Endocrine Diseases Flashcards

1
Q

Adrenal Insufficiency causes :

  1. primary
  2. secondary and tertiary
  3. acute
  4. chronic
A

primary–addisons disease–MCC is autoimmune destruction of adrenal gland–>lack of cortisol and aldosterone

secondary–pituitary failure to secrete ACTH or suppression of HPA axis–>lack of androgens and cortisol

tertiary–hypothalamic disease and decr in CRH

acute–addisonians crisis

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2
Q

what happens if a PT is abruptly stopped on steroid tx?

A

adrenal insufficiency

  • bc steroids provide exogenous negative feedback to the pituitary
  • if steroids are stopped…the pituitary takes time to recover function–and during that time–adrenal insufficency can occur
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3
Q

in secondary adrenal insufficiency– ACTH is H/L and aldosterone is H/L??

A

ACTH–low
aldosterone–not affected so its normal
*of course low cortisol

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4
Q

MCC for acute adrenal insufficiency–Addisonians crisis

A

abrupt withdrawl of corticoid tx or a skipped dose of steroids

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5
Q

precipitating factors for addisonian crisis?

A

stressful event

  • surgery
  • illness
  • trauma
  • volume loss
  • hypothermia
  • MI
  • fever
  • hypoglycemia
  • steroid withdrawl
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6
Q

MCC for addisonian crisis

A

abrupt withdrawl of glucocorticoids

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7
Q

imaging for chronic and acute adrenal insufficiency

A

CT: of the adrenal glands if unsure if insuff is autoimmune or not

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8
Q

CT imaging findings for Addison disease

A

small noncalcified adrenal glands

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9
Q

when do you see adrenal calcifications?

A
  • tuberculous addison dz
  • hemorrhage
  • fungal infection
  • pheochromocytoma
  • melanoma
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10
Q

how to test for adrenal insufficiency (AI)

A
  1. order basic metabolic panel and do 8am measure of serum cortisol
    - ->If results inconsistent with AI: consider other diagnosis
    - ->If low cortisol levels, normal to high K and low to normal Na are found then go to:
  2. Cosyntropin ACTH stimulation test: where we measure basal ACTH levels B4 administering IV ACTH–then we measure the cortisol levels after 30-60 mins
    - –>if normal: consider other diagnosis
    - –>LOW cortisol and HIGH acth–PRIMARY AI
    - –>LOW cortisol and LOW acth–secondary AI
  3. If primary AI:
    - measure 21-hydroxylase antibody
    - CT of adrenal glands
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11
Q

lab findings for primary adrenal insuff

  • CRH
  • ACTH
  • cortisol
  • Aldosterone
  • Renin
  • what would the ACTH stimulation test results show?
A
high CRH
high ACTH 
low cortisol 
Low aldosterone 
high renin  

ACTH stim tests would show: high ACTH

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12
Q

lab findings for secondary adrenal insuff

  • CRH
  • ACTH
  • cortisol
  • aldosterone
  • Renin
  • what would the ACTH stimulation test results show?
A
CRH: high 
ACTH: low 
Cortisol: low 
aldosterone: low 
Renin: normal to low 

ACTH stim test: absent/low ACTH

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13
Q

lab findings for tertiary adrenal insuff

  • CRH
  • ACTH
  • cortisol
  • aldosterone
  • Renin
  • what would the ACTH stimulation test results show?
A
CRH: low
ACTH: low 
Cortisol: low
Aldosterone: low 
Renin: normal to low 

ACTH stim test: exaggerated or prolonged

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14
Q

BMP results for adrenal insufficiency

  • k
  • na
  • glucose
A

hyponatremia
hyperkalemia
hypoglycemia

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15
Q

list the disorders of HYPOfunction of adrenal glands

-both primary and secondary

A

PRIMARY

  • ACUTE adrenal insufficiency–addisonian crisis
  • addison’s disease

SECONDARY:
-pituitary failure of ACTH secretion–aka CHRONIC adrenocortical insufficiency

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16
Q

List the disorders of HYPERfunction of adrenal glands

-primary and secondary

A
  • Cushing’s disease–SECONDARY
  • Cushing’s syndrome
  • Primary hyperaldosteronism
  • Pheochromocytoma
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17
Q

Manifestations of ________ cause Cushing’s syndrome

A

Hypercortisolim

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18
Q

Hypercortisolism aka?

A

Cushing Syndrome

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19
Q

Different b/w Cuhsing’s DZ and Syndrome?

A

Disease: Pituitary Gland overprodues ACTH(due to hyperplasia or adenoma)—secondary cause of Hypercortisolim

Syndrome: s/s related to cortisol excess…..does not specify a cause of source of why excess cortisol.. has 4 main causes.. .ONE Of them is Cushing Disease

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20
Q

Four main causes of Cushing Syndrome

A
  1. Exogenous sources: long-term high dose glucocorticoids tx—-MCC overall!!!**
  2. Endogenous:
    - over secretion of ACTh from AP—-cushing’s disease–MC endogenous cause!!!!!*******
    * secondary

or

  • Ectopic ACTH producing tumor/adenoma (MEN, SCLC)
  • secondary

or

-Adrenal Tumor/adenoma (primary)

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21
Q

MC place for an ectopic tumor secreting ACTH

A

lungs—small cell lung Ca

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22
Q

low dose dexamethasone test is used as?

A

screening test for Cushing syndrome

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23
Q

when do we do high dose dexamethasone test??

A

after we get a negative result on low dose—- aka elevated cortisol levels
**used to distinguish a pituitary cause AKA cushing dz from an adrenal cause/other cause

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24
Q

Dexamethasone test results below indicate what cause of Cushing Syndrome:

  1. high ACTH with suppression of Cortisol
  2. High ACTH with no suppression of cortisol
  3. Low ACTH with no suppression of cortisol
A
  1. Cushing Dz (bc adrenals are sending neg feedback to AP—but AP is not listening)
  2. Ectopic ACTH producing tumor
  3. Adrenal tumor and/or exogenous steroids
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25
Q

list the three screening tests for cushing syndrome

*which is the most specific

A
  1. 24 hour urine test to test for cortisol-MOST SPECIFIC
  2. Nighttime salivary cortisol (11pm)
  3. Low dose 1 mg overnight dexamethasone test
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26
Q

if a low dose dexamethasone test does NOT suppress ACTH…..

A

indicates that cushing syndrome exists

but does not tell us the SOURCE of the increased cortisol—– why we do the high dose dex test

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27
Q

does an ectopic ACTH producing tumor respond to the negattive feedback?

A

NO

*why this test result will show as HIGH acth and no suppression of cortisol

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28
Q

When localizing the ACTH for dex test—- _____ responds to the negative feedback and _____ does not

A

Cushings disease DOES respond to neg feedback (why cortisol is supressed)
ECtopic ACTH prod tumor does not (why cortisol not supressed)

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29
Q

MCC of primary hyperaldosternoism

A

Bilateral adrenal hyperplasia

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30
Q

primary hyperaldosternoism is renin indep or dependen?

A

independent

Renin levels are NOT increased.. only seen with secondary

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31
Q

Conn syndrome is?

A

Adrenal Aldosternonoma—tumor in the zona glomerulosa secreting aldosterone
*primary form of hyperaldosteronism

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32
Q

triad for hyperaldosteronsm?

A

HTN— very very very drug resistant
HyPOkalemia
Metabolic alkalosis

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33
Q

PTs usually present how for hyperaldosteronism?

A

usually asympto

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34
Q

lab results for primary hyperaldosternoism?

A
HIGH aldosterone and normal renin 
20:1 ratio 
-Hypok 
-hypernatremia 
high ph
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35
Q

labs for secondary hyperaldosternoism?

A

High aldosteron
high plasma renin levels—–because RAAS is activated due to renal artery stenosis– and increase in RAAS–increase renin–increase aldosterone

**NOT an adrenal issue here

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36
Q

define adenoma

A

a tumor that is non cancerous

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37
Q

Most common place for neuroendocrine tumors to arise?

why?

A

lungs and GI tract
WHY? because THEY LOVE BLOOD– love to grow in vascularized areas

**but since they are from neuroendocrine cells– they can arise technically anywhere

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38
Q

Characteristics of carcinoid tumors can cause?

A

carcinoid syndrome

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39
Q

carcinoid syndrome manifestations

A

flushing
diarrhea
wheezing

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40
Q

TSH secreting pituitary adenoma

  • what is it
  • size?
  • invasive?
A

TSH producing adenoma… rare

  • large
  • very invasive
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41
Q

presentation for TSH secreting pituitary adenoma

A

diffuse goiter >95% of time

  • hyperthyroid s/s
  • pituitary adenoma s/s
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42
Q

lab work for tsh secreting pit adenoma

A

High TSH and High free T3/T4

  • also can have some vision disturbances if its obstruction optic chiasm
  • **because it is secondary hyperthyroidism
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43
Q

how to diagnose TSH secreting pituitary adenoma

A

MRI***

2. radioactive iodine uptake scan–will note diffuse uptake

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44
Q

radioactive iodine uptake scan–how does it work and for what hormone

A

TSH
-when TSH rises–thyroid gland uses iodine to make the T hormones–RAIU tests use a radioactive tracer (iodine) to measure how much tracer the thyroid gland absorbs

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45
Q

what disease will have diffuse uptake for RAIU

A

graves or TSH secreting pituitary adenoma

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46
Q

what disease will have decreased uptake for RAIU

A

thyroiditis

-hashimoto, postpartum

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47
Q

what disease will have “hot nodule or hot spot” uptake for RAIU

A

toxic adenoma

hot spot= focal area of increased uptake

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48
Q

what disease will have multiple nodules uptake for RAIU

A

toxic multinodular goiter

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49
Q

list the well differentiated thyroid CAs

A

papillary throid carcinoma

follicular thyroid Carcinoma

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50
Q

list the invasive and poorly differentiating thyoid CAs

A

Medullary thyroid carcinoma

anaplastic thyroid carcinoma

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51
Q

if she shows a pathology pic– which thyroid CA would it be?

A

papillary thyroid carcinoma

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52
Q

pathology shows “orphan Annie eye Nuclei”— what CA?

A

papillary thyroid carcinoma

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53
Q

which the MC thyroid CA?

A

papillary thyroid carcinoma

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54
Q

who have a poorer prognosis for papillary thyroid carcinoma.. men or women?

A

MEN**

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55
Q

who has a higher incidene rate for papillary thyroid CA?

A

WOMEN

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56
Q

which of the thyroid cancers is least aggressive and highest cure rate?

A

papillary thyroid carcinoma

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57
Q

which of the subtypes for DM1 is MC?

A

subtype 1A

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58
Q

when does 1A usually peak for onset?

A

young… ages 4-14

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59
Q

trigger for subtype 1A?

A

outside factors

  • infection
  • gene mutation: HLA DR3-DQ2 and DR4
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60
Q

MC clin man for DM1

A

hyperglycemia without acidosis

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61
Q

second MC clin man for DM1

A

DKA

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62
Q

normal body ph

A
  1. 35-7.45

* **7.40

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63
Q

DKA is MC seen with? and Hyperglycemic Hyperosmolar state MC seen with?

A

DKA–DM1

HHS–DM2

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64
Q

anion gap equation
+
normals for anion gap

A

[NA+] - [Cl-] - [HCO3]

normals range from 3-11 or 8-16

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65
Q

explain the presentation of diabetic neuropathy

A

stocking glove distribution–finger tips–fingers–hands—arms—–
or
toe tip–toes—foot–calfs—etc
*progresses distal–>proximal SYMMETRICALLY

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66
Q

what test is done to test for DM neuropathy

A
  1. monofilament test
  2. also can use the vibration sense test with tuning fork—if the PT cannot feel the vibrations from the fork… then move the fork proximally until they do feel it to sense their degree of neuropathy
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67
Q

target A1C to be below??

A

7

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68
Q

lab vlaues for DKA

A
pH <7.3 
Bicarb <22 
\+ketones in urine 
BGL >250... but usually not above 600 
increased serum osmolarity
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69
Q

dawn phenomenon

  • define
  • describe patho behind it
  • management
A
  • normal glucose levels UNTIL
  • ->2-8am

*results from decrease insulin sensitivity and nightly surge of counterregulatory hormones during nighttime fasting–>cortisol, glucagon, GH

  • tx:
  • bedtime injection of insulin (NPH) to blunt morning hypergycemia
  • avoid nighttime snacks or CHO snacks late at night
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70
Q

Somogyi effect

  • define
  • describe patho behind it
  • management
A

nocturnal hypoglycemia followed by rebound hyperglycemia

*due to surge in GH after the early AM hypoglycemia

tx:
- decrease nighttime insulin (NPH) dose
- give bedtime snack
- move evening dose of NPH to earlier

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71
Q

insulin waning

  • define
  • describe patho
  • tx
A

progressive rise in glucose from bed–> morning

  • seen when NPH evening dose is administered before dinner
  • due to ineffective dosing of NPH insulin

tx:
-move NPH insulin dose to bedtime
or
-increase the evening dose

*happens a lot with newly diagnosed diabets who are unsure how todo nightttime dose

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72
Q

what is the main reason for delayed diagnosis of DM2

A

lack of overt s/s in the early disease process

**many PTs are diagnosed during anual screeings or incidentally with blood tests

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73
Q

ADA screening for DM

A

all adults greater than or equal to 45 X3 years
OR
BMI >25 in adults

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74
Q

explain patho behind poor wound healing in DM

A

DM patients have poor circulation bc their BVs are narrower–>glucose damages endothelium (constant inflammation)–>not enough oxygen is bound to hemoblogin–>less going to the area to be fixed

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75
Q

four diagnotic criteria for DM

A
  1. random glucose >200
  2. fasting glucose >126
  3. 2-hour postprandial glucose >200
  4. HgA1c>6.5%
76
Q

differences b/w DM 1 and DM 2

  • onset
  • age of onset
  • body habitus
  • ketoacidosis
  • Autoantibodies
  • endogenous insuli
  • concordance in ID twins
  • Prevalence
A

DM1:

  • onset=sudden
  • age of onset=mostly under 30
  • body habitus=thin or normal
  • ketoacidosis=common
  • autoantibodies=usually present
  • endogenous insulin=low or absent
  • twins=50%
  • prevalence=less prev than DM2

DM2:

  • gradual
  • mostly adults
  • often obese
  • rare DKA
  • absent antibodies
  • insulin is normal decreased or increased
  • 90% for twins
  • more prevant—– 90-95% of US diabetics are type 2
77
Q

is there a cure for DM1 or DM2?

A

NOPE

only maintenance

78
Q

TOC for DM?

A

fasting plasma glucose levels

**check notes for the exact levels to diagnose preDM and DM

79
Q

define impaired fasting glucose (IGF)

A

fasting glucose level of 100-125

80
Q

define impaired glucose tolerance test (IGT)

A

plasma glucose levels 140-199 2 hours after a 75 gram glucose load

81
Q

patients with IFG and IGT have DM?

A

no

-but are at very very high risk of developing DM2 and CVD in future

82
Q

how to diagnose somogyi effect vs dawn? *what do we want to measure?

A
AM VMA (b/d of epinephrine) in the urine levels 
WHY?? 

because in somogyi—the hypoglycemia in middle of the night is a stressful event— so the body goes into FIGHT OR FLIHGT mode and secretes EPI, cortisol, glucagon etc….. compard to the dawn– no epi is releeasd

83
Q

DKA is usually precipitated by?

A

recent infection

84
Q

very commonly how do DM1 patients initially present?

A

in DKA

85
Q

how often should DM patient get food exam

A

1-2 times per year

86
Q

how often should DM get HBA1 checked

A

2-4 times/year by doctor
AND
DAILLLYYY by the PT

87
Q

how often should DM get eye exam

A

annual or biannual

88
Q

how often should DM get screening for neuropathy

A

annual

89
Q

BP screening for DM done how often

A

quarterly

90
Q

Which immunications is VERY imp for DM to get?

A

influzena
pneumococcal
Hep B

91
Q

What is the MC cause of HHS and WHY

other precipitating factors

A

infection
*bc illness will lead to dehydration—->increased serum osmolarity–>leads to HHS

OTHEER:

  • mi
  • stroke
  • surgery
92
Q

what is the plasma glucose range in Pt with HHS

A

> 600

*DKA was lower like 250

93
Q

plasma osmolarity for HHS?

A

> 320

94
Q

what is not seen with HHS that is seen with DKA?

A

metabolic acidosis

95
Q

HHS frequently occurs with?

A

mild or occult (“hidden”) DM

96
Q

name meds that can cause HHS

A

phenytoin
diazoxide
corticosteroids
diuretics

97
Q

typical pt population who gets HHS

A

middle-aged to eldery PTs

WHY? bc they are more prone to forget to take meds

98
Q

onset of HHS?

A

insidious… usually over several days

99
Q

clinical manifestations of HHS

A

weakness
polyuria
polydipsia
dehydration

AMS only when super advanced and serum osmolarity is over 310

convulsions occurs when serum osmolarity >320-330

100
Q

PE findings for HHS

A

severe dehydration
lethargy
or coma (severe)

KUSSMUAL RESPS*****

101
Q

general definition of pituitary adenomas

A

benign tumors that arise from one of the 5 AP cell types
*may cause clinical effects from either OVER prodcution of the hormone OR supression by compressive effects of structures

basically can cause:
-hypopituitaryism
or
-hyperpituitarism

**MC is over production

102
Q

list the four cell types that pituitary adenomas can rise from

A
  1. somatotroph—->GH
  2. Lactotroph—>prolactin
  3. Corticotroph—> ACTH
  4. Thyrotrope—>TSH
103
Q

which hormone secreting Pit tumor is MC?

A

prolactinomas—50%

104
Q

what size of adenoma do you start seeing s/s?

A

2-10 cm

105
Q

Lab values for prolactinoma

A

HIGH prolactin
LOW FSH and LH

**TSH, GH and ACTH levels are always ordered too bc prolactinomas can cause hyper or hyposecretion of these hormones

106
Q

Lab values for Somatotroph adenoma

A

increase GH

107
Q

about ____ of all pituitary adenomas are nonfucntions and do not secrete hormones

A

1/3

108
Q

define microadenoma

A

<10mm

109
Q

define macroadenoma

A

> 10mm

110
Q

which pituitary adenomas are common to see in MEN1

A

prolactin and GH secreting tumors

111
Q

general s/s for pituitary adenoma either hypo or hyper secreting

A
HA 
vision changes ---- bitemporal hemianopsia 
diplopia
ptosis
opthalmoplegia 
decreased facial sensation 

can see hypopituitarism OR hormonal excess

112
Q

MC cause of hyperprolactinemia

other causes

A

prolactinoma

primary HYPOthyroidism— because Increase TRH stimulates prolactin

aromegaly

pharmacologic: dopamine antagonists, 1st and 2nd gen antipsychotics, estrogen

physiologic:
- pregnancy
- stess
- exercise

113
Q

s/s of hyperprolactinemia

  1. men
  2. women
A
  1. Men—hypogonadism (bc prolactin inhibits GnRH)
    - Ed
    - decr libido
    - infertitlity
  2. women–hypogonadism–oligomenorrhea, amenorrhea, infertility, vagina ddryness, galactorrhea
114
Q

prolactin inhibits what hormone

A

GnRH

115
Q

somatotroph adenoma causes?

A

acromegaly–>adults

gigantism–>kids

116
Q

corticotroph adenoma causes?

A

cushing’s DISEASE

117
Q

thyrotroph adenoma causes

A

hyperthyroidism

118
Q

lab values for cortitotroph adenoma?

A

CUSHINGS DZ
so….
high cortisol
high acth

119
Q

GH is a counterregulatory hormone that increases what?

A

glucose!

120
Q

increase GH stimulates hepatic productino of?

A

IGF-1

*insulin like growth factor

121
Q

lab values for gigantism/acromegaly

A

IGF-1 elevated (3-10 fold)

GH typically elevated–

122
Q

which hormone do you use for diagnostic lab values to diagnose giantism/acromegaly

A

IGF-1 bceacuse it is more consistenly elevated compared to GH

123
Q

complications from gigantism/acrpmegaly

A
LV diastolic HF 
cardiomegaly--cardiomyopathy 
glucose intolernce and DM 
colonic malignancy 
HTN
124
Q

initial screening test of choice for gigantism/acromegaly

A

insluin-like growth factor lab values

125
Q

what is the mortality rate for PT with giagantism

A

increases 3 fold compared to PT w.o

*survival rate 10 years less

126
Q

confirmatory test for gigantism/acromegaly?

*results compared to pt w.o

A

oral glucose suppression test

-pt with disease will have elevated GH (bc normal response would be decreased)

127
Q

image of choice for acromegaly or gigantism

A

MRI to check for pituitary lesions

128
Q

high dose dexamethasone test results for cushings disease

A

cortisol will be suppressed

ACTH increased

129
Q

TOC for cushings dz

A

MRI

130
Q

dwarfism is?

A

GH deficiency–form of hypopituitarism

131
Q

etiology for dwarfism

A

congenital or acquired

acquired—GH deficiecny from tumors, infiltrative diseases or pitutary infarction or radaition tx

  • *pituitary does not make enough GH
  • -can be in isolation or with generalized hypopituitarism
132
Q

how to diagnose dwarfism

A

arginine and sleep stimulation test

133
Q

Lab values for dwarfism

A

Low GH

Low IGF-1

134
Q

arginine and GH

A

arginine stimulates GH

and inhibits somatostatin

135
Q

arginine sleep study test–how does it work

if somene has dwarfism– what will results show

A

done after overnight fasting

samples are collected at the same time that GH would be peak stimulated
intervals when GH is measured: 0, 30, 60, 90, 120 minutes
MAX GH peak is around 60 minutes

+dwarfism will have no change in GH release

136
Q

what is the diagnostic lab value to diagnose dwarfism

A

low serum IGF-1

137
Q

osmolarity define

expressed as?

measured in?

changes with?

A

[ ] of solution

expressed as the total number of solute particles per liter

measured as milimoles/liters

changes with tempterature

138
Q

define osmolality

measurd in??

affect with temp?

A

measure of the number of dissolves particles in a kg of the liquid they are dissolved in
*amt of dissolved substance (K NA CL Urea) in a sample of blood or fluid

measured in miliosmoles/kg

does not change with temperature

prefered in medicine

139
Q

normal serum osmolality?

A

280-295 mOsm/kg

140
Q

serum osmolality compared to osmolality inside cells

A

they are very close

141
Q

what body fluid is used to measure osmolality in humans? and why

A

serum*****
urine too

it is very very very close to the osmolality inside the cells

142
Q

define serum

A

what is left from blood once the cells and proteins have been removed

143
Q

define serum osmolality

A

how much water is in the blood compared to how many solutes are in the blood

144
Q

etiology for Central diabetes insipidus

A

NOOO production of ADH from PP

  • **idiopathic MC
  • head trauma
  • not hereditary
  • not genetic
  • not autoimmune
145
Q

what happens when there is no ADH production?

A

no reabsoprtion of water at the DCT back into the blood

  • so volume regulation is out of whack
  • body cannot concentrate urine–>large amounts of diluted urine–>increases serum osmolality
146
Q

function of ADH

A

decrease urine production
decrease sweating
increase BP

*increases water absorption–>increasing intravascular volume–>dilutes serum sodium

147
Q

clin man of DI

A

polyuria * like up to 20 times a day
polydipsia
* excessssive thirst becayse body wants to maintian water balance with all the peeing
**high volume nocturia

Neuro s/s are from hypernatremia: 
confusion
lethargy-
disorientation
seizures
coma
148
Q

PE findings for DI

A

dehydration
hypotension
rapid vascular collapse in severe cases

HYPOtensive

149
Q

labs for central DI

A

increased serum osmolality >295 with inappropr diluted urine

decreased urine osmolality (<300) and Specific gravity +increased urine volume

HYPERnatremia

150
Q

how to calculate serum osmolarity

A

(2x9Na+k) +(BUN/2.8) + (glucose/18)

151
Q

definitive diagnosis of DI? what test

A

Fluid deprivation test: dont give the PT water….and a normal response is progressive urine [ ] (since the body is getting dehydrated)

BUT in DI:
they still produce large amounts of dilute urine with a low urine osmolality

152
Q

how to differentite b/w DI central and nephorgenic? what test is don

A

Desmopressin ADH stimulation test

central= reduction in urine output + increase in urine osmolality (responding to ADH)

nephrogenic=contined production of large amts of diluted urine (No response to ADH)

153
Q

define SIADH

causes what?

A

non-physiologic excess from ADH over secretion from AP
OR
from ectopic source

causes FREE WATER RETENTION AND HYPOnatremia—because retaining more and more water which is decreasing the sodium in plasma

*kidneys cannot excrete the excess water

154
Q

what is the [ ] of urine for a pt with SIADH

A

very very concentrated
INCREASED urine osmolality
*urine sodium [ ] is very very high

155
Q

etiologies for SIADH

MC?

A

MC: is CNS related–SAH, stroke, Head trauma, meningitis, CNS tumors, Post-op, hydrocephalus

Pulmonary causes: small cell lung CA** secreting ectopic ADH, infection (Legionella pneumonia), HIV

MEDS: Anticonvulsants, Carbamazepine, Hydrocholorothiazide, NSAIDS, chlorpropamide, antidepressants (TCAs/SSRIs), high dose IV Cyclophosphamide, MDMA, narcotics

OTHER: HIV, Conn syndrome and hypothyroidism

*mechanically ventilated patients are at risk for it too

156
Q

Small cell lung CA.. always thikn of?

A

SIADH

**ectopic tumor producing ADH

157
Q

Clinical Manifestations of SIADH

A

S/s vary depending on how rapidly the condition develops:

Nausea/Vomiting 
Neurologic s/s are due to hyPOnatremia & cerebral edema: 
-HA
-weakness
-lethargy 
-confusion 
-disorientation 
-Seizures **
-Coma 

others:
* HTN

158
Q

lab values for SIADH

A
Decreased serum osmolarity 
Decreased BUN 
decreased serum NA+ 
***in the setting of normovolemia aka no s/s of edema
HIGH ADH 
Increased Urine somolarity with NA+ >20 

**diagnosis made in absence of renal, adrenal, pituitary, thyroid diseases or diuretic usage

159
Q

differences b/w Cenrtral DI and SIADH

  1. ADH and water
  2. urine output
  3. sodium
  4. serum osmolairty
  5. Risk of developing___?
  6. Tx
A

for Central DI:

  1. low ADH and low water in body
  2. very high UO +polyuria
  3. serum NA high–hypernatremia
  4. high serum osmolalty due to dehydration
  5. risk to develop hypovolemic shock
  6. DDAVP –synthetic ADH

SIADH:

  1. high ADH and high water in body
  2. decreased UP—Oliguira
  3. low soidum–hyponatremia
  4. low serum osmolarity
  5. risk of developing seizures from hyponatremia
  6. Hypertonic Saline
160
Q

oliguria

A

little urine prod

161
Q

CDI and SIADH pneumonics

A

SIADH—- Soaked Inside

DI—Dry Inside

162
Q

etiologies for hypocalcemia

MC?

A

MCC hypoparathyroidism ***
chronic renal disease or liver disease
Vit D deficiency–osteomalacia and rickets
Hypomagnesia
MEDS: diruetics, Ca chelators, bisphosphonates, denosumab

163
Q

hypocalcemia occurs at a level below____ mg/dl

A

8.0

164
Q

functions of CAclicum

A

blood coagulation
neuromusc actiivty
cellular acitivty
bone integrity

165
Q

most of CA is bound or unbound?

A

BOUND to albumin **why we get “corrected” levels*

166
Q

Calcium levels are controlled by?

A

PTH–increaeses levels
Calcitonin–decreases levels
Vit D–increases levels

167
Q

if calcium is low and PTH is high… explain some etiologies behind this

A
  1. VIt D deficiency is causing hypocalcemia—the parathyroid is releasing PTH in response
  2. PTH itself may be abnormal/non functional
  3. PTH receptors may be resistant to PTH–leading to elevated serum PTH and ineffective hormone–also called pseudohypoparathyroidism
168
Q

pseudohypoparathyroidism

A

when PTH receptors are resistant to PTH–leading to increases levels of PTH and hypocalcemia

*caused by G protein and malfunction of the signal transduction inside the cell

169
Q

s/s of hypocalcemia

A

most are asympto

CNS: fatigue, irritability, depression, anxiety, congnitive impairmnt, lethargy, paraesthesias–hands/feet also at circumoral area, also parkinsonian s/s due to brain calcification

MSK: increased muscular contractions—bc hypocal decreased excitation threshold–increased muscle and nerve excitability—>MUSCLE CRAMPS, convulsions, BRONCHOSPASMS with stridor, FINGER PARESTHESIAS, carpopedal spasms, Chvostek sign, increased DTR

Arrythmias

dry skin, psoriasis

Diarrhea, abd pain, or cramps

abnormal dentintion, osteomalacia

cataracts

170
Q

ECG findings for hypocalcemia?

A

prolonged QT

171
Q

two main PE findings for hypocalcemia/hypoparathyroidism

A
  1. Chvostek sign: facial muscle contraction/spasm occuring when you tap on the facial nerve
  2. trousseau’s sign: carpal spasm with inflation of a BP cuff above the SBP
172
Q

CATS-G

A

s/s for hypocalcemia

convulsions 
arrhytmias: prolonged QT--torsades, CHF 
tetany and DTR increased 
spasms and stridor 
GI--N/V/ constipation,
173
Q

Etiologies for hypoparathyroidism ? MC?

A

RARE

Primary MC: autoimmune destruction of the parathyroid glands
issues with parathyroid synthesis

Seconary MC: post thyroidectomy surgery via accidental removal of parathyroid gland OR parathyroidectomy—–accquired

**surgical reason is more common than the auto immune destruction

OTHERS:

  • hypo or hypermagneisum–REVERSIBLE
  • radiation therapy
  • congential pseudohypoparathyroidsm, parathyroid hypoplasia (DiGeorge Syndrome)
174
Q

clinical manifestations of hypoparathyroidism

A

RELATED TO HYPOCALCEMIA:

  1. CNS: fatigue, irritability, depression, anxiety, cognitive impairment, lethargy, paraesthesias @circumoral area and hands +feet, seizures, increased DTR
  2. MSK: weakness, cramps, carpaldpedal spasms, convulsions, tetany, laryngospasms and stridor
  3. Cardio: prolonged QT—torasdes
  4. Skin: dry, skin psoriasis
  5. GI: diarrhea, cramping/abd pain,
175
Q

long term hypocalcemia with hyperphosphatemia causes ?

A

calciications in the soft tissues like joints skin artieries

brain calcifications in BG

176
Q

PE findings for hypoparathyroidism

A

Chvostek sign

Trousseuas sign

EKG can show prolonged QT

177
Q

labs for hypoparathyroidsm

A

TRIAD:
decreasd intact PTH
hypocalcemia
increased phosphate

urine studies:

  • ca low
  • alkaline phosphate normal

always measure serum mag too beacuse hypo or hyper mag can exacerbate symptoms

178
Q

hypocalemia + HIGH PTH can be from?

A

renal or liver diz **
vit d deficinecy
hypomagnesium

179
Q

hypocalcemia + low PTH etiology?

A

hypoparathyroidism MC

180
Q

etiologies for hyperparathyroidism

A

PRIMARY:

  • parathyroid adenoma–screting PTH— MC cause
  • Lithium
  • MEN 1 and MEN 2A (rare)

SECONDARY:
-incr PTH by physiologic response to hypocalcemia or vit D deficiency—CHRONIC KIDNEY DZ MC ***

181
Q

CM of primary hyperparathyroidism

A

most asymptomatic

But, get s/s of hypercalcemia

STONES: kidney stones from renal loss of CA and phosphate, NEPHROLITHIASIS–ca oxalate and phosphate deposition

BONES: increasd osteoclastic activity causing:

  • decalcification of bone –PAIN
  • easily fractured
  • pseudotumors in the jaw, skul, and phalanges
  • osteopenia
  • osteoporosis
  • decreased DTR

ABD GROANS: incr CA stimulates gastrin release–causeing ulcers

  • abd pain
  • acute pancreatitis
  • increase gallstones
  • constipation
  • N/V

PSYCHCI MOANS:

  • depression
  • anxiety
  • behaviroal changes

HTN

182
Q

lab values for primary hyperparathyroidism

both blood work and urine studies

A

TRIAD: for blood work
HIGH Calcium
high intact PTH
LOW phosphate

urine:
- hyperphosphaturia
- hypercalciruria

183
Q

Lab values for secondary hyperparathyroidism

A

normal-low CA
high phosph
high PTH

super low Vit D

184
Q

diagnostic tests for hyperparathyroidism

A

labs
bone density scan– will show osteoporosis
Ultrasound to see if PTH adenomas

185
Q

how does high PTH raise blood ca?

A
  1. breaking down the bone– taking our the CA from bone
  2. increasing body’s ability to absorb CA from GI tract
  3. increasing kidneys ability to HOLD onto CA that otherwise wouldve been lost in urine

increase serum and urine CA*

186
Q

EKG findings for hypercalcemia?

A

shorteend QT interval **
Prlonged PR
QRS widening

187
Q

lab values for CA and PTH in the following:

  1. hyperparathyrodism
  2. hypoparathyroidism
  3. hypercalcemia of malignancy
  4. secondary hyperparathyroidism in renal dz
A
  1. high for both
  2. low for both
  3. high CA and low PTH
  4. low CA and high PTH