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CSI > Kidney Stones > Flashcards

Kidney Stones Flashcards

1
Q

What brought Mr Stanworth in?

A

Fatigue

He thought it could be related to thyroid

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2
Q

What were his abnormal test results?

A

Kidney function
High serum creatinine
High urine protein
Higher HBA1c

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3
Q

What does the doctor request?

A

Referral to kidney clinic
Ultrasound of kidney
Write to diabetes specialist

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4
Q

What long term condition does Mr Stnaworth have?

A

Type 2 diabetes

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5
Q

What is important in Mr Stanworth’s management?

A

Blood pressure control

Blood sugar control

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6
Q

What is diabetic nephropathy?

A

Kidney damage caused by diabetes

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7
Q

What is diabetic nephropathy also known as?

A

Kidney disease

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8
Q

What proportion of those with diabetes need treatment for kidney disease?

A

1 in 5

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9
Q

What causes kidney disease?

A

High blood glucose damages the small blood vessels and filters in the kidney
High blood pressure also does this
Causes leaks and abnormal amounts of protein leaves body via urine

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10
Q

What are the symptoms of kidney disease?

A 
Swollen ankles, feet and hands
Blood in urine
Fatigue
Shortness of breath
Nausea
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11
Q

How can the risk of kidney disease be reduced?

A 
Keep blood sugar within target range
Keep blood pressure down
Stop smoking
Eat healthily and keep active
Go to all medical appointments
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12
Q

What are the tests for kidney disease?

A 
Both included in 15 healthcare essentials
Urine test (ACR)
Blood test (eGFR)
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13
Q

What is the urine test called?

A

Albumin: creatinine ratio

Looks for signs that protein is leaking into urine

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14
Q

What does the blood test look for?

A

Tests for creatinine

Used to estimate glomerular filtration rate

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15
Q

How long does it take to receive blood test results?

A

A week

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16
Q

How is kidney disease treated?

A

High blood pressure managed by: ace inhibitors or a ARBs

Possible advice to avoid certain foods

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17
Q

How is late stage kidney disease treated?

A

Kidney transplant

Dialysis

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18
Q

What support is available to those with kidney disease?

A 
Diabetes team
National kidney Federation
British kidney patient Association
Diabetes.org helpline
Kidney research UK
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19
Q

What is the glomerulus?

A

Bowl of capillaries surrounded by the Bowmans capsule into which urine is filtered

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20
Q

What does the filtration barrier consist of?

A

Endothelial cells is glomerular capillaries
Glomerular basement membrane
Epithelial cells of Bowmans capsule (podocytes)

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21
Q

What are Perforations in the glomerular capillaries endothelium called?

A

Fenestra

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22
Q

How big are fenestrae?

A

70no

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23
Q

What is the role of these pores?

A

Do not restrict the movement of water and proteins or large molecules
But instead limit the filtration of cellular components e.g. RBCs

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24
Q

What surrounds the luminal surface of the endothelial cells?

A

Glycocalyx

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25
Q

What does glycocalyx consist of?

A

Negatively charged glycosaminoglycan is which function to hinder the diffusion of negatively charged molecules

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26
Q

What is the basement membrane made up of?

A

Mainly type IVcollagen
Heparan sulphate proteoglycans
Lamina

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27
Q

What are the three layers of the glomerular basement membrane?

A

And inner layer: lamina rara interna
A thick layer: lamina densa
An outer dense layer: lamina rara externa

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28
Q

What are podocyte?

A

Specialised epithelial cells of Bowmans capsule which form the visceral layer of the capsule

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29
Q

What projects from the podocytes?

A

Foot like processes which interdigitate to form filtration slits
The filtration slits abridged by a thin diaphragm Which has very small paws preventing large molecules from crossing

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30
Q

What is around the podocytes?

A

Negatively charged glycoproteins

Restrict filtration of large and anions

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31
Q

What percentage of nephrotic syndrome is minimal change glomerulonephritis?

A

10 to 25%

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32
Q

What triad of symptoms is experienced in a nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia
Oedema

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33
Q

How do the glomeruli appear under a light microscope in minimal change disease?

A

Normal

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34
Q

How do the glomeruli appear under an electron microscope in minimal change disease?

A

Diffuse effacement of the foot processes of podocyte

Microvillous change seen on the podocytes

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35
Q

What is the pathology a minimal change disease?

A

Uncertain and considered idiopathic

Thought to be due to a T-cell derived factor

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36
Q

What do patients with minimal change disease often respond well to?

A

Steroid therapy
Symptoms may relapse if the patient comes of steroid therapy
Some patients become steroid dependent but most do not progress to chronic renal failure
Those that do usually have focal segmental glomerulosclerosis as well

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37
Q

What is Alport syndrome?

A

Genetic disease characterised by progressive chronic kidney disease

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38
Q

So the symptoms of Alport syndrome?

A

Heamateria
Sensorineural deafness
Ocular abnormalities

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39
Q

What is the genetic mutation and inheritance of Alport syndrome?

A

In majority of patients inheritance is X-linked

With mutations of the gene coding for alpha five chain of type 4 collagen

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40
Q

What does the mutation in Alport syndrome result in?

A

Thinning of the lamina densa

Multilayering produces a basket weave appearance

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41
Q

What occurs in the later stages of Alport syndrome?

A

Glomerulosclerosis
Interstitial fibrosis
Tubular atrophy

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42
Q

What is the treatment for Alport syndrome?

A

No definitive treatment

But ACE Inhibitors are given to reduce proteinuria and progression of renal disease and also to control hypertension

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43
Q

What is the renin angiotensin aldosterone system?

A

Call moon system within the body that is essential for the regulation of blood pressure and fluid balance

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44
Q

What three hormones comprise the RAAS system?

A

Renin
Angiotensin II
Aldosterone

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45
Q

What is the system primarily regulated by?

A

Rate of renal blood flow

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46
Q

What is the first stage of the system?

A

Release of renin From the granular cells of the renal juxtaglomerular apparatus

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47
Q

What three factors trigger renin release?

A

Reduced sodium delivery to the distal convoluted tubule detected by macula densa cells

Reduced perfusion pressure in the kidney detected by Barrow receptors in the afferent arteriole

Sympathetic stimulation of the JGA via beta one adrenoreceptors

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48
Q

What is the release of Renin inhibited by?

A

Atrial naturetic peptide which is released by stretched atria in response to increased blood pressure

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49
Q

What is angiotensinogen?

A

Precursor protein produced in the liver and cleaved by renin to form angiotensin I

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50
Q

How is angiotensin I converted to angiotensin II?

A

Angiotensin converting enzyme

This conversion occurs mainly in the lungs where ACE is produced by vascular endothelial cells

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51
Q

How does angiotensin II exert its action?

A

Binds to various receptors throughout the body
Binds to one of 2G protein coupled receptors, AT1 and AT2
Most actions occur via the AT1 receptor

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52
Q

What is the action of angiotensin II on arterioles?

A

Vasoconstriction

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53
Q

What is the action of angiotensin II on the kidney?

A

Stimulates sodium reabsorption

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54
Q

What is the effect of angiotensin II on the sympathetic nervous system?

A

Increased release of noradrenaline

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55
Q

What is the effect of angiotensin II on the adrenal cortex?

A

Stimulates release of aldosterone

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56
Q

What is the effect of angiotensin II on the hypothalamus?

A

Increases thirst sensation and stimulates antidiuretic hormone release

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57
Q

What are the cardiovascular effects of angiotensin II?

A

Acts on AT1 receptors
Signalling occurs via Gq protein to activate phospholipids C
Increases intracellular calcium

Net effect: Increase in total peripheral resistance and consequently blood pressure

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58
Q

What are the neural effects of angiotensin II?

A

Thirst and secretion of ADH from the posterior pituitary gland increases circulating volume and therefore blood pressure

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59
Q

What is the effect of noradrenaline on the system?

A

Increase in cardiac output
Vasoconstriction of arterioles
Release of renin

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60
Q

How is vasoconstriction achieved in the renal artery and afferent arteriole?

A

Voltage gated calcium channels open and allow an influx of calcium ions

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61
Q

How is vasoconstriction achieved in the efferent arteriole?

A

Activation of AT1 receptor?

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62
Q

What effect does angiotensin II have on mesangial cells?

A

Contraction, leading to decreased filtration area

Achieved by activation of GQ receptors and opening of voltage gated calcium channels

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63
Q

How does angiotensin II increase sodium reabsorption in the proximal convoluted tubule?

A

Increased sodium hydrogen antiporter activity

Adjustment of the starling forces in peritubular capillaries to increase paracellular reabsorption

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64
Q

What does tubuloglomerular feedback do?

A

Helps to maintain a stable glomerular filtration rate
The release locally of prostaglandins which results in a preferential vasodilation to the afferent arterial is vital to this process

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65
Q

What is aldosterone and where is it released from?

A

It is a mineralocorticoid released from the Zona glomerulosa of the adrenal cortex

66
Q

What cells does aldosterone act on?

A

Principal cells of the collecting ducts in the nephron
Increases the expression of apical epithelial sodium channels to reabsorbed urinary sodium
Activity of the basolateral sodium potassium ATPase is increased

67
Q

What can increase levels of aldosterone produce with regards to potassium?

A

Reduce levels of potassium in the blood

68
Q

What are ACE inhibitors?

A

Class a drug typically used in the treatment of hypertension and heart failure

69
Q

Some examples of ace inhibitors

A

Ramipril
Lisinipril
Enalapril

70
Q

What do ace inhibitors do?

A

Inhibit the action of angiotensin converting enzyme

Reduce levels of angiotensin II within the body

71
Q

What is the physiological effects of ace inhibitors?

A

Decreased arteriolar resistance
Decreased arteriolar vasoconstriction
Decreased cardiac output
Reduced potassium excretion in the kidneys

72
Q

What are the side-effects of ACE inhibitors?

A 
Dry cough
Hyperkalaemia
Headache
Dizziness
Fatigue
Renal impairment
Rarely Angioedema
73
Q

What are the two most important prognostic factors in chronic kidney disease?

A

Hypertension

Proteinuria

74
Q

How do you ACE inhibitors reduce proteinuria?

A

Inhibition of the preferential vasoconstriction that occurs in the efferent arterial in the glomerulus
Thus reducing GFR and reducing urinary protein excretion

75
Q

In which patients should ace inhibitors be with held from or used with caution?

A

Bilateral renal artery stenosis

Acute kidney injury

76
Q

What is the function of the kidney?

A

Reabsorption
Secretion
Filtration
Excretion

77
Q

What is the functional unit of the kidney?

A

Nephron

78
Q

What makes up the nephron?

A 
Afferent arteriole
Glomerulus
Efferent arteriole
PCT
Loop of Henle
DCT
Collecting duct
79
Q

What is initial filtration dependent on?

A

Size and charge

80
Q

How is the nephron smart?

A

Salvaging on the basis of requirement

Secretion according to need

81
Q

What are the main features of creatinine?

A

Non protein molecule
Filtered freely
Not reabsorbed
High serum levels shows problems with filtration

82
Q

By what mechanism does proteinuria occur?

A

Proteins filtered through glomerulus with smaller ones passing through easily
Renal epithelial cells reabsorb proteins via endocytosis particularly in PCT
Normally all filtred proteins are reabsorbed

83
Q

What is the exception?

A

Secreted proteins e.g. Uromodulin

84
Q

What is overflow proteinuria?

A

Rhabdomyolysis: rapid breakdown of skeletal muscle
Results in muscle constituents being released to blood stream e.g. myoglobin
OR excess Haemoglobin due to excessive haemolysis
Excess of blood in bloodstream
Only so much reabsorption so protein is lost in urine

85
Q

What is glomerular proteinuria?

A

Diabetic nephropathy
More protein let through
-Secondary glomeruopathy (secondary to disease or drug)
- Primary glomerulopathy (intrinsic)

86
Q

What is the difference between haemoglobinuria and heamateria?

A

Free Haemoglobin vs. Bleeding from the urinary the tract itself also has intact red blood cells

87
Q

What type of protein is predominantly lost in glomerular proteinuria?

A

Albumin
Intermediate size protein roughly same size as glomerular pore
Flexible

88
Q

What are the main features of tubular protein area?

A

Acute tubulointerstitialnephritis
Can be acute or chronic
Acute- nephrotoxic drugs

89
Q

Which for drugs are the most common cause of acute kidney injury in hospitalised patients?

A

Amino glycosides
Contrast
NSAIDS
ACE inhibitors

90
Q

Which of these mechanisms do you think is capable of the biggest protein loss?

A

All of them

91
Q

Which arterioles hyperglycaemia particularly affect?

A

Efferent

92
Q

Which system does hyperglycaemia directly activate?

A

RAA

93
Q

What does afferent arteriolar narrowing do?

A

Increases upstream pressure in the glomerulus

94
Q

What does hypertension cause in the glomerulus?

A

Increased flow through the afferent arteriole, further increasing glomerulal pressure

95
Q

What with the glomerulus usually be protected by?

A

Auto regulation and afferent arteriolar constriction

But this feedback mechanism is altered in diabetes

96
Q

Why does diabetes increase sodium reabsorption?

A

Proximal tubule is work hard to reabsorbed excess glucose increased sodium reabsorption because sodium is Co transported with glucose

97
Q

What does low-sodium uptake by macula densa cells cause?

A

Less stimulation of afferent arteriole vasoconstriction

98
Q

What happens to patients early and diabetic nephropathy?

A

Patients have increased filtration rates

99
Q

What is glomerulosclerosis?

A

Excessive extracellular matrix that leads to the hardening and scarring of the glomerulus
Results in reduced capacity for filtration

100
Q

What intrinsic changes to the basement membrane are seen in those with diabetes?

A

It becomes thickened and structural changes means it also becomes leaky

101
Q

What is nephrin?

A

Key protein component of podocytes

102
Q

What are the most common causes of chronic kidney disease in the western world?

A

Diabetes
Hypertension
Glomerulonephritis

103
Q

What happens in the kidneys when around 50% of nephrons are damaged regardless of pathophysiology?

A

Adaptive hyperfiltration- blood flow shunted to functioning nephrons and away from damaged ones

104
Q

What does adaptive hyperfiltration lead to in originally healthy nephrons?

A

Glomerulosclerosis
Ischaemic injury
Loss of filtration
Nephron loss

105
Q

What’s the best way to monitor or screen for proteinuria in diabetes?

A

Albumin: creatinine

Ratio of urine sample

106
Q

What is the issue with a urine dip stick test?

A

Detects albumin
But poor sensitive
Might miss cases
Does not detect some proteins e.g. myoglobin

107
Q

How much albumin lost today is normal?

A

Less than 30mg a day

Usually 5-10mg a day

108
Q

What is the issue with a 24 hour urine test?

A

Relied on patient to accurately collect all urine
Impractical
Often not collected accurately
Total protein should be less than 150mg a day

109
Q

What is the issue with random albumin concentration?

A

Unreliable
Depends on urinary concentration
Depends on patients hydration

110
Q

Why is in albumin creatinine ratio of urine sample used?

A

Account for differences in urine concentration
Provides reasonable estimate of protein loss
Used in diabetes: greater sensitivity

111
Q

Why do you check for proteinuria in diabetes?

A

Cardiovascular risk
Identification and early diagnosis
Often a sign of damage in other areas and can predict those that are more likely to progress to chronic kidney disease

112
Q

What is microalbumiuria?

A

Albumin loss between 30-300mg a day

Predictive and prongnostic marker of CKD

113
Q

What is macroalbuminuria?

A

Greater than 300mg lost a day

Now moderate and severe are the proffered terms

114
Q

What is GFR?

A

Glomerular filtration rate

115
Q

How can GFR be estimated?

A

What volume of fluid is filtered from the glomerular capillaries to the bowman capsule per unit time

Proportional to clearance of a certain substances

116
Q

Why is creatinine used?

A

Freely filtered
Not reabsorbed
Ideally not secreted but a little it (5-10%)
Considered roughly proportional to GFR

117
Q

What is clearance equal to?

A

Urinary [substance] x urine production rate divided by plasma [substance]

118
Q

What is done clinically to estimate GFR?

A

Evidence Based formula is that you serum creatinine without need for urinary creatinine
More practical

119
Q

What is the most commonly used formula?

A

MDRD formula
Origin: the modification of diet in renal disease study
Tracer injected IV (isotopic]

120
Q

What is considered in the MDRD formula?

A

Age
Ethnicity
Gender

121
Q

Why are these demographic data important?

A

Different serum creatinine depends on amount produced which is higher with increasing creatinine
Also depends on dietary protein consumption

122
Q

In who should this formula be used carefully?

A 
High protein diets
Extremes of weight
Amputees
Body builders
Muscle wasting conditions 
Pregnant women
123
Q

What do you aim to catch early?

A

Albuminuria

124
Q

What are the markers of chronic kidney disease?

A 
Albuminorrhoea
Electrolyte abnormalities
Abnormal abnormalities on histology
Structural abnormalities
Kidney transplantation
125
Q

What else must be considered when using Creatine to estimate GFR?

A

When serum creatinine is unstable

E.g. acute kidney injury

126
Q

What factors in an acutely unwell patient might impact the serum creatinine?

A 
Drugs
Trauma
Malnutrition 
Muscle wasting
Sepsis
127
Q

Why is it not reliable in pregnant lady?

A

Filtration rate increases

GFR estimate unreliable

128
Q

Why is it not reliable and should be used with caution in those with end stage kidney disease?

A

In end stage kidney failure

As GFR falls the proportion of Creatine secreted increases and the amount actually filtered decreases

129
Q

What is Mr. Stanworth’s diagnosis?

A

3A A2 CKD

130
Q

What medication should Mr. Stanworth be started on?

A

Ramipril- ACE inhibitors reduced glomerular pressure
Atorvastatin
Insulin

Target the modifiable risk factors
Hypertension
dyslipidepia
Hyperglycaemia

131
Q

What causes symptoms of CKD?

A

Decreased excretion
Decreased biosynthesis
Altered metabolism

132
Q

Main features of decreased excretion

A 
Increased sodium and water: volume overload
Hyperkalemia: increased potassium
Increased H+: metabolic acidosis
Increased urea
Increased uric acid: gout
Increased phosphates: renal bone disease
133
Q

Main features of decreased biosynthesis

A

Anaemia due to reduced erythropoietin synthesis
Normocytic, normochromic

Vitamin D decreasing- renal bone disease

134
Q

Main features of altered metabolism

A

Abnormal lipid metabolism

Sex hormones: sexual dysfunction

135
Q

What is released By the kidneys to aid absorption?

A

Vitamin D

136
Q

What do the kidneys aid absorption of?

A

Calcium

137
Q

What senses a decrease in the absorption of this molecule?

A

Parathyroid gland

138
Q

What is used to hydrolyse stores of this molecule?

A

Parathyroid hormone

139
Q

Where is this molecule stored?

A

Bone

140
Q

What is molecule Y?

A

Phosphate

141
Q

What is molecule Z?

A

FGF23
Bone derived hormone
Elevated in CKD
Decreases reabsorption and increases secretion of phosphate

142
Q

What is the likely progression for Mr Stanworth’s chronic kidney disease?

A

He has CKD stage two with eGFR of 61
Has moderate albuminuria
Expect to progress to 3a within 2 years
3b within 10 years

Improvement in first year or so due to drug interventions

143
Q

What is the take home message?

A

Early detection is key

144
Q

What does the general management for CKD involve?

A

Treatments of reversible causes
Preventing or slowing the progression
Treatments of complications of renal failure
Adjusting drug doses when appropriate for the level of eGFR
Identification and adequate prep of patient in whom renal replacement therapy will be required

145
Q

What are the reversible causes of renal failure?

A

Decreased renal perfusion
Administration of nephrotoxic drugs
Urinary tract obstruction

146
Q

What causes decreased renal perfusion?

A

Hypovolemia
Hypotension
Infection
Administration of drugs

147
Q

What drugs can interfere with creatinine secretion and the creatinine assay?

A

Trimethoprim (UTI antibiotic)

148
Q

How do drugs interfere with creatinine assays?

A

Does not change glomerular filtration rate

may reuse tin increased serum creatinine

149
Q

Why may a urinary tract infection always be considered?

A

Inhibits the flow of urine

150
Q

What can cause a UTI?

A

prostate enlargement
kidney stone
ureteric scars
strictures

151
Q

What is hydronephrosis?

A

Where the kidney is swollen due to inability to drain properly

152
Q

What therapeutic modalities can be used to offer renal protection?

A

Protein restriction
Stopping smoking
Treatment of chronic metabolic acidosis
Control of blood glucose

153
Q

How do you treat volume overload?

A

Combination of dietary sodium restriction

Diuretic therapy

154
Q

In which patients is hyperkalaemia seen?

A

Oliguiric patients
High-potassium diet
Increased tissue breakdown
Hypoaldosteronism

155
Q

How is metabolic acidosis treated?

A

Bicarbonate supplementation

156
Q

What is phosphate retention related to?

A

Secondary hyperparathyroidism

157
Q

What changes in bone structure are seen in progressive CKD?

A

osteitis fibrosa
osteomalacia
dynamic bone disease

158
Q

How are the bone disorders treated?

A

dietary phosphate restriction
administration of oral phosphate binders
calcitriol

159
Q

What percentage of CKD patients have hypertension?

A

80-85%

160
Q

What are the big six?

A 
Eating healthily
Regular exercise 
Give up smoking
Reduce alcohol intake 
Keep blood pressure down
Control diabetes

CSI (17 decks)

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