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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
what are the causes of hyperkalaemia?
excess intake reduced excretion shift of K out of the intracellular compartment (NaK ATPase problem, requires insulin)
26
what investigations are required to determine the cause of metabolic acidosis?
serum lactate serum ketones plasma glucose U&E (for renal failure)
27
what is the management of cardiogenic shock caused by LV MI?
high flow oxygen PCI IV furosemide insulin administration (lower blood glucose and stop ketoacid production)
28
what acid-base disorder can be caused by vomiting?
metabolic alkalosis | loss of acid/H+ in gastric secretions
29
what acid-base disorder can be caused by narcotic drugs?
respiratory acidosis | depression of respiratory centre; hypoventilation
30
describe Kussmaul's respiration
deep, rapid breathing pattern indicates (metabolic) acidity the body tries to expel CO2
31
describe vasculitis
inflammatory leucocytes in the blood vessel walls causing damage loss of the normal immune tolerance mechanisms
32
what are the lifestyle requirements for dialysis?
``` low Na diet and restrict PO4 and K fluid restriction time commitment psychological impact (high mortality rate) ```
33
describe CKD-related bone disease
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
34
what are the causes of sodium and water losses?
GI losses - vomiting, diarrhoea renal losses - osmotic diuresis, diuresis secondary to drugs dermal losses
35
what are the causes of sodium and water retention?
``` pregnancy heart failure liver failure renal failure nephrotic syndrome ```
36
what are the signs of fluid retention?
pulmonary oedema pitting oedema volume mediated hypertension
37
what are the consequences of reduced renal perfusion?
RAAS activation | sodium and water retention
38
what is the treatment of fluid retention?
salt and fluid restriction diuretics (spironolactone/eplerenone) ACEi/ARB sympathetic nervous system blockade (cardioselective beta blocker)
39
what are the causes of secondary hypertension?
``` chronic renal disease renal vascular disease endocrine disorders co-arctation of the aorta NSAIDs alcohol ```
40
why does pulse pressure increase with age?
reduction of elastic recoil in the arteries
41
what are the complications of renal artery stenosis?
chronic hypoperfusion of nephrons compensation by activation of the RAAS system hypertension to maintain renal perfusion
42
what are the complications of very rapid correction of BP?
AKI; compromised renal perfusion
43
define AKI
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
what does normal renal function depend on?
perfusion with adequate pressure and oxygen intact nephrons free urinary drainage
45
define oliguria
UO <400-500mls/day
46
what are the causes of an AKI?
true volume depletion; GI loss, haemorrhage hypotension; septic or cardiogenic shock oedematous states; advanced cardiac and liver failure
47
what are the causes of ATN?
severe pre-renal insults (hypotension associated with sepsis or during surgery) drugs radiocontrast dye haem pigments (myoglobin)
48
what are the consequences of ATN?
limited reabsorption of solutes decreased excretion of toxins low urine osmolality increased urine sodium levels
49
what are the risk factors for an AKI?
``` age previous AKI hypotension hypovolaemia sepsis medication diabetes HF ```
50
what are the consequences of pre-renal AKI?
sodium and water retention
51
what medications should be stopped in a pre-renal AKI (septic shock)?
ACEi ARB NSAIDs interfere with dilatation of afferent arterioles to maximise blood flow into glomeruli and constriction of efferent arterioles to reduce outflow
52
what are the causes of renal AKI?
ATN | glomerulonephritis (suspect if blood and protein on urinalysis)
53
what are the causes and management of post-renal AKI?
renal tract obstruction | urgent USS and consider urinary catheter
54
describe the pathology of DKD
efferent and afferent arteriole constriction and vasodilation increased glomerular capillary pressure GBM becomes more porous to albumin podocytes become damaged by hyperglycaemia albuminuria
55
why does glomerular hypertension lead to progressive renal failure?
glomeruli are lost due to raised pressure and gradual scarring
56
define albuminuria
urinary ACR >30mg/mmol
57
what are the components of DKD
albuminuria hypertension decreasing eGFR
58
what is the treatment of DKD?
``` ACEi ARB BP control blood glucose control transplant ```
59
describe ADPKD
a clonal disorder of epithelial cell growth | inactivation of 2 copies of a PKD gene (1 and 2) through germline and somatic mutations
60
what are the risk factors for ADPKD?
smoking folic acid deficiency DNA polymorphisms
61
what are the complications of ADPKD?
``` cerebral aneurysm (SAH) hepatic cysts cardiac valve disorders umbilical and inguinal herniae kidney stones CKD HTN ```
62
what are the symptoms of ADPKD?
haematuria flank and abdominal pain asymptomatic
63
what is the management of ADPKD?
ACEi/ARB (aim <130/90mmHg) tolvaptan (ADH receptor antagonist) manage CVD risk
64
define the glomerulus
a specialised network of capillaries supported by mesangial cells
65
describe the pathology of glomerulonephritis
alteration of the GBM properties leading to protein loss from the circulation into the urine (proteinuria)
66
what is the clinical presentation of glomerulonephritis?
``` asymptomatic visible haematuria HTN proteinuria post-infectious AKI (nephritic syndrome) CKD peripheral and peri-orbital oedema ```
67
what are the clinical features of nephrotic syndrome?
``` oedema (massive leg oedema) hypoalbuminaemia proteinuria xanthelasma (secondary hyperlipidaemia) vasculitis (vasculitic rash) ```
68
why does oedema occur in nephrotic syndrome?
hypoalbuminaemia causes a reduction in plasma oncotic pressure hydrostatic pressure > plasma oncotic pressure so net fluid movement into interstitium
69
what is the treatment of nephrotic syndrome?
``` dietary salt/fluid restriction diuretics ACEi biopsy may need immunosuppressant therapy ```
70
what are the causes of a raised anion gap (increased acid) in metabolic acidosis?
``` lactic acidosis renal failure ketoacidosis methanol ethylene glycol aspirin ```
71
what are the causes of a normal anion gap (bicarbonate loss) in metabolic acidosis?
GI loss | renal loss
72
what is the treatment of a metabolic acidosis with a raised anion gap?
treat the cause | improve oxygenation
73
describe hyperkalaemia on an ECG
peaked T waves wide QRS complexes near sinusoidal pattern PR prolongation
74
what is the treatment of hyperkalaemia?
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
what are the indications for dialysis in those with AKI/CKD?
refractory hyperkalaemia
76
what are the features of nephritic syndrome?
haematuria oliguria proteinuria fluid retention
77
describe glomerulosclerosis
scarring in the tissue of the glomerulus | can be caused by glomerulonephritis, obstructive uropathy or focal segmental glomerulosclerosis
78
describe IgA nephropathy/Berger's disease
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
describe membranous glomerulonephritis
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
describe post-streptococcal glomerulonephritis
``` typically <30yrs 1-3 weeks post streptococcal infection develop nephritic syndrome usually make a full recovery low complement ```
81
describe good pasture syndrome
anti-IgM antibodies attack the glomerulus and pulmonary basement membrane causes glomerulonephritis and pulmonary haemorrhage can present with AKI and haemoptysis
82
describe Wegener's granulomatosis
vasculitis associated with ANCA can present with AKI, haemoptysis, wheeze, sinusitis, saddle shaped nose
83
describe rapidly progressive glomerulonephritis
histology; cresenteric glomerulonephritis very acute illness, sick patients responds well often secondary to good pastures syndrome
84
what are the clinical features of post-streptococcal glomerulonephritis?
``` headache malaise visible haematuria proteinuria HTN oliguria low C3 raised ASO titre ```
85
what are the causes of acute interstitial nephritis?
``` NSAIDs antimicrobial agents salicylates ACE inhibitors diuretics ```
86
what are the USS features of CKD?
bilateral shrunken kidneys exceptions; ADPKD, DKD, amyloidosis, HIV associated nephropathy
87
what are the causes of focal segmental glomerulosclerosis?
``` idiopathic secondary to other renal pathology; IgA nephropathy HIV heroin alports syndrome sickle cell ```

Clinical Practice (14 decks)

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