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Final review for Step 2 Ck > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Diagnostic criteria (3 different ways for DM1 and Dm2)?

A

Random BS > 200 with Syx, HbA1c > 6.5%, 2 hour GTT >200, fasting Bs (8 hours) > 126

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2
Q

What is diagnosed with fasting BS > 126, random glucose > 200 with syx, HbA1c > 6.5% or 2 hour GTT > 200?

A

DM

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3
Q

First step in suspected HHS or DKA?

A

Start IVF and get a fingerstick BS

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4
Q

What does insulin due to K+

A

Insulin puts K+ into cells

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5
Q

Why does DKA and HSS cause low K+ despite high/normal serum levels

A

No insulin means all the K+ is out of cells, and the hyperosmolar state and dehydration causes K+ diuresis, actually K depleted

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6
Q

Greatest factor in metabolic syndrome?

A

Greatest factor in metabolic syndrome is insunlin resistance

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7
Q

S/s of DM gastroparesis

A

DM gastroparesis has n/v, constipation and perhaps overflow incontinence

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8
Q

how is diabetic gastroparesis treated

A

treat diabetic gastroparesi with erythromycin and metoclopramide or cirapride`

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9
Q

What is first line insulin tx in DM?

A

Metformin

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10
Q

What do you nee to check before giving metformin?

A

Metformin is C/I in kidney failure due to lactic acidosis

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11
Q

What are AE of sulfonylureas

A

Sulfonyulreas cause hypoglycemia and weight gain as they cause constant secretion of endog insulins

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12
Q

Sulfonylurea name

A

G-ides (glipizide, glyburide, glimepirde)

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13
Q

What are the drugs glipizide, glyburide, glimepiride?

A

The G-rides glipizide glyburide and glimepiride are sulfonylureas

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14
Q

Thy are the glitazones used?

A

Glitazones are thiazolindinediones that increases sensitivity to insulin via PPARy and cause edema and worsens heart failure and are CI in CHF failure

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15
Q

AE of a-glucosidase inhibitors?

A

Bloating and diarrhea/farting. Cannot absorb the sugar and it causes osmotic discomfort

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16
Q

What are the incretins?

A

incretin cause more release of insulin with an oral meal and decrease glucagon and decrease gastric absorption. They are the GLP agonists and are the “Tides” (exena, liraglutide)

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17
Q

What are AE of Incretins?

A

Incretins are the “tides” lira, exenaglutide and cause weight loss as the slow gastric absorption, increase insulin release with a meal and decrease glucagon release

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18
Q

When would you use GLP 1 incretin lira or exaglutide?

A

The incretins lira and exaglutide cause weight loss and are second line for weight loss and in insulin resistant diabetes

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19
Q

What are the flozins?

A

The flozins are SGLT2is

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20
Q

what are the name fo the SGLT2i

A

The flozins are SGLT2is

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21
Q

AE of the SGLT2i flozins?

A

UTI and weight loss with vandidiatsis

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22
Q

When to offer BRCA testing?

A

Offer BRCA in ovarian CA below age of 50

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23
Q

What increased risk do PCOS (cancer) do these patients have?

A

They have endometrial CA risk

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24
Q

What is initial tx of DKA

A

For DKA you give IVF and insulin unless K+ is low and add K+ when it is 4.5

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25
Q

when do you give K+ in DKA and HHS?

A

Give IVF and insulin in DKA unless K+ is low or once it reaches 4.5mol

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26
Q

Key factor for metabolic syndrome development (what causes insulin resistance which is the issue?

A

Truncal obesity and with increased waist to hip ratio

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27
Q

What are the GLP1 lira and exenaglutides used for?

A

Lira and exenaglutide are GLP1 agonists that are second line after metformin and cause weight loss. The next line is DPP4i which are the liptins and are weight neutral, so GLp1 agonism with exenatide/liraglutide are used before liptins (DPP4i)

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28
Q

What is a AE of sulfonylurea and why are GLP1 agonists better

A

Sulfonylureas cause weight gain from constant endogenous insulin release (the G-rides) and GLP1 agonism with liraglutide and exenaglutide cause weigh tgain

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29
Q

How are diabetic ulcers on feet treated?

A

They need antibiotics AND debridement or won’t heal

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30
Q

When do you hospitalize for diabetic foot ulcer?

A

Osteomyelitis or Gangrene

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31
Q

When does a diabetic start statins?

A

ALL DM patients need statins older than 40 regardless of lipid levels

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32
Q

A DM is older than 40 with lipids WNL, what do they need?

A

ALl DM patients older than 40 need a statin regardless of lipid levels

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33
Q

BP goal in DM

A

Goal is 140/80

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34
Q

Who gets screened for DM

A

all patients over 45 and esp those with increased risk (obese, sedentary life, lots of waist to hop obesity)

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35
Q

Does HHS have ketones or acidosis?

A

No, HHS does not have ketones or acidosis as they have some insulin, but BS is extremely high over 600 and around 1000. Vision changes are comon

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36
Q

Does HHS have acidosis?

A

HHS often do NOT have acidosis, but are extremely volume deplete and IVF alone helps lower BS by dilution which is very volume depleted, then add K+ once K is WNL from its elevated value

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37
Q

Is there an anion gap in HHS?

A

HHS does NOT have acidosis, an anion gap or ketones. Just a HIGH serum omsomlarity

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38
Q

S/s of HHS

A

Mental status, dry mucous membranes, NO acidosis and NO ketones and no anion gap, just high serum Osmo. Vision changes are common

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39
Q

What does HbA1c correlate with clinically to patient?

A

Microvascular disease and survival time

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40
Q

Can Hba1c tell microvascular disease risk?

A

yes, it tells SMALL vessel disease risk, but not overall survival and CAD risk

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41
Q

How is HHS treated?

A

First step is volume replacement! Then add regular insulin, then add K once K is WNL, then add 1/2NS + 5% dextrose once 250BS to repvent cerebral edema

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42
Q

How is cerebral edema prevented in DKA/HHS tx?

A

Add 5% dextrose in 1/2 NS once BS is 250 mg to prevent cerebral edema

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43
Q

What happens if 5% dextrose 1/2 NS is not added onc BS is 250 in DKA and HHS?

A

cerebral edema

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44
Q

Foot spur, asymmetric in a DM patient with neuropathy, loose bodies on XR, cause?

A

Diabetic neurogenic arhtorpathy, degenerative, asymmetric joint dieases with functional imitation and due to neuropathy

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45
Q

What is best way to prevent DM nephropathy?

A

BP control below 140/80 with ACEI

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46
Q

How is DM retinopathy fixed?

A

Laser coagulation

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47
Q

S/s of DM retinopathy

A

There is cotton wool spots or microanueryms, hemorrhage and exudates with neovascularization

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48
Q

First change in DM nephropathy?

A

Hyperfilitration

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49
Q

What is pathognomonic for DM nephropathy?

A

Nodular sclerosis (Kimmestiel - Wilson nodules)

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50
Q

Who gets ACEi in DM?

A

DM patients with microalbuin get ACEi, EVEN if BP is WNL.

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51
Q

Do DM patients need ACEi with microalbumin in urine even if BP is WNL?

A

YES! Give ACEi with microalb, not just with high BP. Need to reduce GFR hyperfiltration, BP is just added effect

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52
Q

What defects does neuropathy in DM cause?

A

neuropathy in DM causes sensation and late late loss of propieception, UMN mean it is NOT related to DM neuropathy and MRI of spine or brain is indicated

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53
Q

what is the type of neuropathy in DM?

A

Symmetric, distal polyneuropathy (stocking glove)

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54
Q

How are foot ulcers predicted in DM?

A

Monofilament for distal neuropathy and small vascular disease

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55
Q

Does HbA1c decrease all cause mortalty?

A

Keep it below 7, but lower causes death form hypoglycemia. It predicts SMALL vessel, not large vessel and cAD death risk

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56
Q

HbA1c control think?

A

Micro, NOT macro vascular control of complications

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57
Q

Best test for DM nephropathy?

A

Microabl : Cr RATIO.

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58
Q

The Microalb : Cr ratio is the best?

A

Dm nephropathy screen.

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59
Q

Aterial ulcers are due to?

A

Large vessel disease, at end of toes and necrosis (unlike diabetic neuorpathy which is ulcers over pressure points) and unlike venous ulcers near /above the medial malleolus

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60
Q

Cause of Mucomycosis in DM?

A

Rhizopus

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61
Q

s/s of rhizopus in DM?

A

Proptosis, nasal turbinate damage and necrosis, headache, high BS

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62
Q

Odd rhizopus syx?

A

Causes mucormycosis which needs surgery and antibiotics and in patients with very high HbA1c, fever, necrotic turbinates, headache and proptosis of the eyes. may cause cavernous sinus disease

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63
Q

GAD antibodies (glutamic acid decarboxylase) in what disease?

A

Glutamic acid decarboxylase Ab in Dm1

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64
Q

Key sign of Graves?

A

Exopthlamos = graves specific as is bruit

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65
Q

What type of disease is Graves?

A

Autoimmune from stimulating TSH-R antibodies on the thyroid

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66
Q

Can hyperthyroid cause angina?

A

Hyperthyroid increases MyO2 demand and HR can causes palps which can result in angina in CAD patients

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67
Q

Key Syx in thyroid storm/disease?

A

LID LAG and/or exophthalmos

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68
Q

Thyroid hormone effects? General–

A

BONE AND CNS maturation (can increase risk of beon disease), increased BMR and RR and HR and MyO2 demand and B1 effects

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69
Q

How is primary hyperthyroidism worked up?

A

Primary hyperthyroidism is worked up to see if it is due to Graves/or nodular adenoma or thyroiditis– measure TSH and T4 with s/s, if TSH low and T4 high (primary) look for s/s or Graves (Exophthalmos, pretibial mxedema) = diagnosis of Graves. If no Graves s/s,then you do a RAI and look for diffuse versus nodular uptake. If not uptake, then it is either exogenous or it is thyroiditis, and measure thyroglob. Low thyroglobulin = exogenous

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70
Q

When is thyroglobulin measurement used?

A

Thyroglobulin tells you that there is cell lysis or thyroid and that there is thyroiditis versus exogenous hormone use after a hyperthyroid workup without Graves s/s gets RAI and there is no uptake

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71
Q

First step in secondary hyperthyroidism?

A

MRI of pituitary

72
Q

High TSH and T3/4 and s/s of hyperthyroid, next?

A

MRI pit

73
Q

Euthyroid/hypothyroid and s/s of thyroid disease?

A

FNA to r/o cancer versus hyperthyroid s/s (low TSH high T3/4) in which you look for Graves syx, then do RAI and if RAI equivocal, measure for thyroglobulin

74
Q

Where it thyroglobulin?

A

Within thyroid cells, high = lysis

75
Q

A person has hyperthryoid s/s and low TSH and high T3/4. No Graves exopth, get RAI with single uptake point, cause?

A

Adenoma, no s/s Gravies with one uptake point that suppresses TSh in rest of follicle

76
Q

Cause of Euthyroid sick snydrome?

A

Low T3, rT3 doesn’t work, you do not treat it so you do not test for it, happens in acutely ill patients

77
Q

What happens in pregnancy requiring dosing changes for thyroid disease?

A

TBG is increased and hypothyroid patients need more levothyrox

78
Q

When else is TBG up?

A

In high estrogen states, people on hormone replacement may need increased doses of thyroid hormone

79
Q

What happens to thyroid production during prengnacy?

A

high estrogen states increase TBG, but the bhcg alpha subunit cross reacts and causes thryoid to increase total and free T4 (although WNL)

80
Q

What other disease than thyroid (hyper) present as?

A

Hyperthyroidism is often confused with MG as patients have proximal muscle fatigue, but s/s pointing to thyroid are tremor, RR, BP, sweatin, etc

81
Q

Lid lag is a hint for?

A

Hyperthyroid (exopthlamos is a hint for Graves’ disease)

82
Q

Tx of thyroid storm

A

Tx is Bblock with PTU and then steroids (decreases peripheral T3 conversion)

83
Q

What causes thyroid storm precipitation?

A

Surgery, infection, stress, pregnancy and birth

84
Q

key sign for thyroid disease?

A

Lid lag! lid lag in thyroid disease think hyperthyroid is going on

85
Q

When do you get RAI versus FNA?

A

Do FNA when TSH and T4 comes back eu or hypothyroid (normal TSH and t4 or low T4 and high TSH) to rule out cancer. Get RAI in hyperthyroidism. Also get FNA if there is a COLD nodule

86
Q

How is hyperthyroid treated?

A

Hyperthyroid is best treated initially with BB to reduce syx of anxiety, palps and HR. Can also used PTU while waiting for definitive Tx of RAI uptake. do NOT use RAI in pregnancy as it can hurt fetus too, need to use PTU (not methimazole)

87
Q

Tx of hyperthyroidism first line while waiting for definitive RAI?

A

BB block.

88
Q

What are the CI to RAI definitive ablation for hyperthyroid?

A

Pregnancy and severe exopthalmos (as it worsens exopthalmos and affects fetal thyroid) use PTU in pregnancy

89
Q

MCC of AE after RAI ablation?

A

MC AE is hypothyroidism, give levothyroix

90
Q

Risk of untreated hyperthyroid?

A

Tachyarrhytmia, Afib and bone loss

91
Q

Does thyroid affect bone?

A

Hyperthyroidism increases osteoclastic activity and increases bone loss if untreated along with afib and heart dsyarrhythmia

92
Q

What causes exopth?

A

Graves disease due to retro orbital tissue infiltration with lymphotcytes from a direct result of antiTSH-R Ab

93
Q

What is the MC AE of PTU (propylthiouracil) and MTE (methimazole)

A

The MCC of PTU and MTE AE is allergic reaction, but both causes agranulocytosis. PTU is also a cause of vasculitis and LFT increases and MTE is a teratogen

94
Q

What is euthyroid sick syndrome (EuSS)?

A

EuSS is due to LOW t3 with normal T4 and TSH, happens in acutely ill and is not treated so it is not followed

95
Q

What classicall increases TBG?

A

TBG is clasically increases by high estrogen states like pregnancy or HRT

96
Q

AntiTPO or anti thyroglobulin ab?

A

Hashimoto (hypOthyrO)

97
Q

Unexplained CK elevation, suspect?

A

Always have hypothyroid on unexplained CK increases. Remember that hyperthyroidism causes muscle fatigue confused with MG and that hypothyroidism increases CK and needs a TSH test

98
Q

What does high CK indicated in low thyroid?

A

Unexplained myopathy think TSH and low thyroid

99
Q

Two common lab issues in hypothyroid

A

high LDL and high CK

100
Q

Complication of prolonged hypothyroidism (hashimoto with antiTPO/Thyroglobulin Ab)

A

High risk of thyroid lymphoma

101
Q

How is myxedema coma treated and why

A

Myxedema coma can present similar to adrenal insuff with low BP, low HR, obtunded, hypoventilation = treat for AI and hypothyroid = IV levo + IV steroids

102
Q

How is thyroiditis treated?

A

Thyroiditis is usually self-limiting, suspect with low uptake on RAI with high thyroglobulin, treat SYX with BB (don’t use PTU as when it normalizes bc it is self limiting you make them hypothyroid ) +/- NSAIDs

103
Q

What is the MCC thyroid malignancy

A

Papillary is the most common thyroid malignancy

104
Q

Papillary CA occurs how often in thyroid CA?

A

Papillary CA occurs in 80% of thyroid cancer, papillary is the MCC

105
Q

What history is the MCC thyroid malignancy papillary assoc with?

A

Family or PMHx of radiation

106
Q

PMHx of radiation and neck ondule with compressive syx an dhoarseness, most likley cause?

A

Follicular thyroid CA is MCC of thyroid CA with history of radiation or family history

107
Q

Papillary thyroid CA is most?

A

Papillary is most papillary

108
Q

How does papillary spread?

A

Papillary is most popular and spreads with lymphatics

109
Q

What is often involved in papillary lymph spread?

A

LNs

110
Q

How does follicular spread (thyroid CA?)

A

It spreads via blood, not lymph. papillary is most popular and spreads via lymph

111
Q

How is follicular diagnosed?

A

Follicular thyroid ca needs capsule invasions as diagnosis so you have to remove the whole thyroid to diagnos it

112
Q

What do you suspect in a thyroid C cell tumors with calcitonin deposits?

A

Screen for MEN2 and2B

113
Q

What is causes of osteomalacia

A

Osteomalacia causes poor bone mineralization

114
Q

Imaging findings for osteomalacia

A

Pseudofractures and thin cortex where the hydroxyapatite is mineralized

115
Q

osteomalacia labs?

A

Low vitamin D with low PO4,3- and low calcium and high PTH

116
Q

When do you see secondary PTH

A

secondary PTH with kidney disease, it cannot make Vit D so active 1,25 OH D3 is low and you cannot excrete PO4 and you have

117
Q

Who gets hypocalcemia due to magnesium

A

Alcoholics get low magnesium and then low calcium

118
Q

What are hypomagnesium labs

A

HypoMg in an alcholc has low PTH – low Ca and low PO4 (gut absorption low)

119
Q

How is hypomagnesium treated?

A

Treat hypomagneisum by calcium and magnesium; if you only give Mg the PTH will remain low and calicum helps to supplement at first

120
Q

How is osteoporosis diagnosed?

A

Labs in osteoporosis are normal and it is a screen at 65 in women or 70 in men with DEXA, must use DEXA, XR will not show lower BMD

121
Q

How is osteoporosis treate?

A

Osteoporosis is treated with bisphosphonates and with Vit D and calcium

122
Q

What is the other name for Paget?

A

Osteitis deformans

123
Q

What is osteitis deformans?

A

Osteitis deformans is another name for Paget disease

124
Q

What is the bone lesion in primary PTH called versus Paget

A

Paget is osteitis deformans and osteitis fibrosa cystia is due to primary PTH disease

125
Q

Paget have increased risk of?

A

Fracture, osteosarcoma and neuro syx

126
Q

Dx of osteoporosis?

A

DEXA NOT XR

127
Q

Cause of Paget?

A

CLASTS

128
Q

What is the tx for primary aldosteronism?

A

It depends on the laterality, unilateral = surgery, b/l= aldosterone antagonism; dx with ald/renin ratio >20 and CT to see laterality

129
Q

In a patient with primary hyperaldost, s/s of first line aldosterone antagnosim (spirono/eplerenone)

A

Gynecomastia, breat issues, menstrual changes

130
Q

In severe hyperthyroidism, first step in treatment?

A

Control HR/RRR and use BB then figure out if truly thyroid and treat and diagnose accordingly

131
Q

Name metagolic derangements in hypothyroid

A

LDL high, Na LOW and CK 10x normal at times

132
Q

what happens to LDL, Na and CK in hypothyroid

A

LDL high, Na LOW and CK 10x normal in hypothyroid

133
Q

Can thyroid storm have fever?

A

Yes, thyroid storm can have fever

134
Q

At quick glance, how is thyroid storm diff from malignant hyperthermia

A

while both have seizure, altered mental status, thyroid storm has palps, high heart rate NO rigidity and other s/s like LID LAG, goiter, PMHx of thyroid disease
Malignant hyperthermia also has muscle rigidity resulting in muscle destruction such as high potassium, high CK

135
Q

How is acute adrenal insuff treated?

A

IVF with steroids

136
Q

What is addison’s?

A

A-ddisons is primary AI

137
Q

what is the name of primary AI?

A

Primary Adrenal insuff is due to A-dd-I-son’s

138
Q

How do you test for suspected AI? (A-ddison)

A

Addison disease is primary adrenal insuff and you test for it with cosyntropin (ACTH analog) stim, ACTH levels and urinary cortisol levels, which can tell you the cause of any etiology

139
Q

PCOS patients at risk for?

A

DM2 and endometrial hyperplasia and need 2 hour GTT/ diabetes screening

140
Q

When does PCOS get metformin?

A

consider screening for DM2 in PCOS and give metformin for first line therapy in sugar control

141
Q

What does PCOS get OCP

A

OCP in PCOS first line, if they have DM2 = metformin and ovulation desired = clomiphene citrate

142
Q

Initial testing for Cushing

A

early am cortisol, 24 hour urinary cortisol or low dose dexa suppression test

143
Q

what is the utility of low dose dex suppression test?

A

low dose dexa suppression test is an initial screen for Cushing’s along with 24hour urinary cortisol and early morning cortisol levels

144
Q

Endocrine Cushing diagnostic algorithm: initial –> FU and –> confirmatory ?

A

Initial: Dexa (low dose) suppression test, 24 hour urinary cortisol or early am cortisol
FU with ACTH (Dependency)
If ACTH dependent = do high dose dexa to see if ectopic

145
Q

PTU has a bad AE other than agranulocytosis what is it

A

Beware of PTU hepatic failure and beware of methimazole teratogenicity

146
Q

How is opthomopathy prevented in RAI in Graves which can worsen it initially?

A

Pretreat with steroids

147
Q

Steroids, PTU or BB prevent opthalmopathy from worsening in Grave’s disease when treated with RAI

A

it is STEROIDS, not PTU that prevent the worsening opthalopmathy that occurs with people when Graves’ is treated (Antithyroid drugs take weeks to take effect, which is also why BB is first line in thyroid storm)

148
Q

How is hypercalcemia of immobilization treated?

A

Hypercalcemia of immobilization is treated with bisphosphonates and oral hydration

149
Q

A person is immobilized for a long time, how are their calcium levels controlled?

A

Immobilization causes hypercalcemia and can be prevented with IVF and bisphosphonates

150
Q

Screen for DM?

A

Risks and over 45, or sustained BP >135

151
Q

What is the algorithm for calcium high / syx tx?

A

High calciuim = measure a diff time and correct for alb = if high, then get PTH – if PTH high, then check urinary calcium for FHH versus parathyroid syndrome causes, if PTH normal, consider PTHrP and VitD3 testig

152
Q

If PTH is high after 2 confirmed high CA, next step?

A

measure urinary CA

153
Q

If PTH is WNL or low after 2 confirmed calcium levels that are high, next?

A

Consider VitD, PTHrP, etc

154
Q

What is first step for GH hormone escess

A

IGF1

155
Q

If IGF1 is high with acromegaly, next test?

A

After IGF1 eleavtion, you do glucose suppression test. GH release should be suppressed by glucose load

156
Q

If IGF1 is high, GH is not suppressed by glucose load, then what?

A

MRI the brain for adenoma

157
Q

How is Acromegaly treated?

A

Treated with pegvimosant or octreotide medically versus sphenoidal transresection surgically

158
Q

when do you operate in prolactinoma

A

operate with COMPRESSIVE SYX or when >3cm, otherwise medically manage with cabergoline and bormocriptine

159
Q

When is PRL level diagnostic

A

over 200 and s/s

160
Q

What is a common cause of nephrogenic DI (medicatin)

A

Lithium commonly causes nephrogenic DI

161
Q

What are the other AE of lithium

A

Ebstein, movement, hypothyroid and nephro DI

162
Q

What is primary DI?

A

Primary DI is pyschogenic DI

163
Q

How is central DI treated?

A

Central DI is treated with DDAVP

164
Q

How is nephro DI treated?

A

Nephro DI is treated with fluid and slat restriction with HCTZ

165
Q

What does sodium tell you in DI?

A

DI in a nonhospitalized patient is central or peripheral, versus a hospitalized patient when it is pirmary (pscyogenic). LOW NA (

166
Q

Two ways to follow resolution of DKA?

A

DKA resolution is followed by anion gap or direct betahydroxybutyrate assay

167
Q

What other entitey, less commoly used can follow DKA?

A

DKA can be followed with anion gap and direct betahydroxybutyrate assay

168
Q

Best way to diagnose MEN syndromes?

A

If suspected, Get RET oncogene PCR as it is very sensitive compared to biochem measurement

169
Q

What are complications of hyper PTH?

A

Complications of hyper PTH are osteoporosis/penia and kidney function decrease/nepholithiasis

170
Q

other than s/s, what things (think complications) are strong indication to operate from hyperparathyrodism

A

Decreased renal function, frequent kidney stones and osteoporosis (BMD

171
Q

Who should be suspected for Vit D def?

A

Suspect in malabsorption (pancreatitis, CF, ileal/gatroresection and Crohn’s)

172
Q

What are levels in Vit D def?

A

Suspet in malabsorption with low PO4 and low Ca

173
Q

Classic XR finding for Vit D def?

A

Pseudofractures

174
Q

What are key differentiators of osteomalacia from porosis

A

osteomalacia HAVE lab issues and low calcium and vitamin D = bone pain d/t pseudofractures and poor mineralization, weakness from hypocalcemia and muscle weakness, ostoporosis doesn’t have pseudofractures and dont’ complain of bone pain

175
Q

Pancreatic tumors are associated with?

A

MEN, suspect in VIPoma, glucagonoma, gastrinoma

176
Q

What can T4/T3 do to the heart?

A

They can cause increased MyO2 demand and lead to angina, along with atrial fibrillation and atrial flutter as arrhythmias

Final review for Step 2 Ck (12 decks)

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