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CPR Test II > Renal approach to CP, SOB/DOE, Palpitations > Flashcards

Renal approach to CP, SOB/DOE, Palpitations Flashcards

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1
Q

how is hyponatremia defined?

A

< 135 mEq/L

mild hyponatremia: 130-134
moderate hyponatremia: 120-129
severe hyponatremia: <120

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2
Q

what patient are common for Hyponatremia? and what are some risk factors

A

Very common electrolyte disorder
-more common in hospitilized patients especially in the ICU

Risk factors:

  • CHF
  • Cirrhosis
  • Nephrotic syndrome
  • Pneumonia (legionella especially)
  • Postop state
  • ICU
  • Geriatric
  • Medications
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3
Q

what is the normal Serum Osmolarity

what are the 2 systems that regulate?

A

280-290 mOsm/L

ADH system
thirst mechanism

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4
Q

what are the two stimuli that cause the release of ADH

A

Osmotic stimuli: from increases in serum osmolarity detected by osmoreceptors in the anterior hypothalamus

Non-osmotic stimuli: from decreases in blood pressure or blood volume detected by blood baroreceptors

  • also: Nausea, Hypoxia, Pain (especially post op)
  • medications (opiates, antidepressantss (SSRI’s))
  • PRegnancy
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5
Q

what is the pathogenesis of Hyoponatremia

A

Results primarily from increases in TBW and less from changes in total body sodium

Increases in TBW results from either

  • excessive intake of water (oral or IV)
  • decreased renal excretion of water (usually from inability to suppress ADH release)
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6
Q

when do symptoms appear for Hyponatremia and what are those symptoms?

A

<125

  • HA
  • Fatigue/lethragy
  • dizziness
  • Nausea
  • Gait instabillity/falls
  • Confusion
  • psychosis
  • seizures
  • coma from cerebral edema
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7
Q

what is considered Acute vs Chronic Hyponatremia

A

Acute Hyponatremia: < 48 hours

Chronic hyponatremia: >48 hours or unknown duration

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8
Q

what is the systemic approach to Hyponatremia?

A

First measure Serum Osmolarity:
-determine if hypotonic, isotonic, or hypertonic hyponatremia is present

if patient hasHypotonic hyponatremia then assess volume status of the patient

  • measure random urine sodium level and urine osmolarity
  • consider a serum uric acid to determine SIADH
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9
Q

Should you draw labs first or treat first?

A

Best to avoid treatment until labs are drawn so it is important to draw all labs simultaneously

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10
Q

Hypovolemia exam findings

A
  • Hypotension
  • orthostatic vital signs
  • tachycardia
  • Poor capillary refill
  • Increased skin tugor
  • Dry oral mucosa or tongue fissuring
  • Flat JV
  • Hx of decreased urine output
  • > 50% collapse of IVC during inspiration on ECHO
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11
Q

Hypervolemic exam findings

A

Hypertension

  • sacral or LE edema
  • JVD
  • Dilated IVC on ECHO
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12
Q

after assessing the ECF VOlume status as Hypovolemic Hyponatremia, Urine osm >300 and urine Na+ is >20 mEq/L what is the DDx

A

Renal fluid losses

  • Diuretic excess
  • adrenal insufficiency
  • Osmotic diuresis
  • post-obstructive diuresis
  • RTA
  • Cerebral salt wasting
  • salt losing nephropathy
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13
Q

after assessing the ECF VOlume status as Hypovolemic Hyponatremia, Urine osm >300 and urine Na+ is <20 mEq/L what is the DDx

A

Extrarenal fluid loss

  • vomiting
  • diarrhea
  • third spacing of fluids (burns, pancreatitis)
  • blood excess
  • excessive sweating
  • lung losses
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14
Q

after assessing the ECF VOlume status as Euvolemic Hyponatremia, Urine osm >300 and urine Na+ is >20 mEq/L what is the DDx

A 
SIADH
-tumor
-CNS or pulmonary disorder
-drugs
-nausea
-pain
hypoxia

Hypothyroidism
Adrenal insufficiency
thiazides

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15
Q

after assessing the ECF VOlume status as Euvolemic Hyponatremia, Urine osm <100 what is the DDx

A

Primary polydipsia

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16
Q

after assessing the ECF VOlume status as Hypervolemic Hyponatremia, Urine osm >300 and urine Na+ is <20 mEq/L what is the DDx

A

Nephrotic syndrome
Heart failure
Cirrhosis

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17
Q

after assessing the ECF VOlume status as Hypervolemic Hyponatremia, Urine osm >300 and urine Na+ is >20 mEq/L what is the DDx

A

Acute or chronic kidney failure (Low GFR)

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18
Q

after assessing the serum osmolarity it is >305 but the patient is hyponatremia what is the DDx

A 
Hyperglycemia 
Hypertonic infusions
	-Glucose		-Glycerol
	-Mannitol		-Sorbitol
	-Glyceine		-Ethanol
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19
Q

how is the diagnosis of SIADH (syndrome of inappropriate antidiuretic hormone) made

A

Diagnosis of exclusion

must rule out cortisol deficiency, hypothyroidism, and other causes

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20
Q

what are the two causes of SIADH that I need to be aware of

A

Postoperative state

Small cell lung cancer: most common malignancy associated with ectopic ADH production

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21
Q

what are some drug classes that are associated with SIADH

A 
Antidepressants
Anticonvulsants
Antipsycotics
Anticancer drugs: cyclophosphamide
Misc: opiates, MDMA(extasy)
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22
Q

what is the rate of sodium correction in acute vs chronic hyponatremia

A

General rule of thumb is serum Na+ should be corrected over the same period for the time it took to get low

Acute <48 hours
-can have rapid correction little risk

Chronic: >48hrs

  • must be careful due to osmotic demyelination syndrome (ODS)
  • raise serum sodium 8-10 mEq/L a day and no more than 18 in first 48 hrs
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23
Q

what to give symptomatic patients who are hyponatremic

A

Give hypertonic saline (3%) to quickly raise sodiume

-3-4 mEq/L raise just to stop seizures then continue to raise slowly

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24
Q

what to do if you over correct the sodium

A

raise to fast, lower back down with:

  • 5% dextrose in water aka free water
  • DDAVP
  • D5W and DDAVP
  • discontinue some therapies that are raising sodiums
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25
how to treat Hypovolemic Hyponatremia: Renal fluid losses or extrarenal fluid losses
``` Isotonic saline (no symptoms) Hypertonic saline (symptoms) ```
26
How to treat Primary Polydipsia
Water restriction Hypertonic saline (symptoms)
27
How to treat SIADH
Hypertonic saline for symptoms SIADH: - Water restriction! - furosemide! - salt or urea tablets! - vaptans - Demeclocycline
28
How to treat Hypervolemic Hyponatremia
Water restriction | Furosemide
29
What are the major complications of Hyponatremia
``` Osteoprosis falls Seizures Coma Death from brain herniation Osmotic demylination syndrome (ODS) -occurring with rapid Na serum correction ```
30
how does Osmotic demyelination syndrome (ODS) | present and what are its diagnosis
demyleination occurs in the pontine and extrapontine neurons Clinical manifestations occur 2-6 days after Na correction: - dysarthria - dysphagia - Paraparesis - behavioral disturbances - Pseudobulbar palsy - seizures - coma - locked in syndrome - death Diagnosis: Head MRI but can be negative up to 4 weeks
31
what happens in the brain when given NA too quickly ffor ODS
initially brain swells due to decrease of osm and then will adapt by losing organic osmolytes and electrolytes -if correction is too fast brain cells will shrink and axonal shear damage occurs and there is disruption of blood brain barrier
32
how is Hypernatremia characterized? what patients is this common i? and what are some risk factors?
Hypernatremia: serum sodium is >145 mEq/L seen in infants and elderly risk factors: - trauma - burns - ICU - Dementia - Uncontrolled diabetes
33
what re the 2 processes that the indivdual becomes hypernatremia:
Unreplaced water loss (dehydration) - most common cause - Gastrointestinal water loss (vomiting, diarrhea) - renal water loss (DI, diuretics) - Insensible water loss (excessive sweating or in burn patients, respiratory loss) - impaired thirst mechanism Sodium overload - less common - Hypertonic saline infusion, hemodialysis, sodium bicarbonate infusion
34
what are the differences between acute and chronic hypernatremia and what are the clinical manifestation of hypernatremia?
acute: <48 hrs chronic: >48 hrs duration Hypernatremia results in cellular shrinkage since ther is an osmotic gradient for H20 to move out of the cells - irritabillity - altered mental status - letharagy - ataxia - seizures - hyperreflexia - intracerebral hemorrhages, subarachnoid, or subdural hematomas
35
what is the rate sodium correction of acute and chronic hypernatremia
acute: can have rapid correction of serum sodium with little risk of cerebral edema chronic: must be careful of rapid correction of serum sodium as patient is at higher risk for cerebral edema - goal is to lower serum sodium by 10-12 mEq/day
36
what are the 2 steps in treatment of hypernatremia?
Replace the water deficit - 5% dectrose in water (D5W) - other hypotonic solutions (1/2NS) Correct underlying cause leading to water loss
37
how does cerebral edema occur in hypernatremia rapid correction
due to the high osmolarity water leaves the brain and it rapidly adapts by accumulating electrolytes and organic osmolytes if rapid water enters and sodium the brain will rush with fluid and cause a hypertonic state and swell leading to cerebral edema
38
what are the primary regulators of the serum potassium (what cells, and what do they do) and how are immediate and long term responses controlled
THe kidney is the primary regulator of serum potassium '-principle cells (secretion) -a-intercalated cells (reabsorption) immediate response: transcellular shift long term control: renal excretion
39
what part of the nephron regulates urinary K+ secretion?
distal part of the nephron
40
how is hyperkalemia described and what are some risk factors?
Hyperkalemia is defined as serum potassium of >5.0 or 5.5 mEq/L risk factors: - AKI - CKD - DM - Medications(NSAIDS, ACE/ARB, aldosterone antagonists, heparin, etc) - Malignancy - Rhabdomyolysis - older age - acidosis
41
Clinical Manifestations of Hyperkalemia
Can range from asymptomatic to mild symptoms to life threatening Cardiac Arrhythmia - high enough potassium can lead to ventricular fibrillation - bradycardia from AV block - Asystole Skeletal muscle weakness -severe hyperkalemia can lead to respiratory failure from diaphragm weakness Metabolic acidosis - K+ ions enter the cells and H+ exit the cells to maintain electroneutrality - decreases ammoniagenesis and thus decreases ammonium chloride excretion in the kidneys therefore less net acid excretion
42
what is the effect of K+ on resting Membrane Potential?
High K+ concentration makes membrane potential less negative - initially increase excitabillity - however long term persistent depolarization leads to inactivation of sodium channels and cause decrease in membrane excitability leading to impaired cardiac conduction and or neuromuscular weakness/paralysis
43
what are some ECG changes in Hyperkalemia
6-7: peaked T waves 7-8: Flattened P wave, prolonged PR interval, depressed ST segment, peaked T waves 8-9: atrial standstill, prolonged QRS duration, further peaking T waves >9: sinusoid wave pattern = ventricular fibrillation
44
what are the two main reasons for hyperkalemia
Transcellular shift (increased K+ release from cells) Decreased Renal K+ excretion
45
what can cause a Transcellular shift causing increased K+ release from cells
- Pseudohyperkalemia - Metabolic acidosis - Insulin deficiency, hyperglycemia, hyperosmolality - increased tissue catabolism - Medications: B2 blockers, a1 adrenergic agonist, digoxin, succinylcholine, minoxidil - Exercise - Blood transfusions
46
what are some examples of Pseudohyperkalemia?
Results from an artificial increase in serum K+ due to K+ release from cells - RBC hemolysis - serum blood samples: due to clotting released from cells - leukocytosis
47
what are some of the causes for decreased renal K+ excretion?
Low aldosterone secretion -medications (ACEi, ARBs, Renin inhibitors, NSAIDS, Heparin, Ketoconazole) adrenal insufficiency Aldosterone resistance: - Potassium sparing diuretics (aldosterone receptor blockers, spironolactone or eplerenone) - sodium channel blockers (amiloride or triamterene) or antibiotics like trimethoprim AKI or CKD -Low GFR Hypovolemia Ureterojejunostomy Intrinsic renal defect
48
how is the diagnosis of Hyperkalemia made?
based on history and exam Laboratory tests are guided by suspected cause per history Fractional excretion of K+ (FEK)
49
how to interpret Fractional excretion of K+ (FEK)
< 10 percent indicates renal etiology >10% indicates extrarenal etiology
50
Hyperkalemia treatment for peaked T waves
Calcium gluconate which stabilizes cardiac membrane
51
Hyperkalemia treatment for transcellular shift
Insulin and dextrose B2 agonist (albuterol nebuilzer) Bicarbonate infusion
52
Hyperkalemia treatment for Potassium removal
Loop diuretic or thiazide Exchange resins: - Sodium polystyrene sulfonate (kayexalate) which exchanges Na+ ions for potassium primarily in the colon - zirconium cycloslicate (exchanges Na+ and H+ ions for ppotassium throughout intestines - Patiromer (exchanges Ca+ for potassium primarily in the colon Hemodialysis Low K+ diet discontinue medications that increase K+ (ACEi, ARB, ALdosterone blockers, potassium supplements, etc)
53
what is the characteristic of Hypokalemia and what are the risk factors?
Hypokalemia is defined by a serum potassium < 3.5 mEq/L risk factors include: - diarrhea - viomiting - medications: diuretics, insulin
54
Clinical Manifestations of Hypokalemia
usually not symptomatic until serum K< 3.0 mEq/L Cardiac Arrhythmias - Premature atrial contractions (PAC) - Premature ventricular contractions (PVC) - Tachycardia - Brady cardia - Ventricular fibrillation Skeletal muscle weakness -including diaphragmatic weakness Rhabdomyolysis Metabolic alkalosis Nephrogenic diabetes insipidous
55
what are the effects of K+ on resting Membrane potential
Low K+ concentration makes membrane more negative
56
what are ECG changes in hypokalemia
3. 5: low T wave 3: Low t wave and high U wave 2. 5: Low T wave, high U wave, low ST segment
57
3 main reasons for hypokalemia?
Transcellular shift (increased K+ uptake by cells) Extrarenal loss (GI loss, sweat, etc) Renal loss
58
what are the most common causes of hypokalemia via a Transcellular shuft
increased K+ uptake by cells Insulin -DM treatment or refeeding syndrome B2 agonist -Albuterol, catecholamines, etc Metabolic alkalosis Pseudohypokalemia Hypokalemic periodic paralysis barium toxicity
59
causes of Hypokalemia via extrarenal loss
Gastrointestinal loss: - Upper GI losses (vomiting, NG suctioning both leading to volume depletion leading to activation of RAAS thus aldosterone leads to Na+ reabsorption and secondarily increases K + secretion - Lower GI losses (intestinal K+ concentration is higher so diarrhea, laxatives, drains, fistulas Cutaneous loss -sweating Plasmapheresis Dialysis
60
causes of Hypokalemia via renal loss
Diuretics Increased mineralcorticoid activity - primary hyperaldosteronism (conns syndrome), hypercortisolism (cushing syndrome) - aldosterone increases Na+ reabsorption via ENaC that makes the lumen more negative and more K+ secreted by ROMK Hypomagnesemia Increased distal delivery of Na+ and water - nonreasorbable anions (bicarbonate, DKA, Hippurate toluene glue sniffing, penicillin derivative - polyuria RTA type 1 or 2 Intrinsic renal defect (bartter, gitleman, lpiddle syndrome
61
what are the diagnostic measures of Hypokalemia
laboratory tests per suspected history - Primary hyperaldosteronism - Hypercortisolism - Renal artery stenosis - RTA - ABG - Serum magnesium - Hypokalemic periodic paralysis Urinary K+ excretion: - 24 hour urine potassium - Urine K/Cr ratio
62
what does values on a 24 hour urine potassium test tell you that is below 25-30 mEq/day
>25-30 mEq/day suggest renal K+ wasting
63
what is considered K renal wasting in urine K/Cr ratio
Urine K/Cr ratio is normally below 13 mEq/g higher values seen in renal K wasting
64
what is the treatment for Hypokalemia?
Treat the underlying cause Replace the potassium deficit - give Potassium chloride - general rule is K level increases 0.1 mEq/L for every 10 mEq of KCl given Replace magnesium if low - magnesium sulfate - magnesium oxide

CPR Test II (6 decks)

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