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Pathology > Infections > Flashcards

Infections Flashcards

1
Q

Neisseria meningitides

A

G-ve diplococci
Transmission: resp droplets
ROS: usually just mild “flu” sx’s (carrier)
Complication: invasion of blood stream causing septicemia and meningococcemia
*meningitis in some pt’s

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2
Q

Meningitis Pathogenesis

A

Pathology: pyogenic inflamm of leptomeninges and SA space
Gross: meninges are dull, congested w/ purple to exudate
Microscopically: PMN cells, fibrin, vascular congestion (acute inflamm)

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3
Q

Meningitis Clinical Features

A

ROS: fever, HA, cloudy consciousness, nuchal rigidity
Dx: CSF w/ PMNs and increased protein, low glucose
Other causes: TB, viral or fungal

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4
Q

Meningitis Course Features

A

Complications: shock, purpura, toxemia, DIC
Epidemiology: N. meningiditis common at all stages except neonates

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5
Q

Waterhouse Friderichsen Syndrome

A

Bilateral adrenal hemorrhages

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6
Q

Neisseria gonorrhoeae Features (and male sx’s)

A

G-ve diplococci, sexually transmitted
Male ROS: urethritis, epididymitis, urethral d/c, dysuria
Homosexual male ROS: oropharyngitis and proctitis

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7
Q

Neisseria gonorrhoeae (female sx’s)

A

ROS: cervicitis, salpingitis, peritonitis, vaginal d/c, dysuria, intermenstrual bleeding, PID,
Course: chronic can cause scarring of Fallopian tubes leading to infertility

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8
Q

Gonorrhea Course

A

Rarely hematogenous - can cause tenosynovitis, arthritis, hemorrhagic skin lesion, endocarditis, rarely causes meningitis

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9
Q

Ophthalmia Neonatorum (Gonorrhea)

A

Transmission: during parturition
ROS: purple to conjunctivitis
Tx: erythromycin/silver nitrate eye drops after birth for prevention

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10
Q

Salmonella typhi Features

typhoid fever

A

G-ve bacilli
Transmission: ingestion of contaminated food/water
Mechanism: enters ileal wall, enters blood stream and causes bacteremia during (week 1)

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11
Q

Typhoid Fever Organ Affects

A

Hepatomegaly: typhoid nodules composed of Kupffer cell hyperplasia, minute fo i of hemorrhagic necrosis, collections of macrophages during (week 2)
Splenomegaly: soft spleen w/ splenetic, typhoid nodules

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12
Q

Typhoid Fever Course

A

Excretion through bile into gut, re-enter gut wall through ileum, sensitization has occurred an contact w/ the organism produces lymphoid hypertrophy and necrosis in the mucosa (week 3)

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13
Q

Typhoid (enteric) Fever Lesions

A

Ileum: lymphoid hypertrophy of Peyer’s patches, necrosis, ulceration
Features: no PMNs, only macrophages, erythrophagocytosis, mesenteric LN enlarged, hemorrhagic necrosis

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14
Q

Typhoid (enteric) Fever Clinical Features

A

ROS: fever, toxic appearance, leucopenia*, bradycardia, endotoxin produces depression of heart and bone marrow, ulcers heal w/o scarring
Complications: perforation peritonitis, bleed (week 3 and 4)

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15
Q

Typhoid Fever Diagnosis

A

Week 1: blood culture (lysis of macrophages release large # of bacilli)
Week 2: organisms can be demonstrated in feces and sometime sin urine
Week 3: demonstrate Ab’s (Widal test)

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16
Q

Typhoid Carrier State

A

Persistent/chronic infection leads to colonization of gallbladder, carrier has no sx’s but can shed the bacteria in feces/urine
Tx: need to undergo choelcystectomy

17
Q

G-ve Sepsis

A

ROS: fever, DIC, hypotension, shock
Organisms: normally commensalism but become pathogenic in situations (immunodeficiency, break in mucous membrane)
E.g. - E. coli, h influenzae, pseudomonas aergunosa, klebsiella, proteus, serratia

18
Q

Staphylococci

A

G+ve, normally colonize human skin
Infectious: most commonly S. aureus
Lesions: inflammatory or toxin mediated

19
Q

Inflammatory Staphylococci Lesions

A

Skin, postpartum mastitis, bacteremia, endocarditis (tricuspid valve, common in drug addicts), osteomyelitis, pneumonia, bacteremic abscess
*MRSA

20
Q

Toxin Mediated Staphylococci Lesions

A

Food poisoning (enterotoxin), TSS, Scalded Skin Syndrome (exfoliatintoxin)

21
Q

Streptococci

A

G+ve cocci, present in pairs or chains, hemolytic

Lancefield grouping: Group A are beta hemolytic (e.g. - S. pyogenes), Group B are hemolytic

22
Q

Streptococci Infection

A

Direct damage: suppurative - cellulitis, abscess, pneumonia
Exotoxins mediated: Scarlet Fever
Indirect damage: caused by immune response

23
Q

Strep Pneumonia (pneumococcal pneumonia)

A

Causes: lobar pneumonia in healthy young adults
ROS: cough, fever, CP, hemoptysis
Early stage: exudate rich in fibrin, RBCs, few PMNs seen in lumen of alveoli
Progression: bronchioles and alveolar walls not damaged bc pt is immunocompetent
Spread: via pores of Kohn to involve the entire lobe
Course: total resolution w/in 10 days

24
Q

Red Hepatization

A

Exudate consists of RBCs, fibrin, more PMNs

- lung loses spongy consistency and feels solid and red like liver

25
Q

Grey Hepatization

A

Congestion and fibrin disappear, PMNs replaced by macrophages
Resolution: macrophages clear up the debris a few days later
Tx: abx accelerate the process
Complications: rare dev of abscess, fibrosis, emphysema

26
Q

Rheumatic Fever Course

A

Initial: streptococcal ST, or skin infection
Lag: 2-3 wks after initial infection
Mechanism: Ab’s generated to M protein of the bacteria cross react w/ tissue glycoproteins in joints, heart, skin, etc.

27
Q

Rheumatic Fever Sx’s

A

ROS: fever, poly arthritis, carditis, chorea, skin nodules, erythema (ACCNE)
Complication: carditis showing Aschoff bodies on biopsy, can become chronic and cause mitral stenosis
Tx: to prevent chronic rheumatic heart dz give pt prophylactic abx tx s/p RF

28
Q

Post-Streptococcal Glomerulonephritis Course

A

Initial: steptococcal ST or skin infection
Lag: 1-4 wks after initial infection
Mechanism: Ab-ag immune complexes form and get deposited in BM of glomeruli, activates complement and induce acute inflammation
*type III hypersensitivity

29
Q

Post-Streptococcal Glomerulonephritis Sx’s

A

ROS: acute malaise, fever, oliguria, hematuria, azotemia (👆🏽BUN, Creatinine and 👇🏽GFR)
Resolution: resolves spontaneously in most pt’s as immune complexes are cleared

30
Q

Diphtheria

A

Myocarditis is the complication

31
Q

Pseudomembranous Colitis (C. diff)

A

Clostridium difficult: G+ve bacillus
Cause: tx w/ broad spectrum abx is assoc w/ colitis bc they eliminate the normal flora of the gut that normally afford protection

32
Q

C. difficile Mechanism

A

Exotoxin causes severe mucosal suppurative inflamation, small vascular thrombosis, necrotic mucosa forms pseudomembrane

33
Q

Rickettsia Infections

A

Small, obligate intracellular, resemble G-ve

34
Q

Epidemic Typhus

A

Organism: Rickettsia prowazeki
Transmission: head/body lice
ROS: hemorrhagic nodules on skin, vasculitis, thrombosis, hemorrhage
Complications: pneumonia, hepatitis, CNS involvement (typhus nodule)
Severe: necrosis of earlobes, scrotum, nose, finger
Dx: immunofluorescence and Weil Felix test (Ab’s cross react w/ Proteus ag)

35
Q

Rocky Mountain Spotted Fever

A

Organism: Rickettsia rickettsii
Transmission: tick bite
Geography: OK, TN, AR, GA
ROS: fever, HA, myalgia followed by skin rash
Complications: vascular necrosis, hemorrhage, vasculitis, thrombosis (severe lung and CNS involvement)
Dx: immunofluorescence on biopsy

36
Q

Q Fever

A

Organism: Cloxiella burnetti
Transmission: airborne droplets from sheep/cattle
ROS: no skin rash, pneumonia (affects liver, spleen and bone marrow)
Biopsy: ring granuloma in liver biopsy - central fat, fibrinoid material surrounded by epithelioid cells
Dx: immunofluorescence, serology

Pathology (14 decks)

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