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NUNP531 Applied Pathophysiology > FINAL resp/eent > Flashcards

FINAL resp/eent Flashcards

1
Q

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.

A

Dendritic cells

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2
Q

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

A

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.

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3
Q

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?

A

Eosinophils.

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4
Q

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

A

4 - 8 hours

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5
Q

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

A

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

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6
Q

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

A

Airway remodeling.

(subethelial fibrosis, smooth muscle hypertrophy)

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7
Q

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

A

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

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8
Q

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

A

Chest constriction

Expiratory wheezing

Dyspnea

Nonproductive coughing

Prolonged expiration

Tachycardia

Tachypnea

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9
Q

What is a pulsus paradoxus?

When might this occur in a person living with asthma?

A

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.

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10
Q

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.

A

Status asthmaticus.

Acidosis.

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11
Q

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

A

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.

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12
Q

Risk factors for PE (pulmonary embolism)

A

Virchows triad- venous stasis, endothelial injury, and hypercoaguabilty

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13
Q

Examples of venous stasis

A

immobilization, heart disease

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14
Q

Examples of endothelial injury

A

Trauma, inflammation, infection, smoking

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15
Q

Examples of hypercoaguability

A

Coag disorders, malignancy, hormone replacement, oral contraceptives

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16
Q

What is a PE?

A

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.

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17
Q

Patho of PE?

A

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

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18
Q

Does a PE cause dead space or shunting?

A

Dead space- ventilated but not perfused :(

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19
Q

S&S PE?

A

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.

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20
Q

Dx of PE?

A

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)

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21
Q

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

A

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

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22
Q

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

A

More prevalent in the very old and very young

Incidence and mortality are highest in the elderly

viral more common in young

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23
Q

What are risk factors for CAP?

A

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

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24
Q

What are the most common causative agents of CAP?

A

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

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25
Q

What is the patho of pneumonia

A

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

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26
Q

What precedes most cases of CAP?

A

URTI

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27
Q

S/S of pneumonia

A

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

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28
Q

What finding confirms diagnosis of pneumonia?

A

Chest x-ray shows infiltrates

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29
Q

What are other diagnostic considerations?

A

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

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30
Q

Treatment of pneumonia depends on ______

A

Causative agent

May include antibiotics, may be supportive treatment

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31
Q

What are some supportive treatments for CAP?

A

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

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32
Q

What are some CAP prevention strategies?

A

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

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33
Q

“Dizziness caused from crystals moving into semicircular canals that obstruct the normal flow of endolymph.”

Is this BPPV, Meniere’s Disease, or Labyrinthitis?

A

BPPV

34
Q

“Dizziness, hearing loss, tinnitus caused by build up of fluid – endolymph in inner ear.”

Is this BPPV, Meniere’s Disease, or Labyrinthitis?

A

Meniere’s Disease

35
Q

“Viral or post-viral inflammatory disorder affecting the inner ear. Inflammation causes vertigo AKA Vestibular Neuritis.”

Is this BPPV, Meniere’s Disease, or Labyrinthitis?

A

Labyrinthitis

36
Q

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

A

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

37
Q

The eye has three layers, what are they?

A

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

38
Q

What is Uveitis?

A

also known as iritis

inflammation of the uveal tract (iris, ciliary body, and choroid)

39
Q

What causes uveitis?

A

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

40
Q

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

A

The uvea (iris, ciliary body, choroid)

41
Q

What are predisposing factors for uveitis?

A

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

42
Q

S/S of uveitis

A

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

43
Q

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

A

Needs immediate referral to ophthalmologist

44
Q

What will be diagnostics included for uveitis?

A

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.

45
Q

What does treatment look like for uveitis?

A

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

46
Q

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

A

recurrent attacks are common and require immediate attention

47
Q

What are the three categories of conjunctivitis?

A

Bacterial, viral, allergic

48
Q

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

A

Allergic

49
Q

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?

A

Viral

50
Q

What are other S/S for viral conjunctivitis?

A

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.

51
Q

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

A

Bacterial

52
Q

What other S/S for Bacterial conjunctivitis?

A

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

53
Q

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

A

Allergic

54
Q

What are other S/S for allergic conjunctivitis

A

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

55
Q

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

A

staphylococcus or streptococcus

spread through poor hygiene or contact with other people or insects

56
Q

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

A

Adenoviruses

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

57
Q

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

A

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

58
Q

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

A

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.

59
Q

Outline treatment for bacterial conjunctivitis

A

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)

60
Q

Outline treatment for viral conjunctivitis

A

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

61
Q

Outline treatment for allergic conjunctivitis

A

Cold compress.

Artificial tears.

Anti-allergy eye drops or oral medications (over the counter or prescription).

62
Q

Which condition involving vertigo has “drop attacks”

A

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

63
Q

BPPV - what age group and sex is most affected?

A

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

64
Q

Risk factors for BPPV

A

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

65
Q

Patho of BPPV

A

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

66
Q

How long does BPPV take to resolve?

A

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

67
Q

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

A

True

68
Q

S&S of BPPV

A

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

69
Q

WHat maneuver is done to diagnose posterior canal BPPV?

A

Dix-Hallpike maneuver

70
Q

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

A

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

71
Q

Horizontal canal BPPV - what maneuver is used to diagnose?

A

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

72
Q

What 2 Particle Repositioning Maneuvers are used to treat BPPV?

A

Epley and Semont

73
Q

Describe the Epley maneuver

A

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

74
Q

Describe Semont maneuver

A

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

75
Q

Patient teaching for episodes of BPPV?

A

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

76
Q

When is onset of symptoms for Meniere’s disease?

A

20-40 years typically

77
Q

Risk factors for Menieres

A

Family history

Autoimmune disease (diabetes, lupus or rheumatoid arthritis

Head injury, especially if it involved the ear

Viral infection of inner ear

Allergies

78
Q

Patho of Meniere’s

A

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

79
Q

Time course of Meniere’s

A

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

80
Q

What is the triad of symptoms in Meniere’s

A

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

81
Q

Dx of Meniere’s

A

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

NUNP531 Applied Pathophysiology (24 decks)

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