Pratap sagar Tiwari, MD, Internal Medcine,

Lecturer, NMCTH

UNDERSTANDING DIABETES..PART 2

DIABETES KETOACIDOSIS

•RECAP

CASE SUMMARY

• A 30 yrs old M was brought in ERD in the state of unconsciousness.

(Note: Coma is a symptom, not a diagnosis.)

Pic taken from http://censorbugbear-reports.blogspot.com/2010/03/shocking-neglect-of-comatose-patient-at.html

RECAP

• Causes of patient in state of coma

• Definition of terms related to consciousness

• Causes of Coma in a Diabetic Patient

• Insulin Synthesis/ Secretion

• Regulation of Glucose hemostasis

• Response of hypoglycemia in normal & DM

• Hypoglycemia & symptoms

DKA

• DKA is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 DM, but it is not uncommon in some patients with type 2 DM.

• This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.

Hyperglycemia Ketoacidosis

DKAInsulin def/ resistance

Inhibition of “insulin inhibition of Glucagon”

↑ Glucagon

↑ fat/muscle breakdown

↑ Hepatic gluconeogenesis

↑ delivery of gluconeogenetic precursors to Liver

↑ Glycerol/ Alanine

Glycosuria

↓ Glucose excretion

↓ GFR

Osmotic Diuresis

Volume Depletion

↑ Blood GLucose

Action of Insulin:

↑ utilisation of peripheral glucose in skeletal muscle ↑ Blood Sugar

XInsulin↓/ Resistance

(Note: Insulin resistance is a condition in which cells fail to respond to the normal actions of the hormone insulin. The body produces insulin, but the cells in the body become resistant to insulin and are unable to use it as effectively, leading to hyperglycemia.)

Insulin def/ resistance

Glucose utilization is impaired

Alternate source of Energy : KETONES

↑ Lipolysis

TG

FFA

Normally

Plus increased catecholamines

DEVELOPMENT OF KETOACIDOSIS

• The development of ketoacidosis requires a specific alteration in hepatic metabolism so that free fatty acyl CoA can enter the mitochondria, where conversion to ketones occurs.

• Mitochondrial entry is regulated by the cytosolic enzyme carnitine palmitoyltransferase I (CPT I), the activity of which varies inversely with malonyl CoA [1].

• Glucagon decreases the production of malonyl CoA, thereby increasing CPT I activity and ketogenesis [2].

• Insulin does not appear to directly affect hepatic ketogenesis [3].1. McGarry JD, Woeltje KF, Kuwajima M, Foster DW. Regulation of ketogenesis and the renaissance of carnitine palmitoyltransferase. Diabetes Metab Rev 1989; 5:271.

2. Cook GA, Nielsen RC, Hawkins RA, et al. Effect of glucagon on hepatic malonyl coenzyme A concentration and on lipid synthesis. J Biol Chem 1977; 252:4421.

3. Miles JM, Haymond MW.. Effects of free fatty acid availability, glucagon excess, and insulin deficiency on ketone body production in postabsorptive man. J Clin Invest 1983; 71:1554.

NOTE

• Moderate insulin deficiency, as seen in HHS, might be associated with sufficient insulin to block lipolysis (and therefore ketoacid formation) but not enough to promote glucose utilization and prevent the development of hyperglycemia [1].

1. Hillman K. Fluid resuscitation in diabetic emergencies--a reappraisal. Intensive Care Med 1987; 13:4.

BREATHING PATTERNS: CHEYNE-STOKE

• characterized by periods of respirations during which the tidal volume starts shallow and gets progressively deeper, and then gets progressively shallower.

• This shallow-deep-shallow pattern is followed by periods of significant apnea that can last up to 30 seconds or longer, then the cycle starts over.

BIOT’S BREATHING (CLUSTER RESPIRATION)

• A respiratory pattern characterized by periods or “clusters” of rapid respirations of near equal depth or followed by regular periods of apnea.

• damage to the medulla oblongata by stroke (CVA) or trauma.

ATAXIA RESPIRATIONS

• Completely irregular breathing pattern with irregular pauses and increasing episodes of apnea.

• caused by damage to the medulla oblongata secondary to trauma or stroke.

KUSSMAUL’S RESPIRATIONS

• A type of labored or hyperventilation characterized by a consistently deep and rapid respiratory pattern.

• Most of the time a respiratory pattern secondary to a metabolic acidosis is rapid and shallow and a true kussmaul breathing pattern is rarely reached before the acidosis is corrected

APNEUSTIC RESPIRATIONS

• have a prolonged inspiratory phase followed by a prolonged expiratory phase commonly believed to be apneic phases.

• damage to the upper part of the pons

FEATURES OF HYPEROSMOLARITY

• Excessive thirst despite frequently taking water / other liquids

• Continued high level of blood sugar

• Dry and/ or parched mouth

• Frequency of urination increases

• Pulse rate becomes rapid

• Shortness of breath with exertion

• Skin becomes dry and warm and there is no sweating

• Sleepiness and/ or a condition of confusion

http://www.mayoclinic.org/diseases-conditions/diabetic-hyperosmolar-syndrome/basics/definition/con-20026142

END OF SLIDESReferences:

1. Harrison's Principles of Internal Medicine, 18th Edition

2. Davidson Practice of Medicine

3. Uptodate 20.3

4. Standards of Medical Care in Diabetesd 2014. American Diabetes Association. Diabetes Care Volume 37, Supplement 1, January 2014

5. Medscape.com

6. Mercksmanual