Week 7: Type 1 DM Flashcards by Jay Sandoval

Type 1 DM mechanism

autoantibodies against beta cells of pancreas resulting in loss of insulin secretion

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Course og Type 1 DM

over months to years, β cells are destroyed until they reach a point where a normal blood sugar can’t be maintained

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Describe Islet cell autoimmunity

Type 1 DM is actually T cell mediated and not B cell mediated

People without B cell function can still have Type 1 DM

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What causes Islet cell autoimmunity

Genetics but there also seems to be something else

more Type 1 DM Dxd in the winter months versus summer

more Type 1 DM further from the equator

Low prevalence zone to high prevalence zone increases chances

Cocksakie virus / enterovirus

Molecular mimicry GAD

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How to screen for Islet cell autoimmunity

Historically were detected this way

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Screening for the autoantibodies against β cells

4 listed

GAD autoantibodies (Glutamic acid decarboxylase)
Insulin autoantibodies (only on someone not on insulin yet because if exposed to injected insulin can develop antibodies)
IA-2 autoantibodies (Insulinoma associated antigen)
ZnT8 (Zinc Transporter 8)

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GAD AKA

Glutamic acid decarboxylase

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IA-2 AKA

Insulinoma associated antigen 2

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ZnT8 AKA

Zinc Transporter 8

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Treatment of type 1 DM

mimic the bodies tendency to use glucagon to raise fasting sugars and the insulin for when we are in the fed state

use insulin regimen 1/2 long-acting mimics gradual gluconeogenesis
Short-acting insulin to cover the meals in the fed state

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Basal-Bolus insulin regiments

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Describe the risks of insulin therapy

can be work to maintain proper dosing

Severe hypoglycemia can be life-threatening

Can switch regimens to longer-acting insulins to help prevent spikes or troughs

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Severe hypoglycemia treatment

Rescue Glucagon (injection or new intranasal glucagon powder)

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Acute complications of Type 1 DM

DKA

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DKA AKA

Diabetic Ketoacidosis

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What is DKA?

End-result of an insulin deficiency in the setting of a counterregulatory hormone surge like from pneumonia or from a trauma

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DKA triad

*Classically* All 3 of these things need to be present for a Dx of DKA

Hyperglycemia
Ketosis
Acidosis

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Describe the Mechanism of DKA

deficiency of insulin in the setting of counterregulatory hormone surge

high glucagon, GH, cortisol, catecholamines

increases hormone-sensitive lipase activity leading to FA and glycerol mobilization

glycerol further metabolized to more glucose via gluconeogenesis adding to the already hyperglycemia

FFAs metabolized by the liver to make ketoacids (acetoacetic acid, β-hydroxybutyrate)

This happens very rapidly and the body cannot compensate especially with a deficiency of insulin or insulin signaling

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DKA prevalence

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New Mexico DKA prevelance

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Mortality from DKA

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Who is most likely to die from DKA?

Elderly

And usually not DKA itself but is the precipitating event itself

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Clinical presentation of DKA

sugars pouring out of the kidney and pulling water with it (osmotic diuresis) urinating frequently and very thirsty
malaise, fatigue
NV
Abdominal pain
Altered sensorium in severe cases (altered mental status

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Physical exam of DKA

* Tachycardia * Postural hypotension * Kussmaul respirations (deep irregular breathing) * Fruity breath (acetone) * Abdominal tenderness (can look like acute surgical abdomen or acute pancreatitis)

Diagnostic criteria for DKA

* Glucose High (250 mg/dL) HHS is even higher * pH low (less than 7.3) * bicarb low (less than 18 mEq/L) * Ketones + in the urine or serum

Electrolytes and hydration statues of DKA

Serum K+ can fool because often elevated and it can be caused by a transcellular shift in K+ in the setting of an acidosis (total body K+ can be deficit but appears high in serum)

Precipitating factors of DKA

* Infection * Noncompliance * New-onset DM * MI * Stroke * Trauma * PRegnancy * Pancreatitis * EtOH abuse * Medications (that can cause hormone surge like steroids)

Management of DKA

* IV fluids * Insulin * K+ * Assess for need of HCO3-

IV fluids

Depends on the degree of dehydration (can use pressors if necessary)

Pressors for?

if so depleted their BP is dropping despite fluid level is full can give pressors to increase BP

When blood glucose is below 200

add sugar to the IV fluids (Dextrose) because run the risk of low blood sugar by adding so much fluid if they were fluid depeleted

Key mechanism of DKA

Lipolysis from hormone-sensitive lipase

Insulin administration in DKA

don't target normal blood sugars (target high 150-200) because want to avoid fluid shifts like cerebral edema

K+ administration for DKA

Hold off on K+ and follow it closely because insulin itself will lower K+ When K+ drops to normal range start giving K+ because total body depletion of K+ Unless K+ is low in serum then give fluids and K+ and no insulin

Assess need for HCO3-

if pH is really low no evidence for improved outcomes

Risk of DKA treatment

Cerebral edema from rapid correction of serum osmolality 1% of children with DKA PRevent by targeting higher than normal blood sugars High mortality 40-90%

Cerebral edema clinical manifestations

* Lethargy * seizures * Bradycardia * Respiratory arrest

Chronic Complications of Type 1 DM

microvascular (eyes, nerves, kidneys, etc...) not unique to Type 1 DM

Most frequent cause of new cases of blindness

Diabetic Retinopathy

Diabetic Retinopathy prevalence

Diabetic Retinopathy classification

* Non-proliferative Diabetic Retinopathy * Proliferative Diabetic Retinopathy Macular Edema can occur in proliferative or non-proliferative Diabetic Retinopathy

Non-proliferative Diabetic Retinopathy gross histology

No new blood vessels but abnormal and have hemorrhages hard exudate (lipids) white areas infarcted retina (cotton wool spots) macular edema thickening of the retina fluid has leaked out of the vessels and is accumulating in the retina Proliferative on the bottom (abnormal blood vessels VEGF) in response to hypoperfusion of the retina (hypoxia)