Option H: Further Human Physiology

H 1.1 State that hormones are chemical messengers secreted by endocrine glands into the blood and are transported to specific target cells.

H 1.2 State that hormones can be steroids (progesterone), proteins (insulin) and tyrosine derivatives (thyroid hormone).

H 1.3 Distinguish between the mode of action of peptide hormones and steroid hormones. 

Peptide hormones	Steroid hormones
Do not enter cell	Do enter the cell
Attach to cell surface receptor	Attach to receptor in cytoplasm
Act through secondary messenger	Act directly on DNA
Affect enzyme activity	Affect gene transcription

H 1.4 Outline the relationship between the hypothalamus and the pituitary gland.

• Portal veins connect hypothalamus to the anterior pituitary gland.
• Neurosecretory cells connect hypothalamus to posterior pituitary gland
• Neurosecretory cells secrete releasing factors into bloodstream which travel to posterior pituitary for storage.

 H 1.5 Explain the control of ADH secretion by negative feedback.

ADH secreted by hypothalamus; by neurosecretory cells; transport of ADH to posterior pituitary for storage; through axon; osmoreceptor cells monitor concentration of blood plasma; if blood plasma too concentrated, ADH released; kidney produces a small volume of hypertonic urine / reabsorption of water in collecting ducts; if plasma too dilute, ADH level of blood drops; kidney produces a large volume of hypotonic urine / little water reabsorbed from collecting ducts; controlled by negative feedback; 6 max

H 2.1 Digestive juices are secreted into the alimentary canal by glands, including salivary glands, gastric glands in stomach wall, the pancreas and the wall of the small intestine.

H 2.2 Explain the structural features of exocrine gland cells.

• Secretory cells grouped into acini and ducts
• Large amount of rough endoplasmic reticulum for synthesis of digestive enzymes
• Large amount of mitochondria to supply ATP for protein synthesis
• Large amount of vesicles in ducts to store digestive enzymes prior to secretion
• Secretory vesicles release their contents by exocytosis.

(b) Label the indicated structures in the micrograph of exocrine gland cells below.

I. ............................acinus cell/secretory cell/secretory cell............................

II. ......................................................duct..........................................................

H 2.3 Compare the composition of saliva, gastric juice and pancreatic juice.

Saliva - W E L M  S

• Water
• Electrolytes
• Lysozymes
• Mucus
• Salivary amylase

Gastric juice - WH P RM 

Water

HCl

Pepsin

Rennin enzymes

Mucus

Pancreatic juice - WACLBT

Water

Amylase

Bicarbonate

Carboxypeptidase

Lipase

Trypsinogen

H 2.4 Outline the control of digestive juice secretion by nerves and hormones, using the example of secretion of gastric juice.

• Gastric juice secretion involves both nerve impulses and gastrin hormone;
• Sight/smell of food causes nerve impulses to be sent via reflex action;
• Food in stomach stimulates chemoreceptors, that cause release of more gastric juice;
• Stretching of stomach stimulates secretion of hormone gastrin;

H 2.5 Outline the role of membrane-bound enzymes on epithelial cell surfaces in the small intestine during digestion.

• Some digestive enzymes, e.g. maltase) are immobilized in exposed plasma membranes of epithelial cells in intestinal villi.
• These digestive enzymes include disaccharidase enzymes which break down disaccharides.

H.2.6  Outline the reasons for cellulose not being digested in the alimentary canal.

Cellulase enzyme digests cellulose.
Human gut does not produce cellulase.
Thus cellulose remains undigested.
Instead cellulose is dietary fibre which plays a role in strengthening the gut muscles.

H 2.7 Explain why pepsin and trypsin are initially synthesized as inactive precursors and how they are subsequently activated.

Pepsinogen secreted by gastric glands in stomach wall;
Pepsinogen conversion to pepsin activated by HCl;
Autocatalytic reaction - pepsin causes conversion of pepsinogen to more pepsin;
Inactive precursor pepsinogen needed to prevent damage to stomach wall/selfdigestion;

H 2.8 Discuss the roles of gastric acid and Helicobacter pylori in the development of stomach ulcers and stomach cancers.

• Stomach ulcers are open sores in the stomach wall.
• Helicobacter pylori are bacteria that can inhabit various areas of the stomach and duodenum, causing mild inflammation of the stomach lining and possibly ulcers and stomach cancer.
• A strong relationship between H. pylori infection and ulcers has been identified.
• When in the gut lumen, H. pylori produces urease, an enzyme that neutralizes HCl, allowing the bacterium to form colonies in the stomach lining, living in the mucosa.
• As a result, helicobacter pylori survives in acidic conditions of stomach.
• H.pylori secretes protease which allows gastric acids to damage the stomach lining. 
• H. pylori produces cytotoxins that damage and form pores in the epithelial cell membrane of the stomach wall, causing inflammation.
• H. pylori is now treated as an infectious disease and antibiotics are administered in order to control the bacterium and to treat stomach ulcers.
• The prolonged presence of stomach ulcers can lead to tumour formation.
• A correlation between H. pylori infection and stomach cancer has been identified.

ulcers are sores/inflamed/infected/damaged areas in the stomach wall;
strong relationship/association between H. pylori infection and ulcers;
H. pylori survives acid conditions in the stomach;
H. pylori lowers acidity of stomach / secretes urease which lowers acidity;
H. pylori secretes protease which damages stomach lining/protective mucus;
H. pylori allows damage of stomach lining by gastric acids;
H. pylori now treated as infectious disease / controlled as treatment for ulcers;
(prolonged) presence of stomach ulcers may lead to the formation of
tumours/cancer;
association/correlation between H. pylori infection and stomach cancer; 6 max


H. pylori is a bacterium which causes gastritis;
stomach ulcers are open sores in the stomach wall;
prolonged presence of ulcers may lead to the formation of tumours;
cancer of the stomach is a malignant tumour in the stomach wall;
about 80% of gastric ulcers are caused by H. pylori;
H. pylori survives in the stomach mucosa;
producing urease;
which neutralizes gastric acid;
colonization by H. pylori opens up/weakens the (protective)
(mucosal/mucus) lining;
for digestive attack by gastric acid/HCl causing ulcers;
linking H. pylori to stomach ulcers was a paradigm shift in medicine;
cause was previously thought to be stress/lifestyle/diet;
H. pylori now thought to be primary cause / now treated as
infectious disease; 5 max

State the major role of Helicobacter pylori in the development of stomach ulcers.

causes increased acid secretion / produces toxins / forms pores in
epithelial cell membrane / produces urease which produces ammonia
(which is toxic) / resides in gastric mucous protected from immune
system reactions but cause inflammation and increase acid
production / destroys mucus lining exposure to acid/causing inflammation

Explain the control of thyroxine by negative feedback.

thyrotropin releasing hormone TRH produced in the hypothalamus;
transported to the anterior pituitary in the portal vein;
secretion of thyroxine stimulating hormone TSH by the anterior pituitary;
thyroxine stimulating hormone brings about the secretion of thyroxine from the thyroid gland;
two forms exist / T3, T4;
released into the bloodstream;
causes an increase in metabolic rate;
thyroxine inhibits the production / release of thyroxine releasing
hormone / thyroxine stimulating hormone;
increased metabolic rate / rise in body temperature monitored by
hypothalamus / causes decreased production of TRH;
thyroxine levels maintained within narrow limits;


H.2.9 Explain the problem of lipid digestion in a hydrophilic medium and the
role of bile in overcoming this.

• Lipid molecules tend to coalesce (join together).
• Enzyme lipase needs to have an active site to which a hydrophobic substrate binds.
• Lipids are only accessible to lipase at the lipid - water interface. 
• Bile molecules have a hydrophilic end and a hydrophobic end, and thus prevent lipid droplets coalescing.

H 3.1 Draw and label a diagram showing a transverse section of the ileum as seen under a light microscope.

H 3.2 Explain the structural features of an epithelial cell of a villus as seen in electron micrographs, including microvilli, mitochondria, pinocytotic vesicles and tight junctions.
Microvilli:

• LARGE surface area for absorption
• Facilitated diffusion channels for hydrophilic molecules
• Active transport pumps for moving molecules against concentration gradient

Mitochondria

• Provide ATP for active transport of molecules against concentration gradient.

Pinocytotic vesicles

• Formed by endocytosis, allow absorption of large numbers of molecules from digestion.

Tight junctions

• Proteins in membranes of adjacent cells lock together
• This forms a seal that prevents molecules from digestion passing between villus cells.

H 4.1 Outline the circulation of blood through liver tissue, including the hepatic artery, hepatic portal vein, sinusoids and hepatic vein. (Include difference in structure between sinusoids and capillaries).

• Hepatic artery brings oxygenated blood;
• Hepatic portal vein brings nutrients from small intestine;
• Hepatic artery and portal vein merge to form sinusoids where liver cells store and regulate nutrients;
• Hepatocytes regulate blood sugar level by storing glucose as glycogen; under influence of insulin carried by hepatic artery;

H 4.2 Explain the role of the liver in regulating levels of nutrients in the blood.

H4.3 Outline the role of the liver in the storage of nutrients, including vitamin A, vitamin D, iron and carbohydrate.

H 4.4 State that the liver synthesises plasma proteins and cholesterol. State that the liver has a role in detoxification. (contains catalase for breakdown of hydrogen peroxide).

H 4.6 Describe the process of erythrocyte hemoglobin breakdown in the liver, including phagocytosis, digestion of globin and bile pigment formation.

• erythrocytes rupture after 120 days; and absorbed by phagocytosis from blood by Kupffer cells in liver;
• Hemoglobin split into globin and heme groups;
• Globin digested to form amino acids
• Iron removed from heme groups leaving bile pigment bilirubin;
• bilirubin released into alimentary canal

erythrocytes rupture when they reach the end of their life span / after 120 days;
absorbed by phagocytosis / Kupffer cells in liver from blood;
hemoglobin split into globin and heme groups;
iron removed from heme leaving bile pigment / bilirubin;
bilirubin released into alimentary canal;
digestion of globin to produce amino acids;

H. 4.7 Explain the liver damage caused by excessive alcohol consumption.

• Alcohol abuse can cause liver inflammation; and nutritional deprivation
• Products of alcohol metabolism toxic to liver cells causing replacement of healthy liver cells with scar tissue; 
• alcohol abuse blocks blood flow through liver 
• cholesterol (product of alcohol metabolism) blocks bile duct, preventing removal of toxins via the bile;

can cause inflammation/fatty liver/cirrhosis of the liver from alcohol abuse;
usually from prolonged/excessive drinking / OWTTE;
products of alcohol metabolism toxic to cells / alcohol consumption reduces antioxidant activity;
replacement of healthy liver cells with fibrous/scar tissue;
blocks blood flow through liver / loss of functional liver cells / blocks normal metabolic carbohydrates/fats/proteins;
decreased ability to remove toxins (through bile)/bacteria / production of bile and blood proteins;
nutritional deprivation / susceptible to infection/hepatic viruses; 5 max

H 5.1 Explain the events of the cardiac cycle, including atrial and ventricular systole and diastole, and heart sounds.

H. 5.3 Outline the mechanisms that control the heartbeat, including the roles of the SA (sinoatrial) node, AV (atrioventricular) node and conducting fibres in the ventricular walls.

• SA node is located in wall of right atrium of heart muscle, consisting of both nerve and muscle tissue.
• SA node is myogenic and initiates each impulse, acting as pacemaker of heart
• Impulses from SA Node spread out in all directions through walls of atria
• SA node connected to nerves which slow/accelerate heart rate.

SA node is located in the wall of right atrium of heart muscle;

has characteristics of both nerve and muscle tissue;

SA node initiates each impulse;

acts as pacemaker of the heart;

no nerve impulses needed for contraction / myogenic;

connected to nerves which slow/accelerate heart rate;

impulses spread out in all directions through walls of atria;

stimulates atrial systole/contraction;

fibres in walls of atria prevent impulses from reaching ventricles;

impulses reach AV node (after atrial contraction); 6 max


H. 5.4 Outline atherosclerosis and the causes of coronary thrombosis.
Atherosclerosis 

Coronary thrombis 

H 5.5 Discuss factors that affect the incidence of coronary heart disease.

Gas exchange

H 6.1 Define partial pressure

Amount of pressure that a gas exerts in a mixture of gases, dependent on the number of gases in the mixture.

H 6.2 Explain the oxygen dissociation curves of adult hemoglobin, fetal hemoglobin and myoglobin.

adult hemoglobin: [2 max]
rapid saturation of oxygen in the lungs;
rapid dissociation of oxygen as the oxygen concentration decreases;
oxygen released in the tissues where needed;

fetal hemoglobin: [2 max]
fetal hemoglobin curve to the left of adult hemoglobin;
higher affinity for oxygen than adult hemoglobin;
oxygen moves from adult hemoglobin to fetal hemoglobin;

myoglobin: [2 max]
myoglobin to the left of fetal hemoglobin;
higher affinity for oxygen than adult hemoglobin;
only releases oxygen at very low oxygen concentrations/in tissues;
oxygen reserve;

curve shows saturation level at each partial pressure of oxygen;
curve is to the left of hemoglobin/rises steeply;
myoglobin’s affinity for O2 is greater than hemoglobin;
becomes saturated at low oxygen concentrations;
provides oxygen when it is very low;
curve not sigmoid because myoglobin only has one heme group/globin;

H 6.3 Describe how carbon dioxide is carried by the blood, including the action of carbonic anhydrase, the chloride shift and buffering by plasma proteins.



H 6.4 Explain the role of the Bohr shift in the supply of oxygen to respiring tissues.

H 6.5. Explain how and why ventilation rate varies with exercise.

Exercise uses ATP through aerobic respiration, causing the CO2 concentration to increase, resulting in a lower pH content of blood. This is detected by chemoreceptors in the aorta and carotid arteries that send nerve impulses to breathing centre of brain. Nerve impulses are then sent to diaphragm and intercostal muscles to increase contraction/relaxation rates.

Exercise uses ATP, causing an increase in CO2 concentration, leading to lowering of pH. This is detected by chemoreceptors in the aorta and carotid arteries that send nerve impulses to the breaching centre of the brain. Nerve impulses are then sent to the diaphragm and intercostal muscles to increase contraction/relaxation rates.

H 6.6 Outline possible causes of asthma and its effects on gas exchange system

H6.7 Explain the problem of gas exchange at high altitudes and the way the body acclimatizes.
lung capacity can increase so that O2 intake becomes more efficient
per breath;
heart rate can increase so that available O2 is circulated around
bound more quickly to counter the reduced O2 availability;
increased number of red blood cells allow greater carrying capacity
(greater amount of hemoglobin);
muscles produce more myoglobin to bind more O2;