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JMP Semester 2 > Week 20 > Flashcards

Week 20 Flashcards

1
Q

What are the functions of the liver?

A
  1. Metabolism- interconversion of carbohydrates, fats and proteins- storage of glycogen and Vitamin A.
    1. Drug processing- metabolism/detoxification/excretion
    2. Biosynthesis- bile, cholesterol, phospholipids
    3. Immune function- screening of intestinal blood with Kupffer cells.
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2
Q

How can the blood supply to the liver be described?

A

Dual

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3
Q

What are the arteries supplying the liver?

A

Left and Right hepatic

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4
Q

What does the blood from the digestive organs drain into and then go on to form?

A

Mesenteric veins –> merge into the portal vein –> travels to the liver

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5
Q

What is the functional units of the liver?

A

Hepatic lobule

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6
Q

What is the general structure of a hepatic lobule?

A

Hepatocytes occupy bulk, central vein

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7
Q

What is the portal triad?

A

The hepatic artery, hepatic vein and bile duct

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8
Q

Where is bile produced and how does it get to the gall bladder?

A

Produced by the hepatocytes, travels down the bile duct

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9
Q

What is the flow of blood from the digestive system to the heart?

A
  1. Portal vein
    1. Hepatic venules
    2. Filter past hepatocytes
    3. Drain to central vein
    4. Hepatic vein
    5. Inferior vena cava
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10
Q

What are the components of bile?

A
  1. Water (97%)
    1. Bile salts (0.7%)
    2. Bile acid
    3. Fats (0.51%) mostly cholesterol
    4. Bilirubin (0.2%)
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11
Q

How does bile get from the hepatocytes to the bile duct?

A

Collected into bile canaliculi

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12
Q

What is the main action of bile?

A

To emulsify fats which aids the function of pancreatic lipase

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13
Q

What are some excretions (waste elimination) in bile?

A

Steroid hormones
Calcium
Drugs/drug metabolites
Bilirubin

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14
Q

What is Bilirubin?

A

Bilirubin is converted Haem from dead erythrocytes.

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15
Q

What is the steps from dead erythrocytes to bilirubin excretion?

A
  1. Dead erythrocytes are taken from circulation via phagocytosis (including Kupffer cells in the liver)
    1. Iron and protein recycled, whereas haem is for elimination
    2. Haem converted to bilirubin
    3. Bilirubin is transported to the liver and conjugated
    4. Conjugated bilirubin is secreted in bile
    5. Bacteria in large intestine metabolise bilirubin to sterobilin (to give faeces its brown colour.
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16
Q

What is the function of the Gall Bladder?

A

Storage site for bile salts (60ml)

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17
Q

What regulates gall bladder contraction?

A

Cholecystokinin (CCK)

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18
Q

What is the Sphincter of Odi?

A

The major duodenal papilla (site at which bile and pancreatic secretions enter the duodenum)

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19
Q

What happens relating to the gall bladder during a non digestive period?

A
  1. Sphincter of Oddi is contracted

2. Bile flows from the liver to the gall bladder

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20
Q

What happens relating to the gall bladder during a non digestive period?

A
  1. Intestinal phase triggers release of CCK (cholecytokinin) and secretin
    1. Secretin stimulates the hepatic duct cells to release bicarbonate
    2. CCK triggers relaxation of the Sphincter of Oddi and contractions of the gall bladder
    3. Bile is released into the duodenum
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21
Q

How are bile salts recycled?

A

Transporters in the terminal ileum (end of small intestine) take up bile sales and transport them to the liver via the hepatic portal vein.

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22
Q

What percentage of bile salts are recycled?

A

95%

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23
Q

What does returned bile salts to the liver stimulate?

A

The liver to produce more bile salts

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24
Q

What is the importance of recycled of bile salts in drug pharmacokinetics?

A

Molecules bound to bile salts remain in the body for longer.

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25
Q

How is bile acids/salts reabsorbed in the small intestine?

A
  1. Uptake is mediated by the sodium-dependent bile salt transporter proteins (which are only in the ileum)
  2. 95% of bile salts absorbed here
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26
Q

How is bile salts absorbed in the large intestine?

A
  1. Not reabsorbed

2. Degraded by bacteria and eliminated

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27
Q

What is the consequence of too much bile acid/salt entering the large intestine?

A

Bile acid mediated diarrhoea

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28
Q

What can happen if insufficient bile is produced?

A

Steatorrhea (fatty faeces)

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29
Q

What is the location of the pancreas?

A

Posterior to the stomach - retroperitoneal

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30
Q

What is the two functional divisions of the pancreas?

A
  1. Endocrine

2. Exocrine

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31
Q

What are the endocrine and exocrine functions of the pancreas?

A
  1. Endocrine
    - produces insulin (Beta cells),
    -produces glucagon (alpha cells)
    - produces somatostatin (gamma cells)
    All are released into circulation.
  2. Exocrine
    - produces digestive zymogens (activate in the duodenum)
    - amylase, lipase, proteases etc
    All are released into the duodenum through the pancreatic duct (exits into duodenum via duodenal papilla)
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32
Q

What is the microscopic arrangements of exocrine cells?

A
  1. Arranged into acini (clusters)
    1. Pyramidal cells surround a central duct (eventually drains into pancreatic duct)
    2. Exocrine cells contain darker secretory granules
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33
Q

What is the microscopic arrangements of endocrine cells?

A
  1. Regions found throughout
    1. Make up “islets of Landgerhans”
    2. Mostly contain Beta cells (insulin)- special stains are required to distinguish islet cell populations.
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34
Q

In what form does the exocrine pancreas secrete its pro-digestive enzymes?

A

Zymogens (inactive enzyme)

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35
Q

What are the 5 main pancreatic zymogens released and their corresponding active forms?

A
  1. Trypsinogen –> trypsin (active – protein digestion)
    1. Chymotrypsinogen –> chymotrypsin (active – protein digestion)
    2. Proelastase –> elastase (active – protein digestion)
    3. Procarboxypeptidase –> carboxypeptidase (active – protein digestion)
    4. Prolipase –> lipase (active – fat digestion)
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36
Q

Where are digestive (zymogens) enzymes produced in the pancreas?

A

Acinar cells

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37
Q

Where is bicarbonate fluid produced in the pancreas?

A

Epithelial cells lining the pancreatic ducts

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38
Q

How does the pancreas prevent auto-digestion?

A
  1. Enzymes are synthesised as zymogens and packaged in granules
    1. Produces bicarbonate rich fluid to flush pancreatic ducts and prevent zymogen activation
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39
Q

Why does chyme need to be neutralised?

A
  1. Very acidic, from stomach, pH 2
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40
Q

What is released in the duodenum in response to chyme?

A

CCK and secretin

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41
Q

What is the mechanism of action for CCK and secretin in response to chyme?

A
  1. CCK drives release of bile from the gall bladder (pH 6-7)

2. Secretin drives release of bicarbonate fluid from the pancreas (pH 7-8)

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42
Q

What is the effect of secretion in the duodenum on pH?

A
  1. Neutralises pH to 7-8.5

2. Allows function of pancreatic enzymes at correct pH

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43
Q

How are zymogens activated in the small intestine?

A
  1. Brush border enzyme removes a peptide fragment from trypsinogen to convert it to activated trypsin
    1. Trypsin then cleaves peptide fragments from the other zymogens to activate them
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44
Q

What is an example of neural regulation of pancreatic exocrine function?

A
  1. Cephalic phase and gastric phases
    1. Trigger vagal signalling
    2. Triggers acinar cells to release zymogen granules
    3. Triggers duct epithelial cells to release bicarbonate fluid
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45
Q

What are examples of endocrine regulation of the pancreatic exocrine function?

A
  1. Gastrin produced in the stomach (in gastric phase) - increases secretion of zymogen granules
    1. Luminal contents release CCK and secretin - increase zymogen and fluid secretion
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46
Q

What is an Erythrocyte?

A

Red blood cell

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47
Q

What is the life span of an Erythrocyte?

A

120 days

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48
Q

How are Erythrocytes removed from circulation?

A

Phagocytosis (macrophages mainly in spleen, but also bone marrow and liver)

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49
Q

What is Bilirubin from and what colour is it?

A
  1. Breakdown product of haemoglobin

2. Yellow

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50
Q

What are the key events in Haeme breakdown?

A
  1. Haeme catabolised –> GREEN biliverdin (happens mainly in spleen, marrow, liver)
    1. GREEN biliverdin rapidly reduced into –> YELLOW bilirubin (complexed with albumin (blood protein)
    2. Yellow bilirubin conjugated with glucuronic acid in liver hepatocytes
    3. Secreted into intestines ant converted to urobilinogen by intestinal bacteria
    4. Urobilinogen –> Oxidised to Yellow urobilin in kidneys OR BROWN stercobilin by intestinal bacteria and excreted in faeces.
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51
Q

What are the colour changes and chemical changes in Haeme breakdown?

A
  1. Haem –> Green biliverdin
    1. Green biliverdin –> Yellow bilirubin
    2. Yellow bilirubin –> conjugated bilirubin
    3. Conjugated bilirubin –> Urobilinogen
    4. Urobilinogen –> Yellow Urobilin or Brown Stercobilin
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52
Q

How is bilirubin taken up by the liver?

A

Facilitated diffusion from the blood

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53
Q

What is bilirubin conjugated with in the liver?

A

Glucuronic acid

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54
Q

How is conjugated bilirubin secreted from the liver?

A

In bile into the intestines.

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55
Q

What are the purposes of bile salts?

A
  1. Emulsify fats so fats and fat soluble vitamins may be absorbed
  2. Elimination of waste products such as bilirubin
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56
Q

What are the two potential end points of bilirubin that enters the GIT?

A 
1. Kidney excretion (as Urobilin)
Faecal excretion (as Stercobilin)
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57
Q

What is the structure of cholesterol?

A

Lipid with four fused hydrocarbon rings to form the bulky steroid structure.

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58
Q

What functional roles does cholesterol have in the body?

A
  1. Cell membrane - permeability and fluidity
    1. Vitamin D synthesis
    2. Steroid hormone synthesis
      Manufacture of bile salts
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59
Q

What are the sources of cholesterol?

A
  1. Diet (animal fats)

2. Synthesized

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60
Q

Where is cholesterol synthesized?

A

Liver (80%), peripheral tissues (20%)

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61
Q

How is cholesterol synthesized?

A
  1. Glucose, fatty acids, Amino acids –> Acetyl CoA
    1. Acetyl CoA processed by HMG-CoA reductase (rate limiting step)
    2. Few intermediate units before cholesterol
    3. Cholesterol has a negative feedback loop back onto HMG-CoA reductase.
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62
Q

What is the target of statins in term of cholesterol synthesis?

A

HMG-CoA (rate limiting step)

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63
Q

What is the effect of intracellular cholesterol on cholesterol synthesis?

A
  1. High = reduction in synthesis

2. Low = increase in synthesis

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64
Q

How are bile acids produced from cholesterol?

A

Oxidation of cholesterol mediated by cytochrome P450.

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65
Q

How are lipids and cholesterol transported in the blood?

A

Packaged in lipoproteins

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66
Q

How are lipoproteins classified?

A

Density

67
Q

What does a low density lipoprotein mean?

A

High lipid content, low protein content as protein is more dense.

68
Q

What is an example of a lowest density lipoprotein?

A

Chylomicrons

69
Q

What are apolipoproteins?

A

They are lipid proteins that can bind to lipids and cholesterol to form lipoproteins

70
Q

What are the important roles of apolipoproteins?

A
  1. Facilitate lipid solubility
    1. Maintain structural integrity of lipoprotein
    2. Serve as ligands for lipoprotein receptors (allow lipids to be deposited where needed)
    3. Regulate enzyme activity involved in lipoprotein catabolism
71
Q

What are the general classes of lipoproteins?

A

Chylomicrons –> VLDL –>IDL (intermediate density lipid) –>LDL –>HDL

72
Q

Why is LDLs considered bad and HDLs considered good?

A
  1. LDLs full of lipid –> will travel the body and deposit that lipid
    HDL not full of lipid –> will travel the body and harvest excess lipids to bring back to the liver for processing
73
Q

What does pharmacokinetics describe?

A 
Absorption
Distribution
Metabolism
Excretion
ADME!
74
Q

What factors affect drug absorption orally?

A
  1. Nature of absorbing surface
    1. Lipid solubility and pH of environment
    2. Drug formulation (sustained release or enteric coating)
    3. Lipophilic vs hydrophilic
    4. Blood flow
    5. Food in stomach
    6. Motility of gut
75
Q

What is the easiest type of drug to cross a lipid membrane?

A

Lipid soluble drugs (lipophilic drugs) - they diffuse easily

76
Q

What do large drugs typically require to cross a membrane?

A

Carrier proteins

77
Q

Where are most orally administered drugs absorbed?

A

Small intestine

78
Q

What does an enteric coating do?

A
  1. Prevents drug breakdown in stomach (pharmacologically inactive)
    1. Prevents stomach irritation
      What type of acids and bases are many drugs and what does this mean for their species?
    2. Many are Weak acids or bases
    3. This means they can be present as both non-ionized and ionised species
79
Q

Is ionised or non-ionised dug species more lipid soluble?

A

Non-ionised- Hence they are able to diffuse across cell membranes better
Non-ionised can also be describes as protonated

80
Q

What is pKa?

A

pH at which half of the number of drug molecules are in their ionised form.

81
Q

What happens when pH is less than the pKa value of a weak acid?

A

Protonated form predominates (non ionised)

82
Q

What happens when the pH is greater than the pKa of a weak acid?

A

The unprotonated (ionised) form predominates

83
Q

What is pH trapping and how does it work?

A

A drug is effectively trapped in the circulatory system plasma

1. Weak acid (pKa 4) 
2. Enters stomach pH 1-2
3. Weak acid hence in a mostly protonated form (non-ionised = neutral)
4. Neutral change means lipid solubility --> diffuses across lipid membrane into blood
5. Blood pH is 7 
6. Drug hence becomes mostly deprotonated and ionised (lipid insoluble)
7. Drug is trapped in plasma
84
Q

What happens if the pH is less than the pKa value of a weak base?

A

Unprotonated form predominates (ionised) –> weaker absorption across lipid layer

85
Q

What happens when pH is greater than the pKa value of a weak base?

A

Protonated form predominates (non ionised) –> better absorption thus better in SI

86
Q

For solid drugs what has to be considered first for what effects its absorption?

A

Rate of drug dissolution (how well drug dissolves in aqueous solutions)

87
Q

What is a enteric coating typically made of and what is a standard threshold pH?

A

Cellulose polymers with threshold of dissolution pH 5-6

88
Q

What is another benefit of enteric coatings outside of being inactive in stomach and reducing irritation?

A

Enable drug to be presented to sites of action in ileum and colon.

89
Q

What is controlled/sustained release drugs designed for?

A

Produce slow uniform absorption of drug for 8 hours or longer

90
Q

What is the benefits of controlled/sustained release drugs?

A
  1. Reduces how often a patient needs to take it (improves compliance)
    1. Maintains therapeutic effect overnight
    2. Decreased incidence and/or adverse effects by reducing peaks in drug concentration
    3. Reduces chance of nontherapeutic blood levels (eliminates troughs in concentration)
    4. Delayed absorption - capsules can be designed to remain intact for hours
  2. Mix slow and fast - can have slow and fast release particles to produce rapid but sustained absorption.
91
Q

What is the effect of blow flow on absorption and why?

A
  1. Fast blood flow –> steeper concentration gradient (drug concentration in blood kept low) –> faster absorption
    1. Slow blood flow –> smaller gradient (high drug concentration in vessels) –> slower absorption
92
Q

Increase gastric emptying =?

A

Faster drug absorption in small intestine

93
Q

Decreased gastric emptying =?

A

Slower drug absorption in the small intestine

94
Q

Effects of fatty food on gastric emptying?

A

Delays gastric emptying –> reduces SI drug absorption

95
Q

How does food in stomach change the pH?

A

Food in = lower pH (good for drugs needing acid activation) (antifungals)
Empty = higher pH (good for acid sensitive drugs)

96
Q

What are specific metabolic impact on drugs in the intestinal lumen?

A
  1. Inactivation by metabolic enzymes (before being absorbed)
    1. Gut microbiota metabolisation
    2. Cytochrome P450 enzymes located in epithelium can metabolise drugs
      N.B all these reduce the amount of drug absorbed, represent natural mechanisms to reduce absorption of foreign chemicals.
97
Q

What is exsorption?

A

Movement of materials from the blood/cells back into the lumen of the intestines.

98
Q

What is a efflux transporter example for the intestinal epithelium?

A

P-glycoprotein -has an ATP binding cassette (ABC) requiring ATP energy.

99
Q

Where was P-glycoprotein first identified?

A

Tumour cells –> pumps out chemotherapy drug –> leading to multi-drug resistance

100
Q

What is the effect of P-glycoprotein on drugs in the intestinal epithelium?

A

Pumps drugs back into the lumen of the intestines –> reduces drug amount reaching the systemic circulation

101
Q

What is the family of and structure of the Hepatitis A virus?

A
  1. Family- Picornaviridae - Pico = small (small RNA virus)
    1. Structure- non-enveloped genome packaged into a protein shell (capsid) (icosahedron shaped)
    2. There are 6 subtypes
102
Q

What is the family and structure of the Hepatitis B virus?

A
  1. Family- Hepadnaviridae - Hepa = liver (DNA virus)
    1. Structure- Virus particle (Dane particle) - consists of nucleocapsid protein core inside a lipid envelope derived from host membrane. (icosahedron shaped)
    2. There are 8 known genotypes and 24 subtypes
103
Q

What is the family of and structure of the Hepatitis C virus?

A
  1. Family- Flaviviridae- flavus = yellow
    1. Structure- Genome surrounded by a protein capsid and lipid envelope (derived from host membranes) (icosahedral-like capsid structure)
    2. There are 7 major genotypes and 67 subtypes
104
Q

What Hepatitis virus has only a capsid?

A

Hep A

105
Q

What hepatitis virus has an envelope?

A

Hep B and C

106
Q

What are some mechanisms that virus structure can impact on?

A
  1. Viral entry

2. Virion release

107
Q

What are some general features of non-enveloped virus like Hep A?

A
  1. Surface consists of viral derived proteins
    1. More stable- can last longer in the environment
    2. Transmission routes - faecal-oral, contaminated food and water.
108
Q

What are some general features of enveloped virus like Hep B and C?

A
  1. Sensitive- limited survival outside host environments - desiccation, heat
    1. Entry method - fusion
    2. Coated in cell membrane during release, longer time to replicate
    3. Transmission route- directly from host to host eg blood, bodily fluids
    4. Envelope enables adaption and integration of different surface proteins (both host and viral) to evade immune response in persistent infection.
109
Q

What is the replication cycle of the HAV hepatitis A virus?

A
  1. Attachment (via receptors) and entry into host via endocytosis
    1. Its +ssRNA is translated to viral polyproteins by host ribosomes
    2. Polyproteins are cleaved to form structural viral proteins
    3. +ssRNA is transcribed into -ssRNA to make new viral genomes
    4. New virions are assembled
    5. Intact HAV is released from the cell via lysis
110
Q

What are some downsides of HAV replication method?

A
  1. HAV requires functional eukaryote initiating factor 4G for translation
    1. Cannot shut down host protein synthesis
    2. Must compete for cellular translational machinery
111
Q

What is the replication cycle of HBV hepatitis B virus?

A
  1. Attachment to surface proteins and entry via clathrin or caveolin dependant endocytosis
    1. Virus membrane fuses with cell membrane to release virus core into cytoplasm
    2. Vural genomic DNA is transferred to cell nucleus
    3. Host DNA polymerase converts the partially dsDNA to fully dsDNA
    4. Fully dsDNA transformed into covalently closed circular DNA for use a viral mRNA transcription template
    5. Longest mRNA used to make new genomes, capsid, core protein and DNA polymerase
    6. Assembles at the endoplasmic reticulum
    7. Released from the cell
112
Q

What is the replication cycle of HCV hepatitis C virus?

A
  1. Attachment - receptor mediated endocytosis
    1. ssRNA released into cytoplasm
    2. ssRNA translated into single protein
    3. Viral proteases cleave protein into functional viral proteins
    4. Viral polymerase produces -ssRNA as template for genome
    5. Assembles - genome packaged into capsid
    6. Virus packaged within host membrane envelop and released.
113
Q

What is hepatitis?

A

Inflammation of the liver

114
Q

What is the two forms of hepatitis?

A
  1. Acute- (self-limiting)
    1. Chronic- inflammation of hepatocytes lasting longer than 6 months –> can progress to fibrosis, cirrhosis, liver cancer
115
Q

What is the most common cause of hepatitis?

A

Hepatitis viruses- A,B,C,D,E

116
Q

What are some non-viral causes of hepatitis?

A
  1. Other infections - bacterial, parasitic
    1. Toxins- alcohol, certain medications
    2. Autoimmune diseases
117
Q

What is the general progression to hepatocellular carcinoma?

A
  1. Chronic Hepatitis- ongoing injury to hepatocytes (inflammation)
    1. Cirrhosis- results from long term tissue damage and fibrosis
    2. Hepatocellular carcinoma - most common primary liver cancer, most common cause of death in individuals with cirrhosis
118
Q

What is some symptoms of chronic and acute hepatitis? (chronic can show similar symptoms)

A
  1. Fatigue
    1. Nausea, vomiting
    2. Poor appetite
    3. Joint paint
    4. Jaundice
119
Q

What is some symptoms of cirrhosis? (Slow development to pathology)

A
  1. Jaundice
    1. Weight loss
    2. Coagulopathy (impaired blood clotting)
    3. Ascites (abdominal fluid collection)
    4. Peripheral oedema
120
Q

What is some symptoms of Hepatocellular carcinoma (HCC)?

A

Generally associated with worsening cirrhosis symptoms:

1. Jaundice
2. Abdominal swelling and pain due to ascites
3. Bruising from clotting abnormalities
4. Appetite loss
5. Weight loss
6. Nausea, vomiting 7. Fatigue
121
Q

What is the transmission modes for Hep A,B,C?

A
  1. Hep A- faecal-oral, contaminated food/water, direct contact with infected person
    1. Hep B- (can persist 7 days outside host) mother-child at birth, blood, body fluids, sexual transmission
    2. Hep C- (blood borne virus) - used needles, unsterilised medical equipment, transfusion, sexual intercourse, mother to baby
122
Q

Which Hepatitis virus’ are more likely to result in chronic hepatitis?

A

Hep B,C, NOT A

123
Q

How does the transmission mode of Hep A relate to the “at risk” groups for the virus?

A
  1. Unsanitary conditions is a big factor in the virus spread
    1. Hence the at risk groups consist of
      people in poorer living/working conditions
      -cannot look after themselves properly (intellectually disabled)
      -Men-men intercourse (increased bleeding risk)
      -Injecting drug users etc
124
Q

How does the transmission mode of Hep B relate to the “at risk” groups for the virus?

A

Similar at risk groups for Hep A

1. Especially dangerous for infants as a large proportion of them will develop chronic hepatitis B if exposed 80-90% - this is compared to 5% in adults
2. As can survive outside the body can be a risk to people living with a Hep B positive individual etc.
125
Q

How does the transmission mode of Hep C relate to the “at risk” groups for the virus?

A
  1. Blood borne infection
    1. Hence risk groups are those that are in environments exposed to blood/sexual contact with infected persons.
      Drug users
      Health care workers
      Sex workers
      Used needles
      Children born to infected mothers
      Etc
126
Q

How does Hep C cause its damage and go onto being a chronic infection?

A
  1. Causes direct liver damage through activation of non specific immune inflammation
    1. To establish chronic infection it subverts the immune system by:
      Altering hepatic chemokine expression
      Impairing cell mediated immunity (T-cells)
      Chronic tissue inflammation
127
Q

What are the treatment options for Hepatitis A?

A

There is no treatment options!
Only prevention:
1. Hygiene/sanitation
2. Passive and active immunisation

128
Q

What is the difference between passive and active immunisation?

A

Passive - done on everyone say at a certain age regardless

Active- done on at risk populations

129
Q

What are the treatment options for Hepatitis B?

A
  1. Antiviral agents - reduce symptoms - does not cure chronic HBV - antiviral agents block reverse transcriptase but can have a side effect of viral mutation and subsequent antiviral resistance.
    1. Antiviral (interferon)- used to treat chronic infection but can have many side effects:
      - cause/aggravate mental problems
      - flu like symptoms
      - not recommended for people who (use drugs, alcohol, organ transplant recipient or have advanced cirrhosis)
130
Q

What are the treatment options for Hepatitis C?

A
  1. There is new oral direct acting antivirals
    1. There is an array of antiviral therapies that target various points of the HCV life cycle
    2. All patients with Hep C are considered for antiviral therapy
    3. Goal is to accomplish SRV (sustained virological response) (undetectable in blood “cure”)
131
Q

How is the Hep A vaccine used?

A
  1. Passive and active immunisation (2 dose to enable long term protection)
    1. Can be given after exposure as well.
132
Q

How was the Hep B vaccine developed?

A

Subunit vaccine containing hepatitis B surface antigen produced by recombinant DNA technology

133
Q

How is the Hep B vaccine used?

A

Infants - birth dose, 2,4,6 months of age
Children/adolescents - 3 dose schedule 0,1,6 months from start
Adults - 2 dose schedule
Given as part of standard vaccine schedule.

134
Q

Is Hep C vaccinated against?

A

No, no vaccine exists

135
Q

What is a blood borne virus?

A

A bloodborne disease is a disease that can be spread through contamination by blood and other body fluids. (this is the primary mode of transmission for the virus)

136
Q

What are some common causes for RUQ pain?

A
  1. Renal problems - stones , UTI, infection, cancer
    1. Liver conditions- hepatitis, liver abscess, cancer
    2. Preeclampsia
    3. Gall bladder problems- gallstones (choledocholithiasis),
    4. GIT- Dyspepsia (heartburn), gastritis, peptic ulcers
    5. Pancreatic conditions- pancreatitis
137
Q

How would you clinically distinguish these causes?

A
  1. Renal problems- radiating pain to lower back or groin, urination changes/pain
    1. Liver- jaundice
    2. Preeclampsia- rise in blood pressure
    3. Gallbladder problems- pain occurs after a large meal
    4. GIT- dull burning pain, bloating, burping or gas
  2. Pancreatic conditions- pain worsens with time
138
Q

What are the common causes/diagnoses causing jaundice?

A
  1. Acute hepatitis
    1. Cholangitis (bile duct inflammation)
    2. Choledocholithiasis (bile duct stone)
    3. Haemolytic anaemia (bilirubin increased as lots of blood cell broken down)
    4. Gilbert’s syndrome (genetic condition that impairs enzymes that process bilirubin)
  2. Cholestasis - bile flow interrupted, conjugated bilirubin remains in the liver and is not excreted
139
Q

What is pre hepatic jaundice?

A

Excess production of bilirubin (more than the liver can process efficiently)

140
Q

What is intra hepatic jaundice?

A

Inability of the liver to conjugate or excrete bilirubin

141
Q

What is post hepatic jaundice?

A

There is an impediment to the flow of bile due to partial or complete obstruction of the biliary passage on its way to the duodenum

142
Q

How would you distinguish pre, intra and post hepatic jaundice?

A
  1. Pre - primarily findings of high levels of unconjugated bilirubin (most commonly caused by hemolytic anemia)
    1. Intra - fraction of bilirubin varies - if viral predominately unconjugated - if cholestasis (flow impede) from drugs or biliary cholangitis will be high conjugated bilirubin. - can lead to dark urine also
    2. Post - high conjugated bilirubin caused by a mechanical obstruction of bile in the biliary ducts or within the pancreas
      - Can have dark urine
      - Stool deficient of bile
143
Q

How do gallstones form?

A 
Gallstone can form from bile stasis in the gallbladder or the cystic duct/bile ducts
High cholesterol (hypercholesterolemia) increases risk of gallstones.
144
Q

What are some reasons for bile stasis?

A
  1. Anatomy of the bile duct (may be kinked etc.) usually an issue for the cystic duct
    1. Fasting
    2. Inflammation
145
Q

What is the composition of gallstones?

A

Cholesterol, Bile salts and bilirubin

146
Q

What are the two main forms of gallstones?

A
  1. Cholesterol- 80% of gallstones (predominately cholesterol) yellow-green in colour.
  2. Pigment stones- predominantly made of bilirubin (small and dark in colour
147
Q

What are the symptoms of gallstones?

A
  1. 80% of people do not get any symptoms from gallstones
    1. Pain in RUQ
    2. Nausea/vomiting
    3. Jaundice
    4. Clay colored stool
148
Q

What are the complications of gallstones in the gallbladder vs the biliary tract?

A
  1. Gallbladder - inflammation of the gallbladder (cholecystitis) a gallstone blocks the gallbladder duct, leading to infection and inflammation of the gallbladder.
  2. Biliary tract - biliary cholic (obstruction in cystic duct)
    - Pancreatitis (biliary obstruction near pancreas)
    Cholangitis (biliary duct inflammation)
149
Q

What is biliary colic?

A

Biliary colic, also known as a gallbladder attack or gallstone attack, is when a colic (sudden pain) occurs due to a gallstone temporarily blocking the cystic duct.

- often after a big meal or during the night. (as gall bladder starts to contract there is increased intra gall bladder pressure)
- not true colicy pain as it is not in waves due to peristaltic movement
- No fever associated
150
Q

What is cholecystitis?

A

Inflammation of the gallbladder
Can be diagnosed by murphy’s sign - patient breathes in and if they wince when the gall bladder hits your hand
- reasonably constant pain but will elevate with eating etc
- Fever
- tachycardic

151
Q

What is ascending cholangitis/acute cholangitis?

A

Inflammation of the bile duct- from bacteria in the duodenum

152
Q

What is a bloodborne disease?

A

A bloodborne disease is a disease that can be spread through contamination by blood and other body fluids. Bloodborne pathogens are microorganisms such as viruses or bacteria.

153
Q

What are the most common blood borne disease?

A

The most common examples are HIV, hepatitis B (HVB), hepatitis C (HVC) and viral haemorrhagic fevers.

154
Q

What are the clinical illness associated with Hep A,B,C?

A 
Fatigue
Jaundice
Nausea/vomiting
Abdominal pain RUQ
Clay colored stool
Loss of appetite
155
Q

What is the general risks of chronic illness from Hep A,B,C?

A

Hep A - Temporary most people clear virus
Hep B - Most adults clear virus but infants and children are at much greater risk of chronic infection
Hep C - Most people cannot clear virus

156
Q

How are blood borne diseases transmitted?

A

Blood products or bodily fluids

157
Q

How are bloodborne diseases prevented in healthcare settings?

A
  1. PPE

2. Limit exposure to blood products and bodily fluids

158
Q

Within a liver function test what values help indicate degree of cholestasis?

A

Bilirubin
GGT
ALP
etc

159
Q

Liver functional mass?

A

reported by Albumin levels

160
Q

Why is urinalysis done in a liver evaluation?

A

If bilirubin is present in urine it can indicate hepatic issues

161
Q

What are some screening questions for cardiac issues?

A
  1. Any chest pain
    1. Any cardiac history
    2. Any SOB shortness of breath
162
Q

What are some screening questions for malignancy

A
  1. Any weight loss

2. Any night sweats

163
Q

What are some screening questions for UIT?

A
  1. Any dysuria (pain on urination)

2. Noticed any increase in urination

164
Q

When is the pain normally worst for billarycholic

A

after a meal

JMP Semester 2 (8 decks)

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