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CPR > Path: Lung and Renal > Flashcards

Path: Lung and Renal Flashcards

1
Q

What is the mechanism of barotrauma while diving?

A

Air spaces in the body are compressed at increased depth, which can cause tissue injury if normal volumes are not restored.

Can cause: eardrum rupture, dental pain, lung squeeze, pneumothorax, or air gas embolism

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2
Q

What is nitrogen narcosis?

A

Gas percentage at depth stays constant, but partial pressures increase with total pressure. This causes more nitrogen to be dissolved in blood at greater depths. As pN2 increases, effects increase in intensity. Mild intoxication, drunk equivalent, auditory/visual hallucinations, and finally loss of consciousness.

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3
Q

How does O2 cause problems at depth?

A

Similar to N2, increased pressure causes an increased amount of O2 to be dissolved in blood. As the amount increases, CNS and pulmonary toxicity can ensue. This is mitigated by reducing O2 percentage at depth or taking air breaks.

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4
Q

How do dissolved gases cause problems for divers?

A

As the partial pressure of a gas in the lung increases, the amount of that gas in the tissue increases, and vice versa. When returning from depth, the gas in the tissue cannot be transported away quickly enough. The gas then comes out of solution in the tissue or venous blood, causing harmful bubbles (“the bends”). These bubbles cause problems if they reach the arterial circulation, perhaps through a patent foramen ovale.

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5
Q

What is the mechanism by which bubbles in decompression sickness (the bends, or DCS) cause damage to tissue?

A
  1. stretching tissue and directly blocking blood flow.
  2. activation of Hageman factor and subsequent activation of kinin and complement system, platelet aggregation, vascular permeability, and relative ischemia.
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6
Q

How does decompression sickness (DCS) present? How are cases treated?

A

Depends on where the bubbles occur. Joint pain, neurologic decompensation (divers: spinal; aviators: brain), lung problems (dyspnea, nonproductive cough, substernal pain), cutaneous rash.

Responds to hyperbaric O2 therapy

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7
Q

How does flying DCS differ from diving DCS?

A

Air expands on ascent, which may cause pain at altitude (gut, intracranial, intraocular, intrathoracic, tooth abscess). If atmosphere drops to 50% of ambient, N2 can bubbles out of solution.

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8
Q

What are the symptoms of altitude sickness?

A

decreased exercise tolerance (10%@5000ft, 10% per subsequent 1000ft)
decreased alcohol tolerance
increased fluid loss (respiratory and urinary)
disturbed sleep
periodic breathing
resp alkalosis => apnea => incr. CO2, decr. O2 => hypervent
altered judgment

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8
Q

What illnesses are possible to due altitude?

A
  • peripheral edema
  • thromboembolism
  • retinopathy
  • acute mountain sickness (AMS)
  • high altitude pulmonary edema (HAPE)
  • high altitude cerebral edema (HACE)
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9
Q

What are the symptoms of acute mountain sickness (AMS)?

A
  • throbbing, bi-temporal headache
  • axorexia, possibly associated with nausea
  • fatigue, 25% with rales (dyspnea at rest suggests HAPE)
  • dizziness (when severe or with ataxia suggests HACE)
  • difficulty sleeping
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10
Q

How does one prevent and treat altitude illness?

A

Prevent: slow ascent, supplemental O2, avoid alcohol/sedatives
Medications: acetazolamide, dexamethasone, phosphodiesterase

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11
Q

What are the symptoms of high altitude cerebral edema (HACE)?

A
  • ataxic gate (defines)
  • severe lassitude
  • altered consciousness (confusion, drowsiness, stupor, coma)
  • headache, nausea, vomiting
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12
Q

What causes high altitude cerebral edema (HACE)?

A

Normal brain autoregulation in an abnormal environment.

  • brain increases blow flow to compensate decr. O2 content
  • increased flow causes increased hydrostatic pressure leading to edema, causing regional ischemia and cell death
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13
Q

What are the symptoms of high altitude pulmonary edema (HAPE)?

A
  • dyspnea at rest
  • persistent dry cough and fever
  • cyanosis
  • HACE/AMS symptoms
  • often affects the fittest individual
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14
Q

What causes high altitude pulmonary edema (HAPE)?

A
  • Normal low ventilation response in an abnormal environment
  • decreased O2 causes vasoconstriction throughout lungs => pressure rises to systolic levels => pressure causes fluid leak across membrane (climber’s pneumonia)
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15
Q

What pathogens commonly cause disease in the nasopharynx?

A

mainly viruses, i.e. rhinoviruses, coronaviruses, etc.

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16
Q

What pathogens commonly cause disease in the oropharynx?

A 
streptococcus pyogenes (GAS)
corynebacterium diptheriae
Epstein-Barre virus
adenovirus
enterovirus
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17
Q

What pathogens commonly cause disease in the middle ear and parasinuses?

A

streptococcus pneumoniae
haemophilus influenzae
also, streptococcus pyogenes (GAS)

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18
Q

What pathogens commonly infect the epiglottis?

A

haemophilus influenzae type b

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19
Q

What are the major features of streptococcus pyogenes (GAS)?

A
  1. Gram+ cocci that tend to occur in chains
  2. catalase negative (distinguishes strept. from staph.)
  3. beta-hemolytic on blood agar plates (pale)
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20
Q

What disease states are associated with strept. pyogenes (GAS)?

A

Suppurative

  • pharyngitis (uncommonly w/ scarlet fever)
  • pyoderma (impetigo, erysipelas, cellulitis, necrotizing fasciitis)
  • Non Suppurative streptococcal disease
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21
Q

What are the symptoms of pharyngitis?

A

nausea, vomiting, abdominal pain, oropharyngeal inglammation, petichiae

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22
Q

What are the complications of pharyngitis?

A

peritonsillar abscess, scarlet fever, cervical adenitis, otitis media, streptococcal toxic shock syndrome

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23
Q

How is streptococcus pyogenes infection related to rheumatic heart disease?

A

M-protein (on the surface of strep pyo.) mimics molecules found in the leaflets of the heart valves. These antibodies create deposits and fibrosis of the valves of the heart.

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24
Q

What are the characteristics of haemophilus influenzae?

A
  • Gram-
  • coccobacilli (curved ends on short rods)
  • requires X (hemin) and V (NAD or NADP) to grow (chocolate agar)
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25
Q

What H. influenzae strain is responsible for the majority of disease in humans? What is the antigen associated with this capsule?

A

H. Influenzae type B

polyribose-ribitol phosphate (PRP or Hib)

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26
Q

What disease states are associated with H. Influenzae infections?

A

-meningitis: primarily toddlers who are not vaccinated
-epiglottitis: obstructive, cherry red epiglottis
-pneumonia
Others: bacteremia, cellulitis, septic arthritis

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27
Q

How does one treat H. influenzae infections?

A

3rd gen cephalosporins, switch to ampicillin if organism is susceptible

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28
Q

How can young infants be vaccinated to prevent disease?

A

Hib-conjugate vaccines. Babies’ immune systems cannot form antibody to carbohydrate, however the Hib carbohydrate antigen can be coupled to a protein, such as diptheria toxin

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29
Q

what is the causative agent of diphtheria?

A

Corynebacterium diptheriae

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30
Q

What is the pathogenesis of diphtheria?

A

organism colonizes mucosa => produces diphtheria toxin => causes necrosis and the formation of a pseudomembrane => death by obstruction

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31
Q

What types of infection does non encapsulated haemophilus cause?

A
  • otitis media
  • sinusitis
  • conjunctivitis
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32
Q

What are the characteristics of corynebacterium diphtheriae?

A
  • Gram+ rods
  • form “chinese letters”
  • catalase+
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33
Q

What are the primary viruses that cause the common cold?

A

rhinoviruses

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34
Q

What are the primary viruses that cause pharyngitis?

A

adenovirus

Epstein-Barre Virus (EBV)

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35
Q

What are the general characteristics of rhinovirus?

A
  • non enveloped
  • +ssRNA genome (RNA replicates in cytoplasm)
  • more than 100 serotypes
  • ICAM-1 is the primary infectious cell receptor
  • flourishes best at 88-90 deg F (the nose)
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36
Q

What is the pathogenesis of respiratory syncytial virus?

A
  • infections lasts 7-10 days
  • runny nose
  • fever
  • rapid breathing
  • wheezing and/or loud whistling on exhale
  • breathlessness
  • abdominal contraction while breathing
  • continuous coughing
  • lips turn blue
  • immunity does not last long => repeat infxns possible
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37
Q

What are the characteristics of respiratory syncytial virus?

A
  • enveloped
  • -ssRNA genome (replicates in cytoplasm)
  • helical capsid
  • two major envelope proteins: F = fusion protein; G = attachment
  • encodes its own RNA-dependent RNA polymerase
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37
Q

What does “syncytial” in RSV’s name mean?

A

It indicates that the disease forms syncytia. These are cytoplasmic masses or cells with multiple nuclei/inclusions.

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37
Q

How is respiratory syncytial virus diagnosed?

A

DFA, IFA, or ELISA are used to detect antigen in nasal washing/aspirates/swab samples.

Viral culture is carried out in certain cell lines.

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38
Q

What are useful first line drugs against tuberculosis?

A
  • isoniazid
  • rifampin
  • rifapentine
  • rifabutin
  • ethambutol
  • pyrazinamide
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39
Q

What respiratory diseases can be caused by adenovirus?

A
  • febrile, undifferentiated URTI (young children and infants)
  • pharyngoconjunctival fever
  • acute respiratory disease (military recruits esp.)
  • pertussis-like syndrome (infants, young children)
  • pneumonia (infants, young children, military recruits, immunocompromised patients)
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40
Q

What cells does epstein-barre virus target to replicate in?

A

epithelial and B cells

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41
Q

What is a disease caused by epstein-barre virus (EBV) that commonly affects adolescents?

A

infectious mononucleosis

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42
Q

What is the general structure of epstein-barre virus (EBV)?

A
  • enveloped
  • linear dsDNA (replicates inside nucleus)
  • large genmone, encodes numerous proteins for replication and immune evasion
  • CD21 is the prinary receptor
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43
Q

What is the pathophysiology of infectious mononucleosis?

A

The virus infects B cells, which are then killed by CD8+ T cells in the acute phase. This makes the host immune compromised. Some of the infected cells may survive, and create a persistent phase.

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44
Q

What are the symptoms of infectious mononucleosis? Which of these occur in nearly every case?

A
  • soreness and reddening of throat**
  • cervical lymphadenopathy**
  • atypical lymphocytosis**
  • reddened, swollen tonsils with white patches
  • fatigue, malaise, loss of appetite, headache
  • cough
  • splenic enlargement and pain
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45
Q

How is infectious mononucleosis diagnosed?

A
  1. atypical lymphocytes (irregular borders)
  2. agglutination test for herterophile antibodies
  3. EBV antibody ELISA
  4. PCR for EBV genes
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46
Q

What are the major components of the mycobacterial cell envelope?

A
  • waxes
  • mycolic acids
  • polysaccarides
  • peptidoglycan (murein)
  • phenolic glycolipid I (PGL-1)
  • lipoarabinomannan (LAM)
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47
Q

How is TB transmitted?

A
  • inhalation

- ingestion via contaminated milk/milk products (M. bovis)

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48
Q

Describe the stages of Pulmonary TB

A

Stage 1: inhalation and seeding into the mid/lower lung
bacteria multiply in alveolar space
macrophages ingest bacteria (some killed, some grow)
Stage 2: logarithmic growth of bacteria in phages (kill by lysis)
arrival of new macrophages, and subsequent infxn
infected phages spread through bloodstream
Stage 3: bacterial growth finally countered by CD8+ CTL
formation of granulomas and ghon complexes at primary
infxn site
Stage 4: bacterial multiply within granulomas, protected from
immune response
granulomas become necrotic
lesions heal, but organisms may remain viable

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49
Q

What groups are at high risk for TB infection or exposure?

A
  • close contacts with people known or suspected to have TB
  • foreign born people from areas where TB is common
  • residents and employees of high risk congregate settings (retirement homes)
  • health care workers who serve high risk clients
  • medically underserved, low income populations
  • high risk racial or ethnic populations
  • children exposed to adults in high risk categories
  • people who use illicit IV drugs
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50
Q

What groups are at higher risk for developing disease after being infected with TB?

A
  • HIV infected
  • recently infected
  • people with certain medical conditions (immune comp, etc)
  • illicit IV drug users
  • history of poorly treated TB
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51
Q

How is TB diagnosed?

A
  • sputum smear
  • culture (gold standard; takes 2-3 weeks to form colony)
  • tuberculin skin test (Mantoux or PPD)
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52
Q

What is the pathogenesis of a primary influenza infection?

A
  1. short incubation period
  2. virus replicates locally in respiratory epithelium
  3. damage to the epithelium and ciliated columnar cells causes susceptibility to bacterial infection
  4. no viremia
  5. macrophage and lymphocyte infiltration
  6. interferons and cytokines cause fever, aches, edema
  7. direct virus damage and immune response kills infected cells
  8. antibodies and virus specific T cells formed
  9. virus cleared
  10. IgA in respiratory tract mediates immunity to reinfection by same strain
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53
Q

Why do we take cultures even if they take so long to develop?

A
  • drug susceptibility testing

- genotyping

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54
Q

What are two possible outcomes of a secondary influenza virus infection?

A
  1. asymptomatic, limited infection mediated by IgA

2. mild symptoms, but still sheds enough virus to infect others

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55
Q

What are the clinical features of influenza virus?

A
  • abrupt onset
  • headache
  • high fever(100-103 degF)
  • chills
  • myalgia
  • malaise
  • sore throat
  • non productive cough
  • runny or stuffy nose
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56
Q

What are three possible complications of influenza infection?

A

secondary bacterial pneumonia: following improvement, fever reappears, cough,purulent sputum (S. pneumoniae, S. aureus, H. influenzae)

viral pneumonia: relentless progression of illness, dyspnea, hypoxia, cyanosis, severe alveolar inflammation,edema => ARDS

CNS or muscle involvement

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57
Q

What are the high risk populations for influenza complications?

A
  • people over 65yo
  • nursing home residents (& other chronic care facilities)
  • anyone with a chronic pulmonary or CV disorder (incl. asthma)
  • anyone who requires regular medical follow-up/hospitalization
  • anyone 6mo-18yo who has long term aspirin therapy (Reye Syn.)
  • women in the 2nd or 3rd trimester during flu season
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58
Q

What are the general characteristics of influenza virus?

A
  • -RNA virus
  • enveloped
  • haemagglutinin and neuraminidase spikes
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59
Q

What are the three types of influenza virus, and which undergo antigenic shift and drift?

A

Type A: shit and drift
Type B: drift only
Type C: stable (no disease in humans)

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60
Q

What are the functions of the M2 ion channel, hemagglutinin, and neuraminidase in influenza virus?

A

hemagglutinin (HA): viral attachment and membrane fusion

neuraminidase (NA): virus release and disaggregation

M2: facilitates virus disassembly and HA maturation

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61
Q

What triggers hemagglutinin conformational change and virus release in the cell?

A

low pH (when bound to an endosome)

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62
Q

How is influenza virus diagnosed?

A
  1. isolated from clinical specimens (throat swab/wash, nasal wash, nasopharyngeal aspirate)
  2. virus grown in eggs or cell cultures
  3. serotype determined
    OR
    -rapid diagnosis by RT-PCR based tests
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63
Q

What is antigenic shift and drift?

A

shift: occurs as segments of the virus genome are rearranged in large animal reservoirs
drift: occurs when mutations are introduced during replication

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64
Q

What are the two types of influenza vaccination?

A 
trivalent inactivated virus (TIV)
   -intramuscular injection
   -chemically inactivated
   -induces serum antibodies
   -6mo and older
live attenuated influenza vaccine (LAIV)
   -nasal spray
   -induce mucosal immunity (IgA)
   -5-49yo (healthy)
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65
Q

What proteins on influenza are the target of antiviral therapies, and what drugs are associated with each?

A

neuraminidase (NA): prevents viral release
-oseltamivir
-zanamivir
M2 ion channel: block channel and prevent H+ entry and viral disassembly
-amantadine
-rimantadine

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66
Q

What is the presentation of a typical pneumonia?

A

high fever
shaking chills
chest pain
lobar consolidation on CXR

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67
Q

What organisms are responsible for most typical pneumonias, and which are community acquired vs nosocomial?

A
  • streptococcus pneumoniae (most common cause of CAP)
  • staphylococcus aureus (CAP)
  • haemophilus influenzae (CAP)
  • gram negative enterics (E. coli) (nosocomial)
68
Q

What are the common features of atypical pneumonia?

A
  • less severe illness (“walking pneumonia”)
  • dry cough
  • headache
  • other systemic complaints
  • CXR is diffuse consolidation (looks worse than illness suggests)
  • no predominant organisms in sputum sample
  • hospitalization not required
69
Q

What organisms are responsible for atypical pneumonia?

A

bacteria

  • mycoplasma pneumoniae
  • chlamydia pneumoniae, c. psittaci
  • legionella pneumophila
  • influenza and other viruses (adeno, EBV, RSV)
  • coxiella burnetti
70
Q

What are the bacterial characteristics of streptococcus pneumoniae?

A
  • alpha hemolytic (green)
  • mucoid, shiny, smooth colonies
  • Gram+, lancet shaped, diplococci
  • catalase negative
  • bile soluble
  • optochin susceptible
  • encapsulated
71
Q

What is the major virulence factor of streptococcus pneumoniae, and what it its mechanism of function?

A

virulence factor: capture
function: anti-phagocytic by blocking the interaction between C3b (on the organism) and C3b receptor (on the white cells)

72
Q

What factors predispose a person to pneumococcal infection?

A

-viral infection of the upper respiratory tract (esp. influenza)
-compromised pulmonary function (alcohol, general anesthesia)
-age (elderly, or under 2yo)
-ethnicity/race: per CDC: “blacks, native Amer., Alaska natives)
-basic immunity impaired: sickle cell anemia, splenectomy,
hypogammaglobulinemia, granulocytopenia, HIV, multiple
myeloma, lymphoma, chronic lymphocytic leukemia, C3b
complement deficiency
-serotype of infecting S. pneumoniae (esp. type 3)

73
Q

What is the pathogenesis of pneumococcal pneumonia?

A

organism colonises pharynx and gains lung access => alveoli =>
phagocytized by macrophages => stop OR multiply in edematous fluid => exudate spills into bronchioles and adjoining alveoli => inflammatory response, air displaced => centrifugally spreading lesion => resolution OR death

74
Q

What are the signs and symptoms of pneumococcal pneumonia?

A
  • usually lobar

- sudden onset of chills, fever, pleuritic pain, rusty sputum/+blood culture in 30% of cases

75
Q

Describe the vaccine currently used to protect young children against pneumococcal pneumonia.

A

PCV13

  • conjugate vaccine
  • for use ages 6wo - 71mo
76
Q

What are possible complications of pneumococcal pneumonia infection?

A
  • lung abscess
  • bacteremia
  • meningitis
  • otitis media
77
Q

What is the difference between a mycoplasma and a mycobacterium?

A

A mycobacterium has a cell wall, where a mycoplasma does not.

78
Q

What are the properties of mycoplasma?

A
  • small
  • no cell wall, no peptidoglycan (therefore no suscept. to penicillin)
  • unit membrane containing sterols
  • pliable membrane (require sterols)
  • slow growing
  • facultative aerobes
79
Q

What are the symptoms of infection with mycoplasma pneumoniae?

A
  • “walking pneumonia”
  • flu-like symptoms (fever, sore throat, headache, myalgia, nasal congestion, general malaise)
  • non productive cough
  • self limiting
  • chronic, insidious nature
80
Q

What molecules are responsible for mycoplasma pneumoniae’s tight attachment to respiratory epithelium?

A

on bacterium: P1 adhesin

on cell: neuraminic acid-containing glycoprotein

81
Q

What are the primary pathogenic mechanisms of mycoplasma pneumoniae infection?

A

-production of CARDS toxin
causes vacuolation and ciliostasis
-immune pathology when cell mediated response is too vigorous

82
Q

How is Mycoplasma pneumoniae diagnosed?

A

culture: difficult, restricted to certain labs
serology: greater than or equal to a 4 fold rise in specific Ab
test for cold hemagglutinins (not specific)

83
Q

What are the antibiotics of choice for use against Mycoplasma pneumoniae?

A
  • tetracycline
  • erythromycin or azithromycin

-beta-lactams are NOT effective

84
Q

What are the properties of Chlamydiaceae?

A
  • obligate intracellular
  • DNA, RNA
  • binary fission
  • carry plasmids
  • cell envelope (no detectable peptidoglycan, but evidence present)
85
Q

What forms of chlamyia are implicated in pneumonias?

A

C. pneumoniae

C. psittici

86
Q

What are the primary pathogenic mechanisms of Chlamydiae?

A

cytopathic effect on host cells (cell death)

tissue damage due to immune response

  • conjuctival scarring
  • fallopian tube scarring
87
Q

How is C. pneumoniae diagnosed?

A

IgM titer of greater than or equal to 1:64, or a four fold rise in the IgG titer in acute serum and convalescent serum (measured 4 weeks apart)

88
Q

What is the reservoir for C. psittaci, and what does this imply about at risk populations?

A
  • birds

- Any population that has exposure to infected birds (bird owners, poultry industry workers, vets, etc)

89
Q

What are the clinical features of C. psittaci infection (Psittacosis)?

A
  • abrupt onset
  • fever, headache, myalgia, mild cough
  • abnormal chest exam
  • confusion/altered conscious state
90
Q

How is C. psittaci infection diagnosed?

A
  • greater than 4 fold rise in antibody titer

- single IgM titer of greater than or equal to 1:16

91
Q

What drugs are effective against C. psittaci?

A
  • doxycycline
  • azithromycin
  • erythromycin
92
Q

What are the symptoms of infection by Legionella pneumophila and other Legionella species?

A
  • interstitial pneumonia
  • fever
  • headache
  • malaise
  • GI symptoms**
  • nausea**
  • diarrhea**
93
Q

What groups are significantly at risk for Legionella infection, and where can the organism commonly be found?

A

-older patients with underlying disease or otherwise weakened cell mediated immunity

The organism is associated with water sources and air conditioning esp. in hotels and hospitals

94
Q

What are the virulence strategies of Legionella?

A
  • survival in macrophages
  • biofilm production
  • LPS
95
Q

What labs help to diagnose Legionella?

A
  • specific LPS antigen in urine via ELISA
  • culture of bronchoalveolar lavage on buffered charcoal yeast extract agar
  • nucleic acid probes
  • NO gram stain
96
Q

How is Legionella treated?

A
  • macrolides (erythromycin, azithromycin)
  • fluoroquinilones (ciprofloxacin, levofloxacin)

Most strains produce beta-lactamase

97
Q

What are some diseases associated with Pseudomonas aeruginosa infection?

A
  • pneumonia in cystic fibrosis patients
  • burn infections
  • nosocomial infections
  • cellulitis
  • folliculitis
  • urinary tract infection
  • swimmers ear (otitis externa)
98
Q

What are the symptoms of pseudomonas aeruginosa infection?

A
  • fever
  • sepsis
  • tissue damage in airways
  • location dependent for non respiratory diseases
99
Q

What groups are particularly vulnerable to Pseudomonas infection?

A
  • patients with cystic fibrosis

- patients in hospitals

100
Q

What are the pseudomonas virulence strategies?

A
  • capsule (very sticky, mucoid capsule. Extremely difficult to penetrate with macrophages/antibiotics. Countered with surfactant)
  • LPS
  • biofilm production (see capsule)
  • exotoxins and proteases
101
Q

What are the characteristics of Pseudomonas aeruginosa?

A
  • Gram-
  • flagella
  • capsulated
  • strict aerobes
102
Q

How is Pseudomonas infection diagnosed?

A
  • culture (lactose- on MacConkey agar)
  • oxidase positive
  • green pigment producing
  • grape-like odor
103
Q

What antibiotics are useful in the treatment of Pseudomonas?

A
  • aminoglycosides (amikacin, gentamicin, tobramycin)
  • carbapenems (imipenem, meropenem)
  • carboxypenicillins (ticarcillin)
  • ureidopenicillins (piperacillin)
  • extended spectrum cephalosporins (ceftazidime, cefepime, cefoperazone)
  • fluoroquinolones (ciprofloxacin)
  • monobactam (aztreonam)
104
Q

What is a dimorphic fungi? What part of the life cycle occurs in what environment?

A

A dimorphic fungi has two forms to its life: mold and yeast. Mold forms outside tissue, where it is generally cooler. Yeasts form inside warm environments, such as tissue.

105
Q

What are the important features of endemic mycoses?

A
  • acquired by spore inhalation
  • specific to geographical regions
  • acute and/or reactivation disease
  • range of severity
106
Q

What is the morphology of Histoplasma?

A 
mold:
   -white or brown hyphal colonies
   -large, spiky spherical spores
   -small, ovoid spores
   -slow growing on cycloheximide
yeast
   -intracellular
   -uninucleate
   -ovoid
107
Q

Where is Histoplasma located?

A

The Mississippi and Ohio River valleys

108
Q

How common is histoplasmosis infection in the United States?

A

Significantly common, however most cases do not produce disease.

109
Q

What is the pathogenesis of Histoplasmosis, and what disease process does it mirror?

A

spores => lungs => yeast form => taken into macrophages => can spread through body via reticuloendothelial system

after 2-3 weeks, macrophages become fungicidal => granulomas with central necrosis => eventually, calcium deposition and calcified granulomas (mirrors TB infection)

110
Q

What is the most common clinical presentation of Histoplasmosis?

A

None. Most individuals are asymptommatic

111
Q

Characterize the pulmonary symptoms associated with Histoplasmosis in the acute, subacute, and chronic settings.

A

acute: mild, self limited illness
-fever, sweats, cough, occasional GI complaints
-may have diffuse pulmonary infiltrates, +/- hilar nodes
subacute: (presents over weeks)
-fever, sweats, cough, weight loss
-hilar or mediastinal lymphadenopathy
-possible focal or patchy infiltrates
chronic
-fever, cough, sweats, weight loss
-interstitial or consolidative infiltrates, +/- bullae, +/- calcification

112
Q

How does Histoplasmosis infection affect the heart?

A

The infection can lead to acute pericarditis, fibrosis of the pericardium, and cardiac tamponade.

113
Q

What are the symptoms of progressive disseminated histoplasmosis? What patients are at higher risk to develop it?

A
  • fever, weight loss, sweats
  • hepatosplenomegaly and lymphadenopathy (but less than 50%)
  • hematologic abnormalities due to bone marrow involvement
  • respiratory distress
  • possible GI, adrenal, CNS, and mucosal involvement
114
Q

What methods are used in histoplasmosis diagnosis?

A

Culture (low sensitivity, 2-4 weeks to get results)
Fungal stain (rapid, low sensitivity)
Serology (rapid, high sensitivity, False- (immune comp., 1st few
weeks after exposure, false+ cross reactivity, cant differentiate
current or prior infection)
Antigen (rapid, good for disseminated Dx, low sensitivity for
localized Dx)

115
Q

How is Histoplasmosis treated?

A

Mild: self limited
Moderate: itraconazole
Severe: amphotericin B

HIV patients may require lifelong suppressive Rx

116
Q

What is the morphology of Blastomyces yeast?

A
  • very characteristic double contoured walls
  • multinucleated
  • spherical
  • reproduce by formation of single buds
117
Q

Where is Blastomyces located?

A

In the southern Mississippi River valley (Mississippi, Arkansas,
Kentucky)

118
Q

What is the clinical presentation of blastomycosis?

A 
Usually asymptomatic/subclinical.
Most common manifestations are:
   -pulmonary
   -cutaneous
   -bone
   -genitourinary
119
Q

How does blastomycosis manifest in the lungs?

A

Acute pneumonia
-atypical pneumonia with alveolar infiltrates that dont respond to
usual antibiotics
-mass-like lesions frequently diagnosed as cancer
Subacute & chronic pneumonia
-fever, sweats, weight loss, fatigue
Radiology: varied (alveolar infiltrate, mass-like lesion, multiple nodules, lobar infiltrates, cavitary lesions can all be seen)

120
Q

Why is blastomycosis difficult to diagnose?

A

It can present with any number of manifestations, commonly including cutaneous lesions (verrucous or ulcerative), genitourinary tract infection, and osteomyelitis. There are many less common presentations as well.

121
Q

How is blastomycosis diagnosed?

A
  • histopathology
  • culture
  • serology is not helpful (poor specificity)
122
Q

How is blastomycosis treated?

A

Mild: itraconazole
Severe: amphotericin B

123
Q

What is the morphology of coccidioides immitis?

A

In mold form, it forms long stalks. Spores are separated by dividing cells that dry out and break to form wings to carry the spores.

In yeast form, spherules are formed that produce endospores. Rupture releases endospores, which can form new spherules.

124
Q

Where are the two species of coccidiodes found?

A

immitis: Southern California and along the border of Mexico
posadasii: few areas in South America

125
Q

What is the clinical presentation of coccidioidomycosis?

A
  • 50-70% with no symptoms
  • most commonly, self limited pneumonia
  • fever, fatigue, chills, night sweats, weight loss
  • cough
  • myalgias
  • dyspnea
  • chest pain
  • 5-10% develop persistent symptoms and residual sequelae suc as nodules or peripheral thin walled cavities
126
Q

How is coccidioidomycosis diagnosed?

A
  • direct microscopic evaluation of sputum or tissue

- serology

127
Q

How is coccidioidomycosis treated?

A

mild to moderate: fluconazole or itraconazole

Severe: amphotericin B

128
Q

What is the morphology of the yeast form of paracoccidioides?

A

-oval to round with multiple buds (“pilot wheel”)

129
Q

Where is paracoccidioides found?

A

tropical and subtropical central and S. America

130
Q

What are the clinical manifestations of paracoccidioidomycosis?

A
  • usually asymptommatic
  • acute, subacute, or chronic pneumonia
  • if disseminated, lymphadenopathy, organomegaly, bone marrow involvement
  • chronic mucocutaneous ulcers
  • meningitis
131
Q

How is paracoccidioidomycosis treated?

A

Usually itraconazole
In severe cases, amphotericin B

TMP/SMX suppression for HIV+ patients

132
Q

Define azotemia. What is prerenal and postrenal azotemia? How is uremia related?

A

elevation of blood urea nitrogen (BUN) and creatinine levels, largely due to glomerular filtration rate (GFR).
Prerenal: due to kidney hypoperfusion
Postrenal: due to an obstruction in urinary outflow after exiting the kidney
Uremia: the constellation of signs and symptoms associated with azotemia; including metabolic, hematoligic, endocrine, gastrointestinal, neural, and cardiovascular effects

133
Q

What is associated with acute nephritic syndrome?

A
  • hematuria or RBC casts in urine
  • azotemia
  • variable proteinuria (<3.5 g/day)
  • oliguria
  • facial edema/hypertension (due to Na retention)
134
Q

What are the features of rapidly progressive glomerularnephritis?

A
  • acute nephritis
  • proteinuria
  • acute renal failure
135
Q

What are the features of nephrotic syndrome? What is nephrotic syndrome associated with?

A

> 3.5 g/day proteinuria

  • hypoalbuminemia
  • hyperlipidemia
  • lipiduria or fatty casts
  • associated with a hypercoagulable state (thromboembolism) and increased risk of infection (loss of immunoglobulins)
  • generalized edema
136
Q

What are the characteristics of chronic renal failure?

A

azotemia => uremia (progressing for years)

137
Q

Characterize the four stages of renal failure in terms of glomerular filtration rate (GFR).

A
  1. Diminished renal reserve: up to 50% normal GFR
    • pts asymptomatic
    • BUN/creatinine levels normal
  2. Renal insufficiency: 20-50% normal GFR
    • azotemia with anemia and hypertension
  3. Chronic renal failure: less than 20% normal GFR
    • edema
    • metabolic acidosis
    • hyperkalemia
  4. End stage renal disease: less than 5% normal GFR
138
Q

What are the clinical features of adult polycystic kidney disease (ADPKD)?

A
  • hematuria
  • flank pain
  • urinary tract infection
  • renal stones
  • hypertension
139
Q

What are the pathologic features of adult polycystic kidney disease (ADPKD)?

A
  • large, multicystic kidneys (bilat)
  • liver cysts
  • berry aneurysms (brain)
  • mitral prolapse
140
Q

What are the major complications of childhood polycystic kidney disease (ARPKD)?

A
  • hepatic fibrosis
  • oliguria
  • oligohydramios leading to Potter’s facies
141
Q

What are the pathologic features of childhood polycystic kidney disease?

A

enlarged, cystic kidneys at birth

cysts appear as striations perpendicular to the smooth capsule of the kidney

142
Q

What is the chromosome mutation is involved in adult polycystic kidney disease (ADPKD)?

A
  • chromosome 16p13.3 (PKD1: encoding polycystin 1 in most cases)
  • chromosome 4q21 (PKD2: encoding polycystin 2 in the remainder)
143
Q

What long term therapy can result in the development of cortical and medullary cysts? What long term risk is increased with this condition?

A
  • dialysis (acquired cystic disease)

- renal cell carcinoma risk is increased

144
Q

What are the features of simple cysts in the kidney?

A
  • benign, common lesion
  • solitary, asymptomatic
  • may cause flank pain
145
Q

What are the hallmarks and consequences of medullary cystic disease?

A
  • medullary cysts can lead to fibrosis, renal insufficiency, and inability to concentrate urine
  • small kidney on ultrasound
  • high rate of kidney stone development
146
Q

What are the symptoms of acute poststreptococcal glomerulonephritis? Is it a nephrotic or nephritic syndrome?

A
  • follows or accompanies streptococcal infection
  • peripheral/periorbital edema
  • enlarged, hypercellular, bloodless glomeruli (incr. mesangial c.)
  • electron dense humps on the epithelial side of the basement membrane (subepithelial localization)
  • course granulofluorescence for IgG or C3
147
Q

What causes acute acute poststreptococcal glomerulonephritis?

A

-deposition of immune complexes formed by anti-streoptococcal antibodies that deposit in the glomerular network

148
Q

What diseases can result in rapidly progressive glomerulonephritis (RPGN)?

A
  • Goodpasture syndrome
  • Wegener’s granulomatosis
  • microscopic polyangiitis
149
Q

What is the defining histological feature of rapidly progressing glomerulonephritis?

A

Formation of a crescent of fibrin and proteins between bowman’s capsule and the glomerular tuft

(crescenteric glomerulonephritis)

150
Q

What is the cause of rapidly progressing glomerulonephritis? What disease is it commonly secondary to? Nephrotic or nephritic?

A
  • deposition of immune complexes in Bowman’s space
  • often (50%) poststreptococcal

-nephritic

151
Q

What is Goodpasture syndrome, and how is it related to rapidly progressive glomerulonephritis? What is the major hallmark of Goodpasture? Nephrotic or nephritic?

A

Goodpasture syndrome is a syndrome affecting men in their mid-20s in which IgG (antiglomerular basement membrane antibodies) deposits linearly on glomerular basement membranes. Linear immunofluorescence

The symptoms of Goodppasture are nephritic syndrome and lung involvement (pneumonitis with hemoptysis)

It causes a crescent morphology similar to rapidly progressing glomerulonephritis.

152
Q

What causes IgA nephropathy (Berger’s Disease)? Nephrotic or nephritic?

A

IgA deposition in the mesangium causes recurrent hematuria in children (usually no more than 1-2 days) following an infection

nephritic

153
Q

What causes Alport syndrome? Nephrotic or nephritic?

A

A mutation in collagen IV causes a split basement membrane

nephritic

154
Q

What are the clinicopathologic features of minimal change disease? Nephrotic or nephritic?

A
  • occurs often in young children
  • on light microscope, normal appearing glomeruli
  • electron microscope: fused/effaced foot processes
  • high amounts of lipid in renal cortex
  • nephrotic
155
Q

What are the clinicopathologic features of focal segmental glomerulosclerosis? Nephrotic or nephritic?

A
  • usually occurs in older patients
  • sclerosis of juxtamedullary glomeruli capillaries
  • can be either focalor segmental in distribution
  • nephrotic
156
Q

What are the clinicopathologic features of membranous nephropathy? Nephrotic or nephritic?

A
  • immune complex disease of unknown etiology
  • diffuse capillary and glomerular basement membrane thickening
  • “spike and dome” on EM
  • nephrotic syndrome accompanied by azotemia
  • granular immunofluorescence
  • nephrotic
157
Q

What are the clinicopathologic features of membranoproliferative glomerulonephritis? Nephrotic or nephritic?

A
  • slow progression to chronic renal disease
  • hypercellularity and basement membrane proliferation
  • “tram track” appearance of basement membrane
  • can present as either nephrotic or nephritic
158
Q

What is the stain for amyloidosis? Where are the deposits found in the kidney? Nephrotic of nephritic?

A
  • congo red
  • mesangial space or subepithelial
  • nephrotic
  • can be associated with multiple myeloma
159
Q

What histological features accompany diabetic glomerulonephropathy? Nephrotic or nephritic?

A
  • thickened basement membrane
  • proliferated mesangium, can be nodular or diffuse
  • arteriolosclerosis of efferent and afferent
  • nephrotic
160
Q

What are the clinicopathologic features of acute tubular necrosis? Describe the stages of the disease.

A

-associated with renal ischemia(shock,sepsis), crush injury, toxins
-muddy brown casts in urine
-3 stages
1. inciting event
2. maintenance phase - oliguric (risk of hyperkalemia) (highest
death rate)
3. recovery phase - polyuric (BUN and creatinine fall; risk of
hypokalemia)

161
Q

What causes acute interstitial renal nephritis?

A
  • drug induced
    • often penicillin derivatives, NSAIDs, or diuretics
  • acute interstitial renal inflammation
162
Q

What are the general characteristics of a urinary obstruction?

A

-renal colic: excruciating pain caused by acute distension of the
ureter
-hydronephrosis: distention of the the renal pelvis and calyces
-infection: localized proximal to the site of obstruction

163
Q

What are the four types of kidney stone and their causes?

A
  1. calcium: hypercalciuria and conditions that cause it (cancer,
    increased PTH)
  2. ammonium magnesium phosphate: associated with certain
    infections (proteus mirabilis, staphylococcus, klebsiella)
  3. uric acid: associated with hyperuricemia (e.g. gout) and disease
    with high cell turnover (like leukemia)
  4. cystine: secondary to cystinuria; often genetic problem with
    AA resorption
164
Q

What are the clinicopathologic features of renal cell carcinoma?

A
  • most common in men 50-70yo (high incidence in smokers)
  • hematuria
  • palpable mass
  • flank pain
  • fever, weight loss
  • invades IVC and spreads hematogenously
    • metastasize to bone and lung
  • histology: clear cells
165
Q

What are the clinicopathologic features of Wilm’s tumor?

A
  • peak incidence 2-4yo
  • huge, palpable flank mass
  • hematuria
  • can be part of WAGR complex (Wilm’s tumor, Aniridia, Genitourinary malformations, motor/mental Retardation) WT-1 gene
166
Q

What are the clinicopathologic features and associations of a transitional cell carcinoma?

A
  • associated with Pee SAC problems: Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide
  • papillary growth originating in renal calyces, renal pelvis, ureters, or bladder
167
Q

What are the clinicopathologicfeatures of small cell carcinoma? What is its associated paraneoplastic syndrome?

A
  • located centrally
  • undifferentiated (small dark blue cells)
  • associated with ectopic production of ACTH or ADH
168
Q

What are the clinicopathologic features of squamous cell carcinoma? What is its associated paraneoplastic syndrome?

A
  • located centrally (hilar mass)
  • associated with smoking (think epithelial change)
  • cavitation
  • contains keratin pearls and visible desmosomes
  • parathyroid like activity - production of PTHrP
169
Q

What are the clinicopathologic features of adenocarcinoma? What is its associated paraneoplastic syndrome?

A
  • located peripherally
  • two types: bronchial and bronchioalveolar
  • bronchial
    • develops in site of previous inflammation/injury
  • bronchioalveolar
    • not linked to smoking
    • grows along airways
    • can present like pneumonia
170
Q

What are the clinicopathologic features of large cell carcinoma?

A
  • located peripherally

- pleomorphic giant cells with leukocyte fragments inside

171
Q

What are the clinicopathologic features of ARDS?

A

-secondary to trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, or amniotic fluid embolism
-diffuse alveolar damage => increased capillary permeability =>
proteinaceous leakage into alveoli
-forms intra-alveolar hyaline membrane

CPR (3 decks)

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