L 29 CKD Flashcards
1
Q
What is acute kidney injury?
A
An abrupt as a result of decrease in kidney function occurs over a period of 7 days or less.
2
Q
What is the amount of patients admitted to ICU for kidney injury ?
A
50%
3
Q
What is Chronic Kidney disease?
A
More than 90 days suffering with kidney abnormalities.
4
Q
What are the risk factors for Acute and Chronic Kidney disease?
A
Age
Diabetes
Hypertension
Diabetes mellitus
5
Q
What is the epidemiology of Kidney disease?
A
High BMI Diabetes Chronic Liver disease Nephrotoxic agents Poisoning
6
Q
What are the pre gestational mother risk factors of AKI?
A
Poverty Low Education Underweight CKD Environment Covid 19
7
Q
What is triple Whammy?
A
ACE=> Vasodilation result glomerular filtration
ARB=> cause vasodilation result glomerular filtration
NSAIDs=> arteriole vasoconstriction
Overall can increase the risk of AKI by 31 %
8
Q
What are the Risk factors in childhood and young adult life?
A
Catch up growth
Diabetes
Nephrotoxic medication
9
Q
Average renal blood flow
A
~1200-1500mL/min
10
Q
Average GFR
A
~100mL/min
11
Q
How to diagnose AKI?
A
Decrease urine volume
Increase in serum creatinine
12
Q
How does AKI develop or pathogenesis?
A
Cause Endothelial monolayer injury as a result causes inflammation thus formation of microthrombi and cause an influx of inflammatory cells. Cause fluid overload and cause electrolyte imbalance.
13
Q
What are the risk factors of CKD?
A
Diabetes Hypertension Obesity Chemicals like medications Environment Cancer
14
Q
When a patient is 3 fold high for the risk of CKD?
A
If a patient is already suffering AKI then it has a 3 fold higher chance of CKD.
15
Q
What is the Average urine output?
A
800-2mL/min
16
Q
What is the CKD risk in NZ?
A
Age Female Ethnicity Diabetes Deprivation
17
Q
What does RAAS stand for?
A
Renin-angiotensin-aldosterone system((RAAS) is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance.)
18
Q
Purpose of RAAS?
A
Homeostasis (Homeostasis is the ability to maintain a relatively stable internal state that persists despite changes in the world outside)
19
Q
What happens when RAAS becomes impaired?
A
- Impaired K+ homeostasis
- Impaired Na+ and H2O homeostasis
- Hypertension
- Cardio-renal syndrome
20
Q
Where is renin stored?
A
In juxtaglomerular cells of the afferent arteriole
Half life of renin
~15 minutes
21
Q
What is renin?
A
A protease that converts angiotensin to angiotensin I
22
Q
What are the 3 determinants of increased renin release?
A
- Decreased Na+ concentration in macula densa (of distal tubule)
- Decreased blood pressure or renal blood flow
- B2 receptor activation on juxtaglomerular cells by norepinephrine
23
Q
What converts ATI to ATII?
A
ACE (angiotensin converting enzyme)
24
Q
What does Angiotensin II cause and what does it produce?
A
Angiotensin II causes vasoconstriction.
Angiotensin II produces aldosterone.
25
What is the pathogenesis of CKD?
First nephrons generate utero which leads to atrophy which further get worse due to environmental and genetic factors as a result increase in nephron size and lose its barrier function and impaired filtration result in inflammation and scar formation result in damage of nephron.
26
What would be the systemic effect because of CKD?
```
Electrolyte imbalance
Anaemia
Mineral bone disorder
Hypertension
Dyslipidemia
```
27
What are the guidelines for diagnosis of CKD in NZ?
GFR
| And to identify structural damage we have to do Ultrasound imaging and biopsy.
28
What stage of G3 and G4 and G5 for CKD?
Management of Blood pressure , Diabetes, cardiovascular risk. But in G5 kidney failure so no way to survive.
29
What are the effects of aldosterone?
Aldosterone increases Na+ and water reabsorption and promotes K+ excretion from the kidneys
(Na+ and water in, K+ out)
30
The RAAS system is a compensatory mechanism that aims to...
Aims to maintain plasma volume and cardiac output.
31
RAAS activators (renin release activators)
Low blood volume
Low blood pressure
Low Na+
B2 receptor activation
32
Examples of ACEI's
Enalapril, lisinopril, quinapril, cilazapril, perindopril, captopril
33
Examples of Angiotensin Receptor Blockers (ARBs)
Losartan
Candesartan
Irbesartan
Valsartan
34
Most ACEI are ... and most are
....
Most ACEI are prodrugs and most are renally cleared
Most ARBs are ... and most have ......
Most ARBs are highly protein bound and most have low oral bioavailability
35
MoA of ACEI
ACEI inhibits angiotensin converting enzyme, therefore reducing the production of ATII, and reducing aldosterone secretion.
36
MoA of ARBs
Bind to and block angiotensin II receptors
37
Systemic effects of ACEI and ARBs
- Decrease systemic vascular resistance and therefore blood pressures
- Increase renal blood flow by dilating efferent and afferent arterioles.
38
What is a renoprotective effect?
An effect that prevents or delays the progression of renal disease
39
Which 2 drug classes are renoprotective? Why?
ACEI and ARBs are renoprotective.
They cause vasodilation of efferent arterioles = reduced glomerular pressure and GFR = reduced proteinuria = slower CKD progression = improved CV outcomes
40
Which 2 drugs can cause acute renal injury, AKI?
ACEI and ARBs if you overdose them, the glomerulus pressure is so low that it wont actually work.
41
Loop diuretic examples x2
Furosemide, bumetamide
42
Thiazide examples x2
Bendrofluazide, hydrochlorothiazide
43
Potassium sparing diuretic examples x2
Triamterene, amiloride
44
Aldosterone antagonist example x1
Spironolactone
45
Big picture actions of diuretics
Increase urine flow rate, increase water & Na+ excretion (natriuresis), reduces ECF.
46
Diuretics are used in ... but are not actually ....
Diuretics are used in hypertension but are not anti-hypertensives.
47
Diuretics work in the...
Loop of Henle and the distal tubule
48
Thiazides work in the ...
Distal tubule
49
Potassium sparing and aldosterone antagonists work in the ...
Distal tubule and collecting duct
50
Loop diuretics MoA. Max effect is...
Inhibit Na/K/2Cl cotransporter (NKCC2) in thick ascending loop of Henle.
Max effect is ~20-25% (as 25% of filtered Na+ has already been reabsorbed)
51
Thiazide diuretics MoA. Max effect is....
Inhibit Na/Cl cotransporter (NCCT) in distal tubule.
| Max effect ~5%
52
K sparing diuretics MoA. Max effect is...
Inhibit activity of epithelial Na+ channels in late distal tubule and collecting duct.
Max effect ~2% (very limited efficacy)
53
Aldosterone antagonists MoA
Competitively inhibit aldosterone binding to mineralocorticoid receptor
54
What is different about aldosterone antagonists?
Only diuretic class that enter the tubule from the blood side rather than tubular side.
55
What type of dose-response do loop diuretics have? Do they have a maximum effect?
Loop diuretics have a steep dose-response with a maximum high ceiling effect
56
What type of dose-response do thiazides have? Do they have a maximum effect?
Thiazides have a flat dose-response and a much lower maximum effect
57
Increasing the dose of .... may not increase the effect
Increasing the dose of thiazides may not increase the effect
58
Very large doses of .... can be given in some settings
Very large doses of furosemide can be given in some settings
59
Which drug is not usually recommended in renal impairment?
Thiazides are not usually recommended with worsening renal function.
60
Larger doses of ... are required in CKD
Larger doses of loop diuretics are required in CKD.
61
Loop diuretics have a ... and therefore have a .... than thiazides
Loop diuretics have a steep dose-response, therefore, have a greater maximum effect than thiazides.
62
The diuretic effect is reduced in renal impairment therefore requiring...
An increased dose of loop diuretics.
63
Which cavity Kidney are situated in our body?
retroperitoneal cavity
64
How many nephrons approx in our kidney?
One million nephrons
65
The nephron comprises two structures what are they?
renal Corpuscle and renal tubules
66
What are the functions of the Kidney?
```
Excretory function
Regulatory function
Electrolyte balance
Urinie volume and composition
Maintain pH
```
67
What is the purpose of RAAS?
The purpose of Renin angiotensin aldosterone system(RAAS) is Homeostasis
68
What RAAS do in terms of the cardiovascular system?
Regulation of Blood pressure
69
Why do we need to understand RAAS?
Because they play a major role in human pathologies like Hypertension, Heart failure, Myocardial Infarction, Diabetic nephropathy
70
If RAAS impaired what will happen?
Impaired potassium homeostasis
Impaired sodium and water homeostasis
Hypertension
Cardiorenal syndrome
71
Where renin is stored?
Justaglomerular cells within afferent arterioles
Its half-life is 15 minutes
its primary substrate is circulating angiotensinogen
72
What are the 3 determinants of renin release if they INCREASE?
i) Decrease Na+ concentration in the macula densa
ii) Decrease BP or Renal Blood flow
iii) B2 receptor activation on Juxtaglomerular cells by norepinephrine
73
How RAAS works? MoA
Renin release then converts to ATS=>ATI=> ATI ii =>Aldosterone which then increases Water and Na reabsorption and K excretion
74
What ATI II causes?
vasoconstriction
75
What are the drugs which may Perturb(alter) the RAA system?
```
ACE
ARB
NSAIDs
Loop diuretics
Vasodilators
Beta Blockers
```
76
Does RAAS can be activated by low blood volume?
Yes they can by low blood volume and low BP Low Na B2 receptor activation
77
What aldosterone can increase K loss in the distal tubules in exchange for increased?
Na reabsorption
78
What increases K loss in the distal tubules? how?
aldosterone increases K loss in distal tubules in exchange for increased Na reabsorption
79
Examples of ACE inhibitors?
Captopril Enalapril Fosinopril Cilazapril
80
What is the example of ARBs?
Candesartan
Losartan
Valsartan (use as a combo only)
81
What is the Mechanism of ACE inhibitors?
Inhibit Angiotensin-converting enzyme thus reduce the production of ATI II, aldosterone secretion and reverses renin induced vasocostriction
82
MoA of ARBs?
Bind and block Angiotensin II receptors
83
What ACE and ARB used for?
Reduce vascular resistance diastolic and systolic blood pressure
Increase Renal blood flow by dilating efferent and afferent arterioles
Used for hypertension cardiovascular disease heart failure and diabetic nephropathy
84
How ace and ARB protect renal effect?
Renoprotection: ACE Prevent or delay the progression of renal disease
Improve CV outcome: by causing vasodilation of the efferent arterioles>reduce glomerular pressure> reduceGFR>reduce protenuria>Slower progression of CKD
85
Paradoxically ACE and ARB may cause
acute renal injury AKI while its used to protect the kidney but they slow the progression.
86
Diuretics Types?
Loop Diuretics
Thiazides
Potassium sparing diuretics
Aldosterone antagonists
87
What are the example of Loop diuretics?
Furosemide Bumetamide
88
Examples of Thiazides?
Bendrofluazide, hydrochlorothiazide
89
Example of Potassium-sparing diuretics?
Triamterene, amiloride
90
Example of Aldosterone antagonists?
Spironolactone
91
How do diuretics work?
Increase rate of urine flow
Increase Na, which flows the water (remember)
Reduce the extracellular fluid volume
92
How do loop diuretics work?
They inhibit Na K and 2CL transport in the ascending loop of Henle
93
What amount of Na reabsorbed and what amount of effect we can get of using Loop diuretics?
By the time 75 percent of the Na filtered by loop of henly and reabsorbed back into the plasma and only
20-25 percent only excrete.
94
How Thiazide diuretics work?
Inhibit Na and CL in the distal tubule
Hre 95 percent filtered Na reabsorbed and the only 5 percent interect
