U: Edema, Salt Retaining

Front 1

What is edema?

Is generalized edema associated with any changes in how the kidneys regulate salt and water?

Back 1

an increase in the interstitial fluid compartment of the ECF, manifested as palpable swelling of subQ tiss.

yes, Na and H20 retention.

Front 2

What is the equation that details the net filtration across capillary walls?

Back 2

Net filtration = Kf [(Pcap-Pif) – sigma x (∏cap-∏if)]
- the weird "n's" are "mean oncotic pressure"

Front 3

What is the most common cause of increased movement of fluid from the intravascular compartment to the interstitium? What causes this?

Back 3

^^hydrostatic pressure.

Salt and water retention, with transmission of the increased hydrostatic pressure to the capillaries by way of the venule end (remember, they have a sphincter on the arterial end which protects them from arterial P changes)
-- kidney, Ht fail, and liv dz are the main sources of this.

Front 4

This is seen in conditions causing protein loss from the kidney (nephrotic syndrome) or the intestine (protein-losing enteropathy) and in malnutrition... what is seen? Result?

Back 4

decrease in intravascular oncotic pressure.
- movement of fluid from intravascular --> interstitium

Front 5

In pregnancy, with local inflammation, with the administration or release of interleukin-2 and perhaps other factors such as interleukin 8, tumor necrosis factor, histamine and oxygen free radicals released during inflammatory or allergic reactions, sepsis and the adult respiratory distress syndrome.... what can be seen re: capillary fluid abs/filtration?

Back 5

increase in porousness of capillaries --> interstitial edema.

Front 6

What safeguards are in place to protect against interstitial edema?

Back 6

body can increase the hydrostatic pressure of the interstitial cmpt, which is usually ~0.
- can also increase lymphatic clearance.
- can decrease interstitial oncotic pressure as well.

Front 7

How does the kidney respond to low and high output Ht fail?

Back 7

similarly; by retaining Na and water despite expansion of the ECF in an effort to shore up the EABV / BP.

Front 8

Differentiate between the forward and backward mechanisms of edema formation in ht failure.

Back 8

forward: Na and water retention in an attempt to shore up EABV / BP
backward: venous pressure backup --> capillary fluid --> insterstitium.

Front 9

What is the difference between the effects of RAAS and SNS in compensated Ht fail vs decompensated ht fail?

Back 9

comp: tend to be useful in that they help restore CO and maintain tiss perfusion; work in conjunction with ANP and local vasodilatory prostaglandins.

decomp: maladaptive, counteract the effects of ANP.

Front 10

Do persistently high lvls of AngII and aldosterone damage the ht?

Back 10

increasing evidence suggests so, yes.

Front 11

What are the two theories that have been postulated to explain the pathogenesis of sodium and water retention in liver dz?

Back 11

- underfill: postulates that increased sinusoidal pressure with pooling of blood in splanchnic bed, peripheral vasodilation, and to a lesser degree, hypoalbuminemia --> formation of ascities at the expense of the intravascular volume --> \EABV

- overfill: initiating event re: liver Na retention is renal Na and H20 rtn -->^ECF --> ^Venous pressure --> increase capillary hydraulic pressure --> ascities.

Front 12

What is the postulated stim for the overfill pathogenesis in liver dz?

Back 12

The stimulus for primary sodium and water retention by the kidney is a postulated hepatorenal neural reflex owing to increased intrasinusoidal pressure rather than increased portal pressure.

Front 13

What are the three most common causes of edema?

Back 13

Ht Fail, liver failiure, nephrotic syndrome (renal dz)

Front 14

Explain the pathogenesis of nephrotic syndrome. Complications?

Back 14

increase in the permeability of the glomerular capillary wall to proteins, including large molecular weight proteins, leading to an increase in urinary protein excretion exceeding 3.5 grams of protein in 24 hours.
--> hypoalbuminemia
--> edema
--> lipiduria
--> dyslipidemia

atherosclerosis, ^ increase DVT risk, can also be a decrease in GFR, hematuria.

Front 15

Which, underfill or overfill is the major mechanism responsible for Na rtn in nephrotic syndrome?

Back 15

overfill: primary Na and H20 rtn by kidney w/o \EABV or neural/hormonal factors.

Front 16

Explain underfill theory in relation to Na retention in nephrotic syndrome.

Back 16

Increased proteinuria --> decreased interstitial oncotic pressure --> arterial underfilling --> SNS, RAAS, ADH, altered kidney blood flod / GFR --> Na retention

Front 17

What is expanded in most patients in nephrotic syndrome? what does this mean re: tx?

Back 17

ECFV; it means that diuretics aren't a good idea. Should tx to reverse the glomerular dz with corticosteroid/cytotoxic agents, low Na diet, *cautious* diuretic use, ACE inhibitors, etc.