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268 Cards in this Set
- Front
- Back
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What is the physiological path of corticosteroid production
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"Hypothalamus secretes Corticotropin Releasing Hormone
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Which drugs show about equal levels of Anti inflam and salt retention
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"Hydrocortisone
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What drug has strong anti inflammatory with little salt retention
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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
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"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
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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
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"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
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PCT
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Mercuric Chloride
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Acidophillic inclusions
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Carbon tetrachloride
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"Neutrla lipids in injured site and necrosis, also get liver injury"
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Ethylene Glycol
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Ballooning of PCT and calcium oxalate crystals
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What occurs in the initiation phase of toxic ATN
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"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
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"Flank pain, fever, malaise, dysuria, pyuria, + Murphy Test.
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Ascending pyelonephritits
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"Yellow abscesses, papillary necrosis, bladder involved"
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Descending pyelonephritis
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"Comes from a bacteriemia, usually involves whole kidney"
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aka Reflux Neuropathy"
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"Recurrent inflammation and scarring
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Acute drug induced interstitial nephritis
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"Fever, eosiniophilia, skin rash"
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Benign Nephrosclerosis
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"gradual inc in BP over years, some hyaline ateriosclerosis, rough subcapsular section of kidneys"
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Malignant Nephrosclerosis
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Fibrinoid necrosis of arterioles w inflammatory infiltrates. ONION SKIN
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Adult polycystic kidney disease
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"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
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"Auto Recessive
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What is the most important function of the kidney
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Maintaining homeostasis by regulating volume status
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How fast should you decrease the pressure in a cuff?
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2-3 mm Hg/sec
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Whats the normogram look like
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"Na Cl BUN
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Characteristics of Creat
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"Serum levels due to muscle metabolism
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Creat ________ as age increases
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decreases
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Females have _______ Creat
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lower
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African americans have _________ creat
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increased
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"What is worse Creat from 1 to 2, or from 4 to 5"
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"1 to 2
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What should the specific gravity and osmolality be for urine
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"1.003- 1.035
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Microscopic analysis of urine looks for
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"RBC, WBC, Casts, Crystals, Orgs"
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What is a cast
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reflection of the tubules
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RTE Cast
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Casts with squamous looking cells (larger and more symmetrical)
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What can cause pyuria
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"intersitial nephritis
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Hyaline Cast
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"Tamm-Horsfall cast, not pathologic. can see in volume contracted pts"
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RBC cast
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"always pathologic
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Coarse Granular Cast
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"Acute tubular necrosis, acute injury or failure
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Waxy Cast
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Nephrosis
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Who gets renal biopsy
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"2 kidneys
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What medications are used in Stage I Hypertension
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"Thiazide
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Medication for Stage II
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Thiazide and ACEI/ARB/BB/CCB
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What will u see in a pt with pre renal AKI
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"Evidence of fluid loss, diminished intake, low CO
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What is post renal AKI
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"Bladder outlet obstruction (BPH, Stones)
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Lab profile for ATN
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"not really high BUN/Creat
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Azotemia
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Elevated BUN
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Oliguria
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less than 400 mL urine output
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Anuria
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less than 100mL urine output
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Intact Nephron Hypothesis
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"nephrons are not destroyed globally, some are some remain intact"
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What is the main reason albumin is not found in urine
|
negative charge of the molecule keeps it from being filtered
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What is the normal loss of albumin in urine
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20-30 mg/day
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Glomerular Proteinuria is
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"change in pore size, hemodynamics or charge of glomerulus allowing proteins into urine"
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Tubular Proteinuria
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B2 microglobulin is reabsorbed by tubular cells. in disfunction find lots of b2Mg
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Overflow proteinuria
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nothing wrong w kidneys but too much protein in blood (multiple myeloma)
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Range for microalbuminuria
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30-300 mg/day
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Range for clinical albuminuria
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>500 mg/day
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What does a neg dipstick and positive SSA indicate
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non albumin protein is in the urine and need to do UPEP
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What proteinuria level is considered nephrotic
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>3.5g/day
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What secondary complications can occur with nephrotic syndrome
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"Renal Failure
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How is nephrotic syndrome managed
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"Na restrict
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Hallmarks of Minimal Change Disease
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"fusion of footprocesses.
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what are the 3 important causes of nephrotic syndrome
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"Minimal change disease
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what causes membranous glomerulopathy
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"Idiopathic
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What is the most common cause of nephrotic syndrome
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focal segmental glomerulosclerosis
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Stage 1 Diabetic nephropathy
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"Increase GFR
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Stage 2 Diabetic nephropathy
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"Thick basement membrane
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Stage 3 Diabetic Nephropathy
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"Incipient nephropathy
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Stage 4 DN
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"Clinical nephropathy
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Management of DN
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"Glu control
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Nephritic Syndrome
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Destruction of filtering units
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What occurs when Vit D levels decline
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"GI Ca absorbtion drops
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Primary Hyperparathyroidism
|
"Hypercalcemia
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Characteristics of Early Renal disease
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"PTH high
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Characteristics of advanced Renal failure
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"Low Ca
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How does Vit D metabolism go wrong
|
"accumulation of FGF23 stops hydrolyzation of 1,25 D
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What occurs in the PT to enhance its abnormal function
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nodules lose Ca receptors and lose ability to downregulate PTH synthesis
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Definition of Acute TIN
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"intense accumulation of WBCs with symptoms of fever, rash and eosinophilia"
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How does acute tubular necrosis lead to decreased gfr
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cells die in the tubules and slough off and block the tubes and create and obstruction
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Causes of Acute TIN
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"Drugs (#1), drugs form complex with proteins in body that mimics structure of antigen in kidney, ABs attack kidneys"
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How is TIN caused by drugs differentiated from other causes of low renal function
|
"Hx. Clinical Dx.
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What are infectious causes of TIN
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"Legionella
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Autoimmune TIN causes
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"Sarcoid, TIN and uveitis syndrome"
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Clinical sx of TIN
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"WBC in urine
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Tx for TIN
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"Remove causative agent
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what does a kidney in chronic failure look like
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starts to look like a thyroid
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What is the mechanism for renal fibrosis
|
"chronic hypoxia converts tubular cells into fibroblasts
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What are the consequences of tubular fibrosis
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"Less NH4- metabolic acidosis
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How does chronic TIN present
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"Uremia
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what causes chronic TIN
|
"DM, HTN, Heavy metals, analgesic, reflux nephropathy, UTI w stones"
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what is normal serum Na Range?
|
135-145 mEq/L
|
|
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what is the most dilute the body can make urine
|
at maximal ADH activity urin is 50-100 mOsm/kg
|
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what is normal urine osmolarity
|
280-300 mOsm/kg
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what does isothenuria mean
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conc of urine is same as the plasma
|
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how is adh released in relation to serum osmolaltiy
|
linear increase to a point
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if the body is losing volume how does ADH release increase
|
exponentially
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what is the hallmark of euvolemic hyponatremia
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concentrated urine despite the absence of any stimulus for ADH release
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what is the fastest you can replace a pt's Na
|
".5 mEq/L per hr
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|
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Hallmark of Hyperaldosterone State
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Hypokalemic Metabolic Alkalosis
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Classic Triad of Renal Tumor
|
"Hematuria
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What paraneoplastic symptoms show up in renal CA
|
"Hypercalcemia, HTN, Gynecomastia, polycythemia, cushing syndrome, von hippel lindau"
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Von Hippel Lindau
|
"hemangioblastomas of CNA and retina, cysts in kidney, liver and pancreas, pheochromoctycoma"
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What is the typical route of metastasis of renal tumors
|
"renal vein
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Clear Cell"
|
"Clear cytoplasm
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Papillary Type"
|
"Highly Vascularized
|
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Chomophobe"
|
"Prominent nuclear membranes, pale cytoplasm, halo around nucleus
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|
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Collecting Duct CA"
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"rare
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Where do Renal Cell CA tend to metastasize
|
Lung and bone
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|
Renal papillary adenoma
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"benign
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Oncocytoma
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"mahogany brown w central scar
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angiomyolipoma
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"benign but can lead to hemorhage
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Transitional Cell CA
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"Renal Pelvis, associated w papillary necrosis and analgesic abuse
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|
|
Most common primary bladder tumor
|
Transitional cell CA
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|
|
Stauffer's syndrome
|
high LFTs due to cholestasis
|
|
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Ddx for Hematuria
|
"UTI
|
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what is vital capacity
|
max insp to max exhale
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FRC
|
"functional residual capacity
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FVC
|
"forced vital capacity
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FVC1
|
"Forced expired volume at 1 second
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|
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What is the criteria for obstructive disease
|
FEV1/FVC <70%
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|
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What is the criteria for restriction
|
all lung volumes are decreased
|
|
|
where are rhonchi heard
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bronchi
|
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Sibilant
|
high pitched
|
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|
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
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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
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Where in the nephron is the fluid most hypertonic
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at the tip of the loop of henle
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most common primary glomerulopathy worldwide
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"IgA nephropaty
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Wire and Loop Lesions
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Membranous GN
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What has a Hep association
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Membranous Glomerulopathy
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5 GNs with nephrotic syndrome
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"Membranous Glomerulopathy
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3 primary nephritic causes
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"Post infectious
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Dense ribbon deposit
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Type II MPGN
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"C3, IgG, C1, C4 granular in periphery"
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MPGN Type I
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If blood becomes acidemic which way does the O2 curve shift
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to the right
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Aveolar gas equation
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PA O2=(0.21)(760-47) – PaCO2/R
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What is normal blood pH
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"7.4
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What is normal pCO2
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"36-44
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What is normal HCO3
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"21-27
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High pCO2
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acidosis
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Low HCO3
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Acidosis
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Metabolic Acidosis
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Low Bicarb
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Metabolic Acidosis
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High Bicarb
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Resp Acidosis
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High pCO2
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Resp Alkalosis
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Low pCO2
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and their pCO2 is lower than the compensation should be what is going on w the pt"
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they have a resp acidosis with an additional 1' resp alkalosis
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Causes of increased anion Gap
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"Methanol
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Causes of a normal anion gap
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"Hyperalimentation
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Decreased anion gap caused by
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"Bromide
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Delta delta issssss
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"Change in AG / change in bicarb
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D/D < 1
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HARD UP + MUDPILES
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D/D = 1 to 2
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MUDPILES
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D/D >2
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MUDPILES and Met Alkalosis
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