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Mech. 2 > digestive disorderas > Flashcards

digestive disorderas Flashcards

1
Q

Normal Liver-stroma

A

Reticular fibers

  • chomphor cell
  • eto cell
  • endoth. cell
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2
Q

Normal Liver-parenchyma

A 
Hepatocytes
-lrg cells w/ lots of organelles 
-stem cells like=Divide/regen. during lost hepatocyte 
-Function 
  :detox 
  :bile production 
  :blood prot. 
  :glycogen storage
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3
Q

Normal liver-received blood from which organ

A

Directly from GIT

-perfusion determine susceptibility to toxin

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4
Q

Normal liver-vasculature and system

A

Supportive via proper hepatic artery

Incre. O2 level

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5
Q

Normal Liver-Vasculature function

A

Digestive tract

Via Portal Vn=incre. Nutrients

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6
Q

Normal liver-blood flow

A

Blood–>sinusoid-parenchyma(b/w hepatoxyte) –>central vn(sublobular vn–>hepatic vn–>exit liver)

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7
Q

Normal liver-portal triad

A 
Liver receives BF from 3 BV 
-bile duct=bile produce b/w hepatocyte and flow periphers (away central vn) 
-hepatic art=incre. O2 
  :goes to central vn. 
-Portal vn=incre. nutrients 
  :goes to central vn
  :from GIT 
  :kaupffer cells=liver res. MAC (w/ endoth. cells)
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8
Q

Normal liver-liver perfusion

A

Classic hepatic lobule
-drain blood from portal vn/hep. art.–>central vn
Portal lobules=bile drain from hepatocyte to bile duct
:b/w caniculus central vn as pt. in lobules
Portal acinus=supplies O2 blood to hepatocyte
-dif. zone=Z1, Z2, Z3
:incre. O2 and nurtrients=Z1
:decre. O2 and nutrients=Z3
:incre. toxic affect=Z.3 b/c least support

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9
Q

normal liver-liver perfusion parenchyma is divided into how many lobules

A

3

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10
Q

Liver dis. response to injury

A 
Hepatocytes
-degen./intracellular accumulation 
-death= necrosis/apoptosis 
Inflammation
Regeneration 
Fibrosis
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11
Q

Clinical Liver Syndromes

A 
Hepatic Failure 
-no general functions
-cells dnt function properly 
Cirrhosis
-disrupt architecture 
-fibrosis w/ nodules of hepatocytes  
Portal HTN=incre. R to BF in liver  
Bilirubin metabolism failure
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12
Q

Can Cirrhosis maintain function and not know

A

Yes
Functional tissue nodules r suff. for maintenance
Greenish color=bile accum. (b/c bilirubin)
End stg. alcoholic liver~ cirrhosis resulting from other causes

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13
Q

Bilirubin Normally cleared

A

Senescent RBC r destroyed by phago.
-w/in spleen, liver, BnM
Color=yellowish
W/in fading bruises as RBCs from hemorrhage r removed
-hem brk dwn=produce billirubin (excreted by bile)
Not H2O soluble (pH=7.4)
Bound to albumin
Conj. Biliruben to glucoronic acid from excreted in bile=incre. solubility
-eventually fecal matter
-bile salts in bile is recycled

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14
Q

Bilirubin-abnormal

A

Cholestasis=impaired bile formation/flow

Incre. Bilirubin=jaundice and Icterus

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15
Q

The cells involved in fibrosis normal actions (when inhibit.)

A

Quiescent Stellate cel
-b/w space of disse=b/w endoth. and hepatocyte
-lipid droplet w/ vit. A storage
Inactive kupffer cell

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16
Q

Fibrosis pathogenesis

A 
Foreign memb. comp.(carb/lipid) or secretion of memb. outter leaflet +MAC
Release cytokine
-prolif.=PDGF, TNF 
-contract=ET-1
-chemotaxis=MCP-1, PDGF
Activation of stellate cells 
-+myofibrils prolif. 
-contraction 
-chemotaxis(influx comp.) 
-fibrogenesis=2ndry to +MAC
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17
Q

Causes hepatitis

A

Virus=infects hepatocytes
liver damage 2ndry to systemic infection
DONT need virus for hepatitis

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18
Q

Hepatitis-acute clinical synd.

A

Submassive hepatic necrosis
-Asymp.
:serological evidence
:acute w/ recovery
-Acute symptomatic hepatitis w/ recovery=anicteric or icteric
-acute liver failure=massive hepatic necrosis

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19
Q

Hepatitis-acute Pathology/pathogenesis

A 
Pathology
-necrosis (massive hepatocyte damage) 
Pathogenesis 
-lymphocyte infiltrate(mononuclear infiltrate)
-hepatic damage 
-maybe bridging necrosis
S/S
-fatigue, decre. blood sugar, edema and decre. blood prot.
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20
Q

Hepatitis-chronic clincal synd.

A

Clinical synd.
-w/ or w/o progression cirrhosis
~ presentation to toxic liver injury

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21
Q

Hepatitis-chronic hep. pathology and pathogenesis

A 
Pathology 
-end. stg. prog. hepatocyte damage 
-liver recovers from initial inj. 
Pathogenesis
-dense mononuclear-infiltrate
-bridging necrosis
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22
Q

Viral hepatitis-3 steps of expression

A

Virus infects hepatocyte
Hepatocytes express viral antGN
Immune system targets hepatocytes

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23
Q

Viral hepatitis-Cirrhosis is linked to which cancer

A

hepatocellular carcinoma

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24
Q

Viral hepatitis-acute and chronic basics

A 
Acute 
-Primary viral=hepatitis A, B, C, D, E
-Systemic viral (yellow fever, mononucleosis-EBV)
Chronic=unresolved acute injury or from subacute injury 
-MC=hep. C
-Mini.=Hep B/D 
-immunocomp.=Hep E
-NEVER hep A
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25
Q

Viral hepA

A 
2-6wks=fecal HAV 
-fecal oral infection 
2-12 wks
-anti-HAV IGM=decre. overtime 
-anti-HAV IgG 
Mo. to recover
s/s=jaundice
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26
Q

Hep. B infection

A 
1st acute infection 
-subclinical=recovery
-acute hepatitis=recov. or falminant hepatitis (acute hep. fail) 
-death/transplant 
-Chronic
  :western=spont. clear of HbsAg
  :cirrhosis and/or hepatocellular carcinoma=death/transplant 
Histo
-necrosis hepatocyte 
  :also seen in hep. A
-MAC cluster w/ eosinophilic cytoplasm 
Test
-IHC for HbsAg
-ground glass app. for HBsAg eosinophilic accum.
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27
Q

Hep C

A 
Both acute and chronic 
-serum transaminase
-2-26 wls=serum marker for HCV-RNA 
Acute
-recovery w/ anti-HCV
for mo. or years 
Chronic 
-no recovery
-reactivate endogenous HCV strain
-new mutant strains
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28
Q

Hep C-immune/histo.

A

Acidophil body=apoptotic cells

Mononuclear infiltrate=surrounding damage hepatocytes

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29
Q

Viral hep.-consequences

A 
Loss liver function
-hypoproteinemia
-hyperbilirubinemia 
-anemia  
Infection/stress=more damage 
-cirrhosis may be undx
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30
Q

Chronic hepatitis symp.

A 
S/S=fatigue, malaise, loss of appetite, mild jaundice 
Blood tests 
-Serum transaminase is elevated 
-Hyperglobulinemia
-Hyperbilirubinemia
Minor hepatomegaly/splenomegaly 
Hepatic tenderness 
Tx=symp. and allow it to pass
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31
Q

Drug and toxin liver injury-dis.

A 
cholestatic 
cholestatic hepatitis 
-morphology
  :cholestasis w/ lobular necroinflammatory activity 
  :may shouw bile duct destruction 
Hepatocellular necrosis 
-morphology-massive necrosis 
-assoc. =acetaminophen 
Fatty liver dis. 
-morphology=steatohepatitis w/ mallory-denk bodies 
-assoc. ethanol
Fibrosis and cirrhoss
-morphology=periportal and pericellular fibrosis 
-assoc. alcohol 
Neoplasms 
-morphology=hepatocellular carcinoma 
-assoc.=alcohol
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32
Q

Can you have both toxic and viral liver damage

A

Yes
Produce acute or chronic dis.
Immune response
Hepatocytes are destroyed=cirrhosis
B/C=liver is primary detox organ for the body
-toxins must be eliminated as a potential cuase

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33
Q

Toxic liver Injury

A 
Z. 3=zonal necrosis
Portal acinus=perfusion 
Toxins criteria 
-predictable/dose dependent
  Ej=acetaminophen very toxic to liver
-idiosyncratic is not does dep. 
  :Isoniazid (Tx TB)
  :Lovastatin(decre. cholesterol)
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34
Q

Toxic liver inj.-necrosis in liver

A 
Necrotic liver 
-congested (expand BV and incre. blood
-bile accum. 
-incre. necrosis not fibrosis [
  :smaller liver
  :feel softer(should be tougher)
Acetaminophen overdoes
-confluent necrosis 
-zone 3 
-surround central vn.
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35
Q

Common liver toxins-acetaminophen

A 
Liver convert reactive intermed. 
-incre. cell killing in Z. 3 b/c less R to intermed 
Chlopromazine=dopa antag.
-~ to acetaminophen
-tx Schizo
-form insoluble complex in bile
  :cholestasis in bile ducts 
-Metabolites 
  :inhib. memb.-enzyme 
  :improper function
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36
Q

Common liver toxin-ethanol w/ mild and serious injury

A 
Mild injury=mod. alcohol intake(6 beer/8oz. of 80prof.)
-liver inj. 
-steatosis=fatty deposit w/in liver
-inhib. liver function 
-normally clear but accum. w/ chronic alcoholic intake 
Serious 
-massive intake/chronic effect 
-hepatitis
37
Q

Toxic liver inj.-alcoholic hepatitis

A

Ethanol w/ multiple hepatocyte effect
-chemically=effect memb. function
:ethanol–>memb. =decre. memb. fluidity(ICF) and impair cell function
-induce/inhib. enzymes detoxying foreign comp.
:accum. foreign comp. and ROS(incre. O2 toxicity)
-Oxidation of Ethanol–>acetaldehyde
:inhib. prot. export/metab.
:alters redox potential

38
Q

Toxic liver damage-alcoholic hepatitis hepatocyte damage

A 
Necrosis=inflam infiltrate and visible fat pockets 
Mallory body formation
-come from inhib. prot. degradation--
>IF prot. w/ ubiquitin 
-histologically=eosinophilic conc.
39
Q

Toxic liver damage-alcoholic steatosis

A

Fat deposit w/in liver cell
Lrg/small fat droplets
MC around central vn in Z. 1

40
Q

Toxic liver damage-alcoholic steatofibrosis

A

fibrotic changes from + steallet cell

41
Q

Toxic liver Injury-for alcoholic hepatitis can steatosis, cirrhosis and hepatitis occur indi.

A

Yes BUT also in correlation from each other

Recovery w/ no alcoholic intake

42
Q

Hepatitis-non alcoholic fatty liver dis.

A

80%=isolated fatty liver
-inhib. or decre. cirrhosis
-MAINLY steatosis
-no incre. risk of death compared to gen. pop.
Non-alcoholic steatophepatitis (NASH)
-prog. cirrhosis=hepatocell carcinoma or decom.

43
Q

Hepatic vascular dis.-hepatic circulatory disorder (impaired blood inflow)

A 
Inhib. BF/pre hep. 
Portal vn obstruction
-intra/extrahepatic thombosis 
Manifestation 
-esoph. varieces 
-spleenomeg. 
-intesteinal cong.
44
Q

histo. what is seen in sickle cell dis. and liver

A

occlusion of sinusoid

45
Q

portal HTN causes

A

Prehep
-obstructive thrombosis of portal vn.
-structural abnorm. narrow of portal vn.
Intrahep.=anything incre. P.(mainly fibrosis.)
-cirrhosis of any cause
-Primary biliary cirrhosis (even w/o cirrhosis)
-massive fatty change
-diffuse, fibrosing granulomatous dis.(sarcoidosis)
-amyoidosis
Posthep.
-Cor pulmone

46
Q

Where is liver found respective to thrombosi?

A

dwn stream from thrombosis while necrosis and hem is upstres

47
Q

Preeclampsia/eclampsia-S/S

A

Maternal HTN
Proteinuria
Peripheral edema
Coag. abnorm. (hypercoag.)

48
Q

Preeclampsia/eclampsia-liver dis manifestation as HELLP SYND.

A

H=hemolysis
EP=elevated liver enzymes
LP=Low platelets
(coag. impacted=fatal)

49
Q

Preeclampsia/eclampsia-other S/S

A

Hemorrhage W/IN SPACE OF DIS
Fibrin deposits w/in periportal sinus
Develop coagulative necrosis of hepatocytes
Hematoma=under glisson’s capsulse(liver CT capsule)
-cn result in catastrophic hepatic rupture

50
Q

BF to liver

A

portal vn.

51
Q

can bilirubin damage liver?

A

Yes b/c excreted by liver

52
Q

Cholestatic synd.

A

bile move. damage liver

53
Q

Cholestatic synd.- Cholestasis and systemic retention of bilirubin and other solutes

A 
Excess cholesterol
Xenobiotics
Other wast products NOT H2O soluble
-cnt be eliminated in urine(h2o solb. goes to urine)
-bile-->duodadenal and not absob=fecal
54
Q

Cholestatic synd.- cholestasis and impaired bile formation and flow

A

Accum. of bile in hepatitis
Obstruction of bile channels (extra/intrahep.)
Defects in hepatocyte bile secretion

55
Q

Cholestatic synd.- cholestasis and s/s

A 
Jaundice=no inhib. biliruben
Pruritis= bile sats deposit in skin 
-very itchy
Skin xanthomas(cholest. accum.)
Malabsop.
-b/c no bile salts in duoad.=no absop. 
-no absop. of Vit. DEKA
56
Q

Cholestasis-hist.

A

Enlarged hepatocyte
Dilated Canaliculus(channel b/w cells)
Apoptotic hepatocyte
Kupffer cells digest pig.

57
Q

Cholestasis-acute larg duct obstruction

A

W/in hepatocellular parenchyma
Ductular rxn w/in PMN
Edema in portal tract stroma
NOT w/in caniculi

58
Q

Cholestasis-caused by sepsis?

A

yes

59
Q

Cholestasis-sepsis and the 3 diff. mech.

A

Diff. effects b/c infect w/in liver(abcess or cholangitis)
-cholangitis=bile duct lining is inflamed
-block bile flow
Circulating microbial products
-main cause leading to cholestasis(esp. gram neg.bact.)
Hypotension=ischemia(esp. if already cirrhotic)

60
Q

Cholestasis-sepsis and commonly leading to canalicular cholestasis

A

Bile plugs w/in centrilobular bile canaliculi
+Kupffer cell
Mild portal inflam.

61
Q

Cholestasis-sepsis and ductular cholestasis

A

Canal of hering is dilated an bile plugs in bile ductules
Edema/presence of PMN in stroma
Hepatocyte cell=death

62
Q

Norm. gall bladder

A

Located=under liver and shares bile duct to go to duodenal
Food enter duodenal
-incre. bile by sphincter of odd into duodenal to mix w/ food
Dnt need bile
-goes to cystic duct and is store in gall bladder
:gall bladder store excess bile by special epith.

63
Q

Cholecystitis-s/s

A 
Inflammed gall bladder
Acute or chronic or both
Mainly assoc. w/ gall stones
-incre. Bile conc. by ball bladder 
-cholesterol or pigment(bilirubin) stones
64
Q

Cholecystitis-acute

A

Enlarged/tense gall bladder
Thick wall and fluid-filled (edematous)
Serosa=hem. under it
Fibrinous exudate coverage on gall bladder surface
-fibrinosuppurative(pus)=more severe dis.

65
Q

Cholecystitis-Chronic

A 
Mucosal inflam. infiltrate
-incre. P. on wall forming sinuses 
Sinuses=rokitansky-aschoff sinus
-disrupts muscularis of gall bladder 
-assoc. w/ prolife. of cells=PRE CANCEROUS LESION
66
Q

Neuroendocrine tumors

A 
Endocrine pancreas issues 
Benign 
-2% of pancreatic tumors 
-s/s relate to excessive hormone release 
Overgrowth of specific cell types(3 types)
-Glucagonoma
-Insulinoma
-Somatostinoma
67
Q

Neuroendocrine tumors-Glucagonoma

A 
Alpha cells hyperplasia
Glucagon=incre. gluco. 
Excessive gluc.=hyperglycemia
S/S=Rash
-malnutrition 
-AA--> to gluconegenesis not prot. production
68
Q

Neuroendocrine tumors-insulinoma

A 
beta cells hyperplasia 
Clinically
-hypoglycemia=neuro sysmpt. 
-Incre. by fasting/excersi
-incre. insulin=incre. gluc. uptake
Tx=food/gluc.
69
Q

Neuroendocrine tumors-somatostinoma

A

delat cells hyperplasia=inhib. alpha and beta cells
Diabetes=change gluc. uptake
cholethiasis=impaired bile secretion(gall stone)
Steatorrhea= inhib. pancreatic excretion (decre. glucagon)
-decre. fat brk dwn

70
Q

Diabetes mellitus-insulin action

A 
Adipose tissue
-incre. gluc. uptake and lipogenesis
-decre. lipolysis
Striated muscle 
-incre. gluc uptake, glycogen/port. synth. 
Liver
-decre. gluconeogenesis 
-incre. glycogen synth./lipogenesis
71
Q

Diabetes mellitus- type I

A 
Beta cell destroy 
-cn be absolute insulin def. 
Pathology
-autoimmune rxn to islet beta cell(islet langerhan cells)
-form insulitis
72
Q

Diabetes mellitus-type II

A

Comb. of inulin R and B cell dysfunction
Pathology-Amyloidosis in islet
-cn be seen w/ normal age
-decre. islet cells

73
Q

Pancreatic cells for a,b and d

A

alpha=glucagon
Beta-inulin
Delat=somatostatin

74
Q

Diabetes mellitus-diabetic glomerulonephrophaty

A

diffuse mesangeial matrix incre. b/c endoth. uptake of gluc.
Incre. uptake by endoth. cells
-Hyperglycemia w/in insulin R=effect endoth. cell/function
-Incre. atherscloerosis
-Lipidemia=change function of (glycoprot.)
-Fibrinogen= thrombosis

75
Q

Diabetes mellitus-clinically of no insulin or def./R

A

Pholyphagia
-incr. lipolysis(free FA)
-incre. prot. catoblisim(aa) w.in sk.muslce
-incre. glucagon
:gluconeogen
Hyperglycemia
-incre. gluconeogen
-insulin R.
-effect on endoth. cells=incre. renal vascular def.
:athrosclorsis
:dislipidemia after liver production of lipoprotein
:fibronolysis (incre. thrombosis)
Ketoacidosis=incre. lypolysis->ketogensis
-diabetic coma
Kid. issues from hyperglycemia and ketoacidosis
-ketonuria glycosuria
-polyuria
-volume depletion=polydispsia
:cn also cuases diabetic coma

76
Q

exocrine pancreas dis.

A

Pancreatitis
Acute=reversible
Chronic=irrevers. exposure of unresolved acute damage that is not full resolved from prev. incidents
-cn be progressive and

77
Q

Acute pancreatitis-CUASES

A 
MC
-Biliary tract dis.=b/c share the same duct ampuella w/ pancreas 
-Alcohol=MC 
-Toxin 
-Trauma 
-Vascular dis. 
Metabolic
-mainly alcohol and drugs
-hyperCa+emia and hyperlipoprotenemia 
Genetic=trypsin
Mechanical
-gallstone blocking the ampulla duct 
-Iatrogenic injury=surgery injury
  :endoscopic procedure w/ dye injection 
Vascular
-shock b/c low BP 
Infection=mumps
78
Q

Acute pancreatitis-pathogenesis

A 
3 ways of the beginning 
-Ductal obstruction
  :ie gall stones
  :chronic alcohol 
-Acinar cell injury=alcohol
-defective intracel transport=mainly alcohol
All of them cause acinar cell injury 
Irreg. act. enzymes=causes acute pancreatitis
79
Q

how is trypsin normally

A

An active pancreatic enzymes secretes and goes to duodenal to activate trypsin
Trypsin will active other enzymes

80
Q

Acute pancreatitis-trypsin irreg.

A

Changes in assoc. w/ acute pancreatitis=autodigestion of pancreas by own digestive enzymes
Trypsin is activated in pancreas not duod.
-cuased mutation of cleavage site that usually deactivate(ie fail safe)
-mutation in trypsin inhib. =always active trypsin

81
Q

Acute panreatitis-autodigestion

A

Elastase damages vsl walls=Microvasc. leakage(edema)
Activate lipases=fat necrosis
Proteases(trpsin, chemotryps etc.)=parenchymal degrade
Clotting defect.=thromboses damage wk vessl
Kallikrein=hem
-type of kinin
-related to BP and inflammation
-envolve plasma=degrad clots and +clotting factors

82
Q

Acute pancreatits=pancreatic necrosis

A

Focal Parenchymal necrosis

Fat necrosis

83
Q

Chronic pancreatitis-basic

A 
Inflammation and irrev. destruction of acinar cells
Fibrosis impact endocrine parenchyma
-affect alpha, beta and delta cells
MC=long term alcohol abuse
-incre. excretion-->duct obstruction
-directly toxic to acinar cells
84
Q

Chronic pancreatitis -pathogenesis

A 
~acute=duct obstruction and cell inj. 
Oxidative stress
Repeated acute episodes=fiborsis and parenchyma loss 
-pelilobular fibrosis 
-duct distortion 
-altered secretion
85
Q

Chronic pancreatitis -pathology

A

Parenchymal fiborsis
Reduce exocrin acini (not endocrin islets)
Duct dilation/conc.

86
Q

Hepatic vascular dis.-hepatic circulatory disorder (impaired intrahepatic BF)

A 
Inhib. intrahepatic BF 
Cirrhosis
Sinusoid occlusion
Manifestation
-acites=2ndry to cirrhosis by accum. of fluid b/c assoc. w/ hypoalminemia from liver damage(no edema)
-esophageal varices(cirrhosis)
-hepatomegaly
-elavated aminotransferases
87
Q

Clinical pancreatitis

A 
Upper abdo pain. 
-b/c inflam pancreas. (behind stomach)
Nausea
Vomit
Fever
Tachycardia
Sweating
Icterus/jaundice=gall bladder of ampula
88
Q

Pancreatitis-tx

A

IV fluid
No food b/c activate pancreatic enzymes
Med. for pain/suppor

89
Q

Hepatic vascular dis.-hepatic circulatory disorder (Hepatic vn. outflow obstruction-post hep.)

A 
Hepatic vn. Thrombosis (bud-chirai synd.)
Sinsusoidal obstruction synd. 
Manifestation
-ascites
-hepatomeg.
-elevated= aminotrasnferase
-jaundice

Mech. 2 (8 decks)

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