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int med exam 0828 > Endocrinology - Adrenal, Diabetes > Flashcards

Endocrinology - Adrenal, Diabetes Flashcards

1
Q

where specifically does each zone of the adrenal cortex contain?

A
  • Outer zone glomerulsa - aldosterone
  • middle zona fasciulata - cortisol
  • inner zone reticularis - androgens
  • GFR - ACR
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2
Q

where in the adrenal glands is epinephrine produced?

A

chromaffin cells in the adrenal medulla

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3
Q

what is the function of mineralocorticoids function ?

A

aldosterone normally increase sodium absorption and K+/H+ excretion so high levels cause hypertension, hypokalemia, and alkalosis.

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4
Q

what is the function of glucocorticoids?

A
  • cortisol stimulates lipolysis
  • release of amino acid from muscles
  • liver glucogenesis
  • inhibits inflammatory process
  • Inhibits T-cells and associated DTH and cell-mediated immunity\
  • excess cortisol can stimulate mineralocorticoids and androgen receptors with a similar appearance to aldosterone excess (HTN, hypokalemia, alkalosis)
  • It does not bind to androgen receptors.
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5
Q

what are the androgens produced by the adrenals?

A

DHEA and small amounts of testosterone.

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6
Q

what is the effect of excess adrenal androgens in a woman?

A
  • during gestation - ambiguous genitalia
  • Postnatally - excess hair and abnormal menses
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7
Q

Describe signs and symptoms of Cushing syndrome?

A

excessive adrenal glucocorticoid production causing:

  1. proximal muscle weakness and fatigue
  2. amenorrhea, hirsutism, acne
  3. easy bruising
  4. emotional liability/frank psychosis
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8
Q

what are the physical exam findings of Cushing syndrome?

A

facial plethora (redness of face/fullness due to increased blood flow)

thin skin with pink to purple striae

cervicodorsal fat pad

truncal obesity

moon facies

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9
Q

what are the comorbid conditions associated with Cushing syndrome?

A

DM2 and osteoperosis

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10
Q

what are the causes of cushing syndrome from most to least frequent?

A
  • iatrogenic cortisol adminsitration
  • ACTH - secretuing pituitary adenoma (cushing disease)
  • ectopic ACTH secretuing tumor: (bronchogenic, pancreatic, thymic (if age>60), SCLC
  • bilateral adrenal hyperplasia
  • adrenal tumors
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11
Q

what would you expect to see on a BMP with cushing syndrome?

A

hypokalemia and metabolic alkalosis

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12
Q

what can mimic the phenotypic features of cushing’s syndrome? why is this important?

A
  • obesity, alcoholism, and depression can mimic
  • important as they can result in slightly increased 24-hour urine cortisol and/or abnormal low-dose suppression test
  • this is called pseudo-cushing’s.
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13
Q

what does ACTH do again?

A

increases cortisol, androgens, and mineralocorticoids.

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14
Q

what is the difference between Cushing disease and Cushing syndrome?

A
  • Cushing disease is a disease in the head, caused by a pituitary microadenoma which has increased ACTH stimulating the production of adrenal DHEA.
  • Females can present with virilization (hirsitusim and acne)
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15
Q

what endocrinology labs would you expect to see with an adrenal adenoma that is producing cortisol?

A

ACTH and DHEA would be low.

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16
Q

what are the initial tests to get for Cushing syndrome workup?

A
  • 24 hour urine free cortisol
  • late-night salivary cortisol and/or
  • low dose dexamethasone suppression test to confirm excess cortisol
  • abnormal tests should be confirmed at least once.
  • note that urinary cortisol reflects plasma free cortisol levels
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17
Q

how do you identify pseduo-Cushing’s?

A

elevated cortisol levels (urine) with suppression with low dose dexamethasone suppression of cortisol

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18
Q

what is your next step in working up Cushing’s syndrome if you have elevated cortisol with failure to suppress cortisol with low dose dexamethasone test?

A
  • identify if this is ACTH dependent or ACTH independent disease by measuring ACTH.
  • Normally, a high cortisol completely suppresses ACTH production
  • Any measurable ACTH indicates ACTH dependent Cushing syndrome (Cushing disease or ectopic ACTH production)
  • ACTH to low to be measured indicates ACTH independent Cushing syndrome - (nonpituitary adrenal hyperplasia or adrenal mass)
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19
Q

what if your next step if you have a high urinary cortisol, measurable ACTH?

A
  • this is an ACTH dependent Cushing syndrome so either pituitary tumor (Cushing disease) or ectopic ACTH secreting tumor.
  • Next step is to image the pituitary with a gadolinium-contrasted MRI
  • Can also image chest/abdomen with high res CT.
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20
Q

what is the next step if you have high cortisol, low/unmeasurable ACTH ?

A
  • this is likely ACTH independent cushing syndrome from an adrenal tumor (adenoma or carcinoma)
  • Would measure DHEA and testosterone concentrations
  • Adrenal adenomas have low ACTH and modest DHEA levels
  • carcinomas have low ACTH and high DHEA and urine 17 ketosteroids.
  • adrenal tumors do not usually suppress cortisol production in response to high dose dexamethasone test.
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21
Q

what is the difference between primary and secondary adrenal insufficiency in terms of labs?

A
  • primary (abnormal cosyntropin stim, high ACTH, low aldosterone, hyponatremia, hyperkalemia,
  • secondary (abnormal cosyntropin stim, low ACTH production by pituitary or withdrawal of glucocorticoids, normal aldosterone)
  • all adrenal insufficiency does not respond to ACTH stimulation
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22
Q

why do you have hyperkalemia with primary adrenal insufficiency and not secondary?

A

primary AI would affect both the zona glomerulosa and zona fasiculata causing a hyperreninemic hypoaldosteronism.

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23
Q

what labs do you get to test for adrenal insufficiency?

A
  • baseline cortisol, serum aldosterone, ACTH
  • Cosyntropin stimulation test 0,30.60.
  • If ACTH not >18-20, diagnostic.
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24
Q

what is the treatment for AI?

A

corticosteroids and mineralcorticoids like fludrocortisone

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25
Q

what is schmidt syndrome? what is the treatment?

A
  • combination of primary adrenal insufficiency and hypothyroidism and often type I DM.
  • Must replace cortisol first because giving thryoid replacement as this can increase metabolic demand and cause or worsen shock.
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26
Q

what is the function of aldosterone?

A
  • increases sodium resorption and hence potassium and hydrogen excretion in distal tubules.
  • Increase in sodium resorption means increased water retention and hypertension.
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27
Q

what is primary aldosteronism? associated diseases?

A
  • too much aldosterone produced by adrenal gland.
  • associated with hyporeninemia, hypertension, and hypokalemia
  • associated with Cushing syndrome and licorice ingestion
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28
Q

what is secondary aldosteronism?

A
  • overactivity of the RAAS in the kidney
  • associated with high renin, increased aldosterone
  • this causes decreased renal blood flow, increased renin, increased Ang II, increased aldosterone.
  • See hypertension and hypokalemia
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29
Q

what conditions are associated with a PAC: PRA ratio?

A
  1. primary aldosteronism: PAC elevated, PRA supression, with elevated ratio. Think adrenal tumor or hyperplasia
  2. Secondary aldosteronism: PAC and PRA both icnreased with ratio<10. Think kidney disease (renoovascular or renal tumor)
  3. Cushing, and block licorice: PAC and PRA both decreased with PAC:PRA normal or elevated.
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30
Q

what is the most common cause of hypoaldosteronism?

A
  • decreased production of renin in diabetic patients with mild renal failure
  • this is hyporeninemic hypoaldosteronism
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31
Q

what lab findings do you see in hypoaldosteronism?

A
  • hyperkalemia
  • normal anion gap metabolic acidosis
  • low renin and low aldosterone
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32
Q

what do you do for work up for hypoaldosteronism? treatment?

A
  • exclude AI as a cause of hyperkalemia
  • perform ACTH stimulation test.
  • Low aldosterone response indicates primary hypoaldosteronism of the adrenals
  • large response indicates secondary hypoaldosteronism
  • Tx with mineralocorticoid (fludrocortisone( and/or furosemide
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33
Q

when do you suspect catecholamine-secreting tumor?

A

spells of headaches, sweating, chest palpitations

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34
Q

what is the most sensitive biochemical screening test for pheochromocytoma?

A
  • fractioned metanephrines and catecholamines on 24 hour urine. Wean off TCA and cyclobenazprine 2 weeks before testing)
  • plasma fractionated metanpehrines has a high sensitivity but low specificity.
  • if concern for false positive with plasma metanephrine increase, can do clonidine suppression test.
  • If after a dose of clonidine, plasma metanephrine levels fall, it is due to HTN.
  • If after a dose of clonidine, plasma metanephrines still elevated, likely due to pheo.
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35
Q

what do you do after biochemical tets are positive for pheochromocytoma?

A

CT or MRI of abd/pelvis to find the tumor.

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36
Q

what is the treatment for pheochromocytoma?

A
  • combined alpha and beta blockade preoperatively.
  • phonoxybenzamine for 2 weeks prior to surgery, and 3 days before surgery beta-blocker.
  • Never use beta-blocker first due to unopposed alpha stimulation and potential for HTN crisis.
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37
Q

what tests should patient have for adrenal incidentaloma?

A
  • BP and potassium. Add PAC:PRA if HTN or hypokalemia present. testing for hyperaldosteronism
  • 24 hour urinary free cortisol or low dose dex for Cushing
  • plasma fractionated metanephrines for adrenal medulla for pheochromocytoma
  • estrogens and androgens if feminization or virilization present.
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38
Q

what are the 3 indicatinos for adrenalectomy of incidentaloma?

A
  1. functioning tumor
  2. mass is >4-6cm
  3. imaging suspicious for malignancy
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39
Q

define primary amenorrhea? cause?

A
  • lack of menstruation by age 16 or lack of development of secondary sex characteristics by age of 14.
  • uterine outflow tract abnormality/absence or ovulatory abnormality.
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40
Q

what are the common causes of primary amenorrhea?

A
  • if short stature, wide space nipples, web neck, decreased pubic and axillary hair, think turner (45,XO)
  • if no palpable cervix and no uterus, androgen insensitivity (see elevated testosterone) or genetic absence of uterus.
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41
Q

define secondary amenorrhea?

A

absence of menses for 3-6 months

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42
Q

most common causes of secondary amenorrhea?

A

pregnancy

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43
Q

what are the initial labs do you want to get for secondary amenorrhea?

A
  • pregnancy test, FSH, and LH
  • If virilization, get serum total testosterone and DHEA.
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44
Q

what does increased FSH and LH levels tell you in the amenorrheic women?

A
  • it tells you that the pituitary has lost negative feedback from the ovaries.
  • this suggest ovarian failure either premature ovarian failure<40 like turner syndrome, galactosemia, or autoimmune polyglandular syndrome
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45
Q

what does decreased GSH and LH levels tell you in an amenorrheic woman?

A

it tells you that the pituitary is not making hormones either it is diseased or because the hypothalamus is not sending out GnRH.

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46
Q

what do you need to check on a amenorrheic women with low FSH and low LH?

A
  • meds - antiepilpeitic or psychotropic meds - functional hypothalamic amenorrhea
  • prolactin level
  • TSH
  • MRI
  • If young patient, consider estrogen testing for functional hypothalamic amenorrhea from stress/athletes.
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47
Q

ddx for amenorrheic women with virilizing signs?

A
  • PCOS
  • adrenal or ovarian tumors
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48
Q

what is the MOA behind POCS?

A
  • ovaries and adrenal produces excess androgen and estrogens
  • continuous secretion of estrogen decreases FSH secretions but enhances LH so the LH:FSH ratio is more than 2.
  • LH causes ovarian stromal hyperplasia (more theca cells) and more production of androgens.
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49
Q

what is the primary treatment for PCOS?

A
  1. First line treatment is education and weight loss.
  2. No hirsutism and no pregnancy: OCP or medroxypgrogesterone 1-3 months to induce withdrawal bleeding and to protect the endometrium from hyperplasia
  3. Hirsute and no desire for pregnancy: combined estrogen-progesteorne OCP, metformin
  4. Hrisute and describes pregnancy: induce ovulation with clomiphene with or without metformin.
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50
Q

define virilization? define hirsutism?

A
  • clitoromegaly,
  • voice deepending
  • male pattern balding
  • de-feminization (breast atrophy)
  • Hirsutism - abnormal growth of hair
51
Q

ddx for histutism?

A
  • Cushing disease (central)
  • adrenal cancer
  • ovarian cancer (stromal)
  • congenital adrenal hyperplasia
  • PCOS
52
Q

what labs with hirsutism are suggestive of PCOS?

A
  • mild elevations of DHEA
  • mild elevation of testosterone
  • LH:FSH >2
53
Q

what labs with hirsutism are suggestive of congenital adrenal hyperplasia?

A
  • normal to mild testosterone level
  • normal to mild DHEA or urinary 17 ketosteroids
  • normal LH:FSH
54
Q

what labs are suggestive of adrenal carcinoma with hirsutism?

A
  • normal to mild testosterone
  • very high DHEA or urinary 17 ketosteroids
  • normal LH:FSH
55
Q

what labs with hirsutism are suggestive of ovarian cancer (stromal)?

A
  • elevated testosterone level
  • normal to mild DHEA/urinary 17 ketosteroids
  • normal LH:FSH
56
Q

what labs with hirsutism is suggestive of Cushing disease (central)?

A

normal to mild testosterone

normal to mild DHEA level/urinary 17 ketosteroids

normal LH:FSH

57
Q

what drugs are associated with hirsutism?

A
  • minoxidil
  • cyclosporine
  • phenytoin
58
Q

what does LH do?

A

stimulates Leydig cells (L stimulates L) to produce testosterone which inhibits FSH and LH secretion.

59
Q

what does FSH do?

A

FSH stimulates sertoli cells to secrete inhibin B and androgen binding globulin which in turn binds to testosterone.

60
Q

what is the most common cause of primary hypogonadism?

A

usually due to Klinefelter syndrome, which results in defective testosterone synthesis by the Leydig cells.

61
Q

what is the gene mutation associated with klinefelter syndrome?

A

47XXY or mosaic 46XY/47,XXY

62
Q

what labs are associated with klinefelters and treatment?

A
  • low testosterone, high LH and high FSH
  • tx is testosterone
63
Q

what is the ddx of secondary hypogonadism?

A
  • hyperprolactinemia (high prolactin)
  • anabolic steroids
  • cushing syndrome (excessive glucocorticoids)
  • congenital gonadotropin deficiency (kallman syndrome)
  • hemochromatosis (high ferritin)
64
Q

what endocrine labs do you see with secondary vs primary hypogonadism?

A
  1. primary has defective testosterone synthesis, so low testosterone, high FSH and high LH
  2. secondary has low testosterone, low FSH and low LH
65
Q

ddx of gynecomastia ? lab abnormalities likely to be seen?

A
  • altered estrogen:androgen ratio
  • advanced age
  • obesity
  • cirrhosis
  • hyperthyroidism
  • kleinfelters
  • germ cell tumors
  • meds
66
Q

what does high cholesterol mean?

A

high LDL

67
Q

what is the primary endpoint of lipid screening? Formula?

A
  • LDL
  • LDL = TC - HDL - VLDL
  • LDL = TC - HDL - TGL/5 (provided TGL<400)
68
Q

what is the secondary target once LDL target achieved for primary prevention of lipid screening? formula?

A
  • non-HDL
  • non-HDL = TC - HDL
69
Q

lipid profile effect of changing diet to hydrogenated vegatable oils (trans)?

A

increase LDL, decrease HDL

70
Q

lipid profile effect of changing diet to decreasing saturated fats?

A

decrease LDL, decrease HHDL, same or increase LDL/HDL ratio. Neutral/bad.

71
Q

lipid profile effect of changing diet to change diet to polyunsaturated fats?

A

decrease LDL, decrease HDL, same or increase. this is bad.

72
Q

lipid profile effect of changing diet to monounsaturated fats?

A

decrease LDL, may increase HDL, decrease LDL/HDL. This is good.

73
Q

what are the 4 statin benefit groups? and which statin?

A
  1. age 21 with ASCVD. age<75 high intensity; age>75 - moderate staitn
  2. age 21 with LDL>190 - high intensity statin
  3. age 40-75 with DM and LDL 70-189; ASCVD<7.5% - moderate, ASCVD >7.5 - high intensity
  4. age 40-75 with no ASCVD or diabetes with ASCVD of 7.5% higher - moderate/high statin
74
Q

if you can’t use a statin, what 3 drugs can you use that are not statins? (generally)

A

PCSK9 inhibitors, Ezetimibe, bile acid sequestrants

75
Q

what is the adverse effect of statins?

A

myalgias, myositis, elevated transaminases

76
Q

define MODY vs LADA?

A
  • MODY is mature onset diabetes of the young and rare genetic defect in beta cells.
  • LADA is latent autoimmune diabetes in adults is a late-onset of immune-mediated course in non-obese adults due to autoantibodies targeting pancreas
77
Q

what are the components of whole blood, serum, and plasma?

A
  • whole blood = cells + clotting factors + watery part of blood
  • serum = watery part of blood - (cells + clotting factors)
  • Plasma = (watery part + clotting factors) - cells
78
Q

how do you diagnose prediabetes?

A
  • One of the following:
  • impaired fasting glucose between 100-125
  • impaired glucose tolerance between 140-199 after 75gm oral glucose load. (more sensitive)
  • A1c of 5.7-6.4 is supportive, but you need to retest patients with OGTT or FPG
79
Q

how do you diagnose DM?

A
  • FPG>126
  • random plasma glucose>200 with symptoms
  • A1c>6.5%
  • 2 hour plasma glucose>200 after 75g OGTT
  • confirm diagnose with the same test used initially
  • the best test to diagnose overt T2DM is fasting plasma glucose
80
Q

what diseases can lead to false value of HbA1c?

A
  • anything that alters abnormal blood turnover.
  • iron-deficiency anemia
  • thalassemias
  • hemolytic anemias
  • hepatic or renal diseases
81
Q

what autoantibodies are associated with Type I DM? which is the most important?

A
  • islet cells
  • insulin
  • glutamic acid decarboxylase (most clinically useful)
  • tyrosine phosphatases IA-2 and IA-2B
82
Q

what autoimmune diseases are associated with T1DM? MHC?

A
  • HLA Dr3 and DR4
  • thyroid, adrenal celiac, vitiligo, b12 deficiency, and myasthenia
83
Q

name the long acting insulins?

A

glargine (lantus) and detemir (levemir)

84
Q

explain the honeymoon effect?

A

improvement of hyperglycemia after diagnosis and treatment for a short while, but eventually require reinstitution of treatment

85
Q

explain the dawn phenomenon?

A
  • increased blood glucose between 4 and 7 AM with no preceding hypoglycemia.
  • The cause is transient, mild insulin resistance due to normal early-morning rise in cortisol and GH.
86
Q

explain the Somogyi effect? treatment?

A
  • nocturnal hypoglycemia stimulates adrenal to release glucocorticoids that increase early morning glucose.
  • INCORRECT to reduce evening NPH
  • delay the long evening acting insulin bedtime if NPH used
  • or substitute NPH for a long-acting insulin analog
87
Q

what conditions are associated with acanthosis nigricans? what is it?

A
  • velvety dark rash on flexural surfaces
  • associated with insulin-resistant conditions like PCOS, Cushing, acromegaly, meds like niacin or corticosteroids
  • rapid onset of widespread acanthosis nigricans in older patients suggest GI malignancy
88
Q

what are the oral meds associated with treatment of T2DM?

A
  • BATS
  • biguanide (metformin)
  • alpha glucosidase inhibitors (acarbose, miglitol)
  • Thiazolidinediones/glitazones
  • secretagogues (sulfonyulureas, meglitinidies)
89
Q

MOA, weight effect, mortality and disadvantage of insulin?

A
  • MOA: decrease hepatic glucose production, increase peripheral glucose uptake, suppress ketogenesis
  • increased weight gain
  • hypoglycemia, weight gain, training,
  • decrease in microvascular events.
90
Q

MOA, weight effect, mortality and disadvantage of sulfonylureas?

A
  • glipizide, glyburide
  • stimulate insulin secretion
  • increase weight gain
  • hypoglycemia, weight gain
  • decrease in microvascular events, possible increase in CVD events
91
Q

MOA, weight effect, mortality and disadvantage of biguanides?

A
  • decrease hepatic glucose production, increase insulin-mediated uptake of glucose in muscles
  • neutral weight gain
  • GI effect, vitamin b12 deficiency, lactic acidosis
  • Contraindicated with liver, kidney or cardiac failure
  • decrease in CVD events
92
Q

MOA, weight effect, mortality and disadvantage of alpha -glucosidase inhibitors?

A
  • acarbose, miglitol
  • inhibit polysaccharide absorption
  • neutral weight gain
  • GI effect
  • possible decrease in CVD events in prediabetes
93
Q

MOA, weight effect, mortality and disadvantage of thiazolidinediones?

A
  • rosiglitazone, pioglitazone
  • increase peripheral uptake of glucose
  • increase weight gain
  • fluid retention, heart failure, edema, possible increase risk of bladder cancer with pioglitazone
  • possible decrease in CVD events with pioglitazone
94
Q

MOA, weight effect, mortality and disadvantage of meglitinides?

A
  • repaglinide
  • stimulate insulin release
  • increase weight gain
  • hypoglycemia, weight gain, frequent dosing
95
Q

MOA, weight effect, mortality and disadvantage of amylin mimetic?

A

slows gastric emptying, suppresses glucagon secretion, increases satiety

decrease effect on weight

nausea, vomiting, worsens gastroparesis, injectable, frequent dosing

no effect on mortality

96
Q

MOA, weight effect, mortality and disadvantage of GLP-1 receptor agonist?

A
  • exenatide, liraglutide, “glutide”
  • glucose-dependent increase in insulin secretion. glucose-dependent glucagon secretion slows gastric emptying, increases satiety
  • decrease weight
  • GI effects, hypoglycemia with sulfonyureas, possible pancreatitis, injectable, possible medullary thyroid tumors
  • decrease in CVD events and mortality with DM2 with liraglutide
97
Q

MOA, weight effect, mortality and disadvantage of DPP4 inhibitors?

A
  • sitagliptin, saxagliptin, linagliptin
  • glucose-dependent increase in insulin secretion, glucose-dependent suppression of glucagon secretion
  • neutral weight
  • hypoglycemia with sulfonylureas, increased risk of infections, possible pancreatitis, dermatologic reactions
  • increased heart failure hospitalizations
98
Q

which pharmacologic agents used for DM2 decrease weight?

A

GLP-1 receptor agonists, amylin mimetic, SGLT2 inhibitors

99
Q

MOA, weight effect, mortality and disadvantage of SGLT2 inhibitors?

A
  • canaglifozin, empagliflozin
  • increase kidney excretion of glucose
  • decrease weight
  • hypoglycemia with insulin secretagogues, hypersensitivity reactions, increased candida infections and UTI, euglycemic DKA, hyperkalemia, fractures, amputations
  • bladder cancer with dapagliflozin
  • CVD and mortality
100
Q

MOA, weight effect, mortality and disadvantage of bile acid sequestrants?

A
  • colesevelam
  • MOA not understood, possible decrease hepatic glucose production, possible increase in incretin levels
  • neutral weight
  • constipation, dyspepsia, increased TGL
  • no effect long term
101
Q

MOA, weight effect, mortality and disadvantage of dopamine 2 agonists?

A
  • bromocriptine quick release
  • increases insulin sensitivity, alters metabolism via the hypothalamus
  • neutral weight gain
  • nausea, orthostasis, fatigue
  • possible decrease in CVD events
102
Q

when is monotherapy used for DM2?

A

A1c less than 8

103
Q

when should you initiate dual therapy for DM2?

A

A1c 7.5-9% or higher or after 3 months of metformin therapy not achieving the target

104
Q

how often should you monitor glycemic control?

A
  1. q3 months with adjustments until target achieved.
  2. q6 months if at goal
105
Q

what/when do you need to screen for DM1?

A
  • retinopathy - start 5 years after diagnosis, then annually
  • nephropathy - start 5 years after diagnosis, then annually
  • Neuropathy - start 5 years after diagnosis, then annually
  • CVD - hypertension at diagnosis, screen every visit
  • CVD - dyslipidemia - at diagnosis and prior to initiating statin, screen annually
106
Q

when should insulin be instituted early instead of starting oral drugs for DM?

A
  • DM1 always insulin
  • consistently high random plasma glucose
  • A1c>10-12 without symptoms
  • A1c>9 with symptoms
  • signs of ketosis on physical exam
  • hyperglycemia symptoms or history of DKA
107
Q

what can you do to lower LDL cholesterol?

A

intensity statin, add ezetimibe, PCSK9, colesevelam, or niacin

108
Q

what can you do to lower Non-HDL-C, TG?

A

intensity statin, and/or add R-grade omega 3 FA, fibrate and/or niacin

109
Q

if you have a diabeticwith ASCVD, CKD3 or HFrEF, what should you do?

A

start long acting GLP-1 or SLGLT2

110
Q

how do you diagnose hypoglycemia?

A
  • whipple triad of:
  • signs and symptoms with hypoglycemia
  • associate low glucose level<55
  • relief of symptoms with glucose
111
Q

what are the 2 categories of hypoglycemia and it’s breakdown?

A
  1. reactive (postprandial) - requires Whipple triad, never order OGTT, post-GI surgical patients
  2. non-reactive (fasting)
112
Q

what is the ddx of non-reactive hypoglycemia?

A
  • factitious: insulin or sulfonylureas
  • autoimmune
  • insulinoma
  • hormone deficiencies like adrenal insufficiency
113
Q

what 4 tests are used in the work up of confirmed, nonreactive hypoglycemia?

A
  • serum insulin
  • serum proinsulin
  • c-peptide
  • urinary/plasma sulfonylurea test
114
Q

define fasting non-reactive hypoglycemia and most common causes?

A
  • fasting/factitious type - patient unable to maintain glucose levels with fasting
  • MCC - alcohol abuse, drugs, sepsis, and renal failure
115
Q

what suggests a factitious insulin injection?

A

low C-peptide for insulin level

116
Q

what suggests oral hypoglycemic injection for cause of hypoglycemia?

A
  1. C-peptide that parallels insulin level
  2. high urinary/plasma sulfonyurea level
117
Q

what suggests an insulinoma for the cause of hypoglycemia?

A
  • c-peptide that parallels insulin level (1:1)
  • no urinary/plasma sulfonyurea
  • proinsulin level greater than 20%
  • insulin level usually >3-6 whiel hypoglycemia
118
Q

what suggests an autoimmune cause of hypoglycemia?

A
  • c-peptide that parallels insulin level
  • no urinary/plasma sulfonyurea
  • proinsulin level normal (around 10%)
  • autoantibody to insulin present
119
Q

Cushing syndrome work up?

A
120
Q

How do you treat adrenal crisis?

A
121
Q

summary of labs in interpretation of Adrenal insufficiency?

A
122
Q

alogirithim in suspected primary aldosteronism?

A
123
Q
A

int med exam 0828 (24 decks)

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