M103 T3 L10

Question 1

Why isn’t bp mainly measured at the GP?

Answer 1

white coat syndrome

Question 2

What are the two main methods for measuring bp over a 24 hour period?

Answer 2

ambulatory bp monitoring

home bp monitoring

Question 3

What is the range for a high and a normal bp?

Answer 3

high: x > 150 / 95 mmHg over 24hrs
normal: 120 / 80 mmHg

Question 4

What is the equation for bp?

Answer 4

bp = cardiac output x total peripheral resistance

Question 5

What is the equation for cardiac output?

Answer 5

cardiac output = stroke volume x heart rate

Question 6

What is the process by which the symp NS constricts arterioles to increase bp?

Answer 6

baroreceptors detect low cardiac output and low bp in the aorta
sends messages to medulla oblongata
symp NS activated
releases noradrenaline and adrenaline from adrenal glands
noradrenaline binds to alpha-1 receptors present on the smooth muscle of the arterial
causes constriction of the arterioles
increase in afterload
causes the left ventricle to have to contract with more force to pump blood into the systemic circulation
bp increases

Question 7

Which receptors does noradrenaline bind to?

Answer 7

a & b-1 receptors

Question 8

In what three ways can the symp NS increase bp?

Answer 8

constricting arterioles / venules
increasing peripheral resistance
increasing the frequency and force of contraction of the heart

Question 9

What is the process by which the symp NS constricts venules to increase bp?

Answer 9

noradrenaline binds to a-1 receptors present on the smooth muscle of the venules
constricts the veins - blood is squeezed back up which helps it return to the heart, increases preload
as preload increases, the force of contraction of the heart will increase to get rid of the additional blood that is returning
so cardiac output will increase

Question 10

What is the relationship between preload and the force of contraction?

Answer 10

the greater the preload, the more powerful the contraction is

Question 11

What types of drugs are used to treat hypertension?

Answer 11

a-1 antagonist

b-1 antagonist / beta blockers

Question 12

What three things do a-1 antagonists reduce?

Answer 12

arterial constriction
peripheral resistance
preload

Question 13

What effect do b-1 antagonists have on hypertension?

Answer 13

reduce the ability of the symp NS to increase the frequency and or to increase the force of contractility in the heart

Question 14

What effect does the symp NS have on the heart?

Answer 14

increases frequency of contraction

increases force of contraction

Question 15

What effect does the parasymp NS have on the heart?

Answer 15

decreases frequency of contraction

decreases force of contraction

Question 16

How does the symp NS increase force and rate of contraction?

Answer 16

(nor)adr < b1 receptors < cAMP < ca2+ < SA node cells

releases adr and noradr that act on β1 receptors
increases cAMP which increases intracellular calcium in the SA node cells (increases rate) and in the ventricular myocytes (increases force of contraction)

Question 17

How does the symp NS decrease the rate of contraction?

Answer 17

releases NT ACh
binds to M2 receptor
this decreases cAMP
which decreases the frequency of heart contractions

Question 18

What are the two types of receptors that respond to ACh?

Answer 18

muscarinic

nicotinic

Question 19

How are IP3 levels increased?

Answer 19

noradrenalin acts on a-1 receptors

Question 20

How does IP3 control calcium movement?

Answer 20

increases calcium influx into the muscle cell from the outside
drives the release of calcium from intracellular stores

Question 21

What are the effects of the release of calcium from intracellular stores?

Answer 21

the muscle cells constrict
the blood vessels constrict
increase in the amount of blood returning to the heart
peripheral resistance increases

Question 22

What system is activated when the bp is low?

Answer 22

the RAAS system

Question 23

What does the RAAS do on activation?

Answer 23

causes a decrease in renal perfusion

signals cells in the juxtaglomerular apparatus

Question 24

What is the function of renin?

Answer 24

to catalyse angiotensinogen into Ang I

Question 25

What happens to Ang I?

Answer 25

circulates in the bloodstream | is converted into Ang II - its active form by ACE

Question 26

Where does Ang I converted into II by ACE?

Answer 26

bc the lungs and kidneys have such a rich vascular supply, most of the conversion occurs here

Question 27

Where is ACE found?

Answer 27

in endothelial cells lining the blood vessels all over the body

Question 28

What receptor does Ang II bind to?

Answer 28

AT-1 receptor

Question 29

What happens when Ang II binds to the AT-1 receptor?

Answer 29

stimulates the release of the steroid aldosterone from the adrenal cortex facilitates the release of noradrenaline from symp terminals into blood vessels arteriolar vasoconstriction

Question 30

What are the effects of increased salt and water absorption?

Answer 30

blood volume, stroke volume and bp ics in a knock on effect

Question 31

What is the effect of aldosterone release?

Answer 31

stimulates the kidney to preserve salt and water in the body

Question 32

Where is ADH located?

Answer 32

made by the hypothalamus | stored in the posterior pituitary gland

Question 33

What are the effects of ADH?

Answer 33

makes the tubules in the kidneys more permeable towards collecting water increases blood volume increases the amount of blood returning to the heart increases stroke volume and bp causes renal perfusion to increase negative feedback system turns off the signal for ADH

Question 34

What types of drugs reduce bp?

Answer 34

ACE inhibitors AT1-receptor blockers renin inhibitors

Question 35

What are the effects of ACE inhibitors?

Answer 35

block the action of ACE this reduces the amount of Ang II produced reduce Ang II's effects on all of these systems will reduce bp

Question 36

What is the mechanism by which Ang II is released?

Answer 36

``` dcs in cardiac output, bp and in renal blood flow dcs'd pressure in the glomerulus reduces filtration in the kidneys kidney function is impaired the kidneys activate the RAAS Ang II released ```

Question 37

How does Ang II regulate peripheral resistance?

Answer 37

acts on AT-1 receptor to increase IP3 levels increases intracellular calcium, arteriolar vasoconstriction increases peripheral resistance, bp

Question 38

How does blood travel through the nephron?

Answer 38

enters the glomerulus via the affterent arteriole filtered out into Bowman's capsule the glomerular filtrate passes into the PCT down through the LoH, into the DCT into the collecting duct where it'll drain into the ureta and the bladder exits via the effterent arteriole

Question 39

Where does salt and water reabsorption occur in a nephron?

Answer 39

PCT, DCT | loop of Henle

Question 40

What is the mechanism for how aldosterone works?

Answer 40

aldosterone activates cytoplasmic receptors bind to the nucleus increases the expression of Na+ channels increased Na+ and water retention

Question 41

Where are aldosterone receptors located?

Answer 41

inside the cytoplasm | not on the outside of the cell membrane

Question 42

How does aldosterone reach its receptor?

Answer 42

aldosterone is a steroid - very lipophilic so can easily pass through the cell membrane to get inside of the cytoplasm

Question 43

What happens when aldosterone binds to its mineralocorticoid receptors?

Answer 43

causes the receptor and the ligand (aldosterone ) to translocate to the nucleus there aldosterone binds to various response elements on DNA drives the transcription and translation of two proteins

Question 44

Where is ENaC located?

Answer 44

it sits in the membrane of the DCT cell that lines the lumen where urine is being formed

Question 45

What cells make up the lining of the DCT?

Answer 45

simple cuboidal cells

Question 46

How does ATPase transfer ions into and out of the cell?

Answer 46

pumps 3Na+ into the cell via the ENaC, 2K+ out of the cell | as the concentration of na rises inside the DCT, gets pumped out into the blood - reversed

Question 47

What patient features will guide a decision on choosing which drug to treat high bp?

Answer 47

Age, Race | Co-existing diseases

Question 48

What two drug options are under 55s likely to be prescribed as 1LT when treating hypertension?

Answer 48

ACE inhibitor | Ang receptor blockers

Question 49

How does race influence what drug is most effective when treating high bp?

Answer 49

ACE inhibitors / beta blockers may be less efficacious in black people even if under 55, treated with ca channel blocker

Question 50

How do co-existing diseases influence what drug is most effective when treating high bp?

Answer 50

the side effects of drugs in the treatment might make existing coexisting conditions that the patient is suffering from, worse

Question 51

What two drug options are over 55s likely to be prescribed as first line treatment when treating high bp?

Answer 51

ca2+ channel blockers

Question 52

How do calcium channel blockers work in over 55s to treat high bp?

Answer 52

Ca's important for vasoconstriction, so if Ca channel blockers are used, blood vessels relax peripheral resistance and bp decreases

Question 53

Why might using other drugs that aren't calcium channel blockers for over 55s be dangerous?

Answer 53

some of these drugs can reduce the rate and the force of contraction of the heart

Question 54

What is another term for adrenaline?

Answer 54

epinephrine

Question 55

How is bp measured instead of at the GP?

Answer 55

it is mostly measured over a 24hr period bc of white coat syndrome

Question 56

Why is it called the juxtaglomerular apparatus?

Answer 56

bc it is next to (juxta-) the glomerulus

Question 57

What is the role of the juxtaglomerular apparatus?

Answer 57

Quality Control | to maintain bp and to act as a quality control mechanism to ensure proper GFR and efficient Na+ reabsorption