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USMLE Step 2 - Top 5% > Endocrinology 💊 > Flashcards

Endocrinology 💊 Flashcards

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USMLE® Step 1 flashcards
1
Q

Metabolic syndrome aspects and diagnosis

A

WEIGHHT
waist size, impaired glucose tolerance, hypertension, HDL, TG

> =3/5 of above

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2
Q

Best initial Tx for metabolic syndrome

A

Lifestyle

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3
Q

If patient has impaired fasting glucose in metabolic syndrome, can give what??

A

Metformin

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4
Q

Main treatments for diabetic retinopathy

A

Anti VEGF agents and laser photocoagulopathy

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5
Q

Main Tx for diabetic nephropathy

A

ACEi

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6
Q

Which CN is most seen in diabetic neuropathy

A

CN3

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7
Q

Neuropathic pain in DM can be Mx with

A

TCA or SNRI or gabapentin

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8
Q

Gastroparesis Tx

A

Metoclopromide or erythromycin

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9
Q

How to Dx micro albuminuria in DM

A

Spot urine ACR (30-300). Otherwise cannot see in routine UA

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10
Q

Dx for DM

A

Random glucose at >=200 with symptoms.
Or fasting glucose >=126
Or >=200 after OGTT
Or HbA1c > 6.5%

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11
Q

Screening for T2 DM in age > 45

A

Check HbA1c every 3 years. If 5.7-6.4 then do yearly recheck. Do yearly check up on high glucose generally/positive OGTT, if they didn’t quite make Dx

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12
Q

Excserize advice to DM patient

A

Moderate intensity for 30-60 mins, 5 days a week

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13
Q

When to give statin your DM patient

A

All aged 40-75 regardless of lipid level

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14
Q

Aside from routine, which Vx’s should be given to DM patients

A

Pneumococcal (above 19)

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15
Q

If patient on insulin struggling with intermittent dosing… can give what?

A

Insulin infusion pump

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16
Q

Out of Metformin and sulfonylureas, which decreases microvasc events and which decreases CVD

A

Metformin decreases CVD and sulfons reduce microvasc

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17
Q

Goal HbA1c for adults and children

A

Adults - <7%
Children - <7.5%

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18
Q

Does tight glycemic control reduce risk more for macro or micro vasc complications

A

More for microvasc complications

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19
Q

DKA vs HHS
Glucose-
Acidosis-
Ketones-
Anion gap-
Osmolality-

A

Glucose- >250 DKA. >600 HHS
Acidosis- only in DKA
Ketones- only in DKA
Anion gap- raised in DKA
Osmolality- raised in HHS

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20
Q

Mx for DKA
-consider K+ being low to start
-consider if glucose goes down but AG remains

A

NS, insulin (check for low K+) until AG closes. If K+ <3.3 then give K+ before starting insulin. If glucose goes below 200, but acidosis remains, give dextrose with the Insulin

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21
Q

Mx of HHS

A

NS first, insulin (check for low K+).. DVT prophlx

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22
Q

When to further evaluate patients with hypoglycemia

A

If Whipple triad is present only!

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23
Q

Hypoglycemia after meals only… consider what disease

A

Consider dumping syndrome

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24
Q

If patient has hypoglycemia after fasting, then what should we do to Invx

A

Do a fast, then take glucose, Insulin, c peptide.

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25
Q

Patient conscious and has hypoglycemia. Mx?

A

Oral sugar/drink

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26
Q

Patient with altered mental state and has hypoglycemia. Mx?

A

IV dextrose. Or IM glucagon if no IV access

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27
Q

Best initial test to screen for thyroid disease

A

TSH

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28
Q

Best initial tests to screen for pituitary-based thyroid disease

A

TSH and T4

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29
Q

Euthyroid sick syndrome findings (TFTs)

A

Low T3, but high rT3 (T4 converted to rT3)

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30
Q

Thyroid bruits can be a sign of what disease

A

Graves

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31
Q

Which kind of thyroid nodules need biopsy and further workup for CA

A

Non functioning nodules

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32
Q

Dx
Hyperthyroid signs, low thyroglobulin, low uptake on RAI scan.

A

⬆️ Exogenous thyroid hormone

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33
Q

DDx
Hyperthyroid signs, high thyroglobulin, low uptake on RAI scan.

A

Acute thyroiditis, iodine exposure, extra glandular exposure

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34
Q

Graves opthalmopathy Tx

A

Steroids

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35
Q

Definitive Tx for hyperthyroidism. When is this CI’d

A

I 131. Not if large and obstructive goiter, or graves (worsens ophthalmopathy). Do thyroidectomy for these cases

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36
Q

Mainstay symptomatic treatment for hyperthyroidism

A

Bb

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37
Q

First line agent to tackle the high TH in hyperthyroidism

A

Methimazole (recall 1st trim rule)

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38
Q

Thyroid storm Tx

A

Bb, then anti thyroid meds (PTU due to rapid action), GCs, then KI
(+-) cholestyramine

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39
Q

Most common cause of congenital hypothyroidism

A

Thyroid dysgenesis

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40
Q

High CK seen in hypo or hyper thyroidism

A

Hypo

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41
Q

Mx of myxedema coma

A

ICU admission. IV levo and IV hydrocortisone (unless excluded adrenal crisis)

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42
Q

De quervain thyroiditis Mx

A

Self limited, but give NSAID for pain

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43
Q

Thyroiditis Mx (generally)

A

Anti thyroid meds if hyperT, and levo if hypoT. Anti thyroid meds not indicated

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44
Q

Why does levo dose need to be increased in pregnancy

A

Because E. increases, increasing TBG, decreasing free T3/T4

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45
Q

Appreciate diagnostic workup for thyroid nodule

A
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46
Q

Thyroid nodule:
Next two things to do

A

TSH and neck US

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47
Q

Thyroid nodule:
TSH low. Do what?

A

Scintigraphy

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48
Q

Thyroid nodule:
TSH low. And RAI shows hot nodule. How to Mx

A

I131, or Sx excision

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49
Q

Thyroid nodule:
TSH low. And RAI shows cold nodule. How to Mx

A

Check if needs FNA criteria on US. Then proceed to FNA

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50
Q

Thyroid nodule:
TSH high/normal.
How to Mx

A

See if meets FNA criteria on US. Then do FNA

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51
Q

Tx for malignant thyroid CA

A

Hemi or total thyroidectomy. +- RAI

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52
Q

Tx for indeterminate thyroid nodule (risk of CA)…. FNA not 100%

A

Balance watch and wait with hemithyroidectomy

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53
Q

Mx for patient with confirmed benign thyroid nodule

A

Exam and US follow up

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54
Q

Diagnostic test for osteoporosis.
When should this be done

A

DEXA scan. This should be done for all women above 65 and older men above 70. And in patients with signs and symptoms or risk factors

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55
Q

When and what to treat osteoporosis

A

Treat all osteoporosis patients. Do you lifestyle modifications and bisphosphonates are first line.

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56
Q

Supposed cause of Padgetts disease

A

Latent viral infection in susceptible patience

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57
Q

Best initial test for Paget’s disease

A

Plain x-ray, to see the lytic and sclerotic lesions

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58
Q

Aside from plain x-ray, what to other tests can be done in Paget’s disease

A

Radionucleotide bone scan is needed to characterise the extent of the disease. And bloods (LP, calcium, phosphate)

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59
Q

Treatment for PAgets

A

Usually no treatment. But may need to reduce pain. Is phosphonate our first line pharmacologically, calcitonin second line.

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60
Q

Bone pain and hearing loss, think what disease

A

Paget’s disease

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61
Q

General hypercalcaemia treatment. Consider if secondary to malignancy

A

IV fluids and calcitonin. If secondary to malignancy, add bisphosphonate

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62
Q

Treatment of solitary parathyroid adenoma, and parathyroid hyperplasia

A

If adenoma can remove. If hyperplasia remove 3.5 of the glands

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63
Q

Management of hyperPTH in the setting of chronic kidney disease

A

Oral phosphate binders and diet phosphate restriction. Consider cinacalcet

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64
Q

What is the diagnosis. Profound hypocalcaemia following a parathyroidectomy in a patient who had hyper parathyroidism

A

Hungry bone syndrome

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65
Q

What inhibits GnRH

A

Prolactin

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66
Q

What is the main inhibition and stimulation for prolactin secretion

A

Dopamine inhibits and TRH stimulates

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67
Q

Dopamine inhibit secretion of which two anterior pituitary hormones

A

Prolactin and TSH

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68
Q

What is panhypopituitarism

A

Where are the anterior and posterior pituitary are affected

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69
Q

Diagnose this. Asymptomatic patient, has high calcium, PTH as normal, urinary calcium is low.

A

Most likely FHH

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70
Q

Which hormones are most affected in pituitary diseases

A

Gonadotropins and growth hormone. So children often have growth retardation an adult often have hypogonadism

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71
Q

What are the routine hypopituitarism testings

A

8 am cortisol (on two occasions), three T4, testosterone and oestrogen, urine and plasma osmolality. Once that is established do an MRI of the brain

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72
Q

Watery diarrhoea, low potassium and hypochlorhydria. What is the diagnosis

A

VIPoma 

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73
Q

What are the 4 Ss Of adrenal crisis management

A

Salt (0.9% saline), steroids (IV hydrocortisone), support (resus and 50% dextrose), and search for underlying illness

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74
Q

Do you have a concern for adrenal insufficiency, what is the first investigation

A

8 am cortisol

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75
Q

Do you have a patient where you are suspicious for Adrenal insufficiency. The cortisol results are indeterminate. How do you manage next

A

Do a cosyntropin stimulation test

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76
Q

In an adrenal insufficiency suspicion. Cosyntropin test shows minimal cortisol response. What do you do

A

Measure ACTH. At this rate adrenal insufficiency is confirmed. Now we just want to know where the secondary or primary

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77
Q

If you have a concern for adrenal insufficiency, you do an 8 am cortisol test.

It comes back with low cortisol levels. Is this diagnostic

A

Yes and you can now measure ACTH

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78
Q

When do you do a cosyntropin stimulation test

A

When you suspect adrenal insufficiency, and your 8 am quarts or test shows indeterminate results. If the 8 am cortisol tests show low cortisol, adrenal insufficiency is confirmed

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79
Q

Hi suspicion of adrenal insufficiency, what takes precedent giving steroids or diagnostic testing

A

Giving steroids

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80
Q

Best initial test for pheochromocytoma

A

24 hour urine metanephrines and catecholamines

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81
Q

When do you do imaging for pheochromocytoma

A

After labs. Can do CT or MRI of the adrenals, and nuclear MIBG scam to localise extra adrenal lesions

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82
Q

Talk to me about the treatment of pheochromocytoma

A

Surgical resection. However you must give phenoxybenzamine prior. Beta blockers never given first due to unopposed alpha vasoconstriction

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83
Q

3 diagnostic tests for Cushing’s syndrome

A

24 hour urine 3/4 or or low-dose dexamethasone suppression test or late night salivary cortisol

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84
Q

Once diagnosed Cushing’s syndrome what do you do next

A

Measure ACTH to know whether it is adrenal or extra adrenal

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85
Q

Patient diagnosed with Cushing syndrome, ACTH is suppressed. Next investigation?

A

Adrenal CT

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86
Q

Patient diagnosed with Cushing’s syndrome and has elevated ACTH. How did we manage the patient

A

MRI of pituitary. If more than 6 mm Adenoma than this is Cushing’s disease. Note that the US Emily algorithm does not include high-dose dexamethasone suppression test

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87
Q

Patient diagnosed with Cushing’s syndrome, has high ACTH, and no adenoma (or less than 6 mm adenoma) is seen on MRI. How to investigate next

A

Do Petros or sinus sampling with CRH. If there is a central to peripheral ACTH gradient it is Cushing’s disease, if there is no gradient is likely ectopic ACTH

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88
Q

Why do some patients with hyperaldosteronism get muscle weakness and Ileus

A

Due to hypokalaemia

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89
Q

Main way to diagnose primary hyperaldosteronism

A

 I give sodium load and measure urine aldosterone. Failure to suppress aldosterone indicates diagnosis. Can also do plasma renin activity to calculate the aldosterone to plasma renin activity ratio

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90
Q

Went to do imaging for primary hyperaldosteronism

A

Only after labs. And a CT/MRI usually is used

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91
Q

Management of con syndrome. What about management of bilateral hyperplasia (Hyperaldosteronism)

A

For constant room you can do surgical resection (done after correction of potassium and blood pressure).

Hyperplasia is usually treated with spironolactone

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92
Q

Diagnostic marker for 21 hydroxylase deficiency

A

17 hydroxyprogesterone elevation 

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93
Q

General management for congenital adrenal hyperplasia

A

Fluid resource and salt repletion. Cortisol to decrease the ACTH.

An antigen is. Fludrocortisone can be given in severe 21 hydroxylase deficiency cases. Consider surgery for ambiguous genitalia

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94
Q

Main way to differentiate between CAH and aromatase defficiency

A

They present very similarly in females. But CAH will have blood pressure and electrolyte problems

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95
Q

Initial lab test for diabetes insipidus

A

Serum osmolality, urine osmolality, serum sodium, urine sodium

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96
Q

Confirmation test for diabetes insipidus, and how to differentiate them (Central and nephrogenic)

A

Water deprivation test. Then give desmopressin

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97
Q

Treatment for central diabetes insipidus

A

Desmopressin IV or intranasally or orally

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98
Q

Treatment regime for nephrogenic diabetes insipidus

A

Salt restriction, thiazide, amiloride, low protein diet

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99
Q

You clinically suspect acromegaly, what is the first test to do. Interpret what are the results with mean

A

IGF – 1 levels. If normal rules out acromegaly, if elevated must do further testing

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100
Q

Patient had a suspicion for acromegaly, IGF levels were elevated. What must be done next

A

Oral glucose suppression test. If there is adequate growth hormone suppression this rules out acromegaly. If inadequate must do MRI

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101
Q

Patient had suspicion for acromegaly. IGF-I was elevated and oral glucose suppression test was inadequate (i.e. positive). What must be done next

A

MRI of the brain.

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102
Q

What is the surgical and medical therapy for acromegaly

A

Surgery is transphenoidal surgical resection. Medical therapy is ocreotide or pegvisomant

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103
Q

What diagnostic tests must be done in suspected hyperprolactinaemia

A

Serum prolactin. MRI of the brain. And a pregnancy test

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104
Q

Best initial treatment for hyperprolactinaemia

A

Dopamine agonists (cabergoline or bromocriptine)

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105
Q

If Prolactinoma is resistant to medication. Or has compressive effects. How can we manage

A

Transphenoidal surgery

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106
Q

Mainstay treatment for SIADH

A

Restriction of fluids

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107
Q

Patient with SIADH. You have restricted fluids. But it is persistent and symptomatic. How do you manage

A

Try IV hypertonic saline therapy

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108
Q

Aside from restriction of fluids and IV hypertonic saline. What to therapies can be given for either severe SIADH or chronic SIADH

A

Severe can be given tolvaptan. Chronic can be given Demeclocycline

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109
Q

Initial test for pheochromocytoma suspicion. And then the diagnostic test

A

Initial test is plasma metanephrines. If they are high do a CT.

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110
Q

Why might glucose be elevated in pheochromocytoma

A

Because epinephrine and norepinephrine inhibit insulin

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111
Q

Diagnosis of nonclassic congenital Adrenal hyperplasia. What’s the treatment

A

Diagnosed by doing And ACTH stimulation test, which will see an increase in 17 0HPROG. Treat with Hydro Cortizone believe it or not

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112
Q

Why estrogen will recquire more levothyroixine

A

Because increase estrogen means more TBG. Usually in normal people this will equilibrate, but since a hypothyroidism patient cannot increase TH when TSH increases, it doesn’t. So that’s why more Levo needed.

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113
Q

Babies with CAH… do they have electrolyte abnormalities at birth?

A

No. 2-3 weeks after, since maternal adrenal hormones are still present

114
Q

Hyperparathyroid like symptoms… high urine Ca excretion vs low? DDx

A

Low = FHH. High = HyperPTH (so much Ca that even though PTH increases reab, there is net excretion)

115
Q

Precocious puberty, one of the best things to do first

A

Bone age test

116
Q

Precocious puberty, if bone scan shows same bone age as chronological age

A

Benign pubertal variant

117
Q

Precocious puberty, if bone scan shows higher bone age as chronological age, measure what?

A

LH, to see if the precoc is central or peripheral

118
Q

How does the location of the diabetes inspires impact the Na levels

A

If the hypothalamus or pituitary are effected, then The thirst centre is kinda fucked, so Na levels can go up more. If it’s nephrogenic then the thirst centre is intact and Na is ok often

119
Q

Neuropathic pain Tx…. Say if patient is old and has MI Hx

A

Preg abalone or gabapentin. Avoid TCA here

120
Q

Patient who is young and has HTN. Given thiazide and suddenly gets low K. What’s occurring here and what to do next

A

Likely hyper aldosterone. These patients are very susceptible to low K. Do Aldo:PRA to Dx.

121
Q

Values of Na and K in central adrenal insuff

A

Na is low, since cortisol usually inhibits ADH. K is normal

122
Q

Why might CF patient (or other chronic pancreatitis cases) with pancreatic insuff and DM, be as risk for hypos

A

Since alpha cells are usually damaged too, we get lack of glucagon…. Causing hypos

123
Q

Myopathy of hyperthyroidism

A

Weakness, can be distil but more likely proximal, muscle atrophy, reflexes often normal, no pain, other signs of hyperthyroidism. Usually resp and bulbar muscles normal

124
Q

Neonatal hyperthyroidism cause . TX?

A

Mums graves antibodies cross placenta. Cannot be from mums levothyroxine since it cannot cross placenta. Give methimazole and a BB, will resolve in 3 mo.

125
Q

What changes in TSH, and total T3/T4 do we see in pregnancy and why

A

Due to high TBG, we see increase in total T3/T4. Because of hCG being high, it stimulates TSHr and negatively feeds back on TSH (lowering it).

126
Q

Findings of TFTs in euthyroid sick syndrome

A

Low total and free T3. Normal TSH and T4

127
Q

Neuroblastoma facts

A

Usually in adrenal medulla or sympathetic plexus. Usually young young child. If in Cervicle plexus then can cause horners. Can mets to orbit and cause periorbital bruising. Can cause opsiclonus myoclonus syndrome. Small blue cells and schwaaniana stroma . N myc amplification

128
Q

Harlequin sign

A

when a child cries, they flush only on one side of the face. Due to horners in a child

129
Q

How to monitor for recurrence after papillae, follulcar and medullary thyroid cancer

A

TG for the first two. And calcitonin for the last

130
Q

What is postpartum thyroiditis in relation to Hashimoto

A

Postpartum firelighters is a type of Hashimoto, that is not chronic. And of course after pregnancy

131
Q

Galactosaemia, mention signs and symptoms, genetic defect, management

A

GALT mutation. Patient will have vomiting, low glucose, Portone, hepatomegaly, bilateral cataracts, jaundice. Will be part of newborn screening, we’ll see reducing sugars in the urine, GALT activity in red blood cells will be low. Managed bye reducing milk, going to soy diet

132
Q

What is subclinical hypothyroidism

A

High TSH, yet normal T4

133
Q

What is euthyroid sick syndrome. How do you manage

A

In ill patients are cytokines cause a decrease in T4 to T3 conversion. This means we will have normal TSH, normal T4, low T3. rT3 struggles to get degraded to, so is elevated. For treatment thyroid hormone does not work, so we just observe. Later on TSH may decrease, and then near the end of the disease it starts to increase (which can appear like hypothyroidism). So wait a bit before retesting

134
Q

What is the equation to calculate the calcium corrected for albumin

A

Ca + (0.8 * (4 - alb))

135
Q

What is pseudo gynaecomastia

A

Essentially lipomastia. Fat accumulates in the chest, and does not have clear define borders like normal mammary glands. The man will have no hypogonadal problems or cancer signs. It’s benign so just advise weight loss

136
Q

If diagnose somebody with high blood pressure what other tests should be done initially

A

ECG, UandEs, urinanalysis, complete blood count, diabetes testing, cholesterol testing. Essentially checking for comorbidities and complications

137
Q

What’s the definition of resistant hypertension

A

Blood pressure that persists even with three classes of antihypertensives

138
Q

What is the diagnostic/investigation steps for pheochromocytoma

A

Plasma metanephrines, then ct or pet to confirm and locate tumour

139
Q

Why do we see gynaecomastia more in primary gonad issues, rather than central courses.

A

Because in primary gonadal issues, we get increased LH and FSH, which increase the aromatisation of testosterone to oestrogen.

In central cause as we don’t have this so gynaecomastia is less prominent

140
Q

Can opioids cause hypogonadism

A

Yes! They can suppressed secretion of GnRH and LH

141
Q

Name a couple of key differences between symptoms in polymyositis and thyroid myopathy

A

Polymyositis usually has reserved the tendon reflexes, where is thyroid problems will show varying signs. Polymyositis have weak muscles not myalgia.

142
Q

A patient with diabetes and persistent albumuria Is said to have diabetic nephropathy when what is present (two potential things)

A

Had type one for five or more years, or type two for a significant time

Has proliferative diabetic retinopathy

143
Q

How to diagnose premature adrenarche or premature thelarche

A

Patient will have signs of high androgen (pubic hair and acne) or the patient will have breast development respectively. Both of these will have normal bone age, versus precocious puberty which has advanced bone age 

144
Q

How to diagnose central versus peripheral precocious puberty

A

Patient has advanced bone age, to distinguish between the two must do GnRH stimulation test. If LH is low it’s preferable if LH is high its central

145
Q

Describe the relationship between calcium and. Albumin

A

Albumin will bind calcium (free), And lower it.

So maybe you will have hypocalcaemia on labs, but the actual calcium might be normal. Or you may have normal on labs, but may have a slightly high calcium in reality

146
Q

Treatment for hypercalcaemia due to immobilisation

A

Bisphosphonate (make sense)

147
Q

Constitutional delay of growth and puberty versus familial short stature, in terms of bone age

A

Bone age will be less than actual age in the prior, And bone age will be the same as actual age in the latter. Also there’s usually a fam history in the latter

148
Q

Talk to me a bit about constitutional delay of growth of puberty

A

Patient would have had normal-ish growth around six months to 3 years, then it will have come down to around the second percentile (but it will be on the same trajectory for a very long time).

Bone age less than actual age. Tanner will be one. Maybe a family history of delayed puberty. Manage with watch and wait

149
Q

Went to do partial lobectomy versus total thyroidectomy.

And when do we give radioactive iodine

A

If the cancer is less than one to 2 cm and there is no lymph node or local invasion, we can do partial lobectomy. If it’s greater than 2 cm old is lymph nodes all this invasion we do total thyroidectomy. Radioactive iodine is given after. Third hormone is required (to replace the hormone but also to inhibit TSH). TSH is our market of choice for follicular carcinoma

150
Q

If a woman has increased hair and acne on the face. Also has temporal balding, enlarged clitoris, muscular build.

What does this tell us about the aetiology

A

Since it’s virilisation, It’s most likely a testosterone or DHE a producing tumour

151
Q

DHEAS versus DHEA versus testosterone producing Tumour in women

A

DHEAS (sulphated = partially metabolised), DHEA, T from adrenal,

T and DHEA from ovary

152
Q

Presentation of CAH in newborns do not have salt changes, why

A

Mothers hormones are present. So salt wasting only seen in 1-2 weeks

153
Q

Why does secondary adrenal insufficiency cause low sodium

A

Loss of cortisol can prevent its natural inhibition on ADH. So we can an SIADH. Lowering sodium

154
Q

What are some of the things that can trigger Phae attack

A

Surgery, anaesthetics, abdominal pressure, BB

155
Q

Graves Tx details

A

If mild can do remission with methimazole. If severe do thyroidectomy or RAI (give GCs with it to stop opthalmopathy)

156
Q

Overview of invx and Dx of primary hyperaldo

A

Basic labs, then plasma aldo to renin ratio (almost Dx’ic). Urine aldo after Na loading is Dx’ic. Abdominal CT or adrenal venous sampling to determine bilateral or unilateral

157
Q

Patient in PTU or methimazole, and gets sore throat, what to do?

A

Stop med, and take WBC count. If less than 1000, stop indefinitely. No need to do WBC screening however

158
Q

Hooklike osteophytes are seen where

A

Hemochromatosis (in fingers )

159
Q

How to adjust insulin for long and short excserize

A

If short burst, can reduce short acting dose of insulin. If long duration, reduce both long and short acting

160
Q

Why is sodium
Low in HHS

A

Osmolality will draw water into vessels causing diltional low Na

161
Q

Risks for HHS

A

CSs, thiazide, skipping insulin, MI, infx

162
Q

Does aggressive DM medical management and HBA1C refutation improve micro or macro vasc complications

A

Micro, macro not so much. And it can even increase all cause cardiac mortality. Aim for 7

163
Q

Pathophys and cause of milk alkali syndrome

A

Intake of calcium and absorbable alkali. Can even be just CaCO4 as a whole. Causes renal Vasoconstriction and reab of bicarbonate. Causing high Ca signs. And met alk. Give ISOtonic fluid and then furosemide

164
Q

When to do statins for primary prevention

A

LDL >190, age > 40 and DM,

165
Q

What effect does E therapy have on hypothyroid patients on Levo

A

As we know, TBH increases, free T4 decreases, TSH increases… but hypoT patients cannot increase the TH, so they need bigger dose of Levo

166
Q

Decrease libido and pubic hair in primary adrenal insufficiency are seen in men or women? Why?

A

Women. Men have testes still

167
Q

Central Precocious puberty treatment

A

If ideopathic give GnRH ag therapy. Surgery if adenoma

168
Q

Osteomyelitis and patient has foot puncture wound. Bacteria cause?

A

Pseudomonas

169
Q

Osteomyelitis in diabetes patients. What are the causes bacterial level

A

Polymicrobial. Gram-positive and anaerobic coverage needed

170
Q

Is first trimester thyroid hormone changes

A

Thyroid finding population increases which increases total thyroid hormone. Also the increase in HCG (due to close alpha subunit mimicry) can decrease TSH via negative feedback and further increase forward hormone production

171
Q

When do you do adrenal Veena sampling for high aldosterone

A

Do either when the CT comes back normal, and you need to know whether it’s bilateral adrenal hyperplasia or Conns syndrome. Or if the patient about 40 years old

172
Q

Pro insulin level percentage compared to insulin. What is the significance of this value when comparing hypoglycaemia due to sulphonylurea versus insulinoma

A

In insulinoma pro insulin is more than 20% of the total insulin level. Where is it usually less than 20% in sulphonylurea. However you do need to take sulphonylurea levels to diagnose

173
Q

Quick contrast between metoclopramide and erythromycins for diabetic gastroparesis

A

Metoclopramide obviously has extra promote effects. Erythromycins exhibits tachyphylaxis, and it’s only really used for less than a month

174
Q

Is chronic GC then withdrawal a secondary or primary AI. and why does the Na decrease

A

Secondary, and Na decreases due to increase ADH… Aldo is normal

175
Q

If you have low T. Or E. And the LH and FSH are normal…. Is this primary or secondary

A

Secondary apparently

176
Q

HHS mainstay Tx

A

IV insulin. aggressive fluids, do NS regardless of Na, then 0.45 NS if sodium high. Give K if it’s less than 5.3

177
Q

DKA Tx overview

A
178
Q

Thyroid storm vs phae… which has fever

A

Thyroid storm (sometimes 40°c plus)

179
Q

Causes of hypoglycaemia without DM

A

Drugs: quinolones, quinine, beta blockers
Alcohol (usually with prolonged starvation)
Sepsis/critical illness
Adrenal insufficiency
Insulinoma
Surreptitious insulin, sulfonylurea, or meglitinide use
Depleted glycogen stores (anorexia nervosa)
Severe hepatic failure

180
Q

HB A1c levels above 45 years old. When and how often to recheck the levels

A

If below 5.7 recheck every three years. If between 5.7 and 6.4 recheck yearly

181
Q

On top of giving levothyroxine treatment to a myxedema coma patient, what else do we have to give him why

A

Give hydrocortisone. Unless you have ruled out adrenal crisis, as they present similarly

182
Q

In what circumstances do we give levothyroxine, even if the patient is subclinically presenting

A

If the TSH is above 10, or if the patient has Hashimoto (treat anyway)

183
Q

In the work up for Cushing’s, if the ACTH is high and you’ve done the MRI, what millimetre adenoma cut off would signify Cushing’s disease

A

6 mm. Bigger than 6 mm adenoma is Cushing’s disease. Less than 6 mm, must do petrosal sinus CRH sampling

184
Q

Milk alkali syndrome Tx

A

IV fluids then loops. and stop offending cause

185
Q

Milk alkali symptoms

A

High Ca, alkalosis, AKI

186
Q

Meds that worsen milk alkali

A

Mainly thiazides. Makes sense

187
Q

Why might celiacs patient have bone pain

A

Vit D deficiency. Got Q wrong based on this…

188
Q

Infant with low low BP and signs of hypovolemia. Na very low, K very high. Dx?

A

Most likely CAH salt wasting

189
Q

Long standing CKD patient. Calcium starts to rise. po4 still high, PTH very very high.

A

Maybe 3° hyperPTH

190
Q

3° hyperPTH usual Tx

A

Parathyroidectomy

191
Q

Causes of acute hypocalcemia

A

Citrate chelation, EDTA, surgical PTectomy, major resp alkalosis, sepsis, pancreatitis, TLS

192
Q

Diagnostic tests for PKU. Consider if the newborn screening, versus suspected later on.

A

Newborn screening is with mass spectrometry. Later on you can do amino acid analysis.

193
Q

TFT results in preg

A

Increase Estrogen, and thus TBG. This will increase the total T3 and T4. Because the HCG is high, this mimics TSH, so TSH often is decreased. So increase thyroxine if they are hypothyroidism patient

194
Q

Diagnosed this condition. Pancytopenia, bone pain, delayed puberty, hepatic splenic Meg.. 14-year-old.

A

G A,UCHER 

195
Q

Before doing plasma, rennin and aldosterone testing, what medications need to be withdrawn?

A

All of the thiazide, spironolactone diuretics. And they should be withdrawn one month before testing.

196
Q

What Aldo:renin suggests 1° hyperaldo

A

20

197
Q

What is the rough schedule for medical therapy prior to surgical reception of the phaechromocytoma? 

A

Roughly 2 weeks before start irreversible, non-selective, alpha blocker therapy. Then roughly a couple of days before the operation can initiate beta-blockade as well.

198
Q

Why might a diabetic gastroparesis patient have increased hypoglycaemic episodes when taking insulin

A

Because there is delayed transit into the duodenum, the patient may misstime the insulin doses 

199
Q

Compare and contrast the benefits and drawbacks to erythromycin versus metoclopramide

A

metoclopramide can cause extra pyradimal side-effects. Erythromycin has tachyphylaxis, and can diminish effect overtime. 

200
Q

Tx of these prolactinomas

Micro (<1cm) and no symptoms

2cm and no symptoms

0.5cm and symptoms

Above 3cm

Failed cabergoline

A

No Tx

DA ag

DA ag

Sx

Sx

201
Q

For how long can someone be on GC before withdrawal Adrenal insuff is a risk

A

3 weeks only!

202
Q

Polyuria is how many L in 24 hr

A

3hr

203
Q

Why are pregnant women at risk of D.I.

A

Placenta produces vasopressinase. Which breaks down ADH. It can either unmask DI or cause transient DI

204
Q

Once established polyuria… what do I want to know next

A

Is it osmotic or non osmotic.

Osmotic: DM, urea
Non osmotic: DI, psychogenic polydyp

205
Q

Best way to look at whether something is primary or secondary (axis wise)

A

Primary disorders will always cause major feedback to the central system. So primary hypogonadism will need high LH and FSH. If we have primary hypergonadism, we will see very low FSH and LH. If the FSH or LH are normal, it’s usually central

206
Q

What two things do I give to a patient in myxedema, and why?

A

IV. Thyroid hormone replacement. An IV hydrocortisone (unless you have excluded adrenal insufficiency)

207
Q

What is cinacelet

A

 PTH analog. It’s a calcium and can be used in hyperparathyroidism to decrease the PTH.

208
Q

Exercise recommendation for diabetics

A

Moderate intensity exercise for 30 to 60 minutes, five times per week

209
Q

What is the statin rule for diabetics

A

40 to 75-year-olds year olds should be placed on a statin

210
Q

Three contraindications for Met Forman

A

Heart failure, renal failure, hepatic failure

211
Q

Do DKA and HHS both have high serum osmolality

A

No, only HHS

212
Q

Some rules about potassium and DKA treatment

A

If potassium is low (less than 3.3) don’t give insulin, replete potassium first. If potassium is in normal range, often give potassium with insulin. If potassium hi give insulin, and monitor potassium

213
Q

When you reach around 250 to 300 glucose levels when treating DKA with insulin. What should we do

A

Consider adding 5% dextrose, just to avoid hypoglycaemia

214
Q

What is mixed meal testing for dumping syndrome

A

Consume nonliquid meal, and then do glucose, C-peptide, insulin.

215
Q

Best initial test if suspect thyroid disease, versus if suspect hypothalamic/pituitary thyroid disease

A

TSH

TSH and free T4

Not sure how important is it

216
Q

In essence what is euthyroid sick syndrome

A

A physiological adaptation, where T4 is not shunted T3, but rather a rT3. this avoids excess catabolism. So do not supplement thyroid hormone

217
Q

In essence what is subclinical hypothyroidism

A

Beginning stages/compensated hypothyroidism. TSH is elevated and can compensate (T3 and T4 are normal).

218
Q

Thyroid bruit is specific for what disease

A

Graves disease

219
Q

If a patient has large obstructive goitre, or Graves ophthalmopathy. Can we do radioactive iodine

A

No.

220
Q

What is the role of bile acid finding resins for thyroid storm

A

Because the right hormone is excreted in bile, BABR can prevent its reabsorption

221
Q


Delayed relaxation of deep tendon reflexes are seen in which disease

A

Hypothyroidism

222
Q

LDL triglycerides CK and sodium levels in hypothyroidism

A

Hi, hi, hi, low

223
Q

In subclinical hypothyroidism when do we give levothyroxine

A

When the TSH goes above 10

224
Q

De quervain thyro

Lymphocytic or granulomatous

TX?

A

Granulomatous

NSAID or CS for pain

225
Q

How to manage an indeterminate FNA of a thyroid nodule

A

Watch and wait versus hemithyroidectomy

226
Q

Vertebral compression fractures in osteoporotic patient presentation

A

Usually asymptomatic, often shows lots of height and progressive thoracic kyphosis

227
Q

Osteoporosis patients, who get bis phosphonate. Osteopenic patients who gets bisphosphonate

A

All osteoporosis patients. Osteopenic patients with high calculated fracture risk based on FRAX

228
Q

Where is consequence of osteoporosis

A

Hip fracture. Carries the highest mortality in a

229
Q

If intolerant to bisphosphonates, what is the second line treatment for Paget’s disease

A

Calcitonin, and of course analgesia for the pain

230
Q

Recall the general criteria for parathyroidectomy, given that the patient is asymptomatic (every symptomatic patient gets a parathyroidectomy)

A

Very high calcium, high creatinine, low bone mineral density, less than 50

231
Q

Two circumstances that cinacalcet is used 

A

Hyper parathyroidism secondary to renal disease or when no Sx can be done on PT gland

232
Q

Which two hormones are primarily affected in panhypopituitarism

A

Growth hormone and gonadotropins

233
Q

Why do we give levothyroxine and cortisol in Myxoedema coma?

A

We must do this unless we have ruled out adrenal insufficiency. Because levothyroxine can increase cortisol clearance and worsen the adrenal crisis

234
Q

Most common cause of death in acromegaly

A

Left ventricle hypertrophy and thus diastolic heart failure

235
Q

Some other random complications of acromegaly

A

Type two diabetes, diverticulosis, colon cancer

236
Q

Dopamine and TRH control of prolactin

A

Dopamine inhibits, TRH stimulates

237
Q

MEN2A has which of the Ps??

A

Parathyroid stuff

238
Q

Acid-base disorder that adrenal insufficiency causes

A

None annoying gap metabolic acidosis (due to low aldosterone)

239
Q

Morning plasma cortisol level of what value is considered low (Low enough to skip the synacthen test)

A

Less than three. In this case go straight to ACTH levels to see if primary or secondary

240
Q

If you have low 8 am cortisol level, but not lower than three. What investigation do you do

A

Synacthen test

241
Q

Hi suspicion of adrenal insufficiency. What comes first diagnostic testing or steroids

A

Steroids

242
Q

What’s more common, pituitary or adrenal Cushing’s

A

Pituitary

243
Q

K levels in cushings

A

Low

244
Q

My three diagnostic tests for Cushing syndrome

A

Low dose dexa surp , late nights delivery cortisol, 24 hour urine cortisol

245
Q

Cushing’s disease adenoma less than 6 mm (or can’t see on MRI) what investigation do we do

A

Petros will sign a sampling with CRH. Central peripheral gradient indicates crushing disease. Takes the place of high dose Dexa surp

246
Q

High dose dexamethasone suppression test will suppress cortisol in Cushing’s disease or ectopic ACTH production

A

Cushing’s disease

247
Q

Why is it extra important to screen for pheochromocytoma (urine VMA) prior to surgery for medullary thyroid cancer

A

Obviously to check for con commitment pheochromocytoma, but also to avoid risk of hypertensive crisis during surgery

248
Q

If have severe salt wasting in 21 hydroxylase deficiency, aside from fluid resource, salt repression, cortisol what can we add

A

Fludrocortisone. Remember this is the only CAH associated with low mineralocorticoid

249
Q

Remember the side effect that Savvas mentioned about SGL T2 inhibitors

A

Eug lycaemic ketoacidosis

250
Q

Out of pheochromocytoma and thyroid storm which has an elevated temperature

A

Thyroid storm

251
Q

We all know that in the euthyroid state sick syndrome, T3 is low, T4 and TSH is normal. What happens in severe cases

A

All of them can become low, but T3 come become very low

252
Q

Why would a patient with severe pancreatic damage have specifically bad diabetes, in terms of risk of hypoglycaemia

A

Alpha cells are damaged, glucagon cannot be made. Causing unopposed insulin one treated

253
Q

Woman with acne, increase hair growth on face, secondary aminuria. You also find that they are muscular and build and have a large clitoris

A

Most likely a testosterone or DHE a tumour. PCOS does not cause rapid visualisation

254
Q

In C8H when do we get salt wasting, in assault wasting type

A

One to 2 weeks after birth. Don’t expect in a couple of days-year-old infant. Really tough question we had on ambiguous genitalia XX.

Had high testosterone, but sodium and potassium are normal. This is not a Leydig cell tumour this is CAH

255
Q

How can I use DHEAS levels to know a androgen producing tumour and a woman is in the adrenal or the gonad

A

DHEA and testosterone are produced in both the ovary and the adrenal. DHEAS is only produced in the adrenal.

256
Q

As we know patients with PT you can get a granulocytosis. We don’t need to do regular monitoring, however what do we do if a patient get a sore throat or signs of infection

A

Immediately come off the medication. If the white blood cells are less than 1000 we never go back onto it

257
Q

General rules for diabetics on insulin, wanting to do exercise. Mention just the insulin dose changes. Consider if short or long distance

A

If short: just decrease the short acting

If long: decrease the long and the short acting

258
Q

HHS, why can we see sodium being low

A

 hi osmolality can cause a shift of sodium into cell

259
Q

Which osteoporotic medication can cause milk alkaline

A

Calcium carbonate

260
Q

Cance previous severe chronic hypoglycaemic episode cause eventual unawareness

A

Yes

261
Q

Which medications are risk factors for milk alkaline

A

Thiazides especially, anything else that decreases intravascular volume

262
Q

You see low LA, low TSH, high prolactin. What are you thinking

A

Non-functioning adenoma in the pituitary

263
Q

What is considered a low urine specific gravity

A

Less than 1.006

264
Q

What changes to systemic vascular resistance and heart contraction does thyroid hormone make

A

Drops systemic vascular resistance increases contraction. Increasing pulse pressure

265
Q

When discussing albumin to creatinine ratio. What is an okay milligram per gram

A

Less than 30

266
Q

Man with osteoarthritis, hepato-megaly, history of diabetes, loss of libido

A

Haemochromatosis

267
Q

Site induces can have affect on what vitamin di

A

It can induce vitamin di breakdown

268
Q

Is gynaecomastia more of a primary or central problem in men

A

Peripheral. Because then the increase subsequent LH will stimulate testosterone and oestrogen

269
Q

For deficiencies. Mothers milk is low in what, cows milk is low in what

A

Mums milk is low and a lot of things commonly seems to be low in vitamin D. And can cause Ricketts. Cows milk is low in iron

270
Q

Treatment for hypercalcaemia secondary to immobilisation

A

Bisphosphonate

271
Q

Galactosaemia patients are at increased risk for infection

A

E. coli sepsis

272
Q

Calcium levels in chronic pancreatitis

A

Usually normal

273
Q

General centimetres for when you would do a total thyroidectomy for thyroid cancer

A

1 to 2 cm or less you do parcel. More than two you do total

274
Q

General cut off to do oral versus IV calcium in hypocalcaemia

A

7.5

275
Q

Very rarely mentioned, but bear in mind somebody with primary adrenal insufficiency can also have androgen deficiency, so decrease the decrease libido

A
276
Q

Mayway to tell between constitutional Grace delay and family or short stature

A

Burnage. Burnage will be less than actual age in constitutional.

Burnage will equal actual age and family.

277
Q

Is HbA1c reliable in pregnancy

A

No, that is increase red blood cell turnover

278
Q

The link usually between coeliac’s and endocrine in terms of vitamins

A

Vitamin di deficiency. Causing an osteomalacia

279
Q

Remember diabetes insipidus 300 room (for remembering osmolality

A

 Serum osmolality above 300, urine osmolality below 300

280
Q

Recall some of my calcium chelating things that’s causing hypocalcaemia

A

EDT A, for Scarlett, lactate, blood transfusion i.e. citrate

281
Q

If I have established precocious puberty. Is it when my LH is high or low that I would continue to do the GnRH stimulation test

A

If LH is low. Give GnRH see whether I can increase it, which would mean it central

USMLE Step 2 - Top 5% (34 decks)

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