PATHOGENESIS GROSS MICRO

LUNG PATHOLOGY
Congenital Anomalies Severe – fatal
during early period
Pulmonary Hypoplasia Defect on both lungs
↓ lung sized
- caused  compressed the
lungs  impede expansion

Eg. Diaphragmatic Hernia,

oligohydramnios

Foregut Cyst From primitive foregut Ciliated Rarely connected to

MC: hilum/ middle pseudostratified tracheobronchial
mediastinum columnar tree
(+) wall glands
Classes: (wall based)
- bronchogenic (MC)
- esophageal
- enteric

Pulmonary Descrete lung tissue NOT Two types:

Sequestration connected to airway
- with abnormal blood Extralobar – outside
supplies arises from aorta the lungs = common
on infants ; mass
Assoc with other
congenital anomalies

Intralobar – inside
lungs
- older children
- due to recurrent
infection
Atelectasis Incomplete expansion or
collapse of the lungs
 PATHOGENESIS GROSS MICRO
Resorption atelectasis (+) obstruction of aiways  - ipsilateral shifting of REVERSIBLE
excessive secretion ( mucus the mediastinum
plug)
Aspiration of foreign bodies
- impairment of blood flows
Compression Significant fluid volume - contralateral shift Reversible
Atelectasis (transudate/exudate (blood mediastinum shift
or air (pneumothorax) in the away from the
PLEURAL CAVITY affected lungs

Contraction Atelectasis (+) Fibrosis Irreversible

- focal or generalized
Pulmonary edema Due to congestive heart Fluid on the
failure dependent portion

Hemodynamic Edema –due to LHF

Cause:
* ↑ HP – volume overload;
pulmonary vein obstruction
* ↓ OP – hypoalbunemia
Liver, nephrotic
* Lymph dse

Microvascular (alveolar Non-cardiogenic

injury) (+) damage vascular
epithelium  ARDS

Chronic Bronchitis Smoking  damage to lining Location: Hypremia, swelling, Persistent CTFR -dysfunction --
cells  inflamm Bronchus edma productive scanty < abdnomal
protective response: Cough, sputum secretion
submucosal glands ↑ Mucus gland
hyperhtopy mucous hyperplasia Blue bloaters Reid index 0.4 (n) ↑
hypersection
Tobacco
-impaired cilary actions 
 PATHOGENESIS GROSS MICRO
cannot remove excess
mucus ↑ risk for infection
Bronchiectasis Persistent or severe Destruction of Cystic fibrosis – CFTR Purulent cough Compli:
infections leads to smooth muscles  defect  defect ion
permanent dilation of brochi Airways dilation transport – thick sec  Cor pulmonale
and bronchioles scarring defective and aiways
Location: obs
Bronchus Primary Ciliary
(dyskinesia (Kartagener
syndrome) – defect in
Lower lobes ciliary motor poretins –
bilaterally dynein( retention of
secrations  chronic
inf,
Allergic
Bronchopulmonary
aspergillosis - a.
fumigatus -- act TH2
helper t cells
Asthma Episodic Location: Types: Wheeze, dyspnea
bronchoconstriction bronchus Acute dever asthma –
(reversible) status asmathicus
Smooth m. hyperplasia Criteria –
↑ mucus prod; inflammation Atopic asthma – mc,
IgE med, (childhood) ↑ airflow obstuction
Immune Non-atopic- adult (-) all Diff with exalation
Pherireal blood
Drug induced asthma – eonophila
aspirin, nsaid, Finding eos,
Chr. 5 – susceptible locus (aspirin uncommon chrushmann
located here. spiralus (atomic),
trigger by inhibiting
cyclooxygenase charcot leyden
Class HLA II – linked to prod
patheawy of crytals in sputum
of ige AB
arachidonic acid metab
– rapid ↓ of pge2 =
IL 33 – th2 production
 PATHOGENESIS GROSS MICRO
TSLP – initiating allergic (inhibit inflamm med)
react from the epithelium Occupational asthma –
fumes , minute qty.
(type1, direct
bronchoconstrictionm
unknown)
Emphysema 1.toxic injury & inflamm  Location: acinus Types: Other forms: Dyspnea Cxr, alkalosis 
smoke damage respiratory acidos
epithelium  inflamm Airspace enlargement Centriacinar – 1.compensatory Pink puffers ↑ residual volume
Fibrosis is small ( diff 2.Protease release Wall destroy affected is central and hyperinflication – ↑ LC
from chronic 3.Oxidative stress = ROS = proximal;spared desginated dilation of ↓ FEV1
bronchisis) tissue damage Loss of elastic tissue distal; upper lobe; alveoli in resoonse of
4. Infection (not initiating  clog  copd; heavy smokers loss lung subs. ( ff. Tx:
byt exacerbate) hyperthropy of SM – removal of lung lobe) Smoking cessation,
thinkening of Panacinar – affected is 2.Bullouse oxygen, long acting
tobacco bronchial wall respiratory bronhiole emphysema-large bronchodilators,
 teminal bl; subpleural bleb >1cm coticodsteroidds ,
lowerzone; a1- 3.obstructive Bullectemoy
antitypsin overinflation-lung Some; lung volume
expands bec of air reduction sx,
Distal (Paraseptal) trapping( cause by transplant
- affected is distal, tumor of FB)
spare proximal; adj 4.Interstinal
pluera, upper half; emphysema- entrance
spon. Pneumothorax of air to connective
Cyst like structure tissue (+) alveolar
tears0
Irregular – no
predilections, scarring
Small airway/ Inflammation Inflammation Cough, dyspnea
bronchiolitis Scarring Scarring

Tobacco
Fibrosing dieasee
Pneumoconioses Nonneoplastic
 PATHOGENESIS GROSS MICRO
Inhalation of mineral dust 1-
5um
Coal workers Inhalation of coal particles Simple CWP – coal
Penumoconiosus Asymptmatic anthacosis dust macules with
(mc) carbon laden
macrophages
(conitain small amt of
collagen fiber)
Compli/massice –
years; black scab: w/
dense collagen
pigments
SIlicosis Inhalation of pro-inflamm MOST PREVALENT
crystalline silicon dioxide or CHORNIC
silica OCCUPATIONAL DSE
IN WORLD
Asbestos – related Localized Pleural placques
DIease
Granulomatosis Dse
Sarcoidosis Unknown cause, systemic Asteroid body – star DX by EXCLUSION
Disordered immune shape
regulation gen predisposed Schaummann bodies
indi expose to - classificationb
environmental agenst
Vascular in origin
Pulmonary Embolism Impt for bedridden Linexahn Saddle embolus MC sourse – deep leg RF: hypercoaguble Dx: CT angiogram
vein thrombosis states Duplexx UTZ
Predisposing condtion:
thrombophilia Dyspneam pleuritic CXR = 12-36hrs after
pain, cough -- wedge shape
w/ plueritis – infiltate
friction rub
Pulmonary Mean pulmonary ≥ 22mmhg Medial hyperthorphy: Group 1: autoimmune
hypertension at rest pulmo mus and elastic BMPR2
a. >> RV hyperthophy Group2: heart fail
 PATHOGENESIS GROSS MICRO
G3: lung dse
G4: chronic thrombo
G5 unclear; multi
PULMONARY infections
Bronchopneumonia P Patchy
Consolidated are if
acute suppurative
Neutrophul rich
Lobar penumoniua Congestion
Red patization (pms)
Gray hepatization
(fibronusupporative
resolutiobn
Bacteria pneumonia Neutrophilic, intraalveolar
Viral Mononuclear
interstitail
Tumors Mc: carcnimoa M ost frequesnt dx RF: smoking, industrial
hazard, air pollution,
acruire mutation
Adenocarcinoma Most common Glandular Mucin production ; Precursor lesion: KRAS none for
Pheripheral differationm lepidic less cured by surgery atypical adenomatous smoker
Common in never smokrers (crawl) papilary, hyperplasia EGFR - smokers
micropapillat, solid Adenocar in SITU IHC= TTF 1, napsin a

Squamous cell 2nd most common Keratixation From: squamous meta Chromosome del
Center Intercellular bridges  in situ tp53, cdkna
In smokers FGFR1 amplification
IHC: p40, p63
Small cell 3rd Small cells, scant High mitosis No precusior Highest mutation,
KULCHITSKY CELLS cytoplasama, ill Azzopardy effect tp532 and rb deacti
MOST adrressive Almost always defined borders, Chr, 3p loss
No site predilection smokers nuclear molding MYC ampliu
Salf and pepper (fine IHC: chromogranin
granulation)
 PATHOGENESIS GROSS MICRO
Pareneoplastic In small cells ca SIADH: ADH
syndrome Cushing ACTH
Hypercal – PTH pthrp
PGE cytokines
(squamous_
Hypoal – calcitonin
Carcnioid – serotonin
brady
GIT
Tracheoesophageal And particiton of trachea A: both atreasia Mc: type c – distal
fistula and esophagus by B prox fistula, distal TEF with proximal
tracheoesophaegeal spetum atresia eso atrecia
c. distal fistula, pro
atresia
d. both fistula
e. no atresia with
connection to trachea
Imporferate anus X cloacal membrane X meconium Mc: congenital
involution intestinal atresia

Diaphargmatic hernia Incomplete diaph Type: bochadelc =

development, herniate abdn posterolat defect, left
into thoracic caivity  side
pulmo hypo Morgagni –
anteromedial defect
omphalocele Failuteof vidcera to return –With sac Related to aother
6-10 aog ch, abdnomalities
Gastrochisis Herniation of interstine  ALL LAYERS incolve ISOLATED
amniotic cavity
Meckels diveticulum Fail involution of True -all layer May (+) ectopic Mc congenital of 2% pop
vitelline/omphalomesenteric pancreas or gastric the GI tract Within 2 feet
duct Lining: intestinal ulceration (60cm) of ileocecal
Loc: antimedenteric side Ddx; appendicitis 2 inches long
2times in male
2 yo asympt
 PATHOGENESIS GROSS MICRO
Pyloric stenosis Erythromycin/Azythromycin Hyperthopic Turner symdrome, New regur, non
– 1st 2 weeks of life (hyperplasia) 45Xo, Trisonomy 18 bilou vomiting,
muscularis propria OLIVE SHAPE 3-5x male
abdominal mass

Hisrhpruing diease Absence of myenteric
(aurbach) and submucosal
(meissners) to due abnormal
migration or neural crest or
premature death
Esophagus
Functiona esophageal Nutrcucker esophagus –
obstruction high amplitude
MOST COMMON
Mechanical Stemosis – luminal
obstrcution narowning
Achalasia Prim: degeneration of NO-
producing neurons
2nd: Chagas ( T, cruzi)
Tx: myotomy
Angalionic segments_ RET mutations Failure to pass AChase – IHC stain
constricted meconium to acces gangling
Normal; dilated Abd ditention cells
Preforation  Intraoperatice
peritonitis frozen section
Diffuse esiphageal LES dysfuntion ; high Sewuale – fals
Spasm ( DES) – resting pressure or diverticula
Corkscrew incomplete relaxation
Repetitive in isolation or Epiphrenic above LES
simultations nomal together with the Pharyngoesophael
ampli - forms (zenker) – above UES –
DESmoothmuscle regur, halitosis
Mucosal webs – semi Esophageal Rings
circumferential ledge (Schatsxki ring) –
like protrutions circumferentioal
AssocL proturions, THICKER,
Plummer VInsion mau contain all three
Syndrom – (triad) layers
- UEwebs A ring – AbOVE GEJ
-IDA B rings – SCJ of lower
-Glositis, chelosis eso
TRAID: Incomolete
LES relax
Increase LES stone
Eso aperistalsis

CM: dysphagiam
 PATHOGENESIS
LACARATIONS Malory wise – long hutidinal
tear near GEJ
sever retshing , vomit
ALCHOL INTOX
Esdo fail to relax 
aperistatlic
(+) hematemesis
Esophageal varices Dilation of esophageal
anastomosis (esophageal
branch of left gastric vein
and azygos to portal
hypertension
Cause: liver cirrhosis 2nd
Alcoholic liver dse
Hepatic Schistomsomiasis
Barretth esophagus
Squamous cell ca More common
Tobacoo and albohol
Diet low un fruits and veg
Hot drink
Orevious radion
Achalasia
GROSS MICRO
diff in belching
Chest pain
Booehavve syndrome Reflux esophagitis Eosinophilc esophagitis
- MC GERD – eesoniphils in
Transmural rupture & Transien LES relax epithelial
tearing of sital eso
Eosinophils in Refractory high dose
Leaking eso content – squamosu mucosa, PPI
mediastintius basal xone hyperplasi,
elongation od lamina Atopic
CM chest pain, shock prop papillae -- allergen prevention
(MI) and corticosteroids
Heartburn, dysphagia,
reguritation
Dilated mucosal and Compliation:
sub mu bleeding
Hallmark: (+) goblet  adenocarcinoma
cells
MIDDLE THIRD Swuamous dysplasia
Well defirentiated
 PATHOGENESIS GROSS MICRO
Plummer vinsion

Adenocarcinoma Chronic GERD tobacco DISTAL THRID barret Both:

Radation Upper: cervical nodes
Gland forming Middle: medist, para
trache,
tracheobronchial
Lowe: gastic nad celiac
STOMACH
Gastritis Indlamm response Gastropathy: absent
Actue: neurophilic infiltrate or rare inflamm cells
Chrnic: mononuclear
infiltrate

Stress related Stress ulcer: pt shock sepsis, Curling ulcers: Cushing ulcers – All: PEPTIC ULCERS:
trauma, proximal Duodenal Intracranial pathology SOLITARY, antrum
↓ intravascular voume, ↓ ulcers seen in burns Direct vagal Multiple lesions in
vasoconstrcinc ( splanchinic) stimulation different locationsl
↓ mucosal bf hypersecretion of with blood vessels
gastric acid thickening and absent
scaring
- healing: re-
epithelization
Chronic Gatritis Mc cause: H. pylori H. pylori: CagA – gastric Antrum
-secreates urease  urea to Multifocal atrophic adenoma Superficial
nh3 ammonia ↑ ph – allows gatritis Pmns
growth Partchy

If diffuse: autoimmune
gastritis (mc but <10%)

Autoimmune Atrophic Antibodies to parietal cells Spares ANTRUM Body

Gastritis and intrinsic factor Deep
↓ pepsinogenI Lymphocytes ,
Endocrine cell hyperplasia macropgahes,
 PATHOGENESIS GROSS MICRO
Vit. 12 def. Diffuse and
extensive
CD4 Tcells  parietal cell
Autoantibodies 
protonpump
Peptic ulcer disease Chronic mucosal ulceration Burning epigastric Solitary, Gsastric Duodenal
pain Pround to ovalm Mucosal atrophy, Antral predominant
Perforated: referred sharply punched corpus ↑ gastric acid
to back, LUQ, or chest ↓ gastric acid Pain several hours
(MI) Heaped up margins- Pain with meals or after meals
pnbeumoperitonium supect malignancy shortly after meals (+) nocturnal
Compli: bleeding (-) Nocturnal awakening
awakening AdenoCA assoc: NO
AdenoCA assoc: YES

Hypertrophic Menetrier disease Zollinger Ellison

Gastropathies Diffuse foveolar hyperplasia Syndrome
+ protein losing enteropathy Parietal cell
Excessice TGF-a secretion hyperplasia +
consequent acid
hypersecretion 
gastrin secreting
tumor – peptic
ulceration
Gastic polyps Risk of consequence Inflammatory/ Fundic polyp glands Gastric adenoma
depends on size hyperplastic
PPI use ↓ gastric acid - Dysplastic
h.pylori  reactive ↑ gastrin – parietal cell
hyperplasia overgrowth Assoc chronic gast,
inflamed polyps atrophy, intertinal
Min. to absent metaplasia
mc inflame

Gastric tumors Mc: adenocarcinoma

Mc site – stomach
 PATHOGENESIS GROSS MICRO
Most commn mesenchymal:
GIST
Gastric Antrum lesse> Prognostic factors. Lauren classification
adenocarcinoma Invation and Intestinal Diffuse infitlratice
nodal/distant mets ↑ WNT signaling CDH1 Ecadherin
Bulky, ulcerative loss
Glandular Dyscohesuve
Intra- apical mucin Signer ring
Extra: gland Intra: signer ring
Extra lakes
Lymphoma Mc extranodel marginal Lympthoepithelaol MALT lymph – MLT
zone be cell lesion and BCL10 not
MALT is usuallt absent, byt responsive to h, pylori
can be induced in chronic
gastritis
Gastrointerinal stromal Carney tiad L GIST, Spindle cell, thin elong IHC: CD117
tumors parangalioma, pulmonary Epitheloiod - Tyrosin kinase
chindroma ephithelial activation
NFT1
Small intestine Mc adhesion Mc <3 Vomiting, abd pain,
intussusception distention
Ischemic Bowel disease Hemorrhagic infart (red) Mc site: colon Surface epi most
Splenic and vulnerable
Acute vas obstraction rectosigmoid Mucosal
Heart mc source of emboli Mural sub and
Athrerosclerosis--RF mucosal
transmural
Diarrhea ↑ frequency Osmotic Malabsorptive Secretory Exudative
>200g/day Unabsorbed solutes, Fail nutrient absopr Isotonic stools - Purulent bloody
seen in lactase def Steatorrhea: bulky, cholera stools – amoebic
greasy, stools
Cealiac dse , CMI
(gliadin – in gluten)
Cholera Vibrio cholerae Rice water stools
Cholera toxin ↑ adp Fishy odor
 PATHOGENESIS GROSS MICRO
stimulatory g protein ↑ camp
Opens cftr channel ↑chloride
sec
↓na and cl reabsorption
Amoebic dysntery Entamoeba hystolitica Cecum and ascending Compli- amoebic liver
colon absess
Ingestion of cyst
Flasked shape ulcer
IBS Chrons Ulcerative colitis
Transmural Mural mucosa
Skip Fiffuse
Ileum + colon Colon
Thick wall Thin wall
Yes all exp Toxic mega Toxi mega
Polyps
Nonneoplastic plyps Hyperplastic polyps Hamartomatous Hamartomatous
Benigh Juvenile Polyp Peutz-jeghers polyp
Serrated archi  delayed Rectum MC AD
shedding of surfaced epi AD juvenile polyposis SI MC
(both in Sesiile serated syn Multiple polyps and
lesions) Multiple mucucoteneos
↑ risk Malignant ↑ malignancy for other
Mc; LEFT colon Extraintestinal: sites
Upper third of crypt serrated pulmonary amvs
(-) lat growth Aborizing networks
Mixed inflammatory for connective titiue,
infiltrate with cilated sm, lamina prop
dilated glands
N looking glands
Neoplatics polyps Sessile serated lesions Colorectal edenoma
With malignant potential (+) dyplasia
Mc RIGHT colon Risk size >4cm
Entire gland serrated lesion Intramycosal ca:
(+)Lateral growth extend to lamina
prop and muscularis
 PATHOGENESIS GROSS MICRO
muc bit the beyond
Familial Tumor Syn Familial adenomatous Hereditary Non-
polyposis (FAP) polyposis Colon
Cancer (HNPCC)
Multiple colorectal Mismatch repair
adenomas as teenages MSH2 MLH1
APC gene ch 5 mutation Amsterdam cri (3-2-1)
Dx atleast 100 polyps Vertified lynch
If untrated  100 symdrome assoc with
adenocarcinoma 3 members (1 should
be 1st degree)
2 generation
1 dx under 50
Colorectal MC malignancy of gi tract Dysplastic columnar Commn mets: Liver Right sided : Left T1: submu
Adenocarcinoma RF: low fiber, high carbo dn epithelial cells with IDA weakness fatigue Change in bowel 2L muscu
fat strong desmoplastic Prognosis: depth Bulky, exophytic habits, bowel 3 pass muc
NSAIDs: protective Mucin producing invatsionm LN mets obstruction 4a visceral peri
Molecular gene: loss of APC (poor prog) ↑msi Annular napkin ring 4b adjacent
Microsatellite instability Signet ring cell type N1a 1
(MSI) (Rare) N1b 2-3
N1c no (+) nodes
But with tumor
deposite serosa
N2a 4-6
N2b 7 or more
M1a 1 site without
peri
M1b 2 or more site
without
M1c
peritoneal ,mets
Anus
Hemorrhoids ↑ venous pressour Internal: External
Ma be assoc portal hpn Superior Inferior
hemorrhoidal plexus Below dentate
 PATHOGENESIS GROSS MICRO
Above dentate SSNK
Dilated submucoal vessels Interstinal type lining Usually present pain
No pain
Appendix Acute ppendicitis Tumors:
Obstcution – stasis – Carcinoid
inflammation
PMNs
Fecalith common
obstruction
Blood Vessels
Vasculitides Iflmmation of bv Large vessels – Undergpes fibroid
Infectious and non granulomatous necrosis
infectious Medium vessels: If immune – type 3
predominantly
necrotizing
Major Non Infectious
Large vesskes Giant cell arthritis (temporal Takayasu arteritis Both: Same micro = dx is
artheritis) <50 yrs old based on age
Common in elderly in the Aortic arch, great Intimal thickening,
west vessels, ↓ dm
Temporal, othalmic Ocular disturbances Medial
Aorta Pulseless disease granulomatous with
Headache elastic lamina
Pain along superficial fragmentation
temporal Tcell infiltrate
Dipload or vision loss CD4>cd8,
multinucleated giant
cell
Medium vessel Polyatheris nodosa Kawasaki Fibrinoid  luminal
Assoc hep b MI in children thrombosis
Vessels: kid>heart>liver>git Coronary atreties
Temp heterogenicity
Abd pain, HPN Feverm conjutival
injection
PROMINENT fibronoid necro Mucosal erythema
 PATHOGENESIS GROSS MICRO
Cevercal LAD
Polymorphus
exanthem

LESS PROMINENT
fibrinoid nec
Small vessles Microscopic polyangiitis Chrug-strauss Granulomatosis with
syndrom angiitis
Henoichschinlein purpyra Allergic Wegeners
and conncective tissue d/o granulomatosis
PAN + pulmonary
involvement
Mpo-anca (p anca) Mpo anca (p anca) Pr3 anca (c anca)
Kidney lung MC Cutaneous, GIT renal Small and medium,
Hemoptysis Palpable purpouro, GI renal
Hematuria proteinuria bleed Oenumonitis,
PAN but temporally FGSG sinusitism
homogenous Cardiomyopathy Acute necrotizing
Keukocytoclastic vasculitis PAN + extravacular granulomatous respi
Infiltrating and fragmenting necrotizing tract
neutrophils granuloma and Vascultucs
eosinophils Focal anf necrotizing
glomeruloneppritis
Cresenteric GN
Buerger Disease Vessels of the extremities,
THrombioangitis tibial, radial
Obliterans Reynaud phenomenon
Instep claudication
Phlebitis
Ulceration  gangrene
Thrombus with
microabcesses
Tumors
Glomus stumor Smooth buscle cells of Look like hamagioma
glomus bodies
 PATHOGENESIS GROSS MICRO
Painful beneath finger nails
Kaposi sarcoma Borderline tumors Most common Patch
Vascular neoplasm by hhpv malignancy related to Red purple dilared
8 HIV Plaque – large
Assoc with aids violacoeus rasce
HHV  infect endothelial Pathch plawue Noudule violet
cells nodules
ANgisarcoma Malignant IHCL CD31 vWf
Soft tiisues, skinm breast
liver
Benign
Hemangiona Cappilary Cavernous
Thin walled capillaries scant Uncapsulated,
stroma infiltrative borders
(+) regression Large cavernous
Juvenytle type (strawberry) blood filled vascular
Pyogenic granuloma =, red space
peduculated lesions on the Vin hippel lindau
skin or oral mucosa disease (AD)
Granuloma gravidaru, (+) VHL vh 3  loss of
pregnancy, regress after function ↑ HIF 1
bbith ↑VEGF – excessive
growth
Thins without RBC
Hemangiomba anf
cavernous
hemangiomas

Massice dilated with

aggregates of
lymphoid

TURNER SYNDROM
(neck)
KIDNEY
 PATHOGENESIS GROSS MICRO
Nephritic Glomerula INFLAMMATION
 loss integrity of filtration
barrier, hematuria >
proteinuria
Obliteration of capillary
lumen  ↓ GFR
PSAGN Type 3 Tuboloiintestinal Enlarge hypercellular Granular deposits of Azotemia in adults
Mc nephritic in children edema, inflamm, rbc glomeruli IgG, C3 and some iGm mostly
GABHS infection cast Cresent in the mesangium and Progression on
M12,4, 1 strain Capillary lumina GBM adults
obliteration ↑ anti streptococcal
titers
↓C3 and other
complements
Rapidly Progressing Progressice loss of renal CRESENTS Type 1 ( Type 2 Type 3
Glomerulonepthitis function  nephritic (cresenteric GN  +) antibodies agains 2- complication of - pauci-immune
syndrome with severe hallmark GBM immune mediated (+) ANCA
oliguria - anti gbm dse glomerular injury - anca vasculatidd
Parietal epithelial Goodpasture - psagn lupus neph, LM cresents
3 typres: celss admixed with - LM cresents hsp,Berger EM none
1 (+) antibodies agains GBM leukocytes infiltrating IF: linear LM cresents IF negative
the glomerulus EM lumpy bumby
IF Granular
Goodpasture Antibodies against the non Male predominance 20s smoker male
syndrome collagenous domain of a1 Active smokiers hyemoptysis and
Collagen type 4 (alveoli and 20s renail falue
gbm antiden)
*anti GBM limited to kidney
Nephrotic Loss intergrity of filtration ↓ globulin = ↑ Minimal Change Membarnoproliferative
barrier  ↑ permeability  infections Disease (lipoid glomerulonephritis
proteinuria↓ aldbumin Loss of prthrobin 3 nephrosis) (MPGN Type I)
edema ↑ hepatic lipoprotein Focal Segmental Dense deposit disease
syn  hyperlipidemia Glomerusclorosis (MPGN type 2)
 lipiduria (FSGS)
Membranous
 PATHOGENESIS GROSS MICRO
Nephropahty/
Glopmerulopathy
Minimal change diease LM: Normal Assoc respi infection Steroid responsive Most common
glomerulus icause in children
EM: unifier and Prophylactic
diffuse effacement of immunization NSAIDs
food processes of the
podocytes, lipid
nephroisis
IF: none
Membranous LM:Uniform diffuse Penicillamin, Not steroid responsive Second most
Nephropathy thickening of cap wall Captopril, NSAID commin in adult
EM: subepithelial dep
in GBM (spike and
dome)
Effacement of foot
processes
IF: granular immune
complex
Focal segmental LM:Collapse capillary Heroin (+) azotemia Most common
glomerulsclerosis loops and hyalinosis cause in adults
↑ mesangial matrix
(both)
Collapsing
glomerulopathy – in
HIV
EM: Diffuse
effacement of foot
process
Focal epithelial cell
detachment and
GBM denudation
IF: IgM, C3 in sclerotic
areas
Membranoproliferative (+) immune deposit complex Activate classical and LM: tram track, Sle, hbv, hvc,
 PATHOGENESIS GROSS MICRO
Glomerulonephritis alternative double contour endocarditism AV
(MPGN type 1 ) EM: Subendothelial shunt infected HIV
electron -dense shcitosomiasis, CLL
deposits
IF: Granular c3
deposits with igG and
early components (C1-
c4)
Dense Deposit Dse (-) immune deposit complex alnetative LM: variable
(MPGN 2) EM: ribbon like
IF: granular or linear
c3 without IgG and
early complement
IgA Nephrophaty igA deposit in mesangial LM: Mc; Older children,
regions (loc to kid) mesagnioproliferative: glumerolonephritis gross hematuria
mesangial widening worlwide after a respi, gi or
and endocap gu tract inf
proliferation, focal 2nd: celiac dse, liver
proliferative GN dse
FSGS; focal
cresenteric GN
EM: mesangial
elecrion – dense
IF: meangial
deposition of IgA with
c3 an properdin and
smaller IgM. IgG no
complements
Henoch-schonlein Systemic igA deposition Mc in children 3-8 Purpuric skin
purpura Sever in adults lesions, abd pain
and intestinal
bleeding and
athralgia with renal
abn ff. RTI
PATHOGENESIS GROSS MICRO