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Urinary > 7. Blood Pressure > Flashcards

7. Blood Pressure Flashcards

1
Q

Below what mean arteriole pressure is cerebral blood flow severely and quickly impaired?

A

55 mmHg.

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2
Q

What cells release renin?

A

Granular cells of the juxtaglomerular apparatus.

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3
Q

What stimulates renin release?

A

Reduced NaCl delivery to distal tubule.
Reduced perfusion pressure detected by baroreceptors in the afferent arteriole.
Sympathetic stimulation to JGA.

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4
Q

What actions does angiotensin II have on the kidney?

A

Vasoconstriction of efferent arteriole.
Enhanced Na+ reabsorption at the PCT (NHE3 exchanger).
Release of aldosterone and ADH.

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5
Q

Where is aldosterone released from?

A

Adrenal cortex.

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6
Q

What are the main actions of aldosterone?

A

Increased ENaC and Na/K/ATPase expression in the principle cells of the collecting duct, so stimulates Na+ and therefore water reabsorption.

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7
Q

What effect do high levels of sympathetic stimulation have on renal blood flow?

A

Reduction of renal blood flow by vasoconstriction of arterioles and decreased GFR to increase BP.
Activation of NHE3 exchanger and Na/K/ATPase in PCT.
Stimulation of renin release from granular cells.

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8
Q

What stimulates the release of prostaglandins?

A

Angiotensin II.
Noradrenaline.
ADH.

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9
Q

What is the effect of prostaglandins in the kidney?

A

Very local actions, cause vasodilation of afferent arteriole of buffer the effects of excessive vasoconstriction produces by RAAS, SNS and ADH.

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10
Q

What do prostaglandins released locally enhance the release of? Why?

A

Renin.
Net effect of prostaglandin and RAAS is systemic vasoconstriction, vasoconstriction of the efferent arteriole, but vasodilation of the afferent arteriole to preserve GFR.

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11
Q

What stimulates the release of ADH?

A

Increases in plasma osmolarity.

Severe hypovolaemia.

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12
Q

What is the main function of ADH?

A

Increases water reabsorption in the collecting duct by AQP2, so forming concentrated urine.

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13
Q

What is renal autoregulation? What two systems does it involve?

A

Regulation of renal blood flow to maintain a stable GFR despite changes in systemic blood pressure (between 80 and 180 mmHg mean arterial BP).
Myogenic reflex.
Tubuloglomerular feedback.

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14
Q

Where is atrial natriuretic peptide released from?

A

Atrial myocytes in response to stretch.

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15
Q

What are the two main actions of atrial natriuretic peptide (ANP)?

A

Vasodilation - systemic circulation to decrease BP and of the afferent arteriole to increase GFR.
Inhibits Na+ reabsorption in the collecting duct.

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16
Q

What is seen in all patients with hypertension?

A

Pressure-natriuresis.

17
Q

What is primary hypertension?

A

Hypertension with no definable cause. Is 95% of hypertensive patients.

18
Q

What is secondary hypertension?

A

Hypertension due to a secondary cause.

19
Q

What are the two main types of renal artery stenosis?

A

Atheroma.

Fibromuscular dysplasia.

20
Q

How does renovascular disease lead to secondary hypertension?

A

Decreased kidney perfusion pressure, increased renin, activation of RAAS, vasoconstriction and aldosterone release causing Na+ retention.

21
Q

What is seen clinically in coarctation of the aorta?

A

Hypertension due to reduced perfusion of kidneys.
Radio-femoral delay.
Low blood pressure in legs.

22
Q

How does Conn’s syndrome cause secondary hypertension?

A

An aldosterone secreting adenoma, causing increased Na+ reabsorption, arterial stiffness and cardiac remodelling.

23
Q

Other than Conn’s syndrome, what else can cause primary hyperaldosteronism leading to secondary hypertension?

A

Adrenal hyperplasia.

24
Q

How would you diagnose primary hyperaldosteronism?

A

Measure aldosterone:renin ratio.

Ct scan - adenoma.

25
Q

How would you treat primary hyperaldosteronism?

A

Surgery for adenoma.

Mineralcorticoid receptor antagonist.

26
Q

How does Cushing’s disease lead to secondary hypertension/

A

Excess cortisol secretion, which at high concentrations acts on aldosterone receptors.

27
Q

How can liquorice cause hypertension?

A

Increased aldosterone and cortisol in distal nephron - increasing Na+ reabsorption.

28
Q

What is oedema?

A

Excess salt and water in the interstitium.

29
Q

Name 3 causes of generalised oedema.

A 
Heart failure.
Chronic kidney disease.
Nephrotic disease.
Liver disease.
Pregnancy.
30
Q

Give 3 pathological mechanisms for oedema.

A

Increased capillary hydrostatic pressure.
Increased interstitial fluid osmotic pressure.
Tumour blocking lymphatic drainage.
Decreased capillary osmotic pressure eg low blood albumin.

31
Q

What is the difference between transudate and exudate?

A

Transudate - increased hydrostatic capillary pressure (eg congestive heart failure) or decreased capillary osmotic pressure, is low in protein (eg decreased protein production in liver disease or increased protein loss in kidney disease). Low protein content. Causes pitting oedema.
Exudate - increased inter-endothelial spaces in inflammation. High protein content. Causes non-pitting oedema.

32
Q

What 3 factors influence the effective arterial blood volume?

A

Cardiac output.
Systemic vascular resistance.
Intravascular volume.

33
Q

How does chronic kidney disease lead to secondary hypertension?

A

Inability to excrete excess salt and water due to reduced kidney function (decreased GFR).

34
Q

How does nephrotic syndrome lead to secondary hypertension?

A

Reduce oncotic pressure (hypoalbuminemia), causing reduced perfusion pressure and activation of RAAS, SNS and ADH.
Alterations in Na+ and H2O excretion fun to reduced kidney function.

35
Q

What clinical triad is seen in nephrotic syndrome?

A

Proteinuria >350 mg/mmol.
Hypoalbuminaemia.
Oedema.

36
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change disease.

Urinary (14 decks)

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