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Endocrine > EXAM #2: REVIEW > Flashcards

EXAM #2: REVIEW Flashcards

1
Q

What is the mnemonic to remember the parents vessels of the suprarenal arteries?

A

IPAR

Inferior phrenic= superior suprarenal a.
Aortic= middle suprarenal a.
Renal= inferior suprarenal a.

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2
Q

What is the expected gross finding in the setting of ACTH excess i.e. Cushing’s? Be specific.

A

Hypertrophy of the adrenal cortex limited to the Fasiculata and Reticularis

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3
Q

What is the order in which the catecholamines are synthesized?

A 
Tyrosine 
DOPA 
Dopamine 
NE 
Epi
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4
Q

What capillaries receive the hormones from the adrenal cortex?

A

Sinusoidal capillaries

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5
Q

What is the origin of the cortical and medullary arteries?

A

Supracapsular arterial plexus

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6
Q

Draw the synthesis pathway of the cortical steroids.

A

N/A

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7
Q

What are the physiologic actions of cortisol? What is the mnemonic to remember these actions?

A

Mnemonic= BIG FIB

B= Blood pressure increase 
I= Insulin resistance 
G= Gluconeogenesis, lipolysis, proteolysis 
F= Fibroblast activity increased 
I= Immunosuppression 
B= Bone resorption
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8
Q

How does ACTH increase adrenal steroid synthesis?

A

Activation of the Melanocortin-2 Receptor

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9
Q

What is the function of 11β-HSD type II?

A

Inactivation of cortisol to corticosterone in mineralcorticoid rich tissues

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10
Q

What is the function of 11β-HSD type I?

A

Activation of corticosterone to cortisol in glucocorticoid rich tissue

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11
Q

How does cortisol increase blood glucose?

A

1) Increases gluconeogenesis

2) Decreases glucose utilization by cells

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12
Q

Where do adrenal carcinomas commonly metastasize?

A

1) Lungs

2) Lymph nodes

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13
Q

What are the two primary cortical neoplasms?

A

1) Cortical adenoma

2) Cortical carcinoma

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14
Q

How are cortical adenomas typically described grossly?

A

Well circumscribed, yellow-orange lesions

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15
Q

How are cortical adenomas typically described histologically?

A

Vacuolated with mild nuclear pleomorphism

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16
Q

What is the underlying pathology of Addison’s Disease?

A

Chronic autoimmune destruction of the adrenal cortex

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17
Q

How will secondary adrenal insufficiency appear grossly?

A

Atrophy of the adrenal gland, with sparing of the Glomerulosa and Adrenal Medulla

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18
Q

What morphological features differentiate a cortical adenoma from a cortical carcinoma?

A

1) Metastasis
2) Large size
3) Necrosis
4) Mitotic figures
5) Vascular invasion

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19
Q

What are three clinical manifestations of a Neuroblastoma?

A

1) Abdominal mass
2) Diastolic hypertension
3) Blue-berry muffin baby

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20
Q

Describe the gross appearance of adrenal hyperplasia.

A

Yellow, thickened, and multinodular

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21
Q

What are the 10% rules of pheochromocytomas?

A

10% of pheochromocytomas are:

1) Bilateral
2) Familial
3) Malignant
4) Afunctional
5) Extraadrenal

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22
Q

Describe the gross appearance of a cortical carcinoma.

A
  • Yellow on cut surface

- Large with areas of hemorrhage, cystic change, and necrosis

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23
Q

Describe the gross appearance of a pheochromocytoma.

A
  • Pale gray-brown
  • Associated with hemorrhage, necrosis, cystic change
  • Highly vascular
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24
Q

Describe the morphology of the adrenal gland in Addison’s Disease.

A

1) Small glands
2) Lipid depletion of the adrenal cortex
3) Variable lymphocytic infiltrate in the adrenal cortex

*Note that the adrenal medulla is SPARED

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25
Q

List six features of an adrenal tumor that are concerning for malignancy.

A

1) Irregular
2) Large (greater than 4cm)
3) Calcification
4) Unilateral
5) High CT attenuation (greater than 20 HU)
6) Extension into local structures

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26
Q

How is Conn Syndrome diagnosed?

A

1) Urine aldosterone

2) Saline suppression test

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27
Q

How is adrenal cancer treated?

A

Surgery if possible; otherwise, palliative measures

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28
Q

What do you need to remember about the clinical presentation of adrenal cancer?

A

B/c of local invasion, can have a mix of adrenal syndromes at presentation

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29
Q

If CT is equivocal in a patient with likely pheochromocytoma, what is the next best step?

A

Fluoroscope guided renal vein sampling

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30
Q

If you suspect an adrenal cancer in a patient, what labs should you check?

A

1) Cortisol
2) Catecholamines
3) Androgens

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31
Q

What is the algorithm for diagnosing Cushing Syndrome?

A

1) Cortisol levels
2) Follow-up high cortisol with ACTH
3) Dexamethasone suppression
4) Imaging

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32
Q

Specifically, how is IPA treated?

A

Medically with aldosterone antagonist (spironolactone)

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33
Q

What is the expected response to a Cortrosyn stimulation test?

A

Cortisol greater than 18 mcg/dL

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34
Q

When treating primary adrenal insufficiency, what end points do you want to monitor?

A

1) Weight
2) Blood pressure
3) Electrolytes
4) Sense of well-being

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35
Q

What four stimuli will cause the secretion of CRH, leading to increased cortisol?

A

1) Stress
2) Hypoglycemia
3) Cold temperatures
4) Pain

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36
Q

What are the diagnostic criteria for primary adrenal insufficiency?

A

1) Random cortisol less than 5mcg/dL or am less than 3 mcg/dL
2) Simultaneously elevated ACTH
3) Positive Cortrosyn stimulation test

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37
Q

How is an adrenal crisis treated? What is the mnemonic?

A

5 S’s

1) Saline
2) Sugar
3) Steroids
4) Support
5) Search for cause

38
Q

What are the two major etiologies of secondary adrenal insufficiency?

A

Transient= iatrogenic–abrupt glucocorticoid cessation

Permanent= panhypopituitarism

39
Q

What are the expected hormone findings in primary adrenal insufficiency?

A

1) Decreased cortisol with elevated ACTH
2) Decreased aldosterone with increased renin
3) Decreased DHEA

40
Q

How is secondary adrenal insufficiency treated?

A

Cortisol replacement without aldosterone

41
Q

What is the most common cause of ACTH-independent Cushing’s (non-iatrogenic)?

A

Adrenal adenoma producing cortisol

42
Q

How do the clinical manifestations of Cushing’s from ectopic ACTH differ from a pituitary adenoma or iatrogenic Cushings?

A

1) Rapid onset
2) Hyperpigmentation
3) Hirsutism

43
Q

List three drugs that reduce cortisol levels for symptomatic relief of Cushing’s Disease.

A

1) Aminoglutethimide
2) Ketoconazole
3) Mitotane

44
Q

How is ectopic ACTH treated?

A

1) Surgical resection
2) Chemo/radiation
3) Bilateral adrenalectomy
4) Medications

45
Q

What are the expected lab and hormone findings in a child with Congenital Adrenal Hyperplasia due to 21 hydroxylase deficiency?

A

1) High 17-OH progesterone
2) High ACTH
3) High Renin

46
Q

When will a child typically present with Addison’s Disease?

A

Between 10 and 14 years old

47
Q

How is Congenital Adrenal Hyperplasia treated?

A

1) Hydrocortisone
2) Fludricortisone
3) Surgical correction of genitalia

48
Q

What are the classic electrolyte and glucose findings in Congenital Adrenal Hyperplasia?

A

1) Hyponatremia
2) Hyperkalemia
3) Hypoglycemia

49
Q

What does APS stand for?

A

Autoimmune Polyglandular Syndrome

50
Q

What is APS1?

A

Adrenal insufficiency +

  • Hypoparathyroidism
  • Mucocutaneous candidiasis
51
Q

What is APS2?

A

Adrenal insufficiency +

  • Thyroiditis
  • DM-I
52
Q

What are the four principles of basic carb counting?

A

1) Become aware of foods containing carbs
2) Understand portion sizes
3) Avoid sweeteners
4) Maintain carbohydrate consistency

53
Q

What are the goals of Medical Nutrition Therapy (MNT) in treating DM?

A

1) Healthy eating
2) Individualized goals i.e.
- Glycemic
- Blood pressure
- Lipids
3) Achieve/ maintenance of body weight goals
4) Delay/prevent DM complications

54
Q

What fats have been shown to be healthy for DM patients?

A

1) Monosaturated

2) Long-chain omega 3 fatty acids

55
Q

What blood glucose levels “sinch” the diagnosis of DM in kids?

A
  • Random greater than 300 mg/dL

- Fasting greater than 200 mg/dL

56
Q

A pediatric patient has an exquisitely tender thyroid and a toxic appearance, what is the most likely diagnosis?

A

Acute suppurative thyroiditis

57
Q

What are the clinical manifestations of PKU in a child?

A

1) Choking spells
2) Difficulty feeding
3) Vomiting
4) Abnormal neuro develop e.g. autism-like

58
Q

What should you do to work up a suspected metabolic disorder?

A

1) Electrolytes, glucose and ammonia levels
2) Blood, urine, and CSF cultures
3) Head CT/MRI

59
Q

What causes Galactosemia?

A

Galactose 1-phosphate uridylultransferase deficiency

60
Q

List the clinical manifestations of Galactosemia.

A

1) Vomiting
2) Diarrhea
3) Hepatospleomegaly
4) Jaundice
5) Anemia

61
Q

How is Galactosemia diagnosed?

A

1) Red cell enzyme tests

2) Urine with reducing substrate

62
Q

What product accumulates in Galactosemia?

A

Galactose 1-phosphate

63
Q

What does MCAD stand for?

A

Medium chain acyl-CoA dehydrogenase deficiency

64
Q

When should you suspect a metabolic disorder in a child?

A

1) Any neonate with unexplained, overwhelming, or progressive disease after a normal pregnancy
2) Any kid with acute deterioration after routine illness
3) Any kid with acidosis or hypoglycemia

65
Q

What chromosome are the HLA antigens located on that lead to DM-I susceptibility? What does this region code for?

A

Chromosome 6; MHC II on macrophages

66
Q

What are the two classes of drugs that can induce DM?

A

1) Glucocorticoids

2) Atypical antipsychotics

67
Q

How is DM diagnosed?

A

1) Oral glucose tolerance test
2) Classical presentation of DKA
3) Antibodies
4) C-peptide

68
Q

In DM I-a, what antibody is positive in most patients?

A

GAD65, glutamic acid decarboxylase

69
Q

What are the four treatment goals in DM-I?

A

1) Normoglycemia
2) Normal HbA1c
3) Normal growth in children
4) Treatment of cardiac risk factors

70
Q

What is the MOA of pramlitide?

A

Amylin mimic that:

1) Slows GI transit
2) Decreases glucagon
3) Decrease appetite

71
Q

List six signs of PVD in the DM patient.

A

1) Claudication
2) Rest pain
3) Atrophic shiny skin
4) Diminished hair growth
5) Dependent rubor
6) Pallor on elevation

72
Q

What is Charcot Arthropathy?

A

Described as a “neurogenic arthropathy,” it is the progressive degeneration of a weight bearing joint with marked boney destruction/deformity

73
Q

How do you treat/manage Charcot Arthropathy?

A

1) Non-weight bearing
2) Cast/immobilization
3) Obtain serial x-rays
4) Address blood glucose and HbA1c

74
Q

What is the most common location for Charcot Arthropathy?

A

Midfoot

75
Q

What two types of bone scans can differentiate between Charcot Arthropathy and Osteomyelitis?

A

1) Indium
2) Ceretec

*BOTH will be positive in Charcot Arthropathy

76
Q

What do AGEs, DAG, and oxidative stress activate to induce the injurious pattern seen in DM?

A

PKC beta

77
Q

What steps can be taken to prevent DM retinopathy?

A

1) Dilated eye exam 5 years s/p T1DM dx and at time of T2DM dx
2) Glycemic control
3) Blood pressure control

78
Q

Outline the natural history of DM nephropathy.

A

1) Glomerular HYPERperfusion, hypertrophy and INCREASED GFR
2) Thickening of the BM and normalization of the GFR
3) Microalbuminuria
4) Nephropathy
5) End Stage Renal Disease

79
Q

When a DM patient’s GFR is between 45-60, what steps should you take in their treatment?

A

1) Refer to nephrology
2) Consider medication dose adjustments
3) GFR every 6 months
4) Monitor electrolytes
5) Check Vitamin D and bone density

80
Q

When a DM patient’s GFR is between 30-45, what steps should you take in their treatment?

A

1) Consider medication dose adjustments
2) Check GFR every 3 months
3) Monitor electrolytes

81
Q

How do you treat CKD in DM patients?

A

1) ACE-inhibitors
2) ARBs
3) Modest protein restriction

82
Q

What drugs can be used to treat DM nerve pain?

A

1) TCAs
2) Anticonvulsants
3) Duloxetine
4) Capsaicin

83
Q

What is the general purpose of the PreOp eval in an emergent patient? What things should be done? What is your goal

A

Generally, you’re trying to establish a baseline and the goal is to optimize the things that you can prior to surgical intervention. At a minimum you should get:

1) EKG
2) Blood work

84
Q

List four reasons why wound infections are rampant in DM patients.

A

1) Reduced capillary perfusion
2) Reduced oxygen and nutrient delivery
3) Impaired circulation of antimicrobials
4) Hyperglycemia “feeds” bacteria

85
Q

In post-op DM patients, what cardiovascular complication do you need to have a high index of suspicion for?

A

Silent MI

86
Q

What two classes of medications can have an adverse effect on DM patients in the hospital?

A

1) Glucocorticoids

2) TPN

87
Q

What effect does insulin have on K+ and phosphate?

A

Insulin increases the UPTAKE of K+ and phosphate INTO the cells

88
Q

What are the three most common causes of hypoglycemia in non-DM patients?

A

1) Alcohol
2) Critical illness
3) Hormone deficiency

89
Q

What critical illnesses can precipitate hypoglycemia?

A

1) Hepatic failure
2) Renal failure
3) Cardiac failure
4) Sepsis

90
Q

What are the causes of post-parandial hypoglycemia?

A

1) Gastric resection
2) Islet cell tumor
3) Glycogen Storage Disease
4) Hereditary Fructose Intolerance
5) Galactosemia

91
Q

What are the three unique features of MODY compared to other forms of DM?

A

1) No insulin resistance
2) No GAD65 antibodies
3) No loss of beta cell numbers

Endocrine (34 decks)

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