Topic 6 Flashcards

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1
Q

Benefits of a double circulatory system

A
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2
Q

3 types of capillary walls + functions/why [3]

A
  • 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) `
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3
Q

Describe the structural elements of capillary that aid its function [4]

A
  • 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
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4
Q

features of how the blood flow/material exchange in capillaries works [2] (hydrostatic pressure - wise)

A
  • 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
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5
Q

Structural features of venules that aid its function [3]

A
  • large lumen –> low pressure
  • valves to prevent backflow
  • thin walls (little elastic and muscle fibre)
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6
Q

How does blood move in veins [4]

A
  • 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
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7
Q

Layers of the 3 different blood cells [3]

A
  • 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
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8
Q

Explain how heart rate is controlled [7]

A
  • 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
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9
Q

Explain a heart disease that can be caused by unregulated diet

A
  • 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
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10
Q

Factors affecting heart disease exposure

A
  • Age, Genetics, Obesity, Diet, Diseases, Exercise, Sex (males more predisposed), Smoking

( A Goddess)

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11
Q

Describe the surface barriers to pathogen entry []

A

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

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12
Q

Describe how the coagulation cascade occurs [5]

A
  • 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
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13
Q

Describe/Explain the processes in the second line of defence to prevent infection

A
  • 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)
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14
Q

Describe the functioning of the third line of defence/adaptive immune system [7]

A
  • 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
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15
Q

Describe the functioning of immunoglobulins

A
  • 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
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16
Q

Explain how antibiotics provide protection from certain forms of infectious diseases [4]

A
  • 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
17
Q

Why antibiotic resistance more common + briefly (don’t get into the evolution rabbit hole rn) why it occurs at large scale

A

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)

18
Q

Florey and Chain (and alexander fleming despite him being highkey useless) experiments with penicillin

A
  • 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
19
Q

How HIV works and is spread

A
  • 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
20
Q

Ventilation v. gas exchange v. respiration

A

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

21
Q

Air pathway through the lungs

A

nose, pharynx, trachea, bronchi (connect to lungs - RL 3 lobes, LL 2 lobes bc heart) , bronchioles, alveoli clusters

22
Q

structural features of alveoli

A
  • 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
23
Q

Describe the structure and function of T1 & 2 pneumocytes [6]

A

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

24
Q

Which muscle sets contract and relax during inspiration and expiration

A

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

25
Q

Causes, symptoms and factors affecting lung cancer

A

Causes:
- uncontrolled growth of cells –> forms a tumour
- can be in one place (benign) or move to different parts of the body (malignant)

Why its dangerous:
- lungs are very critical to the body’s functioning so anything that impedes that is v harmful
- lungs possess rich blood supply –> easy to metastasise

symptoms:
- coughing up blood, wheezing, weight loss, respiratory distress

factors affecting LC:
asbestos, smoking, pollution, passive smoking, radiation exposure, genetically predisposed, age, occupation (exposure), diseases (eg COPD)

26
Q

Explain what happens when a person develops type 1 diabetes [2]

A
  • insulin needed to regulate blood GLUCOSE levels;
  • AUTOIMMUNE RESPONSE/ANTIBODIES destroy beta pancreas cells/pancreas do not produce enough insulin;
  • reduced uptake of glucose from the blood;