Pathophysiology and Pharmacology Book PDF

24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Pathophysiology and Pharmacology Book Site: Federation University Moodle Printed by: Dajou Buloba...

24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Pathophysiology and Pharmacology Book Site: Federation University Moodle Printed by: Dajou Buloba NURBN 2027 SEM2 2024: Nursing Context 7: Date: Thursday, 24 October 2024, 7:32 PM Course: Pathophysiology and Pharmacology Applied to Person- Centered Nursing Practice B Combined 001 Book: Pathophysiology and Pharmacology Book Table of contents 1. Introduction 2. Scenario 3. Disorders of the renal and urinary system 3.1. Revision of Anatomy and Physiology Key Concepts 3.2. Renal calculi 3.3. Urinary tract infection 3.4. Glomerulonephritis 3.5. Acute Kidney Injury 3.6. Chronic Renal Disease https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 1/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 1. Introduction  Intended Learning Outcomes Upon the completion of this Moodle content and with further reading you will be able to 1. Demonstrate understanding of the structure and function of the kidneys 2. Demonstrate understanding of the structure and function of the nephron 3. Discuss the structure and function of the ureters, bladder and urethra 4. Identify two causes of renal calculi, discuss the pathophysiology, pharmacology, signs and symptoms and diagnosis 5. Discuss the cause, pathophysiology, pharmacology , signs and symptoms and diagnosis of urinary tract infection 6. Discuss the cause, pathophysiology and treatment, signs and symptoms and diagnosis of Glomerular disorders (focus on acute glomerulonephritis and nephrotic syndrome) 7. Discuss the cause, progression, outcome and treatment of Acute Kidney Disease - List a cause of pre, intra and post renal failure, discuss the pathophysiology of AKI, discuss clinical manifestations/complications that occur due to AKI, discuss treatment options - List three causes of CKD, discuss the pathophysiology of CKD, discuss the impact of CKD on at least three body systems (such as cardiovascular), discuss three management/treatment options 8. Discuss the cause, progression, outcome and treatment of Chronic Kidney Disease  Alignment to Assessment Information in this Week will assist in the successful completion of Assessment Task : Asynchronous Video Presentation and Assessment : Practical Exam  Time Allocation Reading through this book and completing all associated activities is expected to take approximately 4-6 hours and must be done PRIOR to attending any scheduled synchronous class. https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 2/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 2. Scenario  Activity - Scenario Complete the scenario to prepare for the pathopthysiology book: https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 3/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3. Disorders of the renal and urinary system Overview In this week, we will be covering the renal and urinary disorders. We will start by reviewing some anatomy and physiology key concepts appertaining to the renal system then discuss the pathophysiology of some disorders along with medications to treat these conditions. The urinary system is composed of the kidneys, ureters, bladder and urethra. Urine is formed within the nephrons, and from there, it flows into the ureter. The ureter is a fibromuscular tube, approximately 24 – 30cm long and connects each of the kidneys to the bladder. It’s important you understand the anatomy of the ureter, namely the areas in which it narrows as there will be a propensity for obstruction. Obstructions of the ureter will be covered in more detail later in this module. Once urine enters the ureter, it moves into the bladder via peristaltic waves from smooth muscle contraction of the ureter wall. The urethra arises from the base of the bladder. For males, it passes through the penis, and females it opens anterior to the vagina. The bladder is under control of the internal sphincter (involuntary smooth muscle) and external sphincter (voluntary smooth muscle) Kidney Function Test Also you need to know the pathology tests that are undertaken to ascertain the function of the kidneys; these are called the Renal Function Tests and the values are as follows: https://www.researchgate.net/profile/Marwa-Hamed- 3/publication/311398426/figure/tbl1/AS:670380918312967@1536842674241/Commonly-used-renal-function-tests-with-their- references-values.png (Links to an external site.) When these values are deranged, this is an indicator that the kidneys are not functioning normally which may be attributed to any of the disease conditions covered in this module. https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 4/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Micturiton Furthermore, Micturition (urination) is the process of urine excretion from the urinary bladder. Most of the time, the bladder (detrusor muscle) is used to store urine. As it fills, the rugae distend and a constant pressure in the bladder (intra-vesicular pressure) is maintained. This is known as the stress-relaxation phenomenon. Smooth muscle stretch initiates the micturition reflex by activating stretch receptors in the bladder wall. This autonomic reflex causes the detrusor muscle to contract and the internal urethral sphincter muscle to relax, allowing urine to flow into the urethra. Micturition Reflex - Neural Control of Urination Animation Video. https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 5/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3.1. Revision of Anatomy and Physiology Key Concepts Revision of Anatomy and Physiology Key Concepts The focus for this week will be the urinary system, including the kidneys, bladder, ureters, and urethra. The primary function of the kidney and urinary system is to maintain homeostasis by controlling the fluid and electrolyte balance within the body and removing wastes as required. This waste is removed via our urine, which is produced through a highly complex process involving excretion and re-absorption. We are going to review the renal system’s normal anatomy and physiology before we get into the pathophysiology of this system. If this knowledge is already familiar to you, feel free to skip ahead to where we commence our content on the pathophysiology of the renal system. For those of you who would like a refresher, keep on reading below. Let’s start by looking at the kidney. There are two kidneys, a left and a right, located retroperitoneally on the posterior wall of the abdomen. The kidney is considered the workhouse of the renal system. Several hormones are produced by the kidneys, a hormone (erythropoietin) produced by the kidneys stimulates red blood cell production by the bone marrow. Other hormones produced by the kidneys help regulate blood pressure (renin) via the renin angiotensin aldosterone system or are released during stress (cortisol) causing a retention of sodium and subsequent retention of water. To sum up, the kidneys are powerful chemical factories that perform the following functions: remove waste products from the body remove drugs from the body balance the body's fluids release hormones that regulate blood pressure produce an active form of vitamin D that promotes strong, healthy bones control the production of red blood cells regulate the acid-base balance The following image depicts the anatomy of the kidney, ensure you have a good grasp of the different parts of the kidney https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 6/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle This image summarises how the nephron performs reabsorption, secretion and excretion of fluids and electrolytes through its different parts. Have a look Watch this video which provides an overview of the function of the nephron, the functional unit of the  kidney https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 7/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Nephron Function https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 8/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3.2. Renal calculi  Overview Urinary calculi that occur in the urinary tract, usually in the renal pelvis, is due to the ions precipitating from solutions in the urine. It is referred to as nephrolithiasis or urolithiasis. It is usually caused by calcium ions (Ca2+ ) which forms precipitates with oxalate (most common), phosphate or urate ions to form calcium oxalate, calcium phosphate or calcium urate. The other types of stones can include uric acid crystals, cystine and struvite. Stones can also form when there is a deficiency of substances that normally prevent crystallisation in the urine, such as citrate, magnesium, nephrocalcin and uropontin. Stones can occur due to reduced water content of urine due to dehydration or it can occur during treatment with medications such as lop diuretics. a summary of the four types of stones is presented below: Calcium - The most common stones are formed when calcium combines with other minerals like oxalate or phosphate Struvite - Struvite stones are caused by urinary tract infections (UTI’s) and can be quite large Uric Acid - Uric acid stones are often caused by eating very large amounts of protein foods and are often softer than other types of stones Cystine stones - Cystine stones are a rare inherited condition where the protein cysteine can build up in urine and form stones If stones are small enough then the person may be asymptomatic and the stones can remain where they are or be passed through the urinary system. Larger stones can cause urinary tract obstruction and damage to structures of the urinary tract that causes intense pain that can originate near the ureters and can radiate. Chills and fever can occur and as the stone passes through structures and damages them, blood can appear in the urine. 4-8% of Australians develop symptomatic kidney stones over their lifetime; 1 in 10 men and about 1 in 35 women. Watch the following video detailing the pathophysiology of renal calculi Urinary/Kidney Stones - Overview (signs and symptoms, risk factors, pathophysiology, tre… tre… Signs and Symptoms https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 9/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle The main sign and symptom for these patients is pain. Pain is usually due to a stone being present in the ureter which distends the ureteral wall. Onset of pain is usually abrupt and severe - referred to as ureteral colic. As the urine flow becomes more obstructed the pain becomes more intense and the ureteral wall becomes more and more distended by a build-up of urine behind the stone. The pain tends to by rhythmic and ipsilateral. the pain begins in the flank area and then can radiate down into the groin. The patient can experience nausea and vomiting. The patient may also experience diarrhoea and abdominal discomfort due to renointestinal reflexes and due to the anatomical location of the kidneys to the stomach, pancreas, and large intestine. If a stone lodges in the bladder, it usually produces symptoms of irritation and can be associated with UTI and haematuria. It may also cause urinary retention if it obstructs the neck of the bladder. Diagnosis and Treatment Imaging include the use of KUB x-rays, CT, US. Occasionally and IVP can be beneficial. Blood tests that look at FBC, U&Es and renal function (urea and creatinine) is beneficial to determine any issues with renal functionality. In order to diagnose renal calculi a 24 hour urine test and blood test looking at the levels of calcium, uric acid, creatinine,sodium and pH as these are indicative of stone formation. Most stones will pass spontaneously, however, some require intervention. The stone is surgically removed if it is causing severe obstruction, infection, unrelieved pain or serious bleeding. A common procedure is a lithotripsy: the use of sound or shock waves to crush a stone. A ureteral stent may be inserted into the affected ureter tomaintain its patency. Apart from removal of the stone which would require pre and post op management, the other side of nursing management is related to the acute attack. Therefore, the focus should be on treating any infection and pain management. The use of heat packs and encouraging fluids to add in the passage of the stone and dilute the urine should be considered. Patients may require intravenous therapy due to dehydration. The other reason to improve fluid intake is to increase hydrostatic pressure within the urinary tract to promote passage of the stone. It is important to strain the urine to detect the presence of the any stones that may have passed. https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 10/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3.3. Urinary tract infection Urinary tract infection The kidneys, ureters, bladder and proximal ureter are sterile. Sterility is maintained through several different mechanisms. It is by the frequent flushing action of the urine when you go to the toilet. The bladder also have specific immune protection through the lining of the bladder that secrete antibody IgA. In the distal urethra near the external opening, a resident microbial community exists. These include Gram positive Skin bacteria S. epidermidis and Gram-negative enteric bacteria E coli. The sterile urine in the bladder becomes contaminated with microbes during its passage through the urethra. However, only when the mechanical, chemical and immune defences of the urinary tract as a whole are compromised that the risk of an infection is increased. The presenting features of lower urinary tract infection include frequent urination or an urgent need to urinate, dysuria, suprapubic pain and turbid or foul smelling urine. Fever and non-specific lower back pain may be present. Loin pain accompanied by systemic symptoms such as fevers, rigors, nausea and vomiting may suggest an ascending infection or pyelonephritis. In elderly patients, confusion may be the only presenting symptom. Urinary Tract Infections (UTIs) usually occur due to the patient's own bowel flora. Bacteria from faeces enters the urinary tract at the urethral opening and ascends to the bladder and sometimes makes it to the kidneys (ascending UTI).The Australian Institute of Health and Welfare (2016) reported that diseases of the kidney and urinary tract were the 10th leading cause of death in Australia, with 3,352 deaths annually. When a pathogenic microbe enters the urinary tract, it attaches to the urethral epithelial cells and damages the lining of the urethra. This precipitates an inflammatory state referred to a urethritis (inflammation of the urethra). The E Coli then continues to ascend the urinary tract, entering the urinary bladder where it attaches to the bladder epithelial cells. Damage to the epithelial lining of the bladder in the form of cell apoptosis (death) and exfoliation elicits inflammation referred to as cystitis (inflammation of the urinary bladder). Both of these conditions highlighted above are considered to be lower UTIs. Patients with urethritis and cystitis will usually present with dysuria (pain on urination) and increased frequency and urgency of urination. There may also be urethral discharge present and the patient may experience suprapubic tenderness and haematuria. Ultimately, a UTI may ascend to the kidney causing an upper UTI and pyelonephritis (inflammation of the renal pelvis and parenchyma/kidney). A patient with an upper UTI will present as acutely unwell with additional and more severe symptoms than a lower UTI such as fever, tachycardia, chills, flank pain, bacteriuria, leucocytosis and pyuria. If a patient becomes septic they will develop profound hypotension, yet they will remain peripherally warm. Peripheral vasoconstriction will be counteracted by the inflammatory mediators responsible for the systemic inflammatory response that occurred in the first place exacerbating distributive shock. https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 11/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Diagnosis Investigation for UTI begins on the ward. Initially when you receive a sample from a patient it may have an offensive smell and its colour may be abnormal and it could be turbid (cloudy). These are all things that you can notice just by using your senses. But then we need to use a dipstick and test the urine for any abnormalities. After collecting a MSU (midstream urine) and we look for the following : Neutrophils - pus cells (pyuria) a high concentration of bacteria - Nitrites - characteristic product of bacterial metabolism Blood - haematuria in some cases We send the MSU off for culture and sensitivities to identify the pathogen and determine its antibiotic sensitivity. If the patient is suspected of becoming septic then a blood test is also completed which would show an increase in white blood cells (leucocytosis ) with elevation of neutrophils (neutrophilia). It may be required to undertake an IV pyelogram, US or CT to rule out other diseases. Antibiotic treatment may be commenced empirically for symptomatic cystitis if clinically warranted. However, formal microscopy, culture and susceptibility testing should be performed in most circumstances to ensure patients receive appropriate antimicrobial therapy, especially given the rising incidence of antibiotic resistance. This is particularly important in men, pregnant women and patients with recurrent infections. A midstream urine is considered clinically positive if there are more than 103 colony forming units (cfu)/mL in acute uncomplicated infections in women. In complicated urinary tract infections, more than 105 cfu/mL in a midstream sample of urine in women and more than 104 cfu/mL in men or in an in-out catheter urine in women are clinically significant. There is an associated pyuria (>100 white blood cells/high power field). Contamination of the sample with epithelial cells is indicative of poor collection technique. Blood cultures should be taken if the patient has signs of sepsis or has an unusual organism in the urine, such as S. aureus, suggesting a haematogenous source. Ultrasound of the urinary tract is indicated in patients with recurrent infections to check for upper tract abnormalities and urinary stones. It is also indicated in older men to check for bladder outlet obstruction and residual urine volume post-voiding. Patients with macroscopic haematuria or persistent microscopic haematuria following resolution of a urinary tract infection should have a cystoscopy and evaluation of the upper tracts. This is usually done with a CT urogram. Watch the following video, it provides an overview of UTI, signs and symptoms, treatment and  diagnosis Urinary Tract Infection - Overview (signs and symptoms, pathophysiology, causes and treatment) UTI PHARMACOLOGY 1. Urinary symptoms relief agents https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 12/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Commonly used agents given to provide relief of urinary symptoms (like spasm or dysuria) that are experienced by persons with urinary conditions, such as urinary tract infections and incontinence. Anticholinergics (hmmm, that reminds me of week 1), like oxybutynin (Ditropan), provide relief of bladder spasms by inhibiting bladder contraction muscle. Why? Because these agents block the muscarinic receptors found in the detrusor muscles of the bladder neck; therefore, resulting in relaxation. Sodium citrotartrate (Ural®) sachets are another medication that alkalises the urine to decrease the pain experienced with more acidic urine. These products with contain sodium (as suggested in their generic name) so need to be avoided in people with sodium restricts. They can also interact with some medications like lithium, nitrofurantoin, and quinolones. 2. Antibacterials to treat urinary tract infection (UTI) Drugs commonly recommended for simple UTIs include: Trimethoprim/sulfamethoxazole (Bactrim): selectively interferes with bacterial synthesis of nucleic acids and proteins, common side effects are rash, nausea , vomiting and abdominal pain, caution as it may potentiate the anticoagulant action of warfarin, has an increased risk of nephrotoxicity if given with other antibiotics and hyperkalemia if given with ACE inhibitors. Cephalexin: first generation cephalosporin General uses: infections where organisms are not resistant to cephalosporins including upper and lower respiratory tract infections, skin infections, bone and joint infections, septicaemia, febrile neutropenia, meningitis, ear nose and throat infections, urinary tract infections. General adverse effects: nausea, vomiting, hypersensitivity reaction, dizziness, headache, leucopenia (low white cell count), neutropenia, anaphylaxis, elevated liver enzymes, nephritis, neurotoxicity, phlebitis. General interactions:affect the stability of oral anticoagulants, increased risk of kidney damage if used wityh other nephrotoxic drugs, absorption is decreased with antacids, chemical incompatibility with aminoglycosides General Nursing considerations: monitor WBC count , liver and renal function tests, therapy should be continued for 2 days after signs and symptoms resolve, donot mix with other drugs in the same syringe, monitor for allergic reaction. Amoxicillin: A penicillin, β-lactam ANTIBIOTIC and is considered the drugs of choice for many infections General action: inhibits the formation of a rigid bacterial cell wall, bactericidal, moderate spectrum General uses: infections where the microorganism is not resistant to penicillins such as upper and lower respiratory tract infection, urinary tract infection, septicemia, intraabdominal infections, sexually transmitted infection, bacterial endocarditis, obstetric and colorectal prophylaxis, group A streptococci General adverse effects: hypersensitivity reaction including urticaria, pruritis; prolongation of bleeding and prothrombin time, headache, nausea, vomiting, diarrhea, rapid IV convulsion, phlebitis, allergic reaction. General interactions: incompatible with aminoglycosides with increased risk of nephrotoxicity, may cause failure of oral contraceptive, absorption may be decreased by antacids, not recommended with alcohol General Nursing considerations: handle carefully to avoid self sensitisation, treatment should continue 48-72 hrs after symptoms have abated, should not exceed 14 days. monitor blood counts, prothrombin time, liver and renal functions, contraindicated for patients with known allergies. M onitor for hypersensitivity reaction, nausea, vomiting and diarrhea. Ceftriaxone: third generation cephalosporin incompatible with Hartmann's solution, review the general actions and interactions of cephalosporins again! https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 13/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3.4. Glomerulonephritis Glomerulonephritis (nephritic syndrome) is an inflammation of the glomerulus caused by primary glomerular injury perpetuated by immunologic responses, drugs, toxins and infections. Immune mechanisms and inflammation are a major causes. Immune injury includes 1) the deposition of circulating antigen-antibody immune complexes on the glomerulus (type III hypersensitivity reaction); 2) antibodies reacting against antigens within the glomerulus; 3) action of antibodies directed against the capillary walls. Nephrotic syndrome involves the excretion of 3 grams of protein per day , hypoalbuminemia and peripheral oedema. Many clinical manifestations are related to loss of protein and retention of sodium such as oedema, vitamin D deficiency due to loss of serum transport protein and decreased activation of vitamin D by the kidney. Hypothyroidism may result due to loss of thyroid binding proteins and alteration in coagulation due to kidney injury may result in thromboembolic events.This differs from nephritic syndrome which has a presenting symptom of hematurea, proteinuria which is not severe. Signs and symptoms of glomerulonephritis Pink or cola-colored urine from red blood cells in your urine (hematurea) Foamy or bubbly urine due to excess protein in the urine (proteinuria) High blood pressure (hypertension) Fluid retention (oedema) with swelling evident in your face, hands, feet and abdomen Urinating less than usual Nausea and vomiting Muscle cramps Fatigue Diagnosis Urine test: This test will determine if there is protein or blood in the urine. Blood test: This test will measure the level of creatinine (waste product filtered by the kidneys) in a blood sample. It also checks other kidney function tests such as urea, electrolytes and glomerular filtration rate. Kidney biopsy: a tiny piece of kidney tissue is removed under guided ultrasound. The tissue gets examined under a microscope. Ultrasound: An ultrasound to check the size of kidneys, for blockages and identifies any problems. Treatment Treatment depends on what caused the glomerulonephritis. A mild case may not need any treatment. At other times, it is recommended to have Changes to diet: less protein, salt and potassium Corticosteroids such as prednisone. Dialysis to filter the blood from toxins, removes extra fluid and control blood pressure. Diuretics (water pills) to reduce swelling Immunosuppressants if the problem with the immune system causes the glomerulonephritis. Antihypertensives such as blood such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers. Plasmapheresis, a special process that filters protein from the blood.  Watch the following video regarding glomerulonephritis and how it differs from nephrotic syndrome Nephrotic vs. Nephritic syndrome | Symptoms, diagnosis, causes, treatment | Visual explanation https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 14/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3.5. Acute Kidney Injury Acute Kidney Injury (AKI) is classified as prerenal; intrarenal (intrinsic) and postrenal. Prerenal AKI develops upstream of the kidneys and usually due to disruptions in the renal blood supply. Intrarenal AKI develops when the injury occurs within the kidneys itself; and then Postrenal AKI is due to an obstruction of urine flow that is distal to the kidneys. The following image depicts the causes for acute kidney injury. Prerenal AKI This is most often caused by renal ischaemia causing an abrupt decrease in the glomerular filtration rate (GFR). Causes of prerenal AKI are described in the diagram above. The most significant result of this ischaemic damage to the kidney is referred to as tubular necrosis. If the glomerular blood supply can be restored then the person can be supported through dialysis and it is expected that their kidney function will return to normal over several weeks. Therefore prerenal AKIs are usually reversible. Intrarenal AKI This is when kidney tissue is directly affected. Causes of intrarenal AKI are described in the diagram above. What we see here is that the GFR falls greatly leading to a decreased urine volume. Therefore the glomerular membrane becomes permeable to blood or protein resulting in either haematuria or proteinuria. Postrenal AKI This type of AKI is caused by an obstruction of the flow of urine from both the kidneys. Causes of postrenal AKI are described in the diagram above. Formed urine proximal to the obstruction causes urinary stasis. This causes an increase in hydrostatic pressure within the renal pelvises and calyces causing them to distend. If not rectified the additional pressure compromises vascular supply leading to permanent loss of nephrons. In different types of AKI - a common anomaly is a reductions in GFR and elevations in serum creatinine levels and urea. In prerenal AKI a person may also have hypotension and possibly tachycardia. When we move onto intrarenal or postrenal forms, the person may commonly have hypertension. Commonly the person will demonstrate flank pain and may have hyperkalaemia. Hyperkalaemia results from protein catabolism which releases cellular potassium in to the body fluids. Hyperkalaemia can lead to arrhythmias (VT) and even cardiac arrest. The reduction in the GFR means that the person may also have significant oedema due to a response in the altered blood osmotic pressure and associated proteinuria. Overall almost every system of the body is affected when there is failure of the normal renal regulatory mechanisms. The patient may appear critically ill, lethargic, have nausea and vomiting and associated diarrhoea. The skin and mucous membranes can become very dry from dehydration and the person's breath may have the odour or urine (uraemic fetor). CNS symptoms include drowsiness, headache, muscle twitching and seizures. Major complications include the development of potentially life-threatening metabolic complications including metabolic acidosis, fluid and electrolyte imbalances. Metabolic acidosis occurs in AKI because patients cannot eliminate the daily metabolic load of acid-type substance produced by normal metabolic processes. Also normal renal buffering mechanisms fails reflected by a decrease in the serum CO2-combining power and blood pH. Other things that can be affected include an increase in blood https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 15/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle phosphate concentrations; calcium levels may be low due to decreased absorption of calcium from the intestine and as a compensatory mechanism for elevated phosphate levels. Usually patients will also have anaemia due to decreased EPO production, uraemic GI lesions and a reduced RBC life span and blood loss from the GIT. Clinical phases of AKI There are four clinical phases of AKI: initiation, oliguria, diuresis and recovery. Initiation - begins with the initial insult and ends when oliguria develops Oliguria - accompanied by a rise in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids and the intracellular cations [potassium and magnesium]). It is in this phase that uraemic symptoms first appear and life- threatening conditions, such as hyperkalaemia develop. Diuresis - the patient experiences gradually increasing urine output, which signals that glomerular filtration has started to recover. The patient must be closely observed for dehydration during this phase. Recovery - signals the improvement of kidney function and may take 3-12 months. Usually patients will have a permanent 1-3% reduction in their overall GFR which is not clinical significant. Diagnosis and treatment AKI is strongly associated with a sudden drop in GFR and as such testing blood for FBC, U&Es and renal function in conjunction with a urinalysis is important in the clinical diagnosis of AKI. The classification system that is widely use is the RIFLE system and this measure the serum creatinine levels, GFR and urine output. Check this image depicting the RIFLE classification system In terms of management of these kidney injuries it is important that any plan is directed at the type of AKI and the causative agents. Initially once the cause of the injury is removed then the repair process can begin, renal function can begin to recover. however normal kidney function can take months to be restored and full recovery may not be possible. Prerenal AKI Treatment - correction of fluid volume deficits or improvement of heart failure using inotropic agents. Intrarenal AKI Treatment - manage the cause of the kidney damage and if necessary changes to medications need to occur - eliminate nephrotoxic agents Postrenal AKI Treatment- managing the cause of the obstruction https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 16/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle Management 1. Monitor fluid and electrolyte imbalances - monitor serum electrolyte levels and physical indicators of these complications during this disorder and its phases. Monitor for excessive K+ intake and monitor cardiac and musculoskeletal status. Note the patient's input and output, noting oedema, jugular veins, changes in heart sounds and breath sounds, difficulty in breathing. Also obtain an accurate daily weight. 2. Reduce the metabolic rate - helps to reduce catabolism and subsequent release of potassium and accumulation of endogenous waste products (urea & Creatinine) 3. Prevent infection - practicing asepsis with nursing care and avoiding the using of invasive devices such as IDCs 4. Providing skin care - skin may be dry or susceptible to breakdown due to oedema or excoriation and irritation to uraemia. PAC and good skin hygiene are essential. 5. Psychological support - may require treatment with haemodialysis, PD or CRRT to prevent serious complications. Role of the nurse is to provide education, information and support to the patient and their family https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 17/18 24/10/2024, 19:32 Pathophysiology and Pharmacology Book | Moodle 3.6. Chronic Renal Disease It is a state of progressive loss of kidney function ultimately resulting in the need for renal replacement therapy (dialysis or transplantation). The most common primary diseases causing CKD and ultimately end-stage renal disease (ESRD) are as follows Diabetes mellitus type 2 Diabetes mellitus type 1 Hypertension Primary glomerulonephritis x Chronic Tubulointerstitial nephritis Hereditary or cystic diseases Secondary glomerulonephritis or vasculitis Neoplasm CKD may result from disease processes in any of the three categories: prerenal (decreased renal perfusion pressure), intrinsic renal (pathology of the vessels, glomeruli, or tubules-interstitium), or postrenal (obstructive). Chronic and sustained insults from chronic and progressive nephropathies evolve to progressive kidney fibrosis and destruction of the normal architecture of the kidney. This affects all the 3 compartments of the kidney, namely glomeruli, the tubules, the interstitium, and the vessels. The steps are Infiltration of damaged kidneys with extrinsic inflammatory cells Activation, proliferation, and loss of intrinsic renal cells (through apoptosis, necrosis, mesangiolysis, and podocytopenia) Activation and proliferation of extracellular matrix (ECM) producing cells including myofibroblasts and fibroblasts Deposition of ECM replacing the normal architecture Signs and Symptoms Some common symptoms and signs at these stages of CKD are: Nausea Vomiting Loss of appetite Fatigue and weakness Sleep disturbance Oliguria Decreased mental sharpness Muscle twitches and cramps Swelling of feet and ankles Persistent pruritus (itchiness) Chest pain due to uremic pericarditis Shortness of breath due to pulmonary oedema from fluid overload Hypertension that's difficult to control Physical examination is often not helpful, but patients may have Skin pigmentation Uremic frost, where high levels of BUN result in urea in sweat, uremic breath Treatment Once the CKD progression is noted, the patient should be offered various options for renal replacement therapy. Haemodialysis Peritoneal dialysis (continuous or intermittent ) Kidney transplantation (living or deceased donor): It is the treatment of choice for ESRD given better long-term outcomes. Patients who do not want renal replacement therapy should be provided with information about conservative and palliative care management. The haemodialysis is performed after stable vascular access is placed in a nondominant arm. In this arm, intravenous cannulas are avoided to preserve the veins. The preferred vascular access is AV fistula. The patency rates of AV fistula is good, and infections are very infrequent https://moodle.federation.edu.au/mod/book/tool/print/index.php?id=7654061 18/18