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SA urinary > S4) Blood Pressure and The Kidney > Flashcards

S4) Blood Pressure and The Kidney Flashcards

1
Q

What is the formula for calculating blood pressure?

A

mean arterial BP = CO x TPR

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2
Q

What is the formula for calculating cardiac output?

A

CO = SV x HR

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3
Q

Explain the 2 actions which allow for the short term regulation of blood pressure

A

Baro-receptor reflex:

  • Adjust sympathetic and parasympathetic inputs to the heart to alter CO
  • Adjust sympathetic input to blood vessels to alter TPR
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4
Q

Describe the long term regulation of blood pressure

A

Neurohormonal response to affect salt and water balance

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5
Q

Identify 4 processes which act on the kidney to regulate blood pressure

A
  • Renin-angiotensin-aldosterone system
  • Sympathetic nervous system (B-adrenergic receptors in heart and a adrenergic receptors in blood vessels)
  • Prostaglandins
  • ADH
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6
Q

Describe the events which occur in RAAS

A
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7
Q

Identify 3 factors which stimulate renin release from the JGA cells in the kidney

A
  • Reduced NaCl delivery to macula densa in distal tubule
  • Reduced perfusion pressure in the kidney (detected by baroreceptors in afferent arteriole)
  • Sympathetic stimulation to JGA increases release of renin
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8
Q

What are the direct effects of Angiotensin II on the kidney?

A
  • Vasoconstriction of efferent arteriole (AA > EA)
  • Enhances Na+ reabsorption at the PCT (stimulates Na-H exchanger in apical membrane)
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9
Q

Angiotensin II stimulates aldosterone release from the adrenal cortex.

Identify 2 of its actions on the kidney

A

Acts on principal cells of collecting duct:

  • Stimulate Na+ and water reabsorption by increasing expression of the apical Na+ channel (ENaC)
  • Increases basolateral Na+ extrusion via Na/K/ATPase
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10
Q

How does the sympathetic nervous system act on the kidney?

A
  • Reduce renal blood flow (vasoconstriction of renal artery)
  • Stimulates Na+ reabsorption (NHE3 & Na/K ATPase) in PCT
  • Stimulates renin release from JGA
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11
Q

In normal situations, prostaglandins have little effect.

Regardless, how does it act in RAAS?

A
  • Vasodilates the afferent arteriole
  • Enhances renin release
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12
Q

What stimulates the release of prostaglandins?

A

Release stimulated by vasoconstrictors:

  • Angiotensin II
  • Noradrenaline
  • ADH
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13
Q

Prostaglandins and RAAS interact to stimulate each other.

What is the net effect of both of these substances?

A
  • Systemic vasoconstriction
  • Vasoconstriction of the efferent arteriole
  • Vasodilation of afferent arteriole
  • Preservation of GFR
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14
Q

What is the main role of ADH?

A
  • Increases water reabsorption in distal nephron (AQP2) in order to control plasma osmolarity through water retention
  • Concentrated urine formed
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15
Q

What stimulates the release of ADH?

A
  • Plasma osmolarity
  • Severe hypovolaemia
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16
Q

ADH is also called arginine vasopressin.

Why is this?

A

ADH also causes vasoconstriction

17
Q

Atrial Natriuretic Peptide acts in the opposite direction of other neurohormonal regulators.

What are its 2 main actions?

A
  • Causes vasodilation of afferent arteriole, increasing GFR
  • Inhibits Na+ reabsorption especially in collecting duct, causing natriuresis

ANP has a vasodilatory effect and helps to decrease blood pressure and increase urine output by inhibiting the RAAS, including the production of renin.

produced in the atria if the heart

18
Q

What stimulates the release of ANP and what inhibits its release?

A
  • Low circulating blood volume = inhibits ANP release
  • High circulating blood volume = stimulates ANP release
19
Q

In terms of evolution, why is hypertension an anticipated problem?

A
  • Mechanisms which increase/maintain BP are stronger than the mechanisms which reduce BP when it is too high
  • Hence, volume depletion (dehydration or blood loss or sepsis) is more of a risk than hypertension
20
Q

What is hypertension?

A

Hypertension is a persistent increase in blood pressure

21
Q

Identify 2 pathological processes involving RAAS

A
  • Secondary hypertension
  • Secondary hyperaldosteronism (oedema)
22
Q

Identify 4 clinical conditions resulting in secondary hypertension

A
  • Renovascular hypertension
  • Coarctation of the aorta
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Cushing’s syndrome
23
Q

Describe the pathophysiology of renovascular disease

A
  • Renal artery stenosis
  • 1/both kidneys affected
  • Due to atheroma (75%) or fibromuscular dysplasia (25%)
24
Q

Identify 5 endocrine causes of hypertension

A
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Cushing’s syndrome
  • Liquorice
  • Phaeochromocytoma
  • Hyperthyroidism / Hypothyroidism
25
Q

What is apparent mineralocorticoid excess syndrome?

A

AME is a condition resulting in an excess amount of aldosterone and cortisol in the distal nephron of the kidney due to excessive liquorice ingestion

26
Q

What is oedema?

A

Oedema is the accumulation of excessive salt/water in the interstitium

27
Q

Identify 5 causes of generalised oedema

A
  • Heart failure
  • Chronic kidney disease
  • Nephrotic disease
  • Liver disease
  • Pregnancy
28
Q

What is Chronic Kidney Disease?

A
  • CKD is a condition leading to the inability to excrete excess salt and water due to reduced kidney function (↓ GFR)
  • It results in hypertension and oedema
29
Q

Which 2 underlying processes lead to Nephrotic syndrome?

A
  • Reduced oncotic pressure causing reduced perfusion pressure and activation of RAAS / SNS / ADH
  • Alterations in sodium and water excretion due to reduced kidney function (hypertension & reduced GFR)
30
Q

Identify 3 symptoms of Nephrotic Syndrome

A
  • Proteinuria > 350 mg/mmol (>3.5 g / 24 hr)
  • Hypoalbuminaemia
  • Oedema

SA urinary (25 decks)

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