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268 Cards in this Set
- Front
- Back
What is the physiological path of corticosteroid production
|
"Hypothalamus secretes Corticotropin Releasing Hormone
|
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Which drugs show about equal levels of Anti inflam and salt retention
|
"Hydrocortisone
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What drug has strong anti inflammatory with little salt retention
|
prednisone
|
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what drugs are moderately stong antinflamatories with no salt retention
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"Methylprednisolone
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What are the drugs that are very strong antiinflammatories with no salt retention
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"Dexamethasone
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What do glucocorticoids increase in metabolism
|
"Gluconeogenesis
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What metabolic processes decrease with glucocorticoids
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"Osteoblast formation and activity
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How do glucocorticoids affect the immune system
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"Decrease cytokines, prostaglandins and interleukins
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Musculoskeletal ADRs of corticosteroids
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"Weakness, myopathy, tendon rupture, osteoporosis, fracture, asceptic necrosis of femoral/humeral heads"
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how can corticosteroids affect fluid and electrolyte balance
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"Na retention
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GI ADR for corticosteroids
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"GI ulceration with perforation
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Enzyme inducers
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"Phenytoin
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Mepristine
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"Corticosteroid antagonist
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Mitotane
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"Corticosteroid antag
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Ciclesonide
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"intranasal
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Aldosterone
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"Acts on DCT, inc Na reabsorption and K excretion"
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Mineralocorticoid actions
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"Na absorption, K excretion, elevates BP, can inhibit adrenals, pituitary and thymus
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Primary use of mineralocorticoids
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"Addison's Disease
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Mineralocorticoid drug interactions
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"Barbituates
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What is Renal Plasma Flow
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RPF= (1-Hct) x RBF
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What is the definition of GFR
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filtration rate of all the glomeruli of the total nephron population of the kidneys
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Definition of Filtration Fraction
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How much plasma per unit time was transported across the glomerular barrier
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How is FF calculated
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"GRF/RPF
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How is GFR calculated
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Kf((Pc-Pi)-s(Pip-Pii))
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A positive value for GFR means
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Filtration is occuring
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What is the first barrier in glomeruli and what size are the openings
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endothelial cells (50-100 nm)
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What is the 2nd barrier in glomeruli
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"lamina rara interna, lamina densa, lamina rara externa
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Third barrier and size
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Podoyctes of the epithelial cells (20-30 nm)
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What does a filterability of 1 mean
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that it is filtered as freely as water
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How are negatively charged particles filtered in relation to positive charged
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A positively charged molecule will be filtered more easily than a negatively charged molecule of equal size
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What is the major determinant of GFR
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"Hydrostatic forces
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how is clearance calculated
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"Cs=Us x V/Ps
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How can GFR be calculated using inulin
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"Amount Filtered= amount excreted
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Why does creatine clearance stabilize after it rises
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"Even though the filtration volume drops, it is offset by a rise in plasma conc of creatine"
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On the luminal membrane of the PCT what is the direction of passive Na movement
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"into the tubular cells
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Na movement on the Basolateral membrane of the PCT
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"Active transport out of cell into interstitum against ECG.
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What is the only method of Na control in the PCT
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antiotensin II can stim Na-H antiporters but for most part Na is just absorbed in large amounts by itself
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Cl movement across the luminal membrane in the PCT
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"Moves into cell against Elec Grad but with Conc Grad. unknown mechanism, anion exchange?"
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Cl movement in PCT on basolateral membrane
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Passive diffusion with electrical gradient
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Water Movement in PCT
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"Aquaporins
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Transport in the Ascending limb
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"impermeable to water all the time
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What active transport systems are in the ascending loop
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"Luminal: Na, K, Cl cotransport
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How is the remaining Na absorbed in the DCT
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Na-Cl cotransport (inhibitted by Thiazides)
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What hormones affect transport in the collecting tubules and ducts
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"ADH, Aldosterone, and ANP"
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How do the collecting ducts specifically control Na reabsorbtion
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Na is absorbed passible from the lumen but Na specific channels are increased through hormones. Na is moved into the interstitum by the Na-K ATPase
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How does GFR affect Na reabsorbtin
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increased GFR increases Na reabsorbtion to a point. Too high GFR leads to lower Na reabsorbtion
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What does ANP do
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"dilates renal vasc and increases GFR, and increases excretion of Na and as a result more water also"
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How does inhibitting H secretion affect Na reabsorbtion
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Will decrease Na reabsorbtion
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Why doesnt the body become hyperkalemic after ingesting high levels of K
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80% temporarily moves into the intracellular compartment
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Where does automatic K reabsorbtion occur
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PCT
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Movement of K in the PCT
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"Lumenal side: no to little movement either direction
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K movement in the Loop of Henle
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"Passive secretion into the tubular fluid as a result of high medullary K conc. Some reabsorption in the ascending portion via Elec grad, and Na,K, Cl cotransporter and the K-Cl cotransport on basolateral mem"
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K and the DCT
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"Steep Conc Gradient into lumen. Mostly secretion.
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How does aldosterone affect K movement
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Increases Na-K ATPases increasing the K conc inside the cells and then increasing passive secretion
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How is K affected by dehydration
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Water is drawn into the interstitium and K is concentrated in the cells leading to increased secretion
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Acidosis and K
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Acidosis leads to hyperkalemia. H moves into tubular cells and K is moved into interstium
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Alkalemia and K
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"H moves out of Cell, K moves in and is secreted
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Bicarb cycle
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"NaHCO3 filtered in glom
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Where does most bicarb get reabsorbed
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PCT
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What happens to bicarb in the DCT
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HCO3 combines with K in the lumen and KHCO3 gets stuck and excreted
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How is bicarb affected by alkalemia
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H is transported to insterstitium leaving lots of bicarb in the cell triggering the Cl-HCO3 increasing bicarb secretion
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How is titratable acid exreted
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Na2HPO4 dissociates to NaHPO4. H is secreted into the tubules and NaH2PO4 is formed and is excreted.
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what cells are especially important in controlling [H] and [bicarb]?
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alpha intercallated cells
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at what pH are the H pumps working at maximum
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4.4
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How does the body get rid of additional acid once the urine is at its lowest pH
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converts amino acids to ammonia and makes non titratable acids
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How does the ammonia system work
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as ammonia diffuses passively into the tubule it combines with H and is trapped. it then combines with sulfate and is excreted
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what movement is occuring as the vasa recta descend into the medulla
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"NaCL and urea enter as water leaves. All passive diffustion. But the blood flow is so fast, equilibrium never occurs"
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How do cortical nephrons fit into kidney function
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they are responsible for producing hypoosmotic fluid which is concentrated in the medulla
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What are the basic features in glomerular disease
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"Basement Membrane thickens
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Diffuse Disease
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involves all glomeruli
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Focal
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invovles only some glomeruli in a section
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Global
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entire individual glomerulus
|
|
segmental
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part of each glomerulus
|
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Anti GBM AB induced nephritis
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"Non collagenous domain of Collagen Type IV
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Heyman Nephritis
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"EDD along subepithelial aspect of BM (lumpy bumpy)
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Circulating Immune Complex Nephritis
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"Trapping of Antigen-AB complexes in glomerulus
|
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Where do cationic complexes deposit
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subepitheial
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where to anionic complexes deposit
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subendothelial
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where do neutral complexes deposit
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mesangium
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What is the typical progression of Glomerular disease
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Focal Segmental Glomerular Disease followed by tubulointerstitial fibrosis
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Focal Segmental Glomerulosclerosis
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"Adaptive change, hypertrophy maintains fx but proteinuria and glomerulosclerosis occur. folllowed by macrophage and ECM accumulations"
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Tubulointersitial fibrosis
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as ischemia and inflammation progress begin to get fibrosis
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Acute Post Infectious Glomerulonephritis
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"B-hemolytic Strep
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Acute Post Infectious Glomerulonephritis
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"LM: very hypercellular
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Rapidly Progressive Glomerulonephritis
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"Severe oliguria and death
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Type I RPGN
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"Goodpasture
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type II RPGN
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"Secondary disease
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Type III RPGN
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Pauci Immune and ANCA
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IgA nephropathy (Berger's)
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"Hematuria w/wo proteinuria
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Henoch-Schonlein Purpura
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"Rash, Abd pain, Arthralgia, Palp Purpura in legs, Renal issues.
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SLE
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"Nephritic, Young, african american women, sub endothial depots of anti-dna.
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SLE WHO Class I
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"No Proteinuria, normal glom, no visible changes, normal renal fx"
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Mesangial Glomerulonephritis"
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"No clinical sx
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SLE WHO Class III
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"Focal and Segmental
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SLE WHO Class IV
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"Diffuse Proliferative Glomerulonephritis
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SLE WHO Class V
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"Membranous Glomerulonephritis
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What classes of SLE have better prognosis
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II and V
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What classes of SLE have worse prognosis
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III and IV
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Alport's Nephritis
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"Eye problems
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What defines nephritic disease
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"hematuria
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What defines nephrotic syndrome
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massive proteinuria which can lead to hypoalbuminemia and edema
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How are lipids affected by nephrotic syndrome
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"hyperlipidemia and lipiduria, lipoproteins get excreted and as a result synthesis increases."
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What infections are common in nephrotic syndrome
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"Staph, pneumococcus"
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Why are infections common in nephrotic syndrome
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Losing complement in the urine
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Membranous Glomerulopathy
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Most Common Cause of Nephrotic Syndrome in Non Diabetic Adults
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What are secondary causes of membranous glomerulopathy
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"Lupus, drugs, malignancies, hep B and C, autoimmune"
|
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Spike and Dome
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Membranous Glomerulopathy
|
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Minimal Change Disease
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"Most common nephritic syndrome in children
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Focal Segmental Glomerulosclerosis
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"HIV, IVDA
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Membranoproliferative Glomerulonephritis (MPGN)
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Basement membrane and mesangial thickening. Nephrotic syndrome. 2 types
|
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MPGN type I
|
"unknown antigen complexted with AB depot'd in the subendothelium. granular C3, C1, C3, IgG depots"
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MPGN Type II
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"Infrequent circulating immune complexes. C3 acts as a nephritic factor. Dense deposit disease, thick hazy ribon "
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LM changes in MPGN
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tram track changes. caps have double contour
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Prognosis for MPGN
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"Not good, II a little worse
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Diabetic Glomerulosclerosis
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"Proteinuria, injury to arterioles, papillary necrosis
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Kimmelstiel Wilson Disease
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Nodular sclerosis in mesangium
|
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what are common causes of Acute Tubular Necrosis
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"Ischemia, Toxins, Acute tubulointerstitial nephritis, Urinary obstruction, DIC"
|
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what is characteristic of ATN
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acute diminuation/loss of renal function with a quick onset of change in lab values
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Characteristics of Ischemic ATN
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"Focal Tubular Epithelial Necrosis
|
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Where is Toxic ATN most obvious
|
PCT
|
|
Mercuric Chloride
|
Acidophillic inclusions
|
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Carbon tetrachloride
|
"Neutrla lipids in injured site and necrosis, also get liver injury"
|
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Ethylene Glycol
|
Ballooning of PCT and calcium oxalate crystals
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What occurs in the initiation phase of toxic ATN
|
"Inc Urine output
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What occurs in the maintanance phase of toxic ATN
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"Dec Urine volume, salt and water overload, rising BUN, hyperkalemia, metabolic acidosis"
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What occurs in the recovery phase of toxic ATN
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"Inc Urine volume
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Acute Pyelonephritis
|
"Flank pain, fever, malaise, dysuria, pyuria, + Murphy Test.
|
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Ascending pyelonephritits
|
"Yellow abscesses, papillary necrosis, bladder involved"
|
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Descending pyelonephritis
|
"Comes from a bacteriemia, usually involves whole kidney"
|
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aka Reflux Neuropathy"
|
"Recurrent inflammation and scarring
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Acute drug induced interstitial nephritis
|
"Fever, eosiniophilia, skin rash"
|
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Benign Nephrosclerosis
|
"gradual inc in BP over years, some hyaline ateriosclerosis, rough subcapsular section of kidneys"
|
|
Malignant Nephrosclerosis
|
Fibrinoid necrosis of arterioles w inflammatory infiltrates. ONION SKIN
|
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Adult polycystic kidney disease
|
"Autosomal dominant. Destruction of parenchyma. assymptomatic til 4th decade. flank pain, hematuria, HTN, UTI. berry aneurysms in C of Willis"
|
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Childhood Polycystic Kidney Disease
|
"Auto Recessive
|
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What is the most important function of the kidney
|
Maintaining homeostasis by regulating volume status
|
|
How fast should you decrease the pressure in a cuff?
|
2-3 mm Hg/sec
|
|
Whats the normogram look like
|
"Na Cl BUN
|
|
Characteristics of Creat
|
"Serum levels due to muscle metabolism
|
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Creat ________ as age increases
|
decreases
|
|
Females have _______ Creat
|
lower
|
|
African americans have _________ creat
|
increased
|
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"What is worse Creat from 1 to 2, or from 4 to 5"
|
"1 to 2
|
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What should the specific gravity and osmolality be for urine
|
"1.003- 1.035
|
|
Microscopic analysis of urine looks for
|
"RBC, WBC, Casts, Crystals, Orgs"
|
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What is a cast
|
reflection of the tubules
|
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RTE Cast
|
Casts with squamous looking cells (larger and more symmetrical)
|
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What can cause pyuria
|
"intersitial nephritis
|
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Hyaline Cast
|
"Tamm-Horsfall cast, not pathologic. can see in volume contracted pts"
|
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RBC cast
|
"always pathologic
|
|
Coarse Granular Cast
|
"Acute tubular necrosis, acute injury or failure
|
|
Waxy Cast
|
Nephrosis
|
|
Who gets renal biopsy
|
"2 kidneys
|
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What medications are used in Stage I Hypertension
|
"Thiazide
|
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Medication for Stage II
|
Thiazide and ACEI/ARB/BB/CCB
|
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What will u see in a pt with pre renal AKI
|
"Evidence of fluid loss, diminished intake, low CO
|
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What is post renal AKI
|
"Bladder outlet obstruction (BPH, Stones)
|
|
Lab profile for ATN
|
"not really high BUN/Creat
|
|
Azotemia
|
Elevated BUN
|
|
Oliguria
|
less than 400 mL urine output
|
|
Anuria
|
less than 100mL urine output
|
|
Intact Nephron Hypothesis
|
"nephrons are not destroyed globally, some are some remain intact"
|
|
What is the main reason albumin is not found in urine
|
negative charge of the molecule keeps it from being filtered
|
|
What is the normal loss of albumin in urine
|
20-30 mg/day
|
|
Glomerular Proteinuria is
|
"change in pore size, hemodynamics or charge of glomerulus allowing proteins into urine"
|
|
Tubular Proteinuria
|
B2 microglobulin is reabsorbed by tubular cells. in disfunction find lots of b2Mg
|
|
Overflow proteinuria
|
nothing wrong w kidneys but too much protein in blood (multiple myeloma)
|
|
Range for microalbuminuria
|
30-300 mg/day
|
|
Range for clinical albuminuria
|
>500 mg/day
|
|
What does a neg dipstick and positive SSA indicate
|
non albumin protein is in the urine and need to do UPEP
|
|
What proteinuria level is considered nephrotic
|
>3.5g/day
|
|
What secondary complications can occur with nephrotic syndrome
|
"Renal Failure
|
|
How is nephrotic syndrome managed
|
"Na restrict
|
|
Hallmarks of Minimal Change Disease
|
"fusion of footprocesses.
|
|
what are the 3 important causes of nephrotic syndrome
|
"Minimal change disease
|
|
what causes membranous glomerulopathy
|
"Idiopathic
|
|
What is the most common cause of nephrotic syndrome
|
focal segmental glomerulosclerosis
|
|
Stage 1 Diabetic nephropathy
|
"Increase GFR
|
|
Stage 2 Diabetic nephropathy
|
"Thick basement membrane
|
|
Stage 3 Diabetic Nephropathy
|
"Incipient nephropathy
|
|
Stage 4 DN
|
"Clinical nephropathy
|
|
Management of DN
|
"Glu control
|
|
Nephritic Syndrome
|
Destruction of filtering units
|
|
What occurs when Vit D levels decline
|
"GI Ca absorbtion drops
|
|
Primary Hyperparathyroidism
|
"Hypercalcemia
|
|
Characteristics of Early Renal disease
|
"PTH high
|
|
Characteristics of advanced Renal failure
|
"Low Ca
|
|
How does Vit D metabolism go wrong
|
"accumulation of FGF23 stops hydrolyzation of 1,25 D
|
|
What occurs in the PT to enhance its abnormal function
|
nodules lose Ca receptors and lose ability to downregulate PTH synthesis
|
|
Definition of Acute TIN
|
"intense accumulation of WBCs with symptoms of fever, rash and eosinophilia"
|
|
How does acute tubular necrosis lead to decreased gfr
|
cells die in the tubules and slough off and block the tubes and create and obstruction
|
|
Causes of Acute TIN
|
"Drugs (#1), drugs form complex with proteins in body that mimics structure of antigen in kidney, ABs attack kidneys"
|
|
How is TIN caused by drugs differentiated from other causes of low renal function
|
"Hx. Clinical Dx.
|
|
What are infectious causes of TIN
|
"Legionella
|
|
Autoimmune TIN causes
|
"Sarcoid, TIN and uveitis syndrome"
|
|
Clinical sx of TIN
|
"WBC in urine
|
|
Tx for TIN
|
"Remove causative agent
|
|
what does a kidney in chronic failure look like
|
starts to look like a thyroid
|
|
What is the mechanism for renal fibrosis
|
"chronic hypoxia converts tubular cells into fibroblasts
|
|
What are the consequences of tubular fibrosis
|
"Less NH4- metabolic acidosis
|
|
How does chronic TIN present
|
"Uremia
|
|
what causes chronic TIN
|
"DM, HTN, Heavy metals, analgesic, reflux nephropathy, UTI w stones"
|
|
what is normal serum Na Range?
|
135-145 mEq/L
|
|
what is the most dilute the body can make urine
|
at maximal ADH activity urin is 50-100 mOsm/kg
|
|
what is normal urine osmolarity
|
280-300 mOsm/kg
|
|
what does isothenuria mean
|
conc of urine is same as the plasma
|
|
how is adh released in relation to serum osmolaltiy
|
linear increase to a point
|
|
if the body is losing volume how does ADH release increase
|
exponentially
|
|
what is the hallmark of euvolemic hyponatremia
|
concentrated urine despite the absence of any stimulus for ADH release
|
|
what is the fastest you can replace a pt's Na
|
".5 mEq/L per hr
|
|
Hallmark of Hyperaldosterone State
|
Hypokalemic Metabolic Alkalosis
|
|
Classic Triad of Renal Tumor
|
"Hematuria
|
|
What paraneoplastic symptoms show up in renal CA
|
"Hypercalcemia, HTN, Gynecomastia, polycythemia, cushing syndrome, von hippel lindau"
|
|
Von Hippel Lindau
|
"hemangioblastomas of CNA and retina, cysts in kidney, liver and pancreas, pheochromoctycoma"
|
|
What is the typical route of metastasis of renal tumors
|
"renal vein
|
|
Clear Cell"
|
"Clear cytoplasm
|
|
Papillary Type"
|
"Highly Vascularized
|
|
Chomophobe"
|
"Prominent nuclear membranes, pale cytoplasm, halo around nucleus
|
|
Collecting Duct CA"
|
"rare
|
|
Where do Renal Cell CA tend to metastasize
|
Lung and bone
|
|
Renal papillary adenoma
|
"benign
|
|
Oncocytoma
|
"mahogany brown w central scar
|
|
angiomyolipoma
|
"benign but can lead to hemorhage
|
|
Transitional Cell CA
|
"Renal Pelvis, associated w papillary necrosis and analgesic abuse
|
|
Most common primary bladder tumor
|
Transitional cell CA
|
|
Stauffer's syndrome
|
high LFTs due to cholestasis
|
|
Ddx for Hematuria
|
"UTI
|
|
what is vital capacity
|
max insp to max exhale
|
|
FRC
|
"functional residual capacity
|
|
FVC
|
"forced vital capacity
|
|
FVC1
|
"Forced expired volume at 1 second
|
|
What is the criteria for obstructive disease
|
FEV1/FVC <70%
|
|
What is the criteria for restriction
|
all lung volumes are decreased
|
|
where are rhonchi heard
|
bronchi
|
|
Sibilant
|
high pitched
|
|
sonorous
|
lou pitched
|
|
rales
|
alveolus popping against fluid
|
|
excretion =
|
filtration - reabsorption + secretion
|
|
TBW=
|
TBW = 0.6 x body weight (kg)
|
|
filtered load
|
gfr x plasma conc
|
|
summarize Na and H2O transport in the PCT
|
various Na+ transporters bring Na+ and water (follows passively) into the cell Na+/K+-ATPase pumps intracellular Na+ into the lateral sac area lateral sacs build up hydrostatic pressure peritubular interstitium peritubular capillaries
|
|
Where in the nephron is the fluid most hypertonic
|
at the tip of the loop of henle
|
|
most common primary glomerulopathy worldwide
|
"IgA nephropaty
|
|
Wire and Loop Lesions
|
Membranous GN
|
|
What has a Hep association
|
Membranous Glomerulopathy
|
|
5 GNs with nephrotic syndrome
|
"Membranous Glomerulopathy
|
|
3 primary nephritic causes
|
"Post infectious
|
|
Dense ribbon deposit
|
Type II MPGN
|
|
"C3, IgG, C1, C4 granular in periphery"
|
MPGN Type I
|
|
If blood becomes acidemic which way does the O2 curve shift
|
to the right
|
|
Aveolar gas equation
|
PA O2=(0.21)(760-47) – PaCO2/R
|
|
What is normal blood pH
|
"7.4
|
|
What is normal pCO2
|
"36-44
|
|
What is normal HCO3
|
"21-27
|
|
High pCO2
|
acidosis
|
|
Low HCO3
|
Acidosis
|
|
Metabolic Acidosis
|
Low Bicarb
|
|
Metabolic Acidosis
|
High Bicarb
|
|
Resp Acidosis
|
High pCO2
|
|
Resp Alkalosis
|
Low pCO2
|
|
and their pCO2 is lower than the compensation should be what is going on w the pt"
|
they have a resp acidosis with an additional 1' resp alkalosis
|
|
Causes of increased anion Gap
|
"Methanol
|
|
Causes of a normal anion gap
|
"Hyperalimentation
|
|
Decreased anion gap caused by
|
"Bromide
|
|
Delta delta issssss
|
"Change in AG / change in bicarb
|
|
D/D < 1
|
HARD UP + MUDPILES
|
|
D/D = 1 to 2
|
MUDPILES
|
|
D/D >2
|
MUDPILES and Met Alkalosis
|