Genitourinary Objectives

7/30/2019 Genitourinary Objectives

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Genitourinary Objectives

Objective #1

State the indications, significance of abnormal findings and complications of the following Imaging and Laboratory studies.

Urinalysis, serum BUN and creatinine, creatinine clearance and GFR, IVP, cystoscopy, US of bladder kidney and prostate, Urine

culture and sensitivity, renal biopsy

Urinalysis: (types)

Random = looks for protein and blood (typically for screening) First morning specimen = looks for by products of stuff like antigens, protein, etc. 24 hour specimen = (pee into a jug for 24 hours and put in fridge to keep cool) looks for creatinine, used to look for muscle

break down.

Indications:

Used in the diagnosis of:o Calculio Urinary tract infection (UTI)o Malignancyo Systemic dz affecting the kidney

Used to screen for:o Pregnancy

Significance of abnormal findings and complications:

Color and odor:o Cloudy urine = precipitated phosphate crystals in alkaline urine or pyuriao Normal urine = urinoid odor doesnt imply infectiono Fruity/sweet urine = diabetic ketoacidosiso Ammoniacal odor = alkaline fermentation after prolonged bladder retention

Specific gravity (hydration status/concentrating ability of kidneys):o Normal USG 1.003-1.030o Value < 1.010 = relative hydrationo Value > 1.020 = relative dehydrationo Increased USG = glycosuria and SIADHo Decreased USG = diuretic use, diabetes insipidus (DI), adrenal insufficiency, aldosteronism, & impaired renal fxn.

Urine pH (generally reflects the serum pH, except in pt with renal tubular acidosis):o Possible range 4.5-8.0 normally slightly acidic (5.5-6.5)o Inability to acidify urine to a pH of < 5.5 despite an overnight fast and administration of an acid load = HALLMARK of renal

tubular acidosis (RTA)

o Alkaline urine in pt with UTI suggest urea splitting organism which may be associated with magnesium-ammoniumphosphate crystals and can form staghorn calculi (struvite stones)

o Uric acid calculi are associated with acidic urine Hematuria:

o proteinuria, erythrocyte casts, and dysmorphic RBCs = Glomeular hematuriao proteinuria without erythrocyte casts or dysmorphic RBCs = Renal (nonglomerular) hematuriao absence of proteinuria, dysmorphic RBCs, and erythrocyte casts = Urologic hematuria

Proteinuria (3 types):o Glomerular = (MC type) albumin is the primary urine proteino Tubular = results when malfxning tubule cells no longer metabolize or reabsorb normally filtered protein. Therefore low

molecular weight proteins predominate over albumin

o Overflow = low-molecular weight proteins overwhelm the ability of the tubules to reabsorb filtered protein. Glycosuria:

o When the filtered load of glucose exceeds the ability of the tubule to reabsorb it = glycosuria common causes Diabetesmellitus, cushings syndrome, liver and pancreatic dz, and Fanconis syndrome


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Ketonuria:o MC associated with uncontrolled diabetes, also occurs during pregnancy, carbohydrate-free diets, and starvation

Nitrites:o Result of bacteria converting nitrates to nitrites, mostly gram negative but some gram positive organismso Test is specific but not sensitive therefore doesnt rule out a UTI

Leukocyte esterase (product of neutrophils):o If pyuria present usually associated with UTIo

Causes of pyuria with negative cultures are Chlamydia, Ureaplasma ureanylticum, balanitis, urethritis, tuberculosis, bladdertumors, viral infxns, nephrolithiasis, foreign bodies, exercise, glomerulonephritis, and corticosteroid and cyclophosphamide.

Bilirubin and urobilinogen:o Bilirubin in urine = Indicates further evaluation for liver dysfxn and biliary obstructiono Urobilinogen = hemolysis and hepatocellular dz elevate urobilinogen, abx and bile duct obstruction decrease urobilinogen

in urine.

Microscopic urinalysis:o Used to identify cells, casts, crystals, and bacteria

Cells: Squamos epithelial cells indicate contamination Transitional epithelial cells is normal Renal tubule cells indicates significant renal pathology Dysmorphic RBC suggest glomerular dz

Casts: Coagulum of Tamm-Horsfall mucoprotein and the trapped contents of tubule lumen indicate DCT or collecting duct

issues dealing with urinary concentration or stasis, or when urinary pH is very low

Types of casts = hyaline, erythrocyte, leukocyte, epithelial, granular, waxy, fatty, broad Crystals:

Calcium oxalate = refractile square envelope Uric acid = yellow to orange-brown diamond or barrel shaped Triple phosphate = associated with alkaline urine and UTIs or may be normal coffin lid Cystine = colorless, hexagonal shape, present in acidic urine, which is diagnostic of cystinuira

Bacteruria: Colony count of as low as CFU per mL suggest UTI Presence of bacteria in a male specimen is suggestive of infection and a culture should be obtained.

CMDT says

Certain patterns are associated with renal dzo Bland urine sediment = chronic kidney dz and prerenal and postrenal disorderso Heavy proteinuria and lipiduria = nephrotic syndromeo Hematuria with dysmorphic RBCs, RBC casts, and proteinuria = glomerulonrphritiso Pigmented granular casts and renal tubular epithelial casts = acute tubular necrosiso WBCs, neutrophils, eosinophils, WBC casts, RBC, and small amounts of protein = interstitial nephritis and

pyelonephritis

o Pyruia alone = UTI***Sorry I didnt summarize the 17 page monster NNB gave us****

Serum BUN and Creatinine

Indications:

Urea is an index used to measure renal fxn Synthesized mainly by the liver and is the end product of catabolism Urolithiasis/ureteral stones Renal cystic dz


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Drug induce nephropathy Chronic renal dz


Conditions that cause increased BUN: dehydration, reduced effective circulating blood volume (prerenal azotemia),catabolic states (gastrointestinal bleeding, corticosteroid use), high protein diets, tetracycline,

Conditions that decrease BUN: liver dz, malnutrition, sickle cell anemia, SIADH Complications of renal cystic dz = pain, hematuira, renal infections, renal stones, HTN, cerecral aneurysms Complications of chronic renal dz = HTn or hypOten, castrointestinal hemorrhage, Adult respiratory distress syndrome

Creatinine Clearance/GFR

Indicatioins

Useful index of overall renal fxn Adults with proteinuria > grams per 24 hrs require this measurement Renal cystic dz Drug induce nephropathy Chronic renal dz


Creatinine clearance is one way to estimate GFR, creatinine is a product of muscle metabolism produced at a normal rateand cleared by renal excretion, and excretion and production are normally equal.

Conditions that elevate creatinine: ketoacidosis, cephalothin, cefoxitin, flucytosine, other drugs such as aspirin, cimetidine,probenecid, trimethoprim

Conditions that decrease creatinine: advanced age, cachexia, liver disease **With ESRD an average of creatinine clearance and urea clearance is more accurate than creatinine clearance alone** If creatinine clearance is reduced renal failure is a possibility Complications of renal cystic dz = pain, hematuira, renal infections, renal stones, HTN, cerecral aneurysms Complications of chronic renal dz = HTn or hypOten, castrointestinal hemorrhage, Adult respiratory distress syndrome

Intravenous Pyelogram

Indications: (X-Ray with contrast) Functional exam of the kidney to see how fast it can filter Used as an anatomical exam Used to evaluate hematuria, urolithiasis/ureteral stones, renal cystic dz, drug induce nephropathy


With renal cystic dz there are filling defects With drug induced nephropathy there is egg in cup focal necorsis, lobster claw calyces, scarring, sloughing and

calcification of papilla and renal stones.

Complication of IVP = one of the biggest causes of renal failure due to toxicity of the contrast used in the procedureCystoscopy

Indications: Used to assess for bladder or urethral neoplasm, benign prostatic enlargement, and radiation or chemical cystitis Bladder Vesical stones


With vesical stones there can be a back pressure develop due to obstructionUltrasound of the Kidneys, bladder & prostate

Indications:

Hematuria,


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No specifics with this.Urine culture and sensitivity

Indications:

Cystitis, Pyelonephritis Prostatitis,Significance of abnormal findings and complications:

Demonstrates infecting organism (culture is NOT requires for an acute uncomplicated episode in a young woman)

Renal biopsy

Indications:

Unexplained acute renal failure or chronic kidney dz Acute nephritic syndrome Unexplained proteinuria and hematuria Previously identified and treated lesions to plan future therapy Systemic dz associated with kidney dysfunction such as SLE, Goodpasture syndrome, Wegener granulomatosis Suspected transplant rejection Guide to treatment Used to determine subtypes in nephritic syndrome


Contraindications: solitary or ectopic kidney (exception transplant allograft), horseshoe kidney, uncorrected HTN, renalinfection, renal neoplasm, hydronephrosis, ESRD, congenital anomalies, multiple cysts, or uncooperative pt

After biopsy = nearly all pt have hematuria After percutaneous kidney biopsies a blood transfusion will be necessary due to significant blood loss and more than half of

the pt will have a small hematoma

Nephrectomy and mortality (0.06-0.08% chance)

Objective #2

State the usual etiologies, presentation, associated lab findings by etiology & management for:A. HematuriaB. DysuriaC. Proteinurea

Hematuria

Essentials to diagnosiso May be either grossly visible or microscopic; both require evaluationo The upper urinary tract should be imaged, and cystoscopy should be performed if there is hematuria in the

absence of infection

Etiologieso Upper tract sources (kidneys & ureters)

10% of cases 40% are stone diseases 20% renal disease (medullary sponge kidney, glomerulonephritis, papillary necrosis) 10% renal cell carcinoma 5% urothelial cell carcinoma of the ureter or renal pelvis

Drug ingestion and associated medical problems may provide diagnostic clues Analgesic use= papillary necrosis Cyclophosphamide= chemical cystitis Abx= interstitial nephritis DM, sickle cell trait or disease= papillary necrosis

o In the absence of infection, gross hematuria from a lower tract infection is most commonly from urothelial cellcarcinoma of the bladder

o Microscopic hematuria in the male is most commonly from benign prostatic hyperplasia


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o Hematuria in pts receiving anticoagulation therapy cannot be ascribed to the anticoagulation; a completeevaluation is warranted

o Hematuria may be macroscopic or microscopic Microscopic is defined as excretion of >3 RBCs per high-power field in a centrifuged specimen

o Common causes Glomerular

Glomerulonephritis Medications (esp. NSAIDs)

Hemolytic-uremic syndrome Strenuous exercise

Non-glomerular Renal tumors Cystic kidney disease Papillary necrosis

o Often medications Renal stones Infections Trauma Indewelling catheters

Presentationo If gross hematuria occurs, a description of the timing (initial, terminal, total) may provide a clue to the localization

of disease.

o Associated symptoms should be investigated renal colic, irritative voiding symptoms, constitutional symptoms

o Physical examination should emphasize signs of systemic disease fever, rash, lymphadenopathy, abdominal or pelvic masses & signs of medical kidney disease

(hypertension, volume overload)

o Urologic evaluation may demonstrate an enlarged prostate, flank mass, or urethral diseaseo Severe dehydration- renal vein thrombosiso Peripheral edema- nephritic syndrome, vasculitiso Cardiovascular

MI- renal artery disease HTN- glomerulosclerosis

o Abdomen Bruit- renal artery disase Enlarged prostate- prostatitis, prostatic hypertrophy Flank tenderness- renal stone, infarction

Lab findings by etiologyo Initial laboratory investigations include a urinalysis and urine cultureo Proteinuria and casts suggest renal origino Irritative voiding symptoms, bacteriuria, and a positive urine culture in the female suggest urinary tract infection,

but follow-up urinalysis is important after treatment to ensure resolution of the hematuria

o Further evaluation includes urinary cytology to assist in the diagnosis of bladder neoplasm Management

o In the absence of infection, hematuria (either gross or microscopic) requires evaluationo

Referral to nephrologist or pts with Significant proteinurea (>1g/day) Red cell casts or a predominance of dysmorphic red cells Renal insufficiency

Dysuria

Etiologieso Women

Urethritis, cystitis (all types) & pyelonephritis Vaginitis

o Men Urethritis, cystitis (all types) and pyelonephritis


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Prostatitis Obstruction (prostatic hypertrophy) Arthritis syndromes (reiters syndrome, bechets syndrome)

Presentationo The sensation of pain or burning on urination

Lab findings by etiology Management

Proteinurea(From the article & her notes only, she said not to refer to CMDT for proteinurea)

Etiologies

o Normal urinary proteins include: albumin, serum globulins, and proteins secreted by the nephrono Proteinurea is defined as the excretion of more than 150mg per day (10 to 20mg per dL) & is the hallmark of renal

disease

o Microalbuminuria is defined as the excretion of 30-150mg of protein per day and is a sign of early renal disease,esp. in diabetic pts

o Can be classified as transient or persistento See table 5, p.1157 of the article for a complete list of common causeso The majority of proteinuria is benign, this is termed functional

Dehydration, emotional stress, most acute illnesses or fevers, inflammatory processes, orthostaticdisorders, intense activity, heat injuries

Presentationo Transient

A temporary change in glomerular hemodynamics causes the protein excess Folloes a benign, self-limited course

o Orthostatic (postural) proteinuria is a benign condition that can result from prolonged standing; it is confirmed byobtaining a negative U/A result after 8 hours of recumbancy

o Persistent Divided into 3 general categories: 1. Glomerular 2. Tubular 3. Overflow

Glomerular (most common)o Albumin is the primary urinary proteino Increased glomerular capillary permeability to proteins

Tubularo Results when malfunctioning tubule cells no longer metabolize or reabsorb normally

filtered protein

o Low-molecular weight proteins predominate over albumin and rarely exceed 2g per day Overflow

o Low-molecular weight proteins overwhelm the ability of the tubules to reabsorb filteredproteins (hemoglobin, myoglobin, or immunoglobins)

Further evaluation inclused determination of 24-hour urinary protein excretion or spot urinary protein-creatinine ratio, microscopic examination of the urinary sediment, urinary protein electrophoresis, and

assessment of renal function

Lab findings by etiologyo Dipstick analysis is used for screening and a crude estimate of quantity

False positives can occur from a variety of conditions It preferentially detects the larger proteins, such as albumin

o Twenty-four hour urine collection is used for a more specific quantitative evaluationo Microscopic analysis of the patient with persistent proteinuria is done to assess for etiology by demonstration of

abnormal by-products

Leukocytes or leukocytes casts with bacteria occur in Infections Dysmorphic erythrocytes occur in kidney disease, normal erythrocytes are lower system. Erythrocyte casts

demonstrate glomerular disease

Eosinophiluria demonstrates drug-induced interstitial nephritis Waxy, granular or cellular casts appear in advanced renal disease of any cause. Hyaline casts appear with

dehydration or diuretic therapy

o Adults with proteinuria > 2 grams per twenty-four hours requires measurement of creatinine clearanceo Creatinine Clearance

If creatinine clearance is reduced renal failure is a major possibility and therefore a nephrologyconsultation is in order


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If creatinine clearance is normal, and the patient has a clear diagnosis such as diabetes or congestiveheart failure, treat the underlying disease

Managemento Transient proteinuria

Treat any underlying conditions and reassureo Orthostatic proteinuria

Blood pressure measurement and repeat urinalysis every 1-2 years if under 30 years old and < 2 g/dayo Isolated Proteinuria

If the patient is over 30 years old or have proteinuria not associated with posture, they are higher risk andneeds blood pressure measurements, urinalysis and creatinine clearance every 6 months.

o If they have more than 2 grams per day this is more serious and needs a nephrology consultation.Objective #3

State the etiology, clinical presentation, evaluation, lab and imaging findings, management and complications of the following types

of urinary system infections:

a. Acute Pyelonephritis d. Bacterial Prostatitis (all types)

b. Acute Cystitis e. Nonbacterial Prostatitis

c. Interstitial Cystitis

Acute Pyelonephritis

Essentials of Diagnosiso Fevero Flank Paino Irritative voiding sxo Positive urine culture

Etiologyo Acute pyelonephritis is an infectious inflammatory disease involving the kidney parenchyma and renal pelviso Gram-negative bacteria are the most common causative agents including E coli, Proteus, Klebsiella, Enterobacter

and Pseudomonas

o Gram-positive bacteria are less commonly seeno The infection usually ascends from the lower urinary tract

with the exception of S aureus, which usually is spread by a hematogenous route Clinical Presentation

o Symptoms include fever, flank pain, shaking chills, and irritative voiding symptoms (urgency, frequency, dysuria)o

Associated nausea and vomiting and diarrhea are commono Signs include fever and tachycardiao Costovertebral angle tenderness is usually pronounced

Evaluation Lab findings

o CBC shows leukocytosis and a left shifto Urinalysis shows pyuria, bacteriuria, and varying degrees of hematuriao White cell casts may be seeno Urine culture demonstrates heavy growth of the offending agent, and blood culture may also be positive

Imaging Findingso In complicated pyelonephritis, renal ultrasound may show hydronephrosis from a stone or other source of

obstruction

Managemento Severe infections or complicating factors require hospital admissiono Urine and blood cultures are obtained to identify the causative agent and to determine antimicrobial sensitivityo IV ampicillinand an aminoglycoside are initiated prior to obtaining sensitivity resultso In the outpatient setting, quinolones ornitrofurantoin may be initiatedo Fevers may persist for up to 72 hours

failure to respond warrants imaging (CT or ultrasound) to exclude complicating factors that may requireintervention

o Catheter drainage may be necessary in the face of urinary retention and nephrostomy drainage if there is ureteraobstruction

o In inpatients, IV antibiotics are continued for 24 hours after the fever resolves, and oral antibiotics are then givento complete a 14-day course of therapy
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o Follow-up urine cultures are mandatory following the completion of treatment Complications

o Sepsis with shocko In diabetic patients, emphysematous pyelonephritis resulting from gas-producing organisms may be life

threatening if not adequately treated

o Healthy adults usually recover complete kidney function, yet if coexistent kidney disease is present, scarring orchronic pyelonephritis may result

o Inadequate therapy could result in abscess formationAcute Cystitis

Essentials of Diagnosiso Irritative voiding sxo Pt. usually afebrileo + urine culture, blood cultures may also be +

Etiologyo Acute cystitis is an infection of the bladder most commonly due to the coliform bacteria (especially Escherichia

coli) and occasionally gram-positive bacteria (enterococci)

o The route of infection is typically ascending from the urethrao Viral cystitis due to adenovirus is sometimes seen in children but rare in adultso Cystitis in men is rare and implies a pathologic process such as infected stones, prostatitis, or chronic urinary

retention requiring further investigation

Clinical Presentationo Irritative voiding symptoms (frequency, urgency, dysuria) and suprapubic discomfort are commono Women may experience gross hematuria, and symptoms in women may often appear following sexual intercourseo PE may elicit suprapubic tenderness, but examination is often unremarkableo Systemic toxicity is absent

Evaluation Lab findings

o Urinalysis shows pyuria and bacteriuria and varying degrees of hematuriao The degree of pyuria and bacteriuria does not necessarily correlate with the severity of symptomso Urine culture is positive for the offending organism

Imaging Findingso Because uncomplicated cystitis is rare in men, clarification of the underlying problem with appropriate

investigations, such as abdominal ultrasonography or cystoscopy (or both) is warranted

o F/U imaging using CT scanning is warranted if pyelonephritis, recurrent infections, or anatomic abnormalities aresuspected Management

Infections typically respond rapidly to therapy, and failure to respond suggests resistance to the selecteddrug or anatomic abnormalities requiring further investigation

Uncomplicated cystitis in women can be treated with short-term abx therapy Fluoroquinolones and nitrofurantoin are the drugs of choice for uncomplicated cystitis

In men, uncomplicated UTI is rare & the duration of abx therapy depends on the underlying etiology Hot sitz baths or urinary analgesics may provide symptomatic relief

ComplicationsInterstitial Cystitis

Essentials of Diagnosiso Pain with a full bladder or urinary urgencyo Submucosal petechiae or ulcers on cystoscopic examinationo Dx of exclusion

Etiologyo Characterized by pain with bladder filling that is relieved by emptying and is often associated with urgency and

frequency

o This is a diagnosis of exclusion, and patients must have a negative urine culture and cytology and no other obviouscause such as radiation cystitis, chemical cystitis (cyclophosphamide), vaginitis, urethral diverticulum, or genita

herpes

o Up to 40% of patients referred to urologists for interstitial cystitis may actually be found to have a differentdiagnosis after careful evaluation

o Most patients are women, with a mean age of 40 years at onset
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o Patients with interstitial cystitis are more likely to report bladder problems in childhood, and there appears to be ahigher prevalence in white and Jewish women

o Up to 50% of patients may experience spontaneous remission of symptoms, with a mean duration of 8 monthswithout treatment

o Etiology is unknown, and it is most likely not a single disease but rather several diseases with similar symptomso Associated diseases include severe allergies, IBS, or inflammatory bowel diseaseo Theories regarding the cause of interstitial cystitis include increased epithelial permeability, neurogenic causes

(sensory nervous system abnormalities), and autoimmunity

Clinical Presentationo Most common sx: Pain with bladder filling that is relieved with urination or urgency, frequency, & nocturiao Exposures such as pelvic radiation or prior cyclophosphamideshould be inquired about

Evaluationo Examination should exclude genital herpes, vaginitis, or a urethral diverticulum

Lab findingso Urinalysis and urine culture are obtained to exclude infectious causeso Urinary cytology is obtained to exclude bladder malignancyo Urodynamic testing assesses bladder sensation and compliance and excludes detrusor instability

Imaging Findingso The bladder is distended with fluid to detect glomerulations (submucosal hemorrhage), which may or may not be

present

o Biopsy should be performed to exclude other causes such as carcinoma, eosinophilic cystitis, and tuberculouscystitis

o The presence of submucosal mast cells is not needed to make the diagnosis of interstitial cystitis Management

o There is no cure, but most patients achieve symptomatic relief from one of several approaches Hydrodistention (which is usually done as part of the diagnostic evaluation)

Approximately 2030% of patients will notice symptomatic improvement following thismaneuver. Measurement of bladder capacity during hydrodistention, since patients with very

small bladder capacities (< 200 mL) are unlikely to respond to medical therapy.

o Amitriptyline is often used as first-line medical therapy in patients with interstitial cystitis Complications

Bacterial Prostatitis (all types)

Acute Bacterial Prostatitiso Essentials of Diagnosis

Fever Irritative voiding sx Perineal or suprapubic pain; exquisite tenderness common on rectal exam Positive urine culture

o Etiology Acute bacterial prostatitis is usually caused by gram-negative rods (esp. E coli and Pseudomonas) and less

commonly by gram-positive organisms enterococci)

The most likely routes of infection include ascent up the urethra and reflux of infected urine into theprostatic ducts

Lymphatic and hematogenous routes are rareo Clinical Presentation

Perineal, sacral, or suprapubic pain, fever, and irritative voiding complaints are common. Varying degrees of obstructive symptoms may occur as the acutely inflamed prostate swells, which may

lead to urinary retention

High fevers and a warm and often exquisitely tender prostate are detected on examination Care should be taken in performing a gentle rectal examination, as vigorous manipulations may result in

septicemia

Prostatic massage is contraindicatedo Evaluationo Lab findings

CBC shows leukocytosis and a left shift Urinalysis shows pyuria, bacteriuria, and varying degrees of hematuria
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Urine cultures will demonstrate the offending pathogeno Imaging Findingso Management

Hospitalization may be required, and parenteral antibiotics should be initiated until organism sensitivitiesare available

After the patient is afebrile for 2448 hours, oral antibiotics are used to complete 46 weeks of therapy If urinary retention develops, urethral catheterization or instrumentation is contraindicated, and a

percutaneous suprapubic tube is required

F/U urine culture and exam of prostatic secretions should be performed after the completion of therapyto ensure eradication

o Complications With effective treatment, chronic bacterial prostatitis is rare

Chronic Bacterial Prostatitiso Essentials of Diagnosis

Irritating voiding sx Perineal or suprapubic discomfort, often dull & poorly localized Positive expressed prostatic secretions & culture

o Etiology Although chronic bacterial prostatitis may evolve from acute bacterial prostatitis, many men have no

history of acute infection

Gram-negative rods are the most common etiologic agents only one gram-positive organism (Enterococcus) is associated with chronic infection

Routes of infection are the same as for acute infectiono Clinical Presentation

Clinical manifestations are variable Some patients are asymptomatic, but most have varying degrees of irritative voiding symptoms Low back and perineal pain are not uncommon Many pts report a history of UTIs PE is often unremarkable, though the prostate may feel normal, boggy, or indurated

o Evaluationo Lab findings

Urinalysis is normal unless a secondary cystitis is present Expressed prostatic secretions demonstrate increased numbers of leukocytes However, this finding is consistent with inflammation and is not diagnostic of bacterial prostatitis Leukocyte and bacterial counts from expressed prostatic secretions do not correlate with severity of

symptoms

Culture of the secretions or the postprostatic massage urine specimen is necessary to make the diagnosiso Imaging Findings

Imaging tests are not necessary, though pelvic radiographs or transrectal ultrasound may demonstrateprostatic calculi

o Management Few antimicrobial agents attain therapeutic intraprostatic levels in the absence of acute inflammation Trimethoprim-sulfamethoxazole is associated with the best cure rates Optimal duration of therapy remains controversial, ranging from 6 to 12 weeks Symptomatic relief may be provided by anti-inflammatory agents and hot sitz baths

o Complications Chronic bacterial prostatitis is difficult to cure, but its symptoms and tendency to cause recurrent urinary

tract infections can be controlled by suppressive antibiotic therapy

Nonbacterial Prostatitis

Essentials of Diagnosiso Irritative voiding sxo Perineal or suprapubic discomfort, similar to that of chronic bacterial prostatitiso + Expressed prostatic secretions, but culture is negative

Etiologyo The most common of the prostatitis syndromes, and its cause is unknowno Speculation implicates chlamydiae, mycoplasmas, ureaplasmas, and viruses, but no substantial proof existso Sometimes nonbacterial prostatitis may represent a noninfectious inflammatory or autoimmune disorder


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o Because the cause of nonbacterial prostatitis remains unknown, the diagnosis is usually one of exclusion Clinical Presentation

o The clinical presentation is identical to that of chronic bacterial prostatitis, however, no history of UTI is present Evaluation Lab findings

o Increased numbers of leukocytes are seen on expressed prostatic secretionso All cultures are negative

Imaging Findings Management

o Because of the uncertainty regarding the etiology of nonbacterial prostatitis, a trial of antimicrobial therapydirected against Ureaplasma, Mycoplasma, or Chlamydia is warranted

o Symptomatic relief may be obtained with anti- inflammatory agents or sitz bathso Dietary restrictions are not necessary unless the patient relates a history of symptom exacerbation by certain

substances such as alcohol, caffeine, and perhaps certain foods

ComplicationsObjective 4

State the etiology, clinical presentation, pathophysiology, evaluation, lab and imaging findings, management and complications of

the following types of urinary obstruction or stasis:

a) urinary stone disease b) benign prostatic hypertrophy

Urinary Stone Disease p. 833

Essentials of Diagnosis

Flank pain Nausea and vomiting Identification on noncontrast CTEtiology &

Pathophysiology

Men > women Most commonly presents in 3rd or 4th decade Men = women in 6th and 7th decade 5 major types of stones:

Calcium oxalate Calcium phosphate Struvite Uric acid Cystine

Stone formation requires saturated urine that is dependent on: pH Ionic strength Solute concentration Complexation

Geographic factors: areas of high humidity and elevated temperatures Incidence is greatest during hot summer months

Diet and fluid intake: Increased sodium intake will:

Increase sodium and calcium excretion Increase monosodium urate saturation Increase relative saturation of calcium phosphate Decrease urinary citrate excretion

All of these factors encourage stone growth Increased protein load can also increase calcium, oxalate, and uric acid excretion and

decrease urinary citrate excretion

Carbs and fats have no impact on stone formation Bran decreases urinary calcium

Persons in sedentary occupations have higher incidence than manual laborers Genetic factors may contribute: cystinuria & distal renal tubular acidosis

Clinical Presentation Usually present with colic Pain occurs suddenly and may awaken patients from sleep
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Localized to the flank, severe, may be associated with N/V May be episodic and radiate anteriorly over the abdomen

Pts constantly moving As the stone progresses down the ureter pain may be referred to the ipsilateral testes or labium If lodged at the ureterovesicular junction: urinary urgency and frequency Stone size does not correlate with severity of symptoms

Evaluation Stone analysis should be performed on recovered stones 1st time stone-formers:

blood screening for:

calcium phosphate electrolytes uric acid

Recurrent stone-formers or those with a family hx: 24-hour urine collection

volume urinary pH calcium uric acid oxalate phosphate sodium citrate

Serum parathyroid and calcium load tests can be doneLab & Imaging

Findings

Urinalysis Microscopic or gross hematuria (but the absence of microhematuria does not exclude

urinary stones)

pH is a valuable clue to the cause of the stone persistent pH below 5.5 is suggestive of uric acid or cystine stones a pH above 7.2 is suggestive of a struvite infection stone

Plain film of the abdomen and renal ultrasound will diagnose most stones CT scan is 1st line for evaluating flank pain (all stones are visible on CT)

Management Medical tx One must attempt to achieve a stone-free status

Small stone fragments may serve as a nidus for future stone development Increase fluid intake

During meals, 2 hours after each meal, prior to going to sleep, and throughout thenight

Tx underlying reason why stones formed Calcium nephrolithiasis

o Hypercalciuric Cellulose phosphate Thiazides

o Hyperuricosuric Purine dietary restrictions Allopurinol

o Hyperoxaluric Oral calcium supplements

o Hypocitraturic Potassium citrate supplements

Uric acid calculio Potassium citrate

Struvite calculio Appropriate abx

Cystine calculio Increased fluid intake


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o Monitor urine pHo Penicillamine and tiopronin

Surgical tx Ureteral stones

Stones < 6mm will usually pass spontaneously Conservative observation with appropriate pain meds is appropriate for the first 6

weeks

Distal ureteral stoneso

Ureteroscopic stone extractiono In situ extracorpeal shock wave lithotripsy (SWL)

Proximal and midureteral stoneso SWL or ureteroscopy

Renal stones Those that present without pain, urinary tract infections, or obstruction need not

be treated

Growing calculi or symptomatic pts should be treatedo < 2 cm: SWLo Larger diameter: percutaneous nephrolithotomy

Complications UnknownBenign Prostatic Hyperplasia p. 842


Obstructive or irritative voiding symptoms May have enlarged prostate or rectal examination Absence of urinary tract infection, neurologic disorder, stricture disease, prostatic or bladder malignancyEtiology &

Pathophysiology

Most common benign tumor in men Incidence is age related Symptoms of prostatic obstruction are also age related

55 yo: 25% report voiding sx 75 yo: 50% report a decrease in force and caliber of stream

Risk factors poorly understood Heritable form most likely autosomal dominant

Clinical Presentation Obstructive complaints Hesitancy Decreased force and caliber of stream Sensation of incomplete bladder emptying Double voiding: urinating a second time within 2 hours Straining to urinate Postvoid dribbling

Irritative symptoms Urgency Frequency Nocturia

Evaluation AUA symptom index: single most important tool for evaluation Should be calculated in all patients before starting therapy Score can range from 0-35

Detailed hx focusing on the urinary tract to rule out: UTI, neurogenic bladder, or urethral stricture Physical exam, DRE, neurologic exam

Prostate size does not correlate with the severity of symptoms or degree of obstruction Benign: smooth, firm, elastic enlargement of the prostate Cancer: induration

Lower abdomen exam should be done to assess the bladderLab & Imaging

Findings

Urinalysis Serum PSA Upper tract imaging (IVU, CT, ultrasound) Flow rates, postvoid residual urine determination, pressure-flow studies


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optionalManagement Watchful waiting: Pts with mild symptoms (AUA score 0-7)

Some men undergo spontaneous improvement or resolution of sx Medical Therapy

a-blockers prazosin, terazosin, doxazosin

5a-reductase inhibitors finasteride

Combination therapy

Phytotherapy The use of plants or plant extracts for medical purposes Saw palmetto berry, bark of pygeum africanum, etc. (p. 846 if youre really

interested)

Surgery: refractory urinary retention, large bladder diverticula, recurrent UTIs, recurrent grosshematuria, bladder stones, or renal insufficiency

Transurethral resection of the prostate (TURP) Transurethral incision of the prostate (TUIP) Open simple prostatectomy Laser therapy Transurethral needle ablation of the prostate (TUNA) Transurethral electrovaporization of the prostate Hyperthermia

Complications UnknownObjective 5


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Diabetic Nephropathy

Essentials of Diagnosis:

*prior evidence of diabetes mellitus

* albuminuria (micro or macroscopic) not due to another renal disorder

*signs of diabetic nephropathy on renal biopsy, if done.

*other end organ damage common, such as diabetic retinopathy, but not required.

History -Most common cause of ESRD in U.S.

-ESRD is much more likely to develop in persons with type 1 diabetes mellitus

-High risk pts: males, AA, Native Americans

Clinical Presentation

&

Examination

-Pts will usually have enlarged kidneys due to cellular hypertrophy and proliferation.

-The most common lesion is diffuse glomerulosclerosis

-Nodular glomerulosclerosis is PATHOGNOMONIC!! (aka Kimmelstiel-Wilson nodules)

-Diabetic retinopathy is often present

Work-up -Initial screening of diabetics should always include urine examination for microalbuminuria.

-24 hour urine collection is the accepted standard measure.

-Can also test via an early morning spot urine albumin or albumin-creatinine ratio. (more than 30mg-1g is

abnormal)

Complications -Pts prone to other renal dzs such as papillary necrosis, chronic intersititial nephritis, and type 4 renal tubularacidosis

-Pts more susceptible to acute renal failure from contrast material

Prognosis -poor prognosis once dialysis has begun.

Management -Aggressive tx during the onset of microalbuminuria (before onset of clinical proteinuria)

-Strict glycemic control

-tx of HTN with ACE and ARBs

Analgesic Nephropathy p 822

**dont need to worry about other types ofdrug induced nephropathy**

History-Most commonly seen in pts who ingest a large amt of analgesic combinations; esp for chronic HA, muscular pains, a

arthritis.

-Causative drugs: phenacetin, paracetamol, aspirin, and NSAIDs.

-Ingestion of 1g/d X 3 yrs si the typical amt needed for renal dysfxn.

S/Sx -~50% present in acute renal failure

-flank pain, hematuria, fever

-+/- polyuria w/ dehydration

-anemia

-edema (if Na+ retention)

-Nephrotic syndrome if dz is advanced

Clinical

Presentation

&Examination

-Tubulointerstitial inflammation and papillary necrosis are seen on pathologic examination.

-Papillary tip and inner medullary concentrations of some analgesic are 10 fold higher than in the renal cortex.

-Aspirin and other NSAIDs may worsen the damage by decreasing medullary blood flow and decreasing glutathionelevels.

-May have sloughed papillae in the urine.

-Ring Shadow sign at the papillary tip

-broad waxy casts are often present.

-Hyperkalemic

-Hyperchloremic renal tubular acidosis is characteristic

-Pts can exhibit hematuria, mild proteinuria, polyuria, anemia, and sterile pyuria

-Na+ retention and edema

-acute renal insufficiency or failure

-Nephortic syndrome with interstitial nephritis


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Objective 6

State the etiology, clinical presentation, laboratory and imaging findings, management and complications of:

a) acute tubular necrosis b) interstitial nephritis c) glomerulonephritis (both types)

Acute Tubular Necrosis p. 799


Acute kidney injury Clinical scenario consistent with diagnosis (ischemic or toxic insult) Urine sediment with pigmented granular casts and renal tubular epithelial cells is pathognomonic but not essentialEtiology &

Pathophysiology

Acute renal failure due to tubular damage Accounts for 85% on intrinsic acute renal failure 2 causes: ischemia and nephrotoxin exposure

Ischemia: causes damage from states of low perfusion and is often preceded by a state ofprerenal azotemia

inadequate GFR and renal blood flow to maintain parenchymal cellular formation prolonged hypotension or hypoxemia (dehydration, shock, sepsis) Major surgical procedures can involve prolonged periods of hypoperfusion

Nephrotoxins: exogenous > endogenous Exogenous: anminoglycosides, amphotericin B, radiographic contrast material,

NSAIDs, ACE inhibitors, cyclosporine, heavy metals

Endogenous: myoglobinuria (from rhabdomyolysis), hemoglobin, hyperuricemia,Bence Jones protien (multiple myeloma)

Clinical Presentation Same as acute renal failureEvaluation/

Lab & Imaging

Findings

Urinalysis Urine may be brown May show pigmented granular casts or muddy brown casts

Renal tubular epithelial cells and epithelial cell casts may also be present Hypekalemia and hyperphosphatemia common

Management Preventative measures: to avoid volume overload and hyperkalemia Loop diuretics (furosemide)

When to refer: Pt with acute renal failure should be referred to a nephrologist when the etiology is unclear

or renal fxn continues to worsen despite intervention

If fluid, electrolyte, and acid-base abnormalities are recalcitrant to interventions Nephrology referral improves outcome in acute renal failure

o When to admit: When pt has signs or symptoms of acute renal failure that require immediate intervention

-Papillary necrosis

Work-up -Urinalysis

-Renal Fxn test

-IVP

-Radiographs

Labs -Urinalysis: hematuria, low levels of proteinuria and proteinaceous casts. Neutrophils and cellular debris

-Renal Fxn test: Elevated BUN and Creatinine

-Radiographs: non-specific, KUB may show small flecks of Ca++ in the kidney (dystrophic calcification)

-IVP: egg in cup focal necrosis, lobster claw calyces, scarring, sloughing and calcification of papilla and renal stoneComplications -HTN, obstruction from necrotic papillae or calcium, anemia, frequent UTIs, medication toxicities

Prognosis

Management -W/drawl from analgesics

-stablization or improvement of renal fxn may occur if significant interstitial fibrosis is not present.

-Hydration during exposure of analgesics may help.

-Mostly supportive.

-Dialysis if severe poisoning is present


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such as IV fluids, dialytic therapy, or a team approach cannot be coordinated as an

outpatient

Complications UnknownInterstitial Nephritis p. 801


Fever

Transient maculopapular rash Acute renal insufficiency Pyuria (including eosinophilia), whit blood cell casts, and hematuriaEtiology &

Pathophysiology

10-15% of intrinsic renal failure Interstitial inflammatory response with edema and possible tubular damage

T lymphocytes can cause direct cytotoxicity or release lymphokines that recruit monocytesand inflammatory cells

Drugs account for 70% of cases PCN, cephalosporins, sulfonamides and sulfonamide-containing diuretics, NSADIs, rifampin,

phenytoin, allopurinol, PPIs

Can also be caused by: infectious diseases, immunologic disorders, or idiopathic condition Infections: streptococcal infxn, leptospirosis, cytomegalovirus, histoplasmosis, Rocky

Mountain spotted fever

Immunologic: glomerulonephritis, systemic lupus erythematosus, Sjogren syndrome,sarcoidosis, cryoglobulinemia

Clinical Presentation Fever Rash Arthralgias

Evaluation UnknownLab & Imaging

Findings

Peripheral blood eosinophilia Urinalysis

Red cells, white cells, and white cell casts Modest proteinuria (usually NSAID induced) Eosinophiluria

Management Supportive measures and removal of the inciting agent Short course of corticosteroids may be used

Prednisone or methylprednisoloneComplications None. Good prognosis. Rarely, some progress to ESRDGlomerulonephritis

Acute Glomerulonephritis p. 802


Hematuria, dysmorphic red cells, red cell casts, and mild proteinuria Dependent edema and hypertension Acute renal insufficiencyEtiology &

Pathophysiology

Uncommon cause of renal failure (5%) Inflammatory glomerular lesions

Mesangioproliferative, focal and diffuse proliferative, and crescentric lesions Categorization of acute glomerulonephritis can be done by serologic analysis

Cytoplasmic antibodies Moderate antigen excess over antibody production occurs Causes include:

o IgA nephropathy (Bergers disease)o Peri-infectious or post-infectious glomerulonephritiso Endocarditiso Lupus nephritiso Cryoglobulinemic glomerulonephritis (hep C virus)


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o Membranoproliferative glomerulonephritis Anti-GBM antibodies

Confined to kidneys or associated with pulmonary hemorrhage Goodpasture syndrome autoantibodies aimed against type IV collagen in the GBM rather than to immune

complex deposition

Other immune markers of disease Pauci-immune acute glomerulopnephritis

o Due to cell-mediated immune processes Vascular causes

o Malignant HTNo Thrombotic microangiopathies (hemolytic uremic syndrome & TTP)

Clinical Presentation Pts are usually hypertensive and edematous Edema first presents in body parts with low tissue tension (periorbital and scrotal regions)

Evaluation 24 hour urine for protein excretion and creatinine clearance however, in cases of rapidly changing serum creatinine values, urinary creatinine clearance

is an unreliable marker of GFR

Further tests: Complement levels (C3, CA, CH50) ASO titer Anti-GBM antibody levels ANCAs Antinuclear antibody titers Cryoglobulins Hepatitis serologies Blood cultures Renal ultrasound Renal biopsy (occasionally)

Lab & Imaging

Findings

Urinalysis Hematuria Moderate proteinuria (usually < 3 g/d) Cellular elements: red cells, red cell casts, and white cells Red cell casts are specific for glomerulonephritis

Management High dose corticosteroids and cytotoxic agents (cyclophosphamide)Complications Postinfectious Glomerulonephritis p. 811


Proteinuria Glomerular hematuria Symptoms 1-3 weeks after infectionEtiology &

Pathophysiology

Most often due to infxn with nephritogenic group A B-hemolytic strep, especially type 12 Onset occurs within 1-3 weeks after infection (average 7-10 days) Other causes:

Bacteremic states (systemic S. aureus ifxn), infective endocarditis, shunt infections, heptatisB or C, cytomegalovirus, mononucleosis, coccidioidmycosis, malaria, toxoplasmosis


& Evaluation

Pt is oliguric, edematous, and variably hypertensiveLab & Imaging

Findings

Serum complement levels low ASO titers can be high in strep infxn Urinalysis

Cola-colored urine Red blood cells and red cell casts Proteinuria < 3.5 g/d

Immunofluorescence IgG and C3 in granular pattern in the capillary basement membrane


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Electron microscopy Large, dense subepithelial deposits or humps

Management Supportive Appropriate abx should be used Antihypertensives, salt restriction, and diuretics if needed

Complications Adults prone to crescent formation and chronic renal insufficiency Rapidly progressive glomerulonephritis in < 5% Smaller percentage will progress to ESRD

Objective 7

State the etiology, risk factors, clinical presentation, laboratory and imaging findings, management and complications of Nephritic

and Nephrotic Syndrome.

Nephritic Syndrome


Edema Hypertension Hematuria (with or without dysmorphic red cells, red blood cell casts)Etiology Due to an acute inflammatory process in the glomeruli that causes renal dysfunction over days to weeks

and may or may not resolve.

Subtypes (based on how dz presents)o If severe (rapidly progressive glomerulonephritis)= 50% loss of nephron fxn over just a few

weeks. Can cause permanent damage to glomeruli (necrosis, fibrosis, etc.).

RPGN I: Anti-GBM dz (Goodpastures, Masugi, etc.) (20% of RPGN cases) The patient makes antibodies against an antigen uniformly distributed along

the GBM.

RPGN II: Severe immune complex disease (any of these diseases can produce RPGN if itis severe enough)

o Acute (postinfectious) glomerulonephritis = produces the nephritic syndrome two weeksfollowing a respiratory or skin infection with streptococcus.

Commonly appears after pharyngitis or impetigo (1-3 weeks post-infection; average 7-10 days)

o Prolonged inflammation = chronic glomerulonephritis with persistent renal abnormalities thatlead to ESRD.

Clinical

Presentation

&

Examination

Mild edema in low tissue pressure areas (periorbital, scrotal area). Hypertension due to volume overload not vasoactive substances (angiotensin II - this substances are low

in the body).

Oliguria Proteinuria (3-5g/day) RPGN I: Patients experience hemoptysis, dyspnea, and possible respiratory failure. RPGN II:

o Causes: Lupus vasculitis, Henoch-Schonlein (IgA nephropathy = gross hematuria turning to coca-cola colored urine, and purpura on the skin), and the vasculitis of subacute bacterial

endocarditis.

RPGN III: the vasculitis syndromeso Systemic inflammatory disease symptoms, including fever, malaise, and weight loss.

Work-up Laboratory Findings: No serum chemistries characteristic of nephritic syndrome. Special tests: complement levels, antinuclear antibodies (ANA), cryoglobulins, hepatitis

serologies, ANCA, anti-GBM antibodies (diagnostic), antistreptolysin O (ASO) titers, and C3

nephritic factor.

Urinalysis: Hematuria: dysmorphic red blood cells and red blood cell casts. Proteinuria (3-5 g/day) **If you place the patient in the lordotic position for an hour it increases the sensitivity for


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finding red cell casts in the next urine sample.

Biopsy: Do if no contraindications (bleeding disorder, thrombocytopenia, uncontrolled HTN) When > 50% of the glomeruli contain crescents = rapidly progressive glomerulonephritis Type of dz can be categorized based on the immunofluorescent pattern and appearance on

electron microscopy from biopsy.

Complications Renal failureManagement Reduction of HTN and fluid overload

Salt and water restriction Diuretic therapy (cautiously; inpatient) Possibly dialysis Possibly corticosteroids and cytotoxic agents (if glomerular injury is present) Treatment of uremia Specific therapeutic maneuvers aimed at the underlying cause.

Nephrotic Syndrome


Urine protein excretion > 3.5 g/1.73 m2 per 24 hours. Hypoalbuminemia (albumin < 3 g/dL). Peripheral edema.Etiology Indicates excessive permeability of the filtration membrane to plasma proteins.

1/3 of patients with nephrotic syndrome have a systemic renal dz such as DM, amyloidosis, or systemiclupus erythematosus.

Subtypes of nephritic syndrome (need biopsy for dx) Minimal change disease: seen in children or adults with Hodgkins lymphoma (good prognosis) Focal Segmental Glomerulosclerosis: seen in HIV, heroin abuse and chronic reflux nephropathy

(poor prognosis)

Membranous nephropathy: seen in carcinoma, Hodgkins lymphoma, lupus erythematosis Membranoproliferative Glomerulonephropathy

Clinical

Presentation

&

Examination

Heavy proteinuria (> 3.5 g/1.73 m2 per 24 hours) Frothy urine Hypoalbuminemia ( 3.5g/day) Frothy urine Hypoalbuminemia (


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Useful for prognosis and treatment of systemic renal dz Blood chemistries:

Decreased serum albumin (


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U/A may show hematuria and mild proteinuria Anemia, Elevated BUN & Creatinine in serum Dilute urine late in disease If infected bacteriuria and pyuria

Imaging

In patients with PKD1, Ultrasonography confirms the Dx- 2+ cysts in Pts < 30yo (sensitivity is 88.5%). 2+ cysts in each kidney in Pts 30 -59 (sensitivity 100%). 4 or more in Pts 60

years or older is diagnostic of autosomal dominant polycystic kidney disease.

If sonography is unclear, a CT scan is highly recommended and highly sensitiveManagement Fluid intake at 3000mL + low protein diet (0.5-0.75g/kg/d) is indicated as BUN rises. Avoiding caffeine may help prevent cysts. To treat the PAIN bed rest & analgesics are recommended. Cyst decompression (only if obstructing urine flow, otherwise not

effective) can help with chronic pain.

HEMATURIA typically resolves in 7d with bed rest an hydration RENAL INECTION CT scan can be helpful to diagnose. Bacterial cyst infxns are difficult to treat Abx with cystic penetration

should be used, eg, fluoroquinolones, TMP-SMX, and chloramphenicol. Tx may be 2 weeks parenteral + long term oral therapy

NEPHROLITHIASIS primarily calcium oxalate stones. Treat with hydration (2-3L/day) HTNshould be treated aggressively because is will prolong the time to ESRD (diuretics should be used cautiously) CEREBRAL ANEURYSM elective surgery Supportive Tx in for renal function (dialysis in late stage due to renal insufficiency)

Complications Abdominal or flank PAIN caused by infxn, bleeding into cysts and nephrolithiasis HEMATURIA caused by cyst rupture into renal pelvis, but can be caused by renal stone or UTI.

- Recurrent bleeding may suggest the possibility of underlying renal cell carcinoma (especially age > 50)

RENAL INFECTION suspected in Pt with flank pain, fever, and leukocytosis. Blood culture may be (+) while urinalysis is (-) becausethe cyst does not contact the urinary tract directly.

NEPHROLITHIASIS HTN(50% of Pts have at time of presentation) cyst induced ischemia causes activation of the rennin-angiotensin system, and

cyst decompression can lower BP temporarily. HTN and cardiac complication controlled with antihypertensives

10-15% of Pts have arterial CEREBRAL ANEURYSMS in the circle of Willis. Screening Arteriography not recommended unless Pthas a FHx or is undergoing elective surgery

Other problems mitral valve prolapsed in up to 25% of Pts, aortic aneurysms, aortic valve abnormalities, colonic diverticulaMedullary Sponge Kidney**dont confuse this with Medullary Cystic disease which is rare and autosomal recessive

Caused by autosomal dominant mutation in the MCKD1 or MCKD2 genes on chromosomes 1 and 16 respectively Relatively common and benign d/o that is not usually Dx until the 4 th or 5th decade, usually found incidentally on exam or X-ray It is a result of cystic dilation in the collecting tubules


Kidneys have a marked irregular enlargement of the medullary and interpapillary collecting ducts- This is associated with diffuse medullary cysts that give a Swiss cheese appearance

Present with gross or microscopic hematuria, recurrent UTIs or kidney stones Common abnormalities are a decreased urinary concentrating ability and nephrocalcinosis Incomplete type I distal renal tubular acidosis is a less common occurrence Colicky renal pain (generally from stones) Hematuria Resistant UTIs

Lab findings

Labs are usually normal, with occasional bacteriuria, hematuria, and crystals. Renal functions are NORMAL X-rays demonstrate lucencies on KUB and filling defects on IVP. Ultrasound demonstrates the small cysts well. CT scan is excellent at demonstrating the cyst.

Imaging

Dx is confirmed with IVP this shows striations in the papillary portions of the kidney produced by the accumulation of contrastin the dilated colleting ducts

Management


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There is no known therapy Adequate fluid intake (2L/d) helps prevent stone formation If hypercalciuria is present thiazide diuretics are recommended because they decrease calcium excretion Alkali therapy is recommended is renal tubular acidosis is present Management needed for the complicating factors of increased stone formation and resistant UTIs Underlying disease is usually benign, only a small %,


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Etiology Affects up to 20 million Americans OR 1 in 9 adults Most are unaware of the condition because they remain asx until disease has significantly progressed >70% of cases of late stage (stage 5) are due to DM or HTN Glomerulonephritis, cystic diseases and other urologic diseases account for 12% 15% of pts have other/unknown causes Rarely reversible and leads to progressive decline in renal fxn Reduction in renal mass lead to hypertrophy of remaining nephrons w/ hyperfiltration GFR transiently at supranormal levels in hypertrophied nephrons Burden placed on remaining nephrons progressive glomerular sclerosis/interstitial fibrosis Hyperfiltration may worsen renal fxn BUTdecreased renal mass in kidney donors NOT assoc. w/ chronic kidney disease

Clinical

Presentation

Sxs often develop slowly and are nonspecific (see Table 22-7 Below) Individuals can remain asx until renal failure is far advanced (GFR < 10-15 mL/min) Manifestations:

- Fatigue- Weakness- Malaise

GI complaints (common):- Anorexia- N/V- Metallic taste in mouth- Hiccups

Neuro problems:- Irritability- Difficulty concentrating- Insomnia- Subtle memory defects- Restless legs- Twitching

Pruritus is common and difficult to tx As uremia progresses you see:

- Decreased libido- Menstrual irregularities- Chest pain from pericarditis- Paresthesias

Sxs of drug toxicity esp. for drugs renally excreted inc. as renal clearance worsens Physical exam

- Pt appears chronically ill- Yellow skin and easy bruisability- HTN common- Uremic fetor characteristic fishy odor of the breath- Cardiopulmonary signs rales, cardiomegaly, edema, & pericardial friction rub- Mental status varies from decreased concentration to confusion, stupor, & coma- Myoclonus and Asterixis are additional signs of uremic fx on CNS

Uremia used for this clinical syndrome but exact cause remains unknown BUN & SCr considered markers for unknown toxins In any pt it is important to identify and correct all reversible causes UTIs, obstruction, ECF volume depletion, Nephrotoxins, HTN, and CHF should be excluded (can worsen underlyin

chronic renal failure

Laboratory

&

Imaging

Findings

Labs:

Dx of renal failure made by documenting elevations of BUN & SCr concentrations Evidence of previously elevated BUN & Cr, abnormal prior urinalyses, and stable but abnormal SCr on successive

days is most consistent w/ chronic process

Anemia, metabolic acidosis, Hyperphosphatemia, hypocalcemia, and hyperkalemia can occur with bothacute/chronic renal failure

U/A shows Isosthenuria


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Urinary sediment can show broad waxy casts as a result of dilated, hypertrophic nephronsImaging:

Small echogenic kidneys bilaterally (< 10cm) by U/S supports dxManagement

&

When to Refer

Protein restriction- Slows progression of ESRD- Must be careful of Cachexia

Salt and water restriction- Kidney unable to adapt to large changes in Na intake- Daily intake of 1-2L of fluid maintains water balance

Potassium restriction- Needed once GFR has fallen below 10-20mL/min

Phosphorus restriction- Should be kept below 4.6mg/dL predialysis and 5.5 mg/dL when on dialysis- Limits foods rich in phosphorus (colas, eggs, dairy products, & meat)

Magnesium restriction- Excreted mainly by kidneys- All Mg-containing laxatives/antacids are contraindicated in renal failure

Dialysis Kidney Transplant

Complications Hyperkalemia

Acid-Base Disorders Cardiovascular Complications

- Hypertension- Pericarditis- CHF

Hematologic Complications- Anemia- Coagulopathy

Neurologic Complications Disorders of Mineral Metabolism Endocrine Disorders

Table 22-7: Symptoms and signs of uremia (she said to know this)

Organ System Symptoms Signs

General Fatigue, weakness Sallow-appearing, chronically ill

Skin Pruritis, easy bruisability Pallor, ecchymoses, excoriations,

xerosis

ENT Metallic taste in mouth, epistaxis Urinous breath

Eye Pale conjunctiva

Pulmonary Shortness of breath Rales, pleural effusion

Cardiovascular Dyspnea on exertion, retrosternal pain

on inspiration (pericarditis)

Hypertension, cardiomegaly, friction

rub

Gastrointestinal Anorexia, nausea, vomiting, hiccups

Genitourinary Nocturia, impotence Isosthenuria*Neuromuscular Restless legs, numbness and cramps in

legs

Neurologic Generalized irritability to concentrate,

decreased libido

Stupor, Asterixis, myoclonus,

peripheral neuropathy

*Isosthenuria = a fixed specific gravity because the kidney is unable to dilute or concentrate the urine

Acute Renal Failure (ARF) aka Acute Kidney Injury



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*Sudden increase in BUN or serum creatinine

*Oliguria often associated

*Symptoms and signs depend on cause

Etiology Defined as a sudden decrease in renal fxn, resulting in an inability to maintain fluid and electrolyte balance and toexcrete nitrogenous wastes

SCr is a convenient marker- SCr will inc. by 1-1.5 mg/dL daily in absence of fxning kidneys- Can inc more rapidly in conditions like Rhabdomyolysis (up to 9x)

Can be divided into three categories:- Prerenal azotemia

o Most common cause of ARF (40-80% of cases)o Due to renal hypoperfusiono Appropriate physiologic changeo If immediately reversed w/ renal blood flow restored renal parenchymal damage does NOT occuro If hypoperfusion persists ischemia intrinsic renal failureo Decreased renal perfusion occurs in one of three ways:

Dec. in intravascular volume Causes of volume depletion include:

o Hemorrhageo GI losseso Dehydrationo Excessive diuresiso Extravascular space sequestrationo Pancreatitiso Burnso Traumao Peritonitis

Change in vascular resistance Occur systematically with:

o Sepsiso Anaphylaxiso Anesthesiao Afterload-reducing drugs (ACEIs, NSAIDs, EPI, NorEPI, high-dose dopamine,

cyclosporine) Renal artery stenosis causes increased resistance and decreased perfusion

Low cardiac output State of low effective renal arterial blood flow Occurs in states of:

o Cardiogenic shocko CHFo PEo Pericardial tamponadeo Arrhythmias & valvular disorderso Positive pressure ventilation (ICU setting)

- Intrinsic renal diseaseo Account for 50% of all cases of ARF o Aka parenchymal dysfxno Considered after prerenal & postrenal causes excludedo Sites of injury include:

Tubules Insterstitium Vasculature Glomeruli

- Postrenal azotemiao Least common cause of ARF (5-10% of cases)o Important to detect because of its reversibilityo Occurs when urinary flow from both kidneys, or single fxning kidney, is obstructed


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o Each nephron has elevated intraluminal pressure dec. GFRo Causes include:

Urethral obstruction Bladder dysfxn/obstruction Obstruction of both ureters/renal pelvises In men, benign prostatic hyperplasia is most common cause Pts taking anticholinergic are at higher risk Bladder, prostate, & cervical cancers Retroperitoneal processes Neurogenic bladder

o Less common causes blood clots, bilateral ureteral stones, urethral stones/stricture, bilateral papillarynecrosis

Clinical

Presentation

Uremic milieu of ARF can cause specific sx When present, sx often due to azotemia or underlying cause Azotemia can cause:

- N/V- Malaise- Altered sensorium

HTN rare, but fluid homeostasis often altered Hypovolemia can cause prerenal disease Hypervolemia results from intrinsic/postrenal disease

- May cause rales during lung exam Pericardial effusions/friction rub may be present with azotemia may result in cardiac tamponade Arrhythmias occur (hyperkalemia) Nonspecific diffuse abdominal pain/ileus and platelet dysfxn may be present bleeding more common in these p Neuro exam

- Encephalopathic changes- Asterixis- Confusion- Seizures

Postrenal Azotemia- Pts may be anuric or polyuric- May complain of lower abdominal pain- Obstruction can be partial, intermittent, or complete- Pt may have enlarged prostate, distended bladder, or mass detected on pelvic exam

Laboratory

&

Imaging

Findings

Elevated BUN & creatinine present (does not distinguish ARF from CRF) Hyperkalemia occurs from impaired renal K+ excretion ECG

- Peaked T waves- PR prolongation- QRS widening- Long QT segment seen with hypocalcemia

Anion gap metabolic acidosis Hyperphosphatemiaoccurs when phosphorus cant be secreted by damaged tubules w/ or w/o cell catabolism Hypocalcemia w/ metastatic Ca phosphate deposition may be observed when product of Ca and phosphorus >

70mg/dL Anemia occurs as result of dec. EPO production over wks assoc. platelet dysfxn Prerenal Azotemia

- BUN:creatinine ratio will exceed 20:1 bc of inc. urea reabsorption- With dec. GFR the kidney will reabsorb water/salt avidly if no intrinsic tubular dysfxn

Postrenal Azotemia- May initially reveal high urine osmolality, low urine Na, & high BUN:creatinine ratio- Urine Na will inc. after several days as kidneys fail and cannot concentrate urine isosthenura- Urine sediment usually benign- Pts should undergo bladder ultrasonography and bladder cath of hydroureter/hydronephrosis present with

enlarged bladder


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Management

&

When to Refer

Identifying cause is 1st step towards tx the pt Prerenal Azotemia

- Depends on cause but always:o Maintenance of euvolemiao Pay attn to serum K+o Avoid nephrotoxic drugs

- Careful assessment of volume status, drug usage, and cardiac fxn Postrenal Azotemia

-Pts usually undergo postobstructive diuresis

care should be take to avoid dehydration

- Prompt tx of obstruction w/in days by cath, stents, or other surgical procedures can result in complete reversaof acute process

Table 22-4: Classification & Differential Diagnosis of ARF

Prerenal

Azotemia

Postrenal

Azotemia

Intrinsic Renal Disease

Acute Tubular

Necrosis

Acute

Glomerulonephritis

Acute Interstitial

Nephritis

Etiology Poor renal

perfusion

Obstruction of

urinary tract

Ischemia,

Nephrotoxins

Poststreptococcal;

collagen-vascular

disease

Allergic rxn; drug rxn

Serum

BUN:Cr ratio

>20:1 >20:1 20:1 500


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Normochloremic MA usually results from addition to blood of nonchloride acids like- Lactate- Acetoacetate- Beta-hydroxybutyrate- Exogenous toxins

Lactic Acidosis- Lactic acid formed from pyruvate in anaerobic glycolysis- Most lactate produced in tissues with high rates of glycolysis (gut, skeletal muscle, brain, skin, and RBCs)-

Normal Functiono Lactate levels stay low (1 mEq/L)o Metabolism by liver thru gluconeogenesis or oxidationo Kidneys metabolize ~30%

- Lactic Acidosiso Lactate levels are at least 4-5 mEq/L but commonly up to 10-30 mEq/Lo Mortality exceeds 50%o Two types of lactic acidosis (both assoc. w/ inc. lactate production & dec. lactate utilization):

Type A (hypoxic) More common type Results from

o Poor tissue perfusiono Cardiogenic, septic, or hemorrhagic shocko Carbon Monoxide or cyanide poisoning

Cause lactic acid production to inc. peripherally AND hepatic metabolism of lactate to decreaas liver perfusion declines

Severe form impairs liver to extract perfused lactate Type B

May be due to metabolic causeso DMo Ketoacidosiso Liver diseaseo Renal failureo Infectiono Leukemiao

Lymphomao Toxicity (ethanol, methanol, salicylates, metformin)

Nutritional problems are an important cause (parenteral nutrition w/o thiamine is cause bc oderanged metabolism of pyruvate)

Seen in AIDS pts Idiopathic seen in debilitated pts and has extremely high mortality rate

Diabetic Ketoacidosis- Characterized by hyperglycemia and MA (pH


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- Common d/o of chronically malnourished pts who consume large quantities of alcohol daily- Usually have mixed acid-base d/o- Decreased bicarb is usual- 50% of pts have normal or alkalemic pH- Three types of MA seen in alcoholic ketoacidosis:

o Ketoacidosis due to beta-hydroxybutyrate and acetoacetate excesso Lactic acidosis inc. NADH:NAD ratio causes inc. production/dec. utilization of lactateo Hyperchloremic acidosis from bicarb loss in urine assoc. with ketonuria

- of the pts have either hyperglycemia or hypoglycemia- When serum glucose levels are >250 mg/dL, the distinction from diabetic ketoacidosis is hard- Dx of alcoholic ketoacidosis supported by absence of DM hx and by no evidence of glucose intolerance after ini

therapy

Toxins- Multiple toxins/drugs can inc. anion gap by inc. endogenous acid production (ethanol, methanol, salicylates,

metformin)

Uremic Acidosis- At GFR < 20mL/min, the inability to excrete H+ w/ retention of acid anions results in inc. anion gap acidosis (rar

severe)

- Unmeasured anions replace bicarb- Hyperchloremic normal anion gap acidosis develops in earlier stages of CKD

Normal Anion Gap Acidosis Hallmark of this d/o is that the low bicarb of MA is assoc. with hyperchloremia, so anion gap remains normal Most common causes GI bicarb loss and defects in renal acidification (renal tubular acidosis RTA)

- Urinary anion gap helps differentiate b/w the two GI HCO3- Loss

- Bicarb is excreted in multiple areas in GI tract (small bowel/pancreatic secretions contain large amts)- Massive diarrhea or pancreatic drainage can result in bicarb loss bc of inc. excretion/dec. absorption- Hyperchloremia occurs bc ileum/colon secrete bicarb in 1:1 exchange for Cl- (countertransport)- Resultant vol. contraction causes further inc. Cl- retention by kidney in setting of dec. anion bicarb

Renal Tubular Acidosis (RTA)- Hyperchloremic acidosis w/ normal anion gap and normal GFR, and in absence of diarrhea defines RTA- Defects

o Inability to excrete H+o Inappropriate reabsorption of bicarb

- Three major types differentiated by clinical setting, urinary pH, urinary anion gap, and serum K+ level (type III Rnot used anymore):

o Classic distal RTA (type I) characterized by hypoK hyperCl MA due to selective deficiency in H+ secretioin alpha intercalated cells in the collecting tubule

o Proximal RTA (type II)hypoK hyperCl MA due to selective defect in proximal tubules ability to adequatreabsorb filtered bicarb (HCO3

-)

o Hyporeninemic hypoaldosteronemic RTA (type IV) Most common form of RTA in clinical practice Only type characterized by hyperK, hyperCl acidosis Defect is aldosterone deficiency/antagonism impairs distal nephron Na+ reabsorption and K+/H+

excretion

Dilutional Acidosis rapid dilution of plasma vol by 0.9% NaCl mild hyperCl acidosisAssessment of Hyperchloremic Metabolic Acidosis by Urinary Anion Gap

Inc. renal NH4+Cl- excretion to enhance H+ removal is a normal physiologic response to MA Normal daily urinary excretion of NH4Cl of about 30 mEq can be inc. up to 200 mEq in response to acid load Urinary anion gap from random urine sample reflects ability of kidney to excrete NH4Cl

- Helps distinguish b/w renal and GI causes of hyperchloremic acidosis- If cause of MA is GI bicarb loss (diarrhea) the renal acidification ability remains normal and NH4Cl excretion inc.

response to acidosis (urinary anion gap is negative)

- If cause is distal RTA, urinary anion gap is positive bc the basic lesion in d/o is the inability of kidney to excrete Hand so inability to inc. NH4Cl excretion


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- If cause is proximal RTA the urinary anion gap is negative bc kidney has defective bicarb reabsorption, leading tinc. bicarb excretion

When vol. depletion is present, the urinary anion gap is a better measurement of ability to acidify urine than urinarpH (if large amts of other anions present in urine urinary anion gap may not be reliable)

Signs

&

Symptoms

Sx of MA are mainly those of the underlying disorder Compensatory hyperventilation is an important clinical sign

- May be misinterpreted as primary respiratory disorder- When severe, Kussmaul respirations seen (deep, regular, sighing respirations)

Lab Findings Blood pH, serum HCO3-, and PCO2 are decreased Anion gap may be normal (Hyperchloremic) or increased (normochloremic) HyperK may be seen

Complications ?

Metabolic Alkalosis (See table 21-15, pg. 791)


*High HCO3-with alkalemia

*Evaluate effective circulating volume by physical examination and check urinary chloride concentration. This will help differentiate

saline-responsive metabolic alkalosis from saline-unresponsive alkalosis

Etiology Characterized by high bicarb Initiation factors - abnormalities that generate bicarb w/in the body Maintenance factors abnormalities that promote renal conservation of bicarb Metabolic alkalosis may remain even after initiation factors disappear Classified into two groups based saline responsiveness (urinary Cl -) which are markers for volume status Saline-Responsive Metabolic Alkalosis (extracellular volume contraction)

- More common disorder- Characterized by normotensive extracellular vol. contraction and hypokalemia (hypotension or orthostatic

hypotension may be seen)

- Vomiting/nasogastric suction loss of acid (HCl) causes alkalosiso Vol contraction from loss of Cl- sustains alkalosis bc decline in GFR cause avid renal Na+ and bicarb

reabsorption

o Cl- depletion from stomach so available anion is bicarb which has inc. reabsorption proximally and urine may be acidic (paradoxic aciduria)

- Urinary Cl- is preferred to urinary Na+ as a measure of extracellular volume- Generally assoc. w/ hypokalemia (direct fx on renal excretion of K+ and hyperaldosteronism from vol. depletion

o HypoK worsens metabolic alkalosis by inc. bicarb reabsorption in proximal tubule and H+ ion secretion indistal tubule

o Repletion of KCl reverses d/o Saline-Unresponsive Alkalosis (implies a volume expanded state)

- Hyperaldosteronismo 1 hyperaldosteronism causes expansion of extracellular vol. with HTNo Metabolic alkalosis with hypoK results from renal mineralocorticoid fxo High levels of NaCl excreted (urinary Cl- is high >20 mEq/L) bodies attempt to dec. extracellular vol.

- Alkali administration with decreased GFRo Enhanced bicarbonaturia prevents pts w/ normal renal fxn from developing metabolic alkalosis (even wit

large bicarb ingestion)

o Pts with CKD have inadequate urinary excretion of bicarb (if antacids are consumed metabolic alkalosis woccur)

o Volume contraction from renal hyperCa fx further exacerbate alkalosisSigns

&

Symptoms

No characteristic signs/sx Orthostatic hypotension may be seen Weakness and hyporeflexia occur is serum K+ is markedly low Tetany and neuromuscular irritability (rare)


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Lab Findings Arterial blood pH & bicarb are elevated Arterial PCO2 increased Serum K+ and Cl- decreased May be increased anion gap

Complications ?

Hypernatremia

Essential of Diagnosis:*Increased thirst and water intake is the first defense against hypernatremia

*Urine osmolality helps differentiate renal from nonrenal water loss

Etiology Defined as sodium concentration > 145 mEq/L All pts have hyperosmolality Pt is typically hypovolemic due to free water losses (but can see hypervolemic hypernatremia) Excessive Na intake is a rare cause Mild in primary aldosteronism (usually no sx) Intact thirst mechanism and access to water are primary defense Hypothalamus senses minimal changes in serum osmolality, triggering thirst mechanism and inc. water intake Underlying disorders include dehydration, lactulose/Mannitol therapy, central/nephrogenic diabetes insipidus Excess water loss can cause hypernatremia only when adequate water intake not possible unconscious pts

Signs&

Symptoms

Dehydrated pt orthostatic hypotension/oliguria are common findings Sx may be delayed since water shifts from cells to intravascular space to protect volume status Early signs:

- Lethargy- Irritability- weakness

Sx seen with severe hypernatremia (Na > 158 mEq/L):- Hyperthermia- Delirium- Seizures- Coma

Sx in elderly nonspecific- Recent change in consciousness poor prognosis

Lab Findings Urine osmolality > 400 mosm/kg - renal water conserving ability is fxning- Nonrenal losses hyperNa occurs if water intake falls behind hypotonic fluid losses from excessive sweating,

respiratory tract, or bowel movt & lactulose causes osmotic diarrhea with loss of free water

- Renal losses severe hyperglycemia is cause and progressive vol. depletion from osmotic glucosuria, osmoticdiuresis occurs with use of Mannitol or urea

Urine osmolality < 250 mosm/kg- Dilute urine characteristic of central/nephrogenic DI- Result from renal insensitivity to ADH- Common causes lithium, Demeclocycline, relief of urinary obstruction, interstitial nephritis, hypercalcemia, a

hypokalemia

Complications Osmotic demyelination is an uncommon consequence of severe hypernatremia

Volume Overload(pg. 772)


*Disorder of excessive sodium retention in the setting of low arterial underfilling (e.g., CHF or cirrhosis)

*Hyponatremia from water retention in edematous states is associated with sodium retention

Hallmark of volume overloaded state is sodium retention Abnormally low arterial filling (CHF or cirrhosis) activates neurohumeral axis Renin-angiotensin-aldosterone system, SNS, & ADH release are stimulated Na retention with edema results ADH release stimulus is nonosmotic ADH released in response to baroreceptors activation (dec. in arterial baroreceptors stretch)


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ADH stimulates renal V2 receptors inc. water reabsorption Hyponatremia can develop in edematous state

Hyponatremia


*The patients volume status and serum osmolality are essential to determine etiology

*Hyponatremia usually reflects excess water retention relative to sodium rather than sodium deficiency

*Hypotonic fluids commonly cause hyponatremia in hospitalized patients*Treatment strategy should be based on pathophysiology, symptoms, severity, and acuity

Etiology Defined as a serum sodium concentration < 135 mEq/L Most common electrolyte abnormality in hospitalized pts Mismanagement can result in catastrophic neurologic consequences due to cerebral osmotic demyelination Etiology of most cases apparent thru H&P, and basic labs Most cases are hypotonic Total body water and total body Na can be low, normal, or high in hyponatremia since the kidney can regulate Na a

water homeostasis independently

Most cases reflect water imbalance/abnormal water handling, NOT Na imbalance Eval starts w/ careful hx:

- New meds-

Changes in fluid intake (polydipsia, anorexia, IV fluid rates and composition)- Fluid output (N/V/D, ostomy output, polyuria, oliguria, insensible losses)

Physical exam categorize pts vol. status into hypovolemia, euvolemia, or hypervolemiaHypovolemic Hypotonic Hyponatremia

Occurs with renal or extrarenal volume loss and hypotonic fluid replacement Total body Na and total body water are decreased ADH secretion inc. to maintain intravascular volume causes free water retention from hypotonic fluid replaceme Body sacrifices serum osmolality to preserve intravascular volume Losses of water/Na are replaced by water alone Cerebral salt wasting is rare subset of diseaseEuvolemic Hypotonic Hyponatremia

Broad differential dx (only need to focus on hormone abnormalities hypothyroid) Hormone abnormalities

- Hypothyroidism/adrenal insufficiency can cause hyponatremia (may be related to ADH)Signs

&

Symptoms

Sx depend on severity/acuity Chronic disease can be severe (Na concentration < 110 mEq/L) but may be asx bc brain adapts by decreasing tonicit

over wks/mos

Acute disease develops over hours to days and can be severely sx w/ relatively moderate hyponatremia Mild cases (Na concentrations of 135-135 mEq/L) is usually asx Mild sx of nausea/malaise progress to:

- Headache- Lethargy- Disorientation

Most serious sx include:- Respiratory arrest- Seizure- Coma- Permanent brain damage- Brain stem herniation- Death

Premenopausal women more likely than menopausal women to die/suffer permanent brain injury from hyponatremencephalopathy

Lab Findings Serum electrolytes SCr


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Serum osmolality Urine sodium May need to do thyroid/adrenal fxn tests

Complications Most serious complication is iatrogenic cerebral osmotic demyelination from overly rapid/inappropriate Na correct

Hyperkalemia


*Hyperkalemia may develop in patients taking ACE inhibitors, ARBs, potassium sparing diuretics, or their combination, even with no only mild renal dysfunction

*The ECG may show peaked T waves, widened QRS and biphasic QRS-T complexes, or may be normal despite life-threatening

hyperkalemia

*Measurement of plasma potassium level differentiates potassium leak from blood cells in cases of clotting, leukocytosis, and

thrombocytosis from elevated serum potassium

*Rule out extracellular potassium shift from the cells in acidosis and assess renal potassium excretion

Etiology Usually develops in pts with advanced renal dysfxn but can also develop w/ no/mild renal dysfxn Intracellular K+ shifts to ECF in hyperK associated with acidosis

- Serum K+ concentration rises ~0.7 mEq/L for every decrease of 0.1 pH unit Repeatedly clenching/unclenching fist during venipuncture may raise K+ concentration by 1-2 mEq/L by causing

acidosis and K+ loss from cells

Absence of acidosis serum K+ concentration rises ~1 mEq/L when total body K+ excess of 1-4 mEq/kg The higher the serum K+ concentration, the smaller the excess necessary to raise K+ levels further Mineralocorticoid deficiency in Addison disease or CKD is another cause w/ decreased renal excretion of K+ ACEI/ARBs used for pts with CHF or CKD is a cause Simultaneous use of Spironolactone, Beta-blockers further increases risk Thiazide/loop diuretics, Na bicarb may help minimize hyperK Milder hyperK that recurs in pts NOT on ACEIs is usually due type IV renal tubular acidosis (RTA) Heparin is another cause (inhibits aldosterone production) TMP inhibits renal excretion of K+ causing hyperK but K+ concentration returns to baseline when stop drug Immunosuppressive drugs can cause hyperK in organ transplant pts (esp. kidney transplant) Severe hyperK and cardiovascular disturbances caused by use of drugs with KATP channel opening properties (K-

channel syndrome)

Commonly seen in HIV ptsSigns

&

Symptoms

Elevated K+ concentration interferes with normal neuromuscular fxn producing- Muscle weakness- Flaccid paralysis (rare)- Abdominal distention- Diarrhea-

Lab Findings ECG is not a sensitive method for detecting hyperK bc of pts w/ serum concentration > 6.5 mEq/L will not have anECG changes

ECG changes- Peaked T waves of increased amplitude- Widening of QRS and biphasic QRS-T complexes- Inhibition of atrial depolarization may occur- Heart rate may be slow

Complications VFib and cardiac arrest (terminal events)

Hypokalemia


*Severe hypokalemia may induce dangerous arrhythmias and Rhabdomyolysis

*Transtubular potassium concentration gradient (TTKG) can distinguish renal from nonrenal loss of potassium

Etiology Most common cause (esp. in developing countries) is GI loss due to infectious diarrhea K+ concentration in intestinal secretion is 10x higher (80mEq/L) than gastric juice Aldosterone is most important regulator of body K+ content


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Can occur as re

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