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Endocrine Pathophys Flashcards

1
Q

SIADH

dorwart chalmers formula

A

serum osmolality = (1.86(Na)) + (Glucose/18) + (BUN/2.8) + 9

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2
Q

SIADH

smithline and gardner formula

A

serum osmolality = 2(Na) + glucose/18 + BUN/2.8

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3
Q

SIADH

normal serum osmolality ranges

A

275 mOsm/Kg to 295 mOsm/kg

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4
Q

SIADH

what to do after checking serum osmolality?

A

UA (for urine osmolality)

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5
Q

SIADH

normal response to water deprivation

A
  1. H2O deprivation
  2. increased plasma osmolarity
  3. osmoreceptors stimulated to increase ADH secretion from post pit
  4. increased H2O permability of cells increase H2O reabsorption
  5. increased urine osmolarity and volume
  6. decreased plasma osmolarity toward normal
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6
Q

SIADH

Effect of ADH

A
  • increase H2O permeability in late distal tubule collecting duct
  • increase activity of Na K 2Cl transporter (increase Na intake, H2O follows)
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7
Q

SIADH

volume change of what? causes shift of ADH levels?

A
  • > 10% volume change
  • shock would trigger ADH secretion to maintain vol
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8
Q

SIADH

what can happen if you too rapidly correct hyponatremia

A

Locked In Syndrome

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9
Q

SIADH

overall characterize SIADH

A
  • ADH is secreted independently of osmoreceptors
  • Produces Hyperosmotic urine, Hypoosmotic Plasma, and Abnormally High levels of ADH
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10
Q

Male Hypogonadism

role of sertoli cells

A

Sertoli cells are a type of sustentacular “nurse” cell found in human testes which contribute to the process of spermatogenesis

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11
Q

Male Hypogonadism

Leydig Cells

A

produce testosterone in the presence of LH

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12
Q

Male Hypogonadism

key players in male HPG axis

A
  • Hypothalamus produces GnRH
  • Ant Pituitary produces FSH and LH (neg feedback to the hypothalamus)
  • Testes produce testosterone and inhibin (neg feedback to the ant pit)
  • testosterone can neg feedback of the hypothalamus
  • LH stimulates Leydig cells to make testosterone
  • FSH stimulates Sertoli cells to produce ABP and inhibin
  • Sertoli cells to support sperm production
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13
Q

Male Hypogonadism

which are gonadotropins?

A
  • FSH and LH are glycoproteins secreted by gonadotrophs of the APG
  • secretion is regulated by GnRH of the hypothalamus
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14
Q

Hyperaldosteronism

overall what does RAAS regulate?

A

BP (slowly)

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15
Q

Hyperaldosteronism

RAAS pathway

A
  1. angiotensinogen (liver)
  2. renin (kidney)- converts-
  3. angiotensin I
  4. antiongensin converting enzyme (ACE) - (lungs/kidney) - converts-
  5. angiotensin II
  6. systemic effects
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16
Q

Hyperaldosteronism

RAAS direct renal mechanism

A
  • increase of mean arterial pressure causes increased filtration rate in the tubules
  • this means the kidney cannot reabsorb filtrate fast enough –> more fluid leaves the body in the urine –> blood volume decreases –> lower BP
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17
Q

Hyperaldosteronism

RAAS indirect renal mechanism

A

reduced mean arterial pressure & Na+ concentration decreases kidney perfusion leading to…
* cells of macula densa stimulate renin production from the juxtaglomerular cells after sensing change in osmolarity
* ACE stimulates secretion of aldosterone from the glomerulosa cells of adrenal gland which increases Na+ reabsorption & increases blood osmolality
* Angiotensin II increases Na+ reabsorption, ADH secretion, thirst, and vasoconstricts arterioles to increase peripheral resistance

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18
Q

Hyperaldosteronism

two components of fetal adrenal gland? what do they do?

A
  • definitive: principal site of glucocorticoid and mineralcorticoid synthesis
  • fetal: androgenic precursors which the placenta converts to various types of estrogens
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19
Q

Hyperaldosteronism

Mature adrenal gland histology

A
  • cortex (zona glumerulosa, fasciculata, reticularis)
  • medulla
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20
Q

Hyperaldosteronism

function of zona glomerulosa

A
  • produces mineralcorticoids (aldosterone)
  • sodium reabsorption in the kidney, electrolyte balance, intravascular volume, blood pressure
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21
Q

Hyperaldosteronism

function of zona fasciculata

A
  • produces glucocorticoids (cortisol)
  • uniquitous physiologic regulators, influences variety of body functions
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22
Q

Hyperaldosteronism

function of zona reticularis

A
  • produces sex steroids (androgens)
  • too much can cause secondary sex characteristics in women
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23
Q

Hyperaldosteronism

what regulates aldosterone?

A
  • renin-angiotensin system
  • hyperkalemia
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24
Q

Endocrine System Overview

endocrine system is collective term for?

A

all endocrine glands and hormone secreting cells distributed throughout the body

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25
Q

Endocrine System Overview

differentiate endocrine glands/cells versus neuroendocrine/neurosecretory cells

A
  • endocrine: lacks a duct, secretes their hormone into surrounding tissue/fluid and it is taken up by the blood and carried throughout the body
  • neuro: neurons that produce and release their secretions/hormones in response to signals from the nervous system
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26
Q

Endocrine System Overview

what are hormones

3 things

A
  • chemical messenger secreted into bloodstream
  • produces a response only in certain target cells that possess a receptor
  • control and coordinate body’s metabolism, energy level, reproduction, growth/development, response to injury/stress/mood
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27
Q

Endocrine System Overview

Hypothalamus location

A

region of forebrain located below the thalamus and posterior to optic chiasma

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28
Q

Endocrine System Overview

hypothalamus connects to what? via what?

A

connects to pituitary gland via neural and circulatory connections

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29
Q

Endocrine System Overview

major functions of hypothalamus

A
  • hormone regulation and secretion from pit gland
  • autonomic regulation
  • thermoregulation
  • food/water/sleep/circadian rhythm
  • memory
  • emotional behavoirs
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30
Q

Endocrine System Overview

Pituitary Gland (hypophysis) location

A
  • seated in the SELLA TURCICA of the sphenoid bone below hypothalamus
  • attached to the hypothalamus by the infundibulum
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31
Q

Endocrine System Overview

names of two pituitary lobes

A
  • anterior pituitary (adenohypophysis)
  • posterior pituitary (neurohypophysis)
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32
Q

Endocrine System Overview

pituitary gland job

A

secretes severeal hormones and regulates the acitivity of other hormone secreting glands

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33
Q

Endocrine System Overview

nerve fiber connections between hypothalamus and pituitary

A

Hypothalamohypophysial Tract
* synthesized in the hypothalamus, stored in the post pit
* neurons in the paraventricular and supraoptic nuclei have direct projections that end in the post pit
* paraventricular nuclei: produce oxytocin (stimulate uterine contractions + releases during lactation)
* supraoptic nuclei: primarily produce ADH/vasopressin (vasoconstrictor that increases absorption of Na+/H2O from renal tubules)

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34
Q

Endocrine System Overview

bloodstream connection between the hypothalamus + post pit

A

Hypothalamohypophysial Portal System
* formed from branches off the internal carotid arteries
* arteries travel through median eminence (pituitary stalk) into the capillaries that surround cells within anterior pituitary
* Releasing hormones: corticotropin-releasing hormone (CRH), thyrotropin releasing hormone (TRH), gonadotropin-releasing hormone (GnRH), growth hormone-releasing hormone (GHRH)
* Release Inhibiting hormones: somatostain, dopamine

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35
Q

Endocrine System Overview

Anterior pituitary hormones

A

synthesizes and secretes 6 hormones
* Non-tropic Hormone: prolactin (PRL), growth hormone (GH)
* Tropic Hormones: Follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH)

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36
Q

Endocrine System Overview

which part of pituitary gland actually produces its own hormones?

A

anterior

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37
Q

Endocrine System Overview

differentiate tropic and non-tropic hormones

A
  • Non-tropic: directly stimulates target cells to induce effects
  • Tropic: pituitary hormone who target organ is another endocrine gland
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38
Q

Endocrine System Overview

which two hormones does the post pit store? how do they travel from hypothalamus to post pit?

A
  • stores: ADH, OT
  • travel: down the hypothalamohypophyseal tract via infundibulum
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39
Q

Endocrine System Overview

control of pituitary secretion

A
  • timing and the amoung of pituitary secretion is regulated by the hypothalamus, higher brain structures, feeback from target organs
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40
Q

Endocrine System Overview

Anterior Pituitary control of secretion

A
  • releasing hormones: stimulate secretion by pituitary cells
  • inhibiting hormones: suppress secretion from pituitary cells
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41
Q

Endocrine System Overview

Posterior pituitary control of hormone secretion

A
  • controlled by neuroendocrine reflexes
  • ADH: released when there is increase in blood plasma osmolality or decrease in blood volume
  • Oxytocin (OT): released during labor + after nipple stimulation
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42
Q

Endocrine System Overview

release of oxytocin breastfeeding

A
  1. suckling stimulates nerves in nipple to signal hypothalamus
  2. hypothalamus stimulates the posterior pituitary to release oxytocin & anterior pituitary to release prolactin
  3. oxytocin simtulates lobules in the breast to release milk, prolactin stimulates milk production

pos feedback

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43
Q

Endocrine System Overview

oxytocin in birth

A
  1. head of baby pushes against cervix
  2. nerve impulses to the brain
  3. pituitary releases oxytocin
  4. oxytocin stimulates uterine contractions
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44
Q

Endocrine System Overview

what is pitocin

A
  • synthetic substance that mimics oxytocin
  • given to induce labor
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45
Q

Endocrine System Overview

ADH overview

A
  • aka vasopressin
  • wants blood osmolality 275-295 mOsm/L
  • increased osmolality (dehydration) is detected by the hypothalamuc neurons (osmoreceptors) and release ADH from post pit
  • ADH acts on distal tubule to reabsorb water (lowers urine volume and stimulates thirst)
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46
Q

Pituitary Adenomas

types of secretory adenomas

A
  • lactotroph (increased prolactin -> hyperprolactinemia)
  • somatotroph (increased GH –> acromegaly/gigantism)
  • corticotroph (increased cortisol –> Cushing’s)
  • thyrotroph (increased TSH –> secondary hyperthyroidism)
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47
Q

Pituitary Adenomas

what is seen w/ CN III palsy

A
  • ptosis (inactivation of levator palpebrae)
  • mydriasis (decreased tone of constrictor pupillae muscle)
  • down & out (unopposed left superior oblique and lateral rectus muscles)
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48
Q

Gigantism & Acromegaly

Growth Hormone is also known as?

A

somatotropin

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49
Q

Gigantism & Acromegaly

growth hormone is produced by?

A

anterior pituitary

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50
Q

Gigantism & Acromegaly

what signals the release of GH?

A

growth hormone releasing hormone (GHRH)

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51
Q

Gigantism & Acromegaly

major effects of growth hormone

A
  • stimulates the liver to produce insulin like growth factors (IGFs- 4types)
  • tells adipose cells to break down stored fat (lipolysis)
  • Liver to break down glycogen into glucose (glycogenolysis)
  • liver to produce glucose (gluconeogenesis)
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52
Q

Gigantism & Acromegaly

impact of GH on insulin?

A

increased insulin resistance in the tissues –> not moving glucose into cells –> increased blood glucose levels

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53
Q

Gigantism & Acromegaly

Describe insulin-like growth factor 1

A
  • aka somatomedin C
  • produced by liver with inc. GH
  • binds IGF-1 receptors to: promote cellular metabolism, muscle growth, long bone growth
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54
Q

Gigantism & Acromegaly

describe oral glucose tolerance test/GH suppression test

A
  • helps determine if the pituitary is releasing too much GH
  • drink w/ 75g glucose
  • measure serume GH before and after 2 hrs
  • > 1 ng/mL is abnormal (with an increase in blood glucose, GH should be suppressed)
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55
Q

Gigantism & Acromegaly

which is in kids? which is in adults?

A
  • kids: gigantism (growth plates open during sx onset)
  • adults: acromegaly (growth plates already closed)
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56
Q

Dwarfism

define short stature

A
  • height vertex below 2SD or in 3rd percentile for given age/sex
  • adult height < 4 ft 10 in
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57
Q

Dwarfism

which type is achondroplasia

A
  • disproportionate dwarfism
  • average sized torso, short limbs, large head
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58
Q

Dwarfism

which presentation is associated with GH deficiency

A

proportionate dwarfism

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59
Q

Thyroid Gland

anatomy of thyroid gland

A
  • largest endocrine gland
  • located below larynx and wraps around anterior/lateral sides of trachea
  • two large lobes connected by narrow anterior isthmus
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60
Q

Thyroid Gland

anatomy of thyroid follicles

A
  • filled w/ colloid
  • lined by follicular cells
  • secrete thyroxine (T4) and triiodothyronine (T3)
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61
Q

Thyroid Gland

anatomy of parafollicular cells

A
  • aka C cells
  • located between follicular cells
  • secrete calcitonin and decrease blood Ca+ levels
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62
Q

Thyroid Gland

describe T3/T4 homeostasis loop

A
  • Homeostasis: normal T3 and T4 concentrations, normal body temp
  • disturbances: decreased T3/T4
  • hypothalamus releases TRH –> adenohypophysis releases TSH –> thyroid follicles release T3 and T4
63
Q

Thyroid Gland

differentiate T3 and T4

A
  • T3: primary active thyroid hormone
  • T4: circulates blood, converted as needed to T3
64
Q

Thyroid Gland

other name for TSH?

A

thyrotropin

65
Q

Thyroid Gland

where are thyroid hormones stored?

A
  • stored in the follicular lumen
  • bound to protein (thyroglobulin- TG)
  • bound hormones can’t diffuse into cells, unbound/free hormone can bind thyroid receptors and exert effects
66
Q

Thyroid Gland

what inhibits the conversion of T4 to T3?

A
  • aging
  • fasting/calorie restriction, obesity
  • inflammation
  • sleep deprivation
  • stress
  • acute/chronic conditions of liver, kidney, intestines
  • alcohol
  • meds: amiodarone, propranolol, propylthiouracil
67
Q

Thyroid Gland

factors which can increase conversion of T4 to T3

A
  • zinc
  • selenium
  • vitamin A
  • vitamin E
68
Q

Thyroid Gland

4 functions of thyroid hormones

A
  • increased metabolism
  • growth & development
  • interrelated actions w/ catecholamines
  • regulates pituitary hormone synthesis
69
Q

Hypothyroidism

levothyroxine

dose, when to take, avoid

A
  • 1.6 mcg/kg PO QD
  • 30 min before eating or bedtime
  • check TSH level every 4-6 wks until reach goal of 1-2
  • avoid: calcium, iron supplements w/in 4 hrs
70
Q

Thyroiditis

generally what is it

A

inflamamtion of the thyroid gland

71
Q

Thyroiditis

2 types of thyroiditis

A
  • Hashimoto’s (autoimmine, crhonic lymphocytic thyroiditis)
  • painful subacute thyroiditis
72
Q

Hashimoto’s Thyroiditis

pathophys

A
  • trigger leads to autoimmune destruction causing progressive depletion of thyroid epithelial cells
  • thyroid cell destruction is mediated by CD8+ cytotoxic cells + local production of cytokines
  • antibodies made to thyroglobulin (Tg) and/or thyroid peroxidase (TPO)
  • lymphocytic infiltration and fibrosis of thyroid cells –> distruption of follicles and release of stored thyroid hormones
73
Q

Thyroid

describe thyroid uptake scans + potential results

A
  • evaluates thyroid function + pathology
  • uses radioactive iodine
  • hyperthyroidism: very black, increased uptake in both lobes
  • toxic goiters: uneven uptake
  • toxic adenomas: increased uptake in one area
  • thyroiditis: decreased or absent uptake
74
Q

Thyroid Nodules

high risk US features of thyroid nodules

A
  • solid
  • hypoechoic (indicates solid mass of dense tissue)
  • microcalcifications
  • irregular margins
  • extrathyroidal extension
75
Q

Hyperthyroidism

describe production of thyroid hormones

A
  • tetraiodothyronine (T4, thyroxine) –> 2 tyrosine + 4 iodine
  • Triiodothyronine (T3, most metabolically active) –> 2 tyrosine + 3 iodine
  • convert T4 to T3 PRN
76
Q

Hyperthyroidism

review HPT axis

A
  • hypothalamus: TRH which stimulates….
  • pituitary: TSH which stimulates….
  • thyroid: T4 + T3
  • T4 + T3: inhibit hypothalamus (TRH) + pituitary (TSH)
77
Q

Hyperthyroidism

causes

3

A
  • increased synthesis of thyroid hormones (primary)
  • excessive passive release of thyroid hormones (primary)
  • extrathyroidal source (pituitary adenoma, secondary)
78
Q

Hyperthyroidism

which patients CANNOT get the RAIU + thyroid scan? what do you do instead?

A
  • cannot be used in pregnancy or while lactating
  • use US to detect diffuse enlargement, solitary/multiple nodules, and increased vascularity of the gland
79
Q

Hyperthyroidism

which tissues do these work on?
* Beta-1 blockers
* Beta-2 blockers
* Beta-3 blockers

A
  • beta 1: heart/kidney
  • beta 2: lung, muscles
  • beta 3: adipose tissue
80
Q

Hyperthyroidism

differentiate selective and non-selective?

A
  • selective: only block beta-1 receptors (atenolol, metoprolol, carvedilol, nebivolol)
  • non-selective: block both beta 1 and beta 2 receptors (nadolol, propranolol, pindolol, sotalol)
81
Q

Hyperthyroidism

contraindications of BBs

A
  • bradycardia, hypotension
  • uncontrolled HF
  • 2nd or 3rd degree AV blocks
82
Q

Hyperthyroidism

purpose of BBs

A
  • block beta receptors which prevents the catecholamines norephinephrine and epinephrine from binding and activating them which decreases sympathetic nervous system response
83
Q

Hyperthyroidism

MOA anti-thyroid meds

A
  • inhibit oxidation and organic binding of thyroid iodine by inhibiting thyroid peroxidase
  • inhibits extrathyroidal conversion of T4 to T3
84
Q

Hyperthyroidism

antithyroid meds- baseline labs required and why?

A
  • baseline CBC
  • liver function
  • due to risk of agranulocytosis
85
Q

Hyperthyroidism

what is agranulocytosis

A

acute, drug induced blood disorder characterized by severe reduction in number of WBCs in circulation

86
Q

Hyperthyroidism

when to use methimazole? when to use propylthiouracil?

A
  • methimazole: preferred except during first trimester of pregnancy due to birth defectsm can be used during thyroid storm
  • propylthiouracil: used in 1st trimester of pregnancy or if TTC or thyroid storm; BBW for severe liver damage
87
Q

Hyperthyroidism

describe use of radioactive iodine (I-131) ablation

A
  • contraindicated in pregnancy or lactation
  • most pts will become hypothryoid within 2-6 mo
  • PO capsule which progressively destroys thyroid cells
88
Q

Multiple Endocrine Neoplasia

what can you not give a diabetic pt who has MEN?

A

GLP-1 inhibitors (increases risk for development of medullary thyroid cancer)

89
Q

Hypoglycemia

what happens to glucagon response after 5 yrs of DM?

A

pts lose glucagon response (glucagon increases glucose in the blood when it senses low sugars)
pts do not MAKE glucagon, they can still be responsive to it

90
Q

Hypoglycemia

how can this occur in pt w/out DM?

A
  • requires full workup to see what is happening
  • potential causes: eating less/exercising more, alcohol consumption, meds, hypermetabolic states (sepsis, burns), tumors (insulinomas)
91
Q

Hypoglycemia

Glucose homeostasis

A
  • serum glucose levels should be 71-99 mg/dL fasting
  • homeostasis coordinated between insulin, glucagon, and SNS
92
Q

Hypoglycemia

body response to insulin less than 80? less than 68? less than 66?

A
  • 80: insulin secretion decreases
  • 68: glucagon, norephinephrine, and epinephrine secreted
  • < 66: growth hormone and cortisol secreted (increases lipolysis, ketogenesis, and gluconeogenesis)
93
Q

Hypoglycemia

role of glucagon in response to hypoglycemia? norephinephrine?

A
  • glucagon: mobilizes glycogen from liver to increase blood glucose by ~36 mg/dL in 15 min
  • norephinephrine: acts systematically to cause adrenergic symptoms of hypoglycemia including tachycardia/diaphoresis
94
Q

Hypoglycemia

role of epinephrine in response to hypoglycemia?

A
  • stimulates glycogenolysis and gluconeogenesis in the liver
  • decreases insulin secretion
  • increases glucagon secretion from pancreatic islet cells
  • increases lipolysis in adipose tissue (provides glycerol for gluconeogenesis)
  • decreases glucose uptake by muscle cells
95
Q

Hypoglycemia

differentiate glycogenolysis, gluconeogenesis, lipolysis

A
  • Glycogenolysis: process by which glycogen breaks down into glucose PRN for energy when fasting
  • Gluconeogenesis: process that allows the body to form glucose from non-hexose precursors, particularly glycerol, lactate, pyruvate, propionate, and glucogenic amino acids
  • Lipolysis: process through which triacylglycerols (TAGs) break down via hydrolysis into their constituent molecules (glycerol and FFA)
96
Q

Hypoglycemia

meds causing hypoglycemia

A
  • insulin
  • meglitinides (repaglinide, nateglinide)
  • sulfonylureas (glipizdie, glimepiride, glyburide)
  • BBs
  • ethanol
  • quinolones
  • salicylates (ASA)
  • MAO-I
97
Q

Hypoglycemia

MOA of insulin

A

increase glucose uptake by skeletal muscle and adipose tissue

98
Q

Hypoglycemia

when does coma/death occur?

A

< 40 mg/dL

99
Q

Hypoglycemia

Whipple Triad

A

hypoglycemia in non-diabetic pts
* confirmed glucose concentration < 70 mg/dL
* signs/sx associated w/ hypoglycemia
* resolution of sx after correcting hypoglycemia

100
Q

Type 1 DM

endocrine fucntion of pancreas

A
  • islet of langerhans cells secrete hormones and hormone like messangers
  • Insulin: secreted by beta cells in response to increased glucose
  • Glucagon: secreted by alpha cells in response to decreased glucose
101
Q

Type 1 DM

exocrine function of pancreas

A

digestive enzymes secreted by acinar cells

102
Q

Diabetes Mellitus

disorder is characterized by what two things?

A
  • poor insulin production
  • resistance to insulin
103
Q

Type 1 DM

simpilifed pathophys

A
  • T cell immune mediated destruction of insulin producing pancreatic islet cells leading to absence of insulin production

AUTOIMMUNE

104
Q

Type 1 DM

which two antibodies are most commonly present?

A
  • glutamic acid decarboxylase antibodies (GAD- adults)
  • insulin autoantibodies (IAA, children)
105
Q

Type 1 DM

describe the three stages

A
  • Stage 1: asx, characterized by normal fasting glucose/glucose tolerance, but presence of >2 pancreatic autoantibodies
  • Stage 2: asx, characterized by pancreatic autoantibodies (multiple); dysglycemia (impaired fasting glucose/glucose tolerance, abnormal HbA1c)
  • Stage 3: evidence of diabetes defined as hyperglycemia w/ clinical sx
106
Q

Type 1 DM

how do 1/3 of pediatric patients present intially?

107
Q

Type 1 DM

in children how can polyuria present?

A
  • enuresis (can’t hold pee –> wetting the bed)
  • nocturia (urination at night)
108
Q

Type 1 DM

interpret results of fasting plasma glucose (FPG)

A
  • no calories for > 8 hrs
  • > 126 mg/dL at least 2 times = DM
  • 100-125 would be prediabetic (T2 DM)
109
Q

Type 1 DM

describe dawn phenomenon

A
  • in the early AM, hormones (GH, cortisol, catecholamines) cause the liver to release large amounts of glucose into blood stream
  • in pts w/ DM, the body does not produce enough insulin which causes high blood sugar in the morning
  • if blood sugar is normal to high at 2-3am, it is this phenomenon. Avoid eating carbs late at night.
110
Q

Type 1 DM

describe somogyi effect

A
  • blood sugar level drops too low in the early morning hours, hormones (GH, cortisol, catecholamines) are released to reverse low blood surgar levels
  • in DM - pts who takes insulin and do not eat a bedtime snack will experience drops in sugar during night and the body will respond by releasing hormones
  • low blood sugar in early AM = this!
111
Q

Type 1 DM

components of DexCom for management

A
  • continuous glucose monitoring system
  • measures glucose continuously in the interstitial fluid for 7-14d
  • data can be transmitted to Dr. offices prior to appts
  • alarms can be set for levels
112
Q

Type 1 DM

which meds are rapid acting insulin? Basal insulin?

A
  • rapid: glulisine, lispro, aspart
  • basal: glargine, detemir
113
Q

Hyperglycemic Crises

compare and contrast HHS & DKA

A
  • hyperglycemia (more severe in HHS)
  • dehydration
  • hyperosmolality (more severe in HHS)
  • electrolyte abnormalities
  • ketoacidosis (only in DKA)
114
Q

Hyperglycemic Crises

normal physioloigc response to increased serum glucose

A
  • high sugar detected by pancreatic beta cells to release insulin
  • insulin will decrease glucagon secretion from pancreatic alpha cells; stop gluconeogenesis/glycogenolysis in the liver; increase glucose uptake by muscle/adipose cells
115
Q

Hyperglycemic Crises

pathophys

A
  • results from problems relating to insulin: decreased glucose utilization by periph tissues; increased glycogenolyssi/gluconeogenesis by the liver
  • this leads to increased plasma osmolality (high solute- glucose) which draws water out of the cells and dilutes the Na+ concentration in the interstitial space
116
Q

Hyperglycemic Crises

when would glucosuria occur?

A

serum glucose levels are >180 mg/dL

117
Q

Hyperglycemic Crises

what are the effects of glucosuria?

A
  • increase in osmotic pressure of urine leading to polyuria
  • loss of water –> dehydration –> hyperosmolality –> K+ shifts out of cells –> increased extracellular potassium, decreased intracellular potassium
  • impaired renal function, AKI
118
Q

Diabetes Mellitus Type 2

effects of chronic hyperglycemia

A
  • high serum glucose level >180 mg/dL exceeds renal threshold causing glucosuria, polyuria (increase in urine osmolality), polydipsia (dehydration)
  • intracellular glucose deficiency causing polyphagia
  • chronic complications: CV disease, neuropathy, nephropathy, retinopathy
119
Q

Adrenal Insufficiency

anatomy of adrenal glands

A
  • adrenal medulla (inner portion, responds to sympathetic stimulation by secreting catecholamines)
  • adrenal cortex (thicker outer portion, synthesizes 25 steroid hormones- corticosteroids)
  • 3 layers of adrenal cortex: zona glomerulosa (outer), zona fasciculata (middle), zona reticularis (inner)
120
Q

Adrenal Insufficiency

three types of corticosteroids

A

mineralocorticoids, glucocorticoids, sex steroids

121
Q

Adrenal Insufficiency

describe mineralocorticoids

A
  • secreted by zona glomerulosa
  • control electrolyte balance
  • act on kidney
  • primary is aldosterone
122
Q

Adrenal Insufficiency

describe glucocorticoids

A
  • secreted by zona fasciculata
  • stimulate fat/protein catabolism
  • gluconeogenesis (synthesis of glucose from non-carb sources) in the liver
  • release FA and glucose into blood, help body adapt to stress
  • main glucocorticoid is cortisol
123
Q

Adrenal Insufficiency

describe sex steroids

A
  • secreted by zona reticularis
  • androgens and estrogens
  • main androgen is dehydroepiandrosterone (DHEA)
124
Q

Adrenal Insufficiency

describe aldosterone

A
  • operates in RAAS
  • secreted directly in response to hyperkalemia and via RAAS in response to low blood volume/pressure
  • works to move Na+ into blood (H2O follows) thus increasing blood volume/pressure
125
Q

Adrenal Insufficiency

primary, secondary, and tertiary causes of adrenal insufficiency

A
  • primary: dysfunction or destruction of adrenal cortex
  • secondary: conditions that cause deficiency in pituitary adrenocorticotrophic hormoen (ACTH) secretion
  • tertiary: conditions that cause deficiecny in the hypothalamic secretion of corticotropin-releasing hormone (CRH)
126
Q

Adrenal Insufficiency

causes of primary insufficiency

A

Addison’s
* autoimmune (most common): adrenal cortex gradually destroyed –> loss of mineralocorticoids, glucocorticoids, and adrenal androgen hormone production
* could also be infection (TB), hemorrhage (rupture of adrenal cortex blood vessles due to increased BP causing tissue ischemia), metastatic cancers

127
Q

Adrenal Insufficiency

secondary causes of insufficiency

A
  • hypopituitarism (decreased ACTH)
  • pituitary tumors/surgery
128
Q

Adrenal Insufficiency

causes of tertiary insufficiency

A
  • prolonged high dose glucocorticoid use suppresses HPA axis
  • treating Cushing’s
129
Q

Adrenal Insufficiency

describe HPA axis

A
  • hypothalamus secretes CRH –> release of ACTH from anterior pituitary
  • ACTH release is pulsatile via circadian rhythm (increases in early AM, peaks at 8:30am, decreased in evening)
  • ATCH stimulates zona fasciculata (cortisol) and zona reticularis (androgens) in the adrenals
  • the zona glomerulosa is regulated by the renin-angiotensin system & K+ level
130
Q

Cushing Syndrome

which hormone is out of wack?

131
Q

Cushing Syndrome

differentiate primary, secondary

A
  • primary: increased production of glucocorticoids by adrenal glands (tumors)
  • secondary: Cushing’s disease (subtype of cushing syndrome); increased pituitary ACTH production leading to adrenal gland hyperplasmia (commonly see pituitary adenoma)
  • secondary: ectopic ACTH syndrome; increased ACTH production outisde pituitary and adrenal glands (e.g. paraneoplastic syndromes like SCLC)
132
Q

Cushing Syndrome

describe exogenous cushing syndrome

A
  • most common form of hypercortisolism
  • medical use of glucocorticoids
  • expgenous cortisol causes neg feedback at level of hypothalamus and ant pit (reduced CRH and ACTH)
  • due to: long term use of glucocortioids (fasciculata atrophy, cortisol no longer produced by body) or abrupt discontinuation of glucocorticoids (body can’t produce it anymore –> adrenal crisis)
133
Q

Cushing Syndrome

differentiate ACTH dependent and ACTH independent Cushing’s

A
  • Dependent: body makes too much ACTH which subsequently increases production of cortisol
  • Independent: adrenal glands produce cortisol without stimulation from ACTH
134
Q

Diabetes Insipidus

types

4

A
  1. central diabetes insipidus (CDI)
  2. nephrogenic diabetes insipidus (NDI)
  3. gestational diabetes insipidus
  4. dipsogenic diabetes insipidus (primary polydipsia)
135
Q

Diabetes Insipidus

pathophys of central (neurogenic)

A

decreased production by hypothalamus or decreased release of ADH from posterior pituitary causing polyuria

136
Q

Diabetes Insipidus

pathophys of nephrogenic

A

decrease in urinary concentrating ability as a result of resistance to the action of ADH

137
Q

Diabetes Insipidus

causes and pathophys of nephrogenic DI

3

A
  • Hereditary- X-linked inheritance, mutation in vasopressin V2 receptor, mutation in aquaporin-2 gene
  • Drug Induced: chronic lithium use (causes dysfunction of aquaporin-2 water channel)
  • Acute/Chronic Kidney Diseases: reduction in maxiumum renal concentrating ability due to fewer nephrons/damage to tubules
138
Q

Diabetes Insipidus

use of desmopressin in central DI

A
  • synthetic form of ADH/vasopressin
  • first line med for central
  • give at minimum dose to prevent nocturia, take at bedtime
  • risk for hyponatremia- nausea, vomiting, HA, lethargy, seizure, coma
139
Q

Diabetes Insipidus

use of thiazide diuretics (hydrochlorothiazide) for nephrogenic DI

A
  • increases proximal tubule sodium and water reabsorption and less water delivered to ADH sensitive collecting tubules
140
Q

Diabetes Insipidus

use of indomethacin (NSAID) for nephrogenic DI

A

increase renal concentration of urine by inhibiting renal synthesis of prostaglandins (ADH antagonists)

141
Q

Parathyroid Disorders

use of calcium in the body

A
  • all intake is dietary
  • strong bones/teeth
  • smooth muscle contraction
  • cofactor for enzymatic rxns
  • regulation of clotting
142
Q

Parathyroid Disorders

storage of calcium in the body

A
  • 45% free ionized form
  • 40% bound to albumin/protein
  • 15% complexed w/ anions
143
Q

Parathyroid Disorders

components of parathyroid glands

A
  • 4 total glands located posterior to thyroid gland
  • Chief cells synthesize, secrete, and store PTH
144
Q

Parathyroid Disorders

general job of PTH? via what cells?

A

regulates calcium levels in the blood through calcium sensing receptors within chief cells

145
Q

Parathyroid Disorders

3 functions of PTH (patho, more specific)

A
  • increases calcium and phosphate releases from bones via osteoclast formation
  • increases calcium reabsorption and phosphate excretion in the distal tubule of the kidney
  • increases synthesis of 1,25 dihydroxyvitamin D (active vit D) which will increase calcium absorption from the gastrointestinal tract
146
Q

Parathyroid Disorders

relationship between calcium &
* phosphate
* vitamin D
* magnesium

A
  • phosphate: inverse
  • vitamin D: direct
  • magnesium: direct

“commit to memory” :-)

147
Q

Parathyroid Disorders

what stimulates secretion of PTH?

A
  • decreased serum calcium
  • low levels of 1, 25 dihydroxyvitamin D (active vit D- calcitriol)
  • as levels of phosphorus increase, levels of free calcium in the blood decrease because phosphorus binds to calcium
  • low magnesium
148
Q

Parathyroid Disorders

what is calcitonin produced by? functions?

A
  • produced by parafollicular cels (c cells) of thyroid gland
  • secretion stimulated by increased serum calcium
  • function: inhibits activity of osteoclasts (prevent calcium release from bone) and decreases calcium reabsorption in the kidneys

calcitonin = too much calcium = tell the bones to keep their Ca2+ and tells the kidneys to get rid of Ca2+

149
Q

Parathyroid Disorders

differentiate primary, secondary, tertiary diseases

A
  • Primary: elevated PTH independent of Ca2+ levels
  • Secondary: elevated PTH due to chronic hypocalcemia
  • Tertiary: long-standing secondary hyperthyroidism or autonomous functioning of parathyroid glands
150
Q

Parathyroid Disorders

causes of primary hyperparathyroidism

A
  • most common cause of hyperparathyroidism
  • 95% occur sporadically (benign adenomas 85%, hyperlasia 15%, carcinoma < 1%)
  • 5% due to familial genetic mutations (MEN 1/4)
151
Q

Parathyroid Disorders

causes of secondary hyperparathyroidism

A
  • chronic renal failure
  • bypass surgery
  • malabsorption (celiac/crohn’s)
  • severe vitamin D deficiency
152
Q

Parathyroid Disorders

what is Tc99 sestamibi scan?

A

radioactive substance absorbed by hyperactive parathyroid gland

153
Q

Parathyroid Disorders

when to use total serum Ca2+ for evaluation of serum calcium? when to use ionized Ca2+ for evaluation of serum calcium?

A
  • Total: normal albumin
  • Ionized: low albumin
154
Q

Parathyroid Disorders

causes of hypoparathyroidism

A
  • autoimmune destruction
  • thyroiditis
  • tissue resistance to PTH (pseudohypoparathyroidism)
  • radiation/damage to thyroid or parathyroid
  • heavy metal overload (iron overload (hemochromocytosis) or copper (Wilson’s disease))

CMT (78 decks)

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