ID Flashcards

1
Q

How are community and hospital acquired pneumonia defined?

A
  • community occurs in the community or within the first 72 hours of hospitalization
  • hospital occurs during hospitalization after the first 72 hours
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2
Q

Typical Community Acquired Pneumonia

A
  • that which occurs outside the hospital setting or within the first 72 hours of hospitalization
  • most commonly caused by S. pneumoniae, H. influenzae, and aerobic gram-negatives like Klebsiella
  • presents with acute onset of fever and shaking chills, cough productive of thick purulent sputum, pleuritic chest pain, and dyspnea
  • patients are typically tachycardic, tachypneic, and have late inspiratory crackles on exam
  • CXR typically shows lobar consolidation
  • treat with a fluoroquinolone or a second or third generation cephalosporin in the outpatient setting
  • treat with a fluoroquinolone or a third generation cephalosporin with a macrolide in the inpatient setting
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3
Q

Atypical Community Acquired Pneumonia

A
  • a community acquired pneumonia caused by an organism that is not visible on gram stain and is not culturable on standard blood agar
  • more common in younger, healthy patients
  • common agents include Mycoplasma pneumoniae, chlamydia pneumoniae, Coxiella burnetii, Legionella, and viruses such as flu, adenovirus, parainfluenza, etc.
  • presents with a more insidious onset including headache, sore throat, fatigue, myalgias, dry cough, and fever without chills
  • notably, they often have pulse-temperature dissociation in that their pulse is normal in the setting of a very high fever
  • CXR typically shows diffuse reticulonodular infiltrates with minimal or without consolidation
  • treat with macrolides or doxycycline
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4
Q

How do typical and atypical community acquired pneumonias differ?

A
  • atypical are those that can’t be visualized using gram stain or cultured using standard blood agar
  • typical includes S. pneumonia, H. influenza, and some aerobic, gram-negative rods while atypical includes Mycoplasma pneumoniae, Chlamydia pneumoniae, Coxiella, Legionella, and viruses
  • typical will present with a more acute onset while atypical has a more insidious onset
  • typical will usually have tachycardia while atypical is likely to have temperature-pulse dissociation
  • typical usually presents with a productive cough while atypical presents with a dry cough
  • on CXR typical demonstrates consolidation while atypical has diffuse reticulonodular infiltrates
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5
Q

What specific etiologic agents are associated with pneumonia in alcoholics and in immigrants?

A
  • alcoholics: think Klebsiella

- immigrants: think TB

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6
Q

Which etiologic agents are most likely to be the cause of a secondary pneumonia?

A

Strep pneumo followed by S. aureus

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7
Q

Describe the role of CXR in the diagnosis of pneumonia.

A
  • a PA and lateral CXR are required to confirm the diagnosis
  • additionally it is considered sensitive, so if the CXR does not suggest pneumonia, do not treat with antibiotics
  • CXR may take 6 weeks after clinical change to demonstrate resolution
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8
Q

How long after clinical resolution of a pneumonia may it take for the CXR to show resolution?

A

up to 6 weeks

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9
Q

False-negative CXRs looking for pneumonia are most often caused by what four things?

A
  • neutropenia
  • dehydration
  • infection with PCP
  • early disease (less than 24 hours)
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10
Q

What is unique about Legionella pneumonia?

A
  • it is common in organ transplant recipients, patients with renal failure, patients with chronic lung disease, and smokers
  • it presents with a pneumonia accompanied by GI symptoms and hyponatremia
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11
Q

How is the decision about whether or not to hospitalize a patient with pneumonia made?

A

using the pneumonia severity index, which takes into account demographics, comorbid illness, physical exam findings, lab findings, and radiographic findings

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12
Q

How is community acquired pneumonia treated?

A

outpatients require treatment for at least 5 days and until they have been afebrile for at least 48 hours
- for patients younger than 60 in the outpatient setting, we’re worried about S. pneumonia, Mycoplasma, Chlamydia, and Legionella: treat with macrolide or doxy as first-line agents and add a fluoroquinolone as an alternative therapy
- for patients over 60, who have a comorbid condition, or who have been treated with antibiotics in the last three months we’re worried about more typical agents: start with a fluoroquinolone and add on a second- or third-generation cephalosporin
for hospitalized patients, use a fluoroquinolone alone or a third-generation cephalosporin plus a macrolide

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13
Q

How is hospital-acquired pneumonia treated?

A

treatment is aimed at gram-negative rods:

  • cephalosporins with pseudomonas coverage including ceftazidime or cefepime
  • carbapenems
  • zosyn
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14
Q

What are the most common complications of pneumonia?

A
  • pleural effusions
  • pleural empyema
  • acute respiratory failure
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15
Q

How is pleural effusion in the setting of pneumonia managed?

A
  • usually they are uncomplicated and resolve with treatment of the pneumonia
  • a thoracentesis is needed only if it is more than 1 cm on lateral decubitus film
  • it rarely progresses to an empyema but this requires chest tube drainage if it does
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16
Q

Ventilator Associated Pneumonia

A
  • mechanical ventilation is a risk factor because it imapirs normal mucociliary clearance
  • a bronchoalveolar lavage is performed to get cultures
  • treat with a combination of two of the following: cephalosporin/penicillin/carbapenem, aminoglycoside/fluroquinolone, and vanc/linezolid
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17
Q

Lung Abscess

A
  • defined as one or more suppurative cavitary lesions more than 2 cm in diameter
  • results when infected lung tissue becomes necrotic, typically in the setting of inadequately treated pneumonia
  • the most common agents are oral anaerobes Prevotella, Peptostreptococcus, Fusobacterium, and Bacteroides and other bacteria like S. aureus or S. pneumoniae
  • because aspiration is the biggest risk factor, these abscess most commonly arise in the posterior segments of the RUL and the superior segments of the RLL
  • has an indolent onset with cough productive of foul-smelling sputum, shortness of breath, fever, chills, and constitutional symptoms
  • CXR reveals a thick-walled cavitation with air-fluid levels but a CT may be necessary to differentiate it from an empyema
  • sputum stain or culture is unreliable and a bronchoscopy or transtracheal aspiration may be needed
  • treat with hospitalization, postural drainage, and a long course of antibiotics until the cavity is gone
  • antibiotics selection: ampicillin or vanc for gram-positive cocci, clindamycin or metronidazole for anaerobes, and a fluoroquinolone or ceftazidime for gram-negatives
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18
Q

Primary TB

A
  • an infection due to inhalation of aerosolized M. tuberculosis
  • this initial infection is known as primary TB and affects predominately the middle or lower lobes of the lungs
  • although asymptomatic in most cases, primary TB will lead to a positive PPD
  • the organism replicates in macrophages and may spread via the lymphatics to the hilar nodes, causing lymphadenopathy
  • involvement of the hilar nodes forms a Ghon complex, which is the combination of hilar lymphadenopathy and a parenchymal, caseating granuloma in the subpleural space
  • in most cases, the bacteria are walled off in these granulomas, fibrosed, and calcified, forming a Ranke complex with the infection becoming latent
  • rifampin and isoniazid can be used as prophylaxis to prevent reactivation
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19
Q

Secondary TB

A
  • a symptomatic stage of TB caused by reactivation of the bacteria, typically following application of TNFa inhibitors or the onset of some other immune compromised state
  • reactivated bacteria tend to involve the upper lobes of the lungs where O2 content is highest and presents with cough, hemoptysis, night sweats, weight loss, and apical rales on exam
  • the hematogenous spread of progressive primary or secondary TB is known as miliary TB
  • spread to the brain forms cavitary lesions known as tuberculomas; spread to the vertebral column, most often the lower thoracic or upper lumbar, is known as Pott disease
  • sputum culture is the definitive method for diagnosis but requires 4-8 weeks, PCR is more rapid, and AFB on microscopy is supportive of diagnosis
  • rifampin, isoniazid, pyrazinamide and ethambutol is the preferred treatment combination
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20
Q

Primary TB is characterized by what type of granulomas?

A

caseating granulomas in the subpleural space of the lower lobe of the lung, which stain with AFB

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21
Q

What is the difference between a Ghon focus, Ghon complex, and Ranke complex?

A

they are progressive stages of a TB lesion

  • a Ghon focus is a small area of granulomatous inflammation
  • it is said to be a Ghon complex if it also involves the adjacent lymphatics or hilar lymph nodes
  • when the Ghon complex fibroses and calcifies, it becomes known as a Ranke complex
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22
Q

What is primary progressive TB?

A

a primary TB infection that involves pulmonary and constitutional symptoms because the immune response is incomplete or inadequate, so it never enters a latent phase

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23
Q

Describe TB skin testing.

A
  • a screening test to detect those who may have been exposed to TB
  • it is for the diagnosis of latent TB, not active TB (if active TB is suspected, get a sputum acid-fast test and CXR)
  • 15 mm induration is positive in those with no risk factors
  • 10 mm induration is positive in those who live in a high-prevalence area, are immigrants from within the last 5 years, are homeless, prisoners, healthcare workers, nursing home residents, alcoholics, or diabetics, and those with a close contact with primary TB
  • 5 mm induration is positive in those who are HIV-positive, steroid users, transplant recipients, in close contact with someone with active TB, or who have radiographic evidence of TB
  • should repeat the test after 1-2 weeks if it is the individuals first time being tested
  • follow up a positive test with a CXR to evaluate for active disease
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24
Q

How is TB treated?

A
  • a positive PPD without CXR evidence of active TB should be followed by 9 months of isoniazid, even if the patient has a history of BCG vaccination
  • those with active TB must be isolated and treated with isoniazid, rifampin, pyrazinamide, and ethambutol or streptomycin for two months followed by four more months of INH and rifampin
  • remember that all these agents can cause hepatotoxicity but should only be discontinued if liver transaminases rise to 3-5 times the upper limit of normal
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25
Q

Isoniazid should always be given alongside what other agent? Why?

A
  • it should always be started with vitamin B6, aka pyridoxine
  • this helps prevent symptoms of B6 deficiency including stomatitis, glossitis, cheilosis, convulsions, hyper irritability, peripheral neuropathy, and sideroblastic anemia
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26
Q

Why is the diagnosis of TB challenging in patients with HIV?

A
  • PPD skin testing may be falsely negative due to anergy
  • patients have atypical CXR findings
  • sputum smears are more likely to be negative
  • granuloma formation may not be present in the later stages
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27
Q

What is an adverse reaction that can be caused by all TB medications? What is the indication to stop these meds?

A
  • all can cause hepatotoxicity

- they should be discontinued only if liver transaminases rise to 3-5 times the upper limit of normal

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28
Q

Influenza

A
  • caused by orthomyxovirus, divided into two antigenic types A and B, which is transmitted via respiratory droplets during the winter months
  • annual epidemics are due to minor genetic reassortment while rare pandemics are due to major genetic recombination and are more often fatal
  • presents with rapid onset fever, chills, malaise, headache, nonproductive cough, and sore throat
  • treatment is supportive; antivirals, primarily neuraminidase inhibitors, are indicated only in severe disease or in those with a high risk of complications and must be given in the first 48 hours of illness
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29
Q

What is zanamivir and oseltamivir?

A

they are neuraminidase inhibitors which prevent the enzyme from cleaving budding viral progeny from their cellular envelope attachment points (neuraminic acid) just prior to release

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30
Q

Meningitis

A
  • inflammation of the meningeal membranes that envelope the brain and spinal cord
  • classified as acute, onset within hours to days, versus chronic, onset within weeks to months
  • the cause of acute meningitis varies heavily by age but agents include GBS, E. coli, S. pneumoniae, H. influenzae, and N. meningitidis
  • chronic meningitis is most often caused by mycobacteria, fungi, Lyme disease, or parasites
  • aseptic meningitis is cased by a variety of nonbacterial pathogens such as enterovirus and HSV
  • it may also be caused by non-infectious processes such as medications, SLE, and sarcoidosis
  • presentation includes the classic triad of fever, nuchal rigidity, and change in mental status as well as n/v, malaise, photophobia, and headache
  • signs include the manifestations of increased ICP, Kernig sign, and Brudzinski sign
  • diagnosed based on LP, but should get a CT first if there are focal neurologic signs or evidence of increased ICP
  • treat meant should be started immediately following the LP or before the LP if there will be a delay such as the need for a CT
  • treat with empiric antibiotics, usually requiring some combination of cephalosporins, vancomycin, and ampicillin; add steroids if cerebral edema is present
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31
Q

Give the likely pathogens and the empiric treatment for acute bacterial meningitis in the following:

  • less than 3 months (neonates)
  • 3 months to 50 years old
  • over 50 years old (elderly)
  • immunocompromised
A
  • neonates: GBS, E. coli, and Listeria treated with cefotaxime, amp, and vanc
  • 3-50: N. meningitidis, S. pneumoniae, and H. influenzae treated with ceftriaxone/cefotaxime and vanc
  • elderly: S. pneumoniae, N. meningitis, Listeria treated with ceftriaxone/cefotaxime, amp, and vanc
  • immunocompromised: S. pneumoniae, N. meningitidis, Listeria, and aerobic gram-negative bacilli like Pseudomonas treated with ceftazidime, amp, and vanc
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32
Q

What are the Kernig and Brudzinski signs?

A

they are signs of meningitis

  • Kernig is an inability to fully extend the knees when patients are supine with hips flexed
  • Brudzinski is flexion of the legs and thighs brought on by passive flexion of the neck
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33
Q

What will an LP show for the following types of meningitis:

  • bacterial
  • viral
  • fungal/TB
A
  • bacterial: elevated opening pressure, cloudy appearance, increased cell count of predominately PMNs, increased protein, and reduced CSF-to-serum glucose ratio
  • viral: normal or slightly elevated opening pressure, clear appearance, increased cell count of predominately lymphocytes, slightly increased protein, and normal clugose
  • fungal/TB: elevated opening pressure, cloudy appearance, increased cell count of predominately lymphocytes, elevated protein, and diminished glucose
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34
Q

How does the treatment of aseptic meningitis differ from that of acute bacterial meningitis?

A

aseptic is self-limited and does not require anything more than supportive care, including analgesics and antipyretics

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35
Q

Encephalitis

A
  • a diffuse inflammation fo the brain parenchyma
  • most often viral in origin, including HSV-1, arboviruses such as West Nile, and enteroviruses such as polio
  • may also be caused by toxoplasmosis, cerebral aspergillosis, metabolic encephalopathies, and T-cell lymphoma
  • presents with a prodrome of headache, malaise, and myalgias; often complicated by meningitis and associated symptoms; typically progresses to altered mental status and behavioral abnormalities; focal neurologic deficits and seizures may be occur
  • MRI brain is the imaging study of choice; increased areas of T2 signal in frontotemporal region is consistent with HSV encephalitis
  • CSF PCR is the most specific and sensitive test for diagnosing many of the viral encephalitis causes
  • treat with supportive care, antivirals (acyclovir for HSV and ganciclovir or foscarnet for CMV), and management of possible complications
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36
Q

How is cerebral edema treated?

A

hyperventilation, osmotic diuresis, and steroids to reduce ICP

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37
Q

Which agents are likely to cause a brain abscess in in those who have AIDS or are neutropenic?

A
  • AIDS: toxoplasma gondii and fungi

- neutropenic: Candida, aspergillus, and zygomycosis

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38
Q

What is the differential diagnosis for altered mental status?

A

MOVE STUPID

  • metabolic (B12, thiamine, serotonin, thyroid)
  • oxygen (cardiopulmonary, anemia)
  • vascular (HTN, CVA, vasculitis)
  • electrolyte/endocrine
  • seizure
  • tumor/trauma/temperature
  • uremia (renal or hepatic)
  • psychiatric
  • infection
  • drugs, including withdrawal
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39
Q

How are the hepatitis viruses transmitted?

A
  • A and E via the fecal-oral route
  • B parenterally or sexually
  • C parenterally
40
Q

How are acute and chronic viral hepatitis defined?

A
  • acute is that with less than 6 months of liver inflammation
  • chronic is that with more than 6 months of liver dinflammation
41
Q

Which types of hepatitis can potentially progress to chronic disease and which is most likely to?

A

B, C, and D are all possible causes; however, hepatitis C is the most likely

42
Q

Describe the presentation of acute hepatitis.

A

can vary from subclinical and asymptomatic to fulminant liver failure, but generally presents with:

  • jaundice
  • dark colored urine as a result of conjugated hyperbilirubinemia
  • RUQ pain
  • n/v and malaise
  • hepatomegaly
43
Q

What are the major complications of fulminant hepatitis?

A
  • hepatic encephalopathy
  • hepatorenal syndrome
  • bleeding diathesis
44
Q

Describe the presentation of chronic hepatitis.

A
  • on the one hand, patients may be asymptomatic and chronic carriers; they may only present with the late complications such as cirrhosis and HCC
  • in other cases it can present as an extension of the acute phase with jaundice, direct hyperbilirubinemia, RUQ pain, hepatomegaly etc.
45
Q

How is HCV infection diagnosed?

A

PCR to detect viral RNA

46
Q

Describe hepatitis A serology.

A

anti-HAV is detectable during acute infection and persists for life so IgG cannot distinguish the two

47
Q

Describe hepatitis B serology.

A
  • HBsAg is present in acute or chronic infection until the infection is cleared
  • HBeAg is present during active viral replication and it’s presence indicates contagiousness of the host
  • anti-HBs is present after vaccination or resolution of an infection and is protective
  • anti-HBc is present only in those who have been infected (not those who were vaccinated) and can be helpful because it may be present in the window between HBsAg disappearance and anti-has formation but it is not protective
48
Q

How is viral hepatitis treated?

A
  • treatment for A and E are supportive
  • IFNa or lamivudine are used to treat chronic HBV
  • IFNa and ribavirin are used to treat chronic HCV
  • may eventually require a liver transplant
49
Q

Botulism

A
  • a disease caused by ingestion of preformed toxins produced by the spores of C. botulinum in improperly stored food
  • presents with symmetric, descending flaccid paralysis that starts a dry mouth, diplopia, and dysarthria; abdominal cramps, n/v, and diarrhea are common
  • diagnosed by a toxin assay of stool, serum, or gastric contents
  • treat by monitoring their respiratory status and administration of an antitoxin as soon as laboratory specimens are collected
50
Q

How are intra-abdominal abscesses treated?

A
  • begin with drainage of the abscess

- use an antibiotic regiment that covers gram-negative rods, enterococci, and anaerobes

51
Q

Cystitis

A
  • risk factors are female gender, sexual intercourse, pregnancy, indwelling urinary catheters, and diabetes; males who are uncircumcised or have anal intercourse are more at risk
  • most often due to E. coli; Staph saprophyticus is characteristically seen in young, sexually active women; enterococcus and K. pneumoniae are common; Proteus mirabilis is likely if the urine is alkaline with an ammonia scent
  • presents with dysuria, frequency, urgency, and suprapubic pain; systemic symptoms like fever are absent
  • urine is cloudy with more than 10 WBC/uL, dipstick is positive for leukocyte esterase and potentially nitrites, culture grows greater than 100K colonies
  • sterile pyuria (cystitis with a negative urine culture) suggests urethritis due to Chlamydia trachomas or Neisseria gonorrhoeae
  • treat uncomplicated cases with 3 days of bactrim, nitrofurantoin, fosfomycin single dose, or ciprofloxacin
52
Q

What does the following in urine indicate:

  • leukocyte esterase:
  • nitrites:
  • squamous cells
A
  • positive leukocyte esterase reflects pyuria
  • positive nitrite test is sensitive and specific for enterobacteriaceae
  • squamous cells reflex vulvar or urethral contamination
53
Q

What is the most important finding on UA when trying to diagnose UTI?

A

WBCs, specifically more than 10 leukocytes per uL

54
Q

What is asymptomatic bacteriuria and when should it be treated?

A
  • it is defined as two successive positive cultures (more than 100K bacteria)
  • treat only in pregnancy or before urologic procedures
55
Q

What is considered to be a complicated UTI?

A

any UTI that spreads beyond the bladder or is caused by structural abnormalities, metabolic disorder, or neurologic dysfunction

  • those occurring in men, diabetics, and those with renal failure
  • those during pregnancy
  • those in the setting of pyelonephritis within the last year
  • those in the setting of an obstruction, indwelling catheter, stent, or nephrostomy tube
  • those that are in immunocompromised patients
56
Q

How is acute, uncomplicated cystitis treated?

A

with any of the following:

  • oral bactrim for 3 days
  • fosfomycin single dose (unless pyelonephritis is possible)
  • amoxicillin (falling out of favor due to resistance)
  • ciprofloxacin for 3 days
57
Q

What is phenazopyridine?

A

a urinary analgesic that can be used to treat dysuria in the setting of cystitis

58
Q

How are UTIs treated if during pregnancy, found in men, or are recurrent?

A
  • pregnancy: treat with ampicillin, amoxicillin, or oral cephalosporins for 7-10 days, avoiding fluoroquinolones which may cause fetal arthropathy
  • men: treat as you would uncomplicated (bactrim, fosfomycin, amoxicillin, ciprofloxacin) but for 7 days
  • recurrent: if within 2 weeks, continue normal treatment for two more weeks; if outside 2 weeks, treat as normally
59
Q

What is the preferred chemoprophylaxis for recurrent UTI?

A

single dose of bactrim after intercourse or at the first signs of symptoms

60
Q

Acute Pyelonephritis

A
  • an infection of the kidney
  • usually due to ascending infection secondary to vesicoureteral reflux
  • most common agents are E. coli, Enterococcus faecalis, and Klebsiella
  • presents with fever, flank pain, WBC casts, and leukocytosis in addition to the symptoms of cystitis
  • UA is likely to demonstrate pyuria, bacteriuria, and leukocyte casts; hematuria and mild proteinuria may be present
  • treat with bactrim or ciprofloxacin for 10-14 days in the outpatient setting after a single dose of ceftriaxone or gentamicin
  • treat with ampicillin plus gent or cipro for inpatient management
  • failure to respond to therapy suggests a functional or structural abnormality which should be evaluated
61
Q

Chronic Pyelonephritis

A
  • recurrent pyelonephritis, usually due to vesicoureteral reflux or obstruction
  • leads to interstitial fibrosis and atrophy of the tubules
  • atrophic tubules contain eosinophilic proteinaceous material and resemble thyroid follicles (referred to as thyroidization of the kidney)
  • cortical scarring at the upper and lower poles with blunted calyces is indicative of vesicoureteral reflux
62
Q

Acute Prostatitis

A
  • usually bacterial; Chlamydia trachomatis and Neisseria gonorrhoeae are common in younger males while E. coli and Pseudomonase are common in older adults (from spread of UTI)
  • presents with dysuria, fever, and chills, urgency, and low back pain
  • the prostate will feel warm, tender, boggy, and enlarged on digital rectal exam; this should be avoided when possible for fear of causing bacteremia
  • prostatic secretions will show WBCs and culture will reveal bacteria
  • bactrim or fluoroquinolone plus doxycycline for 4-6 weeks is the preferred treatment
63
Q

Chronic Prostatitis

A
  • chronic inflammation of the prostate
  • presents with dysuria and pelvic or low back pain; the prostate is often enlarged and non-tender on DRE
  • prostatic secretions show WBCs but cultures are usually negative
  • treat with a fluoroquinolone but eradication is very difficult and recurrence common
64
Q

How does acute differ from chronic prostatitis in clinical presentation?

A
  • acute is usually bacterial so prostatic secretions contain WBCs and are culture positive; however, secretions from those with chronic prostatitis are likely culture negative
  • additionally, acute presents with dysuria, fever, and chills whereas chronic presents with dysuria and pelvic or low back pain
65
Q

Chlamydia trichomadis

A
  • the most common bacterial STD and often accompanied by a gonorrheal infection
  • serotypes A-C are transmitted via hand-to-eye contact or via fomites and cause trachoma, a chronic infection leading to blindness (#1 cause of blindness worldwide)
  • serotypes D-K are sexually transmitted and cause urethritis with a watery discharge, PID, scrotal pain with swelling, and intermenstrual or postcoital bleeding
  • this PID is why chalmydia is the leading cause of infertility in women and is responsible for cases of epididymitis and proctitis in men
  • serotypes D-K also cause neonatal pneumonia with a staccato cough and neonatal conjunctivitis
  • serotypes L1-L3 cause lymphogranuloma venereum, which manifests as a painless genital ulcer followed weeks later by painful inguinal lymphadenopathy
  • all serotypes can be complicated by Reiter’s syndrome of uveitis, urethritis, and arthritis
  • diagnosed using nucleic acid amplification test (NAAT)
  • treat with single dose azithromycin or 7 days of doxycycline
66
Q

Gonorrhea

A
  • men are typically have symptoms involving the urethra including purulent discharge, dysuria, erythema and edema of the urethral meatus, and urinary frequency
  • most women are asymptomatic although it can produce symptoms of urethritis and cervicitis (dyspareunia or intermenstrual bleeding)
  • disseminated gonoccal infection may present with fever, arthralgia, tenosynovitis, migratory polyarthritis, endocarditis, etc.
  • complications include PID with possible infertility and chronic pelvic pain, epididymitis, prostatitis, salpingitis, tuba-ovarian abscess, and Fitz-Hugh-Curtis syndrome
  • it is facultative intracellular with a tropism for PMNs and gram stain showing gram negative diplococci within leukocytes is highly specific
  • grown on chocolate agar or VPN, also known as Thayer-Martin agar, with vancomycin, polymyxin, and nystatin
  • treat with ceftriaxone and add a macrolide or doxycycline to treat presumed co-infection with chlamydia
67
Q

What is the preferred treatment for chlamydia and for gonorrhea?

A
  • chlamydia: doxycycline or azithromycin

- gonorrhea: ceftriaxone plus doxy or azithromycin

68
Q

What are the four phases of HIV infection?

A
  • primary infection (mono-like syndrome)
  • asymptomatic infection
  • symptomatic infection
  • full-blown AIDS
69
Q

What defines AIDS in contrast to HIV?

A

AIDs is defined by marked immune suppression (CD4 count less than 200) or an AIDS defining illness

70
Q

How are CD4 cell counts and HIV viral loads used in management of HIV?

A
  • CD4 counts are the best indicator of immune status and risk for HIV-related diseases, it is used to determine when to initiate antiretroviral therapy and PCP prophylaxis
  • viral load is used to assess the response to and adequacy of antiretroviral therapy such that if the load is more than 50 after four months of treatment, the regimen should be altered
71
Q

Describe how the diagnosis of HIV is made.

A
  • PCR RNA viral load is the first test that will be positive
  • seroconversion occurs 3-7 weeks after infection and the diagnosis can be made with ELISA
  • western blot should be used to confirm seroconversion
72
Q

What pulmonary infection is often the initial opportunistic infection that establishes the diagnosis of AIDS?

A

P. carnii pneumonia

73
Q

What is the recommended prophylaxis for PCP in those with AIDS?

A

oral bactrim once CD4 cell count is less than 200

74
Q

When is antiretroviral therapy initiated in patients with HIV?

A
  • symptomatic patients regardless of CD4 count

- asymptomatic patients with CD4 count less than 500

75
Q

What are the components of HAART therapy?

A
  • two nucleoside reverse transcriptase inhibitors

- and either a non nucleoside reverse transcriptase inhibitor or a protease inhibitor

76
Q

What are the following for HIV therapy:

  • “navir”
  • raltegravir
  • enfuvirtide
  • maraviroc
A
  • navir is a suffix for protease inhibitors
  • raltegravir is an integrase inhibitor
  • enfuvirtide is a gp41 inhibitor that prevents entry
  • maraviroc is a CCR-5 inhibitor that blocks the interaction with gp120 for entry
77
Q

What is the recommended prophylaxis for the following in patients with HIV:

  • PCP
  • TB
  • MAC
  • Toxoplasmosis
A
  • PCP: bactrim when CD4 count is less than 200
  • TB: isoniazid plus pyridoxine if the patient has a positive PPD
  • MAC: clarithromycin or azithromycin when CD4 count is less than 100
  • toxoplasmosis: bactrim when CD4 count is less than 100
78
Q

Candidasis

A
  • budding yeast which form hyphae and long pseudohyphae
  • risk factors are antibiotic use, diabetes, immunosuppression, OCP use
  • presents as a thick, white vaginal discharge without pain; thrush; cutaneous candidiasis in the form of erythematous, eroded patches with satellite lesions; esophagitis with odynophagia; or disseminated disease causing multiple abscess, shock, or meningitis
  • KOH prep is used for diagnosis
  • treat with nystatin mouthwash for oral candida; oral ketoconazole or fluconazole for esophagitis; miconhzole or clotrimazole cream for vaginal candida; and amphotericin B or fluconazole for systemic cases
79
Q

Cryptococcus

A
  • a budding, round yeast with a thick polysaccharide capsule
  • associated with pigeon droppings and most commonly seen in patients with advanced AIDS
  • pulmonary infection is common but it may also affect the CNS causing meningitis or meningoencephalitis with brain abscesses
  • diagnose with an LP and a latex agglutination or india ink test
80
Q

How is fever of unknown origin defined and what are some frequent causes?

A
  • defined as having a fever continuing on several occasions for at least three weeks without a diagnosis despite one week of inpatient workup
  • causes are most often infectious; other causes include lymphoma and leukemia, collagen vascular disease, granulomatous diseases like Crohn’s or sarcoidosis, drug fevers, PE, familial mediterranean fever, gout, subacute thyroiditis, etc.
81
Q

How does fever differentiate from hyperthermia?

A
  • a fever, but not hyperthermia, is the result of an elevation in the hypothalamic set-point
  • instead, hyperthermia is usually the result of an inability fo the body to dissipate heat
  • as a result, fever will generally respond to antipyretics but hyperthermia requires external cooling measures
82
Q

Toxic Shock Syndrome

A
  • a disease caused by an enterotoxin of S. aureus or S. pyogenes that affects at least three organ systems
  • risk factors include tampon use, surgical wounds, burns, and infected insect bites
  • the onset of symptoms is abrupt and include flu-like symptoms, a diffuse macular, erythematous rash, hyperemic mucous membranes, strawberry tongue, warm skin and hypotension due to peripheral vasodilation
  • then during the convalescent phase the rash usually desquamates over the palms and soles
  • it is largely a clinical diagnosis
  • use fluids and pressers for stabilization, remove the source of the toxin, and give anti-staphylococcal therapy along with clindamycin
83
Q

Catheter-Related Sepsis

A
  • most often occurs with a central venous catheter and rarely with peripheral lines
  • risk factors are emergent placement, femoral lines, and prolonged indwelling of the line
  • usually caused by S. aureus or S. epidermidis
  • rarely presents with signs of infection at the site of line placement
  • when suspected, immediately remove the catheter and send it for culture this will often lead to improvement and antibiotics are an adjuvant
84
Q

Neutropenic Fever

A
  • defined as a fever in someone with an ANC less than 1500/mm3
  • causes include bone marrow failure, bone marrow invasion, hypersplenism, AIDS, SLE, and drug reactions
  • because neutropenia compromises the inflammatory response of the host, fever may be the only manifestation of a severe infection
  • the most infectious processes occurring are septicemia, cellulitis, and pneumonia
  • obtain a CXR, panculture, CBC, and CMP for evaluation while placing the patient in reverse isolation
  • begin treatment with broad spectrum antibiotics, give antifungals if the fever persists more than 4-5 days, and consider G-CSF
85
Q

Infectious Mononucleosis

A
  • caused by EBV and less commonly by CMV, which are transmitted through infected saliva
  • typically seen in adolescents, especially college students and military recruits, since most adults are carriers or have immunity
  • presents with fever, fatigue, sore throat, tonsillarpharyngitis, lymphadenopathy, splenomegaly, maculopapular rash, lymphocytosis, and elevated aminotransferases
  • may be complicated by hepatitis, meningoencephalitis, splenic rupture, thrombocytopenia, hemolytic anemia, and upper airway obstruction secondary to LAD
  • the mono spot test is used for diagnosis of EBV-mono as it detects heterophile antibiodies not produced in cases of CMV-mono
  • a peripheral blood smear usually reveals lymphatic leukocytosis with large, atypical lymphocytes
  • treat with supportive care and avoidance of strenuous or contact activities
86
Q

What does a negative mono-spot testing mean in the setting of high clinical suspicion for infectious mono?

A
  • it could be that it is CMV-mono, in which case heterophile antibodies aren’t produced
  • it could be that it is too early since heterophiles may not be produced in EBV-mono until 4 weeks after infection
87
Q

Chancroid

A
  • a sexually transmitted disease caused by Haemophilus ducreyi
  • it presents with painful genital ulcers that are deep with ragged borders and a purulent base along with unilateral tender inguinal lymphadenopathy that appears 1 to 2 weeks later
  • it is a clinical diagnosis
  • treat with azithromycin, ceftriaxone, erythromycin, or ciprofloxacin
88
Q

Syphilis

A
  • primary syphillus arises as the bacteria damage blood vessels leading to an area of ischemic necrosis seen as a a painless chancre
  • secondary syphillus is a systemic disease characterized by a rash that affects the hands and feet and condyloma late, which are flat-topped cutaneous lesion
  • tertiary syphillus presents with soft growths with firm necrotic centers known as gummas, aortitis leading to “tree-barking” and possibly a thoracic aortic aneurysm, damage to the posterior columns known as tabes dorsalis, and Argyll Robertson pupils, which accommodate but do not react to light
  • RPR and VDRL are screening tests that look for antibodies against treponema but false-positives are frequent
  • the confirmatory test is the more specific FTA-Abs
  • treatment can lead to Jarisch-Herxheimer reaction: dying spirochetes release lots of LPS with a cytokine storm hours after treatment
89
Q

Cellulitis

A
  • an inflammation of the skin and subcutaneous tissue
  • it is most commonly caused by S. pyogenes or S. aureus
  • presents with erythema, warmth, pain, and swelling; fever may or may not be present
  • it is a clinical diagnosis but blood and tissue cultures should be collected
  • treat with IV staphylococcal penicillins or a cephalosporin until there are signs of improvement and then continue with two weeks of oral antibiotics
90
Q

Why does cellulitis increase the risk of recurrence in that area?

A

because the inflammation and infection lead to damage of local lymphatic vessels that increase the risk of subsequent infection

91
Q

Erysipelas

A
  • a cellulitis that is confined to the dermis and lymphatics
  • it is usually caused by S. pyogenes
  • risk factors are lymphatic obstruction (post-mastectomy), local trauma or abscess, fungal infections, diabetes, and alcoholism
  • it presents as a well-demarcated, fiery red, painful lesion with high fever and chills
  • treat with IM or oral penicillin or erythromycin
92
Q

Necrotizing Fasciitis

A
  • a life-threatening infection of deep soft tissues that rapidly tracks along fascial planes
  • it is most often caused by S. pyogenes and C. perfringens
  • risk factors are recent surgery, diabetes, trauma, and IV drug use
  • presents with fever and pain out of proportion to the appearance of the skin; extension of the infection leads to thrombosis of microcirculation which causes tissue necrosis, discoloration, crepitus, and cutaneous anesthesia
  • it may rapidly progress to sepsis, toxic shock syndrome, or multi organ failure
  • surgical intervention is required along with broad spectrum IV antibiotics
93
Q

Lymphadenitis

A
  • an inflammation of one or more lymph nodes
  • usually caused by local skin or soft tissue bacterial infection
  • presents with fever, tender lymphadenopathy of regional lymph nodes, and red streaking of skin from the wound or area of cellulitis
  • may be complicated by thrombosis of adjacent veins or sepsis
  • treat with appropriate antibiotics but wound drainage may eventually be necessary
94
Q

Osteomyelitis

A
  • an inflammatory destruction of bone due to infection
  • can be either from direct spread or hematogenous seeding and risk factors include open fractures, diabetes, use of IV drugs, and sepsis
  • the most common organisms are S. aureus and coagulase-negative staphylococci; salmonella is a common cause in those with HbS and nosocomial infections are often caused by pseudomonas
  • presents with pain, erythema, warmth, and swelling over the bone as well as systemic findings of fever, headache, fatigue
  • needle aspiration of the infected bone is the most direct and accurate means of diagnosis but MRI is the most commonly used as it is non-invasive
  • notably, the earliest radiographic changes are not seen for at least 10 days on plain radiograph
  • treat with surgical debridement and 4-6 weeks of antibiotics: empiric therapy includes cephalosporins, fluoroquinolones, vancomycin, linezolid, daptomycin, and clindamycin
95
Q

Acute Infectious Arthritis

A
  • an infection of a joint space by a microorganism that releases endotoxins to trigger cytokine release and neutrophil infiltration, which leads to erosion and destruction of the joint
  • usually caused by S. aureus but gonococcal arthritis is another important cause as are pseudomonas and salmonella in patients with risk factors
  • presents with a warm, swollen, very painful joint; passive and active range of motion are severely limited by pain
  • may be complicated by avascular necrosis or sepsis
  • diagnose with a joint aspiration: likely to find more than 50K WBC/mm with >80% PMNs
  • treat with surgical drainage and antibiotics: empiric treatment with IV staph penicillin or first generation cephalosporin in most cases