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Biology HL > Option D: Human Physiology > Flashcards

Option D: Human Physiology Flashcards

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1
Q

essential nutrients

A
  • nutrients that can’t be synthesized by the body

- yet are necessary for function

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2
Q

dietary minerals

A
  • inorganic substances required by living organisms
  • they can be recycled but not with 100% efficiency
  • thus small amounts of those minerals in our diet are necessary
  • as most of them are soluble in water, they are generally referred to as “electrolytes”
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3
Q

why are Ca2+ ions necessary?

A
  • they are used in the growth and repair of bones

- bones require constant repair so small amounts of Ca ions are always being lost and must be replaced

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4
Q

why are Fe2+ ions necessary?

A
  • Fe2+ ions are an important component of haemoglobin, found in erythrocytes (RBCs)
  • RBCs have a lifespan of 4 months and its components are recycled in the liver after it reaches its limit
  • however not all iron can be recovered
  • so it has to be replaced in the diet
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5
Q

vitamins

A
  • chemically diverse carbon (organic) compounds)
  • not all vitamins can be synthesized by a particular organism
  • so it relies on vitamin intake from other organisms
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6
Q

vitamin C as an essential vitamin

A
  • it’s not an essential vitamin for most vertebrates but it is for humans
  • if humans go without vit C for extended periods, they become afflicted with the deficiency disease scurvy
  • it’s produced from glucose in the kidneys of some animals and in the livers of others
  • its synthesis requires 4 enzymes in a metabolic pathway
  • the 4th enzyme’s gene coding is defective in all humans
  • this makes it an essential vitamin
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7
Q

vitamin D as an essential vitamin

A
  • along with Ca2+, vit D is necessary for proper formation of bones
  • going without adequate vit D during adolescence may lead to rickets, a disease causing bone deformities
  • bones near growth plates (areas at the end of developing bones) don’t mineralize properly
  • this leads to irregular, thick, and wide bone growth
  • children with rickets won’t reach their optimal height and their legs are bowed inwards/outwards at the knees
  • adults don’t develop rickets but will instead develop osteomalacia (i.e. soft bones)
  • the human skin epidermis contains precursors that can synthesize vit D when stimulated by UV rays in sunlight
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8
Q

essential fatty acids

A
  • alpha linolenic acid (omega-3)

- linoleic acid (omega-6)

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9
Q

cholesterol as an indicator of coronary heart disease

A
  • people may develop plaque on their arteries
  • sufficient build-up of plaque on coronary arteries leads to coronary heart disease (CHR)
  • if enough build-up occurs to block a coronary artery, a heart attack occurs
  • one component of plaque is cholesterol
  • thus monitoring blood cholesterol levels can reduce the risk of heart attacks
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10
Q

no. of essential amino acids to humans

A

9 out of 20

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11
Q

importance of having essential amino acids in diet

A
  • lack of essential amino acids affects protein synthesis

- human body has no storage mechanism for amino acids

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12
Q

phenylketonuria (PKU)

A
  • genetic disease causing inability to metabolize the amino acid phenylalanine
  • due to mutation of gene carrying information on the enzyme phenylalanine hydroxylase, which breaks down phenylalanine
  • this inability causes excess buildup of phenylalanine in the bloodstream and in tissues
  • resulting in seizures, mental deficiencies, behavioural problems, etc
  • the PKU gene is recessive
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13
Q

treating phenylketonuria

A

having a diet that limits protein sources high in phenylalanine

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14
Q

malnutrition

A
  • nutritional problems

- caused by deficiencies/imbalances/excess of nutrients in the diet

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15
Q

malnutrition due to deficiency

A
  • growth becomes stunted/irregular

- in the case of Ca2+/vit D, children contract rickets

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16
Q

malnutrition due to imbalance

A

1 or more essential amino acids may be lacking

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17
Q

malnutrition due to excess

A

obesity

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18
Q

autonomic activities

A

activities occurring at the subconscious level

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19
Q

appetite control center

A

hypothalamus

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20
Q

how does the hypothalamus regulate appetite?

A
  • full stomach –> electrical impulses sent to hypothalamus
  • intestines + pancreas produce hormones to transmit info to the hypothalamus
  • adipose (fat) tissues produce the hormone leptin to transmit info to the hypothalamus
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21
Q

health implications of anorexia

A
  • anorexia is an eating disorder characterized by having an unhealthy body ideal
  • tendencies include starving oneself, coupled with excessive exercise
  • insufficient amount of essential nutrients –> body systems are negatively affected
  • without adequate essentials, the heart gets smaller and weaker over time
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22
Q

health risks of obesity

A

more likely to develop hypertension and type II diabetes

hypertension:

  • high blood pressure
  • increased strain on heart and arteries
  • some factors of HBP are uncontrollable (e.g. age) but others are (e.g. BMI)

type II diabetes:

  • resistance to insulin = can’t metabolize glucose correctly
  • glucose can no longer be stored effectively and remains at higher concentrations in the bloodstream
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23
Q

what happens during starvation?

A
  • body tissues are digested for their stored nutrients
  • their own skeletal muscles are used as a source of amino acids to make other proteins
  • the skeletal muscles are still there but barely noticeable
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24
Q

digestion

A
  • chemical process
  • requires secretion of digestive fluids
  • these secretions are controlled by the nervous and endocrine systems
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25
Q

importance of regulating digestive fluids

A

would be wasteful + possibly harmful to continuously secrete digestive juices

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26
Q

exocrine glands

A
  • secretes into ducts (NOT into bloodstream)

- the ducts take the secretion either out of the body or into the lumen of the gut

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27
Q

examples of exocrine glands

A
  • lacrimal glands
  • gastric glands
  • pancreas
  • liver
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28
Q

function of lacrimal glands

A
  • secretes tears
  • taken by ducts to outer section of the eye
  • for lubrication
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29
Q

function of gastric glands

A
  • secretes gastric fluid
  • taken to stomach lumen
  • mucus secretions protect stomach lining
  • HCl denatures proteins and its pH kills some pathogens
  • the enzyme pepsin breaks down proteins
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30
Q

function of pancreas (exocrine gland only)

A
  • secretes pancreatic fluid
  • taken to the duodenum
  • contains digestive enzymes and a bicarbonate solution to neutralize partially-digested food

(NOTE: as the pancreas also secretes hormones into the bloodstream, it’s also an endocrine gland)

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31
Q

function of liver (exocrine gland only)

A
  • secretes bile
  • taken to the gallbladder and duodenum
  • for emulsification of lipids
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32
Q

mechanisms regulating digestive fluids

A
  • nervous system: seeing/smelling/thinking about food triggers digestive secretions
  • endocrine system: includes all glands that secrete hormones into the bloodstream
  • the two systems control the volume and content of secretions e.g. in the stomach lumen
33
Q

gastric pit

A
  • numerous small exocrine glands in the stomach lining
  • pit-like structures lined with cells that secrete substances into the lumen
  • secretions include: mucus, HCl, pepsinogen
34
Q

gastric fluid

A

the overall secretions of gastric pits

35
Q

gastrin

A
  • hormone released by certain stomach cells
  • secretions are controlled by the nervous system
  • gastrin stimulates the production of more gastric juice
36
Q

how does the nervous system regulate gastric juice during digestion?

A
  • the thought/smell/sight/taste of food sends an electrical impulse to the medulla oblongata in the brain stem
  • action potentials are sent by the vagus nerve to the stomach to stimulate the secretion of gastric juices and gastrin
  • as gastrin joins the bloodstream, it stimulates more production of gastric juice in other areas of the stomach
  • when food enters the stomach, the stomach walls become distended (expanded)
  • more messages are sent to the medulla oblongata, which sends back impulses to maintain/increase gastric juice secretion
  • when the chyme (partially-digested food) passes into the duodenum, a set of signals stimulates the secretion of the hormone secretin
  • it terminates the secretion of HCl and pepsinogen
37
Q

how are the acidic conditions of the stomach suitable for digestion?

A
  • HCl helps prevent food poisoning by destroying many pathogens
  • also provides a pH that favors certain hydrolysis reactions
  • pepsinogen is an inactive enzyme that activates in low pH to become the enzyme pepsin, which breaks down proteins into amino acids
  • however, the highly acidic conditions also cause health problems
  • acid reflux is a condition in which oesophagus walls are damaged by gastric fluids
  • stomach ulcers are made worse by the acidic gastric juice
38
Q

how have health problems caused by gastric juices been mitigated?

A
  • proton pump inhibitor drugs were developed

- they inhibit the production of HCl in gastric pits

39
Q

what causes stomach ulcers

A
  • it was believed that nothing could survive in the pH 2 conditions of the stomach
  • but H. pylori bacteria can survive by burrowing into the mucous layer to infect stomach lining cells
  • they then neutralize stomach acid using the enzyme urease to create ammonia
  • infection leads to gastritis and stomach ulcers
40
Q

how are villi adapted to their function?

A
  • each villus has epithelial cells with microvilli for increased SA
  • digested molecules pass through these cells before entering a villus
  • one side of each epithelial cell is in direct contact with the fluid in the lumen (i.e. digested molecules)
  • tight junction: epithelial cells are held tightly together by shared proteins
  • this prevents undigested food from entering the villus without passing through a plasma membrane
  • some molecules are absorbed via active transport, so each epithelial cell contains numerous mitochondria
  • near the epithelial cells is a capillary bed for absorption into the bloodstream
41
Q

importance of fibre in diet

A
  • the higher the fibre content, the more efficiently undigested material moves through the large intestine
  • bc fibre can’t be digested
  • high fibre content helps all solid waste to continue moving
  • this prevents the waste from remaining in the large intestine for long
42
Q

symbiotic conditions in the large intestine

A
  • a large amount of bacteria lives in the large intestine
  • they thrive due to the water, warmth, and food material provided
  • in turn they provide vit K, which is necessary for blood clotting
43
Q

circulation of blood to and from the liver

A
  • hepatic artery: supplies oxygenated blood
  • hepatic portal vein: brings absorbed nutrients from intestines
  • hepatic vein: brings blood from liver to vena cava, then right atrium
44
Q

hepatic portal vein

A
  • receives blood from all the capillaries in the small intestine

unlike other blood vessels arriving at an organ, it:

  • is filled with low-pressure deoxygenated blood
  • contains a variable amount of nutrients depending on the type of food ingested and the timing of ingestion/digestion/absorption
45
Q

hepatocyte

A
  • liver cells that filter toxins in the bloodstream

- they chemically alter toxins so they either become useful or are added back to be eliminated via kidney filtration

46
Q

role of the liver with relation to RBCs

A
  • as RBCs don’t have a nucleus, their lifespan is short (4 months)
  • a single RBC contains 250 mil haemoglobin proteins
  • each haemoglobin contains 4 polypeptides that contains a non-protein haem group at the centre
  • the liver makes sure the RBCs’ components are recycled as much as possible
47
Q

how is each RBC component recycled?

A
  • sinusoids are lined with Kupffer cells (specialized WBCs)
  • they remove RBCs via phagocytosis
  • all 4 polypeptides are hydrolysed into amino acids in the Kupffer cell
  • amino acids are returned to the bloodstream or deaminated by the liver (depending on blood conc)
  • haem groups are separated from the globin chain and sent to nearby hepatocytes for further modification
  • the iron is removed from each haem group and sent to the bone marrow
  • iron-less haem groups are modified to bilirubin (an important component of bile)
48
Q

role of the liver with relation to cholesterol

A
  • lipids are not water-soluble, so they combine together
  • this forms lipid droplets in the lumen of the stomach and small intestine
  • the enzyme lipase can break down lipids, but only whatever is on the surface
  • bile, a fluid secreted by the liver, helps emulsify lipids (i.e. breaks them into smaller droplets), increasing their SA for faster digestion
  • bile is made up of 2 components: bile salts and bilirubin
  • bilirubin is synthesized from the remains of a haem group after Fe2+ is removed
  • bile salts are synthesized in the liver from surplus cholesterol
49
Q

plasma proteins

A

proteins circulating in blood plasma

50
Q

examples of plasma proteins

A
  • albumin

- fibrinogen

51
Q

albumin

A
  • protein regulating the osmotic balance of blood

- used as a carrier molecule for bile salts and other fat-soluble molecules

52
Q

fibrinogen

A
  • protein used in blood clotting
  • when a blood vessel is damaged, the inactive enzyme prothrombin activates into thrombin and converts fibrinogen to fibrin
  • the fibrin mesh traps blood clots to seal in the cut area
53
Q

role of the liver in plasma protein production

A

hepatocytes secrete plasma proteins using golgi apparatus and the endoplasmic reticulum

54
Q

role of the liver in the regulation of nutrients

A
  • the hepatic portal vein transports nutrients directly from the small intestine
  • the liver regulates the nutrient levels so that nutrient levels are more stable and consistent in the hepatic vein compared to the hepatic portal vein
55
Q

sinusoids

A
  • capillaries of the liver

- where exchanges occur between blood and hepatocytes

56
Q

differences between sinusoids and regular capillaries

A
  • sinusoids are wider than regular capillaries
  • they’re lined with endothelial cells with gaps in between
  • the gaps allow large molecules (e.g. proteins) to be exchanged
  • as hepatocytes are in direct contact with blood components, exchanges are more efficient
  • sinusoids contain Kupffer cells
  • they receive a mixture of oxygen-rich and nutrient-rich blood
57
Q

how does alcohol cause liver damage?

A
  • alcohol can be mistaken for useful nutrients and brought to the liver hepatocytes
  • each time blood passes through the liver, the hepatocytes attempt to remove the alcohol
  • over time the exposure incurs damage to the liver cells
58
Q

types of liver damage due to alcohol

A
  • cirrhosis: scar tissue where hepatocytes have been destroyed due to alcohol exposure – areas with cirrhosis no longer function
  • fat accumulation: damaged areas may build up fat instead of normal liver tissue
  • inflammation: swelling of damaged liver tissue due to alcohol exposure (i.e. alcoholic hepatitis)
59
Q

nutrients stored by the liver

A
  • glycogen: polysaccharide of glucose
  • iron: removed from haemoglobin and later sent to bone marrow
  • vit A: associated with good vision
  • vit D: associated with healthy bone growth
  • vit B12/K
60
Q

jaundice

A
  • condition caused by excess bilirubin in bloodstream
  • as bilirubin is a yellow pigment, people with jaundice have a yellow tinge to their skin and whites of their eyes
  • if untreated, may cause acute bilirubin encephalopathy
  • because excess bilirubin levels are toxic to brain cells
61
Q

types of jaundice

A
  • infant jaundice: found in babies born prematurely (their liver can’t fully process bilirubin into bile)
    treatment: exposure to blue-green light spectrum – this changes the shape and structure of bilirubin molecules
  • adult jaundice: similar symptoms and consequences, but the cause is not an immature liver (obviously) but to liver damage
62
Q

how are heart muscles adapted to their function?

A
  • cardiac muscle cells are connected via intercalated discs
  • discs contain small holes called gap junctions where cytoplasm and electrical impulses can be transmitted/shared
  • muscle cells form branches, so they can chemically communicated with one another
  • result: all the cells work together to contract as a unit
63
Q

how do the SA and AV nodes work?

A
  • the SA node (group of cells in the right atrium) creates an impulse that extends across muscle cells in the atria via intercalated disks and branches
  • however, these disks and branches don’t extend into the ventricles
  • the ventricles get their signal from the AV node, which doesn’t act spontaneously but transmits the signal to contract from the SA node after a brief delay
64
Q

what happens during the delay between the SA and AV impulse?

A
  • both atria have enough time to complete atrial systole (process of contracting and forcing blood into the ventricles) before the AV valves close
  • heart valves open and close based on pressure differences on either side of the valve
  • after the delay, the ventricles contract as the AV valves close and SL valves open, forcing the blood out of the ventricles into the aorta
65
Q

how is ventricle contraction coordinated?

A
  • ventricle muscular walls are very thick (thicker than atrial walls)
  • there are too many cells in the ventricular walls for efficient cell-to-cell communication
  • thus the ventricles rely on nerve fibres to quickly spread the impulse from the AV node
  • this is done via a system of conducting fibres from the AV node to the septum between the two ventricles
  • from there, branches called Purkinje fibres are spread out into the thick cardiac muscle tissue of the ventricles
  • the impulse is carried from the conducting fibres to the muscle fibre
  • gap junctions conduct them across the ventricles
66
Q

how are normal heart sounds made?

A
  • the thumping sounds are caused by the opening and closing of the SL and AV valves
  • the first sound is the AV valves closing
  • the second sound is the SL valves closing
67
Q

systolic pressure

A

measurement of pressure in arteries when ventricles contract (undergo systole)

68
Q

diastolic pressure

A

measurement of pressure in arteries when ventricles are at rest and refilling with blood

69
Q

hypertension: causes, effects, and treatment

A 
- consistent HBP
cause:
- loss of elasticity in blood vessels
- build-up of plaque in arteries
effect: increased risk of heart attack/stroke
treatment:
70
Q

thrombosis: causes, effects, and treatment

A
  • thrombus (clot) develops and breaks loose within a blood vessel
    cause: usually plaque build-up – the thrombus is a formed from a part of the plaque breaking away
    effect: can be fatal if the thrombus gets stuck in lung or coronary arteries
    treatment: anticoagulant medications – prevents blood clotting from occurring as quickly
71
Q

artificial pacemakers and their use

A
  • small battery-operated device implanted under the
    skin
  • sets the heart rate in the same way that a healthy SA node would
  • connected to one or more wires (leads) that are threaded into a blood vessel leading directly into the interior of the heart
  • a very small electrical shock occurs at regular intervals, each shock triggering a cardiac cycle
  • placement of lead(s) is dependent on the patient’s heart problem and how many leads are being placed
72
Q

defibrillation devices and their use

A
  • heart attack can mean the heart has stopped (cardiac arrest) or is no longer in sequence with the set of electrical impulses typical of a cardiac cycle (arrhythmia)
  • effect: blood is not being pumped effectively to the rest of the oxygen-deprived body
  • defibrillation: process involving a device that delivers an electric shock to the heart
  • it resets the electrical signals starting with the SA node
  • the heart will continue beating on its own once the electrical shock has been delivered
73
Q

factors contributing to risk of coronary heart disease (CHD)

A

CHD: plaque build-up in arteries and the problems associated with them

risk factors:

  • obesity
  • stress
  • HBP
  • cholesterol problems
  • remember that these risk factors have a cascading effect (one factor affects another)
    e. g. stress → smoking and overeating → obesity → HBP, cholesterol problems, etc
74
Q

steroid hormones

A
  • controls protein production within the target cell
  • synthesized from cholesterol
  • in a cell, it binds with a receptor protein to form a receptor–hormone complex
  • the complex passes through the nuclear membrane and selectively binds to 1+ specific gene(s)
  • can inhibit or promote transcription
  • target cell(s) have their biochemistry dramatically altered due to the presence of the hormone
75
Q

peptide hormones

A
  • composed of amino acids
  • upon reaching a target cell, it binds to a receptor protein on the outer surface of the cell membrane
  • the presence of the receptor protein determines whether or not a cell is a target cell
  • similar mechanics with enzyme-substrate specificity
  • a peptide hormone’s chemical binding to a receptor protein activates a secondary messenger molecule in the cytoplasm
  • the secondary messenger chemically activates 1+ other messenger molecule(s) in the cytoplasm in a cascade of reactions
  • the final messenger either activates an enzyme in the cytoplasm (thus allowing a rxn that was not possible before), or activates a transcription factor that enters the nucleus and either promotes or inhibits transcription in general
76
Q

how does the posterior lobe of the pituitary gland communicate with the hypothalamus?

A
  • hormones produced in the hypothalamus are secreted in the posterior pituitary
  • posterior lobe of the pituitary contains axons of neurosecretory cells (very long cells whose dendrites and cell bodies are located in the hypothalamus)
  • hormones are produced in the hypothalamus and secreted in the posterior pituitary gland (in a similar way to the release of a neurotransmitter)
77
Q

how does the anterior lobe of the pituitary gland communicate with the hypothalamus?

A
  • target cells of hormones produced + secreted in the hypothalamus are the anterior pituitary cells
  • hypothalamus contains capillary beds that take in hormones produced by the hypothalamus itself (also
    produced by neurosecretory cells, but the kind entirely within the hypothalamus)
  • these hormones are often referred to as releasing hormones (e.g. gonadotropin-releasing hormone, GnRH)
  • capillary beds join together into a blood vessel (portal vein) extending down into the anterior pituitary
  • the portal vein branches into a second capillary bed that allows the releasing hormones to leave the bloodstream for their target cells (anterior pituitary cells)
  • releasing hormones stimulate the anterior pituitary cells
    to secrete specific hormones
78
Q

how hormones control milk secretion

A
  • the pituitary hormones prolactin (anterior) and oxytocin (posterior)
  • during pregnancy, increasing prolactin levels → development of milk-producing cells
  • naturally high levels of oestrogen during pregnancy inhibit those cells from releasing milk
  • after birth, 2 things occur: drastically lowered levels of oestrogen (due to birth), and high levels of oxytocin (needed to stimulate uterine contractions)
  • without oestrogen to inhibit, milk-producing cells begin releasing milk
  • oxytocin stimulates contraction of smooth muscle tissue surrounding milk ducts → milk ejection
  • production of both hormones is increased by the stimulation of the nipple caused by a suckling infant
  • i.e. positive feedback
79
Q

examples of hormones produced by pituitary gland

A
  • LH
  • FSH
  • ADH
  • prolactin
  • oxytocin

Biology HL (12 decks)

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