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163 Cards in this Set

  • Front
  • Back
Autoimmunity Succeptibility" genes
HLA class II antigen linkage
HLA B27 induction
Costimulation, INfection induced AI mechanism
1- microbe stimulates APC that also shows Self, activated T-cell sees self- attacks
2- self reactive T-cell is activated when shown microbe particles- attacks self
Antinuclear antibodies
antibodies against nuclear cytoplasm components
Generic ANA
RNA, DNA, Protein reactive
ANA test
dsDNA, Smith Ag, Antihistone
Sensitive for SLE
SOme Tp and some Fp
NOT specific
Major SLE factors
Genetic, Non-genetic, B cell hyperactivity
Non- genetic SLE factors
Drugs, sex hormones, UV light damage changes DNA to anti-DNA
B Cell involvment with SLE
CD4+ cells cause self reactive B cells to make antibodies
or something like that
SLE type II hypersensitivity
Abs are direct mediators of damage
Hematologic: WBC, RBC, Platelet
Type III hypersensitivity
Lesions mediated by immune complexes
Arthritis, skin, feve3r, fatigue
Glomerular (anti-DNA complex)
SLE and small blood vessels
Acute- necrotizing vasculitis w/ fibrinoid deposits involving small AA IgDNAC3 in vessel walls
Chronic- fibrosis and intimal thickening
SLE and Skin
lesions exacerbated by sunlight, basal layer liquefaction,
mononuclear cell infiltrate around the BVs
Butterfly Rash
Kidney and SLE
DNA and antiDNA are not filterable- cause damage
Type III hypersensitivity
Late- Changes to Type IV
Kidney and SLE WHO class I to III
I-normal
II- Mesengeial lupus
III- focal Glomerular nephritis
Kidney and SLE WHO class IV,V
IV diffuse proliferative GN,
V Membranous GN
SLE and serosa
pericardial and serous effusions, fibrous exudates, opacification
SLE cardiovascular
Pericarditis, Myocarditis, vascular endocarditis,
Libman Sachs
Atherosclerosis
Warty Vegitations on heart valves
SLE Libman Sachs
SLE and Joints
like the ganja, reefer, stank, stash, hashish, weed, clo,

Artritis, mononuclear infiltrates, no deformity
CNS and SLE
Microvascular injury
Multiforcal cerebral microinfarcts due to microvascular injury
Drug induced lupus
like SLE
HIP drugs suckas
ANA+ for HISTONE
Stop RX
ANA+ for histone
Drug induced SLE/Lupus
Sicca syndrome
Sjorgen w/o other AI disease
Pic- enormous parotid glands
Sjorgen ANAs
Anti SS-A
Anti SS-B
Sjorgen Pt increased risk for
B-cell lymphoma in glands
Def: Systemic Sclerosis
Inflammatory and fibrotic ghanges throughout interstitium of many organs
Systemic Sclerosis and GI
Can't swallow
CREST
Systemic Sclerosis
Calcium (something)
Raynauds
Esophageal dysmotility
Sclerodactyly
Telangiectasia
Unique ANAs to systemic scleroderma
Anticentromere- limited to CREST
SCL-70 DNA topoisomerase- in diffuse S.S.
JO-1
inflammatory myopathy Ab against T. RNS synthetase
Dermatomyositis, polymyositis
Inflammatory myopathies
Dermatomyositis, polymositis
inflammatory disorder that injures skeletal muscle
B-Cell Marker
CD: 19, 20, 21
NK cell markers
CD16, CD56
CD4 T helper cell Role
inflammation, stimulation of B lymphocytes, Cytokines released, acitvation of macrophages
Two types of CD4 and MHC class
TH1-CMI
TH2- Humoral
Both: MHC, II (HLA DP, DR, DQ)
TH1 cell function and cytokine
CMI- IL1 IFN
TH2 Cell function and Cytokine
HUM- IL 4,5
CD8 MHC complex
MHC1 (ALA A,B,C)
HLA-B2
Ankylosing spondylitis
Type I hypersensitivity Rxn
IgE regulated, immediate
Peniciillin, or hives- Urticaria
Local/Atopic
Type II hypersensitivity Rxn
Antibody Mediated
SLE,
Type III hypersensitivity Rxn
Immune complex mediated
SLE- Kidney Probs
Type IV hypersensitivity Reactin
CD4
Cell mediated - Delayed
Poison oak, contact dermititis
Immediate hypersensitivity prototype disorder
Anaphylaxis
immediate hypersensitivity immune mech
IgE antibodiy mediate release of vasoactive amines
Recruit inflammatory cells
Immediate hypersensitivity immune pathology
Tissue injury, inflammation
Vascular dilation, SmM contraction, mucus production
Type II Hyp Prototype
Aemolytic anemia
Goodpasture syndrome
type II Hyp Immune mech
IgG, M bind to targe cell/tissue- phagocytosis or lysis by activated complement or FC receptors
Type II hyp immune lesion pathology
PhagoC and lysis of cells
Type III hypersesitivity
Prototype
Mech
Pathologic lesion
SLE: glomerular nephritis
Deposition of complexes-> complement activated-> leukocytes release enzymes and toxins
INflammation, necrotizing vasculitis
CM hypersensitivity prototype
Mecha
lesion
Contact dermititis, MS, type I DM, RA, IBS, TB (all the acronyms)
activated CD4 t lymphocyte does 2 things
1-cytokines- inflammation
2- T-cell mediated cytotoxicity
Perivascular infiltrates, edema, granuloma, cell destruction
Type I local vs systemic
Hives/Urticaria vs Penicillin anaphylaxis
Myasthenia Gravis
Type II block of NMJ
Graves' disease
Type II antibodies activate thyroid stimulating hormone
Transplant rejection hyperacute
recepient has pre-formed antidonor antibodies, minutes to hours for rxn
Acute vasculits
Dead organ
Transplant rejection acute
days to weeks
need to give immune suppressin
also has associated complications
Transplant rejection chronic
Late presentation
Vascular change and interstitial fibrous deposits
Dead organ- no salvage
increase graft sufvival
HLA/Immunosuppression
INcreased risk of EBV induced lymphoid tumors
Transplant major complication
GVH disease
GVH disease complications Sx
Graft vs host
jaundice, bloody diarrhea, generalized rash
Brutons
B cell maturation problem
lack of mature B cells
X-linked
Recurrent baacterial infections
Rudimentary Appendix and tonsils
IgA dificiency major complication
Serous anaphylactic reaction due to blood transfusion
Hyper IgM pathogenicity
Mutation in CD40, CD40L
(t cells fail to induce B cells to produce other immunogloblulin
no macro activation, no isotope switch)
Job syndrome
Hyper IgE, eiosinophelia, hyper rxn to allergens
Recurrent STAPH infections
Wiskott Aldrich Pathogenesis
Wasp Protein cytoskeleton defect in signal
C1q, C2, C4 deficiency
SLE, AI
C3 deficiency
serious pyogenic infections and glomerular nephritis
C5-C8 deficiency
Lysing loss
Nisseria infections
C1q esterase inhibior
Hereditary angioedema, autosomal dominant
stress edema, increase complement cascade
AL
RA- most common cause, acute phase reactant
liver, kidney, spleen
AB2
Alzheimers
Not dialized in kidneys- transmembrane glycoproteins APP-apoE complex increases in blood
ATTR
Prealbumin
Cardiac and neural sx
AB2M
Pt on long term dialysis
Tendon deposition- carpal tunnel
Class I MHC
Hereditary ATTR
Prealbumin, causes polyneuropathy
Acal
Thyroid gland C cell
Some boloney about calcium in the blood
look for bifrigence!
What does amyloidosis do
deposits all over the place- imagine the organ- now imagine the organ stuffed with deposits- it simply don't work that well anymore
Congo Red
amyloidosis dx
Gp120, 41
HIV envelope glycoproteins
HIV infectious mechanism
enter mucosa- infect T cell, macrophage, dendritic cells- moves to and establishes in lymph tissues where it remains the reservoir for infections
HIV must.... to enter cell
bind- CD4-gp12o binding causes conform change in gP41
T-CXCR, increases virulence and emergence
M-CCR5 (Macro, mono, lymph)
CD4 vs 8 Ratio in HIV
should be 1:1 or greater (2:1)
less than 1-1 is HIV
MORE FOUR
Mucosal vs Dendritic follicular cells
mucosal- entrance to infection
dend- reservoir of HIV in lymph nodes
HIV- why no granulomas?
No CD4= no granuloma or killing
Foamy cells loaded with bacteria
Acute HIV clinical
Low blood virus- present in lymph nodes
Fever, mono-like, diarrhea, enlarged lymph nodes
aseptic meningitis
Middle HIV phase
HIV + ab test
7-10 yrs
Late Stage HIV
fever longer than a month
gharacteristic increase in virus
CD4<200
AIDs
Late HIV confirmed and one opportunisti infection
HIV Elisa Test
Ab present- LATE
HIV candidiasis
Late HIV- oral and vulvovag
AIDS- esophageal, tracheal, pneumonitis
CMV + HIV
Causes disease in areas outside of normal:
lymph, liver, spleen, GI colitis w/ ulcers
Chorioretinitis
Chorioretinits
Blindness w/ decreased CD4 and CMV
Bartonella lesions
bacillary antiomatosis
erythomatous papules and nodules
liver spleen lymphnodes
Aids squamous carcinoma
HPV warty warts
Lipodystrophy syndrome
Fat redistribution to buffalo hump when using HIV antiretrovirals
Immune reconstitution inflammatory disease
Appearance of sx from a previous infection in HIV during Antiretroviral therapy
Oligohydraminos will appear bilaterally
And diaphragm hernia will be unilateral- like your mom, it will be on the L
Lung cystic adenomatous malformation
Hamartomatous dilated bronchioles
CPAM= cysts in cycstic pupm ad....
CPAM= CYSTS dangitt
absorptive/resorptive atelactassis
complete airway obstruction
Post-op fever w/in 24 hrs (everything else takes longer)
mucus plugs in small airways
Mediastinal shift TOWARDS atelactaisis
Compression/relaxation atelactasis
due to accumulation in pleural space
effusion or pneumo
Mediastinum moves AWAY FROM atelactasis
Microvascular injury edema pathway
capillary injuyr in alveoli, cap perm increases
- edema (in any location as well)
ARDS
pulmonary lesions (DAD) that manifest as congestion, edema, surfactant disruption, atelactasis injury
__++++==== interstitial fibrosis
ARDS morph
Diffuse alveolar damage (increase perm= edema)
Gross: Airless, heavy, consolidated
Micro: Alveolar necrosis, neutrphil, hyaline membrane from exudates
FEV1 and Ratio in
COPD vs Restrictive
Decreased FEV and ratio
vs
Decreased FVC no change in ratio (note FVC)
Centriacinar emphysema
Central part; Respiratory bronch
Starts at apex of lung from inhaled irritants (smoking)
Panacinar emphysema
Resp bronchioles, entire panacinus
PIzz- a1 antitrypsin
PiZZ/PiMM
Panacincar Emphyzema/ normal genotype
Bullous
Supleural bleb or bullae (balloon) >1cm
in all types of emphysema
Rupture = PneumoT
Chronic Bronchitis featurs
Sputum increase
increase CO2, cyanosis, heart failure
Blue bloater
increase airway resistance, large heart
Bronchioloitis appearance vs Emphysema
Blue vs Pink
Atopic Asthma
Type I hypersensitivity due to exposure to simulatnts
Intrinsic asthma
Rhinovirus/parainfluenza- decrease vagal receptor threshold
Asthma Morphology
Mucus plug, Eosinophils, eosinophils
smm mhyperplasia. Sub basement membrane fibrosis
Bronchiectasis
Chronic necrotizing infection of bronchi and bhronchioles
leading to an associated permenant abnormal dilation of bronchi
Restrictive Lung Disease Clinical Features
Vasc Damage
decreased vent/perfusion ratio
decresed CO diffusinon capacity
no abscesses, decreased compliance
RLD radiographic findings
Reticulonodular or Ground Glass pattern
Ground glass Pattern
Restrictive lung disease
Idiopathic fibrosis appearance
Cobblestone surface
Cold-Stone Creamery
Silicosis Clinic/morph
Gelatinous sputum,
nodules of upper lungs, Massive fibrosis,
lymph node calcification
polarized bifringent
Prussian Blue
Asbestis
Ferruginous bodies
Asbestos bodies: golden brown fusiform rods coated iby iron containing protein
Pleural plaques
Flat- well circumscribed rubbery
on parietal pleura, often calcified
THICK WHITE covering
Schaumann bodies
Concretions in sarcoidosis
Asteroid bodies
stellate structures within the giant cell in sarcoidosis
Sarcoid plaques and nodules
Sarcoid granules- systemic even to feet
Sarcoidosis lab
POLYclonal hypergammaglobulinemia
Desqamation interstitial Pneumonia
DIP- smokers, macrophages plug alveoli
stop smoking= good prognosis
Pulm Embolism consequences
pulm htn
sudden death, hemorrages, infarct, effusionsS
Smoking Path
increased necrosis in alveoli
Resp bronchiolitis
smoke increases macrophages which induce all sorts of nasty
Any chronic lung disease
leads to pulmonary HTN
Idiopathic pulmonary HTN
2 hit theory BMPR2
BMPR2
inhibits proliferation of SmM and favors apoptosis
w/o it- sm m proliferation in arterioles
Pumonary A HTN morphology
Large A- Atheroma
Small A- Plexiform lesions
Inhibits prolif of SmM
Goodpasture syndrome
lung injury via type II hypersensitivity
Hemoptysis and diffuse hemmorhage
Antiglomerular basement membrane Agbs in Kidney/lung
Wegeners SLE
C-ANCA
Vasculitis associated hemmorhage
epistaxis, sinusitis, scattered granulomas
Bronchopneumonia place/cause
clinical
Lobular. H Inf, SAureus,
Patchy, lung abscesses, empyema- can disseminate to H valve
Lobar pneumonia place/cause
clinical
Lobar (entire lobe) S. Pneumoniae
1-congestion
2- red hepatization
3- grey hepatization (fibrous supparitive exudates)
Complications of Pneumonia
Abscess, empyima, change to scar tissue, decrease in air space, sepsis
Atypical pneumonia symptoms
cause
Hacking cough, no sputum secondary to bacterial infection
Coxiella Burnetti, virus, infA,B,RSV
Atypical Bronchopneumonia
No alveolar exudates= viruses in wall of alveolae
Lung Abscesses
Klebsiella, staph,
Aspiration of oral contents can cause septic embolus
LAst a long time
Squamous Cell Carcimoma
Closest Correlation with smoking
Small Cell Carcinoma Paraneoplastic syndromes
Cushings, SAIDH (decrease Na), Calcitionin- decrease ca, Gastric lcer, Lambert eaton (m weakness)
Small Cell Carcinoma Molecule
Cyanptophysin
Chronogranuin
Squamous cell carcinoma Morph
polyclonal, eosinophylic cytoplasm
Pearls may cavitate
Squamous cell carcinoma PNP
Makes PTH- HYPERcalcemia
Adenocarcinoma
Female >male
no connection to smoking
early metastasis/airborne mets
Adenocarcinoma Morphology
Glands/tubes
Bronchoalveolar (cancer) morphology
Grows along the alveolae orderly
Bronchal carcinoid
Seratonin 5HT
Pancoasts Tumor
superior sulcus- apex of lung
compression of sympathetic ganglion
Lambert Eaton Mesentaric
small cell carcinoma
Biphases of mesothelioma
Sarco- fibrosarcoma-- fibrous
Epithelial- adenocarcinoma- round
Viral URTI morphology
nasal/mucosal swelling
OTITIS media
TBxray
bilateral upper lobe sclerotic image
Abscess
Air fluid level
Ground Glass
Restrictive lung disease
Apical disease
TB
Flat Diaphragm
Emphysema
Lower fluid accumulation
Compression- effusion
Hilar lymphadenopathy
Sarcoidosis
Xray w/o air lin lobe
atelactasis- everything shifted in x-ray
penumonia- filled w/ neutrophils
Pattchy w/o air
1-bronchopneumonia
2-ARDS