Hdm Week 17

Front 1

epidermis (thin) =>

Back 1

dermis (thick) => subcutaneous tissue (lots of adipose)

Front 2

macule =

(2),

Back 2

flat, <1cm

Front 3

papule =

(2)

Back 3

raised, <1cm

Front 4

plaque =

(3)

Back 4

raised, flat top, >1cm

Front 5

nodule =

(2)

Back 5

rounded/domed, >1cm

Front 6

pustule =

Back 6

pus-filled lesion

Front 7

vesicle =

(3)

Back 7

elevated,

<1cm,

serous fluid

(from serous glands)

Front 8

bulla =

(3)

Back 8

elevated,

>1cm,

serous fluid

Front 9

petechiae =

(3)

Back 9

1. purpuric macules

2. < 2mm

3. do NOT blanch

Front 10

pupuric ~

Back 10

subcutaneous bleeding

Front 11

palpable purpura =

Back 11

elevated, flat, hemorrhagic papules/plaques

Front 12

hemmorhage =

Back 12

escape of blood from its vessel

Front 13

morbiliform =

Back 13

measles-like

Front 14

scarlitiniform =

Back 14

sandpaper-like

Front 15

cellulitis, furuncles, and other skin lesions are a result of:

Back 15

primary bacterial infections

(toxins or immune resp)

Front 16

cellulitis =

Back 16

inflammation of dermis and subcutaneous tissue

Front 17

cellulitis ~~

(4)

Back 17

1. erythema

2. warmth

3. tenderness

4. edema

Front 18

symptoms of cellulitis =

(3)

Back 18

1. fever

2. chills

3. malaise

Front 19

**2 most common causes of cellulitis = **

Back 19

1. Staph auerus

2. Strep pyogenes

Front 20

cellulitis is often associated with bites; most common bact. causes of bite cellulitis =

(4)

Back 20

1. pasteurella (dog/cat)

2. anaerobes

3. Staph aureus

4. Strep pyogenes

Front 21

bite cellulitis is often:

Back 21

polymicrobial

Front 22

periorbital cellulitis is most often caused by:

(4)

Back 22

1. Strep pneumoniae

2. H. influenza

3. M. catarrhalis

4. Staph aureus

Front 23

3 other skin lesions associated with primary bacterial infection:

Back 23

1. erysipelas

2. necrotizing fasciitis

3. toxin-associated skin disease

Front 24

erysipelas =

Back 24

superficial cellulitis with lymphatic involvement

Front 25

erysipelas is commonly caused by:

Back 25

Strep pyogenes

Front 26

necrotizing fasciitis:

(3)

Back 26

1. spreads rapidly

2. painful to the touch, even in early stages

3. requires surgical removal

Front 27

necrotizing fasciitis is most often caused by:

Back 27

Strep pyogenes

(GAS)

Front 28

2 examples of toxin-associated skin disease:

Back 28

1. TSS

2. SSSS

Front 29

impetigo:

(2)

Back 29

1. honey crust, esp. in infants

2. CAN be bullous

Front 30

impetigo is usually caused by:

(2)

Back 30

1. GAS

2. Staph aureus

Front 31

scarlet fever =>

Back 31

sandpaper rash

Front 32

scarlet fever is caused by:

Back 32

GAS

Front 33

macules and papules are COMMON with:

Back 33

acute febrile illness, esp. if of viral etiology

- e.g. measles

Front 34

**wrt macuoles/papules, it's often unnecessary to:**

Back 34

identify the pathogen

Front 35

exanthem =

Back 35

eruption of the skin

Front 36

exanthems ~~

Back 36

development of immunity to virus

Front 37

2 examples of exanthems:

Back 37

Rosela, Parvovirus slapped-cheek

Front 38

petechiae, purpura ~~

Back 38

extravasation of RBC's into the skin, usually due to vasculitis or vascular disorder

Front 39

vasculitis =

Back 39

vascular *injury*

Front 40

when you see petechiae/purpura, **make sure that** :

Back 40

febrile patients don't have a life-threatening illness

Front 41

3 life-threatening illnesses associated with petechiae/purpura:

Back 41

1. meningococcemia

2. RMSF

3. spesis

Front 42

but majority of petechiae/purpura corresponds to:

Back 42

viral etiology

Front 43

there are many causes of vesicles and bulla, but the long list starts with:

(5)

Back 43

1. HSV

2. VZV

3. enteroviruses

4. Staph aureus

5. GAS

Front 44

caution with vesicles/bulla: you need to:

Back 44

*control* the shedding/spread of virus

Front 45

HFM disease ~~

Back 45

enteroviruses

Front 46

slapped cheek ~~

Back 46

5th disease / B19 parvovirus

Front 47

Rosella ~~

Back 47

HSV (HHV-6)

Front 48

molluscum contagiosum ~~

Back 48

MCV1, a pox virus

- not terrible

Front 49

staph scalded skin syndrome ~~

Back 49

sloughing off of skin at touch due to Staph. toxin

Front 50

Staphylococci aureus:

(2)

Back 50

1. coagulase +

2. golden on plate

Front 51

Staph aureus infects:

Back 51

hariy/moist parts of the body, including skin

Front 52

5 areas of the body that Staph aureus infects:

Back 52

1. nares

2. armpits

3. perineum

4. pharynx

5. GI tract

Front 53

Staph aureus can cause folliculitis, an infection of:

Back 53

hair follicles/sebaceous glands

Front 54

furuncle =

Back 54

deeper folliculitis

Front 55

carbuncle =

Back 55

coalescence of neighboring furuncles

Front 56

treatment of folliculitis =

(2)

Back 56

1. drainage

2. ab's for carbuncles

Front 57

what's one anti-Staph aureus antibiotic?

Back 57

clindamycin

Front 58

non-bolus impetigo =

Back 58

honey crust version

Front 59

non-bolus impetigo has historically been caused by ________________, but now is caused by _____________________________

Back 59

GAS;

*mix of GAS and Staph aureus*

Front 60

treatment for honey crust impetigo is no longer:

Back 60

penicillin, due to MRSA;

now it's Ery, mupirocin

Front 61

4 toxin-mediated Staph aureus diseases:

Back 61

1. bullous impetigo

2. SSSS

3. TSS

4. Stphylococci food poisoning

Front 62

SSSS =

Back 62

Staphylococci scalded skin syndrome

Front 63

both bullous impetigo and SSSS are caused by:

Back 63

exfoliative toxins

Front 64

what are 2 exfoliative Staph toxins?

Back 64

Eta, Etb

Front 65

what do Eta and Etb do?

Back 65

as serine proteases, they cut desmoglein-1

Front 66

desmoglein-1 is the:

Back 66

dominant desmosome of the corneal layer

Front 67

TSS is caused by:

Back 67

TSS-1, a superantigen

Front 68

TSS =>

Back 68

organ failure

Front 69

Staphylococci food poisoning is caused by:

Back 69

emetix toxins (SEA through SEU)

Front 70

emetic toxins (SEA-SEU) are:

Back 70

superantigens

=> T-cell OVER-activation

Front 71

other Staph aureus diseases:

(4)

Back 71

1. bacteriemia

2. necrotizing pneumonia

3. small colony variants

4. septic arthritis (rare)

Front 72

to cause bacteremia, needs:

(3)

Back 72

1. capsule

2. antimicrobial R

3. ability to survive in neutrophils

Front 73

**Staph aureus bacteremia can lead to:**

Back 73

endocarditis

(colonization of the heart) => heart troubles

Front 74

necrotizing pneumonia:

(3)

Back 74

1. caused by Staph aureus

2. rare

3. associated with PVL-pos strains

Front 75

small colony variants of Staph aureus:

(3)

Back 75

1. slow-growing

2. difficult to diagnose

3. R to many antibiotics

Front 76

SCV's can cause chronic infections like:

(2)

Back 76

1. CF

2. osteomyelitis

Front 77

in osteomyelitis, which bones of children and which of adults are affected?

Back 77

long bones of children,

vertebrae of adults

Front 78

3 virulence factors of Staph aureus:

Back 78

1. lots of hemolytic toxins

2. surface structures

3. immune evasion

Front 79

what do the hemolytic toxins of Staph aureus do?

(3)

Back 79

1. kill leukocytes/RBC's

2. avoid phag

3. release nutrients

Front 80

4 important surface structures of Staph aureus, and their functions:

Back 80

1. sortase anchor

2. MSCRAMMS (adhesion)

3. SpA (immune modulation)

4. Isd (iron acquisition)

Front 81

immune evasion of Staph aureus: what do CHIPS, SCIN, and SAK do?

Back 81

resist opsonophagocytosis

Front 82

immune evasion of Staph aureus: what do Dlt and Mpr do?

Back 82

protect against antimicrobial peptides

Front 83

immune evasion of Staph aureus: carotenoid pigment =

Back 83

antioxidant

Front 84

immune evasion of Staph aureus: it's inherently resistant to:

(2)

Back 84

ROS, RNS

Front 85

Staph aureus can bind Fc r's in:

Back 85

the *wrong orientation*

=> re-infection b/c you can't opsonize it

Front 86

plasmid =

Back 86

extra-chromosomal DNA that replicates separately

Front 87

Staph aureus adaptations:

(2)

Back 87

1. drug R (HA-MRSA, CA-MRSA)

2. virulence factors

Front 88

drug resistance and virulence factors are acquired:

Back 88

horizontally, via phages and plasmids

Front 89

how did Staph aureus become R to methycillin?

Back 89

by acquiring mecA, from poultry

Front 90

CA-MRSA:

(3)

Back 90

1. different from HA-MRSA

2. dominant version = USA300

3. USA300 is entering health-care settings

Front 91

CA-MRSA infects:

(2)

Back 91

skin and oropharynx

Front 92

treatment for CA-MRSA =

(3)

Back 92

1. TMP-SMX

2. vancomycin

3. Clindamycin

Front 93

**warning with using clindamycin on CA-MRSA:**

Back 93

it could induce R

Front 94

CA-MRSA are generally more susceptible to:

Back 94

treatment than HA-MRSA

Front 95

fungal infections fall into 3 categories:

Back 95

1. superficial infections of skin/mm

2. self-limiting, mild flu-like symptoms

3. invasine, life-trheatening infections

Front 96

2 examples of superficial fungal infection:

Back 96

1. oral thrush

2. candida vaginitis

Front 97

self-limiting, mild fungal infections are caused by:

(2)

Back 97

1. Cryptococcus

2. dimorphs

Front 98

invasive, life-threatening infections tend affect:

(2)

Back 98

1. diabetics

2. imm-comp'd

Front 99

yeast:

(3)

Back 99

1. unicellular

2. reproduce by budding

3. some produce pseudohyphae

Front 100

2 best examples of yeast:

Back 100

1. Candida

2. Cryptococcus

Front 101

fungi can look:

Back 101

very similar to bact, just bigger

Front 102

mold:

(2)

Back 102

1. multicellular

2. hyphae

Front 103

mold reproduce by:

Back 103

sporulation

Front 104

2 best examples of mold:

Back 104

1. Aspergillus

2. Zygomycetes

Front 105

conidia =

Back 105

fungal spores

Front 106

***dimorphic fungi***

Back 106

mold at ambient temp's (infectious),

yeast at body temps (pathogenic)

Front 107

2 best examples of dimorphic fungi:

Back 107

1. Histoplasma capsulatum

2. blastomyces dermatitidis

Front 108

hyphae can be:

Back 108

septate (cross-walled) or aseptate,

hyaline or dematiaceous

Front 109

hyaline hyphae means

Back 109

colorless hyphae

- dmatiaceous = brown/black

Front 110

identify fungi via:

(2)

Back 110

1. microscope

2. culture isolation

Front 111

features of fungi that don't apply to bacteria:

(5)

Back 111

1. true nucleus

2. mit.

3. cell wall = **chitin**

4. ***cyto memb contains sterols***

5. reproduce via budding, hyphael extensions

Front 112

prophylactic antifungals can actually increase:

Back 112

your risk of being infected with other fungi

- it's a cost-benefit question

Front 113

4 classes of anti-fungal drugs:

Back 113

1. polyenes

2. pyrimidine analogues

3 azoles

4. echinocandins

Front 114

**what do polyenes do?**

Back 114

target the fungal cell membrane

Front 115

3 kinds of polyenes:

Back 115

1. Amphotericin

2. Nystatin

3. Natamycin

Front 116

pyrimidine analogues:

(3)

Back 116

1. very limited use

2. primarily for cryptococcal meningitis

3. inhibits fungal DNA synth

Front 117

**what do azoles do?**

Back 117

inhibit cell membrane formation

Front 118

**what do echinocandins do?**

Back 118

inhibit fungal cell wall function

(ends in "fungin")

Front 119

***what is the drug of choice for superficial skin/mm infections:***

Back 119

*fluconazole*

Front 120

3 features of fluconazole:

Back 120

1. can be taken orally (rare)

2. comparatively low toxicity

3. comparatively inexpensive

Front 121

***what is Amphotericin (liposomal form) given for?***

Back 121

1. invasive infections

2. dimorphic infections

Front 122

Amphotericin features:

(3)

Back 122

1. must be given parenterally

2. **high renal toxicity**

3. expensive

Front 123

***echinocandins are used to combat:***

(2)

Back 123

1. invasive Candida

2. invasive Aspergillus

Front 124

what are the 2 most important fungal pathogens of the imm-comp'd?

Back 124

Candida and Aspergillus

Front 125

echinocardin features:

(3)

Back 125

1. IV only

2. very expensive

3. less toxic than Amphotericin

Front 126

Candida albicans:

(3)

Back 126

1. an oval yeast

2. may form pseudohyphae

3. =normal flora of skin and mm

Front 127

pseudohyphae =

Back 127

pinched off instead of walled

Front 128

which fungus infects the imm-comp almost exclusively?

Back 128

C. albicans

Front 129

risk factors for C. albicans infection include:

(4)

Back 129

1. ab therapy

2. catheters

3. ventilators

4. IV's

Front 130

2 major Candida species that cause fungemia:

Back 130

1. C. albicans

2. C. glabrata

Front 131

C. albicans is VERY susceptible to:

Back 131

fluconazole

Front 132

C. glabrata is NOT susceptible to fluconazole; instead, use:

Back 132

echinocandins

Front 133

diagnosing Candida infection: most reliable method =

Back 133

blood culture, for *invasive* Candida spp

PNA-fish differentiates between albicans and glabrata

Front 134

**what is the role of serology in diagnosing C. albicans infection?**

Back 134

NO place

Front 135

HBeAg = marker of replication ~~

Back 135

highly-infectious Hep B

Front 136

anti-HBsAB =

Back 136

*immunity*

Front 137

IgM antiHBc =

Back 137

*acute infection*

Front 138

HBsAg =

Back 138

current infection

Front 139

HBcAB =

Back 139

current OR past infection

Front 140

the BBB is a barrier to which immune cells?

(2)

Back 140

1. *resting* B cells

2. naive/resting T cells

Front 141

the BBB is reinforced by:

(2)

Back 141

astrocytes,

special tight junctions

Front 142

the CNS is immune privileged, which means that it's able to:

Back 142

tolerate antigens *without initiating the inflammatory response*

Front 143

there are NO lymphatics in the brain, but the CSF and brain fluids flow:

Back 143

TO the lymphatics

Front 144

getting things OUT of the CNS is:

Back 144

easy;

getting things in is much harder

Front 145

which 2 innate immune system facets are low in the CNS?

Back 145

1. complement

2. MHC expression

Front 146

exception to low MHC expression: these cells DO express MHC frequently:

Back 146

microglia

Front 147

Innate Immune cells of the CNS:

(3)

Back 147

1. microglia

2. astrocytes

3. mast cells

Front 148

microglia =

Back 148

macrophages of the CNS

Front 149

microglia features:

(4)

Back 149

1. highly phag

2. poor APC's

3. express TLR4

4. can produce inflammatory mediators

Front 150

astrocytes:

(3)

Back 150

1. express TLR4

2. express TGF-B, a pro-inflammatory cytokine

3. but also *suppress* inflammation (paradoxical)

Front 151

mast cells:

(3)

Back 151

1. found near meninges

2. release mediators that increase permeability of the blood vessels

3. => allowing T cells to get into CNS

Front 152

improper mast cell activity =>

(2)

Back 152

1. seizures

2. autism

Front 153

T cells stimulated by an antigen in the periphery can:

Back 153

enter the CNS,

in sickness OR health

Front 154

B cells can enter the CNS IF:

Back 154

*inflammation* is occurring

=> mature to plasma cells in the CNS

Front 155

2 types of inflammation of the brain parenchyma:

Back 155

1. encephalitis

2. brain abscesses

Front 156

abscess =

Back 156

swollen area, usually with pus

Front 157

encephalitis is an ________ problem

Back 157

acute

Front 158

which 3 CNS diseases can be acute OR chronic?

Back 158

1. brain abscesses

2. meningitis

3. myelitis

Front 159

myelitis =

Back 159

inflammation of the SC

Front 160

bacterial causes of acute meningitis:

(4)

Back 160

1. encapsulated bact

2. arboviruses

3. enteroviruses

4. HSV2

Front 161

microbial causes of chronic meningitis:

(3)

Back 161

1. Myco TB

2. Cryptococcus neofromans

3. other fungi

Front 162

ability to disseminate =

Back 162

prerequisite to infecting the CNS

Front 163

bacteria RARELY cause:

Back 163

meningitis

- viral cause much more common

Front 164

viral causes of meningitis:

(7)

Back 164

1. herpes viruses

2. adenovirus

3. Influenza A

4. enteroviruses

5. MMR

6. Rabies

7. arboviruses

Front 165

microbial causes of acute brain abscesses:

(3)

Back 165

1. Staphylococci

2. mixed flora

3. GAS

Front 166

microbial causes of chronic brain abscesses:

(4)

Back 166

1. Myco TB

2. Cryptococcus neoformans

3. T. solium

4. Toxoplasma gondii (protozoan)

Front 167

**what's the most common way for an organism to get into the CNS?**

Back 167

through circulation, by way of **choroid plexus**

Front 168

the choroid plexus is found between:

Back 168

the cerebellum and the pons

Front 169

what quality of the choroid plexus makes it the main point of entry?

Back 169

it's semi-fenestrated

=> microorganisms are able to extravasate, then infect the nearby cells of the BBB

Front 170

2 other forms of entry into the CNS:

Back 170

1. trafficing along peripheral nerves

2. entering through the olfactory nerves

Front 171

***for babies between 0 and 3 months, the most likely causes of meningitis are:***

(3)

Back 171

1. GBS

2. E. coli

3. Listeria monocytogenes

Front 172

if you're >3 months old, the 2 most likely causes of meningitis are:

Back 172

1. Strep pneumoniae

2. N. minigitidis

Front 173

in the imm-comp, the most likely causes of meningitis are:

(2)

Back 173

1. Listeria

2. GN rods

Front 174

temporal lobe encephalitis =>

(3)

Back 174

1. personality changes

2. visual field defects

3. hemiparesis

Front 175

paresis =

Back 175

weakness

Front 176

meningitis =>

(4)

Back 176

1. headache

2. stiffness

3. diplopia

4. CN palsies

Front 177

7 PE findings in CNS infections:

Back 177

1. neck, back rigidity

2. headache

3. vomiting

4. photophobia

5. Brudzinski's sign

6. Kernig's sign

7. dec. BP

Front 178

Brudzinski's sign =

Back 178

lift neck,

legs will bend or pain will increase

Front 179

Kernig's sign =

Back 179

flex hip to 90 degrees,

pt will be unable to straighten leg

Front 180

diagnosis of CNS infection:

(3)

Back 180

1. immediately treat

2. 2 blood cultures

3. lumbar puncture to examine CSF
(CT first if brain abscess suspected)

Front 181

the CSF is normally:

Back 181

clear, colorless

Front 182

***CSF glucose should be:

Back 182

> 50-66% of blood glucose

Front 183

there is NO vaccine against:

Back 183

serotype B of N. meningitidis

Front 184

why is there no vaccine against N. meningitidis serotype B?

Back 184

b/c it posses mlcls that are similar to fetal brain carbs

=> concern that AB against it might be autoreactive

Front 185

virulence factors of N. meningitidis:

(4)

Back 185

1. **capsule**

2. pili

3. Opa prot's

4. LOS

Front 186

infection by N. meningitidis: adhere to non-ciliated epithelial cells =>

Back 186

internalized => intracellular replication => transcytosis through basolateral tissue => dissemination

Front 187

N. meningitidis can cause:

Back 187

skin lesions

Front 188

skin lesions of N. meningitidis are:

(2)

Back 188

macular or non-blanching petechiae

Front 189

CSF profile of N. meningitidis infection:

(3)

Back 189

1. CSF is cloudy due to bact/WBC's

2. glucose is dec.

3. prot is elevated

Front 190

***organisms with capsules***

(7)

Back 190

1. N. meningitidis

2. E. coli

3. H. influenza

4. S. pneumoniae

5. GBS

6. Staph aureus

7. C. neoformans

Front 191

***3 NON-encapsulated bact. that can infect the CNS:***

Back 191

1. Listeria monocytogenes

2. Myco TB (rare)

3. spirochetes

Front 192

2 specific spirochetes:

Back 192

1. T. pallidum

2. B. burg

Front 193

Listeria monocytogenes causes:

Back 193

atypical meningitis

Front 194

how is Listeria meningitis atypical?

(3)

Back 194

it causes a sub-acute course, in which symptoms can be going on for >24 hrs without having to do to the hospital

~ altered consciousness, abnormal movements

~ sometimes there are no CSF findings

Front 195

CNS tuberculosis takes the form of:

(3)

Back 195

1. meningitis (most common)

2. encephalitis

3. Pott's syndrome

Front 196

**principal target of CNS by Myco TB =

Back 196

microglial cells

Front 197

what allows the spirochetes to get through the BBB?

Back 197

their spiral motility

Front 198

B. burg causes:

Back 198

Lyme disease

Front 199

spirochetes tend to be cleared by people pretty quickly, but become a problem for the imm-comp, causing:

Back 199

neurosyphilis, for example

Front 200

what does the orbital septum divide?

Back 200

the lids/soft tissue from the neurovasculature

Front 201

4 signs of orbital cellulitis:

Back 201

1. proptosis

2. pain moving eye

3. problems with CN's 2, 3, 4, 6

4. protrusion of conjunctiva

(fever)

Front 202

peri-orbital cellulitis =

Back 202

*pre-septal* cellulitis

- infection/inflammation is confined to eyelid and soft tissue

Front 203

orbital infections are often the result of:

Back 203

spread from sinuses

Front 204

in adults, orbital infections tend to be caused by *multiple* organisms, which usually include:

(3)

Back 204

1. GP cocci

2. H. influenza

3. anaerobes

Front 205

**the imm-comp are susceptible to _________ orbital infections**

Back 205

***fungal***

- needs aggressive treatment - life-threatening

Front 206

Neisseria meningitis:

(3)

Back 206

1. GN

2. diplococci

3. upper respiratory tract

Front 207

E. coli

(3)

Back 207

1. GN

2. rods

3. GI tract

Front 208

H. influenza

(3)

Back 208

1. GN

2. coccobacilli (pleomorphic)

3. upper resp. tract

Front 209

Strep agalacticae (GBS)

(4)

Back 209

1. GP

2. cocci in short chains

3. GI tract and female genital tract

4. subtle B hemolytic

Front 210

Strep. pneumoniae

(4)

Back 210

1. GP

2. cocci in short chains

3. upper resp. tract

4. alpha-hemolytic

Front 211

Staph aureus

(4)

Back 211

1. GP

2. cocci in clusters

3. skin, nares

4. B-hemolytic

Front 212

Listeria monocytogenes

(3)

Back 212

1. GP

2. facultative intracellular rods

3. GI tract

Front 213

Myco TB:

(3)

Back 213

1. acid-fast

2. bacillus

3. lower resp. tract

Front 214

Treponema pallidum:

(2)

Back 214

1. spirochete

2. disseminates from urogenital tract

Front 215

Borrelia burgdorferi:

(2)

Back 215

1. spirochetes

2. arthropod-borne transmission

Front 216

lots of Neutrophils =

Back 216

bacterial infection

Front 217

inflammatory cells in the CSF =

Back 217

meningitis