Renal- Disordes Of Volume Regulation

Front 1

Weight change
1) ECF Volume depletion
2) ECF Volume Expansion

Back 1

1) quick loss
2) quick gain

Front 2

Intravascular Signs of Mild ECF volume depletion
1) supine BP
2) orthostatic fall in BP
3) orthostatic rise in HR
4) JVP

Back 2

1) normal
2) increased > 15mmHg
2) increased > 15 BPM
4) increased 5-7 cm @ 45 degrees

Front 3

Intravascular Signs of Severe ECF volume depletion
1) supine BP
2) extremities
3) Echo finding
4) PCWP

Back 3

1) Hypotensive <80 systolic
2) cold and weak pulses (shock_
3) low filling of IVC
4) Reduced

Front 4

findings upon palpation for:
1) ECF Volume depletion
2) ECF Volume Expansion

Back 4

1) diminished skin turgor
2) dependant pitting edema, hepatic congestion (enlargement)

Front 5

ECF colume expansion pulmonary finding

Back 5

Rales, wheezing (Cardiac asthma)

Front 6

Findings for ECF volume depletion:
1) mucous membranes
2) IOP
3) axilla

Back 6

1) dry
2) reduced
3) no diapheresis

Front 7

Findings for ECF volume overload
1) abdominal
2) XRay

Back 7

1) ascites
2) Pleural effusion

Front 8

Localized edema suggests:

Dont not mistake these for signs of volume overload

Back 8

damage to local capillary bed (ARDS, burns, allergy, rhabdomyolysis)

lymph obstruction or removal of veins

Front 9

Extensive non-pitting soft tissue edema is a sign of:

Back 9

Myxedema for hypothyroidism- accumulations of mucopolysaccharides which trap water

Front 10

Pitting edema requires how much extra fluid accumulation

Back 10

3L in the ECF so 9L total

Front 11

1) TBW is what % of Total body mass
2) ICV is what % of TBW
3) ECV is what % of TBW
4) Intravascular volume is what percent of ECV?

Back 11

1) 60%
2) 67%
3) 33%
4) 25%

Front 12

Three factors needed for pitting edema to develop:

Back 12

1) Alteration in Starling forces across a Capillary
2) Continued intake of salt and increased thist
3)Renal retention of salt and water as governed by the CVMP

Front 13

Ways in which ECF can be lost

Back 13

1) vomit, diarrhea, GI tube drainage
2) SubQ tissue (burns)
3) Bleeding into gut
4) Oozing into peripheral wounds
5) Urine with high Na++
6) Third spaces

Front 14

Thirsd spaces in the body where ECG can be lost to.

Back 14

intestinal lumen
skeletal muscle [rhabdomyolysis], lymphatics
pancreas during inflammation
bleeding into a body cavity (hematoma)

Front 15

4 ways to develop inefective intravascular volume

Back 15

1) Functional Arterial Underfilling-
Central baroreceptors cannot adequately sense volume (slow upstroke)
2) Funtional Vasodialtion- shunting to a compartment where thee are few baroreceptors and a large capacitance
3) Filtration failure- Kidney as an end organ canot filter
4) Functional Nephron misdirection- mized signals to remain avid even when not directed to do so by the CVMP. i.e. CVMP is off, but the kidney is stimulated from another source

Front 16

Two causes of functional arterial underfilling

Back 16

1) Myocardial Dysfunction
2) Nephrotic Syndrome, wherein albumin is lost, and the IVV is lost to the ISV

Front 17

Three causes of functional vasocialtion

Back 17

1) preganancy
2) Large AV fistula
3) Sepsis or cirrhosis with large amounts of shunt through low resistance abdominal beds

Front 18

Causes of Filration Failure

Back 18

Renal Artery blockage
clogged or damaged glomerlui
Rena Artery constriction

Front 19

Intinsic heart failure- Pathway to edema

Back 19

1) Decreased Contractility
2) Decreased stimulation of phasic barorceptor
3) Perception of decreased IVV
4) CVMP activated-releases catecholamines
5) Causes Increased CO and renin release by JGA, and also ADH secretion by posterior pituitary
6) ANP is also stimulated by resultant atrial stretch but this is insufficienct to overcome effects above
7) sensitization to ADH and desensitization to tonically high ANP
8) Increased salt and water retention

Front 20

How is ANP desensitization mediated

Back 20

more expression of renal endopeptidases that degrade ANP

Front 21

How does Severe nephrotic syndrome (albumin filtration) cause HTN

Back 21

1) Increased PCT absorbtion of albumin binds a receptor that otherwise would bind submembrane vesicles containing Na+/H+ exchangers and keep them from entering the membrane.

2) Dont understand this, but it seems as though ANP insensitivity is also involved

Front 22

How does Severe liver disease cause HTN?

Back 22

Portal HTN causes dilation of other ateries to produce shunt pathways. This shunts blood past the renal circulation and into slowly perfused tissuew where fluid can have a difficult time reentering capillaries once it has left. Reduced GFR and CVMP overactivation cause massive fluid and salt retentiosn

Front 23

Pre-renal azotemia is characterized by what important parameter regarding IVV?

Back 23

Reduced EFFECTIVE IVV resulting in CVMP activation.
This may be due to truly decreased IVV, or inneffective IVV due to Heart failure

Front 24

Genereal symptoms of pre-renal azotemia

Back 24

1) hyponatremia
2) azotemia
3) oliguria (small urine output)
4) metabolic alkalosis
5) Hypokalemia (activation of thirst and ADH secretion overcome increased salt appetite and retention.)

Front 25

Reasons that these symptoms are seen in Pre-Renal Azotemia:
Hyponatremia

Back 25

CVMP activates ADH and thirst to increase IVV even though electrolytes are at normal concentrations. This will dominate the activation of salt appetite and salt conservation because of the primacy of volume over osmolality

Front 26

Reasons that these symptoms are seen in Pre-Renal Azotemia:
azotemia

Back 26

ADH causes insertion of Urea channels into TALH which ensures a high concentration gradient by reabsorbing NH3 into the interstitium.

Front 27

Reasons that these symptoms are seen in Pre-Renal Azotemia:
oliguria

Back 27

3) oliguria- ADH secretion

Front 28

Reasons that these symptoms are seen in Pre-Renal Azotemia:
Metabolic Alkalosis

Back 28

Aldo indirectly sitmulates H+ ATPase of MCD and PCT ammoniagenesis.
AII stimulates PCT Na/H exchanger.

all of these promote H+ excretion

Front 29

Reasons that these symptoms are seen in Pre-Renal Azotemia:
Hypokalemia

Back 29

Na+ reclamation leads to K+ excrection. Basal Na+/K+ ATPase increases intracellular K+ when driving Na+ into the interstitium. This K+ can leak back out in to the lumen through K+ permeable apical pore

Front 30

1) Most common volume disorder
2-4) pharmacological treatment and justification

Back 30

1) Acute exacerbation of Heart failure
2) IV loop diuretic (furosemide)
3) Positive inotrope (dobutamine, cardiac glycosides)
4) preload and afteroad reducers (Nitrates and ARBs)

Front 31

These three pharmacological treatments for acute CHF exacerbation can have reflex side effects that are counterproductive. Describe the Reflex
1) Loop diuretics
2) inotropes- dobutamine
3) preload and afterload reducers (Nitrates and ARBs)

Back 31

1) by increasing Na+ presentation to the Macula Densa can cause TGF, reducing renal perfusion

2) Dobutamine activates Adenylate cyclase which increases Cardiac expenditure and predisposes to arrythmias

3)Preload and afterload reducers can perpetuate low BP when it is already low and renal autoregulation ca least accomodate it.

Front 32

New agent available for the treatment of CHF:
Describe Ca++ sensitizers

Back 32

Increase sensitivity if cardiac troponin to Ca++

Front 33

New agent available for the treatment of CHF:
Cardiac Lusitropy stimulators

Back 33

Speed cardiac myocyte relaxation by stimulating Ca++ ATPase of Sarcplasmic reticulum

Front 34

New agent available for the treatment of CHF:
Endothelin antagonists

Back 34

reduce renal vasoconstriction

Front 35

New agent available for the treatment of CHF:
Adenosine receptor agonists

Back 35

Decrease TGF which is normally caused by increased presentation of Na+ (as in natriuresis) to macula densa. When this drug is given, Macla densa stimulation will not result in constriction of afferent arteriole via adenoside stimulation of mesangial cells

Front 36

The DCT sensory at the macula densa which senses Na+ is what kind of protein

Back 36

Na/K/Cl channel

Front 37

Treatment for Hypovolemia:
1) if severe blood loss and crit<25
2) if less blood loss and normal crit

Back 37

1) packed RBC transfusion
2) saline infusion

Front 38

2 days post MI with reduction in C.O.
1) Plasma Volume
2) ECF volume
3)Effective circulating volume
4) Urinary Na+ excretion

Back 38

1)up
2)up
3)down (flattened pressure wave--> CVMP)
4)down (CVMP--> SIAD)

Front 39

1 week high salt diet
1) Plasma Volume
2) ECF volume
3)Effective circulating volume
4) Urinary Na+ excretion

Back 39

1)up
2)up
3)up
4)up

Front 40

ADH administration for a week
1) Plasma Volume
2) ECF volume
3)Effective circulating volume
4) Urinary Na+ excretion

Back 40

1) small up
2) up
3)small up
4)up (dissipation of Na+ interstitial gradient to try and lose water)

Front 41

Cirrhosis with ascites:
1) Plasma Volume
2) ECF volume
3)Effective circulating volume
4) Urinary Na+ excretion

Back 41

1)variable
2)up
3)down (shunt)
4) down (CVMP due to shunt and hepatorenal reflex)