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M103 T3 > M103 T3 L10 > Flashcards

M103 T3 L10 Flashcards

1
Q

Why isn’t bp mainly measured at the GP?

A

white coat syndrome

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2
Q

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

A

ambulatory bp monitoring

home bp monitoring

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3
Q

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

A

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

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4
Q

What is the equation for bp?

A

bp = cardiac output x total peripheral resistance

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5
Q

What is the equation for cardiac output?

A

cardiac output = stroke volume x heart rate

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6
Q

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

A

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

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7
Q

Which receptors does noradrenaline bind to?

A

a & b-1 receptors

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8
Q

In what three ways can the symp NS increase bp?

A

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

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9
Q

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

A

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

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10
Q

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

A

the greater the preload, the more powerful the contraction is

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11
Q

What types of drugs are used to treat hypertension?

A

a-1 antagonist

b-1 antagonist / beta blockers

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12
Q

What three things do a-1 antagonists reduce?

A

arterial constriction
peripheral resistance
preload

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13
Q

What effect do b-1 antagonists have on hypertension?

A

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

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14
Q

What effect does the symp NS have on the heart?

A

increases frequency of contraction

increases force of contraction

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15
Q

What effect does the parasymp NS have on the heart?

A

decreases frequency of contraction

decreases force of contraction

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16
Q

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

A

(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)

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17
Q

How does the symp NS decrease the rate of contraction?

A

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

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18
Q

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

A

muscarinic

nicotinic

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19
Q

How are IP3 levels increased?

A

noradrenalin acts on a-1 receptors

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20
Q

How does IP3 control calcium movement?

A

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

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21
Q

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

A

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

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22
Q

What system is activated when the bp is low?

A

the RAAS system

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23
Q

What does the RAAS do on activation?

A

causes a decrease in renal perfusion

signals cells in the juxtaglomerular apparatus

24
Q

What is the function of renin?

A

to catalyse angiotensinogen into Ang I

25
Q

What happens to Ang I?

A

circulates in the bloodstream

is converted into Ang II - its active form by ACE

26
Q

Where does Ang I converted into II by ACE?

A

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

27
Q

Where is ACE found?

A

in endothelial cells lining the blood vessels all over the body

28
Q

What receptor does Ang II bind to?

A

AT-1 receptor

29
Q

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

A

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

30
Q

What are the effects of increased salt and water absorption?

A

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

31
Q

What is the effect of aldosterone release?

A

stimulates the kidney to preserve salt and water in the body

32
Q

Where is ADH located?

A

made by the hypothalamus

stored in the posterior pituitary gland

33
Q

What are the effects of ADH?

A

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

34
Q

What types of drugs reduce bp?

A

ACE inhibitors
AT1-receptor blockers
renin inhibitors

35
Q

What are the effects of ACE inhibitors?

A

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

36
Q

What is the mechanism by which Ang II is released?

A 
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
37
Q

How does Ang II regulate peripheral resistance?

A

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

38
Q

How does blood travel through the nephron?

A

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

39
Q

Where does salt and water reabsorption occur in a nephron?

A

PCT, DCT

loop of Henle

40
Q

What is the mechanism for how aldosterone works?

A

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

41
Q

Where are aldosterone receptors located?

A

inside the cytoplasm

not on the outside of the cell membrane

42
Q

How does aldosterone reach its receptor?

A

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

43
Q

What happens when aldosterone binds to its mineralocorticoid receptors?

A

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

44
Q

Where is ENaC located?

A

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

45
Q

What cells make up the lining of the DCT?

A

simple cuboidal cells

46
Q

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

A

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

47
Q

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

A

Age, Race

Co-existing diseases

48
Q

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

A

ACE inhibitor

Ang receptor blockers

49
Q

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

A

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

50
Q

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

A

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

51
Q

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

A

ca2+ channel blockers

52
Q

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

A

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

53
Q

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

A

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

54
Q

What is another term for adrenaline?

A

epinephrine

55
Q

How is bp measured instead of at the GP?

A

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

56
Q

Why is it called the juxtaglomerular apparatus?

A

bc it is next to (juxta-) the glomerulus

57
Q

What is the role of the juxtaglomerular apparatus?

A

Quality Control

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

M103 T3 (21 decks)

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