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Internal Medicine > Symptom to Diagnosis - Acid-Base Abnormalities > Flashcards

Symptom to Diagnosis - Acid-Base Abnormalities Flashcards

1
Q

Step 2 in evaluation of acid-base disorders?

A

Determine whether the primary disorder is due to a metabolic or respiratory process. Check HCO3 and PaCO2.

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2
Q

Step 3 in evaluation of acid-base abnormalities?

A
  1. Calculate whether compensation is appropriate. 2. Formulas predict the expected degree of compensation. 3. Greater or less than predicted compensation suggests that an additional process is affecting the compensating system.
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3
Q

Step 4 in evaluation of acid-base abnormalities?

A

Calculate the anion gap –> Na -(HCO3+Cl). If ELEVATED –> Anion gap metabolic acidosis!

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4
Q

When does anion gap acidosis occur?

A

When an acid is produced and the associated unmeasured anion accumulates - ie ketones, lactate, sulfates, phosphates, or organic anions –> Increasing the anion gap.

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5
Q

Anion gap is affected by?

A

Serum albumin level –> Albumin is negatively charged so that lower serum albumin levels are associated with a lower anion gap.

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6
Q

What is the expected drop in the normal value for the anion gap?

A

2.5mEq/L for every 1g/dL drop in the serum albumin (below 4.4g/dL).

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7
Q

Step 1 in evaluation of acid-base abnormalities?

A

Check pH: PRIMARY disorder is acidosis. >7.4 –> PRIMARY disorder is alkalosis.

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8
Q

Compensation in respiratory acidosis - Acute?

A

HCO3 UP 1mEq/L per 10mmHg UP PaCO2.

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9
Q

Compensation in metabolic alkalosis (either acute or chronic)?

A

PaCO2 UP 0.7mmHg per 1 mEq/L HCO3 increase.

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10
Q

Compensation in acid-base disorders - Metabolic acidosis (either acute or chronic)?

A

Expected compensation: PaCO2 DOWN 1.2mmHg per 1mEq/L HCO3 decrease. To a MINIMUM of 10-15mmHg PaCO2.

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11
Q

Compensation of respiratory acidosis - Chronic?

A

HCO3 UP 3.5mEq/L per 10mmHg UP PaCO2.

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12
Q

Metabolic or respiratory compensation is slower and becomes more complete with time?

A

Metabolic.

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13
Q

Compensation in respiratory alkalosis - Chronic?

A

HCO3 DOWN 4mEq/L per 10mmHg DOWN PaCO2.

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14
Q

Normal baseline of PaCO2 and HCO3?

A

40mmHg and 24mEq/L.

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15
Q

Non anion gap metabolic acidosis occurs when?

A

HCO3 is lost in the urine or stool.

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16
Q

The normal anion gap is due to?

A

Negatively charged proteins such as albumin, phosphates, and sulfates.

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17
Q

Etiology of metabolic acidosis - Anion gap acidoses?

A
  1. Ketoacidosis - DKA, starvation, alcoholic. 2. Lactic acidosis - 2o to any impairment of aerobic metabolism. 3. Uremia - associated with sulfate and phosphate accumulation. 4. Toxin, drugs, and miscellaneous - Aspirin, methanol, ethylene glycol, rhabdomyolysis, D-lactic acidosis.
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18
Q

The DDX of lactic acidosis includes?

A

Any disease that interrupts O2 transport from the environment to the cell’s mitochondria –> Common causes include hypoxia and hypotension (shock).

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19
Q

Non anion gap metabolic acidosis - Etiology?

A
  1. Diarrhea. 2. Renal tubular acidosis (RTA) (type IV most common in adults). 3. Carbonic anhydrase inhibitor. 4. Dilutional - large volume normal saline administration. 5. Early renal failure.
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20
Q

Metabolic alkalosis - Etiology?

A
  1. Vomiting or nasogastric tube. 2. Volume depletion - Diuretics, vomiting. 3. Hypokalemia. 4. Incr. mineralocorticoid activity –> Primary hyperaldosteronism/Hypercortisolism/Excessive licorice ingestion (!).
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21
Q

Respiratory acidosis - Etiology?

A

Any process that participates in normal ventilation - brain, brainstem, spinal cord, nerve, neuromuscular junction, muscle, chest wall, or lung.

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22
Q

Respiratory acidosis - Specific etiology?

A
  1. Brain –> Stroke, drugs, hemorrhage, trauma, sleep apnea. 2. Brainstem herniation. 3. Spinal cord –> Trauma, ALS, polio. 4. Nerve –> Gullain-Barre. 5. Neuromuscular junction –> Myasthenia gravis. 6. Chest wall or muscle –> Flail chest, muscular dystrophy. 7. Pleural disease –> Effusions, pneumothorax.
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23
Q

Respiratory acidosis - MCC?

A

Lung diseases: 1. COPD. 2. Asthma. 3. Pulm. edema. 4. Pneumonia.

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24
Q

Respiratory alkalosis - Etiology?

A
  1. Hypoxemia. 2. Pulm. disorders - via both hypoxic and vagal mechanisms. 3. Extrapulmonary disorders.
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25
Q

Respiratory alkalosis - Pulmonary disorders?

A
  1. Pneumonia. 2. Asthma. 3. Pulm. embolism. 4. Pulm. edema. 5. Interstitial lung disease. 6. Mechanical ventilation.
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26
Q

Respiratory alkalosis - Extrapulmonary disorders?

A
  1. Anxiety. 2. Pain. 3. Fever. 4. Pregnancy. 5. CNS insult. 6. Drugs (salicylates, nicotine, catecholamines). 7. Cirrhosis.
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27
Q

Textbook presentation of DKA:

A

Often begins as an acute illness (ie pneumonia, UTI, MI) in a type I diabetic.

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28
Q

DKA precipitants in type II diabetes:

A
  1. Severe stress. 2. Marked hyperglycemia that may transiently impair insulin secretion.
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29
Q

DKA incidence:

A

4.6-8 cases/1.000 person years in patients with diabetes.

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30
Q

General precipitants of DKA:

A
  1. Low insulin. 2. High insulin counter-hormones (cortisol, Epi, glucagon, GH). 3. BOTH.
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31
Q

DKA - MC precipitants:

A
  1. New-onset type I DM. 2. Non compliance with insulin. 3. Infection (UTI and pneumonia are MC. Patients may be AFEBRILE).
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32
Q

DKA - Other precipitants:

A
  1. Other infections. 2. MI. 3. CVA. 4. PE. 5. Acute pancreatitis. 6. GI hemorrhage. 7. Severe emotional stress. 8. Drugs (eg steroids, thiazides, cocaine).
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33
Q

Most frequent cause of mortality in DKA:

A

The precipitant.

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34
Q

DKA Pathogenesis:

A

Marked decrease in insulin levels together with an increase in counterregulatory hormones.

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35
Q

DKA - Following events:

A
  1. Hyperglycemia. 2. Ketoacidosis. 3. Volume depletion. 4. Hypokalemia. 5. Hyperkalemia. 6. Hyponatremia.
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36
Q

DKA - Hyperglycemia:

A
  1. Reduced glucose uptake by cells leads to hyperglycemia. 2. Increased hepatic glycogenolysis and gluconeogenesis –> augment hyperglycemia. 3. Glucosuria helps prevent extreme hyperglycemia (>500-600mg/dL). 4. More extreme hyperglycemia occurs if urinary output falls.
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37
Q

DKA - Ketoacidosis:

A
  1. Marked insulin deficiency increases acetyl CoA production within the liver. 2. Massive production of acetyl CoA overwhelms Krebs cycle –> Ketone production and ketonemia (primarily β hydroxybutyric acid and to a lesser extent acetoacetic acid). 3. Ketonemia leads to anion gap metabolic acidosis.
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38
Q

DKA - Volume depletion:

A

Ketonemia and hyperglycemia result in OSMOTIC DIURESIS which results in profound dehydration and typical fluid losses of 3-6L.

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39
Q

DKA - Hypokalemia:

A
  1. Osmotic diuresis also causes significant K losses. 2. Dehydration-induced hyperaldosteronism –> K loss. 3. Typical K deficit is 3-5mEq/kg body weight.
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40
Q

DKA - HYPERkalemia:

A
  1. Despite the total body K, hyperkalemia is frequent. 2. Etiology is multifactorial. a. Insulin normally drives glucose + K INTO the cells. Insulin def. causes HYPERkalemia. b. Plasma hypertonicity drives H2O + K OUT of the cell –> HYPERkalemia. c. Acidosis –> K OUT of the cells –> HYPERkalemia.
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41
Q

DKA - Hyponatremia:

A

Hyperglycemia leads to an osmotic shift of water from the intracellular space to intravascular space, resulting in hyponatremia.

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42
Q

DKA mortality rate:

A

5-15%.

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43
Q

Compensation in respiratory alkalosis - Acute?

A

HCO3 DOWN 2mEq/L per 10mmHg DOWN PaCO2.

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44
Q

DKA - Main symptoms/signs:

A
  1. Polyuria and increased thirst are common. 2. Lethargy and obtundation may be seen with markedly increased effective osmolality (>320mOsm/L). 3. Abdominal pain. 4. Nausea and vomiting are common and nonspecific.
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45
Q

DKA - Diagnostic criteria established by the American Diabetes Association (ADA):

A
    1. Glucose >250mg/dL.
    1. pH
    1. HCO3
    1. Positive serum ketones.
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46
Q

DKA - Effective osmolality can be calculated:

A

2x Na + Gluc/18.

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47
Q

DKA - Abdominal pain:

A

Present in 50-75% of DKA cases.

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48
Q

DKA - Abdominal pain due to:

A

2o to the DKA or another process precipitating DKA (appendicitis, pancreatitis, cholecystitis, abscess). –> Increasingly common with increasing severity of DKA.

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49
Q

DKA - When to consider an intra-abdominal cause?

A

Always, especially if the abdominal pain persists, occurs in patients with mild acidosis (HCO3 >10mEq/L), or in patients older than 40yrs.

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50
Q

DKA - Patients with glucose

A

15% - Particularly in pregnancy or with poor oral intake.

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51
Q

Sensitivity of glucose >250 for DKA?

A

POOR (11%).

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52
Q

DKA - 3 ketones:

A
  1. β-hydroxybutyrate. 2. Acetoacetate. 3. Acetone.
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53
Q

DKA - Use of nitroprusside reaction?

A

To detect ketones - Acetoacetate but NOT beta-hydroxybutyrate.

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54
Q

Prominent ketone in severe DKA:

A

Beta hydroxybutyrate.

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55
Q

Which drug causes a false(+) nitroprusside reaction?

A

Captopril.

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56
Q

DKA diagnosis - Measurement of beta hydroxybutyrate:

A

Directly and rapidly. 98% sensitive. 85% specific. LR+ 6.5. LR- 0.02.

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57
Q

DKA diagnosis - urine ketones helpful?

A

Sensitive for DKA but NOT specific (69%). Blood measurement is preferred.

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58
Q

Anion gap - In patients with DKA and glucose >250 in the ED - Sensitivity/specificity, LR+, LR-?

A

84-90% sensitive. 85-99% specific. LR+ 6-84. LR- 0.11-0.16.

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59
Q

If anion gap is positive and ketones are negative - Next step?

A
  1. βOHB measurements. 2. Lactic acid should be measured to rule out lactic acidosis.
60
Q

DKA - Non specific findings:

A
  1. Amylase - non specific elevations in amylase are common. 2. Leukocytosis: a. Mild leukocytosis (10.000-15.000) - May be secondary to stress or infection. b. One study documented higher WBCs in patients without major infection. c. Bands also higher.
61
Q

DKA - Treatment:

A

Must include the following: 1. Initial evaluation and frequent monitoring. 2. Detection and therapy of the underlying precipitant. 3. Fluid/ resuscitation. 4. Insulin. 5. K replacement.

62
Q

MCC of death in DKA:

A

The underlying PRECIPITANT. Find it and treat it.

63
Q

DKA - Initial evaluation and monitoring:

A
  1. Check electrolytes, glucose, ketones, ABG, anion gap, renal function. 2. Serum Cr may be artificially elevated due to interference of assay by ketones. 3. Serum glucose should be check hourly - Electrolytes should be measured frequently (2-4h) and the anion gap calculated.
64
Q

DKA - detection and therapy of the underlying precipitant:

A
  1. Urinalysis, chest film, CBC with differential, blood cultures, lipase, ECG, Troponin levels. 2. β-HCG should be measured in women of childbearing age.
65
Q

DKA treatment - Steps in fluid resuscitation:

A

Step 1: Evaluate dehydration - Check BP, Orthostatic BP, pulse, urinary output. Step 2: IV normal saline 0.5-1.5L bolus initially. Step 3: Reevaluate after each liter by checking BP, orthostatic BP and pulse, urinary output, cardiac and pulmonary exams. Repeat boluses until hypotension and Oliguria resolve. Step 4: Normal saline should be switched to 0.45% normal saline when Intravascular volume improves to restore free water deficit.

66
Q

DKA treatment - Do I give insulin?

A
  1. ADA recommends an IV bolus of regular insulin (0.1units/kg) followed by IV regular insulin 0.1units/kg/hr. 2. Exclude marked HYPOkalemia before starting insulin. 3. Administer in monitored setting. 4. HOURLY glucose monitor –> Target is 75-90 - Adjust accordingly. 5. Insulin should be continued until the AG normalizes and serum HCO3 is >18.
67
Q

Insulin importance in DKA treatment:

A

In DKA, it is important to continue IV insulin until the anion gap returns to normal. –> Administer glucose as necessary to prevent hypoglycemia.

68
Q

HCO3 therapy in DKA:

A
  1. Use is controversial; if used, monitor patient for HYPOkalemia. 2. HCO3 has NOT been shown to improve outcomes in pH>6.9. It may also paradoxically LOWER CNS pH. 3. ADA recommends HCO3 therapy in patients with a pH
69
Q

Phosphate therapy in DKA:

A
  1. Hypophosphatemia is common and may develop during therapy. 2. Replacement in those with MARKED hypophosphatemia (
70
Q

Uremic acidosis - Textbook presentation.

A

Patients with chronic renal failure, low HCO3, high creatinine (often 4-5), and elevated BUN and phosphate. Constitutional symptoms: fatigue, nausea, vomiting, anorexia, and Pruritus.

71
Q

Uremic acidosis - Disease highlights:

A
  1. Each day, ingested nonvolatile acids neutralize HCO3. 2. In health, the kidneys regenerate the HCO3 and maintain the acid-base equilibrium. 3. Renal impairment results in failed HCO3 regeneration –> Metabolic acidosis.
72
Q

AG or non AG metabolic acidosis in renal failure?

A

Either.

73
Q

Early renal failure - AG or non AG metabolic acidosis?

A

NON AG metabolic acidosis. Ammonia-genesis is impaired, resulting in reduced acid secretion and a non anion gap metabolic acidosis.

74
Q

Advanced renal failure - AG or non AG metabolic acidosis?

A

AG metabolic acidosis. Kidneys remain unable to excrete the daily acid load and also become unable to excrete anions (sulfates, phosphates, urate). –> AG. HCO3 levels stabilize between 12-20.

75
Q

Uremic acidosis - Side effects:

A
  1. Increased calcium loss from bone. 2. Increased skeletal muscle breakdown.
76
Q

Uremic acidosis - Treatment:

A
  1. NaHCO3 replacement. 2. Hemodialysis.
77
Q

Lactic acidosis 2o to sepsis - Textbook presentation:

A
  1. Patients with septic shock typically have fever, Tachypnea, Tachycardia, hypotension. 2. Warm extremities and BOUNDING pulses after fluid resuscitation - widened pulse pressure. 3. Mentation may be impaired and urinary output decreased.
78
Q

Sepsis more common in whites or non whites?

A

More common in non whites RR 1.90.

79
Q

Sepsis - MC sources of infection are:

A
  1. Lung. 2. Intra-abdominal infections. 3. Urine, and IV catheters.
80
Q

Commonly overlooked sources of sepsis:

A
  1. Sinusitis (associated with nasogastric tubes). 2. Acalculous cholecystitis. 3. C.difficile colitis.
81
Q

Certain life threatening infections may produce?

A

Characteristic rashes –> Meningococcemia, Rocky Mountain Spotted fever, or staph toxic shock syndrome. Rapid recognition is vital.

82
Q

Sepsis - Pathophysiology:

A
  1. Occurs when an infection (bacterial, fungal, mycobacterial, or viral) triggers a proinflammatory reaction that is poorly regulated and becomes SYSTEMIC. 2. A non infectious process (acute pancreatitis) may also trigger a similarly dysregulated immune response called SIRS.
83
Q

Early sepsis - Immune response:

A

HYPERimmune response may play a role in the organ dysfunction and cause multiple organ dysfunction syndrome (MODS), hypotension, DIC, and death.

84
Q

Late sepsis - Immune response:

A

HYPOimmune –> Infection and death.

85
Q

Hypotension in sepsis?

A

Vasodilation - DOWN SVR due to NO, PGs, low vasopressin.

86
Q

Cardiac output in sepsis:

A

Increased or decreased. 1. Drop in SVR decreases afterload –> UP CO. 2. 3rd space loss –> DOWN Venous return –> DOWN CO. 3. Myocardial function can be reduced and also decrease CO.

87
Q

Initial response in cardiac output?

A

Decreased SVR initially –> Increased CO (particularly after fluid resuscitation).

88
Q

Sepsis and Multiple Organ Dysfunction Syndrome (MODS):

A
  1. Lung involvement: ARDS due to increased permeability. 2. Renal failure. 3. DIC.
89
Q

Renal failure in sepsis:

A
  1. Hypotension. 2. Renal vasoconstriction. 3. Increased TNF.
90
Q

Sepsis and lactic acidosis:

A
  1. Microcirculatory lesion impairs O2 delivery. 2. Hypotension impairs O2 delivery. 3. Mt injury impairs O2 utilization. 4. Decreased hepatic clearance of lactate contributes to lactic acidosis.
91
Q

Definition of sepsis:

A

Infection and AT LEAST 2 of the following: 1. Temperature >38.5 or 90. 3. RR> 20 or PaCO2 12.000 or 10% bands.

92
Q

Mortality associated with sepsis:

A

16%.

93
Q

Definition of SEVERE sepsis:

A

Sepsis and AT LEAST one of the following signs of inadequate tissue perfusion: 1. Altered mental status. 2. OLIGURIA. 3. Lactic acidosis. 4. Platelets

94
Q

Definition of septic shock:

A

Severe sepsis with a mean BP

95
Q

Increased risk for septic shock in patients with:

A
  1. Bacteremia (21%). 2. Age >65. 3. Impaired immune system. 4. CAP. 5. Abdominal infection. 6. Markedly elevated WBC.
96
Q

Mortality of severe sepsis:

A

20%.

97
Q

Mortality of septic shock:

A

46%.

98
Q

Predictors of mortality in sepsis include:

A
  1. Age >40. 2. Comorbidities: Immunosuppression, hepatic failure, heart failure, DM, Cancer. 3. Temperature
99
Q

Fever in sepsis:

A
  1. Higher in bacteremics (38.8) than non bacteremic(38.1). 2. 5% with Gram(-) bacteremia are normothermic (
100
Q

Sepsis and chills:

A
  1. Can vary. 2. Some kind of chills are common in bacteremic patients (88% sensitivity). 3. Shaking chills (rigors) are less sensitive but more SPECIFIC for bacteremia (sens 45%, spec 90%, LR+ 4.7, LR- 0.61).
101
Q

Predictors of bacteremia:

A
  1. Shaking chills. 2. Injection drug use. 3. Central venous catheter. 4. Acute abdomen. 5. WBC>15.000. 6. WBC 1.500. 8. Any type of chills. 9. Comorbidity.
102
Q

A normal WBC…?

A

Does NOT RULE OUT bacteremia.

103
Q

Incidence of bacteremia is low (2%) in patients without ANY of the following risk factors:

A
  1. Temperature >38.3. 2. Shaking chills. 3. Injection drug use. 4. Acute abdomen on exam. 5. Major comorbidity.
104
Q

Catheter site infections - Signs of inflammation?

A

Uncommon in patients with venous catheter infections (sensitivity 27%). Erythema is present in only 3% of patients with catheter-related bloodstream infections.

105
Q

Certain specific findings for catheter infection?

A

Gross pus at the catheter insertion site, cellulitis >4mm around the site, or tunnel tract infection.

106
Q

Sepsis diagnosis - Serum lactate or anion gap is more sensitive?

A

Serum lactate. AG is 44-67% sensitive.

107
Q

Cultures can be negative in … of patients with sepsis?

A

10%.

108
Q

ACUTE Respiratory acidosis - HCO3 compensation?

A

1mEq for every 10mmHg PaCO2 increase.

109
Q

CHRONIC respiratory acidosis - HCO3 compensation:

A

3.5mEq/L for every 10mmHg PaCO2.

110
Q

Why is it vital to distinguish acute from chronic respiratory acidosis?

A

Because the former is more likely to progress rapidly to COMPLETE respiratory failure.

111
Q

MCC of respiratory acidosis:

A

Underlying lung or heart diseases (ie COPD and HF). Such patients are typically in extreme respiratory distress.

112
Q

How is ventilation assessed in respiratory acidosis?

A

By measuring PaCO2. NEVER pulse oximetry to assess adequate ventilation

113
Q

Etiology of respiratory acidosis:

A

Although most commonly due to lung or heart disease, respiratory acidosis may result from any disease affecting ventilation, from the brain to the alveoli.

114
Q

Respiratory acidosis manifestations:

A

Primarily CNS: 1. Severity depends on acuity. Acute has more symptoms than chronic. 2. Anxiety, irritability, confusion, and lethargy. 3. Headache may be prominent in the morning due to the worsening hypoventilation that occurs with sleep. 4. Stupor and coma may occur when the PaCO2>70-100mmHg. 5. Tremor, asterixis, slurred speech, Papilledema may be seen.

115
Q

A normal PaCO2 during respiratory acidosis suggests?

A

Respiratory failure.

116
Q

How to distinguish hypercapnia due to pulmonary disease from HYPERCAPNIA due to CNS disease (central hypoventilation)?

A

Via the A-a gradient.

117
Q

Normal A-a gradient is around?

A

10.

118
Q

Pulsus paradox - Definition:

A

Defined as >10mmHg drop in systolic BP during inspiration.

119
Q

Pulsus paradox may be seen in?

A

In patients using unusually strong inspiratory effort.

120
Q

Pulsus paradox - Sensitivity for asthma?

A

Insensitive for asthma.

121
Q

When pulsus paradox is marked?

A

There is a high LR of severe disease

122
Q

Treatment of respiratory acidosis:

A
  1. Treat underlying disease process (bronchodilators for asthma, naloxone for narcotic overdose). 2. Supplement O2 - Not in severe COPD, asthma, sleep apnea (generally hypoxic). 3. Avoid HYPOkalemia and dehydration that may worsen metabolic alkalosis.
123
Q

Mechanical ventilation in the treatment of respiratory acidosis?

A
  1. When pH80-90mmHg. 2. In general –> Patients with ACUTE hypoventilation require mechanical ventilation with MILDER hypercapnia than patients with chronic hypoventilation.
124
Q

Textbook presentation of lactic acidosis:

A

Presentation of lactic acidosis depends on the underlying etiology. MCCs are: 1. Hypoxemia. 2. Septic shock. 3. Cardiogenic shock. 4. Hypovolemic shock.

125
Q

What can cause lactic acidosis (generally)?

A

Any disease that interferes with O2 delivery.

126
Q

Etiology of lactic acidosis - low O2 carrying capacity:

A
  1. Hypoxemia - from pulmonary or cardiac disease. 2. Severe anemia. 3. CO poisoning (interferes with O2 binding).
127
Q

Etiology of lactic acidosis - Inadequate tissue perfusion (shock):

A
  1. Hypovolemic shock. 2. Cardiogenic shock. 3. Septic shock.
128
Q

Etiology of lactic acidosis - other causes:

A
  1. Regional obstruction to blood flow (ischemic bowel). 2. Inadequate cellular utilization of O2 (cyanide poison). 3. Occasionally - develops 2o to unusually high demand exceeding O2 supply (eg intense exercise, seizures).
129
Q

Problem with lactic acidosis and shock?

A

Substantially increased mortality. 70% compared to 25-35% in patients with shock without lactic acidosis.

130
Q

Should we order a serum lactate level in critically ill patients?

A

Yes - Regardless of the anion gap.

131
Q

Treatment of lactic acidosis:

A

Should target the underlying condition. A variety of buffering agents (ie NaHCO3) have been tried and failed to demonstrate improved hemodynamics or survival.

132
Q

MC type of RTA?

A

IV - Hyporenin hypoaldosterone.

133
Q

Textbook presentation of hyporenin hypoaldosterone RTA:

A

Patients have long-standing diabetes, mild renal insufficiency, a mild non AG metabolic acidosis (HCO3=17) and HYPERkalemia.

134
Q

Etiology of RTA IV:

A

Numerous: 1. Diabetes with mild renal impairment is common. 2. Drugs. 3. Addison. 4. SLE. 5. AIDS nephropathy. 6. Chronic interstitial renal disease.

135
Q

Treatment of RTA IV:

A

Dietary K restriction, loop diuretics, fludrocortisone.

136
Q

D-lactic acidosis - Where to see it?

A

Rare disorder - in some patients with jejunoileal bypass or short bowel.

137
Q

D-lactic acidosis - presenting manifestations:

A

Encephalopathy and metabolic acidosis after carbohydrate ingestion.

138
Q

Alcoholic ketoacidosis - when?

A

Usually in advanced alcoholism when the majority of calories are from the alcohol.

139
Q

Alcoholic Ketoacidosis - Precipitants:

A
  1. Decreased intake. 2. Pancreatitis. 3. GI bleeding. 4. Infection.
140
Q

Metabolic alkalosis - Textbook presentation:

A

MC clinical situations that give rise to metabolic alkalosis are: 1. Recurrent vomiting. 2. Diuretics. Usually ASYMPTOMATIC - Muscle cramping due to COEXISTENT HYPOkalemia may be seen.

141
Q

What is the essential basis for metabolic alkalosis to occur:

A

BOTH an increased production of HCO3 + A renal stimulus to reabsorb NaHCO3. In the absence of a concomitant renal stimulus to reabsorb NaHCO3, overproduction simply results in increased renal HCO3 excretion.

142
Q

MC mechanism that promotes NaHCO3 reabsorption is?

A

Decreased renal perfusion.

143
Q

Respiratory alkalosis - Textbook presentation:

A

Depends on the underlying disorder: Most –> Associated with tachypnea, which can be dramatic or subtle.

144
Q

MCC of respiratory alkalosis:

A
  1. Pulmonary disease. 2. Fever. 3. Pain. 4. Anxiety. –> Hyperventilation.
145
Q

Respiratory alkalosis and CNS function:

A

Hypocapnia –> ACUTELY reduces CNS blood flow. Symptoms: 1. Paresthesias. 2. Vertigo. 3. Dizziness. 4. Anxiety. 5. Hallucinations. 6. Myalgias.

146
Q

Respiratory alkalosis - Adverse effects:

A
  1. Decreased cerebral blood flow. 2. Hypokalemia. 3. Hypocalcemia. 4. Lung injury. 5. Seizures. 6. Angina. 7. Arrhythmias.
147
Q

DKA - Risk factors for death:

A
  1. Severe coexistent disease - OR 16.3. 2. pH300 after 12hrs - OR 8.3. 5. Depressed mental status after 24hr - OR 8.6. 6. Fever >38 after 24hr - OR 5.8. 7. Increasing age - Mortality rate 55.

Internal Medicine (106 decks)

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