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Acid-Base and Nutrition > ECF Volume and Water Metabolism > Flashcards

ECF Volume and Water Metabolism Flashcards

1
Q

How do you calculate/estimate total body water? ICF? ECF? Plasma Water? Blood volume?

A

TBW= 60% BW in kg 9in women or elderly it is only 50%; 2/3 TBW; 1/3 TBW; 1/4 EC water; plasma water/(1-Hct)

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2
Q

What is hypovolemia?

A

loss of salt and water

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3
Q

What is hypervolemia?

A

gained both water and salt

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4
Q

What is the major determinant of ECF volume? What happens as it increases? decreases?

A

sodium in ECF; ECF volume increases and volume overload will result; decrease in ECF resulting in volume depletion

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5
Q

What are the three systems responsible for regulating body sodium? How?

A

RAAS (funct. of renal renin release), SNS (catecholamines: NE, Epi), ANP and renal vasodilators; all promotes renal Na retention

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6
Q

What is effective circulating volume (effective arterial blood volume)?

A

blood volume detected by volume sensors; not directly measurable; pressure perfusing the arterial baroreceptors

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7
Q

Where can effective circulating volume be sensed? How?

A

atria of heart (ANP), carotid sinus and aortic arch (SNS), afferent glomerular arterioles (Renin); arterial perfusion pressure or stretch in tissues

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8
Q

what are the two systems that are effectors of volume? What are there components?

A

systemic hemodynamics: SNS, Ang II; Renal Na excretion: GFR, Ang II, Peritubular capillary hemodynamics, aldosterone, SNS, ANP, pressure natriuresis

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9
Q

How and where is renin released?

A

JG cells sense changes in renal perfusion and respond by producing changes in release of renin; dec. ECF-> inc renin-> sodium retention

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10
Q

What stimuli increase aldosterone? What does aldosterone do?

A

inc. plasma Ang II levels, dec. Pna, inc Pk; inc Na reabsorption by CD

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11
Q

What stimuli increase catecholamines? What does catecholamines do?

A

SNS activation; inc. Na reabsorption by PCT

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12
Q

What stimuli causes release of ANP? What is ANPs action?

A

atrial stretch; dec. Na reabsorption by CD

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13
Q

What hormone is primarily responsible for osmoregulation? Derangement in osmoregulation results in what?

A

ADH; hypo or hypernatremia

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14
Q

What are the sensors in osmoregulation? Effectors? What’s affected?

A

plasma osmolality by hypothalamic osmoreceptors and effective circulating volume depletion; ADH and thirst; water excretion and intake

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15
Q

what does serum sodium levels tell us?

A

tonicity not volume status, function of renal water handling

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16
Q

What happens when ADH is increased?

A

increased permeability of renal CT to water, water flow down gradient to be reabsorbed into medullary interstitium, renal water retention

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17
Q

What are some things that can be evaluated clinically to assess fluid balance?

A

intake & output, weight change, skin turgor/edema, mucous membranes, lung sounds (crackles/dullness), JVD & Hepato-Jugular Reflux, Orthostatic BP & HR, CVP (8-10), CO, Urine Na & Osm, Serum Nitrogen:Creatinine

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18
Q

What are signs and symptoms of hypovolemia?

A

orthostatic decrease in BP with increase HR, decreased pulse volume, venous pressure, skin turgor, and dry mucous membranes

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19
Q

what are some extra renal causes of hypovolemia?

A

(urinary Na low); GI (Vomit, diarrhea, NG or bowel aspiration, intestinal fistulae), skin/resp (burns, heat, skin disease, CF, drainage pleural effusion)

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20
Q

What are some renal causes of hypovolemia?

A

high urinary Na; Extrinsic (Solute or Osmotic diuresis- diabetic ketoacidosis, diuretics, adrenal or aldosterone insufficiency), Intrinsic (diuretic phase of acute RF, post obstructive diuresis, salt wasting nephropathy- barters & gitlemans

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21
Q

How do you treat hypovolemia?

A

IV normal saline, oral and enteral- salty food and broth, salt tablets, encourage fluids

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22
Q

What are clinical manifestations of hypervolemia?

A

hypertension, edema, pulmonary crackles, edema, pleural effusion, ascites, JVD

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23
Q

What are causes of hypervolemia?

A

primary or secondary Renal sodium retention

24
Q

What are causes of primary renal sodium retention?

A

hyperaldosteronism, Cushing’s Syndrome, Inherited Hypertension, Renal Failure, Nephrotic Syndrome

25
Q

What are causes of secondary renal sodium retention?

A

Hypoproteinemia, Low cardiac output, Peripheral Vasodilation

26
Q

Causes of hypoproteinemia?

A

nephrotic syndrome, protein losing enteropathy, cirrhosis w/ ascites

27
Q

Causes of low cardiac output?

A

Pericardial effusion, CHF, Constrictive pericarditis, Valvular disease, Pulmonary Hypertension, Cardio-myopathy

28
Q

Causes of peripheral vasodilation?

A

shunt flow away from kidney; pregnancy, sepsis, anaphylaxis, arteriovenous fistula, trauma, cirrhosis, idiopathic edema, vasodilating drugs

29
Q

How do you treat hypervolemia?

A

slat and fluid retention, low Na diet, diuretics, drainage of sequestered fluid, correction of hemodynamics, Dialysis of fail medical management

30
Q

What is the serum sodium level indicative of hyponatremia? Hypernatremia?

A

< 135 mEq/L; > 145 mEq/L

31
Q

What is the most common electrolyte abnormality in hospitalized patients? Incidence rate in other populations?

A

hyponatremia (15-20%), 7% in ambulatory population, up to 53% in elderly

32
Q

what is the difference between acute and chronic hyponatremia?

A

acute48 hours, brain excretes intracellular osmolytes to avoid cerebral edema

33
Q

what are the stages and changes seen with brain adaptation and therapeutic correction with hyponatremia?

A

immediate- water gain in brain-> low osm-> rapid adaptation-loss of Na, K, and Cl-> slow adaption- loss of organic osmolytes; if improper therapy (rapid correction)-> osmotic demyelination

34
Q

What are the three classes of hyponatremia?

A

psuedohyponatremia, hyperosmolar (translocation) hyponatremia, hypo-osmolar hyponatremia (true)

35
Q

What are the causes of pseudo-hyponatremia?

A

hyperlipidemia (familial dyslipidemia in thousands), hyperparaproteinemia; iso-osmolar condition, mostly historical interest; false result cuz measure [Na] in whole plasma not just liquid phase

36
Q

What are the causes of iso or hyperosmolar hyponatremia?

A

shift from intracellular to extracellular compartments, effective osmoles drag water out: glucose (100mg/dL above 100= fall of 1.6mEq/L Na, mannitol

37
Q

what are the hypovolemic causes of hyponatremia?

A

Renal- osmotic diuresis or diuretic excess, Extra renal- Vomit, diarrhea, 3rd spacing- burns, pancreatitis, trauma, and hemorrhaging

38
Q

How do you treat Hypovolemic Hyponatremia?

A

asymptomatic- normal saline, restore ECF (Watch), symptomatic- 3% saline Slow, hypertonic fluid helps decrease cerebral edema (intracranial pressure)

39
Q

What are causes of hypervolemic hyponatremia?

A

CHF, Cirrhosis, Nephrotic syndrome

40
Q

How do you treat hypervolemic hyponatremia?

A

asymptomatic- decrease dietary Na, fluid restrict, loop diuretics; symptomatic- 3% saline and loop diuretics

41
Q

what are causes of Euvolemic hyponatremia?

A

glucocorticoid deficiency (Addison’s), hypothyroidism, psychosis-> due to meds or increased thirst perception (psychogenic polydipsia)

42
Q

what is psychogenic polydispsia?

A

hyponatremic by overwhelming kidneys ability to excrete H2O, ADH appropriately depressed, UNa < 100mOsm, > 10-12 L per day H2O

43
Q

What is post-operative hyponatremia?

A

excessive infusion of electrolyte free water (hypotonic saline or D5W) and presence of vasopressin which prevents its excretion

44
Q

what causes SIADH? diagnostic criteria?

A

carcinoma, pulmonary disorders, CNS disorders, Drugs; Posm100, euvolemia, elevated UNa despite normal Na and H2O intake, absence of: adrenal, thyroid, pituitary or renal insufficiency or diuretic use

45
Q

How do you treat euvolemic hyponatremia?

A

Neuro symptoms- 3% saline, no neuro- SIADH: fluid restrict, high Na diet/high protein diet, others: treat underlying cause

46
Q

What is osmotic demyelination?

A

most commonly affects central pons (CPM), all ages esp pre-menopausal women, common after liver transplant, risk related to severity and chronicity of hyponatremia; seen T2 MRI 2wks later

47
Q

when is a patient dehydrated?

A

hypernatremic (>145mEq/L) and hypovolemic

48
Q

what populations are at risk for developing hypernatremia and why?

A

impaired thirst- elderly, hypothalamic lesion, psychosis or impaired access to water- dementia, delirium, infants

49
Q

What are the causes of hypovolemic hypernatremia?

A

renal loss (osmotic or loop diuretic, post-obstruction diuresis) or extra renal loss (burns, sweating, diarrhea, fistulas)

50
Q

How do you manage hypernatremia?

A

calculate water deficit, desired correction no greater than 0.5mEq/L/hr or 8-10 mEq/L/day

51
Q

What are iatrogenic and other causes of hypervolemic hypernatremia?

A

administration of sodium bicarb, NCl or blood products may increase TBNa and TBW

52
Q

What is diabetes insipidus?

A

defect in renal H2O conservation, Central: impaired synthesis, transport, storage or release of ADH (hypothalamus/pituitary) or Nephrogenic: reduced response to ADHin CT (hereditary or acquired- RF, hypercalcemia, drugs)

53
Q

How do you tell the difference between Central and Nephrogenic DI?

A

Pavp- C- not detectable, N >5pg/mL; water restrict loss 3-5% BW, aqueous AVP; inc. Uosm w/ AVP- C- substantial, N- little or none

54
Q

How do you treat CDI? NDI?

A

Central- desmopressin 5-20mcg 1-2 per day, low Na and protein diet; NDI- remove offending drugs (lithium), HCTZ or Amiloride, Low Na and protein diet

55
Q

How does the brain adapt to hypernatremia?

A

H2O moves extracellularly and electrolytes intracellularly to maintain brain volume; chronic-accumulate organic osmolytes increase brain volume; rapid correction may cause cerebral edema

56
Q

How is hypernatremia managed?

A

calculate water defecit, desired rate of correction no greater than 0.5mEq/L/hr or 8-10mEq/day

Acid-Base and Nutrition (6 decks)

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