DM-Complications Flashcards

1
Q

EuglycemicDKA must be considered in

A

Pregnancy

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2
Q

Precipitating factors

A

Infection (pneumonia / UTI / gastroenteritis / sepsis)
• Infarction (cerebral, coronary, mesenteric, peripheral)
• Pancreatitis
• Drugs (cocaine)
• Pregnancy ( EuglycemicDKA must be considered)
• Omission or inadequate insulin
• Mental health disorders

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3
Q

Pathophysiology of DKA

A

counterregulatory hormone excess (glucagon, catecholamines,cortisol, and growth hormone)

Gluconeogenesis+Glycogenolysis

Hyperglycaemia

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4
Q

Laboratory abnormalities in DKA

A

hyperglycemia (serum glucose > 250 mg/dL)
• Ketosis
• Metabolic acidosis (serum bicarbonate <15–18 mmol/L)

Arterial pH usually ranges between 6.8 and 7.3
• Serum potassium at presentation may be mildly elevated
• Total-body stores of potassium, sodium, chloride, phosphorus, and
magnesium are reduced in DKA
• Leukocytosis, Hypertriglyceridemia, Hyperamylasemia
• Ketone body: β-hydroxybutyrate, acetoacetate.

Administer long-acting insulin as soon as patient is eating. Allow for a 2- to 4-h
overlap in insulin infusion and SC long-acting insulin injection.

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5
Q

DKA treatment

A

Salin or ringer lactate

change to 5% glucose and 0.45% saline or lactated Ringer’s when blood
glucose reaches 250 mg/dL

Administer short-acting regular insulin,
• Then continuous IV infusion
• increase two- to three fold if no response by 2–4 h

If the initial serum potassium is <3.3 mmol/L (3.3 meq/L), do not administer
insulin

Subcutaneous insulin may be used in uncomplicated, mild-moderate DKA with close monitoring.

. Replace K+:

• If initial serum potassium is >5.2 mmol/L (5.2 meq/L), do not supplement K+

Despite a bicarbonate deficit, bicarbonate replacement is not usually necessary.
• just In the presence of severe acidosis (arterial pH <7.0);

Continue above until patient is stable, glucose goal (150–
200 mg/dL), and acidosis is resolved. Insulin infusion may be decreased.

Administer long-acting insulin as soon as patient is eating. Allow for a 2- to 4-h
overlap in insulin infusion and SC long-acting insulin injection

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6
Q

HHS=Hyperosmolar hyperglycaemia state

A

elderly individual with type 2 DM,
with a several-week history of polyuria, weight loss, and diminished oral intake that
culminates in mental confusion, lethargy, or coma.

A debilitating condition (prior stroke or dementia) or social situation
• Profound dehydration > hyperosmolality,
hypotension, tachycardia,
confusion,
Pathophysiology (Relative insulin deficiency and inadequate fluid intake).

The marked hyperglycemia (plasma glucose may be > 1000 mg/dL)
• Hyperosmolality (>350 mOsm/L),
The measured serum sodium may be normal or slightly low despite the marked hyperglycemia.
• In contrast to DKA, acidosis and ketonemia are absent or mild.

**HHS has a substantially higher mortality rate than DKA **

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7
Q

HHS Treatment

A

Fluid replacement should initially stabilize the hemodynamic status of the patient
(1–3 L of 0.9% normal saline over the first 2–3 h).

• The calculated free water deficit (which can be as great as 9–10 L) should be
reversed over the next 1–2 days (200–300 mL/h of hypotonic solution).

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8
Q

Management of hospitalized DM patients

A

The target range in the perioperative period should be 80–180 mg/dL.

either an insulin infusion or SC insulin.
1/Insulin infusions are preferred in the ICU or in a clinically unstable setting

2/In patients who are not critically ill or not in the ICU, basal or
“scheduled” insulin is provided by SC,

Insulin infusion is the preferred for managing type1 DM over a prolonged (several hours) perioperative period or whenserious concurrent illness is present (regular insulin).

• If the diagnostic or surgical procedure is brief (<4 h), a reduced dose of
SC insulin may suffice with short-acting bolus insulin

Individuals with type 2 DM can be managed with either an insulin
infusion or SC long-acting insulin (20–50% reduction) plus preprandial,
short-acting insulin.
• Oral glucose-lowering agents should be discontinued upon admission (or
up to a week prior to planned admission for SGLT2 inhibitors).
• Moreover, these oral agents may be dangerous if the patient is fasting
(e.g., hypoglycemia with sulfonylureas,
Euglycemic DKA with SGLT2 inhibitors)
or at risk for declining kidney function due to, for example,radiographic contrast media or unstable CHF
(lactic acidosis with metformin).

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9
Q

TPN
TEN

A

DM TPN or TEN greatly increases insulin requirements.
• In addition, individuals not previously known to have DM
may become hyperglycemic during TPN or TEN and require insulin
treatment.
• For TPN, IV insulin infusion is the preferred treatment for hyperglycemia.

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10
Q

steroid-induced diabetes.

A

If new-onset hyperglycemia remains during chronic treatment with
supraphysiologic doses of glucocorticoid (>5 mg of prednisone or
equivalent), the DM may be called “steroid-induced diabetes.”
Most pronounced in the postprandial period

If the FPG is near the normal range, oral diabetes agents (e.g., sulfonylureas, metformin)
may be sufficient to reduce hyperglycemia.
If the FPG is > 200 mg/dL oral agents are usually not efficacious, and insulin therapy is
required.

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11
Q

DIABETES MANAGEMENT IN OLDER ADULTS

A

In an individual with complex/poor health or cognitive impairment, an HbA1c goal of <8.0–8.5% would be reasonable.

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12
Q

Periproductive issues

A

Pregnancy is associated with marked insulin resistance; the increased
insulin requirements often precipitate DM and lead to the diagnosis of
gestational diabetes mellitus (GDM).

• Glucose, which at high levels is a teratogen to the developing fetus,
readily crosses the placenta, but insulin does not.

• Hyperglycemia from the maternal circulation may stimulate insulin
secretion in the fetus. The anabolic and growth effects of insulin may
result in macrosomia.
Screening for glucose intolerance: between weeks 24 and 28 of pregnancy in
women not known to have diabetes.
• Oral glucose-lowering agents are not approved for use during pregnancy.

• Individuals who develop GDM are at marked increased risk for developing type
2 DM in the future
• Children of women with GDM appear to be at risk for obesity and glucose
intolerance and have an increased risk of diabetes beginning in the later stages
of adolescence.
Intensive insulin therapy and near-normalization of the HbA1c (<6.5%)
are essential for individuals with existing DM who are planning pregnancy.

The most crucial period of glycemic control is soon after fertilization.

• Maintenance of the HbA1c <6.0–6.5% reduces the incidence and severity
of fetal macrosomia and neonatal hypoglycemia related to fetal
hyperinsulinism at delivery driven by elevated maternal glucose pre-delivery .

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13
Q

DM Complications

A

Diabetes-associated microvascular complications usually do not appear until the second decade of hyperglycemia.

• In contrast, diabetes-associated CHD risk, related in part to insulin resistance and its
resultant dyslipidemeia, may develop before hyperglycemia is established.

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14
Q

The microvascular (retinopathy, neuropathy, nephropathy )complications of both type 1 and type 2 DM

A

Result from chronic hyperglycemia.

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15
Q

…………..and …………..also play important roles in macrovascular complications.
(CHD, peripheral arterial disease [PAD], cerebrovascular disease).

A

dyslipidemia and hypertension

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16
Q

strict……………. control significantly reduced both macro- and microvascular complications

A

blood pressure

ADA recommends blood pressure control <130/80 mmHg for individuals with high
cardiovascular risk and <140/90 mmHg for individuals with lower cardiovascular risk.

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17
Q

despite long-standing DM, some individuals never develop retinopathy or nephropathy,

A

suggesting a genetic susceptibility for developing particular complications.

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18
Q

The reduction of cellular glucose entry in certain tissues such as myocardium and renal
tubular epithelium through inhibition of the……………..may contribute to the reduction in CHD events and renoprotective effects.

A

sodium glucose co-transporter-2 (SGLT-2)

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19
Q

…………..may play an important role in some diabetes-related microvascular
complications; For example,……………. is increased locally in diabetic proliferative retinopathy.

A

Growth factors

vascular endothelial growth factor A (VEGF-A)

20
Q

Diabetic retinopathy is classified into two stages:
Nonproliferative
• Proliferative

A

The appearance of neovascularization in response to retinal hypoxemia is the hallmark of proliferative diabetic retinopathy.

These newly formed vessels appear near the optic nerve and/or macula and rupture
easily, leading to vitreous hemorrhage, fibrosis, and ultimately retinal detachment.

• Clinically significant macular edema can occur in the context of nonproliferative or
proliferative
retinopathy.

21
Q

Paradoxically, during the first 6–12 months of improved glycemic control,……………
may transiently worsen.

A

retinopathy

22
Q

Individuals with known retinopathy may be candidates for………….. when initiating intensive therapy.

A

Prophylactic laser photocoagulation

23
Q

Treatment of severe nonproliferative or proliferative retinopathy or macular edema

A

Controling hyperglycemia and BP

Lowering elevated levels of triglycerides with fenofibrate may reduce the progression
of retinopathy.

With laser photocoagulation and/or anti-VEGF therapy (intravitreous injection)
usually is successful in preserving vision

24
Q

RENAL COMPLICATIONS OF DM

A

Individuals with diabetic nephropathy commonly have diabetic retinopathy.

The presence of CKD in individuals with DM and no retinopathy should prompt
investigation for alternative causes of kidney disease

25
Q

Renal complication with DM

A

The mechanisms by which chronic hyperglycemia leads to diabetic nephropathy,
involve the effects of soluble factors (growth factors, angiotensin II, endothelin,
AGEs), hemodynamic alterations in the renal microcirculation (glomerular
hyperfiltration or hyperperfusion, increased glomerular capillary pressure), and
structural changes in the glomerulus (increased extracellular matrix, basement
membrane thickening, mesangial expansion, fibrosis).
• Smoking accelerates the decline in renal function.

albuminuria as a persistently increased urinary albumin-to creatinine ratio >30 mg/g on a spot specimen.

Diabetic kidney disease refers to albuminuria and reduced GFR (<60 mL/min)
Once there is marked albuminuria and a reduction in GFR, the pathologic changes
are likely irreversible
.

26
Q

……………. may occur in type 1 or 2 DM. (hyperkalemia and acidemia)

A

Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism)

27
Q

Radiocontrast-induced nephrotoxicity.

A

Patients with DM are predisposed to .
Risk factors are preexisting nephropathy and volume depletion.
• Individuals with DM undergoing radiographic procedures with contrast dye should be:
• well hydrated before and after dye exposure, and
• the serum creatinine should be monitored for 24–48 h following the procedure.
Metformin should be held.

28
Q

Treatment of renal complications in DM

A

• (1) improved glycemic control,
• (2) strict blood pressure control,
• (3) administration of an ACE inhibitor or ARB

• If use of either ACE inhibitors or ARBs is not possible or the blood pressure is not
controlled, then diuretics, calcium channel blockers (nondihydropyridine class), or
beta blockers
may be used.
Mineralocorticoid receptor antagonists can help reduce blood pressure and
albuminuria in refractory cases but require monitoring of the serum potassium.

• (4) in individuals with type 2 DM, administration of a SGLT-2 inhibitor.
/SGLT1i can prescribed until eGFR declined to 20 in T2DM.

Because of the elevated risk of euglycemic diabetic ketoacidosis with SGLT-2
inhibitors, use in individuals with type 1 DM and insulin-deficient type 2 DM is not
recommended.
• Some glucagon-like peptide-1 (GLP-1) receptor agonists
Insulin is choice and only the permitted drug in advanced CKD.

• Dyslipidemia should also be treated.

29
Q

During the later phase of declining renal function, …………… requirements may fall as
the kidney is a site of its degradation.

• As the GFR decreases with progressive nephropathy, the use and dose of……….. should be reevaluated.

Some glucose-lowering medications …………………are contraindicated in advanced renal insufficiency, while others may require dose adjustment (glinides and DPP-4 inhibitors).

A

Insulin

glucose lowering agents

sulfonylureas and metformin

30
Q

GFR declined to 20

A

SGLT1i can’t be prescribed anymore

Referral for transplant evaluation should be made

31
Q

Why Autonomic neuropathy cause hypoglycemia unawareness

A

may reduce counterregulatory hormone release (especially epinephrine), leading to an inability to sense hypoglycemia appropriately

32
Q

diabetic amyotrophy

A

Involvement of the lumbar plexus or femoral nerve may cause severe
pain in the thigh or hip and may be associated with muscle weakness in
the hip flexors or extensors.

33
Q

Neuropathy Involving of the ………cranial nerve is most common.

A

Third

ptosis and ophthalmoplegia with normal pupillary constriction to light .

34
Q

Treatment of neuropathy in DM

A

Controlling glycemia +BP+ Triglycerides

Avoid neurotoxins (including alcohol) and smoking, and consider supplementation with vitamins for possible deficiencies (B12,folate)

Metformin may reduce intestinal absorption of vitamin B12 in type 2 DM, and pernicious anemia
is more common in type 1 DM

. duloxetine and pregabalin, or gabapentin is usually initially used for pain.

• Diabetic neuropathy may respond to tricyclic antidepressants, venlafaxine, carbamazepine, tramadol, or topical capsaicin products.

35
Q

may be one of the earliest signs of diabetic neuropathy

A

Erectile dysfunction and retrograde ejaculation

36
Q

glucose control had limited benefit on…………… outcomes in individuals
with established the disease, suggesting the importance of insulin
resistance and dyslipidemia.

A

cardiovascular

37
Q

………….plus optimal medical management likely has better outcomes than
PCI for individuals with diabetes.

A

CABG

38
Q

In patients with CHF,…………… should not be used.

A

thiazolidinediones

39
Q

Some newer glucose-lowering therapies also have cardiovascular benefit, including:

A

• the GLP-1 analogues
• the SGLT-2 inhibitor

40
Q

A possible increased risk of lower limb amputation and Fournier’s
gangrene has been reported with ……………therapy

A

SGLT-2 inhibitor

41
Q

DM itself does not increase levels of……….., but the small particles found in type 2 DM are more atherogenic.

A

LDL

42
Q

…………..use for treating dyslipidemia is associated with an even greater increased risk for type2 DM or worsening glycemic control and is not recommended because of a lack of
improvement in cardiovascular outcomes.

A

Niacin

43
Q

Treating dyslipidemia

A

If statin intolerant or the LDL cholesterol goal is not met, consider the
addition of Ezetimibe or a PCSK9 inhibitor.

Statin usage is associated with a mild increase in the risk of developing type 2 DM.

44
Q

Providers should consider screening for asymptomatic PAD in individuals >50 years of
age who have diabetes and other risk factors using …………testing.

A

ankle-brachial index

45
Q

Bacteriuria occurs frequently in individuals with diabetic cystopathy and does not require antibiotic therapy except in specific circumstances such as ………….and …………

A

pregnancy or a planned urologic procedure.