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Week 19: Jaundice > General Jaundice > Flashcards

General Jaundice Flashcards

1
Q

A) What is gastritis?
B) Causes?
C) What are its clinical presentations?
D) What would you prescribe to someone with gastritis?

A

A) Inflammation of the lining of the stomach
B) Helicobacter pylori bacterial infection, alcohol, stress
C) Indigestion, burning stomach pain, nausea and vomiting
D) Proton pump inhibitor (Omeprazole)

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2
Q

Define jaundice.

A

A clinical sign due to the accumulation of bilirubin in the blood, and the deposition in the skin, sclera and the mucous membranes leading to yellowing of the skin

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3
Q

Name three causes of pre-hepatic jaundice.

A
  • Haemolytic anaemia
  • Haemolytic drugs (e.g NSAIDs)
  • Blood transfusion (blood transfusion reaction if the type is not right)
  • Sickle cell crisis
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4
Q

Name three causes of hepatic jaundice.

A
  • Hepatitis
  • Hepatocellular Carcinoma
  • Cirrhosis
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5
Q

Name three causes of post-hepatic jaundice.

A
  • CBD Stones (common bile duct stones)
  • Carcinoma of the head of the pancreas
  • Sclerosing cholangitis (Inflammation of the bile ducts inside and outside the liver leading to fibrosis and narrowing)
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6
Q

A patient presents with symptoms that indicate blockage of the bile ducts. An ultrasound is requested which shows some bile duct dilatation and a stone in the duct. To confirm the diagnosis, which of the following should be requested and why:

A) MRCP or ERCP?
B) What are the possible complications of an ERCP?

A

A) MRCP (should be used to confirm the diagnosis as it gives an accurate idea of the anatomical position of the stones)

Because ERCP is an invasive procedure

B) Bleeding, pancreatitis, perforation, infection

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7
Q

What are the possible complications of an ECRP?

A
  • Bleeding
  • Perforation
  • Pancreatitis
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8
Q

Define Digestion.

A

Breakdown of molecules into absorbable molecules

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9
Q

Define absorption.

A

Movement of nutrients, water, and electrolytes from the gut lumen to the internal environment

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10
Q

Describe how the structure of the small intestine allows for efficient absorption.

A

The lumen arranged in the circular folds of keckring –> Villi projects from folds –> surface of villi = enterocytes + goblet cells –> surface of epithelial cells has microvilli brush border = large surface area for absorption

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11
Q

What is the most vital part of the GI in terms of digestion and absorption?

A

Small Intestine

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12
Q

State the constituents of the following product of carbohydrate breakdown:

A) Lactose
B) Sucrose
C) Maltose

A

A) Galactose + Glucose (lactose is broken down by lactase)
B) Glucose + Fructose (Sucrose is broken down by sucrase)
C) Glucose + Glucose (Maltose is broken down by maltase)

So remember: products of carbohydrate digestions is glucose, fructose, and galactose

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13
Q

What enzymes break down carbohydrates?

A

Salivary amylase and pancreatic amylases

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14
Q

When carbohydrates are broken down they produce these smaller constituents called a-limit dextrin (two disaccharides linked together) which is broken down by which enzyme?

A

Isomaltase

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15
Q

What is the mechanism of absorption of glucose, galactose and fructose into capillaries?

A
  • Glucose + Galactose: Na+-Dependent Co-Transport

- Fructose: Facilitated Diffusion

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16
Q

In summary, describe protein digestion and absorption.

A
  • Protein break down products: amino acids, dipeptides, and tripeptides
  • Absorbed in the small intestine
  • Aminoacids are absorbed through Na+ dependent cotransport
  • Dipeptides through H+-Dipeptide dependent cotransport
  • Tripeptides = through H+-tripeptide dependent co-transport
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17
Q

In summary, describe lipids digestion and absorption.

A
  • Lipid breakdown products: fatty acids, monoglycerides, cholesterol
  • Absorption in the small intestine
  • Bile salts attach to lipid molecules –> pancreatic lipases and colipase breakdown fats into monoglycerides and fatty acids stored in micelles –> monoglycerides and fatty acids move out of the micelles and enter cells by diffusion + cholesterol from the molecules is transported in by a membrane transporter –> re-esterification of fats into triglycerides + cholesterol –> absorbed fat + cholesterol + protein = chylomicron –> chylomicrons are released into the lymphatic system
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18
Q

Why are bile salts important in lipid break down and absorption?

A
  • Lipids are hydrophobic (not soluble in water)

- Hence solubilisation is important

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19
Q

What are the three main enzymes involved in lipids digestion?

A

Lipases, phospholipases, and esterases (pancreatic enzymes)

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20
Q

Which vitamin is required for the absorption of calcium?

A

Vitamin D

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21
Q

The intrinsic factor is required for the absorption of which vitamin?

A

Vitamin B12

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22
Q

State 4 functions of the liver.

A
  • Metabolism of proteins, fats, and carbohydrates
  • Storage of iron
  • Storage of B12
  • Synthesis and secretion of bile
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23
Q

Describe the clinical signs of pre-hepatic jaundice.

A
  • Raised unconjugated bilirubin
  • Normal colour/brown stool
  • Normal colour urine
  • Normal/increased urobilinogen (remember conjugated bilirubin gets to the duodenum and gets transformed into urobilinogen some of getting reabsorbed into the blood, increased in Unconjugated bilirubin means an increase in conjugated bilirubin as more is made and hence more gets to the duodenum and gets transformed into urobilinogen)
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24
Q

Describe the clinical signs of hepatic jaundice

A
  • Raised both unconjugated and conjugated bilirubin
  • Slightly pale/normal colour stool (when the hepatocytes die or are damaged a lot of the conjugated bilirubin goes back into the bloodstream rather than to the intestine where it usually gets transformed into stercobilin which gives stool its colour)
  • Dark urine (this is because of the water-soluble conjugated bilirubin that goes back into the bloodstream and gets into the urine)
  • Decreased urobilinogen
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25
Q

Describe the clinical signs of post-hepatic jaundice

A
  • Raised conjugated bilirubin
  • Pale stool
  • Dark urine (all conjugated bilirubin that cant get to the duodenum diffuses back into the blood and gets excreted in the urine)
  • Decreased/negative urobilinogen
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26
Q

A) What is cirrhosis?
B) Describe Pathophysiology of cirrhosis.
C) What are the causes of cirrhosis?
D) How does cirrhosis lead to oesophageal varices?

A

A) An irreversible chronic disease of the liver marked by degeneration of cells, inflammation and fibrous thickening due to fibrosis
B)Defenestration and capillarization of
liver sinusoidal epithelial cells -> Repeated cycles of apoptosis and regeneration of hepatocytes -> characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules
C) Hep B and C, Alcoholism, NAFLD
D) Cirrhosis = scarring –> increased portal hypertension due to increased resistance by fibrous tissue –> pressure builds up back up the venous system

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27
Q

Why might someone with alcoholic liver disease:

A) have bruises?
B) develop a fatty liver?

A

A) damaged liver will damage the liver’s ability to synthesise clotting factors
B) damaged liver cells mean they cannot metabolise fat anymore and hence it will build up.

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28
Q

A) Describe the features of HIV.
B) Describe the mode of transmission.
C) Describe the main clinical symptoms.

A

A) RNA Genome, retrovirus which uses reverse transcriptase to make DNA copy from viral RNA (it inserts itself into host cell DNA)
B) Via blood/blood products or contaminated needles + sexually + perinatally during delivery or ingestion of milk
C) Depending on stage: Acute stage (flu-like symptom such as muscles pain, rash, headache, swollen glands) –> Chronic Stage (no symptoms) –> AIDs (untreated chronic HIV becomes AIDs (serious danger of infections and cancers due to a low number of CD4+ cells))

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29
Q

How would you diagnose HIV?

A
  • ELISA: specific antibodies

- NAAT: measures viral load

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30
Q

Describe the pharmacological treatment of HIV.

A

Anti-retroviral therapy

(A combination of:
- NRTI’s (nucleoside reverse transcriptase) or NNRTI’s (non-nucleoside reverse transcriptase) or protease inhibitors)

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31
Q

Describe prevention methods of HIV.

A
  • Screening of blood products
  • Needle Exchange programmes
  • Anti-retroviral prophylaxis for post-exposure (e.g needle stick injuries)
  • Avoiding high risk partners
32
Q

Describe the following regarding Hepatitis B.

A) Features of the virus
B) Mode of transmission
C) Stages of Hep B
D) Treatment of Hep B

A

A) Hepadnavirus, double-stranded DNA genome, enveloped
B) Blood products/transfusions, IVDU, tattoos and piercings, bodily fluids in sexual intercourse
C) 6 months incubation –> Acute hepatitis –> either self-limiting or becomes chronic
D) Pegylated Interferon (suppresses viral replication) and Anti-viral medication (Oral Lamivudine - for low liver function)

33
Q

A) State methods of diagnosis of Hepatitis.

B) State methods of prevention of Hepatitis.

A

A) Serologic testing for antibodies, LFT, and liver biopsy to assess damage
B) HBsAg vaccine (3 injections over 6 months), Blood screening, Needle exchange programme, sexual health education

34
Q

Describe the following regarding Hep C:

A) Features
B) Transmission
C) Prevention

A

A) Flavivirus, single-stranded genome, enveloped, primarily replicates in hepatocytes
B) Blood products/transfusions, IVDU, tattoos and piercings, bodily fluids in sexual intercourse
C) NAAT screening on all blood samples for transfusion, needle exchange, and sex ed

35
Q

What is the cause of malaria and how is it transmitted?

A
  • Plasmodium (genus) parasite

- Transmitted by female Anopheles mosquitos which inject sporoza into the bloodstream - hence it is a zoonotic disease

36
Q 
A) What are the clinical features of Malaria?
B) What are the stages of malaria?
C) How do you diagnose malaria?
D) Treatment of malaria?
E) Methods of Prevention of malaria?
A

A) Fever, Flu-Like symptoms (headache, muscle pains), vomiting, diarrhoea, fatigue
B) Symptoms appear 7-18 days after infection
C) Blood testing by a Minimum of 3 blood films at three different times
D) Chemotherapy kills blood stages of malaria (as it later can spread to cerebellum and liver), but combination therapy is the norm and hospital admission in the risk of deterioration
E) sleep under bed nets, cover exposed skin between dusk and dawn, use mosquito repellent

37
Q

State factors that affect oral absorption of a drug.

A
  • Particle size and formulation
  • GI Motility ( in general foods tend to slow down the rate of gastric emptying, hence better absorption?)
  • First-pass metabolism (First pass metabolism by the gut wall or hepatic enzymes)
  • Physiochemical factors (e.g environment pH)
38
Q

What are an advantage and a disadvantage of intranasal administration?

A

Advantage: Avoids hepatic first pass metabolism
Disadvantage: limited drugs are suitable, and irritants cannot work

39
Q

Name factors that affect the distribution of drugs.

A
  • Cardiac output and blood flow
  • Lipid solubility
  • Degree of drug ionisation
  • pH of compartments
  • Capillary permeability
40
Q

Name complications of IV Drug administration.

A
  • Infection/Sepsis
  • Extravasation/infiltration
  • Anaphylaxis
  • Psychosocial effects (phobia)
  • Overdose
41
Q

Describe how portal hypertension occurs.

A 
- Increase in intrahepatic vascular
resistance due to massive structural
changes associated with fibrosis and
the increased vascular tone in the hepatic
microcirculation
-  blocking of blood through the liver occurs
and blood bypasses back towards
oesophagus and gastric vein, splenic
vein
- Eventually leading to oesophageal
varices, ascites, splenomegaly,
haemorrhoids
 (in severe cases hepatic encephalopathy
because ammonia is not broken down
in liver)
42
Q

What are the key diagnostic findings of

cirrhosis?

A 
Presence of risk factors: alcohol
misuse, IV drug use, obesity,
unprotected sex, obesity, blood
transfusion
 Abdominal distention (decompensated
cirrhosis 2ndary to ascites in portal HTN
and hepatomegaly)
Jaundice
 Jaundice and pruritus (decompensated
cirrhosis 2ndary to reduced hepatic
excretion of conjugated bilirubin into
the biliary tree)
 Coffee-ground vomitus and black stool
(melaena)
 Leukonychia, palmar erythema, spider
angiomata
 Abdo features: collateral circulation,
hepatosplenomegaly
43
Q

What are the key diagnostic findings of

cirrhosis?

A 
Presence of risk factors: alcohol
misuse, IV drug use, obesity,
unprotected sex, obesity, blood
transfusion
 Abdominal distention (decompensated
cirrhosis 2ndary to ascites in portal HTN
and hepatomegaly)
Jaundice
 Jaundice and pruritus (decompensated
cirrhosis 2ndary to reduced hepatic
excretion of conjugated bilirubin into
the biliary tree)
 Coffee-ground vomitus and black stool
(melaena)
 Leukonychia, palmar erythema, spider
angiomata
 Abdo features: collateral circulation,
hepatosplenomegaly
44
Q

What are the symptoms of Hepatitis?

A
  • Fever
  • Malaise
  • Anorexia
  • Nausea
45
Q

Why is it good to take some drugs with food?

A

Slows gastric emptying –> better absorption

46
Q

The liver is the major organ of enzymic
biotransformation/ metabolism. Name some
other sites of metabolism

A
  • gut lumen
  • gut wall
  • plasma
  • lungs
  • kidneys
  • nerves
47
Q

How do inhalation drugs exert local effects?

A 
Modified structure (ipratropium)
 Particle size (salbutamol)
 Selectivity for receptors (salbutamol)
 Rapid breakdown in plasma
(fluticasone)
48
Q 
Which of the following methods of IV
administration has the highest risk of
hypersensitivity?
a) Bolus injection
b) continuous infusion
c) intermitted infusion
A

a) bolus injection

  • rapid response required
  • incompatibilities
  • unstable drug
49
Q

You prescribe dobutamine to a pt with severe
heart failure to increase the force and rate of
the heart. The drug itself is unstable with a
half-life of only 2 minutes. What method of
administration would you give this drug?

A

Continuous IV infusion
*because it is unstable you would expect to
give via intermittent infusion. However, the
half-life indicates that the drug needs to be
given continuously - but usualy unstable drugs are given by intermitten infusion but they need a long half-life

50
Q

In phase I of metabolism, certain mechanisms are used in the liver for functionalisation (revealing a functional group) in order to increase polarity making more reactive product and facilitate excretion in urine. List three of these mechanisms.

A
  • Oxidation (cytochrome P450, alcohol dehydrogenase, xanthine oxidase)
  • Reduction (ketone reductions, anaerobic cytochrome P450 metabolism)
  • Hydrolysis (ester hydrolysis e.g. cholinesterase, amide hydrolysis) resulting in a more water-soluble metabolite
51
Q

A) What is metabolism phase II?

B) Give an example of Phase II.

A

A) It is conjugation reaction = Increases the drug’s polarity and turns it into a detoxified, water-soluble easily secreted product for excretion in bile or urine

B) Glucuronidation (-OH, -COOH, -NH2)

52
Q

Which drugs are more easily eliminated, hydrophilic or lipophilic during the excretion stage of?

A
  • Hydrophilic drugs are eliminated more readily than hydrophobic
53
Q

A) State three methods of excretion of drugs in the body.

B) Which organ is the most important in the excretion of drugs in the body?

A

A) Urine (major method), breath, faeces (perspiration etc…)
B) Kidneys

54
Q

What enzyme is involved in the metabolism of MOST drugs?

A

Cytochrome P450

55
Q

A) Describe Enterohepatic conjugation.

B) How does this affect the dose of a drug that is required for an effect?

A

A) The drug in intestine –> enters blood –> conjugated in the liver in metabolism –> it is conjugate in bile –> conjugate back in intestine –> hydrolysis of conjugation can occur which means the drug is reabsorbed and less is excreted and it goes through the cycle again
B) The drug will stay in circulation longer than anticipated however at the same time if this is taken into account, but another drug kills the bacteria which usually hydrolyses the other drug, then the other drug will be in circulation less than expected and so will be less effective (e.g oral contraceptives and antibiotics where antibiotics stop this circulation)

56
Q

During the metabolism of a drug, there is a potential for competition and saturation. Explain Why?

A 
- Drugs and endogenous compounds for
same enzyme
- Different enzymes for the same substrate
- Enzyme can be saturated, conjugate
depleted
57
Q

How would a high albumin concentration affect the distribution of a drug?

A

Reduced distribution (protein-binding affects distribution, a lipid soluble drug binds non-specifically)

58
Q

A) How would an intra-hepatic cause of jaundice present itself in an LFT?
B) How would you differentiate alcoholic hepatitis from other hepatic causes?

A

A) Raised ALT and AST - enzymes found in hepatocytes which are released into the blood when hepatocellular damage occurs (Rather than ALP, which is found in bile duct cells)

B) ALT and AST never raised above 500 and 300 respectively in alcoholic hepatitis, while they raise into the 1000s for other hepatic causes such paracetamol toxicity

59
Q

A) How would an intra-hepatic cause of jaundice present itself in an LFT?
B) How would you differentiate alcoholic hepatitis from other hepatic causes?

(Unsure whether this stuff would come up!)

A

A) Raised ALT and AST - enzymes found in hepatocytes which are released into the blood when hepatocellular damage occurs (Rather than ALP, which is found in bile duct cells)

B) ALT and AST never raised above 500 and 300 respectively in alcoholic hepatitis, while they raise into the 1000s for other hepatic causes such paracetamol toxicity

60
Q

What is the most common cause of acute hepatic failure?

A

Paracetamol toxicity

61
Q

What is the most common cause of acute hepatitis?

A

Hepatitis A Virus (followed by B)

62
Q

How would you recognise an obstructive cause of jaundice from LFT results?

A

Raised ALP and GGT (BUT GGT is actually mostly raised in alcoholic hepatitis, check if they have a history of alcoholism if GGT is raised before deciding it is obstructive)

63
Q

Reduced ALBUMIN levels in the blood, and raised Prothrombin Time would indicate which kind of liver disease, chronic or acute?

A

Chronic as the liver has reduced synthetic function

64
Q

Name 5 risk factors for developing gallstones disease.

A
  • Overweight or obesity
  • Older Age
  • Sedentary lifestyle
  • Female
  • Rapid weight loss
65
Q

List the stages of liver damage starting with inflammation/

A

Hepatitis (Inflammation) –> Fibrosis –> Cirrhosis –> Hepatocarcinoma

66
Q

State 3 pieces of advice you would give to someone with liver disease/or to reduce the risk of NAFLD.

A
  • Change to a Mediterranean diet
  • 150/200mins of moderate exercise per week
  • Calorie restriction (aim to lose 7% of body weight )
67
Q

List three deficiencies common in alcoholic liver disease/

A
  • Thiamine
  • B12
  • Folate
68
Q

Which of the following is most likely to occur in
a liver disease patient with malnutrition?
a) sarcopenia
b) pyrexia
c) dyspnoea
d) arthralgia

A

a) sarcopenia

-preferential use of lipids as fuels (fat loss) and
decreased protein synthesis (muscle atrophy)
in heavy drinkers

69
Q 
Ursodeoxycholic acid (UDCA) can be used to
minimalize the risk of what?
A

Gall stones due to rapid w.loss e.g.

after bariatric surgery

70
Q 
Describe the clinical presentations of the following:
A) Cholelithiasis 
B) Biliary Colic
C) Cholecystitis 
D) Cholangitis
A

A) no pain or problems (Gallstones in the gallbladder chilling)
B) Occurs after a meal, lasts <6hrs, epigastric/RUQ pain radiates to the scapula/shoulder, nausea + vomiting, usually after consuming fat, stops suddenly (the stone goes into the cystic duct and back upon contraction)
C) RUQ pain/epigastric >6 radiates to shoulder, Fever, RUQ tenderness (Murphy’s sign!), tachycardia, + may have raised WBC, T, CRP etc… (Stone goes into cystic ducts and gets stuck -> inflammation of the gallbladder)
D) Positive Charcot’s triad (RUQ pain and tenderness, obstructive jaundice, fever +/- rigours), Reynold’s Pentad (Charcot’s triad + hypoperfusion and loss of consciousness) you will get some amylase as pancreas affected too, medical emergency, the person will be very ill (Inflammation of the whole biliary tree)

71
Q

What is the relevance of depression in jaundice?

A

Paracetamol overdose (Most common cause of acute hepatitis)

72
Q

Jaundice, no pain, and weight loss. Likely cause?

A

Tumour

73
Q

What is the usual management of suspected obstructive jaundice?

A
  • Blood Tests
  • USS (followed by CT or MRCP)
  • ERCP (if confirmed for removal)
74
Q

Describe the management of a patient presenting with a charcots triad.

A
  • Medical Emergency
  • IV Fluids
  • IV Antibiotics
  • ERCP for biliary decompression once well enough
75
Q

A patient comes in with acute epigastric pain
that is persistent and spreads to the right
shoulder. They complain of recent vomiting and
on examination, you notice they are pyrexia and
tender on palpation.
1. What is the likely diagnosis?
2. What differentiates this diagnosis from
biliary colic?
3. How would the chronic condition
differ?
4. Would the patient have jaundice?

A 
Acute cholecystitis
 Inflammatory component (local
peritonism, fever, prob increase in
WCC)
 In chronic cholecystitis there is chronic
inflammation +/- colic. Flatulent
dyspepsia: vague abdominal
discomfort, distention, nausea,
flatulence and fat intolerance
 Mild jaundice MAY occur for someone with cholecystitis, but it will definitely occur if the stone moves to the CBD then you have obstructive jaundice
76
Q

Management of biliary colic?

A
  • Analgesia
  • Low-fat diet
  • weight loss

Week 19: Jaundice (1 decks)

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