MET EOYS1 Flashcards
Explain why a patient with cholestatic problem would have pale stools [1] and dark urine [1]
Pale stools: no bilirubin reaches the gastrointestinal tract
Dark urine: reflux of conjugated bilirubin into blood which is excreted in the urine
Paul is a 47-year-old with a long history of alcohol abuse.
Which of the following LFT results would be most likely?
Very high AST, high ALT, high GGT
Very high AST, high ALT, low GGT
High AST, very high ALT, high GGT
Low AST, high ALT, high GGT
High AST, very high ALT, low GGT
Paul is a 47-year-old with a long history of alcohol abuse.
Which of the following LFT results would be most likely?
Very high AST, high ALT, high GGT
The typical LFT pattern in alcoholic liver disease is high AST and ALT (with AST typically twice as high as ALT).
In the context of acute liver damage, ALT and AST are also raised, however, ALT tends to be significantly higher than AST.
A 43-year-old lady attends A&E at 8pm with right upper quadrant (RUQ) pain, nausea and vomiting. On examination, you note she has a BMI of 33kg/m2, yellowing of the sclera and she states the pain is worse after eating.
Given the likely diagnosis, what pattern would you expect to see on her blood tests?
High unconjugated bilirubin, low conjugated bilirubin, low haemoglobin
Normal unconjugated bilirubin, high conjugated bilirubin, normal haemoglobin
High unconjugated bilirubin, high conjugated bilirubin, normal haemoglobin
Low unconjugated bilirubin, low conjugated bilirubin, low haemoglobin
Normal unconjugated bilirubin, high conjugated bilirubin, low haemoglobin
A 43-year-old lady attends A&E at 8pm with right upper quadrant (RUQ) pain, nausea and vomiting. On examination, you note she has a BMI of 33kg/m2, yellowing of the sclera and she states the pain is worse after eating.
Given the likely diagnosis, what pattern would you expect to see on her blood tests?
High unconjugated bilirubin, low conjugated bilirubin, low haemoglobin
Normal unconjugated bilirubin, high conjugated bilirubin, normal haemoglobin
Gallstones are most common in middle-aged women and are associated with an increased BMI.
They typically cause pain after eating a fatty meal. Large gallstones may become stuck in the common bile duct and block the flow of bile. This can cause post-hepatic jaundice as conjugated bilirubin from the liver is not excreted and the concentration increase in the blood. Unconjugated bilirubin is usually at a normal level as the hepatocytes are not damaged. Low haemoglobin in the context of jaundice is an indicator of a pre-hepatic cause, such as haemolytic anaemia. The most likely pattern of blood results for this patient is, therefore, normal unconjugated bilirubin, high conjugated bilirubin and normal haemoglobin.
The following LFT results indicate a problem in which area of the body?
Normal ALT
Normal AST
High ALP
Normal GGT
Hepatocytes
Blood
Biliary tree
Bones
Intestines
Bones
An isolated raised ALP is suggestive of extrahepatic disease. The osteoblastic activity can cause raised ALP: recent fracture, bone cancer or metastasis, vitamin D deficiency. Therefore, bones would be the best answer here.
If there was a problem with the hepatocytes, LFTs would demonstrate a very raised AST/ALT.
A raised GGT in addition to the raised ALP would indicate a problem in the biliary tree.
Whilst a problem in the intestines could lead to a blockage of the bile duct and deranged LFTs, this answer is less likely here.
The following LFT results indicate a problem in which area of the body?
Normal ALT
Normal AST
High ALP
Raised GGT
Hepatocytes
Blood
Biliary tree
Bones
Intestines
The following LFT results indicate a problem in which area of the body?
Normal ALT
Normal AST
High ALP
Raised GGT
Hepatocytes
Blood
Biliary tree
Bones
Intestines
Excess aldosterone would lead to
Metabolic acidosis
Metabolic alkalosis
Resp. acidosis
Resp. alkaloisis
Metabolic alkalosis
The physiologic increase in aldosterone secretion contributes to the development of metabolic alkalosis as salt retention by the kidneys is linked to increased bicarbonate reabsorption and acid excretion
The level of the ratio of AST:ALT can be helpful: in diagonsis:
A ratio of AST: ALT >2 suggests which pathology? [1]
A a ratio of AST: ALT <1 suggests which pathology? [1]
A ratio of AST: ALT >2 suggests alcoholic liver disease
A a ratio of AST: ALT <1 suggests non-alcoholic liver disease
Chronic liver diesease would present with which of the following?
AST > ALT
ALT > AST
ALT = AST
Raised ALP
Chronic liver diesease would present with which of the following?
AST > ALT
ALT > AST
ALT = AST
Raised ALP
Chronic alcohol abuse would present with which of the following?
AST > ALT
ALT > AST
ALT = AST
Raised ALP
Chronic alcohol abuse would present with which of the following?
AST > ALT - 2:1
ALT > AST
ALT = AST
Raised ALP
An ALT/AST 10-50 x greater than normal would indicate
Alcoholic hepatitis
Acute obstructive
Acute viral
Toxic
Ischaemic
An ALT/AST 10-50 x greater than normal would indicate
Alcoholic hepatitis
Acute obstructive
Acute viral
Toxic
Ischaemic
An ALT/AST 10x greater than normal would indicate
Alcoholic hepatitis
Acute obstructive
Acute viral
Toxic
Ischaemic
An ALT/AST 10x greater than normal would indicate
Alcoholic hepatitis
Acute obstructive
Acute viral
Toxic
Ischaemic
A patient presents with damage to their liver. What score of Child-Pugh would indicate that their liver is decompensated?
> 5
6
7
8
9
A patient presents with damage to their liver. What score of Child-Pugh would indicate that their liver is decompensated?
> 5
6
> 7
8
9
Metabolic alkalosis is usually accompanied by [hypokalemia / hyperkalemia]
Metabolic alkalosis is usually accompanied by hypokalemia
How does liver disease progress? (is similar for no. of pathologies)
- Primary Injury: liver cells are damaged.
2.This causes inflammation
- This causes liver cell injury / death from primary injury or inflam. response
- Fibrosis occurs if cell death is too advanced / regen capacity is exhausted / process has been to extensive: causes pathological scar tissue (fibrosis).
- Eventually fibrotic nodules are formed: this is when we classify as cirrhosis
- A liver can function normally with cirrhosis (& be asymptomatic) but can lead to liver failure or cancer
Symptoms of liver disease?
Systemic [2]
Cholestatic? [2]
None
Systemic:
* Weight loss
* Tiredness
Cholestatic (reduction in bile flow)
* Pruritis (itchy skin; Cholestatic liver disease increases levels of bile salt which accumulate under the skin causing itch)
* Pale stools/dark urine
Complications of underlying disease
Signs of Chronic Liver Disease? [5]
Palmar erythema
Spider naevi
(most specific)
Hair loss
Gynaecomastia (man boobs)
Leuchonychia / Clubbing
Proximal wasting
Scratch marks
Xanthelasma
Indicators of liver status:
Which blood tests would be useful to indicate liver function? [2]
Which blood tests would be useful to indicate stage of liver disease? [2]
Which blood tests would be useful to indicate liver function? [2]
* Albumin
* INR (Prothrombin Time)
Which blood tests would be useful to indicate stage of liver disease? [2]
* Platelet count (as spleen enlarges, can have consumption of platelets)
* ALT/AST
What would be indicated if ALT / AST is raised? [1]
Elevated ALT / AST indicates source is hepatic problem
What would be indicated if Alk Phos AND γGT/ GGT is raised? [1]
Elevated Alk Phos / γGT indicates cholestatic problem
What could be ruled out of causing ALT > 500?
What would ALT of 500-100 indicate is the source?
What would ALT of 1500+ indicate?
ALT:
Alcohol doesn’t put ALT > 500
500 – 1500: autoimmune hepatitis
more than 1500: hepatitis viruses / drugs / ischaemia
First Imaging used for liver disease? [1]
What are alternatives? [4]
Ultrasound:
* Biliary tree
* Liver lesions
* Ascites
* Spleen
* Veins
* Other pathology
CT
MRI
ERCP / MRCP
Explain how portal hypertension causes ascites
Liver malfunction:
* Liver breaks down vasodilatory peptides (if not working, then doesn’t)
* Cirrhosis reduces ease of blood flow
* If liver is also not producing albumin, decreases oncotic pressure and pushes liquid out
Causes splachnic vasodilation
Causes reduction in circulating volume in portal system.
(sensed by the kidney (by JGA))
Activates renin system: causes activation of RAAS. Leads to salt and water reab. at kidney
Leads to ASCITES
How can you treat variceal bleeding [4]
What can you give as primary and secondary prophylaxis for variceal bleeding? [2]
Treatment:
Resuscitation
Terlipressin (inhibits portal hypertension with simultaneous reduction of blood circulation in portal vessels) and Antibiotics
Banding or injection sclerotherapy
TIPSS
Primary + secondary prophylaxis beta blockers
Propranolol / Carvedilol
Banding
How is ammonia produced in health? What happens after this?
NH3 is produced when glutamine converted to glutamate
In health: NH3 is converted to urea & excreted in kidney OR in reverse of reaction, back to glutamine
How can you stop the production of NH3 to treat encephalopathy? [2]
Rifaximin: reduces the production of NH3 in the gut
L-Ornithine L-arginine: stops the conversion of glutamate to glutamine
What scoring system do you use to assess if have decompensated liver? [1]
What score would classify a decompensated liver? [1]
Child-Pugh score:
over 7 points: decompensated
Explain how insulin resistance causes a higher risk of developing fatty liver disease [3]
Insulin Resistance causes high risk of developing fatty liver disease.
Patient resistant: have high levels of circulating glucose: causes de novo lipogenesis in liver cells
Also causes inappropriate gluconeogenesis, impaired glycogen synthesis AND decreases the suppression of lipids in the liver
Overall: causes more glycerol, long chain fatty acids that make way to liver and hepatic fats accumulate. Also get impaired clearance of via VLDL formation
Which three process due to fat accumulating in the liver causes the progression to fatty liver disease? [3]
Oxidative Stress (lioptoxicity)
Inflammation
Innate immune activation
Which pathology is commonly associated with ALD? [1]
What does this pose a risk or when re-feeding? [2]
Nutritional deficiency
* Poor oral intake and ‘empty calories’
* Possible re-feeding risk
* Thiamine and vitamin deficiencies
What effect does low pH on the body if it is out of control acutely? [4]
Acutely:
* Negatively inotropic
* ‘Air hunger’: panting away
* Part of critical illness syndrome – generalised cellular dysfunction
* Affects body K+ distribution (net shift of K+ from the intracellular to the extracellular space)
What happens when low pH is out of control chronically? [3]
- Effect of bones and stone formation
- Associated with progression of kidney disease
- Paradoxical relationship with mortality
What is Henderson-Hasselbach equation in the body for pH blood plasma? [1]
Which imaging modality is normally used first for assessing liver disease?
CT
Ultrasound
MRI
ERCP / MRCP
Which imaging modality is normally used first for assessing liver disease?
CT
Ultrasound
MRI
ERCP / MRCP
How does infusing a Ptx with acid effect the Ptx? [1]
Causes decrease of serum bicarbonate. Drives equation to left: causes increase in PCO2: blow off the acid as CO2 because now hyperventilation
Hyperventilation causes acid / alkolosis?
Hypoventilation causes acid / alkolosis?
Hyperventilation causes alkolosis: expelling more CO2
Hypoventilation causes acidosis
How can you cause metabolic acodosis? [4]
Adding Acid to your body:
- Ingestion of acid (Aspirin)
- Generation of acid (lactic acid, ketones)
- Retention of acid (renal failure)
Loss of bicarbonate:
- Gut – eg diarrhoea, Kidneys - RTA
What is hyperchloremic metabolic acidosis?
What is the most common cause? [1]
More rare cause? [1]
Normal anion gap acidosis is an acidosis that is not accompanied by an abnormally increased anion gap.
Caused by loss of HCO3- WITH a compensatory rise in Chlorine
Most common cause: diarrhoea
Also caused by: renal tubular acidosis
What is metabolic alkalosis caused by? [4]
Occurs mostly due loss of chloride: so get HCO3- rise:
- Chloride (HCl) – in vomiting/NG aspiration
- Chloride – through diuretic use
- Potassium – through the effect of aldosterone
- Ingestion of alkali
*
What is Normal anion gap acidosis aka? [1]
= hyperchloremic metabolic acidosis
What are the characteristics of compensated resp acidosis:
pH? [1]
pCO2? [1]
HCO3-? [1]
- Normal pH
- high pCO2
- compensatory high HCO3-
How does lactic acidosis / ketoacidosis commonly present with regards to:
- pH
- HCO3-
- CO2
Low pH, low HCO3-, often low CO2
What does lactic acidosis / ketoacidosis commonly present as? [3]
Low pH, low HCO3-, often low CO2
What happens to serum K+ levels in severe acidosis?
Go up (as exchange of H+ causes to go otherway)
What are normal anion gap, metabolic acidosis characterised by? [1]
Increased Chlorine levels / = ‘Hyperchloraemic metabolic acidosis’
Compensatory rise in chloride to maintain electrical neutrality
Hes losing bicarbonate
What would cause normal anion gap metabolic acidosis?
= ‘Hyperchloraemic metabolic acidosis’
Usually due to bicarbonate loss
* Kidneys: Renal tubular acidosis
* Gut: diarrhoea
Compensatory rise in chloride to maintain electrical neutrality
Why might HCO3- rise in Ptxs? [4]
As H+ is lost:
* Diarrhoea
* Diuretics
* Mineralocorticoid excess
* Vomiting/NG drainage
As H+ moves into cells: Hypokalaemia
The best liver function test is:
a. AST/ALT
b. Alkaline phosphatase
c. Bilirubin
d. INR
The best liver function test is:
a. AST/ALT
b. Alkaline phosphatase
c. Bilirubin
d. INR
Of the above, only the INR is a true liver function test as it examines the capacity of the liver to synthesize clotting factors. AST and ALT are enzymes that are elevated in hepatocellular injury. Alkaline phosphatase is an enzyme that is elevated in cholestatic injury. Bilirubin is a pigment secreted by the liver that is elevated with liver dysfunction but can also be elevated with bile obstruction (even though liver function is normal).
The following statements are all true, except:
a. Hepatic stellate cells produce bile
b. Bile formed in the liver is transported to the gut
c. Bile helps digest fat
d. Cholesterol forms a part of bile
The following statements are all true, except:
a. Hepatic stellate cells produce bile
b. Bile formed in the liver is transported to the gut
c. Bile helps digest fat
d. Cholesterol forms a part of bile
