Topic 6- Human Physiology Flashcards

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1
Q

Pathogen

A
  • a disease causing organism

Can be cellular (living) or acellular (non living)

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2
Q

Bacteria

A
  • unicellular prokaryote that can reproduce quickly through binary fission and compete with host cells for space and/or nutrition
  • some even form mutualistic relationships with its host, ex; normal gut flora

Ex; salmonella, ear and eye infections

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3
Q

Viruses

A
  • needs a host cell to carry out functions of life, including reproduction, hence are ‘non living’
  • can either be DNA or RNA based
  • mutate, evolve and recombine quickly

Ex; flu, herpes, common cold etc..

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4
Q

Fungi

A

-are eukaryotes and reproduce with spores

Ex; athletes foot, ringworm

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5
Q

Protozoa

A

‘Described a simple parasites’, an organism that grows and feeds on an organism to the detriment of the hosts survival

Ex; malaria

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6
Q

Methods of transmission of pathogens

A
  • inhaled droplets, ex; influenza virus
  • direct contact, ex; herpes
  • bodily fluids, ex; HIV
  • animal vectors, ex; rabies, malaria
  • blood contact, ex; hepatitis B
  • ingested/swallowed, ex; salmonella
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7
Q

First line of defence

A

surface barriers that prevent the entry of pathogens into the body
(Skin and mucous membranes)

Skin:

  • protects external structures when intact
  • secretes lactic acid and fatty acids to lower the PH
  • contains biochemical defense agents

Mucuos membranes:

  • protects internal structures
  • contains biochemical defense agents, ex; lysozyme
  • consists of a thin region of living surface cells that release fluids to wash away the pathogens, ex; saliva, mucus, tears etc..
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8
Q

Clotting (haemostasis)

A

Mechanism by which broken blood vessels are repaired when damaged, blood clots at the site of a wound prevents blood loss and the entry of pathogens.

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9
Q

Platelets (small cell fragments)

A

Release clotting factors in response to a wound, in the presence of air the clot dries to form a scab which shields the healing tissue wound

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10
Q

Coagulation cascade

A

(Blood clotting is an example of a metabolic pathway/chain of biochemical reaction)

Draw diagram/structure of process with clear labels
Description:
1. Damaged tissue releases clotting factors
2. Clotting factors convert inactive prothrombin to active thrombin
3. Fibrinogen to insoluble fibrin
4. Fibrin forms mesh —> clots
5. Clots dry —-> scab

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11
Q

Coronary thrombosis

A

Formation of clot within blood vessels that supply and sustain the heart tissue.

Blood clots form in coronary arteries when the vessels are damaged as a result of the deposition of cholesterol.
Fatty deposits develop in the arteries—> lumen narrows—> restricts blood flow—> increase in pressure in the artery—> damage to arterial wall—> damaged region is repaired with fibrous tissue (significantly reduces the elasticity of the vessel wall)—> plaque and lesions start to form—> if plaque ruptures blood clotting is triggered—-> form a thrombus that restricts blood flow—> coronary muscle tissue dies as a result of a lack of blood and oxygen

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12
Q

Leukocytes (white blood cells)

A
  • phagocytes (provides body with a non specific immune response to any material judged to be foreign)
  • lymphocytes (B cells, T cells, killer cells)
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13
Q

Phagocytic Leukocytes

A

(Process by which solid materials, such as pathogens, dust, pollen or other allergens, are ingested by a cell via endocytosis)

  1. Phagocytic leukocytes circulate in the blood and move into body tissue in response to infection
  2. Damaged tissue releases chemicals which draws white blood cells to the site of infection (via chemotaxis)
  3. Pathogens are engulfed when cellular extensions surround the pathogen and then fuse to form an internal vesicle
  4. Vesicle is then fused to a lysosome (forming a phagolysosome) and pathogen is digested (by digestive enzymes), waste products are expelled (by exocytosis)
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14
Q

Second line of defense

A

Innate immune system, which is non-specific in its response
(Responds to an infection the same way every time)

Example: phagocytic leukocytes

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15
Q

Antigen

A

A substance or molecule often found on a cell/virus surface that causes antibody formation

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16
Q

Antibody

A

A globular protein that recognises a specific antigen and binds to it as part of an immune response (triggered by non-self cells)

(Antibodies are specific to certain antigens)

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17
Q

ABO blood group

A

Type A:
Antigen A
Anti B antibody
(Can have A or O blood, no to B or AB)

Type B:
Antigen B
Anti A antibody
(Can have B or O blood, no to A or AB)

Type AB:
Antigens A+B
Neither antibody
(Universal recipient)

Type O:
Neither A or B antigen
Both antibodies
(Universal donor, but can only have O blood)

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18
Q

Production of antibodies

A
  • many different lymphocytes exist, each type recognises one specific antigen
  • when the immune system is challenged by the invasion of a pathogen, the corresponding lymphocyte responds. It makes many clones of itself, each of which produces antibodies to the pathogen. This process is called ‘clonal selection’, as the right lymphocyte is selected and then cloned.
    (Some cloned cells remain as memory cells, ready for a second invasion by the pathogen— this is immunity)
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19
Q

Third line of defense

A

Adaptive immune system, which is specific in its response

Example: production of antibodies.

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20
Q

Antibiotics

A
  • are drugs used in the treatment and prevention of prokaryotic bacteria
  • are designed to disrupt structures or metabolic pathways
    (Targeted features include cell walls and membranes, protein and DNA/RNA synthesis)

(Can either kill the bacteria or suppress its potential to reproduce)
However as viruses do not possess a metabolism (uses the eukaryotic host cells metabolism) and have different ‘features’ (no cell wall and membrane to attack), antibiotics have no effect and must instead be treated with specific antiviral agents.

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21
Q

Antibiotic resistance

A

Caused by:

  • over prescription of antibiotics
  • patients not finishing their treatment
  • over use of antibiotics in livestock and fish farming
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22
Q

Antibiotic resistance is an example of evolution by natural selection

A
  • bacteria mutates and resistance to an antibiotic naturally arises
  • bacteria divides rapidly and therefore a resistant strain of bacteria can quickly proliferate
  • over time, strains of bacteria can become resistant to multiple strains of bacteria

Example: MRSA (methicillin resistant) and MSSA (methicillin susceptible)

MSSA is killed, MRSA survives.
MRSA reproduces and resistant gene proliferates/ MRSA population increases and becomes the dominant strain.

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23
Q

Penicillin

A

Howard Florey and Ernst Chain (test on mice)
8 mice were injected with haemolytic streptocci and 4 of these mice were subsequently injected with doses of penicillin, the untreated mice died of bacterial infection while those treated with penicillin all survived- demonstrating its antibiotic potential.

Fleming:
A penicillin mould began to grow and a halo of inhibited bacterial growth was observed around the mould, Fleming concluded that the mould was releasing a substance (penicillin) that was killing the nearby bacteria.

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24
Q

Human Immunodeficiency Virus (HIV)

A
  • gradually attacks T- helper cells (which helps produce antibodies) thus gradually attacked the immune system (our body’s natural defence again illness)
  • AIDS is a symptom caused by HIV (develops when the HIV is advanced), reduction in T cells leads to antibodies not being produced which leads to lowered immunity, body becomes susceptible to opportunistic infections, eventually resulting to death
  • HIV is a retrovirus: inserts its own RNA into the host cell, which then incorporates the RNA in its DNA.
    Once CD4 (T-cells) cells drop below a critical level (2–cells/mm3), the immune system is ineffective and the patient has AIDS
  • HIV is transmitted through the exchange of bodily fluids (such as unprotected sex, blood transfusion, breast feeding etc..)
25
Q

Neuronas

A

Nerve cells that transmit (rapid) electrical impulses

26
Q

Central Nervous System (CNS)

Peripheral Nervous System (PNS)

A
CNS= brain and spinal cord
PNS= everything outside of CNS
27
Q

Sensory neuron

Motor neuron

A

Sensory neuron: carries impulses from the sense organs to CNS
Motor neuron: carries impulses from the CNS to the effector (muscle or a gland), thus travels away from the body

28
Q
Cell body
Dendrites
Axon
Schwann cells
Nodes of ranvier
Myelin sheath 
(Draw labelled diagram)
A

Cell body (soma): contains nucleus and organelles
Dendrites: converts chemical information into electrical signals/transmits impulses
Axon: transmits electrical signals to terminal regions
Schwann cells despite myelin (double layer of phospholipid) which insulates the axons which allows the impulses to travel more quickly
Nodes of ranvier is the gap between the myelin insulation of Schwann cells

29
Q

Resting potential

A

(-70mv), the sodium potassium pump expels 3NA+ ions for every 2K+ ions admitted, this makes the cell interior relatively negative compared to the extra cellular environment.
- is the electrical potential across the plasma membrane of a cell that is not conducting an impulse (maintained by active transport- the exchange of ions requires the hydrolysis of ATP)

30
Q

Action potential

Draw graph diagram

A
  • is the reversal (depolarisation) and restoration (repolarisation) of the membrane protecting as an impulse travels along it.

Graph diagram explanation:
1. The sodium potassium pump maintain the electrochemical gradient of the resting potential, -70mv
2. In response to a stimulus, voltage gated NA+ channels open and sodium enters the neuron by diffusion. The entry of NA+ causes membrane potential to become positive (depolarisation= changes from - to +)
3. The depolarisation causes NA+ channels to close and voltage gated K+ channels open, K+ diffuses out of the neuron rapidly and the membrane potential becomes negative again (repolarisation)
4. Before neuron is ready to propagate another impulse, the distribution of NA+ and K+ needs to be reset, hence returning neuron to resting potential.
This enforced rest (refractory period) ensures the impulses can only travel in a single direction.

31
Q

Propagation (spreading/movement) of nerve impulses

A
  • causes the next part of the axon to reach the threshold potential

(Depolarisation at one axon segment triggers the opening of ion channels in the next segments, consequently the action potential spreads along the axon as a ‘wave’ of depolarisation)

32
Q

Myelinated axons & Saltatory conduction

A

-only allows action potential to occur at the un-myelinated nodes of ranvier, this forces action potential to ‘jump’ from node to node (Saltatory conduction)

Result of Saltatory conduction:
- impulses travels much more quickly, x100
- reduces degradation of the impulse, hence allows impulse to travel larger distances
- reduces energy expenditure over the axon
Disadvantage:
- takes up significant amount of space within an enclosed environment

33
Q

Synapse

A

Junction between neuronas and receptor (which impulses cannot travel past on its own)

34
Q

Diagram of synaptic transmission and explanation

A

Explanation:
As the nerve impulse reaches the terminal end of a pre-synaptic neuron, it triggered an influx of Ca+ (depolarisation causes the voltage gated calcium channels to open and Ca+ ions rushes in). This influx causes the vesicles containing neurotransmitters to move to the pre-synaptic membrane and fuse with it. The neurotransmitters are then released into the synaptic cleft (gap between neurons) by exocytosis. NT the diffuses across and binds to specific NT receptors on the post synaptic neuron. This causes sodium channels to open, causing sodium ions to enter, leading to depolarisation, ultimately initiating action potential.
The enzymes in the synaptic cleft then break down the NT. the products of this breakdown are taken back up by the pre-synaptic neuron by active transport (hence the large number of mitochondria)

35
Q

Acetylcholine

A

(Commonly released at neuromuscular junctions and binds to receptors on muscle fibres to trigger muscle contraction/activate muscle)

  1. Acetylcholine (ACh) is made from chloline and acetyl group
  2. In the synapse, ACh is rapidly broken down by the enzyme acetylchlolinesterase (AChE)
  3. Choline is transported back into the axon terminal and used to make more ACh

(Acetylcholine must be continually removed from the synapse as overstimulation can lead to fatal convulsions and paralysis)

36
Q

Neonicotinoid pesticides

A
  • cannot be broken down by acetylcholinesterase, resulting in permanent overstimulation of target cells
    As insects have a different composition of acetylcholine receptors (overstimulation and blocking of the receptors leading to paralysis and eventual death), they are significantly more toxic to insects than mammals, making them a globally used highly effective pesticide.

Disadvantage of such pesticide:

  • reduction in bird population (due to the loss of insects as a food source)
  • reduction in honey bee population

Advantage:
Protections of crops from pest species

37
Q

Hormones

A

Proteins that act as chemical messengers, secreted by endocrine glands into the bloodstream.

38
Q

Insulin & Glucagon

A
  • responsible for regulating blood glucose concentrations

- released from pancreatic pits called ‘islets of langerhans’ & act principally on the liver

39
Q

When blood glucose levels are high (ex:after eating)

A
  • insulin is released from B cells of the pancreas and cause a decrease in blood glucose concentration
  • may involve stimulating glycogen synthesis in the liver, and promoting glucose updates by the adipose tissue and liver, and increasing rate of glucose breakdown
40
Q

When blood glucose levels are low (ex: after exercise)

A
  • glucagon is released from A cells of the pancreas and cause an increase in blood glucose concentration
  • may involve stimulating glycogen breakdown in the liver, promoting glucose release but he liver and adipose tissue, and decreasing rate of glucose breakdown
41
Q

Diabetes Type 1

A
  • body not producing enough insulin
  • usually occurs during childhood (early onset)
  • requires insulin injections to regulate blood glucose
42
Q

Diabetes Type 2:

A
  • failing to respond to insulin production
  • controlled by managing diet and lifestyle
  • usually occurs during adulthood (late onset)
43
Q

Thyroxin

A

(Hormone secreted by the thyroid gland- targets most body cells)

  • increases metabolic rate/protein synthesis rate
  • helps control body temperature/increase heat production

Example: colder temp. Causes hypothalamus to stimulate thyroxine release which increases metabolic rate of the body to generate heat (raising body temp.)

44
Q

Leptin

A

(Hormone produced by adipose cells- targets apetite control centre of the hypothalamus)
- increase in adipose tissue increases leptin secretion into the blood, causing apetite inhibition and hence reduced food intake. Conversely, periods of starvation leads to a reduction in adipose tissue and hence less leptin is released, triggering hunger.

Mice experiment:
When obese mouse with no leptin was parabiotically fused to a healthy mouse, leptin in the blood of healthy mouse was transferred to the obese mouse. Hence obese mouse began to lose weight (demonstrating potential viability of leptin treatment)
But when obese mouse with a defective leptin receptor was parabiotically fused to a healthy mouse, leptin was transferred to the healthy mouse. Hence obese mouse remained obese and healthy mouse became emaciated.

45
Q

Human experiment

A
  • most cases of obesity are caused by unresponsiveness and not deficiency of leptin, hence very few experience significant weight loss in response to leptin injections
46
Q

Melatonin

A

(Hormone produced by the pineal gland in response to changes in light)
- affects synchronisation of the circadian rhythms including sleep timing and blood pressure regulation

Jet lag: pineal glad continues to secrete melatonin according to the ‘old’ time zones so that the sleep schedule is not synchronised to the new time zone

47
Q

Female

Male

A
Female= XX
Male= XY
48
Q

Y chromosome

A

Includes a gene called the SRY gene which leads to male development.
SRY gene codes for a testis-determining factor (TDF) that causes an embryonic gonad to form into testes, in the absence of TDF protein, the embryonic gonad will develop into ovaries

49
Q

Testosterone

A

(Secreted by the testes= main male reproductive hormone)

  • responsible for the pre-natal development of male genitalia
  • involved in sperm production
  • aids in the development of secondary sex characteristics (body hair, depending voice, muscle mass etc..)
50
Q

Estrógeno and Progesterone

A

(Secreted by the ovaries= main female reproductive hormones)

  • responsible for the development of secondary sex characteristics (breast development, growth of pubic hair etc..)
  • promotes the pre natal development of the female reproductive organs
  • involved in monthly preparation of egg release following puberty

(Initially, secreted by mothers ovaries and then the placenta, until female reproductive organs develop which occurs in the absence of testosterone)

51
Q

Label and Draw female reproductive system

A

Uterus: provides protection, nutrients and waste removal for the developing fetus, muscular walls contract to aid birthing process

Fallopian tube (oviduct): connects the ovary to the uterus, fertilisation of the egg occurs here

Ovary: produces estrógeno and progesterone, eggs stored to develop and mature

Endometrium (lining of the uterus): develops each month in readiness for the implantation of a fertilised egg (site of implantation becomes the placenta)

Vagina: accepts the penis during sexual intercourse and sperm is received here

Urether
Urethra
Kidney
Bladder

Cervix: entrance to the uterus, closes to protect the developing fetus and opens to form the birth canal

52
Q

Label and draw the male reproductive system

A

Vas Deferens (sperm duct): carries sperms to the penis during ejaculation

Prostate gland: adds alkaline fluids that neutralises the vaginal acids

Urethra: delivers semen during ejaculation and urine during excretion

Penis/ erectile muscle: muscle becomes erect to penetrate the vagina during sexual intercourse, delivers sperm to the top of the vagina

Epididymis: sperm mature here and become able to move, sperm stored awaiting ejaculation

Scrotum: protects and holds the testes outside of the body (to maintain a lower optimum temperature for sperm production)

Seminal vesicle: adds nutrients including fructose sugar for respiration, adds mucus to protect sperm

Testis: produces sperms and testosterone

53
Q

Pituitary hormones

A

FSH and LH

FSH: stimulates follicular growth in ovaries and stimulates estrógeno secretion

LH: surge causes ovulation

54
Q

Ovarian hormones

A

Estrogen and progesterone

Estrogen: thickens uterine lining, inhibits FSH and LH for most of cycle, stimulates FSH and LH release pre-ovulation

Progesterone: maintainers uterine lining, inhibits FSH and LH

55
Q

Follicular phase (day 1-4)

A
  • FSH is secreter from the pituitary gland and stimulates the growth of ovarian follicles
  • dominant follicle produces estrogen (acts on the uterus to stimulate the thickening of the endometrial layer), which inhibits FSH secretion (negative feedback) to prevent other follicles growing
56
Q

Ovulatory phase (day 5-14)

A
  • estrogen stimulates the pituitary gland to secrete hormones (positive feedback), which results in a large surge of LH and a decrease of FSH
  • LH causes dominant follicle to rupture and release an egg/ovulation
57
Q

Luteal phase (day 14-28)

A
  • ruptured follicle develops into a slowly degenerating corpus luteum (secretes high levels of progesterone and lower levels of estrogen)
  • estrogen and progesterone act on the uterus to thicken the endometrial lining (in preparation for pregnancy), also inhibits secretion of FSH and LH, preventing any follicles from developing

If fertilisation occurs, the developing embryo will implant in the endometrium.
If fertilisation doesn’t occur, corpus luteum will degenerate, resulting in estrogen and progesterone levels to drop and triggering menstruation and FSH cycle (cycle begins again)

58
Q

In vetro fertilisation (IVF)

A

Suspends normal ovulation (down regulation)
Collect multiple eggs (super ovulation)

Down regulation:
- drugs are used to halt the regular secretion of FSH and LH, which stops the secretion of estrogen and progesterone (takes about 2 weeks)

Super ovulation:
- injected with a large amount of FSH to stimulate the development of many follicles. Follicles are then treated with HCG, a hormone usually produced by a developing embryo. HCG stimulates follicles to mature and egg is then collected.

Fertilisation:
Extracted eggs are then incubated in the presence of a sperm sample (approximately 36 hours later).
Successfully fertilised eggs are then incubated before implantation.
For approximately 2 weeks before implantation, woman takes progesterone which maintained endometrium to aid implantation.

(Multiple embryos are transferred to improve chances of successful implantation, hence multiple births are a possible outcome)

59
Q

William Harvey’s Investigation of sexual reproduction

A
  • ‘seed and soil’ theory of Aristotle states that the male produces a seed which forms an egg when mixed with menstrual blood. The egg then develops into a fetus inside the mother.

Harvey studied animal reproduction, particularly in chickens and deers.

  • dissected female deer after mating to observe changes in the sexual organs and found none.
  • came to understand that menstrual blood did not contribute to the formation of a fetus, putting Aristotles idea to rest.