Patho review stuff!!! Flashcards
Types of gastric polyps
- hyperplastic (80%) 2. fundal gland polypes (10%) 3. adenomatous polypes (5%)
which tutors elict desmoplastic reactions?
- gastric adenocarcinoma 2. breast 3. breast 4. ledt sided Large intestine
difference of interstitial and diffused gastric adenocarcinoma?
interstitial: precancerous lesion is intesterstial metaplasia of gastric mucosa, better differentiated, associated with chronic gastritis and H. pylori. diffused: de novo mutation of gastric mucosal cells, associated with rear e-cadherin mutation, poorly differentiated.
main metastatic sides of Gastric carcinomas
via lymph bc carcinoma… 1. virchows ln 2. liver 3. peritoneum 4. ovaries (kruckenberg tumor)
how do we classify GIST? and what’s wrong in GIST? where is is Gist most common?
not by being or malignant by mitotic number and size of tumor High and big = aggressive low and small= chill mutation of cKIT (CD117) leading to ligand less activation and therefore unstopped proliferation and growth. most common in stomach, then small intestine, then colon and rectum
why does HCC can cause ischemic bowl disease?
Bc in HCC low levels of Protein s and c are presents leading to a hypercoagulative state causing vinous thrombosis and therefore leading to Ischemic bowl disease.
classification of Ischemic bowl disease
- transmural: entire thickness 2. mural: mucosal & submucosal 3. mucosal: mucosal…
classification of malabsorption
- intraluminal (pancreatic enzymes are broken) 2. mucosal (damaged cell surface transporters(lactose intolerance), intestinal surface reduction(Celiac and Crohns), mucosal infection (whipples)) 3. nutrient delivery
extra intestinal complication of Crohns disease
- uveitis 2. sacroilitis 3. polyarthritis 4. erythema nodosum 5. blue duct inflammation 6. obstructive uropathy
morphology of crohns disease
- sharp demarcation of diseased bowl segments 2. non-caveating granulomas 3. fistula formation (connection between bowl parts)
Etiology of hepatocellualr carcinoma?
- HBV, HCV 2.chronic alkoholism 3. Alfatoxin 4. hemochrombtosis
Hepatic malignant tumors
- HCC 2. Cholangiocelular carcinoma 3. hepatoblastoma
most common hepatic tumor?
metatasatis from portal organs… can get tumors for virtually any organ tho
benign tumros of the liver?
- cavernous hemangioma 2. hepatocellular adenoma
ethology of hepatucellular adenoma
associated with oral contraceptives and steroids
most common hepatic benign tutors?
cavernous Hemangioma
what is a cavernous hemanigoma?
large dilated vessels, infiltrative, no capsule,
what is von hippel Lindau disease?
genetic multi systemic disease of the epidymes, benign tumors called cavernous hemagnionomas…
what is a cholangiocellular carcinoma?
adenocarcinoma arraising from cholangiocytes in intrahepatic ducts. pre disposition for ppl with PSC
changes in a cirrhotic liver
- death of hepatocytes loss of microvilli– problems taking up and secreting proteins 2. extracellular matrix deposition in space of disse form stalate cells 3. vascular reorganisation loss of fenestration hypo perfusion leads to atrophy
what does stalate cells normally do? and fnx in cirrhosis?
normally: storage of Vitamin A cirrhosis: production of Collagen in disse space
what activates stalate cells of liver in cirrhosis?
endothelial cells, Kupffer cells, hepatocytes cytokines: IL1, TNF
Etiology of Cholangitis?
alsmot always Bacterial infection via oddi also obstruction
forms of cholangitis?
- ascending 2. Suppurative cholangitis – most severe from, purulent bile fills bile ducts, attacks ducts, and causes liver abscess
what’s the most severe from of Cholangitis?
Suppurative: causes pus bile to attack lining and liver abscess formation
most common tumor of the biliary tract?
Carcinoma of the gallbladder
ethology of gallbladder carcinoma?
- gallstones 2. bacterial 3. parasitic
what histological form do gallbladder carcinomas have?
Adenocarcinoma.
what are hepatic bile duct tumors in hilum of the liver called?
KLATSKIN tumor is a cholangiocarinoma of the hepatic bile ducts
pathogenisis of cholecystitis?
obstruction– lecithin– isolecthin– toxic disruption of mucosa– bile aggressive eon mucosa too– PGI= inflammation yay
types of pankreatitis and its subclassifications
- acute 1.1. intestinal 1.2. hemorragic 2. chronic 2.1. fibrotizing 2.2 obstructive 2.3 autoimmune
ethology of acute pancreatitis
- cholelithiasis 2. alcohol 3. idiopathic 4. trauma from surgery 5. ruptured posterior duodenal ulcer 6. infections 7. hypercalemia: enzyme activaor
pathogenesis of acute interstitial pancreatitis
enzymatic destruction of fat cells– FA released – combine with Ca– insoluble salts
pathogenesis of acute hemorraghic pancreatitis
affects ascinar and ductal cells and langerhans affects blood vessels– hemorrhage
Pthaogeneis of Acute pancreatitis
increased pressure will lead to damage of acing cells which will release enzymes duodenal pancreatic refulx bilo pancreatic refulx epithelial dame due to bile salts hyper activation of enzymes
what causes acinar injury in acute pancreatitis?
Alcohol virus trauma hypercalcemia
what causes ductal obstruction in acute pancreatitis? and pathogenesis?
stones CF tumors oddin edema pathogenesis: obstruction– high intraluminal pressure- – accumulation of enzyme rich fluid– lipase is active– fat necrosis– injury and pro inflammatory enzymes
which enzymes are active in acute pancreatitis?
Amylase: Lipase: Free FA bind with Ca= fat necrosis Proteases: digest vessels, parenchyme etc.
consequences of acute pancreatitis
- recovery 2. fat necrosis 3. pseudocysts (liquified fat necrosis) Becomes pancreatic Abscess 4.Abcess 5. Pancreatic Apoplexia
systemic consequences of acute pancreatitis?
- paralytic ileus 2. shock 3. peritonitis 4. DIC 5. ARDS 6. DM 7. hypocalcemia
forms of chronic pancreatitis?
general idea: acing cells don’t fucntion so fibrosis 1. chronic autoimmune 2. chronic obstructive 3. chronic fibrotizing
explain chronic autoimmune pancreatitis
high IgG4 infiltration of T cells in PERIDUCTAL AREA massive periductal myofibroblastic proliferation ASSOCIATED WITH SJÖRGENS SYNDROME
explain chronic obstructive pancreatitis.
periductal fibrosis
explain chronic fibrotizing pancreatitis
most frequent chronic alcoholism fibrosis due to no enzyme production
what is duct ectasia of the breast?
dilated ducts, filled with green viscid matter nipple discharge significant degree of fibrosis mimics carcinoma
what are fibrocystic changes?
cyct formation and fibrosis
due to cyclic change of breast in menstrual cycle
subdivieded into non proilferative and prolfiverative
classification of fibrocystic chances in Brest.
- non proliferative– fibrosis without hyperplasia
- proliferative– hyperplasia, scleorisng adenosis
explain non-proliferative fibrocystic changes in the breast
+ diseases considered non proliferative fibrocystic
most common type
increased fibrous storm no hyperplasia dilation of ducts–> cysts form Bilateral
diseases:
- Duct ectasia
2. Cycst
3. Apocrine change
4. mild hyperplasia
5. Adenosis
6. Fibroadeoma with out complex features
explain proliferative fibrocystic changes in breast
epithelial hyperplasia (2 layers in duct instead of one) Ductal papillomatosis- papillary processes in lumen atypical lobular hyperplasia- resebeles carcinoma in situ sclerosing adenosis- enlarge meant of lobules with many acini and hardening
what is atypical lobular hyperplasia in fibrocystic changes?
proliferative carcinoma in situ (doesn’t fill all acini) very high risk for carnimoa development calcification may appear
what is sclerosing adenosis in fibrocystic changes?
proliferative enlargement of lobules with acini proliferation of fibroblasts along the ducts causing the compression of lumina of the ducts
benign tumours of the breasts
Fibrocystic changes
Fibroadenoma adenoma
Phyllodes
intraductal papilloma
malignant tumors of the breast
- non invasive (insitu) carcinoma
- 1 DCIS ductal carcinoma in situ
- 2 LCIS Lobular cis
- invasive carcinoma
- 1 invasive ductal carcinoma NST
- 2 invasive lobular carcinoma
- 3 Special types
- 4 Rear and salivary gland type
- 5 neuroendocrine tumors
- 6 inflammatory carcinoma
Explain fibroadenoma
most common benign tumor do to high levels of oestrogen raises from CT enlarges during mesntrual cycle and pregnancy due to Estrogen
explain Phyllodes tumor
mixed epithelium and stromal tumor
hypercellular stroma
classification: being, borderliner, mallignant
Arises from periductal storma leaflike appearance increased stomal cellularity and high mitotic activity
explain intraductal papilloma
solitary lesion in larger ducts serous + bloody nipple discharge papillary growth into lumen of duct double layers epithelium single elation stays benign, multiple can get malignant
inflammatory disorders of the breast
- Acute mastitis
- Mammary duct ectasia
- Fat necrosis
- Lymphocytic mastopathy
- granulomatous mastitis
ethology of Acute mastitis
usually doing 1st moth of lactation bacterial infection due to nipple cracy and fissures self resolved by breast feeding or antibiotics
What is peridcutal mastitis?
duct plugging; duct dilation; rupture; intese chronic+granulamotaous inflammation due to squamous metaplasia of the nipple shedding keratin in ducts
what is zuska disease?
Periductal mastitis due to squamouscell metaplasia of nipple
what is Lymphocitic mastopathy?
Autoimmune?! collagenized storma around atrophic ducts with shitloads of Lymphocytes associated with DM1 and AI thyroid diseases
which fiibrocystic leasions have minimal to no rsik to become breast carinoma?
- fibrosis
- cycst
- apporcine metaplasia
which fibrocystic leasion have slight risk in becomming breast carinomas?
- ductal hyperplasia (no atypia)
- scleoring adenosis
which fibrocystic changes have high risk in becomming breast carinomas
atypical hyperplasia of ducts and lobles
most common type of invasive breast cancer?
invasive ductal carinoma
NST
most common breast tumor?
fibroadenoma
special features of invasive ductal carinomas NST of the breast:
- tubular carinoma
- mucinous carinoma
- medullary carinoma
- inflammatory carinoma
classification of Phyllodes tumors?
benign
borderline
malligantn
which genes are mutated in breast carinomas?
- BRCA 1/2
- p53
- ataxia teleangiectasia (ATM) gene
- Cowdens disease (10q mutation)
- Her 2
- Ras
- MYC
what do we use the notingham grading system for?
invasive breast carinoma
3 components
- how many tubukles are there
- polymorphism
- mitotic acitvity
whats the recent classificaton of breast carinoma WHO?
Insitu
- ductal/DCIS
- Lobular/LCIS
Invasive
- nospecial type NST
- Invasive lobular ca
- special types
- rear/salivary gland type ca
- Neuroendocrine neoplasms
what is the Van Nuys grading?
for DCIS
a bit simpler then the perfect grading system
based on necrosis and grade of the cells
what are the different ‘looks’ of the NST Carinomas of the breast?
with medullary features
with NE differntiation
glycogen rich
Lipid rich
etc
what is the classificaiton based on gentic prifile of breast carinoma
Based on Estrogen receptor positive or negative
gerneally: over stimulation of E causes low grade Ca
E+: Luminal A/B : low grade
E-: her2, Normal breast like, basal like: high grade
classification of Rhinitis?
- allergic
- infectious
- chronic
what type of reaction is alleric rhinits?
type 1 hypersensitivity
allergen activates b cell which produces IgE which then causes degranulation of mast cells
important formes of Laryngitis
- tuberculoid
- diphteric
risk factors for vainous thrombosis
- prolonged bed rest
- post surgery
- severe trauma
- Contraceprive
- pregnancy
- CHF
- overweight
- SMOkER
What is Atelectatic lung?
forms of atelectasis
- Resorption
- Compression
- Contraction
what is resorption atelectasis
follows compleat airway obstruction
leads to decreased O2 that makes it to the alveoli
may be due to exessive mucus production etc.
Mediastinum goes towards lung
what is Compression Atelectasis?
when pleural space is expanded
pressure on lung
mediasitum goes away from collapsed lung (‘mass effect’)
what is contraction Atelectasis?
due to local fibrotic change
holds the lung to gether
what is ARDS?
end reult of acute alveolar injury
imbalance of pro and anti inflammatory mediators
what casues ARDS?
imbalace of Pro and anti inflamamtory state
increase IL1, IL8 and TNF
Pathogenesis of ARDS
- damage to vesel wall or alveolar epithel
- acitve pulmo macrophages (IL1, IL8, TNF)
- Neutrophiles due to chemotactic cytokines
- neutrophioes damage walles even more (ROS, Lysozym, AA)
- leads to loss of surfactant and increased vascular permability
Results in: lungs not able to expand
what are restricive lung diseases chracterized by?
the loss of compliance
for example due to fibrosis
type of pneumoconiosis
- coal workers
- silicosis
- berylliosis
- asbestosis
types of chronic bronchitis
- simple chronic bronchitis
- chronic asthmatic bronchits
- chronic obstructive broncitis
what is chrnic brnochitis
mucosal gland metaplasia
mucus hypersecretion
what causes obstrction of airways in chronic bronchtis
what is the index called to histologically classify chronic bronchitis?
Reid index
what is bronchiectasis?
permanent dialatrion of bronchi due to destrctuion of msucle and elastic tissue, results in chronic necrosis
its a secodnary disease
what casues bronchiectasis?
parthogenesis ob bronchiectasis?
obstruction or infection is the etiology
due to obstrcution we will get an infection and inflammation opccours eventually leading to tissue damage
types of emphysema
what is the differecne between Centriacinar and pan acinar emphysema
pathogenesis of emphysema
imbalacne of oxidants and antioxidants
tabbaco– macrophages– NFkB transcription– neutrophils release proteases– destruction of CT oof alveolar walls
effect of Cystic Fibrosis on lung
- viscous mucus
- hyperplasia and hypertrophy
- obstrctuion
What is chronic bronchitis?
COPD
Hypertrophy of the mucus glads (reid index)
Excress of mucus prodctuion ( productive cough)
Cyanosis due to CO2 trapping in blood
Smiking associated
what is COPD?
air has issues leaving the lungs due to a condtion:
- Chronic bronhitis
- Ashma
- Emphysema
- Bronchioectasis
increases TLC due to air trapping
decreased FEV1/FVC ratio
what leads to destrcution of alveolar walls in emphysema?
either exessive inflammation or antitrypsin deficnecy
A1AT inhibts proteases which is secreated by neurotphils. so if lack of A1AT neutropphils will destroy the walls
smoking causes excessive inflammation
what is asthma?
Reversible airway bronchoconstriction
hypersensitivity type 1
Pathogeneseis of Asthma.
- allergen activates Th2 cells
- release of IL4(class switch to IgE) IL5(eosinophils come) IL10(inhibits Th1 cells)
- rexeposure leads ti IgE activation of mast cells
- Histamine release
- brconhospasm
what is in the mucus of an asthma patient?
Spiral shaped mucus plugs (= Curschmann spirales)
Eosinophil derived crystals (= Charcot-lyden crystals)
what causes bronchiectasis?
Cystic fibrosis
Kartagner syndrom (due to dynein arm, no cillilary movement)
tumor
necrotiszing infection
what is Kartagerner syndrom?
mutation of dynein arm
no cilia movement
results in bronchiectasis, infertility, sinusitis etc
etiology of sialoadenitis?
- traumatic
- viral
- bacterial
- Autoimmune
traumatic pathogegesis of sialoadenitis
blockadeg or rupture of salivary duct.
saliva attacks neighbour tissue
Mucocele
Viral etiology of sialoadenisits
- Mumps
- CMV
what are the autoimmune causes for Sialoadinatis?
- sjorgen sydnrom
- sarcoidosis
What is a warthin tumor?
Salivary gland tissue trapped in regional LN
only in parotid
mucus cysts
Papillary cystadenoma lymphomatosum
what is a pleimophic adenoma?
most commmon benign tumor of salivary glands
classic gross phases of Lobar pneumonia?
- Congestion
- Red hepatization with exudate
- gray hepatization
- resolution
histological soectrum of Pneumonia?
- fibrinopurulent alveolar exudate (acute bacterial)
- Mononuclear interstial infultate( atypical/Viral)
- Granulomatous (chronic benumonia)
Patterns of pneumonia
describe Bronchopneumonia
patchy distribution
more the one lobe
inital infection of bronchi extednig to alvolus
caused by: Staph, Haemophilus, pseudomona, moraxrlla, legionella
describe Lobar pneumonia:
consolidation of entire lobe
bacterial: strep pneumonia, klepsiella
Congestion– red hepatization– grey hepatization– resolution
tumors of the nose
- squamous cell ca
- adenoca
- malignant melanoma
- inverting papiloma
- esthesioneuroblastoma (olfactory)
histological variants of nasopharyngeal carinoma
- keratinizing squamous cell ca
- non keratinizing squamous cell ca
- undifferentiated ca
pathogeneisis of nasopharyngeal carinoma?
EBV associated
replicates in nasopharynx mucoa, then ifects tonsils
epithelium changes of tonsisl= carinmoam
anatomical sites of laryngeal carinoma
- supraglottic
- glottic
- infraglottic
spuraglottic: rich in lymphatics– early spread to cervial LN
Glottic: more common, directly on vocal chords, keratinizing, better prognosis not rich in Lympahtics
Infraglottic: least common, worst prognosis, no early symptoms, goot Lympahtic spread
what are aschoff bodeis?
found in heard in reumatic fever
T lymphocyte accumulations
what is mamrantic endocarditis?
non-bacterial thrmoboctic endocaridits
deposition of fibrin
