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PSBIM > Endocrinology: Diabetes Mellitus > Flashcards

Endocrinology: Diabetes Mellitus Flashcards

1
Q

Type of DM where onset of hyperglycemia is usually <25 yo or neonatal period (onset <6 months of age), AD inheritance, Impaired insulin secretion

A

Maturity-onset diabetes of the young (MODY) and monogenic diabetes –>

MODY-associated genes are an uncommon (<5%) cause of type 2 DM

Genetic defects of b cell devt or function 
Mutations:
MODY 1 - HNF-4a
MODY 2 - Glucokinase 
MODY 3 - HNF-1a
MODY 4 - panc. and duo. homeobox
MODY 5 - HNF-1b, NeuroD1

*HNF (Hepatocyte nuclear transcription factor) - LIVER, ISLETS, KIDNEY

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2
Q

Diseases where islets are damaged by 1° pathologic process originating in pancreatic exocrine tissue causing DM

A

CF (Cystic Fibrosis), Chronic Pancreatitis

Other diseases of exocrine pancreas:
Pancreatectomy
Neoplasia
Hemochromatosis
Fibrocalculous Pancreatopathy
Mutations is carboxyl ester lipase
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3
Q

Endocrinopathies involving hormones that antagonize insulin action causing DM

A 
Cushing's 
Hyperthyroidism
Acromegaly
Somatostatinoma
Pheochromocytoma
Aldosteronoma
Glucagonoma
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4
Q

Acute-onset Type 1 DM that may be related to viral infection of the islets

A

Fulminant Diabetes

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5
Q

Gestational DM is glucose intolerance developing during ___ - ___ trimester of pregnancy

Insulin resistance related to metabolic changes of pregnancy: increased insulin demands

A

2nd to 3rd trimester

35-60% risk to develop DM in the next 10-20 years. Screen at least every 3 YEARS.

Child: inc. risk to develop Met. syndrome & T2 DM later

1st trimester: Preexisting pregestational DM

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6
Q

In Asia, prevalence of DM increasing rapidly, phenotype, onset: (4 answers)

A

lower BMI
younger age
greater visceral adiposity
reduced insulin secretory capacity

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7
Q

Diseases with genetic defects in insulin action

A

Type A Insulin resistance
Rabson-Medenhall syndrome
Leprechaunism
Lipodystrophy

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8
Q

Drug or chemical induced hyperglycemia

multiple answers

A

(aaabc – depp – gh – mn – tv)

antipsychotics
asparaginase
a-interferon
B-adrenergic agonists
calcineurin inhib (tacrolimus, cyclosporine)

diazoxide
epinephrine
pentamidine
protease inhibitors (ritonavir, saquinavir..)

glucocorticoids
hydantoins

mTOR inhibitors (everolimus..)
nicotinic acid

thiazides
vacor (a rodenticide)

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9
Q

Infections that can cause DM

A

Congenital Rubella
CMV
Coxsackie

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10
Q

immune-mediated beta cell destruction
lean, ketosis-prone

↑ risk of autoimmune do
(autoimmune thyroid disease, adrenal insufficiency, pernicious anemia, celiac dse, vitiligo)

A

Type 1 DM

  • genetic + envt’l + immunologic
  • African American and Asian
  • insulin deficiency, insulin-requiring at onset
  • common before 20 yo, onset <30yo
  • islet-directed autoimmunity
  • triggered by infectious or envt’l stimulus that inc. insulin requirements &raquo_space; autoantibodies against beta cells antigen appear&raquo_space; loss of insulin secretion&raquo_space; DM
  • unknown non-immune mechanisms
  • ketosis-prone
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11
Q

Genetic syndromes assoc. with DM

A

Down
Turner
Klinefelter

Friedreich ataxia
Huntington chorea
Prader-Willi
Myotonic dystrophy

Porphyria
Laurence-moon-biedl
Wolfram

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12
Q

Glucose >70 mg/dl stimulate insulin synthesis →
Glucose transport into beta cell by GLUT2

For Normal Glucose Homeostasis, give the values for:
FPG
2-hr PG
HbA1C

A

Normal Glucose Homeostasis

FPG: <5.6 mmol/L *18 (100 mg/dl)
2-hr PG: <7.8 mmol/L (140 mg/dl)
HbA1C: <5.6%

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13
Q

Impaired Glucose Homeostasis cause increased risk of DM (Intermediate Hyperglycemia, Prediabetes)

Give the values for IFG, IGT:
FPG
2-hr PG
HbA1C

A

Impaired Glucose Homeostasis

FPG: 6.6-6.9 mmol/L *18 (100-125 mg/dl)
2-hr PG: 7.8-11 mmol/L (140-199 mg/dl)
HbA1C: 5.7% - 6.4%

ANNUAL monitoring: IFG, IGT, HbA1c of 5.7–6.4%

Transition from IGT to DM triggered by inc. insulin reqt:
Puberty, Infections

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14
Q

Criteria for diagnosing Diabetes Mellitus

In the absence of unequivocal hypergly or acute metab decompensation, repeat testing on a diff. day to confirm

A

Symptoms of Diabetes (polyuria, polydipsia, weight loss) plus:

FPG: >/= 7 mmol/L (126 mg/dl) OR
RPG: >/= 11 mmol/L (200mg/dl) OR
2-hr PG: >/= 11 mmol/L (200mg/dl) OR
HbA1C: >/= 6.5%

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15
Q

Screening for DM for all individuals > 45yo every ___ years

A

> 45yo - every 3 years, use FPG or HbA1C

Earlier if overweight (BMI >/= 25kg/m2) and have 1 addtl risk factor

Do ANNUAL screening for Distal Symmetric Polyneuropathy starting at time of diagnosis

For Autonomic Neuropathy,

  • 5 years after diagnosis of T1 DM
  • at time of diagnosis for T2 DM
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16
Q

Risk Factors for DM

Insulin resistance → Insulin secretory defect → Inadequate insulin → DM

Latinos: insulin resistance
Asians: beta cell dysfunction
Obese: ketosis-prone

A
  1. Fam hx (parent or sibling with T2 DM)
    T2 stronger genetic comp. than T1
  2. Race (African Am, Latino, Native Am, Asian-Am, PI)
  3. Overweight (BMI >/= 25, >/= 23 if Asian)
  4. Physical Inactivity
  5. GDM
  6. IFG, IGT or HbA1c 5.7-6.4
  7. HPN or cardiovasc dse
  8. HDL <35 mg/dl, Trigly >250 mg/dl
  9. PCOS
  10. Acanthosis nigricans
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17
Q

Most Important regulator of Glucose is INSULIN:
50% secreted to portal circulation, degraded by liver
50% enters systemic circulation, bind to receptors → stimulate tyrosine kinase → receptor autophosphorylation → → GLUT4 glucose uptake by skeletal muscle and fat

Marker of Endogenous Insulin secretion

A

C-Peptide

Other regulators of glucose other than Insulin:
neural input
metab signals
hormones (glucagon)

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18
Q

Rate-limiting step that controls glucose-regulated insulin secretion

A

Glucose phosphorylation by GLUCOKINASE

ATP produced during Glycolysis 
→ inhibit ATP-sensitive K channel 
→ beta cell membrane depolarization 
→ influx of Ca 
→ insulin secretion
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19
Q

Food induces release of these hormones from GIT neuroendocrine L cells (or from intraislet production from alpha cells), that bind specific receptors on beta cell to stimulate/amplify glucose-stimulated insulin secretion through cyclic AMP production.

They also suppress glucagon production and secretion.

*only when blood glucose is above fasting

Most potent is ________.

A

Incretins

Most potent incretin: GLP-1 (Glucagon-like peptide)

  • from L cells in SI
  • stimulate insulin when blood glucose is above fasting level

Other incretin: GIP glucose-dependent insulinotropic peptide

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20
Q

Fasting state vs Postprandial

A

FASTING

  • Low Insulin; Glucagon release from pancreatic a cells
  • Glycogenolysis
  • Hepatic Gluconeogenesis
  • Mobilization of stored precursors: aa, ffa (Lipolysis)
  • Reduce glucose uptake in skeletal muscle and fat

POSTPRANDIAL / FED

  • Rise in Insulin, fall in Glucagon
  • Carbohydrate and fat and protein synthesis
  • Utilization by skeletal muscle via GLUT4 (insulin-stimulated transport)

BRAIN: utilize glucose insulin-independent

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21
Q

Type1 Pathophysiology

abnormalities in cellular and humoral immunity

A
  1. islet cell autoantibodies
  2. activated lymphocytes in the islets, peripancreatic LD and systemic circulation
  3. T lymphocyte proliferation when stimulated with islet proteins
  4. cytokine release within the insulitis (TNFa, interferon y, IL1) – beta cells particularly susceptible
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22
Q

Pathologic changes in Type 1 DM:

type of cell that infiltrates islets

A

lymphocytic infiltration of pancreatic islets (insulitis), peripancreatic LN, systemic circulation
(T lymphocytes)

abates after destruction of beta cells, atrophy of islets

cytokines within the insulitis
TNF a, IFNy, IL1 → Beta cell death

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23
Q

Marker of autoimmune process of Type 1 DM?

A

Islet cell autoantibodies

of ICA = Inc risk of DM

ICA positivity:
New onset T1 DM: >85%
Newly diagnosed T2 DM: 5-10%
GDM: <5%
1st degree rel. of T1 DM: 3-4%

ICA + impaired insulin secretion after IV GT: >50% risk of devt of T1 DM within 5yrs

children with multiple ICA, 70% developed T1 DM after 10years, 80% after 15years

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24
Q

Environmental triggers for T1 DM

A 
Viruses: Coxsackie, Rubella, Enteroviruses
Early exposure to bovine milk proteins
Nitrosourea compounds
Vit D deficiency
environmental toxins
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25
Q

Metabolic abnormalities in T2 DM?

  1. Amyloid deposition
  2. Lipotoxicity worsen islet function
  3. ↓ Beta cell mass
  4. Hepatic steatosis = NAFLD = Dyslipidemia
A

↓ Maximum glucose utilization = Postprandial Hypergly

↑ Hepatic glucose output = ↑ FPG

Accelerated atherosclerosis

Central of visceral obesity = ↑ FFA and adipokines = iIsulin resistance

↓ production of adiponectin (insulin-sensitizing peptide) = hepatic insulin resistance

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26
Q

Components of Metabolic Syndrome

Feature:
Acanthosis nigricans
Hyperandrogenism (hirsutism, acne, oligomen.)

A 
Insulin resistance
Hypertension + accelerated CV disease
Dyslipidemia ↓ HDL ↑ TG
Central or visceral adiposity
T2 DM, IFG or IGT
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27
Q

Syndromes of Severe Insulin resistance in adults

Type A vs Type B

A

hyperandrogenism
severe hyperinsulinemia

Type A
young, obese women
undefined defect in the insulin-signaling pathway

Type B
middle-aged women
autoimmune disorders
autoantibodies directed at insulin receptor, may block insulin-binding or stimulate the receptor = intermittent hypogylcemia

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28
Q

Aside from intensive lifestyle changes (diet and exercise), what can prevent or delay DM

A

Metformin, by 31% compared to placebo

Consider giving to those with IFG, IGT, at high risk of progression to DM:
< 60 yo
BMI >35
GDM hx

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29
Q

Glucokinase gene mutation –> altered set point for insulin secretion –>
higher glucose levels required to elicit insulin secretory response

Mild to moderate but stable hyperglycemia
Does not respond to OHA

A

MODY 2

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30
Q

HNF-1a mutation

Progressive decline in glycemic control but may respond to SU

A

MODY 3

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31
Q

Mutation in the transcription factor ____ : most common cause of pancreatic agenesis

A

GATA6

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32
Q 
Type of DM
onset >30yo
>/= 80% obese, visceral or central (hip-waist ratio)
elderly may be lean
initially not insulin-requiring

presence of other assoc. conditions (HPN & CV disease, dyslipidemia, PCOS, insulin resistance)

PCOS –> inc risk for t2 dm independent of effects of obesity

A

Type 2 DM

  1. genetic susceptibility: transcription factor 7–like 2 gene
    polymorphisms: peroxisome proliferator–activated receptor γ, inward rectifying potassium channel, zinc transporter, IRS, and calpain 10
  2. environmental factors -obesity, poor nutrition, and physical inactivity
  3. increased or reduced birth weight
  4. children of GDM moms
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33
Q

Rare variant caused by mutations in pancreatic and duodenal homeobox 1, a transcription factor that regulates pancreatic devt and insulin gene transcription

inactivating mutations: pancreatic agenesis heterozygous mutations: DM

A

MODY 4

34
Q

Complications related to CHRONIC hyperglycemia typically appear during the ____ decade of hyperglycemia

A

2nd decade

Complications secondary to ACUTE hyperglycemia while occur at any stage of the disease

Those with undetected T2 DM may present with chronic complications at the time of diagnosis

35
Q

Symptoms of hyperglycemia

A

polyuria
polydipsia
weight loss

fatigue
weakness
blurry vision (results from changes in the water content of the lens, resolves as hyperglycemia is controlled

frequent superficial infections: vaginitis, fungal skin infections
slow healing of lesions after minor trauma

36
Q

Once insulin is secreted into the portal venous system, 50% is degraded by the

A

liver.

Unextracted insulin enters systemic circulation and binds to receptors on target sites –> stimulate intrinsic TK activity –> receptor autophosphorylation –> intracellular signaling –> mitogenic/metab effect of insulin

e.g. activation of PI-3-kinase = translocation of GLUT4 to cell surface –> glucose uptake by sk. muscle and fat

activation of other signaling pathways = glycogen synthesis, protein synthesis, lipogenesis

37
Q

Uncommon forms of immune-mediated diabetes include.. (2 answers)

A

Stiff person syndrome

anti-insulin receptor antibodies

38
Q

fasting hyperglucagonemia
hyperglucagonemia in the post-prandial state
impaired glucagon response to hypoglycemia

A

alpha cell dysfunction

39
Q

honeymoon phase in T1 DM in the first 1-2years

A
  • fleeting phase of endogenous insulin prod from residual beta cells
  • glycemic control is achieved with modest doses of insulin or insulin not needed

– sometimes 70-80% beta cell mass at presentation of T1 DM but variable

40
Q

The concordance of T2 DM in identical twins is ___% - ___%

A

T1 DM 40-60%
T2 DM 70-90%

Both parents with T2 DM: 40% risk in offspring

41
Q

The concordance of T1 DM in identical twins is ___% - ___%

A

T1 DM 40-60%

T2 DM 70-90%

42
Q

Atypical Ketosis-prone T2 DM presents with DKA but no autoimmune markers, treat with ____

A

Ketosis-prone T2 DM presents with DKA but no autoimmune markers, treat with OHA, NOT Insulin

43
Q

Major susceptibility gene for T1 DM is located in the _____

A 
HLA region on Chromosome 6
- contains genes that encode class II MHC (major histocompatibility complex) molecules --> present antigen to helper T cells --> initiate immune response

Polymorphisms in the HLA complex account for 40-50% of genetic risk of developing T1 DM

Most with T1 DM have HLA DR3 or DR4 haplotype
DQA10301 DQB10302 DQB1*0201 strongly associated, but most with it do not develop DM

44
Q

What is the % risk of developing Type 1 DM among relatives?

A

3-4% risk if parent has T1 DM
5-15% risk in a sibling

Tenfold increase risk to develop T1 DM in relatives

75% do not have first-degree relative with T1 DM

45
Q

pancreatic islets with modest infiltration of lymphocytes

A

Insulitis

Once beta cells desytroyed, inflammation abates and islets become atrophic

46
Q

mechanisms of beta cell death

A

not known

may involve

  • formation of nitric oxide metabolites
  • apoptosis
  • direct CD8+ T cell cytotoxicity
47
Q

islet destruction is mediated by _____

Thus, increased emphasis has now been placed on interventions earlier in the disease course (i.e., during Stage 1 and 2 disease

A

T lymphocytes

NOT islet autoantibodies

  • do not react with cell surface of islet cells
  • not capable of transferring DM to animals

Efforts to suppress the autoimmune process ineffective or only temporarily effective in slowing beta cell destruction

48
Q

Stages of T1 DM

intervene earlier in the disease course (i.e., during Stage 1 and 2 disease

A

Stage 1 : development of two or more islet cell autoantibodies / normoglycemia

Stage 2 : continued autoimmunity / dysglycemia

Stage 3 : hyperglycemia that exceeds the diagnostic criteria for the diagnosis of diabetes

49
Q

Pancreatic islet molecules targeted by the autoimmune process

autoantigens not beta cell–specific

autoimmune process directed at one beta cell > spreads to other islet molecules > secondary autoantigens > modified proteins or “neoantigens” that serve as additional immune targets

A
  • proinsulin
  • insulin
  • glutamic acid decarboxylase (GAD)
  • biosynthetic enzyme for the neurotransmitter GABA)
  • ICA-512/IA-2 (homology with tyrosine phosphatases)
  • beta cell–specific zinc transporter (ZnT-8)
50
Q

NO intervention have delayed or prevented DM

New-onset T1 DM: ________ slowed decline in C-peptide levels

A

anti-CD3 monoclonal antibodies

51
Q

If

both parents have type 2 DM, the risk approaches __ %

A

If

both parents have type 2 DM, the risk approaches 40 %

52
Q

Pathophysiology of T2 DM

A
  1. impaired insulin secretion
  2. insulin resistance 3. excessive hepatic glucose production
  3. abnormal fat metabolism
  4. systemic low-grade inflammation
53
Q

the decreased ability of insulin to act effectively on target tissues (muscle, liver, and fat)

prominent feature of type 2 DM, results from genetic susceptibility and obesity

A

Insulin resistance: impairs glucose utilization

Insulin dose-response curves : rightward shift

reduced sensitivity
reduced maximal response
decrease in max glucose utilization (30–60% lower than in normal individuals)

54
Q

Increased hepatic glucose output = increased ___

decreased peripheral glucose utilization = ___

A

Increased hepatic glucose output = increased FPG

decreased peripheral glucose utilization = postprandial hyperglycemia

55
Q

In addition to regulating body weight, appetite, and energy expenditure, _____ also modulate insulin sensitivity.

A

In addition to regulating body weight, appetite, and energy expenditure, adipokines also modulate insulin sensitivity. = insulin resistance in skeletal muscle and liver

56
Q

Dyslipidemia found in type 2 DM

A

HIGH triglycerides, LDL

LOW HDL –> retention leads to liver steatosis –> NAFLD

57
Q

Metabolic syndrome, the insulin resistance syndrome, and syndrome X

A
  1. insulin resistance
  2. type 2 DM or IGT/IFG
  3. hypertension
  4. accelerated cardiovascular disease
  5. dyslipidemia (decreased HDL and elevated triglycerides)
  6. central or visceral obesity
58
Q

physical features of insulin resistance

A
  1. acanthosis nigricans

2. hyperandrogenism: hirsutism, acne, oligomenorrhea

59
Q

heterogeneous disorders characterized by selective loss of adipose tissue, leading to severe insulin resistance and hypertriglyceridemia

A

Lipodystrophies

inherited or acquired

60
Q

Diabetes Prevention Program (DPP)

A

diet and exercise for 30 min/day 5x/week
delayed the development of type 2 DM by 58%

metformin prevented or delayed diabetes by 31% compared to placebo

61
Q

This drug should be considered in individuals with IFG and IGT who are at very high risk for progression to DM (<60 years, BMI ≥35 kg/m2, history of GDM)

A

Metformin

62
Q

HNF-1b mutation

  • progressive impairment of insulin secretion, insulin resistance
  • require insulin treatment
  • minimal response to sulfonylureas
A

MODY 5
- have other abnormalities: renal cysts
mild pancreatic exocrine insufficiency
abnormal liver function tests

63
Q

Homozygous glucokinase mutations cause a severe form of ______, WHILE mutations in mitochondrial DNA are associated with diabetes and deafness

A

neonatal diabetes

64
Q

mutations identified in the coding sequence of the insulin gene have been found to interfere with proinsulin folding, processing, and bioactivity

A

Mutant Ins-gene- induced Diabetes of Youth (MIDYs)

65
Q

complications related to related to chronic hyperglycemia typically begin to appear during

A

second decade of hyperglycemia

66
Q

phenotypic appearance of type 2 DM, do not have absolute insulin deficiency but have autoimmune markers (GAD and other ICA autoantibodies) suggestive of type 1 DM

A

latent autoimmune diabetes of the adult

<50
thinner
personal or family history of other auto-immune disease
more likely to require insulin treatment within 5 years

67
Q

type of DM, have associated defects such as deafness, pancreatic exocrine disease

A

type 3c DM

68
Q

Ketones, an indicator of DKA, should be measured in individuals with type 1 DM when the plasma glucose is ___

Serum ketones are usually positive at serum dilution of ≥1:8

A

> 13.9 mmol/L (250 mg/dL), during a concurrent illness, or with symptoms such as nausea, vomiting, or abdominal pain.

Blood measurement of β-hydroxybutyrate preferred (synthesized at a threefold greater rate) over

urine testing with nitroprusside tab (measure only acetoacetate and acetone, captopril or penicillamine may cause false-positive)

69
Q

disorders associated with absolute or relative insulin deficiency, volume depletion, acid-base abnormalities

A

DKA and HHS

cytokines and CRP elevated

70
Q 
Glucose: 13.9–33.3 (250–600)
Na: 125–135
K: N to H / Crea: Sl. H
Mg: N / Cl: N / Phos: N
Osmolality: 300-320
Plasma Ketones: ++++
HCO3: <15
pH: 6.8-7.3
PCO2: 20-30
AG: H
(Na-[Cl+HCO3])

Elevated BUN and Crea = intravascular volume depletion

Leukocytosis
hypertriglyceridemia
hyperlipoproteinemia

In DKA, the amylase is usually of salivary origin and thus is not diagnostic of pancreatitis. Request for LIPASE.

A

DKA
components:
1. relative or absolute insulin deficiency
2. counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone)

decreased insulin:glucagon = gluconeogenesis
= glycogenolysis
= ketone body formation in the liver
= increase substrate delivery from fat and muscle (free fatty acids, amino acids) to the liver

Classic signs:

  • Kussmaul respirations
  • Fruity odor on the patient’s breath
71
Q 
Glucose: 33.3–66.6 (600–1200)
Na: 135–145
Crea: Mod. H
K/Mg/Cl/Phos: N
Osmolality: 330-380
Plasma Ketones: +/-
HCO3: N to Sl. L
pH: >7.3
PCO2: N
AG: N to Sl. H
(Na-[Cl+HCO3])
A

HHS

72
Q

Symptoms of DKA

A

Nausea/vomiting Thirst/polyuria
Abdominal pain
Shortness of breath

73
Q

Precipitating events for DKA

Reduced insulin + elevated catecholamines and growth hormone -> increase lipolysis -> release of FFA -> (normally converted to VLDL in the liver) but due to H glucagon -> ketone body synthesis in the liver

Inc FFA = Inc VLDL-trigly
VLDL clearance low because of decreased insulin-sensitive lipoprotein lipase in muscle and fat

A
  • Inadequate insulin administration
  • Infection (pneumonia/UTI/ gastroenteritis/sepsis)
  • Infarction (cerebral, coronary, mesenteric, peripheral)
  • Drugs (cocaine)
  • Pregnancy
74
Q

Physical Findings in DKA

A
  • Tachycardia
  • Tachypnea/Kussmaul respirations/respiratory distress
  • Dehydration/hypotension (volume depletion + peripheral vasodilatation)
  • Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen)
  • Lethargy/obtundation/cerebral edema (seen more common in children)/possibly coma
75
Q

This enzyme is crucial for regulating fatty acid transport into the mitochondria, where beta oxidation and conversion to ketone bodies occur.

At physiologic pH, ketoacids are neutralized by bicarbonate. As bicarbonate stores are depleted = metabolic acidosis

Increased lactic acid = acidosis

A

carnitine palmitoyltransferase I

76
Q

In DKA, the measured serum sodium is reduced as a consequence of the hyperglycemia

Normal Na in DKA indicates a more profound water deficit

Formula for Corrected Sodium?

A

1.6-mmol/L [1.6-meq] reduction in serum sodium

for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose)

77
Q

Formula for serum osmolality

In DKA, it is mildly to moderately elevated, although to a lesser degree than that found in HHS

A

2 × (Na + K) + Gl in mg/dL/18 + BUN/2.8

78
Q

Hydration in DKA

fluid deficit is often 3–5 L

A

first 1–3 h:
2–3 L of 0.9% saline
(10–20 mL/kg per hour)

hemodynamic stability and adequate urine output are achieved: 0.45% saline at 250–500 mL/h

plasma glucose reaches 250 mg/dL (13.9 mmol/L): 5% glucose and 0.45% saline at 150–250 mL/h

initial use of LR may reduce hyperchloremia

Measure CBG Q1–2 h 
Measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4h for first 24h
79
Q

Insulin in DKA

If the initial serum K is <3.3, do not administer insulin until K is corrected!!

A

short-acting regular insulin IV (0.1 units/kg)

then 0.1 units/kg/hr by continuous IV infusion,
increase 2-3 fold if no response by 2-4 h

80
Q

K replacement in DKA

A

K: <5.0–5.2
normal ECG, w/UO & crea
10 meq/h or 20–30meq/L

K: <3.5, bicarb given
40–80 meq/h

K: >5.2 mmol/L (5.2 meq/L), do not supplement K+ until the potassium is corrected ??

81
Q

IV regular insulin continued until..

A
  • Patient is stable
  • Glucose goal: 8.3–11.1 mmol/L (150–200 mg/dL), - Acidosis resolved

Insulin drip may be decreased to 0.02–0.1u/kg/hr

Administer long-acting insulin & SC short-acting insulin as soon as patient is eating

2–4hr overlap in insulin drip and SC long-acting insulin

PSBIM (2 decks)

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