10b.) CKD Flashcards
1
Q
Describe adult polycystic kidney disease, include:
A
- Abnormal cysts (swellings filled with fluid) form on kidneys and other organs
- Autosomal dominant
- Mutation in:
- PKD 1 gene (85%)
- PKD 2 gene
- Diagnosed via ultrasound (but may do genetic testing if family history)
- Prognosis depends on rate of increase in kidney size and age- eventually leads to kidney failure
- Symptoms:
- Pain in kidneys
- Haematuria if cyst bursts
- High blood pressure
- Infection
- Renal stones
- Any other symptoms of kidney failure
2
Q
Explain why adult polycycstic kidney disease generally presents in adulthood
A
- Cysts grow with age and we diagnose on ultrasound so cysts might not be visible till adulthood (this is why you can’t exclude APCKD with ultrasound if patient under 30 years old)
- Takes time for renal failure to develop
3
Q
For adult polycystic kidney disease, the mutation can be in PKD 1 gene or PKD 2 gene; which mutation causes earlier disease?
A
PKD 1 gene (it is also more common ~85%)
4
Q
What happens to the size of kidneys in adult polycytic kidney disease?
A
Increase
5
Q
Hypertension is often the first sign of adult polycystic kidney disease and it occurs before renal function changes; true or false?
A
True
6
Q
Patients with adult polycystic kidney disease have an increased incidence of what 2 conditions?
A
- Intra-cranial aneurysm
- Heart valve abnormalities
7
Q
Describe the managemetn of adult polycystic kidney disease, including pharmacological and general management
A
- Treat hypertension: block RAAS e.g. ACE inhibitor, angiotensin blocker
- Diet:
- Lots of fluid (4L)
- Low salt
- Normal but not excessive protein
- Tolvaptan: vasopressin II antagonist hence causes increased urination (a lot therefore can have low compliance)
- Others e.g. somatostain analogues
8
Q
Describe how GFR and hence the general aims of treatment changes as you progress through stages of chronic kidney disease
A
9
Q
How many nephrons do humans have in total?
How many do we need to survive?
A
- 2 x106 nephrons (1 x106 in each kidney)
- Only need 40,000 to survive
IDEA IS JUST TO SHOW SCALE OF DAMAGE NEEDED TO CAUSE RENAL FAILURE
10
Q
Define chronic kidney disease
A
Progressive and irreversible loss of renal function over a period of months to years
11
Q
Describe what happens to renal tissue in CKD
A
Damaged renal tissue is replace by extracellular matrix (fibrosis) histologically giving rise to glomerulosclerosis and tubuler interstitial fibrosis
12
Q
CKD is associated with substantial cardiovascular morbidity and mortality even with mild CKD; true or false?
A
True
13
Q
Describe how we stage CKD
A
We look at GFR in combination with albuminuria
14
Q
State 4 categories of people that CKD is more common in
A
- Elderly
- Ethnic minorities
- Multi-morbid
- Social deprivation
15
Q
What % of population in UK have CKD?
A
6.1%
16
Q
State some common causes of CKD
A
- Diabetes (MOST COMMON)
- Arteriopathic kidney disease
- Hypertension
- Immunological e.g. glomerulonephritis
- Infection e.g. pyelonephritis
- Other systemic diseases e.g. lupus
- Obstructive and reflux nephropathies
- Genetics (family history of CKD stage 5 or adult polycystic kidney disease)
17
Q
If a child presents with polycystic kidney disease what is the inheritance pattern likely to be?
A
Autosomal recessive
18
Q
Describe what happens to size of kidney in CKD
A
Kidney size decreases (renal cortex size decreases)
Histology shows fibrosis
19
Q
What are the two most common causes of CKD?
A
- Diabetes (45%)
- Hypertension (33%)
20
Q
State some factors, other than the underlying disease process, that may cause progressive renal injury (3)
A
- Any form of AKI (including nephrotoxins or decreased perfusion)
- Proteinuria
- Hyperlipidaemia
21
Q
State some symptoms of CKD
A
- Tirendess
- Breathlessness
- Restless legs
- Sleep reversal
- Aches & pains
- Nausea & vomitting
- Ithcing
- Chest pain
- Seizures
22
Q
CKD is a systemic disease; state effects on:
- General effects
- Cardiovascular
- Haematology
- Bone
- CNS
- GI
- Endocrine
- Metabolic
A
23
Q
What happens to the:
- Life expectancy
- Quality of life
… of patients with CKD?
A
Both decrease
24
Q
When investigating CKD what 5 things must we do?
A
- Define degree of renal impairment
- Defince cause of reanl impairment
- Provide patient with diagnosis & prognosis
- Identify complications of CKD
- Plan long term treatment (delay progression & plan for for dialysis and transplantation)
25
What 2 things MUST you measure/investigate in someone with CKD?
* Blood pressure
* Urien dipstick
26
eGFR is accurate in children; true or false?
FALSE
27
eGFR is not useful in CKD but it is useful in AKI; true or false?
FALSE- useful in CKD (it actually defines CKD!) but not useful in AKI as it takes time for it to change and AKI is too quick to notice much change
28
State some blood tests you would do for a patient with CKD (think about why)
* Urea & electrolytes
* Bone biochemistry
* Liver function (albumin)
* FBC
* CRP
* +/- Fe levels
* +/- PTH
29
If you suspect an auto-immune disease as a cause of CKD would you do futher tests?
Yes
30
Alongside blood tests, state some other investigations you can do for CKD
31
State some risk factors for CKD that we can try to elimate/reduce
* Smoking
* Obesity
* Lack of exercise
* Poorly controlled diabetes
* Hypertension
* Proteinuria
* Lipids (due to already increased CVS disease risk)
32
Remind yourself of some of the functions of the kidney
33
If someone with CKD has proteinuria what drug should they be on?
ACE inhibitor or antgiotensin receptor blocker as long as their kidney disease isn't so far advanced that they are at risk of hyperkalaemia
34
80-85% of CKD patients are hypertensive; state 3 ways we can manage hypertension
* Anti-hypertensive drugs
* Diuretics
* Fluid restriction
35
Explain why someone with CKD may need to be on fluid restriction
* If their GFR decreases then their maximum urine output for the day will be increased
* Say their maximum urine output was 1-2L a day and they drank 4L the other 2-3L would go into interstitium
36
Explain why someone with CKD may complain of nocturia
Have small glomerular filtrate rate but still have same solute load that they need to excrete; the high solute load reduces repsonse to ADH. At night, ADH usually kicks in to stop us needing to urinate throughout night.
37
Hyperkalaemia can occur in CKD patients once eGFR \<20mls/min; state 3 things we can do to manage hyperkalaemia
* Stop ACE inhibitor/angiotensin receptor blocker
* Avoid drugs that increase K+ (e.g. spironalactone)
* Alter diet to avoid foods with high potassium
38
Explain why metabolic acidosis may occur in CKD patients
How do we treat metabolic acidosis in CKD patients?
* CKD= renal failure
* Less re-absorption of bicarbonate
* Loss of bircarbonate
Treat with oral NaHCO3 tablets
39
State some symptoms of acidosis
40
State some possible causes of anaemia in CKD
41
Treating anaemia in CKD can help slow progression of renal disease; true or false?
True
42
Describe how we would treat anaemia in CKD (think about the order we would do things in)
1. Check Fe stores (if low replace)
2. If Hb still low start erythropoietin stimulating agent
43
Describe how CKD can lead to mineral bone disease
* Kidneys ability to excrete PO4- decreases
* Increases CaPO4 deposition
* Decreases plasma [Ca2+]
* Increased PO4- and Ca2+ stimulates parathyroid glands
* Increase PTH
* Increase bone resoprtoin
* Increase in bone resorption increases FGF23 which inhibits activation of vitamin D in kidneys
* Decreases Ca2+ absorption
* Decrease bone mineralisation
* Further stimulate PTH
* Renal klotho production falls in CKD and klotho deficiency may contribute to tissue & vascular calcification
44
State some consequenes of renal bone disease
* Weak bones
* Calcium deposits elswhere e.g. joints, skin
45
State how we manage CKD-mineral bone disease
* Reduce phosphate intake
* Phosphate binders
* One-alpha-calcidol (vitamin D analogue)
46
Lots of drugs require dose alteration in CKD; true or false?
True because there may be:
* Reduced drug metabolims
* Reduced excretion
* Increased drug sensitivity
47
CKD leads to accumulation of waste products; what symptoms can the accumulation of waste products cause?
Uremic syndrome symptoms e,g:
* Nausea and vomitting
* Reduced appetite
* Pruritis
48
# Define end stage renal failure
What is the eGFR at ESRF?
* Renal failure at a point where death is likely without renal replacement therapy
* eGFR \<15mls/min
49
When do we start renal replacement therapy?
When renal function declines to a levle no longer adequete to support health
50
State some symptoms of ESRD
* Overwhelming fatigue
* Physically and mentallly incapacitated
* Difficulty sleeping
* Difficulty concentration
* Signs & symptoms of volume overload
* Nausea & vomitting
* Restless legs
* Pruritis
* Sexual dysfunction/infertility
* Increased infections
51
State 3 treatment options when kidneys fail
* Haemodialysis
* Peritoneal dialysis
* Transplant
52
Briefly describe how haemodialysis works
* Blood taken out of artery
* Blood flows into machine where it is separted from a suitable fluid by semipermeable membrane
* Electrolytes and solutes diffuse acorss membrane until equilibrium is reached
53
Describe the practicalities of haemodialysis
* 4 hours (minimum), 3x per week
* Designated slot
54
Briefly describe how peritoneal dialysis works
* Put fluid into peritoneum (4-5 bags per day)
* Peritoneal membrane acts as semi-permeable membrane allowing substances to diffuse across
* Waste drainage collected
55
Discuss advantages and disadvantages of peritoneal dialysis and haemodialysis
56
Discuss advantages and disadvantages of a kidney transplant to treat CKD
For disadvantages also:
* Immunosupressants increase infection and malignancy risk
* Risk of diabetes, hypertension from medications required after transplant
57
Where are transplanted kidneys "plumbed into"?
Iliac vessels
58
Explain why CKD leads to hypertension
Reduced GFR, increases Na+ and hence water retetion, increase intravascular volume
59
Describe how you can differentiate between AKI and CKD, include:
* Similarities
* Differences
60
Describe how remaining nephrons compensate when there is loss of functioning nephrons
Hypertrophy and increase filtration and solute reabsorption but this causes damage to nephrons and ultimately leads to further loss
61
What is fibromuscular dysplaisia?
State some symptoms
Can it lead to CKD?
* Non-atherosclerotic, non-inflammatroy disease of blood vessels that causes abnormal growth within wall of artery- often occurs in renal arteries leading to renal stenosis
* Symptoms:
* Heart: chest pain, SOB
* Abdo: pain after eating, weight loss
* Limbs: weakness, cold limbs
* Yes
62
How do we define oliguria in:
* Infants
* Children
* Adults
* Infants: \<1ml/kg/h
* Children: \<0.5ml/kg/h
* Adults: \<400 or 500ml per 24 hours
