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Surgical Physiology Flashcards

(33 cards)

1
Q

total body water (TBW) & distribution

A

*TBW varies from 45-70%, depending on age/gender/diseases/IV fluids
*distributed into several compartments:
1. extracellular compartment (40% TBW):
1a. intravascular/plasma space (25% of extracelluar)
1b. extravascular/interstitial space (75% of extracellular)
2. intracellular compartment (60% TBW)

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2
Q

extracellular vs. intracellular water electrolyte composition

A

*extracellular water: primarily sodium, chloride, bicarbonate
*intracellular water: primarily potassium, organic phosphate, and sulfate

recall: salty banana = sodium outside, potassium inside

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3
Q

fluid maintenance requirements - in a healthy adult

A

approximately 30 mL/kg body weight/24 hours

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4
Q

fluid maintenance requirements after volume resuscitation

A

4-2-1 formula:
4 mL/kg for the first 10 kg body weight
2 mL/kg for the second 10 kg body weight
1 mL/kg for all additional weight

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5
Q

hypernatremia - clinical manifestations

A

*thirst, restlessness, irritability, ataxia, altered mental status
*commonly seen in free water deficit (diabetes insipidus, significant renal conditions)

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6
Q

hyponatremia - clinical manifestations

A

*headache, delirium, nausea, malaise, lethargy, confusion; if more severe, acute seizures & coma

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7
Q

hypokalemia - clinical manifestations

A

*if severe ( < 3.0): fatiuge, weakness, cramps, constipation, ileus
*EKG changes: flat T-waves, ST depression, appearance of U waves
*may occur as a result of isotonic fluid loss (SIADH, adrenal insufficiency, hyperglycemia)
*increased K+ loss can result from emesis, diarrhea, diuretic use, DI, and metabolic alkalosis

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8
Q

hyperkalemia - clinical manifestations

A

*if severe: weakness, flaccid paralysis
*EKG changes: peaked T-waves, prolonged PR and QRS intervals
*can result from any catabolic state (trauma, burns, prolonged illness, hemolysis, renal failure, adrenal insufficiency)

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9
Q

treatment of hyperkalemia

A

*varies based on rapidity of rise of serum K+ and underlying cause
1. IV glucose + IV regular insulin (shifts K+ intracellularly)
2. sodium bicarb (corrects metabolic acidosis)
3. calcium gluconate (stabilizes the cardiac membrane)

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10
Q

acid-base status and serum potassim

A

*alkalosis→ shifts K+ into cells
*acidosis → shifts K+ out of cells

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11
Q

hypercalcemia - clinical manifestations

A

*chronic/classically: nephrolithiasis (stones), pathologic fractures (bones), moans, groans
*EKG changes: short QT interval
*if severe ( > 12) and acute: weakness, confusion, vomiting, anorexia, abd pain, polyuria
*common causes include hyperparathyroidism, cancer, hyperthyroidism, renal insufficiency, and prolonged immobilization

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12
Q

hypocalcemia - clinical manifestations

A

*confusion, seizures, carpopedal spasm, perioral paresthesias, tetany, Trousseau sign (inflating BP cuff causes carpopedal spasm), Chvostek sign (tapping facial nerve causes face twitches)
*EKG changes: QT prolongation with severe deficits
*common causes include hypoparathyroidism, pancreatitis, severe trauma/crush injuries, nec fasc, and severe renal failure

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13
Q

hypermagnesemia - clinical manifestations

A

*occur when mag > 4
*hyporeflexia, weakness, lethargy, paralysis, ileus, respiratory failure
*EKG changes: prolonged PR, QRS, and QT intervals

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14
Q

hypomagnesemia - clinical manifestations

A

*occur with levels < 1.2
*confusion, tetany, seizures
*EKG changes: prolonged PR and QT intervals, wide QRS, presence of U waves, Torsades de pointes

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15
Q

hyperphosphatemia - clinical manifestations

A

*s/s attributable to hypocalcemia (confusion, seizures, spasms, etc)
*common causes include severe crush injury, muscle breakdown, and severe renal failure

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16
Q

hypophosphatemia - clinical manifestations

A

*if severe ( < 1): weakness, impaired diaphragmatic function, ileus, confusion, stupor
*common causes include hyperparathyroidism and malnourishment (eg. alcoholics)

17
Q

expected compensations in metabolic acid-base disorders

A

*metabolic acidosis: PCO2 expected to decrease 1.2 mmHg for every 1 decrease in HCO3
*metabolic alkalosis: PCO2 expected to increase 0.7 for every 1 increase in HCO3

18
Q

solute concentrations of normal saline (0.9%)

A

Na+: 154
Cl+: 154

K+:
HCO3-:
Ca+:
Glucose:

19
Q

solute concentrations of lactated ringers (LR)

A

Na+: 130
Cl+: 1-9
K+: 4
HCO3-: 28
Ca+: 2.7

Glucose:

20
Q

solute concentrations of D5 1/2 NS

A

Na+: 77
Cl+: 77

K+:
HCO3-:
Ca+:
Glucose: 50

21
Q

solute concentrations of D5 1/2 NS + 20 KCl

A

Na+: 77
Cl+: 97
K+: 20

HCO3-:
Ca+:
Glucose: 50

22
Q

normal saline (0.9%) crystalloid fluid

A

*ubiquitously used for dehydration and hypovolemia
*considered an “isotonic fluid”
*concentration of NaCl is higher than found in humans
*typically the first-line fluid used in trauma resuscitations, head injuries, acute neurologic conditions where hyponatremia should be avoided

23
Q

lactated ringers (LR) crystalloid fluid

A

*commonly used for resuscitation
*more isotonic than NS, with less NaCl
*widely used with equal efficacy as NS in most circumstances
*advantages: more physiologic levels of sodium & chloride
*considerations: think before using in pts with hyperkalemia or renal dysfunction

24
Q

D5 1/2 NS (5% dextrose in 1/2 normal saline)

A

*a common IV fluid used for maintaining fluid balance & providing calories
*a combination of 5% dextrose in 0.45% NaCl
*dextrose helps decrease hypotonicity and provides caloric content, stimulating insulin release and preventing protein catabolism

25
D5 1/2 NS + 20 KCl (5% dextrose in 1/2 NS with 20 mEq of KCl)
*addition of KCl results in an almost isotonic solution with solute concentrations approach that of stomach fluid
26
hypertonic saline
*solutions range from 2% to > 23% *can be used to treat pts with head injury, hypovolemic shock, spontaneous subarachnoid hemorrhage, or refractory hyponatremia *advantages: volume expansion, reduction of cerebral edema via osmotic effects, scavenging of oxygen free radicals *use with caution
27
hemostasis - review of steps
1. vasoconstriction 2. platelet aggregation 3. coagulation 4. fibrinolysis
28
prothrombin time (PT)
*measures the EXTRINSIC factors that lead to clotting (esp. factors II, V, VII, or XI) *also used as a surrogate to reflect the function of the liver (INR) *more affected by warfarin / vitamin K
29
partial thromboplastin time (PTT)
*measures the function of the INTRINSIC factors that lead to clotting (esp. factors VIII, IX, XI, or XII) *more affected by heparin *elevated in pts with hemophilia
30
heparin
*anticoagulant agent *accelerates the effects of **antithrombin III** → a systemically anticoagulated state *the heparin-antithrombin III-complex inactivates several factors in the coag cascade, esp. **thrombin & factor X** *level of anticoagulation cnan be measured by checking the PTT
31
low-molecular-weight-heparin (LMWH)
*acts primarily by **inhibiting factor Xa** *does not prolong PTT
32
warfarin
*leads to a deficiency of vitamin K, leading to a **decrease in production by the liver of factors II, VII, IX, and X; proteins C and S** *level of anticoagulation is measured by checking the PT/INR
33
acute hemolytic transfusion reaction
*a life-threatening reaction that occurs during or within 24h of a blood transfusion *mechanism: ABO incompatibility *caused by the recipient's antibodies attacking and destroying the donor RBCs *common sx: anxiety, chest pain, chills, flank pain, headaches *tx: stop transfusion, alert blood bank, ensure adequate hydration and diuresis