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General Medicine sara > Renal > Flashcards

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

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2
Q

What staging system is used in AKI

A

KDIGO

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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

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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

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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

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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

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7
Q

What are the most commonest causes of AKI?

A

Ischaemia
Sepsis
Nephrotoxins: most commonly gentamicin , NSAIDs, ACEi and iodinated contrast

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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
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9
Q

How can the renal causes of AKI be divided?

A

Tubular
Glomerular
Vascular
Interstitial

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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

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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

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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

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13
Q

What are the vascular causes of renal AKI

A

Vasculitis, thrombotic emboli, pre- eclampsia and malignant hyperthermia

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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

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15
Q

How can the post renal causes of AKI be divided?

A

Intraluminal
Intramural
External

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16
Q

Relatively how common are the post renal causes of AKI

A

Least common

More likely to affect elderly

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17
Q

What are the intraluminal causes of post renal AKI

A

Tumour

Stone

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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
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19
Q

What are the external causes of post renal AKI?

A

Benign prostatic hyperplasia
Malignancy- bladder /prostate
Aortic aneurysm
Gravid uterus

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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

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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
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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

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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

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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
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25
Q

When should you refer a suspected AKI case to a nephrologist?

A 
Hyperkalaemia in oligoruic patient 
High k , fluid overload or acidaemia unresponsive to treatment 
Bad signs of uraemia 
Indication for dialysis 
Glomerulonephritis
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26
Q

What are the indications for dialysis in AKI?

A 
Refractory pulmonary oedema
Persistent hyperkalaemia 
Severe metabolic acidosis 
Uraemic complications such as pericarditis and encephalopathy
Drug overdose
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27
Q

What is the prognosis of AKI ?

A

Greatly depends on cause and severity
Outcome can be predicted by comorbidities
some fully recover, others go on to have CKD

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28
Q

How may someone present with AKI ?

A

Vague symptoms
Reduced urine output
Vomiting and confusion

Signs associated with cause- sepsis, dehydration

Signs associated with complications - uraemic syndrome (itchy, tired, nausea, palpitations )

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29
Q

What would you find on examination for a
A) hypovolaemic patient
B) cardiac failure patient
c) septic patient (systemic vasodilation )

A

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

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30
Q

What electrolyte disturbances can alkalosis lead to ? Acidosis?

A

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

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31
Q

What’s the normal range for serum sodium ?

A

135 to 145 mM

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32
Q

What are the problems with hypernatraemia?

A

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

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33
Q

What are the causes of hypernatraemia ?

A 
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
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34
Q

What is diabetes insipidus ?

A

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

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35
Q

What are the symptoms of hypernatraemia?

A

Signs/ symptoms of cerebral dehydration:

  • thirst
  • apathy
  • confusion
  • reduced consciousness
  • seizures and coma

Signs of dehydration

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36
Q

What investigations are carried out if you suspect someone is hypernatraemic?

A

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

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37
Q

What is the treatment for hypernatraemia ?

A

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 )
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38
Q

What are the categories for the causes of hyponatraemia ?

A
  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
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39
Q

What are the renal causes of hypovolaemic hyponatraemia?

A

Diuretics (thiazides in particular )
Osmotic diuretics (glucose)
Salt wasting nephropathy (chronic tubular dysfunction)
Addison’s disease

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40
Q

What are the non renal causes of hypovolaemic hyponatraemia ?

A

Sweating, diarrhoea
Pancreatitis
Brain injury leads to release of brain natriuretic peptide

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41
Q

What are the causes of hypervolaemic hyponatraemia?

A

Nephrotic syndrome
Congestive heart failure
Cirrhosis

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42
Q

What are the causes of euvolemic hyponatraemia?

A

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

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43
Q

What is the main complication of hyponatraemia?

A

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

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44
Q

What are the signs and symptoms of hyponatraemia?

A

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

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45
Q

What investigations would you do if you suspected hyponatraemia ?

A

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

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46
Q

How is hyponatraemia managed ?

A

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
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47
Q

What is pseudo hyponatraemia ?

A

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

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48
Q

What two drugs can be used to treat SIADH release and explain how the first works?

A

Demeclocycline : induced nephrogenic diabetes insipidus

Lithium ( also known to induce nephrogenic diabetes insipidus)

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49
Q

What is hypoosmolar hyponatraemia caused by?

A

Defect in renal water excretion
- volume depletion , advanced renal failure, SIADH
Water intake exceeding normal excretory capacity

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50
Q

What is translocational hyponatraemia ?

A

Water comes out into ECG due to osmotic drive

Caused by Hyperglycaemia and exogenous solutes such as mannitol

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51
Q

State what value is classed as hyperkalaemia

A

More than 5 mM

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52
Q

What is pseudohyperkalaemia

A

Venepuncture can cause localised hyperkalaemia

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53
Q

What are the causes of hyperkalaemia ?

A 
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
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54
Q

Which drugs can cause hyperkalaemia?

A 
Spironolactone, eplerone, amiloride
digoxin
ACEi 
NSAIDs - decreased renal excretion
B blockers 
Heparin / LMWH (can inhibit aldosterone release )
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55
Q

What are the complications of hyperkalaemia?

A

Membrane potential disturbances

  • arrhythmia
  • heart block
  • paralytic ileus

Acidosis

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56
Q

What are the signs and symptoms of hyperkalaemia

A 
Palpitations 
Chest pain 
Irregular and fast heart rate 
Light headed 
Weakness
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57
Q

How can you manage someone if you suspect hyperkalaemia?

A

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 )

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58
Q

What ECG changes are seen in hyperkalaemia?

A 
Peaked T wave
Flattened p 
Prolonged PR interval 
Depressed ST segment 
Prolonged QRS 
Sine wave pattern
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59
Q

What value is given for hypokalaemia?

A

Less than 3.5 mM

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60
Q

What are the causes of hypokalaemia ?

A

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

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61
Q

What is bartters and gitelmans syndrome ?

A

Autosomal recessive tubular hypo Mg and hypo k metabolic alkalosis with hypo ca

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62
Q

What is liddles syndrome?

A

Autosomal dominant in ENaC channels leading to over expression

Leads to hypertension, oedema, hypokalaemia and metabolic alkalosis

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63
Q

What are the complications of hypokalaemia?

A

Paralytic ileum
Arrhythmia
Muscle weakness
Nephrogenic diabetes insipidus

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64
Q

What are the signs and symptoms of hypokalaemia ?

A 
Fatigue
Constipation 
Proximal muscle weakness
Cardiac arrhythmia 
Hypotonia and hyporeflexia 
Cramps 
Light headed
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65
Q

What investigations should be carried out if you suspect hypokalaemia ?

A

U&Es
Venous pH and anion gap
K: creatinine ratio in urine
ECG

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66
Q

What does the KCR show (k: creatinine ratio )

A

Less than 1 : extrarenal
More than 1 and low/normal BP: tubular/extrarenal
More than 1 and high blood pressure : mineralocorticoid axis

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67
Q

What ecg changes are found in hypokalaemia ?

A

Small T waves
U waves
Increased PR

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68
Q

How do potassium levels affect vasculature

A

Low k leads to vasoconstriction

High k leads to vasodilation

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69
Q

What is the treatment for hypokalaemia ?

A

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

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70
Q

What is the normal range for pH

A

7.35 to 7.45

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71
Q

How can metabolic acidosis occur?

A

Increased bicarbonate loss
Increased acid retention
Excess production of acid

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72
Q

What are the clinical features of acidosis ?

A

Kussmaul breathing - increased tidal volume with deep sighing inspiration and hyperventilation to blow off excess CO2

Reduced myocardial contractility

Resistant arrhythmias

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73
Q

Why is there reduced myocardial contractility in acidosis

A

Acidosis causes vasodilation
Acidosis reduced binding of NA to receptors
Reduced release of calcium from ER

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74
Q

What investigations should be carried out if you suspect acidosis

A 
U&amp;E 
Venous pH
ABG 
Urine pH
Lactate , ketones and blood glucose 
Urine dipstick
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75
Q

How is the anion gap calculated? What is the normal value?

A

AG = [Na+k] - [cl + hco3 ]

Usually 8 to 16

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76
Q

What affect does albumin have on th anion gap?

A

Albumin is negatively charged so underestimates the anion gap

So if hypoalbuminic then need to correct for this

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77
Q

What are the causes of acidosis with a normal anion gap?

A

Due to increased HCl or H2CO3

Diarrhoea
Renal bicarbonate loss - renal tubular acidosis
Failure of renal acid excretion - renal tubular acidosis
Addisons

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78
Q

Causes of acidosis with increased anion gap?

A

Kusmal

  • K ketoacidosis (diabetes , starvation, alcohol)
  • U uraemia (CKD)
  • S salicylates
  • M methanol
  • A aldehydes
  • L lactic acid
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79
Q

What are the causes of lactic acidosis ?

A 
Cardiogenic shock
Sepsis
Hypovolaemia 
Severe anaemia 
Ischaemia 
Extreme exercise 
Seizures
Malignant hyperthermia
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80
Q

What is the treatment for acidosis ?

A

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

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81
Q

Why is sodium bicarbonate not given unless acidosis is severe?

A

Can actually worsen intracellular acidosis and may cause hypo ca

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82
Q

What are the causes of metabolic alkalosis ?

A

With low chloride :

  • vomiting
  • diuretics (thiazides and loop)
  • cystic fibrosis

With low k

  • hyperaldosteronism
  • bartters, Liddell and gitelmans
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83
Q

What are the signs and symptoms of metabolic alkalosis ?

A

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)

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84
Q

How is alkalosis treated ?

A

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
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85
Q

How do b blockers and insulin lead to hyperkalaemia

A

Block Na k ATPase

Block renin production

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86
Q

what is CKD?

A

progressive loss of renal function >3 months based on structure /function or eGFR <60ml/min

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87
Q

what are the different stages of CKD?

A 
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

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88
Q

what are the different causes of CKD?

A

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
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89
Q

how does myeloma cause CKD?

A

light chains of Ig (kappa chains) deposit into kidneys
chemotherapy can damage kidneys
chemotherapy can cause N&V which can damage the kidneys

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90
Q

what is alports syndrome?

A

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

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91
Q

how does polycystic kindeys result in kidney failure?

A

fluid filled sacs press on nephrons blocking them.

92
Q

what are the complications of CKD

A

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
Q

how do bone disorders result from CKD? what bone abnormalities are found?

A

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
Q

what are the symptoms of CKD?

A

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
Q

what are the signs of CKD?

A 
peripheral oedema
yellow tinge - uraemia
anaemia - palor 
peripheral vascular disease
pleural effusion 
left ventricular hypertrophy 
pericardial rub
96
Q

what could you ask in the history of someone with suspected CKD?

A

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
Q

what investigations could you carry out for someone with CKD?

A

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
Q

what does USS tell us for renal disease?

A 
CKD - small kindeys
polycystic kidneys
any stones
tumours
hydronephrosis
99
Q

when is a renal biopsy indicated?

A

unexplained AKI/CKD where knowing the cause would change treatment/management

100
Q

what are the contraindications to a renal biopsy?

A 
neoplasm
one kidney
horseshoe kidney
hypertension
abnormal clotting 
CKD with small kidneys
101
Q

what is the conservative management for CKD?

A

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
Q

what is the pharmacological management of CKD?

A 
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
Q

what regular check ups do CKD patients need?

A

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
Q

what is the ultimate treatment for CKD

A

dialysis or transplant

usually CKD stage 5

105
Q

when do you refer to a nephrologist?

A 
stage 4/5
rapidly declining GFR
BP poorly controlled despite antihypertensives 
proteinuria and haematuria 
suspected renal artery stenosis 
known rare genetic cause
106
Q

why is eGFR used and not GFR?

A

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
Q

which patients should be screened for CKD?

A

high risk groups:

  • hypertension
  • diabetes
  • family history
  • known stones or BPH
  • CVS disease
  • recurrent UTIs
  • vasculitis and SLE
108
Q

what is glomerulonephritis?

A

collection of diseases causing pathology/inflammation to the glomerulus

109
Q

how can glomerulonephritis present?

A

may be isolated haematuria/proteinuria
may be nephrotic or nephritic syndrome
may present as AKI/CKD

110
Q

what is nephrotic syndrome?

A

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
Q

what are the complications of nephrotic syndrome?

A

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
Q

name some conditions that lead to nephrotic syndrome?

A 
minimal change glomerulonephritis 
membrane glomerulonephritis
focal segmental glomerulosclerosis
diabetic nephropathy
other:
  - amyloidosis 
  - mesangiocapillary glomerulonephritis 
  - membranoproliferative glomerulonephritis type 1/2
  - SLE 
  - Hep B/C
113
Q

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

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
Q

what is membrane glomerulonephritis?

- what is it caused by and associations?

A

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
Q

what is the most common cause of nephrotic syndrome ?

A

membrane glomerulonephritis

116
Q

what is the prognosis of membrane glomerulonephritis?

A

1/3 get better, 1/3 stay the same, 1/3 progress to CKD

117
Q

how is membrane glomerulonephritis treated?

A

corticosteroids +/- ACEi

118
Q

what is focal segmental glomerulosclerosis?

A

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
Q

what is the prognosis of focal segmental glomerulosclerosis ?

A

> 50% progress to renal failure

doesn’t respond well to steroids.

120
Q

what is amyloidosis associated with?

A

crohns, RA and myeloma

121
Q

what is meant by non-proliferative glomerulonephritis?

A

the number of cells within the glomerulus remain unchanged e.g. NEPHROTIC syndrome

122
Q

what is nephritic syndrome?

A

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
Q

name different conditions that lead to nephritic syndrome?

A 
IgA nephropathy
Thin basement membrane disease
good pastures syndrome 
vasculitis 
Henoch Schonlein Purpura 
post streptococcal GN
mesangiocapillary GN
124
Q

what is IgA nephropathy?

A

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
Q

is there a cure for IgA nephropathy?

A

no - there is no way of removing the IgA complexes that have been deposited in the glomerulus

126
Q

what are the two examples of thin basement membrane disease?

A
  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
Q

how does vasculitis lead to nephritic syndrome?

A

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
Q

what is meant by proliferative glomerulonephritis?

A

increase number of cells in the glomerulus - NEPHRITIC syndrome

129
Q

what is Henoch- Schonlein purpura?

A

this is a variant of IgA nephropathy

it causes small vessel vasculitis -purputic rash especially on extensor surface of legs. Also causes nephritis.

130
Q

what is post- streptococcal glomerulonephritis?

A

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
Q

what is rapidly progressive glomerulonephritis?

A

the most aggressive form of glomerulonephritis
results in ESRF within days

different causes e.g. good pastures, IgA, SLE

132
Q

how is rapidly progressive glomerulonephritis treated?

A

high dose steroids + cyclophosphamide + plasmaphoresis

133
Q

what is good pastures syndrome?

A

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
Q

how is goodpastures syndrome treated?

A

immunosuppression and plasmaphoresis

135
Q

what blood tests might you want to do in someone with glomerulonephritis?

A

FBC, U&Es, LFTs, ESR/CRP
IgA levels - raised in IgA nephropathy
Complement levels
autoAbs - autoimmune disease e.g. SLE

136
Q

how would you manage someone with glomerulonephritis?

A

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
Q

how is proteinuria defined?

A

presence of protein in urine >300mg/day

138
Q

What is microalbuminaemia?

A

protein between 30-300mg / day.

standard dipsticks will be negative for this level of protein.

139
Q

what are the signs and symptoms of proteinuria?

A

usually asymptomatic

but if hypoalbuminaemia develops, it can lead to .. ankle swelling, ascites and pleural effusion

140
Q

what are the causes of proteinuria ?

A

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
Q

what investigations would you want to do for proteinuria?

A

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
Q

how do you treat proteinuria?

A

treat the cause
e.g. if hypertension - ACEi
treat diabetes - also with ACEi and other diabetic treatment.

143
Q

How can we classify haematuria ?

A
  1. visible haematuria /macroscopic
  2. non-visible - microscopy
    a) symptomatic
    b) asymptomatic
144
Q

how is significant haematuria defined?

A

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
Q

what are the causes of haematuria?

A
  • 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
Q

what do you want to ask someone with haematuria?

A

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
Q

what further investigations would you do in someone with haematuria?

A 
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
Q

what are the indications of urological referral in someone with haematuria?

A

all patients with visible haematuria unless GN is suspected
all patients with symptomatic NVH
all patients with asymptomatic NVH that are 40 +

149
Q

what are the indication for nephrology referral in someone with haematuria?

A

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
Q

Name some nephrotoxic drugs?

A
  • 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
Q

what organic substances are toxic to the kidneys?

A 
urate
haemoglobin - in haemolysis 
myoglobin - in rhabdomyolysis 
Igs in myeloma (light chains)
streptococcus 
TB
clamidyia 
salmonella 
campylobacter
HIV, adeno, measles
taxoplasmosis and leishmania
152
Q

how can we help prevent kidney injury during the use of radiocontrast material?

A

stop other nephrotoxins
pre-hydrate
ask nephrologist for advice.

153
Q

what increases the risk of AKI with nephrotoxic drugs?

A

age, dose, CKD, long term treatment, other nephrotoxins too

154
Q

what are the causes of rhabdomyolysis?

A 
burns
excessive exercise
statins
seizures 
crush injury 
alcohol
ecstasy 
myositis 
infection
duchennes muscular dystrophy
155
Q

what are the symptoms of rhabdomyolysis?

A

muscle pain
swelling
red/brown urine (coca cola urine)

156
Q

What are the indications of renal replacement therapy?

A 
severe metabolic acidosis
hyperkalaemia 
pericarditis
encephalopathy
intractable volume load
peripheral neuropathy
intractable GI symptoms 
end stage renal failure (GFR <15ml/min)
157
Q

how does haemodialysis work?

A

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
Q

How is haemodialysis performed?

A

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
Q

what are the advantages of haemodialysis?

A

less responsibility
days off
better survival

160
Q

what are the disadvantages of haemodialysis?

A

travel time

deformities of the arm

161
Q

what are the complications of haemodialysis?

A

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
Q

what are the contraindications to haemodialysis?

A

heart failure
coagulopathy
failed vascular access

163
Q

what is peritoneal dialysis?

A

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
Q

how is peritoneal dialysis carried out?

A

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
Q

what are the advantages of peritoneal dialysis?

what are the disadvantages?

A

can be performed at home, holiday , at work - independence

however time consuming and responsibility

166
Q

what are the contra-indications to peritoneal dialysis?

A
  • 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
Q

what are the complications of peritoneal dialysis?

A
  • 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
Q

what are the 3 forms of renal replacement therapy?

A

peritoneal dialysis
haemodialysis
renal transplant

169
Q

what are the different types of renal transplant?

A
  • cadaveric: brainstem death
  • non-heart beating donor: no active circulation
  • live related:
    • optimal surgical timing
    • HLA matched
    • improved graft survival
  • Live unrelated
170
Q

how is a transplant carried out e.g. before and after care?

A
  • 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
Q

what are the indications of renal replacement therapy?

A

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
Q

what are the contraindications of renal transplant?

A 
cancer 
active infection 
uncontrolled ischaemic heart disease
acquired immunodeficiency disease with opportunity infections 
active viral hepatitis 
extensive peripheral vascular disease
mental incapacity
173
Q

what are the risks of transplantation?

A

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
Q

what is hyperacute rejection?

A

occurs within minutes of insertion - rare now due to cross matching
the graft has to be removed
ABO incompatibility

175
Q

what is accelerated rejection?

A

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
Q

what is acute cellular rejection?

A

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
Q

what is chronic rejection?

A

gradual rise in serum creatinine and proteinuria, resistant hypertension
biopsy shows vascular changes, fibrosis and tubular atrophy.
not responsive to increasing immunosuppressive therapy.

178
Q

what are the differential diagnosis for rise in creatinine in transplant patients?

A

rejection
obstruction
acute tubular necrosis
drug toxicity

179
Q

what are the acute and chronic nephrotoxic effects of tacrolimus

A

acute: reversible afferent arteriole constriction - reduced GFR
chronic: tubular atrophy and fibrosis

180
Q

how does pregnancy effect renal function?

A

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
Q

what are the pathological renal effects of pregnancy?

A

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
Q

what Abx are given to UTIs in pregnancy?

A

Trimethroprim is preferred throughout

nitrofurantoin should definitely be avoided in last trimester

183
Q

what are the effects of CKD on pregnancy?

A

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
Q

what are the predictors of pregnancy in those with CKD?

A

BP
serum creatinine
proteinuria

185
Q

what are the effects of transplant on pregnancy?

A

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
Q

what is the pathophysiology of a UTI?

A

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
Q

what are the symptoms of a UTI?

A

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
Q

what is the difference between a complicated and non-complicated UTI?

A

uncomplicated - normal healthy women

complicated: men, children, pregnancy, staph aureus, reflux nephropathy, immunocompromised.

189
Q

what is the treatment for UTIs?

A

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
Q

what is the treatment for pyelonephritis?

A

14 days of co-amoxiclav, gentamicin/ciprofloxacin

NOT nitrofurantoin because no systemic action

191
Q

what prophylactic treatment can be given to those who have >3 UTIs/ yr?

A

Trimethroprim/nitrofurantoin as single nightly dose

192
Q

what would investigations show if someone has a UTI?

A

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
Q

what are the risk factors for UTIs?

A

sexual intercourse
menopause
pregnancy
stones

194
Q

what is the pathophysiology behind renal stones?

A

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
Q

80% of renal stone are due to hypercalciuria. What are the causes of hypercalciuria and hypercalcaemia?

A 
hyperparathyroidism - squamous cell carcinoma
destruction of bone - tumour, pagets
excess vitamin D
thiazide diuretics
increased calcium intake
196
Q

what are the two types of calcium based stones?

A

calcium oxaloate and calcium phosphate

197
Q

hyperoxaluria can cause renal stones. what are the causes of hyperoxaluria?

A

increased oxaloate absorption from the gut = crohns
diet: spinach, tea, nuts
short bowel syndrome

198
Q

hyperuraciamia can cause renal tones what are the causes of this?

A

thiazide diuretics
tumour lysis
idiopathic

(also presents as gout)

199
Q

where are the 3 common sites for renal stones to form?

A

uretopelvic junction
uretovesicle junction
pelvic brim

200
Q

what are the symptoms of renal stones?

A 
may be asymptomatic
renal colic - excruciating pain for 20 mins in L1 dermatome (groin, iliac fossa and inner thigh) 
N&amp;V, pallor and sweating 
haematuria 
recurrent UTIs
201
Q

what are the complications of renal stones?

A

acute pyelonephritis +/- sepsis
AKI
UTI
hydronephrosis

202
Q

what is the treatment for renal stones?

A

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
Q

what are the causes of bladder stones?

A

caused by outflow obstruction - urethral stricture, prostate, neuropathic bladder

204
Q

what are the types of incontinence?

A

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
Q

what are the causes of urinary incontinence?

A

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
Q

how do we manage stress urinary incontinence?

A

pelvic floor exercises
Duloxetine (pharmacological)
surgery - intramural bulking agents e.g. collagen

207
Q

how do we manage urge incontinence?

A

bladder training

anticholinergic agents

208
Q

what fluid balance should you aim for in AKI? and why?

A

aim for +30-50ml to account for insensible losses.

209
Q

how do you conduct fluid resuscitation in patients at risk of fluid overload?

A

give 250ml bolus over 15 mins (rather than 500ml)

210
Q

during pelvic surgery which structures should you be careful of?

A

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
Q

explain the link between an aortic aneurysm and testicular varices

A

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
Q

name 3 embryological kidney abnormalities

A

horseshoe kidney - migration defect
renal agenesis - may be unilateral/bilateral
pelvic kidney

213
Q

why is infection in polycystic kidneys more problematic?

A

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
Q

how is clearance calculated and defined?

A

volume of plasma completely cleared of a substance per unit time

conc in urine x urine flow rate
divided by plasma conc

215
Q

what is the GFR?

A

volume of plasma filtered by bowmans capsule per minute

216
Q

describe the methods of renal blood flow regulation

A

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
Q

where are the osmolarity receptors located in brain?

A

OVLT in hypothalamus

218
Q

what drugs stimulate the Na/K ATPase?

A

K+
insulin
aldosterone (increases expression of Na/K ATPase)
catecholamines

219
Q

what factors promote K out of cells?

A

exercise - repolarisation and muscle tears
cell lysis - chemotherapy
acidosis - H/K exchanger
increased osmolality - draws K+ out along with water

220
Q

what are the effects of acidaemia and alkalaemia?

A

Alkalaemia: low Ca - increased neuronal excitability,paraesthesia and tetani . also hypo K
acidaemia - hyperkalaemia and denatures proteins.

221
Q

describe the physiological regulation of blood pressure

A

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
Q

explain the RAAS

A

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
Q

how does Hypoalbumin lead to AKI and how to does AKI lead to hypoalbumin?

A

leaky glomerulus can result in protein loss –> hypoalbumin

hypoalbumin reduces circulating volume which can reduce kidney perfusion and result in damage

224
Q

how are ACEi linked to AKI? so why are ACE sometimes used in kidney failure?

A

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
Q

what is renal failure in myeloma due to?

A
  • Light chain deposition
  • Hypercalcaemia
  • Sepsis
  • Use of NSAIDs
  • Chemotherapies.
226
Q

what treatment can be given in most drug overdoses?

A

IV intralipid - lipid soluble drugs will dissolve into this which will reduce their systemic effects

General Medicine sara (4 decks)

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