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59 Cards in this Set
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What are the corresponding blood glucose levels to HbA1c of:
1. 6 2. 7 3. 8 4. 9 |
1. 120
2. 150 3. 180 4. 210 |
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Definition:
Hyperglycemia resulting from the autoimmune distruction of the insulin-producing beta cells of the pancreas |
DM-1
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most common HLA genotypes in DM-1
(2) |
HLA DR3
HLA DR4 |
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Dx:
woman has a recurrent vaginal candidiasis that is refractory to treatment what test should be done? |
Diabetes mellitus
Get a blood glucose |
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Antibody types for DM-1
(2) |
Anti-cytoplasmic Ab against:
Beta cells and Glutamic Acid Carboxylate (GAD) |
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(2) environmental factors that may play a role in the etiology of DM-1
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Viral infection
Exposure to cow's milk during infancy |
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(3) Viral infections that may play a role in the etiology of DM-1
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Congenital Rubella
Mumps Coxsackie B |
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Dx:
polyuria, polydipsia, weight loss, dehydration, blurred vision, fatigue |
DM-1
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Dx tests for Diabetes
(3) |
1. Fasting glucose > 126
2. Random plasma glucose > 200 3. HbA1c > 7% |
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(4)* Bugs that occur in DM patients due to their decreased efficacy of granulocytes
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MA and PA:
Mucormycoses; Actinomycoses; Pseudomonas; Aspergillosis (pneumonia) |
MA and PA
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How do you determine the time the daily dose of insulin (NPH or 70/30 preparations) is given for a DM-1 patient?
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Give 2/3 daily dose before breakfast
Give 1/3 daily dose before dinner |
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How should new DM-1 patients monitor their glucose?
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Finger-stick levels 5 times a day:
morning fasting; breakfast postprandial; lunch postprandial; dinner postprandial; before bed |
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Which insulin preparation is considered "Rapid-acting" and used right before meals?
(2) List: - Onset of action - Peak action - Duration of action |
Humalog or Lispro
Onset of action = 15 min Peak action = 60 min (ave 30-90 min) Duration of action = 3 hr (ave 2-4 hr) |
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Regular insulin:
- Onset of action - Peak action - Duration of action |
Onset of action = 30-60 min
Peak action = 2-4 hr Duration of action = 6-8 hr |
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(2) Intermediate-acting Insulin preparations
List: - Onset of action - Peak action - Duration of action |
NPH and Lente
Onset of action = 1-3 hr Peak action = 6-12 hr Duration of action = 18-26 hr |
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(2) Long-Acting Insulin preparations
List: - Onset of action - Peak action - Duration of action |
Ultralente and PZI
Onset of action = 4-8 hr Peak action = 14-24 hr Duration of action = 24+ |
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Longest acting Insulin preparation
(2 names) List: - Onset of action - Peak action - Duration of action |
Glaragine (Lantus)
Onset of action = 1 hr Peak action = no peak Duration of action = 24+ |
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Definition:
exaggeration of the normal tendancy of plasma glucose to rise in the early morning hours before breakfast what may it be caused by? First step in Tx? |
Dawn phenomenon
By: inc in GH secretion Tx: move nighttime insulin closer to bedtime |
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what is "postprandial"?
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2 hours after meal
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Definition:
nighttime hypoglycemia followed by dramatic inc in fasting glucose levels and inc plasma ketones what confirms dx? Tx? |
Somogyi Effect
confirms: Hypoglycemia at 3am Tx: give Long-acting insulin at bedtime (instead of NPH) |
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Dx:
patient presents w/ persistent morning hyperglycemia, despite increasing his nighttime NPH insulin dose. He complains of frequent nightmares and his wife witnessed him having a seizure in the middle of the night |
Somogyi effect
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MC negative complication w/:
1. DM-1 2. DM-2 |
1. DKA
2. Non-Ketonic Hyperglycemic Hyperosmolar Coma (NKHC) [either can occur w/ either DM] |
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What type of immunity is impaired w/ diabetes?
what type of infections can this lead to? |
Cell-mediated immunity
leads to: Fungal infections |
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What should be done if the am finger-sticks show hypoglycemia?
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decrease the bedtime NPH even if the bedtime finger-sticks are high
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(3) causes of DM-2 hyperglycemia
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1. Impaired secretion of Insulin
2. Decreased insulin effectiveness at glucose uptake 3. Impaired inhibition of hepatic gluconeogenesis |
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How can hyperglycemia cause further glucose intolerance?
(2) |
1. it Decreases insulin sensitivity
2. it Increases hepatic glucose production |
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Drug class of Metformin
MOA (3) AE |
Biguanides
MOA: sensitizes skeletal muscle and fat to insulin; Dec hepatic gluconeogenesis; Dec GIT absorption AE: Lactic Acidosis |
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(4)* drugs in Sulfonylurea class
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Goes To Cancel Glucose:
Glyburide; Tolbutamide; Chlorpropamide; Glipizide |
Goes To Cancel Glucose
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MOA of Sulfonylureas
AE |
MOA:
increase postprandial insulin secretion from beta cells AE: Hypoglycemia |
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(3) drugs in the Thiazolidinediones class
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GLITAZONES:
Troglitazone; Rosiglitazone; Pioglitazone |
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(2) MOA of the Thiazolidinediones
AE |
MOA:
Reduces insulin resistance; dec. hepatic glucose output AE: Hepatotoxicity |
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Example of an Alpha-glucosidase inhibitor
MOA AE |
Example:
Acarbose MOA: inhibits monosaccharides and oligosaccharide hydrolysis in the small intestines AE: Diarrhea and nausea (and farting) |
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MC combination of DM oral drugs
(plus 2 drugs in it) |
Glucovance
(Metformin + Glyburide) |
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Basic Etiology behind DKA
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Severe insulin deficiency causes body to switch from metabolizing carbs to metabolizing and oxidizing lipids
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What (2) ketones are produced w/ DKA?
what is normal raio of these two? ratio in DKA? |
Beta-hydroxybutyric Acid (BOH)
Acetoacetic Acid Normal ratio: 3:1 DKA ratio: 8:1 |
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Pathophysiology of DKA and how it leads to "fruity breath"
(4) |
1. insulin deficiency causes hyperglycemia -> osmotic diuresis
2. loss of fluids, Na and K 3. inhibition of FFA oxidation in liver -> ketosis 4. Met Acidosis results in respiratory compensation and blowing off of breakdown products (acetone) |
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Dx:
dehydration, polyuria, N/V, rapid deep (Kussmal) breathing, + anion gap, scent to breath |
DKA
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(3) main parts of Dx DKA
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D: high glucose (400-800 mg)
K: + Ketones A: pH < 7.3 (inititially casues K to rise) |
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(3) Tx rules for DKA
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1. Hydrate (usu 3-4L loss): replace w/ NS
2. Insulin (and glucose if pt becomes normoglycemic) 3. Replace K |
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Causes of death w/ DKA
(3) |
circulatory failure;
HypoK; Infection |
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MC DM-2 patient profile to get Nonketotic Hyperosmolar Coma
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DM-2 nursing home patient
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Etiology of Nonketotic Hyperosmolar Coma
(4--2 are drugs) |
Sepsis;
Dehydration; Diuretics; Glucocorticoids |
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Sx:
Altered mental status, signs of profound dehydration, neurologic deficits, DM-2 |
Nonketotic Hyperosmolar Coma
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What is serum glucose levels for Nonketotic Hyperosmolar Coma?
serum Osmolarity? what is the other indicator, with relation to the kidneys? |
glucose > 1000 mg/dL
serum osmloarity around 385 mOsm/kg Pre-renal Azotemia: BUN/creatinine levels are increased |
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Tx for Nonketotic Hyperosmolar Coma
(3) |
1. Expand IV volume: infuse 2-3L NS over 1-2hrs
2. K replacement 3. withhold insulin therapy for up to 1 hour (to help w/ IV osmolality) |
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Whipple's triad of Hypoglycemia
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1. plasma glucose < 60mg/dL
2. Sx of hypoglycemia 3. improvement of Sx w/ Glucose |
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MCC of altered mental status in Healthcare environments
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Hypoglycemia
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Etiology of Hypoglycemia
(6)* |
DIAL HI:
1. Drug induced 2. Islet cell tumor/adenoma 3. Adrenal insufficiency 4. Liver/renal Dz (severe) 5. Hypopituitarism from low GH and cortisol 6. Insulin receptor Ab |
DIAL HI
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Dx:
possible Hx of insulin or sulfonylurea Tx, adrenergic Sx (diaphoresis, anxiety, tremor, hunger, palpitations); confusion, inappropriate behavior, mistaken for alcohol intoxication |
Hypoglycemia
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Dx Tests for Hypoglycemia
(2) |
1. Low serum glucose < 50mg/dL
2. ask lab to test C-peptide to distinguish b/t Endogenous insulin (high C-peptide) or Exogenous insulin(low) |
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If alcoholism or nutritional deficiency is a suspected reason for hypoglycemia, what should be placed w/ the IV of dextrose?
Why? |
Thiamine
to prevent Wernicke's encephalopathy |
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Hospital Tx for Hypoglycemia
(3 steps) |
1. IV amp of 50% dextrose
2. if no improvement, give a second amp 3. continue to infuse 10% dextrose until serum glucose is > 100mg/dL |
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if hypoglycemia is refractory after Tx and there are associated signs of adrenal insufficiency, what is Tx?
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give Hyrdocortisone 100-200mg IV
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what is used to resuscitate hypoglycemic coma?
what type of patient will this Tx not work on? |
Glucagon IM
won't work on Alcoholic w/ liver failure |
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What does a glucagonoma present with?
(3) |
1. new-onset DM
2. weight loss 3. characteristic rash (necrolytic migratory erythema) |
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How is insulin related to Catecholamines?
(2) |
1. Inc insulin leads to hypoglycemia, leading to tachycardia, sweating and anxiety
2. Pheochomocytoma patient have inc risk of hyperglycemia and DM |
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How does Cortisol relate to glucose levels?
(2) |
1. Too much cortisol (Cushings) leads to hyperglycemia and DM
2. Too little cortisol (Addisons) leads to hypoglycemia |
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How does GH relate to glucose levels?
(2) |
1. high GH in acromegaly, leads to hyperglycemia and DM
2. neonatal hypoglycemia is a cardinal sign of GH deficiency |
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List the 5 signs (any 3 of which can confirm Dx) to properly Dx Metabolic syndrome
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1. Fasting glucose > 110 mg/dL
2. Abdominal obesity 3. Serum TG > 150 mg/dL 4. HDL-C < 40 in men and < 50 in women 5. Blood Pressure > 130/85 (or on BP meds) |
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