Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3b general care > nephrology > Flashcards

nephrology Flashcards

1
Q

what does the RAAS system control?

A

regulates blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what controls RAAS?

A

Juxtaglomerular apparatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what produces BNP?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do loop diuretics work?

A

act on thick descending loop of henle

prevent Na/K/Cl channels from functioning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do thiazide diuretics work?

A

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

SE- hypokalaemia, glucose intolerance, hypercalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

features of renal stones?

A 
lion pain, intermittent 'colicky' pain 
N&V
haematuria
dysuria
secondary infection may cause fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

differentials of renal stones?

A 
AAA
pancreatitis
gallstones
MSK pain
pyelonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is nephritic syndrome?

A

a type of GN

haematuria with red cell casts. proteinuria, hypertension, oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

causes of nephritic syndrome?

A

rapidly progressive glomerulonephritis
IgA nephropathy
post-strep GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

causes of rapidly progressive GN

A

goodpastures syndrome- associated haemopytysis
Wegener’s granulomatosis
SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ix of rapidly progressive GN

A

renal biopsy- crescenteric GN

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mx of rapidly progressive GN

A

aggressive immunosuppression e.g. ciclosporin, corticosteroids, cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is membranous GM and its causes?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is seen in renal biopsy of membranous GN?

A

basement membrane thickened with electron dense deposits- ‘spike and dome appearance’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

mx of membranous GN?

A

ACEi or ARB
Immunosuppression- steroid and cyclophosphamide
anticoagulants for high risk patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

prognosis of GN?

A

1/3 spontaneous remission
1/3 proteinuric
1/3 ESRF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Features of nephrotic syndrome?

A

proteinuria
hypoalbuminaemia
oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

causes of nephrotic syndrome?

A

membranous GN
minimal change disease
focal segmental GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is minimal change disease?

A

most common in children, T-cell mediated condition, damage to GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

causes of minimal change disease?

A

idiopathic in majority
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

mx of minimal change disease?

A

steroid responsive (80%)
steroid resistant- cyclophosphamide
furosemide
ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is good pasture’s syndrome?

A

caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen
causes pulmonary haemorrhage and rapidly progressive GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

mx of good pasture’s syndrome?

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the most common renal cell carcinoma?

A

adenocarcinoma

arises from proximal tubular convoluted tubular epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

RFs for renal cell carcinoma?

A 
2x M>F
average onset is 65-75 years
smoking
obesity
long term dialysis
Von Hippel-lindau syndrome
tuberous sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

features of renal cell carcinoma?

A

triad of haematuria, loin pain and abdo mass

endocrine effects- secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

mx of RCC?

A

partial of total nephrectomy

alpha-interferon or IL2 to reduce tumour size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

common mets to bone?

A 
breast
prostate
kidney
lung
thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what does proteinuria show in an AKI?

A

it must be a renal cause

42
Q

what does nitrites show in an AKI?

A

Rules out infection

43
Q

causes of pre-renal AKI?

A

hypovolaemia secondary to D&V
renal artery stenosis
hypotension

44
Q

renal causes of AKI?

A 
acute tubular necrosis
nephrotoxicity
renal parenchyma disease
GN
rhabdomyolysis
tumour lysis syndrome
45
Q

post-renal causes of AKI?

A

Kidney stone
BPH
external compression of the ureter

46
Q

RFs for AKI?

A
  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
Q

causes of acute tubular necrosis?

A

renal ischaemia e.g. shock, sepsis
toxins e.g. aminoglycoside, myoglobin secondary to rhabdomyolysis
no known treatments

48
Q

urinalysis of acute tubular necrosis?

A

muddy brown casts
urine osmolality low
urinary sodium high

49
Q

diagnostic criteria of AKI?

A

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
Q

Ix of AKI?

A

U&Es
urinalysis
renal USS

51
Q

mx of AKI?

A 
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
Q

criteria for renal replacement therapy?

A 
hyperkalaemia
metabolic acidosis
symptoms or complications or uraemia (encephalopathy or pericarditis)
fluid overload
pulmonary oedema
53
Q

staging of CKD?

A 
1- GFR >90
2- GFR 60-90
3a- GFR 45-59
3b- GFR 30-44
4- 15-29
5- <15
54
Q

RFs for CKD progression?

A 
CV disease
proteinuria
AKI
hypertension
DM
Smoking
Afro-Caribbean
NSAIDs
untreated urinary tract outflow obstruction
55
Q

mx of CKD?

A

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
Q

what levels is hyponatraemia?

A

serum sodium <136mmol/L

57
Q

signs and symptoms of hyponatraemia?

A

confusion
lethargy
seizures
coma

58
Q

classification of hyponatraemia?

A

concentration of solutes in the blood

calculated by: 2(Na) + glucose + urea (all in mmol/L)

59
Q

what is hypotonic hyponatraemia?

A

low serum osmolality hyponatraemia

can be wither hypovolaemia, euvolaemic or hypervolaemic (judge clinically)

60
Q

what is isotonic hyponatraemia?

A

normal serum osmolality

caused by hyperproteinaemia or hyperlipidaemia

61
Q

what is hypertonic hyponatraemia?

A

caused by hyperglycaemia
mannitol, sorbitol, glycerol, maltose
radiocontrast agents

62
Q

what are the causes of hypotonic hypovolaemic hyponatraemia?

A

if urinary Na <10-> dehydration, diarrhoea, vomiting

if urinary Na >20 -> diuretics, ACEi, nephropathies, mineralocorticoid deficiency

63
Q

causes of hypotonic euvolaemic hyponatraemia?

A 
SIADH
post-op
hypothyroidism
psychogenic polydipsia
thiazide diuretics, ACEi
endurance exercise
adrenocorticotropin deficiency
64
Q

causes of hypotonic hypervolaemic hyponatraemia?

A

caused by hyperglycaemia
congestive HF
liver disease/ CKD
nephrotic syndrome

65
Q

mx of hypotonic hypovolaemic hyponatraemia?

A

treat underlying cause, replace lost fluid with 0.9% saline according to degree of dehydration
stop diuretics

66
Q

mx of hypotonic euvolaemic hyponatraemia?

A

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
Q

mx of hypotonic hypervolaemic hyponatraemia?

A

treat underlying cause

68
Q

what is central pontine myelinosis?

A

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
Q

what is SIADH?

A

Urine Na >20

euvolaemic hyponatraemia

70
Q

causes of SIADH?

A

Malignancy- SCLC, pancreas, prostate
Neuro- stroke, SAH, SDH, meningitis/encephalitis
Infections- TB, pneumonia
Drugs- sulphonylureas, SSRIs, TCAs, carbamazepine

71
Q

diagnosis of SIADH?

A

Urine osmolality >500, plasma osmolality <275
no recent diuretics
clinically euvolaemic
urinary sodium >20mmol/L

72
Q

mx of SIADH?

A

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
Q

causes of hypernatraemia?

A 
dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline
iatrogenic
Conn's syndrome
74
Q

symptoms and signs of hypernatraemia?

A

symptoms- anorexia, nausea, weakness, hyper-reflexia, confusion, decreased GCS
signs- assess fluid balance, volume status, neurological deficit

75
Q

Ix of hypernatraemia?

A

plasma osmolality
urine osmolality
CT head if suspected central cause

76
Q

tx of hypernatraemia?

A

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
Q

what is the opposite of SIADH?

A 
diabetes insipidus (reduced ADH secretion)
very dilute urine= low urinary sodium
very concentrated blood= high serum osmolality
78
Q

what are the 2 types of diabetes insipidus?

A

1) cranial- idiopathic, post head-injury, pituitary surgery, craniopharyngiomas
2) nephrogenic DI- AVPR2 gene defect, hypercalcaemia, hypokalaemia, tubulo-interstitial disease

79
Q

features of diabetes insipidus?

A

polyuria
polydipsia
dehydration
symptoms of hypokalaemia or hypernatraemia

80
Q

diagnosis of diabetes insipidus?

A

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
Q

MX of diabetes insipidus?

A

nephrogenic- treat cause, bendroflumethazide, low salt/protein diet
cranial- desmopressin

82
Q

what causes polycystic kidney disease?

A

Mutations in PKD1 and PKD2

83
Q

renal and non-renal manifestations of PKD?

A

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
Q

mx of PKD?

A 
Avoid nephrotoxic drugs
low salt diet
sufficient fluids
control BP
tolvaptan slows GFR

screen for cerebral aneurysm at the time of diagnosis

85
Q

what are maintenance fluids in an adult?

A

25-30ml/kg/day of water (NaCl)
1mmol/kg/day K/Na/Cl
50-100g/day glucose- 0.18% in 4% glucose

86
Q

when should hartmann’s not be used?

A

in patients with hyperkalaemia as it contains potassium

87
Q

what is the risk of 0.9% saline if large volumes are used?

A

hyperchloraemic metabolic acidosis

88
Q

what is fibromuscular dysplasia?

A

young females who develop AKI after the initiation of an ACE inhibitor
gives a ‘string of beads’ appearance of the renal arteries

89
Q

what is the anion gap

A

done in patients with metabolic acidosis

(Na +K)- (HCO3 +Cl)= 8-14mmol/L

90
Q

causes of metabolic acidosis with normal anion gap?

A

diarrhoea
renal tubular acidosis
Addison’s disease

91
Q

causes of metabolic acidosis with raised anion gap?

A

lactate: shock, hypoxia, sepsis
ketones: DKA, alcohol
Urate: renal failure
salicylate poisoning

92
Q

what renal disease has sterile pyuria and white cell casts?

A

acute interstitial nephritis
secondary to Abx use- NSAIDs, salicylates, ACEi, diuretics
allergy-type reaction

93
Q

how are diabetic patients screened for diabetic nephropathy?

A

screened annually using urinary albumin:creatinine ratio (ACR)- urine protein
ACR >2.5 = Microalbuminaemia

94
Q

what are DAMN drugs?

A 
drugs that can cause acute renal failure when elderly are dehydrated/infected
Diuretics
ACEi
Metformin
NSAIDS
95
Q

different causes of polyuria/polydipsia?

A

DM
SIADH
hypercalcaemia
Drugs-diuretics

96
Q

symptoms of PKD?

A 
flank pain
haematuria
hypertension 
with a positive FH
renal USS to diagnose
97
Q

conditions that cause large kidneys on USS?

A

ADPKD
chronic HIV- associated nephropathy
diabetic nephropathy
amyloidosis

98
Q

functions of the kidney?

A
  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
Q

what form of AKI do ACEi and NSAIDS produce?

A

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
Q

why does renal failure cause anaemia?

A

erythropoietin deficiency

mx= give EPO parenterally

101
Q

how does renal bone disease work?

A

reduced phosphate stimulates PTH secretion

reduced Vit D activation- decreases dietary calcium absorption- hypocalcaemia- PTH release

monitor PTH levels to check

3b general care (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions