Exam 3: DM and Thyroid Flashcards
What are the risk factors that lead to metabolic syndromes
waist circumference
Triglycerides
HDL
BP
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
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
Glucagon
hormone important in glucose regulation
prevents hypoglycemia by triggering the release of glucose from storage site in liver and skeletal muscle
Gluconeogensis
protein substances into glucose
Glycogenesis
production and storage of glycogen
Glycogenolysis
glycogen into glucose
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
ketogenesis
conversion of fats to acid products
Lipolysis
breakdown of fats, TGs into 1 glycerol and 3 fatty acids
proteolysis
breakdown of body proteins
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
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
DKA: clinical manifestions
3 p’s, rotting citrus fruit odor to the breath, kussmaul respirations, N/V, abdominal pain (cramps), weakness, confusion, shock, coma
DKA: treatment
fluids, regular insulin (watch the potassium)
HHNK: clincial manifestations
severe dehydration and hyper-osmolality, decreased BP, increased HR, altered LOC
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
What are the retinal changes with diabetes
cotton woot spots, microaneurysms, edema, exudate, neuvascularization
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%
Pre meal glucose goal
70-130
peak after meal glucose level goal
180 or less
Rapid acting insulins
aspart (Novolog), Lispro (humalog)
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
