Module 4 EB #3 Flashcards
Diverticular disease
-essentials of dx
-patho
-etiology
-diverticulosis increases w/ age
-involves sigmoid and descending colon
-unknown
Diverticulosis disease
-who is predisposed?
-non-specific sx
-physical exam
-patients w/ abnormal connective tissue: predisposed to development of diverticulosis
*most pts w/ diverticulosis has uncomplicated disease and no specific sx
-chronic constipation, abd pain, fluctuating bowel habits
-usually normal; may reveal mild left lower quad tenderness w/ a thickened, palpable sigmoid and descending colon
Diverticulosis disease
-lab studies
-dx
-dx imaging
-screening labs should be normal in uncomplicated diverticulosis
-often found during medical procedures done for other reasons (routine colon cancer screenings - colonoscopy; exam for rectal bleeding/abdominal pain)
-no reason to perform imaging studies for purpose of dx asymptomatic uncomplicated disease
*barium enema, colonoscopy, CT scan: diverticula are seen well
diverticulosis disease
-tx
-bleeding
-high-fiber diet or fiber supplements
-1/2 of all cases of acute lower GI bleeding are attributable to diverticulosis
diverticulosis disease
-risk factors
age
obesity
smoking
lack of exercise
diverticula/diverticulum
-def
small pockets that form in the wall of the bowel. diverticula is pleural (more than one) and diverticulum is singular (one pocket)
diverticulosis
-def
formation of diverticula in the lining of the bowel
-diverticula can be small (pea-sized) or larger
-the formation occurs because of increased pressure from fluid, waste, or gas on weak spots of the bowel wall
-diverticulosis is common but rarely causes sx or problems during a pt’s lifetime
-it’s found most often during a test for other reasons like a colonoscopy or sigmoidoscopy
diverticulitis
-def
when one or more diverticula become infected or inflamed
-this occurs most often when waste blocks the small pockets which allow bacteria to multiply and develop into an infection
diverticular bleeding
-def
when a small artery in the diverticulum breaks into the colon
-diverticular bleeding is usually painless and causes bleeding from the rectum
-pts may see maroon or bright red blood during bowel movements
diverticulosis disease - symptomatic
-essentials of dx
-def
-acute abd pain; LLQ tenderness + mass, leukocytosis
-macroscopic inflammation of diverticulum that may reflect a spectrum from inflammation alone, to microperformation w/ localized paraoclic inflammation, to macroperforation w/ either abscess or generalized peritonitis
-thus, there is a range from mild to severe disease
diverticulosis disease - symptomatic
-sx
-physical exam
-localized inflammation or infection: mild-moderate aching abd pain (LLQ)
*constipation or loose stools
*frequent N/V are frequent (sx are so mild that pt may not seek medical attention until several days after onset)
-low-grade fever, LLQ tenderness, palpable mass; + stool occult blood (hematochezia is rare)
diverticulosis disease - symptomatic
-imaging
-NOTE
-mild sx and presumptive dx of diverticulitis: empiric medical therapy is started w/o further imaging in acute phase
-respond well should undergo colonic evaluation w/ colonoscopy or radiologic imagining (CT colonography or barium enema)
-AFTER resolution of clinical sx to corroborate the dx or exclude other disorders such as colonic neoplasms
-pts who DON’T improve rapidly 2-4d of empiric tx and those with severe disease: CT scan of abd
*presence of colonic diverticula and wall thickening, pericolic fat infiltration, abscess formation, or extraluminal air or contrast suggests diverticulitis
-Endoscopy and colonography contraindicated during initial stages of acute attack because of risk of free perforation
diverticulosis disease - symptomatic
-prevention
-complications
-diets high in fruits, vegetables, and whole grains than diets high in red meat and refined grains
-chronic inflammation or untreated abscess –> fistula formation (involve the bladder, ureter, vagina, uterus, bowel, and abd wall)
*acute or chronic inflammation –> stricturing of colon w/ partial or complete obstruction
diverticulosis disease - symptomatic
-tx (mild sx + NO peritoneal signs)
-tx (severe)
-manage outpatient on clear liquid diet
*antibiotics: use selectively for uncomplicated disease
*once the acute episode has resolved, high-fiber diet is often recommended
-high fevers, leukocytosis, peritoneal signs + elderly, immunocompromised, severe comorbid disease = hospitalization, NP, IV fluids, NG tube for ileus, IV abx
diverticulosis disease - symptomatic
-surgical management
-prognosis
-connection to colorectal cancer?
-surg consult + repeat CT on all pts w/ severe disease or those who do not improve after 72hr of medical management
-recurs in 15-30% patient population over 10-20yrs
-diverticulosis is NOT associated w/ increased risk of colorectal CA
Hemorrhoids
-essentials of dx (3)
-bright red blood per rectum
-protrusion, discomfort
-characteristic findings on external anal inspection and anoscopic exam
Hemorrhoids
-internal hemorrhoids
-subepithelial vascular cushions consisting of connective tissue, smooth muscle fibers, and arteriovenous communications between terminal branches of the superior rectal artery and rectal veins
-normal anatomic entity, occurring in all adults, that contribute to normal anal pressures and ensure a water-tight closure of the anal canal
*commonly occur in 3 primary locations: right anterior, right posterior, left lateral
Hemorrhoids
-external hemorrhoids
arise from inferior hemorrhoidal veins located below the dentate line and are covered w/ squamous epithelium of the anal canal or perianal region
Hemorrhoids
-when do they become symptomatic?
-risk factors
-may become symptomatic as a result of activities that increase venous pressure –> distention and engorgement
-straining at stool, constipation, prolonged sitting, pregnancy, obesity, and low-fiber diets
*time, redundancy and enlargement of venous cushions may develop and result in bleeding or protrusion
Hemorrhoids
-S/S
*internal hemorrhoids
*chronically prolapsed hemorrhoids
-bleeding, prolapse, mucoid discharge
*bleeding; bright red blood; may range from streaks of blood visible on toilet paper or stool to bright red blood that drips into toilet bowl after BM
-sense of fulness or discomfort and mucoid discharge –> irritation of perianal skin and soiling of underclothes
**pain is unusual w/ internal hemorrhoids (only occurs with extensive inflammation and thrombosis)
Hemorrhoids
-physical exam
*external hemorrhoids
*nonprolapsed internal hemorrhoids
*prolapsed hemorrhoids
-digital exam
-external hemorrhoids: readily visible on perianal inspection
-Nonprolapsed internal hemorrhoids: not visible; may protrude through anus w/ gentle straining while clinician spreads buttocks
-prolapsed hemorrhoids: visible as protuberant purple nodules covered by mucosa
*examine perianal region for other signs of disease (fistulas, fissures, skin tags, condyloma, anal cancer, or dermatitis)
-digital exam: uncomplicated internal hemorrhoids are neither palpable nor painful
-anoscopic evaluation: best performed in prone jackknife position, provides optimal visualization of internal hemorrhoids
Hemorrhoids
-treatment
*conservative measures
-patients with early (stage I and stage II) disease
*decrease straining w/ defecation: initiate high fiber diet and increased fluid with meals
*dietary fiber: supplement with bran powder or commercial bulk laxatives
*suppositories and rectal ointments
*mucoid discharge: local application of cotton ball tucked next to anal opening after BMs
Hemorrhoids
-treatment for stage I, stage II, and stage III hemorrhoids + recurrent bleeding
-treatment for edematous, prolapsed (stage IV) internal hemorrhoids
-rubber band ligation is preferred (recurrence is common)
-emollients, topical anesthetics, vasoconstrictors, astringents and corticosteroids
Cholelithiasis
-key findings
-often asymptomatic, classic biliary sign “episodic gallbladder pain” characterized by infrequent episodes of steady severe pain in the epigastric of RUQ with radiation to right scapula
*detected on ultrasound
Cholelithiasis
-prevention
-rapid weight loss component and prevention
low carb diet, mediterranean diet, physical activity, cardiorespiratory fitness
-protect against gallstones in women: consuming caffeine/coffee
-reduce risk of gallstones in men: high mag intake and polysaturated/monosaturated fats
-reduces risk of gallbladder removal in women: high fiber diet rich in fruits/veggies and statin use
-protect against gallstones: aspirin and NSAIDs
-reduce risk of gallstone formation in those with rapid weight loss: ursodeoxycholic acid and diets high in fat
Cholelithiasis
-prevalence
more common in women than men
-increasing incidence in both sexes and all races with age >60yrs
Cholelithiasis
-associated with:
increase overall mortality, CV mortality, and cancer mortality
-attributable to hemolysis in >1/3 of those with SSD
*Native Americans: high rate of cholesterol gallstones r/t predisposition to “thrifty” LITH genes (promote efficient caloric utilization and fat storage)
Cholelithiasis
-how are gallstones classified?
by chemical composition
-cholesterol or calcium bilirubinates
Cholelithiasis
-dx studies
gallstones detected by ultrasound
Cholelithiasis
-risk factors for developing sx/complications
-female sex, young age, awareness of having gallstones, and large, multiple, and older stones
-small intestinal obstruction due to “gallstone ileus” or Bouveret syndrome (when the obstructing stones is in pylorus or duodenum) –> presents as initial manifestations of cholelithiasis
Cholelithiasis
-recurrence?
1/2 of patient recurs w/i 5 years of tx cessation
Cholelithiasis
-risk factors
-obesity (esp women), rapid weight loss (after bariatric surgery), DM, glucose intolerance, insulin resistance
-high dietary glycemic load increases risk of cholecystectomy (women)
-hypertriglyceridemia (promotes gallstones formation by impairing gallbladder mortality)
-increased incidence of gallbladder disease in men with cirrhosis/hep C
-high incidence in those with Crohns
-certain meds; prolonged fasting (formation of biliary sludge which resolves with refeeding)
-pregnancy (obese women); hormone replacement
-increased with right-sided colon CA
Cholelithiasis
-treatment of choice for symptomatic gallbladder disease
-lap cholecystectomy
Cholelithiasis
-tx of biliary pain in pregnancy
conservative approach
-perform cholecystectomy in 2nd trimester if suffering from repeated attacks of biliary pain or acute cholecystitis
Cholelithiasis
-ursodeoxycholic acid
dissolves cholesterol stones
-used in select pts who refuse lap chole
-most effective in pts with functioning gallbladder
acute cholecystitis
-key findings
steady, severe pain and tenderness in right hypochondrium or epigastrium; N/V, fever & leukocytosis
acute cholecystitis
-acalculous cholecystitis
*when to consider this as dx
*multiorgan failure?
-consider when unexplained fever and RUQ pain occurs w/i 2-3 weeks or major surgery or critically ill patient with no oral intake for prolonged period
**multi-organ failure is often present!!!
acute cholecystitis
-etiology
*patho
*other causes
-stones become impacted in cystic duct –> inflammation develops behind obstruction
-infectious agents in pts with AIDS; vasculitis
acute cholecystitis
-diagnostic imaging
*plain XR films
-gallstones
acute cholecystitis
-diagnostic imaging
*Tc hepatobiliary imaging/HIDA scan
-demonstrates obstructed cystic duct (cause of acute cholecystitis)
-reliable test if bilirubin is <5mg/dL
-FALSE positives occur with: prolonged fasting, liver disease, and chronic cholecystitis
-IMPROVE SPECIFICITY with: IV morphine (induces spasm of sphincter of Oddi)
acute cholecystitis
-diagnostic imaging
*RUQ abd US
*CT scan of abd
*diagnostic findings of acute cholecystitis
-often performed 1st - may show gallstones NOT SPECIFIC FOR ACUTE CHOLECYSTITIS
-shows complications of acute cholecystitis –> perforation of gangrene
-gallbladder wall thickening, pericholecystic fluid, and sonographic Murphy sign
acute cholecystitis
-S/S
*caused by:
*characterized by:
-large or fatty meal
-sudden steady pain localized to epigastrium or right hypochondrium (gradually subside over a period of 12-18hr)
*vomiting, fever (typical), RUQ tenderness (+murphy sign); palpable gallbladder 15% of pts; jaundice (25% of cases)
STRONGLY FAVORABLE SIGNS OF DX: definite localization of pain/tenderness in RUQ, with radiation to intrascapular area (true cholecystitis w/o stones = a calculous cholecystitis)
acute cholecystitis
-lab findings
-WBC elevated
-total serum bili (1-4): seen in absence of bile duct obstruction
-elevated serum aminotransferase and alkaline phosphatase
-moderately elevated serum amylase
acute cholecystitis
-tx
*conservative regimen
*pain management
*recurrent attacks
*non-surgical tx
*surgical tx
-sx usually subside on conservative regimen by withholding oral feedings, IV alimentation, analgesics, and IV abx
-morphine or meperidine
-high risk of recurrent attacks = refer for lap cholecystectomy (performed w/i 24hr of admit to hospital
-watch pt carefully for recurrent sx, evidence of gangrene of gallbladder, or cholangitis
-high risk pt; US guided aspiration of gallbladder OR percutaneous or EUS-guided cholecystostomy OR endoscopic insertion of stent or nasobiliary drain into gallbladder
Acute pancreatitis
-key findings
abrupt onset of deep epigastric pain (radiating into back); hx of previous episodes (related to ETHO intake); N/V, sweating, weakness
-abd tenderness and distention, fever; leukocytosis
*elevated serum amylase and serum lipase
Acute pancreatitis
-prevalence
-prevention
-most cases related to biliary tract disease OR heavy ETOH intake
-vegetable consumption, dietary fiber, and use of statins
*coffee drinking –> reduce risk of nonbiliary pancreatitis
Acute pancreatitis
-associated with: (9)
-hypercalcemia
-HLD
-drugs
-vasculitis infections (mumps, CMV, etc.)
-peritoneal dialysis
-cardiopulmonary bypass
-single- or double-balloon enteroscopy
-ERCP
-abdominal trauma (surgery)
Acute pancreatitis
-pathogenesis
exact cause unknown
-may include edema or obstruction of ampulla of vater, reflux of bile into pancreatic ducts, and direct injury or pancreatic acina cells
Acute pancreatitis
-S/S
-physical exam
-epigastric abd pain (abrupt onset, steady, boring, and severe; made worse by walking and lying supine; made better by sitting and leaning forward; usually radiates to back
*N/V, weakness, sweating, anxiety; history of ETHO intake or heavy meal immediately preceding the attack
-tender, upper abd (often W/O guarding, rigidity, or rebound; may be distended with absent bowel sounds due to associated ileus
*fever, tachy, hypotension, pallor, cool clammy skin
*AKI (usually prerenal azotemia) may occur early in course of acute pancreatitis
Acute pancreatitis
-diagnostic imaging
*plain XR of abd
*ultrasound
*unenhanced CT scan
-shows calcified gallstones, “sentinel loop”, “colon cutoff sign”
-not helpful in dx acute pancreatitis, but CAN ID gallstones in gallbladder
-shows enlarged pancreas, provides initial assessment of prognosis (but often unnecessary early in course)
Acute pancreatitis
-diagnostic imaging
*CT scan w/ contrast
*MRI
*EUS
*ERCP
-valuable after the first 3 days of severe acute pancreatitis for identifying areas of necrotizing pancreatitis and assessing the degree of necrosis
**avoid when serum creatinine is >1.5mg/dL
-suitable alternative to CT
-ID’s occult biliary disease; present in majority of pts with idiopathic acute pancreatitis and indicated in >40 years to exclude malignancy
*following single attack of idiopathic acute pancreatitis = negative EUS exam predicts a low risk of relapse
-not indicated after 1st attack unless associated with cholangitis or jaundice or bile duct stone known to be present
*EUS or MRCP should be considered, exp after repeated attacks of idiopathic acute pancreatitis
Acute pancreatitis
-assessment of severity
labs + severity of acute alcoholic pancreatitis can be assessed using several scoring systems –> ranson criteria
Acute pancreatitis
-lab findings
-inc serum amylase and lipase
*lipase remains elevated longer than amylase and is slightly more accurate for the dx of acute pancreatitis
-leukocystosis, proteinuria, granular casts, glycosuria, hyperglycemia, inc serum bilirubin
-inc BUN and serum alkaline phosphatase and coagulation tests abnormal
-disease severity
*dec serum calcium = correlates with severity of disease
*inc c-reactive protein = severe disease
-inc serum creatinine level; rise in hematocrit –> pancreatic necrosis
-biliary pancreatitis: serum ALT >150u/L + clear evidence of acute pancreatitis
-acute pancreatitis due to hypertriglyceridemia
Acute pancreatitis
-mild disease
*how to manage
*refer or treat outpatient?
-rest the pancreas: NPO, bed rest; possible NG suction
-early fluid resuscitation with LR
-pain management with meperidine (or morphine as alternative if kidney or liver dysfunction)
-resume eating/drinking when free of pain and bowel sounds present
*begin with clear liquids
*gradual advancement to low-fat diet
-treat hypertriglyceridemia with acute pancreatitis –> use combo of insulin, heparin, apheresis, and hemofiltration
-refer
Acute pancreatitis: mild disease
-following recover from acute biliary pancreatitis, what test is performed?
laparoscopic cholecystectomy
Acute pancreatitis: severe disease
-what is occurring?
-refer or treat outpatient?
-necrotizing pancreatitis
-refer!!
Acute pancreatitis: severe disease
-RF for high levels of fluid sequestration
-hemodynamic monitoring in an ICU is required
-enteral nutrition via a nasojejunal or possibly NG tube: pts who will otherwise be without oral nutrition for at least 7-10 days
*reduces risk of MODS and mortality when started w/i 48 hours of admission
*parenteral nutrition
acute pancreatitis - severe disease
-antibiotics (when to administer)
sterile necrotizing pancreatitis - don’t administer abx in pt with less than 30% pancreatic necrosis!
*abx of choice >30%: imipenem and cefuroxime
Hematuria
-essentials of dx
*gross vs microscopic - which require evaluation?
*what should occur with hematuria in absence of infection?
-both gross and microscopic hematuria require evaluation
-hematuria in absence of infection –> upper urinary tract should be imaged, and cystoscopy be performed
Hematuria: clinical findings
-upper tract source (kidney/ureters)
-can be identified in 10% of patients with gross or microscopic hematuria
*40% stone disease
*20% medical kidney disease (glomerulonephritis, papillary necrosis)
*10% renal cell carcinoma
*5% urothelial cell carcinoma or the ureter or renal pelvis
Hematuria: clinical findings
-lower tract source (in absence of infection)
*most common cause?
*what commonly causes microscopic hematuria (male)?
*hematuria in pts receiving antiplatelet or anticoagulation therapy
-most commonly from urothelial carcinoma of the bladder
-most commonly from BPH
-cannot be presumed to be d/t medication; a complete evaluation is warranted consisting of upper tract imaging, cystoscopy, and urine cytology
Hematuria
-S/S
*gross hematuria
*associated sx
*physical examination
*urologic evaluation
-must obtain description of timing –> can provide clue to localization of disease
-renal colic, irritative voiding sx, constitutional sx = INVESTIGATE THIS!
-emphasize signs of systemic disease (fever, rash, lymphadenopathy, abd or pelvic masses) as well as signs of medical kidney disease (HTN, volume overload)
-enlarged prostate, flank mass, or urethral disease
Hematuria: diagnostic studies
-Obtain diagnostic clues from medical ingestion and associated medical problems
-abd and pelvic CT scan (with & w/o IV contract) or upper tract
-cystoscopy
Hematuria: lab findings
-urinalysis and urine culture
-proteinuria and casts
-females: irritative voiding sx, bacteriuria, + urine cs = UTI
-eGFR: obtain since intrainsic kidney disease has implications for further evaluation and management of pts with hematuria
Hematuria: follow-up
-repeat evaluations?
-urinary cytology
-imaging repeated how often?
-patients with negative evaluations, repeat evaluations may be warranted to avoid a missed malignancy
-urinary cytology can be obtained after initial negative evaluation or in persons with risk factors
-cystoscopy and upper tract imaging may be repeated 1 year after an initial negative evaluation
Hematuria: when to refer
absence of infection or other benign etiology, hematuria (either gross or microscopic) requires evaluation
Acute Cystitis: essentials of dx
-sx
irritative voiding sx, usually afebrile, positive urine culture; blood cultures may be positive
Acute Cystitis
-common cause
-route of infection
-viral cystitis
-uncomplicated cystitis (men)
-coliform bacteria (e coli) and occasionally gram-positive bacteria (enterococci)
-typically ascending from urethra
-viral cystitis: adenovirus; seen in children; RARE IN ADULTS
-rare; implies pathologic process (infected stones, prostatitis, chronic urinary retention) –> requires investigation!!!!!
Acute Cystitis
-S/S
-physical examination
-irritative voiding sx (frequency, urgency, dysuria) and suprapubic discomfort (common)
*gross hematuria (women): sx may often appear following sexual intercourse
-suprapubic tenderness, but examination is often unremarkable. Systemic toxicity is absent!!!!!
Acute Cystitis: prevention
-women
-how to assess?
->3 episodes of cystitis per year = considered candidates for prophylactic abx therapy (prevent recurrence after tx of UTI)
-begin starting therapy: perform thorough urologic exam –> exclude anatomic abnormality (stones, reflux, fistula)
*most common PO abx agents: bactrim, nitrofurantoin, cephalexin
*dose schedule: single dosing at bedtime or at the time of intercourse
Acute Cystitis: diagnostic studies
-abd US or cystoscopy (or both): men with uncomplicated cystitis (to determine underlying problem)
-follow-up CT scan: pyelonephritis, recurrent infections or anatomic abnormalities are suspected
Acute Cystitis: lab findings (2 tests)
-urinalysis: pyuria, bacteriuria, and varying degrees of hematuria
-positive urine culture: + for offending organism
Acute Cystitis: differential dx
-women
-men
-noninfectious causes of cystitis-like sx
-distinguish infectious processes (vulvovaginitis and PID) by pelvic examination and urinalysis
-distinguish urethritis and prostatitis by physical examination (urethral discharge or prostatic tenderness)
-pelvic irradiation, chemotherapy (cyclophosphamide), bladder carcinoma, interstitial cystitis, voiding dysfunction disorders, and psychosomatic disorders
Acute Cystitis: prognosis
responds rapidly to therapy, and failure to respond suggests resistance to the selected medication - REQUIRES FURTHER EVAL!!
Acute Cystitis: treatment
-uncomplicated cystitis in women
-uncomplicated urinary tract infection in men
-cephalexin, nitrofurantoin, and trimethoprim-sulfamethoxazole
**Black Box Warning: restricting fluoroquinolone to use for uncomplicated infections, including uncomplicated UTIs; local patterns of bacterial resistance should be consulted to identify best treatment options
-rare; duration of antibiotic therapy depends on underlying etiology
*hot sitz baths or urinary analgesics may provide symptomatic relief
Acute Cystitis: when to refer
-suspicion or radiographic evidence of anatomic abnormality
-evidence of urolithiasis
-recurrent cystitis due to bacterial persistence
Acute Pyelonephritis: clinical findings
-def
-most common cause
-route of infection
-an infectious inflammatory disease involving the kidney parenchyma and renal pelvis
-gram-negative bacteria (E coli, proteus, Klebsiella, enterbacter, and pseydomonas; gram-positie bacteria are less common (enterococcus faecalis and staphylococcus aureus)
-ascends from lower urinary tract - with exception of S aureus, which is usually spread by hematogenous route
Acute Pyelonephritis: essentials of dx
fever, flank pain, irritative voiding sx, POSITIVE URINE CULTURE
Acute Pyelonephritis: dx studies
renal US: complicated pyelonephritis to evaluate hydronephrosis from a stone or other source of obstruction
Acute Pyelonephritis: lab findings
-complete CBC
-urinalysis
-urine culture
-blood culture
-leukocytosis and left shift
-pyuria, bacteriuria, and varying degrees of hematuria; white cell casts may be seen
-heavy growth of the offending oragnism
-may also be positive
Acute Pyelonephritis
-S/S
-fever, flank pain, shaking chills, and irritative voiding sx (urgency, frequency, dysuria)
-associated nausea and vomiting, and diarrhea (common)
-fever and tachycardia; costovertebral angle tenderness is usually pronounced
Acute Pyelonephritis: prevention
-women
-most common PO abx agents
-when to take abx
->3 episodes of cystitis per year –> considered candidates for prophylactic abx therapy (prevent recurrence after tx of UTI)
*begin starting therapy: perform a thorough urologic exam –> exclude any anatomic abnormality (stones, reflux, fistula)
-MOST common PO abx agents: bactrim, nitrofurantoin, cephalexin
-single dosing at bedtime or at time of intercourse
Acute Pyelonephritis: differential dx (5)
-distinguish acute intra-abd disease (appendicitis, cholecystitis, pancreatitis, or diverticulitis): normal urinalysis (usually seen in GI disorders)
-inflammation from adjacent bowel (appendicitis or diverticulitis) –> hematuria or sterile pyria –> differentiate with abnormal liver biochemical tests or inc amylase levels
-lower-lobe pneumonia: dx with abnormal chest XR
-epididymitis/acute prostatitis (males): physical exam and location of the pain should permit this distinction
-DM: gas-producing organism –> emphysematous pyelonephritis (may be life-threatening if not adequately treated; healthy adults usually recover comple`te kidney fx, yet if coexistent kidney disease is present, scarring or chronic pyelonephritis may result –> inadequate therapy –> abscess formation
Acute Pyelonephritis: prognosis
-what can lead to less favorable outcome?
-complications
-with prompt dx and appropriate tx, acute pyelonephritis carries a good prognosis
-complicating factors, underlying kidney disease, and inc patient age may lead to a less favorable outcome
-complications: sepsis with shock
Acute Pyelonephritis: treatment
-ID causative agent
-outpatient or inpatient tx?
-follow-up cultures?
-obtain urine/blood sample; ID causative agent and determine antimicrobial sensitivity
-outpatient tx: empiric therapy - cipro/levaquin/bactrim
-antibiotics are adjusted according to sensitivities
*fevers may persist for up to 72hrs even with appropriate antibiotics; failure to respond w/i 48 hours warrants imaging (CT or ultrasound) to exclude complicating factors that may require intervention
-follow-up urine cultures are mandatory following the completion of treatment
Acute Pyelonephritis
-when to refer
evidence of complicating factors (urolithiasis, obstruction)
-absence of clinical improvement in 48 hours
Acute Pyelonephritis
-when to admit
severe infections or complicating factors, evidence of sepsis or need for parenteral antibiotics
-need for radiographic imaging or drainage of urinary tract obstruction
Urinary Stone Disease
-key findings
-occur more in men or women?
-urinary calculi (made of what?)
-5 major types of stone
-severe flank pain; N/V; identification on non-contrast CT or US
-occurs more in men (30-50yrs)
-polycrystalline aggregates composed of amounts of crystalloid and a small amount of organic matrix
*stone formation requires saturated urine that is dependent on pH, ionic strength, solute concentration, and complexation
-calcium oxalate, calcium phosphate, struvite (mag ammonium phosphate), uric acid, and cystine
Urinary Stone Disease
-most common type of stone
-how do urinary stones appear on xrays?
-calcium (85%)
-most urinary stones are RADIOPAQUE on plain abd xrays
*uric acid stone = radiopaque
*PURE uric acid stones = radiolucent
*cystine stones = radiolucent
Urinary Stone Disease
-geographic factors contribute to development of stones
-high humidity and elevated temperatures (hot summer months); sedentary lifestyle, HTN, carotid calcification, CV disease
Urinary Stone Disease
-dietary factors
-genetic factors
-high protein, high salt intake, inadequate hydration
-50% of calcium-based stones have heritable component
*cystinuria = autosomal recessive disorder
*distal renal tubular acidosis = transmitted as hereditary trait; urolithiasis occurs in >75% of affected pts
Urinary Stone Disease
-diagnostic findings (4)
-plain abd x-ray and renal US examination –> dx up to 80% of stones
-spinal CT: most accurate imaging to eval flank pain; BUT US is safer d/t no radiation and has good accuracy
-hounsfield units (HU) on CT scans: estimate stone density to help determine stone type
-non-contrast CT scan: all stones (radiopaque or radiolucent on plain abd x-rays) will be visible
*EXCEPTION: rare protease inhibitor calculs
Urinary Stone Disease: labs
-urinalysis
-urinary pH
-microscopic or gross hematuria: absence of microhematuria DOES NOT EXCLUDE urinary stones
-valuable clue to cause of possible stone (normal is 5.8-6.2)
*persistent pH < 5.5 = uric acid stone
*persistent pH > 7.2 = struvite (infection-related) stone
*pH > 7.5 = calcium phosphate stone
*pH between 5.5-6.8 = calcium oxalate-based stones
Urinary Stone Disease: S/S
-obstructing urinary stones
-stone progresses down ureter
-stone becomes lodged at uretero-vesicular junction
-after stone passes into bladder
-acute, unremitting, and severe colic, occurs suddenly, may awaken pt from sleep; typically localized to the flank, associated with N/V
*pt will constantly move around trying to find comfortable position; occurs episodically and may radiate anteriorly over abd
-pain may be referred into ipsilateral groin
-complaints of marked urinary urgency and frequency and in men, pain may radiate to the tip of the penis
-minimal pain with passage through urethra
*stone size DOES NOT CORRELATE with severity of sx
Urinary Stone Disease: stone evaluation
-stone analysis (how to help dec stones)
uncomplicated first-time stones should undergo dietary counseling + optional complete metabolic evaluation
-general dietary counseling
*reduce sodium
*reduce non-dairy animal protein intake
*ingest adequate fluid to achieve a voided volume of 2.5L/day of urine
Urinary Stone Disease
-stone evaluation: tests to run
-24 hour urine collection
-serum parathyroid hormone (PTH): check for pt w/ suspected hyperparathyroidismUrinary Stone Disease
-serum uric acid (check for pt w/ suspected gout)
Urinary Stone Disease: treatment
-metabolic evaluation
-recurrence of stones
-follow-up
-reduce recurrence with dietary modification
*metabolic evaluation: identifies a modifiable risk factor that can further reduce stone recurrence rates; medical therapy is initiated based on metabolic evaluation findings)
*some stone types (uric acid, cystine) are more prone to rapid recurrence than others: increased fluid intake is of greatest importance in reducing stone recurrence –> ensure a voided volume of 2.5L/day
-every 6-8 months
Urinary Stone Disease: diet
-restrict…?
-animal protein…?
-limit intake of…?
-dietary calcium intake
-restrict sodium intake –> keep urinary sodium levels less than 150mEq/day
-animal protein intake should be spread out through the day (not all consumed during any individual meal) - best limited to 1g/kg/day
*increase calcium, oxalate, and uric acid excretion and decrease urinary citrate excretion
-limit intake of oxalate and purines
-DO NOT ROUTINELY dec dietary calcium or calcium supplements
Calcium Nephrolithiasis
-etiology
-how many different types?
-increased absorption of calcium at the level of the small bowel (jejunum)
-can be subdivided into types I, II, III
Calcium Nephrolithiasis
-hypercalciuric
*cause
*tx
->250mg/24h; greater than 4mg/kg/24h
-absorptive, resorptive, and renal disorders
-administer thiazide diuretics offered to patients with high urinary calcium and recurrent calcium stones
Calcium Nephrolithiasis
-hyperuricosuric
*def
*tx
*labs (urinary pH #)
-secondary to dietary purine excess or endogenous uric acid metabolic defects
-dietary purine restriction can reduce hyperuricosuria in 85% of cases
*pts with hyperuricosuria, normocalciuria, and recurrent calcium oxalate stones –> allopurinol
-urinary pH >5.5
Calcium Nephrolithiasis: hyperoxaluric
-cause
-patho
-primary intestinal disorders (hx of chronic diarrhea frequently associated with IBS)
-increased bowel fat or bile (or both) combine with intraluminal calcium –> form soap-like product –> calcium cannot bind to oxalate in gut –> oxalate is freely and rapidly absorbed –> any small increase in oxalate absorption significantly increases stone formation
Calcium Nephrolithiasis: hyperoxaluric
-tx
-avoid
-caution
-if diarrhea or steatorrhea cannot be effectively curtailed = PO calcium should be taken with meals (either ingest dairy products or taking calcium carbonate supplements
-excess ascorbic acid
-pts w/ significant dietary ingestion of oxalate-rich foods can reduce their oxalate intake, but this should not be routinely recommended
Calcium Nephrolithiasis
-type I
*cause
*tx
-absorptive hypercalciuria
*independent of calcium intake
*thiazide diuretics can be used to dec renal calcium excretion
Calcium Nephrolithiasis
-type II
*cause
*tx
-absorptive hypercalciuria
*diet-dependent; rare
*decreasing calcium intake by 50%
Calcium Nephrolithiasis
-type III
*cause
*tx
-absorptive hypercalciuria
*secondary to a renal phosphate leak –> inc vitamin D synthesis –> increased small bowel absorption of calcium
*readily reversed by orthophosphates
Prescription: orthophosphates = inhibit vit D synthesis
Calcium Nephrolithiasis: resorptive hypercalciuria
-cause
-labs
-tx
-secondary to hyperparathyroidism
-hypercalcemia, hypophosphatemia, hypercalciuria, and elevated serum PTH value
-sx resection of the parathyroid adenoma cures the disease
Renal Hypercalciuria
-cause
-labs
-tx
-renal tubules cannot efficiently reabsorb filtered calcium –> hypercalciuria; spilling calcium in the urine results in secondary hyperparathyroidism
-normal serum calcium
-thiazides = effective long-term therapy in pts with disorder
Hypocitraturic
-secondary to?
-patho
-associated with:
-treatment patho:
-secondary to chronic diarrhea, type I renal tubular acidosis, chronic hydrochlorothiazide tx, or in any condition that results in metabolic acidosis
-metabolic acidosis enhances citrate transport into the proximal tubular cells –> consumed by citric acid cycle in their mitochondria –> hypocitraturia
=calcium stone formation
-calcium stone formation
-urinary citrate is decreased in acidosis and inc during alkalosis
*med: potassium citrate supplements (corrects hypokalemia and corrects acidosis)
*60mEq total daily divided into 3x or 2x daily (can also drink lemonade)
Uric Acid Calculi
-cause
-tx
-urinary pH is >5.5 in persons who form pure uric acid stones
-inc urinary pH to >6.2
*urinary alkalization with potassium citrate or an equivalent agent is the key to stone dissolution and prophylaxis (target should be a urinary pH greater than 6.2 and less than 7.5)
Uric Acid Calculi
-other causes (besides pH inc)
-diagnosis
-hyperuricemia, myeloproliferative disorders, malignancy with increased uric acid production, abrupt and dramatic weight loss, and uricosuric medications (hyperuricemia + hyperuricosuria: tx with allopurinol (given to prevent stone formation)
-pure uric acid stones are relatively radiolucent; most have some calcium components and can be visualized on plain abd radiographs
Struvite calculi
-def
-prevalence
-dx
-struvite stones are radiodense magnesium-ammonium-phosphate stones
-most common in women with recurrent UTIs with urease-producing organisms (proteus, pseudomonas, providencia)
*rarely present as ureteral stones w/ colic w/o prior upper tract endourologic intervention
-most are discovered as a large staghorn calculus forming a cast of the renal collecting system
Struvite calculi
-labs
-stone analysis
-treatment
-recurrence
-urinary pH is HIGH (>7.2)
-relatively soft
-percutaneous removal; order the REQUIRED perioperative antibiotics
-recur rapidly
what kind of calculi require perioperative antibiotics?
struvite calculi
Cystine calculi
-cause
-tx
-prevention
-abnormal excretion of cystine
-difficult to manage medically
-marked increased fluid intake during day and evening to achieve volume of 3-4L/day; urinary pH greater than 7.0, disulfide inhibitors such as tiopronin or penicillamine)
**there are no known inhibitors of cystine calculi
which calculi type has no known inhibitors?
cystine calculi
which calculi requires potassium citrate or equivalent agent to help with stone dissolution and prophylaxis?
uric acid calculi
six types of calcium nephrolithiasis?
- hypercalciuric
- hyperuricosuria
- hyperoxaluric
- resorptive hypercalciuria
- renal hypercalciuria
- hypocitraturia
Ureteral Stones
-sites of urine obstruction with stone
-stones that pass spontaneously
-stones that require surgical removal (and with what?)
-ureteropelvic junction, crossing ureter over iliac artery, ureterovesicular junction
-5-6mm on abd XR
-mid-distal ureter stones
Ureteral Stones: proximal and intrarenal stones
-how to increase rate of spontaneous stone passage
-when do small stones require surgical intervention?
-tamsulosin PO + ibuprofen + with or without short course of prednisone PO = most effective for distal stones
-stone fails to pass w/i 4wk, fever, intolerable pain, persistent N/V, must return to work/travel: REQUIRES SURGICAL INTERVENTION
Ureteral Stones: mid-distal ureter stones
*how are stones removed?
*obstructed stone fragments post-SWL conservative management
*fragments not passed within 6 weeks
-removed with ureterscopic stone extraction
*SWL or ureteroscopy
-spontaneous resolution w/ eventual passage of stone fragments
-unlikely to do so w/o intervention
Ureteral stones: medical & surgical tx
-acute setting
-signs of infection
*when is it a medical emergency?
-achieve a euvolemic state with IV fluids (forced diuresis can be counterproductive and exacerbate pain)
-fever, tachycardia, or inc WBC –> UTI behind obstructing stone = MEDICAL EMERGENCY = refer to urology stat for prompt drainage by ureteral stent or percutaneous nephrostomy tube
*abx alone are inadequate and only used as an adjunct to urinary drainage of the obstruction
Renal Calculi
-without pain/UTI/obstruction
-intervene when symptomatic?
-<2cm
*how to tx
-what happens when SWL/stones do not pass?
-may not warrant surgical tx
*watch and wait; monitor with serial abd XR or renal US exams q3-12MO
-calculi are growing to become symptomatic = INTERVENTION REQUIRED
-tx w/ SWL or ureteroscopic extraction
*calculi of larger diameter, located in inferior calices, and staghorn stones: percutaneous nephrolithotomy
-pt who cannot have SWL/stones do not fragment and pass = laparoscopic, open, or robotic-assisted stone removal may be sondiered
*ADMIN perioperative abx coverage for ANY STONE PROCEDURE - based on preoperative urine cx
Urinary Stone Disease: when to refer
-evidence of urinary obstruction
-urinary stone with associated flank pain
-anatomic abnormalities or solitary kidney
-concomitant pyelonephritis or recurrent infection
Urinary Stone Disease:
