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Clinical Practice > Nephrology > Flashcards

Nephrology Flashcards

1
Q

what are the causes of breathlessness and ankle swelling?

A 
CCF
cor pulmonale
liver disease
kidney disease
nephrotic syndrome
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2
Q

describe pitting oedema

A

salt and water retention
ECF volume is increased
interstitial fluid displacement

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3
Q

how does the RAAS combat a reduction in CO?

A 
BP falls (BP = CO x PR)
prostaglandins dilate the afferent arterioles
angiotensin II constricts the efferent arterioles
GFR increases due to auto regulation of glomerular blood flow
increased aldosterone levels cause sodium and water retention
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4
Q

describe hypervolaemic hyponatraemia and its prognosis

A

retention of salt and (excess) water

poorer prognosis in heart failure

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5
Q

describe RAAS activation

A 
reduced renal perfusion and GFR
sensed by the macula
juxtaglomerular apparatus
renin release
angiotensin I
angiotensin II (lungs)
aldosterone released from adrenal glands (Na retention)
Cl and water reabsorption

chronically exacerbates cardiac dysfunction by increasing the workload

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6
Q

describe natriuretic peptide activation in HF and how this is associated with the kidneys

A

atrial and ventricular stretch associated with ECF volume expansion
natriuretic peptides released from the heart and act on renal tubules to promote Na excretion
NT-proBNP released in HF

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7
Q

describe sympathetic nervous system activation in HF

A

BP drop; baroreceptor activation
catecholamine release; increases SV and HR
initially increase PR

chronic; aberrant re-modelling of cardiomyocytes (fibrosis)

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8
Q

describe vasopressin activation in HF

A

baroreceptor activation
released from posterior pituitary
increases peripheral resistance
increases water reabsorption from the collecting ducts

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9
Q

why does hyponatraemia develop in advanced HF?

A

Na retention by aldosterone

excess water retention by vasopressin and RAAS

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10
Q

describe the causes and complications of renal artery stenosis

A

atherosclerotic plaques in the renal arteries

reduced perfusion pressure to the kidneys
RAAS activation
= secondary hypertension

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11
Q

what drugs should be stopped in an AKI?

A

diuretics
ACEi or ARBs
metformin
NSAIDs

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12
Q

how do NSAIDs affect renal function?

A

they block the vasodilator prostaglandin synthesis

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13
Q

what is the sepsis 6 bundle?

A 
give IV fluids
give IV antibiotics
give oxygen
take blood cultures
take urine output volume
take blood lactate levels
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14
Q

what is the pathology of peripheral vascular disease?

A

poor oxygen delivery to bones and soft tissue of the lower limb
tissue hypoxia leads to skin breakdown, poor wound/ulcer healing, poor defence against infection

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15
Q

what are the risk factors for an AKI?

A 
age
hypotension
sepsis
hypovolaemia/fluid losses (diarrhoea, diuretic)
drugs (abx, NSAIDs, ACEi)
pre-existing CKD
co-morbidities (diabetes, HF)
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16
Q

what is the treatment of diabetic kidney disease?

A

ACEi or ARB 1st line

lower glomerular capillary pressure, reduce proteinuria and slow progression of proteinuria renal disease

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17
Q

name some potassium-sparing drugs

A

ACEi
ARB
spironolactone
eplerenone

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18
Q

what are the indications to start dialysis?

A

hyperkalaemia refractory to conservative management
fluid overload refractory to conservative management
severe hypertension
severe GI symptoms
severe neurological symptoms
eGFR <10ml/min

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19
Q

what are the common types of shock?

A 
septic
hypovolaemic
cardiogenic (pump)
anaphylactic
obstructive
neurogenic
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20
Q

what is the stepwise approach to determining the type of acid-base disorder?

A

academic/alkalaemic
ventilation compensating for or contributing to the pH change
bicarbonate
anion gap (is acidosis present due to acid gain or bicarbonate loss)

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21
Q

define an anion gap

A

(Na + K) - (Cl + HCO3)

normal is 10-14mmol/L

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22
Q

what are the causes of a metabolic acidosis with a raised anion gap?

A 
lactic acidosis
ketoacidosis
renal failure
certain poisons (methanol, ethylene glycol, aspirin)
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23
Q

why is the bicarbonate concentration reduced in metabolic acidosis?

A

excess acid is being partly buffered by HCO3 = H2O and CO2 generation
excess acid; overwhelming the ability of the lungs to compensate
excess acid; overwhelming the ability of the kidneys to excrete H+ and regenerate HCO3

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24
Q

how does renal failure contribute to acidosis?

A

no H+ excretion and HCO3 generation

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25
Q

what are the causes of hyperkalaemia?

A

excess intake
reduced excretion
shift of K out of the intracellular compartment (NaK ATPase problem, requires insulin)

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26
Q

what investigations are required to determine the cause of metabolic acidosis?

A

serum lactate
serum ketones
plasma glucose
U&E (for renal failure)

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27
Q

what is the management of cardiogenic shock caused by LV MI?

A

high flow oxygen
PCI
IV furosemide
insulin administration (lower blood glucose and stop ketoacid production)

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28
Q

what acid-base disorder can be caused by vomiting?

A

metabolic alkalosis

loss of acid/H+ in gastric secretions

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29
Q

what acid-base disorder can be caused by narcotic drugs?

A

respiratory acidosis

depression of respiratory centre; hypoventilation

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30
Q

describe Kussmaul’s respiration

A

deep, rapid breathing pattern
indicates (metabolic) acidity
the body tries to expel CO2

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31
Q

describe vasculitis

A

inflammatory leucocytes in the blood vessel walls causing damage
loss of the normal immune tolerance mechanisms

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32
Q

what are the lifestyle requirements for dialysis?

A 
low Na diet and restrict PO4 and K
fluid restriction
time commitment
psychological impact (high mortality rate)
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33
Q

describe CKD-related bone disease

A

vitamin D cannot be activated in CKD
calcium cannot be absorbed from the gut
parathyroid glands secrete PTH in response to falling serum Ca levels
PTH stimulates osteoclasts to reabsorb bone which releases Ca

benefits; avoid cardiac arrhythmias
chronically; secondary hyperparathyroidism and weakened bone structure

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34
Q

what are the causes of sodium and water losses?

A

GI losses - vomiting, diarrhoea
renal losses - osmotic diuresis, diuresis secondary to drugs
dermal losses

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35
Q

what are the causes of sodium and water retention?

A 
pregnancy
heart failure
liver failure
renal failure
nephrotic syndrome
36
Q

what are the signs of fluid retention?

A

pulmonary oedema
pitting oedema
volume mediated hypertension

37
Q

what are the consequences of reduced renal perfusion?

A

RAAS activation

sodium and water retention

38
Q

what is the treatment of fluid retention?

A

salt and fluid restriction
diuretics (spironolactone/eplerenone)
ACEi/ARB
sympathetic nervous system blockade (cardioselective beta blocker)

39
Q

what are the causes of secondary hypertension?

A 
chronic renal disease
renal vascular disease
endocrine disorders
co-arctation of the aorta
NSAIDs
alcohol
40
Q

why does pulse pressure increase with age?

A

reduction of elastic recoil in the arteries

41
Q

what are the complications of renal artery stenosis?

A

chronic hypoperfusion of nephrons
compensation by activation of the RAAS system
hypertension to maintain renal perfusion

42
Q

what are the complications of very rapid correction of BP?

A

AKI; compromised renal perfusion

43
Q

define AKI

A

GFR decrease in hours-weeks that is potentially reversible

abrupt reduction in renal function associated with an increase in serum creatinine and/or a reduction in urine output

44
Q

what does normal renal function depend on?

A

perfusion with adequate pressure and oxygen
intact nephrons
free urinary drainage

45
Q

define oliguria

A

UO <400-500mls/day

46
Q

what are the causes of an AKI?

A

true volume depletion; GI loss, haemorrhage
hypotension; septic or cardiogenic shock
oedematous states; advanced cardiac and liver failure

47
Q

what are the causes of ATN?

A

severe pre-renal insults (hypotension associated with sepsis or during surgery)
drugs
radiocontrast dye
haem pigments (myoglobin)

48
Q

what are the consequences of ATN?

A

limited reabsorption of solutes
decreased excretion of toxins
low urine osmolality
increased urine sodium levels

49
Q

what are the risk factors for an AKI?

A 
age
previous AKI
hypotension
hypovolaemia
sepsis
medication
diabetes
HF
50
Q

what are the consequences of pre-renal AKI?

A

sodium and water retention

51
Q

what medications should be stopped in a pre-renal AKI (septic shock)?

A

ACEi
ARB
NSAIDs

interfere with dilatation of afferent arterioles to maximise blood flow into glomeruli and constriction of efferent arterioles to reduce outflow

52
Q

what are the causes of renal AKI?

A

ATN

glomerulonephritis (suspect if blood and protein on urinalysis)

53
Q

what are the causes and management of post-renal AKI?

A

renal tract obstruction

urgent USS and consider urinary catheter

54
Q

describe the pathology of DKD

A

efferent and afferent arteriole constriction and vasodilation
increased glomerular capillary pressure
GBM becomes more porous to albumin
podocytes become damaged by hyperglycaemia
albuminuria

55
Q

why does glomerular hypertension lead to progressive renal failure?

A

glomeruli are lost due to raised pressure and gradual scarring

56
Q

define albuminuria

A

urinary ACR >30mg/mmol

57
Q

what are the components of DKD

A

albuminuria
hypertension
decreasing eGFR

58
Q

what is the treatment of DKD?

A 
ACEi
ARB
BP control
blood glucose control
transplant
59
Q

describe ADPKD

A

a clonal disorder of epithelial cell growth

inactivation of 2 copies of a PKD gene (1 and 2) through germline and somatic mutations

60
Q

what are the risk factors for ADPKD?

A

smoking
folic acid deficiency
DNA polymorphisms

61
Q

what are the complications of ADPKD?

A 
cerebral aneurysm (SAH)
hepatic cysts
cardiac valve disorders
umbilical and inguinal herniae
kidney stones
CKD
HTN
62
Q

what are the symptoms of ADPKD?

A

haematuria
flank and abdominal pain
asymptomatic

63
Q

what is the management of ADPKD?

A

ACEi/ARB (aim <130/90mmHg)
tolvaptan (ADH receptor antagonist)
manage CVD risk

64
Q

define the glomerulus

A

a specialised network of capillaries supported by mesangial cells

65
Q

describe the pathology of glomerulonephritis

A

alteration of the GBM properties leading to protein loss from the circulation into the urine (proteinuria)

66
Q

what is the clinical presentation of glomerulonephritis?

A 
asymptomatic
visible haematuria
HTN
proteinuria
post-infectious
AKI (nephritic syndrome)
CKD
peripheral and peri-orbital oedema
67
Q

what are the clinical features of nephrotic syndrome?

A 
oedema (massive leg oedema)
hypoalbuminaemia
proteinuria
xanthelasma (secondary hyperlipidaemia)
vasculitis (vasculitic rash)
68
Q

why does oedema occur in nephrotic syndrome?

A

hypoalbuminaemia causes a reduction in plasma oncotic pressure
hydrostatic pressure > plasma oncotic pressure so net fluid movement into interstitium

69
Q

what is the treatment of nephrotic syndrome?

A 
dietary salt/fluid restriction
diuretics
ACEi
biopsy
may need immunosuppressant therapy
70
Q

what are the causes of a raised anion gap (increased acid) in metabolic acidosis?

A 
lactic acidosis
renal failure
ketoacidosis
methanol
ethylene glycol
aspirin
71
Q

what are the causes of a normal anion gap (bicarbonate loss) in metabolic acidosis?

A

GI loss

renal loss

72
Q

what is the treatment of a metabolic acidosis with a raised anion gap?

A

treat the cause

improve oxygenation

73
Q

describe hyperkalaemia on an ECG

A

peaked T waves
wide QRS complexes
near sinusoidal pattern
PR prolongation

74
Q

what is the treatment of hyperkalaemia?

A

10ml 10% calcium gluconate IV (stabilises myocardium)
10 units short acting glucose (Actrapid) IV (shift K into cells)
50ml 50% glucose IV
nebullised beta 2 agonist (10mg salbutamol)

loop diuretcs
dialysis
calcium resonium

75
Q

what are the indications for dialysis in those with AKI/CKD?

A

refractory hyperkalaemia

76
Q

what are the features of nephritic syndrome?

A

haematuria
oliguria
proteinuria
fluid retention

77
Q

describe glomerulosclerosis

A

scarring in the tissue of the glomerulus

can be caused by glomerulonephritis, obstructive uropathy or focal segmental glomerulosclerosis

78
Q

describe IgA nephropathy/Berger’s disease

A

most common cause of primary glomerulonephritis
peak age of presentation in 20s
develops 1-2 days post URTI
histology; IgA deposits and glomerular mesangial proliferation

79
Q

describe membranous glomerulonephritis

A

most common cause of glomerulonephritis overall
peak age between 20-60
histology; IgG and complement deposits on basement membrane
causes; idiopathic, malignancy, rheumatoid disorders, drugs (NSAIDs)

80
Q

describe post-streptococcal glomerulonephritis

A 
typically <30yrs
1-3 weeks post streptococcal infection
develop nephritic syndrome
usually make a full recovery
low complement
81
Q

describe good pasture syndrome

A

anti-IgM antibodies attack the glomerulus and pulmonary basement membrane
causes glomerulonephritis and pulmonary haemorrhage
can present with AKI and haemoptysis

82
Q

describe Wegener’s granulomatosis

A

vasculitis
associated with ANCA
can present with AKI, haemoptysis, wheeze, sinusitis, saddle shaped nose

83
Q

describe rapidly progressive glomerulonephritis

A

histology; cresenteric glomerulonephritis
very acute illness, sick patients
responds well
often secondary to good pastures syndrome

84
Q

what are the clinical features of post-streptococcal glomerulonephritis?

A 
headache
malaise
visible haematuria
proteinuria
HTN
oliguria
low C3
raised ASO titre
85
Q

what are the causes of acute interstitial nephritis?

A 
NSAIDs
antimicrobial agents
salicylates
ACE inhibitors
diuretics
86
Q

what are the USS features of CKD?

A

bilateral shrunken kidneys

exceptions; ADPKD, DKD, amyloidosis, HIV associated nephropathy

87
Q

what are the causes of focal segmental glomerulosclerosis?

A 
idiopathic
secondary to other renal pathology; IgA nephropathy
HIV
heroin
alports syndrome
sickle cell

Clinical Practice (14 decks)

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