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Endocrine Flashcards

1
Q

Where does the thyroid gland develop?

A

thyroid diverticulum arises from floor of primitive pharynx, descending into neck. It is connected to tongue by thyroglossal duct which norally disappears but may persist as pyramidal lobe of thyroid.

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2
Q

What is the normal remnant of the thyroglossal duct?

A

foramen cecum

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3
Q

What is the most common site of ectopic thyroid tissue?

A

tongue - lingual thyroid

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4
Q

How does a thyroglossal duct look like?

A

an anterior midline neck mass that MOVES w/ swallowing. Make sure you remove it b/c it can get infected

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5
Q

Tell me about the fetal adrenal gland?

A
  • consists of an outer adult zone and inner active fetal zone.
  • Adult zone is dormant during early fetal life but begins to secrete cortisol late in gestation.
  • Cortisol secretion is controlled by ACTH and CRH from fetal pituitary and placenta.
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6
Q

Why is cortisol necessary for the fetus?

A
  • responsible for fetal lung maturation and surfactant production
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7
Q

What is the embryonic derivative of the adrenal cortex and medullar?

A
  • cortex = mesdoerm

- medulla = neural crest

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8
Q

What is produced in the adrenal medulla?

A

it’s stimulated by pregangionlic sympathetic fibers to make catecholamines via chromaffin cells

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9
Q

What is produces in the adrenal cortex?

A
  1. Renin-Angiotensin activates Zone Glomerulosa to make Aldosterone
  2. ACTH, hypothalamic CRH stimulates Zone Fasciculata to make cortisol and some sex hormone
  3. ACTH, hypothalamic CRH stimulates Zona Reticularis to make sex hormones
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10
Q

How do the adrenal glands drain?

A
  1. Left adrenal –> left adrenal vein – > left renal vein –> IVC
  2. Right adrenal –> right adrenal vein –> IVC
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11
Q

What is the most common tumor of the adrenal medullar for an adult?

A

pheochromcytoma

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12
Q

What is the most common tumor of the adrenal medulla in kids?

A

neuroblastoma

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13
Q

What is stored in the posterior pituitary? (neurohypophysis)

A
  • secretes ADH and oxytocin

- remember derived from neuroectoderm

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14
Q

What is released from the anterior pituitary? (adenohypophysis)

A

Secretes FSH, LH, ACTH, TSH, prolactin, GH, MSH

- Remember derived from oral ectoderm (Rathke’s pouch)

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15
Q

There are some hormones who have alpha and beta subunits. What are they and what is the importance of the subunits?

A
  • FSH, LH, TSH, bhCG
  • all the alpha subunits are the same
  • the Beta subunits determines hormone specificity
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16
Q

What are the acidophilic hormones?

A

GH, prolactin

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17
Q

What are the basophilic hormones?

A

FSH, LH, ACTH, TSH

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18
Q

What makes up the endocrine pancreas?

A
  1. alpha cells- make glucagon
  2. beta cells- make insulin
  3. delta cells- make somatostatin
    - islets of langerhans are made up of peripheral alpha cells w/ central beta cells and interspersed delta cells
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19
Q

What are all the hormones involved in the HP and HPA axis?

A
  1. TRH –> TSH and prolactin
  2. Dopamine inhibits prolactin
  3. CRH –> ACTH, MSH, beta-endorphin
  4. GHRH –> GH
  5. Somatostatin inhibits GH, TSH
  6. GnRH –> FSH, LH
  7. Prolactin inhibits GnRH
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20
Q

What is the precursor molecule for ACTH?

A

-POMC which also contains sequences for other hormonal peptides. eg MSH and beta-endorphin

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21
Q

Where is somatostatin made?

A

throughout the GI Tract notably by delta cells in pancreas and GI mucosa
- also made by nervous system

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22
Q

What effect do somatostatin have?

A
  1. decrease endocrine and exocrine secretions
  2. decrease splanchnic blood flow
  3. decrease GI motility and gallbladder contraction
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23
Q

What are the clinical uses of somatostatin? eg octreotide

A
  1. pituitary excess - acromegaly, thyroitropinoma, ACTH secreting tumor
  2. GI endocrine excess: ZE syndrome, carcinoid syndrome, VIPoma, glucagonoma, insulinoma
  3. Need to decrease splanchnic circulation : portal HTN and bleeding peptic ulcers, esophageal varicies
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24
Q

What is the function of prolactin?

A
  1. stimulates milk production in breast

2. inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release

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25
Q

How is prolactin regulated?

A
  1. tonically inhibited by dopamine
  2. prolactin in turn inhibits its own secretion by increasing dopamine synthesis and secretion
  3. TRH increases prolactin secretion
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26
Q

What can be used to treat prolactinomas?

A

dopamine agonists - bromocriptine b/c they inhibit prolactin secretion

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27
Q

What can stimulate prolactin secretion?

A

Dopamine antagonists - most antipsychotics; and estrogens (OCPs, pregnancy)

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28
Q

What happens to females and males when they have hyperprolactinemia?

A
  1. Premenopausal W - hypogonadism, infertility, oligo/amenorrhea, rarely galactorrhea
  2. Postmenopausal W - non since they are already hypogonadal
  3. Male - hypogonadism (low T) = decreased libido, impotence, infertility, gynecomastia, rarely galactorrhea
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29
Q

What is the function of GH?

A

Stimulates linear growth and muscle mass through IGF1/somatomedian secretion. Increases insulin resistance (diabetogenic)

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30
Q

How is GH regulated?

A
  • Released in pulses in response to GHRH
  • secretion increases during exercise and sleep
  • Secretion inhibited glucose and somatostatin
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31
Q

What are all the steps to make aldosterone?

A 
Cholesterol to Pregnenolone (Desmolase)
Preg to Progesterone (3BHSDH)
Prog to  11DOC (21hydroxylase)
11DOC to corticosterone (11Bhydroxylase)
Corticosterone to Also (Aldo synthase)
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32
Q

What are the steps to make Corisol?

A

Cholesterol to Preg (desmolase)

  • essentially you NEED 17 alpha hydroxylase and 3BHSDH to make 17hydroxyprogresterone
  • 17 hydroxyprog to 11deoxycortisol (21OHlase)
  • 11 deoxycortisol to cortisol (11BOHlase)
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33
Q

What are the steps to make Testosterone?

A

need 17 hydryoxylase and 3Bhydroxysteroid DH

  • to get to DHT you need 5 Alpha reductase
  • Use aromatase to make Estrone and estradiol
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34
Q

What happens w/ a 17 alpha hydroxylase deficiency?

A
  • increased mineralcorticoids
  • HTN, hypokalemia
    XY - decreased DHT = pseudohermaphroditism (variable, ambiguous genitalia, undescended testes)
    XX - externally phenotypic female w/ normal internal sex organs, lacks primary sex characteristics
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35
Q

What happens w/ a 21 hydroxylase deficiency?

A
  • increased sex hormones
  • hypotension, hyperkalemia, increased renin activity, volume depletion
  • masculinization leading to pseudohermaphroditism in females
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36
Q

What happens w/ a 11 B hydroxylase deficiency?

A
  • increased sex hormones
  • decreased aldosterone
  • increased 11 DOC
    HTN and masculinization
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37
Q

What are all of the congenital bilateral adrenal hyperplasia characterized by?

A

enlargement of BOTH adrenal glands due to increased ACTH stimulation b/c of decreased cortisol

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38
Q

What are all the functions of cortisol?

A
  1. Maintains blood pressure - upregulates alpha1 receptors and increases sensitivity to NE and E
  2. decreases bone formation
  3. Anti-inflammatory/immunosuppresives
  4. Increases insulin resistance (diabetogenic)
  5. Increases gluconeogenesis, lipolysis, proteolysis - catabolic hormone
  6. inhibits fibroblasts (causes striae) - decreases collagen synthesis
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39
Q

What are all the anti-inflammatory/immunosuppresive effects of cortisol?

A
  1. inhibits production of LT and PGs
  2. inhibits leukocyte adhesion –> neutrophilia
  3. blocks histamine release from mast cells
  4. reduces esoinophils
  5. blocks IL 2 production
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40
Q

How is cortisol regulated?

A
  1. CRH stimulates ACTH causing cortisol production in adrenal zona fasciculata.
  2. excess cortisol decreases CRH, ACTH, and cortisol secretion
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41
Q

What are the side effects for excess cortisol?

A
  1. thinning of skin
  2. easy bruisability
  3. osteoporosis
  4. adrenal cortical atrophy
  5. peptic ulcers
  6. diabetes
  7. immunosuppression
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42
Q

What are the effects of stress?

A
  1. gluconeogenesis
  2. increased lipolysis - increased FFA
  3. immunosuppression
  4. higher cortisol levels, more catecholamines
  5. affects water absorption
  6. proteolysis = poor muscle tone
  7. more frequent bowel movements
  8. viscous secretions
  9. Sympathetics!!!!
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43
Q

What hormones use the Gs pathway?

A

FSH, LH, ACTH, TSH, CRH, hCG, ADH (v2), MSH, PTH, calcitonin, GHRH, glucagon
- FLAT ChAMP

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44
Q

What hormones use the cGMP pathway?

A

NO and ANP

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45
Q

What hormones use the IP3 pathway?

A

GnRH, GHRH, oxytocin, ADH (V1), TRH, Angiotensin II, gastrin
- GGOAT

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46
Q

What hormones use steroid receptors?

A

Vit D, Estrogen, T, T3/T4, Cortisol, Aldosterone, Progesterone

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47
Q

What hormones use the intrinsic tyrosine kinase receptor?

A

Insulin, IGF1, FGF, PDGF, EGF

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48
Q

What hormones use the receptor associated tyrosine kinase?

A

Prolactin, Immunomodulators (eg cytokines IL2/6/8)

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49
Q

What is the signaling pathway of steroid hormones?

A

Steroid hormones are lipophilic and therefore must circulate bound to specific binding globulins which increase their solubility.

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50
Q

What happens to T when SHBG increases in men?

A

lowers free T

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51
Q

What happens to W when SHBG decreases?

A

raises free T leading to hirsutism

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52
Q

What happens to SHBG during pregnancy?

A

increases

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53
Q

What is the hormone responsible for controlling the body’s metabolic rate?

A

TH

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54
Q

What is the source of TH?

A

follicles of thyroid. Most T3 formed in target tissues

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55
Q

What is the function of TH?

A
  1. bone growth (synergism w/ GH)
  2. CNS maturation
  3. INcrease B1 receeptors in heart = increased CO, HR, SV, contractility
  4. Increased basal metabolic rate via Increased NaKAPTase activity = increases O2 consumption, RR, Body temp
  5. Increased glycogenolysis, gluconeogenesis, and lipolysis
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56
Q

What regulates TH?

A

TRH stimulates TSH which stimulates follicular cells.

  • negative feedback by free T3 to anterior pituitary decreases sensitivity to TRH
  • Thyroid stimulating Igs (TSIs) like TSH stimulates follicular cells – Grave’s
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57
Q

What is the Wolff-Chaikoff effect?

A

excess Iodine temporarily inhibits thyroid peroxidase = decreases iodine organification = decreases T3/T4 production

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58
Q

What happens to TBG in hepatic failure? in pregnancy?

A
  1. failure = decreased so decrease in total TH
  2. pregnancy = increased so increase in total TH
  3. OCP = increases TBG
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59
Q

What is better T4 or T3?

A

T4 is the major thyroid product but it’s converted to T3 in peripheral tissues by 5’deiodinase.
- T3 binds receptors w/ greater affinity

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60
Q

What are the steps to make TH?

A
  1. I` is taken into follicular cells and oxidized via peroxidase
  2. Then I2 is added to Thyroglobulin to form MIT and DIT = organification (also done by peroxidase), Y residues are added
  3. T3/T4 is stored in colloid of thyroid gland
  4. Follicular cells proteolyze T3/T4 before sending it out into the blood
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61
Q

What inhibits the initial uptake of I` into the follicular cells?

A

anions - perchlorate, pertechnetate

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62
Q

What inhibits the organification of TH?

A

antithyroid drugs - PTU, methimazole

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63
Q

What is Cushing’s Syndrome?

A

increased cortisol due to many reasons

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64
Q

What is the most common cause of Cushing’s syndrome?

A

exogenous steroids = decreased ACTH, both adrenal glands are atrophic

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65
Q

What are some endogenous causes of Cushing’s Syndrome?

A
  1. Cushing’s Disease (75%)
  2. Ectopic ACTH (15%)
  3. Adrenal (15%)
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66
Q

What is Cushing’s disease?

A

due to ACTH secretion from pituitary adenoma. Slight increase in ACTH
- both adrenals will be big

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67
Q

What are causes of ecotopic ACTH?

A

small cell lung cancer, bronchial carcinoids

- high levels of ACTH

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68
Q

What are causes of adrenal Cushings?

A

adenoma, carcinoma, nodular adrenal hyperplasia (one adrenal is big, other is atrophic)
- here you have decreased ACTH

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69
Q

What are the clinical findings for Cushing’s syndrome?

A
  1. HTN
  2. WT gain
  3. Moon facies
  4. Truncal obesity
  5. buffalo hump
  6. hyperglycemia
  7. skin changes (thinning, striae)
  8. osteoporosis
  9. amenorrhea
  10. immune suppression
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70
Q

How is the dexamethasone suppression test used to ID cushing’s syndrome?

A
  1. Normal - should have suppressed levels of cortisol at high and low doses
  2. ACTH pituitary tumor - will only be suppressed at high doses
  3. Ecotopic ACTH Tumor and Adrenal producing cortisol tumor - both will have elevated levels of cortisol even at high and low doses of dexamethasone
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71
Q

What is primary hyperaldosteronism?

A

Caused by adrenal hyperplasia or an Aldosterone secreting adrenal adenoma (Conn) - may be bilateral of unilateral

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72
Q

What are the clinical presentations of primary hyperaldosteronism?

A
  1. HTN
  2. Hypokalemia
  3. metabolic alkalosis
  4. Low plasma renin
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73
Q

What is the treatment for a primary hyperaoldosteronism?

A

Surgery to remove tumor and spironolactone (K sparing diuretic that works by acting as an Aldo antagonist)

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74
Q

What is secondary hyperaldosteronism?

A
  • renal perception of low IV volume results in overactive RAAS
  • due to renal artery stenosis, chronic renal failure, CHF, cirrhois, or nephrotic syndrome
  • HIGH PLASMA RENIN
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75
Q

What is Addison’s Disease?

A

Chronic primary adrenal insufficiency due to adrenal atrophy or destruction of disease
- deficiency of aldo and cortisol

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76
Q

What are the clinical findings of Addison’s Dz?

A
  1. hypotension (hyponatremic volume contraction)
  2. hyperkalemia
  3. acidosis
  4. skin hyperpigmentation (due to increased MSH from ACTH)
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77
Q

What happens in secondary adrenal insuffiency?

A
  • problem is at the pituitary
  • no hyperpigmentation or hyperkalemia
  • low cortisol b/c of low ACTH
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78
Q

What happens in tertiary adrenal insufficiency?

A

abrupt withdrawal of exogenous steroids

- mild HTN

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79
Q

What is Waterhouse Friderichsen syndrome?

A

Acute primary adrenal insufficiency due to adrenal hemorrhage associated w/ Neisseria meningitidis

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80
Q

What are symptoms of Waterhouse Friderichsen syndrome?

A

septicemia, DIC, endotoxic shock, petechial rash

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81
Q

What is pheochromocytoma?

A

Secretes E, NE, and dopamine which can cause episodic HTN

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82
Q

How can a pheochromocytoma be Dxed?

A
  • Urinary VMA, metanephrine, HVA

- plasma catecholamines are elevated

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83
Q

what else is pheochromocytoma associated with?

A
  • neurofibromatosis type 1

- MEN 2A and 2B

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84
Q

What is the treatment for Pheochromocytoma?

A

remove tumor only after effective alpha and beta blockers is achieved.

  • irreversible alpha antagonists must be given first to avoid a hypertensive crisis
  • Beta blockers are then given to slow the heart rate
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85
Q

What are the symptoms of a pheochromocytoma?

A
  1. High BP
  2. Pain (headache)
  3. Perspiration
  4. Palpitations
  5. Pallor
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86
Q

What is the rule of 10’s for pheochromocytoma?

A 
10% malignant
10% bilateral
10% extra-adrenal -- bladder
10% calcify
10% kids
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87
Q

Where can a neuroblastoma occur?

A

anywhere along the sympathetic chain

- less likely to develop HTN

88
Q

What are things associated w/ a neuroblastoma?

A
  1. N-myc oncogene
  2. Bombesin tumor marker
  3. Neurofilament stain
  4. Homer-Wright pseudorosette
89
Q

What are the signs/symptoms of Hypothyroidism?

A
  1. cold intolerance (decreased heat production)
  2. Wt gain, decreased appetite
  3. Hypoactivity, lethargy, fatigue, weakness
  4. constipation
  5. decreased reflexes
  6. myxedema (facial/periorbital)
  7. dry, cook skin. coarse brittle hair
  8. bradycardia, dyspnea on exertion
90
Q

What are the signs/symptoms of Hyperthyroidism?

A
  1. heat intolerance (increased heat production)
  2. wt loss, increased appetite
  3. Hyperactivity, sweating
  4. Diarrhea
  5. increased reflexes
  6. pretibial myxedema (grave’s)
  7. warm, moist skin. fine hair
  8. chest pain, palpitations, arrhythmias, increased Beta adrenergic receptors
91
Q

What are the lab findings for hypothyroidism?

A

increased TSh
decreased free T4
High cholesterol

92
Q

What are the lab findings for hyperthyroidism?

A

decreased TSH if primary
increased free/total T4
increased free/total T3
low cholesterol

93
Q

What are some causes of hypothyroidism?

A
  1. Hashimoto’s thyroiditis
  2. Cretinism
  3. Subacute Thyroiditis (de Quervain’s)
  4. Riedel’s Thyroiditis
  5. Other causes - congenital hypothyroidism, iodine deficiency, goitrogens, Wolff-Chaikoff effect, painless thyroiditis
94
Q

What is Hashimoto’s thyroditis?

A

MCC of hypothyroidism.

  • autoimmune disorder (against peroxidase and thyroglobulin)
  • may be hyperthyroid early in course. thyrotoxicosis during follicular damage
95
Q

What is associated a/ Hashimoto’s thyroiditis?

A

HLA-DR5

- increased risk of non-Hodgkin’s lymphoma ( B cell)

96
Q

What is seen on histology for Hashimoto’s thyroiditis?

A

lymphocytic infiltrate w/ germinal centers

- Hurthle cells: enlarged epithelial cells w/ increased eosinophilic cytoplasm

97
Q

What are the clinical findings of Hasimoto’s thyroiditis?

A

moderately enlarged, nontender thyroid

98
Q

What is Cretinism?

A
  • due to severe fetal hypothyroidism
  • endemic ones are seen wherever endemic goiters are prevalent (lack of dietary iodine)
  • sporadic cretinism is caused by defect in T4 formation or development failure in thyroid formation
99
Q

What are the clinical findings for Cretinism?

A
  1. pot-bellied
  2. pale
  3. puffy face child
  4. protruding umbilicus
  5. protuberant tongue
    short stature, mental retardation, coarse facial features
100
Q

What is subacute thyroiditis (de Quervain’s)?

A

self-limited hypothyroidism often following a flu-like illness
- may be hyperthyroid early in course

101
Q

What are the histology findings for De Quervains?

A

granulomatous inflammation

102
Q

What are the clinical findings for De Quervains?

A

increased ESR, jaw pain, early inflammation, very tender thyroid

103
Q

What is Riedel’s Thyroiditis?

A

thyroid replaced by fibrosis tissue

104
Q

What are the findings for Riedel’s thyroditis?

A

fixed, hard, rock-like , and painless goiter

- macrophages and eosinophils

105
Q

What is a toxic multinodular goiter?

A

focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor

  • increase release of T3 and T4
  • hot nodule - so takes up radioactive I
106
Q

What is Jod Basedow phenomenon?

A

thyrotoxicosis if a pt w/ iodine deficiency goiter is made iodine replete

107
Q

What is Grave’s disease?

A

Autoimmune hyperthyroidism w/ TSI

  • Type III HSR
  • Increase T3/T4 but decreased TSH
  • scalloped colloid
108
Q

What are some clinical findings of Grave’s?

A
  1. pretibial myxedema
  2. ophthalmopathy - proptosis, EOM swelling
  3. increased CT deposition
  4. diffuse goiter
109
Q

What is a thyroid storm?

A

stress induced catcholamine leading to death by arrhythmia (afib)

  • serious complication of Grave’s and other hyperthyroid disorders
  • may see increase ALP due to increase bone turnover
110
Q

What are some symptoms of thyroid storm?

A

hyperthermia, vomiting, hypovolemic shock

111
Q

What is the treatment for thyroid storm?

A
  1. PTU
  2. steroids
  3. Beta blockers
  4. methimazole
112
Q

What is the MC thyroid cancer?

A

papillary carcinoma

113
Q

Tell me about papillary carcinoma of thyroid?

A
  1. good prognosis
  2. empty- appearing nuclei (ground glass; Orphan Annie eyes)
  3. Psammoma bodies - layered calcification
  4. nuclear grooves
    - increased risk w/ childhood irradiation
  5. spreads to nearby lymph nodes
114
Q

Tell me about follicular carcinoma of thyroid?

A
  1. good prognosis
  2. uniform follicles
  3. spreads via blood
115
Q

Tell me about medullary carcinoma of thyroid?

A
  1. from parafollicular C cells - produce calcitonin
  2. sheets of cells in amyloid stroma
  3. Associated w/ MEN 2A and 2B
116
Q

What are the various mutations seen w/ thyroid cancers?

A
  1. papillary - Ret
  2. follicular -Ras
  3. Medullary - Ret
117
Q

Tell me about undifferentiated/anaplastic thyroid cancer?

A

older pts, very poor prognosis

- invade local structures= dysphagia or respiratory problems

118
Q

What are some goitrogens that can cause hypothyroidism?

A

Brasscia Veg

Cruciferous Veg

119
Q

What is the major regulator of insuline release?

A

glucose

120
Q

How is insulin made?

A

it’s made as a preproinsulin. The finally product is cleaved into C peptide and insulin.
- Insulin has disulfide bonds b/w alpha and beta chains

121
Q

How is insulin released from the beta cells of the pancreas?

A
  1. Glu enters via Glut 1
  2. Glu undergoes glycolysis and increases the ATP:ADP ratio
  3. HIgh levels of ATP close the ATP sensitive K channel
  4. The cell is depolarized
  5. Voltage gated Ca channels open
  6. Ca causes exocytosis of insulin granules
122
Q

What are all the organs that have insulin- independent glucose uptake?

A

BRICK -L

Brain, RBCs, Intestine, Cornea, Kidney, Liver

123
Q

Where are Glut 1 receptors found?

A
  • insulin independent

RBCs, Brain

124
Q

Where are Glut 2 receptors found?

A
  • Beta islet cells, liver, kidney, small intestine
125
Q

Where are Glut 4 receptors found?

A

=insulin dependent

Adipose tissue and skeletal muscle

126
Q

What are all of the anabolic effects of insulin?

A
  • increase glucose transport in skeletal muscle and adipose
  • increase glycogen synthesis and storage
  • increase TG synthesis and storage
  • increase Na retention (kidneys)
  • increase protein synthesis (muscles)
  • increase cellular uptake of K and amino acids
  • decrease glucagon rlease
127
Q

What regulates insulin?

A
  1. Hyperglycemia, GH, and Beta2 antagonists - increase insuline
  2. Hypoglycemia, somatostatin, and alpha agonists - decrease insulin
128
Q

What are the effects of glucagon?

A
  • catabolic
    Glycogenolysis, gluconeogenesis
    Lipolysis and ketone production
129
Q

When is glucagon released?

A

in response to hypoglycemia

- inhibited by insulin, hyperglycemia, and somatostatin

130
Q

What are the acute manifestation of DM?

A
  • polydipsia, polyuria, polyphagia, wt loss, DKA (type I), hyperosmolar coma (type 2), unopposed secretion of GH and E (exacerbating hyperglycemia)
131
Q

What happens with insulin deficiency and glucagon excess?

A
  1. Decreased glucose uptake = hyperglycemia, glycosuria, osmotic diuresis, electrolyte depletion –> dehyrdation, acidosis –> coma/death
  2. Increased protein catabolism -= increased plasma AA, nitrogen loss in urine, and above
  3. Increased lipolysis = increased plasma FFAs, ketogenesis, ketonuria, ketonemia –> dehydration and acidosis –> coma/death
132
Q

What are the chronic manifestations of DM due to?

A
  1. Nonenzymatic glycosylation

2. Osmotic damage

133
Q

What is affected by nonenzymatic glycosylation?

A
  1. Small vessels - diffuse thickening of basement membranes –> retinopathy ( hemorrhages, exudates, microaneurysms, vessel proliferation), glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to HTN)
  2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, and gangrene –> limb loss, cerebrovascular disease
134
Q

What is affected by osmotic damage?

A
  • sorbital accumulation in organs w/ aldose reductase
  • Neuropathy (motor, sensory, and autonomic degeneration) b/c Schwann cells affected
  • Cataracts b/c lens of eye is affected
135
Q

What are the tests to Dx DM?

A

Fasting serum glucose
oral glucose tolerance test > 200
HBA1c

136
Q

What is acanthosis nigracans seen in?

A

DM and visceral malignancies

137
Q

What are the special types of nodules seen in DM?

A

Kimmerlstiel Wilson nodules in the kidneys

138
Q

what is the primary defect in type 1 DM?

A

autoimmune destruction of Beta cells of pancreas

139
Q

What is the primary defect in type 2 DM?

A

increased resistance to insulin, progressive pancreatic Beta cell failure

140
Q

What is the age that is associated w/ Type 1 and 2 DM?

A

Type 1 - less than 30

Type 2 - greater than 40 usually

141
Q

What is the genetic predisposition with Type 1 and 2 DM?

A

Type 1 - relatively weak

Type 2 - relatively strong genetic

142
Q

What type of DM has a HLA association? What is the HLA?

A

Type 1, HLA DR3 and 4

143
Q

What is the level of glucose intolerance w/ Type 1 and 2 DM?

A

Type 1 - severe

Type 2 : mild to moderate

144
Q

What type of DM has insulin sensitivity?

A

type 1

145
Q

What type of DM is ketoacidosis common in?

A

type 1

146
Q

Which type of DM do the classic symptoms of polyuria, polydipsia, polyphagia, and wt loss present in?

A

type 1

147
Q

What is the histology of type 1 and 2 DM?

A

Type 1 - islet leukocyte infiltrate

Type 2 - islet amyloid (AIAPP deposit)

148
Q

What is diabetic ketoacidosis?

A

one of the most important complications of DM (usually type 1).

  • Usually due to increased insulin requirement from increased stress (eg infxn)
  • excess fat breakdown and increase ketogenesis from increased FFA which are then made into ketone bodies
149
Q

What are the main ketone bodies?

A

B-hydroxybutyrate > acetoacetate

150
Q

What are the signs and symptoms of Diabetic ketoacidosis?

A
  • Kussmaul respirations
    N/V, abdominal pain, psychosis/delirium, dehydration,
  • fruity breath order (due to exhaled acetone)
151
Q

What are kussmaul respirations?

A

rapid regular deep breathing that is meant to exhale the extra CO2

152
Q

What are the labs of diabetic ketoacidosis?

A
  • hyperglycemia, increased acid, decreased Bicarb (anion gap metabolic acidosis)
  • increased blood ketone levels, leukocytosis, hyperkalemia but depleted intracellular K due to transcellular shift from decreased insulin
153
Q

What are the complications of Diabetic ketoacidosis?

A
  • life threatening mucormycosis

Rhizopus infxn, cerebral edema, cardiac arrhythmias, heart failure

154
Q

What is the treatment of diabetic ketoacidosis?

A
  • IV fluids, IV insulin, and K (to replete intracellular stores), glucose if necessary to prevent hypoglycemia.
155
Q

What is carcinoid syndrome?

A
  • rare syndrome caused by carcinoid tumors (neuroendocrine) especially metastatic small bowel tumors, which secrete high levels of serotonin (5HT)
  • not seen if tumor is limited to GI tract (5HT undergoes first pass metabolism in liver
156
Q

What are the symptoms of carcinoid syndrome?

A
  • recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular disease
157
Q

What are the labs of carcinoid syndrome?

A

increased 5HIAA in urine and niacin deficiency

158
Q

What is the treatment for carcinoid syndrome?

A

somatostatin analog – octreotide

159
Q

What is the rule of 1/3s for carcinoid syndrome?

A
  • 1/3 metastasize
  • 1/3 present w/ 2nd malignancy
  • 1/3 multiple
  • it’s the most common tumor of appendix
160
Q

What is ZE syndrome?

A

gastrin secreting tumor of pancreas of duodenum

  • stomach shows rugal thickening w/ acid hypersecretion
  • causes recurrent ulcers
  • may be associated w/ MEN type 1
161
Q

What is MEN 1? (werner’s syndrome?

A

3 P’s: Parathyroid, pituitary (prolactin or GH), and pancreatic endocrine tumors (ZE syndrome, insulinomas, VIPomas, glucagonomas
- Commonly presents w/ kidney stones and stomach ulcers

162
Q

What is MEN 2A? (sipple’s syndrome)?

A
  • Medullary thyroid carcinoma (secretes calcitonin)
  • pheochromocytoma
  • parathyroid tumors
163
Q

What is MEN 2 B?

A

Medullary thyroid carcinoma
Pheochromocytoma
Oral/intestinal glanglioneuromatosis (associated w/ marfanoid habitus) - mucsoal neuroma

164
Q

What gene mutations is associated w/ MEN 2A and 2b?

A

ret

165
Q

What is the mode of inheritance for the MEN syndromes?

A

AD

166
Q

What is the treatment strategy for Type 1 DM?

A

low sugar diet, and insulin replacement

167
Q

What is the treatment strategy for Type 2 DM?

A

dietary modification and exercise for wt loss, oral hypoglycemic and insulin replacement

168
Q

What are the different types of insulin?

A
  1. Lispro (rapid acting
  2. Aspart (rapid acting)
  3. Glulisine (rapid acting)
  4. Regular (short acting)
  5. NPH (intermediate)
  6. Glargine (long acting)
  7. Determir (long acting)
169
Q

What is the action of insulin for treatment purposes?

A
  1. binds insulin receptor
    Liver - increases glucose stores as glycogen
    Muscle - increase glycogen and protein synthesis and K uptake
    Fat - aids TG storage
170
Q

What is the clinical use for insulin?

A

Type 1 DM, type 2 DM, gestational diabetes, life threatening hyperkalemia, stress induced hyperglycemia

171
Q

What are the toxcities of insulin?

A

hypoglycemia, very rarely HSR rxn, lipodystrophy, wt gain

172
Q

MOA of biguanides (metformin)

A

decreased gluconeogenesis, increased glycolysis, increased peripheral glucose uptake (insulin sensitivity)
- acts in liver

173
Q

What is the clinical use for metformin?

A

Oral - first line therapy in type 2 DM

can be used in pts w/out islet function

174
Q

What are the toxicities of metformin?

A 
GI Upset
LACTIC ACIDOSIS (thus contraindicated in renal failure and IV contrast)
175
Q

MOA of sulfonylureas?

A

closes K channel in beta cell membrane so cell depolarizes and triggers insulin release via increase Ca influx

176
Q

clinical uses of sulfonylureas

A

stimulates release of endogenous insulin in type 2 DM. Requires some islet function, so useless in type 1 DM
- very useful in early type 2 DM

177
Q

What are the 1st gen sulfonylureas?

A

Tolbutamide

Chlorporpamide

178
Q

What are the 2nd gen sulfonylureas?

A

Glyburide
Glimepriride
Glipizide

179
Q

toxicites of 1st gen sulfonylureas

A

disulfiram-like effects

180
Q

toxicities of 2nd gen sulfonylureas

A

hypoglycemia can be long lasting

181
Q

MOA of glitazones/thiazolidinedionines (TZD)

A

increase insulin sensitivity in peripheral tissues

- binds to PPAR-gamma nuclear transcription regulator

182
Q

What is the clinical use of TZD?

A

uses as monotherapy in type 2 DM or combined w/ other hypoglycemics

183
Q

ADE of TZD?

A

wt gain, ededma, hepatoxiticity, heart failure

184
Q

What are examples of TCD?

A

Pioglitazone and Rosiglitazone

185
Q

What hypoglycemic increases risk of MI?

A

rosiglitazone

186
Q

MOA of alpha-glucosidase inhibitors?

A

inhibit intestinal brush border alpha-glucosidase

  • delayed sugar hydrolysis and glucose absorptino
  • decreased postprandial hyperglycemia
  • used in type 2 DM
187
Q

ADE of alpha-glucosidase inhibitors?

A
  • GI disturbances
188
Q

Examples of alpha-glucosidase inhibitors

A

Acarbose, Miglitol

189
Q

MOA of amylin analog (pramlintide)

A

decreased glucagon and decrease gastric emptying

- used in type 1 and 2 DM

190
Q

ADE of amylin analog

A

hypoglycemia, nausea, diarrhea

191
Q

MOA of GLP1 analogs

A
  • increase insulin
  • decrease glucagon release
  • Type 2 DM
192
Q

ADE of GLP1 analog

A

N/V, pancreatitis

193
Q

examples of GLP1 analogs

A
  1. exenatide - exendin analog

2. liraglutide - synthetic analog

194
Q

DPP-4 inhibitors MOA

A

increases insulin
decreases glucagon release
- affects GLP1, prolongs incretin action
- Type 2 DM

195
Q

DDP4 inhibitors ADE

A

mild urinary or respiratory infxns

196
Q

Examples of DDP4 inhibitors?

A
  1. linagliptin
  2. saxagliptin
  3. sitagliptin
197
Q

What is PPAR-gamma used for?

A

gene activated by PPAR gamma regulate fatty acid storage and glucose metabolism
- increases insulin sensitivity and levels of adiponectin

198
Q

MOA of PTU

A

blocks peroxidase, thereby inhibiting organification of iodide and coupling of TH synthesis
- blocks 5’deiodinase = decreases peripheral conversion of T4 to T3

199
Q

MOA of methimazole

A

blocks peroxidase, thereby inhibiting organification of iodide and coupling of TH synthesis

200
Q

clinical use of PTU and methimazole

A

hyperthyroidism

PTU can be used in pregnancy

201
Q

PTU ADE

A

skin rash, aganulocytosis, aplastic anemia, hepatoxcity

202
Q

Methimazole ADE

A

skin rash, agranulocytosis, aplastic anemia

possible teratogen

203
Q

MOA of levothyroxine and triiodothyronin

A

thyroxine replacement

204
Q

clinical uses of levothyroxine and triiodothyronin

A

hypothyrodism and myxedema

205
Q

ADE of levothyroxine and triiodothyronin

A

tachycardia, heat intolerance, tremores, arrhythmias

206
Q

Clinical use of GH

A

GH deficiency, Turner syndrome

207
Q

Clinical use of somatostatin (octreotide)

A

acromegaly, carcinoid, gastrinoma, glucagonoma, esophgeal varices

208
Q

Clinical uses of oxytocin

A

stimulates labor, uterine contractions, milk let down, controls uterine hemorrhage

209
Q

clinical uses of ADH (desmopressin)

A

pituitary (central, not nephrogenic) DI

210
Q

MOA of demeclocyclin

A

ADH antagonist (member of tetracycline family)

211
Q

clinical use of demeclocyclin

A

SIADH

212
Q

ADE of demeclocyclin

A

nephrogenic DI, photosensitivity, abnormalities of bone and teeth

213
Q

MOA of glucocorticoids?

A

decrease production of LTs and PGs by inhibiting PLA2 and expression of COX 2

214
Q

examples of gluocorticoids

A 
Hydrocortisone
prednisone
triamcinolone
Dexamethaosone - long acting
Beclomethasone -long acting
215
Q

clinical uses of glucorticoids

A

Addison’s dz, inflammation, immune suppression, asthma

216
Q

ADE of glucocorticoids?

A

Iatrogenic cushing’s syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic),
- Adrenal insufficienc when drug stopped abruptly after chronic use

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