endocrine Flashcards

1
Q

Type one

A

ketone development occurs
weight loss
believed to be the result of an ifectious or toxic envrionment insult to pancreatic B cells

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2
Q

type two

A

random over 200

fasting x 2 > 126

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3
Q

bun

A

10-20 fluctuates indipendant of kidney function

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4
Q

creat

A

.5-1.5

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5
Q

metabolic syndrome

A
waist circumferance >40 in men and 35 in women
BP >130/85
Triglycerides >150
FBG >100
HDL <40 in men and <50 in women 

any 3 equals + diagnosis

super high rish of sudden cardiac death

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6
Q

AIC

A

5.5-7 6 is goal

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7
Q

normal fasting glucose

A

60-99

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8
Q

dm diet

A

total carbs 55-60%
fats 20-30
fiber 25g or 1000ca
protein 10-20%

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9
Q

if pt presents with ketons then

A

insulin is most likely warented

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10
Q

insulin admin split dose

A

05u kg/da 2/3 am (2/3 nph and 1/3 R)pm (1/2 nph 1/2 regular)

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11
Q

type two therapy for obese

A

start with weight loss

consider early oral antidiabetics

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12
Q

oral antadiabetics sulfonyureas

A

most widley prescribed stimulate pancreasee to produce insulin (glipizide, glyburide lglimiperide)

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13
Q

biguanides

A

good adjunc but can be used alone for obese pts

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14
Q

standard of care oral on type two diagnosis

A

etformin (biguininide-glucaphage) Lactic acidosis is a potential side effect.

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15
Q

symogi effect

A

nocturnal hypoglycemia leads to surge of counter regulatory hormones which increase the blood sugar, low at 0300 but high at 0700 - dc or reduce bedtime dose

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16
Q

dawn phenomenon

A

tissue becomes desentized to insulin nocturnally progressive increase through the day and elevated glucose at 0700 the dawn is rising - add or increase pm insulin dose.

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17
Q

syndrome x

A

HTN obesity and abnormal liid profile Hig trig and low HDL’s

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18
Q

DM 2 beyond the polys

A

recurrant vaginitis
blurred vision
neruopathy
chronic skin infections including prutius

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19
Q

sulfonyureas

A

stim pancreas to release insulin

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20
Q

alpha glucosidase inhibitors -

A

less sugar absorption in the gut

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21
Q

thiazolidediones

A

decrease glycogeniss - less production of glucose
avandia - increase in heart failure
actos same

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22
Q

non sulfonurea insulin reales stims –

A

mimics the effect of insulin - prandid and starliz

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23
Q

Major complication of Type 1

A

DKA

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24
Q

Type one DKA what is it

A

intracellular dehydration as a result of elevated blood glucose levels

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25
Q

type one DKA S&S

A
poly and nocturia
weak
N&amp;V
Kussmals 
altered LOC
orthostatic hypo
poor turgur
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26
Q

Type one DKA labs and diagnosits

A
Hyperglycemia- serum glu >250-300
Ketones
acidosis ph <7.30
low bicarb
low pco2
elevated hct
elevated BUN
Hyperkalemia
leukocytosis
Hyperosmololity 2(nameq/L +Kmeq/L+Glucose/18)
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27
Q

type one DKA managemnt

A

protect airway
admin 02
isotonic flu (NS) at least 1 L in he frist hr and then 500ml per hr
is glu is less that 500 use 1/2 after first hour
when glu is below 250 change to d51/2 to preent hypoglycemia

0.1u/kg rugular insulin bolus followed by 0.1u/kg/hr if glucose dose not fall bu at least 10% after the first hours, repeat the bolus

correct acidosis- if PH <7.1 with bicarb gtt 44-48meqin 900ml 1/2nss untill ph goes >7.1

do not treat hyperkalemia
monitor hourly uop

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28
Q

normal serum osmo

A

thumbnail is like 2 times the NA 140x2 is 280

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29
Q

HHNK

A

no ketones greatley elevated glu like >1000

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30
Q

HHNK (2) signs

A

normal anion gap,crazy high glucose

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31
Q

HHNK treatment

A

NS IV for massive fluid recussitation

ns then 1/2 then D51/2

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32
Q

may give insulin but this is contraversial

A

HHNK II

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33
Q

HYPER thyroid

A

most common in women 8:1
young onset 20-40
GRAVES DISEASE IS MOST COMMON PRESENTATION
other causes of hyper- toxic adenoma, subacute thyroiditis, TSH secreting tumor of pituitary, high dose amiodarone

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34
Q

HYPER thyroid S and S

A
UP -
nervous
sweaty
(tired) 
emotion
temor
hyper reflexes
increased appetite
weight loss
SMOOTH WARM MOIST VELVETY SKIN
FINE/THIN HAIR
lid lag
tacchy
heat intolerance
increased a-fib
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35
Q

Labs, diagnostics for HYPER thryroid

A

TSH assay is the most sensitive test and is LOW in most cases
sometimes T4 is normal but T3 is elevated 80-230ng/dl)
sereum ANA usually up (no lupus or collagen disease)

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36
Q

HYPER thyroid and iodine

A

high iodine uptake is graves

low iodine uptkae is subacute thyroiditis

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37
Q

prefered exam to visualize the eyes in graves

A

MRI of the orbitz

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38
Q

HYPO thyroid

A
primary disease of the tyroid gland
pituitary defficiency of tsh
hypothalmic defficiency of TRH
iodine deficiency
hashimotos thryroiditis
damage to gland
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39
Q

HYPOTHYROID

A
down 
extreme weakness
muscle fatigue 
arthalgias 
COLD INTOLERANCE
briiittle nails
edema in hads and face
slowed DTRs
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40
Q

HYPO thryoid LABS

A

TSH is elevated in HYPO
T4 is low or normal
hyponatremia and hypoglycemia

41
Q

most common presentation of hyper thryorid

A

graves

42
Q

most common presentation of HYPO thyroid

A

hashimotos thyroids

43
Q

HYPERthyroid labs

A

TSH down T3 is up

44
Q

Hyperthyroid meds-

A

propanolol - 10-80mg four times daily treats the shakes

thiourea drugs for small goiters and fear of isotopes

45
Q

Hyper thyroid meds methimazole

A

tapazole - 30-60 daily in 3 divided doses

46
Q

HYPERTHYROID meds radioactive iodine

A

131 used to destroy goiters

47
Q

HYPERTHYROID meds lugols solution

A

2-3 drops por every day x10 days to reduce vascularity of the gland

48
Q

patients with subacute thyroiditis are treated with

A

propanolol

49
Q

treatment of thyroid crisis

A

propylthiouracil 150-250- q6 or
methimazole or tapazole 15-25mg q6 with the followign in one hour

lugols solution 10gtt
sodium iodine 1g slow iv
propanolol 05-2gm iv q4 or 20-120 po q6
hydrocortizone 50 q6 with reduction on improvment.

50
Q

HYPER THYROID cRISIS Avoid

A

ASA

51
Q

HYPO thyroid meds

A

SYNthroid, 50-100 mcg Qday, increasing dose by 25mcg, every 1-2 weeks untill symptoms stabelize, >60 years of age decrease dose

52
Q

HYPO thyroid in patient manageet of myxedema coma

A
protect airway
fluid replacement
synthroid 400mcgIVx1 then 100mcg qday
support hypotension
slow rewrm
53
Q

cushings

A

ATCH is hyperselected by the pituitary
adrenal tumors
chronic admin of glucocorticoids

54
Q

Cushings s and s

A
central obesity 
MOON FACE AND BUFFALO HUMP 
acne 
poor wound healing 
purple straie
hirstuism
hypertension
weakess
amenorrhea
impotence
headache
polyuria and thirst
labile mood frequent infections
55
Q

lab and diagnostics cushings

A
hyperglycemia 
hypernatremia
hyperkalemia
glycosuria
leukocytosis
ELEVATED PLASMA CORTISOL IN AM
serum ACTH 
Dexamethasone supression test to differentiate cause
56
Q

cushings treatment

A
depends on the cause
discontinue meds inducing the symptoms 
transphenoidal resection of a pituitary adenoma
surgical removal of adrenal tumor
resection of ACTH secreting umor 
treat E imbalance
57
Q

myxedema is functionally

A

a varried breathing state

58
Q

Adreno cortico trophic hormone

A

ACTH

59
Q

cushings pressure

A

high

60
Q

cushings lab triad

A

HIgh sodium K and sugar

61
Q

addisons cause

A

low cortisone (rare)
destriction of adrenal glan
defficiencey of cortisol , aldosterone and androgen
anticoag adrenal hemmorage

62
Q

Addisons s and s

A

hyperpigmentation in the buccal mucosa and skin creases: knuckels nipples skin creases palms
diffuse tanning anf freckles,
orthostasis and hypotension
scant axillary and pubic hari

63
Q

addisons acute

A

fever, change in LOC, rapid change in chronic symptoms

64
Q

addisons lab

A

Low sugar, NA and K

elevated ESR

PLASMA CORTICOL <5mcg/dl at 8a
cosyntropin

65
Q

addisons management

A

secilist referral
GLUCOCORTICOID AND MINERALOCORTICOID REPLACEMENT

hyrodcortisone
flroinef

66
Q

addisons inpatient management

A

HYDROCORTISONE (SOLUCORTEF 100-300MCG iv WITH NSS

REPLACE VOLUME WITH d5nss at 500cchr/4hrs and then taper

67
Q

addisons and vasopressors

A

usually dont work

68
Q

assisons common underlying cause

A

infections

69
Q

SIADH

A
release of ADH occurs independent of osmolaity or volume dependent stim
INNAPRORIATE WATER RETENTION
tumors producing ADH 
skull frx or head trauma
CNS disorder
chronic lung disease
70
Q

Siadh

A

low NA and temp
COLD INTOLERENCE
decreased DTR

71
Q

SIADH volume and sodium

A

euvolemic by low sodium

72
Q

SIADS serum osmo vs urine osmo

A

<280mOsm/kg (Low)
urine osmo >100mOsm/kg (high)
normal renal cardiac and thyroid function

73
Q

DI Central

A

related to pituitary or hypothalmus damage resulting in ADH defficiency

damage to above
infection
surgical damage
metastatic tumor

74
Q

Di Nephrogenic

A

due to a defect in the real tubules where renal tubules are insensitive to ADH antidiuretic hormone
x-link trait
aquired due to pylenephrotis, sickle cell anemia, chronic hyper K

75
Q

SIADH treatmet >120

A

If serum NA is Less than 120 1000ml fluid restrictions for24hrs

76
Q

SIADH NA 110-120

A

without symptoms 500 fluid restriction q24

77
Q

SIADH NA <110

A

or neuro symptoms present
replace with hypertonic na and lasix
at 1-2meq/hr
monitor NA and k

78
Q

DI s and S

A
Thirst 5-10 L per day 
2-20L per day peeing 
weigh loss fatigue
changes in LOC
dizzy 
HIGH TEMP
tacchy 
hypotension
poor turgor and dry 

THIRST
PEEING
DRY

79
Q

Nephrogenic DI caused by meds

A

lithium and methicillin

80
Q

DI labs

A

DRY

HIgh NA
elevated BUN and creat

81
Q

DI LABS

A

serum osmo high >290
urine osmo is low <100
urine specific gravity <1.005 peeing water

82
Q

DI determination if central is suspected

A

DDAVP vasopressen test- 0.05-0.1ml nasally or 1 uq sq or iv with measurement of urine volume. if urine osmo goes up its central if it does not then its nephro

83
Q

urine normal specific gravity

A

1.10-1.03

84
Q

if no clear cause for DI then

A

MRI

85
Q

DI tx NA over 150

A

if serum na is over 150 then D5w to replace 1/2 volume deficit in 24 hours, dont lower na quickly can cause neuro damage

86
Q

DI tx NA less than 150 substitute 1/2 or .9nss

A

substitute 1/2 or .9nss

87
Q

DI maintence dose of DDAVP

A

10ug every 12-24hrs intranasal

88
Q

DI acute DDAVP dose

A

1-4ug IV or sq Q24

89
Q

pheocromocytoma

A

rare but serious disease from excess catecholamine release causing parox or sustained HTN almost always from ADRENAL MEDULLA TUMOR

90
Q

pheocromocytoma S and S

A
labile HTN
sweating
high sugar
SEVERE HA
palpitations 
tremor tacchy 
postural hypotension
91
Q

pheocromocytoma LAB AND DIAG

A

TSH NORMAL

NORMATENEPHRINE AND METANEPHERINELEVATED

92
Q

pheocromocytoma DIAG

A

CT OF ADRENALS USED TO CONFIRM AND LOCALIZE TUMOR

93
Q

Pheocromocytom vs hyperthyroid differentiation

A

check TSH

94
Q

pheocromocytoma lab test

A

plasma free metanephrine

95
Q

pheocromocytoma non emergent

A
test urine 24hrs
chatacholimine
creat
VMA and
metaniphrine
96
Q

pheocromocytoma TX

A

surgical removal of tumor is treatment of choice

97
Q

Pheocromocytoma

A

alpha adrenergic meds can be used pre op

98
Q

Pheocromocytoma post op

A

HYPOtension
adrenal insufficiency (HYpotension)
hemmorhage