CKD RENAL Flashcards

1
Q

Ckd is characterized b

A

IFTAGS

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2
Q

Clinical definition of ckd

A

Abnormalities of kidney str present for more than 3 months with implications for health
Gfr less than 60 ml/min
Albuminuria more than 30 mg / 24 hr

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3
Q

CTID

Primary CTID features are

A

IF TA
IF when more than 5 % of cortical area is connective tissue
TA when diameter drops by 50%

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4
Q

Most potent fibrogenic cytokine which is also responsible for ctid

A

Tgf beta

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5
Q

TGF BETA sources are

A

Pericytes converted to fibroblast
Fibroblast progenitors activation (Gli -I cells)
Hypoxia triggers fibrosis

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6
Q

Balkam nephropathy occurs due to

A

Toxin -aristolochic acid chinese herbal poisoning

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7
Q

Ouch ouch nephropathy occurs due to

A

Cadmium

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8
Q

Hyperuricemia and htn due to lead is k a

A

Saturnine gout

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9
Q

Drugs responsible for ctid

A

Lithium

Calcineurin inhibitors

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10
Q

Vacuolation of pct >dct due to

A

Hypokalemia

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11
Q

Metabolic causes of ctid

A

Hypokalemia
Hypercalcemia
Hyperoxaluria
Hyperuricemia

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12
Q

Rate of fall in gfr in ctid

A

2-4ml/min/yr

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13
Q

Mcc cause of Anemia in cld is ctid why

A

Because erythropoetin is produced from peritubular interstitial fibroblast and fibrosis leads to very low levels of erythropoetin

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14
Q

Defective concentration capacity of kidney lead to

A

Polyuria nocturia

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15
Q

Proximal tubular dysfunction leads to

A

Fanconi syndrome rickets like feature

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16
Q

Salt wasting syndrome is seen in

A

Ctid

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17
Q

Type 4 RTA aka pseudohypoaldosteronism lead to
Potassium levels?
Urine output

A

Hyperkalemia which is disproportionate to degree and duration of ckd
And nephrogenic diabetes insipidus

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18
Q

Salt sensitive hypertension occurs due to

A

Hypertrophy of jga as it is last to fibrose

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19
Q

Microcystic changes in DT without interstitial inflammation

A

Lithium

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20
Q

Characterstic changes in calcineurin inhibitors toxicity

A

Patchy interstitial fibrosis in striped pattern

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21
Q

Afferent arteriolar hyalinosis is seen in

Afferent and efferent arteriolar hyalinosis is seen in

A

Calcineurin inhibitors

Diabetes

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22
Q

Treatment of ctid

A

Transplant

Doesn’t recur post transplant

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23
Q

Characteristics feature of IgG4 related kidney disease

A

Lymphoplasmocytic infiltration of any organ

Tumifactive storiform fibrosis

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24
Q

Bird eye /maple wood grain pattern is seen in

A

IgG4 related kidney disease

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25
Autoimmune pancreatitis salivary gland swelling ctid | Reidel thyrditis are c/f of
IgG4 related kidney disease
26
Incidence of ckdu is seen in
Working age male (Agricultural ) Heat stress
27
Areas of ckd u belt
El salvador Egypt Sri lanka india
28
Mesoamerican nephropathy is seen in
Sugar cane worker | Also known as heat stress nephropathy
29
Factors affecting ckd u
Water high fluoride, cyanobacterial toxin Pesticides Aluminum utensil
30
Heat wave nephropathy in India is known as
UDDANAM
31
Primary Vesicoureteric reflux occurs in
Boys during antenatal pd and is of grade 4-5
32
Grading of VUR
1 reflux to ureter 2 reflux to ureter and pelvicalyceal sys no dilatation 3mild to moderate dilatation no blunting of fornices 4severe dilatation blunting of fornices Papillary impression intact 5 Papillary impression lost
33
Diagnosis of congenital VUR
Antenatal usg - fetal renal pelvis >5mm
34
Patho of congenital VUR
Retrograde flow of urine from bladder to kidney | Shortening of intravesical submucosal length of ureter
35
When to suspect VUR
Hydroureteronephrosis in mother Vur in sibling Uti in less than 7 yr child
36
Most common cause of CKD | Rate of fall of gfr /yr
Diabetic NEPHROPATHY | 8-10ml/mt /yr
37
Grading of ckd is done on the basis of
``` GFR Grade 1 to 5 GFR 90 to 15 ml/ mt Albumin secretion Albumin creatine ratio A1 <30mg /g A2 30-300 mg/g A3 >300mg/g ```
38
Mechanism of damage in ckd
When more than 50% nephrons are lost kidney independently progresses towards ckd
39
Most important risk factor for kidney disease progression
Proteinuria
40
Nephron loss leads to glomerular capillary hypertension what are sequlae of this
Mechanical stretching leads to mesangial endothelial podocyte cell proliferation and sclerosis Protein accumulation in Podocyte leads to ang 2 release and gene activation tgf beta release Foot process effacement Glomerular permeability to protein increase
41
Strongest morphological predictor of ckd progression
IF | TA
42
Problem ass with ckd
Anemia CV manifestation Bone mineral changes Others
43
Substance which largely depend on gfr for excretion | Inversely related
Urea creatinine
44
Substance which do not show change in plasma conc with renal failure because rate of excretion per surviving nephron increase
Sodium
45
How to define anemia in ckd
Acc to KDIGO | Hb less than 13 male &12 female in ckd pt is anemia
46
Erythopoietin independent phases in erythropoiesis
Pleuripotent stem cell to burst forming unit erythroid
47
Erythopoietin dependant phases in erythropoiesis
BFU -E to CFU-E first step | CFU-E to erythroblast to reticulocyte
48
Iron dependant phases of erythropoiesis
Erythroblast to erythrocyte
49
When to start erythopoietin simulating agents in ckd pt
Hb less than 10 | Target hb is 11-12gm/dl
50
Indication for iron therapy in ckd
Percentage saturation of transferrin less than 30 % | Sr ferritin less than 500ng/ml
51
Iron is given through which route amd composition
I/V iron - fe sucrose, ferric carboxymaltose, iron isomaltose
52
Erythopoietin simulating agents are given by | Name first and second gen esa
Subcutaneous or intravenous First gen Epoietin alpha Second gen Darbepoietin alpha CERA (continuous erythroid receptor activator )
53
When do we say pt is resistant to esa because hb levels are not improving
Even after 300 unit /kg/wk ESA THERAPY | HB fails to improve it is resistance
54
Major causes of resistance to ESA THERAPY
Iron deficiency Infection Underdialysis Inflammation
55
When do we treat anemia in ckd by epo mimetic as there are anti epo antibodies in blood
Epo mimetic- peginesatide | Pure red cell aplasia is ass with anti epo antibodies
56
Complications of epo therapy
Stroke HTN Thrombosis Malignancy
57
Classification of mineral bone ds in ckd
High bone turnover ds -Osteitis fibrosa cystica 90% Low bone turnover ds-Adynamic bone disease 10% Miscellaneous Osteomalacia abnormal mineralization Osteoporosis decrease bone density
58
Major cause of high bone turnover ds
Secondary hyperparathyroidism | Gfr less than 50-70
59
Role of fgf in mineral bone ds as well as cardiovascular manifestation in ckd
As gfr decrease in ckd phosphorus level in blood increase but this is prevented by FGF 23 It also inhibits 1alpha hydroxylase which converts 25(OH) D3 to 1,25 (OH) D3 causing decrease calcium and phosphorus absorption from git
60
Receptor for FGF 23
Klotho receptor
61
Features of ckd pt with secondary hyperparathyroidism
Decrease serum calcium due to abnormal mineralization Decrease calcitriol due to FGF Increase klotho resistance leading to increase phosphorus level
62
``` Formation of woven bone Medial calcification Easy fracture, BONE PAIN Increase PTH PHOSPHORUS DECREASE SR CALCIUM AND CALCITRIOL ```
Osteitis fibrosa cystica -high bone turnover ds
63
Low turnover ds is characterized by
PTH low due to increase calcium from exogenous an d calcium dialysate Vit D sr calcium phosphate increased
64
Widespread medial calcification is seen in
Adynamic bone disease Medial calcification means tunica media calcification Leads to decrease arterial distension and LVH
65
How to manage low bone turnover ds
Stop ca and vit d Zero calcium dialysate Vit K2 analogue
66
Mgt of high bone turnover ds
If Sr calcium low phosphorus high Dietary restrictions on phosphorus Phosphate binders preferred If sr calcium high and phosphorus high Seen in 3 degree hyper PTH Cinacalet -calcium sensing receptor agonist helps pth to sense calcium and inhibit pth
67
Names of phosphate binders
``` Lanthanum Sevelamer carbonate Sucroferric oxyhydoxide Niacin Tenapanor Ferric citrate ```
68
Leading cause of mortality in ckd
Cardiac cause - 50% esrd pt die from cvs manifestation