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Urinary > Week 4 - Control of BP > Flashcards

Week 4 - Control of BP Flashcards

1
Q

What are the 4 mechanisms of long-term control of blood pressure?

A
  • Renin-Angiotensin-Aldosterone-System
  • Sympathetic Nervous System
  • Anti-Diuretic Hormone
  • Atrial Natiuretic hormone
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2
Q

Where is renin released from? What 3 mechanisms stimulate its release?

A
  • Granular cells of JGA
    1) Reduced NaCl in DCT detected by MD ->Cause afferent arteriole to release PGs ->PGs cause granular cells to release renin
    2) Reduced perfusion pressure detected by baroreceptors in afferent arteriole
    3) Sympathetic stimulation of JGA
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3
Q

What is angiotensinogen and where is it made?

A
  • Precursor

- In the liver at a constant rate

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4
Q

Where is angiotensin I in high conc?

A

-Lungs

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5
Q

What are the functions of angiotensin II?

A
  • Stimulates aldosterone production from adrenal cortex
  • Stimulates Na resorption in PCT (stimulate NHE)
  • Stimulates vasoconstriction of afferent and efferent arteriole to decrease GFR and thus decrease excretion
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6
Q

Describe the pathway of aldosterone stimulation by RAAS

A
  • Angiotensinogen->Angiotensin I by renin
  • Angiotensin I ->Angiotensin II by Angiotensin Converting Enzyme
  • Angiotensin II stimulates aldosterone
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7
Q

What is the aim of RAAS?

A

-To increase BP by increasing fluid volume

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8
Q

What is the main angiotensin II receptor? What type of receptor is it?

A
  • AT1

- GPCR

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9
Q

Describe the actions of aldosterone on the kidney

A
  • Acts on principle cells of collecting duct and stimulates Na and thus water resorption
  • Increases expression of ENaC and NaKATPase and apical K channel
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10
Q

How does aldosterone reach the priciple cells?

A

-Can diffuse directly through cell membrane as steroid hormone

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11
Q

Why does an ACE inhibitor cause a dry cough?

A

-Decreased bradykinin in lungs as ACE breaks it down

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12
Q

What is bradykinin?

A

-Vasodilator

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13
Q

Explain how the sympathetic nervous system stimulates renin release from JGA

A
  • In response to low bp, High levels of sympathetic stimulation reduces renal blood flow via vasoconstriction of the arterioles
  • This causes a decrease in GFR and thus a decrease in the filtration fraction
  • This causes less Na to be delivered to DCT which is detected by MD of JGA
  • MD causes afferent arteriole to release prostaglandins which cause vasodilation and stimulates the release of renin from granular cells
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14
Q

In what 3 ways does the sympathetic nervous system reduce Na excretion

A
  • Directly acts on PCT to activate NHE and NaKATPase
  • Causes vasoconstriction of afferent arteriole to reduce GFR -> reduced Na Excretion
  • Stimulate Renin release from JGcells
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15
Q

How does antidiuretic hormone act as a long-term regulator of BP?

A

-ADH stimulates Na resorption in thick ascending limb through NKCC2

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16
Q

How does atrial natiuretic peptide act as a long-term regulator of BP?

A
  • ANP acts to reduce bp by promoting Na excretion and thus water excretion
  • ANP (which is sythesised and stored in atrial myocytes) is released from atrial cells in response to stretch -> Increased blood volume -> increased SV -> increased stretch
  • When corculating vol reduced -> less stretch -> less ANP released
  • ANP acts as a vasodilator of afferent arteriole which increases renal perfusion = increased GFR = increased excretion
  • ANP also inhibits Na reabsorption along the nephron
17
Q

What is the general action of prostaglandins?

A

-Vasodilator

18
Q

What effect do NSAIDs have on prostaglandins?

A

-Inhibit cyclo-oxygenase pathway involved in prostaglandin synthesis -> decreased PGs

19
Q

What is the danger of adminstering NSAIDs in Acute Kidney Injury?

A

-Further increase the injury by inhibiting PGs and causing a reduction in renal blood flow -> decreases GFR further

20
Q

What effect does dopamine have on the BP?

A
  • Dopamine formed locally in the kidney from L-DOPA
  • Acts on dopamine receptors on renal BVs and cells of PCT and TAL
  • Causes vasodilation and increases renal blood flow
  • Causes reduces reabsorption of NaCl by inhibiting NHA and NaKATPase
21
Q

What is hypertension?

A

-Sustained increase in BP over 140/90

22
Q

What is primary hypertension?

A

-Hypertension with no definitive cause

23
Q

What is secondary hypertension?

A

-Hypertension secondary to disease eg cushings, chronic renal disease

24
Q

How does renovascular disease cause hypertension?

A
  • Occlusion of renal artery/renal artery stenosis causes a fall in perfusion pressure
  • Decreased perfusion leads to an increase in renin
  • Increase in renin results in an increased aldosterone
  • Increased Na and Water reabsorption -> Hypertension
25
Q

What is Conn’s syndrome?

A

-Hypertension and hypokalaemia caused by an aldosterone secreting adenoma

26
Q

Why does pheochromocytoma cause hypertension?

A
  • Excess production of NA and A
  • Increased action of sympathetic nervous system
  • Increased vasoconstriction -> Hypertension
27
Q

What is the eqn for calculating BP? What is the eqn for calculating CO?

A
  • CO x TPR

- CO=SV x HR

28
Q

How is hypertension treated pharmacologically?

A
  • ACE inhibitors
  • AngIIR antagonists
  • Thiazide Diuretics or Spironolactone
  • L-Type Ca Channel blockers
  • a1-receptor blockers
  • b-blockers if previous MI
29
Q

How do L-type Calcium Channel blockers reduce hypertension?

A
  • Reduce Ca entry into vascular smooth muscle of cells

- Relaxation of vascular smooth muscle

30
Q

How do a1-receptor blocers decrease hypertension?

A

-Reduce sympatheric tone by blocking NA

31
Q

Describe non-pharmacological approaches to treating hypertension

A
  • Diet
  • Exercise
  • Stop smoking
  • Reduce alcohol intake
  • Reduced Na intake
32
Q

What is the short-term regulator of BP? Explain it

A
  • Baroreceptor reflex
  • Baroreceptors are stretch receptors located in aortic arch and the carotid which adjust symp and parasymp input to the heart to alter CO and adjust symp input to vessels
  • They are sensitive to pressure. Increased pressure on the receptors causes increased signals to be sent to the medulla -> increased parasympathetic input -> decreased CO and TPR
  • Decrease in blood pressure decreases signals sent to medulla -> decreased parasymp and increased symp (if needed) and vasoconstriction occurs

Urinary (21 decks)

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