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Internal Med - Jesse > Endocrine > Flashcards

Endocrine Flashcards

0
Q

For the average person, approximately ______ of ingested food energy is used for basal processes such as maintaining normal body temperature; approximately ______ is used for exercise, and ______ is used for digestion and metabolism itself.

A

Half
40%
10%

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1
Q

Involuntary weight loss of _____ or more of body weight in <12 months should prompt medical evaluation.

A

5%

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2
Q

_______ acts on receptors in the hypothalamus to increase hunger, and _______ acts on the same cells to reduce hunger (increase satiety).

A

Ghrelin

Leptin

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3
Q

Elderly patients are at risk for a number of conditions that limit intake of calories, including the five Ds:

A

depression, dementia, poor dentition, dysgeusia (altered taste), and side effects of drugs

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4
Q

Weight loss, fever and night sweats are associated with _________

A

tuberculosis and lymphoma

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5
Q

_________ are the most common etiologies detected in patients with weight loss. (3)

A

Malignancy, depression, and benign (nonmalignant) GI causes

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6
Q

Symptoms of _________ (2) should be assessed for all elderly patients with involuntary weight loss since they may have atypical presentations of _________________. (2)

A

depression and TSH; depression and hyperthyroidism

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7
Q

Hyperthyroidism results from _________. (4)

A

1 autonomous thyroid nodules (eg multinodular goiter)
2 diffuse thyroid hormone overproduction (Grave’s disease)
3 damage to the thyroid (subacute thyroiditis: granulomatous/de Quervain/viral/painful or lymphocytic/painless/autoimmune/postpartum) - hyperthyroid often followed by hypothyroid state before resolution; may lead to Hashimoto’s
4 rarely, TSH overproduction (pituitary disease).

  • these 2 are the most common
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8
Q

Sx (7) and signs (6) of hyperthyroidism

A 
Sx:
Heat intolerance
Palpitations
Weight loss
Nervousness
Fatigue and weakness
Oligomenorrhea
Frequent or loose bowel movements

Signs:
Tachycardia (irreg rhythm may be due to AFib)
Fever (in viral subacute thyroiditis)
Warm, moist skin
Lid lag (upper eyelid does not cover sclera above iris with downward gaze)
Tremor
Goiter (may/may not be present; may be tender; may have nodules)

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9
Q

2 signs seen exclusively in Graves’ disease

A

Proptosis, pretibial myxedema

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10
Q

Hyperthyroidism DDx with high uptake on thyroid scan (4)

A

Grave’s disease
Toxic multinodular goiter
Solitary adenoma
TSH-secreting pituitary tumor (rare)

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11
Q

Hyperthyroidism DDx with low uptake on thyroid scan (4)

A

Thyroiditis
Exogenous thyroid hormone use/abuse
Ovarian teratoma (struma ovarii)
Metastatic functional thyroid cancer

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12
Q

High TSH and high FT4 is ____________
Low TSH and high FT4 is _____________
Low TSH and normal FT4 is _____________

A

Secondary hyperthyroidism
Primary hyperthyroidism
T3 thyrotoxicosis (elevated T3 levels) or subclinical hyperthyroidism

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13
Q

Antithyroid drugs (2)

A

methimazole, propylthiouracil

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14
Q

Tx for relief of hyperthyroid Sx

A

Beta blockers: Propranolol (also prevents conversion of T4 to T3) or atenolol (DIE dosing, more convenient).

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15
Q

Low FT4 and high TSH is ___________
High TSH, normal FT4 is _______________
Low FT4, low TSH is _____________

A

Primary hypothyroidism
Subclinical hypothyroidism
Secondary hypothyroidism

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16
Q

Profound hypothyroidism may present with _________.

A

myxedema coma

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17
Q

Hashimoto thyroiditis gland suffers ___________. (Pathogenesis; 3)

A

lymphocytic infiltration, follicular atrophy, and cytotoxic thyroid cell destruction

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18
Q

___________ can cause both hyper and hypothyroidism (drug)

A

Amiodarone

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19
Q

_________ (2 drugs) can cause hypothyroidism

A

Amiodarone and lithium

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20
Q

Hypothyroidism Sx (10) and findings (12)

A 
Sx:
Cold intolerance
Weight gain
Fatigue
Constipation
Hoarseness
Memory loss
Menstrual changes
Decreased libido
Dry skin
Sx mistakenly attributable to aging (carpal tunnel, anemia)

Findings:
Diastolic blood pressure (BP) is often mildly elevated
Bradycardia (severe cases)
Hypothermia (severe cases)
dry skin
coarse hair
retarded nail growth
thinning of the lateral third of the eyebrows.
Goiter (Hashimoto - firm and sometimes lobulated); may not be palpable after radiation or ablative therapy
Delayed relaxation of deep tendon reflexes.
Carpal tunnel syndrome, with median nerve compromise.
Myxedema: edematous face, periorbital edema, nonpitting pretibial edema.
Myxedema coma (late, severe - depression of all organ systems including cardiac, respiratory, and CNS).

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21
Q

Infiltration disorders that can cause primary hypothyroidism include _________ (3)

A

amyloidosis, sarcoidosis, scleroderma

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22
Q

Nonthyroid test findings useful to confirm Dx of hypothyroidism (5)

A 
Hypercholesterolemia
hypertriglyceridemia
Elevated creatine phosphokinase
Anemia
Abnormal ECG (decreased voltage, T-wave flattening)
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23
Q

Thyroid autoantibodies found in Hashimoto thyroiditis; useful in confirming the autoimmune diagnosis. (2)

A

TPO antibody and thyroglobulin antibody

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24
Q

Drug used to treat hypothyroidism

A

Levothyroxine

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25
Q

Patients with highly suspected panhypopituitarism and patients with myxedema coma should always begin hydrocortisone treatment prior to thyroid replacement therapy due to a danger of _______

A

Adrenal crisis; they have adrenal insufficiency and thyroid replacement may increase the metabolism of the small amount of the body’s remaining cortisol

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26
Q

Met common cause of hypothyroid in USA and in world

A

USA: hashimoto’s
World: iodine deficiency

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27
Q

Thyroid replacement therapy is monitored by measuring _______ levels every _______ (duration) at the beginning; Once a stable replacement dose is achieved, TSH can be monitored every _______. (duration)

Overreplacement increases the risk of ________. (2)

A

TSH
4-6 weeks
6 months
atrial fibrillation and excessive bone loss (danger in elderly)

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28
Q

Without insulin, DM1 patients are prone to develop ketoacidosis, which is caused by the lack of insulin and the increased release of ___________. This leads to increased gluconeogenesis, release of fatty acids, and oxidation of fatty acids to form ketone bodies. __________ (same answer as prev) accelerates the oxidation of fatty acids by ___________.

A
  • Glucagon

- increasing their carnitine-mediated transport into the mitochondria, where the oxidation occurs

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29
Q

Presenting Sx of DM1 pt with diabetic ketoacidosis (4)

A

nausea, vomiting, and polyuria, maybe diffuse abdominal pain

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30
Q

Underlying disorders that may cause diabetes mellitus (4)

A

Hemochromatosis

Pancreatic exocrine insufficiency (acute or chronic pancreatitis, pancreatectomy, cystic fibrosis)

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31
Q

Hyperglycemia DDx (5)

A

DM
Drugs (e.g., corticosteroids, thiazide diuretics, protease inhibitors)
Administration of dextrose-containing IV fluids
Excess secretion of the counterregulatory hormones (acromegaly, Cushing syndrome, pheochro-mocytoma)
Stress (via catecholamine release)

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32
Q
  • To make the diagnosis of DM, one of the following criteria must be present, and to confirm the Dx, one of the criteria should be confirmed on a subsequent day (3).
  • What is impaired fasting glucose?
A 
Fasting glucose (FG) level >125 mg per dL (normal 200 mg per dL with symptoms (polyuria, polydipsia, unexplained weight loss)
2-hour glucose level >200 mg per dL during a 75-g oral glucose tolerance test (OGTT)

Impaired fasting glucose (defined by fasting glucose from 100 to 125 mg per dL) is a predictor of the progression to DM and should be formally diagnosed for patient education and intervention.

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33
Q

The general goals for diabetic patients attempting tight control are a fasting glucose of ________ and an HbA1c of ____.

A

80 to 120 mg per dL (4.4 to 6.7 mmol/L)

<7%

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34
Q

In DM patients, a balanced diet of ___% carbohydrates, ____% protein, and ____% fat (saturated fats limited to ___%) is recommended.

A

55%
15%
30%
7%

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35
Q

Oral hypoglycemics (6 classes)

A 
1 Biguanides (“insulin-sensitizing” - Metformin also decreases circulating insulin levels, avoiding weight gain (1st line in obese). There is no risk of hypoglycemia.  Metformin should not be used in patients with renal disease or hepatic disease (increased risk of lactic acidosis))
2 Sulfonylureas (bind to sulfonylurea receptors on beta cells, stim insulin release. 1st-line in nonobese. 2nd-gen agents (glyburide, glipizide, glimepiride) most popular. 
3 Meglitinides (repaglinide and nateglinide - nonsulfonylurea but equipotent to sulfonylureas. Repaglinide is not renally secreted - preferred in renal failure.)
4 Thiazolidinediones (pioglitazone, rosiglitazone - increase insulin sensitivity in the liver and muscle. Safety questioned; reserved for patients who fail combination therapy and refuse insulin therapy.)
5 Alpha-glucosidase inhibitors (acarbose, miglitol - inhibit carb absorption by preventing the breakdown of oligosaccharides in the small intestine - used in combination).
6 Sitagliptin (Dipeptidyl peptidase-4 inhibitor, increases its substrate, glucagon-like peptide-1 (GLP-1), which increases beta cell production of insulin and decreases pancreatic alpha cell production of glucagon. Used only in combination.)
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36
Q

________ is a natural substance produced by pancreatic beta cells that reduces glucagon production. ________ is a synthetic injectable form of this substance given preprandially in some DM1 and DM2 pts.

A

Amylin

Pramlintide

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37
Q

________ is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also renal failure. It is a form of hyperventilation.

A

Kussmaul breathing

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38
Q

DKA is generally seen in type ____ DM. It may be precipitated by ______(4). Tx consists of ________(2).

A

1
infections, vascular events (stroke, myocardial infarction), cessation of insulin, or dehydration
volume repletion and insulin replacement - Insulin therapy is adjusted based on the improvement in the anion gap. Add dextrose to IV fluid when glucose under 250 mg/dL and intravenous insulin still required.

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39
Q

Although serum potassium levels are often initially _______ in DKA, these pts are always potassium _________.

A

Elevated
Depleted

Potassium must be added to the replacement fluid as soon as urine output is established and serum potassium approaches normal levels.

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40
Q

_____________ coma is usually seen in patients with type 2 DM when progressive hyperglycemia leads to an osmotic diuresis and worsening dehydration. Mortality is _____%.

A

Hyperosmolar nonketotic coma

Mortality = 50%

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41
Q

Sx of hypoglycemia - 2 categories

A

Adrenergic Sx from epinephrine release (tachycardia, diaphoresis, tremulousness, palpitations, and anxiety)
Neuroglycopenic Sx from CNS dysfunction (develop later; headache, blurred vision, confusion, seizures, LOC).

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42
Q

Screening for ________ is used for early detection of diabetic nephropathy; If it develops, Tx with _________ decreases the rate of progression to overt nephropathy.

A

microalbuminuria

an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker

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43
Q

____________ therapy should be given to diabetic patients over 40 years old, or to younger patients at above average risk for macrovascular disease.

A

Prophylactic aspirin therapy (81 mg) and statin therapy

44
Q

The two most common etiologies of hypercalcemia are ________. Measurement of _______ can successfully discriminate these two etiologies.

A

primary hyperparathyroidism and malignancy (together, 90% of all cases)
PTH

45
Q

Immediate and long-term Tx of hypercalcemia

A

1 Immediate: hydration with IV NS (restores the depleted intravascular volume and increases renal calcium excretion)
2 Once volume is OK and Ca excretion is maximized, calcitonin subQ may be used short-term.
3 Long-term: treat the underlying disease, or use bisphosphonates.

46
Q

Tx of primary hyperparathyroidism

A

Treated surgically, most commonly with resection of a solitary parathyroid adenoma.

47
Q

Disorders involving _______ may manifest as hypercalcemia. (5)

A

increased bone destruction, decreased renal excretion, increased gastrointestinal (GI) absorption, unregulated secretion of PTH, and vitamin D abnormalities

48
Q

Action of PTH (3)

A

increases serum calcium by:

  • activating bone resorption
  • increasing renal tubular resorption of calcium
  • increasing activation of vitamin D, which assists in increasing calcium reabsorption from the gut.
49
Q

Malignancy may cause hypercalcemia by two mechanisms - what are they and which cancers are assoc with each?

A

1 Direct bone destruction, believed to be mediated by an osteoclast-activating factor. Assoc cancers: Breast, nonsmall cell lung, and multiple myeloma.

2 Humoral hypercalcemia of malignancy (HHM): a PTH-related protein (PTHrP), is secreted by the tumor. Assoc cancers: Lung (especially squamous cell), Head and neck, Renal, T-cell leukemia (assoc with HTLV-1)

50
Q

3 groups of less common causes of hypercalcemia

A

1 Vitamin D Mediated (Increased vitamin D ingestion; Granulomatous disease (e.g., sarcoid, tuberculosis)—granulomas activate vitamin D through production of α1-hydroxylase; Hodgkin disease and NHL)

2 Increased Bone Turnover (Hyperthyroidism, Immobilization (usually in association with underlying high bone turnover, as seen in Paget disease); Vitamin A intoxication)

3 Decreased Renal Excretion of Calcium (Thiazide diuretics; Milk-alkali syndrome)

51
Q

What is milk-alkali syndrome (incl mechanism)?

A
  • Caused by excessive ingestion of antacids or calcium supplements (mostly calcium carbonate).
  • Resulting alkalosis leads to greater renal absorption of calcium, which in turn induces volume depletion and renal insufficiency.
  • Cycle continues (more alkalosis and calcium reabsorption as long as ingestion persists) leading to increasing hypercalcemia.
52
Q

Difference betw primary hyperparathyroidism and familial hypocalciuric hypercalcemia

A

Both involve increased PTH secretion. In familial hypocalciuric hypercalcemia (FHH) (autosomal dominant), urine calcium excretion remains low despite hypercalcemia, but in primary hyperparathyroidism, hypercalciuria occurs with the rising calcium levels.

53
Q

Mechanism of hypercalcemia assoc with lithium intake or familial hypocalciuric hypercalcemia

A

Both lithium and FHH involve a decreased activity in the calcium-sensing receptor, leading to elevated calcium levels in order to activate the receptor and decrease PTH secretion.

54
Q

hyperparathyroidism mnemonic

A

“stones, bones, and groans” - refers to nephrolithiasis, bone resorption, and constitutional/GI symptoms.

55
Q

Excess ingestion of which vitamins can lead to hypercalcemia?

A

A and D

56
Q

Hypercalcemia Sx

A

Nonspecific!

  • fatigue, anorexia, and drowsiness
  • more severe: confusion and stupor.
  • GI: nausea, vomiting, and constipation.
  • polyuria (Inhibition of renal-concentrating ability).
  • recurrent nephrolithiasis or peptic ulcer disease (in patients with primary hyperparathyroidism and chronic hypercalcemia)
57
Q

Calcium exists in three forms in the extracellular fluid: protein bound (___%), free ions/active form (___%), and complexed with anions (___%)

A

40
50
10

58
Q

Acidemia _________ calcium binding to albumin, and therefore ________ the ionized calcium.

A

decreases

increases

59
Q

What are blood phosphate levels in hypercalcemia mediated through PTH or PTHrP?

A

Hypophosphatemia is seen in hypercalcemia mediated through PTH or PTHrP

60
Q

Normal to high PTH level can be due to: (3)

A

1 primary hyperparathyroidism (solitary parathyroid adenoma; parathyroid hyperplasia)
2 FHH (familial hypocalciuric hypercalcemia)
3 lithium ingestion

61
Q

If PTH is low or undetectable, ________ is most likely and ______ may be measured to confirm the diagnosis of _______.

A

malignancy
PTHrP
HHM (humoral hypercalcemia of malignancy)

62
Q

Bone manifestations of longstanding primary hyperparathyroidism (3)

A

Osteitis fibrosa cystica
Subperiosteal resorption in phalanges
Chondrocalcinosis with associated pseudogout

63
Q

Cardiac manifestation of hypercalcemia (1)

A

shortened QT interval on ECG

64
Q

The adrenal cortex:
Glucocorticoids (e.g., cortisol): produced in the zona ________
Mineralocorticoids (e.g., aldosterone): produced in the zona _______
Androgens (e.g., dehydroepiandrosterone [DHEA]): produced in the zona _________

A

fasciculata
glomerulosa
reticularis

65
Q

Primary adrenal insufficiency (aka __________ ) can be caused by/assoc with: (6)

A

Addison disease (usually autoimmune)
Polyglandular autoimmune syndromes type I & II
tuberculosis
human immunodeficiency virus (HIV) infection
metastatic carcinoma
adrenal hemorrhage
X-linked adrenoleukodystrophy

66
Q

Secondary adrenal insufficiency can be caused by: (2)

A
  • glucocorticoid withdrawal

- panhypopituitarism

67
Q

Adrenal insufficiency Sx (5) and findings (2)

A

Insidious; nonspecific Sx: fatigue, weight loss, nausea, anorexia, and abdominal pain.
Acute adrenal insufficiency (adrenal crisis) can occur in the patient with poor adrenal reserve who is exposed to surgery, infection, or injury; have nausea and abdominal pain.

O/E:

  • Orthostatic hypotension (adrenal insufficiency) or shock (adrenal crisis).
  • Hyperpigmentation in skin folds and scars, due to excess production of pro-opiomelanocortin (the precursor to ACTH). Unique to Addison. Hyperpigmentation is often seen in skin folds and in scars.
68
Q

Na, K levels in primary adrenal insufficiency

A

Hyperkalemia and hyponatremia, due to the lack of mineralocorticoid production.

69
Q

Na, K levels in secondary adrenal insufficiency

A

Hyperkalemia is not present, but hyponatremia may occur as a manifestation of syndrome of inappropriate antidiuretic hormone (SIADH)

70
Q

Lab findings in adrenal insufficiency (besides Na, K levels) (4)

A

Mild hypercalcemia
Eosinophilia
Normochromic, normocytic anemia
Mild acidosis

71
Q

The ___________ test is used to diagnose glucocorticoid deficiency. What are the requirements to Dx adrenal insufficiency?

A

cosyntropin (synthetic ACTH) stimulation test

Dx of adrenal insufficiency: suboptimal one hour cortisol response to cosyntropin (cortisol less than 20 µg/dL).

72
Q

1 Tx of chronic adrenal insufficiency (drug)

2 additional Tx (drug) for primary adrenal insufficiency

A

1 Hydrocortisone replacement (10 to 25 mg daily) with stress doses (100 to 300 mg) used for illness or surgery.

2 Fludrocortisone is used for mineralocorticoid replacement. (High doses of hydrocortisone used for illness/surg also have mineralocorticoid FX, so fludrocortisone is not required)

73
Q

Overproduction of cortisol in Cushing syndrome: ACTH-dependent (2) and ACTH-independent (2)

A

ACTH-dep:

  • Pituitary adenomas (mostly from microadenomas) = Cushing disease
  • Ectopic ACTH production (usually from small cell lung cancer)

ACTH-indep: cortisol is autonomously produced by the adrenal glands:

  • Adrenal tumor (adenoma or carcinoma)
  • Micronodular adrenal disease
74
Q

Cushing syndrome vs Cushing disease

A

Cushing syndrome is caused by excess levels of circulating cortisol.

Pituitary adenomas (mostly from microadenomas) = Cushing disease

75
Q

Physical examination findings suggestive of Cushing syndrome include ________ (7).

A

moon facies, truncal obesity, “buffalo hump,” proximal muscle weakness, wide purple striae, muscle atrophy, hypertension

76
Q

Cushing syndrome is characterized by excess cortisol production as well as _________ (2). Therefore, initial diagnostic work-up of Cushing syndrome includes __________ (2). __________ (1) can also be used.

Once hypercortisolism is confirmed, __________(1) distinguishes between primary (i.e., adrenal) and secondary (i.e., pituitary or ectopic) causes of hypercortisolism. Intermediate (indeterminate) values from this test may require _________ (another test).

A

lack of response to usual feedback mechanisms, and lack of normal circadian rhythm of cortisol

measurement of urine free cortisol (24h) or late-night salivary cortisol

Overnight dexamethasone suppression (1 mg) of cortisol

a serum ACTH level

CRH stimulation to assess the ACTH response

77
Q

Actions of cortisol on each of: Glucose metabolism, Adipose tissue, Connective tissue, Bone, immunologic function, Kidney

A

Tissue dependent.

Glucose metabolism—increased gluconeogenesis and decreased peripheral glucose uptake, leading to hyperglycemia
Adipose tissue—increased lipolysis; lipogenic effects of associated insulin release lead to central fat deposition
Connective tissue—inhibition of fibroblasts, leading to skin atrophy and easy bruising, and increased breakdown of muscle protein
Bone—Increased bone resorption, inhibition of intestinal calcium absorption, and increased urinary calcium excretion
Immunologic function—decreased prostaglandin synthesis and neutrophil migration
Kidney—Increased sodium retention through the mineralocorticoid activity of cortisol (cortisol is usually metabolized to inactive cortisone by 11 β-hydroxysteroid dehydrogenase type 2, but this enzyme is overwhelmed in Cushing syndrome)

78
Q

Most pituitary adenomas are nonfunctioning; the most common functioning adenomas are ________, which often present as _________ (2) in women. Diagnosis is confirmed by _______ (2). Treatment in most cases is _______ (1).

A

prolactinomas
amenorrhea and galactorrhea
the combination of an elevated prolactin level (>150 µg per L) and pituitary mass
a dopamine agonist (Bromocriptine, Cabergoline)

79
Q

Acromegaly (excess GH) often presents as _______(2), sometimes in association with common disorders such as _________ (3). ________ (1) levels are elevated.

A

fatigue and arthralgias
diabetes mellitus (DM), hypertension, or carpal tunnel syndrome
IGF-1

80
Q

_________ is suspected in patients with hypogonadism who have low levels of FSH and LH. _______ is also low or normal. Causes include __________ (3).

A

Hypopituitarism
TSH
large (nonfunctioning) pituitary adenomas, radiation exposure, and granulomatous disease

81
Q

undersecretion of vasopressin produces ___________.

Tx? (2)

A

diabetes insipidus

Patients with DI and hypernatremia need replacement of free water, either orally or with a hypotonic IV solution such as D5W. 
Desmopressin acetate (DDAVP), a synthetic vasopressin, is used to control polyuria in central DI.
82
Q

Diseases assoc with MEN type I include (3)

A

Pituitary adenomas, parathyroid hyperplasia, and pancreatic islet cell tumors.

83
Q

Sheehan syndrome is:

A

postpartum infarction of the pituitary, often caused by hypotension during delivery. Lack of lactation following pregnancy may be the first suspicion.

84
Q

Classic visual field deficit because of compression from a large pituitary adenoma.

A

bitemporal hemianopia

85
Q

DDx for the patient with amenorrhea and hirsutism (4)

A

Pituitary disorders (Cushing disease, acromegaly)
Polycystic ovary syndrome
Congenital adrenal hyperplasia
Pregnancy (rule out)

86
Q

Lab results in panhypopituitarism (4)

A
  • IMPORTANT: because prolactin secretion is under chronic inhibition, prolactin level may be normal or slightly elevated in hypopituitarism.
  • Low free T4 (thyroxine) and T3 (triiodothyronine) in the setting of low or low-normal TSH
  • Low testosterone or estrogen with low FSH and LH
  • Suboptimal ACTH stimulation test
87
Q

Vitamin Tx to lower cholesterol

A

Niacin - large (gram) doses

88
Q

Vitamin K is an important cofactor in the γ-carboxylation of clotting factors _________ (4)

A

II, VII, IX, and X

89
Q

Names of the following vitamins: B1, B6, B12, C, E

A 
B1: thiamine
B6: Pyridoxine
B12: cobalamin
C: ascorbic acid
E: tocopherol
90
Q

Thiamine deficiency may result in: (3)

A

B1 Deficiency syndromes are classified into cardiovascular (wet beriberi) and nervous system (Wernicke-Korsakoff syndrome) dysfunction.

Wet beriberi presents with high-output cardiac failure, peripheral vasodilation, and edema.

Wernicke encephalopathy is the acute neurologic presentation of thiamine deficiency, with delirium, ataxia, nystagmus, and ophthalmoplegia. This may be reversed with thiamine.

Chronic deficiency often results in Korsakoff syndrome, which is notable for anterograde amnesia (inability to form new memory) and confabulation.

91
Q

Alcoholics and malnourished patients should always receive a dose of __________ before a glucose load.

A

Thiamine; to avoid Wernicke encephalopathy.

In these patients, a glucose load (such as IV dextrose) may precipitate Wernicke encephalopathy by using the little remaining thiamine with glucose catabolism.

92
Q

_______ is the classic niacin deficiency syndrome

A

Pellagra (diarrhea, dementia, dermatitis)

93
Q

B12 deficiency results in _______ (2)

A

Megaloblastic anemia, posterior column neuropathy

94
Q

Folate deficiency results in (2)

A

Megaloblastic anemia, neural tube defects

95
Q

Excess _______ intake leads to a predisposition to bleeding in patients on warfarin

A

Vit E

96
Q

Screening for dyslipidemia consists of a _________ (3); desirable values are based on __________.

A

fasting total cholesterol, HDL, and calculated LDL

the total CHD risk factor profile

97
Q

Secondary causes of dyslipidemia include ________ (5).

A

DM, liver disease, chronic renal failure, nephrotic syndrome, and hypothyroidism.

98
Q

Treatment of dyslipidemia is initially dietary restriction when ______% LDL reduction is needed.

A

<25%

99
Q

Drug Tx of dyslipidemia consists of _______ (5)

A 
statin drugs (First line; most evidence for prevention of cardiovascular events.)
ezetimibe
niacin
bile acid sequestrants
fibric acid derivatives.
100
Q

Patients with known CHD have a goal of LDL below _______.

A

100 mg per dL (2.6 mmol/L) or lower

101
Q

____________ is characterized by a defective hepatic LDL receptor, resulting in LDL elevations. ________ is a more common disorder that may present with elevation in cholesterol, triglycerides, or both.

A

Familial hypercholesterolemia

Familial combined hyperlipidemia

102
Q

Dietary factors that may increase cholesterol include ____________ (2). Alcohol increases __________ by inhibiting their metabolism.

A

high intake of saturated fats and exogenous cholesterol

triglycerides

103
Q

Risk factors for CHD (6) and one protective factor

A

Men older than 45 years or women older than 55 years
Family history of premature CAD (men younger than 55 or women younger than 65)
Current smoking
Hypertension (blood pressure [BP] >140/90 or on medication)
Diabetes mellitus (DM)
High HDL cholesterol (60 mg per dL) is considered a protective factor; patients with high HDL are considered to have one less risk factor.

104
Q

Physical examination is almost always normal in dyslipidemia, except in cases of extreme elevation of cholesterol, as seen in hereditary disorders. Physical findings include: (3)

A 
Tendinous xanthomas (subcutaneous painless nodules located on extensor tendons or Achilles tendon)
Eruptive xanthomas (smaller yellowish papules occurring on buttocks and pressure-sensitive surfaces)
Xanthelasmas (yellowish plaques located on eyelids)
105
Q

Once the diagnosis of dyslipidemia is made, always consider other disorders that may increase lipid levels, such as: (5)

A 
Hypothyroidism
Nephrotic syndrome or chronic renal failure
DM
Cholestatic liver disease
Drugs (thiazides, oral contraceptives)
106
Q

The initial screening test for dyslipidemia in healthy patients is __________ and LDL is calculated by the following equation: ________. This calculation is accurate only under the following conditions: ___________ (2)

A

a fasting lipid profile (total, HDL, LDL, and triglycerides)

LDL = Total Cholesterol - HDL - (Triglycerides ÷ 5)

In the fasting state and if the triglyceride level is

107
Q

A total cholesterol of ____ mg per dL are desirable values. All other patients should be managed according to the LDL level and the associated risk factors.

A

Total Chol 40 mg per dL (1 mmol/L)

108
Q

HMG-CoA reductase inhibitors: Effects on Lipid Profiles (HDL, LDL, TG)

A

HDL up, LDL down, TG unchanged

Internal Med - Jesse (8 decks)

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