Hepatitis Internal Non-Infectious Diseases

Hepatovirus

Structure and composition

Structure

• doesn't have an envelope
• proteins, made up of capsimirs that makes up the capsid structure
• inside of that capsid you have different types of enzymes
• inside of this there's a nucleic acid structure that is a single stranded rna virus +ve sense

Structure of Hepadnaviridae

structure

• does have an envelope, it does have a lipid bilayer
• inside of this it's going to have capsomers which makes up the capsid
• double stranded dna

Structure of Flaviviridae

• it does have an envelope
• Has a capsid and capsimears
• Inside of that it has it's nucleic acid structure
• single stranded rna, specifically - positive sense single stranded rna

Structure

Structure

• It has an envelope and it has a circular stranded structure that is not double stranded but a circular stranded rna.
• Called single stranded rna but is a negative sense RNA

Structure

Structure of Hepeviridae

• no envelope present
• capsomers and capsid proteins present
• Inside it has a nucleic acid which is single stranded rna positive sense

Structure

Ribosomes

The virus's nucleic acid goes down to the host's cell's ribosomes and uses the host cell's ribosome to synthesize proteins. It's going to make proteins such as maybe capsomeres which are important because they make up the capsid it might make certain types of antigens that they put on the surface.

It will synthesize rna or dna polymerases.

Then it will send these molecules to the golgi or endoplasmic reticulum-like complex and they'll get synthesized and will make these vesicles that will contain all these different proteins.

All these components will come together and make virus particles, then it just release these viruses out of the hepatocyte and go cause it to damage other nearby hepatocytes.

Hepatocyte Lysis

Whenever these viruses start being developed they cause destruction of the cell so whenever they actually accumulate within a cell they do lead to lysis.

Another way that the hepatocyte can get damaged, all of these proteins that are being synthesized. Cells here will actually make antigens, and send these antigens and put them onto a protein that we express on our cell membrane - MHC1

Cell Death

when you're having this infection your body releases different types of interferons which activate macrophages which activate t cells those t cells are then going to come to this area of where this infection is. These cytotoxic T cells come over to this area and have a specific protein that they use to recognize this mhc-1 molecule. A specific molecule which is going to hook onto MHC1 is called cd8. When this cytotoxic T cell doesnt recognise any self antigens present, it sends a signal to secrete molecules - perforins! which will make holes in the cell membrane. another molecule called granzymes will leak into the pores and induces apoptosis - Cell Death

Cell Death

Conversely our immune system can respond to this infection, when these hepatocytes are damaged, damaged they can secrete interferons and the particular type is interferon gamma, that activates macrophages.

Then the macrophages will then come and stimulate these different t cells, particularly a cytotoxic t cell. They'll come and cause destruction of these cells. This is how you get inflammation and destruction

of the liver cells.

Dehydration

Hypovolemia

GI Tract

Electrolyte loss

Once the chemo trigger zone stimulates the ammetic centre, this will activate

nerves that are going to go to the

gastrointestinal tract.

This will cause a retro peristaltic

action and this retro peristaltic action

is going to cause certain types of food

and gastrointestinal contents to be pushed in the opposite direction - Vomiting

Weight loss

Diarrhea

Inside the cells

Haem

Further

Liver cells continue to get more and

more damaged, more problems occur.

when hemoglobin is broken down:

Unconjugated bilirubin is then taken to the liver where it reacts with an enzyme and this enzyme is called ugt uridine glucoronicile transferase.

it stimulates the conversion of unconjugated bilirubin into conjugated bilirubin

Billirubin

UCB

3 main types:

1:Primary photosensitivity

2:Secondary (Hepatogenous) photosensitivity

3.Genetic Photosensitivity

Primary photosensitivity

• Ingestion of St Johns Wort (Hypericum Perforatum) – which contains the photo-toxic pigment Hypercin
• This becomes toxic when exposed to direct sunlight (UV) via the blood stream in unpigmented skin
• Highest levels of Hypercin occurs during flowering

• Other plants implemented- Buckwheat, Bishop’s weed, Spring Parsley, clover and alfalfa

Secondary Photosensitivity

Due to liver damage-reducing the removal of the phototoxin Phylloerythrin from the blood stream.

Some causes:

-Ragwort Poisoning (pyrrolizidine alkaloids)

-Liver Fluke

-Liver Abscess

-Brassica toxicity

What even is Phylloerythrin?

• Phylloerythrin comes from the breakdown of chlorophyll (found in grass) by microorganisms in the Gut.

• Phylloerythrin is normally excreted by the liver into the bile.

• If the liver is incapable of excretion it reaches the skin becomes phototoxic when it interacts with UV light

Genetic photosensitivity

Bovine congenital erythropoietic protoporphyria (BCEPP).

Reported in Limousin cattle, Blonde d’ Aquitane and Holsteins.

This condition is caused by a deficiency in an enzyme which causes excessive photo-toxins in the body.

Treatment

Treatment: supportive

• Remove animal from direct sunlight- Dark Shed
• Pain relief (Steroids or NSAIDs if pregnant)
• Liver support tonics