Renal Flashcards
1
Q
Define AKI
A
A rapid decline in kidney function over hours to days resulting in the failure to maintain fluid/electrolyte and acid/base homeostasis and a build up of nitrogenous waste in the blood.
The decline in kidney function is measured by serum creatinine and urea levels
2
Q
What staging system is used in AKI
A
KDIGO
3
Q
How is stage one AKI defined
A
Serum creatinine 1.5-1.9 above baseline OR a riwszse of 26.5uM in 48 hours
AND
Urine output <0.5ml/kg/hr for last 6-12 hours
4
Q
How is stage 2 AKI defined
A
Serum creatinine 2-2.9x baseline
And urine output <0.5ml/kg/hr for more than 12 hours
5
Q
How is stage 3 AKI defined ?
A
Serum creatinine 3x baseline
Or serum creatinine of 353.6uM
Or initiation of renal replacement therapy
Or if <18yrs and EGFR of <35ml/min
And urine output of <0.3ml/kg/hr for >24 hours or anuria for >12 hours
6
Q
How can the causes of AKI be categorised ?
A
Pre renal - reduced perfusion of the kidneys
Renal - affecting the kidney itself
Post renal- affecting the urology system e.g. Some blockage
7
Q
What are the most commonest causes of AKI?
A
Ischaemia
Sepsis
Nephrotoxins: most commonly gentamicin , NSAIDs, ACEi and iodinated contrast
8
Q
What are the pre-renal causes of AKI?
A
Hypovolaemia: dehydration, burns, pancreatitis, hypoaldosteronism, cirrhosis
Hypotension: sepsis, anaphylaxis
Low CO: heart failure
Vascular: renal artery stenosis
Drugs:
- NSAIDs cause vasoconstriction afferent
- ACEi cause vasodilation of efferent
9
Q
How can the renal causes of AKI be divided?
A
Tubular
Glomerular
Vascular
Interstitial
10
Q
What are the causes of acute tubular necrosis (renal cause of AKI)?
A
Ischaemia (all the pre renal causes can lead to ischaemia and ATN)
Nephrotoxins:
-Endogenous: haemoglobinaemia (DIC due to sepsis or haemolysis), rhabdomyolysis, light chain Ig in myeloma, urate and bilirubin.
- exogenous: NSAIDs, ACEi, contrast medium, aminoglycosides and amphotericin
11
Q
Why should you be aware of AKI in someone on statins with CKD?
A
Risk factors include CKD itself, the fact they are on statins means they have high lipids and thus vascular risk factors and finally statins can lead to rhabdomyolysis esp if CKD and impaired excretion of statins
12
Q
What are the glomerular causes of AKI (part of renal causes)
A
Autoimmune: SLE, wegeners
Nephrotic, nephritic syndromes
Drugs, infections, thrombocytopenia
Pre eclampsia- high blood pressure leads to BM damage
13
Q
What are the vascular causes of renal AKI
A
Vasculitis, thrombotic emboli, pre- eclampsia and malignant hyperthermia
14
Q
What are the renal interstitial causes of AKI?
A
Drugs: NSAIDs, penicillins and diuretics
Infections: pyelonephritis , TB and haemorrhagic fever
Sjogrens
Infiltration with lymphoma
15
Q
How can the post renal causes of AKI be divided?
A
Intraluminal
Intramural
External
16
Q
Relatively how common are the post renal causes of AKI
A
Least common
More likely to affect elderly
17
Q
What are the intraluminal causes of post renal AKI
A
Tumour
Stone
18
Q
What are the intramural causes of post renal AKI?
A
Structures- post TB Tumours Reflux nephropathy Neurological disorders: MS, Diabetes, spinal cord injury Drugs: Levo dopa and anticholinergics
19
Q
What are the external causes of post renal AKI?
A
Benign prostatic hyperplasia
Malignancy- bladder /prostate
Aortic aneurysm
Gravid uterus
20
Q
How does post renal AKI lead to reduced renal function
A
A blockage leads to build up of fluid and thus pressure
This leads to dilation of renal pelvis (hydronephrosis)
The build up in pressure reduces glomerular filtration
21
Q
List the general risk factors for AKI
A
Age Diabetes Sepsis Dehydration Cancer Peripheral vascular disease Cardiac failure CKD Chronic liver failure Drugs Female Anaemia
22
Q
What are the complications of AKI?
A
Regulation of fluid, electrolytes, pH and blood pressure are all disturbed
- hyperkalaemia, hyponatraemia, hyperphosphataemia, hypocalcaemia
- acidaemia
- uricaemia- itchy, nausea, impotence, tired, weak. More severe is pericarditis and encephalopathy
Spontaneous haemorrhage - GI
Hypertension
Increased half life of medication
23
Q
How can we avoid AKI
A
Identify high risk patients: CKD, diabetes, nephrotoxins, cardiac or liver disease, vascular disease
Monitor them regularly - creatinine, urinalysis
Educate on hydration and other risk factors
If creatinine rises stop metformin
If in hospital ensure monitoring is more regular, oxygenate, get nephrologist opinion before any contrast medium
24
Q
How would you initiate management of someone with suspected AKI (write down answers - big answer)
A
Start with ABCDE
- in C ensure you cover JVP, lung crepitations and oedema (assess volume status). Also venous k+ and ECG because if hyperkalaemia this can kill them.
Take full history:
- look for risk factors of pre renal, renal and post renal
- this includes a detailed PMH and drug history
- CVS risk factors
- any known autoimmune conditions or symptoms of autoimmune
- symptoms of cancer- ask this to rule out
- double check UTI symptoms and history of renal stones , history of malignancy
- any haematuria or loin pain (sign of stones)
Examination:
Look for signs of fluid overload/ depletion, signs of the cause
- feel peripheries- cool (shut down), warm (sepsis)
- capillary refil - long suggests cardiac failure
- JVP
- signs of dehydration
- check peripheral oedema and lung bases - volume overload
- check lungs for signs of pneumonia - source of sepsis
- check abdomen for shifting dullness- source of sepsis
- feel for polycystic kidneys, palpable bladder and renal bruit
- if you suspect renal cause look for rashes, oral ulcers, epistaxis in case of autoimmune
- if you suspect post renal check for abdo masses, rectal exam for prostate in men.
Investigations
- urinalysis
If low sodium then pre renal AKI
If blood is present may be stones, vasculitis, glomerulonephritis
White cells: infection, acute interstitial necrosis
Protein: glomerulonephritis, myeloma
If normal does not exclude AKI
- bloods
FBC, U&Es, LFT
Clotting due to DIC in sepsis
Blood cultures if suspect sepsis
CK and myoglobin - in case rhabdomyolysis
Venous blood gas and ABG
- immunology
Screen for autoantibodies in case of autoimmune
SLE: ANA and anti phospholipid
Wegeners: ANCA
Anti GBM : goodpastures
- electrophoresis for bence jones proteins in myeloma
- imaging:
CXR: pulmonary oedema and haemoptysis
USS of renal track ASAP esp if hydronephrosis is suspected
- renal biopsy - only if unknown cause and the cause would alter the management
Management:
- Treat cause where possible and monitor electrolytes and fluids regularly. This means catheterising the patient so fluids can be monitored closely.
- stop nephrotoxins
- aim for euvolaemia. Either by restricting fluids (fluid overload) or giving crystalloid / Hartmanns (fluid deplete)
- management of complications
Hyperkalaemia
Pulmonary oedema:
sit up and high flow oxygen
Give venous dilator - diamorphine
Give furosemide
Consider CPAP
Dialysis if unresponsive
Uraemia: treat symptoms such as itching. Dialysis needed if severe complications such as pericarditis and encephalopathy
Acidaemia: NaHC03 oral or IV otherwise dialysis - treat cause
Sepsis - Abx
Inotropes in ICU if in shock
Fluid resuscitation if volume deplete
Renal causes sometimes respond to steroids but often need referral because may be myeloma, autoimmune or glomerulonephritis
Post renal - catheterise and refer to urology - may need stent etc
25
When should you refer a suspected AKI case to a nephrologist?
```
Hyperkalaemia in oligoruic patient
High k , fluid overload or acidaemia unresponsive to treatment
Bad signs of uraemia
Indication for dialysis
Glomerulonephritis
```
26
What are the indications for dialysis in AKI?
```
Refractory pulmonary oedema
Persistent hyperkalaemia
Severe metabolic acidosis
Uraemic complications such as pericarditis and encephalopathy
Drug overdose
```
27
What is the prognosis of AKI ?
Greatly depends on cause and severity
Outcome can be predicted by comorbidities
some fully recover, others go on to have CKD
28
How may someone present with AKI ?
Vague symptoms
Reduced urine output
Vomiting and confusion
Signs associated with cause- sepsis, dehydration
Signs associated with complications - uraemic syndrome (itchy, tired, nausea, palpitations )
29
What would you find on examination for a
A) hypovolaemic patient
B) cardiac failure patient
c) septic patient (systemic vasodilation )
A) low blood pressure , low JVP, cool peripheries
B) low blood pressure, high JVP, cool peripheries, oedema
C) low blood pressure, low JVP, warm peripheries and wide pulse pressure
30
What electrolyte disturbances can alkalosis lead to ? Acidosis?
Hypokalaemia - due to H/K exchanger
Hypocalcaemia - as pH rises transport proteins such as albumin become more ionised so calcium binds more strongly to them
Opposite for acidosis
31
What's the normal range for serum sodium ?
135 to 145 mM
32
What are the problems with hypernatraemia?
Water is drawn out of cells - cellular dehydration
If sodium is high due to loss of volume then this loss of volume creates vascular sheer stress which can result in bleeding and thrombosis
33
What are the causes of hypernatraemia ?
```
Excess hypertonic fluids:
-IV fluids, TPN, sea water drowning, excess salt
Excess water loss:
- renal: diabetes insipidus , diuretics, osmotic diuresis (DKA)
- Cushing's and cons
- gut: diarrhoea , vomiting , fistula
- skin: sweating and burning
Decreased thirst :
- elderly and unwell
- psychotic medication
```
34
What is diabetes insipidus ?
Group of disorders where there is excess water loss but not due to diabetes but a problem with water conservation mechanism of the body
Central diabetes insipidus - problem with the hypothalamus/ posterior pituitary whereby not enough ADH is released.
This may be caused fracture to base of skull, tumour, TB, meningitis , cerebral vasculitis (wegeners) or aneurysm
Nephrogenic diabetes insipidus- kidneys are not sensitive to ADH
May be congenital, due to lithium, hypokalaemia/hypercalcaemia
35
What are the symptoms of hypernatraemia?
Signs/ symptoms of cerebral dehydration:
- thirst
- apathy
- confusion
- reduced consciousness
- seizures and coma
Signs of dehydration
36
What investigations are carried out if you suspect someone is hypernatraemic?
Check serum sodium, glucose and osmolality
Check urine sodium and osmolality - i.e. Deciding on cause because if diabetes insipidus then urine will be very dilute and increased urine output (assuming no diuretic medication )
Then could do a fluid deprivation test to further check for diabetes insipidus - I.e. If dilute urine is still being produced then supports diagnosis
37
What is the treatment for hypernatraemia ?
Seek expert help
Depends on cause
Diabetes insipidus:
- cranial: intranssal desmopressin (ADH nasal spray) , ADH can also be given IV
- nephrogenic thiazide diuretic (improves environment for ADH sensitivity)
Dehydration
- should be corrected slowly over 48 hours this is because excessively rapid rehydration may result in cerebral odema
- can give water orally or via IV fluids ( but hypotonic fluids should be avoided )
38
What are the categories for the causes of hyponatraemia ?
1. Age - with age the kidneys become less efficient and there is reduced capacity to excrete water. This is exacerbated by drugs that reduce renal function e.g. NSAIDS
2. Hypovolaemic hyponatraemia
3. Hypervolaemic hyponatraemia
4. Euvolaemic hyponatraemia
39
What are the renal causes of hypovolaemic hyponatraemia?
Diuretics (thiazides in particular )
Osmotic diuretics (glucose)
Salt wasting nephropathy (chronic tubular dysfunction)
Addison's disease
40
What are the non renal causes of hypovolaemic hyponatraemia ?
Sweating, diarrhoea
Pancreatitis
Brain injury leads to release of brain natriuretic peptide
41
What are the causes of hypervolaemic hyponatraemia?
Nephrotic syndrome
Congestive heart failure
Cirrhosis
42
What are the causes of euvolemic hyponatraemia?
Syndrome of inappropriate ADH release (SIADH) - increase ADH from pituitary or other source
Hypothyroidism: due to reduced GFR due to systemic effects of thyroid hormones on vascular resistance and cardiac output
43
What is the main complication of hyponatraemia?
Osmotic pressure of blood is reduced which can lead to cerebral oedema
If the drop in sodium is acute, it is much more of a problem.
If over a long period of time, the brain can adapt to prevent cerebral oedema
44
What are the signs and symptoms of hyponatraemia?
Most hyponatraemic patients are assymptomatic because it slowly occurs and body adapts. However if it occurs more rapidly or if sodium gets very low then there are symptoms:
- anorexia, nausea and malaise unitially
- then weakness, perception disturbances and gait disturbances (risk of fracture)
- headache, confusion, apathy
- can lead to seizures and coma
These symptoms may be due to cerebral oedema and encephalopathy
45
What investigations would you do if you suspected hyponatraemia ?
On examination look for signs:
- fluid level: oedema , JVP
- stigmata of addisons : pigmentation
U&Es
- if k and mg are low this can potentiate ADH release
- high k could indicate addisons , diuretic use
TSH and 9am cortisol
Albumin and glucose
46
How is hyponatraemia managed ?
Try to make a diagnosis for cause
Stop giving giving drugs and fluids that are causing it
Correct Mg and K if incorrect
Assymptomatic
- hypovolaemic: resuscitate with 0.9% saline
- euvolaemic: usually due to SIADH. Restrict fluid intake and give sodium tablets and furosamide. Demeclocycine and lithium to treat SIADH
- hypervolaemic : fluid restriction
Acute ( encephalopathy )
- take to ICU
- give hypertonic saline and could give furosamide to reduce fluid depending on cause
47
What is pseudo hyponatraemia ?
Sodium concentration is actually normal but appears to be less because the volume of plasma is made up by addition of products e.g. Hyperlipidaemia , hyperproteinaemia (myeloma) and hyperglycaemia
48
What two drugs can be used to treat SIADH release and explain how the first works?
Demeclocycline : induced nephrogenic diabetes insipidus
| Lithium ( also known to induce nephrogenic diabetes insipidus)
49
What is hypoosmolar hyponatraemia caused by?
Defect in renal water excretion
- volume depletion , advanced renal failure, SIADH
Water intake exceeding normal excretory capacity
50
What is translocational hyponatraemia ?
Water comes out into ECG due to osmotic drive
| Caused by Hyperglycaemia and exogenous solutes such as mannitol
51
State what value is classed as hyperkalaemia
More than 5 mM
52
What is pseudohyperkalaemia
Venepuncture can cause localised hyperkalaemia
53
What are the causes of hyperkalaemia ?
```
Kidneys : AKI or CKD
Increased intake - bananas
Drugs
Addisons
metabolic acidosis
Increased release from cells : DKA ( acid and low insulin ), acidosis, tumour lysis, rhabdomyolysis (trauma, statins), exercise and haemolysis
```
54
Which drugs can cause hyperkalaemia?
```
Spironolactone, eplerone, amiloride
digoxin
ACEi
NSAIDs - decreased renal excretion
B blockers
Heparin / LMWH (can inhibit aldosterone release )
```
55
What are the complications of hyperkalaemia?
Membrane potential disturbances
- arrhythmia
- heart block
- paralytic ileus
Acidosis
56
What are the signs and symptoms of hyperkalaemia
```
Palpitations
Chest pain
Irregular and fast heart rate
Light headed
Weakness
```
57
How can you manage someone if you suspect hyperkalaemia?
stop taking anything that may cause it.
Do an ECG and take bloods
Calcium gluconate - stabilises cardiac membrane potential - then 10ml every 10mins until ECG stable.
Insulin and dextrose
B agonist (increases Na/k ATPase)
Sodium bicarbonate
Resins - bind k in gut and prevent absorption
Dialysis
Diuresis (furosamide )
58
What ECG changes are seen in hyperkalaemia?
```
Peaked T wave
Flattened p
Prolonged PR interval
Depressed ST segment
Prolonged QRS
Sine wave pattern
```
59
What value is given for hypokalaemia?
Less than 3.5 mM
60
What are the causes of hypokalaemia ?
Inadequate intake
Increased losses from gut: vomiting, diarrhoea, ileostomy or fistula
Increased uptake by cells: alkalosis , exercise , b agonists
Endocrine :
- cons syndrome
- renin secreting tumour
- bilateral adrenal hyperplasia
- cushings disease
- secondary hyperaldosteronism - liver disease , heart failure and nephrotic syndrome
Diuretics
Bartters and liddle's amd gitelmans syndrome
61
What is bartters and gitelmans syndrome ?
Autosomal recessive tubular hypo Mg and hypo k metabolic alkalosis with hypo ca
62
What is liddles syndrome?
Autosomal dominant in ENaC channels leading to over expression
Leads to hypertension, oedema, hypokalaemia and metabolic alkalosis
63
What are the complications of hypokalaemia?
Paralytic ileum
Arrhythmia
Muscle weakness
Nephrogenic diabetes insipidus
64
What are the signs and symptoms of hypokalaemia ?
```
Fatigue
Constipation
Proximal muscle weakness
Cardiac arrhythmia
Hypotonia and hyporeflexia
Cramps
Light headed
```
65
What investigations should be carried out if you suspect hypokalaemia ?
U&Es
Venous pH and anion gap
K: creatinine ratio in urine
ECG
66
What does the KCR show (k: creatinine ratio )
Less than 1 : extrarenal
More than 1 and low/normal BP: tubular/extrarenal
More than 1 and high blood pressure : mineralocorticoid axis
67
What ecg changes are found in hypokalaemia ?
Small T waves
U waves
Increased PR
68
How do potassium levels affect vasculature
Low k leads to vasoconstriction
| High k leads to vasodilation
69
What is the treatment for hypokalaemia ?
Mild (>2.5mM) : oral slow release KCl
Severe (<2.5mM)
- IV KCl - never give it fast
- cardiac monitor
- check Mg (often hypoMg) - give mg replacement
- avoid glucose containing solutions or bicarbonate
Need to keep checking k+ in case of hyperkalaemia
70
What is the normal range for pH
7.35 to 7.45
71
How can metabolic acidosis occur?
Increased bicarbonate loss
Increased acid retention
Excess production of acid
72
What are the clinical features of acidosis ?
Kussmaul breathing - increased tidal volume with deep sighing inspiration and hyperventilation to blow off excess CO2
Reduced myocardial contractility
Resistant arrhythmias
73
Why is there reduced myocardial contractility in acidosis
Acidosis causes vasodilation
Acidosis reduced binding of NA to receptors
Reduced release of calcium from ER
74
What investigations should be carried out if you suspect acidosis
```
U&E
Venous pH
ABG
Urine pH
Lactate , ketones and blood glucose
Urine dipstick
```
75
How is the anion gap calculated? What is the normal value?
AG = [Na+k] - [cl + hco3 ]
Usually 8 to 16
76
What affect does albumin have on th anion gap?
Albumin is negatively charged so underestimates the anion gap
So if hypoalbuminic then need to correct for this
77
What are the causes of acidosis with a normal anion gap?
Due to increased HCl or H2CO3
Diarrhoea
Renal bicarbonate loss - renal tubular acidosis
Failure of renal acid excretion - renal tubular acidosis
Addisons
78
Causes of acidosis with increased anion gap?
Kusmal
- K ketoacidosis (diabetes , starvation, alcohol)
- U uraemia (CKD)
- S salicylates
- M methanol
- A aldehydes
- L lactic acid
79
What are the causes of lactic acidosis ?
```
Cardiogenic shock
Sepsis
Hypovolaemia
Severe anaemia
Ischaemia
Extreme exercise
Seizures
Malignant hyperthermia
```
80
What is the treatment for acidosis ?
Consider sodium bicarbonate if pH is less than 7 with impaired cardiac performance. Except for ketoacidosis (reduces removal of ketone bodies) and can't be given if resp function impaired
To treat lactic acidosis - treat cause e.g. Improve oxygenation and resuscitate the shock
81
Why is sodium bicarbonate not given unless acidosis is severe?
Can actually worsen intracellular acidosis and may cause hypo ca
82
What are the causes of metabolic alkalosis ?
With low chloride :
- vomiting
- diuretics (thiazides and loop)
- cystic fibrosis
With low k
- hyperaldosteronism
- bartters, Liddell and gitelmans
83
What are the signs and symptoms of metabolic alkalosis ?
Not specific but related to hypokalaemia, hypocalcaemia and hypovolaemia
With severe alkalosis there can be a reduction in cerebral and myocardial blood flow leading to headaches, confusion and seizures , angina and arrhythmias
O2 to tissues is reduced (dissociation curve and vasoconstriction)
84
How is alkalosis treated ?
Depends on cause:
- vomiting : antiemetic
- diuretics: stop/ change to k sparring
- treat low Cl with cal replacement
- treat low k with KCl
- acetazolamide daily will help remove NaHCO3
Urgent reversal of metabolic alkalosis (ITU)
- needed if bicarbonate is very high, hepatic encephalopathy , arrhythmia , confusion , seizure
- IV HCL via central line
85
How do b blockers and insulin lead to hyperkalaemia
Block Na k ATPase
| Block renin production
86
what is CKD?
progressive loss of renal function >3 months based on structure /function or eGFR <60ml/min
87
what are the different stages of CKD?
```
G1 - GFR <90
G2 -60-89
G3 - 30 -59
G4 - 15-29
G5 (endstage) <15
```
ACR - albumin: creatinine ratio
A1 - <3
A2 3-30
A3 >30
88
what are the different causes of CKD?
3 main causes:
- hypertension leads to nephrosclerosis
- diabetes
- glomerulonephritis - IgA nephropathy mainly but also SLE and vasculitis
other:
- reflux nephropathy (urine reflux - infection - eventual damage)
- Age
- AKI
- pyelonephritis
- myeloma/neoplasm
- renal artery stenosis
- alports
- polycystic kidney
89
how does myeloma cause CKD?
light chains of Ig (kappa chains) deposit into kidneys
chemotherapy can damage kidneys
chemotherapy can cause N&V which can damage the kidneys
90
what is alports syndrome?
genetic condition with abnormal collagen IV. leads to progressive scarring of BM (glomerulonephritis) allowing blood and protein into urine (nephritic syndrome). also affects ears and eyes
91
how does polycystic kindeys result in kidney failure?
fluid filled sacs press on nephrons blocking them.
92
what are the complications of CKD
Acidosis
Anaemia - less erythropoietin and less sensitive to this in uraemia background. reduced platelet function too and bleeding
Dehydration/volume overload - reduced conc ability and low eGFR so can quickly become overloaded
uraemic
increased risk of AKI
bone disorders
Increased risk of heart disease and stroke (due to uraemia, hypertension and hyperlipid
93
how do bone disorders result from CKD? what bone abnormalities are found?
less vitamin D produced by the kidneys
failing kidneys means less Ca is reabsorbed therefore calcium levels drop and phosphate rises.
Phosphate draw Ca into bones and structures - calcification of aorta and rugger jersey spine
levels of calcium drop further
This stimulates PTH release
this leads to osteomalacia and osteitis fibrosa cystica - (excessive bone resorption and replacement by fibrotic tissue. )
also can get periarticular calcifications
94
what are the symptoms of CKD?
fairly mild symptoms/asymptomatic until >stage 3
At stage 4 get symptoms associated with complications:
- anaemia: tiredness, poor exercise tolerance and SoB
- uraemia: anorexia, pruritus, N&V, weak, palpitations/chest pain (pericarditis) and confusion (encephalopathy)
- acidosis: muscle cramps
- fluid retention: puffy eyes, peripheral oedema, dyspnoea from pulmonary oedema
General: tired, insomnia, headaches, nocturia and polyuria
if severe: hiccups, sizures, pericarditis and coma
95
what are the signs of CKD?
```
peripheral oedema
yellow tinge - uraemia
anaemia - palor
peripheral vascular disease
pleural effusion
left ventricular hypertrophy
pericardial rub
```
96
what could you ask in the history of someone with suspected CKD?
presenting complaint - cover any worrying symptoms e.g. chest pain or difficulty breathing
previous UTI, IHD, renal stones, diabetes, hypertension
family history e.g. polycystic
drug history
systems review in case of malignancy
97
what investigations could you carry out for someone with CKD?
Renal function:
- --U&Es, GFR, urate - kidney function
- --urine collection - MC&S, A:C ratio
causes:
- --glucose - diabetes
- --immunology to check for autoimmune causes
- -- LFTs including albumin
- --- USS
- -- renal biopsy
complications:
- -- FBC - in case of anaemia, infection
- --- INR because hypoalbumin can lead to hypercoag
- -- bone function blood test : ca, po4, ALP, PTH to check for renal osteodystrophy
- --- Xray of bones
- --- CXR
- --- ECHO/ECG - ventricular hypertrophy
98
what does USS tell us for renal disease?
```
CKD - small kindeys
polycystic kidneys
any stones
tumours
hydronephrosis
```
99
when is a renal biopsy indicated?
unexplained AKI/CKD where knowing the cause would change treatment/management
100
what are the contraindications to a renal biopsy?
```
neoplasm
one kidney
horseshoe kidney
hypertension
abnormal clotting
CKD with small kidneys
```
101
what is the conservative management for CKD?
dietician to help with diet: restrict K, PO4 and Na (BP) and increase Ca
educate patient of possible complications and to look out for them and seek medical attention when needed
educate patient to limit progression by good glycaemic control in diabetes and controlling CVS risk factors.
educate patient to avoid risk factor: loose weight, keep hydrated, avoid nephrotoxins, stop smoking
102
what is the pharmacological management of CKD?
```
maintain BP with antihypertensives
CVS modifications: statins, aspirin
renal bone disease:
- PO4 binders
- give active Vit D analogs - alfacalcidol
- give Ca supplements
- give bisphosphonates
```
Abx for recurrent UTIs
iron for anaemia. or can give EPO 3x a week
Bicarbonate supplements for acidosis however be careful in those with high BP as Na can raise BP
furosemide for oedema
gabapentin and clonazepam for restless legs and cramps.
influenza vaccine every yr
103
what regular check ups do CKD patients need?
BP, HbA1c, PTH, Ca/PO4 level, FBC
eGFR measured annually to monitor progression (unless recently diagnosed then 3 reading over 90 days)
proteinuria measured anually
104
what is the ultimate treatment for CKD
dialysis or transplant
| usually CKD stage 5
105
when do you refer to a nephrologist?
```
stage 4/5
rapidly declining GFR
BP poorly controlled despite antihypertensives
proteinuria and haematuria
suspected renal artery stenosis
known rare genetic cause
```
106
why is eGFR used and not GFR?
standardised for age, sex race
because some races and males have more body muscle and thus will have a higher creatinine value
however still individual differences.
107
which patients should be screened for CKD?
high risk groups:
- hypertension
- diabetes
- family history
- known stones or BPH
- CVS disease
- recurrent UTIs
- vasculitis and SLE
108
what is glomerulonephritis?
collection of diseases causing pathology/inflammation to the glomerulus
109
how can glomerulonephritis present?
may be isolated haematuria/proteinuria
may be nephrotic or nephritic syndrome
may present as AKI/CKD
110
what is nephrotic syndrome?
the glomerulus becomes leaky and there is loss of proteins (proteinuria). There may be some haematuria too.
Due to loss of albumin there is reduced oncotic pressure and thus oedema.
The liver works hard to replace albumin and it is thought that this leads to hyperlipidaemia. Patients may have fat bodies in urine.
GFR may be normal.
in summary : proteinuria, oedema, hypoalbuminaemia and hyperlipidaemia
111
what are the complications of nephrotic syndrome?
proteinuria leads to hypoalbuminaemia and oedema - reduces kidney perfusion - can lead to AKI and also RAS activated - fluid retention and more oedema (including pulmonary oedema)
loss of protein - loss of Ig - increased risk of infection
loss of protein - imbalance of clotting factors - increased clearance of AT3, increased hepatic synthesis of clotting factors - risk of clots/bleeds. (thromboembolic disorder) (low albumin also leads to hypercoaguable state)
negative nitrogen balance
hyperlipidaemia
112
name some conditions that lead to nephrotic syndrome?
```
minimal change glomerulonephritis
membrane glomerulonephritis
focal segmental glomerulosclerosis
diabetic nephropathy
other:
- amyloidosis
- mesangiocapillary glomerulonephritis
- membranoproliferative glomerulonephritis type 1/2
- SLE
- Hep B/C
```
113
what is minimal change glomerulonephritis?
- what does it lead to
- what is it caused by?
- who is it most common in ?
- what does it look like
- how well does it respond to treatment
A disease that results in nephrotic syndrome
unknown cause - due to circulating factor but not Ab. Associated with NSAIDs and allergy in adults. Also in adults may be paraneoplastic to Hodgkin's lymphoma
Most common in children and teens.
light microscopy shows no change but under electron microscopy you can see loss of podocyte foot processes
responds very well to steroids
rarely progresses to renal failure and may reoccur.
114
what is membrane glomerulonephritis?
| - what is it caused by and associations?
IgG binds to podocyte receptors.
associated with NSAIDs, hep B/C, malaria, lupus, malignancy (breast, lung, lymphoma), penicillin.
this can lead to nephrotic syndrome (but also nephritic syndrome)
115
what is the most common cause of nephrotic syndrome ?
membrane glomerulonephritis
116
what is the prognosis of membrane glomerulonephritis?
1/3 get better, 1/3 stay the same, 1/3 progress to CKD
117
how is membrane glomerulonephritis treated?
corticosteroids +/- ACEi
118
what is focal segmental glomerulosclerosis?
A disease that can lead to nephrotic syndrome.
There is sclerosis of segments of glomeruli due to unknown circulating factor.
most common in adults.
associated with HIV and heroin abuse.
119
what is the prognosis of focal segmental glomerulosclerosis ?
> 50% progress to renal failure
| doesn't respond well to steroids.
120
what is amyloidosis associated with?
crohns, RA and myeloma
121
what is meant by non-proliferative glomerulonephritis?
the number of cells within the glomerulus remain unchanged e.g. NEPHROTIC syndrome
122
what is nephritic syndrome?
Proliferation of cells in the glomerulus results in 'blocking up' the glomerulus. The GFR reduces. Inflammatory cells damage the lining of the glomerulus leading to haematuria. increased pressure due to the blockage also leads to haematuria.
due to reduced GFR, RAS is activated, further hypertension
OVERAL: reduced GFR, haematuria, hypertension, oligiouria and some proteinuria.
usually abrupt onset.
123
name different conditions that lead to nephritic syndrome?
```
IgA nephropathy
Thin basement membrane disease
good pastures syndrome
vasculitis
Henoch Schonlein Purpura
post streptococcal GN
mesangiocapillary GN
```
124
what is IgA nephropathy?
A disease where IgA immune complexes form elsewhere (e.g. respiratory tract mucosal infection) and then circulate and deposit in the mesangial/glomerulus. This results in damage. Can lead to nephritic syndrome but not always.
This can occur at any age.
A significant proportion go onto renal failure.
presents as haematuria +/- proteinuria.
125
is there a cure for IgA nephropathy?
no - there is no way of removing the IgA complexes that have been deposited in the glomerulus
126
what are the two examples of thin basement membrane disease?
1. genetically thin BM
- haematuria but no complication - no renal failure or proliferative disease.
2. Alports syndrome.
- X linked disease. abnormal collagen IV. progresses to renal failure and deafness.
127
how does vasculitis lead to nephritic syndrome?
there is inflammation of blood vessels and this will effect the kidneys because they are highly vascular.
holes appear in the endothelium of blood vessles and so they leak blood - haematuria.
128
what is meant by proliferative glomerulonephritis?
increase number of cells in the glomerulus - NEPHRITIC syndrome
129
what is Henoch- Schonlein purpura?
this is a variant of IgA nephropathy
| it causes small vessel vasculitis -purputic rash especially on extensor surface of legs. Also causes nephritis.
130
what is post- streptococcal glomerulonephritis?
occurs 1-2 weeks after a sore throat or skin infection.
streptococcal antigens are deposited into the glomerulus and host immune complexes form (IgG and C3).
supportive treatment is required and 95% recover fully.
131
what is rapidly progressive glomerulonephritis?
the most aggressive form of glomerulonephritis
results in ESRF within days
different causes e.g. good pastures, IgA, SLE
132
how is rapidly progressive glomerulonephritis treated?
high dose steroids + cyclophosphamide + plasmaphoresis
133
what is good pastures syndrome?
uncommon condition where there are autoantibodies (IgG) to collagen IV. This leads to inflammation of the basement membrane.
leads to acute onset of nephritic syndrome and rapid progression.
associated with pulmonary haemorrhage too (collagen IV also found in lungs)
134
how is goodpastures syndrome treated?
immunosuppression and plasmaphoresis
135
what blood tests might you want to do in someone with glomerulonephritis?
FBC, U&Es, LFTs, ESR/CRP
IgA levels - raised in IgA nephropathy
Complement levels
autoAbs - autoimmune disease e.g. SLE
136
how would you manage someone with glomerulonephritis?
refer to a nephrologist
treat underlying cause - often with steroid, plasmophoresis
oedema: fluid restriction, furosemide, salt restriction
proteinuria/hypertension: ACEi, prostaglandins.
hypercoaguable state - TED stocking, aspirn/warfarin/heparin
hyperlipid - statins, fibrates
Dialysis
137
how is proteinuria defined?
presence of protein in urine >300mg/day
138
What is microalbuminaemia?
protein between 30-300mg / day.
| standard dipsticks will be negative for this level of protein.
139
what are the signs and symptoms of proteinuria?
usually asymptomatic
| but if hypoalbuminaemia develops, it can lead to .. ankle swelling, ascites and pleural effusion
140
what are the causes of proteinuria ?
minimal change GN, membranous GN, diabetes
drug induced: lithium, ciclosporin, NSAIDs, cisplatin
genetic: polycystic kidneys
immune: IgA nephropathy, sarcoidosis
infection e.g. TB
metabolic: raised Ca, raised urea.
vascular: diabetes, hypertension, sickle cell
neoplasm: bence jones proteins in myeloma (light chain Ig) (may be undetectable on a dipstick)
141
what investigations would you want to do for proteinuria?
3 samples tested by dipstick
- remember microalbuminaemia (diabetes) and bence jones are not usually detected by dipstick so need MSU sample.
if proteinuria by dipstick is present:
- rule out UTI
- BP recording
- check U&Es
- check for diabetes
- measure albumin: creatinine in urine
- if >100mg/mM - refer
- if >45 + haematuria - refer
could do USS, Auto Ab screen, maybe biopsy.
142
how do you treat proteinuria?
treat the cause
e.g. if hypertension - ACEi
treat diabetes - also with ACEi and other diabetic treatment.
143
How can we classify haematuria ?
1. visible haematuria /macroscopic
2. non-visible - microscopy
a) symptomatic
b) asymptomatic
144
how is significant haematuria defined?
a) any episode of visible haematuria
b) any episode of symptomatic non-visible haematuria (in absence of UTI or any transient cause)
c) reoccurring asymptomatic non-visible haematuria (in absence of UTI)
145
what are the causes of haematuria?
- infective: cystitis, TB, prostatitis, schistosomiasis, pyelonephritis
- tumour: Renal cell carcinoma, bladder cancer, prostate cancer
- traumatic: catheter
- Inflammatory: glomerulonephritis (IgA nephropathy)
- structural: stones, polycystic kidneys.
- haematological: sickle cell, warfarin
- surgical
- drugs: cephalosporins, furosemide, NSAIDs, sulphonamides
- menstruation
146
what do you want to ask someone with haematuria?
how often? when in stream? any pain?
any other symptoms? e.g. Mass, weight loss, night sweats
any recent travel ? schistosomiasis and TB
PMH: stones, cancer, diabetes and hypertension?
drug history? Warfarin? chemotherapy?
family history - alports?
147
what further investigations would you do in someone with haematuria?
```
exclude UTI and period
measure eGFR, serum creatinine, FBC
BP
A:C ratio in urine
cytological exam of the urine - any inflammatory cells, dysmorphic erythrocytes suggest renal origin
USS kidneys
renal angiography
CT scan
biopsy
```
148
what are the indications of urological referral in someone with haematuria?
all patients with visible haematuria unless GN is suspected
all patients with symptomatic NVH
all patients with asymptomatic NVH that are 40 +
149
what are the indication for nephrology referral in someone with haematuria?
urology causes have been excluded
low GFR
stage 4/5 CKD
significant proteinuria or A:C
haematuria in absence of proteins and hypertension in 40+
visible haematuria and recurring infection.
150
Name some nephrotoxic drugs?
- analgesics: NSAIDs
- antimicrobials: aminoglycosides (gentamicin), sulphonamides, penicillin, rifampicin, amphotericin, acyclovir
- anticonvulsants: phenytoin, valproate
- others: furosemide, thiazides, ACEi, ARBs, omeprazole, calcinurin inhibitors, cisplatin.
radiocontrast media
151
what organic substances are toxic to the kidneys?
```
urate
haemoglobin - in haemolysis
myoglobin - in rhabdomyolysis
Igs in myeloma (light chains)
streptococcus
TB
clamidyia
salmonella
campylobacter
HIV, adeno, measles
taxoplasmosis and leishmania
```
152
how can we help prevent kidney injury during the use of radiocontrast material?
stop other nephrotoxins
pre-hydrate
ask nephrologist for advice.
153
what increases the risk of AKI with nephrotoxic drugs?
age, dose, CKD, long term treatment, other nephrotoxins too
154
what are the causes of rhabdomyolysis?
```
burns
excessive exercise
statins
seizures
crush injury
alcohol
ecstasy
myositis
infection
duchennes muscular dystrophy
```
155
what are the symptoms of rhabdomyolysis?
muscle pain
swelling
red/brown urine (coca cola urine)
156
What are the indications of renal replacement therapy?
```
severe metabolic acidosis
hyperkalaemia
pericarditis
encephalopathy
intractable volume load
peripheral neuropathy
intractable GI symptoms
end stage renal failure (GFR <15ml/min)
```
157
how does haemodialysis work?
blood is pumped through an artificial kidney in which the blood is surrounded by a solution of electrolytes (the dialysate). diffusion occurs between substances in blood and dialysate (set the concentration of dialysate how you want e.g. high calcium to correct hypoCa
the blood is drawn from a arteriovenous fistula - out of the radial artery and back into the cephalic vein.
by altering the pressures on either side of the membrane between blood and dialysate we can alter the ultrafiltration to regulate how much water is removed from the patients blood.
158
How is haemodialysis performed?
fistula must be created between a peripheral artery and vein. The fistula takes several weeks to mature and should ideally be fashioned 3-6 months before starting dialysis.
Alternatively a plastic catheter can be inserted into the internal jugular or subclavian vein
heparin is constantly infused to prevent clotting.
can be carried out at hospital or patients home
for CKD usually 3 x a week for 4 hours.
some patients prefer better control (6 days/ week) - optimal fluid balance/biochemistry.
159
what are the advantages of haemodialysis?
less responsibility
days off
better survival
160
what are the disadvantages of haemodialysis?
travel time
| deformities of the arm
161
what are the complications of haemodialysis?
Access related: local infection, endocarditis, osteomyelitis, creation of stenosis, thrombosis or aneurysm
hypotension, cardiac arrhythmias, air embolism
N&V, headache, cramps
fever: infected central lines
anaphylactic reaction to sterilising agents.
steal syndrome - ischaemia of the hand due to fistula
heparin induced thrombocytopenia or haemolysis
disequilibrium syndrome: restless, headache, tremors, fits and coma
depression
162
what are the contraindications to haemodialysis?
heart failure
coagulopathy
failed vascular access
163
what is peritoneal dialysis?
A dialysate is infused into the peritoneal cavity and the blood flowing through peritoneal capillaries acts as the blood source. diffusion occurs across the peritoneal membrane.
fluid balance/ultrafiltration is controlled by altering the osmolarity of the dialysate solution.
164
how is peritoneal dialysis carried out?
catheter is inserted into the patients peritoneum under local/general anaesthetic
the dialysate is added through the catheter and waste is removed after 20 mins. (this catheter remains there permanently)
this needs to be performed 4 x a day by the patient OR overnight and one/two throughout the day.
165
what are the advantages of peritoneal dialysis?
| what are the disadvantages?
can be performed at home, holiday , at work - independence
however time consuming and responsibility
166
what are the contra-indications to peritoneal dialysis?
- intra-abdominal adhesions
- abdominal wall stoma
- scarring of the peritoneum e.g. previous peritonitis
- obesity/ large muscle mass (peritoneal cavity is small) , hernia, intestinal disease, respiratory disease, previous abdominal surgery, ascites = relative contraindications
167
what are the complications of peritoneal dialysis?
- peritonitis, sclerosing peritonitis
- catheter problems: infection, blockage, kinking, leaks (scrotum) or slow drainage.
- constipation, fluid retention , hyperglycaemia (add glucose to dialysate to remove more water) , weight gain
hernias - incision, inguinal, umbilical
back pain
malnutrition
depression
168
what are the 3 forms of renal replacement therapy?
peritoneal dialysis
haemodialysis
renal transplant
169
what are the different types of renal transplant?
- cadaveric: brainstem death
- non-heart beating donor: no active circulation
- live related:
- optimal surgical timing
- HLA matched
- improved graft survival
- Live unrelated
170
how is a transplant carried out e.g. before and after care?
- matched ABO and HLA haplotype
- waiting time depends on tissue match, age and how long you have waiting.
- native kidney is not usually removed, new kidney is placed extra-peritoneally in iliac fossa
- kidney can be stored up to 1 hour at room temperature and 30hours in ice.
- frequent follow ups (2-3 times a week initially and then for life - screening for cancer, drug toxicity and CVS disease.
- to prevent rejection the recipients receive induction at the time of transplant with either depleting or non-depleting monoclonal or polyclonal Ab directed against T cells e.g. antithymocyte globulin , basiliximab or alemtuxumab
- maintainane immunosuppression - triple therapy (calcineurin inhibitor, antimetabolite and prednisolone)
171
what are the indications of renal replacement therapy?
ESRD
fit enough to have surgery
good prognosis after e.g. if cause is prerenal then new kidney may also fail
not too old or too young - young will need immunosupressants for long time and old will only make little use of kidney (although co-morbidities is a better predictor)
172
what are the contraindications of renal transplant?
```
cancer
active infection
uncontrolled ischaemic heart disease
acquired immunodeficiency disease with opportunity infections
active viral hepatitis
extensive peripheral vascular disease
mental incapacity
```
173
what are the risks of transplantation?
operative complications: local infection, pain, pneumonia, DVT
rejection
arterial/venous thrombosis in the transplant
infections
cancer (skin, lymphoma)
reoccurance of original disease in transplant
side effects of drugs e.g. hypertension and atherosclerosis , diabetes (calcineurin inhibitors) , bone marrow suppression (infections and malignancy) , hirsutism (ciclosporin), agranulocycotosis and hepatitis (mycophenylate)
174
what is hyperacute rejection?
occurs within minutes of insertion - rare now due to cross matching
the graft has to be removed
ABO incompatibility
175
what is accelerated rejection?
aggressive and mainly T cell mediated
occurs within a few days
patient presents with fever, swollen kindey, rapidly increasing serum creatinine. -
can be salvaged by high dose steroids or antilymphocyte Ab however long term survival is affected
176
what is acute cellular rejection?
occurs in 25% usually in 1-3 days (but can occur up to 12 weeks)
clinical signs include fluid retention, rising BP, rapid increase in creatinine
treated with IV steroids
177
what is chronic rejection?
gradual rise in serum creatinine and proteinuria, resistant hypertension
biopsy shows vascular changes, fibrosis and tubular atrophy.
not responsive to increasing immunosuppressive therapy.
178
what are the differential diagnosis for rise in creatinine in transplant patients?
rejection
obstruction
acute tubular necrosis
drug toxicity
179
what are the acute and chronic nephrotoxic effects of tacrolimus
acute: reversible afferent arteriole constriction - reduced GFR
chronic: tubular atrophy and fibrosis
180
how does pregnancy effect renal function?
structural changes: increased renal blood flow and vasodilation. smooth muscle relaxation and the effect of the gravid uterus results in ureter dilation.
functional changes:
- reduced systemic resistance - increases CO and blood volume which increases GFR - proteinuria, reduced serum urate and creatinine. increased bicarbonate excretion (acidosis)
- however net Na resorption and increased ADH so fluid retention
- reduced renal threshold for glucose reabsorption so glucosuria (gestational diabetes also adds to this)
181
what are the pathological renal effects of pregnancy?
UTIs: glucosuria and urinary stasis (due to dilation)
- this can lead to pyelonephritis (can be lifethreatening to baby and mum)
- can precipitate preterm labour
- asymptomatic bacteruria should be treated
stones: structural changes promote stone formation
pre-eclampsia can lead to AKI due to hypertension and DIC
182
what Abx are given to UTIs in pregnancy?
Trimethroprim is preferred throughout
| nitrofurantoin should definitely be avoided in last trimester
183
what are the effects of CKD on pregnancy?
ESKD - fertility is reduced, increased risk of pre-eclampsia, small fetus, pre-term labour
haemodialysis needs to be increased to 6-7x a week
184
what are the predictors of pregnancy in those with CKD?
BP
serum creatinine
proteinuria
185
what are the effects of transplant on pregnancy?
need to wait 2 years post transplant before pregnancy
renal function needs to be closely monitored throughout
some drugs are unsafe e.g. mycophenolate
prednisolone, azathioprine, ciclosporin and tacrolimus are safe.
186
what is the pathophysiology of a UTI?
mainly caused by gram negative rods e.g. Ecoli
more common in women - shorter urethra so shorter distance from the anus
more common in:
- benign prostatic hyperplasia
- pregnancy
- stones
- neurological problem and incomplete emptying e.g. MS or spinal cord injury
- reflux nephropathy
187
what are the symptoms of a UTI?
cystitis: dysuria, frequency, pain
pyelonephritis - above + fever, loin pain, nausea
septicaemia /shock (UTIs are a major cause of gram negative septicaemia)
asymptomatic in pregnancy
188
what is the difference between a complicated and non-complicated UTI?
uncomplicated - normal healthy women
complicated: men, children, pregnancy, staph aureus, reflux nephropathy, immunocompromised.
189
what is the treatment for UTIs?
water
sodium citrate - prevents attachment to the wall (in cranberry juice)
uncomplicated:
- trimethroprim (200mg/day) or nitrofurantoin (50mg/6hrs) for 3 days
complicated: 5-7 days of the above.
190
what is the treatment for pyelonephritis?
14 days of co-amoxiclav, gentamicin/ciprofloxacin
| NOT nitrofurantoin because no systemic action
191
what prophylactic treatment can be given to those who have >3 UTIs/ yr?
Trimethroprim/nitrofurantoin as single nightly dose
192
what would investigations show if someone has a UTI?
urine may look cloudy - WBCs
leucocyte-esterase positive on dipstick - indicates WBCs (specific to UTIs)
nitrates may also be positive however not specific
haematuria
proteinuria
culture urine:
- MSU sample or catheter sample - can test sensitivities for complicated cases
193
what are the risk factors for UTIs?
sexual intercourse
menopause
pregnancy
stones
194
what is the pathophysiology behind renal stones?
solution contains more solute than it can hold so stone forms and adheres to urothelium.
caused by:
1. dehydration
2. increased mineral content - hypercalcaemia/uria, hyperuricaemia, hyperoxaluria ,
3. urinary stasis - infection/obstruction
4. polycystic kindyes
5. infection - struvite stones (more in women)
195
80% of renal stone are due to hypercalciuria. What are the causes of hypercalciuria and hypercalcaemia?
```
hyperparathyroidism - squamous cell carcinoma
destruction of bone - tumour, pagets
excess vitamin D
thiazide diuretics
increased calcium intake
```
196
what are the two types of calcium based stones?
calcium oxaloate and calcium phosphate
197
hyperoxaluria can cause renal stones. what are the causes of hyperoxaluria?
increased oxaloate absorption from the gut = crohns
diet: spinach, tea, nuts
short bowel syndrome
198
hyperuraciamia can cause renal tones what are the causes of this?
thiazide diuretics
tumour lysis
idiopathic
(also presents as gout)
199
where are the 3 common sites for renal stones to form?
uretopelvic junction
uretovesicle junction
pelvic brim
200
what are the symptoms of renal stones?
```
may be asymptomatic
renal colic - excruciating pain for 20 mins in L1 dermatome (groin, iliac fossa and inner thigh)
N&V, pallor and sweating
haematuria
recurrent UTIs
```
201
what are the complications of renal stones?
acute pyelonephritis +/- sepsis
AKI
UTI
hydronephrosis
202
what is the treatment for renal stones?
conservative: drink lots of water, change diet (more fruit /veg - K+ promotes urinary citrate excretion). limit salt and sugar.
treat underlying cause
NSAIDs and bed rest
thiazide diuretics - reduce calcium excretion
potassium cirtrate if hypocitramia Abx for struvite stones
percutaneous nephrolithotomy - hole in skin and remove stone
extracorporeal shockwave lithotripsy - break down stone.
203
what are the causes of bladder stones?
caused by outflow obstruction - urethral stricture, prostate, neuropathic bladder
204
what are the types of incontinence?
stress urinary incontinence - most prevalent due to weak pelvic floor muscles. involuntary leak on exertion e.g. cough/sneeze
urge incontinence - involuntary leakage immediately proceeded by urge
mixed urinary incontinence
overflow incontinence - lower MN lesion
205
what are the causes of urinary incontinence?
spinal cord lesions
weak pelvic floor muscles e.g. after birth
diabetic neuropathy - effects parasympathetic nerves - therefore retrograde ejaculation
UTI - irritates parasympathetic fibres - urgency and frequency
206
how do we manage stress urinary incontinence?
pelvic floor exercises
Duloxetine (pharmacological)
surgery - intramural bulking agents e.g. collagen
207
how do we manage urge incontinence?
bladder training
| anticholinergic agents
208
what fluid balance should you aim for in AKI? and why?
aim for +30-50ml to account for insensible losses.
209
how do you conduct fluid resuscitation in patients at risk of fluid overload?
give 250ml bolus over 15 mins (rather than 500ml)
210
during pelvic surgery which structures should you be careful of?
uterine artery bridges over the ureter. therefore during a hysterectomy uterine artery needs to be ligated but need to be careful not to damage the ureter.
similarly vas deferens during vasectomy need to be careful of ureter
211
explain the link between an aortic aneurysm and testicular varices
renal vein runs inbetween aorta and superior mesenteric. if there is an aortic aneurysm this can pinch and obstruct the renal vein resulting in ineffective drainage of kidney. The left testicle drains via the left renal vein into the IVC. therefore this results in inproper drainage of left testicle resulting in a varice
212
name 3 embryological kidney abnormalities
horseshoe kidney - migration defect
renal agenesis - may be unilateral/bilateral
pelvic kidney
213
why is infection in polycystic kidneys more problematic?
there is an increased risk of infection in polycystic kidneys and also if you get an infection it is harder to treat because of infection getting into cysts and being walled off.
214
how is clearance calculated and defined?
volume of plasma completely cleared of a substance per unit time
conc in urine x urine flow rate
divided by plasma conc
215
what is the GFR?
volume of plasma filtered by bowmans capsule per minute
216
describe the methods of renal blood flow regulation
myogenic response: increase pressure - dilation of afferent arteries - reflex vasoconstriction to maintain a flow
tubuloglomerular feedback:
- increased GFR means more NaCl reaches macula densa (TAL). this causes release of adenosine which vasoconstriction of afferent and dilation of efferent to reduce GFR
- reduced delivery releases prostaglandins instead with vasodilates afferent.
217
where are the osmolarity receptors located in brain?
OVLT in hypothalamus
218
what drugs stimulate the Na/K ATPase?
K+
insulin
aldosterone (increases expression of Na/K ATPase)
catecholamines
219
what factors promote K out of cells?
exercise - repolarisation and muscle tears
cell lysis - chemotherapy
acidosis - H/K exchanger
increased osmolality - draws K+ out along with water
220
what are the effects of acidaemia and alkalaemia?
Alkalaemia: low Ca - increased neuronal excitability,paraesthesia and tetani . also hypo K
acidaemia - hyperkalaemia and denatures proteins.
221
describe the physiological regulation of blood pressure
blood pressure is too high:
- aortic arch and carotid body have baroreceptors which fire when BP Is high - via vagus nerve to medullar and then via vagus/glossopharyngeal to induce bradycardia
ADH can cause vasoconstriction
blood pressure too high:
- opposite of above mechanism and instead -->
sympathetic NS: stimulates vasoconstriction , increased HR and renin release to reduce GFR. overall increase in BP
Atrial natureitic peptides (ANP) - stored in myocytes and released in response to stretch - vasodilation of afferent - increased GFR to reduce BP
reduced NaCL delivered to macula densa due to reduced GFR therefore increased renin release - vasoconstriction, thirst, aldosterone
222
explain the RAAS
low NaCL detected by macula densa and renin released.
renin can convert angiotensinogen (made by liver) to angiotensin 1. AT1 to AT2 by ACE in lungs. (ACE also breaks down bradykinin)
AT2 leads to vasoconstriction, aldosterone release, thirst, increased Na absorption.
aldosterone increases expression of ROMK, ENaC and Na/K ATPase - increased sodium reabsorption and thus BP.
223
how does Hypoalbumin lead to AKI and how to does AKI lead to hypoalbumin?
leaky glomerulus can result in protein loss --> hypoalbumin
hypoalbumin reduces circulating volume which can reduce kidney perfusion and result in damage
224
how are ACEi linked to AKI? so why are ACE sometimes used in kidney failure?
Not nephrotoxic but can cause AKI
lead to vasodilation of efferent arteriole and thus reduce flow rate through kidneys and thus reduce GFR
ACEi can help reduce proteinuria and thus can be useful: if good volume status but leaky glomerulus e.g. nephrotic then ACE is useful however if volume deplete, reducing GFR further with ACE can be problematic
225
what is renal failure in myeloma due to?
- Light chain deposition
- Hypercalcaemia
- Sepsis
- Use of NSAIDs
- Chemotherapies.
226
what treatment can be given in most drug overdoses?
IV intralipid - lipid soluble drugs will dissolve into this which will reduce their systemic effects
