NON-VASCULAR COMPLICATIONS OF DIABETES Flashcards
What is Diabetic Ketoacidosis (DKA)?
What is it characterized by?
3
An absolute insulin deficiency
Potentially fatal if not treated properly
Characterized by a biochemical triad of hyperglycemia, ketonemia, and anion gap metabolic acidosis
(extra glucose in blood is pulling all the fluid out from your cells)
HOw does DKA usually evolve? (onset)
DKA usually evolves rapidly,
over a 24-hour period.
Pathophysiology:
Reduction in what?
Elevation in what? 3
This results in? 3
Reduction in net effective concentration of circulating insulin
Elevation of counter-regulatory hormones
Glucagon
Cortisol
Growth hormone
Hyperglycemia
Osmotic diuresis
dehydration
What causes the ketonuria in DKA?
3 steps
- Insulin deficiency causes the inability to drive glucose into the cells.
- Cell starvation so we have to break down fats for energy instead.
- These fats are converted to ketone and we make too many
PRECIPITATING FACTORS
The most common events associated with DKA?
4
Other less common?
7
- inadequate insulin therapy
- infection
- pneumonia
- urinary tract infection
Severe dehydration Acute major illnesses myocardial infarction cerebrovascular accident pancreatitis New onset type 1 diabetes Drugs that affect carbohydrate metabolism
Diabetic Ketoacidosis (DKA) CLINICAL PRESENTATION
Thirst, polydipsia Polyuria Nausea, vomiting Abdominal pain Weakness Fatigue Anorexia Tachycardia Orthostatic hypotension Poor skin turgor Dry skin and mucous membranes Kussmaul’s respirations Fruity breath (ketones) Altered mental status or coma Hypothermia
Diabetic Ketoacidosis (DKA) Lab findings?
What will be high? 3
What will be low? 2
- Blood glucose 250 - 800
- Serum osmolality normal to high
- Serum K+ high ( >5)
- Serum Na+ normal to low (130-145)
- Serum Bicarb low 12 meq/L
pH
Hyperosmolar Hyperglycemic State (HHS) occurs almost exclusively in what type of pts and why?
Occurs almost exclusively in Type 2 DM
Elderly and physically impaired
Limited access to free water!!
How is HHS distinguished from DKA?
6
- Severe hyperglycemia >600
- Hyperosmolality
- Develops more insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission
- Greater degree of dehydration
- Relative absence of acidosis and ketones
- Mortality rates 5-20%
Hyperglycemia is the constant between HHS and DKA what makes them diiferent according to the medscape chart?
3 things
DKA- hyperlipidemia
HHS- hyperosmolarity
absence of ketogenesis
Hyperosmolar Hyperglycemic State causes?
4
- Catabolic Stress
- Infection
- Non-compliance
- Drugs
Hyperosmolar Hyperglycemic State clinical persentation?
Polyuria Polydipsia Weight loss Vomiting Dehydration Weakness Mental status changes Slower progression Tachycardia Hypotenstion Severe dehydration Dry skin and mucous membranes Extreme thirst
WHat are the neuro signs of HHS?
Neuro signs: Lethargy to coma Sensory impairment Seizures Hyperthermia
Hyperosmolar Hyperglycemic State lab findings:
What will be high? 3
What will be normal? 4
What can this state be complicated by?
Lab findings:
- Blood glucose > 600
- Serum osmolality >320 (too much solute/sugar in the blood)
- Serum Na+ - normal to high (135-145)
- Serum K+ - normal (4-5)
- Serum Bicarb >20 (no acidosis)
- pH > 7.3
- Ketones – negative
Can be complicated by thromboembolic events arising because of the high serum osmolality.
Prognosis less favorable than DKA.
Treatment of DKA:
Initial assessment? 3
After that what are the two things that we do? 2
Initial assessment:
- Airway, breathing, and circulation (ABC) status
- Mental status
- Volume status
- IV fluid and electrolyte replacement
- -Slower rate and greater volume needed for HHS - Insulin therapy
- -Insulin replacement starts after rehydration is in progress
HHS vs DKA differ clinically how?
according to the presence of ketoacidosis and usually the degree of hyperglycemia
Significant overlap between DKA and HHS has been reported in more than one-third of patients
HHS has some insulin although minimal
What biochemical processes are involved with HHS? (what does this lead to?)
What biochemical processes are involved with DKA 1? (what does this lead to? 2)
Glycogenolysis and gluconeogenesis leading to hyperglycemia causing osmotic diuresia and dehydration
Ketone body production leading to hyperglycemia causing decreased alkaline buffer and acidosis
Hypoglycemia as a side effect is more common in what kind of DM?
Type 1, especially those receiving intensive therapy
What are the two kinds of functional hypoglycemia?
Fasting
Postprandial (reactive)
Hypoglycemia causes?
5
- Insulin injections
- Oral hypoglycemic agents
- Gastroparesis
- Hepatic and renal dysfunction
- Malnutrition
Hypoglycemia Clinical Presentation onset:
Neurogenic symptoms from what and what do they cause? 2
Neuroglycopenic symptoms? 5
- catecholamine-mediated/adrenergic
- –Tremor, palpitations, and anxiety/arousal - acetylcholine-mediated/cholinergic
- -sweating, hunger, and paresthesias - cognitive impairment,
- behavioral changes,
- psychomotor abnormalities and,
- at very low plasma glucose,
- seizure and coma
Hypoglycemia Clinical Presentation signs?
4
- Diaphoresis
- Pallor
- Tachycardia
- Elevated blood pressure
Hypoglycemia Unawareness in Diabetes is what?
Absent symptoms of hypoglycemia, which is thought to be the result of reduced sympathoadrenal, predominantly sympathetic neural, responses to a given degree of hypoglycemia
What is Hypoglycemia Unawareness caused by?
3
- Loss of autonomic warning
- –caused by recent antecedent hypoglycemia, prior exercise, or sleep - Autonomic neuropathy
- – so the epinephrine response diminished or lost - Medications
- -Beta-Blockers (lowers HR, blood pressure etc, tired, fatigued)
Management of Hypoglycemia
Outside the hospital? 2
Hospital setting? 2
Oral
SQ/IM
IV
1 amp of D50 (20-50mL)
In the patient without diabetes, the definition of hypoglycemia is based upon the presence of what?
3
Whipple’s triad:
- Symptoms and signs consistent with hypoglycemia
- a low plasma glucose at the time of symptoms
- and resolution of those signs and symptoms after raising the plasma glucose
Surreptitiously Induced Hypoglycemia or Factititious hypoglycemia occurs secondary to what?
What levels will be low and high in this type?
(who will also be like this?)
surreptitious use of insulin or insulin secretagogues. The term factitious hypoglycemia has been used in medical parlance to imply covert human activity.
plasma insulin is high while C-peptide is low
(Type 1)
What levels will be almost undetectable in Type 1 pts?
C-peptide levels
What causes hypoglycemic coma?
How long does it have to last to be called a coma?
Recovery from hypoglycemia may be delayed, because of 1. cerebral edema.
Unconsciousness lasting more than 30 minutes after plasma glucose is corrected is called post-hypoglycemic coma
When does the dawn phenomenon occur?
Between 5 and 9am
Counter-regulatory hormones released
How to tell the difference between Dawns and Somogyi?
if the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect.
If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it’s likely the dawn phenomenon.
Although part of a spectrum of diabetic complications DKA and HHS primarily differ according to what?
the presence of ketoacidosis and the degree of hyperglycemia.
Neurologic complications, related to higher glucose levels and serum osmolality, are more common which, HHS or DKA?
HHS
The triad of DKA consists of what?
hyperglycemia, anion gap metabolic acidosis, and ketonemia.
A precipitating event can usually be identified in patients with DKA or HHS. The most common are what? 2
The initial evaluation of patients with hyperglycemic crises should include assessment of what?
3
- infection or
- inadequate insulin therapy.
- cardiorespiratory status,
- volume status, and
- mental status.
