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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
Definition:
Hyperglycemia resulting from the autoimmune distruction of the insulin-producing beta cells of the pancreas
DM-1
most common HLA genotypes in DM-1
(2)
HLA DR3

HLA DR4
Dx:
woman has a recurrent vaginal candidiasis that is refractory to treatment

what test should be done?
Diabetes mellitus


Get a blood glucose
Antibody types for DM-1
(2)
Anti-cytoplasmic Ab against:

Beta cells

and

Glutamic Acid Carboxylate (GAD)
(2) environmental factors that may play a role in the etiology of DM-1
Viral infection


Exposure to cow's milk during infancy
(3) Viral infections that may play a role in the etiology of DM-1
Congenital Rubella

Mumps

Coxsackie B
Dx:
polyuria, polydipsia, weight loss, dehydration, blurred vision, fatigue
DM-1
Dx tests for Diabetes
(3)
1. Fasting glucose > 126

2. Random plasma glucose > 200

3. HbA1c > 7%
(4)* Bugs that occur in DM patients due to their decreased efficacy of granulocytes
MA and PA:

Mucormycoses;

Actinomycoses;

Pseudomonas;

Aspergillosis (pneumonia)
MA and PA
How do you determine the time the daily dose of insulin (NPH or 70/30 preparations) is given for a DM-1 patient?
Give 2/3 daily dose before breakfast

Give 1/3 daily dose before dinner
How should new DM-1 patients monitor their glucose?
Finger-stick levels 5 times a day:
morning fasting;
breakfast postprandial;
lunch postprandial;
dinner postprandial;
before bed
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)
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
(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
(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+
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+
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
what is "postprandial"?
2 hours after meal
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)
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
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]
What type of immunity is impaired w/ diabetes?

what type of infections can this lead to?
Cell-mediated immunity


leads to: Fungal infections
What should be done if the am finger-sticks show hypoglycemia?
decrease the bedtime NPH even if the bedtime finger-sticks are high
(3) causes of DM-2 hyperglycemia
1. Impaired secretion of Insulin

2. Decreased insulin effectiveness at glucose uptake

3. Impaired inhibition of hepatic gluconeogenesis
How can hyperglycemia cause further glucose intolerance?
(2)
1. it Decreases insulin sensitivity

2. it Increases hepatic glucose production
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
(4)* drugs in Sulfonylurea class
Goes To Cancel Glucose:

Glyburide;

Tolbutamide;

Chlorpropamide;

Glipizide
Goes To Cancel Glucose
MOA of Sulfonylureas

AE
MOA:
increase postprandial insulin secretion from beta cells

AE:
Hypoglycemia
(3) drugs in the Thiazolidinediones class
GLITAZONES:

Troglitazone;

Rosiglitazone;

Pioglitazone
(2) MOA of the Thiazolidinediones

AE
MOA:
Reduces insulin resistance;
dec. hepatic glucose output

AE:
Hepatotoxicity
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)
MC combination of DM oral drugs
(plus 2 drugs in it)
Glucovance

(Metformin + Glyburide)
Basic Etiology behind DKA
Severe insulin deficiency causes body to switch from metabolizing carbs to metabolizing and oxidizing lipids
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
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)
Dx:
dehydration, polyuria, N/V, rapid deep (Kussmal) breathing, + anion gap, scent to breath
DKA
(3) main parts of Dx DKA
D: high glucose (400-800 mg)

K: + Ketones

A: pH < 7.3 (inititially casues K to rise)
(3) Tx rules for DKA
1. Hydrate (usu 3-4L loss): replace w/ NS

2. Insulin (and glucose if pt becomes normoglycemic)

3. Replace K
Causes of death w/ DKA
(3)
circulatory failure;

HypoK;

Infection
MC DM-2 patient profile to get Nonketotic Hyperosmolar Coma
DM-2 nursing home patient
Etiology of Nonketotic Hyperosmolar Coma
(4--2 are drugs)
Sepsis;

Dehydration;

Diuretics;

Glucocorticoids
Sx:
Altered mental status, signs of profound dehydration, neurologic deficits, DM-2
Nonketotic Hyperosmolar Coma
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
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)
Whipple's triad of Hypoglycemia
1. plasma glucose < 60mg/dL

2. Sx of hypoglycemia

3. improvement of Sx w/ Glucose
MCC of altered mental status in Healthcare environments
Hypoglycemia
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
Dx:
possible Hx of insulin or sulfonylurea Tx, adrenergic Sx (diaphoresis, anxiety, tremor, hunger, palpitations); confusion, inappropriate behavior, mistaken for alcohol intoxication
Hypoglycemia
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)
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
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
if hypoglycemia is refractory after Tx and there are associated signs of adrenal insufficiency, what is Tx?
give Hyrdocortisone 100-200mg IV
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
What does a glucagonoma present with?
(3)
1. new-onset DM

2. weight loss

3. characteristic rash (necrolytic migratory erythema)
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
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
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
List the 5 signs (any 3 of which can confirm Dx) to properly Dx Metabolic syndrome
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)