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BDS1 > Kidney 3 - regulation in health and disease > Flashcards

Kidney 3 - regulation in health and disease Flashcards

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1
Q

Which hormones act on the DCT?

A

ADH (vasopressin), aldosterone, atrial natriuretic peptide (ANP)

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2
Q

Effect of ADH

A

inserts aquaporins which increases fluid reabsorption so a small volume of concentrated urine is produced

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3
Q

Effect of aldosterone

A

inserts Na+ channels (Na+ reabsorbed and water follows) leading to fluid reabsorption so a small volume of concentrated urine is produced

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4
Q

Effect of atrial natriuretic peptide

A

counteracts ADH and aldosterone therefore inhibiting insertion of aquaporins and Na+ channels. So water and Na+ remain in filtrate and are excreted in a large volume of dilute urine.

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5
Q

What function of the kidney do ADH, aldosterone and ANP regulate?

A

homeostatic regulation of blood volume and pressure

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6
Q

What does the body detect for the release of ADH/aldosterone/ANP?

A

changes in BP

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7
Q

Which hormones are released when high BP is detected?

A

atrial natriuretic peptide

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8
Q

Which hormones are released when low BP is detected?

A

ADH and aldosterone

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9
Q

Glomerular Filtration Rate (GFR) definition

A

the rate at which blood plasma is filtered through the glomerulus into the Bowman’s capsule

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10
Q

What factors influence the glomerular filtration rate?

A

Glomerular HP, Capsular HP, Glomerular OP, systemic BP, RAAS, disease

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11
Q

What do kidneys measure as a proxy for systemic BP?

A

GFR

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12
Q

What is the effect of high systemic BP on [Na+] in filtrate as it enters DCT?

A

A high systemic BP means a higher GFR so filtrate flows faster and there is less time for Na+ reabsorption. Therefore filtrate has a higher [Na+]

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13
Q

What is the effect of a lower systemic BP on [Na+] concentration as it enters the DCT?

A

A lower BP means a lower GFR so filtrate flows more slowly meaning there is more time for Na+ reabsorption. Therefore, [Na+] is lower in the filtrate.

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14
Q

What structure measures and responds to changes in Na+ conc in the filtrate?

A

juxta-glomerular apparatus

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15
Q

Location of juxta-glomerular apparatus

A

connects the DCT with the glomerulus

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16
Q

What are the 3 cell groups within the juxta-glomerular apparatus?

A

macula densa, juxtaglomerular cells, mesangial cells

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17
Q

Function of macula densa

A

detects Na+ concentration in filtrate as it passes through DCT and sends impulses to juxtaglomerular cells

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18
Q

Where is the macula densa located?

A

in the DCT proximal to juxtaglomerular cells / renal corpuscle

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19
Q

Appearance of macula densa

A

darker pink coloured cells (of DCT epithelium)

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20
Q

What type of cell makes up the juxtaglomerular cells?

A

specialised smooth muscle cells

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21
Q

Function of juxtaglomerular cells

A

adjust diameter of the afferent arteriole hence regulating GFR

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22
Q

Function of mesangial cells

A

supporting cells

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23
Q

Location of mesangial cells

A

extra and intraglomerular

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24
Q

How does BP influence Na+ filtrate concentration?

A

BP influences glomerular HP which influences GFR which determines how much Na+ is reabsorbed

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25
How is normal homeostatic BP maintained?
Macula densa detects a Na+ filtrate concentration within normal limits. Juxtaglomerular cells maintain the large diameter of the afferent arteriole. Glomerular HP is maintained.
26
What is tubuloglomerular feedback?
mechanism of changing the diameter of the afferent arteriole to protect glomerular capillaries from fluctuations in BP
27
Sequence of events in tubuloglomerular feedback when BP is high
High BP increases glomerular HP which increases GFR leading to an increased [Na+] in filtrate. Na+ and water enter macula densa causing cells to swell which triggers the release of adenosine. This signals to the juxtaglomerular cells to constrict the afferent arteriole. Therefore, glomerular HP, GFR, [Na+] return to normal.
28
What chemical signal is released by the macula densa to juxtaglomerular cells when [Na+] in the filtrate is high?
adenosine
29
What chemical signal is released by the macula densa cells when [Na+] in the filtrate is low?
prostaglandins
30
What is the effect of prostaglandins on juxtaglomerular cells?
Vasodilate (minimal effect) and release renin into the circulation (activating RAAS to increase systemic BP)
31
What is the effect of adenosine on juxtaglomerular cells?
Vasoconstrict
32
When does the tubuloglomerular feedback regulate systemic BP?
When systemic BP is low, tubuloglomerular feedback stimulates RAAS
33
Effect of low systemic BP on tubuloglomerular feedback
low BP leads to low glomerular HP which reduces GFR therefore [Na+] in filtrate is decreased. Na+ and water leave the macula densa as a result causing the cells to shrivel which triggers prostaglandins release. Stimulates vasodilation of juxtaglomerular cells and renin release. RAAS activated
34
Which system restored blood pressure?
Renin angiotensinogen system restores BP via angiotensin II
35
How does the renin angiotensinogen restore BP?
Renin converts angiotensinogen (inactive in circulation) into angiotensin I. As angiotensin I passes through vascular endothelium of the lung, it is cleaved by angiotensin converting enzyme into angiotensin II which is a potent vasoconstrictor.
36
Where is angiotensinogen produced?
liver
37
Where is ACE (angiotensin converting enzyme) produced?
vascular endothelium of the lungs
38
Where is renin released from?
Juxtaglomerular cells
39
Under what conditions do juxtaglomerular cells release renin?
When prostaglandins are released by macula densa (due to low [Na+] in filtrate)
40
Why is the renin angiotensinogen system a short term solution to increase BP?
Body needs to increase fluid volume to address the root cause of low BP
41
Which system restored blood volume?
renin angiotensin aldosterone system
42
Location of target receptors for angiotensin II
arterioles (constrict), hypothalamus (thirst), pituitary gland (ADH release), adrenal cortex (aldosterone release)
43
How does the renin angiotensin aldosterone system restore blood volume?
angiotensin II triggers release of (ADH and) aldosterone which increases Na+ and fluid retention in DCT
44
Where is aldosterone released from?
adrenal cortex
45
Which hormone counteracts RAAS?
atrial natriuretic peptide
46
Which hormone is released when systemic BP is elevated?
Atrial natriuretic peptide
47
Which cells release atrial natriuretic peptide?
endothelial cells lining the atria
48
How do atrial endothelial cells detect blood pressure?
the endothelial cells express baroreceptors
49
Function of baroreceptors
detect rise in BP
50
How does atrial natriuretic peptide reduce BP?
ANP inhibits ADH and aldosterone and removes aquaporins and Na+ channels from the DCT. Therefore, excess fluid is excreted
51
Effect of chronic kidney disease on GFR
CKD reduces GFR
52
In CKD patients, what do the kidneys misinterpret reduced GFR as?
reduced systemic BP (use GFR as a proxy for BP)
53
What is the consequence of reduced GFR in CKD patients?
inappropriate activation of RAAS and inadequate removal of fluid and metabolic waste products
54
Why are patients with chronic kidney disease (CKD) at greater risk of developing cardiovascular disease?
CKD causes build up of waste products in blood which can damage vasculature. Inappropriate activation of RAAS in CKD can cause hypertension which increases risk of CVD.
55
Why can hypertension be both a cause and a symptom of CKD?
Hypertension can damage glomerular capillaries causing CKD. Activation of RAAS in CKD can lead to hypertension.
56
What is the leading cause of death for patients with CKD?
cardiovascular disease
57
Why can diabetes increase risk of CKD and CVD?
hyperglycaemic blood can harm vasculature including glomerular capillaries
58
Up to _?_ % of diabetic patients can develop CKD
40%
59
Why may having CKD and diabetes be restrictive for patients?
need to monitor sugar intake as well as salt and fluids
60
What are the causes of CKD?
hypertension, diabetes, high cholesterol, kidney infections, glomerulonephritis, polycystic kidney disease, kidney stones, long-term use of NSAIDs
61
Why can high cholesterol cause CKD?
accumulation of plaque in glomerular capillaries can reduce GFR
62
What are the possible sources of kidney infections?
UTIs, oral bacterial (e.g. Staphylococci, Streptococci)
63
What is glomerulonephritis?
inflammation of glomerular capillaries
64
What is polycystic kidney disease?
genetic disease in which renal tubules are unable to properly form. As patient ages, fluid-filled cysts accumulate. Require renal transplant or dialysis
65
Causes of kidney stones
crystallisation of waste products which can accumulate
66
What is the effect of kidney stones?
painful blockages and increases risk of kidney infections
67
What are NSAIDs?
non-steroidal anti-inflammatory drugs e.g. ibuprofen, aspirin
68
Why are kidney transplant patients not recommended NSAIDs?
NSAIDs can cause CKD
69
Symptoms of CKD
hypertension, nausea, oedema, blood/protein in urine, anaemia, weak/painful bones
70
Why can CKD cause nausea?
due to accumulation of waste products in circulation
71
Why can CKD cause oedema?
build up of solutes in blood cause water retention
72
Common location of oedema due to CKD
ankles, hands or feet and around lungs
73
Why can CKD lead to anaemia (low RBCs)?
erythropoietin release from the kidneys is affected which leads to unregulated RBC production in bone marrow
74
Why can CKD lead to weak/painful bones?
Kidneys are important in Ca2+ regulation. Removal of too much Ca2+ can weaken bones
75
How is CKD regulated?
by treating hypertension
76
How is hypertension treated?
reducing salt intake in diet / weight loss in combination with anti-hypertensive treatments
77
Examples of anti-hypertensive treatments for CKD
diuretics (e.g, furosemide), ACE inhibitors / angiotensin receptor blockers (ARBs), aldosterone agonists
78
How do ACE inhibitors reduce hypertension?
prevents the conversion of angiotensin I into angiotensin II which is a vasoconstrictor
79
How do angiotensin receptor blockers (ARBs) reduce hypertension?
prevent the action of angiotensin II hence downregulating RAAS
80
How do aldosterone agonists reduce hypertension?
block aldosterone nuclear receptors or sodium channels, preventing Na+ and water reabsorption in DCT
81
Which pump does furosemide target?
NKCC2 (apical surface of epithelium lining thick ascending limb of loop of Henle)
82
How does furosemide act as a diuretic?
Inactivates NKCC2 cotransporter therefore less Na+, K+ and Cl- is reabsorbed from the filtrate into IF. Results in a lower solute concentration in medulla so less water is reabsorbed / drawn out of thin descending limb. So more Na+ and water remain in filtrate and are excreted.
83
What effect does furosemide have on reabsorption of Na+ and water from the filtrate?
Reduces Na+ and water reabsorption due to inactivation of NKCC2 which reduces solute concentration in medulla.
84
What effect does furosemide have on fluid and electrolyte balance of blood?
Decreases water and electrolytes in blood. As less Na+, K+, Cl- ions are transported out of the filtrate in the thick ascending limb (due to inactivation of NKCC2), fewer solutes are reabsorbed into the blood. In addition, as less water is drawn out of the thin descending limb, less water is reabsorbed into the blood.
85
What effect does furosemide have on symptoms of hypertension?
acts as a diuretic as more water and sodium are excreted in urine. This reduces blood volume hence reducing hypertension.
86
Which stage of CKD is known as kidney failure?
stage 5 (aka end-stage renal disease)
87
What percentage of kidney function do kidney failure patients have?
less than 15%
88
Treatment for kidney failure
dialysis or kidney transplant
89
What is dialysis?
artificial removal of waste, solutes, water and toxins from blood
90
What are the 2 types of dialysis?
Haemodialysis and peritoneal dialysis
91
What happens in haemodialysis?
Patients must have their blood filtered by a machine in hospital 2-3 times a week for 4 hours at a time
92

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