Renal Pathophysiology Flashcards

Question

Heat and Acetic Acid for urine test?

Answer 1

take a specimen of urine and heat it up and if there’s protein you will see it form at the bottom of the test tube The test tube has been heated (left) and as it cools you see the protein on the bottom This is with heat and acetic acid but with sulfosalicylic acid it will look very similar We don’t do this often, usually send sample off to the lab and they can measure protein or albumin

Answer 2

detects all proteins in the urine

Answer 3

dipsticks not positive until rel high to find smaller amounts - use direct measrements of albumin secretion microalbumin - to - creatinine ratio!

Answer 4

protein electrophoresis

Answer 5

increase in permeabilty of glomerular capillary wall leads to increased glomerular filtration of protein

Answer 6

impaired reabsorption of normally filtered proteins

Answer 7

increased production of smaller proteins in multiple myeloma and ther plasma cell issues

Answer 8

massive loss of normal serum proteins in the urine 1. heavy proteinuria (\>3.5) 2. hypoalbuminemia 3. edema 4. hyperlipidemia 5. sometimes HTN

Answer 9

urinary loss of protein liver is making more but can't keep up with loss

Answer 10

overfill hypothesis glomerular disease/tubular inflammation leads to increased renal sodium retention (reabsorb mostly in collecting tubules

Answer 11

Na retention USUALLY results in hypertension but nephrotic patients to not MAY be secondary to hypoalbuminemia

Answer 12

elevated cholesterol, TG, phospholipids low plasma albumin? increased lipoprotein synthesis

Answer 13

oval fat bodies (tubular cells w fat drops) maltese crosses (fat drops under polarized light) on urinalysis

Answer 14

oval fat bodies in neprhotic synd urine ## Footnote 1: oval fat body (tubular cell that is filled with fat)

Answer 15

maltese crosses - polarized light on fat lipid in urine in nephrotic If you think a patient has nephrotic syndrome it is important to look at the urine for oval fat bodies and then look under polarized light

Answer 16

in nephrotic syndrome! hypercoagulable state DVT and renal vein thrombosis

Answer 17

acute onset variable fluid retention HTN infrequent renal function is normal EDEMA and protein in the urine!

Answer 18

proteinuria (ALBUMIN - selective) oval fat bodies few cells

Answer 19

high dose steroids - usually remission in 2-4 wks

Answer 20

insidious - asymptomatic proteinuria or microscopic hematuria

Answer 21

massive proteinuria (non selective - not just albumin) HTN and azotemia if late

Answer 22

follows GSA - pharyngitis or skin gross hematuria and oligouria edema and pulmonary congestion flank pain hypertension

Answer 23

nephritic!! renal retention of salt and water decreased urine output dyspnea, orthopnea, cardiomegaly, rales, gallop

Answer 24

GAS rxn hematuria (coca cola) RBCs, RBC casts prteinuria (low) low urine sodium (retaining, vol overload) very concentrated urine

Answer 25

treat HTN manage fluids and electrolytes treat renal failure/dialysis

Answer 26

gross - nephritic only microscopic - sometimes nephrotic, always nephritic

Answer 27

sometimes in nephrotic, always in nephritic

Answer 28

sometimes nephrotic always nephritic

Answer 29

only nephritic

Answer 30

always nephrotic rarely nephritic

Answer 31

pyuria and WBC casts bacteria

Answer 32

WBCs and WBC casts

Answer 33

eosinophils granular or WBC casts

Answer 34

nephrotic diabetes, amyloid

Answer 35

nephrotic minimal change fsgs membranous

Answer 36

SLE Endocarditis MPGN ANCA

Answer 37

post infectious IgA

Answer 38

finnish severe NS at birth - all ESKD need dialysis and transplant because mutation in nephrin (in the podocyte slit diapragm) how we learned about it!

Answer 39

malignancy (Hodgkin and non-hodgkin lymphoma drugs (NSAID, lithium, rifampin) Infections (syphilis, malaria)

Answer 40

mostly children explosive onset - edema, hypoalbuminemia kidney biopsy to make diagnosis

Answer 41

prednisone - usually dramatic and quick response treat underlying secondary disease

Answer 42

role in FSGS

Answer 43

steroids first line most are steroid resistant second = calcineurin inhibitors some targetted thereapy? recur post transplant!

Answer 44

secondary to other kidney disease and obesity

Answer 45

NS or asymp prteinuria normal or elevated BP

Answer 46

NON-nephrotic preinuria, decreased GFR

Answer 47

ACEI/ATR blocker

Answer 48

variant of FSGS characterized by dedifferentiation and proliferation of podocytes with collapse of glomerular tuft HIV nephropathy (infects podocytes causing proliferation) or infections, meds, malignanc

Answer 49

anti retroviral correct underlying ACEI/ARBs

Answer 50

worse prognosis in FSGS, more likely to develop kidney failure in african americans 1 risk allele = prptection from trypanosomes 2 = risk for kidney failure

Answer 51

characterized by C3, IgG deposits SUBEPITHELIAL

Answer 52

NS or asymptomatic proteinuria

Answer 53

25% spontaneous remission 50% persistent proteinuria 25% renal failure

Answer 54

ACEI/ARB prednisone/calcineuron?

Answer 55

IgG antibody to podocyte ag (PLA2R) Ab fixes compliment and C3 is present in renal tissue Here would be the podocyte (brownish stuff) - Expresses the antigen (phospholipase A2 receptor) - Ab is generated to that autoimmune antibody receptor that binds the receptor - That then activates complement à destroys the podocyte and gives you this disease - To remind you, an Ag-Ab complex can activate complement à which ultimately can form this membrane attack complex

Answer 56

phospholipase A2 receptor on the membrane of the podocyte IgG ab bonds to it and fixes comp Here would be the podocyte (brownish stuff) - Expresses the antigen (phospholipase A2 receptor) - Ab is generated to that autoimmune antibody receptor that binds the receptor - That then activates complement à destroys the podocyte and gives you this disease - To remind you, an Ag-Ab complex can activate complement à which ultimately can form this membrane attack complex

Answer 57

trapping of preformed antibody-angigen complexes leading to fixation of complement and podycte damage SLE syphilis malaria hep B drugs tumor

Answer 58

presentations OF nephritic syndrome that are emergent based on percent of cresecents (not time!!) require urgent treatment

Answer 59

small circulating immune complexes of low-avidity antibody an oligovalent angigen (any infection can cause)

Answer 60

nephritic syndrome 1-2 wks after strep infection (skin, throat)

Answer 61

subepithelial deposition of immune complexes granular on immunoflorscence

Answer 62

most recover in a couple weeks control - BP, diuresis, infection

Answer 63

mesangial IC deposits with IgA and usually C3 and IgG - Shown biopsy with immunofluorescence - Slice of kidney à primary Ab against IgA, IgG or IgF à secondary Ab with something that can be detected fluorescently - In this case see IgA deposited in kidney in mesangium and around glomerular capillaries (L piecture) - You also see complement (R picture) - This would be enough to give you a dx of IgA nephropathy

Answer 64

1. incrased levels of galactose deficienct IgA 2. production of unique auto antibodies 3. formation of pathogenic IgA contianing ICs circulating 4. mesangial deposition and glomerular injury Somehow you get this galactose-deficient IgA à produce unique auto antibody à some systemic (maybe driven by a third factor like infection) à deposition of immune complex à activate immune response à inflammation

Answer 65

hep B, hep C, malignancy, eds can present w systemic signs of vasculitis and renaly insufficiency and nephritic syndrome skin rash etc treat underlying

Answer 66

antibodies to proteins expressed in neutrophil binding of abs to neutrophil plasma membrane leads to neutrophil activation which causes kidney disease get autiantibodies by molecular mimicry - present protein that looks like self

Answer 67

cancer model inductions (steroids and abs) plasmapheresis if severe renal impairment interfere w immune system

Answer 68

i.e. goodpastures (+ pulmonary hemorrhage) auto antibodies against alpha3 chain of collagen IV in renal and lung BM ab activates compliment

Answer 69

oliguria advanced renal failure

Answer 70

recovery of renal function is rare can use aggressive drugs if fewer crescents

Answer 71

alports! hereditary nephritis

Answer 72

1. hematuria 2. proteinuria 3. eskd (30s, 40s)

Answer 73

genetic mutation in alpha 3/4 (ch 2) or alpha 5 or type IV collagen inflammation

Answer 74

ACEI (before proteinuria) to protect GBM from damage from deposition transplant

Answer 75

primary deposition of C3 in absence of IgG was referred to MPGN2 or dense deposit disease DDD alternative pathway!!!

Answer 76

C3GN - DDD, C3GN without IC post infectious GN other

Answer 77

DDD - younger, many more ESKD faster, more C3 C3GN - older, less end stage both recur!!

Answer 78

monoclonal abs

Answer 79

alternate day steroids abs ACEI/ARB

Answer 80

sense osmolality control thirst secrete/suppress ADH (post pit)

Answer 81

prinipal cell ## Footnote AQP2, 3, and 4 are all affected by ADH. ADH attaches to the V2 receptor on the basolateral surface of principle cells in the collecting duct. That activates GTP-associated protein which activates adenylate cyclase. cAMP activates PKA in the cytoplasm and PKA in the nucleus. In the nucleus, PKA phosphorylates various transcription factors and increases the synthesis of AQP2, 3, and 4. Activation of PKA in the cytoplasm phosphorylates AQP2. AQP2 is located in a subapical region (in vesicles) and when it is phosphorylated, the aquaporin 2 moves to the apical membrane, fuses with it, and makes it water permeable. When AQP2 in the membrane is dephosphorylated, it moves back to the subapical region and vesicles accumulate. There is a shuttling of AQP2 between apical membrane and subapical region that is ultimately under the influence of ADH. AQP3 and 4 are located on the basolateral surface and are not thought to shuttle between sub-basolateral membrane and membrane; they tend to stay on the membrane. You can see that water flows in the CD across AQP2 on the apical surface and out the basolateral membrane via AQP3 and 4. Exactly how water transport occurs through the cytoplasm is currently unknown.

Answer 82

AQP2 is located in a subapical region (in vesicles) and when it is phosphorylated, the aquaporin 2 moves to the apical membrane, fuses with it, and makes it water permeable. When AQP2 in the membrane is dephosphorylated, it moves back to the subapical region and vesicles accumulate. There is a shuttling of AQP2 between apical membrane and subapical region that is ultimately under the influence of ADH.

Answer 83

AQP2 is located in a subapical region (in vesicles) and when it is phosphorylated, the aquaporin 2 moves to the apical membrane, fuses with it, and makes it water permeable. When AQP2 in the membrane is dephosphorylated, it moves back to the subapical region and vesicles accumulate. There is a shuttling of AQP2 between apical membrane and subapical region that is ultimately under the influence of ADH. AQP3 and 4 are located on the basolateral surface and are not thought to shuttle between sub-basolateral membrane and membrane; they tend to stay on the membrane. You can see that water flows in the CD across AQP2 on the apical surface and out the basolateral membrane via AQP3 and 4. Exactly how water transport occurs through the cytoplasm is currently unknown.

Answer 84

requires loss of hypotonic body fluid AND Absence of thirst OR inability to get sufficient water

Answer 85

replace water rapidly if acute (less than three days) slowing if greater than 3 days or unknown if there is hypernaturemia + Na deficit - replace sodium first (isotonic fluids) and then replace water

Answer 86

without insulin - glucose is in blood - shifts water from ICF to ECF lowers Na by 1.6 mEq per 100 mg/dl glucose hyperglycemia can entirely account for hyponaturemia or not

Answer 87

((Na/144) -1) x TBW

Answer 88

what degree hyperglycemia accounts for hyponaturemia 1.6 mEq/L for 100 mg/dL

Answer 89

hyperglycemia!!

Answer 90

indicator of the relative roles of the kidney's ability to dilute and fluid intake ans contributors to the hyponaturemia

Answer 91

high!! kidney is not having trouble - problem is likely intake

Answer 92

50-100 mosm

Answer 93

hyponaturemia despite max dilution of urine! episodic drinking in excess of normal kidney's ability to excrete water polyuria, low Na in urine

Answer 94

failure of defense of Posm after water intake - hyponautemia primary polydipia tea and toast diet (poor intake of protein and salt drinking beer renal failure (can't dilute) failure to suppress ADH (SIADH) There are also patients that dilute normally but have a limitation in the amount of urine they can excrete. This is because they have a decrease in the number of osmoles in their urine– elderly people that eat tea and toast, very low protein diets or diets that primarily consist of beer— very low in Na, K; lots of sugars and very little or no protein. The number of osmoles in their urine are very low, a total of maybe 100 mOsm/day. These people can only excrete 2 L/day even though the urine has a Uosm of 50. This is a group of patients with dilute urine that becomes hyponatremic. 2 groups: primary polydipisa and decreased urinary solute.

Answer 95

diarrhea glycosuria diuretics hyponaturemia

Answer 96

cirrhosis, CHF, nephrotic syndrome

Answer 97

evidence of ADH effect

Answer 98

replenishment of decreased ECFV or decreased EABV with relatively more water than Na in the presence of reduced water (and Na) excretion due to failure to filter normal amts of water (decreased GFR) failure to deliver water and solute to TALH (increased proximal Na reabsorption) failure to suppress ADH

Answer 99

intake of more water than Na in presence of reduced water (and Na excretion) due to ARF or CRF failure to filture nomral amts of water due to decreased GFR

Answer 100

if exclude other causes of euvolemic hyponaturemia - increased hypothalamic release of ADH (pain, stress, pulm disease, drugs) or ectopic release of ADH (tumors) hyponaturemia high Uosm clinically normal ECFV suppression of Na reabsorption by water expansion of ECFV - effect on vol receptors high urine Na! DECREASED serum uric acid!!

Answer 101

low ECFV - give NS to turn of ADH secretion high ECFV - water restrict, diuretics, ACEI

Answer 102

3% saline and sometimes Lasix increase Osm enough t get rid of yptoms desmopressin (DDAVP) to slow rate of correction

Answer 103

water restrict Tolvaptam (ADH antagonist) correct slowly!!! brain swelling

Answer 104

increase Na - opens BBB - C3 and cks get in and attack oligodendrocytes - demylination rate of correction of chronic hyponaturemia is a risk

Answer 105

immediate funtion longer lifespan rapidly transplantable/able to plan can avoid dialysis elective scheduling

Answer 106

delayed funtion shorter lifespan waitlist unpredictable

Answer 107

longer in living donors

Answer 108

GFR \< 20 eval safety of immune suppression eval safety ensrure patient will be able to comply w regimen

Answer 109

O - most common

Answer 110

the new kidney is placed in the iliac fossa, native kidney remains in place

Answer 111

1. innunosuppresants (3) 2. anti fungal, anti-viral, antibiotic 3. anti hypertensives

Answer 112

low sodium low potassium low phosphate limited fluids

Answer 113

once activated, t cells clonally expand - induce cytotoxic t cell activity, help b cellss make antibodies and help macrophages induce delayed hypersensivity MHC!!

Answer 114

NSAIDs, ACEi, vascular disase, CKD, chronically elevated BP

Answer 115

when MAP \<80 mm - autoregulation can't work and GFR falls

Answer 116

ABRUPT fall in GFR by increase creatinine by .5 or 50% over baseline oliguria decline in GFR to require dialysis

Answer 117

pre-renal intrinsic post-renal (obstruction)

Answer 118

fall in RBF leading to fall P of glomerulus

Answer 119

fall in K(f) fall in RBF increase in P(t) * Intrinsic acute renal failure, which may result from anything happening in the kidney tissue/parenchyma itself * This may affect the ultrafiltration coefficient, e.g. the permeability or surface area of the membrane It may result in a fall in renal blood flow, or a rise in tubular pressure

Answer 120

increase in Pt * Post-renal acute renal failure is typically caused by an obstruction to the flow of urine in the renal pelvis or distal to that * Obstruction initially increases the tubular pressure—the pressure increases proximal to the obstruction When tubular pressure equals the glomerular pressure, filtration will stop

Answer 121

percentage of filered Na that is excreted in the urine U(na) x P(cr) / P(na) x U(cr) x100

Answer 122

min protein no micro high osmolarity (low water) lower Na

Answer 123

tubular protein, casts, RBC, WBC low Uosm (a lot of water) \>1% Na - getting rid of Na

Answer 124

min protein everything varies

Answer 125

hypovolemia low CO distributive (sepsis, vasodilators) renal (renal artery stenosis, drugs)

Answer 126

effective treatment of vol loss, infection, reversible causes of impaired autoregulation avoid additional insults (toxins, infections)

Answer 127

ischemia and toxins

Answer 128

pre renal - normal or occ hyaline ATN - epithelial cells, grnular and muddy casts

Answer 129

ischemia or toxins damage the tubular cells - leads to sloughing of brush border and cells into lumen w cast formation decrease in GFR is out of proportion to pathological changes

Answer 130

hemodynamic (hypoperfusion or vasoconstriction of outer medulla) alteration of tubule cell structure (necrosis and apoptosis) tubular obstruction activation of Tubulo Glomerular feedback

Answer 131

the outer medulla! relatively hypoxic oxygen demand is high because of transport * The cartoon shows the cortex, medulla and the thick ascending limb * In this portion of the kidney, in the thick ascending limb, there is a high oxygen demand because this is where the NKCC transporter lives * This transport takes up a lot of oxygen * In addition, the vasa recta are shunting blood around the ascending limb * This is how the medullary interstitial gradient is generated, which allows for concentration of the urine * In this segment of the kidney particularly, the balance between oxygen delivery and oxygen demand is pretty precarious * This segment is very sensitive to any decrease in oxygen supply * When oxygen demand exceeds oxygen supply, there is ischemic damage, ischemic reperfusion injury, free radicals, etc. * This is one possibility as to why ischemia causes tubular damage

Answer 132

* This is a little more detailed view of the various mechanisms that are proposed to explain why GFR falls so much in tubular injury * Note: the peritubular capillary is shown at left * If you have shock, toxins, you have endothelial damage, an increase in adhesion molecules, and the inflammatory cells can enter the tubular lumen * There are cytokines that damage the tubular cells * In the proximal tubule (to the right of the peritubular capillary), you either lose the integrity of the cells, or lose cells entirely * When this occurs, there is nothing to protect the basement membrane from allowing the filtrate in the lumen to leak back into the circulation * You can filter urea, for example, but if it leaks back, it will not be excreted * These cells lose microvilli, some become necrotic or apoptotic and slough off in the tubular lumen à they no longer function like normal tubular cells * The image at right shows a region later on in the distal portion of the nephron * That image is a picture of tubular cells now contacting Tamm-Horsfall proteins, polymerizing with the protein, adhering to one another and forming a cast that now obstructs the tubular lumen and will prevent urine flow It is a combination of ischemic damage, necrosis, loss of normal polarization of the tubular cells, cast formation, back leak à these all lead to renal failure when you have toxic or ischemic damage to the tubules

Answer 133

loss of brush border and polarity necrosis and apoptosis sloughing off of cells w lumenal obstruction dedifferentiation of viable cells

Answer 134

decreased Na reabsorption in the proximal tubule increases delivery to the MD signalling the glomerulus to reduce GFR

Answer 135

treat infection, support BP, avoid insults duiretics to increase urine output bicarb for acidosis if needed limit Na, water, K intake adjust meds for reduced GFR

Answer 136

GFR falls when tubular pressure rises and gradient favoring filtration falls for renal failure, obst must be bilat or in patient w only one kidney - not ruled out w normal urine output

Answer 137

remove obstruction

Answer 138

* The kidneys are designed to protect themselves * The first thing that happens in obstruction is the tubular pressure goes up * The kidneys think they may need more blood flow in order to overcome that * Afferent resistance will go down * Glomerular pressure will rise in an attempt to balance tubular pressure * Depending on how severe the obstruction is, the glomerular filtration rate (GFR) may not initially fall * If the tubular pressure stays very high, the kidney now knows any further perfusion will deleterious * Therefore, you have renal vasoconstriction that causes glomerular pressure to be lower and GFR falls still further * After you relieve the obstruction, it takes some time—not too long, but a little while—for the decrease in tubular pressure to be reflected in a decrease in afferent resistance * This is less than 24 hours, but you may not see an immediate increase in GFR * It may take time because the tubular obstruction has set off all of these compensatory mechanisms to try to initially maintain GFR and then prevent further damage * The take-home message in obstruction: tubular pressure goes up, GFR goes down * When you relieve the obstruction, this recovers within 24 hours

Answer 139

GFR \< 60 for 3 months with or without kidney damage OR kidney damage for greater than 3 months with or without decreased GFR manifested by either pathologic abnormalities or markers of kidney damage

Answer 140

CKD requiring dialysis or transplant

Answer 141

1 - GFR \> 90 2 60-89 3 GFR 30-59 4 15-29 5 less than 15

Answer 142

african americans - 1 allele protects against trypanosomes 2 alleles increase the risk for kidney disease, FSGS and HIV nepropathy circulating domain that pokes holes in trypanosimes

Answer 143

cardiovascular disease

Answer 144

low cholesterol, low LDL, high TG treat with a statin - lowers all cause mortality, CV death, non CV mortality what is uremic toxin leads to heart disease?

Answer 145

diabetes, GSFS MPGN IgA, membranous. post strep always treat underlying kidney disease!

Answer 146

once a critical reduction of renal mass occurs, either by initiating disase or surgical removal of a kidney tissue, progressive rena; failure can ensue by a set of common mechanisms

Answer 147

lose nephrons as units what remain are intact functional nephrons that must compensate for the loss of function of the lost neprons try to compensate and damage themselves increase single nephron GFR by increasing glomerular capillary P - hypertrophy glomerular plasma low, pressure, filtrtion rate increases

Answer 148

endothelial cells: mechanical stretch activate EC to secrete factors that cause fibrosis mesangial cell - mechanical stretch - narrowing

Answer 149

1. control BP 2. use ACEI as first line therapy

Answer 150

inhibiting RAS

Answer 151

RAAS! antiprtoeinuric effects are due to direct effect of ATII on permeability barrier (podocyte) and decreas intraglomerular P

Answer 152

increased filtered albumin is taken up by PT accumulate in cytoplasm - perturbation of cell function - recruit macrphages and T cells, activate TGF beta - bind to cells fibroblast proliferation and matrix depositioon

Answer 153

metabolic acidosis high phosphate smoking obesity hyperlipidemia african american

Answer 154

CKD causes acidemia - increase interstitial fibrosis ## Footnote This is just to highlight, because it is really important, that a lot of the things that you do, there’s not good data. There is good data for angiotensin system for progression. There is good data if you can decrease proteinuria. There is also data for treating the acidosis, for preventing progression. I mean, controlled trials that if you treat with bicarbonate and get the serum bicarbonate to normal, you will preserve kidney function. So ammonia can increase renal acid production, can activate complement, can activate a cytokine called endothelin.

Answer 155

uremic symotms hyperkalemia and acidosis fluid overload or HTN

Answer 156

for GFR 30 - educate, referral for transplant 20 - create fistula 10 - start HD

Answer 157

There is a transcription factor regulated by oxygen called HIF-1 (hypoxia inducible factor), which under normal conditions when oxygen is present, it is degraded. When oxygen is very low, the enzyme that causes it to get degraded, a prolyl hydroxylase, gets inhibited, and so HIF-1 is not degraded. It accumulates, it goes to the nucleus. It turns on erythropoietin, which then circulates and goes to the bone marrow, and commits RBCs to differentiate. If you don’t have kidney’s, your erythropoietin levels are low.

Answer 158

kidney makes erythrpoetin - interstitial fibroblast senses O2 content/RBCs and if it decreases turns on erythropoetin give recombinant erythropoeitin

Answer 159

binds to same receptors with same mechanism as endogenous erythropoeitin carb chains to increase half life guidelines: do NOT go to Hgb\> 12

Answer 160

So here is sort of the standard idea. As you lose kidney function, phosphorus goes up, it then will combine with calcium and precipitate in the bone. (Something about lay down in the bone and could be … go other ways? Could not make out sentence/clause). So high phosphorus will eventually lower in the serum the free ionized calcium. That sets (?) by the parathyroid gland and the parathyroid gland will make PTH, which then goes and circulates, and will stimulate and tell the osteoclasts to break down more bone and release calcium.

Answer 161

vitamin D needs to be activated by 2 ways, there is a 25 hydroxylase in the liver and then a one (hydroxylase?) in the kidney. So 1,25 (OH)2D is your active vitamin D. If you don’t have kidney function your 1,25 is decreased. That’s important for calcium reabsorption for the gut. So that’s another reason why your calcium could be low. directly suppresses PTH in parathyroid

Answer 162

decreased nephron mass - decrease PO4 clearance - increased PO4 - decrease C, decreased D - increased PTH also high FGF 23

Answer 163

, fibroblast growth factor 23, this is actually one of the major stimuli for the kidney to decrease reabsorption of phosphorus. And it blocks phosphorus reabsorption by the kidney. So what happens is as you lose kidney function, phosphorus goes up, FGF23 is made to try to… is one of the other… maybe more important than PTH. FGF23 then causes increased phosphate loss, but FGF23 does a lot of other things. It can lower 1,25. It blocks the 1 hydroxylase. So it lowers vitamin D, which has its other effects.

Answer 164

increased osteoclast activation and bone resorption

Answer 165

painful bones - increased osteoclast - fractures ## Footnote The disease that you get from hyperparathyroidism is a disease called osteitis fibrosa cystica where the osteoclasts are activated. They resorb bone and you get really painful bones, the patients will tell you their body aches all over. They can develop actual cysts in the bone and it can actually be crippling. That should never happen anymore, we can actually treat it. How do you treat it, really quickly?

Answer 166

restrict phosphorus oral phosphate binders (bind phosphate so not absorbed) give vit d (decreases PTH syntehsiss and serum Ca levels)

Answer 167

creatinine and urea surrigates for uremic toxins

Answer 168

2.5 years major COD is cardiovascular - HF, SCD, arrhythmias atherolsclerosis but not by traditional risk factors

Answer 169

OATs on cell membranes in PT and endothelium transport many small protein bound solutes (? uremic toxins)

Answer 170

candidate for uremic toxins - when administered to nephrectomized rats - accelerated renal scarring and changed the expression of many genes mimics the effect of uremia on gene expression gene dysregulation not corrected by dialysis (leading to cardiac death) may be due to IS which is poorly dialyzable!!!

Answer 171

signals gene transcription (like a steroid hormone) in nucleus transported by OAT in proximal tubule

Answer 172

patients with end stage renal disease who rentain residual renal function (continue to produce urine) have better survival and less CV disease than patients who do not produce urine ? reflects activtiy of PT transporters and the small quantity of urine produced has IS (or another uremic toxin) elim of toxic products could serve survival function

Answer 173

in the gut! gut derived binds albumin

Answer 174

gain of HCl!! RTA (I, II, IV) Diarrhea (loss of HCO3 = gain of HCl)

Answer 175

gain of HA, A is not Cl ingestions ketoacidosis lactic acidosis renal failure

Answer 176

hyperchloemic metabolic acidosis loss of stool (NaCl, KCl, NaHCO3) = gain of H+ decrease serum HCO3, decrease amt filtered Kidney must reabsorb Na (esp bc high renin, low vol) Renal Na reapsorption is accompanied by more Cl becaue no HCO3 is available!

Answer 177

anion gap metabolic acidosis (gain of acid w non-Cl anion) anaerobic metabolism H+lactate- added to the plasma H+ titrates HCO3 - decrease HCO3 - lactate replaces HCO3 in serum

Answer 178

electroneutrlity requires that cations = anions Na + UC = Cl + HCO3 + UA even thugh everything is measured we pretend it is not

Answer 179

Na - Cl - HCO3 = UA-UC = Anion Gap nl = 6-12 (major UA is albumin)

Answer 180

M — Methanol U — Uremia (chronic kidney failure) D — Diabetic ketoacidosis P — Propylene glycol ("P" used to stand for Paraldehyde but this substance is not commonly used today) I — Infection, Iron, Isoniazid, Inborn errors of metabolism L — Lactic acidosis E — Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.) S — Salicylates

Answer 181

distal tubular defect in H+ ion secretion (congenital or acquired) decreased rate of H+ ion secretion - can't get rid of daily proton load urine pH \> 5.5 (can't acidify) hyperchloremic metabolic acidosis (like gain of HCl) H+ + Bone --\> hypercalciuria and osteoporosis

Answer 182

high urine pH high urine calcium low urine citrate calcium phosphate stones common bc citrate stops it!!

Answer 183

proximal tubular defect in H+ ion secretion impaired HCO3 reabsorption in the PT congenital or acquired - ocular abnormalities still able to max acidify urine (pH \< 5.5) hyperchloremic acidosis but patients are in acid balance! To maintain Na - reabsorb Cl (really low HCO3) No hypercalciuria or stones if give HCO3 - pee it right out bc can't reabsorb

Answer 184

can max acidify urine! hyperchloremic acidosis but still in acid balance (unlike distal) - no hypercalciuria or stones reabsorb Cl with Na because no HCO3

Answer 185

hyporenin/hypoaldo is primary defect conmmon in DM and with spiro/ACEI hypoaldo --\> hyperkalemia hyperkalemia inhibits glutaminase activity and NH4 generation - no urinary buffer so urine is acidic hyperchloremic metabolic acidosis

Answer 186

lack of urinary buffer (no NH3) leads to acidified urine

Answer 187

GFR \< 30 results from impaired ammonia synthesis because of reduced nephron mass in CKD max acidified urine though patients are not in acid balance!! (remaining intact nephrons acidify urine) lower GFR means less nephrons to get rid of acid anion gap variable - depeneds on retention of SO4, PO4

Answer 188

decrease in H due to increase in HCO3 2 components: generation (cause of increased HCO3) maintenence (reason kidney's can't excrete it) i.e. eat HCO3 - usually NO maintenence (volume expansion - decrease in RAS - rapid excretion of HCO3\_

Answer 189

generation: Lose H, Cl usually when secrete H into stomach, HCO3 goes into blood but in balance because HCO3 into duodenum so in balance instead - no H entry into duodenum and no balance high HCO3 in serum - urinary losses of Na and K - filtred HCO3 exceeds threshold of of PT maintenence: since lost Na and K - decrease in ECFV - increase in renin and aldo increase serum HCO3 - Cl is low so reabsorb Na with HCO3 Cl responsive metabilic alkalosis (low Cl)

Answer 190

low Cl! Cl responsive!!

Answer 191

during maintenence phase of vomiting, filtered HCO3 is being reabsorbed in proximal tubule - HCO3 is high but none in urine bc reabsorbing all of it

Answer 192

K loss leads to shift K out of cells and H in despite alkalosis stim ammoniagenesis - H is being secreted so HCO3 reabsorption

Answer 193

loss of fluid relatively high in Cl leads to a higher [HCO3] does not account for the kidney! diuretics cause

Answer 194

Cl responsive metabolic alkalosis 1. generation phase - loss of NaCl in TALK, higher [HCO2] results ue to loss of Cl - contraction alkalosis 2. maintenance phase - decrease EABV - renin and AII and Aldo - Na distally leads to hypokalemia

Answer 195

like taking thiazides hypokalemic metabolic alkalosis - salt losing (hyperrenin/aldo)

Answer 196

like taking furosemide hypokalemic hetabolic alkalosis salt losing hypomag NOT hypocalciuria

Answer 197

Cl unresoonsive metabilic acidosis continued NaCl delivery to CCD Renin, ATII suppressed - turns off proximal Na reabsorption NOT cl depleted so it' won't help

Answer 198

vomiting diuretics (when not acting) CF low chloride intake

Answer 199

primary hyperaldo diuretics (acting) alklai admin bartters/gitelmans severe hypokalemia

Answer 200

replete ECFV replete Cl (NaCl, KCl)

Renal Pathophysiology Flashcards

(235 cards)