Diabetes Mellitus Part 2 Flashcards by Nicole Quinn

Diabetes is a

disease of hyperglycemia due to insulin loss or resistance

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T1DM usually seen in

young and lean pts

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T2DM is usually seen in

older & overwt/ obese pts
pts with Fhx

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DM dx

fasting plasma glucose (HbA1c*, random glucose, OGTT)

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Regardless of type of DM, management starts with

diet and exercise

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Type 1 DM is when

insulin production is absent due to autoimmune pancreatic beta cell destruction
usually develops in childhood/ adolescence, may develop in adults (latent autoimmune diabetes of adulthood, initially appears like T2DM)

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T1DM pathophysiology

T-cell mediated response resulting in beta-cell destruction (insulitis)

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T1DM presentation

sx hyperglycemia (random glucose > 200)
may present in diabetic ketoacidosis (DKA)
polyuria, polydipsia, dehydration, nausea, unexplained wt loss, weakness, blurry vision

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T1DM workup/dx

random serum glucose
fasting glucose
glucose tolerance testing
urinalysis

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T1DM treatment

insulin induction (lifetime insulin therapy)
electrolyte management
diet/ exercise - consult nutritionist
consult endo

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T1DM treatment: Insulin

dose based on wt
basal insulin (single injection)
Pre-prandial (divided doses given before a meal, each does is determined by estimating carbohydrate content of meal, insulin to carb ratio = 1:20 insulin sensitive to 1:5 insulin resistant)

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T1DM glycemia control HgA1c should be

less than or equal to 7 for most

individualized on basis of age, comorbidities, duration of disease

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T1DM treatment - Insulin adverse reactions

Lipoatrophy - loss of fat at injection site; may allow for incidental intramuscular injection
Hypertrophy - increase in fat mass at site, leads to erratic insulin absorption
Resistance - require larger amounts of insulin to get desired effect, due to antibody formation

need to rotate sites

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DKA can result in

Cerebral Edema

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DKA diagnostic criteria

Diabetic (Glucose > 200)
Ketonuria
Acidosis (pH < 7.3)
venous bicarb < 15

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T1DM Complications - DKA IV fluid management

patient WITH signs of shock (tachycardia, hypotension, poor profusion, AMS) = bolus 2-3 liters of Normal saline -> STAT

patient WITHOUT signs of shock = Normal saline over 1 hour

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T1DM Complications - DKA steps 1-3:

1 - fluid replacement (approx fluid loss 6-9 L in DKA)
2 - electrolyte replacement (correct hypokalemia, if you start insulin therapy before electrolyte replacement you will worsen hypokalemia - cause of morbidity/ mortality from cardiac arrhythmias and resp muscle weakness, correct serum sodium)
3 - insulin drip (GO SLOW, goal is to close anion gap acidosis)

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Once DKA has resolved:
pH >
glucose < or equal to
Bicarb level is > or equal to

pH > 7.3
Glucose < or equal 200 mg/dL
Bicarbonate > or equal to 18 mEq/L

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once levels achieved, oral fluids tolerated, start –>

start insulin regimen that includes intermediate or long-acting insulin AND short or rapid-acting insulin

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Leading cause of death in children presenting in DKA

Cerebral Edema

Suspect Cerebral Edema with DKA when pt presents with

sudden HA with neurological deterioration (altered LOC and Lethargy) - usually within 4-12 hours treatment onset

The ________ the patient the _______ you go (pertaining to insulin)

sicker, slower
no insulin bolus/ lower insulin drip
judicious use of IV fluids

What is insulin based off?

wt
0.5 units/kg/day

The more units per mL the ______ it will be absorbed

slower

How is insulin usually administered?

SubQ usually in the abdomen

T2DM etiology

adult onset or non-insulin dependent DM Glucose intolerance - insulin secretion inadequate to overcome resistance insulin levels are very high, esp early in the disease, later insulin production may fall, further exacerbating hyperglycemia

T2DM is when

hyperglycemia develops when insulin secretion can no longer compensate for insulin resistance

Hyperglycemia may cause

impairment of insulin secretion or desensitize beta cells and cause beta cell dysfunction (glucose toxicity) or both

Changes typically takes years to develop the presence of insulin resistance --> usually ______ years before clinical diagnosis of DM

4-7 years

What are two determinants of insulin resistance

obesity wt gain (adipose tissue functions as an endocrine organ; releases multiple factors that favorable and adversely influence glucose metabolism)

T2DM risk factors

age greater than or equal to 45 overwt or obesity FHx DM PCOS Hx HTN Dyslipidemia Gestational diabetes mellitus

DKA provocation

infection infarction (CVA or MI) iatrogenic surgery intoxication initial onset of dx not good insulin management (gave themselves too little or none at all)

Signs and symptoms of DM

hyperglycemia: polyuria, polydipsia progress to orthostatic hypotension, dehydration (severe dehydration: weakness, fatigue, mental status changes) polyphagia wt loss, n/v, blurred vision, hx of bacterial/ fungal infections

DM diagnostic criteria:

fasting plasma glucose > 126 mg/dL random glucose > 200 mg/dL with sx of hyperglycemia or hyperglycemia crisis 2-hr plasma glucose > 200 mg/dL during 76 g OGTT

Pre-diabetic dx criteria:

FPG > 100-125 mg/dL 2-hr OGTT plasma glucose of 140-199 mg/dL HbA1c 5.7-6.4%

_______ is not recommended for diagnosing T1DM or gestational DM

HbA1c

T2DM initial pharmaceutical treatment/management:

preferred - metformin additional medications are added in stepwise pattern - GLP-1, SGLT2 inhibitors preferred over insulin inless sx hyperglycemia

T2DM management:

Blood Pressure Management if > 120/80 lifestyle management ACE/ARB if > 160/100 add thiazide or dihydropyridine CCB (amlodipine, diltiazem, nifedipine) Lipid Management: statins, Omega 3 fish oils

Maturity Onset DM of Youth (MODY) is

usually seen in adolescents with obesity: Peripheral insulin sensitivity 50% overwt and obese children > 10 years should be screened (include pancreatic autoantibodies to rule out T1DM)

MODY treatment

lifestyle management consider metabolic surgery if fails multidisciplinary team needed: endo, nutrition, behavioral health

Hyperosmotic Hyperglycemic Nonketotic Syndrome (HHNK) is

metabolic complication characterized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness often occurs in T2DM - think 'type 2 DKA'

Treatment of HHNK

IV saline solution and insulin

Complications of HHNK

coma seizures death

Presentation of HHNK

primary sx = altered mental status varies from confusion or disorientation to coma usually extreme dehydration with or without prerenal azotemia, hyperglycemia, hyperosmolality

Unlike DKA, HHNK can lead to

focal or generalized seizures and transient hemiplegia may occur

HHNK dx

blood glucose level - elevated serum osmolarity urine tested for ketones arterial pH usually > 7.3

Treatment for HHNK

IV isotonic saline 15-20 mL/kg/hour Correction of any hypokalemia IV insulin (if potassium is less than or equal to 3.3 mEq/L)

T2DM final treatment plan

routine follow up and lab testing oral agents with/without insulin ACE/ARB (renal vs HTN dosing) Statin (pending ASCVD risk) annual flu shot and pneumonia vaccine