Module 5-Path Continued: Men, Salmonella Flashcards

1
Q

What are the 4 different etiologies of Meningitis?

A

Bacterial
Viral
Fungal
Tuberculous

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2
Q

What is meningitis ?

A

Inflammation of leptomeninges (pia and arachnoid)

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3
Q

How is meningitis spread?

A

Via inhalation of respiratory droplets == colonizes in nasopharynx —- spreads directly to brain via sinuses to meninges but can also spread via blood (via thoracic duct into lymphatics to bloodstream to CSF)

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4
Q

What are the symptoms of meningitis?

A

Headache, fever, stiff neck and photophobia

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5
Q

What is the best investigation for meningitis?

A

Spinal Tap

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6
Q

What examination should you do on a patient before spinal tapping the patient?

A

Fundoscopy to check for papilledema
if a patient has papilledema and you as the physician do a lumbar puncture the patient will get an uncal herniation (or transtentorial herniation)
CNIII is damage so patient pupil is dilated (mydriasis)

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7
Q

What would you find in the CSF of a patient with bacterial meningitis?

A

Increased Protein
Decreased Glucose (Bacteria eats it)
Increased PMNs
CSF will also be cloudy due to pus – exudate

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8
Q

What would you find in the CSF of a patient with viral meningitis?

A

Slightly Increased Protein
Slightly low/normal glucose
Increased lymphocytes (CD8 T cells –remember its viral thats why)

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9
Q

What would you find in the CSF of a patient with fungal meningitis?

A

Increased protein
Slightly decreased glucose
Mix of PMNs and lymphocytes (remember acute and chronic cells for fungal)

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10
Q

What would you find in the CSF of a patient with TB meningitis?

A

Increased Protein
Decreased Glucose
Increased CD4 T lymphocytes

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11
Q

A neonate up to 2 months, what bacterial meningitis would you find?

A

Strep. Agalactiae (group B) (gram positive bacteria)

group B colonizes the vagina of a pregnant women so baby can get meningitis during birth in the birth canal.

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12
Q

Infancy through childhood, what bacterial meningitis would you find?

A

Strep. Pneumoniae (gram positive bacteria, diplocci)

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13
Q

In adolescences what bacterial meningitis would you find?

A

Neisseria meningitides (gram negative bacteria)

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14
Q

During adulthood what bacterial meningitis would you find?

A

Strep Pneumoniae (gram positive bacteria, diplocci)

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15
Q

on gross image of the brain of a patient with bacterial meningitis what do you find?

A

Hyperemic (increased active blood volume) blood vessels

purulent exudate in subarachnoid space

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16
Q

What is one of the best investigations for TB?

A

Acid fast stain for CSF

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17
Q

What is the first investigation for TB?

A

xray

18
Q

What is one complication to bacterial meningitis?

A

Gram negative septic shock (aka neisseria meningitides )

N. meningitides leads to gram negative septic shock from meningococcal septicemia

19
Q

Meningococcal Septicemia can lead to DIC how?

A

LPS binds to LBP and this complex is now taken up by macrophages , secrete —- TNFalpha, recruits —– neutrophils, secrete —- IL-1 and procoagulant which causes endothelial damage —– systemic microthrombi —- DIC

20
Q

How does a gram positive bacteria cause DIC?

A

Via superantigens

21
Q

What are the internal and external bleeding spots in DIC?

A

Internal: adrenal glands hemorrhage
External: purpura and petechiae and ecchymosis
this leads to Waterhouse-Friderichsen Syndrome which can lead to Addison’s disease.

22
Q

What investigations would you do for Meningococcal Septicemia?

A

Increased D-dimer
Increased bleeding time
Increased PT and PTT

23
Q

So the first complication of Bacterial meningitis was meningococcal septicemia due to N. meningitides, what are the other 3 complications of bacterial meningitis?

A
  1. Deafness
  2. Communicating Hydrocephalus
  3. Spread of infection can cause encephalitis (these patients are usually immunocompromised)
24
Q

Clostridium Perfringens is a gram positive bacilli, anaerobic bacteria that produces spores and is found in the soil and invades traumatic and surgical wounds. what type of infection does this bacterial cause?

A

Myonecrosis aka gas gangrene
gas forming organisms: degradative enzymes produce gas in tissues
Deadly form of gangrene –> medical emergency
Perfringens perforates a gangrenous leg

25
Q

Clostridium Perfringens secretes 12 exotoxins= necrosis

most important is alpha toxin (lecithinase) what exactly do these exotoxins do?

A

Degrade lecithin – a major component cell membrane
Destroys RBCs, platelets, muscle fibers (myonecrosis)
Enzymes released from necrotic tissue

26
Q

Schistosoma is a parasite that has what significant effects on the body if contracted?

A

Bladder carcinoma
hepatomegaly, fibrosis and portal HTN
Eggs induce granulomas –> fibrosis and this leads to liver failure and hence ascites

27
Q

Staphylococci lesions can either be inflammatory mediate or toxin mediated. Name some inflammatory mediated examples:

A
  1. Skin- folliculitis, furuncle, carbuncle, cellulitis, impetigo, paronychia, surgical wound infection
  2. Post Partum-mastitis
  3. Bacteremia
  4. Endocarditis: tricupsid valve
  5. Osteomyelitis
  6. Pneumonia: bronchopneumonia, abscess wit hwatery pus
  7. Bacteremic abscess- lung, kidney, brain
  8. MRSA
28
Q

What are examples of toxin mediated staphylococci lesions?

A
  1. Food poisoning: enterotxoin
  2. Toxic Shock Syndrome (TSS)- intravaginal tampon if left in longer leads to growth of staph – release of exotoxin into circulation —rash, conjunctivitis and vomiting
  3. Scaled skin Syndrome
29
Q

Neisseria gonorrhoeae is a gram negative, diplococci, sexually transmitted disease. What are the signs and symptoms in males, homosexual males and females?

A

Males:
1. Urethritis and Epididymitis
–urethral discharge and dysuria
Homosexual Males:
1. oropharyngitis and proctitis (inflammation of rectum)
Females:
1. Cervicitis, salpingitis (infection/inflammation of fallopian tubes) and peritonitis, PID (pelvic inflammatory disease)
–vaginal discharge, inter menstrual bleeding
–if untreated can lead to scaring of the fallopian tubes

30
Q

Neisseria gonorrhoeae disseminated via what methods?

A
  1. Rare via hematogenous (carried in blood)
  2. Tenosynovitis (inflammation of the lining of sheath that surrounds tendon), arthritis
  3. Hemorrhagic skin lesions
  4. Endocarditis
  5. Rarely meningitis
31
Q

Neisseria gonorrhoeae can occur in a newborn, explain the mechanism for this

A
infections acquired during passage of the fetus through cervix during labor 
purulent conjunctivitis (opthalmia neonatorum)
use of erythomycin/silver nitrate eye drops after birth can prevent this
32
Q

How does one diagnosis Neisseria gonorrhoeae in males and females

A

Males: microscopy of exudate: PMNs and gram - diplococci
Females: culture of exudate - essential b/c gram - diplococci are normal part of vaginal flora
could yield false negative result if there are fewer organism

33
Q

What other STI can produce similar signs and symptoms as Neisseria gonorrhoeae?

A

Chlamydial infection

34
Q

Typhoid fever = Enteric Fever and it is caused by Salmonella Typhi: gram negative bacilli. how is this bacteria acquired?

A

Through ingestion of contaminated food, water (transferred in feces)

35
Q

Typhoid fever (Enteric fever) affects the body differently with each week, explain the effects of the bacteria during week one

A

Enter ileal wall (no lesions at this time) – enter bloodstream — bacteremia

36
Q

What is the effect of the salmonella typhi in week two?

A

Liver enlarged = typhoid nodules: composed of Kupffer cell hyperplasia
–minute foci of hemorrhagic necrosis, collections of macrophages
–Typhoid nodules: macrophages that contain bacteria, RBCs, degenerated lymphocytes
Spleen: enlarged soft spleen with splenitis, typhoid nodules

37
Q

What is the effect of salmonella typhi in week three?

A

Bacteria excreted through gall bladder in bile – lumen of gut — re-enter gut wall through ileum
–sensitization has occurred during this period — contact with organisms produces lymphoid hypertrophy (increase lymph tissue) and necrosis in the mucosa

38
Q

What are the clinical features of Enteric/Typhoid fever?

A
  • –Fever, toxic appearance, leukopenia (decreased WBCs) and bradycardia
  • –Endotoxin = depression of heart and bone marrow
  • –Ulcers heal without scarring
  • -Complications: perforation peritonitis bleed (3rd and 4th week)
39
Q

What are the lesions of enteric/typhoid fever?

A

ileum — lymphoid hypertrophy (Peyer’s patches), necrosis, ulceration

  • –no PMNs (Excrete a protein called invasion, that allows non phagocytic cells to take up the bacteria, where it is able to live intracelluarly; also inhibit oxidative burst of leukocytes = innate (Acute) immune response infected)
  • -only macrophages, erythrophagocytosis (phagocytosis of RBCs)
  • -mesenteric LN enlarged, hemorrhagic necrosis
40
Q

How would you diagnosis Enteric/Typhoid fever with each week?

A

End of week 1: blood culture – lysis of macrophages release large number of bacilli into circulation
Week 2: organisms in feces/ urine
Week 3: Widal test (demonstrate antibodies ) — bacteria are mixed with serum containing specific antibodies from an infected individual

41
Q

In some patients with Enteric/Typhoid fever, they develop chronic colonization of gallbladder, in what kind of patients does this develop?

A

Asymptomatic carries

42
Q

Gram negative bacteria septicemia leads to septic shock, what are some features of septic shock?

A

Common Clinical Situation
Fever, septicemia, DIC, Shock
Normally commensual organsims — become pathogenic
immune deficiency, break in mucous membranes