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Module 10: Mali: Endocrine > CM Endo > Flashcards

CM Endo Flashcards

1
Q

what is the purpose of the endocrine system?

speed?

A

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)

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2
Q

what are 7 endocrine glands in the body?

A

pituitary

thyroid

parathyroid

adrenal glands

pancreas

gonads

hypothalamus

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3
Q

endocrine hormones

what are they?

A

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

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4
Q

paracrine hormones

what are these?

A

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

ex: sex steroids on the ovary

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5
Q

autocrine hormones

what are these?

A

acts on the tissue it comes from

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

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6
Q

hormones

4 properties

A
  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
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7
Q

what are the transportation mechanisms for hormones?

A

free

bound

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8
Q

free or unbound molecules

what is this?

A

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

free=water soluble

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9
Q

hormones bound to carriers

what are these? (2)

what do they come from?

length of activity?

A

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

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10
Q

what are 3 ways hormones are degredated?

1

1

3

A
  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)
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11
Q

protein and peptide/polypeptide hormones

solbulity?

size?

how eliminated?

length of life?

receptor binding mechanism?

4 example hormones?

A
  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
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12
Q

steroid hormones

what does it come from?

membrane permeability?

receptor location?

type of messenge?

ultimate effect?

5 hormones

A
  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
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13
Q

amines/amino acids

made from?

behave like?

2 hormone examples? made from?

A
  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
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14
Q

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

A

BEHAVE LIKE PROTEINS AND PEPTIDES

  1. water soluble
  2. bind with receptor on surface and use secondary messangers
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15
Q

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

A

3-200 amino acids

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16
Q

explain how proteins and polypeptides are synthesized?

4

A

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
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17
Q

what is the most prominent class of hormones?

A

proteins and poly peptides

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18
Q

explain the synthesis of steroid hormones?

what to keep in mind about this process?!

A

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****
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19
Q

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

A

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)

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20
Q

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

class that uses this method?

4 hormones that use this?

A

pass through membrane and bind to intracellular receptor

example:

steroids

  1. aldosterone
  2. cortisol
  3. estradiol
  4. testosterone
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21
Q

amino acid hormones (proteins + peptides/polypeptides)

what is there ultimate effect?

speed?

duration of effect?

A

use cell membrane receptors to alter existing proteins in target cells

fast-acting

shor duration of effects

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22
Q

steroid hormones

what is their ultimate effect?

speed of effect?

duration of effect?

A

use intracellular receptors to synthesize new proteins

slow acting

long lasting effects

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23
Q

hormone receptors

where are they?

what do they do?

response is dependent on? 2

can they number increase or decrease?

A
  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

  1. the number of receptors changes for number of reasons
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24
Q

upregulation of hormone receptors

what are two ways this can occur?

A
  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
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25
Q

down regulation of hormones

what is 1 thing that causes this?

A

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

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26
Q

cell surface receptors

what are 2 things this method requires?

binding of hormone can signal what 2 things?

A

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

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27
Q

what is the most widely distributed secondary messenger system?

A

cyclic adenosine monophosphate system (cAMP)

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28
Q

secondary messenger system:

cyclic adenosine monophosphate system

what are the 5 steps in creating this pathway?

A
  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 cconverts 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**

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29
Q

what is the advantage of the secondary messenger system?

A

amplification

allows a small amount of hormone to have a large effect

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30
Q

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

A

uses secondary messenger system using cAMP system

epi binds to the

beta adrenergic receptor

EFFECTS IN TARGET CELL:

  1. smooth muscle relaxation
  2. vasodilation
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31
Q

secondary messenger system:

inositol-phospholipid calcium plathway

A
  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

  1. DAG activates protein kinase C
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32
Q

norepinephrine

what pathway does it initiate?

what receptor does it bind to?

what two effects does it have on the target cell?

A

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
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33
Q

nuclear receptors

what are the 5 steps that occur when these are stimulated?

A
  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***

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34
Q

hypophysis

what is this?

A

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

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35
Q

hypothalmus/hypothalmic hormones

4 things it controls?

regulated by what two things?

A

CONTROLS:

  1. PAIN
  2. EMOTION
  3. BODY TEMP
  4. NEURAL INPUT

regulated by BOTH hormonal feedback mechanisms and neural input (neurotransmitters)

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36
Q

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

A

released into hypophyseal portal to anterior pituitary:

  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
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37
Q

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

A
  1. ADH
  2. oxytocin
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38
Q

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

A
  1. FSH/LH-gonads
  2. ACTH-adrenal glands
  3. TSH-thyroid
  4. GH-long bones and muscles
  5. prolactin-breasts
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39
Q

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

A

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!!**

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40
Q

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

A

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

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41
Q

what are the 4 regulation methods of hormones?

A
  1. negative feedback regulation
  2. positive feedback regulation
  3. exogenous feedback mechanism
  4. regulation via hormone they produce
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42
Q

negative feedback mechanism of hormones

how does this work?

ex?

A

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

ex: TSH

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43
Q

positive feedback mechanism of hormones

how does this work?

example?

A

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

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44
Q

exogenous hormones

what can these do?

example?

A

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

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45
Q

regulation via substance the hormone produces

what is this?

2 examples?

A

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

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46
Q

what are the 8 functions of the hypothalamus?

A
  1. temp
  2. osmolarity
  3. blood nuitrients
  4. inflammation mediatiors
  5. emotions
  6. pain
  7. blood hormone levels
  8. rgulates secretion of pituitary gland
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47
Q

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

A
  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
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48
Q

anterior pituiary hormones

where are they released?

act on what?

A

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**

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49
Q

types of anterior pituitary hormones:

  1. trophic (3)
  2. direct (2)

what do each of these mean?

A

trophic: stimulate other endocrine cells

  1. FSH/LH
  2. ACTH
  3. TSH

direct: act directly on effector

  1. GH
  2. prolactin

*****PNEUMONIC: FLAT PEG******

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50
Q

radioimmunoassay

what is this?

what do you use?

what one dxs is particullary important?

A

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

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51
Q

urine tests

what type do you wnana do?

A

24 hour urine sample provides better picture than an isolated sample

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52
Q

stimulation tests

when do you use this?

what do you do in this test?

1 example?

result interpreation?

A

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*

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53
Q

suppression test

when do you do this?

what happens in these conditions?

1 example? what happens in normal people? in disease?

A

used when hyperfunction of an endocrine disorder 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
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54
Q

thyroid physiology

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?

A

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!!

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55
Q

thyroid hormone synthesis

what does this require?

what is converted?

what is it linked with?

2 things it makes?

how does this make T3/T4?

A

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****

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56
Q

Formation of thyroid hormone:

MIT+DIT+thyroglobulin=

A

monotyrosine (MIT)+diiodotyrosine (DIT)+thyroglobulin=T3

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57
Q

formation of thyroid hormones:

DIT+DIT+thyroglobulin=

A

diodotyrosine (DIT)+diodotyrosine (DIT)+thyroglobulin= S4

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58
Q

which one is produced more….T4 or T3?

so what happens with this?

which one causes more effecT?

A

T4!!!!!!! 13x more T4 than T3!!!

50% of this is deiodinated for form T3

***it is primaryily T3 that enters cells and exhibits effects***

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59
Q

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?

A

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

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60
Q

what happens to the majority of T4?

this accounts for what percent?

A

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!!

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61
Q

thyroid hormone transporters

(3)

what can changes in the most common transporter cause?

what is an example of this?

A
  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

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62
Q

thyroid hormone

where does it bind?

2 major functions?

essenital for 3 things?

A

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

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63
Q

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

A

leads to severe mental retardation “cretinism”

**this is why we screen in all newborns**

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64
Q

what is the most common cause of thyroid disorders?

2 CAUSES?

A

result of autoimmune process

cause:

1. GLANDULAR DESTRUCTION AND UNDER PRODUCTION

2. STIMULATE OVERPRODUCTION OF THYROID HORMONE

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65
Q

what is this?

A

goiter

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66
Q

TSH

controlled by what type of mechanism?

what instance would it be increased or decreased relative to thyroid function?

sensitive? means?

A

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

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67
Q

the TSH is always ______ with hypo/hyper thyroidism

normal/abnormal values?

A

the TSH is always abnormal with hypo/hyper thyroidism

normal: less than 3
abnormal: 3-6….consider hypothyroidism

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68
Q

Free T4

when is this needed?

what does it measure?

what is it helpful in?

normal?

A

occasionally needed to confirm hypo/hyperthyroidism

directly measures free T4

helpful in management of thyrotoxicosis

normal 9-24

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69
Q

anti-thyroid antibodies

what are 2 conditions this is elevated in?

what is the anyibody name?

what does it cause

A

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

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70
Q

RAI uptake/scan

what is used in this study?

what does it tell you?

what can the two different patterns tell you?

A

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

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71
Q

what is the definitive test for thyroid cancer or nodule?

A

fine needle aspiration! KEY and NEEDED for dx!!

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72
Q

hyperthyroidism:

thyrotoxicosis

what is this?

what is elevated, what id decreased?

what is the most common cause of this?

A

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!!!

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73
Q

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

A
  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)
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74
Q

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

A

amiodarone!!!

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75
Q

what is the most common cause of hyperthryoidism?

A

GRAVES DISEASE!!!

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76
Q

hyperthyroidism:

Graves disease

what is important to knwo about this?

who is it common in?

what causes this?

3 things it leads to?

A

MOST COMMON CAUSE OF HYPERTHYROIDISM

women more common 20-40 years old!!

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

leads to: hypertrophy, hyperplasia, commonly goiter!!

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77
Q

hyperthyroidism:

graves disease

13 sxs

2 3 key ones you need to remember

A
  1. hyperactivity, irritability, restlessness

2. heat intolerance, sweating

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

8. goiter

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

-proptosis/exopthamos

-lid lag

  1. dermopathy
    - pretibial myxedema
  2. hyperreflexes
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78
Q

hyperthyroidism:

Graves disease

OPTHALMOPATHY

3 things causes?

why?

A

unique to graves disease

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

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

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79
Q

hyperthyroidism:

Graves Disease

DERMOPATHY

what is the name for this?

what does this cause?

apperance?

A

3% occurance

“pre-tibial myxedema”

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

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80
Q

hyperthyroidism:

Graves disease

2 tests to check

what don’t you need to check?

A
  1. very low TSH

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

2. total and T4 elevated

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

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81
Q

hyperthyroidism:

Graves disease

9 tx options?

what is the toc?

who do you use each in?

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

-monitor WHB, pruirits, and FT4

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

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

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82
Q

hyperthyroidism:

Graves disease

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

A

radioactive iodine

used to destroy the gland because it concentrates here

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

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

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83
Q

hyperthyroidism:

Graves disease

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

(propylithiouricil or methimazole)

A

50%

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

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84
Q

what are 4 complications that can come from graves disease?

A
  1. CV
  2. ocular
  3. psychological complications
  4. post tx hypothyroidism common, but easily txed
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85
Q

thyroid storm

what is this?

3 labs?

4 sxs?

3 tx options?

A

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

elevated T3 and T4

decreased TSH

high fever

tachycardia

sweating

delierum

tx:

  1. satruated iodine solution
  2. iodinated contrast agents
  3. glucocorticoids
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86
Q

what are the 5 causes of hypothyroidism?

A
  1. hasimotos thyroiditis

2. congenital hypothyroidism

  1. idiopathic
  2. iatrogenic
  3. drug induced- amiodarone
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87
Q

hypothyroidism:

Hashimoto’s thyroiditis

what is important to remember about this?

what type of disease?

how does it show up?

2 things ath cause this

what to keep in mind?

A

MOST COMMON CAUSE OF HYPOTHYROIDISM

AUTOIMMUNE, with insidious onset

thyroperoxidase and thyroglobulin antibodies present in high titers

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

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88
Q

hypothyroidism:

Hashimoto’s thyroiditis

5 early sxs

8 late sxs

A

early:

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

late:

  1. slow speech

2. hoarse voice

3. weight gain

3. goiter

4. alopecia

4. facial and eyelip puffiness

5. bradycardia

6. edema non pitting

7. myxedema

8. pleural/pericardial effusion

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89
Q

hypothyroidism:

hashimotos thyroiditis

myxedema

what can this lead to?

5 sxs?

A

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

can lead to mydxedema crisis EMERGENCY:

severe form of hypothyroidism

  • bradycardia
  • CNS depression (coma)
  • respiratory depression
  • hypotension
  • hypothermia
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90
Q

hypothyroidism:

hashimotos thyroiditis

2 complications

4

1

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

coma/confusion

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91
Q

hypothyroidism:

Hashimotos thyroiditis

5 dx?

A
  1. High TSH
  2. low T3/T4
  3. increased triglycerides
  4. decreased HDL
  5. anti-thyroid antibodies
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92
Q

hypothyroidism:

hashimoto’s thyroiditis

what is the tx?

how is it dosed?

monitoring?

goal? time frame?

A

levothyroxine (synthetic T4)

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

GOAL: clinically euthyroid state (normal)

**sxs improve slowly over months**

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93
Q

hypothyroidism:

iatrogenic (we caused it)

tx?

A

radioative iodine for initial hyperthyroidism that leads to gland destruction

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94
Q

hypothyroidism:

congenital

what testing?

why is it key to identify?

A

screening of TSH in newborns should elimate disease

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

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95
Q

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

A

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

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96
Q

thyroiditis:

suppurative

what is this caused by?

3 sxs?

1 dx?

1 tx?

A

caused by gram positive bacteria

STAPH AUREUS

1. tender thyroid

  1. fever
  2. pharyngitis

DX:

fine needle aspiration

Tx:

drainage

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97
Q

thyroiditis:

De quervains aka granulomatous

what is this?

when is it most common?

when does it occur?

explain the progression?

2 dx?

  1. tx?
A

MOST COMMON CAUSE OF PAINFUL THYROID GLAND

***peaks in the summer….weird****

MC POST VRAL INFECTION

thyrotoxicosis initially presents followed by hypothyroidism and euthyroid within 12 months

DX:

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

Tx:

TOC=aspirin!!!

bb

ionated constrast agent

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98
Q

thyroiditis:

drug induced amiodarone

what does the medication contain?

what percent get this?

3 progression steps?

A

contains 37% iodine by weight or 75 mg per tablet

causes thyroid dysregulation in 20% of patients

Progression:

  1. can cause rise in T4 during first month of tx
  2. causes cellular resitsance to T4
  3. hypothyroid picture ensues with elevated TSH
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99
Q

thyroiditis:

fibrous thryoiditis (riedel)

who is this in?

what hapens to the thyroid?

key description

what happens to RAI?

ab?

1 dx method

1 tx method?

A

rarest form of thyroiditis, 80% are in females

formation of dense fibous tissue in the thyroid

causes

hard “woody” asymmetric thyroid feeling

the fibrosis can spread outside of the thyroid

radioactive iodine is decreased in involved areas of the thyroid

antibodies may be present in 45%

DX:

BIOPSY

tx:

tomoxifan

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100
Q

thyroid nodules

how are these found?

2 types? which MC?

why do we care?

2 dx methods? (interpreation)

TOC?

A

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***

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101
Q

toxic thyroid nodules

what do they present with?

number?

3 tx groups?

A

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

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102
Q

thyroid cancer

what are the two MC types?

appearance?

speed?

what to keep in mind about how it effects thyroid?

description of PE finding

A

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”

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103
Q

thyroid cancer

2 dx techniques?

2 tx?

what must you make sure to do?

A

DX:

1. fine needle aspiration

  1. 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***

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104
Q

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

A

childhood irradiation to head and neck increases risk 25x

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105
Q

parathyroid hormone

what is the main function?

what are the 4 actions it has on the body to achieve this?

A

regulates and maintains calcium homeostasis in the serum/body

  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
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106
Q

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

A

parathyroid hormone

  1. increases osteoclast and BONE resorbtion
  2. activates vitmin D (1,25-dihydroxy vD3, calcitriol)
  3. resportion of Ca at the DCT in kidney
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107
Q

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

A
  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
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108
Q

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

A
  1. PTH
  2. vitamin D
  3. calcitonin (opposit effect of PTH, used when the serum Ca levels are high)
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109
Q

calcium metabolism

what are the 3 forms it comes in?

what should you do if the total Ca appeares low?

A

50% ionized

40% protein bound

10 complexed with anions

**important to measure serum albumin and “correct” total Ca if albumin is low”

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110
Q

hyperparathyroidism

what are 2 most common causes?

what is hypersecreted?

2 hallmark lab findings?

what are 5 things this can lead to?

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

hypersecretion of PTH

HALLMARK:

1. elevated PTH

2. elevated serum total and ionized Ca

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

osteopenia

osteoporosis

pathologic fractures

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111
Q

hyperparathyroid:

how is this normally found?

pneumonic for sxs?

leads to what what 6 presentations?

A

often discovered as incidental lab finding

“moans, groans, stones, bones”

  1. skeletal: loss of cortical bone with bone pain and arthalgias
  2. nephrologic disorders:
    - decreased sensitivity to ADH with polyuria and poly dipsea
    - increased calcium stones from saturation
    - nephrosclerosis
    - renal failure
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112
Q

hyperparathyroidism:

5 lab findings

what is important to do?

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

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

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113
Q

hyperparathyroidism:

4 tx options

what are the indications for the last?

1

4

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

3 biphosphonate stop osteoclast bone resorption

  1. parathyroidectomy

symptomatic:

presence of bone or kidney disease

asymptomatic:

1. hypercalcemia with significant hypercalcuria

2. BD ovr 2 SD below normal

3. age less than 50

4. pregnancy

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114
Q

what is a complication from thyroidectomy used to tx hyperparathyroidism?

tx?

A

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

RX: calcium supplements

until parathyroid resumes function

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115
Q

what are five complications of hyperparathyroidism?

A
  1. pathologic fractures, esp in women
  2. urinary stones, obstruction, UTIs
  3. if Ca rises rapidly-CNS changes, renal failure
  4. PUD and pancreatitis form high CA levels
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116
Q

hypoparathyroidism

what are the 3 causes?

MC?

hallmark

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

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

HALLMARK:

low ionized Ca

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117
Q

hypoparathyroidism

6 acute sxs

5 chronic sxs

A

acute:

muscle cramps

irritability

tetany

seizures

paresthesias of hands and feet

carpopedal spasm

chronic:

  1. personaity changes
  2. decrease cognitive function
  3. cataract
  4. dry brittle nails
  5. chevosteks sign-twitching of facial nerve with tapping
  6. trousseaus sign-blow up BP cuff around arm and hand will twitch
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118
Q

hypoparathyroidism

4 lab findings

A

1. low serum total and ionized Ca

  1. elevated PO4
  2. decreased PTH
  3. prolonged QT and arrythmias
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119
Q

hypoparathyroidism tx:

1 acute

3 chronic

A

acute

IV CALCIUM GLUCONATE

do until tetant and other sxs resolve

chronic

1. oral calcium

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

3. magnesium supplement

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

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120
Q

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

A

cortex

glerulosa=aldosterone

fasiculata=cortisol

reticularis=androgens (sex hormones)

medula

catecholamines (NE, epi)

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121
Q

adrenal cortex:

aldosterone

what is this secreted by?

what is it regulated by?

what effect does it have?

A

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

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122
Q

adrenal cortex:

cortisol

what is this?

where is it released from?

what is it nessacary for?

what prompts its release?

A

major glucocorticoid secreted by the middle and inner adrenal cortex (FASICULATA)

NESSACARY FOR LIFE

secretion is regulated by ACTH secreted from antierior pituitary

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123
Q

adrenal cortex:

androgens

where is this released from?

what are 4 things that are released?

A

androgens more than estrogens

released from the reticularis (inner most)

testosterone

androstenedione

DHEA

estradiol

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124
Q

cortisol increases….5 things

A
  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**

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125
Q

steroid hormones:

cortisol

what are the 7 functions of this?

A
  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

  1. required for production of angiotensin II
  2. nessacary for normal boldily function
  3. lower serum calcium
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126
Q

steroid hormones:

cortisol

what are 4 things this is released in response to?

what is it nicknamed?

2 things it does

A

released in response to stress, trauma, infection, major surgery

nicknamed “the permissive hormone”: required for bodily function

supports normal circulatory function and hemodynamic stability

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127
Q

cushing syndrome

what are the 2 endogenous causes of cushings?

what is the 1 exogenous cause of cushings?

*which is most common*

A

endogenous

  1. over production
  2. tumors secreting cortisol or ACTH

exogenous

  1. glucocorticoid administration by medical providers

**MOST COMMON**

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128
Q

endogenous glucocorticoid excess

CUSHING SYNDROME

3 causes

CUSHING DISEASE

1 cause

A
  1. endogenous cushing syndrome

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!

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129
Q

exogenous glucocorticoid excess

what should you know about this?

what happens tha causes this?

what does it lead to?

what is developement dependent on?2

MC offender?

A

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!

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130
Q

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

A

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

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131
Q

cushings syndrome

5 main sxs

4

4

1

A
  1. central obesity
    - moon faces
    - central protuberance
    - buffalo hump

-supraclavicular fat

  1. catabolic effects
    a. thin skin with easy bruising and striae!
    b. THIN EXTREMITIES
    c. MUSCLE WASTING
    d. hirsuitism
  2. glucose intolerance/DM

increased thirst and polydipsia

  1. HTN
  2. osteopenia/osteoporosis
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132
Q

cushing syndrome

what are the 5 tests you want to do?

2 key?

A

1. elevated cortisol levels with loss of diurnal pattern (in day)

  1. dexamethasone suppression
  2. low ACTH level (since suppressed with high cortisol levels)
  3. hyperglycemia
  4. MRI of head, CT chest and abdomen
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133
Q

cushing syndrome

3 tx options?

A
  1. transphenodial resection of pituitary adenoma (increased ACTH)
  2. laproscopic resecection of adrenal tumor (increased cortisol)

**good prognosis if resection complete**

  1. ketoconazole and metryaprone used for METASTATIC adrenal cancer** by **inhibiting 11 B-hyrdoylase

(decreases cortisol synthesis)

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134
Q

what do you see morbiditiy with endogenous cushings disease? 5

A
  1. diabetes
  2. HTN

3 osteoporosis

  1. infections
  2. fractures
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135
Q

what is the only way you could call the disease “cushings” disease?

A

if the excess cortisol originated with pituitary increase in ACTH secretion

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136
Q

what is the most common overall cause of cushing syndrome?

A

iatrogenic

whe did it with high does corticosteroid drugs

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137
Q

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

A

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!!***

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138
Q

adrenal cortical insufficiency

3 causes of this

what do you find in each?

A
  1. primary adrenal insufficiency
    - ADDISONS

TB or autoimmune destruction of adrenal cortex

High levels of ACTH as results because trying to stimulate release

  1. secondary adrenal insufficiency

HYPOPITUITARISM

hypopituitarism (low levels of ACTH)

  1. acute adrenal crisis
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139
Q

what are 4 things that can cause corticoadrenal insufficiency?

0

0

2

2

A
  1. taking exogenous corticosteroids supresses the hypothalmic-pituitiary-adrenal axis
  2. requirement for corisol increases
  3. chronic adrenal insuffiiciency

addisons disease

billtareal adrenal hemmorage

  1. acute adrenal insufficiency

corticosteroid cessation

adrenal sugery/pituiary sugery

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140
Q

corticoadrenal insufficiency:

increased cortisol need

*can’t meet demand*

4 causes

A
  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
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141
Q

chronic corticoadrenal insufficiency:

2 causes

A
  1. addisons disease
  2. billateral adrenal hemmorage
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142
Q

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

A

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
  2. 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)
  3. orthostasis/low BP
  4. hyperpigmentation “Bronzed” skin
    - knuckles
    - palmar creases
    - elbows
    - knees

nailbeds

nipples

***reduction in axillary and pubic hair***

143
Q

chronic adrenal insufficiency:

pituitary failure/destruction

A

pituitary injury/failure causes a ACTH deficiency** which means the facicularis of the adrenal cortex **isn’t stimulated to make cortisol leadingto deficiency

144
Q

chronic adrenal insufficiency:

addisons disease

6 labs

1 diagnostics

A
  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

  1. high ACTH since trying to stimulate cortisol release

(only the adrenal are effected not pituitary)

  1. lymphocytosis
  2. hypoglycemia
  3. hyperkalemia
  4. hyponatremia
  5. abdominal CT-_small non-calcified adrenals_
145
Q

chronic adrenal insufficiency:

what is the tx option fo this?

what must you do for a patient in this situation and when is it indicated? 3

A
  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*****

146
Q

what are the 2 causes of acute adrenal insufficiency?

A
  1. corticosteroid use with increased bodily cortisol need or abruptly stopping medication without taper

**doens’t allow axis to recover**

  1. post adrenal or pituitary surgery
147
Q

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/

A

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!!***

148
Q

acute adrenal insufficiency

6 sxs?

2 key?

A
  1. headache
  2. N/V
  3. cyanosis
  4. dehydration
  5. hemodynamic collapse
  6. hypotension/shock unresponsive to iV fluids and pressors
149
Q

acute adrenal insufficiency:

what are the 2 txs for this?

A
  1. RAPID INFUSION OF ISOTONIC FLUIDS
    - normal saline
  • ringers lactate
    2. IV hydrocortisone Q 6 hours until stable

***oral hydrocortisone once stable***

150
Q

pheochromocytoma

what is this?

what does it increase?

4 sxs?

3 sxs pneumonic?

A

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
151
Q

pheochromocytoma

1 DX?

2 tx options (1 TOC)?

A

DX:

24 hour urine for catecholamines and emtanephedrines

TX:

1. TOC laproscopic removal of the tumor

  1. preoperative administration of alpha block and beta blockers can reduce complications
152
Q

pheochromocytoma

4 complications?

A
  1. HTN crisis

  1. stroke
  2. intracerebral bleed
  3. cardiomyopathy
153
Q

incidentaloma

what is this?

what do you need to determine? why?

what commonly goes here?

removal suggestions?

A

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
154
Q

osteoporosis

what is this?

what type of bone is lost more commonly?

percentages

A

MOST COMMON METABOLIC BONE DISEASE

comprimised bone strength leading to an increased risk for fracture

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

Net bone loss over 10 years:

trabecular 25-30% and MC!!

cortical 10-15%

155
Q

bone density

describe the progression throughout life? 5

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

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

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

156
Q

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

A
  1. sex hormone deficiency, esp post menopause

  1. excess glucocorticoids (cushings)
  2. hyperparathyroidism-increased PTH stimulates bone breakdown
  3. thyrotoxicosis-increased bone metbolism
  4. alcoholism
  5. anorexia
  6. vit d deficency
157
Q

opsteopenia definition

A

BMD 1-2.5 SD below peak bone density

158
Q

osteoporosis definition

A

BMD over 2.5 SD from normal

159
Q

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

A

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

160
Q

do men get osteoporosis?

how many?

A

YEP!!

1 out of 5 dxed people are men

hip fracture is a significant predictor for mortality!!

161
Q

what are 7 RF that increase your risk for osteoporosis?

A
  1. prior fractures
  2. FH of osteoporosis related fractures
  3. low body weight
  4. cigarette consumption
  5. excessive ETOH use
  6. chronic inflammation: RA
  7. patients at high risk for falls or frailty
162
Q

osteoporosis

what are 4 sxs you may see with this?

what is usually the inital presentation?

A

1. many asymptomatic till fracture (often spontaneous)

  1. ******may see back pain, decrease in height, or kyphosis***
  2. dietary calcium, vit D deficiency
163
Q

osteoporosis

4 texts for dx

1 TOC? interpretation

A
  1. DEXA is TOC!!!

includes spine, femur

T-score: SD away from young healthy adults

over 2.5=osteoporosis

over 2: osteopenia

  1. check calcium levers
  2. check vitamin D levels (25-hydroxy vit D)
  3. consider checking putuiary hormones when indicated
164
Q

who do you screen for osteoporosis in?

A
  1. early menopause

  1. RF

FH

malnourished

alcoholism

renal failure

  1. 65+
165
Q

can you reverse established osteoporosis?

A

no

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

166
Q

osteoporosis

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

A

1. bisphosphonates-DOC

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

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

inhibits osteoclasts

dental care important-jaw issues

very long half-life, in bone 10 years

  1. SERMS

serum estrogen receptor agonist/antagonist

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

  1. calcitonin
  2. Vitamin D; calcium

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

  1. PTH synthetic analog

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

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

6.estrogen replacement

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

167
Q

pagets disease

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?

A

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

168
Q

pagets disease

what are the 4 body systems that are effected? 7 sxs?

what is worst case senario?

A

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

169
Q

pagets disease

4 dx

4 tx

A

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
170
Q

what are the 6 hormones released from the anterior pituitary?

two from posterior pituitary?

A

anterior

GH

prolactin

ACTH

TSH

LH

FSH

posterior

ADH

oxytocin

171
Q

what are 8 possible cause sof hypopituitarism?

A
  1. genetic defects
  2. tumors
  3. autoimmune
  4. trauma
  5. irradiation
  6. stroke
  7. hemmorage
  8. peri-partum
172
Q

what is sheehan’s syndrome?

A

pituitary infarction from chock or hemmorage during/post delivery

173
Q

hypopituitarism:

decrease LH/FSH

what is this?

8 sxs?

dx?

A

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

174
Q

hypopituitarism:

Decreased TSH

what does this lead to?

6 sxs of this?

A

hypothyroidism

  1. decreases thyroid hormone
  2. weakness/cold intolerance
  3. constpation
  4. skin atrophy
  5. hair loss
  6. dyslipidemia
    dx: decreased free T4
175
Q

hypopituitarism:

ACTH decrease

what becomes decreased?

4 sxs?

A

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

176
Q

when suspecting hypopituitarism, what do you need to do?

A
  1. MRI: look for neoplasms

  1. if tumor: transphenoid pituitary surgery followed by endocrine replacement therapy
177
Q

diabetes insipidus

4 types

(2 for the last)

A
  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

178
Q

diabetes insupidus

1 dx?

tx if central?

tx if nephrogenic

A

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

179
Q

what are two complications that can come from diabetes insipidus?

A
  1. severe dehydration
  2. hypernatremia
180
Q

prolactin

what is its function?

what is the production pattern mediated by?

A

induces lactation during pregnancy (along with estrogen and progesterone)

control:

production is inhibitory mediated by dopamine

181
Q

hyperprolactinemia:

5 causes?

(3 main)

A
  1. pituitary microadenoma
  2. Drugs- SSRIs
  3. hypothyroidism
  4. renal failure
  5. cirrohosis
182
Q

hyperprolactinemia:

what do high prolacitn levels do?

4 overall sxs?

4 sxs in women?

3 sxs in men?

A

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

183
Q

hyperprolactinemia

3 DX

4 TX OPTIONS(when do you use each?)

A
  1. baseline labs including TSH, prolactin levels

prolactin level over 250 is high suspicious/diagnostic

  1. 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)

  1. SURGERY RESERVED FOR VISION CHANGES FROM COMPRESSION OF THE OPTIC NERVE CHIASM
184
Q

acromegaly/gigantism

what is in excess?

MC from what?

what alllows these effects to happen?

what else do these commonly secrete?

A

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***

185
Q

acromegaly/gigantism

difference between children and adults?

what caues each?

sxs in adults? 7

5 associated sxs that are common?

A

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)

186
Q

acromegaly/gigantism

4 dx?

A
  1. overnight fasting IGF-1 (5x normal) (alsomay see high prolactin if tumor secretes it or elevated glucose if progressed to diabetes)

  1. TSH (of low suggestes additional pituitary pathology
  2. glucose challenge test post fast-suppresses GH levels to confirm dx

4. MRI to find tumor

187
Q

acromegaly/gigantism

2 tx

A
  1. transphenoidal microsurgery toc

**keep in mind this can cause permanent hypopituiarism and may need replacement tx**

  1. octreotide-samatostatin (shrinks tumor and suppres GH secretion)

***used in patients who continue to have excessive GH release post op**

188
Q

pituitary dwarfism

what are the 3 types of this?

what does each one lack?

middle: sxs6
last: who mos common in? 3

2 measureable levels

A

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

189
Q

what is psychosocial dwarfism?

3 sxs?

who does it occur in?

A

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

190
Q

dwarfism

(green book)

what is the most common type?

occurs from?

10 sxs?

tx

A

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

191
Q

achondroplasia:

what is the gene that is mutated?

A

FGFR3

192
Q

pituitary dwarfism can present with what two clues?

A

micropenis

hypoglycemia

193
Q

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

A

pituitary adenoma

lactorophic is the most common type of pituitary adenoma and secrete prolactin

194
Q

too little hormone:

3 general causes

A
  1. congenital defects
  2. damage from disease
  3. atrophy from aging or drugs
195
Q

too much hormone:

3 general causes

A
  1. excess stimulation of the gland
  2. hormone producing tumor
  3. administration of exogenous hormone
196
Q

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

A

remember it

197
Q

GH → ________→ _______

A

GH → stimulates the liver → IGF-1

198
Q

TSH → ______→ ________

A

TSH → stimulates the thyroid → thyroid hormones

199
Q

ACTH →_________→ __________

A

ACTH → stimulates adrenal cortex → cortisol

200
Q

FSH and LH → ________ → _________

A

FSH and LH → stimulate gonads → sex hormones

201
Q

Prolactin → _______→ _________

A

Prolactin → stimulates breast → milk production

202
Q

where does a primary hormone disorder occur?

A

at the level of the periphreal gland

203
Q

where does a secondary hormone disorder occur?

A

at the level of the anterior pituitary

204
Q

where does a tertiary hormone abnormality occur?

A

at the level of the hypothalmus

205
Q

what is another name for growth hormone?

A

somatotropin

THEY ARE THE SAME THING!!

206
Q

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

A
  1. growth promoting effects

stimulates the liver to produce IGF-1** with increases **protein synthesis and growth** in the_:_**

1. bone and cartilate

2. body organs

3. muscle

  1. anti-insulin effects

adipose tissue: increased lipolysis and decreased adipositiy

carbohydrate metabolism: increases blood glucose

207
Q

growth hormone:

stimulated by?4

inhibited by?4

A

stimulated by:

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

208
Q

what do follicular cells release?

A

THYROID HORMONES T3 AND T4

209
Q

PARATHYROID HORMONE

what is the overall effect?

2 ways it accomplishes this

A

INCREASES BLOOD CA LEVELS

1. STIMULATES RELEASE OF CA FROM BONE (RESORPTION)

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

210
Q

calcitonin

what secretes this?

overall funciton?

3 ways it accomplishes this?

A

secreted by the thyroid c-cells

**decreases blood Ca levels**

1. inhibits intestinal Ca absorption

2. inhibits osteoclast and stimulates osteoblast activity

3. inhibits renal tubular reabsorption of Ca

211
Q

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

A

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
  3. thyroglobulin becomes iodinated and formes MIT and DIT
  4. MIT and DIT form different combinations

MIT + DIT= T3 (triiodothyronine)

DIT+DIT=T4 (thyroxine)

  1. secreted into the blood, mostly bound to thyroixine binding globulin (TBG), to travelto target cell and promote mRNA to increase metabolic rate
212
Q

is T4 active?

A

nope, it is converted to T3

***T4 is secreted more than T3****

213
Q

Lack of what component can cause thyroid insufficiency?

A

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

214
Q

cortisole is a ______ that effects ______

A

glucocorticoid

effects METABOLISM

215
Q

aldosterone is a ______ that effects _______

A

mineralcorticoid that effects Na absorption and K excretion

216
Q

pharmacokinetics

A

what the body does to the drug

217
Q

pharmachodynamics

A

what the drug does to the body

218
Q

how many people world wide are obese?

A

1.9 billion

219
Q

how many people have diabetes and prediabetes?

A

diabetes: 25.8 milllion
prediabetes: 57 million

220
Q

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

A
  1. african americans

2. american indians

3. hyspanics

4. alaska natives

221
Q

what are the percent prevalence of T1DM and T2DM?

A

T1DM=10%

T2DM=90%

222
Q

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

A

insulin deficiency

hyperglycemia

dyslipidemia

metabolic wasting

ketoacidosis

223
Q

what are 4 brief features of T2DM?

A

hypoinsulinemia

hyperglycemia

dyslipidemia

obestiy often

224
Q

what do most of the complications from diabetes stem from?

A

micro and macrovascular disease from uncontrolled sugars

225
Q

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?

A
  1. amylin via beta cells

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

226
Q

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

A

promote insulin release

aka

“incretin effect”

227
Q

explain how glucose stimulates the beta pancreatic cell?

6 steps

A
  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 influx of Ca causes INSULIN RELEASE

BOOM!

228
Q

anabolic effects:

insulin/glucose on muscle

3

A
  1. increase glucose uptake

2. increase glycogen storage

3. increased protein synthesis

229
Q

anabolic effects:

glucose/insulin on fat

3

A

1. increased glucose intake

2. triglyceride synthesis

3. decreased lipolysis

230
Q

anabolic effects:

glucose/insulin on liver

A

1. increase glycogen synthesis

2. increase triglyceride synthesis

3. decrease glucose production

231
Q

what is the clinical importance of the insulin structure?

A

contrains C peptide

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

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

232
Q

when insulin is released there is ______ nervous system activity

A

when insulin is released there is parasympathetic nervous system activity

233
Q

what are 5 overall broad functions of insulin secretion?

A
  1. decrease blood glucose
  2. decrease blood fatty acid
  3. decrease blood amino acid
  4. increase protein syntheisi
  5. increase fuel storage
234
Q

anabolic means

A

building things up

235
Q

anti-catbolic means…

A

preventing from being broken down

236
Q

LIVER

1 anabolic

3 anti-catabolic

A

anabolic:

Stimulation of glycogen synthesis

catabolic

iinhibition of:

glycogenolysis

gluconeogensis

ketogenesisi

237
Q

glycogenolysis

A

breakdown of glycogen to glucose

(occurs at liver, and less commonly muscles)

238
Q

gluconeogensis

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

A

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

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

239
Q

ADIPOSE TISSUE

3 anabolic

1 anit- catabolic

A

anabolic

increase glucose uptake

increase triglyceride synthesis

increase fatty acid uptake and synthesis

catabolic

inhibition of lipolysis

240
Q

muscle tissue

4 anabolic

2 anticatabolic

A

anabolic

1. increase glucose uptake

2. increase glycogen storage

3. increase protein synthesis

4. increase amino acid uptake

anticatbolic

1. inhibition of proteolysis

2. decrease amino acid output (wants to build)

241
Q

what cells secrete glucagon?

A

alpha cells of the pancreas when blood glucose was low

242
Q

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

A

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

**negative feedback once BS increase**

243
Q

glucagon

A

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

244
Q

amylin

3 functions

A
  1. slows glucose absorption in the duodenum

  1. supresses glucagon secretion
  2. metabolizes carbs
245
Q

somatostatin

(not somatoropin=GH)

2 functions

A
  1. decreased GI activity
  2. suppresses glucagon and insulin secretion
246
Q

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

A
  1. epi
  2. glucagon
  3. cortisol
  4. GH

**all of these work under sympathetic control and want the BS to increase**

247
Q

counterregulatory:

epinephrine

3 effects?

how long does it take?

A

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(**

248
Q

counterregulatory:

glucagon

3 functions?

how long

A

increase hepatic glucose output

lipolysis

ketones

***intermediate acting***

249
Q

counterregulatory:

cortisol

3 functions

time?

A
  1. increase gluconeogensis
  2. decrease muscle glucose uptake and glycogensis
  3. increase lipolysis

***takes hours***

250
Q

counter regulatory:

GH

2 fxns

A
  1. increase hepatic glucose output
  2. decrease muscle glycogenesis
251
Q

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

A

GLUT4 translocation

252
Q

causes of diabetes:

type 1:

type 2:

gestational

Type 4:

A

type 1: autoimmune

type 2: hereditary-offspring

gestational

Type 4: drug induced

253
Q

who do you typically find diabetic ketoacidosis in?

A

TYPE 1

(can be in late stage 2)

254
Q

who do you typically find acute hypoglycemia in?

A

type 1 post insulin without eating

255
Q

who do you typically find hyperglycemia in?

A

type 1 and type 2

256
Q

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

A

HYPOglycemia!!

257
Q

metabolic syndrome

5 risk factors

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

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

258
Q

Metabolic Syndrome

what is this called?

what does it indicated for the patient?

what type of diabetes?

A

aka insulin resistance; syndrome X

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

associated with T2DM

259
Q

metabolic syndrome:

waist circumference RF

A

men over 102

women over 88

260
Q

metabolic syndrome:

triglycerides RF

A

over 150

261
Q

metabolic syndrome:

HDL RF

A

men less than 40

women less than 50

262
Q

metabolic syndrome:

BP RF

A

over 130 SBP

over 85 DBP

263
Q

metabolic syndrome:

fasting glucose RF

A

over 100

264
Q

visceral fat is ____

subcutaneous fat ____

A

visceral fat is BAD

subcutaneous fat GOOD

265
Q

T2DM:

Visceral Fat

what does it do? (hence why bad)

4 steps that make this bad!

A

bad because it secretes adipokines/cytokines

theses increase insulin resistance

insulin resistance can also increase DYSLIPDEMIAS

dyslipidemias lead to

MI, STROKE, HYPERTENSION

266
Q

what is the goal preprandial glucose?

post prandial?

A

pre: 80-130
post: less than 180

267
Q

what is the goal BP for a diabetic?

A

less than 140/90

268
Q

what is the goal of LDL for diabetics?

A

less than 100

269
Q

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

4

A

4 qualifications:

1. clinical athlerosclerotic CVD

2. DM type 1 or type 2 and age 40-75 and LDL 70-190

if 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

270
Q

sulfonylureas

what are they ment to work like?

what do they do?

what are 3 things they cause as SE?

A

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

since made to act like insulin can cause:

hypoglycemia

hyperinsulinemia

increased body weight

271
Q

insulin secretagogues

sulfonylureas

what part do they work on?

what type of diabetic do you use this in

what are the two drugs name

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

A

THIS IS THE SECOND DRUG OF CHOISE AFTER METFORMIN

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

T2DM, in adjunct to metformin

glypizide, glyburide

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

272
Q

biguandines-Metformin

what to keep in mind?

4 things that it does in the body?

MC SE?

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

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

A

first drug you give for T2DM

1. decreases hepatic glucose production

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

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

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

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

273
Q

thaiazolidinediones

what do they do?

1 drug we use?

2 problems with them?

avoid in? 1

**remember**

A

improves insulin sensitivity and signaling

plioglitazone

problems:

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

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

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

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

274
Q

alphacglucosisase inhibitors

what doe these do?

what do they cause as SE? why?

when is it used?

A

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

275
Q

pramlinitide

what is this?

when is it normally secreted?

3 functions?

what does it improve?

which diabetes do you use it in?

A

synthetic analogue of amylin

amylin is normally co-secrete with insulin and

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

**modulates post prandial glucose**

type 1 and type 2

276
Q

where are the most reliable injection sites for pramlintide?

A

abdomen and thigh

277
Q

where is the most reliable injection site for insulin?

A

thigh and abdomen

278
Q

GLP-1 receptor agonist

what is this?

how is it given?

what is unique that this is thought to do?

4 things it stimualtes

3 things it decreases

A

exanatide, liraglutide

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

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

stimulates:

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

decreases:

  1. decreased gastric empyting
  2. decrease appetite
  3. decrease glucagon release
279
Q

DDP-4 inhibitors

name of the drug?

what does ths drug do?

why is complance better?

how is this drug used?

A

sitagliptin

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

(stimulates insulin, inhibits glucagon)

overall, this drug decreases blood sugar

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

280
Q

SGLT2 inhibitors

what do they do?

what is the drug name?

because of this what are you at increased risk for?

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

WHAT IS THERE A WARNING ABOUT?

A

NEWEST CLASS

canaglifozin

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

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

UTIS since increasing sugar excretion

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

281
Q

what is more efffective than any oral antidiabetic drug?

A

exercise!!!

282
Q

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

A
  1. insulin
  2. repaglinide (increase insulin secertion) ***causes less weight gain than the others****
  3. sulfonyureas (increase insulin secretion)
283
Q

what are the ABCDEs of diabetes?

A

A=aspirin reduce platelets

B=bloood pressure ACE

C=cholesterol

D=diet, diabetes control

E=exercise, improves glucose and lipids

284
Q

why do we care about foods that cause inflammation? 4

3 exampls

A

because they increase risk of CV disease, insulin resistance, hypertension, and central adiposity

processed foods

white foods

simple sugars

285
Q

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

A
  1. medditerean diet (breads, fibers, fruits and veggies)

  1. fish oils- 3 omega fatty acids
  2. red juices (blueberries, back tea, nuts)
  3. modest alcohol consumption
  4. ACE
  5. STATINS
  6. ASA
286
Q

stages of resistance for Type 2 diabetes

4 stages

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

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

  1. impaired glucose tolerance

hyperglycemia/hyperinsulinemia

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

  1. early diabetes-B cell burn out

hyperglycemia/hypoinsulemia

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

4. late diabetes

hyperglycemia/hypoinsulemia

BETA CELLS BURN OUT!!

287
Q

what is insulin resistance?

A

unknown mechanism

suspected etiology:

feuled by proinflammatory respons from cytokines and adipokines

288
Q

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

A

25-50 mg

289
Q

what are 3 microvascular long term complications of diabetes?

1 macrovacular long term complication of diabetes?

A

microvascular:

  1. retinopathy
  2. nephropathy
  3. neuropathy

macrovascular:

  1. athlerosclerosis

(CHD, CVD/stroke, PAD)

290
Q

diabetes complications:

retinopathy

what are the 2 types?

what is each characterized by?

what is key to prevent this?

A

Non-proliferative:

microaneurysms, hemorrhases, exudates, retinal edema

Proliferative:

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

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

worse with HTN and smoking

291
Q

how often do diabetics need eye exams?

A

annually

292
Q

diabetic complications:

nephropathy

what are 2 things that cause this?

who is this worse in?

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

3 tx options?

A

developes from chronic hyperglycemia and uncontrolled HTN

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

worse in smokers!!

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

RX:

1. tight glycemic control

2. tight BP controll less than 140/90

3. early institution of ACEI

293
Q

how do you check for nephropathy in diabetic?

3 ranges

A

want to check MICROALBUMINURIA 30-300

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

normal less than 30

microalbiumemia: 30-300

albumenmia: over 300

294
Q

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

A
  1. dialysis
  2. transplantation from living related donor is preferable to dialysis
295
Q

ACE initiation in diabetics

who do you start in and when?

what are 4 things it prevents the progression of?

A

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

EVEN IF THE BP IS NORMAL!!!!!

decreases risk for

glomerulrar hemodynamics

death

dialysis

transplantation

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

296
Q

diabetic complications: athlerosclerosis

what are 5 things this can lead to?

what is diabetes a equivalent to?

what should you consider putting them on?

A

CHD

MI

CHF

PVD

Suddent death

diabetes is a coronary risk equivalent

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

297
Q

diabetes is a…

A

CVD risk factor equvalent!!

298
Q

Periphreal vascular disease in diabetics

what vessels effected?

lleads to 4 things?

4 tx options?

A

Large and small vessel disease

leads to:

claudications

ulcerations

amputations

RX:

regular foot exams

tight glycemic contro.

podiatric care

STOP SMOKING

299
Q

diabetic complications:

neuropathy

3 presentations?

3 tx options for medication?

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

TX

  1. gabapentin (neurontin)
  2. duloxetine (cymbalta)
  3. pregabalin (lyrica)
300
Q

diabetes complications:

autonomic neuropathy

5 presentations

A
  1. gastroparesis

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

tx: metoclopropramide

  1. diarreah/constapation
  2. orthostatic hypotension

fludrocortisone and elastic stockings

  1. impotence, sexual dysfunction
  2. decreased bladded sensation
301
Q

diabetic ketoacidosis

what is this?

who does it occur in?

why?

4 potenital causes?

2 critical things it can lead to?

A

lifethreatenig emergency

TYPICALLY TYPE 1 DM

need for insulin increases from trigger

triggers:

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

can progress to coma and death

302
Q

diabetic ketoacidosis

5 general sxs?

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

A

polyuria

abominal pain

nausea

vomiting

fatigue

PROGRESSIVE DKA:

  1. decrease mentation

2. stupor

3. coma

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

form of hyperventilation to blow off the CO2

303
Q

diabetic ketoacidosis pathophysiology

4 steps

results in?

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

results in metabolic acidosis with increase anion gap

304
Q

diabetic ketoacidosis:

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

A

production of FFA and conversion to

1. acetoacetic (ketoacid)

and

2. B-hydroxybutyric acid

305
Q

diabetic ketoacidosis:

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

A
  1. osmotic diuresis
  2. volume and electrolyte loss/imbalance
306
Q

explain why diabetic ketoacidosis is INCREASED ANION GAP ACIDOSIS?

A

the anion gap equation is

Na-(Cl+HCO3)

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

Henced increases metabolic acidosis

307
Q

diabetic ketoacidosis:

7 lab findings

A
  1. pH less that 7.3

  1. low HCO3 with increased anion gap
  2. increased urine osmolarity
  3. BS usually over 300
  4. elevated amylase
  5. elevated WBC over 10,000 without infxns
  6. initial serum K often high but total body ky low from fluid and electrolyte losses
308
Q

diabetic ketoacidosis tx:

4 tx options

A
  1. estalish flowsheet ot measure all levels

  1. insulin regular

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

4. replace K by KCL IB

309
Q

hyperglycemic nonketotic hyperosmolar state

which diabetics is this in?

what is the patho of this?

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

A

type 2 DM

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

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

310
Q

hyperglycemic hyperosmolar nonketoic acidosis:

what happens here that complicates thsi?

2 tx options?

A

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

TX:

  1. 0.9% normal saline
  2. insulin
311
Q

what is the mortality seen with hyperglycemic hyperosmolar nonketotic acidosis?

A

50% mortality

312
Q

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

A

infection most common

313
Q

what is the differences between DKA and HHNK?

A

DKA=TYPE 1, presensce of ketones

HHNK= TYPE 2, way higher BS

314
Q

Type 1 DM

what is your typical patient? 2

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

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

A

typical patient:

non-obese and insulin dependent

primarily autoimmune

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

catabolic disorder where absence of insulin leads to:

1. hypergylcemia

2. fat and protein breakdown lead to

KETOACIDOSIS

315
Q

type 1 DM

patho

what promps this start of this?

5 triggers

A

infectious or toxic insult

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

triggers:

viruses

mumps

coxsackie

rubella

toxic chemicals

316
Q

how many diabetic patients are there in the uS?

A

over 25 million

317
Q

what four populations hae increased predisposition to DM?

A

african americans

hispanics

native americans

318
Q

type 1 DM treatment

what is the medication you tx with?

combination and percent of diffreent insulins? 2

A

tx: INSULIN only!!

SMBG 4-6x daily

combination of:

basal insulin= 40-50% intermediate/long acting

(NpH, glargine, detemir)

prandial needs=40-50%

short term or rapid (regular or INSULIN LISPRO)

**alernative is insulin pump**

319
Q

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

A

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

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

320
Q

what is the total insulin need for someone with T1DM?

A

0.4-1 Units/kg

321
Q

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

A

hypoglycemia

322
Q

hypoglycemia

what are two drugs that are known for doing this?

5 sxs?

what sugar correlates with this?

A

most common complication seen with insulin or sulfonylurea

SXS:

1. sweating

2. tachycardia

3. hunger

4. tremulousness

5. nausea

less than 50 BS

323
Q

what drug can mask hypoglycemia because it produces similar sxs

A

non selective beta blockers

324
Q

Type 2 DM

characteristics of patient? 4

what is the goal? how to accomplish? 2

2 first line tx options?

A

typical patient:

non-insulin dependent

obese

increase triglycerides

insulin resistance

MOST IMPORTANT TO REGAIN INSULIN SENSITIVITY

1. WEIGHT REDUCTION

2. DIET AND EXERCISE

TX:

  1. LIFESTYLE THEN
  2. METFORMIN
325
Q

type 2 DM prevents….

A

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

326
Q

who does T2DM occur in?

A

obese 70%

non obese 30%

327
Q

explain the role of central/visceral obesity in T2DM?

A

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

328
Q

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

A

gluconeogensisi

329
Q

glucotoxicity

what does this come from?

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

A

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

worsens insulin resistance and destroys the B cell function

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

330
Q

what is nessacary to preserve B cell function?

A

control BS

331
Q

how does diet and exercise improve insulin resistance?

A

exercise increases blood flow to the muscles

increases muscle mass and decreases muscle fat storage

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

332
Q

Type 2 DM

7 sxs associated with this?

A
  1. often no sxs early
  2. polyuria
  3. thirst
  4. skin infections
  5. vulvovaginits
  6. abnormal fat distribution
  7. hyperglycemia
333
Q

diabetic dyslipidemia is defined as what?

A

high triglycerides 300-400

low HDL less than 30

334
Q

glycated HB (A1c)

what does this show you?

how often should you check in diabetic?

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

what is the goal for diabetic?

A

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

normal= 4-6%

prediabetes= 5.7-6.4%

diabetes=over 6.4%

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

335
Q

what are the values for A1c?

normal

prediabetes

diabetes

A

normal= 4-6%

prediabetes= 5.7-6.4%

diabetes=over 6.4%

336
Q

self monitoring blood sugar

A

standard of care for all diabetics

requires a lot of education about meter, when to take it, cost, everything!

337
Q

what are the four qualifications/options for diabetes dx?

A
  1. FBS over 126 (normal under 100)

  1. A1C over 6.5%
  2. 2 hr GTT over 200
  3. Random BS over 200 (need fasting to confirm but highly likely)
338
Q

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

A
  1. FBS 100-125

  1. 2 hr GTT BS of 140-199
  2. A1c 5.7-6.4%
339
Q

what are the goal levels for:

preprandial

postprandial

bedtime

a1c

A

preprandial=90-130

postprandial=less than 180

bedtime=100-140

a1c=less than 7

340
Q

what are the goal target percentages for diabetics:

protein

fat

carbohydrates

fiber

A

protein 10-35%

fat 25-35%

carbohydrates 45-65%

fiber 20-35

341
Q

what is the 3 tx algorithm used fot T2DM?

A

Step 1 tre​at at dx: lifestyle and metformin

step 2:

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

ORRRR

metformin + sulfonylure

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

342
Q

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

A
  1. poultry
  2. fish
  3. artificial sweetners aspartame and saccharin
343
Q

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

A
  1. NPH/reg in 70:30 mixture

  1. insulin glargine
344
Q

what do you need to consider when dosing insulin?

A

need

diet

activity

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

345
Q

what is the goal of txing with insulin? 2

A

tight control to prevent hypoglycemia

prevent long term complications

346
Q

rapid acting insulin

what is the name?

onset?

peak?

what is it ideal for?

how can it be used?

A

Lispro

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

ideal for pre-meal and rapidly deals with glucose load

**can be used with insulin pump**

347
Q

regular insulin

how long does it take?

onset?

peak?

how is it delivered? unique fact?

A

short acting

onset: 30-60 mins
duration: 6-8

SC/IM/IV

only IV so used to tx diabetic ketoacidosis

348
Q

neutral protamine

how long does this last?

onset?

duration?

A

intermediate acting

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

349
Q

insulin glargine

how long does this last?

how long is the coverage?

when is it dosed?

why is this good?

what can’ you do?

A

long acting insulin

24 hour coverage with steady state insulin levels

dosed at bedtime

**causes less hypo/hyperglycemia**

**can’t mix with other insulins**

350
Q

insulin mixes

what is this a mix of?

who is it good for?

what does it allow for?

A

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

351
Q

insulin pumps

what insulin can you use it with?

how does it work?

1 benefit?

3 drawbacks?

A

can be used with lispro or regular

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

Benefits: tight glycemia control

drawbacks: cost, skin infections, and DKA

352
Q

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

A
353
Q

why is moderate exercise essential?

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

Module 10: Mali: Endocrine (5 decks)

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