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Block 34 metabolic -Ellen > Acute kidney injury Pt2 > Flashcards

Acute kidney injury Pt2 Flashcards

1
Q

when in renal failure does uraemia start (GFR)

A

<15ml

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2
Q

symptoms of uraemia (9)

A
  • pruitus
  • nausea and vomiting
  • lethargy
  • confusion
  • restless legs
  • metallic taste
  • neuropathy
  • bleeding
  • chest pain
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3
Q

acidosis symptoms (2)

A

breathlessness

confusion

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4
Q

hyperkalaemia symptoms

A

palpitations
chest pain
weakness

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5
Q

ECG signs of hyperkalaemia (5)

A
  • peaked T waves
  • flattered P waves
  • lengthened PR interval
  • widened QRS
  • sine wave pattern (VF)
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6
Q

vitamin D deficiency symptoms

A

bone pain

fractures

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7
Q

anaemia symptoms

A

breathlessness
lethargy
faintness
tinnitus

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8
Q

presentations of renal failure (6)

A
  • uraemia
  • protein loss and Na+ retention
  • acidosis
  • hyperkalaemia
  • anaemia
  • vit d deficiency
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9
Q

electrolyte balances in AKI

A 
hyponatremia (low Na+)
hypocalcaemia (low Ca+)
Hyperkalaemia (high K+) 
hypermagnesemia (high Mg) 
Hyperphosphatemia (high phosphate)
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10
Q

why do you get hyponatremia and hyperkalaemia

A

reduction in GFR means that less sodium is being filtered into the tubules, this decreases the activation of the sodium-potassium co-transporters in the distal convoluted tubule, decreasing the tubular secretion of potassium.

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11
Q

what does high serum K+ do to cell membranes

A

activates the potassium-proton pumps on cells so they release protons into the blood leading to metabolic acidosis

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12
Q

fraction of excreted sodium=

A

percentage of sodium filtered by the kidneys which is excreted in urine

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13
Q

a low FeNa <1% indicates

A

pre-renal or contrast induced nephropathy

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14
Q

FeNa >1% indicates

A

intrinsic AKI -sodium wasting

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15
Q

what happens to amylase in renal insufficiency

A

elevation in serum amylase when creatinine falls below certain threshold

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16
Q

low urine sodium leads to ____ osmolarity

A

high

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17
Q

which AKIs cause high urine osmolarity

A

pre-renal

post-renal

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18
Q

which AKIs cause low urine osmolarity

A

intrinsic

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19
Q

what detects fall in Bp

A

baroreceptors and macula densa cells

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20
Q

where are baroreceptors

A

carotid sinus

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21
Q

what do macula densa sense

A

filtrate sodium chloride

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22
Q

what do macula densa signal to

A

granular cells of the JGA

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23
Q

what does renin do

A

converts angiotensinogen (from liver) to angiotensin 1

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24
Q

what does ACE do

A

converts angiotensin 1 to 2

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25
Q

where does angiotensin 2 act

A

efferent arteriole constriction increasing GFR

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26
Q

aldosterone role

A

released from adrenal cortex causing Na+ reabsorption

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27
Q

what happens to drugs in renal failure (5)

A
  • reduced clearance rate
  • longer half life
  • reduced plasma binding of acidic drugs
  • reduced non-renal clearance (decreased activity of CYP450 enzymes)
  • takes longer to reach steady state
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28
Q

how can hypertension progress kidney disease

A

afferent arteriole thickens via atherosclerosis reducing perfusion to kidneys and causing ischaemic injury –> deposition of extracellular matrix leading to glomerulosclerosis

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29
Q

extra glucose effect on kidneys

A

binds to vessels via non-enzymatic glycation leading to vessel wall thickening -by hyaline arteriosclerosis obstructing blood flow in efferent vessel and causing an increased GFR

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30
Q

kidney vessel most affected by glucose in diabetes

A

efferent arteriole

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31
Q

what is the direct effect of ACEi

A

cause efferent arteriolar dilation

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32
Q

extra effect of ACEi

A

inhibits breakdown of bradykinin to increase antihypertensive effects

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33
Q

can ARBs and ACEi further exacerbate renal hypoperfusion

A

yes

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34
Q

nephrotic syndrome (4) symptoms

A

proteinuria >3g/day
Oedema
hypoalbuminemia
hyperlipidaemia

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35
Q

nephritic syndrome (4) symptoms

A

haematuria
hypertension
raised creatinine
oliguria

36
Q

why hyperlididaemia in nephrotic syndrome

A

occurs secondary to hypoproteinemia stimulation of protein synthesis in the liver overproduces lipoproteins

37
Q

main site of damage in nephrotic syndrome

A

epithelial podocytes - loss of the pedible foot processes

38
Q

name 3 primary causes of nephrotic syndrome

A
  • minimal change nephritis
  • focal segmental glomerulosclerosis
  • membranous glomerulonephritis
39
Q

most common nephrotic syndrome in children

A

minimal change nephritis

40
Q

pathology of minimal change

A

T cells secrete cytokines damaging pedicle foot processes causing loss of negative charge and effacement

41
Q

what can minimal change be associated with

A

Hodgkin’s lymphoma

42
Q

symptoms of minimal change (4)

A
  • foamy urine
  • poor appetite
  • swelling eyes, ankles, abdomen
  • weight gain
43
Q

most common nephrotic syndrome in adults

A

focal segmental glomerulosclerosis

44
Q

how is focal segmental glomerulosclerosis characterised histologically

A

localised areas of scarring within the glomerulus

45
Q

secondary FSGS associated with which diseases

A
  • sickle cell disease
  • HIV
  • retrovirus
  • heroin abuse
46
Q

what happens to some of the filtered proteins and lipids in FSGS

A

they deposit into the interstitium causing hyalinosis and giving a glassy histological appearance -cause scarring

47
Q

what is membranous GN

A

diffuse inflammation and thickening of the basement membrane by autoantibodies

48
Q

what do immune deposits in membranous GN do

A

activate complement and the membrane attack complex causing cell damage

49
Q

pattern of the basement membrane in membranous GN

A

spike dome pattern of the basement membrane

50
Q

rule of 3s for membranous GN

A

1/3 resolve
1/3 respond to cytotoxics
1/3 develop CKD

51
Q

name 4 causes of nephritic syndrome

A
  • post-streptococcal GN
  • Henoch-scholen purpura GN
  • Vasculitis
  • IgA nephropathy
52
Q

when does post-strep GN occur post sore throat infection

A

1-2 weeks

53
Q

main agent of post-strep GN

A

A streptococcus

54
Q

when else can post-strep GN occur

A

4-6 weeks after a skin infection

55
Q

pathology of post-strep GN

A

immune complex deposition of strep antigen deposited into kidney and transported into peritubular space -inducing a state of inflammation damaging glomerular basement membrane

56
Q

symptoms of post-strep GN (5)

A
  • dark urine
  • peripheral oedema
  • dyspnoea
  • general malaise/headache
  • weakness, anorexia, N&V
57
Q

what is Henoch-scholen purpura GN

A

an acute IgA mediated vasculitis disorder

58
Q

what is vasculitis

A

a group of disorders that destroy blood vessels by inflammation

59
Q

where is the vessel damage in henoch-scholen (4)

A

skin
GI tract
joints
kidney

60
Q

what age in Henoch Scholen purpura GN common in

A

3-10 years old

61
Q

Henoch scholen purpura GN symptoms

A
  • leg and arm purpura rash
  • arthritis joint pain
  • abdo pain, N&V
  • GI bleeding
  • nephritis
62
Q

name 4 vasculitis’s

A

SLE
Small vessel
good pastures
ANCA

63
Q

good pastures pathophysiology

A

anti-glomerular basement membrane antibodies specific to alpha-3 subunit of type 4 collagen

64
Q

associations of Good pastures in rest of body

A
  • pulmonary haemorrhage (haemoptysis)

- rapidly progressing GN

65
Q

renal biopsy of Good pastures shows

A

IgG deposits on membrane

66
Q

ANCA vasculitis associated with

A

small vessel vasculitis

67
Q

clinical signs of ANCA

A

affects various organs

-skin lesions such as purpura and urticaria

68
Q

IgA nephropathy also called

A

Berger’s disease/ mesangioproliferative GN

69
Q

in IgA nephropathy where does it deposit

A

in the mesagium (smooth muscle surrounding capillaries)

70
Q

typical presentation of IgA nephropathy

A
  • young male recurrent episodes of macroscopic haematuria
  • mucosal infection -upper respiratory tract
  • renal failure
71
Q

which has low complement levels IgA nephropathy or post-strep GN

A

post-strep GN

72
Q

in which -post strep GN or IgA nephropathy is the main symptom proteinuria

A

post-strep GN

73
Q

interval between respiratory tract infection and IgA nephropathy

A

1-2 days

74
Q

% of patient with IgA nephropathy developing ESRF

A

25%

75
Q

what marks a good prognosis in IgA nephropathy

A

frank haematuria

76
Q

what marks a bad prognosis in IgA nephropathy (5)

A 
male gender 
proteinuria 
hypertension 
smoking 
hyperlipidaemia
77
Q

6 complications of CKD

A 
anaemia 
renal bone disease 
hyperphosphatemia 
acidosis 
oedema 
uraemia
78
Q

nephritic condition occuring in childhood following diarrhoea-inducing GI infection

A

haemolytic uremic syndrome

79
Q

what cancer can cause AKI

A

myeloma

80
Q

why can myeloma cause AKI

A

unregulated secretion of antibodies leading to protein filtration through the kidney coordinating damage

81
Q

treatment of AKI

A

depends on cause

82
Q

treatment of hyperkalaemia

A
  • 10ml of 10% calcium gluconate

- 50ml of 50% glucose with 6-10 units of insulin (actrapid)

83
Q

what does calcium gluconate do

A

protects the heart from life threatening arrhythmias

84
Q

what does insulin do (in AKI)

A

encourages intracellular movement of potassium

85
Q

signs and symptoms of AKI

A
  • oliguria
  • N&V
  • Dizziness
  • orthopnoea
  • PND
  • oedema (pulmonary and peripheral)
  • tachycardia
  • hypotension

Block 34 metabolic -Ellen (8 decks)

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