ENDO Portion Flashcards
(135 cards)
1
Q
what is the most common cause of hyperthryoidism?
A
GRAVES DISEASE!!!
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!!
3
Q
hyperthyroidism:
graves disease
13 sxs
2 3 key ones you need to remember
A
- hyperactivity, irritability, restlessness
2. heat intolerance, sweating
- palpatations
- increased appetite, weight loss
- tachycardia
- arrythmia
- fine tremor
8. goiter
- warm, oily hair
- proximal muscle weakness
- opthalmopathy
-proptosis/exopthamos
-lid lag
-
dermopathy
- pretibial myxedema - hyperreflexes
4
Q
hyperthyroidism:
Graves disease
OPTHALMOPATHY
3 things causes?
why?
A
unique to graves disease
- proptosis/exopthalmos “lid lag”
- conjunctival inflammation/edema
- corneal drying
******occurs because the lympocytes infiltrate the orbit, muscles, eyelids and may cause diplopria and compression of optic nerve*****
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*****
10
Q
hyperthyroidism:
Graves disease
2 tests to check
what don’t you need to check?
A
- 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**
11
Q
hyperthyroidism:
Graves disease
9 tx options?
what is the toc?
who do you use each in?
A
- endocrinology consult essential
- propanolol for sxs
-
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
- propylithiouricil (PTU) (thiourea) if pregnant
- saturated iodine solution- severe
- iodinated contrast agens- severe or thyroid storm
- prevents conversion of T4 to T3 - glucocorticoids-severe
- prevents conversion -
radioative iodine-DEFINITIVE TX and TREATMENT OF CHOICE IN THE US!!
- destroys the overactive gland because concentrates here
- uses I-131 - thyroidectomy
no longer TOC but used in children or pregnancy or those that can’ be controlled with medication
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***
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*****
14
Q
hypothyroidism:
Hashimoto’s thyroiditis
5 early sxs
8 late sxs
A
early:
- cold intolerance
- dry hair, hair loss
- headaches
- mennorhagia
- thin, brittle nails
late:
- 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
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
16
Q
what are 4 complications that can come from graves disease?
A
- CV
- ocular
- psychological complications
- post tx hypothyroidism common, but easily txed
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:
- satruated iodine solution
- iodinated contrast agents
- glucocorticoids
18
Q
what are the 5 causes of hypothyroidism?
A
- hasimotos thyroiditis
2. congenital hypothyroidism
- idiopathic
- iatrogenic
- drug induced- amiodarone
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
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
23
Q
hypothyroidism:
hashimotos thyroiditis
2 complications
4
1
A
-
Cardiovascular
- pericardial effusions
- cardiomyopathy
- accerlerated CHD
- HF - encephalopathy
coma/confusion
24
Q
hypothyroidism:
Hashimotos thyroiditis
5 dx?
A
- High TSH
- low T3/T4
- increased triglycerides
- decreased HDL
- anti-thyroid antibodies
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**
26
Q
hypothyroidism:
iatrogenic (we caused it)
tx?
A
radioative iodine for initial hyperthyroidism that leads to gland destruction
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
- fever
- pharyngitis
DX:
fine needle aspiration
Tx:
drainage
28
Q
thyroiditis:
De quervains aka granulomatous
what is this?
when is it most common?
when does it occur?
explain the progression?
2 dx?
- 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:
- markedly increase ESR
- very low anti-thyroid bodies
Tx:
TOC=aspirin!!!
bb
ionated constrast agent
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:
- can cause rise in T4 during first month of tx
- causes cellular resitsance to T4
- hypothyroid picture ensues with elevated TSH
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
31
hyperparathyroidism
## Footnote
what are 2 most common causes?
what is hypersecreted?
2 hallmark lab findings?
what are 5 things this can lead to?
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_
33
hyperparathyroid:
## Footnote
how is this normally found?
_pneumonic for sxs_?
leads to what what _6 presentations_?
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_**
34
hyperparathyroidism:
## Footnote
5 lab findings
what is important to do?
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_**\*\*\*
35
hyperparathyroidism:
## Footnote
4 tx options
what are the indications for the last?
1
4
1. **_normal saline_** to increase intravascular space
2. **_furosemide_** facilitates Ca excretion
3 **_biphosphonate_** stop osteoclast bone resorption
4. **_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**
36
what is a complication from thyroidectomy used to tx hyperparathyroidism?
tx?
rapid drop of PTH levels and can lead to **_acute hypocalcemia post-op_**
RX: **_calcium supplements_**
until parathyroid resumes function
37
what are five complications of hyperparathyroidism?
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
38
hypoparathyroidism
## Footnote
what are the 3 causes?
MC?
hallmark
1. MC_-post-thyroidectomy_ or removal of parathyroid adenoma
## Footnote
2. rarely **_polyglandular autoimmune_**
3. _chronic magnesium deficiency_ which impairs PTH release
**_HALLMARK:_**
low ionized Ca
39
hypoparathyroidism
## Footnote
6 acute sxs
5 chronic sxs
_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
4. chevosteks sign-twitching of facial nerve with tapping
5. trousseaus sign-blow up BP cuff around arm and hand will twitch
40
hypoparathyroidism tx:
1 acute
3 chronic
acute
## Footnote
**_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\*\*
41
hypoparathyroidism
## Footnote
4 lab findings
_1. low serum total and ionized Ca_
2. elevated PO4
3. decreased PTH
4. _prolonged QT and arrythmias_
43
PARATHYROID HORMONE
## Footnote
what is the overall effect?
2 ways it accomplishes this
INCREASES BLOOD CA LEVELS
## Footnote
**_1. STIMULATES RELEASE OF CA FROM BONE (RESORPTION)_**
**_2. STIMULATES VITAMIN D ACTIVATION BY KIDNEY TO INCREASE INTESTINAL CA ABSORPTION_**
44
calcitonin
what secretes this?
overall funciton?
3 ways it accomplishes this?
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_**
45
osteoporosis
## Footnote
what is this?
what type of bone is lost more commonly?
percentages
**_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%_
46
bone density
## Footnote
describe the progression throughout life? 5
what do people suggest about the tx based on this progression?
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*_**\*\*\*\*
47
what are 7 conditions that increase the risk someone will develop osteoporosis?
1. **_sex hormone deficiency, esp post menopause_**
## Footnote
2. excess glucocorticoids (cushings)
3. hyperparathyroidism-increased PTH stimulates bone breakdown
4. thyrotoxicosis-increased bone metbolism
5. alcoholism
6. anorexia
7. vit d deficency
48
opsteopenia definition
BMD **_1-2.5 SD_** below peak bone density
49
osteoporosis definition
BMD **_over 2.5 SD_** from normal
50
when classifying between osteopenia, osteoporosis, or just normal person, what do you NEED to keep in mind?
presence of fracture without S&S or trauma indicates severe osteoporosis regardless of what the SD is!!
51
do men get osteoporosis?
how many?
YEP!!
1 out of 5 dxed people are men
hip fracture is a significant predictor for mortality!!
52
what are 7 RF that increase your risk for osteoporosis?
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
53
osteoporosis
## Footnote
what are 4 sxs you may see with this?
what is usually the inital presentation?
**_1. many asymptomatic till fracture (often spontaneous)_**
2. \*\*\*\*\*\*may see back pain, decrease in height, or kyphosis\*\*\*
3. dietary calcium, vit D deficiency
55
osteoporosis
## Footnote
4 texts for dx
1 TOC? interpretation
1. _DEXA is TOC!_!!
## Footnote
includes spine, femur
**_T-score:_** SD away from young healthy adults
**_over 2.5_**=osteoporosis
**_over 2:_** osteopenia
2. check calcium levers
3. check vitamin D levels (25-hydroxy vit D)
4. consider checking putuiary hormones when indicated
56
who do you screen for osteoporosis in?
1. early menopause
## Footnote
2. RF
FH
malnourished
alcoholism
renal failure
3. 65+
57
can you reverse established osteoporosis?
no
can increase BD, decrease fractures, and hald or slow progression
58
osteoporosis
## Footnote
what are the 5 drug classes used to tx this? First DOC? how is it taken? key things to know?
**_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_**
2. SERMS
serum estrogen receptor agonist/antagonist
_alternative to estrogen in postmenopausal woman with decreased risk of adverse effects since no BC risk_
3. calcitonin
4. Vitamin D; calcium
**_always supp vit D, Ca only if it is low!_**
5. 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_**
59
what are the percent prevalence of T1DM and T2DM?
T1DM=10%
## Footnote
T2DM=90%
60
what are 5 brief features you find in Type 1 diabetes?
**_insulin deficiency_**
hyperglycemia
dyslipidemia
**_metabolic wasting_**
**_ketoacidosis_**
61
what are 4 brief features of T2DM?
**_hypoinsulinemia_**
hyperglycemia
dyslipidemia
**_obestiy often_**
62
what is the clinical importance of the insulin structure?
contrains C peptide
## Footnote
**_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_**
63
what are 5 overall broad functions of insulin secretion?
1. decrease blood glucose
2. decrease blood fatty acid
3. decrease blood amino acid
4. increase protein syntheisi
5. increase fuel storage
64
**_LIVER_**
1 anabolic
3 anti-catabolic
anabolic:
**_Stimulation of glycogen synthesis_**
catabolic
i**_inhibition of:_**
**_glycogenolysis_**
**_gluconeogensis_**
**_ketogenesisi_**
65
glycogenolysis
breakdown of glycogen to glucose
(occurs at liver, and less commonly muscles)
66
gluconeogensis
\*\*WHAT TO KEEP IN MIND...WHAT DOES THIS OCCUR WITH?\*\*\*
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
**_ADIPOSE TISSUE_**
## Footnote
3 anabolic
1 anit- catabolic
anabolic
## Footnote
**_increase glucose uptake_**
**_increase triglyceride synthesis_**
**_increase fatty acid uptake and synthesis_**
catabolic
**_inhibition of lipolysis_**
68
**_muscle tissue_**
4 anabolic
2 anticatabolic
anabolic
## Footnote
**_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
what cells secrete glucagon?
alpha cells of the pancreas when blood glucose was low
70
if there is a decrease in blood sugar...what is released and ffrom where? what does it cause
glucagon is released from the alpha cells of the pancrease which causes liver glycolysis and gluconeogenisis
## Footnote
\*\*negative feedback once BS increase\*\*
71
glucagon
causes relase of stored glycogen (glucose stored) into the blood
72
who do you typically find diabetic ketoacidosis in?
TYPE 1
(can be in late stage 2)
73
who do you typically find acute hypoglycemia in?
type 1 post insulin without eating
74
if you find a diabetic in a stoke like coma or passed out...what can you almost always believe it is?
HYPOglycemia!!
75
metabolic syndrome
## Footnote
5 risk factors
1. abdominal obesity
2. triglycerides
3. HDL
4. fasting glucose
5. HTN
\*\*\*must have 3 of the five qualifications\*\*\*
76
Metabolic Syndrome
## Footnote
what is this called?
what does it indicated for the patient?
what type of diabetes?
aka insulin resistance; syndrome X
## Footnote
classified as a constellation of sxs findings that **_significantly increase risk of athlerosclerosis_**
**_associated with T2DM_**
79
metabolic syndrome:
waist circumference RF
men over 102
women over 88
80
metabolic syndrome:
triglycerides RF
over 150
81
metabolic syndrome:
HDL RF
men less than 40
women less than 50
82
metabolic syndrome:
BP RF
over 130 SBP
over 85 DBP
83
metabolic syndrome:
fasting glucose RF
over 100
84
T2DM:
Visceral Fat
what does it do? (hence why bad)
4 steps that make this bad!
bad because it **_secretes adipokines/cytokines_**
theses **_increase insulin resistance_**
insulin resistance can also increase **_DYSLIPDEMIAS_**
dyslipidemias lead to
**_MI, STROKE, HYPERTENSION_**
86
sulfonylureas
## Footnote
what are they ment to work like?
what do they do?
what are 3 things they cause as SE?
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
what is the goal preprandial glucose?
post prandial?
pre: 80-130
post: less than 180
89
insulin secretagogues
## Footnote
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!
**_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
biguandines-Metformin
## Footnote
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?
first drug you give for T2DM
## Footnote
**_1. decreases hepatic glucose production_**
2. i**_ncreases insulin sensitivity and promotes uptake by skeletal muscle (what is left will work better)_**
3. improves lipid profile
4. 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
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
exanatide, liraglutide
## Footnote
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
3. insulin production
4. increase beta cell production
5. muscle uptake and and storage
decreases:
6. decreased gastric empyting
7. decrease appetite
8. decrease glucagon release
92
thaiazolidinediones
## Footnote
what do they do?
1 drug we use?
2 problems with them?
avoid in? 1
\*\*remember\*\*
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
SGLT2 inhibitors
## Footnote
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?
**_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
pramlinitide
## Footnote
what is this?
when is it normally secreted?
3 functions?
what does it improve?
which diabetes do you use it in?
synthetic analogue of amylin
## Footnote
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
stages of resistance for Type 2 diabetes
## Footnote
4 stages
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
2. **_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_*
3. **_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
DDP-4 inhibitors
## Footnote
name of the drug?
what does ths drug do?
why is complance better?
how is this drug used?
**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
what is more efffective than any oral antidiabetic drug?
exercise!!!
100
what are the ABCDEs of diabetes?
A=aspirin reduce platelets
B=bloood pressure ACE
C=cholesterol
D=diet, diabetes control
E=exercise, improves glucose and lipids
102
what is insulin resistance?
unknown mechanism
suspected etiology:
feuled by proinflammatory respons from cytokines and adipokines
103
what are 3 microvascular long term complications of diabetes?
1 macrovacular long term complication of diabetes?
**_microvascular:_**
1. retinopathy
2. nephropathy
3. neuropathy
**_macrovascular:_**
1. athlerosclerosis
(CHD, CVD/stroke, PAD)
105
diabetes complications:
retinopathy
what are the 2 types?
what is each characterized by?
what is key to prevent this?
**_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
how often do diabetics need eye exams?
annually
107
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?
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
how do you check for nephropathy in diabetic?
3 ranges
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
what are two ways to tx diabetic nephropathy once they have reached ESRD?
1. dialysis
2. transplantation from living related donor is preferable to dialysis
110
ACE initiation in diabetics
who do you start in and when?
what are 4 things it prevents the progression of?
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
diabetic complications: athlerosclerosis
## Footnote
what are 5 things this can lead to?
what is diabetes a equivalent to?
what should you consider putting them on?
CHD
MI
CHF
PVD
Suddent death
**_diabetes is a coronary risk equivalent_**
\*\*\*put patient on ASA if they these RF\*\*\*
112
diabetes is a...
CVD risk factor equvalent!!
113
Periphreal vascular disease in diabetics
what vessels effected?
lleads to 4 things?
4 tx options?
Large and small vessel disease
leads to:
**_claudications_**
**_ulcerations_**
**_amputations_**
RX:
regular foot exams
tight glycemic contro.
podiatric care
**_STOP SMOKING_**
114
diabetic complications:
neuropathy
3 presentations?
3 tx options for medication?
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
diabetes complications:
autonomic neuropathy
5 presentations
1. gastroparesis
## Footnote
slow gastric emptying incuding early saiety, nausea, and vomitying 1-3 hours after meal
**_tx: metoclopropramide_**
2. diarreah/constapation
3. orthostatic hypotension
**_fludrocortisone and elastic stockings_**
4. impotence, sexual dysfunction
5. decreased bladded sensation
116
diabetic ketoacidosis
## Footnote
5 general sxs?
once havd it for a while....6 sxs? 1 buxx word!!
polyuria
abominal pain
nausea
vomiting
fatigue
**_PROGRESSIVE DKA:_**
1. decrease mentation
**_2. stupor_**
**_3. coma_**
4. tachycardia
5. **_RAPID BREATH WITH FRUITY BREAHT (accumulation of ketones)_**
6. **_kussmauls respiration_**
form of hyperventilation to blow off the CO2
117
diabetic ketoacidosis
## Footnote
what is this?
who does it occur in?
why?
4 potenital causes?
2 critical things it can lead to?
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
diabetic ketoacidosis pathophysiology
## Footnote
4 steps
results in?
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
diabetic ketoacidosis:
what 2 products does the fat breakdown or lipolysis create for products?
production of FFA and conversion to
**_1. acetoacetic (ketoacid)_**
**_and_**
**_2. B-hydroxybutyric acid_**
121
diabetic ketoacidosis:
## Footnote
2 things it leads to because of glycosuria from glucse wasting from hyperglycemia?
1. osmotic diuresis
2. volume and electrolyte loss/imbalance
122
diabetic ketoacidosis:
## Footnote
7 lab findings
1. pH less that 7.3
## Footnote
2. low HCO3 with increased anion gap
3. increased urine osmolarity
4. BS usually over 300
5. elevated amylase
6. elevated WBC over 10,000 without infxns
7. initial serum K often high but **_total body ky low from fluid and electrolyte losses_**
123
diabetic ketoacidosis tx:
## Footnote
4 tx options
1. _estalish flowsheet ot measure all levels_
## Footnote
2. **_insulin regular_**
**_3. replace lost fluids with 0.9% NaCL\*\*\*give 3-4 L over 8 hours\*\*\*_**
**_4. replace K by KCL IB_**
124
hyperglycemic nonketotic hyperosmolar state
## Footnote
which diabetics is this in?
what is the patho of this?
what is the sugars like? what isn't present?
**_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
hyperglycemic hyperosmolar nonketoic acidosis:
## Footnote
what happens here that complicates thsi?
2 tx options?
the profound ostmotic diuresis causes severe dehydration (10-11L) is complicated by the ensuring pre-renal azotemia
## Footnote
TX:
1. 0.9% normal saline
2. insulin
126
what is the mortality seen with hyperglycemic hyperosmolar nonketotic acidosis?
50% mortality
127
explain why diabetic ketoacidosis is INCREASED ANION GAP ACIDOSIS?
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
what is the differences between DKA and HHNK?
DKA=TYPE 1, presensce of ketones
## Footnote
HHNK= TYPE 2, way higher BS
129
type 1 DM
patho
what promps this start of this?
5 triggers
**_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
Type 1 DM
## Footnote
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_?
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
type 1 DM treatment
## Footnote
what is the medication you tx with?
combination and percent of diffreent insulins? 2
tx: INSULIN only!!
## Footnote
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
what do you use as insulin to tx Type 1 DM?
combination of basal (Long acting) and prandial (shorter acting) insulin
## Footnote
covers them throughout the day and also when they have their specific meals
133
what is the total insulin need for someone with T1DM?
0.4-1 Units/kg
134
what is the most common seen complication with insulin or sulfonylurea use?
hypoglycemia
135
hypoglycemia
## Footnote
what are two drugs that are known for doing this?
5 sxs?
what sugar correlates with this?
most common complication seen with insulin or sulfonylurea
**_SXS:_**
**_1. sweating_**
**_2. tachycardia_**
**_3. hunger_**
**_4. tremulousness_**
**_5. nausea_**
**_less than 50 BS_**
136
what drug can mask hypoglycemia because it produces similar sxs
non selective beta blockers
137
Type 2 DM
## Footnote
characteristics of patient? 4
what is the goal? how to accomplish? 2
2 first line tx options?
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
explain the role of central/visceral obesity in T2DM?
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
glucotoxicity
## Footnote
what does this come from?
what mechanism does it cause to be faulty? what does this lead to?
comes from chronic hyperglycemia that ***inhibits the increase in insulin secretion normally seen in response to hyperglycemia***
## Footnote
worsens insulin resistance and _destroys the B cell function_
*\*\*THE MECHANISM GETS RUINED WITH CHRONIC INCREASED GLYCEMIA\*\**
140
how does diet and exercise improve insulin resistance?
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
Type 2 DM
## Footnote
7 sxs associated with this?
1. **often no sxs early**
2. polyuria
3. thirst
4. skin infections
5. vulvovaginits
6. _abnormal fat distribution_
7. hyperglycemia
143
glycated HB (A1c)
## Footnote
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?
describes the state of glycemia over prior 8-12 weeks, **_recheck every 3-4 months_**
## Footnote
normal= **_4-6%_**
prediabetes= **5.7-6.4%**
diabetes=**over 6.4%**
**\*\*\*\*goal in diabetic for A1c is less than 7%\*\*\*\*\***
144
what are the values for A1c?
normal
prediabetes
diabetes
normal= **4-6%**
prediabetes= **5.7-6.4%**
diabetes=**over 6.4%**
145
what are the four qualifications/options for **_diabetes_** dx?
1. FBS over 126 (normal under 100)
## Footnote
2. A1C over 6.5%
3. 2 hr GTT over 200
4. Random BS over 200 (need fasting to confirm but highly likely)
146
what are the 3 qualifications/options for **_imparied glucose tolerance aka pre diabetes?_**
1. FBS 100-125
## Footnote
2. 2 hr GTT BS of 140-199
3. A1c **_5.7-6.4%_**
147
what is the 3 tx algorithm used fot T2DM?
**Step 1 treat at dx:** lifestyle and metformin
## Footnote
**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
what are the goal levels for:
## Footnote
preprandial
postprandial
bedtime
a1c
preprandial=90-130
postprandial=less than 180
bedtime=100-140
a1c=less than 7
149
rapid acting insulin
## Footnote
what is the name?
onset?
peak?
what is it ideal for?
how can it be used?
**_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
regular insulin
## Footnote
how long does it take?
onset?
peak?
how is it delivered? unique fact?
short acting
## Footnote
onset: 30-60 mins
duration: 6-8
**_SC/IM/IV_**
**_only IV so used to tx diabetic ketoacidosis_**
151
neutral protamine
## Footnote
how long does this last?
onset?
duration?
intermediate acting
onset: 1-3 hours
duration: 14-18 hours
152
insulin glargine
how long does this last?
how long is the coverage?
when is it dosed?
why is this good?
what can' you do?
long acting insulin
## Footnote
**_24 hour coverage with steady state insulin levels_**
dosed at bedtime
\*\*causes less hypo/hyperglycemia\*\*
\*\*can't mix with other insulins\*\*
153
insulin pumps
## Footnote
what insulin can you use it with?
how does it work?
1 benefit?
3 drawbacks?
can be used with _lispro or regular_
## Footnote
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
things you should be checking every 3-6 months and annuually for diabetics?
