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CMN568 > Module 4 EB #3 > Flashcards

Module 4 EB #3 Flashcards

1
Q

Diverticular disease
-essentials of dx
-patho
-etiology

A

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

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2
Q

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

A

-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

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3
Q

Diverticulosis disease
-lab studies
-dx
-dx imaging

A

-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

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4
Q

diverticulosis disease
-tx
-bleeding

A

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

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5
Q

diverticulosis disease
-risk factors

A

age
obesity
smoking
lack of exercise

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6
Q

diverticula/diverticulum
-def

A

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

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7
Q

diverticulosis
-def

A

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

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8
Q

diverticulitis
-def

A

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

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9
Q

diverticular bleeding
-def

A

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

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10
Q

diverticulosis disease - symptomatic
-essentials of dx
-def

A

-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

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11
Q

diverticulosis disease - symptomatic
-sx
-physical exam

A

-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)

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12
Q

diverticulosis disease - symptomatic
-imaging
-NOTE

A

-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

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13
Q

diverticulosis disease - symptomatic
-prevention
-complications

A

-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

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14
Q

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

A

-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

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15
Q

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

A

-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

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16
Q

Hemorrhoids
-essentials of dx (3)

A

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

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17
Q

Hemorrhoids
-internal hemorrhoids

A

-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

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18
Q

Hemorrhoids
-external hemorrhoids

A

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

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19
Q

Hemorrhoids
-when do they become symptomatic?
-risk factors

A

-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

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20
Q

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

A

-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)

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21
Q

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

-digital exam

A

-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

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22
Q

Hemorrhoids
-treatment
*conservative measures

A

-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

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23
Q

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

A

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

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24
Q

Cholelithiasis
-key findings

A

-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

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25
Q

Cholelithiasis
-prevention
-rapid weight loss component and prevention

A

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

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26
Q

Cholelithiasis
-prevalence

A

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

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27
Q

Cholelithiasis
-associated with:

A

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)

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28
Q

Cholelithiasis
-how are gallstones classified?

A

by chemical composition
-cholesterol or calcium bilirubinates

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29
Q

Cholelithiasis
-dx studies

A

gallstones detected by ultrasound

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30
Q

Cholelithiasis
-risk factors for developing sx/complications

A

-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

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31
Q

Cholelithiasis
-recurrence?

A

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

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32
Q

Cholelithiasis
-risk factors

A

-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

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33
Q

Cholelithiasis
-treatment of choice for symptomatic gallbladder disease

A

-lap cholecystectomy

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34
Q

Cholelithiasis
-tx of biliary pain in pregnancy

A

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

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35
Q

Cholelithiasis
-ursodeoxycholic acid

A

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

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36
Q

acute cholecystitis
-key findings

A

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

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37
Q

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

A

-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!!!

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38
Q

acute cholecystitis
-etiology
*patho
*other causes

A

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

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39
Q

acute cholecystitis
-diagnostic imaging
*plain XR films

A

-gallstones

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40
Q

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

A

-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)

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41
Q

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

A

-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

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42
Q

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

A

-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)

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43
Q

acute cholecystitis
-lab findings

A

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

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44
Q

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

A

-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

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45
Q

Acute pancreatitis
-key findings

A

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

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46
Q

Acute pancreatitis
-prevalence
-prevention

A

-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

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47
Q

Acute pancreatitis
-associated with: (9)

A

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

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48
Q

Acute pancreatitis
-pathogenesis

A

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

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49
Q

Acute pancreatitis
-S/S
-physical exam

A

-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

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50
Q

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

A

-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)

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51
Q

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

A

-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

52
Q

Acute pancreatitis
-assessment of severity

A

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

53
Q

Acute pancreatitis
-lab findings

A

-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

54
Q

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

A

-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

55
Q

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

A

laparoscopic cholecystectomy

56
Q

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

A

-necrotizing pancreatitis
-refer!!

57
Q

Acute pancreatitis: severe disease

A

-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

58
Q

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

A

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

59
Q

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

A

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

60
Q

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

A

-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

61
Q

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

A

-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

62
Q

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

A

-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

63
Q

Hematuria: diagnostic studies

A

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

64
Q

Hematuria: lab findings
-urinalysis and urine culture

A

-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

65
Q

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

A

-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

66
Q

Hematuria: when to refer

A

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

67
Q

Acute Cystitis: essentials of dx
-sx

A

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

68
Q

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

A

-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!!!!!

69
Q

Acute Cystitis
-S/S
-physical examination

A

-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!!!!!

70
Q

Acute Cystitis: prevention
-women
-how to assess?

A

->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

71
Q

Acute Cystitis: diagnostic studies

A

-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

72
Q

Acute Cystitis: lab findings (2 tests)

A

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

73
Q

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

A

-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

74
Q

Acute Cystitis: prognosis

A

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

75
Q

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

A

-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

76
Q

Acute Cystitis: when to refer

A

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

77
Q

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

A

-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

78
Q

Acute Pyelonephritis: essentials of dx

A

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

79
Q

Acute Pyelonephritis: dx studies

A

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

80
Q

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

A

-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

81
Q

Acute Pyelonephritis
-S/S

A

-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

82
Q

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

A

->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

83
Q

Acute Pyelonephritis: differential dx (5)

A

-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

84
Q

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

A

-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

85
Q

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

A

-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

86
Q

Acute Pyelonephritis
-when to refer

A

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

87
Q

Acute Pyelonephritis
-when to admit

A

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

88
Q

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

A

-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

89
Q

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

A

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

90
Q

Urinary Stone Disease
-geographic factors contribute to development of stones

A

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

91
Q

Urinary Stone Disease
-dietary factors
-genetic factors

A

-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

92
Q

Urinary Stone Disease
-diagnostic findings (4)

A

-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

93
Q

Urinary Stone Disease: labs
-urinalysis
-urinary pH

A

-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

94
Q

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

A

-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

95
Q

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

A

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

96
Q

Urinary Stone Disease
-stone evaluation: tests to run

A

-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)

97
Q

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

-follow-up

A

-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

98
Q

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

A

-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

99
Q

Calcium Nephrolithiasis
-etiology
-how many different types?

A

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

100
Q

Calcium Nephrolithiasis
-hypercalciuric
*cause
*tx

A

->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

101
Q

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

A

-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

102
Q

Calcium Nephrolithiasis: hyperoxaluric
-cause
-patho

A

-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

103
Q

Calcium Nephrolithiasis: hyperoxaluric
-tx
-avoid
-caution

A

-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

104
Q

Calcium Nephrolithiasis
-type I
*cause
*tx

A

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

105
Q

Calcium Nephrolithiasis
-type II
*cause
*tx

A

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

106
Q

Calcium Nephrolithiasis
-type III
*cause
*tx

A

-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

107
Q

Calcium Nephrolithiasis: resorptive hypercalciuria
-cause
-labs
-tx

A

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

108
Q

Renal Hypercalciuria
-cause
-labs
-tx

A

-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

109
Q

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

A

-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)

110
Q

Uric Acid Calculi
-cause
-tx

A

-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)

111
Q

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

A

-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

112
Q

Struvite calculi
-def
-prevalence
-dx

A

-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

113
Q

Struvite calculi
-labs
-stone analysis
-treatment
-recurrence

A

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

114
Q

what kind of calculi require perioperative antibiotics?

A

struvite calculi

115
Q

Cystine calculi
-cause
-tx
-prevention

A

-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

116
Q

which calculi type has no known inhibitors?

A

cystine calculi

117
Q

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

A

uric acid calculi

118
Q

six types of calcium nephrolithiasis?

A
  1. hypercalciuric
  2. hyperuricosuria
  3. hyperoxaluric
  4. resorptive hypercalciuria
  5. renal hypercalciuria
  6. hypocitraturia
119
Q

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

A

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

120
Q

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

A

-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

121
Q

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

A

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

122
Q

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

A

-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

123
Q

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

A

-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

124
Q

Urinary Stone Disease: when to refer

A

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

125
Q

Urinary Stone Disease:

A

CMN568 (10 decks)

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