Test 3, NP 614 - Sheet1 Flashcards

1
Q

Labs to order for a 54-yo female experiencing unusual fatigue, Hct 38%, and fasting glucose of 130

A

Chemistry panel, fasting LFT, CK, Hgb A1C, and TSH

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2
Q

Best medication/rationale for a female with BMI of 50

A

Metformin / improves insulin sensitivity

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3
Q

Why does even a small weight loss (as little as 10 lbs) help diabetes

A

Helps improve sensitivity to insulin receptors

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4
Q

According to the ADA, a HbgA1c should be at least

A

<7

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5
Q

A common side effect of metformin therapy is

A

Gastrointestinal problems

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6
Q

The goal for someone with diabetes and HTN is

A

Treatment to a systolic blood pressure goal of less than 140 mmHg and diastolic pressure less than 80 mmHg

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7
Q

Besides a beta-blocker (that a patient has taken for years), what other HTN medication should be started

A

ACE inhibitor

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8
Q

Annual screenings for a patient who has had diabetes for 5 years includes

A

Fasting LFT, urine albumin, serum creatinine, dilated and comprehensive eye exam, neuropathy screening, comprehensive foot exam

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9
Q

Appropriate pharmacological management for a 77 yo female who has stable angina, increased TSH and normal T4

A

Levothyroxine 12.5 mcg q d

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10
Q

Diagnosis of 32 yo female who reports menstrual irregularities, fatigue, elevated TSH, normal free T4 and normal T3

A

Sub-clinical hypothyroidism

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11
Q

Consideration of Graves disease

A

Should be considered if patient has a-fib

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12
Q

Length of time to take medication for a patient diagnosed with Grave’s disease who elects treatment with anti-thyroid medications

A

6-12 months

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13
Q

The main reason for goiter in the U.S. is

A

Chronic autoimmune thyroiditis disease

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14
Q

A 56 yo man who reports fatigue, loss of weight, nausea and vomiting, muscle cramps, with hyperpigmentation at the elbows and knees would lead you to do a work-up for:

A

Addison’s disease

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15
Q

Initial medication for a patient who is hyperthyroid and complaining of fatigue and palpitations

A

Atenolol 50 mg daily

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16
Q

The response to a patient who asks you to increase her synthroid in order for her to lose weight

A

Excessive thyroid medication can lead to osteoporosis

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17
Q

Caution to tell patients regarding medication for hypothyroidism

A

This medication can increase the risk of fracture years from now if not monitored

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18
Q

Is insulin ever used for first-line treatment of Type II diabetes?

A

Yes

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19
Q

Early work-up for a suspected thyroid nodule includes:

A

TSH and serum free T4, ultrasound of suspected nodule, and a fine-needle biospy

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20
Q

Indication of elevated TSH

A

Hypothyroid

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21
Q

Indication of low TSH

A

Hyperthyroid

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22
Q

A gland

A

Anything in the endocrine system that sends out hormones

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23
Q

Hormones

A

Diffuse throughout the body and bump into cells

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24
Q

Water soluble hormones

A

Example - epinephrine. Docks on the surface of a cell and set up a signal transmission pathway in order to cause the desired effect

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25
Q

Lipid soluble hormones

A

Exampe - testosterone. Is transported directly into the cell membrane and can be moved into the nucleus

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26
Q

Pineal - hormone and action

A

Melatonin and circardian rhythm. Only secreted at night

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27
Q

Anterior pituitary - one hormone and action

A

Growth hormone and cell growth

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28
Q

Posterior pituitary - one hormone and action

A

ADH (antidiuretic hormone) and water balance

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29
Q

Thyroid gland - hormones and actions

A

T3/T4 - metabolism: calcitonin - lowers blood calcium and calcium goes back into the bones

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30
Q

Parathyroid gland - one hormone and action

A

PTH (parathyroid hormone) and raises blood calcium if calcium level gets too low

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31
Q

Pancreas - hormones and actions

A

Insulin - lowers blood sugar. Glucagon - raises blood sugar

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32
Q

Adrenal cortex - one hormone and action

A

Glucocorticoids - anti-inflammatory response

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33
Q

Adrenal medulla - one hormone and action

A

Epinephrine - fight or flight response

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34
Q

Ovaries - one hormone and action

A

Estrogen - female sex characteristics

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35
Q

Testes - one hormone and action

A

Testosterone - male sex characteristics

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36
Q

Hypothalamus

A

A member of the brain and the endocrine system. Nerve signals funnel into the brain and this gland sends them into the pituitary gland. Makes ADH and oxytocin.

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37
Q

Pituitary gland

A

Called the Master Gland because it takes the stimulation from hypothalamus and directs them to most of the other endocrine glands.

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38
Q

Thyroid gland

A

Wraps around the trachae and it helps in regularing metabolism by using T3 and T4

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39
Q

Parathyroid glands

A

Main role is reguation of blood calcium levels.

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40
Q

Adrenal glands

A

Located on top of kidneys

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41
Q

Adrenal cortex responsibility

A

Makes the adrenocorticosteroids - cortisol (stress hormone and increases blood sugar) and aldosterone (major regulator of blood fluid volume)

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42
Q

Adrenal medulla responsibility

A

Makes catecholamines - epinephrine and norepi and are involved in the body’s fight or flight response

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43
Q

Gonads - ovaries and testes

A

Release sex hormones that are involved in making the secondary sex characteristics and progressing us through the life stages

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44
Q

Pancreas

A

Located in upper abdomen and is uses hormones to stimulate control of the blood sugar through hormones insulin and glucoagan

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45
Q

Hormones and receptors

A

The receptors and their locations respond specifically to certain hormones

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46
Q

Autocrine hormones

A

Function at the cell that makes them. Example T-cells and the immune system

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47
Q

Paracrine hormones

A

Function regionally. Example - hormones released by hypothalamus that direct the thyroid

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48
Q

Endocrine hormones

A

Function at a distance - example pituitary gland stimulating the gonads

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49
Q

Incretin hormones

A

Located in the gut and are glucagon-like peptide-1 and glucose-dependent insulin-otropic polypeptide that regulate the secretion of insulin by stimulating beta cells to produce and secrete insulin, but only when glucose levels are increased.

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50
Q

Incretin hormone medications

A

Januvia - taken once daily with metformin. Byetta - injectable twice daily and causes nausea - biggest side effect pancreatitis.

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51
Q

When to start insulin as first-line glucose treatment

A

When Hgb A1C >9.0% and they are taking no meds.

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52
Q

Aspirin for CAD prevention in diabetics

A

Little evidence, focus on minimizing risks.

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53
Q

Facts about diabetes

A

7th leading cause of death, leading cause of blindness and kidney failure, >60% have nerve damage and amputations secondary to diabetes, 2x more likely to have periodontal disease and depression

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54
Q

Criteria for diagnosis of diabetes

A

A1C >6.5% or FPG > 126 mg/dl or 2-h plasma glucose > 200 or a random plasma glucose of >200 in a patient with classic symptoms of hyperglycemia

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55
Q

Categories of increased risk for Prediabetes

A

FPA 100-125 mg/dL or 2-h plasma glucose in the 75-g OGTT 140-199 mg/dl or A1C 5.7-6.4%

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56
Q

Testing in asymptomatic patients

A

All patients with BMI > 25 who have any additional risk factors. Begin testing at age 45 if BMI is normal (If normal and not diabetic or prediabetic recheck in 3 years). If patient is prediabetic, screen annually for progression to diabetes.

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57
Q

Test patients with a BMI >25 and any of the following risk factors for diabetes

A

Sedentary: first degree relative: high-risk ethnicity; previous GDM; delivery of infant >9 lbs; HTN; HDL 250; PCOS; prediabetes; clinical conditions associated with insulin resistance; history of CVD

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58
Q

Prevention of type 2 diabetes

A

Screen for any modifiable risk factors. At least 150 min/week of moderate physical activity. Weight loss of 7% of body weight. Appropriate referrals. Consider metformin for any prediabetics 35.

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59
Q

Microvascular considerations of patient with diabetes

A

Assess for retinopathy, nephropathy, and neuropathy

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60
Q

Sensory neuropathy considerations of patient with diabetes

A

Include history of foot lesions

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61
Q

Autonomic neuropathy considerations of patient with diabetes

A

Include sexual dysfunction and pastroparesis

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62
Q

Macrovascular considerations of patient with diabetes

A

CHD, CVA, PAD

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63
Q

Other medical conditions to consider in patient with diabetes

A

Psychosocial problems and dental disease

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64
Q

Comprehensive foot exams in patient with diabetes

A

Inspection. Palpation of dorsalis pedis and posterior tibial pulses. Presense/absence of patellar adn Achilles reflexes. Determination of proprioception, vibration, and monofilament sensation

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65
Q

Diagnostics to consider in patient with diabetes

A

A1C if not avaialble within last 3 months. Each year - fasting lipids, LFTs, urine albumin, serum creatinine with GFR, TSH in type 1 or dyslipidemic patients or women over 50

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66
Q

When to order A1C

A

At initial assessment. Every 6 months in patients at goal and who are stable. Every 3 months in patients not at goal. Use point of care if avaialble

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67
Q

A1C goal in non-pregnant adult

A

7%

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68
Q

Preprandial (fasting glucose) ideal reading

A

70-130 mg/dL

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69
Q

Postprandial (1-2 hr after meal) ideal reading

A

<180

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70
Q

Pt centered approach to diabetes - Key points

A

Glycemic targets and glucose lowering therapies must be individualized. Diet, exercise, and education remain the foundation of therapy. Metformin is 1st line. After metformin data is iffy. Most pts will require insulin alone or in combo with oral agents. All treatment decisions must be made with the patient. CVD risk reducation is overall goal.

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71
Q

Weight loss and diabetes

A

All pts with prediabetes or diabetes should receive nutritional counseling. Modest weight loss produces significant benefit. Limit ETOH, limit sodium, and increase fiber

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72
Q

Immunizations recommended for diabetics

A

Influenza, pneumococcal, and Hep B

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73
Q

BP >140-80 treatment and diabetes

A

Should be advised on lifestyle changes and began on med - ACE is 1st line

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74
Q

Consider low dose ASA for these diabetic patients

A

History of CVD or other major risk factors such as: FH or CVD, HTN, smoking, dyslipidemia or albuminuria. Increased risk for stroke. Most men >50. Most women >60

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75
Q

When to refer a diabetic patient with chronic kidney disease based on GFR

A

<30

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76
Q

LDL goals of patient with known CVD diabetes

A

<70

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77
Q

LDL goals of patient without CVD with risk factors and diabetes

A

<100

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78
Q

5 clinical manifestations of metabolic syndrome

A

Central obesity (waist >39 in men, >35 women), elevated fasting glucose >100 or drug treatment for elevated glucose, elevated triglyceridea >150 or treatment, reduced HDL-C 130 systolic or >85 diastolic or treatment

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79
Q

Number of clinical manifestations required for diagnosis of metabolic syndrome

A

3 of 5

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80
Q

Microvascular changes in diabetes

A

Caused by the long-standing hyperglycemia and results in neuropathy, nephropathy, and retinopathy. They are not part of metabolic syndrome.

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81
Q

Risk of CV disease in diabetics

A

2-4 fold increased risk

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82
Q

Primary prevention of CV in diabetics patients

A

Aspirin (75-162 mg/d) especially in pts >40 with additional risk factors (family hx of CVD, HTN, smoking, dyslipidemia, or albuminuria)

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83
Q

Possible best combo for patients with type 2 DM

A

Basal insulin and 1-2 daytime oral medications - Metformin with insulin

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84
Q

Race with greater insulin resistance

A

Latinos

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85
Q

Danger of hypoglycemia

A

Exacerbates MI and may cause dysrhythmias and possibly brain dysfunction with repeated episodes

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86
Q

Adverse effects of diabetes

A

Cardiovascular disease, renal failue, blindness, and nontraumatic lower limb amputation. Lower life expectancy and significant morbidity

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87
Q

Target organ damage of diabetes

A

Eyes, kidneys, heart, blood vessels, and nerves

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88
Q

Pathophysiology of type 1 diabetes

A

Caused by the autoimmune destruction of the beta cells within the islets of Langerhans in the pancreas in a genetically predisposed individual

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89
Q

Pathophysiology of type 2 diabetes

A

More obscure and hallmarks are insulin resistance and impaired beta cell function

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90
Q

Typical symptoms of untreated type 1 diabetes

A

Polyuria, polydipsia, polyphagia, weight loss, blurred vision, and fatigue

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91
Q

Signs of ketoacidosis

A

Glycosuria increases, nausea, vomiting, abdominal pain, rapid shallow breathing, hypotension, and dehydration

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92
Q

Symptoms of untreated type 2 diabetes

A

May have no symptoms or subtle ones that last for weeks to years. Polyuria, polydipsia, blurred vision, fatigue, slowly healing wounds, and frequent infections.

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93
Q

Focus of physical exam in diagnosis of diabetes

A

Dehydration, weight loss, and precipitating causes, such as illness, infection, or stress. May appear dry and flushed. Assess skin, eyes, heart, lungs, thyroid.

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94
Q

Labs related to diagnosis of diabetes

A

Serum glucose (random or fasting), oral glucose tolerance test, HbA1C, and urinalysis

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95
Q

Treatment of diabetes

A

Health diet, regular exercse, medication, monitoring, self-care education, and periodic follow-up by the PCP and diabetes care team.

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96
Q

Goal of nutritional therapy regarding diabetes

A

Development of a meal plan, balancing insulin with food intake and activity to achieve glycemic control

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97
Q

Exercise and type 2 diabetes

A

Decreases insulin resistance and increases glucose uptake into the cell. This can cause the exercise lag effect and can last up to 48 hrs after exercise.

98
Q

Treatment of type 2 diabetes includes…

A

Management of dyslipidemia, hypertension, obesity, insulin resistance, and hypercoagulability as well as glycemic control, education, diet, exercise, adn achievement and maintenance of a desirable body weight.

99
Q

The most common reason for use of insulin in type 2 diabetes

A

Failure to respond to the oral antihyperglycemic agents

100
Q

Symptoms of mild hypoglycemia

A

Shaking/trembling, sweating, hunger, tachycardia, weakness, lightheadedhess, pallor, irritability, but no change in mental status: individual able to treat self

101
Q

Symptoms of moderate hypoglycemia

A

Decreased thinking, increased emotions (anger, irritability), inability to complete tasks, some changes in mental status: individual may be able to treat self

102
Q

Symptoms of severe hypoglycemia

A

Confusion, drowsiness; may progress to unconsciousness, impaired neurologic function; individual requires assistance

103
Q

Diabetic ketoacidosis

A

Caused by insulin deficiency and is characterized by hyperglycemia, ketonemia, and acidemia

104
Q

Clinical presentation of DKA

A

Rapid development of abdominal pain, nausea, vomiting, Kussmaul respirations, dehydration, fruity odor to breath, tachycardia, hypotension, and changes in consciousness

105
Q

Treatment of DKA

A

Fluid resuscitation, IV insulin, electrolyte monitoring and replacement, and treatment of underlying illness or infection

106
Q

Acanthosis nigricans

A

A diffuse, hyperpigmented, velvety thickening of the skin that is found on the neck and axillae. Sign of insulin resistance

107
Q

How to calculate BMI

A

Weight divided by height squared

108
Q

Labs of metabolic syndrome

A

Glucose tolerance test - fasting blood glucose, fasting plasma insulin concentration, fasting lipid profile, urinalysis (for protein), and C-reactive protein

109
Q

Complications of metabolic syndrome

A

CVD, atherosclerotic vascular disease, ischemic heart disease, coronary artery disease, MI, and stroke

110
Q

Causes of goiter

A

Hormonal or immunologic stimulation or may result from inflammatory, infiltrative, or metabolic conditions, including iodine deficiency or excess, neoplasia, Graves’ disease, and thyroiditis

111
Q

Diagnosis of goiter

A

TSH, free T4, antimicrosomal antibodies, radionuclide scannin, thyroid ultrasound

112
Q

Hyperthyroidism

A

A clinical syndrome caused by the excess production or release of thyroid hormone and its clinical manifestations

113
Q

Most common cause of hyperthyroidism

A

Graves’ disease

114
Q

Pathophysiology of Graves’ disease

A

An autoimmune disorder in which thyroid-stimulating antibodies compete with TSH for TSH receptors on the thyroid and activate the production of cyclic adenosine monophosphate, which increases the synthesis and release of thyroid hormones

115
Q

Symptoms of hyperthyroidism

A

Dry eyes, SOA, palpitation, tachycardia, weight loss, goiter, amenorrhea, tremor, sweaty palms, anxiety, irritability, sleeplessness, anorexia

116
Q

TSH level in hyperthyroidism

A

TSH will be low or undetectable

117
Q

Pharmacological treatment of Graves’ disease

A

Beta blockers for tremor and tachycardia.

118
Q

Medical treatment of Graves’ disease

A

PTU and radioiodine therapy

119
Q

Subclinical hyperthyroidism

A

Suppressed TSH with normal serum T4 and T3 levels and most elderly patients have multinodular goiters

120
Q

Clinical findings of thyroid storm or thyrotoxic crisis

A

Temp 102-105, profuse sweating, pulse above 120-140, a-fib, restlessness, confusion, agitation, coma, severe vomiting, diarrhea, and hepatomegaly, jaundice

121
Q

Hypothyroidism

A

Results from synthesis of thyroid hormone that is insufficient to meet the body’s needs and is the most common disorder of the thyroid.

122
Q

Clinical presentation of hypothyroidism

A

Myxedema, slowed mentation, the most comon is fatigue. Increased sensitivity to cold, weight gain, hoarseness, puffiness of the face and hands, heavy and irregular menstrual periods, dry skin, dry and brittle hair, depression, paresthesias, muscle aches, and constipation.

123
Q

Lab tests of hypothyroidism

A

Elevated TSH

124
Q

Treatment of hypothyroidism

A

Levothyroxine

125
Q

Subclinical hypothyroidism

A

Elevated TSH in the presence of normal thyroid hormone levels

126
Q

Myxedema coma

A

Hypothermic stuporous state that may be characterized by respiratory depression and eventually death is the result of untreated hypothyroidism and can be triggered by environmental stressors such as cold exposure or trauma and infection

127
Q

Thyroid hormone and metabolism

A

Stimulates metabolic activities in cells, leading to increased basal metabolic rate

128
Q

Lipids and thyroid hormone

A

Increased thyroid hormone leads to an increased concentration of fatty acids in plasma

129
Q

Cholesterol levels and thyroid hormone

A

Cholesterol and triglycerides are inversely realted to thyroid hormone levels

130
Q

Carbohydrates and thyroid hormone

A

Stimulates their metabolism, and stimulates the insulin-dependent entry of glucose into cells

131
Q

Glucose production and thyroid hormone

A

Increased levels result in increased gluconeogenesis and glycogenolysis resulting in increased production of glucose

132
Q

Growth hormone and thyroid hormone

A

Closely related to the effects of growth hormone and is necessary for normal growth and development in children

133
Q

Thyroid hormone and cardiovascular effects

A

It increases HR, contractility and cardiac output

134
Q

Thyroid hormone and CNS effects

A

Derangements in thyroid hormone can lead to changes in mental statue; fatigue if too low and anxiety if too high

135
Q

Thyroid hormone and reproductive system effects

A

Normal levels are necessry for the functioning of the reproductive system, and low levels are associated with infertility

136
Q

T4 and T3

A

Hormones released by the thyroid gland itself and circulates through the bloodstream to other “target cells”. 80% if T4 and most of T4 is converted to T3

137
Q

Feedback loop of thyroid hormone production

A

Negative loop

138
Q

Diagnosing Graves’ disease

A

The TSH will be low and the free T4 will be high. No further workout needed especially if ophthalmic signs and symptoms are present

139
Q

Toxicosis

A

Low TSH, low T4 and high T3

140
Q

Radioiodine uptake patterns

A

High update - Graves’ disease. Low uptake - thyroiditis

141
Q

Treatment of hyperthyroidism

A

Depends on multiple factors: age of pt, size of goiter, other medical conditions, severity of symptoms, and wishes of pt

142
Q

Iodine preparations and treatment of Graves’ disease

A

Dose is 1 gm/day for up to 12 weeks and not used long-term because can increase thyroid hormone release

143
Q

Low term effects of thyroxine

A

Decreased bone density, cardiac arrhythmias

144
Q

TSH and disgnosis of hypothyroidism

A

TSH elevated and free T4 decreased

145
Q

Diseases classified under Alzheimer’s disease

A

Parkinson’s-associated dementia, Lewy Body Dementia, Frontal Lobe Dementia

146
Q

Questions to ask yourself when considering dementia

A

Is this a reversible problem? How best to treat the patient and the family?

147
Q

Changes in brain regarding Alzheimer’s

A

Senile plaques develop between neurons. Neurofibrillary tangles develop within the neurons

148
Q

Pathophysiology of Alzheimer’s

A

Involvement of cholinergic neurons causes level of acetylcholine within synapses to drop. Levels of acetylcholinesterase also drop. Butylcholinesterase levels increase which metabolizes acetylcholinesterase and the disease progresses. Glutamate is also thought to be involved, is a chemical that causes brain cell death.

149
Q

Vascular dementia - clinical manifestations

A

Caused by multi-infarcts. Sudden onset, stepwise deterioration. Difficulty retrieving works, organizing and solving complex problems. Relatively preserved language skills. More depressed component. Numerous CV risk factors. MRI - periventricular white matter disease

150
Q

Lewy Body Dementia - clinical manifestations

A

Dementia presents first followed by physical changes. Recurrent visual hallucinations and delusions. Often walks with a stoop (similiar to Parkinson’s). Frequent falls are common. More flactuating attention problems. Increased sensitivity to conventional anti-psychotics. Performs better on verbal recall than Alzheimer’s pts. Poor organizational skills

151
Q

Progression of Alzheimer’s

A

Mild cognitive impairment- 7 yrs - short-term memory loss. Mild - 2 yrs - problems reading, poor object recognition, poor directional sense. Moderate - 2 yrs - poor judgment, impulsivity, short attention. Severe - 2 yrs - visual problems

152
Q

Diagnosis of Alzheimer’s dementia

A

Memory impairment and one or more of the following - asphasia, apraxia, agnosia, and disturbances in planning, organizing, sequencing, abstracting

153
Q

Diagnostic studies to consider when diagnosing Alzheimer’s

A

CBC - anemia or infection. Vit B12 - anemia. Folate - anemia. Homocystine - supports B12 and folate. Thyroid function - reversible cause. Metabolic panel - rule out liver or renal and is reversible. Electrolytes and calcium - hypo/hypernatremia or hypo/hypercalcemia. Glucose. Lipid - vascular cause. ECG - a-fib. RPR - latent syphilis

154
Q

Prevelance of stroke

A

Major cause of permanent disability and 3rd leading cause of death in U.S.

155
Q

Definition of stroke

A

Symptoms lasting 24 hrs or imaging of an acute clinically relevant brain lesion in patients with rapidly vanishing symptoms.

156
Q

Definition of TIA

A

Brief episode of neurological dysfunction caused by a focal disturbance of brain or retinal ischemia, wich clinical symptoms typically lasting less than 1 hr and without evidence of infarction”. Important determinant of stroke with 90-day risk reported as high as 10.5% and greatest risk in first week.

157
Q

Diagnosis of epilepsy

A

When they have had two unprovoked seizures and all other possible causes have been ruled out

158
Q

Physiological signiture of Parkinson’s disease

A

Progressive death of neurons, and the presence of tiny dense structures called Lewy bodies, in the substantia nigra of the brain’s basal ganglia that produce dopamine

159
Q

Cardinal signs of Parkinson’s disease

A

Non-intentional tremors at rest (pill-rolling), bradykinesis, muscle ridigity, and postural instability.

160
Q

Early symptoms of Parkinson’s disease

A

Small handwriting, slowness in walking, reduced speech volume with montony, reduced arm swing, reduced blinking and swallowing, and seborrheic dermatitis

161
Q

Later symptoms of Parkinson’s disease

A

A shuffling, stooped gait, instability, propulsive gait, retropulsion, and postural hypotention leads to falls, dysphagia, impotence, and urgent micturition or incontinence

162
Q

Diagnosis of Parkinson’s

A

Made by history and physical exam. No specific labs

163
Q

Pharmacologic therapy of Parkinson’s

A

Drugs that lower central dopamine concentrations - Levadopa, Requip, MAO inhibitors, Amantadine

164
Q

Levadopa/Carbidopa

A

Often initial choice for Parkinson’s - greater effect on bradykinesia and rigidity. Sinemet

165
Q

Where in the back does the spinal cord end?

A

T12-L1

166
Q

Conus Medullaris

A

Lower end of the spinal cord

167
Q

Cauda Equina

A

Division of multiple nerve roots beginning at the level of L1

168
Q

Discs commonly involved in lower back problems

A

L4-L5 and L5-S1

169
Q

Types of disc herniation

A

Protrusion/bulge, disc herniation, and sequestration

170
Q

Protrusion/bulge of disc

A

A bulgin disc with intact annular and posterior longitudinal ligament fibers

171
Q

Categories of disc herniation

A

Type A - disruption of inner annular fibers with intact outer annular fibers. Type B - disrupted annulus with tail of disc material extending into the disc space.

172
Q

Sequestration

A

Free fragment without tail extending into disc space. Fragment may be reabsorbed spontaneously.

173
Q

Typical locations of disc herniation

A

Central, posterolateral, and foraminal

174
Q

Central disc herniation

A

Rare and affects multiple nerve roots, back pain more than leg, cause incontinence of bladder and bowel, requires immediate treatment.

175
Q

Posterolateral disc herniation

A

Usual location, most commonly involving one nerve root (the lower one)

176
Q

Foraminal disc herniation

A

Occurs in 8-10% of cases and involves the exiting nerve. Usually the top nerve

177
Q

Discogenic back pain internal disc disruption

A

Annular tears. Early disc degeneration. Pain worsens with flexion/sitting. Slightly better with extension. Forward flexion limited on exam. No radicular symptoms.

178
Q

Straight leg raise with back pain

A

Wanting to see if pt can actively lift leg more than 30 degrees. Passively lift pt leg until point of pain is reached. Looks for nerve root impingement

179
Q

Braggard stretch leg test for back pain

A

Stop at point of pain with straight leg pain and lower until pain stops. Then dorsiflex the foot to reproduce the pain in the buttock and back

180
Q

Hoover test for leg pain

A

Measures ability of pt to more or not be able to move leg. Put hands under heels and ask pt to lift leg. When they are faking, you will feel counter force to the opposite foot.

181
Q

Benign essential tremors

A

Get worse with intentional activity and they respond really well to beta blockers

182
Q

Goal of parkinson’s disease treatment

A

Reduce symptoms, minimize complications, maintain independence. The foundation of treatment is individualization and education.

183
Q

Freezing phenomenon with Parkinson’s

A

A motor block, is a transient inability to perform active movements. Usually affects legs, but can involve eyelid opening, speaking, and writing

184
Q

Wearing off effect of parkinson’s

A

The period of effectiveness after each dose may begin to shorten

185
Q

On/off effect of Parkinson’s

A

Sudden fluctuations in movement, from normal or dyskinesia to parkinsonian slowness and stiffness and back again. The responses to a drug is changing as the disease progresses

186
Q

Risk stratification for risk of early recurrence of stroke

A

ABCD - Age, blood pressure, clinical symptoms of focal weakness or speech impairment without weakness, diabetes.

187
Q

When to discontinue anti-thrombotic therapy

A

When risks of bleeding become greater than the beneift. Pre-procedures - must weigh risk of hemorrhage about risk of thromboembolism. The decisions about stopping treatment pre-surgery/procedure are made on the basis of type of therapy, pts bleeding risk, and degree of inherent in the procedure. Consult

188
Q

Type of dementia associated with neurofibrillary tangles

A

Alzheimer’s

189
Q

Question to ask when assessing for memory loss

A

What did you have for dinner yesterday?

190
Q

Acetylcholinesterase inhibitors works by…

A

Shown to slow progression of memory loss

191
Q

Principle of antiepileptic drug therapy

A

Titrate medication slowly

192
Q

A construction worker who suffered a new seizure should be advised…

A

To avoid work on any roof until fully evaluated

193
Q

Earliest presentation of Parkinson’s Disease that is often misdiagnosed

A

Resting tremor in the distal extremities

194
Q

Best way to diagnose Parkinson’s disease

A

Giving a small dose of Levadopa /carbidopa (Sinemet)

195
Q

Spinal stenosis should be suspect when…

A

Walking or prolonged standing causes pain in legs

196
Q

Diagnosis of a patient who suffered from right side facial and arm numbness for a few hrs and resolved

A

TIA

197
Q

A nonmodifiable risk factor for stroke is

A

HTN

198
Q

An appropriate antiplatelet therapy post TIA without a-fib and no other contraindications/risk factors

A

Low dose aspirin

199
Q

Essential tremor

A

Benign, chronic neurologic condition that involves symmetric, rhythmic trembling of the upper extremities, head, or voice. Legs are less common. Emotional stress will increase symptoms.

200
Q

Multiple sclerosis

A

Chronic progressive inflammatory and neurodegenerative disease affecting the CNS. Hallmark lesion is called a plaque

201
Q

Onset of MS

A

Usually between 20-50, more women than men

202
Q

Pathophysiology of MS

A

Thought to be triggered by an event, probably environment, that activates the inflammatory process outside the CNS

203
Q

Four clinical courses of MS

A

Relapsing-remitting (RRMS), primary-progressive (PPMS), secondary-progressive (SPMS), and progressive-relapsing(PRMS). RRMS is most common

204
Q

Common initial symptoms of MS

A

Sensory symptoms (paresthesias), optic neuritis, limb weakness, diplopia, nystagmus, unsteady gait, myelopathy, and trigeminal neuralgia

205
Q

Diagnosis of MS

A

Clinical diagnosis. Events must be at least two distinct episodes lasting more than 24 hrs occuring at least 30 days apart and occur in two different locations. The symptoms must be not explained by another pathologic process.

206
Q

Gold standard of MS diagnosis

A

MRI of brain

207
Q

Drugs to treat MS

A

Interferons (Betaseron, extavia, avonex, rebif), copaxone, mitoxantrone

208
Q

Pathophysiology of Parkinson’s

A

Develops after widespread depletion of dopamine in the substantia nigra and the nigrostriatal pathway to the caudate and putamen

209
Q

Clinical presentation of Parkinson’s

A

Asymmetric or unilateral tremor, rigidity, bradykinesia with freezing, and flexed posture with loss of postural reflexes. Cogwheel feeling with passive movement of joint

210
Q

Status epilepticus

A

Defined as more than 30 minutes of continuous seizure activity or two or more seizures without a baseline consciousness between attacks

211
Q

Partial seizures

A

Begin in a limited region of one cerebral hemisphere and how focal EEG abnormalities. Consciousness may vary

212
Q

Simple partial seizures

A

No alteration in consciousness and are usually the aura, or warning, that the patient experiences before a larger seizure

213
Q

Complex partial seizure

A

The seizure activity spreads and involves the brainstem or both hemispheres, consciousness becomes altered

214
Q

Primary generalized seizure

A

Occur when the initial electrical activity begins in both cerebral hemispheres. Consciousness is almost always imapired and may be convulsive or nonconvulsive

215
Q

Clinical presentation of seizure

A

Accurate and detailed history is important New onset seizures require determination of any recent history of headache, illness, trauma, or focal neurologic deficit

216
Q

Goal of seizure management

A

Control seizures with minimum adverse effects

217
Q

Types of stroke

A

Ischemic (more prevalent) and hemorrhagic (more deadly)

218
Q

Relapse of back pain

A

75% in the 12 months after recovery

219
Q

Chronic low back pain

A

Defined as pain that lasts for more than 12 weeks, making the recovery time less certain

220
Q

Categories of lumbar spine disorders

A

Axial low back pain and radicular pain

221
Q

Mechanical back pain causes

A

Atrributed to direct injury, deformity, imbalance, or overuse of identifiable structures

222
Q

Structural causes of mechanical low back pain

A

Intervertebral disks, facet joints, vertebral bodies, ligamentous structures, and sacroiliac joing as well as imbalances of the muscles supporting the lumbar spine

223
Q

Neuropathic causes of low back pain

A

Typically attributed to direct compression of the spinal cord or spinal nerve roots as well as alteration of the neurologic pathways involving the brain and spinal cord.

224
Q

Lumbar radiculopathy

A

Refers to involvement of the spinal nerve root with resultant neurologic symptoms, such as pain, weakness, numbness, tingling, and change in reflexes involving a specific dermatomal or myotomal distribution associated with an affected lumbar spinal nerve root

225
Q

Clinical presentation of lumbar radiculopathy

A

Often present with significant leg and thigh pain greater than low back pain and may include neurologic symptoms

226
Q

Clinical presentation of spinal stenosis

A

Typically present with thigh, calf, and back pain, typically worsened by standing and walking and alleviated with sitting

227
Q

Most widely used imaging study for back pain

A

MRI of brain

228
Q

Management of back pain

A

Bed rest for no more than 2 days with frequent position changes

229
Q

Acute cerebral vascular syndreom (ACVS)

A

Used to be called TIA and refers to events that are manifested as neurologic deficits that resolve completely within a few hrs but no more than 24 hrs.

230
Q

Population typically affected by ischemic strokes

A

Typically older persons with other disease processes

231
Q

Population typically affected by hemorrhagic strokes

A

Typically healthy individuals between 40-60

232
Q

Risk factors for ischemic stroke

A

HRN, age, smoking, male, family history, race, previous stroke, carotid stenosis of more than 80%, a-fib, CHF, mitral stenosis, prosthetic cardiac valves, MI, and cocaine use, diabetes, sedentary lifestyle, and elevated cholesterol

233
Q

Risk factors for hemorrhagic stroke

A

Intracranial vascular anomalies, HTN, family history, PCOS, Ehler-Danlos syndrome, lupus, neurofibromatosis, tuberous schlerosis, pregnancy, smoking, atherosclerosis, acute ETOH intoxication, and cocaine use.

234
Q

Most common cause of hemorrhagic stroke

A

Trauma

235
Q

Common signs and symptoms of stroke

A

Hemiparesis, hemisensory loss, visual field defects, ataxia, dysarthria, relfex asymmetry, and Babinski’ssign

236
Q

Presentation of ischemic stroke

A

May occur over a few hours in a stepwise or shuttering fashion involving one area and progressing until the stroke is fully developed

237
Q

Presentation of hemorrhagic stroke

A

Usually begins with the abrupt onset of a severe headache (“worst headache of my life”), nausea and vomiting, signs of meningeal irritation, and varying degrees of neurologic dysfunction, loss of consciousness, dizziness, seizures, with or without neurologic dysfunction

238
Q

Presentation of HTN intracerebral hemorrhage

A

May have no warning signs, HTN, headache, followed within a few minutes by unilateral facial sag, slurred speech, weakness in an arm and leg, and eye deviation away from the paretic limbs occurring during 5-30 minutes

239
Q

Preferred diagnostic test for stroke

A

CT

240
Q

Management of TIA

A

If seen days after event and has no current signs or symptoms - out-pt management is adequate. If symptoms, should be treated as a medical emergency

241
Q

Management of ischemic stroke

A

Careful monitoring of BP - labetalol. tPA for selected pts if administered within 3 hrs of onset. Antiplatelet agents - ASA, Coumadin, Plavix

242
Q

Patient education regarding stroke

A

Risk factor reduction and stroke symptom recognition and emergency treatment. HTN is most important independent and modifiable risk factor