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PATHOANA 2 > Liver > Flashcards

Liver Flashcards

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1
Q

no invasive

A

Ultra
elastormetry
ct

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2
Q

semiinvasiev

A

cholecustocholangiography
ercp-endoscopic retrograde choalngiopankreticography

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3
Q

acute liver injury non specooc enzymes

A

ALT, AST

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4
Q

chonic liver ezyme

A

GMt-glutamyltranferase

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5
Q

oncomakekers

A

AFP by hepatocellular carcinoma
CEA(carcinoembryonal antigen) by cholangiocellular ca

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6
Q

INASIVE

A

ANGIOGRAPHY
LIVER NIPSY

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7
Q

developmental abnormalities of over

A

-common, not serois

1.liver cyst
2. congenital heptic fibrosis

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8
Q

liver/bilary cyst

A

-AD
-bile duct dilation is reason

POLYCYSTIC liver disease
-AD-
-ADPKD
-cyst in pancrea, spleen, oavries, ling
-ALLTID OF KIDNEY OGSP

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9
Q

congentialheptic fibrosis

A

-AR
-PORTAL HYPERTENSION
-fucntion normla

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10
Q

Inborn metabolic diases

A

-tesaurismoses
-deficinecy of a1-antitrypsin
-def of a1-antichymotrypsin
-fibrin storage disease

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11
Q

tesaursismoses

A

storage disorder

.amyloidosis, lipidoses, glykogenosis

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12
Q

deficiency of a1 antitrypsin

A

-AR
-hepatitis, choelstasis, fibrosis/cirrhoiss
-lung ephysmea+resp fialureee

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13
Q

Inbron metabolic lover disease

A

Wilson disease
porphyria
IRON: inborn haemochromatosis and haemosiderosis

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14
Q

wilson

A

-damaged liver + iris/lens
-acc of copper
-normal: rabsorption of copper from intestine –>by albumin–>liver tissue and then by cerruplasmin to stool
-cerruplasmin dont work
-Liver injury: ACUTE lover failure, haemolytic aneima w kindey filure, chronic liver disease->fibrosis/cirrhosis

brian
irisl/lens_->kayser-fleischers ring

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15
Q

porphyria

A

hepatic:
-inborn
-acquired(80%): alchol, HIV, msoking,

erythropoeitic

clinic:liver injurt and sking signs:blister/erythema
- photodermatoses

-acc of uv light

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16
Q

haemochromatosis

A

-AR
- eat–>^abs or iron from intesitines–>overload–>iron acc in liver and so on
-BRONZE DIABETES: cirrhosis+DM+skin pigmetation

congetial
kupher cells
ACC MAINLY IN HEPTOCYTES

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17
Q

haemosiderosis

A

-ext/int ron overload
types
1. internal bc of hemolysis
2.external: alcholo, repeted blood transfusuin

typucally reversible
NOT inhertited obvi
Kupcher cells
ACC OF IRON MAINLY IN MACROPHAGES/KUPFER

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18
Q

toxic liver isease

A

-alco and drugs

  1. Intrinsic=predicitible
    -^durgs=înjury
    -serious ness depent of dose
    -know durg and tocins
    -direct=injury of heptocytes
    -indirtc=incorporation into metabolism
    -quick symtoms
  2. idosyncratic=unpredictable
    -individual dororder of metabolsim of toxin/interaction w immune
    -toxin ecssesd base dose=NOT DOSE DEPENDANT
    -d,w,month for clinical manifestaiton

liver injuty:
-ACUTE HEPATITIS, chronic, csteatosis, fibrosis, choelstssis, GRANULOMATOUS

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19
Q

Steatosis

A

calssifiction
-AFLD:alcoholic fatty liver disease
-NAFLD

etiology of NAFLD
- obestity, DM, hyeprlidpidemina, tocins, durgs, hepttis, meta liver disease

LARGE LIVER, SOFT, YELLOW

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20
Q

Chronic liver venous steasiss/hyperemia

A

Chronic hepatic venous stasis is a manifestation of long-term venous hyperemia in chronic venous liver disease right heart failur

Macroscopically has an image of the nutmeg liver - hepar moschatum

Cyanotic induration of the liver is also accompanied by chronic venostasis of the spleen and kidneys

Necrosis in zone 3(around central vein)(hyperemia), steatosis more peripherally(around the CENTRILOBULAR veins)
Shows increase amount of collagen and reticular fibers around the central veins (so-called “cardiac fibrosis”)

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21
Q

alchol injury liver

A

-most common
-injurt: stetosis, steotheptitis, cirr, fibro, choelstatsis

HARD

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22
Q

acute hepatitis

A

-acute injury +NECROSIS
-is reverrsibøe, regenreraiton can happens
-SELF limiting
-flu, jaundive, nasue, abd pain, heptomegalu
-asymptoamtic

NO FIBROOS-so therefore NO CIRRHOSIS HAPPENING

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23
Q

chronic heptitis

A

-persisent
-chornic infla of protal tract+parenchymal infla+fibrosis–>cirhosis
->6monts

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24
Q

hepatotorphic viruses

A

HAV, HBV,C,D,E

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25
Accompaniying heptis
herpes, adenoviruses, CMV, EBV
26
unifectious heptotis
acute choelstiss, durg, autoimmune, alcholl injury
27
serousness of acute heptitis
amount of necrosis
28
cyryptogenous hepatitis
unknown etiology
29
acute viral heptotis according to type of virys
DNA: bare HBV resten RNA
30
acute viral heptotis according to INCUBATION
hav: 3-6 w hbv:1-6m hcv:15-150days
31
acute viral heptotis according to transtition
F-O route: A OG E resten parenteral
32
acute viral heptotis according to chronic hepatitis
NO: A OG E retsen JA
33
Worl most common HV
HBV sex, no gloves, nlood transfusion
34
most common in europe
HCV- no vacciantion
35
most common in slovakia
HAV: dirty hands
36
acute viral heptitic
Most common is subclinical(60%) and acute hepatits(25%) most common and mostly cured-60-90%
37
acute viral hepatitis C
least comon, more severe -chronic hepatitic (85%%)
38
B and C contribuye to
heaptocellular caricnoma
39
acute viral hepatitis D
-incomplete viral particle -need B for replicaiton -WORST DIAGNOSIS 1. confection:HBV+HDV: most cured w no consequence 2. superinfect HDV : chronic B virus+new D virus infection-->chornicn hepatitis -70-80%
40
chronci viral hepatitis-grading anstaging
garding-grade of activity aka extend of necrosis and infla infiltrate staging-stage of disease aka amoth og fibrosis and cirrhosis
41
choelssrtasis
-acc of bile in body complete: both bile and salt=>ICTERUS incomplete: no biliruben, bare BA+SALT intrahepatal7extahepatal CLINICAL: -Yellow color os skina dn scleras: complete -dark urine + alcholoc stool -skin itching
42
icterus-jaundice
-acc of biirubin +BA in body -un 1.hemolytic/preheptic: -ûrobilinogen 2. hepatocellualr icterus ^conjuagted, biles salt âst, alt 3. choelstatic icterus: -disorder of bielexcretion -CLAY colored stool -^conjuagted+bile salt
43
primary bilairy cirrhosos(cholangitis)
aff bile dcuts w/o hepatocyte injury -intra Probably of Autoimmune origin - amboss says it is has autoimmune origin
44
primary scleorising cholangitis
aff bile ducts W hepatocyte injury
45
secondayr scelrosing cholangitis
known etio after surgery, choelslithiasis, infection, inborn, isnchemic biel ducts
46
obstruction of extrahepatal bile ducts-gallstone
-mostt common gallstone neoplasmi strictures PSC atresis parasitic
47
purulent cholangitis
-bacteri go for inetsine up into bile duct-->infla-->pus -reason bile duct obstruction -ascendent spread for extraheptic biliary tract complication:rupture, abscess, postinfla stenoses
48
liver absecc
-localizeed purulent infla of liver - MTS by lump or vv by purulent ifn of GIT
49
parasitic infections of liver
-echinnococus granulosos -infl of intestines -dogs/foc->humans cyst development filled w infectius agenst called scotex
50
vascular disease of liver
acute arterial blockage closuer of heptoc veins ACUTE BLOCAGE OF INTRAHEPATIC BRANCHE SOF PROTAL VEINS CHORNIC LIVER VENOSTASIS
51
acute arterial bloacge
of hepatic a-->necrosis -smaller-->w/o injury bc anastomose
52
closure of hepatic veins
-ACUTE BUDD CHIARI SYNDROME(acute stasis of blood in liver-->enlargemed)) -pyelephlebitis, tumors -hypercoagualitve conditions, aucte liver fialure, haemorrahic inftction of intesine chornic budd chiary syndri -post infla stenosis of veins -thromboses -cardic disease=HF Budd chiari syndrome is a post-hepatic and intra-hepatic cause of portal hypertension
53
SCUTE BLOCAGE OF INTRAHEPTIC BRANCHES OF PORTAL VEINS
-NO necrosis -pale/congested -lievr cells alive
54
chonic liver venostais
-CYANOTIC INDURATION OF LIVER=NUTMEG symttoms: -heptomegaly, ascites, jaundince, fatigue, cardial cirrhosis etiology: RHFFFFFF, chronic budd chiari
55
liver cirrhossi
final cons of chronic liver injury classificaiton -micronodualr: <3mm, macro >3mm, bilaru -result: liverfaiulre + portal hypertension liver nelarged but afuncitonal micro: -uniform zise and snamll -most common of cirrhosis -chronic injury macro: -irr size of noduls -potato - after acute necroiss -patocytes abnormal arrangment bILIARY: -MICRONODULAR +DISTINH CHOLESTSIS -BILE DUCT INJURT -YELLOW/GREN
56
PORTAL HYPERTENSION
^pressure of bllod in hepatic porta-->problem leaving thorugh liver and is acc in abd cavity site of blockage 1.prehepatal: -blockage of protal veins -MPN, hypercoagulaiton 2. intahepatal: -most common -cirrhosis, fibrosis,venoocclusive disease 3. post hepatal: -heptic veins-->vena cava -budd chiari -mpn, pregnancy, constrictive pericarditis rsult: -collaterals - splenomegaly+hypersplenism+ascites compli: eso varices bleeding and gaemorrodes hypocoagulaion state
57
hepatal failuremclinical
encephalopathy haemorragic diatesis: dec coagualtion facots icterus hypaalbunemy, oedema arterial hypotension renal failure hypoventilation hormonal dosrpder:gynecomastia, vascualr spiders, female escutcheon, testicular atrophy
58
compliction f liver failure
brain edema, bleeding into GIT by varieses, hypoglycemy, heptorenal failure, sepsis
59
being tumor of liver
-not comon 1. focal nodular hyperplasa -patho blood supply -pver prolif of parenchyme -not ture. pseudotumorus 2. hepatocellualr adenoma -TRUE BEING -women yougn - estrogen and corticoids 3.hemangioma: MOST COMMON, TRUE BEING
60
most common malignatn tumor of liver
HEPATOCELLULAR CARCINOMA -aplpha fetoprotein etiology: alfatoxine, acohol chronic hepatitis, oral contrceptivem smokin, chronic metabolic disease -aplhatocin+HBV clincial: abd pain+discomfort, hepatomegaly, veingt loss, cirrhosis deompensaiton MTS: liver, lung,LN
61
most common malignnt ymor in chilhoord
hepatoblastoma - solitay -no cirrhosis -MTS:lung and brains
62
inheriteed abnormalitis of gallbaldder and bile ducts
stenosis or atresia of ectraheptic bile ducts abnormalitis of cyst duct+anomlies of blood supply
62
othe rmalingnt tumor
cholangiocellualr caricnoma -chronic infla bile duct disease -tumor of white color, not weel demercated, macro dsitint infiltartove growth
63
cholecystolithasis
most common affecting gallbaldder etio: chole strones, pigment sotnes-haemolysis, alchohol, cirrhosis, 4XF rule complication: cholcystitis clincial: -asym - subcostal reion pain -no fatty food
64
cholesterolosis
common lesion w no clinical imoact acc of chol crystls in mucosa-->white/yellow -STRAWBERRY GALL
65
acute choelcysttitis
-acutye infla of bile sac -95% accompaniend by choleites clincial: right ypper quadrant pain, tenderness, fever complicaiton: ascending extra or intarheptic choalngitis, gallbladder emphysema, liver abscess, rupture-->peritonints, fistulation
66
chronci cholecystits
-acc omapnied by cholelites clinical: abd discomfort/pain after fodd complication: porcelian gallbrllader, mucocela, carcinoma
67
malignant utmor og gallbladder
-main risk factor: cholecystolithiass ADENOCARCINOMA OF GALLBALDDER -female - etiologt: stone, often chron infla clinical': silent and unsepcific,a bd pain, weight loss, fever, jaundice, cholestasis
67
being tumor og gall
-cholesterol polyps -adenomatous hyperplasoa: fundus of gall, dilation of glands+smooth m prolif, not ture -adneoma of gallbladder:pyloric gland/intestinal, ture
68
most imp inborn disease of pancreas
mucoviscidosis/cystic fibrosis -AR inherited -production of thick mucus everywhere in body-->multiorgan consequence
69
acute pancreatitis-etio and pathogenesis
etiologt: -mechnaical:bile stones, tumor, duodenal stenossi -toxi: alcohol -trauma:abd truam, operaiton -iscehmic -idiopathic pathogeneis: act of proenzymes by regurgaitaiton of duodenal content-->tissue autodigesiton by yrypis-->>act of resting snzymes
70
acute pancreatitis-types, clinical, complicaiotn
types: - acute intestitial pancratitis-NO NECROSIS, odema, infl, tissue injurt, ALCHO ABUSE, -acute hemmorgahic/necrotixin clinic -acute abd pain, nause, vomiting, meteorism complic: - pancretic abscess-->pseudocyst-->duo obstruciton -spesi, abscess, DIC, shock(ARDS),a cute renal failure, bleeding in git, thromboses
71
chronic pancretitis
-alchol mostlyyyy -stones -genetic -autoimmuinue -idiotpathi clincial: abd pain, inotlerance to food complicaiton: maldigestion, dm , acute appendicits
72
most common and most aggresive tumor of pancrea
ductal pancreatic carcinoma etio: hereditaru, chronic pancreatitis, dm, smokin clinical: -silent, epiagstric pain, weight loss, icterus
73
other pancreatic tumors
1.acinar adenocarcinoma -5y survival 6& 2. nerudndocrine neoplasme -hormonally active 3. pancreatoblastoma-rare - in childhood -50% curability

PATHOANA 2 (14 decks)

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