15: Diseases Of The Respiratory Tract And CVS Flashcards

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1
Q

Sinusitis

A

Infection of the upper respiratory tract
-sinuses are normally air filled
-inflammation reaction ass. w/ the virus produce fluid, mucus, and edema that cannot drain

-when the fluid gets trapped in the sinuses, it becomes a great growth medium for bacteria and fungi. This happens because the trapped fluid, which is usually mucus, is warm and moist—ideal conditions for pathogens to thrive.

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2
Q

Acute cases of sinusitis are caused by

A

Often caused by a viral infection, such as the common cold
Haemophilus influenza
Streptococcus pneumoniae

Which are OPPORTUNISTIC INFECTIONS
Pre-disposing factors
-previous URT infection deviated septum
-enlarged lymph nodes
-Allergies
-cystic fibrosis

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3
Q

Ottis media

A

Infection of the middle ear
URI
Bacteria from nasopharynx colonize and multiply
Fluid builds up in the middle ear.
normally fluid in the middle ear drains into the through through a tube called the Eustachian tube. But during an infection, swelling blocks off the tube, so fluid builds up.

Eustachian tube dysfunction is often the underlying problem in otitis media. The eustachian tube connects the middle ear to the back of the throat and helps equalize pressure and drain fluids from the middle ear.

The middle ear is the air-filled space behind the eardrum that contains the tiny bones responsible for hearing. Otitis media is a common condition, particularly in children, and can be caused by bacteria or viruses. It often follows an upper respiratory infection, such as a cold or sinus infection, where the fluid gets trapped behind the eardrum.

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4
Q

Who is more at risk for Eustachian tube obstruction and reflux and why?

A

Children >3yo
Because infants and younger children have shorter, more horizontal tubes, immature floppy elastic cartilage and larder adenoids compared to adults which places the a at a higher risk therefore can get easily blocked by the inflammation of the middle ear (Ottis media)

Most acute cases are caused by Streptococcus pneumonia and Haemophilus influenza

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5
Q

Pharyngitis and causative pathogen

A

Infection of the throat
bacteria
Mostly due to Streptococcus pyogenes - “strep throat”
Less common due to Fusobacterium necrophorum

Viruses as well and some fungi

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6
Q

Streptococcus pyogenes
-gram +/-
-shape
-w/ or w/o O2
-lab identification

A

-gram -
-cocci
-facultative anaerobic
-B-hemolytic, catalase (-), coagulase (-)

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7
Q

Strep pharyngitis CLINICAL MANIFESTATIONS

A

Redness and swelling (inflammation) of the pharynx and tonsils
White pus nodules may appear
Fever, malaise, headache, throat pain

The reddened appearance and pus pockets of a throat with pharyngitis.

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8
Q

Strep Pharyngitis DIAGNOSIS

A

-direct latex agglutination from throat swab specimen (10min)
-Direct culture of pharyngeal specimen on blood agar (takes at least 18 hrs to get results)

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9
Q

Strep pharyngitis treatment

A

Penicillin V
Or amoxicillin

Cephalosporin if allergic to penicillin

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10
Q

Complications/sequela of Strep pyogenes infection

A

-Rheumatic fever
An autoimmune response that can occur after untreated or inadequately treated strep throat. Inflammation affecting the heart, joints, skin (subcutaneous tissue)
-scarlet fever
strain of S. pyogenes that produces a erythrogenic toxin (superantigen). Characterized by a red, sandpaper-like rash, high fever, and a strawberry tongue.
-acute glomerulonephritis
A kidney inflammation that develops after a streptococcal skin (impetigo) or throat infection (pharyngitis). It can cause permanent kidney failure, low urine output, and swelling (edema).

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11
Q

How does Rheumatic fever occur after a strep. Pyogenes infection is left untreated or mistreated ?

A

Strep Throat (S. pyogenes infection):
The initial infection, often in the form of pharyngitis (strep throat), triggers an immune response.

Immune Response (Antibody production):
The body produces antibodies against the M protein of S. pyogenes.

Molecular Mimicry:
The structural similarity between M protein and cardiac myosin leads to a cross-reactive immune response.

Rheumatic fever:
Occurs about 1-5 weeks after an untreated or inadequately treated strep infection.

Chronic Rheumatic Heart Disease:
The immune system attacks heart valves and tissues.

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12
Q

How does Acute Glomerulonephritis occur after a strep. Pyogenes infection is left untreated or mistreated ?

A

Streptococcal Infection:
After an infection with certain strains of S. pyogenes (particularly those producing nephritogenic M proteins), the body produces antibodies against the bacterial antigens.

Antigen-Antibody Complex Formation in the kidneys:
The antigens from S. pyogenes bind to the antibodies produced by the immune system. This creates immune complexes that can grow larger as more antigens and antibodies accumulate.

Complex Deposition in the Kidneys:
These antigen-antibody complexes circulate through the bloodstream. They get deposited in the glomeruli—the tiny filtering units within the kidneys responsible for filtering blood.

Inflammatory Response:
The deposition of these complexes triggers a complement system activation and an inflammatory response. Immune cells like neutrophils and macrophages are recruited to the site, which results in glomerular inflammation and damage.
Cause low urine output, edema, can lead to permanent kidney failure

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13
Q

Pertussis (whooping cough)
-gram +/-
-shape
-w/ or w/o O2
-transmission
-special characteristic

A

Gram -
Coccoc-bacillus
aerobic
Respiratory droplets (highly infectious)
Strict human pathogen, and Fastidious

Pertussis, commonly known as whooping cough, is a highly contagious respiratory infection caused by the bacterium Bordetella pertussis

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14
Q

Pertussis Pathogenesis

A

attaches to the ciliated epithelial cells of the respiratory tract and produces toxins that interfere with normal respiratory function.
=immobilizes cilia = inability to remove particles
pertussis toxin
Xs mucus production
tracheal cytotoxin
Destroys ciliated cells

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15
Q

Pertussis clinical manifestations

A

-Whooping sound
-Patient is contagious from beginning of catarrhal stage
through the 3rd week after onset of paroxysms

Pertussis progresses through three stages, each with distinct symptoms:
Catarrhal Stage (1-2 weeks):
Symptoms resemble the common cold: mild cough, runny nose, sneezing, low-grade fever.
This is the most contagious phase of the disease, though symptoms are nonspecific and often mistaken for a regular upper respiratory infection.

Paroxysmal Stage:
Severe coughing fits (paroxysms) develop. The coughing is often uncontrollable, followed by a “whooping” sound as the patient breathes in air after the coughing fit.
The intense coughing can lead to vomiting, exhaustion, and even broken ribs in severe cases.

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16
Q

What is the gold standard for diagnosing pertussis

A

Culture
Samples from posterior nasopharynx (NOT THE THROAT)
PCR
ELISA

17
Q

How can we prevent pertussis?

A

DTap vaccine - children <7yoa
Tdap vaccine - older children/adults

18
Q

Pneumonia
-what is it?
-acquired?

A

Infection of the lung involving the alveoli
Fluid fills the alveoli
Can be caused by bacteria, viruses, fungi and helminths
Community acquired, hospital acquired, animal/environmental acquired

19
Q

Pneumonia pathogenesis

A

Bacteria is inhaled or aspirated into the bronchi and alveoli
=induces inflammatory response
=infiltration of immune cells
=produce mucus and exudate w/ pus

20
Q

Pneumonia community acquired (person-to-person) mostly caused by

A

40% - streptococcus Pneumonia
30% - viruses
10% - mycoplasma pneumonia

Haemophilus influenza used to be the major cause but now we have vaccines

21
Q

Pneumonia nosocomial acquired mostly caused by

A

Commonly ass. w/ mechanical ventilation = tracheotomy
Mortality rate 30-50%

Pseudomonas aeruginosa
Klebsiella pneumoniae
Stenotrophomonas maltophilia
Acinetobacter baumannii
Burkholderia cepacia

22
Q

Pneumonia clinical manifestations

A

-Lobar pneumonia
-bronchial pneumonia
-atypical pneumonia (walking pneumonia)

23
Q

Infective endocarditis (IE)

A

Inflammation of endocardium
Most of the time is infection of the heart valves (mitral or aortic)

Most infection occur on damaged or prosthetic valves

24
Q

Oral predisposing factors of infective endocarditis

A

Dental disease
Recent dental or surgical procedure

25
Q

Acute infective endocarditis caused by what bacteria

A

-S.aureus (most of staph causing IE)
-S.pneumoniae

26
Q

Subacute infective endocarditis caused by what bacteria

A

-Viridans strep (most of strep cases causes IE)
-enterococcus
-S.epidermidis
-HACEK organisms
-fungi

27
Q

Infective endocarditis pathogenesis

A

Endothelial Injury:
Pre-existing heart damage: Individuals with pre-existing valvular damage (e.g., from rheumatic heart disease, congenital heart defects, or mitral valve prolapse) or the presence of prosthetic heart valves are more susceptible to IE. Damage to the endocardial surface, especially on the heart valves The endothelial damage stimulates platelet and fibrin deposition, leading to the formation of clots. This fibrin-platelet matrix provides an ideal environment for microorganisms to adhere and proliferate forming vegetations

28
Q

Cardiac conditions ass. w/ the highest risk of Infective endocarditis

A

MUST PRESCRIBE PROPHYLAXIS W/ DENTAL PROCEDURE

-previous history of IE
-prosthetic cardiac valves
-congenital heart disease

29
Q

Recommended antibiotics prophylaxis regimens for periodontal procedures in adults at risk for infective endocarditis for a standard oral regimen?

A

amoxicillin (2.0g 30-60min before procedure)
For standard oral regimen

clindamycin (600mg 30-60min before procedure)
Allergic to pen

30
Q

Recommended antibiotics prophylaxis regimens for periodontal procedures in adults at risk for infective endocarditis for patients unable to take oral medications?

A

Ampicillin (2.0g intramuscularly or intravenous w/n 30min before procedure

Allergic to pen
clindamycin (600mg - inject slowly and dilute) or cefazolin (1.0g)

31
Q

Clinical manifestations for sepsis

A

Drop in blood pressure (hypotension) = shock
Organs start to dysfunction
Death

bacteremia - sepsis - septic shock
Sources of infection - bacteria enter blood (bacteremia)- leaking blood vessels -organ dysfunction - death

32
Q

Sepsis diagnosis

A

-Blood cultures to detect pathogen before antibiotic treatment
-gram stain for identification of bacteria
-antibiogram to determine antibiotic resistance

33
Q

Sepsis treatment

A

Empiric antibiotic treatment until agent is known and susceptibilities are determined.

Measures to correct shock and poor oxygen