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ACNP805: Acute Diagnostic Reasoning > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Alcoholic ketoacidosis

A

Wide anion gap metabolic acidosis associated with acute cessation of alcohol consumption after chronic abuse

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2
Q

True or false: Alcoholic ketoacidosis is found only in chronic drinkers.

A

False. Usually found in chronic, but has been reported in first-time binge drinkers.

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3
Q

Alcoholic ketoacidosis symptoms

A

typically associated with nausea, vomiting, abdominal pain, shortness of breath and vague GI complaints. Signs: tachypnea, tachycardia, heme+ stool, hepatomegaly, altered mental status, hypotension

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4
Q

What is the mechanism of alcoholic ketoacidosis?

A

Occurs when NAD is depleted by ethanol metabolism, resulting in inhibition of the aerobic metabolism in the Krebs cycle, depletion of glycogen stores, ketone formation, and lipolysis stimulation.

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5
Q

Diagnostic criteria for alcoholic ketoacidosis

A

Ω Low, normal or slightly elevated glucose Ω Binge drinking ending in nausea, vomiting, decreased intake Ω Wide anion gap metabolic acidosis Ω Positive serum ketones Ω Wide anion gap metabolic acidosis without alternate explanation

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6
Q

Alternative diagnoses for alcoholic ketoacidosis

A

% Lactic acidosis % Uremia % Secondary lactic acidosis *sepsis *hypotension *salicylic acid ingestion *toxic alcohol ingestion % DKA % Starvation ketosis

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7
Q

Alternative or concomitant diagnoses for alcoholic ketoacidosis

A

% Methanol ingestion % Ethylene glycol ingestion % Isopropanol ingestion % Pancreatitis % Gastritis % upper GI bleed % Seizures % Ethanol withdrawal (detoxing) % Pneumonia % Sepsis % Hepatitis

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8
Q

Alcoholic ketoacidosis treatment

A

Hydration with D5 NS # Carbs + fluids reverse alcoholic KA by increasing insulin levels & suppressing glucagon. Better than fluid alone. # Thiamine supplementation as prophylaxis for Wernicke’s encephalopathy # Replace electrolytes #Bicarb only in severe life-threatening acidosis unresponsive to fluid & glucose therapy

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9
Q

Common causes of primary hypothyroidism

A

$ Autoimmune (Hashimoto) $ Thyroiditis (subacute, silent, postpartum) $ Iodine deficiency $ Ablation $ External radiation $ Infiltrative disease (lymphoma, sarcoid, amyloidosis, tuberculosis) $ Congenital $ Drugs: amiodarone, lithium, potassium perchlorate, iodine, alpha interferon, interleukin-2 $ Idiopathic

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10
Q

Common causes of secondary hypothyroidism

A

$ Panhypopituitarism $ Pituitary adenoma $ Infiltrative causes (hemochromatosis, sarcoidosis) $ Tumors impinging on hypothalamus $ History of brain irradiation $ Infection (tuberculosis)

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11
Q

What is myxedema crisis/coma?

A

Myxedema coma (also called myxedema crisis) is the end spectrum of severe hypothyroidism and is an emergency.

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12
Q

What are the clinical signs/symptoms of myxedema crisis?

A

In addition to usual hypothyroid signs: % Bradycardia % Hypotension % Hypothermia % Altered mental status or coma

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13
Q

Almost 90% of myxedema crisis cases are among what demographic?

A

Elderly women during the winter

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14
Q

Signs & symptoms of hypothyroidism

A

Symptoms: # Hair loss # Fatigue # Depression # Shortness of breath # Weight gain # Constipation # Menstrual irregularities # Infertility # Muscle cramps # Joint pain # Cold Intolerance

Signs: #periorbital puffiness # loss of outer 1/3 of eyebrow # Pallor # Macroglossia # Bradycardia # Hoarseness # Hypoventilation # Absent or decreased bowel sounds # Non-pitting edema # Delayed relaxation of ankle jerk # Peripheral neuropathy # Cool, rough, dry skin # Hypothermia

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15
Q

Differentiation of primary vs. secondary hypothyroid

A

Obesity: Common in primary, less in secondary

Hypothermia: Common in primary, less in secondary

Coarse voice: Common in primary, less in secondary

Pubic hair: Present in primary, absent in secondary

Skin: Dry & coarse in primary, fine & soft in secondary

Heart size: Increased in primary, normal in secondary

Menses & lactation: Normal in primary, absent in secondary

Sella turcica: Normal in primary, enlarged in secondary

Serum TSH: increased in primary, decreased in secondary

Plasma cortisol: Normal in primary, decreased in secondary

Response to TSH: None in primary, good in secondary

Levothyroxine without steroids: Good in primary, none in secondary

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16
Q

Constitutional symptoms of hypothyroidism

A
  • Cold intolerance & hypothermia: due to the decreased basal metabolic rate and absence of shivering.
  • Weight gain
  • Weakness
  • Lethargy
  • Fatigue
  • Vocal changes: hoarse deep voice, slow speech. Husky voice due to mucopolysaccharide infiltration of vocal chords
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17
Q

Cardiopulmonary findings of hypothyroidism

A
  • Angina
  • Bradycardia
  • Distant heart sounds
  • Low voltage ECG
  • Pericardial/pleural effusions
  • Cardiomyopathy
  • Hypoventilation
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18
Q

Dermatologic findings of hypothyroidism

A
  • Dry skin
  • Hair loss
  • Non-pitting edema
  • Facial swelling
  • Ptosis
  • Macroglossia
  • Periorbital edema
  • Generalized non-pitting edema (myxedema): secondary to hyaluronic acid deposition and is characteristically not initially found in dependent areas.
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19
Q

Myxedema coma

A

Myxedema coma is a state of metabolic and multi-organ decompensation characterized by preexisting uncorrected hypothyroidism, mental status changes or coma, hypothermia [usually <35.5°C (95.9°F)], and precipitating stressor(s).

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20
Q

Clinical presentation of myxedema coma

A

The characteristic hypothyroid habitus is evident, as well as bradycardia, hypotension, hypothermia, hypoventilation, and altered mental status or coma.

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21
Q

What might normal temperature indicate in a patient with myxedema coma?

A

Hypothermia is so common in myxedema that a normal temperature, present in up to 25% of patients, should suggest an underlying infection.

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22
Q

Precipitating factors for myxedema coma

A

In hypothyroid patients, myxedema crisis can be precipitated by a number of conditions, including infection, anesthetic agents, cold exposure, trauma, myocardial infarction or congestive heart failure, cerebrovascular accident, GI hemorrhage, metabolic conditions (hypoxia, hypercapnia, hyponatremia, and hypoglycemia), surgery, burns, medications (e.g., -blockers, sedatives, narcotics, phenothiazine, amiodarone), or thyroid medication noncompliance.

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23
Q

Primary hypothyroidism (thyroid gland etiology) is confirmed by…

A

High TSH with low total or free thyroxine (T4 ) and triiodothyronine (T3)

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24
Q

secondary hypothyroidism (hypothalamic-pituitary etiology) is confirmed by…

A

Low TSH with low total or free T4 and T3

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25
Q

What are the supportive treatments for myxedema coma?

A
  • Airway, breathing, circulation
  • IV therapy: dextrose for hypoglycemia, water restrict for hyponatremia
  • Vasopressors: if indicated (ineffective without thyroid hormone therapy)
  • Hypothermia: passive rewarming with blankets
  • Steroids: hydrocortisone (bc of increased metabolic stress; 100-200 mg IV
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26
Q

Describe hormone replacement therapy for myxedema coma.

A
  • IV T4 (levothyroxine) at 4 micrograms/kg, followed in 24 h by 100 micrograms IV, then 50 micrograms IV until oral medication is tolerated. (Switch to 50–200 micrograms/d PO when patient is ambulatory.
  • IV T3 (liothyronine or triiodothyronine) for myxedema coma at 20 micrograms followed by 10 micrograms IV every 8 h until the patient is conscious (given because of the risk of decreased T3 generation from T4 in severely hypothyroid patients). Start with no more than 10 micrograms IV for the elderly or those with coronary artery disease.
  • Either T4 or T3 can be used, but in severe myxedema coma, T3 should be considered (either combined with T4 or used alone) but with cautious use on patients with myocardial compromise.
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27
Q

Precipitating factors that may need to be treated in myxedema coma

A
  • Infections
  • Sedatives
  • Anesthetic agents (e.g., etomidate)
  • Cold exposure
  • Trauma
  • Myocardial infarction or congestive heart failure
  • Cerebrovascular accident
  • GI hemorrhage
  • Contributing metabolic conditions include hypoxia, hypercapnia, hyponatremia, and hypoglycemia
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28
Q

Why are thyroid hormones given IV instead of PO during myxedema coma?

A

Decreased GI motility; decreased absorption

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29
Q

Advantages & disadvantages of T4 administration

A

The advantages of T4 are a smooth, slow, and steady onset of action. Disadvantages include the fact that extrathyroidal conversion of T4 to T3 may be reduced in myxedema coma. The onset of action of T4 is also slower.

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30
Q

Advantages & disadvantages of T3 administration

A

The advantages of T3 therapy include more rapid onset of action and no need for extrathyroidal conversion. T3 crosses the blood–brain barrier more readily than does T4 in an animal study using baboons.11 Disadvantages of T3 include rapid action and highly fluctuating serum levels, which may not be desirable in patients who have underlying coronary atherosclerosis.

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31
Q

Prognosis in myxedema coma?

A

Myxedema coma carries a high mortality, ranging from 30% to 60% depending on comorbid diseases. Factors such as advanced age, bradycardia, and persistent hypotension suggest a poor prognosis. All patients with myxedema coma require intensive care unit admission.

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32
Q

Relationship between T3 & T4

A

Two major types of thyroid hormones are thyroxine (T4 ) and triiodothyronine (T3). T4 is the major form of thyroid hormone. The ratio of T4 to T3 released in the blood is 20:1. Peripherally, T4 is converted to the active T3, which is three to four times more potent than T4 .

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33
Q

What is the difference between hyperthyroidism & thyrotoxicosis?

A

Hyperthyroidism refers to excess circulating hormone resulting only from thyroid gland hyperfunction whereas

thyrotoxicosis refers to excess circulating thyroid hormone originating from any cause (including thyroid hormone overdose).

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34
Q

Definition of thyroid storm

A

Thyroid storm is the extreme manifestation of thyrotoxicosis. This is an acute, severe, life-threatening state of thyrotoxicosis caused either by adrenergic hyperactivity or altered peripheral response to thyroid hormone following the presence of one or more precipitants.

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35
Q

Mortality of thyroid storm

A

The mortality of thyroid storm without treatment is between 80% and 100%, and with treatment, it is between 15% and 50%.

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36
Q

Causes of primary hyperthyroidism

A
  • Graves disease: most common; 85% of all cases. Associated with diffuse goiter, opthalmopathy, local dermopathy
  • Toxic multinodular goiter: 2nd most common
  • Toxic nodular (adenoma) goiter: enlarged thyroid gland that contains a small rounded mass or masses called nodules with overproduction of thyroid hormone
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37
Q

Common causes of secondary hyperthyroidism

A
  • Thyrotropin-secreting pituitary adenoma: thyroid overstimulated
  • Thyroiditis: inflammation of thyroid gland
  • Hashimoto thyroiditis: inititally state of hyperthyroid, but then progresses to hypothyroid
  • Subacute painful thyroiditis (de Quervain thyroiditis)
  • Subacute painless thyroiditis
  • Radiation thyroiditis
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38
Q

Other causes of hyperthyroidism

A
  • Ectopic thyroid tissue: rare form of teratoma
  • Metastatic thyroid cancer
  • Human chorionic gonadotropin (secreting hydatidiform mole)
  • Drug induced
  • Iodine
  • Amiodarone (contains iodine)
  • alpha-interferon (during treatment for other illnesses)
  • interleukin-2 (during treatment for other illnesses)
  • excessive thyroid hormone ingestion
  • thyrotoxicosis factitia (Munchausen-like; intentional overdose)
  • Ingestion of beef containing thyroid tissue
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39
Q

Primary hyperthyroidism is caused by…

A

Primary hyperthyroidism is caused by the excess production of thyroid hormones from the thyroid glands.

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40
Q

Secondary hyperthyroidism is caused by…

A

Secondary hyperthyroidism is caused by the excess production of thyroid-releasing hormones or thyroid-stimulating hormones (TSHs) in the hypothalamus and pituitary, respectively.

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41
Q

Precipitants of thyroid storm

A
  • Systemic insult:
    • Infection # trauma # general surgery # hyperosmolar coma
  • Cardiovascular insult:
    • myocardial infarct # CVA # PE
  • Obstetric:
    • Parturition # Eclampsia
  • Endocrine:
    • DKA
  • Drug or hormone related:
    • Withdrawal of thyroid medication
    • Iodine administration
    • Thyroid gland palpation
    • Ingestion of thyroid hormone
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42
Q

Constitutional signs & symptoms of thyroid storm

A
  • Lethargy
  • Weakness
  • Heat intolerance
  • Diaphoresis
  • Fever
  • Weight loss
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43
Q

Neuro S&S of thyrotoxicosis

A
  • Emotional lability
  • anxiety
  • confusion
  • coma
  • psychosis
  • fine tremor
  • muscle wasting
  • hyperreflexia
  • periodic paralysis
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44
Q

Opthalmologic S&S of thyrotoxicosis

A
  • Diplopia
  • lid lag
  • eye irritation
  • dry eyes
  • exopthalmos
  • opthalmoplegia
  • conjunctival infection
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45
Q

Endocrine S&S of thyrotoxicosis

A
  • Neck fullness
  • Tenderness
  • Thyroid enlargement
  • bruit
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46
Q

Cardiorespiratory S&S of thyrotoxicosis

A
  • Dyspnea
  • Palpitations
  • Chest pain
  • Widened pulse pressure
  • Systolic hypertension
  • Sinus tachycardia
  • Atrial fib or flutter
  • CHF
47
Q

GI S&S of thyrotoxicosis

A
  • Diarrhea
  • Hyperactive bowel sounds
48
Q

Gynecologic S&S of thyrotoxicosis

A
  • Oligomenorrhea
  • Decreased libido
  • Gynecomastia
  • Telangiectasia
49
Q

Hematologic S&S of thyrotoxicosis

A
  • Pale skin
  • Anemia
  • Leukocytosis
50
Q

True or false: all hyperthyroid patients present with goiter.

A

False.

51
Q

Burch & Wartofsky’s Scoring System for Thyroid Storm

A

Score of ≥ 45: highly suggestive of thyroid storm

Score of 25-55: Suggestive of impending storm

Score of <25: Unlikely to represent thyroid storm

52
Q

In primary hyperthyroidism, the TSH will be (high/low).

A

In primary hyperthyroidism, the TSH level is low as a result of the negative feedback mechanism of a high thyroid hormone level.

53
Q

In secondary hyperthyroidism, the TSH is (high/low).

A

In secondary hyperthyroidism, TSH is increased because of increased production in the pituitary.

54
Q

What do free T4 & T3 levels indicate re: thyrotoxicosis?

A
  • A low TSH with an elevated free thyroxine (FT4) confirms thyrotoxicosis.
  • On the other hand, a low TSH with a normal FT4 but elevated free triiodothyronine (FT3 ) is also diagnostic of T3 thyrotoxicosis.
55
Q

Are total T4 & T3 levels generally measured in suspected thyrotoxicosis? Why or why not?

A

No. Only a small fraction of the hormones are free and unbound. Laboratory measurement of total T3 and total T4 measures mainly protein-bound hormone concentrations. Therefore, results may be affected by conditions that affect protein binding. With the improved assays for FT4 and FT3, there is now little indication to measure total T3 and total T4.

56
Q

What lab should be ordered if Graves disease is suspected?

A

If Graves disease is suspected, thyroid antibody titers (to thyroid peroxidase or thyroglobulin) will help determine diagnosis. Thyroid-stimulating antibodies are detected in Graves disease.

57
Q

What imaging could be done in the case of suspected thyroid storm?

A

A thyroid sonogram with Doppler flow can be done to assess thyroid gland size, vascularity, and the presence of nodules.

  • Thyroid gland secreting excessive hormones would be enlarged and have enhanced Doppler flow.
  • Subacute, postpartum thyroiditis, silent thyroiditis, or exogenous causes of hyperthyroidism, the thyroid gland would be expected to be small with decreased Doppler flow.
  • Nuclear medicine imaging with iodine-131 would reveal a greatly increased uptake of radioiodine as early as 1 or 2 hours after administration of the agent.
58
Q

What are some common ECG findings in thyrotoxicosis?

A
  • A fib (10-35% of cases)
  • A flutter
  • PVCs
  • Sinus tach (40% of cases)
59
Q

Treatment of thyrotoxicosis

A
  • General: oxygen, telemetry
  • Fever: external cooling, tylenol (no aspirin: increases T4)
  • Dehydration: IV fluids; D5W if hypoglycemic
  • Nutrition: glucose, multivitamin, thiamine & folate
  • Cardiac: rate control, inotrope, diuretic & sympatholytic as required
  • Inhibition of thyroid hormones with thonamides:
    • PTU loading 600-1000 mg PO followed by 200-250 mg Q4H. (Preferred, as blocks peripheral conversion of T4 to T3)
    • Methimazole 40 mg PO loading dose followed by 25 mg Q4H.
  • Inhibition of new thyroid hormone production
    • Lugol solution 8-10 gtt PO Q6-8H
    • Potassiom iodide (SSKI) 5 gtt PO Q6H
    • IV opanoic acid 1 gram Q8H for 24H, then 500mg BID
    • Ipodate 0.5-3 grams daily PO (esp useful with thyroid hormone overdose)
60
Q

5 treatment aims for thyroid storm

A
  1. Supportive care
  2. Inhibition of thyroid hormone release
  3. Inhibition of new thyroid hormone production
  4. Prevention of T4 to T3 conversion
  5. beta-adrenergic receptor blockade
61
Q

Adrenal crisis is…

A

Adrenal crisis is a life-threatening exacerbation of adrenal insufficiency due to increased physiologic demand (e.g., infection) or decreased supply (e.g., discontinuation of steroid therapy) of cortisol.

62
Q

Most frequent iatrogenic cause of adrenal crisis…

A

The most frequent iatrogenic cause of acute adrenal crisis is rapid withdrawal of steroids in patients with adrenal atrophy secondary to long-term steroid administration.

63
Q

Define Addison’s disease/primary adrenal insufficiency.

A

Primary adrenal insufficiency, or Addison disease, is due to intrinsic adrenal gland dysfunction and results in decreased cortisol and aldosterone production.

  • Approximately 90% of the gland must be destroyed for clinical adrenal insufficiency to develop.
  • The causes include infection [e.g., tuberculosis, human immunodeficiency virus (HIV)], drugs, adrenal hemorrhage (from use of warfarin, sepsis, and trauma), sarcoidosis, autoimmune disorders, metastases, and congenital adrenal hyperplasia.
64
Q

Define secondary adrenal insufficiency.

A

Secondary adrenal insufficiency is due to hypothalamic-pituitary dysfunction causing inadequate ACTH production.

  • This results in cortisol deficiency only.
  • This may be caused by withdrawal of prolonged steroid therapy, pituitary disease, head trauma, or postpartum pituitary necrosis (Sheehan syndrome).
65
Q

Adrenal cortex produces…

A

Steroid hormones

3 categories

  • Glucocorticoids (cortisol)
  • mineralocorticoid (aldosterone)
  • gonadocorticoids (sex hormones: testosterone and estrogen).
66
Q

Adrenal medulla produces…

A

Catecholamines

67
Q

Cortisol is secreted in response to…

A

Direct stimulation by ACTH.

68
Q

True or false: ACTH is secreted (thus cortisol stimulated) consistently throughout the day.

A

False. Diurnal rhythm: greater in AM, less in PM.

69
Q

Aldosterone secretion is controlled by…

A

The renin-angiotensin system and the serum potassium concentration.

Thus it maintains sodium & potassium levels.

70
Q

Causes of Primary Adrenal Insufficiency

A
  • Autoimmune: Isolated, or as part of polyglandular syndrome
  • Adrenal hemorrhage or thrombosis
    • Necrosis; coag disorder; overwhelming sepsis
  • Drugs
    • Adrenolytic agents; metyrapone; amioglutethimide; mitotane; ketoconazole
  • Infections involving adrenal glands
    • Tuberculosis; fungal or bacterial sepsis; AIDS involving adrenal glands
  • Infiltrative disorders involving adrenal glands
    • sarcoidosis; hemochromatosis; amyloidosis; lymphoma; metastatic cancer
  • Surgery: bilateral adrenalectomy
  • Hereditary
    • adrenal hypoplasia, accquired or congenital; adrenoleukodystrophy; familial glucocorticoid deficiency
  • Idiopathic
71
Q

Primary adrenal insufficiency:

Most common cause worldwide?

Most common cause in the U.S.?

A

Worldwide: tuberculosis

U.S.: HIV/AIDS

72
Q

Most common cause of secondary adrenal insufficiency?

A

Long-term therapy with pharmacologic doses of glucocorticoids for autoimmune or inflammatory conditions.

73
Q

A high index of suspicion for adrenal crisis should be given in case of…

A

Unexplained hypotension

  • especially in patients with increased risk such as
    • acquired immunodeficiency syndrome
    • prior glucocorticoid therapy
    • known autoimmune diseases
    • history of chronic fatigue and hyperpigmentation, severe head trauma, and those displaying acute symptoms related to the diseases known to cause acute adrenal crisis
74
Q

Primary adrenal insufficiency (labwork to differentiate from secondary)

A

Primary adrenal insufficiency is typically characterized by hyponatremia and hyperkalemia due to aldosterone deficiency.

75
Q

Secondary adrenal insufficiency (labwork to differentiate from primary)

A

Secondary adrenal insufficiency is characterized by either hypernatremia (aldosterone functioning causing sodium reabsorption in kidney) or hyponatremia (following water retention) and hypokalemia.

76
Q

Clinical presentation of adrenal crisis

A
  • Severe hypotension (refractory to vasopressors)
  • Dehydration
  • Weakness
  • Circulatory collapse
  • Delirium, confusion, disorientation, lethargy
  • Abdominal pain, nausea & vomiting (mimicking an acute abdomen)
  • Associated sepsis
77
Q

Describe the rapid ACTH test.

A

Cosyntropin (synthetic ACTH) is used to stimulate production of cortisol after the basal blood level is taken.12 A dose of 0.25 milligrams is given IV, and, subsequently, the cortisol level is taken at 30 minutes and 1 hour later.

Dexamethasone has less cross-reactivity than hydrocortisone.

78
Q

Drug of choice for adrenal crisis?

A

Hydrocortisone. Provides both glucocorticoid & mineralocorticoid effects.

79
Q

Adrenal crisis treatment plan

A
  1. IV fluids: D5NS for hypoglycemia & hyponatremia
  2. Steroids: hydrocortisone (100mg bolus) or dexamethasone (4mg bolus)
  3. Vasopressors: after steroid therapy in pt unresponsive to fluid resuscutation (neo-epi, epi, or phenylephrine prefered)
  4. Supplementation: may require lifelong gluco/mineralocorticoid supplementation
  5. Maintenance: increased maintenance doses are required during periods of stress re: increased need for cortisol
80
Q

What precautions should be taken pre-surgically in adrenal insufficiency patients?

A

Additional supplementation therapy before surgical procedures or other medical stress, to prevent progression to adrenal crisis

81
Q

Recommendations on adrenal supplementation for patients with recent history of corticosteroid therapy

A

As of this writing, there are no evidence-based recommendations in terms of dosage or duration of steroid supplementation for patients with past corticosteroid treatment.

  • Because hypothalamus–pituitary–adrenal axis function should recover within 1 month after the last dose of steroids, a reasonable recommendation is to consider steroid supplementation for 3 to 4 weeks in patients who have received oral steroids in the preceding 12 months.
  • Patients who receive steroids by topical, intranasal, inhalational, or PR routes are not thought to be at risk for hypothalamus–pituitary–adrenal axissuppression, and supplemental steroids are not recommended for this group for minor or moderate stress.
82
Q

Recommendations for patients with known adrenal insufficiency presenting to ED with minor illness or injury

A

In normal circumstances, 20 to 30 milligrams/d of hydrocortisone is needed, with or without mineralocorticoid replacement. For a minor illness or injury, double the daily glucocorticoid dose for 24 to 48 hours until symptoms improve. Increasing the mineralocorticoid dose is usually not necessary.

83
Q

Heat-related illness is…

A

Set of preventable conditions ranging from mild (heat exhaustion, heat cramps) to potentially fatal heat stroke

84
Q

Cellular damage occurs at what core body temperature?

A

104˚F or 40˚C

85
Q

Initial treatment of heat injury

A

Lowering core temp through cold water immersion

Alternative: applying ice packs to head, neck, axilla, groin

86
Q

Populations at risk for heat related illness

A
  • Older persons
  • Children
  • People performing strenuous outdoor activity
  • Heart & lung diseases
  • chronic mental disorders
  • taking medications that interfere with salt/water balance
87
Q

Heat exhaustion definition

A

Inability to continue activity bc of environmental conditions.

Cause: believed to be central mechanism protecting body in times of overexertion

88
Q

Heat stroke definition

A

Elevated core temperature of 104˚F/40˚C or above

and

CNS disturbance

89
Q

Classic heat stroke:

  1. Time frame
  2. Temperature range
  3. Population at risk
A
  1. Slowly, develops over days
  2. Lower core temp than exertional
  3. Older persons, chronic illness
90
Q

Exertional heat stroke

  1. Time frame
  2. Temp range
  3. Population at risk
A
  1. Rapid onset
  2. Higher core temperatures than classic
  3. Young, healthy people
91
Q

Why is cold water immersion most effective?

A

More body surface area is immersed, which increases conductive potential

92
Q

Why does wearing pale clothing help heat exhaustion?

A

Absorbs less heat because it reflects radiant energy

93
Q

What is the most effective way humans release heat?

A

Perspiration/evaporation

94
Q

Why does air permeable/loose clothing help with heat loss?

A

Because it allows air circulation, which increases convective heat loss

95
Q

Where is thermoregulation coordinated?

A

CNS Centers: hypothalmus, spinal cord

Peripheral centers: skin & organs

96
Q

What happens at 104˚F/40˚C?

A

Cellular damage, leading to SIR, increased cell wall permeability & endotoxin release, then tissue hypoxia, metabolic acidosis, and severe organ dysfunction

97
Q

How can a person work at levels of heat previously intolerable or life threatening?

A

Successive increments of increasing exposure over weeks

Physiologic adaptations:

  • Improved sodium retention
  • increased glomerular filtration rate
  • enhanced CV performance
98
Q

Why are children at increased risk for heat related illness?

A
  • Greater surface area to body mass ratio. Permits greater heat exchange.
  • Slower sweat rates
  • Higher temp threshold for sweating
  • Produce more dilute sweat
99
Q

Mild heat-related illness S&S

A

Symptoms: Diarrhea, dizziness, headache, irritability, loss of coordination, nausea/vomiting, syncope, weakness

Signs: core temp < 104˚F, normal MS, goose flesh, pallor, tachycardia, hypotension

100
Q

Heat stroke S&S

A

Symptoms: Confusion, dizziness, hallucination, headache, nausea/vomiting, syncope

Signs: Core temp ≥ 104˚F, altered MS, hot skin w/ or w/out perspiration, hypotension, tachycardia, seizure

101
Q

Major risk factors for heat-related illness

A
  • Age: older than 65, younger than 15
  • Cognitive impairment
  • Heart &/or lung disease
  • Limited access to AC
  • Mental illness
  • Obesity
  • Physical disability/impaired mobility
  • Poor fitness level
  • Sickle cell trait
  • Strenuous outdoor activity during hottest daytime hours
  • Urban residence or living on higher floor
102
Q

Medications/substances that contribute to heat-related illness

A
  • Alcohol
  • Alpha-adrenergic agents
  • Amphetamines
  • Anticholinergics
  • Antihistamines
  • Benzos
  • Betablockers
  • Calcium channel blockers
  • cocaine
  • diuretics
  • ephedra-containing supplements
  • laxatives
  • neuroleptics
  • phenothiazines
  • stimulants
  • thyroid receptor agonists
  • tricyclic antidepressants
103
Q

Who is at highest risk among high school athletes?

A

Football players, especially during August pre-season conditioning

104
Q

When should cooling be started in heat stroke?

A

On-site cooling before transfer to ED

105
Q

Survival rate of exertional heat stroke with water cooling

A

Almost 100%

106
Q

True or false: fans provide similar benefits to AC re: heat-related illness.

A

False. Spending time in air-conditioned areas is among strongest factors in preventing heat-related deaths. Fans do not provide same benefit.

107
Q

Recent analysis of 140 OHCA patients in TH-capable hospital reported…

A
  • 56% overall survival to discharge
  • 92% of survivors with favorable neuro outcomes
108
Q

What do experiments indicate about the timing of TH induction?

A

Progressively larger IS reduction with progressively earlier initiation of TH

109
Q

Studies show which one may be more important: temperature of myocardial tissue, or temperature of reperfusing blood?

A

Reperfusing blood

110
Q

Barriers to overcome regarding the use of TH for STEMI

A
  • Must be achieved rapidly before reperfusion, but not significantly delay reperfusion
  • Discomfort, shivering, & stress among alert patients
111
Q

Indications for rapid vs. delayed TH

A
  • Rapid: necessary for cardioprotection
  • Delayed: can convey neuroprotection
112
Q

Methods of initiating & maintaining therapeutic hypothermia

A
  • Ice packs
  • Cooling helmet
  • Surface cooling
  • Endovascular heat exchange catheters
  • Refrigerated IV fluids
  • Total liquid ventilation
  • Automated peritoneal lavage
113
Q
A

ACNP805: Acute Diagnostic Reasoning (7 decks)

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