McNeil's notes: lytes, physiology, toxicology, hypothermia, burns, embolism, radiology, potpourrie(-stats/epi/ethics) Flashcards Preview

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1

Labs in diabetes insipidus show:
a. Hyponatremia.
b. Hypoglycemia.
c. High urine specific gravity.
d. Low urine osmolarity
e. Urine specific gravity

e. Urine specific gravity

2

1) patient post transsphenoidal resection pituitary tumour. Now has mild DI . Just complain of thirst and Na 145. Best treatment option is:
a. fluids ad lib
b. R/L at 150 cc / hour
c. D5 at 150 cc/ hr
d. DDAVP

a. fluids ad lib

DDAVP for Na > 150

3

The body system MOST sensitive to changes in sodium homeostasis is:
A. CVS
B. CNS
C. Respiratory
D. Musculoskeletal

Answer: CNS

The clinical features of acute hyponatremia are related to osmotic water shift leading to increased ICF volume, specifically brain cell swelling. Therefore, the symptoms are primarily neurologic, and their severity is dependent on the rapidity of onset and absolute decrease in plasma [Na+ ].

The major symptoms of hypernatremia are neurologic and include altered mental status, weakness, neuromuscular irritability, focal neurologic deficits, and occasionally coma or seizures.
- Washington Manual of Medical Therapeutics, 30th ed., Copyright © 2001

4

In a patient diagnosed with multiple myloma, had the following lab result, Creatinine 178, Urea 5, Na 128, K 3.5 & Albumin 22. the cause of hyponatremia is:
a. SIADH
b. Pseudohyponatremia
c. Renal failure
d. Volume overload
e. Dehydration

Answers given:
pseudohyponatremia

pseudohyponatremia seem with MM and high TG, and hyperglycemia

Pseudohyponatremia is a laboratory artifact that is present when the plasma contains very high concentrations of protein (multiple myeloma, intravenous immunoglobulin infusion) or lipid (hypertriglyceridemia, hypercholesterolemia). It does not occur when a direct ion-selective electrode determines the sodium concentration, a technique that is increasingly used in clinical laboratories. In true hyponatremia, the measured osmolality is low, whereas it is normal in pseudohyponatremia.
- Kliegman: Nelson Textbook of Pediatrics, 18th ed.

Depends on the osmolality

There are two situations in which sodium can be fictitiously low as a result of the presence of substances that alter the volume of plasma water in which sodium is measured.
Pseudohyponatremia is common in the setting of hyperglycemia or the use of some other restricted solute that causes high plasma osmolality.
Pseudohyponatremia also can occur as a result of an increase in relatively high-molecular-weight substances, such as occurs with Bence-Jones proteins in multiple myeloma or in hyperlipidemia.
- Abeloff: Abeloff's Clinical Oncology, 4th ed.

Adrenal insufficiency - orthostatic hypotension and hyponatremia are common; hyperpigmentation and hyperkalemia and volume depletion occur in primary adrenal failure (disease of adrenal glands versus secondary which is caused by disorders the pituitary or hypothalamus); may become pre-renal; multiple myeloma-monoclonal malignancy of plasma cells that produce paraprotein and is characterized by replacement of bone marrow and bone destruction; often presents with bone pain, anemia and infection; labs: rouleaux/rare plasma cells/pancytopenia, monoclonal protein, heavy and light chains on SIE, decreased normal immunoglobulins, BJ proteins, hyperCa, increased Cr, increased ESR, and narrow anion gap; renal failure secondary to: myeloma kidney (light chain deposition), hypercalcemic nephropathy, pyelo, amyloid, obstruction, plasma cell infiltration, hyperuricemia, and hyperviscosity of renal blood flow; diuretics-side effects depend on class; thiazides cause hypokalemia, hypoMg, hyperlipidemia, hyperCa, hyperglycemia, hyperuremia, hyponatremia, and rarely azotemia; loop diuretics cause hypoMg, hypoCa, and hypoK; K-sparing diuretics of course cause hyperK!

5

65 year old male patient presents with symptomatic hyponatremia his NA is 117.What is the best way to treat his hyponatremia:
a. Slow infusion hypertonic saline
b. Rapid infusion of hypertonic saline
c. D5W
d. D5 ½ NS
e. D5 ¼ NS

a. Slow infusion hypertonic saline

Risk central pontine demyelination

Hyponatremia can be either hypovolemic, hypervolemic, and euvolemic. The treatment will usually vary depending on which of these is present. In a patient with severe hyponatremia however, (Na

6

Calculate the approximate sodium deficit in a 70kg man with a serum sodium of 120mmol/L.
a. 280
b. 410

this only seems to have been asked 1 year so probably low yield.

Sodium Deficit = Total Body Water * Normal Wt in kg * (Desired Na - Pt's Na) (TBW = 0.6 if male and 0.5 if female)

70*0.6 = 42kg water = 42L water
(140-120)mmol/L*42L = 840mmol needed

7

Post-op laryngectomy, headache, decreased LOC. AVSS, normal urine output. Sodium 118. What is the most likely diagnosis
a) SIADH
b) Dilutional hyponatremia
c) Depletional hypokalemia

b) Dilutional hyponatremia (seems like a long surgery)

??? or could be DKA with pseudohyponatremia? depends on the question

8

1) Hyponatremia: when do you treatment it with Na replacement (When pt is symptomatic or if Na less than 120)
a.

a.

9

In patient with cirrhosis and ascites, hyponatremia is associated with:
a. Expanded extravascular fluid volume
b. Expanded intravascular fluid volume
c. Renal loss of Na
d. Depleted intravascular volume

Answer: Expanded intravascular fluid volume

The net effect is avid renal sodium and water retention because the patient is effectively volume depleted even though extracellular sodium stores, the plasma volume, and the cardiac output are increased. The sodium retention leads to the development of ascites unless the patient is adequately treated with dietary sodium restriction and diuretics.
- Up To Date 2007 Hyponatremia in Cirrhosis

proteins go extravascular-->intravascular hypovolemia
ADH increases as cirrhosis gets worse-->retain salt and water
lose ability to excrete water as cirrhosis worsens

end up hyponatremic with increased total body sodium. worsened by those that continue to drink alcohol. Better to be on low sodium diet.
initially would be vascular low volume but as things get worse can't pee water so would be hypervolemic hyponatremic.

10

Hypercalcemia causes all of the following except:
a) Polyuria
b) carpopedal spasm
c) proximal mm weakness
d) coma

b) carpopedal spasm

11

IV lasix is associated with all except:
All are complications of Lasix therapy EXCEPT:
a. Hyperuricemea.
b. Hyponatremia.
c. Hypercalcemia.
d. Metabolic alkalosis

c. Hypercalcemia.

actually can be used for tx of hyperCa

Loop diuretics inhibit the Na+/K+/2Cl- cotransporter in the ascending limb of the loop of Henle (see Fig. 136-1 ). They are highly protein bound and not filtered by the glomerulus. Loop diuretics are actively secreted into the proximal tubule by the organic anion pathway and reach their site of action intraluminally. They also indirectly inhibit reabsorption of calcium and magnesium by their effect on transepithelial potential difference.
- Walsh: Palliative Medicine , 1st ed.

12

Which of the following is the site of calcium and iron absorption in the gastrointestinal tract?
1. duodenum
2. distal ileum
3. proximal ileum
4. jejunem

1. duodenum

13

Which of the following will NOT cause hypercalcemia?
A. Thiazide diuretics
B. Sarcoidosis
C. Paget’s disease
D. Multiple fractures

Answer: Multiple fractures

Common question. This is always the answer

[Paget's] may also cause hypercalcemia, especially if the patient becomes bed-bound.
- Bradley: Neurology in Clinical Practice, 5th ed.

In addition to the well-known association of hypercalcemia in sarcoidosis ....
- Abeloff: Abeloff's Clinical Oncology, 4th ed.

Young, normally active patients with high bone turnover rates are subject to the development of hypercalcemia when suddenly forced into immobility, as may occur during forced bed rest after injury or major illness.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

14

In Paget’s disease, the following abnormality is MOST likely to occur:
a. elevated serum calcium
b. elevated alkaline phosphatase
c. elevated serum phosphate

Answer: elevated alkaline phosphatase

High alk phos.normal or high calcium ,normal phos

Paget's disease can cause bone pain and deformity. An elevated bone-specific alkaline phosphatase and characteristic radiographic changes can help make the diagnosis. Joint pain caused by secondary osteoarthritis in areas of involvement of bone from Paget's disease most commonly occurs in the hip, knee, or vertebrae. Spinal stenosis from Paget's disease of the spine has been reported.
- Goldman: Cecil Medicine, 23rd ed.

Extracellular calcium homeostasis is almost invariably normal despite the massive increase in bone turnover. Hypercalciuria and more rarely hypercalcemia may occur with prolonged immobilization or fracture.

15

A 40 yo presents with hypocalcemia and hyperparathyroidism. What is the MOST likely diagnosis?
A. Renal Failure
B. Osteomalacia
C. Parathyroid Adenoma
D. Vitamin D Deficiency

D. Renal failure

Secondary hyperparathyroidism is caused by any condition that gives rise to chronic hypocalcemia, which in turn leads to compensatory overactivity of the parathyroid glands. Renal failure is by far the most common cause of secondary hyperparathyroidism, although several other diseases, including inadequate dietary intake of calcium, steatorrhea, and vitamin D deficiency, may also cause this disorder.
- Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition , 8th ed.


Uptodate 2016: Vitamin D deficiency osteomalacia is the only osteomalacia in their table that has both hypocalcemia and hyperparathyroidism

Parathyroid adenoma = hypercalcemia

16

All of the following are used in the treatment of hypercalcaemia except:
a. Steroid
b. Rehydration
c. Lasix
d. Calcitonin
e. None of the above

a. none of the above (although steroid is only used in granulomatous disease : lymphoma, sarcoidosis)

Other EXCEPT answers:
-Thiazide (avoid as may increase reabsorption of calcium in DCT)
-Insulin

MANAGEMENT (9)
1. Forced diuresis with isotonic saline and lasix (mainstay in those with normal kidneys, dialysis possible in those with RF)
2. Bisphosphonates
3. Mithramycin
4. Calcitonin
5. Corticosteroids (in sarcoidosis)
6. IV phosphates (disodium or monopotassium phosphate, use as absolute last resort)
7. Gallium nitrate
8. Chloroquine phosphate (in sarcoidosis)
9. Surgical excision of excess functioning tissue
- Morell Notes

17

A patient with Trousseau's sign, prolonged QT interval and hyperactive DTR. He has :

Answer given: Hypocalcemia

But more likely hypomagnesemia.
- Trousseau’s sign is seen in hypocalcemia and hypomagnesemia.
- Hyperactive DTRs are somewhat more specific for hypomagnesemia
- QT shortening is seen with hypocalcemia

Hypocalcemia
Hypercalcemia can produce a number of nonspecific findings, as follows:
* Hypertension and bradycardia may be noted in patients with hypercalcemia, but this is nonspecific.
* Abdominal examination may suggest pancreatitis or the possibility of an ulcer.
* Patients with long-standing elevation of serum calcium may have proximal muscle weakness that is more prominent in the lower extremities; they also may have bony tenderness to palpation.
* Hyperreflexia and tongue fasciculations may be present.
* Anorexia or nausea may occur.
* Polyuria and dehydration are common.
* Lethargy, stupor, or even coma may be observed.

Hypercalcemia may produce ECG abnormalities related to altered trans-membrane potentials that affect conduction time. QT interval shortening is common, and, in some cases, the PR interval is prolonged. At very high levels, the QRS interval may lengthen, T waves may flatten or invert, and a variable degree of heart block may develop. Digoxin effects are amplified.
- http://emedicine.medscape.com/article/766373-diagnosis

Hypomagnesemia
Physical
# Neuromuscular irritability
* Hyperactive deep tendon reflexes
* Muscle cramps
* Muscle fibrillation
* Trousseau and Chvostek signs
* Dysarthria and dysphagia from esophageal dysmotility
# CNS hyperexcitability
* Irritability and combativeness
* Disorientation
* Psychosis
* Ataxia, vertigo, nystagmus, and seizures (at levels

18

Hypomagnesemia MOST likely causes:
A. Decreased deep tendon reflexes
B. Tremor
C. Constipation
D. Muscle paralysis

B. Tremor

Tip: Hypoeverything makes you slow
EXCEPTION: hypoMg and hypoCa make you twitch

Clinical and laboratory manifestations:
a. Neuromuscular: weakness, hyperreflexia, fasciculations, tremors, convulsions, delirium, coma
b. Cardiovascular: cardiac arrhythmias
c. Hypokalemia refractory to potassium replacement
d. Hypocalcemia refractory to calcium replacement
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.

At serum magnesium levels less than 1 mEq/L, patients have tremor, hyperactive deep-tendon reflexes, hyperreactivity to sensory stimuli, muscular fibrillations, positive Chvostek and Trousseau signs, and carpopedal spasms progressing to tetany. Mental status changes may become evident and may include irritability, disorientation, depression, and psychosis. Cardiac arrhythmias and reversible respiratory muscle failure can also occur in severe hypomagnesemia.
- http://emedicine.medscape.com/article/922142-overview

Clinical Manifestations of hypomagnesemia
Cardiac manifestations (7):
1. tachyarrhythmias (unstable VT)
2. digitalis toxicity enhanced as both inhibit the membrane pump
3. prolonged QT
4. T-wave flattening
5. prolonged PR interval
6. A. fib
7. Torsades de pointes
Neurologic manifestations: Changes in mental status, seizures, Tremors, Hyperreflexia
All uncommon, non-specific and have little clinical value
Tremor is the most characteristic finding with hypomagnesemia but tetany is first sign.
- Morell Notes

19

35 year old male patient with ulcerative colitis and chronic diarrhoea presents with hypocalcaemia, and you prescribed calcium gluconate two weeks later present with tetany. What is the most likely diagnosis:
a. Hypomagnesaemia
b. Hyponatremia
c. Hypokaemia
d. Exacerbation of ulcerative colitis
e. None compliance to medication

a. Hypomagnesaemia

Tetany associated with hypocalcemia.
Hypocalcemia in this case caused by hypomagnesemia, causing decreased PTH secretion and inhibition of PTH effect on bone.

20

Hypomagnesaemia is caused by all of the following except:
a. Cisplastin
b. Loop diuretics
c. Cyclosporine
d. Aminoglycosides
e. Malabsorbtion

Sources mention all answers!

I refuse to learn this list, but here it is for you keeners:

Primary nutritional disturbances
Inadequate intake, total parenteral nutrition, refeeding syndrome
Gastrointestinal disorders
Specific absorptive defects, malabsorption syndromes, prolonged diarrhea, prolonged nasogastric suction, pancreatitis
Endocrine disorders
Hyperparathyroidism, hypoparathyroidism, hyperthyroidism, primary hyperaldosteronism, Bartter's syndrome, diabetic or alcoholic ketoacidosis, administration of epinephrine, SIADH, hungry bone syndrome after parathyroidectomy
Chronic alcoholism, alcoholic withdrawal, increased renal excretion
Ethanol ingestion; idiopathic; after renal transplantation; drugs (cisplatin, aminoglycoside, amphotericin B, diuretics, pentamidine, theophylline); recovery phase of acute tubular necrosis; colony-stimulating factor therapy
-Miller: Miller's Anesthesia, 7th ed.

HYPOMAGNESEMIA (Etiology)
a Gastrointestinal and nutritional
i. Defective gastrointestinal absorption (malabsorption)
ii. Inadequate dietary intake (e.g., alcoholics)
iii. Parenteral therapy without magnesium
iv. Chronic diarrhea, villous adenoma, prolonged nasogastric suction, fistulas (small bowel, biliary)
b Excessive renal losses
i. Diuretics
ii. RTA
iii. Diuretic phase of ATN
iv. Endocrine disturbances (diabetic ketoacidosis, hyperaldosteronism, hyperthyroidism, hyperparathyroidism), SIADH, Bartter's syndrome, hypercalciuria, hypokalemia
v. Cisplatin, alcohol, cyclosporine, digoxin, pentamidine, mannitol, amphotericin B, foscarnet, methotrexate
vi. Antibiotics (gentamicin, ticarcillin, carbenicillin)
c Redistribution: hypoalbuminemia, cirrhosis, administration of insulin and glucose, theophylline, epinephrine, acute pancreatitis, cardiopulmonary bypass
d. Miscellaneous: sweating, burns, prolonged exercise, lactation, “hungry-bones” syndrome
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.

Loop diuretics inhibit the apical membrane Na+/K+/2Cl− cotransporter of the TAL and abolish the transepithelial potential difference, thereby inhibiting paracellular Mg2+ reabsorption. Hypomagnesemia is therefore a frequent finding in patients receiving chronic loop diuretic therapy
- Brenner: Brenner and Rector's The Kidney, 8th ed

21

The earliest clinical sign of hypermagnesemia is:
a. stupor
b. convulsion/seizure
c. decreased DTRs
d. something else

Answer: these something elses: hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus. BUT These are so common so I would say they shouldn't clinically make you think of hyperMg unless you're an internal medicine resident and listing your top 100 DDx

If those aren't there, probably decreased DTR

Causes of hypermagnesemia:
renal insufficiency, antacid overuse, adrenal insufficiency, hypothyroidism, excessive intake (e.g. tx of eclampsia).
Signs and symptoms
Clinical: nausea, vomiting, weakness, mental status changes, hyperreflexia, hyperventilation
EKG findings include AV block and prolonged QT interval
Treatment
1- discontinue or remove external sources; large amounts found in antacids and cathartics
2- IV calcium gluconate for emergent symptoms
3- dialysis in renal failure patients
- Mont Reid Surgical Handbook, pg 26

Magnesium toxicity is a serious and potentially fatal condition. Mild hypermagnesemia (serum magnesium level >4 to 6 mg/dL) causes hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus. Above serum magnesium levels of 8 to 12 mg/dL, flaccid skeletal muscular paralysis and hyporeflexia may ensue, together with bradyarrhythmias, respiratory depression, coma, and cardiac arrest. A low, or even negative serum anion gap may sometimes be seen.
- Goldman: Cecil Medicine, 23rd ed.

22

Cardiac toxicity in hyperkalemia would be BEST treated with:
A. Insulin
B. Metoprolol
C. Calcium
D. Bicarbonate

Intravenous calcium is used to stabilize the myocardium by lowering the threshold potential. It has no effect on the serum potassium level. Improvement in the ECG is usually evident within 2 to 5 minutes.
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.

23

The following are clinical signs of hyperkalemia except:
a. peaked T waves
b. wide QRS
c. diarrhea
d. tetany

Answer: diarrhea

In hyperkalemia, there is a depolarizing effect on the resting membrane potential and potassium channel conductance is increased, leading to the classic electrocardiographic changes of hyperacute peaked T waves associated with rapid repolarization ( Fig. 118-2). Because of the increased potassium conductance, hyperkalemia antagonizes the normal slow depolarization of pacemaker tissue that is usually associated with a decrease in potassium conductance. Hyperkalemia, like acetylcholine, commonly results in sinus bradycardia. Heart block, loss of P waves on the electrocardiogram, and prolonged QRS intervals are all seen in cases of severe hyperkalemia, usually in excess of 6 mmol/L.
- Goldman: Cecil Medicine, 23rd ed

Neuromuscular signs and symptoms of hyperkalemia include muscle cramps, weakness, paralysis, paresthesias, tetany, and focal neurologic deficits, but these are rarely specific enough to suggest the diagnosis in themselves
- Marx: Rosen's Emergency Medicine, 7th ed.

EKG Summary:
- loss of P wave
- prolonged QRS
- hyperacute T wave

24

2) What are the signs of hypokalemia?
a) Depressed ST, inverted T, wide QRS
b) Depressed ST, inverted T, narrow QRS
c) Elevated ST, inverted T, wide QRS
d) Elevated ST, inverted T, narrow QRS

A) Depressed ST, inverted T, wide QRS

Low serum potassium not only hyperpolarizes most cells, leading to an increase in the resting potential, but also has effects on certain potassium channels required for repolarization. Thus, hypokalemia decreases or slows potassium conductance, the prolonged repolarization phase accounting for the characteristic electrocardiographic findings of broad, flattened T waves. U waves are also indicative of this delay in repolarization.
- Goldman: Cecil Medicine, 23rd ed.

Electrocardiographic changes in hypokalemia include broad flat T waves, ST depression, and QT prolongation; these are most marked when serum K+ is

25

3) Which of the following is a sign of hypokalemia:
a. U wave
b. Peaked T waves
c. ST segment elevation
d. Increased deep tendon reflexes
e. None of the above

U wave

26

All of the following may cause hypokalemia EXCEPT:
A. Vitamin B12
B. Ventolin
C. Insulin
D. Digoxin
E. Corticosteroids

Answer: digoxin can lead to malignant hyperkalemia (Digibind, used for digoxin toxicity, is a cause)

Etiology and classification:
a. Cellular shift (redistribution) and undetermined mechanisms
i. Alkalosis (each 0.1 increase in pH decreases serum potassium by 0.4 to 0.6 mEq/L)
ii. Insulin administration
iii. Vitamin B12 therapy for megaloblastic anemias, acute leukemias
iv. Hypokalemic periodic paralysis: rare familial disorder manifested by recurrent attacks of flaccid paralysis and hypokalemia
v. β-Adrenergic agonists (e.g., terbutaline), decongestants, bronchodilators, theophylline, caffeine
vi. Barium poisoning, toluene intoxication, verapamil intoxication, chloroquine intoxication
vii. Correction of digoxin intoxication with digoxin antibody fragments (Digibind)
b. Increased renal excretion
i. Drugs
(a) Diuretics, including carbonic anhydrase inhibitors (e.g., acetazolamide)
(b) Amphotericin B
(c) High-dose sodium penicillin, nafcillin, ampicillin, or carbenicillin
(d) Cisplatin
(e) Aminoglycosides
(f) Corticosteroids, mineralocorticoids
(g) Foscarnet sodium
ii. Renal tubular acidosis (RTA)
iii. Diabetic ketoacidosis, ureteroenterostomy
iv. Magnesium deficiency
v. Postobstruction diuresis, diuretic phase of acute tubular necrosis (ATN)
vi. Osmotic diuresis (e.g., mannitol)
vii. Bartter's syndrome: hyperplasia of juxtaglomerular cells leading to increased renin and aldosterone, metabolic alkalosis, hypokalemia, muscle weakness, and tetany (seen in young adults)
viii. Increased mineralocorticoid activity (primary or secondary aldosteronism), Cushing's syndrome, or physiologic increases in mineralocorticoid activity (dehydration)
ix. Chronic metabolic alkalosis from loss of gastric fluid (increased renal potassium secretion)
c. Gastrointestinal loss
i. Vomiting, nasogastric suction
ii. Diarrhea
iii. Laxative abuse
iv. Villous adenoma
v. Fistulas
d. Inadequate dietary intake (e.g., anorexia nervosa)
e. Cutaneous loss (excessive sweating)
f. High dietary sodium intake, excessive use of licorice
g. Hypomagnesemia
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed

27

What is the commonest cause of hypokalemia associated with INCREASED urine potassium?
a. prolonged thiazide diuretic use
b. spironolactone use
c. primary hyperaldosteronism

Answer: A vs C (thiazide more common than 1 hyperaldosteronism)

"The most common causes of hypokalemia due to urinary potassium losses include diuretic use, a primary increase in mineralocorticoid activity, increased distal delivery of nonreabsorbable anions, and loss of gastric secretions." uptodate 2016

The four most common causes of hypokalemia are reduced intake, gastrointestinal losses, excessive renal losses of potassium (e.g., with excess of mineralocorticoids or diuretics), and potassium shifts from the ECF to the intracellular fluid (e.g., owing to insulin administration).
- Miller: Miller's Anesthesia, 7th ed.

Renal loss of K+ is by far the most common cause of hypokalemia. With rare exceptions, hypokalemia due to increased renal wasting of potassium can be attributed to an increased activity of aldosterone or other mineralocorticoids. Increased aldosterone could be a primary disorder as in primary hyperaldosteronism or due to increased renin secretion as in secondary hyperaldosteronism.
Examples of secondary hyperaldosteronism that result in hypokalemia include renal artery stenosis, diuretic therapy, and malignant hypertension, and congenital defects in renal salt transport such as Bartter's syndrome and Gitelman's syndrome.
- McPherson & Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed.

28

Normal hemodynamic changes during pregnancy include all of the following except:
a) Hemodilution
b) increased red cell mass
c) leukocytosis
d) eosinophilia

d) eosinophilia

Turns out babies are not parasites

Increase in TBW (by 40%) – 2/3 increase in extravascular. Increase in plasma volume. Disproportionate increase in plasma volume over RBC volume – hemodilution. Despite erythrocyte production there is a physiologic fall in the HB and hematocrit readings. (likely Eosinophilia)

As a consequence of the increased minute ventilation, maternal Pao2 levels during late pregnancy range from 104 to 108 mm Hg, and maternal Paco2 ranges from 27 to 32 mm Hg.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

Physiologic leukocytosis during pregnancy makes it more difficult to evaluate infectious abdominal processes, particularly late in the 3rd trimester, when the WBC is even higher.
- Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed.

29

Which is not associated with pregnancy?
a. low CO2
b. metabolic acidosis
c. decreased Hct
d. leukocytosis
e. high ESR

b. metabolic acidosis

Minute ventilation begins to rise by the end of the first trimester and continues to increase until term. Progesterone mediates this response by direct stimulation of respiratory drive and by increasing sensitivity of the respiratory center to CO2.[16] This results in a mild respiratory alkalosis—Pco2 falls to approximately 27 to 32 mm Hg—and a compensatory increase in renal excretion of bicarbonate. This large increase in minute ventilation allows maintenance of high-normal Po2 despite the 20% to 33% increase in oxygen consumption in pregnancy.
- Brenner: Brenner and Rector's The Kidney, 8th ed.

Physiology maternal hyperventilation causes a compensatory metabolic acidosis with a decrease in maternal Hco3. The mother therefore has less buffering capacity for metabolic acidosis

ESR elevated in: inflammatory states (acute-phase reactant), collagen-vascular diseases, infections, myocardial infarction, neoplasms, hyperthyroidism, hypothyroidism, rouleaux formation, elderly, pregnancy
- Rakel: Textbook of Family Medicine, 7th ed.

Hematocrit is 30–50% normal
- Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed

30

Resistant is proportional to:
a. Length and 1/radius to power of 4
b. Radius and 1/ length to power of 4
c. Length to power of 4 and 1/radius
d. Radius to power of 4 and 1/length

a. Length and 1/radius to power of 4