Nephrology Flashcards
(167 cards)
1
Q
Water and electrolytes are taken in by food and water and lost in urine and sweat. What other, insensible water losses are there?
A
500ml lost by expiration per day
2
Q
What percentage of an adult’s body weight is water?
A
50-60%
3
Q
In the healthy 70kg male, total body water is approx. how many litres?
A
42L
4
Q
What are the three major body fluid compartments?
A
Intracellular, extracellular and plasma
5
Q
Which is the largest of the body fluid compartments?
A
Intracellular
Approx. 28L (35% of lean body weight)
6
Q
Describe the extracellular fluid compartment
A
The extracellular fluid compartment comprises of the interstitial fluid that bathes the cells (9.4L/12% of body weight)
7
Q
What is osmotic pressure?
A
The primary determinant of the distribution of water among the three major compartments
8
Q
What is osmolality?
A
Defined as the number of osmoles per KILOGRAM of solution
Measurement of the osmotic concentration
9
Q
What is osmolarity?
A
Defined as the number of osmoles per LITRE of solution
10
Q
What electrolyte predominates in the intracellular compartment?
A
Potassium
11
Q
What electrolytes predominates in the interstitial fluid?
A
Sodium salts
12
Q
What molecules determine the oncotic pressure within the plasma?
A
Proteins
13
Q
What are the daily water requirements?
A
25-30ml/kg/day
14
Q
What are the daily requirements for sodium, potassium and chloride?
A
1mmol/kg/day
15
Q
What are the daily requirements for glucose?
A
50-100 grams/day
16
Q
What two forces balance to maintain plasma within the vasculature?
A
Hydrostatic pressure (forcing plasma into the interstitium)
Oncotic pressure (pressure exerted by plasma proteins to retain fluid in the vasculature)
17
Q
What is the definition of oedema?
A
Increase in the interstitial fluids due to one of a number of different aetiologies
18
Q
Outline some causes of oedema
A
Increased hydrostatic pressure e.g. sodium and water retention in cardiac failure
Reduced oncotic pressure e.g. as a result of nephrotic syndrome with hypoalbuminaemia
Obstruction to lymphatic flow
Increased permeability of the blood vessel wall e.g. local inflammation
19
Q
What are crystalloids?
A
Sodium chloride 0.9% containing low molecular weight salts or sugars that dissolve completely in water and pass freely between intravascular and interstitial compartments
20
Q
What are colloids?
A
E.g. dextran 70, gelatin
Contain larger molecular substances and remain for a longer period in the intravascular space than crystalloids
21
Q
What are colloids used for?
A
Used to expand circulating volume in haemorrhage, burns and sometimes septicaemia
22
Q
What side effects may accompany administration of colloids?
A
Hypersensitivity reactions including anaphylaxis and a transient increase in bleeding time
23
Q
What clinical observations may indicate a patient is ‘dry’ (hypovolaemic)?
A
Skin turgor, capillary refill, jugular venous pressure, pulse, lying and standing blood pressure
24
Q
Why should urine output not be considered alone in the assessment of fluid balance post-operatively?
A
Post-operatively there is a physiological oliguria and an impaired ability of the kidneys to dilute urine; increasing the risk of dilutional hyponatraemia
25
Before the prescription of IV fluids, clinical assessment of what needs to be undertaken?
Establish fluid and electrolyte needs
Identify the type of fluid needed
Does the patient need resuscitation, maintenance etc
Work out the appropriate rate of administration
26
Regulation of the extracellular volume is determined by the tight control of what electrolyte in particular?
Sodium
27
What is the effective arterial blood volume (EABV)?
The fullness of the vasculature; determines the control of renal sodium and water excretion
28
What two types of volume receptors detect changes in the effective arterial blood volume?
Extrarenal: in the large vessels near the heart
Intrarenal: in the afferent renal arteriole
29
Intrarenal volume receptors have direct control over what hormonal system?
The renin-angiotensin-aldosterone system (RAAS)
30
What hormones counteract the effects of the renin-angiotensin-aldosterone system?
Atrial natriuretic peptide - increases sodium excretion
31
Increased extracellular volume is a result of increased sodium retention/impaired excretion by the kidneys. Outline the symptoms.
Interstitial volume overload - ankle oedema, pulomary oedema, pleural effusion and ascites
Intravascular volume overload - raised JVP, cardiomegaly and a raised arterial pressure
32
List some aetiologies of extracellular volume expansion
Cardiac failure
Cirrhosis
Nephrotic syndrome
Sodium retention
33
How does cirrhosis lead to extracellular volume expansion?
Complex pathophysiology leading to vasodilation and under perfusion of the volume receptors.
Hypoalbuminaemia may contribute
34
List some common causes of decreased extracellular volume?
Haemorrhage
Plasma loss in burns
Pathological diuresis
35
Signs of volume depletion may occur in a patient with a normal volume. Give an example of when this occurs?
Sepsis (due to vasodilation and increased capillary wall permeability)
36
What is the most potent class of diuretics? Give an example
Loop diuretics e.g. furosemide
37
What is the mechanism of action of loop diuretics?
Reduce Na+/Cl- reabsorption from the ascending loop of Henle in the glomeruli
38
What is the mechanism of action of thiazide diuretics? Give an example
Reduced Na+ reabsorption at the distal convoluted tubule of the glomeruli
Bendroflumethiazide
39
Spironolactone is an example of what class of diuretics?
Aldosterone antagonists
40
Give an example of a potassium-sparing diuretic
Amiloride
41
Give common signs and symptoms of volume depletion
Symptoms - thirst, nausea, dizziness (postural)
Signs - loss of skin tugor, peripheral vasoconstriction, tachycardia, low JVP, postural hypotension
42
What are the dangers of severe volume depletion?
Impaired cerebral perfusion leading to confusion and eventual coma
43
What device allows the measurement of the central venous pressure?
Central venous line
44
If the kidneys are working well, what is the expected normal value of urinary sodium?
<20mmol/L
45
How is circulating volume depletion treated?
Outline the specific treatments for haemorrhage, loss of plasma, loss of sodium/water and loss of water alone
Overall principle: Replace what is lost.
Haemorrhage - initial treatment with crystalloid/colloid until packed red cells are available
Loss of plasma (burns/peritonitis) - replace with human plasma/colloid
Loss of sodium and water (vomiting/diarrhoea) - saline or glucose electrolyte solutions
Loss of water - water w. 5% glucose solution to avoid osmotic lysis of red cells
46
What is the normal value for plasma osmolality?
285-300 mosmol/kg
47
What receptors sense changes in plasma osmolality? Where are they located?
Osmoreceptors in the hypothalamus
48
What mechanisms does the hypothalamus activate on detection of a raised osmolality?
Thirst mechanism and release of anti-diuretic hormone (ADH)
49
What is the action of anti-diuretic hormone?
Increases renal reabsorption of water from the collecting ducts
50
What non-osmotic stimuli may also cause secretion of ADH?
Hypovolaemia
Stress (surgery/trauma)
Nausea
51
What is the other name for the hormone ADH?
Vasopressin
52
What physiological phenomena occurs at a plasma osmolality of less than 275 mosmol/kg?
Complete suppression of ADH secretion
53
What is the definition of hyponatraemia?
Reflects too much water in relation to sodium.
Serum sodium < 135 mmol/L
54
List four aetiologies of hyponatraemia
1. Water excess (dilutional hyponatraemia)
2. Salt loss e.g. diarrhoea
3. Pseudohyponatraeia (hyperlipidaemia causing spuriously low sodium - no treatment required)
4. Artefactual hyponatraemia - blood sample taken from an arm where a low sodium drip is being infused e.g. glucose
55
What is the essential distinction a clinician must make when assessing the hyponatraemia patient?
Is the patient either:
Hypovolaemia
Euvolaemic
Hypervolaemic
56
How is hypovolaemic hyponatraemia treated?
Restoration of extracellular volume crystalloids or colloids normalises serum sodium
57
What is the most common cause of hypovolaemia hyponatraemia?
Diuretics over-use
58
What is the most common cause of dilutional hyponatraemia (hypovolaemic)?
Overuse of 5% glucose in post-operative patients
59
What three pathologies often precipitate dilutional hyponatraemia?
Severe cardiac failure, cirrhosis, nephrotic syndrome
60
What are the consequences of not correcting dilutional hyponatraemia?
Due to the movement of water into brain cells (cerebral oedema)
Headache, confusion, convulsions and coma
61
How is dilutional hyponatraemia managed?
Most cases managed by water restriction
Review of diuretic treatment may be indicated
Vasopressin V2 receptor antagonists e.g. tolvaptan produces free water diuresis
62
What is central pontine myelinolysis?
Over-rapid correction of sodium concentration leading to severe neurological damage causing quadriparesis, respiratory arrest, pseudobulbar palsy, mutism, seizure
63
What is the most common cause of hypernatraemia?
Reduced water intake or water loss in excess of sodium
64
What are the clinical features of hypernatraemia?
Nausea, vomiting, confusion
65
Serum levels of potassium are regulated by what three factors?
1. Uptake of K+ into cells
2. Renal excretion - mainly controlled by aldosterone
3. Extrarenal losses e.g. gastrointestinal
66
What is the definition of hypokalaemia?
Serum potassium concentration of <3.5 mmol/L
67
What are the most common causes of hypokalaemia?
Diuretic treatment
| Hyperaldosteronism
68
What are the clinical features of hypokalaemia?
Usually asymptomatic
Muscle weakness and cardiac arrhythmias if severe
69
How is hypokalaemia managed?
Assessment of diuretic treatment
Replacement with oral potassium chloride
70
What other electrolyte must be normalised before hypokalaemia can be normalised?
Magnesium
Hypomagnesaemia makes hypokalaemia difficult/impossible to correct
71
Under what circumstances may IV potassium be indicated?
Severe hypokalaemia associated with cardiac arrhythmias and hypokalaemia diabetic ketoacidosis
72
What is the definition of hyperkalaemia?
>5mmol/L
73
What are the most common causes of hyperkalaemia?
```
Renal impairment (e.g. AKI)
Diabetic ketoacidosis
Addison's disease
```
74
What are the clinical features of hyperkalaemia?
Produces few symptoms until it causes cardiac arrest
Causes progressive ECG changes
75
How is mild hyperkalaemia managed?
Mild disturbance causes dietary potassium restriction
76
What ECG changes may be seen in hyperkalaemia?
Reduced P wave
Wide QRS complex
Tented T waves
'Sine wave' pattern
77
How is severe hyperkalaemia treated?
Protection of myocardium - 10ml of 10% calcium gluconate
Drive K+ into cells - Soluble 10 units of insulin and 50ml of 50% dextrose
Deplete body K+ - polystyrene sulphonate resin orally
78
What are the two effects magnesium has on potassium and PTH?
Increases renal excretion of potassium
| Leads to parathyroid hormone resistance
79
What is the management of hypomagnesaemia?
Underlying causes must be corrected
Oral supplements in mild disease
IV supplementation in severe disease (plus loading dose)
80
What is the most common cause of hypermagnesaemia?
Usually iatrogenic in patients with renal failure who have been given magnesium-containing antacids/laxatives
81
What are the clinical features of hypermagnesaemia?
Neurological,respiratory and cardiovascular depression
82
How is hypermagnesaemia treated?
Mild - stopping magnesium-containing drugs
Severe - IV calcium gluconate with dextrose/insulin to lower plasma magnesium
83
What is the normal range of pH?
7.35-7.45
84
What molecule is the main plasma and extracellular fluid buffer?
Bicarbonate
85
Where is bicarbonate excreted and reabsorbed respectively?
Filtered out at the glomerulus and reabsorbed at the proximal and distal renal tubules
86
What enzyme facilitates the bicarbonate equilibrium?
Carbonic anhydrase
87
What compensatory mechanism is triggered by metabolic acidosis? What receptors detect and trigger this?
Hyperventilation
Via medullary chemoreceptors
88
What compensatory mechanism is triggered by respiratory acidosis?
Renal bicarbonate retention
89
The measurement of what three things reveal the nature of an acid/base disturbance? What clinical procedure does this describe?
pH
PaCO2
[HCO3-]
All measured in an arterial blood gas sample
90
What is metabolic acidosis? What is the most common cause?
Accumulation of any acid other than carbonic acid.
Most commonly lactic acidosis following shock or cardiac arrest
91
What are the clinical features of metabolic acidosis?
Hyperventilation, hypotension and cerebral dysfunction (fits and confusion)
92
What is the first step in the differential diagnosis of metabolic acidosis?
Measure the anion gap.
Essentially tells you whether the acidosis is due to retention of HCl or another acid.
93
What are the most common causes of metabolic acidosis with a normal anion gap?
(ABCD)
Addison's
Bicarbonate loss e.g. diarrhoea or renal tubular damage
Chloride
Drugs- acetazolamide
94
What are the most common causes of metabolic acidosis with an increased anion gap?
```
Lactic acidosis (sepsis)
Uraemic acidosis
Diabetic ketoacidosis
Alcohol
Acid poisoning (methanol, Salicylates)
```
95
Outline lactic acidosis
Occurs when cellular respiration is anaerobic (type A) or due to metabolic abnormality (type B).
Type A occurs in septicaemia and cardiogenic shock
96
Outline diabetic ketoacidosis
Accumulation of acetoacetic and hydroxybutyric acids
97
Outline renal tubular acidosis
Failure of the kidney to acidify urine properly
98
Outline uraemic acidosis
Reduction of the capacity to secrete H+ and NH4+.
Associated with hypercalcaemia and renal osteodystrophy
99
Metabolic alkalosis is most often associated with what two pathologies?
1. Volume depletion
| 2. Potassium depletion
100
What are the main causes of metabolic alkalosis?
Persistent vomiting, diuretic therapy or hyperaldosteronism
101
What is one of the earliest signs of alkalosis?
Cerebral dysfunction
102
How is metabolic alkalosis managed?
Fluid replacement
103
What is the functional unit of the kidney?
Nephron
104
What structure regulates elimination of potassium and non-volatile hydrogen ions?
Distal tubules
105
What are the two most common diseases of the kidney or urinary tract in men and women respectively?
Men - BPH
| Women - UTI
106
List some symptoms indicative of renal tract disease?
Dysuria, frequency of micturition, haematuria, urinary retention, alteration of urine volume (oliguria, polyuria)
107
What may be the presenting symptoms/incidental findings of chronic kidney disease?
Lethargy, anorexia, pruritis
Incidental finding of hypertension, raised serum urea, proteinuria/ haematuria
108
What are the vasa recta?
Vessels supplying the loop of Henle
109
List the causes of dysuria
1. Inflammation of urethra (urethritis) or bladder (cystitis)
2. Inflammaiton of the vagina/glans by candida albicans or gardnerella vaginalis
110
Outline management of the oliguric patient
1. Exclude obstruction - due to acute retention (great discomfort, dull blader to percussion)
2. Assess for hypovolaemia (BP, pulse, JVP, urinary electrolytes)
3. Management of established AKI (diagnosed after 1. and 2. have been ruled out)
111
Outline some causes of loin/flank pain
Acute pyelonephritis
Upper urinary tract obstruction
Occlusion of the renal artery
Thrombosis/emboli
112
How is renal function assessed?
Estimation of glomerular filtration rate (eGFR)
113
What equation is used to calculate eGFR from serum creatinine?
Cockrof-Gault equation
114
Outline what is possible to test for with urinary dipstick testing
Blood, protein, glucose, ketones, bilirubin, urobilinogen, pH, nitrates, leukocytes
115
What is considered to be normal urinary protein excretion?
<150mg/day
116
What is the nephrotic range of proteinuria?
>3.5g per day (PCR >350mg/mm)
117
What is microalbuminuria?
Increase above the normal range of urinary albumin excretion that is undetectable by conventional dipsitcks
118
What is the clinical usefulness of testing for microalbuminuria?
Predictor in the development of diabetic nephropathy
119
How is microalbuminuria measured?
Albumin/creatinine ratio (ACR) >2.5mg/mmol in men and >3.5mg/mmol in women
120
Haematuria can arise from several sites. Outline how the bleeding pattern can indicate different sites
Blood at the beginning of micturition - urethral disease
Blood at the end of micturition - bladder/prostate disease
Blood seen as even discolouration - bleeding above the bladder (e.g. ureters/kidneys)
121
List some transient causes of haematuria
UTI
| Contamination of urine from menstruation
122
List some imaging techniques of renal pathology
```
Plain X-ray
US
MRI
Excretion Urography (IVU)
Renal angiography
Anterograde pyelography (outlines
Retrograde pyelography
Renal scintigraphy
```
123
What is the difference between glomerulonephritis and glomerulopathy?
On microscopic examination of renal biopsies, if inflammation is predominant, it can be described as glomerulonephritis. Otherwise, it is glomerulopathy
124
In term of renal disease description, what is meant by the term 'focal'?
Some, but not all of the glomeruli are affected
125
In term of renal disease description, what is meant by the term 'diffuse'?
Approx. >75% of glomeruli contain the lesion
126
In term of renal disease description, what is meant by the term 'segmental'?
Only a part of the glomerulus is affecte
127
In term of renal disease description, what is meant by the term 'global'?
All glomeruli involved
128
In term of renal disease description, what is meant by the term 'proliferative'?
An increase in cell numbers due to hyperplasia of one or more of the resident glomerular cells
129
In term of renal disease description, what is meant by the term 'membrane alterations'?
Capillary wall thickening due to deposition of immune complexes in the basement membrane
130
In term of renal disease description, what is meant by the term 'crescentic'?
Epithelial cell proliferation with mononuclear infiltration in Bowmann's space
131
What is the typical history of a person with glomerular disease?
Suspected in patients presenting with haematuria, red cell casts and proteinuria
132
Glomerular disease can be classified into four main syndromes; what are they?
1. Nephrotic syndrome
2. Acute glomerulonephritis (acute nephritic syndrome)
3. Rapidly progressive glomerulonephritis
4. Asymptomatic haematuria/ proteinuria (or both)
133
What is nephrotic syndrome?
Massively increased filtration fo macromolecules resulting in:
1. Hypoalbuminaemia - a consequence of massive proteinuria
2. Oedema (due to sodium retention in renal collecting tubules)
3. Hypercholesterolaemia (due to increased synthesis)
134
What is the difference between active and bland sediments?
Sediments are precipitates in your urine. Active sediments have cellular components e.g. RBCs, WBCs, casts - usually indicate an active process of renal damage
Bland sediments are proteins, crystals or casts
135
What are the differential diagnoses for a patient with nephrotic syndrome and bland urinary sediments?
Membranous nephropathy and focal segmental glomerulosclerosis in adults
Minimal-change nephropathy in children
136
What is membranous nephropathy?
Deposition of IgG and C3 in the basement membrane attributed to a number of causes including drugs (e.g. NSAIDs, penicillamine etc.), autoimmune processes (e.g. SLE), malignancy, infections (hepatitis B/C, schistosomiasis)
137
What is focal segmental glomerulosclerosis?
A particularly common cause of nephrotic syndrome in black adults. Similar histological types in HIV infection
138
What is minimal change nephropathy?
Accounts for over 90% of nephrotic syndrome in children.
Unknown pathogenesis with no immunofluorescent immune complexes.
Glomeruli appear normal on light microscopy
139
Outline some non-immune mediated causes of nephrotic syndrome
Renal amyloid and diabetes mellitus
140
What are the differential diagnoses for a patient with nephrotic syndrome and active urinary sediments?
Mesangiocapillary (membranoproliferazive glomerulonephritis)
Mesangial Proliferative Glomerulonephritis
141
What is Mesangiocapillary (membranoproliferazive glomerulonephritis)?
Occurs with chronic infection (e.g. abscesses, infective endocarditis, hepatitis C) and leads to progressive renal failure
142
What is Mesangial Proliferative Glomerulonephritis?
Heavy proteinuria with minimal changes on microscopy. Glomerular mesangium deposition of IgM and/or complement
143
What are the clinical features of nephrotic syndrome?
Oedema of the ankles, genitals, abdominal wall
144
What are the differential diagnoses for nephrotic syndrome?
Other causes of oedema and hypoalbuminaemia e.g. heart failure, cirrhosis
145
How is nephrotic syndrome managed?
General oedema - salt restriction, thiazide diuretic e.g. bendroflumethiazide (followed by furosemide and amiloride in unresponsive patients)
Proteinuria reduced by ACEIs
Specific treatment - minimal change is always steroid-responsive in children
146
What baseline investigations are indicated in glomerular disease?
eGFR, urinary protein, serum ureas and electrolytes, serum albumin
147
What are some diagnostically useful tests in glomerular disease?
Urine microscopy (to look for red cell casts)
Throat/skin swab culture (for recent strep. infection)
Serum antistreptolysin-O titre (for recent strep. infection)
148
List three complications of glomerular disease (or its treatment) which may occur:
1. Venous thrombosis (renal pain, haematuria, decreasing kidney function - Dx by US)
2. Sepsis (due to loss of immunoglobulins)
3. AKI (usually consequence of diuretic therapy)
149
What is acute glomerulonephritis?
Often caused by an immune response triggered by an infection or other diseases.
Typically a post-streptococcal GN develops 1-3wks after infection (pharyngitis/cellulitis) with a group A beta-haemolytic strep. bacteria
150
What are the clinical features of acute GN?
```
Haematuria (visible or non-visible)
Proteinuria
Hypetension and oedema
Oliguria
Uraemia
```
151
What diseases are associated with acute GN?
Post-infective GN (strep. or others including staph, malaria etc.)
SLE
Infective endocaritis
Henloch-Schönlein Purpura
152
How is acute GN managed?
Hypertension treated with salt restriction, loop diuretics and vasodilators
Fluid balance monitored (fluid restriction may be necessary if oedematous)
153
What are the three main causes of rapidly progressive glomerulonephritis?
1. On a background of acute nephritic syndrome
2. ANti-glomerular basement membrane disease (lung involvement = Goodpasture's syndrome)
3. Antibeutrophilic cytoplasmic antibody (ANCA)-associated antibodies
154
List some causative organisms for UTIs
E. coli
Proteus mirabilis
Klebsiella aerogenes
Enterococcus faecalis
155
What is meant by the term 'uncomplicated UTI'?
UTI in the otherwise healthy, non-pregnant woman with a functionally normal urinary tract
156
What is urethral syndrome?
Occurs in women and presents with dysuria and frequency but in the absence of bacteriuria
May be associated with vaginitis in post-menopausal women, irritant chemicals (e.g. soaps) and sexual intercourse
157
What is bacterial prostatitis?
A relapsing infection which presents as perineal pain, recurrent epididymo-orchitis and prostatic tenderness, with pus in expressed prostatic secretion
158
How is bacterial prostatitis treated?
Treatment is for 4-6 weeks with drugs that penetrate into the prostate, such as trimethoprim or ciprofloxacin.
159
What are the complications associated with bacterial prostatitis?
Prostadynia (prostatic pain in the absence of active infection)
160
What is tubulointerstitial nephritis?
Primary injury to the renal tubules and interstitium that results in decreased renal function.
Both acute and chronic
161
Describe acute tubulointerstitial nephritis
Mostly due to drug allergy (e.g. NSAIDs, penicillins)
Patients present with fever, eosinophilia and eosinophiluria. proteinuria
Renal biopsy show intense interstitial cellular infiltrate and variable necrosis
Treated by removing the offending drug and high dose prednisolone
162
What is chronic tubulointerstitial nephritis?
Many causes including prolonged consumption of large doses of analgesics (particularly NSAIDs)
Presentation is with polydipsia, polyuria and uraemia
163
What are the two main mechanisms by which hypertension complicated bilateral renal disease?
1. Activation of the renin-angiotensin-aldosterone system
| 2. Retention of salt and water
164
How does renal vascular disease increase blood pressure?
Renal perfusion pressure is reduced and renal ischaemia results in increased renin production and blood pressure
165
How is renal artery stenosis investigated and managed?
Renal arteriography
| Treated with transluminal angioplasty and stent placement
166
What is nephrocalcinosis?
Diffuse renal parenchymal calcification that is detectable radiologically
Sx: Painless, hypertension and renal impairment
167
List some causes of nephrocalcinosis
Hypercalcaemia
Renal tubular acidosis
Tuberculosis
