Water, Electrolytes, Acid/base, Hemodynamics

Front 1

What is the major extracellular fluid cation? Anion?
What is the major intracellular cation? Anion?

Back 1

Extra: Na, Cl
Intra: K, Phosphorus

Front 2

How do you ruffly calculate plasma osmolality (POsm) and what is a normal value?

Back 2

POsm = 2*Na + serum glu/18 + serum BUN/2.8 = 275-295 mOsm/kg.

Front 3

What is edema? What are the four types of edema, and which one pits?

Back 3

Excess fluid in the interstitial space. Exudate, transudate (only one that pits), lymphedema, and glycosaminoglycans (increase in hyaluronic acid and chondroitin sulfate - nonpitting edema called myxedema).

Front 4

What is the protein concentrations of a transudate and a exudate?

Back 4

Transudate (protein-poor) < 3 g/dL and cell poor.
Exudate > 3 g /dL and cell rich.

Front 5

What Starling pressures are responsible for these edemas:
(1) Hypoalbuminemia
(2) Pulmonary edema in left-side heart
(3) Right-sided heart failure
(4) Cirrhosis
(5) Renal retention of sodium and water

Back 5

(1) Decreased vascular oncotic pressure
(2) Increased vascular hydrostatic pressure
(3) Increased vascular hydrostatic pressure
(4) Both increase in hydrostatic and decreased oncotic Starling forces
(5) Increases hydrostatic pressure and decreases oncotic pressure (dilutional effect on albumin).

Front 6

What is the pathophysiology of exopthalmos in Grave's disease?

Back 6

T-cell cytokines stimulate fibroblasts to synthesize GAGs in the eye. Increased syn. of GAGs causes preorbital myxedema.

Front 7

What is the most common cause of lymphedema in the US? What is the most common cause in 3rd world countries?

Back 7

Radical mastectomy (risk of lympangiosarcoma).
Wuchereria bancrofti.
Dont forget: scrotal and vulvar lymphedema due to lymphogranuloma venereum.

Front 8

What are the fluid compartments of the body and how do their sizes relate?

Back 8

ECF = interstitial fluid and vascular compartment (2:1).
ICF = intracellular fluid (ICF to ECF is 2:1).

Front 9

In what fluid compartments of the body does sodium, glucose and urea reside?

Back 9

ECF = sodium and glucose
Urea equilibrates between ECF and ICF.

Front 10

What is TBNa, serum Na and TBW, and how are they related?

Back 10

Serum Na ~ TBNa/TBW

Front 11

What are the signs of volume depletion (decreased TBNa)?

Back 11

Dry mucous membranes, decreased skin turgor, drop in BP and increase in pulse when sitting up from a supine position (positive tilt test).

Front 12

What effect does hyponatremia have on the ECF and ICF?

Back 12

Water osmotically flows into the ICF. ECF contracts and ICF expands.

Front 13

What effects does an isotonic loss of fluid have on the ECF and ICF? Name some causes of isotonic loss of fluid.

Back 13

ECF: contracts. ICF: remains the same (no osmotic gradient change).
Causes: adult diarrhea, hemorrhage.

Front 14

What effect does Addison's disease have on the ECF and ICF compartments?

Back 14

Addison's results in a loss of ALD, therefore a hypertonic loss of sodium (loss of more salt then water). ECF: contracted. ICF: expanded

Front 15

What effect could small cell carcinoma secreting ADH have on the ECF and ICF?

Back 15

Gain of free water. ICF and ECF both expand.

Front 16

What are the main causes of a hypotonic gain of Na? What are the effects on the ICF and ECF?

Back 16

ECF: expand. ICF: expand.
Causes: right-sided heart failure, cirrhosis, nephrotic syndrome. These states cause pitting edema.

Front 17

What happens to the ICF compartment in a hypertonic condition?

Back 17

ICF contracts. Hypernatremia and hyperglycemia are the most common causes of increased POsm.

Front 18

What happens to the ICF and ECF in osmotic diuresis?

Back 18

Glucose loss in the kidney. This pulls extra water: hypotonic loss of sodium. ICF and ECF volumes contract.

Front 19

What are the main causes of hypotonic loss of Na? How do you treat?

Back 19

Osmotic diuresis, sweating, infant diarrhea. Give the patient what they lost, a hypotonic salt solution. Remember, gatorade must have glucose to reabsorb Na (cotransport pump in the SI).

Front 20

What happens to the ICF and ECF compartments in:
(1) diabetic ketoacidosis
(2) infusion of Na

Back 20

(1) ICF and ECF contract
(2) ECF expands, ICF contracts

Front 21

During hypovolemic shock the primary response of the body is initiated by the baroreceptors in the carotids (IX) and aorta (X) which cause a release of catecholamines. What are the effects of the catecholamines?

Back 21

Increase heart rate, contractility (beta 1). Vasoconstriction of smooth muscle arterioles (alpha 1). Cause renin to release, angiotensin II is a vasoconstrictor. Ang II causes 18-hydroxylase to convert corticosterone to aldosterone which reabsorbs salt and water.

Front 22

During hypovolemic shock the primary response of the body is initiated by the baroreceptors in the carotids (IX) and aorta (X) which cause a release of catecholamines. What are the effects of the catecholamines?

Back 22

Increase heart rate, contractility (beta 1). Vasoconstriction of smooth muscle arterioles (alpha 1). Cause renin to release, angiotensin II is a vasoconstrictor. Ang II causes 18-hydroxylase to convert corticosterone to aldosterone which reabsorbs salt and water.

Front 23

In hypovolemic shock, what fluids should be given to the patient to keep the blood pressure up?

Back 23

Normal saline (0.9%), because its isotonic and it stays in the ECF.

Front 24

What is the nonpharmacological treatment of pitting edema? Pharmacological?

Back 24

Restrict salt and restrict water.
Diuretics.

Front 25

Can diabetes insipidus cause hypovolemic shock? Name some causes that can cause hypovolemic shock.

Back 25

No, your only losing pure water.
Causes: sweating, diarrhea, hemorrhage.

Front 26

What is a positive tilt test?

Back 26

Normal blood pressure when in a supine position. When the patient sits up, the blood pressure decreases and the pulse increases.

Front 27

How is CO, LVEDP, and PVR effected by septic shock?

Back 27

CO is increased due to rapid blood fow through dilated arterioles, causing increased return of blood to the heart. LVEDP is decreased due to neutrophil transmigration through the pulmonary capillaries into alveoli producing noncardiogenic pulmonary edema.
Decreased PVR due to vasodilation of peripheral resistance arterioles.

Front 28

What causes the vasodilation seen septic shock?

Back 28

Endotoxins damage endothelial cells which releases NO and PGI2.
Endotoxins activate the alternative pathway: anaphylatoxins (C3a and C5a) are produced which stimulate histamine release from mast cells.
IL-1 and TNF are released from macrophages which activate neutrophil adhesion molecules.

Front 29

What effect does shock have on the kidneys?

Back 29

Ischemic acute tubular necrosis: coagulation necrosis of proximal tubule cells and cells in the thick ascending limb. Signs/labs: oliguria, increased BUN and creatinine, renal tubular casts.

Front 30

What is the easiest way to determine the cause of pH change in the body? What is the normal pH?

Back 30

pH = HCO3 / PCO2.
7.35-7.45

Front 31

How does the body compensate for respiratory acidosis?

Back 31

Via metabolic alkalosis: serum HCO3 < 30 in acute respiratory acidosis, HCO3 > 30 mEq/L indicates renal compensation in chronic respiratory acidosis.

Front 32

What are the main causes of respiratory acidosis involved with the following systems:
(1) CNS
(2) Upper airway
(3) Muscles of respiration
(4) Lungs

Back 32

(1) Depression of respiratory center in medulla due to trauma or barbiturates
(2) Obstruction: due to acute epiglottitis (H. influenzae) or croup (parainfluenza virus)
(3) Paralysis: ALS, phrenic nerve injury, Guillain-Barre, hypokalemia, hypophosphatemia
(4) Obstructive disease: chronic bronchitis, CF; other: pulmonary edema, ARDS, RDS, bronchial asthma.

Front 33

What are the main causes of respiratory alkalosis involved with the following systems:
(1) CNS
(2) Muscles of respiration
(3) Lungs

Back 33

(1) Anxiety, high altitude, normal pregnancy, salicylate poisoning, endotoxic shock, cirrhosis.
(2) Rib fracture: hypoventilation from pain.
(3) Restrictive disease: sarcoidosis, asbestosis; other: pulmonary embolism, mild bronchial asthma.

Front 34

What is the PaCO2 level in respiratory acidosis? What are the clinical findings?

What is the PaCO2 level in respiratory alkalosis? What are the clinical findings?

Back 34

Acidosis: PaCO2 > 45. Somnolence, cerebral edema (VD of cerebral vessels).
Alkalosis: PaCO2 < 33. Light-headed and confusion, signs of tetany (thumb adduction, peioral twitching - Chvostek sign, perioral numbness).

Front 35

How does alkalosis cause tetany?

Back 35

Alkalosis increases the number of negative charges on albumin, therefore, calcium is displaced from the ionized calcium fraction and is bound to albumin, causing a decrease in ionized calcium levels. Decrease calcium makes neurons more permeable to sodium (threshold easier to reach).

Front 36

What is the anion gap (AG) equation and what is the normal value?

Back 36

AG = serum Na - (serum Cl + serum HCO3) = 12 +/- 2
Na - 135-147
Cl - 95-105
HCO3 - 22-28

Front 37

When would metabolic acidosis have an increase in the AG and when would the AG be normal?

Back 37

AG is increased when excess H+ ions of an acid are buffered by HCO3, which decreases serum HCO3.
AG remains the same when HCO3- is lost or unable to be synthesized (in the kidney) and Cl anions increase to counterbalance the loss of HCO3 - hyperchloremic normal AG metabolic acidosis.

Front 38

Name some general causes of metabolic acidosis with an increase AG.

Back 38

Lactic acidosis (hypoxia with concomitant anaerobic glycolysis - e.g. shock, CN poising, CO poisoning), ketoacidosis (diabetic, alcoholic, starvation), salicylate poisoning, ethylene glycol poisoning, methyl alcohol poisoning.

Front 39

Why does alcoholism cause ketoacidosis and why cant standard test for ketone bodies detect the ketoacidosis?

Back 39

Acetyl CoA in alcohol metabolism is converted to ketoacids: increase in NADH causes acetoacetate to convert to beta-hydroxybutyrate which is not detected with standard tests for ketone bodies.

Front 40

What is the most common cause of metabolic acidosis with a normal AG in children?

Back 40

Diarrhea. Loss of HCO3 in the stool.

Front 41

What is the pathogenesis of:
(1) type I renal tubular acidosis
(2) type II renal tubular acidosis
(3) type IV renal tubular acidosis

Back 41

(1) Inability to synthesize HCO3 in the H/K ATPase pump in the collecting tubules.
(2) Renal threshold for reclaiming HCO3 is lowered from 24 to 15.
(3) Destruction of the JG apparatus (e.g. hyaline arteriolosclerosis).

Front 42

What are the most common causes of metabolic alkalosis?

Back 42

Vomiting: loss of HCL.
Mineralocorticoid excess: enhances Na/H channels increases the synthesis of HCO3.
Thiazide and loop diuretics: Block in Na reabsorption leads to augmented late distal/collecting duct reabsorption of Na and secretion of H.

Front 43

What are the clinical findings in metabolic acidosis?

Back 43

Hyperventilation - Kussmaul breathing.
Warm shock - acidosis vasodilates peripheral resistance arterioles.
Osteoporosis - bone buffers excess H ions.

Front 44

How come patients are at risk of ventricular arrhythmias in metabolic alkalosis?

Back 44

Metabolic alkalosis left-shifts the binding curve and its compensation, respiratory acidosis, decreases arterial PO2 causing hypoxia to cardiac muscle.

Front 45

What is the pathogenesis of decompression sickness (caissons disease)? How do you treat?

Back 45

Atm pressure increases by 1 every 33 ft descended in water. N gas is forced out of the alveoli and dissolves in blood and tissues. Rapid ascent causes nitrogen to expand and form gas bubbles in tissue and vessel lumens. Tx: recompression (nitrogen forced into solution) followed by slow decrompression.

Front 46

What are the clinical findings in caissons disease?

Back 46

Pain develops in joints, muscles, and bones (bends).
Pneumothorax: rupture of subpleural bleb.
Pulmonary embolus: pressure on lower extremities produces stasis and thrombus formation.

Front 47

What would the electrolyte profile of a person with SIADH look like?

Back 47

Serum Na, K, and Cl would all be decreased. HCO3 would be near the lower end of normal range.

Front 48

Serum Na - 130 (136-145); serum K, 2.9 (3.5-5); serum Cl 80 (94-105); serum HCO3 36 (22-28). How can this profile be explained by vomiting?

Back 48

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Front 49

Serum Na - 130 (136-145); serum K, 2.9 (3.5-5); serum Cl 80 (94-105); serum HCO3 36 (22-28). How can this profile be explained by thiazide use?

Back 49

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