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Endocrinology > Review Part 1 > Flashcards

Review Part 1 Flashcards

1
Q

What is needed for a diagnosis of DKA?

A

ketonemia and metabolic acidosis

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2
Q

What is the management for DKA?

A
  • insulin
  • fluid replacement (normal saline) add 5% glucose once BG reaches 250 mg/dL
  • replace potassium prophylactically with IV fluids
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3
Q

What is HHNS (hyperosmolar hyperglycemic nonketotic syndrome)?

A

a state of severe hyperglycemia, hyperosmolarity, and dehydration

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4
Q

Who is HHNS typically seen in?

A

elderly with type II diabetics

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5
Q

What are common findings with HHNS?

A

CNS and focal neurologic signs

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6
Q

What is the management for HHNS?

A
  • fluid replacement is most important

- low-dose insulin infusion

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7
Q

What are the autonomic complications of diabetes?

A
  • impotence in men

- gastroparesis - chronic nausea and vomiting, early satiety

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8
Q

What is the most common cause of end-stage renal disease?

A

diabetic nephropathy

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9
Q

What is pathognomonic for DM?

A

nodular glomerular sclerosis - hyaline deposition in one area of glomerulus

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10
Q

What increases the risk of progression of diabetic nephropathy to ESRD?

A

hypertension

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11
Q

What is the treatment used to decrease the rate of progression of nephropathy

A

ACE inhibitor or ARB

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12
Q

What is the leading cause of blindness in the US?

A

diabetic retinopathy

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13
Q

What does fundoscopic examination show of diabetic retinopathy?

A

hemorrhages, exudates, micro aneurysms, and venous dilation

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14
Q

What is the leading cause of visual loss in diabetic patients?

A

edema of the macula

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15
Q

Peripheral Neuropathy

A
  • AKA: distal symmetric neuropathy
  • “stocking/glove pattern”
  • begins in feet, later involves the hands
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16
Q

What symptoms are common in peripheral neuropathy?

A

numbness and paresthesia

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17
Q

Painful diabetic neuropathy

A
  • hypersensitivity to light touch

- severe “burning” pain (especially at night)

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18
Q

Treatment for diabetic neuropathy

A

pregablin, gabapentin, duloxetine, TCAs

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19
Q

What Cranial Nerve is most often effected by diabetes?

A 
CN III (oculomotor)
-diabetic third nerve palsy
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20
Q

What macrovascular complications is the most common cause of death in diabetic patients?

A

coronary artery disease

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21
Q

What is the treatment of diabetic polyneuropathy?

A
  • complex management
  • pharmacologic agents: NSAIDs, pregablin, gabapentin, duloxetine, TCAs
  • gastroparesis: promotility agent, such as metoclopramide, exercise, and low-fat diet
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22
Q

What are the renal complications of diabetes?

A

diabetic nephropathy

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23
Q

What is the prophylactic management of renal compilations of diabetes?

A

Control BP aggressively

-prescribe an ACE inhibitor or ARB if urine test is positive for microalbuminuria

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24
Q

What are the manifestations of diabetes?

A
  • polyuria (peeing a lot)
  • polydipsia (constantly thirsty)
  • polyphagia (constantly feeling the need to eat)
  • fatigue
  • weight loss
  • blurred vision
  • fungal infections
  • numbness, tingling of hands and feet
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25
Q

What is normal Hemoglobin A1c value?

A

<5.6%

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26
Q

What is impaired fasting glucose Hemoglobin A1c value?

A

5.7% - 6.4%

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27
Q

What is diabetes Hemoglobin A1c value?

A

> 6.5%

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28
Q

What is the somogyi effect?

A

glucose is low at 3 am glucose check

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29
Q

What is the treatment for somogyi effect?

A

evening insulin should be decreased

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30
Q

What is dawn phenomenon?

A

glucose is elevated at 3 am glucose check

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31
Q

What is the management of dawn phenomenon?

A

evening insulin should be increased to provide additional coverage in the overnight hours

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32
Q

What are the risk factors for diabetes?

A
  • obesity (greatest risk factor)
  • genetics
  • age
  • physical inactivity
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33
Q

How do you diagnosis diabetes?

A

perform any of the following tests on two separate days

  • sxs of diabetes + a random glucose concentration of >200 mg/dL (not fasting)
  • a fasting BG of >126 mg/dL
  • a BG of >200 mg/dL 2 hours after a 75 g glucose load during an oral glucose tolerance test
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34
Q

What is the contraindications for metformin?

A

renal failure

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35
Q

What are the clinical manifestations of insulinoma?

A

sympathetic activation
-diaphoresis, palpitations, tremors, high blood pressure, anxiety
neuroglycopenic symptoms
-headache, visual disturbances, confusion, seizures, coma

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36
Q

What is the diagnosis for insulinoma?

A

-72 Hour Fast

Whipple Triad

  • hypoglycemic symptoms brought on by fasting
  • blood glucose <50 mg/dL during symptomatic attack
  • glucose administration brings relief of symptoms
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37
Q

What is the mechanism of action of HMG CoA reductase inhibitors (statins)?

A
  • rate-limiting step in cholesterol synthesis

- deplete intracellular supply of cholesterol

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38
Q

What are the indications for high-intensity statin therapy?

A
  • Clinical ASCVD + age <75
    (and candidate for high-intensity statin)
  • LDL >190 mg/dL
  • Age 40 - 75 w/ type 1 or 2 DM + estimated 10 year ASCVD risk >7.5%
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39
Q

What is the medication effectiveness for high-intensity statin therapy?

A

daily doses lowers LDL-C by about 50% on average

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40
Q

What is the indication for moderate-intensity statin therapy?

A
  • Established ASCVD risk >7.5%

- Age 40-75 w/type 1 or 2 DM + no estimated 10 year ACVD risk >7.5%

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41
Q

What is the medication effectiveness for moderate-intensity statin therapy?

A

daily doses lowers LDL-C by 30-50% on average

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42
Q

What are the indications for low-intensity statin therapy?

A

for patients who cannot tolerate a high or moderate dose statin

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43
Q

What is the medication effectiveness of low-intensity statin therapy?

A

daily doses lowers LDL-C by less than 30% on average

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44
Q

What are the contraindications of statin therapy?

A

pregnancy category X

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45
Q

What are the side effects of statins?

A
  • elevated liver function tests

- myopathy and rhabdomyolysis

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46
Q

What is the most effective agent for increasing HDL-C?

A

nicotinic acid (niacin)

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47
Q

What is the MOA of nicotinic acid?

A

strongly inhibits lipolysis in adipose tissues, thereby reducing the free fatty acid production

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48
Q

What are the side effects of nicotinic acid?

A
  • intense cutaneous flushing (with uncomfortable sensation of warmth) and pruritus
  • hepatotoxicity
49
Q

What is the mechanism of action of fibric acid derivatives?

A
  • lowers serum triglycerides and increases HDL-C

- fenofibrate >gemfibrizol in lowering triglyceride levels

50
Q

What are the indications of fibric acid derivatives?

A

treatment of hypertriglyceridemia

51
Q

What are the side effects of fibric acid derivatives?

A
  • gallstone formation due to increased biliary cholesterol excretion
  • contraindicated gemfibrizol + simvastatin
52
Q

What is the mechanism of action for bile acid-binding resins?

A
  • lowers bile acid concentration

- keeps you from absorbing fats

53
Q

What are the indications for bile acid-binding resins?

A
  • cholestyramine can relieve pruritus related to bile acid accumulation in patients with biliary stasis
  • colesevelam is also indicated for DMII due to glucose-lowering effects
54
Q

What is the drug name in the Cholesterol Absorption Inhibitor class and ASEs?

A
  • ezetimibe

- adverse effects are uncommon

55
Q

What is the MOA of Omega-3 Fatty Acids and what is the indication?

A
  • MOA: inhibits VLDL and triglyceride synthesis in the liver

- Lower triglyceride levels

56
Q

What is the management for hypertriglyceridemia?

A
  • primary therapy: diet and exercise
  • secondary therapy: nicotinic acid and fibric acid derivatives are most effective
  • omega-3 fatty acids in adequate doses may be beneficial
57
Q

What are the laboratory testing done to look for complications from antihyperlipidemic agents?

A
  • AST
  • ALT
  • CK levels
  • eGFR
  • INR
58
Q

What are the physical exam findings related to hyperlipidemia?

A
  • most patients are asymptomatic
  • Xanthelasma: yellow plaques on eyelids
  • Xanthoma: hard, yellowish masses found on tendons
59
Q

What is the goal number for cholesterol?

A

< 200 mg/dL

60
Q

What is high risk number for cholesterol?

A

> 240 mg/dL

61
Q

What is goal number for HDL?

A

> 45 mg/dL (males)

> 55 mg/dL (females)

62
Q

What is a negative risk factor number for HDL?

A

> 60 mg/dL

63
Q

What is high risk number for HDL?

A

< 40 mg/dL

64
Q

What is goal number for LDL?

A

< 100 mg/dL

65
Q

What is normal LDL for diabetics?

A

< 70 mg/dL

66
Q

What is normal for triglycerides?

A

< 150 mg/dL

67
Q

What are the causes of elevated LDL?

A
  • hypertriglycerides
  • low HDL levels
  • obesity
  • DM II
  • metabolic syndrome
  • infection or inflammatory states
68
Q

What is the cause of elevated VLDL?

A

hypertriglycerides

69
Q

What are the causes of elevated HDL?

A
  • exercise

- moderate consumption of alcohol

70
Q

What are the causes of elevated triglycerides?

A
  • DM
  • obesity
  • alcohol intake
  • high fat meals lead to formation of large Chylomicrons particles due to the increased amount of triglyceride being transported
71
Q

What medication has the best effect on elevated LDL?

A

statins

72
Q

What are the potential complications of Statins?

A
  • elevates liver function
  • pregnancy category X
  • myopathy and rhabdomyolysis
  • increase effects of warfarin
73
Q

What medication has the best effect on increasing HDL?

A

niacin

74
Q

What are the potential complications of niacin?

A
  • intense cutaneous flushing and pruritus

- hepatotoxicity

75
Q

What is the best treatment for isolate hypertriglyceridemia?

A

fibric acid derivatives (fenofibrate and gemfibrizol)

76
Q

What are the potential complications of fibric acid derivatives?

A
  • gallstone formation due to increased biliary cholesterol excretion
  • gemfibrizol + simvastatin is contraindicated
77
Q

What antihyperlipidemic drug is excreted by the kidneys?

A

nicotinic acid (niacin)

78
Q

What antihyperlipidemic drug is excreted by the liver?

A

statins

79
Q

What antihyperlipidemic drug is excreted by the feces?

A

bile acid-binding resins

80
Q

What antihyperlipidemic is contraindicated for pregnancy?

A

HMG CoA Reductase inhibitors (statins)

81
Q

Why are statins contraindicated during pregnancy?

A

cholesterol is an essential component of fetal development, including steroid synthesis and membrane development

82
Q

What are high potency statins?

A
  • rosuvastatin

- atorvastatin

83
Q

What are low potency statins?

A
  • lovastatin
  • fluvastatin
  • pitavastatin
84
Q

What is the MCC of Cushing’s disease?

A

Pituitary adenoma

  • producing large amounts of ACTH, which elevate cortisol.
  • use MRI to visualize
85
Q

What are pheochromocytomas? and what is the presentation of pheochromocytoma?

A
  • Catecholamine producing tumors, Arise sporadically or inherited.
  • palpitations
  • headaches
  • episodic sweating (diaphoresis)
86
Q

What are the Rule of 10’s for pheochromocytoma?

A
  • 10% are bilateral
  • 10% are extra-adrenal
  • 10% are malignant
87
Q

What is the presentation of Cushing’s syndrome?

A
  • fatty deposits between shoulders: buffalo hump and supraclavicular fat deposits
  • rounded face: moon face
  • pink or purple stretch marks: striae
  • male pattern hair distribution (hirsutism)
  • hypertension
  • psych disturbances: depression, anxiety, euphoria, psychosis
88
Q

What is the presentation of Addison’s?

A
  • hyperpigmentation
  • insidious onset
  • mood/personality change
  • joint and muscle pain
  • hypoglycemia
  • fatigue
  • weight loss
  • vomiting, diarrhea
  • headache
  • sweating
89
Q

What is the presentation of hirsutism?

A

androgen-dependent terminal hair (sexual hair) following a male-pattern hair growth

  • face
  • chest
  • abdomen
  • back
90
Q

What are the hormones produced by adrenal medulla?

A

chromaffin cells of the medulla secrete both norepinephrine and epinephrin, but norepinephrine is usually the predominant amine

91
Q

What are the hormones produced by adrenal cortex?

A
  • mineralocorticoids: aldosterone
  • glucocorticoids: cortisol
  • adrenal androgen precursors: 5 androgens
92
Q

What are the effects of androgens?

A

DHEA are converted in the gonads and peripheral target cells to sex steroids acting via androgen and estrogen receptors

93
Q

What are the effects of mineralocorticoids and glucocorticoids?

A

regulate aspects of physiological stress, blood pressure, and electrolyte homeostasis

94
Q

What labs are used to diagnosis pheochromocytoma?

A

Biochemical testing
-plasma and urine catecholamines and metanephrines: elevated

Imaging

  • CT and MRI
  • radioactive tracers can localize tumors
95
Q

What labs are used to diagnose adrenal insufficiency?

A

ACTH (cosyntropin) stimulation test

  • baseline ACTH and cortisol levels are drawn
  • injection of cosyntropin, repeat cortisol levels at 30 and 60 minutes
  • <18 = confirms insufficiency

Hyponatremia

96
Q

What labs are used to diagnose Cushing’s disease?

A
  • late night salivary cortisol
  • 24 hour urinary free cortisol excretion
  • dexamethasone suppression test
97
Q

Parathyroid hormone and how it interacts with vitamin D

A
  • PTH acts directly on kidneys where it synthesizes 1,25-dihydroxyvitamin D hormone
  • serum PTH levels are tightly regulated by a negative feedback loop where vitamin D is acting through its nuclear receptor to reduce PTH release and synthesis
  • low vitamin D = high PTH
  • high vitamin D = low PTH
98
Q

What is the clinical presentation of hyperparathyroidism?

A
  • stones: renal - loss of calcium and phosphate
  • bones: pain - diffuse bone demineralization, trabecular bone increase
  • groans: increased GI absorption and abdominal cramps
  • moans: irritability and depression
99
Q

What is the presentation of pseudohypoparathyroidism?

A
  • short stature
  • rounded face
  • shortened 4th and 5th MCP
  • obesity
  • dental hypoplasia
  • soft-tissue calcifications or ossifications
  • developmentally delayed
100
Q

What is the presentation of hypoparathyroidism?

A
  • hypocalcemia (Chvostek’s and Trousseau sign)
  • muscle cramping
  • paraesthesia in extremities
  • hyperactive DTR’s
  • confusion
  • seizures
101
Q

How is Hirsutism graded?

A

Grade 0-4 (0 = no hirsutism, 4 = severe)

  • > 9 in Mediterranean, Hispanic, and middle eastern
  • > 8 in black and white
  • > 6 South American
  • > 2 in Asians
  • 8-15 = mild
  • 15-25 = moderate
  • > 25 = severe
102
Q

What is Primary hyperaldosteronism?

A

Excess aldosterone secretion which is independent of renin-angiotensin system (Conn’s Syndrome)

103
Q

What are the causes of primary hyperaldosteronism?

A
  • Aldosterone secreting adenoma (conns)
  • Bilateral hyperplasia of the cortex
  • Rarely carcinoma
104
Q

What is the complete workup for cushing’s?

A
  • Determine if ACTH dependent or independent
  • ACTH level <20 suggests adrenal tumor, hyperplasia or carcinoma
  • Dexamethasone suppression test: Serial measurements of 2 or 3, 24hr urinary free cortisol
  • MRI: if pituitary tumor suspected (Cushing’s Dz)
  • CT: if Adrenocortical or other tumor suspected (Cushing’s Syndrome)
  • Endocrine referral
105
Q

What is the high dose and low dose dexamethasone suppression test observing?

A

High dose: assess between ectopic ACTH and Cushing’s disease:

  • Ectopic ACTH tumor: Suppression absent
  • Cushing’s disease: suppression (of ACTH and cortisol) present

Low dose: R/o pseudo-crushing’s syndrome:

  • Healthy pt: Suppression present
  • Cushing syndrome: Suppression absent
106
Q

Where is hyperpigmentation usually found in a pt with Addisons?

A
  • Palmar creases
  • Buccal mucosa
  • Vermilion border of the lips
  • Around scars
  • Nipples
107
Q

What are the lab results for a pt w/ Addisons?

A
  • Low serum cortisol levels at 8 a.m. < 3 mcg/dL
  • Hyponatremia
  • Hyperkalemia
  • Elevated plasma renin level
  • Increase in ACTH
108
Q

What is the tx for Addisons?

A

Hydrocortisone, Fludrocortisone, DHEA(for women)

109
Q

What are the sxs of Addisonian Crisis?

A

Adrenal insufficiency presenting as

  • Shock
  • HypoTN
  • Weakness
  • Abdominal pain
  • N/V
  • Confusion
  • Volume depletion
110
Q

Addisonian Crisis may occur in pts with?

A

Primary adrenal insufficiency who have been subjected to:

  • Serious infxn or other major stress
  • Bilateral adrenal infarction/hemorrhage
  • Abrupt w/d from glucocorticoid therapy
111
Q

What is the tx of Addisonian Crisis?

A

1mg ACTH stimulation test: plasma cortisol level is drawn at baseline and 30 minutes
- <25 and <9 elevation over baseline = inadequate adrenal response

DO NOT delay therapy while waiting for response

112
Q

What is the difference between a macroadenoma and a microadenoma in a pt presenting with a pituitary adenoma?

A
  • Macroadenoma: greater than 1 cm

- Microadenomas: less than 1 cm

113
Q

What is the MC secretory pituitary adenoma?

A

Prolactinomas

114
Q

What are the sxs of a Prolactinoma?

A
  • Irregular menstrual periods
  • HA
  • Fatigue
  • Breast discharge
  • Vision loss: Bitemporal hemianopsia (optic chiasms)
115
Q

What is the management of a Prolactinoma?

A
  • Get MRI and full endocrine testing and therapy
  • Tx: Dopaminergic drug: Bromocriptine and Cabergoline.
  • Surgical: TSS
116
Q

What is a common DDx of Pheochromocytoma?

A

Panic Attacks

117
Q

What are the S/Sxs and lab results of primary hyperaldosteronism?

A

S/Sxs: HTN and Hypokalemia

Labs: increased aldosterone and low renin

118
Q

What are the side effects of bile-acid binding resins?

A

GI-related: constipation, nausea, flatulence

Endocrinology (18 decks)

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