IBD and DKA vignettes

Question 1

How does tobacco use affect risk for Crohn’s and ulcerative colitis?

Answer 1

Smokers are at increased risk for Crohn’s disease; former smokers and nonsmokers are at greater risk for ulcerative colitis (cigarette smoking is protective).

Question 2

What is hematochezia?

Answer 2

Blood in the stool/diarrhea?

Question 3

Is hematochezia seen in Crohn’s or UC?

Answer 3

Crohn’s: Rarely. UC: Commonly

Question 4

What is the usual location of Crohn’s and UC?

Answer 4

Crohn’s: almost always in the Ileum. UC: almost always in the rectum

Question 5

What is the pattern in Crohn’s and UC?

Answer 5

Crohn’s: discontinuous (skip lesions). UC: continuous

Question 6

Is Crohn’s or UC found in the upper GI tract?

Answer 6

C: Yes. UC: No

Question 7

Are extra-GI manifestations common in C’s or UC?

Answer 7

Yes. Common in both

Question 8

Are fistulas common in C’s or UC?

Answer 8

Commin C’s. Rare in UC

Question 9

What kind of inflammation is seen in Crohn’s and UC?

Answer 9

C’s: Transmural. UC: Mucosal

Question 10

What kind of extra-intestinal manifestations are seen in IBD?

Answer 10

Lots of -itis. Pleuritis; myocarditis; pancreatitis; arthritis; tendinitis; etc.

Question 11

What is IBD?

Answer 11

General term. Encompasses crohn’s plus UC. Inappropriate inflammatory response to intestinal microbes in a genetically susceptible host

Question 12

What are genetic factors of IBD?

Answer 12

Nucleotide oligomerization domain 2 (NOD2). Interleukin-23�type 17 helper T-cell (Th17) pathway. Autophagy genes

Question 13

What factors could explain the rising prevalence of IBD?

Answer 13

Changes in diet; antibiotic use; Altered intestinal colonization (e.g. the eradication of intestinal helminths); tobacco

Question 14

How is DKA defined?

Answer 14

hyperglycemia; metabolic acidosis; ketonemia/ketonuria. DKA = Diabetes (high blood sugar); Ketones in the blood and urine; Acidosis. Also see potassium derangements and dehydration

Question 15

What is the presentation of a child in DKA?

Answer 15

Polyuria; polydypsia; polydispasia. Thin. Tachycardic. Tachypneic (Kussmaul respirations). Dehydrated. May have nausea and vomiting

Question 16

What cells produce insulin?

Answer 16

Beta cells of pancreas

Question 17

What happens to beta cells in type 1 DM?

Answer 17

Autoimmune process leads to destruction of beta cells and results in insulin deficiency

Question 18

Describe the pathway for insulin release from the beta cells

Answer 18

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.

Question 19

What is the name of the transporter that allows glucose into the Beta cells?

Answer 19

GLUT2 transporter

Question 20

In general what does insulin do?

Answer 20

It is a signal to “lock up” energy. Stimulates uptake of glucose and triglycerides while promoting synthesis of fats; proteins; and glycogen

Question 21

What is the action of insulin in the liver?

Answer 21

It signals for + glucose uptake + glycogen synthesis + lipogenesis - gluconeogenesis - ketogenesis

Question 22

What is the action of insulin in the muscle?

Answer 22

Triggers + glucose uptake + glycogen synthesis + protein synthesis

Question 23

What is the action of insulin in adipose tissue?

Answer 23

Triggers + glucose uptake + triglyceride uptake + lipid synthesis

Question 24

What are the two cardinal sins in DKA management?

Answer 24

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).

Question 25

What causes the acidosis seen in DKA?

Answer 25

Result of beta oxidation of fatty acids. Process generates H+ and ketone bodies. To compensate for the excess acid the body increases respiratory volume and rate to hasten the elimination of carbon dioxide. Takes advantage of this equation H+ + HCO3- H2CO3 H20 + CO2

Question 26

What causes the dehydration seen in DKA?

Answer 26

Largely the result of osmotic diuresis 2ndary to hyperglycemia.

Question 27

What process leads to an overall depletion of potassium in Pts in DKA?

Answer 27

As Pt fights dehydration the body compensates by holding onto sodium more avidly. Increased sodium conservation comes at the expense of potassium. A lot of potassium is lost in the urine and Pts in DKA are depleted in the total body potassium.

Question 28

Why can Pts in DKA still present with hyperkalemia? What happens as they are treated with insulin?

Answer 28

Acidosis leads to increased H+ ions in the cells; so potassium leaves the cell. This is why Pts in acidosis can have hyperkalemia. As they are treated with insulin the K+ will return to the cell and may then reveal their hypokalemia.

Question 29

What is the leading cause of death with pediatric DKA?

Answer 29

Cerebral edema

Question 30

What process may lead to cerebral edema as you rehydrate Pts in DKA?

Answer 30

Rapidly decreased blood osmolarity may cause osmosis across the BBB

Question 31

How can cerebral edema be prevented?

Answer 31

Slowly rehydrating and not using too hypotonic IV fluid

Question 32

How does cerebral edema present?

Answer 32

Mental status changes; headache; Cushing’s triad; fixed/dilated pupils.

Question 33

What is treatment for cerebral edema?

Answer 33

Raise the osmolality of the blood