Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
patho exam 2
disorders of kidney and urinary tract function
| Question | Answer |
|---|---|
| urinary tract function | produces, stores and eliminates urine |
| urinary tract is composed of | bladder, two kidneys, two ureters and the urethra |
| kidneys are responsible for | homeostasis via urine production and elimination |
| kidney impacts multiple body functions like | blood pressure (secretes renin to start RAAS which raises BP), electrolyte and acid-base balance, RBC production and bone health (controls amt of Ca) |
| acute kidney injury (AKI) | rapid decrease in kidney function |
| chronic kidney injury (CKD) | loss of kidney function over time, results from a failure of the body to remove waste productions |
| end stage renal disease (ESRD) | occurs if CKD is not treated, results from a failure of the body to remove waste products |
| how to prevent ESRD if pt has CKD | use other strategies to remove waste to prevent ESRD from happening |
| elimination of waste products | without blood flow to the kidneys, urine output decreases AKA decreased BF to kidneys = decreased urine output |
| acid-base balance | bicarbonate acts as buffer to maintain acid-base balance |
| in acidosis, | kidneys reabsorb bicoarbonate |
| in alkalosis | kidneys excrete more bicarbonate |
| glomerulonephritis (GN) causes | acute and chronic kidney injury/disease |
| glomerulonephritis (GN) is | the inflammation of the glomeruli and capillaries |
| glomerulonephritis (GN) is characterized by | proteinuria, hematuria and edema |
| etiology and pathogenesis of glomerulonephritis (GN) | postinfectious (accumulation of immune complex which triggers hypersensitivity type III), systemic disease, toxin exposure, thrombosis (thrombus stuck in glomerulus), genetics (make you more prone) |
| acute postinfectious glomerulonephritis (GN) decreases | the ability to get rid of waste |
| nephritic syndrome (inflammation) | hematuria, mild proteinuria, RBC casts/dysmorphic RBCs |
| nephrotic syndrome | hyperlipidemia, proteinuria, hypoalbuminemia, edema, urinary fatty casts |
| diagnosis of glomerulonephritis (GN) | biopsy and urine analysis |
| treatment of glomerulonephritis (GN) | blood pressure control, blood cholesterol control, control of rising creatinine: immunosuppression |
| diabetic nephropathy | CKD resulting from hyperglycemia |
| diabetic nephropathy is the leading cause of | end stage renal disease |
| diabetic nephropathy is characterized by | proteinuria and hyperfiltration (induced by blood glucose) |
| risk factors of diabetic nephropathy | poor glycemic control, uncontrolled HTN, obesity, smoking, genetic factors, race (minorities) |
| diabetic nephropathy is more prevalent in | african american, hispanic, american indian, and asian individuals |
| progression of diabetic nephropathy | hyperglycemia, polyuria, increased renal blood flow, glomerular hypertrophy (more cells divided in glomerulus), glomerular hypertension (secrete renin, adapt vasculature to high BP), hyperfiltration |
| CMs of diabetic neuropathy | albuminuria (albumin in the urine and problems with filtration), hyperfiltration, hypertension (constriction in vessels) |
| diagnosis of diabetic neuropathy | renal biopsy may not be necessary pt having diabetes, HTN and albuminuria leads to Dx |
| treatment of diabetic neuropathy | maintain BP under 140/90 blood cholesterol control - using statins maintain A1C under 7% |
| how to maintain BP under 140/90 | use ACE inhibitors and ARBs (angioreceptor blockers that stop formation of angio II) |
| how to maintain A1C under 7% | lifestyle modifications and glucose lowering medications |
| A1C above 7% is a marker of | chronic blood glucose |
| hypertensive nephropathy is | CKD resulting from long standing HTN |
| hypertensive nephropathy is the second leading cause of | end stage renal disease |
| hypertensive nephropathy affects | glomerulus, tubules and vasculature of kidneys |
| hypertensive nephropathy leads to | nephrosclerosis which is the hardening of blood vessels due to chronic high BP |
| risk factors of hypertensive nephropathy | genetics, diabetes, previous renal disease, more prevalent in african americans |
| etiology of hypertensive nephropathy | genetics, lifestyle choices (exercising avoids this disease), activation of RAAS (increases BP), arterial stiffness (artery can't constrict or dilate) |
| pathogenesis of hypertensive nephropathy | activation of RAAS! atherosclerosis, reduced BF to glomeruli, SNS stimulation, activate RAAS, renal renin production (increased secretion of renin, angio I to angioi II, aldosterone stimulates reabsorption of NA and increases BP), increased systemic BP |
| CMs of hypertensive nephropathy | left ventricular hypertrophy, opthalamic changes, mild proteinuria , increased BUN and creatine over time |
| BUN is | blood urea nitrogen |
| diagnosis of hypertensive nephropathy | past medical history, HTN, increased BUN/creatinine |
| treatment of hypertensive nephropathy is the same as | diabetic nephropathy bc interconnected diseases |
| treatment of hypertensive nephropathy | maintain BP under 140/90 blood cholesterol control - using statins lifestyle modifications |
| lifestyle modifications for treatment of hypertensive nephropathy | regular exercise, smoking cessation, maintain BMI under 25, restrict dietary sodium to less than 2.4g/day |
| UTI | infection of lower urinary tract of the bladder, upper urinary tract or the kidney (can migrate here) |
| who is more prone to get UTIs | women |
| what do you need to control UTIs | medications |
| cystitis | infection of the bladder |
| cystitis is the most common | bacterial infection |
| risk factors of cystitis | diabetes mellitus, familial predisposition, obstruction (kidney stones), neurogenic bladder (can't vascontrict/dilate the bladder), use of spermicides and diaphragms |
| what is affected by cystitis | the bladder wall |
| pyleonephritis | infection of the renal pelvis and parenchyma (functional tissue) of the kidney |
| pyleonephritis risk factors | female gender - sexually active, use of spermicides or diaphragm, pregnancy genitourinary tract abnormalities (anything that blocks the bladder) neurogenic bladder immunosuppresion diabetes |
| ascending bacterial colonization from urethra to bladder is most caused by | E. coli |
| ascending bacterial colonization from urethra to bladder is classified as | complicated or uncomplicated |
| other causes of ascending bacterial colonization from urethra to bladder | obstruction in flow of urine (stones or papillary necrosis), residual urine retention, bacteremia, instrumentation, back flow of urine (vesicoureteral reflux - VUR) |
| cystitis CMs | dysuria, urgency, frequency, confusion in older adults cannot control pee! |
| Dx of cystitis | based on clinical symptoms, urinalysis, urine culture as needed |
| pyelonephritis CMs | costovertebral angle pain (pain on the kidneys) fever and chills bc inflam process is induced which stimulates a systemic response WBC is urine = BAD |
| Dx of pyelonephritis | urine culture - check for WBC which are indicative of pyelonephritis and CT scan |
| Dx of UTIs | based on clinical symptoms, urinalysis and culture |
| Tx of UTIs | antibiotic therapy - any regimen of antibiotics |
| neprholithiasis aka | kidney stones |
| kidney stones result from | formation of urinary crystals into larger stones |
| kidney stones are a common | obstruction that usually affect maes |
| risk factors of kidney stones | previous stones, dehydration, hypercalcuria, hyperoxaluria (from high vitamine and Ca), high sodium diet bc Na will induce dehydration |
| main cause of kidney stones | dehydration |
| composition of kidney stones | majority are calcium based less common: uric acid, struvite, cyestine stones |
| stone formation | damage to lining of urinary tract, crystal aggregation, slow urine flow to allow crystallization, excretion of large amounts of calcium in urine |
| CMs of kidney stones (renal calculi) | acute, unilateral flank pain nausea vomiting severe pain that comes and goes |
| can kidney stones move | yes, thats why the pain comes and goes |
| Dx of kidney stones | based on clinical symptoms, ultra sound, x-ray |
| Tx of kidney stones | thiazide diuretic (makes you pee more) or allopurinol, percutaneous nephrolithotomy - PCNL (tube to drain), surgery as needed |
| urinary incontinence is most common in | caucasian women |
| urinary incontinence risk factors | pregnancy, older age (decreases elasticity), obesity, HTN, smoking, alcohol consumption, postmenopausal diabetes, neurogenic bladder |
| type of incontinence: stress (usual) | physical activity, sneezing, coughing |
| type of incontinence: urgency | feeling urgency with loss of urine |
| type of incontinence: postural | position change |
| type of incontinence: nocturnal enuresis | during sleep |
| type of incontinence: mixed | all together! stress, urgency, or postural features |
| type of incontinence: continuous | always! continuous loss of urine |
| type of incontinence: insensible | can't tell unawareness of loss of urine |
| type of incontinence: coital | occurs with coitus (sexual activity) |
| Dx of urinary incontinence | report loss of urine in various situations |
| Tx of urinary incontinence | weight loss, bladder training, pelvic floor muscle training, pessary, surgery, antimuscarinics/anticholinergics |
| chronic kidney disease | either kidney damage or GFR <60mL/min/1.73 m2 for 3 months or more |
| chronic kidney disease incidence continues to | rise in US and worldwide |
| chronic kidney disease use of dialysis | 25% of people starting dialysis die within the first year of treatment |
| diabetic nephropathy pathogenesis | most frequent cause of CKD in ESRD moderate albuminuria=early indicator basement membrane thickening, mesangial expansion, increased glomerular permeability, decreased GFR |
| hypertensive nephrosclerosis pathogenesis | increased pressure in the glomerulus > damage of glomerular cells > glomerulosclerosis damage of small vessels in kidney > inadequate blood supply > decreased BP to glomeruli > glomerulosclerosis hyperfiltration > thickening of glomerular vessels |
| chronic glomerulonephritis pathogenesis | direct injury to the glomerulus, pathogenesis to diabetic nephropathy, antibody deposition > glomerular inflammation, chemokines and cytokines > mesangial cells promote inflammation |
| polycystic kidney disease pathogenesis | onset at 30 y/o, another cause of CKD and 3rd cause of ESRD, cysts develop from collecting duct of nephron, cysts increase in number and size with age, macrophrage infiltration/neurovascularitzation, progressive fibrosis, and decreased renal function, |
| 90% of polycystic kidney disease caused by | PKD1 gene mutation |
| complications of CKD | cardiovascular disease (CVD) metabolic acidosis chronic kidney disease-mineral and bone disorder (CKD-MBD) anemia hyperkalemia hypervolemia uremia |
| cardiovascular disease (CVD) CMs | most common causes of death in CKD HTN, dyslipidemia, and chronic inflammatory state |
| metabolic acidosis | in CKD, kidneys retain H+ ions decreased kidney function leads to increased ammonia and retained H+ ions decreased kidney function decreases resorption of sodium bicarbonate |
| chronic kidney disease-mineral and bone disorder (CKD-MBD) CMs | bone disease in CKD resulting from mineral and hormonal changes, causes bone pain, deformities and fractures, results from abnormal bone turnover, hypocalcemia, hyperphosphatemia, and hyperparathyroidism |
| anemia CMs | decreased erythropoietin, worsens with worsening CKD, leads to increased cardiac preload, decreased afterload and increased cardiac output |
| hyperkalemia CMs | develops as oliguria develops, results from decreased aldosterone secretion and decreased excretion of potassium |
| aldosterone function | acts at collecting duct and will absorb Na and K is eliminated |
| hypervolemia CMs | once GFR falls, renal secretion of sodium and water decreases, exacerbates CVD and LVH |
| uremia CMs | results from waste product accumulation in blood |
| diagnosis of CKD | national kidney foundation guidelines blood and urine tests - check fro abnormals (proteinuria) additional laboratory tests - liver profile (enzymes), thryoid function tests (cells), electrolyte panel imaging |
| imaging Dx of CKD | KUB (kidney, urinary, bladder), renal ultrasound, arteriogram, CT, MRI |
| stages of CKD are decided by level of GFR | the lower the GFR, the more severe the stage of CKD |
| treatment of CKD | anti-hypertensives, lipid-lowering agents, hemodialysis, peritoneal dialysis, renal transplantation |
| anti-hypertensives | ACE/ARB medications - deal with BP |
| lipid lowering agents | statin therapy - deal with lipids |
| hemodialysis | removal of toxins and excess fluid from the blood, filtrate the blood so number of toxins decrease |
| peritoneal dialysis | removal of toxins and excess fluid by utilizing the peritoneum, dialysis fluid is injected at the peritoneal cavity and the bad collection comes out |
| renal transplantation | most common! encouraged in those who have the potential of a good quality of life after transplantation |
| what to do first and second to treat CKD | control the BP first, then decrease lipids |
Created by:
leh195