FINAL resp/eent

Question 1

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.

Answer 1

Dendritic cells

Question 2

Inflammatory mediators (histamine, prostaglandins, platelet-aggravating factor, interleukins) released during the early asthmatic phase cause which physical presentations?

Answer 2

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.

Question 3

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?

Answer 3

Eosinophils.

Question 4

The late asthma response begins _____ hours after the onset of the early asthma response.

Answer 4

4 - 8 hours

Question 5

What is happening in the late asthma response, approx. 4 - 8 hours after the onset of the early asthma response?

Answer 5

Latent release of inflammatory mediators, once again inciting bronchospasm, edema, and mucous secretion causing airflow obstruction.

Question 6

In a person with asthma, untreated inflammation can lead to long-term airway damage that is irreversible and is known as ______.

Answer 6

Airway remodeling.

(subethelial fibrosis, smooth muscle hypertrophy)

Question 7

Asthmatic airway obstruction causes decreased airflow, especially expiratory flow. Impaired expiratory airflow causes _______?

Answer 7

Air trapping, hyperinflation distal to obstructions, and increased work of breathing.

Question 8

What are the clinical manifestations of the onset of an asthma attack?

Answer 8

Chest constriction

Expiratory wheezing

Dyspnea

Nonproductive coughing

Prolonged expiration

Tachycardia

Tachypnea

Question 9

What is a pulsus paradoxus?

When might this occur in a person living with asthma?

Answer 9

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.

Question 10

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.

Answer 10

Status asthmaticus.

Acidosis.

Question 11

The diagnosis of asthma is supported by________, and further evaluated through ______.

Answer 11

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.

Question 12

Risk factors for PE (pulmonary embolism)

Answer 12

Virchows triad- venous stasis, endothelial injury, and hypercoaguabilty

Question 13

Examples of venous stasis

Answer 13

immobilization, heart disease

Question 14

Examples of endothelial injury

Answer 14

Trauma, inflammation, infection, smoking

Question 15

Examples of hypercoaguability

Answer 15

Coag disorders, malignancy, hormone replacement, oral contraceptives

Question 16

What is a PE?

Answer 16

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.

Question 17

Patho of PE?

Answer 17

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

Question 18

Does a PE cause dead space or shunting?

Answer 18

Dead space- ventilated but not perfused :(

Question 19

S&S PE?

Answer 19

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.

Question 20

Dx of PE?

Answer 20

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)

Question 21

Community acquired pneumonia (CAP) is the ___th leading cause of death in Canada

Answer 21

The 8th One of most common reasons for hospitalization. 36% of those with CAP require CCU admit and have mortality range of 21-58%

Question 22

In terms of age, who is most likely to get CAP?

Answer 22

More prevalent in the very old and very young

Incidence and mortality are highest in the elderly

viral more common in young

Question 23

What are risk factors for CAP?

Answer 23

older adults, immunocompromised, underlying lung disease, alcoholism, altered consciousness, impaired swallowing/coughing, smoking, malnutrition, immobilization, underlying cardiac or liver disease, and LTC residence

Question 24

What are the most common causative agents of CAP?

Answer 24

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

Question 25

What is the patho of pneumonia

Answer 25

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

Question 26

What precedes most cases of CAP?

Answer 26

URTI

Question 27

S/S of pneumonia

Answer 27

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

Question 28

What finding confirms diagnosis of pneumonia?

Answer 28

Chest x-ray shows infiltrates

Question 29

What are other diagnostic considerations?

Answer 29

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

Question 30

Treatment of pneumonia depends on ______

Answer 30

Causative agent May include antibiotics, may be supportive treatment

Question 31

What are some supportive treatments for CAP?

Answer 31

Establishing adequate ventilation and oxygenation, good hydration, pulmonary hygiene, rest  

Question 32

What are some CAP prevention strategies?

Answer 32

hand hygiene, vaccination, avoidance of aspiration, isolation for infectious/immunocompromised individual

Question 33

"Dizziness caused from crystals moving into semicircular canals that obstruct the normal flow of endolymph." Is this BPPV, Meniere's Disease, or Labyrinthitis?

Answer 33

BPPV

Question 34

"Dizziness, hearing loss, tinnitus caused by build up of fluid – endolymph in inner ear." Is this BPPV, Meniere's Disease, or Labyrinthitis?

Answer 34

Meniere's Disease

Question 35

"Viral or post-viral inflammatory disorder affecting the inner ear. Inflammation causes vertigo AKA Vestibular Neuritis." Is this BPPV, Meniere's Disease, or Labyrinthitis?

Answer 35

Labyrinthitis

Question 36

Vertigo occurs in both Menieres and BPPV. How long does it last in each?

Answer 36

Each attack usually only lasts under 1 minute in BPPV. In Meniere's: can last from 20 minutes to 24 hours

Question 37

The eye has three layers, what are they?

Answer 37

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

Question 38

What is Uveitis?

Answer 38

also known as iritis inflammation of the uveal tract (iris, ciliary body, and choroid)

Question 39

What causes uveitis?

Answer 39

specific cause is unknown, underlying causes include infections, viruses, and arthritis

Question 40

Which layer of the eye is inflamed in Uveitis? **exam hint**

Answer 40

The uvea (iris, ciliary body, choroid)

Question 41

What are predisposing factors for uveitis?

Answer 41

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

Question 42

S/S of uveitis

Answer 42

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

Question 43

Is referral needed for suspected uveitis or can this be managed by primary care?

Answer 43

Needs immediate referral to ophthalmologist

Question 44

What will be diagnostics included for uveitis?

Answer 44

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.

Question 45

What does treatment look like for uveitis?

Answer 45

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

Question 46

What is a patient teaching point that should be included with uveitis?

Answer 46

recurrent attacks are common and require immediate attention

Question 47

What are the three categories of conjunctivitis?

Answer 47

Bacterial, viral, allergic

Question 48

Which conjunctivitis (bacterial, viral or allergic) involves an IgE-mediated hypersentitivity reaction?

Answer 48

Allergic

Question 49

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?

Answer 49

Viral

Question 50

What are other S/S for viral conjunctivitis?

Answer 50

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.

Question 51

Which conjunctivitis (bacterial, viral or allergic) has sticky, often yellowish discharge?

Answer 51

Bacterial

Question 52

What other S/S for Bacterial conjunctivitis?

Answer 52

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

Question 53

Which conjunctivitis (bacterial, viral or allergic) causes “ropey discharge”

Answer 53

Allergic

Question 54

What are other S/S for allergic conjunctivitis

Answer 54

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

Question 55

What are common causative agents for bacterial conjunctivitis? How is this spread?

Answer 55

staphylococcus or streptococcus spread through poor hygiene or contact with other people or insects

Question 56

What are common causative agents for viral conjunctivitis? How is it spread?

Answer 56

Adenoviruses Most viruses that cause conjunctivitis spread through hand-to-eye contact by hands or objects that are contaminated with the infectious virus

Question 57

True or false: antibiotics or antivirals are needed to resolve conjunctivitis which is not caused by allergies

Answer 57

False. Most cases are self-limited. Bacterial self-resolve and clear within 10 days, viral usually in 7-14 days

Question 58

Which disorder involving vertigo has hearing loss and tinnitus associated? Is the hearing loss permanent?

Answer 58

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.

Question 59

Outline treatment for bacterial conjunctivitis

Answer 59

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)

Question 60

Outline treatment for viral conjunctivitis

Answer 60

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

Question 61

Outline treatment for allergic conjunctivitis

Answer 61

Cold compress. Artificial tears. Anti-allergy eye drops or oral medications (over the counter or prescription).

Question 62

Which condition involving vertigo has "drop attacks"

Answer 62

Meniere's “drop attacks” or sudden fall that occurs without warning while standing or walking.

Question 63

BPPV - what age group and sex is most affected?

Answer 63

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

Question 64

Risk factors for BPPV

Answer 64

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

Question 65

Patho of BPPV

Answer 65

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

Question 66

How long does BPPV take to resolve?

Answer 66

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

Question 67

T/F in both Meniere's and BPPV, patients may feel sense of disequilibrium or imbalance between attacks

Answer 67

True

Question 68

S&S of BPPV

Answer 68

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

Question 69

WHat maneuver is done to diagnose posterior canal BPPV?

Answer 69

Dix-Hallpike maneuver

Question 70

Dix-Hallpike maneuver: what will you see for nystagmus?

Answer 70

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

Question 71

Horizontal canal BPPV - what maneuver is used to diagnose?

Answer 71

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

Question 72

What 2 Particle Repositioning Maneuvers are used to treat BPPV?

Answer 72

Epley and Semont

Question 73

Describe the Epley maneuver

Answer 73

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

Question 74

Describe Semont maneuver

Answer 74

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

Question 75

Patient teaching for episodes of BPPV?

Answer 75

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

Question 76

When is onset of symptoms for Meniere's disease?

Answer 76

20-40 years typically

Question 77

Risk factors for Menieres

Answer 77

Family history Autoimmune disease (diabetes, lupus or rheumatoid arthritis Head injury, especially if it involved the ear Viral infection of inner ear Allergies

Question 78

Patho of Meniere's

Answer 78

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

Question 79

Time course of Meniere's

Answer 79

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

Question 80

What is the triad of symptoms in Meniere's

Answer 80

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

Question 81

Dx of Meniere's

Answer 81

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