Dibetic Emerg IN CLASS Flashcards
Insulin promotes absorption of glucose from the blood to:
skeletal muscles and fat tissue.
Normally insulin allows glucose transport into the cells for energy or storage as glycogen. Also stimulates protein synthesis and free fatty acid storage in adipose tissue
Is pancreatitis always a result of alcohol use?
Pancreatitis can result from leaky gall bladder (autodigestion) – don’t assume pacnreatitis is result of alcohol
Diabetes is risk factor for what conditions?
MI, stroke, renal failure, retinopathy, peripheral and autonomic neuropathy and peripheral vascular disease
Type 1 DM. When does it usually occur?
How is it managed?
usually occurs before age 30 (can occur at any age)
Patient is usually thin and requires exogenous insulin and dietary management to achieve control
Type 2 DM
Who gets it?
Tx?
Common in overweight adults over 40
Treated with exercise, meal planning and anti diabetic drugs, may include insulin
Increasingly diagnosed in adolescents and young people
What’s more common, type 1 or 2 DM?
type 2
Cause of Type II DM?
may result from impaired insulin secretion, peripheral insulin resistance, increased basal hepatic glucose production obesity, hormonal contraceptives, pregnancy, insulin antagonists i.e. phenytoin over the counter regulatory hormones
From class: body may just be too big, [pancreas can’t produce enough insulin for it}
Contraceptives + pregnancy affects sugar levels
Type I cause?
autoimmune disease strongly associated with leukocyte antigens DR3 and DR4. May be associated with certain viral infections
T/F Glucagon secretion is inhibited by increasing glucose levels with or without insulin
F - ONLY when insulin is present
DKA and HHS occur in environment where there is a lack (relative or absolute) of insulin so that glucagon cannot be turned off thereby increasing the blood glucose further.
How do DKA + insulin differ in terms of insulin secretion + how does this affect acid involved?
DKA – no insulin therefore gluconeogenesis and lipolysis
Production ketone bodies (acetone breath) and ketoacidosis (can be severe)
HHS – insulin still present therefore gluconeogenesis and lipolysis mainly inhibited
Ketones mild/absent and pH normal/mild
Is pH abnormal in HHS? How is fluid loss affected?
no ketones and normal pH but typically greater fluid loss
Causes of DKA/HHS?
Usually a stressful event that causes the release of glucagon, cortisol and catecholamines:
- Infection
- MI
- Treatment errors with insulin
- Diarrhea and vomiting
- Stroke
- Trauma
- Pancreatitis
- Unknown etiology
How does stress r/t glucose levels?
Acute Stress –> hormone release including counter regulatory hormones (corticosteroids, catecholamines)
All attempt to increase glucose further to deal with the stress –> fight or flight) –> All worsen an already high blood glucose level
Signs + symptoms of DKA?
acetone breath, ketones in urine, acidosis, confusion/coma all from ketone production
Kussmaul breathing (deep rapid breathing) and abdominal pain from metabolic acidosis
polyuria from high glucose (osmotic diuresis) glc in urine
polydipsia and tachycardia from dehydration
sodium may be increased/ decreased or normal
Hypotension from dehydration
Polyuria, Polydipsia, Blurred vision, Weakness, Headache, Orthostatic hypotension, frank hypotension (volume depletion),anorexia, nausea, vomiting, abd pain, acetone breath, hyperventilation, mental status changes
S+S of HHS
HHS – negative ketone breath and ketone in urine because no ketone bodies produced
stupor/coma from hyperosmolar state
fluid imbalance dehydration, high sodium
polyuria from high glucose (osmotic diuresis) glc in urine
polydipsia and tachycardia from dehydration
Hypotension from dehydration
What is Kussmaul breathing?
KUSSMAUL RESPS = trying to blow off CO2; DEEP and FAST breathing