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150 Cards in this Set
- Front
- Back
Excretory Functions of the Kidney (3)
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1 - Remove waste products that came from the body's metabolism
2 - Regulate the composition of blood by controlling the amount of water, acid-base balance, and quantity and concentration of ions 3 - Excrete foreign substances |
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-bean shaped organ in the back of abdomen
-one on each side -level of the lower ribs -each weighs about 1/4 pound Approx. 4 inches long by 2.5 inches wide by 1.5 inches thick |
Kidney
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-Blood returns to the heart through the inferior vena cava
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Renal Vein
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-major branch from aorta
-receives = 20% of blood from heart -blood flows through kidneys at about 1.2 liters/min |
Renal Artery
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-enters at hilus
-conncets kidney to bladder -urine collection duct |
Ureter
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-contains light colored cone shaped masses known as the pyramids
-towards the middle of the kidney -where active transport and inactive transport occur along with filtration |
Medulla
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-part of the medulla
-made up of all tubules |
Pyramids
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-falt funnel shaped cavity that collects the urine into the ureters
-near hilus -pool to collect urine |
Pelvis
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-outer 1/3 of kidney
-contains most of filtration units -very active blood filtration area |
Cortex
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-found in cortex and medulla
-perpendicular to surface of kidney -1 million in each kidney -each one produces urine -main function is to clean the blood -ball of capillaries at end of artery -long thin tube with a hair-pin loop -closed at one end -surrounded by peribulbar capillaries |
Nephron
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Main Parts of Nephron (6)
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1 - Glomerulus
2 - Proximal convoluted tubule 3 - Descending Loop of Henle 4 - Ascending Loop of Henle 5 - Distal Tubule 6 - Collecting Duct |
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-part of nephron
-about the size of pinhead -contain Bowman's capsule and Juxtaglomerular cells -ball of capillaries -like having your hand in a closed balloon |
Glomerulus
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-part of glomerulus
-located in cortex -the tissue that surrounds the glomerular capillaries |
Bowman's capsule
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-closed end at the beginning of the nephron
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Vascular Pole
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-open end of nephron
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Urine Pole
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-artery bringing blood into glomerulus
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Afferent arteriole
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-vessel that takes blood out/away from glomerulus
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Eferent arteriole
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-part of glomerulus
-baroreceptors -enlarged smoothe muscle cells of afferent arteriole -produce, store, and excrete renin, which results in vasoconstriction |
Juxtaglomerular cells
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-has fenestrated endothelium and incomplete basement membrane supported by podocytes
-held together by mesangial cells that have a phagocytic function and contractile capabilities to control blood flow |
Glomerular Capillaries
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-part of glomerular capillaries
-epithelial cells -allow the filtration to occur easily -similar structure to choriocapillaris and RPE cells -have space between them and spaces contain nephrin which forms slit diaphragm |
Podocytes
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-helps control the blood flow of nephron
-causes the constriction of afferent arteriole and release of renin from juxtaglomerular cells -constriction causes slower blood flow and less filtration pressure |
Sympathetic system
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-helps control the blood flow of nephron
-renin-->angiotensin II, which causes constriction of efferent arteriole -helps achieve a constant rate of filtration in glomerulus |
Renin system
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-helps control the blood flow of the nephron
-influence renal blood vessels -PGs, NO, Endothelin |
Chemical mediators
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-cause dilation of blood vessels
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PGs
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-cause constriction of vessels
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NO and Endothelin
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-part of nephron
-first twisted region after Bowman's capsule -in cortex -almost all of glucose, bicarbonate, aa, and other metabolites are actively reabsorbed here -approx 2/3rds of Na is actively reabsorbed from the tubules here - depends on angiotensin -Cl and water reabsorbed passively by following the sodium -K actively reabsorbed -some meds actively excreted at this point -filtrate is isotonic here |
Proximal convoluted tubule
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-part of nephron
-at entrance the filtrate is isotonic -osmolarity increases becase the only thing that can be reabsorbed here is water -"water falls out" passively -this water will be reabsorbed by peritubular capillaries |
Descending Loop of Henle
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-part of nephron
-long hairpin loop after proximal tubule -extend from cortex into medulla and back out to cortex -at entrance filtration is hypertonic -"water can't flow up stream" -cells lining this tube are impermeable to water -active reabsorption of sodium, potassium, and chloride occur here -another major site for salt reabsorption -this reabsorption of salt makes the medulla very hypertonic -at exit filtrate is hypotonic |
Ascending Loop of Henle
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-part of the nephron
-second twisted part of nephron in cortex -cells of early one also impermeable to water -reabsorption of chloride -calcium excretion regulated here by PTH -active K excretion also occurs partly in exchange for Na -filtrate remains hypotonic |
Distal Tubule
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-at the junction between ALH and distal tubule
-chemoreceptors that respond to decreased concentration of sodium and chloride in filtrate to encourage release of renine from juxtaglomerular cells -respond to too little Na and too little Cl by telling the body to release renin |
Macula densa cells
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-part of nephron
-sodium reabsorbed by active processes -potassium excreted by exchange with Na - aldosterone increases this activity -urea passively reabsorbed here -presence of ADH allows water to pass through walls of collecting ducts and be reabsorbed -makes urine hypertonic in the end -long straight portion after the distal tubule that is the open end of nephron -extends from cortex to medulla -collects fluid from several nephrons |
Collecting Duct
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Processes of Kidney (3)
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1 - Filtration
2 - Reabsorption 3 - Excretion |
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-process of kidney
-occurs as blood passes through glomerulus --> pressure in glomeruli is 2-3 times higher than other capillary beds of the body -glomerulus shows selective permeability influenced by the size, charge, and configuration of the substance -higher concentration of substance in capillaries increases concentration in filtrate -filtrate in water, ions, glc, aa, bicarbonate |
Filtration
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-process of kidney
-ions, glc, aa get reabsorbed from lumen of nephron -specialized transporters on membranes of epithelial cells of nephrons -different transporter types located in different parts of nephrons -some transporters are active and some passive process -reabsorption of most substances related to Na reabsorption- by exchange, via share transporters or via solvent drug -also occurs along tubules -usually passive -this is huge! -only 1% of total filtrate volume becomes urine |
Reabsorption
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Two Major Modifiers of Absorption
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1 - Concentration of molecules
2 - Rate of flow of filtrate |
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-addition of substance to filtrate
-unwanted components such as ammonia -can be a function of transporter cells or passive process -these processes try to maintain a balance in your blood stream |
Excretion
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Follow the Filtrate!
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Glomerulus --> Proximal Tubule --> Descending LoH --> Ascending LoH --> Distal Tubule --> Collecting ducts
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-controlled by two main mechanisms
--> structure and transport properties of the nephron -->ADH secreted by the pituitary |
Water balance maintainance
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-major stimulus for secretion is decreased blood volume
--> baroreceptors in many places --> decreased bp causes release of ADH - next is increased osmolarity of blood --> osmoreceptors located in ant hypothalamus --> most responsive to Na and mannitol -> Glc also has some effect -more of this increases water reabsorption |
ADH
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-increase the blood flow to kidney
--> prevent vasoconstriction -impair water reabsorption by several mechanisms --> block ADH in collecting duct --> prevents water and sodium reabsorption --> prevents K excretion -can be countered by NSAIDs and steroids and cause decreased initial filtration which results in edema |
Renal PGs
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-type of kidney endocrine function
-manufactured by kidney -released in response to hypoxia -stimulates bone marrow to produce RBCs |
Erythropoietin
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-type of kidney endocrine function
-conversion of Vit D to active metabolic form -impt for absorbing Ca from intestine |
Calcitrol
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-type of kidney endocrine function
-combines with angiotensin --> angiotensin I --> angiotensin II -produced and released by juxtaglomerular cells -also causes the release of aldosterone from adrenal cortex -increases release of ADH from neurohypophysis -also stimuates thirst -helps regulate blood pressure |
Renin
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-increases Na reabsorption at distal tubules and collecting ducts which increase water reabsorption
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Aldosterone
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-kidney function
-remember that body keeps blood at a relative pH of 7.4 -excess hydrogen ions combine with bicarbonate -kidney helps control this --> regeneration of bicarbonate --> excretion of hydrogen ions when blood is too acidic --> excretion of bicarbonate ions when blood is too alkaline |
Acid-base balance
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-type of kidney function test
-amt of filtrate formed in all nephrons -about 20% of renal plasma flow is filtered -normal rate is 125ml per min -used to assess renal functions -measured clinically by collecting timed blood and urine samples |
Glomerular filtration rate
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-type of kidney function test
- a product of creatine metabolism of muscle -filtered by kidney but not reabsorbed out of tubules -urine is collected for 24 hours with blood draw at end -normal is about 100ml per min - less than 60 is significant indicator of kidney disease |
Creatinine clearance rate
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-type of kidney function test
-normal = 1.0mg/100mL -depends on gender and size of individual -if value doubles consider GFR and kidney function to have fallen to half of normal state -if value triples it suggests 25% of normal kidney function |
Serum creatinine level
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-type of kidney function
-an end product of protein metabolism -filtered and controlled by kidney function - about 50% is excreted and 50% is reabsorbed -if glomerular filtration rate is slow the excretion of urea goes way down because more is reabsorbed the longer the tubular fluid stays in the kidney -normal value is 7-20 mg/dL -increases with decreasing kidney function |
Urea
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-kidney function test
-expect no protein, blood or glc -if found, suggest kidney disease -a gross test |
Urinalysis
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-type of serum lab test
-tend to increase with kidney failure |
Potassium and phosphate
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-type of serum lab test
-tend to decrease with kidney failure |
Calcium, pH, bicarbonate
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-future test
-has advantage because it is good at showing when someone has had acute trauma to the kidney -used to look for acute problems as can be caused by sx - some forms of acute renal failure can be reversed if found quickly and doing right things |
Neutrophil gelatinase assoc lipcalin
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-type of imaging
-visualize the urethra, bladder, and ureteral orifices -allows for biopsy |
Cystoscopy
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-type of imaging
-for evaluation of structure, tumors, abnormalities |
Ultrasound
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-type of imaging
-CAT scan detect tumors -radiopaque iodine contrast medium allows visualization of urinary structures -IV pyelogram allos xray visualization of renal tissues as injected dye is cleared by kidneys |
Radiologic exams
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-4-16% of US adults has some kind of chronic of this
-84,000 deaths per year due to renal problems -more than 335,000 americans suffer fom failure and need dialysis or transplantation to live -more than 74,000 pts are waiting for transplants but only 17000 receive them each year because of shortage of donors -increasing in the US |
Kidney Disease
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-these underlie the most causes of primary kidney disease
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Immune Mechanisms
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-most common cause of kidney failure - 40% of cases
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Diabetes
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-commonly results from kidney problems
-always damages the kidneys to some extent -second most common cause of chronic kidney failure in the US |
Hypertension
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Common First Symptoms of Kidney Disease (10)
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1 - HTN
2 - Swelling of legs 3 - Pulmonary edema 4 - Fatigue 5 - Headaches 6 - Weight loss 7 - N and V 8 - Itching 9 - Increased tendency to bleed 10 - Cognitive Impairment |
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Diseases that cause ocular and renal effects (6)
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1 - Diabetes
2 - HTN 3 - TINU 4 - MPGN 5 - Von Hippel-Lindau 6 - Wilms' |
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Ocular symptoms that renal disease can present with first (7)
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1 - Eyelid edema
2 - Ca deposits on lids or conj 3 - Aniridia 4 - Uveitis 5 - ONH edema 6 - Drusen around macula 7 - Retinal changes |
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-leads to increased risk of cardiovascular death and increased risk of stroke
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Impaired renal function
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-an abrupt decrease in renal function that leads to retention of nitrogenous waste products in body over a few days
-multiple causes -signs and symptoms reflect loss of regulatory, excretatory, and endocrine functions of kidney -if pt survives this, 90% change of full recovery of kidney function --> intial survival depends on cause and severity |
Acute Renal Failure
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-part of ARF
-decreased blood flow from volume loss or occlusion -kidney would still function if had enough fluid -hemorrhage, heart failure, shock, burns, diarrhea and vomiting, and thromboemboli |
Pre-Renal
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Diseases that Involve Kidney structures (3)
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1 - Vessels
--> malignant HTN --> Vasculitis 2 - Glomerulus --> Infectious --> Immune mediated 3 - Tubular --> Toxicity |
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-most common instrinsic cause of ARF
-abrupt decline in GFR -occurs within min to days -response to acute ischemic or neprotoxic insult -destruction of tubular epithelial cells decreases ion transport -damages vasculature --> increases endothelin, decreases nitric oxide and decreases PG --> vasoconstriction -causes reduced volume of urine and increased waste products in blood -due to medical illness: 30% mortality rate -due to prego: 10-15% mortality rate -if pt survives original cause there is a 90% chance of recovery -later death most likely due to infection |
Acute Tubular Necrosis
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-uncommon form of HTN
-diastolic BP -> 120mm Hg -ON head edema -encephalopathy -CV abnormalities -renal failure -True medical emergency -immediate and aggressive anti-HTN therapy -vascular damage to kidney -increased permeability of small vessels -leads to fibrosis which causes narrowing of vessl lumen -results in ischemia to kidney -causes release of renin which causes further vasoconstriction -develops vicous cycle |
Malignant Hypertension
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Specific Agents that cause ARF (4)
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1 - Radiographic contrast agents
2 - Aminoglycosides 3 - NSAIDS 4 - Ethylene Glycol |
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-specific agent that causes ARF
-reported rates in literature vary from 0-76% -especially at risk are patients with pre-existing renal insufficiency -dehydration also a risk |
Radiographic contrast agents
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-specific agent that causes ARF
-nephrotoxicity occurs in about 10% of pts taking these meds -avoiding overdoes is impt -typically comes within 1 week of treatment -prognosis for recovery is very good |
Aminoglycosides
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-specific agent that causes ARF
-inhibit PG synthesis -discontinuation often allows resolution |
NSAIDs
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-specific agent that causes ARF
-anti-freeze -maifests after 48-72 hours -pts are disoriented -develop stupor, coma, cardiovascular collapse -often fatal |
Ethylene Glycol
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-clinical manifestations are variable
-tend to manifest when GFR is less than 10mL/min -related to toxic effects of: --> retained products normally excreted by kidneys --> normal products such as hormones that are now present at higher than normal levels --> loss of normal products of kidneys ( loss of erythropoietin) |
Chronic Renal Failure
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-when the pt has clinical signs and symptoms of azotemia
-affects every organ system --> likely due to multiple factors being out of balance not just excess urea -includes fatigue, N,V,D, headache, and azotemia |
Uremia
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GI signs of Uremia (4)
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1 - Metallic taste
2 - anorexia 3 - NVD 4 - GI bleeding |
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-tend to be freq and occur early
-start with subtle changes in cognitive ability -poor memory and sleep disturbance also common -progresses to lethargy, irritability, confusion, seizures -can have loss of peripheral sensation in glove and stocking distribution -decreased deep tendon reflexes -can improve with dialysis |
Neurological Manifestations of Uremia
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Musculoskeletal Manifestations of Uremia (2)
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1 - Late in disease
2 - Osteoporosis |
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Hematologic Problems with Uremia (2)
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1 - Anemia
2 - Bleeding disorders |
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Endocrine Abnormalities (3)
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1 - thyroid disease
2 - Enlarged thyroid is found in as many as 1/3 of uremic pts 3 - Decreased libido |
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Immunological function in Uremia (2)
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1 - Immunosuppressed
2 - Increased risk of infections of all kids |
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-diabetics show decreased insulin requirements as kidney function decreases
-decreased sensitivity to insulin in peripheral tissues - due to electrolyte dysfunction |
Metabolic disorders and Uremia
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Dermatologic Manifestations and Uremia (4)
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1 - Ca Sulfate and PO4 precipitate in the sweat
2 - Itching 3 - Yellow discoloration of skin 4 - Odor |
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Types of Glomerular Disease (2)
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1 - Nephritic syndrome
2 - Nephrotic syndrome - membranoproliferative glomerulonephritis |
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Types of tubule and interstitial disease (3)
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1 - TIN
2 - Pyelonephritis 3 - Interstitial nephritis |
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-constitutes some of the major problems in nephrology
-characterized by altered glomerular function - could be faster or slower but usu slower -changes in filtration rate -changes in permeability of glomerular capillaries partly due to nephron that makes small slits in capillaries -can be caused by immunologic mechanisms -can be caused by injury often secondary to metabolic imbalances such as in DM |
Gomerular Disease
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Initial nonspecific Manifestions of Glomerular Disease (5)
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1 - HTN
2 - Edema 3 - Malaise 4 - Proteinuria 5 - Hematuria |
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-type of glomerular disease
-acute inflammation of glomeruli -abrupt onset of hematuria and proteinuria with impaired renal function that results in small amts of urine -one of first manifestations may be oliguria -retention of salt causes fluid retention and HTN -mild edema usually of the eyelids and face first -less urine volume, less glom filtration, and blood in urine |
Nephritic Syndrome
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-prior stretococcal infection
--> 10-14 days after acute strep infection --> inflammation from Ag-Ab reaction -more common in children -more common in summer and fall - post strep throat infection in northern US --> <5% of individuals -post strep pyoderma in southern US --> As many as 50% develop this -SLE --> consider if no prior strep infection - subacute bacterial endocarditis - can be idiopathic |
Common causes of nephritic syndrome
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-cause of nephritic syndrome
- an infection of heart tissue -usually valvular and end up where pooling of blood occurs with bacteria that grow in it and is caused by blood isn't getting pushed out like it should |
Subacute bacterial endocarditis
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-salt restriction
-diuretics and other anti-hypertensives -complete recovery in 90-95% -can take 1-2 years in some individuals -rarely progresses to chronic renal failure |
Treatments of Nephritic syndrome
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-type of glomerular disease
-derangement of capillary walls of glomerulus -massive PROTEINURIA - seen as bubbly and frothy urine by patients - generalized EDEMA - eyelids first and very extensive - HYPOALBUMINEMIA triggers the production of all plasma proteins including lipoproteins - HYPERLIPIDEMIA and HYPERLIPIDURIA - peripheral breakdown of lipoproteins also impaired that causes an increase risk of thromboembolism -not inflammation of glomerulus -get huge amt of protein -can develop into pitting edema |
Nephrotic syndrome
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-beleived to be immune mediated
-diabetes, SLE, NSAID induced, Membranoproliferative glomerulonephritis, and idiopathic |
Common causes of Nephrotic syndrome
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-ACE inhibitors or ARB decrease protein by decreasing glomerular filtration rate, improve charge and size selectivity of glomerular BM
- more than 90% of pts respond to corticosteroids - proteinuria recurs in more than 66% of initial responders - use is controversial as may become steroid dependent -other immune suppressive meds can be used -thrombro-prophylaxis during first 6 months -place pt on meds to alter renin-angiotensin because who renin cascade will end up causing vasoconstriction of efferent arteriole which increases the pressure and makes the glom leaky |
Treatment for Nephrotic syndrome
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- a very specific form of nephrotic syndrome
-immune system damages capillaris and supporting mesangium - at least two subtypes often of unknown cause - can cause HTN and signs of nephrotic syndrome - Type II assoc with bilateral central clustered DRUSEN -often found in teens -initially VA of VF unchanged - long term = poor night vision, SRNVM, Macular detachment, central serous retinopathy, and retinal atrophy |
Membranoproliferative glomerulonephritis - dense deposit disease
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- a group of inflammatory kidney diseases that primarily involve the interstitium and tubules
- spares the glomeruli and renal vessels - can be acute or chronic |
TIN
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-type of TIN
-often caused by bacterial infection of the renal pelvis - due to infection |
Pyelonephritis
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-type of TIN
-if noninfection in origin -drugs and metabolic disorders -physical injury |
Interstitial nephritis
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- type of TIN
- in young adults between 10 and 33 - occurs in females more than males - bilaterial uveitis in majority - conjunctival injection, fine KP, iridocyclitis - ocular symptoms occur first in about 35% - often recurrent - fever, weight loss, fatigue that is very nonspecific - oral corticosteroids |
Acute idiopathic tubulointerstitial nephritis and uveitis
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-inflammation of kidney and renal pelvis
- almost always bacteria getting to kidney retrograde via the bladder and ureters - almost exclusively in women due to length and location of urethra - esp common in pregos - clinically there is fever, dysuria, flank/back pain, and pyuria -usually very responsive to abxs |
Acute pyelonephritis
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- slowly progressing and insidious disease which slowly destroys the kidney due to retrograde flow of urine
- often the only signs and symptoms are "fatigue, dont feel well" and other vague symptoms so ususally diagnosed late -there is usually some pus in urine -primary underlying disorder is frequent UTI from obstruction, vesicoureteric reflux, or diabetic nephropathy, many of these pts wind up on renal dialysis - pts with diabetes have reduced immune system and glc in urine allows bacteria to grow easily - something causes urine to go back into kidneys |
Chronic pyelonephritis
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-common cause of acute renal failure
- kidney based hypersensitivity reaction - type 4 - primarily includes tissue surround glom and tubules |
Acute interstitial nephritis
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-med that can cause acute interstitial nephritis
- body breaks these meds and is carried through glom they combine with proteins of kidney and get stuck within the kidney and we get haptun form - byproduct of something that attaches itself to protein and sets up immune response of the body (3) |
1 - Abx
--> PCN, sulfonamides, ciprofloxacin 2 - NSAIDs --> Ibuprofen, indomethacin 3 - Diuretics --> Thiazides, furosemide |
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-classic presentation of acute renal failure, fever, rash, arthralgias, and eosinophilia
- mild to no proteinuria - no edema - no HTN - treat by removing causative agent |
Acute interstitial nephritis
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- causes include drugs such as analgesics, and cytotoxic/immunosuppressive agents
- gout - lead exposure - immune disorders |
Chronic interstitial nephritis
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- single most impt cause of ERSD in US
- direct result of metabolic changes in DM - good glood sugar control is protective against this disease - ACE inhibitors and angiotensin II receptor blockers are protective - microalbuminuria and proteinuria even early on in diagnosis - nephrotic syndrome and azotemia develop 3-5 years after proteinuria - end stage renal disease 1-5 years after that - accelerated decline with HTN, infection, nephrotoxins - glomerulus capillary basement membrane thickening - renal athersclerosis --> affects both afferent and efferent arterioles --> changes blood flow to kidneys - pyelonephritis --> increased susceptibility to infection due to warm env, poor wbcs, and sugar in urine that allows bacteria to grow |
Diabetic neuropathy
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-epithelium lined cavities filled with fluid or semisolid debri
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Cystic diseases of the kidney
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-present in up to 505 of pts over 50 and are often asymptomatic
- can be confused with tumors - ultrasound and CT scan help differentiate - part of cystic diseases of the kidney |
Simple Cysts
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-type of cysitc diseases of the kidney
- multple cysts throughout the kidneys with enlargement of kidneys - can be inherited - can result in chronic renal failure |
PKD
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-type of PKD
- autosomal dominant PKD - most common heriditary disease in US - M=F - progresses slowly - accts for about 10% of pts on dialysis - HTN = most common cardiovascular manifestation |
Adult PKD
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-type of PKD
- autosomal recessive - universally fatal by third decade - often fatal within first year as it occurs with congenital hepatic fibrosis -much more concerning but much less common - involves liver and other internal organs, not just kidney - very often causes death |
Childhood PKD
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- type of urinary outflow obstruction
- formation of a calculus in the collecting system - travels down stream until too large for duct - usually occurs in the ureters - blockage of flow of urine - due to coalition of ions and or minerals - get pushed down until it gets to a tube that is too smale and stops the urine flow -occur with symptoms in 1 out of 20 people at some time in their life - a frequent disorder found in about 1% of all autopsies - peak incidence is between 20 and 45 years of age - symptomatic urolithiasis is more common in males |
Nephrolithiasis
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-usually occurs when pt becomes dehydrated
- meds and gout |
Polygenic Nephrolithiasis
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Composition of Nephrolithiasis (3)
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1 - Calcium - 75%
2 - Magnesium - 15% 3 - Uric acid or cystine - 10% |
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- hematuria
- pain is common because stone is impinging on ureter -sudden onset, very severe - diagnosed with CAT scan |
Signs and Symptoms of Nephrolithiasis
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- 90% of stones pass spontaneously
- pain relief - meds to allow spontaneous passage --> alpha adrenergic blockers, calcium channel blockers - dietary modifications - antibiotics given after they are passed - shockwave lithotripsy - extremely strong sound wave applied to kidney area to break up large stones into smaller ones and tend to develop HTN - very large stones may require surgery if shockwave doesnt work |
Treatment of Nephrolithiasis
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- causes kidney stones and we use it for ONH edema and angle closure glaucoma
- remain well hydrated to decrease the effect of kidney stones - if pt has angle closure glaucoma you dont want them to drink alot so you can decrease IOP |
Acetazolamide
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- accounts for 80-90% of all malignant tumors of the kidney
- 2/1 male dominated - accts for 2% of all cancers in adults --> greater freq in cig smokers - assoc with Von-Hippel Lindau disease - long standing fever - elevated sedimentation rate - systemic signs of cancer like weight loss and fatigue - develops from proximal tubules - highly vascular - usually treated by surgical removal of kidney - percutaneous cryoablation and VEGF being explored - 5 year survival rate about 70% if no metastasis --> metastasize via bloodstream --> the metastases may remit when primary tumor is removed - will occasionaly spontaneously remit and nobody knows why |
Renal cell carcinoma
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- causes vascular tumors in many places
- has to do with renal cell carcinoma |
Von Hippel Lindau disease
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- most common presenting manifestation of Renal Cell Carcinoma
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Painless hematuria
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Classic Triad of Renal Cell Carcinoma
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1 - Hematuria
2 - Dull flank pain 3 - Palpable flank mass |
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- second most common kidney malignancy
- third most common organ cancer in children less than 10 - can grow to an incredible size and result in abdominal distention - high incidence of this in kids with aniridia - treated with radiotherapy, nephrectomy, and chemotherapy - good prognosis --> 90% survival for 2 years |
Wilms' tumor
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-part of Wilm's tumor
- loss of iris or failure of iris to develop properly - can be absent or just part of it is missing - 20% of children with this have Wilms' |
Aniridia
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-remove or treat cause if known
-treatment of HTN - decreases the progression of renal failure -treatment of secondary manifestations - heart disease, HTN, edema, anemia -restriction of dietary protein -avoid toxic meds -short or long term dialysis -renal transplantation -has to be both the dr and pt decision |
Treatments for chronic renal failure
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-diuretics
-beta blockers -ACE inhibitors -angiotensin II antagonists -Calcium channel blockers -Renin inhibitors -some of the most common and impt meds taken by pts in your practice |
Antihypertensive drugs
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-shown to be renal protective in diabetics beyond level expected from blood pressure drop
-and some say in all with kidney disease -three anti hypertensive drugs |
1 - ACE inhibitors
2 - Angiotensin II antagonists 3 - Renin inhibitors |
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-type of antihypertensive
-decrease the re-absorption of Na in kidneys -therefore increased urine output -initially reduce blood volume -but blood volume may return to normal with time --> especially if kidney function is normal -very useful in pts with HTN due to chronic renal disease |
Diuretics
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Types of diuretics that are typically used for kidney, heart, and bp treatment (3)
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1 - Thiazide
2 - Loop 3 - Potassium sparing |
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-types of Thiazide diurectics (2)
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1 - Hydrochlorothiazide
2 - Chlorthalidone |
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-Types of Loop Diuretics
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1 - Bumetanide
2 - Furosemide |
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Types of K sparing diuretics
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1 - Spironolactone
2 - Triamterene |
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-type of diuretic that is commonly used in eye care for glaucoma or disc edema
-acetazolamide |
CAI
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-type of diuretic that is used for glaucoma
-includes mannitol, urea, and isosorbide |
Osmotic diuretics
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-current criteria for initiation for dialysis
-glomerular filtration rate --> 15ml/min for diabetics --> <10ml/min for nondiabetics -uremia -edema not responsive to diuretics -acidosis -persistent hyperkalemia -heart failure -encephalopathy -two choices -any combo of these things can cause you to do this -decision is based on lifestyle, what symptoms pt has, and how close they live to a hospital -want to decrease the load on kidneys in diabetics |
Renal Replacement therapy
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-Types of Replacement Therapies (4)
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1 - Hemodialysis
2 - Peritoneal dialysis 3 - Renal treansplantation 4 - Choice depends on many factors: age, underlying disease, pt preference and motivation, donor availability, and accessibility of dialysis sites |
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-type of renal replacement therapy
->100,000 pts with ERSD are maintained on this -most common tx in US -blood circulates out of body into artificial kidney machine -another fluid called dialysate is pumped through machine in opposite direction of blood -semi-permeable membrane separates these two fluids -allows diffusion of ions and low mw substances from blood into dialysate -blood circulated back into the body -requires 3.5 hours of dialysis three times a week -yields minimal creatinine clearance -strict dietary modification also needed espeically dealing with protein and phosphorous and calcium -studies have shown that more visual impairment in pts on dialysis than expected for age - includes VA, contrast sensitivity, and depth perception -pts don't feel the greatest -use about 20-25% of kidney function -risks are anemia, ionic dysfunction, heart dysfunction, pulmonary edema, and infection |
Hemodialysis
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-type of renal replacement therapy
-pt has indwelling catheter in peritoneal cavity -installation of 1-3ml of dialysate into peritoneal cavity -stays in peritoneal cavity for specific period of time -peritoneum acts as semipermeable membrane to remove solute -dialysate removed and more added -in continuous ambulatory PD, fluid is constantly in peritoneum -treated differently when prescribing meds - |
Peritoneal Dialysis
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Adv of Peritoneal dialysis over Hemodialysis (4)
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1 - Less time spent in dialysis activities per se
2 - Less dietary restrictions 3 - Generally more consistent filtration 4 - Residual kidney function retained longer |
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Risks of Peritoneal Dialysis (2)
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1 - Peritonitis: not easy infection to tx
2 - Death: two times more common than with hemodialysis esp if cardiovascular disease is present and unsure why |
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-most satisfactory treatment for ESRD
-kidney recipients have improved health related quality of life -preferred method of renal replacement therapy -kidney is from a living related donor or cadaver --> donor and recipient method for HLA type, blood type, gender --> living donation has a better chance of graft and pt survival -most pts take immunosuppressive durg therapy as prophylaxis for life |
Renal Transplantation
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-types of immunosuppressants taken with renal transplantation (3)
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1 - Corticosteroids
2 - Cyclosporine 3 - Rapamune sirolimus - acute rejection |
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-type of immunosuppressant
-previously discussed by dr. smith -some centers are moving away from using them due to side effects but more than 50% still use them -ocular side effects include cats, increased risk of glaucoma, and papilledema due to increase in intracranial pressure |
Corticosteroids
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-type of immunosuppressant
-comes from soil fungus -introduced in early 1980s -increased graft survival rate by 20% for the first year -works by suppressing cell mediated immune reactions -prevents cytokines from activating T lymphocytes -ususally administered concurrently with glucocorticoids |
Cyclosporine
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-nephrotoxicity
-hepatotoxicity -HTN -increased risk of infections -increased risk of lymphoma -interacts with many meds - increased levels of cyclosporine to toxic levels |
Adverse effects of cyclosporine
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-immunosuppressive disorders
-secondary HTN due to prednisone and native kidney renin production -infections such as UTI, hepatitis, and pneumonia -malignancy --> 100 times greater than general population --> skin cancer --> kaposi's sarcoma --> ocular sq cell carcinoma -graft rejections are known to occur |
Transplantation Complications
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-a transplantation complication
-very common to show up in conj and looks like a sub-conjunctival hemorrhage -wont change colors if it is this -decreased with Rapamune |
Kaposi's sarcoma
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-try to avoid meds toxic to kidney such as aminoglycosides and tetracyclines except docycycline
-adjust amt of meds gived based on the creatinine clearance result -can be decreased dose or increased interval |
Prescribing meds for Renal Transplanation pts
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Two possible formulas for dosing meds on kidney pts
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Dose = (pts CrCl/ normal CrCl) x normal dose
Dosing interval = (normal CrCl/pts CrCl) x normal interval |
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-drug used for infection
-excretion: bile primarily -epocrates indicates no renal adjustment but caution advised if severe impairment |
Azithromycin
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