Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 6: Microbio, ID, Derm, Heme-Onc > Antiparasitics, TB, Leprosy, Derm (Week 6) > Flashcards

Antiparasitics, TB, Leprosy, Derm (Week 6) Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

Treatment for visceral leishmaniasis

A

Liposomal amphotericin B

Sodium stibogluconate (pentavalent antimony)

Miltefosine

Paromomycin is alternative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Malaria prophylaxis

A

Chloroquine (where there are sensitive strains)

Mefloquine (Lariam)

Doxycycline

Atovaquone proguanil (Malarone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Malaria treatment

A

Uncomplicated: atovaquone proguanil, artemether/lumafantrine (Coartem), artesunate (only available through CDC)

Also…? Quinine sulfate plus doxycycline or clindamycin (toxicity: cinchonism = flushing, tinnitus, confusion, cardiac conduction problems)

Severe malaria: quinidine gluconate IV, artesunate, plasma exchange in severe malaria, monitor vol status to avoid pulmonary edema due to capillary leak syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatment for lice, scabies (ectoparasites)

A

Topical: permethrin, malathion

Systemic: ivermectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fever

A

Increased core temperature in response to infection, usually 1-4 C

Triggered by cytokine release (IL-1, IL-6, TNF-alpha, INF-beta, INF-gamma) and ultimately results in PGE2 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Markers of inflammation

A

Erythrocyte sedimentation rate (ESR)

C-reactive protein

Ferritin

Quantitative IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of fever other than infection

A

Malignancy (“B symptoms”)

Collagen vascular diseases (auto-immune)

Drugs (malignant hyperthermia of anesthetics, neuroleptic malignant syndrome)

“Central fever” (head trauma with CNS blood, stroke)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Antipyretics

A

Acetaminophen (Tylenol), NSAIDs (block/reduce cytokine-activated increase in core temperature)

Cooling blankets, ice packs (external cooling measures)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What could be some causes of fever of unknown origin (FUO)?

A

Infection

Malignancy

Collagen vascular (auto-immune)

Other: PE, DVT, hematoma, drugs, Familial Mediterranean fever, factitious fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Septicemia

A

Bacteremia (bacteria in blood) with clinical manifestations (fever, chills)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Systemic inflammatory response syndrome (SIRS)

A

Any two or more of:

1) T>38 or <36
2) HR > 90 bpm
3) Respiratory rate >20 or PaCO2 <32
4) WBC > 12,000/ul, <4,000/ul or >10% bands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Septic shock

A

SIRS plus hypotension even with adequate fluid resuscitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Severe sepsis

A

Septic shock + end-organ dysfunction (renal, pulmonary, CNS, liver, impaired glucose metabolism)

Can have consumptive coagulopathy to disseminated intravascular coagulation (DIC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is sepsis just a hyperactivation of the immune system?

A

No

LPS (gram negative endotoxin) and cytokine storm are present, but may be some immunosuppression (hypoimmunity) as well (loss of delayed type hypersensitivity, inability to clear infection, increased susceptibility to nosocomial infection, apoptosis of CD4 T-cells/B-cells/DCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathophysiology of sepsis

A

Decreased tissue perfusion, oxygen delivery (decreased SVR, vasodilation)

Myocardial depression (even though total cardiac output increased, not enough to compensate for decreased SVR)

Increased leukocyte-endothelial interaction

Metabolic acidosis (frequently lactic acidosis from tissue ischemia)

DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for sepsis

A

Empiric antimicrobial therapy

Hemodynamic support (volume expansion, vasopressors)

Ventilatory support

Early goal-directed therapy (CVP, oxygenation, urine output)–> less organ dysfunction, less sudden circulatory collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Infectious disease history taking

A

Travel history

Social history (work, hobbies, pets, sick contacts)

Foodborne disease

Medical history (immunocompromise (diabetes, cancer chemotherapy, chronic corticosteroids, HIV), past infections/exposures (TB, histo), immunizations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Papulosquamous rash

A

Scaly papules or plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does it mean that papulosquamous rashes are raised and scaly?

A

Raised: inflammatory infiltration and swelling of dermis and/or epidermis; proliferative thickening of epidermis called “acanthosis” or “epidermal hyperplasia”

Scaly: thickening of stratum corneum is “hyperkeratosis”; defective maturation of epidermis called “parakeratosis” and is abnormal retention of keratinocyte nuclei in stratum corneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Differential for an annular plaque

A

Dermatophyte

Granuloma annulare

Discoid lupus

Sarcoidosis

Pityriasis rosea (herald patch)

Erythema annulare centrifigum

Urticaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Psoriasis

A

Chronic relapsing inflammatory skin disease

Pathogenesis: immune based disease involving T cells (Th1 and Th17), neutrophils, and epidermal hyperproliferation/dysmaturation

Primary lesion: erythematous plaques that are sharply demarcated, silvery scale, typically symmetrical

Treatments: topical, systemic, biologics

On extensor surfaces (elbows, knees)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Auspitz sign

A

Pinpoint bleeding upon removal of scale

Thinning of epidermal plate above capillaries is what causes this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Different clinical presentations of psoriasis

A

Plaque-type psoriasis: most common; scaly plaques

Inverse psoriasis: common in axilla, groin, umbilicus; no scale because wet; prone to secondary infection

Guttate psoriasis: scattered scaly papules; can be associated with strep infection

Erythrodermic psoriasis: diffusely red scaly skin; fluid and electrolyte imbalances

Pustular psoriasis: sudden onset of erythematous macules and papules with sterile pustules; fevers, chills, arthralgias, leukocytosis (lots of neutrophils); often seen after discontinuation of systemic glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Psoriatic arthritis

A

Seronegative spondyloarthropathy

Symmetrical polyarthritis, oligoarticular, DIP, arthritis mutilans, axial/spondyloarthritis

Sausage fingers

Enthesitis (inflammation at site of tendon insertion into bone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Exacerbating factors of psoriasis

A

Medications: lithium, beta-blockers, anti-malarials, indomethacin, quinidine, interferon

Withdrawal of systemic steroids

Infection/stress

Physical trauma to skin (Koebner phenomenon)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Diseases associated with psoriasis

A

Depression

Alcoholism

Diabetes

MI

Stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Treatment of psoriasis

A

Localized disease: topical: steroids, calcineurin inhibitors, vitamin D analogues (calcipotriene), retinoids (tazarotene), tar, anthralin, keratolytics (salicylic acid), emollients

Generalized disease: phototherapy, retinoids (acitretin), methotrexate, cyclosporine, tacrolimus, hydroxyurea, 6-thioguanine, anti-TNF, biologic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Biologic therapies

A

Anti-TNFalpha therapies: adalimumab, golimumab, etanercept, infliximab

Anti CD-2 therapy: alefacept

Anti-IL 12/23 therapy: ustekinumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pityriasis rosea

A

Acute, self-limited (6-8 weeks) exanthematous skin disease (Christmas tree distribution)

Slighly inflammatory, oval, papulosquamous lesions (scaly papules and plaques) on the trunk and proximal areas of extremities

“Herald patch” is annular plaque that precedes eruption

Mistaken for tinea corporis

Presumed viral etiology (HHV6 or UUV7)

Treatment: none, topical steroids, UV, erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pityriasis (tinea) versicolor

A

Dyschromic (hyper/hypopigmented) macules or papules with fine scale, often on trunk and proximal extremities

Pathophysiology: overgrowth of M. furfur (pityrosporum) with minimal inflammation and production of dicarboxylic acid moiety that interacts with melanin synthesis pathway

Treatment: topical selenium sulfide, topical ketoconazole, oral ketoconazole; may resolve over months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Eczema and dermatitis

A

Synonyms!

Descriptive, and not a diagnosis

Broad range of conditions that begin as spongiosis and may progress to lichenified stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Types of dermatitis

A

Contact dermatitis

Seborrheic dermatitis

Stasis dermatitis

Atopic dermatitis

Nummular dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Nummular dermatitis

A

AKA nummular eczema, discoid eczema

Very itchy, coin-shaped scaly plaque sometimes with crusts or vesicles on extremities

Treatment: emollients and topical anti-inflammatories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Atopy

A

Hereditary tendency to develop allergies to food and inhalant substances and in general to develop over-reactive epithelial surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Atopic dermatitis

A

Chronic, itchy eczema associated with personal or family history of atopy

Itching often precedes appearance of lesions and get into vicious itch-scratch cycle

Pathophysiology: skin is hypersensitive; langerhans cells directly stimulate T cells without presence of antigen; Th2 response

Usually starts after age 2 months, and most who will have it get it by age 5

Treatment: topical steroids, antibiotics or systemic medications depending on severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Atopic dermatitis and family history

A

Affected families may have asthma, allergic rhinitis (hay fever) as well

If one parent atopic, more than half of their children will have allergic symptoms by age 2

Associated with defective skin barrier, in many cases in conjunction with mutations in FLG gene (codes filaggrin, key constituent of cornified cell envelove essential for skin barrier function)

Tendency to Th2 driven immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Exacerbations/triggers for atopic dermatitis

A

Food allergies

Skin infections

Irritating clothes or chemicals

Heat or cold (sweating causes itching)

Dry skin (overbathing)

Staph aureus

Itch-scratch (treat with antihistamines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Stages of atopic dermatitis

A

Infantile (2mo - 2 years): head, diaper area, flexor and extensor surfaces; central face spared = headlight sign; ill-marginated scaly plaques, excoriations

Childhood (2 - 10 years): antecubital fossae, popliteal fossae, face, neck, upper chest

Adult: antecubital fossae, popliteal fossae, face, neck, upper chest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Associated findings with atopic dermatitis

A

Infra-orbital folds (Dennie-Morgan lines)

Hyperlinearity of palms

Lichen simplex chronicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Labs to diagnose atopic dermatitis

A

Elevated IgE

Elevated eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How to treat atopic dermatitis flares

A

Topical steroids (stronger if worse disease or thicker skin)

Antibiotics if evidence of impetiginization (weey, crusted, doesn’t have to be cellulitis)

Systemic medications if severe (cyclosporine, azathioprine, mycophenolate mofetil, methotrexate, PUVA, nbUVB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

3 topical steroids to know

A

Low: desonide 0.05% (mild problems or face/axilla/groin)

Medium: triamcinolone 0.1% (workhorse for most dermatitis, but avoid on face or prolonged on groin/axilla)

High: fluocinonide 0.05% (for contact dermatitis, psoriasis, lichenified eczema, but avoid face/groin/axilla prolonged use)

43
Q

Side effects of potent topical corticosteroids

A

Atrophy of skin

Telangiectasias

Striae

Acneiform eruption

Rosacea-like dermatitis

Exacerbation of periorificial dermatitis

Pruitus

Hypopigmentation

Cataracts/glaucoma (controversial)

Adrenal suppression

Cushingoid syndrome (moon facies, buffalo hump, truncal obesity, hypertension)

Exacerbation of some infections, dermatophytosis

44
Q

Topical tacrolimus and pimecrolimus

A

Topical calcineurin inhibitors

Inhibit inflammation by preventing cytokine release

Weaker than steroids

Put patient on topical steroid first, then transition over

Don’t use in kids

45
Q

What kind of skin condition gets superinfected?

A

Atopic dermatitis gets frequently superinfected (because decreased antimicrobial peptide production)

Psoriasis does not get superinfected (because increased antimicrobial peptide production)

46
Q

Seborrheic dermatitis

A

Erythematous plaque with greasy scale

Prefers scalp, eyebrows, eyelids, nasolabial folds, ears but can also involve sternal area, axilla, umbilicus, groin, gluteal crease

Dandruff = mild seborrheic dermatitis

M. furfur/pityrosporum overgrowth plays a role

Associated with HIV, Parkinson’s

Can overlap with psoriasis (seboprosiasis)

Treatment: mild steroids, topical antifungals, selenium sulfide, zinc pyrithione

47
Q

Contact dermatitis

A

Allergic contact dermatitis, or irritant contact dermatitis

Something from the outside get onto your skin

Blister beetles, poison oak, OTC antifungal, topical 5-FU, lip-licking

48
Q

Can you use short course of oral steroids for skin disease?

A

No, never <10 days of oral steroids for skin disease!

49
Q

Hints for differentiating papulosquamous diseases

A

Early childhood onset –> atopic dermatitis

Very itchy –> atopic dermatitis, other eczema, contact

Burning/stinging –> irritant contact dermatitis

“Outside job” shapes –> contact dermatitis

Psoriasis has better demarcated plaques than eczema

“Christmas tree” –> pitryiasis rosea

Seborrheic dermatitis –> typical locations and scale

50
Q

What should you do if you’re not sure if it’s dermatitis or dermatophyte?

A

Treat dermatitis first (steroid) and schedule patient back

If steroid doesn’t help, then do KOH or culture fo dermatophyte (which you can then treat with antifungal)

51
Q

Symptoms and findings with primary infection with tuberculosis

A

Symptoms: fever, fatigue, chest discomfort

CXR: hilar adenopathy, transient infiltrates, pleural effusion

PPD not positive until 1-3 months after primary infection!

52
Q

With TB, will you always see acid fast bacilli (AFB; M. tuberculosis) on sputum sample?

A

No, sometimes won’t see the actual organism

But if you see caseating granuloma or multinucleated giant cell (Langerhans cell), can diagnose TB anyway!

53
Q

Ghon complex

A

Seen in tuberculosis

Calcified pulmonary tubercle + hilar lymph node

54
Q

Pathogenesis of active tuberculosis

A

Usually due to reactivation of primary infection (which was probably asymptomatic)

Cough, hemoptysis, fever, night sweats, weight loss

Slow onset

Focal or widespread pneumonia (upper lobes, apex of lower lobes in reactivation), pulmonary nodules, caseation/liquefaction/cavitation, bronchogenic spread

Pleural involvement (empyema, pneumothorax, bronchopleural fistula)

Disseminated disease (Miliary tuberculosis, Pott’s disease, scrofula)

55
Q

Other sites affected by TB

A

Reactivation of extrapulmonary tubercles or dissemination from lung can cause:

Pott’s disease: vertebral bodies

Scrofula: lymph nodes

Kidneys, GI, pericarditis, CNS

56
Q

How do you tell Pott’s disease from staph aureus infection?

A

TB goes to vertebral body itself and not discs

S. aureus arises in disc then travels to 2 adjacent vertebral bodies

57
Q

What means you will be more contagious?

A

Infection in lungs, airways, larynx

AFB positive sputum (increased burden of organisms)

Cavitary disease (higher number of bacteria, easier to transmit)

58
Q

Reading PPD test

A

Test positive at >5mm induration: HIV +, recent contact of TB, patients with fibrotic changes on chest radiograph, patients with organ transplant/immunocompromise

Test positive at >10mm induration: recent arrival from high-prevalence countries, IV drug users, medical pesonnel, mycobacteriology lab personel, patients with clinical conditions that place them at high risk (silicosis, diabetes, renal failure, cancer, gastrectomy), children <4 or those exposed to adults in high-risk categories

Test positive at >15mm induration: no known risk factors for TB

59
Q

How would you get a false positive or false negative on PPD?

A

False positive: had BCG vaccine within 5 years; non-tuberculous mycobacterial infection

False negative (anergy): other recent overwhelming infection, recent live virus vaccination, under 6 months old, HIV, immunosuppression

60
Q

Booster phenomenon

A

Some people with latent infection may have negative PPD when tested years after primary infection, but that initial skin test will stimulate (boost) ability to react to tuberculin so SECOND skin test is then positive

This does NOT indicate new infection, just that first PPD was false negative!

61
Q

Two step testing

A

Use this for initial skin testing of adults who will be retested periodically (health care workers)

If first test positive then person is infected (duh)

If first test negative, perform second test 1-3 weeks later –> if second test positive, consider person infected but if second test negative consider person uninfected

62
Q

Anti-TB drugs

A

INH-SPIRE (or RIPE)

Isoniazid (INH)

Streptomycin (injected)

Pyrazinamide

Rifampin

Ethambutol

Second-line (just for MDR strains): paramino salacylic acid (PAS), ethionamide, cycloserine, capreomycin

New drug: rifapentine

63
Q

How to treat TB

A

Use multiple drugs (INH-SPIRE)

As bacteria decrease, can decrease number of drugs

NEVER add single drug to failing regimen

Failure usually due to non-adherence

Patient isolation until non-infectious on treatment (respiratory AFB smear-negative)

Initial phase with RIPE drugs daily for 2 months; continuation phase with Isoniazid and rifampin daily for 4 months (longer in compromised hosts/disseminated disease)

64
Q

Multidrug resistant TB

A

Multidrug resistant (MDR): resistant to isoniazid and rifampin

Extensive drug resistant (XDR): MDR also resistant to at least 3 of 6 second line drugs

65
Q

TB drug toxicities

A

Isoniazid: hepatotoxicity, neuropathy

Rifampin: hepatotoxicity, orange discoloration or urine, contact lenses (all secretions), drug interactions

Ethambutol: optic neuritis

66
Q

Non-tuberculous mycobacteria

A

M avium intracellulare (MAI, MAC): infections look like TB, but arise in AIDS patients at end stage disease

M. abscessus (local disease or dissemination in immunosuppression)

M. chelonae (other pulmonary disease)

M. fortuitum (other pulmonary disease)

M. kansasii (environmental, pulmonary disease similar to TB)

M. marinum (in fish tanks, local infection of soft tissue, lymphatics)

M. leprae

M. bovis (ingestion of contaminated milk, causes GI tuberculosis or pulmonary similar to TB if inhaled)

67
Q

Mycobacterium avium complex (Mycobacterium avium-intracellulare)

A

Similar clinical presentation to TB, but usually in AIDS patients at end stage disease

Causes chronic lung disease (bronchiectasis), cavitary nodular disease

Disseminated disease in AIDS/immunosuppression (fever, night sweats, severe weight loss, diarrhea, bone marrow infiltration)

68
Q

ESKAPE bacteria

A

Bacteria that have become very antibiotic resistant

Enterococcus (VRE)

Staphylococcus aureus (MRSA)

Klebsiella

Acinetobacter

Pseudomonas

ESBL (E. coli, Enterobacter; resistant to all oral agents)

Note: gram - are the biggest problem–we have no drugs for ESBL and very few drugs for others!

69
Q

What drug do we use to treat very drug resistant gram - bacteria?

A

Colistin

Lots of toxicities (nephrotoxicity) so stopped using in 1960’s but had to start using it again once bacteria started becoming so resistant

70
Q

Reasons why we’re not making good, new antibiotics

A

1) Science: difficult to do
2) Economics: not good investment ($-50 million)
3) Regulatory: R&D too risky/expensive

71
Q

The non-inferiority problem of RCTs for antibiotics

A

In order to prove efficacy in RCT by non-inferiority, need previous RCTs of older drugs

However, older drugs are SO old that they didn’t have RCTs back then so there never were and never will be RCTs for older antibiotics!

72
Q

Why is the bacterial capsule anti-phagocytic?

A

1) Some capsules are rich in sialic acid, which has an affinity for serum protein H, which is a complement regulatory protein that leads to degradation of opsonin C3b (by factor I and formation of C3 convertase)
2) Some capsules cover C3b that does bind to bacterial surface (so prevent C3b from binding its receptor on phagocytes)

73
Q

Why are splenectomized patients at risk for bacteremia by encapsulated organisms?

A

Because spleen removes opsonized bacteria (and senescent RBCs and antibody-coated cells) from the blood stream

If no spleen, will still have encapsulated (though opsonized?) bacteria in the blood stream

74
Q

Tuberculoid vs. lepromatous leprosy

A

Tuberculoid leprosy: person has good strong immune response; granuloma forms and limits spread of microorganism; localized damage to superficial nerves and skin; thickened (palpable) nerves; hypopigmented/hairless lesions; elevated, sharply defined plaques, decreased sensitivity to sharp/dull and hot/cold; multi-nucleated giant cells; acid fast stain is negative

Lepromatous leprosy: person has weak immune response; host cannot contain microorganism; inflammatory damage at cooler skin, nerves, testes, sensory loss at face/extremities; get secondary infections/burns; lose eyebrows, saddle-nose deformity, leonine facies, infertility; disseminated nodules; foamy macrophages and few lymphocytes; many bacilli on acid fast stain

75
Q

Why do you lose hair in leprosy?

A

Nerve innervating hair follicle is infected with mycobacterium leprae and causes hair to fall off

76
Q

How is leprosy transmitted?

A

Human to human via nasal discharge

From armadillos!

77
Q

Acne

A

Caused by propionibacterium acnes, which is normal bacterial commensal

78
Q

Important childhood exanthems

A

Rubeola

Scarlet fever

Rubella (German measles)

Erythema infectiosum (fifth disease)

Roseola

Hand-Foot and Mouth Disease

Varicella

79
Q

What causes the inflammatory response that produces the exanthem?

A

Not yet known!

Possibly:

1) Direct invasion of blood vessel walls by virus
2) Immune complex deposition
3) Cell-mediated immune responses

80
Q

Measles (Rubeola)

A

Downward progression from face, and resolves in that order too

Becomes confluent on face

Koplik’s spots on buccal mucosa

Subacute sclerosing panencephalitis causes personality changes (very rare)

81
Q

Scarlet fever

A

Group A strep (beta-hemolytic)

White strawberry tongue then red strawberry tongue

Enanthem (inside) of palatal petechiae, bright red oropharynx

Sandpaper-like fine papules

Pastia’s lines (flexular accentuation with petechiae)

Desquamation

82
Q

Rubella (German Measles)

A

Enanthem during prodrome (Forschheimer’s spots)

Downward spread from face

83
Q

Erythema infectiosum (fifth disease)

A

Slapped cheeks

Lacy, reticulated pattern of erythema on trunk and extremities

No enanthem

In adults can cause arthritis

In pregnant women can cause hydrops fetalis

84
Q

Roseola infantum (HHV6)

A

Enanthem of erythema of soft palate and oropharynx

Febrile seizures

85
Q

Hand foot and mouth disease

A

Coxsackie A16 virus

Enanthem of small vesicles and erosions on gingivae, lingual and buccal mucosae–painful!

Gray-white vesicles on hands, feet, butt

86
Q

Varicella (chicken pox)

A

Enanthem of mucosal vesicles and erosions

Exanthem occurs in crops (macules to papules to vesicles to pustules to crusts)

Begins on trunk

87
Q

Verrucae (warts)

A

HPV

Verrucae vulgaris (3D warts)

Verruca plana (flat warts)

Verruca plantaris (on soles of feet)

88
Q

How do arthropods (insects) cause disease?

A

1) Direct, nonallergic local tissue damage (stings, bites, tissue invasion)
2) Allergic reactions (papular urticaria) to secretions, skins, scales
3) Producing systemic toxicity
4) Transmitting disease (malaria, other parasites)

89
Q

Clinical presentation of scabies

A

Primary lesion (burrows) about half a centimeter long, pinkish

Involves interdigital spaces, flexular aspect of wrists, axillae, waist, ankles, feet, butt, belt area

Nodules, pustules, papules, crusted plaques

Erythematous scaly plaque in diaper distribution

Intense pruitus accentuated at night and exacerbated by hot bath or shower

Can get secondary bacterial infections with group A strep pyogenes and S. aureus

90
Q

Scabies

A

Sarcoptes scabei, variety hominis

Female mite burrows in epidermis, takes blood meal and lays eggs which hatch and propagate infestation

Transmission from CLOSE skin to skin contact

91
Q

If scabies mites are only found in a few places, what causes systemic immune response (papules everywhere)?

A

Poop (scabela) from scabies mite causes immune response

92
Q

Crusted scabies

A

AKA Norwegian scabies

In immunocompromised (HIV, elderly, transplant)

Lesions are hyperkeratotic, crusted, cover large areas

Marked scaline

Sometimes no pruitis

Tons of mites and eggs in these lesions!

93
Q

Treatment for scabies

A

Wash bed linens, clothing in hot water

Permethrin (Elimite) 5% cream

Sulfur in petrolatum 10% concentration

Ivermectin

Permethrin kills adults but not eggs so must treat now and one week later to kill eggs that have hatched after 1 week

All family members and close contacts must receive treatment too

94
Q

Myiasis

A

Infestation of skin by larvae of botfly (Dermatobia hominis), or just any larvae in open wound

95
Q

Cutaneous larva migrans

A

Caused by Ancylostoma braziliense or caninum (cat and dog hookworms)

Infection caused by walking/laying on ground contaminated with feces

Skin lesions are serpiginous and very itchy

Treat with topical tiabendazole

96
Q

Tungiasis

A

Female flea in skin is full of eggs and train of poop coming out of skin

Treat by anesthetizing and gauging it out

97
Q

Pediculosis capitis (head lice)

A

Live on hairs of head and feed on scalp

Female lays 300 eggs in 30 day life cycle

Causes itchy scalp and see eggs (nits) in the hair

Treat with permethrin cream rinse 1%, lindane shampoo 1%, or if resistant: malathion, ivermectin

98
Q

Pediculosis corporis (body lice)

A

Pruitus and excoriations

Body lice are vectors (via their poop!) for trench fever (bartonella quintana) and epidemic typhus (rickettsia prowazekii)

99
Q

Pediculosis pubis (crab lice)

A

STD, but occasional transmission via fomites

Infestation of pubic hair, mustache, axillae, eyelashes, eyebrows (coarse hairs)

Maculae coeruleae (gray to bluish macules 1cm in size)

100
Q

Papular urticaria

A

Very general term, but refers to bug bites

Erythematous papule, very pruitic, excoriated

Can be seen in linear groups of 3 (breakfast, lunch, dinner)

101
Q

Bedbugs

A

Cimex lectularius

Bites in lines of 3 (breakfast, lunch and dinner)

Treat with topical steroids

102
Q

Allergic reactions to insect stings

A

Bee, hornet, wasp have melittin (protein) antigen in venom that causes degranulation of basophils and mast cells releasing histamine, Phospholipase A, hyaluronidase

Normal reaction: itch and pain for hours

Severe local reaction: itch and pain + swelling

Toxic reaction: >10 stings, headache, fever, GI symptoms

Anaphylactic reaction: urticaria, bronchospasm, hypotension (will carry epinephrine pen)

103
Q

Brown recluse spider

A

Loxosceles reclusa

Characteristic violin-case pattern on cephalothorax

Venom contains sphingomyelinase D

Bite is not very painful

Erythema with central ischemia then surrounding edema, necrosis, can lead to fever, DIC, shock

Treatment: prednisone, dapsone, surgical excision

104
Q

Black widow spider

A

Latrodectus mactans

Red hourglass on underside of abdomen

Venom contains alpha latrotoxin (neurotoxin that depolarizes neurons and stimulates uncontrolled exocytosis of NTs)

Abdominal rigidity, muscle cramps

Treatment: antivenom, IV calcium gluconate, muscle relaxants

Block 6: Microbio, ID, Derm, Heme-Onc (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions