Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Urinary > Blood Pressure and The Kidney > Flashcards

Blood Pressure and The Kidney Flashcards

1
Q

Which two organs are intimately related to regulate blood pressure?

A

heart and kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outline how RAAS works.

A

Low BP stimulates JGA to release renin. Renin converts angiotensinogen–> angiotensin1 ACE will then convert angiotensin 1–> angiotensin 2 Angiotensin 2 causes vasoconstriction Angiotensin 2 stimulates adrenal glands to release aldosetrone. Aldosterone promotes Na+ and water reabsorption in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What four thing will help the kidney deal with poor perfusion?

A

RAAS SNS Prostaglandins ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

If the perfusion in the kidney rises what peptide will be released in response?

A

ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

recall the equation for mean arterial pressure?

A

SV x HR x TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can the kidney effect cardiac out put?

A

Increase in circulating blood volume will increase the SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Recall from CVS the short term control of blood pressure.

A

Baraoreceptor reflex - adjust heart rate (SAN) and force (myocytes) of contraction by the ANS via the medulla oblongata. Symathetics will effect vascular tone to adjust TPR Thirst is also stimulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does the kidney control BP changes more long term?

A

Thirst Increase NaCl and water reabsorption So over all it acts to increase circulating volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does the kidney control BP changes more long term?

A

Thirst Increase NaCl and water reabsorption So over all it acts to increase circulating volume (increase ECF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where are the baroreceptors?

A

Aortic Arch and carotid sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 3 factors stimulate RAAS?

A

Reduced NaCl delivery to distal tubule Reduced perfusion pressure in kidney Sympathetic stimulation of the JGA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which cells release renin?

A

Juxtaglomerular granular cells of the afferent arteriole in response to poor perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What 3 components make up the juxtaglomerular apparatus?

A

Macula Densa, granule cells and surrounding mesangial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where are the macula densa?

A

Glomerular edge of DCT - detects changes in [NaCl] stimulates renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List the effects of angiotensin 2.

A

Activates sympathetics– vasoconstriction ADH release Thirst Stimulates adrenal cortex to release aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does angiotensin 2 effect the kidney.

A

vasoconstriction of efferent>afferent (preserve GFR in low perfusion) PCT absorbs more na+ as NA-H stimulated collecting duct stimulated by ADH and aldosterone (indirect effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which RAAS receptor is in the PCT?

A

AT2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the effects of aldosterone?

A

Acts on principle cells of CD- stimulates Na (and H2O) reabsorption by increasing expression of apical ENaC and K+ channels Also upregulates basolateral Na/K ATPase to get the sodium into the blood for water to follow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What would high levels of sympathetic innervation do to GFR?

A

Lots of vasoconstriction would decrease GFR because renal blood flow would drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What effect does sympathetic innervation have in the kidney?

A

Apical Na/H exchanger activated Na/K ATPase activated Renin released from JGA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why do we need prostaglandins when we have lost of sympathetic stimulation, ADH and RAAS activation?

A

Protect the kidney for excessive vasoconstriction leading to hypoxia in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Normally whats the effect of prostaglandins in the kidney?

A

Minimal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the local action of prostaglandins in the nephron?

A

Afferent arteriole dilation (lets blood flow to avoid hypoxia - increases filtration pressure gradient to conserve GFR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the effect of local prostaglandin release on renin?

A

Local prostaglandin release STIMULATES renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does ADH do in times of low blood volume?

A

Forms concentrated urine by increasing H2O reabsorption in the distal nephron (more AQP2 channels) Also tightens vessels (vasopressin is the other name)

26
Q

What stimulates ADH release?

A

Hypovolaemia or increase in osmolality of plasma (it needs diluting)

27
Q

If blood pressure acutely increases- how does the body respond?

A

Baroreceptor reflex Renal autoregulation- to avoid huge increase in GFR ANP

28
Q

What are the two types of renal auto-regulation?

A

Myogenic Tubulo-glomerular feedback

29
Q

With in what range of mean arterial BP can renal autogregulation control GFR?

A

80-180

30
Q

What is tubule-glomerular feedback and how does it aid increasing BP?

A

GFR up Macula densa detects higher [NaCl] Paracrine to afferent arteriole - constriction stimulated GFR down

31
Q

What are the 2 major actions of ANP?

A

Vasodilation and Inhibition of Na+ reabsorption in the CD

32
Q

How does ANP increase GFR?

A

If circulating volume is high ANP secreted. Vasodilation systemically and of the afferent arteriole increases GFR. Na+ reabsorption goes down so you get a nature’s Diuresis

33
Q

What mechanisms do we as humans favour- the ones that increase BP or reduce?

A

Increase (historically thats what we needed)

34
Q

Why do we get persistent hypertension?

A

abnormality between arterial pressure and renal salt and water excretion (pressure-naturesis)

35
Q

name the two pathological processes that involve RAAS and BP

A

Secondary hypertension Oedema (secondary hyperaldosteronisms)

36
Q

Name the four types of secondary hypertension

A

Renovascular hypertension Coarctation of the aorta Primary hyperaldosteronism Cushings

37
Q

What would you need to consider when working out if hypertension is primary or secondary.

A

>95% are primary Young patient, especially females with a borderline low potassium- investigate secondary causes

38
Q

What is renovascular disease?

A

Poor renal perfusion because of renal artery pathology- stenosis or narrowing. Caused by atheroma (75%), fibromuscular dysplasia or rarer ones. Can be unilateral or bilateral

39
Q

Why might a kidney with renovascular disease be small?

A

Ischaemia from lack of blood flow leads to shrunken kidney

40
Q

Outline how renovascular disease leads to secondary HTN

A

Perfusion to kidney reduced Kidney tries to compensate by increasing blood volume- RENIN released. Angiotensin 2 levels rise Vasconstriction and aldosterone released Hypertension

41
Q

Why in primary aldosteronism is Renin low but aldosterone high?

A

The adrenal is affected so anything down stream of the adrenal is upregulated but anything higher is lower than expected.

42
Q

List the endocrine causes of hypertension that involve RAAS

A

Primary Aldosteronsim

Cushing’s Syndrome

Liquorice (minerolaocorticoid excess)

43
Q

Which endocrine causes of HTN are independent of RAAS?

A

Phaeochromocytoma

Acromegaly

Thyroid problems

44
Q

What happens if one kidney suffers renovascular disease?

A

The affected kidney will increase RAAS

The unaffected kidney will get hyper-perfused and act to counter act this- induce naturesis and supress RAAS

45
Q

List 3 clinical signs of coarctation of the aorta?

A

Hypertension

Radio-femoral delay

Low BP in legs

(note- normal U&E normal)

46
Q

What leads to a primary hyperalosteronism?

A

Adrenal adenoma

Adrenal hyperplasia

47
Q

How do you diagnose someone with primary hyperaldosteronism?

A

Measure the aldosterone:renin

Look for adenoma on CT

48
Q

How might you treat a primary hyeraldosteronism?

A

Surgery to remove adenoma

If surgery isn’t an option then block aldosterone (mineralocorticoid antagonists)

49
Q

How does liquorice effect the distal nephron?

A

Inhibits the enzyme that degrades cortisol to cortisone.

If high cortosl persists it will bine mineralocortiocoid recptors and give similar effects to aldosterone

50
Q

Why are Cushings patients hypertensive?

A

Cortisol binds mineralocorticoid recepetor

Reabsorb more sodium (means we have lose K+ remember) and water will follow the sodium

51
Q

Why do we get oedema?

A

Excess salt and water in interstitium

52
Q

List causes of oedema

A
53
Q

How at the cpaillary bed might you get oedema?

A

Increase in vascular hydrostatic pressure

Albumin leaks to interstitium (oncotic pull of interstitium goes up)

Blocked lymphatics- non pitting

Nephrotic syndorm- loss of protein in urine so reduced vacular oncotics

54
Q

What is the difference betwenn transudate and exudate?

A

Trasudate- fluid leaks

Exudate - fluid and protein leak

55
Q

What 3 factors effect the effective arterial blood pressure?

A

Cardiac output

Intravascular volume

Systemic Vascular Resistance

56
Q

Why do we retain water in heart failure?

A

The heart pump is no longer effective.

Renal blood flow drops- Kidney acts to increase blood Volume (sympathetic, juxtaglomerular feedback and RAAS)- water and sodium retained

Effective circulatory volume dropped becaue pump failed so volume receptor in left atrium and throaci vessel drops- ADH secreted to retain water

57
Q

How might a chronic kindey disease pateint develope oedema?

A
58
Q

How do nephrotic syndrome pateints get oedema?

A

Nephrotic syndrome- leads to proteinuria so reduced vascular oncotic pressure– Kidney compensates to increase blood volume as its getting poorly perfused

Reduced GFR from kindey damage

59
Q

What is the clinical triad for a nephrotic syndrome?

A

Proteinuria >350mg/mmol

Hypoalbunaemia

Oedema

60
Q

Minimal change disease is a common cause of nephrotic syndrome in children, why do they get oedema?

A

Reduced effective arterial blood volume

GFR tends to be ok

61
Q
A

Year 2 Urinary (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions