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Rotation 2: IM Outpatient > ENDO Portion > Flashcards

ENDO Portion Flashcards

1
Q

what is the most common cause of hyperthryoidism?

A

GRAVES DISEASE!!!

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2
Q

hyperthyroidism:

Graves disease

what is important to knwo about this?

who is it common in?

what causes this?

3 things it leads to?

A

MOST COMMON CAUSE OF HYPERTHYROIDISM

women more common 20-40 years old!!

autoimmune TSH-R AB-IgG antibodies aka TSI directed to TSH receptor over-activate gland leading to hypersecretion

leads to: hypertrophy, hyperplasia, commonly goiter!!

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3
Q

hyperthyroidism:

graves disease

13 sxs

2 3 key ones you need to remember

A
  1. hyperactivity, irritability, restlessness

2. heat intolerance, sweating

  1. palpatations
  2. increased appetite, weight loss
  3. tachycardia
  4. arrythmia
  5. fine tremor

8. goiter

  1. warm, oily hair
  2. proximal muscle weakness
  3. opthalmopathy

-proptosis/exopthamos

-lid lag

  1. dermopathy
    - pretibial myxedema
  2. hyperreflexes
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4
Q

hyperthyroidism:

Graves disease

OPTHALMOPATHY

3 things causes?

why?

A

unique to graves disease

  1. proptosis/exopthalmos “lid lag”
  2. conjunctival inflammation/edema
  3. corneal drying

******occurs because the lympocytes infiltrate the orbit, muscles, eyelids and may cause diplopria and compression of optic nerve*****

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5
Q

hyperthyroidism:

Graves Disease

DERMOPATHY

what is the name for this?

what does this cause?

apperance?

A

3% occurance

“pre-tibial myxedema”

*******noninflammatory induration and plaque formation of the pre-tibial area leading to thickened skin, and orange skin appereance*****

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10
Q

hyperthyroidism:

Graves disease

2 tests to check

what don’t you need to check?

A
  1. very low TSH

since the T3 and T4 high, negative causes this to be low

2. total and T4 elevated

**don’t need to check TSH-R AB for dx**

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11
Q

hyperthyroidism:

Graves disease

9 tx options?

what is the toc?

who do you use each in?

A
  1. endocrinology consult essential
  2. propanolol for sxs
  3. methimazole (thiourea) -MILD TO MOD 12-18 months!
    - inhibits thyroid peroxidases and block organification of iodine to decrease hormone production

-monitor WHB, pruirits, and FT4

  1. propylithiouricil (PTU) (thiourea) if pregnant
  2. saturated iodine solution- severe
  3. iodinated contrast agens- severe or thyroid storm
    - prevents conversion of T4 to T3
  4. glucocorticoids-severe
    - prevents conversion
  5. radioative iodine-DEFINITIVE TX and TREATMENT OF CHOICE IN THE US!!
    - destroys the overactive gland because concentrates here
    - uses I-131
  6. thyroidectomy

no longer TOC but used in children or pregnancy or those that can’ be controlled with medication

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12
Q

hyperthyroidism:

Graves disease

what do you need to keep in mind about the toc for this? what is it? what might worsen?

A

radioactive iodine

used to destroy the gland because it concentrates here

permanent hypothyroidism often develops within 1 year and may need replacement tx FOR LIFE!!!!

***opthalmopathy may worsen esp in smokers with this tx***

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13
Q

hypothyroidism:

Hashimoto’s thyroiditis

what is important to remember about this?

what type of disease?

how does it show up?

2 things ath cause this

what to keep in mind?

A

MOST COMMON CAUSE OF HYPOTHYROIDISM

AUTOIMMUNE, with insidious onset

thyroperoxidase and thyroglobulin antibodies present in high titers

*****keep in mind, this can itially cause a hyperthyroidism from release of stored hormone, but the end result is hypothyroisim*****

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14
Q

hypothyroidism:

Hashimoto’s thyroiditis

5 early sxs

8 late sxs

A

early:

  1. cold intolerance
  2. dry hair, hair loss
  3. headaches
  4. mennorhagia
  5. thin, brittle nails

late:

  1. slow speech

2. hoarse voice

3. weight gain

3. goiter

4. alopecia

4. facial and eyelip puffiness

5. bradycardia

6. edema non pitting

7. myxedema

8. pleural/pericardial effusion

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15
Q

hyperthyroidism:

Graves disease

in txing it with thiourea drugs what percent will have reccurance?

(propylithiouricil or methimazole)

A

50%

reccurence are common if tx is only with thiourea, propylthiouracil or methimazole

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16
Q

what are 4 complications that can come from graves disease?

A
  1. CV
  2. ocular
  3. psychological complications
  4. post tx hypothyroidism common, but easily txed
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17
Q

thyroid storm

what is this?

3 labs?

4 sxs?

3 tx options?

A

rare, but life-threatening of extreme hyperthyroidism, can be fatal and need to be admitted and txed STAT

elevated T3 and T4

decreased TSH

high fever

tachycardia

sweating

delierum

tx:

  1. satruated iodine solution
  2. iodinated contrast agents
  3. glucocorticoids
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18
Q

what are the 5 causes of hypothyroidism?

A
  1. hasimotos thyroiditis

2. congenital hypothyroidism

  1. idiopathic
  2. iatrogenic
  3. drug induced- amiodarone
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20
Q

hypothyroidism:

congenital

what testing?

why is it key to identify?

A

screening of TSH in newborns should elimate disease

early detection is key to prevent cretinism** and **hypodevelopment

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22
Q

hypothyroidism:

hashimotos thyroiditis

myxedema

what can this lead to?

5 sxs?

A

abnormal interstitial fluid acculuation in skin giveing it a waxy/coarsened (non-pitting) appearence

can lead to mydxedema crisis EMERGENCY:

severe form of hypothyroidism

  • bradycardia
  • CNS depression (coma)
  • respiratory depression
  • hypotension
  • hypothermia
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23
Q

hypothyroidism:

hashimotos thyroiditis

2 complications

4

1

A
  1. Cardiovascular
    - pericardial effusions
    - cardiomyopathy
    - accerlerated CHD
    - HF
  2. encephalopathy

coma/confusion

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24
Q

hypothyroidism:

Hashimotos thyroiditis

5 dx?

A
  1. High TSH
  2. low T3/T4
  3. increased triglycerides
  4. decreased HDL
  5. anti-thyroid antibodies
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25
Q

hypothyroidism:

hashimoto’s thyroiditis

what is the tx?

how is it dosed?

monitoring?

goal? time frame?

A

levothyroxine (synthetic T4)

a. start 50-100 ug/day and titrate to full dose over time, following TSH levels
b. recheck TSH levels every 2-3 months until normal

GOAL: clinically euthyroid state (normal)

**sxs improve slowly over months**

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26
Q

hypothyroidism:

iatrogenic (we caused it)

tx?

A

radioative iodine for initial hyperthyroidism that leads to gland destruction

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27
Q

thyroiditis:

suppurative

what is this caused by?

3 sxs?

1 dx?

1 tx?

A

caused by gram positive bacteria

STAPH AUREUS

1. tender thyroid

  1. fever
  2. pharyngitis

DX:

fine needle aspiration

Tx:

drainage

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28
Q

thyroiditis:

De quervains aka granulomatous

what is this?

when is it most common?

when does it occur?

explain the progression?

2 dx?

  1. tx?
A

MOST COMMON CAUSE OF PAINFUL THYROID GLAND

***peaks in the summer….weird****

MC POST VRAL INFECTION

thyrotoxicosis initially presents followed by hypothyroidism and euthyroid within 12 months

DX:

  1. markedly increase ESR
  2. very low anti-thyroid bodies

Tx:

TOC=aspirin!!!

bb

ionated constrast agent

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29
Q

thyroiditis:

drug induced amiodarone

what does the medication contain?

what percent get this?

3 progression steps?

A

contains 37% iodine by weight or 75 mg per tablet

causes thyroid dysregulation in 20% of patients

Progression:

  1. can cause rise in T4 during first month of tx
  2. causes cellular resitsance to T4
  3. hypothyroid picture ensues with elevated TSH
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30
Q

thyroiditis:

fibrous thryoiditis (riedel)

who is this in?

what hapens to the thyroid?

key description

what happens to RAI?

ab?

1 dx method

1 tx method?

A

rarest form of thyroiditis, 80% are in females

formation of dense fibous tissue in the thyroid

causes

hard “woody” asymmetric thyroid feeling

the fibrosis can spread outside of the thyroid

radioactive iodine is decreased in involved areas of the thyroid

antibodies may be present in 45%

DX:

BIOPSY

tx:

tomoxifan

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31
Q

hyperparathyroidism

what are 2 most common causes?

what is hypersecreted?

2 hallmark lab findings?

what are 5 things this can lead to?

A
  1. MC cause parathyroid adenoma
  2. parathyroid hyperplasia/enlargement

hypersecretion of PTH

HALLMARK:

1. elevated PTH

2. elevated serum total and ionized Ca

  1. increased excretion of Ca and PO4 by the kidney overwhlems the tubular Ca absorptive capacity leading to hypercalciURIA
  2. chronic bone reabsorption
  3. sever leads to

osteopenia

osteoporosis

pathologic fractures

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33
Q

hyperparathyroid:

how is this normally found?

pneumonic for sxs?

leads to what what 6 presentations?

A

often discovered as incidental lab finding

“moans, groans, stones, bones”

  1. skeletal: loss of cortical bone with bone pain and arthalgias
  2. nephrologic disorders:
    - decreased sensitivity to ADH with polyuria and poly dipsea
    - increased calcium stones from saturation
    - nephrosclerosis
    - renal failure
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34
Q

hyperparathyroidism:

5 lab findings

what is important to do?

A
  1. serum Ca over 10.5
  2. increased ionized calcium over 5.4
  3. PO4 low
  4. alk phos increase if presence of bone disease
  5. PTH assay via radioimmunoassay

**important to do a 24 hour urine to quantify***

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35
Q

hyperparathyroidism:

4 tx options

what are the indications for the last?

1

4

A
  1. normal saline to increase intravascular space
  2. furosemide facilitates Ca excretion

3 biphosphonate stop osteoclast bone resorption

  1. parathyroidectomy

symptomatic:

presence of bone or kidney disease

asymptomatic:

1. hypercalcemia with significant hypercalcuria

2. BD ovr 2 SD below normal

3. age less than 50

4. pregnancy

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36
Q

what is a complication from thyroidectomy used to tx hyperparathyroidism?

tx?

A

rapid drop of PTH levels and can lead to acute hypocalcemia post-op

RX: calcium supplements

until parathyroid resumes function

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37
Q

what are five complications of hyperparathyroidism?

A
  1. pathologic fractures, esp in women
  2. urinary stones, obstruction, UTIs
  3. if Ca rises rapidly-CNS changes, renal failure
  4. PUD and pancreatitis form high CA levels
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38
Q

hypoparathyroidism

what are the 3 causes?

MC?

hallmark

A
  1. MC_-post-thyroidectomy_ or removal of parathyroid adenoma

  1. rarely polyglandular autoimmune
  2. chronic magnesium deficiency which impairs PTH release

HALLMARK:

low ionized Ca

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39
Q

hypoparathyroidism

6 acute sxs

5 chronic sxs

A

acute:

muscle cramps

irritability

tetany

seizures

paresthesias of hands and feet

carpopedal spasm

chronic:

  1. personaity changes
  2. decrease cognitive function
  3. cataract
  4. dry brittle nails
  5. chevosteks sign-twitching of facial nerve with tapping
  6. trousseaus sign-blow up BP cuff around arm and hand will twitch
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40
Q

hypoparathyroidism tx:

1 acute

3 chronic

A

acute

IV CALCIUM GLUCONATE

do until tetant and other sxs resolve

chronic

1. oral calcium

2. active metabolite of vitamin D 1,25-dihyrdroxycholecalciferole AKA CALCITROL

3. magnesium supplement

**goal: maintain serum Ca in low normal range**

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41
Q

hypoparathyroidism

4 lab findings

A

1. low serum total and ionized Ca

  1. elevated PO4
  2. decreased PTH
  3. prolonged QT and arrythmias
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43
Q

PARATHYROID HORMONE

what is the overall effect?

2 ways it accomplishes this

A

INCREASES BLOOD CA LEVELS

1. STIMULATES RELEASE OF CA FROM BONE (RESORPTION)

2. STIMULATES VITAMIN D ACTIVATION BY KIDNEY TO INCREASE INTESTINAL CA ABSORPTION

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44
Q

calcitonin

what secretes this?

overall funciton?

3 ways it accomplishes this?

A

secreted by the thyroid c-cells

**decreases blood Ca levels**

1. inhibits intestinal Ca absorption

2. inhibits osteoclast and stimulates osteoblast activity

3. inhibits renal tubular reabsorption of Ca

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45
Q

osteoporosis

what is this?

what type of bone is lost more commonly?

percentages

A

MOST COMMON METABOLIC BONE DISEASE

comprimised bone strength leading to an increased risk for fracture

bone resorption occurs most commonly in the trabecular bone** **“spongy bone” than the corical bone

Net bone loss over 10 years:

trabecular 25-30% and MC!!

cortical 10-15%

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46
Q

bone density

describe the progression throughout life? 5

what do people suggest about the tx based on this progression?

A
  1. increases dramatically in puberty due to gonadal steroids
  2. peaks in early 20s
  3. bone loss beings before menses creases
  4. accelerated bone loss in the 1st 5-10 years post menopause
  5. slows after age 60

***this is why people think that you could theoretically prevent with estrogen, and might be helpful in subsets like hypogonadism or premature menopause** **but NOT as long term option due to adverse outcome risks****

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47
Q

what are 7 conditions that increase the risk someone will develop osteoporosis?

A
  1. sex hormone deficiency, esp post menopause

  1. excess glucocorticoids (cushings)
  2. hyperparathyroidism-increased PTH stimulates bone breakdown
  3. thyrotoxicosis-increased bone metbolism
  4. alcoholism
  5. anorexia
  6. vit d deficency
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48
Q

opsteopenia definition

A

BMD 1-2.5 SD below peak bone density

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49
Q

osteoporosis definition

A

BMD over 2.5 SD from normal

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50
Q

when classifying between osteopenia, osteoporosis, or just normal person, what do you NEED to keep in mind?

A

presence of fracture without S&S or trauma indicates severe osteoporosis regardless of what the SD is!!

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51
Q

do men get osteoporosis?

how many?

A

YEP!!

1 out of 5 dxed people are men

hip fracture is a significant predictor for mortality!!

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52
Q

what are 7 RF that increase your risk for osteoporosis?

A
  1. prior fractures
  2. FH of osteoporosis related fractures
  3. low body weight
  4. cigarette consumption
  5. excessive ETOH use
  6. chronic inflammation: RA
  7. patients at high risk for falls or frailty
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53
Q

osteoporosis

what are 4 sxs you may see with this?

what is usually the inital presentation?

A

1. many asymptomatic till fracture (often spontaneous)

  1. ******may see back pain, decrease in height, or kyphosis***
  2. dietary calcium, vit D deficiency
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55
Q

osteoporosis

4 texts for dx

1 TOC? interpretation

A
  1. DEXA is TOC!!!

includes spine, femur

T-score: SD away from young healthy adults

over 2.5=osteoporosis

over 2: osteopenia

  1. check calcium levers
  2. check vitamin D levels (25-hydroxy vit D)
  3. consider checking putuiary hormones when indicated
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56
Q

who do you screen for osteoporosis in?

A
  1. early menopause

  1. RF

FH

malnourished

alcoholism

renal failure

  1. 65+
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57
Q

can you reverse established osteoporosis?

A

no

can increase BD, decrease fractures, and hald or slow progression

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58
Q

osteoporosis

what are the 5 drug classes used to tx this? First DOC? how is it taken? key things to know?

A

1. bisphosphonates-DOC

ALENDRONATE: take 30 mins before AM meal with 8ox water and remain upright 30 minutes after

-increased risk of unusual fracture so not longer than 5 years

inhibits osteoclasts

dental care important-jaw issues

very long half-life, in bone 10 years

  1. SERMS

serum estrogen receptor agonist/antagonist

alternative to estrogen in postmenopausal woman with decreased risk of adverse effects since no BC risk

  1. calcitonin
  2. Vitamin D; calcium

always supp vit D, Ca only if it is low!

  1. PTH synthetic analog

***normally PTH stimulates osteoclasts BUT when given in synthetic form it increases osteoblast activity and new bone formation=paradox**

INCREASES BONE DENSITY MORE THAN ANY OTHER DRUG BUT IS NEW AND CAN LEAD TO BONE CANCERS SO NOT USED AS MUCH NOW

6.estrogen replacement

only used in patients with premature menopause or hypogonadism**…dose related issues and increased risk for BC, DVT, endometrial cancer etc and **short term use only

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59
Q

what are the percent prevalence of T1DM and T2DM?

A

T1DM=10%

T2DM=90%

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60
Q

what are 5 brief features you find in Type 1 diabetes?

A

insulin deficiency

hyperglycemia

dyslipidemia

metabolic wasting

ketoacidosis

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61
Q

what are 4 brief features of T2DM?

A

hypoinsulinemia

hyperglycemia

dyslipidemia

obestiy often

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62
Q

what is the clinical importance of the insulin structure?

A

contrains C peptide

this is present only on endogenous insulin so measuring this will tell you how much insulin the Beta cells are actually producing and how much of their function is lef

WE MEASURE THIS TO TELL US HOW WELL THE BETA CELLS ARE WORKING

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63
Q

what are 5 overall broad functions of insulin secretion?

A
  1. decrease blood glucose
  2. decrease blood fatty acid
  3. decrease blood amino acid
  4. increase protein syntheisi
  5. increase fuel storage
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64
Q

LIVER

1 anabolic

3 anti-catabolic

A

anabolic:

Stimulation of glycogen synthesis

catabolic

iinhibition of:

glycogenolysis

gluconeogensis

ketogenesisi

65
Q

glycogenolysis

A

breakdown of glycogen to glucose

(occurs at liver, and less commonly muscles)

66
Q

gluconeogensis

**WHAT TO KEEP IN MIND…WHAT DOES THIS OCCUR WITH?***

A

generation of glucose from glycogen (most commonly from the liver)

****KEEP IN MIND THAT GLYCOGENOLYSIS AND GLUCONEOGENESIS BOTH OCCUR AT THE SAME TIME BECAUSE THE FIRST MUST OCCUR TO ALLOW THE SECOND!!!***

67
Q

ADIPOSE TISSUE

3 anabolic

1 anit- catabolic

A

anabolic

increase glucose uptake

increase triglyceride synthesis

increase fatty acid uptake and synthesis

catabolic

inhibition of lipolysis

68
Q

muscle tissue

4 anabolic

2 anticatabolic

A

anabolic

1. increase glucose uptake

2. increase glycogen storage

3. increase protein synthesis

4. increase amino acid uptake

anticatbolic

1. inhibition of proteolysis

2. decrease amino acid output (wants to build)

69
Q

what cells secrete glucagon?

A

alpha cells of the pancreas when blood glucose was low

70
Q

if there is a decrease in blood sugar…what is released and ffrom where? what does it cause

A

glucagon is released from the alpha cells of the pancrease which causes liver glycolysis and gluconeogenisis

**negative feedback once BS increase**

71
Q

glucagon

A

causes relase of stored glycogen (glucose stored) into the blood

72
Q

who do you typically find diabetic ketoacidosis in?

A

TYPE 1

(can be in late stage 2)

73
Q

who do you typically find acute hypoglycemia in?

A

type 1 post insulin without eating

74
Q

if you find a diabetic in a stoke like coma or passed out…what can you almost always believe it is?

A

HYPOglycemia!!

75
Q

metabolic syndrome

5 risk factors

A
  1. abdominal obesity
  2. triglycerides
  3. HDL
  4. fasting glucose
  5. HTN

***must have 3 of the five qualifications***

76
Q

Metabolic Syndrome

what is this called?

what does it indicated for the patient?

what type of diabetes?

A

aka insulin resistance; syndrome X

classified as a constellation of sxs findings that significantly increase risk of athlerosclerosis

associated with T2DM

79
Q

metabolic syndrome:

waist circumference RF

A

men over 102

women over 88

80
Q

metabolic syndrome:

triglycerides RF

A

over 150

81
Q

metabolic syndrome:

HDL RF

A

men less than 40

women less than 50

82
Q

metabolic syndrome:

BP RF

A

over 130 SBP

over 85 DBP

83
Q

metabolic syndrome:

fasting glucose RF

A

over 100

84
Q

T2DM:

Visceral Fat

what does it do? (hence why bad)

4 steps that make this bad!

A

bad because it secretes adipokines/cytokines

theses increase insulin resistance

insulin resistance can also increase DYSLIPDEMIAS

dyslipidemias lead to

MI, STROKE, HYPERTENSION

86
Q

sulfonylureas

what are they ment to work like?

what do they do?

what are 3 things they cause as SE?

A

minic the function of insulin by closing the K channels so that insulin is secreted

since made to act like insulin can cause:

hypoglycemia

hyperinsulinemia

increased body weight

87
Q

what is the goal preprandial glucose?

post prandial?

A

pre: 80-130
post: less than 180

89
Q

insulin secretagogues

sulfonylureas

what part do they work on?

what type of diabetic do you use this in

what are the two drugs name

what are the 3 side effects that you might see with this!

A

THIS IS THE SECOND DRUG OF CHOISE AFTER METFORMIN

work on the K pump as well but are less likely to cause hypoglycemia but are very expensive

T2DM, in adjunct to metformin

glypizide, glyburide

****caution can cause hypoglycemia, hyperinsulinemia, and weight gain***

90
Q

biguandines-Metformin

what to keep in mind?

4 things that it does in the body?

MC SE?

who do ou not use this in? 3 senarios? why?

what is a senariou you don’t want to give this medication?

A

first drug you give for T2DM

1. decreases hepatic glucose production

  1. increases insulin sensitivity and promotes uptake by skeletal muscle (what is left will work better)
  2. improves lipid profile
  3. decrease carbohydrate absorption in the gut

MC common SE is GI distrubances so start low go slow to get to max dose of 2000-2500

_*****contraindicated for patients with renal insufficiency, liver failure, and major surgery because of increased risk of lactic acidosis***_

(so hold on same day as contrast and 48 hours after so if kidneys shut down don’t get poisioned)

91
Q

GLP-1 receptor agonist

what is this?

how is it given?

what is unique that this is thought to do?

4 things it stimualtes

3 things it decreases

A

exanatide, liraglutide

since thought that GLP-1 can cause Beta cell proliferation it is though that this medication could help to regain beta cell function when the beta cells start to burn out

**alternative to insulin w/o weight gain** SC admin

stimulates:

  1. insulin secretion
  2. insulin production
  3. increase beta cell production
  4. muscle uptake and and storage

decreases:

  1. decreased gastric empyting
  2. decrease appetite
  3. decrease glucagon release
92
Q

thaiazolidinediones

what do they do?

1 drug we use?

2 problems with them?

avoid in? 1

**remember**

A

improves insulin sensitivity and signaling

plioglitazone

problems:

weight gain (don’t wanna give to type 2 patients)

heart failure from edema around the the hear***favoritism going out because of this!!!

AVOID: liver dysfunction, so need to get a LFT before intitiating

***try staying away from these drugs because of the side effects but if you have to go with one of them go with pioglitazone***

93
Q

SGLT2 inhibitors

what do they do?

what is the drug name?

because of this what are you at increased risk for?

why is one benefit to this drug and who can this help?

WHAT IS THERE A WARNING ABOUT?

A

NEWEST CLASS

canaglifozin

blocks reabsorption of glucose in the proximal tubule and causes it to be excreted in the urine

BENEFIT: can cause weightloss of 5-10 pounds since diuresis, lowers bp (good for T2DM!)

UTIS since increasing sugar excretion

*****FDA WARNING ABOUT KETOACIDOSIS since more sugar secreted in the urine****

94
Q

pramlinitide

what is this?

when is it normally secreted?

3 functions?

what does it improve?

which diabetes do you use it in?

A

synthetic analogue of amylin

amylin is normally co-secrete with insulin and

  • suppresses glucagon secretion
  • slows gastric emptying
  • improves glycemic control

**modulates post prandial glucose**

type 1 and type 2

96
Q

stages of resistance for Type 2 diabetes

4 stages

A
  1. obesity leads to insulin resistance
    - euglycemia/hyperinsulinemia

body pumps out a lot of insulin to overcome the resistance and initially it is able to keep the BS within normal range

  1. impaired glucose tolerance

hyperglycemia/hyperinsulinemia

eventually resistance increase to a point where B cells work overtime to pump out more insulin through Beta cell hyperplasia to try to get sugar down but the resitance grows so despite elevated insulin, the surgar stays high

  1. early diabetes-B cell burn out

hyperglycemia/hypoinsulemia

B cells start to burn out so the insulin production decreases but the sugar is still high EARLY DIABETES CAN’T MEET DEMANDS

4. late diabetes

hyperglycemia/hypoinsulemia

BETA CELLS BURN OUT!!

97
Q

DDP-4 inhibitors

name of the drug?

what does ths drug do?

why is complance better?

how is this drug used?

A

sitagliptin

breaks down the DDP-4 enzyme that breaks down GLP-1 increasing increatin hormones

(stimulates insulin, inhibits glucagon)

overall, this drug decreases blood sugar

**oral so better compliance…but used as an adjunt

99
Q

what is more efffective than any oral antidiabetic drug?

A

exercise!!!

100
Q

what are the ABCDEs of diabetes?

A

A=aspirin reduce platelets

B=bloood pressure ACE

C=cholesterol

D=diet, diabetes control

E=exercise, improves glucose and lipids

102
Q

what is insulin resistance?

A

unknown mechanism

suspected etiology:

feuled by proinflammatory respons from cytokines and adipokines

103
Q

what are 3 microvascular long term complications of diabetes?

1 macrovacular long term complication of diabetes?

A

microvascular:

  1. retinopathy
  2. nephropathy
  3. neuropathy

macrovascular:

  1. athlerosclerosis

(CHD, CVD/stroke, PAD)

105
Q

diabetes complications:

retinopathy

what are the 2 types?

what is each characterized by?

what is key to prevent this?

A

Non-proliferative:

microaneurysms, hemorrhases, exudates, retinal edema

Proliferative:

formation of new blood vessels** **leading to BLINDNESS

*********TIGHT GLYCEMIC CONTROL ESSENTIAL TO PREVENTION OF RETINOPATHY*****

worse with HTN and smoking

106
Q

how often do diabetics need eye exams?

A

annually

107
Q

diabetic complications:

nephropathy

what are 2 things that cause this?

who is this worse in?

what is important to know as a fact abou prevalance in the US?

3 tx options?

A

developes from chronic hyperglycemia and uncontrolled HTN

***to prevent…control both of these***

worse in smokers!!

leading cause of ESRD in the US!!!!! diabetic nephropathy

RX:

1. tight glycemic control

2. tight BP controll less than 140/90

3. early institution of ACEI

108
Q

how do you check for nephropathy in diabetic?

3 ranges

A

want to check MICROALBUMINURIA 30-300

BUT A DIPSTICK ISN’T SENSITIVE ENOUGH SO NEED TO ORDER A RADIOIMMUNOASSAY SPOT AM URINE

normal less than 30

microalbiumemia: 30-300

albumenmia: over 300

109
Q

what are two ways to tx diabetic nephropathy once they have reached ESRD?

A
  1. dialysis
  2. transplantation from living related donor is preferable to dialysis
110
Q

ACE initiation in diabetics

who do you start in and when?

what are 4 things it prevents the progression of?

A

start in Type 1 and Type 2 with the presence of microalbuminuria

EVEN IF THE BP IS NORMAL!!!!!

decreases risk for

glomerulrar hemodynamics

death

dialysis

transplantation

GOAL: less than 140/90, often requires multipe agents

111
Q

diabetic complications: athlerosclerosis

what are 5 things this can lead to?

what is diabetes a equivalent to?

what should you consider putting them on?

A

CHD

MI

CHF

PVD

Suddent death

diabetes is a coronary risk equivalent

***put patient on ASA if they these RF***

112
Q

diabetes is a…

A

CVD risk factor equvalent!!

113
Q

Periphreal vascular disease in diabetics

what vessels effected?

lleads to 4 things?

4 tx options?

A

Large and small vessel disease

leads to:

claudications

ulcerations

amputations

RX:

regular foot exams

tight glycemic contro.

podiatric care

STOP SMOKING

114
Q

diabetic complications:

neuropathy

3 presentations?

3 tx options for medication?

A
  1. distal symmetric polyneuropathy-decrease sensation in “stocking glove” distribution
  2. motor involvement late
  3. PAIN COMMON

TX

  1. gabapentin (neurontin)
  2. duloxetine (cymbalta)
  3. pregabalin (lyrica)
115
Q

diabetes complications:

autonomic neuropathy

5 presentations

A
  1. gastroparesis

slow gastric emptying incuding early saiety, nausea, and vomitying 1-3 hours after meal

tx: metoclopropramide

  1. diarreah/constapation
  2. orthostatic hypotension

fludrocortisone and elastic stockings

  1. impotence, sexual dysfunction
  2. decreased bladded sensation
116
Q

diabetic ketoacidosis

5 general sxs?

once havd it for a while….6 sxs? 1 buxx word!!

A

polyuria

abominal pain

nausea

vomiting

fatigue

PROGRESSIVE DKA:

  1. decrease mentation

2. stupor

3. coma

  1. tachycardia
  2. RAPID BREATH WITH FRUITY BREAHT (accumulation of ketones)
  3. kussmauls respiration

form of hyperventilation to blow off the CO2

117
Q

diabetic ketoacidosis

what is this?

who does it occur in?

why?

4 potenital causes?

2 critical things it can lead to?

A

lifethreatenig emergency

TYPICALLY TYPE 1 DM

need for insulin increases from trigger

triggers:

  1. infection
  2. trauma
  3. sugery
  4. MI

can progress to coma and death

119
Q

diabetic ketoacidosis pathophysiology

4 steps

results in?

A
  1. inadequate insulin resulting in increased BS** that promps **increase in abnormal fat breakdown
  2. increase in BS also increases catechols, cortisol, glucagon, and GH** resulting in **gluconeogenisis and glycogenolysis
  3. fat breakdown or lipolysis** produces **free fatty acids and conversion of acetoacetic (ketoacid) and B=hydroxybutyric acid leading to ACIDOSIS
  4. increases ketogenesis in the liver also contributes to ketoacidosis

results in metabolic acidosis with increase anion gap

120
Q

diabetic ketoacidosis:

what 2 products does the fat breakdown or lipolysis create for products?

A

production of FFA and conversion to

1. acetoacetic (ketoacid)

and

2. B-hydroxybutyric acid

121
Q

diabetic ketoacidosis:

2 things it leads to because of glycosuria from glucse wasting from hyperglycemia?

A
  1. osmotic diuresis
  2. volume and electrolyte loss/imbalance
122
Q

diabetic ketoacidosis:

7 lab findings

A
  1. pH less that 7.3

  1. low HCO3 with increased anion gap
  2. increased urine osmolarity
  3. BS usually over 300
  4. elevated amylase
  5. elevated WBC over 10,000 without infxns
  6. initial serum K often high but total body ky low from fluid and electrolyte losses
123
Q

diabetic ketoacidosis tx:

4 tx options

A
  1. estalish flowsheet ot measure all levels

  1. insulin regular

3. replace lost fluids with 0.9% NaCL***give 3-4 L over 8 hours***

4. replace K by KCL IB

124
Q

hyperglycemic nonketotic hyperosmolar state

which diabetics is this in?

what is the patho of this?

what is the sugars like? what isn’t present?

A

type 2 DM

adequate circulate insulin to breakdown fat but not enough to control hyperglycemia **aka there is some insulin so the body doesn’t think it is starving itself**

progressive development of very high BS 600-2400 in absence of ketoacidosis

125
Q

hyperglycemic hyperosmolar nonketoic acidosis:

what happens here that complicates thsi?

2 tx options?

A

the profound ostmotic diuresis causes severe dehydration (10-11L) is complicated by the ensuring pre-renal azotemia

TX:

  1. 0.9% normal saline
  2. insulin
126
Q

what is the mortality seen with hyperglycemic hyperosmolar nonketotic acidosis?

A

50% mortality

127
Q

explain why diabetic ketoacidosis is INCREASED ANION GAP ACIDOSIS?

A

the anion gap equation is

Na-(Cl+HCO3)

in diabetic ketoacidosis, the HCO3 decreases to buffer the acid produced by the muscle breakdown to make the intermediate, since this is decreases according toe the equation the total amount is increase

Henced increases metabolic acidosis

128
Q

what is the differences between DKA and HHNK?

A

DKA=TYPE 1, presensce of ketones

HHNK= TYPE 2, way higher BS

129
Q

type 1 DM

patho

what promps this start of this?

5 triggers

A

infectious or toxic insult

in genetically predisposed people causing autoimmune response against altered pancreatic B cell antigens

triggers:

viruses

mumps

coxsackie

rubella

toxic chemicals

130
Q

Type 1 DM

what is your typical patient? 2

what is the primary cause of this? (what happens)

what type of disorder is this? lead s to 2 things?

A

typical patient:

non-obese and insulin dependent

primarily autoimmune

mediated with presence of islet cell antibodies that lead to destruction of the B cells in pancrease

catabolic disorder where absence of insulin leads to:

1. hypergylcemia

2. fat and protein breakdown lead to

KETOACIDOSIS

131
Q

type 1 DM treatment

what is the medication you tx with?

combination and percent of diffreent insulins? 2

A

tx: INSULIN only!!

SMBG 4-6x daily

combination of:

basal insulin= 40-50% intermediate/long acting

(NpH, glargine, detemir)

prandial needs=40-50%

short term or rapid (regular or INSULIN LISPRO)

**alernative is insulin pump**

132
Q

what do you use as insulin to tx Type 1 DM?

A

combination of basal (Long acting) and prandial (shorter acting) insulin

covers them throughout the day and also when they have their specific meals

133
Q

what is the total insulin need for someone with T1DM?

A

0.4-1 Units/kg

134
Q

what is the most common seen complication with insulin or sulfonylurea use?

A

hypoglycemia

135
Q

hypoglycemia

what are two drugs that are known for doing this?

5 sxs?

what sugar correlates with this?

A

most common complication seen with insulin or sulfonylurea

SXS:

1. sweating

2. tachycardia

3. hunger

4. tremulousness

5. nausea

less than 50 BS

136
Q

what drug can mask hypoglycemia because it produces similar sxs

A

non selective beta blockers

137
Q

Type 2 DM

characteristics of patient? 4

what is the goal? how to accomplish? 2

2 first line tx options?

A

typical patient:

non-insulin dependent

obese

increase triglycerides

insulin resistance

MOST IMPORTANT TO REGAIN INSULIN SENSITIVITY

1. WEIGHT REDUCTION

2. DIET AND EXERCISE

TX:

  1. LIFESTYLE THEN
  2. METFORMIN
138
Q

explain the role of central/visceral obesity in T2DM?

A

increased central visceral fat causes increased waist/hip fat of the omentum and this contributes to insulin resitsance** which **snowballs and makes the central obesity worse

139
Q

glucotoxicity

what does this come from?

what mechanism does it cause to be faulty? what does this lead to?

A

comes from chronic hyperglycemia that inhibits the increase in insulin secretion normally seen in response to hyperglycemia

worsens insulin resistance and destroys the B cell function

**THE MECHANISM GETS RUINED WITH CHRONIC INCREASED GLYCEMIA**

140
Q

how does diet and exercise improve insulin resistance?

A

exercise increases blood flow to the muscles

increases muscle mass and decreases muscle fat storage

***this improves glucose resistance because of the decreased fats that release the cytokines and adipokines***

141
Q

Type 2 DM

7 sxs associated with this?

A
  1. often no sxs early
  2. polyuria
  3. thirst
  4. skin infections
  5. vulvovaginits
  6. abnormal fat distribution
  7. hyperglycemia
143
Q

glycated HB (A1c)

what does this show you?

how often should you check in diabetic?

what are the values for normal, prediabetic, and diabetes?

what is the goal for diabetic?

A

describes the state of glycemia over prior 8-12 weeks, recheck every 3-4 months

normal= 4-6%

prediabetes= 5.7-6.4%

diabetes=over 6.4%

****goal in diabetic for A1c is less than 7%*****

144
Q

what are the values for A1c?

normal

prediabetes

diabetes

A

normal= 4-6%

prediabetes= 5.7-6.4%

diabetes=over 6.4%

145
Q

what are the four qualifications/options for diabetes dx?

A
  1. FBS over 126 (normal under 100)

  1. A1C over 6.5%
  2. 2 hr GTT over 200
  3. Random BS over 200 (need fasting to confirm but highly likely)
146
Q

what are the 3 qualifications/options for imparied glucose tolerance aka pre diabetes?

A
  1. FBS 100-125

  1. 2 hr GTT BS of 140-199
  2. A1c 5.7-6.4%
147
Q

what is the 3 tx algorithm used fot T2DM?

A

Step 1 tre​at at dx: lifestyle and metformin

step 2:

metformin + basal insulin (long)******(this is the better option according to handler lecture)

ORRRR

metformin + sulfonylure

step 3: metformin + intensive insulin (basal + prandial)

148
Q

what are the goal levels for:

preprandial

postprandial

bedtime

a1c

A

preprandial=90-130

postprandial=less than 180

bedtime=100-140

a1c=less than 7

149
Q

rapid acting insulin

what is the name?

onset?

peak?

what is it ideal for?

how can it be used?

A

Lispro

onset: 5-15 mins, peak 1-2 hours

ideal for pre-meal and rapidly deals with glucose load

**can be used with insulin pump**

150
Q

regular insulin

how long does it take?

onset?

peak?

how is it delivered? unique fact?

A

short acting

onset: 30-60 mins
duration: 6-8

SC/IM/IV

only IV so used to tx diabetic ketoacidosis

151
Q

neutral protamine

how long does this last?

onset?

duration?

A

intermediate acting

onset: 1-3 hours
duration: 14-18 hours

152
Q

insulin glargine

how long does this last?

how long is the coverage?

when is it dosed?

why is this good?

what can’ you do?

A

long acting insulin

24 hour coverage with steady state insulin levels

dosed at bedtime

**causes less hypo/hyperglycemia**

**can’t mix with other insulins**

153
Q

insulin pumps

what insulin can you use it with?

how does it work?

1 benefit?

3 drawbacks?

A

can be used with lispro or regular

continuous SQ insulin infusion, maintains basal insulin infusion and times bolus delivery before meals

Benefits: tight glycemia control

drawbacks: cost, skin infections, and DKA

154
Q

things you should be checking every 3-6 months and annuually for diabetics?

A

Rotation 2: IM Outpatient (12 decks)

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