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Endocrinology > Diabetes Mellitus Part 2 > Flashcards

Diabetes Mellitus Part 2 Flashcards

1
Q

Diabetes is a

A

disease of hyperglycemia due to insulin loss or resistance

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2
Q

T1DM usually seen in

A

young and lean pts

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3
Q

T2DM is usually seen in

A

older & overwt/ obese pts
pts with Fhx

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4
Q

DM dx

A

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

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5
Q

Regardless of type of DM, management starts with

A

diet and exercise

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6
Q

Type 1 DM is when

A

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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7
Q

T1DM pathophysiology

A

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

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8
Q

T1DM presentation

A

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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9
Q

T1DM workup/dx

A

random serum glucose
fasting glucose
glucose tolerance testing
urinalysis

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10
Q

T1DM treatment

A

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

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11
Q

T1DM treatment: Insulin

A

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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12
Q

T1DM glycemia control HgA1c should be

A

less than or equal to 7 for most

individualized on basis of age, comorbidities, duration of disease

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13
Q

T1DM treatment - Insulin adverse reactions

A

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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14
Q

DKA can result in

A

Cerebral Edema

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15
Q

DKA diagnostic criteria

A

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

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16
Q

T1DM Complications - DKA IV fluid management

A

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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17
Q

T1DM Complications - DKA steps 1-3:

A

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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18
Q

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

A

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

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19
Q

once levels achieved, oral fluids tolerated, start –>

A

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

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20
Q

Leading cause of death in children presenting in DKA

A

Cerebral Edema

21
Q

Suspect Cerebral Edema with DKA when pt presents with

A

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

22
Q

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

A

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

23
Q

What is insulin based off?

A

wt
0.5 units/kg/day

24
Q

The more units per mL the ______ it will be absorbed

A

slower

25
Q

How is insulin usually administered?

A

SubQ
usually in the abdomen

26
Q

T2DM etiology

A

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

27
Q

T2DM is when

A

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

28
Q

Hyperglycemia may cause

A

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

29
Q

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

A

4-7 years

30
Q

What are two determinants of insulin resistance

A

obesity
wt gain

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

31
Q

T2DM risk factors

A

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

32
Q

DKA provocation

A

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

33
Q

Signs and symptoms of DM

A

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

34
Q

DM diagnostic criteria:

A

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

35
Q

Pre-diabetic dx criteria:

A

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

36
Q

_______ is not recommended for diagnosing T1DM or gestational DM

A

HbA1c

37
Q

T2DM initial pharmaceutical treatment/management:

A

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

38
Q

T2DM management:

A

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

39
Q

Maturity Onset DM of Youth (MODY) is

A

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)

40
Q

MODY treatment

A

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

41
Q

Hyperosmotic Hyperglycemic Nonketotic Syndrome (HHNK) is

A

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

42
Q

Treatment of HHNK

A

IV saline solution and insulin

43
Q

Complications of HHNK

A

coma
seizures
death

44
Q

Presentation of HHNK

A

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

45
Q

Unlike DKA, HHNK can lead to

A

focal or generalized seizures and transient hemiplegia may occur

46
Q

HHNK dx

A

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

47
Q

Treatment for HHNK

A

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)

48
Q

T2DM final treatment plan

A

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

Endocrinology (5 decks)

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