295 First Aid Ch 15 Renal Flashcards

8/13/2019 295 First Aid Ch 15 Renal Flashcards

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www.natures.ir3-year-old boy presents with facialedema, malaise, and proteinuria.

Steroids for minimal changedisease.

oman presents with UTIpositive for Proteus vulgaris. What type of

kidneystones is she at risk for?

Ammonium magnesium

phosphate (struvite).

Patient describes a 2-yearhistory of acetaminophen use. What is

she at risk for?Renal papillary necrosis.

_ X-ray film shows massivelyenlarged kidneys bilaterally.

Adult polycystic kidney disease.

Patient taking enalaprilcomplains of constant coughing.

Alternative

Losartanangiotensin IIreceptor blocker.

Ureters: course

Ureters pass under uterine artery andunder ductus

Water (ureters) under the

deferens (retroperitoneal). bridge (artery,ductus

deferens).


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The ????? kidney is taken duringtransplantation because ????

left

has a longer renal vein.

Ions in ECF vs ICFECF: NaCl, K+

ICF: K+, NaCl

ECF PV = interstitial volume.

TBW ECF = ICF.

604020 rule (% of body weight):60% total body is water

40% ICF20% ECF

Plasma volume measured by?

Extracellular volume measuredby?

radiolabeled albumin.

inulin.

plasma Osmolarity is approximately 290 mOsm


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Renal clearanceequation

Cx= UxV/Px= volume of plasma from which the

substance is completely cleared per unittime.

Cx= clearance of X.Ux= urine conc of X.

Px= plasma conc of X.V = urine flow rate.

If Cx< GFR,

If Cx> GFR,

If Cx= GFR,

-If Cx< GFR, then there is net tubularreabsorption of X

-If Cx> GFR, then there is net tubularsecretion of X.

-If Cx= GFR, then there is no netsecretion or reabsorption.

Responsible for filtration of plasmaaccording to size and net charge.

Glomerular filtration barrier

Glomerular filtration barrier is responsiblefor

Responsible for filtration of plasmaaccording to size and net charge.

Glomerular filtration barrieris composed of

1. Fenestrated capillary endothelium (size

barrier)2. Fused basement membrane with

heparan sulfate

(negative charge barrier)3. Epithelial layer consisting of podocytefoot processes

Glomerular filtration barrierwhat is lost in nephrotic syndrome and

what does that lead to

The charge barrier is lost innephrotic syndrome,

Resulting in:albuminuria, hypoproteinemia,

generalized edema, andhyperlipidemia.


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When is the negative chare barrier lost onthe Glomerular filtration barrier

nephrotic syndrome,

Glomerular filtration ratethings used to measure

Inulinor

Creatinine

Inulin can be used to calculate GFR

because

it is freely filtered and is neither

reabsorbed nor secreted.

Inulin GFR calculation

GFR = Uinulin V/Pinulin = Cinulin=

Kf[(PGC PBS) (GC BS)].

(GC = glomerular capillary; BS =Bowmans space.)

BS normally equals zero.

Effective renal plasma flow things used to measure

PAH (para-Aminohippurate)

Effective renal plasma flowcalculation and blood flow

ERPF = UPAH V/PPAH = CPAH.

RBF = RPF/1 Hct.

ERPF underestimates true RPF by ~10%.

ERPF can be estimated using PAH

because

ERPF can be estimated using PAHbecause it is both filtered and actively

secreted in theproximal tubule. All PAH entering the

kidney is excreted.


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Filtration fraction = GFR/RPF. GFR/RPF.

GFR/RPF = Filtration fraction

Filtered load = GFR plasma concentration.

GFR plasma concentration = Filtered load

Free water clearancedescribe and calculate

Given urine flow rate, urine osmolarity,and plasma osmolarity, be able to

calculate free water clearance:

CH2O = V Cosm.

V = urine flow rate; Cosm =UosmV/Posm.

Glucose clearancedifferent levels wrt blood Glc

-At plasma glucose of 200 mg/dL,glucosuria begins

(threshold).-At 350 mg/dL, transport mechanism

is saturated (Tm).

Glucose clearancewhat hapens to Glc at normal levels

Glucose at a normal plasma level iscompletely reabsorbed in proximal tubule.


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Amino acid clearancedescribe

Reabsorption by at least 3 distinct carriersystems, with competitive inhibition within

each group.2 active transport occurs in proximal

tubule and is saturable.

Early proximal convoluted tubulewhat is resorbed and what is secreted

Reabsorbs all of the glucose and aminoacids and most of the bicarbonate,

sodium,and water.

Secretes ammonia, which acts as a bufferfor secreted H+.

workhorse of the nephron. A. Early proximal convoluted tubule

Thin descending loop of Henlewhat is resorbed and what is secreted

passively reabsorbs water via medullaryhypertonicity (impermeable to sodium).

Thick ascending loop of Henlewhat is resorbed and what is secreted

actively reabsorbs Na+,K+, and Cl

and indirectly induces the reabsorptionof

Mg2+ and Ca2+.

Impermeable to H2O.

Early distal convoluted tubulewhat is resorbed and what is secreted

actively reabsorbsNa+, Cl

. Reabsorption of Ca2+ is under thecontrol of PTH.

Collecting tubule

what is resorbed and what is secreted

reabsorb Na+ in exchange forsecreting K+ or H+ (regulated by

aldosterone).

Reabsorption of water is regulated byADH/vasopressin


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What part of the nephron is

Reabsorbs all of the glucose and aminoacids and most of the bicarbonate,

sodium,and water. Secretes ammonia, which acts

as a buffer

for secreted H+.

Early proximal convoluted tubule


Reabsorbs most of the bicarbonate ,sodium, and water.



Secretes ammonia, which acts as a bufferfor secreted H+.



passively reabsorbs water via medullary

hypertonicity (impermeable to sodium).

Thin descending loop of Henle


Impermeable to H2O.Thick ascending loop of Henle


actively reabsorbs Na+ K+, and Cl

and indirectly induces the reabsorption ofMg2+ and Ca2+.

Thick ascending loop of Henle


actively reabsorbsNa+, Cl-

Reabsorption of Ca2+ is under thecontrol of PTH.

Early distal convoluted tubule


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Reabsorption of Ca2+ is under thecontrol of PTH.

Early distal convoluted tubule


reabsorb Na+ in exchange forsecreting K+ or H+ (regulated by

aldosterone).

Collecting tubules


reabsorption of water is regulated byADH/vasopressin

Collecting tubules

Osmolarity of medulla can reach1200 mOsm/L H2O.

1200 mOsm/L H2O.

Renin-angiotensin systemMechanism

Renin is released by the kidneys uponsensing BP and cleaves

angiotensinogen toangiotensin I. Angiotensin I is thencleaved by angiotensin-converting

enzyme (ACE), primarily in the lungcapillaries, to angiotensin II.

Actions of angiotensin II

1. Potent vasoconstriction2. Release of aldosterone from the

adrenal cortex3. Release of ADH from posterior pituitary

4. Stimulates hypothalamus thirst

Overall, angiotensin II serves to intravascular volume and BP.


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??? released from atria may act as acheck on the renin-angiotensin system

(e.g., inheart failure). Decreases renin and

increases GFR.

ANP

ANP as a check on renin-angiotensin

ANP released from atria may act as acheck on the renin-angiotensin system

(e.g., inheart failure). Decreases renin and

increases GFR.

JG cells

What type . JG cells secrete

(modified smooth muscle of afferent

arteriole)

macula densaWhat does it sense and where is it

(Na+ sensor, part ofthe distal convoluted tubule)

JG cells secrete renin

what cells secrete renin JG cells

(Na+ sensor, part of

the distal convoluted tubule)

macula densa


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Juxtaglomerular apparatus (JGA)

main purpose

GA defends glomerularfiltration rate via the renin-

angiotensin system.

Juxtaglomerular apparatus (JGA)

components

JG cellsand

macula densa

Kidney endocrine functions

in general

epoVit D

ReninProtaglandins

What causes JG cells to secrete renin renal blood pressure,

Na+ delivery to distal tubule, sympathetic tone (via 1)

Kidney endocrine functionsdescribe mech of

EPO

Endothelial cells of peritubular capillariessecrete erythropoietin in response to

hypoxia


Vit D

Conversion of 25-OH vitamin D to 1,25-(OH)2vitamin D by 1-hydroxylase, which

isactivated by PTH


prostaglandins

Secretion of prostaglandins thatvasodilate

the afferent arterioles to GFR


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how can NSAIDS cause kidney problems

NSAIDs can cause acute renal failure invascoconstrictive states by inhibiting the

renalproduction of prostaglandins,

which keep the afferentarterioles vasodilated to

maintain GFR.

causes of

Respiratory acidosis

Acute lung diseaseChronic lung diseasOpioids, narcotics,

Weakening of respiratory

musclesAirway obstruction

causes of

Metabolic acidosis with increased aniongap

MUD PILES:MethanolUremia

Diabetic ketoacidosisParaldehyde or Phenformin

Iron tablets or INHLactic acidosisEthylene glycol

Salicylates

causes of

Metabolic acidosis with normal anion gap

HyperchloremiaDiarrhea

Glue sniffingRenal tubular acidosis

causes of

Respiratory alkalosis

HyperventilationAspirin ingestion (early)

causes of

metabolic alkalosis

VomitingDiuretic useAntacid use

Hyperaldosteronism


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Anion gap = Na+ (Cl + HCO3

)Na (Cl + HCO3)

Lab values for

Respiratory acidosis

pH < 7.4PCO2 > 40 mmHg

Lab Values For

Metabolic acidosis with compensation

pH < 7.4

PCO2 < 40 mmHg

Lab Values For

Respiratory alkalosis

pH > 7.4PCO2 < 40 mmHg

Lab Values For

Metabolic alkalosis with compensation

pH > 7.4PCO2 > 40 mmHg

Potters syndromecause

Bilateral renal agenesis oligohydramnios

Caused by malformation of ureteric bud.

Potters syndrome

clinical findings

limb deformities, facial deformities,pulmonary

hypoplasia.


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Bilateral renal agenesis oligohydramnios

limb deformities, facial deformities,pulmonaryhypoplasia.

Potters syndrome

Horseshoe kidneydescribe

Inferior poles of both kidneys fuse. Asthey ascend

from pelvis during fetal development,horseshoe

kidneys get trapped under inferiormesenteric artery

and remain low in the abdomen.

Horseshoe kidneywho females with Turner Syndrome

What casts in urine mean

RBC casts

glomerular inflammation (nephriticsyndromes), ischemia, or malignant

hypertension.


WBC casts

tubulointerstitial disease, acutepyelonephritis, glomerular disorders.


Granular castsacute tubular necrosis.


Waxy castsadvanced renal disease/CRF.


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Hyaline castsnonspecific.

Presence of casts indicatesthat hematuria/pyuria is

is of renal origin.

What type of cast is seen in

nephritic syndromesRBC casts


acute pyelonephritisWBC casts


acute tubular necrosis.Granular casts


advanced renal disease/CRF.Waxy casts

Characteristics of

NephrItic syndrome

I = inflammation.hematuria,

hypertension,

oliguria,azotemia.


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Characteristics ofNephrOtic syndrome

O = prOteinuria.massive proteinuria (frothy urine),

hypoalbuminemia,peripheral and periorbital edema,

hyperlipidemia.

6 examples ofNephrItic syndrome

1. Acute poststreptococcalglomerulonephritis

2. Rapidly progressive(crescentic)glomerulonephritis3. Goodpastures syndrome

4. Membranoproliferativeglomerulonephritis

5. IgA nephropathy (Bergers disease)6. Alports syndrome

6 examples ofNephrOtic syndrome

1. Membranous glomerulonephritis

2. Minimal change disease (lipoidnephrosis)

3. Focal segmental glomerular sclerosis.4. Diabetic nephropathy

5. SLE6. Amyloidosis

LM/EM/IF findings in

Acute poststreptococcalglomerulonephritis

glomeruli

enlarged and hypercellular, neutrophils,lumpy-bumpy.


Rapidly progressive glomerulonephritis

LM and IF:crescent-moon shape.


Goodpastures syndrome

(type II hypersensitivity)IF: linearpattern,

anti-GBM antibodies.


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Membranoproliferative glomerulonephritis

EM: subendothelialhumps, tram track.


IgA nephropathy (Bergers disease)

IF and EM: mesangial depositsof IgA.


Alports syndromesplit basement membrane.


Membranous glomerulonephritis

LM: diffuse capillary and basementmembrane thickening.IF: granular pattern.

EM: spike and dome.


Minimal change disease

LM: normal glomeruli.

EM: foot process effacement

LM/EM/IF findings inFocal segmental glomerular sclerosis

LM: segmental sclerosisand hyalinosis.


Diabetic nephropathy

LM: Kimmelstiel-Wilson wire looplesions,

basement membrane thickening (seeColor Image 95).


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5. SLE

(5 patterns of renal involvement)

LM: In membranousglomerulonephritis pattern, wire-loop

lesion with subepithelial deposits.


Amyloidosis

IF: Congo red stain, apple greenbirefringence.

Name the Glomerular pathology

LM: crescent-moon shape.

Rapidly progressive (crescentic)

glomerulonephritis


LM: glomeruli enlarged and hypercellular,neutrophils,



lumpy-bumpy.



EM:subepithelial humps. IF: granularpattern.



IF: crescent-moon shape.

Rapidly progressive (crescentic)

glomerulonephritis


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IF: linear pattern antibodies.

Goodpastures syndrome (type IIhypersensitivity)


EM: subendothelial humps, tram track.Membranoproliferative glomerulonephritis


tram track.Membranoproliferative glomerulonephritis


IF and EM: mesangial depositsof IgA.



split basement membrane.Alports syndrome


LM: diffuse capillary andbasement membrane thickening.



IF: granular pattern. EM: spikeand dome.



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spike and dome.Membranous glomerulonephritis


EM: foot process effacement

2. Minimal change disease (lipoidnephrosis)


LM: segmental sclerosisand hyalinosis.

Focal segmental glomerular sclerosis


LM: Kimmelstiel-Wilson wire looplesions,

basement membrane thickening

Diabetic nephropathy


(5 patterns of renal involvement)LM: Inmembranous

glomerulonephritis pattern, wire-looplesion with subepithelial deposit

SLE


IF: Congo red stain, apple greenbirefringence.

Amyloidosis

clinical features of Glomerular pathology


Most frequently seen in children.Peripheral and periorbital edema.

Resolves spontaneously.


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Rapidly progressive (crescentic)glomerulonephritis

Rapid course to renal failure.Number of crescents indicates

prognosis.


Goodpastures syndrome

(type II hypersensitivity)anti-GBM antibodies

Hemoptysis, hematuria.


Membranoproliferative glomerulonephritis

Slowly progresses to renal

failure.



Mild disease.Often postinfectious.

Collagen IV mutation. Nervedeafness and ocular disorders.

Alports syndrome


Alports syndrome

Collagen IV mutation. Nervedeafness and ocular disorders.



Most common cause of adult

nephrotic syndrome.


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Most common cause of adultnephrotic syndrome.




Most common cause of childhoodnephrotic syndrome. Responds well to

steroids.


Focal segmental glomerular sclerosisMore severe disease in HIV patients.


Diabetic nephropathyDM

Most common cause of childhoodnephrotic syndrome. Responds

well to steroids.

Minimal change disease (lipoidnephrosis)

Glomerular pathology

Amyloidosis associations

Associated with multiple myeloma,chronic conditions,TB, rheumatic arthritis.

Glomerular pathology

Associated with multiple myeloma,chronic conditions,TB, rheumatic arthritis.

Amyloidosis


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Minimal change diseaseaka

lipoid nephrosis

lipoid nephrosisaka


Kidney stones

which are Radilucent.

I cant C U on XRay. for Cystine and

Uric acid stones.

Kidney stoneswhich are Radopaque

Calcium

Ammonium magnesium phosphate(struvite)

Most common kidney stonesCalcium (7585%):

Calcium oxalate, calcium phosphate, orboth.

2nd most common kidney stoneAmmonium magnesium phosphate

(struvite)

Conditions that cause hypercalcemia(??????) can lead to hypercalciuria and

stones.

cancer, PTH, vitamin D, milk-alkali

syndrome


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Kidney stones that tend to recur Tend to recur.

Kidney stones

Radiopaque and Worsened by alkaluria.


Kidney stones

Radiolucent and Worsened by aciduria.Uric acid

Kidney stones

cause of Ammonium magnesiumphosphate (struvite)

Caused by infectionwith urease-positive bugs (Proteus

vulgaris,) Staphylococcus, Klebsiella).

Kidney stones

Can form staghorn calculi


Kidney stones

Uric acid associations

Strong association with hyperuricemia(e.g., gout).

Kidney stones

Strong association with hyperuricemia(e.g., gout).

Uric acid stone


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Kidney stones

Uric acidwho

Often seen as a result of diseases withcell

turnover, such as leukemia andmyeloproliferative disorders.

cause of Cystine Kidney stones Most often 2 to cystinuria.

Most common renal malignancy Renal cell carcinoma

Renal cell carcinoma

who gets it and risk factors

Most common in men ages 5070. incidence with

smoking and obesity.


associations

von HippelLindauand

gene deletion in chro-mosome 3.


Histo

Originates in renal tubule cells polygonal clear cells.


Clinical findings

hematuria, palpable mass,2 polycythemia, flank pain, fever, and

weightloss.


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invasion features

Invades IVC and spreadshematogenously.


wrt paraneoplastic syn-dromes

(ectopic EPO, ACTH, PTHrP, andprolactin)

Most common renal malignancy of early

childhood Wilms tumor

Wilms tumor

who

Most common renal malignancy of earlychildhood (ages 24)

Wilms tumor

presentation

Presents with huge,palpable flank mass, hemihypertrophy.

Wilms tumor

genetics

Deletion of tumor suppression gene WT1on chromosome 11.

Wilms tumor

WRT a complex

WAGR complex:Wilms tumor,

Aniridia,

Genitourinary malformation,and mental-motor Retardation.


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WAGR complex

WAGR complex:Wilms tumor,

Aniridia,Genitourinary malformation,

and mental-motor Retardation.

Most common tumor of urinary tractsystem

Transitional cell carcinoma


where

(can occur in renal calyces, renal pelvis,

ureters, and bladder).

Painless hematuria is suggestive of bladder cancer


associations

problems in your Pee SACS: Phenacetin,Smoking,

Aniline dyes,Cyclophosphamide,

Schistosomiasis

Acute Pyelonephritis

what is effected

Affects cortex with relative sparing ofglomeruli/vessels.

pathognomonic for Acute Pyelonephritis White cell casts in urine


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Acute Pyelonephritis

presentationPresents with fever, CVA tenderness.

Chronic Pyelonephritis

gross

Coarse, asymmetric corticomedullaryscarring, blunted calyx.

Chronic Pyelonephritis

castseosinophilic

thyroidization of kidney Chronic Pyelonephritis

Acute generalized infarction of cortices ofboth kidneys

Diffuse cortical necrosis

what isDiffuse cortical necrosis

Acute generalized infarction of cortices ofboth kidneys

Diffuse cortical necrosis

causes

Likely due to a combination of vasospasmand DIC. Associated with obstetric

catastrophes (e.g., abruptio placentae)and septic shock.


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what isDrug-induced interstitial nephritis

Acute interstitial renal inflammation.

Drug-induced interstitial nephritis

presentation

Fever, rash, eosinophilia, hematuria 2weeks

tis after administration.

Drug-induced interstitial nephritis

causes and mech

Drugs (e.g., penicillin derivatives,

NSAIDs, diuretics) act as haptensinducing hypersensitivity.

Most common cause of acute renalfailure.

Acute tubular necrosis


course

Reversible, but fatal if left untreated.Recovery in 23 weeks.


causes

Associated with renal ischemia (e.g.,shock), crush injury (myoglobulinuria),

toxins.


when do people die

Death most often occurs during initial

oliguric phase.


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mech

Loss of cell polarity,epithelial cell detachment, necrosis,

granular casts.


stages

Three stages:inciting event maintenance (low urine)

recovery.

Renal papillary necrosis

associations

1. Diabetes mellitus2. Acute pyelonephritis

3. Chronic phenacetin use(acetaminophen is phenacetin derivative)

4. Sickle cell anemia

what is Acute renal failureAbrupt decline in renal function withcreatinine and BUN over a period of

several days.

Abrupt decline in renal function withcreatinine and BUN over a period of

several days.Acute renal failure

Acute renal failure

Prerenal azotemia

Mech

decreased RBF (e.g., hypotension) GFR.

Na /H2Oretained by kidney.

Acute renal failure

Intrinsic

mech

generally due to acute tubular necrosis orischemia/toxins. Patchy necrosis leads to

debris obstructing tubule andfluid

backflow across necrotic tubule GFR.


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Acute renal failure

Intrinsic

casts

Urine has epithelial/granular casts.

Acute renal failure

Post renal

mech

3. Postrenaloutflow obstruction (stones,BPH, neoplasia). Develops only with

bilateral obstruction.

Consequences of renal failure

0. Uremia1. Anemia

2. Renal osteodystrophy

3. Hyperkalemia,4. Metabolic acidosis

5. Uremic encephalopathy6. Sodium and H2O excess

7. Chronic pyelonephritis8. Hypertension

mechanisms for the consequences ofrenal failure

Uremia

clinical syndrome marked by BUN

and creatinine and associatedsymptoms.


Anemia

(failure of erythropoietin production)


Renal osteodystrophy

(failure of activevitamin D production)

consequences of renal failure

Hyperkalemia

can lead to cardiac arrhythmias


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Metabolic acidosis

acid secretionand

generation of HCO3

consequences of renal failure

Sodium and H2O excess

CHF andpulmonary edema

2 forms of renal failure with causes

acute renal failure (often due

to hypoxia) and chronic renal failure (e.g.,due to HTN and diabetes).

what is Fanconi's syndrome

Defect in proximal tubule transport ofamino acids, glucose, phosphate, uric

acid,protein, and electrolytes.

Defect in proximal tubule transport ofamino acids, glucose, phosphate, uric

acid,protein, and electrolytes.

what is Fanconi's syndrome

Fanconi's syndrome

complications

rickets,osteomalacia,hypokalemia,

metabolic acidosis.

Adult polycystic kidney disease

gross

Multiple, large, bilateral cysts that

ultimately destroy the parenchyma.


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presentation

flank pain, hematuria, hypertension,urinary infection, progressive renal failure.


GenesAutosomal dominant mutation in APKD1


Associated with

polycystic liver disease,berry aneurysms,

mitral valve prolapse,diverticulosis


cause of deathfrom uremia or hypertension.

Juvenile polycystic kidney disease

grossradial cysts presentation in parenchyma


genesAutosomal recessive.


Associated with

hepatic cysts

and fibrosis.


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Ca2+

Low serum concentrationvs

High serum concentration

Tetany, neuromuscular irritability

Delirium, renal stones, abdominal pain

Mg2+



Neuromuscular irritability, arrhythmiasDelirium,

DTRs, cardiopulmonary arrest

PO4 2



Low-mineral ion product causes boneloss

High-mineral ion product causesmetastatic

calcification, renal stones

Name the Electrolyte disturbances

Disorientation, stupor, comaLow Na+


2 to metabolic alkalosisLow Cl


U waves on ECG, flattened T waves,arrhythmias, paralysis

Low K+


Tetany, neuromuscular irritability

Low Ca2+


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Neuromuscular irritability, arrhythmiasLow Mg2+


Low-mineral ion product causes boneloss

Low PO42


Neurologic: irritability, delirium, comaHigh Na+


2 to nonanion gap acidosisHigh Cl


Peaked T waves, arrhythmiasHigh K+


Delirium, renal stones, abdominal painHigh Ca2+


Delirium, DTRs, cardiopulmonary arrest

High Mg2+


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High-mineral ion product causesmetastatic calcification, renal stones

High PO42

MannitolMechanism

Osmotic diuretic, tubular fluidosmolarity, producing urine flow.

Mannitol

Clinical use

Shock, drug overdose,

intracranial/intraocular pressure

MannitolToxicity

Pulmonary edema, dehydration.Contraindicated in anuria, CHF.

AcetazolamideMechanism

Carbonic anhydrase inhibitor. Causesself-limited NaHCO3 diuresis and

reduction in total-body HCO3 stores.

AcetazolamideClinical use

Glaucoma, urinary alkalinization,metabolic alkalosis, altitude sickness.

Acetazolamide

Toxicity

Hyperchloremic metabolic acidosis(ACIDazolamide causes

ACIDosis),

neuropathy,NH3 toxicity,sulfa allergy.


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FurosemideMechanism

Sulfonamide loop diuretic. Inhibitscotransport

system (Na+, K+, 2 Cl) of thick ascending limb

of loop of Henle. Abolishes hypertonicityof medulla, preventing concentration of

urine.

FurosemideClinical use

Edematous states (CHF, cirrhosis,nephrotic syndrome, pulmonary edema),

hypertension,hypercalcemia.

FurosemideToxicity

OH DANG!Ototoxicity,

Hypokalemia ( Ca2+ excretion. Loops

Lose calcium.)Dehydration,

Allergy (sulfa),Nephritis (interstitial), Gout.

Ethacrynic acidMechanism

Phenoxyacetic acid derivative (NOT asulfonamide).

Essentially same action as furosemide.

Ethacrynic acidClinical use

Diuresis in patients allergic to sulfa drugs.

Ethacrynic acidToxicity

Similar to furosemide; can be used inhyperuricemia,

acute gout (never used to treat gout).

Hydrochlorothiazide

Mechanism

Thiazide diuretic. Inhibits NaClreabsorption in early distal tubule,

reducing diluting capacity of the nephron. Ca2+ excretion.


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HydrochlorothiazideClinical use

Hypertension, CHF, idiopathichypercalciuria, nephrogenic diabetes

insipidus.

HydrochlorothiazideToxicity

Hypokalemic metabolic alkalosis,hyponatremia,Sulfa allergy.

HyperGLUC:hyperGlycemia,hyperLipidemia,hyperUricemia,hyperCalcemia.

K+-sparing diureticsnames

EATS K+

Eplereone.Amiloride,

Triamterene,Spironolactone,

K+-sparing diuretics

Mechanism

Spironolactone is a competitivealdosterone receptor

antagonist in the cortical collecting tubule.

Triamterene and amiloride act at thesame part ofthe tubule by blocking Na+ channels in

the CCT.

K+-sparing diureticsClinical use

Hyperaldosteronism, K+ depletion, CHF.

K+-sparing diureticsToxicity

Hyperkalemia, endocrine effects (e.g.,spironolactone

causes gynecomastia, antiandrogen

effects).


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Which diuretic causes gynecomastia,antiandrogen effects

Spironolactone

Diuretics: electrolyte changes

Urine NaCl

(all diureticscarbonic anhydraseinhibitors, loop diuretics, thiazides, K+-

sparingdiuretics).


Urine K+ (all except K+-sparing diuretics).


Blood pH

(acidosis)carbonic anhydraseinhibitors, K+-sparing diuretics;

(alkalosis)loopdiuretics, thiazides.


Urine Ca+

loop diuretics,

thiazides.

ACE inhibitorsMechanism

Inhibit angiotensin -converting enzyme,

reducinglevels of angiotensin II and preventing

inactivation of bradykinin, a potentvasodilator. Renin release is due to loss

of feedback inhibition.

ACE inhibitors

Clinical use

Hypertension, CHF, diabetic renal

disease.


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ACE inhibitorsToxicity

CHAPTOPRIL.

Cough,hyperkalemia,Angioedema,

Proteinuria,Taste changes,

hypOtension,Pregnancy problems (fetal renaldamage),

Rash,Increased renin,

Lower angiotensin II.

ACE inhibitors

when to avoid thembilateral renal artery stenosis.

Order of diuretic action as you go thoughthe nephron

1. Acetazolamide2. Osmotic agents (mannitol)

3. Loop agents (e.g., furosemide)4. Thiazides

5. Potassium sparing6. ADH antagonists

Name the diuretic by its toxicity

Pulmonary edema, dehydration.Contraindicated in

anuria, CHF.

Mannitol


Hyperchloremic metabolic acidosis,Acetazolamide


ototoxicity

Furosemide


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NephritisFurosemide


Hypokalemic metabolic alkalosisHydrochlorothiazide


hyperGlycemiaHydrochlorothiazide


HyperkalemiaK+-sparing diuretics


endocrine effectsspironolactone


gynecomastiaspironolactone


antiandrogen

spironolactone


42/43

Name the diuretic used for

HyperaldosteronismK+-sparing diuretics


K+ depletionK+-sparing diuretics


Shock and drug overdoseMannitol


intracranial/intraocular pressure.Mannitol


Glaucoma,Acetazolamide


urinary alkalinization and metabolicalkalosis

Acetazolamide


altitude sickness.

Acetazolamide


43/43


Edematous states (CHF, cirrhosis,nephrotic

syndrome, pulmonary edema),

Furosemide


hypertension andhypercalcemia.

Furosemide

or

Hydrochlorothiazide


Diuresis in patients allergic to sulfa drugs.Ethacrynic acid


nephrogenic diabetes insipidus.Hydrochlorothiazide

Types of renal tubular acidosis

all (ecxept type 4) have high urine pH-Type 1: defect in H+ pump

-Type 2: Renal loss of Bicarb-Type 3: genetic defect in type 2 carbonic

anhydrase

-Type 4: Hypoaldosteronism leading tohyperkalemia leading to inhibition of

ammonia excretion

what is renal tubular acidosis

a medical condition that involves anaccumulation of acid in the body due to a

failure of the kidneys to appropriatelyacidify the urine

a medical condition that involves an

Documents

295 First Aid Ch 15 Renal Flashcards