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Boards 2 > Renal > Flashcards

Renal Flashcards

1
Q

Fluid Compartments

A

2/3 ICF

  • 1/3 ECF with 1/4 being plasm
  • Manitol and inulin measure ECF
  • D2O measures total body water
  • Radioactive albumin measures Plasma
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2
Q

Volume determinants

A

ECF volume is a function of solute, if Na/Cl are lost the ECF will contract. The ICF will spill fluid there to maintain equal osmolarity

  • 2*Na+glucose/18+BUN/2.8
  • Osmolarity of compartments is always the same.
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3
Q

Expansions and Contractions

A
  • Expansions and Contractions refer to the ECF volume
  • Osmolarity effects the ICF volume
  • Isoosmotic Expansion: ICF stays same volume and ECF expands by volume added (Isotonic saline infusion)
  • Hyperosmotic expansion: ECF expands and ICF will shrink to maintain osmolarity. NaCl igestions
  • Hypoosmotic expansion: ECF expands and ICF expands to maintain osmolarity. SIADH, free water resorbed without resporbtion in Na. ICF shrniks, throws off concentrations in nuerons leads to siexures
  • Isoosmotic contraction: Diahhrea/burns/trauma
  • Hyperosmotic contracction: Los of free H20 (DI, sweating (More dilute than plasma))
  • Hypoosmotic Contraction: Loss of solute without water, aldosterone deficency (Addisons)
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4
Q

Clearance

A
  • The ammount of plasma cleared of a given substance per unit time
  • Ammount excreted in urine/plasma concentration
  • (urine concentration time flow rate)/(Plasma concentration)
  • Units are volume/time
  • Inulin is GFR, PAH is RPF, glucose and albumin are zero
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5
Q

Renal Blood Flow

A
  • Calculated using PAH clearance to get renal plasma flow

- Then can correct for hematocrit

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6
Q

Regulators of Renal Blood Flow

A
  • SANS: Through alpha 1 receptors lead to a constriction of afferent and efferent. Decreases both RPF and GFR
  • Ang II: Preferetial Constriction of efferent over afferent, leads to a decrease in RPF with a maintained GFR (graded response)
  • ANP: Causes dilation of all arterioles and constriction of efferent only. Leads to increased renal flow and significantly increased GFR (Escape from aldosterone, lower Na content and lower ECF)
  • Prostaglandins: Cause dilation of afferent and efferent. Allow escape from SANS/AngII contriction. If NSAIDs, decrease this effect leads to decreased GFR
  • Myogenic: Stretch of smooth muscle cells leads to constriction and increased GFR
  • Tubuloglomerular: Increased delivery of solutes to macula densa signals and increase in GFR, release vasoactive substance to constrict afferent and decrease GFR
  • Dopamine: Causes contriction of skeletal muscle and dilation of renal, splanchinic, and cerebral vessels. Hemorrhage leads to preservation of vital organs in exchange for skeletal muscle
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7
Q

Filtration barrier

A
  • Endothelial cells have pores that keep RBC but allow proteins to get through
  • Basement membran, doesn’t allow proteins through
  • Podocyte processes generate filtration slits to further reinforce boundary
  • Negative chage from GAG’s and heparin decrease plasma protein filtration
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8
Q

Changes in GFR and Filtration

A
  • Constriction of the ureter leads to decreased hydrostatic pressure and decreased GFR and filtration fraction at a given RPF
  • Protein concentratoin in plasma will also effect GFR and FF without altering RPF
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9
Q

Filtration equilirium

A

At the end of the glomerular cappilary there is often quilibrim reached because loss of fluid leads to relative increase in plasma protein concentration and increase in osmotic pressure. Hydrostatic is little changed.

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10
Q

Pre-renal Azotemia

A

Decreased RPF will lead to a decreased GFR

  • Creatinine is nor resorbed while urea is
  • pre renal azotemia will lead to increased BUN/Cr ratio
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11
Q

Glucose Reabsorption

A
  • Tm System, governed by sturation of carriers
  • Carriers with 2 Na and one glucose on apical, basal is glut1, glut2
  • Splay is the begining period of glucose in urine, haven’t completely saturated transporters, but have partially
  • DM
  • Physiologic glucosuria of pregnancy caused by an increase in GFR leading to an increase in filtered load
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12
Q

Urea

A
  • Passively reabsorbed and secreted, flows down conentration gradient and highly dependednt on H20 Reabsorption
  • In PCT H20 resprobtion leads to 50% of urea to be reabsorbed
  • At the bottome of thin desceding limb, water has been resorbed and urea concentration in interstitial fluid is high, some is secreted. Total concentration is 110% o filtered load
  • Impermiable in DCT, Ascending limb, and proximal collectin duct
  • Distal collecting duct H20 will be resorbed leading to an increase in urea concentration and some will be reabsorbed.
  • UT1 is a transported that increases permiablity
  • Dependent on ADH mediated H2O resorption
  • Eventuall approximatly 40% is excreted
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13
Q

PAH

A
  • Organic anion transporter secretes into urine
  • Freely filtered but Tm system
  • At low plasma PAH concentrations, all PAH is secreted, at high plasma PAH secretion, saturation occurs and some is reabsorbed. no longer useful clincal measure of GFR
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14
Q

Weak acids and bases

A
  • Ionization state effects lipid solublty and ability to diffuse back into paratubular capillaries
  • Acids are ionized at high pH and trapped in urine
  • Treat ASA and TCA overdose with NaHCO3
  • Amphetamines and opiods are bases, charged at high pH, increase seccretion with NH4Cl leading to acidified urine
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15
Q

Tf/P

A
  • Ratio of tubular fluid concentration to plasma concentration
  • Dependednt almost exclusively on water reabsorption
  • If equal 1 then resorbed with water (Na)
  • If less than one, resorbed faster than water (glucose)
  • If greater than one: Slowly resorbed or secreted (Inulin, urea, etc)
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16
Q

(Tf/P)/(Tf/Pinulin)

A

-Measureing the ratio when compared to inulin will give a measurment of the fraction of the filtered load that has beeen resorbed

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17
Q

Na Balance

A
  • Na balance is primarily driven by Na/K ATPase gradient

- Coupled to the transport of many molecules

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18
Q

Early part of PCT

A
  • Na is cotransported with Glucose, AA, HCO3, citrate, Lactate, etc
  • Na is also antiporterd with H
  • All metabolic necessary products are resorbed with Na but very little Cl is resporbed
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19
Q

Late PCT

A
  • Na is resorbed antiport with H still
  • Cl- is also resorbed in a Cl antiporter
  • High Concentration leads to Cl- transcellular absorption
  • Na follows charge difference
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20
Q

Isomotic absortion

A

-As solutes are absorbed actively water will follow

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21
Q

Tubuloglomerular feedback

A
  • Assuming plasma concentrations remain the same, 67% of water and filtered load will be absorbed
  • As GFR increases and filtered load increases there will be a higher oncotic pressure int he paratubular cappilay
  • This higher oncotic pressure will lead to increased waater resorption keeping the total resorption constant
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22
Q

Thin Descending limb

A

-Permiable to water but impermiable to other solutes leads to concentration of solute

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23
Q

Thick ascending limb

A
  • Na/K/2Cl, impermiable to water
  • Some K leaks back into lumen generating a positive intraluminal electrical gradient
  • Leads to a paracellular push of cations into the paratubular capillaries
  • Transporter can be blocked with furosemide which binds to Cl site
  • Normally resorbs 25% of filtered Na load, strong diuretic
  • Absorption in thick ascending limb is load dependeny, if there is elevated Na, more will be resorbed and so on. Therefore proximal tubule diuretics are weaker
  • Diluting segment
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24
Q

Early DCT

A
  • Contains load dependent Na/Cl cotransporter
  • Further dilutes urine
  • Blocked by thiazides (Cl binding site)
  • Macula Densa
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25
Q

Late DCT and Collecting Duct

A
  • Alpha intercalated (acid)
  • Principle (Na/K)
  • Principle cell is responsive to aldosterone and synthesizes ENaC channels
  • Can be blocked by Amilioride, Triameterene, and Spironolactone
  • Dirutics are weaker due to only 3% of Na resorbed
  • Normally Na and K reabsorption are opposed, increase Na leads to more K secretion. Blockers prevent this and spare K
  • Load dependent, especially with K
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26
Q

Regulation

A
  • Na is mainly funtional in maintaining ECF and effective blood volume.
  • Decreases in blood volume lead to SANS activation and decreased GFR and RPF. Na is load dependent and so Na loss is reudced
  • Elevated blood volumes leads to ANP secretion leads to afferent dilation and efferent constricion leading to increased GFR and increased secretion.
  • Ang II will synthesize H/Na channels in PCT
  • Aldosterone synthesizes ENaC in principle cells
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27
Q

K Balance

A
  • More passive and depends on Na

- Depends primarilry on electrochemical gradient

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28
Q

PCT

A

-Isoosmotic reabsorption follows water

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29
Q

Thick ascending limb

A
  • Na/K/2Cl transporter

- K leaks back into luminal side to allow positive charge and transcellular Ca and Mg absrption

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30
Q

Internal K regulation

A

-Put into cells: Insulin and beta agonists cuase increase in ATPase. Acidosis causes a transcellular shift to buffer acid, H in exchange for K. If ECF is hyposomolar then fluid wil leave cells and K will follow to keep osmolarities the same

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31
Q

Internal regulaion K excretion from cells (Hyperkalemia)

A
  • Skeletal muscle exsercise or cellular death leads to increae K
  • Lack of insulin or beta blockers
  • Alkalosis will shift H out of cells in exchange for K
  • Hyperosmolar ECF will caues water to rush out of cells and K will follow
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32
Q

Intercalated cell

A

Intercalated cell is crucial in acid base base balances and uses a pimary active transport H/K antiporter

  • Acidotic states will lead to increased H secreted and increased K resorbed hyperkalemia
  • Alkolotic state will lead to decreased H secreted and decreased K resorbed leading to hypokalemia
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33
Q

Principle Cell

A
  • Main cell in K regulation. K secretion dependent on the ammount of Na absorbed. More Na absorbed, more K excreted
  • Na resorption dependent on delivery and presence of ENaC channels
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34
Q

Aldosterone

A

-Increased ENaC channels and increased intracellular Na leading to increaed K secretion and hypokalemia

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35
Q

Diruteics

A
  • Loops inhibit absorption and also increase Na delivery lead to major K loss
  • Thiazides: increase Na deilvey and increase K excretion
  • K sparing: Block ENaC and prevent increased intracellular Na leading to decreased secretion
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36
Q

Phosphate metabolism

A
  • All is absorbed in the PCT
  • Coupled to Na/P secondary active transport
  • Function of transport is inhibited by PTH through Gs and cAMP leading to phosphate excretion
  • Elevated PTH levels lead to elevated cAMP and P in urine
  • Important role as a titratable acid
  • PseudohypoPTH is from defective Gs leading to no response to PTH. Blood levels will be high in PTH but P will be up and Ca will be down. There will be no cAMP in urine
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37
Q

Ca metabolism

A
  • 67% is absorbed in PCT with Na
  • In TAL increased luminal charge from K leak drives Ca and Mg paracellular transport
  • Loop diuretics abolish this action and lead to Ca wasting. Can precipitate a stone, or can treat hypercalcemia
  • Regulation occurs in DCT
  • Not coupled to Na and contains own transporter that is increased with PTH through cAMP
  • Thiazides will increase Ca resporption, used to treat Ca stones and hypercalemiuria
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38
Q

Mg Metabolism

A

Minimally absorded in PCT

  • Majority of absorptin occurs in the TAL through paracellular transport
  • Loop diuretics cause hypomagnesiumemia
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39
Q

ADH actions

A
  1. Increase function of Na/K/2Cl transporter to increase the corticomedullary gradient
  2. Increased production of aquaporins in the collecting duct (medullary and cortical and inner)
  3. increase inner collecting duct urea transporters to increase urea contribution to gradient
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40
Q

Nephrogenic DI

A

Treatemtn with thiazides serves to increase the concentration of the urine and decrease fluid volume

  • This will decrease GFR
  • It will also decrease Na levels, whichs is a major risk factor for problems
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41
Q

Free Water clearance

A
  • Free water is the volume of urine minus the clearance (volume) of solute
  • Calculate solute clearance (Cosm) and then subtract that number from urine flow rate
  • 0 is seen in loop diuretics. abolish diluting capabilities
  • positive is seen in hyposomolar urine (Elevated hydration)
  • Negative is seen in high ADH states, when there is lots of water being resorbed, dehydration.
42
Q

Bicarbonate handling

A
  • in PCT Na/H+ exchanger puts H into lumen which combines with HCO3- to generate H2O and water
  • CO2 resorbed and intraluminal CA converts to HCO3 and H. H goes back to lumen, HCO3 goes to blood
  • Net Na/HCO3 through H
  • Acetazolamide inhibits this and inhibits HCO3 absorpotion leading to metabolic alkalosis
43
Q

Titratable acid

A
  • urine pH can only get to 4.4 therfore buffers exist to allow uring
  • Most important is phosphate
  • Also NH3 produced from urea cycle when necessary, trapped in lumen as NH4
  • In intercalated cell, CA converts H2O and CO2 to HCO3 and H
  • HCO3 is absorbed with Cl and H is excreted onto titratable acids
44
Q

RTA

A
  • Type 1 is impaired secretion of H in intercalated cells. leads to alkaline urine
  • Type 2 is inability to resorb HCO3 in PCT, low urine pH
  • Type 4 hypoaldosteronism leads to hyperkalemia which impairs aminogenesis in PCT leading to decreased buffering capacity. pH will be low in urine
45
Q

Acidosis

A

-Anion GAP: MUDPILES
-DKA, Methanol and ethylene glycol (Osmolar gap)
-Iron or INH
Uremia
Lactic acidosis
-Salicytlate: early incourse will have respiratory alkalosis later is metabolic acidosis
-Type 2 RTA (Fanconi’s sundrome) and diahrrea will have a normal gap hyperchloremic acidosis

46
Q

Contraction Alkalosis

A
  • Thiazides and loops cause a volume contraction which will lead to a decreased GFR and increased resorption time for HCO3 leading to alkalosis
  • Also plays a role in vommiting
47
Q

Congential Maldevelopments

A
  • Most common is at the ureteropelvic junction and leads to hydronephrosis
  • There can also be a posterior urethral diaphragm with similiar presentation
48
Q

Multicystic Dysplastic Kidney

A
  • imparied signalling between ureteric bud (collecting sysyem) and Metanephric mesoderm (Nephron) leads to a kidney that is CT and cysts
  • Usually unilateral and other kidney hypertrophies and functionality is maintained
49
Q

Fanconi Syndrome

A
  • Impaired function of PCT
  • Usually presents with defect in HCO3 resporbtion leading to acidosis (type 2)
  • Type 1 is secretion by alpha intercalated (others have low pH, this one has high urine pH)
  • Type 4 is hypoaldosteronism, hyperkalemia impairing PCT NH3 produciton and reducing titratable acid concentraiont
50
Q

Waxy Casts

A

Chronic renal Failure

-Hyaline casts mean nothing

51
Q

Nephritic

A
  • PSGN
  • RPGN
  • Alport
  • Bergers
  • Proliferative (Signals hypercellularity and nephritic potential)
52
Q

Nephrotic

A 
Minimal Change
DM
Amyloidosis
Membranous
FSGN
-Membranoproliferative and diffuse membranoproliferative can be both nephritic and nephrotic
53
Q

FSGN

A
  • Most common in adults, especially IV drugs, Black, Hispanic, HIV, IFN, Obese, or lack of other kidney. Many causes
  • Thickening of BM and loss of foot processes
  • No IF
  • Treat with steroids, but prognosis is likely ESRD
54
Q

Minimal Change Disease

A
  • Lipoid nephrosis
  • Mos common cuase seen in kids
  • Ovoid fat casts
  • Caused by foot process effacement, most commonly due to cytokines (can follow illness)
  • Tx with steroids and rapid good response
  • Selective proteinuria only involves albumin, will spare clotting factors and others
55
Q

Membranous Nephropathy

A

-Granular IF with spike and dome appearance on EM
-Subepitheilial dposits without cellular proliferation
-Common in adults
Treat with steroids
-SLE’s nephrotic presentation, also Hep B,C, tumors, drugs. Many other causes

56
Q

Amyloidosis

A
  • Most commonly secondary to MM but can be RA or TB

- Amyloid deposits with congo red, leads yo nephrotic syndrome

57
Q

Membranoproliferative glomerulonephritis Type I

A
  • Subendothelial deposits with tram track appearance from mesangial proliferation
  • Generally is a nephrotic presentation
58
Q

Diabetic Nephropathy

A
  • NEG of basement membrane and protein deposition leads to large kimmelstein wilson bodies
  • Also NEG of effeernt areteriole leads to arterioscelerosis and hyperfiltration injury due to increaed GFR
  • Begins with microalbuminuria and progresses to chronic failure eventually
  • Treat with ACEI to minimize hyperfiltration injury
  • Hypertensive arteriolosclerosis of efferent arteriole can also cause elevated GFR and hygperfiltration injury, but not as bad or as common as DM
  • Will progress to ESRD
59
Q

Membranoproliferative Glomeruolonephritis Type 2

A
  • Intralaminar complex deposition
  • Associated with C3 nephritic factor which stabalizes C3 convertase and leads to inflammation
  • More likely to cause Nephritic syndrome
60
Q

Nephritic Syndrome

A
  • HTN, Oliguria, Hematuria
  • RBC casts are ~pathognemonic
  • Neutrophil and macrophage infiltration lead to inflammation and damage leading to renal failure
61
Q

Acute Poststreptococcal (Acute proliferative)

A
  • Type 3 hypersensitivity post strep infection (generally skin)
  • Most common in kids
  • Subepithelial depsosits and neutrophilic infiltarte
  • Positive ASO titers and maybe low C3 levels
  • Can become RPGN, but
62
Q

FSGN

A
  • Most common in adults, especially IV drugs, Black, Hispanic, HIV, IFN, Obese, or lack of other kidney. Many causes
  • Thickening of BM and loss of foot processes
  • No IF
  • Treat with steroids, but prognosis is likely ESRD
63
Q

Minimal Change Disease

A
  • Lipoid nephrosis
  • Mos common cuase seen in kids
  • Ovoid fat casts
  • Caused by foot process effacement, most commonly due to cytokines (can follow illness)
  • Tx with steroids and rapid good response
  • Selective proteinuria only involves albumin, will spare clotting factors and others
64
Q

Membranous Nephropathy

A

-Granular IF with spike and dome appearance on EM
-Subepitheilial dposits without cellular proliferation
-Common in adults
Treat with steroids
-SLE’s nephrotic presentation, also Hep B,C, tumors, drugs. Many other causes

65
Q

Amyloidosis

A
  • Most commonly secondary to MM but can be RA or TB

- Amyloid deposits with congo red, leads yo nephrotic syndrome

66
Q

Membranoproliferative glomerulonephritis Type I

A
  • Subendothelial deposits with tram track appearance from mesangial proliferation
  • Generally is a nephrotic presentation
67
Q

Diabetic Nephropathy

A
  • NEG of basement membrane and protein deposition leads to large kimmelstein wilson bodies
  • Also NEG of effeernt areteriole leads to arterioscelerosis and hyperfiltration injury due to increaed GFR
  • Begins with microalbuminuria and progresses to chronic failure eventually
  • Treat with ACEI to minimize hyperfiltration injury
  • Hypertensive arteriolosclerosis of efferent arteriole can also cause elevated GFR and hygperfiltration injury, but not as bad or as common as DM
  • Will progress to ESRD
68
Q

Membranoproliferative Glomeruolonephritis Type 2

A
  • Intralaminar complex deposition
  • Associated with C3 nephritic factor which stabalizes C3 convertase and leads to inflammation
  • More likely to cause Nephritic syndrome
69
Q

Nephritic Syndrome

A
  • HTN, Oliguria, Hematuria
  • RBC casts are ~pathognemonic
  • Neutrophil and macrophage infiltration lead to inflammation and damage leading to renal failure
70
Q

Acute Poststreptococcal (Acute proliferative)

A
  • Type 3 hypersensitivity post strep infection (generally skin)
  • Most common in kids
  • Subepithelial depsosits and neutrophilic infiltarte
  • Positive ASO titers and maybe low C3 levels
  • Can become RPGN, but normally resolves when infection is cleared
71
Q

RPGN

A
  • Goodpastures
  • Vasculitis
  • Alports
  • Bergers
  • PSGN
72
Q

Goodpastures

A

Type 2 to type 4 collagen

  • Effects lungs (Hemoptysis) and lens, and kidney
  • Treat with plasmaphoresis and steroids
73
Q

Wegners

A

-Small vessel vasculitis, granulomatous, C-ANCA

74
Q

Alports

A
  • X linked defect in collagen type 4

- Leads to membrane splitting, also assocaited neural deafness and blindness/cataracts

75
Q

Bergers

A
  • IgA deposition in mesangium leads to mesangial proliferation
  • Often associated with HSP
  • Usually presents as a relapsing and remitting disease each time there is an infection
  • Eventually is progressive
76
Q

Lupus

A
  • Renal involvment is inevitable and is common cause of death
  • Begins with membranous nephropathy that is nephrotic and subepithelial spike and dome
  • Eventually becomes diffuse proliferative
77
Q

Diffuse Proliferative glomerulonephritis

A
  • Later in lupus course
  • Wire loop glomeruli
  • Subendothelial deposits often low C3 or C4 levels
  • Neutrophil infiltartion and nephritic syndrome
78
Q

Calcium Oxalate Stones

A
  • Most common, form in acidic urine
  • Most common cause is idiopathic increase in urine Ca, can also be associated with cancer
  • Treat with hydration, Thiazides (Decrease Ca in urine) and citrate
  • Can be caused by increase in oxalate (Crohns disease) or vitamin C abuse (Acid in urine)
  • Other causes of increased Ca (Sarcoid, hyperPTH)
79
Q

Calcium Phosphate stones

A
  • Form in alkaline urine, type 2 RTA, acetazolamide
  • Elevated Ca levels is a cause
  • Treat with citrate, hydration and thiazides
80
Q

Struvite

A
  • Form in alkaline urine in the presence of urease positive bugs (CO2 and NH3). Proteus, Klebsiella, Pseudomonas, Staph
  • Staghorn caliculi that are often nidus for infection
81
Q

Uric Acid

A
  • Seen with acid urine or increased cell turnover (tumor lysis syndrome)
  • Treat with hydration, alkalinization of urine (Acetazolaminde) or decreaese uric acid production. Allopurinol
82
Q

Cysteine

A
  • Form from congenital deficency in basic amino acid transport (ornithin, lysine, argenine)
  • Form in acidurine, treat with alkalinzatin of the urine and hydration
83
Q

Hydronephrosis

A

Cause by ureteral or junctional obstruction leading to dilation of pyramids and calyces
-Can cause cortical parenchymal thinning

84
Q

Renal Cell Carcinoma

A
  • Tumor of PCT epithelium
  • Associated with smoking, Dialysis, obesity
  • Clear cells filled with lipid and glycogen
  • Often have VHL muitation and congential is bilateral (3)
  • Present with flank pain and mass with hematuria
  • Hemotogenous spread to L renal vein (varicocele) also to lungs, bone
  • EPO, ACTH, PTHrP paraneoplastic syndromes
85
Q

Wilms Tumor

A
  • Tumor of primitive glomeruloid like cells
  • Seen with mutation in WT1 on chrom 11
  • Associated with WAGR and Beckwith Wiederman
  • Large abdominal mass in child
86
Q

Transitional Cell Carcinoma

A
  • Most common carcinoma and of cells from calyx to bladder
  • Associated with smoking, dyes, cyclophosphamide, phenacetin
  • Presents with painless hematuria and may obstruct ureter leading to hydronephrosis
  • Field defect, means whole area was mutated and recurrence is common
87
Q

SCC

A
  • Chonic inflammation and squamous metaplasia

- Associated with schistosoma haematobium (middle eastern man)

88
Q

Adenocarcinoma

A

-Urachal remnant on superior pole of bladder

89
Q

Acute Pyelonephritis

A
  • Ascending infection of parenchyma that spares glomeruli
  • CVA and systemic symptoms
  • WBC casts are pathognemonic
  • Tx with cipro IV. Beware of sepsis
  • Can be nidus of stones (Struvite)
90
Q

Chronic Pyelonephritis

A
  • Structural problem leads to recurrent infections (VUR, recurrent stones)
  • Leads to scarring, calyx blunting and eosinophilic deposits in tubules leading to thyroidization of kidney
91
Q

Drug induced interstitial nephritis

A
  • Hypersensitivity (type 1) to drugs
  • Eosinophils, pyuria, and azotemia
  • NSAIDs (Months after), Diuretics, Beta Lactams, antibiotics etc
  • Fever rash hematuria and CVT
92
Q

Diffuse Cortical Necrosis

A
  • Caused by DIC
  • Commonly related to obstetric complications (abruptio placentae and eclampsia)
  • Also related to Septic shock
93
Q

Renal Papillary necrosis

A

Ischemic injury to renal papilla

  • Sickle Cell is classic
  • Also diabetes, NSAIDs, and pyelo
94
Q

ATN

A
  • Muddy brown casts and oliguria or anuria
  • Leads to azotemia, hyperkalemia, uremia, fluid overload (Pulmonary Edema). treat with dialysis if out of control
  • Ischemic: Leads to death of straight PCT and medullary segment of TAL. Disruption of BM leads to difficult recovery
  • Toxic: Damage to tubular cells, BM intact
  • Drugs, myoglobin, radiocontrast, multiple myeloma, gout
  • 1-3 week oliguric period with risks mentioned above (Hyperkalemia)
  • Followed by recovery phase with massive excretino and risk of hypokalemia
95
Q

Prerenal Azotemia

A
  • Hypoperfusion leading to decreased GFR. BUN absorptin increased so BUN/Cr is increased
  • FeNa less than 1, most is resorbed
  • Tubular cells are still functional urine osmolarity is still high
96
Q

Intrarenal

A
  • ATN is cause usually. Can also be RPGN

- Decreased BUN/Cr ratio as cells are dead

97
Q

Postrenal

A
  • Obstruction leads to backup and increase in bowmans space hydrostatic pressure leading to decreased GFR
  • Blockage must be bilateral as one kidney can compensate for other
  • BPH, Stones, Congenital defects, Tumor (Ovarian commonly metastasize)
98
Q

Renal Failure Consquences

A

-Uremia: Encephalopathy and asterixis, platelet dysfunction, anemia, pericarditis, N/V
-Renal Osteodystrophy
-Hyperkalemia
-Fluid overload and HTN. CHF and pulmonary edema
-Anemia, decreased EPO
-Acidosis
Dyslipidemia

99
Q

Renal Osteodystrophy

A
  • Decreased vitamin D, increased Ca wasting and elevated Phosphate in serum. Also elevated PTH
  • Leads to subperiosteal bone resporption and pain
  • Also precipitation of CaP in tissues
100
Q

ADPKD

A

AD
-Presents with hematuria, flank pain, HTN (Renin is elevated)
Family history
-Also increased risk for SAH and berry anyeurism
-MVP and benign hepatic cysts

101
Q

ARPKD

A

-Presnts in infancy and is AR
-Fibrosis of kidney and liver leads to HTN and portal hypertension
If survive have pHTN, HTN, and renal failure
-Potters syndrome from oligohydramnios

102
Q

Medullary Cystic Kidney Disorder

A

Medullary cysts lead to interstitial fibrosis and kidney dysfunction

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