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Stuff Thats Would Be Cool To Remember > Patho review stuff!!! COPY > Flashcards

Patho review stuff!!! COPY Flashcards

1
Q

Types of gastric polyps

A
  1. hyperplastic (80%) 2. fundal gland polypes (10%) 3. adenomatous polypes (5%)
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2
Q

which tutors elict desmoplastic reactions?

A
  1. gastric adenocarcinoma 2. breast 3. breast 4. ledt sided Large intestine
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3
Q

difference of interstitial and diffused gastric adenocarcinoma?

A

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.

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4
Q

main metastatic sides of Gastric carcinomas

A

via lymph bc carcinoma… 1. virchows ln 2. liver 3. peritoneum 4. ovaries (kruckenberg tumor)

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5
Q

how do we classify GIST? and what’s wrong in GIST? where is is Gist most common?

A

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

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6
Q

why does HCC can cause ischemic bowl disease?

A

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.

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7
Q

classification of Ischemic bowl disease

A
  1. transmural: entire thickness 2. mural: mucosal & submucosal 3. mucosal: mucosal…
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8
Q

classification of malabsorption

A
  1. 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
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9
Q

extra intestinal complication of Crohns disease

A
  1. uveitis 2. sacroilitis 3. polyarthritis 4. erythema nodosum 5. blue duct inflammation 6. obstructive uropathy
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10
Q

morphology of crohns disease

A
  1. sharp demarcation of diseased bowl segments 2. non-caveating granulomas 3. fistula formation (connection between bowl parts)
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11
Q

Etiology of hepatocellualr carcinoma?

A
  1. HBV, HCV 2.chronic alkoholism 3. Alfatoxin 4. hemochrombtosis
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12
Q

Hepatic malignant tumors

A
  1. HCC 2. Cholangiocelular carcinoma 3. hepatoblastoma
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13
Q

most common hepatic tumor?

A

metatasatis from portal organs… can get tumors for virtually any organ tho

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14
Q

benign tumros of the liver?

A
  1. cavernous hemangioma 2. hepatocellular adenoma
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15
Q

ethology of hepatucellular adenoma

A

associated with oral contraceptives and steroids

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16
Q

most common hepatic benign tutors?

A

cavernous Hemangioma

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17
Q

what is a cavernous hemanigoma?

A

large dilated vessels, infiltrative, no capsule,

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18
Q

what is von hippel Lindau disease?

A

genetic multi systemic disease of the epidymes, benign tumors called cavernous hemagnionomas…

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19
Q

what is a cholangiocellular carcinoma?

A

adenocarcinoma arraising from cholangiocytes in intrahepatic ducts. pre disposition for ppl with PSC

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20
Q

changes in a cirrhotic liver

A
  1. 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
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21
Q

what does stalate cells normally do? and fnx in cirrhosis?

A

normally: storage of Vitamin A cirrhosis: production of Collagen in disse space

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22
Q

what activates stalate cells of liver in cirrhosis?

A

endothelial cells, Kupffer cells, hepatocytes cytokines: IL1, TNF

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23
Q

Etiology of Cholangitis?

A

alsmot always Bacterial infection via oddi also obstruction

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24
Q

forms of cholangitis?

A
  1. ascending 2. Suppurative cholangitis – most severe from, purulent bile fills bile ducts, attacks ducts, and causes liver abscess
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25
Q

what’s the most severe from of Cholangitis?

A

Suppurative: causes pus bile to attack lining and liver abscess formation

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26
Q

most common tumor of the biliary tract?

A

Carcinoma of the gallbladder

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27
Q

ethology of gallbladder carcinoma?

A
  1. gallstones 2. bacterial 3. parasitic
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28
Q

what histological form do gallbladder carcinomas have?

A

Adenocarcinoma.

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29
Q

what are hepatic bile duct tumors in hilum of the liver called?

A

KLATSKIN tumor is a cholangiocarinoma of the hepatic bile ducts

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30
Q

pathogenisis of cholecystitis?

A

obstruction– lecithin– isolecthin– toxic disruption of mucosa– bile aggressive eon mucosa too– PGI= inflammation yay

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31
Q

types of pankreatitis and its subclassifications

A
  1. acute 1.1. intestinal 1.2. hemorragic 2. chronic 2.1. fibrotizing 2.2 obstructive 2.3 autoimmune
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32
Q

ethology of acute pancreatitis

A
  1. cholelithiasis 2. alcohol 3. idiopathic 4. trauma from surgery 5. ruptured posterior duodenal ulcer 6. infections 7. hypercalemia: enzyme activaor
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33
Q

pathogenesis of acute interstitial pancreatitis

A

enzymatic destruction of fat cells– FA released – combine with Ca– insoluble salts

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34
Q

pathogenesis of acute hemorraghic pancreatitis

A

affects ascinar and ductal cells and langerhans affects blood vessels– hemorrhage

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35
Q

Pthaogeneis of Acute pancreatitis

A

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

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36
Q

what causes acinar injury in acute pancreatitis?

A

Alcohol virus trauma hypercalcemia

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37
Q

what causes ductal obstruction in acute pancreatitis? and pathogenesis?

A

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

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38
Q

which enzymes are active in acute pancreatitis?

A

Amylase: Lipase: Free FA bind with Ca= fat necrosis Proteases: digest vessels, parenchyme etc.

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39
Q

consequences of acute pancreatitis

A
  1. recovery 2. fat necrosis 3. pseudocysts (liquified fat necrosis) Becomes pancreatic Abscess 4.Abcess 5. Pancreatic Apoplexia
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40
Q

systemic consequences of acute pancreatitis?

A
  1. paralytic ileus 2. shock 3. peritonitis 4. DIC 5. ARDS 6. DM 7. hypocalcemia
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41
Q

forms of chronic pancreatitis?

A

general idea: acing cells don’t fucntion so fibrosis 1. chronic autoimmune 2. chronic obstructive 3. chronic fibrotizing

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42
Q

explain chronic autoimmune pancreatitis

A

high IgG4 infiltration of T cells in PERIDUCTAL AREA massive periductal myofibroblastic proliferation ASSOCIATED WITH SJÖRGENS SYNDROME

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43
Q

explain chronic obstructive pancreatitis.

A

periductal fibrosis

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44
Q

explain chronic fibrotizing pancreatitis

A

most frequent chronic alcoholism fibrosis due to no enzyme production

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45
Q

what is duct ectasia of the breast?

A

dilated ducts, filled with green viscid matter nipple discharge significant degree of fibrosis mimics carcinoma

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46
Q

what are fibrocystic changes?

A

cyct formation and fibrosis

due to cyclic change of breast in menstrual cycle

subdivieded into non proilferative and prolfiverative

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47
Q

classification of fibrocystic chances in Brest.

A
  1. non proliferative– fibrosis without hyperplasia
  2. proliferative– hyperplasia, scleorisng adenosis
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48
Q

explain non-proliferative fibrocystic changes in the breast

+ diseases considered non proliferative fibrocystic

A

most common type

increased fibrous storm no hyperplasia dilation of ducts–> cysts form Bilateral

diseases:

  1. Duct ectasia

2. Cycst

3. Apocrine change

4. mild hyperplasia

5. Adenosis

6. Fibroadeoma with out complex features

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49
Q

explain proliferative fibrocystic changes in breast

A

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

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50
Q

what is atypical lobular hyperplasia in fibrocystic changes?

A

proliferative carcinoma in situ (doesn’t fill all acini) very high risk for carnimoa development calcification may appear

51
Q

what is sclerosing adenosis in fibrocystic changes?

A

proliferative enlargement of lobules with acini proliferation of fibroblasts along the ducts causing the compression of lumina of the ducts

52
Q

benign tumours of the breasts

A

Fibrocystic changes

Fibroadenoma adenoma

Phyllodes

intraductal papilloma

53
Q

malignant tumors of the breast

A
  1. non invasive (insitu) carcinoma
  2. 1 DCIS ductal carcinoma in situ
  3. 2 LCIS Lobular cis
  4. invasive carcinoma
  5. 1 invasive ductal carcinoma NST
  6. 2 invasive lobular carcinoma
  7. 3 Special types
  8. 4 Rear and salivary gland type
  9. 5 neuroendocrine tumors
  10. 6 inflammatory carcinoma
54
Q

Explain fibroadenoma

A

most common benign tumor do to high levels of oestrogen raises from CT enlarges during mesntrual cycle and pregnancy due to Estrogen

55
Q

explain Phyllodes tumor

A

mixed epithelium and stromal tumor

hypercellular stroma

classification: being, borderliner, mallignant

Arises from periductal storma leaflike appearance increased stomal cellularity and high mitotic activity

56
Q

explain intraductal papilloma

A

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

57
Q

inflammatory disorders of the breast

A
  1. Acute mastitis
  2. Mammary duct ectasia
  3. Fat necrosis
  4. Lymphocytic mastopathy
  5. granulomatous mastitis
58
Q

ethology of Acute mastitis

A

usually doing 1st moth of lactation bacterial infection due to nipple cracy and fissures self resolved by breast feeding or antibiotics

59
Q

What is peridcutal mastitis?

A

duct plugging; duct dilation; rupture; intese chronic+granulamotaous inflammation due to squamous metaplasia of the nipple shedding keratin in ducts

60
Q

what is zuska disease?

A

Periductal mastitis due to squamouscell metaplasia of nipple

61
Q

what is Lymphocitic mastopathy?

A

Autoimmune?! collagenized storma around atrophic ducts with shitloads of Lymphocytes associated with DM1 and AI thyroid diseases

62
Q

which fiibrocystic leasions have minimal to no rsik to become breast carinoma?

A
  1. fibrosis
  2. cycst
  3. apporcine metaplasia
63
Q

which fibrocystic leasion have slight risk in becomming breast carinomas?

A
  1. ductal hyperplasia (no atypia)
  2. scleoring adenosis
64
Q

which fibrocystic changes have high risk in becomming breast carinomas

A

atypical hyperplasia of ducts and lobles

65
Q

most common type of invasive breast cancer?

A

invasive ductal carinoma

NST

66
Q

most common breast tumor?

A

fibroadenoma

67
Q

special features of invasive ductal carinomas NST of the breast:

A
  1. tubular carinoma
  2. mucinous carinoma
  3. medullary carinoma
  4. inflammatory carinoma
68
Q

classification of Phyllodes tumors?

A

benign

borderline

malligantn

69
Q

which genes are mutated in breast carinomas?

A
  1. BRCA 1/2
  2. p53
  3. ataxia teleangiectasia (ATM) gene
  4. Cowdens disease (10q mutation)
  5. Her 2
  6. Ras
  7. MYC
70
Q

what do we use the notingham grading system for?

A

invasive breast carinoma

3 components

  1. how many tubukles are there
  2. polymorphism
  3. mitotic acitvity
71
Q

whats the recent classificaton of breast carinoma WHO?

A

Insitu

  1. ductal/DCIS
  2. Lobular/LCIS

Invasive

  1. nospecial type NST
  2. Invasive lobular ca
  3. special types
  4. rear/salivary gland type ca
  5. Neuroendocrine neoplasms
72
Q

what is the Van Nuys grading?

A

for DCIS

a bit simpler then the perfect grading system

based on necrosis and grade of the cells

73
Q

what are the different ‘looks’ of the NST Carinomas of the breast?

A

with medullary features

with NE differntiation

glycogen rich

Lipid rich

etc

74
Q

what is the classificaiton based on gentic prifile of breast carinoma

A

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

75
Q

classification of Rhinitis?

A
  1. allergic
  2. infectious
  3. chronic
76
Q

what type of reaction is alleric rhinits?

A

type 1 hypersensitivity

allergen activates b cell which produces IgE which then causes degranulation of mast cells

77
Q

important formes of Laryngitis

A
  1. tuberculoid
  2. diphteric
78
Q

risk factors for vainous thrombosis

A
  1. prolonged bed rest
  2. post surgery
  3. severe trauma
  4. Contraceprive
  5. pregnancy
  6. CHF
  7. overweight
  8. SMOkER
79
Q

What is Atelectatic lung?

A
80
Q

forms of atelectasis

A
  1. Resorption
  2. Compression
  3. Contraction
81
Q

what is resorption atelectasis

A

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

82
Q

what is Compression Atelectasis?

A

when pleural space is expanded

pressure on lung

mediasitum goes away from collapsed lung (‘mass effect’)

83
Q

what is contraction Atelectasis?

A

due to local fibrotic change

holds the lung to gether

84
Q

what is ARDS?

A

end reult of acute alveolar injury

imbalance of pro and anti inflammatory mediators

85
Q

what casues ARDS?

A

imbalace of Pro and anti inflamamtory state

increase IL1, IL8 and TNF

86
Q

Pathogenesis of ARDS

A
  1. damage to vesel wall or alveolar epithel
  2. acitve pulmo macrophages (IL1, IL8, TNF)
  3. Neutrophiles due to chemotactic cytokines
  4. neutrophioes damage walles even more (ROS, Lysozym, AA)
  5. leads to loss of surfactant and increased vascular permability

Results in: lungs not able to expand

87
Q

what are restricive lung diseases chracterized by?

A

the loss of compliance

for example due to fibrosis

88
Q

type of pneumoconiosis

A
  1. coal workers
  2. silicosis
  3. berylliosis
  4. asbestosis
89
Q

types of chronic bronchitis

A
  1. simple chronic bronchitis
  2. chronic asthmatic bronchits
  3. chronic obstructive broncitis
90
Q

what is chrnic brnochitis

A

mucosal gland metaplasia

mucus hypersecretion

91
Q

what causes obstrction of airways in chronic bronchtis

A
92
Q

what is the index called to histologically classify chronic bronchitis?

A

Reid index

93
Q

what is bronchiectasis?

A

permanent dialatrion of bronchi due to destrctuion of msucle and elastic tissue, results in chronic necrosis

its a secodnary disease

94
Q

what casues bronchiectasis?

A
95
Q

parthogenesis ob bronchiectasis?

A

obstruction or infection is the etiology

due to obstrcution we will get an infection and inflammation opccours eventually leading to tissue damage

96
Q

types of emphysema

A
97
Q

what is the differecne between Centriacinar and pan acinar emphysema

A
98
Q

pathogenesis of emphysema

A

imbalacne of oxidants and antioxidants

tabbaco– macrophages– NFkB transcription– neutrophils release proteases– destruction of CT oof alveolar walls

99
Q

effect of Cystic Fibrosis on lung

A
  1. viscous mucus
  2. hyperplasia and hypertrophy
  3. obstrctuion
100
Q

What is chronic bronchitis?

A

COPD

Hypertrophy of the mucus glads (reid index)

Excress of mucus prodctuion ( productive cough)

Cyanosis due to CO2 trapping in blood

Smiking associated

101
Q

what is COPD?

A

air has issues leaving the lungs due to a condtion:

  1. Chronic bronhitis
  2. Ashma
  3. Emphysema
  4. Bronchioectasis

increases TLC due to air trapping

decreased FEV1/FVC ratio

102
Q

what leads to destrcution of alveolar walls in emphysema?

A

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

103
Q

what is asthma?

A

Reversible airway bronchoconstriction

hypersensitivity type 1

104
Q

Pathogeneseis of Asthma.

A
  1. allergen activates Th2 cells
  2. release of IL4(class switch to IgE) IL5(eosinophils come) IL10(inhibits Th1 cells)
  3. rexeposure leads ti IgE activation of mast cells
  4. Histamine release
  5. brconhospasm
105
Q

what is in the mucus of an asthma patient?

A

Spiral shaped mucus plugs (= Curschmann spirales)

Eosinophil derived crystals (= Charcot-lyden crystals)

106
Q

what causes bronchiectasis?

A

Cystic fibrosis

Kartagner syndrom (due to dynein arm, no cillilary movement)

tumor

necrotiszing infection

107
Q

what is Kartagerner syndrom?

A

mutation of dynein arm

no cilia movement

results in bronchiectasis, infertility, sinusitis etc

108
Q

etiology of sialoadenitis?

A
  1. traumatic
  2. viral
  3. bacterial
  4. Autoimmune
109
Q

traumatic pathogegesis of sialoadenitis

A

blockadeg or rupture of salivary duct.

saliva attacks neighbour tissue

Mucocele

110
Q

Viral etiology of sialoadenisits

A
  1. Mumps
  2. CMV
111
Q

what are the autoimmune causes for Sialoadinatis?

A
  1. sjorgen sydnrom
  2. sarcoidosis
112
Q

What is a warthin tumor?

A

Salivary gland tissue trapped in regional LN

only in parotid

mucus cysts

Papillary cystadenoma lymphomatosum

113
Q

what is a pleimophic adenoma?

A

most commmon benign tumor of salivary glands

114
Q

classic gross phases of Lobar pneumonia?

A
  1. Congestion
  2. Red hepatization with exudate
  3. gray hepatization
  4. resolution
115
Q

histological soectrum of Pneumonia?

A
  1. fibrinopurulent alveolar exudate (acute bacterial)
  2. Mononuclear interstial infultate( atypical/Viral)
  3. Granulomatous (chronic benumonia)
116
Q

Patterns of pneumonia

A
117
Q

describe Bronchopneumonia

A

patchy distribution

more the one lobe

inital infection of bronchi extednig to alvolus

caused by: Staph, Haemophilus, pseudomona, moraxrlla, legionella

118
Q

describe Lobar pneumonia:

A

consolidation of entire lobe

bacterial: strep pneumonia, klepsiella

Congestion– red hepatization– grey hepatization– resolution

119
Q

tumors of the nose

A
  1. squamous cell ca
  2. adenoca
  3. malignant melanoma
  4. inverting papiloma
  5. esthesioneuroblastoma (olfactory)
120
Q

histological variants of nasopharyngeal carinoma

A
  1. keratinizing squamous cell ca
  2. non keratinizing squamous cell ca
  3. undifferentiated ca
121
Q

pathogeneisis of nasopharyngeal carinoma?

A

EBV associated

replicates in nasopharynx mucoa, then ifects tonsils

epithelium changes of tonsisl= carinmoam

122
Q

anatomical sites of laryngeal carinoma

A
  1. supraglottic
  2. glottic
  3. 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

123
Q

what are aschoff bodeis?

A

found in heard in reumatic fever

T lymphocyte accumulations

124
Q
A

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