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Rapid Review Pathology > Chapter 5 - Water, Electrolyte, Acid-Base, and Hemodynamic Disorders > Flashcards

Chapter 5 - Water, Electrolyte, Acid-Base, and Hemodynamic Disorders Flashcards

0
Q

What are the major ECF and ICF cations?

A

Na+, K+: major ECF and ICF cations, respectively

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1
Q

Describe how water compartment sizes compare to one another.

A

Compartment sizes: ICF > ECF; interstitial > vascular

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2
Q

Describe how plasma osmolality differs between isotonic, hypotonic and hypertonic states.

A

Isotonic, hypotonic, hypertonic: normal POsm, ↓POsm, ↑POsm, respectively

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3
Q

What is the plasma osmolality equation?

A

POsm = 2 (serum Na+) + serum glucose/18 + serum BUN/2.8 = 275–295 mOsm/kg

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4
Q

What is the equation for effective osmolality? How does this equation differ from the plasma osmolality equation?

A

EOsm = 2 (serum Na+) + serum glucose/18; urea diffuses between ECF and ICF

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5
Q

Describe two features of osmosis.

A

Osmosis: H2O moves between ECF and ICF; Na+ controlled movement

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6
Q

Describe osmosis in hyponatremia.

A

Hyponatremia: H2O moves from ECF to ICF (expanded)

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7
Q

Describe osmosis in hypernatremia/hyperglycemia.

A

Hypernatremia/hyperglycemia: H2O moves from ICF (contracted) to ECF

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8
Q

What does the serum sodium concentration approximate?

A

Serum Na+ ~ TBNa+/TBW

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9
Q

List four clinical findings with decreased total body sodium.

A

↓TBNa+: ↓skin turgor, dry mucous membranes, ↓blood pressure, ↑pulse when sitting/standing up

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10
Q

List two clinical findings with increased total body sodium.

A

↑TBNa+: pitting edema, body cavity effusions

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11
Q

How does an increase in total body sodium affect Starling forces?

A

↑TBNa+: alteration of Starling forces (↑HP and/or ↓OP)

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12
Q

What do Starling forces do?

A

Starling forces: control fluid movements in ECF compartment

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13
Q

What is the most common cause of weight gain in a hospitalized person?

A

↑Patient weight in hospital: ↑TBNa+

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14
Q

How does an isotonic loss or gain affect serum sodium concentration?

A

Isotonic loss or gain: serum Na+ normal

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15
Q

If there is a gain in fluid, how does the ECF respond?

A

Gain in fluid: ECF always expands

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16
Q

If there is a loss of fluid, how does the ECF respond?

A

Loss in fluid: ECF always contracts

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17
Q

How does an isotonic loss of fluid affect TBNa+ and TBW? Provide an example.

A

Isotonic loss: ↓TBNa+/↓TBW; secretory diarrhea

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18
Q

What is the treatment for an isotonic loss of fluid?

A

Rx isotonic loss: normal saline

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19
Q

What results from a normal saline infusion?

A

Normal saline: ↑BP; equilibrates between vascular/interstitial space

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20
Q

How does an isotonic gain of fluid affect TBNa+ and TBW? Provide an example.

A

Isotonic gain: ↑TBNa+/↑TBW; ↑↑isotonic saline infusion

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21
Q

What is the treatment for an isotonic gain of fluid?

A

Rx isotonic gain: restrict water; loop diuretics

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22
Q

What is always present in hypotonic disorders? How does the ICF respond?

A

Hypotonic disorders: hyponatremia always present; ICF expansion

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23
Q

How does a hypertonic loss of fluid affect TBNa+ and TBW?

A

Hypertonic loss: ↓↓TBNa+/↓TBW

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24
Q

List three examples of a hypertonic loss of fluid.

A

Hypertonic loss: loop diuretics/thiazides (excessive), Addison, ↓21-hydroxylase

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25
Q

What is the treatment for a hypertonic loss of fluid?

A

Rx hypertonic loss: infuse normal saline or equivalent

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26
Q

What may result in central pontine myelinolysis?

A

Central pontine myelinolysis: rapid correction of hyponatremia with saline in alcoholic

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27
Q

How does a hypotonic gain of water affect TBNa+ and TBW? Give two examples.

A

Hypotonic gain water: TBNa+/↑↑TBW; SIADH, compulsive water drinker

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28
Q

What is the treatment for a hypotonic gain of water?

A

Rx hypotonic gain water: restrict water

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29
Q

How does a hypotonic gain of Na+ affect TBNa+ and TBW?

A

Hypotonic gain water + Na+: ↑TBNa+/↑↑TBW

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30
Q

List three different pitting edema states. How is cardiac output affected?

A

Pitting edema states: RHF, cirrhosis, nephrotic syndrome; ↓cardiac output

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31
Q

What is the treatment for pitting edema states?

A

Rx pitting edema states: restrict water/sodium; diuretics

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32
Q

Name two hypertonic disorders. How does the ICF respond?

A

Hypertonic disorder: hypernatremia/hyperglycemia; ICF contraction

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33
Q

How does the ICF always respond in hypertonic conditions?

A

Hypertonic conditions: ICF always contracted

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34
Q

How does a hypotonic loss of Na+ affect TBNa+ and TBW?

A

Hypotonic loss Na+ + water: ↓TBNa+/↓↓TBW

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35
Q

List four examples of hypotonic loss of Na+.

A

Hypotonic loss Na+ + water: osmotic diuresis/diarrhea, sweating, vomiting

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36
Q

How does loss of pure water affect TBNa+ and TBW?

A

Hypotonic loss water: TBNa+/↓↓TBW

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37
Q

List two examples of loss of pure water.

A

Hypotonic loss water: diabetes insipidus; insensible water loss

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38
Q

How does hypertonic gain of Na+ affect TBNa+ and TBW?

A

Hypertonic gain Na+: ↑↑TBNa+/↑TBW

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39
Q

Provide two examples of hypertonic gain of Na+.

A

Hypertonic gain: ↑NaHCO3, Na+-containing antibiotic infused

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40
Q

What is DKA and what does it cause?

A

DKA: hypertonic state with dilutional hyponatremia; osmotic diuresis

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41
Q

What occurs in the proximal tubule?

A

Proximal tubule: reabsorb Na+, reclaim HCO3−

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42
Q

How does decreased EABV affect FF, PO and PA?

A

↓EABV → ↑FF → PO > PH

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43
Q

How does increased EABV affect FF, PH and PO?

A

↑EABV → ↓FF → PH > PO

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44
Q

What is reclaiming HCO3-?

A

Reclaiming HCO3−: retrieving filtered HCO3−

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45
Q

What is the effect of decreasing the threshold for reclaiming HCO3-? Provide an example.

A

↓Threshold for reclaiming HCO3− (carbonic anhydrase inhibitor): lose HCO3− in urine, ↓HCO3− in blood (metabolic acidosis)

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46
Q

What is the effect of increasing the threshold for HCO3-? Provide an example.

A

↑Threshold for reclaiming HCO3− (vomiting): reclaim more HCO3− from urine, ↑HCO3− in blood (metabolic alkalosis)

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47
Q

Heavy metal poisoning results in what?

A

Heavy metal poisoning: Fanconi syndrome

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48
Q

What are the functions of Na+-K+- 2Cl− symporter?

A

Na+-K+- 2Cl− symporter: generates fH2O, reabsorbs Ca2+

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49
Q

What type of water does ADH reabsorbs?

A

ADH: only reabsorbs fH2O not oH2O

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50
Q

What do loop diuretics do?

A

Cl− binding site in Na+-K+-Cl− symporter: inhibited by loop diuretics

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51
Q

What electrolyte abnormalities may loop diuretics produce?

A

Loop diuretic: hyponatremia, hypokalemia, metabolic alkalosis

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52
Q

What do thiazides do?

A

Thiazide: inhibits Cl− site Na+-Cl− symporter; ↑Ca2+ reabsorption

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53
Q

How do thiazides affect electrolytes?

A

Thiazide: ↓serum Na+, ↓K+; ↑HCO3− (metabolic alkalosis), ↑Ca2+ (if ↑PTH)

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54
Q

How do thiazides affect Na+ and K+? What is there danger of?

A

Thiazides: ↑Na+ reabsorption, ↑K+ excretion (danger of hypokalemia)

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55
Q

How does hypokalemia affect H+ and HCO3-? What is there risk for?

A

Hypokalemia: ↑H+ excretion → ↑HCO3− in blood; risk for metabolic alkalosis

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56
Q

Name two potassium-sparing diuretics.

A

Amiloride, triamterene: K+-sparing diuretics

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57
Q

How do proximally-acting diuretics affect distal delivery of Na+? What results from this effect?

A

↑Distal delivery Na+ (proximally-acting diuretics): ↓K+, metabolic alkalosis

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58
Q

Give an example of a titratable acid.

A

Titratable acid: NaH2PO4

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59
Q

What is the most effective way of removing H+?

A

NH4Cl: most effective way of removing H+

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60
Q

What does the H+-K+-ATPase pump excrete and regenerate?

A

H+-K+-ATPase pump: excretes excess H+; regenerates HCO3−

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61
Q

What is spironolactone and what does it do?

A

Spironolactone: aldosterone inhibitor; spares K+

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62
Q

How does an ACE inhibitor affect afterload and preload?

A

ACE inhibitor: ↓afterload (↓ATII), ↓preload (↓aldosterone)

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63
Q

How does Addison disease affect electrolyte levels?

A

Addison disease: hyponatremia, hyperkalemia, metabolic acidosis

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64
Q

What is primary aldosteronism most frequently caused by?

A

1° Aldosteronism: adenoma in zona glomerulosa

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65
Q

What electrolyte abnormalities are present in primary aldosteronism?

A

1° Aldosteronism: hypernatremia, hypokalemia, metabolic alkalosis

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66
Q

How does primary aldosteronism affect renin levels and blood pressure?

A

1° Aldosteronism: low renin hypertension

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67
Q

Why is pitting edema absent in mineralocorticoid excess states?

A

Absence pitting edema: escape phenomenon (PH > PO; lose Na+ in urine) + ↑ANP/BNP

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68
Q

What results from the absence of ADH?

A

Absence of ADH → dilution → loss of fH2O

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69
Q

How does CDI/NDI affect urine concentration?

A

CDI/NDI: always diluting, never concentrating

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70
Q

In CDI/NDI, how do UOsm and POsm compare?

A

CDI/NDI: UOsm < POsm

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71
Q

List one lab finding and two clinical findings in CDI/NDI.

A

CDI/NDI: hypernatremia, polyuria, polydipsia

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72
Q

Describe the results of water deprivation studies in CDI and NDI.

A

CDI: desmopressin ↑UOsm (concentration); NDI: desmopressin no change in UOsm

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73
Q

What is the treatment for CDI?

A

Rx CDI: desmopressin acetate

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74
Q

What is the treatment for NDI? How does the treatment work?

A

Rx NDI: thiazides; volume depletion decreases polyuria

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75
Q

How is the normal concentration of urine affected in CRF?

A

CRF: loss of concentration and dilution

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76
Q

What is a common cause of hyponatremia in a hospitalized patient?

A

SIADH: common cause of hyponatremia in hospitalized patient

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77
Q

What is the most common neoplasm ectopically producing SIADH?

A

SIADH: MCC small cell carcinoma of lung

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78
Q

How does SIADH affect the normal concentration of urine?

A

SIADH: always concentrating never diluting

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79
Q

In SIADH, how do UOsm and POsm compare?

A

SIADH: UOsm greater than POsm

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80
Q

What is diagnostic of SIADH? How are TBNa+ and TBW affected?

A

SIADH: serum Na+ <120 mEq/L; TBNa+/↑↑TBW

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81
Q

How are UOsm and random UNa+ affected in SIADH?

A

UOsm and random UNa+ increased in SIADH

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82
Q

How is mild SIADH treated?

A

Rx SIADH: restrict water

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83
Q

What does demeclocycline do and produce?

A

Demeclocycline: inhibits ADH; produces NDI

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84
Q

How does hypokalemia affect insulin secretion?

A

Hypokalemia inhibits insulin secretion

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85
Q

How does hyperkalemia affect insulin secretion?

A

Hyperkalemia stimulates insulin secretion

86
Q

What has primary control of potassium?

A

Aldosterone has primary control of K+

87
Q

How does arterial pH affect potassium levels? What is there the potential for?

A

Alkalosis causes K+ to move into cells; potential for hypokalemia

88
Q

How does acidosis affect potassium levels? What is there the potential for?

A

Acidosis causes K+ to move out of cells; potential for hyperkalemia

89
Q

How do insulin and β2-agonists affect potassium levels?

A

Insulin, β2-agonists enhance Na+/K+-ATPase pump: K+ moves into cell; hypokalemia

90
Q

How do digitalis, β-blockers and succinylcholine affect potassium levels?

A

Digitalis, β-blockers, succinylcholine inhibit Na+/K+-ATPase pump: K+ moves out of cell; hyperkalemia

91
Q

What is the most common cause of hypokalemia?

A

Loop/thiazide diuretics: MCC hypokalemia

92
Q

List four clinical and laboratory findings of hypokalemia.

A

Hypokalemia: muscle weakness; ECG shows U wave
Hypokalemia: polyuria; NDI due to vacuolar nephropathy
Hypokalemia: rhabdomyolysis

93
Q

List two clinical findings of hyperkalemia.

A

Hyperkalemia: ECG shows peaked T waves; heart can stop in diastole

94
Q

What is the benefit of calcium gluconate?

A

Calcium gluconate cardioprotective in hyperkalemia

95
Q

If there is no compensation, the expected compensation remains where?

A

No compensation: expected compensation remains in normal range

96
Q

If there is partial compensation, where is the expected compensation and pH?

A

Partial compensation: expected compensation outside normal range; pH outside normal range

97
Q

If there is full compensation, how is the pH affected? How often does full compensation occur?

A

Full compensation: compensation brings pH into normal range; rarely occurs

98
Q

What does pH define?

A

pH defines the primary disorder versus the compensation

99
Q

What do formulas for compensation help with?

A

Formulas for compensation: help recognize single versus multiple acid-base disorders

100
Q

Respiratory acidosis is due to what?

A

Respiratory acidosis: alveolar hypoventilation

101
Q

What is the PaCO2 in respiratory acidosis? How are the pH, HCO3-, and PCO2 affected?

A

Respiratory acidosis: Paco2 >45 mm Hg; ↓pH ~ ↑HCO3−/↑↑PCO2

102
Q

What is the compensation for metabolic alkalosis?

A

Metabolic alkalosis: compensation for respiratory acidosis

103
Q

What is the most common cause of respiratory acidosis?

A

Chronic bronchitis: MCC respiratory acidosis

104
Q

What is the PaCO2 in respiratory alkalosis? How are the pH, HCO3, and PCO2V affected?

A

Respiratory alkalosis: PaCO2 <33 mm Hg; ↑pH ~ ↓HCO3−/↓↓PCO2v

105
Q

What is respiratory alkalosis characterized by?

A

Respiratory alkalosis: alveolar hyperventilation eliminating CO2

106
Q

What is the compensation for respiratory alkalosis?

A

Metabolic acidosis: compensation for respiratory alkalosis

107
Q

What is the most common cause of respiratory alkalosis?

A

Anxiety: MCC respiratory alkalosis

108
Q

Tetany commonly occurs in what acid-base disorder?

A

Tetany: commonly occurs in acute respiratory alkalosis

109
Q

How is albumin affected in alkalosis?

A

Alkalosis: ↑COO− groups in acidic amino acids on albumin

110
Q

What is the serum HCO3- in metabolic acidosis? How are the pH, HCO3-, and PCO2 affected?

A

Metabolic acidosis: serum HCO3− <22 mEq/L; ↓pH ~ ↓↓HCO3−/↓PCO2

111
Q

What is the compensation for metabolic acidosis?

A

Respiratory alkalosis: compensation for metabolic acidosis

112
Q

What is the formula for calculating anion gap?

A

AG = serum Na+ − (serum Cl− + serum HCO3−) = 12 mEq/L ± 2

113
Q

What does increased anion gap signify?

A

↑AG: additional anions are present that should not be there

114
Q

Describe how is HCO3- affected in metabolic acidosis.

A

Metabolic acidosis: ↓HCO3− due to buffering of excess H+ from an acid

115
Q

In increased AG metabolic acidosis, what replaces buffered HCO3-?

A

↑AG metabolic acidosis: anions of acid replace buffered HCO3−

116
Q

What is the most common increased AG metabolic acidosis?

A

Lactic acidosis: most common ↑AG metabolic acidosis

117
Q

What is the osmolal gap useful for?

A

Osmolal gap: useful in diagnosing methanol or ethylene glycol poisoning

118
Q

In normal AG metabolic acidosis, what replaces HCO3-?

A

Normal AG metabolic acidosis: Cl− anions replace HCO3−

119
Q

List three clinical findings in metabolic acidosis.

A

Clinical findings: hyperventilation, warm shock, osteoporosis

120
Q

Metabolic alkalosis is due to what?

A

Metabolic alkalosis: lose H+ or gain HCO3−

121
Q

What is the serum HCO3- in metabolic alkalosis? How are the pH, HCO3-, and PCO2 affected?

A

Metabolic alkalosis: serum HCO3− >28 mEq/L; ↑pH ~ ↑↑HCO3−/↑PCO2

122
Q

What is the compensation for metabolic alkalosis?

A

Respiratory acidosis compensation for metabolic alkalosis

123
Q

What are the characteristic findings of chloride responsive metabolic alkalosis?

A

Cl− responsive: volume depletion, ↓serum/urine Cl−, ↑reclaiming HCO3−, corrects with normal saline

124
Q

List two examples of chloride responsive metabolic alkalosis.

A

Cl− responsive: vomiting, loop/thiazide diuretics

125
Q

Describe the characteristic findings of chloride resistant metabolic alkalosis.

A

Cl− resistant: volume overload, ↑serum/urine Cl−, no correction with normal saline

126
Q

What is the cause of chloride resistant metabolic alkalosis?

A

Cl− resistant: mineralocorticoid excess (e.g., 1° aldosteronism)

127
Q

What is a clinical findings of metabolic alkalosis?

A

Clinical findings: ↑risk ventricular arrhythmias

128
Q

What is a mixed acid-base disorder?

A

Mixed acid-base disorder: two or more primary acid-base disorders

129
Q

Describe salicylate intoxication as an example of a mixed acid-base disorder.

A

Salicylate intoxication: mixture 1° metabolic acidosis and 1° respiratory alkalosis; normal pH

130
Q

Describe chronic bronchitis and loop diuretic use as a mixed acid-base disorder.

A

Chronic bronchitis + loop diuretic = 1° chronic respiratory acidosis + 1° metabolic alkalosis and normal pH

131
Q

Describe cardiorespiratory arrest as a mixed acid-base disorder.

A

Cardiorespiratory arrest = 1° respiratory acidosis + 1° metabolic acidosis = extreme acidemia

132
Q

What are the clues for a mixed disorder?

A

Clues for mixed disorder: normal pH; extreme acidemia or alkalemia

133
Q

What is edema?

A

Edema: excess fluid in interstitial space

134
Q

What is a transudate?

A

Transudate: protein-poor and cell-poor fluid

135
Q

Transudates are associated with what?

A

Transudate: pitting edema, body cavity effusions; alteration in Starling forces

136
Q

What is an exudate?

A

Exudate: protein-rich and cell-rich fluid

137
Q

What does hydrostatic pressure do?

A

HP: move transudate out of capillaries/venules

138
Q

What does the oncotic pressure equate with and what does it do?

A

OP (albumin): opposes filtration out of capillaries/venules

139
Q

What are three clinical examples of increased HP?

A

↑HP: pulmonary edema, pitting edema RHF, ascites due to PH

140
Q

What are four clinical examples of decreased OP?

A

↓OP: nephrotic syndrome, malnutrition, cirrhosis, malabsorption

141
Q

Give an example of increased HP and decreased OP.

A

Ascites in cirrhosis: ↑HP (portal vein hypertension), ↓OP (hypoalbuminemia)

142
Q

How does renal retention of sodium and water affect HP? Give two examples.

A

Renal retention sodium and water: ↑hydrostatic pressure; renal failure, glomerulonephritis

143
Q

When is vascular permeability increased?

A

↑Vascular permeability: acute inflammation

144
Q

What does lymphatic obstruction produce?

A

Lymphedema: lymphatic obstruction

145
Q

List three examples of lymphedema.

A

Lymphedema: modified radical mastectomy and radiation; inflammatory carcinoma breast; filariasis

146
Q

What is the pathogenesis of thrombi?

A

Thrombi: endothelial injury, stasis of blood flow, hypercoagulability

147
Q

What is the pathogenesis of venous thrombi?

A

Pathogenesis venous thrombi: stasis blood flow, hypercoagulable state

148
Q

What is the most common site for venous thrombosis?

A

MC site for venous thrombosis: deep veins, lower extremity below the knee

149
Q

Where do thrombi in the lower extremity deep veins propagate toward?

A

Deep veins lower extremity: thrombi propagate toward the heart

150
Q

What is the composition of a venous thrombus?

A

Composition venous thrombus: entrapped RBCs, platelets, white blood cells

151
Q

What are heparin and warfarin?

A

Heparin/warfarin: anticoagulants that prevent venous thrombosis

152
Q

What is the pathogenesis of arterial thrombi?

A

Arterial thrombi: endothelial cell injury points of bifurcation/overlying atherosclerotic plaques

153
Q

What is the most common arterial thrombus?

A

MC arterial thrombus: coronary artery thrombus overlying an atherosclerotic plaque

154
Q

What is the composition of an arterial thrombus?

A

Composition arterial thrombus: fibrin clot composed of platelets

155
Q

What prevents arterial thrombi?

A

Prevention arterial thrombi: aspirin, other agents that prevent platelet aggregation

156
Q

Where are mixed thrombi located?

A

Mixed thrombus: heart chambers and aneurysms in aorta

157
Q

What is the composition of mixed thrombi?

A

Mixed thrombus: laminated; pale areas platelets, red areas predominantly RBCs

158
Q

Give two examples of thrombi that develop in heart chambers.

A

Heart chamber thrombi: left ventricle (post acute myocardial infarction), left atrium (mitral stenosis)

159
Q

What are the complications of arterial thrombi?

A

Arterial thrombi complications: infarction, embolization

160
Q

Describe the composition of postmortem clots.

A

Postmortem clot: nonadherent fibrin clot of plasma without cells

161
Q

Describe the site of origin of PE,

A

PE: majority originate in deep veins of lower extremities and pelvis

162
Q

What are the clinical findings of PE?

A

PE clinical: sudden death, pulmonary infarction

163
Q

Why is pulmonary infarction uncommon?

A

Pulmonary infarction uncommon: dual blood supply—pulmonary arteries, bronchial arteries

164
Q

What is a paradoxical embolus?

A

Paradoxical embolus: venous embolus passing thru ASD/VSD into systemic circulation

165
Q

Where do systemic emboli originate?

A

Systemic embolism: majority originate in left side of heart

166
Q

What are two sources for noncardiogenic embolization?

A

Noncardiogenic embolization: aortic aneurysms, ulcerated atherosclerotic plaques

167
Q

What are the target sites of systemic emboli?

A

Target sites: upper/lower extremities, spleen, kidneys, small bowel

168
Q

What are the clinical findings of systemic embolism?

A

Clinical findings systemic embolism: pale and hemorrhagic infarctions

169
Q

What is the most common cause of fat embolism?

A

Fat embolism: fracture of long bones most common (e.g., femur), pelvis

170
Q

Describe the pathogenesis of fat embolism.

A

Marrow fat enters ruptured marrow sinusoids and venules

Fat emboli initially trapped in pulmonary capillaries: enter arteriovenous shunts to disperse to distant sites

171
Q

When do symptoms/signs of fat embolism occur?

A

Symptoms/signs of fat embolism occur in 1−3 days

172
Q

What are the clinical findings of fat embolism?

A

Fat embolism: dyspnea, tachypnea, petechiae over chest/upper extremities

173
Q

What are the lab findings of fat embolism?

A

Fat embolism: hypoxemia, ↑A-a gradient, thrombocytopenia

174
Q

Describe the epidemiology of AF embolism.

A

AF embolism: occurs during labor or immediately postpartum

Maternal mortality 80%

175
Q

What is the pathogenesis of AF embolism?

A

Pathogenesis: tear placental membrane, rupture uterine veins

176
Q

What are the clinical findings of AF embolism?

A

Clinical: abrupt onset dyspnea, hypotension, bleeding
Clinical: ARDS, DIC

177
Q

What are the autopsy findings in AF embolism?

A

Autopsy: pulmonary vessels—fetal squames, lanugo hair, vernix

178
Q

What is the prognosis in AF embolism?

A

Prognosis: permanent neurologic impairment 85%

179
Q

What are the lab findings in AF embolism?

A

Laboratory: hypoxemia, respiratory acidosis, ↑PT

180
Q

Describe the epidemiology of DCS.

A

DCS: form of gas embolism; scuba diving, deep sea diving

181
Q

What is the pathogenesis of DCS?

A

DCS: nitrogen gas goes into solution in blood and tissue with descent
DCS: rapid ascent causes nitrogen gas bubbles in vessel lumens and tissue (e.g., joints)

182
Q

What are the clinical findings in DCS?

A

The bends: nitrogen gas in skeletal muscle vessels and joints
Nervous system: mimics spinal cord trauma
Pneumothorax: rapid ascent; rupture preexisting subpleural/intrapleural bleb; dyspnea pleuritic chest pain
PE: ↑pressure on lower extremity veins → stasis → thrombosis → embolism; dyspnea, pleuritic chest pain

183
Q

What is caisson disease?

A

Caisson: persistent nitrogen gas bubbles in bone; aseptic necrosis femur, tibia, humerus

184
Q

What is the treatment from DCS?

A

Rx DCS: recompression in high pressure chamber followed by slow decompression

185
Q

What is hypovolemic shock due to?

A

Hypovolemic shock: excessive fluid loss (blood/sweat/sodium in urine)

186
Q

What loss of blood volume produces shock?

A

Loss of >20% of blood volume produces shock

187
Q

What are two causes of external bleeding?

A

External bleeding: penetrating trauma, gastrointestinal bleeding

188
Q

What are causes of internal bleeding?

A

Internal bleeding: trauma to solid organs (liver/spleen), ruptured abdominal aortic aneurysm

189
Q

How are Hb and Hct affected in blood loss?

A

Blood loss: no initial drop in Hb and Hct

190
Q

What uncovers RBC deficit immediately in blood loss?

A

Normal saline uncovers RBC deficit immediately

191
Q

When does reticulocyte response to RBC deficit begin?

A

Reticulocyte response to RBC deficit begins in 5-7 days

192
Q

What is the best indicator of tissue hypoxia?

A

MVO2: best indicator of tissue hypoxia

193
Q

How are CO, LVEDP, PVR, and MVO2 affected in hypovolemic shock?

A

Hypovolemic shock ↓CO, ↓LVEDP, ↑PVR, ↓MVO2

194
Q

What are the clinical findings in hypovolemic shock?

A

Clinical: cold/clammy skin, hypotension, tachycardia,↓urine output

195
Q

What are the lab findings in hypovolemic shock?

A

Laboratory:↑AG metabolic acidosis due to lactic acidosis

196
Q

What is the most common cause of cardiogenic shock?

A

Cardiogenic shock: MCC AMI

197
Q

How are CO, LVEDP, PVR, and MVO2 affected in cardiogenic shock?

A

Cardiogenic shock: ↓CO, ↑LVEDP, ↑PVR, ↓MVO2

198
Q

What are the lab findings in AMI?

A

Laboratory findings in AMI: ↑CK-MB, ↑troponin I and T

199
Q

What is the most common site for infection leading to sepsis?

A

MC site for infection leading to sepsis is the lungs

200
Q

What is the most common cause of death in intensive care units?

A

MCC of death in intensive care units is septic shock

201
Q

What is the most common cause of septic shock?

A

Septic shock: MCC sepsis due to gram-positive organisms (coagulase-negative Staphylococci)

202
Q

What is the most common cause of gram-negative septic shock?

A

Escherichia coli: MCC of gram-negative septic shock

203
Q

What is the most common fungal cause of septic shock?

A

Candida species: MC fungal cause septic shock

204
Q

What is the most important factor producing septic shock in gram-positive pathogens?

A

Lipoteichoic acid: most important factor producing septic shock in gram-positive pathogens

205
Q

What does IL-1 do?

A

IL-1: fever, activate neutrophil adhesion molecules (neutropenia)

206
Q

What does TNF do?

A

TNF: damages endothelial cells (releases vasodilators; NO, PGI2)

207
Q

What do endotoxins do?

A

Endotoxins: activate macrophages, complement system, tissue thromboplastin (DIC)

208
Q

How are CO, LVEDP, PVR, and MVO2 affected in the initial phase of septic shock?

A

Septic shock (initial phase): ↑CO, ↓LVEDP, ↓PVR, ↑MVO2

209
Q

What are the clinical findings in early septic shock?

A

Clinical: warm skin, strong peripheral pulses, hypotension, DIC

210
Q

What is there increased risk for developing in septic shock?

A

Septic shock: ↑risk for ARDS

211
Q

What are the hematologic findings in early septic shock?

A

Hematologic findings: anemia, thrombocytopenia, neutropenia

212
Q

What is the most common cause of death in shock?

A

MODS: MCC of death in shock

Rapid Review Pathology (14 decks)

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