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endocrine Flashcards

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1
Q

What are the classical endocrine glands?

A
  • hypothalamus
  • pituitary
  • thyroid
  • parathyroid
  • pancreas(islet of langerhans)
  • adrenal glands
  • gonads
  • placenta
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2
Q

What are the organs with endocrine function?

A

brain<br></br>heart<br></br>liver<br></br>GI tract<br></br>kidneys<br></br>adipose

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3
Q

What are the 4 basic functions of the endocrine system(whole body regulation)?

A

<ol><li>maintain homeostasis</li><li>help body cope with stressful enviro</li><li>regulate cell metabo and energy balance</li><li>regulate mood, growth, devo and repro</li></ol>

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4
Q

What are the effects of hormones acting at the cellular level?

A

<ul><li>cell division, growth, diff and death</li><li>motility</li><li>secretion</li><li>nutrition uptake, storage & utilization</li></ul>

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5
Q

What are the effects of hormones at the molecular level?

A

<ul><li>gene transcription</li><li>protein synthesis & degregation</li><li>enzyme and protein activity</li><li>protein conformation</li><li>interaction bw molecules</li></ul>

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6
Q

What is the classical endocrine model?

A

chemical synth & secreted by glands → blood vessels(µg to pg) → target tissue (bind to receptors) → target tissue has physio repsonse<br></br><br></br>*homone acts as paracine or autocrine fnx

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7
Q

what is a paracrine function?

A

affects neighboring cells

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8
Q

what is an autocrine function?

A

works on same cells that produce them

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9
Q

How are hormones excreted from the body?

A

<ul><li>degraded by target tissue, blood, kidney/liver</li><li>via bile or urine</li></ul>

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10
Q

How does negative feedback effect hormone secretion?

A

hormones produce physio response that inhibit futher secretion<br></br><ul><li>elevated or dimished release</li></ul>

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11
Q

What are the 3 major classes of hormones?

A

<ul><li>steroids</li><li>protiens + protein derivites</li><li>tyrosine</li></ul>

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12
Q

What are steroid hormones?

A

lipids derived from cholesterol

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13
Q

What are the chemical properties of steroids?

A

lipophilic and hydrophobic

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14
Q

what are the chemical properties of protien hormones?

A

lipophobic and hydrophilic

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15
Q

what are tyrosine derivatives?

A

<ul><li>similar to steriods</li><li>catecholemines (protiens)</li></ul>

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16
Q

why is hormone chemistry important?

A

<ul><li>it determines how they can be taken for efficacy</li><li>how long it stays in your system</li></ul>

<br></br>

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17
Q

What are the functions of hormone receptors?

A

<ul><li>cell response based on receptor types available</li><li>up/down regulated</li><li>agonist/antagonist pharm manipulation</li></ul>

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18
Q

what is circhoral hormone secretion?

A

released every hr

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19
Q

what is ultradian horome secretion?

A

longer than 1 hr but less than 24 hrs

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20
Q

what is circadian hormones secretion?

A

released every 24 hrs

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21
Q

what is dinural secretion?

A

episodes at defined periods of the day

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22
Q

what is circatrigintan secrection?

A

released ~ 30 days

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23
Q

what type of secrection of GnRH & LH undergo?

A

cichoral<br></br>hypothalamus releases GnRH → LH release from anterior pituitary

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24
Q

What are the effects of GnRH pulsatility on pituitary gonadotropes?

A

pulses 60-90 min apart → upregulate GnRH receptors → stimulate gonadotropin release (LH, FSH)

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25
What occurs with the continuous administration of GnRH?
down regulation of receptors → supress release and function 
26
How does endocrine disease develop? 
front and back ends 

endocrine tissue: hypo/hypersecretion 
target tissue: sensitivity defects 
27
What is the bottom line of endocrine hypofunction?
dimished production and secretion of one or more hormones
28
What are examples of primary deficiency disorders?
hashimoto's thyroiditis
addison's disease
29
What is a primary deficiency disorder?
elevated hormone levels b/c of normal feedback response
30
What are examples of secondary deficiency disorders?
2º adrenal insufficiency 
2º hypothyroidism 

* developed from primary hypopituitarism 
31
What is secondary deficiency disorder?
trophic hormone for target organ is deficient 
32
what is tertiary deficiency disorder? 
one step above secondary deficiency 
33
what are examples of tertiary deficiency disorders?
3º adrenal insufficiency
3º hypothyroidism 
34
what are the 4 main etiologies of endocrine hypofunction? 
  • destruction of endocrine tissue
  • lack of gland devo as fetus
  • defects in hormone biosynthesis 
  • idiopathic 
35
What are the 4 etiologies of destruction of endocrine tissue?
  1. autoimmune 
  2. neoplasms 
  3. trauma/ removal 
  4. ischemia/inflamm/infarction
36
what is the pathophysiology of the autoimmune phenomena?
antibodies produced against target organ → destruction
37
What two factors are required for the autoimmune phenomena?
  • genetic predisposition
  • environmental trigger
38
What are examples of endocrine neoplasms?
  • craniopharyngiomas (slow growing, rathke's pouch) 
  • null-cell tumors 
39
What is the pathophysiology of endocrine neoplasms? 
hypersecretion if cells are cancerous 

if non-hormone producing tissue in gland → infiltrates gland → destroy hormone producing cells → deficiency 
40
What are the biggest types of hormones? 
protiens 
smallest: TRH(3)
30-225 = protiens 
41
What are examples of Ischemia/Infarction/ Inflamm/ Infiltrative disease?
  • Sheehan's syndrome 
  • pancreatitis
  • hemochromotosis
42
What is Sheehan's syndrome?
postpartum pituitary necrosis or infarction 
43
What develops because of chronic pancreatitis?
develop transient DM type 1 from insufficient insulin secretion 
44
What happens in hemochromotosis?
hypopituitarism 
from hypogonadotropic hypogonadism 
45
What type of endocrine tissue damage can occur with severe head trauma? 
hypophysectomy: tearing of pituitary stalk → 2º hypopituitarism 
46
What is the most common gland that fails during embryo development?
thyroid glands
gonads
47
What causes defects in hormone bio synthesis and what are the results?
cause: congenital defects 
results: mutations in hormones or hormone- producing enzymes 
48
What are the basic treatment principles for endocrine hypofunction?
  • treat underlying cause 
  • hormone supplementation 
49
What are the types of endocrine hyperfunction? 
1st, 2nd, 3rd
50
What is Cushing's Syndrome and its cause in primary form?
disorder of glucocorticoid excess caused by adrenocorticol hypersecretion
51
What is the cause of secondary form Cushings Syndrome?
hypersecretion of ACTH 
52
What the 5 etiologies of endocrine hyperfunction?
  1. tumors/neoplasm
  2. autoimmune stimulation
  3. ectopic production of hormone
  4. hyperplasia
  5. iatrogenic/factitious problems 
53
What is the pathophysiology of hyperplasia?
↑ cellularity and hormone overproduction

54
What is the pathophysiology of autoimmune stimulation for Graves' disease?
antibodies bind and activate TSH receptors on thyroid 
55
what is the causes and types of hormones can be ectopically produced?
polypeptides:
ACTH, ADH, calcitonin

insulin(rare)

*caused by tumors that do not usually produce the hormone
56
What is an iatrogenic problem and an example?
intentional exogenous administration of the hormone

ex: steroids for anti-inflamm conditions 
57
What is a factitious problem and an example?
exogenous administration of hormone by pt w/o clinician's knowledge

ex: thyroid hormone to induce weight loss 
58
What are the treatments for endocrine hyperfunction?
  • removal
  • radiation
  • pharmacologic intervention (block production, reception, sequelae control)
59
what does hormone response require?
  • normal receptor protein structure
  • receptor available 
  • intact receptor signaling 
  • normal post receptor events 
60
What can cause tissue resistance/ insenseitivity?
  • receptor defects/lack of availability 
  • post receptor defects 
  • target tissue damage
61
What types of assays are available for hormone levels?
  • RIA
  • ELISA
  • RRA
  • FIA
62
What else can assays measure?
hormone metabolites 
63
What are qualities of a good assay?
both sensitive and specific 
64
What is dynamic testing?
endocrine test that provide info about function beyond regular testing 
65
what is dynamic testing based off of and what is the goal of it?
stimulation or supression of endogenous hormone production

goal: response to target tissue in vivo
66
what are stimulation tests used?
hypofuction of gland is suspected and look at reserved capacity of hormone 
67
How are stimulation test performed?
  • admin of exogenous hormone → look at capacity of target gland ↑ hormone production 
  • admin of drug → secreation of endogenous hormone → effects on target gland hormone levels 
68
What is an example of dynamic testing for adrenal insufficiency diagnosis?
rapid ACTH test (cortrosyn IV/IM)
cortisol measured at 30-60 mins 

↑ cortisol: 2/3º AI
↓ cortisol: 1º AI
69
When are suppression tests used?
hyperfunction suspected and check negative feedback intact (GH,glucose)
70
What types of testing/imaging can be used for endocrine diagnosis?
  • MRI, CT
  • biopsy
  • genetic testing 

71
What is some advice for endo? 
  • know chemistry of hormone → unlock info
  • know what hormone does physio, then excess and deficient 
  • dont jump to conclusions with labs 
72
what is hypothalamus part of ?
diencephalon
73
What are the two main parts of the pituitary?
anterior lobe(andeohypophysis)
posterior lobe(neurohypophysis)

*in sella turcica
74
what are the 2 important hypothalmic nuclei? 
  • paraventricular
  • supraoptic 
75
What are the 5 cell types of the anterior pituitary?
  • Thyrotropes (5% TSH)
  • Lactotropes (15% Prolactin)
  • Corticotropes (15% ACTH) 
  • Somatotropes (20% GH) 
  • Gonadotropes (15% FSH, LH) 
76
how many different hormones are secreted by the anterior pituitary and hypothalamus?
anterior (6) influenced by (6/7) of hypothalamus 
77
What are the main regulators of GH secretion?
GHRH and GHIH 
aka somatostatin 
78
How is GH secretion regulated? 
  • indirectly through somatomedins (IGFs) production in liver
  • negative feedback
  • effects of target tissues

79
How often is GH secreted? 
pulses at  2-2.5 hrs
80
when does the largest secretory burst of GH occur?
w/in 1 hr of falling asleep
81
How does GH secretion vary over a lifetime?
childhood: stable 
puberty: secretory burst 
after puberty: stable
elderly: lowest level
82
What are the physiological functions of GH?
  • more bone laid down for long bones(epiphys plates)
  • ↓ glucose uptake and utilization (muscle and adipose) 
83
How is prolactin secretion regulated?
not pregnant: inhibited by dopamine (PIH) from hypothalamus 

pregnant: stimuli for secretion 
84
what are the physiological effects of prolactin in pregnant and post partum women?
post partum
  • stimulates milk production 
  • synth + secretion of GnRH → inhibits ovulation → ↓fertility during breastfeeding 
preg
  • PRL ↑ → additional breast development → milk production prep
85
what are the physiological effects of prolactin in males?
hyperprolactinemia → inhibit GnRH → ↓spermatogenesis→ infertility 

galactorrhea
86
What does LH do in male testes?
stimulates leydig cell →  makes testosterone →  spermatogenesis
87
What does FSH do in male testes?
stimulates Sertoli cells → secrete seminal fluid 
88
What should be given to people who make too much GH?
glucose
89
What does FSH and LH do in females?
menstrual cycle: stimulates ovaries

1st half: synth and secrete estradiol

2nd half: synth and secrete progesterone 
90
What are the 3 phases of post- natal growth pattern?
  • infantile (2yrs 30-35 cm)
  • childhood( 5-7cm/yr, prepubertal dip)
  • pubertal phase (8-14 cm/yr, ↑ gonadal steroids + GH secretion)
91
What is constitutional short stature?
variation of normal 

2 SDs + ↓ mean height for kids of that age and sex
92
what are the hormones made in posterior pituitary and what nuclei do they originate from ? 
ADH (SON) and Oxytocin (PVN)
93
How is ADH stimulated? 
↑ plasma osmolality (most important) 
hypovolemia
↓ in ECF vol 10% +
↓ in aBP
94
What does ADH do? 
  • water reabsorbtion by kidneys (V2 receptor bind → ↑h20 permeability) 
  • contraction of arteriolar vascular smooth muscle (V1 receptor bind → vasocontruction, ↑BP)
95
What is the pathophysiology associated with ADH?
neurogenic DI → decrease ADH secretion 

nephrogenic DI → renal insensitivity to ADH (defect in V2 receptor/ signaling) 

96
What are the major clinical manifestations of DI in adults?
  • large volumes of dilute urine 
  • excessive/intense thrist
  • ↑fluid ingestion
* can also happen with primary polydipsia (complulsive water drinking)
97
What test is used to diagnose DI?
water deprivation test 

(2-3hrs dep→ measure urine and plasma osmolality → synth ADH given) 

desmo, urine and plasma osmo measured
98
How is neurogenic DI treated?
desmopressin
99
how is nephrogenic DI tx'd?
HCTZ
100
What is SIADH and what signs and symptoms are associated with it?
↑ ADH secretion 

  • hyponatremia
  • plasma hyposmolality
  • ↑ urinary Na+ excretion 
  • lung cell carcinoma 
101
How does oxytocin function in lactation?
suckling on nipple → oxytocin secretion → contracts mammry alveoli/ ducts → milk ejection 
102
How does oxytocin work in birth?
oxytocin → initiates and ↑ contractions in active uterus 
103
How does oxytocin affect males/females?
  • cuddle/love hormone
  • facilitation of trust 
  • antidepressant 
  • empathy
104
What is genetic short stature?
consitutional short stature in kids with short parents (@ or ↓ 3-5th percentile)
105
What are the 3 basic steps to diagnose short stature?
  • hx and presentation
  • IGF-1 levels
  • GH stimulation tests
106
What are some causes of short stature?
  • genetics/ maternal drug, alchy use/ fetal growth retardation
  • GH deficiency 
  • chronic systemic dz/infection
  • psychosocial dwarfism 

107
What is a key finding in clinical presentation for short stature?
slow growth that progressively deviates from previously defined precentile (2+SD's  ↓ mean)
108
What can cause dysmorphic/disproportinate features associated with short stature?
  • chromosomal abnormalities 
  • intrauterine infection 
  • maternal exposures 
  • dysplasia/rickets 
109
What is are key tests to determine short stature?
  • x-ray: hand and wrist 
  • IGF 1 levels (GH deficiency)
  • GH stimulation tests (10ng normal) 
110
What is the gold standard to dx GH deficiency?
GH stimulation tests 
  • Insulin- induced hypoglycemia (15-120 min after injection)
  • Arginine (serum GH 0-120 min after) 
*correct thyroid def 1st 
111
What are the hypothalamic causes of GH deficiency?
idopathic(GHRH secretion)
hypothalmic tumors
112
What are the pituitary causes of GH def?
  • abnormal GH secretion
  • tumor, radiation
  • trauma/removal
  • idiopathic
113
What are the signs of tall stature?
  • variation from normal
  • accelerated growth
  • genetics
  • advanced bone age
  • taller than peers
114
what are genetic causes of tall stature?
Klinefelte's syndrome (2+ X chromosomes in male phenotype)

Marfan's syndrome (inherited autosomal dominate disorder of connective tissue) 
115
What are the features of klinefelter's syndrome?
  • long arms and legs 
  • learning disabilities (language)
  • small testes and gynecomastia 
MC cause of congenital hypogonadism 
116
What are the features of Marfan's syndrome?
  • tall
  • long, thin fingers
  • hyperextension of joints 
117
What are the endocrine causes of tall stature?
  • pituitary giantism
  • precociois puberty
  • hyperthyroidism 
118
What is the clinical manifestation of  pituitary giantism?
(rare) 
  • GH excess
  • Height 3-4 SDs from normal
  • headache + VF involvement (tumors)
  • rapid growth rate 
  • excess size for age 
119
What are the features of precocious puberty? 
  • tall
  • early epiphys closure
  • advanced bone age 
  • more common in girls 
  • short adult 
120
what are the causes of precocious puberty?
  • congenital adrenal hyperplasia 
  • virilizing adrenal tumors 
  • testicular and ovarian tumors 
  • ovarian cysts 
121
What are the features of hyperthyroidism?
overproduction/tx w/ exogenous thyroxine 
↑ growth and advanced bone age 
122
How is pituitary giantism dx'd?
  • bone age 
  • TFT
  • sex steroid hormone [conc]
  • karyotype
  • GH studies (IFG 1 Levels, OGTT, MRI) 
123
What is the most common cause of acromegaly?
GH secreting adenoma of the pituitary 
124
what is acromegaly?
excessive GH after puberty 
125
What are other causes of acromegaly?
  • excess secretion of GHRH by hypothalamic or small cell lug cancers 
  • ectopic secretion by non- endocrine tumors 

126
What are the clinical features of acromegaly? 
  • stimulation of tissue growth 
  • insulin antagonism and lipogenesis 
  • adenoma
    • headache 
    • visual field defects 
    • cranial nerve palsies

127
What are 3 examples of anopsias?
  • total blindness (left eye, L optic nerve)
  • bitemporal hemianopsia (optic chiasm) 
  • right homonymous hemianopsia(L optic tract)
128
What are the clinical features of acrial overgrowth?
  • enlarged jaw 
  • enlarged, swollen hands and feet 
  • enlarged nose and frontal bones 
  • teeth spread apart 
129
What are the clinical features of articular overgrowth?
  • enlarged synovial tissue 
  • hypertophic arthropathy (knees, ankles, hip, spine)
  • back pain and kyphosis
130
What are the clinical features of acromegaly for pituitary function?
macroadenoma: ↓secretion of other pituitary hormones (gonadotropins MC)

131
What are the clinical features of skin and hear with acromegaly?
  • thickened skin and skin tags
  • hyperhidrosis
  • ↑ hair growth and hitsutism 
132
what are the soft tissue clinical features of acromegaly?
  • macroglossia (sleep apnea)
  • deepened voice 
  • hand paresthesias
133
what are the clinical manifestations of tumors, viscera and others  in acromegaly?
Tumors
  • ↑ uterine tumors (benign)
  • colonic adenomatous polyps 
  • adenocarinoma ~10%
Viscera
  • enlarged organs 
Other
  • sleep apnea, CV dysfunction, neuropathy, hypogonadism
134
What are the lab abnormailites of acromegaly? 
  • hyperglycemia
  • hyperprolactinemia 
135
What is the mortality of acromegaly?
2-3x expected (CV and CA) 
↓10 yr survival average 
lower GH → normal mortaility rate 
136
What are the dental aspects of acromegaly?
  • macroglossia(indentations from teeth)
  • enlarged jaw 
  • malocclusion (over/underbite) 
  • teeth spacing 
137
What are other oral aspects of acromegaly?
  • thick lips 
  • salivary gland enlargement 
  • skin folds (face) 
  • enlarged nasal sinus 
138
what is the best test to dx acromegaly?
IGF-1 [conc]
139
what other tests can be used to dx acromegaly?
GH supression test(>2ng/ml in 85% post gluc)
Pituitary MRI
140
what is the presentation for a male with Hyperprolactinemia?
  • impotence/ ↓ libido
  • infertility 
  • headache 
  • perph vision loss 
  • mood changes 
  • galactorrhea
  • gynecomastia 
141
what is the presentation of females with Hyperprolactinemia? 
same as male + : 
  • irregular menstruation 
  • menopausal symptoms 
  • weight gain 
  • increased androgens 
142
what are the causes of hyperprolactinemia?
  • prolactinoma 
  • pituitary tumors 
  • thypothalamic disease 
  • CKF 
  • severe 1º hypothyroidism 
  • med SEs 
  • idiopathic 
143
What types of meds can cause hyperprlactinemia (PRL level <50-100 ng/mL)?
  • dopamine receptor antagonist 
  • dopamine depleting agents 
  • trycyclic antidepressants 
  • verapmil 
  • estrogens and antiantdogens 
  • opiates 
144
what is a highly suggestive PRL secreting adenoma for a fasting serum? 
>200ng/mL 
prolactinomas(~1% of pop) 
  • microadenoma in women(<10mm)
  • macroadenoma in men (>10mm)
145
what are common clinical features of women with hyperprolactinemia?
  • amenorrhea 
  • galactorrhea 
  • infertility 
146
what are common clinical features of males with hyperprolactinemia?
  • ↓ libido
  • headache/vision changes 
  • impotence/infertility 
147
What is the workup for hyperprolactinemia? 
  • Serum Assays: PRL, FSH, LH, estradiol, testosterone, TSH, renal/hepatic panels, 𝛃 -hCG (females) 
  • MRI of brain and pituitary 
  • VF exam 
  • neuro testing 
148
What is hypopituitarism? 
disease of pituitary gland or hypothalamus→ decreased pituitary hormone secretion → multiple hormone deficits 
149
What is the most common cause of hypopituitarism?
pituitary tumor or tx of tumor 
150
What are other causes of hypotiuitarism? 
  • pituitary radiation (exposed to all pituitary) → new ACTH, TDH or LH/FSH defs (4yrs) 
  • hemochromotosis (infiltrative) 
  • infarction(Sheehan's syndrome)
  • pituitary apoplexy (spontaneous hemorrhage into pituitary) 
151
What is the presentation and treatment of pituitary apoplexy? 
  • severe headache, visual deficits due to pressure (tumor) 
  • w/o tx: permenant visual damage, hypopituitarism, death 
  • emergency pituitary decompression 
152
what are the order hormones fall in hypopituitarism?
GH ↓ → LH/FSH → ACTH → TSH → prolactin
153
How does ACTH definiency present in hypopituitarism?
cortisol deficiency 
154
how does TSH deficiency present in hypopituitarism?
T3/T4 deficiency → lethargy, ↓ appetite, facial puffiness, dry skin, brady, anemia 
155
How does LH/FSH deficiency present in hypopituitarism?
  • hypogonadism 
    • women: ovarian hypofunction 
    • men: testicular hypofunction 
156
how does GH deficiency present in hypopituitarism?
children: short 
adults:
  • ↓ muscle mass, ↑ fat mass
  • ↑LDL 
  • ↑CVD risk 
  • ↓ bone density  
157
how does PRL deficiency present in hypopituitarism?
inability to lactate after delivery(preg) 
158
How is hypopituitarism dx'd? 
  • ↓secretion documentation of hormones 
  • test each hormone seperately 
  • consider lesions 
159
how is hypopituitarism treated?
depends on hormone deficit 
160
Where are the adrenal glands located?
Retroperitoneal cavity above each kidney
161
what are the 3 primary sources the aterial supply arises from? 
  1. superior suprerenal arteries 
  2.  middle suprarenal artery 
  3. inferior suprarenal arteries 

162
what is the largest part of the adrenals?
Cortex (80%) 
163
what are the 3 distinct cells of the adrenal cortex?
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
164
what are the adrenal medulla cells?
chromaffin cells
165
What hormones are produces in the zona glomerulosa? 
mineralocorticocoids → aldosterone
166
What hormones are produces in the zona fasciculata?
glucocorticoids → cortisol
167
what hormones are produced in the zona reticularis?
adrenal androgens → DHEA anf Androstenedione
168
what hormones are produced in the medulla?
epi and norepi
169
what is the basis for why each layer makes a different steroid?
the presence or absence of certain enzymes 
170
What is the main role of cortisol?
"coping with adversity"
171
How does cortisol work? 
increase glucose (gluconeogenesis, liver) → increase protein + fat breakdown → protect against hypoglycemia 
172
what are the other actions of cortisol?
  • anti-inflammation 
  • immune response suppression 
  • maintain vascular response to NE/Epi
  • inhibit bone formation
  • maintain/promote ↑ GFR
173
what is Cushing Syndrome?
excess cortisol due to problem(tumor) in adrenal cortex
174
what is Cushing Disease?
excess cortisol due excess ACTH (tumor) in anterior pituitary 
175
what is addisons disease (primary adrenal insufficiency)?
↓ cortisol secretion due to AI or fungal infections in adrenal cortex 
176
what is secondary adrenal insufficiency?
↓ ACTH secretion 
177
What are plasma ACTH levels in Cushing Syndrome and Addison disease?
they are high 
178
what is the clinical features of Cushing Syndrome?
hyperglycemia 
osteoporosis 
HTN 
179
why does pathophysiology of addisons cause hyperpigmentation?
it results from elevated ACTH and subsequent metabolism to ⍺-MSH
180
Does hyperpigmentation occur in 2º adrenal insufficiency 
no, they have lower levels of ACTH
181
which situations can cause an adrenal crisis?
  • undx'd with serious infection/stress 
  • dx'd + infection + vomiting(GI, gastroenteritis)
  • after bilateral adrenal infarction or hemorrhage
  • abrupt withdrawl from steroids
182
what is the predominant manifestation of adrenal crisis?
shock
183
what are more common symptoms of adrenal crisis?
  • anorexia
  • N,V, ab pain
  • weak/fatigue
  • lethargy/fever
  • confusion
  • coma
184
what is aldosterone and what is its major function? 
a primary mineralocorticoid and controls body fluid volume by ↑ reabs of Na+ in kidneys and ↑ K+ and H+ excretion.
185
what is the most common cause of conn syndrome (primary hyperaldosteronism)?
adenonma (75%)
186
what is the cause of idiopathic hyperaldosteronism?
adrenal hyperplasia
187
what are the two main clinical findings of primary hyperaldosteronism?
HTN and hypokalemia
188
How is Conn Syndrome treated?
spirolactone + tumor removal 
189
what are the other clinical findings of primary hyperaldosteronism?
  • EFC volume expansion
  • Na+ plasma NOT elevated ( only if dehydrated) 
  • headaches
  • muscle fatigue and weakness (hypokalemia) 
190
How is primary hyperaldosteronism diagnosed?
  • aldosterone:renin ratio >25ng/dL
  • ↑aldosterone + ↓ renin(PRA)

191
What is the saline suppression test?
a test to measure aldosterone excess
  • 2L saline x 4 hrs
  • aldosterone measured before + after 
  • >10ng/dL → primary hyperaldosteronism
192
what is the next step in primary hyperaldosterone diagnosis after aldosertone:renin and saline suppression?
CT/MRI
  • if high aldosterone levels, consider solitary tumor (MC)
  • if MILD → bilateral adrenal hyperplasia
193
If MRI/CT is inconclusive, what is the next step in primary hyperaldosteronism diagnosis?
adrenal venous sampling (taken from each gland)
  • if one side higher → functional adrenal tumor 
  • same bilaterally → hyperplasia

194
how is primary hyper aldosteronism treated?
sugically (take out tumor) or with spirolactone (hyperplasia)
195
what are the physiological effects of adrenal androgens on women?
it is responsible for pubic and axillary hair devo and libido
196
what occurs in adrenogenital syndrome (congenital 21𝛃 -hyroxylase deficiency) and what is it caused by?
  • females become masculinized and virilized 
  • supressed gonadal function in both sexes 
it is caused by an ↑ synth of adrenal androgens (↑DHEA and androstenedione levels) 
197
what causes congenital 17⍺-hydroxylase deficiency and what occurs?
  • cause: lack of cortisol and adrenal androgens 
  • occurance: production shunted toward mineralocortocoid pathway 
198
what are the physiological effects of the adrenal medulla hormones?
the effects of epi (synth'd) 
199
what is phenochromocytoma?
a tumor on the adrenal medulla → epi and norepi secretion 
200
what is the etiology of phenochromocytoma?
  • 90% benign tumor 
  • 10% outside adrenals 
  • 10% malignant 
  • 0.1-0.2% w/ HTN 
201
what are the clinical findings of phenochromocytoma and how do they typically present?
  • HTN
  • Headache
  • palpatations/tachy/sweaty
  • anxiety/tremors
  • weight loss/ hypermetabo
  • hyperglycemia 
usually wax and wane 
202
what is phenochromocytoma commonly misdiagnosed as? 
  • HTN/myocarditis 
  • anxiety/cocaine/ meth
  • unstable angina
  • hyperthyroidism 
203
what occurs if phenochromocytoma goes untreated?
  • MI/Stroke/arrythmia 
  • shock/renal failure 
  • dissecting aortic aneurysm 
  • death 
204
how is phenochromocytoma diagnosed?
  • 24 hr urine catecholamine + metabolites (metanephrine, normetanephrine, wanillymandelic acid VMA)
  • plasma catecholamines >2000pg/mL (+)
  • imaging(MRI/CT)
205
what is a clonidine supression test?
clonidine admin to test for phenochromocytoma 
  • 92% accurate 
  • NO fall in levels if phenochromocytoma present (wait 3 hrs after admin to test)
206
how is a phenochromocytoma treated?
surgery 
  • no carvedilol before 
possbile outcome → vascular instability/shock (excess catecholamines are gone) 
207
how is GH administered and what are the brand names? 
subQ

brands
  • -tropin/trope
  • saizen

208
What is the indication for IGF-1 prep and what is it's name?
growth failure from primary IGF-1 deficiency 
  • mecasermin
209
what is the main adverse effect of IGF-1 prep?
hypoglycemia 
(eat right before or after) 
210
what is GHIH (somatostatin) prep indicated for and what are their names?
indicated for acromegaly 
  • octerotide (sandostatin)
  • lanreotide
211
what will acromegaly provoke that causes the need to administer a dopaine agonist? 
secretion of high prolactin → cabergoline 
212
What is the inidcation for GHR antagonist and what is its name?
indication: acromegaly 
name: Pegvisomant 
213
what is the MOA of GHR antagonist?
blocks GH receptors and ↓ IGF1 blood levels 
214
what testing is done for pegvisomant(somavert) prior to administration?
LFT's 
215
what are the names of the dopamine agonist and what are they indicated for?
name: cabergoline, bromocriptine
indication: prolactinoma 
216
what is the MOA of dopamine agonist?
minic dopamine(PIH)
217
which dopamine agonist is more effective and why?
cabergoline: more selective for D2 receptors on lactoropes (anterior pituitary)
218
what is the indication for oxytocin prep and what is its name?
indication:
  • ↑ contraction in labor 
  • prevent hemorrhage after labor 
name: pitocin
219
what is the indication for oxytocin in regards to breastfeeding?
stimulate lactation reflex
220
what is the indication for ADH(vasopressin) and what is its name?
indication: neurogenic (central) DI, primary noctural enuresis(+6yo)
name: desmopressin 
221
how can DDAVP be administered?
nasal
oral (only 5% abs)
IV(control bleeding)
222
what is the indication for mineralocorticoid and what is its name?
indication: adrenal insufficiency 
name: hyrdocortisone (30-35.7mg/day)
223
what is the indication for increasing the dose of hydrocortisone?
minor or major stress 
224
what are the indications for low potency hydrocortisone/cortisone?
  • replacement therapy 
  • minor inflamm conditions 
225
what are the indications for prednisone/prednisolone? 
  • inflamm/allergies 
  • asthma 
  • AIs 
226
what are the indications for bethmethasone/budesonide/dexamethasone?
  • skin disorders
  • asthma 
  • adrenal axis testing 
227
what other mineral corticoid replacement can be used if hydrocortisone is not sufficient replacement?
fludrocortisone(50-200 mg/day oral)
228
what are the adverse signs that indicate for more mineralocorticoid?
  • hypotension
  • hyperkalemia
  • hyponatremia
* opposite indicates for less
229
what are the names and MOAs of the drugs for Cushing's syndrome 
  • aminoglutethimide, MOA: inhibit cholesterol → pregnenolone conversion 
  • metyrapone, MOA: inhibit 11𝛃-hydroylase
  • ketoconazole + fluonazole, MOA: antifugal have some 11𝛃-hydroylase inhibition
230
what are the names of aldosterone receptor antagonist and what is thier indication?
name: eplerenone(more selective to aldosterone receptors) and spirolactone
indication: hyperaldosteronism 
231
what is the most common alpha blocker and its indication?
phenoxybenzamine 
indication: pre-op (10-14 days) to normalize BP
232
what is the most common beta blocker and when is it administered?
propanolol
given AFTER alpha andrenergic 
233
what is the adverse effect of giving propanolol before phenoxybenzamine and why?
perph 𝛃-adrenergics receptors are blocks → vasodilation blocked → greatly ↑ BP 
234
What are the functions of ADH?
↑ serum osmlarity or ↓ intravascular volume 
235
where is ADH synthesized and secreted from?
synthesized: hypothalamus 
secreted: anterior pituitary
236
what occurs with abnormal ADH levels?
too little/ receptor issues: DI
too much: SIADH 
237
which type of body composition has has more total body water?
lean (60%)
238
what are they key differences in fluid volume between infants/children and elderly?
children:
  • higher turnover and lost more h2o (immature kidneys)
  • more SA, ↑ insensible losses 
elderly
  • ↓ thirst response 
  • meds influence inbalances 
239
what is defined as orthostatic hypotension?
↓ SBP of 20mmHg
↑DBP of 10mmHG w/in 3 min of standing
240
what labs are used to test ADH?
  • BMP (BUN, K+, Na+, Creatinine, gluc)
  • H + H & CBC
  • Urine osmolality (sp. gravity)


241
what is the hematocrit range for both sexes?
male: 40-54%
female: 38-47%
242
what does specific gravity measure?
weight of a substance compared to pure water at same temp
243
what is the normal range for SG? 
1.005-1.030
(more [conc] ↑ the number)
244
what is the clinical presentation for someone who is hypovolemic?
  • ↑ thirst 
  • oliguria
  • ↓skin turgor + dry membranes 
  • CNS ↓
  • weak + muscle cramps 
  • ↓BP, postural hypotension, ↑pulse
245
what are causes of hypovolemia?
  • GI, renal and skin loss
  • sequestration w/o loss 
246
what are clinical features of hypervolemia?
  • SOB, HTN, tachy
  • crackles
  • JVD
  • edema, weight gain
  • orthopnea, PND
  • hepatojugular reflux
247
what are the causes of hypervolemia?
  • overhydration
  • ↑ Na+ intake 
  • 1º renal Na+ retention (1º hyperaldosteronism/ cushings dz)
  • 2º renal Na+ retention (heart + liver failure)
248
what is osmolality, its solutes and normal ranges?
solute or particle [conc] of a fluid
solutes: Na+, gluc, urea
range: 280-295mOsm/kg
249
what are other osmotically active stubstances?
mannitol
antifreeze, ethanol, methanol 
250
what is water retention influeced by?
thirst and ADH
251
what is salt retention influenced by?
RAAS, ANP and catacholamines
252
what does an electrolye panel consist of?
Na+ (135-145)
K (3.5-5.0)
Cl- (98-106)
Co₂ (22-32)
253
what should be considered when looking at sodium levels?
  • abnormal ECFV b/c of Na+ control mechanisms 
  • abnormal [Na+] b/c of water control 
*both can coexist 
254
what are the two types of DI?
neurogenic (central)
nephrogenic
255
what are the etiologies of neurogenic DI?
  • idiopathic
  • tumors
  • neurosx/ trauma
  • FHx/congenital
  • hypercal or hypoK
  • lithium 
  • sickle cell
256
what is the pathophysiology of DI?
neurogenic: low synth + secretion of ADH
nephrogenic: kidney not responding to ADH in blood 
257
who is at risk for nephrogenic DI?
  • elderly 
  • sick
  • acute/chronic renal insufficiency 
258
what are the clinical manifestations of DI?
  • large vol. of DILUTE urine (2.5-20L/day)
  • excessive/intense thirst (cold drinks)
259
How is DI diagnosed?
  • 24 hr urine 
  • blood 
  • plasma + urine osmolality w/ h₂o deprivation 
260
what are differential diagnosis for polyuria?
  • DM (1st)/DI (SG <1.005, osmo<200) 
261
what are normal results of a water deprivation test?
  • ↑ADH w/ plasma osmolality ↑
  • ↑ in urine osmolality
262
what is the treatment for neurogenic DI?
↓urine output (↑ADH)
replace fluid loss 
DDAVP
263
What are other drugs that could be given if patient is unresponsive to DDAVP?
  • chlorpropamide 
  • carbamazepine/clofibrate
264
how is nephrogenic DI treated?
  • treat underlying cause 
  • hypercal → normalize Ca²+
  • lithium → IRREVERSIBLE if renal damage present 
265
what medications can be used to treat nephrogenic DI?
thiazides + low Na+ diet 
266
what is SIADH?
high ADH plasma levels w/o stimulus 
267
what type of patients are suspected to have SIADH?
  • hyponaturemic
  • serum hyposmolality
  • Na+ urine excretion >20mmol/24hr
268
what are the etiologies of SIADH?
  • tumors
  • pulm disease 
  • major sx
  • CNS disturbance
  • drugs induced 
269
what is the pathophysiology of SIADH?
water retained → blood diluted → aldosterone ↓ → Na+ + urine removes excess H₂O
270
what are the main clinical manifestations of SIADH?
hyponatremia
271
what are signs and symptoms of SIADH?
early 
  • N,V 
  • headache 
  • muscle cramps/ tremors 
Late
  • confusion/miid swings 
  • hallucinations 
  • seizure/coma 
  • death
272
what is the treatment for SIADH?
water restriction and salt administration 
* rapid corrrection → neuro complications* 
273
what are other treatment options for SIADH?
  • Na+ + loop diuretic 
  • demeclocycline/lithium
  • ADH receptor agonist 
274
How does the thyroid receive blood flow?
external carotids → superior thyroid arteries 
subclavian → inferior thyroid arteries 
275
what causes bruits on the thyroid?
goiter 
276
what is the uncommon variant of blood supply to the thyroid?
brachiocephalic trunk, right common carotid or aortic arch → thyroid IMA artery (7.5% of people)
277
what are the 2 thyroid cells and what does one secrete?
TGB(thyroglobulin)
C cells(parafollicular cells) → secretes calcitonin 
278
what are the 2 types of thyroid hormones, how is it converted and which is the most potent? 
T₃ (triiodothyronine) + T₄ (thyroxine) 

thyroid gland → T₄ → T₃ in target tissue 
T₃ most potent 
279
what is necessary for normal thyroid hormone synthesis?
iodine (75-150 mcg/day)
280
what is the difference b/w 1º, 2º and 3º hypothyroidism?
need to enter 
281
what is the 1st and 2nd step of thyroid synthesis? 
1. gather ingredients: C cells synth + TGB(↑ tyrosine) → dump into colloide

2. iodine trapped in Na+/I- pump
  • pump inhibition 
    • thyocyanate + perchlorate (no clinical use) 
282
what is the 3-5th step of thyroid synthesis what is required for this process?
Thyroid peroxidase 
3. oxidize I- →I₂
4. I₂ + tyrosine TGB → MIT +DIT (organification)
5. Coupling + colloid storage 
  • MIT+ DIT → T₃
  • DIT + DIT → T₄
283
what are the drugs that inhibit thyroid peroxidase 
methinmazole
propylthiouracin (PTU, also inhibits T₄ → T₃ in perph tissue)
284
what are the 6-8th step of thyroid synthesis?
6. colloid → follicular cells 
7. cleave T₃, T₄, DIT/MIT → blood (T₃, T₄)
8. deiodination of residual MIT/DIT (via thyroid deiodinase) & recycle I- and tyrosine 
285
what are the actions of TSH?
  • stimulate TGB synth
  • stimulate Na+/I- pump 
  • activate thyroid peroxidase 
  • stimulate thyroid follicles (too high → goiter)
286
what can cause goiters?
hypo/hyperthyroidism
287
what is the major clinical correlation to TSH/TSI binding?
graves disease 
288
what are the 3 major transport proteins? 
  1. thyroxine-binding globulin
  2. thyroxine- binding pre-albumin(TBPA)
  3. albumin
289
what is the general effect of thyroid hormones?
activate nuclear transciption of genes → protein and receptor synthesis
290
when is the critical period CNS maturation? 
perinatal 
291
what occurs in utero with congenital hypothyroidism? 
maternal T₄ crosses placenta to allow normal fetus development
292
when does fetal thyroid gland function begin?
10-12 weeks 
1º source of thyroid hormone after 1st trimester
293
what occurs if congenital hypothyroidism goes untreated?
growth retardation and delayed cogitive development
294
what are the 3 screenings for congenital hypothyroidism and when is it done?
1. low T₄ → for high TSH
2. high TSH
3. low T₄ + high TSH

2-5 days after birth 
295
what are the CNS effects of thyroid hormone in adults?
alertness, concentration/focus 
296
what else does thyroid hormone promote in adults and what occurs with hypothyroidism?
ossification and fusion of bone plates and maturation 
intestinal motility

hypothyoidism: bone age is less than chronologic age
297
what would the TSH plasma levels look like in each hyperthyroid disease?
  • graves → low 
  • neoplasms → low
  • TSH-secreting adenoma → high
  • factitious administration → low
298
what is a thyroid storm?
FATAL
exaggeration of usual hyperthyroid symptoms
  • resting tachy or arrythmia (>140,aFib)
  • hypotension/shock
  • high fever(104-106)
  • severe N,V,D, ab pain 
  • anxiety/delirium/psychosis/coma
  • ↑T₃ & T₄, ↓TSH
299
what causes a thyroid storm?
  • surgery
  • trauma/partition
  • infection
300
what are the clinical manifestations of hypo/hyperthyriodism?
based on what thyroids normally do
301
what are causes of hyperthyroidism?
  • graves
  • neoplasms
  • TSH-secreting adenoma
  • facticious admin
302
what causes hypothyroidism?
  • hashimotos/thyroiditis
  • iodine deficiency 
  • thyroidectomy
  • lack of TSH
303
what would plamsa levels look like in each primary hypothyroid cause?
  • hashimotos
  • iodine deficiency 
  • thyroidectomy
  • lack of TSH
 HIGH TSH → LOW T₄
304
what is myxedema?
deposition of mucopolysaccharides in dermis → swelling in affected areas 

*severe hypothyroidism*
305
what is myxedema coma?
Medical emergency (30-40% mortalility, rare)
↓CNS and hypothermia 
(shock-like symptoms also present)
306
what are symptoms associated with myxedema coma?
  • puffy hands and face 
  • thick nose 
  • swollen lips and tongue 
  • non-pitting extremities 
307
how is myxedema coma managed?
supportive 
  • correct hypothermia
  • electrolytes + glucose 
  • vent
  • IV T₄
308
what are the two mechanisisms hyperthyroidism is caused by and what is used to determine treatment?
1.↑ thyroid function
2. not associated with ↑ thyroid function

diagnositc:24 hr radioactive irodine uptake (RAIU +/-) scan
309
what labs are done BEFORE RAIU and scan?
TSH
Free T₃ + T₄
preg test 
310
what is a RAIU and scan? What are normal values?
pt ingest iodine and is scanned
10-30% @ 24 hrs
311
when is RAIU contraindicated?
pregnancy and breastfeeding 
312
what is a high RAIU and what does it indicate?
>30% @ 24 → increased thyroid function
313
what are autoimmune thyroid diseases and what causes them?
diseases: AI hyperthyroidsim/graves
cause: TSH antibodies → TSI (thyroid stim immunoglobs) 
  • TSI thyroid activity stimulates thyroid independent of TSH
314
what is the most common cause of hyperthyroidism and what are the lab results? What is a common sign?
graves
↓TSH ↑T₄
exopthalmos
315
what do autonomous thyroid tissue do and what are the labs?
toxic adenoma/multinodular goider develop auto function → make excess thyroid 

labs:↓TSH,↑T₄
316
what is a rare cause of hyperthyroidism
↑TSH via TSH-producing macoradenomas?
317
what does TSH-producing adenomas cause and what are their labs?
cause: secondary hyperthyroidism 
labs: ↑TSH and T₄
318
what is the inidcation for low RAIU and what is it not associated with?
low: <10% @24hrs

indication: inflamm or destruction of thyroid tissue → released of pre-formed/extra thyroidal source hormone to circulation

NOT ASSOCIATED: ↑ thyroid function
319
what does thyroiditis result from and what does it cause?
result from: inflammation

cause:  injury from thyroid follicular cells → transient hyperthyroidism due to pre-formed T₃/T₄
320
What are the labs for thyroiditis?
↓TSH
↑T₄
321
what forms of thyroiditis present with pain and tenderness and what causes it?
subacute(viral,URI)
infectious(bacterial, staph/strep)
322
what are forms of thyroiditis that present w/o pain and tenderness?
painless(AI, NOT hashis/graves)
postpartum
drug-induced(amnio,lithium)
323
what is the initial presention of thyroiditis followed by?
hypothyroid phase → thyroid fnx recovery (possible)
324
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what can give rise to exogenous or ectopic hyperthyroidism and when can it occur?
rise: external/interal sources of excess thryroid hormone
 
cause:
  • factitious
  • levo overdose
  • struma ovarii
  • large metastases from follicular carcinoma
330
what is struma ovarii?
functioning thyroid tissue in ovarian neoplasm
331
what causes high RAIU?
↑ thyroid function causes 
332
what causes low RAIU
causes not associated with ↑ thyroid function 
333
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// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
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336
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
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337
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338
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Toggle Masks
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339
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340
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341
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342
what happens to thyroid function during chronic AI thyroiditis?
gradual, permanent loss of function 

*NO initial hyperthyroid phase*
343
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344
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345
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346
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347
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348
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349
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350
what is rare in the western world but still occurs worldwide?
iodine deficiency 
351
what is an example of infiltrative 1º hypothyroidism?
hemochromatosis
352
what are the two major disorders of the adrenal cortex?
1. adrenal hyperfunction
2. excess circulating levels
353
What are the 3 adrenal hyperfunction disorders?
1. hyperaldosterism(↑aldosterone)
2. cushings syndrome(hypercortisolism)
3. phenochromocytoma(↑ catecholamines)
354
what are the two forms of hyperaldosteronism and where do they originate from?
primary → adrenal gland
secondary→ not from gland
355
what is aldosterone secretion mediated by?
Angiotension II, ACTH and K+ levels
356
what does aldosterone do?
  • active reabs of Na+
  • passive reabs of H₂O
  • active excretion of K+(↑BP/ blood vol. and hypoK)
357
what happens if there is too much aldosterone?
Na+ retention and K+ loss 
358
what are the primary causes of 1º hyperaldosteronism?
  • adrenal adenoma/carcinoma
  • bilateral hyperplasia of adrenal gland
359
what is the clinical presentation of hyperaldosteronism and why?
HTN (aldosterone controls BP)
muscle weakness and paralysis (hypoK)
360
what are the etiologies of primary hyperaldosteronism?
  • conn's
  • bilateral adrenal hyperplasia
  • familial hyperaldosteronism(rare)
361
what is the cause of Conn's syndrome?
a benign cortical adenoma
362
how is primary hyperaldosteronism diagnosed? 
  • plasma aldosterone (AM)
  • CMP
  • PRA(plasma renin activity) blood test 
  • Imaging(CT/MRI)
  • EKG(AFib)
363
what are the symptoms of hyperaldosteronism?
  • ↑ BP
  • headache/vertigo
  • muscle weakness/ fatigue
  • periodic paralysis 
  • polydipsia
  • weight gain 
364
when are patients screened for hyperaldosteronism?
If hypoK with ↑K+ doses
resistant HTN
365
what are complications of yperaldosteronism?
MI, HF, Stroke
366
What is the treatment for hyperaldosteronism?
  • treat cause 
  • removal (benign adenoma) 
  • diuretics (bilateral hyperplasia)

367
what is secondary hyperaldosteronism?
↑ aldosterone adrenal production from extra-adrenal stimuli
368
what are the causes of secondary hyperaldosteronism?
  • liver cirrhosis w/ ascities 
  • shock
  • renin secreting tumors
  • HF
  • Renal stenosis (resistant HTN)
369
what is hypercortisolism?
Cushing syndrome/ disease 
370
what are the endogenous causes of cushing syndrome?
tumor in adrenal cortex or pituitary 
371
what are the exogenous causes of cushing syndrome?
medication
adrenal hyperplasia
372
what are the endogenous causes of cushing diease?
tumor in the anterior pituitary
excess ACTH production
pituitary hyperplasia
373
what do both cushing syndrome and disease have in common?
THEY ARE THE SAME
both hypercortisolism and affected by ACTH
374
Is Cushing syndrome endogenous or exogenous?
exogenous (MC) and temporary 
375
what are the clinical manifestations of Cushings?
  • HTN
  • Moonface/obesity
  • osteoporosis/ecchymosis easily 
  • insulin resistant
  • irregular menstration/ body hair
  • thin skin
  • major depression/mood swings/memory loss/ ↓ [conc]
376
what are the key symptoms of cushings?
abnormal fat distribution (buffalo hump)
moon face 
hirsutism
stretch marks/ thin skin
377
what is the most common cause of endogenous cushing syndrome and what does it do?
adrenal/pituitary adenoma → ectopic ACTH production
378
what is the most common cause of exogenous Cushing syndrome?
cortisol like meds
379
what are the most common causes of Cushings disease? 
anterior pituitary adenoma(benign) 
pituitary hyperplasia → too much ACTH
380
who commonly gets cushings syndrome?
women 20-40 yo
381
arenal carcinomas are [...] and produce [...] of androgens 
arenal carcinomas are larger and produce excessive amounts of androgens 
382
adrenal adenomas are [...] and mostly produce [...]
adrenal adenomas are benign, small and mostly produce cortisol
383
ectopic causes of [...] are [...] and are NOT inhibited by [...]
ectopic causes of ACTH secretion are malignant tumors, bilateral adrenal hyperplasia and are NOT inhibited by cortisol or other steroids
384
the most common cause of [...] cushing syndrome is [...] because they i[...] secretion → [...]
the most common cause of exogenous cushing syndrome is chronic use of steroids because they inhibit CRH and ACTH secretion → bilateral adrenocorticol atrophy 
385
the 3 components of glucocorticoids are [...], [...] and [...] 
the 3 components of glucocorticoids are cortisone, cortisol and cotricosterone 
386
gluconeogenesis occurs mainly in the [...] and makes [...] from [...]
gluconeogenesis occurs mainly in the liver and makes glucose from non-carb sources
387
glycoysis is the [...] → [...] and [...]
glycoysis is the breakdown of glucose → pyruvate and energy 
388
glycogenolysis is the [...] to release glucose which occurs on the [...] and is stimulated by [...]
glycogenolysis is the breakdown of glycogen to release glucose which occurs on the liver and muscle and is stimulated by epi and glucagon
389
gluconeogenesis is stimulated by [...], [...] and [...] that have [...] and [...]
gluconeogenesis is stimulated by mobilized amino acids from extrahepatic tissues, fat breakdown in adipose and inhibits glucose uptake in muscle and adipose tissue that have anti-inflammatory and immunosuppressive properties
390
mineralocorticoids and glucocorticoids are released from the adrenal cortex via the [...] of the [...] that releases [...] → [...]
mineralocorticoids and glucocorticoids are released from the adrenal cortex via the feedback loop cycle of the hypothalmic-pituitary-adrenal axis that releases CRH from hypothalamus → ACTH from pituitary
391
CRH is produced by the [...] and is carried via [...] to pituitary that [...] in pituitary
CRH is produced by the hypothalamus and is carried via hypophysial artery to pituitary that stimulates ACTH in pituitary
392
ACTH follows the [...] and is [...]. They control the [...] and [...]
ACTH follows the circardian rhythm and is undetectable by midnight. They control the production and release of sterids and stimulate cholesterol to pregnenolone(precursor)
393
adrenal insufficiency is caused by [...] that is caused by [...] at any level of [...]
adrenal insufficiency is caused by insufficient circulating gluco/mineralcorticoid hormone that is caused by abnormailites at any level of hypothalamic-pituitary-adrenal axis
394
what are the risk factors for adrenal insufficiency?
  • genetics
  • medications(rifampin)
  • withdrawl
  • hypercoagulable states
  • severe sepsis 
395
what are the etiologies of primary adrenal insufficiency?
  • autoimmune (80%)
  • infection
  • metastatic invasion
  • adrenal hemorrhage(sepsis)
  • inflintrative (sarcoidosis, hemochromatosis)
  • bilateral adrenalectomy
396
primary adrenal insufficiency is the [...] with [...] that are [...]
primary adrenal insufficiency is the inability for the adrenal gland to release hormone with skin manifestations that are common but not diagnostic 
397
what are common clinical manifestations of primary adrenal insufficiency?
  • insidious
  • chronic malaise
  • fatigue (worse with exertion, better with rest)
  • anorexia/weight loss
  • GI
  • hypotension 
398
what are key clinical manifestations of primary adrenal insufficiency?
  • hyponatremia(salt craving)
  • hyperK
  • hypoglycemia
  • hyperpigmentation (hair, nails, freckles become darker, patchy)
399
Addison's is the [...] due to [...] that results from the [...] where at least [...]
Addison's is the hyposecretion of cortisol and aldosterone due to adrenal gland failure that results from the progresive destruction of the adrenal cortex where at least 90% of the cortex is destroyed 
400
Addisons dieases is [...] and usually occurs at [...]
Addisons dieases is uncommon and usually occurs at 30-50 yo
401
Addisons is diagnosed with [...] consisting of [...] along with [...] and [...] 
Addisons is diagnosed with labs consisting of Na+,K+, AM cortisol and ACTH along with chest/ab x-ray and flu test  
402
the treatment for Addison's is [...], [...] and [...]
the treatment for Addison's is IV hydorcortison, fluid restiction and steroid replacement
403
they key differences in clinical presentation of 2º and 3º adrenal insufficiency are [...] or [...], [...] and less common [...]
they key differences in clinical presentation of 2º and 3º adrenal insufficiency are no hyperpigmentation or ACTH↑, no hyperK and less common GI, hyponatremia and hypotension
404
what are the eitologies for 2º adrenal insufficiency?
  • hypopituitarism
  • pituitary infiltrative disease
  • Sx
  • acute interruption of prolonged steroid use
405
what are the etiologues of 3º adrenal insufficiency?
  • head trauma
  • sepsis
  • hypothalamus insufficiency 
  • invasive neoplasms
406
2º and 3º adrenal insufficiency is diagnosed with [...], [...], [...], t[...], [...], [...]
2º and 3º adrenal insufficiency is diagnosed with ↓cortisol levels in morning <3, ACTH stim test, cortisol <5, thyroid panel+ TSH, CT/MRI/CXR, Renin and Aldosterone
407
Increaced [...] with low [...] helps confirm [...]
Increaced ACTH with low cortisol helps confirm 1º adrenal insufficiency
408
2º and 3º adrenal insufficiency is treated with [...] in mild cases and [...] for moderate/sev cases. Treatmet for severe cases like adrenal crisis calls for [...]
2º and 3º adrenal insufficiency is treated with hydrocortisone in mild cases and hydrocortisone/prednisone + florinef for moderate/sev cases. Treatmet for severe cases like adrenal crisis calls for admission to ICU
409
Adults with adrenal insufficiency are monitered [...] and ped every [...] by endo. They are screened [...] for [...]. Pts are educated in regards to steroids during [...]. Genetic counseling is recommonened for [...]
Adults with adrenal insufficiency are monitered every month and ped every 6-12 months by endo. They are screened annually for thyroid, DM, premature ovarian failure, celiac disease, and vit B12 def. Pts are educated in regards to steroids during illness, fever and stress. Genetic counseling is recommonened for 1º
410
the three 1st line test to diagnose hypersortisolism are [...], st[...], and [...]
the three 1st line test to diagnose hypersortisolism are urine(24hr), steroid supression(overnight LDDST), and saliva(11pm-12pm, ↑ if cushings)
411
a standard 2 day low dose [...] test consist of dexamethasone admin [...] x [...]. A [...] is obtained and repeated [...] of test. If [...], [...] with [...]
a standard 2 day low dose dexamethasone test consist of dexamethasone admin every 6 hrs x 8 doses. A 24 hr UFC baseline is obtained and repeated 2nd day of test. If abnormal, cortisol is not suppressed by dexamethasone with cushings
412
When diagnosis Cushings, if there is an [...] cause, the next test after labs and suppression test is [...] with [...], [...], or [...]
When diagnosis Cushings, if there is an endogenous cause, the next test after labs and suppression test is imaging with CT of adrenals, MRI of pituitary, or CT/MRI of thorax and abdomen(ectopic ACTH producing tumor)
413
the treatment for cushing's syndrome is to [...].
In order to reverse clinical manifestations, [...]
If there is a tumor → [...]

When treating, [...] should be conidered
the treatment for cushing's syndrome is to treat the 1º cause.
In order to reverse clinical manifestations, steroid taperring is used.
If there is a tumor → surgery

When treating, avoiding permenent med/ hormone dependence should be conidered
414
A trans-spehnoidal/pituitary endoscopic surgery is approached through [...] or [...]. The potential risks of the surgery are [...]. The most direct approach is a [...]. 
A trans-spehnoidal/pituitary endoscopic surgery is approached through upper lip or endonasally. The potential risks of the surgery are CSF leak. The most direct approach is a craniotomy. 
415
When tumor is not found or not cured by trans- sphenoidal resection, [...] and/or [...] is used. 

When tumor is not found or not cured by trans- sphenoidal resection, pituitary irradiation and/or cytotoxic chemotherapy is used. 


416
If irradiation fails to normalize cortisol secretion, a [...] is performed. It will be followed by l[...]
If irradiation fails to normalize cortisol secretion, a surgical bilateral total adrenalectomy is performed. It will be followed by lifelong glucocorticoid & mineralocorticoid replacement

417
the treatment for exogenous Cushing's syndrome is to [...] with [...]. Be cautious with [...] and [...] when steroids are stopped

the treatment for exogenous Cushing's syndrome is to stop glucocorticoid administration with gradual withdrawl. Be cautious with withdrawl and peroid insufficiency when steroids are stopped


418
The improvements that occur with effective therapy for Cushing's syndrome are the [...], [...] and [...]
The improvements that occur with effective therapy for Cushing's syndrome are the manifestations disappear over 2-12 months, HTN and glucose intolerance improve and osteoporosis improves over 6 mos
419
Untreated Cushing's is [...] becuase of C[...]. [...] or [...] have [...] prognosis
Untreated Cushing's is fatal becuase of CV, clots, HTN complications or bacterial infections. Ectopic ACTH seretion or adrenocortical carcinoma have poor prognosis
420
[...] is the appearance of [...] and have some [...] but with a different [...].
Psueod-Cushing syndrome is the appearance of cushingoid and have some silimar biochemical abnormailites but with a different etiology.
421
Etiologies of Pseudo-Cushing's Syndrome are severe [...], [...], [...], [...] or [...]
Etiologies of Pseudo-Cushing's Syndrome are severe major depression, alcoholism, PCOS, morbid obesity or ESRD 
422
Pseudo-Cushing’s syndrome is also called [...] and is defined as a [...] that is not related to a [...]
Pseudo-Cushing’s syndrome is also called non-neoplastic hypercortisolism (NNH) and is defined as a mild to moderate hypercortisolism that is not related to a ACTH tumor 

423
what are the transient 5 P's of the clinical manifestations of phenochromocytoma?
  • pressure
  • palpatations
  • perspiration
  • pain 
  • pallow
424
What are the other non-speficic clinical manifestations of phenochromocytoma?
  • weight loss
  • anxiety/ tremors
  • flank pain
  • cardiac arrythmia/cardiomyopathy
  • nausea/weakness
425
a phenochromocytoma is a [...] but [...] tumor on the [...] and causes [...] hormone secretion
a phenochromocytoma is a rare but benign tumor on the adrenal medulla(epi and norepi secretion) and causes paroxysmal/continuous hormone secretion
426
A phenochromocytoma is diagnosed with [...] and labs via [...]
A phenochromocytoma is diagnosed with CT/MRI and labs via catecholamine urine and plasma levels 
427
A phenochromocytoma is managed with [...] or [...]
A phenochromocytoma is managed with ⍺/𝛃 blockers or surgical resection
428
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429
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// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
430
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
431
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
432
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
433
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
434
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
435
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
436
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
437
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
438
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
439
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
440
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
441
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
442
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
443
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
444
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
445
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
446
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
447
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
448
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
449
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
450
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
451
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
452
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
453
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
454
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
455
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
456
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
457
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
458
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
459
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
460
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
// Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
461
// Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = "visible"; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); }
Toggle Masks
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Hyperthyroidism is an [...] that can present with [...] and [...]
Hyperthyroidism is an excess of thyroid hormone cirulating in the blood that can present with increased heat production and adrenergic sensitivity (tachy,tremor)
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What are the causes of hyperthyroidism?
  • graves 
  • ectopic production
  • toxic multinodular goiter/adenoma
  • subacute thyroiditis
  • exogenous ingestion
  • TSH-mediated
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the ophthamlmic manifestations of graves result from [...] causing [...] and the [...]
the ophthamlmic manifestations of graves result from AI binding of IGF 1 receptors causing inflammation, edema, increased pressure in the orbit and the accumulation of glycoaminoglycans(GAG)
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the ophthalmic presentation of graves can consist of [...]
the ophthalmic presentation of graves can consist of possible vision loss, corneal irritation and diplopia
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the most common skin site affected by graves is the [...] and presents as a [...] of [...]
the most common skin site affected by graves is the shin and presents as a raised, hyperpigmented, orange peel texture of papules 
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Other common skin signs of graves are [...]. The only symptom that is indicitive of graves is [...]
Other common skin signs of graves are sweating, onycholysis, pruritis, and thin hair. The only symptom that is indicitive of graves is infiltrative dermopathy
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Myxedema is [...] caused by [...] seen in [...].
Myxedema is skin changes from edema caused by severe hypothyroidism seen in myxedema coma.
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Myxedema coma can present with [...] and [...] → [...]
Myxedema coma can present with edema, mental change, hypotension/brady and low temp → death

graves/hyperthyroidism → pretibial myxedema 
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the cardio effects of graves → [...], [...] and [...]. Another finding more commonly found in eldery is [...]
the cardio effects of graves → increased CO + HR, wide pulse pressure and ↓ perph vasc resistance. Another finding more commonly found in eldery is AFib
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Respiratory sypmtoms of graves can present as [...] or [...] due to the [...]
Respiratory sypmtoms of graves can present as dyspnea or dyspnea on exertion due to the trachial obstruction of a goiter
472
GI symptoms of graves presents as [...], [...] and [...]
GI symptoms of graves presents as weight loss, ↑ gut motility and diarrhea/malabsorption

Endocrine (2 decks)

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