Radiology and ENT CIS Flashcards
rules for x-rays are for what kind of film?
P-A
Inspiration vs Expiration
good inspiration –> less superior-inferior height, wider chest width, smaller heart shadow, less dense lung parenchyma
Poor inspiration–> more superior-inferior height, narrower chest width, larger heart shadow, more dense (whiter- less air in the alveoli) lung parenchyma
ABCDEFGHI Approach to reading x-rays
Assessment of quality
- Position : AP, PA, or Lateral?
- Inspiration: You should see 10 to 11 posterior ribs with a good inspiration
- Exposure: good lung detail and an outline of the spinal column
- Rotation: space between clavicle and adjacent vertebrae should be roughly equal
Bones and soft tissues
- Scan the bones for symmetry, fractures, osteoporosis, or metastatic lesions. Evaluate the soft tissues for foreign bodies, edema, or subcutaneous air.
Cardiac
- Evaluate the heart size: the heart should be less than 50% of the chest diameter on PA films and <60% on AP films. Check for heart shape, calcifications, and prosthetic valves.
Diaphragms
- Check diaphragms for position (the right is slightly higher than the left due to the liver) and shape (may be flat in asthma or COPD). Look below the diaphragms for free air.
Effusions
- Check the costophrenic angles for sharpness
Check a lateral film for small posterior effusions
Fields and fissures
- Check for infiltrates (interstitial vs. alveolar), masses, consolidation, air bronchograms, pneumothoraces, and bronchovascular markings.
Evaluate the major and minor fissures for thickening or fluid.
Great vessels
- Check aortic size and shape and the outlines of pulmonary vessels.
Hila and mediastinum
- Evaluate the hila for lymphadenopathy, calcifications, and masses. The left hilum is normally higher than the right. Check for widening of the mediastinum (which may indicate aortic dissection) and tracheal deviation (which may indicate a mass effect or tension pneumothorax).
Impression
- In most cases an impression is worthwhile as it not only forces you to synthesize all the findings together but acts as double check.
Things that look white on an x-ray
Effusions/Hemothorax
Consolidation (all white)
- +/- air bronchogram
Ground glass (all gray) - Mosaic pattern (patchy normal black and abnormal white or gray)
Reticular (increased lines) - spiderweb looking
- Reticulonodular (bumpy reticular pattern)
- Crazy paving (reticular plus ground glass)
Nodular/tumors/masses
things that look black on x-ray
Pneumothorax
Emphysema
Cystic spaces with air
- Honeycoming
A 6 year old male presents with a severe sore throat. He has no other complaints (picture of infection on tonsils)
What should be done next on this patient?
Treatment? complications?
Streptococcal screen and/or cultures
Oral penicillin V or amoxicillin
complications:
Acute infectious: Retropharyngeal abscess, peritonsillar abscess, sinusitis, cervical lymphadenitis, otitis media, mastoiditis
Subacute autoimmune: Acute rheumatic fever (carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules) and poststreptococcal glomerulonephritis (hematuria, edema, and hypertension)
Chronic sequela of autoimmune reaction: Rheumatic heart disease
Group A Streptococcal Disorders: Acute
Purulent and self-limited: Pharyngitis Tonsillitis Sinusitis Otitis media Arthritis Osteomyeilitis Impetigo Cellulitis Pneumonia Necrotizing fasciitis Sepsis
–> Toxin mediated:
Scarlet fever
(Erythrogenic toxin)
Toxic shock syndrome
(Toxic shock synd. toxin)
Group A streptococcal disorders: delayed
Immunological:
Acute rheumatic fever
(M protein)
Rapidly progressive acute (crescentic) glomerulonephritis
(Pyogenic exotoxin B)
Scarring:
Rheumatic valvular disease
Chronic renal failure
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
A 13 y/o girl diagnosed with T- ALL was treated with chemotherapy and steroids. A few days after starting the third intensification block, she developed steroid induced diabetes mellitus, which was controlled with insulin. A week later she presented with a one day history of headache, fever, right orbital pain and impaired vision in the right eye. A day later, she developed proptosis with a round necrotic lesion over right nasal bridge. A CT scan and MRI of brain showed right paraorbital cellulitis, and bilateral ethmoidal and maxillary sinusitis with intracerebral fungal mass. The patient was placed on appropriate emperic medication but died within within 7 days of further spread of the disorder.
rhinocerebral mucormycosis
A 37 y/o male with presented with history of four months left sided nasal blockage and discharge associated with left facial pain and two episodes of large amount of epistaxis from left nostril. The left nasal cavity was occupied by a pinkish polypoid mass that did not extend to nasopharynx . No mass was seen in right nasal cavity.
CT scan reported as heterogeneous soft tissue mass seen in left maxillary sinus and nasal cavity with no extension to nasopharynx. Erosion of medial and posterolateral wall of left maxillary sinus noted. The mass was surgically removed. The tumor was reported as having two distinct components. The first was composed of nests of squamous epithelium with minimal atypia within a fibrous stroma invaginating into the underlying tissues and the second of a proliferation of vessels within a dense fibrous stroma.
Diagnoses and prognosis?
SINONASAL INVERTED PAPILLOMA AND ANGIOFIBROMA
Poor prognosis with recurrences.
A 57 y/o male presents with several hard lymph nodes in the right neck. A biopsy of one of the lymph nodes demonstrates nests of cells in a swirling pattern that have abundant eosinophilic cytoplasm and intercellular bridges
diagnosis… and where is the primary?
Metastatic well-differentiated squamous cell carcinoma.
Primary most likely in the neck region.
Examine skin (including the scalp and ear), nasal cavity and major salivary glands in the region Do radiographic studies and examine mucosae of the mouth, pharynx and larynx with biopsies off all regions, including the tonsils
An 11-year-old male patient presented with anorexia, weight loss and persistent cough with nocturnal paroxysms for the previous 4 weeks with occasional wheezing and chest tightness. No fever, chills, myalgia, sore throat, or rhinorrhea. Treated with amoxicillin, ebastine and bronchodilator therapy but did not improve. The cough was severe with occasional emesis and an end inspiratory whoop. PMHx unremarkable and he was vaccinated according to the National Vaccine Program.Examination temp 37°C , oxygen saturation 96%. Frequent, violent paroxysms of cough. The mucous membranes were moist and the pharynx was slightly injected without exudates. On auscultation had diffuse crackles and expiratory wheezes. A chest x ray was obtained.
Pneumonitis with whooping cough
Tuberculin skin test was negative. Gastric sample (no sputum) sent for microbiological studies and Mycobacterium tuberculosis and Bordetella pertussis DNA by PCRPCR was positive for Bordetella pertussis DNA
Clarithromycin for patient and all who came in direct contact with the patient. (Two family members developed symptoms of Bordetella pertussis infection)
Bordetella pertussis - Virulence factors
adhesins: filamentous hemagglutinin, pertactin, pertussis toxin PT subunits, fimriae
Toxins: Pertussis toxin (toxoid form in vaccine) (inactivates Gi –> increased cAMP and respiratory secretions), adenyl cyclase, tracheal cytotoxin, LPS
A 23-year-old man was found to have congenital bilateral absence of the vas deferens during investigations for infertility. A detailed history revealed several previous episodes of acute pancreatitis.
cystic fibrosis
What studies should be performed?
Normal sweat test
Normal nasal potential difference study
Homozygosity for CFTR gene mutation
What is the location of the abnormal gene
Chr 7q31.2
Why was this patient not diagnosed earlier
Variable presentation of CF with mutations other than Δ508 or modifier genes
Mannose binding lectin 2, TGFβ1, interferon related developmental regulator 1, etc.
CYSTIC FIBROSIS Spectrum
Class I: complete lack of CFTR protein
Class II: most common (delta F508 gene mutation in 70%). CFTR degrades with complete lack on surface. Abnormal trafficiking, folding, processing.
Class III: defective regulation
Class IV: reduced function
Class V: reduced amount of normal
Class VI- altered regulation of separate ion channels; affect regulatory role of CFTR
Classic cystic fibrosis phenotype: two “severe” (I, II, or III) mutations
Less severe phenotype: “mild” (IV or V) mutation on one or both alleles
