Gastrointestinal Infections III Flashcards

1
Q

What is the name for inflammation of the angles of the mouth?

What are te usual etilogical agents responsible?

A

Angular Cheilitis

Angular stomatitis or perleche

  • Etiology:
    • Candida albicans- usually
    • Yellow crusting – Staphylococcus aureus
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2
Q

Angular Cheilitis is most common in which demographic?

A
  • elderly, children who suck their digits, adn in people with riboflavin or irion deficiency
  • Elderly
    • sagging facial muscles adn ill filling dentures
    • causes maceration of skin resultin in inflammation
  • can be sign of anemia or vitamin deficiency
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3
Q

Angular Ceilitis Diagnosis?

Treatment?

Prevention?

A
  • Diagnosis
    • swab & culture
      • S. aureus - blood plates/others
      • C. albicans - sabouraud dextrose agar
  • Treatment
    • Antigungal or antibacterial agent depending on cause
    • hydrocortizone if chronic
  • Prevention
    • proper nutrition
    • proper fitting dentures
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4
Q
A
  • Oral candidiasis

Oral hairy leukoplakia usually occurs at the corners of themouth & you cannot remove it

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5
Q
A

Oral hairy leukoplakia

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6
Q

What is the most common cause of benign viral parotitis?

A

Paramyxovirus

mumps

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7
Q

What are the possible complicated associated with mumps?

A
  • Aseptic meningitis (parotitis absent up to 50%)
    • asymptomatic infections occur in 40-50% mumps
    • symptomatic CNS infections occur in 10% clinical cases
    • adults & boys at higher risk
    • perminant sequelae occur in 25% – 1% die
    • can result in encephalitis (fatal 1.4%)
  • Oophoritis and Epididymoorchitis
    • testicular swelling, tenderness, nausea, vomiting, and fever
    • most common complication postpubertal males
    • ovarian inflammation in 5% postpubertal females
  • Deafness
    • 1 in 15,000– usually unilateral
    • sudden onset & damage is permanant
  • During pregnancy can lead to fetal death in 1st trimeser
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8
Q

Incubation period for Mumps?

Symptoms?

A
  • Incubation: 14-25 days
  • Usually asymptomatic
    • may present as lower respiratory tract infection– esp in preschool children
  • If symptomatic
    • prodrome: myalgia, headache, anorexia, malaise, low-grade fever
    • parotitis: swollen and tender salivary glands with earache (30-40% patients)
    • can be bilateral or unilateral
    • symptoms occur w/in first 2 days, usually gone after 10 days
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9
Q

How is mumps transmitted?

What is the most affected demographic?

A
  • highly contagious
    • airborne transmission w/ infected droplet nuclei or saliva
    • direct person-person contact
    • most common in winter-spring
    • infections 3 days before symptoms & 9 days after symptoms disappear
  • primarily childhood infection w/ 60% cases occurring in children <15 years of age
  • no carrier state is known
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10
Q

Mumps Pathogenesis

A
  • Virus replicates in nasopharynx and regional lymph nodes
  • viremia 12-25 days later
  • multiple tissues infected durign viremia
    • hemagglutinin-neuraminidase or virus binds to trisaccharids (alpha2,3-linked sialic acid) on host cells
  • Tropisms for glandular tissue & CNS
    • meninges, salivary glands, testes, ovaries, pancreas, kidneys, thyroid, eyes, and mammary glands
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11
Q

Mumps diagnosis

A
  • clinically obvious
    • jelly-like feel; NOT warm
  • isolate virus from saliva, urine, and CSF
  • serology EIA fro IgM and IgG
    • IgM: first few days (acute)
    • IgG: requies 2 samples 2 weeks apart
      • if titer is rising, indication acute case
      • not rising = past case/immunized
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12
Q

Mumps treatment and prevention

A
  • Treatment
    • treat the symptoms
  • Prevention
    • MMR vaccine (live attenuated)
      • not given to pregnant people
    • 95% develop immune response – given 12-15 months
    • booster 4-6 years
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13
Q

What is the etilogical agent of acute bacterial parotitis?

Manifestations?

A
  • Etilogy
    • S. aureus
  • Manifestations
    • swellign salivary glands
    • chewing increases pain
    • skin- erythema, warm
    • massage- purulent saliva (differentiate bacterial vs. viral)
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14
Q

What demographic is most commonly affected by acute bacterial parotitis?

A
  • elderly- takign medications that affect flow of saliva
  • dehydrated
  • choronically ill
  • postoperative patients
  • patients with dry mouth
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15
Q

Pathogenesis of Acute bacterial parotitis

A
  • flow of saliva affected
  • bacteria enter duct
  • ascend to gland
  • inflammation adn pain
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16
Q

Diagnosis of actue parotitis?

Treatment?

Prevention?

A
  • Diagnosis
    • skin erythematous, warm
    • massage to express purulent material
    • gram stain and culture
  • Treatment
    • IV antibiotic
    • rehydrate patient
    • may need surgery
  • Prevention
    • proper hydration of chronically ill, elderly and postoperative patients
17
Q
A

Ludwig’s angina

  • w/ bacterial parotitis, movement of the tongue wouldn’t cause pain– chewing will, though
18
Q
A

Viral Parotitis

19
Q
A

bacterial parotitis

20
Q
A

Oral hairy leukoplakia– caused by Epstein Barr

21
Q

What is the name for inflammation of the esophagus?

It is associated with what two specific symptoms?

Possible causes?

A

Esophagitis

  • Associated with
    • dysphagia (trouble swallowing)
    • odynophagia (painful swallowing)
  • causes
    • GERD
    • Infections
    • Medications
22
Q

Etilogical infectious agents responsible for esophagitis?

A
  • Candida albicans
  • CMV (cytomegalovirus)
  • HSV (herpes simplex virus)
  • HIV
  • VZV (varicilla zoster virus)
23
Q

Esophagitis symptoms?

What demographic is most commonly affected?

A
  • Symptoms
    • dysphagia, odynophagia, heatburn, retrosternal discomfort or pain, nausea, vomiting, fever, sepsis, abdominal pain, epigastric pain, cough
  • Epidemiology
    • most common in immunosuppressed
      • AIDS, Leukemia,Lymphoma, diabetes, alcoholism, motility disorders, patients undergoing ratiation and chemotherapy)
      • rare in general population <5%
24
Q

Patogenesis of esophagitis?

–with relation to the most common causes

A
  • C. albicans - most common all patients
  • HIV- low CD4- more liekly to get fungal
  • HSV and CMV- AIDS & transplant patients
    • CMV more common than HSV in AIDS patients
    • Transplant
      • HSV early
      • CMV 2-6 months after transplant
25
Q

How is esophagitis diagnosed?

A
  • odynophagia is unique to infectious esophagitis
  • Esophagogastroduodenoscopy (EGD)
    • to see and biopsy the esphagus
    • Candida albicans
      • thrush
      • plaques in esophagus, creamy white or pale yellow w/ underlying raw base
      • stain & look for yeast
    • HSV
      • abrupt onset
      • early lesions- small vesicles middle to distal esophagus
      • later- ulcers with raised edge (volcano lesions
      • Lok for Tzanck cells
    • CMV
      • onset of symptoms gradual
      • only in immnocompromised hosts
      • large solitary shallow ulcer or multiple discrete lesions at distal end esophagus
      • culture
    • HIV
      • multple small thrush-lie lesions
      • durign priamry HIV infection
      • later on giand deep uncers
      • fistula, perforation, hemorrhage or superinfections
    • VZV
      • usually has skin lesions consisten w/ chicken pox or shingles
26
Q

Treatment esophagitis?

Prevention?

A
  • Tratment
    • Antifungal or antiviral agent depending on the cause of the infection
    • Steriods to lower inflammation
  • Prevention
    • Don’t get immuno-suppressed if you don’t have to
27
Q

What is the most common etilogical cause of chronic active gastritis and peptic ulcer disease?

What are the two kinds of peptic ulcer disease?

A
  • Etiology
    • Helicobacter pylori
  • Peptic ulcer disease
    • gastric ulcer disease
    • duodenal ulcer disease
28
Q

Symptoms of Chronic active gastritis?

A
  • often asymptomatic
  • moderate
    • pain or discomfort in pit of stomach
    • pain in left upper abdomen
      • travels to back of belly
    • burning, gnawing, sore, vague discomfort
    • belching w/o relief, nausea, vomiting
  • critically ill
    • pale and sweaty
    • may have tachycardia
    • severe illness- bleeding from stomach, faint or feel like fainting
    • vomit blood
    • blood or dark sticky, foul smelling stools
29
Q

Symptoms of peptic ulcer disease

A
  • Gnawing or burign pain inepigastrium
  • bleeding that may result in anemia, weakness, and fatigue
  • hematemesis, melena or hematochezia
  • gastric ulcers
    • pain made worse by eating
  • duodenal ulcers
    • pain relieved by eating or antacids
30
Q

Why does eating food increase pain caused by gastric ulcers but decrease pain caused by duodenal ulcers?

A
  • Nerves respond to protons (exposed by ulcer)
    • at lower pH, more protons, more pain stimulus
  • In the stomach, when you are eating acid is being made,
    • increasing pain
  • However, the duodenum produced bicarbonate in response to eating (b/c it does not like low pH), so it increases the pH while you are eating
    • decreasing pain