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Renal Part II Flashcards

1
Q

Sx of associated with hematuria

A

Colic
Frequency/burning
Intermittent

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2
Q

Med hx associated with hematuria

A

Anticoagulants
Analgesics
Sickle cell
Abx

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3
Q

Work up for hematuria

A 
U/A with microscopy= casts often make the dx
-Red cell cast= glomerulus
-White cell cast= acute pyelonephritis
-Hyaline casts= not pathognomonic for anything
-Muddy brown casts= ATN
-Fatty casts= nephrotic syndrome
-Protein = kidneys
-WBCs = infection
Upper tract imaging= CT abdomen/pelvis
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4
Q

Albumin in proteinuria

A

Pathognomonic of CKD

Increases BEFORE the GFR drops

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5
Q

Overflow proteinuria (paraproteins)

A 
Monoclonal gammopathies
Myeloma
Amyloidosis
Hemoglobinuria
Myoglobinuria
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6
Q

Glomerular proteinuria

A 
Pregnancy
Lupus
IgA
Minimal change dz
Malignancy
Familial
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7
Q

Tubular proteinuria

A

Drugs
Toxins
Fanconi syndrome

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8
Q

Diagnosis of CKD

A

GFR < 60 mL/min for 3 or more mos (if shorter it is acute)
Albuminuria > 30 mg
Anatomical d/os
Abnormal urine sediment (on repeated labs)
-Hematuria, RBC casts
Electrolyte or tubule disorders
Hx of kidney transplantation or donation

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9
Q

Stage I CKD

A

Kidney damage with nl or increased GFR
GFR greater than or equal to 90
Dx/tx of underlying condition and comorbidities

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10
Q

Stage II CKD

A

Mild
GFR 60-89
Estimate the rate of progression

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11
Q

Stage III CKD

A

Moderate
GFR 30-59
Evaluate and treat complications

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12
Q

Stage IV CKD

A

Severe
GFR 15-29
Prepare for renal replacement therapy

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13
Q

Stage V CKD

A

Kidney failure
GFR <15 or dialysis
Dialysis or transplantation if uremic

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14
Q

Causes of CKD

A 
DM
HTN
Meds
Glomerulonephritis
Trauma
AKI
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15
Q

Diabetic nephropathy

A 
MCC of ESRD in the US
High GFR
Microalbuminemia
Frank proteinuria
Decline in GFR
Typically diabetic for >10 yrs
Other end organ damage is common
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16
Q

Tx of diabetic nephropathy

A

Strict glycemic control and tx of HTN
BP goal of <130/80
ACE and ARBs used in early stages as they carry some renal protective benefit

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17
Q

Tx of CKD

A 
Attempt to slow progression of dz
BP < 130/80
HgbA1c <7.0%
LDL <100 mg/dL
Tobacco cessation, wt control
ACE or ARB, esp in DM or those with proteinuria
Avoidance of nephrotoxic agents
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18
Q

Prognosis of CKD

A

Albuminuria is most predictive
Albuminuria occurs BEFORE a drop in GFR
GFR less than or equal to 15= kidney failure, but no dialysis until sx occur

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19
Q

ESRD

A

Most pts do not develop sx until late in dz and often nonspecific
-Fatigue, malaise, insomnia, HA
-Anorexia, metallic taste, hiccups, nausea
-Pruritis
Signs include:
-Cachexia, wt loss, altered mentation, asterixis, foamy urine
-In severe cases, pericardial rub

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20
Q

Renal artery stenosis

A

Caused by atherosclerotic occlusive dz (80-90%), fibromuscular dysplasia, HTN, CKD, DM, smoking
HTN refractory to multiple meds
Pulmonary edema with poorly controlled HTN
Increased BUN-Cr with significant renal ischemia
Audible abdominal bruit on affected side
AKI with starting of ACE/ARB is often how you diagnose

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21
Q

Dx of renal artery stenosis

A

Doppler u/s
CTA
MRA
Gold standard diagnostic= renal angiography

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22
Q

Tx of renal artery stenosis

A

Antihypertensive meds

Angioplasty with or without stenting

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23
Q

Fibromuscular dysplasia

A

Seen almost exclusively in women under 40

Treatment- percutaneous transluminal angioplasty and is often curative

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24
Q

Autosomal dominant polycystic kidney dz

A 
MC genetic dz in US
Commonly found at 30-40 yoa with new-onset HTN
Within a family, there are variations in age of presentation, progression of dz
Clinical findings:
-Hematuria
-Abdominal pain
-Central or abdominal enlargement
--Similar to PCOS presentation
-HTN
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25
Diagnostic criteria for autosomal dominant polycystic kidney dz
Renal u/s after age 30 Associated hepatic, splenic, pancreatic cysts Associated aneurysm in Circle of Willis, evaluate for HA Renal calculi are common Aggressive tx of HTN may slow progression of the dz At end stage, transplant, dialysis, or medical management
26
Dietary risks for nephrolithiasis
High sodium Protein Oxalates Purines
27
What are the types of kidney stones?
Calcium oxalate, calcium phosphate= MC Struvite= infection Uric acid= radiolucent, not seen on KUB Cystine= genetic, rare
28
S/sx of nephrolithiasis
Renal or ureteral colic, intermittent, cannot sit still -Back pain, abdominal pain, flank pain -Radiates to groin (testicle, labia) = lower ureter/UVJ Nausea, vomiting, gross or microscopic hematuria
29
Imaging for nephrolithiasis
Gold standard= spiral CT without contrast May demonstrate hydronephrosis -Distention of the renal calyces and pelvis with urine d/t obstructive outflow
30
Organisms of pyelonephritis
``` Gram negs MC E. coli Proteus Klebsiella Enterobacter Pseudomonas ```
31
S/sx of pyelonephritis
``` Fever Rigors N/V CVA tenderness Frequency Urgency Burning Hematuria Possible sepsis with shock ```
32
Labs for pyelonephritis
``` Leukocytosis with left shift Blood cx may be positive Pyuria Bacteriuria Hematuria +/- white cell casts Urine cx positive with heavy growth ```
33
Tx of pyelonephritis
Inpt- ampicillin and aminoglycoside IV initially Outpt- FQ PO and prompt f/u Failure to respond- kidney u/s or CT scan
34
Renal cell carcinoma
``` RF- smoking Hematuria is MC presentation Often found incidentally on radiography Flank pain/abdominal mass Metastatic sx present in 20-30% Imaging- CT abdomen/pelvis, workup for mets ```
35
Where is the compensatory mechanism when the primary illness is in ventilation?
Kidneys
36
Where is the compensatory mechanism when the primary illness is metabolic?
The lungs
37
Causes of metabolic acidosis
DKA Severe diarrhea Renal failure Shock
38
S/sx of metabolic acidosis
``` HA Decreased BP Hyperkalemia Muscle twitching Warm, flushed skin N/V/D Changes in LOC Kussmal respirations ```
39
Causes of metabolic alkalosis
Severe vomiting Excessive GI suctioning Diuretics Excessive sodium bicarb
40
S/sx of metabolic alkalosis
Restlessness followed by lethargy Dsyrhythmias Compensatory hypoventilation Confusion (decreased LOC, dizzy, irritable) N/V/D Tremors, muscle cramps, tingling of fingers and toes Hypokalemia
41
Causes of respiratory acidosis
Decreased respiratory stimuli (anesthesia, drug overdose) COPD Pneumonia Atelectasis
42
S/sx of respiratory acidosis
``` Hypoventilation leads to hypoxia Rapid, shallow respirations Decreased BP with vasodilation Dyspnea HA Hyperkalemia Dysrhythmias (Increased K) Drowsiness, dizziness, disorientation Muscle weakness, hyperreflexia ```
43
Causes of respiratory alkalosis
Hyperventilation (anxiety, PE, fear) | Mechanical ventilation
44
Conditions associated with lowered bicarb
CKD Ingestion of methanol, ethylene glycol, excessive ASA Diarrhea Starvation
45
Conditions associated with elevated carbon dioxide
``` Acute respiratory failure Drug overdose COPD Morbid obesity Neuromuscular dz ```
46
Conditions associated with increased bicarb
Vomiting Gastric suctioning Loop or thiazide diuretics
47
Anion gap
The difference between measured cations and anions in serum (Na - (Cl + HCO3)) Used in diagnosis of metabolic acidosis Nl anion gap acidosis= HCO3 loss Elevated anion gap acidosis = generation of new acid -Ketoacids, lactic acid, ingestions
48
Causes of normal anion gap acidosis
Addisons Bicarb loss Chloride excess Diuretics
49
Formula for urine anion gap
(Na + K) - Cl
50
Cause of increased urine anion gap
Renal causes increased urine HCO3
51
Cause of decreased anion gap
GI causes increased urine NH4 excretion
52
What anion gap levels are consistent with renal issues like renal tubular acidosis when kidneys cannot properly excrete ammonia?
>20 mEq/L
53
What is the source most likely to be when the urine anion gap is zero or negative, but the serum anion gap is positive?
GI (diarrhea or vomiting)
54
Causes of high anion gap metabolic acidosis
Lactate Toxins Ketones Renal
55
What does the MUD PILERS acronym stand for?
``` Methanol, metformin Uremia DKA (or alcoholic or starvation ketoacidosis) Paraldehyde, propylene glycol Infection, iron, isoniazid Lactic acidosis Ethylene glycol Rhabdo Salicylates ```
56
Other tests to consider to find root cause of high anion gap metabolic acidosis
``` Lactate (LA) Glucose (DM) Beta-hydroxybutyrate (DM, starvation) BUN/creatinine (Renal failure) Urine ketones (DKA, starvation) Serum levels of: -Methanol -Ethanol -Acetaminophen -Salicylates -Ethylene glycol ```
57
Osmolar gap
This is a clinical aid to evaluate the difference between the measured osmolality and the calculated serum osmolarity Osmolar gap > 25 suggests methanol or ethylene glycol poisoning
58
Nl serum osmolality
275-295 mosm/kg
59
What occurs with increased aldosterone, leading to Na retention
Primary hyperaldosteronism
60
What occurs with increased ADH that leads to water retention?
SIADH
61
Hyponatremia
Serum Na < 135 mEq/L Reflects excess water retention rather than Na deficiency Hypo-osmolar, volume excess, edema forming states SIADH, pituitary mass, meds (SSRI, SNRI) Psychogenic polydipsia
62
Sx of hyponatremia
``` HA Lethargy N/V Disorientation Seizures Coma ```
63
Management of acute hyponatremia
Restrict water intake Correct Na balance slowly (1-1.5 mEq/L/hr) Severe sx: 100 cc 3% NaCl Mild to moderate sx: 3% NaCl at 0.5-2 cc/kg/h
64
Management of chronic hyponatremia
Goal is to prevent central pontine myelinosis = iatrogenic cerebral osmotic demyelination Chronic means known duration >48 hrs Minimum 4-8 mmol/L per day Max 10-12 mmol/L/day or 18 mmol/L/48 hr For pts at high risk max 8 mmol/L/day High risk: alcoholics, those with VERY low serum sodium levels, concomitant hypokalemia, liver dz, and malnutrition
65
Lab findings of SIADH
Serum Na down Urine Na up Urine osmolality up Serum osmolality down
66
PE of SIADH
BP elevated | Pos edema
67
Tx of SIADH
Water restriction Treat underlying dz Induce DI by giving demeclocycline
68
Sx of DI
Polydipsia, polyuria
69
Labs of DI
Neg urine glucose | Nl serum glucose
70
Dx of DI
Water deprivation test: they continue to pee dilute urine despite no water Then give ADH: it gets better= central DI If not = nephrogenic DI
71
Tx for central DI
DDAVP
72
Tx of nephrogenic DI
HCTZ, if due to lithium toxicity, reverse cause
73
Hypernatremia
Serum Na > 145 mEq/L
74
Euvolemic hypernatremia
Renal losses, DI, lithium toxicity
75
Hypovolemic hypernatremia
With urine Na < 20: GI loss, sweating, burns | With urine Na > 20: loop diuretics, laxative abuse
76
Hypervolemic hypernatremia
Primary aldosteronism Bicarb infusion or pushes Hypertonic dialysis Cushing's
77
Sx of hypernatremia
Lethargy Irritability Weakness Thirst
78
Management of hypernatremia
Slow correction over 48 hrs Hypovolemia: isotonic nl saline Euvolemia: 5% dextrose IV or water ingestion Hypervolemia: 5% dextrose IV, loop diuretics, possibly dialysis
79
What can hypokalemia result from?
``` Insufficient intake Increased excretion (diuretics, hyperaldosteronism) Shift from extracellular to intracellular space GI losses via vomiting or diarrhea ```

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