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CAM III > Renal Part II > Flashcards

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
Q

Diagnostic criteria for autosomal dominant polycystic kidney dz

A

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

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26
Q

Dietary risks for nephrolithiasis

A

High sodium
Protein
Oxalates
Purines

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27
Q

What are the types of kidney stones?

A

Calcium oxalate, calcium phosphate= MC
Struvite= infection
Uric acid= radiolucent, not seen on KUB
Cystine= genetic, rare

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28
Q

S/sx of nephrolithiasis

A

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

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29
Q

Imaging for nephrolithiasis

A

Gold standard= spiral CT without contrast
May demonstrate hydronephrosis
-Distention of the renal calyces and pelvis with urine d/t obstructive outflow

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30
Q

Organisms of pyelonephritis

A 
Gram negs MC
E. coli
Proteus
Klebsiella
Enterobacter
Pseudomonas
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31
Q

S/sx of pyelonephritis

A 
Fever
Rigors
N/V
CVA tenderness
Frequency
Urgency
Burning
Hematuria
Possible sepsis with shock
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32
Q

Labs for pyelonephritis

A 
Leukocytosis with left shift
Blood cx may be positive
Pyuria
Bacteriuria
Hematuria +/- white cell casts
Urine cx positive with heavy growth
33
Q

Tx of pyelonephritis

A

Inpt- ampicillin and aminoglycoside IV initially
Outpt- FQ PO and prompt f/u
Failure to respond- kidney u/s or CT scan

34
Q

Renal cell carcinoma

A 
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
Q

Where is the compensatory mechanism when the primary illness is in ventilation?

A

Kidneys

36
Q

Where is the compensatory mechanism when the primary illness is metabolic?

A

The lungs

37
Q

Causes of metabolic acidosis

A

DKA
Severe diarrhea
Renal failure
Shock

38
Q

S/sx of metabolic acidosis

A 
HA
Decreased BP
Hyperkalemia
Muscle twitching
Warm, flushed skin
N/V/D
Changes in LOC
Kussmal respirations
39
Q

Causes of metabolic alkalosis

A

Severe vomiting
Excessive GI suctioning
Diuretics
Excessive sodium bicarb

40
Q

S/sx of metabolic alkalosis

A

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
Q

Causes of respiratory acidosis

A

Decreased respiratory stimuli (anesthesia, drug overdose)
COPD
Pneumonia
Atelectasis

42
Q

S/sx of respiratory acidosis

A 
Hypoventilation leads to hypoxia
Rapid, shallow respirations
Decreased BP with vasodilation
Dyspnea
HA
Hyperkalemia
Dysrhythmias (Increased K)
Drowsiness, dizziness, disorientation
Muscle weakness, hyperreflexia
43
Q

Causes of respiratory alkalosis

A

Hyperventilation (anxiety, PE, fear)

Mechanical ventilation

44
Q

Conditions associated with lowered bicarb

A

CKD
Ingestion of methanol, ethylene glycol, excessive ASA
Diarrhea
Starvation

45
Q

Conditions associated with elevated carbon dioxide

A 
Acute respiratory failure
Drug overdose
COPD
Morbid obesity
Neuromuscular dz
46
Q

Conditions associated with increased bicarb

A

Vomiting
Gastric suctioning
Loop or thiazide diuretics

47
Q

Anion gap

A

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
Q

Causes of normal anion gap acidosis

A

Addisons
Bicarb loss
Chloride excess
Diuretics

49
Q

Formula for urine anion gap

A

(Na + K) - Cl

50
Q

Cause of increased urine anion gap

A

Renal causes increased urine HCO3

51
Q

Cause of decreased anion gap

A

GI causes increased urine NH4 excretion

52
Q

What anion gap levels are consistent with renal issues like renal tubular acidosis when kidneys cannot properly excrete ammonia?

A

> 20 mEq/L

53
Q

What is the source most likely to be when the urine anion gap is zero or negative, but the serum anion gap is positive?

A

GI (diarrhea or vomiting)

54
Q

Causes of high anion gap metabolic acidosis

A

Lactate
Toxins
Ketones
Renal

55
Q

What does the MUD PILERS acronym stand for?

A 
Methanol, metformin
Uremia
DKA (or alcoholic or starvation ketoacidosis)
Paraldehyde, propylene glycol
Infection, iron, isoniazid
Lactic acidosis
Ethylene glycol
Rhabdo
Salicylates
56
Q

Other tests to consider to find root cause of high anion gap metabolic acidosis

A 
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
Q

Osmolar gap

A

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
Q

Nl serum osmolality

A

275-295 mosm/kg

59
Q

What occurs with increased aldosterone, leading to Na retention

A

Primary hyperaldosteronism

60
Q

What occurs with increased ADH that leads to water retention?

A

SIADH

61
Q

Hyponatremia

A

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
Q

Sx of hyponatremia

A 
HA
Lethargy
N/V
Disorientation
Seizures
Coma
63
Q

Management of acute hyponatremia

A

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
Q

Management of chronic hyponatremia

A

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
Q

Lab findings of SIADH

A

Serum Na down
Urine Na up
Urine osmolality up
Serum osmolality down

66
Q

PE of SIADH

A

BP elevated

Pos edema

67
Q

Tx of SIADH

A

Water restriction
Treat underlying dz
Induce DI by giving demeclocycline

68
Q

Sx of DI

A

Polydipsia, polyuria

69
Q

Labs of DI

A

Neg urine glucose

Nl serum glucose

70
Q

Dx of DI

A

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
Q

Tx for central DI

A

DDAVP

72
Q

Tx of nephrogenic DI

A

HCTZ, if due to lithium toxicity, reverse cause

73
Q

Hypernatremia

A

Serum Na > 145 mEq/L

74
Q

Euvolemic hypernatremia

A

Renal losses, DI, lithium toxicity

75
Q

Hypovolemic hypernatremia

A

With urine Na < 20: GI loss, sweating, burns

With urine Na > 20: loop diuretics, laxative abuse

76
Q

Hypervolemic hypernatremia

A

Primary aldosteronism
Bicarb infusion or pushes
Hypertonic dialysis
Cushing’s

77
Q

Sx of hypernatremia

A

Lethargy
Irritability
Weakness
Thirst

78
Q

Management of hypernatremia

A

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
Q

What can hypokalemia result from?

A 
Insufficient intake
Increased excretion (diuretics, hyperaldosteronism)
Shift from extracellular to intracellular space
GI losses via vomiting or diarrhea

CAM III (12 decks)

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