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Abdo year 3-K > Biliary tree and Cirrhosis + pancreas > Flashcards

Biliary tree and Cirrhosis + pancreas Flashcards

1
Q

What happens in a healthy liver?

A 
Balanced fatty acids
Hepatic fatty acids (FFAs) uptake
Lipogenesis in liver
FFA oxidation in liver
FFA export within liver by lipoproteins
Rate of FFA input = output
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2
Q

What happens when we take too much drugs, ethanol & fatty foods?

A

Simple steatosis

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3
Q

Is it reversible?

A

Yes
Once you stop the “good” life..
Eat healither, no drugs, no good taste fatty foods.

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4
Q

What happens in simple steatosis?

A

Fat accumulation in the liver
Initially ariund zone 3’, near central veins
Later, throughout the parenchyma.
Xs fat from diet, ethanol, from adipose tissue,
↪️ there is less oxidation, so Triglycerides (TG) will accumulate as lipid venules

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5
Q

What happens to triglycerides?

A

Lipase hydrolyses TGs (from fiet, adipose tissue) to FFAs that go to hepatocytes and are stored as TGs or undergo oxidation.

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6
Q

What happens in fat accumulation?

A

Rate of fatty acid input(uptake & synthesis of lipids)> rate of FFAs output. (Oxidation & secretion of lipids)
↪️ impaired fat metabolism leads to lipid accumulation in vesicles.

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6
Q

What happens if we continue with the bad habbits? After simple steatosis. Is it reversible?

A

Steatohepatitis- termed now as fatty liver disease.
Its still feversible
.

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7
Q

What happens in steatohepatitis?

A 
Fat accumulation
Liver cell nevrosis
Inflammation
(Mallon-1- Boujet) 
Fibrosis
↪️inflammation is associated w/ fatty changes
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8
Q

What is cirrhosis? Is it reversible?

A

This is the last stage of fatty liver disease. IRRIVERSIBLE
Fibrosis
Hyperplastic noduels
Subendothelial or pericentral fibrosis (hepatic fibrosis)
Progresses to panlodular fibrosis w/ nodule formation (cirrhosis)
❌ shrunk liver, smaller.

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9
Q

Whats alcohol related cirrhosis?

A

Typically micronodular

W/ steatosis

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10
Q

Whats beta oxidation of fatty acids? Where does it happen?

A

In the matrix of mitochondria,
Fatty acids provide more ATP than glycerol.
Catabolic process by which fatty acids broken down to generate Acetyl-CoA, entering Krebs–> NADH + FADH2 –> ETC–> energy.
However, ketone bodies also produced.

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11
Q

Whats lipid anabolism?

A

Lipid anabolism: lipogenesis
Stimulated by insulin
Liver & adipose tissue
Make lipids from glucose and amino acides (lipoproteins)

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12
Q

Whats ketogenesis?

A

Kerone bodies mainly produced in hepatocytes’ mitochondria, and their synthesis - response to unavailability of blood glucose.
After glycogen stores exhausted.

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13
Q

What else triggers ketogenesis?

A

When High levels of blood glucose that cannot be stored as glycogen in hepatocytes or muscles.
Then, makes availability of enerfhy, stored as fatty acids.

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14
Q

What else stimulates steatosis?

A

PPAR-gamma receptor sensor- when Xs energy = fat oxidation.
When defective- ⬇️ fat oxidation.
↪️ steatosis
PPAR-g stimulates steatosis.

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15
Q

What are the types of Fatty Liver Disease?

A

Alcoholic fatty liver diease and Non-Alcoholic Fatty Liver disease (NAFLD)

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16
Q

What hapoens in Alcoholic fatty liver disease?

A

Ethanol–> acetaldehyde by alcohol degydrohenase giving off NADH
↪️ Acetic acid –> Acetyl-CoA –> fatty acids in Liver

17
Q

So.. Alcohol fatty liver disease:

A
  1. Xs reduced NADH+ formed–> lipid synthesis
    –> from Xs alcohol
  2. Impaired secretion of lipoproteins
    ↪️ lipids accumulate in liver
  3. Increased peripheral catabolism of Fat
    (+ ketone bodiess…..)
18
Q

NAFLD- what is it and how is it tx?

A
  1. “Diet involved” high intake of dietary fats, e.g. fructose–> glyceraldehyde..–> G3P..
  2. Higher fat uptake
  3. Reduced fat secretion
  4. Reduced secretion of lipoproteins
  5. Increased storage of FFAs
    ↪️FATTY ACIDS IN LIVER.

Ask for alcohol to exclude this fx.
Dx- ⬆️⬆️AST +ALT , CHECK HEP C- causes fat to accumulate.
H/w these do not discriminate from simple steatosis.
Refer to hepatologist for amount of fat- USS and CT, again not specifi for scarring and inflammation present.
Definite: Liver biopsy.
Non alcoholic steatohepatitis.
Sx:
Silent, no sx. Maybe pain in RUQ,
O/E slight hepatomegaly and acanthiosis nigricans (patch dark discolouration of skin over neck and upper arms. )
Progression to cirrhosis is slow.
Tx
Usually there are obese, so lose wt, oprimise DM, HTN and hyperlipidaemia if present.

Drugs used in DM help, simce its a metabolic disorder of the liver to metabolise insulin.
Insulin sensitisers - clinical studies in completion almost.

19
Q

Whats Metabolic syndrome?

A

3/5 of these:

  1. HTN
  2. Obesity
  3. Resistance
  4. Dylipidaemia
  5. Impaired glucose tolerance
20
Q

Causes of Liver Cirrhosis

A
  1. Alcoholic Liver disease, alcohol steatohepatitis
    Fat in liver, steatosis, inflammation, fibrosis,
    ⬆️⬆️ AST, ALT, fever, Hepatomegaly, jaundice.
  2. Non-alcoholic + steatohepatitis, metabolic syndrome, DM, obesity, drugs, steatosis, inflammation % fibrosis. ↪️LONGER.
3. Hep C >6 months --> cirrhosis
Blood to blood, asymptomatic, 
Acute: hepatitis
Chronic: fibrosis & cirrhosis
Abs- cannot detect antigen, hard diagnosis, no vaccine, interferons. 
4. Hep B > 6 months --> cirrhosis
Blood, sex, semen, vagina
Acute infx: jaundice, hepatitis, vomiting
Chronic: cirrhosis, liver cancer 
Interferons vaccine.
21
Q

Complications of liver cirrhosis

FUCK

A 
Portal Hypertension
Oesophageal varices --> bleeding (PHTN) through portal vein.
Hepatic encephalopathy. 
Hepatic pulmonary syndrome
Hepatocellular carcinoma
Oedema
Itching- ⬆️ levels of uric acid
Hepatorenal syndrome
Jaundice
Haemorrhoids- rectal varices or backflow
Slpinomegaly- back flow to splenic veins - accumulation of cells- WBCs, RBCs, platelets..
22
Q

Whats portal Hypertension (PHTN)

A

Portal vein–> liver–> hepatic vein–> IVC–> RA
Pressure is increasing, blood flows backwards,
Stomach –> gastric veins,
Rectum- rectal veins

23
Q

Whats hepatopulmonary syndrome?

A

(Endothelin 1 –> vasoconstriction) – vasodilation by NO in abscence of endothelin 1.
So, pulmonary vasodilation induced NO, enthothelin-1 secreted by liver.

24
Q

Why is hepatic encephalopathy a sx?

A
  • ammonia not detoxified, loss of memmory, concentration, coma, death, confusion
25
Q

Sx of hepatocellular carcinoma?

A

Hepatomegaly
Wt loss
Pain
Swelling

26
Q

Pathogensis of hepatorenal syndrome

A

⬇️ kidney hypoperfusion, PTHN/onstruction
⬆️ perfusion in Abdo cavity : Ascites (so Na+ & H2O not foow through liver)
Stomach: big
Infxs
Fluid not to heart –> Hypovolaemia
Then–> arterial systemic vasodilatation
RAAS
reabs Na + H2O to compensate for Hypovolaemia= low fluid in blood.

27
Q

Why Jaundiced?

A

Intrahepatic onbstruction of bile to intestines

Bilirubin accumulates in plasma

28
Q

Some systemic features of cirrhosis?

A

Low platelet count, anaemia

29
Q

PSC

A

Leads to cirrhosis
Progressive fibrosis of intra and extra hepatic ducts.
Common: episodes of ascending cholangitis and jaundice.
ERCP- shows multiple strictures
AIDS common.
Eventully liver transplant. 🚑

30
Q

How is acute pancreatitis distinguished from chronic pancreatitis?

A 
Acute- isolate or recurent attcks- pancreas returns back to normal structurally and functionally.
Causes: 
Gall stones
Poison- venom scorpion 
Alcohol 
Neoplasia- obstruction
Metabolic: hypercalcaemia,hyperlipidaemia
Iatrogenic: post -surgical, post ERCP, 
Drugs- cosricosteroids,

Chronic:
Alcohol, idiopathic, protein energy malnutrition, hereditary, CF, Autoimmune.

Acute- inflammation

31
Q

Acute Pancreatitis

A

Patho: initiating event-> 1. acinar cell injury -> 2. Activated proteases released in pancreatic interstitium.

  1. Disruption of acinar cells-> promotes migration of inflamatory cells - from microcirculation into interstitium.
  2. mediators and cytokines released cause a Local inflamatory response. And smts SIRS –>~ multiple or single organ F due to hypoperfusion (shock)

CF
Cardinal sx- epigastric or UQ pain radiating to back. N+V and in severe: multiorgan F. O/E - 1. Epigastric tenderness, 2. Guarding. 3. Rigidity.
Severe necrotising P- cullens sign(?Ecchymoses round umbilicus) or Grey Turners sign (in flanks).

Dx
⬆️ serum amylase + hx. If late: normal, urinary amylase or serum lipase are still up.
FBC, CRP, U+E, LFTs, plasma Ca2+ and ABGs done for severity.
Radiology: erect CXR to exclude Perf DUlcer and high serum amylase.
Abdo USS to search for GS and inflammation of pancreas, may also show swelling. CT and MRI in mildest.

Mx
Most are mild- interstitial inflammation and recover in 5-7 days.
Severe: assc w/ multiorgan F like renal and resp F.
2. Impaired coagulation
3. Disseminated intravascular coagulation (DIC)
4. Necrosis usually- CT- focal areas of reduced tissue perfusion.

Severe- ABC, Medical therapy (pain control, tramedol choice NBM, IV fluids, NG tube (mild)to empty stomach?)
Consider ITU nursing
Prophylactic antibiotcs - cefuroxime, or aztreonam (⬇️ risk of infected necrosis)
Naso- jejunal feeding or TPN if not tolerated.
ERCP within 48hts if GS P and or cholangitis.
⬇️⬇️
Contrast enhanced Abdo CT scan /MRI within 3-7 days
⬇️
Monitor for complications.
Hyperglycaemia (no B cells to make insulin), hypocalcaemia, renal F and shock.

Prognosis:
Mortality:50% in seve cases.

32
Q

⬆️ serum amylase

A

PUD
Acute cholecystitis
X3 pancreatitis

33
Q

Pancreatic severity scoring system based on initial admission and subsequent repeat tests over 48hrs??

A 
Glascow scoring system
Age >55
WCC >15x109/L
Glucose >10 mmol/L
Urea >16 mmol/L
PaO2 100 units/L

Severe P >_3 +ve criteria

34
Q

Why is Morphine avoided in Pancreatitis?

A

Increases the pressure of the sphincter of Oddi

35
Q

Some words about chronic Pancreatitis

A

Continuing inflammatory response of pancreas, characterised by irriversible morphological change and permanent functional impairmenent.
Developed: chronic calcifying P, uusually by alcohol. If stop drinking, can arrest condition tho.

CF
Central abdo pain in epigastrium and radiates to back. May be intermittent or constant, exacerbations by alcohol binging.
Pain accompined by severe wt loss as result of anorexia,mdiff to distinyuish from P cancer pain.
DM may develop and steatorrhoea when the secretion of oancreatic lipase is reduced by 90%.

Occasionally pt presents with jaundice with biliary obstruction and cholangitis.
Ddx cancer
Consider when short hx and localised ductular abnormalities on imaging,

36
Q

Carcinoma of the pancreas

A

5th cancer death in West.
M>F , age increases, peak 7th decade.
Aetiology unknown, but alcohol, coffee, smoking and fat ingestion implicated.

CF
Head of pancreas: painless jaundice due to CBD obstr + wt loss.
O/E : jaundice and distended GB.

37
Q

Whats Courvoisier’s law?

A

In case of painless jaundice, and a palpable GB, the case is not GS.
Cz GS cause pain: colicky due to peristaltic waves. In GB.
In GS disease, chronic inflammation and fibrosis prevent distention of the GB.

Cancer of body or tail:
Abdo pain, wt loss + anorexia.

DM may occur and there is an increased risk of thrombophlebitis.

Invx
Dx- USs or CT Abdo.
Duodenoscopy or ERCP may detect tumor at head or ampulla.
Endoscopic ultrasound used for staging + difficult cases.

Mx
Cure: resection, but some resectable disease at dx cz presents LATE.
?
If not fit for surgery- chemo + radio.
5-Flurorouracil + gemcitabine - improve survival in advanced disease + survivL benefit agaianst pancreatic resection.

Pallative tx for unresectable to relieve obstructive jaundice (stent by ERCP across the obstructed distal CBD) , gastric outflow obstruction and pain.

Prognosis
Surgical resection-3Y :30-40% .
Median treated: 8-12M with advanced D.
Metastatic D: 3-6M.

38
Q

What makes resection impossible in pancreatic cancer??

A

Tumour adherence and invasion into adjacent structures esp major blood vessels (locally advanced disease) , makes complete resection diff.
Theses patients are treated w/ combined chemo + radiotherapy.

39
Q

Neuroendocrine tumours

A

Arise in pancreas from APUD- amine precursor uptake and decarbozylation cells.

Usually produce 1 hormone- most tumors express lots of somatostatin receptors- IV injection of octretide- uptaken- localises tumor.

Abdo year 3-K (13 decks)

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