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Endocrine Exam > Adult Endocrinology > Flashcards

Adult Endocrinology Flashcards

1
Q

What is basal insulin?

A
  • The long acting insulin to achieve more steady state of glucose control (to mimic baseline insulin levels in non-diabetics)
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2
Q

What is bolus insulin?

A
  • Can be adjusted at mealtime and based on FSG (sliding scale) +/- carbohydrate count anticipated
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3
Q

What are some signs and symptoms of DM?

A
  • Polyuria
  • Polydipsia
  • Nocturia
  • Blurred vision
  • Weight loss (unintentional)
  • Frequent recurrent infections even with appropriate treatment and documented clearance
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4
Q

What are the guidelines for diagnosis of DM?

A
  • Fasting plasma glucose values ≥126 mg/dL
  • Two hour plasma glucose values of ≥200 mg/dL during a 75g OGTT
  • HbA1C values ≥6.5 percent
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5
Q

What are some ways to get an average 3 months glucose?

A
  • Hemoglobin A1C
  • HbA1C
  • GHbA1C
  • Glycosylated hemoglobin
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6
Q

How is an A1C retrieved?

A
  • Typically venipuncture sample, but fingerstick machines available
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7
Q

What is the acronym for the differential diagnosis for mental status changes?

A
  • AEIOUTIPS
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8
Q

What does AEIOUTIPS stand for?

A
  • Alcohol
  • Epilepsy with seizure activity
  • Infection
  • Overdose
  • Uremia
  • Trauma
  • Insulin (high or low blood sugar)
  • Poisoning/psychosis
  • Stroke
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9
Q

What is the acronym for the differential diagnosis for abdominal pain?

A
  • BAD GUT PAINS
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10
Q

What does BAD GUT stand for?

A
  • Bowel obstruction
  • Appendicitis, adenitis
  • Diverticulitis, Diabetic ketoacidosis, dysentery
  • Gastroenteritis
  • UTO/UTI
  • ## Testicular torsion/toxins
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11
Q

What does PAINS stand for?

A
  • Pneumonia/pleurisy/pancreatitis/ perforated bowel/peptic ulcer/porphyria
  • Abdominal aneurysm
  • Infarcted bowel, infarcted myocardium, incarcerated hernia, IBD
  • Splenic rupture/infarction
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12
Q

What are some acute complications seen in DM?

A
  • DKA
  • Non-ketotic hyperosmolar state (NKHS) –> AKA: Hyperosmolar non-ketotic coma (HNKC) or hyperglycemic hyperosmolar state (HHS)
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13
Q

Who is DKA more likely seen in?

A
  • Type 1 diabetics but could occur in type 2
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14
Q

Who is NKHS more likely seen in?

A
  • Type 2 diabetics
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15
Q

What are some etiologies of DKA?

A
  • Inadequate insulin administration
  • Infection (pneumonia, UTI, gastroenteritis, sepsis)
  • Infarction in any location (coronary, cerebral, mesenteric, peripheral)
  • Surgery
  • Drugs (cocaine)
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16
Q

What are some initial symptoms of DKA?

A
  • Anorexia
  • Nausea
  • Vomiting
  • Polyuria
  • Thirst
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17
Q

What are some progression of symptoms of DKA?

A
  • Abdominal pain
  • Altered mental function
  • Coma
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18
Q

What are some signs of DKA?

A
  • Kussmaul respirations
  • Acetone (fruity) breath odor
  • Dry mucous membranes
  • Poor skin turgor
  • Tachycardia
  • Hypotension
  • Fever
  • Abdominal tenderness
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19
Q

What does MUDPILES stand for?

A
  • Methanol
  • Uremia
  • Diabetic ketoacidosis
  • Paraldehyde
  • Isopropyl alcohol, iron, INH
  • Lactic acidosis
  • Ethylene glycol
  • Salicylates
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20
Q

What is MUDPILES an acronym for?

A
  • High anion gap acidosis
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21
Q

What is the treatment of DKA?

A
  • ICU
  • Frequent monitoring of general status, vital signs, glucose and other labs
  • Acid base status
  • Renal function
  • Potassium and other electrolytes
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22
Q

What is the 1-2-3 rule?

A
  • 2-3 liters normal saline over first 1-3 hours
  • Then 1/2 strength saline at 150 ml/hr
  • When glucose reaches 250 mg/dl, switch to D51/2 NS at 100-200 ml/hr
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23
Q

What is the fluid deficit in DKA?

A
  • Often 3-5 liters
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24
Q

What is the initial insulin administration in DKA?

A
  • 10-20 units IV or IM
  • Then, 5-10 units/hr continuous IV
  • Increase if no response in 1-2 hours - orders can be written with guideline to titrate
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25
Q

What initial monitoring is done in DKA?

A
  • Bloodwork: BSG at least hourly and electrolytes q2-4 hours

- Clinical status at least hourly: VS, Mental status, Fluid I&O

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26
Q

When should you consider potassium replacement in DKA?

A
  • When serum K is <5.5 mEq/L
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27
Q

What do you need to keep in mind when supplementing potassium?

A
  • Renal function
  • Baseline EKG and continuous cardiac monitoring for changes
  • Verify urinary output and measure hourly – likely will need indwelling foley catheter initialy
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28
Q

What are the treatment goals for DKA?

A
  • Increase the rate of glucose utilization in insulin dependent tissues (glucose goal is 150-250)
  • Reverse ketonemia and acidosis
  • Correct depletion of water and electrolytes
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29
Q

When is intermediate or long acting insulin started?

A
  • When patient is able to eat as shown by mental status improved, no N/V, or no abdominal pain
  • Anion gap normalized
  • Allow overlap timing of IV with SQ insulin
30
Q

What are some etiologies of NKHS?

A
  • Insulin deficiency
  • Inadequate fluid intake
  • Osmotic diuresis induced by hyperglycemia
31
Q

What are some precipitating factors for NKHS?

A
  • Sepsis
  • Myocardial infarction
  • Glucocorticoids
  • Phenytoin
  • Thiazide diuretics
  • Impaired access to water
32
Q

What are some symptoms of NKHS?

A
  • Polyuria
  • Thirst
  • Altered mental status
33
Q

What is absent in NKHS that is typically seen in DKA?

A
  • N/V
  • Abdominal pain
  • Kussmaul respirations
  • Acidosis and ketonemia
34
Q

What is the fluid deficit in NKHS?

A
  • Often 8-10L
35
Q

What is the fluid replacement in NKHS?

A
  • 2-3 liters NS over first 1-3 hours

- When glucose reaches 250 mg/dl, switch to D51/2 NS at 100-200 ml/hr

36
Q

What is the treatment for NKHS?

A
  • Regular insulin at 5-10 units IV bolus or 3-7 units continuous infusion
  • Transition when eating as with DKA
  • Monitor, replace K, investigate, and address underlying causes as with DKA
37
Q

What are some differences between DKA and HHS?

A
  • Fluid deficit is much greater in NKHS

- Some drugs can contribute to NKHS

38
Q

What are some similarities between DKA and HHS?

A
  • Insulin deficiency – absolute or relative
  • Glucagon excess – absolute or relative
  • Volume depletion
  • Mental status change
  • Both are critical conditions that need invasive monitoring
39
Q

What is the major cause of mortality in T2DM?

A
  • Cardiovascular disease
40
Q

What is the average increase in glucose with each percentage of the A1C?

A
  • Starts at 5% = 80 mg/dl

- Each percentage is 30 mg/dl higher

41
Q

What is seen in diabetic gastropathy?

A
  • Pacemaker area of stomach is dysfunctional

- Since gastric emptying varies, the absorption also varies

42
Q

What can diabetic gastropathy?

A
  • Causes insulin requirements to also be extremely variable and unpredictable
43
Q

What is the screening for proteinuria?

A
  • Spot (random) urine sample

- Standard urine dipstick not sensitive if proteinuria <300 mg/24 hr

44
Q

What is the most common type of protein in diabetic nephropathy?

A
  • Albumin
45
Q

What is the earliest measurable sign of proteinuria?

A
  • Microalbumin/creatinine ratio
46
Q

What is microalbuminemia?

A
  • 30mg-300mg
47
Q

What is 24 hour urine collection used for?

A
  • More advanced/complex kidney disease
48
Q

What can be problematic in 24 hours urine collection?

A
  • Difficult to remember to save all urine
  • Dexterity required to get it into container
  • Leak in container
49
Q

What is done in the quarterly diabetes monitoring?

A
  • Hgb A1C
  • Review SGM log
  • Foot inspection for ulcerations
50
Q

What is done in the annual diabetes monitoring?

A
  • Dilated eye exam
  • Urine protein screening (microalbumin/creatinine ratio)
  • Monofilament testing
51
Q

What is the foot care for diabetes?

A
  • Daily inspection – often difficult for patient with dexterity and visual problems
  • Never go barefoot
  • Moisturize – but NOT in between or under toes
  • Prescription shoes
  • Podiatry
52
Q

What are some lifestyle modifications for diabetes treatments?

A
  • Physical activity
  • Dietary modification
  • Weight loss
  • Psychosocial
  • Initial and follow-up diabetic education
53
Q

What are some common complications of diabetes?

A
  • Retinopathy
  • Heart disease, widespread vascular disease (cigarette smoking is the single most additive risk for vascular disease)
  • Neuropathy: autonomic, peripheral
54
Q

What are some qualities of T1DM?

A
  • Insulin deficiency - absolute
  • Glucagon excess - absolute
  • Volume depletion
  • Mental status changes
  • Autoimmune
55
Q

What are some qualities of T2DM?

A
  • Insulin deficiency - relative
  • Glucagon excess - relative to body’s utilization/formation
  • Volume depletion
  • Mental status changes
  • Obesity/inactivity/lifestyle
56
Q

What are some signs and symptoms of hyperthyroidism?

A
  • Lid lag/exophthalmos
  • Bruits
  • Goiter vs. nodules
  • Heart rate and rhythm quality
  • Tremor
  • Warm, moist skin
  • Gynecomastia
  • Muscle weakness
57
Q

What are some additional findings to look for in hyperthyroidism?

A
  • Perspiration
  • Diarrhea
  • Polyuria
  • Weight loss
  • Fatigue and weakness
  • Oligomenorrhea
  • Hyperactivity
  • Heat intolerance, sweating
  • Palpitations
58
Q

What is the dysfunction in primary thyroid disorder?

A
  • Organ itself is the source of dysfunciton
59
Q

What is the dysfunction in secondary thyroid disorder?

A
  • Pituitary dysfunction
60
Q

What is the dysfunction in tertiary thyroid disorder?

A
  • Hypothalamic dysfunction
61
Q

What are the TSH and FT4 levels in primary hypothyroidsim?

A
  • TSH: increase

- FT4: decrease

62
Q

What are the TSH and FT4 levels in primary hyperthyroidism/

A
  • TSH: decrease

- FT4: increase

63
Q

What are the TSH and FT4 levels in TSH producing tumor?

A
  • TSH: increase

- FT4: increase

64
Q

What are the TSH and FT4 levels in central hypothyroidism?

A
  • TSH: decrease

- FT4: decrease

65
Q

What is euthyroid sick?

A
  • Critically ill patient

- Lab results don’t fit a pattern for primary, secondary, or tertiary dysfunction

66
Q

What may cause euthyroid sick?

A
  • May be due to protein shifts, protective effect of decreased metabolism or a maladaptive process – all of which are still being studied
67
Q

What is a concern with surgery of the thyroid?

A
  • Recurrent laryngeal nerve damage
68
Q

What are the different classification of causes of hypercalcemia?

A
  1. Parathyroid-related
  2. Malignancy-related
  3. Vitamin D related
  4. Associated with high bone turnover
  5. Associated with renal failure
69
Q

What is the treatment for hypercalcemia of malignancy with mental status changes &/or EKG changes?

A
  • Aggressive volume expansion with isotonic saline is the first measure
70
Q

What is done for bone density testing?

A
  • DEXA scan for osteoporosis and excessive bone turn-over

Endocrine Exam (11 decks)

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