CM Endo

Question 1

what is the purpose of the endocrine system?

speed?

Answer 1

uses hormones released from glands into the blood and transports them throughout the body to influence the activity in other tissues

slow speed

longer results

(takes longer than neurotransmitters but sticks around for longer)

Question 2

what are 7 endocrine glands in the body?

Answer 2

pituitary

thyroid

parathyroid

adrenal glands

pancreas

gonads

hypothalamus

Question 3

endocrine hormones

what are they?

Answer 3

released into the bloodstream, this is most common, circulates to distant targets,

Question 4

paracrine hormones

what are these?

Answer 4

hormone acts locally on other cells other than the ones that produce it

ex: sex steroids on the ovary

Question 5

autocrine hormones

what are these?

Answer 5

acts on the tissue it comes from

ex: release on insulin from pancreatic beta cells since the release inhibits these same cells

Question 6

hormones

4 properties

Answer 6

1. blood borne signals released by endocrine glands
2. may be transported free or bound to carrier protein
3. different cells can respond differently to the same hormone
4. cells can have the same response to different hormones

Question 7

what are the transportation mechanisms for hormones?

Answer 7

free

bound

Question 8

free or unbound molecules

what is this?

Answer 8

peptide hormones and protein hormones are water soluble so therefore don’t need a carrier

free=water soluble

Question 9

hormones bound to carriers

what are these? (2)

what do they come from?

length of activity?

Answer 9

steroid hormones and thyroid hormones are carried by specific carrier proteins synthesized in the liver and cross membrane because lipid soluble

***the more binding that is present, the longer it stays in the system**

bound hormone=lipid soluble

Question 10

what are 3 ways hormones are degredated?

1

1

3

Answer 10

1. may be destroyed by enzymes at the receptor site (epi)
2. may be taking up by cells and destroyed (peptide hormones)
3. may be destroyed in the liver and excreted in the bile (steroid hormones, T3, T4)

Question 11

protein and peptide/polypeptide hormones

solbulity?

size?

how eliminated?

length of life?

receptor binding mechanism?

4 example hormones?

Answer 11

1. water soluble and circulate freely in the blood
2. small to large
3. degraded by enzymes in the blood or tissue and excreted by kidneys and liver
4. short lifespan in circulation
5. bind with RECEPTORS on the surface and use secondary messangers

Ex:

1. insulin
2. glucagon
3. hypothalmus hormones
4. pituitary hormones

Question 12

steroid hormones

what does it come from?

membrane permeability?

receptor location?

type of messenge?

ultimate effect?

5 hormones

Answer 12

1. come from cholesterol
2. can pass through lipid membrane
3. interacts with intracellular receptors in cytoplasm or on nucleus
4. primary messenger since enters cell
5. effect is transcription and translation of new gene

ex:

1. estradiol
2. testosterone
3. aldosterone
4. cortisol
5. glucocorticoids

Question 13

amines/amino acids

made from?

behave like?

2 hormone examples? made from?

Answer 13

1. derived from tyrosine
2. behave like proteins and peptides

ex:

1. NE and EPI
   - made from 1 single amino acid tyrosine
2. thyroid hormones
   - makde from 2 tyrosines

Question 14

T3/T4 and NE/EPI, although being amines, behave like? what does this mean?

Answer 14

BEHAVE LIKE PROTEINS AND PEPTIDES

1. water soluble
2. bind with receptor on surface and use secondary messangers

Question 15

what is the range in size for the polypeptides/proteins?

Answer 15

3-200 amino acids

Question 16

explain how proteins and polypeptides are synthesized?

4

Answer 16

vessicle mediated

1. synthesizied in the rough endoplasmic reticulum into precursor hormone called “prohormone”
2. moves to golgi appartus** and **packaged into vessicles
3. prohormones are converted to hormones once in the vessicle, if present
4. once endocrine cell is stimulated** the **vessicles go to the surface to release hormone

Question 17

what is the most prominent class of hormones?

Answer 17

proteins and poly peptides

Question 18

explain the synthesis of steroid hormones?

what to keep in mind about this process?!

Answer 18

nonvessicle mediated

1. synthesized in the smooth endoplasmic reticulum (hence why steroid producing tissues have a large amouth of SER)
2. some steroids serve as precursors for production of other hormones
3. *****process not completely understood****

Question 19

what type of receptors do polar, water soluble hormones bind to?

what two types of hormones use this methode?

example hormones within that class?

3

4

Answer 19

bind to plasma membrane receptors on outside of cell

1. proteins and peptides/polypeptides

-hypothalmus and pituitary hormones

-glucagon

-insulin

2. amines

(epi, NE, dopamine, T3, T4)

Question 20

what type of receptors do non-polar, lipid soluble molecules bind to?

class that uses this method?

4 hormones that use this?

Answer 20

pass through membrane and bind to intracellular receptor

example:

steroids

1. aldosterone
2. cortisol
3. estradiol
4. testosterone

Question 21

amino acid hormones (proteins + peptides/polypeptides)

what is there ultimate effect?

speed?

duration of effect?

Answer 21

use cell membrane receptors to alter existing proteins in target cells

fast-acting

shor duration of effects

Question 22

steroid hormones

what is their ultimate effect?

speed of effect?

duration of effect?

Answer 22

use intracellular receptors to synthesize new proteins

slow acting

long lasting effects

Question 23

hormone receptors

where are they?

what do they do?

response is dependent on? 2

can they number increase or decrease?

Answer 23

1. located intracellularly or on membrane
2. recognize a specific hormone and translate it into cellular response

3. response varies with number of receptors present and affinity

4. the number of receptors changes for number of reasons

Question 24

upregulation of hormone receptors

what are two ways this can occur?

Answer 24

1. decreased hormone levels increases the number of receptors so the cell is more sensitive to the decreased levels of hormone, negative feedback
2. sometimes the receptors can increase in response to increase hormone, causing a positive feedback

Question 25

down regulation of hormones ## Footnote what is 1 thing that causes this?

Answer 25

increased hormone levels cause the number of receptors to decrease and therefore decreasing the sensitivity to the hormone

Question 26

cell surface receptors ## Footnote what are 2 things this method requires? binding of hormone can signal what 2 things?

Answer 26

require: 1. first messenger 2. second messenger binding of hormone can cause: **_1. cause intracellular cascade_** **_2.direct effect on opening ion channel in cell membrane which influx becomes the secondary messenger_** ex: calcium

Question 27

what is the most widely distributed secondary messenger system?

Answer 27

cyclic adenosine monophosphate system (cAMP)

Question 28

secondary messenger system: cyclic adenosine monophosphate system what are the 5 steps in creating this pathway?

Answer 28

1. **_first messenger**_ _**hormone**_ binds with the _**surface receptor_** 2. the binding activates the **_G protein and converts ADP to ATP_** 3. this conversion cause the G protein to move through the membrane and **_activate adenylate cyclase_** 4. this activation c**_converts ATP to cAMP which is the SECOND MESSENGER_** 5. **_cAMP goes on to activate OTHER PROTEIN_** \*\*phosphidesterase breaks down the cAMP which causes the actions of the hormone to stop and shuts the effect off\*\*

Question 29

what is the advantage of the secondary messenger system?

Answer 29

amplification ## Footnote allows a small amount of hormone to have a large effect

Question 30

EPINEPHRINE what type of receptor pathway does it use? what recptor type does it bind to? what is its effect on the targe cell? 2

Answer 30

uses **_secondary messenger system using cAMP system_** epi binds to the beta adrenergic receptor EFFECTS IN TARGET CELL: 1. smooth muscle relaxation 2. vasodilation

Question 31

secondary messenger system: inositol-phospholipid calcium plathway

Answer 31

1. hormone binds to the **_plasma membrane receptor_** 2. activates **_G protein_** 3. G protein acitvates **_phospholipase C**_ which cleaves and creates _**inositol triphosphate and Diacylglycerol (DAG)_** .4. inositol triphosphate causes **_release of Ca ions from intracelluar stores_** 5. DAG **_activates protein kinase C_**

Question 32

norepinephrine ## Footnote what pathway does it initiate? what receptor does it bind to? what two effects does it have on the target cell?

Answer 32

binds to plasma membrane receptors and activates **_inisitol-phosphilipid-calcium pathway_** BINDS WITH _ALPHA-ADRENERGIC RECEPTOR_ effect on the target cell: 1. smooth muscle contraction 2. vasoconstriction

Question 33

nuclear receptors ## Footnote what are the 5 steps that occur when these are stimulated?

Answer 33

1. passively diffuse through the membrane and **_bind to receptors in on the nuclear membrane or in the cytoplasm_** 2. enter the nucleus as **_hormone receptor complexes_** 3. they **_bind to the DNA reponse elements or "HORMONE RESPONSE ELEMENTS**_ whic is the _**promoter site that initiates transcription_** 4. transcription produces **_mRNA_** 5. mRNA moves into the cytoplams to be **_translated to proteins_** \*\*\*these proteins either work internaly or externally and can have an inhibitory or promotionary overall effect\*\*\*

Question 34

hypophysis what is this?

Answer 34

the combination of the hypothalamus and pituitary gland connected by the hypophysial portal system which goes from the hypothalamus and drains into the anterior pituitary

Question 35

hypothalmus/hypothalmic hormones 4 things it controls? regulated by what two things?

Answer 35

CONTROLS: 1. PAIN 2. EMOTION 3. BODY TEMP 4. NEURAL INPUT **regulated by BOTH _hormonal feedback mechanisms_ and _neural input (neurotransmitters)_**

Question 36

what are the 7 hypothalmic hormones? what part of the pituitary do they go to? how do they get there?

Answer 36

released into hypophyseal portal to anterior pituitary: ## Footnote 1. gonadotropin releasing hormone (GnRH) 2. corticotropin releasing hormone (CRH) 3. thyroid releasing hormone (TRH) 4. growth hormone releasing hormone (GHRH) 5. prolactin inhibitory factor made in hypothalmus, travel down axon, stored in posterior piruitary: 1. ADH 2. oxytosin

Question 37

what are the two hormones that are made in the hypothalmus and stored the posterior pituitary?

Answer 37

1. ADH 2. oxytocin

Question 38

what are the 5 anterior pituitary hormones and their locations of function?

Answer 38

1. **FSH/LH**-gonads 2. **ACTH**-adrenal glands 3. **TSH**-thyroid 4. **GH**-long bones and muscles 5. **prolactin**-breasts

Question 39

what is the difference between the types of tissues in the anterior and posterior pituitary? nickanems for these?

Answer 39

ANTERIOR: **_endocrine/glandular_** tissue **_adenophypopphysis_** POSTERIOR: **_neural tissue_**, connection and extension of the hypothalmus also called "**_neurohypophysis"_** \*\*the tissues between the two are very different!!\*\*

Question 40

what are the 5 types of cells in the anterior pituitary? what do they produce and where does it go?

Answer 40

**_1. thyrotrophs_**: TSH to thyroid **_2. corticostrophs:_** ACTH to glucocorticoid levels **_3. gonadotrophs_**: LH and FSH to gonads **_4. somatotrophs:_** GH to metabolism and growth **_5. lactotrophs:_** prolactin to breast growth and milk production

Question 41

what are the 4 regulation methods of hormones?

Answer 41

1. negative feedback regulation 2. positive feedback regulation 3. exogenous feedback mechanism 4. regulation via hormone they produce

Question 42

negative feedback mechanism of hormones ## Footnote how does this work? ex?

Answer 42

higher levels of hormone cause negative feedback on the hypothalmic system and decrease production ex: TSH

Question 43

positive feedback mechanism of hormones ## Footnote how does this work? example?

Answer 43

higher levels of hormone cause positive feedback and increase the levels are are secreted ex: estradiol, during the follicular phase once it reaches threshold it increases the amount that is produced to reach the LH surge

Question 44

exogenous hormones ## Footnote what can these do? example?

Answer 44

can influence the normal feedback control of hormone production and release ex: administration of corticosteroids hormones causes suppression of the hypothalamic-pituitary-target cell system that regulates the production of these hormones

Question 45

regulation via substance the hormone produces ## Footnote what is this? 2 examples?

Answer 45

regulated by the level of substance they regulate ex: insulin; insulin levels are regulated in response to to blood glucose levels ex: aldosterone; levels change in response to the blood levels of sodium and potassium

Question 46

what are the 8 functions of the hypothalamus?

Answer 46

1. temp 2. osmolarity 3. blood nuitrients 4. inflammation mediatiors 5. emotions 6. pain 7. blood hormone levels 8. rgulates secretion of pituitary gland

Question 47

what are the two ways the hypothalmus releases (neuro)hormones?

Answer 47

1. **_neurosecretory neurons extend into posterior pituitary_** and secrete **_neurohormones ADH and oxytocin_** into **_SYSTEMIC CIRCULATION_** 2. neurosecretory neurons **_secrete RELEASING HORMONES_** into **_PORTAL CIRCULATION_** that stimulate the **_anterior pituitary endocrine cells appropriate receptors_**

Question 48

anterior pituiary hormones ## Footnote where are they released? act on what?

Answer 48

enter **systemic circulation** and **act on receptors on the cell** \*\*many targets of pituitary hormones also act on endocrine cells causing them to release hormones\*\*

Question 49

types of anterior pituitary hormones: 1. trophic (3) 2. direct (2) what do each of these mean?

Answer 49

**_trophic_**: stimulate other endocrine cells ## Footnote 1. FSH/LH 2. ACTH 3. TSH **_direct_**: act directly on effector 1. GH 2. prolactin \*\*\*\*\*PNEUMONIC: FLAT PEG\*\*\*\*\*\*

Question 50

radioimmunoassay ## Footnote what is this? what do you use? what one dxs is particullary important?

Answer 50

radiolabeled form of the hormone antibody to quantify the hormone level in the sample decreases as the amount of unlabeled hormone in the sample is increased **_antithyroid peroxidases (anti-TPO)_** measured in the initial work up and followup for patients with **_hashimoto thyroiditis_**

Question 51

urine tests what type do you wnana do?

Answer 51

24 hour urine sample provides better picture than an isolated sample

Question 52

stimulation tests ## Footnote when do you use this? what do you do in this test? 1 example? result interpreation?

Answer 52

used when **_hypofunction of an endocrine organ_** is suspected a stimuating hormone is given to see the ability for the organ to produce that hormone is measured ex: the hypothalmic-pituitary-adrenal system can be evalauged through stimulation tests *using ACTH and measuring the cortisol response* * -failure to increase cortisol levels after ACTH stimulation test suggests an inadequate capacity to produce cortisol by the adrenals*

Question 53

suppression test when do you do this? what happens in these conditions? 1 example? what happens in normal people? in disease?

Answer 53

used when **_hyperfunction_** of an **_endocrine disorde_**r is suspected the negative feedback process isn’t functioning appropriately so the excessive secretion of of hormone continues ex: when a GH secreting tumor is suspected, the GH repsonse to glucose load is measured - - normally a high glucose level would suppress GH levels - however, in adults with tumor producing hormones, the levels remain high

Question 54

thyroid physiology ## Footnote what system does this depend on? what is the hormone that controls this and where does it bind? what does this process require to function appropriately?

Answer 54

dependent on **hypothalamic-pituitary-thyroid acis** **_TSH**_ turns thyroid on and off by binding to the _**follicular cells of the thyroid_** the process of creating T3 and T4 **_requires iodine!!_**

Question 55

thyroid hormone synthesis ## Footnote what does this require? what is converted? what is it linked with? 2 things it makes? how does this make T3/T4?

Answer 55

requires **_iodide trapping**_ followed by _**thyroid peridoxidase conversion to IODINE**_ and linking it to _**thyroglobulin (tyrosine)**_ to make _**MIT and DIT_** \*\*\*the different combinations of MIT and DIT make T3 and T4 which are released into the blood\*\*\*\*

Question 56

Formation of thyroid hormone: MIT+DIT+thyroglobulin=

Answer 56

monotyrosine (MIT)+diiodotyrosine (DIT)+thyroglobulin=**_T3_**

Question 57

formation of thyroid hormones: DIT+DIT+thyroglobulin=

Answer 57

diodotyrosine (DIT)+diodotyrosine (DIT)+thyroglobulin= **_S4_**

Question 58

which one is produced more....T4 or T3? so what happens with this? which one causes more effecT?

Answer 58

T4!!!!!!! 13x more T4 than T3!!! 50% of this is deiodinated for form T3 \*\*\*it is primaryily T3 that enters cells and exhibits effects\*\*\*

Question 59

what percent of T3 and T4 are bound and ree? which enter the cell to exert their activity? which one is more active? by how much?

Answer 59

T4: 99.98% bound, 0.25% free T3: 99.7% bound, 0.3% free \*\*\*only the free T4 or T3 can enter the cell and exert its biological activity\*\* **T3 is 3-4 times more biologically active than T4**

Question 60

what happens to the majority of T4? this accounts for what percent?

Answer 60

T4 gets converted to T3 in the tissues, especially liver brain and hear by _deiodinase enzymes_ 80-90% of the avaliable T3 was created by this conversion manner!!

Question 61

thyroid hormone transporters (3) what can changes in the most common transporter cause? what is an example of this?

Answer 61

1. 80% by thyroxine binding globulin (TBG) 2. TBPA 3. albumin \*\*\*\*\*changes in the TBG leads to changes in the total T3 and T4 levels in the _absence of disease_ so need to look at this!!\*\*\* Ex: TBG levels increase with estrogen in pregnancy so to TOTAL T4 levels with be _increased_ but the free levels will _remain normal_

Question 62

thyroid hormone ## Footnote where does it bind? 2 major functions? essenital for 3 things?

Answer 62

BINDS WITH NUCLEAR OR INTRACELLULAR RECEPTORS 1. **_crucial role in cell differentiation and maturation in developement_** 2. **_maintains thermogenic and metabolic homeostasis in adult_** essential for **_metabolism, protein synthesis , and organ function_**

Question 63

what can happen if thyroid hormones aren't present at birth?

Answer 63

leads to severe mental retardation "cretinism" \*\*this is why we screen in all newborns\*\*

Question 64

what is the most common cause of thyroid disorders? 2 CAUSES?

Answer 64

result of autoimmune process ## Footnote cause: **_1. GLANDULAR DESTRUCTION AND UNDER PRODUCTION_** **_2. STIMULATE OVERPRODUCTION OF THYROID HORMONE_**

Question 65

what is this?

Answer 65

goiter

Question 66

TSH ## Footnote controlled by what type of mechanism? what instance would it be increased or decreased relative to thyroid function? sensitive? means?

Answer 66

controlled by **_negative feedback_** \*\*THINK ABOUT THIS SINCE NEGATIVE FEEDBACK\*\* DECREASED in HYPERTHYROIDISM INCREASED in HYPOTHYROIDISM extremely sensitive **_indicator of thyroid function so NORMAL RESULT EXCLUDES HYPO/HYPER THYROIDISM_**

Question 67

the TSH is always ______ with hypo/hyper thyroidism normal/abnormal values?

Answer 67

the TSH is always **_abnormal_** with hypo/hyper thyroidism normal: less than 3 abnormal: 3-6....consider hypothyroidism

Question 68

Free T4 ## Footnote when is this needed? what does it measure? what is it helpful in? normal?

Answer 68

*occasionally* needed to confirm hypo/hyperthyroidism directly measures free T4 helpful in **_management of thyrotoxicosis_** normal 9-24

Question 69

anti-thyroid antibodies ## Footnote what are 2 conditions this is elevated in? what is the anyibody name? what does it cause

Answer 69

autoimmune thyroid disease antibodies elevated in **_hashimotos and graves disease**_-most common thyroid disease and _**stimulated thryoid gland to release more hormone_** TSH-R AB (TSAb) aka thryoid stimulating hormone receptor antibodies

Question 70

RAI uptake/scan ## Footnote what is used in this study? what does it tell you? what can the two different patterns tell you?

Answer 70

oral I-131 take up by the thyroid......the **_% uptake indicates the gland activity_** and provides a picture of the gland helpful in differentiating the types of thyrotoxicosisc diffuse uptake=graves localized=toxic nodule with high specific uptake \*\*think about it: if an area is making a large amount of hormone, then it will require a large amount of iodide to make it so it wil concentrate in the specific area (nodule) or diffuse (entire thyroid) and indicate the issue

Question 71

what is the definitive test for thyroid cancer or nodule?

Answer 71

fine needle aspiration! KEY and NEEDED for dx!!

Question 72

hyperthyroidism: thyrotoxicosis what is this? what is elevated, what id decreased? what is the most common cause of this?

Answer 72

clinical syndrome caused by **_excess circulating thyroid hormone**_ (T4 or T3) causing the _**TSH to be decreased/suppressed_** (occurs becauseit is negative feedback so if high levels of T3 or T4 causes TSH to be low) GRAVES DISEASE IS THE MOST COMMON CAUSE!!!

Question 73

what are 6 causes of hyperthyroidism? which is most common?

Answer 73

1. **_graves disease MOST COMMON_** 2. toxic/hot **adenomas/nodules** 3. **early phase of hashimotos or sub-acute (viral) thyroiditis-** 4. factitious-**excessive thyroid hormone intake** 5. **TSH secreting adenoma** 6. **amiodarone (both hypo and hyperthyroidism)**

Question 74

what is one particular drug that can cause hyper and hypo thyroidism?

Answer 74

amiodarone!!!

Question 75

what is the most common cause of hyperthryoidism?

Answer 75

GRAVES DISEASE!!!

Question 76

hyperthyroidism: Graves disease what is important to knwo about this? who is it common in? what causes this? 3 things it leads to?

Answer 76

**_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!!

Question 77

hyperthyroidism: graves disease 13 sxs 2 3 key ones you need to remember

Answer 77

1. **_hyperactivity, irritability, restlessness_** **_2. heat intolerance, sweating_** 3. palpatations 4. increased appetite, weight loss 5. tachycardia 6. arrythmia 7. **_fine tremor_** **_8. goiter_** 9. warm, oily hair 10. proximal muscle weakness 11. _opthalmopathy_ **-proptosis/exopthamos** **-lid lag** 12. _dermopathy_ - **pretibial myxedema** 13. hyperreflexes

Question 78

hyperthyroidism: Graves disease OPTHALMOPATHY 3 things causes? why?

Answer 78

_unique to graves disease_ ## Footnote 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\*\*\*\*\*

Question 79

hyperthyroidism: Graves Disease DERMOPATHY what is the name for this? what does this cause? apperance?

Answer 79

3% occurance "_pre-tibial myxedema_" \*\*\*\*\*\*\*noninflammatory **_induration_** and **_plaque_** formation of the pre-tibial area leading to **_thickened skin_**, and **_orange skin appereance_**\*\*\*\*\*

Question 80

hyperthyroidism: Graves disease 2 tests to check what don't you need to check?

Answer 80

1. very low TSH ## Footnote 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\*\*

Question 81

hyperthyroidism: Graves disease 9 tx options? what is the toc? who do you use each in?

Answer 81

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** 4. propylithiouricil (PTU) (thiourea) if pregnant 5. saturated iodine solution- severe 6. iodinated contrast agens- severe or thyroid storm - prevents conversion of T4 to T3 7. glucocorticoids-severe - prevents conversion 8. **_radioative iodine-DEFINITIVE TX and TREATMENT OF CHOICE IN THE US!!_** - destroys the overactive gland because concentrates here - uses I-131 9. thyroidectomy no longer TOC but used in children or pregnancy or those that can' be controlled with medication

Question 82

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

Answer 82

radioactive iodine ## Footnote 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\*\*\*

Question 83

hyperthyroidism: Graves disease in txing it with thiourea drugs what percent will have reccurance? (propylithiouricil or methimazole)

Answer 83

50% reccurence are common if tx is only with thiourea, _propylthiouracil_ or _methimazole_

Question 84

what are 4 complications that can come from graves disease?

Answer 84

1. CV 2. ocular 3. psychological complications 4. _post tx hypothyroidism_ _common, but easily txed_

Question 85

thyroid storm ## Footnote what is this? 3 labs? 4 sxs? 3 tx options?

Answer 85

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

Question 86

what are the 5 causes of hypothyroidism?

Answer 86

1. **_hasimotos thyroiditis_** **_2. congenital hypothyroidism_** 3. idiopathic 4. iatrogenic 5. drug induced- **_amiodarone_**

Question 87

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?_

Answer 87

**_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 **_hypo_**thyroisim\*\*\*\*\*

Question 88

hypothyroidism: Hashimoto's thyroiditis 5 early sxs 8 late sxs

Answer 88

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_**

Question 89

hypothyroidism: hashimotos thyroiditis _myxedema_ what can this lead to? 5 sxs?

Answer 89

**_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

Question 90

hypothyroidism: ## Footnote hashimotos thyroiditis 2 complications 4 1

Answer 90

1. **_Cardiovascular_** - pericardial effusions - cardiomyopathy - accerlerated CHD - HF 2. **_encephalopathy_** coma/confusion

Question 91

hypothyroidism: Hashimotos thyroiditis 5 dx?

Answer 91

1. **_High TSH_** 2. low T3/T4 3. **_increased triglycerides_** 4. **_decreased HDL_** 5. anti-thyroid antibodies

Question 92

hypothyroidism: hashimoto's thyroiditis what is the tx? how is it dosed? monitoring? goal? time frame?

Answer 92

levothyroxine (synthetic T4) ## Footnote 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\*\*

Question 93

hypothyroidism: iatrogenic (we caused it) tx?

Answer 93

radioative iodine for initial hyperthyroidism that leads to gland destruction

Question 94

hypothyroidism: ## Footnote congenital what testing? why is it key to identify?

Answer 94

screening of TSH in newborns should elimate disease early detection is key to prevent **_cretinism**_ and _**hypodevelopment_**

Question 95

what is really important to keep in mind about the initial phase of hypothyroidism???

Answer 95

early phase can present as hyperthyroidism (release of stored hormone) because of lymphocytic infiltration of the gland but end result is hypothyroidism

Question 96

thyroiditis: suppurative what is this caused by? 3 sxs? 1 dx? 1 tx?

Answer 96

**_caused by gram positive bacteria_** STAPH AUREUS **_1. tender thyroid_** 2. fever 2. pharyngitis DX: **fine needle aspiration** Tx: drainage

Question 97

thyroiditis: ## Footnote De quervains aka granulomatous what is this? when is it most common? when does it occur? explain the progression? 2 dx? 3. tx?

Answer 97

**_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

Question 98

thyroiditis: drug induced amiodarone what does the medication contain? what percent get this? 3 progression steps?

Answer 98

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

Question 99

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?

Answer 99

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

Question 100

thyroid nodules ## Footnote how are these found? 2 types? which MC? why do we care? 2 dx methods? (interpreation) TOC?

Answer 100

single or multiple most found incidently on PE or imaging follicular adenoma-MC papillary adenomas-rare when single found usually **benign adenoma or colloid cyst** _but cancer is a possibility (5%)_ DX: 1. **_radioactive iodie thryroid scan_** **COLD NODLULE**: **NO UPTAKE** meaning they aren't functiong like normal thyroid tissue would, so more likely to be cancerous **REMOVE, HIGHLY SUSPICIOUS** **HOT NODULE:** UPTAKE, means functioning like the tissue nromally would and less likely to be cancerous since still functioning \*\*\*FINE NEEDLE ASPIRATION IS THE TOC FOR INITIAL NODULE..MUST RULE OUT THYROID CANCER\*\*\*

Question 101

toxic thyroid nodules ## Footnote what do they present with? number? 3 tx groups?

Answer 101

present with **_thyrotoxicosis aka high secretion of T3 and T4_** single (young), multiple (elderly) Tx: **over 40:** Radioactive iodine **less than 40**: radioative iodine or surgery **multinodular goiter:** radioactive iodine

Question 102

thyroid cancer ## Footnote what are the two MC types? appearance? speed? what to keep in mind about how it effects thyroid? _description of PE finding_

Answer 102

papillary MC-76% (rare mets) follicular-16% ( distant mets) **well differentaited** **slow growing** **curable** **DO NOT EFFECT THYROID FUNCTION** **"_painless neck swelling, firm, nontender nodule"_**

Question 103

thyroid cancer ## Footnote 2 dx techniques? 2 tx? what must you make sure to do?

Answer 103

DX: **_1. fine needle aspiration_** 2. US of neck TX: **_1. surgery_** -near total thyroidectomy with preservation of the parathyroid glands **_2. post-op suppression therapy with stimulation of any remaining thyroid tissue_** \*\*\*radioactive iodine scan to detect and remaining thyroid tissue/metastasis with further tx of I-131 if indicated....looking for cold spots!!!...can't uptake the iodine like normal tissue\*\*\*

Question 104

what is the most common risk factor for thyroid cancer??

Answer 104

childhood irradiation to head and neck increases risk 25x

Question 105

parathyroid hormone ## Footnote what is the main function? what are the 4 actions it has on the body to achieve this?

Answer 105

regulates and maintains calcium homeostasis in the serum/body ## Footnote 1. **_increases osteoclas activity_**-increasing PO4 and Ca 2. **_increase renal tubular absorption of Ca_** 3. **_increase PO4 excretion in the urine_** 4. **_activates 1,25-dihydroxycholecalciferol (activated vitamin D) absorption of Ca from GI tract_**

Question 106

when there is low levels of ca in the serum, what is released and what 3 things does it directly cause?

Answer 106

parathyroid hormone ## Footnote 1. **_increases osteoclast and BONE resorbtion_** 2. **_activates vitmin D (1,25-dihydroxy vD3, calcitriol)_** 3. **_resportion of Ca at the DCT in kidney_**

Question 107

what are the four things that activated vitamin D (calcitriol, 1-25-dihydroxy) does?

Answer 107

1. **_increase osteoclast activity_** 2. **_negative feedback to PTH_** (decreases the release) 3. **_increase Ca and PO4 absorption from the GI tract_** 4. **_Ca resorption from PCT_**

Question 108

what are the 3 hormones involved in regulating the calcium levels?

Answer 108

1. PTH 2. vitamin D 3. calcitonin (opposit effect of PTH, used when the serum Ca levels are high)

Question 109

calcium metabolism ## Footnote what are the 3 forms it comes in? what should you do if the total Ca appeares low?

Answer 109

_50% ionized_ 40% protein bound 10 complexed with anions \*\*important to measure serum albumin and "correct" total Ca if albumin is low"

Question 110

hyperparathyroidism ## Footnote what are 2 most common causes? what is hypersecreted? 2 hallmark lab findings? what are 5 things this can lead to?

Answer 110

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_

Question 111

hyperparathyroid: ## Footnote how is this normally found? _pneumonic for sxs_? leads to what what _6 presentations_?

Answer 111

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_**

Question 112

hyperparathyroidism: ## Footnote 5 lab findings what is important to do?

Answer 112

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_**\*\*\*

Question 113

hyperparathyroidism: ## Footnote 4 tx options what are the indications for the last? 1 4

Answer 113

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**

Question 114

what is a complication from thyroidectomy used to tx hyperparathyroidism? tx?

Answer 114

rapid drop of PTH levels and can lead to **_acute hypocalcemia post-op_** RX: **_calcium supplements_** until parathyroid resumes function

Question 115

what are five complications of hyperparathyroidism?

Answer 115

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

Question 116

hypoparathyroidism ## Footnote what are the 3 causes? MC? hallmark

Answer 116

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

Question 117

hypoparathyroidism ## Footnote 6 acute sxs 5 chronic sxs

Answer 117

_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

Question 118

hypoparathyroidism ## Footnote 4 lab findings

Answer 118

_1. low serum total and ionized Ca_ 2. elevated PO4 3. decreased PTH 4. _prolonged QT and arrythmias_

Question 119

hypoparathyroidism tx: 1 acute 3 chronic

Answer 119

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\*\*

Question 120

what are 3 things that are secreted by the adrenal cortex? and one thing by the medula?

Answer 120

cortex ## Footnote glerulosa=aldosterone fasiculata=cortisol reticularis=androgens (sex hormones) medula catecholamines (NE, epi)

Question 121

adrenal cortex: aldosterone what is this secreted by? what is it regulated by? what effect does it have?

Answer 121

secretion localized to **_glomerulosa_** regulated by the **_RAAS system of the kidneys_** **_mineral corticoid effects on the renal tubules_** reabsorption of Na, K, etc leading to water reabsorption

Question 122

adrenal cortex: cortisol what is this? where is it released from? what is it nessacary for? what prompts its release?

Answer 122

major **_glucocorticoid_** secreted by the middle and inner adrenal cortex (**_FASICULATA)_** NESSACARY FOR LIFE secretion is regulated by **_ACTH secreted from antierior pituitary_**

Question 123

adrenal cortex: androgens where is this released from? what are 4 things that are released?

Answer 123

*androgens more than estrogens* released from the **_reticularis_** (inner most) **_testosterone_** **_androstenedione_** **_DHEA_** **_estradiol_**

Question 124

cortisol increases....5 things

Answer 124

1. increase catabolism of fat and muscle tissue 2. increases free fatty acids 3. increases gluconeogenesis (glucose secretions) 4. increases blood glucose levels 5. increases sympathetic nervous system \*\*think about it when you are stressed out everything ramps up...this is why stress is bad in diabetes from glucose excretion from liver\*\*

Question 125

steroid hormones: cortisol what are the 7 functions of this?

Answer 125

1. **_carbohydrate metabolism_** 2. **_inhiits insulin secretion_** 3. increases hepatic **gluconeogenisis** 4. **dampens immune response** 5**_. inhibts production or action of many mediatiors of inflammation_** 6. required for production of **_angiotensin II_** 7. **_nessacary for normal boldily function_** 8. **_lower serum calcium_**

Question 126

steroid hormones: cortisol what are 4 things this is released in response to? what is it nicknamed? 2 things it does

Answer 126

released in response to _stress, trauma, infection, major surgery_ ## Footnote nicknamed "the permissive hormone": _required for bodily function_ _supports normal circulatory function and hemodynamic stability_

Question 127

cushing syndrome ## Footnote what are the 2 endogenous causes of cushings? what is the 1 exogenous cause of cushings? \*which is most common\*

Answer 127

**_endogenous_** 1. over production 2. tumors secreting cortisol or ACTH **_exogenous_** 1. glucocorticoid administration by medical providers \*\*MOST COMMON\*\*

Question 128

endogenous glucocorticoid excess ## Footnote CUSHING SYNDROME 3 causes CUSHING DISEASE 1 cause

Answer 128

1. _endogenous_ _cushing syndrome_ ## Footnote a. **_adrenal tumor adenoma 32% that secretes excess cortisol, causing low ACTH from negative feedback loop_** \*\*direct increase of the cortisol levels\*\* most common endogenous cause b.ECTOPIC ACTH: **_non pituitary neoplasms_** like small cell lung cancer also secrete ACTH _2. endogenous cushing disease_ **_puituiary adenoma: that secretes excess ACTH!_**

Question 129

exogenous glucocorticoid excess ## Footnote what should you know about this? what happens tha causes this? what does it lead to? what is developement dependent on?2 MC offender?

Answer 129

**_most common cause of CUSHINGS SYNDROME_** **_\*\*\*patient is taking prolonged administration of synthetic exogenous glucocorticoid in supraphysiologic doses\*\*\*_** \*\*\*leads to suppression of ACTH and clinical picture of hypercorticolism\*\*\* developement is dependent on _dose duration_ and timing mc=prednisone use!

Question 130

what is important to remember if a pt is taking glucocorticoids?

Answer 130

MUST TAPER!!! the glucocorticoids have caused chronis suppression of the adrenal glands so if you discontinue you must table to give the adrenal glands time to make their own cortisol

Question 131

cushings syndrome ## Footnote 5 main sxs 4 4 1

Answer 131

1. **_central obesity_** - _moon faces_ - _central protuberance_ - _buffalo hump_ _-supraclavicular fat_ 2. catabolic effects a. **_thin skin with easy bruising and striae!_** b. **_THIN EXTREMITIES_** c. MUSCLE WASTING d. hirsuitism 3. glucose intolerance/DM increased thirst and polydipsia 4. HTN 5. osteopenia/osteoporosis

Question 132

cushing syndrome ## Footnote what are the 5 tests you want to do? 2 key?

Answer 132

_1. elevated cortisol levels with loss of diurnal pattern (in day)_ 2. _dexamethasone suppression_ 3. low ACTH level (since suppressed with high cortisol levels) 4. hyperglycemia 5. MRI of head, CT chest and abdomen

Question 133

cushing syndrome ## Footnote 3 tx options?

Answer 133

1. **_transphenodial resection of pituitary adenoma_** (increased ACTH) 2. **_laproscopic resecection of adrenal tumor_** (increased cortisol) \*\*good prognosis if resection complete\*\* 3. **_ketoconazole and metryaprone used for METASTATIC adrenal cancer**_ by _**inhibiting 11 B-hyrdoylase_** (decreases cortisol synthesis)

Question 134

what do you see morbiditiy with endogenous cushings disease? 5

Answer 134

1. diabetes 2. HTN 3 osteoporosis 4. infections 5. fractures

Question 135

what is the only way you could call the disease "cushings" disease?

Answer 135

if the excess cortisol _originated with pituitary increase in ACTH secretion_

Question 136

what is the most common overall cause of cushing syndrome?

Answer 136

iatrogenic whe did it with high does corticosteroid drugs

Question 137

explain the dexamethasone suppression test that is used to dx cushings?

Answer 137

dexamethasone is 4x more potent than cortisol...therefore giving this at 11 pm should cause the cortisol to be lower in the morning because it suppresses ACTH \*\*\*\*if you don't get this response and cortisol is still elevated means that there is a tumor secreteing it because the quantities is so high that the dexamethasone does nothing!!\*\*\*

Question 138

adrenal cortical insufficiency ## Footnote 3 causes of this what do you find in each?

Answer 138

1. primary adrenal insufficiency - ADDISONS **_TB or autoimmune destruction of adrenal cortex_** **_High levels of ACTH as results because trying to stimulate release_** 2. secondary adrenal insufficiency HYPOPITUITARISM **_hypopituitarism (low levels of ACTH)_** 3. acute adrenal crisis

Question 139

what are 4 things that can cause corticoadrenal insufficiency? 0 0 2 2

Answer 139

1. taking _exogenous corticosteroids_ supresses the hypothalmic-pituitiary-adrenal axis 2. requirement for corisol increases 3. chronic adrenal insuffiiciency **_addisons disease_** **_billtareal adrenal hemmorage_** 4. acute adrenal insufficiency **_corticosteroid cessation_** **_adrenal sugery/pituiary sugery_**

Question 140

corticoadrenal insufficiency: increased cortisol need \*can't meet demand\* 4 causes

Answer 140

1. infection 2. MI 3. surgery 4. glucocorticoid (prednisone) tapered too quickly for suppressed adrenal gland to resume normal secretion leaidng to no enough cortisol

Question 141

chronic corticoadrenal insufficiency: ## Footnote 2 causes

Answer 141

1. addisons disease 2. billateral adrenal hemmorage

Question 142

chronic adrenal insufficiency: addisons disease what is the MC cause of this in US and worldwide? what hormones does it cause a decrease in? what are 4 sxs? location 7

Answer 142

**_autoimmune destruction of the adrenal cortex_** that develops over time and leads to **_decreased CORTISOL, ALDOSTERONE, ADRENAL ANDROGENS_** autoimmune cause: MC in industeralized world tuberculosis: MC worldwide sxs: 1. fatigue, weakness, arthalgias, myalgias, anxiety _all nonspecific so mush have index of suspcion_ 1. hypotension that doesn't respond to fluid (since RAAS system damaged since relies on aldosterone from the adrenal cortex but it is damanged from autoimmune) 2. orthostasis/low BP 3. hyperpigmentation "Bronzed" skin - knuckles - palmar creases - elbows - knees nailbeds nipples \*\*\*reduction in axillary and pubic hair\*\*\*

Question 143

chronic adrenal insufficiency: pituitary failure/destruction

Answer 143

pituitary injury/failure causes a **_ACTH deficiency**_ which means the facicularis of the adrenal cortex _**isn't stimulated to make cortisol_** leadingto deficiency

Question 144

chronic adrenal insufficiency: addisons disease 6 labs 1 diagnostics

Answer 144

1. _low AM cortisol level less than 5_ _2. cosyntropin (synthetic ACTH) stimulation test_ given IV/IM-serum cortisol obtained in 30-60 minutes...normally would see rise in serum cortisol **_measure of adrenal reserve, however, here doesn't rise_** 3. high ACTH since trying to stimulate cortisol release (only the adrenal are effected not pituitary) 2. lymphocytosis 3. hypoglycemia 4. hyperkalemia 5. hyponatremia 6. abdominal CT-_small non-calcified adrenals_

Question 145

chronic adrenal insufficiency: ## Footnote what is the tx option fo this? what must you do for a patient in this situation and when is it indicated? 3

Answer 145

1. **_glucocorticoid replacement following diurnal pattern_** hydrocortisone 15-20 in AM 5-10 PM \*\*\*\*\***_MUST**_ increase 8-10x maitenance cortisol dose during periods of _**STESS like infection, MI, surgery to AVOID acute adrenal insufficiency/crisis_**\*\*\*\*\*

Question 146

what are the 2 causes of acute adrenal insufficiency?

Answer 146

1. corticosteroid use with increased bodily cortisol need or abruptly stopping medication without taper ## Footnote \*\*doens't allow axis to recover\*\* 2. post adrenal or pituitary surgery

Question 147

acute adrenal insufficiency: exogenous corticosteroids is this serious? how does this occur? what do you do to prevent this? what does it allow? 3 things that increase cortisol demand? what must you do it pt taking high level of glucocorticoids/

Answer 147

**_LIFETHREATENING MEDICAL EMERGENCY_** MC from _supressed gland from exogenous glucocorticoids is MC scenario of acute where stopped too quickly/abruptly--MUST TAPER BECAUSE OF THIS!!_ \*\*allows the adrenal pituitary axis time to recover\*\* MC in patients with suppressed adrenal glad who develop a need for additional cortisol - infection - MI - surgery etc. \*\*\*MUST HAVE HIGH INDEX OF SUSPICION IN ALL PATIENTS TAKING GLUCOCORTICOIDS!!\*\*\*

Question 148

acute adrenal insufficiency ## Footnote 6 sxs? 2 _key_?

Answer 148

1. headache 2. N/V 3. cyanosis 4. dehydration 5. hemodynamic collapse 6. _hypotension/shock unresponsive to iV fluids and pressors_

Question 149

acute adrenal insufficiency: ## Footnote what are the 2 txs for this?

Answer 149

1. **_RAPID INFUSION OF ISOTONIC FLUIDS_** - normal saline - ringers lactate 2. _IV hydrocortisone Q 6 hours until stable_ \*\*\*oral hydrocortisone once stable\*\*\*

Question 150

pheochromocytoma ## Footnote what is this? what does it increase? 4 sxs? 3 sxs pneumonic?

Answer 150

RARE cause of secondary HTN adrenal medulla tumor secretes large amounts of catecholamines (NE and EPI) into circulation SXS: 1. HTN 2. "PHE"-_Palpatations, headache, excessive sweating_

Question 151

pheochromocytoma ## Footnote 1 DX? 2 tx options (1 TOC)?

Answer 151

DX: **_24 hour urine for catecholamines and emtanephedrines_** TX: **_1. TOC laproscopic removal of the tumor_** 2. preoperative administration of _alpha block and beta blockers can reduce complications_

Question 152

pheochromocytoma ## Footnote 4 complications?

Answer 152

1. HTN crisis ## Footnote 2. stroke 3. intracerebral bleed 4. cardiomyopathy

Question 153

incidentaloma ## Footnote what is this? what do you need to determine? why? what commonly goes here? removal suggestions?

Answer 153

_adrenal_ mass found incidently on imaging (need to know if it is malignant!) Primary adrenal carcinoma is rare **_but other cancers metastasize here esp LUNG CANCER_** 1. risk high if mass over 6cm 2. surgical removal over 4 cm esp is younger

Question 154

osteoporosis ## Footnote what is this? what type of bone is lost more commonly? percentages

Answer 154

**_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%_

Question 155

bone density ## Footnote describe the progression throughout life? 5 what do people suggest about the tx based on this progression?

Answer 155

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*_**\*\*\*\*

Question 156

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

Answer 156

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

Question 157

opsteopenia definition

Answer 157

BMD **_1-2.5 SD_** below peak bone density

Question 158

osteoporosis definition

Answer 158

BMD **_over 2.5 SD_** from normal

Question 159

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

Answer 159

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

Question 160

do men get osteoporosis? how many?

Answer 160

YEP!! 1 out of 5 dxed people are men hip fracture is a significant predictor for mortality!!

Question 161

what are 7 RF that increase your risk for osteoporosis?

Answer 161

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

Question 162

osteoporosis ## Footnote what are 4 sxs you may see with this? what is usually the inital presentation?

Answer 162

**_1. many asymptomatic till fracture (often spontaneous)_** 2. \*\*\*\*\*\*may see back pain, decrease in height, or kyphosis\*\*\* 3. dietary calcium, vit D deficiency

Question 163

osteoporosis ## Footnote 4 texts for dx 1 TOC? interpretation

Answer 163

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

Question 164

who do you screen for osteoporosis in?

Answer 164

1. early menopause ## Footnote 2. RF FH malnourished alcoholism renal failure 3. 65+

Question 165

can you reverse established osteoporosis?

Answer 165

no can increase BD, decrease fractures, and hald or slow progression

Question 166

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

Answer 166

**_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_**

Question 167

pagets disease ## Footnote what is this? who is it most common in? what does it come from? what happens in this condition? what 2 things does it lead to? which 3 bones are most common?

Answer 167

**_second most common metabolic bone disease after osteoporosis_** more common in Northern European genetic **_RANK GENE_** and environmental influences "collage of matrix madness" massive/furious osteoclast-mediated bone reabsorption followed by disorganized osteoblast repair that replaces bone with weak and poor quality bone making **_JIG SAW PUZZLE OR CEMENT LINES**_=_**fractures and bowing_** **_skill, spine, pelvis: axial skeleton_**

Question 168

pagets disease ## Footnote what are the 4 body systems that are effected? 7 sxs? what is worst case senario?

Answer 168

most commonly found incidently on radiograph **_skull: headaches, tinnitis, vertigo, eventual hearing loss_** **_spine:_** causes **_kyphosis_**, nerve compression **_legs:**_ _**bowed femur, tibia, fibia_** **_skin:_** **_warm_** overlying the skin from hypervascularity of paget bones worst case sarcoma

Question 169

pagets disease 4 dx 4 tx

Answer 169

DX: 1. **_bone deformities and xray changes_** 2. **_elevated alk phos_** 3. bone scans to detect rapid bone turnover and monitor response to tx 4. bone bx to differentiate from cancer TX: 1. NSAIDS 2. biphosphonates (suppressive) 3. calcitonin (suppressive) 4. vitamin D and calcium

Question 170

what are the 6 hormones released from the anterior pituitary? two from posterior pituitary?

Answer 170

**_anterior_** GH prolactin ACTH TSH LH FSH **_posterior_** ADH oxytocin

Question 171

what are 8 possible cause sof hypopituitarism?

Answer 171

1. genetic defects 2. tumors 3. autoimmune 4. trauma 5. irradiation 6. stroke 7. hemmorage 8. peri-partum

Question 172

what is sheehan's syndrome?

Answer 172

pituitary infarction from chock or hemmorage during/post delivery

Question 173

hypopituitarism: decrease LH/FSH what is this? 8 sxs? dx?

Answer 173

**_decreased sex hormones_** 1. loss of secondary sex characteristics 2. beard 3. axillary hair 4. pubic hair 5. libido 6. ammenoreah 7. infertility 8. low testosterone/estrogen DX: **_decreased LH and FSH leads to decreased testosterone and estradiol_**

Question 174

hypopituitarism: Decreased TSH what does this lead to? 6 sxs of this?

Answer 174

**_hypothyroidism_** 1. decreases thyroid hormone 2. **_weakness/cold intolerance_** 3. constpation 4. skin atrophy 5. hair loss 6. dyslipidemia dx: **_decreased free T4_**

Question 175

hypopituitarism: ACTH decrease what becomes decreased? 4 sxs?

Answer 175

**_decreased cortisol levels and adrenal insuffiency_** 1. weakness 2. fatigue 3. weight loss 4. hypotension DX: **_ACTH leads to decreased cortisol leading to hyponatremia and hypoglycemia_**

Question 176

when suspecting hypopituitarism, what do you need to do?

Answer 176

1. MRI: look for neoplasms ## Footnote 2. if tumor: **_transphenoid pituitary surgery followed by endocrine replacement therapy_**

Question 177

diabetes insipidus ## Footnote 4 types (2 for the last)

Answer 177

1. central: deficient ADH/AVP 2. primary: autoimmune 3. secondary: damage to pituitary 4. nephrogenic: inability of kidneys to respond to ADH **_congenital:_** total lack of ADH receptors **_acquired_**: pyelonephritis obstructive drug induced (lithium) hyercalcemia

Question 178

diabetes insupidus ## Footnote 1 dx? tx if central? tx if nephrogenic

Answer 178

dx: **_vasopressin challange_** desmopressin administered SC or intranasal results in a _drastic decrease in urine volume indicating central cause_ or lack of original ADH (allows for water reabsorption at the kidneys) TX: central: **_partial deficiency:_** just fluids **_complete deficiency:_** desmopressed at lowest effective dose nephrogenic: **_INDOMETHACIN_** MAKES THE KIDNEYS MORE SENSITIVE TO ADH/AVP BY **blocking prostaglandin E**

Question 179

what are two complications that can come from diabetes insipidus?

Answer 179

1. severe dehydration 2. hypernatremia

Question 180

prolactin ## Footnote what is its function? what is the production pattern mediated by?

Answer 180

induces lactation during pregnancy (along with estrogen and progesterone) control: production is **_inhibitory mediated by dopamine_**

Question 181

hyperprolactinemia: 5 causes? (3 main)

Answer 181

1. **_pituitary microadenoma_** 2. Drugs- SSRIs 3. hypothyroidism 4. renal failure 5. cirrohosis

Question 182

hyperprolactinemia: ## Footnote what do high prolacitn levels do? 4 overall sxs? 4 sxs in women? 3 sxs in men?

Answer 182

high prolactin levels **_supress GnRH and lead to decreased LH/FSH resuling in hypogonadotropin_** vision changes from compression of optice nerve, N/V and headache **_PLUS_** women: **_galactorreah_** **_amoenorrhea_** _infertility_ _decreased libido_ \*\*since these sxs are so bothersome in women it is usually detected earlier\*\* men _decreased libido_ _erectile dysfunction_ _gynecomastia_

Question 183

hyperprolactinemia ## Footnote 3 DX 4 TX OPTIONS(when do you use each?)

Answer 183

1. baseline labs including **_TSH, prolactin_** levels **_prolactin level over 250 is high suspicious/diagnostic_** 2. **_MRI_** tx: 1. DC the offending drug if present 2. microprolactinomas grow very slowly so can monitor if asymptomatic 3. **_if sxs of hypogonadism and infertility**_ _**or large:_** **_dopamine agonist (Cabergoline)_** (shrinks tumor and ts sxs) 4. SURGERY **_RESERVED FOR VISION CHANGES FROM COMPRESSION OF THE OPTIC NERVE CHIASM_**

Question 184

acromegaly/gigantism ## Footnote what is in excess? MC from what? what alllows these effects to happen? what else do these commonly secrete?

Answer 184

**_excessive GH release, almost always from pituitary adenoma_** and effects are mediated by _insulin like growth factor-1 (IGF-1) in liver_\*\*causes growth in bons or visceral organs\*\* \*\*often times these tumors also secrete prolactin which cause additionaly sxs\*\*\*

Question 185

acromegaly/gigantism ## Footnote difference between children and adults? what caues each? sxs in adults? 7 5 associated sxs that are common?

Answer 185

**_gigantism in children:_** - unfused long bones - effects everything **_acromegaly in adults:_** - ​after boes fuse - **enlarged hands lips, face, feet, deep voice, coarse facial hair, visceral organs** ASSOCIALTED FINDINGS: **_1. HTN_** **_2. CARDIOMEGALY_** **_3. INSULIN RESISTANCE AND DIABETES_** (GH counteracts the actions of insulin) **_4. cardiovascular disease and premature death_** **_5. hypogonadism_** (if tumor cosecretes prolactin which is common)

Question 186

acromegaly/gigantism ## Footnote 4 dx?

Answer 186

1. overnight fasting **_IGF-1_** (5x normal) (alsomay see high prolactin if tumor secretes it or elevated glucose if progressed to diabetes) ## Footnote 2. TSH (of low suggestes additional pituitary pathology 3. **_glucose challenge test post fas_**t-suppresses GH levels to confirm dx 4**_. MRI_** to find tumor

Question 187

acromegaly/gigantism ## Footnote 2 tx

Answer 187

1. **_transphenoidal microsurgery toc_** ## Footnote \*\*keep in mind this can cause permanent hypopituiarism and may need replacement tx\*\* 2. octreotide-samatostatin (shrinks tumor and suppres GH secretion) \*\*\*used in patients who continue to have excessive GH release post op\*\*

Question 188

pituitary dwarfism ## Footnote what are the 3 types of this? what does each one lack? middle: sxs6 last: who mos common in? 3 2 measureable levels

Answer 188

**_1. idiopathic GH deficiency_** lack of hypoathalmc **_GHRH_** *includes those with familial short stature and delay in growth or puberty* **_2. pituitary tumors, agenesis of pituitary_** Lack GH * shorter than normal birth length* * decreased growth rate first 1-2 years* *_normal intelligence_* * obesity and immature facial features* * delay in skeletal muscle* *_micophallus-abnormmal small penis_* **_3. laron-type dwarfism_** Rare, abnormal GH receptor **_high levels of GH and low levels of IGF-1_** **_meditterean descent esp sepharidic jews**_ _**and african pygmies_**

Question 189

what is psychosocial dwarfism? 3 sxs? who does it occur in?

Answer 189

hypopituitarism that is seen in emotionally deprived children 1. poor growth 2. potbelly 3. poor eating and drinking habits \*\*usually in those who hare severely neglected or disciplined\*\* child returns to normal removed from situation

Question 190

dwarfism (green book) what is the most common type? occurs from? 10 sxs? tx

Answer 190

**_achondroplasia is the most common non-lethal type_** most common type of short-limbed dwarf and occurs from **_failure of the cartilage to ossify_** average height of ~4 ft sxs: 1. short limbs 2. long narrow trunks 3. large heads with medface hyperplasia 4. prominent brows 5. delayed motor milestones 6. _intelligence is normal_ 7. bowing of the legs 8. obesity 9. dental problesm 10. _frequenct ottis media_ TX: orthopedic problems fixed with orthopedic intervention

Question 191

achondroplasia: ## Footnote what is the gene that is mutated?

Answer 191

FGFR3

Question 192

pituitary dwarfism can present with what two clues?

Answer 192

micropenis hypoglycemia

Question 193

what is the most common cause of hyperpituitarism? what is the most common within this group?

Answer 193

pituitary adenoma **_lactorophic is the most common type of pituitary adenoma and secrete prolactin_**

Question 194

too little hormone: ## Footnote 3 general causes

Answer 194

1. congenital defects 2. damage from disease 3. atrophy from aging or drugs

Question 195

too much hormone: 3 general causes

Answer 195

1. excess stimulation of the gland 2. hormone producing tumor 3. administration of exogenous hormone

Question 196

Releasing hormones → anterior pituitary → secretion of hormones into blood → signal specific peripheral glands or target tissues

Answer 196

remember it

Question 197

GH → \_\_\_\_\_\_\_\_→ \_\_\_\_\_\_\_

Answer 197

GH → stimulates the liver → IGF-1

Question 198

TSH → \_\_\_\_\_\_→ \_\_\_\_\_\_\_\_

Answer 198

TSH → stimulates the thyroid → thyroid hormones

Question 199

ACTH →\_\_\_\_\_\_\_\_\_→ \_\_\_\_\_\_\_\_\_\_

Answer 199

ACTH → stimulates adrenal cortex → cortisol

Question 200

FSH and LH → ________ → \_\_\_\_\_\_\_\_\_

Answer 200

FSH and LH → stimulate gonads → sex hormones

Question 201

Prolactin → \_\_\_\_\_\_\_→ \_\_\_\_\_\_\_\_\_

Answer 201

Prolactin → stimulates breast → milk production

Question 202

where does a primary hormone disorder occur?

Answer 202

**_at the level of the periphreal gland_**

Question 203

where does a secondary hormone disorder occur?

Answer 203

**_at the level of the anterior pituitary_**

Question 204

where does a tertiary hormone abnormality occur?

Answer 204

**_at the level of the hypothalmus_**

Question 205

what is another name for growth hormone?

Answer 205

somatotropin THEY ARE THE SAME THING!!

Question 206

explain the function of GH and the different parts of the body it effects

Answer 206

1. growth promoting effects ## Footnote stimulates the liver to produce **_IGF-1**_ with increases _**protein synthesis and growth**_ in the_**:_** **_1. bone and cartilate_** **_2. body organs_** **_3. muscle_** 2. anti-insulin effects **_adipose tissue_**: increased lipolysis and decreased adipositiy **_carbohydrate metabolism_**: increases blood glucose

Question 207

growth hormone: stimulated by?4 inhibited by?4

Answer 207

stimulated by: ## Footnote **_hypoglycemia_** **_fasting_** **_starvation_** **_stress_** inhibited by: **_increased glucose levels_** (hense in testing why if you give someone glucose GH should go down, and if you give them insulin it should go up) **_free fatty acid release_** **_obesity_** **_cortisol_**

Question 208

what do follicular cells release?

Answer 208

THYROID HORMONES T3 AND T4

Question 209

PARATHYROID HORMONE ## Footnote what is the overall effect? 2 ways it accomplishes this

Answer 209

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_**

Question 210

calcitonin what secretes this? overall funciton? 3 ways it accomplishes this?

Answer 210

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_**

Question 211

what is the general steps involded in the formation of T3 and T4?

Answer 211

IN THYROID FOLLCIULAR CELLS 1. SIMOTANOUSELY: iodide is taken in from the blood and converted **to iodine by peroxidase** 2. WHILE: amino acids are combined in the **RER into thyroglobulin** 2. _thyroglobulin becomes iodinated_ and formes MIT and DIT 3. MIT and DIT form different combinations _MIT + DIT= T3 (triiodothyronine)_ _DIT+DIT=T4 (thyroxine)_ 4. secreted into the blood, mostly bound to _thyroixine binding globulin (TBG)_, to travelto target cell and promote mRNA to **_increase metabolic rate_**

Question 212

is T4 active?

Answer 212

nope, it is converted to T3 \*\*\*T4 is secreted more than T3\*\*\*\*

Question 213

Lack of what component can cause thyroid insufficiency?

Answer 213

iodide since this is nessacary to iodinate the thyroglobulin and turn it into MIT and DIT which makes T3 and T4...if iodide is absent then this process can't occur and no T3 and T4 is made\*\*\* no negative feedback, so TRH and TSH increase to try to simulate production of T3 and T4....causes the thyroid to grow because it becomes stimulated by its own TSH

Question 214

cortisole is a ______ that effects \_\_\_\_\_\_

Answer 214

glucocorticoid ## Footnote effects METABOLISM

Question 215

aldosterone is a ______ that effects \_\_\_\_\_\_\_

Answer 215

mineralcorticoid that effects **_Na absorption and K excretion_**

Question 216

pharmacokinetics

Answer 216

what the body does to the drug

Question 217

pharmachodynamics

Answer 217

what the drug does to the body

Question 218

how many people world wide are obese?

Answer 218

1.9 billion

Question 219

how many people have diabetes and prediabetes?

Answer 219

diabetes: 25.8 milllion prediabetes: 57 million

Question 220

what are four populations that have increased risk/prevalence of diabetes?

Answer 220

1. **_african americans_** ## Footnote **_2. american indians_** **_3. hyspanics_** **_4. alaska natives_**

Question 221

what are the percent prevalence of T1DM and T2DM?

Answer 221

T1DM=10% ## Footnote T2DM=90%

Question 222

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

Answer 222

**_insulin deficiency_** hyperglycemia dyslipidemia **_metabolic wasting_** **_ketoacidosis_**

Question 223

what are 4 brief features of T2DM?

Answer 223

**_hypoinsulinemia_** hyperglycemia dyslipidemia **_obestiy often_**

Question 224

what do most of the complications from diabetes stem from?

Answer 224

micro and macrovascular disease from uncontrolled sugars

Question 225

when food enteres the body, what are the four hormones that are released that play a role in insulin secretion? of these 4....two of them preform 3 additional funcions which are they and what do they do?

Answer 225

1. amylin via beta cells ## Footnote **_carbohydrate metabolism_** **_INHIBITS_** a. gastric emptying b. glucagon release c. appetite 2. insulin via B beta cells 3. GIP by K cells in SI 4. GLP-1 by L cells in jejunum **_inhibits (like amylin):_** a. gastric emptying b. glucagon release c. appetite

Question 226

what is the combined function of GLP-1 and GIP?

Answer 226

promote insulin release aka "incretin effect"

Question 227

explain how glucose stimulates the beta pancreatic cell? 6 steps

Answer 227

1. glucose stimulates the Beta pancreatic cell 2. glucose is **_metabolized_** via glycolysis to make **_ATP_** 3. ATP release **_facilitates closure of the K channels_** 4. closure of the channels makes the **_inside have a postivie charge because K is postivie and the cell depolarizes_** 5. depolarization causes the **_Ca channel to open_** 6. the i**_nflux of Ca_** causes **_INSULIN RELEASE_** BOOM!

Question 228

anabolic effects: insulin/glucose on muscle 3

Answer 228

1. **_increase glucose uptake_** **_2. increase glycogen storage_** **_3. increased protein synthesis_**

Question 229

anabolic effects: glucose/insulin on fat 3

Answer 229

**_1. increased glucose intake_** **_2. triglyceride synthesis_** **_3. decreased lipolysis_**

Question 230

anabolic effects: glucose/insulin on liver

Answer 230

**_1. increase glycogen synthesis_** **_2. increase triglyceride synthesis_** **_3. decrease glucose production_**

Question 231

what is the clinical importance of the insulin structure?

Answer 231

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_**

Question 232

when insulin is released there is ______ nervous system activity

Answer 232

when insulin is released there is parasympathetic nervous system activity

Question 233

what are 5 overall broad functions of insulin secretion?

Answer 233

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

Question 234

anabolic means

Answer 234

building things up

Question 235

anti-catbolic means...

Answer 235

preventing from being broken down

Question 236

**_LIVER_** 1 anabolic 3 anti-catabolic

Answer 236

anabolic: **_Stimulation of glycogen synthesis_** catabolic i**_inhibition of:_** **_glycogenolysis_** **_gluconeogensis_** **_ketogenesisi_**

Question 237

glycogenolysis

Answer 237

breakdown of glycogen to glucose (occurs at liver, and less commonly muscles)

Question 238

gluconeogensis \*\*WHAT TO KEEP IN MIND...WHAT DOES THIS OCCUR WITH?\*\*\*

Answer 238

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!!!\*\*\*

Question 239

**_ADIPOSE TISSUE_** ## Footnote 3 anabolic 1 anit- catabolic

Answer 239

anabolic ## Footnote **_increase glucose uptake_** **_increase triglyceride synthesis_** **_increase fatty acid uptake and synthesis_** catabolic **_inhibition of lipolysis_**

Question 240

**_muscle tissue_** 4 anabolic 2 anticatabolic

Answer 240

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)

Question 241

what cells secrete glucagon?

Answer 241

alpha cells of the pancreas when blood glucose was low

Question 242

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

Answer 242

glucagon is released from the alpha cells of the pancrease which causes liver glycolysis and gluconeogenisis ## Footnote \*\*negative feedback once BS increase\*\*

Question 243

glucagon

Answer 243

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

Question 244

amylin ## Footnote 3 functions

Answer 244

1. slows glucose absorption in the duodenum ## Footnote 2. supresses glucagon secretion 3. metabolizes carbs

Question 245

somatostatin ## Footnote (not somatoropin=GH) 2 functions

Answer 245

1. decreased GI activity 2. suppresses glucagon and insulin secretion

Question 246

what are four counter-regulatory hormones of insulin (mean it works against insulin and does the opposit)?

Answer 246

1. epi 2. glucagon 3. cortisol 4. GH \*\*all of these work under sympathetic control and want the BS to increase\*\*

Question 247

counterregulatory: epinephrine 3 effects? how long does it take?

Answer 247

**_1. increase hepatic glucose output_** **_2. decrease insulin output_** **_3. increase glucagon release_** \*\*only takes minutes\*\* \*\*think about it, epi gets you ready for flight or fight so they want to increase the sugar avaliable(\*\*

Question 248

counterregulatory: glucagon 3 functions? how long

Answer 248

**_increase hepatic glucose output_** **_lipolysis_** **_ketones_** \*\*\*intermediate acting\*\*\*

Question 249

counterregulatory: cortisol 3 functions time?

Answer 249

1. increase gluconeogensis 2. decrease muscle glucose uptake and glycogensis 3. increase lipolysis \*\*\*takes hours\*\*\*

Question 250

counter regulatory: GH 2 fxns

Answer 250

1. increase hepatic glucose output 2. decrease muscle glycogenesis

Question 251

what is the name of the _insulin regulated glucose transporter_ that is activated when insulin is released to take up the extra glucose?

Answer 251

GLUT4 translocation

Question 252

causes of diabetes: type 1: type 2: gestational Type 4:

Answer 252

type 1: autoimmune type 2: hereditary-offspring gestational Type 4: drug induced

Question 253

who do you typically find diabetic ketoacidosis in?

Answer 253

TYPE 1 (can be in late stage 2)

Question 254

who do you typically find acute hypoglycemia in?

Answer 254

type 1 post insulin without eating

Question 255

who do you typically find hyperglycemia in?

Answer 255

type 1 and type 2

Question 256

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

Answer 256

HYPOglycemia!!

Question 257

metabolic syndrome ## Footnote 5 risk factors

Answer 257

1. abdominal obesity 2. triglycerides 3. HDL 4. fasting glucose 5. HTN \*\*\*must have 3 of the five qualifications\*\*\*

Question 258

Metabolic Syndrome ## Footnote what is this called? what does it indicated for the patient? what type of diabetes?

Answer 258

aka insulin resistance; syndrome X ## Footnote classified as a constellation of sxs findings that **_significantly increase risk of athlerosclerosis_** **_associated with T2DM_**

Question 259

metabolic syndrome: waist circumference RF

Answer 259

men over 102 women over 88

Question 260

metabolic syndrome: triglycerides RF

Answer 260

over 150

Question 261

metabolic syndrome: HDL RF

Answer 261

men less than 40 women less than 50

Question 262

metabolic syndrome: BP RF

Answer 262

over 130 SBP over 85 DBP

Question 263

metabolic syndrome: fasting glucose RF

Answer 263

over 100

Question 264

visceral fat is \_\_\_\_ subcutaneous fat \_\_\_\_

Answer 264

visceral fat is BAD subcutaneous fat GOOD

Question 265

T2DM: Visceral Fat what does it do? (hence why bad) 4 steps that make this bad!

Answer 265

bad because it **_secretes adipokines/cytokines_** theses **_increase insulin resistance_** insulin resistance can also increase **_DYSLIPDEMIAS_** dyslipidemias lead to **_MI, STROKE, HYPERTENSION_**

Question 266

what is the goal preprandial glucose? post prandial?

Answer 266

pre: 80-130 post: less than 180

Question 267

what is the goal BP for a diabetic?

Answer 267

less than 140/90

Question 268

what is the goal of LDL for diabetics?

Answer 268

less than 100

Question 269

what are the rules regarding statin use that apply to diabetics? 4

Answer 269

4 qualifications: ## Footnote **_1. clinical athlerosclerotic CVD_** **_2. DM type 1 or type 2 and age 40-75 and LDL 70-190_** **_i_**f over 7.5 high intensity if less than 7.5 low intensity **_3. age 40-75 and LDL 70-189 \*\*calculate risk\*\*_** **_4. LDL over 190_**

Question 270

sulfonylureas ## Footnote what are they ment to work like? what do they do? what are 3 things they cause as SE?

Answer 270

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_**

Question 271

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!

Answer 271

**_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\*\*\*_**

Question 272

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?

Answer 272

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)

Question 273

thaiazolidinediones ## Footnote what do they do? 1 drug we use? 2 problems with them? avoid in? 1 \*\*remember\*\*

Answer 273

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\*\*\*

Question 274

alphacglucosisase inhibitors ## Footnote what doe these do? what do they cause as SE? why? when is it used?

Answer 274

inhibit the hydrolysis of comple carboydrates so it can be absorbed form the small intestine by inhibiting **_the alpha glucodaise enzyme_** acrabose causes **_massive**_ _**diarreah and flatulence_** since the stool osmolarity is increased so patients \*don't like this\* _only used in combination_

Question 275

pramlinitide ## Footnote what is this? when is it normally secreted? 3 functions? what does it improve? which diabetes do you use it in?

Answer 275

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

Question 276

where are the most reliable injection sites for pramlintide?

Answer 276

abdomen and thigh

Question 277

where is the most reliable injection site for insulin?

Answer 277

thigh and abdomen

Question 278

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

Answer 278

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

Question 279

DDP-4 inhibitors ## Footnote name of the drug? what does ths drug do? why is complance better? how is this drug used?

Answer 279

**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_**

Question 280

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?

Answer 280

**_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\*\*\*\*

Question 281

what is more efffective than any oral antidiabetic drug?

Answer 281

exercise!!!

Question 282

of the diabetic meds which 3 cause hypoglycemia and hyperinsulinemia and weight gain?

Answer 282

1. insulin 2. repaglinide (increase insulin secertion) \*\*\*causes less weight gain than the others\*\*\*\* 3. sulfonyureas (increase insulin secretion)

Question 283

what are the ABCDEs of diabetes?

Answer 283

A=aspirin reduce platelets B=bloood pressure ACE C=cholesterol D=diet, diabetes control E=exercise, improves glucose and lipids

Question 284

why do we care about foods that cause inflammation? 4 3 exampls

Answer 284

because they increase risk of CV disease, insulin resistance, hypertension, and central adiposity ## Footnote **_processed foods_** **_white foods_** **_simple sugars_**

Question 285

what are 7 things we can do to minimize the inflammation cause by food intake or diabtes?

Answer 285

1. medditerean diet (breads, fibers, fruits and veggies) ## Footnote 2. fish oils- 3 omega fatty acids 3. red juices (blueberries, back tea, nuts) 4. modest alcohol consumption 5. ACE 6. STATINS 7. ASA

Question 286

stages of resistance for Type 2 diabetes ## Footnote 4 stages

Answer 286

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!!

Question 287

what is insulin resistance?

Answer 287

unknown mechanism suspected etiology: feuled by proinflammatory respons from cytokines and adipokines

Question 288

how much does 15 g of glucose increase the BS by?

Answer 288

25-50 mg

Question 289

what are 3 microvascular long term complications of diabetes? 1 macrovacular long term complication of diabetes?

Answer 289

**_microvascular:_** 1. retinopathy 2. nephropathy 3. neuropathy **_macrovascular:_** 1. athlerosclerosis (CHD, CVD/stroke, PAD)

Question 290

diabetes complications: retinopathy what are the 2 types? what is each characterized by? what is key to prevent this?

Answer 290

**_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_

Question 291

how often do diabetics need eye exams?

Answer 291

annually

Question 292

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?

Answer 292

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_**

Question 293

how do you check for nephropathy in diabetic? 3 ranges

Answer 293

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_**

Question 294

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

Answer 294

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

Question 295

ACE initiation in diabetics who do you start in and when? what are 4 things it prevents the progression of?

Answer 295

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_

Question 296

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?

Answer 296

CHD MI CHF PVD Suddent death **_diabetes is a coronary risk equivalent_** \*\*\*put patient on ASA if they these RF\*\*\*

Question 297

diabetes is a...

Answer 297

CVD risk factor equvalent!!

Question 298

Periphreal vascular disease in diabetics what vessels effected? lleads to 4 things? 4 tx options?

Answer 298

Large and small vessel disease leads to: **_claudications_** **_ulcerations_** **_amputations_** RX: regular foot exams tight glycemic contro. podiatric care **_STOP SMOKING_**

Question 299

diabetic complications: neuropathy 3 presentations? 3 tx options for medication?

Answer 299

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)

Question 300

diabetes complications: autonomic neuropathy 5 presentations

Answer 300

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

Question 301

diabetic ketoacidosis ## Footnote what is this? who does it occur in? why? 4 potenital causes? 2 critical things it can lead to?

Answer 301

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

Question 302

diabetic ketoacidosis ## Footnote 5 general sxs? once havd it for a while....6 sxs? 1 buxx word!!

Answer 302

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

Question 303

diabetic ketoacidosis pathophysiology ## Footnote 4 steps results in?

Answer 303

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_**

Question 304

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

Answer 304

production of FFA and conversion to **_1. acetoacetic (ketoacid)_** **_and_** **_2. B-hydroxybutyric acid_**

Question 305

diabetic ketoacidosis: ## Footnote 2 things it leads to because of glycosuria from glucse wasting from hyperglycemia?

Answer 305

1. osmotic diuresis 2. volume and electrolyte loss/imbalance

Question 306

explain why diabetic ketoacidosis is INCREASED ANION GAP ACIDOSIS?

Answer 306

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_**

Question 307

diabetic ketoacidosis: ## Footnote 7 lab findings

Answer 307

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_**

Question 308

diabetic ketoacidosis tx: ## Footnote 4 tx options

Answer 308

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_**

Question 309

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?

Answer 309

**_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_**

Question 310

hyperglycemic hyperosmolar nonketoic acidosis: ## Footnote what happens here that complicates thsi? 2 tx options?

Answer 310

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

Question 311

what is the mortality seen with hyperglycemic hyperosmolar nonketotic acidosis?

Answer 311

50% mortality

Question 312

in DKA and HHNK, what is the most common cause of increased need of insulin that prompts this to occur?

Answer 312

infection most common

Question 313

what is the differences between DKA and HHNK?

Answer 313

DKA=TYPE 1, presensce of ketones ## Footnote HHNK= TYPE 2, way higher BS

Question 314

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_?

Answer 314

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_**

Question 315

type 1 DM patho what promps this start of this? 5 triggers

Answer 315

**_infectious or toxic insult_** in genetically predisposed people causing **_autoimmune response against altered pancreatic B cell antigens_** triggers: viruses mumps coxsackie rubella toxic chemicals

Question 316

how many diabetic patients are there in the uS?

Answer 316

over 25 million

Question 317

what four populations hae increased predisposition to DM?

Answer 317

african americans hispanics native americans

Question 318

type 1 DM treatment ## Footnote what is the medication you tx with? combination and percent of diffreent insulins? 2

Answer 318

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_**\*\*

Question 319

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

Answer 319

combination of basal (Long acting) and prandial (shorter acting) insulin ## Footnote covers them throughout the day and also when they have their specific meals

Question 320

what is the total insulin need for someone with T1DM?

Answer 320

0.4-1 Units/kg

Question 321

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

Answer 321

hypoglycemia

Question 322

hypoglycemia ## Footnote what are two drugs that are known for doing this? 5 sxs? what sugar correlates with this?

Answer 322

most common complication seen with insulin or sulfonylurea **_SXS:_** **_1. sweating_** **_2. tachycardia_** **_3. hunger_** **_4. tremulousness_** **_5. nausea_** **_less than 50 BS_**

Question 323

what drug can mask hypoglycemia because it produces similar sxs

Answer 323

non selective beta blockers

Question 324

Type 2 DM ## Footnote characteristics of patient? 4 what is the goal? how to accomplish? 2 2 first line tx options?

Answer 324

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

Question 325

type 2 DM prevents....

Answer 325

ketosis (DKA) because the small amount of insulin that is present prevents this breakdown process, however it doens't prevent hyperglycemia

Question 326

who does T2DM occur in?

Answer 326

obese 70% ## Footnote non obese 30%

Question 327

explain the role of central/visceral obesity in T2DM?

Answer 327

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_**

Question 328

presence of hepatic insensitivity or from insulin resistance causes there into be a increase in...

Answer 328

gluconeogensisi

Question 329

glucotoxicity ## Footnote what does this come from? what mechanism does it cause to be faulty? what does this lead to?

Answer 329

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\*\**

Question 330

what is nessacary to preserve B cell function?

Answer 330

control BS

Question 331

how does diet and exercise improve insulin resistance?

Answer 331

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\*\*\*

Question 332

Type 2 DM ## Footnote 7 sxs associated with this?

Answer 332

1. **often no sxs early** 2. polyuria 3. thirst 4. skin infections 5. vulvovaginits 6. _abnormal fat distribution_ 7. hyperglycemia

Question 333

diabetic dyslipidemia is defined as what?

Answer 333

high triglycerides 300-400 low HDL less than 30

Question 334

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?

Answer 334

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%\*\*\*\*\***

Question 335

what are the values for A1c? normal prediabetes diabetes

Answer 335

normal= **4-6%** prediabetes= **5.7-6.4%** diabetes=**over 6.4%**

Question 336

self monitoring blood sugar

Answer 336

standard of care for all diabetics ## Footnote requires a lot of education about meter, when to take it, cost, everything!

Question 337

what are the four qualifications/options for **_diabetes_** dx?

Answer 337

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)

Question 338

what are the 3 qualifications/options for **_imparied glucose tolerance aka pre diabetes?_**

Answer 338

1. FBS 100-125 ## Footnote 2. 2 hr GTT BS of 140-199 3. A1c **_5.7-6.4%_**

Question 339

what are the goal levels for: ## Footnote preprandial postprandial bedtime a1c

Answer 339

preprandial=90-130 postprandial=less than 180 bedtime=100-140 a1c=less than 7

Question 340

what are the goal target percentages for diabetics: protein fat carbohydrates fiber

Answer 340

protein 10-35% fat 25-35% carbohydrates 45-65% fiber 20-35

Question 341

what is the 3 tx algorithm used fot T2DM?

Answer 341

**Step 1 tre​at 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)**

Question 342

what are 3 dietary changes a diabetic should consider making to help maintain sugar?

Answer 342

1. poultry 2. fish 3. artificial sweetners aspartame and saccharin

Question 343

when txing T2DM with metformin and insulin, what are the two common preparations you might see?

Answer 343

1. NPH/reg in 70:30 mixture ## Footnote 2. insulin glargine

Question 344

what do you need to consider when dosing insulin?

Answer 344

need diet activity since this is dose before when we are guessing their sugars will be later

Question 345

what is the goal of txing with insulin? 2

Answer 345

**_tight control to prevent hypoglycemia_** ## Footnote **_prevent long term complications_**

Question 346

rapid acting insulin ## Footnote what is the name? onset? peak? what is it ideal for? how can it be used?

Answer 346

**_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\*\*_**

Question 347

regular insulin ## Footnote how long does it take? onset? peak? how is it delivered? unique fact?

Answer 347

short acting ## Footnote onset: 30-60 mins duration: 6-8 **_SC/IM/IV_** **_only IV so used to tx diabetic ketoacidosis_**

Question 348

neutral protamine ## Footnote how long does this last? onset? duration?

Answer 348

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

Question 349

insulin glargine how long does this last? how long is the coverage? when is it dosed? why is this good? what can' you do?

Answer 349

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\*\*

Question 350

insulin mixes ## Footnote what is this a mix of? who is it good for? what does it allow for?

Answer 350

mix of intermediate PLUS short or rapid for T1DM and good for those who have hard time mixing insulins allow for both basal and post meal requirements

Question 351

insulin pumps ## Footnote what insulin can you use it with? how does it work? 1 benefit? 3 drawbacks?

Answer 351

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_**

Question 352

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

Answer 352

Question 353

why is moderate exercise essential?

Answer 353

1. increases effectiveness of insulin 2. stabilizes insulin dosages 3. improves utilization of fats and carbohydrates regardless of weight