Inflammation, Vasculitis, and Neoplasia are 3 hallmarks of Pathology

Inflammation
Activation of fibrin dissemination of clot scar tissue
Pusneutrophils PMNmulti-lobed nuclei
o Subacute inflammation
o Bacteria and Necrosis [Dead Tissue] where Neutrophils are seen
Lymphocytes
o Viral infection
o Chronic Infection
o BacteriaBordatella
o B lymphocytesantibodiesplasma cells
Plasma Cells
o Plasmocytomamultiple myeloma
o Lamina propriayou find plasma cells
o Helicobacter pylori
In this infectionplasma cells infiltrate the lamina propria
Eosinophils
o Asthma
o Helminthic
Release Major Basic Protein
Destruction of Helminths
Endocarditis
MacrophagesGranulomatous Infection/Response
o Macrophage= histiocytes
o Chronic inflammation
o 3-5 days of inflammation
o Acid fast bacilli, suture, fungi, etc
Multinucleated GIANT cells
o Langhans---nuclei in periphery
o Its a cell that is dividingso many nuclei are seen
o Cytoplasm is not dividing
o Haphazard nucleiForeign Body Cell Giant Cell
GranulomaNon-necrotic
o Early stages of Granulomaits TB but not caseous necrosis yet because its early
o So just because we dont see the hallmark caseous necrosis we cant rule out TB
GranulomaNecrotic
o LymphocytesTh1 lymphocytes activate macrophages by releasing IFN-gamma
o Where do you see Necrotic granulomas-
TB
HIV
Hansens/Leprosy
Crohns
Sarcoidosis
Ischemic Necrosis [Kidney]
o Atheroma Thrombi
o Deathsee outline
Cellular Response
o PMN abundancefirst 24 hours
o 36-72 hourslarge mononuclear cells-macrophages
o 1
st
weekgranulation tissue, capillaries
o 1 monthresolution or scar
Ischemic Necrosis of Heart
o Neutrophilswithin 24 hours
Enzymatic Fat Necrosis
o Pancreatitisactivate of pancreatic enzymes
o Tissue destruction
o Fat is broken downhas charged groups on itattracts CALCIUMcalcium depositsstains BLUE
o Chronic Pancreatitis and Enzymatic Fat Necrosis
Presents with MALABSORPTION
Rheumatoid Nodule
o Fibrinoid Necrosis
o Subcutaneous nodules in Rheumatoid Arthritis
o Setting of Vasculitis
o Type III Hypersensitivity
o Macrophages
Postmortem necrosis
o Ultimate formno cellular response at all
o No cellular features, just dead tissue
o Gangrenedead tissue attached to a viable host
Where would you see it? Dead Tissue in the Periphery, not infiltrated
Granulation Tissue
o Found in tissues that cannot regenerate themselves
o Earliest collage deposition is Type III
o Later is Type I
o 80% tensile strength after one monthcollagen type I
o Neovascularization
o Spindle-shaped cells are seen fibroblasts
Granulation tissue
o Hypocellular
o Less cells, more collagen
Atrophy
o Normal hepatic cell
o Atrophicshrunken
Chapter 8 of RobbinsInfectious Diseases
o Bacterial colonies
o Gram + diplocci
Dyspnea, fever
Strep. Pneumoniae
o Gram diplococci
Neisseria meningitis
o Acid Fast bacilli
Red Snappers
Thick waxy coat
AIDS patientsno macrophage activationMAC complex
o Aspergillus
Branching septum hyphae
o CMV
Intranuclear inclusions
Looks like Reed-Sternberg
PCR!!
Nuclear Amplification AT
o HSV 1 and 2
Viral inclusions
Tzanck Smear
Neoplasia
Uterine Leiomyoma Fibroids
o Benign proliferation of Smooth muscle cells
o NEVER become neoplasticno malignancy risk
o If woman tried to conceivehard time
o Histo: WHORLED appearance
Intraductal papilloma
o Number one cause of bloody nipple discharge in person younger than 50
o Lactiferous duct
o Finger like projections off the gland
Infiltrating carcinomabreast
o Irregular stellate border
o Area of hemorrhage**
o Grow so fast run out of blood supplyhallmark of malignancy
Carcinoma
o Why is it palplable? Desmoplastic responsedeposition of collagenhost response
o Dysplasiaway to malignancy; atypical nuclei
Invasive Carcinoma
o Broken past basal membrane
o SCC of esophagus
Plummer Vinson syndrome
Tired and listlessanemia deficiency
Spooning of nails-- koilonychia
Difficulty swallowingdysphagia [esophagus]
o Patient presents with Right sided CHF
Metastatic Carcinoma
o Boney trabeculae
o Glandular structure inside boneAdenocarcinoma metastasizes to bone
Carcinoma implantsSeeding
o Severely distended abdomen
o Gelatinous material inside
o Mucinous materialseeding
Pseudomyxomal Peritonii**
Cervix derived
Jelly Belly**
Osteoscarcoma
o Bone making tumors
o Malignant tumor arising from MESENCHYMAL tissuevimentin staining tissue
o Osteogenic Sarcomamakes bone
High Yield Topics they will definitely ask
o TB
o Tissue Repair and Regenerationhow many days
o Different types of Necrosis
CARDIO
o Pulmonary artery embolus
Usually arise from DEEP VEIN THROMBOSIS
Post operative patient
R sided heart failurepulmonary embolus
o Perimortem clot
Lines of ZahnPRIOR TO patient dying
Strata
Perimortem clot
Thrombo/Embolus
Clot, lay RBCs and platelets on top, another clot, lay RBCs and platelets continous
o Postmortem clot
Gravitysedimentationheaviest in bloodRBCS!
Then plasma
Then buffy coat
o Organization/Recanalization of Thrombus/Embolus
Re-estblished blood flow via endothelial progenitor cells
o Renal infarct
Neutrophils
Hyperemia
Histomore pinkeosinophil dye
Necrotic tubulesinfarct
End organend arterial bloody supplyPALE infarct with coagulative necrosis
o Cornonary thrombosis
Hypercholesteremiacholesterol plaqueAtheroma plaqueNOT OCCULSION of vessel that
causes thrombosis its the RUPTURE
It can rupture lots of Tissue factorFactor 3 activate EXTRINSIC Coagulation Factor
FORM Coronary Thrombosis
o Ischemic Necrosis
Pus-likeneutrophils
Free Wall rupture
1-2 weeksgranulation tissuecollagen 3less likely to rupture
o MI complications
0-24 hours--#1 complication is arrythmia
Acute suppurative
Free Wall Rupture
Granulation Tissue
Heart Failure/Forward Failure
o Constrictive Pericarditis---Dresslers within 1-2 weeks of MIAutoimmune
If there is Pericarditis within 3 days of MI it is not autoimmune/Dresslers
o Myocardial Infarct
Subendocardial ST depression
Transmural ST elevation
Aortic Stenosis/ Hypertension
MIfibrosis
Patients Ejection FractionDecreased
Complications
Dilation ventricular aneurysms
Or Mural thrombi
o Atherosclerosis
Initial stepFATTY STREAK
Fibrous cap; cleftscholesterol
Foam Cells macrophages and Smooth muscle cells ***
Both of these cells can form foam cells
Calcified deposits
o Aortic Aneurysm
Walldilationsaneurysm
Atheroma increase pressure
Law of La Place
Law of tension is directly proportional to radius
o Aortic dissection
Tearing of intima
Inner 2/3
Outer 1/3
In people with connective tissue disorders
Increase in mucopolysaccharides--MPS
Used to be called Cystic Medial necrosis deposition of MPS
o Myocardial hypertrophy
Boxcar nuclei
Hyaline Vascular Arteriolosclerosis
Diabetes
Non-enzymatic glycosylation
Hyperplastic ArteriolosclerosisOnion Skinning
o Rhemuatic Fever
Autoimmune
Poststrep
Pancarditis
Sterile vegetations
No bugs
Jones Criteria
Aschof Bodygranuloma
Marcophages, plasma cells, etc
Anistchow Cells
o Myocarditis [Viral]
Virus: Coxsackie
Foreign: Trapanosoma; Chagas
Drug induced eosinophils
o Bacterial Endocarditis
Healthy: S. aureus
Damaged: Virdians group
Chordae tendinaeshort and fused
Gram StainGram +
Clusters
Staph aureus
o Non-Bacterial thrombotic endocarditis [Marantic Endocarditis]
SLE
Lupus anticoagulantin vitroacts as a anticoagulant
In vivoacts a coagulant hypercoagulable state
Most common cause of hypercoagulable state
Factor 5 mutation
Prothrombin mutation
Respiratory
o Lobar Pneumonia
1. Consolidation
2. Red Hepatizationneutrophils, RBCS
3. Gray Hepatization
Intense congestion--suppurative
o Pneumonia
Pus and neutrophils
Dialted Blood Vesselsin the SEPTUM
o Calcified GranumolaTB
Scarring
Ghon Foci
o Reactivation of Tuberculosis---when immunocompromised
Apical Lobe
Simon Foci
o Miliary TB
Blood seed back into the lungs
Cheesy-white caseous necrosis
Necrotic granuloma
o Emphysemaauto-digestion
Smoker
Primarily neutrophils
Destruction of septa
Large empty spaces
Alveolar spacesnormally 1-2 mm; in emphysema they are HIGHE
Hyper-radiolucency on X-Ray; tympanic on percussion
o Bronchiecatasis
Inflammation and of bronchioles
Collection of mucous and pus PLUGlots of Gram negative, oxidative positive
BacteriaPseudomonas aeruginosa
Rareamyloidosis can occur
o Asthma
Eosinophils
Increased number of globet cells
Release inflammatory mediatorsLTE, LTB4, LTC4anaphylaxis
o Asbestos bodies
Iron/Salt Material covers
o Broncial Carcinoid
Benign variant of small cell
Neuroendocrine
Secrete Serotonin---
o Carcinoidsalt and pepper appearance
Lymohocyte APPEARING
o Bronchogenic carcinoma
Squamous cell carcinoma
Pearly white appearance; KERATIN
Smoking
Squamous cell and Small cells
**Most common diagnosisAdenocarcinoma in Non-smoker, woman
2ndary bronchiectasis due to obstruction of lumen by tumor
o Squamous Cell Carcinoma
Hypercalcemia Paraneoplastic syndrome
PTHrP
o Adenocarcinoma
Hyperchromatic, irregular shaped glands
Desmosplastic
K-RAS gene more specific
o Small Cell Carcinoma
Neuroendocrine cells
Chromagranin and Synaptophysin +
Paraneoplastic Syndrome
Cushings Syndrome
HyponatremiaSIADH
o Pulmonary Infarction
Hemorrhagic
Histo: RBCs
Dual supply
Recanalization of thromboemboli
o MCC of pulmonary edemaforward failure, Left sided heart failure
o Right Sided Heart FailureLiver affected
o Chronic Congestion
Hemosiderin macrophages
o Diffuse Aleveolar Damage
ARDS/Noncardiogenic pulmonary edema
type I pneumocyte damage
Blood air barried
Damage of basement membrane and endothelial cells
Potential space becomes real space
Hyalinization
o Protein
o Cellular debris
o Lamellar bodiesfrom Type II pneumocytes
Derm
o Verricca vulgariscommon wart
HPV 6 and 11
o Veruccakeratohylaine granules
o Compound Nevus
At dermo-epidermal junction + dermis compound nevus
Melanocytes from neural crest neurofilament like structures as they progress
Round, raised, DOME-shaped
If they progress dysplastic changescould change into mela noma
o Basal cell Carcinoma
MCC of cancer
UV light exposure
Never become metastatic; they just burrow; so can be excised
Nests of Basal cells
Neoplastic transformation
Host Responselymphocytes
o Squamous cell Carcinoma
Keratin
Actinic Keratinosisputs you at risk for squamous cell
Metastatic
Hyperchromic, nuclei, pleomorphichallmarks of Dysplasia
o Malignant Melanoma
Epidermisvery irregular, asymmetrical
Poor prognosis
Vertical growth
o Psoriasis
Abnormal proliferation on non-neoplastic cells
Parakeratosis
Collection of PMNsMunros abscess
Auspitz signbleeding if plaque scratched off
o Corey Likes Girls in String BikinisLayers of the skin
Barrets Esophagus
Chronic Gastritis
o Plasma Cells infiltrates in Lamina Propria
o H.pyloridown regulates bicarb production
o MC location to find ulcers for H. pyloriDuodenum
o Long term H. Pylori infection
Gastric Adenomcarcinoma
Low Grade B cell Lymphoma or Marginal Zone Lymphoma
o MCC of ulcerH. pylori
Benign Gastric Peptic Ulcer
o Ulcer baseclotted up with blood
o Rugal folds
o Rupturefree air in Peritoneal cavity
o Presentmassive hematemesis
Ulcerated gastric carcinoma
o Heaped up borders!
Gastric Adenocarcinoma
o Earlyvery few dysplastic cells
Ulcerative Colitis
o Spreads Proximallyall the way to Ileo-cecal valve
o Limited to MUCOSA
o Famous complicationTOXIC Megacolon
Deep ulcersbacteria gets in mucosa submucosadamage myenteric plexus
No more peristalisis
Toxic Megacolon
o Barium EnemaLEAD PIPE sign
Crohns Disease
o Transmural inflammation
o Chronic inflammationstricture
o Barium EnemaSTRING sign
o Colonoscopyskipped lesions
o Wallthick fibrosis
o If ruptures fistula
Pseudomembranous Colitisresponse to a toxic
o C. difficile or E. coli
o Antibiotic treatmentprofuse watery diarrhea
Ischemic Colitis
o Of mesenteric vessels
o Complicationsbowel infarction
Pedunculated colonic adenoma
o Starts to grow
Adenoma
o Based on # of glands that are dysplastic
o Cellular atypia
o No goblet cellsdue to severe neoplasia
FAP with secondary carcinomas
o High probability of carcinoma
o Prophylactic colectomy
Colonic adenocarcima
o Right sided lesionsIron deficiency anemia occult blood
o Left- sided lesions pencil stools
Invasice adenocarcinomavia lymphatics
Carcinoid of small bowel
o Has to metastasize to LIVERto metabolize serotonin
o Salt and pepper appearance
Acute Appedicitis
o Increase pressurecut off blood supply acute appendicitis
o Ischemicinvaded with bacteria
Fatty ChangeSteatosis
o Reversible
o Lipids packed in cytoplasm
o ALCOHOLIC patient
CholestasisBile plugs
o Elevated Alk Phosphatase
Central Zonal hemorrhagic necrosisnutmeg liver
Intact portal zone surrounded by central zone
o Zone 3 is closes to central vein
Hemorrhage and encrosis
o Hemosiderophage!
Alcoholic Liver Disease
o Mallory Bodies
Made of: cytokeratin
Viral Hepatitis
o AcutePUS
o Ballooning degeneration
o Chroniclymphocytes
Massive Hepatic collapse
o Nodular changes in response to toxic insult
o Micro/Macronodular changes
o Hepatitis B; CCl4, other toxins
Regular Cirrhosis
o Cells die off; some regeneratescar [cycle]
Hemochromatosis
o HLA gene codes for MHC gene on chromosome 6
o HFE gene on Chromosome 6
Esophageal Varices
o Cirrhosiscomplications
o Cause of deathrupture MASSIVE HEMATEMESIS
Cholelithiasis
o Pigment
o Cholesterolfat, forty, fertile, females
Chronic Cholecysitis
o Aschoff Rokitansky sign
Pancreasscystic fibrosis
o Obstruction of ampulla of Vater
Chronic Pancreatitis
o Activated in pancreasautodigestion
Enzymatic Fat necoris
Adenocarcinoma of the pancreas
o Rugal foldsduodenum
o Head of pancreasproximal to duodenum
o Conjugated bilirubinJaundice
o Whipple!!!! Surgeryremoval of head of pancreas and part of duodenum removed due to shared
blood supply
MSK
Rib fracture
o Increase osteoclastic activityReactive bone formation
o Prostheticosteoblastic
Fractureendochondral bone formation
o Epiphyseal growth plate; cartilage and bone growth on either side of cartilage
Osteomyelitis
o Suppurative
o MCC Staph. Aureus
o Bone destroyedand necrotic: Sequestrum
o Reactive bone formation around the area of necrotic tissueInvolucrum
o Sickle Cell PatientMCC is Salmonella
Pagets Disease
o Polyoma virus
o Affects Osteoclast
o Lysing of bone
o Haphazard/Squiggly cement linesmosaic patternnormally should be LINEAR
o Osteoclasts with SO many nucleiabnormal infected with virus
o Prone to fracture
Osteogenic Sarcoma
o Occurs in young teen males, distal end of femur or proximal tibia
o Codmans Triangle
o Sunburst appearance
Chondroscarcoma
o Elderly patients
o Flat bones
o Chrondo-rick material; bi-nuclei chondrocytes
Multiple MyelomaRib
o Malignant
o IL-`1 and IL-6 [Acute phase reactants] activate osteoblast punched out lesions
Osteoid Osteoma
o Reactive bone formation
o Thickened trabeculae
o Young patient, at night, asprin helps
Osteochondroma
o Epiphyseal plate broke off early, so formed its own normal bone
o Its normal bone
Osteoarthritis
o Femoral head
o Wearing down of cartilage
o Bone on bone articulation
o Ebraunation of bonepolishing
o NO INFLAMMATION
Rheumatoid Arthritis
o Lymphocyte and
o Affecting Synvovial membranePANNUSgranulomatous infiltrations
Macrophages, lymphocytes, and plasma cells
Kelpid
o Hypertrophic scarstays within confines of initial insult
o Increasee collagen
o Extend outside of the region of initial insult
GoutTophus
o Ear
o Monosodium Urate Crystals
o Negative bifringence crystals from synovial fluids

NEURO
Acute Infarcations-24 hours
o Swollen, edema in Acute Infarction of CNS
o 24 hoursdense neutrophils infiltration
o Hippocampal, CA1 neurons MOST prone to ischemic insulta lot of stress ; wont remember
o CerebellumPurkinje cells will not be able to see themvery prone to ischemia
o Red Neurons, dead tissue within 24 hours
17 days laterInfarction
o NecrosisLiquefactive
Related to lysosomal enzyme activation
CNS tissuehas a lot of lysosomes hence why CNS has liquefactive necrosis
o Buxmol blue stain
o Macrophagesmyelin tissues degraded within the macs stained with Luxol blue
o No fibrocytes in CNSinstead astrocytesyou get instead GLIOSIS!
BRAIN TUMORS
o Astrocytoma
Low grade
Irregular mass pushing on corpus callosum
No sharp borders
No inflammatory cells; just astrocytes
o Glioblastoma
High grade neoplasm
Very deadly
Hemorrhage
Butterfly appearance
Histovery abnormal looking nuclei, hyperchromatic, mitotic figures
Endothelial proliferationangiogenesisto avoid hemorrhage
Histo: serpentile; pseudopalisading
o Oligodendroglioma
Peripheral clearing
o Meningoma
Psammomma bodies
Papillary carcinoma of thyroid
Pale, tan-like
NF-2!! High association
Mainly benign
Can be bad if grows in places its not supposed to because compression of BV, etc
o Global ischemia
Swelling, atrophy, changes of gyri
Histored neurons
Mutiple Sclerosis
o Luxol stain
o Demyelination
o Lymphocytes Th17 lymphocytes; IL 22 and 23 activate Th17]
o [Th17implicated in autoimmune; so it is Targets in Autoimmune drugsPsoriasis]
Subactue Sclerosisng Panencephalitis
o Seen in measles
o Deadly, no treatment
o PreventativeMMR vaccine
o Early manifestationacute behavior/personality changes
o Histo: inclusion due to virus
Acute Meningitis
o 0-2: Strep B, E.coli, and Listeria
o Teens: N. meningitis
o Elderly: Strep. Pneumoniae
Cerebral Abscess
o Can be walled off
Alzheimers
o Prominent atrophy
o Neurofibrillary tangles and plaques
o Cerebral-Amyloid Angiopathy
o Hirano bodies
o Granulo-macular degeneration
o May have association with
Lewy Body demential
o Alpha-synuclein
Parkinsons Disease
o Loss of dopaminergic neurons in substantia nigradepigmentation
Creutzfeldt-Jakob Disease
o Spongiform Encephalitis
o Neuropathologists
o Presents with RAPIDLY PROGRESSIVE DEMENTIA
ALS
o Is PURELY motor!!!!
o If there is Motor and SENSORYSyringomyelia
Huntigntons Disease
o ANTICIPATIONEARLY ONSET IN SUBSQUENT generations
o Dilated lateral ventricles
o CAG repeats
o Autosomal Dominant

Endocrine
Diabetes Type 1
o Dense cellular infiltrates
o Young kid
Diabetes Type 2
o Pink, amorphic materialamyloid deposition
o Antibody mediated destruction
o Obesity
o Autoimmune disorder
Islet cell Tumors of pancreas
o Malegynaceomastia and hypercalcemia; presented with bout of hematemesis
Upper GI endoscopymultiple GI ulcers
Diagnosis: MEN 1
Multiple ulcers, Ademocarcinoma of pancreas
o Necrotizing epidermylsis--GLUCAGON
Pituitary adenemaprolactin
Parathyroid tumors Hypercalcemia
MEN 2
Pheochromocytoma
Medulllary carcinomaproduces calcitonin amyloid
MEN2BMarfan habitus; oral Neuromas
o Small, round, blue, cells, uniformsneuroendocrine
Pituatry adenoma
o Bitemporal heminanopsia
o Presents with amenorrha
o MCC of primary amenorrheaTurners syndrome
AdrenalitisAutoummune
o JFKprimary adrenal disorder increase ACTHincrease MOMA
o MCCTB back in the day; now its autoimmune
Nodular hyperplasia of adrenal [Diffuse]
o Cushings Disease **pituitary release of ACTHtrophic hormone can cause HYPERPLASIABilateral in
this case
o Histo:
Multinodular hyperplasia of thyroid
o Goiterdue to
Hashimotos thyroidits
o Small, round, blue cellslymphoid follicule appearance
o Destruction of
Papillary carcinoma of thyroid
o TSHsky high level
o Histo: Psammoma bodies
Areasclear cytoplasm- Orphan Annie Aniridia

Graves Disease
o Pretibial myxedma
o MPS deposition
o Exophthalmus MPS deposits in orbital cavity or fat goes away
o Histoscalloping
Pheochromocytoma
o UrineVMA or metanephrins
o Rule of 10s
o BETA BLOCKERS ARE CONTRAINDICATED IN PHEOCHROMOCYTOMA!!! Creates an HYPERTENSIVE
EMERGENCY
Repro
Squamous Metaplasia
o Cervical epithelium
Severe dysplasia of cervix
o 1/3 of thickenss-mild
o 2/3moderate
o Whole but not BMin situ
o DIC and cuttrage
o Basal cell layer is stem cell for cervical
Endometrial hyperplasia
o Estrogenhyper
o Fertile ground for malignancy
o Hx: Polycystic Ovarian SYNDROME
Endometrial adenocarcinoma
o Glandular tissue
o Tamoxifendownregulates breast tissue, but upregulates endometrial tissue
o Desmoplastic response
o Can be ulcerated
Endometriosis of ovarychocolate cyst
o Rectouterine pouch is another placedysperineum, or painful defecation
Mucinous cystadenoma of ovary
o Ovarian surface derived tumors
o Brenerstransitional cellsassociated with teratoma
o Mucinousresembles intestinalseeds peritoneumJELLY BELLY
o Goblet cells
o PAS stain-bright pink
Ovarian carcinoma
Granulosa cell tumors
o Make hormonesestrogen
o Gross: yellow
o Can put at risk for
o Call-Exner bodiesprimitive endodermal cells
o SeminomasSchuller duvall bodiesresemble primitive glomeruli
Mature cystic teratomadermoid
o See teeth, hair, nails, etc
Struma ovarii thyroid tissue and
Seminoma
o Normal looking cells
o No crowding
Chronic salpingitis
Ectopic [tubal gestation]
o Ampulla
Leiomyoma-fibroids
Hyaditifroms
o Hydorphilc swollen villi
o Complete choricarcinoma
Follicular carcinoma of thyroid, RCC, and Hepato and ChorioHEMATOGENOUS spread
Fibrocystic changes
o Blue dome
Intraductal papilloma
o Stalkfibrovascular core
o MCC of blleding from nipple in woman
Intraductal carcinoma of breast



Renal/Urinary Q-bank notes
o SLE
Antibodies against Smith Antigen
Type III HSR
Type II HSRhemolytic anemia
o Wegeners Granulomatosisupper airways, vasculitis, and renal diseasnecrotizing granulomas
C-ANCA
Serum proteinase 3confirmatory
o CREST
Anti-centromere
o Goodpasture syndorm
Antiglomerular basement membrane antibibodies
o Churg-Strauss, Primary sclerosing cholangitis,Ulcerative colitis, and Microscopic polyangitis
Antibodies against Myeloperoxidase
P-anca possible
o Diffuse Cortical Necrosis of the Kidney
DIC
Overwhelming sepsishyoptension and vasoconstriction
o Multiple Myeloma
Renal deposition of amyloid protein and damage to both glomeruli and tubules
o APCKD
Enlarged kidneys kidneys filled with cystic masses
o Pyelonephritis
Inflammation, renal pelvis
o Sickle Cell Anemia
Affects MEDULLA most severely, and can cause papillary necrosis
o Minimal Change Diseas
Associated with abnormal secretion of lymphokines by T cellsreduces the production of
anions in the glomerular BM increasing the glomerular permeability to albumin and other
proteins
Other conditions, such Hodgkin disease and T-cell lymphoma, are sometimes associate with
minimal change diseases
o Membranoproliferative GN
Consumption of complement factors
o IMMUNE COMPLEX DEPOSITION
Postinfectious glomerulonephritis, Lupus Nephritis, Henoch- Schonlein purpura,
cryoglobulinemia, and bacterial endocaritiis
o Fibroelastic hyperplasia
Reduplication of elastic lamina and fibrosis of the media affects media of Larger interlobular
and arcuate arteries
Benign nephrosclerosisHYPERTENSIVE PATIENTS
Hyaline arteriosclerosis and sometimes patchy ischemic aatropy
o Diabtic nephropathy
Mesangial prolferation, nodular deposits of mesangial matrix, and thickened BM
o E. coli
Childhood HYS with microangiopathic hemolytic anemia
Blood
o CML
Characteristic t(9;22)
Bcr-abl translocation
CML
Results in abnormal proteinchimeric protein
Doesnt exist in body
Activity of tyrosine kinasepromotes growth
Tyrosine can be inhibited by imatinib
In CMLPMNS have decreased LAP
LAP is increased in inflammatory response
CML==myeloproliferative syndrome
Increase neutrophilscharacteristicdecreased enzymatic activity of Leuko Alk Phosphatase
Histo
Abundance of neutrophils
Precursorsmetomyelocytes and myelocytes
o Myeloproliferative syndromes
BM: increased all lineages
Peripheral blood
Increased PMNS/neutrophilsCML
Increased RBCsPCV
Increased plateletsET essential thrombocytopenia
o Increased lymphocytes in PBCLL
o Numerous lymphoblastsacute leukemia
Found in BM biopsy!
Assoc with ALL
o Numerous myeloblasts
Acute leukemias
BM
Late phases of chronic leukemia
o Pancytopenia
Myelodysplastic syndrome
Ineffective hematopoiesis
o Target cells
Thalassemia
Abnormalities of Hb synthesisalpha or beta chain and numerous target cells
Hemoglobin C disease
Liver disease
o Hereditary spherocytosis
Abnormality of red cell cytoskeleton
o Sickle Cell Anemia
Sickling of cells when exposed to low Oxygen
Autosplenectomy may cause some target cells
o Microcytic anemia of iron deficiency
Anemia due to mineral deficiency
o Macrocytic anemias of B12 and folate deficiences
Anemia due to vitamn deficiency\
o DIC
Develop secondary to abruption of placenta
In DICconsumption of all the coagulation factors and platelets
Labsincreased PT, PTT, and TBT
D-dimer assay confirms diagnosis
o WV disease
Increased BT and PTT; normal platelets and PT
Abnormal response to ristocetin
o ITP
Decreased platelet count
Increased BT
Normal PT and PTT
Females in childbearing age with PBS with megathrombocyte
o TTP
Decreased platelets
Increased BT
Pentadfever, thrombocytopenia, MAHA, neurologic symptoms, renal failure
o HUS
Decreased platelts
Increased BT
Following infectious gastroenteritis; E. coli O157:H7
o Bernard-Soulier
Normal or decreased platelets
Increased BT
Defect in GpIb [no adhesion].
Abnormal response to riscocetindoesnt correct with plasma
o Glanzmann thrombastenia
Normal Pts
Increased BT
Defect in GpIIb-IIIano aggregation
o Vitamin K deficiency
Normal platelets, BT
Increased PT and PTT
Decreased clotting factors, 2,7,9,10
Vitamin K injection
o Liver disease
Increased PT and PTT
Decrease ALL clotting factors
o Hemophilia A
Increased PTT
Decrease of factor VIII
Endocrine
o MEN IIA
Medulalry carcinoma of thyroid
Pheochromocytoma
Parathyroid hyperplasia
Adenoma
o MEN IIB
Medullar carcinoma of the thyroid
Pheochromocytoma
Mucocutaneous neuroma
o