NURBN2027 Exam Concept Maps PDF

Kidneys Module 1: Renal and Urinary disorders UTIs Demonstrate understanding of the structure and function Describe the Di...

Kidneys Module 1: Renal and Urinary disorders UTIs Demonstrate understanding of the structure and function Describe the Discuss the cause, pathophysiology of urinary tract infection The pathogenic microbe entering the urinary tract attaching to of the kidneys pathophysiology epithelial cells and damaging lining of urethra. This inflammatory The kidneys are located just above waist between the state referred as urethritis. E.coli or bacteria ascends urinary peritoneum and back of abdomen. The two kidneys are tract, enters bladder, attaching to the bladder epithelial cells being the liver and intestines in the small of back partially causing cell apoptosis (death) & exfoliation = inflammation protected by 11th and 12th pair of ribs. The function of the considered lower UTIs. An upper UTI is when this ascends to the kidneys is to excrete waste & foreign substances in the kidney/s & pyelonephritis (renal pelvis + parenchyma/kidney). urine, regulate properties of blood; ionic composition, pH, homeostatic functions such as regulation of electrolytes, Glomerular Disorder acid-base balance and BP by producing enzyme renin and Discuss the cause, pathophysiology of Glomerular produce hormones Vitamin D and erythropoietin. disorders Acute glomerulonephritis = structural and functional Nephron changes; cellular proliferation leads to increase in Demonstrate understanding of the structure number of cells in glomerular tuft due to proliferation and function of the nephron of endothelial, mesangial and epithetlial cells. Each nephron consists of two parts: renal Nephrotic syndrome is inflammation of the glomerulus corpuscle and a renal tubule. The nephrons are caused by primary glomerular injury exacerbated by the functional units of the kidneys. Nephrons and immunologic responses, drugs, toxins, and infections, collecting ducts perform three basic functions: resulting in type III hypersensitivity reactions, filtration of the blood, re-absorption of water and antibodies, and inflammation. solutes, and secretion of wastes from the blood. AKI Filtered liquid passes through the proximal Discuss the cause of pre, intra and post renal failure, discuss convoluted tubule, Loop of Henle (neprhon loop) the pathophysiology of AKI and distal voncoluted tubule Pre-renal occurs upstream of the kidneys due to renal blood supply disruptions & caused by renal ischaemia, causing a Ureters, bladder and urethra decrease in GFR and tubular necrosis. Intrarenal occurs within the kidneys glomerular membrane becomes permeable to blood Structure and function of the ureters, bladder and or protein resulting in either haematuria or proteinuria, and urethra post-renal occurs due to obstruction of urine flow that is distal There are two ureters positioned behind the peritoneum, to the kidneys & compromises vascular supply, leading to one for each kidney which transports urine from renal nephron loss. Four clinical phases of AKI: initiation, oliguria, pelvis to the bladder. Gravity & hydro-static pressure, diuresis and recovery muscular contractions push urine = ureters as bladder fills compresses opening of ureters preventing back flow. The Renal Calculi CKD urinary bladder is in the pelvic cavity a hollow, muscular List 3 causes of CKD pathophysiology impact of CKD Identify two causes of renal calculi, on 3 body systems organ in males in front of rectum, females in front of the discuss the pathophysiology. Occurs in vagina + below uterus held in place by folds of peritoneum the urinary tract, usually in the renal pelvis, 1. Prerenal (decreased renal perfusion pressure), 2. with 700-800 ml capacity smaller in females due to uterus. intrinsic renal (pathology of the vessels, glomeruli, or is due to the ions precipitating from 3. tubules-increases. Cardiovascular risks due to fluid The stretch receptor in bladder transmit nerve impulses to solutions in the urine. It is referred to as spinal cord = trigger of reflect and urethral sphincter and buildup in the heart and causing blood pressure to nephrolithiasis or urolithiasis. Calcium; rise. respiratory; altering fluid homeostasis, acid- pelvic muscles controls this. Urethra carries urine out of stones formed when it combines with body, small tube leads from bladder to exterior; females base balance and vascular tone. Endocrine; oxalate or phosphate, struvite caused by deficiency of: calcitriol, testosterone, insulin-like (4 cm length), males (approx 20 cm). UTI’s, Uric acid and cystine stones growth factor and, erythropoietin (EPO).  Kidneys Module 1: Renal and Urinary disorders UTIs Diagnostic tests or investigations Clinical manifestations - Symptoms: Dysuria, Imaging Studies Define and discuss clinical frequent urination, urgency, and lower abdominal Ultrasound: Non-invasive, assesses kidney manifestations pain. In more severe cases, fever, chills, and flank size, structure, and the presence of stones pain. Signs: May present with fever, or obstruction. CT Scan: Provides detailed costovertebral angle (CVA) tenderness, and images for identifying stones, tumours, or cloudy or foul-smelling urine. structural abnormalities. X-rays: Diagnostic tests - see urinalysis testing Sometimes used to detect certain types of kidney stones. Glomerular Disorder Clinical manifestations - Symptoms: Hematuria (blood in urine), proteinuria (protein in urine), Nephron oedema, hypertension, and in severe cases, renal failure. Signs: Swelling (especially in the face and Diagnostic tests - Kidney Biopsy legs), frothy urine (due to protein), and possible Purpose: Obtains a tissue sample to weight gain due to fluid retention. diagnose specific kidney diseases, Diagnostic tests - urinalysis, serum creatinine such as glomerulonephritis or measurement, and kidney biopsy. interstitial nephritis. Standards: Performed when other tests are AKI inconclusive and specific kidney Clinical manifestations pathology needs to be identified. Symptoms: Decreased urine output, swelling (oedema), fatigue, confusion, shortness of breath, and in severe Ureters, bladder cases, seizures or coma. Signs: Elevated blood pressure, reduced urine output, and potential for fluid overload. and urethra Diagnostic tests - AKI is strongly associated with a sudden drop in GFR and as such testing blood for FBC, Diagnostic tests U&Es and renal function in conjunction with a urinalysis Urinalysis; Purpose: Detects Renal is important in the clinical diagnosis of AKI. abnormalities in the urine such as protein, blood, glucose, and specific Calculi CKD gravity. Helps in diagnosing conditions like infections, glomerulonephritis, and Clinical manifestations Symptoms: Clinical manifestations Symptoms: Fatigue, weakness, anaemia, appetite kidney stones. Standards: Testing for Severe pain (flank pain), hematuria loss, nausea, vomiting and changes in urination patterns (e.g., more proteinuria (e.g., urine protein-to- (blood in urine), frequent urination, frequent or less frequent urination). Signs: Oedema, hypertension, and creatinine ratio), haematuria, and the and nausea or vomiting. Signs: Pain changes in skin pigmentation. Diagnostic tests - Estimated Glomerular presence of casts or crystals. A MSU may radiate to the lower abdomen Filtration Rate (eGFR) Purpose: Estimates kidney function by calculating (midstream urine sample), assess for and groin; sometimes, there’s visible the rate at which the kidneys filter blood. Standards: An eGFR below 60 neutrophils, bacteria, nitrites, and blood in the urine. mL/min/1.73 m² over three months is indicative of CKD. blood, and send it for culture and Diagnostic tests - The primary Discuss three management/treatment options - Lifestyle & dietary sensitivity; if sepsis is suspected, blood diagnostic test for renal calculi is a modifications (restrict protein, sodium, potassium, and phosphorus tests may show leukocytosis and non-contrast CT scan of the intake) to reduce kidney strain. Pharmacological treatments (ACE neutrophilic, with potential imaging US abdomen and pelvis, which inhibitors or ARBs) focus on controlling blood pressure and managing or CT studies to rule out other effectively identifies the presence, symptoms, while renal replacement therapy (dialysis or transplant) is conditions. size, and location of kidney stones. used when kidney function is severely impaired.  Kidneys Module 1: Renal and Urinary disorders UTIs Trimethoprim/sulfamethoxazole (Bactrim) interferes Pharmacological treatment for kidney-related conditions includes antihypertensives like Enalapril Discuss different with bacterial nucleic acid synthesis and can cause rash, nausea, and potential interactions with warfarin and Losartan, diuretics such as Furosemide and pharmacological treatments and nephrotoxic agents. Cephalexin, a first-generation Hydrochlorothiazide, phosphate binders like cephalosporin, is used for various infections and may Sevelamer, and vitamin D analogues such as cause nausea, hypersensitivity, and interactions with Calcitriol. Additionally, Erythropoiesis-stimulating anticoagulants and nephrotoxic drugs. Amoxicillin, a β- agents (Epoetin alfa), immunosuppressants lactam antibiotic, is effective against many infections (Prednisone), and antibiotics (Nitrofurantoin) are but can lead to hypersensitivity reactions and used, all requiring regular monitoring of renal interactions affecting oral contraceptives. Ceftriaxone, function and electrolytes. a third-generation cephalosporin, is noted for its Nephron incompatibility with Hartmann's solution and follows similar general actions and interactions as other cephalosporins. Key nursing considerations include Pharmacological treatment for nephron- monitoring blood counts, renal and liver function, and related conditions includes potential allergic reactions across all these antihypertensives (ACE inhibitors and ARBs), medications. diuretics, phosphate binders, vitamin D analogues, erythropoiesis-stimulating agents, immunosuppressants, and AKI antibiotics, all of which require regular Management of acute kidney injury (AKI) monitoring of renal function and electrolytes. includes monitoring fluid and electrolyte imbalances, reducing metabolic rate to limit Glomerular Disorder potassium and waste buildup, preventing infections with aseptic techniques, ensuring proper skin care, and providing psychological Management of kidney support and education to patients and conditions may include families. Diuretics may help manage volume dietary changes to reduce Renal overload in cases of pre-renal AKI, but if protein, salt, and potassium; unresponsive, renal replacement therapy, corticosteroids like Calculi such as dialysis or filtration, may be prednisone; dialysis to filter toxins and excess fluid; Pharmacological intervention for renal calculi CKD necessary. diuretics for swelling; focuses on pain management with NSAIDs or immunosuppressants for Pharmacological treatment for chronic kidney disease (CKD) opioids, prescribing antibiotics for any urinary immune-related includes managing complications such as hypertension with tract infections, and using alpha-blockers to relax glomerulonephritis; antihypertensives, controlling diabetes with insulin or oral urinary tract muscles for easier stone passage. antihypertensives such as hypoglycemics, and addressing electrolyte imbalances, particularly Patients are advised to increase fluid intake, ACE inhibitors or ARBs; and hyperkalemia. Patients may also receive phosphate binders and possibly receiving intravenous fluids if plasmapheresis to remove vitamin D analogs to manage mineral metabolism. Additionally, dehydrated, and urine should be strained to excess proteins from the those with end-stage renal disease (ESRD) may require renal identify expelled stones. A common procedure is blood. replacement therapies such as hemodialysis or peritoneal dialysis, a lithotripsy: the use of sound or shock waves to with kidney transplantation being the preferred long-term solution. crush a stone. A ureteral stent may be inserted For patients who opt against renal replacement therapy, into the affected ureter to maintain its patency. conservative and palliative care options should be discussed. NURBN2027 - Module 1: Renal and Urinary disorders Diagrams NURBN2027 - Module 1: Renal and Urinary disorders Diagrams NURBN2027 - Module 1: Renal and Urinary disorders Diagrams  Module 2: Endocrine Disorders 1: Diabetes Mellitus Type 1 Diabetes Mellitus Discuss and explain the pathophysiology Diabetes: Micro Diabetes Mellitus can lead to significant microvascular complications, including Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune condition that affects the retinopathy, nephropathy, and neuropathy. Retinopathy results from chronic pancreas, leading to an inability to produce insulin. Cause: Autoimmune destruction of hyperglycemia, damaging retinal vessels and risking blindness. Nephropathy involves pancreatic beta cells (genetic & environmental triggers). Progression: Loss of insulin kidney damage from elevated blood sugar, leading to protein leakage and potential production → hyperglycemia, symptoms (thirst, urination, fatigue, weight loss), risk of kidney failure. Neuropathy affects peripheral nerves, causing numbness and increasing Diabetic Ketoacidosis (DKA). Treatment: Insulin therapy (injections/pump), blood the risk of foot ulcers. Key risk factors include prolonged hyperglycemia, diabetes glucose monitoring, diet & exercise. Complications: Cardiovascular disease, duration, and conditions like hypertension. Effective management through blood glucose neuropathy (nerve damage), retinopathy (vision loss), nephropathy (kidney damage). control, regular screenings, and lifestyle changes is crucial for early detection and prevention of complications. Type 2 Diabetes Mellitus Type 2 Diabetes Mellitus (T2DM) is primarily caused by Diabetes: Macrovascular genetic factors and lifestyle choices, such as poor diet, Type 2 Diabetes Mellitus increases the risk of macrovascular inactivity, and obesity, leading to insulin resistance and complications that affect large blood vessels, leading to elevated blood sugar levels. Over time, the pancreas may serious health issues. Prolonged high blood sugar causes become insufficient in insulin production. Common atherosclerosis, heightening the risk of cardiovascular disease, symptoms include increased thirst, frequent urination, heart attacks, and strokes. Peripheral artery disease (PAD) fatigue, blurred vision, and slow wound healing. Treatment occurs when narrowed arteries restrict blood flow to the limbs, focuses on lifestyle changes—such as a healthy diet, regular causing pain and potentially leading to ulcers or amputations. exercise, and weight management—as well as medications Key risk factors include chronic hyperglycemia, hypertension, like Metformin to improve insulin sensitivity. If poorly dyslipidemia, and obesity. Effective management involves managed, T2DM can lead to serious complications, including maintaining blood glucose levels, controlling blood pressure heart disease, nerve damage, kidney issues, and vision loss. and lipids, and making lifestyle changes. Early intervention and However, with effective management and monitoring, these monitoring are essential to prevent complications and complications can often be delayed or prevented, helping enhance cardiovascular health. individuals maintain a good quality of life. Pathophysiology T1DM Diabetic Ketoacidosis Type 1 Diabetes Mellitus (T1DM) involves autoimmune destruction of Diabetic Ketoacidosis (DKA) is a serious complication of Type 1 Diabetes insulin-producing beta cells in the pancreas, leading to insulin caused by missed insulin injections, illness, or stress, leading to insulin deficiency and elevated blood glucose levels (hyperglycemia). The deficiency. The body breaks down fat for energy, producing ketones and presence of autoantibodies, such as glutamic acid decarboxylase causing metabolic acidosis, dehydration, and electrolyte imbalances. (GAD) antibodies, indicates this autoimmune response. With Symptoms include extreme thirst, frequent urination, nausea, vomiting, insufficient insulin, the body breaks down fat for energy, producing abdominal pain, rapid breathing with a "fruity" odour, fatigue, and ketones that can cause Diabetic Ketoacidosis (DKA). Increased confusion. If untreated, DKA can lead to coma or organ failure. glucose production in the liver worsens hyperglycemia. Chronic high Emergency treatment typically involves hospitalisation with IV insulin, fluids, and electrolyte management. Pathophysiology blood sugar can lead to complications like retinopathy, nephropathy, neuropathy, cardiovascular disease, and stroke, HHNS T2DM highlighting the significant health risks associated with T1DM. Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) is a Type 2 Diabetes Mellitus (T2DM) is marked by insulin resistance and impaired insulin secretion, leading to severe complication of Type 2 Diabetes, often triggered by infections chronic hyperglycemia. Insulin resistance arises when muscle, liver, and adipose tissue cells become less or dehydration. It occurs when blood sugar exceeds 600 mg/dL, responsive to insulin, often due to obesity, reducing glucose uptake. Initially, the pancreas compensates causing severe dehydration and confusion without significant ketone by increasing insulin production, but over time, beta cells become exhausted. The liver also continues to production. Key symptoms include excessive thirst, frequent produce excess glucose, worsening hyperglycemia. Dysfunctional adipose tissue releases inflammatory urination, and potential seizures. Treatment involves IV fluids, insulin cytokines that further promote insulin resistance, while changes in gut hormones disrupt glucose therapy, and electrolyte management. Prompt intervention is regulation. Prolonged hyperglycemia can lead to complications like retinopathy, nephropathy, essential to prevent organ failure or death, particularly in older adults, neuropathy, cardiovascular disease, and peripheral artery disease. Understanding T2DM's but early treatment can enable full recovery. pathophysiology is essential for effective management and lifestyle interventions.  Module 2: Endocrine Disorders 1: Diabetes Mellitus Diabetes: Micro Type 1 Diabetes Mellitus Discuss the clinical Microvascular complications of diabetes mellitus result from Type 1 Diabetes Mellitus (T1DM) rapidly presents with symptoms manifestations, prolonged hyperglycemia and primarily affect small blood vessels, due to acute insulin deficiency, including polyuria (increased urination), polydipsia (excessive thirst), polyphagia (increased investigations, of patients leading to significant morbidity. The three main types are: 1. Diabetic Retinopathy: Damage to retinal blood vessels, causing hunger), unexplained weight loss, and fatigue. Severe cases can with diabetes mellitus symptoms like blurred vision and floaters, potentially leading to lead to Diabetic Ketoacidosis (DKA), with symptoms like nausea, vision loss. Early detection through regular eye exams is crucial. 2. abdominal pain, rapid deep breathing (Kussmaul respirations), Diabetic Nephropathy: Kidney damage that starts with fruity-smelling breath, and altered mental status. Diagnosis microalbuminuria and can progress to proteinuria and end-stage involves blood glucose testing (fasting plasma glucose ≥126 mg/dL renal disease. Regular monitoring of kidney function and urine or random plasma glucose ≥200 mg/dL) and Haemoglobin A1c protein is vital for early intervention. 3. Diabetic Neuropathy: (HbA1c) levels of 6.5% or higher. Urinalysis may show glucose and Affects peripheral and autonomic nervous systems, leading to ketones, while autoantibody testing confirms autoimmune beta- numbness, tingling, pain, and gastrointestinal and cardiovascular cell destruction. Low C-peptide levels indicate insufficient insulin issues. Investigations include eye exams (fundoscopy), urine tests production, consistent with T1DM. Timely diagnosis and for albumin and creatinine, and nerve conduction studies. management are essential to prevent acute and chronic Maintaining tight glycemic control, along with managing blood complications. pressure and lipid levels, is essential to prevent or slow progression. Regular screening and early management are key to Type 2 Diabetes Mellitus reducing the burden of these complications. Type 2 Diabetes Mellitus (T2DM) features a Diabetes: Macrovascular gradual onset of symptoms due to insulin Macrovascular complications of diabetes significantly resistance and impaired insulin secretion. increase the risk of cardiovascular diseases and often Common manifestations include polydipsia present with subtle symptoms. Common manifestations (increased thirst), polyuria (frequent urination), include: 1) Coronary Artery Disease (CAD): May cause chest polyphagia (excessive hunger), fatigue, blurred pain (angina) and fatigue. 2) Cerebrovascular Disease: Can vision, and slow-healing sores. Patients may lead to transient ischaemic attacks (TIAs) or strokes with experience unintended weight loss despite sudden neurological deficits. 3) Peripheral Artery Disease increased appetite due to ineffective glucose (PAD): Characterised by leg pain (claudication) and non- utilization. Diagnosis typically involves blood healing wounds. Investigations involve regular blood glucose testing (fasting plasma glucose ≥126 pressure monitoring, lipid profile assessments, and mg/dL or random plasma glucose ≥200 mg/dL) electrocardiograms (ECGs). Additional diagnostic tools and Haemoglobin A1c (HbA1c) levels of 6.5% or may include stress tests, echocardiograms, carotid higher. An Oral Glucose Tolerance Test (OGTT) ultrasounds, ankle-brachial index (ABI) testing, and may also be used, with a 2-hour plasma glucose level of 200 mg/dL or higher being diagnostic. DKA coronary angiography. Regular blood glucose monitoring, including HbA1c testing, is crucial for managing diabetes Urine tests may show glucose and ketones, and reducing macrovascular risk. especially in uncontrolled cases. Due to the Diabetic Ketoacidosis (DKA) is a severe complication primarily increased cardiovascular risk, routine screening of Type 1 Diabetes but can occur in Type 2 Diabetes during HHNS for commorbidities like hypertension and stress. Symptoms include excessive thirst, frequent urination, Hyperglycemic Hyperosmolar Nonketotic Syndrome dyslipidemia is essential. T2DM is often linked to nausea, abdominal pain, fatigue, confusion, rapid deep (HHNS) is a severe complication of Type 2 Diabetes, obesity and sedentary lifestyles, making lifestyle breathing (Kussmaul respirations), and fruity-smelling breath. characterised by blood glucose levels over 600 mg/dL and interventions crucial. Early diagnosis and DKA results from insulin deficiency, leading to increased hyperosmolarity without significant ketosis. Symptoms management—including lifestyle changes, oral glucose production and fat breakdown, causing ketone include severe dehydration, extreme thirst, polyuria, dry medications, and sometimes insulin therapy—are accumulation and metabolic acidosis. Diagnosis is confirmed mouth, fatigue, and altered mental status. Diagnosis vital to prevent complications such as by blood glucose >250 mg/dL, pH