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SAM 1 > Pulmonary disease > Flashcards

Pulmonary disease Flashcards

1
Q

What are the various pulmonary disorders (list–9)?

A
  • Pneumonia
  • Eosinophilic bronchopneumopathy (EBP)
  • Pulmonary neoplasia
  • Pulmonary edema: non-cardiogenic
  • Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)
  • Pulmonary contusions
  • Pulmonary thromboembolism (PTE)
  • Idiopathic pulmonary fibrosis (progressive interstitial fibrosis)
  • Lung lobe torsion and diaphragmatic hernias
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2
Q

Pulmonary disease–clinical signs

A
  • Difficulty breathing–often expiratory pattern
  • Inc. rate and effort
  • Coughing
  • Exercise intolerance
  • Abnormal pulmonary sounds
    • Compare to pleural disease
  • Abnormal posture–orthopnea
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3
Q

Pneumonia

Overview

A
  • Inflammatory disorder of pulmonary parenchyma
  • Etiology (infectious)
    • Bacterial–most common cause in dogs
    • Viral–most common cause in cats
    • Aspiration
    • Fungal
    • Parasitic (Paragonimus spp, Aelurostrongylus spp)
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4
Q

Pneumonia

Radiographs?

Characterized by?

Other clinical signs?

A
  • Radiographic pattern helps distinguish dif. etiologies
  • Characterized by soft, ineffectual cough
    • Difficulty in breathing on expiration (animals often have both inspiratory and expiratory attern), dyspnea, tachypnea, cyanosis if severe
  • Other clinical signs
    • Nasal discharge
    • Exercise intolerance
    • Systemic signs–pyrexia, lethargy, anorexia
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5
Q

Bacterial pneumonia

More common in?

What occurs?

Primary bac. pneumonia?

A
  • More common in dogs than cats
  • Inflammation and consolidation of pulmonary tissue occurs
  • Primary
    • Younger dogs
      • Bordetella
      • Pasteurella
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6
Q

Bacterial pneumonia

Secondary bac. pneumonia

If history of recent sedation/anesthesia?

A
  • Secondary bac. pneumonia
    • Often older animals
    • Aspiration
      • Iatrogenic, loss of normal airway protection, megaesophagus, cleft palate, nasogastric tube, laryngeal paralysis, consciousness: anesthesia or neuro disease
    • Foreign body (not common in lung tissue)
    • Neoplasia
    • Viral or fungal infection
    • Bronchitis
  • If hx of recent sedation/anesthesia, organism most likely is more resistant b/c it is assoc. w/ hospital infection; hospital/super bug
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7
Q

Bacterial pneumonia

Diagnosis

A
  1. Hematology
    • L shift neutrophilic leucocytosis
    • Monocytosis if more chronic
  2. Thoracic rads
    • Interstitial pattern early in disease
    • Alveolar pattern: air bronchograms are classical
    • Often assoc. w/ R middle lung lobe pathology or cranioventral distribution
    • Look for foreign bodies, megaesophagus, and other thoracic disease
    • Radiographic changes lag behind clinical signs
  3. Transtracheal/endotracheal wash and cytology/culture
  4. Bronchoscopy w/ BAL and culture/cytology
    • Can direct endoscopy to the lesion
    • Usually get BAL samples from R middle and L caudal lung lobes (unless pus is visible elsewhere)
    • Cytology–degen. neut, monocytes, intracellular bac.
  5. Bac. pneumonia can result in sepsis which can lead to ALI and ARDS (death)
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8
Q

Bacterial pneumonia

Treatment: antibiotics

A
  • Begin empirical treatment pending culture results
  • Broad coverage
    • 4 quadrants: gram (+), (-), anaerobes, Mycoplasma spp
  • Begin w/ injectable therapy, then change over to oral medication once under control
  • Long-term therapy usually required–4-8wks, esp. if secondary
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9
Q

Bacterial pneumonia

Treatment: nebulization

Supportive care

A
  • Nebulization
    • Travels all the way down to lungs–> attaches to pus–> easier for animal to cough it up
    • Mobilizes airway secretions
    • Sterile saline +/- gentamycin
    • May result in bronchoconstriction, may need to use a bronchodilator before nebulization
  • Supportive care
    • IV fluids, O2 therapy, and coupage
    • Bronchodilators if required
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10
Q

Mycotic pneumonia

Etiology

A
  • Blastomycosis
  • Histomycosis
  • Coccidiomycosis
  • Aspergillosis
  • Others
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11
Q

Mycotic pneumonia

Respiratory clinical signs

A
  • Similar for all (chronic)
    • Abnormal resp pattern
    • Tachypnea
    • Cough
    • Exercise intolerance
    • Systemic signs
      • Inappetance, weight loss, fever, lameness, lymphadenopathy, chorio-retinitis or anterior uveitis, draining fistula tracts
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12
Q

Mycotic pneumonia

Diagnosis

Treatment

A
  • Diagnosis
    • Urine or serum ag titres
    • Cytology/histopathology (biopsy)
  • Treatment
    • Depends on fungal sensitivity
    • Polyene antifungals–amphotericin B ($$$)
    • Triazoles–itraconazole, posaconazole, voriconazole, fluconazole
    • Imadazoles–clotrimazole, ketoconazole
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13
Q

Mycotic pneumonia

How to tell which fungal organism is causing the clinical signs?

A
  • Geographical location
    • Coccidiomycosis–Arizona
    • Blastomycosis/Histoplasmosis–Ohio river valley
  • Difference in clinical signs or organs that are affected
    • GI signs–histoplasmosis (+/- organism on rectal scrape)
  • Cytology–lymph nodes, draining lesions, TTW, ETW, BAL, pulmonary aspirate
  • Serology
    • Serum antigen titre for Cryptococcus spp., Aspergillosis spp.
    • Urine antigen titre for blastomycosis and histoplasmosis and valley fever (Miravista lab), Aspergillosis
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14
Q

Mycotic pneumonia

Treatment

A
  • Expensive and long-term (4-12 mo)
  • Oral medications
    • Itraconazole more costly, fluconazole generics now avail.
    • Posaconazole very $$–less hepatotoxic, esp. for cats
    • Voriconazole very $$
    • Side effects: inappetance, elevated liver enzymes
  • IV/SC
    • Amphotericin B–nephrotoxic (monitor BUN and Cr)
      • Lipid complex form is more $$ but has fewer side effects, less nephrotoxic
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15
Q

Mycotic pneumonia

Prognosis

A
  • How disseminated is the infection
  • Poorer prognosis if CNS is involved
    • 1st week of treatment–greater chance of worsening resp signs
    • Blastomycosis and cryptococcus–80% effectively treated
    • Histoplasmosis–disseminated form has guarded prognosis, localized form has better prognosis
    • Coccidiomycosis–60% recovery rate but medication often needed for 6-12 mo or longer (lifelong)
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16
Q

Blastomycosis

Geographical distribution?

Mode of infection?

Location in body?

A
  • Distribution–North America
    • Mississippi, Missouri and Ohio river valleys, Mid-Atlantic states and Canadian provinces of Quebec, Manitoba, and Ontario
  • MOI
    • Inhalation of spores from mycelial growth in environment
  • Blastomyces dermatitis establishes in the lungs then disseminates throughout body
    • Lungs
    • Skin, eyes, bones, LN, SQ, nares, brain, testes
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17
Q

Blastomycosis

Clinical findings

A
  • Often show no clinical signs–but then the signs develop and worsen very quickly
  • 40-60% w/ fever
  • Emaciated
  • Lymphadenomegaly common
  • 85% w/ dry harsh cough
  • Exercise intolerance
  • 40% w/ ocular lesions–uveitis, iridic hyperemia, aqueous flare, myosis, chorioretinitis, optic neuritis, retinal detachment
  • 20-50% w/ skin lesions
  • 30% w/ bone lesions
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18
Q

Blastomycosis

Diagnosis

A
  • Imaging–rads, U/S, MRI
  • Hematology and biochemistry
    • Chronic anemia
    • Moderate leucocytosis w/ L shift + lymphopenia
    • Hyperglobulinemia
    • Hypercalcemia
  • Cytology or histopathology
    • LN, skin lesions, TTW (69-76% sensitive), FNA of lung (81% sensitive) (pot. risk of pneumothorax w/ FNA)
  • Serology
  • PCR available
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19
Q

Blastomycosis

Diagnosis–serology

A
  • AGID test
    • Serum and urine samples
    • 41-90% sensitive
    • 90-100%
  • Radioimmunoassays for Blastomyces
    • 92% sensitive
  • ELISA on urine
    • 93.5% sensitive; also cross-react w/ histoplasma and blastomyces
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20
Q

What is this?

A

Blastsomyces dermatitis

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21
Q

Blastomycosis

Pathological findings?

Therapy?

A
  • Pathological findings–pyogranulomatous lesions
  • Therapy
    • Amphotericin B
      • Nephrotoxic–give slowly through IV
      • 0.5mk/kg every other day
      • Accumulated dose of 8-10mg/kg is required to cure blastomycosis
      • Comes in lipid complex (less toxic)
        • Costs more, high dose required
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22
Q

Blastomycosis

Treatment

A
  • Triazole
    • Itraconazole
      • Oral administration 5mg/kg OD for dogs, TD for cats
        • In dogs start w/ TD administration for 5 days to inc. serum conc., then reduce to OD
      • 60-90 days administration
        • 68% response rate
      • Adverse effects, anorexia assoc. w/ hepatotoxicity
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23
Q

Histoplasmosis

Epidemiology

A
  • Histoplasma capsulatum
  • Worldwide
    • Midwestern and Southern US
      • Regions along Mississippi, Missouri and Ohio river
    • Likes soil that is high in bird or bat feces
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24
Q

Histoplasmosis

Clinical findings: dogs vs. cats

A
  • Cats
    • 2nd most common systemic fungal disease
    • Disseminated dz
      • Mental depression, wt. loss, fever, anorexia, pale mm
      • Coughing uncommon, but dyspnea, tachypnea, and abnormal lung sounds are found
  • Dogs
    • Inappetance, wt. loss, fever unresponsive to antibiotics
    • Signs can be limited to resp tract–dyspnea, coughing, abnormal lung sounds
    • Signs are generally disseminated
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25
Q

Histoplasmosis

Diagnosis

A
  • Hematology
    • Chronic anemia
    • Thrombocytopenia (50% dogs, 33% cats)
    • Leukocyte counts vary–often get neutrophilic leucocytosis, monocytosis, and eosinopenia
  • Biochemistry–may show hypoalbuminemia
  • Imaging–rads, U/S
  • TTA/BAL (cytology)
    • Organism found w/in mononuclear-phagocyte system
    • Single or multiple organisms
  • FNA/biopsy–cytology/histo
  • Serology–no test is reliable
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26
Q

What is this?

A

Histoplasmosis

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27
Q

Histoplasmosis

Therapy

A
  • Itraconazole treatment of choice
    • ​10mg/kg once to twice daily (some cats)
    • Treat 4-6mo
  • Fluconazole
    • Better penetration into brain and eye (good for cats w/ neuro signs)
    • But not that effective
  • Voriconazole and posaconazole
    • Penetrates blood brain barrier
  • Amphotericin B used in severe cases
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28
Q

Cryptococcosis

Etiology/epidemiology

A
  • Cryptococcus neoformans and C. gattii
  • Worldwide
  • C. neoformans
    • ​Usually assoc. w/ avian droppings
  • C. gattii
    • ​Assoc. w/ Eucalyptus trees
    • Also found in British Columbia and California
29
Q

Cryptococcosis

Clinical findings (cats and dogs)

A
  • Animals often immunosuppressed
  • Cats
    • Chronic infection, chronic listlessness, wt. loss, poor appetite
    • Bilateral nasal discharge, snuffly
    • Firm to flucuant swelling over bridge of nose
    • Lymphadenopathy–mandibular
    • Neuro signs if CNS affected, ocular lesions
  • Dogs
    • Frequently have disseminated dz
    • 2/3 have neuro signs
30
Q

Cryptococcosis

Diagnosis

A
  • Hematology and biochemistry
    • Usually non-specific
  • Cytology
    • Nasal swab, nasal wash, FNAs, BAL, pleural fluid, CSF, urine
    • Thick capsulated yeast
  • Tissue biopsy
  • Fungal isolation
    • Easy to grow
  • Serology
    • Serum, CSF
    • Latex-agglutination procedure test (90-100% sensitive, 97-100% specific)
  • Nucleic acid detection
    • PCR–highly sensitive and specific (only used if other methods fail)
31
Q

What organism is this?

A

Cryptococcus spp

(Cytology on L, histopathology on R)

32
Q

Cryptococcosis

Treatment

A
  • Surgery
  • Therapy (long–8-9mo)
    • Amphotericin B
    • Fluconazole–10mg/kg BD
    • Itraconazole–10mg/kg OD
    • Voriconazole and posaconazole
  • Monitoring
    • Use LAT–antigen titre should drop at least one dilution (2 fold) per month during effective treatment
    • Continue therapy until LAT is negative
33
Q

Coccidioidomycosis

Organism?

Environment?

Epidemiology?

Known as?

A
  • Coccidioides spp.
  • Likes dry environment
  • Epidemiology
    • Southwestern US
    • A few places w/in South America
  • “Valley fever”
34
Q

Coccidioidomycosis

Clinical findings?

A
  • Dogs
    • Dry, harsh cough–usually due to hilar lymphadenopathy or diffuse pulmonary interstitial disease
    • Fever, partial anorexia, wt. loss, weakness, lameness
    • Can become disseminated
  • Cats
    • Similar signs as dogs, but the cutaneous lesions are most common in cats
35
Q

Coccidioidomycosis–diagnosis

Hematology?

Imaging?

A
  • Hematology
    • Non-regenerative anemia
    • L-shift neutrophilia and monocytosis
    • Eosinophilia–variable
  • Imaging
    • Thoracic rads
      • Diffuse interstitial pattern
      • Miliary to nodular interstitial densities
      • Solitary nodules
      • Hilar lymphadenopathy
    • U/S
    • MRI
36
Q

Coccidioidomycosis–diagnosis

Cytology/histopathology

Fungal culture

Serology

A
  • Cytology or histo
    • Organism found along w/ pyogranulomatous inflammation
    • Round, double-walled structure containing endospores
  • Fungal culture–difficult, use proper labs
  • Serology
    • Tube precipitation antigens (less use today)
      • Body produces IgM antibodies
    • Complement fixation antigens (less use today)
      • Body produces IgG antibodies
    • Latex agglutination for IgM or IgG
    • AGID test for IgM or IgG–antibodies
    • Elisa test for IgM or IgG–antibodies
37
Q

What organism is this?

A

Coccidioides spp

38
Q

Coccidioidomycosis

Treatment

Prognosis

A
  • Treatment
    • Azoles
      • 3-6mo past resolution of clinical signs
      • Ketoconazole, itraconazole, or fluconazole
  • Prognosis
    • Good for resp disease
    • Poor for disseminated disease
39
Q

Parasitic pneumonia

Two main worms (cats/dogs)?

A
  • Aleurostrongylus abstrusus (cat lungworm)
    • Larvae may be found in feces
    • TTW/ETW–cytology
    • BAL–cytology
  • Paragonimus kellicoti (dog/cat lung fluke)
    • Operculated egg
40
Q

Aleurostrongylus abstrusus

What is it?

Signs?

Diagnosis?

Treatment?

A
  • Feline lungworm
  • Can have subclinical to clinical signs similar to asthma
    • Usually younger cats
  • Diagnosis
    • Hematology–poss. eosinophilia
    • Thoracic rads–diffuse nodular densities, caudal lobes
    • TTW/BAL–inc. # of eosinophils and/or larvae
    • Fecal–larvae evident
  • Treatment
    • Fenbendazole
    • Ivermectin
41
Q

Aleurostrongylus abstrusus

Life cycle?

42
Q

Paragonimus spp. pneumonia

Signs?

What forms?

Possible end result?

A
  • Can be subclinical or clinical–cough, wheeze, or resp distress
  • Flukes form cysts w/in lungs
  • Cysts can easily rupture–> pneumothorax
43
Q

Paragonimus spp pneumonia

Diagnosis?

A
  • CBC–eosinophilia
  • Thoracic rads–air-filled cysts
  • TTW/BAL
  • Fecal–zinc sulphate fecal float
    • ​Operculated egg
44
Q

Paragonimus spp

Life cycle?

45
Q

Idiopathic pulmonary fibrosis–progressive interstitial fibrosis

What is it?

Signalment?

A
  • Chronic fibrosis of the lung interstitium characterized by infiltration of fibroblasts; collagen deposits in alveolar septa
  • Signalment
    • West Highland White Terrier
    • Middle or older
    • Some cats
46
Q

Idiopathic pulmonary fibrosis–progressive interstitial fibrosis

History?

Clinical signs?

A
  • History
    • Slow onset, exercise intolerance
  • Clinical signs
    • Depends on severity, resp distress, tachypnea
    • Coughing increases as it progresses
    • Wt. loss in cats
47
Q

Idiopathic pulmonary fibrosis–progressive interstitial fibrosis

Diagnosis

A
  • Very difficult
  • Inspiratory crackles on auscultation (hallmark)
  • Thoracic rads
    • Generalized or diffuse interstitial pattern
  • Arterial blood gas
    • Hypoxemia if severe
  • TTW/BAL
    • Eliminate other differentials
    • Epithelial dysplasia? Non-regenerative neut and lymphocytes
  • Lung FNA
  • Lung biopsies–definitive diagnosis
48
Q

Idiopathic pulmonary fibrosis–progressive interstitial fibrosis

Treatment?

Prognosis?

A
  • Lack of specific treatment
    • Corticosteroids (not very effective alone) + bronchodilators aleviate clinical signs of chronic bronchitis
    • Cyclophosphamide or azathioprine?
    • Colchicine?
  • Prognosis
    • Guarded
    • Progressive resp failure
49
Q

Pulmonary neoplasia

Etiology–primary vs. metastatic vs. multicentric

A
  • Primary
    • Adenocarcinoma (alveolar or bronchogenic)
    • SCC
  • Metastatic
    • Many sources
      • Adenocarcinoma
      • Osteosarcoma/chrondrosarcoma
      • Hemangiosarcoma/oral or digital melanoma
  • Multicentric
    • Lymphoma, malignant histiocytosis, mastocytoma
50
Q

Pulmonary neoplasia

Signalment?

Clinical signs?

A
  • Signalment–usually older animals
  • Clinical signs
    • Wide spectrum
    • Respiratory
      • Abnormal thoracic auscultation, crackles, wheezes, or muffled sounds
      • Cough (from compression), dyspnea, tachypnea, hemoptysis
    • Non-resp signs
      • Wt. loss, inappetance
      • Lameness (hypertrophic osteopathy)
      • Dyshagia/regurgiation (MG)
      • Edema of head/neck (venous obstruction)
51
Q

Pulmonary neoplasia

Radiographs?

Cytology/histo?

A
  • Thoracic rads
    • 3 views essential (2 laterals and DV/VD)
    • Assess LN size
    • Assess pleural space (pneumothorax, effusion)
  • Cytology/histopathology
    • FNA–lung/mass
    • Bronchoscopy (BAL or biopsy)
    • If metastatic find primary mass and sample
52
Q

Pulmonary neoplasia

Treatment

Prognosis

A
  • Treatment
    • Primary
      • Surgical removal–lung lobectomy
    • Metastatic/multicentric
      • Treat primary mass
      • Chemotherapy (lymphoma)
  • Prognosis
    • Guarded to poor
    • If it is a solitary mass or benign mass–prognosis good w/ surgical removal
53
Q

Pulmonary neoplasia

Prognostic factors (common sense)

A
  • Benign better than malignant
  • Primary better than metastatic
  • Adenocarcinoma better than SCC
  • Small tumors better than large tumors
  • Tumors involving one lobe better than mult. lobes
  • No LN involvement is better
54
Q

Pulmonary edema

What is it

2 possible origins

A
  • Accumulation of fluid in alveoli or pulmonary interstitium
  • Cardiogenic or non-cardiogenic in origin
55
Q

Non-cardiogenic pulmonary edema

4 mechanisms?

A
  • Vascular overload/inc. hydrostatic pressure
    • IV fluid overload
  • Decreased plasma oncotic pressure
    • Low albumin
  • Increased alveolar-capillary membrane permeability
    • Pulmonary insults–aspiration, upper airway obstruction, smoke
    • Non-pulmonary insults–sepsis, electric shock, CNS (seizures, head trauma), pancreatitis, DIC
  • Lymphatic obstruction
56
Q

Non-cardiogenic pulmonary edema

Interference?

Can progress to?

A
  • Fluid accumulation interferes w/ ventilation and perfusion
  • Can progress to
    • Accute lung injury and/or
    • ARDS
    • Resp failure
57
Q

Non-cardiogenic pulmonary edema

Thoracic auscultation?

Thoracic rads?

Looks for what?

A
  • Hear crackles–caudal/dorsal area
  • Thoracic rads
    • Alveolar pattern–bilateral
    • Caudo-dorsal lung fields
  • Looks for underlying disease
58
Q

Non-cardiogenic pulmonary edema

Treatment

A
  • Aggressive control of primary/underlying disease
  • Cage rest and O2 therapy
  • Supportive care
    • Sedation–reduce anxiety, O2 requirements and cardiac workload
    • IV fluids–be very careful
    • Positive pressure ventilation–if required
59
Q

Non-cardiogenic pulmonary edema

Prognosis

A
  • Guarded w/ permeability edema pathogenesis
    • Depends on underlying disease
      • Ex: Ehrlichia–more difficult to treat
    • Increase alveolar-capillary membrane permability
  • Better when there is no fluid overload or renal function is intact
60
Q

Respiratory distress

Types?

Commonly secondary to what?

A
  1. Acute lung injury (ALI)–pulmonary inflammation and edema resulting in acute resp failure
  2. Acute resp distress syndrome (ARDS)–severe manifestation of ALI; hypoxemia is worse
  • ALI/ARDS commonly secondary to sepsis, systemic inflmmatory distress syndrome, sock or bac. pneumonia
    • With known FiO2:
      • PaO2/FiO2 < 300 = ALI
      • PaO2/FiO2 <200 = ARDS
    • Raised alveolar-arterial O2 gradient
61
Q

Respiratory distress

Clinical signs?

Current theray?

Prognosis?

A
  • Clinical signs can be delayed 1-4d after inciting event
    • Progressive hypoxemia, resp distress, cyanosis
  • Therapy
    • Aggressive supportive care that requires ICU
    • Positive pressure ventilation
  • Prognosis
    • Mortality rate very high–close to 100%
62
Q

Pulmonary contusions

Various degrees of what?

Thoracic auscultation?

Concurrent pathology w/ trauma?

A
  • Various degrees of resp distress
  • Thoracic auscultation–crackles
  • Concurrent pathology
    • Pneumothorax/hemothorax
    • Herniation
    • Myocarditis
    • Rib fractures
    • Hypotension
63
Q

Pulmonary contusions

Thoracic radiographs

Treatment

A
  • Radiographic evidence can take 2-12hrs to show up
    • Consolidation
  • Treatment
    • Monitor closely for 24-48hrs
    • O2 therapy
    • IV fluids
    • Pain medication for trauma
64
Q

Eosinophilic bronchopneumopathy

What is it?

Antigen?

Signalment?

A
  • Inflammation of lungs–thought to be due to a hypersensitivity to some unknown antigen
    • Lots of eosinophils roduced–>infiltrates to lungs
  • Usually the antigen is not detected, but possibilities include:
    • HW, lung parasites, drugs, inhaled allergens, neoplasia, fungal, bac. infections
  • Signalment
    • Siberian huskies predisposed
    • Young to middle-aged
65
Q

Eosinophilic bronchopneumopathy

Clinical signs

A
  • Harsh cough
  • Progressive resp difficulty, exercise intolerance
  • Some have nasal discharge or anorexia/lethargy
  • Lack of response to antibiotics
66
Q

Eosinophilic bronchopneumopathy

Diagnosis

A
  • Thoracic auscultation–harsh crackles, expiratory wheezes
  • Tracheal palpation may elicit moist productive cough
  • Hematology–50% have inc. neuts or eos
  • Ensure HW (-) and fecal float (-)
    • Eosinophilia often assoc. w/ parasites
  • Pulse oximetry and arterial blood gas
    • Hypoxemia can be marked
    • Can persist post-recovery
  • Thoracic rads
    • Diffuse bronchointerstitial pattern, alveolar infiltrates, bronchiectasis
  • Cytology–eos predominate (>20-25%)
67
Q

Eosinophilic bronchopneumopathy

Treatment

A
  • Find and treat any underlying disease
  • Even if no evidence of lungworms–fenbendazole
  • Corticosteroids
    • Prednisolone–taper over several months depending on clinical radiographic response
    • Often required long-term due to relapses
    • Try inhalation steroids
  • Other immunosuppressives can be tried–cyclosporin, azathioprine
68
Q

Pulmonary thromboembolism (PTE)

Associated with?

A
  • HW
  • Immune-mediated hemolytic anemia
  • Nephrotic syndrome
  • Hyperadrenocorticism–hypercoagulability
  • Pancreatitis
  • DIC
  • Endocarditis
69
Q

PTE

Treatment

Prognosis

A
  • O2 supplementation
  • No stress
  • Treat underlying disease
  • Bronchodilators
  • Prednisolone in IMHA and HW cases
  • Low dose heparin if DIC or hypercoagulable
  • Prognosis–poor to grave

SAM 1 (20 decks)

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