FINAL resp/eent Flashcards
During the early asthmatic response, antigen exposure to the bronchial mucosa activates which kinds of cells?
These cells then present the antigen to T-helper cells that begin the inflammatory process.
Dendritic cells
Inflammatory mediators (histamine, prostaglandins, platelet-aggravating factor, interleukins) released during the early asthmatic phase cause which physical presentations?
Vasodilation
Increased capillary permeability
Mucosal edema
Bronchial smooth muscle contraction (bronchospasm)
Mucous secretion from mucosal goblet cells, with narrowing of the airways and obstruction to air flow.
In an early asthmatic response, what kind of cells cause direct tissue injury and release of toxic neuropeptides that contribute to increased bronchial hyper-responsiveness?
Eosinophils.
The late asthma response begins _____ hours after the onset of the early asthma response.
4 - 8 hours
What is happening in the late asthma response, approx. 4 - 8 hours after the onset of the early asthma response?
Latent release of inflammatory mediators, once again inciting bronchospasm, edema, and mucous secretion causing airflow obstruction.
In a person with asthma, untreated inflammation can lead to long-term airway damage that is irreversible and is known as ______.
Airway remodeling.
(subethelial fibrosis, smooth muscle hypertrophy)
Asthmatic airway obstruction causes decreased airflow, especially expiratory flow. Impaired expiratory airflow causes _______?
Air trapping, hyperinflation distal to obstructions, and increased work of breathing.
What are the clinical manifestations of the onset of an asthma attack?
Chest constriction
Expiratory wheezing
Dyspnea
Nonproductive coughing
Prolonged expiration
Tachycardia
Tachypnea
What is a pulsus paradoxus?
When might this occur in a person living with asthma?
A decrease in systolic blood pressure during inspiration of more than 10 mm Hg.
This may occur in a severe asthma attack when the person is using the accessory muscles of respiration and wheezing is heard.
In a severe asthma attack, is bronchospasm is not reversed by usual treatment measures, the individual is considered to have acute sever bronchospasm, also known as _____.
If it continues, hypoxemia worsens, expiratory flows and volumes/effective ventilation continue to decrease. _______ develops and asthma becomes life threatening.
Status asthmaticus.
Acidosis.
The diagnosis of asthma is supported by________, and further evaluated through ______.
The diagnosis of asthma is supported by history of allergies and recurrent episodes of wheezing, dyspnea and cough or exercise intolerance.
It is further evaluated through spirometry.
Risk factors for PE (pulmonary embolism)
Virchows triad- venous stasis, endothelial injury, and hypercoaguabilty
Examples of venous stasis
immobilization, heart disease
Examples of endothelial injury
Trauma, inflammation, infection, smoking
Examples of hypercoaguability
Coag disorders, malignancy, hormone replacement, oral contraceptives
What is a PE?
Occlusion of pulmonary vasculature by embolus; commonly results from embolization of a clot from DVT in leg. Can also be from tissue fragments, lipids, foreign bodies, air, or amniotic fluid.
Patho of PE?
Thrombus lodged in pulmonary circulation > occlusion of part of pulmonary circulation > hypoxic vasoconstriction, decreased surfactant, release of neurohumoral and inflammatory substances, atelectasis > leads to signs and symptoms
Does a PE cause dead space or shunting?
Dead space- ventilated but not perfused :(
S&S PE?
Sudden onset pleuritic chest pain, dyspnea, tachypnea, tachycardia, anxiety
May develop syncope, hemoptysis
DVT S&S may or may not be present
Massive occlusion= pulmonary HTN, shock
Chronic, recurrent small emboli may not be detected until progressive incapacitation, precordial pain, anxiety, dyspnea, and RV enlargement are exhibited.
Dx of PE?
ABG- resp alkalosis (inc RR breathes off all co2 which is acidic)
Elevated D-dimer (product of clot breakdown)
BNP and trop if suspected RV dysfunction
CT PE (looks blood vessels in lungs with contrast)
Community acquired pneumonia (CAP) is the ___th leading cause of death in Canada
The 8th One of most common reasons for hospitalization. 36% of those with CAP require CCU admit and have mortality range of 21-58%
In terms of age, who is most likely to get CAP?
More prevalent in the very old and very young
Incidence and mortality are highest in the elderly
viral more common in young
What are risk factors for CAP?
older adults, immunocompromised, underlying lung disease, alcoholism, altered consciousness, impaired swallowing/coughing, smoking, malnutrition, immobilization, underlying cardiac or liver disease, and LTC residence
What are the most common causative agents of CAP?
Streptococcus pneumoniae AKA pneumococcus – most common and most lethal since many virulence factors
Influenza virus - most common viral causes in adults
Respiratory syncytial virus – most common viral causes in adults
Staphylococcus aureus – MRSA becoming more common
Mycoplasma pneumoniae - common cause of atypical pneumonia in those living in dorms/young people
inspiration of infected droplet/aerosolized particles
aspiration of oropharyngeal secretions
What is the patho of pneumonia
infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites. Can be categorized: CAP, HCAP (health care), HAP (hospital-acquired), or VAP.
inspiration of infected droplet/aerosolized particles
aspiration of oropharyngeal secretions
pathogens invade/bypass normal defences in the naso/oropharynx and upper airway tract (muco-ciliary clearance, cough reflex) to attack the lower tract (airway epithelial cells)
Inflammation via alveolar macrophage & recruitment of neutrophils
Inflammation and micro-organism toxins can damage respiratory membranes, causing acini and terminal bronchioles to fill with infectious debris & exudate, can lead to consolidation of lung tissue, V/Q mismatch and hypoxia
Viral patho similar but with virus
What precedes most cases of CAP?
URTI
S/S of pneumonia
Common presentation: after URTI, clients develop fever, chills, productive or dry cough, malaise, pleural pain, and sometimes dyspnea, hemoptysis, or rust-colored sputum (bacterial)
Physical examination may show signs of pulmonary consolidation, such as dullness to percussion, inspiratory crackles, increased tactile fremitus
Tachypnoea is the single best predictor of pneumonia in children and the elderly
Hypoxia is an indicator of severity
Individuals also may demonstrate S&S of underlying systemic disease or sepsis
What finding confirms diagnosis of pneumonia?
Chest x-ray shows infiltrates
What are other diagnostic considerations?
Hx and physical examination
Leukocytosis (or leukopenia if individual is immunocompromised)
Oxygenation and pH changes
Pathogen can be identified through stains and cultures of respiratory tract secretions, cultures, or rapid tests
Treatment of pneumonia depends on ______
Causative agent
May include antibiotics, may be supportive treatment
What are some supportive treatments for CAP?
Establishing adequate ventilation and oxygenation, good hydration, pulmonary hygiene, rest
What are some CAP prevention strategies?
hand hygiene, vaccination, avoidance of aspiration, isolation for infectious/immunocompromised individual
“Dizziness caused from crystals moving into semicircular canals that obstruct the normal flow of endolymph.”
Is this BPPV, Meniere’s Disease, or Labyrinthitis?
BPPV
“Dizziness, hearing loss, tinnitus caused by build up of fluid – endolymph in inner ear.”
Is this BPPV, Meniere’s Disease, or Labyrinthitis?
Meniere’s Disease
“Viral or post-viral inflammatory disorder affecting the inner ear. Inflammation causes vertigo AKA Vestibular Neuritis.”
Is this BPPV, Meniere’s Disease, or Labyrinthitis?
Labyrinthitis
Vertigo occurs in both Menieres and BPPV. How long does it last in each?
Each attack usually only lasts under 1 minute in BPPV.
In Meniere’s: can last from 20 minutes to 24 hours
The eye has three layers, what are they?
Sclera: thick fibrous opaque outer layer.
Composed of dense connective tissue.
Sclera transparent at the cornea (allows light to enter the eye)
Protects eye, provides shape, attachment point for ocular muscles
Visible exterior surface of sclera and inner eyelids are lined with conjunctiva (mucous membrane)
Uvea: middle vascular layer, consists of iris+ ciliary body +choroid
Choroid is deeply pigmented (melanin), highly vascular connective tissue layer. Prevents light from scattering inside the eye and provides nutrients/O2.
Anterior part of choroid includes iris (controls pupil size) and ciliary body (produces aqueous humor, and controls lens shape for accommodation [near/far vision])
Retina: innermost light-sensitive layer of nervous tissue
Millions special sensory cells, or photoreceptors called rods & cones
Rods: peripheral + dim light vision (black&white), densest @ periphery
Cones: color + detail vision, densest @ center of retina
Rods and cones transmit impulses to nerve cells in retina–> optical nerve–> visual cortex
What is Uveitis?
also known as iritis
inflammation of the uveal tract (iris, ciliary body, and choroid)
What causes uveitis?
specific cause is unknown, underlying causes include infections, viruses, and arthritis
Which layer of the eye is inflamed in Uveitis? exam hint
The uvea (iris, ciliary body, choroid)
What are predisposing factors for uveitis?
Approximately 15% of clients with sarcoidosis present with uveitis
Predisposing Factors: collagen disorders, Autoimmune disorders, Ankylosing spondylitis, Sarcoidosis, Juvenile rheumatoid arthritis, Lupus, Reiter’s syndrome, Behcet’s syndrome, Syphilis, Tuberculosis, AIDS, Crohn’s disease
S/S of uveitis
Eye pain: Painless to deep-seated ache
Photophobia
Blurred vision with decreased visual acuity
Black spots
Eye redness
Unilateral or bilateral symptoms: Unilateral: The pupil is smaller than that of the other eye because of spasm of the circular muscles of the iris
Ciliary flush
Nausea and vomiting with vagal stimulation
Halos around lights
Hypopyon (pus in anterior chamber)
Limbal flush with small pupil
Is referral needed for suspected uveitis or can this be managed by primary care?
Needs immediate referral to ophthalmologist
What will be diagnostics included for uveitis?
Slit-lamp test: Slit-lamp examination reveals cells in the anterior chamber and “flare,” representing increased aqueous humour protein. Inflammatory cells, called keratic precipitates, can collect in clusters on the posterior cornea.
Penlight examination: Flashlight examination shows a slightly cloudy anterior chamber in the uveitic eye.
What does treatment look like for uveitis?
Treat underlying cause as indicated
Provide immediate referral to an ophthalmologist due to possible complications of cataracts and blindness
Medications are given per ophthalmologist
Uveitis and colitis often flare simultaneously; oral steroids are effective for both
What is a patient teaching point that should be included with uveitis?
recurrent attacks are common and require immediate attention
What are the three categories of conjunctivitis?
Bacterial, viral, allergic
Which conjunctivitis (bacterial, viral or allergic) involves an IgE-mediated hypersentitivity reaction?
Allergic
Which conjunctivitis (bacterial, viral or allergic) causes swelling of the conjunctiva, increased tear production, feeling like a foreign body in the eye, itching, irritation and/or burning?
Viral
What are other S/S for viral conjunctivitis?
Pink or red color in the white of the eye(s)
Swelling of the conjunctiva (the thin layer that lines the white part of the eye and the inside of the eyelid) and/or eyelids
Increased tear production.
Feeling like a foreign body is in the eye(s) or an urge to rub the eye(s)
Itching, irritation, and/or burning.
Which conjunctivitis (bacterial, viral or allergic) has sticky, often yellowish discharge?
Bacterial
What other S/S for Bacterial conjunctivitis?
Burning, itching, a sensation of grittiness, or mild pain or discomfort in the eye
Increased watering of the eye
Thick, sticky, often yellowish discharge from the eye; this can form a “crust” at night, making the eyes feel as if they are glued shut in the morning
Swollen eyelids
Which conjunctivitis (bacterial, viral or allergic) causes “ropey discharge”
Allergic
What are other S/S for allergic conjunctivitis
The body’s release of histamine can produce a number of allergy signs and symptoms, including red or pink eyes. Allergic conjunctivitis may also cause intense itching, tearing and inflammation of the eyes — as well as sneezing and watery nasal discharge
What are common causative agents for bacterial conjunctivitis? How is this spread?
staphylococcus or streptococcus
spread through poor hygiene or contact with other people or insects
What are common causative agents for viral conjunctivitis? How is it spread?
Adenoviruses
Most viruses that cause conjunctivitis spread through hand-to-eye contact by hands or objects that are contaminated with the infectious virus
True or false: antibiotics or antivirals are needed to resolve conjunctivitis which is not caused by allergies
False. Most cases are self-limited. Bacterial self-resolve and clear within 10 days, viral usually in 7-14 days
Which disorder involving vertigo has hearing loss and tinnitus associated? Is the hearing loss permanent?
Meniere’s
Can be temporary or permanent. Usually fluctuates and often initially affects only the lower frequencies. Typically progresses and often results in permanent hearing loss at all frequencies
Some patients have a feeling of pressure or fullness in the ear.
Outline treatment for bacterial conjunctivitis
Possible antibiotic, topically as eye drops or ointment
Antibiotics may help shorten the length of infection, reduce complications, and reduce the spread to others
Antibiotics may be necessary in the following cases: With discharge (pus)
Outline treatment for viral conjunctivitis
Pink eye treatment is usually focused on symptom relief
May benefit from using artificial tears, cleaning
eyelids with a wet cloth and applying cold or warm compresses several times daily.
Stop wearing contact lenses until treatment is complete
Outline treatment for allergic conjunctivitis
Cold compress.
Artificial tears.
Anti-allergy eye drops or oral medications (over the counter or prescription).
Which condition involving vertigo has “drop attacks”
Meniere’s “drop attacks” or sudden fall that occurs without warning while standing or walking.
BPPV - what age group and sex is most affected?
Rarely occurs in people younger than 35 unless there is a history of head trauma
More common in women than men in all age groups
Risk factors for BPPV
Older age
History of head trauma or whiplash
Inflammation of the vestibular nerve
Ear surgery
Residual effect of Meniere’s Disease
Herpes zoster oticus and inner ear ischemia
Patho of BPPV
Crystals in the semicircular canals obstructs the normal flow of endolymph when the head moves in a specific direction
Without normal endolymphatic flow, the semicircular canal cannot properly detect angular acceleration causing vertigo or a sensation of spinning when the head shifts
How long does BPPV take to resolve?
Each attack <1 min
BPPV will usually resolve spontaneously over days to weeks, sometimes longer
If treated with repositioning maneuvers, 85% found single maneuver effective
T/F in both Meniere’s and BPPV, patients may feel sense of disequilibrium or imbalance between attacks
True
S&S of BPPV
Vertigo or a feeling that you are spinning or tilting when you are not which can worsen with certain head movement – like rolling over in bed. Sensation lasts one minute or less
Can be associated with nausea and vomiting
Approximately half of patients complain of imbalance between attacks
Nystagmus during a provoking maneuver
Hearing loss or symptoms typically absent
WHat maneuver is done to diagnose posterior canal BPPV?
Dix-Hallpike maneuver
Dix-Hallpike maneuver: what will you see for nystagmus?
Nystagmus and vertigo usually appear with a latency of a few seconds and lasts less than 30 seconds
Nystagmus has typical trajectory, beating upward and turning to affected side
After nystagmus stops and the patient sits up, the nystagmus will recur but in the opposite direction
If nystagmus is provoked, maneuver should be repeated to the same side, with each repetition, the intensity and duration of nystagmus will diminish
If nystagmus not provoked, maneuver should be repeated with the head turned to the other side
Horizontal canal BPPV - what maneuver is used to diagnose?
Diagnosis is achieved by performing supine-roll maneuver
Patient lies supine. Head is held at 20-30° then the head is turned to the side
If nystagmus beats to the ground this is indicative of horizontal canal BPPV
What 2 Particle Repositioning Maneuvers are used to treat BPPV?
Epley and Semont
Describe the Epley maneuver
Pt is seated upright facing examiner. Examiner places hands on either side of head and patient holds onto examiners forearms for stability
Examiner turns patient’s head to 45° to affected side and quickly lowers patient to supine position with head extending just beyond examining table with outside ear downward
Examiner moves to head of table and repositions hands. Then head is rotated rapidly to the other side with opposite ear now facing down. This position is held for 30 seconds
Patient then rolls onto L side while examiner rapidly rotates head until nose is angled toward floor. Position is held for 30 seconds
Patient is then rapidly lifted into sitting position.
Repeat entire sequency until no nystagmus can be elicited
Describe Semont maneuver
Examiner turns patient head 45° to unaffected side and patient is quickly lowered to the affected side. Position is held for 30 seconds or until any provoked vertigo subsides
Patient is quickly sat up and is rapidly lowered down to other side with head will turned at 45° to unaffected side – face is now partly down into the bed. Position is held for 30 seconds or until vertigo subsides
Patient returns to upright position.
Maneuver is repeated until patient is asymptomatic
Patient teaching for episodes of BPPV?
For acute episodes:
Bedrest with head of bed up and reassurance that most recover spontaneously over a period of several weeks to months
Encourage compliance of bedrest and exercises
Patient can perform repositioning maneuvers on their own tid until vertigo free for 24 hours
When is onset of symptoms for Meniere’s disease?
20-40 years typically
Risk factors for Menieres
Family history
Autoimmune disease (diabetes, lupus or rheumatoid arthritis
Head injury, especially if it involved the ear
Viral infection of inner ear
Allergies
Patho of Meniere’s
Also known as Endolymphatic hydrops – pathologic lesion of Meniere’s disease, which can only be diagnosed by post-mortem histopathologic analysis of the temporal bone
Causes distortion and distension of the membranous, endolymph-containing portions of the labyrinth that disrupts vestibular and hearing functions
Time course of Meniere’s
Comes on quickly and can last from 20 minutes to 24 hours
Most people have repeated attacks over a period of years
Can have disequilibrium between attacks
10% of patients can have disabling symptoms despite treatment and lifestyle changes
Episodes last hours
What is the triad of symptoms in Meniere’s
1) Vertigo – feeling that you or your surroundings are spinning that can minutes to hours often accompanied by severe nausea and vomiting
2) Tinnitus – can be constant or fluctuate. Pitch and intensity vary
3) Hearing loss – can be temporary or permanent.
Usually fluctuates and often initially affects only the lower frequencies
Typically progresses and often results in permanent hearing loss at all frequencies
Dx of Meniere’s
Diagnosis is based on the following:
2 or more spontaneous episodes of vertigo, each lasting 20 min to 12 hours
Low-mild frequency sensorineural hearing loss in affected year – measured with audiometry
Fluctuating symptoms of reduced or distorted hearing, tinnitus or fullness in affected ear
Ruled out other vestibular diagnoses
To meet diagnostic criteria, patients typically have auditory and/or vestibular symptoms for 3-5 days
