354 µmol/L, or initiation of renal replacement therapy | < 0.3 mL/kg/hr for ≥ 24 hours or anuria for ≥ 12 hours |
AKI is a clinical emergency that requires prompt recognition and management to prevent progression to chronic kidney disease or multi-organ failure.
Pathophysiology and Clinical Features of Acute Kidney Injury (AKI)
Pathophysiology:
Acute Kidney Injury (AKI) is a sudden decline in renal function resulting in the accumulation of waste products and fluid imbalance. It is classified as:
- Pre-renal AKI: due to reduced renal perfusion from causes such as hypovolaemia, dehydration, or sepsis.
- Intrinsic AKI: caused by direct renal damage, for example, acute tubular necrosis or nephrotoxic injury.
- Post-renal AKI: resulting from urinary outflow obstruction, such as renal calculi or prostatic enlargement.
These mechanisms lead to decreased glomerular filtration, retention of sodium and water, and raised serum urea and creatinine levels.
Clinical Features:
Common features include oliguria or anuria, fluid overload, peripheral oedema, and dyspnoea. Laboratory findings may show elevated creatinine, urea, hyperkalaemia, and metabolic acidosis. Patients may also experience nausea, fatigue, confusion, or cardiac arrhythmias. Prompt recognition and management are vital to prevent irreversible renal damage and multi-organ failure.
Effective management of Acute Kidney Injury (AKI) necessitates a structured, evidence-based approach, as the condition may progress rapidly and precipitate life-threatening complications. Treatment priorities encompass hemodynamic stabilization, identification and correction of the underlying etiology, prevention of further renal injury, management of metabolic and electrolyte disturbances, and provision of supportive care.
The primary objective is to ensure adequate renal perfusion.
- Volume status assessment and correction:
- Hypovolemia should be managed with intravenous crystalloid administration (e.g., normal saline or balanced solutions).
- Hypervolemia may require cautious diuretic therapy or fluid restriction.
- Blood pressure optimization:
- Maintain mean arterial pressure ≥ 65 mmHg in critically ill patients.
- Initiate vasopressors if hypotension persists despite fluid resuscitation.
- Continuous monitoring of vital signs, urine output, and indicators of fluid overload is essential.
AKI may be classified as pre-renal, intrinsic renal, or post-renal, each requiring targeted intervention:
- Pre-renal AKI (impaired perfusion):
- Etiologies: hypovolemia, heart failure, sepsis, pharmacologic agents
- Management: restore perfusion, discontinue nephrotoxic drugs
- Intrinsic renal AKI (structural renal damage):
- Etiologies: acute tubular necrosis, glomerulonephritis, interstitial nephritis
- Management: condition-specific therapy (e.g., immunosuppressants, appropriate antibiotics)
- Post-renal AKI (obstruction):
- Etiologies: urinary tract stones, tumors, strictures
- Management: relieve obstruction (e.g., catheterization, stenting, nephrostomy
Prevention of Further Renal Injury
- Discontinue or avoid nephrotoxic medications (e.g., NSAIDs, aminoglycosides, contrast agents, ACE inhibitors if appropriate).
- Adjust drug dosages according to renal function.
- Minimize exposure to contrast media or implement prophylactic hydration strategies.
AKI frequently precipitates significant metabolic disturbances:
- Hyperkalaemia: may be life-threatening; requires ECG monitoring and interventions such as calcium gluconate, insulin with glucose, β-agonists, or dialysis if refractory.
- Acid-base disorders: particularly metabolic acidosis, should be corrected.
- Fluid overload: may necessitate diuretic therapy or renal replacement therapy.
- Uremia: symptomatic uremia (e.g., pericarditis, encephalopathy) may require dialysis.
Monitoring of renal function -Serial measurement of serum creatinine and blood urea nitrogen is essential. Urine output should be closely monitored, with oliguria (<0.5 mL/kg/h for more than six hours) serving as a key prognostic indicator. Continuous assessment facilitates early recognition of renal recovery or progression.
AKI can lead to life-threatening electrolyte disturbances, fluid overload, metabolic derangements, uremia, hematologic abnormalities, infection, and cardiovascular complications. Early recognition and management of these complications are crucial to improving patient outcomes.
KSBs addressed:
K24: Know how to support people with commonly encountered symptoms including anxiety, confusion, discomfort and pain
K37: Understand the challenges of providing safe nursing care for people with complex co-morbidities and complex care needs
S3: Recognise and report any factors that may adversely impact safe and effective care provision
S24: Perform a range of nursing procedures and manage devices, to meet people’s need for safe, effective and person-centred care
S28: Support people with commonly encountered symptoms including anxiety, confusion, discomfort and pain
B1: Treat people with dignity, respecting individual’s diversity, beliefs, culture, needs, values, privacy and preferences