Tutorials

Question 1

What is the lysogenic phase of a viruses life cycle?

Answer 1

Where the virus remains dormant in the host

Question 2

What is the lytic phase of a viruses life cycle?

Answer 2

Following lysogenic phase. After stimulation virus forms new virus, self-assembles and bursts out of host cell

Question 3

What is the life cycle of a virus?

Answer 3

1) Entry- Fusion if lipid packaged. Protein packaged interaction with particular protein
2) Endosomal fusion to a lysosome- pH decreases but lysosome supposed to degrade (has proteosomes etc) so virus has to leave quickly
3) Nucleic acid processed- replication and transcription
4) Exit

Question 4

What are the strategies for antiviral drugs? (4)

Answer 4

1) Use immune system
Block with antibodies e.g. vaccinations- block viral action
2) Block proton pump
Stop lysosome
3) Inhibit reverse transcription
Blocking DNA might block normal cells so block reverse transcription
4) Release blocker
Virus not released (has sialic acid). Sialic acids are highly conserved and abundant in most cells so good viral targets. Block neuramidase- cleaves sialic acid (can’t untether)- stops exit

Question 5

What is the mechanism of action of Acyclovir?

Answer 5

Blocks viral DNA replication
Viral thymidine kinase has very high affinity for acyclovir. .
Acyclovir converted to acyclovir monophosphate by viral thymidine kinase. Then converted to acyclovir triphosphate by host cell kinases. Acyclovir triphosphate competitively inhibits and inactivates DNA polymerases preventing viral DNA synthesis without infecting normal cell processes.

Question 6

How would lack of oxygen cause cells to die?

Answer 6

Too little oxygen to cell means there is less ATP being produced in respiration. If ATP drops the ATPase pumps will not work. The ion balance of the cell is disrupted and this means the cell dies.

Question 7

Why is creatine kinase measured to indicate cell death What are the three isoforms?

Answer 7

Creatine kinase- normally present in all cells at very low levels. It is high in metabolically active cells (e.g. brain BB, heart BM, skeletal muscle MM). When cells die it is released into the blood
Cardiac= 70%MM, 30%MB

Question 8

When does serum creatine kinase peak following MI?

Answer 8

24 hours

Question 9

Why can’t you measure CK activity in the serum as a diagnostic test for MI?

Answer 9

Could be any of the three isoforms of CK

After 24 hours the CK depletes and cannot pinpoint what it has decreased from.

Question 10

What serum markers are used to diagnose MI? (4)

Answer 10

Creatine kinase
Serum oxaloacetate transaminase (SGOT)
Lactate dehydrogenase
Cardiac troponin (Ca2+ switch in muscles- I & T are tissue specific)

Question 11

What does red bone marrow indicate?

Answer 11

Not enough oxygen

Increased erythrocyte production

Question 12

How does potassium cyanide (KCN) affect respiration?

Answer 12

It is a cytochrome oxidase inhibitor
It reacts covalently with Fe3+ in cytochrome oxidase, inhibiting the last step of the electron transport chain- this stops respiration

Question 13

How does oligomycin affect respiration?

Answer 13

Interferes with ATPsynthase, reducing it’s ability to utilise the proton gradient in coupled mitochondria leading to inhibition of respiration.
(This does not occur if the mitochondria has been uncoupled)

Question 14

What happens if mitochondria become uncoupled?

Answer 14

Kreb’s cycle and oxidative phosphorylation are running maximally but link to ATP generation is broken free so substrate-released energy is lost as heat.

Question 15

How does DNOC affect respiration?

Answer 15

Uncouples mitochondria (similar to dinitrophenol)
Passes readily across mitochondrial inner membrane in their undissociated form and thus dissipates the proton gradient, disabling gradient formation

Question 16

What is the molecular architecture of collagen?

Answer 16

Glycine as every third amino acid (glycine is the smallest amino acid which sits in the middle of the triple helix)
Contains modified amino acids hydroxyproline and hydroxylysine

Question 17

What is osteogenesis imperfecta?

Answer 17

Repeated fractures of long bones and malformed bones caused by a mutation in COL1A1.
Defective connective tissue or unable to make it.

Question 18

How does a mutation in COL1A1 lead to osteogenesis imperfecta?

Answer 18

Mutation causes glycine to be substituted for cysteine. This is a larger amino acid which causes steric hindrance which generates a kink in the normally straight triple helix resulting in a defect in the fibres.

Question 19

What is a dominant negative disorder?

Answer 19

Because a patient can be heterozygous with a dominant disorder one protein coded by the faulty gene will be disrupted while the other will be normal.

Question 20

What is antibody class switching?

Answer 20

Usually antibody initially secreted is IgM. This switches to IgG as the immune response progresses.
In type I hypersensitivity, activation of CD4+ T helper cells (Th2) causes a switch to IgE production

Question 21

How does IgE cause allergy?

Answer 21

IgE binds to IgE receptors on the surface of mast cells. Causes mast cell degranulation which releases histamine and leukotrienes. These act principally on blood vessels and smooth muscle.
In connective tissue histamine= dilation of vessels, increased blood flow to the surface and increased movement of fluid out of the blood-stream.
Around mucosae= constriction of the airways, contraction of smooth muscle in the walls of the intestine
Subsequent stimulation of these cells by exposure to the allergen

Question 22

What are the symptoms of anaphylaxis?

Answer 22

Rash and oedema. Lowering of blood pressure- leads to shock (dilation of peripheral blood vessels)
Difficulty breathing (constriction of bronchi)
Increased respiration and heart rate
Nausea, abdominal cramps, diarrhoea (effects on the intestines