dysnatremias Flashcards

1
Q

ICF=

A

66% tbw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ECF=

A

33 % tbw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

blood volume=

A

12% tbw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hypovolemic hypernatremia

A

most common. renal losses (osmotic diuresis by means of glucose, urea, mannitol use). insensible losses (through sweating, fever, respiration). GI losses (through diarrhea).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

euvolemic hypernatremias

A

renal losses (through diabetes insipidus nephrogenic or central). variable hypothalamic disorder (primary hypodipsia, resetting of osmostat). normal intravascular status but sodium is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hypervolemic hypernatremia

A

hypertonic saline administration. sodium bicarbonate administration. primary hyperaldosteronism. Too much na related fluid such as IV hypertonic saline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

the 2 defense mechanisms against hypernatremias

A

stimulation of ADH release (resulting in maximal urinary concentraton) and thirst.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypernatremia

A

almost never found in an alert patient who has access to water and a normal thirst mechanism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

concentration of urine requires two basic conditions:

A

a hypertonic medullary interstitium. osmotic equilibrium of urine in the collecting duct that has the hypertonic interstitium (requiring ADH).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Central diabetes insipidus

A

occurs when secretion of ADH is impaired through disruption of the hypothlamic neclei, osmoreceptors. through disruption supraopticohypophysial tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

central DI common causes

A

head trauma, hypoxic or ischemic encephalopathy, idiopathic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

nephrogenic diabetes insipidus

A

the countercurrent mechanism in the kidney is disrupted or the ability to respond to ADH is impaired. lithium. osmotic diuresis. sickle cell anemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clinical manifestations of hypernatremia

A

neurologic manifestations. lethargy, weakness, irritability, hyperreflexia, seizures, coma, and even death, are the result. patients with DI usually do not present with neurologic sxs because of the powerful thirst mechanism which protects them from hypernatremia. instead, these pts complain of polydipsia, polyuria, and nocturia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

diagnosis of hypernatremia

A

H and P:
recent fluid losses, alteration in mental status, and thirst.
assessing the pts volume status and measuring urine osmolality and urine sodium concentration can be helpful in establishing the cause of hypernatremias and in guiding therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

treatment of hypernatremia

A

rapid correction should be avoided because of the brain’s adaptive response to hypernatremia and the potential risk of cerebral edema. the current recommendation is to lower the serum sodium concentration by about .5 meq/l per hour and to replace no more than half the water deficit in the first 24 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hypovolemic hypernatremia treatment

A

normal saline solution is indicated initially to correct the intravascular volume deficit. when that is accomplished, more hypotonic fluids can be used.

17
Q

hypervolemic hypernatremia treatment

A

removing the source of salt excess, administering diuretics, and replacing water are important to successful therapy.

18
Q

manifestations of hyponatremia

A

correlate with the serum sodium concentration and more important, with how rapidly the condition developed. anorexia, nausea, lethargy, and apathy. more advanced sxs include disorientation, agitation, seizures, depressed reflexes, focal neurologic deficits.

19
Q

diagnosis of hyponatremia

A

important hx: medications (particularly thiazide diuretics), recent vomiting, diarrhea or excessive sweating with hypotonic fluid ingestion, recent surgery, and a history of psychiatric illness, CHF, cirrhosis, or nephrotic syndrome with renal failure.

20
Q

hyponatremia physical exam findings

A

assessment of volume status. orthostatic vital signs, skin turgor, mucous membrane appearnace, jugular venous distension, findings of edema, and wedge pressure and central venous pressure.

21
Q

euvolemic hyponatremia

A

adh excess (through syndrome of inappropriate ADH, use of thiazide diuretics or oral hypoglycemic agents). pain, postoperative state, cortisol deficiency. hypothyroidism. decreased solute intake. psychogenic polydispsia. resetting of osmostat (pregnancy, psychiatric disorders)

22
Q

hypovolemic special mention

A

pyschogenic plydispsia. ingest rapidly too much water. related to psychiatric disease or psychiatic drugs. rarely see on other drugs that cause severe dryness of the mouth.

23
Q

treatment failure central pontine myelinolysis

A

demyelination of the pons. mutism, dysphasia, spastic quadriparesis, psedobulbar palsy, delirium, coma, and even death. Key point: raising the serum sodium concentration more than 25 or to a normal or above normal level in the first 48 hours increases the liklihood of central pontine myelinolysis.

24
Q

treatment of hyponatremia

A

eliminate the cause. restrict water. normal saline. may correct up to about 120 fairly rapidly then slow down and increase sodium by about 12 meq every 12-24 hours.