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Clinical Highlights Flashcards

1
Q

Hypopituitarism is rare, what is the most common cause?

• what are some other causes?

A

MOST COMMON: Tx for pituitary Tumor

Other Causes: 
mass lesions
pituitary surgery
pituitary radiation
infiltrative lesions 
infarction => Sheehan syndrome
Apoplexy
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2
Q

T or F: growth hormone levels cannot be used in the diagnosis of GH disorders

A

True, you need to check IGF-1

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3
Q

What are some syndromes that could be associated with GH adenoma?

A
  • MEN1
  • Familial Acromegaly
  • McCune Albright Syndrome
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4
Q

T or F: most patients with GH ademoma present with a MACROadenoma.

A

TRUE, 75% of patients present with this.

*Because its large it may compress other tissue

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5
Q

How do you diagnose Acromegaly?

A
  1. SCREEN:
    • IGF-1 (sensitive, but not specific to GH)
  2. IF IGF-1 is elevated:
    • Oral Glucose Tolerance Test
  3. IF GH>2ng/mL after the test then you have acromegaly (b/c GH isn’t responding the way it should to hyperglycemia)
  4. IMAGING must be done last
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6
Q

How do you treat Acromegaly?

A

SURGERY if possible

If not possible then octreotide (somatostatin)

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7
Q

Who most commonly presents with a prolactinoma?

A

Women around 30 years old who is asymptomatic or may have hypogonadism, menstrual abnormalities, infertility, galactorrhea or bone loss => increase in incidence in pregnancy

Note: prolactinomas are the most common cause of prolactinemia

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8
Q

How do you diagnose a prolactinoma?

A

Prolactin >250 ug/L is very indicative (NL is less than 25 ug/L)

Over 500 ug/L is DIAGNOSTIC

the only thing that could change this is use of antipsychotics that suppress dopamine

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9
Q

What is the treatment for prolactinomas?

A

DOPAMINE Agonists
• Bromocriptine
• Cabergolin

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10
Q

What is typically the clinical manifestation of hypothalamic lesions?

A

Diabetes Insipidus (by disrupting ADH)

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11
Q

What are 4 general reasons that you might get SIADH?

A
  1. Paraneoplastic
  2. Brain
  3. Drugs (nicotine, thiazides, vincas, MAOIs)
  4. Other (Post-op, Hypothyroid, Glucocorticoid insufficiency)
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12
Q

How do people with SIADH present?

A

Na less than 125
N/V/HA

Na less than 120
Seizure, coma, respiratory arrest

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13
Q

How do you diagnose SIADH?

A

Euvolemic (no edema, ascites) hyponatremia (defined as Na < 136), with INAPPROPRIATELY CONCENTRATED urine

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14
Q

What is the treatment of SIADH?

A
  1. Remove underlying cause
  2. Restrict H2O
  3. Demeclocycline, Vaptans, Lithium
  4. Hypertonic Saline (risky)
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15
Q

What are some causes of nephrogenic diabetes insipidus?

A 
Renal Dz
Hypercalcemia
Hypokalemia 
Lithium (messes up glycogen synthase kinase so that ATP can't be made for conversion to cAMP to release AQP2)
Cyclophosphamide, Cisplatin
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16
Q

What are some causes of neurogenic Diabetes Insipidus?

A

WATER DEPRIVATION TESTDO NOT MEASURE ADH**

Restrict Smoking and Overnight H2O

IF urine is still dilute then DI

IF DI then give SQ ADH and check urine

IF urine concentrates then NEUROgenic
IF urine does not concentrate then NEPHROgenic

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17
Q

What is the normal plasma osmolality?

A

290-295 (so NL serum sodium should be about half of that between 136 and 145)

ADH is stimulated around 280
Thrist onset is at 297

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18
Q

T or F: CHF and pregnancy can cause elevated ADH.

A

TRUE

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19
Q

What HLA types are associated with T1DM?

A

HLA-DR3 and 4 (these are found on chromosome 6)

Defects in CTLA-3 and PTPN22 are also possible risk factors

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20
Q

What antibodies are associated with T1DM?

A

Anti-GAD

Anti-ICA512

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21
Q

What are the phases in the development of T1DM?

A
  1. Some kind of environmental insult of ß-cells in the setting of genetic predisposition
  2. Loss of 1st phase in insulin secretion
  3. Loss of Tolerance in OGTT
  4. Overt DM + C-peptide
  5. Over DM without C-peptide
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22
Q

What are normal and DM levels of:
Fasting glucose
Oral GTT
HbA1c

A

NL/DM
FG - less than 100/over 126
OGTT - less than 140/over 200
HbA1C - less than 5.6/over 6.5

Any random BG test above 200 is dx of DM

Anything between is DM

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23
Q

What is the #1 environmental risk factor for T2DM?

A

Central Obesity

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24
Q 
How are the following affected in T2DM? 
•Amylin
• GLP-1
• Glucagon
• SGLT-2
A

Amylin - not secreted after meals to reduce glucagon and gastric emptying

GLP-1 - reduced so less stimulation of insulin release

Glucagon - does not fall after meals

SGLT-2 - resorbs 2x as much glucose (2mg/lb/day)

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25
Q

What is the triad of T1DM?

A
  1. Polyuria
  2. Polydipsia
  3. Polyphagia
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26
Q

What often precipitates the acute stress episode that brings T1DM to clinical attention?

A

Increased: Catecholamines, Glucagon, and Growth Hormone

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27
Q

What is the most common acute metabolic problem in DM?

• what is the precipitating cause?

A

HypOglycemia - caused by failure to take insulin

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28
Q

Why do people need to up their insulin during sickness?

A

Increased Stress Hormones (cortisol, catecholamines)

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29
Q

Why do patients with DM have increased triglycerides?

A

Increased Activity of Lipoprotein Lipase (breaks down VLDL into TGs)

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30
Q

Who is at increased risk of Non-Ketotic Hyperosmolar Syndrome?

A

T2DM patients that are unable to access what (think old, disabled, infection, stroke, etc)

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31
Q 
What lab values indicate Mild, Moderate, and Severe DKA? comment on mental status. 
• Plasma Glc
• pH
• HCO3-
• Urine/Serum Ketons
• Mental Status
A

MILD/MODERATE/SEVERE

PGlc: Over 250 for all
pH: 7.3-7.25 / 7.24-7.0 / less than 7.0
HCO3-: 15-18 / 10-15 / less than 10 
Urine/Serum Ketones: Positive for all 
Mental Stats: Alert / Drowsy / Stupor-coma
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32
Q 
What lab values indicate Non-ketotic Hyperosmolar Syndrome? 
• Plasma Glc
• pH
• HCO3-
• Urine/Serum Ketons
• Mental Status
A 
PGlc: 800-1000
pH: over 7.3
HCO3-: over 18
Ketones: ±
Serum Osm: OVER 330
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33
Q

What is the treatment for both DKA and non-ketotic hyperosmolar syndrome?

A
  1. Fluid Replacement
  2. Insulin Replacement
  3. Patient Education and Prevention
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34
Q

What non-blood glucose controlling medications should you give most diabetics to prevent common complications of DM?

A

Statins - reduce CV risk by 20-25%

BP meds - ACE’s then ARB’s if ace doesn’t work

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35
Q

What is a good marker for determining how much damage has been done to the microvasculature in DM?

A

HbA1c - makes sense given that most microvascular dz can be related to AGEs

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36
Q

What is the number one indicator that a patient may be getting Diabetic Nephropathy?

A

Peeing out albumin

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37
Q

When do we start to see that DM patients are peeing out albumin?
• what other stops do they have on the way to end-stage renal disease?
• How many patients are likely to progress past peeing out albumin?

A

5-15 years into DM we start to see patients get Albuminuria => 1/3 of patients will progress past albuminuria

Albuminuria often progresses to proteinuria (THIS IS OFTEN ACCOMPANIED BY AN INCREASE IN BP)

End-stage renal disease then develops?

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38
Q

Are T1DM or T2DM patients more likely to progress to end-stage renal disease?

A

Technically T2DM patients are more likely to progress to ESRD but this may just be because they are diagnosed later

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39
Q

How much more common is neuropathy in diabetics than the normal population?

A

Neuropathy is 4x as common among diabetics compared to the normal population

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40
Q

What positive and negative symptoms are indicative of lower limb amputation?

A

Positive:
• Pain, Paresthesia, Dysthesia, Allodynia

Negative:
• Temperature, Pain, Touch, Motor invovment (usually lower limbs)

Combination of the symptoms is what causes lower limb amputations

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41
Q

What is the most common type of neuropathy experienced by Diabetics?

A

Persistent Symmetric Polyneuropathy (STOCKING GLOVE SYNDROME)

42
Q

How should you work up a patient with DM when they come to your office?

A
  • H and P
  • HbA1c, Urine Protein, Creatine
  • Eye exam by an opthalmologist
43
Q

How do you workup Hypercalcemia?

A
  1. H and P
  2. Check Albumin and total Ca TWICE
  3. Check PTH
44
Q

What are 2 causes of PTH dependent Hypercalcemia?

A
  1. Hyperparathyroidism

2. Familial Hypercalcinuric Hypercalcemia (FHH)

45
Q

What are some causes of PTH independent Hypercalcemia?

A
  1. Tumor induced (PTHrp or Bone Mets)
  2. Granulomatous (sarcoid/TB)
  3. Multiple Myeloma
  4. Hyperthroidism/Adrenal Failure
  5. Medication (Li+, HCTZ)
  6. Vit D toxicity
46
Q

What Calcium and Phosphate Values would you expect to see in hyperparathyroidism if its:
Primary
Secondary
Tertiary

A

Primary:
• Increased PTH and Ca

Secondary:
• Increased PTH and NL Ca

Tertiary:
• Increased PTH and Increased Ca

47
Q

What are the most common causes of Primary Hyperparathyroidism?

A

Adenoma (80-85%)&raquo_space; Hyperplasia (MEN1, 2A)&raquo_space; parathyroid CA

48
Q

What is the prototypical presentation of a patient with primary hyperparathyroidism?

A

Fatigued Female with stones, moans, groans, and bones

**Remember the majority in real life will be asymptomatic

49
Q

How should you workup a patient with Primary Hyperparathyroidism?

A
  1. LABS:
    •Calcium + Albumin, PTH, 25(OH)VitD, 24 URINE
  2. IMAGING:
    • Thyroid Ultrasound
    • DEXA
50
Q

How do you treat primary Hyperparathyroidism due to Adenoma?

A 
SURGERY IS IDEAL especially if: 
• more than 1mg/dL above UNL
• Under 50 years old
• Osteoporosis
• Renal Insufficiency
MEDs can also be used: 
• WATER
• Bisphosphonates
• Maintain NL vit D
• Cinacalcet 
• Yearly follow-up
51
Q

Familial Hypocalcinuric Hypercalemia:
• inheritance/cause
• DX
• Tx

A

Autosomal Dominant loss of sensitivity of CaSR to detect the presence of Ca2+ so more and more PTH is secreted

Dx: Mild elevation in serum calcium and parathyroid hormone

Tx: no treatment necessary

52
Q

What are some causes of Secondary Hyperparathyroidism?

A
  • Hypocalcemia
  • Hyperphosphatemia
  • Vit D. Deficiency
  • Intestinal Absorption diseases
  • CKD
53
Q

What do you do to workup someone with high PTH but normal Ca?

A 
Secondary Hyperparathyroidism Workup: 
•PTH
• Albumin/total Ca
• Creatinin (B/C CKD is such a common cause)
• Vit D

NO 24 hour urine is necessary

54
Q

How do you treat Secondary Hyperparathyroidism?

A

Treat the underlying cause

55
Q

What are two major causes of PTH INDEPENDENT Hypercalcemia?

A

Malignancy and Granulomatous Disorder

56
Q

What are two ways that malignancy can cause Hypercalcemia even with low PTH?

A

PTHrp secreting tumors
• Most commonly renal, breast and squamous

No PTHrp secreting tumors:
• Bony mets (lung, breast), MM

57
Q

What should your treatment be for Acute Hypercalcemia?

A
  1. Adress Volume Status

ACUTE TX:

  1. Saline ± Furosemide Diuresis
  2. Calcitonin (abs. develop quickly)

LONGER TERM:

  1. Bisphosphonates
  2. Glucocorticoids
  3. Dialysis
58
Q

What is the symptom you should be most concerned about in a patient with Hypocalcemia?

A

Prolonged QT

59
Q

***What are primary, secondary, and “other” causes of hypocalcemia?
• what is the PTH level in each of these?

A

PRIMARY (low PTH):
• Post-thyroidectomy
• Ideopathic/agenesis
• Hyper/Hypomagnesemia (alcoholics, malabsorp, diarrhea)

SECONDARY (high PTH):
• Renal Failure
• Vitamin D Deficiency

Other: 
• Acute Pancreatitis (high PTH)
• Massive transfusion (high PTH)
•Hungry Bone Syndrome (CKD + parthyroidectomy = low PTH) 
• Severe sepsis, TLS/Rhabdomyolysis
60
Q

How should you workup Hypocalemia?

A
  1. H and P
  2. Serum albumin + Ca
  3. check PTH

IF low, look for primary causes
IF high, look for secondary causes

61
Q

What are the acute and long term treatments for Hypocalcemia?

A

ACUTE:

  1. Correct Low Magnesium
  2. Calcium Gluconate

LONG TERM:

  1. Oral Calcium Salts
  2. Vitamin D
  3. Hydrochlorothiazide
62
Q

How does Pseudohypothyroidism present?

A 
Typical Presentation: 
• Short Stature
• Obese
• Rounded Face
•Short 4th and 5th digits
63
Q

Differentiate the inheritance and cause of pseudohypoparathyroidism 1A and pseudopseudohypoparathyroidism?

A

BOTH have GNAS1 mutations

Pseudohypothyroidism:
• AKA Albright Hereditary Osteodystrophy
• Autosomal Dominant from mom

Pseudopseudohypoparathyroidism:
• Autosomal Dominant from DAD - there is no dysfunction of G-alpha subunits in the kidney

64
Q

Differentiate the labs of pseudohypoparathyroidism and pseudopseudohypoparathyroidism.

A

BOTH have all the classical features of short stature, obestity, rounded face, and shortened 4th and 5th digits

Labs
Pseudohypoparathyroidism 1A:
• low urinary cAMP and PO4 after PTH is administered

pseudopseudohypoparathyroidism:
• Normal urinary cAMP and PO4

65
Q

What are markers of bone formation?

A
  • Bone Specific Alkaline Phosphatase
  • Osteocalcin
  • Carboxyterminal Propeptide of Type I collagen
66
Q

What are markers of bone resorption?

A
  • N-telopeptide

* Carboxyterminal of Type I collagen

67
Q

What are the risk factors for bone fracture?

A
  • Femoral Neck T-score
  • Age
  • Previous Low Trauma Fracture
  • Low BMI
  • Current Cigarette Smoking
  • Steriod Use
  • RA
  • High EtOH intake
  • Family History of Fracture
68
Q

How do you treat osteoporosis?

A
  1. Lifestyle Changes: Stop tobacco/EtOH, increase physical activity, adequate calcium, optimal vit. D, Fall prevention
  2. Drugs: Antiresorptive agents, anabolic agents
69
Q

How do you want to monitor a patient with osteoporosis after initiating treatment?

A

N-Telopeptide - tells you short term if treatment is working

DEXA - measures longer term changes

70
Q

What are Medications that increase your fracture risk?

A
  1. Glucocorticoids
  2. Aromatase Inhibitors
  3. Androgen Deprivation Therapy
  4. Any Type of Antipsychotic/Antidepressant
71
Q

Ideopathic post-menopausal osteoporosis is a diagnosis of exclusion. What other conditions should you rule out before diagnosing this?

A
  1. Acromegaly
  2. Hypercalcemia (PTH or Malignancy)
  3. Cushings
  4. Secondary HyperPTH
  5. Hypogonadism (less estrogen)
  6. Hyperthyroidism
72
Q

What would you expect to see in Paget’s Histo?

A
  1. Osteoclasts with more nuclei than normal

2. Morphologically NL osteoblasts

73
Q

What diseases are associated with Osteitis Fibrosa Cystica?

A
  1. Hyperparathyroidism

2. CKD

74
Q

What is a key difference in the pathogenesis of Osteitis Fibrosa Cystica and Osteoporosis?

A

OFC is cortical bone loss and osteoporosis is trabecular bone loss

75
Q

If you se Fibrous Dysplasia in Multiple Bones what should you start thinking could be the cause?
• what age group is most commonly affected?

A

McCune Albright Syndrome - should have strong suspicion in a kid under 10.

***These kids often have precocious puberty

76
Q

Why might you see Hypophosphatemia in Fibrous Dysplasia?

A

• Mesenchymal cells do not differentiate and may secrete lots of FGF23 with works to suppress phosphate levels

77
Q

What are the steps in the diagnosis of Cushings?

A

STEP 1
• 24 hour urine free cortisol or late-night salivary cortisol
• 1mg overnight dexamtehasone suppression test (will only suppress cortisol if the cause is pituitary adenoma)

STEP 2
• Imaging MRI the pituitary if its normal then look for ectopic causes

78
Q

What are the symptoms of acute adrenal insufficiency?

A
  1. Hypotension
  2. Shock
  3. Hypoglycemia
  4. Hyperkalemia
79
Q

How do you diagnose Adrenal Insufficiency? `

A

Standard ACTH stimulation Test

  1. Draw baseline cortisol
  2. Inject 250 mg of ACTH
  3. Check cortisol every 30 min
  4. Cortisol should exceed 18mg/dL

IF cortisol does not exceed 18mg/dL then its adrenal insufficiency

80
Q

How do you treat adrenal insufficiency?

A

Cortisol (this should be your main treatment since it also has some mineralocorticoid activity)

81
Q

How and when do people with non-classic 21ß-hydroxylase deficiency present?

A

Often not noticed until puberty when males and females have premature pubarche, acne, and increased bone age.

Females: may get hirsuitism and menstrual irregularity
Males: May have reduced fertility

82
Q

What labs should you order to diagnose classic and non-classic 21ß-hydroxylase deficiency?

A

Dx Classic:
• Elevated 17-hydroxyprogesterone over 3500mg/dL

Dx non-classic:
• 17-hydroxyprogesterone elevated over 200 mg/dL with an ACTH stimulation test that raises levels to 1500 mg/dL.

83
Q

What Cardiovascular risk is associated with primary hyperaldosteronism?

A

LVH

84
Q

Differentiate the presentation of Bilateral idiopathic hyperaldosteronism and unilateral adenomas that cause Conn’s syndrome?

A

Bilateral Idiopathic:
• Older people with less severe HTN

Unilateral Adenoma:
•Middle aged female with more severe HTN

85
Q

What channel is often mutated in both sporatic (BIH/Conn) and familial (type III) hyperaldosteronism?

A

KCNJ5 potassium channel that allows Ca2+ in to activate calmodulin that works on enzymes that increase Aldosterone synthase activity

86
Q

How do you diagnose Hyperaldosteronism?

A
  1. Simultaneous measurement of aldosterone and renin IF the ratio is greater than 30 then primary hyperaldosteronism is likely
  2. Give 2 liters of Saline IV over 4 hours in the supine position a normal aldosterone level would be below 5 ug/dL
  3. CT scan should be done to look for possible causes
87
Q

What is the healthy BMI range?

A

18.6-29.9, anywhere above or below this is associated with increased risk of mortality.

88
Q

T or F: there is a genetic component to obestity.

A

True, there is 50% twin concordance

89
Q

What are substances that promote weight gain?

A
  1. Neuropeptide Y
  2. Melanin conc. hormone (MCH)
  3. Agouti-related Peptide
  4. Ghrelin
  5. Orexin A and B
  6. NE/E
  7. Endocannabinoids
90
Q

What are substances that promote weight loss?

A
  1. Leptin
  2. Peptide YY (from ileum and colon)
  3. Insulin
  4. Glucagon-Like Peptide 1
  5. CART
  6. CCK
  7. POMC
  8. alpha-MSH
  9. ADIPONECTIN
  10. Amylin
  11. Pancreatic Polypeptide
91
Q

What is the action of endocannibinoids in the peripheral tissue?

A
  1. Insulin Resistance increased
  2. HDL decreased
  3. TG increase
  4. Glucose Uptake decreased
  5. Adiponectin decreased
92
Q

What diseases are associated with obestity?

A

Diabetes, CVD, Cancer, NAFLD, Sleep Apnea, Decreased Fertility, psychosocial, gallstones

93
Q

What 3 general pathologic mechanisms underlie obesity?

A
  1. Insulin Resistance => increased IGF-1 => CA
  2. Steroid Hormone => increased Estrogen
  3. Proinflammatory State => inflammasome activation
94
Q

T or F: its important to look at family history in people with pheochromocytoma.

A

True

95
Q

What do you need to do to diagnose pheochromocytoma?

A
  1. Clinical Triad of epidodic Sweating, Hypertension, Headache

DX:
Acute episode: Blood Catecholamines (normal 24 hr would be 15-80)

Subacute: Urine Metanephrins

96
Q

What are 2 reasons that people in the non-diabetic population might get hypoglycemic?

A
  1. Insulinoma

2. GI surgery

97
Q

What drug could cause someone who is not diabetic to become hypoglycemic?

A

Sulfonamides (quinine, quinolones, and penatmidine are also potential causes)

98
Q

What defines severe hypoglycemia?

A

Someone besides the patient has to take action

99
Q

What are the 4 ways hypoglycemia can kill you?

A
  1. Increased QT interval from hypokalemia (XS insulin pushes all K+ into cells)
  2. Platelet Activation
  3. Increased Inflammation
  4. Increase PAI-I
100
Q

What is Whipple’s Triad?

A

MARKER OF NON-DIABETIC HYPOGLYCEMIA

  1. Symptoms and Signs of Hypoglycemia
  2. Low Plasma Glucose
  3. Resolution of Symptoms after glucose administration

Endocrine (4 decks)

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