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

Acute kidney injury Pt2 Flashcards

(85 cards)

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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
where does angiotensin 2 act
efferent arteriole constriction increasing GFR
26
aldosterone role
released from adrenal cortex causing Na+ reabsorption
27
what happens to drugs in renal failure (5)
- 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
28
how can hypertension progress kidney disease
afferent arteriole thickens via atherosclerosis reducing perfusion to kidneys and causing ischaemic injury --> deposition of extracellular matrix leading to glomerulosclerosis
29
extra glucose effect on kidneys
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
30
kidney vessel most affected by glucose in diabetes
efferent arteriole
31
what is the direct effect of ACEi
cause efferent arteriolar dilation
32
extra effect of ACEi
inhibits breakdown of bradykinin to increase antihypertensive effects
33
can ARBs and ACEi further exacerbate renal hypoperfusion
yes
34
nephrotic syndrome (4) symptoms
proteinuria >3g/day Oedema hypoalbuminemia hyperlipidaemia
35
nephritic syndrome (4) symptoms
haematuria hypertension raised creatinine oliguria
36
why hyperlididaemia in nephrotic syndrome
occurs secondary to hypoproteinemia stimulation of protein synthesis in the liver overproduces lipoproteins
37
main site of damage in nephrotic syndrome
epithelial podocytes - loss of the pedible foot processes
38
name 3 primary causes of nephrotic syndrome
- minimal change nephritis - focal segmental glomerulosclerosis - membranous glomerulonephritis
39
most common nephrotic syndrome in children
minimal change nephritis
40
pathology of minimal change
T cells secrete cytokines damaging pedicle foot processes causing loss of negative charge and effacement
41
what can minimal change be associated with
Hodgkin's lymphoma
42
symptoms of minimal change (4)
- foamy urine - poor appetite - swelling eyes, ankles, abdomen - weight gain
43
most common nephrotic syndrome in adults
focal segmental glomerulosclerosis
44
how is focal segmental glomerulosclerosis characterised histologically
localised areas of scarring within the glomerulus
45
secondary FSGS associated with which diseases
- sickle cell disease - HIV - retrovirus - heroin abuse
46
what happens to some of the filtered proteins and lipids in FSGS
they deposit into the interstitium causing hyalinosis and giving a glassy histological appearance -cause scarring
47
what is membranous GN
diffuse inflammation and thickening of the basement membrane by autoantibodies
48
what do immune deposits in membranous GN do
activate complement and the membrane attack complex causing cell damage
49
pattern of the basement membrane in membranous GN
spike dome pattern of the basement membrane
50
rule of 3s for membranous GN
1/3 resolve 1/3 respond to cytotoxics 1/3 develop CKD
51
name 4 causes of nephritic syndrome
- post-streptococcal GN - Henoch-scholen purpura GN - Vasculitis - IgA nephropathy
52
when does post-strep GN occur post sore throat infection
1-2 weeks
53
main agent of post-strep GN
A streptococcus
54
when else can post-strep GN occur
4-6 weeks after a skin infection
55
pathology of post-strep GN
immune complex deposition of strep antigen deposited into kidney and transported into peritubular space -inducing a state of inflammation damaging glomerular basement membrane
56
symptoms of post-strep GN (5)
- dark urine - peripheral oedema - dyspnoea - general malaise/headache - weakness, anorexia, N&V
57
what is Henoch-scholen purpura GN
an acute IgA mediated vasculitis disorder
58
what is vasculitis
a group of disorders that destroy blood vessels by inflammation
59
where is the vessel damage in henoch-scholen (4)
skin GI tract joints kidney
60
what age in Henoch Scholen purpura GN common in
3-10 years old
61
Henoch scholen purpura GN symptoms
- leg and arm purpura rash - arthritis joint pain - abdo pain, N&V - GI bleeding - nephritis
62
name 4 vasculitis's
SLE Small vessel good pastures ANCA
63
good pastures pathophysiology
anti-glomerular basement membrane antibodies specific to alpha-3 subunit of type 4 collagen
64
associations of Good pastures in rest of body
- pulmonary haemorrhage (haemoptysis) | - rapidly progressing GN
65
renal biopsy of Good pastures shows
IgG deposits on membrane
66
ANCA vasculitis associated with
small vessel vasculitis
67
clinical signs of ANCA
affects various organs | -skin lesions such as purpura and urticaria
68
IgA nephropathy also called
Berger's disease/ mesangioproliferative GN
69
in IgA nephropathy where does it deposit
in the mesagium (smooth muscle surrounding capillaries)
70
typical presentation of IgA nephropathy
- young male recurrent episodes of macroscopic haematuria - mucosal infection -upper respiratory tract - renal failure
71
which has low complement levels IgA nephropathy or post-strep GN
post-strep GN
72
in which -post strep GN or IgA nephropathy is the main symptom proteinuria
post-strep GN
73
interval between respiratory tract infection and IgA nephropathy
1-2 days
74
% of patient with IgA nephropathy developing ESRF
25%
75
what marks a good prognosis in IgA nephropathy
frank haematuria
76
what marks a bad prognosis in IgA nephropathy (5)
``` male gender proteinuria hypertension smoking hyperlipidaemia ```
77
6 complications of CKD
``` anaemia renal bone disease hyperphosphatemia acidosis oedema uraemia ```
78
nephritic condition occuring in childhood following diarrhoea-inducing GI infection
haemolytic uremic syndrome
79
what cancer can cause AKI
myeloma
80
why can myeloma cause AKI
unregulated secretion of antibodies leading to protein filtration through the kidney coordinating damage
81
treatment of AKI
depends on cause
82
treatment of hyperkalaemia
- 10ml of 10% calcium gluconate | - 50ml of 50% glucose with 6-10 units of insulin (actrapid)
83
what does calcium gluconate do
protects the heart from life threatening arrhythmias
84
what does insulin do (in AKI)
encourages intracellular movement of potassium
85
signs and symptoms of AKI
- oliguria - N&V - Dizziness - orthopnoea - PND - oedema (pulmonary and peripheral) - tachycardia - hypotension

Block 34 metabolic -Ellen (8 decks)

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