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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
List six features of an adrenal tumor that are concerning for malignancy.
1) Irregular 2) Large (greater than 4cm) 3) Calcification 4) Unilateral 5) High CT attenuation (greater than 20 HU) 6) Extension into local structures
26
How is Conn Syndrome diagnosed?
1) Urine aldosterone | 2) Saline suppression test
27
How is adrenal cancer treated?
Surgery if possible; otherwise, palliative measures
28
What do you need to remember about the clinical presentation of adrenal cancer?
B/c of local invasion, can have a mix of adrenal syndromes at presentation
29
If CT is equivocal in a patient with likely pheochromocytoma, what is the next best step?
Fluoroscope guided renal vein sampling
30
If you suspect an adrenal cancer in a patient, what labs should you check?
1) Cortisol 2) Catecholamines 3) Androgens
31
What is the algorithm for diagnosing Cushing Syndrome?
1) Cortisol levels 2) Follow-up high cortisol with ACTH 3) Dexamethasone suppression 4) Imaging
32
Specifically, how is IPA treated?
Medically with aldosterone antagonist (spironolactone)
33
What is the expected response to a Cortrosyn stimulation test?
Cortisol greater than 18 mcg/dL
34
When treating primary adrenal insufficiency, what end points do you want to monitor?
1) Weight 2) Blood pressure 3) Electrolytes 4) Sense of well-being
35
What four stimuli will cause the secretion of CRH, leading to increased cortisol?
1) Stress 2) Hypoglycemia 3) Cold temperatures 4) Pain
36
What are the diagnostic criteria for primary adrenal insufficiency?
1) Random cortisol less than 5mcg/dL or am less than 3 mcg/dL 2) Simultaneously elevated ACTH 3) Positive Cortrosyn stimulation test
37
How is an adrenal crisis treated? What is the mnemonic?
5 S's 1) Saline 2) Sugar 3) Steroids 4) Support 5) Search for cause
38
What are the two major etiologies of secondary adrenal insufficiency?
Transient= iatrogenic--abrupt glucocorticoid cessation Permanent= panhypopituitarism
39
What are the expected hormone findings in primary adrenal insufficiency?
1) Decreased cortisol with elevated ACTH 2) Decreased aldosterone with increased renin 3) Decreased DHEA
40
How is secondary adrenal insufficiency treated?
Cortisol replacement without aldosterone
41
What is the most common cause of ACTH-independent Cushing's (non-iatrogenic)?
Adrenal adenoma producing cortisol
42
How do the clinical manifestations of Cushing's from ectopic ACTH differ from a pituitary adenoma or iatrogenic Cushings?
1) Rapid onset 2) Hyperpigmentation 3) Hirsutism
43
List three drugs that reduce cortisol levels for symptomatic relief of Cushing's Disease.
1) Aminoglutethimide 2) Ketoconazole 3) Mitotane
44
How is ectopic ACTH treated?
1) Surgical resection 2) Chemo/radiation 3) Bilateral adrenalectomy 4) Medications
45
What are the expected lab and hormone findings in a child with Congenital Adrenal Hyperplasia due to 21 hydroxylase deficiency?
1) High 17-OH progesterone 2) High ACTH 3) High Renin
46
When will a child typically present with Addison's Disease?
Between 10 and 14 years old
47
How is Congenital Adrenal Hyperplasia treated?
1) Hydrocortisone 2) Fludricortisone 3) Surgical correction of genitalia
48
What are the classic electrolyte and glucose findings in Congenital Adrenal Hyperplasia?
1) Hyponatremia 2) Hyperkalemia 3) Hypoglycemia
49
What does APS stand for?
Autoimmune Polyglandular Syndrome
50
What is APS1?
Adrenal insufficiency + - Hypoparathyroidism - Mucocutaneous candidiasis
51
What is APS2?
Adrenal insufficiency + - Thyroiditis - DM-I
52
What are the four principles of basic carb counting?
1) Become aware of foods containing carbs 2) Understand portion sizes 3) Avoid sweeteners 4) Maintain carbohydrate consistency
53
What are the goals of Medical Nutrition Therapy (MNT) in treating DM?
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
What fats have been shown to be healthy for DM patients?
1) Monosaturated | 2) Long-chain omega 3 fatty acids
55
What blood glucose levels "sinch" the diagnosis of DM in kids?
- Random greater than 300 mg/dL | - Fasting greater than 200 mg/dL
56
A pediatric patient has an exquisitely tender thyroid and a toxic appearance, what is the most likely diagnosis?
Acute suppurative thyroiditis
57
What are the clinical manifestations of PKU in a child?
1) Choking spells 2) Difficulty feeding 3) Vomiting 4) Abnormal neuro develop e.g. autism-like
58
What should you do to work up a suspected metabolic disorder?
1) Electrolytes, glucose and ammonia levels 2) Blood, urine, and CSF cultures 3) Head CT/MRI
59
What causes Galactosemia?
Galactose 1-phosphate uridylultransferase deficiency
60
List the clinical manifestations of Galactosemia.
1) Vomiting 2) Diarrhea 3) Hepatospleomegaly 4) Jaundice 5) Anemia
61
How is Galactosemia diagnosed?
1) Red cell enzyme tests | 2) Urine with reducing substrate
62
What product accumulates in Galactosemia?
Galactose 1-phosphate
63
What does MCAD stand for?
Medium chain acyl-CoA dehydrogenase deficiency
64
When should you suspect a metabolic disorder in a child?
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
What chromosome are the HLA antigens located on that lead to DM-I susceptibility? What does this region code for?
Chromosome 6; MHC II on macrophages
66
What are the two classes of drugs that can induce DM?
1) Glucocorticoids | 2) Atypical antipsychotics
67
How is DM diagnosed?
1) Oral glucose tolerance test 2) Classical presentation of DKA 3) Antibodies 4) C-peptide
68
In DM I-a, what antibody is positive in most patients?
GAD65, glutamic acid decarboxylase
69
What are the four treatment goals in DM-I?
1) Normoglycemia 2) Normal HbA1c 3) Normal growth in children 4) Treatment of cardiac risk factors
70
What is the MOA of pramlitide?
Amylin mimic that: 1) Slows GI transit 2) Decreases glucagon 3) Decrease appetite
71
List six signs of PVD in the DM patient.
1) Claudication 2) Rest pain 3) Atrophic shiny skin 4) Diminished hair growth 5) Dependent rubor 6) Pallor on elevation
72
What is Charcot Arthropathy?
Described as a "neurogenic arthropathy," it is the progressive degeneration of a weight bearing joint with marked boney destruction/deformity
73
How do you treat/manage Charcot Arthropathy?
1) Non-weight bearing 2) Cast/immobilization 3) Obtain serial x-rays 4) Address blood glucose and HbA1c
74
What is the most common location for Charcot Arthropathy?
Midfoot
75
What two types of bone scans can differentiate between Charcot Arthropathy and Osteomyelitis?
1) Indium 2) Ceretec *BOTH will be positive in Charcot Arthropathy
76
What do AGEs, DAG, and oxidative stress activate to induce the injurious pattern seen in DM?
PKC beta
77
What steps can be taken to prevent DM retinopathy?
1) Dilated eye exam 5 years s/p T1DM dx and at time of T2DM dx 2) Glycemic control 3) Blood pressure control
78
Outline the natural history of DM nephropathy.
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
When a DM patient's GFR is between 45-60, what steps should you take in their treatment?
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
When a DM patient's GFR is between 30-45, what steps should you take in their treatment?
1) Consider medication dose adjustments 2) Check GFR every 3 months 3) Monitor electrolytes
81
How do you treat CKD in DM patients?
1) ACE-inhibitors 2) ARBs 3) Modest protein restriction
82
What drugs can be used to treat DM nerve pain?
1) TCAs 2) Anticonvulsants 3) Duloxetine 4) Capsaicin
83
What is the general purpose of the PreOp eval in an emergent patient? What things should be done? What is your goal
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
List four reasons why wound infections are rampant in DM patients.
1) Reduced capillary perfusion 2) Reduced oxygen and nutrient delivery 3) Impaired circulation of antimicrobials 4) Hyperglycemia "feeds" bacteria
85
In post-op DM patients, what cardiovascular complication do you need to have a high index of suspicion for?
Silent MI
86
What two classes of medications can have an adverse effect on DM patients in the hospital?
1) Glucocorticoids | 2) TPN
87
What effect does insulin have on K+ and phosphate?
Insulin increases the UPTAKE of K+ and phosphate INTO the cells
88
What are the three most common causes of hypoglycemia in non-DM patients?
1) Alcohol 2) Critical illness 3) Hormone deficiency
89
What critical illnesses can precipitate hypoglycemia?
1) Hepatic failure 2) Renal failure 3) Cardiac failure 4) Sepsis
90
What are the causes of post-parandial hypoglycemia?
1) Gastric resection 2) Islet cell tumor 3) Glycogen Storage Disease 4) Hereditary Fructose Intolerance 5) Galactosemia
91
What are the three unique features of MODY compared to other forms of DM?
1) No insulin resistance 2) No GAD65 antibodies 3) No loss of beta cell numbers

Endocrine (34 decks)

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