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M.T.B > Internal Med- Endocrinology > Flashcards

Internal Med- Endocrinology Flashcards

1
Q

What is the etiology of Panhypopituitarism

A

Ultimately, anything that damages the brain, from hemochromatosis, sarcoidosis, tumor to stroke to infection to trauma

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2
Q

What are some of the key features of Prolactin deficiency?

A

There are never any symptoms of prolactin deficiency in men. In women, prolactin deficiency inhibits lactation after childbirth.

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3
Q

What are some of the key features of Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) deficiency?

A

Women will not be able to ovulate or menstruate normally and will become amenorrheic. Men will not make testosterone or sperm. Both will have decreased libido and decreased axillary, pubic, and body hair. Men will have erectile dysfunction and decreased muscle mass.

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4
Q

What are some of the key features of Kallmann Syndrome?

A
  • Decreased FSH and LH from decreased GnRH
  • Anosmia
  • Renal agenesis in 50%
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5
Q

What can you say about deficiency disease described Oxytocin

A

There is no deficiency disease described for oxytocin. Oxytocin helps uterine contraction during delivery, but delivery still occurs even if it is absent.

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6
Q

What is Diabetes insipidus (DI)?

A

It is a decrease in either the amount of ADH from the pituitary (central DI) or its effect on the kidney (nephrogenic DI).

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7
Q

What are some of the causes of Nephrogenic DI (NDI)?

A

A few kidney diseases such as chronic pyelonephritis, amyloidosis, myeloma, or sickle cell disease will damage the kidney enough to inhibit the effect of ADH. Hypercalcemia and hypokalemia also inhibit ADH’s effect on the kidney. Lithium is a classic cause of NDI.

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8
Q

How would a Pt with Diabetes insipidus (DI) present clinically?

A 
Polydipsia and Polyuria.
Urine:
osmolality
>Na+
When hypernatremia is severe, there will be neurological symptoms such as confusion, disorientation, lethargy, and eventually seizures and coma. Neurological symptoms occur only when volume losses are not matched with drinking enough fluid.
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9
Q

How do you tell the difference between central and nephrogenic Diabetes insipidus (DI)?

A

Vasopressin (desmopressin) stimulation test.
In central DI, urine volume will decrease and urine osmolality will increase. With nephrogenic DI, there is no effect of vasopressin use on urine volume or osmolality.

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10
Q

How is Diabetes insipidus (DI) Mgx?

A

Central DI is treated with long-term vasopressin (desmopressin) use. Nephrogenic DI is managed by trying to correct the underlying cause (e.g. hypokalemia or hypercalcemia). Nephrogenic DI also responds to hydrochlorothiazide, amiloride, and prostaglandin inhibitors such as NSAIDs (e.g., indomethacin).

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11
Q

What are some of the clinical features that would make Acromegaly the most likely Dx?

A

Acromegaly enlarges soft tissue like cartilage and bone, resulting in:

  • Increased hat, ring, and shoe size
  • Carpal tunnel syndrome and obstructive sleep apnea from soft tissues enlarging
  • Body odor from sweat gland hypertrophy
  • Coarsening facial features and teeth widening from jaw growth
  • Deep voice and macroglossia (big tongue)
  • Colonic polyps and skin tags
  • Arthralgias from joints growing out of alignment
  • Hypertension resistant to treatment for unclear reasons in 50%
  • Cardiomegaly and CHF
  • Hyperglycemia
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12
Q

What is the best initial test when suspecting Acromegaly?

What is the most accurate test?

A

The best initial test is a level of insulinlike growth factor (IGF-1).

The most accurate test is the glucose suppression test. Normally, glucose should suppress growth hormone levels.

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13
Q

What are some of the lab findings consistent with Acromegaly?

A

Glucose intolerance and hyperlipidemia, which contribute to the cardiac dysfunction.
High Prolactin levels- because of cosecretion with growth hormone.

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14
Q

How is Acromegaly Tx?

A
  1. Surgery: Acromegaly responds to transphenoidal resection of the pituitary in 70% of cases. Larger adenomas are harder to cure.
  2. Medications:
    - Cabergoline: Dopamine will inhibit GH release.
    - Octreotide: Somatostatin inhibits GH release.
    - *Pegvisomant: A GH receptor antagonist, it inhibits IGF release from the liver.
  3. Radiotherapy: Radiation is used only in those who do not respond to surgery or medications.
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15
Q

What are some of the causes of Hyperprolactinemia?

A

-Prolactin can be cosecreted with GH, and increase simply because of acromegaly.
-Hypothyroidism leads to hyperprolactinemia because extremely high TRH levels will stimulate prolactin secretion.
-Kidney disease elevates prolactin.
-Cirrhosis elevates prolactin.
-Dopamine inhibits
prolactin release, so some drugs can inhibit dopamine and allow prolactin levels to rise. (Antipsychotic medications, methyldopa, metoclopramide, opioids, tricyclic antidepressants, and verapamil all raise the prolactin level.) *Verapamil is the only calcium blocker to raise prolactin level.
Always exclude pregnancy first in any woman with a high prolactin level.

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16
Q

How would you Tx Hyperprolactinemia?

A
  1. Dopamine agonists: Cabergoline is better tolerated than bromocriptine.
  2. Transphenoidal surgery is appropriate for those not responding to medications.
  3. Radiation is rarely needed.
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17
Q

What is the best initial test when suspecting Hypothyroidism?

A

TSH level

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18
Q

What is the next best step, when TSH is very high (more than double the upper limit of normal) and the T4 is normal?

A

Replace hormone=> thyroxine

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19
Q

What is the next best step, when TSH is less than double the normal and the T4 is normal?

A

Get antithyroid peroxidase/antithyroglobulin antibodies. If antibodies are positive, replace thyroid hormone.

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20
Q

What are some of the differences and or similarities between Graves disease, Toxic Multinodular goiter, Subacute thyroiditis, Exogenous thyroid
hormone use and Pituitary adenoma, in terms of TSH, RAIU (radioactive iodine uptake) and clinical findings

A

Graves disease=> RAIU, Eye (proptosis) (20%–40%) and Positive antibody testing

Toxic Multinodular goiter=> RAIU (focal, not diffuse like Graves)

Subacute thyroiditis=>

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21
Q

How would you Tx Acute Hyperthyroidism and “Thyroid Storm”?

A
  1. Propranolol: blocks target organ effect, inhibits peripheral conversion of T4→T3
  2. Thiourea drugs (methimazole and propylthiouracil): blocks hormone production
  3. Iodinated contrast material (iopanoic acid and ipodate): blocks the peripheral conversion of T4 to the more active T3; also blocks the release of existing hormone
  4. Steroids (hydrocortisone)
  5. Radioactive iodine: ablates the gland for a permanent cure
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22
Q

What is clinical significance of Thyroid Nodules?

A

These are incredibly common, and are palpable in as much as 5% of women and 1% of men. Ninety-five percent are benign (adenoma, colloid nodule, cyst). Thyroid nodules are rarely associated with clinically apparent hyperfunctioning or hypofunctioning.

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23
Q

A 46-year-old woman comes to the office because of a small mass she found on palpation of her own thyroid. A small nodule is found in the thyroid. There is no tenderness. She is otherwise asymptomatic and uses no medications.

What is the most appropriate next step in the management of this patient?

a. Fine-needle aspiration.
b. Radionuclide iodine uptake scan.
c. T4 and TSH levels.
d. Thyroid ultrasound.
e. Surgical removal (excisional biopsy).

A

*C.
If the patient has a hyperfunctioning gland (i.e., the T4 is elevated or the TSH is decreased), the patient does not need immediate biopsy. Malignancy is not hyperfunctioning. Ultrasound of thyroid is done to evaluate the size of the lesion, but does not change the need for either thyroid function testing or needle aspiration.

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24
Q

What is the next best step in a Pt with a thyroid nodule?

A
  1. Perform thyroid function tests (TSH and T4).
  2. If tests are normal, biopsy the gland because Malignancy doesn’t give hyperfunctioning of the thyroid and should be excluded.
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25
Q

What are the 2 most common causes of Hypercalcemia?

A

Primary hyperparathyroidism and cancer account for 90% of hypercalcemia patients.

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26
Q

How would a Pt with Hypercalcemia present clinically?

A

Primary hyperparathyroidism often presents as an asymptomatic elevation in calcium levels found on routine blood testing. When there are symptoms, it can occasionally present with the signs of acute, severe hypercalcemia such as:

  • Osteoporosis
  • Nephrolithiasis and renal insufficiency
  • Muscle weakness, anorexia, nausea, vomiting, and abdominal pain
  • Peptic ulcer disease (calcium stimulates gastrin)
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27
Q

How would you Tx Hypercalcemia?

A
  1. Saline hydration at high volume

2. Bisphosphonates: pamidronate

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28
Q

A 75-year-old man with a history of malignancy is admitted with lethargy, confusion, and abdominal pain. He is found to have a markedly elevated calcium level. After 3 liters of normal saline and pamidronate, his calcium level is still markedly elevated the following day.

What is the most appropriate next step in management?

a. Calcitonin.
b. Zoledronic acid.
c. Plicamycin.
d. Gallium.
e. Dialysis.
f. Cinacalcet.

A

A. Calcitonin inhibits osteoclasts. The onset of action of calcitonin is very rapid, and it wears off rapidly. Bisphosphonates take several days to work. Plicamycin and gallium are older therapies for hypercalcemia that no longer have any place in management. When they are given as choices for therapy, plicamycin and gallium are always wrong. Zolendronic acid is a bisphosphonate and does not add anything to the use of pamidronate. Cinacalcet is an inhibitor of PTH release. If the hypercalcemia is from malignancy, PTH should already be maximally suppressed. Dialysis would be used only for those in renal failure.

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29
Q

How would you Tx hypercalcemia from sarcoidosis or any

granulomatous disease?

A

Prednisone

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30
Q

What are some of the lab findings you would expect to see in a Pt with Hyperparathyroidism?

A

Besides high calcium and PTH levels, you will also find a low phosphate level, high chloride level, EKG with a short QT, and sometimes an elevated BUN and creatinine. Alkaline phosphatase may be elevated from the effect of PTH on bone.

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31
Q

How would a Pt with Hypocalcemia present clinically?

A

Signs of neural hyperexcitability in hypocalcemia:

  • Chvostek sign (facial nerve hyperexcitability)
  • Carpopedal spasm
  • Perioral numbness
  • Mental irritability
  • Seizures
  • Tetany (Trousseau sign)
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32
Q

What ECG finding do you expect to see in Hypocalcemia

A

A prolonged QT that may eventually cause arrhythmia.

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33
Q

How would you Mgx Hypocalcemia?

A

Replace calcium and activated vitamin D.

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34
Q

What are the differences in presentation between Hypercalcemia and Hypocalcemia?

A

Low calcium = twitchy and hyperexcitable

High calcium = lethargic and slow

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35
Q

What is Cushing syndrome?

A

Is a hypercortisol state due to pituitary overproduction of ACTH.

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36
Q

What are some of the clinical features of Cushing syndrome?

A
  • Fat redistribution: “Moon face,” truncal obesity, “buffalo hump,” thin extremities, increased abdominal fat
  • Skin: striae, easy bruising, decreased wound healing, and thinning of skin
  • Osteoporosis
  • Hypertension: from increased sodium reabsorption in the kidney
  • Menstrual disorders in women
  • Erectile dysfunction in men
  • Cognitive disturbance: from decreased concentration to psychosis
  • Polyuria: from hyperglycemia and increased free water clearance
37
Q

What are the steps you would need to take when diagnosing or establishing a hypercortisol state?

A
  1. Establish the Presence of Hypercortisolism:

↑ 24-hour urine cortisol is the best initial test, if this is not in the choices, then the answer;

  • ↑ early morning serum cortisol levels following a low-dose dexamethasone suppression test
  • ↑ midnight salivary cortisol
  • ↑ midnight serum cortisol
  1. Establish the Cause of Hypercortisolism
    ACTH testing is the best initial test to determine the cause (source) or location of hypercortisolism.
    Low ACTH means an adrenal source.
    If the ACTH level is elevated, the source could be from:
    Pituitary (suppresses with high dose dexamethasone)
    Ectopic production: lung cancer, carcinoid (dexamethasone does not suppress)
38
Q

If ACTH level is elevated and does not suppress with high dose
dexamethasone, what is the next best step?

A

Scan the brain with an MRI

39
Q

If ACTH level is elevated and does not suppress with high dose
dexamethasone and the MRI does not show a clear pituitary lesion, what is the next best step?

A

Sample the inferior petrosal sinus for ACTH, possibly after stimulating the patient with corticotropin-releasing hormone (CRH). An elevated ACTH from the venous drainage of the pituitary confirms the pituitary as the source. The petrosal venous sinus must be sampled because some pituitary lesions are too small to be detected on MRI.

40
Q

If ACTH level is elevated and does not suppress with high dose
dexamethasone and you cannot find a defect in the pituitary either by
MRI or by sampling the petrosal sinus, what is the next best step?

A

Scan the chest looking for an ectopic source of ACTH production.

41
Q

Why do we confirm the source of hypercortisolism with biochemical tests before you perform imaging
studies, instead of going straight to imaging?

A

Because at least 10% of the population has an abnormality of the pituitary on MRI. If you start with a scan, you may remove the pituitary when the source is in the adrenals.

42
Q

Why do we confirm the source of hypercortisolism with biochemical tests before you perform imaging
studies, instead of going straight to imaging?

A

Because at least 10% of the population has an abnormality of the pituitary on MRI. If you start with a scan, you may remove the pituitary when the source is in the adrenals.

43
Q

What would you expect to see on the biochemical analysis in a Pt with hypercortisolism?

A

Cortisol is a stress hormone that is an antiinsulin. In addition, there is some aldosteronelike effect of cortisol that has an effect on the kidney.

  • Hyperglycemia
  • Hyperlipidemia
  • Hypokalemia
  • Metabolic alkalosis
  • Leukocytosis from demargination of white blood cells. At least half of white cells in the blood are on the vessel wall waiting for an acute stress to come into circulation. They are like parked police cars waiting to be called.
44
Q

How would you Tx hypercortisolism?

A

Surgically remove the source of the hypercortisolism. Transsphenoidal
surgery is done for pituitary sources whereas laparoscopic removal is done for adrenal sources.
If surgery is not successful, use pasireotide, which is a somatostatin analog.
*Pasireotide controls unresectable pituitary ACTH overproduction.

45
Q

What is the relationship between Addison disease and Adrenal crisis?

A

Chronic hypoadrenalism is Addison disease. Acute adrenal insufficiency is an adrenal crisis. These conditions are different severities of the same disorder.

46
Q

What are some of the etiological factors of Addison disease?

A

It is caused by autoimmune destruction of the gland in more than 80% of cases. Less common causes are:

  • Infection (tuberculosis)
  • Adrenoleukodystrophy
  • Metastatic cancer to the adrenal gland
47
Q

What are some of the etiological factors of Acute adrenal crisis?

A

It is caused by hemorrhage, surgery, hypotension, or trauma that rapidly destroys the gland. The sudden removal of chronic high-dose prednisone (steroid) use can precipitate acute adrenal crisis.

48
Q

What is the biochemical analysis in Hypoadrenalism likely to show?

A
  • Hypoglycemia
  • Hyperkalemia
  • Metabolic acidosis
  • Hyponatremia
  • High BUN
49
Q

What is the most specific test of adrenal function?

A

The Cosyntropin Stimulation Test.
Cosyntropin is synthetic ACTH. You measure the cortisol level before and after the administration of cosyntropin. In a patient whose health is otherwise normal, there should be a rise in cortisol level after giving cosyntropin.
*Treatment is more important than testing in acute adrenal crisis.

50
Q

How would you Mgx Hypoadrenalism?

A
  1. Replace steroids with hydrocortisone.
  2. Fludrocortisone is a steroid hormone that is particularly high in mineralocorticoid or aldosterone-like effect. Fludrocortisone is most useful if the patient still has evidence of postural instability.
51
Q

A patient is brought to the emergency department after a motor vehicle accident in which he sustains severe abdominal trauma. On the second hospital day, the patient becomes markedly hypotensive without evidence of bleeding. There is fever, a high eosinophil count, hyperkalemia, hyponatremia, and hypoglycemia.

What is the most appropriate next step in management?

a. CT scan of the adrenals.
b. Draw cortisol level and administer hydrocortisone.
c. Cosyntropin stimulation testing.
d. ACTH level.
e. Dexamethasone suppression testing.

A

B.
In a patient with suspected acute adrenal insufficiency, it is critical to administer hydrocortisone. This is more important than diagnosing the etiology. Hydrocortisone possesses sufficient mineralocorticoid activity to be life-saving. In addition, hydrocortisone will increase the blood pressure because there is a permissive effect of glucocorticoids on the vascular reactivity effect of catecholamines. BP will come up fast with steroids because norepinephrine will be more effective on constricting blood vessels.

52
Q

What is Primary Hyperaldosteronism?

A

It is the autonomous overproduction of aldosterone despite a high pressure with a low renin activity.

53
Q

What set of clinical features would make Hyperaldosteronism the most likely Dx?

A

High blood pressure in association with a low potassium level.
Features of secondary hypertension;
-HTN under age 30 or above age 60
-HTN not controlled by 3 antihypertensive medications

54
Q

What is the best initial test when suspecting Hyperaldosteronism?

A

It is to measure the ratio of plasma aldosterone to plasma renin. An elevated plasma renin excludes primary hyperaldosteronism.
*Aldosterone-to-renin ratio > 20:1

55
Q

What is the most accurate test to confirm the presence of a unilateral adenoma causing Hyperaldosteronism?

A

It is a sample of the venous blood draining the adrenal. It will show a high aldosterone level.

56
Q

What is the biochemical analysis in Hyperaldosteronism likely to show?

A

Low potassium
High aldosterone despite a high-salt diet
Low plasma renin level
Aldosterone-to-renin ratio > 20:1 and aldosterone > 15 = hyperaldosteronism

57
Q

When can you start with a scan before biochemical testing in endocrinology?

A

Never start with a scan in endocrinology. There are too many incidental lesions of the adrenal.

58
Q

How would you Mgx Hyperaldosteronism?

A
  • Unilateral adenoma is resected by laparoscopy.

- Bilateral hyperplasia is treated with eplerenone or spironolactone.

59
Q

What are some of the side effects of using Spironolactone when Tx Bilateral adrenal hyperplasia?

A

Spironolactone causes gynecomastia and decreased libido because it is antiandrogenic.

60
Q

What is Pheochromocytoma?

A

It is a nonmalignant lesion of the adrenal medulla

autonomously overproducing catecholamines despite a high blood pressure.

61
Q

What set of clinical features would make Pheochromocytoma the most likely Dx?

A
  • Hypertension that is episodic in nature
  • Headache
  • Sweating
  • Palpitations and tremor
62
Q

What is the best initial test when suspecting Pheochromocytoma?

A

The best initial test is the level of free metanephrines in plasma. This is confirmed with a 24-hour urine collection for metanephrines. This is more sensitive than the urine vanillylmandelic acid level. Direct measurements of epinephrine and norepinephrine are useful as well.

63
Q

If after biochemical testing you look for and can’t find the lesion causing high free metanephrines in plasma (Pheochromocytoma) with a CT or MRI, what is the next best step?

A

MIBG scanning (metaiodobenzylguanidine scanning): This is a nuclear isotope scan that detects the location of pheochromocytoma that originates outside the adrenal gland.

64
Q

What is the best initial Tx for Pheochromocytoma?

A

Phenoxybenzamine is an alpha blocker that is the best initial therapy. Calcium channel blocker and beta blockers are used afterwards.
Pheochromocytoma is removed surgically or by laparoscopy.

65
Q

What is Diabetes Mellitus?

A

It is a hyperglycaemic state defined as persistently high fasting glucose levels
>/= 126 mg/dL or 7.0 mmol/L on at least 2 separate occasions.

66
Q

What set of clinical features would make Diabetes Mellitus the most likely Dx?

A 
Polyuria, polyphagia, and polydipsia are the most common presentation. 
Type 1
-Onset in childhood
-Insulin dependent from an early age
-Not related to obesity
Type 2
-Directly related to obesity
-Onset in adulthood
-less likely to present with polyphagia
67
Q

How would you Dx Diabetes Mellitus?

A
  • Two fasting blood glucose measurements greater than 125 mg/dL
  • Single glucose level above 200 mg/dL with above symptoms
  • Increased glucose level on oral glucose tolerance testing

Hemoglobin A1c >6.5% is a diagnostic criterion and is the best test to follow
response to therapy over the last several months.

68
Q

What is significance of Diet, Exercise, and Weight Loss in Tx Diabetes Mellitus?

A

Weight loss can control as much as 25% of cases of Type 2 DM without the need for medications, since decreasing the amount of adipose tissue helps to decrease insulin resistance. Exercising muscle does not need insulin.

69
Q

What is the best initial Drug Tx for Diabetes Mellitus?

A

Oral metformin works by blocking gluconeogenesis. Sulfonylureas are not used as first-line therapy because they increase insulin release from the pancreas, thereby driving the glucose intracellularly and increasing obesity.

70
Q

What is the target when using Oral Hypoglycemic Medication?

A

HgA1c <7%.

71
Q

Pt’s with which disease are contraindicated in using Metformin?

A

Those with renal dysfunction because it can accumulate and cause metabolic acidosis.

72
Q

What is the mechanism of action of DPP-IV inhibitors in relation to Incretins [glucose insulinotropic peptide (GIP) and glucagon-like peptide (GLP)]?
What are some of the examples of such drugs?

A

The incretins (GIP and GLP) increase insulin release and decrease glucagon release from the pancreas. They are secreted into the bloodstream when food (especially carbohydrates) enters the duodenum and is metabolized by dipeptidyl peptidase-IV (DPP-IV). The incretins normally have a half-life of only 1–2 minutes. Giving DPP-IV inhibitors—such as sitagliptin and alogliptin—markedly lengthens the half-life of incretins.

73
Q

What is the mechanism of action of Incretin mimetics?

What are some of the examples of such drugs?

A 
The incretins (GIP and GLP) increase insulin release and decrease glucagon release from the pancreas.
Exenatide and  liraglutide.
74
Q

What is the mechanism of action of Sodium-glucose co-transporter 2 (SGLT2 inhibitors)?
What are some of the examples of such drugs?

A

They inhibit the reabsorption of glucose in the proximal convoluted tubule after it has been filtered. The extra sugar in the urine increases the likelihood of urinary tract infections and fungal vaginitis.
They are added when 2 or 3 other oral hypoglycemic medications have not been effective.
Empagliflozin and Dapagliflozin.

75
Q

What is the mechanism of action of Alpha glucosidase inhibitors?
What are some of the examples of such drugs?

A

They block glucose absorption in the bowel. They add about half a point decrease in HgA1c. They cause flatus, diarrhea, and abdominal pain. They can be used with renal insufficiency.
Acarbose.

76
Q

Why is Metformin the safest drug to start in newly diagnosed diabetics?

A

It does not cause hypoglycemia.

77
Q

When is Insulin indicated in Type 2 diabetics?

A

If the patient is not controlled with oral hypoglycemic agents.

78
Q

How is a diabetic generally Mgx with Insulin?

A

Long-acting insulin is combined with a shortacting insulin such as lispro, aspart, or glulisine.
Long-acting insulin=> Glargine or NPH. Glargine provides much more steady blood levels for 24hrs than NPH insulin, which is dosed twice a day.

79
Q

What set of clinical features would make Diabetic Ketoacidosis the most likely Dx?

A 
Patients present with:
-Hyperventilation
-Possibly altered mental status
-Metabolic acidosis with an increased anion gap
-Hyperkalemia in blood, but decreased total body potassium because of
urinary spillage
-Increased anion gap on blood testing
-Serum is positive for ketones
-Nonspecific abdominal pain
-“Acetone” odor on breath
-Polydipsia, polyuria
Although more common in those with Type 1 diabetes, diabetic ketoacidosis (DKA) can definitely present in those with Type 2 diabetes.
80
Q

In general, how would you Mgx Diabetic Ketoacidosis?

A
  • Treat with large-volume saline and insulin replacement.
  • Replace potassium when the potassium level comes down to a level approaching normal.
  • Correct the underlying cause: noncompliance with medications, infection, pregnancy, or any serious illness.
81
Q

A 57-year-old man is admitted to the intensive care unit with altered mental status, hyperventilation, and a markedly elevated glucose level.

Which of the following is the most accurate measure of the severity of his condition?

a. Glucose level.
b. Serum bicarbonate.
c. Urine ketones.
d. Blood ketones.
e. pH level on blood gas.

A

B.
Hyperglycemia is not the best measure of the severity of DKA. The glucose level can be markedly elevated without the presence of ketoacidosis. Urine ketones mean very little. Although blood ketones are important, they are not all detected. If the serum bicarbonate is very low, the patient is at risk of death. If the serum bicarbonate is high, it does not matter how high the glucose level is, in terms of severity. Serum bicarbonate level is a way of saying “anion gap.” If the bicarbonate level is low, the anion gap is increased.

82
Q

What are some of the Health Maintenance recommendations for all Its with Diabetes Mellitus?

A

All patients with DM should receive:

  • Pneumococcal vaccine
  • Yearly eye exam to check for proliferative retinopathy, which needs laser therapy
  • Statin medication if the LDL is above 100 mg/dL
  • ACE inhibitors or ARBs if the blood pressure is greater than 140/90 mmHg
  • ACEI or ARB if urine tests positive for microalbuminuria
  • Aspirin, used regularly in all diabetic patients above the age of 30
  • Foot exam for neuropathy and ulcers
83
Q

How is Diabetic Nephropathy screened and prevented in diabetics?

A

The dipstick for urine becomes trace positive at 300 mg of protein per 24 hours. But microalbuminuria means levels of albumin between 30 and 300 mg per 24 hours. Patients with DM should be screened annually for microalbuminuria and started on an ACE inhibitor or ARB when it is present. These agents are proven to decrease the rate of progression of nephropathy by decreasing intraglomerular hypertension and decreasing damage to the kidney.

84
Q

Explain the reason/mechanism of Gastroparesis in a Diabetic. How is it Mgx?

A

After several years, DM decreases the ability of the gut to sense the stretch of the walls of the bowel. Stretch is the main stimulant to gastric motility. Gastroparesis is an immobility of the bowels that leads to bloating, constipation, early satiety, vomiting, and abdominal discomfort. Treatment is with metoclopramide and erythromycin, which increase gastric motility.

85
Q

How can you Mgx Diabetic Retinopathy?

A

The only Mgx for nonproliferative retinopathy is tighter control of glucose.
When neovascularization and vitreous hemorrhages are present, it is called proliferative retinopathy. This is treated with laser photocoagulation, which markedly retards the progression to blindness. Vascular endothelial growth factor (VEGF) inhibitors treat severe retinopathy.

86
Q

Explain the reason/mechanism of Diabetic Neuropathy. How is it Mgx?

A

Damage to microvasculature damages the vasonervorum that surrounds large peripheral nerves. This leads to decreased sensation in the feet—the main cause of skin ulcers of the feet which lead to osteomyelitis. When the neuropathy leads to pain, treatment is with pregabalin, gabapentin, or tricyclic antidepressants.

87
Q

What is Polycystic Ovary Syndrome (PCOS)?

What is the diagnostic criteria?

A

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder characterized by hyperandrogenism, oligoovulation/anovulation, and/or the presence of polycystic ovaries.
Dx Criteria:
-Clinical hirsutism and/or high testosterone/DHEA
-Irregular menstruation
-10 cysts on pelvic sonogram with enlarged ovary (> 10 cm)
Only 2 of the above criteria are needed to diagnose PCOS. If the patient meets the other 2 criteria, sonogram is not needed. Also note that LH/FSH ratio is not part of the diagnostic criteria.

88
Q

Why is irregular menstruation clinically a focal point in Pt’s with Polycystic Ovary Syndrome (PCOS)?

A

Irregular menstruation is a problem in these patients because a woman’s uterine lining must be shed regularly; otherwise, there may be conversion to uterine hyperplasia (premalignant) [endometrial cancer]. Oral contraceptives containing progesterone allow monthly menstruation, solving this problem.

89
Q

How is Polycystic Ovary Syndrome (PCOS) Mgx?

A

Spironolactone is given in PCOS patients with hirsutism—however, spironolactone is the last-line therapy and is used only after lifestyle management, metformin, and OCPs have been attempted and found not to help.
Oral contraception pills are indicated in women who do not wish to conceive. The aim of treatment in women who desire to conceive is to normalize ovarian function and stimulate follicular growth (e.g., with clomiphene).

M.T.B (9 decks)

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