Topic 6 Flashcards
(26 cards)
Benefits of a double circulatory system
3 types of capillary walls + functions/why [3]
- Fenestrated: has pores. usually in capillaries suited to absorption
- Continuous: endothelial cells held together tightly by cell junctions
- Sinusoid: large intracellular gaps (for larger molecules to pass) `
Describe the structural elements of capillary that aid its function [4]
- one cell thick wall - lower diffusion distance and maximise the material exchange
- small diameter - allows one RBC at a time, slows down the flow, optimises the material exchange
- basement membrane surrounding - allows necessary materials to pass through
- may have pores/fenestrated: increase material exchange
features of how the blood flow/material exchange in capillaries works [2] (hydrostatic pressure - wise)
- arterioles branch into the capillaries + the lumen narrows to dissipate the pressure
- higher HS pressure at arteriole end –> materials (o2 and nutrients) are forced from bloodstream into tissue fluid
- lower HS pressure at venule end –> urea and co2 exit tissue fluid and enter the bloodstream
Structural features of venules that aid its function [3]
- large lumen –> low pressure
- valves to prevent backflow
- thin walls (little elastic and muscle fibre)
How does blood move in veins [4]
- veins often pass between skeletal muscle groups
- contraction of skeletal muscles parallel to veins compresses them/arteries may run parallel to veins and their pulse may have a similar effect
- pushes the blood in a particular direction
- valves prevent backflow between compressions
Layers of the 3 different blood cells [3]
- A/V: tunica adventitia; tunica media; tunica intima (think adventurous so it’s on the outside; media because in the middle; intima because on the inside) –> in the arteries the layers are v. distinct
- cap: tunica intima
Explain how heart rate is controlled [7]
- medulla oblongata controls the increase/decrease HR
- 2 nerves connected to brain - sympathetic and parasympathetic. S: releases norepinephrine (speeds up HR); PS: releases acetylcholine (slows down HR)
- Sino-atrial node is located in the right atrium and is the primary pacemaker
- SAN sends out the nerve impulse
- Stimulates the contraction of the heart muscle -> causing atria to contract
- stimulates AV node at the junction of the A and V –> sending signals down the septum via Bundle of His (nerve bundle)
- e impulse passes through ventricular walls as Purkinje fibres in walls innervated
- in prep for vigorous physical activity/fight or flight, adrenaline can increase HR by activating same chemical pathways as norepinephrine
Explain a heart disease that can be caused by unregulated diet
- atherosclerosis
- excess cholesterol/fats consumption causes fatty deposits to build up in the arteries
- pressure on arterial walls is increased as the lumen is smaller
- leads to rupture of the artery wall –> to repair it, the wall is replaced with fibrous tissue, which is less elastic than the normal elastic layer
- smooth lining progressively degrades, lesion called atherosclerotic plaques form
- if plaque ruptures, clotting occurs and a thrombus forms
- if dislodged, it can block a smaller artery
Factors affecting heart disease exposure
- Age, Genetics, Obesity, Diet, Diseases, Exercise, Sex (males more predisposed), Smoking
( A Goddess)
Describe the surface barriers to pathogen entry []
Skin:
- May release certain acids/fatty acids to lower pH
- sebum and chemicals released from sebaceous glands to ensure inhibit microbial growth on skin
- thick dry layer of dead cells to protect external structures
Mucous membranes:
- protect internal structure of the body
- releases fluids to wash away pathogens
- thin layer of living cells
- may be ciliated to expel pathogens from the body when trapped by mucus
- biochemical defence agents –> lysozyme to cause sell lysis in pathogens
Describe how the coagulation cascade occurs [5]
- clotting factors are released from damaged cells and platelets
- platelets become sticky and adhere to the wound –> sticky plug formed
- clotting factors cause the conversion of inactive prothrombin to thrombin
- thrombin catalyses fibrinogen to fibrin conversion
- fibrin forms the mesh of fibres around the platelet plug + traps RBC –> clot
- clot is dissolved by plasmin when wound is repaired
Describe/Explain the processes in the second line of defence to prevent infection
- the second line of defence is non-specific
- pathogen enters the system, phagocytic leukocytes move in response to infection
- the damaged tissues release chemicals (histamines) drawing the WBCs to the site
- PL extend arm-like projections (pseudopodia) to engulf the pathogen via endocytosis (forming vesicle)
- vesicle fused into a lysosome to digest the pathogen
- other features: swelling, fever, antimicrobial chemicals release.
- (clotting factors in the coagulation cascade cause vasoconstriction -> reduce exposure of the blood)
Describe the functioning of the third line of defence/adaptive immune system [7]
- once pathogens are engulfed by phagocytes, antigens are displayed on their surface
- phagocytes travel to lymph nodes –> specific T helper lymphocytes are activated
- T helpers release cytokines to activate specific B lymphocytes which divide and differentiate into plasma cells –> to release large amounts of specific antibodies
- antibodies function via: agglutination, neutralising toxins on pathogen
- agglutination –> the phagocytes can recognise and engulf pathogens more easily
- b cells and some t cells then form memory cells -> provide immunity. rapid and specific response upon secondary exposure prevents symptoms
Describe the functioning of immunoglobulins
- made of 4 polypeptide joined by disulphide bonds
- they function as specific antibodies, specific to a certain pathogen
- 2 variable regions where it binds to the antigen
- rest of the molecule is constant -> recognisable by immune system -> aid destruction of pathogen
- attracts phagocytes to engulf bacteria
- ways they function: toxin neutralisation, agglutination, lysing cells
Explain how antibiotics provide protection from certain forms of infectious diseases [4]
- kill bacteria (bactericidal)
- by inhibiting metabolic pathways/membrane proteins/DNA replication
- doesn’t impact eukaryotic metabolism, only prokaryotic, hence can be used on people and animals
- don’t work if bacteria contains the resistant gene
- only work on bacteria, not viruses as viruses are not alive –> don’t have metabolism
Why antibiotic resistance more common + briefly (don’t get into the evolution rabbit hole rn) why it occurs at large scale
why:
- some bacteria have resistant gene -> degrade/block antibiotic
- reproduce quickly -> gene passed on to offspring
- bacterial conjugation –> passed to others via plasmid
why its more common:
- overprescription
- use on animals/in food production
- hospital environments where there is high use –> multi drug resistant bacteria eg:- MRSA (Methicillin resistant staph aureus)
Florey and Chain (and alexander fleming despite him being highkey useless) experiments with penicillin
- fleming’s accident: some penicillium grew on a mouldy dish of s.aureus –> inhibited bacterial growth
- Florey and Chain: injected 8 mice with hemolytic streptococci –> 4 were given antibiotics (penicillin)
- those w the antibiotic didn’t die and the others did basically
How HIV works and is spread
- Is an immunodeficiency disease targetting the T helper cells
- goes through a period of clinical latency when the infected cells divide
- then virus becomes active again -> t helper cells killed in process and no antibodies produced
- the immune system weakened -. body susceptible to opportunistic infections
- progressed form is AIDS
- transmission: reusing needles, unprotected ex, mother’s milk
Ventilation v. gas exchange v. respiration
ventilation: the exchange of air between the atmosphere and the lungs
gas exchange: the exchange of gases between the bloodstream and the air in the alveolus
cellular resp: release of ATP from organic molecules -> enhanced by O2 presence
Air pathway through the lungs
nose, pharynx, trachea, bronchi (connect to lungs - RL 3 lobes, LL 2 lobes bc heart) , bronchioles, alveoli clusters
structural features of alveoli
- Type TWO pneumocytes release a liquid containing a surfactant -> gases diffuse more easily when dissolved
- Gas exchange carried out through type 1 pneumocytes -> one cell thick walls to min diffusion distance
- surrounded by a rich network of capillaries –> maximise the exchange of gases with the blood
- spherical in shape –> increased SA:V for more efficient diffusion
Describe the structure and function of T1 & 2 pneumocytes [6]
T1:
- SQUAMOUS (ew) in shape, and very thin -> min diffusion distance
- the site of the gas exchange
- joined by occluding junctions to ensure no leakage of tissue fluid into the alveoli
- not able divide by mitosis –> formed via the differentiation of T2 cells
T2:
- CUBOIDAL (less ew) in shape
- make up most of the cells (by number) but very little of the lung by SA
- release fluids containing the pulmonary surfactant –> makes it easier for gases to diffuse and reduces surface tension -> prevents alveolar collapse
Which muscle sets contract and relax during inspiration and expiration
Inspiration:
- external intercostal muscles –> pulling ribs up and out, increasing lungs volume
- diaphragm contracts –> increasing the volume (hence lowering pressure) of the lungs -> causing air to rush in
Expiration:
- internal intercostal muscles –> pull lungs in and down
- diaphragm relaxes
- abdominal wall muscles contract –> push diaphragm up during forced exhalation
