Immunology
Innate Immune system: present at birth, non-specific resistance (skin, mucus membrane, salvia, NK cells, monocytes)
Acquired Immunity: developed over time with memory + specificity
WBCS:
 Neutrophils: ↑ if bacterial infection/inflammation
 Bands: baby neutrophils
 Dendritic cells: Skin Macrophages
 Eosinophils: ↑ if allergens, parasites, neoplasm, asthma
 Basophils: secrete histamine + heparin
 Lymphocytes: (T/B cells) ↑ if viral infection
Steroids/ Anti-inflammatory  lower resistance to infection
Fever  ↑cytokines, ↑ metabolic rate, ↑ tissue repair, ↑wbcs
Cytokines  stimulate inflammation + enhance phagocytes
Interferon: polypeptides secreted by cells infected
with viruses (viral warning sign) which activate
NK cells + macrophages
Complement: set of enzymes + plasma proteins that cause
“Cascade rxn” to destroy microbe
MACROPHAGES
 Kupfer cells – liver
 Monocytes- immature macrophages in blood (chemotaxic)
 Histiocytes/Langerhands – skin
 Alveolar- lungs
 Mesangial –kidneys
 Microglial- CNS
The Journey: Margination  Diapedesis  Chemotaxis  Phagocytosis
Acquired Immunity:
a. Passive- Ab/Ig given to a person from an external source
b. Active- you make the Ab (can be from a vaccine with an antigen)
Spleen: destroys old RBCs and removes encapsulated bacteria (H. flu + pneumococcal)
B-Cells: a. Plasma- make Ig b. Memory- reason for vaccines
T-Cells:
a. CD4: secrete cytokines (messengers/activators)
b. CD8: killer cells for virus
c. T suppressor: stops CD8 from killing + decreases function of all immunity cells
Epitope- smallest identifiable portion of antigen
3 types of Antigens:
1. Immunogen- molecule (foreign, large, complex) that stimulates immune response
II. Haptens- need to be coupled with carrier to stimulate response
III. Tolerogen- the more exposure  decreases the immune response
MCH-1 : on all cells (individualized to you) + presents foreign matter to CD8 cells
**CD8 recognize change in MCH-1 and then kill antigen cells
MCH-11: help CD4 cells with recognizing APC (antigen presenting cells - macrophages/B-cells)
Steps:
1. APC kills antigen and holds out prize
2. CD4 recognizes prize by attaching with APC
3. CD4 activates cytokines/immune rxn
4. T-B cell coop: B-cell presents with Ab-Ag complex and T cell CD4 releases cytokines to ↑ B cells division +
production of plasma cells
B-plasma cells make the Antibody: 2 heavy + 2 light chains + Fc
IgG- crosses placenta, inside Ig, 2nd response, blood/lymph/CSF
IgA- outside, neutralizes exotoxins, in breast milk, sweat, saliva, GI secretions, GU secretions, resp. secretions
IgM- primary/early response, agglutination rxn, on surface of B-cells
IgE- allergens, parasites, degranulation of mast cells
IgD- on surface of mature B cells
Humoral Immunity = Bcells = extracellular infection = bacteria
Cell-Mediated immunity = T cells = intracellular infection = viral
Hypersensitivity RXNs
1. Immediate/Anaphylaxis/IgE/allergy to food
2. IgG/IgM (blood transfusions, Rh incompatibility, drug rxn)
3. Ab-Ag circulate and cause tissue damage (SLE) slow + chronic
4. T-Cell mediated (delayed) induced by cytokines (ie: poison ivy, PPD, hepatitis)
Autoimmune Diseases:
1. Exogenous Mechanisms:
a. Molecular Mimicry- Ag looks like host
b. Super-antigenic Stimulation- Ag/Toxin bind to MCH-11 and cause ↑ in Tcell activation
2. Endogenous Mechanisms
a. Neoantigens- altered self antigens
b. Loss of T-cell suppression, cytokine imbalance, increase in B-cell function
Transplants
**The greater the difference in HLA the faster/more aggressive the immune attack
Autograft: transplant from yourself
Allograft: transplant from same species
Xenograft: transplant from different species
**children can get transplant from parents
**parents can NOT get from children
Twins> siblings> parents
** cornea, liver, kidney  don’t need compatibility
Host vs. Graft: your T-cells kill the graft
1. Chronic- organ functions for weeks-years then slowly scar tissue replaces graft (minor MHC diff.)
2. Acute- 7-12 days then rapid destruction (MCH > 50% difference)
3. Hyperacute- antibody mediated b/c of previous exposure to transplants
Graft vs. Host  Bone Marrow Transplant
Rh Dilemma: mom is Rh neg. and first baby is Rh +  mom may develop Rh antibodies and 2nd child will be stillborn
 therefore GIVE Rhogam
Gram Stain
g- does take the saffron dye b/c thin membrane with 2nd lipid layer
g + does NOT take saffron dye b/c of thick membrance
Prion- no DNA or RNA  found in CSF and causes Mad-Cow disease and KURU
Mycoplasm – lack a cell wall, resistant to PCN
Spirochetes – depend on vector transmission
Endemic- disease occurring predictably in specific area
Incidence- # of new cases/time
Prevalence- total # of cases/time
Epidemic- sudden outbreak in region
Pandemic- all over outbreak
Incubation  Prodrome  Acute  Convalescense/Chronic
Sterile fluids: CSF, blood, urine, synovial, bile, pleural, pericardial (need aseptic technique)
Microbial Factors that increase Virulence:
1. Adhesion- bind to cell receptor
2. Evasive- LPS, leukocidin, C-toxins
3. Invasive- phospholipases, elastases, proteases, enzymes that break cell membrane
Staph. Aureus: G+ cocci in clusters
Strep. Pyogenes: G+ cocci in strings
Neisseria Gonorrhea: G- diplococci
Ecoli/Pseudomonas: G- rod
G + cocci = Staph, Strept, Enterococcus
G – cocci = Gonorrhea, N. menigitidis, M. cat
G + rod = Bacillis, Listeria, Corynebacterium
Aerobic g – neg. = Ecoli, Shigella, Proteus, Enterbacter, H flu, Pseudomonas, Klebsiella, V. cholera, H. pylori
Acid Fast = M. leprae, MAC, Tb
Commensalism- one benefits + other has no harm or benefit
Mutualism- both benefit (Ecoli + our colon)
Parasitism- one benefits + the other is harmed/destroyed
Vertical Transmission: mother  fetus (TORCHES)
Ingestion: Hep A+E, cholera, staph (in creams and cakes)
Bloody Diarrhea: Salmonella, Ecoli, Campylobacter (mc), Shigella, Yersina
Viruses- ↑↑ oncogenesis by changing the DNA
Bacteria- reproduce via binary fission
Spirochete- helicial, gMycoplasma- smallest free-living unicellular organism
Rickettsia- small intracellular parasite
Yeasts- monocellular (reproduces via budding)
Molds- multicellular (reproduce via hyphae)
Exotonins- goes into circulation (Diptheria, Botulinum, Tetani, Cholera)
Enterotoxins- GI only (G- neg only)  Ecoli, Clostridium perfinges, Cholerae
Sublinical infection- doesn’t cross clinical threshold
Subacute- btw acute + chronic
Fulminant- abrupt onset of sx w/o prodrome
Bacteremia vs. septicemia (toxins or bacteria or virus in blood)
Latent- dormant
SIRS- systemic inflammatory response syndromes
 Syndrome is sx w/o ID of bacteria OR end organ damage
 SX: tachycardia > 90; tachypnea> 20 breaths/min; WBCs > 12,000, hyperthermia
Sepsis = SIRS + positive blood culture
Wet Mount = ID fungus or trichomonsis
Tzank smear = ID virus
Bandemia = shift to left w/ increase in PMNs
Vaccinations
Active:
 Live- MMR, Varicella, Zoster (CI: pregnant or immunocompromised
 Inactivated- flu, polio, small pox
 Recombiant DNA
Passive:
 TDap, Rabies, Hep B, Hep A, Snake or Spider Anti-venom
PPD:
 False +  BCG
 False – (neg) HIV + (immunocompromised)
o > 5mm = HIV +
o > 10 mm = healthcare worker, homeless, Dm, prison, from endemic region
o > 15 mm= everyone
“Neutropenia with lymphocytosis”  Viral infection with shift to right (virus- mono, HIV, flu)
“Neutrophilia with lymphopenia”  Bacterial infection with shift to left
Eosinophilia: Neoplasm, Asthma/allergies, Addison’s, Collagen Vascular Dz, Parasites
Never (neutrophils)
Let (lymphocytes)
Monkeys (monocytes)
Eat (eosinophils)
Bananas (basophils)
Dermatology
Layers of skin:
1. Epidermis
a. Coreum
b. Lucidum- only in palms + soles of feet
c. Granulosum- has kerito-hyaline
d. Spinosum- w/ dermosomes + Langerhan cells
e. Basal – layer with melanocytes
2. DERMIS- thick w/ collagen + fat
3. Sub-Q- blood vessels + eccrine glands
Hair Growth: Anagen  Catagen  Telogen
Sweat Glands:
1. Eccrine: in dermis on skin surface
2. apocrine- deep and open thru hair follicle (in axilla/groin) **resp. for body odor
Darier sign = rub and make wheal is pos. sign
Auspitz sign = Pt scale is remved + there is pinpoint bleeding
Nikolsky sign desquamation (separation of skin layers)
Koebner phenomenon = minor trauma makes pt scratch (+ in psorias)
Wood lamp = UV light to see tinea capitis
Acetowhitening = acid allows us to see white penile/vaginal warts
Dark Field Exam = spriochetes
Folliculitis: hair follicle infection
Furnucle: acute, deep seated, 1 hair follicle w/ adjacent tissue
 Mcc is staph
 Found in thight, axilla, face, neck, butt
Carbuncle: depper, interconnecting, several hair follicles, into dermis + Sub-Q tissue, draning pus; scarring
 Ass. with systemic sx
 MCC: staph, pseudomonas
 Risks: shaving, waxing, steroids, obesity, poor hygiene, humidity, Dm, increased body temp
 TX: topical mucpirocin (Bacteroban); po antibiotics- Naficillin/Dicloxacillin
Hidradentis Suppurativa: sweat glands w/ pus in axilla or groin
 Chronic infection of apocrine glands
 MC: Africian American females
 Risks: smoking, obesity, genetics, occlusions of follicles and glands
 Occlusion of follicle  duct inflammation leads to infection  ruptures casuing sinus tract formation
 SX: tender/inflammated nodules, abscess, sinus with scar tissue formation
 “DOUBLE OPEN COMEDOMES”
 DX: BX
 TX: steroid injection, I+D, surgery, oral antibiotics, isotretinoin
Impetigo: break in skin  skin infection
 Mc in children  autoinfection
 “Honey Colored Crusts” on face
 Non-bullous: lesions scattered + discrete
 Bullous: vesicles + bulla
 Non-bullous SECONDARY impetigo = has underlying eczema
 Staph is MCC
 Cx: glomerulonephritis w/ strep infection
 Tx: topical mupirocin
Cellulitis: infection of dermis + sub Q with systemic sx and indistinct border
 Red streaks = lymphangitis
SX: red, swollen, hot, tender
 Etiology: staph, strept, DM- polymicrobial
 Risks: trauma, ulcer, Dm, Ca, dermatitis
 DX: g stain, bx, culture, CBC
 CX: Glomerulnephritis w/ strep
 TX: wound care/ topical mupirocin/ systemic antibiotics: (strep-PCN, staph- Diclox/Clox, Dm- Unasyn)
Erysipelas: more superficial cellulitis w/ only superficial dermis tissue involved  more sharply demarcated
Necrotizing Fascitis: flesh eating bacteria ( in Sub-Q + fascia)
 Risk: health pt after trauma
 Etiology: Strep, Staph, Clostridum
 Sx: swollen cellulitis, with quick progression along fascia plane
 Change in color = Red  Purple  Grey  Blue with watery malodorous discharge
 DX: shock; “Gas gangrene”- Clostridium
 If in perineum/genitals- “Fourner’s gangrene”
 TX: surgical debride, po Antibiotics
HPV- codyloma acuminatum (genital warts)
 Sx: + Auspitz
 Plantar warts: increase in depth in foot w/ pressure  painful w/ pressure
 Anogenital- mc STD in US
o HPV that cause cancer: 16, 18, 31
o “cauliflower lesions- small discrete”
o DX: pap smear, BX, PCR
o TX: cryosurgery
HSV-2: MC STD worldwide
 First case is usually worst however, first case could be asymptomatic
 Classic sx: primary infection is worst (in sacral nerves)  hides in dorsal root ganglion
 Reactivates in same area due to: UTI, URI, trauma, HIV, immunocompromised
 Prodrome: tingling, numbness + pain @ site, lymphadenopathy
 SX: grouped painful lesions with pustules which may form ulcers
 Dx: Tzank smera (see Giant multi-nucleated cells); Viral culture
 TX: Acylcovir Cream (tx/prophylaxis)
HSV-1: child/acute gingivostomatitis- around mouth/lips
 On mucus membranes
 On corena of eye  dendritic lesions (do not use steroids)
 Herpetic Whitlow: painful vesicle on finger/hand (autoinoculation)
 Herpetizing ecezema: underlying dermatitis
 Mc is trigeminal nerve
 DX: viral culture, Tzank smear
 TX: acyclovir cream
Varicella: chickenpox
 Varicella is teratogenic in 1-2 trimesters
 Do not give kids ASA  Reye’s
 “a person with herpes zoster can give a PT primary Varicella but not visa versa”
 MC in winter-spring
 Invades dorsal root ganglion; comes in crops
1. Prodrome with systemic sx
2. first crop- disseminated pruritic macules + papules on scalp/face spreading to extremities on mucus membranes 
Vesciular lesions evolve in 12 hrs with clear liquid
Shingles (herpes Zoster): along a dermatome; mc in elderly, HIV, immunocompromised
 prodrome: sharp lancing pain with tingling + tenderness + pruritis
 “Group vesicles along a dermatome unilateral”
 Mc dermatome: thoracic > cervical > trigeminal > lumbar

DX: viral culture, Tzank Smear
 TX: po Acyclovir + acyclovir cream (use po acyclovir as prophylaxis in high risk pt)
 CX:
1.
post herpetic neuralgia
2.
Ophthalmic Zoster (CN V)  blindness (Hutchingson’s sign- vesicle on tip of nose)
3.
Ramsay Hunt Syndrome: CN VIII- in ear canal  deafness
Molluscum Contagiosum: “central umbilication” with molloscum bodies
 Round, firm, skin colored waxy pearly papules; keratotic plug releases exudate w. pressure
 Etiology: pox virus
 MC : in kids on face/eye; in adults- STD on genital
 DX: Bx; keratotic plug
Pityriasis Rosea: herpes virus- hearld patch (large+ red) 1-2 weeks early then Christmas tree pattern on trunk
Cutaneous Tb: ↑ risk in homeless, poverty, HIV
1. Tb chancre- firm, red/brown, painless papule, with LAD
2. Lupus Vulgaris- apple red jelly lesions
DX: BX: caseating granulomas with acid fast bacilli; PPD, CXR, sputum g stain
TX: RIPE
Leprosy (Hansen’s): mc in Africa, South Asia, South America
 Affects skin, mucus membranes, PNS, eyes
 DX: BX- granulomas with nerve involvement and acid-fast bacilli
 First sign = numbness  temp loss  light touch  pain  deep pressure
 SX: plaques are anaesthetic + hypopigmented
 TX: Dapsone, RIF, Clofazimine; steroids; thalidomide
Dermatophyte infections:
 RISKS: steroids, poor hygiene, occlusive clothing, athletes, increased temp
 DX: KOH w/ hyphae, wood lamp
 TX: topical- corporis, cruris, pedis; po- capitis/manuum;
1. Tinea corporis-annular/scaly lesions with central clearing + active border
2. Tinea capitis- crusted/scaling; “black dot” appearance b/c hairs breaks on scalp
a. Hair loss not permanent, may have occipital LAD
b. Kerion: prurlent scalp mass with abscess
c. Tx of choice: griseofluvin
3. Tinea barbea- on beard; looks like folliculitis, but painless when you pull hair
a. Tx of choice: terbinafine
4. Tinea unguim- Nails are lustless ass. with co-infection with tinea pedis
a. TX of choice: terbinafine
5. Tinea Manuum- palms usually unilateral ass. with tinea pedis
6. Tinea Cruris- Jock itch
7. Tinea Pedis – MC (btw 4th and 5th digits)
Tinea Versicolor- Malassezia furfur (not a dermatophyte)
 Pityrosporum yeast infection
 “fine dust scaly covering which does NOT tan in summer”
 TX: topical ketoconazole or selenium sulfide
Candidiasis: muco-cutaneous transmission
 HIV +  ororpharyngeal/ esophageal
 Women  vulvovaginal (thick cottage cheese discharge); pendulous breasts
 Risks: immuncompromised, Dm, Cancer, Antibiotic use, trauma
 Satelite lesions- sharply demarcated w/ white
 TX: Nystatin; po fluconazole
Vesicular Bullae Bullous Pemphigoid: autoimmune rxn
 + Nikolksky
 Subepidermal blister with immune activation

Prodrome: erythema before blisters  then lesions on extremities (flexor)
 2 phases: 1.non-bullous: pruritis/eczema 2. bullous: vesicles; bulla with clear fluids
 Can be drug enduced  diuretics, nsaids, antibiotics
 DX: reveals IgG or C3 at dermal-epidermal junctions
 TX: po + topical steroids + immunosuppressants
Pemphigus Vulgaris- MUCOSAL LESIONS w/ pain and w/o pruritis
 Autoimmune rxn against keritinocytes with loss of adhesion
 Blisters break easily with clear fluid
 DX: immunoflourescence IgG + C3
 Fatal if not treated with steroids (po) + immunosupressants
 Tx: Azathioprine, Methotrexate
ACNE: due to androgens
 Black head- melanin plug
 TX: OTC, po antibiotics, Benzoyl peroxide, sebum suppressants
Rosacea: peaks in 30-40s; ass. with Parkinson’s
 Related to vascular hyperactivity  Red skin on nose, cheeks, forehead
 Ass. with Rhinophyma, Blepharophyam, metrophyma
 TX: Metronidazole; avoid triggers of food, alcohol, humid weather, clonidine
 DO NOT use topical fluorinated steroids on face!!
Hypersensitivity Vasculitis: immune complex rxn- inflammation of arterioles/capillaries/venules
 Immune rxn to drug/infection/molecular mimicry/ Ag-Ab block capillaries
 Leads to vascular damage  ischemia + necrosis
 Hx: drug/strep infection/ SLE/ arthritis (can become systemic)
 “Palpable purpura on legs + ankles with pain  may form ulcers”
 DX: BX
 TX: Antibiotics, dapsone/immunosuppressants + prednisone
Erythema Multiforme: “target iris lesions” 50% idiopathic + 50% drug/infection
 Lesions: involve on hands, feet, face, neck + mucus membranes with oral lesions
 <10% desquamation
 EM-minor: no mucus membranes/ no bulla
 EM-major: SJS is bullous
 SJS is < 30% desquamation with 2+ mucosal sites
TEN: always a drug rxn
 + Nikolsky sign
 > 30% desquamation
 Mc drugs: NSAIDS, sulfa, antibiotics
 TX: 1. stop drug 2. TPN 3. Burn unit 4. debridement 5. systemic steroids
Drug Eruptions: due to clinical situation + drug
 Due to excessive use, pharmacological side effect
 Drugs: PCN, cephalosporins, NSAIDS, INH, streptomycin, sulfa, chloramphenicol
 TX: antihistamine, topical steroids
 PT with mono (EBV)  if you give ampicillin will have drug rxn 4-5 days after therapy
 HIV +  rxn with sulfa drugs
Drug Hypersensitivity- due to Pts genetics
 Drug acts as hapten (↑ eosinophils)
Staph Scalded Skin Syndrome (Ritter’s disease)
 “exfoliative toxin” from staph usually in children < 2 y/o
 DX: bx, g stain
TSS: staph/strep toxin
 Risks: foreign bodies (tampons, nasal packing, trauma, wounds/burns)
 Sx: shock, ↓BP ↓BV  multisystemic organ failure (3 + organ systems involved)
 Non-dependent edema on face, hands, feet

DX: g stain of wound + BX (increase in lactic acid, decrease in perfusion)
Toxic Erythema Nodosum
 “painful, tender, deep nodules on ant. Legs in sub-q fat”
 Felt on palpitation, lesions change in color- “purple  brown  yellow  green”
 Dx: CRP, WBCs, CXR to r/o sarcoidosis
 There is a spontaneous resolution in 6 weeks  does not breakdown or ulcerate
Xerosis: dru skin (rough, scaly)
Sx: pruritis
Atopic Dermatits: type 1 hypersensitivity: IgE/Mast cells  histamine + heparin
 Family hx of atopy
 Chronic  lichenification/fissures
 Infants = extensor surfaces
 Adult =flexor surfaces
 TX: phototherapy
Nummular Eczema: “round coined shaped” lesions do Tzank Smear to r/o tinea
Dyshidrotic Eczema: chronic vesicular hand-foot dermatitis
 Vesicles ass. with atopy, stress, hot weather, extreme pruritis
 “tapioca looking” in clusters
 TX: burrow wet dressings; Triamcinolone
Contact Dermatitis: cell mediated (T cell)
 Delayed hypersensitivity rxn
 Poison Ivy/ poison oak  occur after 2nd exposure
 TX: burrow solution/wet dressings with topical or po steroids
Statis Dermatitis: due to venous HTN and venous insufficiency
 Proteins/rbcs deposit in sub-q tissue  brown hemosiderin deposits because breakdown of RBCs; found on
medial ankles  edema on legs (Venous statis/ulcers on medial ankles)
 DX: Doppler see venous insufficiency
Diaper Dermatitis: candida/fungal  due to exposure of urine/feces
 “satellite lesions”
 TX: nystatin + pt education
Perioral Dermatitis- facial/mouth
 “confluent-papulopustular lesions”
 Hx: young women w/ prolonged used of topical steroids sprays for asthma
 Only around peri-oral + nasal-labial folds
 TX: avoid steroids and give antibiotics
Seborrheic Dermatitis: in axilla, groin, face, hands
 In areas of sebaceous glands
 IN infants: “cradle cap” – thick/yellow brown greasy scaling
 In adults: dandruff on scalp, eyelashes, beardm eyebrows
 TX: selenium sulfide shampoo; ketoconazole shampoo
Lichen Simplex Chronicus: end stage of pruritic/eczema hyperplasia (“thick skin”)
 Hyperpigmentation, hyperkeratosis, plaques with lichenification
 TX: high potent topical steroids + anti-histamines
Psoriasis: genetic T-cell immune rxn
 Increase in epidermal proliferation  hyperkeratosis/ keratinocytes
 Triggers: stress, class 1 steriods, Koebner rxn
 SX: salmon plaque w. distinct border w/ silvery white scales
 On extensor surfaces; “pitting” of nails
 + Auspitz; bx shows increased mitosis of keratinocytes
Lichen Planus: Tcell mediated rxn; destruction of keratinocytes + basal cell layer
 Pruritic, penis, polygonal, purple, plaque with fine white scales on flexor surfaces
 Oral lichen planus- lesions on tongue/buccal mucosa

“Wickham’s striae” – fine white lines in mouth
Seborrheic Keratosis: “pasted on plaque”
 Brown/black velvety/warty/ plugged follicle
 Mc in female > 30 y/o
Actinic Keratosis: pre-malignant lesions to skin cancer
 Sx: yellow-brown/dry rough scales
 TX: topicl 5FU or surgery/debridement
Androgenetic Alopecia: mc in males- occipital  temporal with frontal thinning
 Gradual/genetic; mc in Caucasian males
 Action of androgen on hair follicle (increases in 40s)
 Mc type of hair loss; ↓ anagen phase w/ ↑ telogen phase
 Females: central regression (maintain frontal hairline)
o Ass. with acne, hirsutism, virilization
 TX: minoxidil, finasteride
Telogen Effluvium- triggered by stress (happens 2-4 months after stress)
Anagen effluvium- drug enduced happens immediately (due to chemo)
Alopecia areata- hairloss in round areas w/o inflammation
 No pinpoint dots; “EXCLAMATION POINT hairs”
 Affects any hair on body; mc in young adults/children
 If hair regrows- fine grey/white
 Alopecia totalis- loss of hair on scalp/face
 Alopecia universalis- loss of all body hair
 Etiology- T cells ineract with HLA
 “peri-follicular lymphocyte infiltrate”  autoimmunity
Hutchinson’s sign: back streak on nail- Melanoma
Subungal hematoma: blood under nail b/c of trauma
Splinter Hemorrhages: thin longitudinal red subungal lines; sx of infective endocarditis
Oncholysis: nail is white, detachment of nail from it’s bed @ distal end
Onychomycosis: “2 feet, 1 hand” ass. with tinea manuu + pedis
TX: terbinafine
Felon: Sub-Q infection of pulp of digit b/c of penetrating injury
Etiology: staph/strept TX: I+D
Fleas: “breakfast-lunch-dinner” bites on lower legs (hx of pets)
Bed bugs: nocturnal (pt feels itchy before sunrise)
 Bites are also in groups of threes
 TX: permethrin spray
Pediculosis (lice): transferred by fomite, person-person
 Itching in temporal-occipital lobe
 TXL permetherin/ pyrethin/lindane
Scabies: burrows into hand/groin/axilla/fingers
 Risk: hospital, nursing home work
 Lesions in interdigital web spaces
 May cause secondary rxn from eggs
 Increased pruritis at night
Spiders:
1. Black Widow: black with red hour glass; neurotoxic only- N/V, musclar cramping in back, abdominal
2. Brown Recluse: tissue toxin- fever, chills, N/V/ arthralgia
a. Brown w/ yellow head + violin markings
b. Sx: “red-white-blue” discoloration  skin necrosis
Ticks:
1. Dermacentor: causes RMSF  neurotoxin
2. Ixodes Scapularis  Lymes disease (spirochete) with erythema migrans

Cuteneous mets from cancer:
1. Virchow’s noes (left supraclavicular node)
2. Sister Mary Joesph’s- peri-umblical node
3. Paget’s diease- on unilateral breast cancer
Acanthosis Nigricans: thickening of skin in neck/axilla/groin
 May be associated with carcinoma, obesity, Dm, steroid, INH
Dermatomyositis: symmetric muscle weakening, abnormal electromyogram, ↑ CK
 Heliotrope Rash- periorbital; hypopigmenation
 Gottren papules- over bony prominence on hands
Hyperthyroidism: skin is smooth, flushed, mosit, warm
Hypothyroidism: skin is dry, cool, pale, brittle hair
Scurvy: Vit C deficiency  hyperkeratotic ecchymsis like papules on shins
 Hair twists in corkscrews + breaks easily
Sarcoidosis: erythema nodosum- acute/painful panniculitis
 Inflammation of sub-q tissue on shins
 African American young women
Lupus (SLE):
 Discoid SLE
 “scarring plaques with atrophic scars”
 Subacute- shawl-like annular plaque on sun-exposed area
 Systemic- butterfly rash w/ photosensitivity
Reiter’s Syndrome: “can’t see, can’t pee, can’t dance with me”
 Conjunctivitis, urethritis, arthritis
Scleroderma- autoimmune disease
 C- calcinosis deposits on skin
 R- raynaud’s phenomenon (vasospasm)
 E- esophageal dysmotility
 S- sclerodactyly- thick fingers
 T- Telangietasias
Peutz-Jeghers:
 Lentigines on skin, mouth, mucosa
 Pt has polyps with increased risk for GI Cancer
 DX: Barium study at 10 and colonscopy at 25
Vitiligo: depigmenation, autoimmune, ass. w/ thyroid diease, Dm, addison’s, lack of melanocytes
Xeroderma Pigmentosum: allergy to light
Albinism: lack of tyrosinase in melanocytes
 White skin, white-yellow hair, light blue eyes
 Ass. with nystagmus
Melasma: hyperpigmentation in sun-exposed areas (face)
Cholasma: ass. with pregnancy, hormones, disappears spontaneously
Neurofibromatosis (genetic): Crow’s sign, Lisch nodules in eyes
 1st sign- Café au Lait spots > 3 spots
 Mortality  ass. with cancer
Squamous Cell Cancer: malignant; hx of actinic keratosis
 Risks: UV exposure, outdoor occupation, white skin, HPV virus
 Sx: ulcerated/ crusted/ hyperkeratotic/ pink-red/ top of ear + nose
Basal Cell Cancer: MC skin cancer
 “translucent pearly papules w/ fine telangiectasia with large black ulcerations
Melanoma: enlargement/ elevation of nevi with new mole
 Asymmetry, irregular borders, least common but most fatal
Keloids: hypertrophic scars w/o collagen
Opthomology
Macula- good for detailed vision/ made of cones
Fovea- dense amt of cones
Choroid- provides nutrition to retina thru vessels
Palpebrae fissure- open btw upper and lower lids
Canthus- corners where eyelids meet
Ptosis- drooping of eyelids
Ectropion- lower lid turns out
Entropion- lower lid turns in
Proptosis= exophthalmos  protruding eyes
Hordeolum= sty (mcc: staph)
Chalazion- hard, nontender swelling on lid
Blepharitis- inflammation on lid margins, dandruff on eye lashes
Pinguecula- yellow nodule on conjunctiva
Pterygium- intrusion onto cornea of scarring/nodule
Scotomas- vision field loss
Miosis- constriction of pupil (PNS)
Mydrias- dialation of pupils (SNS)
Anisocoria- large pupil cannot constrict
Adies Tonic pupil- no light rxn
Argyll Robertson pupil= small irregular, no light reaction  sx of syphilis
Cover-uncover test- detects strabismus
Strabismus- can not align eyes  diplopia
1. Non-paralytic- short muscle pulls eye in 1 direction (deviation is constant)
2. paralytic- paralysis of muscles- deviation depends on direction
Esotropia- eye goes in
Exotropia- eye goes outward
Hypertropia- upward deviation
Hypotropia- downward deviation
Amblyopia: “lazy eye” because of poor muscle tone
Myopia- nearsightedness (can’t see far away)  need concave lens
Hyperopia- farsighted- can’t see up close (light focuses behind retina)  need convex lens
Astigmatism- corneal surface not spherical
Grave’s disease (hyperthyroidism)  lid lad/ exophthalmos
Macular Degeneration- MCC of vision loss in US (loss of central vision- gradual)
Viral Conjuctivitis: mcc is adenovirus
 pre-auricular LAD with watery discharge
 no change in vision, no photophobia
Bacterial Conjunctivitis- staph, H. flu, strep pneumo, pseudomonas, gonorrhea, diphtheria
 sx: yellow-green discharge; crusty eyes
 sx: chemosis- membranes that line eyelids- surface of eyes of swollen
 tx: polytrim (tx of choice)
 mcc of neonatal conjunctivitis- Chlamydia
o Tx: Azithromycin + ceftriaxone
Allergic Conjunctivitis- IgE, histamines/LT
 Puffy red conjunctiva, thin watery discharge
 Cobblestne papillae and no LAD
Keratoconjunctivits Sicca (Sjogren’s disease)
 Dry, red, scratchy eyes with irritation  no tear film
 DX: Schirmer test
Pinguecula- caused by trauma, UV exposure, drug windy weather
Dacrocystitis- lacrimal sac infection
 Mcc- staph/strep
 Chronic- staph. Epidermis/ candidia
 Sx: red tear sac, swelling, pain with purulent discharge
 Dx: must do CT scan to r/o tumor
 Tx: antibiotic- Augmentin (po) with warm compresses
Blepharitis: inflammation of eyelid
 Etiology: bacterial or seborrheic
 Lacrimal tearing, photophobia, dry flakes on lid; ass. on meibomian gland
Hordeolum- sty (eyelid margin) blocked meibomian gland
 Etiology- staph, painful
 TX: topical antibitics (bactroban)
Ectropion: ass. with CN VII (Bell’s palsy) palsy
 Drooping eyelid, light sensitive, excessive lacrimation
Corneal Abrasion: due to trauma
 Dx: fluoresicein stain with coabalt blue lamp
 Tx: remove foreign body with cotton tip applicator
Anterior uveitis (iritis)- “ciliary flush w/ small pupils, deep eye pain, photophobia”
Posterior uveitis (choroditis)- painless floaters in eye
Intermediate uveitis- Cilitis
Dx: slit lamp exam Tx: mydriatics/steroids
Subconjunctival Hemorrhage- bleeding in eye
Cause: blunt trauma; Vision is NOT affect but you need to r/o a ruptured globe
Open angle Glaucoma- “PERIPHERAL VISUAL LOSS”
 Increased cup: disc ratio
 IOP > 21
Acute Ancle Glaucoma
 Blurry vision, ocular pain, MID-DIALATED Pupil
 IOP > 40
 Causes: SNS stimulation  relaxation of ciliary body  pulls on suspensory ligament  casues mydraiasis and
iris falls forward
 Cloudy, steamy cornea, halos around lghts
 DX: Schiotz tonometer
 TX: iridotomy, pilocarpine (causes myosis), diuretics, timolol
Ulcerative Keratitis:
1. HSV-I: dendritic lesions on cornea- see with fluorescien slit lamp exam
a. Tx: DO NOT GIVE STERIODS (tx with antivirals)
II. Herpes Zoster (shingles) – CN V = ophthalmic branch
 Hutchinson’s sign- vesicle on tip of nose
 Tx: antivirals + steroids
III. Bacterial Keratitis
 Sx: purulent discharge, ulceration
 HYPOPYON- pus in ant. chamber of eye
 MCC in contact lens users: pseudomonas
 MC protozoa in contact lens users: Acanthomoeba
NON-Ulcerative Keratitis
 Causes: syphilis, Tb, SLE, viral
o TX: topical antibiotics
Corneal Ulcer- cx of keratitis  corneal scarring
Blunt Trauma with Ruptured Globe
 Sx: pear-shaped, teardrop pupils  points to site of rupture
 Orbital ecchymosis, bloody chemosis, conjunctival hemorrhage
 Dx: CT scan; slit lamp exam
Hyphema- hemorrhage in ant. Chamber (assume ruptured globe)
Metal-foreign bodies form  “rust ring” MRI: contra-indicated
Orbital blowout fx.
 Sx: ocular pan  loss of upward gaze; diplopia
 Orbital ecchymoss; palpable bony step offs
 DX: xray of maxillary sinuses: Water’s view
Chemical Eye Burn: alkali burn is more damaging
 Immediate irrigation with Morgan lens
Orbital Cellulitis: can lead to meningitis
 Mcc- staph
 Sx: painful ocular movement, fever, decreased ocular motility; decreased vision
 Sx: proptosis, limited EOM, edema
 DX: CT scan
TX: IV antibiotics
Retinal Detachment: vitreous fluid  lead to more damage (tear flaps)
 Sx: sudden painless unilateral vision loss
 “Dark curtain pulled down over vision”
Central Retinal Artery Occlusion
 Ass. wth cardiovascular disease (embolic)
 Sx: sudden painless unilateral vision loss
 Pale retina with cherry red fovea
Papilledema- caused by venous stasis + HTN
 Sign of increased IOP
 Sx: swollen optic disc ratio with blurred margins + loss of vessels
Nonproliferatve Diabetic Retinopathy:
 Hallmark: MICROANEURYSMS- 1st detectable sign
 Hard exudates, ischema cotton wool spots
 Leading cause of adult blindess
 “hazy disc margins”  macular edema
 Flame-shape hemorrhage  superficial retinal hemorrhage
 Dot + blot hemorrhage  deep retinal hemorrhage
Proliferative:
 NEOVASCULARIZATION
 can result in retinal detachment
 pre-retinal vitreous hemorrhage  boat shaped hemorrhage
HTN retinopathy: prolonged narrowing of arteries
 blurred optic disc  papilledema
 retinal streak hemorrhages; AV nicking; copper wiring
 macular star  soft exudates (infarct)
Otolaryngology
Turbinates:
superior: drain thru sphenoid sinus;
middle: drain thru paranasal sinus;
inferior: drain thru nasal-lacrimal ducts
Paranasal sinuses  drain thru ostia
Parotid duct- Stenson’s duct
Submandibular duct- Wharton’s duct
Conductive hearing loss- external/middle ear
Sensorineural hearing loss- problem with chochlea or nerve (inner ear)
Weber’s test- tuning fork on head
 conductive: lateralized to affected ear
 sensorineural: lateralzes to unaffected ear
Rhinne test- normal if sensioneural hearing loss (AC> BC)
 abnormal- BC> AC (if conductive hearing loss)
Conductive Hearing Loss
I. Cerumen Impaction
II. Otitis Externa
a. Pain on tragus/pinna movement; canal edematous
b. Tx: corticosporin otic solution
III.
Foreign Body- unilateral discharge from ear
a. Tx: insect- lidocaine with mineral oil; removal; prophylactic antibiotics
IV.
Otitis Media- mcc: strep pneumo, H flu, M cat
a. Hearing loss ass with children’s speech impairment  E tubes
b. Tubes if: >3 in 6 months; > 4 in 12 months
c. TX: amoxicillin + Sudafed
V. Serous Otitis Media (Tm retracted)
a. Dx: decreased mobility of Tm
b. Tx: Sudafed + antibiotics
VI.
Tm perforation- from trauma/AOM
a. Tx: topical or po antibiotics + tympanoplasty
VII. Myringosclerosis- white calcium on Tm
VIII. Tympanosclerosis- stiff/fibrosis of Tm
IX.
Otosclerosis- immobilization of stapes bones @ oval window
a. Prevents ossicles from moving (3 bones become 1)
b. Sx: low frequency hearing loss + tinnitus tx: hearing aids
X. Cholesteatoma- benign lesion behind Tm
a. Sx: chronically draining ear (fails to respond to antibiotics tx)
b. Tm perforation with cheesy white debris
Sensorineural Hearing Loss
I. Presbycusis (MCC of sensorineural loss)
a. Sx: bilateral, hx of noise trauma, may have tinnitus
b. Affects high-frequency hearing loss; worsened by nosiy enviroments
II. Acoustic Neuroma (CN VIII tumor)
a. Unilateral hearing loss, tinnitus, vertigo, ass. with ataxia
b. Brain stem dysfunction; ass. with Bell’s Facial Nerve Palsy
III.
Meniere’s disease- hearing loss in 40s; increase in endolymph
a. Unilateral low frequency hearing loss
b. SX: aural fullness, tinnitus, episodic vertigo tx: decrease in salt intake, diuretics, steriods
IV.
Toxin mediated- drug induced, high frequency loss
a. Drugs: ASA, NSAIDS, diuretics, aspirin, chemo
Perforated Tm- hx of diving, airplane flight
Sx: hearing loss w. tinnitus + purulent otorrhea
Acute OM- mc in children b/c ET tubes  can lead to conductive hearing loss
 Mc etiology: strep pneumo, M Cat, H flu
 Can’t see “cone of light” on Tm
 TX: antibiotics, tympanometry, AVOID ANTIHISTAMINES
Recurrent OM 3 n 6 months, 4 in 12 months
Otitis Media Effusion- mc in divers/flights
 Decrease in Tm mobility or retracted
 May have hearing loss dx: tympanometry
Chronic OM- caused by pseudomonas, proteus, staph
 SX: fullness of ears/pain, purulent discharge
Barotrauma- change in pressure btw inner and outer ear
 Inability to equalize pressure  flying/diving
 Tx: decongestants, myringotomy, Valsalva (auto-inflation)
Mastoiditis- “post auricular fluctuance”
 Casues: Strep pneumo, M Cat, H flu
 Edema over mastoid; CT: see bony destruction
Labrynthitis- viral infecton
 Sx: vertigo, hearing loss, decrease in balance, N/V, nystagmus, tinnitus
 CT: r/o tumor or CVA
tx: steroids, sedatives, antivert
Vertigo- motion perceived when there is none
 Causes: peripheral or central brain lesions; CN VIII dysfunction- acoustic neruoma
 Note: nystagmus is horizontal (rotational) with peripheral lesions
 Nystagmus is vertical (bidirectional) with central lesions
Allergic Rhinoconjunctivitis- IgE + mast cells
 Sx: sneezing, rhinorrhea, polyps filled with eosinophils, itching + red eyes
 Risks: family hx of atopy, trees, grass, pollen, ragweed
 Tx: antihistamines, LT antagonists, steroids, vasoconstrictor eye drops
Urticaria- superficial lesions w/ pruritis + blanch with pressure
Angioedema- deep in SUB-Q tissue; edema of eyes, lips, hands, feet (puffy and not pruritic)
Vasomotor Rhinitis- non-allergic
 Increase in cholinergic gland activity (PNS dysfunction)
 Sx: rhinorrhea, all allergy tests are normal, no nasal pruritis, no sneezing
 Blood vessels contract then dialate to increase mucosal secreation
 TX: topical anticholinergics, steroids, antihistamines
Rhinitis Medicamentosa: overuse of topical nasal decongestants (ephedrine, phenylephrine)
Tx: stop nasal medication  take oral decongestants
Atrophic Rhinits: change in cells: ciliated columnar  replaced by stratified squamous
 Dry nasal turbinates; anosmia-loss of smell
 OZENA- foul green discharge/ epistaxis
Sinusitis- mc is Maxillary
 Obstruction of ostia or loss of cilia function
 Risks: recent URI, allergic/chronic rhinitis, polyps
 Etiology:
o
Acute- bacterial (strep pneumo, h.flu, viral, fungal)
 Sx: sinus pain, yellow-green discharge, sinus pressure < 1month
o
Chronic- anaerobes (staph, strep)
 > 3months; no fever, dull HA, cough
o
Fungal- non-fulmnant (increase in eosinophils) only one sinus affected
 Mc-aspergillosis, usually HIV +
 Dx: CT (water’s view-maxillary sinus)
 Cx: osteomyelitis, cellulitis, mucocele, polyps, meninigits
 TX: antibiotics- Amoxicilln, Decongestants
Viral Rhinitis- common cold

Etiology: rhinovirus, parainfluenza, coronavrus, adenovirus

Incubation: 1-5 days (may last 7-2 weeks)

Watery mucosal discharge, sneezing, clear rhinorrhea, low fever, HA

TX: antipyretcs, analgesics, decongestants

CX: secondary bacterial infection
Nasal polyps- small sac, non-tender, grey grape like mass,

Risk factor: cystic fibrosis

Asthmatic + nasal polyps  hypersensitive rxn to ASA
Influenza (the flu)- abrupt onset of high fever

Sx: myalga, HA, photophobia, N/V/ non-productve cough

TX: oseltamivir, zanamivir; flu vaccine (effective 10 days after admin)
EBV (mono): transmission via saliva; one infection- life long immunity

Incubation: 2-5 weeks

Prodrome: LAD, HA, fever, fatgue, splenomegaly

Rash with Amoxacillin

DX: monospot/ throat culture

CX: GBS (Gullan Bare- ascending paralysis)
Herpangina- Coxsackie A virus

Hand, Foot, Mouth disease  vesicular lesions on dorsum of hand/palms (may ulcerate)

Sx: acute fever, sore throat, gray-white papulovesciular lesions on red base that ulcer (on soft palate, tonsils,
uvula)
HSV- herpes

Gingivostomatitis/Pharyngitis  1st episode of HSV

Sx: cervical LAD, fever, malaise, myalgia, grouped vesicles on red skin on buccal mucosa

Tx: acyclovir
Gonococcal Pharyngititis

G neg diplococcus; sore throat with LAD

Risk: sexually active (oral) dx: culture on Thayer Martin Media
Diptheria- sx due to toxin only  forms pseudomembrane on pharynx
CX: aspiration-blocks airwayl; sepsis
DX: DpT vaccine q 10 years
Peritonsillar Abscess/Cellulitis:

Strep pyogenes, H. flu, Strep viridans, Staph

SX: TRISMUS, odynophagia, DEVIATED UVULA, peritonsillar swelling with LAD

TX: I+D, IV PCN or cephalosporin
Retropharyngeal Abscess- deep space infection of neck

Posterior to larynx/ trachea; sx: neck pain, stridor, drooling, stiff neck, swelling, LAD, dysphagia

TX: IV- PCN
CX: pericarditis, airway obstruction
Intra-oral ulcerative Lesions (Necrotizing Gingivitis) “Trench mouth”- painful gingivitis/foul breath

Risks: tobacco, immuno-compromised, stress, poor hygiene (periodontal disease)
Apthous Ulcer- on buccal/labial mucosa

Painful small round ulcer with yellow center with red border
Oral Candidiasis- Thursh “white plaque on mouth/tongue” can be removed tx: Nystatin
Oral Leukoplakia- hyperkeratotosis, precancerous
Risks- trauma, alcohol, tobacco

White and can not be removed

Erythroplakia- red/velvety- more likely to become cancer then leukoplakia
Oral Lichen Planus- autoimmune disease

Sx: purple, polygonal, papules, pruritic

Wickham’s striae- white striations on buccal mucosa

Tx: topical steroids, cyclosporine mouthwash
Glossitis- red, smooth tongue, painful; causes: nutritional def./drug rxn/dehydration
Sialdenitis- infection of submandibular glands
Risk: Sjogren’s syndrome- decreased salivation, pus massaged from duct, swelling of gland
DX: US
Parotidititis- inflammation of Parotid glands (stenson’s); causes: MUMPS sx: preauricular/postauricular LAD
Ludwig’s Angina- Cellulitis of submaxillary space, and sublingual and submental spaces

Sx: tongue displace, edema, dysphonia, trismus, drooling, stridor

Dx: CT, culture tx: IV antibiotics; ICU- b/c risk of airway obstruction

Voice Sounds:
I. Raspy- harsh voice due to edema with low pitch
II. Muffled- talks very low (cause- painful dysphonia)
III.
Shaky- decreased respiratory force (elderly)
IV.
Acute hoarseness- mcc: viral infection or vocal trauma
a. If vesicles on soft palate- coxsackie virus/herpes
Vocal Cord Paralysis- recurrent laryngeal nerve injury; hx of chronic intubation
Vocal Cord Lesions- if smooth + paired  vocal abuse
Leukoplakia on Vocal Cords- premalignant (in smokers, sx of hoarseness w/o pain)
Anterior Epistaxis- mc epistaxis (Kiesselbach’s plexus)

Hx of digital trauma/ foreign body/ URI/ allergies

“unilateral bright red bleeding with no sensation of post-nasal drip”

TX: pinch nose and lean forward  silver nitrate/lidocaine  packing (merocel)
Posterior Epistaxis- mc: sphenopalantine artery

Risks: HTN, bleeding disorder, cocaine abuse

Sx: hemoptysis, hematemesis, no visualzed source

“post nasal drip, bilateral bleed with dark red blood”
Osler-Weber-Renu: disorder of blood vessels- excessive bleeding

Sx: telangiectasias on lips, tongue, nasal mucosa

Cx: hemorrhage  hypovolemic shock
EPIGLOTTITIS- H. flu infection; thumbprint sign;  risk of aspiration/blocked airway; TX: surgery to intubate
CROUP- parainfluenza, viral URI, steeple sign, tx: nebulizer, epinephrine, steroids
Pulmonology
Bronchioltis- RSV in children < 2 y/o; sx: wheezing, dyspnea, SOB, apnea; Peaks in winter

RSV is a risk factor for asthma + allergies

Cx: BOOP- pneumona is interstitial w. scarrng + obstruction

Dx of choice- nasal smear

Tx: epinephrine, humidfer, hospitalize infant < 6 months
Influenza (the flu, most pathogenic-type A)

Most infectious disease of human kind; mc in winter

Inflammatory mediators: THN-alpha, Interleukin-6

Sx: abrupt fever, dry cough, pharyngitis, high fever, cervical LAD

DX of choice- viral culture

TX: zanamivir, oseltamivir
PNEUMONIA
CAP- < 48 hrs of hospital admission; etiology- strep pneumo (mcc), H.flu, Staph, Influenza (viral)

Atypical- mycoplasma, Legionella, Chlamydia
Nosocominal > 72 hrs in hospital/ nursing home

Pathogens- pseudomonas, Ecoli, proteus
PNEUMONIA FACTS …………………………………………………………………………………

Mc in winter; viral mc in children; bacterial mc in adults; infants/neonates don’t have classic sx

Classic sx: rales, cough, ↑tactile fremitis, ↑ vibrations (+ bronchophony/egophony), breath sounds ↓, dullness
to percussion, chest pan

DM- strep, staph

Sickle Cell- strep pneumo, H. flu

COPD- Strep pneumo, H.flu, M Cat

HIV- Tb, PCP

Alcoholic- Klebsiella/ anarerobes

Neonate- mc is bacterial- strepB, Ecoli, staph (then think viral- CMV, HSV)

Infant- mc is atypical (chylamida- has ass. conjunctivitis)

Toddler- mc is viral: RSV, adenovirus (then think bacterial- strep pneumo, h. flu)

Adult- mc is atypical- mycoplasma/ mcc in adults s strep pneumo

DX: CXR (gold standard- but note there may be “lag”- normal CXR with new onset of sx), g stain, sputum
culture, WBC

TX:
o Outpt CAP- macrolide; Outpt CAP w. comorbdities- macrolide + fluroquinolone
o CAP w/ hospitalization- fluoroquinolone
o Cap in ICU- anti-pseudomonal fluroquinolone + AMG
o Nosocominal- anti-pseudomonal fluroquinolone + AMG
PICKING THE RIGHT PATHOGEN IN PNEUMONIA………………………………………………

Strep Pneumo: mcc of CAP; g+ cocci in chains; rust colored sputum; tx: PCN

H. flu: pleomorphic g- coccobacilli; tx: cephalosporin, ampcillin

Staph Aureus: g+ cocci in clusters; risks: CF, IVDA, can by CAP or nosocominal
 CXR: empyema, cavitation in lungs tx: Naf, Ox, Clox, Diclox + RIF

Klebsiella: g- rod; Nosocomal; risks: Dm, alcoholic; “RED APPLE JELLY SPUTUM”
 Found in upper right lung fields; tx: 3 gen cephalosporin

E. Coli: g- rod tx: 3 gen cephalosporin

Pseudomonas: g- rod; RISKS: CF, nosocominal tx: Pipericillin + AMG

Anaerobes: risks: poor dental hygiene, aspiration
 Sx: foul smelling breath/ Bad taste in mouth
 TX: Clindamycin

Mycoplasma pneumonia- walking pneumonia; NO gram stain appearance






 “Bullous myringitis, skin rash”
 Mc in young adults (fall-spring)
 Dx: COLD AGGLUTIN titers tx: erythromycin
Legionella- risks: exposure to water source: air-conditioner
 Dx: Urine Antigen Assay
 TX: macrolide (erythromycin)
Chlaymydia pneumonia- longer prodrome (in neonates) TX: DOXYCYCLINE
Chlaymydia psittaci- hx of exotic birds TX: DOXYCYCLINE
M. Cat- g- diplococci + pre-existing lung disease TX: Macrolide
PCP: HIV + dx: silver sputum stain tx: Bactrim, pentamidine, prednisone
Fungal:
o
Coccidiodes- risks: southwest US
o
Histoplasma- bat/bird feces; travel to Mississippi-Ohio valley
o
Aspergillus: immunocompromised; CXR: fungus ball
o
Cryptococcus: HIV +
o
Blastomyces: travel to MID-WEST US
o
TX for all fungual pneumonia: AMPHOTERCIN B
Pleuritis: mc sx: localized sharp chest pain which increases with breathing

Etiology: young healthy pt wth hx of viral UR

DX: pleural friction rub- “grating sound” on stethoscope
Pleural Effusion: mc sx: SOB/dyspnea

Decreased tacticle fremitus, dullness to percussion

HOOVER sign- lagging expansion on affected side

Etiology: CHF, liver disease, pneumonia, cancer
1. TRANSUDATIVE pleural effusion- ↑ hydrostatis pressure / ↓ oncotic pressure
a. SYSTEMIC factores- capillaries are not inflammated  pleural fluid is PROTEIN POOR
b. Causes: left CHF, PE, liver cirrohosis, pancreatitis (increase in amylase)
2. EXUDATVE pleural effusion- cappilares are inflamed  pleural fluid is Protein rich
a. Cause: decreased lymph clearance; pneumonia, lung infecton, empyema, lung cancer

DX: CXR- blunting of costophrenic angle; cytology to r/o cancer

If continuous effusion  tap to remove fluid or pleurodess- fibrosis with chemicals
Pneumothorax: SOB, chest pain, decreased breath sounds on affected side
1. primary- no lung disease; tall/thin boys w/ family hx
2. secondary- lung disease (COPD, asthma, TB)
3. Tension Pneumo- due to trauma

Mediastinal shift + tracheal deviation; decreased tactile fremitus

Hamman crunch: pre-cordial crunching with heart beat
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TX: immediate needle decompression @ 2nd ICS
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CXR- visceral-pleural line with increased radiolucency
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TX:
1. asymptomatic + <15% hemithorax  observe
2. symptomatic + < 15 % hemithorax  aspiration w/ needle cath
3. Secondary Spontaneous pneumothorax  chest tube
COPD- #1 risk factor is smoking
1. Chronic Bronchitis- Blue Bloater
a. Sx: productive cough x 3 months, rales, ronchi
b. CXR: increase in interstitial markings at base
c. Risks: overwight, frequent chest infections
2. Emphysema- pink puffer/increased AP diameter; Permanent enlargement of air spaces w/ blebs on CXR
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a. Centriacinar- mc in smokers; in upper lobes
b. Panacinar- mc in PT with alpha-1 antitrypsin deficiency
c. Distal Acinar- alveolar ducts/sacs involved; decrease in elastic recoil
i. CXR: hyperlucent, small heart, lungs are lucent w/ blebs + flat diaphragm
COPD in general: ↓↓ FEV-1 with ↑↑ total lung capacity ↑ residual volume
SX: dyspnea, wheezing, barrel chest ↑ AP diameter, clubbing of nails, ↑ rbcs b/c of hypoxa polycythemia
Decreased diaphragmatic excursion/ increased + prolonged expiratory time
Cx: Cor Pulmonale- right sided heart failure
2 TX that alter the course of disease:
o 1. Smoking Cessation
o 2. Oxygen therapy > 15 hrs/ day
o DRUGS only help:
 1. bronchodalators (Ipratropium)
 2. Bronchodialators (Albuterol)
 3. Theophyline (prevent heart failure)
 4. Steriods
Pulmonary HTN > 20 mmHg
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Cor Pulmonale- “right sided heart failure in absence of left”
o MCC: COPD, also: lung fibrosis, PE
o Causes: right ventricular hypertrophy (increase in afterload/ resistance)
o Sx: exertional dyspnea, syncope, hepatomegaly, peripheral edema, ascites, JVD
o DX: EKG- right ventricular hypertrophy/ tall P waves, inverted T waves, right axis deviation
o CXR: prominent pulmonary vessels with increased pulmonary artery pressure
Idiopathic Pulmonary fibrosis
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Pro-inflammatory state- increases fibrosis  O2 perfusion
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Sx: SOB, DOE, clubbing, cyanosis, fine-late inspiratory crackles at base
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CXR: ground-glass patchy appearance, honeycombing
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PFT: restrictive pattern, decreased FEV-1; normal FEV1: FVC ratio
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DX: BX (gold standard)
Sarcoidosis- noncaseating granulomas
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Young African American Female
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SX: erythema nodosum on pre-tibial area, lupus-like butterfly rash
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CXR: bilateral hilar LAD
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PFT: restrictve pattern (↓ FEV-1 with ↑FEV-1: FVC ratio)
Silicosis- DOE, cough, cor pulmonale, clubbing, JVD
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CXR: egg shell calcifications
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Risks: sandblasting, quarry work, metal factory, miner, glass
Asbestosis- cancer causing (mesothelioma)
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Sx: DOE, SOB, cough, rales, cor pulmonale
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CXR: pleural thickening, fibrosis, honey combing pattern
Berylliosis- risks: aerospaces/rocket building/ nuclear weapons/ computers/ oil-gas industry
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Has associated dermatitis rash; dx: BelPT test; CXR: ground glass with hilar LAD
TX of SPN:
1. Low CA risk- serial CXR q 3months x 1year  then q 6 months x 5years
2. Moderate Ca risk  BX
3. HIGH Ca risk  surgical resection
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Malignant: grows 4-8 months
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Benign: fat n nodule w/ halo sign
PE
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Virchow’s triad: venous stasis, hypercoaguable state, endothelial injury
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Mc sx: SOB
V/Q mismatch
Best definitive test: pulmonary angiography
TB
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Risks: homeless, HIV +, endemic areas, crowded living
“soft caseous necrosis” with hilar LAD
Sx: apical rales, anorexia, weight loss, night sweats, productive cough
CXR: ghon’s complex, apical infiltrates w/ cavitations