SIADH
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1. SIADH (syndrome of inappropriate antidiuresis) is a condition characterized by hyponatremia caused by excessive secretion of antidiuretic hormone (ADH). 2. It can be caused by various pulmonary, neurological, oncological and other medical conditions. Common culprit drugs include ADH analogs, SSRIs, antipsychotics and NSAIDs. 3. Management involves fluid restriction and slow correction of sodium levels to avoid osmotic demyelination syndrome, which is a serious complication of too rapid correction. Vasopressin receptor antagonists are also being studied.
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2. Replace sodium and water losses. Administer intravenous saline to restore effective circulating volume.
3. Consider glucocorticoid replacement if due to primary adrenal insufficiency.
4. Monitor sodium levels closely during treatment to avoid overcorrection.
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Here are the key steps in treating hypotonic, hypovolaemic hyponatraemia:
1. Stop the underlying cause of sodium loss if possible (e.g. stop diuretics).
2. Replace sodium and water losses. Administer intravenous saline to restore effective circulating volume.
3. Consider glucocorticoid replacement if due to primary adrenal insufficiency.
4. Monitor sodium levels closely during treatment to avoid overcorrection.
The goal is to restore effective circulating volume and sodium levels slowly to avoid complications from rapid correction. Replacing sodium and water losses is priority over speed of correction.
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This document provides an overview of hyponatremia (sodium concentration < 135 mEq/L), including its introduction, pathophysiology, symptoms, workup, treatment, and perspectives from cardiologists. Hyponatremia is usually caused by increased water retention and can be classified into four types based on volume status and cause: type 1 is hypervolemic, type 2 is hypovolemic, type 3A is euvolemic due to SIADH, and type 3B is euvolemic due to other causes. The workup involves assessing serum and urine osmolality, sodium concentration, and specific gravity to distinguish between impaired water excretion versus excess fluid intake. Treatment depends on
Diabetes insipidus
Diabetes insipidus is a disorder characterized by excessive urine production and thirst due to a deficiency of antidiuretic hormone. There are two main types: central diabetes insipidus caused by issues with the pituitary gland, and nephrogenic diabetes insipidus caused by kidney problems. Symptoms include producing large volumes of dilute urine, excessive thirst, and dehydration. Treatment aims to replace ADH through medications like DDAVP, correct fluid and electrolyte imbalances, and identify and address the underlying cause of the condition.
Cushing's syndrome
this presentation contains the detailed radiological invesstigations and treatment of Cushing's syndrome.
Hypercalcaemia of Malignancy
1) A 10-year-old Labrador presented with PU/PD, lethargy, weight loss, and anorexia. Biochemistry revealed hypercalcemia.
2) Thoracic radiographs and ultrasound identified a cranial mediastinal mass. FNA was non-diagnostic but PCR suggested a mixed population of T-cells, consistent with mediastinal lymphoma.
3) The diagnosis was stage Vb mediastinal T-cell lymphoma, causing hypercalcemia of malignancy through PTHrP secretion and increased bone resorption. Treatment was palliative with steroids to reduce hypercalcemia and improve appetite.
Cushing's syndrome
Cushing's syndrome is caused by prolonged exposure to high levels of the hormone cortisol and results from tumors in the pituitary gland or adrenal glands overproducing cortisol. Symptoms include upper body obesity, high blood pressure, fragile bones, and depression. Treatments depend on the underlying cause but may include surgery, radiation, chemotherapy, or drugs to inhibit cortisol production such as Korlym. Cushing's syndrome is rare, affecting about 10-15 people per million.
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This is my PowerPoint that was presented at pioneer Pacific College. It took alot of work with my failing memory but I did It! I want to get the word out about Cushing's and my journey with this awful disease. The first picture is me now.
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Syndrome of Inappropriate Anti-diuretic Hormone Secretion (SIADH)
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Concept Map of Syndrome of Inappropriate (ly high) Anti-Diuretic Hormone (SIADH)
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This document discusses electrolyte disorders and their management. It covers water and sodium metabolism including hypo- and hypernatremia. It also discusses potassium disorders including hypo- and hyperkalemia. The key mechanisms and renal regulation of electrolytes are explained. Treatment approaches are outlined depending on the electrolyte abnormality and patient volume status. Symptoms, causes, and management strategies are provided for common electrolyte disorders.
Syndrome of inappropriate anti diuretic hormone release (SIADH)
SIADH, or syndrome of inappropriate anti-diuretic hormone release, is characterized by high levels of ADH released in the absence of normal stimuli. It is associated with tumors that secrete ADH, such as small cell lung cancer, as well as pulmonary and neurological disorders. SIADH causes water retention through ADH increasing water reabsorption in the kidneys, leading to hyponatremia and hypo-osmolality as blood is diluted. Clinical features range from mild thirst to seizures depending on sodium level. The diagnosis requires lab tests showing low sodium and osmolality with concentrated urine. Treatment focuses on correcting the underlying cause, restricting fluids, and sometimes using demeclocycline or coniv
Chronic kidney Disease
Chronic kidney disease (CKD) is characterized by a progressive decline in kidney function over time. It ranges from initial kidney damage to end-stage renal disease where the kidneys fail. The main causes of CKD include diabetes, high blood pressure, glomerulonephritis and polycystic kidney disease. As kidney function declines, waste products accumulate in the body leading to complications like anemia, bone disease, heart disease and fluid/electrolyte imbalances. Treatment focuses on slowing progression through blood pressure control and reducing proteinuria with ACE inhibitors. Dialysis or transplantation may be required in late stages to replace kidney function and relieve uremia.
Approach to Acute renal failure.ppt
Acute renal failure (ARF), also known as acute kidney injury (AKI), can have various causes including pre-renal, renal, and post-renal factors. The definition includes an abrupt decline in kidney function over 48 hours seen through rises in creatinine or decreases in urine output. Evaluation involves assessing volume status, obtaining urine and blood tests, and ultrasound. Treatment focuses on identifying and treating the underlying cause, providing supportive care like fluid management, and potentially initiating renal replacement therapy for complications such as fluid overload or electrolyte imbalances. Prognosis depends on the severity and underlying etiology of the AKI.
Diuretics
Diuretics are drugs that increase urine output and sodium excretion. They work by inhibiting sodium reabsorption in different parts of the nephron. Loop diuretics like furosemide work in the loop of Henle, thiazides work in the distal tubule, and potassium-sparing diuretics work in the collecting duct. Diuretics are used to treat conditions caused by fluid overload like hypertension, heart failure, and liver disease. Common side effects include electrolyte imbalances like hypokalemia and hyponatremia. The document also discusses the mechanisms and uses of various classes of diuretics like loop diuretics, thiazides, potassium-sparing diuretics
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Hyponatremia, defined as a serum sodium level below 135 mEq/L, is the most common electrolyte disorder. It can be caused by excess water intake relative to sodium, and inappropriate antidiuretic hormone (ADH) secretion is a common cause. Hyponatremia is categorized as hypervolemic, euvolemic, or hypovolemic based on total body water status. Symptoms range from mild gastrointestinal issues to serious neurological effects like seizures or coma if severe. Diagnosis involves assessing sodium, osmolality, and urine studies. Treatment depends on chronicity and severity, with hypertonic saline used for acute cases and fluid restriction or vasopressin receptor antagon
Etiopathogenesis & Mx Of Chronic Kidney Disease
Chronic kidney disease is defined as glomerular filtration rate below 60 mL/min/1.73m2 or markers of kidney damage. It is staged based on GFR. Common causes include diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and congenital anomalies. Manifestations include electrolyte imbalances, cardiovascular complications, central nervous system effects, peripheral neuropathy, and bone disease like renal osteodystrophy. Treatment depends on stage but may include dialysis, kidney transplantation, and management of complications.
Hyponatremiappt 170315180214
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Chronic kidney diasease
This document summarizes chronic kidney disease (CKD), defining it as abnormalities of kidney structure or function lasting over 3 months that impact health. CKD is classified based on cause, glomerular filtration rate (GFR) category, and albuminuria levels. Key aspects of CKD addressed include pathophysiology, GFR estimation and staging, risk factors, clinical abnormalities associated with decreased kidney function like fluid/electrolyte issues and anemia, leading causes, and management including treating complications and renal replacement therapy for late stages.
Neurology of electrolyte imbalance
The document discusses electrolyte imbalances and their neurology. It covers sodium, potassium, calcium and magnesium disorders. For sodium, it describes hyponatremia and hypernatremia in detail. Hyponatremia can be hypovolaemic, hypervolaemic or euvoleamic. Causes, clinical features and treatment approaches are provided. For potassium, it discusses hypokalemia and its neuromuscular and cardiac manifestations. Causes of hypokalemia include reduced intake, renal and non-renal losses, and intracellular shifting. ECG changes are also outlined.
Inherited tubular disorders
1. Autosomal dominant polycystic kidney disease (ADPKD) is characterized by multiple renal cysts that increase in size and number over time, eventually leading to kidney failure in half of patients by age 60.
2. ADPKD is caused by mutations in genes that regulate renal tubule cell proliferation and results in the monoclonal expansion of tubular epithelial cells.
3. Clinical manifestations include chronic flank pain, urinary tract infections, kidney stones, hypertension, liver cysts, and cerebral aneurysms. Treatment focuses on blood pressure control and management of complications.
CKD.pptx
This document summarizes chronic kidney disease (CKD), dividing it into 5 stages based on glomerular filtration rate (GFR). It describes the etiologies of CKD including primary and secondary glomerular diseases, tubulointerstitial nephritis, obstructive nephropathies, vascular diseases, and hereditary diseases. The clinical features of CKD include fluid and electrolyte imbalance, acid-base disturbances, uremia, disturbances in calcium and phosphate metabolism, anemia, hypertension, dyslipidemia, endocrine dysfunction, and growth impairment. Management involves treating the underlying cause, slowing progression with ACE inhibitors, and treating complications like anemia, fluid overload, hyperkalemia, metabolic acid
Acute Renal Failure Overview
Acute renal failure, also known as acute kidney injury, is defined as an abrupt loss of kidney function that develops within 7 days. It is characterized by a decrease in creatinine clearance and increases in blood urea nitrogen and creatinine levels. Acute renal failure can be caused by pre-renal issues that decrease blood flow to the kidneys, intrinsic renal issues that damage the kidneys, or post-renal issues that obstruct urine flow. The condition is diagnosed through blood and urine tests and imaging and treated by addressing the underlying cause, giving intravenous fluids, and providing renal replacement therapies like hemodialysis in severe cases.
Chronic kidney disease
Chronic Kidney Disease (CKD) is characterized by a progressive decline in kidney function over time and is classified into 5 stages based on glomerular filtration rate. CKD has many potential causes including diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. As kidney function declines, patients experience complications such as anemia, bone disease, electrolyte imbalances, cardiovascular disease, and other systemic effects. Treatment focuses on slowing progression, managing complications, and renal replacement therapy for stage 5 CKD.
Hypernatremia1
Hypernatremic disorders can be caused by a loss of hypotonic fluid or infusion of hypertonic fluid, usually resulting from too little water or too much salt. Hypernatremia is defined as a serum sodium level above 145 mEq/L. It tends to occur in infants or the elderly, particularly those with impaired mental status who are unable to ask for water. Treatment involves replacing the free water deficit with intravenous or enteral fluids at a slow rate to avoid cerebral edema, not exceeding 0.5 mmol/L/hr or 10 mmol/day sodium correction. The volume status and chronicity of the hypernatremia must be assessed to determine appropriate treatment.
Cvs drugs new
This document discusses cardiovascular drugs used to treat issues related to the cardiovascular system. It begins by describing the basic anatomy and physiology of the cardiovascular system. It then discusses different types of malfunctions like heart failure, hypertension, arrhythmia, angina, and myocardial infarction. The remainder of the document focuses on drugs used to treat hypertension, including diuretics, sympathoplegics, vasodilators, calcium channel blockers, ACE inhibitors, and ARBs. It provides details on the mechanisms of action, side effects, and clinical uses of different drug classes and examples within each class.
Hypernatremia
This document discusses hypernatremia, defined as a serum sodium level greater than 150 mEq/L. It describes the normal extracellular and intracellular fluid compartments and how they are affected by hypernatremia. Clinical signs of hypernatremia range from restlessness to seizures and death depending on the serum osmolality level. Common causes include inadequate water intake, excessive sodium intake, renal or GI losses. Treatment involves volume repletion first with isotonic fluids followed by a gradual decrease in sodium levels with hypotonic fluids over 1-2 days. Free water deficits are calculated to determine fluid replacement volumes needed.
Acute renal failure (2)
This document discusses acute renal failure (ARF), also known as acute kidney injury (AKI). It defines ARF, discusses its epidemiology and causes. The main causes of ARF are pre-renal (decreased blood flow/volume), renal (damage within the kidneys), and post-renal (obstruction of urine flow). The most common form of intrinsic ARF is acute tubular necrosis, often due to ischemia or nephrotoxins. Diagnosis involves lab tests of kidney function and urine analysis. Treatment focuses on identifying and reversing the underlying cause, maintaining fluid/electrolyte balance, and potentially initiating renal replacement therapy like dialysis.
ANEMIA
Anaemia is a condition where there is a decrease in the total amount of red blood cells in or haemoglobin in the blood or a lowered ability of the blood to carry oxygen.
ETIOLOGY :blood loss and decreased red blood cell production.
SYMPTOMS : feeling tired, weakness, shortness of breath.
EPIDEMIOLOGY: Anaemia is a common, multifactorial condition among older adults.
RISK FACTORS :chronic infections such as osteomyelitis , SLE
COMPLICATIONS : lack of energy, increased risk of infections, heart and lung problems
Hyponatremia- Fishing in troubled waters.
Hyponatremia is a common electrolyte disorder in diverse fields of medicine. A sound understanding of Physiology is essential for its management. Real life clinical examples are described
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This document contains a coursework cover sheet and assignment for a student named Hiren Divecha on the topic of defining and classifying spondylolisthesis and discussing the management of high grade slips. It includes a 2193 word essay on the topic with sections on the definition of spondylolisthesis, two common classification systems (Wiltse-Newman and Meyerding), and discussion of management approaches for high grade slips in children/adolescents and adults. References are provided at the end.
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2. A literature review and analysis of classification systems for clavicle shaft fractures and AC joint injuries.
3. Discussion of treatment options for various fracture and injury types, outlining biomechanical advantages and disadvantages.
4. The student provides their own analysis and critique of treatment approaches based on the literature.
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analysis of the stress shielding effect of stemmed tibial TKR prostheses and how this effect can be varied/ reduced
Static analysis of the ankle joint
The document is a cover sheet for a student submitting an assignment on static analysis of the ankle joint. It includes the student's personal details, module details, and a signed declaration stating the work is their own. The full assignment analyzes the ankle joint under single leg stance, single leg tip-toe stance, and with the foot suspended in mid-air using free body analysis to determine joint and muscle forces. It finds the joint reaction force is 1.8 times body weight for single leg stance and 2.5 times for tip-toe stance, and only 0.02 times body weight when suspended horizontally.
Biomechanical analysis of external fixation
This document discusses the biomechanics of external fracture fixation devices and their influence on fracture repair. It analyzes the rigidity of a unilateral external fixator frame and how changing variables like pin length, diameter, and material properties affects the overall vertical deflection at the fracture site. Maintaining an optimal level of rigidity is important to ensure proper fracture healing without displacement while encouraging callus formation through controlled strain levels. Too rigid or flexible of a construct can inhibit healing.
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Subtrochanteric fractures
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Legg-Calvé-Perthes Disease
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Femoral shaft fractures
This document summarizes femoral shaft fractures, including:
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2) Clinical presentation includes non-weight bearing, pain, deformity, and leg position with external rotation, abduction and shortening.
3) Treatment options include intramedullary nailing, plate fixation, or external fixation. Intramedullary nailing has union rates over 95% and is the preferred treatment.
Orthopaedic Trauma - The Basics
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Complications after THR
1. Common complications of hip replacement surgery include dislocation (1-2%), nerve injury (1-2% for primary, 3-4% for revision, 5-6% for developmental dysplasia of the hip), infection (<1%), pulmonary embolism (fatal in 0.1-0.5% without prophylaxis), and heterotopic ossification.
2. Risk factors for complications include component malposition, soft tissue imbalance, central nervous system disorders affecting gait and balance, and peripheral nerve or muscle disorders.
3. Long term complications include aseptic loosening due to osteolysis from histiocytic response to wear debris, pseudotumors from metal-on-metal
Clavicle Fractures & ACJ Injuries
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SIADH
- 1. SIADH By Hiren Divecha FY2 Hairmyres Hospital 1/5/2007
- 2. Sodium • Needed for: 1. Nerve conduction 2. Co-transport of metabolites • 135-146 mmol/L • Regulation – Thirst – ADH – RAAS – ANP & BNP
- 3. Euvolaemic Hyponatraemia Hypervolaemic Hypovolaemic
- 4. Hypovolaemic Euvolaemic Hypervolaemic Extracellular Na ↓ N ↑ TBW Slightly ↓ Slightly ↑ ↑↑ Causes Renal Thiazides CCF •Diuretics •Osmotic diuresis SIADH Liver failure (glucose, urea, mannitol) Glucocorticoid def Renal failure •Addison’s •Salt-wasting neph Hypothyroidism Nephrotic syndrome Gut Primary polydipsia •Vomiting Pregnancy •Diarrhoea iv dextrose Other Sodium-free irrigant •Haemorrhage •3rd space loss (BO, burns, peritonitis, pancreatitis)
- 5. Causes of SIADH Neoplastic Pulmonary CNS Drugs Other Lung Infection Infection AVP analogues Idiopathic •Small cell •Pneumonia •Abscess •Desmopressin •Mesothelioma •Abscess •Meningitis •Oxytocin Hereditary •TB •AIDS •Vasopressin (V2 receptor) GI •Aspergillosis •Stomach Bleeds Stimulate AVP •Pancreas Asthma •Subdural release/action •SAH •SSRIs GU Cystic Fibrosis •Antipsychotics •Bladder CVA •Anti-epileptics •Prostate PPV •NSAIDs •Endometrium Head trauma •MDMA Thymoma MS, GBS Leukaemia Lymphoma Shy-Drager Sarcoma
- 6. Clinical Features <120 mmol/l <110 mmol/l – Dysgeusia • Drowsiness – Lethargy • Confusion – Anorexia • Depressed reflexes – Nausea, vomiting • Extensor plantar responses – Irritability • Seizures – Headache • Coma – Cramps • Death – Muscle weakness
- 7. Criteria for SIADH • Bartter and Schwartz (1967) – Hyponatraemia – Clinically euvolaemic – No diuretic use – Serum osmolality <275mOsm/kg – Urine osmolality >100 mOsm/kg – Urine sodium >40mmol/L – Normal thyroid, adrenal and renal function
- 8. Management - acute • Benzodiapines • Aim for 1-2mmol/L/hr initially – Resolution of neurology – Slow replacement (10 mmol/L/day) • Frusemide (free water excretion) • Find and treat cause
- 9. TBW = weight * 0.5 (girls) = weight * 0.6 (guys) Na+ to replace = desired change in Na+ * TBW Rate of Na+ replacement = rate of desired change * TBW Rate infusion = Rate of Na+ replacement / (conc of infusate)
- 10. As a rough guide • To increase Na+ by 1mmol/L/hr – 1 ml/kg/hr of 3% saline – 1.7 ml/kg/hr of 1.8% saline • Max. rate = 70 mmol of Na+/hr • Monitor U&E 2 – 3 hourly
- 11. Management - Chronic • Risk of osmotic demyelination if change is >12mmol/L/day • Symptomatic – Aim for lower rate of correction (0.5mmol/L/hr) • Asymptomatic – Fluid restrict – Demeclocycline – Oral urea
- 12. Fluid restriction (Urinary Na + Urinary K) / Plasma Na • >1 – <500ml/day • 1 – 500-700ml/day • <1 – <1L/day
- 13. Vasopressin Receptor Antagonists • RCTs showed sustained increase in plasma Na compared to placebo • Risk of hypotension with non-selective antagonists • V2 selective antagonists in trials • No reports of osmotic demyelination
- 14. Osmotic Demyelination Syndrome • Central pontine + extrapontine • Over-enthusiastic correction of Na+ • In chronic hyponatraemia – Brain tissue losses inorganic and organic solutes – Takes few days • Predisposing factors – Alcoholism – Malnourishment
- 15. Osmotic Demyelination Syndrome • Demyelination • Pontine symptoms – Dysarthria, dysphagia, pseudobulbar palsy – Flaccid quaraparesis • Extra-pontine – Tremor, ataxia, mutism – Parkinsonism, dystonia • Reversible ? – 5% dextrose and desmopressin
- 17. References 1. “The syndrome of inappropriate antidiuresis”, Ellison et al, NEJM, 2007;356(20):2064-72 2. “Hyponatraemia”, Adrogue & Madias, NEJM, 2000;342(21):1581-89