Nephrology Flashcards

(110 cards)

1
Q

Aldosterone stimulates which part of the renal tubule to reabsorb Na?

A

Cortical collecting duct

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2
Q

ANP affects which part of the renal tubule to inhibit Na reabsorption?

A

Medullary collecting duct

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3
Q

Which part of the tubule is the site for excretion of trimethoprim?

A

Proximal tubule

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4
Q

Dapagliflozin exerts its effect on which part of the renal tubule?

A

Proximal tubule

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5
Q

Why is Gaddolinium avoided in CKD?

A

Nephrogenic systemic fibrosis from gad chelators

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6
Q

Renal Tx, detection of graft rejection risk modalities and when risk is greatest

A

CDC +ve> Flow cytometry > virtual cross matching

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7
Q

Renal transplant x2 induction agents

A

Basilixumab (anti-CD25) and ATG (superior in high risk)

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8
Q

Renal Tx Immunosuppression maintenance

A

Pred + Tac + MMF

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9
Q

CNI pathway affected:

A

Signal 1: TCR/CD3 -> calcineurin -> NFAT -> IL-2,IL2R

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10
Q

mTORi pathway

A

Signal 3: IL2 -> CD25/JAK3 -> mTOR -> cell cycling

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11
Q

What is belatacept?

A

soluble CTLA4-Fc

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12
Q

Tacrolimus side effects

A

Twitchy and shorn, more diabetes, seizures

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13
Q

Cyclosporin side effects

A

Cheesy (gums) and neanderthal (hirsuitism)

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14
Q

MMF MOA

A

Inhibits IMPDH

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15
Q

MMF side effects

A

myelosuppressive, diarrhoea

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16
Q

Everolimus vs. Sirolimus side effects

A

Everolimus less cancer and less infection

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17
Q

Most important HLA group re. rejection

A

HLA-DQ

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18
Q

T cell mediated rejection rx

A

Methylpred and increase maintenance

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19
Q

Ab mediated rejection Rx

A

PLEX or IVIg or Rituximab

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20
Q

CMV prophy duration

A

6/12 if mismatch, 3/12 if R+ irrespective of donor; give if needing ATG

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21
Q

CMV rx

A

double dose valgan or gan

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22
Q

Rx for resistant CMV

A

foscarnet, cidofovir, CMV Ig, reduce anti-metabolite immunosuppression

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23
Q

Change of immunosuppression because of skin cancer

A

cease Aza and use mTORi

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24
Q

pattern of transplant glomerulopathy

A

MPGN

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25
BK nephropathy specific stain
Simian virus 40 stain
26
Areas of kidney most susceptible to AKI
outer medulla and proximal tubules
27
biggest risks for contrast induced nephropathy
CKD and diabetes
28
Mgmt of Contrast induced nephropathy
isotonic IVH, iso/low osmolar contrast low volume
29
MOA of rhabdo
Causes vasoconstriction, direct tubular damage and cast nephropathy
30
Top 3 causes of isolated glomerular haematuria
IgA, Alport's, Thin BMD
31
Nephrotic diseases
Kids- MCD; middle age= FSGS; old- membranous
32
Nephritic diseases
Kids- Post-infectious; young- IgA, SLE; old- AAN
33
What GN often recurs early post Tx?
FSGS
34
Secondary MCD is due to
NSAIDs, infection, allergy, cancer
35
2nd most common Ab in primary membranous
THSD7A (thrombospondin)
36
Secondary causes of membranous GN
cancer or SLE
37
main cell damaged in membranous GN
podocyte
38
Rx for primary membranous GN
Rituximab
39
Primary FSGS MOA
Elevated suPAR (soluble urokinase-type Plasminogen Activator Receptor) gets trapped in BM -> protease results in foot process effacement
40
Causes of secondary FSGS
HIV (collapsing), obesity, heroin, cancer, hyperfiltration
41
What is TINU?
Tubulointerstitial nephritis with uveitis. Occurs in young women, HLA assoc, Rx AIN w. steroids
42
Where go Ig complexes deposit in IgA GN?
mesangium
43
Biggest predictor of ESRF in IgA?
proteinuria >1g/day
44
When to biopsy in SLE?
Any renal involvement unless bland urine with <0.5g/day or creatinine too high to salvage
45
Mgmt of lupus nephritis
steroids + cyclophosphamide -> MMF maintenance
46
classic cause of secondary MPGN
chronic infection, Hep C +/- cryo
47
IN relapsing AAV mgmt
Rituximab better than cyclophosphamide. Argument for Ritux upfront if PR3
48
To what are antibodies directed in Anti-GBM disease?
against noncollagenous domain of alpha 3 chain of type 4 collagen
49
HLA/other links w. Anti-GBM
HLA-DR2; lung damage from smoking, hydrocarbons, influenza A, Alemtuzumab
50
Immunuotactoid GN details
Monoclonal IgG GN. usually IgG1. proliferative. nephritic. forms microtubular structure with HOLLOW tubes on EM. usually assoc. w. lymphoproliferative malignancy
51
Fibrillary GN details
Monoclonal IgG GN. MPGN. IgG in all. Bad nephritic/ RPGN. <20% have MGUS. Assoc. w. Hep C/Ca/AID. Tubules are thick
52
Type 1 cryo =
Monoclonal PTN due to haem usu. CLL/Waldenstroms. Often hyperviscous. TMA presentation
53
Type 2 cryo =
mixed, usually IgM-k mono + polyclonal IgG. Often assoc. infection Hep B/C. present as arthralgia, weakness, rash, neuropathy
54
Type 3 cryo =
mixed. polyclonal from infection/ AID. complement mediated MPGN.
55
PCKD % 1 vs. 2
78% 1 vs. 15% 2
56
PCKD inheritance
AD, complete penetrance
57
PCKD mutation type
point mutations causing either truncating (66%) or non-truncating in rest (milder).
58
Risk factors for progression in PCKD
PKD1 truncating > non-truncating > PKD2. Male, early onset sx, FHx. ESRF, proteinuria, HTN, size on MRI
59
Extra-renal manifestations ADPKD
MCA berry aneurysms/ hepatic cysts/ pancreatic and seminal vesical cysts/ valvular (MVP, AR)/ aorta (Dissection, aneurysm), GI (diverticulae, hernias)
60
PCKD diagnosis
No Fhx: >10 cysts bilateral with renal enlargement. FHx: 15-40yrs 3 cysts total. 40-60 2 cysts each. >60 4 cysts each
61
Tolvaptan MOA
Vasopressin-2 receptor antagonist
62
uOsmol aim of Tolvaptan
<280
63
Causes of death in PCKD
CVD > ICH
64
Dialysis Kt/V aim
HD 1.2, PD 1.7
65
Dialysis adequacy urea reduction ratio
Urea pre-urea post/ urea pre
66
single factor w. biggest impact on longevity of PD
PD peritonitis
67
Biggest factor to improve dialysis adequacy
time on dialysis
68
Best access method of dialysys
AVF
69
Dialysis disequilibrium mechanism
osmotic gradient -> cerebral oedema
70
Ways to improve Peritoneal dialysis
higher dextrose, more bags, higher volume
71
Where are aldosterone receptors located?
cortical collecting duct
72
Where does ANP work?
medullary collecting duct
73
Where are V1 receptors?
On vasculature
74
Where are V2 receptors?
On TAL/DCT/CD
75
V2 receptor activation ->
aquaporin channels and free water re-absorption
76
What does CA-inhibition cause e.g. acetazolamide
metabolic acidosis from excess bicarbonate loss from proximal tubule (form of T2 RTA)
77
Where is Na reabsorbed in kidney
67% PCT, 25% TAL Na-K-Cl. 5% DCT
78
Where do thiazides work?
DCT Na-Cl channel
79
Channel on which loop diuretics work
Na-K-Cl
80
electrolyte changes of Bartters
HypoK, HypoCa,HypoMg, volume depletion, alkalosis; secondary hyperaldosteronism
81
Rx of Bartter's
NSAIDs, Electrolyte replacement
82
Gitelman's inheritance
AR
83
What are prostaglandins in Bartter's
elevated +++ due to poor perfusion
84
Gitelman's sx
polyuria, cramps
85
Liddle's defect
ENaC in collecting tubule permanently turned on -> excessive Na reabsorption -> HTN (like apparent mineralocorticoid excess)
86
Liddle rx
Amiloride
87
Gordon's defect
defect in thiazide sensitive Na-Cl co-transporter, gain of function; excessive Na reabsorption (opposite of Gitelman)
88
Findings in Gordon's
HTN, Acidosis, Hyperkalaemia
89
Rx of Gordon's
Thiazide
90
RTA Type 1 features
NAGMA, hypokalaemia, alkaline urine, nephrolithiasis
91
T1 RTA causes
AID- SS, RA
92
T2 RTA features
NAGMA, hypokalaemia, urine pH low
93
T2 RTA causes
Monoclonal IgG disease, drugs- Tenofovir, Fanconi's
94
T4 RTA features
hypoaldosteronism, low BP, NAGMA, hyperkalaemia
95
T4 RTA causes
adrenal insufficiency, CNIs, NSAIDs, interstitial nephritis, DM nephropathy, acute GN
96
T4 RTA mgmt
fludrocortisone
97
Gentamicin type of nephrotoxicity
ATN
98
Top 4 medications in order of benefit for BP/proteinuria
ACE-i/ARB, diuretics/ CCB/ spiro
99
FIrst biochemical change in CKD-MBD
lose klotho; FGF23 rises
100
why is 1,25-vitD reduced in CKD-MBD?
FGF-23 inhibition of 1-OH and destruction of 25-OH-vitD
101
FGF23 normally suppresses
PO4 and PTH
102
Most common form of CKD-MBD in dialysis patients
adynamic bone disease
103
PTH target in dialysis patients
2-9x ULN
104
Iron target in ESRF
Ferritin >100-200 and TfSat >20%
105
side effects of EPO
pure red cell aplasia with Abs to EPO; stroke
106
Target Hb of ESRF
100-110
107
Diabetic nephropathy biopsy finding
Kimmelstiel-wilson nodules = nodular glomerulosclerosis
108
Lithium action on tubules
Nephrogenic DI- from impaired responsiveness of distal nephron to ADH/ decreased expression AQP2 Hypercalcaemia- impairs CaSR so doesn't inhibit Ca reabsorption in the tubule
109
Response to desmopressin in nephrogenic DI
no/minimal rise in urine osmolality
110
mgmt lithium DI
thiazides and amiloride when urine vol >4L/day