weaknesses Flashcards
strengthen the weaknesses
cystic fibrosis is caused by a mutation of CFTR PROTEIN how does this altered protein result in thick sticky mucus and how this accounts for respiratory symptoms of the desease.
cftr is a channel protein
mutated cftr can block transport and movement of chloride ions out of cells into mucus.
water is retained in cells (no osmosis)
unable to remove mucus in lungs.
narrowing air passage
infections more susceptible.
cystic fibrosis
· Cystic fibrosis is caused by a mutation in the gene for the CFTR protein on chromosome 7
· The CFTR protein is a channel protein for chloride ions
· There is more than 1 mutation that can cause cystic fibrosis
· All mutations affect the transport of Cl- ions out of the cell
· The CFTR protein may be absent, have a non-functioning shape (tertiary /3D structure), or be reduced in number
Mucus has too much water
The Na+ channel is open, Na+ enters cell lowering the water potential in the cell causing water to move out of the mucus into the cell by osmosis. Cl- channel is closed so Cl- follows Na+ down the electrochemical gradient
Mucus has too little water
The Cl- channel opens, Cl- leave the cell lowering the water potential in the mucus causing water to move out of the cell into the mucus by osmosis. Na+ channel is closed so Na+ follow Cl- down the electrochemical gradient
reduced gas exchange
Mucus becomes thicker and sticker.
Mucus blocks the lumen of the airways – Reduced airflow of oxygen through the bronchi / bronchioles to the alveoli (reduced ventilation).
Reduced gas exchange by increasing diffusion distance and decreasing surface area of alveoli
Reduced concentration gradients of O2 and CO2 between the alveoli and capillaries
Reduced surface area and elasticity, decreases diffusion of gases
Reproductive system – causes infertility - Fertilisation of egg is prevented
Males
Thick mucus blocks vas deferens / sperm duct
Sperm cells can’t leave the testes and reach the egg or
Sperm duct / vas deferens is absent, sperm cells can’t pass through so fewer sperm cells in each ejaculate
Females
o Fallopian tubes / cervix are blocked or narrowed by thick mucus
o Sperm cells can’t pass the blockage and are prevented from reaching an egg
o Implantation is impaired
How does HIV infect and replicate in host cells?
· GP120 on the surface of HIV binds to CD4 receptors on the membrane of T helper cells
· Co receptor CCR5 on T helper cells is also involved in binding to HIV
· Viral envelope fuses with cell membrane of T helper cells
· Viral RNA enters host cell
· Reverse transcriptase converts viral mRNA into viral DNA
· Integrase helps the viral DNA integrate into the host DNA
· New virus particles are synthesised using host cell organelles
· New HIV viruses bud from the surface of T helper cells
· T helper cells are killed by virus budding out the cell
B cells (B-lymphocyte)
o Have specific antibodies on their surface
o Recognise specific foreign antigens and become an APC themselves
o Activated by cytokines from T helper-cells to divide by mitosis to produce clones of effector cells
o Effector cells differentiate into genetically identical plasma cells
Ø produce specific antibodies that are complementary to the antigen initially recognised
o Create memory cells for future secondary infections
T helper cells – bind to macrophage APC
o Bind to a specific foreign antigen presented on MHC complexes on macrophages via CD4 receptors on their surface
o Are activated and produce cytokines that
Ø Activate B cells to produce antibodies from plasma cells
Ø Activate T killer cells to destroy / kill infected host cells
o Create memory cells for future secondary infections
T killer cells (also known as cytotoxic T cells)
o Recognise specific foreign antigens on host cells via CD8 receptors e.g., virus infected cells
o Activated by cytokines from T helper cells to divide by mitosis to produce clones on active T killer cells
o Release perforin to create pores in cell membrane of host cell causing cell lysis
o Virus including incomplete viruses are released from host cell allowing antibodies to bind to them
Ø Prevents virus attaching to, and entering more host cells
Ø allows phagocytosis by macrophages
o Create memory cells for future secondary infections
VENA CAVA
- Vena cava – return deoxygenated blood from the cells of the body to the right side of the heart
av valves
- Atrioventricular valve – Tricuspid valve prevents backflow of blood from the right ventricle into the right atria during ventricular systole
RV
- Right ventricle – receives blood from the right atria then moves it out of the heart into the pulmonary artery during ventricular systole via the semilunar valve
semi lunar valve
- Semilunar valve – Pulmonary valve prevents backflow of blood from the pulmonary artery back into the right ventricle during diastole
pulmonary artery
- Pulmonary artery – carries deoxygenated blood away from the heart towards the lungs
Consequences of a hole in the heart
· Oxygenated and deoxygenated blood will mix so more oxygen will be transported to the lungs.
Ø Reduced oxygen concentration gradient between the alveoli and the blood capillaries, Less diffusion of oxygen into the blood and less oxygen transported to the cells of the body.
· Blood pressure will be reduced / lower
why do insects not need blood vessels to transport its blood around its body.
- Have a large surface area to volume ratio 2. Cells are very close to the heart and blood 3. Diffusion is fast enough for gas exchange 4. Low metabolic rate
