Module 6 Renal and Urinary Disorders Past Paper PDF

Module 6 Renal and Urinary Disorders November 20/21, 2024  Overview- Wed Nov 20, 2024 Time Topic Duration 6:00-6:10 Time-check in 10 minutes 6:10-6:30 Normal Kidney anatomy and f...

Module 6 Renal and Urinary Disorders November 20/21, 2024  Overview- Wed Nov 20, 2024 Time Topic Duration 6:00-6:10 Time-check in 10 minutes 6:10-6:30 Normal Kidney anatomy and function 20 min Review quiz 6:35-7:05 Clinical Consult- Chronic Kidney Disease with mineral and bone 15 +5 disorder- Hassan Majeed 7:10-7:30 Clinical Consult- Chronic Kidney Disease and Renal Replacement 15+5 Therapy-Rebecca Valdman 7:30-7:45 Break 15 min 7:45-8:15 Glomerular disorders 30 min Chronic Renal Failure GU Patho- Urinary Obstruction Urinary Incontinence, Urinary Tract Infection, 8:15-8:30 Practice Quiz- GU 15min 8:30-8:50 Midterm prep 20 min LOI prep 8:50-9:00 Wrap up 15 minutes 2  Overview- Thurs. November 21st Time Topic Duration 10:00-10:10 Time-check in 10 minutes Module 5 quiz review 10:10-10:30 Normal Kidney anatomy and function 20 min Review quiz 10:35-11:05 Clinical Consult- Chronic Kidney Disease with mineral and 15 + 5 min bone disorder- Cinol Saneesh 11:10-11;30 Clinical Consult-Microscopic Hematuria 15 + 5 min Jamie Bucknell 11;30-11:45 Break 15 min 11:45-12:15 Glomerular Disorders, Renal failure 30 min GU Patho- Urinary Obstruction Urinary Incontinence, Urinary Tract Infection, 12:15-12:30 Practice Quiz- GU 15min 12:30-12:50 Midterm prep 20 min LOI prep 12:50-13:00 Wrap up 15 minutes 3 1. Kidney Anatomy- The Nephron-Question What is correct order of the some of the components within the filtration system in the nephron? a) Proximal collecting duct, loop of Henle, distal collecting duct b) Glomerulus, Proximal convoluted tubule, Loop of Henle, Distal convoluted tubule c) Proximal collecting duct, Glomerulus, Loop of Henle, Collecting duct d) Glomerulus, Proximal convoluted tubule, Loop of Henle, Distal collecting duct 5  PCT-Proximal convoluted tubule DCT-Distal convoluted tubule Renal Corpuscle- Ascending Loop of Henle Contain the Glomerulus Loop of Henle and Bowman's capsule Descending CD-Collecting Duct 2. Kidney Anatomy- Nephron- Question Where are the nephrons located in the kidney? a) Hilum and renal pelvis b) Renal cortex and renal pelvis c) Renal cortex and renal medulla d) Renal medulla and renal pelvis Renal Corpuscle (contains glomerulus and Bowman’s capsule) Renal cortex Juxtamedullary nephron Cortical nephron Renal medulla The Nephron- Video Lecture slide In my reading, resources indicate 2 types of nephrons (cortical and juxtamedullary) Did anyone find a resource for 3 types of nephrons? 3. Kidney Anatomy-Question What is the role of the renal calyces? a) Receive blood from the renal pelvis b) Deliver blood to the renal pelvis c) Receive urine from the collecting ducts d) Send urine to the collecting ducts 13 4. Renal anatomy-Hilum- Question The renal hilum is the entry/exit area on the medial side of each kidney for the following structures EXCEPT: a) Renal artery and vein b) Renal pelvis c) Lymphatics d) Parasympathetic nerve bundle 5. Renal - Sympathetic stimulation-Question Sympathetic stimulation of the kidney results in: a) Renal artery dilation to increase blood flow to the kidneys b) Release of renin from the juxtaglomerular cells c) Decrease in glomerular filtration rate to preserve kidney function d) Vasodilation of intra-renal arteries in the medulla 15 Secretion of Renin by the Kidney Renal arteriole vasoconstriction in response to sympathetic stimulation AGA- Afferent glomerular arteriole EGA- Efferent glomerular arteriole Video lecture slide 6. Renal filtration and the Nephron- Question What substances are not filtered by the glomerulus in a normal kidney? a) Glucose, Red blood cells, Large proteins b) Large proteins, Calcium, Bicarbonate c) Red blood cells, Large proteins, Hydrogen ions d) Large proteins, Red blood cells, Platelets https://www.youtube.com/watch?v=OEzKQmqV2WQ 7. Renal nephron filtration- Question In the nephron, where are the majority of nutrients reabsorbed from the urine filtrate into the blood stream? a) Bowman’s capsule b) Proximal convoluted tubule c) Distal convoluted tubule d) Loop of Henle e) Collecting Duct 8. Nephron and filtration- Question Antidiuretic hormone (ADH) (Vasopressin) acts on this part of the nephron to increase water reabsorption a) Bowman’s capsule and Proximal convoluted tubule b) Proximal convoluted tubule and Loop of Henle c) Loop of Henle and Distal convoluted tubule d) Distal convoluted tubule and Collecting duct Bonus question! How do loop diuretics (e.g. furosemide, bumetanide) increase urinary output? a) Block the sodium-potassium-chloride co-transporter in the ascending loop of Henle b) Inhibit sodium-potassium-chloride from entering the epithelial wall in the descending loop of Henle c) Inhibit water diffusion through the thin epithelial wall of the ascending loop of Henle d) I am not sure- I just know they must work somewhere in the Loop of Henle since they are called a ‘loop diuretic’ Loop of Henle Ascending Loop of Henle Epithelial cell in ascending A co-transporter molecule Loop of Henle on the luminal side of the epithelium will transport 1 Sodium, 1 Potassium and 2 Chloride molecules from the urine filtrate to the interstitial fluid of the medulla. This requires energy (active transport) Loop diuretics-How do they increase urinary output? Loop diuretics block NA-K-Cl cotransporter Less sodium and other solvents (and K and Cl) can move into the interstitial area in the medulla Medulla not as ‘salty’ Water in the urine filtrate is no longer drawn out of the filtrate in the descending Loop of Henle as the concentration gradient is lost Increase water and sodium (and K+ and CL-) are excreted in the urine https://www.youtube.com/watch?v=5k5btYZTKhQ  Clinical Consult CKD associated with mineral and bone disorder Hassan Majeed Wed, Nov 20, 2024 29  Clinical Consult CKD and renal replacement therapy Rebecca Valdman Wed. Nov 20th, 2024 30  Clinical Consult CKD associated with mineral and bone disorder Cinol Saneesh Thur. Nov 21, 2024 31 Clinical Consult Microscopic Hematuria Jamie Bucknell Thurs. Nov 21, 2024 32 Break Time See you at 33  Identify risk factors for acute and Learning chronic glomerulonephritis Explain the pathophysiology of acute Outcomes and chronic glomerulonephritis. Describe the clinical manifestations of Glomerular acute and chronic glomerulonephritis. disorders Compare and contrast nephrotic and nephritic syndromes 34 Video Lecture slide and content 35  Glomerular filtration in the nephron Capillary endothelium- the endothelial cells have tiny holes (fenestrations) to allow small particles to leak through (Na, Cl-, Glucose) Basement membrane (semi- permeable) (additional barrier, negative charge repels proteins) Podocytes- tubular cell (epithelial cell). Some have legs/feet that wrap around capillaries https://www.youtube.com/watch?v=wWsdcfGta4k 36 Mesangial Cells play a key role in the immune response within the Glomerulus Removing debris: Phagocytic cells that remove debris and trapped residue from the glomerular basement membrane and filtration slit diaphragm. Supporting podocytes: Provide structural support for podocytes in areas where the basement membrane is absent. Regulating glomerular filtration rate: Contractile cells that control glomerular tone, which helps regulate the glomerular filtration rate (GFR). Responding to injury: Synthesize and secrete molecules that help the glomerulus respond to injury. Participating in immune responses: Play a role in cellular immune responses. Signaling: Contribute to cell-to-cell signaling in the glomerulus. 37  Chronic Glomerulonephritis Chronic glomerulonephritis is related to a variety of diseases that cause deterioration of the glomerulus and a progressive course leading to chronic kidney failure. Diabetic nephropathy is the most common cause of glomerular injury progressing to CKD and is related to chronic hyperglycemia, inflammatory mediators, and microvascular and macrovascular complications. 38 Immune response Mechanisms of Glomerular Injury (textbook) Diabetic Glomerulopathy 40 What are some key differences and similarities between nephrotic and nephritic syndromes? 41  Syndrome Selection Quiz Nephrotic Syndrome Nephritic Syndrome Injury to the glomerular filtration membrane leading to increased permeability and loss of electrical negative charge Hypertension Oliguria Massive protein loss Decreased GFR Hyperlipidemia Hematuria Edema Hypoalbuminemia 42 Compare and contrast nephrotic and nephritic syndromes. Glomerulonephritis can lead to either nephrotic syndrome or nephritic syndrome In nephrotic syndrome, injury to the Nephritic syndrome is caused by increased glomerular filtration membrane permeability of the glomerular filtration leads to increased permeability and membrane with pore sizes large enough to loss of an electrical negative charge. allow the passage of red blood cells and protein. The pathophysiology is related to 1. Massive immune injury of the glomerulus proteinuria 1. Hematuria 2. Hypoalbuminemia 3. Edema 2. Oliguria 4. Hyperlipidemia/ 3. Decreased GFR hyperlipiduria 4. Hypertension 43 Supplemental Information- not on exam Ontario Resource- Ontario Renal Network 44  Identify the causes of acute kidney Learning injury, chronic kidney disease and Outcomes end-stage renal disease. 4. Explain the pathophysiology of acute kidney injury, chronic kidney disease Acute Kidney and end-stage renal disease. Injury and Chronic Kidney Describe the clinical manifestations of acute kidney injury, chronic kidney Disease disease and end-stage renal disease. 45 Video Lecture Slide 46  Acute Kidney Injury- Information AKI is a sudden decline in kidney function with a decrease in glomerular filtration caused by a defect in the excretion of water, salts, and nitrogenous waste products, which accumulate in the blood as demonstrated by an elevation in SCr level and decrease in urine volume. AKI is currently broadly classified according to the underlying pathophysiologic process as prerenal (renal hypoperfusion), intrarenal (intrinsic disorders involving renal parenchymal or interstitial tissue), or postrenal (urinary tract obstructive disorders) 47 48 Process leading to Chronic Renal Failure 49 50 Supplemental learning resource 90 minutes 9 minutes https://www.youtube.com/watch?v=Ywe5jjiJJJo https://www.youtube.com/watch?v=fv53QZRk4hs 51 Learning Compare and contrast the causes, Outcomes pathophysiological mechanisms and clinical manifestations of upper and lower urinary tract obstructions. Urinary Tract Describe the clinical manifestations of Obstruction and Urinary urge, stress, overflow and functional Incontinence incontinence. 52 UPPER AND LOWER URINARY OBSTRUCTIONS 53  FIG. 38.1 Urinary Tract Obstruction and Hydronephrosis. (A) Major sites of urinary tract obstruction. (B) Hydronephrosis of the kidney. There is marked dilation of the renal pelvis and calyces with thinning of the overlying cortex and medulla due to compression atrophy. (B, From Kumar V, et al. Robbins and Cotran pathologic basis of disease, 10th edition. Philadelphia: Elsevier; 2021.) Textbook page 1232 Lecture video slide Lecture video slide  Source: Pre-lecture Video Dietary- DASH diet; Mediterranean Diet associated with decreased risk of kidney stones 57  1. Nephrolithiasis local conditions- Question The following conditions are needed to form kidney stones, EXCEPT for: a) Super saturation of one or more salts b) Precipitation of salts from liquid to solid state c) Growth via crystallization or aggregation d) Obstruction of urine flow within the kidney or urinary tract 58  2. Nephrolithiasis Composition-Question In addition to calcium, what are possible contents of kidney stones? a) Uric Acid, Chloride b) Oxalate, Phosphate c) Cholesterol, Uric Acid d) Cholesterol, Phosphate 59 Response- What are gallstones made of? Flashback- Module 5 Components of gall stones can include: A Calcium, cholesterol, carbohydrates B Bilirubin, bile, bicarbonate C Carbohydrates, bile, bacteria D Cholesterol, bilirubin, calcium  3. Nephrolithiasis formation- Question What conditions can influence the precipitation of salts from liquid to solid state in the production of kidney stones? a) Urine filtrate pH too high or too low b) Urine filtrate pH too high c) Urine filtrate pH too low d) Urine filtrate pH does not influence this process 61  4. Nephrolithiasis- Common Stones- Question What is the most common type of kidney stone in adults? a) Uric acid b) Calcium Oxalate c) Calcium Phosphate d) Struvite e) Cystine 62  Supporting information Conditions associated with Calcium Oxalate stone formation- notes 1. Decreased solute- dehydration 2. Decreased stone inhibitors- decreased citrate in the urine filtrate Normally, citrate binds with Calcium and therefore Ca not available to bind with oxalate and form stone. e.g. medication Diamox (Acetazolamide) inhibits reabsorption of bicarbonate in the proximal tubule- extra bicarb in urine leads to increased secretion of protons into the urine (via distal tubule) (e.g. Type II renal tubular acidosis- problem in prox. tubule) Citrate does not like acidic environment in the urine- leads to increased reabsorption of citrate into blood stream Ca now binds with oxalate in the urine as citrate not available for binding 3. Too much calcium in the urine filtrate available to bind to oxalates in the urine filtrate Hypercalcemia (e.g. with increase parathyroid hormone, some cancers) leads to increase calcium filtration High oxalate level in blood (low calcium diet, or malabsorption syndrome with decreased fat absorption) Decreased calcium reabsorption in kidney- e.g. high sodium, high https://www.youtube.com/watch?v=YXFv_5aAh_8 protein diet, loop diuretic) 63  Supporting information How can a low calcium diet can lead to increased risk of calcium oxalate renal stone formation! -notes Low Calcium Diet Oxalate can cross from gut into blood stream. However, if calcium binds to oxalate- it cannot be absorbed into the blood stream. If less calcium in gut, less oxalate to bind and therefore it can cross over into blood stream Fat malabsorption in the gut Calcium loves to bind with fats If extra fat in the gut (malabsorption- e.g. IBD, pancreatic problems)- calcium will choose to bind with fats rather than oxalate Therefore, more oxalate available to cross over from gut into blood stream https://www.youtube.com/watch?v=YXFv_5aAh_8 64 5. Renal Colic- Question Renal colic can be described as: a) Continuous severe flank pain from hydronephrosis b) Continuous severe flank pain due to mucosal ischemia c) Bursts of flank pain due to reflex ureter spasm d) Bursts of flank pain due to ureter dilation 65 Video Lecture slide content 66 Neurogenic Bladder- bladder dysfunction caused by a neurological disorder Lecture Video Slide Sites of Neurologic Injury Associated With Neurogenic Bladder. https://www.news-medical.net/health/Micturition-Reflex-Neural-Control-of-Urination.aspx  The brain ‘blocks’ the bladder reflex so you are not voiding The Bladder reflex- sensory nerves are triggered when every time there is a bit of urine in the bladder. the bladder was is stretched due to urine When you no longer need to ‘hold it’- your brain withdraws Signals go the SACRAL section of the spinal cord and the signal that was holding the bladder reflex tell the bladder to contract. https://www.youtube.com/watch?v=kmcsrNxWEQo Sacral Spinal Cord Injury and urination Lesions below S1 The bladder reflex does not work. No sensation of filling or contraction can occur. Leads to weak detrusor muscle and weak sphincter  Spinal cord injury above the sacral area Impact on urination The bladder reflex is intact The brain’s ability to control the bladder reflex is lost as the nerve signals/pathway between brain to the sacral area are disrupted from injury (e.g. can’t ‘hold’ the bladder reflex) Result: Bladder spasms- urinary spasms, leakage when you don’t want it to happen (urinary incontinence) Textbook Urinary Incontinence Watch video on urinary incontinence” from lecture video Clinical integration video using case studies The material goes beyond the learning objectives for this module; however, case study approach very appliable to primary care setting 1. Type of Incontinence- Question What type of incontinence may occur in men with benign prostatic hyperplasia? a) Stress incontinence b) Overflow Incontinence c) Mixed incontinence d) Urge incontinence  Overflow Urinary Incontinence-notes If the pressure in the urinary bladder exceeds the pressure of the bladder sphincter, a continuous trickle of urine is discharged. The bladder is constantly overfilled and continuously releases small amounts of urine in the absence of any urge Enlarged to urinate (e.g. dribbling) prostrate Reasons for overflow incontinence can be drainage disorders, e.g. due to urinary stones, tumours or nerve damage. In many cases, an enlarged prostate can also cause a blockage of the bladder outlet. Men are more affected by this type of incontinence than women. “Drainage disorder leads to dribbling” 75  2. Incontinence type- question An overactive bladder, or the sudden, intense urge to urinate followed by involuntary loss of urine is considered: a. Urge incontinence b. Spastic neurogenic bladder c. Overflow incontinence d. Detrusor muscle hypertrophy 76  3. Incontinence- Question Urge urinary incontinence can be due to: a) Cystitis b) Loss of cerebral inhibition of detrusor muscle contraction c) Neurological changes from Parkinson’s disease d) All of the above e) None of the above 77  Urge Urinary Incontinence-notes A sudden, irresistible urge to urinate, which can often occur at short intervals and even when the bladder is not full, forces the person concerned to seek a toilet immediately. – Urge symptoms cannot be delayed and there is an involuntary leakage of urine before a toilet can be reached. – A frequent urge to urinate with frequent visits to the toilet at very short intervals (