Nephrology Flashcards
(134 cards)
1
Q
Board answer for BP management
A
Ambulatory blood pressure monitoring
2
Q
How to dose HCTZ
A
Keep it at 25 mg. You don’t get a significant antihypertensive effect beyond this but do get a significant increase in side effects.
3
Q
When to start bicarb in CKD and why
A
- Serum bicarb chronically below 22
- Alkali therapy can delay progression of CKD
4
Q
Treatment of minimal change glomerulopathy
A
High dose prednisone (1-2 mk/kg per day for 8 to 12 weeks, then taper)
5
Q
what is standard treatment of nephrotic syndrome
A
- ACE or ARB
- Diuretics for edema
- Statin
6
Q
Term for renal disorder that can develop from MGUS
A
monoclonal gammopathy of renal significance (MGRS)
7
Q
Labs for MGRS (monoclonal gammopathy of undetermined significance)
A
nephrotic and subnephrotic proteinuria, hematuria, elevated creatinine
8
Q
Treatment of IgA nephropathy
A
ACE or ARB (this inhibits protein production and slows disease progression)
9
Q
Lab features of polydypsia
A
- very low urine osmolality (less than 100)
- low urine sodium
10
Q
serum sodium with diabetes insipidus
A
Typically normal but can be elevated in patients who do not have access to water
11
Q
How to prevent calcium oxalate kidney stones in patients with chronic diarrhea
A
Potassium citrate (urine citrate is reduced because diarrhea causes a metabolic acidosis. Also, calcium binds to fat as opposed to oxalate with chronic pancreatitis due to fat malabsorption which leaves oxalate free to be absorbed and excreted in the urine)
12
Q
Med that will also reduce progression of kidney disease and CV events in patients with CKD from DM2
A
SGLT2
13
Q
Treatment of rhabdo induced AKI
A
Aggressive fluid resuscitation with NS to goal UOP 200-300 mL/h
14
Q
How to reduce incidence of contrast-induced nephropathy
A
Normal saline
15
Q
Presentation of milk alkali syndrome + cause
A
- Ingestion of large amounts of calcium
- hypercalcemia + metabolic alkalosis + AKI
16
Q
Treatment of ethylene glycol toxicity
A
IV hydration
Fomepizole
Hemodialysis (need to dialyze toxin)
17
Q
Presentation of ethylene glycol toxicty
A
CNS depression
Anion gap acidosis
Increased osmolal gap
Kidney failure
18
Q
Evaluation of membranous glomerulopathy
A
Age and sex appropriate cancer screening
Hep B and C, lupus and syphilis testing
19
Q
Anticoagulation for membranous glomerulopathy
A
Is higher risk, particularly when albumin is below 2.8 but there is no conscenus and guidelines generally recommend monitoring rather than anticoagulation
20
Q
How to test for diabetes insipidus + how it works
A
Water deprivation test (response to exogenous ADH supports diagnosis of central DI, whereas lack of response is seen in nephrogenic DI)
21
Q
Why heparin can cause hyperkalemia
A
Hypoaldosteronism
22
Q
clinical outcomes of peritoneal vs. hemodialysis
A
Comparable
23
Q
Important complication of peritoneal dialysis
A
Peritonitis
24
Q
Treatment of stage 2 hypertension
A
Combination therapy with antihypertensives of different classes
25
Stage 2 HTN definition
BP greater than 140 over 90
26
More efficacious antihypertensives in AA patients
Thiazide diuretics or CCBs
27
Renal disease typically caused by multiple myeloma
Cast nephropathy
28
Clinical features of ANCA-associated glomerulonephritis
Vasculitic prodrome (malaise, arthralgia, myalgia, skin findings) + hematuria + proteinuria
29
Biopsy of RPGN
Pauci-immune staining
Linear staining
Granular staining
30
Cause of pyroglutamic acidosis
- Happens in people taking therapeutic doses of acetaminophen chronically in setting of critical illness, poor nutrition, chronic liver or kidney disease
31
Presentation of pyroglutamic acidosis
Mental status changes + gap acidosis
32
Presentation of D-lactic acidosis
Gap acidosis + neuro dysfunction (confusion, slurred speech, ataxia) + patient with short-bowel syndrome
33
Labs for D-lactic acidosis
NORMAL serum lactic (not measured by conventional lab assays)
34
Pathophys of D-lactic acidosis
Patients with short-bowel syndrome following jejunoileal bypass or small bowel resection --> excess carbohydrates reach the colon and are metabolized to d-lactate
35
Presentation of salicylate toxicity
Respiratory alkalosis OR both respiratory alkalosis + gap acidosis
36
Propylene glycol toxicity presentation
gap acidosis + AKI
37
Gap acidosis differential
```
M - Methanol
U - Uremia
D - DKA
P - Paraldehyde
I - Iron, INH
L - Lactic acidosis
E - ethanol, ethylene glycol
S - salicylate/aspirin
```
38
what are the ANCA associated glomerulonephritidis?
GPA + MPA
39
Management of abdominal compartment syndrome
Abdominal compartment decompression
| Correction of positive fluid balance
40
Definition of abdominal compartment syndrome
Sustained intra-abdominal pressure greater than 20 + at least one organ dysfunction
41
Settings in which abdominal compartment syndrome occurs
Abdominal surgery
Large volume fluid resuscitation
Multiple transfusions
42
Presentation of abdominal compartment syndrome
Distended abdomen
Ascites
Sodium-avid AKI (increased pressure compresses the renal parenchyma and vasculature, causing decrease in GFR)
43
AIN clinical features
Hematuria + pyuria + white cell casts
44
Age cutoff for working up hematuria
Age greater than 35 (should also prompt urology referral even if self-limited)
45
Appearance of erythrocyte casts and specificity
- cylindrical or tubular structure + agrunular spherocytes
| - Specific for hematuria of glomerular origin
46
RF' of vancomycin nephrotoxicity
CKD + supra therapeutic troughs + concomitant diuretic use
47
Microscopy findings with ATN
Numerous renal tubular epithelial cells + granular casts
48
Features of AIN
Classic triad = fever + rash + eosinophilia (but only 30% of patients have this)
*UA with hematuria + pyuria + casts
49
Features of contrast-induced nephropathy
Occurs within 48 hours of exposure to contrast
50
Treatment of acute symptomatic hyponatremia
A 100-mL bolus of 3% saline w/ goal increase in sodium of 2-3
- Can be repeated 1-2x until symptoms resolve
51
Why MDMA causes hyponatremia
SIADH + stimulates thirst receptors
52
Goal sodium correction in hyponatremia
Less than 10 in 24 hr period (remember, if the patient isn't symptomatic you have plenty of time to correct sodium)
53
Management of ACS in a patient with CKD
Immediate cath (mortality is far higher with cardiovascular disease than with CKD)
54
Renal clinical features of sarcoidosis
Nephrocalcinosis from hypercalcemia and hypercalciuria
55
Extrapulmonary organ involvement with sarcoid
Skin
arthralgia
eyes
56
Physiology of hyponatremia in pregnancy
Plasma volume increases with water retention greater than sodium retention so mild hyponatremia is common in pregnancy
57
management in dyslipidemia in CKD
All adults over 50 with a GFR less than 60 but not on dialysis, should be on a statin
58
Image type to diagnose nephrolithiasis
NONCON helical abdominal CT
59
Benign causes of increased serum creatinine
Increased muscle mass
Creatine supplements
(creatinine is derived from the metabolism of creatinine produced by muscle)
60
Management of recurrent kidney stones
24 hour urine studies
IF citrate normal --> Thiazide diuretic (will decrease calcium excretion into urine, reducing hypercalciuruia and calcium oxalate stone formation)
IF citrate low --> start potassium citrate
61
Management of membranous glomerulopathy
Observe for 6-12 months while on nephrotic syndrome meds (ACEi, statin, diuretic) to allow time for possible spontaneous remission before initiating immunosuppression (30% have spontaneous remission)
62
First line immunosuppressive therapy for membranous glomerulopathy
Alternating months of steroids and cyclophosphamide
63
Management of renal artery stenosis
Medical management (ACE inhibitor + treat CV risk factors statin because it is due to atherosclerosis)
64
term for kidney injury from contrast
Contrast-induced nephropathy
65
how to reduce incidence of contrast induced nephropathy when cath'ing patient with CKD
IV isotonic fluid before and after cath
66
Type 1 RTA clinical features + pathophys
- Defect in urine acidification in the distal nephron
| - NAGMA (can't secrete hydrogen ions0 + basic urine (pH 7) + hypokalemia + increased calcium phosphate kidney stones
67
Clinical features of kidney injury caused by NSAIDS
Interstitial nephritis (proteinuria)
68
Type 2 RTA clinical features + cause
- Proximal tubular defect in reclaiming bicarb
| - NAGMA + hypokalemia + glycosuria + proteinuria + phosphate wasting
69
How to differentiate NAGMA
Calculate urine anion gap
70
Management of alcoholic ketoacidosis
```
Thiamine first (to decrease risk of precipitating Wernicke's)
D5NS
```
71
management of edema in nephrotic syndrome
Low salt diet + loop diuretic
72
Other causes of secondary FSGS
Premature birth
| Solitary kidney
73
Risk of VTE in membranous glomerulopathy correlates to...
Degree of hypoalbuminemia (albumin less than 2.8)
74
patients with membranous glomerulopathy are at increased risk of...
- gout (true of all CKD patients due to reduced uric acid secretion)
- malignancy
75
Management of HTN in CKD patient
ACE or ARB
76
Preeclampsia clinical features
New-onset hypertension + proteinuria + new onset end-organ damage (liver, kidney, pulmonary edema, HA or visual symptoms, or thrombocytopenia)
77
HELLP syndrome clinical features
Hemolysis
Elevated liver enzymes
Low platelets
78
Fabry disease clinical features
Episodic pain + burning sensation in hands and feet + decreased perspiration + angiokeratomas
79
Management of cardio renal syndrome
Loop diuretics
80
Features of cardio renal syndrome
- Elevated BUN-creatinine ratio
| - Diuretic resistant heart failure (failure to improve CHF symptoms despite increasing diuretic requirement)
81
When do you need to dialyze CHF patients with cardio renal syndrome
Severe volume overload refractory to medical management
82
Goals of anemia management in CKD
Target transferrin saturation greater than 30% + ferritin level greater than 500
83
workup for renovascular hypertension + caveat
Kidney US with doppler (no studies have shown a benefit from percutaneous intervention so should be reserved for people with strong indications such as FMD)
84
Metabolic alkalosis workup
Differentiate saline responsive from saline unresponsive
Urine chloride
- low = vomiting, NG suction, diuretic use (GI losses so reabsorbing chloride)
- high = saline-resistant due to mineralocorticoid excess (Cushing syndrome + primary aldosteronism)
85
IgG4 related disease clinical features
Renal disease + autoimmune pancreatitis + allergic rhinitis + submandibular gland swelling
86
IgG4 related disease lab features
Elevated ANA
Low serum complement
Elevated serum IgG + IgE
Peripheral eosinophilia
87
What are the calcineurin inhibitors
Tacrolimus
| Cyclosporine
88
Hypermagnesemia treatment
Stop magnesium containing medications
NS bolus’s (increase secretion of mag) + furosemide
IV calcium (calcium counteracts neuromuscular effects of magnesium)
89
What you're looking for with urine microscopy for ATN
Granular casts and/or renal epithelial cells
90
What is masked hypertension
BP that is normal in the office but elevated in the ambulatory setting
91
How to differentiate chronic HTN from gestational HTN
Chronic HTN = HTN recognized before 20 weeks gestation
*In normal pregnancy BP declines during the first trimester, decreases further in 2nd trimester, and rises slowly thereafter. Thus, HTN in the first trimester suggests that it predates the pregnancy. Gestational HTN manifests later and resolves within 12 weeks of delivery.
92
Management of BP in pregnant women
Goal 160/105
| *avoid over treatment and associated fetal risk
93
Anti-phospholipase A2 receptor antibodies are associated with...
Membranous glomerulopathy
94
Management of suspected white coat hypertension
Ambulatory blood pressure monitoring
95
Type IV RTA clinical features
Hyperkalemia + NAGMA + impaired urine acidification (positive urine anion gap) + pH <5.5
96
When does hyperkalemia manifest with CKD
Usually stage 4 or worse -- GFR <40-45
97
Management of lupus patient developing kidney disease
Kidney biopsy (guides treatment and to determine class of lupus nephritis. there are multiple classes of lupus nephritis -- focal or diffuse proliferative lupus nephritis, lupus membranous nephropathy)
98
Blood pressure management in advanced CKD
loop diuretics (thiazides become less effective. useful for hyperkalemia and metabolic acidosis. sodium retention and impaired natriuresis lead to volume expansion and increased BP)
99
Most appropriate venous access for a patient with advanced CKD
```
NO PICCS (they can cause vein trauma and venous stenosis). need to protect upper extremity veins.
*Tunneled IJ central line
```
100
initial management of HTN in diabetics
Start ACE/ARB (don't want for trial of lifestyle modification)
101
Medications that reduce proximal tubule secretion of creatinine (causing benign elevation in creatinine/no effect on GFR) + management
Bactrim
Dolutegravir/Bictegravir
Cimetidine
*recheck creatinine in 1 week
102
Kidney stones caused by topamax
Calcium phosphate (carbonic anhydrase inhibitor so causes a decrease in urinary citrate excretion and formation of alkaline urine)
103
Most common type of kidney stone
calcium oxalate
104
tubulontersitial nephritis on UA
Pyuria + proteinuria + hemautira
105
high serum potassium without ECG changes, think..
pseudohyperkalemia
106
Situations in which pseudohyperkalemia can occur
Significant leukocytosis or thrombocytosis (cell lysis can lead to K leakage)
107
Goal hgb in anemia of CKD/esrd
10-11.5
108
Goal ferritin and transferrin sat in anemia of ckd/esrd
transferrin saturation >30% + ferritin >500
109
How to replete iron in anemia of ESRD
IF transferrin saturation >30 percent + patient not stage 3b or 4 → try PO iron → if no improvement, give IV iron
IF transferrin saturation <30 percent → IV iron
110
Medication class inhibits erythryopoesis
ACEis + ARBs
111
definition of allosensitization
exposure to an alloantigen that induces immunologic memory cells
112
Organism most often responsible for infection-related glomerulonephritis
Staph aureus
113
Phos goals in CKD4 and 5 generally
Lower toward reference range (not goal normal since there's no evidence of benefit to aggressively lowering to normal range)
114
Class of medications that commonly elevates blood pressure + mechanism
NSAIDs (increased sodium retention)
115
Diseases associated with membranoproliferative glomerulonephritis
Hep C
116
Lead nephropathy associations
Hyperuricemia + HTN + recurrent gout
117
Nephropathy clinical features from chronic ASA or APAP
chronic tubulointersitial disease
118
Causes of NAGMA
GI bicarbonate loss (diarrhea)
Renal loss of bicarbonate
Inability of kidney to excrete acid
119
Explain physiology of why you calculate a urine anion gap for NAGMA
Normal physiologic response to acidosis is to increase urine acid excretion. Therefore, need to determine whether kidney is appropriately excreting acid or whether impaired acid excretion is the cause. You measure urine chloride as a surrogate of ammonium to determine if acid is being excreted
120
Interpretation of urine anion gap
```
negative = GI cause
positive = RTA
```
121
Treatment of AIN
steroids
122
D-lactic acidosis occurs in which settings
short-bowel syndrome (usually due to small-bowel resection or jejunoileal bypass) (excess carbohydrates reach the colon and are metabolized to D-lactate by bacteria)
123
D-lactic acidosis clinical features
Neuro deficits (confusion, slurred speech, ataxia) + high anion gap acidosis
124
Management of immunosuppressants in kidney transplant recipients planning on having a baby
DC mycophenolate, sirolimus, and everolimus (replace with azathioprine)
*Also should wait 1-2 years after stable allograft
125
Clinical features of light chain cast nephropathy from MM
- Elevated urine protein-creatinine ratio
| BUT Minimal proteinuria by urine dipstick
126
Most common type of kidney disease in multiple myeloma
Light chain cast nephropathy
127
Presentation of IgA nephropathy
Recurrent gross hematuria occurring within days of URI or physical exercision + otherwise benign
128
Other term for IgA vasculitis
HSP - Henoch-Schonlein purpura
129
Features of IgA vasculitis
Abdominal pain + palpable purpura
130
General approach to working up acid base disorder
1) Identify primary disorder
2) Determine if adequate compensatory response
3) If no adequate compensation --> mixed acid-base disorder is present
131
How to determine metabolic compensation for respiratory alkalosis
Bicarb should be reduced by 5 mEq for each 10 decrease in PCO2 (nickel for a dime)
132
Significant proteinuria with minimal proteinuria on urine dipstick suggests...
Bence-Jones (light chain) proteinuria (isn't picked up by dipstick)
133
When CKD patients are referred for transplant evaluation
eGFR <30 (need to plan ahead to find living donor or to be put on early listing if no living donor available)
- transplant is also cheaper than dialysis
134
Management of hepatorenal syndrome
- octreotide + midodrine or levophed
- discontinue diuretics
- IF albumin <2.5 → Albumin 1g/kg q8h x 3 days
