Endocrine - hypo/hyperthyroidism, diabetes Flashcards

1
Q

describe the general flow of thyroid hormones

A

TRH (thyrotropin releasing hormone) from Hypothalamus acts on the anterior pituitary gland, which releases TSH (thyroid stimulating hormone) which stimulates the thyroid gland to produce T4 and T3
Iodine needed for production of T3 and T4

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2
Q

Thyroid tests to determine levels

A

TSH high + T4 low = HYPOthyroidism

TSH low + T4 high = HYPERthyroidism

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3
Q

describe hyperthyroidism

A

thyroid gland produces too much thyroid hormone, causes hypermetabolic syndrome that affects females more than males

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4
Q

Hyperthyroidism causes

A
  1. Grave’s disease - characterized by a goiter, ‘orange-peel’ skin. caused by an antibody-mediated auto-immune reaction that binds to the TSH receptor and chronically stimulates it
  2. thyroiditis
  3. excess ingestion of thyroid hormone
  4. drug-induced - Aminodarone
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5
Q

signs and symptoms of hyperthyroidism

A

intolerance to heat, facial flushing
fine, straight hair, bulging eyes, finger clubbing
tachycardia, tremors, increased systolic BP
diarrhea, weight loss, amenorrhea, edema

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6
Q

hyperthyroidism diagnosis

A

decreased thyroid stimulating hormone and increased thyroid hormones (T3 & T4)

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7
Q

complications associated with hyperthyroidism

A
  1. increased HR, heart failure, muslce wasting, osteopoposis
  2. Thyroid ‘storm’ - rapid onset with high temp, extreme exhaustion, rapid HR, delerium
  3. Death
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8
Q

drug therapy for hyperthyroidism

A
Drug Therapy:
-Methimazole
-Propylthiouracil (PTU)
-Radioactive Iodine
Adjunctive Therapy:
-Beta-blockers
-corticosteroids
Surgery:
-Thyroidectomy
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9
Q

what are the main anti-thyroid drugs and describe

A

Propythiouricil and methimazole
These two drugs block the binding of iodine, therfore prevents the formation of thyroid hormones.
Note: may take weeks to see full effect

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10
Q

A/E to PTU and methimazole

A

granulocytopenia (decrease WBC’s)
rash
peripheral neuritis

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11
Q

common adjuncts (add-ons) to propylthiouracil and methimazole

A

propranolol to supress tachycardia

corticosteroids to reduce immune respose

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12
Q

radioactive iodine and hyperthyroidism

A

suitable for most patients, although some prefer to use mainly for older Pt’s
-used when failed medical therapy or surgery
-medical/surgical therapy is contraindicated
NOTE: contraindicated with PREGNANCY and has high incidence to cause hypothyroidism

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13
Q

describe Iodine-131

A

-radioactive isotope
-concentrates in the thyroid gland
-destruction of thyroid tissue via beta emissions
-reduces thyroid function gradual
Full effects in 2 weeks to 3 months

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14
Q

describe hypothyroidism

A

deficiency of thyroid hormone or decreased activity of the thyroid gland. affects women more than men

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15
Q

Causes of hypothyroidism

A
  1. Hashimoto’s thyroiditis - autoimmune disease where the body’s own antibodies attack the cells of the thyroid
  2. destruction of thyroid gland (trauma)
  3. lack of dietary iodine
  4. drug induced - amiodarone, lithium, interferon-alpha, over-treatment with anti-hyperthyroid drugs
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16
Q

hypothyroidism diagnosis

A

clinical sign and symptoms
increased TSH
T3/T4 is usually low

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17
Q

signs and symptoms of hypothyroidism

A

intolerance to cold, receding hairline, facial and eye-lid edema, thick tongue/slow speech
apathy, lethargy, dull-blank expression, extreme fatigue
dry skin, muscle aches, anorexia,
constipation, menstrual disturbances
ADVANCED: bradycardia, wieght gain, decreased LOC, cardiac complications

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18
Q

Thyroid hormone drug therapy

A
LEVOTHYROXINE (T4 analogue)
-Synthroid
-Eltroxin
LIOTHYRONINE (T3 analogue)
Dosage:
usually start 50-75 mcg/day, increasing dose by 25-50mcg in 6-8 week intervals. 
Usual dose ~ 75-150mcg/day
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19
Q

A/E to thyroid hormone therapy

A

headache, palpations (atrial fibrillation), chest pain, heat intolerance, sweating
monitor clinical status of Pt for 6-8 weeks (TSH, T3, T4)

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20
Q

diseases associated with cortisol

A

too much = Cushing’s Syndrome/Disease

too little = Addison’s disease

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21
Q

what does cortisol do

A

-controls water and sodium balance
-regulates carbohydrate, fat and protein metabolism
-production increases during stress
produced by the adrenal gland, mostly in the a.m. (20mg/day)

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22
Q

describe the cortisol loop

A

hippocampus gets the hypothalamus to release CRH (corticotropin releasing hormone) and acts on the anterior pituitary that then releases ACTH (Adrenocorticotropin hormone) that acts on the adrenal gland to produce more cortisol.
Negative feedback loop. once cortisol levels rise, the hippocampus will not stimulate hypothalamus any further

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23
Q

describe Cushings syndrome/disease

A

too much cortisol produced as a result of too much ACTH released from pituitary gland.
Pituitary tumor = Cushing’s disease
Adrenal tumor = Cushing’s syndrome

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24
Q

signs/symptoms of Cushing’s syndrome/disease

A
moon face, Na+ and fluid retention
hyperglycemia, personality changes
males may develop breasts (gynecomastia)
females may have amenorrhea, hirsutism
thin skin, purple striae, osteoporosis, fat deposits on back
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25
Q

treatment for cushings syndrome/disease

A
  1. reverse the underlying cause
  2. if tumor is identified then it may be removed via surgery. steroid replacement afterwards.
  3. if surgery not suitable, several drugs have been found to inhibit cortisol synthesis (Ketoconazole, antifungal that reduces cortisol production)
26
Q

Describe Addison’s disease

A

Too little cortisol produced when cortex of adrenal gland is damaged, most commonly found by the body attacking itself (autoimmune disease)

27
Q

other causes for adrenal gland failure

A
  • tuberculosis
  • other infections of the adrenal gland
  • spread of cancer to the adrenal glands
  • bleeding into the adrenal glands
28
Q

secondary causes for adrenal insufficiencies

A
  • pituitary gland diseased
  • inadequate production of ACTH can lead to insufficient production of hormones produced by the adrenal gland
  • when Pt’s treating chronic conditions, such as asthma or arthritis, suddenly stop taking corticosteroids
29
Q

signs and symptoms for Addison’s disease (too little cortisol)

A

bronze pigmentation of skin
hyopglycemia, postural hypotension, weight loss
changes in distribution of body hair, weakness
Adrenal CRISIS: profound fatigue, dehydration, vascular collapse (BP), renal shut down, decreased serum Na+, increased Serum K+ (electrolyte imbalance)

30
Q

treatments for Addison’s disease

A

Hydrocortisone
Cortisone
Fludrocortisone

31
Q

what is type 1 diabetes

A

onset usually at a young age
no production of insulin: islet cells of pancreas not working
oral meds are ineffective
Glucose enters the bloodstream, there is little to no insulin in the blood to breakdown the glucose to it build up in the blood stream leading to hyperglycemia

32
Q

what is type 2 diabetes

A

onset in adulthood, usually secondary to obesity
insulin resistance and relative insulin deficiency
Oral meds usually work
**too much fat, not enough exercise, and inherited genes. leads to overwieght and body becomes insulin resistance.. Fatty deposits in pancreas cause damage and prevent insulin from being produced = type 2 diabetes. Insulin produced is resistant to effective use and can’t push the glucose into the interstitial space, resulting in increased glucose in the blood stream

33
Q

signs and symptoms of diabetes

A
tired, thirsty, increased urination, increased hunger
change in body weight (+/-)
blurred vision
vaginal infections in women
balantitis in uncircumcised men
tingling/numbness in hands/feet
34
Q

risk factors for type 1 diabetes

A

generally young
not usually overweight
may not have a family history
prone to developing Ketosis (ketone - fruity breath)

35
Q

risk factors for type 2 diabetes

A
prediabetes
sedentary lifestyle
overweight/obese
hypertension
dyslipidemia (high cholesterol)
40 years old or higher
close relative who has type 2
member of high risk population
heart disease
women who have had gestational diabetes mellitus
36
Q

common diagnosis tools for diabetes

A

FPG - Fasting plasma Glucose - >7.0mmol/L (8 hours w/o caloric intake)
OR
Casual PG - plasma glucose - >11.1mmol/L (taken at any point during the day) must present with signs of diabetes
OR
75g 2hPG OGTT - Oral glucose tolerance test. Used by specialists who administer the FPG then person drinks a glucose sol’n and waits for 2hours and result >11.1mmol/L

37
Q

blood glucose targets for adults

A

A1C (glycosylated hemoglobin) gives average of BG level for last 120days. A1C <6.0 (normal range)

FPG preprandial PG = 4.0-7.0 (diabetic), or 4.0-6.0 (normal range)

2hPG postprandial(after food) = 5.0-10.0 (diabetic), or 5.0-8.0 (normal range)

38
Q

major diabetic compications

A

cerebrovascular disease
retinopathy (blindness)
Coronary heart disease
nephropathy (kidney)
Peripheral neuropathy and vascular disease
Diabetic foot ulcerations and amputations

39
Q

Management of diabetes type 2

A

non-pharmacological therapy (exercise, diet)
achieve desired blood glucose asap (within 6 mos.)
Medications

40
Q

medications for type 2 diabetes

A
  • Secretagogues (Sulfonylureas, Meglitidines)
  • Biguanide
  • Alpha-glucosidase inhibitor
  • Thiazolidinediones (TZD)
  • Incretin agents (DPP-4 inhibitors)
  • Insulin
41
Q

Biguanides and thiazolidinediones mechanisms of action

A

reduce glucose production in Liver

reduce insulin resistance in skeletal muscle and adipose tissue

42
Q

insulin secretagogue (sulphonylureas & Meglitinides)

A

increase insulin production in Pancreas

43
Q

Alpha-glucosidase inhibitor mechanism of action

A

slows the absorption of sucrose and starch in the small intestine

44
Q

sulfonylureas generic names, dose, and risk of hypoglycemia

A

GLYBURIDE - 2.5-5mg at breakfast, MAX 20mg (10mg BID)/day. signficant risk for hypoglycemia
GLICLAZIDE - 40-80mg daily, MAX 320mg (180mg BID). Minimul to moderate risk for hypoglycemia
GLICLAZIDE MR - start 30mg/day, MAX 120mg once daily. minimul/moderate risk for hypoglycemia
GLIMEPIRIDE - 1-2mg daily, MAX 8mg/day at breakfast, moderate risk for hypoglycemia

45
Q

Meglitidine generic names, dose, and risk of hypoglycemia

A

NATEGLINIDE - 120mg w/ each meal. max dose 540mg (180mg TID). minimal to moderate risk for hypoglycemia
REPAGLINIDE - start w/0.5mg at each meal if A1C 8%. Max dose 4mg per meal up to QID.
NOTE:: if meals are skipped these can be used because they can be skipped as well

46
Q

Biguanides generic names, dose, and risk of hypoglycemia and A/E.

A

METFORMIN - 250mg 1-2x/day MAX=2500mg/day. negligible risk for hypoglycemia
METFORMIN HCl - once daily 500mg. Max=2000mg

A/E: abdominal cramping

47
Q

Alpha-glucosidase inhibitors generic names, dose, and risk of hypoglycemia and A/E

A

ACARBOSE - start 25-50mg each meal. MAX = 300mg (100mg TID). negligible risk if used as monotherapy. MUST be taken with first bite of food

A/E - abdominal gas

48
Q

Thiazolidinediones (TZD) generic names, dose, and risk of hypoglycemia and A/E

A

PIOGLITAZONE - start w/ 15mg/daily. MAX=45mg once daily. negligible risk for hypoglycemia
ROSIGLITAZONE - start w/ 4mg/day. MAX = 8mg (4mgBID). negligible risk for hypoglycemia

A/E: weight gain, may induce edema and/or heart failure
not indicated for use with insulin

49
Q

DPP-4 inhibitors generic names, dose, and risk of hypoglycemia and A/E

A

SITAGLIPTIN - start w/ 100mg once daily. Negligible risk for hypoglycemia when used as monotherapy.

A/E: improves postprandial PG, weight neutral, occasionally associated with increased rates of minor infection

50
Q

what is insulin

A

a hormone produced by the pancreas to control the amount of glucose in the blood

51
Q

insulin use in type 1 and type 2 diabetes

A

Type 1 - drug of choice!
Type 2 - may be used in cases of marked hyperglycemia (A1C >9%). May also be used initially or after oral medications deemed ineffective

52
Q

effects of insulin on glucose uptake and metabolism

A

insulin binds to the receptor then

  1. starts many activation cascades
  2. influx of glucose
  3. glycogen synthesis
  4. glycolysis
  5. and fatty acid synthesis
53
Q

types of insulin

A

Prandial (bolus) insulins - rapid/short acting (CLEAR!!!)
Basal insulins - intermediate acting (CLOUDY!!!)
Basal insulins - Long acting (CLEAR!!!)
Pre-mixed insulins - regular and long acting (CLOUDY!!!)
“R” = Clear “N” = Cloudy

54
Q

Rapid acting (Prandial) insulin meds and onset/duration

A
Insulin Aspart (10-15min / 3-5hrs)
Insulin Lispro (10-15min / 3-5hrs)
Insulin Glulisine (10-15min / 3-5hrs)
Humulin R (30min / 6.5hrs)
Novolin ge Toronto (30min / 6.5hrs)
55
Q

Intermediate acting (Basal) insulins

A
Humulin N (1-3hr / up to 18hr)
Novolin NPH (1-3hr / up to 18hr)
56
Q

long acting (basal) insulins

A
Insulin Determir (1.5hr. / 16-24hr)
Insulin Glargine (1.5hr. / 16-24hr)
57
Q

premixed insulins (NPH - cloudy)

A

Humulin 30/70 (rapid-short acting % / intermediate acting %)

Novolin 30/70, 40/60, 50/50

58
Q

insulin storage guidlines

A

30 days at room temp once opened

90 days if refridgerated (once opened)

59
Q

insulin A/E

A

HYPOglycemia
weight gain
Lipohypertrophy at injection site (fat nodules)
allergic reactions (rare)

60
Q

insulin monitoring guidelines

A

Blood glucose
A1C
Hyperglycemia
Hypoglycemia (very important to discuss with diabetic Pt’s)

61
Q

treatment for hypoglycemia

A

mild to moderate: oral ingestion of 15g of carbs (juice, honey, sugar) wait 15 minutes - admin second 15g prn

severe hypoglycemia: 20g of carbs, wait 15 minutes -admin second 15g prn if <4.0mmol/L

severe (unconscious) hypoglycemia: glucagon 1mg SC or IM injection, call for emergency sevices.
If IV access: 10-25g glucose admin over 1-3 minutes

62
Q

symptoms of hypoglycemia

A

shaking, sweating, anxious, dizziness, fast heaertbeat, impaired vision, weakness/fatigue, headache