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Pathology of Liver Failure, Study notes of Pathology

Document contains all the information about pathology of liver failure, starting from general structural and function of hepatic cells. Then mechanism of injury and it’s consequences with progression to liver failure. Explaining by gross and microscopy of hepatic failure. And finally throwing light on portal hypertension and complications of liver failure.

Typology: Study notes

2020/2021

Available from 10/04/2022

Aryadahane
Aryadahane 🇮🇳

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E-PR

# General^ Info^

alot lives
  1. weight^
  • 1400 to^1600 gm

     112kg ≈ 
  1. (^) Blood (^) supply →^ Postal^
vein =^ GO^ to^ 70%

Hepatic art. =^30 to (^) 40% ◦ Anatomy (^) of diner (^) Lobule model connective tissue bubs (^) ← ¥ÉÉ¥¥¥i¥☒→ central^ mien tnterlobular ruin (^) a ← Egg hepatic win) go o mi :::: ]→*.. """ H¥¥p¥i¥÷:ᵗᵈjE "

Feom (^) portal ruin

I puffer cells

B. duty Hepatocytes unsaid É÷g.p.ve¥¥%E J HA.^ I^ { pace of Disse

endothelial stellate^ I,

uh (^) + , cells space bin^ hepatocyte^

Fat. containing sinusoidal tinning

Celts win^ space

endothelial cells

of Iisse

.sn#!Thiouitk ☒☒☒ ¥i¥÷É¥¥☒*÷w " Y,^ hepatitis^ >^ Canal (^) of cholangiocyte (^) Hering

  • Bile^ Flow^ → Bile canaliculi

Duduk ← ⑨ canal^ of Hering ! Hepatocyte cells ↓ Brite ductile ± Tntoelobulwe bite^ duct

☒ EEE^ #☒HUMM^

  • E- ¥ # Alky → Iuiured /^ dysfunctional hepatocyte ↓ Res pongee C Reversible^ changed steatosis ←

, → Buttoning of hepatocyte

Cfut deposit)^ lcholestasis

C. Bilirubin It, deposited HALLMARK OF ① (^) Alcohol induced/ Non - alcohol (^) induced ✗ → (^) Irreversible teatohepatitu Lyiwry ↓ Hepatocytes

  • die →^
Neurosis

§ → Apoptosis In (^) imbalance in necrosis (^) → AT^ the flaw into hepatocyte ◦ → ↓ This (^) swells (^) - H2O

im ; ↓^

ruptures

↑↑ Intracellular Cat

Burst +
+↑ mitochondrial

dysfunct

Now (^) ; stimuli^ for stellate cell^ activate^ is ① TNF^ -^ a^ - produced by buffer^

cells

macrophages

② Altered interact e-

extracellular matrix^ [^ Eeñ ③ Toxins^ → Reactive

oxygen species^

[Ros]

These activates^ PDUF ,^ Ta^ F- P

& IL- 17 , chemokines Released from keiffer^ cells (^) ,^ other^ monsoons which (^) transmits'"aignd to stellate

  • cells which (^) in turn release _uaso active GF factors www.ne/,chemotauhteadinglo-persistence of iuiwy & (^) inflammatory conch

In turn leading to ECM^ deposition ⑨ (^) Spate of Disse^

  • toss^ of sinusoidal endothelium I^2 IN^ CA , PILLARIZA^ -110N

Sinusoidal (^) Capili urination is a HALLMARK of

→ NON
  • ALCOHOLIC
STEATOHEPATITEE

1 HEPATIC CARCINOMA t, ① toss^ of vascular (^) compromise ② Teansfoun into dense^ fibrous^ Septa This fibrous Hepler encircles surviving hepatocyte & give rise to diffuse

  • earring i. (^) e. chief

zedo.fm#yiwy&cwefarmatw is interrupted^ by G- : (^) ① clearance of hepatitis virus ② Cessation^ of alcohol use

stellate cell activate^

_^ stopped &

earring

is

stopped

fibrous septet % (^) broken byMETAuoPRoTEINAS5#

① liver^ transaminases^ are (^) elevated

↓ hepatocyte

smelling

Enlarged him → inflammatory infiltrate

Edema

221 £ (^) II parenchyma dies & (^) liver shrinks ↓

Serum Teams^ aiuiuase

←→

Decrease Elevated^ as^

it ↓ was R^ ↓ :b

sign of ingrown

hepatocyte die

(^) Other (^) main

esfesfatiaws

① Cheek^ stasis^ -^ Bilirubin^ retention due to alteration^ in^ bite formation & (^) flaw. I tending

to

yellows

skin^ → Jaundice sclera →^

icterus

Asterixis is a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements Grade-> Cerebral edema incidence I- Behariar changes, altered sleep-tale gude farely I-@asterixis, lethargy, disorientation farely Ill - more severe 25-25% IV - CoMa 65-75% ② Hepatic Enchaehalopabhy

& (^) pectaumofdistwrbunuocc-i.ir

  1. Consciousness μ fiction behavioral abnormality bᵈ% D (^) iinfusim a) ii. coma I
5) Death

Symptoms can oceans^

① Rigidity

Hyperrefused

a

Asterisms

t.

No☒^ -

rhythmic ,^ eapidenteusth

flexion movement of head + extremities ;^ when arm is^ -^ extended^ + dorsi flexd wrists

COAGULOPATHY ÷

2+5--7 ; 9.10.^

21h

All

are defiant " . Leading to ① (^) Easy bruiseability

② Intracranial^

bleeding

(^) Portal

hypertension

  • More^ commonly

in (^) chronic Intra (^) hep §tic^

obstruction

tower failure

I can lead^ to^ Ascites

(^) tlepulo

renal (^) syndrome - Renal failure^ occurring in (^) pt

. (^) with

liver failure

c- No

fun ctl (^) cause (^) of kidney (^) dysfuutn _

Splanchnic circulation is composed of gastric,small intestine,colonic,pancreatic, hepatic splenic circulation arranged in parallel with one another symptoms ÷^ ① 4 Urine output

② ↑ Urea + Creatinine

③ Farted^ hypertension

⑥ with * vasodilators^ 6% by endothelial^ cells in ←splanchnic^ vasculature ↓ Thus 4 Renal^ output ↓ Renal

perfusion

  • +^ UFR tending to Renal^ failure

(^) Pts (^) develops heputo

renal (^) syndrome

also have portal hypertext due^

to ←

Shure Metastatic

§ Cirrhosis^

Alcoholic Tumor

scarring (^) of him Hepatitis

tissues

i. e.^ Fibrosis^ of^ lines tissue

Regenerative →

Nodules

Microscopically
  • Mousson trichome stain ↓ To stain^ thick fibrous bands of collagen around cirrhotic nochilli

40% individuals^ →^ Asymptomatic for & times^ chieosis lien. Symptoms ① Anorexia

② Weight

loss ③ Weakness causes (^) of Death ① Haepatio encephalopathy ② Bleeding from esophageal^ varies ③ Bacterial (^) infections ⑨ tlaepato

cellular carcinoma
⑤Jon
dice +

encephalopathy

  • co^
  • agile

path✓

acute liver^ failure

of (^) xp

(^) CAUSE

of Resistance (^) El (^) sinusoids ① (^) Contract of

muscular smooth muscles

② & cursing

  • Formation^ of nodule in
liver

parenchyma ③ (^) It, No C^ Nitric^ oxide] + ↑↑ Endothelin I

Auyiotousiogent Eicosanoids ↑ ↑

Release ↑^ A^ Naso^ constriction

⑥ sinusoidal^ remodelling

anastomoses ↑ ↑^ portal hypertension ⑤

✗☒ Portal^ venous blood

flaws ioduelo hyperdynamic circulation

Due to^ **^ splanchnic arterial^ blood^ flow

leading

to increase^ venous^ efflux

☒ ☒^ No = vasodilation

170*1#

¥q☒e

#$#☒ F

  1. (^) Hepatic (^) encephalopathy
  2. Ascites
  3. Format^ of^ porto

systemic venous

shunt

Congestive splenomegaly

¥ #SEE

#& - Ibid accumulation

  1. Peritoneal^ cavity 88 %^ caused^ by chi (^) irons

Fluid accumulate^ >^ so◦^ ml -^ detectable If It's serous (^) fluid

  • <3 gmldl protein denim : as #to^
  1. I^ gmldl Alb.
  • (^) Mesothelial cells^ +^ Mononuclear leukocytes

Neutrophil presence suggests (^) infection ◦ RBC presence intra abdominal cancer