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PHCY 310 > L 29 CKD > Flashcards

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.

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2
Q

What is the amount of patients admitted to ICU for kidney injury ?

A

50%

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3
Q

What is Chronic Kidney disease?

A

More than 90 days suffering with kidney abnormalities.

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4
Q

What are the risk factors for Acute and Chronic Kidney disease?

A

Age
Diabetes
Hypertension
Diabetes mellitus

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5
Q

What is the epidemiology of Kidney disease?

A 
High BMI
Diabetes
Chronic Liver disease
Nephrotoxic agents
Poisoning
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6
Q

What are the pre gestational mother risk factors of AKI?

A 
Poverty 
Low Education
Underweight
CKD 
Environment
Covid 19
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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 %

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8
Q

What are the Risk factors in childhood and young adult life?

A

Catch up growth
Diabetes
Nephrotoxic medication

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9
Q

Average renal blood flow

A

~1200-1500mL/min

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10
Q

Average GFR

A

~100mL/min

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11
Q

How to diagnose AKI?

A

Decrease urine volume

Increase in serum creatinine

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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.

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13
Q

What are the risk factors of CKD?

A 
Diabetes 
Hypertension
Obesity
Chemicals like medications
Environment 
Cancer
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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.

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15
Q

What is the Average urine output?

A

800-2mL/min

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16
Q

What is the CKD risk in NZ?

A 
Age 
Female 
Ethnicity
Diabetes
Deprivation
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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.)

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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)

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19
Q

What happens when RAAS becomes impaired?

A
  • Impaired K+ homeostasis
  • Impaired Na+ and H2O homeostasis
  • Hypertension
  • Cardio-renal syndrome
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20
Q

Where is renin stored?

A

In juxtaglomerular cells of the afferent arteriole
Half life of renin
~15 minutes

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21
Q

What is renin?

A

A protease that converts angiotensin to angiotensin I

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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
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23
Q

What converts ATI to ATII?

A

ACE (angiotensin converting enzyme)

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24
Q

What does Angiotensin II cause and what does it produce?

A

Angiotensin II causes vasoconstriction.

Angiotensin II produces aldosterone.

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25
Q

What is the pathogenesis of CKD?

A

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.

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26
Q

What would be the systemic effect because of CKD?

A 
Electrolyte imbalance 
Anaemia
Mineral bone disorder
Hypertension 
Dyslipidemia
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27
Q

What are the guidelines for diagnosis of CKD in NZ?

A

GFR

And to identify structural damage we have to do Ultrasound imaging and biopsy.

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28
Q

What stage of G3 and G4 and G5 for CKD?

A

Management of Blood pressure , Diabetes, cardiovascular risk. But in G5 kidney failure so no way to survive.

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29
Q

What are the effects of aldosterone?

A

Aldosterone increases Na+ and water reabsorption and promotes K+ excretion from the kidneys
(Na+ and water in, K+ out)

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30
Q

The RAAS system is a compensatory mechanism that aims to…

A

Aims to maintain plasma volume and cardiac output.

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31
Q

RAAS activators (renin release activators)

A

Low blood volume
Low blood pressure
Low Na+
B2 receptor activation

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32
Q

Examples of ACEI’s

A

Enalapril, lisinopril, quinapril, cilazapril, perindopril, captopril

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33
Q

Examples of Angiotensin Receptor Blockers (ARBs)

A

Losartan
Candesartan
Irbesartan
Valsartan

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34
Q

Most ACEI are … and most are

A

….
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

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35
Q

MoA of ACEI

A

ACEI inhibits angiotensin converting enzyme, therefore reducing the production of ATII, and reducing aldosterone secretion.

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36
Q

MoA of ARBs

A

Bind to and block angiotensin II receptors

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37
Q

Systemic effects of ACEI and ARBs

A
  • Decrease systemic vascular resistance and therefore blood pressures
  • Increase renal blood flow by dilating efferent and afferent arterioles.
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38
Q

What is a renoprotective effect?

A

An effect that prevents or delays the progression of renal disease

39
Q

Which 2 drug classes are renoprotective? Why?

A

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
Q

Which 2 drugs can cause acute renal injury, AKI?

A

ACEI and ARBs if you overdose them, the glomerulus pressure is so low that it wont actually work.

41
Q

Loop diuretic examples x2

A

Furosemide, bumetamide

42
Q

Thiazide examples x2

A

Bendrofluazide, hydrochlorothiazide

43
Q

Potassium sparing diuretic examples x2

A

Triamterene, amiloride

44
Q

Aldosterone antagonist example x1

A

Spironolactone

45
Q

Big picture actions of diuretics

A

Increase urine flow rate, increase water & Na+ excretion (natriuresis), reduces ECF.

46
Q

Diuretics are used in … but are not actually ….

A

Diuretics are used in hypertension but are not anti-hypertensives.

47
Q

Diuretics work in the…

A

Loop of Henle and the distal tubule

48
Q

Thiazides work in the …

A

Distal tubule

49
Q

Potassium sparing and aldosterone antagonists work in the …

A

Distal tubule and collecting duct

50
Q

Loop diuretics MoA. Max effect is…

A

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
Q

Thiazide diuretics MoA. Max effect is….

A

Inhibit Na/Cl cotransporter (NCCT) in distal tubule.

Max effect ~5%

52
Q

K sparing diuretics MoA. Max effect is…

A

Inhibit activity of epithelial Na+ channels in late distal tubule and collecting duct.
Max effect ~2% (very limited efficacy)

53
Q

Aldosterone antagonists MoA

A

Competitively inhibit aldosterone binding to mineralocorticoid receptor

54
Q

What is different about aldosterone antagonists?

A

Only diuretic class that enter the tubule from the blood side rather than tubular side.

55
Q

What type of dose-response do loop diuretics have? Do they have a maximum effect?

A

Loop diuretics have a steep dose-response with a maximum high ceiling effect

56
Q

What type of dose-response do thiazides have? Do they have a maximum effect?

A

Thiazides have a flat dose-response and a much lower maximum effect

57
Q

Increasing the dose of …. may not increase the effect

A

Increasing the dose of thiazides may not increase the effect

58
Q

Very large doses of …. can be given in some settings

A

Very large doses of furosemide can be given in some settings

59
Q

Which drug is not usually recommended in renal impairment?

A

Thiazides are not usually recommended with worsening renal function.

60
Q

Larger doses of … are required in CKD

A

Larger doses of loop diuretics are required in CKD.

61
Q

Loop diuretics have a … and therefore have a …. than thiazides

A

Loop diuretics have a steep dose-response, therefore, have a greater maximum effect than thiazides.

62
Q

The diuretic effect is reduced in renal impairment therefore requiring…

A

An increased dose of loop diuretics.

63
Q

Which cavity Kidney are situated in our body?

A

retroperitoneal cavity

64
Q

How many nephrons approx in our kidney?

A

One million nephrons

65
Q

The nephron comprises two structures what are they?

A

renal Corpuscle and renal tubules

66
Q

What are the functions of the Kidney?

A 
Excretory function
Regulatory function
Electrolyte balance 
Urinie volume and composition
Maintain pH
67
Q

What is the purpose of RAAS?

A

The purpose of Renin angiotensin aldosterone system(RAAS) is Homeostasis

68
Q

What RAAS do in terms of the cardiovascular system?

A

Regulation of Blood pressure

69
Q

Why do we need to understand RAAS?

A

Because they play a major role in human pathologies like Hypertension, Heart failure, Myocardial Infarction, Diabetic nephropathy

70
Q

If RAAS impaired what will happen?

A

Impaired potassium homeostasis
Impaired sodium and water homeostasis
Hypertension
Cardiorenal syndrome

71
Q

Where renin is stored?

A

Justaglomerular cells within afferent arterioles
Its half-life is 15 minutes
its primary substrate is circulating angiotensinogen

72
Q

What are the 3 determinants of renin release if they INCREASE?

A

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
Q

How RAAS works? MoA

A

Renin release then converts to ATS=>ATI=> ATI ii =>Aldosterone which then increases Water and Na reabsorption and K excretion

74
Q

What ATI II causes?

A

vasoconstriction

75
Q

What are the drugs which may Perturb(alter) the RAA system?

A 
ACE
ARB
NSAIDs
Loop diuretics
Vasodilators
Beta Blockers
76
Q

Does RAAS can be activated by low blood volume?

A

Yes they can by low blood volume and low BP Low Na B2 receptor activation

77
Q

What aldosterone can increase K loss in the distal tubules in exchange for increased?

A

Na reabsorption

78
Q

What increases K loss in the distal tubules? how?

A

aldosterone increases K loss in distal tubules in exchange for increased Na reabsorption

79
Q

Examples of ACE inhibitors?

A

Captopril Enalapril Fosinopril Cilazapril

80
Q

What is the example of ARBs?

A

Candesartan
Losartan
Valsartan (use as a combo only)

81
Q

What is the Mechanism of ACE inhibitors?

A

Inhibit Angiotensin-converting enzyme thus reduce the production of ATI II, aldosterone secretion and reverses renin induced vasocostriction

82
Q

MoA of ARBs?

A

Bind and block Angiotensin II receptors

83
Q

What ACE and ARB used for?

A

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
Q

How ace and ARB protect renal effect?

A

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
Q

Paradoxically ACE and ARB may cause

A

acute renal injury AKI while its used to protect the kidney but they slow the progression.

86
Q

Diuretics Types?

A

Loop Diuretics
Thiazides
Potassium sparing diuretics
Aldosterone antagonists

87
Q

What are the example of Loop diuretics?

A

Furosemide Bumetamide

88
Q

Examples of Thiazides?

A

Bendrofluazide, hydrochlorothiazide

89
Q

Example of Potassium-sparing diuretics?

A

Triamterene, amiloride

90
Q

Example of Aldosterone antagonists?

A

Spironolactone

91
Q

How do diuretics work?

A

Increase rate of urine flow
Increase Na, which flows the water (remember)
Reduce the extracellular fluid volume

92
Q

How do loop diuretics work?

A

They inhibit Na K and 2CL transport in the ascending loop of Henle

93
Q

What amount of Na reabsorbed and what amount of effect we can get of using Loop diuretics?

A

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
Q

How Thiazide diuretics work?

A

Inhibit Na and CL in the distal tubule

Hre 95 percent filtered Na reabsorbed and the only 5 percent interect

PHCY 310 (65 decks)

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