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Clin med 1 > Endocrine 1-3 > Flashcards

Endocrine 1-3 Flashcards

1
Q

What is the normal range for a fasting glucose?

A

70-100 mg/dL

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2
Q

When can T1D be diagnosed up to?

A

Age 30

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3
Q

Who has a higher risk of T1D?

A

Scandanavians

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4
Q

What is the risk of T1D if its the offspring of an affected mother?

A

1-4%

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5
Q

What is the risk of T1D if its the offspring of an affected father?

A

3-8%

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6
Q

What is the risk of T1D if its a non-twin sibling?

A

3-6%

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7
Q

What is the risk of T1D if its a monozygotic twin?

A

30%

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8
Q

What is the risk of T1D if its a dizygotic twin?

A

8%

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9
Q

What are some environmental factors that can increase your chance of getting T1D?

A

Viral infections (enterovirus), immunizations, cow’s milk early, high SES, obesity, Vit D deficiency

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10
Q

What are some perinatal factors that can increase your chance of getting T1D?

A

Maternal age, preeclampsia, neonatal jaundice

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11
Q

What genetic region is involved in risk factors of T1D?

A

HLA region of genome (Human Leukocyte Antigen)

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12
Q

What happens when genetic and environmental factors trigger T1D?

A

T cells are activated, causes a proinflammatory response. End up with B cells producing autoantibodies

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13
Q

What are the classic signs and symptoms of T1D?

A

Polyuria, polydipsia, weight loss, fatigueq

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14
Q

What is the normal function of insulin?

A

Causes the entry of glucose into tissues, promotes storage of carbohydrates and fat

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15
Q

What does insulin inhibit?

A

Lipolysis, glycogenolysis, and tissues catabolism

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16
Q

What is the normal function of glucagon?

A

Stimulates glycogenolysis and gluconeogenesis

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17
Q

Glucagon stimulates the breakdown of what?

A

Glycogen, used when blood sugar is LOW

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18
Q

What is the pathophysiology behind T1D?

A

Abnormal glucose homeostasis. There is a relative or absolute reduction in insulin secondary to beta cell dysfunction

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19
Q

What are the two factors causing beta cell dysfunction

A

Immune mediated (T cell) and idiopathic

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20
Q

What does polyuria cause?

A

Increased urinary glucose excretion -> osmotic diuresis and hypovolemia

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21
Q

What is the renal threshold for urine in the blood?

A

180

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22
Q

What happens after the renal threshold for glucose is reached?

A

If blood sugar is higher than 180, the kidneys dump the glucose into the urine. Once it goes to urine, water follows, causing excessive peeing

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23
Q

What does polydipsia cause?

A

Increased serum osmolality and hypovolemia

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24
Q

Why does a patient with polydipsia become hypovolemic?

A

Water is leaving the blood volume, patient gets dehydrated. The serum osmolality is increased because there is less water

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25
Q

What does weight loss in T1D cause?

A

Hypovolemia and increased catabolism

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26
Q

How does catabolism cause damage?

A

Causes weight loss, if there are no carbs to use, the body begins to break down fat and protein

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27
Q

What is another classic sign of T1D?

A

Fatigue- there is no sugar left in the cells b/c its all in the blood, no energy!

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28
Q

What si/sx would be noted in an initial diagnosis of T1D?

A

Polyuria, polydipsia, weight loss, fatigue, weakness, blurry vision, frequent infections

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29
Q

Why would someone with T1D have blurred vision?

A

Hyperglycemia causes the eye lens to swell and can distort the vision

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30
Q

Why would someone with T1D have frequent infections?

A

Dysregulated immune system, and bacteria love sugar

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31
Q

What physical exam findings would be noted in an initial diagnosis of T1D?

A

Low BP, hypovolemia, tachycardia, could have a high respiratory rate due to acidosis, ketones on breath, abdominal pain is common

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32
Q

What tools do you need to make a diagnosis of T1D?

A

Check capillary blood (need one of the following):
Random blood glucose >200 with associated symptoms
Fasting blood glucose > 126
>200 on glucose tolerance test

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33
Q

What is the leading cause of morbidity and mortality in children with T1D?

A

Diabetic Ketoacidosis (DKA)

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34
Q

What are the causes of DKA?

A

Hyperglycemia (BS>200), metabolic acidosis (pH <7.3 OR bicarb <15), ketosis

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35
Q

What is ketosis?

A

Ketones spilling into the urine. If in urine, it will also be in the blood

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36
Q

What are some si/sx of DKA?

A

Vomiting, Tachypnea, Abdominal pain, SOB, Mental status changes (change in LOC)

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37
Q

What can someone with DKA appear to have?

A

Influenza!

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38
Q

Why does someone with DKA have abdominal pain?

A

Metabolid decomposition

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39
Q

What will the vitals look like for someone with DKA?

A

Low BP, weak diminished peripheral pulses, elevated pulses

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40
Q

What labs should be ordered for someone with DKA?

A

Blood glucose (>200), Ketones, Electrolytes (Na and K), Lactate, BUN, Creatinine, Venous pH, CBC

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41
Q

Why should a lactate be ordered on someone with DKA?

A

Lactate is released during tissue catabolism

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42
Q

Why should a BUN or Creatinine be ordered on someone with DKA?

A

Kidney function tests to see if in kidney failure, dehydration puts them at risk

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43
Q

What is the venous pH test for in DKA?

A

For the acidosis diagnosis

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44
Q

What 4 things need to be managed when someone has DKA?

A
  1. Dehydration
  2. Hyperglycemia
  3. Sodium
  4. Potassium
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45
Q

How do you manage dehydration when someone is in DKA?

A

Osmotic diuresis (glucose and ketones in urine) need CAUTIOUS fluids:
Gradual rehydration with isotonic fluid
Recommendation: 10mL/kg over 1 hour (max 1000mL)

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46
Q

How do you manage hyperglycemia when someone is in DKA?

A

Insulin infusion of 0.1units/kg/hour

Once <300 change fluids to contain glucose (5% dextrose nl saline)

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47
Q

How do you manage sodium when someone has DKA?

A

Needs to be monitored, as H20 moves into cell, serum Na will rise

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48
Q

How do you manage high potassium when someone has DKA?

A

Give insulin, will go down to normal

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49
Q

How do you manage normal potassium levels when someone has DKA?

A

Give K with insulin, if you give just insulin then the potassium levels will drop

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50
Q

How do you manage low potassium when someone has DKA?

A

Give potassium first, then insulin. If insulin first: they will go into cardiac arrest

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51
Q

What does insulin do to potassium?

A

Insulin drives potassium into the cell, if its low and you give insulin, it will continue to drive it into the cells and cause very low levels. Risk of cardiac issues with low K

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52
Q

What other bloodwork can be considered once the T1D diagnosis has been made?

A

T1D antibodies: anti-pancreatic antibodies like insulin, GAD, IA2
Thyroid antibodies
Celiac: Anti-endomysial antibodies, tissues transglutaminase antibodies

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53
Q

What are the T1D antibodies?

A

GAD: glutamate decarboxylase, enzyme produced by beta cells
IA2: insulinoma autoantibody, produced within beta cells

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54
Q

What medications are used for T1D?

A

Insulin** both basal and prandial to keep glucose levels down and glucagon for emergent cases of hypoglycemia

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55
Q

What type of insulin is basal?

A

Long acting

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56
Q

What type of insulin is bolus?

A

Short acting

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57
Q

What are the examples of Short acting insulins (bolus) (4)

A
  1. Aspart
  2. Glulisine
  3. Lispro
  4. Regular
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58
Q

What are the examples of Long acting insulins (basal) (3)

A
  1. Detemir
  2. Glargine
  3. NPH
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59
Q

What other lifestyle changes will patients with T1D have to make?

A

Frequent blood sugar checks 6-8x/day, nutrition counseling, exercise, need to know when to check ketones (BS>300, sick)

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60
Q

What type of nutrition changes will patients on T1D have to make?

A

CARB counseling: calculating insulin needs based on amount of carbs they are going to eat

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61
Q

What does it feel like to be hypoglycemic?

A

Shaky, teeth chattering, dizzy, tired, thirsty, irritable, going to bathroom frequently, HA, blurred vision zoned out

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62
Q

What is the most common cause for hypoglycemia?

A

Took their mealtime insulin and forgot to eat, exercise

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63
Q

What are the two physiologic causes of hyperglycemia?

A
  1. Dawn phenomenon

2. Somogyi effect

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64
Q

What is the Dawn phenomenon?

A

When the blood sugars are high in the morning. its a surge of hormones daily around 4-5am (Cortisol) which increases blood glucose levels

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65
Q

How do you fix Dawn phenomenon?

A

Adjust the overnight basal insulin to decrease hyperglycemia in the morning

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66
Q

What is the Somogyi effect?

A

The patient goes low around 1-2am, hormones begin to surge (cortisol, catecholamines) in response to hypoglycemia, causing hyperglycemia in the morning

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67
Q

If the patients blood sugar is normal around 1-2am, which problem is it?

A

Dawn phenomenon

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68
Q

If the patients blood sugar is low around 1-2am, what is the problem?

A

Somogyi effect

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69
Q

How do you fix the Somogyi effect?

A

Have to pull back on the basal rate of insulin

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70
Q

What is carb counting?

A

45-60G of carbs at a meal, ratio of insulin for carbs is determined by th emedical provider

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71
Q

What are some examples of 15g of carbs?

A

4oz fresh fruit, 1 slice bread, 1/3 cup of pasta, 8oz milk

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72
Q

What is glycemic index?

A

Carbs with a low GI (0-54) good for T1D

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73
Q

Why are carbs with a low GI good for T1D?

A

Feel less hungry, provide you with more energy, lead to weight loss, provide a reduced risk of diabetes

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74
Q

What needs to be regularly checked for T1Ds?

A

Hypoglycemic events, annual eye checks, foot care, renal bloodwork (BUN, creatinine), lipids (CVD and cholesterol), A1c every 3 mos, dental (cavities), psyc (if needed)

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75
Q

What are some possible complications with T1D?

A

Diabetic retinopathy, peripheral neuropathy, nephropathy, skin complcations

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76
Q

What is non-proliferative diabetic retinopathy?

A

Dilation of small vessels, vascular closure leading to ischemia and increased permability

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77
Q

Which type of diabetic retinopathy is initial?

A

Non-proliferative

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78
Q

Which type of diabetic retinopathy has microaneurysms, hemorrhages, “cotton wool” spots, lipid exudates

A

Non-proliferative

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79
Q

Asymptomatic diabetic retinopathy

A

Non-proliferative

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80
Q

What happens in proliferative diabetic retinopathy?

A

Abnormal vascular proliferation (neovascularization)

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81
Q

Which type of diabetic retinopathy has a worse visual prognosis?

A

Proliferative

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82
Q

Neuropathy from T1D characteristics

A

Symmetrical sensory polyneuropathy, can begin in prediabetes state, effects the distal lower extremities

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83
Q

Where does the neuropathy in T1Ds start?

A

In the longest axons first, the sensory loss ascends. From the mid-calf it begins in the hands

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84
Q

What will be found on an exam with T1D neuropathy?

A

Vibratory sensation loss, altered proprioception, impaired pain, light touch, and temperature, decreased reflexes

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85
Q

What is the pathophys behind nephropathy in T1Ds?

A

Mesangial expansion, glomerular basement membrane thickening, podocyte injury, glomerular sclerosis

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86
Q

What are the si/sx of someone with T1D nephropathy?

A

Albuminuria, sometimes hematuria

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87
Q

T1D and nephropathy

A

Up to 30% will have increased albuminuria after 15 years duration of T1D, less than half of these will progress to nephropathy

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88
Q

What is macrosomia?

A

Increased glucose across the placenta, fetus makes more insulin so the baby is very large.

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89
Q

Insulin resistance, impaired insulin secretion, and increased glucose production are all part of what?

A

Type 2 Diabetes

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90
Q

What is typically a disease of adulthood but now also is seen more frequently in children and adolescents?

A

Type 2 Diabetes

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91
Q

What is T2D associated with?

A

Obesity

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92
Q

Circulating endogenous insulin is usually sufficient for what in T2D?

A

Sufficient to prevent ketoacidosis, but NOT sufficient enough to prevent hyperglycemia

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93
Q

What is the risk associated with T2D and monozygotic twins?

A

Over 40 years old, 70%

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94
Q

How many genetic loci have been associated with an increased risk of T2D?

A

30

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95
Q

What is the most important environmental factor causing insulin resistance?

A

Obesity

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96
Q

What are 3 potential sources of T2D?

A
  1. Dysregulation or deficiency on release of insulin by beta cells
  2. Inadequate or defective insulin receptors
  3. Production of inactive insulin or insulin that is destroyed before it can carry out its function
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97
Q

What causes the starvation of body cells, breakdown of fat and increased protein?

A

The inability to transport glucose into fat and muscle cells (T2D)

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98
Q

T2D is the leading cause of what?

A

ESRD, non-traumatic lower extremity amputations, adult blindness

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99
Q

What screening tests are used to diagnose T2D?

A

FPG >126, random blood glucose >200, A1c >6.5%, two hour plasma glucose >200 during an oral glucose tolerance test

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100
Q

What are the test results for someone with prediabetes (T2)?

A

FPG 100-125, plasma glucose levels 140-199, A1c of 5.7-6.4%

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101
Q

What are prediabetes patients at risk for? (T2)

A

Increased risk of progression to T2D (6% per year), increased risk of CVD

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102
Q

How does the oral glucose tolerance test work?

A

Eat balanced diet (atleast 150g carbs) 3 days prior to test, drink 75-100g glucose, measured every hour after

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103
Q

What are normal glucose test results?

A

Normal BG at 1 hour is <184

Normal BG at 2 hours is <140

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104
Q

What would the result from GTT be if patient was prediabetic?

A

If BG is 140-199 after 2 hours

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105
Q

What would the result from GTT be if patient was diabetic?

A

If BG was >200

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106
Q

What are some risk factors for T2D?

A

Family hx, BMI>25, physical inactivity, native/african americans, hx of gestational diabetes or baby >9lbs, PCOS, HbA1C 5.7-6.4%

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107
Q

Who should be screened for T2D?

A

All individuals >45 years old, if normal every 3 yrs after, earlier in certain individuals

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108
Q

People <30years old should be tested for diabetes if

A

BMI>25 or central obesity, habitually sedentary, 1st degree relative with DM, high-risk ethnic population, delivered baby >9lbs, HTN, HDL <35 or triglycerides >250, hx prediabetes, hx CVD

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109
Q

Which ethnic groups are high risk for T2D?

A

African american, latino/hispanic american, native american, asian american, pacific islander

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5
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110
Q

What are the clinical presentations of T2D?

A

Polyuria, polydipsia, polyphagia

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111
Q

What complications can present with T2D?

A

Neuropathic, CV, chronic skin infections

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112
Q

What are some physical exam findings for T2D?

A

Obesity (central), HTN, eye hemorrhages, exudates, neovascularization, acanthosis nigricans, candida infections, decreased sensation to light touch, temp sensation and proprioception, loss of deep tendon reflexes in ankles, dry feet, muscle atrophy, feet ulcers

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113
Q

What is acanthosis nigricans?

A

Dark discoloration of the skin, hyperkeratotic

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114
Q

Patients with acanthosis nigricans patients also have what?

A

Defect in insulin receptor gene, extreme insulin resistance

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115
Q

What are some treatment goals of T2D?

A

Education, nutrition counseling, weight loss, microvascular and macrovascular complications, glycemic control, CV risk factor modification, increasing insulin secretion and responsiveness

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116
Q

CVD risk management for T2D

A

Smoking cessation, aspirin, BP control, management of dyslipidemia, diet, exercise

117
Q

Routine health maintenance of T2D

A

A1c every 3mos, urine microalbumin yearly (kidney disease), podiatry referral, ophthalmology referral, self-monitoring of glucose levels with glucometer (1-4x/day)

118
Q

What 1% drop in A1c is associated with what?

A

Improved outcomes form microvascular complications

119
Q

Who has higher A1c targets?

A

Elderly, patients with multiple comorbidities and limited life expectancy

120
Q

What are some nonpharmacologic therapies for T2D?

A

Weight reduction: carb controlled diet, regular meals with increase in protein, periodic snacks. No concentrated sugars
Exercise, surgical therapy

121
Q

What is the first line pharmacological therapy for T2D?

A

Metformin (Biguanide)

122
Q

Which two pharmacologic therapies lower glucose levels and improve insulin action?

A

Metformin and Thiazolidinediones

123
Q

What two pharmacologic therapies stimulate insulin secretion from pancreatic beta cells?

A

Sulfonylurea and Meglitinides

124
Q

What is an alternative first line therapy for T2D that can also be added to Metformin?

A

Sulfonylurea

125
Q

Which pharmacologic therapy slows the intestinal absorption of glucose?

A

Alpha-glucosidase inhibitors (Acarbose, Miglitol)

126
Q

Which pharmacologic therapy mimics the incretin effect or prolongs incretin action?

A

Glucagon-like peptide 1 (GLP1) therapies

127
Q

What is the MOA of Metformin?

A

Reduces hepatic gluconeogenesis and improves insulin sensitivity

128
Q

What is a C/I for Metformin?

A

Avoid in pts with renal insufficiency (CrCl <30ml/min)

129
Q

Side effects of Metformin

A

Low risk of hypoglycemia, lactic acidosis (rare)

130
Q

How does Metformin cause lactic acidosis?

A

Impairs lactate uptake by liver (avoid in liver failure)

In renal failure patients, reduction in metformin excretion, lactate excretion

131
Q

What is the mechanism of Sulfonylureas?

A

Stimulates insulin release, reduces serum glucagon, increases insulin binding

132
Q

What are the 3 Sulfonylureas?

A

Glyburide, Glipizide, Glimepiride

133
Q

What are some relative contraindications for sulfonylureas?

A

Hepatic or renal insufficiency (increase risk of hypoglycemia)

134
Q

Side effects of sulfonylureas

A

Weight gain, hypoglycemia

135
Q

What is the mechanism for Meglitinides?

A

Increase insulin secretion at beta cells

136
Q

What are the 2 meglitinides?

A
  1. Repaglinide (Prandin)

2. Nateglinide (Starlix)

137
Q

Where is Repaglinide (Prandin) metabolized?

A

Hepatically and 90% excreted in the feces

138
Q

Where is Nateglinide (starlix) metabolized?

A

Hepatically with renal excretion of active metabolites

139
Q

Side effects of meglitinides?

A

Hypoglycemia, less likely than with sulfonylureas

140
Q

C/Is of meglitinides

A

Nateglinide: renal dysfunction

141
Q

What can meglitinides be added onto?

A

Metformin for patients with allergy to sulfonylurea

142
Q

What is an example of an alpha-glucosidase inhibitor?

A

Acarbose and Miglitol

143
Q

Side effects and C/Is of alpha-glucosidase inhibitors

A

Flatulence, diarrhea

Careful in kidney insufficiency

144
Q

Mechanism of Thiazolidinediones?

A

Sensitize peripheral tissues to insulin

145
Q

Examples of thiazolidinediones?

A

Rosiglitazone (avandia) and Pioglitazone (actos)

146
Q

Side effects of Pioglitazone

A

HF/edema, osteoporosis/fractures, possibly bladder cancer, weight gain

147
Q

Mechanism of GLP-1 agonists

A

Enhance glucose dependent insulin secretion, slow gastric emptying, reduce postprandial glucagon

148
Q

Examples of GLP-1 receptor agonists

A

Exenatide (byetta) and Liraglutide (Victoza)

149
Q

What is the BBW for GLP-1 receptor agonists?

A

Causes medullary thyroid cancer in mice

150
Q

GLP-1 receptor agonists

A

Supresses glucagon secretion, administered by subq injection, low risk of hypoglycemia, $$$

151
Q

What are examples of DPP-4 inhibitors?

A

Sitagliptin (januvia)
Saxagliptin (Onglyza) possibly causes HF
Linagliptin (tradjenta)
Alogliptin (nesina)

152
Q

Are DPP4- inhibitors first line treatment?

A

No, can be monotherapy in pts who cant take Metformin, SUs, or thiazolidinediones

153
Q

When should a second agent be added to someone with T2D?

A

If/when A1c goal <7% is not achieved within 3 mos of initial therapy

154
Q

When should you switch to insulin? T2D

A

When A1c is >8.5

155
Q

What is HHNK?

A

Hyperglycemic Hyperosmolar State (Hyperosmotic Hyperglycemic Non-ketonic State)

156
Q

HHNK results in what?

A

Hypovolemia and electrolyte abnormalities

157
Q

What can cause HHNK?

A

Major illnesses: MI, CVA, sepsis, pancreatitis
Drugs: Glucocorticoids, thiazides, atypical antipsycs
Compliance issues

158
Q

What is the clinical presentation of HHS? (Hyperglycemic Hyperosmolar State)

A

Polyuria, polydipsia, weight loss, lethargy, decreased skin turgor, dry mucous membranes, tachycardia, hypotension

159
Q

What are some abnormal lab results of HHS?

A

> 1000 BS, hyperosmolarity, pre-renal azotemia (volume depletion), low potassium, magnesium and phosphate

160
Q

What lab values are different in HHS (T2D) than in DKA (T1D)?

A

Acidosis and ketonemia are absent or mild in HHS

161
Q

What is the treatment for HHS?

A

Intravenous insulin infusion, IV fluid, electrolyte monitoring and repletion (K, Mg, phosphate)

162
Q

Long term microvascular complications of T2D are what

A

Retinopathy (leading cause of blindness in US), Nephropathy (can progress to ESRD required dialysis), Neuropathy (pain and numbness of lower extremities) and Gastroparesis (ulcers can lead to amp)

163
Q

What are the long term macrovascular complications of T2D?

A

Peripheral vascular disease, lower extremity ulcers, amputations (infected ulcers), CAD, MIs

164
Q

How do you treat the Dawn phenomenon with T1D?

A

Increase the basal insulin

165
Q

How do you treat the somogyi effect with T1D?

A

Decrease the overnight basal insulin

166
Q

What is the adrenal gland separated into?

A

Superficial adrenal cortex and inner adrenal medulla

167
Q

The adrenal cortex is a true what?

A

Endocrine gland

168
Q

The adrenal medulla is a modified what?

A

Sympathetic ganglion

169
Q

What part of the spinal cord innervates the adrenal medulla?

170
Q

What are the 3 main types of hormones produced by the adrenal cortex?

A

Glucocorticoids, Mineralocorticoids, Androgens

171
Q

The Zona Fasciculata produces what?

A

Glucocorticoids

172
Q

The Zona Glomerulosa produces what?

A

Mineralocorticoids

173
Q

The Zona Reticularis produces what?

174
Q

Why type of corticosteroid is involved with DHEA and androstenedione?

A

Androgens (precursors to testosterone)

175
Q

What role does aldosterone play?

A

Causes sodium retention into serum with water and potassium secretion into the renal tubule

176
Q

What does aldosterone maintain?

A

Blood pressure

177
Q

Which corticosteroid is involved with aldosterone?

A

Mineralocorticoids

178
Q

What is gluconeogenesis?

A

An increase in glucose metabolism and glycogen formation, especially in the liver

179
Q

What do glucocorticoids do?

A

Mobilize fat, protein and carbs. Suppress the immune system through anti-inflammatory pathways

180
Q

When is cortisol released?

A

Released at a basal rate with bursts due to a stress response

181
Q

What is cortisol regulated by?

A

Anterior pituitary and ACTH via negative feedback loop

182
Q

Corticosteroids are all synthesized from what?

A

Cholesterol

183
Q

What factors can reduce cortisol levels?

A

Music/massage therapy, omega-3 fatty acids, mg supplementation with aerobic exercise, dancing regularly, high dose VitC

184
Q

What factors can increase cortisol levels?

A

Caffeine, sleep deprivation, intense or prolonged aerobic exercise, trauma/stressful event, subQ adipose, anorexia nervosa, excessive alcohol intake

185
Q

What catecholamines are released by the adrenal medulla?

A

Epinephrine, norepinephrine, dopamine

186
Q

What are chromaffin cells?

A

In the adrenal medulla, they are the modified post-ganglionic neurons that have a direct connection to the sympathetic division of the ANS

187
Q

What is effected with the “fight” response

A

Increased BP, HR, vasoconstriction dermis/GI tract, vasodilation smooth muscle (bronchioles, capillaries), glucose metabolism

188
Q

Why are the medullary/chromaffin cells clustered around large vessels?

A

Cause a direct rapid release of catecholamines that target receptors throughout the body

189
Q

Why is there increased muscle contractility in the fight or flight response?

A

To provide the body with extra speed and strength and faster reflexes

190
Q

Pheochromocytoma is a tumor found where?

A

Rare adrenal medulla tumor

191
Q

What does the pheochromocytoma tumor produce?

A

Produces, stores and secretes catecholamines

192
Q

5% of pheochromocytomas are associated with what?

A

MEN2a and MEN2b

193
Q

What is a common clinical feature of pheochromocytoma?

A

HTN: sustained (60%) or labile

Other sxs: HA, diaphoresis, palpitations

194
Q

What are some other non-common si/sx with pheochromocytoma?

A

Chest pain, N/V, abdominal pain, apprehension.anxiety with feeling of impending doom, pallor and/or flushing, HTN +/= tachycardia

195
Q

What can be used to diagnose pheochromocytoma?

A 
24 hour urine collection metanephrine, VMA, total catecholamines, creatinine (levels should normally be low)
Abdominal CT scan (85-95% sensitivity)
Abdominal MRI (99% sensitivity)
196
Q

What drugs need to be given for pheochromocytoma before surgery and why?

A

Alpha-adrenergic blockade 10-14 days and Beta-adrenergic blockade 2 days prior to prevent intra-operative HTN crisis

197
Q

What alpha blocker can be given for pheochromocytoma patients pre-op?

A

Phenoxybenzamine HCl (Dibenzyline)

198
Q

Which beta blockers can be given for pheochromocytoma patients pre-op?

A

Propranolol or Nadolol

199
Q

Laparoscopic surgery is preferred for pheochromocytoma tumors unless what?

A

Unless >8cm

200
Q

What syndrome is the hypersecretion of aldosterone?

A

Hyperaldosteronism

201
Q

Primary Hyperaldosteronism involves what?

A

Due to a problem with the adrenal glands. Could be due to hyperplasia or an adenoma

202
Q

What level is the plasma renin at in primary Hyperaldosteronism?

A

Low. BP goes up, there is increased flow through the JGA and kidney, causes the renin to DROP

203
Q

Secondary Hyperaldosteronism involves what?

A

Extra-adrenal etiology, plasma renin HIGH

204
Q

Pathophys behind secondary Hyperaldosteronism

A

Appropriate release of aldosterone, patient has low flow through JGA causing HIGH renin and aldosterone

205
Q

What can cause secondary Hyperaldosteronism

A

Liver failure patients with ascites, nephrotic syndrome, chronic low flow

206
Q

What does angiotensin 2 do?

A

Increases sympathetic activity, causes tubular Na and Cl reabsorption, K excretion and water retention, causes aldosterone secretion from adrenal gland, arteriolar vasoconstriction, increase BP, ADH secretion from pituitary gland and water absorption in collecting duct

207
Q

What is the mechanism of an ACE I

A

Angiotensin converting enzyme inhibitors,

208
Q

What is the mechanism for ARBs

A

Angiotensin receptor blocker (angiotensin 2 on receptor)

209
Q

What is Conn’s syndrome?

A

Primary Hyperaldosteronism, adrenal adenoma with bilateral cortical nodular hyperplasia

210
Q

What are the 4 classic findings of Conn’s syndrome?

A
  1. Diastolic HTN (HAs)
  2. Hypokalemia (muscle weakness and fatigue)
  3. Metabolic alkalosis (Excess H+ secretion = HCO3 elevation)
  4. Low plasma renin
211
Q

What does the hypersecretion of aldosterone cause?

A

Increased renal tubular exchange of sodium and H+ secretion

212
Q

What will bloodwork show if someone has primary Hyperaldosteronism?

A

Hypokalemia, hypernatremia, metabolic alkalosis (loss of H+ in urine and shift H+ into cells), low plasma renin
urine: proteinuria

213
Q

What will an EKG show for primary Hyperaldosteronism?

A

U waves, ectopic beats, ST depression, prominent P wave, prolonged PRI, LVH criteria

214
Q

What will a CXR show for primary Hyperaldosteronism?

A

Cardiomegaly

215
Q

What does increased aldosterone do (primary Hyperaldosteronism)

A

Increased aldosterone causes increased sodium retention, increases the volume, drops the renin levels

216
Q

What are some diagnostic tests used for primary Hyperaldosteronism

A

Renin hyposecretion w/volume depletion, failed aldosterone suppression w/volume expansion, Abd/pelvic CT or MRI

217
Q

Therapy for primary Hyperaldosteronism

A

Adenoma: surgical excision

Diet with sodium restriction and aldosterone antagonist (Spironolactone)

218
Q

What is the criteria for diagnosis of primary Hyperaldosteronism?

A

Diastolic HTN without edema, decreased secretion of renin when stimulated, increased secretion of aldosterone that cannot suppress, no diuretic use

219
Q

What are some causes for secondary Hyperaldosteronism?

A

Edema state like nephrotic syndrome, ascites, CHF (severe)

Associated with HTN: renin overproduction

220
Q

What can be a cause of low flow through the JGA?

A

Renal artery stenosis

221
Q

Pathophys of secondary Hyperaldosteronism

A

Decreased volume causes an increase in renin, causing an increased in aldosterone which leads to sodium retention

222
Q

What is the cause of Cushing’s syndrome?

A

Prolonged exposure to endogenous or exogenous glucocorticoids

223
Q

Hypersecretion of cortisol from the adrenal cortex causes what?

A

Pituitary overproduction of cortisol from the adrenal cortex (Cushing’s Disease)

224
Q

Pituitary overproducing cortisol is caused by what?

A

Pituitary tumor

225
Q

What else can a pituitary tumor cause?

A

Bitemporal hemianopsia/optic chiasm compression. Also can cause decreased TSH, FSH, LH, GH, prolactin

226
Q

What are some other endogenous causes of cushings syndrome?

A

Adrenal primary mass (typically adenoma and ACTH independent), SCLCA small cell lung carcinoma producing ACTH, thyroid neoplasm, pancreatic neoplasm

227
Q

Hx of cushings disease would have what in it?

A

Weight gain (buffalo hump), dermis changes, proximal muscle wekaness/wasting, sexual dysfunction, psychiatric manifestation, tumor symptoms, increase infections, poor wound healing, osteoperosis and pathologic fractures

228
Q

What type of sexual dysfunction can happen with Cushings syndrome?

A

Decreased libido, impotence, irregular menstruation, infertility, OR virilization female, feminization male (adrenal mass suggested)

229
Q

What dermis changes can happen with Cushings syndrome?

A

Purple/red striae, think skin, easy bruising

230
Q

What tumor symptoms can be seen with Cushings syndrome?

A

HA, vision changes, polyuria, cognitive dysfunction

231
Q

What can be seen on PE with Cushings syndrome?

A

Adipose deposition/obesity, dermis changes, CV/renal HTN edema, PUD, galactorrhea, hypothyroid sxs, fractures/proximal muscle weakness, psyc manifestations

232
Q

Diagnostic tools for Cushings disease

A

24 hour urine cortisol, 1mg Dexamethasone suppression test, CRH/Dex suppression test if above are inclusive, ACTH level

233
Q

What would a 24hour urine cortisol show if pt had Cushings Dx?

A

> 300mcg/dL

<90 is normal

234
Q

What is the 1mg Dexamethasone-suppression test?

A

Dexamethasone is given at 11pm and the cortisol is then measured at 8am
Cushings will show high cortisol and ACTH

235
Q

What is the CRH/Dex suppression test and what will it show if the patient has Cushings?

A

If the cortisol is >50, diagnostic for Cushings

236
Q

What should the ACTH level be at normally around 4pm?

237
Q

What should you do if the ACTH level is high?

A

Cranial MRI and high dose dex-suppression test

238
Q

What should you do if the ACTH level is normal?

A

Abdominal CT/MRI

239
Q

What are the two ways to treat Cushings

A

Surgical resection and medical management

240
Q

What is the goal of surgical resection in Cushings disease?

A

Culprit tumor is reseted. Typically transphenoidal resection of pituitary mass

241
Q

What can you do if the surgical resection for Cushings Dx does not work?

A

Consider radiation of pituitary

242
Q

What types of meds can be used for Cushings Disease?

A

Ketoconazole: Decreaes cortisol production @p450 enzymes of liver
Metyrapone: Blocks final step of cortisol synthesis

243
Q

What are the SEs of using ketoconazole for Cushings?

A

HA, sedation, N, decreased libido, impotence, gynecomastia, elevated LFTs, irregular menses

244
Q

Addisons disease is what type of insufficiency?

A

Adrenocortical due to destruction or dysfunction of the adrenal cortex

245
Q

What can cause Addisons disease?

A

Idiopathic autoimmunity (80%), TB, hematologic malignancy, AIDS, drugs (methadone, ketoconazole), abdominal radiation therapy, CAH (congenital adrenal hyperplasia)

246
Q

The two most common causes of Addisons disease?

A

Idiopathic autoimmunity and TB

247
Q

What can be seen in the clinical presentation of Addisons?

A

Slow insidious presentation: weakness/fatigue, hypotension orthostasis dehydration, weight loss/anorexia, +/- hyperpigmentation of skin and mucosa, N/V/D/abd pain

248
Q

How can we diagnose Addisons disease?

A

Cortrosyn Stimulation Test (Cosyntropin)

249
Q

What is Cortrosyn stimulation test?

A

ACTH stimulation test-tests functional ability of adrenal cortex to synthesize cortisol

250
Q

How is the Cortrosyn stimulation test done?

A

Check baseline plasma cortisol and aldosterone levels
inject IV ACTH o.25mg
30min and 60min post-injection check plasma cortisol and aldosterone levels

251
Q

What will the results be from the cortrosyn stimulation test if the patient has Addisons?

A

There will be minimal to no change in the cortisol or aldosterone levels

252
Q

What will the electrolytes shows if someone has Addisons?

A

Hyponatremic, Hyperkalemic, increased urine Na, increased BUN/Creatinine

253
Q

Other lab findings for Addisons Disease

A

Elevated TSH, should do CXR and PPD, CT abdomen could see enlarged calcified or atrophic adrenal glands

254
Q

What would the cause be if the abdominal CT showed enlarged adrenals?

A

TB, fungal infection, hemorrhage

255
Q

What would the cause be if the abdominal CT showed calcified adrenals?

A

TB, histoplasmosis

256
Q

What would the cause be if the abdominal CT showed atrophic adrenals?

A

Idiopathic autoimmunity

257
Q

What is primary adrenal insufficiency?

A

Anatomic destruction or metabolic failure of the adrenal cortex

258
Q

What is secondary adrenal insufficiency?

A

Suppression or disease of hypothalamic-pituitary axis (ACTH deficiency)

259
Q

What are the signs for secondary adrenal insufficiency compared to Addisons?

A

Similar symptoms but no hyperpigmentation

260
Q

What can be some causes of secondary adrenal insufficiency?

A

Panyhypopituitarism, prolonged exogenous steroids

261
Q

How do we treat adrenal insufficiency?

A

Glucocorticoid: Hydrocortisone 20-30mg/day divided to stimulate diurnal adrenal rhythm 2/3 am and 1/3 pm
Mineralocorticoid: Fludrocortisone 0.05-0.1mg/day with ample sodium intake

262
Q

If there is a rapid/severe adrenal crisis, what can happen?

A

If untreated, coma and death

263
Q

What causes adrenal crisis typically?

A

Exacerbation of chronic adrenal insufficiency (stress precipitant or sudden withdrawal of chronic steroid)

264
Q

What else can cause adrenal crisis?

A

Acute hemorrhagic destruction of bilateral adrenal glands.

265
Q

What is Waterhouse-Friderichsen Sydrome?

A

Adrenal crisis that can be caused by pseudomonas, meningococcemia septicemia

266
Q

What are some stressors with adrenal crisis?

A

Infection, trauma, surgery, V/D, emotional turmoil

267
Q

Symptoms of adrenal crisis

A

Hypotension -> vascular collapse

N/V/adb pain, hyperpyrexia, lethargy somnolence MS change, hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis

268
Q

How do you treat adrenal crisis?

A

IVF resuscitation 2L NS followed by D51/2Ns

Stress Hydrocortisone 100mg IV q6hours or Dexamethasone 4mg q24hours

269
Q

What are the 3 Ps for MEN type 1

A

Hyperparathyroid, Pancreatic islets, Pituitary

270
Q

MEN

A

Multiple Endocrine Neoplasm

271
Q

Hyperparathyroid in MEN type 1

A

Most common manifestation
Due to hyperplasia or adenoma
Sxs: Hyperglycemia, elevated serum Ca++ and PTH normal

272
Q

Pancreatic islets in MEN type 1

A

Occurs in parallel with hyperparathyroid
Due to: hyperplasia, adenoma, or carcinoma
Increase production of pancreatic islet cell hormones like gastrin, insulin, glucagon, VIP

273
Q

Pituitary in MEN type 1

A

Prolactin-> Prolactinoma
GH -> ACromegaly
ACTH -> Cushings disease

274
Q

How do you diagnose MEN type 1?

A

With hormone/electrolyte assays, provocative tesitng, and radiologic testing

275
Q

Which hormone/electrolyte assays are used to diagnose MEN type 1?

A

Gastrin, glucagon, Ca++ and PTH levels, hypokalemia, hypochloremia, metabolic acidosis, GH, prolactin level, ACTH level

276
Q

Which provocative tests can be used to diagnose MEN type 1?

A

Secretin stimulation test w/gastrin levels, short or 72hour fast w/serum insulin and c-peptide levels, dexamethasone suppression test

277
Q

What radiologic tests can be used to diagnose MEN type 1?

278
Q

Which therapies can be used for MEN type 1?

A

Surgical resection and medical management

279
Q

What type of surgical resection is used for MEN type 1

A

Transphenoidal approach w/ pituitary tumors (often difficult b/c multicentric)
Parathyroidectomy and thyroidectomy

280
Q

What meds are used for MEN type 1?

A 
Dopamine agonists (Bromocriptine/ Cabergoline) for prolactinoma
H2 receptor antagonist, PPI for ZES
281
Q

What is seen in MEN2?

A

Medullary thyroid carcinoma and pheochromocytoma

282
Q

MEN2a usually involves what?

A

MTC, pheo (50%), hyperparathyroidism (15-20%)

most common manifestation

283
Q

When does MTC typically develop in 2a?

A

Childhood and >1cm tumor associated with local and distant metastasis

284
Q

MEN2b involves what

A

MTC, pheo (50%), mucosal neuromas, marfanoid body habitus

285
Q

When does MTC develop in type 2b?

A

Earlier and is more aggressive than 2a

286
Q

MEN2 treatment

A

Early thyroidectomy, genetic testing, annual screening w/urine metanephrine/VMA, measurement with Ca++ PTH q 2-3years, surgery

287
Q

What type of surgery is needed for treatment of MTC?

A

Total thyroidectomy w/central LN dissection

288
Q

What type of surgery is needed for treatment of hyperparathyroidism?

A

Excise 3 1/2 with remnant in neck, full excision with remnant implanted in back of forearm

Clin med 1 (9 decks)

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