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Kofi: Pure Clinical Sem 3 > Urinary: LTReg > Flashcards

Urinary: LTReg Flashcards

1
Q

What is the short term regulation of blood pressure?

A

Baroreceptor reflex

  • Adjust sympathetic and parasympathetic inputs to the heart to alter the cardiac output
  • Adjust sympathetic input to peripheral resistance vessels to alter TPR
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2
Q

What are the hormonal responses to low renal perfusion?

A
  • Renin-angiotensin aldosterone system
  • Sympathetic nervous system
  • Prostaglandins
  • ADH
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3
Q

What is the long term regulation of blood pressure?

A

Neurohormonal resposes to affect salt and water balance

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4
Q

What factors stimulate the renin release?

A
  • Reduced NaCl delivery to the macula densa of distal tube
  • Reduced perfusion pressure in the kidney causes the release of renin
  • Sympathetic stimulation (B1) of the juxtaglomerular increases release of renin
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5
Q

Where is renin released from?

A

Juxtagomerular cells of the afferent arteriole in response to reduced perfusion pressure and stimulation by the sympathetic nervous system

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6
Q

What are the direct actions of angiotensin 2 on the kidney?

A
  • Vasoconstriciton of the efferent and to a lesser extent the afferent arteriole
  • Enhanced sodium reabsorption at the proximal collecting tubule by stimulation of Na-H(NHE3) exchanger in the apical membrane
  • Increase in mesangial matrix
  • Increase in mesangial cell proliferation
  • Glomerular permeability to proteins
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7
Q

What are some indirect effects of angiotensin 2 on the kidney to control blood pressure?

A
  • Release of aldosterone

- Release of ADH

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8
Q

What are the actions of aldosterone on the kidney?

A

Acts on principal cells of distal convoluted tubule and collecting ducts to:

  • Stimulate Na+ and therefore water reabsorption
  • Activates apical Na+ channel and apical K+ channel
  • Increases basolateral Na+ extrusion via Na/K/ATPase
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9
Q

What are the actions of the sympathetic nervous system in response to low blood pressure?

A
  • Reduction of the renal blood flow by vasocontrcitin of arterioles and decrease in the GFR
  • Activates apical Na/H exchanger and basolateral Na/K ATPase in proximal collecting tubule
  • Stimulates renin release from JG cells
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10
Q

What are effects of prostaglandins in the kidney?

A
  • Causes vasodilation of the afferent arteriole

- Enhances renin release

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11
Q

Which hormones trigger the release of prostaglandins in the kidney?

A
  • Angiotensin 2
  • Noradrenaline
  • Anti diuretic hormone
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12
Q

What is the net effect of the interaction of prostaglandins and the RAAS system?

A
  • Systematic vasoconstriction
  • Vasoconstriction of the efferent artriole
  • Vasodilation of the afferent arteriole
  • The GFR is preserved as a result
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13
Q

What is action of ADH?

A
  • Formation of concentrates urine by retaining water to control the plasma osmolarity. Reabsorption of water is increased at the distal nephron. AQ2
  • Vasoconstriction
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14
Q

What stimulate release of ADH?

A
  • Increase in plasma osmolarity stimulates release of ADH

- Severe hypovolaemia stimulates release of ADH

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15
Q

What are the 2 major actions for atrial natriuretic peptide?

A
  1. Causes vasodilation of afferent arteriole and constriction of efferent in order to increase excretion of sodium
  2. Inhibits Na+ reabsorption especially in the collecting duct causing natriuresis
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16
Q

What inhibits ANP release?

A

Low circulating volume in order to support blood pressure

17
Q

What is hypertension?

A

-Persistent increase in blood pressure

18
Q

What is pressure natriuresis?

A
  • Increasing blood pressure gradually resets the kidneys for salt concentrations and water volume and this means the regulatory mechanisms aren’t working as well.
  • It is thought to be one of the causes of hypertension
19
Q

What is hypertension?

A

-Persistent increase in blood pressure

140/90

20
Q

What are some causes of secondary hypertension?

A
  • Reno-vascular hypertension
  • Coarctation of the aorta
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Cushing’s syndrome
21
Q

What are the 2 main causes of renovascualr disease?

A
  • Atheroma

- Fibromuscular dysplasia

22
Q

What is the mechanism behind renovascular disease?

A

-Renal artery stenosis which is narrowing of the renal artery

23
Q

Why does renovascular disease lead to hypertension?

A
  • Lack of blood supply to the kidney causes the kidney to sense hypovolaemia in the body
  • This means that it triggers changes in order to increase the blood pressure
  • This causes hypertension because the mechanism are constantly trying to increase blood pressure even though the blood is normotensive
24
Q

What happens with unilateral renal artery stenosis?

A
  • One kidney triggers mechanism to increase blood pressure by activating the RAAS system because it senses hypovolaemia
  • One kidney works normally and sense the increase in sodium so acts to excrete the sodium. It suppresses the RAAS system.
  • Net effect is hypertension with no fluid overload and salt as the kidney that works normally excrete the extra salt and water
25
Q

What happens with bilateral renal artery stenosis?

A
  • RAAS system is activated
  • Kidney does not get rid of the extra salt and water and hypertension persists
  • Risk of acute pulmonary oedema
26
Q

What is coarctation of aorta?

A

Stenosis in the aorta vessel

27
Q

What is the mechanism that causes hypertension due coarctation of the aorta?

A
  • Less renal blood flow

- Kidney triggers the RAAS system as it senses hypovolaemia wrongly

28
Q

What is primary hyperaldosteronism and the causes?

A

Excess secretion of aldosterone

  • Adrenal adenoma
  • Adrenal hyperplasia
29
Q

What are the clinical features of primary hyperaldosteronism?

A
  • Hypertension

- Can cause hypokalemia

30
Q

What is used in the diagnosis of the the primary hyperaldosteronism?

A
  • Aldosterone:renin ratio is high
  • Look for adenoma with a CT scan and remove if present
  • If no adenoma treat by blockage of aldosterone
31
Q

What is the effect of excess liquorice on the blood pressure?

A
  • Blocks an enzyme
  • Cortisol can’t be converted to cortisone
  • Cortisol interacts with mineralocorticoid receptor triggering the same effect as aldosterone
  • Blood pressure increase
  • Similar mechanism as Cushing’s
32
Q

What is chronic kidney disease?

A

Irreversible and sometime progressive loss of renal function over a period of months to years. Renal injury can cause renal tissue to be replaces by extracellular matrix in response to tissue damage
Leads to hypertension and fluid overload (oedema)

33
Q

Which ion primarily affects the effective circulating volume?

A
  • Sodium ions

- Water in the extracellular fluid compartment depends on the sodium ion content.

34
Q

What would be the effect of changing the amount of sodium that is ingested (without kidney action)?

A
  • Amount of water in the extra cellular fluid would change
  • Effective circulating volume would also change
  • Blood pressure also changes as a result
35
Q

Why does the kidney Na+ excretory rates have to vary over a wide range?

A
  • The kidney needs to match excretion of sodium to ingestion to remain sodium balance.
  • Urinary water excretion can be varied physiologically
36
Q

What can you do to increase the plasma volume?

A

-Add an isosmotic solution

Adding water alone affect plasma osmolarity

37
Q

How can we add or remove an isosmotic solution?

A
  • Movement of osmoles

- Water will follow

38
Q

What can affect the proximal tubule Na+ reabsorption?

A
  • Changes in osmotic pressure and hydrostatic pressure

- RAAS system can stimulate proximal tubule Na+ reabsorption

39
Q

What causes pressure natriuresis and pressure diuresis when renal blood pressure increases?

A
  • Increased renal artery blood pressure
  • Reduced number of Na-H and reduced Na-K ATPase activity in proximal tubule
  • Causes reduction in sodium and water reabsorption in proximal tubule
  • Leads to pressure natriuresis and pressure diruresis together in order for the ECF volume to be decrease and diminish the BP rise.

Kofi: Pure Clinical Sem 3 (44 decks)

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