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Adult health 2 > Exam 3: DM and Thyroid > Flashcards

Exam 3: DM and Thyroid Flashcards

1
Q

What are the risk factors that lead to metabolic syndromes

waist circumference

Triglycerides

HDL

BP

Fasting glucose

A

M: over 40 in
F: over 35 in

over 150 mg/dL

M: under 40 mg/dL
F: under 50 mg/dL

Over 130/85

over 110 mg/dL

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2
Q

What are the pathophysiological issue in type 1 vs type 2

A

In type 1 the beta cells are destroyed so there is little to no insulin but there is normal number of receptors

In type 2 the beta cells are present with varying insulin secretion and some receptor problems

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3
Q

Glucagon

A

hormone important in glucose regulation

prevents hypoglycemia by triggering the release of glucose from storage site in liver and skeletal muscle

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4
Q

Gluconeogensis

A

protein substances into glucose

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5
Q

Glycogenesis

A

production and storage of glycogen

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6
Q

Glycogenolysis

A

glycogen into glucose

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7
Q

Glycosylated hemoglobin

A

standardized test that measures how much glucose permanently attaches to the hemoglobin molecule; is often used to indicate the effectiveness of blood glucose control measures

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8
Q

ketogenesis

A

conversion of fats to acid products

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9
Q

Lipolysis

A

breakdown of fats, TGs into 1 glycerol and 3 fatty acids

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10
Q

proteolysis

A

breakdown of body proteins

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11
Q

Early signs of DM type 1

Late signs of DM type 1

A

early: polyuria, polydipsia, polyphagia, visual blurring, fatigue, weight loss

late: coma, chronic complications

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12
Q

Teach type 1 DM to perform vig exercise only when blood glucose levels are

A

100 to 250 mg/dL and no ketones in the urine

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13
Q

DKA: clinical manifestions

A

3 p’s, rotting citrus fruit odor to the breath, kussmaul respirations, N/V, abdominal pain (cramps), weakness, confusion, shock, coma

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14
Q

DKA: treatment

A

fluids, regular insulin (watch the potassium)

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15
Q

HHNK: clincial manifestations

A

severe dehydration and hyper-osmolality, decreased BP, increased HR, altered LOC

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16
Q

HHNK: treatment

A

IV fluid!!!!

Aggressive rehydration with intravenous (IV) fluids, including 0.9% isotonic saline, is indicated in every patient with hyperosmolar hyperglycemic state (HHS). Insulin therapy and repletion of electr

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17
Q

What are the retinal changes with diabetes

A

cotton woot spots, microaneurysms, edema, exudate, neuvascularization

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18
Q

what is the criteria for DM

A

fasting glu level over 126 mg/dL

s/s and random BS over 200 mg/dL

2 hour post prandial glucose level of over 200 mg/dL

HbA1C over 6.5%

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19
Q

Pre meal glucose goal

A

70-130

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20
Q

peak after meal glucose level goal

A

180 or less

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21
Q

Rapid acting insulins

A

aspart (Novolog), Lispro (humalog)

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22
Q

short acting insulin

A

regular (humulin R)

23
Q

Intermediate acting insulin

A

NPH

24
Q

long acting insulin

A

glargine (lantus), detemir (levemir)

25
Q

aspart (Novolog), Lispro (humalog):

onset

peak

duration

A

onset: 15-30 minutes

Peak: 30 minutes

duration: Lasts between 2 to 4 hours

26
Q

regular insulin:

onset

peak

duration

A

onset: 30 to 1 hour

peak: 1-5 hours

duration: 3-6 hours

27
Q

NPH:

onset

peak

duration

A

onset: 1-2 hours

peak: 6-14 hours

duration: 10-16 hours

28
Q

glargine (lantus), detemir (levemir):

onset

peak

duration

A

onset: 1-2 hours

peak: none

Duration: 24 hours

29
Q

How do we draw up insulin

A

air in NPH (cloudy), air in regular (clear)

draw up clear then cloudy

30
Q

What can we cause a patient if we do not rotate injection sites

A

lipodystrophy

31
Q

Explain a bolus dose vs a basal bose

A

bolus dose is pumped to cover food eaten by the patient to control blood glcuose level

basal dose is pumped continuously at an adjustable basal rate to deliver insulin needed between meals and at night

32
Q

What is the dawn phenomenon

A

The dawn phenomenon occurs when hormones like cortisol and growth hormone signal the liver to produce more glucose, which provides energy to wake up. However, if you have diabetes, your pancreas may not produce enough insulin to respond to the rise in blood sugar.

usually between 5am to 6am

33
Q

How do we manage the dawn phenomenon

A

providing more inslulin for the overnight period

34
Q

What is somogyi phenomenon

A

The Somogyi effect also involves a surge of hormones, but it’s due to a low blood sugar episode overnight. Dawn phenomenon doesn’t happen because of low blood sugar

35
Q

How do we manage somogyi

A

managed by ensuring adequate dietary intake at bedtime and evaluation of insulin dose and exercise programs to prevent conditions that lead to low BS

36
Q

What disease is associated with hyperthyroidism?

A

graves disease AKA toxic diffuse goiters

37
Q

What is thyrotoxicosis

A

toxic effect or manifestations of excess thyroid hormone

HTN, tachy, A-fib, boudning pulse, N/V/D, increased temperature

38
Q

What are the main characteristic of graves (2)

A

exophthalmos aka proptosis

pretibial myedema

39
Q

s/s of hyperthyroid

A

heat intolerance

increaesd body temp

weight loss

muscle fatigue

increased appetite

HTN, a fib

nervousness, insomnia

40
Q

What is thyroid storm caused by

A

stress, trauma, DKA, pregnancy, infection

41
Q

S/S of thyroid storm

A

elevated temperature (104-106), tachy, HTN, N/V, abdominal pain, tremors, altered mental status, agitation, coma, psychosis

42
Q

What is the treatment of thyroid storm

A

propranolol, PTU, iodine, glucocorticoids

43
Q

What is important to know about PTU or tapazole

A

blocks synthesis of thyroid hormone

dose tapered to achieve euthyroid

treatment lasts 12-18 months

monitor WBC (agranulocytosis)

44
Q

Patients taking ______ possible liver toxicity or failure

A

PTU

45
Q

women taking _______ to notify their primary HCP if they become pregnant

A

methimazole: slightly increases the chance of certain birth defects in the baby

46
Q

Why do we monitor calcium levels in thyroid patients

A

Monitoring calcium levels in hyperthyroidism patients is crucial because high levels of thyroid hormone can indirectly lead to elevated blood calcium levels (hypercalcemia), which can be harmful to the body, potentially causing complications like kidney stones, bone loss, and even heart problems

47
Q

What is our most common disease for hypothyroidism

A

hashimoto’s disease –> primary thyroid failure

48
Q

Secondary vs tertiary thyroid failure

A

secondary: pituitary tumors, infections, or infarcts –> TSH deficiency

tertierary: hypotalamic tumor, infection, infarct

49
Q

Clinical manifestations of hypothyroidism

A

cold intolerance

cool, dry skin

weight gain

hoarse voice

depression

infertility

periorbital edema

loss of lateral eyebrows

myxeedema coma

anemia

50
Q

S/S of myedema coma

A

hypotension

hyponatremia

hypothermia

hypoglycemia

51
Q

How do we treat myedema coma

A

secure airway

IV levothjyroxin sodium

IV glucose, steriods

maintain temperature

antibiotics

52
Q

What are goitrogenic factors

A

iodine deficiency

foods with goitrogenic properties (cabbage, turnips, soybeans)

litium

intrinsic abnormality in thyroid hormone synthesis

53
Q

Normal ranges for

TSH

Free T4

Free T3

anti TPO

A

TSH 0.5 to 5.5

free t4: 0.8-1.8

free t3: 79-165

anti tpo: less than 35

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