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Metabolism 2 PBL > PBL2 2 > Flashcards

PBL2 2 Flashcards

1
Q

define firboscan

A

this si a speiclaised ultrasound machine for you liver, it measures the fibrosis and steatosis change in the liver

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2
Q

ilteric

A

presence of jaundice seen in the slcera of the eye

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3
Q

AST/ALT ratio

A

ratio between asparate transaminase and alanine transaminsase, this is used to differenaited between various causes of liver disease

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4
Q

gamma GT

A

transferase enzyme that catlayses the transfer of gamma-glutamyl functional groups from molecules such as glutathione to an acceptor that may be an amino acid, peptide or water

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5
Q

diagnostic tap for ascites

A

needle or caterh placed into the periotoneal cavity to obtain ascitic fluid for diagnostic purposes

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6
Q

Terlipressin

A

it is a vasopressin and is sued as a vasoactive drug in the manegemtn of low blood pressure

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7
Q

encephalopathy

A

disease in which the functioning of the brain is affected by some agent or condition

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8
Q

oral lactulose

A

sugar derived medication used to treat hepatic encephalopathy

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9
Q

empirical antibiotics

A

broad-specturm , given use regular given for many thigns

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10
Q

what is the causes of cirrhosis

A
  • Alcohol
  • Fat/metabolic syndrome
  • HBV/HCV
  • Billary disease – PBC/PSC
  • Autoimmune
  • HC/wilsons/amyloid
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11
Q

what re the signs and symptoms of cirrhosis

A 
Symptoms 
-	Not any specific 
-	Weight loss and tiredness 
-	Cholestatic – pruritis, pale stools/dark urine due to bilirubin increased production
Signs 
-	Clubbing 
-	Glynasematic – failure ot breakdown oestrogen 
-	Leuchonychia – pale nails 
-	Palmar erythema 
-	Spider naevi
-	Hair loss
-	Proximal wasting 
-	Scratch marks
-	Xanthelasma
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12
Q

How do you diagnose cirrhosis

A

liver biopsy
child-turrocte-pugh score
fibroscan
blood tests

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13
Q

describe how to do a liver biopsy

A

– stain for scar tissue and shows how much scarring they have GOLD STANDARD

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14
Q

describe a child turoccote-pugh score

A
  • bilirubin - as the amount of bilirubin increases the score increases
  • albumin - as the amount of albumin increases the score increases
  • prothrombin score as the prothrombin time increases the score increases
  • hepatic encephopahty symptom grade - as this gets more controlled the points increase
  • asicites - as this gets worse the points increase
  • each of the 5 points can be given a mark of 1 to 3 depending on severity
  • the lowest score you can get is 5
  • 5-6 is class A where your. liver is compensated and works normally
  • 7-9 class B and 10-15 class C this is when the liver is decompensated and does not work properly
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15
Q

describe a fibroscan

A
  • Electrography – ultrasound like techniqieu
  • Stiffness of the liver is translated in terms of kilopascal
  • Non invasive, painless alternative to the liver bispy
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16
Q

describe blood tests done

A
  • Bilirubin
  • AST/ALT
  • Alkaline phosphate
  • Gamma GT
  • Platelt count – this is important in checking liver disease progression, as liver disease progressive the platelet count decreases
  • • Bilirubin
  • – Unconjugated vs conjugated
  • • Aspartate aminotransferase (AST) – hepatocyte release
  • – Mitochondrial enzyme
  • – Heart/muscle/kidney
  • – hepatitis
  • • Alanine aminotransferae (ALT) – hepatocyte release – involved in moving amino groups to make new amino acids from keotacids
  • – Liver specific
  • • Alkaline phosphatase
  • – Bile cannalicular + sinusoidal membranes
  • – Bone/placenta it is also present in here, can be high in pregnancy
  • – Cholestasis – intra/extrahepatic
  • • Gamma glutamyl transpeptidase (GGT)
  • – Hepatocellular
  • – Cholestasis
  • – Alcohol often associated
  • – Made in liver and biliary cells
  • If AST>ALT – alcohol
  • If ALT>AST – viruses or non alacolic fatty liver disease
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17
Q

what is compensated liver disease

A
  • This is a pathological diagnosis made from anatomical or histological study
  • Asymptomatic
  • Liver can still function
  • Circles of fibrous seen in the liver
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18
Q

what is decompensated liver disease

A

liver failing to work

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19
Q

what three things happen in decompensated liver disease

A

encephalopathy,
portal hypertension which can lead to ascities,
bleeding

20
Q

what are the causes of decompensated liver disease

A

infections, surgery, constipation, haemorrhage, clotting or portal veins, development of liver cancer

21
Q

what are varcies

A
  • These can form in the oesophagus or in the recutm
  • These are big baggy veins that have dialted
  • Can bleed an dcause haemorrhage
22
Q

what re the treatment for varies

A
  • Resuscitation
  • Terlipressin and antibiotics
  • Banding
23
Q

hat is the difference between ascites and oedema

A

Asities – abnormal accumulation of the fluid in the peroneal cavity
Oedema – excessive accumulation of fluid in the interstitial space

24
Q

what causes ascites

A

Ascites
- 1, portal hyperntesion increases this causes the back up of blood in the splenic vein
- 2, leads to splanchnic vasodilation
- 3, this decreases the effectiveness of the circulatory volume
- 4, this activates the renin-angiontesin-aldosterone system
- 5, leads to renal sodium remaining in the body
- 6, this leads to ascites due to an increase in onoctic pressure
-
- or
- when the renin angiotensin aldosterone system is activated you could have renal vasoconstriction and this leads to hepatorenal syndrome, this increases the secretion of ADH and worsens the excess water retention, hyponatremia
- both sodium and potassium would be low due to water retention and dilutional effect
reduced plasma protein (hypoalbuminemia)
- reduced oncotic pressure therefore less water moves back into the capillaries
therefore, ascites is caused due to either an increased hydrostatic pressure or a reduced oncotic pressure

25
Q

what is hepatic encephalopathy

A
  • neuropsychiatric abnormalities in patients with hepatic disease
  • Due to build up of toxins that are not being removed
26
Q

what are the causes of hepatic encephalopathy

A
  • Sepsis
  • Bleeding
  • Drugs
  • Deteriorating liver function
27
Q

how do you diagnose hepatic encephalopathy

A
  • Via a hepatic flap

- EEG/MRI changes

28
Q

what is the pathophysiology of hepatic encephalopathy

A
  • usually glutamine is converted to glutamate and ammonia
  • ammonia then goes to the liver where it is transformed and converted to urea and passed out through the kidney
  • but when the liver is not working ammonia goes to the muscles where it combines back with glutamate and is converted to glutamine this then goes to the brain
    or thiamine
  • important cofactor in converiosn of pyruvate to acetyl-CoA conversion
  • when B1 is lacking pyruvate forms lactic acid
  • this can cause Wernicke-korsakoffs syndrome
29
Q

what is spontaneous bacterial peritonitis and what are the causes

A
  • due to presence of ascites fluid
  • diagsnosis requires panracentesis – sample of the peritoneal fluid taken from the peritoneal cavity
  • mostly caused by a gram negative E coli followed by klebsiella common gram positive bacteria
  • there is bacterial overgrowth
  • weakend immune system – antibitoics increase the risk
30
Q

what are the signs and symptoms of spontaneous bacterial peritonitis

A
  • fever
  • chills
  • nausea
  • vomiting
  • abdominal apin
  • tenderness
  • worsening ascities
31
Q

explain his blood tests

A
  • Haemoglobin low hypochronic – decompensated liver failure liver is not making polypeptides anymore
  • Thrombocytopenia – platelets are removed from the spleen in portal hypertension, marker of worsening liver disease as the liver disease worsens the platelet count decreases
  • INR – normal is 0.8-1.2, so large 1.9 this means that the blood is less likely to coagulation, reduction int eh production of plasma proteins that are involved in the coagulation cascade shows that the liver is decomensated, may alos be due to Vitmain K deficiency
  • Low albumin – liver makes less albumin due to reduction in amino acids and failure, this means that there is a lower plasma oncotic pressure can cause ascities along with portal hyperntesion
  • Bilirubin is high – shows that the liver cannot conjugate it with glucornic acid, therefore this causes jaundice, splenomegaly and pH lead to increase haemolysis
  • High ALP/AST – hepatocyte damage as they are leaking out the cells
  • Alt/gammaGT due to prehpahs billary issue
  • Urea – high not be excreted, means that there is more protien breakdown being used as urea is product of protein
  • Blood glucose – low range of normal – glucose balance not being maintained
32
Q

explain the treatment that he got

A
  • Resuscitated with fluids and blood
  • Thiamine – given thiamine on admission as malnorushied, if isn’t replaced can lead to wernickes encephaly treatment
  • Intravenous pabrinex – contains B vitmains and thiamine and vitamin C, this helps supply energy and prevent refeeding syndrome, contains B1, riboflavin, B6, Vitmain C, B3, anhydrous glucose
  • Empirical antibtoics- broad spectrum antibotics – used to treat any infection he might have in ascities or in the body
  • Asocities tap – check he doesn’t have spontaneous bacterial periteonitis
  • Terlipressin – reduces blood pressure and the effects of portal hypertension
  • Banding – stop the bleeding
  • Oral lactulose – this reduces the gfludi uptake from the gut as it is an osmotic laxative, and acidifies the contents of the gut in order to reduce the absorption of ammonia
  • Creatine levels – check kidney function
  • Diuretics – clear the fluid in the ascites
33
Q

what is the effect of cirrhosis on the cardiovascular system

A
  • Deficiency of blood coagulation factors and thrombocyotpenai – can cause slow wound healing, bleeding, bruising and haemorrhage
  • High INR – decreased synthesis of plasam proteins
    Portal hypertension
    Mechanism
    • Hepatic portal vain = splenic + SMA veins
    • Normal pressure of 5-10 mmHg.
    • When pressure rises above 14 mmHg = collaterals develop
  • between portal and systemic circulations.
    • Primarily at oesophagus, stomach, rectum, left renal vein, lumbar veins etc…

Results of Portal Hypertension
• Hyper dynamic circulatory stage.
• Production of ascites.
-  Raised capillary hydrostatic pressure.
• Neurohormonal responses
-  Activation of RAAS and sympathetic system (lower preload).
• Release of vasopressin
• Therefore = renal water and sodium retention.

34
Q

what is the effect of cirrhosis on the renal system

A
  • Heptorenal syndrome if you have cirrhsosi – can be reversed using a liver transplant
  • It is the development of renal failure in patients with advance liver failure
  • Increases the activity of the RAAS and sympathetic system
35
Q

what is the effect of cirrhosis on the metabolic state

A
  • Blood glucose is low – liver cannot store glycogen or undergo glycogenolysis or glycogenosis so blood homeostasis is impaired
  • Ketones are high
  • Fats are the main energy source
36
Q

what are the 3 histological features of cirrhosis

A

Loss of normal hepatic architecture

Bridging fibrosis

Nodular regeneration

37
Q

What are the casues of the patients cirrhosis

A
  • chronic alcohol abuse

- HCV

38
Q

What are the 3 steps of alcoholic liver disease

A 
Hepatic steatosis (fatty)
- Metabolised by acetaldehyde, various steps process generates NADH, increase NADH/NAD ratio, induces fatty acid synthesis and reduced FA oxidation. Form triglycerides= fatty.

Alcoholic hepatitis

  • Infiltration - polymorphonuclear leucocytes. Hepatocyte necrosis
  • Dense cytoplasmic inclusions (Mallory bodies), damaged cells

Cirrhosis

39
Q

How do you test for HCV

A
  1. Blood tests- antibodies to HCV (immunoassay,
    immunoblot verifies it). Confirmatory test to
    determine viral load (HCV RNA polymerase chain
    reaction). If no RNA and immunoblot positive=
    previous infection but cleared. If immunoblot
    negative means immunoassay was wrong.

Biopsy

Screening

LFTs – deranged in cirrhosis

40
Q

what are the complications of cirrhosis

A

Hepatic failure:

Coagulopathy (decrease in factors 2,7,9,10=
increase in INR)

Encephalopathy- ie liver flap (asterixis) and
confusion/coma

Hypoalbuminaemia (oedema, leuconychia)

Sepsis (pneumonia; septicaemia)

Spontaneous bacterial peritonitis

Hypoglycaemia

41
Q

what is the difference between compensated and decompensated

A

Compensated cirrhosis means that the liver is
heavily scarred but can still perform many
important bodily functions BUT disease progression
is not linear

Decompensated cirrhosis means that the liver is
extensively scarred and unable to function
properly- Hepatomegaly, jaundice, pruritus, ascites,
GI bleeding, confusion etc

42
Q

what is the sign of paraumbilical porto caval anatomose

A

caput medusae

43
Q

How do you treat spontaenous bacterail peritonitis

A
  • IV antibotics

- it is a gram rod

44
Q

What is hepatorenal syndrome

A

Life-threatening medical condition that consists
of rapid deterioration in kidney function in
individuals with cirrhosis or fulminant liver failure.

Reduced creatinine clearance

Altered liver function, abnormalities in circulation,
and kidney failure

45
Q

What are the types of hepatorenal syndrome

A

Type 1- Quick

Type 2 HRS is slower in onset and progression

46
Q

What are the triggers of hepatorenal syndrome

A

Bacterial infection- SBP,

acute alcoholic hepatitis

Bleeding in the upper gastrointestinal tract.

Metabolism 2 PBL (9 decks)

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