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MS2 Renal > 9/10- Clinical Approach to Body Volume Disturbances > Flashcards

9/10- Clinical Approach to Body Volume Disturbances Flashcards

1
Q

What is normal ECF osmolality? Na?

A

Na = 140 mEq/L

Osm = 285 mOsm/kg

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2
Q

What is normal ICF osmolality? K?

A

K = 140 mEq/L

Osm = 285 mOsm/kg

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3
Q

What is the equation for plasma osmolality?

A

2Na + glucose/18 + BUN/2.8

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4
Q

Water balance (pictures)

A
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5
Q

How is total body water regulated?

A
  • Thirst
  • ADH
  • The kidneys
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6
Q

What are the functions of angiotensin II?

A
  1. Stimulates production of aldosterone
  2. Acts directly on arterioles to cause vasoconstriction
  3. Stimulates Na+/H+ exchange in the proximal tubule
  4. Stimulates thirst center
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7
Q

What are the functions of aldosterone?

A
  1. Stimulates reabsorption of Na+ and excretion of K+ in the late distal tubule and collecting tubule.
  2. Stimulates activity of H+ ATPase pumps in the late distal tubule and collecting tubule.

Also:

  • Increases the water permeability of the collecting tubule
  • Mildly increases vascular resistance
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8
Q

Where is ADH made? How is release regulated?

A
  • Synthesized in the hypothalamus and stored in the posterior pituitary
  • Released in response to plasma hyperosmolality and decreased effective circulating volume
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9
Q

What is the driving force for glomerular filtration rate (GFR)?

A

Hydrostatic pressure

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10
Q

What drugs affect GFR?

A

Drugs that regulate RBF

  • Xanthines (caffeine, theophylline, aminophylline) increase CO and vasodilation, resulting in increased RBF
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11
Q

T/F: Filtration is a nonselective process

A

True

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12
Q

What determines filtration (factors)?

A

Function of:

  • GBM permeability
  • Net filtration pressure across the capillaries
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13
Q

What types of substances undergo filtration? What remains in the blood?

A
  • All small molecules (electrolytes, AAs, glucose, drugs and metabolic waste) undergo filtration
  • Cells and large molecules (lipids and proteins) remain in the blood
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14
Q

How many L get filtered per day? What are the main ions?

A
  • 180 L/day filtered
  • Mostly Na, Cl and bicarbonate ions
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15
Q

What is normal GFR?

A

~120 mL/min

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16
Q

More than __ of filtered water and electrolytes are reabsorbed

A

More than 99% of filtered water and electrolytes are reabsorbed

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17
Q

T/F: water is actively reabsorbed to prevent excessive loss following filtration

A

False

  • Water follows passively (facilitated by water channels AQPs) along the osmotic gradient created by solute reuptake
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18
Q

T/F: Many solutes undergo active transport to be reabsorbed

A

True

  • AA, glucose, phosphate, electrolytes… etc
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19
Q

What are the two main kinds of “pumps” used in active tubular secretion?

A
  • For organic acids (uric acid, p-aminohippuric acid, diuretics, antibiotics, etc…)
  • For organic bases (creatinine, procainamide, choline, etc…)
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20
Q

Where does the process of active tubular secretion mainly take place?

A

Proximal tubule

21
Q

What are the main ion handling functions of the proximal tubule?

A
  • 60% of total NaCl and water reabsorbtion
  • 85% of total NaHCO3 reabsorption occurs in the early PT (dependent upon carbonic anhydrase)
  • Organic acid/base secretion
22
Q

There are competitive interactions between diuretics and what?

A

Uric acid (probenecid) and other organic compounds (may impact diuretic action)

23
Q

What happens in the tDL?

A
  • Does NOT participate in salt reabsorption
  • Passive flux of water through AQP1 (driven by high medullary osmolality)
24
Q

What happens in the TAL?

A

Dilution and concentration segment

  • Responsible for 25% of NaCl reabsorption
  • Impermeable to water
  • NaCl transport system: Na.K.2Cl cotransporter (the target of loop diuretics)
  • Major site of Mg and Ca reabsorption

Solute removal without water uptake results in urine dilution

NaCl uptake increases the medullary interstitial osmolality and contributes to the concentrating mechanism

25
Q

What happens in the DCT?

A

Diluting segment

  • Water impermeable
  • Responsible for 5-10% NaCl re-absorption
  • NaCl transporter is blocked by thiazide diuretics
  • Aldosterone exerts a significant influence on NaCl co-transporter

(Volume depletion)

  • Ca is actively reabsorbed (this process is regulated by parathyroid hormone)
26
Q

What happens in the collecting duct?

A
  • Responsible for 2-5% of Na re-absorption
  • Na transport is mediated by Na channels in principal cells (stimulated by aldosterone)
  • Major site of potassium (K+) secretion (negatively charged lumen)
  • ADH increases water permeability in collecting tubule, through its action on AQP2, causing concentrated urine (ADH determines final urine concentration)
27
Q

Na and H2O transporters along nephron (picture)

A
28
Q

What may cause fluid deficiency (main causes)? Fluid excess?

A

Deficiency:

  • Volume depletion (hypovolemia)
  • Dehydration

Excess:

  • Volume excess
  • Hypotonic hydration
29
Q

What may cause volume depletion?

A

GI losses:

  • Nausea
  • Vomiting
  • Diarrhea

Renal losses: diuretics

Skin or Respiratory losses: burns

Third Spacing

  • Intestinal obstruction
  • Pancreatitis.
30
Q

What history might a pt present with in the cause of volume depletion?

A

Thirst, easy fatiguability, muscle cramps, postural dizziness.

More severe fluid loss can lead to

  • chest pain, (coronary ischemia)
  • abdominal pain (mesentric )
  • lethargy and confusion (cerebral vascular beds)

Weight loss

31
Q

Clinical signs of volume depletion?

A
  • Dry skin including axilla
  • Decreased skin turgor
  • Dry mucus membranes
  • Thready pulse, low arterial blood pressure
  • Orthostatic hypotension
  • Decreased jugular venous distension
32
Q

Lab abnormalities seen with volume depletion?

A
  • Elevated BUN/CR ratio
  • Decreased urine

Sodium

  • FeNa – Fractional excretion of sodium.
  • Hemoconcentration
33
Q

Therapy for volume depletion?

A

Isotonic IVF

  • Normal saline- 0.9% NaCl
34
Q

What is seen in volume overload state

A

Edema- palpable swelling produced by expansion of the interstitial fluid volume

  • Dependent bilateral edema
  • Lymphedema
  • Myxedema
  • Localized edema
35
Q

What is the pathophysiology of edema?

A
  • An alteration in capillary hemodynamics that favors the movement of fluid from the vascular space into the interstitium.
  • The retention of sodium and water by the kidneys.
36
Q

The exchange of fluid between the plasma and the interstitium is determined by what?

A

Hydraulic and oncotic pressures.

Starling’s Law:

Net filtration = LpS x (Δ hydraulic pressure - Δ oncotic pressure) = LpS x [(Pcap - Pif) - s(nx cap - nif)]

37
Q

What factors cause edema/volume overload?

A

1. Increased venous pressure

  • Blood volume expansion (heart failure, renal disease)
  • Venous obstruction (hepatic cirrhosis, deep venous thrombosis)

2. Hypoalbuminemia

  • Loss of albumin in urine (nephrotic syndrome)
  • Decreased hepatic albumin synthesis (hepatic cirrhosis)

3. Increased capillary permeability

  • Burns
  • ARDS
  • Malnutrition syndrome
  • Idiopathic capillary leak syndrome

4. Lymphatic obstruction (lymphedema)

  • Primary: genetic defect
  • Secondary: radiation, parasites

5. Renal sodium retention

  • Inability to excrete the Na and water (pts with kidney disease)
  • Appropriate compensatory response to effective circulating volume depletion, with urine Na under 20 meq/L
38
Q

Clinical manifestations of edematous states?

A
  • Jugular vein distention
  • Pulmonary edema
  • Pleural effusions &/or pericardial effusions
  • Ascites
  • Edema of the lower extremities (> 3L)
  • Puffy eyes
  • Dyspnea (pulmonary congestion): PND, DOE, Orthopnea
39
Q

Describe edema in heart failure: pathogenesis, effect on ions…

A

Perception of low effective arterial blood volume (EABV) due to heart failure

  • Activation of sympathetic nervous system,

Renin-AII- Aldosterone and ADH.

Na and water retention by the kidney

  • Urine studies
  • Low FENa, High SG
40
Q

Describe the problem with systolic heart failure.

Treatment?

A

Problem = Low EF

Treatment:

  • Treat underlying causes
  • Na & water restriction
  • Diuretics

—- loop diuretics

—- Combination of loop diuretic and thiazide

—- Aldosterone antagonists

  • Digoxin
  • ACEi/Angiotensin II receptor blocker
  • Beta blockers
  • Vasodilator: Isosorbide and hydralazine
41
Q

Describe the problem with diastolic heart failure.

Treatment?

A

Problem = Inadequate LV filling (normal EF)

Treatment:

  • Treat underlying causes
  • Control of HTN
  • Control of ventricular rate in patients with tachycardia
  • Control of edema with salt and water restriction and diuretics
42
Q

Describe the problem with cirrhosis: what is sensed? Ion handling?

A

Problem:

  • Perception of low EABV due to perpetual arteriolar vasodilatation (?NO, ?PGs).
  • As in CHF, sympathetic nervous system, Renin-AII-Aldosterone and ADH are activated.
  • Na & water retention follow (low FENA)
  • Hepatic flow obstruction favors the formation of ascites
43
Q

Treatment for edema in cirrhosis?

A
  • Treat underlying causes of hepatic cirrhosis: ETOH, hepatitis
  • Na restriction, water restriction if SNa
44
Q

What is the problem with nephrotic syndrome (NS)?

A

(Nephrotic syndrome: problem with glomerulus so that pt is losing protein…)

  • Activation of the intra-renal renin/angiotensin system, with resultant Na & water retention.
  • The cause for activation of the renal AII-system is unknown.
  • Except in some children with nephrotic syndrome, the EABV is normal in spite of low serum albumin.
45
Q

Treatment in NS (nephrotic syndrome)?

A
  • Treat the primary renal disease.
  • Na and water restriction.
  • High dose loop diuretic.
  • Combination of diuretics.
  • ACE inhibition is useful (reduce glomerular perfusion and thus proteinuria)
46
Q

What is the problem causing edema in renal failure and/or GN?

A

Problem = decreased GFR (decreased number of functioning nephrons), leading to diminished ability to eliminate Na load

47
Q

How to treat edema in renal failure and/or GN?

A
  • Low salt diet
  • Diuretics
48
Q

Conclusions:

  • Disturbances of water balance reflect Dysnatremias.
  • Disturbances of volume

—- reflect sodium content abnormalities

—- involve abnormalities in Thirst mechanism, RAS and ADH.

  • Volume depletion

– IVF

– Saline

  • Volume overload

– Low salt diet and Diuretics. ACEI in Nephrotic Syndrome.

A

(:

MS2 Renal (25 decks)

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