Module 4 EB #3

Question 1

Diverticular disease
-essentials of dx
-patho
-etiology

Answer 1

-diverticulosis increases w/ age
-involves sigmoid and descending colon
-unknown

Question 2

Diverticulosis disease
-who is predisposed?
-non-specific sx
-physical exam

Answer 2

-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

Question 3

Diverticulosis disease
-lab studies
-dx
-dx imaging

Answer 3

-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

Question 4

diverticulosis disease
-tx
-bleeding

Answer 4

-high-fiber diet or fiber supplements
-1/2 of all cases of acute lower GI bleeding are attributable to diverticulosis

Question 5

diverticulosis disease
-risk factors

Answer 5

age
obesity
smoking
lack of exercise

Question 6

diverticula/diverticulum
-def

Answer 6

small pockets that form in the wall of the bowel. diverticula is pleural (more than one) and diverticulum is singular (one pocket)

Question 7

diverticulosis
-def

Answer 7

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

Question 8

diverticulitis
-def

Answer 8

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

Question 9

diverticular bleeding
-def

Answer 9

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

Question 10

diverticulosis disease - symptomatic
-essentials of dx
-def

Answer 10

-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

Question 11

diverticulosis disease - symptomatic
-sx
-physical exam

Answer 11

-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)

Question 12

diverticulosis disease - symptomatic
-imaging
-NOTE

Answer 12

-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

Question 13

diverticulosis disease - symptomatic
-prevention
-complications

Answer 13

-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

Question 14

diverticulosis disease - symptomatic
-tx (mild sx + NO peritoneal signs)
-tx (severe)

Answer 14

-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

Question 15

diverticulosis disease - symptomatic
-surgical management
-prognosis
-connection to colorectal cancer?

Answer 15

-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

Question 16

Hemorrhoids
-essentials of dx (3)

Answer 16

-bright red blood per rectum
-protrusion, discomfort
-characteristic findings on external anal inspection and anoscopic exam

Question 17

Hemorrhoids
-internal hemorrhoids

Answer 17

-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

Question 18

Hemorrhoids
-external hemorrhoids

Answer 18

arise from inferior hemorrhoidal veins located below the dentate line and are covered w/ squamous epithelium of the anal canal or perianal region

Question 19

Hemorrhoids
-when do they become symptomatic?
-risk factors

Answer 19

-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

Question 20

Hemorrhoids
-S/S
*internal hemorrhoids
*chronically prolapsed hemorrhoids

Answer 20

-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)

Question 21

Hemorrhoids
-physical exam
*external hemorrhoids
*nonprolapsed internal hemorrhoids
*prolapsed hemorrhoids

-digital exam

Answer 21

-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

Question 22

Hemorrhoids
-treatment
*conservative measures

Answer 22

-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

Question 23

Hemorrhoids
-treatment for stage I, stage II, and stage III hemorrhoids + recurrent bleeding
-treatment for edematous, prolapsed (stage IV) internal hemorrhoids

Answer 23

-rubber band ligation is preferred (recurrence is common)
-emollients, topical anesthetics, vasoconstrictors, astringents and corticosteroids

Question 24

Cholelithiasis
-key findings

Answer 24

-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

Question 25

Cholelithiasis -prevention -rapid weight loss component and prevention

Answer 25

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

Question 26

Cholelithiasis -prevalence

Answer 26

more common in women than men -increasing incidence in both sexes and all races with age >60yrs

Question 27

Cholelithiasis -associated with:

Answer 27

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)

Question 28

Cholelithiasis -how are gallstones classified?

Answer 28

by chemical composition -cholesterol or calcium bilirubinates

Question 29

Cholelithiasis -dx studies

Answer 29

gallstones detected by ultrasound

Question 30

Cholelithiasis -risk factors for developing sx/complications

Answer 30

-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

Question 31

Cholelithiasis -recurrence?

Answer 31

1/2 of patient recurs w/i 5 years of tx cessation

Question 32

Cholelithiasis -risk factors

Answer 32

-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

Question 33

Cholelithiasis -treatment of choice for symptomatic gallbladder disease

Answer 33

-lap cholecystectomy

Question 34

Cholelithiasis -tx of biliary pain in pregnancy

Answer 34

conservative approach -perform cholecystectomy in 2nd trimester if suffering from repeated attacks of biliary pain or acute cholecystitis

Question 35

Cholelithiasis -ursodeoxycholic acid

Answer 35

dissolves cholesterol stones -used in select pts who refuse lap chole -most effective in pts with functioning gallbladder

Question 36

acute cholecystitis -key findings

Answer 36

steady, severe pain and tenderness in right hypochondrium or epigastrium; N/V, fever & leukocytosis

Question 37

acute cholecystitis -acalculous cholecystitis *when to consider this as dx *multiorgan failure?

Answer 37

-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!!!

Question 38

acute cholecystitis -etiology *patho *other causes

Answer 38

-stones become impacted in cystic duct --> inflammation develops behind obstruction -infectious agents in pts with AIDS; vasculitis

Question 39

acute cholecystitis -diagnostic imaging *plain XR films

Answer 39

-gallstones

Question 40

acute cholecystitis -diagnostic imaging *Tc hepatobiliary imaging/HIDA scan

Answer 40

-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)

Question 41

acute cholecystitis -diagnostic imaging *RUQ abd US *CT scan of abd *diagnostic findings of acute cholecystitis

Answer 41

-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

Question 42

acute cholecystitis -S/S *caused by: *characterized by:

Answer 42

-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)

Question 43

acute cholecystitis -lab findings

Answer 43

-WBC elevated -total serum bili (1-4): seen in absence of bile duct obstruction -elevated serum aminotransferase and alkaline phosphatase -moderately elevated serum amylase

Question 44

acute cholecystitis -tx *conservative regimen *pain management *recurrent attacks *non-surgical tx *surgical tx

Answer 44

-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

Question 45

Acute pancreatitis -key findings

Answer 45

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

Question 46

Acute pancreatitis -prevalence -prevention

Answer 46

-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

Question 47

Acute pancreatitis -associated with: (9)

Answer 47

-hypercalcemia -HLD -drugs -vasculitis infections (mumps, CMV, etc.) -peritoneal dialysis -cardiopulmonary bypass -single- or double-balloon enteroscopy -ERCP -abdominal trauma (surgery)

Question 48

Acute pancreatitis -pathogenesis

Answer 48

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

Question 49

Acute pancreatitis -S/S -physical exam

Answer 49

-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

Question 50

Acute pancreatitis -diagnostic imaging *plain XR of abd *ultrasound *unenhanced CT scan

Answer 50

-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)

Question 51

Acute pancreatitis -diagnostic imaging *CT scan w/ contrast *MRI *EUS *ERCP

Answer 51

-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

Question 52

Acute pancreatitis -assessment of severity

Answer 52

labs + severity of acute alcoholic pancreatitis can be assessed using several scoring systems --> ranson criteria

Question 53

Acute pancreatitis -lab findings

Answer 53

-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

Question 54

Acute pancreatitis -mild disease *how to manage *refer or treat outpatient?

Answer 54

-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

Question 55

Acute pancreatitis: mild disease -following recover from acute biliary pancreatitis, what test is performed?

Answer 55

laparoscopic cholecystectomy

Question 56

Acute pancreatitis: severe disease -what is occurring? -refer or treat outpatient?

Answer 56

-necrotizing pancreatitis -refer!!

Question 57

Acute pancreatitis: severe disease

Answer 57

-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

Question 58

acute pancreatitis - severe disease -antibiotics (when to administer)

Answer 58

sterile necrotizing pancreatitis - don't administer abx in pt with less than 30% pancreatic necrosis! *abx of choice >30%: imipenem and cefuroxime

Question 59

Hematuria -essentials of dx *gross vs microscopic - which require evaluation? *what should occur with hematuria in absence of infection?

Answer 59

-both gross and microscopic hematuria require evaluation -hematuria in absence of infection --> upper urinary tract should be imaged, and cystoscopy be performed

Question 60

Hematuria: clinical findings -upper tract source (kidney/ureters)

Answer 60

-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

Question 61

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

Answer 61

-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

Question 62

Hematuria -S/S *gross hematuria *associated sx *physical examination *urologic evaluation

Answer 62

-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

Question 63

Hematuria: diagnostic studies

Answer 63

-Obtain diagnostic clues from medical ingestion and associated medical problems -abd and pelvic CT scan (with & w/o IV contract) or upper tract -cystoscopy

Question 64

Hematuria: lab findings -urinalysis and urine culture

Answer 64

-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

Question 65

Hematuria: follow-up -repeat evaluations? -urinary cytology -imaging repeated how often?

Answer 65

-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

Question 66

Hematuria: when to refer

Answer 66

absence of infection or other benign etiology, hematuria (either gross or microscopic) requires evaluation

Question 67

Acute Cystitis: essentials of dx -sx

Answer 67

irritative voiding sx, usually afebrile, positive urine culture; blood cultures may be positive

Question 68

Acute Cystitis -common cause -route of infection -viral cystitis -uncomplicated cystitis (men)

Answer 68

-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!!!!!

Question 69

Acute Cystitis -S/S -physical examination

Answer 69

-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!!!!!

Question 70

Acute Cystitis: prevention -women -how to assess?

Answer 70

->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

Question 71

Acute Cystitis: diagnostic studies

Answer 71

-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

Question 72

Acute Cystitis: lab findings (2 tests)

Answer 72

-urinalysis: pyuria, bacteriuria, and varying degrees of hematuria -positive urine culture: + for offending organism

Question 73

Acute Cystitis: differential dx -women -men -noninfectious causes of cystitis-like sx

Answer 73

-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

Question 74

Acute Cystitis: prognosis

Answer 74

responds rapidly to therapy, and failure to respond suggests resistance to the selected medication - REQUIRES FURTHER EVAL!!

Question 75

Acute Cystitis: treatment -uncomplicated cystitis in women -uncomplicated urinary tract infection in men

Answer 75

-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

Question 76

Acute Cystitis: when to refer

Answer 76

-suspicion or radiographic evidence of anatomic abnormality -evidence of urolithiasis -recurrent cystitis due to bacterial persistence

Question 77

Acute Pyelonephritis: clinical findings -def -most common cause -route of infection

Answer 77

-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

Question 78

Acute Pyelonephritis: essentials of dx

Answer 78

fever, flank pain, irritative voiding sx, POSITIVE URINE CULTURE

Question 79

Acute Pyelonephritis: dx studies

Answer 79

renal US: complicated pyelonephritis to evaluate hydronephrosis from a stone or other source of obstruction

Question 80

Acute Pyelonephritis: lab findings -complete CBC -urinalysis -urine culture -blood culture

Answer 80

-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

Question 81

Acute Pyelonephritis -S/S

Answer 81

-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

Question 82

Acute Pyelonephritis: prevention -women -most common PO abx agents -when to take abx

Answer 82

->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

Question 83

Acute Pyelonephritis: differential dx (5)

Answer 83

-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

Question 84

Acute Pyelonephritis: prognosis -what can lead to less favorable outcome? -complications

Answer 84

-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

Question 85

Acute Pyelonephritis: treatment -ID causative agent -outpatient or inpatient tx? -follow-up cultures?

Answer 85

-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

Question 86

Acute Pyelonephritis -when to refer

Answer 86

evidence of complicating factors (urolithiasis, obstruction) -absence of clinical improvement in 48 hours

Question 87

Acute Pyelonephritis -when to admit

Answer 87

severe infections or complicating factors, evidence of sepsis or need for parenteral antibiotics -need for radiographic imaging or drainage of urinary tract obstruction

Question 88

Urinary Stone Disease -key findings -occur more in men or women? -urinary calculi (made of what?) -5 major types of stone

Answer 88

-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

Question 89

Urinary Stone Disease -most common type of stone -how do urinary stones appear on xrays?

Answer 89

-calcium (85%) -most urinary stones are RADIOPAQUE on plain abd xrays *uric acid stone = radiopaque *PURE uric acid stones = radiolucent *cystine stones = radiolucent

Question 90

Urinary Stone Disease -geographic factors contribute to development of stones

Answer 90

-high humidity and elevated temperatures (hot summer months); sedentary lifestyle, HTN, carotid calcification, CV disease

Question 91

Urinary Stone Disease -dietary factors -genetic factors

Answer 91

-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

Question 92

Urinary Stone Disease -diagnostic findings (4)

Answer 92

-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

Question 93

Urinary Stone Disease: labs -urinalysis -urinary pH

Answer 93

-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

Question 94

Urinary Stone Disease: S/S -obstructing urinary stones -stone progresses down ureter -stone becomes lodged at uretero-vesicular junction -after stone passes into bladder

Answer 94

-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

Question 95

Urinary Stone Disease: stone evaluation -stone analysis (how to help dec stones)

Answer 95

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

Question 96

Urinary Stone Disease -stone evaluation: tests to run

Answer 96

-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)

Question 97

Urinary Stone Disease: treatment -metabolic evaluation -recurrence of stones -follow-up

Answer 97

-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

Question 98

Urinary Stone Disease: diet -restrict...? -animal protein...? -limit intake of...? -dietary calcium intake

Answer 98

-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

Question 99

Calcium Nephrolithiasis -etiology -how many different types?

Answer 99

-increased absorption of calcium at the level of the small bowel (jejunum) -can be subdivided into types I, II, III

Question 100

Calcium Nephrolithiasis -hypercalciuric *cause *tx

Answer 100

->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

Question 101

Calcium Nephrolithiasis -hyperuricosuric *def *tx *labs (urinary pH #)

Answer 101

-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

Question 102

Calcium Nephrolithiasis: hyperoxaluric -cause -patho

Answer 102

-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

Question 103

Calcium Nephrolithiasis: hyperoxaluric -tx -avoid -caution

Answer 103

-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

Question 104

Calcium Nephrolithiasis -type I *cause *tx

Answer 104

-absorptive hypercalciuria *independent of calcium intake *thiazide diuretics can be used to dec renal calcium excretion

Question 105

Calcium Nephrolithiasis -type II *cause *tx

Answer 105

-absorptive hypercalciuria *diet-dependent; rare *decreasing calcium intake by 50%

Question 106

Calcium Nephrolithiasis -type III *cause *tx

Answer 106

-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

Question 107

Calcium Nephrolithiasis: resorptive hypercalciuria -cause -labs -tx

Answer 107

-secondary to hyperparathyroidism -hypercalcemia, hypophosphatemia, hypercalciuria, and elevated serum PTH value -sx resection of the parathyroid adenoma cures the disease

Question 108

Renal Hypercalciuria -cause -labs -tx

Answer 108

-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

Question 109

Hypocitraturic -secondary to? -patho -associated with: -treatment patho:

Answer 109

-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)

Question 110

Uric Acid Calculi -cause -tx

Answer 110

-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)

Question 111

Uric Acid Calculi -other causes (besides pH inc) -diagnosis

Answer 111

-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

Question 112

Struvite calculi -def -prevalence -dx

Answer 112

-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

Question 113

Struvite calculi -labs -stone analysis -treatment -recurrence

Answer 113

-urinary pH is HIGH (>7.2) -relatively soft -percutaneous removal; order the REQUIRED perioperative antibiotics -recur rapidly

Question 114

what kind of calculi require perioperative antibiotics?

Answer 114

struvite calculi

Question 115

Cystine calculi -cause -tx -prevention

Answer 115

-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

Question 116

which calculi type has no known inhibitors?

Answer 116

cystine calculi

Question 117

which calculi requires potassium citrate or equivalent agent to help with stone dissolution and prophylaxis?

Answer 117

uric acid calculi

Question 118

six types of calcium nephrolithiasis?

Answer 118

1. hypercalciuric 2. hyperuricosuria 3. hyperoxaluric 4. resorptive hypercalciuria 5. renal hypercalciuria 6. hypocitraturia

Question 119

Ureteral Stones -sites of urine obstruction with stone -stones that pass spontaneously -stones that require surgical removal (and with what?)

Answer 119

-ureteropelvic junction, crossing ureter over iliac artery, ureterovesicular junction -5-6mm on abd XR -mid-distal ureter stones

Question 120

Ureteral Stones: proximal and intrarenal stones -how to increase rate of spontaneous stone passage -when do small stones require surgical intervention?

Answer 120

-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

Question 121

Ureteral Stones: mid-distal ureter stones *how are stones removed? *obstructed stone fragments post-SWL conservative management *fragments not passed within 6 weeks

Answer 121

-removed with ureterscopic stone extraction *SWL or ureteroscopy -spontaneous resolution w/ eventual passage of stone fragments -unlikely to do so w/o intervention

Question 122

Ureteral stones: medical & surgical tx -acute setting -signs of infection *when is it a medical emergency?

Answer 122

-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

Question 123

Renal Calculi -without pain/UTI/obstruction -intervene when symptomatic? -<2cm *how to tx -what happens when SWL/stones do not pass?

Answer 123

-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

Question 124

Urinary Stone Disease: when to refer

Answer 124

-evidence of urinary obstruction -urinary stone with associated flank pain -anatomic abnormalities or solitary kidney -concomitant pyelonephritis or recurrent infection

Question 125

Urinary Stone Disease: