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58 Cards in this Set
- Front
- Back
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Drug group: Sulphonylureats
(MOA, use, s.e.) |
MOA: Potentiate glucose stimulatied insulin release.
Attatch to sulphonylurea receptors on Bcells, which are linked to ATP-dependent potassium channels. They CLOSE potassium channels, depolarising the cell, resulting in influx of Ca2+ and insulin release. USE: Type II diabetes S.E: hypolgycaemia Contrasindications: obesity as these drugs tend to stimulate appetite. |
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Metabolic syndrome is associated with what type of DM
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DM type II
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Drug group: Biguanides
(MOA, use,s.e., example) |
METFORMIN- first line therapy
MOA: - increases glucose uptake into skeletal mucle and fat - appetite supression - decreased intestinal glucose absoprtion - decreased gluconeogenesis USE: Type II diabetes S.E. lactic acidosis if renal function comprimised ( as emtformin is comlpetely excreted via the kidney). Gastric intolerance and diarrhoea (10% patients) Note: does not simulate insulin release. Is fabulous because it assists weight loss! |
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Characteristics of Metabolic Syndrome. Must have 3 or more for Dx.
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1. Obesity
Waist circumfrence: men > 40 inches women >/= 35 inches 2. Hypertension BP =/> 130/85 3. Abnormal HDL men < 40 mg/dl women < 50mg/dl 4.Abnormal Triglycerides 150 mg/dl or greater 5. Fasting blood glucose (FBG) of 100mg/dl or greater (insulin resistance) |
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Drug group:alpha-Glucosidase inhibitors
(MOA, use, s.e, example.) |
e.g. ACARBOSE
MOA:inhibit the enzyme that breaks dow dietary complex carbohydrates to sugars. - reduces the quantity of glucose available for absorption across the intestinal wall. USE: type II diabetes, generally incombination with sulphonylureas or metformin, as it is less effective on it's own S.E.: malabsorption of charbohydrates- which are then fermented by colonic bacteria and produce abdominal distension, pain and flatulence |
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What denfines insulin resistance:
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Fasting Blood Glucose (FBG) of 100 mg/dl or greater
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Drug group: Meglitinides
(MOA, use, s.e, example.) |
e.g. Repaglinide (only one)
MOA: They stimulate the same receptor as sulphonylureas but at a different site. Increase insulin! S.E.: hypolgycaemia Contrasindications: obesity as these drugs tend to stimulate appetite. Note: short acting and needs to be taken at least twice a day. |
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Tx indicated for Type II DM when glucose is not controlled by diet, exercise and oral antidiabetic agents?
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Insulin Therapy
(usually begin with NPH single dose therapy) |
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Drug group: Glitazones
(MOA, use, s.e, example.) |
e.g. rosiglitazone, pioglitazone
MOA: reduce insulin resistence by acting on the Peroxisome Proliferator Receptors (PPARg) in fat cells. SE. can cause substantial weight gain Contraindicated: congestive cardiac failure (cause fluid retention) Note: not a great drug |
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Used when around the clock therapy fails to maintain adequate glucose control
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Insulin sliding scale
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Drug group: DPP-IV inhibitors
(MOA, use, s.e, example.) |
MOA: increase insulin secretion and decrease glucagon secretion by the protection of GLP-1 (glucagon like peptide-1) and GIP (gastric inhibitory peptide). The drug inhibits DPP-IV which breaks down these factors.
Note: well tolerated, are weight neutral and rarely cause hypoglycaemia. |
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Assesses glucose control over the past 2-3 months
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Hemoglobin A1c
Indicated q 3-4 months |
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How is somogyi effect and dawn phenom. diagnosed?
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Check 3.am blood glucose level.
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Diagnosis and Treatment
Hypoglycemic at 3 am Hyperglycemic at 7 am |
Somogyi Effect
Tx: Reduce or omit bedtime dose of insulin |
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Diagnosis and Treatment
Normal or Hyperglycemic at 3 am Hyperglycemic at 7 am |
Dawn Phenomenom
Tx: Add or increase dose of bedtime insulin |
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Major complications of Type I DM
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DKA
Hypoglycemia |
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Candidal vaginitis in women may be an initial manifestation of what condition?
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DM Type 2
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Islet autoantibodies are frequently present in this condition.
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Type 1 DM
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Test used to differentiate b/w Type I and Type 2 DM
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C- peptide insulin level
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Lab test: Serum
Its presence indicates endogenous release of insulin. |
Serum C- Peptide
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Serum C-peptide is decreased or undetectable in this condition.
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Type I DM
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reflects the state of glycemic control of the previous 1-2 weeks.
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Serum fructosamine
1.6-2.6 mmol/L 200-285 mcmol/l |
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Conditions that will lower Serum Fructosimine values
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Reduced albumin:
neprhotic state or hepatic disease |
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Serum Fructosamine is increased in what condition?
> 2.6 mmol/l or > 285 mcmol/l |
Diabetes Mellitus
Norm val vary depending on serum albumin levels |
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hyperpigmented and hyperkeratotic skin on axilla, back of neck, groin.
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acanthosis nigricans
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Acanthosis nigricans is associated with?
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significant insulin resistance and may be seen in DM Type 2 patient
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eruptive xanthomas on the flexor surfaces of the limbs and buttocks....
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Uncontrolled DM 2 and hypertriglyceridemia
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A milky appearance of the veins and arteries of the retina, occurring when the lipids of the blood exceed 5 per cent and in diabetes mellitus and leukemia.
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Lipemia retinalis
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is a complication of type 2 diabetes that involves extremely high blood sugar (glucose) levels without the presence of ketones.
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Diabetic hyperglycemic hyperosmolar syndrome (HHS)
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Ketones
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are byproducts of fat breakdown
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Patient is profoundly dehydrated, hypotensive, lethargic or comatose, But w/o kussmauls respirations
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Hyperglycemic hyperosmolar coma
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State of intracellular dehydration from increased blood glucose level
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DKA
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Hyperglycemia > 600 mg/dL.
Serum osmolality > 310 mosm/kg. No acidosis; blood pH above 7.3. Serum bicarbonate > 15 mEq/L. Normal anion gap (< 14 mEq/L). |
HHNK
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Hyperglycemia > 250 mg/dL.
Acidosis with blood pH < 7.3. Serum bicarbonate < 15 mEq/L. Serum positive for ketones. |
DKA
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Severe acidosis with hyperventilation.
Blood pH below 7.30. Serum bicarbonate < 15 mEq/L. Anion gap > 15 mEq/L. Absent serum ketones. Serum lactate > 5 mmol/L. |
lactic acidosis
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serum phosphate < 1 mg/dL [< 0.32 mmol/L])
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Severe hypophosphatemia
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Severe acidosis with hyperventilation.
Blood pH below 7.30. Serum bicarbonate < 15 mEq/L. Anion gap > 15 mEq/L. Absent serum ketones. Serum lactate > 5 mmol/L. |
Lactic Acidosis
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may be seen after gastrointestinal surgery and is particularly associated with the dumping syndrome after gastrectomy and Roux-en-Y gastric bypass surgery. In some cases, it is functional and may represent overactivity of the parasympathetic nervous system mediated via the vagus nerve. Occult diabetes very occasionally present with postprandial hypoglycemia. Rarely, it occurs with islet cell hyperplasia—the so-called noninsulinoma pancreatogenous hypoglycemia syndrome.
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postprandial hypoglycemia
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is due to hepatic glycogen depletion combined with alcohol-mediated inhibition of gluconeogenesis. It is most common in malnourished alcohol abusers but can occur in anyone who is unable to ingest food after an acute alcoholic episode followed by gastritis and vomiting.
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alcohol induced hypoglycemia
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is an extremely rare condition in which anti-insulin antibodies or antibodies to insulin receptors develop spontaneously. In the former case, the mechanism appears to relate to increasing dissociation of insulin from circulating pools of bound insulin. When antibodies to insulin receptors are found, most patients do not have hypoglycemia but rather severe insulin-resistant diabetes and acanthosis nigricans. However, during the course of the disease in these patients, certain anti-insulin receptor antibodies with agonist activity mimicking insulin action may develop, producing severe hypoglycemia.
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Immunopathologic Hypoglycemia
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is self-induced hypoglycemia due to surreptitious administration of insulin or sulfonylureas
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Factitious hypoglycemia
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Essentials of Diagnosis
Hypoglycemic symptoms—frequently neuroglycopenic (confusion, blurred vision, diplopia, anxiety, convulsions). Immediate recovery upon administration of glucose. Blood glucose < 40 mg/dL with a serum insulin level of 6 microunit/mL or more. |
Hypoglycemia due to pancreatic B Cell tumors
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The hypoglycemia occurs 3–4 hours after meals following an initial postprandial hyperglycemic phase that is due to the antibodies interfering with the exit of insulin from the plasma to reach its target tissues. Later, after most of the meal is absorbed, inappropriate high levels of insulin dissociate from this antibody-bound compartment, resulting in hypoglycemia. Insulin levels in excess of 1000 pmol/L are observed at time of hypoglycemia, and these persons have high titers of insulin autoantibodies.
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Immunopathologic Hypoglycemia
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Weakness, cold intolerance, constipation, depression, menorrhagia, hoarseness
Dry skin, bradycardia, delayed return of deep tendon reflexes Anemia, hyponatremia, hyperlipidemia Free tetraiodothyronine (FT4) low Thyroid-stimulating hormone (TSH) elevated in primary |
Hypothyroidism
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is due to thyroid gland disease
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Primary Hypothyroidism
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hypothyroidism is due to lack of pituitary TSH
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Secondary Hypothyroidism
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Causes of hypothyroidism with goiter
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Hashimoto thyroiditis
Subacute (de Quervain thyroiditis) (after initial hyperthyroidism) Riedel thyroiditis Iodine deficiency Genetic thyroid enzyme defects Hepatitis C Drugs: |
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Sweating, weight loss or gain, anxiety, palpitations, loose stools, heat intolerance, irritability, fatigue, weakness, menstrual irregularity.
Tachycardia; warm, moist skin; stare; tremor. In Graves disease: goiter (often with bruit); ophthalmopathy. Suppressed TSH in primary hyperthyroidism; increased T4, FT4, T3, FT3. |
Hyperthyroidism
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Weakness, abdominal pain, fever, confusion, nausea, vomiting, and diarrhea.
Low blood pressure, dehydration; skin pigmentation may be increased. Serum potassium high, sodium low, BUN high. Cosyntropin (ACTH1–24) unable to stimulate an increase in serum cortisol to 20 mcg/dL. |
Acute Adrenocortical Insufficiency (Adrenal Crisis)
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Weakness, fatigability, anorexia, weight loss; nausea and vomiting, diarrhea; abdominal pain, muscle and joint pains; amenorrhea.
Sparse axillary hair; increased skin pigmentation, especially of creases, pressure areas, and nipples. Hypotension, small heart. Serum sodium may be low; potassium, calcium, and BUN may be elevated; neutropenia, mild anemia, eosinophilia, and relative lymphocytosis may be present. Plasma cortisol levels are low or fail to rise after administration of corticotropin. Plasma ACTH level is elevated. |
Chronic Adrenocortical Insufficiency (Addison Disease)
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disease is an uncommon disorder caused by destruction or dysfunction of the adrenal cortices. It is characterized by chronic deficiency of cortisol, aldosterone, and adrenal androgens and causes skin pigmentation that can be subtle or strikingly dark.
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Addison disease
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Central obesity, muscle wasting, thin skin, hirsutism, purple striae.
Psychological changes. Osteoporosis, hypertension, poor wound healing. Hyperglycemia, glycosuria, leukocytosis, lymphocytopenia, hypokalemia. Elevated serum cortisol and urinary free cortisol. Lack of normal suppression by dexamethasone. |
Cushing Syndrome (Hypercortisolism)
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The easiest screening test for Cushing syndrome
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Dexamethasone test
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Describe dexamethasone test
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the dexamethasone suppression test: dexamethasone 1 mg is given orally at 11 pm and serum is collected for cortisol determination at about 8 am the next morning; a cortisol level < 5 mcg/dL (< 135 nmol/L, fluorometric assay) or < 2 mcg/dL (< 54 nmol/L, high-performance liquid chromatography [HPLC] assay) excludes Cushing syndrome with some certainty. However, 8% of established patients with pituitary Cushing disease have dexamethasone-suppressed cortisol levels < 2 mcg/dL. Therefore, when other clinical criteria suggest hypercortisolism, further evaluation is warranted even in the face of normal dexamethasone-suppressed serum cortisol.
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Hypertension that may be severe or drug-resistant.
Hypokalemia (in minority of patients) may cause polyuria, polydipsia, muscle weakness. Elevated plasma and urine aldosterone levels and low plasma renin level. |
Primary Aldosteronism
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Antidiuretic hormone (ADH) deficiency causes central diabetes insipidus with polyuria (2–20 L/d) and polydipsia.
Hypernatremia occurs if fluid intake is inadequate. |
Diabetes Insipidus
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is an uncommon disease characterized by an increase in thirst and the passage of large quantities of urine of low specific gravity (usually < 1.006 with ad libitum fluid intake). The urine is otherwise normal. It is caused by a deficiency of vasopressin or resistance to vasopressin
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Diabetes insipidus
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is the treatment of choice for central diabetes insipidus
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desmopressin acetat
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