Third Exam - Week 6

Question 1

Impetigo

• how deep is it
• what’s it look like
• how does it feel

Answer 1

• superficial
• golden crusty “stuck on” appearance, not a lot of redness or inflammation
• not itchy, not painful

Question 2

Folliculitis

• how deep is it
• what’s it look like
• how does it feel

Answer 2

• hair follicle disease
• pustule with purulent discharge
• itchy

Question 3

Furuncle

• how deep is it
• what’s it look like
• how does it feel

Answer 3

• deeper folliculitis
• firm tender nodule, sometimes draining, (inside of nose), red and purulent
• painful, tender

Question 4

Carbuncle

• how deep is it
• what’s it look like
• how does it feel

Answer 4

• extensive furuncle into subcutaenous fat
• punched out lesion, lower extremities, not very purulent, has heaped border, inflammation
• painful

Question 5

Erysipelas

• how deep is it
• what’s it look like
• how does it feel

Answer 5

• superficial lymphatic involvement
• face and lower extremities, red, swelling, fairly well demarcated, clear border, can get bacteremia and fever in diabetics
• pain, red, hot

Question 6

Cellulitis

• how deep is it
• what’s it look like
• how does it feel

Answer 6

• spreading infection including sub-cutaneous tissues - deeper
• streaking, lymphanditis, warm, red, tender, ulcer (not escar), warm, acute fever, chills

Question 7

Necrotizing fasciitis

• how deep is it
• what’s it look like
• how does it feel

Answer 7

• 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

Question 8

Clostridial myonecrosis (gas gangrene)

• how deep is it
• what’s it look like
• how does it feel

Answer 8

• deep - musculoskeletal
• see subcutaneous air on xray or CT, sepsis, renal failure, fever - rapid progression, DOESN’T BLEED when cut - pale.
• painful, smelly

Question 9

Medullary osteomyelitis

• how deep is it
• what’s it look like
• how does it feel

Answer 9

• 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

Question 10

Superficial Osteomyelitis

• how deep is it
• what’s it look like
• how does it feel

Answer 10

• 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 -

Question 11

Infectious arthritis

• how deep is it
• what’s it look like
• how does it feel

Answer 11

• 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

Question 12

Septic bursitis

• how deep is it
• what’s it look like
• how does it feel

Answer 12

• 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

Question 13

Impetigo

• what’s it caused by
• who does it affect

Answer 13

• caused by group A strep (pyogenes) or staph aureas, in hot or humid weather
• any age, classic in children, highly communicable

Question 14

Folliculitis

• what’s it caused by
• who does it affect

Answer 14

• hot tub folliculitis, tight work-out clothes, dirty razor, staph aureus
• diabetics, athletes, people with hair

Question 15

Furuncle

• what’s it caused by
• who does it affect

Answer 15

• friction and hair follicles, perspiration, staph aureus

- develop from folliculitis

Question 16

Carbuncle

• what’s it caused by
• who does it affect

Answer 16

• either strep or secondary to lesion, pseudomonas in cancer patients
• extremes of age - children and old people

Question 17

Erysipelas

• what’s it caused by
• who does it affect

Answer 17

• strep pyogenes

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

Question 18

Cellulitis

• what’s it caused by
• who does it affect
• tx

Answer 18

• 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

Question 19

Necrotizing fasciitis

• what’s it caused by
• who does it affect
• tx

Answer 19

• 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

Question 20

Clostridial myonecrosis (gas gangrene)

• what’s it caused by
• who does it affect
• tx

Answer 20

• 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

Question 21

Medullary osteomyelitis

• what’s it caused by
• who does it affect
• tx

Answer 21

• caused by staph aureus - hematogenous spread, sometimes pseudomonas for IV drug users
• IV drug users
• IV tx (might be hard for drug users)

Question 22

Superficial Osteomyelitis

• what’s it caused by
• who does it affect
• tx

Answer 22

• 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.

Question 23

Infectious arthritis

• what’s it caused by
• who does it affect
• tx

Answer 23

• 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

Question 24

Septic bursitis

• what’s it caused by
• who does it affect
• tx

Answer 24

• caused by puncture- acute infection

- antibiotic tx

Question 25

Scabies - mode of transmission - site of infection - route of infection - likely host

Answer 25

- person to person, including STI and fomites - hands and feet, waistline and genitals - female bug burrows in skin and lays eggs (sperpinginous burrows)

Question 26

Scabies - clinical signs - diagnosis

Answer 26

- 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

Question 27

Scabies variants (2)

Answer 27

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

Question 28

Scabies | - treatment

Answer 28

- 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

Question 29

Lice variants (3)

Answer 29

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)

Question 30

Head lice - mode of transmission - site of infection - route of infection - likely host

Answer 30

- 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

Question 31

Body lice - mode of transmission - site of infection - route of infection - likely host

Answer 31

- 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)

Question 32

Pubic lice - mode of transmission - site of infection - route of infection - likely host

Answer 32

- sexual contact - pubic hair - sexual transmission - lice from person to person, same as other lice - sexually active adults

Question 33

Lice - clinical signs - diagnosis

Answer 33

- 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

Question 34

Lice | - treatment

Answer 34

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

Question 35

Bed bugs - mode of transmission - site/route of infection - clinical signs - tx

Answer 35

- 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.

Question 36

Tungiasis - AKA - mode of transmission - site/route of infection - clinical signs - tx

Answer 36

- 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

Question 37

Myasis - AKA - mode of transmission - site/route of infection - clinical signs - tx

Answer 37

- 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

Question 38

Amphotericin B | - molecular mechanism

Answer 38

- binds egosterol forming artificial pores (bad for fungus, good for us)

Question 39

Amphotericin B - use - mode of administration

Answer 39

- broadest spectrum for systemic fungal infections - pregnancy category B - preferred over axoles and capsofungin - NOT through BBB - give IV - no oral absorption

Question 40

Amphotericin B | - toxicity

Answer 40

- long term use associated with neprhotoxicity (later generations have hepatotoxicity instead)

Question 41

Nystatin - mechanism - use

Answer 41

- same as amphotericin - parental administration - can be used topically for thrush

Question 42

Azoles | - mechanism

Answer 42

- egosterol synthesis inhibitor - binds to and inhibits cytochrome p450 in fungi

Question 43

Flucanozole - use - toxicity

Answer 43

- 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

Question 44

Itraconazole - use - toxicity

Answer 44

- poor CNs penetration - good for dimorphic fungi - toxicity, congestive heart disease, CYP3A4 inhibition (many drug-drug)

Question 45

Voriconazole - use - toxicity

Answer 45

- 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)

Question 46

Capsofungin/Echinocandin - mechanism - mode of administration - use - toxicity

Answer 46

- 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

Question 47

Griseofulvin - mechanism - use - toxicity

Answer 47

- 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.

Question 48

Terbinafine - AKA - mechanism - use - administration mode - toxicity

Answer 48

- 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)

Question 49

Flucytosine - mechanism - use - toxicity

Answer 49

- 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)

Question 50

Type 1 hypersensitivity - immune mediator - antigen (soluble? surface?) - effector mechanism - example of reaction

Answer 50

- IgE - soluble antigen - mast-cell activation - allergic rhinitis, asthma, systemic anaphylaxis, atopic dermatitis

Question 51

Type 2 hypersensitivity (2) - immune mediator - antigen (soluble? surface?) - effector mechanism - example of reaction

Answer 51

- 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)

Question 52

Type 3 hypersensitivity - immune mediator - antigen (soluble? surface?) - effector mechanism - example of reaction

Answer 52

- IgG - soluble antigen (immune complex) - complement - phagocytes - serum sickness, arthrus reaction, syphilis treponema

Question 53

Type 4 hypersensitivity (3) - immune mediator - antigen (soluble? surface?) - effector mechanism - example of reaction

Answer 53

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

Question 54

example of genetic succeptability for hypersenstivity reactions

Answer 54

atopic dermatitis - Th2 response, IgE, type 1 hypersensitivty

Question 55

Steps for sensitization in Type 1 hypersensitivity rxn (6)

Answer 55

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

Question 56

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

Answer 56

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

Question 57

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

Answer 57

type 4

Question 58

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

Answer 58

``` vascular leak broncho constriction interstinal hypermotility (histamine) ```

Question 59

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

Answer 59

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

Question 60

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

Answer 60

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

Question 61

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

Answer 61

tissue damage/ remodel CT matrix (tryptase)

Question 62

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

Answer 62

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

Question 63

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

Answer 63

tissue remodeling (eosinophil peroxidase)

Question 64

chronic allergen exposure results in what (4 things)

Answer 64

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

Question 65

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

Answer 65

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

Question 66

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

Answer 66

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

Question 67

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

Answer 67

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

Question 68

2 examples of arthus reaction

Answer 68

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)

Question 69

serum sickness is what kind of hypersensitivity reaction?

Answer 69

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

Question 70

3 types of type 4 hypersensitivity reactions (and examples)

Answer 70

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

Question 71

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

Answer 71

- 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

Question 72

Celiac disease (mechanism, reaction)

Answer 72

- 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

Question 73

Granuloma formation (mechanism, Th mediated, reaction)

Answer 73

- 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

Question 74

2 categories of granulomas

Answer 74

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

Question 75

what molecules mediate signaling for effector function of granuloma

Answer 75

CD40 on macrophage, CD40L on T cell

Question 76

Th17 is related to what disease

Answer 76

psoriasis

Question 77

first generation histamine antagonists

Answer 77

- diphenhydramine - doxylamine - chlorpheniramine

Question 78

second generation histamine antagonists

Answer 78

- loratadine (claritin) - cetirizine (zyrtec) - fexofenadine (allegra)

Question 79

endogenous histamine synthesis and metabolism

Answer 79

- 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

Question 80

what is an autacoid

Answer 80

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

Question 81

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

Answer 81

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

Question 82

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

Answer 82

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

Question 83

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

Answer 83

get O or A | have antibodies to B

Question 84

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

Answer 84

get O or B | have antibodies to A

Question 85

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

Answer 85

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

Question 86

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

Answer 86

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

Question 87

describe the mouse study for histocompatibility (skin transplants)

Answer 87

- 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)

Question 88

why do we have T cells that recognize non-self MHC? | What is the clinical significance of this in terms of transplants?

Answer 88

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)

Question 89

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

Answer 89

- 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

Question 90

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

Answer 90

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)

Question 91

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

Answer 91

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)

Question 92

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)

Answer 92

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.

Question 93

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

Answer 93

- pregnancy - giving birth exposes you to paternal HLA - previous transplant rejection - multiple transfusions

Question 94

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

Answer 94

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

Question 95

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

Answer 95

- 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

Question 96

Graft vs. Host (mechanism, timing, avoidance)

Answer 96

- 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

Question 97

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

Answer 97

- serologic testing (cross-match) - molecular (DNA PCR) - cellular (mixed lymphocyte culture)

Question 98

Cross-match test

Answer 98

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?

Question 99

Mixed Lymphocyte Reaction

Answer 99

- 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)

Question 100

Immunosuppressive therapies to avoid rejection (6)

Answer 100

- 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)

Question 101

genes that are associated with autoimmunity (5)

Answer 101

- AIRE (APECED) - CTLA4 (Graves) - FOXP4 (IPEX) - FAS (autoimmune lymphoproliferative syndrome) - C1q (SLE)

Question 102

molecular mimicry (mechanism and example)

Answer 102

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)

Question 103

bystander activation (mechanism and example)

Answer 103

- 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

Question 104

Epitope spreading (mechanism and spreading)

Answer 104

- 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

Question 105

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

Answer 105

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

Question 106

pemphigus vulgaris is what type of hypersensitivity reaction

Answer 106

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

Question 107

subacute bacterial endocarditis is what type of hypersensitivity reaction

Answer 107

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

Question 108

autoimmune hemolytic anemia is what type of hypersensitivity reaction

Answer 108

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

Question 109

insulin-dependent diabetes mellitus is what type of hypersensitivity reaction

Answer 109

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

Question 110

MS is what type of hypersensitivity reaction

Answer 110

type 4 - T cell destruction of myelin

Question 111

graves disease is what type of hypersensitivity reaction?

Answer 111

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

Question 112

rheumatoid arthritis is what type of hypersensitivity reaction

Answer 112

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

Question 113

myasthenia gravis is what type of hypersensitivity reaction

Answer 113

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

Question 114

psoriasis is what type of hypersensitivity reaction

Answer 114

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

Question 115

genetic pathway therapeutic targets for autoimmune diseases (6)

Answer 115

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

Question 116

Give example of co stimulatory target for therapy against autoimmune disorders

Answer 116

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

Question 117

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

Answer 117

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

Question 118

example of inflammatory mediator for target of therapy against autoimmune disorders

Answer 118

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

Question 119

histamine has 3 roles, what are they

Answer 119

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

Question 120

what does cromolyn do to histamine

Answer 120

cromolyn blocks release of histamine

Question 121

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

Answer 121

- G protein coupled receptor (Gq) - endothelium, CNS - increases NO, increases cGMP, increases IP3

Question 122

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

Answer 122

- G protein coupled receptor (Gs) - vascular smooth muscle - increases cAMP

Question 123

what effect does histamine cause on vascular smooth musche

Answer 123

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

Question 124

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

Answer 124

bronchocontsriction via H1 receptors (increases in asthma)

Question 125

what effect does histamine have on the peripheral nervous system

Answer 125

- acts as autocoid - stimulates primary afferent nerve endings (itch, pain) - H1 receptor

Question 126

what effect does histamine have on cns

Answer 126

- acts as neurotransmitter - regulate wakefulness, appetite and body temp - via post-synaptic H1

Question 127

what effect does histamine have on GI

Answer 127

- acts as secretagogue | - stimulates gastric acid release (H2) and increased motility (H1, H2, H4)

Question 128

histamine toxicity

Answer 128

- found in spoiled tuna, causing nausea vomiting but can be suppressed by H1 receptor blockers

Question 129

is anaphylaxis caused by histamine

Answer 129

no.

Question 130

what local allergic reactions do histamine cause

Answer 130

``` urticaria (hives) allergic rhinitis (hay fever) ```

Question 131

pharmacotherapy for sub-acute and preventative allergies

Answer 131

inhaled steroids (flonase)

Question 132

mast cell stabilizers (pharmacotherapy)

Answer 132

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

Question 133

first generation antihistamines list and notable characteristics

Answer 133

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

Question 134

first generation antihistamines mechanism of action

Answer 134

- inverse agonists - all lipid soluble - crosses BBB, placenta and breast milk - metabolized in liver, cleared in renal

Question 135

first generation antihistamines adverse reactions

Answer 135

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

Question 136

first generation antihistamines vulnerable patients

Answer 136

- renal/liver issues - elderly - pregnancy - nenonates/infants (CNS stimulation)

Question 137

second generation antihistamines list and notable features

Answer 137

- fexofenadine (Excreted unchanged, transported by OATP1A2, don't drink orange, grapefruit, apple juice) - loratidine (24hr duration) - cetirizine (24hr duration, metabolite of hydroxyzine)

Question 138

second generation antihistamines characteristics and uses

Answer 138

- 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

Question 139

second generation antihistamine adverse effects

Answer 139

- less than first gen - no CNS penetration - no sedation

Question 140

promethazine uses

Answer 140

motion sickness and morning sickness (first gen)

Question 141

incidence vs prevalence

Answer 141

``` incidence = new diagnoses over time prevalence = people who have it right now ```

Question 142

quarantine vs isolation

Answer 142

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

Question 143

epidemic triad

Answer 143

host, environment, agent

Question 144

steps for outbreak investiagion (9)

Answer 144

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

Question 145

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

Answer 145

candida aspergillus mucor infections

Question 146

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

Answer 146

``` cryptococcus neoformans pneumocystic jirovecii blastomyces dermatitidis coccidiodes immitis histoplasma capsulatum ```

Question 147

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

Answer 147

-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

Question 148

superficial mycoses diagnosis and treatment

Answer 148

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

Question 149

cutaneous mycoses - characteristics and types (6)

Answer 149

- 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)

Question 150

cutaneous mycoses - diagnosis and treatment

Answer 150

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

Question 151

subcutaneous mycoses - characteristics and types (3)

Answer 151

``` 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 ```

Question 152

lymphocutaneous sporotrichosis - caused by, clinical, dx

Answer 152

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

Question 153

chromoblastomycosis- caused by, clinical, dx

Answer 153

- 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

Question 154

eumycetoma mycetoma - caused by, clinical, dx

Answer 154

- 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

Question 155

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

Answer 155

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

Question 156

blastomyces dermatitidis - geographic distribution, clinical, dx, tx

Answer 156

- 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

Question 157

coccidioides immitis- geographic distribution, clinical, dx, tx

Answer 157

- 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

Question 158

histoplasma capsulatum- geographic distribution, clinical, dx, tx

Answer 158

- 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

Question 159

paracoccidioides brasiliensis - geographic distribution, clinical, dx, tx

Answer 159

- 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

Question 160

Opportunistic infections- characteristics and list (5)

Answer 160

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

Question 161

opportunistic infections that affect hosts with neutrophil defects

Answer 161

- aspergillus - candida - zygomyces (mucor, rhizopus, absidia)

Question 162

opportunistic infections that affect hosts with T cell defects

Answer 162

- cryptococcus neoformans | - pneumocystic jirovecii

Question 163

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

Answer 163

- 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

Question 164

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

Answer 164

- 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

Question 165

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

Answer 165

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

Question 166

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

Answer 166

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

Question 167

pneumocystic jirovecii - characteristics, clinical, dx, tx

Answer 167

- 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)

Question 168

papule

Answer 168

less than 1 cm, raised, erythematous

Question 169

plaque

Answer 169

more than 1 cm with scale

Question 170

maccule

Answer 170

discoloration, flat, less than 1 cm

Question 171

patch

Answer 171

discoloration, flat, more than 1 cm

Question 172

nodule

Answer 172

greater than 1 cm, more elevated than wide

Question 173

vessicle

Answer 173

less than 1 cm, clear fluid

Question 174

bulla

Answer 174

more than 1 cm, clear fluid

Question 175

pustule

Answer 175

less than 1 cm, neutrophilic fluid

Question 176

wheal

Answer 176

plaque or papule, erythematous with pale center

Question 177

lichenification

Answer 177

thickened

Question 178

acanthosis

Answer 178

elongated rete (downward epidermal projections into dermis)

Question 179

parakeratosis

Answer 179

retained nuclei in stratum corneum (seen in psoriasis)

Question 180

urticaria

Answer 180

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

Question 181

erythema multiforme

Answer 181

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

Question 182

spongiosus - eczema

Answer 182

- 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)

Question 183

psoriasiform

Answer 183

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

Question 184

lichenoid

Answer 184

- 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

Question 185

deep lupus erethymatosus

Answer 185

thick plauqes, hard to treat - scarring, hair loss - deep inflitrate, has interface change like erethyma multiforme, but deep inflammation - see Ig in IF

Question 186

acne vulgaris

Answer 186

- comedones - blackheads, follicular obbstruction, sebum obstruction in pilosebaceous apparatus - holocrine secretion

Question 187

seborrheic keratosis

Answer 187

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

Question 188

actinic keratosis

Answer 188

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

Question 189

keratoacanthoma

Answer 189

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

Question 190

SCC

Answer 190

UV risk factor - entire thickness atypical keratinocytes - dermal - nodules, frequently ulcerated - invasive - atypical keratinocytes attached to dermal/epidermal jucntion and extend into dermal stroma

Question 191

BCC

Answer 191

common, slow growing (cant treat with chemo) - associated iwth PTCH gene mutation - tumor cells are basophilic (squamous is pink)

Question 192

nevi

Answer 192

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

Question 193

types of benign nevi

Answer 193

- 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

Question 194

dysplastic nevi

Answer 194

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

Question 195

melanoma

Answer 195

risk - blonde, blue eyed, sun exposure, family hx - ABCD - staging - breslow thickness, ulceration and mitotic rate - BRAF mutation

Question 196

merkel cell carcinoma

Answer 196

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

Question 197

dermatofibroma

Answer 197

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

Question 198

neurofibroma

Answer 198

modified schwann cells, delicate stroma and collagen

Question 199

hemangioma

Answer 199

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

Question 200

cysts

Answer 200

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

Question 201

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

Answer 201

- 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)

Question 202

seborrheic dermatitis - associated pathogen, clinical

Answer 202

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

Question 203

pityriasis rosea - associated pathogen, clinical

Answer 203

- 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)

Question 204

Pityriasis lichenoides

Answer 204

goes from PLEVA to PLC - PLEVA in young children (crusted, vesicular pustules) - PLC (chronica, in adults, red-brown scaley papules)

Question 205

small/large parapsoriasis

Answer 205

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

Question 206

pityriasis rubra pilaris

Answer 206

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

Question 207

lichen planus

Answer 207

- violacious papules - wickhman's striae (mouth) - increased risk of SCC - sometimes caused by drug eruptions (ace inhibitors erc.)

Question 208

atopic dermatitis

Answer 208

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

Question 209

allergic contact dermatitis

Answer 209

- burning, itching acneform eruption - acute (vesicular eruption) - chronic (lichenified plaque)

Question 210

stasis dermatitis

Answer 210

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

Question 211

malaria - species (5)

Answer 211

- plasmodium faciparum (most mortality) - plasmodium vivax (has hypnozoites) - plasmodium ovale (has hypnozoites) - plasmodium malariae - plasmodium knowlesi (monkey and human)

Question 212

malaria - who dies from it

Answer 212

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

Question 213

malaria - life cycle of protozoa

Answer 213

- 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

Question 214

complicated malaria- cause, manifestations (2)

Answer 214

- 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

Question 215

Genetic factors for malaria

Answer 215

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

Question 216

malaria diagnosis

Answer 216

- 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)

Question 217

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

Answer 217

- 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

Question 218

Giardia Intestinalis -transmission, forms, clinical, dx

Answer 218

- 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

Question 219

cryptosporidium - transmission, life cycle, clinical, dx

Answer 219

- 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

Question 220

cyclosporiasis - differences

Answer 220

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

Question 221

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

Answer 221

- 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)

Question 222

trypanosomiasis - types (2),

Answer 222

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

Question 223

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

Answer 223

- 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

Question 224

chagas disease - species, life cycle, clinical, dx

Answer 224

- 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

Question 225

Leishmaniasis - transmission, types (3)

Answer 225

``` transmitted via sand fly 3 types: - visceral - cutaneous - mucocutaneous ```

Question 226

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

Answer 226

- 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

Question 227

cutaneous leishmaniasis - species, clinical, dx

Answer 227

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

Question 228

mucocutaneous leishmanisis - species, clinical

Answer 228

- only braziliensis species - only in S America - causes oral/nasal mucosal lesions as well as cutaneous

Question 229

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

Answer 229

- 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)

Question 230

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

Answer 230

- 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

Question 231

Quinolones - mechanism of action, examples

Answer 231

- weak bases, gets protonated and trapped in food vacuole, inhibiting polymerization of heme -- toxic to plasmodium examples: - chloroquine phosphate - quinine sulfate/quinidine - primaquine

Question 232

Chloroquine - works against, resistance, adverse effects, contraindications

Answer 232

- 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

Question 233

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

Answer 233

- 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

Question 234

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

Answer 234

- 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

Question 235

adjunctive therapies with quinolones

Answer 235

- doxycycline - use for prophylaxis also | - clindamycin

Question 236

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

Answer 236

- 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

Question 237

proguanil - active against, mechanism, use, metabolism

Answer 237

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

Question 238

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

Answer 238

- 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

Question 239

what malaria drugs can you use in pregnancy (3)

Answer 239

- chloro (if not resistant) - clinda and quinine - mefloquine

Question 240

what can you use for prophylaxis (5)

Answer 240

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

Question 241

nematodes: subsets, types (12)

Answer 241

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)

Question 242

Soil transmitted helminths

Answer 242

- ascaris lumbricoides, hookworm, whipworm | "unholy trinity"

Question 243

ascaris lumbricoides - life cycle, clinical, dx

Answer 243

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

Question 244

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

Answer 244

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

Question 245

trichuris trichuria - characteristics, life cycle, clinical, dx

Answer 245

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

Question 246

enterobius vermicularis - geography, life cycle, clinical, dx

Answer 246

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

Question 247

strongyloides stercoralis - geography, life cycle, clinical, dx

Answer 247

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

Question 248

toxocariasis - life cycle, clinical

Answer 248

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

Question 249

anisakiasis - clinical

Answer 249

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

Question 250

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

Answer 250

- 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

Question 251

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

Answer 251

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

Question 252

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

Answer 252

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

Question 253

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

Answer 253

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

Question 254

dracunculus medinensis - transmission, life cycle, clinical, dx

Answer 254

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

Question 255

trematodes - classifications and types (6)

Answer 255

liver flukes: - fasciola hepatica - opsithorchis viverrini - clonorchis sinesis lung flukes: - paragonimus blood flukes: - schistosoma mansoni - schistosoma haematobium

Question 256

fasciola hepatica - geographic distribution, transmission, clinical

Answer 256

- S America, Iran, Egypt - get it by eating watercress - can get blockage of BILE DUCT and abcess formation

Question 257

opsithorchis viverrini - geographic distribution, transmission, clinical

Answer 257

- 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

Question 258

paragonimus - geographic distribution, transmission, clinical

Answer 258

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

Question 259

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

Answer 259

- 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)

Question 260

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

Answer 260

- 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

Question 261

cestodes - kinds (2)

Answer 261

taenia - beef (saginata), pork (solium)

Question 262

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

Answer 262

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

Question 263

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

Answer 263

- 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

Question 264

diphyllobothrium latum - geographic location, transmission, clinical

Answer 264

- fish tapeworm - usually from Scandinavia - from copepod and freshwater fish - association with B12 deficiency

Question 265

echinococcus - transmission, life cycle, clinical, tx

Answer 265

- 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)

Question 266

Benzimidazole -includes, mechanism, use, resistance

Answer 266

- 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

Question 267

mebendazole - use, oral/IV, tox/contraindications

Answer 267

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)

Question 268

albendazole- use, oral/IV tox/contraindications

Answer 268

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)

Question 269

Avermectin - includes, mechanism, use, tox, resistance

Answer 269

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

Question 270

Diethylcarbamazine mechanism, use, tox, resistance

Answer 270

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.

Question 271

pyrantel pamoate -mechanism, use, tox

Answer 271

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

Question 272

praziquantel- mechanism, use, tox, resistance

Answer 272

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

Question 273

Antiherpes/AntiCMV agents (3)

Answer 273

- acyclovir - gancyclovir - foscarnet

Question 274

Anti-influenza (2)

Answer 274

- amantidine (no longer in use) - osetamivir - zanamivir

Question 275

nucleoside reverse transcriptase inhibitors (NRTIs) (3)

Answer 275

- AZT - Abacavir - lamivudine/emtricitibine

Question 276

nucleotide reverse transcriptase inhibitor (NRTI) (1)

Answer 276

-tenofovir

Question 277

non-nucleoside reveres transcriptase inhibitors (1)

Answer 277

- efavirenz

Question 278

protease inhibitors (3)

Answer 278

- ritonavir - darunavir - atazanavir

Question 279

fusion/entry/integration inhibitors (3)

Answer 279

- enfuvirtide - maraviroc - dolutegravir

Question 280

acyclovir - use, mechanism, tox, resistance

Answer 280

- 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

Question 281

gancyclovir- use, mechanism, tox, resistance

Answer 281

- 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

Question 282

Foscarnet- use, mechanism, tox, resistance

Answer 282

- 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

Question 283

oseltamivir- use, mechanism, resistance

Answer 283

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

Question 284

zanamivir

Answer 284

- used for resistant oseltamivir | - approved for children 7 y/o and up

Question 285

abacavir - use, mechanism, resistance, tox

Answer 285

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

Question 286

lamivudine/emtricitibine - use, mechanism, resistance, tox

Answer 286

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

Question 287

tenofovir - use, mechanism, resistance, tox

Answer 287

- 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) ```

Question 288

efavirenz - use, mechanism, resistance, tox

Answer 288

- 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

Question 289

ritonavir - use, mechanism, resistance, tox

Answer 289

- 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

Question 290

Darunavir - use, mechanism, tox

Answer 290

- 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

Question 291

atazanavir- use, mechanism, tox

Answer 291

- 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

Question 292

enfuvirtide- use, mechanism, tox

Answer 292

- 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

Question 293

maraviroc- use, mechanism, tox

Answer 293

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

Question 294

dolutegravir- use, mechanism, tox

Answer 294

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

Question 295

3 categories of drug reactions

Answer 295

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

Question 296

exanthems

Answer 296

- maculopapular, morbilliform or scarlatiniform - 12 weeks after exposure - BLANCHABLE - urticarial but fixed

Question 297

drug hypersensitivity syndrome

Answer 297

- really sick, upset stomach, weakness, fever | - caused by anticonvulsants (prominent edema), sulfa drugs (borderline purpura), allopurinol (CAN BE MONTHS LATER)

Question 298

Anaphylaxis

Answer 298

type 1, IgE mediated | anaphylactoid is NOT immunologically driven

Question 299

Urticarial hives

Answer 299

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

Question 300

angioedema

Answer 300

deeper - see LIP SWELLING, RESP DISTRESS | caused by Ace Inhibitors (can happen at ANY TIME)

Question 301

acute generalized exanthematous pustulosis

Answer 301

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)

Question 302

Steven jonson's syndrome

Answer 302

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

Question 303

TEN

Answer 303

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

Question 304

drug induced vasculitis

Answer 304

``` 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 ```

Question 305

phototoxic rxn

Answer 305

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

Question 306

photoallergic rxn

Answer 306

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

Question 307

where is the separation in pemphigus vulgaris?

Answer 307

above the basal keratinocytes

Question 308

what would direct IF look like for pemphigus vulgaris

Answer 308

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

Question 309

are the bullae fragile or strong from pemphigu vulgaris?

Answer 309

fragile - get erosion

Question 310

where is the separation in pehmphigus folleaceous

Answer 310

more superficial. no mucosal involvement

Question 311

what would direct IF look like for pehmphigus foleaceous

Answer 311

chickenwire, but more superficial. only desmoglein 1

Question 312

bullous pemphigoid affects what patient population mostly

Answer 312

older people

Question 313

where is the separation in bullous pemphigoid

Answer 313

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

Question 314

how does bullous pemphigoid feel in comparison to vulgaris

Answer 314

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

Question 315

what do you see in IF for bullous dermatosis

Answer 315

linear IgA - antibody to proteins in hemidesmosome

Question 316

dermatitis herpetiformis

Answer 316

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

Question 317

epidermolysis bullosa

Answer 317

genetic simplex defect at keratin 5 and 14 different severities (junctional, deep, or dystrophic)

Question 318

what virus is associated iwth oral hairy leukoplakia

Answer 318

EBV

Question 319

oral ulcers are associated with what virus

Answer 319

HSV-1/2 and CMV (usually larger)

Question 320

genital ulcers are associated with what virus

Answer 320

HSV, but you can get secondary bacterial infection

Question 321

Bacillary angiomatosis (cutaneous infection) is associated with what pathogen

Answer 321

bartonella

Question 322

molluseum contagiosum is associated iwth what pathogen

Answer 322

pox-virus. forms umbillicated lesions

Question 323

ocular opportunistic infections are associated iwth what pathogen

Answer 323

CMV retinitis

Question 324

HIV penumonia is caused by what pathogen

Answer 324

pneumocystis jirovecii

Question 325

HIV= related GI infections are related to what pathogen

Answer 325

- CMV (watery diarrhea, odynophagia, cholecystitis, proctitis) - cryptosporidium (unremitting diarrhea, chonecystitis) - parasitic (microsporidium, giardia, entamoeba histolytica)

Question 326

HIV CNS infections are related to what pathogen

Answer 326

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

Question 327

disseminated HIV infection caused by

Answer 327

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

Question 328

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

Answer 328

almost a year

Question 329

what happens to thymus as we age

Answer 329

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

Question 330

pattern of disease for T cell mediated immune defect

Answer 330

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

Question 331

pattern of disease for B cell/humoral immune defect

Answer 331

- URIs | - GI infections

Question 332

pattern of disease for phagocytic immune defect

Answer 332

- bacteria (extracellular strep/staph), fungal, and sometimes mycobacteria if you have neutrophil defect

Question 333

pattern of disease for complement immune defect

Answer 333

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

Question 334

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

Answer 334

phagocyte defect

Question 335

genetic causes of SCID

Answer 335

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

Question 336

DiGeorge's syndrome

Answer 336

- 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

Question 337

Btk deficiency

Answer 337

- 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

Question 338

X-linked Hyper-IgM syndrome

Answer 338

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

Question 339

IgA deficiency

Answer 339

- 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)

Question 340

common variable immunodeficiency (CVID)

Answer 340

seen in teenagers adults - defect in B cell differeitiation - molecular basis unknown - highly associated with autommunity

Question 341

familial hemophagocytic syndromes

Answer 341

- 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

Question 342

X-linked lymphoproliferative disease

Answer 342

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

Question 343

chronic mucucutenous candidiasis

Answer 343

- 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)

Question 344

Hyper IgE syndrome (Job's syndrome)

Answer 344

- 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.

Question 345

Wiskott-Aldrich syndrome

Answer 345

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)

Question 346

Ataxia-Telangiesctasia

Answer 346

multi-system involvement - associated iwth defects in DNA repair - increased malignancies - T cell developmental defect (associated with somatic recombination)

Question 347

FAS mutations cause

Answer 347

autoimmune lymphoproliferative syndrome

Question 348

IPEX mutations cause

Answer 348

Treg deficiency/decreased function

Question 349

Toll-like receptor signalling issues

Answer 349

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

Question 350

IFN-alpha defects

Answer 350

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

Question 351

Chronic granulomatous disease

Answer 351

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

Question 352

Leukocyte adhesion deficiency (LAD-1)

Answer 352

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)

Question 353

Chediak-Higashi syndrome

Answer 353

defects in LYSOSOMAL GRANULE maturation - neutrophils have big granules - get recurrent infections and have melanin deposition issues - can have albinism

Question 354

C3 defect

Answer 354

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

Question 355

C1-q, c2, c4 defects

Answer 355

difficulty with immune clearance

Question 356

membrane attack complexes defects

Answer 356

Neisseria infections, NOT ASSOCIATED WITH IMMUNE COMPLEXES

Question 357

C1 esterase inhibitor defect

Answer 357

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

Question 358

paramyxoviruses types

Answer 358

rubulavirus (mumps) | morbillivirus (measels)

Question 359

togavirus types

Answer 359

``` alpha virus (chikungunya) rubivirus (rubella) ```

Question 360

pneumovirus types

Answer 360

pneumovirus | metapneumovirus

Question 361

F protein is important for

Answer 361

fusion

Question 362

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

Answer 362

- 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

Question 363

mumps- classic clinical, complications

Answer 363

- 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

Question 364

respiratory syncytial virus- classic clinical, complications

Answer 364

- 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

Question 365

metapneumovirus - who/when infected, clinical, dx

Answer 365

- 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

Question 366

Rubela - clinical, seasonality, pattern of infectiousness

Answer 366

- 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

Question 367

congenital rubella syndrome

Answer 367

- 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

Question 368

influenza - clinical, dx

Answer 368

- 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

Question 369

antigenic drift and influenza

Answer 369

H and N antigenicity changes - minor alterations

Question 370

reassortment and influenza

Answer 370

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

Question 371

antigenic shift and influeza

Answer 371

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

Question 372

H5N1 - transmission, mortality

Answer 372

bird to human (need close bird contacts to contract) - limited human-to-human transmission high mortality (50%)

Question 373

arboviruses - include what classes/viruses

Answer 373

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

Question 374

St. Louis encephalitis - transmission, clinical, dx

Answer 374

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

Question 375

West Nile - transmission, clinical, dx

Answer 375

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

Question 376

Dengue

Answer 376

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

Question 377

yellow fever - transmission, clinical, dx

Answer 377

-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

Question 378

Chikungunya - transmission, clinical, dx

Answer 378

"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

Question 379

Zika - transmission, clinical, dx

Answer 379

- 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

Question 380

SARS - type of virus, transmission, clinical, dx

Answer 380

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

Question 381

MERS - type of virus, transmission, clinical, dx

Answer 381

-coronavirus - bats and camels ARABIAN PENINSULA clinical: - severe pneumonia GI, cough fever dx: - PCR lower respiratory

Question 382

Ebola - type of virus, transmission, clinical

Answer 382

- 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)

Question 383

types of adenovirus infections (3)

Answer 383

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

Question 384

pathonmeumonic clinical indications for adenovirus

Answer 384

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

Question 385

parvovirus B19 - cells infected, manifestations

Answer 385

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)

Question 386

5 viral families that cause the common cold

Answer 386

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

Question 387

sinusitis - progression, clinical, dx, tx

Answer 387

- 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

Question 388

pharyngitis - pathogens, clinical, dx

Answer 388

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

Question 389

epiglottitis - pathogen, clinical, dx

Answer 389

- 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

Question 390

croup - pathogen, clinical

Answer 390

only viral affects kids between 3 and 36 months laryngeaotracheal bronchitis, seal bark, preceded by URI, can get spasmodic recurrent croup

Question 391

otitis media - pathogens

Answer 391

H. flu, strep pneumo, common cold viruses

Question 392

otitis externa - manifestations (3)

Answer 392

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)

Question 393

acute bronchitis - clinical

Answer 393

- healthy person with incessant cough, somtimes productive - viral cause. - post-nasal drip, sputum, fever, chest pain due to inflamed trachea NO ANTIBIOTICS

Question 394

Chronic bronchitis - clinical

Answer 394

- 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

Question 395

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

Answer 395

- 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

Question 396

norovirus- who is affected, proteins, clinical, dx

Answer 396

- 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

Question 397

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

Answer 397

- 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

Question 398

types of latency, viruses included, and cell type affected

Answer 398

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

Question 399

glycoproteins in outer envelope of HSV

Answer 399

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

Question 400

acute herpes - primary genital - incubation, clinical

Answer 400

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

Question 401

acute herpes - primary oral - incubation, clinical

Answer 401

short incubation (2-12 days) inflammation of gingiva and mouth, rapid ulceration, cervical lymphadenopathy

Question 402

HSV Keratitis

Answer 402

-corneal invovlement, has dendritic appearance, give topical treatment

Question 403

herpetic whitlow

Answer 403

on finger (dentists) HSV1, looks like bacterial infection

Question 404

dx of HSV

Answer 404

- clinical - look for multinucleated giant cells - PCR

Question 405

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

Answer 405

- 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

Question 406

Shingles - clinical

Answer 406

usually on trunk - DOES NOT CROSS MIDLINE - can get post-herpetic neuralgia (persistent pain) - possible associated meningitis, lung liver and rain dissemination

Question 407

EBV - where is latency, clinical manifestations, dx

Answer 407

-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

Question 408

CMV - where is latency, clinical manifestations, dx

Answer 408

- 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

Question 409

HHV6 - manifestations, complications, dx

Answer 409

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

Question 410

HHV8 - manifestations

Answer 410

Kaposi sarcoma - epithelial cells Castelman's - B lymphocytes (focal or multicentric lymphomas associated with HIV)

Question 411

HIV retrovirus regulatory proteins (3)

Answer 411

tat- turns on replication and elongates viral transcripts rev - promotes nuclear export of viral RNA nef - downregulates host CD4 and MHC1

Question 412

HTLV1 subtypes (5)

Answer 412

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

Question 413

cells that HTLV1 can affect

Answer 413

CD4 CD8 endothelial cells fibroblasts

Question 414

HTLV1 regulatory genes (2)

Answer 414

tax (oncogenic, can lead to human T cell lymphoma) turns on replication rex - promotes nuclear export of viral RNA

Question 415

HTLV1 manifestations (2)

Answer 415

- human T cell lymphoma (bone involvement, hypercalcemia) | - myelopathy (total spastic paraparesis)

Question 416

Immune defects after HIV infection (4)

Answer 416

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

Question 417

primary HIV infection timing

Answer 417

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

Question 418

GI and primary HIV infection

Answer 418

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

Question 419

mechanism of CD4 depletion in HIV

Answer 419

- apoptosis - HIV-mediated syncytia formation - destruction of immune precursor cells

Question 420

founder virus characteristics

Answer 420

CCR5/macrophage tropic, not CXCR4/T lymphocyte tropic

Question 421

elite non-controller polymorphism

Answer 421

CCR5 delta 32 variant - resistant to infection with HIV

Question 422

examples of passive immunization (4)

Answer 422

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)

Question 423

variolation

Answer 423

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

Question 424

types of immunizations/acquired immunity (4)

Answer 424

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)

Question 425

example of live unattenuated vaccine

Answer 425

small pox - unattenuated cow pox

Question 426

examples of live attenuated vaccines (4)

Answer 426

- BCG for TB - measles - rotavirus - intranasal flu

Question 427

examples of inactivated vaccines (3)

Answer 427

- injected flu vaccine - inactivated polio - hepA

Question 428

examples of subunit vaccine

Answer 428

- hep B | - meningococcal (carbohydrate capsule)

Question 429

conjugated capsular vaccines

Answer 429

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

Question 430

guardasil

Answer 430

``` 4 = 6,11,16,18 9 = those + 31,33,45,52,58 ```

Question 431

rotavirus vaccines

Answer 431

rotateq - live attenuated oral vaccine from cow rotavirus - quintavalent rotarix - monovalent, derived from human

Question 432

adverse reaction for rubella vaccine

Answer 432

acute arthopathy

Question 433

adverse reaction for VZV vaccine

Answer 433

rash - can be infectious

Question 434

adverse reaction for previous pertussis vaccine

Answer 434

acute encephalopathy

Question 435

adverse reaction for oral polio

Answer 435

vaccine-associated paralytic poliomyleitis

Question 436

adverse reaction for yellow fever vaccine

Answer 436

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

Question 437

thimersol

Answer 437

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