IBD and DKA vignettes Flashcards
How does tobacco use affect risk for Crohn’s and ulcerative colitis?
Smokers are at increased risk for Crohn’s disease; former smokers and nonsmokers are at greater risk for ulcerative colitis (cigarette smoking is protective).
What is hematochezia?
Blood in the stool/diarrhea?
Is hematochezia seen in Crohn’s or UC?
Crohn’s: Rarely. UC: Commonly
What is the usual location of Crohn’s and UC?
Crohn’s: almost always in the Ileum. UC: almost always in the rectum
What is the pattern in Crohn’s and UC?
Crohn’s: discontinuous (skip lesions). UC: continuous
Is Crohn’s or UC found in the upper GI tract?
C: Yes. UC: No
Are extra-GI manifestations common in C’s or UC?
Yes. Common in both
Are fistulas common in C’s or UC?
Commin C’s. Rare in UC
What kind of inflammation is seen in Crohn’s and UC?
C’s: Transmural. UC: Mucosal
What kind of extra-intestinal manifestations are seen in IBD?
Lots of -itis. Pleuritis; myocarditis; pancreatitis; arthritis; tendinitis; etc.
What is IBD?
General term. Encompasses crohn’s plus UC. Inappropriate inflammatory response to intestinal microbes in a genetically susceptible host
What are genetic factors of IBD?
Nucleotide oligomerization domain 2 (NOD2). Interleukin-23�type 17 helper T-cell (Th17) pathway. Autophagy genes
What factors could explain the rising prevalence of IBD?
Changes in diet; antibiotic use; Altered intestinal colonization (e.g. the eradication of intestinal helminths); tobacco
How is DKA defined?
hyperglycemia; metabolic acidosis; ketonemia/ketonuria. DKA = Diabetes (high blood sugar); Ketones in the blood and urine; Acidosis. Also see potassium derangements and dehydration
What is the presentation of a child in DKA?
Polyuria; polydypsia; polydispasia. Thin. Tachycardic. Tachypneic (Kussmaul respirations). Dehydrated. May have nausea and vomiting
What cells produce insulin?
Beta cells of pancreas
What happens to beta cells in type 1 DM?
Autoimmune process leads to destruction of beta cells and results in insulin deficiency
Describe the pathway for insulin release from the beta cells
1st glucose enters the cell and undergoes glycolysis which leads to increased ATP. This change closes an ATP-sensitive K+ channel so K+ no longer leaks out of cell. The buildup of K+ depolarizes the membrane which activates a voltage-gated Ca++ channel and leads to Ca++ influx. The increased Ca++ in the cell leads to exocytosis of preformed insulin-containing secretory granules.
What is the name of the transporter that allows glucose into the Beta cells?
GLUT2 transporter
In general what does insulin do?
It is a signal to “lock up” energy. Stimulates uptake of glucose and triglycerides while promoting synthesis of fats; proteins; and glycogen
What is the action of insulin in the liver?
It signals for + glucose uptake + glycogen synthesis + lipogenesis - gluconeogenesis - ketogenesis
What is the action of insulin in the muscle?
Triggers + glucose uptake + glycogen synthesis + protein synthesis
What is the action of insulin in adipose tissue?
Triggers + glucose uptake + triglyceride uptake + lipid synthesis
What are the two cardinal sins in DKA management?
Prematurely stopping the insulin infusion and failing to use enough dextrose to bring the blood glucose slowly into the target range (it is counterintuitive to use dextrose).
