nephrology Flashcards

1
Q

what does the RAAS system control?

A

regulates blood pressure

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2
Q

what controls RAAS?

A

Juxtaglomerular apparatus

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3
Q

what is the pathway of RAAS?

A

JG cells -> renin
liver ->angiotensinogen
renin causes angiotensinogen to become Angiotensin I
lungs -> ACE
ACE causes angiotensin I to II (vasoconstrictor)
angiotensin II cause aldosterone release from the adrenal glans (increases resorption)

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4
Q

what is ADH?

A

also known as vasopressin
produced by the hypothalamus and secreted by posterior pituitary
acts on the medullary collecting ducts and makes them more permeable to water -> increases synthesis of aquaporins

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5
Q

what produces BNP?

A

released in ventricles in response to stretching- dilates afferent and constricts efferent arteriole which increases GFR -> lowers BP

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6
Q

how do loop diuretics work?

A

act on thick descending loop of henle

prevent Na/K/Cl channels from functioning

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7
Q

how do thiazide diuretics work?

A

e.g. bendroflumethaside
acts on sodium/chloride transports and decreases reabsorption

SE- hypokalaemia, glucose intolerance, hypercalcaemia

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8
Q

how do potassium-sparing diuretics work?

A

e.g. spironolactone
blocks aldosterone receptors
sodium is lost and potassium is spared
can prevent formation of ascites in patients with chronic liver disease

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9
Q

where do renal stones commonly obstruct?

A
  1. vesico-ureteric junction
  2. mid-ureter where the ureter crosses the iliac vessels
  3. pelvi-ureteric junction
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10
Q

types of renal stones?

A
  • calcium oxalate- stones are radio-opaque (85% of all stones)
  • cystine- relatively radiodense
  • uric acid- radiolucent
  • calcium phosphate- radio-opaque
  • struvite
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11
Q

RFs of renal stones?

A

dehydration
hypercalcaemia, hyperparathyroidism, hypercalciuria
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, PKD
drugs- loop diuretics, steroids, acetazolamide

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12
Q

features of renal stones?

A
lion pain, intermittent 'colicky' pain 
N&V
haematuria
dysuria
secondary infection may cause fever
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13
Q

Ix of renal stones?

A
urine dipstick and culture
Ca and urate
U&Es
FBC/CRP
*non-contrast CT KUB gold standard within 14 hours*
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14
Q

differentials of renal stones?

A
AAA
pancreatitis
gallstones
MSK pain
pyelonephritis
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15
Q

mx of renal stones?

A

NSAIDs e.g. diclofenac
stones <6mm typically pass on their own within 4 weeks
if emergency- nephrostomy tube, ureteric catheters, ureteric stent

if non-emergency- shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy

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16
Q

prevention of renal stones?

A

prevent hypercalcaemia- high fluid intake, low animal protein, low salt diet, thiazide diuretics
prevent urinary acid secretion- cholestyramide, pyridoxine
prevent uric acid stones- allopurinol, urinary alkalinisation

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17
Q

what is nephritic syndrome?

A

a type of GN

haematuria with red cell casts. proteinuria, hypertension, oliguria

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18
Q

causes of nephritic syndrome?

A

rapidly progressive glomerulonephritis
IgA nephropathy
post-strep GN

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19
Q

what is rapidly progressive GN

A

rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli

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20
Q

causes of rapidly progressive GN

A

goodpastures syndrome- associated haemopytysis
Wegener’s granulomatosis
SLE

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21
Q

Ix of rapidly progressive GN

A

renal biopsy- crescenteric GN

bloods- U&E, ESR/CRP, complement, autoantibodies, urine, CXR, renal USS

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22
Q

mx of rapidly progressive GN

A

aggressive immunosuppression e.g. ciclosporin, corticosteroids, cyclophosphamide

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23
Q

features of IgA nephropathy?

A

mesangial deposition of IgA immune complexes
young male, recurrent episodes of macroscopic haematuria
develops 1-2 days after URTI

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24
Q

what is post-streptococcal GN?

A

typically occurs 7-14 days following a group A beta-haemolytic streptococcal infection
immune complexes deposit in glomeruli
young children most commonly affected

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25
what is membranous GM and its causes?
most common GN in adults idiopathic infections- hep B, malaria, syphilis malignancy- lung cancer, lymphoma, leukaemia drugs- gold, penicillamine, NSAIDS autoimmune diseases- SLE, thyroiditis, RA
26
what is seen in renal biopsy of membranous GN?
basement membrane thickened with electron dense deposits- 'spike and dome appearance'
27
mx of membranous GN?
ACEi or ARB Immunosuppression- steroid and cyclophosphamide anticoagulants for high risk patients
28
prognosis of GN?
1/3 spontaneous remission 1/3 proteinuric 1/3 ESRF
29
Features of nephrotic syndrome?
proteinuria hypoalbuminaemia oedema
30
causes of nephrotic syndrome?
membranous GN minimal change disease focal segmental GN
31
what is minimal change disease?
most common in children, T-cell mediated condition, damage to GBM
32
causes of minimal change disease?
idiopathic in majority drugs: NSAIDs, rifampicin Hodgkin's lymphoma, thymoma infectious mononucleosis
33
mx of minimal change disease?
steroid responsive (80%) steroid resistant- cyclophosphamide furosemide ACEi
34
what is good pasture's syndrome?
caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen causes pulmonary haemorrhage and rapidly progressive GBM
35
mx of good pasture's syndrome?
plasma exchange (plasmapheresis) steroids cyclophosphamide
36
what is the most common renal cell carcinoma?
adenocarcinoma | arises from proximal tubular convoluted tubular epithelium
37
RFs for renal cell carcinoma?
``` 2x M>F average onset is 65-75 years smoking obesity long term dialysis Von Hippel-lindau syndrome tuberous sclerosis ```
38
features of renal cell carcinoma?
triad of haematuria, loin pain and abdo mass endocrine effects- secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
39
mx of RCC?
partial of total nephrectomy | alpha-interferon or IL2 to reduce tumour size
40
common mets to bone?
``` breast prostate kidney lung thyroid ```
41
what does proteinuria show in an AKI?
it must be a renal cause
42
what does nitrites show in an AKI?
Rules out infection
43
causes of pre-renal AKI?
hypovolaemia secondary to D&V renal artery stenosis hypotension
44
renal causes of AKI?
``` acute tubular necrosis nephrotoxicity renal parenchyma disease GN rhabdomyolysis tumour lysis syndrome ```
45
post-renal causes of AKI?
Kidney stone BPH external compression of the ureter
46
RFs for AKI?
1. emergency surgery 2. intraperitoneal surgery 3. CKD 4. Diabetes 5. Heart failure 6. age >65 years 7. liver disease 8. Use of nephrotoxic drugs
47
causes of acute tubular necrosis?
renal ischaemia e.g. shock, sepsis toxins e.g. aminoglycoside, myoglobin secondary to rhabdomyolysis no known treatments
48
urinalysis of acute tubular necrosis?
muddy brown casts urine osmolality low urinary sodium high
49
diagnostic criteria of AKI?
Rise in creatitine of 26micromol/L or more in 48 hours OR 50% and rise in creatinine over 7 days OR Fall in urine output to less than 0.5ml/kg/hour for more than 7 hours in adults OR 25% and fall in eGFR in children/ young adults in 7 days
50
Ix of AKI?
U&Es urinalysis renal USS
51
mx of AKI?
``` Get senior help replace fluids carefully palpate the bladder (post-renal AKI0 catheter to monitor urine output stop all nephrotoxic drugs- NSAIDs, aminoglycosides, ACEi (consider stopping metformin, lithium, digoxin) take cultures ->treat sepsis treat hyperkalaemia if pulmonary oedema->Morphine, O2, furosemide consider dialysis- refer to nephrologist manage acidosis refer to urology if obstruction ```
52
criteria for renal replacement therapy?
``` hyperkalaemia metabolic acidosis symptoms or complications or uraemia (encephalopathy or pericarditis) fluid overload pulmonary oedema ```
53
staging of CKD?
``` 1- GFR >90 2- GFR 60-90 3a- GFR 45-59 3b- GFR 30-44 4- 15-29 5- <15 ```
54
RFs for CKD progression?
``` CV disease proteinuria AKI hypertension DM Smoking Afro-Caribbean NSAIDs untreated urinary tract outflow obstruction ```
55
mx of CKD?
Aim to keep SBP <140 and DBP <90 Statins anti-platelet drugs if GFR <30, measure calcium, phosphate and PTH and if indicated offer bisphosphonates measure Hb if eGFR <45 to identify amaemia
56
what levels is hyponatraemia?
serum sodium <136mmol/L
57
signs and symptoms of hyponatraemia?
confusion lethargy seizures coma
58
classification of hyponatraemia?
concentration of solutes in the blood | calculated by: 2(Na) + glucose + urea (all in mmol/L)
59
what is hypotonic hyponatraemia?
low serum osmolality hyponatraemia | can be wither hypovolaemia, euvolaemic or hypervolaemic (judge clinically)
60
what is isotonic hyponatraemia?
normal serum osmolality | caused by hyperproteinaemia or hyperlipidaemia
61
what is hypertonic hyponatraemia?
caused by hyperglycaemia mannitol, sorbitol, glycerol, maltose radiocontrast agents
62
what are the causes of hypotonic hypovolaemic hyponatraemia?
if urinary Na <10-> dehydration, diarrhoea, vomiting | if urinary Na >20 -> diuretics, ACEi, nephropathies, mineralocorticoid deficiency
63
causes of hypotonic euvolaemic hyponatraemia?
``` SIADH post-op hypothyroidism psychogenic polydipsia thiazide diuretics, ACEi endurance exercise adrenocorticotropin deficiency ```
64
causes of hypotonic hypervolaemic hyponatraemia?
caused by hyperglycaemia congestive HF liver disease/ CKD nephrotic syndrome
65
mx of hypotonic hypovolaemic hyponatraemia?
treat underlying cause, replace lost fluid with 0.9% saline according to degree of dehydration stop diuretics
66
mx of hypotonic euvolaemic hyponatraemia?
slow 0.9% saline IV e.g. 1L over 8-10 hours, Na levels should rise over a few days if urine osmolality >500, consider SIADH
67
mx of hypotonic hypervolaemic hyponatraemia?
treat underlying cause
68
what is central pontine myelinosis?
caused by rapid early correction of hyponatraemia causing osmotic demyelination fluid is drawn out the CNS with rapid fluid -> demyelination occurs when replacement exceeds 10-12mmol/1L/24 hours can lead to quadriparesis and bulbar injury, seen on MRI brain
69
what is SIADH?
Urine Na >20 | euvolaemic hyponatraemia
70
causes of SIADH?
Malignancy- SCLC, pancreas, prostate Neuro- stroke, SAH, SDH, meningitis/encephalitis Infections- TB, pneumonia Drugs- sulphonylureas, SSRIs, TCAs, carbamazepine
71
diagnosis of SIADH?
Urine osmolality >500, plasma osmolality <275 no recent diuretics clinically euvolaemic urinary sodium >20mmol/L
72
mx of SIADH?
Correction done slowly to avoid central pontine myelinosis fluid restriction demeclocycline- reduces the responsiveness of collecting tubule cells to ADH vasopressin receptor antagonists- vaptans
73
causes of hypernatraemia?
``` dehydration osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma diabetes insipidus excess IV saline iatrogenic Conn's syndrome ```
74
symptoms and signs of hypernatraemia?
symptoms- anorexia, nausea, weakness, hyper-reflexia, confusion, decreased GCS signs- assess fluid balance, volume status, neurological deficit
75
Ix of hypernatraemia?
plasma osmolality urine osmolality CT head if suspected central cause
76
tx of hypernatraemia?
slow correction of Na if hypovolaemic- give 0.9% saline 1L/6 hours until normovolaemic if normovolaemic- encourage oral fluids or 5% glucose 1L/6 hours
77
what is the opposite of SIADH?
``` diabetes insipidus (reduced ADH secretion) very dilute urine= low urinary sodium very concentrated blood= high serum osmolality ```
78
what are the 2 types of diabetes insipidus?
1) cranial- idiopathic, post head-injury, pituitary surgery, craniopharyngiomas 2) nephrogenic DI- AVPR2 gene defect, hypercalcaemia, hypokalaemia, tubulo-interstitial disease
79
features of diabetes insipidus?
polyuria polydipsia dehydration symptoms of hypokalaemia or hypernatraemia
80
diagnosis of diabetes insipidus?
8 hour water deprivation test desmopressin given- if urine osmolality increases >50%= cranial cause if urine osmolality remains low= nephrogenic cause (desmopressin is a synthetic analogue for ADH)
81
MX of diabetes insipidus?
nephrogenic- treat cause, bendroflumethazide, low salt/protein diet cranial- desmopressin
82
what causes polycystic kidney disease?
Mutations in PKD1 and PKD2
83
renal and non-renal manifestations of PKD?
Renal- progresses to ESRD non-renal- cysts in liver, pancreas, spleen and lungs increased incidence in mitral valve prolapse intracranial berry aneurysms increased frequency of colonic diverticula
84
mx of PKD?
``` Avoid nephrotoxic drugs low salt diet sufficient fluids control BP tolvaptan slows GFR ``` screen for cerebral aneurysm at the time of diagnosis
85
what are maintenance fluids in an adult?
25-30ml/kg/day of water (NaCl) 1mmol/kg/day K/Na/Cl 50-100g/day glucose- 0.18% in 4% glucose
86
when should hartmann's not be used?
in patients with hyperkalaemia as it contains potassium
87
what is the risk of 0.9% saline if large volumes are used?
hyperchloraemic metabolic acidosis
88
what is fibromuscular dysplasia?
young females who develop AKI after the initiation of an ACE inhibitor gives a 'string of beads' appearance of the renal arteries
89
what is the anion gap
done in patients with metabolic acidosis | (Na +K)- (HCO3 +Cl)= 8-14mmol/L
90
causes of metabolic acidosis with normal anion gap?
diarrhoea renal tubular acidosis Addison's disease
91
causes of metabolic acidosis with raised anion gap?
lactate: shock, hypoxia, sepsis ketones: DKA, alcohol Urate: renal failure salicylate poisoning
92
what renal disease has sterile pyuria and white cell casts?
acute interstitial nephritis secondary to Abx use- NSAIDs, salicylates, ACEi, diuretics allergy-type reaction
93
how are diabetic patients screened for diabetic nephropathy?
screened annually using urinary albumin:creatinine ratio (ACR)- urine protein ACR >2.5 = Microalbuminaemia
94
what are DAMN drugs?
``` drugs that can cause acute renal failure when elderly are dehydrated/infected Diuretics ACEi Metformin NSAIDS ```
95
different causes of polyuria/polydipsia?
DM SIADH hypercalcaemia Drugs-diuretics
96
symptoms of PKD?
``` flank pain haematuria hypertension with a positive FH renal USS to diagnose ```
97
conditions that cause large kidneys on USS?
ADPKD chronic HIV- associated nephropathy diabetic nephropathy amyloidosis
98
functions of the kidney?
1. excrete waste products 2. fluid and electrolyte balance 3. acid:base balance- secrete H+ and reabsorb bicarb 4. gluconeogenesis 5. endocrine- produce erythropoietin, convert active form Vit D 6. control BP (secrete renin)
99
what form of AKI do ACEi and NSAIDS produce?
ACEi- causes pre-renal failure with renal artery stenosis due to efferent arteriole vasodilation, reducing GFR pressure NSAIDs- pre renal- reduces GFR due to prostaglandin- mediated afferent arteriole vasodilation renal cause- direct nephrotoxin
100
why does renal failure cause anaemia?
erythropoietin deficiency | mx= give EPO parenterally
101
how does renal bone disease work?
reduced phosphate stimulates PTH secretion reduced Vit D activation- decreases dietary calcium absorption- hypocalcaemia- PTH release monitor PTH levels to check