Exam 3: DM and Thyroid Flashcards by Olivia Lassa

What are the risk factors that lead to metabolic syndromes

waist circumference

Triglycerides

HDL

Fasting glucose

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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What are the pathophysiological issue in type 1 vs type 2

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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Glucagon

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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Gluconeogensis

protein substances into glucose

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Glycogenesis

production and storage of glycogen

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Glycogenolysis

glycogen into glucose

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Glycosylated hemoglobin

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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ketogenesis

conversion of fats to acid products

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Lipolysis

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

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proteolysis

breakdown of body proteins

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Early signs of DM type 1

Late signs of DM type 1

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

late: coma, chronic complications

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

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

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DKA: clinical manifestions

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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DKA: treatment

fluids, regular insulin (watch the potassium)

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HHNK: clincial manifestations

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

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HHNK: treatment

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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What are the retinal changes with diabetes

cotton woot spots, microaneurysms, edema, exudate, neuvascularization

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what is the criteria for DM

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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Pre meal glucose goal

70-130

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peak after meal glucose level goal

180 or less

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Rapid acting insulins

aspart (Novolog), Lispro (humalog)

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short acting insulin

regular (humulin R)

Intermediate acting insulin

NPH

long acting insulin

glargine (lantus), detemir (levemir)

aspart (Novolog), Lispro (humalog): onset peak duration

onset: 15-30 minutes Peak: 30 minutes duration: Lasts between 2 to 4 hours

regular insulin: onset peak duration

onset: 30 to 1 hour peak: 1-5 hours duration: 3-6 hours

NPH: onset peak duration

onset: 1-2 hours peak: 6-14 hours duration: 10-16 hours

glargine (lantus), detemir (levemir): onset peak duration

onset: 1-2 hours peak: none Duration: 24 hours

How do we draw up insulin

air in NPH (cloudy), air in regular (clear) draw up clear then cloudy

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

lipodystrophy

Explain a bolus dose vs a basal bose

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

What is the dawn phenomenon

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

How do we manage the dawn phenomenon

providing more inslulin for the overnight period

What is somogyi phenomenon

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

How do we manage somogyi

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

What disease is associated with hyperthyroidism?

graves disease AKA toxic diffuse goiters

What is thyrotoxicosis

toxic effect or manifestations of excess thyroid hormone HTN, tachy, A-fib, boudning pulse, N/V/D, increased temperature

What are the main characteristic of graves (2)

exophthalmos aka proptosis pretibial myedema

s/s of hyperthyroid

heat intolerance increaesd body temp weight loss muscle fatigue increased appetite HTN, a fib nervousness, insomnia

What is thyroid storm caused by

stress, trauma, DKA, pregnancy, infection

S/S of thyroid storm

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

What is the treatment of thyroid storm

propranolol, PTU, iodine, glucocorticoids

What is important to know about PTU or tapazole

blocks synthesis of thyroid hormone dose tapered to achieve euthyroid treatment lasts 12-18 months monitor WBC (agranulocytosis)

Patients taking ______ possible liver toxicity or failure

PTU

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

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

Why do we monitor calcium levels in thyroid patients

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

What is our most common disease for hypothyroidism

hashimoto's disease --> primary thyroid failure

Secondary vs tertiary thyroid failure

secondary: pituitary tumors, infections, or infarcts --> TSH deficiency tertierary: hypotalamic tumor, infection, infarct

Clinical manifestations of hypothyroidism

cold intolerance cool, dry skin weight gain hoarse voice depression infertility periorbital edema loss of lateral eyebrows myxeedema coma anemia

S/S of myedema coma

hypotension hyponatremia hypothermia hypoglycemia

How do we treat myedema coma

secure airway IV levothjyroxin sodium IV glucose, steriods maintain temperature antibiotics

What are goitrogenic factors

iodine deficiency foods with goitrogenic properties (cabbage, turnips, soybeans) litium intrinsic abnormality in thyroid hormone synthesis

Normal ranges for TSH Free T4 Free T3 anti TPO

TSH 0.5 to 5.5 free t4: 0.8-1.8 free t3: 79-165 anti tpo: less than 35