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I3 > Third Exam - Week 6 > Flashcards

Third Exam - Week 6 Flashcards

1
Q

Impetigo

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • superficial
  • golden crusty “stuck on” appearance, not a lot of redness or inflammation
  • not itchy, not painful
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2
Q

Folliculitis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • hair follicle disease
  • pustule with purulent discharge
  • itchy
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3
Q

Furuncle

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • deeper folliculitis
  • firm tender nodule, sometimes draining, (inside of nose), red and purulent
  • painful, tender
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4
Q

Carbuncle

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • extensive furuncle into subcutaenous fat
  • punched out lesion, lower extremities, not very purulent, has heaped border, inflammation
  • painful
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5
Q

Erysipelas

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • superficial lymphatic involvement
  • face and lower extremities, red, swelling, fairly well demarcated, clear border, can get bacteremia and fever in diabetics
  • pain, red, hot
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6
Q

Cellulitis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • spreading infection including sub-cutaneous tissues - deeper
  • streaking, lymphanditis, warm, red, tender, ulcer (not escar), warm, acute fever, chills
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7
Q

Necrotizing fasciitis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • subcutaneous fat and deep fascia (includes muscle)
  • forms bullae (blue), rapidly progressing skin infection, cutaneous necrosis (sloughing), not well demarcated, dark edema
  • PAIN OUT OF PROPORTION to clinical findings, crepitus, eventual loss of pain due to compression of nerves
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8
Q

Clostridial myonecrosis (gas gangrene)

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • deep - musculoskeletal
  • see subcutaneous air on xray or CT, sepsis, renal failure, fever - rapid progression, DOESN’T BLEED when cut - pale.
  • painful, smelly
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9
Q

Medullary osteomyelitis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • in the bone
  • non-specific tenderness, back pain, see degradation of vertebrae on xray and CT
  • back pain for months, sometimes neurological deficits or throat issues (Depending on direction of spread) +/ fever
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10
Q

Superficial Osteomyelitis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • CONTIGUOUS FOCUS - wound from outside in to bone
  • chronic ulcer (months) sometimes can actually see bone
  • painful (diabetics might not feel it) sometimes with fever and malaise
  • vascular SUFFICIENT - bedsores, pressure sores, screws/metal implant infections - see on CT
  • vascular INSUFFICIENT - diabetic foot ulcers -
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11
Q

Infectious arthritis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • joint infection in synovial fluid
  • usually in knee, fever, palpable joint effusion, limited motion (dont want to extend), warm, swollen, tender, CLOWDY ASPIRATE with high white count
  • painful, tender, don’t want to move
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12
Q

Septic bursitis

  • how deep is it
  • what’s it look like
  • how does it feel
A
  • in the bursae (elbow and knee)
  • focal bursal inflammation with lesion - point of entry
  • tender, inflammed, don’t want to flex - want to stay straight
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13
Q

Impetigo

  • what’s it caused by
  • who does it affect
A
  • caused by group A strep (pyogenes) or staph aureas, in hot or humid weather
  • any age, classic in children, highly communicable
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14
Q

Folliculitis

  • what’s it caused by
  • who does it affect
A
  • hot tub folliculitis, tight work-out clothes, dirty razor, staph aureus
  • diabetics, athletes, people with hair
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15
Q

Furuncle

  • what’s it caused by
  • who does it affect
A
  • friction and hair follicles, perspiration, staph aureus

- develop from folliculitis

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16
Q

Carbuncle

  • what’s it caused by
  • who does it affect
A
  • either strep or secondary to lesion, pseudomonas in cancer patients
  • extremes of age - children and old people
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17
Q

Erysipelas

  • what’s it caused by
  • who does it affect
A
  • strep pyogenes

- ppl with predisposing lymph issues, ppl with lesion or abrasion, infants and elderly, alcoholic, diabetic

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18
Q

Cellulitis

  • what’s it caused by
  • who does it affect
  • tx
A
  • staph and strep, maybe MRSA (hx could point to others - pasteurela, aeromonas (fresh water), eikenella (human bite), vibrio (warm water))
  • MOST COMMON, depends on exposure - burn, injury etc.
  • treat empirically for staph and strep
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19
Q

Necrotizing fasciitis

  • what’s it caused by
  • who does it affect
  • tx
A
  • 2 types of microorganisms (1- polymicrobial mixed anaerobes, or 2- group A strep) secondary to lesion
  • anyone, diabetics
  • might need fasciotomy for compartment syndrome, PROMPT surgical intervention and antibiotics
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20
Q

Clostridial myonecrosis (gas gangrene)

  • what’s it caused by
  • who does it affect
  • tx
A
  • gram pos sporulating anaerobic rod (clost perfring), stool or soil contamination (war wounds)
  • those with preexisting wounds, toxins are everywhere in environment, post surg, war, stool infection
  • surgery and antibiotics
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21
Q

Medullary osteomyelitis

  • what’s it caused by
  • who does it affect
  • tx
A
  • caused by staph aureus - hematogenous spread, sometimes pseudomonas for IV drug users
  • IV drug users
  • IV tx (might be hard for drug users)
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22
Q

Superficial Osteomyelitis

  • what’s it caused by
  • who does it affect
  • tx
A
  • vascular SUFFICIENT - bedsores, pressure sores, stool bacteria from diapers, bone fracture not properly debrieded, screws/metal implant infectons
  • vascular INSUFFICIENT - diabetic foot ulcers - new shoes, toenail clipping, shows mixed anaerobic gram neg culture
  • tx is limited unless you’re able to remove original insult - diabetes, bedrest etc.
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23
Q

Infectious arthritis

  • what’s it caused by
  • who does it affect
  • tx
A
  • synovial fluid is vascular and no BM - so hematogenous spread is easy, adults/adolescent cause is usually STD - gonorrhea, or staph aureus, babies is usually group B strep or staph aureus
  • people who are IV users, have prosthetic joints, have other inflammatory arthritis, systemic infections, or post surgery or trauma
  • tx take fluid out (helps feel better) take culture, and treat with appropriate antibiotic
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24
Q

Septic bursitis

  • what’s it caused by
  • who does it affect
  • tx
A
  • caused by puncture- acute infection

- antibiotic tx

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25
Q

Scabies

  • mode of transmission
  • site of infection
  • route of infection
  • likely host
A
  • person to person, including STI and fomites
  • hands and feet, waistline and genitals
  • female bug burrows in skin and lays eggs (sperpinginous burrows)
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26
Q

Scabies

  • clinical signs
  • diagnosis
A
  • intense itching 3-4 WEEKS AFTER BITE (or sooner for reinfection. also rash, redness, papules, vesicles, red tracks, allergic reaction to the burrowing and eggs
  • dx by history and clinical presentation, or scrape onto microscope slide. also do BURROW INK TEST to see tract
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27
Q

Scabies variants (2)

A
  1. Crusted/Norweigan scabies - immunocompromised patients (HIV, HTLV1, Hep C, Alcohol) presents with uncontrolled replication - millions, highly transmissible
  2. Nodular scabies - intense inflammatory response that causes bumb
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28
Q

Scabies

- treatment

A
  • tx with topical cream or single dose of antiparisitic agent. RETREAT 1 WEEK LATER (drugs only kill adults)
  • treat sexual contacts
  • if kid infected treat all members of house
  • wash fomites with HOT water
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29
Q

Lice variants (3)

A

1) Pediculus humanis capitis (head lice)
2) Pediculus humanis corpus (body lice) - VECTOR for epidemic typhus and relapsing fever
3) Pediculus humanis pubis (pubic lice)

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30
Q

Head lice

  • mode of transmission
  • site of infection
  • route of infection
  • likely host
A
  • person to person (kids)
  • scalp (sometimes beard and eyelashes)
  • adult lice lay nits on hair shaft, feed on blood from scalp
  • children, non-industrialized countries, fomites
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31
Q

Body lice

  • mode of transmission
  • site of infection
  • route of infection
  • likely host
A
  • person-to- person, or fomite to person, adult lice live on clothing
  • chest and back, body hair
  • adult lice live in clothes, come onto body to feed
  • homeless, economically poor, adult, (body louse is vector for epidemic typhus and relapsing fever)
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32
Q

Pubic lice

  • mode of transmission
  • site of infection
  • route of infection
  • likely host
A
  • sexual contact
  • pubic hair
  • sexual transmission - lice from person to person, same as other lice
  • sexually active adults
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33
Q

Lice

  • clinical signs
  • diagnosis
A
  • itchiness - TYPE 1 hypersensitivity rxn to saliva
  • see nits (eggs) (nits hatch no nymphs, which become adults in 1-2 weeks, which live for 1-3 months NEED BLOOD daily)
  • can have secondary bacterial infection due to itching
  • visualize lice or nits with Wood’s lamp - can fluoresce LIVE nits
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34
Q

Lice

- treatment

A

topical pediculocides, gels that stay for a while, retreat later, get rid of fomites (treat sexual parters for pubic lice)

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35
Q

Bed bugs

  • mode of transmission
  • site/route of infection
  • clinical signs
  • tx
A
  • bed bugs live in furniture/fomites
  • anywhere on body, but tend to have clustered bites “breakfast lunch and dinner”
  • nocturnal, will feast at night, attracted to heat and CO2
  • corticosteroids, topical for sympoms. have to kill bugs by heat - hard to get rid of.
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36
Q

Tungiasis

  • AKA
  • mode of transmission
  • site/route of infection
  • clinical signs
  • tx
A
  • AKA “jigger” “chingo”
  • female will penetrate skin of lower extremeties/feet/nailbed and burrown to lay eggs
  • seen in travellers to Africa, Carribean, Central/South America
  • have reaction to flea. can see the rear part stiking out and expelling eggs
  • tx - extract and treat symptoms
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37
Q

Myasis

  • AKA
  • mode of transmission
  • site/route of infection
  • clinical signs
  • tx
A
  • AKA maggots - TUMBU fly in Africa, BOTFLY in South/Central America
  • mode for Tumbu fly, fly lands on damp clothing, lays eggs, maggots hatch and burrow into skin
  • mode for Botfly, fly captures mosquito, lyas eggs, and eggs get transferred during mosquito bite
  • clinical - 3 types of infections (furuncular (most common looks like cellulitis), wound, cavitary)
    tx - suffocate with vaseline etc. iron clothes and prevent mosquito bites
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38
Q

Amphotericin B

- molecular mechanism

A
  • binds egosterol forming artificial pores (bad for fungus, good for us)
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39
Q

Amphotericin B

  • use
  • mode of administration
A
  • broadest spectrum for systemic fungal infections
  • pregnancy category B - preferred over axoles and capsofungin
  • NOT through BBB
  • give IV - no oral absorption
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40
Q

Amphotericin B

- toxicity

A
  • long term use associated with neprhotoxicity (later generations have hepatotoxicity instead)
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41
Q

Nystatin

  • mechanism
  • use
A
  • same as amphotericin
  • parental administration
  • can be used topically for thrush
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42
Q

Azoles

- mechanism

A
  • egosterol synthesis inhibitor - binds to and inhibits cytochrome p450 in fungi
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43
Q

Flucanozole

  • use
  • toxicity
A
  • best CSF penetration (use for cryptococcal meningitis) and prophylaxis for HIV or cancer
  • widest range of use therapeuticaly
  • toxicity: CYP2C9 inhibiton (warfarin and phenytoin), stephen johnson syndrome, alopecia with longer treatment, teratogenic for pregnancy
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44
Q

Itraconazole

  • use
  • toxicity
A
  • poor CNs penetration
  • good for dimorphic fungi
  • toxicity, congestive heart disease, CYP3A4 inhibition (many drug-drug)
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45
Q

Voriconazole

  • use
  • toxicity
A
  • broadest spectrum of all azoles
  • use for invasive asperigillosis (less tocity than amphotericin B)
  • toxicity: produces visual disturbances, inhibits many P450 enzymes (many drug-drug)
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46
Q

Capsofungin/Echinocandin

  • mechanism
  • mode of administration
  • use
  • toxicity
A
  • mech: inhibition of B(1-3) glucan cell wall - disrupts cell wall synthesis
  • IV - water soluble
  • use for candida and asperigillus. can be used for people not responding to voriconazole
  • toxicity: flushing, GI discomfort, hepatotoxicity (esp when used with cyclosporine), embryotoxic
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47
Q

Griseofulvin

  • mechanism
  • use
  • toxicity
A
  • microtubule diruption
  • inhibits mitosis - interferes with microtubule assembly
  • used for onychomycosis (drug is depositied in newly growing keratin)
  • have to be on the drug for 6-9 months. P450 INDUCTION (also rifampin) increases metabolism of drugs - warfarin etc.
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48
Q

Terbinafine

  • AKA
  • mechanism
  • use
  • administration mode
  • toxicity
A
  • aka Lamisil
  • inhibits squalene epoxidase fungal enzyme (increasing squalene levels and decreasing egosterol levels)
  • used for onychomycosis - keratophilic and fungicidal
  • orally administered
  • well tolerated- no P450 interaction, shorter time of use (3mo)
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49
Q

Flucytosine

  • mechanism
  • use
  • toxicity
A
  • gets into cell, gets converted to 5-fluoroacil, which gets incorporated into DNA and RNA - disrupting synthesis and is cytotoxic
  • only works for fungal cells
  • narrow spectrum of action - has to be used in combination with other drugs
  • toxicity: hematotoxicity (anemia, leukopenia)
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50
Q

Type 1 hypersensitivity

  • immune mediator
  • antigen (soluble? surface?)
  • effector mechanism
  • example of reaction
A
  • IgE
  • soluble antigen
  • mast-cell activation
  • allergic rhinitis, asthma, systemic anaphylaxis, atopic dermatitis
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51
Q

Type 2 hypersensitivity (2)

  • immune mediator
  • antigen (soluble? surface?)
  • effector mechanism
  • example of reaction
A
  • IgG
  • platelet/tissue/RBC- associated antigen or cell-surface receptor
  • complement, FcR+ cells (phagocytes, NK), signal altering (receptor-mediated)
  • penicillin allergy, rheumatic fever, HIT, chronic urticaria (receptor)
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52
Q

Type 3 hypersensitivity

  • immune mediator
  • antigen (soluble? surface?)
  • effector mechanism
  • example of reaction
A
  • IgG
  • soluble antigen (immune complex)
  • complement - phagocytes
  • serum sickness, arthrus reaction, syphilis treponema
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53
Q

Type 4 hypersensitivity (3)

  • immune mediator
  • antigen (soluble? surface?)
  • effector mechanism
  • example of reaction
A

1) Th1
- soluble antigen
- macrophage activation
- contact dermatitis, PPD
2) Th2
- soluble antigen
- IgE production, eosinophil activation, mastocytosis
- chronic asthma, chronic allergic rhinitis, granulomas in TB
3) CTL
- Cell-associated antigen
- cytotoxicity
- contact dermatitis

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54
Q

example of genetic succeptability for hypersenstivity reactions

A

atopic dermatitis - Th2 response, IgE, type 1 hypersensitivty

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55
Q

Steps for sensitization in Type 1 hypersensitivity rxn (6)

A
  1. protease (der p1) penetrates barrier tissue and enters dermal space
  2. interacts with resident antigen presenting cells
  3. get immune response, takes antigen to LN, primes T cells
  4. Some T cells become Th2, which help B cells produce IgE
  5. IgE from plasma cells bind to mast cells via FceR1
  6. next time you see antigen you get degranulationu
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56
Q

Steps for effector phase for Type 1 hypersensitivity rxn (4)

A
  1. IgE bound to FceR1 (with ITAM) on mast cells/basophils (from sensitization) is CROSS-LINKED by re-exposure to allergen (protease)
  2. mast cells and basophils are activated to secrete pre-formed granule contents (symptoms w/i 1-5 minutes) and synthesized lipid mediators (5-30 min) and cytokines/chemokines (hours)
  3. chemokines recruit eosinophils to secrete toxins
  4. inflammation and tissue damage occurs
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57
Q

PPD skin test is an example of what type of hypersensitivity reaction

A

type 4

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58
Q

what do mast cell toxic mediators cause (3) (and what’s an example) (1)

A 
vascular leak
broncho constriction
interstinal hypermotility (histamine)
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59
Q

what do mast cell lipid mediators cause (5) (and what are some examples) (5)

A
  • vascular leak
  • broncho constriction
  • intestinal hypermotility
  • mucus secretion
  • inflammation (chemotaxis of eosinophils, basophils and Th2 cells)
    (prostaglandins D2, E2
    leukotrienes C4, D4, E4)
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60
Q

what do mast cell cytokines cause (3) (and what are the cytokines) (4)

A
  • amplify Th2 cell response (Il-4, IL-13
  • promote eosinophil production and activation (IL-5)
  • promote inflammation (TNFalpha)
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61
Q

what do mast cell enzymes do (1) (and what’s an example) (1)

A

tissue damage/ remodel CT matrix (tryptase)

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62
Q

what do eosinophil granule proteins cause (1) (and what’s an example) (2)

A

killing of parasites and host cells (major basic protein, eosinophil cationic protein)

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63
Q

what do eosinophil granule enzymes do (1) (and what’s an example) (1)

A

tissue remodeling (eosinophil peroxidase)

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64
Q

chronic allergen exposure results in what (4 things)

A 
Chronic Th2 mediated inflammation:
- increased mucus production
- remodeling of tissue collagen
- less elasticity
increased airway hyperresponsiveness to allergen
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65
Q

HIT is an example of what kind of hypersensitivity reaction (how does it work)

A

Type 2:
Ab directed at heparin-platelet factor 4 complexes binds to Fc receptors on adjacent platelets, causing aggregation and thromboembolism

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66
Q

Coomb’s test is an example of what kind of hypersensitivity reaction (how does it work)

A

Type 2:
antibodies on RBCs will agglutinate in response to presence of anti-antibody antibody (test for autoimmune hemolytic anemia)

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67
Q

What type of hypersensitivity response is the Arthus reaction? and what are the steps? (4)

A

Type 3 (slower than type 1):

  • previous immune sensitization (pre-existing IgG)
  • when injected with antigen, immune complexes form and activate complement
  • complement recruits additional cells (through C5a)
  • mast cells also have receptors for C5a. C5a binds, causing mast cell to produce proinflammatory cytokines and tissue swelling through FcgammaR3 activation
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68
Q

2 examples of arthus reaction

A

1) vaccine-mediated local dermal necrosis - repetitive vaccines to tetanus
2) hypersensitivity pneumonitis (farmer’s lung) - response to fungal molds in damp hay (also involves Type 4 reaction)

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69
Q

serum sickness is what kind of hypersensitivity reaction?

A

Type 3:

  • patients are treated with immunogenic proteins (polyclonal antibodies, antivenom)
  • after 10 days, they will make antibodies and if there is still antigen (wrong dosing on the doctor’s part), will mount a response and have immune complex deposition in tissues
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70
Q

3 types of type 4 hypersensitivity reactions (and examples)

A

1) delayed-type (mycobacteria, insect venom)
2) contact hypersensitivity (haptens: poison ivy, small metal ions: nickel)
3) gluten-sensitive enteropathy (celiac)

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71
Q

Poison Ivy (mechanism of reaction, Th mediated, end result)

A
  • not a peptide, but modifies proteins in skin, makes chemical reaction and complexes (haptenated proteins), which are presented to T cells by Langerhans and macrophages in the draining LN
  • upon reexposure, T cells migrates to site
  • Th1 cells are activated, which secrete IFN gamma, TNF alpha and chemokines, which recruit macrophages which secrete mediators of inflammation
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72
Q

Celiac disease (mechanism, reaction)

A
  • peptide gets deaminated, deaminated protein gets presented by HLA-DQ2 and DQ8
  • naive T cell responds to deaminated peptide
  • inflammatory effector T cell causes villous atrophy
  • the more you’re exposed to gluten, the more symptoms you have
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73
Q

Granuloma formation (mechanism, Th mediated, reaction)

A
  • Th1 effector cell activation, IFN gamma stimulates macrophage
  • TB evades macrophages causing chronic immune activation
  • get central accumulation of epithelioid macrophages (decreased mobility and phagocytosis) with outer T lymphocyte ring
  • T lymphocytes produce IFN gamma and other cytokines - positive feedback for chronic inflammation
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74
Q

2 categories of granulomas

A

1) (infectious) caseous necrosis - TB, Ghon complex (granuloma in tissue AND lymph node)
2) non-necrotizing - sarcoid, inorganic, fungi - no central region of necrosis

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75
Q

what molecules mediate signaling for effector function of granuloma

A

CD40 on macrophage, CD40L on T cell

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76
Q

Th17 is related to what disease

A

psoriasis

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77
Q

first generation histamine antagonists

A
  • diphenhydramine
  • doxylamine
  • chlorpheniramine
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78
Q

second generation histamine antagonists

A
  • loratadine (claritin)
  • cetirizine (zyrtec)
  • fexofenadine (allegra)
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79
Q

endogenous histamine synthesis and metabolism

A
  • decarboxylation of L-histidine by histidine decarboxylation
  • histamine is rapidly broken down to inactive metabolite methylimidazole acetic acid by monoamine oxidase and excreted into urine
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80
Q

what is an autacoid

A

compound that is released and locally in periphery (histamine, serotonin, prostaglandins, leukotrienes, kinins, etc)

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81
Q

what’s an auto- iso- allo- and xenograft?

A

auto - self
iso - identical twin
allo - other of same species
xeno - different species

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82
Q

if you’re blood type O, what kind of blood types can you receive? What antibodies do you have?

A

get blood from type O - have antibodies to A and B

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83
Q

if you’re blood type A, what kind of blood types can you receive? What antibodies do you have?

A

get O or A

have antibodies to B

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84
Q

if you’re blood type B, what kind of blood types can you receive? What antibodies do you have?

A

get O or B

have antibodies to A

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85
Q

if you’re blood type AB, what kind of blood types can you receive? What antibodies do you have?

A

get blood from any type - have no antibodies against A or B

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86
Q

where do you find blood cell antigens? (anti- A/B etc.)

A

circulating - they’re shed, on RBCs, and on endothelial cells

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87
Q

describe the mouse study for histocompatibility (skin transplants)

A
  • Gave skin transplants from mice with the same MHCa - no rejection
  • Gave MHCa to MHCb - rejection
  • repeated this discordant transplant and rejection was even faster (T cell mediated - memory)
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88
Q

why do we have T cells that recognize non-self MHC?

What is the clinical significance of this in terms of transplants?

A

we have a huge polymorphism in repertoire of T cells. in order to be positively selected in thymus, have to recognize self MHC, but some will also recognize non-self MHC, but won’t be negatively selected because they were never presented with non-self MHC during development

This is important because we need to match MHC 1/2 for graft and transplants (not important for RBC transfusions because RBCs don’t have MHC expression)

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89
Q

classic allograft rejection - timing and cause (think - why do people reject cadaveric transplants more?)

A
  • happens within 2 weeks and intiates memory (second set rejection will be accelerated)
  • require damage to occur first and initiate innate immune cell activation and inflammation which will then lead to lymphocyte (T cell) activation to non-self
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90
Q

Direct allorecognition (what is it, and what MHC/CD is involved)

A

donor antigen presenting cell from transplanted organ migrants to LN, and its MHC (with endogenous donor peptide - MHC1) is recognized by T cells and activates recipient effector function. effector cells migrate to organ and destroy it (CD8 - mediated)

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91
Q

Indirect allorecognition (what is it, and what MHC/CD is involved)

A

self antigen presenting cell will phagocytose endothelium (for example) from donor organ, which contains donor MHC. self MHC will present donor MHC peptides and mount immune response and rejection (exogenous peptide - self MHC class 2 to CD4 cells)

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92
Q

Hyperacute rejection (how long does it take, what causes it, what’s activated in response, what kind of hypersensitivty reaction is it, how can you avoid)

A

happens within minutes or hours.
caused by PRE-FORMED antibodies to donor antigens - causes rapid interaction with antigen on organ endothelial cells, activates COMPLEMENT, causing inflammatory response and tissue destruction. this is an example of TYPE 2 HYPERSENSITIVITY (IgG)- tissue antigen response.
avoid by mixing recipient serum with donor tissue to see if anythign binds or reacts.

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93
Q

what are some reasons people have pre-formed anti HLA antibody?

A
  • pregnancy - giving birth exposes you to paternal HLA
  • previous transplant rejection
  • multiple transfusions
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94
Q

Acute rejection (how long does it take, what causes it, what’s recruited)

A
  • classic rejection
  • happens over days to weeks
  • T cell dependent - causes damage to transplanted organ
  • recruitment of lots of lymphocytes (T cells)
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95
Q

Chronic rejection (how long does it take, what causes it, what happens)

A
  • takes months to years
  • analagous to chronic inflammation - promotes deposition of collagen and fibrotic tissue
  • causes changes in vasculature - more fibrotic, tissue remodeling, IMMUNE COMPLEX DEPOSITION, recruitment of T and B cells
  • recruitment of nuclear cells like macrophages that cause tissue damage
  • causes occlusion of BVs
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96
Q

Graft vs. Host (mechanism, timing, avoidance)

A
  • during bone marrow transplantation, donor immune cells migrate to lymphoid tissue, and alloreact with host dendritic cells and proliferate, causing effector function in inflammed tissues - works through the same mechanism as acute graft rejection, but the opposite way (host vs. donor immune response).
  • can be acute or chronic
  • want better HLA match, however, some graft vs host disease is protective against relapse of leukemia
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97
Q

List 3 categories of lab tests used for identifying HLA type and predicting rejection

A
  • serologic testing (cross-match)
  • molecular (DNA PCR)
  • cellular (mixed lymphocyte culture)
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98
Q

Cross-match test

A

add donor lymphocytes to recipient serum. if you add complement and the cells lyse, then you have a problem (for example, person who expresses B27, their leukocytes will lyse in the presence of anti-B27 antibodies and complement – not a match), OR if you add fluorescent anti-Ig, they will fluoresce. — question! is it donor lymphocyte and recipient antibody or vis versa?

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99
Q

Mixed Lymphocyte Reaction

A
  • mix immune cell lymphocytes (T cells, antigen presenting cells etc.) from donors and recipients to see if they react to each other.
  • If T cells respond to non-self MHC on donor cells, you get activation and proliferation as well as effector function (problematic)
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100
Q

Immunosuppressive therapies to avoid rejection (6)

A
  • corticosteroids (reduce inflammatory response)
  • antibodies that block cytokines/cytokine receptors
  • co-stimulation blockade (CTLA4-Ig)
  • calcineurin inhibitors - block NFAT transcription factor (cyclosporine and tacrolimus)
  • antimetabolites - inhibits guanine nucleotide synthesis in lymphocytes (azathioprine, mycophenolate mofetil)
  • TOR inhibitiors - blocks lymphocyte proliferation (rapamycin)
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101
Q

genes that are associated with autoimmunity (5)

A
  • AIRE (APECED)
  • CTLA4 (Graves)
  • FOXP4 (IPEX)
  • FAS (autoimmune lymphoproliferative syndrome)
  • C1q (SLE)
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102
Q

molecular mimicry (mechanism and example)

A

antigen receptor has CROSS-REACTIVITY between microbial peptide and self-peptide (example: antibodies to S. pyogenes cross-react with epitopes on muscle, kidney and joints causing rheumatic fever)

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103
Q

bystander activation (mechanism and example)

A
  • because of inflammatory microenvironment, you activate self-reactive T-cells - indirect consequence of inflammation.
  • thyroid cells don’t normally express HLA class 2 molecules, but IFN gamma produced during infection/inflammation induces HLA class2 expression on thyroid cells.
  • Activated CD4 T cells recognize thyroid peptides and induce autoimmune thyroid disease
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104
Q

Epitope spreading (mechanism and spreading)

A
  • tissue damage and immune response to self-antigen promotes spreading of immune response to additional self epitopes
  • tissue damage/stress (smoking) changes regulation of post-translational modifications – enzyme PAD converts arginine to citrulline residues, making it susceptible to degradation - residues are presented by HLA class 2 to CD4 T cells - associated with RHEUMATOID ARTHRITIS
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105
Q

MHC/HLA regulation, susceptibility of autoimmune disease (mechanism and associated disorder)

A

MHC haplotype influences both peptide presentation in periphery AND T cell receptor repertoire through pos/neg selection – genetic.

  • changes in MHC (charges/molecules in binding grooves etc) can alter the selectivity of binding and what is presented
  • Celiac - HLA DQ2/DQ8 mutations
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106
Q

pemphigus vulgaris is what type of hypersensitivity reaction

A

Type 2 - direct interaction with cell (desmoglein) causing blistering of skin

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107
Q

subacute bacterial endocarditis is what type of hypersensitivity reaction

A

type 3 - immune complexes cause deposition in vascualture. Neutrophils involved with immune complexes

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108
Q

autoimmune hemolytic anemia is what type of hypersensitivity reaction

A

type 2 - Fc mediated phagocytosis because of Rh blood group antigens

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109
Q

insulin-dependent diabetes mellitus is what type of hypersensitivity reaction

A

type 4- pancreatic beta cell antigen - tissue damage mediated by T cells

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110
Q

MS is what type of hypersensitivity reaction

A

type 4 - T cell destruction of myelin

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111
Q

graves disease is what type of hypersensitivity reaction?

A

type 2 - antibody binds to receptor on thyroid epithelial cells, stimulating production of thyroid hormone, not subject to normal regulation - causes hyperthyroidism

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112
Q

rheumatoid arthritis is what type of hypersensitivity reaction

A

type 4 - autoantibodies and T cells that cause destruction in various tissues

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113
Q

myasthenia gravis is what type of hypersensitivity reaction

A

type 2 -
specific antibody reacting to Ach receptors - antibody binds to receptor and interferes with stimulation - get muscle weakness and paralysis

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114
Q

psoriasis is what type of hypersensitivity reaction

A

type 4 - autoreactive T cell response against skin-associated antigens causing aberrant regulation of skin proliferation

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115
Q

genetic pathway therapeutic targets for autoimmune diseases (6)

A
  1. co-stimulatory molecules
  2. Treg
  3. antigen clearance
  4. antigen presentation/ autoantibody secretion
  5. cytokine polarization
  6. inflammatory mediators
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116
Q

Give example of co stimulatory target for therapy against autoimmune disorders

A

If you block CD28-B7 interaction with CTLA4 (which binds to B7), it blocks T cell activation and promotes tolerance

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117
Q

example of cytokine target for therapy against autimmune disorders (4)

A
  • IL-5 - interfere with eosinophil production
  • IgE - decrease type 1 hypersensitivity reactions
  • IL-6 and IL-17 decreasing Th17
  • IL-12 (proinflammatory)
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118
Q

example of inflammatory mediator for target of therapy against autoimmune disorders

A

interfere with TNF alpha

  • either make antibody to bind to TNF, or make chimeric molecule that adds receptor to TNF binding site and prevents binding to receptors on cells
  • effective anti-inflammatory agent for rheumatoid arthritis that decrease acute phase protein production
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119
Q

histamine has 3 roles, what are they

A

1) immune response (allergic IgE type 1 hypersensitivity via cross-linking and complement activation inflammation)
2) gastric acid secretion
3) neurotransmitter

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120
Q

what does cromolyn do to histamine

A

cromolyn blocks release of histamine

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121
Q

Histamine receptor H1 -what type of receptor is it, where is it located, what is the post-receptor response

A
  • G protein coupled receptor (Gq)
  • endothelium, CNS
  • increases NO, increases cGMP, increases IP3
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122
Q

Histamine receptor H2 -what type of receptor is it, where is it located, what is the post-receptor response

A
  • G protein coupled receptor (Gs)
  • vascular smooth muscle
  • increases cAMP
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123
Q

what effect does histamine cause on vascular smooth musche

A

causes vasodilation/edema

  • decreases blood pressure, increases reflex tachycardia and heart rate
  • via endothelial H1 receptors and NO production
  • via smooth muscle H1 causing calcium increase and contraction
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124
Q

what effect does histamine have on non-vascular smooth muscle (resp. system)

A

bronchocontsriction via H1 receptors (increases in asthma)

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125
Q

what effect does histamine have on the peripheral nervous system

A
  • acts as autocoid
  • stimulates primary afferent nerve endings (itch, pain)
  • H1 receptor
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126
Q

what effect does histamine have on cns

A
  • acts as neurotransmitter
  • regulate wakefulness, appetite and body temp
  • via post-synaptic H1
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127
Q

what effect does histamine have on GI

A
  • acts as secretagogue

- stimulates gastric acid release (H2) and increased motility (H1, H2, H4)

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128
Q

histamine toxicity

A
  • found in spoiled tuna, causing nausea vomiting but can be suppressed by H1 receptor blockers
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129
Q

is anaphylaxis caused by histamine

A

no.

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130
Q

what local allergic reactions do histamine cause

A 
urticaria (hives)
allergic rhinitis (hay fever)
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131
Q

pharmacotherapy for sub-acute and preventative allergies

A

inhaled steroids (flonase)

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132
Q

mast cell stabilizers (pharmacotherapy)

A

cromolyn sodium - directly inhibit mast cell degranulation by blocking ion channels

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133
Q

first generation antihistamines list and notable characteristics

A
  • diphenhydramine (very sedative, very anti Ach, anti-motion sickness)
  • doxylamine (longer lasting, very sedative)
  • chlorpeniramine (less able to cross BBB, somewhat sedative)
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134
Q

first generation antihistamines mechanism of action

A
  • inverse agonists
  • all lipid soluble
  • crosses BBB, placenta and breast milk
  • metabolized in liver, cleared in renal
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135
Q

first generation antihistamines adverse reactions

A
  • cardiac (sinus/reflex tach - dose related)
  • contraindicated for glaucoma or prostatic hypertrophy
  • respiratory depression
  • CNS
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136
Q

first generation antihistamines vulnerable patients

A
  • renal/liver issues
  • elderly
  • pregnancy
  • nenonates/infants (CNS stimulation)
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137
Q

second generation antihistamines list and notable features

A
  • fexofenadine (Excreted unchanged, transported by OATP1A2, don’t drink orange, grapefruit, apple juice)
  • loratidine (24hr duration)
  • cetirizine (24hr duration, metabolite of hydroxyzine)
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138
Q

second generation antihistamines characteristics and uses

A
  • not a neurotransmitter
  • all lipid soluble
  • wide distribution
  • NO BBB
  • metabolized in liver (except fexo)
  • cleared in renal (excpet fexo)
  • use for allergic rhinitis, allergic conjuctivitis and urticaria
  • NOT useful against anaphylaxis, for common cold, sleep aid or anti-motion sickness
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139
Q

second generation antihistamine adverse effects

A
  • less than first gen - no CNS penetration - no sedation
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140
Q

promethazine uses

A

motion sickness and morning sickness (first gen)

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141
Q

incidence vs prevalence

A 
incidence = new diagnoses over time
prevalence = people who have it right now
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142
Q

quarantine vs isolation

A 
isolation = isolate for however long they're contagious
quarantine = exposed but not yet showing illness (for incubation period)
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143
Q

epidemic triad

A

host, environment, agent

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144
Q

steps for outbreak investiagion (9)

A
  1. confirm outbreak
  2. confirm diagnosis
  3. create case definition
  4. count and identify additional cases
  5. perform epidemiological analysis
  6. develop and test hypotheses for risk factors or causal agents
  7. implement control measures to prevent further infections and morbidity
  8. communicate findings
  9. monitor surveillance data
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145
Q

if you have a neutrophil defect, which fungi will cause issues? (3)

A

candida
aspergillus
mucor infections

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146
Q

if you have T cell defect, which fungi will cause issues? (5)

A 
cryptococcus neoformans
pneumocystic jirovecii
blastomyces dermatitidis
coccidiodes immitis
histoplasma capsulatum
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147
Q

superficial mycoses - characteristics, types (4) and causative fungus

A

-limited to outermost layers of hair/skin
- mild infections with little/no inflammation
include:

  • black piedra - gritty brown/black concretions on scalp (piedraia hortae)
  • white piedra - white cranules on hair shaft genital and beards (trichosporon beigelii)
  • tinea nigra - black/brown macules on palms/soles (exophiala werneckii)
  • pityriasis versicolor - hyper/hypo pigmented scaly macules on torso (malassezia furfur) culture on sabouraud’s agar with 1% olive oil
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148
Q

superficial mycoses diagnosis and treatment

A

dx: clinical, wet mount with potassium hydroxide
tx:
- remove hair for black/white piedra
- topical azole or keratolytic agent for tinea nigra
- selenium sulfide for pityariasis versicolor

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149
Q

cutaneous mycoses - characteristics and types (6)

A
  • infect the keratinized tissues and elicit immune response “ring worm”
  • dermatophytes belong to 3 genera (microsporum, trichophyton, epidermophyton)
    include:
  • tinea capitis (head)
  • tinea corporis (body)
  • tinea pedis (feet)
  • tinea barbae (beard)
  • tinea cruris (perineum)
  • tinea unguium (nails)
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150
Q

cutaneous mycoses - diagnosis and treatment

A

dx: clinical - redness around infection, skin sample, drop of potassium hydroxide.
tx: systemic agent for tinea capitis, topical agent for other tineas

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151
Q

subcutaneous mycoses - characteristics and types (3)

A 
below skin - dermis and subcutaneous tissue - need trauma or portan of entry. some have high enough burden of disease to need surgery.
types:
- lymphocutaneous sporotrichosis
- chromoblastomycosis
- eumycetoma mycetoma
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152
Q

lymphocutaneous sporotrichosis - caused by, clinical, dx

A

caused by dimorphous fungus (sporothrix schenckii)

  • requires trauma through skin
  • nodule forms, spreads centrally along lymph tracts
  • dx: look for fungus, culture with sab agar at roomp temp and 37 deg
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153
Q

chromoblastomycosis- caused by, clinical, dx

A
  • caused by fonsecaea or cladosporium
  • happens in the tropics
  • looks warty
  • biopsy for culture - use h&e or black ink, see spherical fungi with copper color - MEDLAR BODIES
  • looks like cauliflower in late stages - NOT purulent
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154
Q

eumycetoma mycetoma - caused by, clinical, dx

A
  • caused by pseudallescheria boydii and madurella grisea
  • true mycetoma (not bacteria)
  • PURULENT as opposed to chromoblast
  • has sinus tract similar to nocaridia and actinomyces
  • have to culture to determine if bacteria or fungus
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155
Q

deep tissue fungal infections - characteristics and types of infections (4)

A
  • acquired from either endogenous or environment
  • invasive
  • dimorphic, primary pathogens in immunocompetent
    types:
  • blastomyces dermatitidis
  • coccidioides immitis
  • histoplasma capsulatum
  • paracoccidiodes brasiliensis
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156
Q

blastomyces dermatitidis - geographic distribution, clinical, dx, tx

A
  • eastern US - E of mississippi
  • spores enter lung - primary infection in lungs, in immune compromised can be dissemminated
  • if left untreated can infect any part of skin, form ulcers, disseminate to prostate and skin, looks like blizzard on CXR
  • on culture with KOH, yeast is much larger thanother cells
  • tx: itraconazole, amphotericin B for disseminated
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157
Q

coccidioides immitis- geographic distribution, clinical, dx, tx

A
  • SW US and NW Mexico (dry parts of SW)
  • get through inhalation
  • LAB TECHS CAN INHALE TOO
  • if left untreated looks like TB, and in immunecompromised can diseminate to CNS, bone and skin - see abnormal spinal x-ray, skin ulceration, sinus tract in knee
  • on culture, see ENDOSPORES - spherule with endospores within - small
  • can do antibody test for recurrent or disseminated infection

tx: flucanosole, amphotericin B for disseminated

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158
Q

histoplasma capsulatum- geographic distribution, clinical, dx, tx

A
  • Ohio river valley (not coastal)
  • found in soil contaminated by BAT and BIRD poop
  • spores inhaled - lungs are first site
  • old lung lesions can calcify when healing
  • chronic lung infections can cause CAVITATION
  • seen in macrophages and monocytes (seen on Giemsa)
  • dimorphic (cold mold heat yeast)
  • causes ulcerations around gums
  • can be acquired by LAB TECHS
  • can see antigen after dissemination and complement fixation

tx - itraconazole, amphotericin B

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159
Q

paracoccidioides brasiliensis - geographic distribution, clinical, dx, tx

A
  • south american distribution
  • spores inhaled - lungs first site
  • likes mucous membrane of entire GI tract
  • see MARINER’S WHEEL on wet mount
  • causes mucosal lesions and ulcerations in GI tract
  • tx - itraconazole, amphotericin B for disseminated
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160
Q

Opportunistic infections- characteristics and list (5)

A 
- associated with neutrophil defects and T cell defects
list:
- candida
- aspergillus
- zygomycosis (mucor, rhizopus, absidia)
- cryptococcus neoformans
- pneumocystis jirovecci
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161
Q

opportunistic infections that affect hosts with neutrophil defects

A
  • aspergillus
  • candida
  • zygomyces (mucor, rhizopus, absidia)
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162
Q

opportunistic infections that affect hosts with T cell defects

A
  • cryptococcus neoformans

- pneumocystic jirovecii

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163
Q

candidiasis - immune cell defect, what does it cause (2), clinical, dx, tx

A
  • endogenous flora
  • chemotherapy or defect reducing neutrophils allows for invasive disease
  • causes:
    1) superfiical disease - mucosal thrush in esophagus, vandida in vagina, skin and nail involvement
    2) chronic mucocutaneous candidiasis in T cell immunocompromised - skin nails and oropharynx
  • spreads hematogenously

dx: culture, germ tube test - C. ALBICANS will form PSEUDOHYPHAE at 37deg
- cottony white spots on oropharynx, chronic coating in mouth, tongue and nails
- liver and spleen abcesses on CT

tx: fluconazole, ampho for disseminated

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164
Q

Aspergillus- immune cell defect, what does it cause (3), clinical, dx, tx

A
  • ubiquitous
  • affect neutorphil deficient hosts
  • spore forming
  • inhaled
    3 disease manifestations:
    1) allergic bronchopulmonary aspergillosis (pts w/ asthma, immediate IgE response to antigen)
    2) aspergilloma (aspergillus makes fungus ball in preexisting lung cavity - can hemorrhage)
    3) invasive aspergillosis (causes invasion into sinuses, lungs, and systemic - causes infarctions in eyes CNS, skin and bone and air crescent in lungs)
  • clinically, CXR aspergilloma that shifts with positioning
  • on culture, aspergillus fumigatus looks like aspergil - sprinkling with holy water. SEPTATED HYPHAE with ACUTE ANGLE BRANCHING

tx- have to restore neutrophil function. then treat with amphotericin B

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165
Q

Zygomycosis - types (3), patient population affected and clinical presentation, dx, tx

A

3 types:

1) mucor
2) rhizopus (bread mold)
3) absidia

patient population and presentation:

  • poorly controlled diabetes (rhinocerebral infection)
  • burn patients (skin infections)
  • neutropenia (pneumonia)
  • chelating therapy (pneumonia)

on culture, see broad, NON-SEPTATED HYPHAE with RIGHT ANGLE BRANCHING - also causes infarctions due to attraction to BVs

tx - also depends on treatment of underlying cause (acidosis or neutropenia), give amphotericin B

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166
Q

Cryptococcus - serotypes (4), clinical presentation,dx, tx

A

4 serotypes

  • A and D (neoformans) from pigeon excreta
  • B and C (gattii) from debris under red gum tree
  • predispotion of AIDS, steroid, lymphoma or nothing (50%)
  • presents with pneumonia and lung cavity, meningitis and dissemination to skin eye bone and prostate
  • UMBILICATED papules
  • dx: india ink staining, see sugar capsule virulence factor (capsule glistens and can be stained with mucicarmine), antigen for dx too
  • tx - amphotericin B +/- 5-fluorocytosine, need to chronically suppress in HIV+ patients with fluconazole/amph B
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167
Q

pneumocystic jirovecii - characteristics, clinical, dx, tx

A
  • related to fungi but no egosterol in membrane (won’t respond to ampho b)
  • all people are carrier s- dormant, but comes out of dormancy if T cell immunocompromised
  • get pneumocystic pneumonia in HIV (PCP) also with bone marrow transplantation
  • dx with lavage to be stained with Giemsa or monoglocal antiboy stain
  • tx with trimethoprim-sulfamethoxazole. give prophylaxis with AIDS diagnosis (primary = risk but no infection, secondary = prevent recurrence)
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168
Q

papule

A

less than 1 cm, raised, erythematous

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169
Q

plaque

A

more than 1 cm with scale

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170
Q

maccule

A

discoloration, flat, less than 1 cm

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171
Q

patch

A

discoloration, flat, more than 1 cm

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172
Q

nodule

A

greater than 1 cm, more elevated than wide

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173
Q

vessicle

A

less than 1 cm, clear fluid

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174
Q

bulla

A

more than 1 cm, clear fluid

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175
Q

pustule

A

less than 1 cm, neutrophilic fluid

176
Q

wheal

A

plaque or papule, erythematous with pale center

177
Q

lichenification

178
Q

acanthosis

A

elongated rete (downward epidermal projections into dermis)

179
Q

parakeratosis

A

retained nuclei in stratum corneum (seen in psoriasis)

180
Q

urticaria

A

just superficial

  • flat, macular
  • erythema and edema
  • lasts 24 hours
  • no scale
  • basketweave surface - normal surface with inflammation
  • mix of eosinophils and neutrophils
181
Q

erythema multiforme

A

interface disease
- target-like configuration - dusky brown area in center - necrosis
- no scale
can become widespread blistering - steven johnson

182
Q

spongiosus - eczema

A
  • edema is between keratinocytes
  • pressure on desmosomal attachments
  • non-discrete lesions
  • serum gets into stratum corneum -WET SCALE
  • different forms of eczema (nummular - coin shaped, allergic contact dermatitis, chronic)
183
Q

psoriasiform

A
  • thickening, acanthosis
  • plaques - DRY SCALE
  • discrete lesions
  • accumulates neutrophils in stratum corneum and epidermis
  • nail changes - matrix involvement
184
Q

lichenoid

A
  • inflammation hugs epidermal/dermal junction
  • pruritic purple polygonal papules - lichen planus
  • saw tooth rete
  • thick granule layer
  • wickham’s striae in mouth
  • will cause hyperpigmentation
185
Q

deep lupus erethymatosus

A

thick plauqes, hard to treat

  • scarring, hair loss
  • deep inflitrate, has interface change like erethyma multiforme, but deep inflammation
  • see Ig in IF
186
Q

acne vulgaris

A
  • comedones - blackheads, follicular obbstruction, sebum obstruction in pilosebaceous apparatus
  • holocrine secretion
187
Q

seborrheic keratosis

A

“wisdom spots”
waxy dark papules
chest, neck face
on face - dermatosis papulos nigra (morgan freedman)
- sudden onset - sign of Leser-Trelat (GI cancers)

188
Q

actinic keratosis

A
  • can evolve into invasive squamous cell carcinoma
  • crusty, erethematous, photoexposed areas (ear etc.)
  • dysplastic keratinocytes only in part of epidermis, NOT full thickness
189
Q

keratoacanthoma

A

inoculous SCC - erupts quickly over a few months, can regress on its own, won’t cause metastasis
grows in a “U” shape

190
Q

SCC

A

UV risk factor

  • entire thickness atypical keratinocytes
  • dermal - nodules, frequently ulcerated
  • invasive - atypical keratinocytes attached to dermal/epidermal jucntion and extend into dermal stroma
191
Q

BCC

A

common, slow growing (cant treat with chemo)

  • associated iwth PTCH gene mutation
  • tumor cells are basophilic (squamous is pink)
192
Q

nevi

A

tumors of melanocytes - 3 types: benign, dysplastic or melanoma

193
Q

types of benign nevi

A
  • junctional - flat maccule, no dermal depth (black color)
  • compound - combo of dermis and epi - raised and brown
  • intradermal - only dermis, raised, no color

as you age, nevi become intradermal

194
Q

dysplastic nevi

A
  • risk for developing into melanoma
  • melanocytes bridge - not discrete nests like in benign nevi
  • well circumscribed, well organized, but some features of melanomas
195
Q

melanoma

A

risk - blonde, blue eyed, sun exposure, family hx

  • ABCD
  • staging - breslow thickness, ulceration and mitotic rate
  • BRAF mutation
196
Q

merkel cell carcinoma

A

virus associated
looks like basal cell
can metastasize
forms cords and nest and trabeculae

197
Q

dermatofibroma

A

benign, scar-like tumor of dermal dendrocytes - arthropod induced
DIMPLE SIGN - attached to dermis, so when you pinch, it depresses

198
Q

neurofibroma

A

modified schwann cells, delicate stroma and collagen

199
Q

hemangioma

A

senile heangioma
red-purple on drunk and back
clusters of thin walled capillaries
can thrombose

200
Q

cysts

A

derived from hair follicles
remain dormant for years, keratin growth is suddenly stimulated, cyst bursts, keratin extrudes into stroma and causes inflammatory response

201
Q

psoriasis - demographics, immune mediator, triggering factors, clinical, tx

A
  • two peak ages (15-25, 50-60)
  • Th1 mediated
  • triggers - friction, infections, stress, meds
  • clinical - pigmentation changes, nail involvement (oil spots, pitting, hyperkeratosis, separation of nail plate) - affects many different areas (palms, soles etc.)
  • tx: molecular targets (anti IL-12/13, anti IL-23, anti TNF, anti IL-17). small molecule inhibitors (phosphodiesterase 4)
202
Q

seborrheic dermatitis - associated pathogen, clinical

A
  • associated iwth malassezia - lipophilic yeast
  • see scaly oily red patches with crust
  • scalp face chest perineum
    increased with parkinsonism, HIV, hep C
203
Q

pityriasis rosea - associated pathogen, clinical

A
  • reactivation of childhood viruses HHV 6/7
  • CHRISTMAS TREE PATTERN on trunk
  • self-limited
  • centrale scale or collarette
  • sometimes confused with secondary syphilis (but no hand/feet involvement in PR)
204
Q

Pityriasis lichenoides

A

goes from PLEVA to PLC

  • PLEVA in young children (crusted, vesicular pustules)
  • PLC (chronica, in adults, red-brown scaley papules)
205
Q

small/large parapsoriasis

A
  • finger-like plaques on trunk
  • CD4 infiltrates
  • 40-50 y/o men
  • can turn into lymphoma
206
Q

pityriasis rubra pilaris

A
  • shiny, red/orange plaques on palms
  • on body - sea of red with islands of sparing
  • treat with phototherapy or retinoids
207
Q

lichen planus

A
  • violacious papules
  • wickhman’s striae (mouth)
  • increased risk of SCC
  • sometimes caused by drug eruptions (ace inhibitors erc.)
208
Q

atopic dermatitis

A
  • prior to age 5
  • genetic and environmental
  • allergy triad for familial predisposition (asthma, allergic rhinitis, atopic dermatitis)
  • LOF MUTATION OF FILAGRIN
209
Q

allergic contact dermatitis

A
  • burning, itching acneform eruption
  • acute (vesicular eruption)
  • chronic (lichenified plaque)
210
Q

stasis dermatitis

A

associated with venous disease
may see pitting edema
patches of dermatitis over varicose veins

211
Q

malaria - species (5)

A
  • plasmodium faciparum (most mortality)
  • plasmodium vivax (has hypnozoites)
  • plasmodium ovale (has hypnozoites)
  • plasmodium malariae
  • plasmodium knowlesi (monkey and human)
212
Q

malaria - who dies from it

A

kids in subsaharan africa (under 5), also pregnant women

213
Q

malaria - life cycle of protozoa

A
  • female mosquito (feeds at night) is the definative host - where sexual reproduction takes place
  • asexual stage (intermediate host) is in humans

cycle:
- mosquito bites, injects larval form into blood, in less than 30 minutes, get to hepatocytes and undergo asexual reproduction, rupture hepatocytes, get into blood stream, invade RBCs, replicate, rupture - causeng massive cytokine release and anemia until host can control the infection or dies

**in vivax and ovale, when larval forms get to liver, some go into dormant phase as hynozoites, can release years later and make host symptomatic

214
Q

complicated malaria- cause, manifestations (2)

A
  • only caused by falciparum
  • parasite proteins are epxressed on RBCs, they become sticky, causing adherence to endothelium and impairing blood flow
  • 2 manifestations:
  • cerebral malaria (seizures, coma)
  • severe anemia (because of hemolysis) - would see BLACKWATER FEVER (urinalysis)

additionally, because of vivax could get splenic rupture upon physical exam

215
Q

Genetic factors for malaria

A

duffy antigen on RBC is the means by which vivax attaches to RBC - if you don’t have antigen, you cant get vivax (reason why vivax isn’t seen in W Africa)

sickle cell trait - won’t get severe disease because infected RBCs don’t last that long because they get destroyed in spleen

216
Q

malaria diagnosis

A
  • finger prick (infected RBCs get stuck in capillaries, so you’re more likely to see malaria in finger tip)
  • thick film blood smear
  • rapid diagnostic (like pregnancy test)
217
Q

Babesiosis - transmission, geographic distribution, clinical, dx, tx

A
  • intraerythrocytic protozoa (like plasmodium)
  • tick transmitted (same for lyme and anaplasma) resevoir is white-footed mouse
  • seen in New England, Wisconsin and Minnesota
  • long lasting fever and generalized symptoms
  • resolves on its own in immune competent
  • dx: look at blood film, see MALTESE CROSS, or do PCR
  • tx: self limited unless HIV or asplenic
218
Q

Giardia Intestinalis -transmission, forms, clinical, dx

A
  • AKA “beaver fever”
  • zoonotic (beaver)
  • trasmitted through ingenstion of contaminated water and sometimes person-to-person
  • noninvasive - adheres to small intestine but doesn’t leave GI tract

2 forms:

  • cyst (round)
  • trophozoite (flagellated binucleated)

clinical

  • non-bloody, fatty “floating” foul-smelling diarrhea
  • interference of fat absorption - can cause impairment of growth if chronic

dx:
- antigen detection on multiplex PCR

219
Q

cryptosporidium - transmission, life cycle, clinical, dx

A
  • contaminated drinking water (chlorine is ineffective)
  • zoonotic - cattle and birds, sometimes person-to-person
  • ingest cysts, release parasite, PARTIALLY EMBEDDED into enterocytes, replicate, and release into feces

clinical

  • seen in kids in developing part of world, HIV infection causing SLIMS DISEASE
  • chronic watery diarrhea - dehydration, weight loss, abdominal pain

dx:

  • PCR
  • MODIFIED ACID FAST
220
Q

cyclosporiasis - differences

A
  • bigger than cryptosporidium
  • similar clinical presentation
  • NOT ZOONOTIC - oubreaks due to imported food
  • dx the same - modified acid fast
221
Q

amoebiasis - causative bug, geographic prevalence, transmission, life cycle, clinical, dx

A
  • caused by entamoeba histolytica
  • seen in tropics, low socioeconomic - high in latino/pacific islander immigrants - more common in men
  • life cycle: contaminated food/water/person-to-person as cyst, then trophozoic form invades mucosa of GI causing ulcers in lining of colon - can disseminate causing significant disease - to liver causing abcesses

clinical:

  • BLOODY diarrhea plus fever
  • liver abcesses
  • FLASK ulcer in colon
  • ANCHOVY PASTE from liver abcess

dx:
- PCR, antibody test

tx- treat trophozoite AND cyst (2x treatment)

222
Q

trypanosomiasis - types (2),

A

1) Human African Trypanosomiasis - trypanosoma BRUCEI - seen in West and central/southern Africa
2) Chagas - trypanosoma CRUZI - seen in South America

223
Q

Human African Trypanosomiasis (HAT) - species, life cycle, clinical, dx

A
  • AKA sleeping sickness
  • trypanosma brucei
  • gambian and rhodesian version (can get both in Uganda)
  • 2 stages of illness:
    1) fever - can visualize parasite in blood or lymph (unudulating tail)
    2) late stage - CNS disease - always fatal

life cycle:
bite into skin, local inflammation (chanchre), gets into blood/lymph, gets into CNS.
has ANTIGEN SWITHCHING - correlates to episodic fever

clinical:

  • lymphadenopathy at posterior cervical lymph nodes
  • diurnal somnolence
  • constant headaches
  • behavior changes
  • enventual coma

dx: microscopy

224
Q

chagas disease - species, life cycle, clinical, dx

A
  • trypanosoma cruzi
  • transmitted by kissing bug (comes out at night and bites face)
  • life cycle:
    bug takes bite, defecates, person scratches, rubs feces into wound, get chancre at site of bite, swelling of eye (Romana’s sign), gets into blood, likes smooth muscle (cardiac and GI muscle)

clinical:

  • acute: fever, facial edema, myocarditis
  • chronic: DILATED CARDIOMYOPATHY, MEGACOLON and MEGAESOPHAGUS

dx:

  • early can see parasite in microscopy
  • chronic - test for antibodies
225
Q

Leishmaniasis - transmission, types (3)

A 
transmitted via sand fly
3 types:
- visceral
- cutaneous
- mucocutaneous
226
Q

visceral leishmaniasis - AKA, geographic distribution, life cycle, clinical, dx

A
  • AKA Kala Azar
  • seen in South Suday and India
  • life cycle:
  • sand fly ingests blood, (dog is reservoir) injects parasite, gets into blood, likes macrophages in liver, spleen and bone marrow

clinical:

  • opportunistic infection in AIDS patients
  • fever, weight loss, LARGE LIVER, pancytopenia, hyperpigmentation (black fever)

dx: PCR or microscopy of spleen/bone marrow aspirate

227
Q

cutaneous leishmaniasis - species, clinical, dx

A
  • sandfly transmission - different species
  • causes chronic lesions at bite site
  • wet/dry ulceration
  • PCR under microscope
228
Q

mucocutaneous leishmanisis - species, clinical

A
  • only braziliensis species
  • only in S America
  • causes oral/nasal mucosal lesions as well as cutaneous
229
Q

artemisins - what stage of life cycle are they effective against, mechanism of action, use, adverse effects

A
  • effective against asexual and gametocyte phases
  • examples (artemether - oral, artesunate - IV)
  • has endoperoxide moity - FREE RADICAL PRODUCTION
  • short half-life (can’t use for prophylaxis, and can’t use as monotherapy - use in ACTS combined therapy)

-adverse effects: well tolerated, but not recommended for 1st trimester, decreases neutrophils and RBCs (rare)

230
Q

Artemesinin-based Combination Therapies (ACT) - example, use, benefits, adverse effects

A
  • Artemether-Lumefantrine - target blood stages
  • 1st line for chloroquine resistant p. falciparum
  • 4-5 day half-life
  • drug-drug interactions with ART protease inhibitors
  • TAKE WITH FATTY FOOD
  • contraindicated in patients with CARDIAC disease
231
Q

Quinolones - mechanism of action, examples

A
  • weak bases, gets protonated and trapped in food vacuole, inhibiting polymerization of heme – toxic to plasmodium

examples:

  • chloroquine phosphate
  • quinine sulfate/quinidine
  • primaquine
232
Q

Chloroquine - works against, resistance, adverse effects, contraindications

A
  • asexual and gametocyte stage
  • resistance due to transporter in food vacuole
  • VISUAL DISTURBANCES, palmar/solar pruritis, nail bed discoloration, hemolysis with G6PD deficiency, tox (CV and CNS)
  • don’t take with epilepsy or myasthenia gravis, liver disease, GI, neurological or blood disordrs
  • CYP INHIBITOR - decreases efficacy of yellow fever vaccine
233
Q

Quinine sulfate/ Quinidine gluconate - works against, resistance, adverse effects, contraindications

A
  • asexual and gametocyte stage
  • combination to decrease duration and tox
  • wide CNS and tissue distribution
  • resistance - efflux pump
  • tox - dose related, CINCHONISM (tinnitus, deafness, visual disturbances) hypersensitivity (BLACKWATER FEVER), narrow therapeutic window
  • contraindicated if they already have tinnitus or optic neuritis or hemolysis
  • CYP inhibition
234
Q

primaquine - works against - stages work against, mechanism, side effects, contraindications

A
  • primary and hypnozoite liver stages, gametocyte blood stage
  • works on HYPNOZOITE
  • gametocydal - doesnt work against asexual blood stages
  • INHIBITS ETC IN MITOCHONDRIA - reactive oxygen species
  • side effects - GI stress
  • contraindicated iwth G6PD- causes hemolytic anemia, contraindicated in pregnancy
235
Q

adjunctive therapies with quinolones

A
  • doxycycline - use for prophylaxis also

- clindamycin

236
Q

atovaquone - effective against, mechanism, drug combo, resistance, drug-drug

A
  • active against p. falciparum asexual blood stages and PRIMARY LIVER STAGES (not p.vivax)
  • inhibits parasite MITOCHONDRIAL ETC
  • combined with proguanil (malarone) - synergy and for prophylaxis
  • not metabolized - biliary excretion
  • resistance - cytochrome b mutations
  • if taken with rifampin will decrease plamsa levels
237
Q

proguanil - active against, mechanism, use, metabolism

A
  • active against blood stages and primary liver
  • prodrug
  • inhibits diydrofolate reductase
  • enhances atovaquone effect - prophylaxis
  • metabolized by CYP
238
Q

mefloquine -effective against what stages, use, metabolism, mechanisms (4)

A
  • active against asexual blood stages
  • better for prophylaxis, and drug-resistant strains of p. falciparum
  • CYP metabolism
  • 4 mechanisms:
    1- inhibit heme degredation
    2- interfere with DNA/RNA synthesis
    3- inhibit ETC
    4- oxidative stress
239
Q

what malaria drugs can you use in pregnancy (3)

A
  • chloro (if not resistant)
  • clinda and quinine
  • mefloquine
240
Q

what can you use for prophylaxis (5)

A
  • chloro if not resistant area
  • atovaquone-proguanil
  • mefloquiine
  • doxycycline
  • primaquine (for vivax and ovale)
241
Q

nematodes: subsets, types (12)

A

nematodes = round worms

INTESTINAL:

  • ascaris lumbricoides
  • hookworm (necator americanus and anclystoma duodenale)
  • whip worm (tricuris tricuria)
  • enterobius vermicularis (pin worm)
  • strongyloides stercoralis
  • anisakiasis (fish ascaris)
  • trichinella spiralis (maybe belongs in tissue)

TISSUE:

  • toxocariasis (maybe belongs in intestinal)
  • lymphatic filariasis (wucheria bancrofti)
  • onchocerca volvulus (african river blindness)
  • loa loa
  • dracunculus medinesis (guinea worm)
242
Q

Soil transmitted helminths

A
  • ascaris lumbricoides, hookworm, whipworm

“unholy trinity”

243
Q

ascaris lumbricoides - life cycle, clinical, dx

A

life cycle:
- get infected by ingesting EGGS in contaminated food or water, eggs reach stomach, frees larvae, larvae penetrates wall of intestine, gets into BV, goes to liver, heart and pulmonary system, ascends bronchial tree, gets up to mouth, swallow, gets into intestine again where larvae develop into adult worms, mate in small intestine, lay eggs, which get expelled in feces

clinical:

  • really HIGH worm burden - can get SURGICAL ABDOMEN
  • eosinophilic pneumonitis - LOEFFLER’S pneumonitis
  • can migrate to biliary tract and cause pancreatitis and cholangitis

dx:
- see eggs in fecal smear

244
Q

hookworm - species, life cycle, clinical, at risk pop, dx

A

2 human species:

  • necator americanus (more prevalent)
  • anclystoma duodenale
  • non-human hookworm can cause cutaneous larva migrans

life cycle:
- larvae in soil, walk around barefoot, penetrate skin, get into BV, go through to liver to heart to lungs, through alveolar space, up bronchial tree, swallow and back down to GI where they become adults, mate, lay eggs, and expelled in feces

clinical:

  • causes anemia - worms feed on blood
  • causes protein deficiency

at risk:

  • pregnant women
  • growing kids
  • menstruating women

dx:
- look for eggs in feces

245
Q

trichuris trichuria - characteristics, life cycle, clinical, dx

A

AKA whip worm
- no long migration phase to lungs, smaller than ascaris

life cycle:
- ingest eggs through mouth, hatch in stomach, likes to live in colon, thin portion embeds in mucosa (thick sticks into lumen and expels eggs)

clinical:

  • leads to inflammation and bleeding
  • bloody diarrhea and fever
  • causes RECTAL PROLAPSE kids are always trying to defecate

dx:
- look for eggs in feces

246
Q

enterobius vermicularis - geography, life cycle, clinical, dx

A

AKA pin worm
ubiquitous around world, seen in kids

lifecycle:
- ingest eggs, release larvae in small intestine, migrate to colon, female worms emerge at night and lay eggs around anus, kid will scratch anus and get eggs on fingers, transmit back to themselves orally or give to other kids

dx:
SCOTCH TAPE TEST

247
Q

strongyloides stercoralis - geography, life cycle, clinical, dx

A

still endemic in US - Appalachia
zoonotic - reservoir dogs and primates

life cycle:
(similar to hookworm) - larvae in soil, penetrate skin, go through lungs, reswallow, ONLY FEMALE WORMS, eggs can hatch in gut, release larvae which can 1) be pooped out, 2) penetrate own intestine and repeat life cycle to lungs or 3) migrate to anus, penetrate skin in perianal region and repeat cycle again

can cause PERSISTANT autoinfection, esp in immunosuppressed

clinical:

  • in functioning immune can see perianal rash, mostly asymptomatic
  • in immunocompromised - acute enteritis, respiratory symptoms, dissemination to CNS and other organs - abcesses with intestinal bacteria

dx:
- see LARVAE in stool sample, can plate on agar and see tracts

248
Q

toxocariasis - life cycle, clinical

A

dog or cat intestinal worms

life cycle:
ingest, hatch, penetrate wall of intestine, get lost because they’re in the wrong host, go to other organs and cause inflammation - brain, eye, liver, lungs, etc.

2 clinical manifestations:

1) visceral larvae migrans - usually in younger kids, see eosinophilia, symptoms depend on migration (lungs etc.)
2) ocular larvae migrans - usually in older kids, can lead to unilateral blindness

249
Q

anisakiasis - clinical

A

ascaris infection of worms - found in sushi

  • larvae get into stomach and try to penetrate wall of stomach - get pain
  • doesn’t disseminate - just wait for it to die or extract it with endoscopy
250
Q

trichinella spiralis - geographic distribution, life cycle, clinical, dx

A
  • found in US too
    zoonotic - big animals in wild (hunting)

life cycle:
- ingest flesh that contains cysts with larvae inside of them, releases larvae in stomach, develop into worms in small intestine, penetrate through and go throughout boyd - likes muscles

clinical:
- first get GI symptoms, then get muscle aches and pains, swelling, edema of muscle - see around FACE/EYES and eosinophilia

dx: muscle biopsy, antibody test

251
Q

lymphatic filiariasis - geography, transmission, life cycle, clinical, dx

A

caused by wuchereria bancrofti

  • most common of the filarial diseases
  • found in tropics
  • vector transmitted - mosquito

life cycle:
- mosquito feeds, ingects micro larvae into bloodstream, adults live in lymphatics (inguinal preferred), male and female mate and live in clusters in nodes, larvae get into bloodstream and another mosquito takes up larvae and transmits to another person

clinical:

  • chronic infections, chronic swelling, hydrocele (Scrotum) breast
  • very stigmatizing, irreversible

dx: see wucheria bancrofti micro filariae (ONLY AT NIGHT) on thick blood smear, can do ultrasound FILARIAL DANCE SIGN, or antigen detection

252
Q

Onchocerca vulvulus- geography, transmission, life cycle, clinical, dx

A

AKA African river blindness

  • W and C Africa
  • transmitted by black fly

life cycle:
- fly will bite and inject microfilariae into skin, stays in skin, develops into adults in nodule nests, produces more larvae, those migrate thorugh subcutaneous tissue, including through the EYE, and causes inflammation and keratitis of cornea, and scarring. another black fly sucks up microfilaria and gives to soemone else

clinical

  • blindness over decades
  • can be pruritic because of migration
  • chronic skin dermatitis
  • CANNOT SEE IN EYE like in loa loa

dx:

  • skin snip of skin nodules, incubate in saline, look for released worms
  • NOT IN BLOOD
253
Q

loa loa - geography, transmission, life cycle, clinical, dx

A

ONLY in Central West Africa
- vector is fly bite

life cycle:
- adult worm lives in skin and they migrate and can see CALABAR SWELLING which is caused by allergic reaction. CAN SEE the worm traversing the eye. releases larvae into blood DURING THE DAY

dx: blood smear during the day

254
Q

dracunculus medinensis - transmission, life cycle, clinical, dx

A

AKA Guinea worm
- lives in tiny COPEPOD CRUSTACEAN that lives in fresh water

life cycle:
- orally ingested, release larvae, penetrate through intestine, travel to legs, female worms pop out through skin to release eggs when you go into fresh water

clinical:
- worm leaving skin - infection, cellulitis, skin/muscle damage

dx:
- see worm, have to twist around a stick slowly

255
Q

trematodes - classifications and types (6)

A

liver flukes:

  • fasciola hepatica
  • opsithorchis viverrini
  • clonorchis sinesis

lung flukes:
- paragonimus

blood flukes:

  • schistosoma mansoni
  • schistosoma haematobium
256
Q

fasciola hepatica - geographic distribution, transmission, clinical

A
  • S America, Iran, Egypt
  • get it by eating watercress
  • can get blockage of BILE DUCT and abcess formation
257
Q

opsithorchis viverrini - geographic distribution, transmission, clinical

A
  • Northern Thailand (koi pla dish)
  • snail is reservoir, infects fish, humans eat fish with parasite in it
  • eat fish, get infected ,adult goes and lives in bile ducts, over time, both clonorhis and opsithorchis cause chronic inflammation of bile duct and cause BILE DUCT CANCER - cholangiocarcinoma
258
Q

paragonimus - geographic distribution, transmission, clinical

A

lung fluke - only in east asia (china, phillipines)

  • get by eating crab or crayfish
  • manifestations - couph up blood, infiltrateson chest xray
    dx: look for eggs in sputum
259
Q

Shistosoma mansoni - geographic distribution, transmission, life cycle, clinical

A
  • South America (only mansoni in SA) and Africa
  • skin contact with fresh water where there are SNAILS

transmission/life cycle
- larvae penetrates skin, migrate to BVs, paired couples mate, produce eggs, eggs get deposited in liver because the adult lives in the intestine

clinical:

  • get rash from penetration of larvae form, swimmer’s itch a day later, month later when worms lay eggs, get allergic reaction - KATAYAMA FEVER - shock analphylaxis, high eosinophilia
  • get PORTAL HYPERTENSION - and enlarged collateral veins to compensate, hepatic fibrosis, GI blood loss and abdominal pain

dx - look at spine (lateral spine)

260
Q

shistosoma haematobium - geographic distribution, transmission, life cycle, clinical

A
  • in Africa
  • skin contact with fresh water where there are SNAILS

transmission/life cycle
- larvae penetrates skin, migrate to BVs, paired couples mate, produce eggs, eggs get deposited in bladder - adults live in venules draining the bladder

clinical:

  • get rash from penetration of larvae form, swimmer’s itch a day later, month later when worms lay eggs, get allergic reaction - KATAYAMA FEVER - shock analphylaxis, high eosinophilia
  • causes hematuria, scarring causes obstruction of bladder - high creatinine, bilateral ureterial obstruction. causes bladder cancer (in women can get deposited in cervix and genital tract)

dx: look at spine (terminal spine)
can see eggs in urine or stool

261
Q

cestodes - kinds (2)

A

taenia - beef (saginata), pork (solium)

262
Q

Taenia Saginata - characteristics, geographic distribution, transmission, life cycle, clinical

A

only in E africa,
long, form segments filled with eggs.

  • ingest larval cysts from eating undercooked beef, worms live in our intestines, segments break off, get released into environment, gets eaten by cow, travels to their muscles, which is how we get it again
  • ONLY ADULT FORM infects human - low pathogenicity in GI system
263
Q

taenia solium - characteristics, geographic distribution, transmission, life cycle, clinical

A
  • see in Mexico, C and S America, Asia and Africa
  • long, form segments filled with eggs.

2 options for transmission:
1- ingest larval cysts from eating undercooked pork, worms live in our intestines, segments break off, get released into environment, gets eaten by pig, travels to their muscles, which is how we get it again
2- humans ingest EGGS from environment, which release larvae, which spread through BVs and disseminate to muscle eye and brain - CYSTISERCOSIS

clinical:
- seizures when cyst dies and causes acute inflammatory response, muscle issues

dx:
CT and antibody testing - might not see anything in feces

tx:
give steroids when trying to kill/remove live cysts

264
Q

diphyllobothrium latum - geographic location, transmission, clinical

A
  • fish tapeworm
  • usually from Scandinavia
  • from copepod and freshwater fish
  • association with B12 deficiency
265
Q

echinococcus - transmission, life cycle, clinical, tx

A
  • normally live in dog intestines and sheep are main intermediate host. humans are accidental host
  • see in places with sheepdogs and farming
  • when you ingest eggs, get dissminated cysts - liver, lung and brain

HYDATID CYST - in liver usually, can get really large, cause obstruction pain and jaundice. if they rupture, cause acute allergic reaction and anaphylaxis - don’t want to rupture. WON’T see eggs in feces

tx: puncture cyst, aspirate, inject chemicals, re-aspirate (PAIR)

266
Q

Benzimidazole -includes, mechanism, use, resistance

A
  • includes mebendazole and albendazole
  • mechanism: inhibiits MICROTUBULE POLYMERIZATION leading to cell death and eath of parasite - selective for parasitic B tubulin
  • used for both GI and systemic NEMATODE infections:
  • one dose good for all nematodes except for tricuris (3 doses) and LF (needs combo of albendazole with ivermectin or diethylcarbamazine)

resistance: change in B tubulin isotope – isotope 1

267
Q

mebendazole - use, oral/IV, tox/contraindications

A

not absorbed in GI - take orally and use for parasitic infections localized in the lumen of the gut

tox: very well tolerated. but when given in high doses over a long period of time, can see BONE MARROW SUPPRESSION, hair loss and liver inflammation
- contraindicated in pregnancy - TERATOGENIC and EMBRYOTOXIC

  • CYP metabolized (inhibitors increase levels - don’t take with cimetidine)
268
Q

albendazole- use, oral/IV tox/contraindications

A

use for systemic infections, CYSTISERCOSIS and liver disease. can penetrate into tissues - larval cysts

oral - erratic absorption take with FATTY FOODS

tox: high doses cause BONE MARROW SUPPRESSION

CYP inhibitors increase levels (don’t take with cimetidine)

269
Q

Avermectin - includes, mechanism, use, tox, resistance

A

Ivermectin
used for LARVAE of FILARIAL infections (onchocerciasis, LF) but NOT for loa loa

mechanism:
interferes with chloride channels, causing hyperpolarization and FLACCID PARALYSIS of nematode

resistance:
mutation in chloride channels or efflux of drug

tox: cyp metabolized - don’t use with cimetidine. potential MAZZOTTI reaction to dying larvae, hypersensitivity reaction, or hyperpolarization in people with impaired BBB

270
Q

Diethylcarbamazine mechanism, use, tox, resistance

A

mechanism: alters surface membrane causing enhanced killing and platelet aggregation. increases arachadonic acid metabolism. causes FLACCID paralysis - decreased muscle activity.

use for FILARIAL infections, particularly LOA LOA - causes both ADULT AND MICROFILARIA death
- do NOT use in ONCHO areas- will get eye damage

take orally

well absorbed systemically. if you have ALKALINE URINE, you’ll get higher drug levels - reabsorption. adjust with renal dysfunction. can get Mazzotti reaction when worms die.

271
Q

pyrantel pamoate -mechanism, use, tox

A

mechanism: stimulates nicotinic Ach receptors, causes release of Ach, inhibits Ach-ase - causing SPASTIC PARALYSIS of worm
- use for pinworm infection (luminal GI nematodes, soil-transmitted)
tox: neuromuscular issues in heart if given in super high doses

272
Q

praziquantel- mechanism, use, tox, resistance

A

mechanism: disrupts outer coating of adult worms - inferering with calcium transport (SPASTIC PARALYSIS)- allows immune system to kill worm because of ANTIGEN EXPOSURE
- use for TENIAE and SHISTO (flat worms). only for ADULT and IMMATURE stages
- tox - GI, nausea, bad taste, contraindicated in preg, cyst in eye could cause inflammation when treated, hepatic diesease prolongs halflife
resistance: not an issue yet, but will be a big one (only drug for shisto) - mutation in voltage gated calcium channel

273
Q

Antiherpes/AntiCMV agents (3)

A
  • acyclovir
  • gancyclovir
  • foscarnet
274
Q

Anti-influenza (2)

A
  • amantidine (no longer in use)
  • osetamivir
  • zanamivir
275
Q

nucleoside reverse transcriptase inhibitors (NRTIs) (3)

A
  • AZT
  • Abacavir
  • lamivudine/emtricitibine
276
Q

nucleotide reverse transcriptase inhibitor (NRTI) (1)

A

-tenofovir

277
Q

non-nucleoside reveres transcriptase inhibitors (1)

278
Q

protease inhibitors (3)

A
  • ritonavir
  • darunavir
  • atazanavir
279
Q

fusion/entry/integration inhibitors (3)

A
  • enfuvirtide
  • maraviroc
  • dolutegravir
280
Q

acyclovir - use, mechanism, tox, resistance

A
  • antiherpes (HSC, VZV)
  • nucleoside analog that has to get phosphate by VIRAL THYMIDINE KINASE, other phosphorlyation steps done by human thymidine kinase
  • inhibits DNA synthesis by competing with normal deoxyGTP - gets into viral DNA
  • tox: nausea, diarrhea, renal tox, neuro tox, cimeditine interaction
  • resistance: mutation in viral thymidine kinase - gives cross resistance to other drugs with same mechanism
281
Q

gancyclovir- use, mechanism, tox, resistance

A
  • anti CMV
  • nucleoside analog that has to get phosphate by VIRAL CMV KINASE, other phosphorlyation steps done by human thymidine kinase
  • inhibits DNA synthesis by competing with normal deoxyGTP - gets into viral DNA
  • prophylaxis for CMV post-transplantation
  • tox: MYELOSUPPRESSION
  • resistance: mutations in kinase
282
Q

Foscarnet- use, mechanism, tox, resistance

A
  • anti CMV agent
  • looks like pyrophosphate - inhibits viral DNA/RNA POLYMERASE and HIV RT
  • doesn’t require activation
  • use for acyclovir resistance

tox: renal tox - electrolyte imbalance

283
Q

oseltamivir- use, mechanism, resistance

A
  • anti-influenza A and B
  • approved for children 1yr and older
  • neuraminidase inhibitor - inhibit the cleavage of influenza progeny
  • resistance is possible
284
Q

zanamivir

A
  • used for resistant oseltamivir

- approved for children 7 y/o and up

285
Q

abacavir - use, mechanism, resistance, tox

A

NRTI
- nucleoside analog, has to be activated by phosphorylation, works by competitive inhibition of RT and incorporation into viral DNA

  • resistance is slower than earlier drugs (AZT) but due to mutation in viral RT
  • tox: increased rsk of MI, fatal systemic hypersensitivity reaction with HLA-B*5701 POLYMORPHISM
286
Q

lamivudine/emtricitibine - use, mechanism, resistance, tox

A

NRTI

  • nucleoside analog, has to be activated by phosphorylation, works by competitive inhibition of RT and incorporation into viral DNA
  • also used to treat Hep B
  • emtricitabine is the same as lamivudine except that it has a fluorine and thus has a longer halflife
  • Truvada has emtricitabine with tenofivir
287
Q

tenofovir - use, mechanism, resistance, tox

A
  • nucleoTide analog
  • don’t need to be phosphorylated, works by competitively inhibiting HIV RT - chain termination after incorporation into DNA

also used for Hep B

tenofovir is co-administered with emtricitabine as first line RTI backbone therapy as truvada

tox:
renal tox (less with alafenamide version)
288
Q

efavirenz - use, mechanism, resistance, tox

A
  • non-nucleoside reverse transcriptase inhibitor
  • bind directly to HIV-1 RT and inhibits all it’s polymerase activity in an ALLOSTERIC fashion – no competition with nucleotide
  • doesn’t require phosphorylation
  • resistance can happen QUICKLY with single mutation in RT (but no cross resistance to NNRTIs)
  • tox: extensively metabolized by CYP3A4 (Drug-drug) have NIGHTMARES/PSYCH DISTURBANCES - eventually resolves, GI and severe hypersensitivity. TERATOGENIC
289
Q

ritonavir - use, mechanism, resistance, tox

A
  • HIV protease inhibitor
  • inhibits the proteolytic cleavage of proteome, don’t require intracellular activation
  • INHIBITOR OF CYP3A4 - used with other PIs to increase their serum levels - boosting
    tox: weird distribution of fat, elevated triglycerides/LDL, elevated serum aminotransferase levels
290
Q

Darunavir - use, mechanism, tox

A
  • use either/or with atazanivir for niave patients
  • HIV protease inhibitor
  • inhibits the proteolytic cleavage of proteome, don’t require intracellular activation
  • tox: rash, sulfa allergies
291
Q

atazanavir- use, mechanism, tox

A
  • either/or with darunavir, treatment of choice for naive patients
  • HIV protease inhibitor
  • inhibits the proteolytic cleavage of proteome, don’t require intracellular activation

tox: rash, KIDNEY STONES

292
Q

enfuvirtide- use, mechanism, tox

A
  • prevents fusion of HIV virus into cell
  • binds GP41 viral envelope glycoprogein - prevents the conformational changes required for fusion - prevents entry pore formation

ONLY for treatment of EXPERIENCED patients

293
Q

maraviroc- use, mechanism, tox

A
  • prevents fusion and entry of HIV virus into cell - works on co-reeceptor CCR5
  • substrate for CYP3A4, used in resistant strains

tox: hepatotox

294
Q

dolutegravir- use, mechanism, tox

A

integrase strand transfer inhibitor

  • binds to integrase and prevents recombination of viral DNA into our genome
  • not firstline treatment - used for resistant strains
  • tox: can be affectd by CYP3A4 induces, used with coinfection with HCV or HBV - can cause increased liver enzymes
295
Q

3 categories of drug reactions

A

type 1: anaphylactic IgE mediated (causes urticaria/angioedema, wheel and flare rxn)

type 2: blistering, cytotoxic reaction. FIXED foreign antigen generates antibody, binds antigen and causes destruction, separation - pemphigus vulgaris (desmoglein target)

type 3: immune complex - SOLUBLE target - deposits on BV causing VASCULITIS with cellular debris,DOESN’T BLANCH - serum sickness, arthus reaction

type 4: delayed type hypersensitivity - exanthematous (red all over), contact dermatitis, tuberculin reaction, stasis dermatitis BLANCHES

296
Q

exanthems

A
  • maculopapular, morbilliform or scarlatiniform
  • 12 weeks after exposure
  • BLANCHABLE
  • urticarial but fixed
297
Q

drug hypersensitivity syndrome

A
  • really sick, upset stomach, weakness, fever

- caused by anticonvulsants (prominent edema), sulfa drugs (borderline purpura), allopurinol (CAN BE MONTHS LATER)

298
Q

Anaphylaxis

A

type 1, IgE mediated

anaphylactoid is NOT immunologically driven

299
Q

Urticarial hives

A

urticaria only lasts a da and then moves. edema, redness, wheel and flare

acute (6 weeks) - food, drug, bug

chronic (over 6 weeks) can’t figure out cause

300
Q

angioedema

A

deeper - see LIP SWELLING, RESP DISTRESS

caused by Ace Inhibitors (can happen at ANY TIME)

301
Q

acute generalized exanthematous pustulosis

A

NOT aossicated iwth follicle

  • 1-2 DAYS after exposure
  • NEUTROPHIL incrase, fever, systemic issues
  • nothing in pusules (no bacteria) besides neutrophils
  • can do PATCH TEST - see petechiae and purpura
  • NOCHOLSKI’S SIGN/ASCOLHANSEN’S SIGN - can push vessicles through epidermis (epidermis is necrotic)
302
Q

Steven jonson’s syndrome

A

really sick, flu, eruptions that start morbilliform then turn dusky
caused by beta lactams and anticonvulsants
mucosal surface involvement

give IV Ig

303
Q

TEN

A

overlaps with steven johnson - see in HIV pop, glutatione deficiency.
see FULL THICKNESS epidermal necrosis

304
Q

drug induced vasculitis

A 
type 3 (circulating/immune complex)
palpable dusky red purpura
NOT blanchable
starts on PRESSURE depedent areas
if given warfarin without heparin first within 3-5 days of starting
305
Q

phototoxic rxn

A 
due to UVA radiation
doxycycline-induced
painful
happens in a matter of minutes
looks like a burn (like lime from ceviche)
306
Q

photoallergic rxn

A

looks like eczema
pruritic, contact dermatitis
happens a day later
scaly, patchy

307
Q

where is the separation in pemphigus vulgaris?

A

above the basal keratinocytes

308
Q

what would direct IF look like for pemphigus vulgaris

A

chickenwire - seeing Ig for desmoglein 3 and sometimes 1 (3 is deeper than 1)

309
Q

are the bullae fragile or strong from pemphigu vulgaris?

A

fragile - get erosion

310
Q

where is the separation in pehmphigus folleaceous

A

more superficial. no mucosal involvement

311
Q

what would direct IF look like for pehmphigus foleaceous

A

chickenwire, but more superficial. only desmoglein 1

312
Q

bullous pemphigoid affects what patient population mostly

A

older people

313
Q

where is the separation in bullous pemphigoid

A

AT basement membrane, so you have intact epidermis with a blister beneath

314
Q

how does bullous pemphigoid feel in comparison to vulgaris

A

pemphigus vulgaris is painful, bullous is itchy - EOSINOPHILS - string of pearls - central clearing

315
Q

what do you see in IF for bullous dermatosis

A

linear IgA - antibody to proteins in hemidesmosome

316
Q

dermatitis herpetiformis

A

depostion of autoantibodies in dermal papillae - IgA mediated
- very itchy - associated iwth GLUTEN ingestion

317
Q

epidermolysis bullosa

A

genetic
simplex defect at keratin 5 and 14

different severities (junctional, deep, or dystrophic)

318
Q

what virus is associated iwth oral hairy leukoplakia

319
Q

oral ulcers are associated with what virus

A

HSV-1/2 and CMV (usually larger)

320
Q

genital ulcers are associated with what virus

A

HSV, but you can get secondary bacterial infection

321
Q

Bacillary angiomatosis (cutaneous infection) is associated with what pathogen

A

bartonella

322
Q

molluseum contagiosum is associated iwth what pathogen

A

pox-virus. forms umbillicated lesions

323
Q

ocular opportunistic infections are associated iwth what pathogen

A

CMV retinitis

324
Q

HIV penumonia is caused by what pathogen

A

pneumocystis jirovecii

325
Q

HIV= related GI infections are related to what pathogen

A
  • CMV (watery diarrhea, odynophagia, cholecystitis, proctitis)
  • cryptosporidium (unremitting diarrhea, chonecystitis)
  • parasitic (microsporidium, giardia, entamoeba histolytica)
326
Q

HIV CNS infections are related to what pathogen

A
  • JC virus (get progressive multifocal leukoencephalopathy)
  • toxo - (get multiple ring enhancing lesions)
  • cryptococcus meningititis
  • CMV (ascending weakness)
327
Q

disseminated HIV infection caused by

A

MAI (mycobacterium avium) - get night sweats, enlarged organs, enlarged LNs, weight loss, pancytopenia

328
Q

how long does it take for a neonate to have functioning plasma cells

A

almost a year

329
Q

what happens to thymus as we age

A

at 35 thymus starts to involude. get decrease in naive T cells and increase in memory cells

more molecular mimicry, more bystander activation, fewer Treg

more chronic stimulation, exhausted cells (don’t proliferate or make IL2 as well) - esp with HIV, CMV, hepatitis

330
Q

pattern of disease for T cell mediated immune defect

A
  • bacteria, fungal, viral, protozoal
  • multiple anatomic sites - systemic, severe, failure to cure
  • opportunistic infections
331
Q

pattern of disease for B cell/humoral immune defect

A
  • URIs

- GI infections

332
Q

pattern of disease for phagocytic immune defect

A
  • bacteria (extracellular strep/staph), fungal, and sometimes mycobacteria if you have neutrophil defect
333
Q

pattern of disease for complement immune defect

A
  • blood bacterial infections (NEISSERIA in C5-9 MAC deficiencies)
  • autoimmunity because immune clearance is defective
334
Q

if you see abcesses or fungi, what class of immune defeciency do you expect

A

phagocyte defect

335
Q

genetic causes of SCID

A

1) X-linked deficiency of common gamma chain - can’t respond to IL-7 (related to IL-7 receptor JAK3 mutations) only affects T cell, not B cell - NO NK CELLS
2) RAG deficiency - no somatic recombination of VDJ - no T or B cell development. can get Omenn’s syndrome - some T and B development- go to periphery and expand in Th2 effector function – leading to atopic dermatitis, eosinophilia, ezcema
3) ADA deficiency - important for nucleoside metabolism, affects both T and B cells. autosomal recessive inheritance

336
Q

DiGeorge’s syndrome

A
  • no development of 3rd or 4th pharyngeal pouch – defect in thymic maturation
  • choromosome 22 deletion
  • usually have some T cells - not as bad as SCID
  • require thymus transplant
337
Q

Btk deficiency

A
  • most common cause of B cell development defects
  • bruton’s tyrosine kinase is important for pre-B cell signalling
  • X-linked
  • T cells are okay
  • URI bacteria, GI viruses, autoimmunity
  • give IV Ig
338
Q

X-linked Hyper-IgM syndrome

A

ISOTYPE SWITCH DEFECT

  • mutation in gene that codes for CD40L
  • IgM is normal, others are decreased or absent
  • have follicles but no germinal centers - no T cell help
339
Q

IgA deficiency

A
  • clinically silent, relatively common
  • associated with CELIAC DISEASE
  • caution repetitive exposure to blood products - mount immune repsonse to any bit of IgA (seen as foreign)
340
Q

common variable immunodeficiency (CVID)

A

seen in teenagers adults

  • defect in B cell differeitiation - molecular basis unknown
  • highly associated with autommunity
341
Q

familial hemophagocytic syndromes

A
  • severe
  • defective granule mediated cytotoxicity (NK and CD8 ineffective) due to perforin mutation
  • chronic stimulation of cytotoxic cells because they aren’t able to kill - get cytokine storm, mass activation of macrophages, which end up eating up normal blood products - pancytopenia
342
Q

X-linked lymphoproliferative disease

A

related to familial hemophagocytic

  • X linked
  • defect in adaptor protein for signalling interations between T and B cells and other cells (CD8 and NK defects too)
  • boys get infected with EBV, get huge amounts of CD8 activity, cytokine production, and macrophage activity
  • risk for lymphoma
343
Q

chronic mucucutenous candidiasis

A
  • normal number of B and T
  • normal T cell response to most other things, and normal B cell humoral repsonse to candida
  • Th17 effector function defect - mutation in IL17 cytokine and receptor signalling or AIRE deficiency (make autoantibodies to IL-17 receptor)
344
Q

Hyper IgE syndrome (Job’s syndrome)

A
  • bad dermatitis
  • staph skin abcesses
  • elevated IgE
  • associated with other system abnormalitlies - osteoclast function for example
  • all use cytokine IL-6 and 10 receptor signalling using STAT3
  • can’t develope Th17 (through IL-6) epithelial cell function and antimicrobial proteins, IL10 down-regulates immune repsonse, so people get ezcema etc.
345
Q

Wiskott-Aldrich syndrome

A

multisystem disease

  • protein that regulates actin polymerization is defective – affects leukocyte migration, platelet formation, cell trafficking etc.
  • linked with platelet issue
  • causes defects in overall T cell function, especially with Treg (increased autoimmunity)
346
Q

Ataxia-Telangiesctasia

A

multi-system involvement

  • associated iwth defects in DNA repair
  • increased malignancies
  • T cell developmental defect (associated with somatic recombination)
347
Q

FAS mutations cause

A

autoimmune lymphoproliferative syndrome

348
Q

IPEX mutations cause

A

Treg deficiency/decreased function

349
Q

Toll-like receptor signalling issues

A

signalling molecule for TLR is adaptor protein called MyD88 - deficiencies in this molecule cause increased infection with bacterial infections (don’t get pro-inflammatory cytokines or stereotypical inflammation) have a “COLD” inflammatory response

350
Q

IFN-alpha defects

A

defects in type 1 cytokine receptor (TLR3) signaling could lead to not getting an antiviral response

351
Q

Chronic granulomatous disease

A

poor phagocytic function due to NADPH oxidase issue - results in chronic inflamation and inability to phagocytose

352
Q

Leukocyte adhesion deficiency (LAD-1)

A

mutations in beta-2 integrins which are important for cell-cell interaction and migration – LFA-1 interacts with ICAM to marginate into tissue – with defect, get defect in leukocyte migration - can’t clear infections get recurrent fungal infections (UMBILICAL STUMP WON’T HEAL)

353
Q

Chediak-Higashi syndrome

A

defects in LYSOSOMAL GRANULE maturation

  • neutrophils have big granules
  • get recurrent infections and have melanin deposition issues - can have albinism
354
Q

C3 defect

A

most severe of the complement defects - all components of complement are affected (opsonization, killing, chemoattaracting)

355
Q

C1-q, c2, c4 defects

A

difficulty with immune clearance

356
Q

membrane attack complexes defects

A

Neisseria infections, NOT ASSOCIATED WITH IMMUNE COMPLEXES

357
Q

C1 esterase inhibitor defect

A

get inappropriate complement activation - inappropriate vasoldiation and mast cell activation causing HEREDIATRY ANGIONEUROTIC EDEMA

358
Q

paramyxoviruses types

A

rubulavirus (mumps)

morbillivirus (measels)

359
Q

togavirus types

A 
alpha virus (chikungunya)
rubivirus (rubella)
360
Q

pneumovirus types

A

pneumovirus

metapneumovirus

361
Q

F protein is important for

362
Q

measles - classic clinical, seasonality, complications, dx, tx

A
  • KOPLIK SPOTS - whitish/bluish punctate lesions in buccal mucosa
  • Morbilliform rash (14-18 days after infection)
  • initially on FACE, then spreads to trunk and extremities, fades in 72 hours

seasonality: winter and spring

complications:
- viral pneumonia, bacterial superinfection, brain involvement - rare subacute sclerosing panenchephalitis (SSPE)

dx: clinical, PCR for RNA in nasal secretions, serology
tx: vitamin A supplementation

363
Q

mumps- classic clinical, complications

A
  • 2-4 week incubation
  • fever, malaise, headache, earache with parotid tenderness (usually bilateral) over 2-3 days
  • resolution in 2-10 days

complications:

  • 25% have post-pubertal epididymo-orchitiis
  • meningitis/encephalitis are rare
  • lose protection over time
364
Q

respiratory syncytial virus- classic clinical, complications

A
  • short incubation 2-8 days
  • inoculation through nose or eye
  • bronchiolitis (peribrochiolar infiltration) with endothelial sloughing and mucus secretion - wheezing and obstruction

complications

  • develop brochiectasis
  • apnea
  • pneumonia in immunocompromized
365
Q

metapneumovirus - who/when infected, clinical, dx

A
  • all age groups, but particularly children in the winter
  • can have co-infection with RSV or influenza
  • similar presentation to Resp syncitial virus and influenza A - need to do PCR to diagnose
366
Q

Rubela - clinical, seasonality, pattern of infectiousness

A
  • togavirus
  • runny nose, fever, rash taht starts on face and progresses to trunk and extremities (similar to measles)
  • joints are painful but not swollen
  • tender LN in posterior vervical and posterior auricular chains
  • similar to measles but not as bad
  • happens in spring
  • MOST INFECTIOUS when rash develops (but may shed before eand after)
  • infants exposed during pregnancy get congenital rubella syndrome
367
Q

congenital rubella syndrome

A
  • occurs when pregnant women are exposed to rublla and don’t have immunity in the 1st and 2nd trimester

clinical:
- low weight, cataracts/claucoma, deagness, heart disease, cognitive impairment, microcephaly, thombocytopenic purpura, hepatomegaly

dx: may have atypical lymphocytes (large and basophilic vacules) - made by serology or PCR of amnio

368
Q

influenza - clinical, dx

A
  • short incubation 1-2 days
  • abrupt onset of chills, myalgias, fever, headache, cough, sore throat
  • can progress to viral and secondary bacterial pneumonia
  • can also progress to GUILLAIN-BARRE - bilateral ascending paralysis

dx: to see subtypes H and N do PCR

369
Q

antigenic drift and influenza

A

H and N antigenicity changes - minor alterations

370
Q

reassortment and influenza

A

recombination of genomic material with 2 different coinfected viruses (how you can have avian and swine and human)

371
Q

antigenic shift and influeza

A

major shifts - no relationship between old and new strains (H3N2 to H5N1 for example)

372
Q

H5N1 - transmission, mortality

A

bird to human (need close bird contacts to contract) - limited human-to-human transmission

high mortality (50%)

373
Q

arboviruses - include what classes/viruses

A

arbo = arthropod-borne

has spherical RNA and includes 4 families:

1) togavirus (chikungunya)
2) flavivirus (dengue, yellow fever, west nile, St. Louis, Japanese enchephalitis, Zika)
3) bunyavirus
4) reovirus

374
Q

St. Louis encephalitis - transmission, clinical, dx

A

bird is reservoir, mosquito is vector, mosquito can’t pick it up again from human (only from bird)

clinical:

  • basic flu
  • encephalitis
  • meningitis
  • acute flaccid paralysis/myelitis

dx: CSF IgM

375
Q

West Nile - transmission, clinical, dx

A

most common arbovirus in north america

  • reservoir is birds, mosquito vector
  • transmission from mosquito or BLOOD TRANSFUSION and VERTICLE TRANSMISSION

clinicla:

  • mostly asymptomatic but likes nervous tissue
  • WN Fever - rever, headache, fatigue, neck stiffness, maculopapular rash, recover in 3-6 days or progress
  • WEST NILE NEUROINVASIVE DISEASE - encephalitis, meningitis (WNM = fever plus meningitis), polio-like flaccid paralysis, elevated WBC, Protein, normal glucose in CSF

dx: CSF IgM upon onset of symptoms, serum IgM after 8 days, convalescent IgG 4-fold rise

376
Q

Dengue

A

humans are main reservoir, will progress to more severe disease if you had prior antibodies

clinical:

  • undifferentiated fever first
  • dengue fever syndrome (fever + RETRO-ORBITAL pain, diffuse, blanching erythematous maculopapular rash with island of sparing, headache, myalgias/arthalgias)
  • dengue hemorrhagic fever (positive TOURNIQUET test, can bleed from anywhere, associated with thrombocytopenia, overwheling cytokine storm, leaky vessels and HEMOCONCETRATION)
  • dengue shock syndrome (worsening of hem fever - BP drops, circulatory failure, high mortality)

dx:
- early on - PCR
- more than 5 days after symptoms IgM
- tourniquet test for hem fever progression

377
Q

yellow fever - transmission, clinical, dx

A

-mosquito borne (Same as dengue)

clinical:

  • BACK-BREAK FEVER - myalgias, sudden high fever, CONJUNCTIVAL SUFFUSION - increased blood flow to eyes, nausea, vomitting.
  • BIPHASIC (antibodies lead to secondary infection - symptoms go a way and then come back)
  • secondary can kill you - renal failure, jaundice, bleeding from everywhere

dx: IgM when symptomatic

378
Q

Chikungunya - transmission, clinical, dx

A

“that which contorts”
alpha togavirus
mosquito borne

2 stage disease:

1) arthralgias, fever, headache, myalgia, EDEMA OF FACE and extremities - resolves in 3 days
2) debilitating POLYARTHALGIAS in PERIPHERAL JOINTS that can last for over a year, TENOSYNOVITIS and raynaud’s syndrome

dx: PCR in intial viermic phase
serology after 2 days of symptoms IgM, or IgG in convalescent rise

379
Q

Zika - transmission, clinical, dx

A
  • mosquito, pregnant to fetus, sex, blood transfusion

clinical:

  • dengue-lite - less severe, fever, mild arthtalgias, mild conjucntivitis
  • but causes microcephaly in first trimester infections
  • also liked to GUILLAIN BARRE - which can make it confused with polio or west nile

dx: acute phase pCR in serum or urine for up to 2 weeks
convalescent phase serum IgM after 14 days, confirm with PRNT

females are transmissible for 8 weeks, men for 6 months

380
Q

SARS - type of virus, transmission, clinical, dx

A

coronavirus
bat transmitted - palm civet in markets

clinical:
- hard to distinguish from flu pneumo.
early = fever, myalgia, chills, DRY COUGH
late = worsening pneumoniaa, water diarrhea

dx: PCR lower respiratory

need to isolate and quarantine contacts

381
Q

MERS - type of virus, transmission, clinical, dx

A

-coronavirus - bats and camels
ARABIAN PENINSULA

clinical:
- severe pneumonia
GI, cough fever

dx:
- PCR lower respiratory

382
Q

Ebola - type of virus, transmission, clinical

A
  • filovirus (are large under EM microscope)
  • reservoir is fruit bat, person to person transmission from contact with body fluid

clinical:

  • multisystem involvement that can lead to hemorrhagic fever
  • rash between day 5-7, if you develop antibodies, the rash will go away, if not, you’ll die
  • post ebola convalescent syndrome (UVEITIS, arthralgias, fatigue, alopecia)
383
Q

types of adenovirus infections (3)

A

1) lytic - kills human EPITHELIAL cells, producing many progeny
2) latent - asymptomatic, stays in LYMPHATIC cells for a long time
3) oncogenic - viral DNA is integrated and replicated in cell’s DNA - no progeny produced

384
Q

pathonmeumonic clinical indications for adenovirus

A

1) pharyngoconjuctival fever - (pus in eyes and tonsils - kids at camp)
2) epidemic keratoconjuctivitis (contagious eye disease, cornea can be involved for months, frequently bilateral)
3) hemorrhagic cystitis (blood in urine, burning, frequency, more common in boys)
4) infantile diarrhea (profuse diarrhea, dehydration - live virus given to military recruits in oral vaccine)
5) intussusception

385
Q

parvovirus B19 - cells infected, manifestations

A

only infects human ERYTHROID PROGENITOR CELLS

manifestations:
1) 5ths disease, AKA erythema infectiosum (prodrome with fever and headaches and SLAP-CHEEK RASH that can spread to trunk and limbs - immune mediated)

2) arthropathy (young women mostly, swelling and stiffness of SMALL joints - looks like rheumatoid arthritis)
3) transient aplastic crisis (in patient with underlying hemolytic disorder - get severe anemia - NOT immune mediated, don’t see IgG)
4) Pure red cell aplasia (in HIV patient - persistent anemia due to lack of parvovirus antibodies - dependent on transfusions)

386
Q

5 viral families that cause the common cold

A

1) parainfluenza
2) respiratory syncicial virus
3) rhinovirus
4) coronavirus
5) enterovirus

387
Q

sinusitis - progression, clinical, dx, tx

A
  • starts out viral and then get bacterial super infection
  • causes inflammation of nasal passages, and get trapped exudate and bacterial infection accordingly

clinical:
-purulent nasal discharge (Green), pressure over sinuses, fever, can extend to proptosis of eyes, meningitis and brain abscesses if left untreated

dx: history, CT
tx: give empiric antibotics

388
Q

pharyngitis - pathogens, clinical, dx

A

viral or bacterial pathogens

clinical:
- with group A strep, can be severe and cause pain, odynophagia, fever, erythematous with exudate, cervical adenopathy and leukocytosis
- with virus, usually mild except flu. EBV and adenovirus can cause exudate, coxackie and HSV have vesicles

dx: strep test, throat culture

389
Q

epiglottitis - pathogen, clinical, dx

A
  • associated with H flu type B

clinical:
-kid leaning forward, drooling, respiratory distress, fever, sore throat

  • dx: visualize epiglottitis, swab or look for organism in blood
390
Q

croup - pathogen, clinical

A

only viral
affects kids between 3 and 36 months

laryngeaotracheal bronchitis, seal bark, preceded by URI, can get spasmodic recurrent croup

391
Q

otitis media - pathogens

A

H. flu, strep pneumo, common cold viruses

392
Q

otitis externa - manifestations (3)

A

1) acute localized (looks like pimple)
2) acute diffuse (swimmer’s ear - edematous and red)
3) invasive/malignant (spread, severe necrotizing infection, related to diabetes, need long term IV antibiotics)

393
Q

acute bronchitis - clinical

A
  • healthy person with incessant cough, somtimes productive
  • viral cause.
  • post-nasal drip, sputum, fever, chest pain due to inflamed trachea

NO ANTIBIOTICS

394
Q

Chronic bronchitis - clinical

A
  • productive cough on most days for at least 3 consecutive months
  • see with COPD and smoker - worse in the morning
  • can get bacterial infection on top - get increased cough, more sputum, fever, don’t feel well
  • if you see eosinophils, think environment
395
Q

rotaviruses - who is affected, proteins, life cycle, clinical, dx

A
  • globally most common for kids under FIVE YERAS OLD - in US kids under 5 get noravirus
  • peak incidence in winter

-SEGMENTED with multiple proteins (VP4 is virulence attachment protein, VP7 is antigen allowing fusion and entrance, VP6 is antibody target, VP2 is structural, VP1 is polymerase, and VP3 is transferase, stabilizing RNA)

life cycle:
- spikes attach, fuse, uncoats, inner and middle enter cell, enzymes 1 and 3 produce and extrude RNA, translation of proteins, gets into vessicle, transcribes new RNA, gets outer coating in ER, exits through vessicle or lysis

clinical:
-nausea, vommiting, WATERY PROFUSE DIARRHEA, dehydration, electrolyte imbalance, LACTIC ACIDOSIS - causing seizures and cardiac arrest

dx: wintertime, clinical, multiplex PCR

396
Q

norovirus- who is affected, proteins, clinical, dx

A
  • most common in humans globally, common from fall to spring. very infectious and resistant to heat and chlorine.
  • NON-SEGMENTED, has 5 geno groups, undergoes genetic drift (immunity not confered) VP1 CAPSID PROTEIN - site of antigenic variation. binds to BLOOD GROUP antigens on GI epithelial cells

clinical:
- no more than 2 days incubation, rapid onset, exposive watery diarrhea and foreceful vomitting, symptoms abate in 2-3 days, but shedding occurs up to a month after

dx: clinical, stool PCR

397
Q

poliovirus - what type of virus is it, kinds of polio, serotypes, transmission, clinical

A
  • enterovirus
  • WT polio, vaccine-associated (mutation in vaccine), vaccine-derived (non-immunized contacts)

3 serotypes - type 1 causes paralysis, no cross-immunity between serotypes, but immunity lasts a lifetime

transmission:
humans host, fecal-oral transmission, replicates in pharynx and gut and dissemiates

clinical:
1-2 week incubation, mostly mild - fever, sore throat, looks like you’re getting better, but then can progress to NONPARALYTIC - aseptic meningitis, stiff neck, lasts 5-10 days, can progress to PARALYTIC POLIO - flaccid paralysis and neural damage

can get CNS poliomyelitis and get respiratory failure and death

398
Q

types of latency, viruses included, and cell type affected

A

1) alpha (HSV 1, 2, VZV) - neuron latency
2) beta (CMV, HHV6, HHV7) monocyte/lymphocute latency
3) gamma (EBV, HHV8) - B lymphocyte latency

399
Q

glycoproteins in outer envelope of HSV

A

gB for infectivity, gD induces neutralizing antibodies (used in vaccine development), gH can trigger cell fusion, leading to multinucleated giant syncial cell formation of epithelial cells

400
Q

acute herpes - primary genital - incubation, clinical

A

5 day incubation

can get inflammation that spreads to meninges and causes urinary retention - ends up in dorsal root ganglia in sacral nerve roots

  • open sores/ulcers, regional lymphadenopathy
401
Q

acute herpes - primary oral - incubation, clinical

A

short incubation (2-12 days)

inflammation of gingiva and mouth, rapid ulceration, cervical lymphadenopathy

402
Q

HSV Keratitis

A

-corneal invovlement, has dendritic appearance, give topical treatment

403
Q

herpetic whitlow

A

on finger (dentists) HSV1, looks like bacterial infection

404
Q

dx of HSV

A
  • clinical
  • look for multinucleated giant cells
  • PCR
405
Q

Varicella Zoster Virus (VZV) - epidemiology, clinical, dx, complications

A
  • chicken pox (or shingles if reactivated)
  • also see multinucleated giant cells and nerve involvement (similar to herpes)

-see in children in late winter/spring - not in tropics

  • 2 week incubation, fever, rash on scalp and trunk that spreads to extremities
  • see vessicles AT DIFFERENT STAGES
  • looks like a dew drop on a rose petal

dx: lesions are characteristic, giant cells, tissue culture, PCR

complications:

  • big 3= hepatitis, pneumonia, encephalitis
  • superinfection with staph aureas
  • Reye’s syndrome (encephalopathy with liver disease)
  • Guilain Barre
406
Q

Shingles - clinical

A

usually on trunk - DOES NOT CROSS MIDLINE

  • can get post-herpetic neuralgia (persistent pain)
  • possible associated meningitis, lung liver and rain dissemination
407
Q

EBV - where is latency, clinical manifestations, dx

A

-latency in B lymphocytes

causes:

  • Mono (tonsillar exudates, anterior/posterior cervical LN, splenomegaly, palette petechiae)
  • Burkitt’s lymphoma (transformation of B lymphocytes causing formation of atypical T lymphocytes)
  • Hodgkin’s, nasopharyngeal carcinoma
  • hemolytic anemia, thrombocytopenia

dx: atypical lymphocytes (large basophilic vacules), elevation of transaminases

408
Q

CMV - where is latency, clinical manifestations, dx

A
  • latency in B lymphocytes (and others) DOWNREGULATES CD8 RESPONSE

clinical:

  • asymptomatic, mono-like, can cause congenital CMV (microcephaly, eye involvement, cerebral calcifications)
  • in immune compromised get (retinitis, pneumonitis, GI colitis, esophagitis, encephalitis, myelitis)

dx:
- OWL EYE INCLUSIONS, aggregates of CMV nuclear protein cores, biopsy, PCR, serology IgM and IgG

409
Q

HHV6 - manifestations, complications, dx

A

causes ROSEOLA and 6th disease

clinical:
abrupt high fever, SUBOCCIPITAL LYMPHADENOPATHY, abrupt dissapearance of fever, THEN RASH development - shot duration

complications:
sezures with high fever

dx: IgM and PCR

410
Q

HHV8 - manifestations

A

Kaposi sarcoma - epithelial cells

Castelman’s - B lymphocytes (focal or multicentric lymphomas associated with HIV)

411
Q

HIV retrovirus regulatory proteins (3)

A

tat- turns on replication and elongates viral transcripts

rev - promotes nuclear export of viral RNA

nef - downregulates host CD4 and MHC1

412
Q

HTLV1 subtypes (5)

A

1) caribbean
2) japanese
3) W Africa
4) C Africa
5) Melanesian

413
Q

cells that HTLV1 can affect

A

CD4
CD8
endothelial cells
fibroblasts

414
Q

HTLV1 regulatory genes (2)

A

tax (oncogenic, can lead to human T cell lymphoma) turns on replication

rex - promotes nuclear export of viral RNA

415
Q

HTLV1 manifestations (2)

A
  • human T cell lymphoma (bone involvement, hypercalcemia)

- myelopathy (total spastic paraparesis)

416
Q

Immune defects after HIV infection (4)

A

1) loss of CD4 number
2) loss of skintest reactivity/delayed type hypersensitivity
3) increased susceptibility to fungal, viral and protozoal infections
4) polyclonal gammopathy

417
Q

primary HIV infection timing

A

happens 2-4 weeks after exposure, would find RNA in blood

418
Q

GI and primary HIV infection

A

GALT can lose up to 60-80% of CD4 and Th17 cells - wipes out memory cells. damage causes leakage of bacteria and antigens into systemic circulation, driving persistent inflammation

419
Q

mechanism of CD4 depletion in HIV

A
  • apoptosis
  • HIV-mediated syncytia formation
  • destruction of immune precursor cells
420
Q

founder virus characteristics

A

CCR5/macrophage tropic, not CXCR4/T lymphocyte tropic

421
Q

elite non-controller polymorphism

A

CCR5 delta 32 variant - resistant to infection with HIV

422
Q

examples of passive immunization (4)

A

1-horse antibody for snake venom
2- tetanus (if you’re not vaccinated and you’re exposed)
3- IV Ig
4- monoclonal antibody preps (anti-eboa)

423
Q

variolation

A

introduction of dried pus from smallpox pustules into skin - first example of vaccination

424
Q

types of immunizations/acquired immunity (4)

A

1) systemic (mostly IgG, some IgM) productionafter injection of antigen
2) mucosal (secretory IgA mediated) oral or intranasal
3) herd immunity
4) secondary immunity (polio transferring to household members)

425
Q

example of live unattenuated vaccine

A

small pox - unattenuated cow pox

426
Q

examples of live attenuated vaccines (4)

A
  • BCG for TB
  • measles
  • rotavirus
  • intranasal flu
427
Q

examples of inactivated vaccines (3)

A
  • injected flu vaccine
  • inactivated polio
  • hepA
428
Q

examples of subunit vaccine

A
  • hep B

- meningococcal (carbohydrate capsule)

429
Q

conjugated capsular vaccines

A 
H flu B
Strep Pneumo (now 13 strains)
Neisseria meningititis (quadrivalent and separate group B for asplenics)
430
Q

guardasil

A 
4 = 6,11,16,18
9 = those + 31,33,45,52,58
431
Q

rotavirus vaccines

A

rotateq - live attenuated oral vaccine from cow rotavirus - quintavalent

rotarix - monovalent, derived from human

432
Q

adverse reaction for rubella vaccine

A

acute arthopathy

433
Q

adverse reaction for VZV vaccine

A

rash - can be infectious

434
Q

adverse reaction for previous pertussis vaccine

A

acute encephalopathy

435
Q

adverse reaction for oral polio

A

vaccine-associated paralytic poliomyleitis

436
Q

adverse reaction for yellow fever vaccine

A

1) neutropenic disease (aseptic meningitis/encephalitis in old and young)
2) viscerotropic (jaundice, renal, with thymus defective patients)

437
Q

thimersol

A

organomercurial preservative in multi-dose vials, been removed from all pediatric vaccines - repordetly associated with autism but not really

I3 (2 decks)

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